PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
17314111-2	2007	In the ESTEEM trial, the oral direct thrombin inhibitor ximelagatran reduced the risk of new ischaemic events when compared with placebo in aspirin treated post myocardial infarction patients.	Aspirin	140-147	coagulation factor II, thrombin	Homo sapiens	37-45
17488476-9	2007	Inhibition of Cox-2 by aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has been found to inhibit proliferation of colorectal cancer cells and in epidemiologic studies has been shown to reduce colon polyp formation in genetically predisposed populations and in the general population.	Aspirin	23-30	prostaglandin-endoperoxide synthase 2	Homo sapiens	14-19
17016059-2	2007	BACKGROUND: The anti-inflammatory actions of acetylsalicylic acid (ASA)/non-steroidal anti-inflammatory drugs (NSAIDs) are thought to be due to inhibition of COX-2, whereas the side effects such as gastric damage and aspirin-induced asthma are mediated through inhibition of COX-1.	Aspirin	45-65	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	158-163
17016059-2	2007	BACKGROUND: The anti-inflammatory actions of acetylsalicylic acid (ASA)/non-steroidal anti-inflammatory drugs (NSAIDs) are thought to be due to inhibition of COX-2, whereas the side effects such as gastric damage and aspirin-induced asthma are mediated through inhibition of COX-1.	Aspirin	67-70	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	158-163
17016059-3	2007	Therefore, a new class of drugs with COX-2 selectivity may be well tolerated by patients with ASA/NSAIDs hypersensitivity.	Aspirin	94-97	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	37-42
17319904-0	2007	Reticulated platelets and uninhibited COX-1 and COX-2 decrease the antiplatelet effects of aspirin.	Aspirin	91-98	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	48-53
17319904-2	2007	Immature (reticulated) platelets may modulate the antiplatelet effects of aspirin through uninhibited cyclooxygenase (COX)-1 and COX-2.	Aspirin	74-81	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	129-134
17319905-10	2007	The CRP levels were independently associated with platelet aggregation and aspirin non-responsiveness (P < 0.001, P < 0.001, respectively).	Aspirin	75-82	C-reactive protein	Homo sapiens	4-7
17319905-13	2007	CRP is an independent predictor of platelet aggregation and aspirin non-responsiveness in the setting of an acute coronary syndrome.	Aspirin	60-67	C-reactive protein	Homo sapiens	0-3
16916603-0	2007	Association between a TGFbeta1 promoter polymorphism and rhinosinusitis in aspirin-intolerant asthmatic patients.	Aspirin	75-82	transforming growth factor beta 1	Homo sapiens	22-30
16916603-5	2007	METHODS: A promoter polymorphism of the TGFbeta1 gene, TGFbeta1-509C>T, and a coding polymorphism (L10P), were genotyped in 203 patients with AIA, 324 patients with aspirin-tolerant asthma (ATA), and 456 normal controls (NC).	Aspirin	168-175	transforming growth factor beta 1	Homo sapiens	40-48
17340471-1	2007	Aspirin irreversibly inhibits platelet cyclooxygenase-1 (COX-1).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	39-55
17340471-1	2007	Aspirin irreversibly inhibits platelet cyclooxygenase-1 (COX-1).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	57-62
17340471-3	2007	Aspirin resistance has to be defined by its inability to inhibit COX-1.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	65-70
17329938-3	2007	The COX-2 pathway was activated by treating with serum-free medium for 12 h. The activated cells were incubated with NS398 (selective COX-2 inhibitor), SC560 (selective COX-1 inhibitor), acetyl salicylic acid (ASA) (nonselective COX inhibitor) at 37 degrees C for 15 min.	Aspirin	187-208	prostaglandin-endoperoxide synthase 2	Homo sapiens	4-9
17329938-3	2007	The COX-2 pathway was activated by treating with serum-free medium for 12 h. The activated cells were incubated with NS398 (selective COX-2 inhibitor), SC560 (selective COX-1 inhibitor), acetyl salicylic acid (ASA) (nonselective COX inhibitor) at 37 degrees C for 15 min.	Aspirin	210-213	prostaglandin-endoperoxide synthase 2	Homo sapiens	4-9
17329906-0	2007	Cytochrome P450 is responsible for nitric oxide generation from NO-aspirin and other organic nitrates.	Aspirin	67-74	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
17308107-4	2007	Here, we investigate the upstream molecular mechanisms responsible for nucleolar targeting of RelA and show that aspirin activates the p38 mitogen-activated protein kinase (MAPK) pathway in colorectal cancer cells.	Aspirin	113-120	mitogen-activated protein kinase 14	Homo sapiens	135-171
17308107-5	2007	We also show that aspirin causes rapid, ubiquitin-dependent degradation of cyclin D1, a known p38 target.	Aspirin	18-25	mitogen-activated protein kinase 14	Homo sapiens	94-97
17308107-6	2007	Aspirin-induced p38 activation preceded cyclin D1 degradation, which was then followed by activation of the NF-kappaB pathway, suggesting a causative link.	Aspirin	0-7	mitogen-activated protein kinase 14	Homo sapiens	16-19
17308107-6	2007	Aspirin-induced p38 activation preceded cyclin D1 degradation, which was then followed by activation of the NF-kappaB pathway, suggesting a causative link.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	108-117
17308107-7	2007	Indeed, chemical p38 inhibition (PD169316) and small interfering RNA directed against p38 blocked aspirin-induced cyclin D1 degradation, nucleolar translocation of RelA, and apoptosis.	Aspirin	98-105	mitogen-activated protein kinase 14	Homo sapiens	17-20
17308107-7	2007	Indeed, chemical p38 inhibition (PD169316) and small interfering RNA directed against p38 blocked aspirin-induced cyclin D1 degradation, nucleolar translocation of RelA, and apoptosis.	Aspirin	98-105	mitogen-activated protein kinase 14	Homo sapiens	86-89
17308107-10	2007	Collectively, these data suggest that aspirin causes inhibition of cyclin D1/CDK4 through the p38 MAPK pathway.	Aspirin	38-45	mitogen-activated protein kinase 14	Homo sapiens	94-97
17218028-10	2007	CONCLUSIONS: We concluded that the frequency of aspirin resistance confirmed in this cohort of patients with metabolic syndrome was higher in patients with a lower diastolic blood pressure, higher hs-CRP levels and atherosclerotic changes in their carotid arteries.	Aspirin	48-55	C-reactive protein	Homo sapiens	200-203
17239863-3	2007	Aspirin inhibited T-cell adhesion to AoSMC activated by interleukin 1beta (IL-1beta) in a dose-dependent manner.	Aspirin	0-7	interleukin 1 beta	Homo sapiens	56-73
17239863-3	2007	Aspirin inhibited T-cell adhesion to AoSMC activated by interleukin 1beta (IL-1beta) in a dose-dependent manner.	Aspirin	0-7	interleukin 1 beta	Homo sapiens	75-83
17239863-5	2007	ICAM-1 and VCAM-1 expression stimulated by IL-1beta was reduced by the treatment with aspirin, whereas the expression of E-selectin was unaffected.	Aspirin	86-93	vascular cell adhesion molecule 1	Homo sapiens	11-17
17239863-5	2007	ICAM-1 and VCAM-1 expression stimulated by IL-1beta was reduced by the treatment with aspirin, whereas the expression of E-selectin was unaffected.	Aspirin	86-93	interleukin 1 beta	Homo sapiens	43-51
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	83-90	nuclear factor kappa B subunit 1	Homo sapiens	15-21
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	83-90	nuclear factor kappa B subunit 1	Homo sapiens	23-32
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	83-90	vascular cell adhesion molecule 1	Homo sapiens	129-135
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	83-90	nuclear factor kappa B subunit 1	Homo sapiens	166-175
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	83-90	nuclear factor kappa B subunit 1	Homo sapiens	166-175
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	191-198	nuclear factor kappa B subunit 1	Homo sapiens	15-21
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	191-198	nuclear factor kappa B subunit 1	Homo sapiens	23-32
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	191-198	interleukin 1 beta	Homo sapiens	59-67
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	191-198	vascular cell adhesion molecule 1	Homo sapiens	129-135
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	191-198	nuclear factor kappa B subunit 1	Homo sapiens	166-175
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	191-198	interleukin 1 beta	Homo sapiens	242-250
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	191-198	nuclear factor kappa B subunit 1	Homo sapiens	166-175
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	191-198	vascular cell adhesion molecule 1	Homo sapiens	338-344
17242094-0	2007	Posttreatment with aspirin-triggered lipoxin A4 analog attenuates lipopolysaccharide-induced acute lung injury in mice: the role of heme oxygenase-1.	Aspirin	19-26	heme oxygenase 1	Mus musculus	132-148
17301265-2	2007	Aspirin also inhibits the cyclooxygenase-2 enzyme and may share with n-3 fatty acids a potential mechanism to decrease the risk of colorectal cancer.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	26-42
16914369-1	2007	BACKGROUND: By inhibiting prostaglandins, aspirin may be deleterious in heart failure (HF) and/or may counteract angiotensin-converting enzyme (ACE) inhibitor efficacy.	Aspirin	42-49	angiotensin I converting enzyme	Homo sapiens	113-142
16914369-1	2007	BACKGROUND: By inhibiting prostaglandins, aspirin may be deleterious in heart failure (HF) and/or may counteract angiotensin-converting enzyme (ACE) inhibitor efficacy.	Aspirin	42-49	angiotensin I converting enzyme	Homo sapiens	144-147
16914369-3	2007	AIM: To investigate the effect of aspirin and clopidogrel on brain natriuretic peptide (BNP) levels in HF patients treated with ACE inhibitors.	Aspirin	34-41	angiotensin I converting enzyme	Homo sapiens	128-131
16914369-9	2007	CONCLUSION: This study demonstrates an adverse effect of aspirin 325 mg/day on BNP plasma levels in HF patients treated with ACE inhibitors.	Aspirin	57-64	angiotensin I converting enzyme	Homo sapiens	125-128
17326708-1	2007	BACKGROUND: Somatic genetic CDKN2A, TP53, and DNA content abnormalities are common in many human cancers and their precursors, including esophageal adenocarcinoma (EA) and Barrett"s esophagus (BE), conditions for which aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) have been proposed as possible chemopreventive agents; however, little is known about the ability of a biomarker panel to predict progression to cancer nor how NSAID use may modulate progression.	Aspirin	219-226	cyclin dependent kinase inhibitor 2A	Homo sapiens	28-34
17258089-6	2007	RESULTS: Endotoxin induction of CXCL16 in human macrophages was attenuated by aspirin, nuclear factor (NF)-kappa-B inhibition and peroxisome proliferator-activated receptor (PPAR)-gamma agonists.	Aspirin	78-85	C-X-C motif chemokine ligand 16	Homo sapiens	32-38
17242290-0	2007	Letter by Kronish et al regarding article, "Residual arachidonic acid-induced platelet activation via an adenosine diphosphate-dependent but cyclooxygenase-1- and cyclooxygenase-2-independent pathway: a 700-patient study of aspirin resistance".	Aspirin	224-231	prostaglandin-endoperoxide synthase 1	Homo sapiens	141-157
17242290-0	2007	Letter by Kronish et al regarding article, "Residual arachidonic acid-induced platelet activation via an adenosine diphosphate-dependent but cyclooxygenase-1- and cyclooxygenase-2-independent pathway: a 700-patient study of aspirin resistance".	Aspirin	224-231	prostaglandin-endoperoxide synthase 2	Homo sapiens	163-179
16678922-7	2007	RESULTS: In both genders, we observed inverse associations between estimated VO2max and levels of CRP after controlling for age, race, body mass index category, hypertension, diabetes, smoking status, alcohol consumption, and use of medications including aspirin, non-steroidal anti-inflammatory drugs, steroid, lipid-lowering agents, antimicrobials, or estrogen/progesterone (in women).	Aspirin	255-262	C-reactive protein	Homo sapiens	98-101
19839181-9	2007	Statins reduce inflammation, modify the composition of atheromatous plaque and promote stabilisation, while acetylsalicylic acid reduces the formation of thrombin, exerts an anti-thrombotic action, reduces endothelial dysfunction and the proliferation of vascular smooth muscle cells, and, like statins, has an anti-inflammatory effect.	Aspirin	108-128	coagulation factor II, thrombin	Homo sapiens	154-162
17369708-6	2007	Interestingly also, IgE antibodies to enterotoxins can be found in the majority of aspirin-sensitive patients, in nasal polyps and severe asthma alike.	Aspirin	83-90	immunoglobulin heavy constant epsilon	Homo sapiens	20-23
17534042-6	2007	In contrast, CRS with NP patients are more likely to have male gender, anosmia/hyposmia, a history of prior sinus surgery, asthma and aspirin sensitivity, allergy to house dust mite, and AFRS.	Aspirin	134-141	twist family bHLH transcription factor 1	Homo sapiens	13-16
17429206-3	2007	The antiplatelet effect of cyclooxygenase-1 inhibitors lasts less than 4 h. Skin and colonic bleeding times are prolonged for 3 and 5 days after aspirin and ticlopidine withdrawal respectively.	Aspirin	145-152	prostaglandin-endoperoxide synthase 1	Homo sapiens	27-43
20306664-0	2007	Role of interleukin-1beta and nitric oxide in the antiinflammatory dynamics of acetylsalicylic acid in carrageenan-induced paw oedema model.	Aspirin	79-99	interleukin 1 beta	Mus musculus	8-25
20306664-7	2007	Pre-treatment with ASA resulted in increase in plasma IL-1beta level, decrease in IL-1beta level at the inflammation site and restoring plasma nitrite concentration to its normal range.	Aspirin	19-22	interleukin 1 beta	Mus musculus	54-62
20306664-7	2007	Pre-treatment with ASA resulted in increase in plasma IL-1beta level, decrease in IL-1beta level at the inflammation site and restoring plasma nitrite concentration to its normal range.	Aspirin	19-22	interleukin 1 beta	Mus musculus	82-90
17211028-2	2007	Taken in combination, aspirin, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins (combination pharmacotherapy) greatly reduce cardiac events.	Aspirin	22-29	angiotensin I converting enzyme	Homo sapiens	77-80
18024618-6	2007	True "aspirin resistance" implies that cyclooxygenase-1 is less sensitive to inactivation by aspirin.	Aspirin	6-13	prostaglandin-endoperoxide synthase 1	Homo sapiens	39-55
18024618-6	2007	True "aspirin resistance" implies that cyclooxygenase-1 is less sensitive to inactivation by aspirin.	Aspirin	93-100	prostaglandin-endoperoxide synthase 1	Homo sapiens	39-55
16473396-0	2007	Acetylsalicylic acid is compounding to antiplatelet effect of C-reactive protein.	Aspirin	0-20	C-reactive protein	Homo sapiens	62-80
16473396-2	2007	In our study, we examined the in vitro effect of C-reactive protein (CRP) on the ASA-mediated inhibition of collagen-stimulated platelet reactivity.	Aspirin	81-84	C-reactive protein	Homo sapiens	49-67
16473396-2	2007	In our study, we examined the in vitro effect of C-reactive protein (CRP) on the ASA-mediated inhibition of collagen-stimulated platelet reactivity.	Aspirin	81-84	C-reactive protein	Homo sapiens	69-72
16473396-3	2007	Influence of CRP on platelet responsiveness to ASA was analysed using classical turbidimetric aggregation and flow cytometry.	Aspirin	47-50	C-reactive protein	Homo sapiens	13-16
16473396-6	2007	In general, our findings showed for the first time the augmenting effect of native C-reactive protein in the antiplatelet action of acetylsalicylic acid.	Aspirin	132-152	C-reactive protein	Homo sapiens	83-101
16473396-7	2007	Thus, we conclude that the effectiveness of aspirin therapy may strongly depend upon the presence of native CRP in circulation.	Aspirin	44-51	C-reactive protein	Homo sapiens	108-111
16581111-0	2007	Genetic polymorphisms of the platelet receptors P2Y(12), P2Y(1) and GP IIIa and response to aspirin and clopidogrel.	Aspirin	92-99	integrin subunit beta 3	Homo sapiens	68-75
16675000-5	2007	RESULTS: Aspirin-depressed thrombin generation in A1 homozygotes (p=0.04), but not in A2 carriers.	Aspirin	9-16	coagulation factor II, thrombin	Homo sapiens	27-35
16780932-0	2007	Aspirin failure course during exercise and its connection with soluble CD40L.	Aspirin	0-7	CD40 ligand	Homo sapiens	71-76
16793119-0	2007	Increased basal platelet activity, plasma adiponectin levels, and diabetes mellitus are associated with poor platelet responsiveness to in vitro effect of aspirin.	Aspirin	155-162	adiponectin, C1Q and collagen domain containing	Homo sapiens	42-53
17200775-4	2007	In this study, we have examined whether an aspirin-triggered lipoxin A (4) analog (ATL-1) modulates ROS generation in endothelial cells (EC).	Aspirin	43-50	atlastin GTPase 1	Homo sapiens	83-88
17241655-2	2007	Possible causes of aspirin resistance include poor compliance, drug interaction, inadequate aspirin dose, increase turnover of platelets, genetic polymorphisms of cyclo-oxygenase-1, and upregulation of alternate (non-platelet) pathways of thromboxane production.	Aspirin	19-26	prostaglandin-endoperoxide synthase 1	Homo sapiens	163-180
17331566-11	2007	CONCLUSIONS: Although the potential mechanisms of aspirin resistance still remains uncertain, we found that platelet responsiveness to aspirin is reduced in patients with high levels of Apolipoprotein B and lipoprotein(a).	Aspirin	135-142	apolipoprotein B	Homo sapiens	186-202
17917621-3	2007	UFH was combined with aspirin to suppress thrombin propagation and fibrin formation in patients presenting with acute coronary syndromes (ACS) or patients undergoing percutaneous coronary intervention (PCI).	Aspirin	22-29	coagulation factor II, thrombin	Homo sapiens	42-50
17087777-8	2006	Compared with the placebo, IgA, IgG subtypes and CRP levels were reduced after aspirin treatment (P = 0.001, P = 0.02, P = 0.04, respectively).	Aspirin	79-86	C-reactive protein	Homo sapiens	49-52
17532367-9	2007	RESULTS AND CONCLUSIONS: Aggrastat, AN51, and aspirin all suppressed thrombin formation.	Aspirin	46-53	coagulation factor II, thrombin	Homo sapiens	69-77
20020969-11	2007	Both the aspirin- and celecoxib-treated DMH groups showed a marked lowering of the lipid peroxide level along with a significant enhancement of CAT activity when compared with the DMH-treated group.	Aspirin	9-16	catalase	Rattus norvegicus	144-147
16785990-5	2006	The recombinant protein, AHNP-SA (ASA) bound to p185(her2/neu) with high affinity, inhibited the proliferation of p185(her2/neu)-overexpressing cells, and reduced tumor growth induced by p185(her2/neu)-transformed cells.	Aspirin	34-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	53-61
16785990-5	2006	The recombinant protein, AHNP-SA (ASA) bound to p185(her2/neu) with high affinity, inhibited the proliferation of p185(her2/neu)-overexpressing cells, and reduced tumor growth induced by p185(her2/neu)-transformed cells.	Aspirin	34-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	119-127
16785990-5	2006	The recombinant protein, AHNP-SA (ASA) bound to p185(her2/neu) with high affinity, inhibited the proliferation of p185(her2/neu)-overexpressing cells, and reduced tumor growth induced by p185(her2/neu)-transformed cells.	Aspirin	34-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	119-127
17087777-9	2006	The percentage reduction of IgA- and IgG-aCL was related to the percentage reduction of CRP after aspirin (P < 0.05).	Aspirin	98-105	C-reactive protein	Homo sapiens	88-91
17136297-9	2006	Selective COX 2 inhibitors can be prescribed in some cases of allergy to aspirin, but they must be used with care.	Aspirin	73-80	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	10-15
17139447-1	2006	Aspirin and other cyclooxygenase inhibitors can increase levels of tumor necrosis factor-alpha and engage pro-apoptosis paths and/or anti-apoptosis paths.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	67-94
16943252-8	2006	Consistent with the tissue distribution of two carboxylesterases human carboxylesterase (HCE) 1 and HCE2, recombinant HCE1 hydrolyzed clopidogrel, whereas recombinant HCE2 hydrolyzed aspirin.	Aspirin	183-190	carboxylesterase 2	Homo sapiens	100-104
16943252-8	2006	Consistent with the tissue distribution of two carboxylesterases human carboxylesterase (HCE) 1 and HCE2, recombinant HCE1 hydrolyzed clopidogrel, whereas recombinant HCE2 hydrolyzed aspirin.	Aspirin	183-190	carboxylesterase 2	Homo sapiens	167-171
16943252-9	2006	In addition, hydrolysis of clopidogrel among liver samples was correlated well with the level of HCE1, and hydrolysis of aspirin with HCE2.	Aspirin	121-128	carboxylesterase 2	Homo sapiens	134-138
17168813-6	2006	It is very well known that pain and inflammation are alleviated through the inhibition of COX-2 inhibitors such as Aspirin, which has resulted in the recent years, in the emergence of a range of COX-2 inhibitors.	Aspirin	115-122	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	90-95
17168813-6	2006	It is very well known that pain and inflammation are alleviated through the inhibition of COX-2 inhibitors such as Aspirin, which has resulted in the recent years, in the emergence of a range of COX-2 inhibitors.	Aspirin	115-122	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	195-200
17218764-9	2006	Furthermore, in comparison to plain ASA, ASA-VitC caused stronger inhibition of cNOS and increase in iNOS expression in the gastric mucosa.	Aspirin	41-44	nitric oxide synthase 2	Homo sapiens	101-105
17218764-13	2006	We conclude that ASA-VitC in comparison with ASA induces less gastric mucosal damage and this protective effect may be due to its inhibitory effect on iNOS expression.	Aspirin	17-20	nitric oxide synthase 2	Homo sapiens	151-155
17080224-7	2006	In the aspirin group we found significantly lower levels of TNFa and MCP-1 after one year; 1.00 versus 1.16 pg/ml (p < 0.001) and 245 versus 261 pg/ml (p < 0.001), respectively.	Aspirin	7-14	tumor necrosis factor	Homo sapiens	60-64
17642204-0	2007	[The thrombin generation is associated with the PIA1/A2 beta3, integrin polymorphism in aspirin-treated patients with coronary artery disease: a role of statins].	Aspirin	88-95	coagulation factor II, thrombin	Homo sapiens	5-13
17642204-14	2007	CONCLUSIONS: In a model of microvascular injury the PIA1/A2 polymorphism influenced thrombin formation but not platelet activation in CAD patients treated with low-dose aspirin.	Aspirin	169-176	coagulation factor II, thrombin	Homo sapiens	84-92
16815474-2	2006	The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST).	Aspirin	71-74	glutathione peroxidase 1	Rattus norvegicus	176-181
16815474-2	2006	The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST).	Aspirin	71-74	catalase	Rattus norvegicus	184-192
16815474-7	2006	The long-term ASA administration partially reversed the decrease in GSHPx activity, but did not influence the activities of catalase and GST in diabetic rats.	Aspirin	14-17	glutathione peroxidase 1	Rattus norvegicus	68-73
17209500-0	2006	[Aspirin for primary prevention of cardiovascular diseases in diabetic patients: focus on gender difference and insulin resistance].	Aspirin	1-8	insulin	Homo sapiens	112-119
17008981-2	2006	Aspirin irreversibly inhibits the cyclooxygenase-1 (COX-1) enzyme, whereas non-steroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit the COX-1 enzyme.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	34-50
17008981-2	2006	Aspirin irreversibly inhibits the cyclooxygenase-1 (COX-1) enzyme, whereas non-steroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit the COX-1 enzyme.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	52-57
16880202-5	2006	Aspirin exposure also resulted in an increase in the half-life of pd1EGFP, a model substrate of proteasome, as well as various intracellular substrates like Bax, IkappaB-alpha, p53, and p27(kip1).	Aspirin	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	162-175
17016788-2	2006	DISCUSSION: Hyphemas can occur after blunt trauma, intraocular surgery, spontaneously and in association with the use of substances that alter platelet or thrombin function (aspirin, ethanol).	Aspirin	174-181	coagulation factor II, thrombin	Homo sapiens	155-163
16952320-4	2006	Aspirin is an inhibitor of COX-2 and has been implicated, with other non-steroidal anti-inflammatory drugs (NSAIDS) in prevention and treatment of breast cancer.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	27-32
16880431-5	2006	Of the compounds that are known to be NF-kappaB antagonists, the most practical for current use may be the nonsteroidal anti-inflammatory drugs aspirin, salicylic acid, and sulindac, each of which binds to and inhibits Ikappa kinase- beta, a central mediator of NF-kappa activation; the low millimolar plasma concentrations of salicylate required for effective inhibition of this kinase in vivo can be achieved with high-dose regimens traditionally used to manage rheumatic disorders.	Aspirin	144-151	nuclear factor kappa B subunit 1	Homo sapiens	38-47
16942942-1	2006	BACKGROUND: Although aspirin is useful in reducing platelet activation and cardiovascular events, its effects on platelet levels of angiogenic factors, such as vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang-1), and markers of platelet activation in hypertension are unknown.	Aspirin	21-28	vascular endothelial growth factor A	Homo sapiens	160-194
16942942-7	2006	After treatment with aspirin for 3 months, there were significant reductions in plasma VEGF (P=.01), pAng-1 (P=.04), sPsel (P=.001), and pPsel (P<.001) levels, but not levels of platelet VEGF and plasma Ang-1.	Aspirin	21-28	vascular endothelial growth factor A	Homo sapiens	87-91
16942942-7	2006	After treatment with aspirin for 3 months, there were significant reductions in plasma VEGF (P=.01), pAng-1 (P=.04), sPsel (P=.001), and pPsel (P<.001) levels, but not levels of platelet VEGF and plasma Ang-1.	Aspirin	21-28	vascular endothelial growth factor A	Homo sapiens	190-194
16865277-0	2006	Acetylsalicylic acid enhances antiproliferative effects of the EGFR inhibitor gefitinib in the absence of activating mutations in gastric cancer.	Aspirin	0-20	epidermal growth factor receptor	Homo sapiens	63-67
16869801-4	2006	Aspirin-treated DCs are partially resistant to phenotypic changes following maturational stimuli, such as lipopolysaccharide (LPS) or TNFalpha, IL-1alpha and PGE2.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	134-142
17699316-9	2006	Serum IL-8 and TNF-alpha concentrations were significantly reduced by aspirin treatment at 4 mo (P = 0.04 and P = 0.007, respectively).	Aspirin	70-77	C-X-C motif chemokine ligand 8	Homo sapiens	6-10
17699316-9	2006	Serum IL-8 and TNF-alpha concentrations were significantly reduced by aspirin treatment at 4 mo (P = 0.04 and P = 0.007, respectively).	Aspirin	70-77	tumor necrosis factor	Homo sapiens	15-24
17699316-10	2006	Serum IL-6 concentration decreased with aspirin treatment but not significantly (P = 0.1).	Aspirin	40-47	interleukin 6	Homo sapiens	6-10
17699316-13	2006	In HD patients, IL-6, IL-8, and TNF-alpha remained suppressed 1 mo after discontinuation of aspirin.	Aspirin	92-99	tumor necrosis factor	Homo sapiens	32-41
16865277-8	2006	Our findings indicate that although gastric cancer does not seem to harbour mutations which render the cancer cells constitutively susceptible to gefitinib, the co-administration of ASA can strengthen RTK inhibitor activity in adenocarcinoma cells by EGFR activation.	Aspirin	182-185	epidermal growth factor receptor	Homo sapiens	251-255
16977569-2	2006	These are all reversible by inhibition of platelet cyclooxygenase 1 with aspirin, and are therefore indicative of platelet activation and platelet-mediated thrombotic processes.	Aspirin	73-80	prostaglandin-endoperoxide synthase 1	Homo sapiens	51-67
16961610-0	2006	Recombinant factor VIIa reverses the inhibitory effect of aspirin or aspirin plus clopidogrel on in vitro thrombin generation.	Aspirin	58-65	coagulation factor II, thrombin	Homo sapiens	106-114
16961610-0	2006	Recombinant factor VIIa reverses the inhibitory effect of aspirin or aspirin plus clopidogrel on in vitro thrombin generation.	Aspirin	69-76	coagulation factor II, thrombin	Homo sapiens	106-114
16961610-3	2006	This study investigated: (a) whether a regimen of aspirin or clopidogrel plus aspirin significantly inhibited platelet thrombin generation (TG); and (b) the reversal of this inhibition by recombinant activated factor VII (rFVIIa).	Aspirin	50-57	coagulation factor II, thrombin	Homo sapiens	119-127
16961610-3	2006	This study investigated: (a) whether a regimen of aspirin or clopidogrel plus aspirin significantly inhibited platelet thrombin generation (TG); and (b) the reversal of this inhibition by recombinant activated factor VII (rFVIIa).	Aspirin	78-85	coagulation factor II, thrombin	Homo sapiens	119-127
16825866-8	2006	SUMMARY: The HLA alleles DRB11302 and DQB10609, and the ALOX5 and FcepsilonRIalpha promoter polymorphisms, may contribute to the pathogenesis of aspirin-induced urticaria/angioedema.	Aspirin	145-152	arachidonate 5-lipoxygenase	Homo sapiens	56-61
17037745-4	2006	RESULTS: RT-PCR showed that the expression COX-2 mRNA was strongly down-regulated in SKOV3 cells after treatment with Celecoxib or Aspirin.	Aspirin	131-138	prostaglandin-endoperoxide synthase 2	Homo sapiens	43-48
17037745-5	2006	FCM and Western blot analysis showed that the protein product of COX-2 was strongly decreased by Celecoxib or Aspirin.	Aspirin	110-117	prostaglandin-endoperoxide synthase 2	Homo sapiens	65-70
16951898-5	2006	Epi-lipoxins (epi-LXs), for instance, are produced from aspirin"s acetylation of inducible cyclooxygenase 2 (COX-2) and together with Resolvins represent an increasingly important family of immuno-regulatory and potentially cardio-protective lipid mediators.	Aspirin	56-63	prostaglandin-endoperoxide synthase 2	Homo sapiens	91-107
16951898-5	2006	Epi-lipoxins (epi-LXs), for instance, are produced from aspirin"s acetylation of inducible cyclooxygenase 2 (COX-2) and together with Resolvins represent an increasingly important family of immuno-regulatory and potentially cardio-protective lipid mediators.	Aspirin	56-63	prostaglandin-endoperoxide synthase 2	Homo sapiens	109-114
16822499-0	2006	Aspirin induces the production of the inflammatory mediator 8-epi-PGF in mast cells.	Aspirin	0-7	placental growth factor	Homo sapiens	66-69
16822499-5	2006	Moreover, we show that exposure of mast cells to aspirin directly induces the production of 8-epi-PGF.	Aspirin	49-56	placental growth factor	Homo sapiens	98-101
16822499-6	2006	Our study suggests that production of 8-epi-PGF by mast cells could contribute to the inflammatory response in e.g. aspirin-sensitive asthma patients.	Aspirin	116-123	placental growth factor	Homo sapiens	44-47
16937749-2	2006	OBJECTIVE: To classify patients with a history of aspirin-induced urticaria as cross-reactors or single-drug reactors by oral challenges with another strong COX-1 inhibitor, namely, ketoprofen.	Aspirin	50-57	prostaglandin-endoperoxide synthase 1	Homo sapiens	157-162
16859832-5	2006	COX-1 and COX-2 inhibition by traditional NSAIDs (for example, aspirin) although chemopreventive have some side effects due to the role of COX-1 in maintaining the integrity of the gastric mucosa.	Aspirin	63-70	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	10-15
16890573-0	2006	Heterogeneity in the suppression of platelet cyclooxygenase-1 activity by aspirin in coronary heart disease.	Aspirin	74-81	prostaglandin-endoperoxide synthase 1	Homo sapiens	45-61
16816107-6	2006	In in vivo studies low-dose aspirin treatment (6 mg/kg.day) induced SR-BI expression in wild-type and PPAR-alpha knockout mice, respectively, whereas the opposite effect was observed upon high-dose aspirin treatment (60 mg/kg.day) in these animals.	Aspirin	28-35	peroxisome proliferator activated receptor alpha	Mus musculus	102-112
16911911-1	2006	BACKGROUND: Aspirin has been associated with adverse heart failure outcomes, probably because of a blunting interaction with angiotensin-converting enzyme (ACE) inhibitors.	Aspirin	12-19	angiotensin I converting enzyme	Homo sapiens	125-154
16911911-1	2006	BACKGROUND: Aspirin has been associated with adverse heart failure outcomes, probably because of a blunting interaction with angiotensin-converting enzyme (ACE) inhibitors.	Aspirin	12-19	angiotensin I converting enzyme	Homo sapiens	156-159
16960142-3	2006	Epilipoxins, for instance, are produced from aspirin"s acetylation of COX-2 and together with Resolvins and COX-2-derived prostaglandins of the D(2) and J(2) series represent an increasingly important family of immunoregulatory lipid mediators with strong implications for disease control and drug discovery.	Aspirin	45-52	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	70-75
16887052-6	2006	Compared with ALI group, the level of NF-KappaB activity and the expression of ICAM-1 and P-selectin were obviously down regulated, and also the pathological lesion and inflammatory response of lung were improved in LMWH and ASA groups.	Aspirin	225-228	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	38-47
16887052-6	2006	Compared with ALI group, the level of NF-KappaB activity and the expression of ICAM-1 and P-selectin were obviously down regulated, and also the pathological lesion and inflammatory response of lung were improved in LMWH and ASA groups.	Aspirin	225-228	selectin P	Rattus norvegicus	90-100
16887052-13	2006	ASA plays the role as an inhibitor of NF-KappaB activation.	Aspirin	0-3	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	38-47
16797507-3	2006	A significant increase in vascular permeability, NOS-2 activity, TNF-alpha, IL-1beta levels and oxidative damage were noted in aspirin administered rats.	Aspirin	127-134	nitric oxide synthase 2	Rattus norvegicus	49-54
16797507-3	2006	A significant increase in vascular permeability, NOS-2 activity, TNF-alpha, IL-1beta levels and oxidative damage were noted in aspirin administered rats.	Aspirin	127-134	tumor necrosis factor	Rattus norvegicus	65-74
16797507-3	2006	A significant increase in vascular permeability, NOS-2 activity, TNF-alpha, IL-1beta levels and oxidative damage were noted in aspirin administered rats.	Aspirin	127-134	interleukin 1 beta	Rattus norvegicus	76-84
16583357-1	2006	In aspirin-intolerant subjects, adverse bronchial and nasal reactions to cyclooxygenase (COX) inhibitors are associated with over-production of cysteinyl-leukotrienes (cys-LTs) generated by the 5-lipoxygenase (5-LO) pathway.	Aspirin	3-10	arachidonate 5-lipoxygenase	Homo sapiens	194-208
16794482-7	2006	At baseline and in individuals who were on one or more antihypertensive medication, regular aspirin use was found to be associated with retinal arterioles on average 3.6 mum (95% confidence interval 1.0, 6.2) wider than those of non-users or occasional aspirin users, after adjusting for age, blood pressure, smoking, diabetes, non-steroidal anti-inflammatory drug use and other variables.	Aspirin	92-99	latexin	Homo sapiens	170-173
16735672-5	2006	On the other hand, users of ACE inhibitors were less likely to die or require HF readmission (HR, 0.87 [0.79 to 0.96]), even if they were using aspirin (HR, 0.86 [0.77 to 0.95]).	Aspirin	144-151	angiotensin I converting enzyme	Homo sapiens	28-31
16862528-6	2006	However, because it is a global test system, and also sensitive to low hematocrit, low platelet counts, and platelet dysfunction (both congenital and acquired; e.g., secondary to medication such as aspirin) it must be recognized that the PFA-100 is neither specific for, nor predictive of, any particular disorder (inclusive of vWD).	Aspirin	198-205	von Willebrand factor	Homo sapiens	328-331
16785341-9	2006	CONCLUSIONS: There is a residual arachidonic acid-induced platelet activation in aspirin-treated patients that (1) is caused by underdosing and/or noncompliance in only approximately 2% of patients and (2) in the remaining patients, occurs via a cyclooxygenase-1 and cyclooxygenase-2 independent pathway, in direct proportion to the degree of baseline platelet activation, and is mediated in part by adenosine diphosphate-induced platelet activation.	Aspirin	81-88	prostaglandin-endoperoxide synthase 1	Homo sapiens	246-262
16785341-9	2006	CONCLUSIONS: There is a residual arachidonic acid-induced platelet activation in aspirin-treated patients that (1) is caused by underdosing and/or noncompliance in only approximately 2% of patients and (2) in the remaining patients, occurs via a cyclooxygenase-1 and cyclooxygenase-2 independent pathway, in direct proportion to the degree of baseline platelet activation, and is mediated in part by adenosine diphosphate-induced platelet activation.	Aspirin	81-88	prostaglandin-endoperoxide synthase 2	Homo sapiens	267-283
16545519-10	2006	Nitric oxide production after 180 min reoxygenation was significantly reduced in aspirin (36.4%), alpha-tocopherol (22.7%) and aspirin-alpha-tocopherol (77.8%) treated rats with respect to diabetic non-treated animals; this was related mainly with a reduction in iNOS activity.	Aspirin	81-88	nitric oxide synthase 2	Rattus norvegicus	263-267
16545519-10	2006	Nitric oxide production after 180 min reoxygenation was significantly reduced in aspirin (36.4%), alpha-tocopherol (22.7%) and aspirin-alpha-tocopherol (77.8%) treated rats with respect to diabetic non-treated animals; this was related mainly with a reduction in iNOS activity.	Aspirin	127-134	nitric oxide synthase 2	Rattus norvegicus	263-267
16600694-6	2006	Together, the findings indicate that in endothelial cells aspirin and PPAR-alpha activators reduce the high glucose-increased expression of MCP-1 by a mechanism that includes the inhibition of reactive oxygen species, and decrease of AP-1 and NF-kB activation.	Aspirin	58-65	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	234-238
16585129-5	2006	RESULTS: Having an angina only diagnosis significantly decreased the likelihood of patients being prescribed aspirin (OR = 0.53; 95% CI = 0.40-0.69), lipid-lowering medication (OR = 0.55; 95% CI = 0.43-0.69) or ACE inhibitors (OR = 0.62; 95% CI = 0.48-0.81).	Aspirin	109-116	angiotensin I converting enzyme	Homo sapiens	211-214
16706971-3	2006	RESULTS: Subjects taking 81 mg of aspirin (n = 50) and controls (n = 38) were evaluated for platelet aggregation and platelet cyclooxygenase-1 (COX-1) activity by measuring collagen-induced thromboxane B2 production.	Aspirin	34-41	prostaglandin-endoperoxide synthase 1	Homo sapiens	144-149
16706971-10	2006	CONCLUSIONS: Aspirin resistance expressed as unsuppressed platelet COX-1 activity is a rare condition in an out-patient population.	Aspirin	13-20	prostaglandin-endoperoxide synthase 1	Homo sapiens	67-72
16792175-9	2006	In aspirin-sensitive polyps the number of eosinophils was significantly higher than in the other patient groups and they had significantly higher eotaxin, eotaxin-2, and -3 protein levels than non-allergic and significantly higher amounts of eotaxin-3 compared with allergic patients.	Aspirin	3-10	C-C motif chemokine ligand 11	Homo sapiens	146-153
16419075-0	2006	Competition of cytarabine and aspirin in binding to serum albumin in multidrug therapy.	Aspirin	30-37	albumin	Homo sapiens	52-65
16675319-4	2006	In addition, NSAIDs, particularly ibuprofen, may interfere with the antithrombotic benefits of aspirin through competitive interaction with platelet cyclooxygenase-1 (COX-1).	Aspirin	95-102	prostaglandin-endoperoxide synthase 1	Homo sapiens	149-165
16675319-4	2006	In addition, NSAIDs, particularly ibuprofen, may interfere with the antithrombotic benefits of aspirin through competitive interaction with platelet cyclooxygenase-1 (COX-1).	Aspirin	95-102	prostaglandin-endoperoxide synthase 1	Homo sapiens	167-172
16635110-9	2006	In coronary artery disease patients, the acetylsalicylic acid-mediated platelet inhibition positively correlated with increased triglycerides (in arachidonic acid-stimulated platelets, r=0.30, P=0.0018), total cholesterol (r=0.33, P<0.0001 in coll and arachidonic acid-activated platelets) and elevated serum C-reactive protein (CRP) (r=0.27, P=0.0024).	Aspirin	41-61	C-reactive protein	Homo sapiens	312-330
16635110-9	2006	In coronary artery disease patients, the acetylsalicylic acid-mediated platelet inhibition positively correlated with increased triglycerides (in arachidonic acid-stimulated platelets, r=0.30, P=0.0018), total cholesterol (r=0.33, P<0.0001 in coll and arachidonic acid-activated platelets) and elevated serum C-reactive protein (CRP) (r=0.27, P=0.0024).	Aspirin	41-61	C-reactive protein	Homo sapiens	332-335
16792983-7	2006	COX-2 inhibitors, collectively called "coxibs" (celecoxib, rofecoxib, valdecoxib, lumiracoxib, etc), held a promise as anti-inflammatory drugs without the some of the side effects of aspirin or non steroidal antiinflammatory agents.	Aspirin	183-190	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
16614756-5	2006	These responses were attenuated by COX-1 knock down, which mimics the beneficial effects of low-dose aspirin.	Aspirin	101-108	cytochrome c oxidase I, mitochondrial	Mus musculus	35-40
16799884-7	2006	Moreover, coadministration of MEL and ASA increased antioxidant enzyme activities after the BDL, and these increases were statistically significant for CAT and GPx.	Aspirin	38-41	catalase	Rattus norvegicus	152-155
16529823-0	2006	Ascorbic acid enhances the inhibitory effect of aspirin on neuronal cyclooxygenase-2-mediated prostaglandin E2 production.	Aspirin	48-55	prostaglandin-endoperoxide synthase 2	Homo sapiens	68-84
16529823-9	2006	Further, these experiments suggest that a combination of aspirin with ascorbic acid constitutes a novel approach to render COX-2 more sensitive to inhibition by aspirin, allowing an anti-inflammatory therapy with lower doses of aspirin, thereby avoiding the side effects of the usually high dose aspirin treatment.	Aspirin	57-64	prostaglandin-endoperoxide synthase 2	Homo sapiens	123-128
16529823-9	2006	Further, these experiments suggest that a combination of aspirin with ascorbic acid constitutes a novel approach to render COX-2 more sensitive to inhibition by aspirin, allowing an anti-inflammatory therapy with lower doses of aspirin, thereby avoiding the side effects of the usually high dose aspirin treatment.	Aspirin	161-168	prostaglandin-endoperoxide synthase 2	Homo sapiens	123-128
16529823-9	2006	Further, these experiments suggest that a combination of aspirin with ascorbic acid constitutes a novel approach to render COX-2 more sensitive to inhibition by aspirin, allowing an anti-inflammatory therapy with lower doses of aspirin, thereby avoiding the side effects of the usually high dose aspirin treatment.	Aspirin	161-168	prostaglandin-endoperoxide synthase 2	Homo sapiens	123-128
16529823-9	2006	Further, these experiments suggest that a combination of aspirin with ascorbic acid constitutes a novel approach to render COX-2 more sensitive to inhibition by aspirin, allowing an anti-inflammatory therapy with lower doses of aspirin, thereby avoiding the side effects of the usually high dose aspirin treatment.	Aspirin	161-168	prostaglandin-endoperoxide synthase 2	Homo sapiens	123-128
16731765-0	2006	Aspirin reduces the outcome of anticancer therapy in Meth A-bearing mice through activation of AKT-glycogen synthase kinase signaling.	Aspirin	0-7	thymoma viral proto-oncogene 1	Mus musculus	95-98
16731765-4	2006	In this work, we tested the ability of aspirin to activate the AKT survival pathway in methylcholanthrene-induced fibrosarcoma cells (Meth A) transplanted into BALB/c nude mice and the clinical effect of aspirin cotreatment during etoposide (VP-16)-based anticancer therapy.	Aspirin	39-46	thymoma viral proto-oncogene 1	Mus musculus	63-66
16731765-5	2006	We found that cotreatment with aspirin reduced VP-16-induced apoptosis and activated AKT in vitro and in vivo.	Aspirin	31-38	thymoma viral proto-oncogene 1	Mus musculus	85-88
16731765-7	2006	Our data suggest that the antiapoptotic effect of aspirin operates in vivo through the activation of AKT-glycogen synthase kinase pathway causing a decrease in the outcome of VP-16-based therapy.	Aspirin	50-57	thymoma viral proto-oncogene 1	Mus musculus	101-104
16419075-1	2006	The aim of this study was to describe a competition between cytarabine (araC) and aspirin (ASA) in binding with bovine serum albumin (BSA).	Aspirin	82-89	albumin	Homo sapiens	119-132
16419075-1	2006	The aim of this study was to describe a competition between cytarabine (araC) and aspirin (ASA) in binding with bovine serum albumin (BSA).	Aspirin	91-94	albumin	Homo sapiens	119-132
16539843-9	2006	Aspirin also decreased the proliferative, migratory, adhesive, and in vitro vasculogenesis capacity of EPC, and also their iNOS levels in a concentration- and time-dependent manner.	Aspirin	0-7	nitric oxide synthase 2	Homo sapiens	123-127
16539843-10	2006	CONCLUSION: Aspirin decreases (1) the number of EPC; (2) the proliferative, migratory, adhesive and in vitro vasculogenesis capacities of EPC; and (3) iNOS levels in EPC.	Aspirin	12-19	nitric oxide synthase 2	Homo sapiens	151-155
16267095-7	2006	The release of NO from NO-ASA, determined with a selective microelectrode was paralleled by the induction of NQO1 and abrogated by NO scavengers; an exogenous NO donor also induced the expression of NQO1.	Aspirin	26-29	NAD(P)H quinone dehydrogenase 1	Homo sapiens	109-113
16267095-7	2006	The release of NO from NO-ASA, determined with a selective microelectrode was paralleled by the induction of NQO1 and abrogated by NO scavengers; an exogenous NO donor also induced the expression of NQO1.	Aspirin	26-29	NAD(P)H quinone dehydrogenase 1	Homo sapiens	199-203
16267095-8	2006	NO-ASA induced concentration-dependently the translocation of Nrf2 into the nucleus as documented by immunofluorescence and immunoblotting; this paralleled the induction of NQO1 and GST P1-1.	Aspirin	3-6	nuclear factor, erythroid derived 2, like 2	Mus musculus	62-66
16267095-9	2006	Thus NO-ASA induces phase II enzymes, at least in part, through the action of NO that it releases and by modulating the Keap1-Nrf2 pathway; this effect may be part of its mechanism of action against colon and other cancers.	Aspirin	8-11	nuclear factor, erythroid derived 2, like 2	Mus musculus	126-130
16489531-0	2006	PPARgamma and colon and rectal cancer: associations with specific tumor mutations, aspirin, ibuprofen and insulin-related genes (United States).	Aspirin	83-90	peroxisome proliferator activated receptor gamma	Homo sapiens	0-9
16630147-0	2006	Cysteinyl leukotriene receptor 1 promoter polymorphism is associated with aspirin-intolerant asthma in males.	Aspirin	74-81	cysteinyl leukotriene receptor 1	Homo sapiens	0-32
16630147-2	2006	CysLTR1-selective antagonists have anti-bronchoconstrictive and anti-inflammatory effects in asthma, particularly aspirin-intolerant asthma (AIA).	Aspirin	114-121	cysteinyl leukotriene receptor 1	Homo sapiens	0-7
16702735-9	2006	The nafamostat hydrolysis in 18 human liver microsomes correlated with aspirin hydrolytic activity specific for carboxylesterase 2 (r=0.815, p<0.01) but not with imidapril hydrolysis catalyzed by carboxylesterase 1 (r=0.156, p=0.54).	Aspirin	71-78	carboxylesterase 2	Homo sapiens	112-130
16613568-3	2006	Acetylation of cyclooxygenase-2 (COX-2) by aspirin can trigger 15-epi-LXA4 (ATL) biosynthesis.	Aspirin	43-50	prostaglandin-endoperoxide synthase 2	Homo sapiens	15-31
16613568-3	2006	Acetylation of cyclooxygenase-2 (COX-2) by aspirin can trigger 15-epi-LXA4 (ATL) biosynthesis.	Aspirin	43-50	prostaglandin-endoperoxide synthase 2	Homo sapiens	33-38
16673274-3	2006	Inhibition of platelet cyclooxygenase-1 by aspirin is followed by relief of microvascular disturbances; correction of shortened platelet survival; correction of increased plasma beta-TG, PF4, and TM levels; and correction of increased TXB2 excretion to normal.	Aspirin	43-50	prostaglandin-endoperoxide synthase 1	Homo sapiens	23-39
16551714-8	2006	However, after aspirin therapy, the percent aggregation to arachidonic acid (the direct COX-1 pathway) decreased more in women than in men (P<.001) and demonstrated near total suppression of residual platelet reactivity in both men and women.	Aspirin	15-22	prostaglandin-endoperoxide synthase 1	Homo sapiens	88-93
16551714-12	2006	However, most women achieved total suppression of aggregation in the direct COX-1 pathway, the putative mechanism for aspirin"s cardioprotection.	Aspirin	118-125	prostaglandin-endoperoxide synthase 1	Homo sapiens	76-81
16484611-0	2006	De novo synthesis of cyclooxygenase-1 counteracts the suppression of platelet thromboxane biosynthesis by aspirin.	Aspirin	106-113	prostaglandin-endoperoxide synthase 1	Homo sapiens	21-37
16484611-1	2006	Aspirin affords cardioprotection through the acetylation of serine529 in human cyclooxygenase-1 (COX-1) of anucleated platelets, inducing a permanent defect in thromboxane A2 (TXA2)-dependent platelet function.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	79-95
16484611-1	2006	Aspirin affords cardioprotection through the acetylation of serine529 in human cyclooxygenase-1 (COX-1) of anucleated platelets, inducing a permanent defect in thromboxane A2 (TXA2)-dependent platelet function.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	97-102
16484611-2	2006	However, heterogeneity of COX-1 suppression by aspirin has been detected in cardiovascular disease and may contribute to failure to prevent clinical events.	Aspirin	47-54	prostaglandin-endoperoxide synthase 1	Homo sapiens	26-31
16519515-1	2006	The two cyclooxygenase enzymes, COX-1 and COX-2, are responsible for the committed step in prostaglandin biosynthesis and are the targets of the nonsteroidal antiinflammatory drugs aspirin and ibuprofen and the COX-2 selective inhibitors, Celebrex, Vioxx, and Bextra.	Aspirin	181-188	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	42-47
16519515-1	2006	The two cyclooxygenase enzymes, COX-1 and COX-2, are responsible for the committed step in prostaglandin biosynthesis and are the targets of the nonsteroidal antiinflammatory drugs aspirin and ibuprofen and the COX-2 selective inhibitors, Celebrex, Vioxx, and Bextra.	Aspirin	181-188	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	211-216
16480405-7	2006	More than two-thirds were aware that aspirin co-therapy decreased the GI safety benefits of the cyclo-oxygenase 2 selective NSAIDs.	Aspirin	37-44	prostaglandin-endoperoxide synthase 2	Homo sapiens	96-113
16480405-8	2006	However, 84% felt that aspirin with a cyclo-oxygenase 2 selective NSAID was safer than aspirin with a non-selective NSAID.	Aspirin	23-30	prostaglandin-endoperoxide synthase 2	Homo sapiens	38-55
16385086-12	2006	Interestingly, treatments with TP receptor antagonists or aspirin hampered the proangiogenic effects of Ang II.	Aspirin	58-65	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	104-110
16516312-0	2006	Aspirin-induced blockade of NF-kappaB activity restrains up-regulation of glial fibrillary acidic protein in human astroglial cells.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	28-37
16516312-3	2006	Aspirin, widely used to prevent NF-kappaB activity, reduced the levels of GFAP mRNA and protein in human astroglial cells including human glioblastoma A172 cells and primary human brain astrocyte cells (HBAs).	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	32-41
16516312-5	2006	We confirmed the repressive effect of aspirin on GFAP transcription by GFAP promoter-driven reporter assay and found that one NF-kappaB binding site conserved in the mouse and human GFAP gene promoters is critical for this effect.	Aspirin	38-45	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	126-135
16469512-4	2006	Thrombin-induced intracellular ROS production was inhibited by NAD(P)H oxidase inhibitors (DPI and apocynin), cyclooxygenase inhibitor (acetylsalicylic acid), and superoxide scavengers (tiron and MnTMPyP).	Aspirin	136-157	coagulation factor II, thrombin	Homo sapiens	0-8
16537708-8	2006	Associations with regular use of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) differed by PGIS genotype.	Aspirin	33-40	prostaglandin I2 synthase	Homo sapiens	108-112
16630404-12	2006	Exposure to nonsteroidal anti-inflammatory drugs/cyclooxygenase-2 inhibitors was associated with a reduced likelihood of prostate cancer (odds ratio [OR], 0.71; 95% confidence interval [CI], 0.58-0.86) as was exposure to aspirin (OR, 0.84; 95% CI, 0.74-0.96).	Aspirin	221-228	prostaglandin-endoperoxide synthase 2	Homo sapiens	49-65
16447059-9	2006	Prostaglandin-endoperoxide synthase 1 (also known as cyclooxygenase 1) inhibitors (acetylsalicylic acid and indomethacin) did not alter the rate of hexose uptake and SCLC2A4 subcellular distribution in L6 myotubes.	Aspirin	83-103	prostaglandin-endoperoxide synthase 1	Homo sapiens	0-37
16384847-0	2006	Acetylsalicylic acid improves lipid-induced insulin resistance in healthy men.	Aspirin	0-20	insulin	Homo sapiens	44-51
16384847-13	2006	CONCLUSIONS: ASA pretreatment attenuated lipid-induced insulin resistance in healthy humans.	Aspirin	13-16	insulin	Homo sapiens	55-62
16384847-14	2006	This acute insulin-sensitizing effect of ASA was unrelated to changes of circulating inflammatory markers.	Aspirin	41-44	insulin	Homo sapiens	11-18
16260580-1	2006	The aim of this study was to assess the effect of chronic administration of NCX4016 [2 acetoxy-benzoate 2-(2-nitroxymethyl)-phenyl ester], a nitric oxide-releasing aspirin derivative on the consequences of coronary artery occlusion in streptozotocin-diabetic rats.	Aspirin	85-103	solute carrier family 8 member A1	Rattus norvegicus	76-79
16260580-1	2006	The aim of this study was to assess the effect of chronic administration of NCX4016 [2 acetoxy-benzoate 2-(2-nitroxymethyl)-phenyl ester], a nitric oxide-releasing aspirin derivative on the consequences of coronary artery occlusion in streptozotocin-diabetic rats.	Aspirin	164-171	solute carrier family 8 member A1	Rattus norvegicus	76-79
16310244-7	2006	The data also showed that NF-kappaB activation and its associated gene expressions, such as COX-2, iNOS, VCAM-1 and ICAM-1, were all suppressed by the low dose aspirin supplementation through the inhibition of phosphorylation and degradation of IkappaBalpha via the NIK/IKK pathway.	Aspirin	160-167	nitric oxide synthase 2	Rattus norvegicus	99-103
16618538-3	2006	NS398, and ASA, can inhibit PGE2 generation via COX-2 inhibition.	Aspirin	11-14	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	48-53
16756193-11	2006	Flowcytometry for P-selectin expression and fibrinogen binding to platelets can be used to monitor antiplatelet therapy with aspirin following acute myocardial infarction.	Aspirin	125-132	fibrinogen beta chain	Homo sapiens	44-54
16310244-8	2006	Our molecular exploration further revealed that aspirin"s suppressive action of NF-kappaB was mediated by its ability to inhibit the nuclear translocation of cytosolic thioredoxin and redox factor-1.	Aspirin	48-55	thioredoxin 1	Rattus norvegicus	168-179
16210341-4	2006	The inhibitory effect of p38 inhibitor is unlikely to be caused by the previous suggested effect on cyclo-oxygenase, as inhibition also was observed in the presence of high concentrations of cyclo-oxygenase inhibitor, aspirin.	Aspirin	218-225	mitogen-activated protein kinase 14	Homo sapiens	25-28
16458133-1	2006	OBJECTIVES: We studied the modifier effect of platelet antigen polymorphism (PlA2) on platelet inhibition by acetylsalicylic acid (ASA, i.e., aspirin), clopidogrel, or their combination in patients with coronary heart disease.	Aspirin	109-129	phospholipase A2 group IB	Homo sapiens	77-81
16458133-1	2006	OBJECTIVES: We studied the modifier effect of platelet antigen polymorphism (PlA2) on platelet inhibition by acetylsalicylic acid (ASA, i.e., aspirin), clopidogrel, or their combination in patients with coronary heart disease.	Aspirin	131-134	phospholipase A2 group IB	Homo sapiens	77-81
16458133-1	2006	OBJECTIVES: We studied the modifier effect of platelet antigen polymorphism (PlA2) on platelet inhibition by acetylsalicylic acid (ASA, i.e., aspirin), clopidogrel, or their combination in patients with coronary heart disease.	Aspirin	142-149	phospholipase A2 group IB	Homo sapiens	77-81
16458133-3	2006	We have shown previously that the effect of ASA on platelets is modified by the glycoprotein IIIa single nucleotide polymorphism PlA2.	Aspirin	44-47	phospholipase A2 group IB	Homo sapiens	129-133
16458133-12	2006	Pl(A2) functions as an important modifier for platelet responsiveness to ASA but not to clopidogrel.	Aspirin	73-76	phospholipase A2 group IB	Homo sapiens	0-5
16493264-4	2006	The anti-tumor effects of aspirin and other NSAIDs are thought to arise primarily from an inhibition of cyclooxygenase-2.	Aspirin	26-33	prostaglandin-endoperoxide synthase 2	Homo sapiens	104-120
16433794-10	2006	In patients of both families with positive aspirin challenge test, deletion of the GSTM1 gene was present.	Aspirin	43-50	glutathione S-transferase mu 1	Homo sapiens	83-88
16175430-0	2006	The renal effects of the addition of low-dose aspirin to COX-2 selective and nonselective antiinflammatory drugs.	Aspirin	46-53	prostaglandin-endoperoxide synthase 2	Homo sapiens	57-62
16141240-0	2006	NO-donating aspirin isomers downregulate peroxisome proliferator-activated receptor (PPAR)delta expression in APC(min/+) mice proportionally to their tumor inhibitory effect: Implications for the role of PPARdelta in carcinogenesis.	Aspirin	12-19	peroxisome proliferator activator receptor delta	Mus musculus	85-95
16141240-0	2006	NO-donating aspirin isomers downregulate peroxisome proliferator-activated receptor (PPAR)delta expression in APC(min/+) mice proportionally to their tumor inhibitory effect: Implications for the role of PPARdelta in carcinogenesis.	Aspirin	12-19	peroxisome proliferator activator receptor delta	Mus musculus	204-213
16141240-4	2006	We studied histochemically the effect of the meta and para positional isomers of NO-ASA on PPARdelta expression in Min (multiple intestinal neoplasia) and wild-type mice, and on cell proliferation and apoptosis.	Aspirin	84-87	peroxisome proliferator activator receptor delta	Mus musculus	91-100
16141240-6	2006	para NO-ASA inhibited intestinal tumor incidence (59%) and PPARdelta expression (55.3%) more than meta NO-ASA (38 and 41.5%, respectively).	Aspirin	8-11	peroxisome proliferator activator receptor delta	Mus musculus	59-68
16493264-6	2006	In addition, some epidemiologic studies have reported that hormone-receptor-positive breast tumors are more responsive to aspirin, which is consistent with these preclinical findings.	Aspirin	122-129	nuclear receptor subfamily 4 group A member 1	Homo sapiens	59-75
16505607-2	2006	RECENT FINDINGS: The overproduction of cysteinyl leukotrienes with the increased expression of cysteinyl leukotriene receptor 1 (CYSLTR1) is a consistent finding in aspirin-induced asthma patients.	Aspirin	165-172	cysteinyl leukotriene receptor 1	Homo sapiens	95-127
16505607-2	2006	RECENT FINDINGS: The overproduction of cysteinyl leukotrienes with the increased expression of cysteinyl leukotriene receptor 1 (CYSLTR1) is a consistent finding in aspirin-induced asthma patients.	Aspirin	165-172	cysteinyl leukotriene receptor 1	Homo sapiens	129-136
16609625-3	2006	The major side effect of aspirin is related to its ability to suppress prostaglandin (PG) synthesis by constitutive cyclooxygenase-1 (COX-1).	Aspirin	25-32	prostaglandin-endoperoxide synthase 1	Homo sapiens	116-132
16609625-3	2006	The major side effect of aspirin is related to its ability to suppress prostaglandin (PG) synthesis by constitutive cyclooxygenase-1 (COX-1).	Aspirin	25-32	prostaglandin-endoperoxide synthase 1	Homo sapiens	134-139
16132039-0	2006	Aspirin-triggered Lipoxin A4 inhibition of VEGF-induced endothelial cell migration involves actin polymerization and focal adhesion assembly.	Aspirin	0-7	vascular endothelial growth factor A	Homo sapiens	43-47
16444599-3	2006	Non-steroidal anti-inflammatory drugs (NSAIDS), piroxicam, aspirin, ibuprofen, naproxen and celecoxib all specifically inhibited tNOX activity of HeLa (human cervical carcinoma) and BT-20 (human mammary carcinoma) cells (IC(50) in the nanomolar range) without effect on ECTO-NOX activities of non-cancer MCF-10A mammary epithelial cells.	Aspirin	59-66	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	129-133
17274466-5	2006	Catalase activity was statistically decreased after both doses of nimesulid and acetylsalicylic acid at the dose of 10 mg/kg body weight.	Aspirin	80-100	catalase	Rattus norvegicus	0-8
16132039-2	2006	We demonstrated previously that an aspirin-triggered lipoxin analog, 15-epi-16-(para-fluoro)-phenoxy-lipoxin A4 (ATL-1), inhibits vascular endothelial growth factor (VEGF)-induced EC migration.	Aspirin	35-42	atlastin GTPase 1	Homo sapiens	113-118
16132039-2	2006	We demonstrated previously that an aspirin-triggered lipoxin analog, 15-epi-16-(para-fluoro)-phenoxy-lipoxin A4 (ATL-1), inhibits vascular endothelial growth factor (VEGF)-induced EC migration.	Aspirin	35-42	vascular endothelial growth factor A	Homo sapiens	130-164
16132039-2	2006	We demonstrated previously that an aspirin-triggered lipoxin analog, 15-epi-16-(para-fluoro)-phenoxy-lipoxin A4 (ATL-1), inhibits vascular endothelial growth factor (VEGF)-induced EC migration.	Aspirin	35-42	vascular endothelial growth factor A	Homo sapiens	166-170
16368345-12	2006	Preserved aspirin sensitivity in the aprotinin group may explain the observed reduction in thrombotic events and might be related to the suppression of perioperative and transmyocardial thrombin formation.	Aspirin	10-17	coagulation factor II, thrombin	Homo sapiens	186-194
16454979-13	2006	CONCLUSIONS: Aspirin plus clopidogrel treatment reduced levels of serum hs-CRP and TNF-alpha in patients with NSTEACS significantly more than aspirin alone.	Aspirin	13-20	tumor necrosis factor	Homo sapiens	83-92
16440541-4	2006	RESULTS: The mean +/- SD values of the semiquantitatively evaluated immunoexpression of ICAM-1, VCAM-1, and VLA-4 were significantly increased in patients with aspirin hypersensitivity compared with aspirin-tolerant patients (1.7 +/- 0.8 vs 0.9 +/- 0.8, P < .003; 1.8 +/- 0.8 vs 0.8 +/- 0.8, P < .001; and 2.2 +/- 0.7 vs 1.3 +/- 0.7, P < .001, respectively), whereas the mean +/- SD values of the expression of lymphocyte function-associated antigen 1 did not differ significantly (2.4 +/- 0.5 vs 2.2 +/- 0.9; P = .57).	Aspirin	160-167	vascular cell adhesion molecule 1	Homo sapiens	96-102
16440541-6	2006	CONCLUSIONS: In nasal polyps of aspirin-hypersensitive patients, up-regulation of the adhesion molecules ICAM-1 and VCAM-1 and the integrin VLA-4 may play an important role in the development of chronic eosinophilic inflammation.	Aspirin	32-39	vascular cell adhesion molecule 1	Homo sapiens	116-122
16607074-3	2006	The possibility was suggested that one of the mechanisms of action of aspirin in thrombotic prevention is through its anti-inflammatory properties in terms of reducing the concentration of CRP.	Aspirin	70-77	C-reactive protein	Homo sapiens	189-192
16326168-7	2006	At the end of the study, LDLR(-/-) mice that had received aspirin had suppressed biosynthesis of thromboxane B2, the major products of COX-1 activity, reduced monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1 levels compared with controls.	Aspirin	58-65	cytochrome c oxidase I, mitochondrial	Mus musculus	135-140
16607074-5	2006	The significant determinants of CRP concentrations included body mass index, oral contraceptives, hormonal replacement therapy, gender, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, physical activity, age, smoking status and the presence of diabetes mellitus but not the use of low dose of aspirin.	Aspirin	334-341	C-reactive protein	Homo sapiens	32-35
17181859-3	2006	We hypothesized that genetic polymorphisms (COX-2 .926, COX-2 .5209, and COX-2 .8473) may reduce overall breast cancer risk or risk for subtypes of breast cancer by modulating the inflammatory response and may interact with aspirin or any NSAID use.	Aspirin	224-231	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	44-49
17181859-3	2006	We hypothesized that genetic polymorphisms (COX-2 .926, COX-2 .5209, and COX-2 .8473) may reduce overall breast cancer risk or risk for subtypes of breast cancer by modulating the inflammatory response and may interact with aspirin or any NSAID use.	Aspirin	224-231	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	56-61
17181859-3	2006	We hypothesized that genetic polymorphisms (COX-2 .926, COX-2 .5209, and COX-2 .8473) may reduce overall breast cancer risk or risk for subtypes of breast cancer by modulating the inflammatory response and may interact with aspirin or any NSAID use.	Aspirin	224-231	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	56-61
16521406-6	2006	Patients with chronic heart failure and with the II genotype of polymorphism I/D ACE were younger, with more frequent administration of betablockers and diuretics, with less regular administration of aspirin and with lower glycemia and plasma TNFalpha level.	Aspirin	200-207	angiotensin I converting enzyme	Homo sapiens	81-84
16373888-4	2006	RESULTS: Insulin-treated diabetic patients were less likely than nondiabetic patients to receive aspirin (adjusted odds ratio 0.83 [95% CI 0.74-0.93]), beta-blockers (0.89 [0.83-0.96]), heparin (0.90 [0.83-0.98]), and glycoprotein IIb/IIIa inhibitors (0.86 [0.79-0.93]).	Aspirin	97-104	insulin	Homo sapiens	9-16
16930084-8	2006	RESULTS: Compared with aspirin-resistant patients, patients who demonstrated effective aspirin inhibition had a significantly lower plasma fibrinogen level (3.3 g/L vs 3.8 g/L; p < 0.05) and significantly lower RBC aggregation values (24.3 vs 28.2; p < 0.01).	Aspirin	87-94	fibrinogen beta chain	Homo sapiens	139-149
16869344-4	2006	Furthermore, concomitant aspirin use substantially reduces the gastrointestinal safety advantage of COX-2-selective drugs.	Aspirin	25-32	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	100-105
16930084-14	2006	The higher rate of hypertension in patients with effective platelet aggregation on aspirin could explain the differences in beta-adrenoceptor antagonist and ACE inhibitor use between these patients and aspirin-resistant patients.	Aspirin	83-90	angiotensin I converting enzyme	Homo sapiens	157-160
16930084-14	2006	The higher rate of hypertension in patients with effective platelet aggregation on aspirin could explain the differences in beta-adrenoceptor antagonist and ACE inhibitor use between these patients and aspirin-resistant patients.	Aspirin	202-209	angiotensin I converting enzyme	Homo sapiens	157-160
20477089-1	2006	Aspirin and other nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase-1 participate in unique pseudoallergic reactions, in which biochemical inhibitions rather than immunoglobulin E antibody direct the cascade of mediators and ultimate reactions.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	68-84
16413386-0	2006	Acetylsalicylic acid-induced release of HSP70 from mast cells results in cell activation through TLR pathway.	Aspirin	0-20	heat shock protein 1B	Mus musculus	40-45
16413386-6	2006	RESULTS: Using BMMC, we show that treatment with heat shock or acetylsalicylic acid results in a selective induction of HSPs, and leads to release of HSP70 into the extracellular environment.	Aspirin	63-83	heat shock protein 1B	Mus musculus	150-155
16399303-0	2006	Endothelial injury and acquired aspirin resistance as promoters of regional thrombin formation and early vein graft failure after coronary artery bypass grafting.	Aspirin	32-39	coagulation factor II, thrombin	Homo sapiens	76-84
16395396-6	2006	Among the questions that remain to be addressed are the following: (a) whether this hazard extends to all or some of the traditional NSAIDs; (b) whether adjuvant therapies, such as low-dose aspirin, will mitigate the hazard and if so, at what cost; (c) whether COX-2 inhibitors result in cardiovascular risk transformation during chronic dosing; and (d) how we might identify individuals most likely to benefit or suffer from such drugs in the future.	Aspirin	190-197	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	261-266
16397290-0	2006	Effect of high-dose aspirin on CYP2E1 activity in healthy subjects measured using chlorzoxazone as a probe.	Aspirin	20-27	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	31-37
16169935-5	2006	NO-aspirin stimulated the phosphorylation of extracellular signal-regulated kinase 1/2 and Akt only marginally.	Aspirin	3-10	AKT serine/threonine kinase 1	Homo sapiens	45-94
16169935-9	2006	Only the dual inhibitor of p38 and JNK and the use of combined siRNA silencing of p38 and cJun abrogated the ability of NO-aspirin to block cell growth.	Aspirin	123-130	mitogen-activated protein kinase 14	Homo sapiens	82-85
16169935-10	2006	Our data indicate that NO-aspirin is dependent on both the p38 and the JNK MAP kinase pathways for its ability to inhibit the growth of colon cancer cells.	Aspirin	26-33	mitogen-activated protein kinase 14	Homo sapiens	59-62
16169935-10	2006	Our data indicate that NO-aspirin is dependent on both the p38 and the JNK MAP kinase pathways for its ability to inhibit the growth of colon cancer cells.	Aspirin	26-33	mitogen-activated protein kinase 8	Homo sapiens	71-74
17392574-2	2006	The aim was to analyze the prevalence of HLA class I phenotypes and HLA-DRB1* genotype in patients with CIU associated with ASA and NSAIDs hypersensitivity (AICU).	Aspirin	124-127	major histocompatibility complex, class II, DR beta 1	Homo sapiens	41-44
17392574-2	2006	The aim was to analyze the prevalence of HLA class I phenotypes and HLA-DRB1* genotype in patients with CIU associated with ASA and NSAIDs hypersensitivity (AICU).	Aspirin	124-127	major histocompatibility complex, class II, DR beta 1	Homo sapiens	68-76
16819430-8	2006	RESULTS: A compounding effect of ASA and PYC to inhibit platelet function recorded in collagen-induced aggregation in PRP was observed, but only when ethanol-dissolved PYC was used.	Aspirin	33-36	prion protein	Homo sapiens	118-121
16179345-0	2005	Aspirin induces platelet receptor shedding via ADAM17 (TACE).	Aspirin	0-7	a disintegrin and metallopeptidase domain 17	Mus musculus	47-53
17154669-7	2006	Selective COX-2 inhibitors (celecoxib and rofecoxib [withdrawn from the market]) are well tolerated by almost all aspirin-sensitive asthmatic patients.	Aspirin	114-121	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	10-15
16179345-0	2005	Aspirin induces platelet receptor shedding via ADAM17 (TACE).	Aspirin	0-7	a disintegrin and metallopeptidase domain 17	Mus musculus	55-59
16179345-3	2005	Recently, aspirin and other anti-inflammatory drugs were shown to induce shedding of L-selectin in neutrophils in a metalloproteinase-dependent manner.	Aspirin	10-17	selectin, lymphocyte	Mus musculus	85-95
16179345-9	2005	These data demonstrate that aspirin at high concentrations induces shedding of GPIbalpha and GPV by an ADAM17-dependent mechanism and that this process can occur in vivo.	Aspirin	28-35	a disintegrin and metallopeptidase domain 17	Mus musculus	103-109
16361798-9	2005	These results suggested that ALOX5 has a differing contribution in two major clinical pathogenesis related to ASA-sensitivity.	Aspirin	110-113	arachidonate 5-lipoxygenase	Homo sapiens	29-34
16199534-0	2005	Pretreatment of acetylsalicylic acid promotes tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by down-regulating BCL-2 gene expression.	Aspirin	16-36	TNF superfamily member 10	Homo sapiens	46-101
16199534-0	2005	Pretreatment of acetylsalicylic acid promotes tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by down-regulating BCL-2 gene expression.	Aspirin	16-36	BCL2 apoptosis regulator	Homo sapiens	139-144
16199534-4	2005	In this study, we observed that pretreatment by acetylsalicylic acid (ASA) augmented TRAIL-induced apoptotic death in human prostate adenocarcinoma LNCaP and human colorectal carcinoma CX-1 cells.	Aspirin	48-68	TNF superfamily member 10	Homo sapiens	85-90
16199534-4	2005	In this study, we observed that pretreatment by acetylsalicylic acid (ASA) augmented TRAIL-induced apoptotic death in human prostate adenocarcinoma LNCaP and human colorectal carcinoma CX-1 cells.	Aspirin	70-73	TNF superfamily member 10	Homo sapiens	85-90
16199534-5	2005	Western blot analysis showed that pretreatment of ASA followed by TRAIL treatment activated caspases (8, 9, and 3) and cleaved poly(ADP-ribose) polymerase, the hallmark feature of apoptosis.	Aspirin	50-53	poly(ADP-ribose) polymerase 1	Homo sapiens	127-154
16199534-6	2005	Most interestingly, at least 12 h of pretreatment with ASA was prerequisite for promoting TRAIL-induced apoptosis and was related to down-regulation of BCL-2.	Aspirin	55-58	TNF superfamily member 10	Homo sapiens	90-95
16199534-6	2005	Most interestingly, at least 12 h of pretreatment with ASA was prerequisite for promoting TRAIL-induced apoptosis and was related to down-regulation of BCL-2.	Aspirin	55-58	BCL2 apoptosis regulator	Homo sapiens	152-157
16199534-7	2005	Biochemical analysis revealed that ASA inhibited NF-kappaB activity, which is known to regulate BCL-2 gene expression, by dephosphorylating IkappaB-alpha and inhibiting IKKbeta activity but not by affecting the HER-2/neu phosphatidylinositol 3-kinase-Akt signal pathway.	Aspirin	35-38	BCL2 apoptosis regulator	Homo sapiens	96-101
16199534-7	2005	Biochemical analysis revealed that ASA inhibited NF-kappaB activity, which is known to regulate BCL-2 gene expression, by dephosphorylating IkappaB-alpha and inhibiting IKKbeta activity but not by affecting the HER-2/neu phosphatidylinositol 3-kinase-Akt signal pathway.	Aspirin	35-38	NFKB inhibitor alpha	Homo sapiens	140-153
16199534-7	2005	Biochemical analysis revealed that ASA inhibited NF-kappaB activity, which is known to regulate BCL-2 gene expression, by dephosphorylating IkappaB-alpha and inhibiting IKKbeta activity but not by affecting the HER-2/neu phosphatidylinositol 3-kinase-Akt signal pathway.	Aspirin	35-38	AKT serine/threonine kinase 1	Homo sapiens	251-254
16199534-8	2005	Overexpression of BCL-2 suppressed the promotive effect of ASA on TRAIL-induced apoptosis and changes in mitochondrial membrane potential.	Aspirin	59-62	BCL2 apoptosis regulator	Homo sapiens	18-23
16199534-8	2005	Overexpression of BCL-2 suppressed the promotive effect of ASA on TRAIL-induced apoptosis and changes in mitochondrial membrane potential.	Aspirin	59-62	TNF superfamily member 10	Homo sapiens	66-71
16199534-9	2005	Taken together, our studies suggested that ASA-promoted TRAIL cytotoxicity is mediated through down-regulating BCL-2 and by decreasing mitochondrial membrane potential.	Aspirin	43-46	TNF superfamily member 10	Homo sapiens	56-61
16199534-9	2005	Taken together, our studies suggested that ASA-promoted TRAIL cytotoxicity is mediated through down-regulating BCL-2 and by decreasing mitochondrial membrane potential.	Aspirin	43-46	BCL2 apoptosis regulator	Homo sapiens	111-116
16371720-2	2005	Aspirin was recently found to have chemopreventive effects on colon cancer and polyps by inhibiting cyclooxygenase-2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	100-116
16020504-6	2005	Although VWF fostered the agglutination of platelets regardless of any additional treatment, the inhibition of mitogen-activated protein kinase kinase (MEK) with U0126 abolished VWF-induced platelet aggregation and thromboxane production in non-aspirin-treated washed platelets.	Aspirin	245-252	mitogen-activated protein kinase kinase 7	Homo sapiens	111-150
16183169-5	2005	Aspirin, which has been shown to block phosphorylation of the IkappaB component of the cytoplasmic NF-kappaB complex, significantly suppressed glutamate-induced cell death, whereas the NF-kappaB decoy oligonucleotide potentiated it.	Aspirin	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	99-108
16183169-5	2005	Aspirin, which has been shown to block phosphorylation of the IkappaB component of the cytoplasmic NF-kappaB complex, significantly suppressed glutamate-induced cell death, whereas the NF-kappaB decoy oligonucleotide potentiated it.	Aspirin	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	185-194
16020504-6	2005	Although VWF fostered the agglutination of platelets regardless of any additional treatment, the inhibition of mitogen-activated protein kinase kinase (MEK) with U0126 abolished VWF-induced platelet aggregation and thromboxane production in non-aspirin-treated washed platelets.	Aspirin	245-252	mitogen-activated protein kinase kinase 7	Homo sapiens	152-155
16020504-6	2005	Although VWF fostered the agglutination of platelets regardless of any additional treatment, the inhibition of mitogen-activated protein kinase kinase (MEK) with U0126 abolished VWF-induced platelet aggregation and thromboxane production in non-aspirin-treated washed platelets.	Aspirin	245-252	von Willebrand factor	Homo sapiens	178-181
16020504-7	2005	However, in platelets treated with aspirin, VWF failed to cause any aggregation.	Aspirin	35-42	von Willebrand factor	Homo sapiens	44-47
16216591-0	2005	Aspirin inhibits thrombin action on endothelial cells via up-regulation of aminopeptidase N/CD13 expression.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	17-25
16267647-6	2005	The superoxide dismutase biosensor was used to determine the antioxidant properties of acetylsalicylic acid-based drugs and the anti-radical activity of healthy and cancerous human brain tissues.	Aspirin	87-107	superoxide dismutase 1	Homo sapiens	4-24
16336399-0	2005	Aspirin induces apoptosis in oesophageal cancer cells by inhibiting the pathway of NF-kappaB downstream regulation of cyclooxygenase-2.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	83-92
16336399-0	2005	Aspirin induces apoptosis in oesophageal cancer cells by inhibiting the pathway of NF-kappaB downstream regulation of cyclooxygenase-2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	118-134
16336399-7	2005	Aspirin dose-dependently decreased the levels of COX-2 mRNA, COX-2 protein and nuclear NF-kappaB protein and increased the cytoplasmic IkappaB protein.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	49-54
16336399-7	2005	Aspirin dose-dependently decreased the levels of COX-2 mRNA, COX-2 protein and nuclear NF-kappaB protein and increased the cytoplasmic IkappaB protein.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	61-66
16336399-7	2005	Aspirin dose-dependently decreased the levels of COX-2 mRNA, COX-2 protein and nuclear NF-kappaB protein and increased the cytoplasmic IkappaB protein.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	87-96
16216591-4	2005	Since activated thrombin receptor is reported to be inactivated by APN/CD13 in vitro, protective actions of aspirin on HUVECs by thrombin stimulation were examined, resulting in the suppression of endothelin-1 and reactive oxygen species productions in HUVECs.	Aspirin	108-115	coagulation factor II, thrombin	Homo sapiens	129-137
16216591-4	2005	Since activated thrombin receptor is reported to be inactivated by APN/CD13 in vitro, protective actions of aspirin on HUVECs by thrombin stimulation were examined, resulting in the suppression of endothelin-1 and reactive oxygen species productions in HUVECs.	Aspirin	108-115	endothelin 1	Homo sapiens	197-209
16216591-6	2005	CONCLUSIONS: Aspirin may exert its anti-atherothrombotic effects in part via the inhibition of thrombin action by up-regulating APN/CD13 on endothelial cells.	Aspirin	13-20	coagulation factor II, thrombin	Homo sapiens	95-103
16304252-0	2005	Comparison of plasma eotaxin family level in aspirin-induced and aspirin-tolerant asthma patients.	Aspirin	45-52	C-C motif chemokine ligand 11	Homo sapiens	21-28
16304252-0	2005	Comparison of plasma eotaxin family level in aspirin-induced and aspirin-tolerant asthma patients.	Aspirin	65-72	C-C motif chemokine ligand 11	Homo sapiens	21-28
16450810-6	2005	All patients post MI require an angiotensin-converting enzyme (ACE) inhibitor and antiplatelet therapy, usually with aspirin.	Aspirin	117-124	angiotensin I converting enzyme	Homo sapiens	32-61
16227351-2	2005	Selective COX-2 inhibitors were seen as successor to non-selective non-steroidal anti-inflammatory drugs, in turn successors to aspirin.	Aspirin	128-135	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	10-15
16412866-10	2006	Soluble CD40L linearly correlated with 11-dehydro-TXB2 (rho = 0.67, p < 0.0001), and both were reduced after one week of aspirin (p < 0.0026), with slow recovery over 10 days after aspirin withdrawal.	Aspirin	124-131	CD40 ligand	Homo sapiens	8-13
16412866-10	2006	Soluble CD40L linearly correlated with 11-dehydro-TXB2 (rho = 0.67, p < 0.0001), and both were reduced after one week of aspirin (p < 0.0026), with slow recovery over 10 days after aspirin withdrawal.	Aspirin	187-194	CD40 ligand	Homo sapiens	8-13
15972451-6	2005	Rate of onset and recovery following aspirin withdrawal was consistent with cyclooxygenase 1 (COX-1) inhibition.	Aspirin	37-44	prostaglandin-endoperoxide synthase 1	Homo sapiens	76-92
15972451-6	2005	Rate of onset and recovery following aspirin withdrawal was consistent with cyclooxygenase 1 (COX-1) inhibition.	Aspirin	37-44	prostaglandin-endoperoxide synthase 1	Homo sapiens	94-99
15972451-9	2005	Comparisons of platelet COX-1 or -2 expression and urinary 11-dehydro-thromboxane B2 excretion suggested that aspirin was less able to block platelet activation in vivo in hypercholesterolemia.	Aspirin	110-117	prostaglandin-endoperoxide synthase 1	Homo sapiens	24-29
16105666-4	2005	NO-ASA also decreased the corresponding steady-state mRNA levels and this reduction preceded the reduction of protein levels by at least 6 h. NO-ASA also reduced the enzymatic activity of NOS2, as determined by a direct enzyme assay (maximal reduction = 80%) and by determining the accumulation of NO in the culture medium (IC50 for this effect = 36 microM).	Aspirin	3-6	nitric oxide synthase 2	Homo sapiens	188-192
15976387-1	2005	This study was undertaken to determine whether the Bcl-2 family proteins and Smac are regulators of aspirin-mediated apoptosis in a gastric mucosal cell line known as AGS cells.	Aspirin	100-107	BCL2 apoptosis regulator	Homo sapiens	51-56
15976387-5	2005	ASA downregulated Bcl-2 protein expression and induced Bax translocation into the mitochondria and cleavage of Bid.	Aspirin	0-3	BCL2 apoptosis regulator	Homo sapiens	18-23
15976387-5	2005	ASA downregulated Bcl-2 protein expression and induced Bax translocation into the mitochondria and cleavage of Bid.	Aspirin	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	55-58
15976387-5	2005	ASA downregulated Bcl-2 protein expression and induced Bax translocation into the mitochondria and cleavage of Bid.	Aspirin	0-3	BH3 interacting domain death agonist	Homo sapiens	111-114
16184416-3	2005	Aspirin induces and acetylates COX-2 to produce 15-(R)-epi-lipoxinA4, an anti-inflammatory mediator thought to protect the gastric mucosa against aspirin-induced injury.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	31-36
16184416-3	2005	Aspirin induces and acetylates COX-2 to produce 15-(R)-epi-lipoxinA4, an anti-inflammatory mediator thought to protect the gastric mucosa against aspirin-induced injury.	Aspirin	146-153	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	31-36
16087788-1	2005	Aspirin is a potent antioxidative agent that reduces vascular production of superoxide, prevents angiotensin II-induced hypertension, and induces NO release.	Aspirin	0-7	angiotensinogen	Homo sapiens	97-111
16132116-6	2005	However, the NF-kappaB inhibitors, such as aspirin, cyclosporin A and dexamethasone, inhibited both the acetaldehyde-induced NF-kappaB activity and the induced cytokine production.	Aspirin	43-50	nuclear factor kappa B subunit 1	Homo sapiens	13-22
16132116-6	2005	However, the NF-kappaB inhibitors, such as aspirin, cyclosporin A and dexamethasone, inhibited both the acetaldehyde-induced NF-kappaB activity and the induced cytokine production.	Aspirin	43-50	nuclear factor kappa B subunit 1	Homo sapiens	125-134
16150050-0	2005	Cyclooxygenase-1 haplotype modulates platelet response to aspirin.	Aspirin	58-65	prostaglandin-endoperoxide synthase 1	Homo sapiens	0-16
16084489-7	2005	Treatment of mice with acetylsalicylic acid or indomethacin at doses effective to cause near-complete inhibition of PGE(2) and PGD(2) biosynthesis in heart ex vivo resulted in enhanced expression of IL-1beta 24h after endotoxin administration.	Aspirin	23-43	interleukin 1 beta	Mus musculus	199-207
16105666-5	2005	These effects of NO-ASA on NOS2 were paralleled by inhibition in cell growth (IC50 = 8.5 microM).	Aspirin	20-23	nitric oxide synthase 2	Homo sapiens	27-31
16168275-2	2005	BACKGROUND: Because of the potential for exacerbating hypertension or renal insufficiency and possible interactions with angiotensin-converting enzyme (ACE) inhibitors, the use of aspirin for secondary prevention of coronary events is controversial in patients with HF.	Aspirin	180-187	angiotensin I converting enzyme	Homo sapiens	121-150
16168275-2	2005	BACKGROUND: Because of the potential for exacerbating hypertension or renal insufficiency and possible interactions with angiotensin-converting enzyme (ACE) inhibitors, the use of aspirin for secondary prevention of coronary events is controversial in patients with HF.	Aspirin	180-187	angiotensin I converting enzyme	Homo sapiens	152-155
16168278-2	2005	BACKGROUND: Previous studies have shown that ASA produces an administration time-dependent inhibition of angiotensin II.	Aspirin	45-48	angiotensinogen	Homo sapiens	105-119
15901601-4	2005	In this study, we investigated whether an aspirin-triggered lipoxin A(4) stable analog, 15-epi-16-(para-fluoro)-phenoxy-lipoxin A(4) (ATL-1) was able to induce endothelial HO-1.	Aspirin	42-49	atlastin GTPase 1	Homo sapiens	134-139
16142873-9	2005	CONCLUSIONS: Higher CRP values and back pain scores and lower BASFI scores at baseline were significant predictors of a higher ASAS 20 response in patients with AS receiving etanercept but predictive value was of insufficient magnitude to determine treatment in individual patients.	Aspirin	127-131	C-reactive protein	Homo sapiens	20-23
16116334-0	2005	Effect of acetylsalicylic acid on nuclear factor-kappaB activation and on late preconditioning against infarction in the myocardium.	Aspirin	10-30	nuclear factor kappa B subunit 1	Homo sapiens	34-55
16116334-2	2005	Acetylsalicylic acid (ASA) blocks NF-kappaB-dependent gene activation in leukocytes and endothelial cells through preventing phosphorylation and subsequent degradation of the inhibitor IkappaB-alpha.	Aspirin	0-20	nuclear factor kappa B subunit 1	Homo sapiens	34-43
16116334-2	2005	Acetylsalicylic acid (ASA) blocks NF-kappaB-dependent gene activation in leukocytes and endothelial cells through preventing phosphorylation and subsequent degradation of the inhibitor IkappaB-alpha.	Aspirin	0-20	NFKB inhibitor alpha	Homo sapiens	185-198
16116334-2	2005	Acetylsalicylic acid (ASA) blocks NF-kappaB-dependent gene activation in leukocytes and endothelial cells through preventing phosphorylation and subsequent degradation of the inhibitor IkappaB-alpha.	Aspirin	22-25	nuclear factor kappa B subunit 1	Homo sapiens	34-43
16116334-2	2005	Acetylsalicylic acid (ASA) blocks NF-kappaB-dependent gene activation in leukocytes and endothelial cells through preventing phosphorylation and subsequent degradation of the inhibitor IkappaB-alpha.	Aspirin	22-25	NFKB inhibitor alpha	Homo sapiens	185-198
16024242-3	2005	Indeed, suppression of aspirin-triggered lipoxin synthesis, through co-administration of a selective COX-2 inhibitor, results in a significant exacerbation of gastric injury.	Aspirin	23-30	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	101-106
16153930-1	2005	OBJECTIVE: The presence of the glycoprotein IIIa allele PlA2 is associated with enhanced thrombin formation and an impaired antithrombotic action of aspirin, which could favor coronary thrombosis.	Aspirin	149-156	phospholipase A2 group IB	Homo sapiens	56-60
16153930-11	2005	When subjects were stratified accordingly to blood platelet glycoprotein IIb/IIIa genotype, in the aspirin group PlA2 carriers had greater blood loss than PlA1 homozygotes (1858 +/- 932 mL vs 1216 +/- 525 mL, P < .05).	Aspirin	99-106	phospholipase A2 group IB	Homo sapiens	113-117
16136765-1	2005	BACKGROUND: The use of selective inhibitors of cyclooxygenase 2 (COX-2) has been shown to be safe in patients with aspirin-induced asthma.	Aspirin	115-122	prostaglandin-endoperoxide synthase 2	Homo sapiens	47-63
16136765-1	2005	BACKGROUND: The use of selective inhibitors of cyclooxygenase 2 (COX-2) has been shown to be safe in patients with aspirin-induced asthma.	Aspirin	115-122	prostaglandin-endoperoxide synthase 2	Homo sapiens	65-70
16187007-2	2005	Low dose aspirin is commonly prescribed in CHF and may attenuate the vasodilator effects of ACE inhibitors.	Aspirin	9-16	angiotensin I converting enzyme	Homo sapiens	92-95
16187007-11	2005	This action of aspirin may reduce the long-term clinical benefits of ACE inhibitors.	Aspirin	15-22	angiotensin I converting enzyme	Homo sapiens	69-72
15955733-6	2005	Thus, epi-lipoxins, produced after aspirin acetylation of inducible cyclooxygenase-2, and glucocorticoid-regulated annexin 1 appear to be important endogenous mediators of their respective anti-inflammatory effects.	Aspirin	35-42	prostaglandin-endoperoxide synthase 2	Homo sapiens	68-124
16101563-9	2005	COX-2 inhibitors, collectively called coxibs (celecoxib, rofecoxib, valdecoxib, lumiracoxib, etc), held a promise of improved treatment of arthritis without the gastrointestinal side effects associated with aspirin and other nonsteroidal anti-inflammatory drugs.	Aspirin	207-214	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
16034127-0	2005	Involvement of the Rho-kinase/myosin light chain kinase pathway on human monocyte chemotaxis induced by ATL-1, an aspirin-triggered lipoxin A4 synthetic analog.	Aspirin	114-121	atlastin GTPase 1	Homo sapiens	104-109
16006977-0	2005	Aspirin, ibuprofen, and other non-steroidal anti-inflammatory drugs in cancer prevention: a critical review of non-selective COX-2 blockade (review).	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	125-130
15978791-2	2005	Originally, the beneficial effects of aspirin were shown to stem from its inhibition of cyclooxygenase (COX 2)-derived prostanoids, fatty acid metabolites that modulate host defense and regulate the cardiovascular system.	Aspirin	38-45	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	104-109
15978791-4	2005	Here, data from a series of comparatively recent experiments exploring aspirin"s unique ability to acetylate the active site of inducible COX 2 and generate a family of lipid mediators called the epi-Lipoxins will be discussed in light of their ability to exert profound modulatory effects on the innate and adaptive immune systems.	Aspirin	71-78	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	138-143
16094491-1	2005	The purpose of this study is to determine whether aspirin can reduce interleukin-1beta(IL-1beta) concentration and exert protective effects against heatstroke.	Aspirin	50-57	interleukin 1 beta	Rattus norvegicus	69-86
16094491-1	2005	The purpose of this study is to determine whether aspirin can reduce interleukin-1beta(IL-1beta) concentration and exert protective effects against heatstroke.	Aspirin	50-57	interleukin 1 beta	Rattus norvegicus	87-95
16094491-3	2005	Three parts were performed in the present experiment: (1) To determine the effects of pretreatment with aspirin against heatstroke;(2) To prove the effects of specifically reducing inducible nitric oxide synthase (iNOS) against rat heatstroke by iNOS selective prohibitor aminoguanidine (AG);(3) To determine the effects of aspirin against heatstroke and fatigue.	Aspirin	104-111	nitric oxide synthase 2	Rattus norvegicus	181-212
16094491-3	2005	Three parts were performed in the present experiment: (1) To determine the effects of pretreatment with aspirin against heatstroke;(2) To prove the effects of specifically reducing inducible nitric oxide synthase (iNOS) against rat heatstroke by iNOS selective prohibitor aminoguanidine (AG);(3) To determine the effects of aspirin against heatstroke and fatigue.	Aspirin	324-331	nitric oxide synthase 2	Rattus norvegicus	181-212
16094491-3	2005	Three parts were performed in the present experiment: (1) To determine the effects of pretreatment with aspirin against heatstroke;(2) To prove the effects of specifically reducing inducible nitric oxide synthase (iNOS) against rat heatstroke by iNOS selective prohibitor aminoguanidine (AG);(3) To determine the effects of aspirin against heatstroke and fatigue.	Aspirin	324-331	nitric oxide synthase 2	Rattus norvegicus	214-218
16094491-15	2005	In conclusion, IL-1betamay contribute to heatstroke through inducing iNOS, which attenuates the tone of peripheral blood vessel, and pretreatment with aspirin can provide preventive effects against heatstroke and reinforce the heat and fatigue endurance, which may be associated with inhibition of systemic IL-1betalevels and local iNOS levels.	Aspirin	151-158	nitric oxide synthase 2	Rattus norvegicus	332-336
15987633-0	2005	Aspirin inhibits NF-kappaB activation in a glycolysis-depleted lung epithelial cell line.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	17-26
15987633-6	2005	Interestingly, aspirin-induced inhibition of NF-kappaB activity was greater in transfectants with restricted glycolysis than in control cells.	Aspirin	15-22	nuclear factor kappa B subunit 1	Homo sapiens	45-54
15987633-7	2005	Our results indicate that aspirin is a suitable complement to therapy based on glycolysis restriction to overcome resistance associated with increased NF-kappaB activity and oxidative stress.	Aspirin	26-33	nuclear factor kappa B subunit 1	Homo sapiens	151-160
16015412-2	2005	Aspirin also inhibits thrombin generation (TG) in platelet-rich plasma (PRP) activated by sodium arachidonate (AA).	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	22-30
16015412-2	2005	Aspirin also inhibits thrombin generation (TG) in platelet-rich plasma (PRP) activated by sodium arachidonate (AA).	Aspirin	0-7	complement component 4 binding protein alpha	Homo sapiens	72-75
15967068-1	2005	In some patients with chronic idiopathic urticaria (CIU), aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase 1 (COX-1) precipitate wheals and swelling.	Aspirin	58-65	prostaglandin-endoperoxide synthase 1	Homo sapiens	135-151
15967068-1	2005	In some patients with chronic idiopathic urticaria (CIU), aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase 1 (COX-1) precipitate wheals and swelling.	Aspirin	58-65	prostaglandin-endoperoxide synthase 1	Homo sapiens	153-158
15967068-3	2005	Skin reactions triggered by aspirin are associated with the inhibition of cyclooxygenase, specifically COX-1, but not COX-2, and are characterized by overproduction of cysteinyl leukotrienes (cys-LTs).	Aspirin	28-35	prostaglandin-endoperoxide synthase 1	Homo sapiens	103-108
15967068-3	2005	Skin reactions triggered by aspirin are associated with the inhibition of cyclooxygenase, specifically COX-1, but not COX-2, and are characterized by overproduction of cysteinyl leukotrienes (cys-LTs).	Aspirin	28-35	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	118-123
16193661-4	2005	No sex-related differences in pharmacodynamics were observed for meloxicam, and ethoricoxib, benzofurocaine, and amison, and acetylsalicylic acid, which are the substrates predominantly for CYP3A.	Aspirin	125-145	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	190-195
16190133-3	2005	On the other hand, aspirin blocks both COX-1 and COX-2 enzymes without decreasing PGI2 but blocks TXA2 synthesis that explains its beneficial action in the prevention of coronary heart disease (CHD).	Aspirin	19-26	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	49-54
16190133-4	2005	The inhibitory action of aspirin on COX-1 and COX-2 enzymes enhances the tissue concentrations of dihomo-gamma-linolenic acid (DGLA), arachidonic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA).	Aspirin	25-32	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	46-51
15988014-4	2005	We demonstrate that the RelA component of NF-kappaB is sequestered in the nucleolus in response to the proapoptotic NF-kappaB stimuli aspirin, serum withdrawal, and UV-C radiation.	Aspirin	134-141	nuclear factor kappa B subunit 1	Homo sapiens	42-51
15817699-6	2005	Furthermore, Ang II and the AT(2) agonist increased prostaglandin E(2) (PGE(2)), which in turn mediated the increase in MMP-1, as shown by the inhibition of MMP-1 by indomethacin or aspirin.	Aspirin	182-189	angiotensinogen	Homo sapiens	13-19
15988014-4	2005	We demonstrate that the RelA component of NF-kappaB is sequestered in the nucleolus in response to the proapoptotic NF-kappaB stimuli aspirin, serum withdrawal, and UV-C radiation.	Aspirin	134-141	nuclear factor kappa B subunit 1	Homo sapiens	116-125
15988014-8	2005	Furthermore, we show that the retention of RelA in the nucleoplasm inhibits this decrease in NF-kappaB-driven transcription and blocks apoptosis induced by aspirin and UV-C radiation.	Aspirin	156-163	nuclear factor kappa B subunit 1	Homo sapiens	93-102
16012551-9	2005	By logistic regression, high age (OR 1.1; 95 % CI 1.0 - 1.2; p = 0.04) and high ASA classification (OR 6.7; 95 % CI 1.4 - 33; p = 0.02) predicted death, and high ASA classification predicted postoperative complications (OR 4.2; 95 % CI 1.7 - 10.2; p = 0.002).	Aspirin	80-83	olfactory receptor family 2 subfamily N member 1 pseudogene	Homo sapiens	100-106
15990700-2	2005	In contrast, aspirin blocks both COX-1 and COX-2 enzymes that, in turn, increases intracellular concentrations of dihomo-gamma-linolenic acid (DGLA), arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and reduced formation of eicosanoids.	Aspirin	13-20	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	43-48
16047057-0	2005	Aspirin reduces serum anti-melanocyte antibodies and soluble interleukin-2 receptors in vitiligo patients.	Aspirin	0-7	interleukin 2	Homo sapiens	61-74
16012551-9	2005	By logistic regression, high age (OR 1.1; 95 % CI 1.0 - 1.2; p = 0.04) and high ASA classification (OR 6.7; 95 % CI 1.4 - 33; p = 0.02) predicted death, and high ASA classification predicted postoperative complications (OR 4.2; 95 % CI 1.7 - 10.2; p = 0.002).	Aspirin	162-165	olfactory receptor family 2 subfamily N member 1 pseudogene	Homo sapiens	100-106
15861417-0	2005	Nuclear factor kappa B activation is a potential target for preventing pancreatic carcinoma by aspirin.	Aspirin	95-102	nuclear factor kappa B subunit 1	Homo sapiens	0-22
15861417-5	2005	RESULTS: Aspirin inhibited constitutive NF-kappaB activity in culture and, in turn, decreased the expression of the NF-kappaB downstream target gene, Cox-2, in PANC-1 or PANC-1/Puro cells, without significantly inhibiting the in vitro growth of PANC-1/Puro cells.	Aspirin	9-16	nuclear factor kappa B subunit 1	Homo sapiens	40-49
15861417-5	2005	RESULTS: Aspirin inhibited constitutive NF-kappaB activity in culture and, in turn, decreased the expression of the NF-kappaB downstream target gene, Cox-2, in PANC-1 or PANC-1/Puro cells, without significantly inhibiting the in vitro growth of PANC-1/Puro cells.	Aspirin	9-16	nuclear factor kappa B subunit 1	Homo sapiens	116-125
15861417-5	2005	RESULTS: Aspirin inhibited constitutive NF-kappaB activity in culture and, in turn, decreased the expression of the NF-kappaB downstream target gene, Cox-2, in PANC-1 or PANC-1/Puro cells, without significantly inhibiting the in vitro growth of PANC-1/Puro cells.	Aspirin	9-16	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	150-155
15861417-8	2005	CONCLUSIONS: Aspirin repressed tumor formation by PANC-1 cells in vivo in a prophylactic setting, suggesting a possible mechanism for aspirin"s preventive effect in pancreatic carcinoma through inhibition of NF-kappaB activation and a mechanistic link between inflammation and tumorigenesis.	Aspirin	13-20	nuclear factor kappa B subunit 1	Homo sapiens	208-217
15861417-8	2005	CONCLUSIONS: Aspirin repressed tumor formation by PANC-1 cells in vivo in a prophylactic setting, suggesting a possible mechanism for aspirin"s preventive effect in pancreatic carcinoma through inhibition of NF-kappaB activation and a mechanistic link between inflammation and tumorigenesis.	Aspirin	134-141	nuclear factor kappa B subunit 1	Homo sapiens	208-217
15882795-2	2005	The aim of this study was to evaluate the effect of high-level aspirin on iNOS expression in cultured rat glial cells treated with lipopolysaccharide (LPS) as pathological stimulator.	Aspirin	63-70	nitric oxide synthase 2	Rattus norvegicus	74-78
15922338-0	2005	Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in growth hormone treated animals.	Aspirin	0-7	insulin receptor substrate 1	Rattus norvegicus	43-71
15922338-2	2005	GH was observed to lead to serine phosphorylation of IRS-1, a phenomenon which was reversed by aspirin in liver, muscle and WAT in parallel with a reduction in JNK activity.	Aspirin	95-102	insulin receptor substrate 1	Rattus norvegicus	53-58
15922338-3	2005	In addition, our data show an impairment of insulin activation in the IR/IRS/PI(3)kinase pathway and a reduction in IRS-1 protein levels in rats treated with GH, which was also reversed in the animals pretreated with aspirin.	Aspirin	217-224	insulin receptor substrate 1	Rattus norvegicus	116-121
15876305-0	2005	Polymorphism of tandem repeat in promoter of 5-lipoxygenase in ASA-intolerant asthma: a positive association with airway hyperresponsiveness.	Aspirin	63-66	arachidonate 5-lipoxygenase	Homo sapiens	45-59
15876305-1	2005	BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA).	Aspirin	177-184	arachidonate 5-lipoxygenase	Homo sapiens	29-34
15876305-1	2005	BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA).	Aspirin	177-184	arachidonate 5-lipoxygenase	Homo sapiens	40-54
15876305-1	2005	BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA).	Aspirin	177-184	arachidonate 5-lipoxygenase activating protein	Homo sapiens	75-82
15876305-1	2005	BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA).	Aspirin	185-206	arachidonate 5-lipoxygenase	Homo sapiens	29-34
15876305-1	2005	BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA).	Aspirin	185-206	arachidonate 5-lipoxygenase	Homo sapiens	40-54
15876305-1	2005	BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA).	Aspirin	185-206	arachidonate 5-lipoxygenase activating protein	Homo sapiens	75-82
15876305-1	2005	BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA).	Aspirin	208-211	arachidonate 5-lipoxygenase	Homo sapiens	29-34
15876305-1	2005	BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA).	Aspirin	208-211	arachidonate 5-lipoxygenase	Homo sapiens	40-54
15876305-1	2005	BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA).	Aspirin	208-211	arachidonate 5-lipoxygenase activating protein	Homo sapiens	75-82
15986848-7	2005	Cells treated with ASA, both alone and in combination with 5-FU, demonstrated apoptotic activity with the up-regulation of Bax protein, which is consistent with 5-FU anticancer treatment.	Aspirin	19-22	BCL2 associated X, apoptosis regulator	Homo sapiens	123-126
15882795-3	2005	Using Western Blotting, we verified that aspirin enhanced LPS-induced iNOS expression and the presence of 15-deoxy-Delta(12,14)-prostaglandin (15d-PGJ2) suppressed this aspirin effect.	Aspirin	41-48	nitric oxide synthase 2	Rattus norvegicus	70-74
15882795-5	2005	These results suggest that aspirin interferes with the cross-talk of prostaglandins and NO, blocking the endogenous negative control exerted by COX products on iNOS expression.	Aspirin	27-34	nitric oxide synthase 2	Rattus norvegicus	160-164
15882795-6	2005	On the other side, aspirin seems to act directly on iNOS reducing its activity, even if it does not completely block NO release by LPS-stimulated glial cells.	Aspirin	19-26	nitric oxide synthase 2	Rattus norvegicus	52-56
15840736-3	2005	OBJECTIVE: To examine the prevalence of the PlA2 allele in patients with ACS and in subjects with or without aspirin resistance.	Aspirin	109-116	phospholipase A2 group IB	Homo sapiens	44-48
15840736-8	2005	The occurrence of the PlA2 allele was significantly higher among patients with aspirin resistance than in subjects who demonstrated an appropriate response to the drug (allele frequencies, 0.21 vs 0.14; p < 0.05).	Aspirin	79-86	phospholipase A2 group IB	Homo sapiens	22-26
15840736-9	2005	All patients homozygous for the PlA2 allele had an inadequate platelet response to aspirin.	Aspirin	83-90	phospholipase A2 group IB	Homo sapiens	32-36
15840736-11	2005	PlA2 homozygosity was associated with an inadequate response to aspirin therapy.	Aspirin	64-71	phospholipase A2 group IB	Homo sapiens	0-4
15746434-5	2005	The addition of anti-inflammatory agents pyrrolidine dithiocarbamate, pentoxifylline, aspirin, and dexamethasone could completely suppress the expression of IL-8 mRNA in fresh/sensitized lung cancer cell cocultures.	Aspirin	86-93	C-X-C motif chemokine ligand 8	Homo sapiens	157-161
15986861-13	2005	Increases in the gastric content of TNF-alpha and IL-1beta after aspirin administration were inhibited by pretreatment with rolipram.	Aspirin	65-72	tumor necrosis factor	Rattus norvegicus	36-45
15986861-13	2005	Increases in the gastric content of TNF-alpha and IL-1beta after aspirin administration were inhibited by pretreatment with rolipram.	Aspirin	65-72	interleukin 1 beta	Rattus norvegicus	50-58
15775706-6	2005	However, at doses of 200 and 300 mg/kg, ASA or ACET significantly and dose-dependently attenuated pain behavior induced by TNF-alpha, IL-1beta or IFN-gamma administered intrathecally.	Aspirin	40-43	tumor necrosis factor	Mus musculus	123-132
15851630-6	2005	Moreover, angiotensin II selectively increased cardiac cyclooxygenase-2 but not cyclooxygenase-1 expression, which was totally prevented by acetylsalicylic acid treatment.	Aspirin	140-160	angiotensinogen	Rattus norvegicus	10-24
15851630-10	2005	Although acetylsalicylic acid and salicylic acid inhibited angiotensin II-induced nuclear factor kappaB (NF-kappaB) activation, nimesulide did not modify NF-kappaB activation.	Aspirin	9-29	angiotensinogen	Rattus norvegicus	59-73
15775706-6	2005	However, at doses of 200 and 300 mg/kg, ASA or ACET significantly and dose-dependently attenuated pain behavior induced by TNF-alpha, IL-1beta or IFN-gamma administered intrathecally.	Aspirin	40-43	interleukin 1 beta	Mus musculus	134-142
15775706-6	2005	However, at doses of 200 and 300 mg/kg, ASA or ACET significantly and dose-dependently attenuated pain behavior induced by TNF-alpha, IL-1beta or IFN-gamma administered intrathecally.	Aspirin	40-43	interferon gamma	Mus musculus	146-155
15775706-7	2005	Our results suggest that orally administered ASA and ACET produce antinociception by inhibiting the nociceptive action of TNF-alpha, IL-1beta or IFN-gamma administered intrathecally.	Aspirin	45-48	tumor necrosis factor	Mus musculus	122-131
15775706-7	2005	Our results suggest that orally administered ASA and ACET produce antinociception by inhibiting the nociceptive action of TNF-alpha, IL-1beta or IFN-gamma administered intrathecally.	Aspirin	45-48	interleukin 1 beta	Mus musculus	133-141
15775706-7	2005	Our results suggest that orally administered ASA and ACET produce antinociception by inhibiting the nociceptive action of TNF-alpha, IL-1beta or IFN-gamma administered intrathecally.	Aspirin	45-48	interferon gamma	Mus musculus	145-154
15870671-1	2005	OBJECTIVE: To evaluate the use of tumor necrosis factor (TNF)-alpha blockade for treatment of patients with Kawasaki syndrome (KS) who fail to become afebrile or who experience persistent arthritis after treatment with intravenous gamma globulin (IVIG) and high-dose aspirin.	Aspirin	267-274	tumor necrosis factor	Homo sapiens	34-67
15894964-3	2005	We investigated whether (a) cigarette smoking is linked to increased cytokine production, which may mediate platelet activation and thrombin generation in chronic coronary artery disease (CAD), and (b) aspirin treatment inhibits smoking-related changes on cytokines, platelets, and thrombin.	Aspirin	202-209	coagulation factor II, thrombin	Homo sapiens	132-140
15894964-3	2005	We investigated whether (a) cigarette smoking is linked to increased cytokine production, which may mediate platelet activation and thrombin generation in chronic coronary artery disease (CAD), and (b) aspirin treatment inhibits smoking-related changes on cytokines, platelets, and thrombin.	Aspirin	202-209	coagulation factor II, thrombin	Homo sapiens	282-290
15811906-1	2005	OBJECTIVE: To report the probable association of angioedema with aspirin therapy and the selective cyclooxygenase-2 (COX-2) inhibitor rofecoxib.	Aspirin	65-72	prostaglandin-endoperoxide synthase 2	Homo sapiens	99-115
15811906-1	2005	OBJECTIVE: To report the probable association of angioedema with aspirin therapy and the selective cyclooxygenase-2 (COX-2) inhibitor rofecoxib.	Aspirin	65-72	prostaglandin-endoperoxide synthase 2	Homo sapiens	117-122
15811906-8	2005	With skin testing and oral rechallenge with aspirin, but not rofecoxib, the allergist determined the cause of the reactions to be aspirin-induced angioedema and selective COX-2 inhibitor intolerance.	Aspirin	44-51	prostaglandin-endoperoxide synthase 2	Homo sapiens	171-176
15811906-11	2005	There are reports of both tolerance and intolerance to selective COX-2 inhibitors in patients with documented allergy-like reactions to aspirin and NSAIDs.	Aspirin	136-143	prostaglandin-endoperoxide synthase 2	Homo sapiens	65-70
15811906-12	2005	CONCLUSIONS: Patients with aspirin and NSAID intolerance may develop intolerance to COX-2 inhibitors, especially with repeated exposure.	Aspirin	27-34	prostaglandin-endoperoxide synthase 2	Homo sapiens	84-89
15806298-0	2005	Aspirin blocks binding of photosensitizer SnET2 into human serum albumin: implications for photodynamic therapy.	Aspirin	0-7	albumin	Homo sapiens	59-72
15681294-5	2005	Recent advances in control of COX-2 transcription by aspirin and salicylate and by a cell cycle-dependent endogenous mechanism are described.	Aspirin	53-60	prostaglandin-endoperoxide synthase 2	Homo sapiens	30-35
15787606-2	2005	It is well documented that insulin sensitizers such as peroxisome-proliferator-activated receptor gamma agonists and aspirin improve insulin action in vivo.	Aspirin	117-124	insulin	Homo sapiens	27-34
15763541-0	2005	Dual effects of acetylsalicylic acid on mast cell degranulation, expression of cyclooxygenase-2 and release of pro-inflammatory cytokines.	Aspirin	16-36	prostaglandin-endoperoxide synthase 2	Homo sapiens	79-95
15763541-4	2005	ASA blocked the expression of cyclooxygenase-2, the production of tumor necrosis factor-alpha and interleukin-6, and the release of granule mediators from mast cells in a concentration-dependent fashion.	Aspirin	0-3	prostaglandin-endoperoxide synthase 2	Homo sapiens	30-46
15763541-4	2005	ASA blocked the expression of cyclooxygenase-2, the production of tumor necrosis factor-alpha and interleukin-6, and the release of granule mediators from mast cells in a concentration-dependent fashion.	Aspirin	0-3	tumor necrosis factor	Homo sapiens	66-93
15763541-4	2005	ASA blocked the expression of cyclooxygenase-2, the production of tumor necrosis factor-alpha and interleukin-6, and the release of granule mediators from mast cells in a concentration-dependent fashion.	Aspirin	0-3	interleukin 6	Homo sapiens	98-111
15763541-5	2005	Concomitantly, ASA inhibited nuclear factor (NF)-kappaB activity, as well as the phosphorylation and breakdown of the inhibitory protein IkappaB-alpha.	Aspirin	15-18	NFKB inhibitor alpha	Homo sapiens	137-150
15763541-6	2005	We thus propose that the anti-inflammatory effects of ASA in mast cells are due to suppression of IkappaB kinase activity, thereby inhibiting subsequent phosphorylation and degradation of IkappaB-alpha, activation of NF-kappaB, and transcription of proinflammatory cytokines.	Aspirin	54-57	NFKB inhibitor alpha	Homo sapiens	188-201
15763541-6	2005	We thus propose that the anti-inflammatory effects of ASA in mast cells are due to suppression of IkappaB kinase activity, thereby inhibiting subsequent phosphorylation and degradation of IkappaB-alpha, activation of NF-kappaB, and transcription of proinflammatory cytokines.	Aspirin	54-57	nuclear factor kappa B subunit 1	Homo sapiens	217-226
15763541-8	2005	Interestingly, the expression of cyclooxygenase-2 was not inhibited at 1mM ASA, but was even enhanced significantly.	Aspirin	75-78	prostaglandin-endoperoxide synthase 2	Homo sapiens	33-49
15546949-7	2005	Src family tyrosine kinase inhibitors also inhibited platelet aggregation and decreased the PAC-1 binding caused by costimulation of G(i) and G(z) signaling pathways in aspirin-treated platelets.	Aspirin	169-176	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	0-3
15769457-0	2005	Aspirin increases CD36, SR-BI, and ABCA1 expression in human THP-1 macrophages.	Aspirin	0-7	GLI family zinc finger 2	Homo sapiens	61-66
15769457-9	2005	CONCLUSIONS: Aspirin produces an increase of CD36 expression in THP-1 macrophages by a PGE(2)-dependent mechanism.	Aspirin	13-20	GLI family zinc finger 2	Homo sapiens	64-69
15762873-12	2005	The influence of aspirin on biochemical pathways induced by IFN-gamma may represent an important part of its broad pharmacological effect.	Aspirin	17-24	interferon gamma	Homo sapiens	60-69
15741988-2	2005	The preventing effect of aspirin and nonsteroidal anti-inflammatory drugs is partly due to inhibition of the COX-2 enzyme.	Aspirin	25-32	prostaglandin-endoperoxide synthase 2	Homo sapiens	109-114
15756426-0	2005	Aspirin, ibuprofen, and other non-steroidal anti-inflammatory drugs in cancer prevention: a critical review of non-selective COX-2 blockade (review).	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	125-130
15811890-9	2005	NSAIDs with or without aspirin use are still associated with a significant risk of upper gastrointestinal bleeding in the era of cyclo-oxygenase 2 selective agents.	Aspirin	23-30	prostaglandin-endoperoxide synthase 2	Homo sapiens	129-146
15770215-0	2005	Aspirin-induced nuclear translocation of NFkappaB and apoptosis in colorectal cancer is independent of p53 status and DNA mismatch repair proficiency.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	41-49
15770215-0	2005	Aspirin-induced nuclear translocation of NFkappaB and apoptosis in colorectal cancer is independent of p53 status and DNA mismatch repair proficiency.	Aspirin	0-7	tumor protein p53	Homo sapiens	103-106
15770215-3	2005	We previously reported that aspirin induces signal-specific IkappaBalpha degradation followed by NFkappaB nuclear translocation in CRC cells, and that this mechanism contributes substantially to aspirin-induced apoptosis.	Aspirin	28-35	NFKB inhibitor alpha	Homo sapiens	60-72
15770215-3	2005	We previously reported that aspirin induces signal-specific IkappaBalpha degradation followed by NFkappaB nuclear translocation in CRC cells, and that this mechanism contributes substantially to aspirin-induced apoptosis.	Aspirin	28-35	nuclear factor kappa B subunit 1	Homo sapiens	97-105
15770215-4	2005	We have also reported the relative specificity of this aspirin-induced NFkappaB-dependent apoptotic effect for CRC cells, in comparison to other cancer cell types.	Aspirin	55-62	nuclear factor kappa B subunit 1	Homo sapiens	71-79
15770215-5	2005	It is now important to establish whether there is heterogeneity within CRC, with respect to the effects of aspirin on the NFkappaB pathway and apoptosis.	Aspirin	107-114	nuclear factor kappa B subunit 1	Homo sapiens	122-130
15770215-8	2005	Here, we set out to determine the p53 and hMLH1 dependency of the effects of aspirin on NFkappaB signalling and apoptosis in CRC.	Aspirin	77-84	tumor protein p53	Homo sapiens	34-37
15770215-8	2005	Here, we set out to determine the p53 and hMLH1 dependency of the effects of aspirin on NFkappaB signalling and apoptosis in CRC.	Aspirin	77-84	nuclear factor kappa B subunit 1	Homo sapiens	88-96
15770215-10	2005	We found that aspirin treatment induced apoptosis following IkappaBalpha degradation, NFkappaB nuclear translocation and repression of NFkappaB-driven transcription, irrespective of p53 and DNA MMR status.	Aspirin	14-21	NFKB inhibitor alpha	Homo sapiens	60-72
15770215-10	2005	We found that aspirin treatment induced apoptosis following IkappaBalpha degradation, NFkappaB nuclear translocation and repression of NFkappaB-driven transcription, irrespective of p53 and DNA MMR status.	Aspirin	14-21	nuclear factor kappa B subunit 1	Homo sapiens	86-94
15770215-10	2005	We found that aspirin treatment induced apoptosis following IkappaBalpha degradation, NFkappaB nuclear translocation and repression of NFkappaB-driven transcription, irrespective of p53 and DNA MMR status.	Aspirin	14-21	nuclear factor kappa B subunit 1	Homo sapiens	135-143
15928593-7	2005	Apart from the inhibition of prostanoid synthesis aspirin shows a variety of pharmacological activities, including reduction of ATP storage pools, increased extracellular adenosine, lowered inducible nitric oxide synthase activity, modulation of mitogen-activated protein kinases, and the expression of a plethora of genes induced under conditions of cell stress via the regulation of transcription factor NFkappaB activity.	Aspirin	50-57	nuclear factor kappa B subunit 1	Homo sapiens	406-414
15786540-5	2005	This mutation, which might be arising from deamination of methylated cytosine in CpG dinucleotide of codon 116 (CGT>TGT), was also detected by the ASA method in the two affected members and a proband"s brother but was not observed in unaffected members and 54 normal control subjects.	Aspirin	150-153	queuine tRNA-ribosyltransferase catalytic subunit 1	Homo sapiens	119-122
15921208-1	2005	BACKGROUND: Cyclooxygenase 1 (Cox-1) plays a key role in arachidonic acid metabolism and in the pathophysiology and immunology of nasal polyposis in patients suffering from aspirin intolerance.	Aspirin	173-180	prostaglandin-endoperoxide synthase 1	Homo sapiens	12-28
15921208-1	2005	BACKGROUND: Cyclooxygenase 1 (Cox-1) plays a key role in arachidonic acid metabolism and in the pathophysiology and immunology of nasal polyposis in patients suffering from aspirin intolerance.	Aspirin	173-180	prostaglandin-endoperoxide synthase 1	Homo sapiens	30-35
15921208-2	2005	We hypothesize that Cox-2 also might be relevant in the etiology of nasal polyps of aspirin-tolerant patients by their effects on inflammatory mediators as well as on microvascular permeability.	Aspirin	84-91	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	20-25
15579484-0	2005	Activation of the caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric cancer.	Aspirin	52-59	BH3 interacting domain death agonist	Homo sapiens	28-31
15579484-0	2005	Activation of the caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric cancer.	Aspirin	52-59	BCL2 associated X, apoptosis regulator	Homo sapiens	36-39
15579484-7	2005	We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release.	Aspirin	15-22	BH3 interacting domain death agonist	Homo sapiens	93-96
15579484-7	2005	We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release.	Aspirin	15-22	BCL2 associated X, apoptosis regulator	Homo sapiens	154-157
15579484-7	2005	We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release.	Aspirin	15-22	cytochrome c, somatic	Homo sapiens	162-174
15579484-10	2005	In conclusion, our results identify a role of caspase-8/Bid and activation of Bax as a novel mechanism for aspirin-induced apoptosis in gastric cancer.	Aspirin	107-114	BH3 interacting domain death agonist	Homo sapiens	56-59
15579484-10	2005	In conclusion, our results identify a role of caspase-8/Bid and activation of Bax as a novel mechanism for aspirin-induced apoptosis in gastric cancer.	Aspirin	107-114	BCL2 associated X, apoptosis regulator	Homo sapiens	78-81
15767339-10	2005	These data suggest that COX-2 expression or activity may be beneficially suppressed, and risk of colorectal polyps reduced, by aspirin or other NSAIDs in PTGS2 -765GG (wild type) individuals and by the -765 CC variant genotype in nonusers of NSAIDs.	Aspirin	127-134	prostaglandin-endoperoxide synthase 2	Homo sapiens	24-29
15767339-10	2005	These data suggest that COX-2 expression or activity may be beneficially suppressed, and risk of colorectal polyps reduced, by aspirin or other NSAIDs in PTGS2 -765GG (wild type) individuals and by the -765 CC variant genotype in nonusers of NSAIDs.	Aspirin	127-134	prostaglandin-endoperoxide synthase 2	Homo sapiens	154-159
15784113-0	2005	The human leucocyte antigen-DRB1*1302-DQB1*0609-DPB1*0201 haplotype may be a strong genetic marker for aspirin-induced urticaria.	Aspirin	103-110	major histocompatibility complex, class II, DR beta 1	Homo sapiens	4-32
15784113-2	2005	OBJECTIVE: In order to uncover the genetic mechanism, we studied the associations of the human leucocyte antigen (HLA) genotypes in patients with aspirin-induced urticaria compared with aspirin-intolerant asthma and normal control in a Korean population.	Aspirin	146-153	major histocompatibility complex, class II, DR beta 1	Homo sapiens	114-117
15784113-7	2005	In haplotype analysis, the HLA-DRB1(*)1302-DQB1(*)0609-DPB1(*)0201 was significantly higher in the aspirin-induced urticaria (8.0%) than in the aspirin-intolerant asthma (0.7%, P=0.0014) and normal controls (2.0%, P=0.0006).	Aspirin	99-106	major histocompatibility complex, class II, DR beta 1	Homo sapiens	27-35
15784113-8	2005	CONCLUSION: These findings suggest that the HLA-DRB1(*)1302-DQB1(*)0609-DPB1(*)0201 may be a strong genetic marker to determine the aspirin-induced urticaria phenotype.	Aspirin	132-139	major histocompatibility complex, class II, DR beta 1	Homo sapiens	44-52
15796213-3	2005	The data indicated that there was decreased NAT activity associated with increased acetylsalicylic acid in the cytosol reaction.	Aspirin	83-103	N-acetyltransferase 1	Rattus norvegicus	44-47
15796213-6	2005	This is the first demonstration of acetylsalicylic acid (Aspirin) inhibition of arylamine N-acetyltransferase activity showing decreases in the N-acetylation of carcinogens in vivo.	Aspirin	35-55	N-acetyltransferase 1	Rattus norvegicus	90-109
15796213-6	2005	This is the first demonstration of acetylsalicylic acid (Aspirin) inhibition of arylamine N-acetyltransferase activity showing decreases in the N-acetylation of carcinogens in vivo.	Aspirin	57-64	N-acetyltransferase 1	Rattus norvegicus	90-109
15787606-2	2005	It is well documented that insulin sensitizers such as peroxisome-proliferator-activated receptor gamma agonists and aspirin improve insulin action in vivo.	Aspirin	117-124	insulin	Homo sapiens	133-140
15746562-4	2005	In this study we wanted to test the impact of the most commonly used anti-inflammatory drugs (acetylsalicylate and prednisolone) on the microglia activation pattern, the rate of caspase-3-dependent photoreceptor apoptosis and the course of the degeneration in the retinal degeneration slow (rds) mouse retina.	Aspirin	94-110	peripherin 2	Mus musculus	264-289
15746562-4	2005	In this study we wanted to test the impact of the most commonly used anti-inflammatory drugs (acetylsalicylate and prednisolone) on the microglia activation pattern, the rate of caspase-3-dependent photoreceptor apoptosis and the course of the degeneration in the retinal degeneration slow (rds) mouse retina.	Aspirin	94-110	peripherin 2	Mus musculus	291-294
15696087-0	2005	Expression of the cysteinyl leukotriene receptors cysLT(1) and cysLT(2) in aspirin-sensitive and aspirin-tolerant chronic rhinosinusitis.	Aspirin	75-82	cysteinyl leukotriene receptor 1	Homo sapiens	50-58
15696570-1	2005	OBJECTIVE: To evaluate the effects of cardiovascular comorbidities and aspirin coprescription on cyclooxygenase (COX)-2 inhibitor (coxib) prescribing patterns among rheumatologists.	Aspirin	71-78	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	97-119
15677512-10	2005	The inverse association between adiponectin and CHD was consistent across strata of aspirin use, family history of myocardial infarction, alcohol consumption, insulin use, duration of diabetes, and levels of HbA(1c), triglycerides, C-reactive protein, and HDL cholesterol.	Aspirin	84-91	adiponectin, C1Q and collagen domain containing	Homo sapiens	32-43
15696087-0	2005	Expression of the cysteinyl leukotriene receptors cysLT(1) and cysLT(2) in aspirin-sensitive and aspirin-tolerant chronic rhinosinusitis.	Aspirin	97-104	cysteinyl leukotriene receptor 1	Homo sapiens	50-58
15696087-3	2005	We previously compared expression of cysLT 1 on mucosal leukocytes in patients with aspirin-sensitive and aspirin-tolerant rhinosinusitis.	Aspirin	84-91	cysteinyl leukotriene receptor 1	Homo sapiens	37-44
15696087-3	2005	We previously compared expression of cysLT 1 on mucosal leukocytes in patients with aspirin-sensitive and aspirin-tolerant rhinosinusitis.	Aspirin	106-113	cysteinyl leukotriene receptor 1	Homo sapiens	37-44
15696087-4	2005	OBJECTIVE: To compare expression of cysLT 1 and cysLT 2 on leukocytes, mucus glands, and epithelium in 32 patients with chronic polypoid rhinosinusitis (21 aspirin-sensitive, 11 aspirin-tolerant) and 9 normal controls.	Aspirin	156-163	cysteinyl leukotriene receptor 1	Homo sapiens	36-43
15696087-6	2005	RESULTS: The percentages of mucosal CD45 + leukocytes expressing cysLT 1 were significantly ( P < .0001) elevated in the aspirin-sensitive but not the aspirin-tolerant patients compared with the controls.	Aspirin	124-131	cysteinyl leukotriene receptor 1	Homo sapiens	65-72
15696087-9	2005	CONCLUSION: Although cysLT 1 expression predominates on inflammatory leukocytes in patients with aspirin-sensitive rhinosinusitis, the effects of cysteinyl leukotrienes on glands and epithelium may be mediated predominantly through cysLT 2.	Aspirin	97-104	cysteinyl leukotriene receptor 1	Homo sapiens	21-28
15767245-7	2005	Concurrent administration of aspirin and other drugs that are metabolized through or are inhibitors of the CYP system may have enhanced the interaction that occurred in this patient.	Aspirin	29-36	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	107-110
15823962-0	2005	Aspirin induces its anti-inflammatory effects through its specific binding to phospholipase A2: crystal structure of the complex formed between phospholipase A2 and aspirin at 1.9 angstroms resolution.	Aspirin	0-7	phospholipase A2 group IB	Homo sapiens	78-94
15823962-0	2005	Aspirin induces its anti-inflammatory effects through its specific binding to phospholipase A2: crystal structure of the complex formed between phospholipase A2 and aspirin at 1.9 angstroms resolution.	Aspirin	0-7	phospholipase A2 group IB	Homo sapiens	144-160
15823962-0	2005	Aspirin induces its anti-inflammatory effects through its specific binding to phospholipase A2: crystal structure of the complex formed between phospholipase A2 and aspirin at 1.9 angstroms resolution.	Aspirin	165-172	phospholipase A2 group IB	Homo sapiens	78-94
15823962-0	2005	Aspirin induces its anti-inflammatory effects through its specific binding to phospholipase A2: crystal structure of the complex formed between phospholipase A2 and aspirin at 1.9 angstroms resolution.	Aspirin	165-172	phospholipase A2 group IB	Homo sapiens	144-160
15823962-2	2005	In order to determine the involvement of phospholipase A2 in the action of non-steroidal anti-inflammatory drugs (NSAIDs), the crystal structure of the complex formed between phospholipase A2 and aspirin has been determined at 1.9 angstroms resolution.	Aspirin	196-203	phospholipase A2 group IB	Homo sapiens	41-57
15823962-2	2005	In order to determine the involvement of phospholipase A2 in the action of non-steroidal anti-inflammatory drugs (NSAIDs), the crystal structure of the complex formed between phospholipase A2 and aspirin has been determined at 1.9 angstroms resolution.	Aspirin	196-203	phospholipase A2 group IB	Homo sapiens	175-191
15604423-11	2005	Moreover, the Cox-2 -765C variant displayed a slightly higher reduction in 11-dTxB2 level on treatment with aspirin.	Aspirin	108-115	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	14-19
15345481-5	2005	Inhibition of COX-2 by acetyl salicylic acid (1 mM), NS-398 (5 microM), or celecoxib (3 microM) abolished the increase in cAMP and markedly reduced alpha(2C)-AR induction in response to serum stimulation.	Aspirin	23-44	prostaglandin-endoperoxide synthase 2	Homo sapiens	14-19
15567157-4	2005	The para isomer of NO-ASA degraded beta-catenin in a dose- and time-dependent manner coinciding with increasing expression of activated caspase-3.	Aspirin	22-25	caspase 3	Homo sapiens	136-145
16168077-4	2005	However, some or all of the gastrointestinal benefit of COX-2 inhibitors may be lost in patients who receive low, cardioprotective doses of aspirin, and recent evidence suggests that some of these agents, at some doses, may be associated with an increased risk for cardiovascular adverse events compared with no therapy.	Aspirin	140-147	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	56-61
15650548-6	2005	When 0.4 IU/ml thrombin was used in samples provided by 10 healthy individuals treated with acetysalicylic acid, Ks levels were increased during versus before therapy.	Aspirin	92-111	coagulation factor II, thrombin	Homo sapiens	15-23
15892673-4	2005	Non-selective cyclooxygenase-1 (COX-1) inhibitors used in periodontal research include compounds such as aspirin, flurbiprofen, ibuprofen, naproxen and piroxicam.	Aspirin	105-112	prostaglandin-endoperoxide synthase 1	Homo sapiens	14-30
15702860-9	2005	The intake of aspirin by patients infected with H. pylori was associated with marked rise in the expression of HD5 and less expression of secretory leukocyte protease inhibitor.	Aspirin	14-21	defensin alpha 5	Homo sapiens	111-114
15813652-3	2005	COX-2 inhibitors increase the risk of serious gastroduodenal adverse reactions but there is evidence that they carry a lower risk for these adverse effects than standard NSAIDs, except when there is concurrent aspirin use.	Aspirin	210-217	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
16491523-0	2005	Does aspirin attenuate the beneficial effect of ACE inhibitors in elderly people with heart failure?	Aspirin	5-12	angiotensin I converting enzyme	Homo sapiens	48-51
16491523-1	2005	BACKGROUND: Several studies have raised concerns over a possible reduction in the beneficial effects of ACE inhibitors on mortality in people also taking aspirin (acetylsalicylic acid).	Aspirin	154-161	angiotensin I converting enzyme	Homo sapiens	104-107
16491523-1	2005	BACKGROUND: Several studies have raised concerns over a possible reduction in the beneficial effects of ACE inhibitors on mortality in people also taking aspirin (acetylsalicylic acid).	Aspirin	163-183	angiotensin I converting enzyme	Homo sapiens	104-107
16491523-2	2005	OBJECTIVE: We performed this study to determine whether there is a reduction in the beneficial effects of ACE inhibitors on mortality in elderly people with heart failure also taking aspirin.	Aspirin	183-190	angiotensin I converting enzyme	Homo sapiens	106-109
16491523-8	2005	Compared with no therapy with ACE inhibitor or aspirin, the HR for death was 0.65 (95% CI 0.31, 1.36) for aspirin users, 0.45 (95% CI 0.27, 0.74) for ACE inhibitor users and 0.37 (95% CI 0.19, 0.70) for ACE inhibitor/aspirin users.	Aspirin	106-113	angiotensin I converting enzyme	Homo sapiens	30-33
16491523-8	2005	Compared with no therapy with ACE inhibitor or aspirin, the HR for death was 0.65 (95% CI 0.31, 1.36) for aspirin users, 0.45 (95% CI 0.27, 0.74) for ACE inhibitor users and 0.37 (95% CI 0.19, 0.70) for ACE inhibitor/aspirin users.	Aspirin	106-113	angiotensin I converting enzyme	Homo sapiens	30-33
15650548-7	2005	Since almost no thrombin generation was found in the samples with the higher dose of exogenous thrombin, we considered that modifications in fibrinogen clotting property by acetysalicylic acid rendered the fibrin network more permeable.	Aspirin	173-192	coagulation factor II, thrombin	Homo sapiens	95-103
15576654-0	2005	Concurrent treatment with renin-angiotensin system blockers and acetylsalicylic acid reduces nuclear factor kappaB activation and C-reactive protein expression in human carotid artery plaques.	Aspirin	64-84	nuclear factor kappa B subunit 1	Homo sapiens	93-114
16201293-9	2005	The hospital stay (days), defervescence time, total fever duration, platelet count, erythrocyte sedimentation rate and C reactive protein were significantly reduced in IVIG+ ASA group as compared with those in the ASA group (P<0.05).	Aspirin	174-177	C-reactive protein	Homo sapiens	119-137
15576654-0	2005	Concurrent treatment with renin-angiotensin system blockers and acetylsalicylic acid reduces nuclear factor kappaB activation and C-reactive protein expression in human carotid artery plaques.	Aspirin	64-84	C-reactive protein	Homo sapiens	130-148
15576654-2	2005	We hypothesized that the combination of RAS blockers (RASb) and ASA reduces NFkappaB and CRP within atherosclerotic plaques.	Aspirin	64-67	nuclear factor kappa B subunit 1	Homo sapiens	76-84
15576654-2	2005	We hypothesized that the combination of RAS blockers (RASb) and ASA reduces NFkappaB and CRP within atherosclerotic plaques.	Aspirin	64-67	C-reactive protein	Homo sapiens	89-92
15489888-1	2004	Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin have been shown to suppress transcription factor NF-kappaB, which controls the expression of genes such as cyclooxygenase (COX)-2 and cyclin D1, leading to inhibition of proliferation of tumor cells.	Aspirin	54-61	nuclear factor kappa B subunit 1	Homo sapiens	111-120
16181986-2	2005	The present study was performed to extend the dose-response curve for effects of ASA on fibrinogen clotting properties and to examine the variability of these effects during a 24-h dose interval.	Aspirin	81-84	fibrinogen beta chain	Homo sapiens	88-98
16137190-13	2005	When patients with AIA need aspirin for specific situations they should receive aspirin desensitization therapy or treatment with selective cyclo-oxygenase 2 inhibitors.	Aspirin	28-35	prostaglandin-endoperoxide synthase 2	Homo sapiens	140-157
15613671-7	2004	Aspirin sensitivity is most often manifested as rhinitis and asthma or urticaria/angioedema induced by cross-reacting nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase 1.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	168-184
15489888-1	2004	Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin have been shown to suppress transcription factor NF-kappaB, which controls the expression of genes such as cyclooxygenase (COX)-2 and cyclin D1, leading to inhibition of proliferation of tumor cells.	Aspirin	54-61	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	169-191
15563357-6	2004	Final results of the celecoxib outcome study (CLASS study) attenuated the initial enthusiasm about the GI safety of selective COX-2 inhibitors, especially in patients concomitantly taking aspirin for cardiovascular prophylaxis.	Aspirin	188-195	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	126-131
16415488-3	2005	Traditional nonsteroidal antiinflammatory drugs (tNSAIDs) and COX-2 inhibitors (coxibs) give rise to antipyretic, analgesic, and antiinflammatory actions, through their reversible clogging of the COX channel of COX-2 - apart from aspirin which modifies irreversibly the catalytic activity of COX-2.	Aspirin	230-237	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	62-67
15569408-6	2004	Aspirin inhibited the increased level of MDA and TNF-alpha induced by LDL.	Aspirin	0-7	tumor necrosis factor	Rattus norvegicus	49-58
15546508-3	2004	ASA and indomethacin triggered apoptosis in cells of all three lines through release of cytosolic cytochrome c, activation of caspase-9 and-3, and cleavage of poly(ADP-ribose) polymerase (PARP), but NS398 induced minimal apoptosis only in Ishikawa cells.	Aspirin	0-3	cytochrome c, somatic	Homo sapiens	98-110
15556053-1	2004	BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAID) or high doses of aspirin (acetylsalicylic acid) can exert detrimental effects on renal function and counteract the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in patients with congestive heart failure.	Aspirin	75-82	angiotensin I converting enzyme	Homo sapiens	195-224
15556053-1	2004	BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAID) or high doses of aspirin (acetylsalicylic acid) can exert detrimental effects on renal function and counteract the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in patients with congestive heart failure.	Aspirin	75-82	angiotensin I converting enzyme	Homo sapiens	226-229
15556053-1	2004	BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAID) or high doses of aspirin (acetylsalicylic acid) can exert detrimental effects on renal function and counteract the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in patients with congestive heart failure.	Aspirin	84-104	angiotensin I converting enzyme	Homo sapiens	195-224
15556053-1	2004	BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAID) or high doses of aspirin (acetylsalicylic acid) can exert detrimental effects on renal function and counteract the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in patients with congestive heart failure.	Aspirin	84-104	angiotensin I converting enzyme	Homo sapiens	226-229
15556053-2	2004	AIMS: The objective of our study was to evaluate the renal effects of low dose aspirin and the NSAID diclofenac in patients with congestive heart failure treated with ACE-inhibitors.	Aspirin	79-86	angiotensin I converting enzyme	Homo sapiens	167-170
15613743-13	2004	ASA and rofecoxib, that significantly suppressed the mucosal prostaglandin (PG) E(2) generation in ulcer area, delayed significantly the rate of ulcer healing and decreased the GBF at ulcer margin, while elevating plasma IL-1beta, TNF-alpha and IL-10 concentrations in non-diabetic rats and these alterations were significantly augmented in diabetic animals.	Aspirin	0-3	interleukin 1 beta	Rattus norvegicus	221-229
15613743-13	2004	ASA and rofecoxib, that significantly suppressed the mucosal prostaglandin (PG) E(2) generation in ulcer area, delayed significantly the rate of ulcer healing and decreased the GBF at ulcer margin, while elevating plasma IL-1beta, TNF-alpha and IL-10 concentrations in non-diabetic rats and these alterations were significantly augmented in diabetic animals.	Aspirin	0-3	tumor necrosis factor	Rattus norvegicus	231-240
15613743-14	2004	In contrast to ASA, the treatment with NO-ASA failed to influence both, the ulcer healing and GBF at ulcer margin and significantly attenuated the plasma levels of IL-1beta, TNF-alpha and IL-10 as compared to those recorded in ASA- or rofecoxib-treated animals.	Aspirin	42-45	interleukin 1 beta	Rattus norvegicus	164-172
15613743-14	2004	In contrast to ASA, the treatment with NO-ASA failed to influence both, the ulcer healing and GBF at ulcer margin and significantly attenuated the plasma levels of IL-1beta, TNF-alpha and IL-10 as compared to those recorded in ASA- or rofecoxib-treated animals.	Aspirin	42-45	tumor necrosis factor	Rattus norvegicus	174-183
15613743-14	2004	In contrast to ASA, the treatment with NO-ASA failed to influence both, the ulcer healing and GBF at ulcer margin and significantly attenuated the plasma levels of IL-1beta, TNF-alpha and IL-10 as compared to those recorded in ASA- or rofecoxib-treated animals.	Aspirin	42-45	interleukin 1 beta	Rattus norvegicus	164-172
15613743-14	2004	In contrast to ASA, the treatment with NO-ASA failed to influence both, the ulcer healing and GBF at ulcer margin and significantly attenuated the plasma levels of IL-1beta, TNF-alpha and IL-10 as compared to those recorded in ASA- or rofecoxib-treated animals.	Aspirin	42-45	tumor necrosis factor	Rattus norvegicus	174-183
15546508-3	2004	ASA and indomethacin triggered apoptosis in cells of all three lines through release of cytosolic cytochrome c, activation of caspase-9 and-3, and cleavage of poly(ADP-ribose) polymerase (PARP), but NS398 induced minimal apoptosis only in Ishikawa cells.	Aspirin	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	159-186
15546508-3	2004	ASA and indomethacin triggered apoptosis in cells of all three lines through release of cytosolic cytochrome c, activation of caspase-9 and-3, and cleavage of poly(ADP-ribose) polymerase (PARP), but NS398 induced minimal apoptosis only in Ishikawa cells.	Aspirin	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	188-192
15546508-5	2004	Both ASA and indomethacin reduced the protein levels of Bcl-2 and Bcl-xl, but upregulated those of Bax and Bcl-xs.	Aspirin	5-8	BCL2 apoptosis regulator	Homo sapiens	56-61
15546508-5	2004	Both ASA and indomethacin reduced the protein levels of Bcl-2 and Bcl-xl, but upregulated those of Bax and Bcl-xs.	Aspirin	5-8	BCL2 like 1	Homo sapiens	66-72
15546508-5	2004	Both ASA and indomethacin reduced the protein levels of Bcl-2 and Bcl-xl, but upregulated those of Bax and Bcl-xs.	Aspirin	5-8	BCL2 associated X, apoptosis regulator	Homo sapiens	99-102
15546508-6	2004	COX-2 protein expression and PGE(2) production were upregulated by ASA and indomethacin in all three cell lines.	Aspirin	67-70	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
15550024-7	2004	Aspirin and clopidogrel were thus found to have similar effects on thrombotic variables and CRP in this patient population.	Aspirin	0-7	C-reactive protein	Homo sapiens	92-95
15544595-3	2004	We hypothesized that this polymorphism, which may result in decreased COX-2 transcription, could be associated with more severe asthma, and/or aspirin-intolerant asthma (AIA).	Aspirin	143-150	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	70-75
15501405-11	2004	NSAIDs examined (aspirin, loxoprofen-SRS, diclofenac sodium, indomethacin and NS398) inhibited m-calpain release and production of prostaglandin E(2) (PGE(2)) induced by 10 ng/ml TNF-alpha.	Aspirin	17-24	calpain 2	Homo sapiens	95-104
15600265-11	2004	In severe kidney disease (GFR 15-29 mL/min/1.73 m2), the hazards risk for death was 0.21 (0.08, 0.53) for aspirin alone, 0.17 (0.06, 0.51) for aspirin with beta-blockers, and 0.35 (0.09, 1.42) for aspirin with beta-blockers and ace-inhibitors.	Aspirin	106-113	CD59 molecule (CD59 blood group)	Homo sapiens	39-44
15576013-7	2004	It is plausible that the COX-2 inhibition is associated with altered homeostasis that is compensated with the cardioprotection effect of COX-1 inhibition that patients receive either through the less COX-2 selectivity of other NSAIDs or through co-administration of low dose aspirin.	Aspirin	275-282	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	25-30
15576013-10	2004	However, based on some available indirect evidence, and unless more clear-cut data become available, the use of highly COX-2 selective NSAIDs without the use of a suitable COX-1 inhibitor, (e.g., low dose aspirin) may be best avoided.	Aspirin	205-212	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	119-124
15461473-2	2004	Specifically, deformations of 1,2-distearoylphosphatidylglycerol(DSPG) membranes induced by interaction with FGF-1, a SPL protein which is released asa function of cellular stress through a nonclassical pathway, have been investigated.	Aspirin	148-151	fibroblast growth factor 1	Homo sapiens	109-114
15297470-1	2004	Administration of selective and nonselective cyclooxygenase (COX)-2 inhibitors to rheumatoid arthritis patients taking low doses of acetylsalicylic acid (ASA) for cardiovascular prevention associates with increased risk of gastrointestinal bleeding.	Aspirin	132-152	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	45-67
15297470-1	2004	Administration of selective and nonselective cyclooxygenase (COX)-2 inhibitors to rheumatoid arthritis patients taking low doses of acetylsalicylic acid (ASA) for cardiovascular prevention associates with increased risk of gastrointestinal bleeding.	Aspirin	154-157	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	45-67
15521369-3	2004	Reactions to aspirin and NSAIDs in patients with AERD are largely due to inhibition of COX-1.	Aspirin	13-20	prostaglandin-endoperoxide synthase 1	Homo sapiens	87-92
15203109-0	2004	Cell cycle arrest and modulation of HO-1 expression induced by acetyl salicylic acid in hepatocarcinogenesis.	Aspirin	63-84	heme oxygenase 1	Mus musculus	36-40
15203109-10	2004	HO-1 induction (65%) provoked by DAB was diminished by ASA administration reaching lower induction levels (23%).	Aspirin	55-58	heme oxygenase 1	Mus musculus	0-4
15203109-11	2004	CONCLUSION: The deregulation of cyclin/CDK expression and the up-regulation of p21 and p27 with the administration of ASA, post-treatment of the carcinogen administration, would block the pass through out to the G0/G1 check point to permit the cells to repair their DNA and HO-1 protected the liver from reactive oxygen species produced from DAB.	Aspirin	118-121	heme oxygenase 1	Mus musculus	274-278
15480320-0	2004	Dynamics of COX-2 in nasal mucosa and nasal polyps from aspirin-tolerant and aspirin-intolerant patients with asthma.	Aspirin	56-63	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	12-17
15480320-0	2004	Dynamics of COX-2 in nasal mucosa and nasal polyps from aspirin-tolerant and aspirin-intolerant patients with asthma.	Aspirin	77-84	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	12-17
15623076-6	2004	Finally, in patients with high cardiovascular risk who should receive a COX-2 selective NSAID, the association with a low dose of acetylsalicylic acid is recommended in order to benefit of a protective antiplatelet effect.	Aspirin	130-150	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	72-77
15471166-8	2004	In the ACE group, FMD was reduced after administration of aspirin (5.3 +/- 4.2%, p<0.05).	Aspirin	58-65	angiotensin I converting enzyme	Homo sapiens	7-10
15381054-11	2004	Aggrenox was associated with a profound reduction of PAR-1 receptors, an observation that may be related to the greater clinical benefit of Aggrenox compared with Aspirin in preventing recurrent stroke.	Aspirin	163-170	coagulation factor II thrombin receptor	Homo sapiens	53-58
15289285-13	2004	Incubation of soluble eNOS for 15 min with 100 microm aspirin or acetylating aspirin analogues increased the l-[(3)H]citrulline yield by 40-80%, while salicylic acid had no effect.	Aspirin	54-61	nitric oxide synthase 3	Homo sapiens	22-26
15289285-13	2004	Incubation of soluble eNOS for 15 min with 100 microm aspirin or acetylating aspirin analogues increased the l-[(3)H]citrulline yield by 40-80%, while salicylic acid had no effect.	Aspirin	77-84	nitric oxide synthase 3	Homo sapiens	22-26
15335302-6	2004	New evidence suggests that selective COX-2 inhibitors may be tolerated in patients with aspirin-sensitive urticaria.	Aspirin	88-95	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	37-42
17043507-7	2004	Aspirin increases the risk of NSAID-related gastrointestinal bleeding in patients taking COX-2 selective inhibitors, with odds ratios ranging from 5.8 to 7.7; however, it is unknown whether this risk is greater than the risk from aspirin alone.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	89-94
15337874-2	2004	Aspirin irreversibly binds cyclooxygenase-1, thereby reducing platelet aggregation for the lifetime of each platelet.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	27-43
15300570-7	2004	Addition of a cyclooxygenase-2 (COX-2) selective inhibitor to low-dose aspirin increased ulcer incidence, to a rate not significantly less than a nonselective nonsteroidal anti-inflammatory drug (NSAID) alone.	Aspirin	71-78	prostaglandin-endoperoxide synthase 2	Homo sapiens	14-30
15300570-7	2004	Addition of a cyclooxygenase-2 (COX-2) selective inhibitor to low-dose aspirin increased ulcer incidence, to a rate not significantly less than a nonselective nonsteroidal anti-inflammatory drug (NSAID) alone.	Aspirin	71-78	prostaglandin-endoperoxide synthase 2	Homo sapiens	32-37
17043507-8	2004	The risks from both traditional NSAIDs and COX-2 inhibitors are increased in the elderly, patients on anticoagulation, and patients with prior gastrointestinal events.Gastroprotective agents have been found to significantly reduce the risk for gastrointestinal injury in patients receiving NSAID therapy, especially those receiving concurrent low-dose cardioprotective doses of aspirin.	Aspirin	378-385	prostaglandin-endoperoxide synthase 2	Homo sapiens	43-48
15240146-0	2004	Aspirin inhibits serine phosphorylation of IRS-1 in muscle and adipose tissue of septic rats.	Aspirin	0-7	insulin receptor substrate 1	Rattus norvegicus	43-48
15240146-3	2004	Sepsis was observed to lead to serine phosphorylation of IRS-1, a phenomenon which was reversed by aspirin in muscle and WAT, in parallel with a reduction in JNK activity.	Aspirin	99-106	insulin receptor substrate 1	Rattus norvegicus	57-62
15188000-3	2004	Here, we explored the hypothesis that cell-type specific effects on NF kappa B signalling are responsible for the observed differences in protection by aspirin against CRC compared to breast and gynaecological cancers.	Aspirin	152-159	nuclear factor kappa B subunit 1	Homo sapiens	68-78
15188000-5	2004	We found that aspirin induced concentration-dependent I kappa B alpha degradation, NF kappa B nuclear translocation and apoptosis in all CRC lines studied.	Aspirin	14-21	NFKB inhibitor alpha	Homo sapiens	54-69
15188000-5	2004	We found that aspirin induced concentration-dependent I kappa B alpha degradation, NF kappa B nuclear translocation and apoptosis in all CRC lines studied.	Aspirin	14-21	nuclear factor kappa B subunit 1	Homo sapiens	83-93
15188000-8	2004	Effects on NF kappa B and apoptosis were observed irrespective of COX-2 expression, or mutation status in APC, beta-catenin, p53 and DNA MMR genes, underscoring the generality of the aspirin effect on NF kappa B in CRC cells.	Aspirin	183-190	nuclear factor kappa B subunit 1	Homo sapiens	11-21
15188000-8	2004	Effects on NF kappa B and apoptosis were observed irrespective of COX-2 expression, or mutation status in APC, beta-catenin, p53 and DNA MMR genes, underscoring the generality of the aspirin effect on NF kappa B in CRC cells.	Aspirin	183-190	nuclear factor kappa B subunit 1	Homo sapiens	201-211
15219202-8	2004	Aspirin (10 mm) treatment of the cells significantly reduced the VCAM-1 response to these APLA.	Aspirin	0-7	vascular cell adhesion molecule 1	Homo sapiens	65-71
15238606-7	2004	Aspirin and 15-epi-lipoxin A(4) were shown to inhibit leukocyte trafficking in an NO-dependent manner using intravital microscopy on IL-1beta-stimulated mouse mesentery.	Aspirin	0-7	interleukin 1 beta	Mus musculus	133-141
15238606-8	2004	Not only did aspirin inhibit leukocyte-endothelial interaction in a manner similar to NO in wild-type mice but both aspirin and 15-epi-lipoxin A(4) had markedly reduced effects on leukocyte-endothelial cell adherence in eNOS- and iNOS-deficient mice compared with wild type.	Aspirin	116-123	nitric oxide synthase 2, inducible	Mus musculus	230-234
15238606-9	2004	Collectively, these data suggest that aspirin triggers the synthesis of 15-epi-lipoxin A(4), which increases NO synthesis through eNOS and iNOS.	Aspirin	38-45	nitric oxide synthase 2, inducible	Mus musculus	139-143
15213311-10	2004	Treatment of mesangial cells with LY294002 and cyclooxygenase-2 inhibitors [N-[2-(cyclohexyloxyl)-4-nitrophenyl]-methane sulfonamide (NS398) and aspirin] effectively inhibited the high glucose-induced mesangial cell proliferation.	Aspirin	145-152	prostaglandin-endoperoxide synthase 2	Homo sapiens	47-63
15157801-10	2004	Inducible NO synthase activity was reduced by 25%, 27% and 30% with triflusal, and 0%, 25% and 24% with ASA.	Aspirin	104-107	nitric oxide synthase 2	Rattus norvegicus	0-21
15213852-12	2004	Pretreatment with aspirin inhibits ERK2 activation induced by 0.1 U/ml thrombin, but has no effect at high concentrations of thrombin.	Aspirin	18-25	mitogen-activated protein kinase 1	Homo sapiens	35-39
15213852-12	2004	Pretreatment with aspirin inhibits ERK2 activation induced by 0.1 U/ml thrombin, but has no effect at high concentrations of thrombin.	Aspirin	18-25	coagulation factor II, thrombin	Homo sapiens	71-79
15188000-0	2004	Evidence for colorectal cancer cell specificity of aspirin effects on NF kappa B signalling and apoptosis.	Aspirin	51-58	nuclear factor kappa B subunit 1	Homo sapiens	70-80
15188000-2	2004	We previously reported that aspirin induces signal-specific I kappa B alpha degradation followed by NF kappa B nuclear translocation in CRC cells, and that this mechanism contributes substantially to aspirin-induced apoptosis.	Aspirin	28-35	NFKB inhibitor alpha	Homo sapiens	60-75
15188000-2	2004	We previously reported that aspirin induces signal-specific I kappa B alpha degradation followed by NF kappa B nuclear translocation in CRC cells, and that this mechanism contributes substantially to aspirin-induced apoptosis.	Aspirin	28-35	nuclear factor kappa B subunit 1	Homo sapiens	100-110
15201075-10	2004	CONCLUSION: Pretreatment with anti-inflammatory dose of aspirin can provide protection against heat stroke in rats, which may be associated with the inhibition of elevation of plasma IL-1beta levels by aspirin.	Aspirin	56-63	interleukin 1 beta	Rattus norvegicus	183-191
15136050-0	2004	Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-alpha stimulated human umbilical vein endothelial cells.	Aspirin	0-7	C-X-C motif chemokine ligand 8	Homo sapiens	56-69
15136050-0	2004	Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-alpha stimulated human umbilical vein endothelial cells.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	84-93
15136050-6	2004	In this study, we found that aspirin inhibited TNF-alpha (10 ng/ml)-induced MCP-1 and IL-8 expression at the RNA and protein levels in human umbilical vein endothelial cells (HUVECs), monocyte adhesion and transmigration, and that its inhibitory effects were not due to decreased HUVEC viability as assessed by MTT test.	Aspirin	29-36	tumor necrosis factor	Homo sapiens	47-56
15136050-6	2004	In this study, we found that aspirin inhibited TNF-alpha (10 ng/ml)-induced MCP-1 and IL-8 expression at the RNA and protein levels in human umbilical vein endothelial cells (HUVECs), monocyte adhesion and transmigration, and that its inhibitory effects were not due to decreased HUVEC viability as assessed by MTT test.	Aspirin	29-36	C-X-C motif chemokine ligand 8	Homo sapiens	86-90
15136050-7	2004	Aspirin at the dose as low as 10 microg/ml significantly inhibited the release of TNF-stimulated MCP-1 by 29.1% (P = 0.008) and IL-8 by 26.9% (P = 0.0146) as compared to TNF-stimulated release.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	82-85
15136050-7	2004	Aspirin at the dose as low as 10 microg/ml significantly inhibited the release of TNF-stimulated MCP-1 by 29.1% (P = 0.008) and IL-8 by 26.9% (P = 0.0146) as compared to TNF-stimulated release.	Aspirin	0-7	C-X-C motif chemokine ligand 8	Homo sapiens	128-132
15136050-7	2004	Aspirin at the dose as low as 10 microg/ml significantly inhibited the release of TNF-stimulated MCP-1 by 29.1% (P = 0.008) and IL-8 by 26.9% (P = 0.0146) as compared to TNF-stimulated release.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	170-173
15136050-9	2004	Furthermore, aspirin (10 microg/ml) inhibited U937 cell adhesion by a 13.4% (P = 0.0119) inhibition as compared to TNF-stimulated alone.	Aspirin	13-20	tumor necrosis factor	Homo sapiens	115-118
15136050-10	2004	Finally, at higher concentration, aspirin also inhibited U937 migration to HUVEC by 89.1% (P = 0.0475) as compared to TNF-stimulated alone.	Aspirin	34-41	tumor necrosis factor	Homo sapiens	118-121
15136050-11	2004	These results in our study suggest that aspirin inhibits TNF-alpha stimulated MCP-1 and IL-8 release in HUVECs, for its additional therapeutic effects of aspirin in causing atherosclerosis.	Aspirin	40-47	tumor necrosis factor	Homo sapiens	57-66
15136050-11	2004	These results in our study suggest that aspirin inhibits TNF-alpha stimulated MCP-1 and IL-8 release in HUVECs, for its additional therapeutic effects of aspirin in causing atherosclerosis.	Aspirin	40-47	C-X-C motif chemokine ligand 8	Homo sapiens	88-92
15136050-11	2004	These results in our study suggest that aspirin inhibits TNF-alpha stimulated MCP-1 and IL-8 release in HUVECs, for its additional therapeutic effects of aspirin in causing atherosclerosis.	Aspirin	154-161	tumor necrosis factor	Homo sapiens	57-66
15201075-10	2004	CONCLUSION: Pretreatment with anti-inflammatory dose of aspirin can provide protection against heat stroke in rats, which may be associated with the inhibition of elevation of plasma IL-1beta levels by aspirin.	Aspirin	202-209	interleukin 1 beta	Rattus norvegicus	183-191
14762100-2	2004	Acetylation of COX-2 by aspirin activates a transcellular biosynthetic pathway that switches eicosanoid biosynthesis from prostaglandin E(2) to 15-epi-lipoxin (LX)A(4) or aspirin-triggered lipoxin (ATL).	Aspirin	24-31	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	15-20
15167166-1	2004	BACKGROUND AND AIMS: Cyclooxygenase 2 (COX-2) is a target of aspirin and other non-steroidal anti-inflammatory drugs and is implicated in the pathogenesis of colorectal cancer.	Aspirin	61-68	prostaglandin-endoperoxide synthase 2	Homo sapiens	21-37
15167166-1	2004	BACKGROUND AND AIMS: Cyclooxygenase 2 (COX-2) is a target of aspirin and other non-steroidal anti-inflammatory drugs and is implicated in the pathogenesis of colorectal cancer.	Aspirin	61-68	prostaglandin-endoperoxide synthase 2	Homo sapiens	39-44
15329003-8	2004	CONCLUSIONS: According to these results the cross-reactivity between aspirin and these COX-2 inhibitors does not occur in subjects with previous respiratory pseudoallergic reactions.	Aspirin	69-76	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	87-92
14762100-2	2004	Acetylation of COX-2 by aspirin activates a transcellular biosynthetic pathway that switches eicosanoid biosynthesis from prostaglandin E(2) to 15-epi-lipoxin (LX)A(4) or aspirin-triggered lipoxin (ATL).	Aspirin	171-178	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	15-20
14762100-3	2004	Here, we demonstrate that exposure of neutrophil (PMN)/human umbilical vein endothelial cell (HUVEC) cocultures to aspirin and NCX-4016 triggers ATL formation and inhibits cell-to-cell adhesion induced by endotoxin (LPS) and interleukin (IL)-1beta by 70 to 90%.	Aspirin	115-122	interleukin 1 beta	Homo sapiens	225-247
15136366-8	2004	CONCLUSION: Patients recovering from ACS had lower levels of CRP and IL-6 at 1 month and lower CRP levels at 3 months when treated with rofecoxib plus aspirin.	Aspirin	151-158	interleukin 6	Homo sapiens	69-73
15056798-6	2004	Inhibition of mitogen-activated protein kinase kinase (MAPKK) and p38 MAPK using PD98059 (20 microM) and SB202190 (5 microM), respectively, attenuated the elevation of COX-2 protein induced by arsenite, whereas physiological concentrations of three COX-2 inhibitors (e.g., NS-398, piroxicam, and aspirin) reduced arsenite-stimulated DNA synthesis.	Aspirin	296-303	mitogen-activated protein kinase 14	Homo sapiens	66-69
15056798-6	2004	Inhibition of mitogen-activated protein kinase kinase (MAPKK) and p38 MAPK using PD98059 (20 microM) and SB202190 (5 microM), respectively, attenuated the elevation of COX-2 protein induced by arsenite, whereas physiological concentrations of three COX-2 inhibitors (e.g., NS-398, piroxicam, and aspirin) reduced arsenite-stimulated DNA synthesis.	Aspirin	296-303	prostaglandin-endoperoxide synthase 2	Homo sapiens	168-173
15346640-1	2004	The antiplatelet effect of aspirin is mostly explained by the irreversible cyclooxygenase-1 inhibition resulting in the suppression of thromboxane A2 synthesis.	Aspirin	27-34	prostaglandin-endoperoxide synthase 1	Homo sapiens	75-91
15120641-6	2004	Aspirin and rofecoxib (non-selective and selective COX-2 inhibitor, respectively) each abolished fibronectin-associated induction of MMP-2 and induced dose-dependent reductions in cellular invasiveness.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	51-56
15120641-6	2004	Aspirin and rofecoxib (non-selective and selective COX-2 inhibitor, respectively) each abolished fibronectin-associated induction of MMP-2 and induced dose-dependent reductions in cellular invasiveness.	Aspirin	0-7	fibronectin 1	Homo sapiens	97-108
15136366-8	2004	CONCLUSION: Patients recovering from ACS had lower levels of CRP and IL-6 at 1 month and lower CRP levels at 3 months when treated with rofecoxib plus aspirin.	Aspirin	151-158	C-reactive protein	Homo sapiens	95-98
15069117-10	2004	An increased concentration of plasma C-peptide was statistically significantly associated with an increased risk of colorectal cancer (relative risk [RR] for the highest versus lowest quintile of plasma C-peptide = 2.7, 95% confidence interval [CI] = 1.2 to 6.2; P(trend) =.047), after adjusting for age, smoking status, fasting, BMI, alcohol consumption, vigorous exercise, and aspirin assignment in the Physicians" Health Study.	Aspirin	379-386	insulin	Homo sapiens	37-46
15242680-4	2004	Mechanistically, NO-aspirin, the best-studied NO-NSAID, has pleiotropic effects on cell signaling (it inhibits Wnt signaling, induces nitric oxide synthase and NF-kappaB activation and induces cyclooxygenase-2 expression), and this mechanistic redundancy might be central to its mode of action against cancer.	Aspirin	20-27	prostaglandin-endoperoxide synthase 2	Homo sapiens	193-209
15853546-6	2004	C-reactive protein is readily amenable to treatment with anti-inflammatory drugs, such as aspirin and statins.	Aspirin	90-97	C-reactive protein	Homo sapiens	0-18
14963632-1	2004	The catalytic reaction of catalase was investigated, by means of a Clark oxygen sensor, in the presence of various concentrations of acetylsalicylic acid.	Aspirin	133-153	catalase	Homo sapiens	26-34
15043523-10	2004	CONCLUSIONS: In patients with increased susceptibility to gastrointestinal adverse events, a lower risk of upper gastrointestinal bleeding was observed in users of cyclo-oxygenase-2 inhibitors compared with users of other non-aspirin, non-steroidal anti-inflammatory drugs.	Aspirin	226-233	prostaglandin-endoperoxide synthase 2	Homo sapiens	164-181
15085062-8	2004	LDL-induced activation of the transcription factor NF-kappaB was inhibited by ASA, and ferritin protein was increased when endothelial cells were incubated with this drug.	Aspirin	78-81	nuclear factor kappa B subunit 1	Homo sapiens	51-60
15060414-4	2004	The phosphorylation of the cytoskeletal enzyme pp60(c-src) increased following PG stimulation, but was blunted by pre-incubation of platelets with aspirin, apyrase, and c7E3, suggesting that tyrosine kinase is important for the signal transduction of platelet aggregation.	Aspirin	147-154	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	52-57
15066917-0	2004	Aspirin, NSAIDs, and colorectal cancer: possible involvement in an insulin-related pathway.	Aspirin	0-7	insulin	Homo sapiens	67-74
15066917-3	2004	We explore the associations between aspirin/NSAIDs, the insulin-related pathway, and the risk of colorectal cancer.	Aspirin	36-43	insulin	Homo sapiens	56-63
15020512-10	2004	Aspirin may prevent transient coronary flow reductions through platelet, thrombin, and cytokine inhibition.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	73-81
15126922-0	2004	Prevention of angiotensin II-induced hypertension, cardiovascular hypertrophy and oxidative stress by acetylsalicylic acid in rats.	Aspirin	102-122	angiotensinogen	Rattus norvegicus	14-28
15126922-8	2004	Similar protective effects were observed in cultured aortic smooth muscle cells, in which increases in O2 production and [H]leucine incorporation (221 and 38%, respectively) induced by Ang II (10 mol/l) were totally prevented by concurrent incubation with ASA (10 mol/l).	Aspirin	256-259	angiotensinogen	Rattus norvegicus	185-191
15126922-12	2004	Chronic concurrent treatment with ASA was found to prevent those Ang II-induced effects on the cardiovascular system, presumably through its antioxidative properties.	Aspirin	34-37	angiotensinogen	Rattus norvegicus	65-71
14991868-5	2004	P-gp over-expression by both transient transfection and aspirin treatment in LNCaP cells showed decreased intracellular DHT accumulation, further suggesting DHT efflux is P-gp regulated.	Aspirin	56-63	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
14991868-5	2004	P-gp over-expression by both transient transfection and aspirin treatment in LNCaP cells showed decreased intracellular DHT accumulation, further suggesting DHT efflux is P-gp regulated.	Aspirin	56-63	ATP binding cassette subfamily B member 1	Homo sapiens	171-175
14725573-4	2004	In 2003, the results of studies suggest, and guidelines recommend, the careful selection of anti-inflammatory drugs - NSAIDs or selective COX-2 inhibitors (coxibs) based upon patients gastrointestinal history and use of aspirin therapy.	Aspirin	220-227	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	138-143
15144225-11	2004	COX-2 inhibitors NS398 and aspirin are capable of inhibiting the benzo[a]pyrene-induced osteoblast proliferation.	Aspirin	27-34	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
15019895-0	2004	Effect of angiotensin-converting enzyme inhibitors, beta blockers, statins, and aspirin on C-reactive protein levels in outpatients with heart failure.	Aspirin	80-87	C-reactive protein	Homo sapiens	91-109
15028355-0	2004	The case for an adverse interaction between aspirin and non-steroidal anti-inflammatory drugs: is it time to believe the hype?	Aspirin	44-51	FIC domain protein adenylyltransferase	Homo sapiens	121-125
15036249-0	2004	Aspirin inhibits TNFalpha- and IL-1-induced NF-kappaB activation and sensitizes HeLa cells to apoptosis.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	17-25
15036249-0	2004	Aspirin inhibits TNFalpha- and IL-1-induced NF-kappaB activation and sensitizes HeLa cells to apoptosis.	Aspirin	0-7	interleukin 1 beta	Homo sapiens	31-35
15036249-0	2004	Aspirin inhibits TNFalpha- and IL-1-induced NF-kappaB activation and sensitizes HeLa cells to apoptosis.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	44-53
15036249-5	2004	Our studies reveal that acetylsalicylic acid (aspirin) prevents TNFalpha- and IL-1-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	24-44	tumor necrosis factor	Homo sapiens	64-72
15036249-5	2004	Our studies reveal that acetylsalicylic acid (aspirin) prevents TNFalpha- and IL-1-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	24-44	interleukin 1 beta	Homo sapiens	78-82
15036249-5	2004	Our studies reveal that acetylsalicylic acid (aspirin) prevents TNFalpha- and IL-1-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	24-44	nuclear factor kappa B subunit 1	Homo sapiens	91-100
15036249-5	2004	Our studies reveal that acetylsalicylic acid (aspirin) prevents TNFalpha- and IL-1-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	24-44	NFKB inhibitor alpha	Homo sapiens	196-208
15036249-5	2004	Our studies reveal that acetylsalicylic acid (aspirin) prevents TNFalpha- and IL-1-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	46-53	tumor necrosis factor	Homo sapiens	64-72
15036249-5	2004	Our studies reveal that acetylsalicylic acid (aspirin) prevents TNFalpha- and IL-1-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	46-53	interleukin 1 beta	Homo sapiens	78-82
15036249-5	2004	Our studies reveal that acetylsalicylic acid (aspirin) prevents TNFalpha- and IL-1-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	46-53	nuclear factor kappa B subunit 1	Homo sapiens	91-100
15036249-5	2004	Our studies reveal that acetylsalicylic acid (aspirin) prevents TNFalpha- and IL-1-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	46-53	NFKB inhibitor alpha	Homo sapiens	196-208
15036249-6	2004	Moreover, aspirin sensitizes HeLa cells to TNFalpha-induced apoptosis.	Aspirin	10-17	tumor necrosis factor	Homo sapiens	43-51
15036249-7	2004	These results suggest that aspirin could be used to potentiate the effectiveness of TNFalpha-based therapeutic interventions in cancer treatment.	Aspirin	27-34	tumor necrosis factor	Homo sapiens	84-92
15163023-1	2004	Cyclooxygenase (COX)-2, the recently described inducible form ofcyclooxygenase, has been shown to be responsible for the inflammatory and tumorigenic effects of prostaglandins; hence the development and expanding clinical use of COX-2 selective inhibitors termed super aspirins.	Aspirin	269-277	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-22
15163023-1	2004	Cyclooxygenase (COX)-2, the recently described inducible form ofcyclooxygenase, has been shown to be responsible for the inflammatory and tumorigenic effects of prostaglandins; hence the development and expanding clinical use of COX-2 selective inhibitors termed super aspirins.	Aspirin	269-277	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	229-234
14769263-1	2004	Aspirin exacerbated respiratory disease (AERD) is an adult onset condition manifested as asthma, rhinosinusitis/nasal polyps, and sensitivity to aspirin and other cyclooxygenase-1 (Cox-1)-inhibitor nonsteroidal anti-inflammatory drugs (NSAIDs).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	163-179
14769263-1	2004	Aspirin exacerbated respiratory disease (AERD) is an adult onset condition manifested as asthma, rhinosinusitis/nasal polyps, and sensitivity to aspirin and other cyclooxygenase-1 (Cox-1)-inhibitor nonsteroidal anti-inflammatory drugs (NSAIDs).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	181-186
14996470-0	2004	Aspirin decreases vascular endothelial growth factor release during myocardial ischemia.	Aspirin	0-7	vascular endothelial growth factor A	Homo sapiens	18-52
14996470-6	2004	RESULTS: Vascular Endothelial Growth Factor levels were significantly lower in patients of the aspirin group compared to those of the non-aspirin group; 94+/-61 vs. 241+/-118 pg/ml, p=0.0003, respectively, this-despite an absence of difference in the platelet count between the groups.	Aspirin	95-102	vascular endothelial growth factor A	Homo sapiens	9-43
14996470-6	2004	RESULTS: Vascular Endothelial Growth Factor levels were significantly lower in patients of the aspirin group compared to those of the non-aspirin group; 94+/-61 vs. 241+/-118 pg/ml, p=0.0003, respectively, this-despite an absence of difference in the platelet count between the groups.	Aspirin	138-145	vascular endothelial growth factor A	Homo sapiens	9-43
14996470-11	2004	CONCLUSIONS: Aspirin treated patients have lower Vascular Endothelial Growth Factor titer levels in the perioperative course.	Aspirin	13-20	vascular endothelial growth factor A	Homo sapiens	49-83
14975599-4	2004	Aspirin and HLA-DRB1*01 were positive predictors of performance on logical memory (aspirin, p=0.04) and verbal fluency tests (HLA-DRB1*01, p=0.018), respectively.	Aspirin	0-7	major histocompatibility complex, class II, DR beta 1	Homo sapiens	126-134
14975599-4	2004	Aspirin and HLA-DRB1*01 were positive predictors of performance on logical memory (aspirin, p=0.04) and verbal fluency tests (HLA-DRB1*01, p=0.018), respectively.	Aspirin	83-90	major histocompatibility complex, class II, DR beta 1	Homo sapiens	12-20
14970279-3	2004	Aspirin may also protect against Hodgkin"s lymphoma by inhibiting transcription factor nuclear factor kappaB (NF-kappaB), which is necessary for immune function and the survival of Hodgkin"s lymphoma cells.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	102-108
14970279-3	2004	Aspirin may also protect against Hodgkin"s lymphoma by inhibiting transcription factor nuclear factor kappaB (NF-kappaB), which is necessary for immune function and the survival of Hodgkin"s lymphoma cells.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	110-119
14970279-11	2004	CONCLUSION: The inverse association between aspirin, but not other NSAIDs, and Hodgkin"s lymphoma suggests that NF-kappaB signaling may play a key role in Hodgkin"s lymphoma pathogenesis.	Aspirin	44-51	nuclear factor kappa B subunit 1	Homo sapiens	112-121
15126922-7	2004	However, concurrent treatment with ASA in Ang II-infused rats completely prevented the Ang II-induced production of O2, in addition to hypertension and cardiac hypertrophy.	Aspirin	35-38	angiotensinogen	Rattus norvegicus	42-48
15126922-7	2004	However, concurrent treatment with ASA in Ang II-infused rats completely prevented the Ang II-induced production of O2, in addition to hypertension and cardiac hypertrophy.	Aspirin	35-38	angiotensinogen	Rattus norvegicus	87-93
14742654-4	2004	In multivariate regression models controlling for age, cigarette smoking, alcohol intake, physical activity, and aspirin intake, self-reported periodontal disease was associated with significantly higher levels of CRP (30% higher among periodontal cases compared with non-cases), t-PA (11% higher), and LDL-C (11% higher).	Aspirin	113-120	C-reactive protein	Homo sapiens	214-217
14742690-0	2004	Aspirin-mediated COX-2 transcript stabilization via sustained p38 activation in human intestinal myofibroblasts.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	17-22
14742690-0	2004	Aspirin-mediated COX-2 transcript stabilization via sustained p38 activation in human intestinal myofibroblasts.	Aspirin	0-7	mitogen-activated protein kinase 14	Homo sapiens	62-65
14742690-2	2004	In human intestinal myofibroblasts, aspirin, at therapeutic doses, had the unexpected effect of inducing prolonged COX-2 expression.	Aspirin	36-43	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	115-120
14742690-3	2004	This induction was especially pronounced when cells were treated with interleukin-1alpha (IL-1) plus aspirin for 24 h. Sodium salicylate, a poor COX inhibitor, likewise enhanced IL-1-mediated COX-2 gene expression whereas 5-aminosalicylic acid (5-ASA) or indomethacin had no effect.	Aspirin	101-108	interleukin 1 beta	Homo sapiens	178-182
14767868-6	2004	A similar reduction in apoAI promoter activity was found after treating the cells with 50 micromol/L acetylsalicylic acid (ASA) (31.8 +/- 1.8%, P <.001), suggesting that the effect of INDO is related to COX inhibition rather than a peculiar effect of INDO.	Aspirin	101-121	apolipoprotein A1	Homo sapiens	23-28
14742690-3	2004	This induction was especially pronounced when cells were treated with interleukin-1alpha (IL-1) plus aspirin for 24 h. Sodium salicylate, a poor COX inhibitor, likewise enhanced IL-1-mediated COX-2 gene expression whereas 5-aminosalicylic acid (5-ASA) or indomethacin had no effect.	Aspirin	101-108	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	192-197
14767868-6	2004	A similar reduction in apoAI promoter activity was found after treating the cells with 50 micromol/L acetylsalicylic acid (ASA) (31.8 +/- 1.8%, P <.001), suggesting that the effect of INDO is related to COX inhibition rather than a peculiar effect of INDO.	Aspirin	123-126	apolipoprotein A1	Homo sapiens	23-28
14742690-4	2004	The COX-2 transcriptional rate, measured by nuclear runoff analysis and heterogeneous nuclear RNA reverse transcription-polymerase chain reaction, was only modestly elevated by aspirin treatment.	Aspirin	177-184	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	4-9
14767868-15	2004	It is concluded that COX inhibition with INDO or ASA downregulates apoAI expression at the transcriptional level.	Aspirin	49-52	apolipoprotein A1	Homo sapiens	67-72
14742690-5	2004	In contrast, aspirin treatment dramatically stabilized the COX-2 message.	Aspirin	13-20	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	59-64
14742690-6	2004	The COX-2 mRNA half-life in IL-1 treated cells was 1 h and was increased in excess of 5 h in IL-1 + aspirin-treated cells.	Aspirin	100-107	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	4-9
14742690-6	2004	The COX-2 mRNA half-life in IL-1 treated cells was 1 h and was increased in excess of 5 h in IL-1 + aspirin-treated cells.	Aspirin	100-107	interleukin 1 beta	Homo sapiens	28-32
14742690-6	2004	The COX-2 mRNA half-life in IL-1 treated cells was 1 h and was increased in excess of 5 h in IL-1 + aspirin-treated cells.	Aspirin	100-107	interleukin 1 beta	Homo sapiens	93-97
14742690-7	2004	Phosphorylation of p38 MAPK was enhanced in aspirin-treated cells (but not in cells treated with 5-ASA or indomethacin) for up to 24 h after treatment.	Aspirin	44-51	mitogen-activated protein kinase 14	Homo sapiens	19-22
14742690-8	2004	Inhibition of p38 activity negated aspirin-mediated COX-2 mRNA stabilization and the resultant increase in COX-2 mRNA and protein levels.	Aspirin	35-42	mitogen-activated protein kinase 14	Homo sapiens	14-17
14742690-8	2004	Inhibition of p38 activity negated aspirin-mediated COX-2 mRNA stabilization and the resultant increase in COX-2 mRNA and protein levels.	Aspirin	35-42	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	52-57
14742690-9	2004	The modest transcriptional response seen in aspirin treated cells was also abolished by p38 inhibition.	Aspirin	44-51	mitogen-activated protein kinase 14	Homo sapiens	88-91
14742690-10	2004	We conclude that aspirin enhances COX-2 expression via sustained activation of p38, which results in prolonged stabilization of the COX-2 message and a slightly elevated transcription rate.	Aspirin	17-24	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	34-39
14742690-10	2004	We conclude that aspirin enhances COX-2 expression via sustained activation of p38, which results in prolonged stabilization of the COX-2 message and a slightly elevated transcription rate.	Aspirin	17-24	mitogen-activated protein kinase 14	Homo sapiens	79-82
14742690-10	2004	We conclude that aspirin enhances COX-2 expression via sustained activation of p38, which results in prolonged stabilization of the COX-2 message and a slightly elevated transcription rate.	Aspirin	17-24	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	132-137
14742690-11	2004	Aspirin also enhanced steady-state mRNA levels of other IL-1 modulated genes (IL-1beta, IL-6, groalpha, and TNFalpha) that are likewise regulated at the level of message stability via p38 activation.	Aspirin	0-7	interleukin 1 beta	Homo sapiens	56-60
14742690-11	2004	Aspirin also enhanced steady-state mRNA levels of other IL-1 modulated genes (IL-1beta, IL-6, groalpha, and TNFalpha) that are likewise regulated at the level of message stability via p38 activation.	Aspirin	0-7	interleukin 1 beta	Homo sapiens	78-86
14742690-11	2004	Aspirin also enhanced steady-state mRNA levels of other IL-1 modulated genes (IL-1beta, IL-6, groalpha, and TNFalpha) that are likewise regulated at the level of message stability via p38 activation.	Aspirin	0-7	interleukin 6	Homo sapiens	88-92
14742690-11	2004	Aspirin also enhanced steady-state mRNA levels of other IL-1 modulated genes (IL-1beta, IL-6, groalpha, and TNFalpha) that are likewise regulated at the level of message stability via p38 activation.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	108-116
14742690-11	2004	Aspirin also enhanced steady-state mRNA levels of other IL-1 modulated genes (IL-1beta, IL-6, groalpha, and TNFalpha) that are likewise regulated at the level of message stability via p38 activation.	Aspirin	0-7	mitogen-activated protein kinase 14	Homo sapiens	184-187
14705149-4	2004	In brain tissue subjected to hypoxia, ASA reduced oxidative stress and iNOS activity (all increased by hypoxia), but only when used at higher concentrations.	Aspirin	38-41	nitric oxide synthase 2	Rattus norvegicus	71-75
15061569-14	2004	ASA inhibits COX-1 and converts COX-2 into an ASA-triggered lipid mediator-generating system that produces an array of novel endogenous local autacoids from dietary omega-3 PUFA.	Aspirin	0-3	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	32-37
14759512-2	2004	In real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and reporter gene assays, we show that indomethacin and aspirin upregulate TFF2 expression in MKN45 gastric cells.	Aspirin	139-146	trefoil factor 2	Homo sapiens	158-162
14759512-4	2004	These results suggest that indomethacin and aspirin upregulate gastric expression of TFF2 through activation of PPARgamma.	Aspirin	44-51	trefoil factor 2	Homo sapiens	85-89
14759512-4	2004	These results suggest that indomethacin and aspirin upregulate gastric expression of TFF2 through activation of PPARgamma.	Aspirin	44-51	peroxisome proliferator activated receptor gamma	Homo sapiens	112-121
15049721-4	2004	Increased platelet thromboxane production as well as activation of platelet receptors for fibrinogen and or adenosine diphosphate (ADP) are often present, and can be treated with aspirin (acetylsalicylic acid) and/or receptor blockers.	Aspirin	179-186	fibrinogen beta chain	Homo sapiens	90-100
15049721-4	2004	Increased platelet thromboxane production as well as activation of platelet receptors for fibrinogen and or adenosine diphosphate (ADP) are often present, and can be treated with aspirin (acetylsalicylic acid) and/or receptor blockers.	Aspirin	188-208	fibrinogen beta chain	Homo sapiens	90-100
14665439-4	2004	Nitric oxide-releasing aspirins, including NCX-4016, have antiplatelet effects similar to aspirin but do not cause gastric damage.	Aspirin	23-31	solute carrier family 8 member A1	Rattus norvegicus	43-46
14665439-4	2004	Nitric oxide-releasing aspirins, including NCX-4016, have antiplatelet effects similar to aspirin but do not cause gastric damage.	Aspirin	23-30	solute carrier family 8 member A1	Rattus norvegicus	43-46
14675411-10	2004	We demonstrate that in vitro aspirin-resistance, revealed by PFA-100 CT prolongation failure, is correlated to increased plasmatic vWF:RCo levels, reinforcing its particular importance in PFA-100 cartridges performance.	Aspirin	29-36	von Willebrand factor	Homo sapiens	131-134
14730251-7	2004	In healthy volunteers, CD40L expression in platelets is not significantly inhibited by acetylsalicylic acid (ASA) alone, but is inhibited after treatment with the ADP-receptor antagonist clopidogrel or with clopidogrel plus ASA.	Aspirin	87-107	CD40 ligand	Homo sapiens	23-28
14730251-7	2004	In healthy volunteers, CD40L expression in platelets is not significantly inhibited by acetylsalicylic acid (ASA) alone, but is inhibited after treatment with the ADP-receptor antagonist clopidogrel or with clopidogrel plus ASA.	Aspirin	109-112	CD40 ligand	Homo sapiens	23-28
14730251-7	2004	In healthy volunteers, CD40L expression in platelets is not significantly inhibited by acetylsalicylic acid (ASA) alone, but is inhibited after treatment with the ADP-receptor antagonist clopidogrel or with clopidogrel plus ASA.	Aspirin	224-227	CD40 ligand	Homo sapiens	23-28
14964479-2	2004	t-PA is reasonably safe if used in a carefully defined manner that ensures close attention to blood pressure, careful patient monitoring, no use of heparin and aspirin during first 24 hours, and appropriate patient selection.	Aspirin	160-167	plasminogen activator, tissue type	Homo sapiens	0-4
14680616-1	2004	Aspirin-exacerbated respiratory disease (AERD) is an adult-onset condition that manifests as asthma, rhinosinusitis/nasal polyps, and sensitivity to aspirin and other cyclooxygenase-1 (COX-1)-inhibitor nonsteroidal anti-inflammatory drugs (NSAIDs).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	167-183
14680616-1	2004	Aspirin-exacerbated respiratory disease (AERD) is an adult-onset condition that manifests as asthma, rhinosinusitis/nasal polyps, and sensitivity to aspirin and other cyclooxygenase-1 (COX-1)-inhibitor nonsteroidal anti-inflammatory drugs (NSAIDs).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	185-190
15383758-14	2004	The use of NSAIDS and aspirin, most likely via inhibition of COX-2 and other inflammatory pathways, is associated with a reduction of adenocarcinoma rates.	Aspirin	22-29	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	61-66
14965321-7	2004	During the past forty years systematic advances in our understanding of the structure, regulation and function of COX isoenzymes have enabled the design and synthesis of COX-2 selective inhibitors as agents intended to lessen the gastrointestinal irritation of aspirin and non-selective NSAIDs.	Aspirin	261-268	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	170-175
14975457-2	2004	Aspirin and older agents in this class are nonselective inhibitors of both COX-1 and COX-2.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	85-90
15482000-9	2004	The COX-2 hypothesis proposes that aspirin causes a structural change in COX-2 that results in the generation of products of the lipoxygenase pathway.	Aspirin	35-42	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	4-9
15205571-9	2004	RESULTS: Immunofluorescence analysis showed a fragmented and granulous ZO-1 staining, after ASA treatment.	Aspirin	92-95	tight junction protein 1	Homo sapiens	71-75
15205571-11	2004	Western blot revealed that ASA inhibited ZO-1 expression and LaLB with its spent culture supernatant counteracted this effect.	Aspirin	27-30	tight junction protein 1	Homo sapiens	41-45
15482000-9	2004	The COX-2 hypothesis proposes that aspirin causes a structural change in COX-2 that results in the generation of products of the lipoxygenase pathway.	Aspirin	35-42	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	73-78
14722849-5	2004	New results have confirmed the preventive effect of long-term aspirin use on adenoma recurrence, but the most cost-effective dosage is not clear; the mechanism of action is also uncertain, but seems to involve cyclooxygenase-2.	Aspirin	62-69	prostaglandin-endoperoxide synthase 2	Homo sapiens	210-226
14753751-0	2003	Aspirin prevents apoptosis and NF-kappaB activation induced by H2O2 in hela cells.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	31-40
14871051-9	2004	Although not discussed in detail, it is acknowledged that both hygienic measures (weight loss and aerobic exercise) and treatment strategies that include aspirin, statins, INS sensitizers, and antihypertensive agents that reduce renin-angiotensin-aldosterone system activity have been shown to reduce inflammation, coagulation abnormalities, endothelial function, proteinuria, and in some cases reduce CVD and renal disease progression.	Aspirin	154-161	renin	Homo sapiens	229-234
14680090-5	2003	In comparison to the control, the aspirin-sensitive rhinitis group had a significant increase of VIP-like immunoreactivity in mucosal nerve fibres.	Aspirin	34-41	vasoactive intestinal peptide	Homo sapiens	97-100
14753751-4	2003	Our studies reveal that a commonly used non-steroid anti-inflammatory drug, acetylsalicylic acid (aspirin) prevents H2O2-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	76-96	nuclear factor kappa B subunit 1	Homo sapiens	129-138
14753751-4	2003	Our studies reveal that a commonly used non-steroid anti-inflammatory drug, acetylsalicylic acid (aspirin) prevents H2O2-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	76-96	NFKB inhibitor alpha	Homo sapiens	234-246
14753751-4	2003	Our studies reveal that a commonly used non-steroid anti-inflammatory drug, acetylsalicylic acid (aspirin) prevents H2O2-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	98-105	nuclear factor kappa B subunit 1	Homo sapiens	129-138
14753751-4	2003	Our studies reveal that a commonly used non-steroid anti-inflammatory drug, acetylsalicylic acid (aspirin) prevents H2O2-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	98-105	NFKB inhibitor alpha	Homo sapiens	234-246
14753751-6	2003	Additionally, aspirin effectively prevents caspase-3 and caspase-9 (cysteinyl aspartate-specific proteases) activation by H2O2.	Aspirin	14-21	caspase 3	Homo sapiens	43-52
14638438-9	2003	There is a complex pattern of PIP isoform variability in seminal plasma from fertile and infertile men but one multimeric form of PIP was absent from the seminal plasma of men with ASA who were fertile.	Aspirin	181-184	prolactin induced protein	Homo sapiens	130-133
14704745-6	2003	Furthermore, high doses of salicylates (aspirin or salicylate) improved insulin sensitivity in patients with type II diabetes.	Aspirin	40-47	insulin	Homo sapiens	72-79
14623265-6	2003	The guanylyl-cyclase inhibitor ODQ partially reversed the suppression of COX-2 activity by NO-aspirin, demonstrating a role of cGMP increase.	Aspirin	94-101	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	73-78
14763357-11	2003	The benefit related to the IN SUMMARY: Cox-2 specific antagonists seems dramatically reduced by the concomitant aspirin intake.	Aspirin	112-119	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	39-44
14597584-5	2003	Thrombin and TXA2 also synergized with P2Y12 in the absence of anticoagulation, because combined treatment of aspirin or C921-78 (a factor Xa inhibitor) with CT50547 or 2-MeSAMP (a P2Y12 antagonist) inhibited the thrombotic process, whereas all treatments failed to inhibit thrombosis when used individually.	Aspirin	110-117	coagulation factor II	Mus musculus	0-8
14633677-0	2003	Growth inhibition of human colon cancer cells by nitric oxide (NO)-donating aspirin is associated with cyclooxygenase-2 induction and beta-catenin/T-cell factor signaling, nuclear factor-kappaB, and NO synthase 2 inhibition: implications for chemoprevention.	Aspirin	76-83	prostaglandin-endoperoxide synthase 2	Homo sapiens	103-119
14633677-5	2003	Interestingly, NO-ASA induced COX-2 expression, although it had no effect on COX-1.	Aspirin	18-21	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	30-35
14640056-2	2003	The mechanisms by which acetylsalicylic acid and other NSAIDs, including COX-2 inhibitors, exert this effect include: inhibition of COX-2, induction of apoptosis and induction of the P21 protein that controls the development of crypt cells.	Aspirin	24-44	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	73-78
14640056-2	2003	The mechanisms by which acetylsalicylic acid and other NSAIDs, including COX-2 inhibitors, exert this effect include: inhibition of COX-2, induction of apoptosis and induction of the P21 protein that controls the development of crypt cells.	Aspirin	24-44	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	132-137
14566053-0	2003	Nitric oxide-donating aspirin inhibits beta-catenin/T cell factor (TCF) signaling in SW480 colon cancer cells by disrupting the nuclear beta-catenin-TCF association.	Aspirin	22-29	hepatocyte nuclear factor 4 alpha	Homo sapiens	67-70
14532966-7	2003	Here we show that aspirin inhibits NF-kappaB, resulting in the suppression of uPA secretion from the highly invasive human prostate cancer cells PC-3.	Aspirin	18-25	nuclear factor kappa B subunit 1	Homo sapiens	35-44
14532966-7	2003	Here we show that aspirin inhibits NF-kappaB, resulting in the suppression of uPA secretion from the highly invasive human prostate cancer cells PC-3.	Aspirin	18-25	plasminogen activator, urokinase	Homo sapiens	78-81
14532966-8	2003	Furthermore, aspirin inhibited migration of PC-3 cells, suggesting an effect on the uPA-uPAR signaling complex.	Aspirin	13-20	plasminogen activator, urokinase	Homo sapiens	84-87
14532966-9	2003	Finally, aspirin suppressed adhesion of PC-3 cells to fibronectin (FN), which binds to an alpha3beta1 integrin receptor, and to vitronectin (VN), which binds to alphavbeta3 integrin receptor.	Aspirin	9-16	fibronectin 1	Homo sapiens	54-65
14532966-9	2003	Finally, aspirin suppressed adhesion of PC-3 cells to fibronectin (FN), which binds to an alpha3beta1 integrin receptor, and to vitronectin (VN), which binds to alphavbeta3 integrin receptor.	Aspirin	9-16	fibronectin 1	Homo sapiens	67-69
14532966-10	2003	Altogether, our data suggests that aspirin inhibits the formation of uPA-uPAR-FN-alpha3beta1 and uPA-uPAR-VN-alphavbeta3 complexes, resulting in the suppression of cell adhesion and cell motility of the highly invasive prostate cancer cells PC-3.	Aspirin	35-42	plasminogen activator, urokinase	Homo sapiens	69-72
14532966-10	2003	Altogether, our data suggests that aspirin inhibits the formation of uPA-uPAR-FN-alpha3beta1 and uPA-uPAR-VN-alphavbeta3 complexes, resulting in the suppression of cell adhesion and cell motility of the highly invasive prostate cancer cells PC-3.	Aspirin	35-42	plasminogen activator, urokinase	Homo sapiens	73-76
14573775-0	2003	Expression of the angiogenic factor thymidine phosphorylase in THP-1 monocytes: induction by autocrine tumor necrosis factor-alpha and inhibition by aspirin.	Aspirin	149-156	GLI family zinc finger 2	Homo sapiens	63-68
14573775-9	2003	An alternative mechanism by which aspirin inhibits gene expression is the modulation of the transcription factor NFkappaB, and the TNFalpha-induced increase in TP mRNA was blocked by a cell-permeable NFkappaB inhibitory peptide.	Aspirin	34-41	nuclear factor kappa B subunit 1	Homo sapiens	113-121
14573775-9	2003	An alternative mechanism by which aspirin inhibits gene expression is the modulation of the transcription factor NFkappaB, and the TNFalpha-induced increase in TP mRNA was blocked by a cell-permeable NFkappaB inhibitory peptide.	Aspirin	34-41	tumor necrosis factor	Homo sapiens	131-139
14573775-9	2003	An alternative mechanism by which aspirin inhibits gene expression is the modulation of the transcription factor NFkappaB, and the TNFalpha-induced increase in TP mRNA was blocked by a cell-permeable NFkappaB inhibitory peptide.	Aspirin	34-41	nuclear factor kappa B subunit 1	Homo sapiens	200-208
14573775-10	2003	Furthermore, TNFalpha increased and aspirin (but not indomethacin) decreased NFkappaB DNA-binding activity in THP-1 cells.	Aspirin	36-43	nuclear factor kappa B subunit 1	Homo sapiens	77-85
14573775-10	2003	Furthermore, TNFalpha increased and aspirin (but not indomethacin) decreased NFkappaB DNA-binding activity in THP-1 cells.	Aspirin	36-43	GLI family zinc finger 2	Homo sapiens	110-115
14566053-0	2003	Nitric oxide-donating aspirin inhibits beta-catenin/T cell factor (TCF) signaling in SW480 colon cancer cells by disrupting the nuclear beta-catenin-TCF association.	Aspirin	22-29	hepatocyte nuclear factor 4 alpha	Homo sapiens	149-152
14566053-2	2003	We studied the ortho, meta, and para (o-, m-, and p-) positional isomers of NO-donating aspirin (NO-ASA), a chemopreventive agent against colon cancer, for their effect on Beta-catenin/T cell factor (TCF) signaling.	Aspirin	88-95	hepatocyte nuclear factor 4 alpha	Homo sapiens	200-203
14504184-8	2003	The change in IL-1beta levels correlated with the change in sP-selectin in patients randomized to either simvastatin (Rho, 0.42; P<0.05) or aspirin (Rho, 0.42; P<0.05).	Aspirin	143-150	interleukin 1 beta	Homo sapiens	14-22
14519044-0	2003	Safety of COX-2 inhibitors in asthma patients with aspirin hypersensitivity.	Aspirin	51-58	prostaglandin-endoperoxide synthase 2	Homo sapiens	10-15
14636445-1	2003	OBJECTIVE: To observe the anti-tumor effect of combination TNF-related apoptosis-inducing ligand (TRAIL) with aspirin on liver cancer cell line, SMMC-7721.	Aspirin	110-117	TNF superfamily member 10	Homo sapiens	98-103
14636445-3	2003	RESULTS: The survival fraction of SMMC-7721 cells treated with 300 ng/ml TRAIL, 3 mmol/L or 10 mmol/L aspirin alone was 82.76%, 81.34% and 71.29% respectively, and the survival fractions of SMMC-7721 cells treated with TRAIL and 3 mmol/L or 10 mmol/L aspirin were 43.54% and 37.8% respectively.	Aspirin	251-258	TNF superfamily member 10	Homo sapiens	73-78
14636445-5	2003	The expression of Bcl-2 in SMMC-7721 cells treated by 3 mmol/L or 10 mmol/L aspirin decreased markedly, but no effect on Bax.	Aspirin	76-83	BCL2 apoptosis regulator	Homo sapiens	18-23
14636445-6	2003	CONCLUSION: The cooperative anti-tumor effect of aspirin and TRAIL may be related to the inhibition of the expression of Bcl-2 by aspirin	Aspirin	49-56	BCL2 apoptosis regulator	Homo sapiens	121-126
14636445-6	2003	CONCLUSION: The cooperative anti-tumor effect of aspirin and TRAIL may be related to the inhibition of the expression of Bcl-2 by aspirin	Aspirin	130-137	TNF superfamily member 10	Homo sapiens	61-66
14636445-6	2003	CONCLUSION: The cooperative anti-tumor effect of aspirin and TRAIL may be related to the inhibition of the expression of Bcl-2 by aspirin	Aspirin	130-137	BCL2 apoptosis regulator	Homo sapiens	121-126
14519044-1	2003	OBJECTIVE: To review the safety of cyclooxygenase-2 (COX-2) inhibitors in asthma patients with aspirin hypersensitivity.	Aspirin	95-102	prostaglandin-endoperoxide synthase 2	Homo sapiens	35-51
14519044-1	2003	OBJECTIVE: To review the safety of cyclooxygenase-2 (COX-2) inhibitors in asthma patients with aspirin hypersensitivity.	Aspirin	95-102	prostaglandin-endoperoxide synthase 2	Homo sapiens	53-58
14519044-6	2003	DATA SYNTHESIS: The literature provides information regarding the safety of COX-2 inhibitors in asthma patients with aspirin-exacerbated respiratory disease (AERD).	Aspirin	117-124	prostaglandin-endoperoxide synthase 2	Homo sapiens	76-81
14519050-5	2003	DATA SYNTHESIS: In randomized clinical trials, low-dose aspirin, high-intensity oral anticoagulants, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins decreased the risk of mortality and reinfarction after MI.	Aspirin	56-63	angiotensin I converting enzyme	Homo sapiens	116-145
14511359-0	2003	Activation of p53 signalling in acetylsalicylic acid-induced apoptosis in OC2 human oral cancer cells.	Aspirin	32-52	tumor protein p53	Homo sapiens	14-17
14511359-2	2003	The aim of this study was to investigate the possible existence of a putative p53-dependent pathway underlying the ASA-induced apoptosis in OC2 cells, a human oral cancer cell line.	Aspirin	115-118	tumor protein p53	Homo sapiens	78-81
14511359-10	2003	In the meanwhile, phosphorylation of p53 at serine 15, accumulation of p53 and increased the expression of its downstream target genes, p21 and Bax induced by ASA.	Aspirin	159-162	tumor protein p53	Homo sapiens	37-40
14511359-10	2003	In the meanwhile, phosphorylation of p53 at serine 15, accumulation of p53 and increased the expression of its downstream target genes, p21 and Bax induced by ASA.	Aspirin	159-162	tumor protein p53	Homo sapiens	71-74
14511359-10	2003	In the meanwhile, phosphorylation of p53 at serine 15, accumulation of p53 and increased the expression of its downstream target genes, p21 and Bax induced by ASA.	Aspirin	159-162	BCL2 associated X, apoptosis regulator	Homo sapiens	144-147
14555553-1	2003	BACKGROUND: Experimental studies and retrospective analyses of mortality trials with angiotensin-converting enzyme inhibitors (ACE-Is) have suggested that aspirin may reduce the beneficial effect of these drugs.	Aspirin	155-162	angiotensin I converting enzyme	Homo sapiens	127-130
14607210-7	2003	The ESTEEM study showed that the oral thrombin inhibitor ximelagatran plus aspirin was more effective than aspirin alone in the prophylaxis of major cardiovascular events following MI.	Aspirin	75-82	coagulation factor II, thrombin	Homo sapiens	38-46
14607210-7	2003	The ESTEEM study showed that the oral thrombin inhibitor ximelagatran plus aspirin was more effective than aspirin alone in the prophylaxis of major cardiovascular events following MI.	Aspirin	107-114	coagulation factor II, thrombin	Homo sapiens	38-46
14584890-2	2003	Significantly higher BMD was found in users of relative COX-2 selective NSAIDs with aspirin (COX-2/ASA) compared with nonusers.	Aspirin	84-91	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	56-61
14584890-2	2003	Significantly higher BMD was found in users of relative COX-2 selective NSAIDs with aspirin (COX-2/ASA) compared with nonusers.	Aspirin	84-91	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	93-98
14584890-2	2003	Significantly higher BMD was found in users of relative COX-2 selective NSAIDs with aspirin (COX-2/ASA) compared with nonusers.	Aspirin	99-102	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	56-61
14584890-12	2003	RESULTS: After adjustment for possible confounders, current use of relative COX-2 selective NSAIDs with aspirin was associated with higher BMD at the whole body (4.2%, 1.2-7.3 CI) and total hip (4.6%, 0.5-8.8 CI) by DXA and at both trabecular (34.1%, 15.4-52.7 CI) and cortical spine (12.8%, 2.3-23.3 CI) by quantitative computed tomography.	Aspirin	104-111	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	76-81
14584890-13	2003	CONCLUSIONS: Our data suggest that the combination of relative COX-2 selective NSAIDs and aspirin is associated with higher BMD at multiple skeletal sites in men and women.	Aspirin	90-97	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	63-68
14521608-0	2003	Aspirin and salicylate inhibit colon cancer medium- and VEGF-induced endothelial tube formation: correlation with suppression of cyclooxygenase-2 expression.	Aspirin	0-7	vascular endothelial growth factor A	Homo sapiens	56-60
14521608-0	2003	Aspirin and salicylate inhibit colon cancer medium- and VEGF-induced endothelial tube formation: correlation with suppression of cyclooxygenase-2 expression.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	129-145
14521608-7	2003	Aspirin or sodium salicylate inhibited VEGF-induced tube formation in a concentration-dependent manner comparable to that of inhibition of colon cancer medium-induced endothelial tube formation.	Aspirin	0-7	vascular endothelial growth factor A	Homo sapiens	39-43
14521608-9	2003	We found that colon cancer medium-induced COX-2 protein expression in EC and aspirin or sodium salicylate suppressed the cancer-induced COX-2 protein levels at concentrations correlated with those that suppressed endothelial tube formation.	Aspirin	77-84	prostaglandin-endoperoxide synthase 2	Homo sapiens	136-141
14521608-10	2003	Furthermore, aspirin and sodium salicylate inhibited COX-2 expression stimulated by VEGF.	Aspirin	13-20	prostaglandin-endoperoxide synthase 2	Homo sapiens	53-58
14521608-10	2003	Furthermore, aspirin and sodium salicylate inhibited COX-2 expression stimulated by VEGF.	Aspirin	13-20	vascular endothelial growth factor A	Homo sapiens	84-88
14521608-11	2003	These findings indicate that aspirin and other salicylate drugs at pharmacological concentrations inhibit colon cancer-induced angiogenesis which is correlated with COX-2 suppression.	Aspirin	29-36	prostaglandin-endoperoxide synthase 2	Homo sapiens	165-170
12960371-0	2003	Interaction of a selective cyclooxygenase-2 inhibitor with aspirin and NO-releasing aspirin in the human gastric mucosa.	Aspirin	59-66	prostaglandin-endoperoxide synthase 2	Homo sapiens	27-43
12960371-0	2003	Interaction of a selective cyclooxygenase-2 inhibitor with aspirin and NO-releasing aspirin in the human gastric mucosa.	Aspirin	84-91	prostaglandin-endoperoxide synthase 2	Homo sapiens	27-43
12960371-1	2003	In addition to inhibiting cyclooxygenase (COX)-1-derived prostanoid biosynthesis, aspirin acetylates COX-2, enabling the conversion of arachidonic acid to 15(R)-epi lipoxin A4, or aspirin-triggered lipoxin (ATL).	Aspirin	82-89	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	101-106
12960371-1	2003	In addition to inhibiting cyclooxygenase (COX)-1-derived prostanoid biosynthesis, aspirin acetylates COX-2, enabling the conversion of arachidonic acid to 15(R)-epi lipoxin A4, or aspirin-triggered lipoxin (ATL).	Aspirin	180-187	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	101-106
13678940-0	2003	Resistance in vitro to low-dose aspirin is associated with platelet PlA1 (GP IIIa) polymorphism but not with C807T(GP Ia/IIa) and C-5T Kozak (GP Ibalpha) polymorphisms.	Aspirin	32-39	integrin subunit beta 3	Homo sapiens	74-81
13678873-12	2003	INTERPRETATION: Oral direct thrombin inhibition with ximelagatran and acetylsalicylic acid is more effective than acetylsalicylic acid alone in preventing major cardiovascular events during 6 months of treatment in patients who have had a recent myocardial infarction.	Aspirin	70-90	coagulation factor II, thrombin	Homo sapiens	28-36
13678873-12	2003	INTERPRETATION: Oral direct thrombin inhibition with ximelagatran and acetylsalicylic acid is more effective than acetylsalicylic acid alone in preventing major cardiovascular events during 6 months of treatment in patients who have had a recent myocardial infarction.	Aspirin	114-134	coagulation factor II, thrombin	Homo sapiens	28-36
14512099-1	2003	The aim of this study was to investigate the capacity of the 2-(acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester (NCX 4016), a nitric oxide (NO)-releaser derivative of aspirin, to decrease blood pressure in spontaneously hypertensive rats (SHR) and to counteract the adrenergic vasoconstriction in perfused tail artery of these animals.	Aspirin	173-180	solute carrier family 8 member A1	Rattus norvegicus	119-122
14512099-5	2003	These vessels, prepared from SHR or WKY rats treated orally with NCX 4016 (10, 30 and 100 micromol/kg for 7 consecutive days), revealed a dose-dependent decrease in vasoconstriction in response to transmural nerve stimulation and norepinephrine, whereas aspirin was ineffective.	Aspirin	254-261	solute carrier family 8 member A1	Rattus norvegicus	65-68
12925472-3	2003	METHODS: Anaesthesia was induced with propofol TCI to obtain loss of consciousness (LOC) in 12 ASA I/II patients.	Aspirin	95-98	latexin	Homo sapiens	47-50
12947436-5	2003	RESULTS: C-reactive protein concentration (dichotomized at the sex-specific 85th percentile) was inversely and significantly associated with concentrations of retinol, retinyl esters, vitamin C, alpha-carotene, beta-carotene, cryptoxanthin, lutein/zeaxanthin, lycopene, and selenium after adjustment for age, sex, race or ethnicity, education, cotinine concentration, body mass index, leisure-time physical activity, and aspirin use.	Aspirin	421-428	C-reactive protein	Homo sapiens	9-27
14511323-3	2003	In the present study, treatment of primary rat mixed glial cell cultures with the common NSAIDs, indomethacin and aspirin, induced significant increases in extracellular apoE protein levels.	Aspirin	114-121	apolipoprotein E	Rattus norvegicus	170-174
14511323-4	2003	Similarly, treatment of primary rat astrocyte cell cultures with aspirin and a cyclooxygenase (COX)-2-selective aspirin derivative also stimulated significant increases in apoE protein.	Aspirin	65-72	apolipoprotein E	Rattus norvegicus	172-176
14511323-4	2003	Similarly, treatment of primary rat astrocyte cell cultures with aspirin and a cyclooxygenase (COX)-2-selective aspirin derivative also stimulated significant increases in apoE protein.	Aspirin	112-119	apolipoprotein E	Rattus norvegicus	172-176
14608518-7	2003	In this article, we review studies, most of them conducted in CHF, that pointed out such a possible deleterious effect and a counteraction of ACE-Is with low-dose aspirin, using various criteria of assessment.	Aspirin	163-170	angiotensin I converting enzyme	Homo sapiens	142-145
14594936-4	2003	Previous clinical trials have shown the effectiveness of the following: polyprenoic acid (acyclic retinoid) for hepatocellular carcinoma; tamoxifen for breast cancer; retinoic acids for head and neck tumor; and aspirin, a COX-2 inhibitor, for colorectal cancer.	Aspirin	211-218	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	222-227
14511359-13	2003	Inhibited the activation of p42/p44 mitogen-activated protein kinase (MAPK) by PD98059, a specific inhibitor of extracellular regulatory kinase (ERK), significantly decreased cell viability and enhanced the expression of p53 induced by ASA.	Aspirin	236-239	mitogen-activated protein kinase 3	Homo sapiens	70-74
14511359-13	2003	Inhibited the activation of p42/p44 mitogen-activated protein kinase (MAPK) by PD98059, a specific inhibitor of extracellular regulatory kinase (ERK), significantly decreased cell viability and enhanced the expression of p53 induced by ASA.	Aspirin	236-239	mitogen-activated protein kinase 3	Homo sapiens	145-148
14511359-13	2003	Inhibited the activation of p42/p44 mitogen-activated protein kinase (MAPK) by PD98059, a specific inhibitor of extracellular regulatory kinase (ERK), significantly decreased cell viability and enhanced the expression of p53 induced by ASA.	Aspirin	236-239	tumor protein p53	Homo sapiens	221-224
14511359-16	2003	Our study presents evidences that activation of p53 signalling involved in apoptosis induced by ASA.	Aspirin	96-99	tumor protein p53	Homo sapiens	48-51
14511359-17	2003	Furthermore, the apoptotic effect was enhanced by blocking the activation of p42/p44 MAPK in response to treatment with ASA, thus indicating a negative role for p42/p44 MAPK.	Aspirin	120-123	mitogen-activated protein kinase 3	Homo sapiens	81-89
14511359-17	2003	Furthermore, the apoptotic effect was enhanced by blocking the activation of p42/p44 MAPK in response to treatment with ASA, thus indicating a negative role for p42/p44 MAPK.	Aspirin	120-123	mitogen-activated protein kinase 3	Homo sapiens	165-173
12898518-6	2003	(3) Dexamethasone as well as acetylsalicylic acid reduced the expression of TNF-alpha in lipopolysaccharide-challenged PIMs, and the decreased expression of TNF-alpha was also consistent with decreased NF-kappaB activation.	Aspirin	29-49	tumor necrosis factor	Homo sapiens	76-85
12917690-7	2003	We show that this effect can be relieved by aspirin derivatives that inhibit NF-kappaB activity, which suggests a therapeutic intervention strategy to restore growth control in patients suffering from familial cylindromatosis.	Aspirin	44-51	nuclear factor kappa B subunit 1	Homo sapiens	77-86
12874188-8	2003	The inducible isoform of cyclooxygenase in platelets, COX-2, has been suggested to confer aspirin resistance.	Aspirin	90-97	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	54-59
12890715-0	2003	Evidence that 5-lipoxygenase and acetylated cyclooxygenase 2-derived eicosanoids regulate leukocyte-endothelial adherence in response to aspirin.	Aspirin	137-144	arachidonate 5-lipoxygenase	Homo sapiens	14-28
12890715-0	2003	Evidence that 5-lipoxygenase and acetylated cyclooxygenase 2-derived eicosanoids regulate leukocyte-endothelial adherence in response to aspirin.	Aspirin	137-144	prostaglandin-endoperoxide synthase 2	Homo sapiens	44-60
12890715-1	2003	(1) Unlike other nonsteroidal anti-inflammatory drugs that inhibit formation of cyclooxygenase (COX)-dependent eicosanoids, acetylation of COX-2 by aspirin switches eicosanoid biosynthesis from prostaglandin E(2) (PGE(2)) to 15-epi-lipoxin A(4) (15-epi-LXA(4) or aspirin-triggered lipoxin, ATL).	Aspirin	148-155	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	139-144
12890715-1	2003	(1) Unlike other nonsteroidal anti-inflammatory drugs that inhibit formation of cyclooxygenase (COX)-dependent eicosanoids, acetylation of COX-2 by aspirin switches eicosanoid biosynthesis from prostaglandin E(2) (PGE(2)) to 15-epi-lipoxin A(4) (15-epi-LXA(4) or aspirin-triggered lipoxin, ATL).	Aspirin	263-270	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	139-144
12890715-3	2003	(2) In the present study, we have examined the role of acetylated COX-2 and 5-LOX in modulating antiadhesive effects of aspirin on adhesion of PMN to endotoxin (LPS)-primed human umbilical endothelial cells (HUVEC).	Aspirin	120-127	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	66-77
12890715-5	2003	Treating HUVEC with selective COX-2 inhibitors, celecoxib and rofecoxib, caused an approximately 70% reversion of antiadhesive effect of aspirin.	Aspirin	137-144	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	30-35
12879250-11	2003	The inhibition of PNF by AsA was associated with decreased intra-islet levels of inflammation-related molecules (IL-1, TNF-alpha, iNOS, COX-2) and chemokines (MCP-1 and MIP-3alpha).	Aspirin	25-28	tumor necrosis factor	Mus musculus	119-128
12879250-11	2003	The inhibition of PNF by AsA was associated with decreased intra-islet levels of inflammation-related molecules (IL-1, TNF-alpha, iNOS, COX-2) and chemokines (MCP-1 and MIP-3alpha).	Aspirin	25-28	nitric oxide synthase 2, inducible	Mus musculus	130-134
12879250-11	2003	The inhibition of PNF by AsA was associated with decreased intra-islet levels of inflammation-related molecules (IL-1, TNF-alpha, iNOS, COX-2) and chemokines (MCP-1 and MIP-3alpha).	Aspirin	25-28	mast cell protease 1	Mus musculus	159-164
12861231-2	2003	We determined whether variation in insulin action is associated with that of ASA on platelets.	Aspirin	77-80	insulin	Homo sapiens	35-42
12861231-10	2003	In vivo insulin sensitivity (r=-0.68, P<0.001 for 1 mmol/l AA) and BMI (r=0.58, P<0.01 for 1 mmol/l AA) were closely correlated with residual aggregation after ASA administration.	Aspirin	166-169	insulin	Homo sapiens	8-15
12861231-12	2003	If this blunted effect is of a single dose of ASA preserved in continuous use, it could contribute to the increased risk of atherothrombosis in insulin-resistant individuals.	Aspirin	46-49	insulin	Homo sapiens	144-151
12769697-8	2003	The first of these relates to the unique mode of action of aspirin, which acetylates the COX-2 enzyme and generates the cancer-suppressing 15R-hydroxyeicosatetraenoic acid at the site of a potential tumour.	Aspirin	59-66	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	89-94
12869645-0	2003	Aspirin protects Caco-2 cells from apoptosis after serum deprivation through the activation of a phosphatidylinositol 3-kinase/AKT/p21Cip/WAF1pathway.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	127-130
12869645-7	2003	The effects of aspirin were mediated at molecular levels, through activation of PI3-kinase/AKT pathway and increase in the p21Cip/WAF1 level.	Aspirin	15-22	AKT serine/threonine kinase 1	Homo sapiens	91-94
12869645-7	2003	The effects of aspirin were mediated at molecular levels, through activation of PI3-kinase/AKT pathway and increase in the p21Cip/WAF1 level.	Aspirin	15-22	cyclin dependent kinase inhibitor 1A	Homo sapiens	130-134
12869645-8	2003	The ability of aspirin to activate AKT protein was observed also in presence of etoposide cotreatment.	Aspirin	15-22	AKT serine/threonine kinase 1	Homo sapiens	35-38
12888880-7	2003	In vitro studies showed TNF alpha dose-dependently (5-40 pg/ml) induced platelet O(2)(-) production, and that this effect was significantly inhibited by its specific inhibitor, WP9QY (1 microM); aspirin (100 microM), AACOCF(3), a specific PLA(2) inhibitor (14 microM), and DPI, an inhibitor of NADPH oxidase, significantly inhibited TNF alpha-mediated platelet O(2)(-) production.	Aspirin	195-202	tumor necrosis factor	Homo sapiens	24-33
12832097-2	2003	However, the mechanism by which ASA exhibits antiproliferative and proapoptotic effects in cyclooxygenase 2 (COX-2)-negative cells remains to be further elucidated.	Aspirin	32-35	prostaglandin-endoperoxide synthase 2	Homo sapiens	91-107
12832097-2	2003	However, the mechanism by which ASA exhibits antiproliferative and proapoptotic effects in cyclooxygenase 2 (COX-2)-negative cells remains to be further elucidated.	Aspirin	32-35	prostaglandin-endoperoxide synthase 2	Homo sapiens	109-114
12714600-0	2003	Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in tumor necrosis factor-treated cells through targeting multiple serine kinases.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	75-96
12714600-3	2003	In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha.	Aspirin	42-49	tumor necrosis factor	Homo sapiens	161-194
12714600-3	2003	In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha.	Aspirin	51-71	tumor necrosis factor	Homo sapiens	161-194
12714600-8	2003	Interestingly, aspirin treatment inhibited the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha.	Aspirin	15-22	mitogen-activated protein kinase 8	Homo sapiens	116-119
12714600-8	2003	Interestingly, aspirin treatment inhibited the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha.	Aspirin	15-22	NFKB inhibitor alpha	Homo sapiens	147-159
12714600-11	2003	Phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha was inhibited by aspirin treatment.	Aspirin	155-162	AKT serine/threonine kinase 1	Homo sapiens	19-22
12714600-11	2003	Phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha was inhibited by aspirin treatment.	Aspirin	155-162	mechanistic target of rapamycin kinase	Homo sapiens	31-60
12714600-11	2003	Phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha was inhibited by aspirin treatment.	Aspirin	155-162	tumor necrosis factor	Homo sapiens	128-137
12714600-12	2003	Finally, aspirin rescued insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha.	Aspirin	9-16	insulin	Homo sapiens	25-32
12714600-12	2003	Finally, aspirin rescued insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha.	Aspirin	9-16	tumor necrosis factor	Homo sapiens	93-102
12714600-13	2003	We conclude that aspirin may enhance insulin sensitivity by protecting IRS proteins from serine phosphorylation catalyzed by multiple kinases.	Aspirin	17-24	insulin	Homo sapiens	37-44
12714600-13	2003	We conclude that aspirin may enhance insulin sensitivity by protecting IRS proteins from serine phosphorylation catalyzed by multiple kinases.	Aspirin	17-24	isoleucyl-tRNA synthetase 1	Homo sapiens	71-74
12867250-6	2003	Benefits from aspirin are more likely in patients whose hs-CRP levels are very high.	Aspirin	14-21	C-reactive protein	Homo sapiens	59-62
12860262-0	2003	Relationship between effects of statins, aspirin and angiotensin II modulators on high-sensitive C-reactive protein levels.	Aspirin	41-48	C-reactive protein	Homo sapiens	97-115
12860262-1	2003	Statins, aspirin and angiotensin II modulators (A II-M: angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type I receptor blockades) may have an anti-inflammatory effect, but the relationship between the effects of statins, aspirin and A II-M on high-sensitive C-reactive protein (hs-CRP) levels remains to be determined.	Aspirin	9-16	angiotensin I converting enzyme	Homo sapiens	56-85
12860262-1	2003	Statins, aspirin and angiotensin II modulators (A II-M: angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type I receptor blockades) may have an anti-inflammatory effect, but the relationship between the effects of statins, aspirin and A II-M on high-sensitive C-reactive protein (hs-CRP) levels remains to be determined.	Aspirin	9-16	angiotensin I converting enzyme	Homo sapiens	87-90
12860262-1	2003	Statins, aspirin and angiotensin II modulators (A II-M: angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type I receptor blockades) may have an anti-inflammatory effect, but the relationship between the effects of statins, aspirin and A II-M on high-sensitive C-reactive protein (hs-CRP) levels remains to be determined.	Aspirin	9-16	angiotensinogen	Homo sapiens	107-121
12860262-1	2003	Statins, aspirin and angiotensin II modulators (A II-M: angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type I receptor blockades) may have an anti-inflammatory effect, but the relationship between the effects of statins, aspirin and A II-M on high-sensitive C-reactive protein (hs-CRP) levels remains to be determined.	Aspirin	9-16	C-reactive protein	Homo sapiens	277-295
12860262-1	2003	Statins, aspirin and angiotensin II modulators (A II-M: angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type I receptor blockades) may have an anti-inflammatory effect, but the relationship between the effects of statins, aspirin and A II-M on high-sensitive C-reactive protein (hs-CRP) levels remains to be determined.	Aspirin	9-16	C-reactive protein	Homo sapiens	300-303
12860262-1	2003	Statins, aspirin and angiotensin II modulators (A II-M: angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type I receptor blockades) may have an anti-inflammatory effect, but the relationship between the effects of statins, aspirin and A II-M on high-sensitive C-reactive protein (hs-CRP) levels remains to be determined.	Aspirin	240-247	angiotensinogen	Homo sapiens	21-35
12860262-1	2003	Statins, aspirin and angiotensin II modulators (A II-M: angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type I receptor blockades) may have an anti-inflammatory effect, but the relationship between the effects of statins, aspirin and A II-M on high-sensitive C-reactive protein (hs-CRP) levels remains to be determined.	Aspirin	240-247	angiotensin I converting enzyme	Homo sapiens	56-85
12860262-1	2003	Statins, aspirin and angiotensin II modulators (A II-M: angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type I receptor blockades) may have an anti-inflammatory effect, but the relationship between the effects of statins, aspirin and A II-M on high-sensitive C-reactive protein (hs-CRP) levels remains to be determined.	Aspirin	240-247	angiotensinogen	Homo sapiens	107-121
12852794-8	2003	CRP levels may also prove useful in targeting therapy for primary and secondary prevention, by identifying patients who would most benefit from medications such as statins and aspirin.	Aspirin	176-183	C-reactive protein	Homo sapiens	0-3
14636445-1	2003	OBJECTIVE: To observe the anti-tumor effect of combination TNF-related apoptosis-inducing ligand (TRAIL) with aspirin on liver cancer cell line, SMMC-7721.	Aspirin	110-117	TNF superfamily member 10	Homo sapiens	59-96
12796127-7	2003	CONCLUSIONS: Among patients with AF who received aspirin, raised levels of vWf (endothelial damage/dysfunction) were predictive of stroke and vascular events, but raised sP-sel levels (platelet activation) were not associated with increased cardiovascular risk.	Aspirin	49-56	von Willebrand factor	Homo sapiens	75-78
12796127-8	2003	Endothelial damage/dysfunction (or vWf itself) may play an important role in the mechanisms behind stroke and cardiovascular outcome among aspirin-treated AF patients and might represent a target for novel therapies or an adjunctive aid to risk stratification in AF.	Aspirin	139-146	von Willebrand factor	Homo sapiens	35-38
12937357-6	2003	The more severe the heart failure, the more likely an appreciable interaction between aspirin and ACE inhibitors will occur.	Aspirin	86-93	angiotensin I converting enzyme	Homo sapiens	98-101
12774247-5	2003	In contrast, ASA aggravated significantly WRS-induced lesions, and this was accompanied by a fall in the GBF, suppression of prostaglandin E(2) generation, and significant rise in ROS chemiluminescence and in plasma TNFalpha and IL-1beta levels.	Aspirin	13-16	tumor necrosis factor	Homo sapiens	216-224
12774247-5	2003	In contrast, ASA aggravated significantly WRS-induced lesions, and this was accompanied by a fall in the GBF, suppression of prostaglandin E(2) generation, and significant rise in ROS chemiluminescence and in plasma TNFalpha and IL-1beta levels.	Aspirin	13-16	interleukin 1 beta	Homo sapiens	229-237
12774247-8	2003	ASA aggravates WRS damage via enhancement of ROS and cytokine generation and suppression of SOD and GPx, and these effects are counteracted by NO released from NO-ASA.	Aspirin	163-166	superoxide dismutase 1	Homo sapiens	92-95
12774247-6	2003	ASA also enhanced significantly the mucosal MDA content and downregulated SOD and GPx mRNA, and these effects were markedly reduced by NO-ASA.	Aspirin	0-3	superoxide dismutase 1	Homo sapiens	74-77
12774247-6	2003	ASA also enhanced significantly the mucosal MDA content and downregulated SOD and GPx mRNA, and these effects were markedly reduced by NO-ASA.	Aspirin	138-141	superoxide dismutase 1	Homo sapiens	74-77
12774247-8	2003	ASA aggravates WRS damage via enhancement of ROS and cytokine generation and suppression of SOD and GPx, and these effects are counteracted by NO released from NO-ASA.	Aspirin	0-3	superoxide dismutase 1	Homo sapiens	92-95
12827217-4	2003	In addition, this compound inhibited cyclooxygenase-2 (COX-2) activity, which was also observed in aspirin-treated human monocytes.	Aspirin	99-106	prostaglandin-endoperoxide synthase 2	Homo sapiens	37-53
12792801-3	2003	Expression of TFF1, TFF2 and TFF3 mRNAs are differentially regulated by FGF2/bFGF, FGF7/KGF, estrogen, aspirin, arachidonic acid, X-ray irradiation, and hydrogen peroxide.	Aspirin	103-110	trefoil factor 1	Homo sapiens	14-18
12792801-3	2003	Expression of TFF1, TFF2 and TFF3 mRNAs are differentially regulated by FGF2/bFGF, FGF7/KGF, estrogen, aspirin, arachidonic acid, X-ray irradiation, and hydrogen peroxide.	Aspirin	103-110	trefoil factor 2	Homo sapiens	20-24
12792801-3	2003	Expression of TFF1, TFF2 and TFF3 mRNAs are differentially regulated by FGF2/bFGF, FGF7/KGF, estrogen, aspirin, arachidonic acid, X-ray irradiation, and hydrogen peroxide.	Aspirin	103-110	trefoil factor 3	Homo sapiens	29-33
12827217-4	2003	In addition, this compound inhibited cyclooxygenase-2 (COX-2) activity, which was also observed in aspirin-treated human monocytes.	Aspirin	99-106	prostaglandin-endoperoxide synthase 2	Homo sapiens	55-60
12883841-23	2003	CONCLUSION: In patients with FA taking aspirin and clopidogrel, selective thrombin injection is more effective than manual compression.	Aspirin	39-46	coagulation factor II, thrombin	Homo sapiens	74-82
12910692-7	2003	Immunohistochemistry and immunoblotting indicated that aspirin effectively decreased COX-2 and c-fos expression in SGC-7901 cell.	Aspirin	55-62	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	85-90
12910692-10	2003	The anti-neoplastic effect aspirin produces may involve the inhibition of COX-2 expression and AP-1 activity.	Aspirin	27-34	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	74-79
14592546-2	2003	It is possible that inhibition of cyclooxygenase (COX)-1 is the major action of aspirin involved in its analgesic and antipyretic effects, and inhibition of COX-2 is responsible for its anti-inflammatory action.	Aspirin	80-87	cytochrome c oxidase I, mitochondrial	Mus musculus	34-56
12904261-6	2003	COX-2 inhibition may decrease endothelial inflammation reducing monocytes infiltration improving vascular cells function, plaque stability and probably resulting in a decrease of coronary atherothrombotic events.Trials including large numbers of patients in prospective double-blind randomized studies worthwhile to confirm the efficacy of NSAID, mainly, COX-2 inhibitors, together with aspirin in the prevention of coronary events in patients with acute coronary disease.	Aspirin	387-394	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
12794159-0	2003	Aspirin-triggered lipoxin A4 and B4 analogs block extracellular signal-regulated kinase-dependent TNF-alpha secretion from human T cells.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	98-107
14592546-5	2003	The antipyretic action of aspirin may be mediated by inhibition of COX-3 in hypothalamic endothelial cells or by inhibition of COX-1 localised close to sensory receptors of peripheral vagal afferents.	Aspirin	26-33	cytochrome c oxidase I, mitochondrial	Mus musculus	127-132
14592555-7	2003	RESULTS: Incubation of HUVECs and PC-12 with 10(-5) mol/l of aspirin increased cNOS expression by 70 +/- 7% and 50 +/- 5, respectively.	Aspirin	61-68	nitric oxide synthase 3	Homo sapiens	79-83
14592556-4	2003	Pretreatment with COX-1 and COX-3 inhibitors (aspirin at a low dose of 1 mg kg(-1), SC 560 and acetaminophen, 0.3-3 mg kg(-1)) slightly augmented thrombolysis by ACE-I, while COX-2 inhibitors (nimesulide and coxibs at doses <1 mg kg(-1) and aspirin at a high dose of 50 mg kg(-1)) or a kinin B2 receptor antagonist (icatibant) abolished it.	Aspirin	46-53	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	18-23
14592556-4	2003	Pretreatment with COX-1 and COX-3 inhibitors (aspirin at a low dose of 1 mg kg(-1), SC 560 and acetaminophen, 0.3-3 mg kg(-1)) slightly augmented thrombolysis by ACE-I, while COX-2 inhibitors (nimesulide and coxibs at doses <1 mg kg(-1) and aspirin at a high dose of 50 mg kg(-1)) or a kinin B2 receptor antagonist (icatibant) abolished it.	Aspirin	244-251	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	18-23
14592562-9	2003	Moreover, in human studies, aspirin seems to be most effective in those with elevated C-reactive protein levels.	Aspirin	28-35	C-reactive protein	Homo sapiens	86-104
12742982-10	2003	(5) Aspirin reduced both the spontaneous and the SFLLRN-stimulated release of IL-7 from platelets, and when administered to healthy control subjects for 7 days (160 mg qd), it reduced plasma levels of IL-7.	Aspirin	4-11	interleukin 7	Homo sapiens	78-82
14592547-0	2003	Control of COX-2 and iNOS gene expressions by aspirin and salicylate.	Aspirin	46-53	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	11-16
14592547-0	2003	Control of COX-2 and iNOS gene expressions by aspirin and salicylate.	Aspirin	46-53	nitric oxide synthase 2	Homo sapiens	21-25
14592549-2	2003	An incomplete suppression of platelet thromboxane (TX) A2 biosynthesis has been assumed to participate in the phenomenon of aspirin resistance, as a consequence of the following possible mechanisms: (i) COX-2 expression in newly formed platelets; (ii) pharmacodynamic interactions between aspirin and coadministered nonsteroidal antiinflammatory drugs (e.g. ibuprofen); (iii) expression of variant isoforms of COX-1 with reduced sensitivity to irreversible inactivation at Ser529.	Aspirin	124-131	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	203-208
14592549-4	2003	Thus, in a subset of patients with unstable angina treated with low-dose aspirin, to almost completely block platelet COX-1 activity, enhanced TXA2 biosynthesis in vivo has been demonstrated, presumably through an increased generation of COX-2-dependent PGH2 in plaque monocytes/macrophages or activated vascular cells.	Aspirin	73-80	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	238-243
14592550-7	2003	Moreover, platelet-neutrophil adhesion induced by thrombin, fMPL or LPS was inhibited by the inhibitor of cyclooxygenase (aspirin), by TXA2 synthase inhibitor (camonagrel), by PAF receptor antagonist (WEB 2170), by the inhibitor of FLAP (MK 886) and by cysLTs receptors antagonist (MK 571).	Aspirin	122-129	coagulation factor II, thrombin	Homo sapiens	50-58
12742982-10	2003	(5) Aspirin reduced both the spontaneous and the SFLLRN-stimulated release of IL-7 from platelets, and when administered to healthy control subjects for 7 days (160 mg qd), it reduced plasma levels of IL-7.	Aspirin	4-11	interleukin 7	Homo sapiens	201-205
12730088-8	2003	Naproxen and aspirin significantly suppressed thrombin generation.	Aspirin	13-20	coagulation factor II, thrombin	Homo sapiens	46-54
12704352-10	2003	In patients with AIA, as opposed to healthy subjects, aspirin challenge invariably precipitated a clinical reaction, accompanied in most patients by a further rise in plasma levels of PGD(2) metabolite and tryptase.	Aspirin	54-61	prostaglandin D2 synthase	Homo sapiens	184-190
12798824-0	2003	Aspirin alters arterial function in patients with chronic heart failure treated with ACE inhibitors: a dose-mediated deleterious effect.	Aspirin	0-7	angiotensin I converting enzyme	Homo sapiens	85-88
12704649-0	2003	Endothelial activation by angiotensin II through NFkappaB and p38 pathways: Involvement of NFkappaB-inducible kinase (NIK), free oxygen radicals, and selective inhibition by aspirin.	Aspirin	174-181	angiotensinogen	Homo sapiens	26-40
12704649-6	2003	In analogy with TNF-alpha-dependent activation of NFkappaB, treatment with either the anti-oxidant N-acetyl cysteine (NAC) or the cyclooxygenase (COX) inhibitor acetyl salicylic acid (aspirin), but not indometacin, prevents the induction of NFkappaB-dependent transcription by AII.	Aspirin	161-182	tumor necrosis factor	Homo sapiens	16-25
12704649-6	2003	In analogy with TNF-alpha-dependent activation of NFkappaB, treatment with either the anti-oxidant N-acetyl cysteine (NAC) or the cyclooxygenase (COX) inhibitor acetyl salicylic acid (aspirin), but not indometacin, prevents the induction of NFkappaB-dependent transcription by AII.	Aspirin	161-182	nuclear factor kappa B subunit 1	Homo sapiens	50-58
12704649-6	2003	In analogy with TNF-alpha-dependent activation of NFkappaB, treatment with either the anti-oxidant N-acetyl cysteine (NAC) or the cyclooxygenase (COX) inhibitor acetyl salicylic acid (aspirin), but not indometacin, prevents the induction of NFkappaB-dependent transcription by AII.	Aspirin	161-182	nuclear factor kappa B subunit 1	Homo sapiens	241-249
12704649-6	2003	In analogy with TNF-alpha-dependent activation of NFkappaB, treatment with either the anti-oxidant N-acetyl cysteine (NAC) or the cyclooxygenase (COX) inhibitor acetyl salicylic acid (aspirin), but not indometacin, prevents the induction of NFkappaB-dependent transcription by AII.	Aspirin	161-182	angiotensinogen	Homo sapiens	277-280
12704649-6	2003	In analogy with TNF-alpha-dependent activation of NFkappaB, treatment with either the anti-oxidant N-acetyl cysteine (NAC) or the cyclooxygenase (COX) inhibitor acetyl salicylic acid (aspirin), but not indometacin, prevents the induction of NFkappaB-dependent transcription by AII.	Aspirin	184-191	nuclear factor kappa B subunit 1	Homo sapiens	50-58
12704649-7	2003	Thus, production of reactive oxygen species, aspirin (asp)-sensitive enzymes of the arachidonate metabolism, and NIK are common transducers of AII- and TNF-dependent pathways to NFkappaB.	Aspirin	45-52	angiotensinogen	Homo sapiens	143-146
12704649-7	2003	Thus, production of reactive oxygen species, aspirin (asp)-sensitive enzymes of the arachidonate metabolism, and NIK are common transducers of AII- and TNF-dependent pathways to NFkappaB.	Aspirin	45-52	tumor necrosis factor	Homo sapiens	152-155
12704649-7	2003	Thus, production of reactive oxygen species, aspirin (asp)-sensitive enzymes of the arachidonate metabolism, and NIK are common transducers of AII- and TNF-dependent pathways to NFkappaB.	Aspirin	45-52	nuclear factor kappa B subunit 1	Homo sapiens	178-186
12704649-7	2003	Thus, production of reactive oxygen species, aspirin (asp)-sensitive enzymes of the arachidonate metabolism, and NIK are common transducers of AII- and TNF-dependent pathways to NFkappaB.	Aspirin	45-48	angiotensinogen	Homo sapiens	143-146
12704649-7	2003	Thus, production of reactive oxygen species, aspirin (asp)-sensitive enzymes of the arachidonate metabolism, and NIK are common transducers of AII- and TNF-dependent pathways to NFkappaB.	Aspirin	45-48	tumor necrosis factor	Homo sapiens	152-155
12704649-7	2003	Thus, production of reactive oxygen species, aspirin (asp)-sensitive enzymes of the arachidonate metabolism, and NIK are common transducers of AII- and TNF-dependent pathways to NFkappaB.	Aspirin	45-48	nuclear factor kappa B subunit 1	Homo sapiens	178-186
12704649-8	2003	AII also activates the inflammatory p38 kinase in endothelial cells, an effect inhibited by exposure to either NAC or asp.	Aspirin	118-121	angiotensinogen	Homo sapiens	0-3
12704649-8	2003	AII also activates the inflammatory p38 kinase in endothelial cells, an effect inhibited by exposure to either NAC or asp.	Aspirin	118-121	mitogen-activated protein kinase 14	Homo sapiens	36-39
12704649-10	2003	These results support a pro-inflammatory effect of the vasoactive peptide AII in endothelial cells, through at least two pathways-NFkappaB and p38-both of which are sensitive to asp and antioxidants.	Aspirin	178-181	angiotensinogen	Homo sapiens	74-77
12704649-10	2003	These results support a pro-inflammatory effect of the vasoactive peptide AII in endothelial cells, through at least two pathways-NFkappaB and p38-both of which are sensitive to asp and antioxidants.	Aspirin	178-181	nuclear factor kappa B subunit 1	Homo sapiens	130-138
12704649-10	2003	These results support a pro-inflammatory effect of the vasoactive peptide AII in endothelial cells, through at least two pathways-NFkappaB and p38-both of which are sensitive to asp and antioxidants.	Aspirin	178-181	mitogen-activated protein kinase 14	Homo sapiens	143-146
12787065-8	2003	Two NF-kappa B inhibitors, aspirin (10 mM) and MG-132 (0.1 microM), blocked basal apoE and apoJ secretion as well as LPS-induced apoJ secretion.	Aspirin	27-34	apolipoprotein E	Rattus norvegicus	82-86
12838187-5	2003	RESULTS: Patients in the IVMP plus ASA/IVIG group, compared with those in the ASA/IVIG alone group, had a shorter mean duration of fever >/=38.3 degrees C after initiation of therapy (1.0 +/- 1.3 vs 2.4 +/- 1.9 days, mean +/- SD, P =.012), shorter hospital stays (1.9 +/- 0.7 vs 3.3 +/- 2.1 days, P =.010), and at six weeks, lower mean erythrocyte sedimentation rate (11.1 +/- 5.7 vs 19.4 +/- 12.4, P =.027) and median c-reactive protein (0.03 vs 0.08, P =.011, Wilcoxon).	Aspirin	35-38	C-reactive protein	Homo sapiens	422-440
12813129-0	2003	Reduction of beta-catenin/T-cell transcription factor signaling by aspirin and indomethacin is caused by an increased stabilization of phosphorylated beta-catenin.	Aspirin	67-74	hepatocyte nuclear factor 4 alpha	Homo sapiens	26-53
12813129-4	2003	Previously, we have shown that the nonsteroidal anti-inflammatory drugs (NSAIDs) aspirin and indomethacin down-regulate beta-catenin/TCF signaling in colorectal cancer cells.	Aspirin	81-88	hepatocyte nuclear factor 4 alpha	Homo sapiens	133-136
12813129-8	2003	The aspirin-induced beta-catenin phosphorylation in colon cancer cells preceded down-regulation of beta-catenin/TCF signaling, suggesting a causal relationship.	Aspirin	4-11	hepatocyte nuclear factor 4 alpha	Homo sapiens	112-115
12894587-4	2003	Inhibitors of the NF kappa B signaling pathway, which is activated by LMP-1, including I kappa B super-repressor and aspirin reduce or cancel induction of MMP-9, COX-2 and invasiveness of LMP-1-expressing cells.	Aspirin	117-124	prostaglandin-endoperoxide synthase 2	Homo sapiens	162-167
12787804-5	2003	Moreover, in the presence of a catalase inhibitor-aminotriazol, ASA showed more apoptotic effect on SKHep-1 cells with increasing intracellular H(2)O(2) level.	Aspirin	64-67	catalase	Homo sapiens	31-39
12787804-6	2003	In conclusion, the present results shows that ASA induced SKHep-1 cell apoptosis has a relation with an early increase in intracellular H(2)O(2) level and catalase inhibitor synergizes to induce this process.	Aspirin	46-49	catalase	Homo sapiens	155-163
12796206-0	2003	Cyclooxygenase-2 inhibitors in aspirin-sensitive asthma.	Aspirin	31-38	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-16
12870263-2	2003	The biological effects induced by aspirin and indomethacin on T98G cells, in which the expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were confirmed by RT-PCR and immunostaining, were investigated by studying cell proliferation and apoptosis assays.	Aspirin	34-41	prostaglandin-endoperoxide synthase 1	Homo sapiens	101-117
12870263-2	2003	The biological effects induced by aspirin and indomethacin on T98G cells, in which the expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were confirmed by RT-PCR and immunostaining, were investigated by studying cell proliferation and apoptosis assays.	Aspirin	34-41	prostaglandin-endoperoxide synthase 2	Homo sapiens	130-146
12870263-2	2003	The biological effects induced by aspirin and indomethacin on T98G cells, in which the expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were confirmed by RT-PCR and immunostaining, were investigated by studying cell proliferation and apoptosis assays.	Aspirin	34-41	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	148-153
12746227-2	2003	Lipoxin (LX) A(4) and aspirin-triggered-LX (ATL) are endogenous lipid-derived mediators that regulate leukocyte trafficking via specific LXA(4) receptors (ALX), and are involved in endogenous anti-inflammation and resolution.	Aspirin	22-29	formyl peptide receptor 2-like	Rattus norvegicus	155-158
12826772-12	2003	There are controversial data about the negative interaction between aspirin and angiotensin-converting enzyme inhibitors in patients with congestive heart failure.	Aspirin	68-75	angiotensin I converting enzyme	Homo sapiens	80-109
12743579-0	2003	Biochemical and clinical evidence that aspirin-intolerant asthmatic subjects tolerate the cyclooxygenase 2-selective analgetic drug celecoxib.	Aspirin	39-46	prostaglandin-endoperoxide synthase 2	Homo sapiens	90-106
12871375-3	2003	ASA ingestion significantly (global P < 0.05) reduced the enhancing effect of epinephrine on LPS-induced IL-8 release by 15-28%.	Aspirin	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	108-112
12841635-6	2003	Treating rabbits with methylene blue or aspirin did not affect TNFalpha secretion but prevented the LPS-induced rise of hydroperoxides and the inactivation of catalase, abolishing fever.	Aspirin	40-47	catalase	Oryctolagus cuniculus	159-167
15199473-4	2003	Aspirin and salicylate at therapeutic concentrations inhibit COX-2 protein expression through interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2 promoter/enhancer.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	61-66
15199473-4	2003	Aspirin and salicylate at therapeutic concentrations inhibit COX-2 protein expression through interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2 promoter/enhancer.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	194-199
15199473-5	2003	Expression of other genes, such as inducible nitric oxide synthase and interleukin-4, may be inhibited by aspirin and salicylate by a C/EBP-dependent mechanism.	Aspirin	106-113	interleukin 4	Homo sapiens	71-84
15199473-5	2003	Expression of other genes, such as inducible nitric oxide synthase and interleukin-4, may be inhibited by aspirin and salicylate by a C/EBP-dependent mechanism.	Aspirin	106-113	CCAAT enhancer binding protein alpha	Homo sapiens	134-139
12767724-1	2003	Anti-thrombotic therapy with aspirin, which at low doses acts as a selective inhibitor of platelet cyclooxygenase 1 (COX-1) activity, is well established.	Aspirin	29-36	prostaglandin-endoperoxide synthase 1	Homo sapiens	99-115
12767724-1	2003	Anti-thrombotic therapy with aspirin, which at low doses acts as a selective inhibitor of platelet cyclooxygenase 1 (COX-1) activity, is well established.	Aspirin	29-36	prostaglandin-endoperoxide synthase 1	Homo sapiens	117-122
12767724-2	2003	However, a major limitation of aspirin treatment is its gastrointestinal toxicity, which is thought to be linked to the suppression of COX-1-mediated production of cytoprotective prostaglandins.	Aspirin	31-38	prostaglandin-endoperoxide synthase 1	Homo sapiens	135-140
12767724-3	2003	Selective COX-2 inhibitors are effective anti-inflammatory agents with lower gastrointestinal toxicity than aspirin.	Aspirin	108-115	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	10-15
12652502-12	2003	In patients with false aneurysms and failed compression therapy under full-dose aspirin, clopidogrel, and heparin, selective thrombin injection is highly effective and safe.	Aspirin	80-87	coagulation factor II, thrombin	Homo sapiens	125-133
12684334-0	2003	Cyclooxygenase-2 inhibitors in aspirin-induced asthma.	Aspirin	31-38	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-16
12668895-6	2003	Cross-reactions between aspirin and other drugs are dependent upon inhibition of the cyclooxygenase-1 isoenzyme.	Aspirin	24-31	prostaglandin-endoperoxide synthase 1	Homo sapiens	85-101
12668895-9	2003	The new highly selective cyclooxygenase 2 inhibitors are well tolerated in AERD asthmatics who have not been desensitized to aspirin.	Aspirin	125-132	prostaglandin-endoperoxide synthase 2	Homo sapiens	25-41
12739030-0	2003	Aspirin use is associated with higher serum concentrations of the anti-oxidant enzyme, paraoxonase-1.	Aspirin	0-7	paraoxonase 1	Homo sapiens	87-100
12665982-2	2003	The aim of the study was to estimate the influence of ASA on the changes in the concentration of ACTH, cortisol and aldosterone (ALD) induced by physical exercise.	Aspirin	54-57	proopiomelanocortin	Homo sapiens	97-101
12665982-12	2003	In both groups after exercise ACTH, cortisol and ALD concentrations were significantly increased, however when compared to the control group, the increase of ACTH in the ASA group was significantly higher, and ALD increase significantly lower.	Aspirin	170-173	proopiomelanocortin	Homo sapiens	30-34
12665982-12	2003	In both groups after exercise ACTH, cortisol and ALD concentrations were significantly increased, however when compared to the control group, the increase of ACTH in the ASA group was significantly higher, and ALD increase significantly lower.	Aspirin	170-173	proopiomelanocortin	Homo sapiens	158-162
12665982-15	2003	That is most likely because the ACTH concentrations in the ASA and control groups were sufficient for almost maximal cortisol secretion.	Aspirin	59-62	proopiomelanocortin	Homo sapiens	32-36
15199473-1	2003	Aspirin acetylates serine-530 of cyclooxygenase-1 (COX-1), thereby blocking thromboxane A (2) synthesis in platelets and reducing platelet aggregation.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	33-49
12622739-0	2003	Transcriptional regulation of COX-2: a key mechanism in the pathogenesis of nasal polyposis in aspirin-sensitive asthmatics?	Aspirin	95-102	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	30-35
15199473-1	2003	Aspirin acetylates serine-530 of cyclooxygenase-1 (COX-1), thereby blocking thromboxane A (2) synthesis in platelets and reducing platelet aggregation.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	51-56
15199473-3	2003	Aspirin is less effective in inhibiting COX-2 activity, whereas celecoxib and rofecoxib selectively inhibit COX-2 activity as they contain a side chain to anchor to the side pocket of COX-2 substrate channel.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	40-45
12618325-6	2003	The possibility of COX-2 as a candidate player in cancer development and progression evolved from the epidemiological studies which suggest that regular use of aspirin or other non-steroidal anti-inflammatory drugs could significantly decrease the risk of developing cancers in experimental animals and in humans.	Aspirin	160-167	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	19-24
12684272-17	2003	8 In conclusion, aspirin suppresses the proliferation of metastatic B16 cells in a JNK-dependent mechanism.	Aspirin	17-24	mitogen-activated protein kinase 8	Homo sapiens	83-86
12612897-10	2003	CONCLUSIONS: In this study, we have proven the concept that addition of an NO-donating moiety to aspirin results in a new chemical entity that maintains cyclooxygenase-1 and platelet inhibitory activity while nearly avoiding gastrointestinal damage.	Aspirin	97-104	prostaglandin-endoperoxide synthase 1	Homo sapiens	153-169
12723895-1	2003	The potential clinical effect of aspirin (ASA) in patients treated with angiotensin converting enzyme (ACE) inhibitors is debatable.	Aspirin	33-40	angiotensin I converting enzyme	Homo sapiens	72-101
12723895-1	2003	The potential clinical effect of aspirin (ASA) in patients treated with angiotensin converting enzyme (ACE) inhibitors is debatable.	Aspirin	33-40	angiotensin I converting enzyme	Homo sapiens	103-106
12723895-1	2003	The potential clinical effect of aspirin (ASA) in patients treated with angiotensin converting enzyme (ACE) inhibitors is debatable.	Aspirin	42-45	angiotensin I converting enzyme	Homo sapiens	72-101
12723895-1	2003	The potential clinical effect of aspirin (ASA) in patients treated with angiotensin converting enzyme (ACE) inhibitors is debatable.	Aspirin	42-45	angiotensin I converting enzyme	Homo sapiens	103-106
12723895-2	2003	Several studies have suggested that ASA attenuates the beneficial effects of ACE inhibitors in hypertension, congestive heart failure (CHF) or coronary artery disease (CAD) and have questioned the safety of using ASA concomitantly with these agents.	Aspirin	36-39	angiotensin I converting enzyme	Rattus norvegicus	77-80
12723895-11	2003	These results indicate that ASA attenuates the beneficial effects of ACE inhibitor on survival in hypertensive rats and this effect was more pronounced at higher dose of ASA.	Aspirin	28-31	angiotensin I converting enzyme	Rattus norvegicus	69-72
12723895-11	2003	These results indicate that ASA attenuates the beneficial effects of ACE inhibitor on survival in hypertensive rats and this effect was more pronounced at higher dose of ASA.	Aspirin	170-173	angiotensin I converting enzyme	Rattus norvegicus	69-72
12676270-13	2003	Findings also revealed that hypothalamic CRH expression was increased when rats were treated with ASA.	Aspirin	98-101	corticotropin releasing hormone	Rattus norvegicus	41-44
12591106-12	2003	We conclude that a single dose of aspirin affects major platelet receptors, presumably directly or indirectly through the inhibition of prostanoids via platelet cyclooxygenase-1 blockade.	Aspirin	34-41	prostaglandin-endoperoxide synthase 1	Homo sapiens	161-177
12644339-10	2003	Furthermore, the benefits of lifestyle modification and drug therapy with aspirin or statins may be most marked among those with elevated CRP levels.	Aspirin	74-81	C-reactive protein	Homo sapiens	138-141
12625225-0	2003	Impact of aspirin on the gastrointestinal-sparing effects of cyclooxygenase-2 inhibitors.	Aspirin	10-17	prostaglandin-endoperoxide synthase 2	Homo sapiens	61-77
12671901-3	2003	Aspirin acetylation of cyclooxygenase 2 also promotes the generation of a series of 15-epimers of LXA(4), known as aspirin-triggered lipoxins (ATL), that may account for some of the bioactivity profile of aspirin and possibly of nonsteroidal anti-inflammatory drugs.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	23-39
12671901-3	2003	Aspirin acetylation of cyclooxygenase 2 also promotes the generation of a series of 15-epimers of LXA(4), known as aspirin-triggered lipoxins (ATL), that may account for some of the bioactivity profile of aspirin and possibly of nonsteroidal anti-inflammatory drugs.	Aspirin	115-122	prostaglandin-endoperoxide synthase 2	Homo sapiens	23-39
12671901-3	2003	Aspirin acetylation of cyclooxygenase 2 also promotes the generation of a series of 15-epimers of LXA(4), known as aspirin-triggered lipoxins (ATL), that may account for some of the bioactivity profile of aspirin and possibly of nonsteroidal anti-inflammatory drugs.	Aspirin	205-212	prostaglandin-endoperoxide synthase 2	Homo sapiens	23-39
14586741-7	2003	Chronic aspirin treatment in diabetic rats significantly attenuated mesangial expansion, and effectively suppressed CTGF induction, as well as inhibiting the upregulation of TGF-beta1 and fibronectin expression.	Aspirin	8-15	transforming growth factor, beta 1	Rattus norvegicus	174-183
12621391-8	2003	CYP3A activity indices increased moderately but significantly by both 7-day and 14-day aspirin treatment (P <.05), but the percentage changes in CYP3A activity indices were not significant.	Aspirin	87-94	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-5
12621391-12	2003	The effect of low-dose aspirin on CYP3A activity awaits further confirmation.	Aspirin	23-30	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	34-39
12723895-3	2003	The present study aims to investigate the possible interaction between ASA and ACE inhibitor in hypertensive rats.	Aspirin	71-74	angiotensin I converting enzyme	Rattus norvegicus	79-82
12566377-8	2003	However, ASA treatment decreased TGF-beta1 transcription and had no significant effect on TGF-beta1 concentration.	Aspirin	9-12	transforming growth factor, beta 1	Rattus norvegicus	33-42
12566377-9	2003	CONCLUSIONS: TGF-beta seems to play an important role in ASA-mediated inhibition of cell proliferation.	Aspirin	57-60	transforming growth factor, beta 1	Rattus norvegicus	13-21
12566377-11	2003	This relationship between ASA and TGF-beta explains many other effects, such as cancer chemoprevention, immunomodulation, and wound healing.	Aspirin	26-29	transforming growth factor, beta 1	Rattus norvegicus	34-42
12622742-1	2003	BACKGROUND: We examined whether a decreased activity of nuclear factor(NF)-kappaB), a transcriptional regulator of cyclooxygenase-2 (COX-2), could account for down-regulation of COX-2 in nasal polyps of aspirin-sensitive asthmatics.	Aspirin	203-210	prostaglandin-endoperoxide synthase 2	Homo sapiens	133-138
12622742-1	2003	BACKGROUND: We examined whether a decreased activity of nuclear factor(NF)-kappaB), a transcriptional regulator of cyclooxygenase-2 (COX-2), could account for down-regulation of COX-2 in nasal polyps of aspirin-sensitive asthmatics.	Aspirin	203-210	prostaglandin-endoperoxide synthase 2	Homo sapiens	178-183
12622742-7	2003	CONCLUSION: This study shows that the low expression of COX-2 mRNA in nasal polyps from aspirin-sensitive patients is associated with a down-regulation of NF-kappaB activity.	Aspirin	88-95	prostaglandin-endoperoxide synthase 2	Homo sapiens	56-61
12527817-3	2003	One of these, triacetylsalicylhydroxamic acid (TriAcSHA) was more effective than aspirin and O-acetylsalicylhydroxamic acid in inactivating both COX-1 and COX-2.	Aspirin	81-88	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	155-160
12852484-10	2003	Correlation of COX-1 and CA-4 expression with ASA sensitivity suggested that embryonic COX-1 and possibly CA4 are much more likely candidates for mediators of ASA developmental toxicity.	Aspirin	46-49	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	15-20
12852484-10	2003	Correlation of COX-1 and CA-4 expression with ASA sensitivity suggested that embryonic COX-1 and possibly CA4 are much more likely candidates for mediators of ASA developmental toxicity.	Aspirin	159-162	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	87-92
12607808-2	2003	This study investigated among smokers the relationship between CRP and use of the anti-inflammatories aspirin and ibuprofen.	Aspirin	102-109	C-reactive protein	Homo sapiens	63-66
12607808-4	2003	Regression models were used to determine the independent relationship between aspirin and ibuprofen use and elevated CRP, controlling for demographics, body mass index, history of CVD, and health status.	Aspirin	78-85	C-reactive protein	Homo sapiens	117-120
12607808-5	2003	RESULTS: Frequency of use of aspirin and ibuprofen among "ever smokers," a population that includes current smokers and quitters, was associated with a decreased likelihood of having elevated CRP.	Aspirin	29-36	C-reactive protein	Homo sapiens	192-195
12607808-6	2003	Ever smokers with low frequency of use of either aspirin or ibuprofen had a lower likelihood of having elevated CRP similar to that for "never smokers."	Aspirin	49-56	C-reactive protein	Homo sapiens	112-115
12535860-0	2003	Anti-thrombin action of low-dose acetylsalicylic acid.	Aspirin	33-53	coagulation factor II, thrombin	Homo sapiens	5-13
12535653-0	2003	Aspirin inhibits human coronary artery endothelial cell proliferation by upregulation of p53.	Aspirin	0-7	tumor protein p53	Homo sapiens	89-92
12535653-9	2003	Western blot analysis revealed that the expression of p53 protein was increased after treatment of the cells with ASA.	Aspirin	114-117	tumor protein p53	Homo sapiens	54-57
12535653-10	2003	These observations indicate that ASA decreases endothelial cell proliferation through cell cycle arrest mediated by enhanced p53 expression.	Aspirin	33-36	tumor protein p53	Homo sapiens	125-128
12490308-0	2003	The combined treatment of aspirin and radiation induces apoptosis by the regulation of bcl-2 and caspase-3 in human cervical cancer cell.	Aspirin	26-33	BCL2 apoptosis regulator	Homo sapiens	87-92
12490308-0	2003	The combined treatment of aspirin and radiation induces apoptosis by the regulation of bcl-2 and caspase-3 in human cervical cancer cell.	Aspirin	26-33	caspase 3	Homo sapiens	97-106
12490308-11	2003	We have demonstrated that combined treatment of aspirin and radiation induces the antitumor effect mediated by bcl-2 and caspase-3 pathway in cervical cancer cells.	Aspirin	48-55	BCL2 apoptosis regulator	Homo sapiens	111-116
12490308-11	2003	We have demonstrated that combined treatment of aspirin and radiation induces the antitumor effect mediated by bcl-2 and caspase-3 pathway in cervical cancer cells.	Aspirin	48-55	caspase 3	Homo sapiens	121-130
12535860-2	2003	Here, we report that treatment of coronary artery patients with 100 mg/day of aspirin does not attenuate thrombin generation, but reduces free thrombin by favouring the formation of thrombin/antithrombin (TAT) complexes.	Aspirin	78-85	coagulation factor II, thrombin	Homo sapiens	143-151
12535860-2	2003	Here, we report that treatment of coronary artery patients with 100 mg/day of aspirin does not attenuate thrombin generation, but reduces free thrombin by favouring the formation of thrombin/antithrombin (TAT) complexes.	Aspirin	78-85	coagulation factor II, thrombin	Homo sapiens	143-151
12515735-2	2003	Given that acetylation of fibrinogen by aspirin can alter its clotting properties and the presence of fibrin stimulates thrombin-mediated activation of FXIII, we have tested the hypothesis that treatment with aspirin differentially modulates the influence of the FXIII Val34Leu polymorphism on its activation in vivo.	Aspirin	209-216	coagulation factor II, thrombin	Homo sapiens	120-128
12515735-5	2003	Although the Leu34-positive and -negative subjects were similar with respect to aspirin-related impairment of thrombin generation, aspirin led to a more pronounced inhibition of the activation of FXIII in the Leu34 carriers as compared with the Val34 homozygotes.	Aspirin	80-87	coagulation factor II, thrombin	Homo sapiens	110-118
14758788-7	2003	Because coxibs do not inhibit platelet aggregation, if prophylaxis against thromboembolic disease is required in patients being treated with a selective COX-2 inhibitor, low-dose aspirin should be used in conjunction with the coxib.	Aspirin	179-186	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	153-158
12409308-1	2003	Salicylates, including aspirin, have been shown to improve insulin sensitivity both in human and animal models.	Aspirin	23-30	insulin	Homo sapiens	59-66
12716445-3	2003	Large outcome studies have shown that patients with OA and RA not taking low-dose aspirin have fewer symptomatic and complicated upper GI events when treated with COX-2 selective inhibitors than with nonselective NSAIDs.	Aspirin	82-89	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	163-168
12545150-0	2003	Genetic variation in cyclooxygenase 1: effects on response to aspirin.	Aspirin	62-69	prostaglandin-endoperoxide synthase 1	Homo sapiens	21-37
12545150-9	2003	CONCLUSIONS: The discovery of a functional single-nucleotide polymorphism in the cyclooxygenase 1 locus may ultimately improve the safe and effective use of acetylsalicylic acid by better tailoring of dosage with an individual"s genetic variation.	Aspirin	157-177	prostaglandin-endoperoxide synthase 1	Homo sapiens	81-97
14583071-10	2003	Moreover, recent data suggest that aspirin and NSAIDs may counteract part of the efficacy of ACE inhibitors and be deleterious in chronic heart failure.	Aspirin	35-42	angiotensin I converting enzyme	Homo sapiens	93-96
14586772-4	2003	Aspirin-induced asthma (AIA) is a typical drug-induced phenotype due to aspirin or nonsteroidal antiinflammatory drugs, and these drugs are metabolized by CYP2C9 and UGT1A6, which are regulated by PXR.	Aspirin	0-7	nuclear receptor subfamily 1 group I member 2	Homo sapiens	197-200
14649387-5	2003	Aspirin is still required for patients with cardiovascular risk who are prescribed a COX-2-selective inhibitor.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	85-90
12871563-0	2003	Aspirin resistance is not a common biochemical phenotype explained by unblocked cyclooxygenase-1 activity.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	80-96
12473561-0	2002	NCX-4016 (NO-aspirin) inhibits lipopolysaccharide-induced tissue factor expression in vivo: role of nitric oxide.	Aspirin	13-20	solute carrier family 8 member A1	Rattus norvegicus	0-3
12891293-14	2003	The use of clopidogrel in similar patients treated with aspirin and enoxaparin was associated with elevated levels of TPA and D-dimer what presumably reflected augmentation of fibrinolytic activity.	Aspirin	56-63	plasminogen activator, tissue type	Homo sapiens	118-121
14593356-13	2003	CONCLUSION: Short term use of ticlopidine in patients with NSTEACS treated with aspirin and unfractionated heparin was associated with lower levels of TAT and fibrinogen (relative to control group) on day 14.	Aspirin	80-87	fibrinogen beta chain	Homo sapiens	159-169
14593356-15	2003	Both ticlopidine and clopidogrel used in regimes with loading doses in NSTEACS patients treated with aspirin and antithrombin prevented acute phase elevation of vWF.	Aspirin	101-108	von Willebrand factor	Homo sapiens	161-164
12853707-6	2003	In PRP, it is diminished in von Willebrand"s disease, but it also shows the effect of platelet inhibitors (e.g. aspirin and abciximab).	Aspirin	112-119	prion protein	Homo sapiens	3-6
15041270-0	2003	Mutations within the cyclooxygenase-1 gene in aspirin non-responders with recurrence of stroke.	Aspirin	46-53	prostaglandin-endoperoxide synthase 1	Homo sapiens	21-37
15041270-1	2003	INTRODUCTION: Aspirin is a common antiplatelet drug used in the prevention of ischemic stroke due to its inhibitory effect on platelet cyclooxygenase-1 (Cox-1).	Aspirin	14-21	prostaglandin-endoperoxide synthase 1	Homo sapiens	135-151
15041270-1	2003	INTRODUCTION: Aspirin is a common antiplatelet drug used in the prevention of ischemic stroke due to its inhibitory effect on platelet cyclooxygenase-1 (Cox-1).	Aspirin	14-21	prostaglandin-endoperoxide synthase 1	Homo sapiens	153-158
15041270-3	2003	In this study, we have searched for variants of the Cox-1 gene that could possibly result in an unblocked and thus, aspirin-resistant Cox-1 enzyme and phenotype.	Aspirin	116-123	prostaglandin-endoperoxide synthase 1	Homo sapiens	52-57
15041270-3	2003	In this study, we have searched for variants of the Cox-1 gene that could possibly result in an unblocked and thus, aspirin-resistant Cox-1 enzyme and phenotype.	Aspirin	116-123	prostaglandin-endoperoxide synthase 1	Homo sapiens	134-139
15041270-4	2003	MATERIALS AND METHODS: The Cox-1 gene was sequenced in 68 patients with recurrent ischemic stroke despite taking aspirin.	Aspirin	113-120	prostaglandin-endoperoxide synthase 1	Homo sapiens	27-32
12705063-3	2003	More than 100 years after aspirin, an inhibitor of cyclooxygenase-1 and -2, was first used for the treatment of rheumatic diseases, analogues were developed for the same and other inclinations that now are available for clinical use.	Aspirin	26-33	prostaglandin-endoperoxide synthase 1	Homo sapiens	51-74
12456256-0	2002	Aspirin use may change cost-effectiveness of COX-2 inhibitors.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	45-50
12473561-1	2002	BACKGROUND: NCX-4016 is an acetylsalicylic acid (ASA) derivative containing a nitric oxide-releasing moiety.	Aspirin	27-47	solute carrier family 8 member A1	Rattus norvegicus	12-15
12473561-1	2002	BACKGROUND: NCX-4016 is an acetylsalicylic acid (ASA) derivative containing a nitric oxide-releasing moiety.	Aspirin	49-52	solute carrier family 8 member A1	Rattus norvegicus	12-15
12466023-12	2002	This extends Aspirin"s mode of action from a covalent modification of COX-2 to the upstream regulation of COX-2 gene expression in neurons.	Aspirin	13-20	prostaglandin-endoperoxide synthase 2	Homo sapiens	70-75
12466023-11	2002	CONCLUSIONS: NF-kappaB regulates neuronal COX-2 gene expression, and acts as an upstream target of Aspirin.	Aspirin	99-106	nuclear factor kappa B subunit 1	Homo sapiens	13-22
12512737-4	2002	Similarly, the use of nonaspirin nonsteroidal antiinflammatory drugs (NSAIDs), including cyclooxygenase (COX)-2 inhibitors, has also been shown to increase the risk of GI effects, and the concomitant use of aspirin and nonaspirin NSAIDs can significantly increase the risk of GI ulceration and bleeding.	Aspirin	25-32	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	89-111
12534448-0	2002	Prior aspirin use in unstable angina patients with modified plasma inflammatory markers and endothelial nitric oxide synthase in neutrophils.	Aspirin	6-13	nitric oxide synthase 3	Homo sapiens	92-125
12534448-2	2002	The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils.	Aspirin	46-53	interleukin 6	Homo sapiens	146-159
12534448-2	2002	The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils.	Aspirin	46-53	interleukin 6	Homo sapiens	161-165
12534448-2	2002	The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils.	Aspirin	46-53	tumor necrosis factor	Homo sapiens	198-207
12534448-2	2002	The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils.	Aspirin	46-53	nitric oxide synthase 3	Homo sapiens	278-311
12534448-2	2002	The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils.	Aspirin	46-53	nitric oxide synthase 3	Homo sapiens	313-317
12534448-7	2002	Plasma levels of both IL-6 and ICAM-1 were reduced in patients taking aspirin.	Aspirin	70-77	interleukin 6	Homo sapiens	22-26
12534448-9	2002	The eNOS protein expression was also higher in neutrophils from the UA patients taking aspirin than in those not taking aspirin.	Aspirin	87-94	nitric oxide synthase 3	Homo sapiens	4-8
12534448-9	2002	The eNOS protein expression was also higher in neutrophils from the UA patients taking aspirin than in those not taking aspirin.	Aspirin	120-127	nitric oxide synthase 3	Homo sapiens	4-8
12534448-10	2002	CONCLUSION: Patients taking aspirin before UA showed a lower systemic inflammatory response and higher eNOS protein expression in their neutrophils	Aspirin	28-35	nitric oxide synthase 3	Homo sapiens	103-107
12468886-15	2002	It seems likely that drugs currently used in the treatment of stroke, such as aspirin, statins, and modulators of the renin-angiotensin-aldosterone system, act at least partly via antiinflammatory mechanisms.	Aspirin	78-85	renin	Homo sapiens	118-123
12421891-6	2002	RESULTS: The absolute number of cells expressing the CysLT1 receptor was significantly higher in the aspirin-sensitive patients than in the non-aspirin-sensitive patients (median, 542 cells per square millimeter [range, 148 to 1390] vs. 116 cells per square millimeter [range, 40 to 259]; P<0.001).	Aspirin	101-108	cysteinyl leukotriene receptor 1	Homo sapiens	53-59
12421891-6	2002	RESULTS: The absolute number of cells expressing the CysLT1 receptor was significantly higher in the aspirin-sensitive patients than in the non-aspirin-sensitive patients (median, 542 cells per square millimeter [range, 148 to 1390] vs. 116 cells per square millimeter [range, 40 to 259]; P<0.001).	Aspirin	144-151	cysteinyl leukotriene receptor 1	Homo sapiens	53-59
12421891-7	2002	The percentage of CD45+ leukocytes expressing the CysLT1 receptor was also higher in the aspirin-sensitive subjects (25 percent of CD45+ leukocytes [range, 4 to 50] vs. 5 percent of CD45+ leukocytes [range, 2 to 11]; P<0.001); the percentage of CD45+ leukocytes expressing the LTB4 receptor did not differ significantly between these two groups.	Aspirin	89-96	cysteinyl leukotriene receptor 1	Homo sapiens	50-56
12421891-9	2002	CONCLUSIONS: The elevated numbers of nasal inflammatory leukocytes expressing the CysLT1 receptor in aspirin-sensitive patients with chronic rhinosinusitis as compared with their non-aspirin-sensitive counterparts and the down-regulation of receptor expression after desensitization to aspirin are probably fundamental in the pathogenesis of aspirin sensitivity and in the mechanism of aspirin desensitization.	Aspirin	101-108	cysteinyl leukotriene receptor 1	Homo sapiens	82-88
12421891-9	2002	CONCLUSIONS: The elevated numbers of nasal inflammatory leukocytes expressing the CysLT1 receptor in aspirin-sensitive patients with chronic rhinosinusitis as compared with their non-aspirin-sensitive counterparts and the down-regulation of receptor expression after desensitization to aspirin are probably fundamental in the pathogenesis of aspirin sensitivity and in the mechanism of aspirin desensitization.	Aspirin	183-190	cysteinyl leukotriene receptor 1	Homo sapiens	82-88
12421891-9	2002	CONCLUSIONS: The elevated numbers of nasal inflammatory leukocytes expressing the CysLT1 receptor in aspirin-sensitive patients with chronic rhinosinusitis as compared with their non-aspirin-sensitive counterparts and the down-regulation of receptor expression after desensitization to aspirin are probably fundamental in the pathogenesis of aspirin sensitivity and in the mechanism of aspirin desensitization.	Aspirin	183-190	cysteinyl leukotriene receptor 1	Homo sapiens	82-88
12421891-9	2002	CONCLUSIONS: The elevated numbers of nasal inflammatory leukocytes expressing the CysLT1 receptor in aspirin-sensitive patients with chronic rhinosinusitis as compared with their non-aspirin-sensitive counterparts and the down-regulation of receptor expression after desensitization to aspirin are probably fundamental in the pathogenesis of aspirin sensitivity and in the mechanism of aspirin desensitization.	Aspirin	183-190	cysteinyl leukotriene receptor 1	Homo sapiens	82-88
12421891-9	2002	CONCLUSIONS: The elevated numbers of nasal inflammatory leukocytes expressing the CysLT1 receptor in aspirin-sensitive patients with chronic rhinosinusitis as compared with their non-aspirin-sensitive counterparts and the down-regulation of receptor expression after desensitization to aspirin are probably fundamental in the pathogenesis of aspirin sensitivity and in the mechanism of aspirin desensitization.	Aspirin	183-190	cysteinyl leukotriene receptor 1	Homo sapiens	82-88
12428645-3	2002	Moreover, cyclooxygenase-2 is markedly downregulated in polyps from aspirin-sensitive patients with asthma.	Aspirin	68-75	prostaglandin-endoperoxide synthase 2	Homo sapiens	10-26
12423318-0	2002	COX-2-independent antiproliferative action of acetylsalicylic acid in human colon cancer cells.	Aspirin	46-66	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
12423325-0	2002	The effects of acetylsalicylic acid on proliferation, apoptosis, and invasion of cyclooxygenase-2 negative colon cancer cells.	Aspirin	15-35	prostaglandin-endoperoxide synthase 2	Homo sapiens	81-97
12423325-3	2002	The aim of this study was to determine the effects of acetylsalicylic acid on proliferation, apoptosis, and invasion in human cyclooxygenase-2 (COX-2) negative colorectal cancer cell lines.	Aspirin	54-74	prostaglandin-endoperoxide synthase 2	Homo sapiens	126-142
12423325-3	2002	The aim of this study was to determine the effects of acetylsalicylic acid on proliferation, apoptosis, and invasion in human cyclooxygenase-2 (COX-2) negative colorectal cancer cell lines.	Aspirin	54-74	prostaglandin-endoperoxide synthase 2	Homo sapiens	144-149
12423325-11	2002	After treatment with ASA, down-regulation of Bcl2 and CD44v6 expression and up-regulation of nm23 expression were observed in SW480 cells.	Aspirin	21-24	BCL2 apoptosis regulator	Homo sapiens	45-49
12423325-14	2002	Down-regulation of Bcl2 expression might represent a potential mechanism by which ASA induces apoptosis in this COX-2 negative colon cancer cell line.	Aspirin	82-85	BCL2 apoptosis regulator	Homo sapiens	19-23
12423325-14	2002	Down-regulation of Bcl2 expression might represent a potential mechanism by which ASA induces apoptosis in this COX-2 negative colon cancer cell line.	Aspirin	82-85	prostaglandin-endoperoxide synthase 2	Homo sapiens	112-117
12398900-1	2002	Previous studies with both intact cells and ram seminal vesicles microsomes have shown that the specific PGHS-2 inhibitors NS-398 (N-[2-(cyclohexyloxy)-4-nitrophenyl]methanesulfonamide) and DuP-697 (5-bromo-2[4-fluorophenyl]-3-[4-methylsulfonylphenyl]-thiophene) attenuate the inhibition of PGHS-1 caused by aspirin and indomethacin.	Aspirin	308-315	prostaglandin-endoperoxide synthase 2	Homo sapiens	105-111
12852480-5	2003	Hence, the developmental toxicity seen in rats after exposure to aspirin may be due to the irreversible inhibition of COX-1 and/or COX-2.	Aspirin	65-72	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	118-123
12852480-20	2003	Such a finding is consistent with the concept that reversible inhibition of COX-1 and/or COX-2 by other NSAIDs would produce weaker developmental toxicity signals than aspirin.	Aspirin	168-175	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	76-81
12852482-2	2003	Aspirin (acetylsalicylic acid, ASA) is a widely used NSAID that irreversibly inhibits cyclooxygenases (COXs) 1 and 2.	Aspirin	0-7	prostaglandin G/H synthase 1	Oryctolagus cuniculus	86-116
12852482-2	2003	Aspirin (acetylsalicylic acid, ASA) is a widely used NSAID that irreversibly inhibits cyclooxygenases (COXs) 1 and 2.	Aspirin	9-29	prostaglandin G/H synthase 1	Oryctolagus cuniculus	86-116
12852482-2	2003	Aspirin (acetylsalicylic acid, ASA) is a widely used NSAID that irreversibly inhibits cyclooxygenases (COXs) 1 and 2.	Aspirin	31-34	prostaglandin G/H synthase 1	Oryctolagus cuniculus	86-116
12529741-3	2002	Even in the presence of aspirin, the platelets from various individuals showed highly different thrombin-induced Ca(2+) responses.	Aspirin	24-31	coagulation factor II, thrombin	Homo sapiens	96-104
12447698-6	2002	RT-PCR analyses showed that NS398 and aspirin up-regulated RECK mRNA level in CL-1 human lung cancer cells.	Aspirin	38-45	reversion inducing cysteine rich protein with kazal motifs	Homo sapiens	59-63
12426218-3	2002	CRP values were adjusted for age, body mass index, vitamin use, statin medication use, aspirin use, the presence of inflammatory disease, cardiovascular disease, and diabetes, and smoking habit.	Aspirin	87-94	C-reactive protein	Homo sapiens	0-3
12451498-7	2002	The fact that aspirin but not H7 blocks the enhancing effect suggests that NF-kappaB might be involved in wogonin-enhanced TNF-alpha gene expression.	Aspirin	14-21	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	75-84
12451498-7	2002	The fact that aspirin but not H7 blocks the enhancing effect suggests that NF-kappaB might be involved in wogonin-enhanced TNF-alpha gene expression.	Aspirin	14-21	tumor necrosis factor	Mus musculus	123-132
12398900-6	2002	This finding indicates that specific PGHS-2 inhibitors are similar to ibuprofen in their ability to compete with aspirin, an irreversible time-dependent inhibitor of PGHS-1 often used for prevention of spontaneous thrombosis.	Aspirin	113-120	prostaglandin-endoperoxide synthase 2	Homo sapiens	37-43
12398900-6	2002	This finding indicates that specific PGHS-2 inhibitors are similar to ibuprofen in their ability to compete with aspirin, an irreversible time-dependent inhibitor of PGHS-1 often used for prevention of spontaneous thrombosis.	Aspirin	113-120	prostaglandin-endoperoxide synthase 1	Homo sapiens	166-172
12398900-7	2002	Importantly, the concentrations at which PGHS-2 inhibitors attenuate the inhibition induced by aspirin and indomethacin are well below those required to cause inhibition of PGHS-1.	Aspirin	95-102	prostaglandin-endoperoxide synthase 2	Homo sapiens	41-47
12391014-1	2002	Aspirin (ASA) is unique among current therapies because it acetylates cyclooxygenase (COX)-2 enabling the biosynthesis of R-containing precursors of endogenous antiinflammatory mediators.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	70-92
12391014-1	2002	Aspirin (ASA) is unique among current therapies because it acetylates cyclooxygenase (COX)-2 enabling the biosynthesis of R-containing precursors of endogenous antiinflammatory mediators.	Aspirin	9-12	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	70-92
12391014-4	2002	Human COX-2 converted DHA to 13-hydroxy-DHA that switched with ASA to 17R-HDHA that also proved a major route in hypoxic endothelial cells.	Aspirin	63-66	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	6-11
12391014-5	2002	Human neutrophils transformed COX-2-ASA-derived 17R-hydroxy-DHA into two sets of novel di- and trihydroxy products; one initiated via oxygenation at carbon 7 and the other at carbon 4.	Aspirin	36-39	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	30-35
12167656-2	2002	Acetylation of Ser-530 of PGHS-1 by aspirin abolishes all oxygenase activity and transforms the peroxide-induced tyrosyl radical from a functional 33-35-gauss (G) wide doublet/wide singlet to a 26-G narrow singlet unable to oxidize AA.	Aspirin	36-43	prostaglandin-endoperoxide synthase 1	Homo sapiens	26-32
12167656-3	2002	In contrast, aspirin-treated PGHS-2 (ASA-PGHS-2) no longer forms prostaglandins but retains oxygenase activity forming 11(R)- and 15(R)-hydroperoxyeicosatetraenoic acid and also retains the EPR line-shape of the native peroxide-induced 29-30-G wide singlet radical.	Aspirin	13-20	prostaglandin-endoperoxide synthase 2	Homo sapiens	29-35
12167656-3	2002	In contrast, aspirin-treated PGHS-2 (ASA-PGHS-2) no longer forms prostaglandins but retains oxygenase activity forming 11(R)- and 15(R)-hydroperoxyeicosatetraenoic acid and also retains the EPR line-shape of the native peroxide-induced 29-30-G wide singlet radical.	Aspirin	13-20	prostaglandin-endoperoxide synthase 2	Homo sapiens	41-47
12167656-3	2002	In contrast, aspirin-treated PGHS-2 (ASA-PGHS-2) no longer forms prostaglandins but retains oxygenase activity forming 11(R)- and 15(R)-hydroperoxyeicosatetraenoic acid and also retains the EPR line-shape of the native peroxide-induced 29-30-G wide singlet radical.	Aspirin	37-40	prostaglandin-endoperoxide synthase 2	Homo sapiens	29-35
12167656-3	2002	In contrast, aspirin-treated PGHS-2 (ASA-PGHS-2) no longer forms prostaglandins but retains oxygenase activity forming 11(R)- and 15(R)-hydroperoxyeicosatetraenoic acid and also retains the EPR line-shape of the native peroxide-induced 29-30-G wide singlet radical.	Aspirin	37-40	prostaglandin-endoperoxide synthase 2	Homo sapiens	41-47
12167656-4	2002	To evaluate the functional role of the wide singlet radical in ASA-PGHS-2, we have examined the ability of this radical to oxidize AA in single-turnover EPR studies.	Aspirin	63-66	prostaglandin-endoperoxide synthase 2	Homo sapiens	67-73
12383982-0	2002	Effects of long-term treatment with angiotensin-converting-enzyme inhibitors in the presence or absence of aspirin: a systematic review.	Aspirin	107-114	angiotensin I converting enzyme	Homo sapiens	36-65
12383982-1	2002	BACKGROUND: Results from a retrospective analysis of the Studies of Left Ventricular Dysfunction (SOLVD) study suggest that angiotensin-converting-enzyme (ACE) inhibitors may be less effective in patients receiving aspirin.	Aspirin	215-222	angiotensin I converting enzyme	Homo sapiens	124-153
12383982-1	2002	BACKGROUND: Results from a retrospective analysis of the Studies of Left Ventricular Dysfunction (SOLVD) study suggest that angiotensin-converting-enzyme (ACE) inhibitors may be less effective in patients receiving aspirin.	Aspirin	215-222	angiotensin I converting enzyme	Homo sapiens	155-158
12383982-6	2002	Overall, ACE inhibitor therapy significantly reduced the risk of the major clinical outcomes by 22% (p<0.0001), with clear reductions in risk both among those receiving aspirin at baseline (odds ratio 0.80, [99% CI 0.73-0.88]) and those who were not (0.71 [99% CI 0.62-0.81], interaction p=0.07).	Aspirin	172-179	angiotensin I converting enzyme	Homo sapiens	9-12
12466023-12	2002	This extends Aspirin"s mode of action from a covalent modification of COX-2 to the upstream regulation of COX-2 gene expression in neurons.	Aspirin	13-20	prostaglandin-endoperoxide synthase 2	Homo sapiens	106-111
12714834-2	2002	In this study, we showed that the combination regimen of clopidogrel with aspirin could downregulate the P-selectin expression on platelets and the plasma concentration of C-reactive protein (CRP) in acute stage of atherosclerotic ischemic stroke.	Aspirin	74-81	C-reactive protein	Homo sapiens	172-190
12714834-2	2002	In this study, we showed that the combination regimen of clopidogrel with aspirin could downregulate the P-selectin expression on platelets and the plasma concentration of C-reactive protein (CRP) in acute stage of atherosclerotic ischemic stroke.	Aspirin	74-81	C-reactive protein	Homo sapiens	192-195
12714834-5	2002	RESULTS: The combined regimen of clopidogrel and aspirin significantly reduced platelet P-selectin expression (93.6 +/- 16.6, p < 0.01) and plasma concentration of CRP (1.2 +/- 1.5 mg/dl, p < 0.01) after 7 days of stroke onset compared with the values (P-selectin; 115.5 +/- 20.7, CRP; 2.5 +/- 2.8 mg/dl) of initial 24 hr.	Aspirin	49-56	C-reactive protein	Homo sapiens	167-170
12714834-5	2002	RESULTS: The combined regimen of clopidogrel and aspirin significantly reduced platelet P-selectin expression (93.6 +/- 16.6, p < 0.01) and plasma concentration of CRP (1.2 +/- 1.5 mg/dl, p < 0.01) after 7 days of stroke onset compared with the values (P-selectin; 115.5 +/- 20.7, CRP; 2.5 +/- 2.8 mg/dl) of initial 24 hr.	Aspirin	49-56	C-reactive protein	Homo sapiens	287-290
12383533-7	2002	Expression of HER-2/neu was likewise reduced in a dose-dependent manner from 87% expression in control cells to 16% in those treated with 5-mmol/L aspirin.	Aspirin	147-154	erb-b2 receptor tyrosine kinase 2	Homo sapiens	14-23
12235371-0	2002	Lipoxin A4 and aspirin-triggered 15-epi-lipoxin A4 inhibit peroxynitrite formation, NF-kappa B and AP-1 activation, and IL-8 gene expression in human leukocytes.	Aspirin	15-22	C-X-C motif chemokine ligand 8	Homo sapiens	120-124
12208780-2	2002	The ability of the nitric oxide (NO)-releasing aspirin, NCX 4016, to control vasoconstrictor responses induced by electrical field stimulation (TNS) or by exogenous norepinephrine (NE) was investigated in perfused rat tail artery with intact endothelium.	Aspirin	47-54	solute carrier family 8 member A1	Rattus norvegicus	56-59
12395741-4	2002	THE INFLUENCE OF A CO-PRESCRIPTION OF ASPIRIN: Patients for whom low-dose aspirin is indicated to offset known thrombotic risk must continue this therapy if a COX-2 selective inhibitor is introduced.	Aspirin	38-45	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	159-164
12395741-4	2002	THE INFLUENCE OF A CO-PRESCRIPTION OF ASPIRIN: Patients for whom low-dose aspirin is indicated to offset known thrombotic risk must continue this therapy if a COX-2 selective inhibitor is introduced.	Aspirin	74-81	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	159-164
12208780-9	2002	Aspirin-moiety released by NCX 4016 inhibited the 6-keto-PGF(1alpha) formation without interfering with the vasorelaxant activity of NCX 4016, while aspirin (100 microM) was devoid of any activity against vasoconstriction induced by both TNS and NE in perfused rat tail artery.	Aspirin	0-7	solute carrier family 8 member A1	Rattus norvegicus	27-30
12208780-9	2002	Aspirin-moiety released by NCX 4016 inhibited the 6-keto-PGF(1alpha) formation without interfering with the vasorelaxant activity of NCX 4016, while aspirin (100 microM) was devoid of any activity against vasoconstriction induced by both TNS and NE in perfused rat tail artery.	Aspirin	149-156	solute carrier family 8 member A1	Rattus norvegicus	27-30
12357134-2	2002	Aspirin interferes with arachidonic acid metabolism in platelets and endothelial cells and thereby reduces thromboxane A2 and prostacyclin.	Aspirin	0-7	ATPase H+ transporting V0 subunit a2	Homo sapiens	119-138
24728118-5	2002	Particularly in patients treated with low-dose of aspirin for cardiovascular prophylaxis, the COX-2 inhibitors seem to have no obvious advantages over conventional NSAIDs.	Aspirin	50-57	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	94-99
12230571-8	2002	Using ASA, a fluorescent fatty acid anthroyloxy analogue as a probe, ASP3c was shown to bind specifically to large fatty acids and ester derivatives, which are brood pheromone components, in the micromolar range.	Aspirin	6-9	chemosensory protein 3	Apis mellifera	69-74
12117719-6	2002	Attenuation of the C pneumoniae-induced activation of NF-kappaB by aspirin also reduced the secretion of interleukin-6 and interleukin-8, indicating efficient inhibition of NF-kappaB gene expression.	Aspirin	67-74	nuclear factor kappa B subunit 1	Homo sapiens	54-63
13679651-4	2002	In PRP it is diminished in thrombopathies, in von Willebrand disease, by antibodies blocking GPIIb-IIIa or GPIb, or by antiplatelet drugs like aspirin and clopidogrel.	Aspirin	143-150	prion protein	Homo sapiens	3-6
12151853-8	2002	Because drugs such as aspirin and statins reduce inflammatory risk, C-reactive protein has the potential to guide the use of these therapies in high-risk individuals for primary prevention.	Aspirin	22-29	C-reactive protein	Homo sapiens	68-86
12425211-3	2002	The authors discuss also possible interactions of acetylsalicyl acid and ACE inhibitors which in retrospective analyses indicate possible veakening of the ACE-I when administered concurrently with ASA in cardiac failure.	Aspirin	197-200	angiotensin I converting enzyme	Homo sapiens	73-76
12425211-3	2002	The authors discuss also possible interactions of acetylsalicyl acid and ACE inhibitors which in retrospective analyses indicate possible veakening of the ACE-I when administered concurrently with ASA in cardiac failure.	Aspirin	197-200	angiotensin I converting enzyme	Homo sapiens	155-158
12225961-5	2002	The nonselective cyclooxygenase inhibitors indomethacin and meclofenamate and the preferential cyclooxygenase-1 inhibitor aspirin augmented NO-induced relaxation specifically in newborns, whereas the selective cycloxygenase-2 inhibitor NS-398 had no effect.	Aspirin	122-129	prostaglandin-endoperoxide synthase 1	Homo sapiens	95-111
12117719-6	2002	Attenuation of the C pneumoniae-induced activation of NF-kappaB by aspirin also reduced the secretion of interleukin-6 and interleukin-8, indicating efficient inhibition of NF-kappaB gene expression.	Aspirin	67-74	interleukin 6	Homo sapiens	105-118
12117719-6	2002	Attenuation of the C pneumoniae-induced activation of NF-kappaB by aspirin also reduced the secretion of interleukin-6 and interleukin-8, indicating efficient inhibition of NF-kappaB gene expression.	Aspirin	67-74	C-X-C motif chemokine ligand 8	Homo sapiens	123-136
12117719-6	2002	Attenuation of the C pneumoniae-induced activation of NF-kappaB by aspirin also reduced the secretion of interleukin-6 and interleukin-8, indicating efficient inhibition of NF-kappaB gene expression.	Aspirin	67-74	nuclear factor kappa B subunit 1	Homo sapiens	173-182
12117719-9	2002	Aspirin exerts an anti-chlamydial effect that is due to the inhibition of C pneumoniae-induced NF-kappaB activation, which might account for some of the cardioprotective activity of aspirin.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	95-104
12117719-9	2002	Aspirin exerts an anti-chlamydial effect that is due to the inhibition of C pneumoniae-induced NF-kappaB activation, which might account for some of the cardioprotective activity of aspirin.	Aspirin	182-189	nuclear factor kappa B subunit 1	Homo sapiens	95-104
11994707-3	2002	OBJECTIVE: The aim of these studies was to investigate Cox-1 and Cox-2 regulation in NPs of aspirin-tolerant human patients compared with that seen in nasal mucosa (NM).	Aspirin	92-99	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	65-70
17608990-5	2002	COX-2 inhibitors may be safe alternatives to traditional NSAIDs for patients with aspirin-sensitive asthma.	Aspirin	82-89	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
12133013-0	2002	Does aspirin attenuate the effect of angiotensin-converting enzyme inhibitors on health outcomes of very old patients with heart failure?	Aspirin	5-12	angiotensin I converting enzyme	Homo sapiens	37-66
12133013-2	2002	We estimated the effect of aspirin use on the rate of mortality, morbidity, and decline in physical functioning in nursing home residents with HF taking angiotensin-converting enzyme (ACE) inhibitors.	Aspirin	27-34	angiotensin I converting enzyme	Homo sapiens	153-182
12133013-2	2002	We estimated the effect of aspirin use on the rate of mortality, morbidity, and decline in physical functioning in nursing home residents with HF taking angiotensin-converting enzyme (ACE) inhibitors.	Aspirin	27-34	angiotensin I converting enzyme	Homo sapiens	184-187
12133028-1	2002	PURPOSE: To determine whether the prostacyclin-inhibiting properties of aspirin counteracts the bradykinin-induced prostacyclin-stimulating effects of angiotensin-converting enzyme (ACE) inhibitors, thereby attenuating the beneficial effects of ACE inhibitors in heart failure patients.	Aspirin	72-79	kininogen 1	Homo sapiens	96-106
12133028-14	2002	METHODS: Data from large clinical trials investigating the interaction between aspirin and ACE inhibitors were analyzed to determine the effect of aspirin on the vasodilatory actions of ACE inhibitors in heart failure patients, and the results were analyzed on the basis of theoretical and laboratory findings.	Aspirin	147-154	angiotensin I converting enzyme	Homo sapiens	186-189
12133028-24	2002	This strong interaction between aspirin and the ACE inhibitor enalapril suggests that the survival benefit of enalapril was significantly lower in patients also taking aspirin than in those taking enalapril alone.	Aspirin	32-39	angiotensin I converting enzyme	Homo sapiens	48-51
12133028-24	2002	This strong interaction between aspirin and the ACE inhibitor enalapril suggests that the survival benefit of enalapril was significantly lower in patients also taking aspirin than in those taking enalapril alone.	Aspirin	168-175	angiotensin I converting enzyme	Homo sapiens	48-51
12133028-27	2002	CONCLUSION: There is a theoretical possibility that the negative interaction between ACE inhibitors and aspirin may reduce the beneficial effects of ACE inhibitors in patients with heart failure, but the information obtained from the existing databases is limited by the retrospective nature of the analyses and does not establish the association definitively.	Aspirin	104-111	angiotensin I converting enzyme	Homo sapiens	85-88
12133028-27	2002	CONCLUSION: There is a theoretical possibility that the negative interaction between ACE inhibitors and aspirin may reduce the beneficial effects of ACE inhibitors in patients with heart failure, but the information obtained from the existing databases is limited by the retrospective nature of the analyses and does not establish the association definitively.	Aspirin	104-111	angiotensin I converting enzyme	Homo sapiens	149-152
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	0-7	nitric oxide synthase 2	Rattus norvegicus	141-172
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	0-7	nitric oxide synthase 2	Rattus norvegicus	174-178
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	9-29	nitric oxide synthase 2	Rattus norvegicus	141-172
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	9-29	nitric oxide synthase 2	Rattus norvegicus	174-178
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	31-34	nitric oxide synthase 2	Rattus norvegicus	141-172
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	31-34	nitric oxide synthase 2	Rattus norvegicus	174-178
12118084-2	2002	Here, we examined if prolonged treatment with an NO-releasing form of aspirin (NO-ASA) can influence neointimal remodeling of femoral arteries of hypercholesterolemic ApoE (-/-) mice.	Aspirin	70-77	apolipoprotein E	Mus musculus	167-171
12118084-2	2002	Here, we examined if prolonged treatment with an NO-releasing form of aspirin (NO-ASA) can influence neointimal remodeling of femoral arteries of hypercholesterolemic ApoE (-/-) mice.	Aspirin	82-85	apolipoprotein E	Mus musculus	167-171
12118084-3	2002	Treatment of ApoE (-/-) mice with NO-ASA, but not aspirin (ASA), improved neointimal remodeling post-injury.	Aspirin	37-40	apolipoprotein E	Mus musculus	13-17
12096151-12	2002	A possible interaction with ACE inhibitors may reduce the efficacy of aspirin, although this evidence is from retrospective analyses of trial cohorts.	Aspirin	70-77	angiotensin I converting enzyme	Homo sapiens	28-31
12065343-0	2002	Safety of a cyclooxygenase-2 inhibitor in patients with aspirin-sensitive asthma.	Aspirin	56-63	prostaglandin-endoperoxide synthase 2	Homo sapiens	12-28
12386502-4	2002	The older standbys of aspirin, heparins, nitrates, beta-blockers, and thrombolytic therapy have given way to vastly improved interventional capabilities (with improved adjunctive pharmacotherapy), low molecular weight heparins, glycoprotein IIb/IIIa antagonists, safer theinopyridines, thrombin inhibitors, and newer generation fibrinolytics.	Aspirin	22-29	coagulation factor II, thrombin	Homo sapiens	286-294
12042422-8	2002	Inhibition of PG synthesis by indomethacin and aspirin significantly suppressed basal as well as Ang II-induced PG levels, but did not significantly affect basal and Ang II-induced leptin secretion.	Aspirin	47-54	angiotensinogen	Homo sapiens	97-103
11986787-7	2002	Furthermore, aspirin treatment is associated with an increase in bcl-2 expression, which persists in the presence of the anticancer drugs.	Aspirin	13-20	BCL2 apoptosis regulator	Homo sapiens	65-70
12126971-4	2002	Acetylsalicylic acid, indomethacin, nimesulide and rofecoxib were all effective in eliminating the increase in endothelin ET(B) receptor-mediated contraction induced by interleukin-1 beta, but only indomethacin and rofecoxib significantly reduced the spontaneous development of this reaction in cultured arteries.	Aspirin	0-20	interleukin 1 beta	Homo sapiens	169-187
11981761-4	2002	Addition of aspirin or NS-398, similar to PD98059, which acts as a specific inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK), an upstream kinase regulating extracellular signal-regulated kinase (ERK)1/2, abrogated such actions of HGF without affecting cell viability.	Aspirin	12-19	mitogen-activated protein kinase kinase 7	Homo sapiens	161-164
11981761-4	2002	Addition of aspirin or NS-398, similar to PD98059, which acts as a specific inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK), an upstream kinase regulating extracellular signal-regulated kinase (ERK)1/2, abrogated such actions of HGF without affecting cell viability.	Aspirin	12-19	mitogen-activated protein kinase 1	Homo sapiens	197-243
11981761-7	2002	In conclusion, our results suggest that aspirin and NS-398 inhibit HGF-induced invasiveness of HepG2 human hepatoma cells through ERK1/2.	Aspirin	40-47	mitogen-activated protein kinase 3	Homo sapiens	130-136
11994707-8	2002	CONCLUSION: These data showing an abnormal regulation of Cox-1 and Cox-2 in NPs from aspirin-tolerant patients reinforce the concept that prostanoid metabolism might be important in the pathogenesis of inflammatory nasal diseases and suggest a potential role for this alteration in the formation of NPs.	Aspirin	85-92	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	67-72
12021247-5	2002	High-dose aspirin treatment resulted in a approximately 25% reduction in fasting plasma glucose, associated with a approximately 15% reduction in total cholesterol and C-reactive protein, a approximately 50% reduction in triglycerides, and a approximately 30% reduction in insulin clearance, despite no change in body weight.	Aspirin	10-17	C-reactive protein	Homo sapiens	168-186
12021247-5	2002	High-dose aspirin treatment resulted in a approximately 25% reduction in fasting plasma glucose, associated with a approximately 15% reduction in total cholesterol and C-reactive protein, a approximately 50% reduction in triglycerides, and a approximately 30% reduction in insulin clearance, despite no change in body weight.	Aspirin	10-17	insulin	Homo sapiens	273-280
12021247-7	2002	Aspirin treatment also resulted in a approximately 20% reduction in basal rates of hepatic glucose production and a approximately 20% improvement in insulin-stimulated peripheral glucose uptake under matched plasma insulin concentrations during the clamp.	Aspirin	0-7	insulin	Homo sapiens	149-156
12021247-7	2002	Aspirin treatment also resulted in a approximately 20% reduction in basal rates of hepatic glucose production and a approximately 20% improvement in insulin-stimulated peripheral glucose uptake under matched plasma insulin concentrations during the clamp.	Aspirin	0-7	insulin	Homo sapiens	215-222
11936556-5	2002	Antipyretic drugs such as acetylsalicylic acid, dexamethasone, and lipocortin 5-(204-212) peptide counteract IL-1beta-induced fever and abolish changes in Ca2+ and PGE2 concentrations in CSF.	Aspirin	26-46	interleukin 1 beta	Homo sapiens	109-117
12011664-1	2002	BACKGROUND: It has been reported that aspirin (ASA) may interfere with the blood pressure (BP)-lowering effect of various antihypertensive agents and attenuate the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in patients with congestive heart failure.	Aspirin	38-45	angiotensin I converting enzyme	Homo sapiens	186-215
12011664-1	2002	BACKGROUND: It has been reported that aspirin (ASA) may interfere with the blood pressure (BP)-lowering effect of various antihypertensive agents and attenuate the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in patients with congestive heart failure.	Aspirin	38-45	angiotensin I converting enzyme	Homo sapiens	217-220
12011664-1	2002	BACKGROUND: It has been reported that aspirin (ASA) may interfere with the blood pressure (BP)-lowering effect of various antihypertensive agents and attenuate the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in patients with congestive heart failure.	Aspirin	47-50	angiotensin I converting enzyme	Homo sapiens	186-215
12011664-1	2002	BACKGROUND: It has been reported that aspirin (ASA) may interfere with the blood pressure (BP)-lowering effect of various antihypertensive agents and attenuate the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in patients with congestive heart failure.	Aspirin	47-50	angiotensin I converting enzyme	Homo sapiens	217-220
12011664-4	2002	Furthermore, the cardiovascular benefits of ASA were of the same magnitude in hypertensive patients receiving or not receiving ACE-inhibitors.	Aspirin	44-47	angiotensin I converting enzyme	Homo sapiens	127-130
11964481-2	2002	Aspirin affords cardioprotection through inhibition of TxA2 formation by platelet cyclooxygenase (COX-1).	Aspirin	0-7	cytochrome c oxidase I, mitochondrial	Mus musculus	98-103
11877318-18	2002	In contrast, phenanthroline and apyrase significantly enhanced the anti-aggregatory effects of aspirin against thrombin-, PAR1AP- and TRAP-induced aggregation suggesting the involvement of ADP- and MMP-2-dependent pathways.	Aspirin	95-102	coagulation factor II, thrombin	Homo sapiens	111-119
11855867-4	2002	Focus formation of PDGF-B-chain-transformed mouse fibroblasts was suppressed by treatment with acetylsalicylic acid (ASA) and salicylic acid, which are known inhibitors of NF-kappaB activation, but other nonsteroidal anti-inflammatory drugs that do not have an effect on NF-kappaB activity did not affect focus formation in these cells.	Aspirin	95-115	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	172-181
11855867-4	2002	Focus formation of PDGF-B-chain-transformed mouse fibroblasts was suppressed by treatment with acetylsalicylic acid (ASA) and salicylic acid, which are known inhibitors of NF-kappaB activation, but other nonsteroidal anti-inflammatory drugs that do not have an effect on NF-kappaB activity did not affect focus formation in these cells.	Aspirin	95-115	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	271-280
11855867-4	2002	Focus formation of PDGF-B-chain-transformed mouse fibroblasts was suppressed by treatment with acetylsalicylic acid (ASA) and salicylic acid, which are known inhibitors of NF-kappaB activation, but other nonsteroidal anti-inflammatory drugs that do not have an effect on NF-kappaB activity did not affect focus formation in these cells.	Aspirin	117-120	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	172-181
11855867-4	2002	Focus formation of PDGF-B-chain-transformed mouse fibroblasts was suppressed by treatment with acetylsalicylic acid (ASA) and salicylic acid, which are known inhibitors of NF-kappaB activation, but other nonsteroidal anti-inflammatory drugs that do not have an effect on NF-kappaB activity did not affect focus formation in these cells.	Aspirin	117-120	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	271-280
11855867-6	2002	Therefore, the transcription factor NF-kappaB plays a vital role in PDGF-B chain transformation of mouse fibroblast cells, and the NF-kappaB activity is sensitive to treatment with ASA.	Aspirin	181-184	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	36-45
11855867-6	2002	Therefore, the transcription factor NF-kappaB plays a vital role in PDGF-B chain transformation of mouse fibroblast cells, and the NF-kappaB activity is sensitive to treatment with ASA.	Aspirin	181-184	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	131-140
11893365-1	2002	PURPOSE: C-reactive protein is an important risk factor for coronary artery disease, and plasma concentrations are lowered by treatment with pravastatin and aspirin.	Aspirin	157-164	C-reactive protein	Homo sapiens	9-27
14561202-4	2002	In this distinct clinical syndrome, aspirin and most other nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase-1 precipitate rhinitis and asthma attacks.	Aspirin	36-43	prostaglandin-endoperoxide synthase 1	Homo sapiens	109-125
14561202-11	2002	New highly specific COX-2 inhibitors appear to be a safe alternative for patients with aspirin-induced asthma.	Aspirin	87-94	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	20-25
11874470-2	2002	Fluorescence ratio imaging indicates that immobilized, aspirin-treated platelets, loaded with Fura-2, respond to inositol 1,4,5-trisphosphate- (InsP3)-generating agonists such as thrombin by high-frequency, irregular rises in cytosolic [Ca2+]i with spikes that vary in peak level and peak-to-peak interval.	Aspirin	55-62	coagulation factor II, thrombin	Homo sapiens	179-187
11821258-7	2002	High-dose aspirin also reduced the expression of CD11a, CD11b, and CD18, whereas meloxicam and etanercept did not.	Aspirin	10-17	integrin subunit alpha M	Rattus norvegicus	56-61
11821258-7	2002	High-dose aspirin also reduced the expression of CD11a, CD11b, and CD18, whereas meloxicam and etanercept did not.	Aspirin	10-17	integrin subunit beta 2	Rattus norvegicus	67-71
11821258-9	2002	Aspirin and meloxicam both lowered retinal TNF-alpha levels.	Aspirin	0-7	tumor necrosis factor	Rattus norvegicus	43-52
11821258-12	2002	High-dose aspirin also suppressed Erk kinase activity, which is involved in CD18 up-regulation.	Aspirin	10-17	integrin subunit beta 2	Rattus norvegicus	76-80
11902853-2	2002	METHODS: We examined whether AsA intake was associated with serum lipids, apolipoprotein A-1 (ApoA1) and apolipoprotein B (ApoB), in 680 Japanese elderly persons.	Aspirin	29-32	apolipoprotein A1	Homo sapiens	74-92
11902853-2	2002	METHODS: We examined whether AsA intake was associated with serum lipids, apolipoprotein A-1 (ApoA1) and apolipoprotein B (ApoB), in 680 Japanese elderly persons.	Aspirin	29-32	apolipoprotein A1	Homo sapiens	94-99
11902853-2	2002	METHODS: We examined whether AsA intake was associated with serum lipids, apolipoprotein A-1 (ApoA1) and apolipoprotein B (ApoB), in 680 Japanese elderly persons.	Aspirin	29-32	apolipoprotein B	Homo sapiens	105-121
11902853-2	2002	METHODS: We examined whether AsA intake was associated with serum lipids, apolipoprotein A-1 (ApoA1) and apolipoprotein B (ApoB), in 680 Japanese elderly persons.	Aspirin	29-32	apolipoprotein B	Homo sapiens	123-127
11902853-4	2002	AsA intake had a significant positive association with serum concentrations of high-density cholesterol and ApoA1, but an inverse association with serum concentrations of low-density cholesterol and ApoB, after adjusting for age, body mass index, total energy, and macronutrients.	Aspirin	0-3	apolipoprotein A1	Homo sapiens	108-113
11902853-4	2002	AsA intake had a significant positive association with serum concentrations of high-density cholesterol and ApoA1, but an inverse association with serum concentrations of low-density cholesterol and ApoB, after adjusting for age, body mass index, total energy, and macronutrients.	Aspirin	0-3	apolipoprotein B	Homo sapiens	199-203
11902853-5	2002	AsA intake was strongly inversely related to ApoA1/ApoB.	Aspirin	0-3	apolipoprotein A1	Homo sapiens	45-50
11902853-5	2002	AsA intake was strongly inversely related to ApoA1/ApoB.	Aspirin	0-3	apolipoprotein B	Homo sapiens	51-55
12402518-4	2002	The inhibition of NO production in PRP significantly reduced the antiaggregant affect of aspirin (IC50 2.64-fold greater), whereas it had no significant effect on the effect of ticlopidine (IC50 1.03-fold greater).	Aspirin	89-96	prion protein	Homo sapiens	35-38
12402518-5	2002	Incubating PMNL in PRP increased the antiaggregant effect of both aspirin (IC50 5.09-fold lower) and ticlopidine (IC50 10.16-fold lower).	Aspirin	66-73	prion protein	Homo sapiens	19-22
11910871-5	2002	The C-reactive protein is predictive for late complications such as restenosis, reinfarction and death due to cardiac events; these patients benefit from close controls and from an anti-inflammatory therapy with acetylsalicyclic acid and statins.	Aspirin	212-233	C-reactive protein	Homo sapiens	4-22
11823092-2	2002	Aspirin, a nonselective COX-1 (cyclo-oxygenase) and COX-2 inhibitor may result in gastric toxicity.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	52-57
11818533-8	2002	Treatment of aged rats with NCX-4016 was associated with increased bioactive NO, compared with ASA.	Aspirin	95-98	solute carrier family 8 member A1	Rattus norvegicus	28-31
11840449-7	2002	The ability of dexamethasone and ASA to suppress IFNgamma and interleukin-1beta (IL-1beta) messenger RNA and protein production was also tested in vitro using T cell clones and monocytes derived from patients with GCA.	Aspirin	33-36	interferon gamma	Homo sapiens	49-57
11840449-7	2002	The ability of dexamethasone and ASA to suppress IFNgamma and interleukin-1beta (IL-1beta) messenger RNA and protein production was also tested in vitro using T cell clones and monocytes derived from patients with GCA.	Aspirin	33-36	interleukin 1 beta	Homo sapiens	62-79
11840449-7	2002	The ability of dexamethasone and ASA to suppress IFNgamma and interleukin-1beta (IL-1beta) messenger RNA and protein production was also tested in vitro using T cell clones and monocytes derived from patients with GCA.	Aspirin	33-36	interleukin 1 beta	Homo sapiens	81-89
11840449-10	2002	While dexamethasone preferentially targeted NF-kappaB-regulated monokines, ASA acted predominantly by suppressing IFNgamma.	Aspirin	75-78	interferon gamma	Mus musculus	114-122
11840449-12	2002	IFNgamma production by T cell clones was highly sensitive to ASA-mediated suppression, whereas IL-1beta production by lipopolysaccharide-stimulated monocytes responded primarily to dexamethasone.	Aspirin	61-64	interferon gamma	Mus musculus	0-8
11826407-3	2002	Inhibition of nuclear factor kappaB (NF-kappaB) activation by aspirin and salicylate has been described in many cells.	Aspirin	62-69	nuclear factor kappa B subunit 1	Homo sapiens	29-35
11826407-3	2002	Inhibition of nuclear factor kappaB (NF-kappaB) activation by aspirin and salicylate has been described in many cells.	Aspirin	62-69	nuclear factor kappa B subunit 1	Homo sapiens	37-46
12036006-3	2002	In this work, acetylsalicylic acid (AAS) was chosen as a model drug, and was mixed with mannitol, a commonly used bulking agent in formulation of tablets.	Aspirin	14-34	FYVE, RhoGEF and PH domain containing 1	Homo sapiens	36-39
11801685-0	2002	Aspirin and salicylates inhibit the IL-4- and IL-13-induced activation of STAT6.	Aspirin	0-7	interleukin 4	Homo sapiens	36-51
11801685-5	2002	We found that treatment of cell lines and primary cells with aspirin and salicylates, but not acetaminophen, inhibited the activation of STAT6 by IL-4 and IL-13.	Aspirin	61-68	interleukin 4	Homo sapiens	146-150
11801685-5	2002	We found that treatment of cell lines and primary cells with aspirin and salicylates, but not acetaminophen, inhibited the activation of STAT6 by IL-4 and IL-13.	Aspirin	61-68	interleukin 13	Homo sapiens	155-160
11801685-9	2002	Because STAT6 activation by IL-4 and IL-13 participates in the development of allergic diseases, our results provide a mechanism to explain the beneficial effects of aspirin and salicylate treatment of these diseases.	Aspirin	166-173	interleukin 4	Homo sapiens	28-32
11801685-9	2002	Because STAT6 activation by IL-4 and IL-13 participates in the development of allergic diseases, our results provide a mechanism to explain the beneficial effects of aspirin and salicylate treatment of these diseases.	Aspirin	166-173	interleukin 13	Homo sapiens	37-42
11804997-7	2002	ASA treatment also completely inhibited the angiotensin II-induced hypertension and O(2)(-) production.	Aspirin	0-3	angiotensinogen	Rattus norvegicus	44-58
11804997-10	2002	These antioxidative properties of ASA are likely involved in the restoration of aortic vasorelaxation, in the attenuation of the development of hypertension in young SHRs, and in the prevention of hypertension following long-term angiotensin II infusion.	Aspirin	34-37	angiotensinogen	Rattus norvegicus	230-244
12013195-2	2002	Topically applied aspirin has recently been reported to decrease histamine-induced itch in human volunteers.	Aspirin	18-25	itchy E3 ubiquitin protein ligase	Homo sapiens	83-87
12013195-8	2002	No difference in itch intensities was found after application of aspirin, mepyramine and vehicle, but more itch was induced in aspirin and mepyramine pretreated sites in inflamed skin compared to normal skin (p<0.05).	Aspirin	127-134	itchy E3 ubiquitin protein ligase	Homo sapiens	107-111
12664642-0	2002	Non-prostaglandin effects of aspirin III and salicylate: inhibition of integrin-dependent human neutrophil aggregation and inflammation in COX 2- and NF kappa B (P105)-knockout mice.	Aspirin	29-36	nuclear factor kappa B subunit 1	Homo sapiens	162-166
11747987-3	2002	We determined whether PKC signals the induction of P-gp in LNCaP human prostate cancer cells, and identified a specific isozyme involved, in a model of aspirin-induced P-glycoprotein expression.	Aspirin	152-159	ATP binding cassette subfamily B member 1	Homo sapiens	168-182
11773732-2	2002	It has been shown that heat shock protein (hsp) expression can be augmented in vivo with the administration of high-dose aspirin before heat treatment.	Aspirin	121-128	selenoprotein K	Rattus norvegicus	23-41
11773732-2	2002	It has been shown that heat shock protein (hsp) expression can be augmented in vivo with the administration of high-dose aspirin before heat treatment.	Aspirin	121-128	selenoprotein K	Rattus norvegicus	43-46
11773732-11	2002	Future studies are needed to investigate further the role of pharmacological therapy combined with hsp induction in improving skin flap survival and to delineate the dose-response relationship between aspirin and hsp.	Aspirin	201-208	selenoprotein K	Rattus norvegicus	213-216
11849193-0	2002	Effect of aspirin on vasodilation to bradykinin and substance P in patients with heart failure treated with ACE inhibitor.	Aspirin	10-17	kininogen 1	Homo sapiens	37-47
11849193-0	2002	Effect of aspirin on vasodilation to bradykinin and substance P in patients with heart failure treated with ACE inhibitor.	Aspirin	10-17	angiotensin I converting enzyme	Homo sapiens	108-111
11849193-1	2002	AIMS: We wanted to examine some of the mechanisms by which aspirin might be responsible for counteraction of the effects of ACE inhibitors.	Aspirin	59-66	angiotensin I converting enzyme	Homo sapiens	124-127
11849193-2	2002	Aspirin has been reported to counteract the effects of ACE inhibitors in patients with heart failure.	Aspirin	0-7	angiotensin I converting enzyme	Homo sapiens	55-58
12086293-4	2002	The gastrointestinal toxicity of nonselective NSAIDs and aspirin derives from the inhibition of the cyclooxygenase (COX) enzyme, COX-1, which synthesizes gastroprotective prostaglandins, while the anti-inflammatory and pain-relieving effects are largely derived from inhibition of COX-2-derived prostaglandins.	Aspirin	57-64	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	281-286
12494116-1	2002	Analysis of results of randomized controlled studies revealed pronounced attenuation of vasodilating, natriuretic, and cardioprotective effects of angiotensin converting enzyme inhibitors (ACEI) by concomitant use with of indomethacin and aspirin in patients with hypertension, chronic heart failure, and acute myocardial infarction.	Aspirin	239-246	angiotensin I converting enzyme	Homo sapiens	147-176
11945152-9	2002	However it is premature to say that the benefit of Cox-2 inhibitors is lost in patients taking aspirin.	Aspirin	95-102	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	51-56
12020174-1	2002	BACKGROUND: Recently, studies have attempted to explore the interaction between ACE inhibitors and aspirin (acetylsalicylic acid) when both drugs are used concomitantly to reduce mortality in patients with coronary artery disease.	Aspirin	99-106	angiotensin I converting enzyme	Homo sapiens	80-83
12020174-5	2002	These data were necessary to calculate the synergy index (S) and its 95% confidence interval (CI) that we used to quantify the effect due to interaction between ACE inhibitors and aspirin.	Aspirin	180-187	angiotensin I converting enzyme	Homo sapiens	161-164
12020174-10	2002	The pooled synergy index S indicates slight but precise antagonism between ACE inhibitors and aspirin (S = 0.91; 95% CI 0.80 to 1.03).	Aspirin	94-101	angiotensin I converting enzyme	Homo sapiens	75-78
12020174-12	2002	CONCLUSION: There seems to be an antagonistic interaction between ACE inhibitors and aspirin.	Aspirin	85-92	angiotensin I converting enzyme	Homo sapiens	66-69
12112002-6	2002	And, NSAIDs aspirin and diclofenase dose dependently inhibited LPS/IFN-gamma-induced HO-1 protein accompanied by suppression of PGE(2) (not NO) production.	Aspirin	12-19	interferon gamma	Homo sapiens	67-76
11755955-0	2001	Epinephrine--via activation of p38-MAPK--abolishes the effect of aspirin on platelet deposition to collagen.	Aspirin	65-72	mitogen-activated protein kinase 14	Homo sapiens	31-34
11717412-8	2001	These results show that a low affinity for Cox-1 and a high degree of Cox-2 selectivity confers a low potential to block aspirin inhibition of platelet Cox-1, consistent with the results of clinical studies.	Aspirin	121-128	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	70-75
12734579-1	2001	In platelets, PGHS-1-dependant formation of thromboxane A(2) is an important modulator of platelet function and a target for pharmacological inhibition of platelet function by aspirin.	Aspirin	176-183	prostaglandin-endoperoxide synthase 1	Homo sapiens	14-20
11717412-0	2001	A high level of cyclooxygenase-2 inhibitor selectivity is associated with a reduced interference of platelet cyclooxygenase-1 inactivation by aspirin.	Aspirin	142-149	prostaglandin-endoperoxide synthase 2	Homo sapiens	16-32
11717412-0	2001	A high level of cyclooxygenase-2 inhibitor selectivity is associated with a reduced interference of platelet cyclooxygenase-1 inactivation by aspirin.	Aspirin	142-149	prostaglandin-endoperoxide synthase 1	Homo sapiens	109-125
11764357-7	2001	Results of the current study suggest that pain induction in osteoid osteoma is related to cyclooxygenase-2, an enzyme that is blocked by acetylsalicylic acid and rofecoxib.	Aspirin	137-157	prostaglandin-endoperoxide synthase 2	Homo sapiens	90-106
11793637-1	2001	OBJECTIVE: To review the literature evaluating the interaction between angiotensin-converting enzyme (ACE) inhibitors and aspirin in patients with congestive heart failure (CHF).	Aspirin	122-129	angiotensin I converting enzyme	Homo sapiens	71-100
11793637-1	2001	OBJECTIVE: To review the literature evaluating the interaction between angiotensin-converting enzyme (ACE) inhibitors and aspirin in patients with congestive heart failure (CHF).	Aspirin	122-129	angiotensin I converting enzyme	Homo sapiens	102-105
11742186-6	2001	Co-administration of the COX-2 selective NSAID, celecoxib, and low-dose aspirin, is associated with the same risk for upper gastrointestinal ulcer complications alone and combined with symptomatic ulcers, as the non-selective NSAIDs, ibuprofen and diclofenac.	Aspirin	72-79	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	25-30
11745453-1	2001	The epidemiologic evidence and rodent studies suggest strongly that nonselective inhibitors of cyclooxygenase (COX) enzymes such as aspirin, inhibiting both COX-1 and COX-2 isoforms, reduce the incidence of and mortality from intestinal tumors.	Aspirin	132-139	cytochrome c oxidase I, mitochondrial	Mus musculus	157-162
11738299-2	2001	BACKGROUND: Aspirin blunts the vasodilation caused by both angiotensin-converting enzyme (ACE) inhibitors and beta-blockers in hypertensive patients and in patients with heart failure.	Aspirin	12-19	angiotensin I converting enzyme	Homo sapiens	59-88
11738299-2	2001	BACKGROUND: Aspirin blunts the vasodilation caused by both angiotensin-converting enzyme (ACE) inhibitors and beta-blockers in hypertensive patients and in patients with heart failure.	Aspirin	12-19	angiotensin I converting enzyme	Homo sapiens	90-93
11738299-3	2001	Several studies suggest that ASA also blunts some of beneficial effects of ACE inhibitors on mortality in patients with heart failure.	Aspirin	29-32	angiotensin I converting enzyme	Homo sapiens	75-78
11917659-0	2001	[Aspirin-ACE inhibitors interaction: myth or reality?	Aspirin	1-8	angiotensin I converting enzyme	Homo sapiens	9-12
11740295-6	2001	RESULTS: The results clearly show that, compared with placebo, ASA ingestion significantly blunted the increased serum ACTH, beta-endorphin, cortisol, and GH levels before exercise (anticipatory response) and was associated with reduced cortisol concentrations after exercise.	Aspirin	63-66	proopiomelanocortin	Homo sapiens	119-123
11740295-6	2001	RESULTS: The results clearly show that, compared with placebo, ASA ingestion significantly blunted the increased serum ACTH, beta-endorphin, cortisol, and GH levels before exercise (anticipatory response) and was associated with reduced cortisol concentrations after exercise.	Aspirin	63-66	proopiomelanocortin	Homo sapiens	125-139
11740295-6	2001	RESULTS: The results clearly show that, compared with placebo, ASA ingestion significantly blunted the increased serum ACTH, beta-endorphin, cortisol, and GH levels before exercise (anticipatory response) and was associated with reduced cortisol concentrations after exercise.	Aspirin	63-66	growth hormone 1	Homo sapiens	155-157
11740295-7	2001	Furthermore, although no differences in the GH response to exercise were shown, a significantly reduced total PRL response to stress condition was observed after ASA.	Aspirin	162-165	prolactin	Homo sapiens	110-113
11740295-8	2001	CONCLUSION: ASA influences ACTH, beta-endorphin, cortisol, GH, and PRL responses to exercise-related stress in humans (preexercise activation/exercise-linked response).	Aspirin	12-15	proopiomelanocortin	Homo sapiens	27-31
11740295-8	2001	CONCLUSION: ASA influences ACTH, beta-endorphin, cortisol, GH, and PRL responses to exercise-related stress in humans (preexercise activation/exercise-linked response).	Aspirin	12-15	proopiomelanocortin	Homo sapiens	33-47
11740295-8	2001	CONCLUSION: ASA influences ACTH, beta-endorphin, cortisol, GH, and PRL responses to exercise-related stress in humans (preexercise activation/exercise-linked response).	Aspirin	12-15	growth hormone 1	Homo sapiens	59-61
11740295-8	2001	CONCLUSION: ASA influences ACTH, beta-endorphin, cortisol, GH, and PRL responses to exercise-related stress in humans (preexercise activation/exercise-linked response).	Aspirin	12-15	prolactin	Homo sapiens	67-70
11723016-0	2001	Pl(A2) polymorphism of beta(3) integrins is associated with enhanced thrombin generation and impaired antithrombotic action of aspirin at the site of microvascular injury.	Aspirin	127-134	phospholipase A2 group IB	Homo sapiens	0-5
11723016-5	2001	In the Pl(A1A1) homozygotes, aspirin ingestion resulted in reductions in the velocity of thrombin B-chain formation (by 32.1%; P=0.007), prothrombin consumption (by 30.4%; P=0.018), factor Va generation (by 28.9%; P=0.014), fibrinogen removal (by 41.2%; P=0.001), and factor XIII activation (by 22.6%; P=0.026).	Aspirin	29-36	coagulation factor II, thrombin	Homo sapiens	89-97
11723016-5	2001	In the Pl(A1A1) homozygotes, aspirin ingestion resulted in reductions in the velocity of thrombin B-chain formation (by 32.1%; P=0.007), prothrombin consumption (by 30.4%; P=0.018), factor Va generation (by 28.9%; P=0.014), fibrinogen removal (by 41.2%; P=0.001), and factor XIII activation (by 22.6%; P=0.026).	Aspirin	29-36	fibrinogen beta chain	Homo sapiens	224-234
11723016-8	2001	CONCLUSIONS: The presence of the Pl(A2) allele is associated with enhanced thrombin formation and an impaired antithrombotic action of aspirin, which might favor coronary thrombosis in the Pl(A2) carriers.	Aspirin	135-142	phospholipase A2 group IB	Homo sapiens	33-38
11728532-9	2001	RESULTS: In a drug free group, digestion of a single tablet of aspirin resulted in a significantly (p<0.05) diminished expression of PECAM-1, GP IIb, fibrinogen binding with PAC-1 antibody, GP Ib, P-selectin, and CD151.	Aspirin	63-70	fibrinogen beta chain	Homo sapiens	153-163
11715180-2	2001	To whatever extent the improvement in symptoms and survival rendered by treatment with ACE inhibitors is attributable to their effects on the circulation and the kidneys, this benefit can be rescinded by concomitant administration of aspirin.	Aspirin	234-241	angiotensin I converting enzyme	Homo sapiens	87-90
11695246-8	2001	Further studies are needed to determine whether COX-2 selective inhibitors are safer than nonselective NSAIDs when used in patients receiving low-dose aspirin.	Aspirin	151-158	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	48-53
11695247-6	2001	They have raised the possibility that use of low dose aspirin may compromise these benefits and appear to have shown differences between (at least some) COX-2 inhibitors and (at least some) NSAIDs with regard to myocardial infarction.	Aspirin	54-61	prostaglandin-endoperoxide synthase 2	Homo sapiens	153-158
11689471-0	2001	Aspirin and salicylate bind to immunoglobulin heavy chain binding protein (BiP) and inhibit its ATPase activity in human fibroblasts.	Aspirin	0-7	heat shock protein family A (Hsp70) member 5	Homo sapiens	31-73
11689471-0	2001	Aspirin and salicylate bind to immunoglobulin heavy chain binding protein (BiP) and inhibit its ATPase activity in human fibroblasts.	Aspirin	0-7	heat shock protein family A (Hsp70) member 5	Homo sapiens	75-78
11687759-1	2001	Aspirin depresses thrombin generation, probably through a mechanism independent of the cyclooxygenase inhibition, but rather related to acetylation of the platelet membrane macromolecules.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	18-26
11674857-6	2001	Binding experiments also revealed that the shear-induced vWF binding to platelets was significantly inhibited by ticlopidine, and less significantly by aspirin, although other indicators of platelet activation, such as shear-induced P-selectin expression and GP Ibalpha translocation were not influenced by either ticlopidine or aspirin.	Aspirin	152-159	von Willebrand factor	Homo sapiens	57-60
11674857-6	2001	Binding experiments also revealed that the shear-induced vWF binding to platelets was significantly inhibited by ticlopidine, and less significantly by aspirin, although other indicators of platelet activation, such as shear-induced P-selectin expression and GP Ibalpha translocation were not influenced by either ticlopidine or aspirin.	Aspirin	329-336	von Willebrand factor	Homo sapiens	57-60
11672762-5	2001	Platelet fibrinogen binding and P-selectin expression were significantly lower in patients treated with ticlopidine but not with aspirin than in those not treated with any antiplatelet agent, and were lowest in those treated with both ticlopidine and aspirin.	Aspirin	129-136	fibrinogen beta chain	Homo sapiens	9-19
11672762-5	2001	Platelet fibrinogen binding and P-selectin expression were significantly lower in patients treated with ticlopidine but not with aspirin than in those not treated with any antiplatelet agent, and were lowest in those treated with both ticlopidine and aspirin.	Aspirin	251-258	fibrinogen beta chain	Homo sapiens	9-19
11679405-7	2001	Furthermore, aspirin and statin therapy appear to be particularly effective among individuals with high CRP levels.	Aspirin	13-20	C-reactive protein	Homo sapiens	104-107
11566042-9	2001	Use of aspirin in the class study has shown that the benefits of COX-2 inhibitors may be reduced by aspirin use.	Aspirin	7-14	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	65-70
11827359-7	2001	Use of low-dose aspirin concurrently with use of a selective cyclo-oxygenase-2 inhibitor may provide some degree of protection against the potential cardiovascular toxicity of the latter but both laboratory and clinical studies suggest that the concomitant use of these two types of drugs results in gastrointestinal ulceration comparable to what is seen with conventional non-steroidal anti-inflammatory drugs.	Aspirin	16-23	prostaglandin-endoperoxide synthase 2	Homo sapiens	61-78
11592792-9	2001	Overall, patients with IFABP elevations had a significantly higher mean ASA class and significant increases in mean CPB and aortic cross-clamp times, mean time to oral intake, median ICU and postoperative lengths of stay, and GI complications.	Aspirin	72-75	fatty acid binding protein 2	Homo sapiens	23-28
11680515-0	2001	The effect of vasodilators on aspirin-induced antagonism of t-PA thrombolysis.	Aspirin	30-37	plasminogen activator, tissue type	Homo sapiens	60-64
11601671-0	2001	Quantifying the interaction between angiotensin-converting enzyme inhibitors and aspirin: are we using the right method?	Aspirin	81-88	angiotensin I converting enzyme	Homo sapiens	36-65
11601671-2	2001	Recently, there has been growing concern about the possible interaction between ACE inhibitors and aspirin.	Aspirin	99-106	angiotensin I converting enzyme	Homo sapiens	80-83
11593435-6	2001	As sulindac and aspirin are the two most important therapeutic/chemopreventative agents demonstrated in colorectal carcinogenesis, in both humans and animals, further investigation revealed that these non-steroidal anti-inflammatory drugs (NSAIDs) target ILK and ILK-mediated events in vivo.	Aspirin	16-23	integrin linked kinase	Homo sapiens	255-258
11593435-6	2001	As sulindac and aspirin are the two most important therapeutic/chemopreventative agents demonstrated in colorectal carcinogenesis, in both humans and animals, further investigation revealed that these non-steroidal anti-inflammatory drugs (NSAIDs) target ILK and ILK-mediated events in vivo.	Aspirin	16-23	integrin linked kinase	Homo sapiens	263-266
11593435-9	2001	Additionally, ILK signaling is shown to undergo modulation by sulindac (and aspirin) for the first time, indicating that it is likely to be one of the targets affected by these agents in vivo.	Aspirin	76-83	integrin linked kinase	Homo sapiens	14-17
11848479-5	2001	Arsenite-induced apoptosis and AP-1 transactivation in JB6 cells were blocked by aspirin and salicylate (SA).	Aspirin	81-88	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	31-35
11848479-8	2001	These results indicate that aspirin and SA inhibit arsenite-induced apoptosis through the inhibition of the Erks/AP-1 pathway.	Aspirin	28-35	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-117
11532860-11	2001	Inhibition of caspase-3 rescued aspirin-induced apoptosis.	Aspirin	32-39	caspase 3	Homo sapiens	14-23
11532860-12	2001	Our results suggest that one of the major pathways which mediates the anti-tumour response of aspirin and indomethacin in gastric cancer cells is through up-regulation of bax and bak and activation of caspase-3.	Aspirin	94-101	BCL2 associated X, apoptosis regulator	Homo sapiens	171-174
11532860-12	2001	Our results suggest that one of the major pathways which mediates the anti-tumour response of aspirin and indomethacin in gastric cancer cells is through up-regulation of bax and bak and activation of caspase-3.	Aspirin	94-101	caspase 3	Homo sapiens	201-210
11496056-0	2001	Does aspirin attenuate the effect of angiotensin-converting enzyme inhibitors in hypertension or heart failure?	Aspirin	5-12	angiotensin I converting enzyme	Homo sapiens	37-66
11496056-1	2001	There is a wealth of data that suggests an important interaction between aspirin and angiotensin-converting enzyme inhibitors in patients with chronic stable cardiovascular disease.	Aspirin	73-80	angiotensin I converting enzyme	Homo sapiens	85-114
11496056-5	2001	There is also considerable evidence that aspirin may entirely neutralize the clinical benefits of angiotensin-converting enzyme inhibitors in patients with heart failure.	Aspirin	41-48	angiotensin I converting enzyme	Homo sapiens	98-127
11496056-10	2001	The combination of aspirin and angiotensin-converting enzyme inhibitors is warranted during this period, after which discontinuation or substitution of aspirin with another agent should be considered.	Aspirin	152-159	angiotensin I converting enzyme	Homo sapiens	31-60
11344169-6	2001	Pleckstrin phosphorylation and serotonin secretion in human platelets stimulated with vWF are blocked by the cyclooxygenase inhibitor acetylsalicylic acid.	Aspirin	134-154	von Willebrand factor	Homo sapiens	86-89
11434828-10	2001	This effect was seen as early as 12 weeks (median reduction in CRP with pravastatin, 14.7%; P<.001) and was present among all prespecified subgroups according to sex, age, smoking status, body mass index, baseline lipid levels, presence of diabetes, and use of aspirin or hormone replacement therapy.	Aspirin	264-271	C-reactive protein	Homo sapiens	63-66
11441320-1	2001	BACKGROUND: Benefits of aspirin and beta-blocker use in patients with coronary artery disease and angiotensin-converting enzyme (ACE) inhibitors in those with left ventricular systolic dysfunction are well documented in all age groups.	Aspirin	24-31	angiotensin I converting enzyme	Homo sapiens	129-132
11476469-8	2001	CONCLUSIONS: Our results indicated that aspirin-induced asthma is associated with overproduction of LT with a shift to the 5-lipoxygenase series of the arachidonate cascade and that leukotriene receptor antagonist are useful for AIA through inhibition of production of LT and eosinophilic inflammation in the airway.	Aspirin	40-47	arachidonate 5-lipoxygenase	Homo sapiens	123-137
11377405-3	2001	For ASA and salicylate, an NF-kappaB inhibitory effect at mM concentrations (pharmacological plasma concentrations reached in vivo) has been shown.	Aspirin	4-7	nuclear factor kappa B subunit 1	Homo sapiens	27-36
11377405-9	2001	Some pharmacological actions of ASA may be ascribed to the inhibition of immune cell proliferation via the inhibition of the transcription factor NF-kappaB.	Aspirin	32-35	nuclear factor kappa B subunit 1	Homo sapiens	146-155
11447381-11	2001	From the standpoint of the mechanisms involved in aspirin-induced respiratory reactions, this study strongly supports inhibition of cyclooxygenase-1 as the essential initiator of these types of reactions.	Aspirin	50-57	prostaglandin-endoperoxide synthase 1	Homo sapiens	132-148
11433182-6	2001	The plasma antiinflammatory cytokine such as IL-1b and oxygen radical-mediated lipid peroxidation was measured in the ulcerated gastric mucosa of ASA and NO-ASA-treated animals.	Aspirin	146-149	interleukin 1 beta	Homo sapiens	45-50
11433182-6	2001	The plasma antiinflammatory cytokine such as IL-1b and oxygen radical-mediated lipid peroxidation was measured in the ulcerated gastric mucosa of ASA and NO-ASA-treated animals.	Aspirin	157-160	interleukin 1 beta	Homo sapiens	45-50
11419884-0	2001	Effects of low-dose aspirin on serum C-reactive protein and thromboxane B2 concentrations: a placebo-controlled study using a highly sensitive C-reactive protein assay.	Aspirin	20-27	C-reactive protein	Homo sapiens	37-55
11419884-1	2001	OBJECTIVES: We performed a placebo-controlled study to evaluate the effect of low-dose aspirin on serum C-reactive protein (CRP) levels.	Aspirin	87-94	C-reactive protein	Homo sapiens	104-122
11419884-1	2001	OBJECTIVES: We performed a placebo-controlled study to evaluate the effect of low-dose aspirin on serum C-reactive protein (CRP) levels.	Aspirin	87-94	C-reactive protein	Homo sapiens	124-127
11419884-3	2001	Moreover, low-dose aspirin therapy has been reported to be more effective in preventing MI in men with higher CRP levels than it is in those with lower levels, raising the possibility that aspirin prevents thrombosis by reducing vascular inflammation.	Aspirin	19-26	C-reactive protein	Homo sapiens	110-113
11419884-3	2001	Moreover, low-dose aspirin therapy has been reported to be more effective in preventing MI in men with higher CRP levels than it is in those with lower levels, raising the possibility that aspirin prevents thrombosis by reducing vascular inflammation.	Aspirin	189-196	C-reactive protein	Homo sapiens	110-113
11419884-4	2001	The effect of low-dose aspirin therapy on serum CRP levels in men has been addressed recently, but the results of the two studies conflict.	Aspirin	23-30	C-reactive protein	Homo sapiens	48-51
11419884-5	2001	METHODS: Effects of aspirin (81 mg every day or 325, 81 or 40 mg every-third-day given for 31 days) on serum CRP, using a highly-sensitive assay, and on serum platelet-cyclo-oxygenase (COX)-1-derived thromboxane (Tx) B2 concentrations were studied simultaneously in 57 healthy volunteers (30 men and 27 women).	Aspirin	20-27	C-reactive protein	Homo sapiens	109-112
11380325-1	2001	BACKGROUND: Neutrophils activation and tumour necrosis factor-alpha (TNF-alpha) induction play a critical role in aspirin-induced gastric mucosal injury.	Aspirin	114-121	tumor necrosis factor	Rattus norvegicus	69-78
11380325-11	2001	The gastric content of TNF-alpha increased and the expression of TNF-alpha mRNA was up-regulated after aspirin treatment.	Aspirin	103-110	tumor necrosis factor	Rattus norvegicus	23-32
11380325-11	2001	The gastric content of TNF-alpha increased and the expression of TNF-alpha mRNA was up-regulated after aspirin treatment.	Aspirin	103-110	tumor necrosis factor	Rattus norvegicus	65-74
11380325-12	2001	However, the peak TNF-alpha mRNA expression 1 h after aspirin administration was inhibited by pioglitazone.	Aspirin	54-61	tumor necrosis factor	Rattus norvegicus	18-27
11356600-8	2001	However, after inhibition of cyclooxygenase and nitric oxide synthase with aspirin and NG-monomethyl-L-arginine, the forearm blood flow response to bradykinin (P = 0.003), but not to sodium nitroprusside (not significant), was significantly suppressed by miconazole.	Aspirin	75-82	kininogen 1	Homo sapiens	148-158
11411740-9	2001	After inhibition of cyclooxygenase with acetylsalicylic acid, the ET-1-induced hypotension was not modified either in P or in TP.	Aspirin	40-60	endothelin 1	Rattus norvegicus	66-70
11405620-1	2001	Observational studies indicate that aspirin may counteract the beneficial effect of angiotensin-converting enzyme (ACE) inhibitors, but the data are not yet sufficient for making firm recommendations.	Aspirin	36-43	angiotensin I converting enzyme	Homo sapiens	84-113
11405620-1	2001	Observational studies indicate that aspirin may counteract the beneficial effect of angiotensin-converting enzyme (ACE) inhibitors, but the data are not yet sufficient for making firm recommendations.	Aspirin	36-43	angiotensin I converting enzyme	Homo sapiens	115-118
11827357-5	2001	Aspirin, a selective platelet cyclo-oxygenase-1 inhibitor still remains the most extensively studied antiplatelet agent, even though there is growing evidence that many other compounds could be valuable either in association, or alternatives in antithrombotic therapy.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	30-47
11509622-0	2001	Lipoxin A(4) and aspirin-triggered 15-epi-lipoxin A(4) antagonize TNF-alpha-stimulated neutrophil-enterocyte interactions in vitro and attenuate TNF-alpha-induced chemokine release and colonocyte apoptosis in human intestinal mucosa ex vivo.	Aspirin	17-24	tumor necrosis factor	Homo sapiens	66-75
11509622-0	2001	Lipoxin A(4) and aspirin-triggered 15-epi-lipoxin A(4) antagonize TNF-alpha-stimulated neutrophil-enterocyte interactions in vitro and attenuate TNF-alpha-induced chemokine release and colonocyte apoptosis in human intestinal mucosa ex vivo.	Aspirin	17-24	tumor necrosis factor	Homo sapiens	145-154
11509622-8	2001	In aggregate, our data demonstrate that lipoxins and aspirin-triggered 15-epi-LXA(4) are potent antagonists of TNF-alpha-mediated neutrophil-enterocyte interactions in vitro, attenuate TNF-alpha-triggered chemokine release and colonocyte apoptosis, and are protective against TNF-alpha-induced morphological disruption in human colonic strips ex vivo.	Aspirin	53-60	tumor necrosis factor	Homo sapiens	111-120
11509622-8	2001	In aggregate, our data demonstrate that lipoxins and aspirin-triggered 15-epi-LXA(4) are potent antagonists of TNF-alpha-mediated neutrophil-enterocyte interactions in vitro, attenuate TNF-alpha-triggered chemokine release and colonocyte apoptosis, and are protective against TNF-alpha-induced morphological disruption in human colonic strips ex vivo.	Aspirin	53-60	tumor necrosis factor	Homo sapiens	185-194
11509622-8	2001	In aggregate, our data demonstrate that lipoxins and aspirin-triggered 15-epi-LXA(4) are potent antagonists of TNF-alpha-mediated neutrophil-enterocyte interactions in vitro, attenuate TNF-alpha-triggered chemokine release and colonocyte apoptosis, and are protective against TNF-alpha-induced morphological disruption in human colonic strips ex vivo.	Aspirin	53-60	tumor necrosis factor	Homo sapiens	185-194
11577463-0	2001	[Cyclooxygenase (COX)-2 selective inhibitors: aspirin, a dual COX-1/COX-2 inhibitor, to COX-2 selective inhibitors].	Aspirin	46-53	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	68-73
11577463-2	2001	During the century after that, aspirin has been found to show its anti-inflammatory, analgesic and anti-pyretic activities by reducing prostaglandins biosynthesis through inhibition of cyclooxygenase (COX); and then COX was found to be constituted of two isoforms, constitutive COX-1 and inducible COX-2.	Aspirin	31-38	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	298-303
11577463-3	2001	Currently, novel NSAIDs, acting through selective inhibition of COX-2, that have efficacy as excellent as aspirin with significantly lower incidence of gastrointestinal adverse effects are available in America and some other countries, but not in Japan.	Aspirin	106-113	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	64-69
11583307-1	2001	As platelet hyperactivity is important in atherosclerosis and smoking, we hypothesized higher levels of soluble platelet membrane glycoprotein V (gpV) in 95 patients with peripheral artery disease (PAD) and 92 with coronary artery disease (CAD) compared to 99 healthy controls, and examined the effects of aspirin and of smoking two cigarettes on soluble gpV and platelet function.	Aspirin	306-313	glycoprotein V platelet	Homo sapiens	130-144
11583307-1	2001	As platelet hyperactivity is important in atherosclerosis and smoking, we hypothesized higher levels of soluble platelet membrane glycoprotein V (gpV) in 95 patients with peripheral artery disease (PAD) and 92 with coronary artery disease (CAD) compared to 99 healthy controls, and examined the effects of aspirin and of smoking two cigarettes on soluble gpV and platelet function.	Aspirin	306-313	glycoprotein V platelet	Homo sapiens	146-149
11493449-7	2001	The defect of GPV null platelets made them more sensitive to inhibition by the anti-GPVI monoclonal antibody (mAb) JAQ1, and this was also the case in aspirin- or apyrase-treated platelets.	Aspirin	151-158	glycoprotein V platelet	Homo sapiens	14-17
11454570-9	2001	However, aspirin reduced the amount of both TNF-alpha and IL-6 mRNA present 30 min after LPS addition by half (P < 0.05).	Aspirin	9-16	tumor necrosis factor	Rattus norvegicus	44-53
11454570-9	2001	However, aspirin reduced the amount of both TNF-alpha and IL-6 mRNA present 30 min after LPS addition by half (P < 0.05).	Aspirin	9-16	interleukin 6	Rattus norvegicus	58-62
11498517-3	2001	In this study, we tested the effects of a gastric-sparing, nitric oxide-releasing derivative of aspirin (NCX-4016) on hypertension in rats.	Aspirin	96-103	solute carrier family 8 member A1	Rattus norvegicus	105-108
11508669-1	2001	The gastric toxic effects of aspirin (ASA) and NCX-4016, a nitric oxide (NO)-releasing ASA, were compared in normal, cirrhotic, and arthritic rats.	Aspirin	87-90	solute carrier family 8 member A1	Rattus norvegicus	47-50
11508669-4	2001	By contrast, NCX-4016 at 190 mg/kg (a dose equimolar to 100 mg/kg of ASA) did not induce damage in normal rat stomachs but caused slight lesions in the gastric mucosa of both cirrhotic and arthritic rats.	Aspirin	69-72	solute carrier family 8 member A1	Rattus norvegicus	13-16
11508669-9	2001	Gastric mucosal application of ASA (100 mg/kg) for 30 min caused a marked reduction of transmucosal potential difference (PD) with a minimal effect on gastric mucosal blood flow in both normal and cirrhotic rats, while that of NCX-4016 did not cause a PD reduction and produced a marked increase in the mucosal blood flow in both groups of rats.	Aspirin	31-34	solute carrier family 8 member A1	Rattus norvegicus	227-230
11508669-10	2001	These results suggest that gastric mucosal susceptibility to ASA-induced damage is increased in both cirrhotic and arthritic rats (the process being partly accounted for by acid hypersecretion in these animals), NCX-4016 has even less gastric toxicity in both cirrhotic and arthritic rats, and the gastric-sparing effect of NCX-4016 is due, at least partly, to an increase of gastric mucosal blood flow, mediated by NO released from this drug.	Aspirin	61-64	solute carrier family 8 member A1	Rattus norvegicus	212-215
11508669-10	2001	These results suggest that gastric mucosal susceptibility to ASA-induced damage is increased in both cirrhotic and arthritic rats (the process being partly accounted for by acid hypersecretion in these animals), NCX-4016 has even less gastric toxicity in both cirrhotic and arthritic rats, and the gastric-sparing effect of NCX-4016 is due, at least partly, to an increase of gastric mucosal blood flow, mediated by NO released from this drug.	Aspirin	61-64	solute carrier family 8 member A1	Rattus norvegicus	324-327
11481242-0	2001	Aspirin inhibits NF-kappaB and protects from angiotensin II-induced organ damage.	Aspirin	0-7	angiotensinogen	Homo sapiens	45-59
11457426-3	2001	In primary cortical neurons, both indomethacin (COX-1/-2 nonselective inhibitor) and aspirin (COX-1 preferential inhibitor) reduced basal and kainic acid-induced PGE(2) production significantly and prevented neuronal cell death after kainic acid treatment.	Aspirin	85-92	cytochrome c oxidase I, mitochondrial	Mus musculus	94-99
11566042-9	2001	Use of aspirin in the class study has shown that the benefits of COX-2 inhibitors may be reduced by aspirin use.	Aspirin	100-107	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	65-70
11453099-6	2001	Moreover, by the tenth day, the delay in ulcer healing caused by aspirin was manifested in a 5.6-fold higher rate of apoptosis and a 5.2-fold higher level of soluble TNF-alpha.	Aspirin	65-72	tumor necrosis factor	Rattus norvegicus	166-175
11453099-7	2001	Treatment with SB 203580 produced dose-dependent reduction (59.5-74.8%) in aspirin-induced increase in the mucosal level of soluble TNF-alpha, evoked 53.2-69.7% decrease in the rate of epithelial cell apoptosis, and led to a marked reversal (51.8-73.9%) in aspirin-induced delay in ulcer healing.	Aspirin	75-82	tumor necrosis factor	Rattus norvegicus	132-141
11376494-2	2001	In this study, we compared gastric mucosal expression of iNOS and COX-2 during 14 days of aspirin ingestion in the same subjects before and 3 months after eradication of H. pylori.	Aspirin	90-97	nitric oxide synthase 2	Homo sapiens	57-61
11376494-5	2001	Independent of H. pylori status, expression of iNOS increased at the beginning of aspirin intake, but then returned to initial values.	Aspirin	82-89	nitric oxide synthase 2	Homo sapiens	47-51
11376495-14	2001	Indomethacin and ASA, which suppressed PGE(2) generation both in the non-ulcerated and ulcerated gastric mucosa, significantly delayed the rate of ulcer healing and this was accompanied by the fall in GBF at ulcer margin and further elevation of plasma IL-1beta and TNFalpha levels, which was sustained up to the end of the study.	Aspirin	17-20	interleukin 1 beta	Rattus norvegicus	253-261
11376495-14	2001	Indomethacin and ASA, which suppressed PGE(2) generation both in the non-ulcerated and ulcerated gastric mucosa, significantly delayed the rate of ulcer healing and this was accompanied by the fall in GBF at ulcer margin and further elevation of plasma IL-1beta and TNFalpha levels, which was sustained up to the end of the study.	Aspirin	17-20	tumor necrosis factor	Rattus norvegicus	266-274
11376496-8	2001	Secretion of PDGF-AB and VEGF increased during the first days of low dose aspirin exposition; higher concentrations led to a depletion of cytokines after an initial liberation in the case of VEGF, mRNA of which was also dose-dependently increased by aspirin.	Aspirin	74-81	vascular endothelial growth factor A	Homo sapiens	25-29
11376496-8	2001	Secretion of PDGF-AB and VEGF increased during the first days of low dose aspirin exposition; higher concentrations led to a depletion of cytokines after an initial liberation in the case of VEGF, mRNA of which was also dose-dependently increased by aspirin.	Aspirin	250-257	vascular endothelial growth factor A	Homo sapiens	191-195
11678602-4	2001	Catalase, a scavenger of H2O2, sodium formate and aspirin, scavengers of hydroxyl radical (*OH), also inhibited the increased tyrosine phosphorylation induced by Cr (VI).	Aspirin	50-57	catalase	Homo sapiens	0-8
11419785-0	2001	Low-dose aspirin as prophylactic therapy for muscle cramp.	Aspirin	9-16	cathelicidin antimicrobial peptide	Homo sapiens	52-57
11328262-7	2001	RESULTS: ASA produced erosions, a marked increase in chemiluminescence, lipid peroxidation, and myeloperoxidase activity.	Aspirin	9-12	myeloperoxidase	Homo sapiens	96-111
11328262-11	2001	CONCLUSIONS: (i) free radical-induced lipid peroxidation and suppression of antioxidizing enzymes play an important role in gastric damage induced by aspirin; (ii) increased myeloperoxidase activity suggests activated neutrophils to be the major source of these radicals; (iii) vitamin C protects against ASA-induced damage due to its anti-oxidizing activity.	Aspirin	150-157	myeloperoxidase	Homo sapiens	174-189
11328262-11	2001	CONCLUSIONS: (i) free radical-induced lipid peroxidation and suppression of antioxidizing enzymes play an important role in gastric damage induced by aspirin; (ii) increased myeloperoxidase activity suggests activated neutrophils to be the major source of these radicals; (iii) vitamin C protects against ASA-induced damage due to its anti-oxidizing activity.	Aspirin	305-308	myeloperoxidase	Homo sapiens	174-189
11305980-2	2001	Because ischemic heart disease is the most common cause of CHF, aspirin is frequently given concomitantly with ACE inhibitors in patients with CHF.	Aspirin	64-71	angiotensin I converting enzyme	Homo sapiens	111-114
11305980-6	2001	Several early reports questioned the safety of aspirin in CHF, and the potential antagonistic interaction between ACE inhibitors and aspirin in patients with heart failure has become the focus of both increasing research and intense debate.	Aspirin	133-140	angiotensin I converting enzyme	Homo sapiens	114-117
11322862-3	2001	At present there is only limited clinical use of some parenteral preparations of thrombin inhibitors in acute situations, especially when the common antithrombotic drugs heparin, warfarin and aspirin are ineffective or associated with side effects.	Aspirin	192-199	coagulation factor II, thrombin	Homo sapiens	81-89
11326011-2	2001	A 423- to 551-bp Acanthamoeba-specific amplimer ASA.S1 obtained with primers JDP1 and JDP2 was the most reliable for purposes i and ii.	Aspirin	48-51	basic leucine zipper ATF-like transcription factor 3	Homo sapiens	77-81
11323279-0	2001	Aspirin inhibits IL-4 production.	Aspirin	0-7	interleukin 4	Homo sapiens	17-21
11235048-0	2001	Successful use of cyclooxygenase-2 inhibitor in a patient with aspirin-induced asthma.	Aspirin	63-70	prostaglandin-endoperoxide synthase 2	Homo sapiens	18-34
11401513-0	2001	Aspirin inhibits matrix metalloproteinase-2 activity, increases E-cadherin production, and inhibits in vitro invasion of tumor cells.	Aspirin	0-7	cadherin 1	Homo sapiens	64-74
11401513-8	2001	Aspirin treatment also increased the production of the cell adhesion molecule, E-cadherin, in Hep G2 cancer cells.	Aspirin	0-7	cadherin 1	Homo sapiens	79-89
11401513-11	2001	These results indicate that aspirin can modulate both MMP-2 and E-cadherin production and therein may possess antimetastatic effect.	Aspirin	28-35	cadherin 1	Homo sapiens	64-74
11316217-1	2001	OBJECTIVE: Increased expression of the inducible cyclooxygenase 2 (COX-2) enzyme has been detected in esophageal and colonic adenocarcinoma, and intake of aspirin and non-steroidal anti-inflammatory drugs, known COX-2 inhibitors, have been associated with reduced tumor formation.	Aspirin	155-162	prostaglandin-endoperoxide synthase 2	Homo sapiens	49-65
11316217-1	2001	OBJECTIVE: Increased expression of the inducible cyclooxygenase 2 (COX-2) enzyme has been detected in esophageal and colonic adenocarcinoma, and intake of aspirin and non-steroidal anti-inflammatory drugs, known COX-2 inhibitors, have been associated with reduced tumor formation.	Aspirin	155-162	prostaglandin-endoperoxide synthase 2	Homo sapiens	67-72
11254909-4	2001	In contrast, aspirin did not affect cP-selectin levels but decreased vWF-Ag levels by -12% (CI: -18 - (-7%); P = 0.005) at 24 h. Neither drug affected cE-selectin levels.	Aspirin	13-20	von Willebrand factor	Homo sapiens	69-72
11330422-5	2001	The gastric concentration of TNF-alpha increased after aspirin administration, and the increase was also inhibited in a dose-dependent manner by treatment with polaprezinc.	Aspirin	55-62	tumor necrosis factor	Rattus norvegicus	29-38
11330422-6	2001	The peak expression of TNF-alpha mRNA 1 hr after aspirin administration was inhibited by 30 mg/kg of polaprezinc.	Aspirin	49-56	tumor necrosis factor	Rattus norvegicus	23-32
11287034-0	2001	Aspirin dose dependently inhibits the interleukin-1 beta-stimulated increase in inducible nitric oxide synthase, nitric oxide, and prostaglandin E(2) production in rat ovarian dispersates cultured in vitro.	Aspirin	0-7	interleukin 1 beta	Rattus norvegicus	38-56
11287034-0	2001	Aspirin dose dependently inhibits the interleukin-1 beta-stimulated increase in inducible nitric oxide synthase, nitric oxide, and prostaglandin E(2) production in rat ovarian dispersates cultured in vitro.	Aspirin	0-7	nitric oxide synthase 2	Rattus norvegicus	80-111
11287034-1	2001	OBJECTIVE: Determine if aspirin inhibits the IL-1 beta-stimulated expression of inducible nitric oxide synthase (iNOS), nitric oxide (NO), and prostaglandin E(2) (PGE(2)) in rat ovarian dispersates cultured in vitro.	Aspirin	24-31	interleukin 1 beta	Rattus norvegicus	45-54
11287034-1	2001	OBJECTIVE: Determine if aspirin inhibits the IL-1 beta-stimulated expression of inducible nitric oxide synthase (iNOS), nitric oxide (NO), and prostaglandin E(2) (PGE(2)) in rat ovarian dispersates cultured in vitro.	Aspirin	24-31	nitric oxide synthase 2	Rattus norvegicus	80-111
11287034-1	2001	OBJECTIVE: Determine if aspirin inhibits the IL-1 beta-stimulated expression of inducible nitric oxide synthase (iNOS), nitric oxide (NO), and prostaglandin E(2) (PGE(2)) in rat ovarian dispersates cultured in vitro.	Aspirin	24-31	nitric oxide synthase 2	Rattus norvegicus	113-117
11287034-10	2001	Aspirin dose dependently reduced the IL-1 beta-stimulated increase in nitrite production from ovarian dispersates after culture for 24 and 48 hours.	Aspirin	0-7	interleukin 1 beta	Rattus norvegicus	37-46
11287034-12	2001	Coadministration of IL-1 beta and aspirin (10 mM) attenuates IL-1 beta-stimulated iNOS expression after culture for 24 and 48 hours.	Aspirin	34-41	interleukin 1 beta	Rattus norvegicus	61-70
11287034-12	2001	Coadministration of IL-1 beta and aspirin (10 mM) attenuates IL-1 beta-stimulated iNOS expression after culture for 24 and 48 hours.	Aspirin	34-41	nitric oxide synthase 2	Rattus norvegicus	82-86
11287034-13	2001	CONCLUSION(S): Aspirin significantly inhibits the IL-1 beta-stimulated expression of iNOS, NO, and PGE(2) in ovarian dispersates cultured in vitro.	Aspirin	15-22	interleukin 1 beta	Rattus norvegicus	50-59
11287034-13	2001	CONCLUSION(S): Aspirin significantly inhibits the IL-1 beta-stimulated expression of iNOS, NO, and PGE(2) in ovarian dispersates cultured in vitro.	Aspirin	15-22	nitric oxide synthase 2	Rattus norvegicus	85-89
11300433-0	2001	The effect of aspirin on C-reactive protein as a marker of risk in unstable angina.	Aspirin	14-21	C-reactive protein	Homo sapiens	25-43
11300433-1	2001	OBJECTIVES: This study was designed to assess the interaction between aspirin and C-reactive protein (CRP) release in unstable angina.	Aspirin	70-77	C-reactive protein	Homo sapiens	82-100
11300433-1	2001	OBJECTIVES: This study was designed to assess the interaction between aspirin and C-reactive protein (CRP) release in unstable angina.	Aspirin	70-77	C-reactive protein	Homo sapiens	102-105
11300433-3	2001	Aspirin has the potential to influence CRP release, either by its anti-inflammatory activity or by reducing myocardial necrosis.	Aspirin	0-7	C-reactive protein	Homo sapiens	39-42
11300433-10	2001	Maximum CRP concentrations were also lower in patients taking aspirin (8.16 mg/l [3.24 to 24.5]) than in patients not taking aspirin (11.3 mg/l [4.15 to 26.1]), although the difference was not significant.	Aspirin	62-69	C-reactive protein	Homo sapiens	8-11
11300433-11	2001	However, there was significant interaction (p = 0.04) between prior aspirin therapy and the predictive value of CRP concentrations for death and myocardial infarction at 12 months.	Aspirin	68-75	C-reactive protein	Homo sapiens	112-115
11300433-12	2001	Thus, odds ratios (95% confidence intervals) for events associated with an increase of 1 standard deviation in maximum CRP concentration were 2.64 (1.22-5.72) in patients not pretreated with aspirin compared with 0.98 (0.60-1.62) in patients pretreated with aspirin.	Aspirin	191-198	C-reactive protein	Homo sapiens	119-122
11300433-12	2001	Thus, odds ratios (95% confidence intervals) for events associated with an increase of 1 standard deviation in maximum CRP concentration were 2.64 (1.22-5.72) in patients not pretreated with aspirin compared with 0.98 (0.60-1.62) in patients pretreated with aspirin.	Aspirin	258-265	C-reactive protein	Homo sapiens	119-122
11300433-13	2001	CONCLUSIONS: The association between CRP and cardiac events in patients with unstable angina is influenced by pretreatment with aspirin.	Aspirin	128-135	C-reactive protein	Homo sapiens	37-40
11259566-0	2001	The nitroderivative of aspirin, NCX 4016, reduces infarct size caused by myocardial ischemia-reperfusion in the anesthetized rat.	Aspirin	23-30	solute carrier family 8 member A1	Rattus norvegicus	32-35
11259566-1	2001	NCX 4016, a nitro-ester of aspirin endowed with antithrombotic activity, appears to have clinical potential in treating cardiac complications related to coronary insufficiency.	Aspirin	27-34	solute carrier family 8 member A1	Rattus norvegicus	0-3
11260389-10	2001	Aspirin-treated platelets formed TXB2 when either RGMCs or intact glomeruli were present in the incubation and formation of TXB2 was approximately fourfold higher with IL-1beta-treated RGMCs or glomeruli.	Aspirin	0-7	interleukin 1 beta	Rattus norvegicus	168-176
11405554-0	2001	Release of tumor necrosis factor-alpha and prostanoids in whole blood cultures after in vivo exposure to low-dose aspirin.	Aspirin	114-121	tumor necrosis factor	Homo sapiens	11-38
11405554-1	2001	BACKGROUND: The preventive effect of low-dose aspirin in cardiovascular disease is generally attributed to its antiplatelet action caused by differential inhibition of platelet cyclooxygenase-1.	Aspirin	46-53	prostaglandin-endoperoxide synthase 1	Homo sapiens	177-193
11405554-2	2001	However, there is evidence that aspirin also affects release of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha).	Aspirin	32-39	tumor necrosis factor	Homo sapiens	98-125
11405554-2	2001	However, there is evidence that aspirin also affects release of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha).	Aspirin	32-39	tumor necrosis factor	Homo sapiens	127-136
11405554-4	2001	METHODS: We assessed the capacity of lipopolysaccharide-activated leukocytes in whole blood cultures of eight healthy subjects following a single oral dose of 80 mg aspirin to release TNF-alpha, prostanoid E2 (PGE2) and prostanoid I2 (PGI2), and thromboxane A2 (TXA2).	Aspirin	165-172	tumor necrosis factor	Homo sapiens	184-193
11405554-6	2001	RESULTS: In seven subjects, TNF-alpha release in blood cultures decreased 24h after intake of aspirin.	Aspirin	94-101	tumor necrosis factor	Homo sapiens	28-37
11405554-8	2001	CONCLUSION: The capacity of activated leukocytes to release TNF-alpha is reduced by ingestion of low-dose aspirin, independent of changes in prostanoid biosynthesis.	Aspirin	106-113	tumor necrosis factor	Homo sapiens	60-69
11273998-3	2001	METHODS AND RESULTS: For dose-finding, the effect of aspirin (1, 2, 5, and 10 mmol/L) on the tumor necrosis factor-alpha-induced upregulation of intercellular adhesion molecule-1 was analyzed in monocultures of human coronary endothelial cells (HCAEC) and the SMCs of the human coronary media (HCMSMC).	Aspirin	53-60	tumor necrosis factor	Homo sapiens	93-120
11273998-7	2001	A dose of 5 mmol/L aspirin inhibited the adherence of monocytes or CD4(+) lymphocytes by 50% (P:<0.01) and the chemotaxis of monocytes by 90% (P:<0.01).	Aspirin	19-26	CD4 molecule	Homo sapiens	67-70
11238116-0	2001	Selective inhibition of interleukin-4 gene expression in human T cells by aspirin.	Aspirin	74-81	interleukin 4	Homo sapiens	24-37
11238116-2	2001	This study is the first in which concentrations of ASA in the therapeutic range were found to significantly reduce interleukin (IL)-4 secretion and RNA expression in freshly isolated and mitogen-primed human CD4+ T cells.	Aspirin	51-54	interleukin 4	Homo sapiens	115-133
11238116-4	2001	ASA inhibited IL-4, but not IL-2, promoter-driven chloramphenicol acetyltransferase expression in transiently transfected Jurkat T cells.	Aspirin	0-3	interleukin 4	Homo sapiens	14-18
11238116-6	2001	The inhibitory effect of ASA on IL-4 transcription was not mediated by decreased nuclear expression of the known salicylate target nuclear factor (NF)-kappaB and was accompanied by reduced binding of an inducible factor to an IL-4 promoter region upstream of, but not overlapping, the NF of activated T cells- and NF-kappaB-binding P1 element.	Aspirin	25-28	interleukin 4	Homo sapiens	32-36
11238116-6	2001	The inhibitory effect of ASA on IL-4 transcription was not mediated by decreased nuclear expression of the known salicylate target nuclear factor (NF)-kappaB and was accompanied by reduced binding of an inducible factor to an IL-4 promoter region upstream of, but not overlapping, the NF of activated T cells- and NF-kappaB-binding P1 element.	Aspirin	25-28	nuclear factor kappa B subunit 1	Homo sapiens	131-157
11238116-6	2001	The inhibitory effect of ASA on IL-4 transcription was not mediated by decreased nuclear expression of the known salicylate target nuclear factor (NF)-kappaB and was accompanied by reduced binding of an inducible factor to an IL-4 promoter region upstream of, but not overlapping, the NF of activated T cells- and NF-kappaB-binding P1 element.	Aspirin	25-28	interleukin 4	Homo sapiens	226-230
11266647-3	2001	Indeed, development of the new "super aspirins," such as Celebrex and Vioxx, that selectively inhibit the inducible COX-2, expressed in areas of inflammation, is a direct outgrowth of this concept.	Aspirin	38-46	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	116-121
11238602-6	2001	Nociceptin-stimulated PMN infiltration was inhibited by treating mice with a synthetic analog of the aspirin-triggered lipid mediator 15-epi-lipoxin A(4).	Aspirin	101-108	prepronociceptin	Homo sapiens	0-10
11238602-7	2001	The present results identify nociceptin as a potent chemoattractant and provide a novel link between the neural and immune systems that are blocked by aspirin-triggered lipid mediators and may be relevant in neurogenic inflammation.	Aspirin	151-158	prepronociceptin	Homo sapiens	29-39
11238289-11	2001	Preventive therapies to attenuate coronary risk in individuals with increased hs-CRP concentrations include aspirin and statin-type drugs.	Aspirin	108-115	C-reactive protein	Homo sapiens	81-84
11260147-8	2001	In contrast, C5a-triggered LTR was significantly higher in ASA (14.4 +/- 12.88 pg/105 cells) and NAA (22.9 +/- 22.61 pg/105 cells) than in AA (9.6 +/- 3.29 pg/105 cells) and controls (7.5 +/- 7.19 pg/105 cells) (P < 0.05).	Aspirin	59-62	complement C5a receptor 1	Homo sapiens	13-16
11260147-9	2001	This difference between ASA and NAA vs. AA and controls was even more pronounced when determining the quotient C5a-/anti-IgE-induced LTR (P < 0.001).	Aspirin	24-27	complement C5a receptor 1	Homo sapiens	111-114
11239649-10	2001	Control cells and cells treated with the lowest concentration of ASA exhibited 2% apoptosis and more than 60% of the population expressed bcl-2.	Aspirin	65-68	BCL2 apoptosis regulator	Homo sapiens	138-143
11173047-2	2001	Aspirin, conventional nonsteroidal anti-inflammatory drugs (NSAIDs), and COX-2-specific inhibitors exhibit different patterns of inhibition of COX-1-mediated thromboxane biosynthesis and COX-2-mediated prostacyclin biosynthesis.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	187-192
11182101-10	2001	The greatest effect of a given therapy was that of aspirin, which accounted for 34% of the decrease in 30-day mortality, followed by thrombolysis (17%), primary angioplasty (10%), beta-blockers (7%), and ACE inhibitors (3%).	Aspirin	51-58	angiotensin I converting enzyme	Homo sapiens	204-207
11165959-6	2001	Diabetic patients, particularly those taking insulin, were less likely to receive aspirin and beta blockers and to undergo coronary revascularization.	Aspirin	82-89	insulin	Homo sapiens	45-52
11964666-10	2001	Preliminary observations indicate that new, highly specific cyclooxygenase-2 inhibitors may soon become a safe alternative for aspirin-intolerant patients with asthma.	Aspirin	127-134	prostaglandin-endoperoxide synthase 2	Homo sapiens	60-76
11182189-2	2001	The aim of the study was to assess the influence of simvastatin and aspirin on serum levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in hypercholesterolemic subjects.	Aspirin	68-75	C-reactive protein	Homo sapiens	95-113
11246058-7	2001	A possible interaction between ACE-I and aspirin might theoretically lead to reduced levels of renin activity in patients on aspirin, but we did not find any such inter-group difference.	Aspirin	41-48	renin	Homo sapiens	95-100
11246058-7	2001	A possible interaction between ACE-I and aspirin might theoretically lead to reduced levels of renin activity in patients on aspirin, but we did not find any such inter-group difference.	Aspirin	125-132	renin	Homo sapiens	95-100
11321509-0	2001	Heat  shock protein 70 (HSP70) in gastric adaptation to aspirin in Helicobacter pylori infection.	Aspirin	56-63	heat shock protein 1B	Mus musculus	24-29
11321509-2	2001	The aim of this study was 1) to evaluate the influence of H. pylori on expression of heat shock protein 70 (HSP70) during ASA ingestion in these subjects and in mice model and 2) to evaluate, whether altered HSP70 expression might be associated with different adaptation to ASA in H. pylori-positive and eradicated subjects.	Aspirin	122-125	heat shock protein 1B	Mus musculus	108-113
11321509-5	2001	During 14 days of ASA treatment, human H. pylori-infected mucosa revealed a decrease of HSP70 expression, while after eradication a higher expression and further increase of HSP70 expression during ASA ingestion were observed.	Aspirin	18-21	heat shock protein 1B	Mus musculus	88-93
11321509-5	2001	During 14 days of ASA treatment, human H. pylori-infected mucosa revealed a decrease of HSP70 expression, while after eradication a higher expression and further increase of HSP70 expression during ASA ingestion were observed.	Aspirin	18-21	heat shock protein 1B	Mus musculus	174-179
11321509-5	2001	During 14 days of ASA treatment, human H. pylori-infected mucosa revealed a decrease of HSP70 expression, while after eradication a higher expression and further increase of HSP70 expression during ASA ingestion were observed.	Aspirin	198-201	heat shock protein 1B	Mus musculus	174-179
11321509-7	2001	Decreased basal and ASA-induced expression of HSP70 may partly be responsible for impaired gastric adaptation to ASA in H. pylori-positive subjects.	Aspirin	20-23	heat shock protein 1B	Mus musculus	46-51
11321509-7	2001	Decreased basal and ASA-induced expression of HSP70 may partly be responsible for impaired gastric adaptation to ASA in H. pylori-positive subjects.	Aspirin	113-116	heat shock protein 1B	Mus musculus	46-51
11321509-9	2001	The HSP70 gene and protein expression is reduced during infection with H. pylori in men and mice and that gastric adaptation to ASA in H. pylori eradicated subjects is accompanied by increased HSP70 expression; 2.	Aspirin	128-131	heat shock protein 1B	Mus musculus	193-198
11321509-11	2001	The expression of HSP70 plays an important role in the mechanism of gastric adaptation to ASA and that H. pylori infection interferes with this adaptation due to decrease of HSP70 expression in gastric mucosal cells.	Aspirin	90-93	heat shock protein 1B	Mus musculus	18-23
11252112-5	2001	In the multivariate analysis, patients who received both aspirin and ACE inhibitors alone had a significantly lower 1-year mortality (adjusted risk ratio [ARR], 0.86 [95% confidence interval (CI), 0.78-0.95] vs 0.85 [95% CI, 0.77-0.93], respectively) compared with patients who received neither aspirin nor ACE inhibitors at discharge.	Aspirin	57-64	angiotensin I converting enzyme	Homo sapiens	307-310
11252112-5	2001	In the multivariate analysis, patients who received both aspirin and ACE inhibitors alone had a significantly lower 1-year mortality (adjusted risk ratio [ARR], 0.86 [95% confidence interval (CI), 0.78-0.95] vs 0.85 [95% CI, 0.77-0.93], respectively) compared with patients who received neither aspirin nor ACE inhibitors at discharge.	Aspirin	295-302	angiotensin I converting enzyme	Homo sapiens	69-72
11171808-0	2001	Platelet glycoprotein IIIa pl(a) polymorphism and effects of aspirin on thrombin generation.	Aspirin	61-68	coagulation factor II, thrombin	Homo sapiens	72-80
11251623-0	2001	Safety of a specific COX-2 inhibitor in aspirin-induced asthma.	Aspirin	40-47	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	21-26
11251623-1	2001	In a subset of patients with asthma, aspirin and several other non-steroidal anti-inflammatory drugs (NSAID) that inhibit simultaneously cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) precipitate dangerous asthmatic attacks.	Aspirin	37-44	prostaglandin-endoperoxide synthase 1	Homo sapiens	137-153
11251623-1	2001	In a subset of patients with asthma, aspirin and several other non-steroidal anti-inflammatory drugs (NSAID) that inhibit simultaneously cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) precipitate dangerous asthmatic attacks.	Aspirin	37-44	prostaglandin-endoperoxide synthase 2	Homo sapiens	166-182
11251623-1	2001	In a subset of patients with asthma, aspirin and several other non-steroidal anti-inflammatory drugs (NSAID) that inhibit simultaneously cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) precipitate dangerous asthmatic attacks.	Aspirin	37-44	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	184-189
11251623-3	2001	In twelve asthmatic patients (seven men, five women, average age 39 years) oral aspirin challenge precipitated symptoms of bronchial obstruction with fall in FEV1 > 20%, and a rise in urinary leukotriene E4 (LTE4) excretion; also in five patients the stable metabolite of PGD2, 9alpha11betaPGF2, increased in urine.	Aspirin	80-87	prostaglandin D2 synthase	Homo sapiens	275-297
11313997-4	2001	We therefore investigated beta-catenin/TCF signaling in response to aspirin or indomethacin, respectively, in four CRC cell lines (SW948, SW480, HCT116, LoVo).	Aspirin	68-75	hepatocyte nuclear factor 4 alpha	Homo sapiens	39-42
11313997-5	2001	Both, aspirin and indomethacin inhibited transcription of a beta-catenin/TCF-responsive reporter gene in a dose dependent manner.	Aspirin	6-13	hepatocyte nuclear factor 4 alpha	Homo sapiens	73-76
11313997-10	2001	These results strongly suggest that aspirin and indomethacin attenuate the transcription of beta-catenin/TCF-responsive genes, by modulating TCF activity without disrupting beta-catenin/TCF complex formation.	Aspirin	36-43	hepatocyte nuclear factor 4 alpha	Homo sapiens	105-108
11313997-10	2001	These results strongly suggest that aspirin and indomethacin attenuate the transcription of beta-catenin/TCF-responsive genes, by modulating TCF activity without disrupting beta-catenin/TCF complex formation.	Aspirin	36-43	hepatocyte nuclear factor 4 alpha	Homo sapiens	141-144
11313997-10	2001	These results strongly suggest that aspirin and indomethacin attenuate the transcription of beta-catenin/TCF-responsive genes, by modulating TCF activity without disrupting beta-catenin/TCF complex formation.	Aspirin	36-43	hepatocyte nuclear factor 4 alpha	Homo sapiens	141-144
11180504-1	2001	To study the possible role of the isoenzymes of cyclooxygenase COX-1 and COX-2 in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson"s disease we used acetylsalicylic acid, a COX-1/COX-2 inhibitor, in comparison with meloxicam, a preferential COX-2 inhibitor.	Aspirin	181-201	cytochrome c oxidase I, mitochondrial	Mus musculus	63-68
11180504-12	2001	In conclusion, the inhibition of either COX-1/COX-2 by acetylsalicylic acid or preferentially COX-2 by meloxicam provided a clear neuroprotection against MPTP-toxicity on the striatal and nigral levels.	Aspirin	55-75	cytochrome c oxidase I, mitochondrial	Mus musculus	40-45
11246536-0	2001	Treatment with simvastatin and low-dose aspirin depresses thrombin generation in patients with coronary heart disease and borderline-high cholesterol levels.	Aspirin	40-47	coagulation factor II, thrombin	Homo sapiens	58-66
11246536-2	2001	We assessed the effects of low-dose aspirin (75 mg daily) on thrombin generation in patients with coronary heart disease and average blood cholesterol levels.	Aspirin	36-43	coagulation factor II, thrombin	Homo sapiens	61-69
11246536-4	2001	Seven-day treatment with low-dose aspirin decreased thrombin generation ex vivo only in patients with total cholesterol < or = 5.2 mmol/L.	Aspirin	34-41	coagulation factor II, thrombin	Homo sapiens	52-60
11246536-6	2001	In these patients, already taking low-dose aspirin, additional three-month simvastatin treatment resulted in a reduction of thrombin generation.	Aspirin	43-50	coagulation factor II, thrombin	Homo sapiens	124-132
11246536-7	2001	This demonstrates that low-dose aspirin depresses thrombin generation only in subjects with desirable blood cholesterol levels, while in others, with borderline-high cholesterol, thrombin formation is being reduced following the addition of simvastatin.	Aspirin	32-39	coagulation factor II, thrombin	Homo sapiens	50-58
11246553-6	2001	In blood from subjects given aspirin for 5 days, abciximab-induced inhibition of the capacity to bind fibrinogen in response to 1 microM ADP was greater when the daily dose had been 325 mg compared with 81 mg (% inhibition: no aspirin 53 +/- 6; 81 mg daily 62 +/- 5; 325 mg daily 69 +/- 6).	Aspirin	29-36	fibrinogen beta chain	Homo sapiens	102-112
11235048-3	2001	Current prescribing information warns to avoid using COX-2 inhibitors in aspirin-sensitive asthma patients.	Aspirin	73-80	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	53-58
11235048-4	2001	New evidence suggests that aspirin sensitivity may be linked to the COX-1 pathway, and COX-2 inhibitors, as a result of their selectivity, may be beneficial in patients with aspirin-induced asthma.	Aspirin	174-181	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	87-92
11180079-7	2001	All four pancreatic cancer cell lines expressed COX-2 protein weakly or strongly, and the inhibitory effect of aspirin on cell growth was correlated with the expression of COX-2.	Aspirin	111-118	prostaglandin-endoperoxide synthase 2	Homo sapiens	172-177
11163773-0	2001	Aspirin promotes TFF2 gene activation in human gastric cancer cell lines.	Aspirin	0-7	trefoil factor 2	Homo sapiens	17-21
11163773-2	2001	In reporter gene assays we show that aspirin (1-12 mM) evokes a six-fold up-regulation of TFF2, but not TFF1 and TFF3 transcription in human gastrointestinal cell lines.	Aspirin	37-44	trefoil factor 2	Homo sapiens	90-94
11163773-4	2001	TFF2 transcription was enhanced by indomethacin and arachidonic acid but repressed by staurosporine, suggesting mediation via protein kinase C. We mapped an aspirin responding element -546 to -758 bp upstream of TFF2.	Aspirin	157-164	trefoil factor 2	Homo sapiens	0-4
11163773-4	2001	TFF2 transcription was enhanced by indomethacin and arachidonic acid but repressed by staurosporine, suggesting mediation via protein kinase C. We mapped an aspirin responding element -546 to -758 bp upstream of TFF2.	Aspirin	157-164	trefoil factor 2	Homo sapiens	212-216
11163773-5	2001	Up-regulation of TFF2 by aspirin may partially explain the chemopreventive potential of low dose aspirin in gastrointestinal carcinogenesis.	Aspirin	25-32	trefoil factor 2	Homo sapiens	17-21
11163773-5	2001	Up-regulation of TFF2 by aspirin may partially explain the chemopreventive potential of low dose aspirin in gastrointestinal carcinogenesis.	Aspirin	97-104	trefoil factor 2	Homo sapiens	17-21
11133489-4	2001	A high dose of ASA blocked IL-1 beta- and TNF-alpha-induced TNF-alpha and IL-8 expression, respectively.	Aspirin	15-18	interleukin 1 beta	Homo sapiens	27-36
11133489-4	2001	A high dose of ASA blocked IL-1 beta- and TNF-alpha-induced TNF-alpha and IL-8 expression, respectively.	Aspirin	15-18	tumor necrosis factor	Homo sapiens	42-51
11133489-4	2001	A high dose of ASA blocked IL-1 beta- and TNF-alpha-induced TNF-alpha and IL-8 expression, respectively.	Aspirin	15-18	tumor necrosis factor	Homo sapiens	60-69
11133489-4	2001	A high dose of ASA blocked IL-1 beta- and TNF-alpha-induced TNF-alpha and IL-8 expression, respectively.	Aspirin	15-18	C-X-C motif chemokine ligand 8	Homo sapiens	74-78
11133489-5	2001	ASA inhibited TNF-alpha-induced activation of NF-kappa B by preventing phosphorylation and subsequent degradation of I kappa B-alpha in a prostanoid-independent manner.	Aspirin	0-3	tumor necrosis factor	Homo sapiens	14-23
11133489-5	2001	ASA inhibited TNF-alpha-induced activation of NF-kappa B by preventing phosphorylation and subsequent degradation of I kappa B-alpha in a prostanoid-independent manner.	Aspirin	0-3	nuclear factor kappa B subunit 1	Homo sapiens	46-56
11133489-5	2001	ASA inhibited TNF-alpha-induced activation of NF-kappa B by preventing phosphorylation and subsequent degradation of I kappa B-alpha in a prostanoid-independent manner.	Aspirin	0-3	NFKB inhibitor alpha	Homo sapiens	117-132
11133489-6	2001	TNF-alpha-induced activation of I kappa B kinase was also suppressed by ASA pretreatment.	Aspirin	72-75	tumor necrosis factor	Homo sapiens	0-9
11133489-7	2001	These observations suggest that the anti-inflammatory effect of ASA in lung epithelial cells may be due to suppression of I kappa B kinase activity, which thereby inhibits subsequent phosphorylation and degradation of I kappa B-alpha, activation of NF-kappa B, and proinflammatory cytokine expression in lung epithelial cells.	Aspirin	64-67	NFKB inhibitor alpha	Homo sapiens	218-233
11133489-7	2001	These observations suggest that the anti-inflammatory effect of ASA in lung epithelial cells may be due to suppression of I kappa B kinase activity, which thereby inhibits subsequent phosphorylation and degradation of I kappa B-alpha, activation of NF-kappa B, and proinflammatory cytokine expression in lung epithelial cells.	Aspirin	64-67	nuclear factor kappa B subunit 1	Homo sapiens	249-259
11141472-8	2001	These results indicate that ATL and LTD(4) bind and compete with equal affinity at CysLT(1), providing a molecular basis for aspirin-triggered LXs serving as a local damper of both vascular CysLT(1) signals as well as ALX receptor-regulated polymorphonuclear leukocyte traffic.	Aspirin	125-132	cysteinyl leukotriene receptor 1	Homo sapiens	83-91
11141472-8	2001	These results indicate that ATL and LTD(4) bind and compete with equal affinity at CysLT(1), providing a molecular basis for aspirin-triggered LXs serving as a local damper of both vascular CysLT(1) signals as well as ALX receptor-regulated polymorphonuclear leukocyte traffic.	Aspirin	125-132	cysteinyl leukotriene receptor 1	Homo sapiens	190-198
11460511-0	2001	Modified clotting properties of fibrinogen in the presence of acetylsalicylic acid in a purified system.	Aspirin	62-82	fibrinogen beta chain	Homo sapiens	32-42
11460511-1	2001	To assess how treatment with acetylsalicylic acid (ASA) alters the fibrin network structure, clotting was initiated in purified fibrinogen incubated with ASA by adding thrombin.	Aspirin	29-49	fibrinogen beta chain	Homo sapiens	128-138
11460511-1	2001	To assess how treatment with acetylsalicylic acid (ASA) alters the fibrin network structure, clotting was initiated in purified fibrinogen incubated with ASA by adding thrombin.	Aspirin	29-49	coagulation factor II, thrombin	Homo sapiens	168-176
11460511-1	2001	To assess how treatment with acetylsalicylic acid (ASA) alters the fibrin network structure, clotting was initiated in purified fibrinogen incubated with ASA by adding thrombin.	Aspirin	51-54	coagulation factor II, thrombin	Homo sapiens	168-176
11460511-1	2001	To assess how treatment with acetylsalicylic acid (ASA) alters the fibrin network structure, clotting was initiated in purified fibrinogen incubated with ASA by adding thrombin.	Aspirin	154-157	coagulation factor II, thrombin	Homo sapiens	168-176
11260838-11	2001	Some data has been published about the safety of drugs used in cardiology: the haemorrhagic risk of LMW heparin in renal failure and of aspirin, even at low doses, drug interactions, aspirin-ACE inhibitors interaction.	Aspirin	183-190	angiotensin I converting enzyme	Homo sapiens	191-194
11145946-11	2001	The superiority of abciximab over aspirin in accelerating fibrinolysis of forming and preformed PRCs is related to its ability to modulate the interactions of fibrinogen and fibrin with platelets.	Aspirin	34-41	fibrinogen beta chain	Homo sapiens	159-169
11437671-4	2001	The development of novel "super aspirins" with high selectivity towards the inhibition of COX-2 showed that this hypothesis was well-founded and that high levels of these drugs could be tolerated without these serious adverse effects.	Aspirin	32-40	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	90-95
12213988-8	2001	Statin class drugs and aspirin appear to modulate CHD risk in those with increased hs-CRP concentration.	Aspirin	23-30	C-reactive protein	Homo sapiens	86-89
11316916-5	2001	The putative aspirin-ACE inhibitor interaction is being tested prospectively in the Warfarin and Antiplatelet Therapy in Chronic Heart Failure (WATCH) trial - a randomized comparison of warfarin, clopidogrel and aspirin in patients with chronic heart failure.	Aspirin	13-20	angiotensin I converting enzyme	Homo sapiens	21-24
11316916-5	2001	The putative aspirin-ACE inhibitor interaction is being tested prospectively in the Warfarin and Antiplatelet Therapy in Chronic Heart Failure (WATCH) trial - a randomized comparison of warfarin, clopidogrel and aspirin in patients with chronic heart failure.	Aspirin	212-219	angiotensin I converting enzyme	Homo sapiens	21-24
11190906-1	2001	Aspirin"s antithrombotic effect is mediated predominately by inhibition of platelet cyclooxygenase-1, leading to a decline in serum thromboxane A2 concentrations.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	84-100
11687189-18	2001	A possible interaction with ACE inhibitors may reduce the efficacy of aspirin, although this evidence is from retrospective analyses of trial cohorts.	Aspirin	70-77	angiotensin I converting enzyme	Homo sapiens	28-31
11347721-4	2001	Some of the beneficial effects of ACE inhibitors might be related to reduced degradation of bradykinin that enhances the synthesis of prostaglandins, while aspirin, through inhibiting the enzyme cyclo-oxygenase, inhibits the production of prostaglandins.	Aspirin	156-163	angiotensin I converting enzyme	Homo sapiens	34-37
11665868-11	2001	In vivo and in vitro studies suggest that NO-aspirin (acetylsalicylic acid) exerts more potent antithrombotic action than aspirin, probably by coupling the ability to inhibit COX-1 with the anti-adhesive effect of NO.	Aspirin	45-52	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	175-180
11665868-11	2001	In vivo and in vitro studies suggest that NO-aspirin (acetylsalicylic acid) exerts more potent antithrombotic action than aspirin, probably by coupling the ability to inhibit COX-1 with the anti-adhesive effect of NO.	Aspirin	54-74	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	175-180
11665868-11	2001	In vivo and in vitro studies suggest that NO-aspirin (acetylsalicylic acid) exerts more potent antithrombotic action than aspirin, probably by coupling the ability to inhibit COX-1 with the anti-adhesive effect of NO.	Aspirin	122-129	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	175-180
11339623-10	2001	In human erythrocytes, SO was unchanged, but GSH-Px and CAT activities were increased after aspirin treatment.	Aspirin	92-99	catalase	Homo sapiens	56-59
11158202-11	2001	Treatment of cells with aspirin, an agent that targets this intracellular pathway and blocks cell inflammatory responses, blocked K1-induced NF-kappaB-dependent promoter activity.	Aspirin	24-31	nuclear factor kappa B subunit 1	Homo sapiens	141-150
11500924-7	2001	Aspirin in the range 3-10 mM decreases the expression of Hsp70 in unstressed and stressed testicular cells, in striking contrast with the effect observed in other tissues as liver.	Aspirin	0-7	heat shock protein family A (Hsp70) member 2	Gallus gallus	57-62
11311545-6	2001	Neuronal injury-induced glial apoE secretion is attenuated by the nuclear factor kappaB inhibitors, aspirin, Bay 11-7082 and MG-132, suggesting that this transcription factor is involved in both constitutive and induced glial apoE expression.	Aspirin	100-107	apolipoprotein E	Homo sapiens	30-34
12094615-7	2001	These effects were preventable by cotreatment with inhibitors of NF-kappa B activity, such as sodium salicylate, aspirin, or pyrrolidine dithiocarbamate.	Aspirin	113-120	nuclear factor kappa B subunit 1	Homo sapiens	65-75
11552047-8	2001	Aspirin is a more potent inhibitor of Cox-1 than of Cox-2, unlike other non-steroidal anti-inflammatory drugs (NSAIDs), which have limited selectivity.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	52-57
11846053-0	2001	Aspirin differentially regulates endotoxin-induced IL-12 and TNF-alpha production in human dendritic cells.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	61-70
11887863-6	2001	Anti-inflammatory doses of aspirin (1-10 mmol/L) restored eNOS expression in LPS-stimulated human peritoneal tissue samples.	Aspirin	27-34	nitric oxide synthase 3	Homo sapiens	58-62
11887863-10	2001	High doses of aspirin protected both eNOS protein expression and sGC in human peritoneum.	Aspirin	14-21	nitric oxide synthase 3	Homo sapiens	37-41
12120179-1	2001	One hundred years after the introduction of aspirin, greater understanding of the mechanism of action of NSAIDs has led to the development of selective COX-2 inhibitors.	Aspirin	44-51	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	152-157
11846053-8	2001	In contrast, the LPS-induced TNF-alpha production was enhanced by aspirin.	Aspirin	66-73	tumor necrosis factor	Homo sapiens	29-38
11846053-9	2001	The differential effects of aspirin on IL-12 and TNF-alpha production may not be due to down-regulation of cyclooxygenase activities.	Aspirin	28-35	tumor necrosis factor	Homo sapiens	49-58
11195467-3	2000	The NSAIDs used in this study include acetylsalicylic acid (ASA) that is anti-inflammatory with COX-1 and COX-2 inhibition and N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS398) that is a specific COX-2 inhibitor.	Aspirin	38-58	cytochrome c oxidase I, mitochondrial	Mus musculus	96-101
11195467-3	2000	The NSAIDs used in this study include acetylsalicylic acid (ASA) that is anti-inflammatory with COX-1 and COX-2 inhibition and N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS398) that is a specific COX-2 inhibitor.	Aspirin	60-63	cytochrome c oxidase I, mitochondrial	Mus musculus	96-101
11112909-0	2000	Selective cyclo-oxygenase 2 inhibitor in patients with aspirin-induced asthma.	Aspirin	55-62	prostaglandin-endoperoxide synthase 2	Homo sapiens	10-27
11121721-0	2000	Synergistic inhibition of cyclooxygenase-2 expression by vitamin E and aspirin.	Aspirin	71-78	prostaglandin-endoperoxide synthase 2	Homo sapiens	26-42
11121721-1	2000	The use of aspirin in rheumatoid arthritis is limited since inhibition of the pro-inflammatory enzyme cyclooxygenase-2 occurs only at higher aspirin doses that are often associated with side effects such as gastric toxicity.	Aspirin	11-18	prostaglandin-endoperoxide synthase 2	Homo sapiens	102-118
11121721-1	2000	The use of aspirin in rheumatoid arthritis is limited since inhibition of the pro-inflammatory enzyme cyclooxygenase-2 occurs only at higher aspirin doses that are often associated with side effects such as gastric toxicity.	Aspirin	141-148	prostaglandin-endoperoxide synthase 2	Homo sapiens	102-118
11121721-3	2000	1A), the present study explores possible synergistic effects of aspirin and vitamin E on the expression and activity of cyclooxygenase-2.	Aspirin	64-71	prostaglandin-endoperoxide synthase 2	Homo sapiens	120-136
11121721-6	2000	Likewise, lipopolysaccharide-induced cyclooxygenase-2 protein and mRNA expression were virtually abolished by the combined treatment of aspirin and vitamin E, whereas the two agents alone were only modestly effective.	Aspirin	136-143	prostaglandin-endoperoxide synthase 2	Homo sapiens	37-53
11121721-9	2000	Our results show that co-administration of vitamin E renders cyclooxygenase-2 more sensitive to inhibition by aspirin by as yet unknown mechanisms.	Aspirin	110-117	prostaglandin-endoperoxide synthase 2	Homo sapiens	61-77
11211927-7	2000	Using the mean of the results for PGE2 and TXB2 inhibition, the COX-1/COX-2 ratios of the IC50 values for aspirin and NS-398 are < 0.1 and > 130, respectively.	Aspirin	106-113	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	70-75
11211927-9	2000	Dose responses to aspirin and NS-398 which are COX- and COX-2 selective inhibitors respectively, confirmed the utility of this system.	Aspirin	18-25	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	56-61
11221592-0	2000	[Interactions between ACE-inhibitors and aspirin].	Aspirin	41-48	angiotensin I converting enzyme	Homo sapiens	22-25
11327313-0	2000	Aspirin ingestion impairs oral mucosal ulcer healing by inducing membrane-bound tumor necrosis factor-alpha release.	Aspirin	0-7	tumor necrosis factor	Rattus norvegicus	80-107
11327313-2	2000	We investigated the effect of aspirin ingestion on the processing of TNF-alpha in rat soft oral tissue during buccal ulcer healing.	Aspirin	30-37	tumor necrosis factor	Rattus norvegicus	69-78
11192938-1	2000	Aspirin therapy inhibits prostaglandin biosynthesis; yet via acetylation of cyclooxygenase 2 (COX-2) it leads to bioactive lipoxins epimeric at carbon 15 (15-epi-LX, also termed aspirin-triggered lipoxin or ATL).	Aspirin	178-185	prostaglandin-endoperoxide synthase 2	Homo sapiens	76-92
11327313-4	2000	Moreover, by the 10th day, the delay in ulcer healing by aspirin was manifested in a 5.6-fold higher rate of apoptosis and a 5.2-fold higher level of soluble TNF-alpha, yet the expression of membrane-bound TNF-alpha showed a 38% decline.	Aspirin	57-64	tumor necrosis factor	Rattus norvegicus	158-167
11327313-4	2000	Moreover, by the 10th day, the delay in ulcer healing by aspirin was manifested in a 5.6-fold higher rate of apoptosis and a 5.2-fold higher level of soluble TNF-alpha, yet the expression of membrane-bound TNF-alpha showed a 38% decline.	Aspirin	57-64	tumor necrosis factor	Rattus norvegicus	206-215
11327313-5	2000	Treatment with metalloprotease inhibitor, Zincov, produced dose-dependent reduction (56.9%) in aspirin-induced increase in the mucosal expression of soluble TNF-alpha, evoked a 62% decrease in the rate of epithelial cell apoptosis, and led to a marked reversal (56.9%) in aspirin-induced delay in ulcer healing.	Aspirin	95-102	tumor necrosis factor	Rattus norvegicus	157-166
11327313-6	2000	Our findings indicate that the impairment in buccal ulcer healing by aspirin is a result of upregulation in the processing of soluble TNF-alpha from its membrane-bound precursor that leads to the amplification of apoptotic events and potentiation of the mucosal inflammatory responses that interfere with healing process.	Aspirin	69-76	tumor necrosis factor	Rattus norvegicus	134-143
11192938-1	2000	Aspirin therapy inhibits prostaglandin biosynthesis; yet via acetylation of cyclooxygenase 2 (COX-2) it leads to bioactive lipoxins epimeric at carbon 15 (15-epi-LX, also termed aspirin-triggered lipoxin or ATL).	Aspirin	178-185	prostaglandin-endoperoxide synthase 2	Homo sapiens	94-99
11192938-3	2000	Also, human endothelial cells, both HUVEC and microvascular, with upregulated COX-2 and treated with ASA converted C20:5 omega-3 to 18R-hydroxyeicosapentaenoic acid (HEPE) and 15R-HEPE.	Aspirin	101-104	prostaglandin-endoperoxide synthase 2	Homo sapiens	78-83
11154121-0	2000	Effect of sodium arachidonate on thrombin generation through platelet activation--inhibitory effect of aspirin.	Aspirin	103-110	coagulation factor II, thrombin	Homo sapiens	33-41
11154121-13	2000	Aspirin administered in vivo produced a decrease of TG in PRP activated with AA.	Aspirin	0-7	prion protein	Homo sapiens	58-61
11078878-4	2000	This effect was more pronounced after inhibition of the cyclooxygenase-2 pathway by acetylsalicylic acid.	Aspirin	84-104	prostaglandin-endoperoxide synthase 2	Homo sapiens	56-72
11027305-6	2000	In the WD or WD + ASA groups, apoE-/- mice had twice the neointimal area than WT mice ( approximately 30,000 vs. 13,000 microm(2) per section; P < 0.0001).	Aspirin	18-21	apolipoprotein E	Mus musculus	30-34
11040851-0	2000	The "aspirin" of the new millennium: cyclooxygenase-2 inhibitors.	Aspirin	5-12	prostaglandin-endoperoxide synthase 2	Homo sapiens	37-53
10992560-0	2000	The importance of COX-2 inhibition for aspirin induced asthma.	Aspirin	39-46	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	18-23
10999979-10	2000	Use of aspirin therapy attenuated the benefit of ACE inhibitors in patients with poor renal function.	Aspirin	7-14	angiotensin I converting enzyme	Homo sapiens	49-52
10999979-12	2000	Use of aspirin therapy may attenuate the benefit of ACE inhibitors in patients with high serum creatinine levels; therefore, further studies are needed to determine whether treatment with aspirin, alternative antiplatelet agents, or anticoagulation is indicated for these patients.	Aspirin	7-14	angiotensin I converting enzyme	Homo sapiens	52-55
10988074-1	2000	Prostaglandin H synthase-1 and -2 (PGHS-1 and -2) catalyze the committed step in prostaglandin synthesis and are targets for nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin.	Aspirin	176-183	prostaglandin-endoperoxide synthase 1	Homo sapiens	35-48
11205285-1	2000	BACKGROUND: We recently found that aspirin induces the expression of P-glycoprotein (P-gp), a protein mediating drug resistance, in human prostate cancer cells.	Aspirin	35-42	ATP binding cassette subfamily B member 1	Homo sapiens	69-83
11205285-1	2000	BACKGROUND: We recently found that aspirin induces the expression of P-glycoprotein (P-gp), a protein mediating drug resistance, in human prostate cancer cells.	Aspirin	35-42	ATP binding cassette subfamily B member 1	Homo sapiens	85-89
11205285-2	2000	The purpose of this study was to evaluate the effect of aspirin on the expression of P-gp in a different human cancer type, i.e., T lymphoma.	Aspirin	56-63	ATP binding cassette subfamily B member 1	Homo sapiens	85-89
11205285-5	2000	RESULTS: aspirin, at plasma attainable levels, induced NF-IL6 DNA-binding activity, and increased MDR1 mRNA expression (by up to 140%), as well as the expression of P-gp, in Molt-4 cells.	Aspirin	9-16	ATP binding cassette subfamily B member 1	Homo sapiens	98-102
11205285-6	2000	CONCLUSIONS: This study suggests that treatment with aspirin induces a cellular signal culminating in the enhancement of P-gp expression in T lymphoma Molt-4 cells.	Aspirin	53-60	ATP binding cassette subfamily B member 1	Homo sapiens	121-125
11046058-0	2000	IL-1 beta converting enzyme is a target for nitric oxide-releasing aspirin: new insights in the antiinflammatory mechanism of nitric oxide-releasing nonsteroidal antiinflammatory drugs.	Aspirin	67-74	caspase 1	Homo sapiens	0-27
11046058-12	2000	Caspase-1 inhibition is a new, cycloxygenase-independent antiinflammatory mechanism of NO-aspirin.	Aspirin	90-97	caspase 1	Homo sapiens	0-9
17018963-12	2000	All aspirinlike drugs have until quite recently been mixed blockers of cyclooxigenases (COX 1 and COX 2) with aspirin itself being the most outstanding COX 1 blocker.	Aspirin	4-11	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	98-103
11228543-0	2000	Aspirin induces apoptosis through release of cytochrome c from mitochondria.	Aspirin	0-7	cytochrome c, somatic	Homo sapiens	45-57
11228543-4	2000	Further analysis of the mechanism underlying this apoptotic event showed that aspirin induces translocation of Bax to the mitochondria and mitochondrial release of cytochrome into the cytosol.	Aspirin	78-85	BCL2 associated X, apoptosis regulator	Homo sapiens	111-114
11228543-5	2000	The release of cytochrome c from mitochondria was inhibited by overexpression of the antiapoptotic protein Bcl-2 and cells that lack Apaf-1 were resistant to aspirin-induced apoptosis.	Aspirin	158-165	cytochrome c, somatic	Homo sapiens	15-27
11228543-5	2000	The release of cytochrome c from mitochondria was inhibited by overexpression of the antiapoptotic protein Bcl-2 and cells that lack Apaf-1 were resistant to aspirin-induced apoptosis.	Aspirin	158-165	apoptotic peptidase activating factor 1	Homo sapiens	133-139
11228543-6	2000	These data provide evidence that the release of cytochrome c is an important part of the apoptotic mechanism of aspirin.	Aspirin	112-119	cytochrome c, somatic	Homo sapiens	48-60
11034940-4	2000	METHODS AND RESULTS: Using washed platelets from normal donors and tyrphostin-A47 and aspirin as tyrosine kinase and COX-1 inhibitors, respectively, we found that tyrphostin-A47 downregulated (1) the thrombin-activated conformational change of alpha(IIb)beta(3), (2) actin polymerization and cytoskeletal reorganization, and (3) the quantity of tyrosine-phospho-rylated proteins associated with the reorganized cytoskeleton.	Aspirin	86-93	coagulation factor II, thrombin	Homo sapiens	200-208
11034610-1	2000	Aspirin therapy inhibits prostaglandin biosynthesis without directly acting on lipoxygenases, yet via acetylation of cyclooxygenase 2 (COX-2) it leads to bioactive lipoxins (LXs) epimeric at carbon 15 (15-epi-LX, also termed aspirin-triggered LX [ATL]).	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	135-140
11034610-1	2000	Aspirin therapy inhibits prostaglandin biosynthesis without directly acting on lipoxygenases, yet via acetylation of cyclooxygenase 2 (COX-2) it leads to bioactive lipoxins (LXs) epimeric at carbon 15 (15-epi-LX, also termed aspirin-triggered LX [ATL]).	Aspirin	225-232	prostaglandin-endoperoxide synthase 2	Homo sapiens	117-133
11034610-1	2000	Aspirin therapy inhibits prostaglandin biosynthesis without directly acting on lipoxygenases, yet via acetylation of cyclooxygenase 2 (COX-2) it leads to bioactive lipoxins (LXs) epimeric at carbon 15 (15-epi-LX, also termed aspirin-triggered LX [ATL]).	Aspirin	225-232	prostaglandin-endoperoxide synthase 2	Homo sapiens	135-140
11034610-3	2000	Human endothelial cells with upregulated COX-2 treated with ASA converted C20:5 omega-3 to 18R-hydroxyeicosapentaenoic acid (HEPE) and 15R-HEPE.	Aspirin	60-63	prostaglandin-endoperoxide synthase 2	Homo sapiens	41-46
11020393-1	2000	BACKGROUND: Several studies have suggested that there may be an interaction between angiotensin-converting enzyme (ACE) inhibitors and aspirin in patients with congestive heart failure, such that their benefits are attenuated when used in combination.	Aspirin	135-142	angiotensin I converting enzyme	Homo sapiens	115-118
11020393-13	2000	After adjusting for confounders, combined use of aspirin and ACE inhibitors was associated with increased mortality in GUSTO-I patients (hazard ratio [HR] = 2.2, 95% confidence interval [CI]: 1.1 to 4.3, P = 0.03) compared with aspirin alone.	Aspirin	228-235	angiotensin I converting enzyme	Homo sapiens	61-64
11020393-14	2000	In EPILOG patients, after adjusting for clinical factors and extent of left ventricular dysfunction, the combination of aspirin and ACE inhibitors was associated with an increased risk of death (HR = 2.1, 95% CI: 1.1 to 3.8, P = 0.02) and of death or nonfatal myocardial infarction (HR = 1.5, 95% CI: 1.1 to 2.5, P = 0.02) compared with aspirin alone.	Aspirin	337-344	angiotensin I converting enzyme	Homo sapiens	132-135
11020393-15	2000	CONCLUSION: These observational findings suggest the possibility of an interaction between aspirin and ACE inhibitors among patients with ischemic heart disease.	Aspirin	91-98	angiotensin I converting enzyme	Homo sapiens	103-106
11078056-5	2000	In contrast, aspirin-like nonselective NSAIDs such as sulindac and indomethacin inhibit not only the enzymatic action of the highly inducible, proinflammatory COX-2 but the constitutively expressed, cytoprotective COX-1 as well.	Aspirin	13-20	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	159-164
11142556-6	2000	Despite inhibiting of PGE2 generation, both nitric oxide-releasing derivatives and native aspirin and naproxen failed to affect expression of cyclooxygenase-1 mRNA but upregulated the cyclooxygenase-2 mRNA.	Aspirin	90-97	prostaglandin-endoperoxide synthase 2	Homo sapiens	184-200
11026650-4	2000	In the condition after pretreatment with the cyclooxygenase inhibitor acetylsalicylic acid, although the vascular effects of TNF-alpha on basal FVR appeared to be blocked (37.1 +/- 5.3 vs. 37.6 +/- 5.2; NS), ACh-induced minimal FVR did not differ between pre- and post-TNF-alpha states.	Aspirin	70-90	tumor necrosis factor	Homo sapiens	125-134
11026650-4	2000	In the condition after pretreatment with the cyclooxygenase inhibitor acetylsalicylic acid, although the vascular effects of TNF-alpha on basal FVR appeared to be blocked (37.1 +/- 5.3 vs. 37.6 +/- 5.2; NS), ACh-induced minimal FVR did not differ between pre- and post-TNF-alpha states.	Aspirin	70-90	tumor necrosis factor	Homo sapiens	269-278
10987821-3	2000	Surprisingly, administration of analgesic doses of morphine or the nonsteroidal antiinflammatory drugs aspirin, metamizol (dipyrone), and indomethacin also increased GPDH mRNA levels in rat spinal cord.	Aspirin	103-110	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	166-170
10970676-9	2000	Pretreatment of the mice with aspirin, an irreversible inhibitor of COX1 and COX2, prevented the hypophagic response to IL-1, 16 h, but not 40 h later.	Aspirin	30-37	cytochrome c oxidase I, mitochondrial	Mus musculus	68-72
10942736-11	2000	Sodium formate and aspirin,.OH radical scavengers, also suppressed p53 activation.	Aspirin	19-26	tumor protein p53	Homo sapiens	67-70
11054089-5	2000	In seven out of 26 PLA2 allele carriers, aspirin shortened BT on average by 30 s, compared with only one among 54 subjects with the PlA1/A1 genotype.	Aspirin	41-48	phospholipase A2 group IB	Homo sapiens	19-23
11054082-7	2000	An increased sensitivity to the anti-aggregatory effect of acetylsalicylic acid was observed in platelets from subjects with the Pl(A2) allele.	Aspirin	59-79	phospholipase A2 group IB	Homo sapiens	129-134
11054089-7	2000	Carriers of the PlA2 allele appear to be more resistant to the antithrombotic action of aspirin.	Aspirin	88-95	phospholipase A2 group IB	Homo sapiens	16-20
11249482-2	2000	Post infarction treatment with aspirin, statins, beta-blockers and angiotensin-converting enzyme (ACE) inhibitors has improved morbidity and mortality and is cost-effective.	Aspirin	31-38	angiotensin I converting enzyme	Homo sapiens	98-101
11022121-0	2000	A short course of oral aspirin increases IL-18-induced interferon-gamma production in whole blood cultures.	Aspirin	23-30	interferon gamma	Homo sapiens	55-71
11022121-2	2000	Four days after cessation of a 3-day regimen of 650 mg of oral aspirin, there was a 70% increase in interferon-gamma (IFN-gamma) production, stimulated by a combination of interleukin-18 (IL-18) plus lipopolysaccharide (p < 0.05).	Aspirin	63-70	interferon gamma	Homo sapiens	100-116
11022121-2	2000	Four days after cessation of a 3-day regimen of 650 mg of oral aspirin, there was a 70% increase in interferon-gamma (IFN-gamma) production, stimulated by a combination of interleukin-18 (IL-18) plus lipopolysaccharide (p < 0.05).	Aspirin	63-70	interferon gamma	Homo sapiens	118-127
11022121-4	2000	TNF-alpha and IFN-gamma production returned to pre-aspirin levels one month after the discontinuation of aspirin.	Aspirin	51-58	tumor necrosis factor	Homo sapiens	0-9
11022121-4	2000	TNF-alpha and IFN-gamma production returned to pre-aspirin levels one month after the discontinuation of aspirin.	Aspirin	51-58	interferon gamma	Homo sapiens	14-23
11022121-4	2000	TNF-alpha and IFN-gamma production returned to pre-aspirin levels one month after the discontinuation of aspirin.	Aspirin	105-112	tumor necrosis factor	Homo sapiens	0-9
11034327-0	2000	Aspirin induces apoptosis through mitochondrial cytochrome c release.	Aspirin	0-7	cytochrome c, somatic	Homo sapiens	48-60
11034327-4	2000	The apoptotic effect of aspirin was analyzed in different cell lines (Jurkat, MOLT-4, Raji and HL-60) showing induction of mitochondrial cytochrome c release and caspases 9, 3 and 8 processing.	Aspirin	24-31	cytochrome c, somatic	Homo sapiens	137-149
11034327-5	2000	Furthermore, early aspirin-induced cytochrome c release was not affected by the caspase inhibitor Z-VAD x fmk and preceded loss of mitochondrial membrane potential.	Aspirin	19-26	cytochrome c, somatic	Homo sapiens	35-47
11034327-6	2000	Therefore, aspirin-induced apoptosis involves caspase activation through cytochrome c release.	Aspirin	11-18	cytochrome c, somatic	Homo sapiens	73-85
10987587-6	2000	Clopidogrel with or without aspirin significantly suppressed expression of platelet activation markers CD 62p, CD 63 and PAC-1 after stimulation with ADP or thrombin (p < 0.001).	Aspirin	28-35	coagulation factor II, thrombin	Homo sapiens	157-165
10987587-10	2000	Clopidogrel in combination with aspirin showed synergistic inhibitory effects after stimulation with collagen and thrombin compared with monotherapies.	Aspirin	32-39	coagulation factor II, thrombin	Homo sapiens	114-122
10973674-0	2000	Inhibitory activity of aspirin on von Willebrand factor-induced platelet aggregation.	Aspirin	23-30	von Willebrand factor	Homo sapiens	34-55
10983857-1	2000	We compared the gastric toxic effect of aspirin (ASA) in both normal and diabetic rats, with that of NCX-4016, a derivative of ASA with nitric oxide (NO) releasing moiety.	Aspirin	127-130	solute carrier family 8 member A1	Rattus norvegicus	101-104
10983857-10	2000	NCX-4016, though absorbed more slowly than ASA, counteracts the injurious effect of aspirin on the gastric mucosa, probably by increasing GMBF mediated by NO.	Aspirin	84-91	solute carrier family 8 member A1	Rattus norvegicus	0-3
10973674-1	2000	The effect of aspirin (ASA) on vWF induced platelet - platelet interaction is unknown.	Aspirin	14-21	von Willebrand factor	Homo sapiens	31-34
10973674-1	2000	The effect of aspirin (ASA) on vWF induced platelet - platelet interaction is unknown.	Aspirin	23-26	von Willebrand factor	Homo sapiens	31-34
10973674-6	2000	Considerable interindividual variability in response to vWF-coated beads was observed, both before ASA and after treatment with ASA.	Aspirin	99-102	von Willebrand factor	Homo sapiens	56-59
10973674-6	2000	Considerable interindividual variability in response to vWF-coated beads was observed, both before ASA and after treatment with ASA.	Aspirin	128-131	von Willebrand factor	Homo sapiens	56-59
10973674-10	2000	Thus, platelet aggregation induced by vWF-coated beads is impaired by ASA.	Aspirin	70-73	von Willebrand factor	Homo sapiens	38-41
10942685-1	2000	OBJECTIVES: the preventive effect of acetylsalicylic acid in cardiovascular disease may be due to inhibition of platelet aggregation mediated by COX-1, but may in addition be due to anti-inflammatory effects by inhibition of COX-2.	Aspirin	37-57	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	225-230
10931797-2	2000	To determine whether smoking influences plaque thrombogenicity, we examined the effect of cigarette smoking and aspirin use on tissue factor (TF) expression in atherosclerotic plaques.	Aspirin	112-119	coagulation factor III	Mus musculus	127-140
10931797-2	2000	To determine whether smoking influences plaque thrombogenicity, we examined the effect of cigarette smoking and aspirin use on tissue factor (TF) expression in atherosclerotic plaques.	Aspirin	112-119	coagulation factor III	Mus musculus	142-144
10931797-9	2000	Aspirin use was associated with reduced TF expression in smokers (9+/-8% versus 3+/-4%; P=0.0017).	Aspirin	0-7	coagulation factor III	Mus musculus	40-42
10931797-11	2000	Treatment with aspirin may reduce TF expression.	Aspirin	15-22	coagulation factor III	Mus musculus	34-36
10977131-10	2000	After incubation with LPS plus acetylsalicylic acid, positive staining was observed for both COX-1-ir and COX-2-ir.	Aspirin	31-51	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	106-111
10933569-0	2000	Intermediate but not low doses of aspirin can suppress angiotensin-converting enzyme inhibitor-induced cough.	Aspirin	34-41	angiotensin I converting enzyme	Homo sapiens	55-84
11798822-2	2000	METHODS: The polymorphisms of CYP1A1 and CYP2E1 gene were analyzed in 158 PD patients and 150 unrelated healthy controls with PCR-RFLP and ASA techniques.	Aspirin	139-142	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	41-47
10923603-2	2000	It was therefore logical to assume that an inhibitor of 5-lipoxygenase (5-LO), such as zileuton, given before and during oral challenges with ASA, might prevent ASA-induced respiratory reactions.	Aspirin	142-145	arachidonate 5-lipoxygenase	Homo sapiens	56-70
10923603-2	2000	It was therefore logical to assume that an inhibitor of 5-lipoxygenase (5-LO), such as zileuton, given before and during oral challenges with ASA, might prevent ASA-induced respiratory reactions.	Aspirin	161-164	arachidonate 5-lipoxygenase	Homo sapiens	56-70
10964725-2	2000	Acetylsalycilic acid, nimesulide, or SQ22536 was used as respective antagonist of COX-1, COX-2, or adenylate cyclase using aortic rings precontracted with phenylephrine and exposed to cumulative concentrations of acetylcholine (ACh).	Aspirin	0-20	cytochrome c oxidase subunit I	Oryctolagus cuniculus	82-87
10933569-1	2000	This self-matched control study aimed to compare the efficiency of two different regimens of active treatment: aspirin in low (100 mg daily) versus intermediate (500 mg daily) doses in abolishing angiotensin-converting enzyme inhibitor (ACEI)-induced cough.	Aspirin	111-118	angiotensin I converting enzyme	Homo sapiens	196-225
10860828-4	2000	The present study was designed to elucidate sequentially the action mechanisms of acetaminophen and salicylates (aspirin and sodium salicylate) on lipopolysaccharide (LPS) plus interferon-gamma (IFN-gamma)-induced iNOS expression in RAW 264.7 macrophages.	Aspirin	113-120	interferon gamma	Homo sapiens	177-204
10862819-6	2000	Catalase activity was significantly augmented in diabetic mice and the long term treatment with aspirin partially reverted it.	Aspirin	96-103	catalase	Mus musculus	0-8
10860828-4	2000	The present study was designed to elucidate sequentially the action mechanisms of acetaminophen and salicylates (aspirin and sodium salicylate) on lipopolysaccharide (LPS) plus interferon-gamma (IFN-gamma)-induced iNOS expression in RAW 264.7 macrophages.	Aspirin	113-120	nitric oxide synthase 2	Homo sapiens	214-218
10912743-3	2000	This study assessed the effects of chronic treatment with low doses of aspirin (100 mg/day) on clinic and ambulatory systolic (SBP) and diastolic (DBP) BP in hypertensives on chronic, stable antihypertensive therapy.	Aspirin	71-78	D-box binding PAR bZIP transcription factor	Homo sapiens	147-150
10868686-6	2000	Bile acids could induce COX-2 expression in six of eight cell lines tested, which was correlated with prostaglandin E2 production, and aspirin could inhibit COX-2 enzymatic activity even after bile acid stimulation but was unable to change the COX-2 protein level in these cell lines.	Aspirin	135-142	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	157-162
10868686-7	2000	Down-regulation of bcl-2 by aspirin was found in the two cell lines tested.	Aspirin	28-35	BCL2 apoptosis regulator	Homo sapiens	19-24
10841227-2	2000	OBJECTIVES: We sought to determine whether the clinical effects of early angiotensin-converting enzyme (ACE) inhibitor (ACEi) treatment for acute myocardial infarction (MI) are influenced by the concomitant use of aspirin (ASA).	Aspirin	214-221	angiotensin I converting enzyme	Homo sapiens	73-102
10841227-9	2000	Angiotensin-converting enzyme inhibitor was associated with similar proportional reductions in 30-day mortality among the 86,484 patients who were taking ASA (6% [SD, 3%] reduction) and among the 10,228 patients who were not (10% [SD, 5%] reduction: chi-squared test of heterogeneity between these reductions = 0.4; p = 0.5).	Aspirin	154-157	angiotensin I converting enzyme	Homo sapiens	0-29
10841227-10	2000	Angiotensin-converting enzyme inhibitor produced definite increases in the incidence of persistent hypotension (17.9% ACEi vs. 9.4% control) and of renal dysfunction (1.3% ACEi vs. 0.6% control), but there was no good evidence that these effects were different in the presence or absence of ASA (chi-squared for heterogeneity = 0.4 and 0.0, respectively; both not significant).	Aspirin	291-294	angiotensin I converting enzyme	Homo sapiens	0-29
10860828-9	2000	Aspirin also dose dependently inhibited iNOS enzyme activity in cell-free extracts, whereas no significant differences were observed in extracts treated with sodium salicylate or acetaminophen.	Aspirin	0-7	nitric oxide synthase 2	Homo sapiens	40-44
10853626-0	2000	Update on the interaction between aspirin and angiotensin-converting enzyme inhibitors.	Aspirin	34-41	angiotensin I converting enzyme	Homo sapiens	46-75
10853626-1	2000	We summarized recent published literature regarding the significance of an interaction between aspirin and angiotensin-converting enzyme (ACE) inhibitors in patients with various cardiovascular diseases.	Aspirin	95-102	angiotensin I converting enzyme	Homo sapiens	107-136
10853626-1	2000	We summarized recent published literature regarding the significance of an interaction between aspirin and angiotensin-converting enzyme (ACE) inhibitors in patients with various cardiovascular diseases.	Aspirin	95-102	angiotensin I converting enzyme	Homo sapiens	138-141
10853626-4	2000	The results of several studies added to our understanding of the clinical ramifications of an aspirin-ACE inhibitor interaction, but also introduced questions.	Aspirin	94-101	angiotensin I converting enzyme	Homo sapiens	102-105
10896240-6	2000	Addition of exogenous PGE2 before incubation nearly abrogated the effect of aspirin on TNF-alpha, substantiating the role of PGE2 as a regulator of TNF-alpha synthesis, whereas the effect on FPA was small.	Aspirin	76-83	tumor necrosis factor	Homo sapiens	87-96
10826452-0	2000	Does aspirin attenuate the beneficial effects of angiotensin-converting enzyme inhibition in heart failure?	Aspirin	5-12	angiotensin I converting enzyme	Homo sapiens	49-78
10826452-2	2000	The issue of possible attenuation of the effect of ACE inhibitors by ASA has been an area of intense debate.	Aspirin	69-72	angiotensin I converting enzyme	Homo sapiens	51-54
10826452-6	2000	Thus, the counteracting effect of ASA on the augmentation of prostacyclin synthesis by ACE inhibitors could result in a potential reduction of the beneficial effects of the ACE inhibitor"s and could be of great importance.	Aspirin	34-37	angiotensin I converting enzyme	Homo sapiens	87-90
10826452-6	2000	Thus, the counteracting effect of ASA on the augmentation of prostacyclin synthesis by ACE inhibitors could result in a potential reduction of the beneficial effects of the ACE inhibitor"s and could be of great importance.	Aspirin	34-37	angiotensin I converting enzyme	Homo sapiens	173-176
10826452-7	2000	This article reviews reports from large clinical trials pertaining to this issue and relates their findings to the currently available theoretical bases for support of the counteracting effect of ASA on augmentation of prostacyclin synthesis by ACE inhibitors.	Aspirin	196-199	angiotensin I converting enzyme	Homo sapiens	245-248
10824632-1	2000	BACKGROUND: There is some evidence that aspirin may be harmful to patients with congestive heart failure treated with angiotensin-converting enzyme (ACE) inhibitors, but there has never been any direct examination of the vascular effects of aspirin in these patients.	Aspirin	40-47	angiotensin I converting enzyme	Homo sapiens	118-147
10824632-1	2000	BACKGROUND: There is some evidence that aspirin may be harmful to patients with congestive heart failure treated with angiotensin-converting enzyme (ACE) inhibitors, but there has never been any direct examination of the vascular effects of aspirin in these patients.	Aspirin	40-47	angiotensin I converting enzyme	Homo sapiens	149-152
10818069-3	2000	Sodium salicylate, aspirin, and indomethacin dose-dependently enhanced nitrite production by interleukin (IL)-1beta-stimulated VSMCs at therapeutic plasma concentration ranges.	Aspirin	19-26	interleukin 1 beta	Rattus norvegicus	93-115
10818069-4	2000	Increased nitrite production by aspirin-like drugs was accompanied by increased iNOS mRNA and protein accumulation in VSMCs.	Aspirin	32-39	nitric oxide synthase 2	Rattus norvegicus	80-84
10818069-8	2000	Our study demonstrates that aspirin and the aspirin-like drugs, sodium salicylate and indomethacin, increase NO synthesis in IL-1beta-stimulated VSMCs by upregulation of iNOS transcription via a 12-LO pathway.	Aspirin	28-35	interleukin 1 beta	Rattus norvegicus	125-133
10818069-8	2000	Our study demonstrates that aspirin and the aspirin-like drugs, sodium salicylate and indomethacin, increase NO synthesis in IL-1beta-stimulated VSMCs by upregulation of iNOS transcription via a 12-LO pathway.	Aspirin	28-35	nitric oxide synthase 2	Rattus norvegicus	170-174
10818069-8	2000	Our study demonstrates that aspirin and the aspirin-like drugs, sodium salicylate and indomethacin, increase NO synthesis in IL-1beta-stimulated VSMCs by upregulation of iNOS transcription via a 12-LO pathway.	Aspirin	44-51	interleukin 1 beta	Rattus norvegicus	125-133
10818069-8	2000	Our study demonstrates that aspirin and the aspirin-like drugs, sodium salicylate and indomethacin, increase NO synthesis in IL-1beta-stimulated VSMCs by upregulation of iNOS transcription via a 12-LO pathway.	Aspirin	44-51	nitric oxide synthase 2	Rattus norvegicus	170-174
10776741-8	2000	Pulmonary embolism or deep-vein thrombosis was confirmed in 105 (1.6%) of 6679 patients assigned aspirin compared with 165 (2.5%) of 6677 assigned placebo, which represents an absolute reduction of 9 (SE 2) per 1000 and a proportional reduction of 36% (19-50; p=0.0003).	Aspirin	97-104	fucosyltransferase 2	Homo sapiens	201-205
10818443-4	2000	Here, we determined the relationship between polyisoprenyl phosphate (PIPP) remodeling and PLD signaling and their impact in activation of PMN receptors by "pro-inflammatory" (leukotriene B4), and "anti-inflammatory" (aspirin-triggered lipoxinA4) ligands.	Aspirin	218-225	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	91-94
10870801-0	2000	A low dose of aspirin (75 mg/day) lowers thrombin generation to a similar extent as a high dose of aspirin (300 mg/day).	Aspirin	14-21	coagulation factor II, thrombin	Homo sapiens	41-49
10870801-1	2000	This randomized, double-blind, parallel-group study was performed to assess the effect of 1-week treatment with 75 and 300 mg aspirin on thrombin generation.	Aspirin	126-133	coagulation factor II, thrombin	Homo sapiens	137-145
10870801-5	2000	At the site of microvascular injury, 75 mg aspirin led to a marked, about 60%, reduction in the total amount of thrombin generated (P = 0.04).	Aspirin	43-50	coagulation factor II, thrombin	Homo sapiens	112-120
10870801-7	2000	We conclude that the thrombin-lowering action of aspirin in the range between 75 and 300 mg daily given for 7 days is not dose dependent.	Aspirin	49-56	coagulation factor II, thrombin	Homo sapiens	21-29
10759852-1	2000	U46619, a thromboxane A2 mimetic, but not ADP, caused activation of p38 mitogen activated protein (MAP) kinase in aspirin-treated platelets.	Aspirin	114-121	mitogen-activated protein kinase 14	Homo sapiens	68-71
10759852-5	2000	Hence, ADP must be generating an agonist, other than thromboxane A2, via an aspirin-sensitive pathway, which is capable of activating p38 kinase.	Aspirin	76-83	mitogen-activated protein kinase 14	Homo sapiens	134-137
10868686-6	2000	Bile acids could induce COX-2 expression in six of eight cell lines tested, which was correlated with prostaglandin E2 production, and aspirin could inhibit COX-2 enzymatic activity even after bile acid stimulation but was unable to change the COX-2 protein level in these cell lines.	Aspirin	135-142	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	157-162
10896240-0	2000	Aspirin potentiates LPS-induced fibrin formation (FPA) and TNF-alpha-synthesis in whole blood.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	59-68
10781899-1	2000	OBJECTIVE: Because the prostaglandin endoperoxide H synthase-1 (PGHS-1)-dependent formation of thromboxane A(2) is an important modulator of platelet function, this pathway represents a pharmacologic target for the inhibition of platelet function by aspirin.	Aspirin	250-257	prostaglandin-endoperoxide synthase 1	Homo sapiens	23-62
10896240-2	2000	Aspirin induced a concentration dependent increase (2.5-5-fold at 5 mM aspirin) in LPS-induced appearance of TNF-alpha and fibrinopeptide A (FPA) in plasma, despite the concomitant increase in the inhibitory cytokine IL-100.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	109-118
10896240-2	2000	Aspirin induced a concentration dependent increase (2.5-5-fold at 5 mM aspirin) in LPS-induced appearance of TNF-alpha and fibrinopeptide A (FPA) in plasma, despite the concomitant increase in the inhibitory cytokine IL-100.	Aspirin	71-78	tumor necrosis factor	Homo sapiens	109-118
10896240-3	2000	Aspirin substantially raised the levels of LPS-induced TF-mRNA and TNFalpha-mRNA in monocytes isolated from whole blood.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	67-75
10781899-1	2000	OBJECTIVE: Because the prostaglandin endoperoxide H synthase-1 (PGHS-1)-dependent formation of thromboxane A(2) is an important modulator of platelet function, this pathway represents a pharmacologic target for the inhibition of platelet function by aspirin.	Aspirin	250-257	prostaglandin-endoperoxide synthase 1	Homo sapiens	64-70
10692466-2	2000	The two isoforms of cyclooxygenase, COX-1 and COX-2, are acetylated by aspirin at Ser-530 and Ser-516, respectively, in the cyclooxygenase active site.	Aspirin	71-78	cytochrome c oxidase I, mitochondrial	Mus musculus	36-41
10727528-2	2000	This study shows that aspirin and sodium salicylate, its major blood metabolite, reverse contractile actions of endothelin-1 (ET-1) in isolated rat aorta and human mammary arteries.	Aspirin	22-29	endothelin 1	Rattus norvegicus	112-124
10727528-2	2000	This study shows that aspirin and sodium salicylate, its major blood metabolite, reverse contractile actions of endothelin-1 (ET-1) in isolated rat aorta and human mammary arteries.	Aspirin	22-29	endothelin 1	Rattus norvegicus	126-130
10692466-6	2000	Site-directed mutagenesis of Val-434, Arg-513, and Val-523 in mouse COX-2 to their COX-1 equivalents resulted in abrogation of 11- and 15-HETE production after aspirin treatment, confirming the hypothesis that these residues are the major isoform selectivity determinants regulating HETE production.	Aspirin	160-167	cytochrome c oxidase I, mitochondrial	Mus musculus	83-88
10671506-4	2000	Aspirin treatment of cyclooxygenase-2 is known to acetylate an active site serine, block prostaglandin biosynthesis, and give 15R-hydroxyeicosatetraenoic acid (15R-HETE) as the only product.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	21-37
10841038-4	2000	When these cells were pretreated with aspirin to inactivate their PGHS-1 and then activated by serum and phorbol ester (TPA) for 6 h, the cells expressed PGHS-2 activity alone.	Aspirin	38-45	prostaglandin-endoperoxide synthase 1	Homo sapiens	66-72
10841038-4	2000	When these cells were pretreated with aspirin to inactivate their PGHS-1 and then activated by serum and phorbol ester (TPA) for 6 h, the cells expressed PGHS-2 activity alone.	Aspirin	38-45	prostaglandin-endoperoxide synthase 2	Homo sapiens	154-160
10639187-4	2000	RESULTS: Incubation with aspirin for 3 days reduced cellular proliferation by up to 35-55% in each cell line studied, but induced a tripling of the percentage of cells expressing P-glycoprotein (an efflux pump conferring multidrug resistance) only in the LNCaP cells.	Aspirin	25-32	ATP binding cassette subfamily B member 1	Homo sapiens	179-193
10639187-7	2000	Furthermore, this protective effect of aspirin was reversed by a specific P-glycoprotein inhibitor, PSC833.	Aspirin	39-46	ATP binding cassette subfamily B member 1	Homo sapiens	74-88
10639187-8	2000	The cellular expression of P-glycoprotein returned to normal within 3 days following the removal of aspirin.	Aspirin	100-107	ATP binding cassette subfamily B member 1	Homo sapiens	27-41
10698490-9	2000	These results suggest that the inhibition of NF-kappaB activity is a plausible mechanism for apoptosis induced by the wt-p53 gene transfer in human colon cancer cells and that anti-NF-kappaB reagent aspirin could make these cells more susceptible to apoptosis.	Aspirin	199-206	nuclear factor kappa B subunit 1	Homo sapiens	181-190
10671506-6	2000	To understand the changes that lead to 15R-HETE synthesis in aspirin-treated COX-2, we employed pro-R- and pro-S-labeled [13-(3)H]arachidonic acids to investigate the selectivity of the initial hydrogen abstraction.	Aspirin	61-68	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	77-82
10671506-7	2000	Remarkably, aspirin-treated COX-2 formed 15R-HETE with removal of the pro-S hydrogen at C-13 (3-9% retention of pro-S tritium label), the same stereoselectivity as in the formation of prostaglandins by native cyclooxygenase.	Aspirin	12-19	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	28-33
10648469-0	2000	NO-aspirin protects from T cell-mediated liver injury by inhibiting caspase-dependent processing of Th1-like cytokines.	Aspirin	3-10	negative elongation factor complex member C/D, Th1l	Mus musculus	100-103
10648469-4	2000	The aim of this study was to investigate whether this NO-aspirin modulates Th1-like response induced by con A.	Aspirin	57-64	negative elongation factor complex member C/D, Th1l	Mus musculus	75-78
10648469-7	2000	At a dose of 100 mg/kg, NO-aspirin caused a 40%-80% reduction of interleukin (IL)-1beta, IL-12, IL-18, interferon (IFN)-gamma, and tumor necrosis factor alpha production without affecting cytokine messenger RNA expression.	Aspirin	27-34	interleukin 1 beta	Mus musculus	65-87
10648469-7	2000	At a dose of 100 mg/kg, NO-aspirin caused a 40%-80% reduction of interleukin (IL)-1beta, IL-12, IL-18, interferon (IFN)-gamma, and tumor necrosis factor alpha production without affecting cytokine messenger RNA expression.	Aspirin	27-34	interferon gamma	Mus musculus	103-125
10648469-7	2000	At a dose of 100 mg/kg, NO-aspirin caused a 40%-80% reduction of interleukin (IL)-1beta, IL-12, IL-18, interferon (IFN)-gamma, and tumor necrosis factor alpha production without affecting cytokine messenger RNA expression.	Aspirin	27-34	tumor necrosis factor	Mus musculus	131-158
10648469-8	2000	NO-aspirin prevented Fas, Fas ligand, and IL-2 receptor up-regulation on spleen lymphocytes and Fas ligand on hepatocytes and caused the S-nitrosylation/inhibition of IL-1beta-converting enzyme-like cysteine proteases (caspases) involved in the processing and maturation of IL-1beta and IL-18.	Aspirin	3-10	interleukin 1 beta	Mus musculus	167-175
10648469-8	2000	NO-aspirin prevented Fas, Fas ligand, and IL-2 receptor up-regulation on spleen lymphocytes and Fas ligand on hepatocytes and caused the S-nitrosylation/inhibition of IL-1beta-converting enzyme-like cysteine proteases (caspases) involved in the processing and maturation of IL-1beta and IL-18.	Aspirin	3-10	interleukin 1 beta	Mus musculus	274-282
10648469-13	2000	Inhibition of Th1-like response is a new anti-inflammatory mechanism of action of NO-aspirin.	Aspirin	85-92	negative elongation factor complex member C/D, Th1l	Mus musculus	14-17
11026496-3	2000	We found that pretreatment of the cultures with aspirin (ASA), which inhibits NF-kappaB activation, resulted in a complete prevention of glutamate-induced p53 immunoreactivity.	Aspirin	48-55	nuclear factor kappa B subunit 1	Homo sapiens	78-87
11026496-3	2000	We found that pretreatment of the cultures with aspirin (ASA), which inhibits NF-kappaB activation, resulted in a complete prevention of glutamate-induced p53 immunoreactivity.	Aspirin	48-55	tumor protein p53	Homo sapiens	155-158
11026496-3	2000	We found that pretreatment of the cultures with aspirin (ASA), which inhibits NF-kappaB activation, resulted in a complete prevention of glutamate-induced p53 immunoreactivity.	Aspirin	57-60	nuclear factor kappa B subunit 1	Homo sapiens	78-87
11026496-3	2000	We found that pretreatment of the cultures with aspirin (ASA), which inhibits NF-kappaB activation, resulted in a complete prevention of glutamate-induced p53 immunoreactivity.	Aspirin	57-60	tumor protein p53	Homo sapiens	155-158
10863553-7	2000	Antioxidants or aspirin inhibit ROS, NF-kappa B and CMV.	Aspirin	16-23	nuclear factor kappa B subunit 1	Homo sapiens	37-47
10966456-2	2000	PGHS-1 and 2 are of particular interest because they are the major targets of nonsteroidal anti-inflammatory drugs (NSAIDs) including aspirin, ibuprofen, and the new COX-2 inhibitors.	Aspirin	134-141	prostaglandin-endoperoxide synthase 1	Homo sapiens	0-12
11055820-10	2000	However, the well known contraindications for NSAIDs, such as late pregnancy, aspirin-induced asthma, congestive heart failure and renal dysfunction, will so far apply also to the COX-2 inhibitors.	Aspirin	78-85	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	180-185
26368635-11	2000	Activation of AP-1 by asbestos or silica was inhibited in both in vitro and in vivo systems by aspirin, which exhibits OH radical scavenging properties.	Aspirin	95-102	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	14-18
10591636-6	2000	The activation of NF-(kappa)B was necessary to promote survival, since its inhibition by acetyl salicylic acid prevented the promoting effect.	Aspirin	89-110	nuclear factor kappa B subunit 1	Homo sapiens	18-29
10983889-5	2000	Aspirin, a well-established antioxidant, substantially inhibited Cr(VI)-induced activation of both NF-kappaB and AP-1.	Aspirin	0-7	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-117
10744037-4	2000	Such phenotypic effect was dose-dependent and partially mediated by NFkappaB, as assessed by functional blockage with acetylsalicylic acid.	Aspirin	118-138	nuclear factor kappa B subunit 1	Homo sapiens	68-76
10590187-0	2000	Effect of short-term aspirin use on C-reactive protein.	Aspirin	21-28	C-reactive protein	Homo sapiens	36-54
10590187-2	2000	In the Physicians Health Study, the magnitude of reduction in the risk of myocardial infarction with aspirin therapy was related to baseline CRP levels, raising the possibility that the protective effect of aspirin may be due to antiinflammatory properties in addition to its antiplatelet effect.	Aspirin	101-108	C-reactive protein	Homo sapiens	141-144
10590187-2	2000	In the Physicians Health Study, the magnitude of reduction in the risk of myocardial infarction with aspirin therapy was related to baseline CRP levels, raising the possibility that the protective effect of aspirin may be due to antiinflammatory properties in addition to its antiplatelet effect.	Aspirin	207-214	C-reactive protein	Homo sapiens	141-144
10590187-3	2000	We therefore investigated whether aspirin therapy lowers CRP levels.	Aspirin	34-41	C-reactive protein	Homo sapiens	57-60
10590187-4	2000	Because heavy physical exertion is a well-known trigger of myocardial infarction, we also investigated the effect of aspirin on CRP levels before and after strenuous exercise.	Aspirin	117-124	C-reactive protein	Homo sapiens	128-131
10585861-8	1999	The production of 8-epi-PGF(2alpha) was also inhibited by indomethacin and aspirin.	Aspirin	75-82	placental growth factor	Homo sapiens	24-27
10585861-9	1999	Exogenous hydrogen peroxide stimulated 8-epi-PGF(2alpha) production by normoxic cells, and aspirin inhibited the hydrogen peroxide-mediated increase in 8-epi-PGF(2alpha) production.	Aspirin	91-98	placental growth factor	Homo sapiens	158-161
10553090-0	1999	Salicylic acid and aspirin inhibit the activity of RSK2 kinase and repress RSK2-dependent transcription of cyclic AMP response element binding protein- and NF-kappa B-responsive genes.	Aspirin	19-26	nuclear factor kappa B subunit 1	Homo sapiens	156-166
10564709-6	1999	Kinetic studies in placentae taken from aspirin-treated pregnancies showed that L-arginine is transported with a significantly higher affinity (Km = 42.5 +/- 5.7 microM), but with a lower capacity (Vmax = 0.064 +/- 0.003 micromol min-1) than in the non-treated group.	Aspirin	40-47	CD59 molecule (CD59 blood group)	Homo sapiens	230-235
10685363-1	1999	The impact of lipoxin A4 (LXA4) and aspirin-triggered-lipoxins (ATL) was investigated in tumor necrosis factor (TNF alpha)-initiated neutrophil (PMN) responses in vitro and in vivo using LX analogs that are metabolically more stable.	Aspirin	36-43	tumor necrosis factor	Homo sapiens	112-121
10698490-0	2000	Overexpression of the wild-type p53 gene inhibits NF-kappaB activity and synergizes with aspirin to induce apoptosis in human colon cancer cells.	Aspirin	89-96	tumor protein p53	Homo sapiens	32-35
10698490-8	2000	We also found that the wt-p53 gene transfer was synergistic with aspirin (acetylsalicylic acid) in inhibiting NF-kappaB constitutive activity, resulting in enhanced apoptotic cell death.	Aspirin	65-72	tumor protein p53	Homo sapiens	26-29
10698490-8	2000	We also found that the wt-p53 gene transfer was synergistic with aspirin (acetylsalicylic acid) in inhibiting NF-kappaB constitutive activity, resulting in enhanced apoptotic cell death.	Aspirin	65-72	nuclear factor kappa B subunit 1	Homo sapiens	110-119
10698490-8	2000	We also found that the wt-p53 gene transfer was synergistic with aspirin (acetylsalicylic acid) in inhibiting NF-kappaB constitutive activity, resulting in enhanced apoptotic cell death.	Aspirin	74-94	tumor protein p53	Homo sapiens	26-29
10698490-8	2000	We also found that the wt-p53 gene transfer was synergistic with aspirin (acetylsalicylic acid) in inhibiting NF-kappaB constitutive activity, resulting in enhanced apoptotic cell death.	Aspirin	74-94	nuclear factor kappa B subunit 1	Homo sapiens	110-119
10698490-9	2000	These results suggest that the inhibition of NF-kappaB activity is a plausible mechanism for apoptosis induced by the wt-p53 gene transfer in human colon cancer cells and that anti-NF-kappaB reagent aspirin could make these cells more susceptible to apoptosis.	Aspirin	199-206	nuclear factor kappa B subunit 1	Homo sapiens	45-54
12749780-6	2000	Also in subjects without cardiovascular risk factors, it is predictable that early and continuous administration of low-dose aspirin, by inhibiting platelet aggregation and thrombin formation, particularly in morning hours, may represent an effective therapy for the prevention of myocardial infarction and morning sudden cardiac death.	Aspirin	125-132	coagulation factor II, thrombin	Homo sapiens	173-181
11149393-6	2000	Both SOD and MDA were significantly higher in the ASA and APA groups compared to controls and AFA group.	Aspirin	50-53	superoxide dismutase 1	Homo sapiens	5-8
11096641-1	1999	Inhibition of thrombin and platelets during percutaneous coronary intervention (PCI), using a combination of unfractionated heparin and aspirin, is designed primarily to minimize the rare but devastating potential acute thrombotic complications of the procedure.	Aspirin	136-143	coagulation factor II, thrombin	Homo sapiens	14-22
10639016-2	1999	Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance.	Aspirin	6-13	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	88-93
10639016-2	1999	Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance.	Aspirin	6-13	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	118-123
10639016-2	1999	Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance.	Aspirin	143-150	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	88-93
10639016-2	1999	Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance.	Aspirin	143-150	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	118-123
10639016-3	1999	However the cellular source(s) of COX-2 possibly responsible for aspirin resistance remains unknown.	Aspirin	65-72	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	34-39
10639016-9	1999	Our results argue against the involvement of COX-2 in TX biosynthesis by activated platelets and consequently dispute platelet COX-2 expression as an important mechanism of aspirin resistance.	Aspirin	173-180	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	127-132
10567380-8	1999	Furthermore, enhanced production, mRNA expression, and gene transcription of apo(a) by interleukin-6 were also inhibited by aspirin.	Aspirin	124-131	interleukin 6	Homo sapiens	87-100
19003147-0	1999	Enhanced CEA production associated with aspirin in a culture of CW-2 cells on some polymeric films.	Aspirin	40-47	CEA cell adhesion molecule 3	Homo sapiens	9-12
19003147-2	1999	By adding aspirin to the media, the production of CEA per cell increased by up to one hundred fold compared to cultivation in normal media containing no aspirin, even though the total cell concentration decreased with the increase in aspirin in the media.	Aspirin	10-17	CEA cell adhesion molecule 3	Homo sapiens	50-53
19003147-2	1999	By adding aspirin to the media, the production of CEA per cell increased by up to one hundred fold compared to cultivation in normal media containing no aspirin, even though the total cell concentration decreased with the increase in aspirin in the media.	Aspirin	153-160	CEA cell adhesion molecule 3	Homo sapiens	50-53
19003147-2	1999	By adding aspirin to the media, the production of CEA per cell increased by up to one hundred fold compared to cultivation in normal media containing no aspirin, even though the total cell concentration decreased with the increase in aspirin in the media.	Aspirin	153-160	CEA cell adhesion molecule 3	Homo sapiens	50-53
19003147-4	1999	The highest production of CEA per cell was observed for the CW2 cells on poly(gamma-benzyl-L-glutamate) and its diblock copolymer films prepared by the Langmuir-Blodgett method in the medium containing 5 mM aspirin after 168 hr of inoculation.	Aspirin	207-214	CEA cell adhesion molecule 3	Homo sapiens	26-29
19003147-6	1999	It is suggested that CW2 cells produce CEA more effectively when the cell growth is suppressed by addition of toxic chemicals such as aspirin or by culture on unfavorable films for cell growth.	Aspirin	134-141	CEA cell adhesion molecule 3	Homo sapiens	39-42
10537081-4	1999	The effect of IL-1beta was Ca(2+)-dependent and significantly inhibited by 100 ng/ml IL-1 receptor-specific antagonist (IL-1r antagonist), cyclooxygenase (COX) inhibitors such as 0.1 mM aspirin, 1 microg/ml indomethacin, and 1 microM NS-398 (specific for COX-2), and 1 microM dexamethasone.	Aspirin	186-193	interleukin 1 beta	Rattus norvegicus	14-22
10527411-0	1999	Orally administered acetylsalicylic acid decreases protein incorporation into the cytoskeleton of thrombin-stimulated platelets.	Aspirin	20-40	coagulation factor II, thrombin	Homo sapiens	98-106
12189305-7	1999	Whereas some studies have shown that the coadministration of NSAIDs including aspirin with ACE inhibitors might diminish the degree of improvement in cardiovascular hemodynamics and adversely affect renal functions, other studies have failed to substantiate this.	Aspirin	78-85	angiotensin I converting enzyme	Homo sapiens	91-94
10480951-4	1999	Recently, we demonstrated that both aspirin and sodium salicylate, but not indomethacin, inhibited the activity of an IkappaB kinase beta (IKKbeta) that is required to activate the nuclear factor-kappaB (NF-kappaB) pathway.	Aspirin	36-43	nuclear factor kappa B subunit 1	Homo sapiens	181-202
10480951-4	1999	Recently, we demonstrated that both aspirin and sodium salicylate, but not indomethacin, inhibited the activity of an IkappaB kinase beta (IKKbeta) that is required to activate the nuclear factor-kappaB (NF-kappaB) pathway.	Aspirin	36-43	nuclear factor kappa B subunit 1	Homo sapiens	204-213
10494034-8	1999	All antithrombotics, be it anticoagulants (e.g. OAC, all heparins or hirudin) or antiplatelet drugs (aspirin, GPIIb/IIIa blockers) diminish thrombin generation.	Aspirin	101-108	coagulation factor II, thrombin	Homo sapiens	140-148
10544957-0	1999	Antioxidant properties of aspirin: characterization of the ability of aspirin to inhibit silica-induced lipid peroxidation, DNA damage, NF-kappaB activation, and TNF-alpha production.	Aspirin	26-33	tumor necrosis factor	Homo sapiens	162-171
11721406-5	1999	Further study indicated that HI117 and SJ9A4-induced Fg binding was reduced by pretreatment of platelets with sphingosine, aspirin, apyrase, and/or PGI2.	Aspirin	123-130	fibrinogen beta chain	Homo sapiens	53-55
10477832-0	1999	PGHS-2 inhibitors, NS-398 and DuP-697, attenuate the inhibition of PGHS-1 by aspirin and indomethacin without altering its activity.	Aspirin	77-84	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-6
10477832-0	1999	PGHS-2 inhibitors, NS-398 and DuP-697, attenuate the inhibition of PGHS-1 by aspirin and indomethacin without altering its activity.	Aspirin	77-84	prostaglandin-endoperoxide synthase 1	Homo sapiens	67-73
10477832-3	1999	In the present study we have tested the effects of DuP-697 and NS-398 on the activity of PGHS-1 and further explored the interactions between these agents and the inhibition of PGHS-1 by aspirin, indomethacin and ibuprofen.	Aspirin	187-194	prostaglandin-endoperoxide synthase 1	Homo sapiens	177-183
10477832-5	1999	The results show that DuP-697 and NS-398, at concentrations ranges which do not inhibit PGHS-1 activity, significantly attenuated the inhibition of PGHS-1 that was caused by aspirin and indomethacin.	Aspirin	174-181	prostaglandin-endoperoxide synthase 1	Homo sapiens	148-154
10477832-8	1999	These results suggest that PGHS-2 inhibitors DuP-697 and NS-398 possibly interact with PGHS-1 at a site different from the enzyme"s catalytic site, thus causing attenuation of PGHS-1 inhibition by aspirin and indomethacin without altering PGHS-1 basal activity or the ibuprofen-induced inhibition.	Aspirin	197-204	prostaglandin-endoperoxide synthase 2	Homo sapiens	27-33
10477832-8	1999	These results suggest that PGHS-2 inhibitors DuP-697 and NS-398 possibly interact with PGHS-1 at a site different from the enzyme"s catalytic site, thus causing attenuation of PGHS-1 inhibition by aspirin and indomethacin without altering PGHS-1 basal activity or the ibuprofen-induced inhibition.	Aspirin	197-204	prostaglandin-endoperoxide synthase 1	Homo sapiens	87-93
10477832-8	1999	These results suggest that PGHS-2 inhibitors DuP-697 and NS-398 possibly interact with PGHS-1 at a site different from the enzyme"s catalytic site, thus causing attenuation of PGHS-1 inhibition by aspirin and indomethacin without altering PGHS-1 basal activity or the ibuprofen-induced inhibition.	Aspirin	197-204	prostaglandin-endoperoxide synthase 1	Homo sapiens	176-182
10477832-8	1999	These results suggest that PGHS-2 inhibitors DuP-697 and NS-398 possibly interact with PGHS-1 at a site different from the enzyme"s catalytic site, thus causing attenuation of PGHS-1 inhibition by aspirin and indomethacin without altering PGHS-1 basal activity or the ibuprofen-induced inhibition.	Aspirin	197-204	prostaglandin-endoperoxide synthase 1	Homo sapiens	176-182
18967757-6	1999	In optimized conditions (flow rate of 2.1 ml min(-1) and volume of injection of 150 mul), the tubular electrode showed a linear response to ASA in the concentration range between 4.0x10(-3) and 4.0x10(-2) mol l(-1).	Aspirin	140-143	CD59 molecule (CD59 blood group)	Homo sapiens	45-51
10458713-9	1999	MCSF, IL-6, and CRP were all reduced after 6 weeks of aspirin treatment (P<0.05).	Aspirin	54-61	interleukin 6	Homo sapiens	6-10
10458713-9	1999	MCSF, IL-6, and CRP were all reduced after 6 weeks of aspirin treatment (P<0.05).	Aspirin	54-61	C-reactive protein	Homo sapiens	16-19
10458713-11	1999	Reduced cytokine and CRP levels by aspirin may explain part of aspirin"s therapeutic action.	Aspirin	35-42	C-reactive protein	Homo sapiens	21-24
10458713-11	1999	Reduced cytokine and CRP levels by aspirin may explain part of aspirin"s therapeutic action.	Aspirin	63-70	C-reactive protein	Homo sapiens	21-24
10404093-8	1999	We also observed a reduction of MSI phenotype after aspirin or sulindac treatment in a hMLH1-defective gastric cancer cell line SNU-1, which lacks COX-2 expression.	Aspirin	52-59	prostaglandin-endoperoxide synthase 2	Homo sapiens	147-152
10426836-3	1999	Angiotensin-converting enzyme (ACE) inhibitors improve diffusion for carbon monoxide and exercise capacity, an effect that is seemingly mediated through prostaglandin activation because it is inhibited by cyclooxygenase blockade with aspirin.	Aspirin	234-241	angiotensin I converting enzyme	Homo sapiens	0-29
10426836-3	1999	Angiotensin-converting enzyme (ACE) inhibitors improve diffusion for carbon monoxide and exercise capacity, an effect that is seemingly mediated through prostaglandin activation because it is inhibited by cyclooxygenase blockade with aspirin.	Aspirin	234-241	angiotensin I converting enzyme	Homo sapiens	31-34
10426836-4	1999	This suggests the possibility that aspirin may disturb the pulmonary function and exercise ability in CHF, at least in those patients who are taking ACE inhibitors.	Aspirin	35-42	angiotensin I converting enzyme	Homo sapiens	149-152
10426836-11	1999	CONCLUSIONS: Aspirin does not affect ventilation efficiency and peak VO(2 ) in patients with CHF not taking ACE inhibitors, but it worsens the pulmonary diffusion for carbon monoxide, VO(2 ), and the ventilatory response to exercise in the presence of ACE inhibition.	Aspirin	13-20	angiotensin I converting enzyme	Homo sapiens	252-255
10426880-4	1999	If tolerated, the treatment should be continued for at least 2 to 3 years and perhaps longer; (2) ACE inhibitor treatment should be started during the first day after myocardial infarction in most patients after timely and careful observation of the patient"s hemodynamic and clinical status and after administration of routinely recommended treatments (thrombolysis, aspirin, and beta-blockers).	Aspirin	368-375	angiotensin I converting enzyme	Homo sapiens	98-101
10480471-2	1999	Inhibition of prostaglandin synthesis with aspirin may therefore theoretically attenuate the antihypertensive effect of ACE inhibitors.	Aspirin	43-50	angiotensin I converting enzyme	Homo sapiens	120-123
10544957-0	1999	Antioxidant properties of aspirin: characterization of the ability of aspirin to inhibit silica-induced lipid peroxidation, DNA damage, NF-kappaB activation, and TNF-alpha production.	Aspirin	70-77	tumor necrosis factor	Homo sapiens	162-171
10390414-0	1999	Cyclooxygenase-2 mRNA is downexpressed in nasal polyps from aspirin-sensitive asthmatics.	Aspirin	60-67	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-16
10426826-0	1999	The interaction of ACE inhibitors and aspirin in heart failure: torn between two lovers.	Aspirin	38-45	angiotensin I converting enzyme	Homo sapiens	19-22
10426836-0	1999	Aspirin worsens exercise performance and pulmonary gas exchange in patients with heart failure who are taking angiotensin-converting enzyme inhibitors.	Aspirin	0-7	angiotensin I converting enzyme	Homo sapiens	110-139
12567448-2	1999	METHODS: Using rosette forming assay to observe the effect of ASA on the binding of platelets to neutrophil and radioimmunoassay to observe the effect of ASA on the thrombin-induced expression of GMP-140 on the surface of human platelets.	Aspirin	154-157	coagulation factor II, thrombin	Homo sapiens	165-173
12567448-6	1999	At high concentration, ASA significantly inhibited thrombin (0.5 U/ml) stimulated platelets binding to neutrophils and expressing GMP-140 on their surface.	Aspirin	23-26	coagulation factor II, thrombin	Homo sapiens	51-59
12567448-7	1999	When the final concentration of ASA was 500,5000 micrograms/ml, the ratio of thrombin-stimulated platelets binding neutrophils was (34.7 +/- 3.8)%, (21.2 +/- 3.6)% respectively (n = 20, P < 0.01); the number of molecular of GMP-140 expressing on the surface of platelet was (1.02 +/- 0.24) x 10(3), (0.68 +/- 0.18) x 10(3) per platelet respectively (n = 9, P < 0.001).	Aspirin	32-35	coagulation factor II, thrombin	Homo sapiens	77-85
10385763-13	1999	CONCLUSION: Addition of abciximab to heparin plus aspirin during PCI was associated with a significant decrease in thrombin generation and a borderline decrease in thrombin activity.	Aspirin	50-57	coagulation factor II, thrombin	Homo sapiens	115-123
10385763-13	1999	CONCLUSION: Addition of abciximab to heparin plus aspirin during PCI was associated with a significant decrease in thrombin generation and a borderline decrease in thrombin activity.	Aspirin	50-57	coagulation factor II, thrombin	Homo sapiens	164-172
10390414-4	1999	We hypothesize that an abnormal regulation of COX-2 will predispose patients with asthma to develop aspirin-intolerant asthma/rhinitis (AIAR).	Aspirin	100-107	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	46-51
10980827-7	1999	Furthermore, preliminary data suggest that the relative efficacy of secondary preventive therapies such as statin drugs and aspirin may depend on the individual patient"s baseline CRP level.	Aspirin	124-131	C-reactive protein	Homo sapiens	180-183
10381514-12	1999	Aspirin treatment abolished the vWF-induced [Ca2+]i signal.	Aspirin	0-7	von Willebrand factor	Homo sapiens	32-35
10400832-1	1999	In some patients with asthma, aspirin (ASA) and all nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase enzymes (cyclooxygenase-1 and -2) precipitate asthmatic attacks and naso-ocular reactions.	Aspirin	39-42	prostaglandin-endoperoxide synthase 1	Homo sapiens	126-149
10400014-0	1999	Effect of acetylsalicylate on cardiac and muscular pain induced by intracoronary and intra-arterial infusion of bradykinin in humans.	Aspirin	10-26	kininogen 1	Homo sapiens	112-122
10400014-1	1999	OBJECTIVES: This study assessed the algesic activity of bradykinin (BK) in humans and the effects of acetylsalicylate on muscular and cardiac BK-induced pain.	Aspirin	101-117	kininogen 1	Homo sapiens	142-144
10400014-13	1999	The BK-induced pain is abolished or reduced by acetylsalicylate, thus suggesting that acetylsalicylate-sensitive mediators, such as prostaglandins, are involved in its pathogenesis.	Aspirin	47-63	kininogen 1	Homo sapiens	4-6
10400014-13	1999	The BK-induced pain is abolished or reduced by acetylsalicylate, thus suggesting that acetylsalicylate-sensitive mediators, such as prostaglandins, are involved in its pathogenesis.	Aspirin	86-102	kininogen 1	Homo sapiens	4-6
10400832-1	1999	In some patients with asthma, aspirin (ASA) and all nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase enzymes (cyclooxygenase-1 and -2) precipitate asthmatic attacks and naso-ocular reactions.	Aspirin	30-37	prostaglandin-endoperoxide synthase 1	Homo sapiens	126-149
10419767-0	1999	Sites of action for future therapy: an adenosine-dependent mechanism by which aspirin retains its antiinflammatory activity in cyclooxygenase-2 and NFkappaB knockout mice.	Aspirin	78-85	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	148-156
10377187-1	1999	The impact of lipoxin A4 (LXA4) and aspirin-triggered lipoxins (ATLs) was investigated in tumor necrosis factor (TNF)-alpha-initiated neutrophil (polymorphonuclear leukocyte) responses in vitro and in vivo using metabolically stable LX analogues.	Aspirin	36-43	tumor necrosis factor	Homo sapiens	90-123
10383505-0	1999	Specific inhibition of cyclooxygenase-2 with MK-0966 is associated with less gastroduodenal damage than either aspirin or ibuprofen.	Aspirin	111-118	prostaglandin-endoperoxide synthase 2	Homo sapiens	23-39
10868495-9	1999	Aspirin was usually or sometimes used for patients with acute ischaemic stroke by 92% of physicians, intravenous heparin by 43%, low-dose subcutaneous heparin by 41%, low-molecular-weight heparin by 25% and tissue-plasminogen activator (t-PA) by 3%.	Aspirin	0-7	plasminogen activator, tissue type	Homo sapiens	207-241
10362194-0	1999	Aspirin and mortality in patients treated with angiotensin-converting enzyme inhibitors: a cohort study of 11,575 patients with coronary artery disease.	Aspirin	0-7	angiotensin I converting enzyme	Homo sapiens	47-76
10362194-1	1999	OBJECTIVES: The purpose of this study was to investigate the significance of the possible negative interaction between aspirin and angiotensin-converting enzyme (ACE) inhibitors.	Aspirin	119-126	angiotensin I converting enzyme	Homo sapiens	131-160
10362194-1	1999	OBJECTIVES: The purpose of this study was to investigate the significance of the possible negative interaction between aspirin and angiotensin-converting enzyme (ACE) inhibitors.	Aspirin	119-126	angiotensin I converting enzyme	Homo sapiens	162-165
10362194-2	1999	BACKGROUND: Several provocative reports have recently suggested that aspirin is unsafe in patients with heart failure and has negative interaction with ACE inhibitors that might attenuate their beneficial effects upon survival.	Aspirin	69-76	angiotensin I converting enzyme	Homo sapiens	152-155
10362194-7	1999	After adjusting for confounders, treatment with aspirin and ACE inhibitors remained associated with lower mortality risk than using ACE inhibitors only (relative risk [RR] = 0.71; 95% confidence interval [CI] = 0.56 to 0.91).	Aspirin	48-55	angiotensin I converting enzyme	Homo sapiens	132-135
10362194-11	1999	CONCLUSIONS: Among coronary artery disease patients with and without heart failure who are treated with ACE inhibitors, the use of aspirin was associated with lower mortality than treatment without aspirin.	Aspirin	131-138	angiotensin I converting enzyme	Homo sapiens	104-107
10362194-12	1999	Our findings contradict the claim that aspirin attenuates the beneficial effect of ACE inhibitors and supports its use in patients with coronary artery disease treated with ACE inhibitors.	Aspirin	39-46	angiotensin I converting enzyme	Homo sapiens	83-86
10362194-12	1999	Our findings contradict the claim that aspirin attenuates the beneficial effect of ACE inhibitors and supports its use in patients with coronary artery disease treated with ACE inhibitors.	Aspirin	39-46	angiotensin I converting enzyme	Homo sapiens	173-176
10433370-5	1999	We further demonstrated that aspirin, but not dexamethasone, suppressed IFN-gamma-induced STAT activation.	Aspirin	29-36	interferon gamma	Homo sapiens	72-81
10381057-16	1999	Aspirin and piroxicam were about 8 times more active against COX-1 than COX-2, indomethacin was 7 times more active, and diclofenac was an equipotent inhibitor of COX-1 and COX-2.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	72-77
10381057-16	1999	Aspirin and piroxicam were about 8 times more active against COX-1 than COX-2, indomethacin was 7 times more active, and diclofenac was an equipotent inhibitor of COX-1 and COX-2.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	173-178
15048267-0	1999	[The in vitro comparison of platelet induced ACC-M cell adhesion with and without Aspirin] ObJECTIVE:Observation the affection of aspirin to adhesion of highly metastatic salivary adenoid cystic carcinoma(ACC-M) cell induced by platelet.METHODS:Adhesive ratios of ACC-M cell induced by platelet with or without aspirin were measured.RESULTS:After the addition of platelet rich plasma(PRP),adhesive ratio of ACC-M cell increased significantly (P<0.01).	Aspirin	130-137	prion protein	Homo sapiens	384-387
15048267-1	1999	The treatment with aspirin after addition of PRP led to a nonsignificant increase of adhesive ratio (P>0.05).The reduction of adhesive ratio by aspirin was found dosage independent within concentration  range of 0.01-0.25g/L of aspirin.	Aspirin	19-26	prion protein	Homo sapiens	45-48
15048267-1	1999	The treatment with aspirin after addition of PRP led to a nonsignificant increase of adhesive ratio (P>0.05).The reduction of adhesive ratio by aspirin was found dosage independent within concentration  range of 0.01-0.25g/L of aspirin.	Aspirin	147-154	prion protein	Homo sapiens	45-48
15048267-1	1999	The treatment with aspirin after addition of PRP led to a nonsignificant increase of adhesive ratio (P>0.05).The reduction of adhesive ratio by aspirin was found dosage independent within concentration  range of 0.01-0.25g/L of aspirin.	Aspirin	147-154	prion protein	Homo sapiens	45-48
10402675-7	1999	The metal chelator, deferoxamine, and hydroxyl (.OH) radical scavengers, sodium formate and aspirin, also inhibited the NF-kappa B activation.	Aspirin	92-99	nuclear factor kappa B subunit 1	Homo sapiens	120-130
10339595-1	1999	The antiinflammatory action of aspirin generally has been attributed to direct inhibition of cyclooxygenases (COX-1 and COX-2), but additional mechanisms are likely at work.	Aspirin	31-38	cytochrome c oxidase I, mitochondrial	Mus musculus	110-115
10339595-2	1999	These include aspirin"s inhibition of NFkappaB translocation to the nucleus as well as the capacity of salicylates to uncouple oxidative phosphorylation (i.e., deplete ATP).	Aspirin	14-21	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	38-46
10218970-6	1999	Dexamethasone, salicylate and aspirin, but not indomethacin, dose dependently inhibited cytokine-stimulated NOx production and iNOS protein expression.	Aspirin	30-37	nitric oxide synthase 2	Rattus norvegicus	127-131
10402163-7	1999	Aspirin and sodium salicylate inhibit activation of NF-KB by blocking IkappaB kinase, a key enzyme in NF-kappaB activation.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	102-111
10233186-5	1999	AIM: To investigate whether acute gastroduodenal injury induced in humans by aspirin can be prevented by the endothelin-1 antagonist, bosentan.	Aspirin	77-84	endothelin 1	Homo sapiens	109-121
10380911-3	1999	Aspirin had minor effects on ex vivo secretion of IL-1beta and no influence on IL-1ra.	Aspirin	0-7	interleukin 1 beta	Homo sapiens	50-58
10218970-10	1999	Aspirin dose dependently inhibited iNOS enzymatic activity, whereas salicylate and dexamethasone had limited effect.	Aspirin	0-7	nitric oxide synthase 2	Rattus norvegicus	35-39
10220501-3	1999	The aim of this study was to investigate whether cysteine endoproteases are involved in the pathogenesis of NSAID gastropathy and are target for NO-aspirin (NCX-4016).	Aspirin	148-155	solute carrier family 8 member A1	Rattus norvegicus	157-160
10220501-13	1999	CONCLUSIONS: Aspirin administration leads to a TNF-alpha-dependent activation of gastric caspases.	Aspirin	13-20	tumor necrosis factor	Rattus norvegicus	47-56
10206978-6	1999	This shift in product profile was accentuated if cyclooxygenase-1 was permanently inactivated with aspirin before cyclooxygenase-2 induction.	Aspirin	99-106	prostaglandin-endoperoxide synthase 1	Homo sapiens	49-65
10220459-0	1999	Suppression of inducible cyclooxygenase 2 gene transcription by aspirin and sodium salicylate.	Aspirin	64-71	prostaglandin-endoperoxide synthase 2	Homo sapiens	25-41
10220459-2	1999	In this report, the effects of aspirin and sodium salicylate on COX-2 expressions in human umbilical vein endothelial cells and foreskin fibroblasts were evaluated.	Aspirin	31-38	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	64-69
10220459-3	1999	Aspirin and sodium salicylate at therapeutic concentrations equipotently blocked COX-2 mRNA and protein levels induced by interleukin-1beta and phorbol 12-myristate 13-acetate.	Aspirin	0-7	interleukin 1 beta	Homo sapiens	122-139
10215736-0	1999	Expression of endothelial cell-derived nitric oxide synthase (eNOS) is increased during gastric adaptation to chronic aspirin intake in humans.	Aspirin	118-125	nitric oxide synthase 3	Homo sapiens	14-60
10215736-0	1999	Expression of endothelial cell-derived nitric oxide synthase (eNOS) is increased during gastric adaptation to chronic aspirin intake in humans.	Aspirin	118-125	nitric oxide synthase 3	Homo sapiens	62-66
10215736-10	1999	eNOS expression started to increase on day 7 in oxyntic mucosa and on day 3 in antral mucosa, reaching its highest values at the end of the consumption of aspirin.	Aspirin	155-162	nitric oxide synthase 3	Homo sapiens	0-4
10215736-12	1999	Increase of mucosal eNOS expression might compensate for reduced prostaglandin synthesis and be responsible for gastric adaptation to chronic aspirin intake in humans.	Aspirin	142-149	nitric oxide synthase 3	Homo sapiens	20-24
12973429-10	1999	This difference is therapeutically significant and selective inhibitors of COX-2 exhibit antiinflammatory potency without the gastric and renal toxicities of the aspirin-like drugs.	Aspirin	162-169	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	75-80
10207634-3	1999	This study was designed to determine whether treatment with 81 mg of aspirin per day for 3 months would alter two putative surrogate end point biomarkers of chemoprevention of colorectal cancer [i.e., mucosal prostaglandin E2 (PGE2) formation and transforming growth factor alpha (TGF-alpha) expression] in normal-appearing rectal mucosa from individuals with a history of adenomatous polyps.	Aspirin	69-76	tumor necrosis factor	Homo sapiens	247-279
10082138-4	1999	Activation of JNK or p38 MAPK by NaSal (or aspirin) was not due to a nonspecific hyperosmotic effect because much higher molar concentrations of sorbitol or NaCl were required to produce a similar activation.	Aspirin	43-50	mitogen-activated protein kinase 8	Homo sapiens	14-17
10193729-2	1999	BACKGROUND: Aspirin inhibits thrombin formation, but its performance is blunted in hypercholesterolemia.	Aspirin	12-19	coagulation factor II, thrombin	Homo sapiens	29-37
10193729-9	1999	RESULTS: Two-week treatment with aspirin had no effect on thrombin markers in vivo, while ex vivo it depressed the total amount of thrombin formed, though not the reaction rate.	Aspirin	33-40	coagulation factor II, thrombin	Homo sapiens	131-139
10193737-10	1999	CONCLUSIONS: Among these apparently healthy U.S. male physicians, fibrinogen is associated with increased risk of future MI independent of other coronary risk factors, atherogenic factors such as lipids and antithrombotics such as aspirin.	Aspirin	231-238	fibrinogen beta chain	Homo sapiens	66-76
10203355-14	1999	It can be concluded that (1) iNOS can be induced without active NF-kappaB; (2) Dex, acetylsalicylic acid, and PDTC inhibit only p65; and (3) JAK2 is involved in iNOS induction, and the contribution of JAK2 to nitrite production is greater than that of NF-kappaB.	Aspirin	84-104	synaptotagmin 1	Rattus norvegicus	128-131
10203355-14	1999	It can be concluded that (1) iNOS can be induced without active NF-kappaB; (2) Dex, acetylsalicylic acid, and PDTC inhibit only p65; and (3) JAK2 is involved in iNOS induction, and the contribution of JAK2 to nitrite production is greater than that of NF-kappaB.	Aspirin	84-104	nitric oxide synthase 2	Rattus norvegicus	161-165
10093990-0	1999	Cyclooxygenase-2 in human platelets as a possible factor in aspirin resistance.	Aspirin	60-67	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-16
10102977-3	1999	AIM: To investigate the effect of aspirin, naproxen and flurbiprofen, and their NO-derivatives, on gastric apoptosis and endothelial cell damage induced by tumour necrosis factor-alpha (TNFalpha).	Aspirin	34-41	tumor necrosis factor	Homo sapiens	186-194
10217529-7	1999	Both HTB and triflusal were more potent than aspirin or salicylate as inhibitors of the nuclear translocation of NF-kappaB.	Aspirin	45-52	nuclear factor kappa B subunit 1	Homo sapiens	113-122
10102747-3	1999	These potentiated effects of captopril and bradykinin were suppressed by Hoe-140, a kinin B2 receptor antagonist, or by concomitant addition of N(G)-nitro arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, and aspirin, a cyclooxygenase inhibitor.	Aspirin	226-233	kininogen 1	Homo sapiens	43-53
10101034-3	1999	However, only triflusal and aspirin inhibited purified COX-2 enzyme.	Aspirin	28-35	prostaglandin-endoperoxide synthase 2	Homo sapiens	55-60
10101034-5	1999	This observation was further confirmed in a rat air pouch model in vivo, in which both aspirin and triflusal inhibited PGE2 production (ID50 = 18.9 and 11.4 mg/kg p.o., respectively) but only triflusal-treated animals showed a decrease in COX-2 expression.	Aspirin	87-94	prostaglandin-endoperoxide synthase 2	Homo sapiens	239-244
10200865-0	1999	Interaction of ACE inhibitors and aspirin in patients with congestive heart failure.	Aspirin	34-41	angiotensin I converting enzyme	Homo sapiens	15-18
10200865-7	1999	Patients with CHF who require therapy with both aspirin and ACE inhibitors may want to consider low doses of aspirin with active monitoring of hemodynamic parameters.	Aspirin	109-116	angiotensin I converting enzyme	Homo sapiens	60-63
10200865-8	1999	However, chronic aspirin therapy in patients with CHF on concomitant ACE inhibitors has not been adequately studied at this time.	Aspirin	17-24	angiotensin I converting enzyme	Homo sapiens	69-72
10200865-11	1999	Further studies are needed to examine the exact mechanism of the interaction between aspirin and ACE inhibitors.	Aspirin	85-92	angiotensin I converting enzyme	Homo sapiens	97-100
10073969-11	1999	Cox-2 and iNOS are coexpressed in native and transplant atherosclerosis, possibly allowing for interaction between the enzymes and suggesting an alternative mechanism for the benefits of aspirin via inhibition of Cox-2 activity.	Aspirin	187-194	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
10073969-11	1999	Cox-2 and iNOS are coexpressed in native and transplant atherosclerosis, possibly allowing for interaction between the enzymes and suggesting an alternative mechanism for the benefits of aspirin via inhibition of Cox-2 activity.	Aspirin	187-194	nitric oxide synthase 2	Homo sapiens	10-14
10073969-11	1999	Cox-2 and iNOS are coexpressed in native and transplant atherosclerosis, possibly allowing for interaction between the enzymes and suggesting an alternative mechanism for the benefits of aspirin via inhibition of Cox-2 activity.	Aspirin	187-194	prostaglandin-endoperoxide synthase 2	Homo sapiens	213-218
10082138-4	1999	Activation of JNK or p38 MAPK by NaSal (or aspirin) was not due to a nonspecific hyperosmotic effect because much higher molar concentrations of sorbitol or NaCl were required to produce a similar activation.	Aspirin	43-50	mitogen-activated protein kinase 14	Homo sapiens	21-24
10667392-4	1999	Pretreatment by two inhibitors of PHS, aspirin and indomethacin, resulted in a dose-dependent inhibition of alpha-naphthol-induced covalent binding, confirming PHS involvement.	Aspirin	39-46	pterin-4 alpha-carbinolamine dehydratase 1	Homo sapiens	34-37
9915793-11	1999	Heterologous TP phosphorylation was observed in aspirin-treated platelets exposed to thrombin, high concentrations of collagen, and the calcium ionophore A 23187.	Aspirin	48-55	coagulation factor II, thrombin	Homo sapiens	85-93
10667392-4	1999	Pretreatment by two inhibitors of PHS, aspirin and indomethacin, resulted in a dose-dependent inhibition of alpha-naphthol-induced covalent binding, confirming PHS involvement.	Aspirin	39-46	pterin-4 alpha-carbinolamine dehydratase 1	Homo sapiens	160-163
10667392-6	1999	Furthermore, combined treatment of aspirin and NDGA almost abolished the increase of alpha-naphthol-induced covalent binding, suggesting that PHS and LPO are both major pathways for xenobiotic activation in platelets.	Aspirin	35-42	pterin-4 alpha-carbinolamine dehydratase 1	Homo sapiens	142-145
10725977-2	1999	The effect of orally administered acetylsalicylic acid to healthy volunteers on incorporation of contractile protein and beta 3 integrin into the cytoskeletal core of thrombin-stimulated platelets was studied.	Aspirin	34-54	coagulation factor II, thrombin	Homo sapiens	167-175
10725977-5	1999	In conclusion, we have shown that acetylsalicylic acid, besides the known inhibitory effect on thromboxane synthesis, promotes changes in the cytoskeletal organization of thrombin-stimulated platelets that could limit thrombus formation.	Aspirin	34-54	coagulation factor II, thrombin	Homo sapiens	171-179
10473982-2	1999	In a vignette describing a hemispheric TIA 1 day prior with ipsilateral bruit, 53% chose admission, 47% elected an outpatient work-up, 28% treated with intravenous heparin and 70% chose aspirin, reflecting the disagreement about medical management of carotid stenosis in the literature.	Aspirin	186-193	TIA1 cytotoxic granule associated RNA binding protein	Homo sapiens	39-44
15512224-4	1999	The aim of this study was to investigate the value of combining low dose aspirin with dietary fatty acid supplementation and its effects on platelet angiotensin II binding in non-pregnant women.	Aspirin	73-80	angiotensinogen	Homo sapiens	149-163
15512224-12	1999	This study found that the combined effect of low-dose aspirin and fish oil causes a significant decrease in platelet angiotensin II binding not caused by either compound taken alone.	Aspirin	54-61	angiotensinogen	Homo sapiens	117-131
10704076-0	1999	Aspirin and some other nonsteroidal anti-inflammatory drugs inhibit cystic fibrosis transmembrane conductance regulator protein gene expression in T-84 cells.	Aspirin	0-7	CF transmembrane conductance regulator	Homo sapiens	68-119
10704076-2	1999	The present study was undertaken to determine whether three nonsteroidal anti-inflammatory drugs (NSAIDs) (aspirin, ibuprofen, and indomethacin) modulate CFTR gene expression in T-84 cells.	Aspirin	107-114	CF transmembrane conductance regulator	Homo sapiens	154-158
9831331-5	1998	The lowest COX-2 selectivities, which means the highest COX-1 selectivities, were observed in indomethacin, aspirin, and oxaprozin.	Aspirin	108-115	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	11-16
9850065-15	1998	Anti-COX-1 and -2, arachidonic acid, ASA, and NS-398 inhibited NNK bioactivation by COX-1 and -2 from 22-49%.	Aspirin	37-40	cytochrome c oxidase I, mitochondrial	Mus musculus	84-96
9851736-5	1998	The in vitro and in vivo anti-platelet studies show that these phenolic esters inhibited (1) arachidonate-triggered human platelet aggregation and (2) thrombin-stimulated rat serum thromboxane A2 production by platelets in the clotting process almost as effectively as aspirin.	Aspirin	269-276	coagulation factor II, thrombin	Homo sapiens	151-159
9916892-7	1998	It is unabated, however, in the presence of substances inhibiting cyclooxygenase-1 and/or cyclooxygenase-2 (e.g., acetyl salicylic acid, SC 58125, L 745337), but is decreased by approx.	Aspirin	114-135	prostaglandin-endoperoxide synthase 1	Homo sapiens	66-82
9916892-7	1998	It is unabated, however, in the presence of substances inhibiting cyclooxygenase-1 and/or cyclooxygenase-2 (e.g., acetyl salicylic acid, SC 58125, L 745337), but is decreased by approx.	Aspirin	114-135	prostaglandin-endoperoxide synthase 2	Homo sapiens	90-106
9951011-1	1998	INTRODUCTION: Different studies have shown that aspirin (AAS), in low doses, may lead to a considerable frequency of hemorrhagic complications when used in the long term.	Aspirin	48-55	FYVE, RhoGEF and PH domain containing 1	Homo sapiens	57-60
9826736-0	1998	Modes of action of aspirin-like drugs: salicylates inhibit erk activation and integrin-dependent neutrophil adhesion.	Aspirin	19-26	mitogen-activated protein kinase 1	Homo sapiens	59-62
9826736-4	1998	Exposure of neutrophils to aspirin or sodium salicylate (poor COX inhibitor) inhibited Erk activity and adhesiveness of formylmethionyl-leucyl-phenylalanine- and arachidonic acid-stimulated neutrophils, consistent with anti-inflammation but not COX inhibition (IC50s = 1-8 mM).	Aspirin	27-34	mitogen-activated protein kinase 1	Homo sapiens	87-90
9840028-0	1998	Influence of low- and high-dose aspirin treatment on thrombin generation in whole blood.	Aspirin	32-39	coagulation factor II, thrombin	Homo sapiens	53-61
9840028-1	1998	The effects of two doses of aspirin (75 and 500 mg/day during 1 week) on thrombin generation was investigated in healthy volunteers.	Aspirin	28-35	coagulation factor II, thrombin	Homo sapiens	73-81
9840028-3	1998	High dose aspirin (500 mg daily) attenuated thrombin generation, whereas low-dose treatment (75 mg daily) failed to attenuate thrombin formation significantly.	Aspirin	10-17	coagulation factor II, thrombin	Homo sapiens	44-52
9840028-5	1998	Our results show that aspirin suppresses thrombin formation in whole blood in a dose-dependent fashion and that the "antithrombin" effects of aspirin require higher doses than the antiaggregating effects.	Aspirin	22-29	coagulation factor II, thrombin	Homo sapiens	41-49
9845404-0	1998	TNFalpha processing enzyme inhibitors prevent aspirin-induced TNFalpha release and protect against gastric mucosal injury in rats.	Aspirin	46-53	tumor necrosis factor	Rattus norvegicus	0-8
9845404-0	1998	TNFalpha processing enzyme inhibitors prevent aspirin-induced TNFalpha release and protect against gastric mucosal injury in rats.	Aspirin	46-53	tumor necrosis factor	Rattus norvegicus	62-70
9845404-1	1998	BACKGROUND: Although previous studies indicate that prevention of tumour necrosis factor alpha (TNFalpha) release protects against NSAID-induced gastric mucosal injury, intracellular pathways by which aspirin causes TNFalpha release are unknown.	Aspirin	201-208	tumor necrosis factor	Rattus norvegicus	96-104
9845404-1	1998	BACKGROUND: Although previous studies indicate that prevention of tumour necrosis factor alpha (TNFalpha) release protects against NSAID-induced gastric mucosal injury, intracellular pathways by which aspirin causes TNFalpha release are unknown.	Aspirin	201-208	tumor necrosis factor	Rattus norvegicus	216-224
9845404-4	1998	AIM: To investigate: (i) molecular events that regulate TNFalpha secretion in response to aspirin in vivo and in vitro; (ii) whether TNFalpha secretion inhibitors prevent aspirin-induced TNFalpha release and protect against gastric mucosal damage; and (iii) whether TNFalpha exerts a direct cytotoxic effect on gastric epithelial cells.	Aspirin	90-97	tumor necrosis factor	Rattus norvegicus	56-64
9845404-8	1998	RESULTS: Aspirin increases intracellular calcium (Ca2+) levels and causes a time and concentration dependent increase in macrophage TNFalpha mRNA accumulation and cytokine release.	Aspirin	9-16	tumor necrosis factor	Rattus norvegicus	132-140
9845404-11	1998	Agents that prevent TNFalpha mRNA transcription, e.g. lisophylline, PGE2, interleukin-10 and 8-BrcAMP, or TACE inhibitors, e.g. EDTA, TAPI-2 and BB-3103, inhibit TNFalpha release and protect rats against gastric mucosal injury induced by oral administration of aspirin.	Aspirin	261-268	tumor necrosis factor	Rattus norvegicus	20-28
9845404-13	1998	CONCLUSIONS: (i) Aspirin directly stimulates TNFalpha gene transcription; (ii) TACE inhibitors protect against aspirin-induced gastric mucosal injury; and (iii) TNFalpha exerts a direct cytotoxic effect on gastric epithelial cells.	Aspirin	17-24	tumor necrosis factor	Rattus norvegicus	45-53
9845404-13	1998	CONCLUSIONS: (i) Aspirin directly stimulates TNFalpha gene transcription; (ii) TACE inhibitors protect against aspirin-induced gastric mucosal injury; and (iii) TNFalpha exerts a direct cytotoxic effect on gastric epithelial cells.	Aspirin	17-24	tumor necrosis factor	Rattus norvegicus	161-169
9845404-13	1998	CONCLUSIONS: (i) Aspirin directly stimulates TNFalpha gene transcription; (ii) TACE inhibitors protect against aspirin-induced gastric mucosal injury; and (iii) TNFalpha exerts a direct cytotoxic effect on gastric epithelial cells.	Aspirin	111-118	ADAM metallopeptidase domain 17	Rattus norvegicus	79-83
9845404-13	1998	CONCLUSIONS: (i) Aspirin directly stimulates TNFalpha gene transcription; (ii) TACE inhibitors protect against aspirin-induced gastric mucosal injury; and (iii) TNFalpha exerts a direct cytotoxic effect on gastric epithelial cells.	Aspirin	111-118	tumor necrosis factor	Rattus norvegicus	161-169
11229224-1	1998	The above discussion on the interaction of aspirin and ACE inhibitors seems to suggest that aspirin in high doses may have adverse interaction with ACE inhibitors in patients with heart failure but the data obtained is not sufficient or conclusive to recommended omission of aspirin in patients with heart failure.	Aspirin	92-99	angiotensin I converting enzyme	Homo sapiens	55-58
11229224-1	1998	The above discussion on the interaction of aspirin and ACE inhibitors seems to suggest that aspirin in high doses may have adverse interaction with ACE inhibitors in patients with heart failure but the data obtained is not sufficient or conclusive to recommended omission of aspirin in patients with heart failure.	Aspirin	92-99	angiotensin I converting enzyme	Homo sapiens	148-151
11229224-1	1998	The above discussion on the interaction of aspirin and ACE inhibitors seems to suggest that aspirin in high doses may have adverse interaction with ACE inhibitors in patients with heart failure but the data obtained is not sufficient or conclusive to recommended omission of aspirin in patients with heart failure.	Aspirin	92-99	angiotensin I converting enzyme	Homo sapiens	55-58
11229224-1	1998	The above discussion on the interaction of aspirin and ACE inhibitors seems to suggest that aspirin in high doses may have adverse interaction with ACE inhibitors in patients with heart failure but the data obtained is not sufficient or conclusive to recommended omission of aspirin in patients with heart failure.	Aspirin	92-99	angiotensin I converting enzyme	Homo sapiens	148-151
9808710-5	1998	Formation of 15-epi-LXA4 was cell ratio-dependent during THP-1 (a monocytic leukemia cell line)-neutrophil interactions with ASA-treated cells, and 15-epi-LXA4 was not detected with either cell type alone.	Aspirin	125-128	GLI family zinc finger 2	Homo sapiens	57-62
9751169-8	1998	Treatment with 3 mM aspirin blocked the NMDA-induced activation of JNK and NF-kappaB.	Aspirin	20-27	mitogen-activated protein kinase 8	Homo sapiens	67-70
9751169-8	1998	Treatment with 3 mM aspirin blocked the NMDA-induced activation of JNK and NF-kappaB.	Aspirin	20-27	nuclear factor kappa B subunit 1	Homo sapiens	75-84
9751169-11	1998	This study also implies that aspirin may exert its neuroprotective action against NMDA through blocking the NMDA-induced activation of NF-kappaB and JNK.	Aspirin	29-36	nuclear factor kappa B subunit 1	Homo sapiens	135-144
9751169-11	1998	This study also implies that aspirin may exert its neuroprotective action against NMDA through blocking the NMDA-induced activation of NF-kappaB and JNK.	Aspirin	29-36	mitogen-activated protein kinase 8	Homo sapiens	149-152
9870835-0	1998	Effects of aspirin treatment on survival in non-insulin-dependent diabetic patients with coronary artery disease.	Aspirin	11-18	insulin	Homo sapiens	48-55
9870835-10	1998	CONCLUSION: Treatment with aspirin was associated with a significant reduction in cardiac and total mortality among non-insulin-dependent diabetic patients with coronary artery disease.	Aspirin	27-34	insulin	Homo sapiens	120-127
9817203-7	1998	Our results indicate that the anti-inflammatory properties of aspirin and salicylate are mediated in part by their specific inhibition of IKK-beta, thereby preventing activation by NF-kappaB of genes involved in the pathogenesis of the inflammatory response.	Aspirin	62-69	nuclear factor kappa B subunit 1	Homo sapiens	181-190
11229224-1	1998	The above discussion on the interaction of aspirin and ACE inhibitors seems to suggest that aspirin in high doses may have adverse interaction with ACE inhibitors in patients with heart failure but the data obtained is not sufficient or conclusive to recommended omission of aspirin in patients with heart failure.	Aspirin	43-50	angiotensin I converting enzyme	Homo sapiens	148-151
9809499-8	1998	Aspirin, but not acetaminophen, inhibits COX-2 activity.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	41-46
9763537-0	1998	Concentration of endogenous tPA antigen in coronary artery disease: relation to thrombotic events, aspirin treatment, hyperlipidemia, and multivessel disease.	Aspirin	99-106	plasminogen activator, tissue type	Homo sapiens	28-31
9763537-7	1998	045), hypertriglyceridemia (P=0.015), and chronic intake of nitrates (P<0.001) were significantly and positively related to tPA antigen concentration, while the chronic intake of aspirin was inversely related to tPA antigen (P<0.001).	Aspirin	182-189	plasminogen activator, tissue type	Homo sapiens	127-130
9763537-13	1998	Therefore, the positive or-in case of aspirin therapy-negative correlation of these parameters with tPA antigen concentration would indicate that thrombus formation and simultaneous endothelial cell activation might be major determinants for tPA antigen concentration in CAD.	Aspirin	38-45	plasminogen activator, tissue type	Homo sapiens	100-103
9763537-13	1998	Therefore, the positive or-in case of aspirin therapy-negative correlation of these parameters with tPA antigen concentration would indicate that thrombus formation and simultaneous endothelial cell activation might be major determinants for tPA antigen concentration in CAD.	Aspirin	38-45	plasminogen activator, tissue type	Homo sapiens	242-245
9831328-9	1998	In addition, the well-known protective action of aspirin on colon cancer may be through an action on COX-2, which is expressed in this disease.	Aspirin	49-56	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	101-106
9798988-8	1998	When platelets were pretreated with aspirin, thrombin-induced secretion of storage granule and lysosomal contents was slightly inhibited, but secretion was inhibited by ethanol to the same extent as the untreated platelets, indicating that this inhibition was independent of thromboxane A2.	Aspirin	36-43	coagulation factor II, thrombin	Homo sapiens	45-53
9748494-13	1998	The bimolecular rate constants for hydrolysis of aspirin by wild-type, D70G and D70K enzymes were found to be close to 1x106 M-1 min-1.	Aspirin	49-56	CD59 molecule (CD59 blood group)	Homo sapiens	129-134
10751796-4	1998	We investigated whether aspirin alone can prevent platelet and thrombin activity induced by catheterization in ten consecutive patients (nine males, mean 50 +/- 8 years) undergoing elective left cardiac catheterization after at least 5 days of oral aspirin (75-300 mg/d).	Aspirin	24-31	coagulation factor II, thrombin	Homo sapiens	63-71
9758314-0	1998	Does aspirin interfere with the therapeutic efficacy of angiotensin-converting enzyme inhibitors in hypertension or congestive heart failure?	Aspirin	5-12	angiotensin I converting enzyme	Homo sapiens	56-85
9758314-1	1998	We conducted a MEDLINE search of published literature from 1966 to January 1998 regarding the impact of aspirin (ASA) on the therapeutic effect of angiotensin-converting enzyme (ACE) inhibitors in hypertension and congestive heart failure.	Aspirin	104-111	angiotensin I converting enzyme	Homo sapiens	147-176
9758314-1	1998	We conducted a MEDLINE search of published literature from 1966 to January 1998 regarding the impact of aspirin (ASA) on the therapeutic effect of angiotensin-converting enzyme (ACE) inhibitors in hypertension and congestive heart failure.	Aspirin	104-111	angiotensin I converting enzyme	Homo sapiens	178-181
9758314-1	1998	We conducted a MEDLINE search of published literature from 1966 to January 1998 regarding the impact of aspirin (ASA) on the therapeutic effect of angiotensin-converting enzyme (ACE) inhibitors in hypertension and congestive heart failure.	Aspirin	113-116	angiotensin I converting enzyme	Homo sapiens	147-176
9758314-1	1998	We conducted a MEDLINE search of published literature from 1966 to January 1998 regarding the impact of aspirin (ASA) on the therapeutic effect of angiotensin-converting enzyme (ACE) inhibitors in hypertension and congestive heart failure.	Aspirin	113-116	angiotensin I converting enzyme	Homo sapiens	178-181
9758314-3	1998	By inhibiting cyclooxygenase, ASA may interfere with the prostaglandin-mediated hemodynamic effects of ACE inhibitors.	Aspirin	30-33	angiotensin I converting enzyme	Homo sapiens	103-106
9758314-5	1998	However, higher dosages of ASA may attenuate the benefits of ACE inhibitors in patients with hypertension and/or congestive heart failure (CHF).	Aspirin	27-30	angiotensin I converting enzyme	Homo sapiens	61-64
9758314-6	1998	Low-dosage ASA appears to interact little with ACE inhibitors, whereas higher dosages may produce a more significant interaction.	Aspirin	11-14	angiotensin I converting enzyme	Homo sapiens	47-50
9727545-2	1998	Negative interaction between aspirin and enalapril has been reported, presumably through inhibition by aspirin of ACE inhibitor-induced prostaglandin synthesis.	Aspirin	29-36	angiotensin I converting enzyme	Homo sapiens	114-117
9727545-2	1998	Negative interaction between aspirin and enalapril has been reported, presumably through inhibition by aspirin of ACE inhibitor-induced prostaglandin synthesis.	Aspirin	103-110	angiotensin I converting enzyme	Homo sapiens	114-117
9727545-4	1998	METHODS AND RESULTS: The objective of this study was to compare the influence of a coadministration of ticlopidine or aspirin on the hemodynamic effects of an ACE inhibitor (enalapril) in patients with chronic heart failure.	Aspirin	118-125	angiotensin I converting enzyme	Homo sapiens	159-162
9694730-7	1998	Both aspirin and salicylate induced DNA fragmentation and the proteolytic cleavage of poly(ADP(adenosine 5"-diphosphate)-ribose) polymerase (PARP), demonstrating that both compounds induce apoptosis of B-CLL cells.	Aspirin	5-12	poly(ADP-ribose) polymerase 1	Homo sapiens	141-145
9694730-8	1998	Finally, inhibition of caspases by Z-VAD.fmk blocked proteolytic cleavage of PARP, DNA fragmentation, and cytotoxicity induced by aspirin.	Aspirin	130-137	poly(ADP-ribose) polymerase 1	Homo sapiens	77-81
9726391-0	1998	Activation of genes for spasmolytic peptide, transforming growth factor alpha and for cyclooxygenase (COX)-1 and COX-2 during gastric adaptation to aspirin damage in rats.	Aspirin	148-155	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	86-108
9726391-13	1998	COX-1 expression was detected in vehicle-control gastric mucosa and after single exposure to ASA or after six consecutive ASA insults, while COX-2 mRNA was not detected in vehicle-control gastric mucosa, but appeared after single ASA insult and was sustained after subsequent ASA doses.	Aspirin	93-96	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	0-5
9726391-13	1998	COX-1 expression was detected in vehicle-control gastric mucosa and after single exposure to ASA or after six consecutive ASA insults, while COX-2 mRNA was not detected in vehicle-control gastric mucosa, but appeared after single ASA insult and was sustained after subsequent ASA doses.	Aspirin	122-125	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	0-5
9726391-13	1998	COX-1 expression was detected in vehicle-control gastric mucosa and after single exposure to ASA or after six consecutive ASA insults, while COX-2 mRNA was not detected in vehicle-control gastric mucosa, but appeared after single ASA insult and was sustained after subsequent ASA doses.	Aspirin	122-125	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	0-5
9726391-13	1998	COX-1 expression was detected in vehicle-control gastric mucosa and after single exposure to ASA or after six consecutive ASA insults, while COX-2 mRNA was not detected in vehicle-control gastric mucosa, but appeared after single ASA insult and was sustained after subsequent ASA doses.	Aspirin	122-125	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	0-5
9723822-0	1998	The effect of aspirin on thrombin stimulated platelet adhesion receptor expression and the role of neutrophils.	Aspirin	14-21	coagulation factor II, thrombin	Homo sapiens	25-33
9723822-3	1998	The aim of the study was to determine the effects of aspirin on thrombin-induced platelet expression of the alpha-granule membrane protein, P-selectin, and the platelet surface glycoprotein required for aggregation, GPIIb-IIIa, and to assess whether this was enhanced by the presence of neutrophils.	Aspirin	53-60	coagulation factor II, thrombin	Homo sapiens	64-72
9723822-9	1998	CONCLUSIONS: These results confirm that thrombin-induced platelet alpha-granule release, with consequent P-selectin expression, and platelet GPIIb-IIIa expression, are not affected by aspirin inhibition of cyclo-oxygenase and suggest that the anti-thrombotic efficacy of aspirin in vivo may partly depend on other mechanisms.	Aspirin	271-278	coagulation factor II, thrombin	Homo sapiens	40-48
9659298-8	1998	Both endotoxin and IL-1 beta increased PGE2 production from the activated aspirin-pretreated membranes during this culture time, but this was transient as after 12 h of culture basal PGE2 production rose to over 200 pg/ml despite aspirin pretreatment.	Aspirin	74-81	interleukin 1 beta	Homo sapiens	19-28
9751197-10	1998	), which, like aspirin and salicylate, has been reported to inhibit the transcription factor NF-kappaB, was also ineffective.	Aspirin	15-22	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	93-102
9664197-8	1998	The Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO-1) study demonstrated a further mortality reduction by early combination therapy of aspirin, intravenous heparin and alteplase vs aspirin, heparin (either intravenous or subcutaneous) plus streptokinase (from 7.3 to 6.3%).	Aspirin	171-178	plasminogen activator, tissue type	Homo sapiens	44-48
9664197-8	1998	The Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO-1) study demonstrated a further mortality reduction by early combination therapy of aspirin, intravenous heparin and alteplase vs aspirin, heparin (either intravenous or subcutaneous) plus streptokinase (from 7.3 to 6.3%).	Aspirin	217-224	plasminogen activator, tissue type	Homo sapiens	44-48
9686761-0	1998	Aspirin attenuates cytomegalovirus infectivity and gene expression mediated by cyclooxygenase-2 in coronary artery smooth muscle cells.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	79-95
9686761-7	1998	Furthermore, by reducing ROS, aspirin and sodium salicylate inhibit CMV-induced NFkappaB activation, the ability of IE72 to transactivate its promoter, CMV IE gene expression after infection of SMCs, and CMV replication in SMCs.	Aspirin	30-37	nuclear factor kappa B subunit 1	Homo sapiens	80-88
9655849-1	1998	The effects of a nitric oxide (NO)-releasing derivative of aspirin, NCX-4016, on gastric functional and ulcerogenic responses in rat stomachs were examined in comparison with those of aspirin.	Aspirin	59-66	solute carrier family 8 member A1	Rattus norvegicus	68-71
9655849-8	1998	These results suggest that, unlike aspirin, the NO-releasing derivative of aspirin NCX-4016 neither had a topical irritating action on the stomach nor exerted a worsening effect on gastric ulcerogenic response to stress, but rather provided gastric protection against ethanol, despite inhibiting cyclo-oxygenase activity and showing anti-inflammatory action much as aspirin does.	Aspirin	75-82	solute carrier family 8 member A1	Rattus norvegicus	83-86
9655849-8	1998	These results suggest that, unlike aspirin, the NO-releasing derivative of aspirin NCX-4016 neither had a topical irritating action on the stomach nor exerted a worsening effect on gastric ulcerogenic response to stress, but rather provided gastric protection against ethanol, despite inhibiting cyclo-oxygenase activity and showing anti-inflammatory action much as aspirin does.	Aspirin	75-82	solute carrier family 8 member A1	Rattus norvegicus	83-86
9659298-8	1998	Both endotoxin and IL-1 beta increased PGE2 production from the activated aspirin-pretreated membranes during this culture time, but this was transient as after 12 h of culture basal PGE2 production rose to over 200 pg/ml despite aspirin pretreatment.	Aspirin	230-237	interleukin 1 beta	Homo sapiens	19-28
9643753-0	1998	PlA2 polymorphism and efficacy of aspirin.	Aspirin	34-41	phospholipase A2 group IB	Homo sapiens	0-4
9554800-4	1998	Aspirin and SQ29548 inhibited and cycloheximide and actinomycin D reduced the time-dependent enhanced response to angiotensin II in rings with endothelium from SHRs.	Aspirin	0-7	angiotensinogen	Rattus norvegicus	114-128
9622204-3	1998	Experiments with acetylsalicylic acid showed that 80% of PGE2 production after 1 h of treatment with LPS is accounted for by COX-1; this figure decreases to about 30% after a 24-h treatment.	Aspirin	17-37	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	125-130
9563738-0	1998	Benefits from adding the 5-lipoxygenase inhibitor zileuton to conventional therapy in aspirin-intolerant asthmatics.	Aspirin	86-93	arachidonate 5-lipoxygenase	Homo sapiens	25-39
9627095-10	1998	Aspirin, but not NCX-4016, markedly suppressed systemic COX-1 and COX-2 activity, and colonic prostaglandin synthesis.	Aspirin	0-7	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	56-61
9641298-0	1998	Oral human spasmolytic polypeptide protects against aspirin-induced gastric injury in rats.	Aspirin	52-59	trefoil factor 2	Homo sapiens	11-34
9641298-5	1998	Human SP (200 micromol/L) administered orally before, or in combination with ASA significantly reduced the fall in PD, the area of microscopic damage, and the number of deep erosions (P < 0.05).	Aspirin	77-80	trefoil factor 2	Homo sapiens	6-8
9509230-5	1998	The beneficial effects of aspirin in reducing the risks of a first MI and stroke are directly related to high plasma concentrations of CRP, whereas small, nonsignificant reductions in risk occurred among patients with low or normal CRP levels.	Aspirin	26-33	C-reactive protein	Homo sapiens	135-138
9515564-1	1998	Aspirin and conventional nonsteroidal anti-inflammatory drugs are nonselective inhibitors of cyclooxygenase-1 (COX-1) and COX-2 enzymes.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	93-109
9515564-1	1998	Aspirin and conventional nonsteroidal anti-inflammatory drugs are nonselective inhibitors of cyclooxygenase-1 (COX-1) and COX-2 enzymes.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	111-116
9515564-1	1998	Aspirin and conventional nonsteroidal anti-inflammatory drugs are nonselective inhibitors of cyclooxygenase-1 (COX-1) and COX-2 enzymes.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	122-127
9472093-0	1998	Inhibition of ultraviolet C irradiation-induced AP-1 activity by aspirin is through inhibition of JNKs but not erks or P38 MAP kinase.	Aspirin	65-72	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	48-52
9472093-2	1998	We demonstrate that aspirin, a promising cancer chemopreventative agent, inhibited UVC-induced AP-1 activity in JB6 cells.	Aspirin	20-27	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	95-99
9472093-4	1998	Since the transcription factor AP-1 is important for the process of tumor promotion, the inhibitory effect of aspirin on AP-1 activation suggests that it can be used as a chemopreventative agent against skin cancer.	Aspirin	110-117	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	31-35
9472093-4	1998	Since the transcription factor AP-1 is important for the process of tumor promotion, the inhibitory effect of aspirin on AP-1 activation suggests that it can be used as a chemopreventative agent against skin cancer.	Aspirin	110-117	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	121-125
9577163-6	1998	Although aspirin and heparin have been the conventionally used agents for inhibiting thrombin and platelet function, newer agents such as hirudin or hirulog and inhibitors of the platelet glycoprotein IIb-IIIa receptors are becoming available, and their clinical application will increase in the future.	Aspirin	9-16	coagulation factor II, thrombin	Homo sapiens	85-93
9551715-4	1998	Triflusal, in the presence of neutrophils, showed a greater antiplatelet potency than acetylsalicylic acid to inhibit thrombin-induced platelet activation.	Aspirin	86-106	coagulation factor II, thrombin	Homo sapiens	118-126
9489975-8	1998	Platelets were activated by tissue-type plasminogen activator or urokinase, and this platelet activation was suppressed with administration of acetylsalicylic acid at 660 mg/day.	Aspirin	143-163	plasminogen activator, tissue type	Homo sapiens	28-61
9427701-5	1998	In aspirin-treated platelets stimulated with high concentrations of collagen, catalase inhibited platelet aggregation, calcium mobilization, and IP3 production.	Aspirin	3-10	catalase	Homo sapiens	78-86
9618042-3	1998	We set out to determine whether p53 overexpression of the colorectum was associated with a patient"s history of aspirin use.	Aspirin	112-119	tumor protein p53	Homo sapiens	32-35
9618042-9	1998	An inverse association of regular aspirin use (two times per week or more) was found both for cases with p53 overexpression (OR: 0.79; 95% CI: 0.39-1.59), and for cases without p53 overexpression (OR: 0.56; 95% CI: 0.25-1.22).	Aspirin	34-41	tumor protein p53	Homo sapiens	105-108
9618042-9	1998	An inverse association of regular aspirin use (two times per week or more) was found both for cases with p53 overexpression (OR: 0.79; 95% CI: 0.39-1.59), and for cases without p53 overexpression (OR: 0.56; 95% CI: 0.25-1.22).	Aspirin	34-41	tumor protein p53	Homo sapiens	177-180
9465844-10	1998	In "responders," aspirin significantly attenuated the renin rise associated with ACE inhibition.	Aspirin	17-24	angiotensin I converting enzyme	Homo sapiens	81-84
9465844-11	1998	CONCLUSIONS: These findings suggest that a number of ACE-inhibited patients are susceptible to 300 mg/day aspirin, regardless of hypertension severity.	Aspirin	106-113	angiotensin I converting enzyme	Homo sapiens	53-56
10608044-0	1998	Prothrombotic Consequences of the Oxidation of Fibrinogen and their Inhibition by Aspirin.	Aspirin	82-89	fibrinogen beta chain	Homo sapiens	47-57
10608044-2	1998	Aspirin can nonenzymatically acetylate fibrinogen"s lysine residues, the functional groups most susceptible to oxidative modification.	Aspirin	0-7	fibrinogen beta chain	Homo sapiens	39-49
10608044-5	1998	Exposure of fibrinogen to aspirin led to acetylation of lysine residues and inhibition of oxidation.	Aspirin	26-33	fibrinogen beta chain	Homo sapiens	12-22
10608044-10	1998	These data show that oxidized fibrinogen manifests prothrombotic effects that can be prevented by acetylation and suggest that inhibition of fibrinogen oxidation may be an additional antithrombotic benefit of aspirin therapy.	Aspirin	209-216	fibrinogen beta chain	Homo sapiens	30-40
10608044-10	1998	These data show that oxidized fibrinogen manifests prothrombotic effects that can be prevented by acetylation and suggest that inhibition of fibrinogen oxidation may be an additional antithrombotic benefit of aspirin therapy.	Aspirin	209-216	fibrinogen beta chain	Homo sapiens	141-151
9718067-0	1998	Aspirin and salicylate enhances the induction of inducible nitric oxide synthase in cultured rat smooth muscle cells.	Aspirin	0-7	nitric oxide synthase 2	Rattus norvegicus	49-80
9718067-1	1998	Aspirin and sodium salicylate enhance to a similar extent the production of nitric oxide (NO) in cultured smooth muscle cells following stimulation by interleukin-1beta (IL-1beta).	Aspirin	0-7	interleukin 1 beta	Rattus norvegicus	151-168
9718067-1	1998	Aspirin and sodium salicylate enhance to a similar extent the production of nitric oxide (NO) in cultured smooth muscle cells following stimulation by interleukin-1beta (IL-1beta).	Aspirin	0-7	interleukin 1 beta	Rattus norvegicus	170-178
9718067-5	1998	Aspirin and sodium salicylate enhance the induction of iNOS expression by IL-1beta.	Aspirin	0-7	nitric oxide synthase 2	Rattus norvegicus	55-59
9718067-5	1998	Aspirin and sodium salicylate enhance the induction of iNOS expression by IL-1beta.	Aspirin	0-7	interleukin 1 beta	Rattus norvegicus	74-82
9718067-7	1998	We investigated the effect of aspirin and sodium salicylate on the response by IL-1beta of VSMCs pretreated with high glucose (25 mM).	Aspirin	30-37	interleukin 1 beta	Rattus norvegicus	79-87
9718067-8	1998	Aspirin and sodium salicylate ameliorate the down-regulation of iNOS expression and the decrease of NO production caused by pretreatment with high glucose (25 mM).	Aspirin	0-7	nitric oxide synthase 2	Rattus norvegicus	64-68
9718067-9	1998	These results suggest a possible therapeutic role in atherosclerotic disease and diabetes mellitus for aspirin and sodium salicylate by enhancing the level of iNOS expression and NO production.	Aspirin	103-110	nitric oxide synthase 2	Rattus norvegicus	159-163
9433378-0	1997	Excessive prolongation of the bleeding time by aspirin in essential thrombocythemia is related to a decrease of large von Willebrand factor multimers in plasma.	Aspirin	47-54	von Willebrand factor	Homo sapiens	118-139
9535546-3	1998	Aspirin, more selective in vitro for the inhibition of COX-1 (10,200 (mg/kg) and nimesulide, a selective in vitro inhibitor of COX-2 (0.5, 5 mg/kg) were dosed p.o.	Aspirin	0-7	cytochrome c oxidase I, mitochondrial	Mus musculus	55-60
9535546-13	1998	CONCLUSION: In this model of chronic inflammation, aspirin, more selective for the inhibition of COX-1 is more effective than the selective COX-2 inhibitors nimesulide and NS-398 at inhibiting granuloma dry weight, vascularity and COX activity.	Aspirin	51-58	cytochrome c oxidase I, mitochondrial	Mus musculus	97-102
9440807-9	1998	Second, the effect of iodide on class I RNA levels and on enhancer A complex formation with Mod-1 and the p50/p65 heterodimer is inhibited by agents that block the inositol phosphate, Ca++, phospholipase A2, arachidonate signal transduction pathway: acetylsalicylate, indomethacin, and 5,8,11,14-eicosatetraynoic acid.	Aspirin	250-266	synaptotagmin 1	Rattus norvegicus	110-113
9355937-15	1997	ASA, DNP and CCCP induced HSP at lower concentrations than substances with a similar lipophilicity, which may be due to effects which add to the misfolding of proteins or to other signal pathways.	Aspirin	0-3	selenoprotein K	Rattus norvegicus	26-29
9627095-12	1998	These results demonstrate that NCX-4016, a nitric oxide-releasing aspirin derivative, exhibited superior chemopreventative effects to aspirin in this model of colon cancer.	Aspirin	66-73	solute carrier family 8 member A1	Rattus norvegicus	31-34
9334204-0	1997	Inhibition of ultraviolet B-induced activator protein-1 (AP-1) activity by aspirin in AP-1-luciferase transgenic mice.	Aspirin	75-82	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	36-55
9383683-7	1997	The increase in NO production in response to IL-1 alpha and TNF-alpha was further stimulated by aspirin and inhibited by exogenous addition of PGE2, suggesting that PGE2 produced by the cytokines, in turn, negatively modulates NO production.	Aspirin	96-103	tumor necrosis factor	Mus musculus	60-69
9334204-2	1997	To study the usefulness of aspirin as a chemopreventative agent for UV-induced human skin cancer, we investigated the effect of aspirin on UVB-induced activator protein-1 (AP-1) activity.	Aspirin	128-135	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	151-170
9334204-2	1997	To study the usefulness of aspirin as a chemopreventative agent for UV-induced human skin cancer, we investigated the effect of aspirin on UVB-induced activator protein-1 (AP-1) activity.	Aspirin	128-135	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	172-176
9334204-3	1997	In the JB6 cell culture system, aspirin or sodium salicylate (SA) inhibited UVB-induced AP-1 activity in a dose-dependent manner; this inhibitory effect occurred only in cells pretreated with aspirin or SA before UVB irradiation but not cells treated with aspirin or SA after UVB irradiation.	Aspirin	32-39	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	88-92
9334204-3	1997	In the JB6 cell culture system, aspirin or sodium salicylate (SA) inhibited UVB-induced AP-1 activity in a dose-dependent manner; this inhibitory effect occurred only in cells pretreated with aspirin or SA before UVB irradiation but not cells treated with aspirin or SA after UVB irradiation.	Aspirin	192-199	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	88-92
9334204-3	1997	In the JB6 cell culture system, aspirin or sodium salicylate (SA) inhibited UVB-induced AP-1 activity in a dose-dependent manner; this inhibitory effect occurred only in cells pretreated with aspirin or SA before UVB irradiation but not cells treated with aspirin or SA after UVB irradiation.	Aspirin	192-199	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	88-92
9326723-12	1997	Similarly, concentrations of aspirin and indomethacin, cyclooxygenase inhibitors that decrease PAF formation, were greater than those reported to block prostaglandin generation.	Aspirin	29-36	PCNA-associated factor	Bos taurus	95-98
9351505-8	1997	The contribution of PGHS-1 was suppressed by pretreatment of the volunteers with aspirin (500 mg; 48 h before venepuncture).	Aspirin	81-88	prostaglandin-endoperoxide synthase 1	Homo sapiens	20-26
9364001-1	1997	Previously, we have reported that aspirin, a cyclooxygenase (COX) inhibitor, can prevent the fibrosis, cirrhosis and generation of oxidative DNA damage, and the associated development of glutathione-S-transferase placental form (GST-P)-positive preneoplastic liver nodules, caused by a choline-deficient, L-amino acid-defined (CDAA) diet in rats.	Aspirin	34-41	glutathione S-transferase pi 1	Rattus norvegicus	187-234
9475035-14	1997	Older nonsteroidal antiinflammatory drugs like aspirin and indomethacin are non selective inhibitors of COX activity and therefore, in addition to inhibiting COX-2 activity, inhibit the formation of eicosanoids by COX-1.	Aspirin	47-54	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	158-163
9289376-11	1997	In them, and not in the remaining patients in each group, aspirin substantially attenuated the renin rise elicited by ACE-inhibition.	Aspirin	58-65	renin	Homo sapiens	95-100
9281601-7	1997	Aspirin at high concentrations of 10 and 20 mM inhibited de novo protein synthesis as demonstrated by inhibition of [35S]methionine incorporation into total islet protein and by inhibition of rabbit reticulocyte expression by Brome mosaic virus mRNA, suggesting that inhibition of iNOS expression at these high concentrations of aspirin may be due to the impairment of the translational machinery.	Aspirin	0-7	nitric oxide synthase 2	Rattus norvegicus	281-285
9281601-8	1997	These findings indicate that inhibition of iNOS expression and NO production may explain, in part, the beneficial effects of aspirin as an anti-inflammatory agent at therapeutic concentrations, whereas inhibition of de novo protein synthesis may possibly explain clinical and side effects of aspirin in the inflamed tissues and organs such as stomach and kidney that may accumulate high concentrations of aspirin.	Aspirin	125-132	nitric oxide synthase 2	Rattus norvegicus	43-47
9281604-2	1997	This observation led us to investigate the role of aspirin in suppressing the activation of the NF-kappaB-regulated tumor necrosis factor-alpha (TNF-alpha) gene expression in primary macrophages.	Aspirin	51-58	tumor necrosis factor	Mus musculus	116-143
9281604-2	1997	This observation led us to investigate the role of aspirin in suppressing the activation of the NF-kappaB-regulated tumor necrosis factor-alpha (TNF-alpha) gene expression in primary macrophages.	Aspirin	51-58	tumor necrosis factor	Mus musculus	145-154
9281604-3	1997	We now report that therapeutic doses of aspirin suppress lipopolysaccharide-inducible NF-kappaB binding to an NF-kappaB binding site in the TNF-alpha promoter, lipopolysaccharide-induced TNF-alpha mRNA accumulation, and protein secretion.	Aspirin	40-47	tumor necrosis factor	Mus musculus	140-149
9281604-3	1997	We now report that therapeutic doses of aspirin suppress lipopolysaccharide-inducible NF-kappaB binding to an NF-kappaB binding site in the TNF-alpha promoter, lipopolysaccharide-induced TNF-alpha mRNA accumulation, and protein secretion.	Aspirin	40-47	tumor necrosis factor	Mus musculus	187-196
9281604-5	1997	The aspirin-initiated stabilization of IkappaB, suppression of induced TNF-alpha mRNA, and NF-kappaB binding to the TNF-alpha promoter are blocked by pretreatment with pertussis toxin.	Aspirin	4-11	tumor necrosis factor	Mus musculus	71-80
9281604-5	1997	The aspirin-initiated stabilization of IkappaB, suppression of induced TNF-alpha mRNA, and NF-kappaB binding to the TNF-alpha promoter are blocked by pretreatment with pertussis toxin.	Aspirin	4-11	tumor necrosis factor	Mus musculus	116-125
9286937-8	1997	In contrast, aspirin could only inhibit monocyte PGHS-2 transiently at very high concentrations.	Aspirin	13-20	prostaglandin-endoperoxide synthase 2	Homo sapiens	49-55
9270062-0	1997	Nitric oxide reverses aspirin antagonism of t-PA thrombolysis in a rabbit model of thromboembolic stroke.	Aspirin	22-29	plasminogen activator, tissue type	Homo sapiens	44-48
9270062-12	1997	Thus, administration of an NO donor (nitroglycerin or nitroprusside) and, to a lesser extent L-arginine, reversed aspirin"s antagonism of t-PA thrombolysis.	Aspirin	114-121	plasminogen activator, tissue type	Homo sapiens	138-142
9215309-9	1997	Aspirin attenuated the stimulatory effect of TPA on PGHS-2 promoter.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	52-58
9215309-11	1997	The activity of PGHS-2 promoter is stimulated by either TPA or cAMP, and the stimulatory effect of TPA is attenuated by aspirin.	Aspirin	120-127	prostaglandin-endoperoxide synthase 2	Homo sapiens	16-22
9191851-9	1997	Sodium salicylate and aspirin, inhibitors of NF-kappa B activation, abolished transcriptional induction of all these cytokines by RSV.	Aspirin	22-29	nuclear factor kappa B subunit 1	Homo sapiens	45-55
9289376-0	1997	[The antagonistic effect of aspirin on the expression of prostaglandin participation in the antihypertensive activity of ACE inhibitors].	Aspirin	28-35	angiotensin I converting enzyme	Homo sapiens	121-124
9289376-2	1997	This provides an explanation for the experimental observation that cycloxygenase blockers (such as aspirin or indomethacin) may counteract the antihypertensive efficacy of the ACE-inhibitors; it may be also possible that hypertensive patients taking aspirin as an antiplatelet agent may fail to benefit from ACE-inhibition.	Aspirin	99-106	angiotensin I converting enzyme	Homo sapiens	176-179
9289376-2	1997	This provides an explanation for the experimental observation that cycloxygenase blockers (such as aspirin or indomethacin) may counteract the antihypertensive efficacy of the ACE-inhibitors; it may be also possible that hypertensive patients taking aspirin as an antiplatelet agent may fail to benefit from ACE-inhibition.	Aspirin	99-106	angiotensin I converting enzyme	Homo sapiens	308-311
9289376-2	1997	This provides an explanation for the experimental observation that cycloxygenase blockers (such as aspirin or indomethacin) may counteract the antihypertensive efficacy of the ACE-inhibitors; it may be also possible that hypertensive patients taking aspirin as an antiplatelet agent may fail to benefit from ACE-inhibition.	Aspirin	250-257	angiotensin I converting enzyme	Homo sapiens	176-179
9151906-3	1997	To explore functions of LXA4 and aspirin-triggered 5(S),6(R),15(R)-trihydroxy-7,9,13-trans-11-cis-eicosatetraenoic acid (15-epi-LXA4) in vivo, we cloned and characterized a mouse LXA4 receptor (LXA4R).	Aspirin	33-40	formyl peptide receptor 3	Mus musculus	179-192
9151906-3	1997	To explore functions of LXA4 and aspirin-triggered 5(S),6(R),15(R)-trihydroxy-7,9,13-trans-11-cis-eicosatetraenoic acid (15-epi-LXA4) in vivo, we cloned and characterized a mouse LXA4 receptor (LXA4R).	Aspirin	33-40	formyl peptide receptor 3	Mus musculus	194-199
9152412-7	1997	After the macrophages were treated with aspirin to inactivate existing COX-1 and COX-2, however, treatment with 12-0-tetradecanoylphorbol 13-acetate increased PGE2 production.	Aspirin	40-47	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	71-76
9175172-3	1997	The IC50S of aspirin, indomethacin and tenoxicam for human COX-1 were 0.41 +/- 0.07 microgram/ml, 0.008 +/- 0.003 microgram/ml, and 7.94 +/- 3.28 micrograms/ml, respectively, and for human COX-20.64 +/- 0.16 microgram/ml, 0.09 +/- 0.05 microgram/ml, and 10.61 +/- 1.50 micrograms/ml, for aspirin, indomethacin, and tenoxicam.	Aspirin	13-20	cytochrome c oxidase assembly factor COX20	Homo sapiens	189-195
9077376-10	1997	Moreover, the reduction associated with the use of aspirin in the risk of a first myocardial infarction appears to be directly related to the level of C-reactive protein, raising the possibility that antiinflammatory agents may have clinical benefits in preventing cardiovascular disease.	Aspirin	51-58	C-reactive protein	Homo sapiens	151-169
9396900-1	1997	OBJECTIVE: Our purpose was to investigate perfusion pressure changes ex vivo induced by angiotensin II on fetoplacental vasculature pretreated with low-dose acetylsalicylic acid.	Aspirin	157-177	angiotensinogen	Homo sapiens	88-102
9396900-10	1997	However, in the cotyledons pretreated with acetylsalicylic acid there was a decrease in the pressor response to 1 x 10(-10) moles of angiotensin II (14.1 +/- 1.4 mm Hg vs 21.5 +/- 3.3 mm Hg, p = 0.05).	Aspirin	43-63	angiotensinogen	Homo sapiens	133-147
9396900-11	1997	CONCLUSIONS: Low-dose aspirin infused into the intervillous space decreases vasoconstriction elicited by angiotensin II in the fetoplacental compartment.	Aspirin	22-29	angiotensinogen	Homo sapiens	105-119
9288002-0	1997	In search of a better aspirin: suppression of intestinal polyposis by targeted inhibition of cyclooxygenase 2.	Aspirin	22-29	prostaglandin-endoperoxide synthase 2	Homo sapiens	93-109
9099752-8	1997	LTC4-[125I]ASA binding to the NAD+ site was confirmed by V8 protease digestion of purified GAPDH labeled with LTC4-[125I]ASA or PNBG-[125I]ASA, with both labels localized to the 6.8-kDa N-terminal fragment.	Aspirin	11-14	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	91-96
9289376-11	1997	In them, and not in the remaining patients in each group, aspirin substantially attenuated the renin rise elicited by ACE-inhibition.	Aspirin	58-65	angiotensin I converting enzyme	Homo sapiens	118-121
9289376-12	1997	These data suggest that: a dosage of 100 mg aspirin is devoid of any inhibitory effect; more that 50% of ACE inhibited patients are, at least in the short term, susceptible to the action of 300 mg aspirin, regardless of the severity of hypertension; counteraction is seemingly mediated through a prostaglandin inhibition and depends on the individual predominance of prostaglandin activation (also as a renin secretory stimulus) or angiotensin inhibition by the ACE-inhibitor.	Aspirin	44-51	angiotensin I converting enzyme	Homo sapiens	105-108
9289376-12	1997	These data suggest that: a dosage of 100 mg aspirin is devoid of any inhibitory effect; more that 50% of ACE inhibited patients are, at least in the short term, susceptible to the action of 300 mg aspirin, regardless of the severity of hypertension; counteraction is seemingly mediated through a prostaglandin inhibition and depends on the individual predominance of prostaglandin activation (also as a renin secretory stimulus) or angiotensin inhibition by the ACE-inhibitor.	Aspirin	197-204	angiotensin I converting enzyme	Homo sapiens	105-108
9289376-12	1997	These data suggest that: a dosage of 100 mg aspirin is devoid of any inhibitory effect; more that 50% of ACE inhibited patients are, at least in the short term, susceptible to the action of 300 mg aspirin, regardless of the severity of hypertension; counteraction is seemingly mediated through a prostaglandin inhibition and depends on the individual predominance of prostaglandin activation (also as a renin secretory stimulus) or angiotensin inhibition by the ACE-inhibitor.	Aspirin	197-204	renin	Homo sapiens	403-408
9289376-12	1997	These data suggest that: a dosage of 100 mg aspirin is devoid of any inhibitory effect; more that 50% of ACE inhibited patients are, at least in the short term, susceptible to the action of 300 mg aspirin, regardless of the severity of hypertension; counteraction is seemingly mediated through a prostaglandin inhibition and depends on the individual predominance of prostaglandin activation (also as a renin secretory stimulus) or angiotensin inhibition by the ACE-inhibitor.	Aspirin	197-204	angiotensin I converting enzyme	Homo sapiens	462-465
9048568-6	1997	Treatment of PGHS-2 with aspirin (acetyl salicylic acid, ASA) was previously shown to result in acetylation of a specific serine residue, cyclooxygenase inhibition, and increased lipoxygenase activity.	Aspirin	25-32	prostaglandin-endoperoxide synthase 2	Homo sapiens	13-19
9057644-7	1997	LPS-induced PGE2 and thromboxane B2 (TXB2) production in aspirin-treated neutrophils was significantly inhibited by IL-10, IL-4, and NS-398.	Aspirin	57-64	interleukin 4	Homo sapiens	123-127
9062488-0	1997	Aspirin inhibits vasopressin-induced hypothalamic-pituitary-adrenal activity in normal humans.	Aspirin	0-7	arginine vasopressin	Homo sapiens	17-28
9062488-4	1997	In this study we administered a single, clinically relevant dose of aspirin before HPA axis stimulation by a bolus dose of iv arginine vasopressin (AVP) to seven normal males using a randomized, placebo-controlled, single blinded design.	Aspirin	68-75	arginine vasopressin	Homo sapiens	148-151
9062488-5	1997	Aspirin significantly reduced the cortisol response to AVP [mean peak increase from basal, 221.1 +/- 20.1 vs. 165.4 +/- 22.5 nmol/L (P = 0.0456); mean integrated response, 11,199.3 +/- 1,560.0 vs. 6,162.3 +/- 1,398.6 nmol.min/L (P = 0.0116) for placebo aspirin/AVP and aspirin/ AVP, respectively].	Aspirin	0-7	arginine vasopressin	Homo sapiens	55-58
9062488-5	1997	Aspirin significantly reduced the cortisol response to AVP [mean peak increase from basal, 221.1 +/- 20.1 vs. 165.4 +/- 22.5 nmol/L (P = 0.0456); mean integrated response, 11,199.3 +/- 1,560.0 vs. 6,162.3 +/- 1,398.6 nmol.min/L (P = 0.0116) for placebo aspirin/AVP and aspirin/ AVP, respectively].	Aspirin	0-7	arginine vasopressin	Homo sapiens	261-264
9062488-5	1997	Aspirin significantly reduced the cortisol response to AVP [mean peak increase from basal, 221.1 +/- 20.1 vs. 165.4 +/- 22.5 nmol/L (P = 0.0456); mean integrated response, 11,199.3 +/- 1,560.0 vs. 6,162.3 +/- 1,398.6 nmol.min/L (P = 0.0116) for placebo aspirin/AVP and aspirin/ AVP, respectively].	Aspirin	0-7	arginine vasopressin	Homo sapiens	261-264
9062488-9	1997	We showed that when normal male volunteers were treated with the PG synthesis inhibitor, aspirin, they had a blunted HPA axis response to the pituitary corticotroph stimulator, AVP.	Aspirin	89-96	arginine vasopressin	Homo sapiens	177-180
9062962-0	1997	Aspirin delays thrombin generation in vitro through interaction with platelet phospholipids.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	15-23
9162173-5	1997	Leukotrienes metabolism is deeply involved in aspirin intolerance or so-called pseudo allergy and, in spite of that the exact mechanism involved is still unknown, leukotriene release in vitro by ASA in the presence C5a represent the first reliable test for this diagnosis.	Aspirin	195-198	complement C5a receptor 1	Homo sapiens	215-218
9071932-4	1997	METHODS: Subjects took aspirin 900 mg twice daily (days 1-3) with bFGF 0.1 mg twice daily or cimetidine 400 mg twice daily or placebo (days 1-14) and then indomethacin 50 mg thrice daily (days 15-21).	Aspirin	23-30	fibroblast growth factor 2	Homo sapiens	66-70
9122273-1	1997	Part 7: Aspirin.	Aspirin	8-15	poly(ADP-ribose) polymerase family member 15	Homo sapiens	0-6
9193008-2	1997	Attention has recently been focused on a possible interaction between ASA and ACE inhibitors.	Aspirin	70-73	angiotensin I converting enzyme	Homo sapiens	78-81
9471925-25	1997	The acetylsalicylic acid had an inhibitory effect on the release of nitrites, PGF2 alpha and TNF alpha (Tab.	Aspirin	4-24	tumor necrosis factor	Mus musculus	93-102
9356662-0	1997	Platelet aggregation in response to collagen and thrombin reliably detects the ingestion of low-dose aspirin.	Aspirin	101-108	coagulation factor II, thrombin	Homo sapiens	49-57
9356662-5	1997	Assessment of collagen-induced platelet aggregation relative to platelet responses of the same subject elicited either by thrombin or by a combination of collagen and thrombin does substantially improve the reliability of functional assays of aspirin.	Aspirin	243-250	coagulation factor II, thrombin	Homo sapiens	167-175
9048568-6	1997	Treatment of PGHS-2 with aspirin (acetyl salicylic acid, ASA) was previously shown to result in acetylation of a specific serine residue, cyclooxygenase inhibition, and increased lipoxygenase activity.	Aspirin	34-55	prostaglandin-endoperoxide synthase 2	Homo sapiens	13-19
9048568-6	1997	Treatment of PGHS-2 with aspirin (acetyl salicylic acid, ASA) was previously shown to result in acetylation of a specific serine residue, cyclooxygenase inhibition, and increased lipoxygenase activity.	Aspirin	57-60	prostaglandin-endoperoxide synthase 2	Homo sapiens	13-19
9048568-7	1997	Acetylation of PGHS-1 by ASA, in contrast, inhibited both lipoxygenase and cyclooxygenase activity.	Aspirin	25-28	prostaglandin-endoperoxide synthase 1	Homo sapiens	15-21
9048568-8	1997	We now have found the ASA-treated PGHS-2 radical to be indistinguishable from that in control PGHS-2.	Aspirin	22-25	prostaglandin-endoperoxide synthase 2	Homo sapiens	34-40
9048568-9	1997	Addition of nimesulide to ASA-treated PGHS-2 inhibited the lipoxygenase and resulted in a narrow radical EPR like that seen in PGHS-2 treated with TNM or nimesulide alone.	Aspirin	26-29	prostaglandin-endoperoxide synthase 2	Homo sapiens	38-44
9048568-9	1997	Addition of nimesulide to ASA-treated PGHS-2 inhibited the lipoxygenase and resulted in a narrow radical EPR like that seen in PGHS-2 treated with TNM or nimesulide alone.	Aspirin	26-29	prostaglandin-endoperoxide synthase 2	Homo sapiens	127-133
9048568-11	1997	Both native and ASA-treated PGHS-2 produced only the R stereoisomer of 11- and 15-HETE, demonstrating that the lipoxygenase stereochemistry was not changed by ASA.	Aspirin	16-19	prostaglandin-endoperoxide synthase 2	Homo sapiens	28-34
9048568-12	1997	Native and ASA-treated PGHS-2 had lipoxygenase K(m) values considerably higher than that of the control PGHS-2 cyclooxygenase.	Aspirin	11-14	prostaglandin-endoperoxide synthase 2	Homo sapiens	23-29
9048568-12	1997	Native and ASA-treated PGHS-2 had lipoxygenase K(m) values considerably higher than that of the control PGHS-2 cyclooxygenase.	Aspirin	11-14	prostaglandin-endoperoxide synthase 2	Homo sapiens	104-110
9048568-13	1997	Taken together, these results suggest that the same PGHS-2 tyrosyl radical serves as the oxidant for both cyclooxygenase and lipoxygenase catalysis and that acetylation of PGHS-2 by ASA favors arachidonate binding in an altered conformation which results in abstraction of the pro-R hydrogen from C13 and formation of 11(R)- and 15(R)-HETE.	Aspirin	182-185	prostaglandin-endoperoxide synthase 2	Homo sapiens	52-58
9048568-13	1997	Taken together, these results suggest that the same PGHS-2 tyrosyl radical serves as the oxidant for both cyclooxygenase and lipoxygenase catalysis and that acetylation of PGHS-2 by ASA favors arachidonate binding in an altered conformation which results in abstraction of the pro-R hydrogen from C13 and formation of 11(R)- and 15(R)-HETE.	Aspirin	182-185	prostaglandin-endoperoxide synthase 2	Homo sapiens	172-178
9042373-12	1997	In the POA a treatment with acetylsalicylic acid (ASA) (33, 66, and 135 micrograms/rat), but not with L-NAME, antagonized the inhibition of drinking behaviour induced by the highest doses of IL-1 beta in the POA.	Aspirin	28-48	interleukin 1 beta	Rattus norvegicus	191-200
9000115-1	1997	The pharmacokinetics of a new ASA-nitroderivative compound, NCX 4016 (ASA-NO2), was evaluated using an HPLC method.	Aspirin	30-33	solute carrier family 8 member A1	Rattus norvegicus	60-63
9042373-12	1997	In the POA a treatment with acetylsalicylic acid (ASA) (33, 66, and 135 micrograms/rat), but not with L-NAME, antagonized the inhibition of drinking behaviour induced by the highest doses of IL-1 beta in the POA.	Aspirin	50-53	interleukin 1 beta	Rattus norvegicus	191-200
9016346-0	1997	Altered sensitivity of aspirin-acetylated prostaglandin G/H synthase-2 to inhibition by nonsteroidal anti-inflammatory drugs.	Aspirin	23-30	prostaglandin-endoperoxide synthase 2	Homo sapiens	42-70
9016346-1	1997	Aspirin (ASA) acetylates Ser516 of prostaglandin G/H synthase-2 (PGHS-2) resulting in a modified enzyme that converts arachidonic acid to 15(R)-hydroxy-eicosatetraeroic acid [15(R)-HETE].	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	35-63
9016346-1	1997	Aspirin (ASA) acetylates Ser516 of prostaglandin G/H synthase-2 (PGHS-2) resulting in a modified enzyme that converts arachidonic acid to 15(R)-hydroxy-eicosatetraeroic acid [15(R)-HETE].	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	65-71
9016346-1	1997	Aspirin (ASA) acetylates Ser516 of prostaglandin G/H synthase-2 (PGHS-2) resulting in a modified enzyme that converts arachidonic acid to 15(R)-hydroxy-eicosatetraeroic acid [15(R)-HETE].	Aspirin	9-12	prostaglandin-endoperoxide synthase 2	Homo sapiens	35-63
9016346-1	1997	Aspirin (ASA) acetylates Ser516 of prostaglandin G/H synthase-2 (PGHS-2) resulting in a modified enzyme that converts arachidonic acid to 15(R)-hydroxy-eicosatetraeroic acid [15(R)-HETE].	Aspirin	9-12	prostaglandin-endoperoxide synthase 2	Homo sapiens	65-71
9016346-2	1997	ASA has pharmacological benefits that may not all be limited to inhibition of prostaglandin synthesis, and this study was initiated to further investigate the properties of ASA-acetylated PGHS-2 and of the mutation of Ser516 to methionine, which mimics ASA acetylation.	Aspirin	173-176	prostaglandin-endoperoxide synthase 2	Homo sapiens	188-194
9016346-2	1997	ASA has pharmacological benefits that may not all be limited to inhibition of prostaglandin synthesis, and this study was initiated to further investigate the properties of ASA-acetylated PGHS-2 and of the mutation of Ser516 to methionine, which mimics ASA acetylation.	Aspirin	173-176	prostaglandin-endoperoxide synthase 2	Homo sapiens	188-194
9016346-3	1997	Both the S516M mutant and ASA-acetylated form of PGHS-2 (ASA-PGHS-2) synthesize 15(R)-HETE and have apparent K(m) values for arachidonic acid within 10-fold of the apparent K(m) value for untreated PGHS-2.	Aspirin	26-29	prostaglandin-endoperoxide synthase 2	Homo sapiens	49-55
9016346-3	1997	Both the S516M mutant and ASA-acetylated form of PGHS-2 (ASA-PGHS-2) synthesize 15(R)-HETE and have apparent K(m) values for arachidonic acid within 10-fold of the apparent K(m) value for untreated PGHS-2.	Aspirin	26-29	prostaglandin-endoperoxide synthase 2	Homo sapiens	57-67
9016346-3	1997	Both the S516M mutant and ASA-acetylated form of PGHS-2 (ASA-PGHS-2) synthesize 15(R)-HETE and have apparent K(m) values for arachidonic acid within 10-fold of the apparent K(m) value for untreated PGHS-2.	Aspirin	26-29	prostaglandin-endoperoxide synthase 2	Homo sapiens	61-67
9016346-8	1997	These results demonstrate that the sensitivity to inhibition by NSAIDs of the 15-HETE production by ASA-treated PGHS-2 is different than that of prostaglandin production by PGHS-2 and that Ser516 plays an important role in the interaction with fenamate inhibitors.	Aspirin	100-103	prostaglandin-endoperoxide synthase 2	Homo sapiens	112-118
8997168-4	1996	Patients treated with IVIG-and-aspirin had by the fourth day developed a highly-significant increase in T cells, CD4 T cells and CD8 T cells and a decrease in B cells.	Aspirin	31-38	CD4 molecule	Homo sapiens	113-116
9017785-4	1997	Both the 5-lipoxygenase inhibitors and the cysLT receptor antagonists have thus far demonstrated the capacity to improve pulmonary function and reduce symptoms in clinical models of asthma, such as exercise-, aspirin-, or antigen-induced bronchoconstriction, and to improve pulmonary function in patients with mild-to-moderate, chronic stable asthma.	Aspirin	209-216	arachidonate 5-lipoxygenase	Homo sapiens	9-23
9263351-3	1997	Aspirin is an approximately 150- to 200-fold more potent inhibitor of the (constitutive) isoform of the platelet enzyme (COX-1) than the (inducible) isoform (COX-2) which is expressed by cytokines, inflammatory stimuli, and some growth factors.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	158-163
9263351-4	1997	This explains the different dosage requirements of aspirin as an antithrombotic (COX-1) and an anti-inflammatory drug (COX-2), respectively.	Aspirin	51-58	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	119-124
8971427-16	1996	Angiotensin II/angiotensin I ratio (index of ACE activity) was significantly decreased by captopril alone or in combination with ASA, but was unaffected by ASA alone.	Aspirin	129-132	angiotensinogen	Homo sapiens	0-14
8971427-16	1996	Angiotensin II/angiotensin I ratio (index of ACE activity) was significantly decreased by captopril alone or in combination with ASA, but was unaffected by ASA alone.	Aspirin	129-132	angiotensin I converting enzyme	Homo sapiens	45-48
8972019-0	1996	Acetylsalicylic acid and sodium salicylate inhibit LPS-induced NF-kappa B/c-Rel nuclear translocation, and synthesis of tissue factor (TF) and tumor necrosis factor alfa (TNF-alpha) in human monocytes.	Aspirin	0-20	nuclear factor kappa B subunit 1	Homo sapiens	63-73
8972019-0	1996	Acetylsalicylic acid and sodium salicylate inhibit LPS-induced NF-kappa B/c-Rel nuclear translocation, and synthesis of tissue factor (TF) and tumor necrosis factor alfa (TNF-alpha) in human monocytes.	Aspirin	0-20	tumor necrosis factor	Homo sapiens	171-180
8941724-0	1996	Aspirin inhibits expression of the interleukin-1beta-inducible group II phospholipase A2.	Aspirin	0-7	interleukin 1 beta	Rattus norvegicus	35-52
8941724-5	1996	We now report that aspirin inhibits the IL-1beta-induced sPLA2 activity in rat mesangial cells in a dose-dependent manner.	Aspirin	19-26	interleukin 1 beta	Rattus norvegicus	40-48
8941724-7	1996	This decrease in sPLA2 activity was not due to direct inhibition of enzymatic activity but rather to the fact that aspirin inhibits the expression of IL-1beta-induced sPLA2 protein and mRNA.	Aspirin	115-122	interleukin 1 beta	Rattus norvegicus	150-158
8941724-8	1996	Furthermore, by electrophoretic mobility shift analysis we demonstrate reduced DNA binding of the nuclear factor kappaB, an essential component of the IL-1beta-dependent upregulation of sPLA2 gene transcription, after treatment of the cells with aspirin.	Aspirin	246-253	interleukin 1 beta	Rattus norvegicus	151-159
8931897-13	1996	In addition, IFN gamma significantly increases the antibacterial activity of ASA and ibuprofen.	Aspirin	77-80	interferon gamma	Mus musculus	13-22
8873691-7	1996	The cyclooxygenase-inhibitor acetylsalicylic acid reduced substance P-induced venodilation from 53% +/- 7% to 34% +/- 8% (p < 0.05), whereas L-NMMA had no effect.	Aspirin	29-49	tachykinin precursor 1	Homo sapiens	58-69
9372101-2	1996	Recent studies suggest that aspirin"s anti-inflammatory effects are mediated via inhibition of an inducible isoform of cyclooxygenase in inflammatory cells (COX-2) and through blockade of the nuclear transcription factor, NF-kappa B.	Aspirin	28-35	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	157-162
9372101-6	1996	A new aspirin derivative is currently being developed that appears to stimulate platelet nitric oxide release, inhibit thrombin-induced platelet aggregation, and lower gastric toxicity.	Aspirin	6-13	coagulation factor II, thrombin	Homo sapiens	119-127
8880021-3	1996	Acetylsalicylic acid, however, also acetylates fibrinogen.	Aspirin	0-20	fibrinogen beta chain	Homo sapiens	47-57
8880021-11	1996	In conclusion, the protective effect of acetylsalicylic acid may be ascribed to its effect not only on platelets but also on fibrinogen.	Aspirin	40-60	fibrinogen beta chain	Homo sapiens	125-135
8883279-2	1996	Smoking was positively associated with fibrinogen, also after adjustment for other lifestyle factors, age, use of anticoagulants and aspirin like drugs, body mass index, and history of myocardial infarction.	Aspirin	133-140	fibrinogen beta chain	Homo sapiens	39-49
8898374-2	1996	We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes.	Aspirin	24-27	prostaglandin-endoperoxide synthase 2	Homo sapiens	184-221
8898374-2	1996	We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes.	Aspirin	24-27	prostaglandin-endoperoxide synthase 2	Homo sapiens	223-229
8898374-2	1996	We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes.	Aspirin	24-27	arachidonate 5-lipoxygenase	Homo sapiens	256-270
8898374-2	1996	We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes.	Aspirin	131-134	prostaglandin-endoperoxide synthase 2	Homo sapiens	184-221
8898374-2	1996	We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes.	Aspirin	131-134	prostaglandin-endoperoxide synthase 2	Homo sapiens	223-229
8898374-2	1996	We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes.	Aspirin	131-134	arachidonate 5-lipoxygenase	Homo sapiens	256-270
8718891-10	1996	ASA-acetylated apo-hCox-2 shows the same fluorescence-quenching behavior in the presence of most of the above inhibitors.	Aspirin	0-3	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	19-25
8870177-0	1996	Is platelet phospholipid-dependent thrombin generation altered by acute myocardial infarction or aspirin?	Aspirin	97-104	coagulation factor II, thrombin	Homo sapiens	35-43
8696958-0	1996	Inhibition of thrombin generation by aspirin is blunted in hypercholesterolemia.	Aspirin	37-44	coagulation factor II, thrombin	Homo sapiens	14-22
8696958-1	1996	Recent evidence indicates that aspirin inhibits thrombin generation in clotting blood.	Aspirin	31-38	coagulation factor II, thrombin	Homo sapiens	48-56
8696958-4	1996	The effects of aspirin on thrombin generation were evaluated in (1) 46 healthy volunteers, 2 hours after ingestion of a single, 500-mg dose and (2) 28 survivors of myocardial infarction who took 300 mg aspirin/d for 2 weeks.	Aspirin	15-22	coagulation factor II, thrombin	Homo sapiens	26-34
8696958-7	1996	Aspirin depressed thrombin generation in the group of subjects with serum cholesterol < 6.2 mmol/L and LDL cholesterol < 4.0 mmol/L but not in the group with high blood cholesterol levels.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	18-26
8865538-9	1996	Responses of aspirin-pretreated platelets to thrombin, SFLLRN, U46619 and PAF were also inhibited by probenecid, indicating that prevention of TXA2 formation does not account for all the inhibitory effects.	Aspirin	13-20	coagulation factor II, thrombin	Homo sapiens	45-53
8863928-6	1996	Simultaneous incubation with ASA 10 micrograms/ml and C5a (10(-8)mol/l) resulted in a cLT concentration of 751 +/- 171 pg/ml in the NI group, 343 +/- 102 pg/ml in the NP group, and 2196 +/- 480 pg/ml in patients with AI (P = 0.0006), whereas simultaneous incubation with ASA 100 g/ml and C5a (10(-8)mol/l) resulted in 268 +/- 51 pg/ml in the NI group, 412 +/- 97 pg/ml in the NP group, and 1701 +/- 368 pg/ml in the AI group (P = 0.005).	Aspirin	29-32	complement C5a receptor 1	Homo sapiens	288-291
8863928-6	1996	Simultaneous incubation with ASA 10 micrograms/ml and C5a (10(-8)mol/l) resulted in a cLT concentration of 751 +/- 171 pg/ml in the NI group, 343 +/- 102 pg/ml in the NP group, and 2196 +/- 480 pg/ml in patients with AI (P = 0.0006), whereas simultaneous incubation with ASA 100 g/ml and C5a (10(-8)mol/l) resulted in 268 +/- 51 pg/ml in the NI group, 412 +/- 97 pg/ml in the NP group, and 1701 +/- 368 pg/ml in the AI group (P = 0.005).	Aspirin	271-274	complement C5a receptor 1	Homo sapiens	54-57
8648609-4	1996	Most of the aspirin-like maleimides inactivated the cyclooxygenase activity of purified ovine PGHS-1 in a time- and concentration-dependent manner similar to that of aspirin.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	94-100
8696958-9	1996	There was a significant correlation between total serum cholesterol or LDL cholesterol and total amount of thrombin generated after aspirin treatment.	Aspirin	132-139	coagulation factor II, thrombin	Homo sapiens	107-115
8662657-1	1996	The presence of prostaglandin (PG) H2 in the supernatant of human umbilical vein endothelial cells (HUVEC) stimulated by thrombin restores the capacity of aspirin-treated platelets to generate thromboxane (TX) B2.	Aspirin	155-162	coagulation factor II, thrombin	Homo sapiens	121-129
8662657-3	1996	HUVEC treated with aspirin lost their capacity to generate PGs but recovery occurred after 3- or 6-h induction of Cox-2 with phorbol ester or IL-1alpha.	Aspirin	19-26	prostaglandin-endoperoxide synthase 2	Homo sapiens	114-119
8662657-4	1996	Enzyme activity of the newly synthesized Cox-2 in aspirin-treated cells, evaluated after immunoprecipitation, was similar to untreated cells but after 18 h of cell stimulation only 50-60% recovery of Cox-1 was observed.	Aspirin	50-57	prostaglandin-endoperoxide synthase 2	Homo sapiens	41-46
8662657-7	1996	Aspirin-treated or untreated cells were incubated in the absence or presence of SC58125 and stimulated by thrombin, the ionophore A23187, or exogenous arachidonic acid.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	106-114
8662657-9	1996	However, in acetylsalicylic acid-treated cells, after 6-h stimulation with IL-1alpha, newly synthesized Cox-2 produced less TXB2 than 6-keto-PGF1alpha compared to untreated cells.	Aspirin	12-32	prostaglandin-endoperoxide synthase 2	Homo sapiens	104-109
8994996-5	1996	Furthermore, important questions about the most effective dose of ACE inhibitor and ACE inhibitor use in conjunction with aspirin and the NSAIDs still have to be answered.	Aspirin	122-129	angiotensin I converting enzyme	Homo sapiens	66-69
8829212-6	1996	Renin caused a more rapid recovery of decidual prostaglandin biosynthesis from acetylsalicylic acid treatment than did control media.	Aspirin	79-99	renin	Homo sapiens	0-5
8691069-1	1996	Aspirin and sodium salicylate each inhibit to a similar extent the production of nitric oxide (NO) in the RAW 264.7 murine macrophage cell line following stimulation by either lipopolysaccharide (LPS) or interferon-gamma (IFN-gamma).	Aspirin	0-7	interferon gamma	Mus musculus	204-220
8691069-1	1996	Aspirin and sodium salicylate each inhibit to a similar extent the production of nitric oxide (NO) in the RAW 264.7 murine macrophage cell line following stimulation by either lipopolysaccharide (LPS) or interferon-gamma (IFN-gamma).	Aspirin	0-7	interferon gamma	Mus musculus	222-231
8691069-5	1996	Aspirin and sodium salicylate inhibit iNOS mRNA induction in LPS-stimulated cells but enhance iNOS mRNA induction in IFN-gamma-stimulated cells.	Aspirin	0-7	nitric oxide synthase 2, inducible	Mus musculus	38-42
8691069-5	1996	Aspirin and sodium salicylate inhibit iNOS mRNA induction in LPS-stimulated cells but enhance iNOS mRNA induction in IFN-gamma-stimulated cells.	Aspirin	0-7	nitric oxide synthase 2, inducible	Mus musculus	94-98
8691069-5	1996	Aspirin and sodium salicylate inhibit iNOS mRNA induction in LPS-stimulated cells but enhance iNOS mRNA induction in IFN-gamma-stimulated cells.	Aspirin	0-7	interferon gamma	Mus musculus	117-126
8691069-7	1996	Concentrations of aspirin in the 3-10 mM range inhibit induced NO production and expression of iNOS protein without inhibiting induction of iNOS mRNA.	Aspirin	18-25	nitric oxide synthase 2, inducible	Mus musculus	95-99
8691069-8	1996	Discordances between effects on NO synthesis and induction of iNOS mRNA indicate that aspirin and sodium salicylate have multiple sites of action in their effects on pathways that are involved in the production of NO by stimulated RAW 264.7 cells.	Aspirin	86-93	nitric oxide synthase 2, inducible	Mus musculus	62-66
8873235-8	1996	ASA provokes an increase in 5-HETE biosynthesis by amnion cells: control media 2.60 +/- 1.5, ASA treatment alone 5.17 +/- 0.20, IL-1 beta alone 6.39 +/- 2.1, and ASA + IL-1 beta 8.95 +/- 1.2 (mean +/- SEM) picograms per microgram protein per 16 hours.	Aspirin	0-3	interleukin 1 beta	Homo sapiens	128-137
8873235-8	1996	ASA provokes an increase in 5-HETE biosynthesis by amnion cells: control media 2.60 +/- 1.5, ASA treatment alone 5.17 +/- 0.20, IL-1 beta alone 6.39 +/- 2.1, and ASA + IL-1 beta 8.95 +/- 1.2 (mean +/- SEM) picograms per microgram protein per 16 hours.	Aspirin	0-3	interleukin 1 beta	Homo sapiens	168-177
8621937-3	1996	Recent work has suggested that some nonsteroidal anti-inflammatory agents, including sodium salicylate and aspirin, can inhibit NF-kappa B-dependent gene activation.	Aspirin	107-114	nuclear factor kappa B subunit 1	Homo sapiens	128-138
8620595-10	1996	These studies implicate cardiac fibroblasts as a source of NO in inflammatory cardiac diseases and suggest a possible therapeutic role for salicylate and aspirin in diminishing the steady state levels of iNOS mRNA.	Aspirin	154-161	nitric oxide synthase 2	Rattus norvegicus	204-208
8616919-0	1996	The protective dose of the potent GPIIb/IIIa antagonist SC-54701A is reduced when used in combination with aspirin and heparin in a canine model of coronary artery thrombosis.	Aspirin	107-114	integrin subunit alpha 2b	Canis lupus familiaris	34-39
8571407-1	1996	Studies were conducted on the mechanism of the ethanol-inducible cytochrome P450 (cytochrome P4502E1, CYP 2E1) induction by acetylsalicylic acid (ASA) or its metabolite salicylate (SAL).	Aspirin	124-144	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	102-109
8571407-1	1996	Studies were conducted on the mechanism of the ethanol-inducible cytochrome P450 (cytochrome P4502E1, CYP 2E1) induction by acetylsalicylic acid (ASA) or its metabolite salicylate (SAL).	Aspirin	146-149	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	102-109
8571407-5	1996	The CYP 2E1 mRNA levels in livers of control rats and rats treated with ASA or SAL were measured by Northern blot analysis.	Aspirin	72-75	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	4-11
8773160-14	1996	Insulin concentrations were increased during the glyburide plus aspirin treatment.	Aspirin	64-71	insulin	Homo sapiens	0-7
8554334-2	1996	Clofibrate, perfluorooctanoic acid, and acetylsalicylic acid all increased the mRNA levels for the mitochondrial-encoded respiratory-chain components cytochrome c oxidase subunit I and NADH dehydrogenase subunit I. Mitochondrial 16S rRNA was also induced by clofibrate.	Aspirin	40-60	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	150-203
8864252-8	1996	After adjustment for age, C4bp levels increased significantly with increasing ASL and ASA.	Aspirin	86-89	complement component 4 binding protein alpha	Homo sapiens	26-30
9125295-6	1996	The platelet thrombin-stimulated TXB2 biosynthesis was inhibited in vitro in the presence of 500 mu M aspirin and 1 mM vitamin E; the erythrocytes from OC animals compared with controls presented an enhanced in vitro susceptibility to free radical-induced hemolysis.	Aspirin	102-109	coagulation factor II	Rattus norvegicus	13-21
8730734-4	1996	LPS-induced nitrite production was markedly attenuated by the nitroxybutylester derivatives of flurbiprofen (FNBE), aspirin, ketoprofen, naproxen, diclofenac and ketorolac, with each compound reducing accumulated nitrite levels by > 40% at the maximum concentrations (100 micrograms ml-1) used.	Aspirin	116-123	toll-like receptor 4	Mus musculus	0-3
8621413-1	1996	Prostaglandin I2 (PGI2) and sodium nitroprusside (SNP) induce a rapid decay of the thrombin-promoted increase of [Ca2+]i in aspirin-treated platelets incubated in the absence of external Ca2+.	Aspirin	124-131	coagulation factor II, thrombin	Homo sapiens	83-91
8629598-0	1996	Effects of aspirin on status of thrombin generation in atrial fibrillation.	Aspirin	11-18	coagulation factor II, thrombin	Homo sapiens	32-40
8735820-4	1996	NCX 4215 and NCX 4016 in a dose-dependent way inhibited also thrombin-induced aggregation of platelets pretreated with acetylsalicylic acid.	Aspirin	119-139	coagulation factor II, thrombin	Homo sapiens	61-69
8631132-4	1996	ASA at a doe of 0.2% almost completely prevented the appearance of cirrhosis, GST-P-positive nodules, 8-OHdG and TBARS in seven out of 11 (63.7%) rats.	Aspirin	0-3	glutathione S-transferase pi 1	Rattus norvegicus	78-83
8600164-6	1996	Inhibition of cyclooxygenase by acetylsalicylic acid augmented the growth response of fibroblasts to all: SP, FGF, and EGF.	Aspirin	32-52	tachykinin precursor 1	Homo sapiens	106-108
8600164-7	1996	In the presence of acetylsalicylic acid, SP combined with FGF enhanced fibroblasts proliferation, whereas a combination with EGF inhibited cellular growth with respect to growth induced by EGF alone.	Aspirin	19-39	tachykinin precursor 1	Homo sapiens	41-43
8533099-0	1995	The effect of sodium salicylate and aspirin on NF-kappa B.	Aspirin	36-43	nuclear factor kappa B subunit 1	Homo sapiens	47-57
21043596-4	1996	In an experimental model in vitro that resembles vessel wall/platelet/PMN interaction in vivo, we found that aspirin (100 muM), a COX inhibitor, but not L-NMMA (100 muM) and a NO-synthase inhibitor, reversed the inhibitory effect of arterial wall on P-selectin mediated platelet/PMN adhesion.	Aspirin	109-116	latexin	Homo sapiens	122-125
21043596-5	1996	The anti-adhesive potency of vessel wall reversed by aspirin was dose-dependently restored by camonagrel (3-100 muM), a new TXA(2) synthase inhibitor.	Aspirin	53-60	latexin	Homo sapiens	112-115
21043650-5	1996	Treatment of endothelial cells on the first coverslip with 100 muM aspirin strongly reduced 6-keto-PGF(1a) levels recovered in the perfusates (118.3 +- 35.8 vs 1038.0 +- 308.5 pg/ml) and significantly increased platelet deposition on the downstream coverslip (% covered surface: 38.6 +- 6.4% vs 14.6 +- 1.8%; P < 0.001).	Aspirin	67-74	placental growth factor	Homo sapiens	99-102
21043667-8	1996	Pretreatment of platelets with acetylsalicylic acid (ASA) before gel-filtration moderately inhibited thrombin-induced dense and alpha-granule release in GFP at a concentration range of 0.01-0.03 U/ml.	Aspirin	31-51	coagulation factor II, thrombin	Homo sapiens	101-109
21043667-8	1996	Pretreatment of platelets with acetylsalicylic acid (ASA) before gel-filtration moderately inhibited thrombin-induced dense and alpha-granule release in GFP at a concentration range of 0.01-0.03 U/ml.	Aspirin	53-56	coagulation factor II, thrombin	Homo sapiens	101-109
9112639-4	1996	Acetylsalicylic acid added to platelet lysate inhibited cathepsin A in the same extent as salicylate.	Aspirin	0-20	cathepsin A	Homo sapiens	56-67
7493972-9	1995	Aspirin is an acid NSAID that inhibits PGHS-1 through a unique covalent acetylation of the enzyme and also showed a reduced rate of inactivation of the mutated enzyme.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	39-45
8825221-1	1995	The in vitro effect of acetylsalicylic acid (ASA) on fibrin gel lysis by exogenous t-PA was studied in 13 patients with angina pectoris.	Aspirin	23-43	plasminogen activator, tissue type	Homo sapiens	83-87
8825221-1	1995	The in vitro effect of acetylsalicylic acid (ASA) on fibrin gel lysis by exogenous t-PA was studied in 13 patients with angina pectoris.	Aspirin	45-48	plasminogen activator, tissue type	Homo sapiens	83-87
8746200-2	1995	This reocclusion is thought to be due to in situ platelet activation mediated by thromboxane (Tx) A2 and thrombin; hence, aspirin and thrombin inhibitors are often used in patients with acute myocardial infarction.	Aspirin	122-129	coagulation factor II, thrombin	Homo sapiens	105-113
7544010-0	1995	The mode of action of aspirin-like drugs: effect on inducible nitric oxide synthase.	Aspirin	22-29	nitric oxide synthase 2, inducible	Mus musculus	52-83
8658372-7	1996	RESULTS: A decrease in both absolute mast cell numbers staining with mast cell tryptase (AA1) and the percentage of mast cells co-immunostaining with 5-lipoxygenase was seen in the ASA patients after lysine aspirin challenge compared with the non-ASA control group.	Aspirin	181-184	arachidonate 5-lipoxygenase	Homo sapiens	150-164
8658372-7	1996	RESULTS: A decrease in both absolute mast cell numbers staining with mast cell tryptase (AA1) and the percentage of mast cells co-immunostaining with 5-lipoxygenase was seen in the ASA patients after lysine aspirin challenge compared with the non-ASA control group.	Aspirin	247-250	arachidonate 5-lipoxygenase	Homo sapiens	150-164
8675638-1	1995	Effects of a nitroxybutylester derivative of aspirin (NCX 4215) on platelet aggregation and prostanoid synthesis were compared to the effects of aspirin.	Aspirin	45-52	solute carrier family 8 member A1	Rattus norvegicus	54-57
8675638-2	1995	NCX 4215 was approximately seven times more potent than aspirin as an inhibitor of thrombin-induced human platelet aggregation in vitro, but did not inhibit platelet thromboxane synthesis or gastric prostaglandin synthesis.	Aspirin	56-63	coagulation factor II, thrombin	Homo sapiens	83-91
7490920-4	1995	Although aspirin, heparin, and warfarin sodium have been the conventionally used agents for inhibiting thrombin and platelet function, newer agents such as hirudin and inhibitors of the platelet glycoprotein IIb-IIIa receptor are becoming available, and their clinical application will increase in the future.	Aspirin	9-16	coagulation factor II, thrombin	Homo sapiens	103-111
8710799-3	1995	The dose-related vasoconstrictor effects of endothelin-1 (ET-1), angiotensin II (A II) and 5-hydroxytryptamine (5 HT) were reduced by graded concentrations of the thromboxane A2 (TXA2) receptor antagonist GR32191 (10(-7)-10(-4)M), aspirin (10(-5)-10(-4)M) and indomethacin (10(-5)M).	Aspirin	231-238	endothelin 1	Homo sapiens	44-56
8710799-3	1995	The dose-related vasoconstrictor effects of endothelin-1 (ET-1), angiotensin II (A II) and 5-hydroxytryptamine (5 HT) were reduced by graded concentrations of the thromboxane A2 (TXA2) receptor antagonist GR32191 (10(-7)-10(-4)M), aspirin (10(-5)-10(-4)M) and indomethacin (10(-5)M).	Aspirin	231-238	endothelin 1	Homo sapiens	58-62
8710799-3	1995	The dose-related vasoconstrictor effects of endothelin-1 (ET-1), angiotensin II (A II) and 5-hydroxytryptamine (5 HT) were reduced by graded concentrations of the thromboxane A2 (TXA2) receptor antagonist GR32191 (10(-7)-10(-4)M), aspirin (10(-5)-10(-4)M) and indomethacin (10(-5)M).	Aspirin	231-238	angiotensinogen	Homo sapiens	65-79
8588198-4	1995	NO-ASA also significantly reduced thrombin-induced (0.04-0.08 U/ml) platelet aggregation in acetylsalicylic acid-treated platelets (basal 70.5 +/- 1.7%; NO-ASA 35.4 +/- 2.2%; P < 0.001; n = 10; IC50 7 x 10(-5) M).	Aspirin	92-112	coagulation factor II	Rattus norvegicus	34-42
8588198-4	1995	NO-ASA also significantly reduced thrombin-induced (0.04-0.08 U/ml) platelet aggregation in acetylsalicylic acid-treated platelets (basal 70.5 +/- 1.7%; NO-ASA 35.4 +/- 2.2%; P < 0.001; n = 10; IC50 7 x 10(-5) M).	Aspirin	3-6	coagulation factor II	Rattus norvegicus	34-42
8588198-5	1995	Methylene blue reduced the effects of NO-ASA on thrombin-induced (NO-ASA 46.7 +/- 5.25%; NO-ASA+MB 59.1 +/- 4.3%; P < 0.01; n = 8), but not arachidonic acid-induced platelet aggregation.	Aspirin	41-44	coagulation factor II	Rattus norvegicus	48-56
8588198-5	1995	Methylene blue reduced the effects of NO-ASA on thrombin-induced (NO-ASA 46.7 +/- 5.25%; NO-ASA+MB 59.1 +/- 4.3%; P < 0.01; n = 8), but not arachidonic acid-induced platelet aggregation.	Aspirin	69-72	coagulation factor II	Rattus norvegicus	48-56
8588198-5	1995	Methylene blue reduced the effects of NO-ASA on thrombin-induced (NO-ASA 46.7 +/- 5.25%; NO-ASA+MB 59.1 +/- 4.3%; P < 0.01; n = 8), but not arachidonic acid-induced platelet aggregation.	Aspirin	69-72	coagulation factor II	Rattus norvegicus	48-56
8772239-4	1995	Pre-treatment of endothelial cells with aspirin, or use of suramin, a broad-specificity inhibitor, prevented the response to P-A1.	Aspirin	40-47	PAXIP1 associated glutamate rich protein 1	Homo sapiens	125-129
8772241-6	1995	When aspirin was administered at 5 mg/kg prior to ET-1 administration at 0.5 microgramoff, ET-1 produced a CFR rating of 2.7 +/- 0.2 (n = 6).	Aspirin	5-12	endothelin 1	Canis lupus familiaris	91-95
8527516-13	1995	Only the combination of mAbs directed to the beta 2-integrin, CD11b (D12/SHCL-3), or CD18 (MHM23) subunits maximally inhibited ASA- and C-mediated sperm adhesion to neutrophils (by 70%) or sperm phagocytosis (by 75%), as well as neutrophil aggregation (by 96%).	Aspirin	127-130	integrin subunit beta 2	Homo sapiens	85-89
8527516-14	1995	These findings strongly implicate the CD11b/CD18 glycoprotein complex (CR3) in the adhesive events involved in ASA- and C-mediated immune destruction of motile sperm by neutrophils.	Aspirin	111-114	integrin subunit beta 2	Homo sapiens	44-48
7587805-3	1995	Aspirin-induced gastric damage and the increase in myeloperoxidase activity were significantly inhibited by the injection of anti-CD11a, anti-CD11b, anti-intercellular adhesion molecule-1 monoclonal antibodies, and the combination of superoxide dismutase and catalase, which are scavengers of active oxygen species.	Aspirin	0-7	integrin subunit alpha M	Rattus norvegicus	142-147
7587805-3	1995	Aspirin-induced gastric damage and the increase in myeloperoxidase activity were significantly inhibited by the injection of anti-CD11a, anti-CD11b, anti-intercellular adhesion molecule-1 monoclonal antibodies, and the combination of superoxide dismutase and catalase, which are scavengers of active oxygen species.	Aspirin	0-7	catalase	Rattus norvegicus	259-267
7587805-4	1995	These results suggest that neutrophil-endothelial adhesive interactions, which occur via CD11a/ CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule-1, and oxygen-derived free radicals produced by neutrophils are implicated in the production of aspirin-induced gastric mucosal injury.	Aspirin	273-280	integrin subunit beta 2	Rattus norvegicus	96-100
7587805-4	1995	These results suggest that neutrophil-endothelial adhesive interactions, which occur via CD11a/ CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule-1, and oxygen-derived free radicals produced by neutrophils are implicated in the production of aspirin-induced gastric mucosal injury.	Aspirin	273-280	integrin subunit alpha M	Rattus norvegicus	106-111
7587805-4	1995	These results suggest that neutrophil-endothelial adhesive interactions, which occur via CD11a/ CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule-1, and oxygen-derived free radicals produced by neutrophils are implicated in the production of aspirin-induced gastric mucosal injury.	Aspirin	273-280	integrin subunit beta 2	Rattus norvegicus	112-116
7589510-5	1995	Acetylsalicylic acid inhibited the secondary aggregation enhanced by TPO, but not the TPO-induced potentiation of the primary aggregation.	Aspirin	0-20	thrombopoietin	Homo sapiens	69-72
7568157-10	1995	These results demonstrate that ASA evokes a unique class of eicosanoids formed by acetylated PGHS-2 and 5-lipoxygenase interactions, which may contribute to the therapeutic impact of this drug.	Aspirin	31-34	prostaglandin-endoperoxide synthase 2	Homo sapiens	93-99
8983933-1	1995	After 4 days of acetysal treatment (160 mg/kg body weight orally), the following were established: a higher acute toxicity of acetysal, an inducing effect on amidopyrin N-demethylase and analgin N-demethylase activity and increases in cytochrome P-450 and cytochrome b5 content.	Aspirin	16-24	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	235-269
7560666-11	1995	A clinical history of aspirin sensitivity was strongly correlated with nonallergic CHS/NP, as well as the nonallergic CHS/NP profile of cytokines, including IFN-gamma.	Aspirin	22-29	interferon gamma	Homo sapiens	157-166
7560666-16	1995	Aspirin sensitivity is strongly correlated with nonallergic CHS/NP and production of the nonallergic CHS/NP profile of cytokines, including IFN-gamma.	Aspirin	0-7	interferon gamma	Homo sapiens	140-149
8749269-6	1995	These results demonstrate that for a wide range of patients without clear contraindications, angiotensin converting enzyme inhibitors started early in acute myocardial infarction prevent further deaths in the first few weeks when added to standard therapy (aspirin, thrombolytic therapy and beta-blockers).	Aspirin	257-264	angiotensin I converting enzyme	Homo sapiens	93-122
7545088-5	1995	We have also demonstrated that the adhesion of tumor cells to IL-1 beta-treated human umbilical vein endothelial cells can be inhibited by anti-NF kappa B reagents such as N-acetyl L-cysteine, aspirin, or pentoxifylline.	Aspirin	193-200	interleukin 1 beta	Homo sapiens	62-71
7545088-5	1995	We have also demonstrated that the adhesion of tumor cells to IL-1 beta-treated human umbilical vein endothelial cells can be inhibited by anti-NF kappa B reagents such as N-acetyl L-cysteine, aspirin, or pentoxifylline.	Aspirin	193-200	nuclear factor kappa B subunit 1	Homo sapiens	144-154
7556619-0	1995	Comparison of recombinant cyclooxygenase-2 to native isoforms: aspirin labeling of the active site.	Aspirin	63-70	prostaglandin-endoperoxide synthase 2	Homo sapiens	26-42
7669029-5	1995	The IIB vWF-evoked (3 micrograms/ml) cytosolic Ca2+ increase was negligibly affected by ADP scavengers or protein kinase C inhibitors; it was drastically reduced by EGTA, La3+, Ni2+ or acetylsalicylate and abolished by the phospholipase A2 inhibitors ONO-RS-082 or oleolyloxyethyl-phosphocholine.	Aspirin	185-201	von Willebrand factor	Homo sapiens	8-11
7573259-3	1995	The angiotensin II-sensitive women were randomized to 60 mg of aspirin or placebo as a subset of a large multicenter, randomized, controlled trial of low-dose aspirin therapy in pregnancy.	Aspirin	63-70	angiotensinogen	Homo sapiens	4-18
7573259-7	1995	RESULTS: Five women had proteinuric preeclampsia in the angiotensin II-sensitive group randomized to aspirin compared with none in the group randomized to placebo.	Aspirin	101-108	angiotensinogen	Homo sapiens	56-70
7544010-2	1995	We report that exposure of lipopolysaccharide-stimulated murine macrophages to therapeutic concentrations of aspirin (IC50 = 3 mM) and hydrocortisone (IC50 = 5 microM) inhibited the expression of iNOS and production of nitrite.	Aspirin	109-116	nitric oxide synthase 2, inducible	Mus musculus	196-200
7544010-5	1995	Immunoblot analysis of iNOS expression in the presence of aspirin showed inhibition of iNOS expression (IC50 = 3 mM).	Aspirin	58-65	nitric oxide synthase 2, inducible	Mus musculus	23-27
7544010-5	1995	Immunoblot analysis of iNOS expression in the presence of aspirin showed inhibition of iNOS expression (IC50 = 3 mM).	Aspirin	58-65	nitric oxide synthase 2, inducible	Mus musculus	87-91
7544010-9	1995	Aspirin and N-acetylimidazole (an effective acetylating agent), but not sodium salicylate or indomethacin, also directly interfered with the catalytic activity of iNOS in cell-free extracts.	Aspirin	0-7	nitric oxide synthase 2, inducible	Mus musculus	163-167
7544010-10	1995	These studies indicate that the inhibition of iNOS expression and function represents another mechanism of action for aspirin, if not for all aspirin-like drugs.	Aspirin	118-125	nitric oxide synthase 2, inducible	Mus musculus	46-50
7544010-10	1995	These studies indicate that the inhibition of iNOS expression and function represents another mechanism of action for aspirin, if not for all aspirin-like drugs.	Aspirin	142-149	nitric oxide synthase 2, inducible	Mus musculus	46-50
8665965-11	1995	These results suggest that the renin-angiotensin II system in the post-acute phase of AMI patients treated with aspirin and beta-blocking agents is correlated with cardiovascular autoregulation during postural manoeuvres.	Aspirin	112-119	renin	Homo sapiens	31-36
8547213-10	1995	In contrast, only additive effects of SIN-1 and iloprost were observed when platelet aggregation was measured in aspirin-treated PRP stimulated by ADP, TRAP, or collagen.	Aspirin	113-120	MAPK associated protein 1	Homo sapiens	38-43
8665965-11	1995	These results suggest that the renin-angiotensin II system in the post-acute phase of AMI patients treated with aspirin and beta-blocking agents is correlated with cardiovascular autoregulation during postural manoeuvres.	Aspirin	112-119	angiotensinogen	Homo sapiens	37-51
7563992-0	1995	[Serum phospholipase A2 activity in patients with aspirin-induced asthma].	Aspirin	50-57	phospholipase A2 group IB	Homo sapiens	7-23
7563992-2	1995	We therefore hypothesized that increased phospholipase A2 (PLA2) activity leads to increased leukotriene synthesis when non-steroidal antiinflammatory drugs inhibit cyclooxygenase in patients with AIA, and that PLA2 activity increases further during an aspirin induced attack.	Aspirin	253-260	phospholipase A2 group IB	Homo sapiens	41-57
7563992-2	1995	We therefore hypothesized that increased phospholipase A2 (PLA2) activity leads to increased leukotriene synthesis when non-steroidal antiinflammatory drugs inhibit cyclooxygenase in patients with AIA, and that PLA2 activity increases further during an aspirin induced attack.	Aspirin	253-260	phospholipase A2 group IB	Homo sapiens	59-63
7641602-2	1995	This remarkable efficacy is rather unexpected, as aspirin selectively inhibits platelet aggregation mediated through activation of the arachidonic-thromboxane pathway, but not platelet aggregation induced by adenosine diphosphate (ADP), collagen and low levels of thrombin.	Aspirin	50-57	coagulation factor II, thrombin	Homo sapiens	264-272
8578530-0	1995	Thrombin generation in myocardial infarction and hypercholesterolemia: effects of aspirin.	Aspirin	82-89	coagulation factor II, thrombin	Homo sapiens	0-8
8578530-8	1995	Recent evidence indicates that antithrombotic effects of aspirin might be explained, partly at least, by its inhibition of thrombin formation.	Aspirin	57-64	coagulation factor II, thrombin	Homo sapiens	123-131
7631591-0	1995	Phenotypes of alpha-1-antitrypsin in intrinsic asthma and ASA-triad patients.	Aspirin	58-61	serpin family A member 1	Homo sapiens	14-33
7628860-6	1995	The aspirin-induced, neutrophil-mediated cell detachment was prevented by a monoclonal antibody directed against CD11/CD18 adhesion integrins on PMNs.	Aspirin	4-11	integrin subunit beta 2	Homo sapiens	118-122
7674234-0	1995	Aspirin modulates interleukin-3 production: additional explanation for the preventive effects of aspirin in antiphospholipid antibody syndrome.	Aspirin	0-7	interleukin 3	Mus musculus	18-31
7674234-0	1995	Aspirin modulates interleukin-3 production: additional explanation for the preventive effects of aspirin in antiphospholipid antibody syndrome.	Aspirin	97-104	interleukin 3	Mus musculus	18-31
7674234-5	1995	Our aim was to examine whether aspirin may exert its beneficial effect in APS not only by its ability to prevent thromboxane A2 production and prostaglandin I2 (PGI2) formation, but also by stimulating IL-3 production.	Aspirin	31-38	interleukin 3	Mus musculus	202-206
7674234-9	1995	RESULTS: When splenocytes and macrophages were cultured in vitro with low dose aspirin (10 micrograms/ml), a marked stimulation of IL-3 production was noted.	Aspirin	79-86	interleukin 3	Mus musculus	131-135
7674234-10	1995	When NDGA was added to mixed cultures of splenocytes and macrophages containing low dose aspirin, it decreased the IL-3 production.	Aspirin	89-96	interleukin 3	Mus musculus	115-119
7674234-14	1995	These results were supported by in vivo studies, in which a higher serum IL-3 level was detected in mice fed low dose aspirin, compared to the control group and to mice fed a higher dose of aspirin.	Aspirin	118-125	interleukin 3	Mus musculus	73-77
7674234-14	1995	These results were supported by in vivo studies, in which a higher serum IL-3 level was detected in mice fed low dose aspirin, compared to the control group and to mice fed a higher dose of aspirin.	Aspirin	190-197	interleukin 3	Mus musculus	73-77
7674234-15	1995	CONCLUSION: Aspirin acts as a potent stimulator of IL-3 through its ability to raise leukotriene production, which induces production of IL-3 both in vitro and in vivo.	Aspirin	12-19	interleukin 3	Mus musculus	51-55
7674234-15	1995	CONCLUSION: Aspirin acts as a potent stimulator of IL-3 through its ability to raise leukotriene production, which induces production of IL-3 both in vitro and in vivo.	Aspirin	12-19	interleukin 3	Mus musculus	137-141
7491348-0	1995	[High levels of cholesterol and lipoprotein (A) in serum decreases the inhibitory effect of aspirin on generation of thrombin].	Aspirin	92-99	coagulation factor II, thrombin	Homo sapiens	117-125
7491348-2	1995	Recently, we have found that aspirin decreases not only platelet aggregation but also thrombin generation.	Aspirin	29-36	coagulation factor II, thrombin	Homo sapiens	86-94
7491348-4	1995	Therefore we decided to examine influence of a single dose of aspirin (500 mg) on thrombin generation in healthy volunteers.	Aspirin	62-69	coagulation factor II, thrombin	Homo sapiens	82-90
7491348-6	1995	Aspirin reduced thrombin generation in persons with normal serum level of lipids.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	16-24
7491348-8	1995	While the mechanism by which aspirin affects thrombin generation remains to be elucidated, our data indicate that hypercholesterolemic subjects might benefit less than others from preventive aspirin treatment.	Aspirin	29-36	coagulation factor II, thrombin	Homo sapiens	45-53
7722147-2	1995	BACKGROUND: Low dose aspirin is frequently prescribed for patients with systolic dysfunction who also benefit from angiotensin-converting enzyme inhibition.	Aspirin	21-28	angiotensin I converting enzyme	Homo sapiens	115-144
7534663-0	1995	Aspirin inhibits nuclear factor-kappa B mobilization and monocyte adhesion in stimulated human endothelial cells.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	17-39
7534663-3	1995	METHODS AND RESULTS: Gel-shift analyses demonstrated dose-dependent inhibition of TNF-induced NF-kappa B mobilization by aspirin at concentrations ranging from 1 to 10 mmol/L.	Aspirin	121-128	tumor necrosis factor	Homo sapiens	82-85
7534663-3	1995	METHODS AND RESULTS: Gel-shift analyses demonstrated dose-dependent inhibition of TNF-induced NF-kappa B mobilization by aspirin at concentrations ranging from 1 to 10 mmol/L.	Aspirin	121-128	nuclear factor kappa B subunit 1	Homo sapiens	94-104
7534663-4	1995	Induction of VCAM-1 and E-selectin surface expression by TNF was dose-dependently reduced by aspirin over the same range, while induction of intercellular adhesion molecule-1 (ICAM-1) was hardly affected.	Aspirin	93-100	vascular cell adhesion molecule 1	Homo sapiens	13-19
7534663-4	1995	Induction of VCAM-1 and E-selectin surface expression by TNF was dose-dependently reduced by aspirin over the same range, while induction of intercellular adhesion molecule-1 (ICAM-1) was hardly affected.	Aspirin	93-100	tumor necrosis factor	Homo sapiens	57-60
7534663-5	1995	Aspirin appeared to prevent VCAM-1 transcription, since it dose-dependently inhibited induction of VCAM-1 mRNA by TNF.	Aspirin	0-7	vascular cell adhesion molecule 1	Homo sapiens	28-34
7534663-5	1995	Aspirin appeared to prevent VCAM-1 transcription, since it dose-dependently inhibited induction of VCAM-1 mRNA by TNF.	Aspirin	0-7	vascular cell adhesion molecule 1	Homo sapiens	99-105
7534663-5	1995	Aspirin appeared to prevent VCAM-1 transcription, since it dose-dependently inhibited induction of VCAM-1 mRNA by TNF.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	114-117
7534663-6	1995	As a functional consequence, adhesion of U937 monocytes to TNF-stimulated HUVECs was markedly reduced by aspirin due to suppression of VCAM-1 and E-selectin upregulation.	Aspirin	105-112	tumor necrosis factor	Homo sapiens	59-62
7534663-6	1995	As a functional consequence, adhesion of U937 monocytes to TNF-stimulated HUVECs was markedly reduced by aspirin due to suppression of VCAM-1 and E-selectin upregulation.	Aspirin	105-112	vascular cell adhesion molecule 1	Homo sapiens	135-141
7534663-8	1995	CONCLUSIONS: Our data suggest that aspirin inhibits NF-kappa B mobilization, induction of VCAM-1 and E-selectin, and subsequent monocyte adhesion in endothelial cells stimulated by TNF, thereby providing an additional mechanism for therapeutic effects of aspirin.	Aspirin	35-42	nuclear factor kappa B subunit 1	Homo sapiens	52-62
7534663-8	1995	CONCLUSIONS: Our data suggest that aspirin inhibits NF-kappa B mobilization, induction of VCAM-1 and E-selectin, and subsequent monocyte adhesion in endothelial cells stimulated by TNF, thereby providing an additional mechanism for therapeutic effects of aspirin.	Aspirin	35-42	vascular cell adhesion molecule 1	Homo sapiens	90-96
7534663-8	1995	CONCLUSIONS: Our data suggest that aspirin inhibits NF-kappa B mobilization, induction of VCAM-1 and E-selectin, and subsequent monocyte adhesion in endothelial cells stimulated by TNF, thereby providing an additional mechanism for therapeutic effects of aspirin.	Aspirin	35-42	tumor necrosis factor	Homo sapiens	181-184
7534663-8	1995	CONCLUSIONS: Our data suggest that aspirin inhibits NF-kappa B mobilization, induction of VCAM-1 and E-selectin, and subsequent monocyte adhesion in endothelial cells stimulated by TNF, thereby providing an additional mechanism for therapeutic effects of aspirin.	Aspirin	255-262	tumor necrosis factor	Homo sapiens	181-184
7895367-5	1995	Aspirin facilitated the inhibitory effect of neutrophils on platelet activation by thrombin, ADP, or epinephrine.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	83-91
7895367-9	1995	The vasoconstricting peptide endothelin-1 (ET-1) reversed the effect of aspirin through the endogenous production of platelet-activating factor (PAF) by neutrophils, as judged by the marked inhibitory effect of the PAF antagonist BN-52021.	Aspirin	72-79	endothelin 1	Homo sapiens	29-41
7895367-9	1995	The vasoconstricting peptide endothelin-1 (ET-1) reversed the effect of aspirin through the endogenous production of platelet-activating factor (PAF) by neutrophils, as judged by the marked inhibitory effect of the PAF antagonist BN-52021.	Aspirin	72-79	endothelin 1	Homo sapiens	43-47
7895367-12	1995	These results add new elements for interpreting the effects of aspirin on the interactions between blood cells, with special reference to high endothelin states (for example, ischemia/reperfusion processes).	Aspirin	63-70	endothelin 1	Homo sapiens	143-153
7612283-7	1995	In some of those trials antiplatelet therapy was also evaluated but only one (SPAF I), showed a significant reduction of stroke with aspirin; the reductions of risk was meanwhile much smaller than with varfarine.	Aspirin	133-140	spermatogenesis associated 5	Homo sapiens	78-82
7612283-10	1995	SPAF II trial directly compare aspirine with varfarine, showing the superiority of the last one but also its greater haemorrhagic risk.	Aspirin	31-39	spermatogenesis associated 5	Homo sapiens	0-4
7872329-4	1995	Similarities with sclerodermatous kidney and an increase in plasma renin activity led us to initiate treatment with aspirin and captopril, with excellent control of the renal syndrome.	Aspirin	116-123	renin	Homo sapiens	67-72
7554708-8	1995	The daily administration of low-dose aspirin (40 mg), a selective inhibitor of platelet PGHS-1, caused a cumulative inhibition of urinary 11-dehydro-TXB2 and whole blood TXB2 production that recovered with a timecourse consistent with platelet turnover.	Aspirin	37-44	prostaglandin-endoperoxide synthase 1	Homo sapiens	88-94
7610986-3	1995	The inducible form of PGHS, termed PGHS-2, has been purified and characterized with respect to substrate specificity, product formation, enzymatic activity, glycosylation, heme content, quaternary structure, and modification by aspirin.	Aspirin	228-235	prostaglandin-endoperoxide synthase 2	Homo sapiens	35-41
7631591-1	1995	The frequency of presence of various phenotypes of alpha 1-antitrypsin was studied in 31 patients with intrinsic asthma and 11 with ASA-Triad, and compared to a group of 200 people representative of the general population.	Aspirin	132-135	serpin family A member 1	Homo sapiens	51-70
7631591-5	1995	Alpha-1-antitrypsin deficiency could be important in the pathogenesis of inflammatory processes and in the clinical manifestations characteristic of patients with intrinsic asthma and ASA-Triad.	Aspirin	184-187	serpin family A member 1	Homo sapiens	0-19
7529028-3	1995	Lower concentrations of TNF alpha (0.3 to 30 pM) had a small, delayed (48-h incubation), stimulatory effect on DNA synthesis that was blocked by dexamethasone (1 microM), aspirin (100 microM), or primaquine (30 microM) pretreatment, indicating that this effect was secondary to the release of cyclooxygenase products.	Aspirin	171-178	tumor necrosis factor	Homo sapiens	24-33
7585737-5	1995	ASL and ASA were positively associated with age, fasting blood sugar levels and plasma fibrinogen levels, and these associations were statistically significant.	Aspirin	8-11	fibrinogen beta chain	Homo sapiens	87-97
7529817-5	1995	Reported here is the effect of aspirin on the platelet thrombi produced by thrombin in this manner.	Aspirin	31-38	coagulation factor II, thrombin	Homo sapiens	75-83
8774994-1	1995	Recent studies have indicated that aspirin promotes neutrophil adherence to endothelium via CD11/CD18-dependent interactions with intercellular adhesion molecule 1, which subsequently leads to neutrophil-mediated cell injury.	Aspirin	35-42	integrin subunit beta 2	Rattus norvegicus	97-101
8774994-7	1995	In addition, pretreatment with anti-CD18 monoclonal antibodies significantly attenuated gastric mucosal damage and inhibited the increases in both MPO activity and TBA-RS in the gastric mucosa after aspirin administration.	Aspirin	199-206	integrin subunit beta 2	Rattus norvegicus	36-40
8774994-8	1995	These observations suggest that CD18-dependent neutrophil-endothelial cell interactions and lipid peroxidation play an important role in the pathogenesis of gastric mucosal lesions induced by aspirin.	Aspirin	192-199	integrin subunit beta 2	Rattus norvegicus	32-36
7815366-6	1995	The reduction elicited by endothelin-3 was unaffected by a phospholipase C inhibitor, neomycin, or a protein kinase C inhibitor, H-7, but was antagonized by pretreatment with phospholipase A2 inhibitors, dexamethasone or methylprednisolone, and by cyclooxygenase inhibitors, aspirin and indomethacin.	Aspirin	275-282	endothelin 3	Canis lupus familiaris	26-38
7584958-4	1995	Aspirin medication correlates with an increase in active TGF-beta concentration, indicating that therapeutic interventions for TGF-beta are possible.	Aspirin	0-7	transforming growth factor beta 1	Homo sapiens	57-65
7584958-4	1995	Aspirin medication correlates with an increase in active TGF-beta concentration, indicating that therapeutic interventions for TGF-beta are possible.	Aspirin	0-7	transforming growth factor beta 1	Homo sapiens	127-135
7529817-7	1995	Actually, the higher doses of aspirin promoted platelet thrombus formation by thrombin even in the absence of protamine.	Aspirin	30-37	coagulation factor II, thrombin	Homo sapiens	78-86
7529817-6	1995	Aspirin was found to inhibit platelet thrombosis by thrombin in low doses (optimum dose 2.5 mg/kg body weight), but at higher doses the aspirin was less effective.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	52-60
21043735-4	1995	There are now at least two systems of platelet activation under intensive study: (a) agonist (e.g. ADP and thrombin) induced platelet activation when fibrinogen is the ligand; this process occurs at low shear forces and is aspirin sensitive; (b) secondly, in marked contrast, at high shear forces, shear itself activates the platelets and von Willebrand"s factor (vWf) is the ligand, and this process is aspirin insensitive.	Aspirin	223-230	coagulation factor II, thrombin	Homo sapiens	107-115
21043735-4	1995	There are now at least two systems of platelet activation under intensive study: (a) agonist (e.g. ADP and thrombin) induced platelet activation when fibrinogen is the ligand; this process occurs at low shear forces and is aspirin sensitive; (b) secondly, in marked contrast, at high shear forces, shear itself activates the platelets and von Willebrand"s factor (vWf) is the ligand, and this process is aspirin insensitive.	Aspirin	223-230	fibrinogen beta chain	Homo sapiens	150-160
21043735-4	1995	There are now at least two systems of platelet activation under intensive study: (a) agonist (e.g. ADP and thrombin) induced platelet activation when fibrinogen is the ligand; this process occurs at low shear forces and is aspirin sensitive; (b) secondly, in marked contrast, at high shear forces, shear itself activates the platelets and von Willebrand"s factor (vWf) is the ligand, and this process is aspirin insensitive.	Aspirin	404-411	coagulation factor II, thrombin	Homo sapiens	107-115
21043735-4	1995	There are now at least two systems of platelet activation under intensive study: (a) agonist (e.g. ADP and thrombin) induced platelet activation when fibrinogen is the ligand; this process occurs at low shear forces and is aspirin sensitive; (b) secondly, in marked contrast, at high shear forces, shear itself activates the platelets and von Willebrand"s factor (vWf) is the ligand, and this process is aspirin insensitive.	Aspirin	404-411	fibrinogen beta chain	Homo sapiens	150-160
7481155-9	1995	However, in spite of improved therapeutical protocols, a normal flow, which is the major criteria for a reduced mortality, is only obtained at the 90th minute in 54% of the patients who were administered the up-to-date treatment ie aspirin-accelerated t-PA-heparin in combination.	Aspirin	232-239	plasminogen activator, tissue type	Homo sapiens	252-256
7996488-2	1994	Heparinized human whole blood samples were incubated with lipopolysaccharide (LPS, 0.1-50 micrograms/ml) for 0 to 24 hr at 37 degrees C. The contribution of platelet PGHS-1 was suppressed by either pretreating the subjects with aspirin (300 mg 48 hr before sampling) or adding aspirin (10 micrograms/ml) in vitro at time 0.	Aspirin	228-235	prostaglandin-endoperoxide synthase 1	Homo sapiens	166-172
7660156-8	1995	The addition of PPP after DDAVP as well as the PPP or PRP after ASA enriched with vWf led to a significant shortening of the IVBT in comparison to the control, indicating that the effect of DDAVP on the prolonged BT seems to be an isolated effect of plasma vWf.	Aspirin	64-67	prion protein	Homo sapiens	54-57
7660156-8	1995	The addition of PPP after DDAVP as well as the PPP or PRP after ASA enriched with vWf led to a significant shortening of the IVBT in comparison to the control, indicating that the effect of DDAVP on the prolonged BT seems to be an isolated effect of plasma vWf.	Aspirin	64-67	von Willebrand factor	Homo sapiens	82-85
7996488-2	1994	Heparinized human whole blood samples were incubated with lipopolysaccharide (LPS, 0.1-50 micrograms/ml) for 0 to 24 hr at 37 degrees C. The contribution of platelet PGHS-1 was suppressed by either pretreating the subjects with aspirin (300 mg 48 hr before sampling) or adding aspirin (10 micrograms/ml) in vitro at time 0.	Aspirin	277-284	prostaglandin-endoperoxide synthase 1	Homo sapiens	166-172
7740476-0	1994	Inhibition of thrombin generation by aspirin.	Aspirin	37-44	coagulation factor II, thrombin	Homo sapiens	14-22
8091447-5	1994	In patients receiving aspirin, the platelet aggregability induced by 2 micrograms/mL collagen and 5 and 10 mumol/L adenosine diphosphate decreased compared with aggregability before medication (P < .005), but the reductions had no significant correlation with the plasma fibrinogen concentration.	Aspirin	22-29	fibrinogen beta chain	Homo sapiens	274-284
7873224-7	1994	However, further studies should be done to test the hypothesis that the association of a 5-HT2-receptor antagonist with aspirin may contribute to decrease myocardial ischemia and prevent coronary occlusion in patients with unstable angina.	Aspirin	120-127	5-hydroxytryptamine receptor 2A	Homo sapiens	89-103
7533066-16	1994	These findings suggest that platelet fibrinogen binding and the release of platelet alpha-granule and lysosomal contents, in response to stimulation with physiological agonists, can continue in patients despite aspirin therapy.	Aspirin	211-218	fibrinogen beta chain	Homo sapiens	37-47
7523416-8	1994	Pretreatment of platelets with acetylsalicylic acid (1 mM) completely abolished vWF-stimulated production of thromboxane A2, dense granule release, and the activation of protein kinase C, without altering the activation and cytoskeletal translocation of PtdIns 3-kinase and pp60c-src.	Aspirin	31-51	von Willebrand factor	Homo sapiens	80-83
7980423-2	1994	In aspirin-treated platelets the thrombin-induced increase of cytosolic Ca2+ ([Ca2+]i) associated with the release from the intracellular stores is followed by a decrease to the baseline which is largely dependent on the re-uptake into the stores.	Aspirin	3-10	coagulation factor II, thrombin	Homo sapiens	33-41
7798537-16	1994	This mediator profile is consistent with mast cell activation during the nasal response to aspirin and suggests that 5-lipoxygenase products are essential for the nasal response to aspirin.	Aspirin	181-188	arachidonate 5-lipoxygenase	Homo sapiens	117-131
7956925-6	1994	Such coculture experiments show that the promoting effect of Ang II on preadipose cell differentiation was strongly reduced by aspirin, antibodies able to neutralize PGI2, and the AT2 receptor antagonist PD123177, but not by the AT1 receptor antagonist losartan.	Aspirin	127-134	angiotensinogen	Rattus norvegicus	61-67
7812637-8	1994	These effects of NPY on the tone and the spontaneous activity remained unaffected by atropine (3 microM), indomethacin (10 microM) and aspirin (100 microM) but were abolished by Ca(2+)-withdrawal from the bathing medium.	Aspirin	135-142	neuropeptide Y	Rattus norvegicus	17-20
7786120-8	1994	A more recent study (SPAF II) confirmed the value of aspirin at the dosage of 325 mg/day which would seem to be a good alternative to anticoagulant therapy when this is contraindicated, although aspirin is less effective.	Aspirin	53-60	spermatogenesis associated 5	Homo sapiens	21-25
7786120-8	1994	A more recent study (SPAF II) confirmed the value of aspirin at the dosage of 325 mg/day which would seem to be a good alternative to anticoagulant therapy when this is contraindicated, although aspirin is less effective.	Aspirin	195-202	spermatogenesis associated 5	Homo sapiens	21-25
8091318-0	1994	Effect of the 5-lipoxygenase inhibitor ZD2138 on aspirin-induced asthma.	Aspirin	49-56	arachidonate 5-lipoxygenase	Homo sapiens	14-28
8091318-3	1994	If the cysteinyl leukotrienes cause aspirin-induced asthmatic reactions, inhibition of the 5-lipoxygenase pathway should prevent aspirin-induced bronchospasm.	Aspirin	129-136	arachidonate 5-lipoxygenase	Homo sapiens	91-105
8091318-11	1994	CONCLUSIONS: In aspirin-sensitive asthma the 5-lipoxygenase inhibitor ZD2138 inhibits the fall in FEV1 induced by aspirin and this is associated with substantial inhibition of 5-lipoxygenase.	Aspirin	16-23	arachidonate 5-lipoxygenase	Homo sapiens	45-59
8091318-11	1994	CONCLUSIONS: In aspirin-sensitive asthma the 5-lipoxygenase inhibitor ZD2138 inhibits the fall in FEV1 induced by aspirin and this is associated with substantial inhibition of 5-lipoxygenase.	Aspirin	114-121	arachidonate 5-lipoxygenase	Homo sapiens	45-59
7912815-4	1994	In this report, a photoactive derivative of rhodamine 123 (Rh123) [125I-azidosalicylic acid (ASA)-Rh123] was synthesized and used in a photoaffinity labeling assay to demonstrate, for the first time, direct and specific binding to P-glycoprotein.	Aspirin	93-96	ATP binding cassette subfamily B member 1	Homo sapiens	231-245
7974380-5	1994	It is also demonstrated that intake of 500 mg of aspirin significantly delays and inhibits thrombin generation in non-anticoagulated, thromboplastin triggered whole blood, whereas it has no effect on the coagulation in citrated plasma.	Aspirin	49-56	coagulation factor II, thrombin	Homo sapiens	91-99
7974380-6	1994	The effect of aspirin intake on thrombin generation in blood is roughly equal to that of 0.03 U/ml of unfractionated heparin.	Aspirin	14-21	coagulation factor II, thrombin	Homo sapiens	32-40
7951139-7	1994	In addition, catalase at a high concentration completely protected both the enzyme from inactivation and AsA from oxidation.	Aspirin	105-108	catalase	Homo sapiens	13-21
8200945-0	1994	Paradoxical inhibition by aspirin of naloxone-induced adrenocorticotropin secretion in myotonic dystrophy.	Aspirin	26-33	proopiomelanocortin	Homo sapiens	54-73
8200945-4	1994	Pretreatment with aspirin reduced the mean integrated ACTH response to naloxone by 33% (P < 0.05).	Aspirin	18-25	proopiomelanocortin	Homo sapiens	54-58
8200945-6	1994	These findings are in contrast to those of a previous study using an identical protocol, in which aspirin increased the ACTH response to naloxone in six normal volunteers.	Aspirin	98-105	proopiomelanocortin	Homo sapiens	120-124
7517181-0	1994	Low dose aspirin in women with raised maternal serum alpha-fetoprotein and abnormal Doppler waveform patterns from the uteroplacental circulation.	Aspirin	9-16	alpha fetoprotein	Homo sapiens	53-70
7517181-1	1994	OBJECTIVE: To investigate the use of low dose aspirin in the reduction of perinatal morbidity and mortality in women with unexplained raised maternal serum alpha-fetoprotein and abnormal uteroplacental Doppler waveform patterns.	Aspirin	46-53	alpha fetoprotein	Homo sapiens	156-173
7517181-13	1994	CONCLUSION: This trial revealed a benefit of low dose aspirin therapy in women with raised maternal serum alpha-fetoprotein and abnormal uteroplacental Doppler waveform patterns, but the effect was smaller than expected.	Aspirin	54-61	alpha fetoprotein	Homo sapiens	106-123
7912815-6	1994	Surprisingly, ASA-Rh123 photoaffinity labeled a 6-kDa V8 peptide in P-glycoprotein that was previously shown to be photoaffinity labeled by another multidrug resistance-associated drug, [125I]iodoarylazidoprazosin.	Aspirin	14-17	ATP binding cassette subfamily B member 1	Homo sapiens	68-82
8114674-7	1994	Recombinant hPGHS-1 and hPGHS-2 both produced 15- and 11-hydroxyeicosatetraenoic acid (HETE) from arachidonic acid, with 15-HETE production by hPGHS-2 being stimulated 5-fold by preincubation with aspirin.	Aspirin	197-204	prostaglandin-endoperoxide synthase 1	Homo sapiens	12-19
8175750-0	1994	Acetylation of human prostaglandin endoperoxide synthase-2 (cyclooxygenase-2) by aspirin.	Aspirin	81-88	prostaglandin-endoperoxide synthase 2	Homo sapiens	21-58
8175750-0	1994	Acetylation of human prostaglandin endoperoxide synthase-2 (cyclooxygenase-2) by aspirin.	Aspirin	81-88	prostaglandin-endoperoxide synthase 2	Homo sapiens	60-76
8175750-1	1994	Aspirin (acetylsalicylate) treatment of human (h) prostaglandin endoperoxide H synthase (PGHS)-1 expressed in cos-1 cells caused a time-dependent inactivation of oxygenase activity.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	50-96
8175750-1	1994	Aspirin (acetylsalicylate) treatment of human (h) prostaglandin endoperoxide H synthase (PGHS)-1 expressed in cos-1 cells caused a time-dependent inactivation of oxygenase activity.	Aspirin	9-25	prostaglandin-endoperoxide synthase 1	Homo sapiens	50-96
8175750-2	1994	Aspirin treatment of hPGHS-2 produced an enzyme which retained oxygenase activity but formed exclusively 15-hydroxy-5,8,11,13-eicosatetraenoic acid (15-HETE) instead of PGH2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	21-28
8175750-4	1994	The Km values for arachidonate of native and aspirin-treated hPGHS-2 were about the same suggesting that arachidonate binds to both aspirin-treated and native hPGHS-2 in a similar manner.	Aspirin	45-52	prostaglandin-endoperoxide synthase 2	Homo sapiens	61-68
8175750-4	1994	The Km values for arachidonate of native and aspirin-treated hPGHS-2 were about the same suggesting that arachidonate binds to both aspirin-treated and native hPGHS-2 in a similar manner.	Aspirin	132-139	prostaglandin-endoperoxide synthase 2	Homo sapiens	61-68
8175750-8	1994	This indicates that Ser-516 is the site of aspirin acetylation of hPGHS-2; this residue is homologous to the "active site" serine of PGHS-1.	Aspirin	43-50	prostaglandin-endoperoxide synthase 2	Homo sapiens	66-73
8175750-8	1994	This indicates that Ser-516 is the site of aspirin acetylation of hPGHS-2; this residue is homologous to the "active site" serine of PGHS-1.	Aspirin	43-50	prostaglandin-endoperoxide synthase 1	Homo sapiens	133-139
8175750-11	1994	An S516M mutant of hPGHS-2 was obtained which resembled aspirin-acetylated hPGHS-2 in that this mutant made 15R-HETE as its major product; however, unlike the aspirin-acetylated hPGHS-2, the Km value of the S516M mutant for arachidonate was 100 times that of native hPGHS-2.	Aspirin	56-63	prostaglandin-endoperoxide synthase 2	Homo sapiens	19-26
8175750-11	1994	An S516M mutant of hPGHS-2 was obtained which resembled aspirin-acetylated hPGHS-2 in that this mutant made 15R-HETE as its major product; however, unlike the aspirin-acetylated hPGHS-2, the Km value of the S516M mutant for arachidonate was 100 times that of native hPGHS-2.	Aspirin	56-63	prostaglandin-endoperoxide synthase 2	Homo sapiens	75-82
8175750-11	1994	An S516M mutant of hPGHS-2 was obtained which resembled aspirin-acetylated hPGHS-2 in that this mutant made 15R-HETE as its major product; however, unlike the aspirin-acetylated hPGHS-2, the Km value of the S516M mutant for arachidonate was 100 times that of native hPGHS-2.	Aspirin	56-63	prostaglandin-endoperoxide synthase 2	Homo sapiens	75-82
8175750-11	1994	An S516M mutant of hPGHS-2 was obtained which resembled aspirin-acetylated hPGHS-2 in that this mutant made 15R-HETE as its major product; however, unlike the aspirin-acetylated hPGHS-2, the Km value of the S516M mutant for arachidonate was 100 times that of native hPGHS-2.	Aspirin	56-63	prostaglandin-endoperoxide synthase 2	Homo sapiens	75-82
8175750-11	1994	An S516M mutant of hPGHS-2 was obtained which resembled aspirin-acetylated hPGHS-2 in that this mutant made 15R-HETE as its major product; however, unlike the aspirin-acetylated hPGHS-2, the Km value of the S516M mutant for arachidonate was 100 times that of native hPGHS-2.	Aspirin	159-166	prostaglandin-endoperoxide synthase 2	Homo sapiens	19-26
7958234-0	1994	Dysfunctional recovery of prostacyclin synthase in aspirin-treated vascular cells: implications for prophylaxis of cardiovascular disease.	Aspirin	51-58	prostaglandin I2 synthase	Homo sapiens	26-47
8061627-3	1994	The first starts from the activation of Phospholipase A-2 that produces Arachidonic acid, which, in turn, undergoes the metabolic pathway leading to Thromboxane A-2; this pathway can be blocked by the intraplatelet Acetylsalicylic acid by irreversible inactivation of Cyclooxygenase but it is insensitive to the extra-platelet Acetylsalicylic acid.	Aspirin	215-235	phospholipase A2 group IB	Homo sapiens	40-57
8061627-3	1994	The first starts from the activation of Phospholipase A-2 that produces Arachidonic acid, which, in turn, undergoes the metabolic pathway leading to Thromboxane A-2; this pathway can be blocked by the intraplatelet Acetylsalicylic acid by irreversible inactivation of Cyclooxygenase but it is insensitive to the extra-platelet Acetylsalicylic acid.	Aspirin	327-347	phospholipase A2 group IB	Homo sapiens	40-57
8143845-0	1994	Mutation of serine-516 in human prostaglandin G/H synthase-2 to methionine or aspirin acetylation of this residue stimulates 15-R-HETE synthesis.	Aspirin	78-85	prostaglandin-endoperoxide synthase 2	Homo sapiens	32-60
8143845-4	1994	While PG synthesis by both isoforms is inhibited by aspirin, 15-R-hydroxyeicosatetraenoic acid (15-R-HETE) synthesis by PGHS-2, but not PGHS-1, is stimulated by preincubation with aspirin.	Aspirin	52-59	prostaglandin-endoperoxide synthase 2	Homo sapiens	120-126
8143845-4	1994	While PG synthesis by both isoforms is inhibited by aspirin, 15-R-hydroxyeicosatetraenoic acid (15-R-HETE) synthesis by PGHS-2, but not PGHS-1, is stimulated by preincubation with aspirin.	Aspirin	180-187	prostaglandin-endoperoxide synthase 2	Homo sapiens	120-126
8143845-5	1994	We have mutated the putative aspirin acetylation site of hPGHS-2, and expressed the mutants in COS-7 cells using recombinant vaccinia virus.	Aspirin	29-36	prostaglandin-endoperoxide synthase 2	Homo sapiens	57-64
8143845-6	1994	Enzyme activity and inhibitor sensitivity studies provide evidence that Ser516 is the aspirin acetylation site of human PGHS-2 and that substitution of a methionine residue at this position can mimic the effects of aspirin acetylation on enzyme activity.	Aspirin	86-93	prostaglandin-endoperoxide synthase 2	Homo sapiens	120-126
8143845-6	1994	Enzyme activity and inhibitor sensitivity studies provide evidence that Ser516 is the aspirin acetylation site of human PGHS-2 and that substitution of a methionine residue at this position can mimic the effects of aspirin acetylation on enzyme activity.	Aspirin	215-222	prostaglandin-endoperoxide synthase 2	Homo sapiens	120-126
8043909-6	1994	These methods permitted to demonstrate that, aspirin, contrary to several other antiplatelet drugs, delay the process of thrombin formation.	Aspirin	45-52	coagulation factor II, thrombin	Homo sapiens	121-129
8043909-7	1994	Continuous dampening of thrombin formation by aspirin might be one of the mechanisms responsible for its prophylactic and therapeutic efficacy.	Aspirin	46-53	coagulation factor II, thrombin	Homo sapiens	24-32
8144103-2	1994	Gastric lesion was induced by the oral administration of acidified aspirin in rats with hepatic cirrhosis produced by N-nitrosodiethylamine (NDA) or carbon tetrachloride (CCl4).	Aspirin	67-74	C-C motif chemokine ligand 4	Rattus norvegicus	171-175
8313551-6	1994	Whole blood platelet aggregation levels in response to 0.050 and 0.075 U of thrombin at baseline were 10.8 +/- 1.0 and 11.9 +/- 1.0 omega; aggregation was inhibited after 7 days of treatment with verapamil to 6.5 +/- 1.1 and 7.8 +/- 0.9 omega (P &lt; .05 versus baseline) and after 7 days of treatment with verapamil and aspirin to 6.1 +/- 1.1 and 7.2 +/- 1.0 omega (P &lt; .05), respectively.	Aspirin	321-328	coagulation factor II, thrombin	Homo sapiens	76-84
8114674-7	1994	Recombinant hPGHS-1 and hPGHS-2 both produced 15- and 11-hydroxyeicosatetraenoic acid (HETE) from arachidonic acid, with 15-HETE production by hPGHS-2 being stimulated 5-fold by preincubation with aspirin.	Aspirin	197-204	prostaglandin-endoperoxide synthase 2	Homo sapiens	24-31
8114674-7	1994	Recombinant hPGHS-1 and hPGHS-2 both produced 15- and 11-hydroxyeicosatetraenoic acid (HETE) from arachidonic acid, with 15-HETE production by hPGHS-2 being stimulated 5-fold by preincubation with aspirin.	Aspirin	197-204	prostaglandin-endoperoxide synthase 2	Homo sapiens	143-150
8114674-8	1994	Chiral phase high performance liquid chromatography analysis showed that aspirin-treated hPGHS-2 produced 15(R)-HETE, with no detectable 15(S)-HETE.	Aspirin	73-80	prostaglandin-endoperoxide synthase 2	Homo sapiens	89-96
8177499-4	1994	A slight yet significant suppression of the bradykinin response was instead observed in the absence of ASA.	Aspirin	103-106	kininogen 1	Canis lupus familiaris	44-54
8187462-11	1994	Aspirin, 325 mg/d, should be administered to patients with ECAD.	Aspirin	0-7	cadherin 1	Homo sapiens	59-63
8067899-0	1994	Acetylsalicylic acid--inducer of cytochrome P-450 2E1?	Aspirin	0-20	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	33-53
8265610-4	1993	Aspirin, indomethacin, and ibuprofen were more potent inhibitors of COX-1 than COX-2 in all models used.	Aspirin	0-7	cytochrome c oxidase subunit I	Ovis aries	68-73
10603518-1	1994	Background: Current strategies in the treatment of patients with acute coronary syndromes include antiplatelet agents and thrombin antagonists, most commonly aspirin and heparin, respectively.	Aspirin	158-165	coagulation factor II, thrombin	Homo sapiens	122-130
18475590-6	1994	Taken together, the immunostimulant effect of ASA shown in the literature as an increased production of interleukin-2 (IL-2) and IFN, could not be confirmed on the basis of the macrophage cytotoxiclty.	Aspirin	46-49	interleukin 2	Homo sapiens	104-117
18475590-6	1994	Taken together, the immunostimulant effect of ASA shown in the literature as an increased production of interleukin-2 (IL-2) and IFN, could not be confirmed on the basis of the macrophage cytotoxiclty.	Aspirin	46-49	interferon alpha 1	Homo sapiens	119-132
8207561-4	1994	RESULTS: Low-dose endothelin-1 infusions resulted in a significant increase in forearm blood flow, indicating vasodilation, which was significantly attenuated by cyclo-oxygenase inhibition using aspirin.	Aspirin	195-202	endothelin 1	Homo sapiens	18-30
8139094-0	1994	Effects of NG-monomethyl-L-arginine, indomethacin, and aspirin on the vasodepressor response to low doses of endothelin-1 and endothelin-3 in rats.	Aspirin	55-62	endothelin 1	Rattus norvegicus	109-121
8153084-4	1993	Amnion cells treated with IL-1 beta recovered rapidly from aspirin pretreatment suggesting an action on fatty acid cyclooxygenase (COX).	Aspirin	59-66	interleukin 1 beta	Homo sapiens	26-35
8256883-0	1993	The pivotal role of 5-lipoxygenase products in the reaction of aspirin-sensitive asthmatics to aspirin.	Aspirin	63-70	arachidonate 5-lipoxygenase	Homo sapiens	20-34
8256883-0	1993	The pivotal role of 5-lipoxygenase products in the reaction of aspirin-sensitive asthmatics to aspirin.	Aspirin	95-102	arachidonate 5-lipoxygenase	Homo sapiens	20-34
8295980-6	1993	TNF alpha consistently induced more rapid recovery from ASA treatment, and protein kinase C inhibition attenuated the stimulatory effects of TNF alpha.	Aspirin	56-59	tumor necrosis factor	Homo sapiens	0-9
7691143-5	1993	PGD2: -80.6%, PGF2: -81.3%) were found after acetylsalicylic acid (ASA)-treatment (0.5 mg 10(-6) cells for 24 h).	Aspirin	45-65	prostaglandin D2 synthase	Homo sapiens	0-4
7691143-5	1993	PGD2: -80.6%, PGF2: -81.3%) were found after acetylsalicylic acid (ASA)-treatment (0.5 mg 10(-6) cells for 24 h).	Aspirin	67-70	prostaglandin D2 synthase	Homo sapiens	0-4
8420330-4	1993	Aspirin at least partially corrects the pathologic increase in angiotensin II sensitivity that precedes the clinical development of preeclampsia.	Aspirin	0-7	angiotensinogen	Homo sapiens	63-77
8222512-8	1993	for aspirin-sensitive asthmatic patients [15.9 (SD 6.9) nmol min-1 mg-1 of protein] was not significantly different from that for the normal subjects.	Aspirin	4-11	CD59 molecule (CD59 blood group)	Homo sapiens	61-71
8103026-6	1993	Incubation of neutrophils with aspirin increased surface expression of CD11b and CD18 on neutrophils.	Aspirin	31-38	integrin subunit beta 2	Homo sapiens	81-85
8103026-7	1993	The aspirin-induced increase in PMN adherence to HUVEC was significantly reduced by monoclonal antibodies against CD18, CD11b, CD11a, and intercellular adhesion molecule 1.	Aspirin	4-11	integrin subunit beta 2	Homo sapiens	114-118
8103026-9	1993	CONCLUSIONS: These studies indicate that aspirin promotes neutrophil adherence to endothelium via CD11a/CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule 1; the adhesion response is partially mediated by leukotriene B4.	Aspirin	41-48	integrin subunit beta 2	Homo sapiens	104-108
8103026-9	1993	CONCLUSIONS: These studies indicate that aspirin promotes neutrophil adherence to endothelium via CD11a/CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule 1; the adhesion response is partially mediated by leukotriene B4.	Aspirin	41-48	integrin subunit beta 2	Homo sapiens	120-124
7690778-8	1993	The neutrophil downregulatory effect on thrombin-induced platelet reactivity was enhanced by aspirin treatment.	Aspirin	93-100	coagulation factor II, thrombin	Homo sapiens	40-48
8339418-9	1993	Oral aspirin 75 mg/d for 14 days abolished bradykinin-induced PGI2 formation, whereas dermal aspirin 750 mg/d had no effect despite similar inhibition of TXA2 biosynthesis.	Aspirin	5-12	kininogen 1	Homo sapiens	43-53
8329564-6	1993	Thrombin overcomes the aspirin inhibition indication that the platelet surface charge reduction is associated with platelet activation.	Aspirin	23-30	coagulation factor II, thrombin	Homo sapiens	0-8
8510013-0	1993	The gastrin/cholecystokinin-B receptor antagonist L-365,260 reduces basal acid secretion and prevents gastrointestinal damage induced by aspirin, ethanol and cysteamine in the rat.	Aspirin	137-144	cholecystokinin B receptor	Rattus norvegicus	12-38
8393884-4	1993	Aspirin pretreatment significantly increased the ACTH response to naloxone [mean peak increase from basal, 8.3 +/- 1.2 vs. 5.9 +/- 0.8 pmol/L (P &lt; 0.05); mean integrated response, 431.9 +/- 51.5 vs. 295.1 +/- 26.6 pmol/L.min (P &lt; 0.005); for aspirin/naloxone and placebo aspirin/naloxone, respectively].	Aspirin	0-7	proopiomelanocortin	Homo sapiens	49-53
8393884-4	1993	Aspirin pretreatment significantly increased the ACTH response to naloxone [mean peak increase from basal, 8.3 +/- 1.2 vs. 5.9 +/- 0.8 pmol/L (P &lt; 0.05); mean integrated response, 431.9 +/- 51.5 vs. 295.1 +/- 26.6 pmol/L.min (P &lt; 0.005); for aspirin/naloxone and placebo aspirin/naloxone, respectively].	Aspirin	248-255	proopiomelanocortin	Homo sapiens	49-53
8393884-4	1993	Aspirin pretreatment significantly increased the ACTH response to naloxone [mean peak increase from basal, 8.3 +/- 1.2 vs. 5.9 +/- 0.8 pmol/L (P &lt; 0.05); mean integrated response, 431.9 +/- 51.5 vs. 295.1 +/- 26.6 pmol/L.min (P &lt; 0.005); for aspirin/naloxone and placebo aspirin/naloxone, respectively].	Aspirin	277-284	proopiomelanocortin	Homo sapiens	49-53
8393884-6	1993	The mean integrated ACTH and cortisol responses were 46% and 26% greater with aspirin, respectively.	Aspirin	78-85	proopiomelanocortin	Homo sapiens	20-24
8393884-9	1993	The action of aspirin on the human HPA axis is probably mediated via inhibition of cyclooxygenase, resulting in changes in arachidonic acid metabolites, which influence ACTH release from corticotrophs.	Aspirin	14-21	proopiomelanocortin	Homo sapiens	169-173
8355292-7	1993	On the other hand, the inoculation of ovalbumin with complete Freund"s adjuvant (CFA) produced positive reaction in both of PCA and ASA.	Aspirin	132-135	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	38-47
8480641-0	1993	Effects of aspirin DL-lysine on thrombin generation in unstable angina pectoris.	Aspirin	11-18	coagulation factor II, thrombin	Homo sapiens	32-40
8480641-8	1993	These results suggest that aspirin rapidly reduces thrombin generation through inhibition of platelet activity in patients with unstable angina with prolonged rest angina.	Aspirin	27-34	coagulation factor II, thrombin	Homo sapiens	51-59
8490165-8	1993	IL-8 synthesis after aspirin ingestion was inhibited by 90% (P &lt; .01) as compared with the preaspirin stimulation.	Aspirin	21-28	C-X-C motif chemokine ligand 8	Homo sapiens	0-4
8482047-5	1993	In further studies, endothelin-1 was co-infused with an inhibitor of nitric oxide production, NG-monomethyl-L-arginine, or after oral administration of the irreversible inhibitor of prostaglandin production, acetylsalicylic acid (aspirin).	Aspirin	230-237	endothelin 1	Homo sapiens	20-32
8482047-10	1993	Prostacyclin was more effective at blocking the venoconstriction in response to endothelin-1 than glyceryl trinitrate (maximum: 12 +/- 3%), and there was substantial potentiation of endothelin-1-induced venoconstriction after pretreatment with aspirin (maximum: 90 +/- 3%).	Aspirin	244-251	endothelin 1	Homo sapiens	182-194
8270561-1	1993	As anti-inflammatory drugs such as acetylsalicylic acid are known to partially restore insulin response to glucose, the possible beneficial effect of colchicine, an anti-gout and anti-inflammatory drug, in non-insulin dependent diabetes mellitus (NIDDM) was studied.	Aspirin	35-55	insulin	Homo sapiens	87-94
8068484-2	1993	After aspirin administration, their serum IgA levels gradually decreased.	Aspirin	6-13	CD79a molecule	Homo sapiens	42-45
8068484-3	1993	After discontinuation of aspirin, their serum IgA levels gradually increased.	Aspirin	25-32	CD79a molecule	Homo sapiens	46-49
8068484-5	1993	The IgA production in vitro of peripheral blood mononuclear cells from a patient taken 3 months of discontinuation of aspirin was markedly inhibited by preincubation with aspirin.	Aspirin	118-125	CD79a molecule	Homo sapiens	4-7
8068484-5	1993	The IgA production in vitro of peripheral blood mononuclear cells from a patient taken 3 months of discontinuation of aspirin was markedly inhibited by preincubation with aspirin.	Aspirin	171-178	CD79a molecule	Homo sapiens	4-7
7509975-6	1993	Prostacyclin was more effective at blocking the venoconstriction to ET-1 than GTN (maximum 12 +/- 3%, p = 0.0001) and there was substantial potentiation of ET-1-induced venoconstriction after pretreatment with aspirin (maximum 90 +/- 3%, p = 0.001).	Aspirin	210-217	endothelin 1	Homo sapiens	156-160
7509975-8	1993	However, substantial potentiation of ET-1-induced venoconstriction by aspirin indicates that endothelial production of prostacyclin modulates responses to ET-1 in human veins in vivo.	Aspirin	70-77	endothelin 1	Homo sapiens	37-41
8121125-5	1993	Fibrinogen level increased from 3.34 +/- 0.15 to 3.95 +/- 0.18 g/l, p &lt; 0.001, and from 3.36 +/- 0.17 to 3.94 +/- 0.17 g/l p = 0.003 in aspirin and heparin groups, respectively.	Aspirin	139-146	fibrinogen beta chain	Homo sapiens	0-10
8105357-5	1993	The somatostatin-induced EDC was attenuated by cyclooxygenase inhibitors (aspirin and indomethacin), thromboxane A2 (TXA2) synthetase inhibitors (OKY-064 and RS-5186), and TXA2 antagonists (ONO-3708 and S-145), which suggests that the endothelium-derived contracting factor is TXA2.	Aspirin	74-81	somatostatin	Canis lupus familiaris	4-16
7686297-0	1993	Effect of indomethacin and aspirin on the TNF-alpha-induced priming and protein tyrosyl phosphorylation of human neutrophils.	Aspirin	27-34	tumor necrosis factor	Homo sapiens	42-51
21043850-0	1993	Release of Choline Metabolites from Human Platelets: Evidence for Activation of Phospholipase D and of Phosphatidylcholine-specific Phospholipase C. In aspirin-treated platelets labelled by preincubation with [(3)H]-choline, enhanced release of both [(3)H]-choline and [(3)H]-choline phosphate resulted from stimulation by collagen or thrombin.	Aspirin	152-159	coagulation factor II, thrombin	Homo sapiens	335-343
1309058-3	1992	Although heparin and aspirin may attenuate ongoing thrombin and thromboxane generation, respectively, a relatively high percentage (10-20%) of patients treated with heparin and aspirin still have complications associated with thrombolysis.	Aspirin	21-28	coagulation factor II, thrombin	Homo sapiens	51-59
1309058-5	1992	Therefore, careful consideration must be given to small molecule, active-site thrombin inhibitors which may prove to be more effective than heparin and to fibrinogen receptor antagonists which block aggregation to all known platelet agonists and have a much broader spectrum of activity than aspirin.	Aspirin	292-299	coagulation factor II, thrombin	Homo sapiens	78-86
1481893-5	1992	Consistent with this concept, indomethacin and aspirin blocked dynorphin- and beta-endorphin-induced vasopressin release.	Aspirin	47-54	vasopressin	Sus scrofa	101-112
1468903-6	1992	Due to the possible involvement of endothelin in headache disorders, the objective of this study was to verify the effects of lithium and cyclooxygenase inhibitors (indomethacin, acetylsalicylic acid and naproxen) on endothelin-1 (ET-1)-induced contractions in isolated human temporal arteries and porcine ophthalmic arteries.	Aspirin	179-199	endothelin 1	Homo sapiens	217-229
1391958-6	1992	Two hours after the ingestion of 500 mg of aspirin, thrombin formation became significantly impaired both in vitro and ex vivo.	Aspirin	43-50	coagulation factor II, thrombin	Homo sapiens	52-60
1391958-9	1992	Thus, aspirin, contrary to other antiplatelet drugs, depresses thrombin formation in clotting blood, a phenomenon that might be of clinical relevance.	Aspirin	6-13	coagulation factor II, thrombin	Homo sapiens	63-71
1390591-9	1992	Similarly, the tissue-type plasminogen activator (t-PA) antigen level was lower in the aspirin + PUFA-treated group.	Aspirin	87-94	plasminogen activator, tissue type	Homo sapiens	15-48
1390591-9	1992	Similarly, the tissue-type plasminogen activator (t-PA) antigen level was lower in the aspirin + PUFA-treated group.	Aspirin	87-94	plasminogen activator, tissue type	Homo sapiens	50-54
1326693-3	1992	Here we examined whether ASA"s effects in nerve growth factor-differentiated PC12 cells were mediated through the Ins1,4,5P3/Ca2+ second messenger pathway by monitoring intracellular Ca2+ (Ca2+i) with Fura2.	Aspirin	25-28	carbonic anhydrase 2	Rattus norvegicus	125-128
1295515-0	1992	[Effect of ASA on the interaction of von Willebrand factor with the platelet membrane].	Aspirin	11-14	von Willebrand factor	Homo sapiens	37-58
1295515-4	1992	A first well known way starts from the activation of Phospholipase A-2 (PL-A2), by which arachidonic acid is produced, that, in turn, undergoes the metabolic pathway leading to Thromboxane A-2; this pathway can be blocked by the intraplatelet ASA by irreversible inactivation of Cyclooxygenase, but it is insensitive to the extra-platelet ASA.	Aspirin	243-246	phospholipase A2 group IB	Homo sapiens	53-70
1295515-4	1992	A first well known way starts from the activation of Phospholipase A-2 (PL-A2), by which arachidonic acid is produced, that, in turn, undergoes the metabolic pathway leading to Thromboxane A-2; this pathway can be blocked by the intraplatelet ASA by irreversible inactivation of Cyclooxygenase, but it is insensitive to the extra-platelet ASA.	Aspirin	243-246	phospholipase A2 group IB	Homo sapiens	72-77
1295515-4	1992	A first well known way starts from the activation of Phospholipase A-2 (PL-A2), by which arachidonic acid is produced, that, in turn, undergoes the metabolic pathway leading to Thromboxane A-2; this pathway can be blocked by the intraplatelet ASA by irreversible inactivation of Cyclooxygenase, but it is insensitive to the extra-platelet ASA.	Aspirin	339-342	phospholipase A2 group IB	Homo sapiens	53-70
1295515-4	1992	A first well known way starts from the activation of Phospholipase A-2 (PL-A2), by which arachidonic acid is produced, that, in turn, undergoes the metabolic pathway leading to Thromboxane A-2; this pathway can be blocked by the intraplatelet ASA by irreversible inactivation of Cyclooxygenase, but it is insensitive to the extra-platelet ASA.	Aspirin	339-342	phospholipase A2 group IB	Homo sapiens	72-77
1403491-5	1992	The encapsulation efficiency of ASA reached a maximum of 9 per cent at DMPC:DCP 1:1 mole ratio.	Aspirin	32-35	decapping mRNA 1B	Homo sapiens	71-81
1510005-5	1992	Administration of aspirin inhibited the insulin-induced increase of plasma prostanoid level.	Aspirin	18-25	insulin	Homo sapiens	40-47
1511739-4	1992	These inhibitors also blocked the platelet aggregation and protein-tyrosine phosphorylation induced with thrombin in aspirin-treated platelets.	Aspirin	117-124	coagulation factor II, thrombin	Homo sapiens	105-113
1326693-7	1992	In Ca(2+)-containing medium the Ca2+ transient induced by ASA was not affected by organic Ca2+ channel blockers, but decreased when Co2+, Mn2+ or Zn2+ were present in the extracellular medium.	Aspirin	58-61	carbonic anhydrase 2	Rattus norvegicus	32-35
1326693-7	1992	In Ca(2+)-containing medium the Ca2+ transient induced by ASA was not affected by organic Ca2+ channel blockers, but decreased when Co2+, Mn2+ or Zn2+ were present in the extracellular medium.	Aspirin	58-61	carbonic anhydrase 2	Rattus norvegicus	90-93
1280631-1	1992	The current study was designed to observe the effects of drugs used for the treatment of inflammatory diseases (glucocorticoid, aspirin, and gamma globulin) on interleukin 6 (IL-6) production in the liver which may be involved in acute phase protein stimulation.	Aspirin	128-135	interleukin 6	Homo sapiens	175-179
1280631-6	1992	At 48 h after addition of glucocorticoid and aspirin, there was a suppression of IL-6 activity in the culture supernatants, which was associated with a decrease of mRNA level in the cells.	Aspirin	45-52	interleukin 6	Homo sapiens	81-85
1280631-8	1992	These data demonstrate that glucocorticoid and aspirin are potent regulators of IL-6 synthesis in the hepatoma cell.	Aspirin	47-54	interleukin 6	Homo sapiens	80-84
1383635-7	1992	At 10(-12) mol/site, intradermally injected PACAP and VIP caused a maximum increase in skin blood flow at 15 min of 379 +/- 96 and 307 +/- 121% (% increase above basal +/- SEM), respectively, and these responses were not significantly affected by oral aspirin (600 mg) taken 1.5 h beforehand.	Aspirin	252-259	vasoactive intestinal peptide	Homo sapiens	54-57
1326693-3	1992	Here we examined whether ASA"s effects in nerve growth factor-differentiated PC12 cells were mediated through the Ins1,4,5P3/Ca2+ second messenger pathway by monitoring intracellular Ca2+ (Ca2+i) with Fura2.	Aspirin	25-28	carbonic anhydrase 2	Rattus norvegicus	183-186
1326693-3	1992	Here we examined whether ASA"s effects in nerve growth factor-differentiated PC12 cells were mediated through the Ins1,4,5P3/Ca2+ second messenger pathway by monitoring intracellular Ca2+ (Ca2+i) with Fura2.	Aspirin	25-28	carbonic anhydrase 2	Rattus norvegicus	183-186
1326693-4	1992	It was found that ASA caused a dose-dependent increase in Ca2+i.	Aspirin	18-21	carbonic anhydrase 2	Rattus norvegicus	58-61
1326693-5	1992	In Ca(2+)-free medium, the increase in Ca2+i elicited by ASA was smaller, but the rise in Ins1,4,5P3 content was not appreciably changed.	Aspirin	57-60	carbonic anhydrase 2	Rattus norvegicus	39-42
1537105-0	1992	High-dose aspirin inhibits shear-induced platelet reaction involving thrombin generation.	Aspirin	10-17	coagulation factor II, thrombin	Homo sapiens	69-77
1643209-7	1992	It is proposed that the increased LPS-induced TF activity and TNF production following aspirin intake may be due to suppressed PGE2 formation.	Aspirin	87-94	tumor necrosis factor	Homo sapiens	62-65
1637110-0	1992	Ibuprofen, indomethacin, and high-dose aspirin, but not low-dose aspirin or imidazole, inhibit CGRP elevations in plasma during endotoxicosis.	Aspirin	39-46	calcitonin related polypeptide alpha	Homo sapiens	95-99
1602386-0	1992	Reduction of aspirin-induced gastric damage in rats by interleukin-1 beta: possible involvement of endogenous corticosteroids.	Aspirin	13-20	interleukin 1 beta	Rattus norvegicus	55-73
1729878-8	1992	Thrombin antagonism and platelet inhibition, primarily with heparin and aspirin, respectively, form the mainstay of conjunctive therapy.	Aspirin	72-79	coagulation factor II, thrombin	Homo sapiens	0-8
1589237-2	1992	We investigated whether aspirin can significantly modulate latencies or durations of the early (ES1) and late (ES2) exteroceptive suppression periods of electrical activity in the temporal muscle.	Aspirin	24-31	glutamine amidotransferase class 1 domain containing 3	Homo sapiens	96-99
1589237-2	1992	We investigated whether aspirin can significantly modulate latencies or durations of the early (ES1) and late (ES2) exteroceptive suppression periods of electrical activity in the temporal muscle.	Aspirin	24-31	ess-2 splicing factor homolog	Homo sapiens	111-114
1589237-7	1992	The administration of placebo as well as aspirin caused a highly significant increase in ES1 duration (P less than or equal to 0.001).	Aspirin	41-48	glutamine amidotransferase class 1 domain containing 3	Homo sapiens	89-92
1589237-8	1992	While aspirin caused a highly significant increase in ES2 duration (P less than or equal to 0.001) the taking of placebo showed no significant effect on ES2 duration.	Aspirin	6-13	ess-2 splicing factor homolog	Homo sapiens	54-57
1589237-9	1992	In giving aspirin as opposed to the placebo, there was a significant interaction between groups and drug effect on the latency of ES1; whereas in migraine patients and in patients with tension-type headache the latency of ES1 was reduced by administration of aspirin, it was increased in healthy subjects (P less than or equal to 0.05).	Aspirin	10-17	glutamine amidotransferase class 1 domain containing 3	Homo sapiens	130-133
1589237-9	1992	In giving aspirin as opposed to the placebo, there was a significant interaction between groups and drug effect on the latency of ES1; whereas in migraine patients and in patients with tension-type headache the latency of ES1 was reduced by administration of aspirin, it was increased in healthy subjects (P less than or equal to 0.05).	Aspirin	10-17	glutamine amidotransferase class 1 domain containing 3	Homo sapiens	222-225
1589237-9	1992	In giving aspirin as opposed to the placebo, there was a significant interaction between groups and drug effect on the latency of ES1; whereas in migraine patients and in patients with tension-type headache the latency of ES1 was reduced by administration of aspirin, it was increased in healthy subjects (P less than or equal to 0.05).	Aspirin	259-266	glutamine amidotransferase class 1 domain containing 3	Homo sapiens	130-133
1589237-9	1992	In giving aspirin as opposed to the placebo, there was a significant interaction between groups and drug effect on the latency of ES1; whereas in migraine patients and in patients with tension-type headache the latency of ES1 was reduced by administration of aspirin, it was increased in healthy subjects (P less than or equal to 0.05).	Aspirin	259-266	glutamine amidotransferase class 1 domain containing 3	Homo sapiens	222-225
1451711-7	1992	Creatinine clearance was 13.2 (95% CI 6.0 to 20.4) ml.min-1 lower in users than non-users of non-aspirin non-steroidal anti-inflammatory drugs.	Aspirin	97-104	CD59 molecule (CD59 blood group)	Homo sapiens	54-59
1309376-1	1992	The etiology of aspirin-sensitive asthma is unknown, but a plausible hypothesis is that the inhibitory effect of aspirin on the cyclooxygenase enzyme increases formation of bronchoconstrictor leukotrienes via "shunting" of unmetabolized arachidonic acid into metabolism by the 5-lipoxygenase enzyme.	Aspirin	113-120	arachidonate 5-lipoxygenase	Homo sapiens	277-291
1446774-4	1992	Unexpectedly, however, IL-3 levels are enhanced in the presence of the prostaglandin PGE2 and conversely, are inhibited by treatment with aspirin, a potent inhibitor of prostaglandin metabolism.	Aspirin	138-145	interleukin 3	Mus musculus	23-27
1310134-5	1992	ASA-ulcers were reduced in a dose-dependent manner by infusion of alpha-CGRP (1-2 nmol kg-1 i.a.	Aspirin	0-3	calcitonin related polypeptide alpha	Homo sapiens	72-76
1310134-11	1992	These results suggest that the inhibitory effects of alpha-CGRP on stimulated acid secretion and aspirin ulcers are mediated by different mechanisms and/or different receptors.	Aspirin	97-104	calcitonin related polypeptide alpha	Homo sapiens	59-63
1913263-7	1991	Two hours after ingestion of 500 mg aspirin, this difference increased up to 150 sec, although the individual responses varied markedly (P = 0.08), while the generation of thrombin became strongly depressed in both groups.	Aspirin	36-43	coagulation factor II, thrombin	Homo sapiens	172-180
1838974-6	1991	In the six patients without azotemia, aspirin inhibited renal prostaglandin E2 synthesis and suppressed renin release from the ischemic kidney, resulting in lowered blood pressure.	Aspirin	38-45	renin	Homo sapiens	104-109
1838974-8	1991	The reduction in blood pressure by angioplasty was correlated with the responses of blood pressure and renin release to aspirin.	Aspirin	120-127	renin	Homo sapiens	103-108
1960551-6	1991	The median times to progression were 1.9 months for the group receiving IFN with ASA and 2.7 months for the group receiving IFN alone (log-rank P = .36).	Aspirin	81-84	interferon alpha 1	Homo sapiens	72-75
1682739-2	1991	During erythropoietin treatment, spontaneous platelet aggregation was significantly higher in these subjects than in non-uraemic controls; concomitant treatment with 300 mg aspirin daily reversed platelet hyperaggregability.	Aspirin	173-180	erythropoietin	Homo sapiens	7-21
1811279-3	1991	At the stable period, low-dose aspirin inhibited platelet aggregation induced by ADP, collagen, or arachidonic acid, and suppressed the increase in intracellular Ca2+ concentration [( Ca2+]i) induced by thrombin significantly.	Aspirin	31-38	coagulation factor II, thrombin	Homo sapiens	203-211
1804603-7	1991	The mechanism of aspirin may be the inhibition of TXA2 and Fn synthesis and decreased consumption of AT-III.	Aspirin	17-24	fibronectin 1	Homo sapiens	59-61
1891022-12	1991	The five- to sixfold increase in the prostacyclin metabolite induced by bradykinin was depressed by pretreatment for four days with 75 mg of immediate-release aspirin, but not by 75 mg of controlled-release aspirin.	Aspirin	159-166	kininogen 1	Homo sapiens	72-82
1910314-5	1991	Furthermore, superoxide dismutase-dependent platelet activation is fully prevented by catalase and/or aspirin, suggesting a role for H2O2 and the involvement of the cyclooxygenase pathway of arachidonic acid in such activation.	Aspirin	102-109	superoxide dismutase 1	Homo sapiens	13-33
1651667-9	1991	Acetylsalicylic acid increased 5-lipoxygenase product formation in the coculture studies but not in the isolated cell experiments.	Aspirin	0-20	arachidonate 5-lipoxygenase	Homo sapiens	31-45
1321263-5	1992	On the other hand, the sensitization of ovalbumin (OVA) with CFA produced positive reactions in all of PCA, ASA, ACA and Schultz-Dale tests.	Aspirin	108-111	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	40-49
1868238-3	1991	Aspirin-treated platelets alone (58 x 10(6)) were fully aggregated by thrombin at 0.05 U/mL or more.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	70-78
1649050-3	1991	This appears to be dependent upon phospholipase A2 activation, since it is well preserved in the presence of aspirin, which completely blocked both intracellular Ca2+ elevation and phosphatidic acid formation which would indicate phospholipase C activation.	Aspirin	109-116	phospholipase A2 group IB	Homo sapiens	34-50
1787232-2	1991	Single or chronic (7-8 days) per os administration to white rats of 0.1% solution of the heparin/acetylsalicylate complex (0.3 ml/200 g body weight) enhanced anticoagulative properties of blood plasma, increased the fibrinolytic activity in respect of stabilized fibrin, and diminished the thrombin-induced platelet aggregation.	Aspirin	97-113	coagulation factor II	Rattus norvegicus	290-298
2035557-1	1991	The hypothesis that an enhanced vasopressor response to angiotensin II in pregnancy may be corrected by suppressing production of platelet thromboxane A2 with low-dose aspirin was tested in a randomized, placebo-controlled, double-blind trial.	Aspirin	168-175	angiotensinogen	Homo sapiens	56-70
1909906-5	1991	Thromboxane A2 was less than 10% of controls in aspirin-treated PRP stimulated with low or high concentrations of collagen or with a pair of agonists.	Aspirin	48-55	prion protein	Homo sapiens	64-67
1680084-0	1991	Low-dose aspirin and vascular response in pregnant patients sensitive to angiotensin II.	Aspirin	9-16	angiotensinogen	Homo sapiens	73-87
1680084-2	1991	After aspirin administration there was a significant decrease in AII sensitivity in sensitive patients with no change in nonsensitive patients.	Aspirin	6-13	NLR family pyrin domain containing 3	Homo sapiens	65-68
1680084-3	1991	Low-dose aspirin favorably affects sensitivity to AII in sensitive patients, thus indicating a reduced vascular reactivity as a consequence of this regimen.	Aspirin	9-16	NLR family pyrin domain containing 3	Homo sapiens	50-53
1896957-5	1991	Aspirin and indomethacin inhibited the formation of the fluorochrome only when platelets were stimulated by thrombin.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	108-116
1903602-4	1991	Furthermore, aspirin-pretreated SMC produced PGI2 in response to arachidonate, ionophore A23187, or thrombin in the presence of platelets but not in their absence.	Aspirin	13-20	coagulation factor II	Rattus norvegicus	100-108
1903602-5	1991	SMC, by themselves unresponsive to thrombin, produced PGI2 during coincubation with thrombin-stimulated aspirin-pretreated platelets.	Aspirin	104-111	coagulation factor II	Rattus norvegicus	84-92
2046403-6	1991	Aspirin inhibits 80% of the adenosine diphosphate-induced platelet vWF surface expression, and the platelet vWF surface expression that is not inhibited by aspirin can be almost totally inhibited by disruption of the platelet cytoskeleton.	Aspirin	0-7	von Willebrand factor	Homo sapiens	67-70
2035557-3	1991	In women taking aspirin, values of thrombin-induced platelet malondialdehyde production were approximately 10% of those determined in the placebo group, indicating marked suppression of thromboxane A2 synthesis.	Aspirin	16-23	coagulation factor II, thrombin	Homo sapiens	35-43
2035557-4	1991	In the aspirin group vascular refractoriness to angiotensin II was restored in 14 of 17 treated women, by comparison with 5 of 15 women in the placebo group who had remained normotensive.	Aspirin	7-14	angiotensinogen	Homo sapiens	48-62
1678031-7	1991	Preincubation of platelets with aspirin (10 mumol/l) reduced the contraction in both vessels, but contraction was abolished only in the presence of both the thromboxane receptor antagonist SQ-30741 and the serotoninergic (5HT2) receptor antagonist ketanserin.	Aspirin	32-39	5-hydroxytryptamine receptor 2A	Homo sapiens	222-236
1674588-2	1991	12-HPETE but not 12-hydroxy-5,8,10,14-eicosatetraenoic acid blocks the U46619- and the thrombin-triggered aggregation of aspirin-treated platelets, dose dependently.	Aspirin	121-128	coagulation factor II, thrombin	Homo sapiens	87-95
1653374-3	1991	Aspirin produced glandular mucosal lesions in the pylorus-ligated rats and caused an increase of the cAMP content in the fundus and a decrease in the antrum.	Aspirin	0-7	cathelicidin antimicrobial peptide	Rattus norvegicus	101-105
1653374-6	1991	Dibutyryl cAMP (dbcAMP) given orally prevented the gastric mucosal lesions induced by aspirin without affecting gastric secretion.	Aspirin	86-93	cathelicidin antimicrobial peptide	Rattus norvegicus	10-14
1653374-7	1991	These results suggest that 1) the changes in the cAMP content of the fundus and antrum induced by aspirin may be associated with the formation of glandular mucosal damage, 2) the antiulcer activity of IM may be related to an increase of the cAMP content in mucous cells, and 3) dbcAMP given orally may penetrate into the surface mucous cells and activate defensive functions.	Aspirin	98-105	cathelicidin antimicrobial peptide	Rattus norvegicus	49-53
1653374-7	1991	These results suggest that 1) the changes in the cAMP content of the fundus and antrum induced by aspirin may be associated with the formation of glandular mucosal damage, 2) the antiulcer activity of IM may be related to an increase of the cAMP content in mucous cells, and 3) dbcAMP given orally may penetrate into the surface mucous cells and activate defensive functions.	Aspirin	98-105	cathelicidin antimicrobial peptide	Rattus norvegicus	241-245
1900222-4	1991	ASA but not the receptor antagonist shortened the time to thrombolysis with t-PA (20 +/- 13 [mean +/- SD] minutes with ASA, 36 +/- 15 minutes with receptor antagonist, and 43 +/- 16 minutes with the saline control).	Aspirin	0-3	tissue-type plasminogen activator	Canis lupus familiaris	76-80
1814850-4	1991	Aspirin, ibuprofen, and phenylbutazone also inhibited IL-6 production by adherent cells stimulated with lipopolysaccharide (LPS).	Aspirin	0-7	interleukin 6	Homo sapiens	54-58
1671747-4	1991	Pretreatment with aspirin significantly attenuated the effects of interleukin-1 beta on both the vasopressin and oxytocin levels.	Aspirin	18-25	interleukin 1 beta	Rattus norvegicus	66-84
1671747-4	1991	Pretreatment with aspirin significantly attenuated the effects of interleukin-1 beta on both the vasopressin and oxytocin levels.	Aspirin	18-25	arginine vasopressin	Rattus norvegicus	97-108
2024888-3	1991	Aspirin-insensitive pathways, mediated by protein kinase C and myosin light-chain kinase, lead to a change of platelet shape, with an attendant striking increase in their surface (pseudopods) followed by exposure of receptors for fibrinogen and vWf on GPIIb-IIIa.	Aspirin	0-7	fibrinogen beta chain	Homo sapiens	230-240
2024888-3	1991	Aspirin-insensitive pathways, mediated by protein kinase C and myosin light-chain kinase, lead to a change of platelet shape, with an attendant striking increase in their surface (pseudopods) followed by exposure of receptors for fibrinogen and vWf on GPIIb-IIIa.	Aspirin	0-7	von Willebrand factor	Homo sapiens	245-248
1899346-2	1991	The present study explored the direct association of membrane-bound fibrinogen with the Triton X-100 (Sigma Chemical Co, St Louis, MO) insoluble cytoskeleton of aspirin-treated, gel-filtered platelets, activated but not aggregated with 20 mumol/L adenosine diphosphate (ADP) or 150 mU/mL human thrombin (THR) when bound fibrinogen had become resistant to dissociation by EDTA.	Aspirin	161-168	fibrinogen beta chain	Homo sapiens	68-78
1725330-4	1991	The reduction elicited by ET-3 was antagonized by pretreatment with phospholipase A2 inhibitors (dexamethasone and methylprednisolone) and cyclooxygenase inhibitors (aspirin and indomethacin).	Aspirin	166-173	endothelin 3	Canis lupus familiaris	26-30
1843906-1	1991	Alpha-1 antitrypsin (A-1-AT) levels were determined in 46 patients with aspirin sensitive asthma using the Eriksson method.	Aspirin	72-79	serpin family A member 1	Homo sapiens	21-27
26487523-5	1991	When 2.8 and 9 muM adenosine diphosphate were used as the aggregants, it became evident that higher ASA doses yielded still further grades of change both in aggregation and disaggregation.	Aspirin	100-103	latexin	Homo sapiens	15-18
1843906-0	1991	[Alpha 1-antitrypsin and its phenotype in patients with asthma and aspirin hypersensitivity].	Aspirin	67-74	serpin family A member 1	Homo sapiens	1-20
1843906-1	1991	Alpha-1 antitrypsin (A-1-AT) levels were determined in 46 patients with aspirin sensitive asthma using the Eriksson method.	Aspirin	72-79	serpin family A member 1	Homo sapiens	0-19
2011121-0	1991	Acetylsalicylate-human serum albumin interaction as studied by NMR spectroscopy--antigenicity-producing mechanism of acetylsalicylic acid.	Aspirin	0-16	albumin	Homo sapiens	23-36
2011121-0	1991	Acetylsalicylate-human serum albumin interaction as studied by NMR spectroscopy--antigenicity-producing mechanism of acetylsalicylic acid.	Aspirin	117-137	albumin	Homo sapiens	23-36
2011121-1	1991	To discover the antigenicity-producing mechanism of acetylsalicylic acid, the interaction of this drug and relevant salicylic acid with human serum albumin (HSA) has been studied by means of nuclear magnetic resonance (NMR) spectroscopy.	Aspirin	52-72	albumin	Homo sapiens	142-155
1776339-3	1991	In contrast to the effects of acetylsalicylic acid, SIN 1 already inhibits aggregation during the first phase of aggregation, and it inhibits aggregations induced by agonists that are not or only marginally influenced by acetylsalicylic acid (such as the aggregation induced by platelet activating factor).	Aspirin	221-241	MAPK associated protein 1	Homo sapiens	52-57
2256495-8	1990	The occurrence of pregnancy-induced hypertension was 100% in the women who remained angiotensin II sensitive during aspirin therapy as compared with 36% and 39% in the other two groups (x2 = 16.14; p less than 0.001).	Aspirin	116-123	angiotensinogen	Homo sapiens	84-98
2256495-9	1990	Thus during low-dose aspirin therapy a failure to develop refractoriness to infused angiotensin II is associated with a nonselective inhibition of eicosanoids and the almost certain development of pregnancy-induced hypertension.	Aspirin	21-28	angiotensinogen	Homo sapiens	84-98
2119831-1	1990	The association between occupancy of the von Willebrand factor (vWf) receptor glycoprotein (GP) Ib, agglutination, and the assembly and composition of the cytoskeletal core was studied in 125I-surface-labeled aspirin-treated washed platelets.	Aspirin	209-216	von Willebrand factor	Bos taurus	64-67
2145839-1	1990	Administration of aspirin (81 mg/day for 2-3 weeks) in nine healthy volunteers (out of an initial ten subjects, only nine qualified) resulted in a greater than 95% decrease of thromboxane B2 production by thrombin-stimulated platelets.	Aspirin	18-25	coagulation factor II, thrombin	Homo sapiens	205-213
1843906-3	1991	In 30 patients with aspirin asthma the phenotype of A-1-AT was determined using the Laurell method.	Aspirin	20-27	serpin family A member 1	Homo sapiens	52-58
1843907-0	1991	[Effect of aspirin on FMLP (formyl-meth-leu-phe)-stimulated leukocytes in patients with asthma and hypersensitivity to aspirin].	Aspirin	11-18	formyl peptide receptor 1	Homo sapiens	22-26
1843907-0	1991	[Effect of aspirin on FMLP (formyl-meth-leu-phe)-stimulated leukocytes in patients with asthma and hypersensitivity to aspirin].	Aspirin	11-18	formyl peptide receptor 1	Homo sapiens	28-47
1843907-0	1991	[Effect of aspirin on FMLP (formyl-meth-leu-phe)-stimulated leukocytes in patients with asthma and hypersensitivity to aspirin].	Aspirin	119-126	formyl peptide receptor 1	Homo sapiens	22-26
1843907-0	1991	[Effect of aspirin on FMLP (formyl-meth-leu-phe)-stimulated leukocytes in patients with asthma and hypersensitivity to aspirin].	Aspirin	119-126	formyl peptide receptor 1	Homo sapiens	28-47
2215033-1	1990	An 11-year retrospective study was conducted to evaluate the surgical treatment of sinusitis in aspirin-triad patients.	Aspirin	96-103	DDB1 and CUL4 associated factor 7	Homo sapiens	0-5
2344576-6	1990	Disorders such as asthma and allergic rhinitis may be provoked by irritants (e.g., cigarette smoke), physical factors (e.g., cold, dry air) and chemical substances (e.g., acetylsalicylic acid) and metabisulfite), none of which involve an IgE-antibody-mediated mechanism.	Aspirin	171-191	immunoglobulin heavy constant epsilon	Homo sapiens	238-241
2198232-1	1990	This study has been planned to investigate some aspects of the interaction between acetylsalicylic acid (ASA) and tolbutamide on insulin secretion.	Aspirin	83-103	insulin	Homo sapiens	129-136
2198232-1	1990	This study has been planned to investigate some aspects of the interaction between acetylsalicylic acid (ASA) and tolbutamide on insulin secretion.	Aspirin	105-108	insulin	Homo sapiens	129-136
2198232-2	1990	In healthy subjects, oral administration of 3.2 g daily of ASA for 3 days significantly enhanced a) basal insulin levels (p less than 0.01), b) arginine-stimulated insulin secretion (25 g i.v.	Aspirin	59-62	insulin	Homo sapiens	106-113
2198232-2	1990	In healthy subjects, oral administration of 3.2 g daily of ASA for 3 days significantly enhanced a) basal insulin levels (p less than 0.01), b) arginine-stimulated insulin secretion (25 g i.v.	Aspirin	59-62	insulin	Homo sapiens	164-171
2198232-7	1990	We conclude that, in case of tolbutamide test, interferences between ASA and tolbutamide on insulin secretion might be dependent, at least in part, on enhancement of free-tolbutamide percentage in plasma and not only on a direct or synergic action of ASA on pancreatic B-cell.	Aspirin	69-72	insulin	Homo sapiens	92-99
2198232-7	1990	We conclude that, in case of tolbutamide test, interferences between ASA and tolbutamide on insulin secretion might be dependent, at least in part, on enhancement of free-tolbutamide percentage in plasma and not only on a direct or synergic action of ASA on pancreatic B-cell.	Aspirin	251-254	insulin	Homo sapiens	92-99
2376868-3	1990	When guinea pigs were sensitized with buspirone or buspirone-OVA emulsified with Freund"s complete adjuvant (FCA), these animals showed negative reactions in active systemic anaphylaxis (ASA), active cutaneous anaphylaxis (ACA), passive cutaneous anaphylaxis (PCA), passive hemagglutination (PHA) and Schultz-Dale test.	Aspirin	187-190	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	61-64
2401523-5	1990	The levels of lipid peroxide also showed a decrease while the activity of superoxide dismutase (SOD) and catalase registered an increase in the aspirin treated animals given isoproterenol when compared to corresponding animals given isoproterenol alone.	Aspirin	144-151	catalase	Rattus norvegicus	105-113
2190817-1	1990	alpha-Thrombin, gamma-thrombin, and platelet-activating factor each stimulated the mobilization of intracellular Ca2+ stores in aspirin-treated human platelets.	Aspirin	128-135	coagulation factor II, thrombin	Homo sapiens	6-14
2303480-7	1990	Therefore, as it appears to be true for thrombin, platelet response upon binding of anti-p24/CD9 is primarily mediated by the activation of phospholipase C. When platelets pretreated with aspirin (200 microM) and apyrase (1 mg/ml) were subsequently exposed to anti-p24/CD9, aggregation still occurred.	Aspirin	188-195	coagulation factor II, thrombin	Homo sapiens	40-48
2303480-7	1990	Therefore, as it appears to be true for thrombin, platelet response upon binding of anti-p24/CD9 is primarily mediated by the activation of phospholipase C. When platelets pretreated with aspirin (200 microM) and apyrase (1 mg/ml) were subsequently exposed to anti-p24/CD9, aggregation still occurred.	Aspirin	188-195	transmembrane p24 trafficking protein 2	Homo sapiens	89-92
2190817-1	1990	alpha-Thrombin, gamma-thrombin, and platelet-activating factor each stimulated the mobilization of intracellular Ca2+ stores in aspirin-treated human platelets.	Aspirin	128-135	coagulation factor II, thrombin	Homo sapiens	22-30
2324733-0	1990	Influence of aspirin and iron(III) tetrasulfonated phthalocyanine on bilirubin binding by human serum albumin.	Aspirin	13-20	albumin	Homo sapiens	96-109
2324733-1	1990	The interaction of bilirubin with aspirin-modified human serum albumin (HSA) and the influence of iron tetrasulfonated phthalocyanine on bilirubin binding by the native protein has been studied by difference spectroscopy and circular dichroism measurements.	Aspirin	34-41	albumin	Homo sapiens	57-70
34893997-1	2022	Derivatives of the cytotoxic cyclooxygenase (COX) inhibitor ((prop-2-ynyl)-2-acetoxybenzoate)dicobalthexacarbonyl (Co-ASS) with a methyl group in the 3, 4, 5, or 6 position of the acetylsalicylic acid (ASS) scaffold were synthesized with the aim to achieve enhanced selectivity for COX-2.	Aspirin	180-200	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	282-287
2107565-7	1990	Aspirin treated platelets aggregated with thrombin demonstrated no thromboxane B2 production and no glutathione disulfide generation.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	42-50
2169174-4	1990	The results of these experiments showed that aspirin and indomethacin cause a marked increase of IFN-gamma production by GO- and SEB-activated PBMC.	Aspirin	45-52	interferon gamma	Homo sapiens	97-106
33794285-0	2021	Effect of pharmacodynamical interaction between nutlin-3a and aspirin in the activation of p53.	Aspirin	62-69	tumor protein p53	Homo sapiens	91-94
33794285-4	2021	In the presented work, we have aimed to investigate the effect of pharmacodynamical interaction between two anti-cancer drugs, nutlin-3a and aspirin in the activation of p53 protein.	Aspirin	141-148	tumor protein p53	Homo sapiens	170-173
33794285-10	2021	When a high dose of aspirin is administered it acts as input disturbance and leads to undesirable over-expression of p53 protein.	Aspirin	20-27	tumor protein p53	Homo sapiens	117-120
33940641-11	2021	Low-dose ASA use was associated with significantly lower peripartum sFLT1 levels (4,650 +- 2,335 vs. 7,870 +- 6,282 pg/mL, p = 0.03) and sFLT1/PlGF ratio (397 +- 196 vs. 1,527 +- 2,668, p = 0.03).	Aspirin	9-12	placental growth factor	Homo sapiens	143-147
33812688-0	2021	Corrigendum to "Aspirin eugenol ester ameliorates paraquat-induced oxidative damage through ROS/p38-MAPK-mediated mitochondrial apoptosis pathway" [Toxicology 453 (2021) 152721].	Aspirin	16-23	mitogen-activated protein kinase 14	Homo sapiens	96-104
26335632-11	2015	Cyclooxygenase-2 gene expression decreased compared to controls during DHA stimulation after 72 h. Treatment with DHA and ASA revealed a decreased 15-lipoxygenase gene expression which was reduced after three days of DHA incubation.	Aspirin	122-125	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-16
26335632-11	2015	Cyclooxygenase-2 gene expression decreased compared to controls during DHA stimulation after 72 h. Treatment with DHA and ASA revealed a decreased 15-lipoxygenase gene expression which was reduced after three days of DHA incubation.	Aspirin	122-125	arachidonate 15-lipoxygenase	Homo sapiens	147-162
25669934-0	2015	Induction of both P-glycoprotein and specific cytochrome P450 by aspirin eventually does not alter the antithrombotic effect of clopidogrel.	Aspirin	65-72	ATP binding cassette subfamily B member 1	Homo sapiens	18-32
25669937-0	2015	Response to "Induction of both P-glycoprotein and specific cytochrome P450 by aspirin eventually does not alter the antithrombotic effect of clopidogrel".	Aspirin	78-85	ATP binding cassette subfamily B member 1	Homo sapiens	31-45
34820927-1	2022	Aspirin-exacerbated respiratory disease (AERD) is a clinical syndrome characterized by asthma, chronic rhinosinusitis with nasal polyposis (CRSwNP), and acute respiratory symptoms following exposure to aspirin and other cyclooxygenase-1 inhibiting nonsteroidal anti-inflammatory drugs (NSAIDs).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	220-236
34942378-6	2022	Inhibition of COX-1 with aspirin, as expected, completely abolished production of TxA2 and PGD/E2, but also significantly inhibited the release of 11-HETE (89 +- 3%) and 9-HODE (74 +- 6%), and reduced 15-HETE and 13-HODE by ~33 %.	Aspirin	25-32	prostaglandin-endoperoxide synthase 1	Homo sapiens	14-19
34693854-5	2022	Subsequent multivariate regression analysis showed heart rate (p <.001, OR = 0.978, 95%CI 0.969-0.987) and albumin (p =.019, OR = 0.658, 95%CI 0.464-0.933) were independent factors for aspirin-therapy after bleeding.	Aspirin	185-192	albumin	Homo sapiens	107-114
34153179-9	2021	Acetyl salicylic acid (ASA), a nonspecific COX inhibitor, was able to mitigate a bradykinin-induced increase in PGE2 in our studies.	Aspirin	0-21	kininogen 1	Homo sapiens	81-91
34875953-0	2022	Combined apocyanin and aspirin treatment activates the PI3K/Nrf2/HO-1 signaling pathway and ameliorates preeclampsia symptoms in rats.	Aspirin	23-30	NFE2 like bZIP transcription factor 2	Rattus norvegicus	60-64
34875953-10	2022	Moreover, the combined treatment upregulated PI3K, Akt, Nrf2, and HO-1 protein levels in the placental tissues from PE rats.Conclusion: Overall, our results suggested that combined treatment of apocyanin and aspirin ameliorates the PE symptoms compared with single-dose apocyanin or aspirin in a PE rat model.	Aspirin	208-215	AKT serine/threonine kinase 1	Rattus norvegicus	51-54
34875953-10	2022	Moreover, the combined treatment upregulated PI3K, Akt, Nrf2, and HO-1 protein levels in the placental tissues from PE rats.Conclusion: Overall, our results suggested that combined treatment of apocyanin and aspirin ameliorates the PE symptoms compared with single-dose apocyanin or aspirin in a PE rat model.	Aspirin	208-215	NFE2 like bZIP transcription factor 2	Rattus norvegicus	56-60
34875953-10	2022	Moreover, the combined treatment upregulated PI3K, Akt, Nrf2, and HO-1 protein levels in the placental tissues from PE rats.Conclusion: Overall, our results suggested that combined treatment of apocyanin and aspirin ameliorates the PE symptoms compared with single-dose apocyanin or aspirin in a PE rat model.	Aspirin	283-290	AKT serine/threonine kinase 1	Rattus norvegicus	51-54
34875953-10	2022	Moreover, the combined treatment upregulated PI3K, Akt, Nrf2, and HO-1 protein levels in the placental tissues from PE rats.Conclusion: Overall, our results suggested that combined treatment of apocyanin and aspirin ameliorates the PE symptoms compared with single-dose apocyanin or aspirin in a PE rat model.	Aspirin	283-290	NFE2 like bZIP transcription factor 2	Rattus norvegicus	56-60
34775204-10	2021	Many of the synthesized agents show enhanced COX-1/2 properties than aspirin with better selectivity index towards COX-2 relative to COX-1.	Aspirin	69-76	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	115-120
34389629-10	2021	Following deconvolution, DEGs included novel putative targets for aspirin such as TRABD2A (q=0.055), a negative regulator of Wnt signaling.	Aspirin	66-73	TraB domain containing 2A	Homo sapiens	82-89
34389629-11	2021	Weighted gene co-expression network analysis identified 12 significant modules, including two that contained hubs for EGFR and PTGES2, the latter being previously implicated in aspirin chemoprevention.	Aspirin	177-184	epidermal growth factor receptor	Homo sapiens	118-122
34389629-11	2021	Weighted gene co-expression network analysis identified 12 significant modules, including two that contained hubs for EGFR and PTGES2, the latter being previously implicated in aspirin chemoprevention.	Aspirin	177-184	prostaglandin E synthase 2	Homo sapiens	127-133
34741187-5	2021	ERK1/2 activated by the combined action of RBD and cytokines crucial for the development of severe COVID-19, i.e. interferon-gamma (IFNgamma) and tumour necrosis factor-alpha (TNFalpha), are more effectively inactivated by CO2 than by dexamethasone or acetylsalicylic acid in human bronchial epithelial cells.	Aspirin	252-272	mitogen-activated protein kinase 3	Homo sapiens	0-6
34707700-9	2021	Moreover, the results indicated that the effects of aspirin treatment on PE might be mediated via the AKT/mTOR signaling pathway.	Aspirin	52-59	thymoma viral proto-oncogene 1	Mus musculus	102-105
34721682-0	2021	Low-doses of aspirin promote the growth of human PC-9 lung cancer cells through activation of the MAPK family.	Aspirin	13-20	mitogen-activated protein kinase 1	Homo sapiens	98-102
34721682-7	2021	An assessment of MAPK inhibitors was performed to further validate the role of JNK, p38 and ERK in aspirin-promoted PC-9 cell growth.	Aspirin	99-106	mitogen-activated protein kinase 1	Homo sapiens	92-95
34864310-6	2022	Aspirin quickly interrupted the STIM1-Orai1 interaction, whereas Sulindac mainly suppressed STIM1 translocation.	Aspirin	0-7	stromal interaction molecule 1	Homo sapiens	32-37
34954768-8	2022	The newly identified rs168753 in F2R gene may influence the efficacy to clopidogrel-aspirin therapy for ischemic stroke patients.	Aspirin	84-91	coagulation factor II thrombin receptor	Homo sapiens	33-36
34935423-10	2021	When tested in our in vitro model, we found evidence that aspirin can blunt cell signaling and endothelial dysfunction caused by bradykinin in these cells.	Aspirin	58-65	kininogen 1	Homo sapiens	129-139
34873925-0	2021	Age-Dependent Effect of Ticagrelor Monotherapy Versus Ticagrelor With Aspirin on Major Bleeding and Cardiovascular Events: A Post Hoc Analysis of the TICO Randomized Trial.	Aspirin	70-77	renin binding protein	Homo sapiens	0-3
34153179-9	2021	Acetyl salicylic acid (ASA), a nonspecific COX inhibitor, was able to mitigate a bradykinin-induced increase in PGE2 in our studies.	Aspirin	23-26	kininogen 1	Homo sapiens	81-91
34153179-10	2021	However, ASA was inflammatory above its therapeutic window, increasing the levels of PGE2 and IL-8 above those seen with bradykinin stimulation alone.	Aspirin	9-12	C-X-C motif chemokine ligand 8	Homo sapiens	94-98
34153179-10	2021	However, ASA was inflammatory above its therapeutic window, increasing the levels of PGE2 and IL-8 above those seen with bradykinin stimulation alone.	Aspirin	9-12	kininogen 1	Homo sapiens	121-131
34153179-13	2021	An ASA-based formula (Biovanta) mitigated bradykinin-induced inflammation more strongly than ASA alone in organotypic human respiratory tissues.	Aspirin	3-6	kininogen 1	Homo sapiens	42-52
34537546-2	2021	Acetylsalicylic acid (ASA/aspirin) is thought to limit growth in PIK3CA-mutated neoplasms through PI3K pathway suppression.	Aspirin	0-20	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	65-71
34537546-2	2021	Acetylsalicylic acid (ASA/aspirin) is thought to limit growth in PIK3CA-mutated neoplasms through PI3K pathway suppression.	Aspirin	22-25	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	65-71
34537546-2	2021	Acetylsalicylic acid (ASA/aspirin) is thought to limit growth in PIK3CA-mutated neoplasms through PI3K pathway suppression.	Aspirin	26-33	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	65-71
34215460-4	2021	A weight-based aspirin dosing regimen for VTE prophylaxis was administered to 1247 patients: patients weighing >=120 kg received 325 mg aspirin twice daily (BID) and those weighing <120 kg received 81 mg aspirin BID for 4 weeks.	Aspirin	136-143	BH3 interacting domain death agonist	Homo sapiens	157-160
34215460-5	2021	In total, 1156 patients in the comparison cohort received 81 mg aspirin BID.	Aspirin	64-71	BH3 interacting domain death agonist	Homo sapiens	72-75
34822026-4	2022	Furthermore, we describe other potential benefits related to aspirin-triggered lipoxins and resolvins while illustrating how NSAIDs interfere with COX-1, COX-2, SARS-CoV-2/ SARS-CoV-2 ORF protein-dependent activation of caspases and their subsequent mitochondrial dysfunction, endoplasmic reticulum stress, apoptosis and necroptosis which were associated with COVID-19 complications.	Aspirin	61-68	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	154-159
34873128-9	2021	Administration of aspirin-triggered (AT) resolvin D1 (AT-RvD1) and AT lipoxin A4 (AT-LXA4), which are agonistic to ALX/FPR2, immediately after reperfusion improved lung function, reduced inflammatory cytokine levels, attenuated lung edema, and decreased neutrophil infiltration 3 h after reperfusion.	Aspirin	18-25	formyl peptide receptor 2-like	Rattus norvegicus	115-118
34868050-8	2021	In the blood, the level of ASA was inversely correlated with the following: the proportion of Th17 expressing HLA-DR (p=0.04), the proportion of effector CD4+ T cells expressing CCR5 (p=0.03) and the proportion of CD8+Tc17 expressing CCR5 (p=0.04).	Aspirin	27-30	CD4 molecule	Homo sapiens	154-157
34868050-9	2021	At the genital tract, ASA use correlated with a decreased of activated CD4+T cells (CD4+CCR5+CD161+ (p=0.02) and CD4+CCR5+CD95+ (p=0.001)).	Aspirin	22-25	CD4 molecule	Homo sapiens	71-74
34868050-9	2021	At the genital tract, ASA use correlated with a decreased of activated CD4+T cells (CD4+CCR5+CD161+ (p=0.02) and CD4+CCR5+CD95+ (p=0.001)).	Aspirin	22-25	CD4 molecule	Homo sapiens	84-87
34868050-9	2021	At the genital tract, ASA use correlated with a decreased of activated CD4+T cells (CD4+CCR5+CD161+ (p=0.02) and CD4+CCR5+CD95+ (p=0.001)).	Aspirin	22-25	killer cell lectin like receptor B1	Homo sapiens	93-98
34868050-9	2021	At the genital tract, ASA use correlated with a decreased of activated CD4+T cells (CD4+CCR5+CD161+ (p=0.02) and CD4+CCR5+CD95+ (p=0.001)).	Aspirin	22-25	CD4 molecule	Homo sapiens	113-116
34762378-13	2021	CONCLUSION: Acupuncture for regulating spleen and stomach combined with aspirin enteric-coated tablets relieve insulin resistance and reduces blood glucose and lipid as well as the recurrence rate of cardiocerebrovascular events in the patients with T2DM, which is probably related to the regulation of insulin resistance and the improvement of vascular endothelial function.	Aspirin	72-79	insulin	Homo sapiens	111-118
34762378-13	2021	CONCLUSION: Acupuncture for regulating spleen and stomach combined with aspirin enteric-coated tablets relieve insulin resistance and reduces blood glucose and lipid as well as the recurrence rate of cardiocerebrovascular events in the patients with T2DM, which is probably related to the regulation of insulin resistance and the improvement of vascular endothelial function.	Aspirin	72-79	insulin	Homo sapiens	303-310
34728445-2	2021	In small studies, aspirin (acetylsalicylic acid (ASA)) has been shown to control immune activation, increase CD4+ count, halt HIV disease progression and reduce HIV viral load (HVL).	Aspirin	18-25	CD4 molecule	Homo sapiens	109-112
34728445-2	2021	In small studies, aspirin (acetylsalicylic acid (ASA)) has been shown to control immune activation, increase CD4+ count, halt HIV disease progression and reduce HIV viral load (HVL).	Aspirin	27-47	CD4 molecule	Homo sapiens	109-112
34728445-2	2021	In small studies, aspirin (acetylsalicylic acid (ASA)) has been shown to control immune activation, increase CD4+ count, halt HIV disease progression and reduce HIV viral load (HVL).	Aspirin	49-52	CD4 molecule	Homo sapiens	109-112
34728718-11	2021	MD simulation validated the stability of four chemicals at the MAPK6 binding pockets, including Assafoetidinol A (ASA), Naringin (NAR), Rutin (RUT), and Tomatine (TOM).	Aspirin	114-117	mitogen-activated protein kinase 6	Homo sapiens	63-68
34725124-0	2021	Correction: Aspirin Suppresses the Growth and Metastasis of Osteosarcoma through the NF-kappaB Pathway.	Aspirin	12-19	nuclear factor kappa B subunit 1	Homo sapiens	85-94
34857988-8	2021	Aspirin also significantly decreased tumor necrosis factor alpha and reactive oxygen species (ROS) levels in the plasma.	Aspirin	0-7	tumor necrosis factor	Mus musculus	37-64
34857988-9	2021	Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin.	Aspirin	304-311	nitric oxide synthase 2, inducible	Mus musculus	84-115
34857988-9	2021	Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin.	Aspirin	304-311	nitric oxide synthase 2, inducible	Mus musculus	117-121
34357562-7	2021	Few pharmacogenomics studies have explored antiplatelet drugs in Brazilian cohorts, finding associations between CYP2C19*2, PON1 rs662 and ABCC3 rs757421 genotypes and platelet responsiveness or clopidogrel PK in subjects with coronary artery disease (CAD) or acute coronary syndrome (ACS), whereas ITGB3 contributes to aspirin PK but not platelet responsiveness in diabetic patients.	Aspirin	320-327	integrin subunit beta 3	Homo sapiens	299-304
34479029-2	2021	The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro.	Aspirin	48-55	mechanistic target of rapamycin kinase	Homo sapiens	183-212
34479029-2	2021	The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro.	Aspirin	48-55	mechanistic target of rapamycin kinase	Homo sapiens	214-218
34705291-1	2022	Aspirin has known effects beyond inhibiting platelet cyclooxygenase-1 (COX1) that have been incompletely characterized.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	53-69
34705291-1	2022	Aspirin has known effects beyond inhibiting platelet cyclooxygenase-1 (COX1) that have been incompletely characterized.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	71-75
34705291-6	2022	In independent cohorts of healthy volunteers and patients with diabetes we validated aspirin"s effects on five genes: EIF2S3, CHRNB1, EPAS1, SLC9A3R2, and HLA-DRA.	Aspirin	85-92	eukaryotic translation initiation factor 2 subunit gamma	Homo sapiens	118-124
34702218-14	2021	Unlike the non-insulin resistance group, the insulin resistance group was independently associated with aspirin HRPR (OR = 1.689, 95% CI 1.14 to 2.51, P = 0.009).	Aspirin	104-111	insulin	Homo sapiens	15-22
34702218-14	2021	Unlike the non-insulin resistance group, the insulin resistance group was independently associated with aspirin HRPR (OR = 1.689, 95% CI 1.14 to 2.51, P = 0.009).	Aspirin	104-111	insulin	Homo sapiens	45-52
34702218-16	2021	Insulin resistance assessed by the TyG index could be an independent risk factor for aspirin HRPR.	Aspirin	85-92	insulin	Homo sapiens	0-7
34700376-7	2021	In HCAE cells, overexpressed genes included EFNA1 and LIF, two genes commonly upregulated in colorectal cancer and associated with poor patient outcomes, and PTGS2 (COX2), a gene associated with the protective effect of aspirin in the colorectal cancer setting.	Aspirin	220-227	prostaglandin-endoperoxide synthase 2	Homo sapiens	158-163
34700376-7	2021	In HCAE cells, overexpressed genes included EFNA1 and LIF, two genes commonly upregulated in colorectal cancer and associated with poor patient outcomes, and PTGS2 (COX2), a gene associated with the protective effect of aspirin in the colorectal cancer setting.	Aspirin	220-227	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	165-169
34641628-5	2021	6.5 times stronger than that of SNT-MLT (43.3% and 6.7% enzyme inhibition, equivalent to the activity of acetylsalicylic acid in conc.	Aspirin	105-125	fibroblast growth factor receptor substrate 2	Homo sapiens	32-35
34245748-6	2021	Moreover, aspirin exerted its inhibitory effects on EndMT in vitro and in vivo by suppressing HIF-1alpha/TGF-beta1/Smads/Snail signaling pathway.	Aspirin	10-17	hypoxia inducible factor 1 subunit alpha	Homo sapiens	94-104
34620931-5	2021	Non-aspirin NSAID users who carry e-NOS intron 4 VNTR polymorphism have lower odds of UGIH (OR: 4.02 (95% CI 1.85, 8.75) than those users with wild type genotype (OR: 6.52 (95% CI 4.09, 10.38)); though the interaction estimates are not statistically significant (RERI: -2.68 (95% CI -6.67, 1.31); S: 0.53 (95% CI 0.18, 1.55)).	Aspirin	4-11	nitric oxide synthase 3	Homo sapiens	34-39
34245748-6	2021	Moreover, aspirin exerted its inhibitory effects on EndMT in vitro and in vivo by suppressing HIF-1alpha/TGF-beta1/Smads/Snail signaling pathway.	Aspirin	10-17	transforming growth factor beta 1	Homo sapiens	105-114
34245748-6	2021	Moreover, aspirin exerted its inhibitory effects on EndMT in vitro and in vivo by suppressing HIF-1alpha/TGF-beta1/Smads/Snail signaling pathway.	Aspirin	10-17	snail family transcriptional repressor 1	Homo sapiens	121-126
34631223-0	2021	Aspirin Positively Contributes to Drosophila Intestinal Homeostasis and Delays Aging through Targeting Imd.	Aspirin	0-7	immune deficiency	Drosophila melanogaster	103-106
34638442-2	2021	Among others, PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha) mutational status was proposed as a molecular biomarker for the response to adjuvant aspirin therapy.	Aspirin	180-187	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	14-20
34638442-7	2021	We observed a significant 10-year overall survival benefit in patients with aspirin use and combined wild-type PIK3CA and mutated-KRAS tumors (HR = 0.38; 95% CI = 0.17-0.87; p = 0.02), but not in patients without aspirin use.	Aspirin	76-83	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	111-117
34638442-8	2021	Our data indicate a benefit of aspirin usage particularly for patients with combined wild-type PIK3CA and mutated-KRAS tumor characteristics.	Aspirin	31-38	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	95-101
34631223-6	2021	Furthermore, our in vivo and in vitro biochemical analyses indicated that aspirin is a negative modulator in control of the K63-linked ubiquitination of Imd.	Aspirin	74-81	immune deficiency	Drosophila melanogaster	153-156
34568314-0	2021	Network Pharmacology and Experimental Validation Reveal the Effects of Chidamide Combined With Aspirin on Acute Myeloid Leukemia-Myelodysplastic Syndrome Cells Through PI3K/AKT Pathway.	Aspirin	95-102	AKT serine/threonine kinase 1	Homo sapiens	173-176
34329734-0	2021	Identification of a potent Nrf2 displacement activator among aspirin-containing prodrugs.	Aspirin	61-68	NFE2 like bZIP transcription factor 2	Homo sapiens	27-31
34329734-2	2021	A library of aspirin derivatives of various scaffolds potentially activating Nrf2 has been tested in Neh2-luc reporter assay which screens for direct Nrf2 protein stabilizers working via disruption of Nrf2-Keap1 interaction.	Aspirin	13-20	NFE2 like bZIP transcription factor 2	Homo sapiens	77-81
34329734-2	2021	A library of aspirin derivatives of various scaffolds potentially activating Nrf2 has been tested in Neh2-luc reporter assay which screens for direct Nrf2 protein stabilizers working via disruption of Nrf2-Keap1 interaction.	Aspirin	13-20	NFE2 like bZIP transcription factor 2	Homo sapiens	150-154
34329734-2	2021	A library of aspirin derivatives of various scaffolds potentially activating Nrf2 has been tested in Neh2-luc reporter assay which screens for direct Nrf2 protein stabilizers working via disruption of Nrf2-Keap1 interaction.	Aspirin	13-20	NFE2 like bZIP transcription factor 2	Homo sapiens	201-205
34329734-2	2021	A library of aspirin derivatives of various scaffolds potentially activating Nrf2 has been tested in Neh2-luc reporter assay which screens for direct Nrf2 protein stabilizers working via disruption of Nrf2-Keap1 interaction.	Aspirin	13-20	kelch like ECH associated protein 1	Homo sapiens	206-211
34329734-10	2021	Hence, the esterase-catalyzed hydrolysis of the prodrug liberates only acetyl groups from aspirin moiety and generates a potent Nrf2 activator.	Aspirin	90-97	NFE2 like bZIP transcription factor 2	Homo sapiens	128-132
34126182-3	2021	ASA and SHL co-administration induced inflammatory responses in HaCat cells, as evidenced by marked increases in the expression of IL-4 and TNF-alpha, and the level of apoptosis.	Aspirin	0-3	interleukin 4	Homo sapiens	131-135
34126182-3	2021	ASA and SHL co-administration induced inflammatory responses in HaCat cells, as evidenced by marked increases in the expression of IL-4 and TNF-alpha, and the level of apoptosis.	Aspirin	0-3	tumor necrosis factor	Homo sapiens	140-149
34568314-8	2021	Pathway enrichment analysis indicated CDM and ASA significantly affected PI3K/AKT signaling pathway.	Aspirin	46-49	AKT serine/threonine kinase 1	Homo sapiens	78-81
34568314-12	2021	Our findings suggested that CDM combined with ASA exerted a synergetic inhibitory effect on cell growth by inactivating PI3K/AKT pathway, which might pave the way for effective treatments of AML-MDS.	Aspirin	46-49	AKT serine/threonine kinase 1	Homo sapiens	125-128
34486255-8	2021	This review summarizes the role of ALOX15 in different phenotypes of asthma, chronic obstructive pulmonary disease, chronic rhinosinusitis, aspirin-exacerbated respiratory disease, and nasal polyps, suggesting new treatment strategies for these airway inflammatory diseases with complex etiology and poor treatment response.	Aspirin	140-147	arachidonate 15-lipoxygenase	Homo sapiens	35-41
34632302-0	2021	Upregulation of IL-1 Receptor Antagonist by Aspirin in Glial Cells via Peroxisome Proliferator-Activated Receptor-Alpha.	Aspirin	44-51	peroxisome proliferator activated receptor alpha	Mus musculus	71-119
34730556-2	2021	In the present study, the antithrombotic effect of ASA in patients with CAD was assessed in platelet-rich plasma (PRP) using integral tests of the hemostasis study: the T-TAS system (Total Thrombus-formation Analysis System) and the thrombin generation test (TGT).	Aspirin	51-54	coagulation factor II, thrombin	Homo sapiens	233-241
34540909-0	2021	Platelet Endothelial Aggregation Receptor 1 Polymorphism Is Associated With Functional Outcome in Small-Artery Occlusion Stroke Patients Treated With Aspirin.	Aspirin	150-157	platelet endothelial aggregation receptor 1	Homo sapiens	0-43
34540909-2	2021	The present study aimed to explore the association between platelet endothelial aggregation receptor 1 (PEAR1) rs12041331 polymorphism and the outcomes in patients with acute ischemic stroke treated with aspirin or dual antiplatelet therapy (DAPT) with clopidogrel.	Aspirin	204-211	platelet endothelial aggregation receptor 1	Homo sapiens	59-102
34575050-5	2021	Aspirin treatment brought the activity of CYP 2E1 to the control level in both tissues, whereas the CYP 3A4 level decreased only in the pancreas.	Aspirin	0-7	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	42-49
34461078-14	2022	CONCLUSIONS: In patients at high risk of a serious adverse pregnancy outcome due to placental disease, the addition of LMWH to aspirin prophylaxis in the early second trimester may restore deficient circulating PlGF to mediate an improved perinatal outcome.	Aspirin	127-134	placental growth factor	Homo sapiens	211-215
34471538-3	2021	Studies reported the genetic polymorphisms of CYP2C19*2, CYP2C19*17, and ITGB3 cause an alteration of the pharmacodynamic and pharmacokinetic profile of aspirin and clopidogrel.	Aspirin	153-160	integrin subunit beta 3	Homo sapiens	73-78
34471538-8	2021	We genotyped aspirin-treated patients with T-ARMS-PCR for missense rs5918 (PlA1/A1) polymorphism of the ITGB3 gene.	Aspirin	13-20	integrin subunit beta 3	Homo sapiens	104-109
34471538-11	2021	On the other hand, among the aspirin-treated patients, polymorphisms of ITGB3 were 84.1% homozygous (PlA1/A1), 15.6% heterozygous (PlA1/A2), and 0.3% mutant homozygous.	Aspirin	29-36	integrin subunit beta 3	Homo sapiens	72-77
34309807-1	2021	PURPOSE: The aim of this study was to examine whether use of regular aspirin and/or other non-steroidal anti-inflammatory drugs (NSAIDs) is associated with the development of age-related macular degeneration (AMD).	Aspirin	69-76	renin binding protein	Homo sapiens	175-178
34373037-6	2021	Moreover, mFI = 1-3 was also associated with higher BMI, non-white race, high ASA, and older age (all p < 0.05).	Aspirin	78-81	melanotransferrin	Mus musculus	10-19
34437574-0	2021	Effect of TGF-beta1 on eosinophils to induce cysteinyl leukotriene E4 production in aspirin-exacerbated respiratory disease.	Aspirin	84-91	transforming growth factor beta 1	Homo sapiens	10-19
34540977-8	2021	Aspirin has been reported to suppress the Wnt pathway by inducing beta-catenin phosphorylation through the activation of glycogen synthase kinase 3 beta via cyclooxygenase-2 pathway inhibition.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	157-173
34428217-5	2021	Experiments demonstrate for the first time that plasma concentrations of Acetylsalicylic acid significantly increased TLR ligand-triggered IL-1beta, IL-10, and IL-6 production in a dose-dependent manner.	Aspirin	73-93	interleukin 6	Homo sapiens	160-164
34428217-6	2021	In contrast, indomethacin did not exhibit this capacity, whereas cyclooxygenase (COX)-2 selective NSAID, celecoxib, induced a similar pattern like Acetylsalicylic acid, suggesting a possible relevance of COX-2.	Aspirin	147-167	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	65-87
34428217-6	2021	In contrast, indomethacin did not exhibit this capacity, whereas cyclooxygenase (COX)-2 selective NSAID, celecoxib, induced a similar pattern like Acetylsalicylic acid, suggesting a possible relevance of COX-2.	Aspirin	147-167	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	204-209
34376069-4	2022	Co-therapy with aspirin reduces the GI benefits of COX-2 selective agents, whereas ibuprofen and naproxen may neglect the antiplatelet effect of aspirin.	Aspirin	16-23	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	51-56
34483913-0	2021	Aspirin Attenuates Cardiac Allograft Rejection by Inhibiting the Maturation of Dendritic Cells via the NF-kappaB Signaling Pathway.	Aspirin	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	103-112
34483913-13	2021	In vitro, aspirin decreased the activation of NF-kappaB signaling of DCs, as well as impeded MHCII and co-stimulatory molecules (CD80, CD86, and CD40) expression on DCs.	Aspirin	10-17	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	46-55
34483913-13	2021	In vitro, aspirin decreased the activation of NF-kappaB signaling of DCs, as well as impeded MHCII and co-stimulatory molecules (CD80, CD86, and CD40) expression on DCs.	Aspirin	10-17	histocompatibility-2, MHC	Mus musculus	93-98
34483913-13	2021	In vitro, aspirin decreased the activation of NF-kappaB signaling of DCs, as well as impeded MHCII and co-stimulatory molecules (CD80, CD86, and CD40) expression on DCs.	Aspirin	10-17	CD80 antigen	Mus musculus	129-133
34483913-13	2021	In vitro, aspirin decreased the activation of NF-kappaB signaling of DCs, as well as impeded MHCII and co-stimulatory molecules (CD80, CD86, and CD40) expression on DCs.	Aspirin	10-17	CD86 antigen	Mus musculus	135-139
34483913-15	2021	Conclusion: Aspirin inhibits the maturation of DCs through the NF-kappaB signaling pathway and attenuates acute cardiac allograft rejection.	Aspirin	12-19	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	63-72
34632302-9	2021	Moreover, we observed that aspirin bound to tyrosine 314 residue of PPARalpha to stimulate IL-1Ra and that aspirin treatment also increased the recruitment of PPARalpha to the IL-1Ra promoter.	Aspirin	27-34	peroxisome proliferator activated receptor alpha	Mus musculus	68-77
34632302-9	2021	Moreover, we observed that aspirin bound to tyrosine 314 residue of PPARalpha to stimulate IL-1Ra and that aspirin treatment also increased the recruitment of PPARalpha to the IL-1Ra promoter.	Aspirin	107-114	peroxisome proliferator activated receptor alpha	Mus musculus	68-77
34632302-9	2021	Moreover, we observed that aspirin bound to tyrosine 314 residue of PPARalpha to stimulate IL-1Ra and that aspirin treatment also increased the recruitment of PPARalpha to the IL-1Ra promoter.	Aspirin	107-114	peroxisome proliferator activated receptor alpha	Mus musculus	159-168
34632302-10	2021	Accordingly, aspirin increased IL-1Ra in vivo in the brain of wild type and PPARbeta-/-, but not in PPARalpha-/- mice.	Aspirin	13-20	peroxisome proliferator activated receptor alpha	Mus musculus	76-84
34127813-7	2021	The suppression of cell apoptosis by ASPN overexpression could be attenuated by LEF1 knockdown or 100 microM aspirin (PTGS2 inhibitor), and siASPN mediated apoptosis could be rescued by LEF1 ectopic expression or adding recombinant IL6.	Aspirin	109-116	asporin	Homo sapiens	37-41
34429873-1	2021	Introduction: Aspirin-exacerbated respiratory disease (AERD) is a phenotype of asthma characterized by eosinophilic inflammation in the airways, mast cell activation, cysteinyl leukotriene overproduction, and acute respiratory reactions on exposure to cyclooxygenase-1 inhibitors.	Aspirin	14-21	prostaglandin-endoperoxide synthase 1	Homo sapiens	252-268
34429873-7	2021	Variations in the expression of cysteinyl leukotriene receptor 1 in the airways could additionally influence the response to long-term aspirin therapy.	Aspirin	135-142	cysteinyl leukotriene receptor 1	Homo sapiens	32-64
34364538-1	2021	Aspirin-exacerbated respiratory disease (AERD) is a condition composed of chronic rhinosinusitis with nasal polyposis and asthma that is defined by respiratory hypersensitivity reactions to the cyclooxygenase 1-inhibitory effects of nonsteroidal anti-inflammatory drugs.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	194-210
34182131-4	2021	The contribution of platelet TXA2 biosynthesis on enhanced blood pressure (BP) and overload-induced cardiac fibrosis was explored in mice by treating with low-dose Aspirin, resulting in selective inhibition of platelet cyclooxygenase (COX)-1-dependent TXA2 generation.	Aspirin	164-171	cytochrome c oxidase I, mitochondrial	Mus musculus	219-241
34358114-2	2021	Our earlier studies showed that novel oleanolic acid oximes (OAO) conjugated with aspirin or indomethacin may enhance their anti-cancer potential through modulation of the Nrf2 and NF-kappaB signaling pathways.	Aspirin	82-89	NFE2 like bZIP transcription factor 2	Homo sapiens	172-176
34358114-2	2021	Our earlier studies showed that novel oleanolic acid oximes (OAO) conjugated with aspirin or indomethacin may enhance their anti-cancer potential through modulation of the Nrf2 and NF-kappaB signaling pathways.	Aspirin	82-89	nuclear factor kappa B subunit 1	Homo sapiens	181-190
34319045-16	2021	Dox-loaded ASA inhibited the proliferation of SW480 cells, because the aptamer facilitated the Dox uptake into these cells which caused the cell apoptosis, indicated by the significant decrease in procaspase-3, apoptosis marker protein.	Aspirin	11-14	caspase 3	Homo sapiens	197-209
34414020-14	2021	In addition, the mRNA levels of CDKN1A, BAX, FOXF1, PUMA, and RRAD in EOC cells were significantly increased by the aspirin treatment.	Aspirin	116-123	cyclin dependent kinase inhibitor 1A	Homo sapiens	32-38
34414020-14	2021	In addition, the mRNA levels of CDKN1A, BAX, FOXF1, PUMA, and RRAD in EOC cells were significantly increased by the aspirin treatment.	Aspirin	116-123	BCL2 associated X, apoptosis regulator	Homo sapiens	40-43
34239315-0	2021	P2X7R in Mast Cells is a Potential Target for Salicylic Acid and Aspirin in Treatment of Inflammatory Pain.	Aspirin	65-72	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	0-5
34239315-8	2021	At last, the effect of salicylic acid (SA) and aspirin (ASA) on the activity of P2X7R was studied by using calcium imaging, electrophysiological technique, ELISA, real-time PCR, behavioral tests, immunofluorescence and molecular docking.	Aspirin	47-54	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	80-85
34239315-8	2021	At last, the effect of salicylic acid (SA) and aspirin (ASA) on the activity of P2X7R was studied by using calcium imaging, electrophysiological technique, ELISA, real-time PCR, behavioral tests, immunofluorescence and molecular docking.	Aspirin	56-59	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	80-85
34239315-13	2021	Interestingly, SA or ASA could reduce high concentrations of ATP-induced inward current, P2X7R upregulation, mediators release, and inflammatory pain.	Aspirin	21-24	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	89-94
34239315-14	2021	SA or ASA also inhibited the inward current evoked by P2X7R agonist, BZATP.	Aspirin	6-9	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	54-59
34239315-15	2021	Molecular docking showed that SA or ASA had affinity for the cytoplasmic GDP-binding region of P2X7R.	Aspirin	36-39	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	95-100
34239315-16	2021	Conclusion: P2X7R in mast cells was involved in inflammation pain by releasing inflammatory mediators, and P2X7R might be a potential target for SA and ASA analgesia.	Aspirin	152-155	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	12-17
34239315-16	2021	Conclusion: P2X7R in mast cells was involved in inflammation pain by releasing inflammatory mediators, and P2X7R might be a potential target for SA and ASA analgesia.	Aspirin	152-155	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	107-112
34127813-7	2021	The suppression of cell apoptosis by ASPN overexpression could be attenuated by LEF1 knockdown or 100 microM aspirin (PTGS2 inhibitor), and siASPN mediated apoptosis could be rescued by LEF1 ectopic expression or adding recombinant IL6.	Aspirin	109-116	prostaglandin-endoperoxide synthase 2	Homo sapiens	118-123
34208905-0	2021	Simultaneous Pretreatment of Aspirin and Omega-3 Fatty Acid Attenuates Nuclear Factor-kappaB Activation in a Murine Model with Ventilator-Induced Lung Injury.	Aspirin	29-36	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	71-92
34208905-4	2021	We compared the lung inflammation after the sequential administration of lipopolysaccharides and mechanical ventilation between the pretreated simultaneous enteral aspirin and omega-3 fatty acid group and the non-pretreatment group, by quantifying NF-kappaB activation using an in vivo imaging system to detect bioluminescence signals.	Aspirin	164-171	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	248-257
34208905-6	2021	Compared to the non-pretreated group, the pretreatment group with simultaneous enteral aspirin and omega-3 fatty acid showed reduced expression of the pro-inflammatory cytokine, tumor necrosis factor-alpha, in bronchoalveolar lavage fluid (p = 0.038).	Aspirin	87-94	tumor necrosis factor	Mus musculus	178-205
34209594-9	2021	Consideration should be given to aspirin"s effect on neutrophils and pregnancy-specific expression of protease-activated receptor 1, as well as additional mechanisms of action to prevent preeclampsia.	Aspirin	33-40	coagulation factor II thrombin receptor	Homo sapiens	102-131
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	tumor protein p53	Homo sapiens	74-77
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	tumor protein p53	Homo sapiens	79-83
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	C-X-C motif chemokine ligand 8	Homo sapiens	86-116
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	C-X-C motif chemokine ligand 8	Homo sapiens	118-123
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	mitogen-activated protein kinase 3	Homo sapiens	126-160
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	mitogen-activated protein kinase 3	Homo sapiens	162-167
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	mitogen-activated protein kinase 1	Homo sapiens	170-204
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	mitogen-activated protein kinase 1	Homo sapiens	206-211
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	mitogen-activated protein kinase 14	Homo sapiens	214-249
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	mitogen-activated protein kinase 14	Homo sapiens	251-257
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	epidermal growth factor receptor	Homo sapiens	260-292
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	epidermal growth factor receptor	Homo sapiens	294-298
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	estrogen receptor 1	Homo sapiens	301-318
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	estrogen receptor 1	Homo sapiens	320-324
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	prostaglandin-endoperoxide synthase 2	Homo sapiens	331-368
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	prostaglandin-endoperoxide synthase 2	Homo sapiens	370-375
34202801-2	2021	In this research, the selected drugs commonly used in diabetes and its comorbidities (gliclazide, cilazapril, atorvastatin, and acetylsalicylic acid) were studied for their interactions with bovine serum albumin-native and glycated.	Aspirin	128-148	albumin	Homo sapiens	198-211
34201817-6	2021	The inhibition of COX-2 enzyme activity, but not protein expression was observed for ASA and one Salix extract.	Aspirin	85-88	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	18-23
34239442-1	2021	Objective: To investigate the impact of albumin levels on the aspirin efficacy, since aspirin inhibits platelet aggregation (PA) by cyclooxygenase one irreversible acetylation that is less effective in patients with type 2 diabetes mellitus (T2DM).	Aspirin	62-69	albumin	Homo sapiens	40-47
34239442-9	2021	Conclusion: In T2DM patients, the efficacy of aspirin varies according to albumin levels.	Aspirin	46-53	albumin	Homo sapiens	74-81
34128956-10	2022	Isolated anti-Ro-52 positivity with cytoplasmic ANA positivity was strongly associated with ASA+-ILD, while ANA negativity was associated with anti-MDA-5+-ILD.	Aspirin	92-95	tripartite motif containing 21	Homo sapiens	14-19
34261702-8	2021	Blocking CTLA4 and IL1B with the specific mAbs significantly suppressed tumor progression and metastasis in the mouse models resistant to anti-PD1 therapy, and the therapeutic efficacy was optimized by blocking cyclooxygenases with aspirin.	Aspirin	232-239	interleukin 1 beta	Mus musculus	19-23
34089489-0	2021	Combined influence of ABCB1 genetic polymorphism and DNA methylation on aspirin resistance in Chinese ischemic stroke patients.	Aspirin	72-79	ATP binding cassette subfamily B member 1	Homo sapiens	22-27
34089489-1	2021	Genetic variants of ABCB1 may affect intestinal absorption of aspirin (ASA).	Aspirin	62-69	ATP binding cassette subfamily B member 1	Homo sapiens	20-25
34089489-1	2021	Genetic variants of ABCB1 may affect intestinal absorption of aspirin (ASA).	Aspirin	71-74	ATP binding cassette subfamily B member 1	Homo sapiens	20-25
34089489-3	2021	Our aims is to investigate the association between ABCB1 polymorphisms and methylation status on the antiplatelet effects of ASA in Chinese Han ischemic stroke patients.	Aspirin	125-128	ATP binding cassette subfamily B member 1	Homo sapiens	51-56
34089489-9	2021	We also found that the methylation status of the ABCB1 promoter correlated positively with arachidonic acid inhibition (AA%) (R = 0.781, p < 0.001).The ABCB1 polymorphism and methylation status was associated with the reduced efficacy of ASA treatment in ischemic stroke.	Aspirin	238-241	ATP binding cassette subfamily B member 1	Homo sapiens	49-54
34089489-9	2021	We also found that the methylation status of the ABCB1 promoter correlated positively with arachidonic acid inhibition (AA%) (R = 0.781, p < 0.001).The ABCB1 polymorphism and methylation status was associated with the reduced efficacy of ASA treatment in ischemic stroke.	Aspirin	238-241	ATP binding cassette subfamily B member 1	Homo sapiens	152-157
34089489-10	2021	Genetic polymorphism and DNA methylation of ABCB1 should be concerned when prescribing ASA.	Aspirin	87-90	ATP binding cassette subfamily B member 1	Homo sapiens	44-49
34078519-0	2021	MiR-877-5p targets PDK-1 to promote aspirin-induced apoptosis in gastric mucosal cells.	Aspirin	36-43	microRNA 877	Homo sapiens	0-7
34078519-1	2021	This study aimed to investigate the role of miR-877-5p in aspirin-induced gastric mucosal injury.	Aspirin	58-65	microRNA 877	Homo sapiens	44-51
34078519-14	2021	Downregulation of miR-877-5p reduced the apoptosis by targeting PDK1 in GES-1 cells treated by aspirin, indicating that miR-877-5p may be a potential therapeutic target for gastric mucosal injury caused by aspirin.	Aspirin	95-102	microRNA 877	Homo sapiens	18-25
34078519-14	2021	Downregulation of miR-877-5p reduced the apoptosis by targeting PDK1 in GES-1 cells treated by aspirin, indicating that miR-877-5p may be a potential therapeutic target for gastric mucosal injury caused by aspirin.	Aspirin	95-102	microRNA 877	Homo sapiens	120-127
34078519-14	2021	Downregulation of miR-877-5p reduced the apoptosis by targeting PDK1 in GES-1 cells treated by aspirin, indicating that miR-877-5p may be a potential therapeutic target for gastric mucosal injury caused by aspirin.	Aspirin	206-213	microRNA 877	Homo sapiens	18-25
34078519-14	2021	Downregulation of miR-877-5p reduced the apoptosis by targeting PDK1 in GES-1 cells treated by aspirin, indicating that miR-877-5p may be a potential therapeutic target for gastric mucosal injury caused by aspirin.	Aspirin	206-213	microRNA 877	Homo sapiens	120-127
35489181-11	2022	Treatment with NAC+ASA increased the levels of glutamate transporters xCT and GLT-1 in nucleus accumbens, while Lactobacillus-GG administration increased those of the dopamine transporter (DAT).	Aspirin	19-22	solute carrier family 1 member 2	Rattus norvegicus	78-83
34121855-5	2021	Combination of aspirin and ginkgolide injection could better reduce brain water content, reduce apoptosis rate of cortical cells P < 0.05, reduce expression levels of caspase-3, Bax and p-REK1/2 proteins in ischemic brain tissue P < 0.05, and increase expression level of Bcl-2 protein than aspirin and ginkgolide injection alone P < 0.05).	Aspirin	15-22	BCL2, apoptosis regulator	Rattus norvegicus	272-277
34121855-5	2021	Combination of aspirin and ginkgolide injection could better reduce brain water content, reduce apoptosis rate of cortical cells P < 0.05, reduce expression levels of caspase-3, Bax and p-REK1/2 proteins in ischemic brain tissue P < 0.05, and increase expression level of Bcl-2 protein than aspirin and ginkgolide injection alone P < 0.05).	Aspirin	291-298	BCL2, apoptosis regulator	Rattus norvegicus	272-277
34122428-4	2021	Celecoxib, a selective COX-2 inhibitor, and aspirin, a non-selective COX-1 and COX-2 inhibitor, are being used as anti-inflammatory, analgesic and anti-pyretic drugs.	Aspirin	44-51	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	79-84
35171329-11	2022	Patients with the phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) mutation profited from postdiagnosis aspirin use (HR = 0.74, 95% CI: 0.56-0.97).	Aspirin	136-143	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	18-89
35535453-8	2022	Both miR-302/367 and aspirin upregulated the expression of FOXD3 protein which is a known inducer of OCT4 and NANOG.	Aspirin	21-28	forkhead box D3	Homo sapiens	59-64
35535453-9	2022	Our results demonstrate that aspirin can enhance miR-302/367-induced reprogramming of breast cancer cells possibly through upregulation of FOXD3 expression.	Aspirin	29-36	forkhead box D3	Homo sapiens	139-144
35258157-4	2022	SlIMP3 demonstrated high affinity with the L-Gal 1-P and D-Ins 3-P, and acted as a bifunctional enzyme in the biosynthesis of AsA and myoinositol.	Aspirin	126-129	inositol monophosphatase 3	Solanum lycopersicum	0-6
35258157-5	2022	Overexpression of SlIMP3 not only improved AsA and myoinositol content, but also increased cell wall thickness, improved fruit firmness, delayed fruit softening, decreased water loss, and extended shelf-life.	Aspirin	43-46	inositol monophosphatase 3	Solanum lycopersicum	18-24
35258157-11	2022	The results support a critical role for SlIMP3 in AsA biosynthesis and cell wall biogenesis, and provide a new method of delaying tomato fruit softening, and insight into the link between AsA and cell wall metabolism.	Aspirin	50-53	inositol monophosphatase 3	Solanum lycopersicum	40-46
35521358-6	2022	Daily administration of aspirin (ASA, 150 mg/kg body weight) for 3 successive days induced a significant increase in gastric juice volume, pepsin activity, serum transaminases, alkaline phosphatase, urea, creatinine, tumor necrosis factor-alpha, myeloperoxidase, and tissue malondialdehyde levels.	Aspirin	24-31	tumor necrosis factor	Rattus norvegicus	217-244
35521358-6	2022	Daily administration of aspirin (ASA, 150 mg/kg body weight) for 3 successive days induced a significant increase in gastric juice volume, pepsin activity, serum transaminases, alkaline phosphatase, urea, creatinine, tumor necrosis factor-alpha, myeloperoxidase, and tissue malondialdehyde levels.	Aspirin	33-36	tumor necrosis factor	Rattus norvegicus	217-244
35171329-11	2022	Patients with the phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) mutation profited from postdiagnosis aspirin use (HR = 0.74, 95% CI: 0.56-0.97).	Aspirin	136-143	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	91-97
35441670-4	2022	Our aims were to compare the effects of low-dose (COX-1 inhibition) and high-dose (dual COX-1 and COX-2 inhibition) aspirin on blood pressure, vascular function, oxidative stress, ET-1 and prostanoid levels and kidney damage during angiogenesis inhibitor therapy in rodents.	Aspirin	116-123	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	98-103
35585040-8	2022	Our results indicate that the neuroprotective effect of HDAC6 inhibition and aspirin treatment results from MIF K78 acetylation; thus, MIF K78 acetylation may be a therapeutic target for ischemic stroke and other neurological diseases.	Aspirin	77-84	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	108-111
35585040-8	2022	Our results indicate that the neuroprotective effect of HDAC6 inhibition and aspirin treatment results from MIF K78 acetylation; thus, MIF K78 acetylation may be a therapeutic target for ischemic stroke and other neurological diseases.	Aspirin	77-84	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	135-138
35441670-4	2022	Our aims were to compare the effects of low-dose (COX-1 inhibition) and high-dose (dual COX-1 and COX-2 inhibition) aspirin on blood pressure, vascular function, oxidative stress, ET-1 and prostanoid levels and kidney damage during angiogenesis inhibitor therapy in rodents.	Aspirin	116-123	endothelin 1	Homo sapiens	180-184
35600474-11	2022	In conclusion, the data of this pilot study indicate an inhibitory effect of rivaroxaban on the thrombin propagation phase of CD36-sensitive platelet thrombin formation in patients with PAD treated with ASA plus rivaroxaban combination therapy, which is associated with decreased PAR-1 but not thrombin-mediated platelet activation.	Aspirin	203-206	coagulation factor II, thrombin	Homo sapiens	96-104
35600474-11	2022	In conclusion, the data of this pilot study indicate an inhibitory effect of rivaroxaban on the thrombin propagation phase of CD36-sensitive platelet thrombin formation in patients with PAD treated with ASA plus rivaroxaban combination therapy, which is associated with decreased PAR-1 but not thrombin-mediated platelet activation.	Aspirin	203-206	coagulation factor II, thrombin	Homo sapiens	150-158
35600474-5	2022	ASA plus rivaroxaban treatment resulted in a significantly decreased thrombin peak in PRP for two triggers, namely, low concentration of tissue factor (TF) and thrombin, compared to ASA monotherapy.	Aspirin	0-3	coagulation factor II, thrombin	Homo sapiens	69-77
35433995-13	2022	Both doses of ASA + CPG decreased pro-inflammatory cytokine interleukin (IL)-6 expression 21 days after stroke.	Aspirin	14-17	interleukin 6	Homo sapiens	60-78
35600474-5	2022	ASA plus rivaroxaban treatment resulted in a significantly decreased thrombin peak in PRP for two triggers, namely, low concentration of tissue factor (TF) and thrombin, compared to ASA monotherapy.	Aspirin	0-3	coagulation factor II, thrombin	Homo sapiens	160-168
35600474-5	2022	ASA plus rivaroxaban treatment resulted in a significantly decreased thrombin peak in PRP for two triggers, namely, low concentration of tissue factor (TF) and thrombin, compared to ASA monotherapy.	Aspirin	182-185	coagulation factor II, thrombin	Homo sapiens	69-77
35600474-6	2022	TF-controlled thrombin generation was additionally characterized by a significantly prolonged lag time in PRP and platelet-free plasma during ASA plus rivaroxaban combination therapy.	Aspirin	142-145	coagulation factor II, thrombin	Homo sapiens	14-22
35600474-7	2022	In comparison, ASA plus clopidogrel treatment presented a significant reduction of the thrombin peak in PRP, which was less pronounced than during subsequent ASA plus rivaroxaban therapy.	Aspirin	15-18	coagulation factor II, thrombin	Homo sapiens	87-95
35629166-8	2022	Our research showed that patients can receive treatment with warfarin and aspirin with a personalized dosage and LVAD complications can be predicted by reference to their genotype polymorphisms in VKORC1, ITGB3 and UGT1A6 genes.	Aspirin	74-81	integrin subunit beta 3	Homo sapiens	205-210
35470674-0	2022	Acetylsalicylic Acid Is Associated With a Lower Prevalence of Ascending Aortic Aneurysm and a Decreased Aortic Expression of Cyclooxygenase 2.	Aspirin	0-20	prostaglandin-endoperoxide synthase 2	Homo sapiens	125-141
35470674-9	2022	In dilated, but not nondilated tricuspid aortic valve aortic specimens, ASA was associated with significantly lower cyclooxygenase-2 levels (P=0.034).	Aspirin	72-75	prostaglandin-endoperoxide synthase 2	Homo sapiens	116-132
35470674-10	2022	Conclusions Our findings are consistent with the hypothesis that ASA treatment may attenuate ascending aortic aneurysmal growth, possibly via cyclooxygenase-2 inhibition in the ascending aortic wall and subsequent anti-inflammatory actions.	Aspirin	65-68	prostaglandin-endoperoxide synthase 2	Homo sapiens	142-158
35416588-12	2022	Likelihood of death following a COVID-19 infection was also higher in those people with a diagnosis of chronic obstructive pulmonary disease (COPD) or severe enduring mental illness but not with asthma, and in people taking aspirin/clopidogrel/insulin.	Aspirin	224-231	insulin	Homo sapiens	244-251
35434898-12	2022	Aspirin abrogated the secretion of VEGF-C in MSCs and also decreased the lymph/angiogenic potential of the MSCs and HCC1954 by tubule formation assay.	Aspirin	0-7	vascular endothelial growth factor C	Homo sapiens	35-41
35434898-13	2022	Furthermore, aspirin decreased the secretion of uPA in HCC1954 cells potentially diminishing its metastatic capability.	Aspirin	13-20	proline rich acidic protein 1	Homo sapiens	48-51
35366826-11	2022	Finally, three compounds for the treatment of glaucoma were obtained in the TCMs database: acetylsalicylic acid, 7-o-methylisomucitol and scutellarin which were applied to molecular docking with the diagnostic biomarker ENO2.	Aspirin	91-111	enolase 2	Homo sapiens	220-224
35366783-7	2022	In COVID-19 patients, aspirin can reduce CRP, IL-6 levels, and platelet aggregation by inhibiting thromboxane A2.	Aspirin	22-29	C-reactive protein	Homo sapiens	41-44
35366783-7	2022	In COVID-19 patients, aspirin can reduce CRP, IL-6 levels, and platelet aggregation by inhibiting thromboxane A2.	Aspirin	22-29	interleukin 6	Homo sapiens	46-50
35000048-0	2022	COX-1, COX-2 and CYP2C19 variations may be related to cardiovascular events due to acetylsalicylic acid resistance.	Aspirin	83-103	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	7-12
35262138-8	2022	Additionally, DHC could attenuate IgE/Ag-induced allergic reactions (dye extravasation and ear thickening) in PCA as well as OVA challenge-induced reactions in ASA mice (body temperature, serum histamine and IL-4 secretion changes).	Aspirin	160-163	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	125-128
35183904-1	2022	BACKGROUND AND AIMS: The platelet inhibitor aspirin reduces inflammation and atherosclerosis in both apolipoprotein E deficient (apoE-/-) mice and low-density lipoprotein receptor deficient (Ldlr-/-) mice.	Aspirin	44-51	apolipoprotein E	Mus musculus	129-133
35373259-3	2022	Compared with colorectal cancer, the role of aspirin in gastric cancer prevention is less well described, however it stands to reason that aspirin and/or other nonsteroidal anti-inflammatory drugs may inhibit gastric cancer progression through the inhibition of COX-2.	Aspirin	139-146	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	262-267
35392432-0	2022	Aspirin Suppressed PD-L1 Expression through Suppressing KAT5 and Subsequently Inhibited PD-1 and PD-L1 Signaling to Attenuate OC Development.	Aspirin	0-7	CD274 antigen	Mus musculus	19-24
35392432-0	2022	Aspirin Suppressed PD-L1 Expression through Suppressing KAT5 and Subsequently Inhibited PD-1 and PD-L1 Signaling to Attenuate OC Development.	Aspirin	0-7	CD274 antigen	Mus musculus	97-102
35392432-5	2022	In this work, we explored the role of ASP in modulating PD-L1 signaling during OC development.	Aspirin	38-41	CD274 antigen	Mus musculus	56-61
35392432-8	2022	ASP treatment also caused downregulated PD-L1 and Ki-67 levels in mice tumors.	Aspirin	0-3	CD274 antigen	Mus musculus	40-45
35392432-9	2022	Moreover, the IFN-gamma-caused PD-L1 accumulation was inhibited by ASP treatment.	Aspirin	67-70	interferon gamma	Mus musculus	14-23
35392432-9	2022	Moreover, the IFN-gamma-caused PD-L1 accumulation was inhibited by ASP treatment.	Aspirin	67-70	CD274 antigen	Mus musculus	31-36
35392432-10	2022	The administration of ASP decreased the expression of PD-L1 of OC cells in a coculture system with activated T cell or unstimulated PBMCs, along with decreased expression of PD-1 by activated T cells.	Aspirin	22-25	CD274 molecule	Sus scrofa	54-59
35392432-11	2022	ASP reversed PD-L1 expression caused by coculture with activated T cells and abolished the suppressed T cells activation and proliferation.	Aspirin	0-3	CD274 molecule	Sus scrofa	13-18
35392432-12	2022	Analysis on molecular mechanisms revealed that KAT5 bonded to the promoter region of PD-L1 and upregulated its expression via enhancing histone H3 lysine 27 acetylation (H3K27ac), whereas ASP downregulated KAT5 expression and blocked this phenomenon.	Aspirin	188-191	CD274 molecule	Sus scrofa	85-90
35392432-14	2022	Hence, we proposed that ASP decreased expression of PD-L1 protein via inhibiting the epigenetic regulation by KAT5 and suppressed the PD-1/PD-L1 signaling to attenuate tumor growth.	Aspirin	24-27	CD274 molecule	Sus scrofa	52-57
35392432-14	2022	Hence, we proposed that ASP decreased expression of PD-L1 protein via inhibiting the epigenetic regulation by KAT5 and suppressed the PD-1/PD-L1 signaling to attenuate tumor growth.	Aspirin	24-27	CD274 molecule	Sus scrofa	139-144
35434414-11	2022	Conclusions: Smaller ASA was an independent risk factor and had significant incremental value for CTRCD in patients with malignant lymphoma who received the CHOP-like regimen.	Aspirin	21-24	DNA damage inducible transcript 3	Homo sapiens	157-161
35401184-0	2022	Association Between Aspirin Usage and Age-Related Macular Degeneration: An Updated Systematic Review and Meta-analysis.	Aspirin	20-27	renin binding protein	Homo sapiens	38-41
35401184-1	2022	Purpose: To investigate the association between long-term use of aspirin and age-related macular degeneration (AMD).	Aspirin	65-72	renin binding protein	Homo sapiens	77-80
35433995-14	2022	Taken together, these results demonstrated that combination treatment with ASA + CPG improved long-term neurological function after stroke and may inhibit platelet-neutrophil interaction by decreasing the concentration of pro-inflammatory cytokine, IL-6.	Aspirin	75-78	interleukin 6	Homo sapiens	249-253
35335908-0	2022	Acetylsalicylic Acid Suppresses Alcoholism-Induced Cognitive Impairment Associated with Atorvastatin Intake by Targeting Cerebral miRNA155 and NLRP3: In Vivo, and In Silico Study.	Aspirin	0-20	NLR family pyrin domain containing 3	Homo sapiens	143-148
35268679-10	2022	Similarly, we found that 4-MU decreased body temperature, serum histamine, and IL4 secretion in OVA-challenged ASA model mice.	Aspirin	111-114	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	96-99
35335908-8	2022	ASA significantly decreased the expression levels of miRNA155, NLRP3, and IL1B, and produced a significant decrease in caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex with a reduction in the process of neuroinflammation and neuronal damage.	Aspirin	0-3	NLR family pyrin domain containing 3	Homo sapiens	63-68
35142767-7	2022	In vitro assays suggested that this combinatory group alleviated LPS-induced inflammation in BV-2 cells, as assessed by the downregulation of nitric oxide, COX-2, and IL-6 compared to 10-HDAA or aspirin treatment alone.	Aspirin	195-202	interleukin 6	Mus musculus	167-171
35335908-8	2022	ASA significantly decreased the expression levels of miRNA155, NLRP3, and IL1B, and produced a significant decrease in caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex with a reduction in the process of neuroinflammation and neuronal damage.	Aspirin	0-3	interleukin 1 beta	Homo sapiens	74-78
35335908-9	2022	To further investigate these findings, we have performed an extensive molecular docking study to investigate the binding affinity of ASA to the binding pockets of the NLRP3 protein.	Aspirin	133-136	NLR family pyrin domain containing 3	Homo sapiens	167-172
35335908-10	2022	Our results indicated that ASA has high binding scores toward the active sites of the NLRP3 NACHT domain with the ability to bind to the NLRP3 pockets by a set of hydrophilic and hydrophobic interactions.	Aspirin	27-30	NLR family pyrin domain containing 3	Homo sapiens	86-91
35335908-10	2022	Our results indicated that ASA has high binding scores toward the active sites of the NLRP3 NACHT domain with the ability to bind to the NLRP3 pockets by a set of hydrophilic and hydrophobic interactions.	Aspirin	27-30	NLR family pyrin domain containing 3	Homo sapiens	137-142
35335908-11	2022	Taken together, the present study highlights the protective pharmacological effect of ASA to attenuate the deleterious effect of alcohol intake and long term ATOR therapy on the cognitive function via targeting miRNA155 and NLRP3 proteins.	Aspirin	86-89	NLR family pyrin domain containing 3	Homo sapiens	224-229
35177224-14	2022	Cyclooxygenase-2 seems to be a downstream mediator between protease-activated receptor 1 and RhoA kinase because aspirin inhibits the nuclear translocation of nuclear factor-kappa B and inhibits neutrophil production of superoxide, thromboxane, and tumor necrosis factor alpha.	Aspirin	113-120	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-16
35067692-4	2022	It has been shown that the biosynthesis of SPMs called eicosapentaenoic acid (EPA)-derived E-series resolvins is initiated by aspirin-acetylated COX-2 from EPA, leading to 18-hydroperoxy-eicosapentaenoic acid (18-HpEPE).	Aspirin	126-133	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	145-150
35067692-7	2022	By contrast, in the aspirin-acetylated COX-2/EPA complex, the H16proS-abstraction energy barriers are somewhat lower than the H13proS energy barriers and much smaller than the H16-transfer barriers in the wild type COX-2/EPA system.	Aspirin	20-27	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	39-44
35067692-7	2022	By contrast, in the aspirin-acetylated COX-2/EPA complex, the H16proS-abstraction energy barriers are somewhat lower than the H13proS energy barriers and much smaller than the H16-transfer barriers in the wild type COX-2/EPA system.	Aspirin	20-27	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	215-220
35067692-9	2022	In the following step of the catalytic mechanism, the calculated O2 addition to C18 is preferred versus the addition to C14 which also agrees with 18R-HEPE and 18S-HEPE being the main products from EPA in aspirin-acetylated COX-2.	Aspirin	205-212	Bardet-Biedl syndrome 9	Homo sapiens	80-83
35067692-9	2022	In the following step of the catalytic mechanism, the calculated O2 addition to C18 is preferred versus the addition to C14 which also agrees with 18R-HEPE and 18S-HEPE being the main products from EPA in aspirin-acetylated COX-2.	Aspirin	205-212	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	224-229
35108049-5	2022	Inhibition of AT-SPM biosynthesis or knockout of the AT-SPM receptor Alx/Fpr2 reversed the immunomodulatory actions of aspirin on macrophages and CD8+ T cells and abrogated its protective effects during I-CRC.	Aspirin	119-126	formyl peptide receptor 3	Mus musculus	69-72
35177224-14	2022	Cyclooxygenase-2 seems to be a downstream mediator between protease-activated receptor 1 and RhoA kinase because aspirin inhibits the nuclear translocation of nuclear factor-kappa B and inhibits neutrophil production of superoxide, thromboxane, and tumor necrosis factor alpha.	Aspirin	113-120	coagulation factor II thrombin receptor	Homo sapiens	59-88
35177224-14	2022	Cyclooxygenase-2 seems to be a downstream mediator between protease-activated receptor 1 and RhoA kinase because aspirin inhibits the nuclear translocation of nuclear factor-kappa B and inhibits neutrophil production of superoxide, thromboxane, and tumor necrosis factor alpha.	Aspirin	113-120	tumor necrosis factor	Homo sapiens	249-276
35197754-9	2022	The linsitinib and aspirin as the IGF1-R antagonists inhibited colon cancer resistance against regorafenib, stem-cell like colon cancer cells growth, decreased expression of CD133, CD44, CD24, and also increased CDX2, PTEN gene expression.	Aspirin	19-26	CD24 molecule	Homo sapiens	187-191
35127290-6	2022	Results: SA-beta-gal staining, PCR, and western blot revealed that aspirin could alleviate the cellular expression of senescence-related indicators of BM-MSCs, including a decrease of SA-beta-gal-positive cells and staining intensity, and downregulation of p16, p21, and p53 expression after aspirin treatment.	Aspirin	67-74	cyclin dependent kinase inhibitor 2A	Homo sapiens	257-260
35127290-6	2022	Results: SA-beta-gal staining, PCR, and western blot revealed that aspirin could alleviate the cellular expression of senescence-related indicators of BM-MSCs, including a decrease of SA-beta-gal-positive cells and staining intensity, and downregulation of p16, p21, and p53 expression after aspirin treatment.	Aspirin	67-74	tumor protein p53	Homo sapiens	271-274
35015330-1	2022	OBJECTIVE: To compare the predictive performance for preterm-preeclampsia (PE) in first-trimester screening by serum placental growth factor (PlGF) vs. pregnancy associated plasma protein-A (PAPP-A), in combinations with maternal risk factors, mean arterial pressure (MAP) and uterine artery pulsatility index (UtA-PI), after adjustment for the effect of aspirin in women receiving this treatment.	Aspirin	355-362	placental growth factor	Homo sapiens	117-140
35111059-0	2021	Aspirin Attenuates Hyperoxia-Induced Acute Respiratory Distress Syndrome (ARDS) by Suppressing Pulmonary Inflammation via the NF-kappaB Signaling Pathway.	Aspirin	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	126-135
35111059-11	2021	However, in vivo imaging revealed that posttreatment with aspirin reduced luciferase expression, suggesting that aspirin might reduce NF-kappaB activation.	Aspirin	58-65	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	134-143
35111059-11	2021	However, in vivo imaging revealed that posttreatment with aspirin reduced luciferase expression, suggesting that aspirin might reduce NF-kappaB activation.	Aspirin	113-120	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	134-143
35111059-12	2021	Posttreatment with aspirin also reduced hyperoxia-induced increases in the numbers of lung macrophages, intracellular ROS levels, and the expression of TNF-alpha, IL-1beta, and IL-4; it also increased CC10, SPC and Nrp-1 levels compared with hyperoxia exposure alone.	Aspirin	19-26	tumor necrosis factor	Mus musculus	152-161
35111059-12	2021	Posttreatment with aspirin also reduced hyperoxia-induced increases in the numbers of lung macrophages, intracellular ROS levels, and the expression of TNF-alpha, IL-1beta, and IL-4; it also increased CC10, SPC and Nrp-1 levels compared with hyperoxia exposure alone.	Aspirin	19-26	sparse coat	Mus musculus	207-210
35111059-12	2021	Posttreatment with aspirin also reduced hyperoxia-induced increases in the numbers of lung macrophages, intracellular ROS levels, and the expression of TNF-alpha, IL-1beta, and IL-4; it also increased CC10, SPC and Nrp-1 levels compared with hyperoxia exposure alone.	Aspirin	19-26	neuropilin 1	Mus musculus	215-220
35015330-1	2022	OBJECTIVE: To compare the predictive performance for preterm-preeclampsia (PE) in first-trimester screening by serum placental growth factor (PlGF) vs. pregnancy associated plasma protein-A (PAPP-A), in combinations with maternal risk factors, mean arterial pressure (MAP) and uterine artery pulsatility index (UtA-PI), after adjustment for the effect of aspirin in women receiving this treatment.	Aspirin	355-362	placental growth factor	Homo sapiens	142-146
34983353-2	2022	By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies.	Aspirin	87-107	prostaglandin-endoperoxide synthase 1	Homo sapiens	17-39
34983353-2	2022	By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies.	Aspirin	87-107	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	51-56
34983353-2	2022	By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies.	Aspirin	109-116	prostaglandin-endoperoxide synthase 1	Homo sapiens	17-39
34983353-2	2022	By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies.	Aspirin	109-116	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	51-56
2697116-7	1989	Our data suggest that coadministration of ranitidine 150 mg bid reduces almost completely gastroduodenal lesions evoked by acetylsalicylic acid 300 mg daily.	Aspirin	123-143	BH3 interacting domain death agonist	Homo sapiens	60-63
2517685-3	1989	Bradykinin-induced relaxation was not inhibited by acetylsalicylic acid (10(-4) M), indomethacin (10(-6) M), and combined treatment with phentolamine (10(-6) M) and propranolol (10(-6) M).	Aspirin	51-71	kininogen 1	Homo sapiens	0-10
2529923-0	1989	Effect of aspirin on platelet-von Willebrand factor surface expression on thrombin and ADP-stimulated platelets.	Aspirin	10-17	von Willebrand factor	Homo sapiens	21-51
2529923-0	1989	Effect of aspirin on platelet-von Willebrand factor surface expression on thrombin and ADP-stimulated platelets.	Aspirin	10-17	coagulation factor II, thrombin	Homo sapiens	74-82
2529923-4	1989	We studied native and ASA-treated platelets for their ability to mobilize and to express platelet-vWF in response to adenosine diphosphate (ADP) or thrombin.	Aspirin	22-25	von Willebrand factor	Homo sapiens	98-101
2529923-4	1989	We studied native and ASA-treated platelets for their ability to mobilize and to express platelet-vWF in response to adenosine diphosphate (ADP) or thrombin.	Aspirin	22-25	coagulation factor II, thrombin	Homo sapiens	148-156
2529923-5	1989	We found that each agonist was effective in promoting increased platelet-vWF surface expression on native and ASA-treated platelets.	Aspirin	110-113	von Willebrand factor	Homo sapiens	73-76
2529923-6	1989	ASA-treated platelets responded identically to native platelets to low (0.01 U/mL) and high (1.0 U/mL) concentrations of thrombin, while the ADP-induced increase in ASA-treated platelets was only 50% to 60% of that for control platelets.	Aspirin	0-3	coagulation factor II, thrombin	Homo sapiens	121-129
2529923-9	1989	In contrast, the increase in platelet-vWF that occurred following ADP stimulation of ASA-treated platelets was largely insensitive to GPIIb/IIIa blockade.	Aspirin	85-88	von Willebrand factor	Homo sapiens	38-41
2529923-11	1989	When platelet shape change was prevented by the addition of cytochalasin D, ADP-induced platelet-vWf surface expression on ASA-treated platelets was reduced by more than 80%.	Aspirin	123-126	von Willebrand factor	Homo sapiens	97-100
2529923-12	1989	Our data indicate that platelets in which the cyclooxygenase pathway is blocked by the action of aspirin can increase surface expression of platelet-vWf as a consequence of platelet shape change.	Aspirin	97-104	von Willebrand factor	Homo sapiens	149-152
2590611-2	1989	Effects of a single intravenous dose of aspirin (600 mg) on bradykinin-stimulated prostaglandin (PG) and on thromboxane (TX) biosynthesis were determined in nine healthy male volunteers.	Aspirin	40-47	kininogen 1	Homo sapiens	60-70
2590611-5	1989	Aspirin inhibited bradykinin stimulated PG and platelet TX biosynthesis 0.5 h after the dose.	Aspirin	0-7	kininogen 1	Homo sapiens	18-28
2621419-7	1989	Moreover, 12-HETE production in the presence of albumin was markedly increased and prolonged after aspirin treatment.	Aspirin	99-106	albumin	Homo sapiens	48-55
2590612-4	1989	This dose of aspirin caused more than a 5 fold increase in gastric bleeding, from control values of 0.5 microliters 10 min-1 (95% confidence limits 0.3-0.8 microliters 10 min-1) to 2.8 microliters 10 min-1 (1.9-4.1 microliters 10 min-1, P less than 0.01) after 5 days of aspirin.	Aspirin	13-20	CD59 molecule (CD59 blood group)	Homo sapiens	119-124
2590612-5	1989	Adaptation did not occur and the gastric bleeding rates remained elevated at 3.4 microliters 10 min-1 (1.9-6.1 microliters 10 min-1) after 12 days of aspirin consumption (P less than 0.01).	Aspirin	150-157	CD59 molecule (CD59 blood group)	Homo sapiens	126-131
2590612-7	1989	Coadministration of ranitidine significantly raised intragastric pH and reduced aspirin induced bleeding to 1.5 microliters 10 min-1 (1.0-2.3 microliters 10 min-1) after 5 days and 1.6 (1.0-2.5 microliters 10 min-1) after 12 days (P less than 0.05).	Aspirin	80-87	CD59 molecule (CD59 blood group)	Homo sapiens	127-132
2590612-4	1989	This dose of aspirin caused more than a 5 fold increase in gastric bleeding, from control values of 0.5 microliters 10 min-1 (95% confidence limits 0.3-0.8 microliters 10 min-1) to 2.8 microliters 10 min-1 (1.9-4.1 microliters 10 min-1, P less than 0.01) after 5 days of aspirin.	Aspirin	13-20	CD59 molecule (CD59 blood group)	Homo sapiens	171-176
2590612-4	1989	This dose of aspirin caused more than a 5 fold increase in gastric bleeding, from control values of 0.5 microliters 10 min-1 (95% confidence limits 0.3-0.8 microliters 10 min-1) to 2.8 microliters 10 min-1 (1.9-4.1 microliters 10 min-1, P less than 0.01) after 5 days of aspirin.	Aspirin	13-20	CD59 molecule (CD59 blood group)	Homo sapiens	171-176
2590612-4	1989	This dose of aspirin caused more than a 5 fold increase in gastric bleeding, from control values of 0.5 microliters 10 min-1 (95% confidence limits 0.3-0.8 microliters 10 min-1) to 2.8 microliters 10 min-1 (1.9-4.1 microliters 10 min-1, P less than 0.01) after 5 days of aspirin.	Aspirin	13-20	CD59 molecule (CD59 blood group)	Homo sapiens	171-176
2746495-0	1989	Aspirin acetylates fibrinogen and enhances fibrinolysis.	Aspirin	0-7	fibrinogen beta chain	Homo sapiens	19-29
2808538-3	1989	When indomethacin or acetylsalicylic acid, an inhibitor of prostaglandin production, was added to FS-4 cells, cell growth stimulated by EGF or TNF was increased, suggesting that prostaglandins induced by these mitogens antagonize their growth stimulatory actions.	Aspirin	21-41	tumor necrosis factor	Homo sapiens	143-146
2529003-1	1989	The observation that aspirin inhibits the increment in tissue plasminogen activator (t-PA) activity induced by venous occlusion of the forearm became controversial with the publication of several nonconfirmatory studies.	Aspirin	21-28	plasminogen activator, tissue type	Homo sapiens	55-89
2789070-7	1989	Aspirin increased bleeding from a rate on placebo of 1.2 microliters 10 min-1 geometric mean (95% confidence limits) (0.7-1.8) microliters 10 min-1 to 20.0 (11.6-34.2) microliters 10 min-1, (P less than 0.01).	Aspirin	0-7	CD59 molecule (CD59 blood group)	Homo sapiens	72-77
2789070-7	1989	Aspirin increased bleeding from a rate on placebo of 1.2 microliters 10 min-1 geometric mean (95% confidence limits) (0.7-1.8) microliters 10 min-1 to 20.0 (11.6-34.2) microliters 10 min-1, (P less than 0.01).	Aspirin	0-7	CD59 molecule (CD59 blood group)	Homo sapiens	142-147
2789070-7	1989	Aspirin increased bleeding from a rate on placebo of 1.2 microliters 10 min-1 geometric mean (95% confidence limits) (0.7-1.8) microliters 10 min-1 to 20.0 (11.6-34.2) microliters 10 min-1, (P less than 0.01).	Aspirin	0-7	CD59 molecule (CD59 blood group)	Homo sapiens	142-147
2789070-8	1989	The rate of bleeding after aspirin preceded by ethamsylate [14.1 (8.5-23.4) microliters 10 min-1] was not significantly different from that after aspirin alone.	Aspirin	27-34	CD59 molecule (CD59 blood group)	Homo sapiens	91-96
2730914-1	1989	Removal of extracellular sodium decreased calcium mobilization from intracellular stores induced by thrombin in aspirin-treated human platelets.	Aspirin	112-119	coagulation factor II, thrombin	Homo sapiens	100-108
2494147-0	1989	Effect of scavengers of active oxygen species and pretreatment with acetyl-salicylic acid on the injury to cultured endothelial cells by thrombin-stimulated platelets.	Aspirin	68-89	coagulation factor II, thrombin	Homo sapiens	137-145
2504679-5	1989	Peak IFN-gamma production by PHA-stimulated PBLs was observed after 24 h of incubation with TF5 and after 72 h with aspirin.	Aspirin	116-123	interferon gamma	Homo sapiens	5-14
2504679-8	1989	Oral administration of aspirin in normal volunteers significantly enhanced production of both IFN-gamma and IL-2.	Aspirin	23-30	interferon gamma	Homo sapiens	94-103
2504679-8	1989	Oral administration of aspirin in normal volunteers significantly enhanced production of both IFN-gamma and IL-2.	Aspirin	23-30	interleukin 2	Homo sapiens	108-112
2504679-9	1989	PHA-stimulated IFN-gamma production was greatest 24 h after aspirin ingestion; in contrast, IL-2 production was optimal 10 h after aspirin ingestion.	Aspirin	131-138	interleukin 2	Homo sapiens	92-96
2653334-6	1989	Substantial evidence already indicates that low-dose aspirin therapy decreases the incidence of preeclampsia; it decreases the maternal systemic arterial pressor response to angiotensin II; and it does not seem to be harmful to the fetus.	Aspirin	53-60	angiotensinogen	Homo sapiens	174-188
2498343-7	1989	With aspirin-treated platelets that had not secreted, EDTA, PGE1, and MB all caused disaggregation and loss of cytoskeletal GP IIIa.	Aspirin	5-12	integrin subunit beta 3	Homo sapiens	124-131
2513995-4	1989	Aspirin selectively stimulates the proliferative responses of T-lymphocytes in part by enhancing IL-2 production.	Aspirin	0-7	interleukin 2	Homo sapiens	97-101
2708229-4	1989	Similarly, methylene blue or aspirin augmented the pressor responses to angiotensin II (0.1-1 microgram).	Aspirin	29-36	angiotensinogen	Rattus norvegicus	72-86
2504679-0	1989	Aspirin and thymosin increase interleukin-2 and interferon-gamma production by human peripheral blood lymphocytes.	Aspirin	0-7	interleukin 2	Homo sapiens	30-43
2504679-0	1989	Aspirin and thymosin increase interleukin-2 and interferon-gamma production by human peripheral blood lymphocytes.	Aspirin	0-7	interferon gamma	Homo sapiens	48-64
2504679-3	1989	Stimulation by oral aspirin of IL-2 and IFN-gamma production by peripheral blood lymphocytes (PBLs) was also studied in healthy human volunteers.	Aspirin	20-27	interleukin 2	Homo sapiens	31-35
2492343-11	1989	Partial inhibition (approximately 50%) of PGI2 production by aspirin (5.6 microM) treatment resulted in a paradoxically decreased vasoconstriction except at the lowest level of serotonin and vasopressin.	Aspirin	61-68	arginine vasopressin	Rattus norvegicus	191-202
2547543-2	1989	Aspirin (100 mg/day)-treated and nontreated rats were fed for 7 days, a mixed diet of 2.5% safflower oil and 7.5% hydrogenated coconut oil (SFO/HCO) or 7.5% fish oil (SFO/FO), or 2.5% gamma-linolenate concentrate and 7.5% fish oil (GLA/FO).	Aspirin	0-7	galactosidase, alpha	Rattus norvegicus	232-235
3189434-4	1988	This study was designed to ascertain if low-dose aspirin therapy (81 mg/day for 1 week) alters vascular refractoriness to angiotensin II and the prostacyclin/thromboxane A2 ratio in pregnant women sensitive to angiotensin II (n = 17).	Aspirin	49-56	angiotensinogen	Homo sapiens	122-136
3146370-19	1988	CONCLUSION: Recombinant tissue type plasminogen activator with heparin and aspirin reduces size of infarct, preserves left ventricular function, and reduces complications and death from cardiac causes but at increased risk of bleeding complications4+	Aspirin	75-82	plasminogen activator, tissue type	Homo sapiens	24-57
3189434-4	1988	This study was designed to ascertain if low-dose aspirin therapy (81 mg/day for 1 week) alters vascular refractoriness to angiotensin II and the prostacyclin/thromboxane A2 ratio in pregnant women sensitive to angiotensin II (n = 17).	Aspirin	49-56	angiotensinogen	Homo sapiens	210-224
3189434-5	1988	Low-dose aspirin increased the effective pressor dose of angiotensin II from 5.9 +/- 2.4 to 10.2 +/- 5.5 ng/kg/min (p less than 0.01, mean +/- SD).	Aspirin	9-16	angiotensinogen	Homo sapiens	57-71
3189434-10	1988	Although low-dose aspirin increases the effective pressor dose of angiotensin II, it does not return to normal pregnancy values.	Aspirin	18-25	angiotensinogen	Homo sapiens	66-80
3147804-5	1988	Contractions induced by bradykinin were also attenuated by indomethacin, aspirin and DPP.	Aspirin	73-80	kininogen 1	Canis lupus familiaris	24-34
3176082-6	1988	Aspirin treatment reduced baseline [Cai2+] as well as thrombin- and collagen-induced [Cai2+] changes.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	54-62
3229444-0	1988	Insulin receptors and glucose homeostasis in type 2 diabetics influenced by acetyl-salicylic acid treatment.	Aspirin	76-97	insulin	Homo sapiens	0-7
3229444-1	1988	The effect of acetyl-salicylic acid administration on insulin receptors on the erythrocytes and the changes of glucose homeostasis examined by hyperglycaemic clamps were evaluated in 8 Type 2 diabetics.	Aspirin	14-35	insulin	Homo sapiens	54-61
3229444-2	1988	Significantly increased number of insulin receptors and decreased insulin affinity constants were found in diabetics after the acetyl-salicylic acid treatment (p less than 0.02).	Aspirin	127-148	insulin	Homo sapiens	34-41
3229444-2	1988	Significantly increased number of insulin receptors and decreased insulin affinity constants were found in diabetics after the acetyl-salicylic acid treatment (p less than 0.02).	Aspirin	127-148	insulin	Homo sapiens	66-73
3229444-3	1988	Significantly decreased tissue sensitivity to insulin and metabolic clearance rate of insulin (p less than 0.02) were observed in Type 2 diabetics after the acetyl-salicylic acid treatment.	Aspirin	157-178	insulin	Homo sapiens	46-53
3229444-3	1988	Significantly decreased tissue sensitivity to insulin and metabolic clearance rate of insulin (p less than 0.02) were observed in Type 2 diabetics after the acetyl-salicylic acid treatment.	Aspirin	157-178	insulin	Homo sapiens	86-93
3229444-4	1988	We conclude that acetyl-salicylic acid may impair glucose homeostasis due to interference with insulin action in peripheral tissues.	Aspirin	17-38	insulin	Homo sapiens	95-102
2455569-7	1988	CP/CPK or aspirin alone reduced fibrinogen binding to 20% to 30%; however, this binding was sufficient to support full platelet aggregation.	Aspirin	10-17	fibrinogen beta chain	Homo sapiens	32-42
2455569-8	1988	Combined treatment with CP/CPK and aspirin abolished fibrinogen binding and aggregation.	Aspirin	35-42	fibrinogen beta chain	Homo sapiens	53-63
3413736-5	1988	Furthermore, the von Willebrand factor (vWF) dependent platelet aggregation induced by 0.6 and 1.0 mg/ml ristocetin was clearly diminished after ASA.	Aspirin	145-148	von Willebrand factor	Homo sapiens	17-38
3413736-5	1988	Furthermore, the von Willebrand factor (vWF) dependent platelet aggregation induced by 0.6 and 1.0 mg/ml ristocetin was clearly diminished after ASA.	Aspirin	145-148	von Willebrand factor	Homo sapiens	40-43
2842885-2	1988	Using a new method in which thrombin-induced platelet aggregation was measured in the presence of endothelial cells, we showed that aspirin-treated endothelial cells inhibited platelet aggregating activity of thrombin in an incubation time- and cell number-dependent manner.	Aspirin	132-139	coagulation factor II, thrombin	Homo sapiens	28-36
2842885-2	1988	Using a new method in which thrombin-induced platelet aggregation was measured in the presence of endothelial cells, we showed that aspirin-treated endothelial cells inhibited platelet aggregating activity of thrombin in an incubation time- and cell number-dependent manner.	Aspirin	132-139	coagulation factor II, thrombin	Homo sapiens	209-217
2845746-5	1988	The different effects of NSAIDs on 5-lipoxygenase activity may be of importance in their therapeutic actions as well as in the appearance of some side-effects, e.g. gastric irritation and "aspirin-induced" asthma.	Aspirin	189-196	arachidonate 5-lipoxygenase	Homo sapiens	35-49
2970689-6	1988	In endotoxin-infused rats pretreated with aspirin the PAA changes induced by endotoxin were prevented or modified; PAI and PI were affected in most organs studied.	Aspirin	42-49	serpin family E member 1	Rattus norvegicus	115-118
3365912-3	1988	The frequency of probably drug-related AST elevations was highest (5%) with aspirin; with oxaprozin, an investigational nonsteroidal antiinflammatory drug, the incidence (3%) fell between that for the other two agents.	Aspirin	76-83	solute carrier family 17 member 5	Homo sapiens	39-42
2970689-10	1988	The results of the present study show that the response of PAA, PAI and PI to aspirin depends on the tissue, the physiological or pathophysiological condition of the tissue and the dose of the aspirin.	Aspirin	78-85	serpin family E member 1	Rattus norvegicus	64-67
2970689-10	1988	The results of the present study show that the response of PAA, PAI and PI to aspirin depends on the tissue, the physiological or pathophysiological condition of the tissue and the dose of the aspirin.	Aspirin	193-200	serpin family E member 1	Rattus norvegicus	64-67
3398694-2	1988	administration of acetylsalicylic acid (ASA) to CCl4-cirrhotic rats to rats which in addition to CCl4 received an oral dose of silymarin throughout the CCl4 treatment to produce cirrhosis and to control groups.	Aspirin	18-38	C-C motif chemokine ligand 4	Rattus norvegicus	48-52
3276731-5	1988	When prostaglandin synthesis was inhibited by indomethacin or aspirin both rIL-1 alpha and beta (greater than or equal to 1 ng/ml) markedly increased SMC growth.	Aspirin	62-69	interleukin 1 alpha	Rattus norvegicus	75-86
3398694-2	1988	administration of acetylsalicylic acid (ASA) to CCl4-cirrhotic rats to rats which in addition to CCl4 received an oral dose of silymarin throughout the CCl4 treatment to produce cirrhosis and to control groups.	Aspirin	40-43	C-C motif chemokine ligand 4	Rattus norvegicus	48-52
2892555-13	1987	Aspirin also inhibited the wheal formed by NKA but not the wheal induced by the other substances.	Aspirin	0-7	tachykinin precursor 1	Homo sapiens	43-46
2892555-12	1987	Aspirin (600 mg orally) significantly inhibited the distant flare response to SP, NKA and CGRP, but not that caused by NKB or histamine; the local erythema induced by CGRP was unaffected by aspirin.	Aspirin	0-7	tachykinin precursor 1	Homo sapiens	82-85
2892555-12	1987	Aspirin (600 mg orally) significantly inhibited the distant flare response to SP, NKA and CGRP, but not that caused by NKB or histamine; the local erythema induced by CGRP was unaffected by aspirin.	Aspirin	0-7	calcitonin related polypeptide alpha	Homo sapiens	90-94
3417210-3	1988	Sodium salicylate (SA) and aspirin also inhibited cathepsin D, although the apparent inhibition was observed at the concentrations of 5 mM or above.	Aspirin	27-34	cathepsin D	Rattus norvegicus	50-61
3417210-5	1988	The maximal inhibitory potencies of indomethacin and aspirin against cathepsin D activity were observed at pH values below 4.0, whereas that of flufenamic acid was at pH values above 7.0.	Aspirin	53-60	cathepsin D	Rattus norvegicus	69-80
2966694-1	1987	This study was designed to examine the effects of aspirin, naloxone and placebo treatment on serum beta-endorphin concentration and joint pain in patients with rheumatoid arthritis (RA).	Aspirin	50-57	proopiomelanocortin	Homo sapiens	99-113
3691277-2	1987	Two enzymatic antioxidants, superoxide dismutase or catalase injected intravenously, reduced mucosal damage either by ethanol or aspirin.	Aspirin	129-136	catalase	Rattus norvegicus	52-60
3130280-7	1987	In the patient group, E produced a significant decrease in aspirin-induced DP Max (11.8 +/- 1.9 vs 6.8 +/- 2.4) (p less than 0.003) and in AUC (117 +/- vs 48 less than 22) (p less than 0.006) as well as in TRB (52 +/- 2 vs 37 +/- 10) (p less than 0.05).	Aspirin	59-66	T cell receptor beta locus	Homo sapiens	206-209
3429760-0	1987	Aspirin disposition in rats acutely intoxicated with CCl4.	Aspirin	0-7	C-C motif chemokine ligand 4	Rattus norvegicus	53-57
2825688-4	1987	This effect of bradykinin was unaffected by aspirin, and was accounted for by the amounts of NO released by the endothelial cells.	Aspirin	44-51	kininogen 1	Homo sapiens	15-25
2889967-3	1987	The inhibitory action of both bradykinin and nitric oxide was abolished by haemoglobin, but not by aspirin, and was potentiated by superoxide dismutase to a similar degree.	Aspirin	99-106	kininogen 1	Homo sapiens	30-40
2822171-10	1987	Aspirin and prostaglandin E1 also inhibited ADP-induced binding of vWf in platelet-rich plasma.	Aspirin	0-7	von Willebrand factor	Homo sapiens	67-70
3555002-6	1987	Indeed, administration of indomethacin or aspirin results in an increased sensitivity to infused AII in normotensive previously AII-refractory women.	Aspirin	42-49	angiotensinogen	Homo sapiens	97-100
3667609-6	1987	Treatment of platelets with aspirin, incubation in the presence of creatine phosphate/creatine phosphokinase, or omission of Ca2+ and fibrinogen do not affect toxin-mediated phospholipase C activation.	Aspirin	28-35	fibrinogen beta chain	Homo sapiens	67-144
3115269-0	1987	Heterogeneity of changes on the disposition of aspirin in rats with CCl4-induced chronic liver damage.	Aspirin	47-54	C-C motif chemokine ligand 4	Rattus norvegicus	68-72
3497679-4	1987	Aspirin and the thromboxane receptor blocker BM 13.177 inhibited these secondary responses to von Willebrand factor, indicating that they require thromboxane A2 formation and feedback amplification by thromboxane A2.	Aspirin	0-7	von Willebrand factor	Homo sapiens	94-115
3435662-6	1987	Aspirin significantly inhibited the phosphorylation of the 47-kDa and actin-binding proteins at 3-8 min after the addition of LPA, but had no effect on protein phosphorylation within the 1st min and had no significant effect on MLC phosphorylation.	Aspirin	0-7	modulator of VRAC current 1	Homo sapiens	228-231
3435662-7	1987	In SPD platelets, aspirin partially inhibited both aggregation and phosphorylation of the 47-kDa protein (less than 30% inhibition) and MLC (less than 40% inhibition) at time points of 1 min or less.	Aspirin	18-25	modulator of VRAC current 1	Homo sapiens	136-139
3036591-1	1987	Aspirin interacts in vitro with human low-density lipoprotein (LDL), which results in a decrease in free amino groups of apolipoprotein B and an increase of electrophoretic mobility of the particle.	Aspirin	0-7	apolipoprotein B	Homo sapiens	121-137
2438305-4	1987	Aspirin treatment of platelets markedly potentiated the ability of t-PA to induce disaggregation.	Aspirin	0-7	plasminogen activator, tissue type	Homo sapiens	67-71
3108319-4	1987	When the prelabeled platelets were suspended together with aspirin-treated lymphocytes and stimulated with ionophore, thrombin, or collagen, a 6KPGF1 alpha peak was detected and enhanced by 1-BI.	Aspirin	59-66	coagulation factor II, thrombin	Homo sapiens	118-126
3617010-6	1987	The calcium response to thrombin was inhibited to a lesser extent by aspirin, and aspirin did not prevent potentiation by epinephrine.	Aspirin	69-76	coagulation factor II, thrombin	Homo sapiens	24-32
3606733-2	1987	This hypersensitivity to thrombin persisted in the presence of CP/CPK to convert released ADP to ATP, and aspirin to block formation of thromboxane A2.	Aspirin	106-113	coagulation factor II	Rattus norvegicus	25-33
3041195-0	1987	[Correlation between dental pulp pain, blood levels of ACTH, cortisol and beta-endorphin and the analgesic efficacy of acetylsalicylic acid].	Aspirin	119-139	proopiomelanocortin	Homo sapiens	55-59
3041195-0	1987	[Correlation between dental pulp pain, blood levels of ACTH, cortisol and beta-endorphin and the analgesic efficacy of acetylsalicylic acid].	Aspirin	119-139	proopiomelanocortin	Homo sapiens	74-88
2439985-7	1987	Aspirin (ASA) (5.5 X 10(-4) M or greater, for more than 4 min) suppressed the responses to BK but not those evoked by hypertonic saline.	Aspirin	0-7	kininogen 1	Canis lupus familiaris	91-93
2439985-7	1987	Aspirin (ASA) (5.5 X 10(-4) M or greater, for more than 4 min) suppressed the responses to BK but not those evoked by hypertonic saline.	Aspirin	9-12	kininogen 1	Canis lupus familiaris	91-93
2439985-8	1987	The ASA effect on the BK response was largely restored by an addition of PG-E2.	Aspirin	4-7	kininogen 1	Canis lupus familiaris	22-24
3555002-6	1987	Indeed, administration of indomethacin or aspirin results in an increased sensitivity to infused AII in normotensive previously AII-refractory women.	Aspirin	42-49	angiotensinogen	Homo sapiens	128-131
2959114-0	1987	Antipain or leupeptin in combination with aspirin or indomethacin synergistically inhibit human platelet activation by thrombin and trypsin.	Aspirin	42-49	coagulation factor II, thrombin	Homo sapiens	119-127
3122775-6	1987	The effects of acetylsalicylic acid, known to act at a step subsequent to PLA2 activation, were completely unlike those of ethanol.	Aspirin	15-35	phospholipase A2 group IB	Homo sapiens	74-78
3799752-0	1987	Effect of low-dose aspirin on angiotensin II pressor response in human pregnancy.	Aspirin	19-26	angiotensinogen	Homo sapiens	30-44
3799752-2	1987	The effect of 80 mg of acetylsalicylic acid on vascular sensitivity to exogenous angiotensin II (Hypertensin, Ciba-Geigy Limited, Basel, Switzerland) was examined in 13 normotensive pregnant patients.	Aspirin	23-43	angiotensinogen	Homo sapiens	81-95
3799752-4	1987	Low-dose aspirin therapy resulted in an enhancement of the pregnancy-acquired refractoriness to angiotensin II.	Aspirin	9-16	angiotensinogen	Homo sapiens	96-110
3110025-0	1987	Effect of single-dose aspirin on TXA2 and PGI2 cyclooxygenases in vivo.	Aspirin	22-29	prostaglandin I receptor (IP)	Mus musculus	42-46
3110025-1	1987	The present study investigated the sensitivities of the thromboxane A2 (TXA2) cyclooxygenase and the prostacyclin (PGI2) cyclooxygenase to aspirin using an in vivo animal model.	Aspirin	139-146	prostaglandin I receptor (IP)	Mus musculus	115-119
3110025-6	1987	These results indicate that the TXA2 and PGI2 cyclooxygenase enzymes are equally sensitive to inhibition by a single dose of aspirin.	Aspirin	125-132	prostaglandin I receptor (IP)	Mus musculus	41-45
3313411-0	1987	Acetyl-salicylic acid impairs insulin-mediated glucose utilization and reduces insulin clearance in healthy and non-insulin-dependent diabetic man.	Aspirin	0-21	insulin	Homo sapiens	30-37
3115070-3	1987	Aspirin-treated platelets aggregated in response to PAF-acether and to 0.25 U/ml thrombin as much as control platelets in absence of detectable thromboxane A2, and were less responsive to 0.05-0.1 U/ml.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	81-89
3115070-4	1987	Thrombin-induced aggregation of aspirin-treated platelets was unaffected by the PAF-acether antagonists BN 52021, CV-3988 and Ro 19-3704.	Aspirin	32-39	coagulation factor II, thrombin	Homo sapiens	0-8
3313411-0	1987	Acetyl-salicylic acid impairs insulin-mediated glucose utilization and reduces insulin clearance in healthy and non-insulin-dependent diabetic man.	Aspirin	0-21	insulin	Homo sapiens	79-86
3313411-0	1987	Acetyl-salicylic acid impairs insulin-mediated glucose utilization and reduces insulin clearance in healthy and non-insulin-dependent diabetic man.	Aspirin	0-21	insulin	Homo sapiens	79-86
3788962-4	1986	The results indicate that thrombin-induced platelet serotonin release, following aspirin ingestion, was subnormal in most hypothyroid patients.	Aspirin	81-88	coagulation factor II, thrombin	Homo sapiens	26-34
2956391-4	1986	Surprisingly, therefore, both indomethacin and aspirin lowered elevated levels of ANP in Bartter"s syndrome to normal, indomethacin achieving this within 24 h. Single doses of indomethacin and aspirin also lowered plasma ANP levels in normal subjects.	Aspirin	193-200	natriuretic peptide A	Homo sapiens	221-224
3797446-1	1986	In vitro salicylates /aspirin, salicylic acid, salicylamide and gentisic acid/ inhibited formation of 12-lipoxygenase products in intact human washed platelets which were stimulated with thrombin or arachidonic acid.	Aspirin	22-29	coagulation factor II, thrombin	Homo sapiens	187-195
2956391-4	1986	Surprisingly, therefore, both indomethacin and aspirin lowered elevated levels of ANP in Bartter"s syndrome to normal, indomethacin achieving this within 24 h. Single doses of indomethacin and aspirin also lowered plasma ANP levels in normal subjects.	Aspirin	47-54	natriuretic peptide A	Homo sapiens	82-85
3091289-0	1986	Beneficial effect of aspirin in maintaining the patency of small-caliber prosthetic grafts after thrombolysis with urokinase or tissue-type plasminogen activator.	Aspirin	21-28	tissue-type plasminogen activator	Canis lupus familiaris	128-161
3021953-6	1986	Acetylsalicylic acid, a specific inhibitor of PG synthesis, completely prevented vasopressin- and arachidonate-evoked increases of cAMP but did not affect basal cAMP concentrations.	Aspirin	0-20	arginine vasopressin	Rattus norvegicus	81-92
2873400-6	1986	These observations lead to the hypothesis that an increased release of TNF in selected young patients treated with aspirin contributes to the development of Reye"s syndrome.	Aspirin	115-122	tumor necrosis factor	Homo sapiens	71-74
3111000-9	1987	The different effect of aspirin on fibrinolytic response during venous occlusion and physical activity suggested that different mechanisms were involved in t-PA release during both stimuli.	Aspirin	24-31	plasminogen activator, tissue type	Homo sapiens	156-160
3010580-4	1986	The present study compares fibrinogen binding to hyperaggregable platelets from diabetic patients and to normal platelets when prostaglandin/thromboxane formation is suppressed by aspirin.	Aspirin	180-187	fibrinogen beta chain	Homo sapiens	27-37
3085729-6	1986	Prior treatment of the platelets with 100 microM acetylsalicylate to block the cyclooxygenase-dependent pathway caused minor reduction in dense-body secretion induced by TPA or thrombin or the combination of both, but otherwise the relative results were comparable to the untreated platelets.	Aspirin	49-65	coagulation factor II, thrombin	Homo sapiens	177-185
3959543-9	1986	Treatment of the platelets with acetylsalicylic acid prior to the experiment depressed the detachment effect of thrombin-stimulated platelets, but did not alter the effect on the release of 51Cr into the ambient fluid.	Aspirin	32-52	coagulation factor II, thrombin	Homo sapiens	112-120
3010580-5	1986	It was found that pre-treatment with aspirin reduced collagen or thrombin-induced binding to platelets from non-retinopathic diabetics to the values seen in controls.	Aspirin	37-44	coagulation factor II, thrombin	Homo sapiens	65-73
3010580-7	1986	The combination of aspirin with apyrase (an ADP scavenger) almost completely inhibited binding and aggregation of platelets from normal controls or non-retinopathic diabetics exposed to collagen or thrombin, whereas it only partially affected binding and aggregation of platelets from retinopathics.	Aspirin	19-26	coagulation factor II, thrombin	Homo sapiens	198-206
3954674-7	1986	After stimulation with thrombin or collagen, the hyperaggregable platelets from FH patients were shown to bind significantly more fibrinogen than control platelets even when PG/Tx formation was suppressed (aspirin) and secreted ADP was scavenged (apyrase).	Aspirin	206-213	coagulation factor II, thrombin	Homo sapiens	23-31
6088878-11	1984	Indomethacin (10(-5) M), piroxicam (10(-6) M), and aspirin, cyclooxygenase antagonists, negated LTB4-, C5a des arg-, and FMLP-induced LAI.	Aspirin	51-58	complement C5a receptor 1	Homo sapiens	103-106
3085277-0	1986	Aspirin and venous occlusion: effects on blood fibrinolytic activity and tissue-type plasminogen activator levels.	Aspirin	0-7	plasminogen activator, tissue type	Homo sapiens	73-106
3085277-8	1986	In contrast, aspirin treatment resulted in a 32% increase in mean individual increments in plasma tPA concentration with occlusion, an effect predominant in men.	Aspirin	13-20	plasminogen activator, tissue type	Homo sapiens	98-101
3905478-2	1985	When in healthy subjects arterial plasma glucose was acutely raised and maintained at +7 mmol/l above fasting level, the plasma insulin response was enhanced by ASA (70 +/- 7 vs. 52 +/- 7 mU/l), whereas the plasma C-peptide response was identical.	Aspirin	161-164	insulin	Homo sapiens	128-135
3905478-3	1985	Despite higher insulin concentrations, glucose utilization was not significantly altered (control, 61 +/- 7; ASA, 65 +/- 6 mumol X kg-1 X min-1) indicating impairment of tissue sensitivity to insulin by ASA.	Aspirin	203-206	insulin	Homo sapiens	192-199
3905478-7	1985	During the hyperglycaemic clamp study, the plasma response of insulin, but not of C-peptide, was enhanced by ASA, whereas tissue sensitivity to insulin was reduced by 30 percent.	Aspirin	109-112	insulin	Homo sapiens	62-69
3931099-0	1985	Effect of aspirin on serum thrombin time and bleeding time.	Aspirin	10-17	coagulation factor II, thrombin	Homo sapiens	27-35
3931099-4	1985	These data indicate that inhibition of cyclooxygenase product formation by aspirin may alter the third stage of coagulation, specifically, endogenous thrombin activity.	Aspirin	75-82	coagulation factor II, thrombin	Homo sapiens	150-158
3926716-2	1985	Effects of aspirin and thymosin on enhancement of IL-2 production.	Aspirin	11-18	interleukin 2	Homo sapiens	50-54
3926716-5	1985	Our studies demonstrate that aspirin, an inhibitor of the cyclooxygenase pathway, given in vivo, or added to cultures in vitro, results in two-fold increased IL-2 production by PHA-stimulated PBL.	Aspirin	29-36	interleukin 2	Homo sapiens	158-162
3926716-9	1985	Augmentation of IL-2 production by aspirin and/or TF5 was prevented by monocyte depletion of the PBL population.	Aspirin	35-42	interleukin 2	Homo sapiens	16-20
3926716-10	1985	These results are interpreted as demonstrating (a) that TF5 and aspirin augment, by distinct mechanisms, IL-2 production by normal human PBL, (b) that the effects of both of these agents are mediated directly or indirectly via a monocyte population and (c) that aspirin, in addition to its analgesic and anti-inflammatory properties, may act as a modulator of immunological responsiveness, either alone or in combination with other biological response modifiers such as thymosin.	Aspirin	64-71	interleukin 2	Homo sapiens	105-109
3888490-9	1985	Both aspirin and salicylic acid are bound to serum albumin (aspirin being capable of irreversibly acetylating many proteins), and both are distributed in the synovial cavity, central nervous system, and saliva.	Aspirin	5-12	albumin	Homo sapiens	45-58
3888490-9	1985	Both aspirin and salicylic acid are bound to serum albumin (aspirin being capable of irreversibly acetylating many proteins), and both are distributed in the synovial cavity, central nervous system, and saliva.	Aspirin	60-67	albumin	Homo sapiens	45-58
3991915-5	1985	Pretreatment with prostaglandin synthetase inhibitors, ketoprofene (KTP) and acetylsalicylic acid (ASA), reduced the magnitude of both the NT- and meal-induced hypermotility responses.	Aspirin	77-97	neurotensin	Canis lupus familiaris	139-141
3991915-5	1985	Pretreatment with prostaglandin synthetase inhibitors, ketoprofene (KTP) and acetylsalicylic acid (ASA), reduced the magnitude of both the NT- and meal-induced hypermotility responses.	Aspirin	99-102	neurotensin	Canis lupus familiaris	139-141
2981130-3	1985	We compared fibrinogen binding to platelets from diabetic subjects with binding to platelets from normal subjects and determined whether aspirin (which inhibits the formation of prostaglandins and thromboxane) would inhibit the binding of fibrinogen to platelets from diabetic subjects and whether this correlated with its effects on platelet aggregation.	Aspirin	137-144	fibrinogen beta chain	Homo sapiens	239-249
3919134-0	1985	Restoration of prostacyclin synthase in vascular smooth muscle cells after aspirin treatment: regulation by epidermal growth factor.	Aspirin	75-82	prostaglandin I2 synthase	Rattus norvegicus	15-36
6518981-4	1984	Changes in lacrimal peroxidase secretion were found after administration of atropine, aspirin, furosemide, indomethacine and pilocarpine.	Aspirin	86-93	peroxidase 42-like	Gossypium hirsutum	20-30
6432882-4	1984	Concentrations of drugs required for 50% inhibition of 5-lipoxygenase were 0.17mM for indomethacin, 0.60mM for ibuprofen, and 3.4mM for aspirin.	Aspirin	136-143	arachidonate 5-lipoxygenase	Homo sapiens	55-69
2936818-8	1986	Exogenously added PGE1, PGE2, and PGI2, but not PGF2 alpha or PGD2, were able to restore the inducing capability of M1-A5 cells, which had been blocked by ASA.	Aspirin	155-158	prostaglandin I receptor (IP)	Mus musculus	34-38
3086606-6	1986	It is suggested that the sex difference in the antiplatelet effect of aspirin results from the difference in the inhibition of Ca2+ mobilization via the inhibition of TXA2 production in thrombin-stimulated rat platelets.	Aspirin	70-77	coagulation factor II	Rattus norvegicus	186-194
3012375-5	1986	After cyclo-oxygenase blockade by acetylsalicylic acid (ASA), PRP was stimulated by a supramaximal concentration of PAF.	Aspirin	34-54	complement component 4 binding protein alpha	Homo sapiens	62-65
3012375-5	1986	After cyclo-oxygenase blockade by acetylsalicylic acid (ASA), PRP was stimulated by a supramaximal concentration of PAF.	Aspirin	56-59	complement component 4 binding protein alpha	Homo sapiens	62-65
3961734-16	1986	In other experiments aspirin (500 microM) inhibited thrombin (0.05 U/ml) induced TXB2 synthesis by 75% in both WKY and SHR platelets but failed to inhibit aggregation or secretion in either WKY or SHR platelets.	Aspirin	21-28	coagulation factor II	Rattus norvegicus	52-60
3943666-6	1986	However, while aspirin (an inhibitor of thromboxane synthesis) reduced the abnormally high fibrinogen binding of platelets from nonretinopathic patients to normal control levels, it did not normalize the high fibrinogen binding of platelets from retinopathic diabetic patients.	Aspirin	15-22	fibrinogen beta chain	Homo sapiens	91-101
3943666-7	1986	The combination of aspirin plus apyrase (an ADP scavenger) almost suppressed fibrinogen binding and aggregation of platelets from normal or nonretinopathic diabetic subjects, whereas it had a somewhat lesser effect on binding and aggregation of platelets from retinopathic subjects.	Aspirin	19-26	fibrinogen beta chain	Homo sapiens	77-87
3080538-8	1986	Creatine phosphate-creatine phosphokinase (CP/CPK) and aspirin completely blocked aggregation and partially blocked the release of granule contents from platelets from control and diabetic rats exposed to this low concentration of thrombin.	Aspirin	55-62	coagulation factor II	Rattus norvegicus	231-239
3080539-8	1986	Except at low concentrations of thrombin, the enhanced sensitivity to thrombin-induced aggregation and release of granule contents from platelets from diabetic rats or their nondiabetic littermates could not be inhibited by creatine phosphate-creatine phosphokinase (CP/CPK) and aspirin (CP/CPK used at concentrations that inhibited aggregation induced by ADP [10 mumol/L] and aspirin at concentrations that inhibited thromboxane B2 production induced by thrombin [1 U/ml] by 99%).	Aspirin	279-286	coagulation factor II	Rattus norvegicus	70-78
3080539-8	1986	Except at low concentrations of thrombin, the enhanced sensitivity to thrombin-induced aggregation and release of granule contents from platelets from diabetic rats or their nondiabetic littermates could not be inhibited by creatine phosphate-creatine phosphokinase (CP/CPK) and aspirin (CP/CPK used at concentrations that inhibited aggregation induced by ADP [10 mumol/L] and aspirin at concentrations that inhibited thromboxane B2 production induced by thrombin [1 U/ml] by 99%).	Aspirin	279-286	coagulation factor II	Rattus norvegicus	70-78
3080539-8	1986	Except at low concentrations of thrombin, the enhanced sensitivity to thrombin-induced aggregation and release of granule contents from platelets from diabetic rats or their nondiabetic littermates could not be inhibited by creatine phosphate-creatine phosphokinase (CP/CPK) and aspirin (CP/CPK used at concentrations that inhibited aggregation induced by ADP [10 mumol/L] and aspirin at concentrations that inhibited thromboxane B2 production induced by thrombin [1 U/ml] by 99%).	Aspirin	377-384	coagulation factor II	Rattus norvegicus	70-78
3080539-8	1986	Except at low concentrations of thrombin, the enhanced sensitivity to thrombin-induced aggregation and release of granule contents from platelets from diabetic rats or their nondiabetic littermates could not be inhibited by creatine phosphate-creatine phosphokinase (CP/CPK) and aspirin (CP/CPK used at concentrations that inhibited aggregation induced by ADP [10 mumol/L] and aspirin at concentrations that inhibited thromboxane B2 production induced by thrombin [1 U/ml] by 99%).	Aspirin	377-384	coagulation factor II	Rattus norvegicus	70-78
2869642-1	1986	The object of the present work was to study the influence of antral pH, of aspirin and indomethacin, and of prostaglandins A2, E1 and E2 on the intragastric output of somatostatin and gastrin induced by electrical vagal stimulation (5 V, 2 ms, 2, 5 and 10 Hz).	Aspirin	75-82	somatostatin	Rattus norvegicus	167-179
2869642-6	1986	When vagal stimulations were performed after the rats had been pretreated with aspirin or indomethacin, more somatostatin than gastrin was detected in the perfusate independently of the perfusate pH.	Aspirin	79-86	somatostatin	Rattus norvegicus	109-121
2869642-7	1986	The vagally induced intraluminal release of somatostatin occurring in aspirin-treated animals was abolished by a low dose of atropine (0.05 mg kg-1) or by a simultaneous infusion of prostaglandin E1 (30 micrograms kg-1 h-1).	Aspirin	70-77	somatostatin	Rattus norvegicus	44-56
3110670-3	1986	Administration of acetylsalicylic acid caused significant antidiuresis (-56%), antinatriuresis (-82%), renin suppression (-26%) and decreased GFR (-41%).	Aspirin	18-38	renin	Homo sapiens	103-108
3903519-0	1985	Aspirin causes short-lived inhibition of bradykinin-stimulated prostacyclin production in man.	Aspirin	0-7	kininogen 1	Homo sapiens	41-51
3903519-7	1985	We report here that an oral dose of aspirin (600 mg) causes rapid and substantial inhibition of bradykinin-stimulated PGI2 production, but recovery occurs within 6 hours; this implies that endothelial PGI2 synthesis would be spared most of the time during dosing once daily with even this relatively large dose of aspirin.	Aspirin	36-43	kininogen 1	Homo sapiens	96-106
4053513-2	1985	As noted by others, aspirin (2.4 g) enhanced the antidiuretic effect of vasopressin, but the fall in potassium excretion was not modified by prior administration of aspirin, which makes it unlikely that the fall was due to the release of endogenous prostaglandins.	Aspirin	20-27	arginine vasopressin	Homo sapiens	72-83
3931686-12	1985	The culture media from endothelial cells inhibited thrombin-induced platelet aggregation, an effect blocked by aspirin.	Aspirin	111-118	coagulation factor II, thrombin	Homo sapiens	51-59
6088878-11	1984	Indomethacin (10(-5) M), piroxicam (10(-6) M), and aspirin, cyclooxygenase antagonists, negated LTB4-, C5a des arg-, and FMLP-induced LAI.	Aspirin	51-58	formyl peptide receptor 1	Homo sapiens	121-125
6418250-5	1983	During the first 5 min after removal of the drugs from the incubation medium, bradykinin-stimulated release remains dose-dependently inhibited (P less than 0.001) in ASA-, but not in dipyrone-treated cultures.	Aspirin	166-169	kininogen 1	Homo sapiens	78-88
3905478-0	1985	Acetyl-salicylic acid impairs insulin-mediated glucose utilization and reduces insulin clearance in healthy and non-insulin-dependent diabetic man.	Aspirin	0-21	insulin	Homo sapiens	30-37
3905478-0	1985	Acetyl-salicylic acid impairs insulin-mediated glucose utilization and reduces insulin clearance in healthy and non-insulin-dependent diabetic man.	Aspirin	0-21	insulin	Homo sapiens	79-86
3905478-0	1985	Acetyl-salicylic acid impairs insulin-mediated glucose utilization and reduces insulin clearance in healthy and non-insulin-dependent diabetic man.	Aspirin	0-21	insulin	Homo sapiens	79-86
3905478-1	1985	The effect of acetyl-salicylic acid (ASA, 3 g per day for 3 days) on glucose utilization and insulin secretion was studied in healthy volunteers and Type 2 diabetic patients using the hyperglycaemic and euglycaemic insulin clamp technique.	Aspirin	37-40	insulin	Homo sapiens	93-100
6235245-8	1984	Aspirin inhibited the rise in TPA activity after venous occlusion by 69% in men (P = 0.004) and 70% in women (P = 0.014).	Aspirin	0-7	plasminogen activator, tissue type	Homo sapiens	30-33
6325550-0	1984	Cyclical abnormalities in the bactericidal function, superoxide production, and lysozyme activity of neutrophils obtained from a healthy woman during menstruation: reversal by pretreatment with aspirin.	Aspirin	194-201	lysozyme	Homo sapiens	80-88
6315524-6	1984	Instillation of acetylsalicylic acid (36 mM, 1300 mg) in 200 ml of 100 mM hydrochloric acid for just 15 min resulted in a mean net hydrogen ion loss of 3.4 mmol/15 min, a net sodium ion gain of 1.9 mmol/15 min, a decrease in the potential difference of 23 mV, and marked gastric mucosal changes.	Aspirin	16-36	ETS transcription factor ELK3	Homo sapiens	127-130
6315524-6	1984	Instillation of acetylsalicylic acid (36 mM, 1300 mg) in 200 ml of 100 mM hydrochloric acid for just 15 min resulted in a mean net hydrogen ion loss of 3.4 mmol/15 min, a net sodium ion gain of 1.9 mmol/15 min, a decrease in the potential difference of 23 mV, and marked gastric mucosal changes.	Aspirin	16-36	ETS transcription factor ELK3	Homo sapiens	171-174
6355137-2	1983	When the plasma glucose concentration was acutely raised and maintained at 125 mg/dl above the basal level after treatment with aspirin (3 g daily for 3 days), acute (0-10 min) and sustained (20-120 min) insulin release were 70% and 45% greater than before treatment.	Aspirin	128-135	insulin	Homo sapiens	204-211
6355137-7	1983	These results demonstrate that aspirin not only enhances beta-cell sensitivity to glucose, but also impairs glucose metabolism in insulin-sensitive tissues.	Aspirin	31-38	insulin	Homo sapiens	130-137
6642786-4	1983	Arginine-induced GH and PRL release was abolished and enhanced, respectively, by ASA pre-treatment.	Aspirin	81-84	growth hormone 1	Homo sapiens	17-19
6326566-0	1984	Effect of epinephrine on fibrinogen receptor exposure by aspirin-treated platelets and platelets from concentrates in response to ADP and thrombin.	Aspirin	57-64	fibrinogen beta chain	Homo sapiens	25-35
6326566-2	1984	Recently epinephrine was reported to induce maximal aggregation of aspirin-treated platelets when combined with ADP or thrombin, and to increase fibrinogen binding of non-aspirin treated platelets stimulated with low doses of ADP.	Aspirin	67-74	coagulation factor II, thrombin	Homo sapiens	119-127
6326566-3	1984	The present study extends these observations to correlate fibrinogen binding in response to various combinations of ADP, epinephrine, and thrombin with platelet aggregation and 14C-serotonin release using aspirin-treated platelets as well as platelets from stored concentrates.	Aspirin	205-212	fibrinogen beta chain	Homo sapiens	58-68
6375609-7	1984	The converting enzyme inhibitor captopril attenuates the acute increase in blood pressure in both control and aspirin treated 2KH - and 1KH -rats pointing to a major role for angiotensin II.	Aspirin	110-117	angiotensinogen	Rattus norvegicus	175-189
6735044-1	1984	Acetyl salicylic acid (AAS) disrupts the gastric mucosal barrier, causing a drop in the transmural potential difference (PD) and mucosal injuries.	Aspirin	0-21	FYVE, RhoGEF and PH domain containing 1	Homo sapiens	23-26
6407547-3	1983	Binding to aspirin-treated platelets was normal in response to U-46619, reduced by 60%-70% in response to ADP, collagen, and thrombin, and absent in response to arachidonic acid.	Aspirin	11-18	coagulation factor II, thrombin	Homo sapiens	125-133
6409111-7	1983	Some known inhibitors of cyclo-oxygenase such as indomethacin, aspirin and sulindac also inhibited human lens aldose reductase.	Aspirin	63-70	aldo-keto reductase family 1 member B	Homo sapiens	110-126
6687979-7	1983	Pretreatment with an aspirin dose of 15 mg/kg 24 hours prior to challenge with endotoxin significantly (p less than 0.05) inhibited thrombin-induced immunoreactive thromboxane B2 synthesis in platelet-rich plasma (in vitro) and endotoxin-induced immunoreactive 6-keto-prostaglandin F1 alpha and immunoreactive thromboxane B2 synthesis by rat peritoneal macrophages.	Aspirin	21-28	coagulation factor II	Rattus norvegicus	132-140
6349864-0	1983	Increased secretion of insulin but unchanged secretion of growth hormone in hyperglycaemic type II diabetics treated with acetyl-salicylic acid.	Aspirin	122-143	insulin	Homo sapiens	23-30
6143813-1	1984	Modifications in prolactin specific binding in the rat liver induced by different non-steroidal anti-inflammatory drugs (indomethacin, piroxicam, ketoprofen, phenylbutazone, mefenamic acid and acetylsalicylic acid) have been studied.	Aspirin	193-213	prolactin	Rattus norvegicus	17-26
6349864-1	1983	The effect of acetyl-salicylic acid (ASA, 3 g/d for three days) on basal and arginine-stimulated concentrations of insulin and growth hormone was studied in seven type II diabetics.	Aspirin	37-40	insulin	Homo sapiens	115-122
6349864-1	1983	The effect of acetyl-salicylic acid (ASA, 3 g/d for three days) on basal and arginine-stimulated concentrations of insulin and growth hormone was studied in seven type II diabetics.	Aspirin	37-40	growth hormone 1	Homo sapiens	127-141
6349864-3	1983	Concentrations of serum insulin in the hyperglycaemic state prior to arginine infusion were increased during treatment with ASA, whereas increments of serum insulin induced by i.v.	Aspirin	124-127	insulin	Homo sapiens	24-31
6401733-5	1983	When aspirin-treated platelets were prelabeled with [14C]- or [3H]arachidonate, the specific activity of phospholipid-bound arachidonate pools remained constant after thrombin stimulation.	Aspirin	5-12	coagulation factor II, thrombin	Homo sapiens	167-175
6309869-5	1983	Acetylsalicylate inhibited the bradykinin- and A23187-evoked increases of cyclic AMP as well as that of prostaglandin E2 synthesis.	Aspirin	0-16	kininogen 1	Canis lupus familiaris	31-41
6864486-7	1983	Acetylation of the lysine-199 residue with aspirin and 5-nitroaspirin decreased the trinitrophenylation rate of albumin with I.	Aspirin	43-50	albumin	Homo sapiens	112-119
6405453-2	1983	We further compared the effects of acetylsalicylic acid, indomethacin, naproxen sodium and diclofenac sodium on platelet TxA2 production in response to thrombin-induced aggregation during spontaneous clotting, and on prostacyclin (PGI2) production by umbilical arteries in a superfusion system by measuring the 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) concentration in the superfusate.	Aspirin	35-55	coagulation factor II, thrombin	Homo sapiens	152-160
6857606-1	1983	The ADP-removing enzyme system creatine phosphate-creatine phosphokinase (CP/CPK) selectively inhibited primary aggregation in response to the thromboxane receptor agonist, U46619, in mouse aspirin-treated platelet-rich plasma.	Aspirin	190-197	cystin 1	Mus musculus	77-80
7174153-6	1982	Repeat studies of plasma t1/2 and AUC for aspirin after discontinuation of oral contraceptive showed values similar to basal levels.	Aspirin	42-49	CD6 molecule	Homo sapiens	25-37
6845354-6	1983	In further studies with clofibrate and a range of other known peroxisome proliferators (nafenopin, tiadenol, BR-931, Wy-14,643, and acetylsalicylic acid), induction of CAT and palmitoyl-CoA oxidation was observed with no increase in activity of another peroxisomal enzyme, D-amino acid oxidase.	Aspirin	132-152	carnitine O-acetyltransferase	Rattus norvegicus	168-171
6757082-0	1982	Discrepant effect of the prostaglandin synthesis inhibitor acetylsalicylic acid on insulin and C-peptide response to glucose in man.	Aspirin	59-79	insulin	Homo sapiens	83-90
6757082-0	1982	Discrepant effect of the prostaglandin synthesis inhibitor acetylsalicylic acid on insulin and C-peptide response to glucose in man.	Aspirin	59-79	insulin	Homo sapiens	95-104
6757082-1	1982	The prostaglandin synthesis inhibitor acetylsalicylic acid (ASA) increases acute insulin response to glucose and improves glucose tolerance in man.	Aspirin	38-58	insulin	Homo sapiens	81-88
6757082-1	1982	The prostaglandin synthesis inhibitor acetylsalicylic acid (ASA) increases acute insulin response to glucose and improves glucose tolerance in man.	Aspirin	60-63	insulin	Homo sapiens	81-88
6757082-4	1982	A daily treatment with 3.0 g ASA over 3 days caused a significant increase of acute (delta IRI area 0-5 min) and late (delta IRI area 30-120 min) insulin response and an improvement of glucose tolerance.	Aspirin	29-32	insulin	Homo sapiens	146-153
6757082-5	1982	By contrast, C-peptide response was in the same range prior to and after ASA treatment.	Aspirin	73-76	insulin	Homo sapiens	13-22
6757082-6	1982	Thus, the C-peptide/insulin ratio was decreased by about 50% due to ASA treatment.	Aspirin	68-71	insulin	Homo sapiens	10-19
6757082-6	1982	Thus, the C-peptide/insulin ratio was decreased by about 50% due to ASA treatment.	Aspirin	68-71	insulin	Homo sapiens	20-27
6757082-8	1982	In summary, the discrepant effect of ASA on C-peptide and insulin responses suggest that changes of insulin metabolism may be involved in the mechanism of ASA induced increase in peripheral insulin levels.	Aspirin	155-158	insulin	Homo sapiens	58-65
6757082-8	1982	In summary, the discrepant effect of ASA on C-peptide and insulin responses suggest that changes of insulin metabolism may be involved in the mechanism of ASA induced increase in peripheral insulin levels.	Aspirin	155-158	insulin	Homo sapiens	100-107
6757082-9	1982	The improvement of glucose tolerance after ASA application seems to be related to the biologic effect of higher circulating insulin levels but not to alteration of insulin antagonists, such as IRG, HGH and NEFA.	Aspirin	43-46	insulin	Homo sapiens	124-131
7048597-5	1982	Platelets isolated from donors who ingested aspirin were incapable of thromboxane synthesis (less than 5 pmol/ml) but remained normally responsive to thrombin-induced activation.	Aspirin	44-51	coagulation factor II, thrombin	Homo sapiens	150-158
6184749-4	1982	Bradykinin treatment of RPCT cells caused an accumulation of intracellular cAMP which was blocked by aspirin and was quantitatively similar to that observed with 10(-5) M PGE2.	Aspirin	101-108	kininogen 1	Homo sapiens	0-10
7048597-8	1982	Furthermore, the fact that cardiac perfusion was preserved during a thrombin challenge of platelets from aspirin-treated donors establishes a fundamental role for the products of cyclooxygenase activity (e.g., thromboxanes) in the genesis of this form of myocardial ischemia.	Aspirin	105-112	coagulation factor II, thrombin	Homo sapiens	68-76
6763430-0	1982	Effect of acetylsalicylic acid on insulin sensitivity in subjects with impaired glucose tolerance.	Aspirin	10-30	insulin	Homo sapiens	34-41
6763430-1	1982	The effect of acetylsalicylic acid (ASA) on tissue sensitivity to insulin was studied in 14 non-obese subjects with impaired glucose tolerance.	Aspirin	14-34	insulin	Homo sapiens	66-73
6763430-7	1982	The metabolic clearance rate of insulin was slightly reduced and the disappearance time of insulin was increased after treatment with ASA.	Aspirin	134-137	insulin	Homo sapiens	32-39
6763430-7	1982	The metabolic clearance rate of insulin was slightly reduced and the disappearance time of insulin was increased after treatment with ASA.	Aspirin	134-137	insulin	Homo sapiens	91-98
6763430-1	1982	The effect of acetylsalicylic acid (ASA) on tissue sensitivity to insulin was studied in 14 non-obese subjects with impaired glucose tolerance.	Aspirin	36-39	insulin	Homo sapiens	66-73
7280120-5	1981	Results of the study demonstrate that aspirin-treated SPD platelets, which cannot form thromboxane or undergo the release reaction on stimulation by arachidonate, can still undergo irreversible aggregation in response to thrombin and ADP if treated first with epinephrine.	Aspirin	38-45	coagulation factor II, thrombin	Homo sapiens	221-229
6897511-3	1982	Moreover, malondialdehyde levels in human PRP after addition of thrombin were inhibited at the same degree by parsalmide, ASA and indometacin.	Aspirin	122-125	prion protein	Homo sapiens	42-45
6897511-3	1982	Moreover, malondialdehyde levels in human PRP after addition of thrombin were inhibited at the same degree by parsalmide, ASA and indometacin.	Aspirin	122-125	coagulation factor II, thrombin	Homo sapiens	64-72
7043491-5	1982	In group I the ASA treatment improved the glucose tolerance associated with sustained rise of plasma insulin significantly, whereas no significant change in glucose tolerance or plasma insulin was observed in group II compared the pretreatment level.	Aspirin	15-18	insulin	Homo sapiens	101-108
6117260-11	1981	The results indicate that Txs modulate cardiac depression, which can be prevented with 650 mg aspirin before operation.	Aspirin	94-101	thromboxane A synthase 1	Homo sapiens	26-29
6894770-4	1981	Pretreatment with aspirin (15 or 100 mg/kg) 30 min before endotoxin significantly (P less than .001) decreased the endotoxin-induced elevations in plasma levels of immunoreactive (i) TXB2, a stable metabolite of TXA2, i6-keto PGF1 alpha, a stable metabolite of PGI2 and significantly (P less than .05) inhibited thrombin-induced in vitro platelet iTXB2 synthesis.	Aspirin	18-25	coagulation factor II	Rattus norvegicus	312-320
7308171-0	1981	[Effect of single doses of indomethacin and aspirin on the serum growth hormone concentration in acromegaly].	Aspirin	44-51	growth hormone 1	Homo sapiens	65-79
7263127-3	1981	The effects of aspirin on cataract formation may result from 1) lowering of plasma tryptophan levels and increased excretion of tryptophan metabolites, 2) inhibition of aldose reductase and sorbitol formation in the diabetic lens, 3) inhibition of tryptophan or kynurenine binding to lens protein.	Aspirin	15-22	aldo-keto reductase family 1 member B	Homo sapiens	169-185
7284687-7	1981	Aspirin was nearly as effective as CCI 17810 against collagen, and adrenaline but about 10 times less active against arachidonic acid; it did not inhibit the primary response to ADP and was only a weak inhibitor of thrombin-induced aggregation.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	215-223
6288146-1	1982	Previous analysis of fibrinogen binding to human aspirin-treated gel-filtered platelets yielded upwardly concave Scatchard plots.	Aspirin	49-56	fibrinogen beta chain	Homo sapiens	21-31
7258182-4	1981	Stimulation of "myeloproliferative" platelets with thrombin after blocking the prostaglandin pathway with aspirin resulted in reduced aggregation, indicating either a deficiency of the storage pool of adenine nucleotides in the platelets or an abnormality of a membrane receptor for thrombin.	Aspirin	106-113	coagulation factor II, thrombin	Homo sapiens	51-59
7245119-6	1981	Although ticlopidine had similar activity in the two species, aspirin and flurbiprofen were considerably less potent in mouse than human PRP as inhibitors of collagen-induced aggregation.	Aspirin	62-69	prion protein	Homo sapiens	137-140
6996497-7	1980	Caution is urged before acceptance of a central role for PGI2, however, because of the capability of microvasculatures and adjacent tissue to synthesize a number of other products whose interaction with platelets and with aspirin and indomethacin remains to be elucidated.	Aspirin	222-229	prostaglandin I receptor (IP)	Mus musculus	57-61
6160349-6	1981	Release of the PGI2-like substance by angiotensin II was reduced after intravenous administration of indomethacin (2, 5, or 10 mg/kg), aspirin (100 mg/kg), aspirin (100 mg/kg), and meclofenamic acid (2 mg/kg), but was not completely eliminated by any of the above inhibitors.	Aspirin	135-142	angiotensinogen	Rattus norvegicus	38-52
6160349-6	1981	Release of the PGI2-like substance by angiotensin II was reduced after intravenous administration of indomethacin (2, 5, or 10 mg/kg), aspirin (100 mg/kg), aspirin (100 mg/kg), and meclofenamic acid (2 mg/kg), but was not completely eliminated by any of the above inhibitors.	Aspirin	156-163	angiotensinogen	Rattus norvegicus	38-52
6776627-3	1980	Labeled cells produced prostacyclin only when exposed to the initiator thrombin: treatment with therapeutic concentrations of aspirin (0.2 millimolar) for 30 minutes completely destroyed the cells" ability to synthesize prostacyclin.	Aspirin	126-133	coagulation factor II	Rattus norvegicus	71-79
6776148-4	1980	To ascertain whether aspirin-treated endothelial cells produce PGI(2) from endoperoxides released by stimulated platelets, [(3)H]arachidonic acid-prelabeled platelets were reacted in aggregometer cuvettes with the calcium ionophore A 23187, thrombin, or collagen in the presence of aspirin-treated endothelial cell suspensions.	Aspirin	21-28	coagulation factor II, thrombin	Homo sapiens	241-249
7403340-2	1980	Concentrations of ADP, thrombin and arachidonate that caused reversible stimulation of aspirin platelets produced irreversible aggregation when the aspirin samples had been pretreated with epinephrine.	Aspirin	87-94	coagulation factor II, thrombin	Homo sapiens	23-31
6995153-2	1980	Treatment of the endothelium with high concentrations of aspirin to block PGI2 formation was associated with increased platelet adherence in a system employing thrombin and 51Cr-labeled platelets.	Aspirin	57-64	coagulation factor II, thrombin	Homo sapiens	160-168
7403340-2	1980	Concentrations of ADP, thrombin and arachidonate that caused reversible stimulation of aspirin platelets produced irreversible aggregation when the aspirin samples had been pretreated with epinephrine.	Aspirin	148-155	coagulation factor II, thrombin	Homo sapiens	23-31
6989847-0	1980	Indomethacin and aspirin prevent the starvation-induced fall in plasma insulin.	Aspirin	17-24	insulin	Homo sapiens	71-78
6989851-3	1980	As both indomethacin and acetylsalicylic acid are potent inhibitors of the endogenous prostaglandin synthesis, these results indicate that the effect of acetylsalicylic acid on insulin and glucagon secretion, as described by others, seems to be unrelated to the suppression of endogenous prostaglandin synthesis.	Aspirin	25-45	insulin	Homo sapiens	177-184
6989851-3	1980	As both indomethacin and acetylsalicylic acid are potent inhibitors of the endogenous prostaglandin synthesis, these results indicate that the effect of acetylsalicylic acid on insulin and glucagon secretion, as described by others, seems to be unrelated to the suppression of endogenous prostaglandin synthesis.	Aspirin	153-173	insulin	Homo sapiens	177-184
6989847-6	1980	By contrast, aspirin and INDO administration prevented the decline in plasma insulin in both lean (INDO, 92 +/- 5%) and obese (INDO, 109 +/- 11%; ASA, 111 +/- 17%) subjects.	Aspirin	13-20	insulin	Homo sapiens	77-84
393296-8	1979	PRP obtained from normal subjects after the ingestion of aspirin exhibited only one wave of aggregation in response to ADP, adrenaline or collagen, PGI2, PGD2 and PGE1 were all powerful inhibitors of this single wave of aggregation.	Aspirin	57-64	prion protein	Homo sapiens	0-3
7001843-4	1980	In both groups an enhanced insulin mobilization was observed, when acetylsalicylic acid has been added.	Aspirin	67-87	insulin	Homo sapiens	27-34
7203849-2	1980	The effect of aspirin (ASP) on the binding of ascorbic acid (AA) to bovine serum albumin (BSA) has been investigated by the method of dynamic dialysis.	Aspirin	14-21	albumin	Homo sapiens	75-88
7203849-2	1980	The effect of aspirin (ASP) on the binding of ascorbic acid (AA) to bovine serum albumin (BSA) has been investigated by the method of dynamic dialysis.	Aspirin	23-26	albumin	Homo sapiens	75-88
6989660-5	1980	No significant changes in either basal or arginine-stimulated glucagon concentrations were observed after ASA; by contrast, the growth hormone peak was significantly reduced after ASA (11.3 +/- 4.2 ng/ml vs 5.1 +/- 1.1 ng/ml, p less than 0.05).	Aspirin	180-183	growth hormone 1	Homo sapiens	128-142
6989660-6	1980	These metabolic effects exerted by ASA in insulin-dependent diabetes seem not to be related to alterations in endogenously secreted insulin since C-peptide circulating levels were similar during the pre- and post-treatment arginine tests.	Aspirin	35-38	insulin	Homo sapiens	42-49
7404479-1	1980	ADP causes human, aspirin-treated, gel-filtered platelets to change from their native discoid shape to spiny spheres with pseudopods, bind 125I-labeled fibrinogen, and aggregate if shaken with sufficient fibrinogen.	Aspirin	18-25	fibrinogen beta chain	Homo sapiens	152-162
7404479-1	1980	ADP causes human, aspirin-treated, gel-filtered platelets to change from their native discoid shape to spiny spheres with pseudopods, bind 125I-labeled fibrinogen, and aggregate if shaken with sufficient fibrinogen.	Aspirin	18-25	fibrinogen beta chain	Homo sapiens	204-214
467810-0	1979	Acetylsalicyclic acid restores acute insulin response reduced by furosemide in man.	Aspirin	0-21	insulin	Homo sapiens	37-44
497917-8	1979	It appears from this study that in these cases prophylaxis against venous thromboembolism using aspirin in a dosage of 600 mg bid is ineffective.	Aspirin	96-103	BH3 interacting domain death agonist	Homo sapiens	126-129
481213-2	1979	Treatment with 3.2 g ASA daily for 3 days caused a significant reduction in basal plasma glucose levels (p less than 0.05); by contrast, basal insulin rose from 23 +/- 2 to 31 +/- 2 microU/ml (p less than 0.01).	Aspirin	21-24	insulin	Homo sapiens	143-150
481213-4	1979	Insulin response to tolbutamide was significantly augmented after ASA (p less than 0.01) while GH response to hypoglycemia was reduced (p less than 0.05).	Aspirin	66-69	insulin	Homo sapiens	0-7
501542-1	1979	Aspirin and four salicylate impurities of aspirin (salicylic acid, acetylsalicylsalicylic acid, acetylsalicylic anhydride, and salicylsalicylic acid) were resolved by silica gell TLC and by high-pressure liquid chromatography (HPLC) on a reversed-phase C18 column.	Aspirin	0-7	Bardet-Biedl syndrome 9	Homo sapiens	253-256
456548-0	1979	Influence of acetylsalicylic acid on insulin, glucagon and growth hormone responses to glucose and arginine in healthy subjects.	Aspirin	13-33	growth hormone 1	Homo sapiens	59-73
227205-0	1979	Effect of two prostaglandin synthesis inhibitors, indomethacin and acetylsalicylic acid, on plasma ACTH and cortisol levels in man.	Aspirin	67-87	proopiomelanocortin	Homo sapiens	99-103
227205-4	1979	Administration of 3.2 g ASA daily depressed ACTH response to hypoglycaemia leaving the cortisol response unchanged, except for a 15 min delay in onset.	Aspirin	24-27	proopiomelanocortin	Homo sapiens	44-48
444675-2	1979	Fibronectin was partially released from washed whole platelets by collagen or thrombin, and its release by collagen was inhibited by aspirin.	Aspirin	133-140	fibronectin 1	Homo sapiens	0-11
485722-5	1979	When these procedures were after pretreatment with the analgesic agents, acetylsalicylic acid or dipyron a reduction in spike discharge was observed only with bradykinin after application of acetylsalicylic acid.	Aspirin	73-93	kininogen 1	Homo sapiens	159-169
485722-5	1979	When these procedures were after pretreatment with the analgesic agents, acetylsalicylic acid or dipyron a reduction in spike discharge was observed only with bradykinin after application of acetylsalicylic acid.	Aspirin	191-211	kininogen 1	Homo sapiens	159-169
376548-2	1979	Aspirin treatment of cultured endothelial cells from the umbilical vein increased the adherence of 51Cr-platelets when thrombin was present.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	119-127
376548-9	1979	The increase in thrombin-induced platelet adherence to 1 mM aspirin-treated monolayers was reversed 2 h after removal of the aspirin solution.	Aspirin	60-67	coagulation factor II, thrombin	Homo sapiens	16-24
376548-9	1979	The increase in thrombin-induced platelet adherence to 1 mM aspirin-treated monolayers was reversed 2 h after removal of the aspirin solution.	Aspirin	125-132	coagulation factor II, thrombin	Homo sapiens	16-24
398985-0	1979	Acetylsalicylic acid augments insulin and C-peptide responses to arginine in diabetes mellitus.	Aspirin	0-20	insulin	Homo sapiens	30-37
34021-6	1979	The results suggest that the hydrolysis of the prodrug to aspirin proceeds by an SN1-type mechanism.	Aspirin	58-65	solute carrier family 38 member 3	Homo sapiens	81-84
399850-0	1979	[Acetylsalicylic acid and hormonal response in insulin induced hypoglycemia].	Aspirin	1-21	insulin	Homo sapiens	47-54
398985-0	1979	Acetylsalicylic acid augments insulin and C-peptide responses to arginine in diabetes mellitus.	Aspirin	0-20	insulin	Homo sapiens	42-51
720774-0	1978	Aspirin stimulates insulin and glucagon secretion and increases glucose tolerance in normal and diabetic subjects.	Aspirin	0-7	insulin	Homo sapiens	19-26
94874-1	1979	In thrombin-induced DIC, acetylsalicylic acid (ASA) prevents the strong initial fall in platelet count and the obturation of the microvasculature of the lung with platelet aggregates.	Aspirin	25-45	coagulation factor II, thrombin	Homo sapiens	3-11
94874-1	1979	In thrombin-induced DIC, acetylsalicylic acid (ASA) prevents the strong initial fall in platelet count and the obturation of the microvasculature of the lung with platelet aggregates.	Aspirin	47-50	coagulation factor II, thrombin	Homo sapiens	3-11
701483-0	1978	Effect of aspirin on thrombin-induced adherence of platelets to cultured cells from the blood vessel wall.	Aspirin	10-17	coagulation factor II, thrombin	Homo sapiens	21-29
362975-0	1978	An analysis of the role of IgE in intolerance to aspirin and tartrazine.	Aspirin	49-56	immunoglobulin heavy constant epsilon	Homo sapiens	27-30
362975-2	1978	Total IgE levels in the aspirin intolerant patients were similar to those expected in a non-atopic population.	Aspirin	24-31	immunoglobulin heavy constant epsilon	Homo sapiens	6-9
701483-6	1978	Platelet adherence induced by thrombin was enhanced significantly by treatment of the endothelial monolayer with 1-2 mM aspirin.	Aspirin	120-127	coagulation factor II, thrombin	Homo sapiens	30-38
701483-8	1978	An aspirin concentration of 0.1 mM was sufficient to block thrombin-induced malonaldehyde production in platelets but it did not interfere with the inhibitory effect of the endothelium against platelet adherence.	Aspirin	3-10	coagulation factor II, thrombin	Homo sapiens	59-67
669099-0	1978	The effect of acetylsalicylic acid on insulin response to glucose and arginine in normal man.	Aspirin	14-34	insulin	Homo sapiens	38-45
103240-6	1978	Thrombin-induced aggregation was inhibited to approximately the same extent by 5-CSA and ASA while meseclazone was inactive.	Aspirin	89-92	coagulation factor II	Rattus norvegicus	0-8
212713-4	1978	Aspirin (10(-4) M) inhibited contraction induced by thrombin at concentration of 0.1 and 0.02 UI/ml (p less than 0.01 at each concentration).	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	52-60
96697-3	1978	However, it recently has been shown that the vascular refractoriness to A-II in normal women can be reduced significantly by the administration of the prostaglandin synthetase inhibitors, indomethacin or aspirin.	Aspirin	204-211	angiotensinogen	Homo sapiens	72-76
669099-2	1978	Pretreatment with ASA augmented the early insulin response to a standard IV glucose tolerance test (25 g) in  7 normal subjects (p is less than 0.05 at 2 min; p is less than 0.02 at 5 min; p is less than 0.01 at 10 min).	Aspirin	18-21	insulin	Homo sapiens	42-49
669099-1	1978	In 14 normal subjects, treatment with acetylsalicylic acid (ASA, 3.2 g daily for 3 days) a well known inhibitor of prostaglandin synthesis, caused a slight but significant decrease (p is less than 0.05) in basal plasma glucose levels; by contrast, basal insulin rose from 5 +/- 1 to 8 +/- 1 muU/ml (p is less than 0.01) after ASA.	Aspirin	38-58	insulin	Homo sapiens	254-261
669099-1	1978	In 14 normal subjects, treatment with acetylsalicylic acid (ASA, 3.2 g daily for 3 days) a well known inhibitor of prostaglandin synthesis, caused a slight but significant decrease (p is less than 0.05) in basal plasma glucose levels; by contrast, basal insulin rose from 5 +/- 1 to 8 +/- 1 muU/ml (p is less than 0.01) after ASA.	Aspirin	60-63	insulin	Homo sapiens	254-261
669099-5	1978	Arginine stimulated insulin levels were increased after ASA (p is less than 0.01 at 15 min; p is less than 0.05 at 30 min; p is less than 0.05 at 45 min), whereas glucose values were lower than under basal conditions at all times, with significant differences at 105 (p is less than 0.02) and 120 (p is less than 0.05) min.	Aspirin	56-59	insulin	Homo sapiens	20-27
624453-7	1978	In addition, use of anti-inflammatory drugs such as aspirin significantly lowers renin levels.	Aspirin	52-59	renin	Homo sapiens	81-86
842682-6	1977	Relaxing effects of BK on canine coronary arterial strips were not altered by atropine, propranolol, metiamide, and aminophylline, but were inhibited by aspirin and indomethacin.	Aspirin	153-160	kininogen 1	Canis lupus familiaris	20-22
602881-3	1977	The inhibition induced by SC 19220 and acetyl salicylic acid was found to be higher for angiotensin III than angiotensin II when the dose-response curves and equipotent concentrations of the peptides were compared before and after the drugs.	Aspirin	39-60	angiotensinogen	Rattus norvegicus	88-102
196696-2	1977	Platelets pre-incubated with acetylsalicylic acid showed only a decrease of cyclic AMP upon addition of thrombin.	Aspirin	29-49	coagulation factor II, thrombin	Homo sapiens	104-112
205238-7	1978	Thrombin decreased the cyclic AMP content of patients" platelets and also that of control platelets pretreated with aspirin.	Aspirin	116-123	coagulation factor II, thrombin	Homo sapiens	0-8
582677-0	1978	The effect of acetylsalicylic acid/salicylic acid mixtures on acetylcholinesterase activity in vitro.	Aspirin	14-34	acetylcholinesterase (Cartwright blood group)	Homo sapiens	62-82
347802-0	1977	[The effect of diclofenac (voltaren) and acetylsalicylic acid (aspirin) on plasma renin activity in man].	Aspirin	41-61	renin	Homo sapiens	82-87
347802-0	1977	[The effect of diclofenac (voltaren) and acetylsalicylic acid (aspirin) on plasma renin activity in man].	Aspirin	63-70	renin	Homo sapiens	82-87
846193-5	1977	Platelets in platelet-rich plasma from control animals aggregated in response to collagen, adenosine diphosphate, and thrombin; platelets from aspirin-, flurbiprofen- and reserpine-treated rats showed markedly diminished aggregation in response to collagen and normal or slightly diminished aggregation in response to ADP and thrombin.	Aspirin	143-150	coagulation factor II	Rattus norvegicus	326-334
834152-0	1977	Effects of acetylsalicylic acid and indomethacin on growth hormone secretion in man.	Aspirin	11-31	growth hormone 1	Homo sapiens	52-66
190267-7	1977	Thrombin treatment of platelets also blocks the acetylation of cyclo-oxygenase by aspirin since the hydrolyzed arachidonic acid competes with aspirin for the active site on cyclo-oxygenase.	Aspirin	82-89	coagulation factor II, thrombin	Homo sapiens	0-8
190267-7	1977	Thrombin treatment of platelets also blocks the acetylation of cyclo-oxygenase by aspirin since the hydrolyzed arachidonic acid competes with aspirin for the active site on cyclo-oxygenase.	Aspirin	142-149	coagulation factor II, thrombin	Homo sapiens	0-8
848248-1	1977	The effect on serum gastrin levels of lysin-acetylsalicylate (LAS), water soluble derivative of acetylsalicylic acid, was investigated in mice.	Aspirin	96-116	gastrin	Mus musculus	20-27
834152-2	1977	In eight subjects, oral administration of 3-2 g daily of ASA for 4 days clearly reached GH response to insulin hypoglycemia (p less than 0.01, ANOVA).	Aspirin	57-60	growth hormone 1	Homo sapiens	88-90
1262333-3	1976	Further, added aspirin, a known inhibitor of the burst in O2 consumption caused by thrombin, also blunted the stimulatory effect of arachidonate on O2 consumption, and eicosatetraynoate, a known inhibitor of arachidonate oxygenation, blunted the burst in O2 consumption initiated by both thrombin and arachidonate.	Aspirin	15-22	coagulation factor II, thrombin	Homo sapiens	83-91
863293-0	1977	Comparable inhibition of aggregation of PRP of neonates and adults by aspirin.	Aspirin	70-77	prion protein	Homo sapiens	40-43
949546-13	1976	Pretreatment of platelets with aspirin in vitro inhibited thrombin-induced release of serotonin but had no effect on the loss of K+ or beta-glucuronidase.	Aspirin	31-38	coagulation factor II, thrombin	Homo sapiens	58-66
949546-14	1976	In contrast, the ingestion of aspirin by mouth inhibited the release of serotonin, beta-glucuronidase, and K+ by thrombin.	Aspirin	30-37	coagulation factor II, thrombin	Homo sapiens	113-121
837964-3	1977	The effect of ASA on urinary sodium excretion was most prominent during day time (8 a.m.-10 p.m.) and on days with low sodium intake, as confirmed by control sodium excretion and plasma renin activity.	Aspirin	14-17	renin	Homo sapiens	186-191
987797-6	1976	The low concentration of bovine factor VIII induces moderate retraction of reptilase-clotted platelet-clotted platelet-rich plasma, which is inhibited by acetylsalicylic acid, indomethacin and apyrase, indicating that it is a consequence of release of platelet adenosine-5"-diphosphate.	Aspirin	154-174	coagulation factor VIII	Bos taurus	32-43
820705-0	1976	The effect of acetylsalicylic acid on TSH and PRL secretion after TRH stimulation in the human.	Aspirin	14-34	prolactin	Homo sapiens	46-49
1262333-3	1976	Further, added aspirin, a known inhibitor of the burst in O2 consumption caused by thrombin, also blunted the stimulatory effect of arachidonate on O2 consumption, and eicosatetraynoate, a known inhibitor of arachidonate oxygenation, blunted the burst in O2 consumption initiated by both thrombin and arachidonate.	Aspirin	15-22	coagulation factor II, thrombin	Homo sapiens	288-296
1260021-3	1976	Acetylsalicylate blocked the formation of malonyldialdehyde completely and partially inhibited the O2 burst induced by thrombin.	Aspirin	0-16	coagulation factor II, thrombin	Homo sapiens	119-127
6719-4	1976	The effects of bradykinin, A I and A II have been shown to be inhibited by aspirin but not by propranolol, metiamide, SC 19220 or a specific, competitive antagonist of A II.	Aspirin	75-82	kininogen 1	Homo sapiens	15-25
6719-4	1976	The effects of bradykinin, A I and A II have been shown to be inhibited by aspirin but not by propranolol, metiamide, SC 19220 or a specific, competitive antagonist of A II.	Aspirin	75-82	NLR family pyrin domain containing 3	Homo sapiens	27-39
6719-4	1976	The effects of bradykinin, A I and A II have been shown to be inhibited by aspirin but not by propranolol, metiamide, SC 19220 or a specific, competitive antagonist of A II.	Aspirin	75-82	NLR family pyrin domain containing 3	Homo sapiens	35-39
1168851-1	1975	Acetylsalicylic acid was shown both in vivo and in vitro to prevent the platelet lipid peroxidation normally induced by the aggregating agents thrombin and epinephrine, and the sulfhydryl inhibitor N-ethylmaleimide.	Aspirin	0-20	coagulation factor II, thrombin	Homo sapiens	143-151
1259204-0	1976	Diabetes mellitus and insulin in an aspirin sensitive asthmatic.	Aspirin	36-43	insulin	Homo sapiens	22-29
178701-2	1976	These effects resemble those produced by ADP, epinephrine, collagen, and thrombin in association with the platelet release reaction but are less  effectively inhibited by aspirin.	Aspirin	171-178	coagulation factor II, thrombin	Homo sapiens	73-81
139704-0	1976	[Change in fibrinogen and enzymatic and nonenzymatic fibrinolytic activity of blood in patients with low-degree rheumatic heart disease under the effect of treatment with acetylsalicylic acid].	Aspirin	171-191	fibrinogen beta chain	Homo sapiens	11-21
1215973-4	1975	125I-fibrinogen half-life was 2.1 days under aspirin and 1.9 days under combined aspirin/heparin therapy.	Aspirin	45-52	fibrinogen beta chain	Homo sapiens	5-15
1215973-4	1975	125I-fibrinogen half-life was 2.1 days under aspirin and 1.9 days under combined aspirin/heparin therapy.	Aspirin	81-88	fibrinogen beta chain	Homo sapiens	5-15
1188708-4	1975	In normal rat, heparin (2.5 mg/kg), acetylsalicylic acid (30 mg/kg) and tranexamic acid (100 mg/kg) suppressed specifically coagulation, platelet aggregation induced by collagen or thrombin and fibrinolysis respectively.	Aspirin	36-56	coagulation factor II	Rattus norvegicus	181-189
810797-4	1975	At 100 muM aspirin, 50% inhibition of prostaglandin synthase and 50% of maximal acetylation are observed after 15 min at 37 degrees.	Aspirin	11-18	latexin	Homo sapiens	7-10
810797-5	1975	Furthermore, the substrate for cyclo-oxygenase, arachidonic acid, inhibits protein acetylation by aspirin at concentrations (50% inhibition at 10-30 muM) which correlate with the Michaelis constant of arachidonic acid as a substrate for cyclooxygenase.	Aspirin	98-105	latexin	Homo sapiens	149-152
1115776-6	1975	Prostaglandin E1 (0.03 mM) and acetylsalicylic acid (0.8 mM) had little effect on basal respiration, but inhibited the thrombin-stimulated burst of oxygen consumption.	Aspirin	31-51	coagulation factor II, thrombin	Homo sapiens	119-127
166481-5	1975	Sodium citrate and aminotriazole and feeding decrease also the activity of hepatic catalase in rats fed ASA.	Aspirin	104-107	catalase	Rattus norvegicus	83-91
5566840-0	1971	[Inhibition of hexokinase activity in normal human lymphocytes by acetylsalicylate].	Aspirin	66-82	hexokinase 1	Homo sapiens	15-25
4480138-0	1974	IgE mediated and non-IgE mediated allergic-type reactions to aspirin.	Aspirin	61-68	immunoglobulin heavy constant epsilon	Homo sapiens	0-3
4480138-0	1974	IgE mediated and non-IgE mediated allergic-type reactions to aspirin.	Aspirin	61-68	immunoglobulin heavy constant epsilon	Homo sapiens	21-24
4458701-0	1974	[Effects of acetylsalicylic acid on reflex cardiocirculatory and respiratory responses induced by injection of bradykinin into the femoral artery].	Aspirin	12-32	kininogen 1	Homo sapiens	111-121
4752265-0	1973	[Effect of aspirin on the response to the intradermal injection of bradykinin].	Aspirin	11-18	kininogen 1	Homo sapiens	67-77
4644711-0	1972	The effect of acetylsalicylic acid on the peripheral and pulmonary vascular responses to thrombin.	Aspirin	14-34	coagulation factor II, thrombin	Homo sapiens	89-97
5055976-0	1972	Effect of defibrinogenation and acetylsalicylic acid on the circulatory response to thrombin.	Aspirin	32-52	coagulation factor II, thrombin	Homo sapiens	84-92
4631526-0	1972	Aspirin potentiates the hydrosmotic effect of antidiuretic hormone in toad urinary bladder.	Aspirin	0-7	arginine vasopressin	Homo sapiens	46-66
4106764-0	1971	Effect of steroids, acetylsalicylic acid and bishydroxycoumarin on prothrombin time.	Aspirin	20-40	coagulation factor II, thrombin	Homo sapiens	67-78
5784642-0	1969	Effect of acetylsalicylic acid and morphine on pressor responses produced by bradykinin.	Aspirin	10-30	kininogen 1	Homo sapiens	77-87
4105907-1	1971	V. The interaction of phenylbutazone, flufenamic acid, and dicoumarol with acetylsalicylic acid-treated human serum albumin.	Aspirin	75-95	albumin	Homo sapiens	110-123
5577976-0	1971	Aspirin inhibition of in vivo effects of intestinal alkaline phosphatase on platelets.	Aspirin	0-7	alkaline phosphatase, intestinal	Homo sapiens	41-72
5531310-1	1970	In rats, administration of acetylsalicylic acid (ASA) by stomach tube two hours before blood removal, or addition of the drug to platelet-rich plasma in vitro, markedly inhibited platelet aggregation induced by thrombin, ADP and collagen.	Aspirin	27-47	coagulation factor II	Rattus norvegicus	211-219
5531310-1	1970	In rats, administration of acetylsalicylic acid (ASA) by stomach tube two hours before blood removal, or addition of the drug to platelet-rich plasma in vitro, markedly inhibited platelet aggregation induced by thrombin, ADP and collagen.	Aspirin	49-52	coagulation factor II	Rattus norvegicus	211-219
5531310-2	1970	Addition of ASA in vitro to human platelet-rich plasma also inhibited platelet aggregation by thrombin, ADP and collagen.	Aspirin	12-15	coagulation factor II, thrombin	Homo sapiens	94-102
5651209-0	1968	Acetylation of human serum albumin by acetylsalicylic acid.	Aspirin	38-58	albumin	Homo sapiens	27-34
5773090-0	1969	Structural changes in human serum albumin induced by ingestion of acetylsalicylic acid.	Aspirin	66-86	albumin	Homo sapiens	34-41
5773090-1	1969	Acetylsalicylic acid (aspirin) acetylates human serum albumin under physiologic conditions in vitro.	Aspirin	0-20	albumin	Homo sapiens	54-61
5773090-1	1969	Acetylsalicylic acid (aspirin) acetylates human serum albumin under physiologic conditions in vitro.	Aspirin	22-29	albumin	Homo sapiens	54-61
5773090-3	1969	Albumin was reacted in vitro with aspirin labeled with (14)carbon at the acetyl-1 or the carboxyl carbon.	Aspirin	34-41	albumin	Homo sapiens	0-7
5773090-10	1969	A transacetylation reaction between aspirin and human albumin occurs in vivo and is similar to that observed in vitro.	Aspirin	36-43	albumin	Homo sapiens	54-61
5651209-1	1968	Human serum albumin is acetylated when exposed to acetylsalicylic acid (aspirin) under physiologic conditions in vitro.	Aspirin	50-70	albumin	Homo sapiens	12-19
5651209-1	1968	Human serum albumin is acetylated when exposed to acetylsalicylic acid (aspirin) under physiologic conditions in vitro.	Aspirin	72-79	albumin	Homo sapiens	12-19
5909493-0	1966	The effect of aspirin on pain and hand blood flow responses to intra-arterial injection of bradykinin in man.	Aspirin	14-21	kininogen 1	Homo sapiens	91-101
33743316-8	2021	We further demonstrated that aspirin inhibited the activation of NF-kappaB signaling and the release of its downstream pro-inflammatory cytokines.	Aspirin	29-36	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	65-74
13050296-0	1953	The ACTH-like effect of acetylsalicylic acid; investigation of combined treatment with acetylsalicylic acid and pantothenic acid.	Aspirin	24-44	proopiomelanocortin	Homo sapiens	4-8
33998099-9	2021	Adjusting for aspirin usage and the interaction between aspirin and chronic hypertension, independent predictors for the development of preterm preeclampsia were PlGF MoM (adjusted odds ratio [aOR]: 0.226; 95% confidence interval [CI]: 0.070-0.723), and estimated risks.	Aspirin	56-63	placental growth factor	Homo sapiens	162-166
33985681-10	2021	CONCLUSION: Ticagrelor plus aspirin yielded generally consistent and favorable net clinical benefit across the diabetes-related factors in THEMIS-PCI but not in the overall THEMIS population.	Aspirin	28-35	thymocyte selection associated	Homo sapiens	139-145
34029712-3	2021	Symptoms due to increased baseline and/or episodic release of PGD2 can be prevented with aspirin, an inhibitor of cyclooxygenase (COX)1 and COX2.	Aspirin	89-96	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	140-144
34016022-10	2021	CONCLUSION: Low-dose aspirin administration lowers AFP early in pregnancy.	Aspirin	21-28	alpha fetoprotein	Homo sapiens	51-54
32299908-0	2021	Identification of a homozygous recessive variant in PTGS1 resulting in a congenital aspirin-like defect in platelet function.	Aspirin	84-91	prostaglandin-endoperoxide synthase 1	Homo sapiens	52-57
33975019-3	2021	The treatment with ASA caused an increase in the gene expression of COX2 and ABCB1 in both MDR cell lines, and a decrease in the expression of ALOX5 in the FEPS cells.	Aspirin	19-22	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	68-72
33975019-3	2021	The treatment with ASA caused an increase in the gene expression of COX2 and ABCB1 in both MDR cell lines, and a decrease in the expression of ALOX5 in the FEPS cells.	Aspirin	19-22	ATP binding cassette subfamily B member 1	Homo sapiens	77-82
33975019-3	2021	The treatment with ASA caused an increase in the gene expression of COX2 and ABCB1 in both MDR cell lines, and a decrease in the expression of ALOX5 in the FEPS cells.	Aspirin	19-22	arachidonate 5-lipoxygenase	Homo sapiens	143-148
33975019-6	2021	Cytometry data showed that there was an increase in ABCB1 protein expression after exposure to ASA.	Aspirin	95-98	ATP binding cassette subfamily B member 1	Homo sapiens	52-57
33975019-7	2021	In addition, the increased activity of ABCB1 in the K562-Lucena cell line indicates that ASA may be a substrate for this efflux pump, corroborating the molecular docking that showed that ASA can bind to ABCB1.	Aspirin	89-92	ATP binding cassette subfamily B member 1	Homo sapiens	39-44
33975019-7	2021	In addition, the increased activity of ABCB1 in the K562-Lucena cell line indicates that ASA may be a substrate for this efflux pump, corroborating the molecular docking that showed that ASA can bind to ABCB1.	Aspirin	89-92	ATP binding cassette subfamily B member 1	Homo sapiens	203-208
33975019-7	2021	In addition, the increased activity of ABCB1 in the K562-Lucena cell line indicates that ASA may be a substrate for this efflux pump, corroborating the molecular docking that showed that ASA can bind to ABCB1.	Aspirin	187-190	ATP binding cassette subfamily B member 1	Homo sapiens	39-44
33975019-7	2021	In addition, the increased activity of ABCB1 in the K562-Lucena cell line indicates that ASA may be a substrate for this efflux pump, corroborating the molecular docking that showed that ASA can bind to ABCB1.	Aspirin	187-190	ATP binding cassette subfamily B member 1	Homo sapiens	203-208
32299908-1	2021	We have identified a rare missense variant on chromosome 9, position 125145990 (GRCh37), in exon 8 in PTGS1 (the gene encoding cyclo-oxygenase 1, COX-1, the target of anti-thrombotic aspirin therapy).	Aspirin	183-190	prostaglandin-endoperoxide synthase 1	Homo sapiens	102-107
32299908-1	2021	We have identified a rare missense variant on chromosome 9, position 125145990 (GRCh37), in exon 8 in PTGS1 (the gene encoding cyclo-oxygenase 1, COX-1, the target of anti-thrombotic aspirin therapy).	Aspirin	183-190	prostaglandin-endoperoxide synthase 1	Homo sapiens	127-144
32955700-8	2021	Subsequent multivariate logistic regression analysis revealed that among these inflammatory cytokines, only IL-6 (P = 0.019) independently predicted higher ASAS 20 response to celecoxib at W12, and it had a fair value for predicting ASAS 20 response to celecoxib at W12 (area under the curve: 0.666, 95% confidence interval: 0.561-0.771) by receiver-operating characteristic curve analysis.	Aspirin	156-160	interleukin 6	Homo sapiens	108-112
33895438-7	2021	RESULTS: The generation of platelet aggregates under flow was significantly increased by the pretreatment of PRP with 100-200 ng/mL C6O4, compared to both the control condition and the experiment performed in presence of ASA.	Aspirin	221-224	complement component 4 binding protein alpha	Homo sapiens	109-112
33444716-17	2021	CONCLUSION: Our studies implicated that NXT could restore HI injury and inhibit thrombosis through COX2-VEGF/NFkappaB signaling, which is consistent with the molecular target of aspirin.	Aspirin	178-185	nuclear factor kappa B subunit 1	Homo sapiens	109-117
33455562-0	2021	Association between insulin resistance and aspirin or clopidogrel resistance in Chinese patients with recent ischemic stroke/TIA.	Aspirin	43-50	insulin	Homo sapiens	20-27
33865015-9	2021	For the first time, aspirin was shown to fully reverse miR-200-mediated trophoblast biology and act through the network signaling of TGF-beta1/ZEB1/miR-200.	Aspirin	20-27	transforming growth factor beta 1	Homo sapiens	133-142
33959001-11	2021	In MSCs, atorvastatin and aspirin combination reduced the release of pro-inflammatory cytokines such as IL-6, IL-8, MCP-1 and IFN-gamma.	Aspirin	26-33	interleukin 6	Homo sapiens	104-108
33959001-11	2021	In MSCs, atorvastatin and aspirin combination reduced the release of pro-inflammatory cytokines such as IL-6, IL-8, MCP-1 and IFN-gamma.	Aspirin	26-33	C-X-C motif chemokine ligand 8	Homo sapiens	110-114
33959001-11	2021	In MSCs, atorvastatin and aspirin combination reduced the release of pro-inflammatory cytokines such as IL-6, IL-8, MCP-1 and IFN-gamma.	Aspirin	26-33	interferon gamma	Homo sapiens	126-135
33959001-13	2021	Combination of atorvastatin and aspirin had additive effect on reducing the secretion of IL-6 from co-cultures of stroke Mo and MSCs.	Aspirin	32-39	interleukin 6	Homo sapiens	89-93
33849034-7	2021	Hence, for optimal CV protection in ET, low dose Aspirin is recommended twice daily in an arterial thrombotic disease like atherothrombotic ischemic stroke in presence of the following risk factors: age > 60 years, Janus kinase2V617F gene mutation, presence of CV risk factors.	Aspirin	49-56	major facilitator superfamily domain containing 11	Homo sapiens	36-38
33819512-1	2021	BACKGROUND: Aspirin Exacerbated Respiratory Disease (AERD) is characterized by the triad of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and intolerance to cyclooxygenase-1 (COX-1) enzyme inhibitors.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	170-186
33918289-6	2021	In this study, we have used cytotoxicity and molecular docking studies to show that NCX4040, a nitric oxide donor related to aspirin, inhibited the functions of ATPase which resulted in significant reversal of resistance to both adriamycin and topotecan in P-gp- and BCRP-expressing human cancer cell lines, respectively.	Aspirin	125-132	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	267-271
33819512-1	2021	BACKGROUND: Aspirin Exacerbated Respiratory Disease (AERD) is characterized by the triad of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and intolerance to cyclooxygenase-1 (COX-1) enzyme inhibitors.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	188-193
33398741-0	2021	Krill oil and low-dose aspirin combination mitigates experimentally induced silicosis in rats: role of NF-kappaB/TGF-beta1/MMP-9 pathway.	Aspirin	23-30	transforming growth factor, beta 1	Rattus norvegicus	113-122
33398741-6	2021	Oral aspirin and krill oil combination significantly attenuated silica-induced oxidative stress through the restoration of reduced glutathione concentration and catalase activity in addition to alleviation of elevated malondialdehyde and total nitric oxide contents.	Aspirin	5-12	catalase	Rattus norvegicus	161-169
33398741-7	2021	Moreover, aspirin and krill oil combination revealed considerable mitigation of silica-induced upregulated expression of the inflammatory and fibrotic mediators: nuclear factor kappa-B, transforming growth factor-beta1, and matrix metalloproteinase-9.	Aspirin	10-17	transforming growth factor, beta 1	Rattus norvegicus	186-218
33558152-1	2021	AIMS: THEMIS (NCT01991795) demonstrated cardioprotective benefits of ticagrelor plus acetylsalicylic acid (ASA) compared with placebo plus ASA in patients with type 2 diabetes (T2D), stable coronary artery disease (CAD) and no history of myocardial infarction (MI) or stroke.	Aspirin	85-105	thymocyte selection associated	Homo sapiens	6-12
32761372-0	2021	ImpaCt of aspirin regimen on THrombin generation in diabEtic patients with acute coronary syndrome: CARTHaGE-ACS trial.	Aspirin	10-17	coagulation factor II, thrombin	Homo sapiens	29-37
33558152-1	2021	AIMS: THEMIS (NCT01991795) demonstrated cardioprotective benefits of ticagrelor plus acetylsalicylic acid (ASA) compared with placebo plus ASA in patients with type 2 diabetes (T2D), stable coronary artery disease (CAD) and no history of myocardial infarction (MI) or stroke.	Aspirin	107-110	thymocyte selection associated	Homo sapiens	6-12
32997790-5	2021	Although the exact mode of action remains unclear, multiple downstream effects of aspirin may interfere with cholangiocarcinogenesis, tumour growth, and metastasis-including inhibiting the COX-2 pathway, preventing platelet aggregation, and modulating certain proteins and signalling.	Aspirin	82-89	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	189-194
33514613-5	2021	The aim of this study was to assess the safety and efficacy of the p48 MW HPC (phenox, Bochum, Germany) to treat distal intracranial aneurysms under the use of aspirin monotherapy.	Aspirin	160-167	interferon regulatory factor 9	Homo sapiens	67-70
33618245-4	2021	OBSERVATIONS: This paper reviews randomized controlled trials that showed that celecoxib, a selective COX-2 inhibitor, or low-dose aspirin, which inhibits COX-1 and inhibits/acetylates COX-2, reduced bipolar symptoms in patients on mood stabilizers.	Aspirin	131-138	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	185-190
33618245-6	2021	CONCLUSIONS: This clinical evidence is consistent with the hypothesis that low-dose chronic aspirin and celecoxib, which can inhibit COX-2 and enter brain, can be repurposed in bipolar disorder to enhance mood stabilizer effects on arachidonic acid metabolism and neurotransmission.	Aspirin	92-99	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	133-138
33657049-4	2021	Platelet aggregation induced by arachidonic acid and assessed with the use of light transmission aggregometry (LTA) was used as a direct measure of the inhibition of COX1 by aspirin.	Aspirin	174-181	prostaglandin-endoperoxide synthase 1	Homo sapiens	166-170
33219556-9	2021	Dabigatran cessation unduly increased platelet aggregability for 2 days after drug cessation, an effect mediated through arachidonic acid or thrombin, which effect was significantly attenuated by single-dose aspirin pretreatment.	Aspirin	208-215	coagulation factor II	Mus musculus	141-149
33318029-7	2021	Of these, aspirin decreased MCM6, RRM2 and ARFIP2 expression and MR analysis showed that a standard deviation increase in mRNA/protein expression was associated with increased CRC risk (OR:1.08, 95% CI:1.03-1.13, OR:3.33, 95% CI:2.46-4.50 and OR:1.15, 95% CI:1.02-1.29, respectively).	Aspirin	10-17	minichromosome maintenance complex component 6	Homo sapiens	28-32
33318029-8	2021	CONCLUSIONS: MCM6 and RRM2 are involved in DNA repair whereby reduced expression may lead to increased DNA aberrations and ultimately cancer cell death, whereas ARFIP2 is involved in actin cytoskeletal regulation indicating a possible role in aspirin"s reduction of metastasis.	Aspirin	243-250	minichromosome maintenance complex component 6	Homo sapiens	13-17
33222458-0	2021	Xuesaitong injection (lyophilized) combined with aspirin and clopidogrel protect against focal cerebral ischemic/reperfusion injury in rats by suppressing oxidative stress and inflammation and regulating the NOX2/IL-6/STAT3 pathway.	Aspirin	49-56	interleukin 6	Rattus norvegicus	213-217
33574709-2	2021	Inhibition of mTORC1 (mechanistic target of rapamycin complex 1) activity upon aspirin treatment has been reported in breast cancer cells harboring PI3KCA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) mutation and is considered to account for anticancer action.	Aspirin	79-86	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	156-226
33633548-7	2020	Nicotine downregulated GLT-1 and xCT gene expression in the prefrontal cortex, an effect reversed by N-acetylcysteine, while acetylsalicylic acid reversed the nicotine-induced downregulation of GLT-1 gene expression.	Aspirin	125-145	solute carrier family 1 member 2	Rattus norvegicus	194-199
33633548-9	2020	Conclusion: Nicotine reinstatement, following post-deprivation of chronic oral nicotine intake, downregulates the mRNA levels of GLT-1 and xCT transporters, an effect reversed by the coadministration of N-acetylcysteine and acetylsalicylic acid, leading to a marked inhibition of nicotine intake.	Aspirin	224-244	solute carrier family 1 member 2	Rattus norvegicus	129-134
33222458-11	2021	Moreover, XST+ASA+CLP group also had lower levels of NOX2, inducible nitric oxide synthase (iNOS), interleukin (IL)-6, and p-STAT3/STAT3.	Aspirin	14-17	nitric oxide synthase 2	Rattus norvegicus	59-90
33222458-11	2021	Moreover, XST+ASA+CLP group also had lower levels of NOX2, inducible nitric oxide synthase (iNOS), interleukin (IL)-6, and p-STAT3/STAT3.	Aspirin	14-17	nitric oxide synthase 2	Rattus norvegicus	92-96
33222458-11	2021	Moreover, XST+ASA+CLP group also had lower levels of NOX2, inducible nitric oxide synthase (iNOS), interleukin (IL)-6, and p-STAT3/STAT3.	Aspirin	14-17	interleukin 6	Rattus norvegicus	99-117
33222458-12	2021	CONCLUSIONS: These results demonstrate that a combination of XST, ASA, and CLP effectively protected rats against middle cerebral artery occlusion/reperfusion (MCAO/R) injury by suppressing the NOX2/IL-6/ STAT3 pathway.	Aspirin	66-69	interleukin 6	Rattus norvegicus	199-203
33512659-0	2021	Pretreatment of Indobufen and Aspirin and their Combinations with Clopidogrel or Ticagrelor Alleviates Inflammasome Mediated Pyroptosis Via Inhibiting NF-kappaB/NLRP3 Pathway in Ischemic Stroke.	Aspirin	30-37	NLR family, pyrin domain containing 3	Rattus norvegicus	161-166
32371071-0	2021	Activation of the 15-Lipoxygenase Pathway in Aspirin Exacerbated Respiratory Disease.	Aspirin	45-52	arachidonate 15-lipoxygenase	Homo sapiens	18-33
32371071-1	2021	BACKGROUND: Aspirin Exacerbated Respiratory Disease (AERD) is characterized by asthma, chronic rhinosinusitis with nasal polyps (CRSwNP), and an intolerance to medications that inhibit cyclooxygenase-1.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	185-201
33009703-0	2021	Risk of Age-Related Macular degeneration in Aspirin Users and Non-Aspirin Users: a population-based cohort study in Taiwan.	Aspirin	44-51	renin binding protein	Homo sapiens	8-11
33009703-1	2021	BACKGROUND: The association between cardioprotective aspirin and risk of age-related macular degeneration (AMD) is still controversial up to date.	Aspirin	53-60	renin binding protein	Homo sapiens	73-76
33358345-8	2021	Intra-arterial tissue plasminogen activator (t-PA) combined with verapamil and eptifibatide was administered within the ASA and the patient had significant neurological improvement immediately postoperatively and at 8-month clinical follow-up.	Aspirin	120-123	plasminogen activator, tissue type	Homo sapiens	15-49
33307284-1	2021	Acetylsalicylic acid (ASA) and type 2 diabetes mellitus (T2DM) affect fibrin clot properties through fibrinogen acetylation or glycation.	Aspirin	0-20	fibrinogen beta chain	Homo sapiens	101-111
33307284-1	2021	Acetylsalicylic acid (ASA) and type 2 diabetes mellitus (T2DM) affect fibrin clot properties through fibrinogen acetylation or glycation.	Aspirin	22-25	fibrinogen beta chain	Homo sapiens	101-111
33307284-2	2021	We aimed to identify glycation and acetylation sites on fibrinogen in plasma fibrin clot of T2DM patients with respect to effects of ASA and fibrin clot properties.	Aspirin	133-136	fibrinogen beta chain	Homo sapiens	56-66
33512659-2	2021	In this study, we investigated the protective efficiency of pretreatment of indobufen or aspirin combined with clopidogrel or ticagrelor (IACT) on cerebral ischemic injury via NF-kappaB/NLRP3 pathway.	Aspirin	89-96	NLR family, pyrin domain containing 3	Rattus norvegicus	186-191
33493277-5	2021	Aspirin attenuated the role of sFlt-1 in oxidative stress and endothelial dysfunction and reduced apoptosis of trophoblasts by inactivating the NF-kappaB signaling pathway in HTR-8/SVneo trophoblast cells.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	144-153
33493277-7	2021	In conclusion, aspirin reverses the endothelial dysfunction and oxidative stress caused by sFlt-1 and thus reduces apoptosis of preeclamptic trophoblasts by inactivating NF-kappaB signaling pathway.	Aspirin	15-22	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	170-179
33493277-4	2021	Serum sFlt-1 and sEng profiles and placental oxidative stresslevels were significantly decreased in preeclampsia patients treated with aspirin compared with untreated patients without it, while serum PLGF and placental SOD profiles were increased in preeclampsia patients with aspirin.	Aspirin	135-142	placental growth factor	Homo sapiens	200-204
33902044-14	2021	A CRP level higher than 15 mg/L may suggest initiation of low-dose aspirin in low-risk pregnancies.	Aspirin	67-74	C-reactive protein	Homo sapiens	2-5
33348283-7	2021	We report that immortalized trophoblast cells express the target proteins of acetaminophen and aspirin: cyclooxygenase (COX) -1 and -2.	Aspirin	95-102	prostaglandin-endoperoxide synthase 1	Homo sapiens	104-134
33093222-8	2021	CONCLUSIONS: Among patients with minor ischemic stroke or TIA who were receiving clopidogrel and aspirin, those carrying the F2R IVSn-14 T allele had a lower rate of recurrent stroke than those who were not.	Aspirin	97-104	coagulation factor II thrombin receptor	Homo sapiens	125-128
33360326-4	2021	The cyclooxygenase-2 enzyme inhibited by Aspirin and other NSAIDs, and which catalyses prostaglandin synthesis and mediates inflammation, is overexpressed in prostate cancer, therefore inhibition of cyclooxygenase-2 may have direct, and indirect, therapeutic effects.	Aspirin	41-48	prostaglandin-endoperoxide synthase 2	Homo sapiens	4-20
33360326-4	2021	The cyclooxygenase-2 enzyme inhibited by Aspirin and other NSAIDs, and which catalyses prostaglandin synthesis and mediates inflammation, is overexpressed in prostate cancer, therefore inhibition of cyclooxygenase-2 may have direct, and indirect, therapeutic effects.	Aspirin	41-48	prostaglandin-endoperoxide synthase 2	Homo sapiens	199-215
33427041-9	2021	COX-independent mechanisms of anticancer effects of aspirin include down-regulation of nuclear factor kappa B activity and Akt activation, modulation of Bcl-2 and Bax family proteins, suppression of vascular endothelial growth factor, induction of apoptosis, disruption of DNA repair mechanisms, and induction of spermidine/spermine N1-acetyltransferase that modulates polyamine catabolism.	Aspirin	52-59	AKT serine/threonine kinase 1	Homo sapiens	123-126
33427041-9	2021	COX-independent mechanisms of anticancer effects of aspirin include down-regulation of nuclear factor kappa B activity and Akt activation, modulation of Bcl-2 and Bax family proteins, suppression of vascular endothelial growth factor, induction of apoptosis, disruption of DNA repair mechanisms, and induction of spermidine/spermine N1-acetyltransferase that modulates polyamine catabolism.	Aspirin	52-59	BCL2 apoptosis regulator	Homo sapiens	153-158
33427041-9	2021	COX-independent mechanisms of anticancer effects of aspirin include down-regulation of nuclear factor kappa B activity and Akt activation, modulation of Bcl-2 and Bax family proteins, suppression of vascular endothelial growth factor, induction of apoptosis, disruption of DNA repair mechanisms, and induction of spermidine/spermine N1-acetyltransferase that modulates polyamine catabolism.	Aspirin	52-59	BCL2 associated X, apoptosis regulator	Homo sapiens	163-166
33427041-9	2021	COX-independent mechanisms of anticancer effects of aspirin include down-regulation of nuclear factor kappa B activity and Akt activation, modulation of Bcl-2 and Bax family proteins, suppression of vascular endothelial growth factor, induction of apoptosis, disruption of DNA repair mechanisms, and induction of spermidine/spermine N1-acetyltransferase that modulates polyamine catabolism.	Aspirin	52-59	vascular endothelial growth factor A	Homo sapiens	199-233
33430037-10	2021	PTGS2/COX2 expression trended lower in aspirin users, but not with tumor response.	Aspirin	39-46	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
33430037-10	2021	PTGS2/COX2 expression trended lower in aspirin users, but not with tumor response.	Aspirin	39-46	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	6-10
31733014-6	2021	Alcohol intake either on the chronic phase or following deprivation and re-access led to a 50% reduction of cortical glutamate transporter GLT-1 levels, while aspirin administration fully returned GLT-1 to normal levels.	Aspirin	159-166	solute carrier family 1 member 2	Rattus norvegicus	197-202
33542757-2	2021	Transforming growth factor beta 1 (TGF-beta1) is reduced not only in the nasal polypoid tissue, but also in the plasma of aspirin-intolerant patients.	Aspirin	122-129	transforming growth factor beta 1	Homo sapiens	0-33
33542757-2	2021	Transforming growth factor beta 1 (TGF-beta1) is reduced not only in the nasal polypoid tissue, but also in the plasma of aspirin-intolerant patients.	Aspirin	122-129	transforming growth factor beta 1	Homo sapiens	35-44
33125972-8	2020	RT-qPCR analysis show that Asp-Sr/beta-TCP, beta-TCP group and Sr/beta-TCP group showed increased BMP2, Smad1, OPG than the OVX group(p < 0.05), while Asp-Sr/beta-TCP exhibited decreased TNF-alpha IFN-gamma and RANKL than the OVX group(p < 0.05).	Aspirin	27-30	tumor necrosis factor	Rattus norvegicus	187-196
33373378-9	2020	Potential risk factors identified in the aspirin group were concomitant insulin medication (p = 0.0006) and elevated C-reactive protein (CRP) (p = 0.0021).	Aspirin	41-48	C-reactive protein	Homo sapiens	117-135
33373378-9	2020	Potential risk factors identified in the aspirin group were concomitant insulin medication (p = 0.0006) and elevated C-reactive protein (CRP) (p = 0.0021).	Aspirin	41-48	C-reactive protein	Homo sapiens	137-140
33293599-6	2020	COX-2 induction was prevented by different antiplatelet agents, i.e., Aspirin, the TP antagonist SQ29,548, or Revacept (a dimeric soluble GPVI-Fc fusion protein).	Aspirin	70-77	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
33184378-6	2020	These effects are initiated by ASA/SA-triggered Akt/mTOR/AMPK-dependent activation of nitric oxide synthase 3 (eNOS), which increases nitric oxide and reactive oxygen species production inducing ER stress response.	Aspirin	31-34	thymoma viral proto-oncogene 1	Mus musculus	48-51
32562573-1	2020	The platelet endothelial aggregation receptor-1 (PEAR1) rs12041331 variant has been identified as a genetic determinant of platelet aggregation in response to antiplatelet therapies, including aspirin.	Aspirin	193-200	platelet endothelial aggregation receptor 1	Homo sapiens	4-47
32562573-1	2020	The platelet endothelial aggregation receptor-1 (PEAR1) rs12041331 variant has been identified as a genetic determinant of platelet aggregation in response to antiplatelet therapies, including aspirin.	Aspirin	193-200	platelet endothelial aggregation receptor 1	Homo sapiens	49-54
33447595-7	2020	Results: Treatment with ASA significantly inhibited the proliferation, invasion, and migration capabilities, and caused a significant decrease in angiogenin and PIGF secretion in both CM and UM.	Aspirin	24-27	phosphatidylinositol glycan anchor biosynthesis class F	Homo sapiens	161-165
32574107-9	2020	Aspirin and dipyridamole may be used, in combination with drugs blocking downstream the activation of the STING pathway, like inhibitors of IL-6R and JAK/STAT pathways.	Aspirin	0-7	interleukin 6 receptor	Homo sapiens	140-145
32930782-12	2020	Adequate adherence with aspirin results in an increase in ATL and IL-10 with reduced IL-8 plasma concentration.	Aspirin	24-31	C-X-C motif chemokine ligand 8	Homo sapiens	85-89
32954579-1	2020	PURPOSE: Magnesium stearate (MgSt) is a widely used excipient in pharmaceutical formulations but should be avoided in aspirin preparations as it hydrolyzes aspirin.	Aspirin	118-125	microsomal glutathione S-transferase 1	Homo sapiens	29-33
32954579-1	2020	PURPOSE: Magnesium stearate (MgSt) is a widely used excipient in pharmaceutical formulations but should be avoided in aspirin preparations as it hydrolyzes aspirin.	Aspirin	156-163	microsomal glutathione S-transferase 1	Homo sapiens	29-33
32954579-2	2020	We hypothesized that preparations of aspirin-containing MgSt (MgSt-ASA) are less effective in preventing thrombosis in clinical settings.	Aspirin	37-44	microsomal glutathione S-transferase 1	Homo sapiens	56-60
32954579-2	2020	We hypothesized that preparations of aspirin-containing MgSt (MgSt-ASA) are less effective in preventing thrombosis in clinical settings.	Aspirin	37-44	microsomal glutathione S-transferase 1	Homo sapiens	62-66
33329515-2	2020	In the current study, we found that both aspirin and 5-aminoimidazole-4-carboxamide-1-beta-riboside (AICAR) siginificantly attenuated virus replication by inhibiting BEFV-induced autophagy via suppressing the BEFV-activated PI3K/Akt/NF-kappaB and Src/JNK pathways as well as inducing reversion of the BEFV-suppressed PI3K-Akt-mTORC1 pathway.	Aspirin	41-48	AKT serine/threonine kinase 1	Homo sapiens	229-232
33329515-2	2020	In the current study, we found that both aspirin and 5-aminoimidazole-4-carboxamide-1-beta-riboside (AICAR) siginificantly attenuated virus replication by inhibiting BEFV-induced autophagy via suppressing the BEFV-activated PI3K/Akt/NF-kappaB and Src/JNK pathways as well as inducing reversion of the BEFV-suppressed PI3K-Akt-mTORC1 pathway.	Aspirin	41-48	nuclear factor kappa B subunit 1	Homo sapiens	233-242
33329515-2	2020	In the current study, we found that both aspirin and 5-aminoimidazole-4-carboxamide-1-beta-riboside (AICAR) siginificantly attenuated virus replication by inhibiting BEFV-induced autophagy via suppressing the BEFV-activated PI3K/Akt/NF-kappaB and Src/JNK pathways as well as inducing reversion of the BEFV-suppressed PI3K-Akt-mTORC1 pathway.	Aspirin	41-48	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	247-250
33329515-2	2020	In the current study, we found that both aspirin and 5-aminoimidazole-4-carboxamide-1-beta-riboside (AICAR) siginificantly attenuated virus replication by inhibiting BEFV-induced autophagy via suppressing the BEFV-activated PI3K/Akt/NF-kappaB and Src/JNK pathways as well as inducing reversion of the BEFV-suppressed PI3K-Akt-mTORC1 pathway.	Aspirin	41-48	mitogen-activated protein kinase 8	Homo sapiens	251-254
33329515-2	2020	In the current study, we found that both aspirin and 5-aminoimidazole-4-carboxamide-1-beta-riboside (AICAR) siginificantly attenuated virus replication by inhibiting BEFV-induced autophagy via suppressing the BEFV-activated PI3K/Akt/NF-kappaB and Src/JNK pathways as well as inducing reversion of the BEFV-suppressed PI3K-Akt-mTORC1 pathway.	Aspirin	41-48	AKT serine/threonine kinase 1	Homo sapiens	322-325
33313269-0	2020	Aspirin alleviates denervation-induced muscle atrophy via regulating the Sirt1/PGC-1alpha axis and STAT3 signaling.	Aspirin	0-7	signal transducer and activator of transcription 3	Mus musculus	99-104
33313269-12	2020	Mitochondrial vacuolation and autophagy were inhibited, as evidenced by reduced level of autophagy related proteins PINK1, BNIP3, LC3B and Atg7 in mice treated with aspirin compared with mice treated with saline.	Aspirin	165-172	autophagy related 7	Mus musculus	139-143
33313269-14	2020	Moreover, aspirin reduced the levels of inflammatory factors interleukin-6, interleukin-1beta and tumor necrosis factor-alpha and decreased the activation of STAT3 signaling pathway.	Aspirin	10-17	interleukin 6	Mus musculus	61-74
33313269-14	2020	Moreover, aspirin reduced the levels of inflammatory factors interleukin-6, interleukin-1beta and tumor necrosis factor-alpha and decreased the activation of STAT3 signaling pathway.	Aspirin	10-17	interleukin 1 beta	Mus musculus	76-93
33313269-14	2020	Moreover, aspirin reduced the levels of inflammatory factors interleukin-6, interleukin-1beta and tumor necrosis factor-alpha and decreased the activation of STAT3 signaling pathway.	Aspirin	10-17	tumor necrosis factor	Mus musculus	98-125
33313269-14	2020	Moreover, aspirin reduced the levels of inflammatory factors interleukin-6, interleukin-1beta and tumor necrosis factor-alpha and decreased the activation of STAT3 signaling pathway.	Aspirin	10-17	signal transducer and activator of transcription 3	Mus musculus	158-163
33313269-15	2020	Conclusions: This is the first study to find that aspirin can alleviate denervation-induced muscle atrophy and inhibit the type I-to-type II muscle fiber conversion and mitophagy possibly through regulating the STAT3 inflammatory signaling pathway and Sirt1/PGC-1alpha signal axis.	Aspirin	50-57	signal transducer and activator of transcription 3	Mus musculus	211-216
33176342-0	2020	PURL:Rethinking daily aspirin for primary prevention.	Aspirin	22-29	phosphoribosylformylglycinamidine synthase	Homo sapiens	0-4
32452885-5	2020	Patients with LDL-C <130 mg/dl were older and were more commonly pretreated with aspirin and statins compared to patients with LDL-C >=130 mg/dl.	Aspirin	81-88	component of oligomeric golgi complex 2	Homo sapiens	14-19
32199913-0	2020	RGS4 promotes allergen- and aspirin-associated airway hyper-responsiveness by inhibiting PGE2 biosynthesis.	Aspirin	28-35	regulator of G-protein signaling 4	Mus musculus	0-4
32199913-12	2020	The RGS4 antagonist CCG203769 attenuated AHR induced by allergen or aspirin challenge of wild type (WT) or ptges1-/- mice, respectively, in association with increased airway PGE2 levels.	Aspirin	68-75	regulator of G-protein signaling 4	Mus musculus	4-8
32199913-13	2020	CONCLUSIONS: RGS4 may contribute to the development of AHR by reducing airway PGE2 biosynthesis in allergen- and aspirin-induced asthma.	Aspirin	113-120	regulator of G-protein signaling 4	Mus musculus	13-17
33170592-4	2020	Platelets from ASA-sensitive patients showed higher expression of the proapoptotic proteins Bak and Bax than those from ASA-resistant patients, although only Bak protein remained different when the results were adjusted by age.	Aspirin	15-18	BCL2 associated X, apoptosis regulator	Homo sapiens	100-103
33038835-4	2020	A focus is also done on single lipoxygenation of mono-hydroxylated products first made by aspirin-treated cyclooxygenase-2.	Aspirin	90-97	prostaglandin-endoperoxide synthase 2	Homo sapiens	106-122
33049446-5	2020	Under salt stress, the SlSOS1/2 and SlNHX1 genes were highly expressed, and the accumulation of Na+ was lower in the transgenic seedlings than in WT, however, ROS accumulated to a greater degree in the former, and the ROS-scavenging-related enzyme activities and AsA content were lower in the transgenic seedlings than WT.	Aspirin	263-266	Na+/H+ antiporter	Solanum lycopersicum	36-42
32956986-0	2020	Concurrent use of aspirin with osimertinib is associated with improved survival in advanced EGFR-mutant non-small cell lung cancer.	Aspirin	18-25	epidermal growth factor receptor	Homo sapiens	92-96
32956986-11	2020	CONCLUSION: Concurrent aspirin use with osimertinib in EGFR-mutant NSCLC patients was associated with improved survival, regardless of lines of therapy, CNS metastatic status, EGFR mutation type, age, gender, TP53, and PD-L1 status.	Aspirin	23-30	epidermal growth factor receptor	Homo sapiens	55-59
32956986-11	2020	CONCLUSION: Concurrent aspirin use with osimertinib in EGFR-mutant NSCLC patients was associated with improved survival, regardless of lines of therapy, CNS metastatic status, EGFR mutation type, age, gender, TP53, and PD-L1 status.	Aspirin	23-30	tumor protein p53	Homo sapiens	209-213
32896555-0	2020	Aspirin restores endothelial function by mitigating 17beta-estradiol-induced alpha-SMA accumulation and autophagy inhibition via Vps15 scaffold regulation of Beclin-1 phosphorylation.	Aspirin	0-7	actin alpha 2, smooth muscle, aorta	Mus musculus	77-86
33111589-5	2021	Results revealed that platelet-like particles (PLPs) derived from ASA-exposed Meg-01 cells, showed higher content of pro-apoptotic proteins Bax and Bak than PLPs from non-ASA incubated Meg-01 cells.	Aspirin	66-69	BCL2 associated X, apoptosis regulator	Homo sapiens	140-143
33111589-7	2021	However, only after calcium ionophore A23187 stimulation, caspase-3 activity, the cytosolic cytochrome C content, and reduction of mitochondrial membrane potential were higher in PLPs from ASA-incubated megakaryocytes than in those from Meg-01 without ASA.	Aspirin	189-192	caspase 3	Homo sapiens	58-67
33111589-9	2021	The L-arginine antagonist, NG-Nitro-L-arginine Methyl Ester, reduced caspase-3 activity in A23187-stimulated PLPs generated from ASA-incubated Meg-01 cells.	Aspirin	129-132	caspase 3	Homo sapiens	69-78
33095767-5	2020	ASA treatment reduced PG synthesis and is associated with decreased expression of components of the Toll and IMD immune pathways, thereby rendering mosquitoes more susceptible to both bacterial and viral infections.	Aspirin	0-3	uncharacterized protein LOC5572865	Aedes aegypti	109-112
33082288-0	2020	SMAR1 repression by pluripotency factors and consequent chemoresistance in breast cancer stem-like cells is reversed by aspirin.	Aspirin	120-127	BTG3 associated nuclear protein	Homo sapiens	0-5
33082288-6	2020	Our findings reveal transcriptional mechanisms regulating SMAR1 that also regulate cancer stemness and chemoresistance and suggest that, by restoring SMAR1 expression, aspirin might enhance chemotherapeutic efficacy in patients with stem-like tumors.	Aspirin	168-175	BTG3 associated nuclear protein	Homo sapiens	58-63
33082288-6	2020	Our findings reveal transcriptional mechanisms regulating SMAR1 that also regulate cancer stemness and chemoresistance and suggest that, by restoring SMAR1 expression, aspirin might enhance chemotherapeutic efficacy in patients with stem-like tumors.	Aspirin	168-175	BTG3 associated nuclear protein	Homo sapiens	150-155
33178183-10	2020	ASA may enhance HCEs migration by decreasing NETs formation through inhibition of NF-kappaB activation and could be a promising strategy for improving the prognosis of corneal alkali burns.	Aspirin	0-3	nuclear factor kappa B subunit 1	Homo sapiens	82-91
33116404-0	2020	Novel Molecular Mechanism of Aspirin and Celecoxib Targeting Mammalian Neuraminidase-1 Impedes Epidermal Growth Factor Receptor Signaling Axis and Induces Apoptosis in Pancreatic Cancer Cells.	Aspirin	29-36	epidermal growth factor receptor	Homo sapiens	95-127
33116404-13	2020	Aspirin blocked Neu-1 desialylation of alpha-2,3-sialic acid expression following 30 min stimulation with EGF.	Aspirin	0-7	G protein-coupled receptor 162	Homo sapiens	39-46
33116404-15	2020	Aspirin inhibited phosphorylation of the EGFR in EGF-stimulated cells.	Aspirin	0-7	epidermal growth factor receptor	Homo sapiens	41-45
33116404-16	2020	Aspirin dose- and time-dependently induced CellEvent caspase-3/7+ cells as well as apoptosis and necrosis on PANC-1 cells.	Aspirin	0-7	caspase 3	Homo sapiens	53-64
32896555-12	2020	Aspirin inhibited alpha-SMA accumulation by enhancing autophagy, reversed endothelial functional impairment caused by E-2, and promoted endothelium-dependent vasodilation.	Aspirin	0-7	actin alpha 2, smooth muscle, aorta	Mus musculus	18-27
31783142-13	2020	CONCLUSION: Our results reveal that "aspirin resistance" is frequently found in T2DM, and is strongly related to insulin resistance and severity of CAD, but weakly related to HbA1c and not at all to inflammatory parameters.	Aspirin	37-44	insulin	Homo sapiens	113-120
32992455-6	2020	Furthermore, by analyses of the soft agar colony formation, 5-ethynyl-20-deoxyuridine (EdU) assay, reactive oxygen species (ROS) imaging, flow cytometry and Western blotting, AsA demonstrated the ability to induce cell cycle arrest in G1 and G1/S phases by increasing ROS generation and decreasing of Akt activity.	Aspirin	175-178	thymoma viral proto-oncogene 1	Mus musculus	301-304
32552387-7	2020	The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were lower in the aspirin group than in the control group after treatment (Both p = .000).	Aspirin	95-102	C-reactive protein	Homo sapiens	45-63
32552387-7	2020	The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were lower in the aspirin group than in the control group after treatment (Both p = .000).	Aspirin	95-102	C-reactive protein	Homo sapiens	65-68
32992455-7	2020	Conversely, ROS inhibitors and overexpression of Akt could decrease cell growth inhibition and cell cycle arrest induced by AsA.	Aspirin	124-127	thymoma viral proto-oncogene 1	Mus musculus	49-52
32992455-8	2020	Therefore, we believe that AsA blocks the cell cycle via an ROS-dependent Akt/Cyclin D1/Rb signaling pathway, which consequently leads to the observed antitumor effect both in vitro and in vivo.	Aspirin	27-30	thymoma viral proto-oncogene 1	Mus musculus	74-77
32994805-0	2020	Aspirin potentiates celecoxib-induced growth inhibition and apoptosis in human non-small cell lung cancer by targeting GRP78 activity.	Aspirin	0-7	heat shock protein family A (Hsp70) member 5	Homo sapiens	119-124
32957311-11	2020	CONCLUSIONS: Our study suggested that aspirin use might be associated with a reduced risk of breast cancer, particularly for reducing the risk of hormone receptor positive tumors or in situ breast tumors, and the risk of breast cancer in postmenopausal women.	Aspirin	38-45	nuclear receptor subfamily 4 group A member 1	Homo sapiens	146-162
32994805-7	2020	Further research showed that the anti-tumor effect of celecoxib combined with aspirin was mainly produced by activating caspase-9/caspase-3, arresting cell cycle and inhibiting the ERK-MAPK signaling pathway.	Aspirin	78-85	caspase 3	Homo sapiens	130-139
32994805-7	2020	Further research showed that the anti-tumor effect of celecoxib combined with aspirin was mainly produced by activating caspase-9/caspase-3, arresting cell cycle and inhibiting the ERK-MAPK signaling pathway.	Aspirin	78-85	mitogen-activated protein kinase 1	Homo sapiens	181-184
32994805-7	2020	Further research showed that the anti-tumor effect of celecoxib combined with aspirin was mainly produced by activating caspase-9/caspase-3, arresting cell cycle and inhibiting the ERK-MAPK signaling pathway.	Aspirin	78-85	mitogen-activated protein kinase 1	Homo sapiens	185-189
32994805-9	2020	Moreover, we identified GRP78 as a target protein of aspirin in NSCLC cells.	Aspirin	53-60	heat shock protein family A (Hsp70) member 5	Homo sapiens	24-29
32994805-10	2020	Aspirin induced an endoplasmic reticulum stress response by inhibiting GRP78 activity.	Aspirin	0-7	heat shock protein family A (Hsp70) member 5	Homo sapiens	71-76
33336182-1	2020	Aspirin-exacerbated respiratory disease (AERD) is characterized by the triad of chronic rhinosinusitis with nasal polyposis, adult-onset asthma and non-IgE mediated reactions to aspirin and other cyclooxygenase-1 (COX-1) inhibitors.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	214-219
32668287-1	2020	Our previous study demonstrated that new oleanolic acid oxime (OAO) derivatives and their conjugates with aspirin (ASP) inhibit NF-kappaB activation.	Aspirin	106-113	nuclear factor kappa B subunit 1	Homo sapiens	128-137
32668287-1	2020	Our previous study demonstrated that new oleanolic acid oxime (OAO) derivatives and their conjugates with aspirin (ASP) inhibit NF-kappaB activation.	Aspirin	115-118	nuclear factor kappa B subunit 1	Homo sapiens	128-137
32668287-4	2020	The results showed the enhanced activation and expression of Nrf2 as a result of treatment with OAO derivatives themselves and to less extent by their ASP conjugates, mainly in HepG2 cells.	Aspirin	151-154	NFE2 like bZIP transcription factor 2	Homo sapiens	61-65
32668287-7	2020	The derivative of OAO (18) substituted with ASP (19) also affected Nrf2 activation and expression, but this effect was less pronounced in comparison with non-conjugated OAO.	Aspirin	44-47	NFE2 like bZIP transcription factor 2	Homo sapiens	67-71
32295429-10	2020	Aspirin induced elevation in the inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-6, and interleukin-1beta.	Aspirin	0-7	tumor necrosis factor	Rattus norvegicus	64-91
33336182-1	2020	Aspirin-exacerbated respiratory disease (AERD) is characterized by the triad of chronic rhinosinusitis with nasal polyposis, adult-onset asthma and non-IgE mediated reactions to aspirin and other cyclooxygenase-1 (COX-1) inhibitors.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	196-212
32360116-0	2020	Aspirin to Reduce Risk for Sudden Cardiac Death in Athletes With Elevated C-Reactive Protein Levels.	Aspirin	0-7	C-reactive protein	Homo sapiens	74-92
32295429-10	2020	Aspirin induced elevation in the inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-6, and interleukin-1beta.	Aspirin	0-7	interleukin 6	Rattus norvegicus	93-106
32295429-10	2020	Aspirin induced elevation in the inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-6, and interleukin-1beta.	Aspirin	0-7	interleukin 1 beta	Rattus norvegicus	112-129
32295429-11	2020	Aspirin enhanced the immunoexpression of inducible nitric oxide synthetase (iNOS) and increased the level of nitrite/nitrate in gastric tissue.	Aspirin	0-7	nitric oxide synthase 2	Rattus norvegicus	41-74
32295429-11	2020	Aspirin enhanced the immunoexpression of inducible nitric oxide synthetase (iNOS) and increased the level of nitrite/nitrate in gastric tissue.	Aspirin	0-7	nitric oxide synthase 2	Rattus norvegicus	76-80
33229758-0	2020	Aspirin-Triggered Lipoxin Protects Lipopolysaccharide-Induced Acute Kidney Injury via the TLR4/MyD88/NF-kappaB Pathway.	Aspirin	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	101-110
32532481-7	2020	RESULTS: After THA, there was a significantly lower risk of VTE associated with the use of direct thrombin inhibitors (0.44%; odds ratio [OR], 0.69; 95% confidence interval [95% CI], 0.55-0.87; P = .002) and factor Xa inhibitors (0.37%; OR, 0.63; 95% CI, 0.47-0.85; P = .003) compared with aspirin (0.63%).	Aspirin	290-297	coagulation factor II, thrombin	Homo sapiens	98-106
32719503-0	2020	Aspirin and ibuprofen could lower risk of LRRK2 Parkinson disease.	Aspirin	0-7	leucine rich repeat kinase 2	Homo sapiens	42-47
32815992-18	2020	Aspirin tended to increase jejunal claudin-1 mRNA expression (P = 0.10), but did not affect mRNA expression of other genes regulating tight junction function (P >= 0.20).	Aspirin	0-7	claudin 1	Bos taurus	35-44
33277869-8	2020	According to Western blotting results, the protein expressions of PI3K, phosphorylated (p)-Akt and p-mTOR were decreased after aspirin treatment.	Aspirin	127-134	AKT serine/threonine kinase 1	Homo sapiens	91-94
33277869-8	2020	According to Western blotting results, the protein expressions of PI3K, phosphorylated (p)-Akt and p-mTOR were decreased after aspirin treatment.	Aspirin	127-134	mechanistic target of rapamycin kinase	Homo sapiens	101-105
33277869-10	2020	It was found in CCK-8 assay that IGF-1 supplementation markedly reversed the inhibition of aspirin on the proliferation of PANC-1 cells in comparison with PBS supplementation.	Aspirin	91-98	insulin like growth factor 1	Homo sapiens	33-38
33277869-11	2020	CONCLUSIONS: Aspirin inhibits the proliferation and promotes the apoptosis of pancreatic cancer cells by inactivating the PI3K/Akt/mTOR signaling pathway.	Aspirin	13-20	AKT serine/threonine kinase 1	Homo sapiens	127-130
33277869-11	2020	CONCLUSIONS: Aspirin inhibits the proliferation and promotes the apoptosis of pancreatic cancer cells by inactivating the PI3K/Akt/mTOR signaling pathway.	Aspirin	13-20	mechanistic target of rapamycin kinase	Homo sapiens	131-135
32535107-5	2020	Hu-COX-2 exposed in vitro to an excess of ASA was acetylated by approximately 40-50% associated with the inhibition of COX-2 activity by 80-90%.	Aspirin	42-45	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	3-8
32854760-9	2020	In regards to the underlying molecular mechanism of action, aspirin reduces histone demethylase (KDM6A/B) expression that mediates histone methylation and suppresses gene expression via a COX-independent manner.	Aspirin	60-67	lysine demethylase 6A	Homo sapiens	97-104
32922301-9	2020	TNF alpha levels could also be reduced by statins, aspirin, and curcumin.	Aspirin	51-58	tumor necrosis factor	Homo sapiens	0-9
33194862-11	2020	LEARNING POINTS: Polycythemia can cause erythromelalgia, which should be treated with aspirin.Primary aldosteronism causes secondary erythropoiesis through activation of the renin-aldosterone system, but the mechanism is not clear.Erythropoiesis may be promoted by concurrent primary aldosteronism and polycythemia vera, resulting in secondary erythromelalgia.	Aspirin	86-93	renin	Homo sapiens	174-179
32353222-11	2020	VWF staining was significantly lower in the ASA+Ticagrelor+UFH group compared with that in the other groups on the 3rd day (p=0.005).	Aspirin	44-47	von Willebrand factor	Homo sapiens	0-3
32325408-0	2020	Interaction between aspirin and vitamin C with human serum albumin as binary and ternary systems.	Aspirin	20-27	albumin	Homo sapiens	59-66
32325408-12	2020	For ternary biological system of (HSA-ASP)-Vit.	Aspirin	38-41	vitrin	Homo sapiens	43-46
32325408-17	2020	Based on the technology combination of voltammetry, infrared, three-dimensional fluorescence and circular dichroism (CD), it is proved that the existence of ASP will influence the binding process of Vit.	Aspirin	157-160	vitrin	Homo sapiens	199-202
32325408-21	2020	C immediately as one have just taken ASP, because the existence of ASP reduce the absorption of Vit.	Aspirin	37-40	vitrin	Homo sapiens	96-99
32325408-21	2020	C immediately as one have just taken ASP, because the existence of ASP reduce the absorption of Vit.	Aspirin	67-70	vitrin	Homo sapiens	96-99
32535107-0	2020	Characterization of cyclooxygenase-2 acetylation and prostanoid inhibition by aspirin in cellular systems.	Aspirin	78-85	prostaglandin-endoperoxide synthase 2	Homo sapiens	20-36
32535107-1	2020	The most recognized mechanism of aspirin(acetylsalicylic acid, ASA) action, at therapeutic dosing, is the inhibition of prostanoid biosynthesis through the acetylation of cyclooxygenase(COX)-isozymes (COX-1 at serine-529 and COX-2 at serine-516).	Aspirin	33-40	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	225-230
32535107-1	2020	The most recognized mechanism of aspirin(acetylsalicylic acid, ASA) action, at therapeutic dosing, is the inhibition of prostanoid biosynthesis through the acetylation of cyclooxygenase(COX)-isozymes (COX-1 at serine-529 and COX-2 at serine-516).	Aspirin	41-61	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	225-230
32535107-1	2020	The most recognized mechanism of aspirin(acetylsalicylic acid, ASA) action, at therapeutic dosing, is the inhibition of prostanoid biosynthesis through the acetylation of cyclooxygenase(COX)-isozymes (COX-1 at serine-529 and COX-2 at serine-516).	Aspirin	63-66	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	225-230
32535107-2	2020	Whether aspirin, also when given at the low-doses recommended for cardiovascular prevention, reduces the risk of colorectal cancer by affecting COX-2 activity in colorectal adenomatous lesions is still debated.	Aspirin	8-15	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	144-149
32535107-3	2020	We aimed to develop a direct biomarker of aspirin action on COX-2 by assessing the extent of acetylation of COX-2 at serine-516 using the AQUA strategy, enabling absolute protein quantitation by liquid chromatography-mass spectrometry.	Aspirin	42-49	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	60-65
32535107-3	2020	We aimed to develop a direct biomarker of aspirin action on COX-2 by assessing the extent of acetylation of COX-2 at serine-516 using the AQUA strategy, enabling absolute protein quantitation by liquid chromatography-mass spectrometry.	Aspirin	42-49	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	108-113
32679592-7	2020	Plasma levels of VWF activity predicted 1-year (hazard ratio [HR]: 2.68; 95% CI: 1.14-6.31; p < 0.024) and long-term (HR: 2.59; 95% CI: 1.10-6.09) mortality despite treatment with potent platelet inhibitors (dual-antiplatelet therapy with aspirin and prasugrel or ticagrelor).	Aspirin	239-246	von Willebrand factor	Homo sapiens	17-20
32933639-11	2020	Compared with the low-dose ginsenoside Rb1 group, the aspirin group and the high-dose ginsenoside Rb1 group had significant reductions in the levels of TNF-alpha, IL-6, and IL-1beta (P<0.05); the high-dose ginsenoside Rb1 group had significant increases in the expression levels of P-PI3K/PI3K and P-AKT/AKT (P<0.05).	Aspirin	54-61	tumor necrosis factor	Mus musculus	152-161
32933639-11	2020	Compared with the low-dose ginsenoside Rb1 group, the aspirin group and the high-dose ginsenoside Rb1 group had significant reductions in the levels of TNF-alpha, IL-6, and IL-1beta (P<0.05); the high-dose ginsenoside Rb1 group had significant increases in the expression levels of P-PI3K/PI3K and P-AKT/AKT (P<0.05).	Aspirin	54-61	interleukin 6	Mus musculus	163-167
32933639-11	2020	Compared with the low-dose ginsenoside Rb1 group, the aspirin group and the high-dose ginsenoside Rb1 group had significant reductions in the levels of TNF-alpha, IL-6, and IL-1beta (P<0.05); the high-dose ginsenoside Rb1 group had significant increases in the expression levels of P-PI3K/PI3K and P-AKT/AKT (P<0.05).	Aspirin	54-61	thymoma viral proto-oncogene 1	Mus musculus	300-303
32847114-7	2020	In this study, we provide a detailed analysis of how resveratrol and its aspirin derivatives can inhibit nuclear factor kappa B (NFkappaB) activation, cytokine production, the growth rate of cancer cells, and in vivo alleviate intestinal inflammation and tumor growth.	Aspirin	73-80	nuclear factor kappa B subunit 1	Homo sapiens	105-127
32847114-7	2020	In this study, we provide a detailed analysis of how resveratrol and its aspirin derivatives can inhibit nuclear factor kappa B (NFkappaB) activation, cytokine production, the growth rate of cancer cells, and in vivo alleviate intestinal inflammation and tumor growth.	Aspirin	73-80	nuclear factor kappa B subunit 1	Homo sapiens	129-137
32835720-5	2022	Aspirin at doses below 300 mg selectively and irreversibly inactivates the cyclooxygenase-1 enzyme, suppressing the production of prostaglandins and thromboxane and inhibiting inflammation and platelet aggregation.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	75-91
32470453-7	2020	Subsequently, overwhelming evidence showed that both metformin and aspirin can ameliorate T-cell mediated inflammation by inducing regulatory T-cells (Tregs) polarisation, inhibiting T-cell trafficking and activation as well as signal transducer and activator of transcription (STAT)3 signalling.	Aspirin	67-74	signal transducer and activator of transcription 3	Homo sapiens	228-284
32535107-5	2020	Hu-COX-2 exposed in vitro to an excess of ASA was acetylated by approximately 40-50% associated with the inhibition of COX-2 activity by 80-90%.	Aspirin	42-45	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	119-124
32535107-6	2020	In the three cell-types expressing COX-2, the extent of COX-2 acetylation and reduction of prostaglandin (PG)E2 biosynthesis by ASA was concentration-dependent with comparable EC50 values(in the low muM range).	Aspirin	128-131	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	35-40
32535107-6	2020	In the three cell-types expressing COX-2, the extent of COX-2 acetylation and reduction of prostaglandin (PG)E2 biosynthesis by ASA was concentration-dependent with comparable EC50 values(in the low muM range).	Aspirin	128-131	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	56-61
32535107-8	2020	In conclusion, we have developed a proteomic assay to evaluate the extent of acetylation of COX-2 at serine-516 by aspirin; its use in clinical studies will allow clarifying the mechanism of action of aspirin as anticancer agent.	Aspirin	115-122	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	92-97
32535107-8	2020	In conclusion, we have developed a proteomic assay to evaluate the extent of acetylation of COX-2 at serine-516 by aspirin; its use in clinical studies will allow clarifying the mechanism of action of aspirin as anticancer agent.	Aspirin	201-208	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	92-97
32802112-10	2020	Flow cytometry analysis showed that the expression of CD62P in platelet-rich plasma in the control group was significantly higher than that in the normal group, while the expression of CD62P in the HYW and aspirin groups was lower than that in the control group (P < 0.05).	Aspirin	206-213	selectin, platelet	Mus musculus	185-190
31420920-0	2020	Aspirin for the prevention and treatment of pre-eclampsia: A matter of COX-1 and/or COX-2 inhibition?	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	84-89
32592197-1	2020	Aspirin prevents thrombosis by inhibiting platelet cyclooxygenase (COX)-1 activity and the production of thromboxane (Tx)A2 , a pro-thrombotic eicosanoid.	Aspirin	0-7	cytochrome c oxidase I, mitochondrial	Mus musculus	51-73
32755957-0	2020	Chitosan nanoparticles loaded with aspirin and 5-fluororacil enable synergistic antitumour activity through the modulation of NF-kappaB/COX-2 signalling pathway.	Aspirin	35-42	nuclear factor kappa B subunit 1	Homo sapiens	126-135
32755957-3	2020	It demonstrated that aspirin inhibited NF-kappaB activation and suppressed NF-kappaB regulated COX-2 expression and prostaglandin E2 (PGE2) synthesis.	Aspirin	21-28	nuclear factor kappa B subunit 1	Homo sapiens	39-48
32755957-3	2020	It demonstrated that aspirin inhibited NF-kappaB activation and suppressed NF-kappaB regulated COX-2 expression and prostaglandin E2 (PGE2) synthesis.	Aspirin	21-28	nuclear factor kappa B subunit 1	Homo sapiens	75-84
32755957-4	2020	Furthermore, the proposed results clearly indicated that the combination of 5-Fu and aspirin by chitosan nanoparticles enhanced the intracellular concentration of drugs and exerted synergistic growth inhibition and apoptosis induction on hepatocellular carcinoma cells by suppressing NF-kappaB activation and inhibition of expression of COX-2.	Aspirin	85-92	nuclear factor kappa B subunit 1	Homo sapiens	284-293
32627038-9	2020	In addition, aspirin upregulated the levels of caspase-cleaved cytokeratin 18, increased the proportion of early apoptotic cells, decreased the levels of clusterin and heat shock protein 70 (HSP 70), upregulated the levels of miRNA-137 and inhibited epidermal growth factor receptor (EGFR) activation.	Aspirin	13-20	heat shock protein 1B	Mus musculus	168-189
32627038-9	2020	In addition, aspirin upregulated the levels of caspase-cleaved cytokeratin 18, increased the proportion of early apoptotic cells, decreased the levels of clusterin and heat shock protein 70 (HSP 70), upregulated the levels of miRNA-137 and inhibited epidermal growth factor receptor (EGFR) activation.	Aspirin	13-20	heat shock protein 1B	Mus musculus	191-197
32848653-11	2020	Accordingly, the lipoxin A4 receptor inhibitor, WRW4, blocked the ASA-induced reduction of ethanol intake.	Aspirin	66-69	formyl peptide receptor 2-like	Rattus norvegicus	17-36
32750030-9	2020	Results showed that aspirin increased eNOS level and reduced injury to the endothelial cells (ECs) caused by ox-LDL, Ang-II, and HG treatment in a dose-dependent manner.	Aspirin	20-27	nitric oxide synthase 3	Homo sapiens	38-42
32750030-9	2020	Results showed that aspirin increased eNOS level and reduced injury to the endothelial cells (ECs) caused by ox-LDL, Ang-II, and HG treatment in a dose-dependent manner.	Aspirin	20-27	angiotensinogen	Homo sapiens	117-123
32750030-11	2020	p-NF-kappaB and p-p38 mitogen-activated protein kinase inhibition, sVCAM-1 and sICAM-1 secretion, and eNOS activity promotion by aspirin treatment were found to be dependent on Beclin-1.	Aspirin	129-136	nitric oxide synthase 3	Homo sapiens	102-106
32750030-12	2020	These results suggested that aspirin can protect ECs from ox-LDL-, Ang-II-, and HG-induced injury by activating autophagy in a Beclin-1-dependent manner.	Aspirin	29-36	angiotensinogen	Homo sapiens	67-73
32752170-1	2020	Sensitivity to acetylsalicylic acid (ASA) is important in the treatment of patients with coronary heart disease (CHD) after coronary artery bypass grafting (CABG).	Aspirin	15-35	RAS p21 protein activator 1	Rattus norvegicus	37-40
32798401-1	2020	OBJECTIVE: To investigate whether Blimp1 plays an anti-apoptosis role in myeloma by interfering with ATF4/CHOP cell apoptosis pathway induced by endoplasmic reticulum stress, and to explore the anti-myeloma mechanism of aspirin.	Aspirin	220-227	PR/SET domain 1	Homo sapiens	34-40
32798401-9	2020	CCK-8 showed that the proliferation activity of U266 cells could be inhibited by aspirin, which showed a time-and dose-dependent manner; at the same time, the expression level of Blimp1 in U266 cells were decreased with the increasing of aspirin concentration, while the expression level of ATF4 and CHOP was increased with the increasing of aspirin concentration.	Aspirin	81-88	PR/SET domain 1	Homo sapiens	179-185
32798401-9	2020	CCK-8 showed that the proliferation activity of U266 cells could be inhibited by aspirin, which showed a time-and dose-dependent manner; at the same time, the expression level of Blimp1 in U266 cells were decreased with the increasing of aspirin concentration, while the expression level of ATF4 and CHOP was increased with the increasing of aspirin concentration.	Aspirin	81-88	DNA damage inducible transcript 3	Homo sapiens	300-304
32798401-9	2020	CCK-8 showed that the proliferation activity of U266 cells could be inhibited by aspirin, which showed a time-and dose-dependent manner; at the same time, the expression level of Blimp1 in U266 cells were decreased with the increasing of aspirin concentration, while the expression level of ATF4 and CHOP was increased with the increasing of aspirin concentration.	Aspirin	238-245	PR/SET domain 1	Homo sapiens	179-185
32798401-9	2020	CCK-8 showed that the proliferation activity of U266 cells could be inhibited by aspirin, which showed a time-and dose-dependent manner; at the same time, the expression level of Blimp1 in U266 cells were decreased with the increasing of aspirin concentration, while the expression level of ATF4 and CHOP was increased with the increasing of aspirin concentration.	Aspirin	238-245	PR/SET domain 1	Homo sapiens	179-185
32798401-10	2020	CONCLUSIONS: Blimp1 may display the anti-apoptosis of myeloma cells through interfering with ATF4/CHOP signaling pathway; low dose of aspirin may play anti-myeloma effect by inhibiting the expression of Blimp1 in myeloma cells.	Aspirin	134-141	DNA damage inducible transcript 3	Homo sapiens	98-102
32798401-10	2020	CONCLUSIONS: Blimp1 may display the anti-apoptosis of myeloma cells through interfering with ATF4/CHOP signaling pathway; low dose of aspirin may play anti-myeloma effect by inhibiting the expression of Blimp1 in myeloma cells.	Aspirin	134-141	PR/SET domain 1	Homo sapiens	203-209
32629916-6	2020	The results revealed that aspirin inhibited macrophage chemoattractant protein (MCP-1), interleukin (IL-6), IL-1beta, and plasminogen activator inhibitor (PAI-1) production in 3T3-L1 adipocytes stimulated by tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS).	Aspirin	26-33	interleukin 6	Mus musculus	101-105
32654613-11	2020	Despite higher cyclooxygenase-1 inhibition, daily aspirin exposure resulted in a paradoxical attenuation of platelet inhibition in response to epinephrine and ADP over time in women but not in men.	Aspirin	50-57	prostaglandin-endoperoxide synthase 1	Homo sapiens	15-31
31904094-7	2020	The negative effect of aspirin on the rate of tumor cell proliferation was more significant in xenograft tumors derived from PIK3CA mutant versus wild-type cells.	Aspirin	23-30	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	125-131
32679712-0	2020	Association between High On-Aspirin Platelet Reactivity and Reduced Superoxide Dismutase Activity in Patients Affected by Type 2 Diabetes Mellitus or Primary Hypercholesterolemia.	Aspirin	28-35	superoxide dismutase 1	Homo sapiens	68-88
32679712-1	2020	Platelet hyperactivation is involved in the established prothrombotic condition of metabolic diseases such as Type 2 Diabetes Mellitus (T2DM) and familial hypercholesterolemia (HC), justifying the therapy with aspirin, a suppressor of thromboxane synthesis through the irreversible inhibition of cyclooxygenase-1 (COX-1), to prevent cardiovascular diseases.	Aspirin	210-217	prostaglandin-endoperoxide synthase 1	Homo sapiens	296-312
32679712-1	2020	Platelet hyperactivation is involved in the established prothrombotic condition of metabolic diseases such as Type 2 Diabetes Mellitus (T2DM) and familial hypercholesterolemia (HC), justifying the therapy with aspirin, a suppressor of thromboxane synthesis through the irreversible inhibition of cyclooxygenase-1 (COX-1), to prevent cardiovascular diseases.	Aspirin	210-217	prostaglandin-endoperoxide synthase 1	Homo sapiens	314-319
32679712-5	2020	To conclude, in T2DM and HC, similarly, the impairment of redox equilibrium associated with a decrease of SOD activity could contribute to a suboptimal response to aspirin.	Aspirin	164-171	superoxide dismutase 1	Homo sapiens	106-109
32646396-13	2020	In addition, the survival benefit of postdiagnosis aspirin use appeared to be confined to patients with mutated PIK3CA tumors [HR = 0.78, 95%CI(0.50, 0.99)] and was positive for PTGS2 (COX-2) expression [HR = 0.75, 95%CI(0.43, 1.30)].	Aspirin	51-58	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	112-118
32646396-13	2020	In addition, the survival benefit of postdiagnosis aspirin use appeared to be confined to patients with mutated PIK3CA tumors [HR = 0.78, 95%CI(0.50, 0.99)] and was positive for PTGS2 (COX-2) expression [HR = 0.75, 95%CI(0.43, 1.30)].	Aspirin	51-58	prostaglandin-endoperoxide synthase 2	Homo sapiens	178-183
32646396-13	2020	In addition, the survival benefit of postdiagnosis aspirin use appeared to be confined to patients with mutated PIK3CA tumors [HR = 0.78, 95%CI(0.50, 0.99)] and was positive for PTGS2 (COX-2) expression [HR = 0.75, 95%CI(0.43, 1.30)].	Aspirin	51-58	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	185-190
32646396-14	2020	CONCLUSIONS: These findings provide further indications that postdiagnosis aspirin use improves overall survival and cancer-specific survival in colorectal cancer, especially for patients who are positive for PTGS2 (COX-2) expression and PIK3CA-mutated tumors.	Aspirin	75-82	prostaglandin-endoperoxide synthase 2	Homo sapiens	209-214
32646396-14	2020	CONCLUSIONS: These findings provide further indications that postdiagnosis aspirin use improves overall survival and cancer-specific survival in colorectal cancer, especially for patients who are positive for PTGS2 (COX-2) expression and PIK3CA-mutated tumors.	Aspirin	75-82	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	216-221
32646396-14	2020	CONCLUSIONS: These findings provide further indications that postdiagnosis aspirin use improves overall survival and cancer-specific survival in colorectal cancer, especially for patients who are positive for PTGS2 (COX-2) expression and PIK3CA-mutated tumors.	Aspirin	75-82	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	238-244
32645080-10	2020	Disease activity measures, including ASDAS-ESR, ASDAS-CRP and BASDAI, had positive correlations with ASAS HI.	Aspirin	101-105	C-reactive protein	Homo sapiens	54-57
32243094-12	2020	CONCLUSION: Certain clinical disease characteristics such as ASA sensitivity, allergic rhinitis and asthma are more associated with CRS patients with eosinophilia when compared to those without eosinophilia.	Aspirin	61-64	twist family bHLH transcription factor 1	Homo sapiens	132-135
32629916-6	2020	The results revealed that aspirin inhibited macrophage chemoattractant protein (MCP-1), interleukin (IL-6), IL-1beta, and plasminogen activator inhibitor (PAI-1) production in 3T3-L1 adipocytes stimulated by tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS).	Aspirin	26-33	tumor necrosis factor	Mus musculus	208-235
32629916-6	2020	The results revealed that aspirin inhibited macrophage chemoattractant protein (MCP-1), interleukin (IL-6), IL-1beta, and plasminogen activator inhibitor (PAI-1) production in 3T3-L1 adipocytes stimulated by tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS).	Aspirin	26-33	tumor necrosis factor	Mus musculus	237-246
32495688-7	2020	Women receiving aspirin therapy had lower median (interquartile range) levels of activin A (8.17 [3.70, 10.36] versus 12.77 [8.37, 31.25] ng/mL; P=0.001) and lower activin/follistatin ratio (0.59 [0.31, 0.93] versus 1.01 [0.64, 2.60] P=0.002) than women who did not receive aspirin, which also remained significant after multivariable analysis.	Aspirin	16-23	follistatin	Homo sapiens	172-183
32366719-9	2020	These effects of ASA and BZ+ASA in chronically infected mice were inhibited by pretreatment with the LXA4 receptor antagonist, Boc-2, indicating that the protective effects of ASA are mediated by ASA-triggered lipoxin.	Aspirin	17-20	formyl peptide receptor 3	Mus musculus	101-114
32366719-9	2020	These effects of ASA and BZ+ASA in chronically infected mice were inhibited by pretreatment with the LXA4 receptor antagonist, Boc-2, indicating that the protective effects of ASA are mediated by ASA-triggered lipoxin.	Aspirin	28-31	formyl peptide receptor 3	Mus musculus	101-114
32366719-9	2020	These effects of ASA and BZ+ASA in chronically infected mice were inhibited by pretreatment with the LXA4 receptor antagonist, Boc-2, indicating that the protective effects of ASA are mediated by ASA-triggered lipoxin.	Aspirin	28-31	formyl peptide receptor 3	Mus musculus	101-114
32366719-9	2020	These effects of ASA and BZ+ASA in chronically infected mice were inhibited by pretreatment with the LXA4 receptor antagonist, Boc-2, indicating that the protective effects of ASA are mediated by ASA-triggered lipoxin.	Aspirin	28-31	formyl peptide receptor 3	Mus musculus	101-114
32544082-2	2020	We aimed to elucidate the combined impact of BMI and dysglycemia expressed by glycated albumin (GA) on efficacy of clopidogrel-aspirin therapy among minor stroke (MS) or transient ischemic attack (TIA) patients.	Aspirin	127-134	albumin	Homo sapiens	87-94
32277415-12	2020	The primary mechanism of ASA and DFC adsorption was justified considering electrostatic interactions and pi-pi interactions between the Cpa-AC and the adsorbate from the solution.	Aspirin	25-28	carboxypeptidase A1	Homo sapiens	136-139
32545774-0	2020	Aspirin Induced Glioma Apoptosis through Noxa Upregulation.	Aspirin	0-7	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	41-45
32545774-3	2020	We found that the human H4 glioma cell-killing effects of aspirin involved mitochondria-mediated apoptosis accompanied by endoplasmic reticulum (ER) stress, Noxa upregulation, Mcl-1 downregulation, Bax mitochondrial distribution and oligomerization, and caspase 3/caspase 8/caspase 9 activation.	Aspirin	58-65	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	157-161
32545774-3	2020	We found that the human H4 glioma cell-killing effects of aspirin involved mitochondria-mediated apoptosis accompanied by endoplasmic reticulum (ER) stress, Noxa upregulation, Mcl-1 downregulation, Bax mitochondrial distribution and oligomerization, and caspase 3/caspase 8/caspase 9 activation.	Aspirin	58-65	BCL2 associated X, apoptosis regulator	Homo sapiens	198-201
32545774-3	2020	We found that the human H4 glioma cell-killing effects of aspirin involved mitochondria-mediated apoptosis accompanied by endoplasmic reticulum (ER) stress, Noxa upregulation, Mcl-1 downregulation, Bax mitochondrial distribution and oligomerization, and caspase 3/caspase 8/caspase 9 activation.	Aspirin	58-65	caspase 3	Homo sapiens	254-263
32545774-4	2020	Genetic silencing of Noxa or Bax attenuated aspirin-induced viability loss and apoptosis, while silencing Mcl-1 augmented the effects of aspirin.	Aspirin	44-51	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	21-25
32545774-4	2020	Genetic silencing of Noxa or Bax attenuated aspirin-induced viability loss and apoptosis, while silencing Mcl-1 augmented the effects of aspirin.	Aspirin	44-51	BCL2 associated X, apoptosis regulator	Homo sapiens	29-32
32172203-5	2020	RESULTS: ASA significantly decreased nitric oxide (NO) production and inducible NO synthase (iNOS) activity, but significantly increased arginase activity.	Aspirin	9-12	nitric oxide synthase 2	Homo sapiens	70-91
32122206-1	2020	Context: In nonallergic (naive) mice, type I cysteinyl-leukotriene receptors (CysLT1R) mediate the stimulatory effects of cytokines (eotaxin/CCL11, interleukin[IL] - 13), and nonsteroidal anti-inflammatory drugs (NSAID; indomethacin, aspirin) on eosinophil production by IL-5-stimulated bone-marrow.	Aspirin	234-241	cysteinyl leukotriene receptor 1	Mus musculus	78-85
32053214-12	2020	Low concentration (0.05mM) ASA reduced inflammatory cytokines IL-6 (p &lt; 0.001), CCL21 (P &lt; 0.05) and MMP-9 (p &lt; 0.05) in an ex vivo pulpitis model.	Aspirin	27-30	interleukin 6	Homo sapiens	62-66
32172203-5	2020	RESULTS: ASA significantly decreased nitric oxide (NO) production and inducible NO synthase (iNOS) activity, but significantly increased arginase activity.	Aspirin	9-12	nitric oxide synthase 2	Homo sapiens	93-97
31060409-0	2020	Development of transferrin-bearing vesicles encapsulating aspirin for cancer therapy.	Aspirin	58-65	transferrin	Homo sapiens	15-26
31060409-4	2020	In this work, we demonstrated that aspirin could be formulated in transferrin-bearing vesicles and that this tumor-targeted formulation could lead to an increase in the anti-proliferative efficacy of the drug in three cancer cell lines in vitro.	Aspirin	35-42	transferrin	Homo sapiens	66-77
31060409-5	2020	The in vitro therapeutic efficacy of aspirin was significantly improved when formulated in transferrin-bearing vesicles, by about 2-fold compared to that of drug solution.	Aspirin	37-44	transferrin	Homo sapiens	91-102
32239624-6	2020	The combination of osimertinib and aspirin induced strong anti-proliferative and proapoptotic effects in osimertinib-resistant NSCLC cells through inhibition of Akt/FoxO3a signaling component phosphorylation and increased Bim expression.	Aspirin	35-42	AKT serine/threonine kinase 1	Homo sapiens	161-164
31897976-7	2020	These findings suggested that the vascular prostanoids, PGI2 and PGE2, exerted significant regulatory influences on neuronal protection (by PGI2), or damage (by PGE2) in the hippocampus, and raised a concern that the wide uses of aspirin in cardiovascular diseases may exert negative impacts on neurodegenerative protection.	Aspirin	230-237	prostaglandin I receptor (IP)	Mus musculus	56-60
32239624-6	2020	The combination of osimertinib and aspirin induced strong anti-proliferative and proapoptotic effects in osimertinib-resistant NSCLC cells through inhibition of Akt/FoxO3a signaling component phosphorylation and increased Bim expression.	Aspirin	35-42	forkhead box O3	Homo sapiens	165-171
31811715-1	2020	AIMS: PEGASUS-TIMI 54 demonstrated that long-term dual antiplatelet therapy (DAPT) with aspirin and ticagrelor reduced the risk of major adverse cardiovascular events (MACE), with an acceptable increase in bleeding, in patients with prior myocardial infarction (MI).	Aspirin	88-95	IKAROS family zinc finger 5	Homo sapiens	6-21
32467498-9	2020	Several pharmacotherapies including lipid-lowering agents and antidiabetic drugs such as insulin sensitizers and incretin mimetics, in addition to antioxidants, ursodeoxycholic acid, semi-synthetic bile acid analogue, acetylsalicylic acid, and renin-angiotensin system inhibitors have been evaluated in the current literature.	Aspirin	218-238	insulin	Homo sapiens	89-96
32546966-9	2020	Tmx treatment of MDA-MB-231 cells in combination with ASA, Met and OP markedly reduced the CD44/CD24 ratio by 6.5-fold compared to the untreated control group.	Aspirin	54-57	CD24 molecule	Homo sapiens	96-100
32429142-0	2020	Anti-Inflammatory and Reactive Oxygen Species Suppression through Aspirin Pretreatment to Treat Hyperoxia-Induced Acute Lung Injury in NF-kappaB-Luciferase Inducible Transgenic Mice.	Aspirin	66-73	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	135-144
32429142-6	2020	This research uses an in vivo imaging system (IVIS) to investigate the mechanisms of aspirin"s anti-inflammatory and antioxidant effects on hyperoxia-induced ALI in nuclear factor kappaB (NF-kappaB)-luciferase transgenic mice.	Aspirin	85-92	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	188-197
32429142-8	2020	An NF-kappaB-dependent bioluminescent signal was used in transgenic mice carrying the luciferase genes to monitor the anti-inflammatory effects of aspirin.	Aspirin	147-154	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	3-12
32429142-9	2020	These results demonstrated that pretreatment with aspirin reduced luciferase expression, indicating that aspirin reduces NF-kappaB activation.	Aspirin	50-57	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	121-130
32429142-9	2020	These results demonstrated that pretreatment with aspirin reduced luciferase expression, indicating that aspirin reduces NF-kappaB activation.	Aspirin	105-112	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	121-130
32429142-11	2020	In addition, we demonstrated that pretreatment with aspirin significantly reduced the protein levels of phosphorylated protein kinase B, NF-kappaB and tumor necrosis factor alpha in NF-kappaB-luciferase+/+ transgenic mice.	Aspirin	52-59	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	137-146
32429142-11	2020	In addition, we demonstrated that pretreatment with aspirin significantly reduced the protein levels of phosphorylated protein kinase B, NF-kappaB and tumor necrosis factor alpha in NF-kappaB-luciferase+/+ transgenic mice.	Aspirin	52-59	tumor necrosis factor	Mus musculus	151-178
32429142-11	2020	In addition, we demonstrated that pretreatment with aspirin significantly reduced the protein levels of phosphorylated protein kinase B, NF-kappaB and tumor necrosis factor alpha in NF-kappaB-luciferase+/+ transgenic mice.	Aspirin	52-59	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	182-191
32429142-12	2020	Thus, the effects of aspirin on the anti-inflammatory response and reactive oxygen species suppressive are hypothesized to occur through the NF-kappaB signaling pathway.	Aspirin	21-28	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	141-150
32704557-1	2020	Background: THEMIS (NCT01991795) showed that in patients with type 2 diabetes (T2D) and stable coronary artery disease (CAD) but with no prior myocardial infarction (MI) or stroke, ticagrelor plus acetylsalicylic acid (ASA) decreased the incidence of ischaemic cardiovascular events compared with placebo plus ASA.	Aspirin	197-217	thymocyte selection associated	Homo sapiens	12-18
32704557-1	2020	Background: THEMIS (NCT01991795) showed that in patients with type 2 diabetes (T2D) and stable coronary artery disease (CAD) but with no prior myocardial infarction (MI) or stroke, ticagrelor plus acetylsalicylic acid (ASA) decreased the incidence of ischaemic cardiovascular events compared with placebo plus ASA.	Aspirin	219-222	thymocyte selection associated	Homo sapiens	12-18
32704557-1	2020	Background: THEMIS (NCT01991795) showed that in patients with type 2 diabetes (T2D) and stable coronary artery disease (CAD) but with no prior myocardial infarction (MI) or stroke, ticagrelor plus acetylsalicylic acid (ASA) decreased the incidence of ischaemic cardiovascular events compared with placebo plus ASA.	Aspirin	310-313	thymocyte selection associated	Homo sapiens	12-18
32351866-8	2020	The transcripts corresponding to AsA-GSH pathway enzymes SOD, APX, GR, DHAR, and MDHAR were up-regulated by 8- to 12-fold under combined drought and heat.	Aspirin	33-36	monodehydroascorbate reductase	Solanum lycopersicum	81-86
32070879-0	2020	Aspirin exerts anti-tumor effect through inhibiting Blimp1 and activating ATF4/CHOP pathway in multiple myeloma.	Aspirin	0-7	PR/SET domain 1	Homo sapiens	52-58
32070879-0	2020	Aspirin exerts anti-tumor effect through inhibiting Blimp1 and activating ATF4/CHOP pathway in multiple myeloma.	Aspirin	0-7	DNA damage inducible transcript 3	Homo sapiens	79-83
32070879-5	2020	Therefore, we aim to explore whether Aspirin could induce AFT4/CHOP apoptosis pathway in MM by inhibiting Blimp1 expression, thereby promoting MM cell apoptosis and exerting anti-tumor effects.	Aspirin	37-44	DNA damage inducible transcript 3	Homo sapiens	63-67
32070879-5	2020	Therefore, we aim to explore whether Aspirin could induce AFT4/CHOP apoptosis pathway in MM by inhibiting Blimp1 expression, thereby promoting MM cell apoptosis and exerting anti-tumor effects.	Aspirin	37-44	PR/SET domain 1	Homo sapiens	106-112
32297484-11	2020	For the mechanism study, we found that the promoter of PD-L1 was inactivated by aspirin via TAZ transcriptional coactivator in the cells.	Aspirin	80-87	tafazzin, phospholipid-lysophospholipid transacylase	Homo sapiens	92-95
32297484-13	2020	CONCLUSIONS: Aspirin suppressed the growth of lung cancer cells via targeting the TAZ/PD-L1 axis.	Aspirin	13-20	tafazzin, phospholipid-lysophospholipid transacylase	Homo sapiens	82-85
32478188-8	2020	Expression of TNF-alpha mRNA, but not IL-1beta mRNA, in the spinal cord following MIA injection was suppressed by ASA administration.	Aspirin	114-117	tumor necrosis factor	Homo sapiens	14-23
32478188-9	2020	Significance: These findings suggest that ASA may have the ability to attenuate secondary hyperalgesia through suppression of ASIC3 and/or TNF-alpha expression.	Aspirin	42-45	tumor necrosis factor	Homo sapiens	139-148
32266013-7	2020	Compared with the model group, rats pretreated with fisetin, quercetin and aspirin showed significant prolongation of clotting time, prothrombin time, thrombin time and activated partial thromboplastin time.	Aspirin	75-82	coagulation factor II	Rattus norvegicus	136-144
32596477-1	2020	Objectives: Aspirin-exacerbated respiratory disease (AERD) is a chronic respiratory condition characterized by a triad of symptoms: asthma, chronic rhinosinusitis with nasal polyposis, and a respiratory reaction to aspirin and other cyclooxygenase-1 inhibitors, also known as nonsteroidal anti-inflammatory drugs.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	233-249
32323728-0	2020	Aspirin inhibits endometrial fibrosis by suppressing the TGF-beta1-Smad2/Smad3 pathway in intrauterine adhesions.	Aspirin	0-7	transforming growth factor beta 1	Homo sapiens	57-66
32323728-7	2020	However, whether aspirin can inhibit endometrial fibrosis through the TGF-beta1-Smad2/Smad3 pathway to prevent postoperative re-adhesion remains to be elucidated.	Aspirin	17-24	transforming growth factor beta 1	Homo sapiens	70-79
32323728-8	2020	The results of the present study suggested that aspirin inhibits endometrial fibrosis by suppressing the TGF-beta1-Smad2/Smad3 pathway, which may provide new hypotheses for the mechanism of action of aspirin in the treatment of IUAs.	Aspirin	48-55	transforming growth factor beta 1	Homo sapiens	105-114
32323728-8	2020	The results of the present study suggested that aspirin inhibits endometrial fibrosis by suppressing the TGF-beta1-Smad2/Smad3 pathway, which may provide new hypotheses for the mechanism of action of aspirin in the treatment of IUAs.	Aspirin	200-207	transforming growth factor beta 1	Homo sapiens	105-114
32270588-11	2020	ASA treatment reduced E2 production, Cyp19a1 expression, glutathione peroxidase (GPx) activity, and estradiol receptor expression in CGCs.	Aspirin	0-3	cytochrome P450 family 19 subfamily A member 1	Homo sapiens	37-44
32270588-11	2020	ASA treatment reduced E2 production, Cyp19a1 expression, glutathione peroxidase (GPx) activity, and estradiol receptor expression in CGCs.	Aspirin	0-3	estrogen receptor 1	Homo sapiens	100-118
32270588-12	2020	The addition of AA prevented the ASA-induced E2 reduction (p < .05) and expression of Cyp19a1.	Aspirin	33-36	cytochrome P450 family 19 subfamily A member 1	Homo sapiens	86-93
31637734-14	2020	In addition, aspirin increased the expression of TNC, TNMD, and Scx and biomechanical properties of the injured tendon.	Aspirin	13-20	tenomodulin	Homo sapiens	54-58
32326897-2	2020	Aspirin use post-diagnosis may modify components of the PI3K pathway, including AKT and mTOR, and has been associated with lower risk of breast cancer recurrence and mortality.	Aspirin	0-7	mechanistic target of rapamycin kinase	Homo sapiens	88-92
32365457-0	2020	Deactivation of Glutaminolysis Sensitizes PIK3CA-Mutated Colorectal Cancer Cells to Aspirin-Induced Growth Inhibition.	Aspirin	84-91	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	42-48
32365457-2	2020	In particular, aspirin has been reported to be effective against PIK3CA-mutated colorectal cancer (CRC); however, little information is available on how the PIK3CA gene status affects its efficacy.	Aspirin	15-22	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	65-71
32365457-3	2020	We found that the growth inhibitory effects of aspirin were impaired upon glutamine deprivation in PIK3CA-mutated CRC cells.	Aspirin	47-54	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	99-105
32365457-4	2020	Notably, glutamine dependency of aspirin-mediated growth inhibition was observed in PIK3CA-mutated cells but not PIK3CA wild type cells.	Aspirin	33-40	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	84-90
32365457-5	2020	Mechanistically, aspirin induced G1 arrest in PIK3CA-mutated CRC cells and inhibited the mTOR pathway, inducing the same phenotypes as glutamine deprivation.	Aspirin	17-24	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	46-52
32365457-5	2020	Mechanistically, aspirin induced G1 arrest in PIK3CA-mutated CRC cells and inhibited the mTOR pathway, inducing the same phenotypes as glutamine deprivation.	Aspirin	17-24	mechanistic target of rapamycin kinase	Homo sapiens	89-93
32365457-6	2020	Moreover, our study including bioinformatic approaches revealed that aspirin increased the expression levels of glutaminolysis-related genes with upregulation of activating transcription factor 4 (ATF4) in PIK3CA-mutated CRC cells.	Aspirin	69-76	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	206-212
32365457-7	2020	Lastly, the agents targeting glutaminolysis demonstrated significant combined effects with aspirin on PIK3CA-mutated CRC cells.	Aspirin	91-98	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	102-108
32365457-8	2020	Thus, these findings not only suggest the correlation among aspirin efficacy, PIK3CA mutation and glutamine metabolism, but also the rational combinatorial treatments of aspirin with glutaminolysis-targeting agents against PIK3CA-mutated CRC.	Aspirin	170-177	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	223-229
32326897-0	2020	Different associations of tumor PIK3CA mutations and clinical outcomes according to aspirin use among women with metastatic hormone receptor positive breast cancer.	Aspirin	84-91	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	32-38
32326897-0	2020	Different associations of tumor PIK3CA mutations and clinical outcomes according to aspirin use among women with metastatic hormone receptor positive breast cancer.	Aspirin	84-91	nuclear receptor subfamily 4 group A member 1	Homo sapiens	124-140
32326897-2	2020	Aspirin use post-diagnosis may modify components of the PI3K pathway, including AKT and mTOR, and has been associated with lower risk of breast cancer recurrence and mortality.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	80-83
32326897-9	2020	PIK3CA mutations were associated with longer TTM among aspirin non-users (HR = 0.60 95% CI:0.44-0.82 p = 0.001) but not among aspirin users (HR = 1.57 0.86-2.84 p = 0.139).	Aspirin	55-62	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	0-6
32326897-9	2020	PIK3CA mutations were associated with longer TTM among aspirin non-users (HR = 0.60 95% CI:0.44-0.82 p = 0.001) but not among aspirin users (HR = 1.57 0.86-2.84 p = 0.139).	Aspirin	126-133	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	0-6
32326897-10	2020	Similarly, PIK3CA mutations were associated with reduced mortality among aspirin non-users (HR = 0.70 95% CI:0.48-1.02 p = 0.066) but not among aspirin users (HR = 1.75 95% CI:0.88-3.49 p = 0.110).	Aspirin	73-80	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	11-17
32323648-11	2020	Furthermore, ASA VI stimulated bone formation on the tension side by enhancing OCN (osteocalcin) expression and RUNX2 (runt-related transcription factor 2) expression, increasing bone volume and density and decreasing in trabecular spacing.	Aspirin	13-16	bone gamma-carboxyglutamate protein	Rattus norvegicus	79-82
32323648-11	2020	Furthermore, ASA VI stimulated bone formation on the tension side by enhancing OCN (osteocalcin) expression and RUNX2 (runt-related transcription factor 2) expression, increasing bone volume and density and decreasing in trabecular spacing.	Aspirin	13-16	bone gamma-carboxyglutamate protein	Rattus norvegicus	84-95
32326897-11	2020	CONCLUSIONS: Among women who develop metastatic breast cancer, tumor PIK3CA mutations are associated with slower time to progression and mortality only among aspirin non-users.	Aspirin	158-165	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	69-75
32323648-11	2020	Furthermore, ASA VI stimulated bone formation on the tension side by enhancing OCN (osteocalcin) expression and RUNX2 (runt-related transcription factor 2) expression, increasing bone volume and density and decreasing in trabecular spacing.	Aspirin	13-16	RUNX family transcription factor 2	Rattus norvegicus	112-117
31951648-5	2020	Additionally, ASA-treated mice had reduced intravascular thrombin activity and microvascular occlusion as compared to untreated S. aureus-infected mice.	Aspirin	14-17	coagulation factor II	Mus musculus	57-65
32323648-11	2020	Furthermore, ASA VI stimulated bone formation on the tension side by enhancing OCN (osteocalcin) expression and RUNX2 (runt-related transcription factor 2) expression, increasing bone volume and density and decreasing in trabecular spacing.	Aspirin	13-16	RUNX family transcription factor 2	Rattus norvegicus	119-154
31915847-1	2020	PURPOSE: Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1).	Aspirin	43-50	prostaglandin-endoperoxide synthase 1	Homo sapiens	73-89
32205444-4	2020	We also show that aspirin-triggered 15-epi-lipoxin A4 (15-epi-LXA4) and 17-epi-resolvin D1 (17-epi-RvD1) through the receptor ALX/FPR2 antagonize cues from CpG DNA, preserve C5aR expression, restore impaired phagocytosis, and redirect human PMNs to apoptosis.	Aspirin	18-25	complement C5a receptor 1	Homo sapiens	174-178
32251451-9	2020	Analysis of eicosanoids in stirred blood demonstrated that administration of ASA at a dose of 12 mg kg-1 to cancer-bearing mice had an effect beyond inhibition of platelet COX-1, suggesting long-term treatment with low-dose aspirin is not a selective murine platelet COX-1/TXA2 pathway inhibitor in cancer-bearing mice.	Aspirin	77-80	cytochrome c oxidase I, mitochondrial	Mus musculus	172-177
32251451-9	2020	Analysis of eicosanoids in stirred blood demonstrated that administration of ASA at a dose of 12 mg kg-1 to cancer-bearing mice had an effect beyond inhibition of platelet COX-1, suggesting long-term treatment with low-dose aspirin is not a selective murine platelet COX-1/TXA2 pathway inhibitor in cancer-bearing mice.	Aspirin	77-80	cytochrome c oxidase I, mitochondrial	Mus musculus	267-272
31453830-8	2020	Our results suggest that, in the setting of durable LVADs, aspirin minimally modulates the biochemical pathway of platelet-mediated thrombin generation.	Aspirin	59-66	coagulation factor II, thrombin	Homo sapiens	132-140
32014718-15	2020	Furthermore low-dose aspirin treatment showed the modest attenuation of the selected Th2 cytokines, IL-10 and IL-13 when compared to low-dose aspirin with metformin (P < 0.01).	Aspirin	21-28	interleukin 10	Mus musculus	100-105
32014718-15	2020	Furthermore low-dose aspirin treatment showed the modest attenuation of the selected Th2 cytokines, IL-10 and IL-13 when compared to low-dose aspirin with metformin (P < 0.01).	Aspirin	21-28	interleukin 13	Mus musculus	110-115
31915847-1	2020	PURPOSE: Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1).	Aspirin	43-50	prostaglandin-endoperoxide synthase 1	Homo sapiens	91-95
31915847-1	2020	PURPOSE: Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1).	Aspirin	52-55	prostaglandin-endoperoxide synthase 1	Homo sapiens	73-89
31915847-1	2020	PURPOSE: Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1).	Aspirin	52-55	prostaglandin-endoperoxide synthase 1	Homo sapiens	91-95
32245119-5	2020	Therefore, the goal of the present study was to determine the influence of prolonged ASA supplementation on the immunolocalization of neuronal nitric oxide synthase (nNOS), vasoactive intestinal peptide (VIP) and cocaine- and amphetamine- regulated transcript peptide (CART) in the porcine jejunum.	Aspirin	85-88	vasoactive intestinal peptide	Homo sapiens	173-202
32289133-0	2020	PURL: Aspirin, Yes, for at-risk elderly-but what about the healthy elderly?	Aspirin	6-13	phosphoribosylformylglycinamidine synthase	Homo sapiens	0-4
32245119-5	2020	Therefore, the goal of the present study was to determine the influence of prolonged ASA supplementation on the immunolocalization of neuronal nitric oxide synthase (nNOS), vasoactive intestinal peptide (VIP) and cocaine- and amphetamine- regulated transcript peptide (CART) in the porcine jejunum.	Aspirin	85-88	CART prepropeptide	Homo sapiens	213-267
32245119-5	2020	Therefore, the goal of the present study was to determine the influence of prolonged ASA supplementation on the immunolocalization of neuronal nitric oxide synthase (nNOS), vasoactive intestinal peptide (VIP) and cocaine- and amphetamine- regulated transcript peptide (CART) in the porcine jejunum.	Aspirin	85-88	CART prepropeptide	Homo sapiens	269-273
32258142-10	2020	Furthermore, aspirin may normalize atherosclerosis and NAFLD by modulating the mannose receptor and CCR2 in macrophages.	Aspirin	13-20	C-C motif chemokine receptor 2	Homo sapiens	100-104
32071459-12	2020	Real-time PCR showed that 1-100 mumol/L meloxicam or 100 mumol/L aspirin down-regulated significantly the mRNA expression of TNF-alpha and IL-6 of LPS-hDPCs (P&lt;0.05), and 100 mumol/L meloxicam down-regulated IL-6 and TNF-alpha more significantly than 100 mumol/L aspirin of LPS-hDPCs (P&lt;0.05).	Aspirin	65-72	tumor necrosis factor	Homo sapiens	125-134
32181121-0	2020	Structural modification of aspirin to design a new potential cyclooxygenase (COX-2) inhibitors.	Aspirin	27-34	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	77-82
32181121-5	2020	Molecular docking and nonbonding interactions have been performed against human cyclooxygenase-2 protein 5F1A to investigate the binding affinity and mode(s) of newly designed aspirin derivatives.	Aspirin	176-183	prostaglandin-endoperoxide synthase 2	Homo sapiens	80-96
32207583-9	2020	In patients untreated with aspirin, AGE-1 positivity was associated with higher C-reactive protein (CRP) level.	Aspirin	27-34	C-reactive protein	Homo sapiens	80-98
32207583-9	2020	In patients untreated with aspirin, AGE-1 positivity was associated with higher C-reactive protein (CRP) level.	Aspirin	27-34	C-reactive protein	Homo sapiens	100-103
32405171-0	2020	Molecular modeling and docking analysis of aspirin with pde7b in the context of neuro-inflammation.	Aspirin	43-50	phosphodiesterase 7B	Homo sapiens	56-61
32405171-3	2020	We document that the amino acid residues such as H186, K190, and G113 of PDE7B protein showed crucial interactions with aspirin for further consideration in this context.	Aspirin	120-127	phosphodiesterase 7B	Homo sapiens	73-78
32258142-0	2020	Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPARdelta-AMPK-PGC-1alpha Pathway in Dyslipidemic Conditions.	Aspirin	0-7	PPARG coactivator 1 alpha	Homo sapiens	111-121
32258142-3	2020	The protein levels of biomarkers (PPARdelta, AMPK, and PGC-1alpha) involved in oxidative phosphorylation in both the vascular endothelial and liver cells were elevated by the aspirin in hyperlipidemic condition.	Aspirin	175-182	PPARG coactivator 1 alpha	Homo sapiens	55-65
32218705-5	2020	Also, aspirin diminished necrosis process (LDH levels), pro-inflammatory mediators (IL-beta and TNF-alpha) and NF-KB protein expression, increasing anti-inflammatory PPAR-gamma protein expression, preventing Abeta1-42 toxic effects.	Aspirin	6-13	tumor necrosis factor	Homo sapiens	96-105
32218705-5	2020	Also, aspirin diminished necrosis process (LDH levels), pro-inflammatory mediators (IL-beta and TNF-alpha) and NF-KB protein expression, increasing anti-inflammatory PPAR-gamma protein expression, preventing Abeta1-42 toxic effects.	Aspirin	6-13	peroxisome proliferator activated receptor gamma	Homo sapiens	166-176
32218705-6	2020	Aspirin inhibited COX-2 and iNOS without changes in COX-1 expression, increasing anti-oxidant protein (Cu/Zn-SOD and Mn-SOD) expression in presence or absence of Abeta1-42.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	18-23
32060649-2	2020	Here, we discuss the interactions of an organometallic complex consisting of an acetylsalicylic acid (ASA) moiety attached to a PtII center via an alkenol linker in a Zeise"s salt-type coordination (ASA-buten-PtCl3) with model peptides angiotensin 1 (AT), substance P (Sub P), and ubiquitin (UQ).	Aspirin	80-100	tachykinin precursor 1	Homo sapiens	256-267
32060649-2	2020	Here, we discuss the interactions of an organometallic complex consisting of an acetylsalicylic acid (ASA) moiety attached to a PtII center via an alkenol linker in a Zeise"s salt-type coordination (ASA-buten-PtCl3) with model peptides angiotensin 1 (AT), substance P (Sub P), and ubiquitin (UQ).	Aspirin	80-100	tachykinin precursor 1	Homo sapiens	269-274
32060649-2	2020	Here, we discuss the interactions of an organometallic complex consisting of an acetylsalicylic acid (ASA) moiety attached to a PtII center via an alkenol linker in a Zeise"s salt-type coordination (ASA-buten-PtCl3) with model peptides angiotensin 1 (AT), substance P (Sub P), and ubiquitin (UQ).	Aspirin	102-105	tachykinin precursor 1	Homo sapiens	256-267
32060649-2	2020	Here, we discuss the interactions of an organometallic complex consisting of an acetylsalicylic acid (ASA) moiety attached to a PtII center via an alkenol linker in a Zeise"s salt-type coordination (ASA-buten-PtCl3) with model peptides angiotensin 1 (AT), substance P (Sub P), and ubiquitin (UQ).	Aspirin	102-105	tachykinin precursor 1	Homo sapiens	269-274
32060649-2	2020	Here, we discuss the interactions of an organometallic complex consisting of an acetylsalicylic acid (ASA) moiety attached to a PtII center via an alkenol linker in a Zeise"s salt-type coordination (ASA-buten-PtCl3) with model peptides angiotensin 1 (AT), substance P (Sub P), and ubiquitin (UQ).	Aspirin	199-202	tachykinin precursor 1	Homo sapiens	256-267
32060649-2	2020	Here, we discuss the interactions of an organometallic complex consisting of an acetylsalicylic acid (ASA) moiety attached to a PtII center via an alkenol linker in a Zeise"s salt-type coordination (ASA-buten-PtCl3) with model peptides angiotensin 1 (AT), substance P (Sub P), and ubiquitin (UQ).	Aspirin	199-202	tachykinin precursor 1	Homo sapiens	269-274
32071459-12	2020	Real-time PCR showed that 1-100 mumol/L meloxicam or 100 mumol/L aspirin down-regulated significantly the mRNA expression of TNF-alpha and IL-6 of LPS-hDPCs (P&lt;0.05), and 100 mumol/L meloxicam down-regulated IL-6 and TNF-alpha more significantly than 100 mumol/L aspirin of LPS-hDPCs (P&lt;0.05).	Aspirin	65-72	interleukin 6	Homo sapiens	211-215
32071459-12	2020	Real-time PCR showed that 1-100 mumol/L meloxicam or 100 mumol/L aspirin down-regulated significantly the mRNA expression of TNF-alpha and IL-6 of LPS-hDPCs (P&lt;0.05), and 100 mumol/L meloxicam down-regulated IL-6 and TNF-alpha more significantly than 100 mumol/L aspirin of LPS-hDPCs (P&lt;0.05).	Aspirin	65-72	tumor necrosis factor	Homo sapiens	220-229
32071459-12	2020	Real-time PCR showed that 1-100 mumol/L meloxicam or 100 mumol/L aspirin down-regulated significantly the mRNA expression of TNF-alpha and IL-6 of LPS-hDPCs (P&lt;0.05), and 100 mumol/L meloxicam down-regulated IL-6 and TNF-alpha more significantly than 100 mumol/L aspirin of LPS-hDPCs (P&lt;0.05).	Aspirin	266-273	tumor necrosis factor	Homo sapiens	125-134
32071459-12	2020	Real-time PCR showed that 1-100 mumol/L meloxicam or 100 mumol/L aspirin down-regulated significantly the mRNA expression of TNF-alpha and IL-6 of LPS-hDPCs (P&lt;0.05), and 100 mumol/L meloxicam down-regulated IL-6 and TNF-alpha more significantly than 100 mumol/L aspirin of LPS-hDPCs (P&lt;0.05).	Aspirin	65-72	interleukin 6	Homo sapiens	139-143
31696583-3	2020	The synthesis of aspirin-triggered lipoxin (ATL) by cyclooxygenase-2 acetylation is an alternative mechanism of ASA, which could explain the effectiveness of ASA treatments.	Aspirin	17-24	prostaglandin-endoperoxide synthase 2	Homo sapiens	52-68
32117036-8	2020	In ASA+CPG mice, the platelet activation marker CD62P was reduced by 40.6 +- 4.2% (p < 0.0001) compared to controls.	Aspirin	3-6	selectin, platelet	Mus musculus	48-53
31696583-3	2020	The synthesis of aspirin-triggered lipoxin (ATL) by cyclooxygenase-2 acetylation is an alternative mechanism of ASA, which could explain the effectiveness of ASA treatments.	Aspirin	112-115	prostaglandin-endoperoxide synthase 2	Homo sapiens	52-68
31696583-3	2020	The synthesis of aspirin-triggered lipoxin (ATL) by cyclooxygenase-2 acetylation is an alternative mechanism of ASA, which could explain the effectiveness of ASA treatments.	Aspirin	158-161	prostaglandin-endoperoxide synthase 2	Homo sapiens	52-68
32134407-1	2020	Although having different rationales and purposes, the PEGASUS-TIMI 54 and COMPASS trials present various points of contact and, especially after the first recommended year of dual antiplatelet therapy (DAPT) from an acute coronary syndrome, pose the clinical question of whether DAPT should be prolonged (PEGASUS strategy) or aspirin should be maintained by combining rivaroxaban 2.5 mg bid (COMPASS strategy).	Aspirin	327-334	IKAROS family zinc finger 5	Homo sapiens	55-70
32009527-0	2020	Aspirin Reduces the Potentiating Effect of CD40L on Platelet Aggregation via Inhibition of Myosin Light Chain.	Aspirin	0-7	CD40 ligand	Homo sapiens	43-48
32009527-3	2020	We hypothesized that in the presence of elevated levels of sCD40L, the efficacy of ASA may vary and aimed to determine the effects of ASA on CD40L signaling and aggregation of platelets.	Aspirin	83-86	CD40 ligand	Homo sapiens	60-65
32009527-4	2020	Methods and Results The effects of ASA on CD40L-treated human platelets, in response to suboptimal concentrations of collagen or thrombin, were assessed at levels of aggregation, thromboxane A2 secretion, and phosphorylation of p38 mitogen-activated protein kinase, nuclear factor kappa B, transforming growth factor-beta-activated kinase 1, and myosin light chain.	Aspirin	35-38	CD40 ligand	Homo sapiens	42-47
32009527-4	2020	Methods and Results The effects of ASA on CD40L-treated human platelets, in response to suboptimal concentrations of collagen or thrombin, were assessed at levels of aggregation, thromboxane A2 secretion, and phosphorylation of p38 mitogen-activated protein kinase, nuclear factor kappa B, transforming growth factor-beta-activated kinase 1, and myosin light chain.	Aspirin	35-38	coagulation factor II, thrombin	Homo sapiens	129-137
32009527-5	2020	sCD40L significantly elevated thromboxane A2 secretion in platelets in response to suboptimal doses of collagen and thrombin, which was reversed by ASA.	Aspirin	148-151	coagulation factor II, thrombin	Homo sapiens	116-124
32009527-7	2020	sCD40L potentiated platelet aggregation, an effect completely reversed and partially reduced by ASA in response to a suboptimal dose of collagen and thrombin, respectively.	Aspirin	96-99	coagulation factor II, thrombin	Homo sapiens	149-157
31693796-1	2020	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is the triad of asthma, nasal polyposis, and sensitivity to cyclooxygenase-1 inhibitors.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	119-135
32010255-0	2020	Clinical efficacy of aspirin combined with clopidogrel in treating cerebral infarction and its effect on serum hs-CRP, sICAM-1 and TNF-alpha.	Aspirin	21-28	tumor necrosis factor	Homo sapiens	131-140
32010255-1	2020	Clinical efficacy of aspirin combined with clopidogrel in treating cerebral infarction and its influence on serum high-sensitivity C-reactive protein (hs-CRP), soluble intercellular adhesion molecule-1 (sICAM-1) and tumor necrosis factor-alpha (TNF-alpha) were explored.	Aspirin	21-28	tumor necrosis factor	Homo sapiens	216-243
32010255-1	2020	Clinical efficacy of aspirin combined with clopidogrel in treating cerebral infarction and its influence on serum high-sensitivity C-reactive protein (hs-CRP), soluble intercellular adhesion molecule-1 (sICAM-1) and tumor necrosis factor-alpha (TNF-alpha) were explored.	Aspirin	21-28	tumor necrosis factor	Homo sapiens	245-254
32010255-7	2020	Combination therapy of aspirin and clopidogrel can improve cerebral infarction effectively, and inhibit the expression levels of hs-CRP, sICAM-1 and TNF-alpha more effectively than aspirin alone.	Aspirin	23-30	tumor necrosis factor	Homo sapiens	149-158
32134407-1	2020	Although having different rationales and purposes, the PEGASUS-TIMI 54 and COMPASS trials present various points of contact and, especially after the first recommended year of dual antiplatelet therapy (DAPT) from an acute coronary syndrome, pose the clinical question of whether DAPT should be prolonged (PEGASUS strategy) or aspirin should be maintained by combining rivaroxaban 2.5 mg bid (COMPASS strategy).	Aspirin	327-334	IKAROS family zinc finger 5	Homo sapiens	55-62
32000660-0	2020	Aspirin has a better effect on PIK3CA mutant colorectal cancer cells by PI3K/Akt/Raptor pathway.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	31-37
32027271-19	2020	After aspirin stimulation of different concentrations for 48 hours, the expression level of Blimp1 in U266 cells decreased with increasing of drug concentration, while the expression levels of ATF4 and CHOP increased with increasing of drug concentration.	Aspirin	6-13	PR/SET domain 1	Homo sapiens	92-98
32027271-19	2020	After aspirin stimulation of different concentrations for 48 hours, the expression level of Blimp1 in U266 cells decreased with increasing of drug concentration, while the expression levels of ATF4 and CHOP increased with increasing of drug concentration.	Aspirin	6-13	DNA damage inducible transcript 3	Homo sapiens	202-206
32027271-21	2020	Aspirin can inhibit the proliferation activity of myeloma cells by down-regulating Blimp1 expression in myeloma cells and up-regulating ATF4 and CHOP expression, therefore plays an anti-tumor rote.	Aspirin	0-7	PR/SET domain 1	Homo sapiens	83-89
32027271-21	2020	Aspirin can inhibit the proliferation activity of myeloma cells by down-regulating Blimp1 expression in myeloma cells and up-regulating ATF4 and CHOP expression, therefore plays an anti-tumor rote.	Aspirin	0-7	DNA damage inducible transcript 3	Homo sapiens	145-149
31608617-11	2020	The group co-administered with DHEA and aspirin showed significant increases in SOD, GST, CAT, GSH, Progesterone, Ca2+ ATPase, Na+ ATPase, H+ ATPase and significant reduction (p<0.05) in malondialdehyde, VEGF, TNF-alpha and estrogen as compared with the DHEA group.	Aspirin	40-47	catalase	Rattus norvegicus	90-93
31608617-11	2020	The group co-administered with DHEA and aspirin showed significant increases in SOD, GST, CAT, GSH, Progesterone, Ca2+ ATPase, Na+ ATPase, H+ ATPase and significant reduction (p<0.05) in malondialdehyde, VEGF, TNF-alpha and estrogen as compared with the DHEA group.	Aspirin	40-47	carbonic anhydrase 2	Rattus norvegicus	114-125
31608617-11	2020	The group co-administered with DHEA and aspirin showed significant increases in SOD, GST, CAT, GSH, Progesterone, Ca2+ ATPase, Na+ ATPase, H+ ATPase and significant reduction (p<0.05) in malondialdehyde, VEGF, TNF-alpha and estrogen as compared with the DHEA group.	Aspirin	40-47	tumor necrosis factor	Rattus norvegicus	210-219
31608617-12	2020	The histopathological analysis showed reductions in cystic fibrosis, atretic ovaries, increased expression of Bcl-2 and E- Cadherin and reduced Bax expression in the group that received Aspirin and DHEA.	Aspirin	186-193	BCL2, apoptosis regulator	Rattus norvegicus	110-115
31997026-7	2020	The THEMIS trial showed a 55% risk reduction for MALE with ticagrelor DAPT compared with aspirin monotherapy (HR 0.45, 95% CI 0.23-0.86).	Aspirin	89-96	thymocyte selection associated	Homo sapiens	4-10
32000660-8	2020	The expression of Bax/Bcl2 increased after treatment indicates that aspirin can induce apoptosis of PIK3CA-mutant CRC cells.	Aspirin	68-75	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	100-106
32000660-11	2020	After treatment with aspirin, as phosphorylation of PI3K and Protein kinase B (PKB, Akt) was decreased, Raptor expression was also decreased.	Aspirin	21-28	AKT serine/threonine kinase 1	Homo sapiens	79-82
32000660-0	2020	Aspirin has a better effect on PIK3CA mutant colorectal cancer cells by PI3K/Akt/Raptor pathway.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	77-80
32000660-11	2020	After treatment with aspirin, as phosphorylation of PI3K and Protein kinase B (PKB, Akt) was decreased, Raptor expression was also decreased.	Aspirin	21-28	AKT serine/threonine kinase 1	Homo sapiens	84-87
32000660-12	2020	CONCLUSION: Aspirin can regulate the proliferation, apoptosis and autophagy of CRC cells through the PI3K/Akt/Raptor pathway, affecting PIK3CA-mutant CRC.	Aspirin	12-19	AKT serine/threonine kinase 1	Homo sapiens	106-109
32000660-1	2020	BACKGROUND: Aspirin, as a non-steroidal anti-inflammatory drug, can improve the survival rate of patients with colorectal cancer, while aspirin is effective in patients with PIK3CA mutant colorectal cancer (CRC).	Aspirin	136-143	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	174-180
32000660-12	2020	CONCLUSION: Aspirin can regulate the proliferation, apoptosis and autophagy of CRC cells through the PI3K/Akt/Raptor pathway, affecting PIK3CA-mutant CRC.	Aspirin	12-19	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	136-142
32000660-2	2020	However, the mechanism of aspirin in the treatment of PIK3CA mutated CRC patients remains unclear.	Aspirin	26-33	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	54-60
32000660-4	2020	To demonstrate that aspirin has a better effect on the CRC of PIK3CA mutations in association with the PI3K/Akt/Raptor pathway, we used aspirin to treat PIK3CA mutant CRC cells (HCT-116 and RKO).	Aspirin	20-27	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	62-68
31992558-6	2020	RESULTS: A total of 6231 respondents in the CARTaGENE study (54.2% of those aged 50-69 yr with no prior history of CVD) were found to be potentially eligible for ASA use for primary CVD prevention.	Aspirin	162-165	CART prepropeptide	Homo sapiens	44-53
32000660-4	2020	To demonstrate that aspirin has a better effect on the CRC of PIK3CA mutations in association with the PI3K/Akt/Raptor pathway, we used aspirin to treat PIK3CA mutant CRC cells (HCT-116 and RKO).	Aspirin	136-143	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	153-159
32000660-8	2020	The expression of Bax/Bcl2 increased after treatment indicates that aspirin can induce apoptosis of PIK3CA-mutant CRC cells.	Aspirin	68-75	BCL2 associated X, apoptosis regulator	Homo sapiens	18-21
32000660-8	2020	The expression of Bax/Bcl2 increased after treatment indicates that aspirin can induce apoptosis of PIK3CA-mutant CRC cells.	Aspirin	68-75	BCL2 apoptosis regulator	Homo sapiens	22-26
31815277-4	2020	In human LECs, the levels of the  EMT markers alpha-smooth muscle actin (alpha-SMA) and fibronectin were drastically reduced by treatment with 2 mM aspirin.	Aspirin	148-155	actin alpha 2, smooth muscle, aorta	Mus musculus	73-82
31815277-4	2020	In human LECs, the levels of the  EMT markers alpha-smooth muscle actin (alpha-SMA) and fibronectin were drastically reduced by treatment with 2 mM aspirin.	Aspirin	148-155	fibronectin 1	Homo sapiens	88-99
31815277-6	2020	In human capsular bags, treatment with 2 mM aspirin significantly suppressed posterior capsule wrinkling and the expression alpha-SMA in capsule-adherent LECs.	Aspirin	44-51	actin alpha 2, smooth muscle, aorta	Mus musculus	124-133
31963688-0	2020	Aspirin Enhances the Protection of Hsp90 from Heat-Stressed Injury in Cardiac Microvascular Endothelial Cells Through PI3K-Akt and PKM2 Pathways.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	123-126
31963688-9	2020	ASA treatment of CMVECs induced a significant expression of Hsp90, which promoted both Akt and PKM2 signals, which are beneficial for relieving HS damage and maintaining the function of CMVECs.	Aspirin	0-3	AKT serine/threonine kinase 1	Homo sapiens	87-90
31815277-10	2020	After lensectomy in mice, we observed an increase in the proliferation and alpha-SMA expression of the capsule-adherent LECs, which was ameliorated by aspirin administration through drinking water.	Aspirin	151-158	actin alpha 2, smooth muscle, aorta	Mus musculus	75-84
31791286-7	2019	RESULTS: It was helpful for clinicians to make a decision for personalized prophylactic aspirin or warfarin in primary MN patients when serum albumin was < 3.2 g/dl to prevent arterial and venous thromboembolic events (VTEs).	Aspirin	88-95	albumin	Homo sapiens	142-149
31905343-0	2020	Aspirin enhances the sensitivity of colon cancer cells to cisplatin by abrogating the binding of NF-kappaB to the COX-2 promoter.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	97-106
31905343-0	2020	Aspirin enhances the sensitivity of colon cancer cells to cisplatin by abrogating the binding of NF-kappaB to the COX-2 promoter.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	114-119
31905343-6	2020	The combined treatment of aspirin and cisplatin suppressed the expression of the anti-apoptotic protein Bcl-2 and the EMT-related proteins, up-regulated the levels of the cleaved PARP and Bax, and blocked the PI3K/AKT and RAF-MEK-ERK signaling pathway.	Aspirin	26-33	BCL2 apoptosis regulator	Homo sapiens	104-109
31905343-6	2020	The combined treatment of aspirin and cisplatin suppressed the expression of the anti-apoptotic protein Bcl-2 and the EMT-related proteins, up-regulated the levels of the cleaved PARP and Bax, and blocked the PI3K/AKT and RAF-MEK-ERK signaling pathway.	Aspirin	26-33	BCL2 associated X, apoptosis regulator	Homo sapiens	188-191
31905343-6	2020	The combined treatment of aspirin and cisplatin suppressed the expression of the anti-apoptotic protein Bcl-2 and the EMT-related proteins, up-regulated the levels of the cleaved PARP and Bax, and blocked the PI3K/AKT and RAF-MEK-ERK signaling pathway.	Aspirin	26-33	AKT serine/threonine kinase 1	Homo sapiens	214-217
31905343-6	2020	The combined treatment of aspirin and cisplatin suppressed the expression of the anti-apoptotic protein Bcl-2 and the EMT-related proteins, up-regulated the levels of the cleaved PARP and Bax, and blocked the PI3K/AKT and RAF-MEK-ERK signaling pathway.	Aspirin	26-33	mitogen-activated protein kinase kinase 7	Homo sapiens	226-229
31905343-6	2020	The combined treatment of aspirin and cisplatin suppressed the expression of the anti-apoptotic protein Bcl-2 and the EMT-related proteins, up-regulated the levels of the cleaved PARP and Bax, and blocked the PI3K/AKT and RAF-MEK-ERK signaling pathway.	Aspirin	26-33	mitogen-activated protein kinase 1	Homo sapiens	230-233
31622780-4	2020	This work demonstrates a proof-of-concept theranostic approach for inflammation based on analyte-kissing induced signaling, whereby a drug (in this report, aspirin) can be released upon the detection of a target level of a proinflammatory cytokine (i.e., interferon-gamma (IFN-gamma)) in real time.	Aspirin	156-163	interferon gamma	Homo sapiens	255-271
31622780-4	2020	This work demonstrates a proof-of-concept theranostic approach for inflammation based on analyte-kissing induced signaling, whereby a drug (in this report, aspirin) can be released upon the detection of a target level of a proinflammatory cytokine (i.e., interferon-gamma (IFN-gamma)) in real time.	Aspirin	156-163	interferon gamma	Homo sapiens	273-282
31622780-9	2020	STATEMENT OF SIGNIFICANCE: We developed an adaptive in vivo sensing device whereby a drug, aspirin, can be released upon the detection of a proinflammatory cytokine, interferon-gamma (IFN-gamma), in real time with a sensitivity of 10 pg mL-1.	Aspirin	91-98	interferon gamma	Homo sapiens	166-182
31764002-7	2020	The mechanism by which a thrombin-like enzyme VLCV (thrombin-like enzyme)-induced platelet aggregation was explored in presence of ticlopidin, clopidogrel and aspirin.	Aspirin	159-166	coagulation factor II, thrombin	Homo sapiens	25-33
31764002-7	2020	The mechanism by which a thrombin-like enzyme VLCV (thrombin-like enzyme)-induced platelet aggregation was explored in presence of ticlopidin, clopidogrel and aspirin.	Aspirin	159-166	coagulation factor II, thrombin	Homo sapiens	52-60
31905343-7	2020	In addition, we demonstrated that the enhanced effect of aspirin on the cisplatin-induced inhibition of tumor cell growth was also mediated through the suppression of the binding activity of NF-kappaB to the COX-2 promoter.	Aspirin	57-64	nuclear factor kappa B subunit 1	Homo sapiens	191-200
31905343-7	2020	In addition, we demonstrated that the enhanced effect of aspirin on the cisplatin-induced inhibition of tumor cell growth was also mediated through the suppression of the binding activity of NF-kappaB to the COX-2 promoter.	Aspirin	57-64	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	208-213
31905343-8	2020	The combination of aspirin and cisplatin effectively attenuated the translocation of NF-kappaB p65/p50 from the cytoplasm to the nucleus, and abrogated the binding of NF-kappaB p65/p50 to the COX-2 promoter, thereby down-regulating COX-2 expression and PGE2 synthesis.	Aspirin	19-26	nuclear factor kappa B subunit 1	Homo sapiens	99-102
31905343-8	2020	The combination of aspirin and cisplatin effectively attenuated the translocation of NF-kappaB p65/p50 from the cytoplasm to the nucleus, and abrogated the binding of NF-kappaB p65/p50 to the COX-2 promoter, thereby down-regulating COX-2 expression and PGE2 synthesis.	Aspirin	19-26	nuclear factor kappa B subunit 1	Homo sapiens	181-184
31905343-8	2020	The combination of aspirin and cisplatin effectively attenuated the translocation of NF-kappaB p65/p50 from the cytoplasm to the nucleus, and abrogated the binding of NF-kappaB p65/p50 to the COX-2 promoter, thereby down-regulating COX-2 expression and PGE2 synthesis.	Aspirin	19-26	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	192-197
31905343-8	2020	The combination of aspirin and cisplatin effectively attenuated the translocation of NF-kappaB p65/p50 from the cytoplasm to the nucleus, and abrogated the binding of NF-kappaB p65/p50 to the COX-2 promoter, thereby down-regulating COX-2 expression and PGE2 synthesis.	Aspirin	19-26	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	232-237
31622780-9	2020	STATEMENT OF SIGNIFICANCE: We developed an adaptive in vivo sensing device whereby a drug, aspirin, can be released upon the detection of a proinflammatory cytokine, interferon-gamma (IFN-gamma), in real time with a sensitivity of 10 pg mL-1.	Aspirin	91-98	interferon gamma	Homo sapiens	184-193
32736893-0	2020	Effect of clopidogrel vs. aspirin on pro-atherosclerotic NLRP1 inflammasome expression in endothelial cells.	Aspirin	26-33	NLR family pyrin domain containing 1	Homo sapiens	57-62
32736893-4	2020	Aspirin could inhibit NLRP1 inflammasome in endothelial cells, and clopidogrel could also provoke a reduction in vascular inflammation.	Aspirin	0-7	NLR family pyrin domain containing 1	Homo sapiens	22-27
32025207-0	2020	Compound C enhances the anticancer effect of aspirin in HER-2-positive breast cancer by regulating lipid metabolism in an AMPK-independent pathway.	Aspirin	45-52	erb-b2 receptor tyrosine kinase 2	Homo sapiens	56-61
32025207-1	2020	Various clinical studies have determined that aspirin shows anticancer effects in many human malignant cancers, including human epidermal growth factor receptor-2 (HER-2)-positive breast cancer.	Aspirin	46-53	erb-b2 receptor tyrosine kinase 2	Homo sapiens	128-162
32025207-1	2020	Various clinical studies have determined that aspirin shows anticancer effects in many human malignant cancers, including human epidermal growth factor receptor-2 (HER-2)-positive breast cancer.	Aspirin	46-53	erb-b2 receptor tyrosine kinase 2	Homo sapiens	164-169
32025207-4	2020	HER-2-positive breast cancer cell lines were treated with aspirin with or without Compound C pre-treatment; their phenotypes and mechanisms were then analyzed in vitro and in vivo.	Aspirin	58-65	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-5
32025207-5	2020	Aspirin exhibited anticancer effects in HER-2-positive breast cancer by inhibiting cell growth and inducing apoptosis through the activation of AMP-activated protein kinase (AMPK).	Aspirin	0-7	erb-b2 receptor tyrosine kinase 2	Homo sapiens	40-45
32025207-9	2020	Aspirin exhibits anticancer effects in HER-2-positive breast cancer by regulating lipid metabolism mediated by c-myc, and Compound C strengthens these effects in an AMPK-independent manner.	Aspirin	0-7	erb-b2 receptor tyrosine kinase 2	Homo sapiens	39-44
32025207-10	2020	Our results potentially provide a novel therapeutic strategy exploiting combined aspirin and Compound C therapy for HER-2-positive breast cancer, which acts by reducing de novo lipid synthesis.	Aspirin	81-88	erb-b2 receptor tyrosine kinase 2	Homo sapiens	116-121
30734682-2	2020	Common therapeutic activity of non-steroidal anti-inflammatory drugs (NSAID), such as aspirin, includes inhibition of two crucial enzymes of AA metabolism - cyclooxygenase-1 and -2 (COX-1/2), with certain risk for gastrointestinal and renal intolerance.	Aspirin	86-93	prostaglandin-endoperoxide synthase 1	Homo sapiens	157-180
31470444-9	2020	Stopping aspirin did not affect markers of P2Y12 reactivity and had no or marginal effects on clot kinetics, but increased markers sensitive to cyclooxygenase-1 blockade.	Aspirin	9-16	prostaglandin-endoperoxide synthase 1	Homo sapiens	144-160
31878351-1	2019	Given to its ability to irreversibly acetylate the platelet cyclooxygenase-1 enzyme, acetylsalicylic acid (ASA) is successfully employed for the prevention of cardiovascular disease.	Aspirin	85-105	prostaglandin-endoperoxide synthase 1	Homo sapiens	60-76
31878351-1	2019	Given to its ability to irreversibly acetylate the platelet cyclooxygenase-1 enzyme, acetylsalicylic acid (ASA) is successfully employed for the prevention of cardiovascular disease.	Aspirin	107-110	prostaglandin-endoperoxide synthase 1	Homo sapiens	60-76
31730866-5	2019	KEY FINDINGS: Results showed that separate treatment with 10 mg/kg BW tofacitinib and 100 mg/kg BW aspirin significantly (P &lt; 0.05) decreased tumour necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and serum amyloid A when compared to diabetic untreated rats.	Aspirin	99-106	tumor necrosis factor	Rattus norvegicus	175-184
31730866-5	2019	KEY FINDINGS: Results showed that separate treatment with 10 mg/kg BW tofacitinib and 100 mg/kg BW aspirin significantly (P &lt; 0.05) decreased tumour necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and serum amyloid A when compared to diabetic untreated rats.	Aspirin	99-106	interleukin 6	Rattus norvegicus	187-200
31730866-5	2019	KEY FINDINGS: Results showed that separate treatment with 10 mg/kg BW tofacitinib and 100 mg/kg BW aspirin significantly (P &lt; 0.05) decreased tumour necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and serum amyloid A when compared to diabetic untreated rats.	Aspirin	99-106	interleukin 6	Rattus norvegicus	202-206
31730866-6	2019	However, the combined therapy (10 mg/kg BW tofacitinib and 100 mg/kg BW aspirin) significantly decreased the levels of TNF-alpha, IL-6, serum amyloid A, HOMA-IR, blood glucose level and SOC-3 gene expression but significantly (P &lt; 0.05) improved glucose homoestasis, insulin secretion, HOMA-beta and GLUT-4 gene expression when compared to diabetic untreated rat.	Aspirin	72-79	tumor necrosis factor	Rattus norvegicus	119-128
31730866-6	2019	However, the combined therapy (10 mg/kg BW tofacitinib and 100 mg/kg BW aspirin) significantly decreased the levels of TNF-alpha, IL-6, serum amyloid A, HOMA-IR, blood glucose level and SOC-3 gene expression but significantly (P &lt; 0.05) improved glucose homoestasis, insulin secretion, HOMA-beta and GLUT-4 gene expression when compared to diabetic untreated rat.	Aspirin	72-79	interleukin 6	Rattus norvegicus	130-134
31544544-6	2019	Antagonists against cysteinyl leukotriene receptor (CysLTR) type 1, including montelukast, pranlukast and zafirlukast, have been widely prescribed in clinical practices; however, some clinical trials have shown insignificant responses to LTRAs in adult asthmatics, while some phenotypes of adult asthma showed more favorable responses to LTRAs including aspirin-exacerbated respiratory disease, elderly asthma, asthma associated with smoking, obesity and allergic rhinitis.	Aspirin	354-361	cysteinyl leukotriene receptor 1	Homo sapiens	52-58
31586705-0	2019	Oleanolic acid oxime derivatives and their conjugates with aspirin modulate the NF-kappaB-mediated transcription in HepG2 hepatoma cells.	Aspirin	59-66	nuclear factor kappa B subunit 1	Homo sapiens	80-89
31586705-1	2019	The aim of this study was to evaluate the effect of new oleanolic acid oxime (OAO) derivatives and their conjugates with aspirin (ASP) on the expression and activation of NF-kappaB in human hepatoma HepG2 cells.	Aspirin	121-128	nuclear factor kappa B subunit 1	Homo sapiens	171-180
31586705-1	2019	The aim of this study was to evaluate the effect of new oleanolic acid oxime (OAO) derivatives and their conjugates with aspirin (ASP) on the expression and activation of NF-kappaB in human hepatoma HepG2 cells.	Aspirin	130-133	nuclear factor kappa B subunit 1	Homo sapiens	171-180
31586705-3	2019	Moreover, conjugation of OAO with ASP led to enhanced downregulation of NF-kappaB expression and activation.	Aspirin	34-37	nuclear factor kappa B subunit 1	Homo sapiens	72-81
31586705-6	2019	The results of this study indicate that the new derivatives of OAO and particularly their conjugates with ASP, downregulate the expression of COX-2 in HepG2 cells by modulating the NF-kappaB signaling pathway and suggest their potential application in the prevention of liver inflammation and cancer.	Aspirin	106-109	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	142-147
31586705-6	2019	The results of this study indicate that the new derivatives of OAO and particularly their conjugates with ASP, downregulate the expression of COX-2 in HepG2 cells by modulating the NF-kappaB signaling pathway and suggest their potential application in the prevention of liver inflammation and cancer.	Aspirin	106-109	nuclear factor kappa B subunit 1	Homo sapiens	181-190
31442000-1	2019	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is a recalcitrant inflammatory disorder defined by asthma, nasal polyposis, and sensitivity to cyclooxygenase-1 inhibitors.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	154-170
31356853-3	2019	The aim of this study was to demonstrate the synthesis of a new compound bearing salicylic acid residue namely 2-((3-(chloromethyl)benzoyl)oxy)benzoic acid, to analyze its potential as a ligand for human cyclooxygenase-2 (COX-2) receptor, to evaluate its toxicity level and its effectiveness for analgesic and antiplatelet agent compared with acetylsalicylic acid.	Aspirin	343-363	prostaglandin-endoperoxide synthase 2	Homo sapiens	204-220
31335509-9	2019	Aspirin also downregulated Akt phosphorylation, and trophoblast invasiveness was facilitated under Akt inhibitor treatment.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	27-30
31335509-9	2019	Aspirin also downregulated Akt phosphorylation, and trophoblast invasiveness was facilitated under Akt inhibitor treatment.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	99-102
31824307-4	2019	Aspirin inhibits BCCMI by attenuating Wnt/beta-catenin signaling and suppressing FMOD expression via inhibiting deacetylation of beta-catenin by histone deacetylase 6 (HDAC6) leading to beta-catenin phosphorylation and cytoplasmic degradation.	Aspirin	0-7	histone deacetylase 6	Homo sapiens	145-166
31824307-4	2019	Aspirin inhibits BCCMI by attenuating Wnt/beta-catenin signaling and suppressing FMOD expression via inhibiting deacetylation of beta-catenin by histone deacetylase 6 (HDAC6) leading to beta-catenin phosphorylation and cytoplasmic degradation.	Aspirin	0-7	histone deacetylase 6	Homo sapiens	168-173
31729451-0	2019	Aspirin suppresses chemoresistance and enhances antitumor activity of 5-Fu in 5-Fu-resistant colorectal cancer by abolishing 5-Fu-induced NF-kappaB activation.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	138-147
31729451-10	2019	Taken together, findings in this study suggest that aspirin can reverse chemoresistance and potentiate the antitumor effect of 5-Fu, which is achieved through abolishing the 5-Fu-induced NF-kappaB activation, suggesting that aspirin may be a promising adjuvant therapeutic agent for CRC.	Aspirin	52-59	nuclear factor kappa B subunit 1	Homo sapiens	187-196
31729451-5	2019	Obviously, aspirin is one of these agents, which has been demonstrated to possess antitumor activities and as an inhibitor of NF-kappaB.	Aspirin	11-18	nuclear factor kappa B subunit 1	Homo sapiens	126-135
31729456-0	2019	Aspirin enhances cisplatin sensitivity of resistant non-small cell lung carcinoma stem-like cells by targeting mTOR-Akt axis to repress migration.	Aspirin	0-7	mechanistic target of rapamycin kinase	Homo sapiens	111-115
31729456-0	2019	Aspirin enhances cisplatin sensitivity of resistant non-small cell lung carcinoma stem-like cells by targeting mTOR-Akt axis to repress migration.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	116-119
31729451-8	2019	In vivo, aspirin markedly enhanced the antitumor activity of 5-Fu in suppressing tumor growth and metastasis, and down-regulating the expression of NF-kappaB-regulated genes in the 5-Fu-resistant cells.	Aspirin	9-16	nuclear factor kappa B subunit 1	Homo sapiens	148-157
31729456-5	2019	A search for the underlying mechanism revealed that aspirin pre-treatment abrogates p300 binding both at TATA-box and initiator (INR) regions of mTOR promoter of CSCs, thereby impeding RNA polymerase II binding at those sites and repressing mTOR gene transcription.	Aspirin	52-59	mechanistic target of rapamycin kinase	Homo sapiens	145-149
31729451-9	2019	Obviously, aspirin completely eradicated the 5-Fu-induced NF-kappaB activation, without inducing pronounced adverse effects.	Aspirin	11-18	nuclear factor kappa B subunit 1	Homo sapiens	58-67
31729456-5	2019	A search for the underlying mechanism revealed that aspirin pre-treatment abrogates p300 binding both at TATA-box and initiator (INR) regions of mTOR promoter of CSCs, thereby impeding RNA polymerase II binding at those sites and repressing mTOR gene transcription.	Aspirin	52-59	mechanistic target of rapamycin kinase	Homo sapiens	241-245
31781346-5	2019	In vitro, aspirin diminished cellular oxygen free radicals (ROS, nitric oxide (NO)) and inflammatory cytokines (interleukin- (IL-) 1beta and IL-6 and tumor necrosis factor alpha (TNF-alpha)) induced by lipopolysaccharides (LPS) in nucleus pulposus cells (NPCs).	Aspirin	10-17	interleukin 6	Rattus norvegicus	141-145
31781346-5	2019	In vitro, aspirin diminished cellular oxygen free radicals (ROS, nitric oxide (NO)) and inflammatory cytokines (interleukin- (IL-) 1beta and IL-6 and tumor necrosis factor alpha (TNF-alpha)) induced by lipopolysaccharides (LPS) in nucleus pulposus cells (NPCs).	Aspirin	10-17	tumor necrosis factor	Rattus norvegicus	150-177
31781346-11	2019	Histological analysis showed that aspirin treatment prevented the loss of COL2 and decreased MMP-3 and MMP-13, inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), IL-1beta, and TNF-alpha expression in the IVD tissues.	Aspirin	34-41	nitric oxide synthase 2	Rattus norvegicus	134-138
31781346-5	2019	In vitro, aspirin diminished cellular oxygen free radicals (ROS, nitric oxide (NO)) and inflammatory cytokines (interleukin- (IL-) 1beta and IL-6 and tumor necrosis factor alpha (TNF-alpha)) induced by lipopolysaccharides (LPS) in nucleus pulposus cells (NPCs).	Aspirin	10-17	tumor necrosis factor	Rattus norvegicus	179-188
31781346-11	2019	Histological analysis showed that aspirin treatment prevented the loss of COL2 and decreased MMP-3 and MMP-13, inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), IL-1beta, and TNF-alpha expression in the IVD tissues.	Aspirin	34-41	interleukin 1 beta	Rattus norvegicus	167-175
31781346-6	2019	We found that aspirin preserved the extracellular matrix (ECM) content of collagen type II (COL2) and aggrecan while inhibiting the expression of matrix-degenerating enzymes, including matrix metalloproteinase 3 and 13 (MMP-3 and MMP-13) and A disintegrin and metalloproteinase with thrombospondin motifs 4 and 5 (ADAMTS-4, ADAMTS-5).	Aspirin	14-21	ADAM metallopeptidase with thrombospondin type 1 motif, 5	Rattus norvegicus	324-332
31781346-11	2019	Histological analysis showed that aspirin treatment prevented the loss of COL2 and decreased MMP-3 and MMP-13, inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), IL-1beta, and TNF-alpha expression in the IVD tissues.	Aspirin	34-41	tumor necrosis factor	Rattus norvegicus	181-190
31781346-11	2019	Histological analysis showed that aspirin treatment prevented the loss of COL2 and decreased MMP-3 and MMP-13, inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), IL-1beta, and TNF-alpha expression in the IVD tissues.	Aspirin	34-41	nitric oxide synthase 2	Rattus norvegicus	111-132
31506320-10	2019	By combining this aspirin treatment with heterozygosity for mutations in actin regulators, we quantitatively identified enhancers and suppressors of COX inhibition.	Aspirin	18-25	Actin 79B	Drosophila melanogaster	73-78
30646422-1	2019	OBJECTIVE:  To assess the effect of aspirin use in low-risk pregnancy on: (1) pregnancy-associated plasma protein-A (PAPP-A) and placental-like growth factor (PLGF); (2) urinary albumin-to-creatinine ratio (ACR) and blood pressure; (3) fetal growth parameters; and (4) placental histopathology.	Aspirin	36-43	placental growth factor	Homo sapiens	129-157
30646422-1	2019	OBJECTIVE:  To assess the effect of aspirin use in low-risk pregnancy on: (1) pregnancy-associated plasma protein-A (PAPP-A) and placental-like growth factor (PLGF); (2) urinary albumin-to-creatinine ratio (ACR) and blood pressure; (3) fetal growth parameters; and (4) placental histopathology.	Aspirin	36-43	placental growth factor	Homo sapiens	159-163
31523846-4	2019	The aim of this study was to investigate A1AT serum levels and the rs1303 (Pi*M3) variant in A1AT gene in patients with ASA.	Aspirin	120-123	serpin family A member 1	Homo sapiens	41-45
31595533-11	2019	Treatment with 5-ASA in CD was associated with higher rates of steroid excess (OR 1.72 [95% CI 1.24-2.09]).	Aspirin	15-20	olfactory receptor family 7 subfamily E member 26 pseudogene	Homo sapiens	79-86
31523846-4	2019	The aim of this study was to investigate A1AT serum levels and the rs1303 (Pi*M3) variant in A1AT gene in patients with ASA.	Aspirin	120-123	serpin family A member 1	Homo sapiens	93-97
31523846-10	2019	A1AT homozygote mutation (PiM3M3) was significantly higher in the ASA group than the control group (21 vs 11, OR (95% CI): 6.68 [2.09-21.40], P = .001).	Aspirin	66-69	serpin family A member 1	Homo sapiens	0-4
31523846-12	2019	CONCLUSION: This preliminary study revealed that homozygote A1AT rs1303 (PiM3M3) variant is significantly higher in patients with isolated ASA and may be associated with ASA development.	Aspirin	139-142	serpin family A member 1	Homo sapiens	60-64
31523846-12	2019	CONCLUSION: This preliminary study revealed that homozygote A1AT rs1303 (PiM3M3) variant is significantly higher in patients with isolated ASA and may be associated with ASA development.	Aspirin	170-173	serpin family A member 1	Homo sapiens	60-64
31106412-7	2019	RESULTS: The administration of omega-3 fatty acids and aspirin significantly inhibited tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in serum of rats.	Aspirin	55-62	tumor necrosis factor	Rattus norvegicus	87-114
31106412-7	2019	RESULTS: The administration of omega-3 fatty acids and aspirin significantly inhibited tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in serum of rats.	Aspirin	55-62	tumor necrosis factor	Rattus norvegicus	116-125
31106412-7	2019	RESULTS: The administration of omega-3 fatty acids and aspirin significantly inhibited tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in serum of rats.	Aspirin	55-62	interleukin 1 beta	Rattus norvegicus	131-148
31106412-7	2019	RESULTS: The administration of omega-3 fatty acids and aspirin significantly inhibited tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in serum of rats.	Aspirin	55-62	interleukin 1 beta	Rattus norvegicus	150-158
31106412-9	2019	Omega-3 fatty acids only, aspirin only, or omega-3 fatty acids plus aspirin also inhibited the protein expressions of COX-2 and iNOS in LPS-stimulated RAW264.7 cells.	Aspirin	26-33	nitric oxide synthase 2, inducible	Mus musculus	128-132
31106412-9	2019	Omega-3 fatty acids only, aspirin only, or omega-3 fatty acids plus aspirin also inhibited the protein expressions of COX-2 and iNOS in LPS-stimulated RAW264.7 cells.	Aspirin	68-75	nitric oxide synthase 2, inducible	Mus musculus	128-132
31220426-11	2019	RESULTS: Overall Mo from control subjects exposed to ASA showed increased secretion of IL-1RA, IL-8, MCP-1, and TNF-alpha and Mo from stroke patients showed greater release of IL-1RA and MCP-1.	Aspirin	53-56	C-X-C motif chemokine ligand 8	Homo sapiens	95-99
31557405-0	2019	Aspirin inhibits adipogenesis of tendon stem cells and lipids accumulation in rat injury tendon through regulating PTEN/PI3K/AKT signalling.	Aspirin	0-7	AKT serine/threonine kinase 1	Rattus norvegicus	125-128
31557405-15	2019	In conclusion, by down-regulating PTEN/PI3K/AKT signalling, aspirin inhibited adipogenesis of TSCs and fatty infiltration in injury tendon, promoted biomechanical properties and decreased rupture risk of injury tendon.	Aspirin	60-67	AKT serine/threonine kinase 1	Rattus norvegicus	44-47
31230127-10	2019	In laparoscopic colorectal surgery, continuation of aspirin is an acceptable strategy for patients with thromboembolic risk caused by interruption of APT.	Aspirin	52-59	LYPLA2 pseudogene 1	Homo sapiens	150-153
31185432-4	2019	All pharmaceuticals except acetylsalicylic acid and sulfathiazole were found in PS1, PS2, and PS3 samples, whereas acetylsalicylic acid, carbamazepine, sulfamethazine, and sulfamethoxazole were found in PS4, most of the pharmaceuticals were not present in PS5.	Aspirin	27-47	taste 2 receptor member 64 pseudogene	Homo sapiens	85-88
31243598-3	2019	Overexpression of CFP-Bcl-XL in Hela and A549 cells observably inhibited aspirin-induced ATP depletion and almost completely inhibited the aspirin-induced cells bubbling, while pharmacological inhibition of endogenous Bcl-XL activity by ABT-737 remarkably promoted aspirin-induced ATP depletion and cells bubbling, suggesting the key inhibitory role of Bcl-XL in aspirin-induced oncosis.	Aspirin	73-80	complement factor properdin	Homo sapiens	18-21
31243598-3	2019	Overexpression of CFP-Bcl-XL in Hela and A549 cells observably inhibited aspirin-induced ATP depletion and almost completely inhibited the aspirin-induced cells bubbling, while pharmacological inhibition of endogenous Bcl-XL activity by ABT-737 remarkably promoted aspirin-induced ATP depletion and cells bubbling, suggesting the key inhibitory role of Bcl-XL in aspirin-induced oncosis.	Aspirin	73-80	BCL2 like 1	Homo sapiens	22-28
31243598-3	2019	Overexpression of CFP-Bcl-XL in Hela and A549 cells observably inhibited aspirin-induced ATP depletion and almost completely inhibited the aspirin-induced cells bubbling, while pharmacological inhibition of endogenous Bcl-XL activity by ABT-737 remarkably promoted aspirin-induced ATP depletion and cells bubbling, suggesting the key inhibitory role of Bcl-XL in aspirin-induced oncosis.	Aspirin	139-146	complement factor properdin	Homo sapiens	18-21
31243598-3	2019	Overexpression of CFP-Bcl-XL in Hela and A549 cells observably inhibited aspirin-induced ATP depletion and almost completely inhibited the aspirin-induced cells bubbling, while pharmacological inhibition of endogenous Bcl-XL activity by ABT-737 remarkably promoted aspirin-induced ATP depletion and cells bubbling, suggesting the key inhibitory role of Bcl-XL in aspirin-induced oncosis.	Aspirin	139-146	BCL2 like 1	Homo sapiens	22-28
31243598-3	2019	Overexpression of CFP-Bcl-XL in Hela and A549 cells observably inhibited aspirin-induced ATP depletion and almost completely inhibited the aspirin-induced cells bubbling, while pharmacological inhibition of endogenous Bcl-XL activity by ABT-737 remarkably promoted aspirin-induced ATP depletion and cells bubbling, suggesting the key inhibitory role of Bcl-XL in aspirin-induced oncosis.	Aspirin	139-146	complement factor properdin	Homo sapiens	18-21
31243598-3	2019	Overexpression of CFP-Bcl-XL in Hela and A549 cells observably inhibited aspirin-induced ATP depletion and almost completely inhibited the aspirin-induced cells bubbling, while pharmacological inhibition of endogenous Bcl-XL activity by ABT-737 remarkably promoted aspirin-induced ATP depletion and cells bubbling, suggesting the key inhibitory role of Bcl-XL in aspirin-induced oncosis.	Aspirin	139-146	BCL2 like 1	Homo sapiens	22-28
31243598-3	2019	Overexpression of CFP-Bcl-XL in Hela and A549 cells observably inhibited aspirin-induced ATP depletion and almost completely inhibited the aspirin-induced cells bubbling, while pharmacological inhibition of endogenous Bcl-XL activity by ABT-737 remarkably promoted aspirin-induced ATP depletion and cells bubbling, suggesting the key inhibitory role of Bcl-XL in aspirin-induced oncosis.	Aspirin	139-146	complement factor properdin	Homo sapiens	18-21
31243598-3	2019	Overexpression of CFP-Bcl-XL in Hela and A549 cells observably inhibited aspirin-induced ATP depletion and almost completely inhibited the aspirin-induced cells bubbling, while pharmacological inhibition of endogenous Bcl-XL activity by ABT-737 remarkably promoted aspirin-induced ATP depletion and cells bubbling, suggesting the key inhibitory role of Bcl-XL in aspirin-induced oncosis.	Aspirin	139-146	BCL2 like 1	Homo sapiens	22-28
31220426-11	2019	RESULTS: Overall Mo from control subjects exposed to ASA showed increased secretion of IL-1RA, IL-8, MCP-1, and TNF-alpha and Mo from stroke patients showed greater release of IL-1RA and MCP-1.	Aspirin	53-56	tumor necrosis factor	Homo sapiens	112-121
31220426-13	2019	In addition, in co-cultures independent of Mo origin, ASA reduced IL-6, IL-8, MCP-1, and TNF-alpha.	Aspirin	54-57	interleukin 6	Homo sapiens	66-70
31220426-13	2019	In addition, in co-cultures independent of Mo origin, ASA reduced IL-6, IL-8, MCP-1, and TNF-alpha.	Aspirin	54-57	C-X-C motif chemokine ligand 8	Homo sapiens	72-76
31220426-13	2019	In addition, in co-cultures independent of Mo origin, ASA reduced IL-6, IL-8, MCP-1, and TNF-alpha.	Aspirin	54-57	tumor necrosis factor	Homo sapiens	89-98
31262687-0	2019	Aspirin Treatment Effect and Association with PIK3CA Mutation in Breast Cancer: A Biomarker Analysis.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	46-52
31262687-10	2019	Also, a subgroup of patients in the low-dose, long-term aspirin group with a PIK3CA mutation showed a small beneficial effect (HR, 0.37; 95% CI, 0.04-3.25; P = .37).	Aspirin	56-63	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	77-83
31262687-12	2019	Future studies should assess the comprehensive mechanism of aspirin for the PIK3CA mutant subgroup in a large study.	Aspirin	60-67	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	76-82
31530062-9	2019	Conclusion: Our findings suggest that SCF and C-kit receptors have a direct effect on the severity of aspirin-induced asthma.	Aspirin	102-109	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-51
31062402-9	2019	The LDL-C achievement rate for three consecutive years after starting treatment with statin and aspirin was 49.7%, 51.4% and 45.9%, respectively.	Aspirin	96-103	component of oligomeric golgi complex 2	Homo sapiens	4-9
31686742-15	2019	Conclusion: The results of the randomized controlled trial of nitric oxide in the prevention of pre-eclampsia (NOPE) showed that in high-risk women receiving standard aspirin prophylaxis from less than 16 weeks, there is no significant reduction in the incidence of hypertensive disorders of pregnancy in the ISMN group, to the desired extent.	Aspirin	167-174	immunoglobulin superfamily DCC subclass member 4	Homo sapiens	111-115
31273781-0	2019	Aspirin up-regulates suppressor of cytokine signaling 3 in glial cells via PPARalpha.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Mus musculus	75-84
31273781-7	2019	While investigating the mechanism, we found that Socs3 gene promoter harbors peroxisome proliferator response element and that aspirin up-regulated SOCS3 in astrocytes isolated from PPARbeta (-/-), but not PPARalpha (-/-), mice.	Aspirin	127-134	peroxisome proliferator activated receptor alpha	Mus musculus	182-190
31273781-8	2019	Accordingly, aspirin increased SOCS3 in vivo in the cortex of wild type and PPARbeta (-/-), but not PPARalpha (-/-), mice.	Aspirin	13-20	peroxisome proliferator activated receptor alpha	Mus musculus	76-84
31273781-10	2019	Finally, recruitment of PPARalpha by aspirin to the proximal, but not distal, peroxisome proliferator response element of the Socs3 promoter suggests that aspirin increases the transcription of Socs3 gene via PPARalpha.	Aspirin	37-44	peroxisome proliferator activated receptor alpha	Mus musculus	24-33
31273781-10	2019	Finally, recruitment of PPARalpha by aspirin to the proximal, but not distal, peroxisome proliferator response element of the Socs3 promoter suggests that aspirin increases the transcription of Socs3 gene via PPARalpha.	Aspirin	155-162	peroxisome proliferator activated receptor alpha	Mus musculus	24-33
31273781-10	2019	Finally, recruitment of PPARalpha by aspirin to the proximal, but not distal, peroxisome proliferator response element of the Socs3 promoter suggests that aspirin increases the transcription of Socs3 gene via PPARalpha.	Aspirin	155-162	peroxisome proliferator activated receptor alpha	Mus musculus	209-218
31273781-11	2019	This study describes a novel property of aspirin in elevating SOCS3 in glial cells via PPARalpha and suggests that aspirin may be further considered for therapeutic application in neuroinflammatory and neurodegenerative disorders.	Aspirin	41-48	peroxisome proliferator activated receptor alpha	Mus musculus	87-96
31442897-3	2019	Expected inhibition of COX1 by ASA was ascertained by a strong decrease in TXB2 production, and its effect on platelet function and hemostasis, by decreased collagen-induced aggregation and increased bleeding time, respectively.	Aspirin	31-34	cytochrome c oxidase I, mitochondrial	Mus musculus	23-27
31554283-6	2019	Interestingly, acetylsalicylic acid, ibuprofen, L-ascorbic acid, and citrate each significantly destabilized HIF1alpha only under normoxia.	Aspirin	15-35	hypoxia inducible factor 1 subunit alpha	Homo sapiens	109-118
31469551-6	2019	Substitution of Arg-513 with histidine (the equivalent residue in COX-1) resulted in a 2-fold potentiation of aspirin inhibition, in support of the hypothesis that the presence of histidine in COX-1 lowers the activation barrier associated with the formation of the initial noncovalent enzyme-inhibitor complex.	Aspirin	110-117	cytochrome c oxidase I, mitochondrial	Mus musculus	66-71
31469551-6	2019	Substitution of Arg-513 with histidine (the equivalent residue in COX-1) resulted in a 2-fold potentiation of aspirin inhibition, in support of the hypothesis that the presence of histidine in COX-1 lowers the activation barrier associated with the formation of the initial noncovalent enzyme-inhibitor complex.	Aspirin	110-117	cytochrome c oxidase I, mitochondrial	Mus musculus	193-198
32123852-7	2019	Moreover, aspirin reduced p53 and p21 accumulation in DOX-treated human and mouse fibroblasts.	Aspirin	10-17	tumor protein p53	Homo sapiens	26-29
31577090-0	2019	Aspirin inhabits proliferation and promotes apoptosis of pancreatic cancer cells via PI3K/Akt/mTOR signaling pathway.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	90-93
31577090-0	2019	Aspirin inhabits proliferation and promotes apoptosis of pancreatic cancer cells via PI3K/Akt/mTOR signaling pathway.	Aspirin	0-7	mechanistic target of rapamycin kinase	Homo sapiens	94-98
31026400-0	2019	Aspirin-exacerbated Respiratory Disease: A Syndrome of Mast Cell-mediated PgD2 Overproduction.	Aspirin	0-7	prostaglandin D2 synthase	Homo sapiens	74-78
31569308-9	2019	The primary aspirin therapy was associated with a significant increase in IgE in nonresponders, but there was no significant increase in IgE after the second aspirin desensitization and treatment.	Aspirin	12-19	immunoglobulin heavy constant epsilon	Homo sapiens	74-77
31569308-11	2019	Patients with higher baseline serum IgE levels may benefit from ESS performed shortly before aspirin desensitization and therapy.	Aspirin	93-100	immunoglobulin heavy constant epsilon	Homo sapiens	36-39
31511539-6	2019	In CAD patients, the PlA2 gene carriers had similar incidence of laboratory aspirin resistance compared to those with PlA1/A1 genotype [29.7% vs 28.3%, OR = 0.94 (95% CI 0.63 to 1.40, P = 0.74)], and there were no significant differences in the adverse clinical outcomes between the PlA2 carriers and the PlA1/A1 genotype patients.	Aspirin	76-83	phospholipase A2 group IB	Homo sapiens	21-25
31510056-0	2019	Effect of Low-Dose Aspirin on Soluble FMS-Like Tyrosine Kinase 1/Placental Growth Factor (sFlt-1/PlGF Ratio) in Pregnancies at High Risk for the Development of Preeclampsia.	Aspirin	19-26	placental growth factor	Homo sapiens	65-88
31510056-0	2019	Effect of Low-Dose Aspirin on Soluble FMS-Like Tyrosine Kinase 1/Placental Growth Factor (sFlt-1/PlGF Ratio) in Pregnancies at High Risk for the Development of Preeclampsia.	Aspirin	19-26	placental growth factor	Homo sapiens	97-101
31510056-7	2019	The use of aspirin showed a trend towards an improvement of the sFlt-1/PlGF ratio in women with preeclampsia in a previous pregnancy and a significant effect on the sFlt-1/PlGF ratio in women with a pathologic first trimester screening for preeclampsia.	Aspirin	11-18	placental growth factor	Homo sapiens	71-75
31510056-7	2019	The use of aspirin showed a trend towards an improvement of the sFlt-1/PlGF ratio in women with preeclampsia in a previous pregnancy and a significant effect on the sFlt-1/PlGF ratio in women with a pathologic first trimester screening for preeclampsia.	Aspirin	11-18	placental growth factor	Homo sapiens	172-176
31510056-8	2019	CONCLUSIONS: Our findings reveal an impact of aspirin on sFlt-1/PlGF ratio in women with a pathologic first trimester screening for preeclampsia, strongly supporting its prophylactic use.	Aspirin	46-53	placental growth factor	Homo sapiens	64-68
31234130-5	2019	Further, a comparative molecular modeling analysis of TM-7 carried out with the crystal structure of aspirin acetylated human COX-2 suggested effectively binding and efficient accommodation inside the active site"s gorge.	Aspirin	101-108	prostaglandin-endoperoxide synthase 2	Homo sapiens	126-131
31813866-4	2019	The aim of the study was to prepare aspirin gel and mouthwash in 1% concentration and use it in patients with periodontal diseases during the non-surgical periodontal treatment and to assess its anti-inflammatory effects on salivary biomarkers PGE2, TNF-alpha, and nitric oxide.	Aspirin	36-43	tumor necrosis factor	Homo sapiens	250-259
30580092-1	2019	BACKGROUND &amp; AIMS: The antiplatelet effect of low-dose aspirin, via inhibition of cyclooxygenase-1, might contribute to its ability to reduce the risk of colorectal cancer (CRC).	Aspirin	59-66	prostaglandin-endoperoxide synthase 1	Homo sapiens	86-102
30328786-8	2019	It has been observed that patients previously stable under ACE inhibitor will most likely develop AE soon after the addition of another medication, including the combination of aspirin or non-steroid anti-inflammatory drugs with ACE inhibitor which has proved to be the most common cause, accounting for close to 50% of all AE cases related to ACE inhibitors.	Aspirin	177-184	angiotensin I converting enzyme	Homo sapiens	59-62
31454281-2	2019	Recently, ASA has demonstrated a promising anti-proliferative effect on GEP-NENs in vitro.	Aspirin	10-13	granulin precursor	Homo sapiens	72-75
31454281-3	2019	However, the direct anti-neoplastic impact of ASA on GEP-NEN clinical outcome is yet to be clarified.	Aspirin	46-49	granulin precursor	Homo sapiens	53-56
31243131-7	2019	Furthermore, acetylsalicylic acid (ASA), a potent inhibitor of the NF-kappaB activator kinase IkappaB kinase beta (IKK-beta), did not significantly diminish reactivation in a primary CD4+ T central memory (TCM) cell latency model.	Aspirin	13-33	nuclear factor kappa B subunit 1	Homo sapiens	67-76
31243131-7	2019	Furthermore, acetylsalicylic acid (ASA), a potent inhibitor of the NF-kappaB activator kinase IkappaB kinase beta (IKK-beta), did not significantly diminish reactivation in a primary CD4+ T central memory (TCM) cell latency model.	Aspirin	35-38	nuclear factor kappa B subunit 1	Homo sapiens	67-76
31243131-12	2019	Our study provides a molecular proof of concept for the use of anti-inflammatory drugs, like aspirin, capable of inhibiting NF-kappaB in patients under combination antiretroviral therapy during the shock-and-kill approach, to avoid potential autoimmune and inflammatory disorders that can be elicited by combinations of LRAs.	Aspirin	93-100	nuclear factor kappa B subunit 1	Homo sapiens	124-133
31429774-10	2019	Palbociclib attenuated body temperature reduction and diminished serum histamine levels in ovalbumin OVA-challenged ASA mice.	Aspirin	116-119	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	91-100
31009712-0	2019	Aspirin-Dependent Platelet Inflammatory Inhibition in Healthy Subjects Decreases NLRP-1 Inflammasome.	Aspirin	0-7	NLR family pyrin domain containing 1	Homo sapiens	81-87
31009712-10	2019	CONCLUSIONS: Data observed in the our study indicate that in HAECs, the intracytosolic NLRP-1 expression is attenuated by the auto/paracrine platelet inhibition by aspirin, without direct platelet-endothelial cell interaction.	Aspirin	164-171	NLR family pyrin domain containing 1	Homo sapiens	87-93
31300475-4	2019	In this article, we present evidence that aspirin"s unique ability to irreversibly inhibit platelet cyclooxygenase-1 is a key mechanism by which aspirin exerts anticancer activity.	Aspirin	42-49	prostaglandin-endoperoxide synthase 1	Homo sapiens	100-116
31300475-4	2019	In this article, we present evidence that aspirin"s unique ability to irreversibly inhibit platelet cyclooxygenase-1 is a key mechanism by which aspirin exerts anticancer activity.	Aspirin	145-152	prostaglandin-endoperoxide synthase 1	Homo sapiens	100-116
31005060-9	2019	CONCLUSIONS:  Aspirin 15 cH acts through the inhibition of the COX-2 pathway producing a clear pro-thrombotic effect.	Aspirin	14-21	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	63-68
31004367-0	2019	Low-dose aspirin reduces hypoxia-induced sFlt1 release via the JNK/AP-1 pathway in human trophoblast and endothelial cells.	Aspirin	9-16	mitogen-activated protein kinase 8	Homo sapiens	63-66
31266078-0	2019	miR-34b-3p May Promote Antiplatelet Efficiency of Aspirin by Inhibiting Thromboxane Synthase Expression.	Aspirin	50-57	thromboxane A synthase 1	Homo sapiens	72-92
31266078-8	2019	Our data demonstrated that the expression of TBXAS1 was higher in the aspirin hyporesponsiveness group than that in the hyperresponsiveness group, suggesting that high expression of TBXAS1 may be associated with aspirin hyporesponsiveness.	Aspirin	70-77	thromboxane A synthase 1	Homo sapiens	45-51
31266078-8	2019	Our data demonstrated that the expression of TBXAS1 was higher in the aspirin hyporesponsiveness group than that in the hyperresponsiveness group, suggesting that high expression of TBXAS1 may be associated with aspirin hyporesponsiveness.	Aspirin	70-77	thromboxane A synthase 1	Homo sapiens	182-188
31266078-8	2019	Our data demonstrated that the expression of TBXAS1 was higher in the aspirin hyporesponsiveness group than that in the hyperresponsiveness group, suggesting that high expression of TBXAS1 may be associated with aspirin hyporesponsiveness.	Aspirin	212-219	thromboxane A synthase 1	Homo sapiens	45-51
31266078-8	2019	Our data demonstrated that the expression of TBXAS1 was higher in the aspirin hyporesponsiveness group than that in the hyperresponsiveness group, suggesting that high expression of TBXAS1 may be associated with aspirin hyporesponsiveness.	Aspirin	212-219	thromboxane A synthase 1	Homo sapiens	182-188
31266078-9	2019	miR-34b-3p may regulate the platelet and aspirin response by suppressing TBXAS1 expression and megakaryocyte proliferation.	Aspirin	41-48	thromboxane A synthase 1	Homo sapiens	73-79
31004367-0	2019	Low-dose aspirin reduces hypoxia-induced sFlt1 release via the JNK/AP-1 pathway in human trophoblast and endothelial cells.	Aspirin	9-16	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	67-71
31248548-7	2019	Among patients with >=1 high-risk feature identified from the CART analysis, rivaroxaban and aspirin prevented 33 serious vascular events, whereas in lower-risk patients, rivaroxaban and aspirin treatment led to the avoidance of 10 events per 1,000 patients treated for 30 months.	Aspirin	93-100	CART prepropeptide	Homo sapiens	62-66
31396016-8	2019	CD34+ cells after six days in culture were stimulated with atorvastatin (AT), acetylsalicylic acid (ASA), sulforaphane (SR), resveratrol (RV), or metformin (Met) for 48 h. Conditioned media from such cells were then used to stimulate human aortic endothelial cells (HAoECs) to enhance tube-like structure formation in a Matrigel assay.	Aspirin	78-98	CD34 molecule	Homo sapiens	0-4
31396016-8	2019	CD34+ cells after six days in culture were stimulated with atorvastatin (AT), acetylsalicylic acid (ASA), sulforaphane (SR), resveratrol (RV), or metformin (Met) for 48 h. Conditioned media from such cells were then used to stimulate human aortic endothelial cells (HAoECs) to enhance tube-like structure formation in a Matrigel assay.	Aspirin	100-103	CD34 molecule	Homo sapiens	0-4
31307465-8	2019	Inhibition of cyclooxygenase by ASA attenuated LPS-mediated P-selectin expression demonstrating that TLR4 signaling in platelets is partially dependent on TxA2 pathway.	Aspirin	32-35	selectin P	Canis lupus familiaris	60-70
31307465-8	2019	Inhibition of cyclooxygenase by ASA attenuated LPS-mediated P-selectin expression demonstrating that TLR4 signaling in platelets is partially dependent on TxA2 pathway.	Aspirin	32-35	toll like receptor 4	Canis lupus familiaris	101-105
31291992-1	2019	Acetylsalicylic acid has been linked to a lower risk for different cancer types, presumably through its inhibitory effect on cyclooxygenase 2.	Aspirin	0-20	prostaglandin-endoperoxide synthase 2	Homo sapiens	125-141
31140860-7	2019	Being a multifunctional molecule, aspirin stimulates the activation of cAMP-response element-binding (CREB) to promote the recruitment of CREB to the IL-11 gene promoter and stimulate the transcription of IL-11 in splenocytes.	Aspirin	34-41	cAMP responsive element binding protein 1	Mus musculus	71-100
31384532-7	2019	We found that aspirin could inhibit NLRP3 inflammasome formation and activation in vitro in dose-dependent manner and has correlation between the NLRP3 inflammasome and the ROS/TXNIP pathway.	Aspirin	14-21	thioredoxin interacting protein	Mus musculus	177-182
31384532-8	2019	We also found that low-concentration aspirin could inhibit the formation and activation of NLRP3 inflammasome and restore the expression of the endothelial tight junction protein zonula occludens-1/2 (ZO1/2).	Aspirin	37-44	tight junction protein 1	Mus musculus	201-206
31225686-0	2019	Aspirin inhibits inflammation and scar formation in the injury tendon healing through regulating JNK/STAT-3 signalling pathway.	Aspirin	0-7	mitogen-activated protein kinase 8	Homo sapiens	97-100
31225686-0	2019	Aspirin inhibits inflammation and scar formation in the injury tendon healing through regulating JNK/STAT-3 signalling pathway.	Aspirin	0-7	signal transducer and activator of transcription 3	Homo sapiens	101-107
31225686-13	2019	CONCLUSIONS: Taken together, the findings suggested that aspirin inhibited inflammation and scar formation via regulation of JNK/STAT-3 signalling and decreased rerupture risk of injury tendon.	Aspirin	57-64	mitogen-activated protein kinase 8	Homo sapiens	125-128
31225686-13	2019	CONCLUSIONS: Taken together, the findings suggested that aspirin inhibited inflammation and scar formation via regulation of JNK/STAT-3 signalling and decreased rerupture risk of injury tendon.	Aspirin	57-64	signal transducer and activator of transcription 3	Homo sapiens	129-135
31140860-7	2019	Being a multifunctional molecule, aspirin stimulates the activation of cAMP-response element-binding (CREB) to promote the recruitment of CREB to the IL-11 gene promoter and stimulate the transcription of IL-11 in splenocytes.	Aspirin	34-41	cAMP responsive element binding protein 1	Mus musculus	102-106
31140860-7	2019	Being a multifunctional molecule, aspirin stimulates the activation of cAMP-response element-binding (CREB) to promote the recruitment of CREB to the IL-11 gene promoter and stimulate the transcription of IL-11 in splenocytes.	Aspirin	34-41	cAMP responsive element binding protein 1	Mus musculus	138-142
31140860-8	2019	Therefore, it appears that low-dose aspirin protects EAE via CREB-mediated stimulation of IL-11-Treg pathway and that aspirin may have therapeutic importance in MS.	Aspirin	36-43	cAMP responsive element binding protein 1	Mus musculus	61-65
31196200-4	2019	RESULTS: Platelet count inversely correlated with blood hemoglobin levels (p < 0.001) and positively correlated with serum levels of CRP and multiple cytokines including IL-1RA, IL-4, IL-6, IL-7, IL-8, IL-12, IFNgamma, and PDGF-BB (p < 0.001 for all), while aspirin use was not associated with the levels of systemic inflammatory markers.	Aspirin	258-265	C-reactive protein	Homo sapiens	133-136
31278071-0	2019	Aspirin targets P4HA2 through inhibiting NF-kappaB and LMCD1-AS1/let-7g to inhibit tumour growth and collagen deposition in hepatocellular carcinoma.	Aspirin	0-7	prolyl 4-hydroxylase subunit alpha 2	Homo sapiens	16-21
31278071-0	2019	Aspirin targets P4HA2 through inhibiting NF-kappaB and LMCD1-AS1/let-7g to inhibit tumour growth and collagen deposition in hepatocellular carcinoma.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	41-50
31278071-4	2019	Here, we tried to decipher whether aspirin (ASA), a classic anti-inflammatory drug, could improve the prognosis of HCC through targeting P4HA2.	Aspirin	35-42	prolyl 4-hydroxylase subunit alpha 2	Homo sapiens	137-142
31278071-4	2019	Here, we tried to decipher whether aspirin (ASA), a classic anti-inflammatory drug, could improve the prognosis of HCC through targeting P4HA2.	Aspirin	44-47	prolyl 4-hydroxylase subunit alpha 2	Homo sapiens	137-142
31278071-5	2019	METHODS: Western blotting, qRT-PCR assay, immunofluorescence staining, luciferase reporter gene assay, and ChIP assay were applied to demonstrate the molecular mechanism of the regulation of P4HA2 expression by aspirin.	Aspirin	211-218	prolyl 4-hydroxylase subunit alpha 2	Homo sapiens	191-196
31278071-6	2019	A mouse xenograft model, cell viability assay, colony formation assay, and immunohistochemistry analysis were used to evaluate the anti-fibrosis effect of aspirin through targeting the NF-kappaB/P4HA2 axis and LMCD1-AS1/let-7g/P4HA2 axis in vitro and in vivo.	Aspirin	155-162	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	185-194
31278071-6	2019	A mouse xenograft model, cell viability assay, colony formation assay, and immunohistochemistry analysis were used to evaluate the anti-fibrosis effect of aspirin through targeting the NF-kappaB/P4HA2 axis and LMCD1-AS1/let-7g/P4HA2 axis in vitro and in vivo.	Aspirin	155-162	arylsulfatase B	Mus musculus	216-219
31571629-1	2019	Background & objectives: Cytochrome P450, P2Y 12, cyclooxygenase-1 (COX1) and glycoprotein V1 (GPVI) gene polymorphisms are known to affect patient responsiveness towards aspirin and clopidogrel dual antiplatelet therapy (DAPT).	Aspirin	171-178	prostaglandin-endoperoxide synthase 1	Homo sapiens	50-66
31571629-1	2019	Background & objectives: Cytochrome P450, P2Y 12, cyclooxygenase-1 (COX1) and glycoprotein V1 (GPVI) gene polymorphisms are known to affect patient responsiveness towards aspirin and clopidogrel dual antiplatelet therapy (DAPT).	Aspirin	171-178	prostaglandin-endoperoxide synthase 1	Homo sapiens	68-72
31090213-7	2019	Aspirin has been found to inhibit cancer cell viability and promote CRC cell apoptosis.Similarly, aspirin has also been found to increase pro-apoptotic protein Bax"s expression.	Aspirin	0-7	BCL2 associated X, apoptosis regulator	Homo sapiens	160-163
31090213-7	2019	Aspirin has been found to inhibit cancer cell viability and promote CRC cell apoptosis.Similarly, aspirin has also been found to increase pro-apoptotic protein Bax"s expression.	Aspirin	98-105	BCL2 associated X, apoptosis regulator	Homo sapiens	160-163
31146130-2	2019	Here we utilized Oncidium cytosolic ascorbate peroxidase (OgCytAPX) as a model to demonstrate that CytAPX of several plants possess dual catalytic activity of both AsA and GSH, compared with the monocatalytic activity of Arabidopsis APX (AtCytAPX).	Aspirin	164-167	peroxidase	Arabidopsis thaliana	46-56
30876584-10	2019	A unique formulation of ASA was found to have a different mass pattern when analyzed with TG-APPI-qMS.	Aspirin	24-27	amyloid beta precursor protein	Homo sapiens	93-97
30187283-7	2019	While investigating mechanisms, we found the presence of cAMP response element (CRE) in the promoter of TH gene and the rapid induction of cAMP response element binding (CREB) activation by aspirin in dopaminergic neuronal cells.	Aspirin	190-197	cAMP responsive element binding protein 1	Mus musculus	139-168
30187283-7	2019	While investigating mechanisms, we found the presence of cAMP response element (CRE) in the promoter of TH gene and the rapid induction of cAMP response element binding (CREB) activation by aspirin in dopaminergic neuronal cells.	Aspirin	190-197	cAMP responsive element binding protein 1	Mus musculus	170-174
30187283-8	2019	Aspirin treatment also increased the level of phospho-CREB in the nigra of C57/BL6 mice.	Aspirin	0-7	cAMP responsive element binding protein 1	Mus musculus	54-58
30187283-9	2019	The abrogation of aspirin-induced expression of TH by siRNA knockdown of CREB and the recruitment of CREB to the TH gene promoter by aspirin suggest that aspirin stimulates the transcription of TH in dopaminergic neurons via CREB.	Aspirin	18-25	cAMP responsive element binding protein 1	Mus musculus	73-77
30187283-9	2019	The abrogation of aspirin-induced expression of TH by siRNA knockdown of CREB and the recruitment of CREB to the TH gene promoter by aspirin suggest that aspirin stimulates the transcription of TH in dopaminergic neurons via CREB.	Aspirin	133-140	cAMP responsive element binding protein 1	Mus musculus	101-105
30187283-9	2019	The abrogation of aspirin-induced expression of TH by siRNA knockdown of CREB and the recruitment of CREB to the TH gene promoter by aspirin suggest that aspirin stimulates the transcription of TH in dopaminergic neurons via CREB.	Aspirin	133-140	cAMP responsive element binding protein 1	Mus musculus	101-105
30187283-9	2019	The abrogation of aspirin-induced expression of TH by siRNA knockdown of CREB and the recruitment of CREB to the TH gene promoter by aspirin suggest that aspirin stimulates the transcription of TH in dopaminergic neurons via CREB.	Aspirin	133-140	cAMP responsive element binding protein 1	Mus musculus	101-105
30187283-9	2019	The abrogation of aspirin-induced expression of TH by siRNA knockdown of CREB and the recruitment of CREB to the TH gene promoter by aspirin suggest that aspirin stimulates the transcription of TH in dopaminergic neurons via CREB.	Aspirin	133-140	cAMP responsive element binding protein 1	Mus musculus	101-105
30487649-7	2019	SNP NR1I2 (rs13059232) was identified as an independent risk factor for the long-term clinical outcomes in the clopidogrel cohorts (P &lt; 0.001), but similar results were not observed in a matched aspirin cohort (P &gt; 0.05).	Aspirin	198-205	nuclear receptor subfamily 1 group I member 2	Homo sapiens	4-9
31098302-8	2019	Two of these transcription factors, Hnf1beta and Hnf4alpha are found down-regulated by aspirin treatment.	Aspirin	87-94	HNF1 homeobox B	Homo sapiens	36-44
31098302-8	2019	Two of these transcription factors, Hnf1beta and Hnf4alpha are found down-regulated by aspirin treatment.	Aspirin	87-94	hepatocyte nuclear factor 4 alpha	Homo sapiens	49-58
31098302-11	2019	In this model we observed that STOX1A and aspirin tended to synergize in the down-regulation of Hnf1beta target genes in trophoblasts.	Aspirin	42-49	HNF1 homeobox B	Homo sapiens	96-104
31018667-0	2019	Impact of Platelet Endothelial Aggregation Receptor-1 Genotypes on Platelet Reactivity and Early Cardiovascular Outcomes in Patients Undergoing Percutaneous Coronary Intervention and Treated With Aspirin and Clopidogrel.	Aspirin	196-203	platelet endothelial aggregation receptor 1	Homo sapiens	10-53
31193169-10	2019	ELISA results showed that ASA VI blocked the release of TNF-alpha, IL-6 and IL-1beta in ADSCs.	Aspirin	26-29	tumor necrosis factor	Rattus norvegicus	56-65
31193169-10	2019	ELISA results showed that ASA VI blocked the release of TNF-alpha, IL-6 and IL-1beta in ADSCs.	Aspirin	26-29	interleukin 6	Rattus norvegicus	67-71
31193169-10	2019	ELISA results showed that ASA VI blocked the release of TNF-alpha, IL-6 and IL-1beta in ADSCs.	Aspirin	26-29	interleukin 1 beta	Rattus norvegicus	76-84
30506894-0	2019	Association between TNF-alpha polymorphisms and the risk of upper gastrointestinal bleeding induced by aspirin in patients with coronary heart disease.	Aspirin	103-110	tumor necrosis factor	Homo sapiens	20-29
30506894-1	2019	OBJECTIVE: To investigate the correlation of tumor necrosis factor alpha (TNF-alpha) polymorphisms with upper gastrointestinal bleeding (UGIB) induced by enteric-coated aspirin in coronary heart disease (CHD) patients.	Aspirin	169-176	tumor necrosis factor	Homo sapiens	45-72
30506894-1	2019	OBJECTIVE: To investigate the correlation of tumor necrosis factor alpha (TNF-alpha) polymorphisms with upper gastrointestinal bleeding (UGIB) induced by enteric-coated aspirin in coronary heart disease (CHD) patients.	Aspirin	169-176	tumor necrosis factor	Homo sapiens	74-83
30506894-9	2019	CONCLUSION: TNF-alpha -863A and -1031C increased the risk of UGIB induction by enteric-coated aspirin in CHD patients, whereas TNF-alpha -857C &gt; T was not correlated with the UGIB risk.	Aspirin	94-101	tumor necrosis factor	Homo sapiens	12-21
30771282-8	2019	Both rivastigmine and 4-bis-nitrophenyl phosphate inhibited plasma esterase activities, suggesting that acetylcholinesterase and carboxylesterase largely contribute to ASA hydrolysis.	Aspirin	168-171	acetylcholinesterase (Cartwright blood group)	Homo sapiens	104-124
31092431-8	2019	CONCLUSION: Plasmatic doses of ASA and celecoxib altered the expression of IL6 and the gene expression of chemokines (ligands and receptors) and cytokines in a dose- and time-dependent manner.	Aspirin	31-34	interleukin 6	Homo sapiens	75-78
30952372-5	2019	RESULTS: ASA accelerates in vitro and in vivo odontogenic differentiation of SCAPs associated with down-regulation of runt-related nuclear factor 2 and up-regulation of specificity protein 7, nuclear factor I C, and dentin phosphoprotein.	Aspirin	9-12	nuclear factor I C	Homo sapiens	192-210
30633827-0	2019	Aspirin suppresses NFkappaB1 expression and inactivates cAMP signaling pathway to treat atherosclerosis.	Aspirin	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	19-28
30633827-12	2019	It was proved that Aspirin increased cell apoptotic rate yet decreased cell proliferation rate of VSMCs to suppress AS progression by down-regulating the expression of NFkappaB1 and its targets, which might well provide us with more therapeutic strategies for treatment of AS.	Aspirin	19-26	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	168-177
30952372-6	2019	ASA up-regulated the phosphorylation of AKT in the odontogenic SCAPs.	Aspirin	0-3	AKT serine/threonine kinase 1	Homo sapiens	40-43
30952372-7	2019	Of interest, pretreatments with phosphoinositide 3-kinase inhibitor LY294402 and small interfering RNA for AKT promoted ASA-induced in vitro and in vivo odontogenic differentiation of SCAPs.	Aspirin	120-123	AKT serine/threonine kinase 1	Homo sapiens	107-110
30952372-8	2019	LY294402 and small interfering RNA for AKT also suppressed the ASA-induced expression of runt-related nuclear factor 2 and enhanced ASA-induced expression of specificity protein 7, nuclear factor I C, and dentin phosphoprotein in SCAPs.	Aspirin	63-66	AKT serine/threonine kinase 1	Homo sapiens	39-42
30952372-8	2019	LY294402 and small interfering RNA for AKT also suppressed the ASA-induced expression of runt-related nuclear factor 2 and enhanced ASA-induced expression of specificity protein 7, nuclear factor I C, and dentin phosphoprotein in SCAPs.	Aspirin	132-135	AKT serine/threonine kinase 1	Homo sapiens	39-42
30952372-8	2019	LY294402 and small interfering RNA for AKT also suppressed the ASA-induced expression of runt-related nuclear factor 2 and enhanced ASA-induced expression of specificity protein 7, nuclear factor I C, and dentin phosphoprotein in SCAPs.	Aspirin	132-135	nuclear factor I C	Homo sapiens	181-199
30944660-0	2019	Aspirin inhibits growth of ovarian cancer by upregulating caspase-3 and downregulating bcl-2.	Aspirin	0-7	caspase 3	Homo sapiens	58-67
30742211-13	2019	Clopidogrel plus aspirin treatment was associated with reduced risk of new stroke in patients with ABCB1 -154 TT and 3435 CC genotype (hazard ratio [HR], 0.43; 95% CI, 0.26-0.71) but not in those with ABCB1 -154 TC/CC or 3435 CT/TT genotype (HR, 0.78; 95% CI, 0.60-1.03) compared with aspirin (P = .04 for interaction).	Aspirin	17-24	ATP binding cassette subfamily B member 1	Homo sapiens	99-104
30742211-13	2019	Clopidogrel plus aspirin treatment was associated with reduced risk of new stroke in patients with ABCB1 -154 TT and 3435 CC genotype (hazard ratio [HR], 0.43; 95% CI, 0.26-0.71) but not in those with ABCB1 -154 TC/CC or 3435 CT/TT genotype (HR, 0.78; 95% CI, 0.60-1.03) compared with aspirin (P = .04 for interaction).	Aspirin	17-24	ATP binding cassette subfamily B member 1	Homo sapiens	201-206
30742211-13	2019	Clopidogrel plus aspirin treatment was associated with reduced risk of new stroke in patients with ABCB1 -154 TT and 3435 CC genotype (hazard ratio [HR], 0.43; 95% CI, 0.26-0.71) but not in those with ABCB1 -154 TC/CC or 3435 CT/TT genotype (HR, 0.78; 95% CI, 0.60-1.03) compared with aspirin (P = .04 for interaction).	Aspirin	285-292	ATP binding cassette subfamily B member 1	Homo sapiens	99-104
30742211-16	2019	Conclusions and Relevance: The ABCB1 polymorphism was associated with the reduced efficacy of clopidogrel plus aspirin treatment compared with aspirin among patients with minor ischemic stroke or TIA.	Aspirin	111-118	ATP binding cassette subfamily B member 1	Homo sapiens	31-36
30742211-16	2019	Conclusions and Relevance: The ABCB1 polymorphism was associated with the reduced efficacy of clopidogrel plus aspirin treatment compared with aspirin among patients with minor ischemic stroke or TIA.	Aspirin	143-150	ATP binding cassette subfamily B member 1	Homo sapiens	31-36
30944655-6	2019	It was also demonstrated that aspirin may be an effective inhibitor of EMT, reducing the viability and migration ability of SW480 tumor cells, including cells induced by TGF-beta1.	Aspirin	30-37	transforming growth factor beta 1	Homo sapiens	170-179
30549041-7	2019	And the bleeding time prolonged by aspirin was also restored by Ft1.	Aspirin	35-42	AKT interacting protein	Homo sapiens	64-67
30944660-0	2019	Aspirin inhibits growth of ovarian cancer by upregulating caspase-3 and downregulating bcl-2.	Aspirin	0-7	BCL2 apoptosis regulator	Homo sapiens	87-92
30811931-6	2019	Here we used US to study the guest aspirin and 1-butanol dissociation processes of beta-cyclodextrin (beta-CD) and an inhibitor SB2 dissociation from a p38alpha mitogen-activated protein kinase (MAPK) complex.	Aspirin	35-42	mitogen-activated protein kinase 14	Homo sapiens	152-160
31014052-3	2019	Western blot was used to detect the expressions of microtubule-associated protein light chain 3 (LC3), p62 and cysteinyl aspartate specific proteinase 3 (caspase-3) after treatment with aspirin, metformin and 3-Methyladenine (3-MA).	Aspirin	186-193	caspase 3	Homo sapiens	111-163
31010006-5	2019	Based on alterations in morphology, modulation of capillary formation, and changes in endothelial and mesenchymal marker profile, our findings demonstrate that higher levels of tumor growth factor-betas and interleukin-6 enhance cancer-associated fibroblast-like cell formation through endothelial-mesenchymal transition and that nonsteroidal anti-inflammatory drug treatment (aspirin and ibuprofen) is able to inhibit this phenomenon.	Aspirin	377-384	interleukin 6	Homo sapiens	207-220
31002695-9	2019	In thrombin-induced acute pulmonary thromboembolism, mice pretreated with aspirin or gelsolin showed 100 and 83.33% recovery, respectively.	Aspirin	74-81	coagulation factor II	Mus musculus	3-11
30888847-4	2019	Acetylsalicylic acid (ASA; also known as aspirin) is known to irreversibly inhibit COX-1, thereby blocking AA-mediated signaling; however, it is unclear whether ASA use alters growth factor release from freshly isolated PRP.	Aspirin	0-20	prostaglandin-endoperoxide synthase 1	Homo sapiens	83-88
31008410-9	2019	Finally, we evaluated this protocol to detect the inhibition of PDMPs generation, washed platelets were incubated with acetylsalicylic acid (10 muM) and an inhibition of 7.7-fold in PDMPs generation for activation of TLR4 was found.	Aspirin	119-139	latexin	Homo sapiens	144-147
30654930-1	2019	Inhibition of the P2Y12 receptor by an oral P2Y12 inhibitor with loading doses along with Cyclooxygenase-1 inhibition by aspirin is considered a first-line treatment strategy in patients with the acute coronary syndrome and patients undergoing percutaneous coronary intervention (PCI).	Aspirin	121-128	prostaglandin-endoperoxide synthase 1	Homo sapiens	90-106
30888847-4	2019	Acetylsalicylic acid (ASA; also known as aspirin) is known to irreversibly inhibit COX-1, thereby blocking AA-mediated signaling; however, it is unclear whether ASA use alters growth factor release from freshly isolated PRP.	Aspirin	22-25	prostaglandin-endoperoxide synthase 1	Homo sapiens	83-88
30888847-16	2019	Although ASA had no effect on TBN-mediated release of VEGF and TGF-beta1 from LR-PRP, ASA did partially block TBN-mediated release of PDGF-AB, although the mechanism remains unclear.	Aspirin	86-89	coagulation factor II, thrombin	Homo sapiens	110-113
30888847-17	2019	CONCLUSION:: Daily use of low-dose ASA reduces VEGF, PDGF-AB, and TGF-beta1 expression in freshly isolated human LR-PRP when activated with AA.	Aspirin	35-38	vascular endothelial growth factor A	Homo sapiens	47-51
30888847-4	2019	Acetylsalicylic acid (ASA; also known as aspirin) is known to irreversibly inhibit COX-1, thereby blocking AA-mediated signaling; however, it is unclear whether ASA use alters growth factor release from freshly isolated PRP.	Aspirin	22-25	complement component 4 binding protein alpha	Homo sapiens	220-223
30888847-17	2019	CONCLUSION:: Daily use of low-dose ASA reduces VEGF, PDGF-AB, and TGF-beta1 expression in freshly isolated human LR-PRP when activated with AA.	Aspirin	35-38	transforming growth factor beta 1	Homo sapiens	66-75
30888847-17	2019	CONCLUSION:: Daily use of low-dose ASA reduces VEGF, PDGF-AB, and TGF-beta1 expression in freshly isolated human LR-PRP when activated with AA.	Aspirin	35-38	complement component 4 binding protein alpha	Homo sapiens	116-119
30888847-4	2019	Acetylsalicylic acid (ASA; also known as aspirin) is known to irreversibly inhibit COX-1, thereby blocking AA-mediated signaling; however, it is unclear whether ASA use alters growth factor release from freshly isolated PRP.	Aspirin	41-48	prostaglandin-endoperoxide synthase 1	Homo sapiens	83-88
30888847-18	2019	CLINICAL RELEVANCE:: Reduction in growth factor release attributed to daily use of low-dose ASA or other COX inhibitors can be mitigated when PRP samples are activated with TBN.	Aspirin	92-95	complement component 4 binding protein alpha	Homo sapiens	142-145
30888847-5	2019	PURPOSE:: To assess the effects of low-dose ASA use on activation of growth factor release from freshly isolated human PRP via AA and thrombin (TBN).	Aspirin	44-47	complement component 4 binding protein alpha	Homo sapiens	119-122
30888847-18	2019	CLINICAL RELEVANCE:: Reduction in growth factor release attributed to daily use of low-dose ASA or other COX inhibitors can be mitigated when PRP samples are activated with TBN.	Aspirin	92-95	coagulation factor II, thrombin	Homo sapiens	173-176
30888847-5	2019	PURPOSE:: To assess the effects of low-dose ASA use on activation of growth factor release from freshly isolated human PRP via AA and thrombin (TBN).	Aspirin	44-47	coagulation factor II, thrombin	Homo sapiens	134-142
30888847-5	2019	PURPOSE:: To assess the effects of low-dose ASA use on activation of growth factor release from freshly isolated human PRP via AA and thrombin (TBN).	Aspirin	44-47	coagulation factor II, thrombin	Homo sapiens	144-147
30814031-2	2019	Aspirin, the most commonly used antiplatelet agent, is a cyclooxygenase-1 inhibitor and considered a mild to moderate inhibitor of platelet function.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	57-73
30585832-8	2019	MEASUREMENTS AND MAIN RESULTS: Acetylsalicylic acid prophylaxis enhanced plasma tumor necrosis factor-alpha concentrations upon the first endotoxin challenge by 50% compared with the control group (p = 0.02) but did not modulate cytokine responses during the second endotoxin challenge.	Aspirin	31-51	tumor necrosis factor	Homo sapiens	80-107
30720135-5	2019	The present authors proposed that aspirin, diaspirin and analogues, and diflunisal (a salicylic acid derivative) may rapidly perturb EGF and EGF receptor (EGFR) internalisation.	Aspirin	34-41	epidermal growth factor receptor	Homo sapiens	141-153
30720135-5	2019	The present authors proposed that aspirin, diaspirin and analogues, and diflunisal (a salicylic acid derivative) may rapidly perturb EGF and EGF receptor (EGFR) internalisation.	Aspirin	34-41	epidermal growth factor receptor	Homo sapiens	155-159
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	62-69	epidermal growth factor receptor	Homo sapiens	250-254
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	62-69	epidermal growth factor receptor	Homo sapiens	342-346
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	182-189	epidermal growth factor receptor	Homo sapiens	250-254
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	182-189	epidermal growth factor receptor	Homo sapiens	342-346
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	182-189	epidermal growth factor receptor	Homo sapiens	250-254
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	182-189	epidermal growth factor receptor	Homo sapiens	342-346
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	182-189	epidermal growth factor receptor	Homo sapiens	250-254
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	182-189	epidermal growth factor receptor	Homo sapiens	342-346
30961940-1	2019	BACKGROUND: We hypothesized that the peculiar mixed interleukin-4 (IL-4/Th2) and interferon gamma INF-gamma (INF-gamma/Th1) inflammatory milieu found in the airways of patients with aspirin-exacerbated respiratory disease (AERD) is responsible for the altered regulation of the IL-1beta/IL-1RI-/EP2/COX-2 autocrine loop also found in these patients.	Aspirin	182-189	interleukin 4	Homo sapiens	52-65
30961940-1	2019	BACKGROUND: We hypothesized that the peculiar mixed interleukin-4 (IL-4/Th2) and interferon gamma INF-gamma (INF-gamma/Th1) inflammatory milieu found in the airways of patients with aspirin-exacerbated respiratory disease (AERD) is responsible for the altered regulation of the IL-1beta/IL-1RI-/EP2/COX-2 autocrine loop also found in these patients.	Aspirin	182-189	interleukin 4	Homo sapiens	67-71
30756509-0	2019	Aspirin ameliorates lung cancer by targeting the miR-98/WNT1 axis.	Aspirin	0-7	Wnt family member 1	Homo sapiens	56-60
30756509-13	2019	After treatment with aspirin the expression of miR-98 was induced and then its target gene, WNT1, was depressed in the cells.	Aspirin	21-28	Wnt family member 1	Homo sapiens	92-96
30756509-14	2019	CONCLUSION: Aspirin targets the miR-98/WNT1 axis to ameliorate lung cancer development.	Aspirin	12-19	Wnt family member 1	Homo sapiens	39-43
30585832-9	2019	In contrast, acetylsalicylic acid treatment resulted in enhanced plasma levels of tumor necrosis factor-alpha (+53%; p = 0.02), interleukin-6 (+91%; p = 0.03), and interleukin-8 (+42%; p = 0.02) upon the second challenge, whereas plasma levels of the key antiinflammatory cytokine interleukin-10 were attenuated (-40%; p = 0.003).	Aspirin	13-33	tumor necrosis factor	Homo sapiens	82-109
30585832-9	2019	In contrast, acetylsalicylic acid treatment resulted in enhanced plasma levels of tumor necrosis factor-alpha (+53%; p = 0.02), interleukin-6 (+91%; p = 0.03), and interleukin-8 (+42%; p = 0.02) upon the second challenge, whereas plasma levels of the key antiinflammatory cytokine interleukin-10 were attenuated (-40%; p = 0.003).	Aspirin	13-33	interleukin 6	Homo sapiens	128-141
30585832-9	2019	In contrast, acetylsalicylic acid treatment resulted in enhanced plasma levels of tumor necrosis factor-alpha (+53%; p = 0.02), interleukin-6 (+91%; p = 0.03), and interleukin-8 (+42%; p = 0.02) upon the second challenge, whereas plasma levels of the key antiinflammatory cytokine interleukin-10 were attenuated (-40%; p = 0.003).	Aspirin	13-33	C-X-C motif chemokine ligand 8	Homo sapiens	164-177
30585832-11	2019	Ex vivo exposure of platelets to acetylsalicylic acid increased production of tumor necrosis factor-alpha (+66%) and decreased production of interleukin-10 (-23%) by monocytes of sepsis patients.	Aspirin	33-53	tumor necrosis factor	Homo sapiens	78-105
30822523-15	2019	CONCLUSION: Preoperative CEA levels were associated with age, BMI, ASA and tumour stage.	Aspirin	67-70	CEA cell adhesion molecule 3	Homo sapiens	25-28
31356179-14	2019	Diabetics" resistance to ASA is associated with increased platelet reactivity, perhaps related to the more frequent ITGB3 PIA1 allele and increased TXB2 generation.	Aspirin	25-28	integrin subunit beta 3	Homo sapiens	116-121
31356179-15	2019	The PIA1 allele may be a potential factor for aspirin resistance with elevated fibrinogen concentration.	Aspirin	46-53	fibrinogen beta chain	Homo sapiens	79-89
30790162-12	2019	Multiple regression analysis revealed that high-sensitive C-reactive protein (p = 0.014) was independent predictor of absolute increase PA. Our study showed that aspirin has limited effect in inhibiting exercise-induced PA, even in the absence of documented CAD.	Aspirin	162-169	C-reactive protein	Homo sapiens	58-76
30611793-9	2019	Here, (1) the chitosan (CS)/beta-sodium glycerophosphate/gelatin hydrogels loaded with aspirin/erythropoietin (EPO) can form at body temperature in 5 min with excellent biocompatibility in vitro and in vivo; (2) The faster release of aspirin than EPO in the early stage is beneficial for anti-inflammation and provides a microenvironment for ensuring the regeneration function of EPO in the following step.	Aspirin	87-94	erythropoietin	Homo sapiens	111-114
31090331-4	2019	Through the study of network pharmacology,12 components of aspirin and Trichosanthis Fructus,including hydroxygenkwanin,quercetin and adenosine,were found to show the anti-platelet aggregation and anti-thrombosis mechanisms through9 common protein targets,such as SRC,RAC1,MAPK14,MAPK1,AKT1,and 14 common signaling pathways,such as VEGF signaling pathway.	Aspirin	59-66	AKT serine/threonine kinase 1	Rattus norvegicus	286-290
30611793-9	2019	Here, (1) the chitosan (CS)/beta-sodium glycerophosphate/gelatin hydrogels loaded with aspirin/erythropoietin (EPO) can form at body temperature in 5 min with excellent biocompatibility in vitro and in vivo; (2) The faster release of aspirin than EPO in the early stage is beneficial for anti-inflammation and provides a microenvironment for ensuring the regeneration function of EPO in the following step.	Aspirin	87-94	erythropoietin	Homo sapiens	247-250
30611793-9	2019	Here, (1) the chitosan (CS)/beta-sodium glycerophosphate/gelatin hydrogels loaded with aspirin/erythropoietin (EPO) can form at body temperature in 5 min with excellent biocompatibility in vitro and in vivo; (2) The faster release of aspirin than EPO in the early stage is beneficial for anti-inflammation and provides a microenvironment for ensuring the regeneration function of EPO in the following step.	Aspirin	87-94	erythropoietin	Homo sapiens	247-250
29921159-0	2019	Aspirin and breast cancer survival: Hope or hype?	Aspirin	0-7	FIC domain protein adenylyltransferase	Homo sapiens	44-48
30482874-1	2019	BACKGROUND: There have been few studies of sufficient size to address the relationship between glioma risk and the use of aspirin or NSAIDs, and results have been conflicting.	Aspirin	122-129	opioid receptor, mu 1	Mus musculus	130-132
30482874-7	2019	RESULTS: A history of daily aspirin use for >=6 months was associated with a 38% lower glioma risk, compared with not having a history of daily use [adjusted meta-OR = 0.62; 95% confidence interval (CI), 0.54-0.70].	Aspirin	28-35	opioid receptor, mu 1	Mus musculus	163-165
30482874-10	2019	In the meta-analysis aggregating GICC data with five previous studies, there was a marginally significant association between use of aspirin and glioma (mOR = 0.84; 95% CI, 0.70-1.02), but no association for NSAID use.	Aspirin	133-140	opioid receptor, mu 1	Mus musculus	153-156
30562044-6	2019	When stratified by tertile of C-reactive protein (CRP), a biomarker of inflammation, treatment with aspirin restored a decrement in the live birth rate in women in the highest CRP tertile (relative risk 1.35, 95% confidence interval 1.08-1.67), increasing to similar rates as women of the lower and mid-CRP tertiles.	Aspirin	100-107	C-reactive protein	Homo sapiens	30-48
30562044-6	2019	When stratified by tertile of C-reactive protein (CRP), a biomarker of inflammation, treatment with aspirin restored a decrement in the live birth rate in women in the highest CRP tertile (relative risk 1.35, 95% confidence interval 1.08-1.67), increasing to similar rates as women of the lower and mid-CRP tertiles.	Aspirin	100-107	C-reactive protein	Homo sapiens	50-53
30562044-6	2019	When stratified by tertile of C-reactive protein (CRP), a biomarker of inflammation, treatment with aspirin restored a decrement in the live birth rate in women in the highest CRP tertile (relative risk 1.35, 95% confidence interval 1.08-1.67), increasing to similar rates as women of the lower and mid-CRP tertiles.	Aspirin	100-107	C-reactive protein	Homo sapiens	176-179
30562044-6	2019	When stratified by tertile of C-reactive protein (CRP), a biomarker of inflammation, treatment with aspirin restored a decrement in the live birth rate in women in the highest CRP tertile (relative risk 1.35, 95% confidence interval 1.08-1.67), increasing to similar rates as women of the lower and mid-CRP tertiles.	Aspirin	100-107	C-reactive protein	Homo sapiens	176-179
30017554-0	2019	COX-1 mediates IL-33-induced extracellular signal-regulated kinase activation in mast cells: Implications for aspirin sensitivity.	Aspirin	110-117	cytochrome c oxidase I, mitochondrial	Mus musculus	0-5
30670536-6	2019	Platelets treated with aspirin did not activate the Akt pathway, resulting in reduced IL-8 secretion and impaired tumor cell invasion.	Aspirin	23-30	C-X-C motif chemokine ligand 8	Homo sapiens	86-90
30240925-5	2019	This pilot study aimed to elucidate the impact of hyperglycaemia on aspirin acetylation of COX-1 using a targeted mass spectrometry approach.	Aspirin	68-75	prostaglandin-endoperoxide synthase 1	Homo sapiens	91-96
30240925-7	2019	Moreover, the functional aspirin-induced inhibition of COX-1 was dose-dependently impaired as glucose concentrations increased.	Aspirin	25-32	prostaglandin-endoperoxide synthase 1	Homo sapiens	55-60
30240925-9	2019	These data provide new insights into the interplay between glucose and aspirin on platelet proteins and their effects on platelet COX-1.	Aspirin	71-78	prostaglandin-endoperoxide synthase 1	Homo sapiens	130-135
30240925-12	2019	SIGNIFICANCE: Deciphering the mutual interplay between glucose and aspirin-mediated acetylation on platelet COX-1, might be of great interest as there is still a lack of information of the mechanism underlying this process that may contribute to the less-than expected response of platelets to aspirin, often observed in diabetes.	Aspirin	67-74	prostaglandin-endoperoxide synthase 1	Homo sapiens	108-113
30240925-12	2019	SIGNIFICANCE: Deciphering the mutual interplay between glucose and aspirin-mediated acetylation on platelet COX-1, might be of great interest as there is still a lack of information of the mechanism underlying this process that may contribute to the less-than expected response of platelets to aspirin, often observed in diabetes.	Aspirin	294-301	prostaglandin-endoperoxide synthase 1	Homo sapiens	108-113
30401649-0	2019	Aspirin in retrieving the inactivated catalase to active form: Displacement of one inhibitor with a protective agent.	Aspirin	0-7	catalase	Homo sapiens	38-46
30401649-2	2019	In the present work, aspirin was considered as a protective agent to retrieve the inactivated catalase by farnesiferol C (FC) through displacement manner.	Aspirin	21-28	catalase	Homo sapiens	94-102
30401649-3	2019	The catalytic assessment revealed that aspirin is able to remarkably retrieve the activity of FC-catalase from 4.2 +- 0.2% to 98 +- 0.1% compare to the control sample.	Aspirin	39-46	catalase	Homo sapiens	97-105
30401649-4	2019	Furthermore, displacement study and CD spectroscopy indicated that aspirin could reduce the stability of FC-catalase complex.	Aspirin	67-74	catalase	Homo sapiens	108-116
30401649-5	2019	Based on the obtained data, it is shown that the binding of aspirin to catalase led to decrease the affinity of catalase to the inhibitor.	Aspirin	60-67	catalase	Homo sapiens	71-79
30401649-5	2019	Based on the obtained data, it is shown that the binding of aspirin to catalase led to decrease the affinity of catalase to the inhibitor.	Aspirin	60-67	catalase	Homo sapiens	112-120
30401649-6	2019	The releasing analysis of FC from the complex showed that the dissociation constant (Kd) of FC-catalase was increased, considerably from 8.9 +- 0.2 muM to 256 +- 01 muM in the presence of aspirin at 298 K. Also, molecular simulation proved the instability of FC-catalase following the binding of aspirin to the complex.	Aspirin	188-195	catalase	Homo sapiens	95-103
30401649-6	2019	The releasing analysis of FC from the complex showed that the dissociation constant (Kd) of FC-catalase was increased, considerably from 8.9 +- 0.2 muM to 256 +- 01 muM in the presence of aspirin at 298 K. Also, molecular simulation proved the instability of FC-catalase following the binding of aspirin to the complex.	Aspirin	188-195	catalase	Homo sapiens	262-270
30401649-6	2019	The releasing analysis of FC from the complex showed that the dissociation constant (Kd) of FC-catalase was increased, considerably from 8.9 +- 0.2 muM to 256 +- 01 muM in the presence of aspirin at 298 K. Also, molecular simulation proved the instability of FC-catalase following the binding of aspirin to the complex.	Aspirin	296-303	catalase	Homo sapiens	95-103
30679550-4	2019	Herein, we tested a commercial drug (acetylsalicylic acid, ASA) and a plant compound with antiophidian properties (rosmarinic acid, RA) using myographic, crystallographic and bioinformatics experiments with a phospholipase A2-like toxin, MjTX-II.	Aspirin	37-57	phospholipase A2 group IB	Homo sapiens	209-225
30604228-13	2019	CONCLUSION: Aspirin attenuates podocyte injury in DN, which may be through COX-2-mediated dysregulation of LDLr pathway.	Aspirin	12-19	low density lipoprotein receptor	Rattus norvegicus	107-111
30737317-9	2019	Nonsteroidal anti-inflammatory drugs (e.g. aspirin, ibuprofen, and naproxen) block PG synthesis by inhibiting COX-1 and COX-2.	Aspirin	43-50	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	120-125
30378182-10	2019	Following inflammatory stimulation and treatment with ASA CM, tenocytes downregulated IL-8 gene expression, a pro-inflammatory cytokine normally elevated during the inflammatory phase of tendon healing.	Aspirin	54-57	C-X-C motif chemokine ligand 8	Homo sapiens	86-90
30378182-11	2019	Additionally, tenocytes treated with ASA CM had significantly lower protein levels of TGF-beta1 compared to controls.	Aspirin	37-40	transforming growth factor beta 1	Homo sapiens	86-95
30401528-9	2019	The rate of death or severe disability was 4.1% in the aspirin group and 3.5% in the placebo group (relative risk, 1.17; 95% confidence interval, 0.76-1.81; P = .48).	Aspirin	55-62	interferon regulatory factor 9	Homo sapiens	157-164
30701538-1	2019	Several clinical studies indicated that the daily use of aspirin or acetylsalicylic acid reduces the cancer risk via cyclooxygenases (Cox-1 and Cox-2) inhibition.	Aspirin	57-64	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	144-149
30701538-1	2019	Several clinical studies indicated that the daily use of aspirin or acetylsalicylic acid reduces the cancer risk via cyclooxygenases (Cox-1 and Cox-2) inhibition.	Aspirin	68-88	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	144-149
30670536-7	2019	Of note, patients with breast cancer receiving aspirin had lower circulating IL-8, and their platelets did not increase tumor cell invasion compared with patients not receiving aspirin.	Aspirin	47-54	C-X-C motif chemokine ligand 8	Homo sapiens	77-81
30326254-0	2019	Activation of catalase via co-administration of aspirin and pioglitazone: Experimental and MLSD simulation approaches.	Aspirin	48-55	catalase	Homo sapiens	14-22
30693272-0	2018	Aspirin Inhibits Natural Killer/T-Cell Lymphoma by Modulation of VEGF Expression and Mitochondrial Function.	Aspirin	0-7	vascular endothelial growth factor A	Homo sapiens	65-69
30693272-3	2018	In this study, we found that aspirin treatment suppresses VEGF expression in NKTCL SNK-6 cells.	Aspirin	29-36	vascular endothelial growth factor A	Homo sapiens	58-62
30693272-4	2018	Further investigation showed that aspirin treatment increases histone methylation in the range of -100~0 that is proximal to the transcription start site on the VEGF promoter, subsequently decreasing the binding ability of Sp1 to the VEGF promoter with VEGF suppression.	Aspirin	34-41	vascular endothelial growth factor A	Homo sapiens	161-165
30693272-4	2018	Further investigation showed that aspirin treatment increases histone methylation in the range of -100~0 that is proximal to the transcription start site on the VEGF promoter, subsequently decreasing the binding ability of Sp1 to the VEGF promoter with VEGF suppression.	Aspirin	34-41	vascular endothelial growth factor A	Homo sapiens	234-238
30693272-4	2018	Further investigation showed that aspirin treatment increases histone methylation in the range of -100~0 that is proximal to the transcription start site on the VEGF promoter, subsequently decreasing the binding ability of Sp1 to the VEGF promoter with VEGF suppression.	Aspirin	34-41	vascular endothelial growth factor A	Homo sapiens	234-238
30693272-6	2018	Aspirin treatment alone slightly inhibits NKTCL SNK-6 tumor growth and EBV replication; while in the presence of histone deacetylase inhibitor (HDACi) chidamide (CDM), aspirin significantly suppresses the VEGF signaling pathway with increased ROS overgeneration and EBV inhibition.	Aspirin	0-7	vascular endothelial growth factor A	Homo sapiens	205-209
30693272-6	2018	Aspirin treatment alone slightly inhibits NKTCL SNK-6 tumor growth and EBV replication; while in the presence of histone deacetylase inhibitor (HDACi) chidamide (CDM), aspirin significantly suppresses the VEGF signaling pathway with increased ROS overgeneration and EBV inhibition.	Aspirin	168-175	vascular endothelial growth factor A	Homo sapiens	205-209
30693272-8	2018	This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation.	Aspirin	56-63	vascular endothelial growth factor A	Homo sapiens	73-77
30693272-8	2018	This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation.	Aspirin	56-63	vascular endothelial growth factor A	Homo sapiens	267-271
30693272-8	2018	This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation.	Aspirin	233-240	vascular endothelial growth factor A	Homo sapiens	73-77
30693272-8	2018	This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation.	Aspirin	233-240	vascular endothelial growth factor A	Homo sapiens	267-271
29925918-4	2019	Interestingly, we identified that GLUT1 and HIF1alpha could be decreased by aspirin.	Aspirin	76-83	hypoxia inducible factor 1 subunit alpha	Homo sapiens	44-53
29925918-7	2019	CoCl2-activated HIF1alpha expression could slightly rescue the GLUT1 expression inhibited by aspirin or PDTC, suggesting that aspirin depressed GLUT1 through targeting NF-kappaB or NF-kappaB/HIF1alpha signaling.	Aspirin	93-100	hypoxia inducible factor 1 subunit alpha	Homo sapiens	16-25
29925918-7	2019	CoCl2-activated HIF1alpha expression could slightly rescue the GLUT1 expression inhibited by aspirin or PDTC, suggesting that aspirin depressed GLUT1 through targeting NF-kappaB or NF-kappaB/HIF1alpha signaling.	Aspirin	126-133	hypoxia inducible factor 1 subunit alpha	Homo sapiens	16-25
29925918-7	2019	CoCl2-activated HIF1alpha expression could slightly rescue the GLUT1 expression inhibited by aspirin or PDTC, suggesting that aspirin depressed GLUT1 through targeting NF-kappaB or NF-kappaB/HIF1alpha signaling.	Aspirin	126-133	nuclear factor kappa B subunit 1	Homo sapiens	168-177
29925918-7	2019	CoCl2-activated HIF1alpha expression could slightly rescue the GLUT1 expression inhibited by aspirin or PDTC, suggesting that aspirin depressed GLUT1 through targeting NF-kappaB or NF-kappaB/HIF1alpha signaling.	Aspirin	126-133	nuclear factor kappa B subunit 1	Homo sapiens	181-190
29925918-7	2019	CoCl2-activated HIF1alpha expression could slightly rescue the GLUT1 expression inhibited by aspirin or PDTC, suggesting that aspirin depressed GLUT1 through targeting NF-kappaB or NF-kappaB/HIF1alpha signaling.	Aspirin	126-133	hypoxia inducible factor 1 subunit alpha	Homo sapiens	191-200
30326254-3	2019	In the present study, the effect of co-administered ASP with PGL was investigated on the structure and catalytic function of catalase as a potential target in the liver.	Aspirin	52-55	catalase	Homo sapiens	125-133
30326254-8	2019	Binding analysis showed that the association constant of catalase-PGL was reduced considerably in the presence of ASP from 12.19 +- 0.1 x 106 M-1 to 6.4 +- 0.2 x 106 M-1 at 298 K. Multiple ligands simultaneous docking (MLSD) also confirmed an increase in the binding affinity of PGL to catalase.	Aspirin	114-117	catalase	Homo sapiens	57-65
30326254-8	2019	Binding analysis showed that the association constant of catalase-PGL was reduced considerably in the presence of ASP from 12.19 +- 0.1 x 106 M-1 to 6.4 +- 0.2 x 106 M-1 at 298 K. Multiple ligands simultaneous docking (MLSD) also confirmed an increase in the binding affinity of PGL to catalase.	Aspirin	114-117	catalase	Homo sapiens	286-294
31039577-12	2019	Additionally, a combination treatment strategy of low-dose aspirin given concomitantly with a selective COX-2 inhibitor may result in a reduced side effect profile compared to aspirin or selective COX-2 inhibitor use alone.	Aspirin	59-66	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	104-109
31820856-9	2019	Ticagrelor and aspirin attenuated the increase in ANP, BNP, collagen-I and collagen-III.	Aspirin	15-22	natriuretic peptide B	Rattus norvegicus	55-58
31039577-12	2019	Additionally, a combination treatment strategy of low-dose aspirin given concomitantly with a selective COX-2 inhibitor may result in a reduced side effect profile compared to aspirin or selective COX-2 inhibitor use alone.	Aspirin	59-66	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	197-202
31039577-12	2019	Additionally, a combination treatment strategy of low-dose aspirin given concomitantly with a selective COX-2 inhibitor may result in a reduced side effect profile compared to aspirin or selective COX-2 inhibitor use alone.	Aspirin	176-183	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	104-109
30888659-6	2019	Resveratrol, rapamycin, metformin and aspirin, showing effectiveness in model organism life- and healthspan extension mainly target the master regulators of aging such as mTOR, FOXO and PGC1alpha, affecting autophagy, inflammation and oxidative stress.	Aspirin	38-45	mechanistic target of rapamycin kinase	Homo sapiens	171-175
30096040-0	2019	Residual cyclooxygenase activity of aspirin-acetylated COX-2 forms 15 R-prostaglandins that inhibit platelet aggregation.	Aspirin	36-43	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	55-60
30096040-6	2019	Aspirin increased 15 R-PGD2 but not 15 R-PGE2 in isolated human leukocytes activated with LPS to induce COX-2.	Aspirin	0-7	prostaglandin D2 synthase	Homo sapiens	23-27
30096040-6	2019	Aspirin increased 15 R-PGD2 but not 15 R-PGE2 in isolated human leukocytes activated with LPS to induce COX-2.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	104-109
30096040-9	2019	15 R-PGs are novel products of aspirin therapy via acetylation of COX-2 and may contribute to its antiplatelet and other pharmacologic effects.-Gimenez-Bastida, J.	Aspirin	31-38	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	66-71
30096040-10	2019	A., Boeglin, W. E., Boutaud, O., Malkowski, M. G., Schneider, C. Residual cyclooxygenase activity of aspirin-acetylated COX-2 forms 15 R-prostaglandins that inhibit platelet aggregation.	Aspirin	101-108	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	120-125
30612679-5	2019	Aspirin pretreatment of HP-diabetic animals is manifested with significantly lower blood and liver glucose, higher G6P concentration, lower G6P-ase and HK activity as well as higher Glk content and GPho-ase activity, compared both to diabetic and HP-diabetic animals.	Aspirin	0-7	galactokinase 1	Rattus norvegicus	182-185
29553866-13	2019	In the EA families, the burden of PEAR1 missense variants was associated with platelet aggregation after aspirin therapy when the platelets were stimulated with epinephrine (p = 0.0009) and collagen (p = 0.03).	Aspirin	105-112	platelet endothelial aggregation receptor 1	Homo sapiens	34-39
29553866-16	2019	We identified additional association of rare missense variants in PEAR1 with platelet aggregation following aspirin therapy.	Aspirin	108-115	platelet endothelial aggregation receptor 1	Homo sapiens	66-71
31336455-10	2019	Drugs that had more interaction with insulin were: acetylsalicylic acid (40%), enalapril (18%), losartan (32%) and hydrochlorothiazide (23%).	Aspirin	51-71	insulin	Homo sapiens	37-44
29227173-6	2019	The aim of this study was to assess the level of AA-, ADP- and thrombin-mediated platelet reactivity in patients on aspirin before, during, and after major vascular surgery, which represents a model of on/off vascular inflammation.	Aspirin	116-123	coagulation factor II, thrombin	Homo sapiens	63-71
30888659-6	2019	Resveratrol, rapamycin, metformin and aspirin, showing effectiveness in model organism life- and healthspan extension mainly target the master regulators of aging such as mTOR, FOXO and PGC1alpha, affecting autophagy, inflammation and oxidative stress.	Aspirin	38-45	PPARG coactivator 1 alpha	Homo sapiens	186-195
30547092-5	2018	Furthermore, administration of acetylsalicylic acid (aspirin) or N-acetylcysteine (NAC) to juvenile ptk7 mutants significantly reduces the incidence and/or severity of scoliosis phenotypes.	Aspirin	31-51	protein tyrosine kinase 7b	Danio rerio	100-104
29520080-13	2018	Among patients with minor stroke or TIA taking clopidogrel-aspirin treatment, CYP2C19 LOF carrier state was associated with higher risk of new stroke in those with eGFR &lt; 75 ml/min/1.73 m2.	Aspirin	59-66	CD59 molecule (CD59 blood group)	Homo sapiens	180-185
30219678-0	2018	Metabolism of liver CYP450 and ultrastructural changes after long-term administration of aspirin and ibuprofen.	Aspirin	89-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	20-26
30219678-16	2018	Long-term administration of enteric-coated aspirin and ibuprofen induced the metabolic activity of the CYP450 enzyme.	Aspirin	43-50	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	103-109
30262158-10	2018	A t-test showed a significant association between cystatin B and PAD at screening, hospital diagnosis of COPD, previous atherosclerotic events, and use of low dose aspirin.	Aspirin	164-171	cystatin B	Homo sapiens	50-60
30221683-0	2018	Aspirin promotes apoptosis and inhibits proliferation by blocking G0/G1 into S phase in rheumatoid arthritis fibroblast-like synoviocytes via downregulation of JAK/STAT3 and NF-kappaB signaling pathway.	Aspirin	0-7	signal transducer and activator of transcription 3	Homo sapiens	164-169
30221683-10	2018	Bioinformatics prediction revealed that aspirin was closely associated with cell proliferation and apoptosis, including the p53 and NF-kappaB signaling pathways.	Aspirin	40-47	tumor protein p53	Homo sapiens	124-127
30221683-12	2018	The expression of Bax increased with aspirin stimulation, while the levels of Bcl-2, PRAP1, Cyclin D1 and P21 decreased; p-STAT3, p-P65 and p-50 levels also decreased while STAT3, P65, P50, p-P105 and P105 remained unchanged.	Aspirin	37-44	BCL2 associated X, apoptosis regulator	Homo sapiens	18-21
30221683-13	2018	From our data, it can be concluded that aspirin is able to promote apoptosis and inhibit the proliferation of RA-FLS through blocking the JAK/STAT3 and NF-kappaB signaling pathways.	Aspirin	40-47	signal transducer and activator of transcription 3	Homo sapiens	142-147
30414472-6	2018	Further, we identified top 50 overexpressed genes of SCLC by Oncomine, and the interconnected genes with the 4 aspirin DPTs in SCLC (IKBKB, NFKBIA, PTGS2 and TP53) by STRING.	Aspirin	111-118	NFKB inhibitor alpha	Homo sapiens	140-146
30414472-6	2018	Further, we identified top 50 overexpressed genes of SCLC by Oncomine, and the interconnected genes with the 4 aspirin DPTs in SCLC (IKBKB, NFKBIA, PTGS2 and TP53) by STRING.	Aspirin	111-118	tumor protein p53	Homo sapiens	158-162
29439623-9	2018	The increased messenger RNA and protein levels of Cox1 and Cox2 induced by T0070907 were markedly reduced by aspirin treatment.	Aspirin	109-116	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	50-54
30144594-0	2018	Aspirin Affects Tumor Angiogenesis and Sensitizes Human Glioblastoma Endothelial Cells to Temozolomide, Bevacizumab, and Sunitinib, Impairing Vascular Endothelial Growth Factor-Related Signaling.	Aspirin	0-7	vascular endothelial growth factor A	Homo sapiens	142-176
30144594-8	2018	RESULTS: Our data reported that ASA affected GBM-EC viability, tube-like structure formation, cell migration, and VEGF releasing in a dose-dependent manner and that combined treatments with TMZ, BEV, and SUN synergized to counteract proangiogenic cell ability.	Aspirin	32-35	vascular endothelial growth factor A	Homo sapiens	114-118
30144594-9	2018	mRNA expression analysis displayed a marked effect of ASA in reducing VEGF, VEGFR-1, HIF-1alpha, RAS, mitogen-activated protein kinase kinase, AKT, and BCL-2, as well a combined anticancer effect of ASA together with TMZ, BEV, and SUN.	Aspirin	54-57	vascular endothelial growth factor A	Homo sapiens	70-74
30144594-9	2018	mRNA expression analysis displayed a marked effect of ASA in reducing VEGF, VEGFR-1, HIF-1alpha, RAS, mitogen-activated protein kinase kinase, AKT, and BCL-2, as well a combined anticancer effect of ASA together with TMZ, BEV, and SUN.	Aspirin	54-57	fms related receptor tyrosine kinase 1	Homo sapiens	76-83
30144594-9	2018	mRNA expression analysis displayed a marked effect of ASA in reducing VEGF, VEGFR-1, HIF-1alpha, RAS, mitogen-activated protein kinase kinase, AKT, and BCL-2, as well a combined anticancer effect of ASA together with TMZ, BEV, and SUN.	Aspirin	54-57	hypoxia inducible factor 1 subunit alpha	Homo sapiens	85-95
30144594-9	2018	mRNA expression analysis displayed a marked effect of ASA in reducing VEGF, VEGFR-1, HIF-1alpha, RAS, mitogen-activated protein kinase kinase, AKT, and BCL-2, as well a combined anticancer effect of ASA together with TMZ, BEV, and SUN.	Aspirin	54-57	AKT serine/threonine kinase 1	Homo sapiens	143-146
30144594-9	2018	mRNA expression analysis displayed a marked effect of ASA in reducing VEGF, VEGFR-1, HIF-1alpha, RAS, mitogen-activated protein kinase kinase, AKT, and BCL-2, as well a combined anticancer effect of ASA together with TMZ, BEV, and SUN.	Aspirin	54-57	BCL2 apoptosis regulator	Homo sapiens	152-157
30120100-0	2018	Aspirin enhances the sensitivity of hepatocellular carcinoma side population cells to doxorubicin via miR-491/ABCG2.	Aspirin	0-7	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	110-115
30482850-6	2018	Aspirin also increased the transcription of Il11 mediated by the transcription factor CREB, which was necessary for the generation of Tregs Neutralization of IL-11 negated the effects of aspirin on Treg development and exacerbated EAE.	Aspirin	0-7	cAMP responsive element binding protein 1	Mus musculus	86-90
30482850-6	2018	Aspirin also increased the transcription of Il11 mediated by the transcription factor CREB, which was necessary for the generation of Tregs Neutralization of IL-11 negated the effects of aspirin on Treg development and exacerbated EAE.	Aspirin	187-194	cAMP responsive element binding protein 1	Mus musculus	86-90
30120100-1	2018	Objective: To explore whether aspirin (ASA) enhances the sensitivity of hepatocellular carcinoma (HCC) side population (SP) cells to doxorubicin (Doxo) via miR-491/ATP-binding cassette sub-family G member 2 (ABCG2).Methods: Non-SP and SP cells were isolated from MHCC-97L cell line using flow cytometry analysis and fluorescence-activated cell sorting.	Aspirin	30-37	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	164-206
30120100-8	2018	In the presence of Doxo, miR-491 inhibitor reduced the inhibitory effect of ASA on the cell viability of SP cells, which was significantly reversed by knockdown of ABCG2 (P&lt;0.05).Conclusion: ASA enhanced the sensitivity of SP cells to Doxo via regulating the miR-491/ABCG2 signaling pathway.	Aspirin	76-79	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	164-169
30120100-8	2018	In the presence of Doxo, miR-491 inhibitor reduced the inhibitory effect of ASA on the cell viability of SP cells, which was significantly reversed by knockdown of ABCG2 (P&lt;0.05).Conclusion: ASA enhanced the sensitivity of SP cells to Doxo via regulating the miR-491/ABCG2 signaling pathway.	Aspirin	76-79	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	270-275
30120100-1	2018	Objective: To explore whether aspirin (ASA) enhances the sensitivity of hepatocellular carcinoma (HCC) side population (SP) cells to doxorubicin (Doxo) via miR-491/ATP-binding cassette sub-family G member 2 (ABCG2).Methods: Non-SP and SP cells were isolated from MHCC-97L cell line using flow cytometry analysis and fluorescence-activated cell sorting.	Aspirin	30-37	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	208-213
30120100-8	2018	In the presence of Doxo, miR-491 inhibitor reduced the inhibitory effect of ASA on the cell viability of SP cells, which was significantly reversed by knockdown of ABCG2 (P&lt;0.05).Conclusion: ASA enhanced the sensitivity of SP cells to Doxo via regulating the miR-491/ABCG2 signaling pathway.	Aspirin	194-197	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	164-169
30120100-1	2018	Objective: To explore whether aspirin (ASA) enhances the sensitivity of hepatocellular carcinoma (HCC) side population (SP) cells to doxorubicin (Doxo) via miR-491/ATP-binding cassette sub-family G member 2 (ABCG2).Methods: Non-SP and SP cells were isolated from MHCC-97L cell line using flow cytometry analysis and fluorescence-activated cell sorting.	Aspirin	39-42	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	164-206
30120100-8	2018	In the presence of Doxo, miR-491 inhibitor reduced the inhibitory effect of ASA on the cell viability of SP cells, which was significantly reversed by knockdown of ABCG2 (P&lt;0.05).Conclusion: ASA enhanced the sensitivity of SP cells to Doxo via regulating the miR-491/ABCG2 signaling pathway.	Aspirin	194-197	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	270-275
30120100-1	2018	Objective: To explore whether aspirin (ASA) enhances the sensitivity of hepatocellular carcinoma (HCC) side population (SP) cells to doxorubicin (Doxo) via miR-491/ATP-binding cassette sub-family G member 2 (ABCG2).Methods: Non-SP and SP cells were isolated from MHCC-97L cell line using flow cytometry analysis and fluorescence-activated cell sorting.	Aspirin	39-42	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	208-213
30456985-4	2018	RESULTS: Higher MPO activity levels were seen in men, smokers, diabetics and those who were taking aspirin.	Aspirin	99-106	myeloperoxidase	Homo sapiens	16-19
30118883-0	2018	Targeting NLRP3 inflammasome via acetylsalicylic acid: Role in suppressing hepatic dysfunction and insulin resistance induced by atorvastatin in naive versus alcoholic liver in rats.	Aspirin	33-53	NLR family, pyrin domain containing 3	Rattus norvegicus	10-15
30118883-10	2018	CONCLUSIONS: Acetylsalicylic acid alleviated the hepatotoxic effects of alcohol and atorvastatin through decreasing the production of NLRP3 inflammasome in rats" liver.	Aspirin	13-33	NLR family, pyrin domain containing 3	Rattus norvegicus	134-139
29969574-13	2018	Aspirin also obviously downregulated the mRNA expressions of IL-6, IL-1beta, and MCP-1 and assuaged the activation of TLR4, MyD88, NF-kappaBp65, and TLR2 in the placental tissue.	Aspirin	0-7	interleukin 6	Rattus norvegicus	61-65
29969574-13	2018	Aspirin also obviously downregulated the mRNA expressions of IL-6, IL-1beta, and MCP-1 and assuaged the activation of TLR4, MyD88, NF-kappaBp65, and TLR2 in the placental tissue.	Aspirin	0-7	interleukin 1 beta	Rattus norvegicus	67-75
29969574-13	2018	Aspirin also obviously downregulated the mRNA expressions of IL-6, IL-1beta, and MCP-1 and assuaged the activation of TLR4, MyD88, NF-kappaBp65, and TLR2 in the placental tissue.	Aspirin	0-7	mast cell protease 1-like 1	Rattus norvegicus	81-86
29969574-13	2018	Aspirin also obviously downregulated the mRNA expressions of IL-6, IL-1beta, and MCP-1 and assuaged the activation of TLR4, MyD88, NF-kappaBp65, and TLR2 in the placental tissue.	Aspirin	0-7	toll-like receptor 4	Rattus norvegicus	118-122
29969574-13	2018	Aspirin also obviously downregulated the mRNA expressions of IL-6, IL-1beta, and MCP-1 and assuaged the activation of TLR4, MyD88, NF-kappaBp65, and TLR2 in the placental tissue.	Aspirin	0-7	toll-like receptor 2	Rattus norvegicus	149-153
29969574-14	2018	Our results indicated that aspirin could assuage preeclampsia-like phenotypes, and this improvement effect is possibly the result of the suppression of pro-inflammatory cytokines via the TLR4, MyD88, NF-kappaBp65, and TLR2 signaling pathway.	Aspirin	27-34	toll-like receptor 4	Rattus norvegicus	187-191
29969574-14	2018	Our results indicated that aspirin could assuage preeclampsia-like phenotypes, and this improvement effect is possibly the result of the suppression of pro-inflammatory cytokines via the TLR4, MyD88, NF-kappaBp65, and TLR2 signaling pathway.	Aspirin	27-34	toll-like receptor 2	Rattus norvegicus	218-222
30332694-5	2018	Despite the use of antiplatelet therapies, including aspirin and P2Y12-receptor antagonists, some patients with artery disease continue to experience recurrent cardiovascular ischaemic events due to excessive thrombin generation beyond the acute period.	Aspirin	53-60	coagulation factor II, thrombin	Homo sapiens	209-217
30276549-11	2018	ELISA analysis showed that aspirin significantly decreased the production of inflammatory cytokines IFN-gamma (p value &lt; 0.05) and IL-8 (p value &lt; 0.001) in PE-DMSCs.	Aspirin	27-34	interferon gamma	Homo sapiens	100-109
30276549-11	2018	ELISA analysis showed that aspirin significantly decreased the production of inflammatory cytokines IFN-gamma (p value &lt; 0.05) and IL-8 (p value &lt; 0.001) in PE-DMSCs.	Aspirin	27-34	C-X-C motif chemokine ligand 8	Homo sapiens	134-138
30108097-0	2018	A Prospective Study of Aspirin Use and Prostate Cancer Risk by TMPRSS2:ERG Status.	Aspirin	23-30	transmembrane serine protease 2	Homo sapiens	63-70
30131302-6	2018	Mechanistic studies revealed that the reduction of cox2 by aspirin in A549 and H1299 was caused by disruption of the chromosomal architecture of the cox2 locus.	Aspirin	59-66	prostaglandin-endoperoxide synthase 2	Homo sapiens	51-55
30131302-6	2018	Mechanistic studies revealed that the reduction of cox2 by aspirin in A549 and H1299 was caused by disruption of the chromosomal architecture of the cox2 locus.	Aspirin	59-66	prostaglandin-endoperoxide synthase 2	Homo sapiens	149-153
30106307-9	2018	Also, it possessed better affinity value, -7.80518 kcal/mol and energy binding -85.08 kcal/mol, in inhibition of COX-2 with PDB Id: 1CVU rather than other compounds and significantly the higher dock score than aspirin, close to celecoxib.	Aspirin	210-217	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	113-118
30106307-9	2018	Also, it possessed better affinity value, -7.80518 kcal/mol and energy binding -85.08 kcal/mol, in inhibition of COX-2 with PDB Id: 1CVU rather than other compounds and significantly the higher dock score than aspirin, close to celecoxib.	Aspirin	210-217	PDB1	Homo sapiens	124-127
29793021-8	2018	Acetylsalicylic acid (ASA) blocked the enhancement of thrombus formation by TPO in both WT and p110alpha KO mice.	Aspirin	0-20	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Mus musculus	95-104
29793021-8	2018	Acetylsalicylic acid (ASA) blocked the enhancement of thrombus formation by TPO in both WT and p110alpha KO mice.	Aspirin	22-25	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Mus musculus	95-104
30108097-0	2018	A Prospective Study of Aspirin Use and Prostate Cancer Risk by TMPRSS2:ERG Status.	Aspirin	23-30	ETS transcription factor ERG	Homo sapiens	71-74
30108097-1	2018	Background: In a case-control study, aspirin use was associated with a lower risk of a common prostate cancer molecular subtype, the TMPRSS2:ERG gene fusion.	Aspirin	37-44	transmembrane serine protease 2	Homo sapiens	133-140
30108097-1	2018	Background: In a case-control study, aspirin use was associated with a lower risk of a common prostate cancer molecular subtype, the TMPRSS2:ERG gene fusion.	Aspirin	37-44	ETS transcription factor ERG	Homo sapiens	141-144
29771821-10	2018	Laminar shear stress, aspirin/LSS combination, and celecoxib/LSS combination were all able to prevent TNFalpha-induced alterations in eNOS levels and prostacyclin/thromboxane ratio.	Aspirin	22-29	tumor necrosis factor	Homo sapiens	102-110
29392539-9	2018	The effects of metformin and aspirin partly relied on cyclooxygenase-2 (COX-2) upregulation, without the production of lipoxins.	Aspirin	29-36	prostaglandin-endoperoxide synthase 2	Homo sapiens	54-70
29392539-9	2018	The effects of metformin and aspirin partly relied on cyclooxygenase-2 (COX-2) upregulation, without the production of lipoxins.	Aspirin	29-36	prostaglandin-endoperoxide synthase 2	Homo sapiens	72-77
29733108-13	2018	WHAT IS NEW AND CONCLUSION: In surgical patients, eGFR frequently underestimates measured CrCl, especially in young patients with low ASA score.	Aspirin	134-137	epidermal growth factor receptor	Homo sapiens	50-54
30280037-9	2018	Analysis using the cBio portal indicated that aspirin might have effects on multiple tumor suppressors, such as TP53, PTEN, and RB1 and that TP53 might play a central role in aspirin-associated genes.	Aspirin	46-53	tumor protein p53	Homo sapiens	112-116
30280037-9	2018	Analysis using the cBio portal indicated that aspirin might have effects on multiple tumor suppressors, such as TP53, PTEN, and RB1 and that TP53 might play a central role in aspirin-associated genes.	Aspirin	175-182	tumor protein p53	Homo sapiens	141-145
30254660-0	2018	MS4A2-rs573790 Is Associated With Aspirin-Exacerbated Respiratory Disease: Replicative Study Using a Candidate Gene Strategy.	Aspirin	34-41	membrane spanning 4-domains A2	Homo sapiens	0-5
29779133-8	2018	The findings also indicate that aspirin may induce HSP60 and HSP47 expression in renal cells.	Aspirin	32-39	serpin family H member 1	Gallus gallus	61-66
29779133-9	2018	Finally, the expression patterns of HSP60 and HSP47 indicated that they may play a renoprotective role, as their expression was higher in the aspirin-treated groups.	Aspirin	142-149	serpin family H member 1	Gallus gallus	46-51
29779133-10	2018	In conclusion, the present findings show that heat stress causes renal damage in poultry and that aspirin may play a protective role against this damage via pathways that involve HSP60 and HSP47.	Aspirin	98-105	serpin family H member 1	Gallus gallus	189-194
29718107-8	2018	However, ASP administration impeded NF-kappaB signaling activation, downregulated COX-2 and inflammatory factor expression, and rescued trophoblast invasion.	Aspirin	9-12	prostaglandin-endoperoxide synthase 2	Homo sapiens	82-87
29775202-12	2018	The response model showed that 0.05% DMSO with 100 muM aspirin would provide platelet aggregation of 3.4 Omega.	Aspirin	55-62	latexin	Homo sapiens	51-54
29775202-14	2018	Overall, the use of 100 muM of aspirin in 0.05% DMSO provides a robust method to test for ex vivo inhibition of platelet aggregation.	Aspirin	31-38	latexin	Homo sapiens	24-27
29554282-0	2018	Effects of Celecoxib and Low-dose Aspirin on Outcomes in Adjuvant Aromatase Inhibitor-Treated Patients: CCTG MA.27.	Aspirin	34-41	chaperonin containing TCP1 subunit 3	Homo sapiens	104-108
29922884-0	2018	Comment on "Targeting AMPK, mTOR and beta-Catenin by Combined Metformin and Aspirin Therapy in HCC: An Appraisal in Egyptian HCC Patients".	Aspirin	76-83	mechanistic target of rapamycin kinase	Homo sapiens	28-32
29473449-12	2018	The effect of acetylsalicylic acid over other anti-inflammatory and anti-platelet agents is possibly attributable to its distinct mechanism of cyclooxygenase-1 inhibition.	Aspirin	14-34	prostaglandin-endoperoxide synthase 1	Homo sapiens	143-159
30013667-0	2018	Synergistic antitumor activity of aspirin and erlotinib: Inhibition of p38 enhanced aspirin plus erlotinib-induced suppression of metastasis and promoted cancer cell apoptosis.	Aspirin	34-41	mitogen-activated protein kinase 14	Homo sapiens	71-74
30013667-0	2018	Synergistic antitumor activity of aspirin and erlotinib: Inhibition of p38 enhanced aspirin plus erlotinib-induced suppression of metastasis and promoted cancer cell apoptosis.	Aspirin	84-91	mitogen-activated protein kinase 14	Homo sapiens	71-74
30013667-4	2018	Furthermore, aspirin plus erlotinib significantly induced the activation of E-cadherin and suppression of p38.	Aspirin	13-20	cadherin 1	Homo sapiens	76-86
30013667-4	2018	Furthermore, aspirin plus erlotinib significantly induced the activation of E-cadherin and suppression of p38.	Aspirin	13-20	mitogen-activated protein kinase 14	Homo sapiens	106-109
30013667-5	2018	The data also indicated that the p38/E-cadherin pathway may be involved in the apoptosis caused by the combination of aspirin and erlotinib.	Aspirin	118-125	mitogen-activated protein kinase 14	Homo sapiens	33-36
30013667-5	2018	The data also indicated that the p38/E-cadherin pathway may be involved in the apoptosis caused by the combination of aspirin and erlotinib.	Aspirin	118-125	cadherin 1	Homo sapiens	37-47
30013667-6	2018	As p38 and E-cadherin also serve a key role in epithelial-to-mesenchymal transition (EMT) and cancer metastasis, we hypothesized that the combination of aspirin and erlotinib may significantly inhibit tumor metastasis.	Aspirin	153-160	mitogen-activated protein kinase 14	Homo sapiens	3-6
30013667-6	2018	As p38 and E-cadherin also serve a key role in epithelial-to-mesenchymal transition (EMT) and cancer metastasis, we hypothesized that the combination of aspirin and erlotinib may significantly inhibit tumor metastasis.	Aspirin	153-160	cadherin 1	Homo sapiens	11-21
29788174-9	2018	In ECS-exposed animals, aspirin induced intense lobular formation, which could indicate that aspirin is counteracting the AHR signaling induced by ECS.	Aspirin	24-31	aryl-hydrocarbon receptor	Mus musculus	122-125
30012602-0	2018	Aspirin binds to PPARalpha to stimulate hippocampal plasticity and protect memory.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Mus musculus	17-26
30012602-2	2018	Here we report that peroxisome proliferator-activated receptor alpha (PPARalpha), a nuclear hormone receptor involved in fatty acid metabolism, serves as a receptor of aspirin.	Aspirin	168-175	peroxisome proliferator activated receptor alpha	Mus musculus	20-68
30012602-2	2018	Here we report that peroxisome proliferator-activated receptor alpha (PPARalpha), a nuclear hormone receptor involved in fatty acid metabolism, serves as a receptor of aspirin.	Aspirin	168-175	peroxisome proliferator activated receptor alpha	Mus musculus	70-79
30012602-3	2018	Detailed proteomic analyses including cheminformatics, thermal shift assays, and TR-FRET revealed that aspirin, but not other structural homologs, acts as a PPARalpha ligand through direct binding at the Tyr314 residue of the PPARalpha ligand-binding domain.	Aspirin	103-110	peroxisome proliferator activated receptor alpha	Mus musculus	157-166
30012602-3	2018	Detailed proteomic analyses including cheminformatics, thermal shift assays, and TR-FRET revealed that aspirin, but not other structural homologs, acts as a PPARalpha ligand through direct binding at the Tyr314 residue of the PPARalpha ligand-binding domain.	Aspirin	103-110	peroxisome proliferator activated receptor alpha	Mus musculus	226-235
30012602-4	2018	On binding to PPARalpha, aspirin stimulated hippocampal plasticity via transcriptional activation of cAMP response element-binding protein (CREB).	Aspirin	25-32	peroxisome proliferator activated receptor alpha	Mus musculus	14-23
30012602-4	2018	On binding to PPARalpha, aspirin stimulated hippocampal plasticity via transcriptional activation of cAMP response element-binding protein (CREB).	Aspirin	25-32	cAMP responsive element binding protein 1	Mus musculus	101-138
30012602-4	2018	On binding to PPARalpha, aspirin stimulated hippocampal plasticity via transcriptional activation of cAMP response element-binding protein (CREB).	Aspirin	25-32	cAMP responsive element binding protein 1	Mus musculus	140-144
30012602-5	2018	Finally, hippocampus-dependent behavioral analyses, calcium influx assays in hippocampal slices and quantification of dendritic spines demonstrated that low-dose aspirin treatment improved hippocampal plasticity and memory in FAD5X mice, but not in FAD5X/Ppara-null mice.	Aspirin	162-169	peroxisome proliferator activated receptor alpha	Mus musculus	255-260
30012602-6	2018	These findings highlight a property of aspirin: stimulating hippocampal plasticity via direct interaction with PPARalpha.	Aspirin	39-46	peroxisome proliferator activated receptor alpha	Mus musculus	111-120
29788174-9	2018	In ECS-exposed animals, aspirin induced intense lobular formation, which could indicate that aspirin is counteracting the AHR signaling induced by ECS.	Aspirin	93-100	aryl-hydrocarbon receptor	Mus musculus	122-125
29967008-0	2018	Aspirin Induces Lysosomal Biogenesis and Attenuates Amyloid Plaque Pathology in a Mouse Model of Alzheimer"s Disease via PPARalpha.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Mus musculus	121-130
29967008-4	2018	Interestingly, aspirin induced the activation of peroxisome proliferator-activated receptor alpha (PPARalpha) and stimulated the transcription of Tfeb via PPARalpha.	Aspirin	15-22	peroxisome proliferator activated receptor alpha	Mus musculus	49-97
29967008-4	2018	Interestingly, aspirin induced the activation of peroxisome proliferator-activated receptor alpha (PPARalpha) and stimulated the transcription of Tfeb via PPARalpha.	Aspirin	15-22	peroxisome proliferator activated receptor alpha	Mus musculus	99-108
29967008-4	2018	Interestingly, aspirin induced the activation of peroxisome proliferator-activated receptor alpha (PPARalpha) and stimulated the transcription of Tfeb via PPARalpha.	Aspirin	15-22	peroxisome proliferator activated receptor alpha	Mus musculus	155-164
29967008-5	2018	Finally, oral administration of low-dose aspirin decreased amyloid plaque pathology in both male and female 5X familial Alzheimer"s disease (5XFAD) mice in a PPARalpha-dependent fashion.	Aspirin	41-48	peroxisome proliferator activated receptor alpha	Mus musculus	158-167
30042442-6	2018	Furthermore, we found that Aspirin could block the activation of NF-kappaB signaling induced by PI3K inhibition, and combined use of GDC-0941 and Aspirin resulted in attenuated cell growth and enhanced apoptosis of 4T1 cells in the in vitro co-culture system with the presence of macrophages.	Aspirin	27-34	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	65-74
29967008-6	2018	This study reveals a new function of aspirin in stimulating lysosomal biogenesis via PPARalpha and suggests that low-dose aspirin may be used in lowering storage materials in Alzheimer"s disease and lysosomal storage disorders.SIGNIFICANCE STATEMENT Developing drugs for the reduction of amyloid beta containing senile plaques, one of the pathological hallmarks of Alzheimer"s disease (AD), is an important area of research.	Aspirin	37-44	peroxisome proliferator activated receptor alpha	Mus musculus	85-94
29967008-6	2018	This study reveals a new function of aspirin in stimulating lysosomal biogenesis via PPARalpha and suggests that low-dose aspirin may be used in lowering storage materials in Alzheimer"s disease and lysosomal storage disorders.SIGNIFICANCE STATEMENT Developing drugs for the reduction of amyloid beta containing senile plaques, one of the pathological hallmarks of Alzheimer"s disease (AD), is an important area of research.	Aspirin	122-129	peroxisome proliferator activated receptor alpha	Mus musculus	85-94
29967008-7	2018	Aspirin, one of the most widely used medications in the world, activates peroxisome proliferator-activated receptor alpha (PPARalpha) to upregulate transcription factor EB and increase lysosomal biogenesis in brain cells.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Mus musculus	73-121
29967008-7	2018	Aspirin, one of the most widely used medications in the world, activates peroxisome proliferator-activated receptor alpha (PPARalpha) to upregulate transcription factor EB and increase lysosomal biogenesis in brain cells.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Mus musculus	123-132
29967008-8	2018	Accordingly, low-dose aspirin decreases cerebral plaque load in a mouse model of Alzheimer"s disease via PPARalpha.	Aspirin	22-29	peroxisome proliferator activated receptor alpha	Mus musculus	105-114
29792865-7	2018	Such aspirin-induced changes of ABT-737 resistance was accompanied by a host of biochemical events like protein phosphatase 2A (PP2A) activation, AKT dephosphorylation, Mcl-1/FLICE inhibiting protein (FLIP)/XIAP downregulation, and Bax mitochondrial redistribution.	Aspirin	5-12	AKT serine/threonine kinase 1	Homo sapiens	146-149
29792865-7	2018	Such aspirin-induced changes of ABT-737 resistance was accompanied by a host of biochemical events like protein phosphatase 2A (PP2A) activation, AKT dephosphorylation, Mcl-1/FLICE inhibiting protein (FLIP)/XIAP downregulation, and Bax mitochondrial redistribution.	Aspirin	5-12	BCL2 associated X, apoptosis regulator	Homo sapiens	232-235
29792865-10	2018	Since PP2A, Akt, and Mcl-1 play critical roles in RCC malignancy and treatment resistance, our present study showed that aspirin, an alternative adjuvant agent, had recalled ABT-737 sensitivity in the RCC cells through processes involving the PP2A/Akt/Mcl-1 axis.	Aspirin	121-128	AKT serine/threonine kinase 1	Homo sapiens	248-251
29792865-10	2018	Since PP2A, Akt, and Mcl-1 play critical roles in RCC malignancy and treatment resistance, our present study showed that aspirin, an alternative adjuvant agent, had recalled ABT-737 sensitivity in the RCC cells through processes involving the PP2A/Akt/Mcl-1 axis.	Aspirin	121-128	AKT serine/threonine kinase 1	Homo sapiens	12-15
29980196-8	2018	In mouse primary microglia, recombinant SAA but not S. pneumoniae stimulated TNFalpha, IL-1beta, IL-6 and CCL-2 expression, and this response was completely blocked by the pro-resolving Fpr2 agonist aspirin-triggered resolvin D1 (AT-RvD1).	Aspirin	199-206	interleukin 1 beta	Mus musculus	87-95
30002310-7	2018	The bioinformatic results revealed that aspirin could inhibit proliferation by blocking the cell cycle, and could reduce migration and invasion via the PI3K-Akt and focal adhesion pathways.	Aspirin	40-47	AKT serine/threonine kinase 1	Homo sapiens	157-160
30002310-9	2018	Furthermore, we found that ASA suppressed the activation of the focal adhesion kinase (FAK) and the phosphorylation of Akt, NF-kappaB, and STAT3.	Aspirin	27-30	AKT serine/threonine kinase 1	Homo sapiens	119-122
30002310-9	2018	Furthermore, we found that ASA suppressed the activation of the focal adhesion kinase (FAK) and the phosphorylation of Akt, NF-kappaB, and STAT3.	Aspirin	27-30	signal transducer and activator of transcription 3	Homo sapiens	139-144
28888067-9	2018	Immunohistochemical staining showed considerable expression of OCN, especially in the TSAH/beta-TCP/BMP-2 and TSAH/beta-TCP/aspirin groups.	Aspirin	124-131	bone gamma-carboxyglutamate protein	Homo sapiens	63-66
28875477-8	2018	Statistical analysis also revealed that aspirin reaction units (ARUs) were significantly associated with PON1 methylation level at CpG site -163 (p = 0.0342).	Aspirin	40-47	paraoxonase 1	Homo sapiens	105-109
29936693-0	2018	Clustering of ABCB1 and CYP2C19 Genetic Variants Predicts Risk of Major Bleeding and Thrombotic Events in Elderly Patients with Acute Coronary Syndrome Receiving Dual Antiplatelet Therapy with Aspirin and Clopidogrel.	Aspirin	193-200	ATP binding cassette subfamily B member 1	Homo sapiens	14-19
28888067-5	2018	At a low concentration (&lt;=100 mug/mL), aspirin did not promote cell proliferation, but enhanced the alkaline phosphatase activity, and osteocalcin (OCN) and collagen I expression of human bone marrow-derived mesenchymal stem cells.	Aspirin	42-49	bone gamma-carboxyglutamate protein	Homo sapiens	138-149
28888067-5	2018	At a low concentration (&lt;=100 mug/mL), aspirin did not promote cell proliferation, but enhanced the alkaline phosphatase activity, and osteocalcin (OCN) and collagen I expression of human bone marrow-derived mesenchymal stem cells.	Aspirin	42-49	bone gamma-carboxyglutamate protein	Homo sapiens	151-154
29873780-11	2018	Finally, using ex vivo culture, we show a strong correlation between degradation of TIF-IA and activation of NF-kappaB in freshly resected, human colorectal tumours exposed to the chemopreventative agent, aspirin.	Aspirin	205-212	RRN3 homolog, RNA polymerase I transcription factor	Homo sapiens	84-90
29873780-11	2018	Finally, using ex vivo culture, we show a strong correlation between degradation of TIF-IA and activation of NF-kappaB in freshly resected, human colorectal tumours exposed to the chemopreventative agent, aspirin.	Aspirin	205-212	nuclear factor kappa B subunit 1	Homo sapiens	109-118
29982425-0	2018	Nitric oxide-donating aspirin (NO-Aspirin) suppresses lung tumorigenesis in vitro and in vivo and these effects are associated with modulation of the EGFR signaling pathway.	Aspirin	22-29	epidermal growth factor receptor	Homo sapiens	150-154
29982425-0	2018	Nitric oxide-donating aspirin (NO-Aspirin) suppresses lung tumorigenesis in vitro and in vivo and these effects are associated with modulation of the EGFR signaling pathway.	Aspirin	34-41	epidermal growth factor receptor	Homo sapiens	150-154
29982425-4	2018	Under in vitro conditions, NO-Aspirin significantly reduced the proliferation and survival of tumorigenic bronchial cell line (1170) and non-small cell lung cancer (NSCLC) cell lines (A549, H1650, H1975 and HCC827) and colony formation by NSCLC cells at sub- or low micromolar concentrations (&lt;=1 microM for 1170 cells and &lt;=6 microM for NSCLC cells) in a COX-2 independent manner.	Aspirin	30-37	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	362-367
30177071-0	2018	The effect of low-dose aspirin on serum placental growth factor levels in a high-risk PREDO cohort.	Aspirin	23-30	placental growth factor	Homo sapiens	40-63
30177071-2	2018	Our second aim was to study the effect of low-dose acetylsalicylic acid (LDA; 100 mg/day), started before the 14th week of gestation, on PlGF concentration.	Aspirin	51-71	placental growth factor	Homo sapiens	137-141
30034291-7	2018	Treatment with aspirin inhibited 4T1 cell growth and migration and MCP-1, PAI-1, and IL-6 production.	Aspirin	15-22	mast cell protease 1	Mus musculus	67-72
30034291-7	2018	Treatment with aspirin inhibited 4T1 cell growth and migration and MCP-1, PAI-1, and IL-6 production.	Aspirin	15-22	interleukin 6	Mus musculus	85-89
30034291-8	2018	In the coculture of both cells, aspirin inhibited secretion of MCP-1, IL-6, and TGF-beta.	Aspirin	32-39	mast cell protease 1	Mus musculus	63-68
30034291-8	2018	In the coculture of both cells, aspirin inhibited secretion of MCP-1, IL-6, and TGF-beta.	Aspirin	32-39	interleukin 6	Mus musculus	70-74
29411531-12	2018	Single nucleotide polymorphisms in serum paraoxonase/arylesterase 1 (PON1) gene was associated with aspirin HoTPR (P = 0.005) while SNP in phospholipase A2, group III (PLA2G3) gene was associated with clopidogrel HoTPR (P = 0.002).	Aspirin	100-107	paraoxonase 1	Homo sapiens	35-67
29557194-7	2018	Administration of aspirin changed the expression patterns of HSF-1, 2 and 3 such that the expression of Hsp90 protein was significantly upregulated (by 2.3-4.1 times compared with that of the non-treated cells).	Aspirin	18-25	heat shock factor protein 3	Gallus gallus	61-75
29411531-12	2018	Single nucleotide polymorphisms in serum paraoxonase/arylesterase 1 (PON1) gene was associated with aspirin HoTPR (P = 0.005) while SNP in phospholipase A2, group III (PLA2G3) gene was associated with clopidogrel HoTPR (P = 0.002).	Aspirin	100-107	paraoxonase 1	Homo sapiens	69-73
29781520-6	2018	A significant association with poor responsiveness to aspirin was observed for GP1BA rs2243093, PTGS1 rs1330344, PTGS2 rs689466 and TBXA2R rs1131882 polymorphisms in overall analyses.	Aspirin	54-61	prostaglandin-endoperoxide synthase 1	Homo sapiens	96-101
29568915-8	2018	Furthermore, it was confirmed that the signaling pathways involving CX3CL1-NF-kappaB, IL-6 and TNF-alpha were partly inhibited by aspirin.	Aspirin	130-137	C-X3-C motif chemokine ligand 1	Homo sapiens	68-74
29568915-8	2018	Furthermore, it was confirmed that the signaling pathways involving CX3CL1-NF-kappaB, IL-6 and TNF-alpha were partly inhibited by aspirin.	Aspirin	130-137	nuclear factor kappa B subunit 1	Homo sapiens	75-84
29568915-8	2018	Furthermore, it was confirmed that the signaling pathways involving CX3CL1-NF-kappaB, IL-6 and TNF-alpha were partly inhibited by aspirin.	Aspirin	130-137	interleukin 6	Homo sapiens	86-90
29568915-8	2018	Furthermore, it was confirmed that the signaling pathways involving CX3CL1-NF-kappaB, IL-6 and TNF-alpha were partly inhibited by aspirin.	Aspirin	130-137	tumor necrosis factor	Homo sapiens	95-104
30149368-3	2018	The cyclooxygenase-2 (COX-2) inhibitory and other direct and indirect pathways of aspirin are translated to inhibition proliferation and enhanced apoptosis of cancer cells.	Aspirin	82-89	prostaglandin-endoperoxide synthase 2	Homo sapiens	22-27
29805582-0	2018	Effects of aspirin on proliferation, invasion and apoptosis of Hep-2 cells via the PTEN/AKT/NF-kappaB/survivin signaling pathway.	Aspirin	11-18	AKT serine/threonine kinase 1	Homo sapiens	88-91
29805582-0	2018	Effects of aspirin on proliferation, invasion and apoptosis of Hep-2 cells via the PTEN/AKT/NF-kappaB/survivin signaling pathway.	Aspirin	11-18	nuclear factor kappa B subunit 1	Homo sapiens	92-101
29805582-6	2018	Aspirin also significantly decreased the expression of B-cell lymphoma 2 (Bcl-2) and caspase-3, and increased the expression of Bcl-2-associated X protein, suggesting that aspirin induced apoptosis through the intrinsic apoptotic pathway.	Aspirin	0-7	BCL2 apoptosis regulator	Homo sapiens	55-72
29805582-6	2018	Aspirin also significantly decreased the expression of B-cell lymphoma 2 (Bcl-2) and caspase-3, and increased the expression of Bcl-2-associated X protein, suggesting that aspirin induced apoptosis through the intrinsic apoptotic pathway.	Aspirin	0-7	BCL2 apoptosis regulator	Homo sapiens	74-79
29805582-6	2018	Aspirin also significantly decreased the expression of B-cell lymphoma 2 (Bcl-2) and caspase-3, and increased the expression of Bcl-2-associated X protein, suggesting that aspirin induced apoptosis through the intrinsic apoptotic pathway.	Aspirin	0-7	caspase 3	Homo sapiens	85-94
29805582-6	2018	Aspirin also significantly decreased the expression of B-cell lymphoma 2 (Bcl-2) and caspase-3, and increased the expression of Bcl-2-associated X protein, suggesting that aspirin induced apoptosis through the intrinsic apoptotic pathway.	Aspirin	0-7	BCL2 apoptosis regulator	Homo sapiens	128-133
29805582-6	2018	Aspirin also significantly decreased the expression of B-cell lymphoma 2 (Bcl-2) and caspase-3, and increased the expression of Bcl-2-associated X protein, suggesting that aspirin induced apoptosis through the intrinsic apoptotic pathway.	Aspirin	172-179	BCL2 apoptosis regulator	Homo sapiens	55-72
29805582-6	2018	Aspirin also significantly decreased the expression of B-cell lymphoma 2 (Bcl-2) and caspase-3, and increased the expression of Bcl-2-associated X protein, suggesting that aspirin induced apoptosis through the intrinsic apoptotic pathway.	Aspirin	172-179	BCL2 apoptosis regulator	Homo sapiens	74-79
29805582-6	2018	Aspirin also significantly decreased the expression of B-cell lymphoma 2 (Bcl-2) and caspase-3, and increased the expression of Bcl-2-associated X protein, suggesting that aspirin induced apoptosis through the intrinsic apoptotic pathway.	Aspirin	172-179	caspase 3	Homo sapiens	85-94
29805582-6	2018	Aspirin also significantly decreased the expression of B-cell lymphoma 2 (Bcl-2) and caspase-3, and increased the expression of Bcl-2-associated X protein, suggesting that aspirin induced apoptosis through the intrinsic apoptotic pathway.	Aspirin	172-179	BCL2 apoptosis regulator	Homo sapiens	128-133
29805582-7	2018	Hep-2 cells treated with aspirin exhibited a significant upregulation of phosphatase and tensin homolog (PTEN) and decreased levels of phosphorylated protein kinase B (AKT).	Aspirin	25-32	AKT serine/threonine kinase 1	Homo sapiens	168-171
29805582-10	2018	These results indicated that the molecular mechanism underlying the antitumor effects of aspirin may be associated with the inhibition of tumor invasion and induction of apoptosis by regulating the activity of the PTEN/AKT/NF-kappaB/survivin signaling pathway.	Aspirin	89-96	AKT serine/threonine kinase 1	Homo sapiens	219-222
29805582-10	2018	These results indicated that the molecular mechanism underlying the antitumor effects of aspirin may be associated with the inhibition of tumor invasion and induction of apoptosis by regulating the activity of the PTEN/AKT/NF-kappaB/survivin signaling pathway.	Aspirin	89-96	nuclear factor kappa B subunit 1	Homo sapiens	223-232
30149368-3	2018	The cyclooxygenase-2 (COX-2) inhibitory and other direct and indirect pathways of aspirin are translated to inhibition proliferation and enhanced apoptosis of cancer cells.	Aspirin	82-89	prostaglandin-endoperoxide synthase 2	Homo sapiens	4-20
29629844-0	2018	Aspirin suppresses components of lymphangiogenesis and lymphatic vessel remodeling by inhibiting the NF-kappaB/VCAM-1 pathway in human lymphatic endothelial cells.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	101-110
29629844-0	2018	Aspirin suppresses components of lymphangiogenesis and lymphatic vessel remodeling by inhibiting the NF-kappaB/VCAM-1 pathway in human lymphatic endothelial cells.	Aspirin	0-7	vascular cell adhesion molecule 1	Homo sapiens	111-117
29629844-8	2018	Western blotting analysis indicated that aspirin decreased expression of vascular cell adhesion molecule-1 (VCAM-1), at both protein and mRNA levels, and these correlated with the reduction of NF-kappaB p65 phosphorylation.	Aspirin	41-48	vascular cell adhesion molecule 1	Homo sapiens	73-106
29629844-8	2018	Western blotting analysis indicated that aspirin decreased expression of vascular cell adhesion molecule-1 (VCAM-1), at both protein and mRNA levels, and these correlated with the reduction of NF-kappaB p65 phosphorylation.	Aspirin	41-48	vascular cell adhesion molecule 1	Homo sapiens	108-114
29781520-6	2018	A significant association with poor responsiveness to aspirin was observed for GP1BA rs2243093, PTGS1 rs1330344, PTGS2 rs689466 and TBXA2R rs1131882 polymorphisms in overall analyses.	Aspirin	54-61	prostaglandin-endoperoxide synthase 2	Homo sapiens	113-118
29769586-5	2018	On multivariable analysis of ASAS+ patients, IL-31 level was associated with sCD40L level (p &lt; 0.0001), modified Stoke AS Spine Score (mSASSS) &lt; 1 (p = 0.035).	Aspirin	29-33	interleukin 31	Homo sapiens	45-50
29381509-12	2018	In conclusion, aspirin induces neuroprotective effects by inhibiting astrocyte activation and apoptosis after SCI through the activation of the Nrf2/HO-1 signaling pathway.	Aspirin	15-22	NFE2 like bZIP transcription factor 2	Rattus norvegicus	144-148
29381509-0	2018	Aspirin suppresses neuronal apoptosis, reduces tissue inflammation, and restrains astrocyte activation by activating the Nrf2/HO-1 signaling pathway.	Aspirin	0-7	NFE2 like bZIP transcription factor 2	Rattus norvegicus	121-125
29698447-9	2018	20-HETE, a prohypertensive androgen-sensitive CYP450 metabolite was higher with celecoxib absent aspirin and was positively associated with SBP in men (P = 0.040) but not women.	Aspirin	97-104	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	46-52
29381509-7	2018	The expression of Nrf2, quinine oxidoreductase 1, and HO-1 proteins was increased in aspirin-treated animals after SCI compared with the vehicle group.	Aspirin	85-92	NFE2 like bZIP transcription factor 2	Rattus norvegicus	18-22
29381509-8	2018	In addition, aspirin simultaneously decreased the expression of inflammation-related proteins, such as tumor necrosis factor-alpha and interleukin-6 after SCI.	Aspirin	13-20	tumor necrosis factor	Rattus norvegicus	103-130
29381509-8	2018	In addition, aspirin simultaneously decreased the expression of inflammation-related proteins, such as tumor necrosis factor-alpha and interleukin-6 after SCI.	Aspirin	13-20	interleukin 6	Rattus norvegicus	135-148
29477135-13	2018	An AC antioxidant has a potential effect as an antiplatelet agent that subsequently can prevent atherosclerosis and CVD and, therefore, AC may be an alternative to other antiplatelet drugs such as aspirin.	Aspirin	197-204	DDB1 and CUL4 associated factor 7	Homo sapiens	3-5
31938370-0	2018	Aspirin-triggered lipoxin A4 attenuates lipopolysaccharide-induced acute lung injury by inhibiting activation of mitogen-activated protein kinases and NF-kappaB in mice.	Aspirin	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	151-160
28948649-0	2018	Association of GPIa and COX-2 gene polymorphism with aspirin resistance.	Aspirin	53-60	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	24-29
28948649-1	2018	OBJECTIVE: This study aimed to explore the association between GPIa, COX-2 gene polymorphisms and aspirin resistance in the ischemic stroke patients from the southern part of Jiangsu province.	Aspirin	98-105	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	69-74
29350433-3	2018	In the present work, we aim to access the effect of two drugs, that is, acetylsalicylic acid and 5-amino salicylic acid on insulin amyloids by using various biophysical, imaging, cell viability assay, and computational approaches.	Aspirin	72-92	insulin	Homo sapiens	123-130
29850157-6	2018	Potential involved molecular pathways in the antitumor activities of aspirin are under studied worldwide for years and the possible mechanisms so far are reviewed in this article as cyclooxygenase (COX)-dependent pathways and COX-independent pathways, involving anti-inflammatory activity, apoptosis, platelet deactivation, PIK3CA mutation specificity and heparanase-related microenvironment changes of tumor cells.	Aspirin	69-76	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	324-330
29599304-0	2018	Aspirin in the Management of Patients with Prostate Cancer Undergoing Radiotherapy: Friend or Foe?	Aspirin	0-7	WAPL cohesin release factor	Homo sapiens	94-97
29599304-1	2018	Aspirin has cyclooxygenase-2 (COX2)-mediated anti-inflammatory and anti-coagulant properties that may confer a positive effect in preventing and limiting the progression of prostate cancer.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	12-28
29599304-1	2018	Aspirin has cyclooxygenase-2 (COX2)-mediated anti-inflammatory and anti-coagulant properties that may confer a positive effect in preventing and limiting the progression of prostate cancer.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	30-34
29599304-2	2018	Prostate cancer has been shown to have poor treatment outcomes due to therapeutic resistance; therefore, COX2 inhibition caused by aspirin could represent an opportunity to augment current therapies.	Aspirin	131-138	prostaglandin-endoperoxide synthase 2	Homo sapiens	105-109
28442495-0	2018	Aspirin prevents NF-kappaB activation and CDX2 expression stimulated by acid and bile salts in oesophageal squamous cells of patients with Barrett"s oesophagus.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	17-26
28442495-2	2018	CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) signalling, which can be inhibited by aspirin.	Aspirin	197-204	nuclear factor kappa B subunit 1	Homo sapiens	148-157
28442495-8	2018	CONCLUSIONS: Differences between NES-B and NES-G cells in NF-kappaB activation by acid and bile salts can account for their differences in CDX2 expression, and their CDX2 expression can be blocked by aspirin.	Aspirin	200-207	nuclear factor kappa B subunit 1	Homo sapiens	58-67
29642568-0	2018	Irradiation-Induced Cardiac Connexin-43 and miR-21 Responses Are Hampered by Treatment with Atorvastatin and Aspirin.	Aspirin	109-116	gap junction protein, alpha 1	Rattus norvegicus	28-39
29642568-7	2018	Treatment with aspirin and atorvastatin prevented an increase in the expression of Cx43 and PKCepsilon without change in the miR-1 levels.	Aspirin	15-22	gap junction protein, alpha 1	Rattus norvegicus	83-87
29642568-11	2018	Treatment with aspirin and atorvastatin interfered with irradiation-induced compensatory changes in myocardial Cx43 protein and miR-21 by preventing their elevation, possibly via amelioration of oxidative stress and inflammation.	Aspirin	15-22	gap junction protein, alpha 1	Rattus norvegicus	111-115
29243196-9	2018	Acetylsalicylic acid totally prevented the effect of homocysteine on acetylcholinesterase activity and catalase activity and immunocontent, as well as the ultrastructural changes, and partially prevented alterations on IL-1beta levels, superoxide dismutase activity, sulfhydryl content, and comet assay.	Aspirin	0-20	interleukin 1 beta	Rattus norvegicus	219-227
29566049-3	2018	The expression of APX1, GRC1, DHAR, MDHAR, GPX1, and GS3 in ASA-GSH cycle was also measured.	Aspirin	60-63	glutathione synthetase, chloroplastic	Triticum aestivum	53-56
29552221-0	2018	TGF-beta1 mediates the effects of aspirin on colonic tumor cell proliferation and apoptosis.	Aspirin	34-41	transforming growth factor beta 1	Homo sapiens	0-9
29552221-3	2018	In the prostaglandin-dependent pathways, inhibition of cyclooxygenase (COX), particularly COX-2, is the primary mechanism known to be involved in aspirin-induced CRC suppression.	Aspirin	146-153	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	90-95
29552221-6	2018	Specifically, aspirin triggers CRC cell apoptosis by inducing the secretion of TGF-beta1, and the increased TGF-beta1 then leads to apoptosis and proliferation inhibition in CRC cells.	Aspirin	14-21	transforming growth factor beta 1	Homo sapiens	79-88
29408091-6	2018	Aspirin disrupted the interaction between Bcl-2 and Beclin-1.	Aspirin	0-7	BCL2 apoptosis regulator	Homo sapiens	42-47
29349624-3	2018	Remarkably, the combined treatment with aspirin and vitamin D3 significantly suppressed the expression of Bcl-2 protein and p-Erk1/2 protein, examined by western blot analysis.	Aspirin	40-47	BCL2 apoptosis regulator	Homo sapiens	106-111
29196297-5	2018	The cytotoxicity of sorafenib and aspirin was blocked by inhibition of the AMPK or ERK pathways through shRNA or via pharmacologic inhibitors of RAF (LY3009120), MEK (trametinib), or AMPK (compound C).	Aspirin	34-41	mitogen-activated protein kinase 1	Mus musculus	83-86
29196297-5	2018	The cytotoxicity of sorafenib and aspirin was blocked by inhibition of the AMPK or ERK pathways through shRNA or via pharmacologic inhibitors of RAF (LY3009120), MEK (trametinib), or AMPK (compound C).	Aspirin	34-41	zinc fingers and homeoboxes 2	Mus musculus	145-148
29196297-7	2018	In vivo treatment of human xenografts in NSG mice with sorafenib and aspirin significantly reduced tumor volume compared with each single-agent treatment.Conclusions: Combination sorafenib and aspirin exerts cytotoxicity against RAS/RAF-mutant cells by simultaneously affecting two independent pathways and represents a promising novel strategy for the treatment of RAS-mutant cancers.	Aspirin	69-76	zinc fingers and homeoboxes 2	Mus musculus	233-236
29196297-7	2018	In vivo treatment of human xenografts in NSG mice with sorafenib and aspirin significantly reduced tumor volume compared with each single-agent treatment.Conclusions: Combination sorafenib and aspirin exerts cytotoxicity against RAS/RAF-mutant cells by simultaneously affecting two independent pathways and represents a promising novel strategy for the treatment of RAS-mutant cancers.	Aspirin	193-200	zinc fingers and homeoboxes 2	Mus musculus	233-236
29402752-0	2018	Aspirin versus placebo in stage III or high-risk stage II colon cancer with PIK3CA mutation: A French randomised double-blind phase III trial (PRODIGE 50-ASPIK).	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	76-82
29402752-2	2018	Two recent retrospective studies strongly suggested that low-dose aspirin used (100 mg/d) after surgical resection of colorectal cancer with a PIK3CA mutation could act as a targeted therapy with a major protective effect on the risk of recurrence.	Aspirin	66-73	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	143-149
29349624-3	2018	Remarkably, the combined treatment with aspirin and vitamin D3 significantly suppressed the expression of Bcl-2 protein and p-Erk1/2 protein, examined by western blot analysis.	Aspirin	40-47	mitogen-activated protein kinase 3	Homo sapiens	126-132
30052978-0	2018	Studies on Prostaglandin-Endoperoxide Synthase 1: Lower Levels in Schizophrenia and After Treatment with Antipsychotic Drugs in Conjunction with Aspirin.	Aspirin	145-152	prostaglandin-endoperoxide synthase 1	Homo sapiens	11-48
30052978-1	2018	Background: Antipsychotic drugs plus aspirin (acetylsalicylic acid), which targets prostaglandin-endoperoxide synthase 1 (PTGS1: COX1), improved therapeutic outcomes when treating schizophrenia.	Aspirin	37-44	prostaglandin-endoperoxide synthase 1	Homo sapiens	83-120
30052978-7	2018	In CCF-STTG1 cells, a human-derived astrocytic cell line, aspirin caused a dose-dependent decrease in PTGS1 that was decreased further with the addition of risperidone.	Aspirin	58-65	prostaglandin-endoperoxide synthase 1	Homo sapiens	102-107
30052978-1	2018	Background: Antipsychotic drugs plus aspirin (acetylsalicylic acid), which targets prostaglandin-endoperoxide synthase 1 (PTGS1: COX1), improved therapeutic outcomes when treating schizophrenia.	Aspirin	37-44	prostaglandin-endoperoxide synthase 1	Homo sapiens	122-127
30052978-8	2018	Conclusions: Our data suggest low levels of dorsolateral prefrontal cortex PTGS1 could be associated with the pathophysiology of schizophrenia, and improved therapeutic outcome from treating schizophrenia with antipsychotic drugs augmented with aspirin may be because such treatment lowers cortical PTGS1.	Aspirin	245-252	prostaglandin-endoperoxide synthase 1	Homo sapiens	75-80
30052978-1	2018	Background: Antipsychotic drugs plus aspirin (acetylsalicylic acid), which targets prostaglandin-endoperoxide synthase 1 (PTGS1: COX1), improved therapeutic outcomes when treating schizophrenia.	Aspirin	46-66	prostaglandin-endoperoxide synthase 1	Homo sapiens	83-120
30052978-8	2018	Conclusions: Our data suggest low levels of dorsolateral prefrontal cortex PTGS1 could be associated with the pathophysiology of schizophrenia, and improved therapeutic outcome from treating schizophrenia with antipsychotic drugs augmented with aspirin may be because such treatment lowers cortical PTGS1.	Aspirin	245-252	prostaglandin-endoperoxide synthase 1	Homo sapiens	299-304
30052978-1	2018	Background: Antipsychotic drugs plus aspirin (acetylsalicylic acid), which targets prostaglandin-endoperoxide synthase 1 (PTGS1: COX1), improved therapeutic outcomes when treating schizophrenia.	Aspirin	46-66	prostaglandin-endoperoxide synthase 1	Homo sapiens	122-127
30052978-2	2018	Our microarray data showed higher levels of PTGS1 mRNA in the dorsolateral prefrontal cortex from subjects with schizophrenia of long duration of illness, suggesting aspirin plus antipsychotic drugs could have therapeutic effects by lowering PTGS1 expression in the cortex of subjects with the disorder.	Aspirin	166-173	prostaglandin-endoperoxide synthase 1	Homo sapiens	44-49
30052978-2	2018	Our microarray data showed higher levels of PTGS1 mRNA in the dorsolateral prefrontal cortex from subjects with schizophrenia of long duration of illness, suggesting aspirin plus antipsychotic drugs could have therapeutic effects by lowering PTGS1 expression in the cortex of subjects with the disorder.	Aspirin	166-173	prostaglandin-endoperoxide synthase 1	Homo sapiens	242-247
29286113-0	2018	Synergistic effect of nutlin-3 combined with aspirin in hepatocellular carcinoma HepG2 cells through activation of Bcl-2/Bax signaling pathway.	Aspirin	45-52	BCL2 apoptosis regulator	Homo sapiens	115-120
29314596-12	2018	Of the patients, 95% were found to be sensitive to ASA, with values under the threshold of normality (400 AU min-1 ).	Aspirin	51-54	CD59 molecule (CD59 blood group)	Homo sapiens	109-114
29286113-0	2018	Synergistic effect of nutlin-3 combined with aspirin in hepatocellular carcinoma HepG2 cells through activation of Bcl-2/Bax signaling pathway.	Aspirin	45-52	BCL2 associated X, apoptosis regulator	Homo sapiens	121-124
29286113-12	2018	Nutlin-3 was able to increase the level of Bax in HepG2 cells treated with aspirin significantly after treatment for 8 h. When treated with a low concentration of aspirin and nutlin-3, the level of Bax in HepG2 cells was enhanced for 2 h. In the animal model, tumor volume and tumor angiogenesis were significantly decreased in combination group compared with other groups (P&lt;0.01).	Aspirin	75-82	BCL2 associated X, apoptosis regulator	Homo sapiens	43-46
29286113-12	2018	Nutlin-3 was able to increase the level of Bax in HepG2 cells treated with aspirin significantly after treatment for 8 h. When treated with a low concentration of aspirin and nutlin-3, the level of Bax in HepG2 cells was enhanced for 2 h. In the animal model, tumor volume and tumor angiogenesis were significantly decreased in combination group compared with other groups (P&lt;0.01).	Aspirin	75-82	BCL2 associated X, apoptosis regulator	Homo sapiens	198-201
29286113-12	2018	Nutlin-3 was able to increase the level of Bax in HepG2 cells treated with aspirin significantly after treatment for 8 h. When treated with a low concentration of aspirin and nutlin-3, the level of Bax in HepG2 cells was enhanced for 2 h. In the animal model, tumor volume and tumor angiogenesis were significantly decreased in combination group compared with other groups (P&lt;0.01).	Aspirin	163-170	BCL2 associated X, apoptosis regulator	Homo sapiens	43-46
29286113-12	2018	Nutlin-3 was able to increase the level of Bax in HepG2 cells treated with aspirin significantly after treatment for 8 h. When treated with a low concentration of aspirin and nutlin-3, the level of Bax in HepG2 cells was enhanced for 2 h. In the animal model, tumor volume and tumor angiogenesis were significantly decreased in combination group compared with other groups (P&lt;0.01).	Aspirin	163-170	BCL2 associated X, apoptosis regulator	Homo sapiens	198-201
29286113-14	2018	Nutlin-3 enhanced the apoptotic effect of a low dose of aspirin by upregulating Bax expression in the HepG2 cell line and in vivo.	Aspirin	56-63	BCL2 associated X, apoptosis regulator	Homo sapiens	80-83
29286113-15	2018	The synergistic effect of nutlin-3 in aspirin antitumor therapy contributed to diminishing the dose of aspirin required and decreased the occurrence of adverse drug events in HCC through targeting the Bcl-2/Bax signaling pathway.	Aspirin	38-45	BCL2 apoptosis regulator	Homo sapiens	201-206
29407631-1	2018	OBJECTIVE: To investigate the association between PEAR1 (platelet endothelial aggregation receptor-1) polymorphisms and cardiovascular outcomes in acute coronary syndrome (ACS) in patients treated with aspirin and clopidogrel.	Aspirin	202-209	platelet endothelial aggregation receptor 1	Homo sapiens	50-55
29407631-1	2018	OBJECTIVE: To investigate the association between PEAR1 (platelet endothelial aggregation receptor-1) polymorphisms and cardiovascular outcomes in acute coronary syndrome (ACS) in patients treated with aspirin and clopidogrel.	Aspirin	202-209	platelet endothelial aggregation receptor 1	Homo sapiens	57-100
29407631-9	2018	CONCLUSIONS: For Chinese patients with ACS treated with aspirin and clopidogrel, genetic mutations in rs822441/rs822442 in PEAR1 correlated significantly with platelet activity after adjusting for CYP2C19 *2/*3 alleles.	Aspirin	56-63	platelet endothelial aggregation receptor 1	Homo sapiens	123-128
29106390-9	2018	Lastly, aspirin markedly attenuates glycolysis and cancer stem-like characteristics by suppressing both H19 and PDK1.	Aspirin	8-15	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	112-116
29153543-13	2018	French prospective randomized study is currently being conducted to investigate postoperative aspirin in colorectal cancers with a PIK3CA mutation.	Aspirin	94-101	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	131-137
29094287-0	2018	Targeting AMPK, mTOR and beta-Catenin by Combined Metformin and Aspirin Therapy in HCC: An Appraisal in Egyptian HCC Patients.	Aspirin	64-71	mechanistic target of rapamycin kinase	Homo sapiens	16-20
29258006-5	2018	Haplotypes of 11-dehydro TxB2 increasing alleles for both PPARGC1B and CNTN4 were significantly associated with 11-dehydro TxB2, explaining 5.2% and 4.5% of the variation in the whole cohort, and 8.8% and 7.9% in participants not taking aspirin, respectively.	Aspirin	237-244	PPARG coactivator 1 beta	Homo sapiens	58-66
29258006-10	2018	If specific protection of PPARGC1B and CNTN4 variant carriers by aspirin is confirmed by additional studies, PPARGC1B and CNTN4 genotyping could potentially assist in clinical decision making regarding the use of aspirin in primary prevention.	Aspirin	65-72	PPARG coactivator 1 beta	Homo sapiens	26-34
29258006-10	2018	If specific protection of PPARGC1B and CNTN4 variant carriers by aspirin is confirmed by additional studies, PPARGC1B and CNTN4 genotyping could potentially assist in clinical decision making regarding the use of aspirin in primary prevention.	Aspirin	213-220	PPARG coactivator 1 beta	Homo sapiens	26-34
29258006-10	2018	If specific protection of PPARGC1B and CNTN4 variant carriers by aspirin is confirmed by additional studies, PPARGC1B and CNTN4 genotyping could potentially assist in clinical decision making regarding the use of aspirin in primary prevention.	Aspirin	213-220	PPARG coactivator 1 beta	Homo sapiens	109-117
29094287-3	2018	OBJECTIVE: The current work aimed to investigate the possibility of targeting AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), and beta-catenin proteins through combined metformin/aspirin treatment in the HepG2 cell line, and to explore such molecular targets in Egyptian HCC patients.	Aspirin	206-213	mechanistic target of rapamycin kinase	Homo sapiens	115-144
29094287-3	2018	OBJECTIVE: The current work aimed to investigate the possibility of targeting AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), and beta-catenin proteins through combined metformin/aspirin treatment in the HepG2 cell line, and to explore such molecular targets in Egyptian HCC patients.	Aspirin	206-213	mechanistic target of rapamycin kinase	Homo sapiens	146-150
29094287-7	2018	RESULTS: Metformin/aspirin combined treatment had a synergistic effect on cell cycle arrest at the G2/M phase and apoptosis induction in a caspase-dependent manner via downregulation of pAMPK and mTOR protein expression.	Aspirin	19-26	mechanistic target of rapamycin kinase	Homo sapiens	196-200
29094287-10	2018	CONCLUSIONS: Targeting AMPK, mTOR and beta-catenin by combined metformin/aspirin treatment could be a promising therapeutic strategy for Egyptian HCC patients, and possibly other HCC patients.	Aspirin	73-80	mechanistic target of rapamycin kinase	Homo sapiens	29-33
29399298-4	2018	RESULTS: APOA5 rs662799 genotype distributions in both the KoGES-ASAS and KNHANES groups were 50.6% for TT, 41.3% for TC, and 8.1% for CC, which are similar to those in previous reports.	Aspirin	65-69	apolipoprotein A5	Homo sapiens	9-14
29399298-9	2018	CONCLUSIONS: The C allele of APOA5 rs662799 was found to be significantly associated with cardiometabolic traits in a large Korean population from the KoGES-ASAS and KNHANES.	Aspirin	157-161	apolipoprotein A5	Homo sapiens	29-34
29378362-9	2018	Plasma level of TXA2 metabolite, TXB2, was lower in both aspirin- and nstpbp5185-treated mice, while the urinary 2,3-dinor-6-keto PGF1alpha (a PGI2 metabolite) and plasma iPF2alpha-III were not altered.	Aspirin	57-64	prostaglandin I receptor (IP)	Mus musculus	143-147
29518782-7	2018	RESULTS: Aspirin significantly suppressed the expression of alpha-smooth muscle actin (alpha-SMA; 1.19+-0.19-fold) and collagen I (0.95+-0.09-fold) in TAC mice.	Aspirin	9-16	actin alpha 2, smooth muscle, aorta	Mus musculus	60-85
29635252-10	2018	CONCLUSIONS: Our findings suggest that PEAR1, P2Y12, and UGT2A1 genetic variants may be potential biomarkers that can be used to guide clinical applications of clopidogrel and aspirin in Chinese patients.	Aspirin	176-183	platelet endothelial aggregation receptor 1	Homo sapiens	39-44
29316620-2	2018	Aspirin is the most commonly used non-steroid anti-inflammatory drugs (NSAIDs), and it irreversibly inhibits cyclooxygenase-1 and -2 (COX1, COX2).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	109-132
29316620-2	2018	Aspirin is the most commonly used non-steroid anti-inflammatory drugs (NSAIDs), and it irreversibly inhibits cyclooxygenase-1 and -2 (COX1, COX2).	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	140-144
29316620-4	2018	The lower aspirin doses causing only minimal gastrointestinal disturbance, ideal for long-term use, can achieve only partial and transitory inhibition of COX2.	Aspirin	10-17	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	154-158
29316620-5	2018	Aspirin"s principal metabolite, salicylic acid, is also found in fruits and vegetables that inhibit COX2.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	100-104
29308184-0	2018	Aspirin inhibited the metastasis of colon cancer cells by inhibiting the expression of toll-like receptor 4.	Aspirin	0-7	toll-like receptor 4	Mus musculus	87-107
29308184-11	2018	Aspirin treatment lead to the downregulation of TLR4 on C26 cells which resulted in the decrease of C26 cells migration and EMT phenotype that induced by LPS.	Aspirin	0-7	toll-like receptor 4	Mus musculus	48-52
29308184-12	2018	Additionally, the inhibitory effect from aspirin on the expression of TLR4 on C26 cells leads to the downregulation of NF-kappaB.	Aspirin	41-48	toll-like receptor 4	Mus musculus	70-74
29308184-12	2018	Additionally, the inhibitory effect from aspirin on the expression of TLR4 on C26 cells leads to the downregulation of NF-kappaB.	Aspirin	41-48	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	119-128
29308184-13	2018	Conclusion: The results of our study indicate that LPS origin from intestinal flora may promote the metastasis of colon cancer to liver and aspirin may inhibit the metastasis of colon cancer by inhibiting the expression of TLR4.	Aspirin	140-147	toll-like receptor 4	Mus musculus	223-227
29518782-7	2018	RESULTS: Aspirin significantly suppressed the expression of alpha-smooth muscle actin (alpha-SMA; 1.19+-0.19-fold) and collagen I (0.95+-0.09-fold) in TAC mice.	Aspirin	9-16	actin alpha 2, smooth muscle, aorta	Mus musculus	87-96
29518782-8	2018	Aspirin, at doses of 100 and 1000 microM, also significantly suppressed angiotensin II-induced alpha-SMA and collagen I in cultured CFs.	Aspirin	0-7	actin alpha 2, smooth muscle, aorta	Mus musculus	95-104
29518782-9	2018	The enhanced phosphorylation of Erk1/2 caused by TAC (p-Erk1, 1.49+-0.19-fold; p-Erk2, 1.96+-0.68-fold) was suppressed by aspirin (p-Erk1, 1.04+-0.15-fold; p-Erk2, 0.87+-0.06-fold).	Aspirin	122-129	mitogen-activated protein kinase 1	Mus musculus	81-85
29518782-9	2018	The enhanced phosphorylation of Erk1/2 caused by TAC (p-Erk1, 1.49+-0.19-fold; p-Erk2, 1.96+-0.68-fold) was suppressed by aspirin (p-Erk1, 1.04+-0.15-fold; p-Erk2, 0.87+-0.06-fold).	Aspirin	122-129	mitogen-activated protein kinase 1	Mus musculus	158-162
28583479-1	2018	BACKGROUND: The pathogenesis of aspirin-exacerbated respiratory disease (AERD) is characterized by the low expression of cyclooxygenase-2 (COX-2) in airway epithelia, which decreases the production of prostaglandin E2 (PGE2).	Aspirin	32-39	prostaglandin-endoperoxide synthase 2	Homo sapiens	121-137
29468963-7	2018	It is important to note that some classical drugs available on the pharmaceutical market, such as acetylsalicylic acid, were also described more recently as NF-kappaB pathway modulators as IKKbeta inhibitors.	Aspirin	98-118	nuclear factor kappa B subunit 1	Homo sapiens	157-166
29195233-5	2018	We show herein that, ASA-BMMSCs treatment reduced inflammatory infiltration and alveolar bone loss in periodontitis rats, reflected by immunohistochemistry staining of OPG/RANK-L and Micro-CT. Levels of TNF-alpha and IL-17 decreased while IL-10 increased after the treatment of ASA-BMMSCs in periodontitis rats.	Aspirin	21-24	tumor necrosis factor	Rattus norvegicus	203-212
28583479-1	2018	BACKGROUND: The pathogenesis of aspirin-exacerbated respiratory disease (AERD) is characterized by the low expression of cyclooxygenase-2 (COX-2) in airway epithelia, which decreases the production of prostaglandin E2 (PGE2).	Aspirin	32-39	prostaglandin-endoperoxide synthase 2	Homo sapiens	139-144
30091133-2	2018	The higher rate of ASA resistance reported in the literature may be mainly due to the cyclooxygenase-1 non-specific assays, non-compliance, and underdosing.	Aspirin	19-22	prostaglandin-endoperoxide synthase 1	Homo sapiens	86-102
28238019-13	2018	NaHS and CORM-2 prevented aspirin-induced gastric mucosal lipid peroxidation via restoration of microcirculation and antioxidative GPx-1 protein expression.	Aspirin	26-33	glutathione peroxidase 1	Rattus norvegicus	131-136
28987816-0	2018	Aspirin increases ferroportin 1 expression by inhibiting hepcidin via the JAK/STAT3 pathway in interleukin 6-treated PC-12 cells.	Aspirin	0-7	solute carrier family 40 member 1	Rattus norvegicus	18-31
30025403-12	2018	Using a transgenic mouse model that imitates human MEN1, this study provides first evidence that aspirin and enalapril are effective chemopreventive agents that aid in the progression of pNENs.	Aspirin	97-104	menin 1	Homo sapiens	51-55
29115440-0	2018	Aspirin ameliorates cerebral infarction through regulation of TLR4/NF-kappaB-mediated endoplasmic reticulum stress in mouse model.	Aspirin	0-7	toll-like receptor 4	Mus musculus	62-66
29115440-0	2018	Aspirin ameliorates cerebral infarction through regulation of TLR4/NF-kappaB-mediated endoplasmic reticulum stress in mouse model.	Aspirin	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	67-76
29115440-6	2018	Aspirin treatment suppressed toll-like receptor (TLR)4 and nuclear factor (NF)-kappaB expression in cerebrovascular endothelial cells.	Aspirin	0-7	toll-like receptor 4	Mus musculus	49-54
29115440-6	2018	Aspirin treatment suppressed toll-like receptor (TLR)4 and nuclear factor (NF)-kappaB expression in cerebrovascular endothelial cells.	Aspirin	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	59-85
29115440-8	2018	It was identified that knockdown of TLR4 inhibited aspirin-mediated downregulation of NF-kappaB signaling pathway and ER stress in cerebrovascular endothelial cells.	Aspirin	51-58	toll-like receptor 4	Mus musculus	36-40
29115440-8	2018	It was identified that knockdown of TLR4 inhibited aspirin-mediated downregulation of NF-kappaB signaling pathway and ER stress in cerebrovascular endothelial cells.	Aspirin	51-58	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	86-95
29115440-11	2018	These results suggested that aspirin may improve cerebral infarction by downregulating TLR4/NF-kappaB-mediated ER stress in a mouse model.	Aspirin	29-36	toll-like receptor 4	Mus musculus	87-91
29115440-11	2018	These results suggested that aspirin may improve cerebral infarction by downregulating TLR4/NF-kappaB-mediated ER stress in a mouse model.	Aspirin	29-36	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	92-101
28987816-4	2018	The data imply that ASA increases Fpn1 expression by inhibiting hepcidin expression via the IL-6/JAK/STAT3 pathway and show that the reduced content of Ft-L is due to the increased Fpn1 and subsequent iron release in the cells.	Aspirin	20-23	solute carrier family 40 member 1	Rattus norvegicus	34-38
28987816-4	2018	The data imply that ASA increases Fpn1 expression by inhibiting hepcidin expression via the IL-6/JAK/STAT3 pathway and show that the reduced content of Ft-L is due to the increased Fpn1 and subsequent iron release in the cells.	Aspirin	20-23	hepcidin antimicrobial peptide	Rattus norvegicus	64-72
28987816-4	2018	The data imply that ASA increases Fpn1 expression by inhibiting hepcidin expression via the IL-6/JAK/STAT3 pathway and show that the reduced content of Ft-L is due to the increased Fpn1 and subsequent iron release in the cells.	Aspirin	20-23	interleukin 6	Rattus norvegicus	92-96
28987816-5	2018	The reduction of iron in neuronal cells by the increased expression of Fpn1 might be partly associated with the beneficial effects of ASA on mood disorders, AD and PD.	Aspirin	134-137	solute carrier family 40 member 1	Rattus norvegicus	71-75
28987816-0	2018	Aspirin increases ferroportin 1 expression by inhibiting hepcidin via the JAK/STAT3 pathway in interleukin 6-treated PC-12 cells.	Aspirin	0-7	hepcidin antimicrobial peptide	Rattus norvegicus	57-65
28987816-2	2018	We demonstrated that IL-6 alone could induce a severe decline in Fpn1 expression and cell viability, and an increase in Ft-L protein, while ASA could markedly diminish the effects of IL-6 on these parameters.	Aspirin	140-143	interleukin 6	Rattus norvegicus	183-187
29172674-0	2017	Single nucleotide polymorphisms in TNF are associated with susceptibility to aspirin-exacerbated respiratory disease but not to cytokine levels: a study in Mexican mestizo population.	Aspirin	77-84	tumor necrosis factor	Homo sapiens	35-38
29204620-2	2017	Aspirin exerts antiplatelet effects through irreversible inhibition of cyclooxygenase-1, whereas its anticancer effects may be due to inhibition of cyclooxygenase-2 and other pathways.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	71-87
29087320-8	2017	Inhibition of NOS2 and COX2 using amino-guanidine and aspirin/indomethacin yielded an additive reduction in the growth of MDA-MB-231 tumor xenografts.	Aspirin	54-61	nitric oxide synthase 2	Homo sapiens	14-18
29087320-8	2017	Inhibition of NOS2 and COX2 using amino-guanidine and aspirin/indomethacin yielded an additive reduction in the growth of MDA-MB-231 tumor xenografts.	Aspirin	54-61	prostaglandin-endoperoxide synthase 2	Homo sapiens	23-27
29131082-2	2018	We previously described that aspirin has effects beyond inhibition of platelet aggregation, as it inhibited thrombin-mediated release of sphingosine-1-phosphate (S1P) from human platelets.	Aspirin	29-36	coagulation factor II, thrombin	Homo sapiens	108-116
29172674-1	2017	AIM: To evaluate the association of three single nucleotide polymorphisms in TNF and one in LTA in Mexican patients with aspirin-exacerbated respiratory disease (AERD) and the correlation of those single nucleotide polymorphisms with serum levels of TNF-alpha.	Aspirin	121-128	tumor necrosis factor	Homo sapiens	77-80
29285098-0	2017	Aspirin suppresses TNF-alpha-induced MMP-9 expression via NF-kappaB and MAPK signaling pathways in RAW264.7 cells.	Aspirin	0-7	tumor necrosis factor	Mus musculus	19-28
29185103-12	2017	Aspirin, ticagrelor, and rosuvastatin decreased serum IL-1beta and IL-6 levels.	Aspirin	0-7	interleukin 1 beta	Mus musculus	54-62
29185103-12	2017	Aspirin, ticagrelor, and rosuvastatin decreased serum IL-1beta and IL-6 levels.	Aspirin	0-7	interleukin 6	Mus musculus	67-71
29185103-14	2017	Aspirin, ticagrelor, and rosuvastatin all decreased TNF-alpha levels.	Aspirin	0-7	tumor necrosis factor	Mus musculus	52-61
29285098-6	2017	It was also observed that aspirin has a suppressive effect on the activation of nuclear factor (NF)-kappaB and inhibits the phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases 1/2, p38 and c-Jun N-terminal kinase.	Aspirin	26-33	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	80-106
29285098-0	2017	Aspirin suppresses TNF-alpha-induced MMP-9 expression via NF-kappaB and MAPK signaling pathways in RAW264.7 cells.	Aspirin	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	58-67
29285098-7	2017	Furthermore, subsequent to inhibition of the MAPK pathway by specific inhibitors (PD98059, SB203580 and SP600125), the expression of MMP-9 was reduced, indicating that the inhibitory effect of aspirin on MMP-9 in TNF-alpha-treated RAW264.7 cells may be, at least in part, through suppression of NF-kappaB activation and the MAPK pathway.	Aspirin	193-200	tumor necrosis factor	Mus musculus	213-222
29285098-3	2017	The present study aimed to investigate the pharmacological effects of aspirin on tumor necrosis factor-alpha (TNF-alpha)-induced MMP-9 expression and the underlying molecular mechanisms in murine macrophage RAW264.7 cells.	Aspirin	70-77	tumor necrosis factor	Mus musculus	81-108
29285098-7	2017	Furthermore, subsequent to inhibition of the MAPK pathway by specific inhibitors (PD98059, SB203580 and SP600125), the expression of MMP-9 was reduced, indicating that the inhibitory effect of aspirin on MMP-9 in TNF-alpha-treated RAW264.7 cells may be, at least in part, through suppression of NF-kappaB activation and the MAPK pathway.	Aspirin	193-200	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	295-304
29285098-3	2017	The present study aimed to investigate the pharmacological effects of aspirin on tumor necrosis factor-alpha (TNF-alpha)-induced MMP-9 expression and the underlying molecular mechanisms in murine macrophage RAW264.7 cells.	Aspirin	70-77	tumor necrosis factor	Mus musculus	110-119
29200971-0	2017	vWF/ADAMTS13 is associated with on-aspirin residual platelet reactivity and clinical outcome in patients with stable coronary artery disease.	Aspirin	35-42	von Willebrand factor	Homo sapiens	0-3
29149707-0	2017	Over-expression of cyclooxygenase-2 in increased reticulated platelets leads to aspirin resistance after elective off-pump coronary artery bypass surgery.	Aspirin	80-87	prostaglandin-endoperoxide synthase 2	Homo sapiens	19-35
29075787-3	2017	Our goal here was to investigate the ability of salicylic acid metabolites, known to be generated through cytochrome P450 (CYP450) enzymes, and its derivatives as cyclin dependent kinase (CDK) inhibitors to gain new insights into aspirin"s chemopreventive actions.	Aspirin	230-237	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	106-121
29075787-3	2017	Our goal here was to investigate the ability of salicylic acid metabolites, known to be generated through cytochrome P450 (CYP450) enzymes, and its derivatives as cyclin dependent kinase (CDK) inhibitors to gain new insights into aspirin"s chemopreventive actions.	Aspirin	230-237	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	123-129
27937053-2	2017	Genetic polymorphisms in platelet endothelial aggregation receptor 1 (PEAR1) were associated with responsiveness to aspirin and P2Y12 receptor antagonists.	Aspirin	116-123	platelet endothelial aggregation receptor 1	Homo sapiens	25-68
27937053-2	2017	Genetic polymorphisms in platelet endothelial aggregation receptor 1 (PEAR1) were associated with responsiveness to aspirin and P2Y12 receptor antagonists.	Aspirin	116-123	platelet endothelial aggregation receptor 1	Homo sapiens	70-75
29200971-2	2017	It has been shown that coronary artery disease (CAD) patients with high on-aspirin RPR have elevated levels of von Willebrand factor (vWF).	Aspirin	75-82	von Willebrand factor	Homo sapiens	111-132
29200971-2	2017	It has been shown that coronary artery disease (CAD) patients with high on-aspirin RPR have elevated levels of von Willebrand factor (vWF).	Aspirin	75-82	von Willebrand factor	Homo sapiens	134-137
29200971-16	2017	Conclusion: These results indicate that ADAMTS13 is of importance for RPR, and that it in combination with vWF also is associated with clinical endpoints in stable CAD patients on aspirin.	Aspirin	180-187	von Willebrand factor	Homo sapiens	107-110
28844979-1	2017	BACKGROUND: The current standard-of-care antiplatelet therapy in cardiovascular disease patients is consisted of cyclooxygenase-1 (COX-1) inhibitor aspirin, along with a platelet receptor P2Y12 antagonist.	Aspirin	148-155	prostaglandin-endoperoxide synthase 1	Homo sapiens	113-129
28844979-2	2017	Recently, the triple antiplatelet therapy with aspirin, a P2Y12 receptor antagonist and a protease activated receptor-1 (PAR-1) antagonist, has been suggested for the secondary prevention of atherothrombotic events, however presented an increased risk of bleeding.	Aspirin	47-54	coagulation factor II thrombin receptor	Homo sapiens	90-119
28866366-1	2017	Interleukin-8 (CXCL8) was originally described asa chemokine whose main function is the attraction of a polymorphonuclear inflammatory leukocyte infiltrate acting on CXCR1/2.	Aspirin	47-50	C-X-C motif chemokine ligand 8	Homo sapiens	0-13
28964633-2	2017	We previously reported radiolabeled asymmetric urea derivatives asa PSMA-targeting radiotracer for single-photon emission computed tomography (SPECT) and positron emission tomography (PET) imaging.	Aspirin	64-67	folate hydrolase 1	Homo sapiens	68-72
28843992-1	2017	The discovery of druggable oncogenic drivers (i.e. EGFR and ALK), along with the introduction of comprehensive tumor genotyping techniques into the daily clinical practice define non-small-cell lung cancer (NSCLC) asa group of heterogeneous diseases, requiring a context-personalized clinico-therapeutical approach.	Aspirin	214-217	epidermal growth factor receptor	Homo sapiens	51-55
28866366-1	2017	Interleukin-8 (CXCL8) was originally described asa chemokine whose main function is the attraction of a polymorphonuclear inflammatory leukocyte infiltrate acting on CXCR1/2.	Aspirin	47-50	C-X-C motif chemokine ligand 8	Homo sapiens	15-20
28866366-5	2017	Thus, IL-8 serum concentrations have been shown to be useful asa pharmacodynamic biomarker to early detect response to immunotherapy.	Aspirin	61-64	C-X-C motif chemokine ligand 8	Homo sapiens	6-10
28936577-9	2017	Aspirin removal on IrO2/Ti-f and cry-Ir/Ti-f after 4h.	Aspirin	0-7	TYRO3 protein tyrosine kinase	Homo sapiens	24-28
28936577-9	2017	Aspirin removal on IrO2/Ti-f and cry-Ir/Ti-f after 4h.	Aspirin	0-7	TYRO3 protein tyrosine kinase	Homo sapiens	40-44
28497369-0	2017	Co-enzyme Q10 and acetyl salicylic acid enhance Hsp70 expression in primary chicken myocardial cells to protect the cells during heat stress.	Aspirin	18-39	heat shock protein family A (Hsp70) member 2	Gallus gallus	48-53
29055792-8	2017	Aspirin reversed the inhibitory effect of TNF-a on trophoblast cell integration into endothelial cellular networks.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	42-47
29055792-9	2017	TNF-a increased PGF1a production (128+-11%, p&lt;0.05), whilst aspirin reversed the TNF-a effect on PGF1a production (19+-4%, p&lt;0.01).	Aspirin	63-70	tumor necrosis factor	Homo sapiens	84-89
29055792-12	2017	Aspirin improves trophoblast cell integration into endothelial cellular networks by inhibiting the effect of TNF-a via PGI2 with no significant effect on antiangiogenic, invasive or endothelial activation markers.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	109-114
28071789-0	2017	Aspirin-triggered lipoxin A4 inhibits atherosclerosis progression in apolipoprotein E-/- mice.	Aspirin	0-7	apolipoprotein E	Mus musculus	69-85
28497369-1	2017	We investigated the effects of co-enzyme Q10 (Q10) and acetyl salicylic acid (ASA) on expression of Hsp70 in the protection of primary chicken myocardial cells during heat stress.	Aspirin	55-76	heat shock protein family A (Hsp70) member 2	Gallus gallus	100-105
28497369-1	2017	We investigated the effects of co-enzyme Q10 (Q10) and acetyl salicylic acid (ASA) on expression of Hsp70 in the protection of primary chicken myocardial cells during heat stress.	Aspirin	78-81	heat shock protein family A (Hsp70) member 2	Gallus gallus	100-105
28497369-2	2017	Western blot analysis showed that Q10 and ASA accelerated the induction of Hsp70 when chicken myocardial cells were exposed to hyperthermia.	Aspirin	42-45	heat shock protein family A (Hsp70) member 2	Gallus gallus	75-80
28497369-5	2017	Quantification of heat shock factors (HSF) indicated that treatment of ASA increased the expression of HSF-1 and HSF-3 during heat stress.	Aspirin	71-74	heat shock factor protein 3	Gallus gallus	103-108
28497369-5	2017	Quantification of heat shock factors (HSF) indicated that treatment of ASA increased the expression of HSF-1 and HSF-3 during heat stress.	Aspirin	71-74	heat shock factor protein 3	Gallus gallus	113-118
28497369-8	2017	Subcellular distribution analysis of HSF-1 and HSF-3 showed that in response to heat stress ASA promoted nuclear translocation of HSF-1 and HSF-3, while Q10 promoted only HSF-1 nuclear translocation.	Aspirin	92-95	heat shock factor protein 3	Gallus gallus	37-42
28497369-8	2017	Subcellular distribution analysis of HSF-1 and HSF-3 showed that in response to heat stress ASA promoted nuclear translocation of HSF-1 and HSF-3, while Q10 promoted only HSF-1 nuclear translocation.	Aspirin	92-95	heat shock factor protein 3	Gallus gallus	47-52
28497369-8	2017	Subcellular distribution analysis of HSF-1 and HSF-3 showed that in response to heat stress ASA promoted nuclear translocation of HSF-1 and HSF-3, while Q10 promoted only HSF-1 nuclear translocation.	Aspirin	92-95	heat shock factor protein 3	Gallus gallus	130-135
28497369-8	2017	Subcellular distribution analysis of HSF-1 and HSF-3 showed that in response to heat stress ASA promoted nuclear translocation of HSF-1 and HSF-3, while Q10 promoted only HSF-1 nuclear translocation.	Aspirin	92-95	heat shock factor protein 3	Gallus gallus	140-145
28497369-8	2017	Subcellular distribution analysis of HSF-1 and HSF-3 showed that in response to heat stress ASA promoted nuclear translocation of HSF-1 and HSF-3, while Q10 promoted only HSF-1 nuclear translocation.	Aspirin	92-95	heat shock factor protein 3	Gallus gallus	130-135
28497369-10	2017	Real-time PCR analysis revealed that ASA induces HSF-1 and HSF-3 binding to Hsp70 HSE, while Q10 only induces HSF1 binding to Hsp70 HSE, in agreement with the impact of HSF1 and HSF3 silencing on Hsp70 expression.	Aspirin	37-40	heat shock factor protein 3	Gallus gallus	49-54
28497369-10	2017	Real-time PCR analysis revealed that ASA induces HSF-1 and HSF-3 binding to Hsp70 HSE, while Q10 only induces HSF1 binding to Hsp70 HSE, in agreement with the impact of HSF1 and HSF3 silencing on Hsp70 expression.	Aspirin	37-40	heat shock factor protein 3	Gallus gallus	59-64
28497369-10	2017	Real-time PCR analysis revealed that ASA induces HSF-1 and HSF-3 binding to Hsp70 HSE, while Q10 only induces HSF1 binding to Hsp70 HSE, in agreement with the impact of HSF1 and HSF3 silencing on Hsp70 expression.	Aspirin	37-40	heat shock protein family A (Hsp70) member 2	Gallus gallus	76-81
28497369-11	2017	These data demonstrate that ASA and Q10 both induce the expression of Hsp70 to protect chicken primary myocardial cells during heat stress, but through distinct pathways.	Aspirin	28-31	heat shock protein family A (Hsp70) member 2	Gallus gallus	70-75
29118740-9	2017	Treatment with ASA or CEL did not affect TNF-alpha, IL-6, IL-8, IL-10, and NO production by infected cells, but increased IL-1beta production by them.	Aspirin	15-18	interleukin 1 beta	Homo sapiens	122-130
29031392-10	2017	After 7 days of aspirin-only ingestion, apoA-I exchange was significantly modified by increasing levels of DHA concentration, with increased apoA-I exchange observed up until log(DHA) of 4.6 and decreased exchange thereafter (p = 0.03).	Aspirin	16-23	apolipoprotein A1	Homo sapiens	40-46
29031392-12	2017	Aspirin"s effects on apoA-I exchange were the greatest when EPA or DHA concentrations were moderate compared to high or low.	Aspirin	0-7	apolipoprotein A1	Homo sapiens	21-27
29260520-9	2017	Occludin expression increased and reached maximum level 120 min after aspirin treatment in brain microvascular endothelial cells.	Aspirin	70-77	occludin	Mus musculus	0-8
29260520-12	2017	CONCLUSION: Aspirin reduced occurrences of the brain metastasis of lung cancer in animal model,which may be caused by inhibition of PGE2 released by lung cancer cells and upregulation of occludin expression therefore leading to decrease in BBB permeability.	Aspirin	12-19	occludin	Mus musculus	187-195
29142602-11	2017	Treatment of MKN45 cells with aspirin reduced the levels of phosphorylated AKT by activating PPARalpha, whereas treatment with apatinib inhibited the phosphorylation of vascular endothelial growth factor receptor 2 and phosphoinositide-3 kinase in MKN45 cells.	Aspirin	30-37	AKT serine/threonine kinase 1	Homo sapiens	75-78
29045972-5	2017	RESULTS: The proliferation of GMSCs and the expressions of CD105, CD146 in GMSCs were increased after ASA treatment.	Aspirin	102-105	melanoma cell adhesion molecule	Mus musculus	66-71
28939073-11	2017	Furthermore, next generation sequencing validated deletion of CDKN2A/p16 and reported it asa common variant with a nonsense mutation having stop /loss of function of the gene in recurrent cases.	Aspirin	89-92	cyclin dependent kinase inhibitor 2A	Homo sapiens	62-68
29042646-4	2017	Aspirin use was associated with a significant reduction of CDH1 methylation in AM (OR: 0.15, 95% CI: 0.06-0.41, p = 0.0002), but was less effective in reversing the methylation that occurred in IM.	Aspirin	0-7	cadherin 1	Homo sapiens	59-63
28948496-6	2017	Recent findings suggest that thrombocytosis carries a higher risk of bleeding than thrombosis in MPN, and aspirin may exacerbate this risk of bleeding, particularly in CALR-mutated ET.	Aspirin	106-113	calreticulin	Homo sapiens	168-172
28707077-0	2017	Association of ABCB1 promoter methylation with aspirin exposure, platelet function, and clinical outcomes in Chinese intracranial artery stenosis patients.	Aspirin	47-54	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
28707077-2	2017	ABCB1 is involved in the intestinal absorption of aspirin.	Aspirin	50-57	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
28707077-3	2017	We aimed to investigate the impact of methylation status of ABCB1 promoter on aspirin exposure, platelet function, and clinical outcomes in Chinese intracranial artery stenosis patients receiving antiplatelet treatment.	Aspirin	78-85	ATP binding cassette subfamily B member 1	Homo sapiens	60-65
28849118-0	2017	Aspirin inhibits the proliferation of human uterine leiomyoma cells by downregulation of K-Ras-p110alpha interaction.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	95-104
29045972-2	2017	METHODS: Flow cytometry analysis were used to analyze the role of ASA in the expression of stem cells surface markers CD146, CD105, CD90, CD34 and CD45 in GMSCs,and the GMSCs proliferation was analyzed by 5-bromo-2-deoxyuridine (BrdU) staining and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.	Aspirin	66-69	melanoma cell adhesion molecule	Mus musculus	118-123
29045972-2	2017	METHODS: Flow cytometry analysis were used to analyze the role of ASA in the expression of stem cells surface markers CD146, CD105, CD90, CD34 and CD45 in GMSCs,and the GMSCs proliferation was analyzed by 5-bromo-2-deoxyuridine (BrdU) staining and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.	Aspirin	66-69	thymus cell antigen 1, theta	Mus musculus	132-136
28899503-10	2017	RESULTS: Under non-inflammatory conditions P. tremula E and ASA increased cellular proteins (P) IL-8 and IL-10; S. virgaurea E modulated IL-1alpha, IL-10, IL-15 and Groalpha (P).	Aspirin	60-63	C-X-C motif chemokine ligand 8	Homo sapiens	96-100
28899503-16	2017	Secretion of IL-8 and IL-6 was reduced by STW1 and ASA.	Aspirin	51-54	C-X-C motif chemokine ligand 8	Homo sapiens	13-17
28899503-16	2017	Secretion of IL-8 and IL-6 was reduced by STW1 and ASA.	Aspirin	51-54	interleukin 6	Homo sapiens	22-26
28687354-0	2017	Aspirin disrupts the mTOR-Raptor complex and potentiates the anti-cancer activities of sorafenib via mTORC1 inhibition.	Aspirin	0-7	mechanistic target of rapamycin kinase	Homo sapiens	21-25
28687354-3	2017	In this study, we revealed the mechanism underlying the effects of aspirin on AMPK-mTOR signaling, and described a mechanism-based rationale for the use of aspirin in cancer therapy.	Aspirin	67-74	mechanistic target of rapamycin kinase	Homo sapiens	83-87
28687354-3	2017	In this study, we revealed the mechanism underlying the effects of aspirin on AMPK-mTOR signaling, and described a mechanism-based rationale for the use of aspirin in cancer therapy.	Aspirin	156-163	mechanistic target of rapamycin kinase	Homo sapiens	83-87
28687354-7	2017	Additionally, the combination of aspirin and sorafenib showed synergetic effects via inhibiting mTORC1 signaling and the PI3K/AKT, MAPK/ERK pathways.	Aspirin	33-40	AKT serine/threonine kinase 1	Homo sapiens	126-129
28687354-7	2017	Additionally, the combination of aspirin and sorafenib showed synergetic effects via inhibiting mTORC1 signaling and the PI3K/AKT, MAPK/ERK pathways.	Aspirin	33-40	mitogen-activated protein kinase 1	Homo sapiens	136-139
28849118-5	2017	Further studies revealed that aspirin blocked the interaction between K-Ras and p110alpha by co-immunoprecipitation and immunofluorescence.	Aspirin	30-37	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	80-89
28849118-6	2017	Western blotting demonstrated K-Ras-p110alpha interaction was required for the effects of aspirin-induced inhibition on cell growth and cell cycle transition via cell cycle regulators, including cyclin D1 and cyclin-dependent kinase 2 (CDK2).	Aspirin	90-97	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	36-45
28849118-7	2017	PI3K/Akt/caspase signaling pathway was involved in human uterine leiomyoma cell growth under aspirin treatment.	Aspirin	93-100	AKT serine/threonine kinase 1	Homo sapiens	5-8
28939079-1	2017	BACKGROUND: To investigate the clinical usefulness of transoral bisected resection (TBR) asa new method to secure adequate deep resection margin in T1-2 oral tongue squamous cell carcinomas (SCC).	Aspirin	89-92	CD6 molecule	Homo sapiens	148-152
28849118-8	2017	Taken together, these results suggest that aspirin inhibited human uterine leiomyoma cell growth by regulating K-Ras-p110alpha interaction.	Aspirin	43-50	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	117-126
29152088-8	2017	Aspirin treatment also led to higher proportions of apoptotic cells and G0/G1 phase arrest in PIK3CA-mutant cells than in PIK3CA-wild-type cells.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	122-128
28849118-9	2017	Aspirin which targeting on interaction between K-Ras and p110alpha may serve as a new therapeutic drug for uterine leiomyoma treatment.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	57-66
29169419-1	2017	Objective To explore the effect of aspirin on the apoptosis and autophagy of human epidermal growth factor receptor 2 (HER2)-positive AU-565 breast cancer cells and triple negative MDA-MB-231 breast cancer cells.	Aspirin	35-42	erb-b2 receptor tyrosine kinase 2	Homo sapiens	83-117
29169419-1	2017	Objective To explore the effect of aspirin on the apoptosis and autophagy of human epidermal growth factor receptor 2 (HER2)-positive AU-565 breast cancer cells and triple negative MDA-MB-231 breast cancer cells.	Aspirin	35-42	erb-b2 receptor tyrosine kinase 2	Homo sapiens	119-123
29152088-0	2017	Aspirin exerts high anti-cancer activity in PIK3CA-mutant colon cancer cells.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	44-50
29152088-9	2017	Aspirin treatment of isogenic SW48 cells carrying a PIK3CA mutation, either c.3140A&gt;G (p.H1047R) or c.1633G&gt;A (p. E545K), resulted in a more significant loss of cell viability compared to wild-type controls.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	52-58
29152088-1	2017	Evidence suggests that nonsteroidal anti-inflammatory drug aspirin (acetylsalicylic acid) may improve patient survival in PIK3CA-mutant colorectal carcinoma, but not in PIK3CA-wild-type carcinoma.	Aspirin	59-66	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	122-128
29152088-1	2017	Evidence suggests that nonsteroidal anti-inflammatory drug aspirin (acetylsalicylic acid) may improve patient survival in PIK3CA-mutant colorectal carcinoma, but not in PIK3CA-wild-type carcinoma.	Aspirin	68-88	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	122-128
29152088-2	2017	However, whether aspirin directly influences the viability of PIK3CA-mutant colon cancer cells is poorly understood.	Aspirin	17-24	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	62-68
29152088-3	2017	We conducted in vitro experiments to test our hypothesis that the anti-proliferative activity of aspirin might be stronger for PIK3CA-mutant colon cancer cells than for PIK3CA-wild-type colon cancer cells.	Aspirin	97-104	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	127-133
29152088-3	2017	We conducted in vitro experiments to test our hypothesis that the anti-proliferative activity of aspirin might be stronger for PIK3CA-mutant colon cancer cells than for PIK3CA-wild-type colon cancer cells.	Aspirin	97-104	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	169-175
29152088-7	2017	Aspirin induced greater dose-dependent loss of cell viability in PIK3CA-mutant cells than in PIK3CA-wild-type cells after treatment for 48 and 72 hours.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	65-71
29152088-7	2017	Aspirin induced greater dose-dependent loss of cell viability in PIK3CA-mutant cells than in PIK3CA-wild-type cells after treatment for 48 and 72 hours.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	93-99
29152088-8	2017	Aspirin treatment also led to higher proportions of apoptotic cells and G0/G1 phase arrest in PIK3CA-mutant cells than in PIK3CA-wild-type cells.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	94-100
28910305-11	2017	The results suggest that aspirin increase metabolism and regulate germline signalling to activate downstream DAF-12 and DAF-16 to extend lifespan.	Aspirin	25-32	Nuclear hormone receptor family member daf-12	Caenorhabditis elegans	109-115
28900541-0	2017	Simultaneous silencing of ACSL4 and induction of GADD45B in hepatocellular carcinoma cells amplifies the synergistic therapeutic effect of aspirin and sorafenib.	Aspirin	139-146	acyl-CoA synthetase long chain family member 4	Homo sapiens	26-31
28900541-9	2017	Importantly, clinical evidence has independently corroborated that survival of HCC patients expressing ACSL4highGADD45Blow was significantly poorer compared to patients with ACSL4lowGADD45Bhigh, thus demonstrating the potential clinical value of combining aspirin and sorafenib for HCC patients expressing ACSL4highGADD45Blow.	Aspirin	256-263	acyl-CoA synthetase long chain family member 4	Homo sapiens	103-108
28900541-10	2017	In conclusion, sorafenib and aspirin provide synergistic therapeutic effects on HCC cells that are achieved through simultaneous silencing of ACSL4 and induction of GADD45B expression.	Aspirin	29-36	acyl-CoA synthetase long chain family member 4	Homo sapiens	142-147
28900541-11	2017	Targeting HCC with ACSL4highGADD45Blow expression with aspirin and sorafenib could provide potential synergistic therapeutic benefits.	Aspirin	55-62	acyl-CoA synthetase long chain family member 4	Homo sapiens	19-24
28912509-4	2017	We found that ASA could downregulate the expressions of iNOS and TNF-alpha both in mouse peritoneum macrophages and RAW264.7 cells induced by LPS via the IkappaK/IkappaB/NF-kappaB pathway and a COX2/PGE2/EP2/NF-kappaB feedback loop, without affecting the expressions of FIZZ/YM-1/ARG1 induced by IL-4.	Aspirin	14-17	nitric oxide synthase 2, inducible	Mus musculus	56-60
28912509-4	2017	We found that ASA could downregulate the expressions of iNOS and TNF-alpha both in mouse peritoneum macrophages and RAW264.7 cells induced by LPS via the IkappaK/IkappaB/NF-kappaB pathway and a COX2/PGE2/EP2/NF-kappaB feedback loop, without affecting the expressions of FIZZ/YM-1/ARG1 induced by IL-4.	Aspirin	14-17	tumor necrosis factor	Mus musculus	65-74
29152088-10	2017	Our findings indicate that aspirin causes cell cycle arrest, induces apoptosis, and leads to loss of cell viability more profoundly in PIK3CA-mutated colon cancer cells than in PIK3CA-wild-type colon cancer cells.	Aspirin	27-34	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	135-141
29152088-10	2017	Our findings indicate that aspirin causes cell cycle arrest, induces apoptosis, and leads to loss of cell viability more profoundly in PIK3CA-mutated colon cancer cells than in PIK3CA-wild-type colon cancer cells.	Aspirin	27-34	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	177-183
29152088-11	2017	These findings support the use of aspirin to treat patients with PIK3CA-mutant colon cancer.	Aspirin	34-41	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	65-71
28692111-6	2017	Addition of either P2Y12 antagonist to ASA did not affect any of the circulating cytokines, except for an attenuation of the ASA-induced increase in TNFalpha by ticagrelor.	Aspirin	125-128	tumor necrosis factor	Homo sapiens	149-157
27506478-8	2017	Antipsychotics, over-the-counter vitamin/supplements, aspirin, selective-serotonin-reuptake-inhibitors and anticholinergics were the leading drug classes for PIM.	Aspirin	54-61	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	158-161
28633086-5	2017	The GSH-AsA related genes including APX, MDHAR, and DHAR were commonly upregulated by melatonin and correlated to the antioxidant enzyme activity as well as the content of GSH and AsA, indicating that the increase of GSH and AsA was attributed to the expression of these genes.	Aspirin	8-11	POD1	Triticum aestivum	36-39
28633086-5	2017	The GSH-AsA related genes including APX, MDHAR, and DHAR were commonly upregulated by melatonin and correlated to the antioxidant enzyme activity as well as the content of GSH and AsA, indicating that the increase of GSH and AsA was attributed to the expression of these genes.	Aspirin	180-183	POD1	Triticum aestivum	36-39
28633086-5	2017	The GSH-AsA related genes including APX, MDHAR, and DHAR were commonly upregulated by melatonin and correlated to the antioxidant enzyme activity as well as the content of GSH and AsA, indicating that the increase of GSH and AsA was attributed to the expression of these genes.	Aspirin	180-183	POD1	Triticum aestivum	36-39
28859704-1	2017	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is a disorder of nasal polyposis, asthma, and hypersensitivity respiratory reactions when on systemic cyclooxygenase 1 blockade.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	161-177
28859705-2	2017	Aspirin-exacerbated respiratory disease (AERD) is defined as asthma, chronic rhinosinusitis with nasal polyposis, and hypersensitivity to cyclooxygenase-1 inhibitors.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	138-154
29084693-8	2017	Prothrombin time was significantly decreased by mixing (10 microg) of ASM (16.67+-1.15 sec), ASH (12.33+-0.57 sec), ASC (15.33+-0.57 sec) and ASA (9.0+-1.0 sec) to that of vehicle (20.0+-1.0 sec).	Aspirin	142-145	coagulation factor II, thrombin	Homo sapiens	0-11
28774396-1	2017	OBJECTIVES: The aim of this study was to determine whether aspirin increases heart failure (HF) hospitalization or death in patients with HF with reduced ejection fraction receiving an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB).	Aspirin	59-66	angiotensin I converting enzyme	Homo sapiens	185-214
28520220-12	2017	CONCLUSION: These results indicate that the pro-inflammatory, oxidative stress, procoagulant, and adhesion properties of MPs can be partly blocked by aspirin via the ERK-NO/O2- and p38 -NF-kappaB-VCAM-1 signal pathway, which clarified other functions beyond anti-atherothrombotic of aspirin.	Aspirin	150-157	mitogen-activated protein kinase 1	Homo sapiens	181-184
28520220-12	2017	CONCLUSION: These results indicate that the pro-inflammatory, oxidative stress, procoagulant, and adhesion properties of MPs can be partly blocked by aspirin via the ERK-NO/O2- and p38 -NF-kappaB-VCAM-1 signal pathway, which clarified other functions beyond anti-atherothrombotic of aspirin.	Aspirin	150-157	nuclear factor kappa B subunit 1	Homo sapiens	186-195
28520220-12	2017	CONCLUSION: These results indicate that the pro-inflammatory, oxidative stress, procoagulant, and adhesion properties of MPs can be partly blocked by aspirin via the ERK-NO/O2- and p38 -NF-kappaB-VCAM-1 signal pathway, which clarified other functions beyond anti-atherothrombotic of aspirin.	Aspirin	150-157	vascular cell adhesion molecule 1	Homo sapiens	196-202
28520220-0	2017	Endothelial damage effects of circulating microparticles from patients with stable angina are reduced by aspirin through ERK/p38 MAPKs pathways.	Aspirin	105-112	mitogen-activated protein kinase 3	Homo sapiens	121-124
28520220-0	2017	Endothelial damage effects of circulating microparticles from patients with stable angina are reduced by aspirin through ERK/p38 MAPKs pathways.	Aspirin	105-112	mitogen-activated protein kinase 1	Homo sapiens	125-128
28774396-1	2017	OBJECTIVES: The aim of this study was to determine whether aspirin increases heart failure (HF) hospitalization or death in patients with HF with reduced ejection fraction receiving an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB).	Aspirin	59-66	angiotensin I converting enzyme	Homo sapiens	216-219
28774396-2	2017	BACKGROUND: Because of its cyclooxygenase inhibiting properties, aspirin has been postulated to increase HF events in patients treated with ACE inhibitors or ARBs.	Aspirin	65-72	angiotensin I converting enzyme	Homo sapiens	140-143
28932294-0	2017	Aspirin-Induced Gastric Lesions Alters EGFR and PECAM-1 Immunoreactivity in Wistar Rats: Modulatory Action of Flavonoid Fraction of Musa Paradisiaca.	Aspirin	0-7	platelet and endothelial cell adhesion molecule 1	Rattus norvegicus	48-55
28932294-15	2017	CONCLUSION: The efficacy of Musa paradisiaca in attenuating the damaging effects of aspirin on the gastric mucosa was observed as there was a significantly increased reactivity for EGFR and PECAM-1 in the gastric corpus in a dose-dependent manner.	Aspirin	84-91	platelet and endothelial cell adhesion molecule 1	Rattus norvegicus	190-197
28636992-8	2017	Interestingly, modulation of SOX2 expression by PGF2alpha agonists and upregulation by fibroblast growth factor 1 (FGF-1) rescued melanoma cells from ASA-induced decreased survival and increased apoptosis.	Aspirin	150-153	fibroblast growth factor 1	Mus musculus	87-113
28636992-8	2017	Interestingly, modulation of SOX2 expression by PGF2alpha agonists and upregulation by fibroblast growth factor 1 (FGF-1) rescued melanoma cells from ASA-induced decreased survival and increased apoptosis.	Aspirin	150-153	fibroblast growth factor 1	Mus musculus	115-120
28636992-9	2017	Moreover, PGF2alpha-receptor antagonist, AL8810 mimics ASA-induced decreased melanoma cells survival which was significantly blocked by PGF2alpha and FGF-1.	Aspirin	55-58	fibroblast growth factor 1	Mus musculus	150-155
28533220-6	2017	While aspirin directly inhibits IkappaB kinases (IKKs) to phosphorylate IkappaBalpha for NF-kappaB activation, triptolide does not directly target IKKs or other factors that mediate IKK activation.	Aspirin	6-13	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	72-84
28717171-3	2017	When the clones were treated with the aspirin metabolite salicylate, Akt phosphorylation was decreased and EMT inhibited.	Aspirin	38-45	AKT serine/threonine kinase 1	Homo sapiens	69-72
28668243-2	2017	Diminished PGE2 regulation in aspirin-exacerbated respiratory disease (AERD) leads to respiratory reactions on cyclooxygenase 1 inhibition.	Aspirin	30-37	prostaglandin-endoperoxide synthase 1	Homo sapiens	111-127
28525374-0	2017	The effect of rapamycin, NVP-BEZ235, aspirin, and metformin on PI3K/AKT/mTOR signaling pathway of PIK3CA-related overgrowth spectrum (PROS).	Aspirin	37-44	mechanistic target of rapamycin kinase	Homo sapiens	72-76
28525374-0	2017	The effect of rapamycin, NVP-BEZ235, aspirin, and metformin on PI3K/AKT/mTOR signaling pathway of PIK3CA-related overgrowth spectrum (PROS).	Aspirin	37-44	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	98-104
28525374-6	2017	We assessed the therapeutic effects of four compounds (rapamycin, NVP-BEZ235, aspirin, and metformin) on PI3K/AKT/mTOR signaling pathway and cell growth.	Aspirin	78-85	AKT serine/threonine kinase 1	Homo sapiens	110-113
28525374-6	2017	We assessed the therapeutic effects of four compounds (rapamycin, NVP-BEZ235, aspirin, and metformin) on PI3K/AKT/mTOR signaling pathway and cell growth.	Aspirin	78-85	mechanistic target of rapamycin kinase	Homo sapiens	114-118
28102731-6	2017	When certain nonsteroidal anti-inflammatory drugs (NSAIDs) are taken orally, they block COX-1 acetylation by aspirin with concomitant reduction of aspirin efficacy against platelets in microfluidic assay.	Aspirin	109-116	prostaglandin-endoperoxide synthase 1	Homo sapiens	88-93
28139830-0	2017	Low-Dose Aspirin Acetylates Cyclooxygenase-1 in Human Colorectal Mucosa: Implications for the Chemoprevention of Colorectal Cancer.	Aspirin	9-16	prostaglandin-endoperoxide synthase 1	Homo sapiens	28-44
28279492-1	2017	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is characterized by tissue eosinophilia and mast cell activation, including abundant production of prostaglandin D2 (PGD2).	Aspirin	12-19	prostaglandin D2 synthase	Homo sapiens	158-174
27297424-3	2017	The results showed that aspirin treatment increased the expression of protein kinase B (Akt), the signal transducer and activator of transcription (STAT)-3 and p-IKKalpha/beta and the colocalization of Akt and STAT-3 with Hsp90 during heat stress, which was accompanied by improved viability and low apoptosis.	Aspirin	24-31	signal transducer and activator of transcription 3	Gallus gallus	98-155
28713783-7	2017	Aspirin, a cyclooxygenase 2 inhibitor, prevented the adhesion of THP-1 cells to HUVECs and did not induce ICAM1 and VCAM1 expression in HUVECs treated with SlaA.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	11-27
27297424-3	2017	The results showed that aspirin treatment increased the expression of protein kinase B (Akt), the signal transducer and activator of transcription (STAT)-3 and p-IKKalpha/beta and the colocalization of Akt and STAT-3 with Hsp90 during heat stress, which was accompanied by improved viability and low apoptosis.	Aspirin	24-31	signal transducer and activator of transcription 3	Gallus gallus	210-216
28713783-7	2017	Aspirin, a cyclooxygenase 2 inhibitor, prevented the adhesion of THP-1 cells to HUVECs and did not induce ICAM1 and VCAM1 expression in HUVECs treated with SlaA.	Aspirin	0-7	GLI family zinc finger 2	Homo sapiens	65-70
28410791-2	2017	We hypothesised that a cyclooxygenase-2-selective NSAID plus proton-pump inhibitor is superior to a non-selective NSAID plus proton-pump inhibitor for prevention of recurrent ulcer bleeding in concomitant users of aspirin with previous ulcer bleeding.	Aspirin	214-221	prostaglandin-endoperoxide synthase 2	Homo sapiens	23-39
28528204-5	2017	Remarkably, aspirin strongly reduced the pro-inflammatory IL-1beta and TNF-alpha production, while it increased the anti-inflammatory IL-10 level in LPS-challenged cells.	Aspirin	12-19	interleukin 1 beta	Homo sapiens	58-66
28618757-9	2017	RESULTS: At the end of the study ASA treatments had decreased the fasting blood glucose levels but had interestingly increased the serum AVP levels in diabetics rats.	Aspirin	33-36	arginine vasopressin	Rattus norvegicus	137-140
28618757-10	2017	CONCLUSION: AVP levels were increased 2-fold by ASA treatment in diabetic rats.	Aspirin	48-51	arginine vasopressin	Rattus norvegicus	12-15
28618757-11	2017	For the first time in this study, the hypoglycemic effect of ASA was attributed to an increase in blood volume by AVP levels.	Aspirin	61-64	arginine vasopressin	Rattus norvegicus	114-117
28528204-5	2017	Remarkably, aspirin strongly reduced the pro-inflammatory IL-1beta and TNF-alpha production, while it increased the anti-inflammatory IL-10 level in LPS-challenged cells.	Aspirin	12-19	tumor necrosis factor	Homo sapiens	71-80
28528204-6	2017	Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1.	Aspirin	10-17	nitric oxide synthase 2	Homo sapiens	151-155
28528204-6	2017	Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1.	Aspirin	10-17	kininogen 1	Homo sapiens	157-161
28528204-6	2017	Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1.	Aspirin	10-17	interleukin 1 beta	Homo sapiens	163-170
28528204-6	2017	Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1.	Aspirin	10-17	prostaglandin-endoperoxide synthase 2	Homo sapiens	172-177
28528204-6	2017	Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1.	Aspirin	10-17	transforming growth factor beta 1	Homo sapiens	272-277
28431615-0	2017	Association between PTGS1 polymorphisms and functional outcomes in Chinese patients with stroke during aspirin therapy: Interaction with smoking.	Aspirin	103-110	prostaglandin-endoperoxide synthase 1	Homo sapiens	20-25
28487961-0	2017	Influence of aspirin on the CX3CL1/CX3CR1 signaling pathway in acute pulmonary embolism.	Aspirin	13-20	C-X3-C motif chemokine ligand 1	Rattus norvegicus	28-34
28487961-1	2017	The present study aimed to explore the influence of aspirin on the CX3CL1/CX3CR1 signaling pathway in acute pulmonary embolism (APE) in rats.	Aspirin	52-59	C-X3-C motif chemokine ligand 1	Rattus norvegicus	67-73
28487961-7	2017	Aspirin significantly decreased pulmonary artery pressure, improve pathological changes in the embolism, and decreased the expression of CX3CL1/CX3CR1 and CX3CL1/NF-kappaB.	Aspirin	0-7	C-X3-C motif chemokine ligand 1	Rattus norvegicus	137-143
28487961-7	2017	Aspirin significantly decreased pulmonary artery pressure, improve pathological changes in the embolism, and decreased the expression of CX3CL1/CX3CR1 and CX3CL1/NF-kappaB.	Aspirin	0-7	C-X3-C motif chemokine ligand 1	Rattus norvegicus	155-161
28487961-8	2017	Moreover, the adenovirus-overexpression CX3CL1 vector aggravated the inflammatory changes in APE, which were improved by aspirin.	Aspirin	121-128	C-X3-C motif chemokine ligand 1	Rattus norvegicus	40-46
28487961-10	2017	In conclusion, aspirin improved pathological changes in rats with APE via the CX3CL1/CX3CR1 signaling pathway.	Aspirin	15-22	C-X3-C motif chemokine ligand 1	Rattus norvegicus	78-84
28516213-0	2017	Expression of Concern: Aspirin attenuates insulin resistance in muscle of diet-induced obese rats by inhibiting inducible nitric oxide synthase production and S-nitrosylation of IRbeta/IRS-1 and Akt.	Aspirin	23-30	AKT serine/threonine kinase 1	Rattus norvegicus	195-198
28005558-2	2017	Oxidative stress reflected by F2-isoprostane [8-iso-prostaglandin-F2alpha (8-IsoPGF2alpha)] is a potential mechanism of failure of aspirin to adequately inhibit cyclooxygenase-1.	Aspirin	131-138	prostaglandin-endoperoxide synthase 1	Homo sapiens	161-177
28346830-7	2017	A combination of DHA and ASA efficiently enhanced heterodimer formations of PPARalpha and RXRalpha and increased the expression of neurotrophic factors PSD-95, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF), while inhibiting NFkappaB and COX2.	Aspirin	25-28	glial cell derived neurotrophic factor	Homo sapiens	206-244
28346830-7	2017	A combination of DHA and ASA efficiently enhanced heterodimer formations of PPARalpha and RXRalpha and increased the expression of neurotrophic factors PSD-95, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF), while inhibiting NFkappaB and COX2.	Aspirin	25-28	glial cell derived neurotrophic factor	Homo sapiens	246-250
28346830-7	2017	A combination of DHA and ASA efficiently enhanced heterodimer formations of PPARalpha and RXRalpha and increased the expression of neurotrophic factors PSD-95, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF), while inhibiting NFkappaB and COX2.	Aspirin	25-28	nuclear factor kappa B subunit 1	Homo sapiens	270-278
28346830-7	2017	A combination of DHA and ASA efficiently enhanced heterodimer formations of PPARalpha and RXRalpha and increased the expression of neurotrophic factors PSD-95, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF), while inhibiting NFkappaB and COX2.	Aspirin	25-28	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	283-287
28346830-8	2017	These findings suggest that a combination of DHA and ASA could significantly improve the expression of PSD-95, BDNF, and GDNF by promoting heterodimerization of PPARalpha and RXRalpha, thus supplying a new therapeutic method for PD.	Aspirin	53-56	glial cell derived neurotrophic factor	Homo sapiens	121-125
28431615-1	2017	PURPOSE: Prostaglandin-Endoperoxide Synthase 1 (PTGS1) and smoking may play important roles in aspirin nonresponsiveness, but the effect of their interaction on stroke outcomes remains largely unknown.	Aspirin	95-102	prostaglandin-endoperoxide synthase 1	Homo sapiens	9-46
28431615-1	2017	PURPOSE: Prostaglandin-Endoperoxide Synthase 1 (PTGS1) and smoking may play important roles in aspirin nonresponsiveness, but the effect of their interaction on stroke outcomes remains largely unknown.	Aspirin	95-102	prostaglandin-endoperoxide synthase 1	Homo sapiens	48-53
28431615-11	2017	CONCLUSIONS: In Chinese Han stroke patients with aspirin therapy, the adverse effect of PTGS1 polymorphisms on functional outcomes may be modulated by the smoking status.	Aspirin	49-56	prostaglandin-endoperoxide synthase 1	Homo sapiens	88-93
28431615-12	2017	PTGS1 gene-smoking interaction might in part reflect the heterogeneity in the prognosis of patients treated with aspirin.	Aspirin	113-120	prostaglandin-endoperoxide synthase 1	Homo sapiens	0-5
28238190-9	2017	At subgroup analyses, lower diabetes duration, aspirin, alcohol use, younger age, female gender, smoking (Resv 500 arm) and female gender and aspirin use (Resv 40 arm) were associated with higher PTX3 increments.	Aspirin	47-54	pentraxin 3	Homo sapiens	196-200
28579807-13	2017	Since cyclooxygenase-2 (COX-2) inhibitors (eg, celecoxib) are associated with important cardiovascular events and gastrointestinal harms, more attention is warranted toward CPAs with a favorable benefit-to-risk ratio, such as low-dose aspirin and calcium.	Aspirin	235-242	prostaglandin-endoperoxide synthase 2	Homo sapiens	24-29
28359761-0	2017	Aspirin suppresses the abnormal lipid metabolism in liver cancer cells via disrupting an NFkappaB-ACSL1 signaling.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	89-97
28359761-3	2017	Aspirin is able to inhibit the growth of cancers through targeting nuclear factor kappaB (NF-kappaB).	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	82-88
28359761-3	2017	Aspirin is able to inhibit the growth of cancers through targeting nuclear factor kappaB (NF-kappaB).	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	90-99
28359761-9	2017	Moreover, we validated that aspirin decreased the nuclear levels of NF-kappaB in HepG2 cells.	Aspirin	28-35	nuclear factor kappa B subunit 1	Homo sapiens	68-77
28359761-12	2017	Thus, we conclude that aspirin suppresses the abnormal lipid metabolism in HCC cells via disrupting an NFkappaB-ACSL1 signaling.	Aspirin	23-30	nuclear factor kappa B subunit 1	Homo sapiens	103-111
28415819-0	2017	Aspirin regulation of c-myc and cyclinD1 proteins to overcome tamoxifen resistance in estrogen receptor-positive breast cancer cells.	Aspirin	0-7	estrogen receptor 1	Homo sapiens	86-103
28415819-3	2017	Here, we demonstrated that aspirin not only inhibits the growth of ER-positive breast cancer cell line MCF-7, especially when combined with tamoxifen, but also has a potential function to overcome tamoxifen resistance in MCF-7/TAM.	Aspirin	27-34	estrogen receptor 1	Homo sapiens	67-69
28415819-7	2017	Our study discovered a novel role of aspirin based on its anti-tumor effect, and put forward some kinds of possible mechanisms of tamoxifen resistance in ER-positive breast cancer cells, providing a new strategy for the treatment of ER-positive breast carcinoma.	Aspirin	37-44	estrogen receptor 1	Homo sapiens	233-235
28238190-9	2017	At subgroup analyses, lower diabetes duration, aspirin, alcohol use, younger age, female gender, smoking (Resv 500 arm) and female gender and aspirin use (Resv 40 arm) were associated with higher PTX3 increments.	Aspirin	142-149	pentraxin 3	Homo sapiens	196-200
27770326-0	2017	Aspirin and paracetamol removal using a commercial micro-sized TiO2 catalyst in deionized and tap water.	Aspirin	0-7	SEC14 like lipid binding 2	Homo sapiens	94-97
28177735-7	2017	Aspirin induced a decrease in cell viability as well as an increase in superoxide dismutase (SOD) and catalase (CAT) activities.	Aspirin	0-7	catalase	Rattus norvegicus	112-115
28177735-8	2017	Contrariwise, the co-exposure of cells to aspirin and EOC alleviated every above syndrome by an increase in cell survival and decrease in SOD and CAT activities.	Aspirin	42-49	catalase	Rattus norvegicus	146-149
28460643-12	2017	This is the first report to suggest that the reduction in risk occurs for low-dose aspirin and not for regular-dose aspirin and only among women with the hormone receptor-positive/HER2-negative subtype.	Aspirin	83-90	erb-b2 receptor tyrosine kinase 2	Homo sapiens	180-184
28060561-11	2017	Correspondingly, aspirin treatment significantly accelerated the decrease of orthodontic force-induced secretion of TNF-alpha and IFN-gamma in serum and the expression of TNF-alpha and IFN-gamma in periodontal ligament during relapse.	Aspirin	17-24	tumor necrosis factor	Rattus norvegicus	116-125
28060561-11	2017	Correspondingly, aspirin treatment significantly accelerated the decrease of orthodontic force-induced secretion of TNF-alpha and IFN-gamma in serum and the expression of TNF-alpha and IFN-gamma in periodontal ligament during relapse.	Aspirin	17-24	tumor necrosis factor	Rattus norvegicus	171-180
28448072-1	2017	OBJECTIVES: The association between aspirin use and improved survival after colorectal cancer diagnosis may be more pronounced in tumors that have PIK3CA mutations or high PTGS2 expression.	Aspirin	36-43	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	147-153
28267249-12	2017	Pooled data showed that the median TXB2 level on day 4 in groups receiving ASA 162 mg twice-daily or 81 mg four times daily was 1.1 ng mL-1 compared with 2.2 ng mL-1 in those receiving ASA 325 mg once-daily.	Aspirin	75-78	2'-5' oligoadenylate synthetase 1B	Mus musculus	135-139
28448072-1	2017	OBJECTIVES: The association between aspirin use and improved survival after colorectal cancer diagnosis may be more pronounced in tumors that have PIK3CA mutations or high PTGS2 expression.	Aspirin	36-43	prostaglandin-endoperoxide synthase 2	Homo sapiens	172-177
28448072-10	2017	The aspirin by PTGS2 interaction was significant for overall survival (PTGS2-high adjusted HR=0.64, 95% CI 0.42-0.98 vs. PTGS2-low adjusted HR=1.28, 95% CI 0.80-2.03, P for interaction=0.04).	Aspirin	4-11	prostaglandin-endoperoxide synthase 2	Homo sapiens	15-20
28448072-10	2017	The aspirin by PTGS2 interaction was significant for overall survival (PTGS2-high adjusted HR=0.64, 95% CI 0.42-0.98 vs. PTGS2-low adjusted HR=1.28, 95% CI 0.80-2.03, P for interaction=0.04).	Aspirin	4-11	prostaglandin-endoperoxide synthase 2	Homo sapiens	71-76
28448072-10	2017	The aspirin by PTGS2 interaction was significant for overall survival (PTGS2-high adjusted HR=0.64, 95% CI 0.42-0.98 vs. PTGS2-low adjusted HR=1.28, 95% CI 0.80-2.03, P for interaction=0.04).	Aspirin	4-11	prostaglandin-endoperoxide synthase 2	Homo sapiens	71-76
28232079-2	2017	METHODS: The activity of rhodanese, 3-mercaptopyruvate sulfurtransferase (MPST) and gamma-cystathionase (CSE), functioning as antioxidant proteins and capable of producing H2S, was investigated in mouse liver and brain after intraperitoneal once a day administration of sodium nitroprusside (5 mg/kg body weight) or acetylsalicylic acid (500 mg/kg body weight) continued for 5 days.	Aspirin	316-336	thiosulfate sulfurtransferase, mitochondrial	Mus musculus	25-34
28285137-11	2017	Hydrolysis levels of the CES2A1-specific substrate aspirin were similar in human iPS cell-derived enterocytes and Caco-2 cells, whereas hydrolysis of the CES1A-specific substrate monoethylglycylxylidine was observed in Caco-2 cells but not in human iPS cell-derived enterocytes.	Aspirin	51-58	carboxylesterase 2	Homo sapiens	25-31
27778192-2	2017	Cumulative relative risk of CVD events can be reduced by 75 % with a combination of aspirin, a beta-adrenoceptor antagonist (beta-blocker), an HMG-CoA reductase inhibitor (statin), and an angiotensin-converting enzyme inhibitor.	Aspirin	84-91	angiotensin I converting enzyme	Homo sapiens	188-217
28139223-2	2017	Aspirin irreversibly inhibits platelet cyclooxygenase-1 and attenuates thromboxane A2 (TXA2)-mediated platelet aggregation, but there is variable suppression of cyclooxygenase-1.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	39-55
28285696-5	2017	The lack of survival benefit in patients with small-cell lung cancer taking long-term aspirin may be due to the low expression of cyclooxygenase-2 in small-cell lung cancer tissue.	Aspirin	86-93	prostaglandin-endoperoxide synthase 2	Homo sapiens	130-146
28060522-9	2017	Cotreatment with aspirin and (or) omega-3 PUFAs reduced convulsive behaviour; reduced levels of LXA4, interleukin-1beta, and nuclear factor-kappaB; and showed a lower percentage of corticohippocampal degenerative cells compared to PTZ-kindled rats.	Aspirin	17-24	interleukin 1 beta	Rattus norvegicus	102-119
27942866-9	2017	Vitamin E, levamisole, ASA, and ASA plus vitamin E inhibited AhR and COX-2 expression in embryos after 7 days and decreased AhR and COX-2 expression in embryos after 13 days.	Aspirin	23-26	prostaglandin-endoperoxide synthase 2	Gallus gallus	69-74
27942866-9	2017	Vitamin E, levamisole, ASA, and ASA plus vitamin E inhibited AhR and COX-2 expression in embryos after 7 days and decreased AhR and COX-2 expression in embryos after 13 days.	Aspirin	23-26	prostaglandin-endoperoxide synthase 2	Gallus gallus	132-137
27942866-9	2017	Vitamin E, levamisole, ASA, and ASA plus vitamin E inhibited AhR and COX-2 expression in embryos after 7 days and decreased AhR and COX-2 expression in embryos after 13 days.	Aspirin	32-35	prostaglandin-endoperoxide synthase 2	Gallus gallus	69-74
27942866-9	2017	Vitamin E, levamisole, ASA, and ASA plus vitamin E inhibited AhR and COX-2 expression in embryos after 7 days and decreased AhR and COX-2 expression in embryos after 13 days.	Aspirin	32-35	prostaglandin-endoperoxide synthase 2	Gallus gallus	132-137
28087411-0	2017	Aspirin prevents TNF-alpha-induced endothelial cell dysfunction by regulating the NF-kappaB-dependent miR-155/eNOS pathway: Role of a miR-155/eNOS axis in preeclampsia.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	17-26
28348498-8	2017	Subgroup and stratified analyses revealed a potential influence of smoking status and aspirin use on the association between CRP levels and colorectal adenoma.	Aspirin	86-93	C-reactive protein	Homo sapiens	125-128
28075528-0	2017	Prospective Evaluation of Genetic Variation in Platelet Endothelial Aggregation Receptor 1 Reveals Aspirin-Dependent Effects on Platelet Aggregation Pathways.	Aspirin	99-106	platelet endothelial aggregation receptor 1	Homo sapiens	47-90
28075528-1	2017	Genetic variation in the platelet endothelial aggregation receptor 1 (PEAR1) gene, most notably rs12041331, is implicated in altered on-aspirin platelet aggregation and increased cardiovascular event risk.	Aspirin	136-143	platelet endothelial aggregation receptor 1	Homo sapiens	25-68
28075528-1	2017	Genetic variation in the platelet endothelial aggregation receptor 1 (PEAR1) gene, most notably rs12041331, is implicated in altered on-aspirin platelet aggregation and increased cardiovascular event risk.	Aspirin	136-143	platelet endothelial aggregation receptor 1	Homo sapiens	70-75
28075528-5	2017	The influence of PEAR1 rs12041331 on platelet aggregation is pathway-specific and is altered by aspirin at therapeutic doses, but not in a dose-dependent manner.	Aspirin	96-103	platelet endothelial aggregation receptor 1	Homo sapiens	17-22
28075528-6	2017	Additional studies are needed to determine the impact of PEAR1 on cardiovascular events in aspirin-treated patients.	Aspirin	91-98	platelet endothelial aggregation receptor 1	Homo sapiens	57-62
27789095-2	2017	METHODS: We prospectively enrolled 112 patients undergoing UKA to determine the incidence of DVT utilizing aspirin 325 mg twice a day (BID) for 4 weeks postoperatively as DVT prophylaxis.	Aspirin	107-114	BH3 interacting domain death agonist	Homo sapiens	135-138
27789095-6	2017	CONCLUSION: Our data suggest that 325 mg of aspirin BID for 4 weeks results in a very low risk of DVT for patients undergoing UKA.	Aspirin	44-51	BH3 interacting domain death agonist	Homo sapiens	52-55
28362840-0	2017	Aspirin-triggered resolvin D1 attenuates PDGF-induced vascular smooth muscle cell migration via the cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) pathway.	Aspirin	0-7	cathelicidin antimicrobial peptide	Homo sapiens	149-157
28362840-2	2017	We sought to investigate the role of the cAMP/PKA pathway in mediating the effects of the aspirin-triggered epimer 17R-RvD1 (AT-RvD1) on VSMC migration.	Aspirin	90-97	cathelicidin antimicrobial peptide	Homo sapiens	41-49
28293429-1	2017	BACKGROUND: Low-dose aspirin irreversibly inhibits platelet cyclooxygenase-1 (COX-1) and suppresses platelet aggregation.	Aspirin	21-28	prostaglandin-endoperoxide synthase 1	Homo sapiens	60-76
28293429-1	2017	BACKGROUND: Low-dose aspirin irreversibly inhibits platelet cyclooxygenase-1 (COX-1) and suppresses platelet aggregation.	Aspirin	21-28	prostaglandin-endoperoxide synthase 1	Homo sapiens	78-83
28293429-3	2017	Because nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly bind with COX-1, the antiplatelet effects of aspirin may be suppressed when NSAIDs are co-administered.	Aspirin	110-117	prostaglandin-endoperoxide synthase 1	Homo sapiens	75-80
28154202-0	2017	Aspirin-Induced Chemoprevention and Response Kinetics Are Enhanced by PIK3CA Mutations in Colorectal Cancer Cells.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	70-76
28154202-5	2017	Aspirin decelerated growth rates and disrupted cell-cycle dynamics more profoundly in faster growing colorectal cancer cell lines, which tended to be PIK3CA mutants.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	150-156
28154202-7	2017	Our study demonstrated what clinical trials have only speculated, that PIK3CA-mutant colorectal cancers are more sensitive to aspirin.	Aspirin	126-133	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	71-77
28154202-8	2017	Aspirin inhibited cell growth in all colorectal cancer cell lines regardless of mutational background, but the effects were exacerbated in cells with PIK3CA mutations.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	150-156
28154202-9	2017	Mathematical modeling combined with bench science revealed that cells with PIK3CA-mutations experience significant G0-G1 arrest and explains why patients with PIK3CA mutant colorectal cancers may benefit from aspirin use after diagnosis.	Aspirin	209-216	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	75-81
28154202-9	2017	Mathematical modeling combined with bench science revealed that cells with PIK3CA-mutations experience significant G0-G1 arrest and explains why patients with PIK3CA mutant colorectal cancers may benefit from aspirin use after diagnosis.	Aspirin	209-216	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	159-165
27538737-1	2017	Aspirin-exacerbated respiratory disease (AERD) refers to the combination of asthma, chronic rhinosinusitis with nasal polyposis, and acute upper and lower respiratory tract reactions to the ingestion of aspirin (acetylsalicylic acid, ASA) and other cyclooxygenase-1 inhibiting non-steroidal anti-inflammatory drugs.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	249-265
27538737-1	2017	Aspirin-exacerbated respiratory disease (AERD) refers to the combination of asthma, chronic rhinosinusitis with nasal polyposis, and acute upper and lower respiratory tract reactions to the ingestion of aspirin (acetylsalicylic acid, ASA) and other cyclooxygenase-1 inhibiting non-steroidal anti-inflammatory drugs.	Aspirin	203-210	prostaglandin-endoperoxide synthase 1	Homo sapiens	249-265
27538737-1	2017	Aspirin-exacerbated respiratory disease (AERD) refers to the combination of asthma, chronic rhinosinusitis with nasal polyposis, and acute upper and lower respiratory tract reactions to the ingestion of aspirin (acetylsalicylic acid, ASA) and other cyclooxygenase-1 inhibiting non-steroidal anti-inflammatory drugs.	Aspirin	212-232	prostaglandin-endoperoxide synthase 1	Homo sapiens	249-265
28057599-8	2017	The in vivo effects of aspirin plus sorafenib on cisplatin therapy were also confirmed in resistant HNC xenograft models, in terms of growth inhibition, GSH depletion, and increased gammaH2AX formation and apoptosis in tumors.	Aspirin	23-30	H2A.X variant histone	Mus musculus	182-191
27567328-1	2017	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is characterized by 3 clinical features: asthma, nasal polyposis, and respiratory reactions to cyclooxygenase-1 inhibitors (nonsteroidal anti-inflammatory drugs).	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	154-170
28087411-5	2017	Aspirin prevented the TNF-alpha-mediated increase in miR-155 biogenesis and decreases in eNOS expression and NO/cGMP production in cultured human umbilical vein endothelial cells (HUVECs).	Aspirin	0-7	tumor necrosis factor	Homo sapiens	22-31
28087411-8	2017	Aspirin recovered the TNF-alpha-mediated decrease in wild-type, but not mutant, eNOS 3"-untranslated region reporter activity, whose effect was blocked by miR-155 mimic.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	22-31
28087411-9	2017	Moreover, aspirin prevented TNF-alpha-mediated endothelial cell dysfunction associated with impaired vasorelaxation, angiogenesis, and trophoblast invasion, and the preventive effects were blocked by miR-155 mimic or an eNOS inhibitor.	Aspirin	10-17	tumor necrosis factor	Homo sapiens	28-37
28087411-10	2017	Aspirin rescued TNF-alpha-mediated eNOS downregulation coupled with endothelial dysfunction by inhibiting NF-kappaB-dependent transcriptional miR-155 biogenesis.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	16-25
27940576-2	2017	Recent epidemiologic studies have suggested a therapeutic benefit from aspirin intake in cancers harboring oncogenic PIK3CA Here, we show that mutant PIK3CA-expressing breast cancer cells have greater sensitivity to aspirin-mediated growth suppression than their wild-type counterparts.	Aspirin	71-78	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	117-123
28219002-7	2017	In addition, the KRAS mutation is a prognostic biomarker and the PIK3CA mutation is a molecular biomarker predicting response to phosphoinositide 3-kinase/AKT/mammalian target of rapamycin inhibitors and response to aspirin therapy in CRC patients.	Aspirin	216-223	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	65-71
28219002-7	2017	In addition, the KRAS mutation is a prognostic biomarker and the PIK3CA mutation is a molecular biomarker predicting response to phosphoinositide 3-kinase/AKT/mammalian target of rapamycin inhibitors and response to aspirin therapy in CRC patients.	Aspirin	216-223	AKT serine/threonine kinase 1	Homo sapiens	155-158
28344655-0	2017	Interactions among COX-2, GPIIIa and P2Y1 variants are associated with aspirin responsiveness and adverse events in patients with ischemic stroke.	Aspirin	71-78	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	19-24
28344655-0	2017	Interactions among COX-2, GPIIIa and P2Y1 variants are associated with aspirin responsiveness and adverse events in patients with ischemic stroke.	Aspirin	71-78	integrin subunit beta 3	Homo sapiens	26-32
27998883-0	2017	Unlocking Aspirin"s Chemopreventive Activity: Role of Irreversibly Inhibiting Platelet Cyclooxygenase-1.	Aspirin	10-17	prostaglandin-endoperoxide synthase 1	Homo sapiens	87-103
27452734-7	2017	In our analyses, metallopeptidase inhibitor 1 (TIMP1) was the single most significantly affected glycoprotein by aspirin treatment.	Aspirin	113-120	TIMP metallopeptidase inhibitor 1	Homo sapiens	47-52
27452734-10	2017	The release of TIMP1 from platelets, which was previously unknown to be affected by aspirin treatment, may play important roles in hemostasis and/or vascular integrity.	Aspirin	84-91	TIMP metallopeptidase inhibitor 1	Homo sapiens	15-20
27998883-2	2017	In this study, using colon cancer as an example, we provide both in vitro (cell culture) and in vivo (chemically induced mouse model of colon cancer) evidence that this profound antineoplastic action may be associated with aspirin"s ability to irreversibly inhibit COX-1-mediated platelet activation, thereby blocking platelet-cancer cell interactions, which promote cancer cell number and invasive potential.	Aspirin	223-230	cytochrome c oxidase I, mitochondrial	Mus musculus	265-270
27940576-2	2017	Recent epidemiologic studies have suggested a therapeutic benefit from aspirin intake in cancers harboring oncogenic PIK3CA Here, we show that mutant PIK3CA-expressing breast cancer cells have greater sensitivity to aspirin-mediated growth suppression than their wild-type counterparts.	Aspirin	71-78	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	150-156
27940576-2	2017	Recent epidemiologic studies have suggested a therapeutic benefit from aspirin intake in cancers harboring oncogenic PIK3CA Here, we show that mutant PIK3CA-expressing breast cancer cells have greater sensitivity to aspirin-mediated growth suppression than their wild-type counterparts.	Aspirin	216-223	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	117-123
27940576-2	2017	Recent epidemiologic studies have suggested a therapeutic benefit from aspirin intake in cancers harboring oncogenic PIK3CA Here, we show that mutant PIK3CA-expressing breast cancer cells have greater sensitivity to aspirin-mediated growth suppression than their wild-type counterparts.	Aspirin	216-223	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	150-156
27940576-3	2017	Aspirin decreased viability and anchorage-independent growth of mutant PIK3CA breast cancer cells independently of its effects on COX-2 and NF-kappaB.	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	71-77
27940576-5	2017	In vivo, oncogenic PIK3CA-driven mouse mammary tumors treated daily with aspirin resulted in decreased tumor growth kinetics, whereas combination therapy of aspirin and a PI3K inhibitor further attenuated tumor growth.	Aspirin	73-80	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Mus musculus	19-25
27940576-5	2017	In vivo, oncogenic PIK3CA-driven mouse mammary tumors treated daily with aspirin resulted in decreased tumor growth kinetics, whereas combination therapy of aspirin and a PI3K inhibitor further attenuated tumor growth.	Aspirin	157-164	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Mus musculus	19-25
30615391-2	2017	The effect of anti-thrombocyte substances on thrombin-induced increasing of the level of cytoplasmic Ca in thrombocytes was analyzed on example of acetylsalicylic acid.	Aspirin	147-167	coagulation factor II, thrombin	Homo sapiens	45-53
26725535-1	2017	The consequences of using aspirin (ASA) for the pathogenesis of Chagas disease are unclear.	Aspirin	26-33	anti-sarcolemmal autoantibodies	Mus musculus	35-38
30615391-4	2017	It is established that in the given test acetylsalicylic acid inhibits thrombin-induced increasing of cytoplasmic Ca at 0.125-5.0 mk/mol concentrations.	Aspirin	41-61	coagulation factor II, thrombin	Homo sapiens	71-79
28356941-8	2017	ASA alone inhibited the levels of phosphorylated AKT (p-AKT) and survivin, whereas BTZ alone augmented the levels of p-AKT and survivin.	Aspirin	0-3	AKT serine/threonine kinase 1	Homo sapiens	49-52
28356941-0	2017	Aspirin enhances the cytotoxic activity of bortezomib against myeloma cells via suppression of Bcl-2, survivin and phosphorylation of AKT.	Aspirin	0-7	BCL2 apoptosis regulator	Homo sapiens	95-100
28356941-8	2017	ASA alone inhibited the levels of phosphorylated AKT (p-AKT) and survivin, whereas BTZ alone augmented the levels of p-AKT and survivin.	Aspirin	0-3	AKT serine/threonine kinase 1	Homo sapiens	56-59
28356941-0	2017	Aspirin enhances the cytotoxic activity of bortezomib against myeloma cells via suppression of Bcl-2, survivin and phosphorylation of AKT.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	134-137
28356941-8	2017	ASA alone inhibited the levels of phosphorylated AKT (p-AKT) and survivin, whereas BTZ alone augmented the levels of p-AKT and survivin.	Aspirin	0-3	AKT serine/threonine kinase 1	Homo sapiens	56-59
28356941-9	2017	Of note, ASA markedly decreased the upregulation of p-AKT and survivin induced by BTZ.	Aspirin	9-12	AKT serine/threonine kinase 1	Homo sapiens	54-57
28356941-11	2017	ASA may potentiate the antimyeloma activity of BTZ against myeloma cells via suppression of AKT phosphorylation, survivin and Bcl-2, indicating the potential of ASA+BTZ in treating MM, particularly for cases of BTZ-refractory/relapsed MM.	Aspirin	0-3	AKT serine/threonine kinase 1	Homo sapiens	92-95
27888917-2	2017	The hallmark of the disease is baseline overproduction of cysteinyl leukotrienes via the 5-lipoxygenase pathway, exacerbated by ingestion of aspirin.	Aspirin	141-148	arachidonate 5-lipoxygenase	Homo sapiens	89-103
28356941-11	2017	ASA may potentiate the antimyeloma activity of BTZ against myeloma cells via suppression of AKT phosphorylation, survivin and Bcl-2, indicating the potential of ASA+BTZ in treating MM, particularly for cases of BTZ-refractory/relapsed MM.	Aspirin	0-3	BCL2 apoptosis regulator	Homo sapiens	126-131
28137499-5	2017	Pre and post-aspirin challenge levels of LTC4 and PGD2 were measured using ELISA.	Aspirin	13-20	prostaglandin D2 synthase	Homo sapiens	50-54
28051316-5	2017	Compounds 6 and 7A inhibited COX-2 by 10% and 8%, respectively, at a concentration of 12.5 muM compared to 12% for 1 mM aspirin (the positive control).	Aspirin	120-127	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	29-34
28168001-10	2017	Rats treated with TRCQT alone (P = 0.021) or in combination with aspirin (P = 0.02) also showed significantly reduced MCAO-induced expression levels of TNF-alpha and pJNK (P &lt; 0.001) in their ischemic regions.	Aspirin	65-72	tumor necrosis factor	Rattus norvegicus	152-161
28125730-0	2017	The Influence of BRAF and KRAS Mutation Status on the Association between Aspirin Use and Survival after Colon Cancer Diagnosis.	Aspirin	74-81	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	17-21
28125730-3	2017	The aim of this study was to investigate the influence of BRAF and KRAS mutation status on the association between aspirin use and overall survival after colon cancer diagnosis.	Aspirin	115-122	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	58-62
28125730-8	2017	In contrast, aspirin use in BRAF mutated tumors was not associated with an improved survival (RR 1.11, 95% CI 0.57-2.16).	Aspirin	13-20	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	28-32
28125730-11	2017	CONCLUSION: Low-dose aspirin use after colon cancer diagnosis was associated with improved survival in BRAF wild-type tumors only.	Aspirin	21-28	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	103-107
28125730-12	2017	However, the large confidence interval of the rate ratio for the use of aspirin in patients with BRAF mutation does not rule out a possible benefit.	Aspirin	72-79	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	97-101
28190074-4	2017	Besides inhibiting the cyclooxygenase 2-prostaglandin axis, ASA"s anti-cancer activities have also been attributed to nuclear factor kB (NFkB) inhibition.	Aspirin	60-63	prostaglandin-endoperoxide synthase 2	Homo sapiens	23-39
27989119-4	2017	Alb forms adducts with many therapeutic drugs or their reactive metabolites such as beta-lactam antibiotics, acetylsalicylic acid, acetaminophen, nonsteroidal anti-inflammatory drugs, chemotherapeutic agents, and antiretroviral therapy drugs.	Aspirin	109-129	albumin	Homo sapiens	0-3
28068952-0	2017	Interaction among COX-2, P2Y1 and GPIIIa gene variants is associated with aspirin resistance and early neurological deterioration in Chinese stroke patients.	Aspirin	74-81	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	18-23
28068952-0	2017	Interaction among COX-2, P2Y1 and GPIIIa gene variants is associated with aspirin resistance and early neurological deterioration in Chinese stroke patients.	Aspirin	74-81	integrin subunit beta 3	Homo sapiens	34-40
28278500-0	2017	Aspirin Inhibits IKK-beta-mediated Prostate Cancer Cell Invasion by Targeting Matrix Metalloproteinase-9 and Urokinase-Type Plasminogen Activator.	Aspirin	0-7	plasminogen activator, urokinase	Homo sapiens	109-145
29098163-1	2017	The aim of the present study was to define changes in the expression of somatostatin (SOM) in the sympathetic perikarya innervating the porcine stomach prepyloric area during acetylsalicylic-acid-induced gastritis (ASA) and experimentally induced hyperacidity (HCL) and following partial stomach resection (RES).	Aspirin	175-195	somatostatin	Sus scrofa	72-84
29098163-1	2017	The aim of the present study was to define changes in the expression of somatostatin (SOM) in the sympathetic perikarya innervating the porcine stomach prepyloric area during acetylsalicylic-acid-induced gastritis (ASA) and experimentally induced hyperacidity (HCL) and following partial stomach resection (RES).	Aspirin	215-218	somatostatin	Sus scrofa	72-84
27555316-15	2017	The vascular endothelial growth factor level was significantly higher in the letrozole-treated group than aspirin-treated group (0.49 +- 0.26 vs 0.42 +- 0.22, P = .029).	Aspirin	106-113	vascular endothelial growth factor A	Homo sapiens	4-38
28034279-9	2017	Inhibition of acetylcholinesterase activity was also potent and was in the following order: celecoxib&gt; piroxicam&gt; diclofenac&gt; aspirin&gt; indomethacin&gt; dexamethasone.	Aspirin	135-142	acetylcholinesterase (Cartwright blood group)	Homo sapiens	14-34
28278500-7	2017	Aspirin treatment significantly resulted in reduction of matrix metalloproteinase-9 (MMP-9) and upregulation of tissue inhibitors of metalloproteinase-1 (TIMP-1) activity, which are the proteolytic enzymes contributing to the degradation of extracellular matrix and basement membrane in cell invasion and metastasis.	Aspirin	0-7	TIMP metallopeptidase inhibitor 1	Homo sapiens	112-152
28278500-7	2017	Aspirin treatment significantly resulted in reduction of matrix metalloproteinase-9 (MMP-9) and upregulation of tissue inhibitors of metalloproteinase-1 (TIMP-1) activity, which are the proteolytic enzymes contributing to the degradation of extracellular matrix and basement membrane in cell invasion and metastasis.	Aspirin	0-7	TIMP metallopeptidase inhibitor 1	Homo sapiens	154-160
28278500-8	2017	Our data further showed that aspirin was able to inhibit both urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) expression in the cells.	Aspirin	29-36	plasminogen activator, urokinase	Homo sapiens	62-98
28278500-8	2017	Our data further showed that aspirin was able to inhibit both urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) expression in the cells.	Aspirin	29-36	plasminogen activator, urokinase	Homo sapiens	100-103
28278500-9	2017	In addition, aspirin treatment caused a strong decrease in nuclear factor-kappa B (NF-kappaB) activation, inhibitor of kappaB (IkappaB)-alpha phosphorylation together with translocation of NF-kappaB p65 to nucleus and IkappaB kinase (IKK)- beta activation.	Aspirin	13-20	nuclear factor kappa B subunit 1	Homo sapiens	59-81
28278500-9	2017	In addition, aspirin treatment caused a strong decrease in nuclear factor-kappa B (NF-kappaB) activation, inhibitor of kappaB (IkappaB)-alpha phosphorylation together with translocation of NF-kappaB p65 to nucleus and IkappaB kinase (IKK)- beta activation.	Aspirin	13-20	nuclear factor kappa B subunit 1	Homo sapiens	83-92
28278500-9	2017	In addition, aspirin treatment caused a strong decrease in nuclear factor-kappa B (NF-kappaB) activation, inhibitor of kappaB (IkappaB)-alpha phosphorylation together with translocation of NF-kappaB p65 to nucleus and IkappaB kinase (IKK)- beta activation.	Aspirin	13-20	nuclear factor kappa B subunit 1	Homo sapiens	189-198
28278500-11	2017	CONCLUSION: The present research concluded that aspirin suppressed prostate cancer cell invasion by reducing MMP-9 activity and uPA expression through decreasing of IKK-beta-mediated NF-kappaB activation, indicating that the ability of aspirin to inhibit cell invasion might be useful in the chemoprevention of metastatic prostate cancer.	Aspirin	48-55	plasminogen activator, urokinase	Homo sapiens	128-131
28278500-11	2017	CONCLUSION: The present research concluded that aspirin suppressed prostate cancer cell invasion by reducing MMP-9 activity and uPA expression through decreasing of IKK-beta-mediated NF-kappaB activation, indicating that the ability of aspirin to inhibit cell invasion might be useful in the chemoprevention of metastatic prostate cancer.	Aspirin	48-55	nuclear factor kappa B subunit 1	Homo sapiens	183-192
28278500-11	2017	CONCLUSION: The present research concluded that aspirin suppressed prostate cancer cell invasion by reducing MMP-9 activity and uPA expression through decreasing of IKK-beta-mediated NF-kappaB activation, indicating that the ability of aspirin to inhibit cell invasion might be useful in the chemoprevention of metastatic prostate cancer.	Aspirin	236-243	nuclear factor kappa B subunit 1	Homo sapiens	183-192
29179207-0	2017	Reduction of NANOG Mediates the Inhibitory Effect of Aspirin on Tumor Growth and Stemness in Colorectal Cancer.	Aspirin	53-60	Nanog homeobox	Mus musculus	13-18
29179207-11	2017	Consistently, aspirin decreased the protein expression of stemness-related transcription factors, including c-Myc, OCT4 and NANOG.	Aspirin	14-21	Nanog homeobox	Mus musculus	124-129
29179207-12	2017	Suppression of NANOG blocked the effect of aspirin on sphere formation.	Aspirin	43-50	Nanog homeobox	Mus musculus	15-20
29179207-13	2017	Conversely, ectopic expression of NANOG rescued the aspirin-repressed sphere formation, suggesting that NANOG is a key downstream target.	Aspirin	52-59	Nanog homeobox	Mus musculus	34-39
29179207-13	2017	Conversely, ectopic expression of NANOG rescued the aspirin-repressed sphere formation, suggesting that NANOG is a key downstream target.	Aspirin	52-59	Nanog homeobox	Mus musculus	104-109
29179207-14	2017	Moreover, we found that aspirin repressed NANOG expression in protein level by decreasing its stability.	Aspirin	24-31	Nanog homeobox	Mus musculus	42-47
29179207-15	2017	CONCLUSION: We have provided new evidence that aspirin attenuates CSC properties through down-regulation of NANOG, suggesting aspirin as a promising therapeutic agent for colorectal cancer treatment.	Aspirin	47-54	Nanog homeobox	Mus musculus	108-113
29179207-15	2017	CONCLUSION: We have provided new evidence that aspirin attenuates CSC properties through down-regulation of NANOG, suggesting aspirin as a promising therapeutic agent for colorectal cancer treatment.	Aspirin	126-133	Nanog homeobox	Mus musculus	108-113
28055284-0	2017	Aspirin attenuates monocrotaline-induced pulmonary arterial hypertension in rats by suppressing the ERK/MAPK pathway.	Aspirin	0-7	Eph receptor B1	Rattus norvegicus	100-103
28163951-8	2017	Aspirin also inhibited the nuclear factor kappa-B (NFkappaB) pathway and decreased the expression of receptor activator of NFkappaB ligand, thus suppressing the formation of osteoclast.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	27-49
27405497-9	2017	Clinical data on aspirin, an irreversible inhibitor of both COX-1 and COX-2, are mainly experimental and hypothetical at this stage, but may be promising in depressed patients with concomitant inflammatory conditions.	Aspirin	17-24	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	70-75
28123464-9	2017	Thus, the results show that, regarding patients with hypertension in pregnancy, 75 mg/day aspirin can decrease the 24-h urinary protein, SOD, and ET-1 level.	Aspirin	90-97	endothelin 1	Homo sapiens	146-150
28286156-1	2017	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) comprises the triad of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and intolerance to inhibitors of the cyclooxygenase-1 (COX-1) enzyme.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	178-194
28286156-1	2017	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) comprises the triad of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and intolerance to inhibitors of the cyclooxygenase-1 (COX-1) enzyme.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	196-201
28128747-1	2017	To evaluate the parameters of the thrombin generation test (TGT) in coronary artery disease (CAD) patients on prolonged aspirin therapy during on-pump coronary artery bypass grafting (CABG) after donor platelet concentrate transfusion.	Aspirin	120-127	coagulation factor II, thrombin	Homo sapiens	34-42
28128747-6	2017	Activation of the endogenous thrombin potential was observed in patients on prolonged aspirin therapy in the pre- and intraoperative periods, as confirmed by high peak thrombin and increased velocity index.	Aspirin	86-93	coagulation factor II, thrombin	Homo sapiens	29-37
28128747-6	2017	Activation of the endogenous thrombin potential was observed in patients on prolonged aspirin therapy in the pre- and intraoperative periods, as confirmed by high peak thrombin and increased velocity index.	Aspirin	86-93	coagulation factor II, thrombin	Homo sapiens	168-176
27800646-1	2017	BACKGROUND/AIM: Data suggest aspirin improves survival in colorectal cancer (CRC) harbouring PIK3CA mutations.	Aspirin	29-36	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	93-99
28163951-8	2017	Aspirin also inhibited the nuclear factor kappa-B (NFkappaB) pathway and decreased the expression of receptor activator of NFkappaB ligand, thus suppressing the formation of osteoclast.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	51-59
28163951-8	2017	Aspirin also inhibited the nuclear factor kappa-B (NFkappaB) pathway and decreased the expression of receptor activator of NFkappaB ligand, thus suppressing the formation of osteoclast.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	123-131
29251761-11	2017	An interesting alternative is the SPC which contains antihypertensive agents along with other drugs used in cardiovascular prevention: statins and acetylsalicylic acid.	Aspirin	147-167	proline rich protein gene cluster	Homo sapiens	34-37
28684123-10	2017	On the other hand, higher aspirin doses have been reported to exert a negative impact on blood pressure due to inhibition of cyclooxygenase-2 activity, which reduces renal blood flow, glomerular filtration rate and sodium and water excretion.	Aspirin	26-33	prostaglandin-endoperoxide synthase 2	Homo sapiens	125-141
30303352-5	2017	Results: It was shown that the antiplatelet effect of aspirin in the preoperative period was manifest as inhibition of the initial stage of blood coagulation accompanied by increased thrombin potential, the total gain of anticoagulant and fibrinolytic activity of the blood.	Aspirin	54-61	coagulation factor II, thrombin	Homo sapiens	183-191
29552640-6	2017	Such integrative research demonstrated potential benefits of aspirin in colorectal carcinoma with PIK3CA mutations, providing the basis for new clinical trials.	Aspirin	61-68	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	98-104
27999284-0	2016	Aspirin down Regulates Hepcidin by Inhibiting NF-kappaB and IL6/JAK2/STAT3 Pathways in BV-2 Microglial Cells Treated with Lipopolysaccharide.	Aspirin	0-7	interleukin 6	Mus musculus	60-63
28514405-7	2017	Twelve (40%) AS patients treated with TNFalpha inhibitors achieved ASAS partial remission.	Aspirin	67-71	tumor necrosis factor	Homo sapiens	38-46
27907814-6	2017	Serum thromboxane B2 was more effectively suppressed at one and three months after the operation with ASA 75mg BID or 160mg OD than with 75mg OD (p&lt;0.001).	Aspirin	102-105	BH3 interacting domain death agonist	Homo sapiens	111-114
27907814-8	2017	Adenosine diphosphate stimulated platelet aggregation in whole blood (Multiplate ) was increased one and three months after the operation, and this was counteracted by ASA 75mg BID but not by 75 or 160mg OD.	Aspirin	168-171	BH3 interacting domain death agonist	Homo sapiens	177-180
28057098-0	2016	[Association of ABCB1 gene polymorphisms with aspirin resistance in patients with ischemic stroke].	Aspirin	46-53	ATP binding cassette subfamily B member 1	Homo sapiens	16-21
28057098-1	2016	Objective: To investigate the relationship of single nucleotide polymorphisms of Multi-drug resistance (ABCB1/MDR1) gene with Aspirin resistance (AR) in patients with ischemic stroke.	Aspirin	126-133	ATP binding cassette subfamily B member 1	Homo sapiens	104-109
28057098-1	2016	Objective: To investigate the relationship of single nucleotide polymorphisms of Multi-drug resistance (ABCB1/MDR1) gene with Aspirin resistance (AR) in patients with ischemic stroke.	Aspirin	126-133	ATP binding cassette subfamily B member 1	Homo sapiens	110-114
27999284-0	2016	Aspirin down Regulates Hepcidin by Inhibiting NF-kappaB and IL6/JAK2/STAT3 Pathways in BV-2 Microglial Cells Treated with Lipopolysaccharide.	Aspirin	0-7	signal transducer and activator of transcription 3	Mus musculus	69-74
27999284-1	2016	Aspirin down regulates transferrin receptor 1 (TfR1) and up regulates ferroportin 1 (Fpn1) and ferritin expression in BV-2 microglial cells treated without lipopolysaccharides (LPS), as well as down regulates hepcidin and interleukin 6 (IL-6) in cells treated with LPS.	Aspirin	0-7	solute carrier family 40 (iron-regulated transporter), member 1	Mus musculus	70-83
27999284-1	2016	Aspirin down regulates transferrin receptor 1 (TfR1) and up regulates ferroportin 1 (Fpn1) and ferritin expression in BV-2 microglial cells treated without lipopolysaccharides (LPS), as well as down regulates hepcidin and interleukin 6 (IL-6) in cells treated with LPS.	Aspirin	0-7	solute carrier family 40 (iron-regulated transporter), member 1	Mus musculus	85-89
27999284-1	2016	Aspirin down regulates transferrin receptor 1 (TfR1) and up regulates ferroportin 1 (Fpn1) and ferritin expression in BV-2 microglial cells treated without lipopolysaccharides (LPS), as well as down regulates hepcidin and interleukin 6 (IL-6) in cells treated with LPS.	Aspirin	0-7	interleukin 6	Mus musculus	222-235
27999284-1	2016	Aspirin down regulates transferrin receptor 1 (TfR1) and up regulates ferroportin 1 (Fpn1) and ferritin expression in BV-2 microglial cells treated without lipopolysaccharides (LPS), as well as down regulates hepcidin and interleukin 6 (IL-6) in cells treated with LPS.	Aspirin	0-7	interleukin 6	Mus musculus	237-241
27999284-4	2016	We demonstrated that aspirin inhibited hepcidin mRNA as well as NO production in cells treated with LPS, but not in cells without LPS, suppresses IL-6, JAK2, STAT3, and P65 (nuclear factor-kappaB) phosphorylation and has no effect on IRP1 in cells treated with or without LPS.	Aspirin	21-28	interleukin 6	Mus musculus	146-150
27999284-4	2016	We demonstrated that aspirin inhibited hepcidin mRNA as well as NO production in cells treated with LPS, but not in cells without LPS, suppresses IL-6, JAK2, STAT3, and P65 (nuclear factor-kappaB) phosphorylation and has no effect on IRP1 in cells treated with or without LPS.	Aspirin	21-28	signal transducer and activator of transcription 3	Mus musculus	158-163
27999284-5	2016	These findings provide evidence that aspirin down regulates hepcidin by inhibiting IL6/JAK2/STAT3 and P65 (nuclear factor-kappaB) pathways in the cells under inflammatory conditions, and imply that an aspirin-induced reduction in TfR1 and an increase in ferritin are not associated with IRP1 and NO.	Aspirin	37-44	interleukin 6	Mus musculus	83-86
27999284-5	2016	These findings provide evidence that aspirin down regulates hepcidin by inhibiting IL6/JAK2/STAT3 and P65 (nuclear factor-kappaB) pathways in the cells under inflammatory conditions, and imply that an aspirin-induced reduction in TfR1 and an increase in ferritin are not associated with IRP1 and NO.	Aspirin	37-44	signal transducer and activator of transcription 3	Mus musculus	92-97
27887602-1	2016	It has been suggested that aspirin may be of benefit in treating sepsis and ARDS in view of its ability to block cyclo-oxygenase-1 (COX-1) and COX-2 activities; inhibit nuclear factor kappa B (NF-kappaB); enhance the production of endothelial nitric oxide (eNO) and lipoxin A4 (LXA4).	Aspirin	27-34	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	143-148
27633788-0	2016	Aspirin inhibits the production of proangiogenic 15(S)-HETE by platelet cyclooxygenase-1.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	72-88
27633788-3	2016	Because the effective doses of aspirin are consistent with the inhibition of cyclooxygenase-1 in platelets, we used liquid chromatography with tandem mass spectrometry analyses and immunoassays of human platelet releasates coupled with angiogenesis assays to search for the mediators of these effects.	Aspirin	31-38	prostaglandin-endoperoxide synthase 1	Homo sapiens	77-93
27633788-9	2016	A., Warner, T. D. Aspirin inhibits the production of proangiogenic 15(S)-HETE by platelet cyclooxygenase-1.	Aspirin	18-25	prostaglandin-endoperoxide synthase 1	Homo sapiens	90-106
27816726-4	2016	In this study, we investigated whether AST-IV could protect rat gastric mucosa against Asp-induced gastric mucosal damage.	Aspirin	87-90	sulfotransferase family 1A member 1	Rattus norvegicus	39-45
27816726-7	2016	The protective mechanism of AST-IV involved the suppression of Asp-induced inhibition of cycloxygenase-1 (COX-1) expression, prostaglandin E2 (PGE2) production, superoxide dismutase (SOD) activity and nitric oxide (NO) production.	Aspirin	63-66	sulfotransferase family 1A member 1	Rattus norvegicus	28-34
27816726-7	2016	The protective mechanism of AST-IV involved the suppression of Asp-induced inhibition of cycloxygenase-1 (COX-1) expression, prostaglandin E2 (PGE2) production, superoxide dismutase (SOD) activity and nitric oxide (NO) production.	Aspirin	63-66	superoxide dismutase 1	Rattus norvegicus	183-186
27816726-8	2016	AST-IV blocked Asp-induced inhibition of SOD activity through preventing Asp from inhibiting the expression of SOD-1, both at the mRNA and protein levels.	Aspirin	15-18	sulfotransferase family 1A member 1	Rattus norvegicus	0-6
27816726-8	2016	AST-IV blocked Asp-induced inhibition of SOD activity through preventing Asp from inhibiting the expression of SOD-1, both at the mRNA and protein levels.	Aspirin	15-18	superoxide dismutase 1	Rattus norvegicus	41-44
27816726-8	2016	AST-IV blocked Asp-induced inhibition of SOD activity through preventing Asp from inhibiting the expression of SOD-1, both at the mRNA and protein levels.	Aspirin	15-18	superoxide dismutase 1	Rattus norvegicus	111-116
27816726-8	2016	AST-IV blocked Asp-induced inhibition of SOD activity through preventing Asp from inhibiting the expression of SOD-1, both at the mRNA and protein levels.	Aspirin	73-76	sulfotransferase family 1A member 1	Rattus norvegicus	0-6
27816726-8	2016	AST-IV blocked Asp-induced inhibition of SOD activity through preventing Asp from inhibiting the expression of SOD-1, both at the mRNA and protein levels.	Aspirin	73-76	superoxide dismutase 1	Rattus norvegicus	41-44
27816726-8	2016	AST-IV blocked Asp-induced inhibition of SOD activity through preventing Asp from inhibiting the expression of SOD-1, both at the mRNA and protein levels.	Aspirin	73-76	superoxide dismutase 1	Rattus norvegicus	111-116
27816726-10	2016	The results clearly showed that AST-IV could neutralize the toxicity of Asp while having no impact on its anti-inflammatory activity.	Aspirin	72-75	sulfotransferase family 1A member 1	Rattus norvegicus	32-38
27638860-10	2016	We also found that both aspirin-PC and aspirin have robust antineoplastic action in the presence of VEGF-blocking drugs.	Aspirin	24-31	vascular endothelial growth factor A	Homo sapiens	100-104
27337950-11	2016	CONCLUSION: The aspirin-enoxaparin short-term protocol may be a good choice after free flap transfer in reconstruction of head and neck surgical defects.	Aspirin	16-23	arachidonate 5-lipoxygenase activating protein	Homo sapiens	87-91
26328807-10	2016	It is also, observed that the gradual addition of HSA has led to a marked increase in fluorescence anisotropy (r) of Amlodipine and Aspirin which can be suggested that the drugs were located in a restricted environment of the protein as confirmed by Red Edge Excitation Shift (REES) studies.	Aspirin	132-139	albumin	Homo sapiens	50-53
26328807-12	2016	CONCLUSIONS: The present experiment showed that the binding of Amlodipine and Aspirin to HSA induced a conformational change of HSA.	Aspirin	78-85	albumin	Homo sapiens	89-92
26328807-12	2016	CONCLUSIONS: The present experiment showed that the binding of Amlodipine and Aspirin to HSA induced a conformational change of HSA.	Aspirin	78-85	albumin	Homo sapiens	128-131
27825819-15	2016	ASA caused hemorrhagic gastric mucosal damage and significantly decreased GBF, H2S production, CO content, mRNA or protein expression for CSE, 3-MST, HO-2 and increased mRNA and/or protein expression for CBS, HO-1, Nrf-2, HIF-1alpha, iNOS, IL-1beta, COX-2 in gastric mucosa and COHb concentration in blood.	Aspirin	0-3	heme oxygenase 2	Rattus norvegicus	150-154
27825819-15	2016	ASA caused hemorrhagic gastric mucosal damage and significantly decreased GBF, H2S production, CO content, mRNA or protein expression for CSE, 3-MST, HO-2 and increased mRNA and/or protein expression for CBS, HO-1, Nrf-2, HIF-1alpha, iNOS, IL-1beta, COX-2 in gastric mucosa and COHb concentration in blood.	Aspirin	0-3	cystathionine beta synthase	Rattus norvegicus	204-207
27825819-15	2016	ASA caused hemorrhagic gastric mucosal damage and significantly decreased GBF, H2S production, CO content, mRNA or protein expression for CSE, 3-MST, HO-2 and increased mRNA and/or protein expression for CBS, HO-1, Nrf-2, HIF-1alpha, iNOS, IL-1beta, COX-2 in gastric mucosa and COHb concentration in blood.	Aspirin	0-3	NFE2 like bZIP transcription factor 2	Rattus norvegicus	215-220
27825819-15	2016	ASA caused hemorrhagic gastric mucosal damage and significantly decreased GBF, H2S production, CO content, mRNA or protein expression for CSE, 3-MST, HO-2 and increased mRNA and/or protein expression for CBS, HO-1, Nrf-2, HIF-1alpha, iNOS, IL-1beta, COX-2 in gastric mucosa and COHb concentration in blood.	Aspirin	0-3	nitric oxide synthase 2	Rattus norvegicus	234-238
27825819-15	2016	ASA caused hemorrhagic gastric mucosal damage and significantly decreased GBF, H2S production, CO content, mRNA or protein expression for CSE, 3-MST, HO-2 and increased mRNA and/or protein expression for CBS, HO-1, Nrf-2, HIF-1alpha, iNOS, IL-1beta, COX-2 in gastric mucosa and COHb concentration in blood.	Aspirin	0-3	interleukin 1 beta	Rattus norvegicus	240-248
27765537-4	2016	Some non-steroidal anti-inflammatory drugs interact with aspirin pharmacodynamics by competing on the drug target, i.e. the platelet"s cyclooxygenase-1 protein.	Aspirin	57-64	prostaglandin-endoperoxide synthase 1	Homo sapiens	135-151
28936833-6	2016	The top 10 important nodes of SAP overlapped with Salvianolate injection and aspirin included MAPK14, MAPK8, IL-6 and IL-8.	Aspirin	77-84	mitogen-activated protein kinase 14	Homo sapiens	94-100
27887602-1	2016	It has been suggested that aspirin may be of benefit in treating sepsis and ARDS in view of its ability to block cyclo-oxygenase-1 (COX-1) and COX-2 activities; inhibit nuclear factor kappa B (NF-kappaB); enhance the production of endothelial nitric oxide (eNO) and lipoxin A4 (LXA4).	Aspirin	27-34	nuclear factor kappa B subunit 1	Homo sapiens	169-191
27887602-1	2016	It has been suggested that aspirin may be of benefit in treating sepsis and ARDS in view of its ability to block cyclo-oxygenase-1 (COX-1) and COX-2 activities; inhibit nuclear factor kappa B (NF-kappaB); enhance the production of endothelial nitric oxide (eNO) and lipoxin A4 (LXA4).	Aspirin	27-34	nuclear factor kappa B subunit 1	Homo sapiens	193-202
27641736-0	2016	Associations of MDR1, TBXA2R, PLA2G7, and PEAR1 genetic polymorphisms with the platelet activity in Chinese ischemic stroke patients receiving aspirin therapy.	Aspirin	143-150	platelet endothelial aggregation receptor 1	Homo sapiens	42-47
27565221-4	2016	We have previously reported the preparation of a novel aspirin derivative that we named Ca-Asp, and showed that it causes less damage to gastric mucosa of rat and inhibits the expression of COX-2 to higher degree than Asp.	Aspirin	55-62	prostaglandin-endoperoxide synthase 2	Homo sapiens	190-195
27683033-0	2016	A novel co-drug of aspirin and ursolic acid interrupts adhesion, invasion and migration of cancer cells to vascular endothelium via regulating EMT and EGFR-mediated signaling pathways: multiple targets for cancer metastasis prevention and treatment.	Aspirin	19-26	epidermal growth factor receptor	Homo sapiens	151-155
27857180-0	2016	Aspirin upregulates alphaB-Crystallin to protect the myocardium against heat stress in broiler chickens.	Aspirin	0-7	crystallin alpha B	Gallus gallus	20-37
27857180-7	2016	ELISAs indicated ASA induced CryAB in vivo to protect against heat stress-induced myocardial damage, but ASA did not induce CryAB in primary chicken myocardial cells.	Aspirin	17-20	crystallin alpha B	Gallus gallus	29-34
27857180-8	2016	The mechanisms by which ASA induces the expression of CryAB in vivo and protects the myocardium during heat stress merit further research.	Aspirin	24-27	crystallin alpha B	Gallus gallus	54-59
27641736-2	2016	Numerous evidence shows that thromboxane A2 receptor (TXA2 receptor, encoded by TBXA2R), lipoprotein-associated phospholipase A2 (Lp-PLA2, encoded by PLA2G7) and platelet endothelial aggregation receptor-1 (PEAR1, encoded by PEAR1) are crucial in regulating platelet activation, and P-glycoprotein (P-gp, encoded by MDR1) influences the absorption of aspirin in the intestine.	Aspirin	351-358	platelet endothelial aggregation receptor 1	Homo sapiens	162-205
27641736-7	2016	MDR1 3435TT genotype carriers, whose arachidonic acid (AA) or adenosine diphosphate (ADP)-induced platelet aggregation was lower than that of CC+CT genotype carriers, were less likely to suffer from aspirin resistance (odds ratio=0.421, 95% CI: 0.233-0.759).	Aspirin	199-206	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
27712763-1	2016	The acute clinical symptoms that develop following the oral ingestion of aspirin, or any other inhibitor of cyclooxygenase-1, are well established in aspirin-exacerbated respiratory disease: nasal congestion, rhinorrhea, and bronchospasm.	Aspirin	150-157	prostaglandin-endoperoxide synthase 1	Homo sapiens	108-124
27475305-2	2016	Aspirin, a nonsteroidal anti-inflammatory drug, inhibits prostaglandin-endoperoxide synthase 2 (PTGS2 or cyclooxygenase-2); PTGS2 promotes inflammation and suppresses T-cell-mediated adaptive immunity.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	57-94
27475305-2	2016	Aspirin, a nonsteroidal anti-inflammatory drug, inhibits prostaglandin-endoperoxide synthase 2 (PTGS2 or cyclooxygenase-2); PTGS2 promotes inflammation and suppresses T-cell-mediated adaptive immunity.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	96-101
27475305-2	2016	Aspirin, a nonsteroidal anti-inflammatory drug, inhibits prostaglandin-endoperoxide synthase 2 (PTGS2 or cyclooxygenase-2); PTGS2 promotes inflammation and suppresses T-cell-mediated adaptive immunity.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	105-121
27475305-2	2016	Aspirin, a nonsteroidal anti-inflammatory drug, inhibits prostaglandin-endoperoxide synthase 2 (PTGS2 or cyclooxygenase-2); PTGS2 promotes inflammation and suppresses T-cell-mediated adaptive immunity.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	124-129
27712764-1	2016	Aspirin-exacerbated respiratory disease (AERD) is characterized by chronic rhinosinusitis with nasal polyps, asthma, and reactions to cyclooxygenase-1-inhibiting drugs.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	134-150
27712766-1	2016	Aspirin-exacerbated respiratory disease (AERD) involves overexpression of proinflammatory mediators, including 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes.	Aspirin	0-7	arachidonate 5-lipoxygenase	Homo sapiens	111-125
27440714-11	2016	In conclusion, a variable delay in the 37  C incubation of blood samples may affect the assessment of platelet cyclooxygenase-1 inhibition by aspirin and confound the characterization of the determinants of aspirin responsiveness.	Aspirin	142-149	prostaglandin-endoperoxide synthase 1	Homo sapiens	111-127
27703200-7	2016	Treatment of mice with aspirin or loxoprofen inhibited the production of 12-HHT and increased the sensitivity toward PLY, which was also ameliorated by the CysLT1 antagonist.	Aspirin	23-30	cysteinyl leukotriene receptor 1	Mus musculus	156-162
27756897-7	2016	In addition, while ASA VI enhanced the expression of ALP, OCN, Col 1 and RUNX2, treatment with LY294002 reduced all of these osteogenic effects and reduced the p-AKT levels induced by ASA VI.	Aspirin	19-22	RUNX family transcription factor 2	Rattus norvegicus	73-78
27653914-11	2016	CONCLUSIONS: Application of the 2013 AHA/ASA Guidelines resulted in a 64% increase in the number of acute ischemic stroke patients treated with TPA at AHMC with no worsening of aggregate outcomes and no increase in bleeds or deaths.	Aspirin	41-44	plasminogen activator, tissue type	Homo sapiens	144-147
27826458-6	2016	Within a binomial logistic regression model, less frequently versus frequently performed flap (odds ratio [OR] = 3.2; confidence interval [CI] = 2.9-3.5; P = 0.000), high-volume versus low-volume surgeon (OR = 0.52; CI = -0.22 to 0.82; P = 0.007), and ASA classification (OR = 2.9; CI = 2.4-3.4; P = 0.033) were retained as independent predictors of severe complications.	Aspirin	252-255	arachidonate 5-lipoxygenase activating protein	Homo sapiens	89-93
27729974-1	2016	BACKGROUND: This experiment was conducted to test the hypothesis that vitamin E (Vit E) and acetylsalicylic acid (ASA), a cyclooxygenase-2 (COX-2) inhibitor, will additively reduce the production of the immunosuppressive molecule prostaglandin E2 (PGE2) and hence reduce inflammatory responses in weaner pigs experimentally infected with an enterotoxigenic strain of E. coli.	Aspirin	92-112	prostaglandin-endoperoxide synthase 2	Sus scrofa	122-138
27729974-1	2016	BACKGROUND: This experiment was conducted to test the hypothesis that vitamin E (Vit E) and acetylsalicylic acid (ASA), a cyclooxygenase-2 (COX-2) inhibitor, will additively reduce the production of the immunosuppressive molecule prostaglandin E2 (PGE2) and hence reduce inflammatory responses in weaner pigs experimentally infected with an enterotoxigenic strain of E. coli.	Aspirin	92-112	prostaglandin-endoperoxide synthase 2	Sus scrofa	140-145
27729974-1	2016	BACKGROUND: This experiment was conducted to test the hypothesis that vitamin E (Vit E) and acetylsalicylic acid (ASA), a cyclooxygenase-2 (COX-2) inhibitor, will additively reduce the production of the immunosuppressive molecule prostaglandin E2 (PGE2) and hence reduce inflammatory responses in weaner pigs experimentally infected with an enterotoxigenic strain of E. coli.	Aspirin	114-117	prostaglandin-endoperoxide synthase 2	Sus scrofa	122-138
27729974-1	2016	BACKGROUND: This experiment was conducted to test the hypothesis that vitamin E (Vit E) and acetylsalicylic acid (ASA), a cyclooxygenase-2 (COX-2) inhibitor, will additively reduce the production of the immunosuppressive molecule prostaglandin E2 (PGE2) and hence reduce inflammatory responses in weaner pigs experimentally infected with an enterotoxigenic strain of E. coli.	Aspirin	114-117	prostaglandin-endoperoxide synthase 2	Sus scrofa	140-145
27393925-3	2016	Aspirin (ASA) as a platelet-inhibiting agent through inactivation of Cyclooxygenase-1 (COX-1) is mostly used for the prevention and treatment of atherothrombotic disorders.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	69-85
27393925-3	2016	Aspirin (ASA) as a platelet-inhibiting agent through inactivation of Cyclooxygenase-1 (COX-1) is mostly used for the prevention and treatment of atherothrombotic disorders.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	87-92
27393925-3	2016	Aspirin (ASA) as a platelet-inhibiting agent through inactivation of Cyclooxygenase-1 (COX-1) is mostly used for the prevention and treatment of atherothrombotic disorders.	Aspirin	9-12	prostaglandin-endoperoxide synthase 1	Homo sapiens	69-85
27393925-3	2016	Aspirin (ASA) as a platelet-inhibiting agent through inactivation of Cyclooxygenase-1 (COX-1) is mostly used for the prevention and treatment of atherothrombotic disorders.	Aspirin	9-12	prostaglandin-endoperoxide synthase 1	Homo sapiens	87-92
27393925-4	2016	ASA inhibits the COX-1 enzyme and therefore blocks platelet thromboxane A2 (TXA2) synthesis.	Aspirin	0-3	prostaglandin-endoperoxide synthase 1	Homo sapiens	17-22
27504605-8	2016	More studies are required to understand the relationship between the role of TNFalpha pathway, aspirin, and colorectal cancer risk.	Aspirin	95-102	tumor necrosis factor	Homo sapiens	77-85
27488919-8	2016	Platelet aggregation studies conducted in the presence of various platelet agonists indicated that the aspirin-lipid conjugates act through inhibition of the cyclooxygenase (COX)-thromboxane synthase (TXAS) pathway.	Aspirin	103-110	thromboxane A synthase 1	Homo sapiens	201-205
27344083-7	2016	The aspirin-mediated inactivation of platelets may restore antitumor reactivity by blocking the release of paracrine lipid and protein mediators that induce COX-2 expression in adjacent nucleated cells at sites of mucosal injury.	Aspirin	4-11	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	157-162
27573422-0	2016	Aspirin-triggered resolvin D1 inhibits TGF-beta1-induced EMT through the inhibition of the mTOR pathway by reducing the expression of PKM2 and is closely linked to oxidative stress.	Aspirin	0-7	transforming growth factor beta 1	Homo sapiens	39-48
27573422-0	2016	Aspirin-triggered resolvin D1 inhibits TGF-beta1-induced EMT through the inhibition of the mTOR pathway by reducing the expression of PKM2 and is closely linked to oxidative stress.	Aspirin	0-7	mechanistic target of rapamycin kinase	Homo sapiens	91-95
27488919-10	2016	We show that although all of the aspirin conjugates act through the COX-TXAS pathway by inhibiting COX-1, the parent fatty acids do not act via this pathway.	Aspirin	33-40	thromboxane A synthase 1	Homo sapiens	72-76
27285781-1	2016	The roles of abscisic acid (ABA) and hydrogen peroxide (H2O2) in inducing glucose-6-phosphate dehydrogenase (G6PDH, EC 1.1.1.49) activity and the possible roles of G6PDH in regulating ascorbate-glutathione (AsA-GSH) cycle were investigated in soybean (Glycine max L.) roots under drought stress.	Aspirin	207-210	glucose-6-phosphate dehydrogenase	Glycine max	109-114
27423494-13	2016	IFN-gamma-matured eosinophil progenitors showed enhanced hPGDS expression and increased levels of PGD2 release at baseline and after aspirin stimulation.	Aspirin	133-140	interferon gamma	Homo sapiens	0-9
27285781-5	2016	Moreover, drought significantly increased the contents of AsA and GSH and the activities of key enzymes in AsA-GSH cycle, while application of G6PDH inhibitor to seedlings significantly reduced the above effect induced by drought.	Aspirin	107-110	glucose-6-phosphate dehydrogenase	Glycine max	143-148
27285781-6	2016	Taken together, these results indicate that H2O2 acting as a downstream signaling molecule of ABA mediates drought-induced increase in cytosolic G6PDH activity, and that enhanced cytosolic G6PDH activity maintains cellular redox homeostasis by regulating AsA-GSH cycle in soybean roots.	Aspirin	255-258	glucose-6-phosphate dehydrogenase	Glycine max	189-194
27557515-0	2016	Therapeutic dosages of aspirin counteract the IL-6 induced pro-tumorigenic effects by slowing down the ribosome biogenesis rate.	Aspirin	23-30	interleukin 6	Mus musculus	46-50
27597145-9	2016	RESULTS: 5-HTT genotype (LL vs *S) was a significant determinant of serum TX level (8.9+-2.6ng/ml vs 6.0+-1.6ng/ml respectively; p&lt;0.02) and 5-HTT LL genotype predicted an incomplete aspirin response (serum TXB2&gt;2.2ng/ml) (p=0.04; OR=2.22, CI=1.03-4.79).	Aspirin	186-193	solute carrier family 6 member 4	Homo sapiens	9-14
27597145-0	2016	Impact of genetic variation in the 5-HT transporter and receptor on platelet function in patients with stable CAD taking aspirin.	Aspirin	121-128	solute carrier family 6 member 4	Homo sapiens	35-51
27597145-6	2016	We hypothesised that 5-HTT and/or HTR2A variation may influence platelet response to aspirin in patients with stable CAD.	Aspirin	85-92	solute carrier family 6 member 4	Homo sapiens	21-26
27597145-6	2016	We hypothesised that 5-HTT and/or HTR2A variation may influence platelet response to aspirin in patients with stable CAD.	Aspirin	85-92	5-hydroxytryptamine receptor 2A	Homo sapiens	34-39
27557515-2	2016	Here we showed that therapeutic dosages of aspirin counteract the pro-tumorigenic effects of the inflammatory cytokine interleukin(IL)-6 in cancer and non-cancer cell lines, and in mouse liver in vivo.	Aspirin	43-50	interleukin 6	Mus musculus	119-136
27557515-3	2016	We found that therapeutic dosages of aspirin prevented IL-6 from inducing the down-regulation of p53 expression and the acquisition of the epithelial mesenchymal transition (EMT) phenotypic changes in the cell lines.	Aspirin	37-44	interleukin 6	Mus musculus	55-59
27713620-8	2016	Aspirin (5.6-560 microM) and cilostazol (5-10 microM) significantly inhibited thrombin-induced increases in [Ca2+]i in a concentration-dependent manner.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	78-86
27557515-8	2016	It is worth noting that aspirin down-regulated ribosome biogenesis, stabilized p53 and up-regulated E-cadherin expression in unstimulated control cells also.	Aspirin	24-31	cadherin 1	Mus musculus	100-110
27713620-12	2016	The combination of aspirin and sodium valproate synergistically inhibited thrombin-induced [Ca2+]i.	Aspirin	19-26	coagulation factor II, thrombin	Homo sapiens	74-82
27262381-5	2016	Our results revealed that 100mg/kg ASA significantly reduced interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha levels in the E groups; however, the IL-10 level was considerably increased.	Aspirin	35-38	interleukin 6	Rattus norvegicus	61-79
27576775-1	2016	BACKGROUND: In the PEGASUS-TIMI 54 trial (Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis in Myocardial Infarction 54), ticagrelor reduced the risk of major adverse cardiovascular events when added to low-dose aspirin in stable patients with prior myocardial infarction, resulting in the approval of ticagrelor 60 mg twice daily for long-term secondary prevention.	Aspirin	170-177	IKAROS family zinc finger 5	Homo sapiens	19-34
27576775-1	2016	BACKGROUND: In the PEGASUS-TIMI 54 trial (Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis in Myocardial Infarction 54), ticagrelor reduced the risk of major adverse cardiovascular events when added to low-dose aspirin in stable patients with prior myocardial infarction, resulting in the approval of ticagrelor 60 mg twice daily for long-term secondary prevention.	Aspirin	311-318	IKAROS family zinc finger 5	Homo sapiens	19-34
27262381-5	2016	Our results revealed that 100mg/kg ASA significantly reduced interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha levels in the E groups; however, the IL-10 level was considerably increased.	Aspirin	35-38	tumor necrosis factor	Rattus norvegicus	84-117
27566955-4	2016	Megakaryocytic cells exposed to aspirin and its metabolite (salicylic acid, a weak COX-1 inhibitor) showed up regulation in the RUNX1 P1 isoform and MYL9, which is transcriptionally regulated by RUNX1.	Aspirin	32-39	myosin light chain 9	Homo sapiens	149-153
27262845-3	2016	Four of the most important HSPs including HspB1 (Hsp27), Hsp60, Hsp70, and Hsp90 were induced by aspirin pretreatment and were suppressed by BAPTA-AM.	Aspirin	97-104	heat shock protein family A (Hsp70) member 2	Gallus gallus	64-69
27566955-5	2016	In human subjects, RUNX1 P1 expression in blood and RUNX1-regulated platelet proteins, including MYL9, were aspirin-responsive and associated with platelet function.	Aspirin	108-115	myosin light chain 9	Homo sapiens	97-101
27394692-0	2016	Addition of aspirin to a fish oil-rich diet decreases inflammation and atherosclerosis in ApoE-null mice.	Aspirin	12-19	apolipoprotein E	Mus musculus	90-94
27318652-0	2016	Interaction between COX-1 and COX-2 Variants Associated with Aspirin Resistance in Chinese Stroke Patients.	Aspirin	61-68	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	30-35
27391154-3	2016	METHODS AND RESULTS: In mice deficient of apolipoprotein E (Apoe-/-), aspirin (20, 50 mg/kg/day) suppressed the progression of atherosclerosis in aortic roots and increased the plaque stability in carotid atherosclerotic plaques induced by collar-placement.	Aspirin	70-77	apolipoprotein E	Mus musculus	42-58
27583400-9	2016	Release of platelet-derived chemokines CCL5 and PF4 and neutrophil extracellular traps was reduced by Aspirin but not by Tirofiban.	Aspirin	102-109	chemokine (C-C motif) ligand 5	Mus musculus	39-43
27583400-9	2016	Release of platelet-derived chemokines CCL5 and PF4 and neutrophil extracellular traps was reduced by Aspirin but not by Tirofiban.	Aspirin	102-109	platelet factor 4	Mus musculus	48-51
27391154-3	2016	METHODS AND RESULTS: In mice deficient of apolipoprotein E (Apoe-/-), aspirin (20, 50 mg/kg/day) suppressed the progression of atherosclerosis in aortic roots and increased the plaque stability in carotid atherosclerotic plaques induced by collar-placement.	Aspirin	70-77	apolipoprotein E	Mus musculus	60-64
27391154-4	2016	In vivo lentivirus-mediated RNA interference of AP-2alpha reversed the inhibitory effects of aspirin on atherosclerosis in Apoe-/- mice.	Aspirin	93-100	apolipoprotein E	Mus musculus	123-127
27391154-5	2016	Mechanically, aspirin increased AP-2alpha phosphorylation and its activity, upregulated IkBalpha mRNA and protein levels, and reduced oxidative stress in cultured vascular smooth muscle cells.	Aspirin	14-21	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	88-96
27391154-6	2016	Furthermore, deficiency of AP-2alpha completely abolished aspirin-induced upregulation of IkBalpha levels and inhibition of oxidative stress in Apoe-/- mice.	Aspirin	58-65	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	90-98
27391154-6	2016	Furthermore, deficiency of AP-2alpha completely abolished aspirin-induced upregulation of IkBalpha levels and inhibition of oxidative stress in Apoe-/- mice.	Aspirin	58-65	apolipoprotein E	Mus musculus	144-148
27391154-7	2016	Clinically, conventional doses of aspirin increased AP-2alpha phosphorylation and IkBalpha protein expression in humans subjects.	Aspirin	34-41	NFKB inhibitor alpha	Homo sapiens	82-90
27391154-8	2016	CONCLUSION: Aspirin activates AP-2alpha to upregulate IkBalpha gene expression, resulting in attenuations of plaque development and instability in atherosclerosis.	Aspirin	12-19	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	54-62
27489545-1	2016	In subjects with non-steroidal anti-inflammatory drugs (NSAIDs)- exacerbated respiratory disease (NERD) symptoms are triggered by acetyl salicylic acid (ASA) and other strong COX-1 inhibitors, and in some cases by weak COX-1 or by selective COX-2 inhibitors.	Aspirin	153-156	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	241-246
27086085-0	2016	Parathyroid Hormone Levels and High-Residual Platelet Reactivity in Patients Receiving Dual Antiplatelet Therapy With Acetylsalicylic Acid and Clopidogrel or Ticagrelor.	Aspirin	118-138	parathyroid hormone	Homo sapiens	0-19
26957558-1	2016	PURPOSE: Prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase-2; a target of aspirin) produces inflammatory mediator prostaglandin E2 (PGE2), and contributes to colorectal neoplasia development.	Aspirin	85-92	prostaglandin-endoperoxide synthase 2	Homo sapiens	9-46
26957558-1	2016	PURPOSE: Prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase-2; a target of aspirin) produces inflammatory mediator prostaglandin E2 (PGE2), and contributes to colorectal neoplasia development.	Aspirin	85-92	prostaglandin-endoperoxide synthase 2	Homo sapiens	48-53
26957558-1	2016	PURPOSE: Prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase-2; a target of aspirin) produces inflammatory mediator prostaglandin E2 (PGE2), and contributes to colorectal neoplasia development.	Aspirin	85-92	prostaglandin-endoperoxide synthase 2	Homo sapiens	55-71
27175028-8	2016	In conclusion, in patients with low-risk, CALR-mutated essential thrombocythemia, low-dose aspirin does not reduce the risk of thrombosis and may increase the risk of bleeding.	Aspirin	91-98	calreticulin	Homo sapiens	42-46
26915678-3	2016	OBJECTIVE: We sought to evaluate the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on T-cell activation of the IL-4 pathway in aspirin-sensitive patients with asthma and control subjects.	Aspirin	138-145	interleukin 4	Homo sapiens	122-126
26915678-15	2016	This inhibition was significantly higher in aspirin-sensitive patients than in aspirin-tolerant subjects and was associated with reduced expression of IL-4.	Aspirin	44-51	interleukin 4	Homo sapiens	151-155
26915678-15	2016	This inhibition was significantly higher in aspirin-sensitive patients than in aspirin-tolerant subjects and was associated with reduced expression of IL-4.	Aspirin	79-86	interleukin 4	Homo sapiens	151-155
27126722-1	2016	Aspirin-exacerbated respiratory disease (AERD) is an adult-onset upper and lower airway disease consisting of eosinophilic nasal polyps, asthma, and respiratory reactions to cyclooxygenase 1 (COX-1) inhibitors.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	174-190
27412561-8	2016	Pretreatment with 20 mug/mL of aspirin in VSMCs could partially block the above-mentioned effects induced by TNF-alpha.	Aspirin	31-38	tumor necrosis factor	Homo sapiens	109-118
27126722-1	2016	Aspirin-exacerbated respiratory disease (AERD) is an adult-onset upper and lower airway disease consisting of eosinophilic nasal polyps, asthma, and respiratory reactions to cyclooxygenase 1 (COX-1) inhibitors.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	192-197
26525539-8	2016	ASA activated the PI3K/Akt-GSK3-mTOR pathway, which phosphorylates ULK1 to prevent autophagy initiation, changes that were inhibited by the PI3K-inhibitor wortmannin.	Aspirin	0-3	AKT serine/threonine kinase 1	Rattus norvegicus	23-26
26969214-0	2016	Aspirin induces Nrf2-mediated transcriptional activation of haem oxygenase-1 in protection of human melanocytes from H2 O2 -induced oxidative stress.	Aspirin	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	16-20
26969214-9	2016	Furthermore, we found ASA dramatically induced NRF2 nuclear translocation, enhanced ARE-luciferase activity, increased both p- NRF2 and total NRF2 levels, and induced the expression of haem oxygenase-1 (HO-1) in human melanocytes.	Aspirin	22-25	NFE2 like bZIP transcription factor 2	Homo sapiens	47-51
26969214-9	2016	Furthermore, we found ASA dramatically induced NRF2 nuclear translocation, enhanced ARE-luciferase activity, increased both p- NRF2 and total NRF2 levels, and induced the expression of haem oxygenase-1 (HO-1) in human melanocytes.	Aspirin	22-25	NFE2 like bZIP transcription factor 2	Homo sapiens	127-131
26969214-9	2016	Furthermore, we found ASA dramatically induced NRF2 nuclear translocation, enhanced ARE-luciferase activity, increased both p- NRF2 and total NRF2 levels, and induced the expression of haem oxygenase-1 (HO-1) in human melanocytes.	Aspirin	22-25	NFE2 like bZIP transcription factor 2	Homo sapiens	127-131
26969214-10	2016	In addition, knockdown of Nrf2 expression or pharmacological inhibition of HO-1 abrogated the protective action of ASA on melanocytes against H2 O2 -induced cytotoxicity and apoptosis.	Aspirin	115-118	NFE2 like bZIP transcription factor 2	Homo sapiens	26-30
26969214-11	2016	These results suggest that ASA protects human melanocytes against H2 O2 -induced oxidative stress via Nrf2-driven transcriptional activation of HO-1.	Aspirin	27-30	NFE2 like bZIP transcription factor 2	Homo sapiens	102-106
26525539-8	2016	ASA activated the PI3K/Akt-GSK3-mTOR pathway, which phosphorylates ULK1 to prevent autophagy initiation, changes that were inhibited by the PI3K-inhibitor wortmannin.	Aspirin	0-3	unc-51 like autophagy activating kinase 1	Rattus norvegicus	67-71
26059811-1	2016	Aspirin, one of the most commonly used anti-inflammatory drugs, has been recently reported to display multiple effects in the central nervous system (CNS), including neuroprotection and upregulation of ciliary neurotrophic factor (CNTF) expression in astrocytes.	Aspirin	0-7	ciliary neurotrophic factor	Rattus norvegicus	202-229
27399131-8	2016	CONCLUSION: Ticagrelor and apixaban with or without ASA inhibit platelet activation and thrombin formation in vivo in healthy subjects.	Aspirin	52-55	coagulation factor II, thrombin	Homo sapiens	88-96
27347106-0	2016	Aspirin inhibits growth of ovarian cancer by upregulating caspase-3 and downregulating bcl-2.	Aspirin	0-7	B cell leukemia/lymphoma 2	Mus musculus	87-92
27347106-10	2016	The relative expression level of caspase-3, bcl-2 protein of the 3 mmol/l aspirin group was significantly improved and reduced, respectively.	Aspirin	74-81	B cell leukemia/lymphoma 2	Mus musculus	44-49
27347106-11	2016	In conclusion, aspirin can inhibit the growth of ovarian cancer of p53S rats due to its upregulation of the expression of caspase-3 protein and downregulation of the expression of bcl-2 protein.	Aspirin	15-22	BCL2, apoptosis regulator	Rattus norvegicus	180-185
27393450-4	2016	We conducted this study to investigate whether previously studied polymorphisms in COX-1, GPIIIa, GPIa and P2RYI genes could be the cause of aspirin resistance in our population.	Aspirin	141-148	integrin subunit beta 3	Homo sapiens	90-96
26059811-1	2016	Aspirin, one of the most commonly used anti-inflammatory drugs, has been recently reported to display multiple effects in the central nervous system (CNS), including neuroprotection and upregulation of ciliary neurotrophic factor (CNTF) expression in astrocytes.	Aspirin	0-7	ciliary neurotrophic factor	Rattus norvegicus	231-235
27083140-1	2016	Due to its ability to inhibit the blood platelet PGHS-1, acetylsalicylic acid (ASA, Aspirin( )) is widely used as a preventive agent in atherothrombotic diseases.	Aspirin	57-77	prostaglandin-endoperoxide synthase 1	Homo sapiens	49-55
27103451-8	2016	Aspirin therapy significantly inhibited platelets since cyclooxygenase 1 derived thromboxane generation levels were reduced by 99%.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	56-72
27083140-6	2016	The prior glycation/carbonylation of PGHS-1 with Glu, 1,6-BPF or MGO decreased the extent of acetylation from 6.4 +- 1.1 down to 2.5 +- 0.2, 3.6 +- 0.3 and 5.2 +- 0.2 mol/mol protein, respectively, but the enzyme still remained susceptible to the subsequent inhibition of its activity with ASA.	Aspirin	290-293	prostaglandin-endoperoxide synthase 1	Homo sapiens	37-43
27083140-1	2016	Due to its ability to inhibit the blood platelet PGHS-1, acetylsalicylic acid (ASA, Aspirin( )) is widely used as a preventive agent in atherothrombotic diseases.	Aspirin	79-82	prostaglandin-endoperoxide synthase 1	Homo sapiens	49-55
27129261-4	2016	The lipid is generated in nanogram amounts by platelets from endogenous arachidonate during physiological activation, with inhibition by aspirin in vitro or in vivo, implicating cyclooxygenase-1 (COX).	Aspirin	137-144	prostaglandin-endoperoxide synthase 1	Homo sapiens	178-194
27083140-1	2016	Due to its ability to inhibit the blood platelet PGHS-1, acetylsalicylic acid (ASA, Aspirin( )) is widely used as a preventive agent in atherothrombotic diseases.	Aspirin	84-91	prostaglandin-endoperoxide synthase 1	Homo sapiens	49-55
27083140-5	2016	When PGHS-1 was incubated with glycating/acetylating agents (glucose, Glu; 1,6-bisphosphofructose, 1,6-BPF; methylglyoxal, MGO, acetylsalicylic acid, ASA), the enzyme was modified in 13.4 +- 1.6, 5.3 +- 0.5, 10.7 +- 1.2 and 6.4 +- 1.1 mol/mol protein, respectively, and its activity was significantly reduced.	Aspirin	128-148	prostaglandin-endoperoxide synthase 1	Homo sapiens	5-11
27083140-5	2016	When PGHS-1 was incubated with glycating/acetylating agents (glucose, Glu; 1,6-bisphosphofructose, 1,6-BPF; methylglyoxal, MGO, acetylsalicylic acid, ASA), the enzyme was modified in 13.4 +- 1.6, 5.3 +- 0.5, 10.7 +- 1.2 and 6.4 +- 1.1 mol/mol protein, respectively, and its activity was significantly reduced.	Aspirin	150-153	prostaglandin-endoperoxide synthase 1	Homo sapiens	5-11
27207670-9	2016	Furthermore, AOM/DSS + ASA inhibited AOM/DSS-induced enrichment of H3K27ac in the promoters of inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) that corresponded to the dramatic suppression of the messenger RNA (mRNA) and protein levels.	Aspirin	23-26	nitric oxide synthase 2, inducible	Mus musculus	95-126
26656902-6	2016	Compared with those of Group 2, patients with aspirin resistance exhibited significantly higher white blood cell counts, neutrophil counts, neutrophil-to-lymphocyte ratios, SUA levels, high-sensitivity C-reactive protein levels, and fasting blood glucose levels.	Aspirin	46-53	C-reactive protein	Homo sapiens	202-220
27207670-9	2016	Furthermore, AOM/DSS + ASA inhibited AOM/DSS-induced enrichment of H3K27ac in the promoters of inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) that corresponded to the dramatic suppression of the messenger RNA (mRNA) and protein levels.	Aspirin	23-26	nitric oxide synthase 2, inducible	Mus musculus	128-132
27207670-9	2016	Furthermore, AOM/DSS + ASA inhibited AOM/DSS-induced enrichment of H3K27ac in the promoters of inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) that corresponded to the dramatic suppression of the messenger RNA (mRNA) and protein levels.	Aspirin	23-26	tumor necrosis factor	Mus musculus	135-162
27207670-9	2016	Furthermore, AOM/DSS + ASA inhibited AOM/DSS-induced enrichment of H3K27ac in the promoters of inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) that corresponded to the dramatic suppression of the messenger RNA (mRNA) and protein levels.	Aspirin	23-26	tumor necrosis factor	Mus musculus	164-173
27207670-9	2016	Furthermore, AOM/DSS + ASA inhibited AOM/DSS-induced enrichment of H3K27ac in the promoters of inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) that corresponded to the dramatic suppression of the messenger RNA (mRNA) and protein levels.	Aspirin	23-26	interleukin 6	Mus musculus	179-192
27207670-9	2016	Furthermore, AOM/DSS + ASA inhibited AOM/DSS-induced enrichment of H3K27ac in the promoters of inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) that corresponded to the dramatic suppression of the messenger RNA (mRNA) and protein levels.	Aspirin	23-26	interleukin 6	Mus musculus	194-198
27207670-11	2016	Collectively, our results suggest that a potential novel epigenetic mechanism underlies the chemopreventive effects of ASA, and this mechanism attenuates CAC in AOM/DSS-induced CF-1 mice via the inhibition of HDACs and the modification of H3K27ac marks that suppress iNOS, TNF-alpha and IL-6.	Aspirin	119-122	nitric oxide synthase 2, inducible	Mus musculus	267-271
27207670-11	2016	Collectively, our results suggest that a potential novel epigenetic mechanism underlies the chemopreventive effects of ASA, and this mechanism attenuates CAC in AOM/DSS-induced CF-1 mice via the inhibition of HDACs and the modification of H3K27ac marks that suppress iNOS, TNF-alpha and IL-6.	Aspirin	119-122	tumor necrosis factor	Mus musculus	273-282
27207670-11	2016	Collectively, our results suggest that a potential novel epigenetic mechanism underlies the chemopreventive effects of ASA, and this mechanism attenuates CAC in AOM/DSS-induced CF-1 mice via the inhibition of HDACs and the modification of H3K27ac marks that suppress iNOS, TNF-alpha and IL-6.	Aspirin	119-122	interleukin 6	Mus musculus	287-291
27074574-6	2016	Platelet COX-1 inhibition by aspirin administration to mice prevented the increased rate of metastasis as well as the enhanced production of TXA2 and PGE2 induced by the in vitro priming of HT29 cells by platelets.	Aspirin	29-36	cytochrome c oxidase I, mitochondrial	Mus musculus	9-14
27161407-16	2016	DHI strengthened the inhibition activity of ASA on both COX-1 and COX-2, which showed that DHI alleviated ASA induced gastric mucosal damage but not antagonized anti-COX effect of ASA.	Aspirin	44-47	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	56-61
27153943-0	2016	Oral treatment with a zinc complex of acetylsalicylic acid prevents diabetic cardiomyopathy in a rat model of type-2 diabetes: activation of the Akt pathway.	Aspirin	38-58	AKT serine/threonine kinase 1	Rattus norvegicus	145-148
27133131-8	2016	Thrombin elevated ~900 lipids &gt;2-fold with 86% newly appearing and 45% inhibited by aspirin supplementation, indicating COX-1 is required for major activation-dependent lipidomic fluxes.	Aspirin	87-94	coagulation factor II, thrombin	Homo sapiens	0-8
26601827-0	2016	The IL-1B Genetic Polymorphism Is Associated with Aspirin-Induced PepticUlcers in a Korean Ethnic Group.	Aspirin	50-57	interleukin 1 beta	Homo sapiens	4-9
26601827-8	2016	On the multivariate analysis after adjustments for age and sex, the CC/CT genotypes of IL-1beta -581C/ T, and the CT/TT genotypes of IL-1beta -1061C/T were positively associated with aspirin-induced peptic ulcers (odds ratio [OR], 4.6, 95% confidence interval [CI], 1.054 to 20.303, p=0.04; OR, 4.6, 95% CI, 1.054 to 20.303, p=0.04).	Aspirin	183-190	interleukin 1 beta	Homo sapiens	87-95
26601827-8	2016	On the multivariate analysis after adjustments for age and sex, the CC/CT genotypes of IL-1beta -581C/ T, and the CT/TT genotypes of IL-1beta -1061C/T were positively associated with aspirin-induced peptic ulcers (odds ratio [OR], 4.6, 95% confidence interval [CI], 1.054 to 20.303, p=0.04; OR, 4.6, 95% CI, 1.054 to 20.303, p=0.04).	Aspirin	183-190	interleukin 1 beta	Homo sapiens	133-141
26601827-9	2016	CONCLUSIONS: The IL-1beta -581C/T and IL-1beta -1061C/T genotypes may be associated with low-dose aspirin-induced peptic ulcers in a Korean ethnic group.	Aspirin	98-105	interleukin 1 beta	Homo sapiens	17-25
26601827-9	2016	CONCLUSIONS: The IL-1beta -581C/T and IL-1beta -1061C/T genotypes may be associated with low-dose aspirin-induced peptic ulcers in a Korean ethnic group.	Aspirin	98-105	interleukin 1 beta	Homo sapiens	38-46
26962983-0	2016	Association of PEAR1 genetic variants with platelet reactivity in response to dual antiplatelet therapy with aspirin and clopidogrel in the Chinese patient population after percutaneous coronary intervention.	Aspirin	109-116	platelet endothelial aggregation receptor 1	Homo sapiens	15-20
26712086-3	2016	Preclinical data show that aspirin down-regulates PI3 kinase (PI3K) signalling activity through cyclo-oxygenase-2 (COX-2) inhibition, leading to the hypothesis that the effect of aspirin might be different according to PIK3CA mutational status, but epidemiological studies have led to conflicting results.	Aspirin	27-34	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	219-225
26712086-4	2016	The aim of this study was to assess the relationship between PIK3CA status and the efficacy of regular use of aspirin after diagnosis on overall survival in colorectal cancer patients.	Aspirin	110-117	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	61-67
26712086-5	2016	MATERIALS AND METHODS: We identified studies that compared post-diagnosis aspirin efficacy in colorectal cancer patients identified by PIK3CA status.	Aspirin	74-81	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	135-141
26712086-12	2016	CONCLUSION: These findings suggest that the benefit of post-diagnosis aspirin treatment on overall mortality in colorectal cancer may be more marked in PIK3CA mutated tumours, although the low number of studies prevents definitive conclusions.	Aspirin	70-77	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	152-158
27018926-12	2016	After RIC during aspirin treatment, changes in thrombin generation were inconsistent; increased peak (p=0.04) and time to peak (p&lt;0.001) and a decrease in lag-time (p&lt;0.001).	Aspirin	17-24	coagulation factor II, thrombin	Homo sapiens	47-55
26873936-5	2016	Aspirin consumption significantly blocked thrombin- and collagen-induced increases in exosome cargo levels of chemokines and HMGB1, without altering total exosome secretion or GPVI cargo.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	42-50
27217606-8	2016	Aspirin decreased lipid peroxidation following SCI as the mean (+- standard error) catalase level was significantly higher in the high-dose aspirin group (46.10+-12.01) than in the sham-treated group (16.07+-2.42) and the vehicle-treated group (15.31+-3.20) (P&lt;0.05; P&lt;0.05, respectively).	Aspirin	0-7	catalase	Rattus norvegicus	83-91
27217606-8	2016	Aspirin decreased lipid peroxidation following SCI as the mean (+- standard error) catalase level was significantly higher in the high-dose aspirin group (46.10+-12.01) than in the sham-treated group (16.07+-2.42) and the vehicle-treated group (15.31+-3.20) (P&lt;0.05; P&lt;0.05, respectively).	Aspirin	140-147	catalase	Rattus norvegicus	83-91
26962983-2	2016	The aim of this study was to investigate whether PEAR1 genetic variations were associated with platelet reactivity as assessed by adenosine diphosphate(ADP)-induced platelet aggregation in Chinese patients treated with aspirin and clopidogrel.	Aspirin	219-226	platelet endothelial aggregation receptor 1	Homo sapiens	49-54
26962983-12	2016	CONCLUSIONS: PEAR1 genetic variations were strongly associated with ADP-induced platelet aggregation in Chinese patients with CHD treated with aspirin and clopidogrel.	Aspirin	143-150	platelet endothelial aggregation receptor 1	Homo sapiens	13-18
26678823-8	2016	ALOX5 was a common predictor of studies on NAR to both aspirin and NSAIDs.	Aspirin	55-62	arachidonate 5-lipoxygenase	Homo sapiens	0-5
26596838-0	2016	Aspirin acetylates wild type and mutant p53 in colon cancer cells: identification of aspirin acetylated sites on recombinant p53.	Aspirin	0-7	tumor protein p53	Homo sapiens	40-43
26596838-0	2016	Aspirin acetylates wild type and mutant p53 in colon cancer cells: identification of aspirin acetylated sites on recombinant p53.	Aspirin	0-7	tumor protein p53	Homo sapiens	125-128
26596838-0	2016	Aspirin acetylates wild type and mutant p53 in colon cancer cells: identification of aspirin acetylated sites on recombinant p53.	Aspirin	85-92	tumor protein p53	Homo sapiens	125-128
26596838-2	2016	We previously demonstrated that aspirin acetylated the tumor suppressor protein p53 at lysine 382 in MDA-MB-231 human breast cancer cells.	Aspirin	32-39	tumor protein p53	Homo sapiens	80-83
26596838-4	2016	We demonstrate that aspirin induced acetylation of p53 in both cell lines in a concentration-dependent manner.	Aspirin	20-27	tumor protein p53	Homo sapiens	51-54
26596838-5	2016	Aspirin-acetylated p53 was localized to the nucleus.	Aspirin	0-7	tumor protein p53	Homo sapiens	19-22
26596838-6	2016	In both cell lines, aspirin induced p21(CIP1).	Aspirin	20-27	cyclin dependent kinase inhibitor 1A	Homo sapiens	40-44
26596838-7	2016	Aspirin also acetylated recombinant p53 (rp53) in vitro suggesting that it occurs through a non-enzymatic chemical reaction.	Aspirin	0-7	tumor protein p53	Homo sapiens	36-39
26596838-10	2016	Our results suggest that aspirin"s anti-cancer effect may involve acetylation and activation of wild type and mutant p53 and induction of target gene expression.	Aspirin	25-32	tumor protein p53	Homo sapiens	117-120
26596838-11	2016	This is the first report attempting to characterize p53 acetylation sites targeted by aspirin.	Aspirin	86-93	tumor protein p53	Homo sapiens	52-55
27096951-15	2016	A mutation of PIK3CA was present in about 20% of patients, and appeared to explain most of the reduction in colon cancer mortality by aspirin.	Aspirin	134-141	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	14-20
26139358-7	2016	From logistic regression, a family history for PFO, ASA, and male gender appeared independent predictors of a RLS.	Aspirin	52-55	RLS1	Homo sapiens	110-113
26847573-1	2016	PURPOSE: The benefit of angiotensin converting enzyme (ACE) inhibition in chronic heart failure (HF) is partially due to its effects on pulmonary function and particularly on lung diffusion, the latter being counteracted by acetylsalicylic acid (ASA).	Aspirin	224-244	angiotensin I converting enzyme	Homo sapiens	24-53
26842876-0	2016	Aspirin Suppresses the Acquisition of Chemoresistance in Breast Cancer by Disrupting an NFkappaB-IL6 Signaling Axis Responsible for the Generation of Cancer Stem Cells.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	88-96
26842876-7	2016	Treatment with aspirin prior to chemotherapy suppressed the acquisition of chemoresistance by perturbing the nuclear translocation of NFkappaB in preexisting CSCs.	Aspirin	15-22	nuclear factor kappa B subunit 1	Homo sapiens	134-142
26843365-1	2016	AIMS: The objective of the present substudy was to examine whether aspirin poor/high responsiveness (APR/AHR) is associated with increased rates of major adverse cardiovascular events (MACE) and serious bleeding after primary percutaneous coronary intervention (PPCI).	Aspirin	67-74	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	101-104
26843365-4	2016	APR/AHR were defined as the upper/lower quintiles of ASPI values, determined 24 h after aspirin loading.	Aspirin	88-95	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	0-3
26847573-1	2016	PURPOSE: The benefit of angiotensin converting enzyme (ACE) inhibition in chronic heart failure (HF) is partially due to its effects on pulmonary function and particularly on lung diffusion, the latter being counteracted by acetylsalicylic acid (ASA).	Aspirin	224-244	angiotensin I converting enzyme	Homo sapiens	55-58
26847573-1	2016	PURPOSE: The benefit of angiotensin converting enzyme (ACE) inhibition in chronic heart failure (HF) is partially due to its effects on pulmonary function and particularly on lung diffusion, the latter being counteracted by acetylsalicylic acid (ASA).	Aspirin	246-249	angiotensin I converting enzyme	Homo sapiens	24-53
26847573-1	2016	PURPOSE: The benefit of angiotensin converting enzyme (ACE) inhibition in chronic heart failure (HF) is partially due to its effects on pulmonary function and particularly on lung diffusion, the latter being counteracted by acetylsalicylic acid (ASA).	Aspirin	246-249	angiotensin I converting enzyme	Homo sapiens	55-58
26635114-0	2016	Aspirin Inhibits LPS-Induced Expression of PI3K/Akt, ERK, NF-kappaB, CX3CL1, and MMPs in Human Bronchial Epithelial Cells.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	48-51
26774572-7	2016	Interestingly, ASP- and PROP-containing substrates not only showed reduced adhesion of platelets and delayed coagulation time, but also drastically reduced the expression level of IL-8 and IL-6.	Aspirin	15-18	C-X-C motif chemokine ligand 8	Homo sapiens	180-184
26774572-7	2016	Interestingly, ASP- and PROP-containing substrates not only showed reduced adhesion of platelets and delayed coagulation time, but also drastically reduced the expression level of IL-8 and IL-6.	Aspirin	15-18	interleukin 6	Homo sapiens	189-193
26635114-8	2016	When compared to the LPS group, expression of PI3K/Akt, ERK, NF-kappaB, and CX3CL1 was significantly decreased in the PD group, PDTC group, and Asp group (P &lt; 0.05).	Aspirin	144-147	AKT serine/threonine kinase 1	Homo sapiens	51-54
26635114-8	2016	When compared to the LPS group, expression of PI3K/Akt, ERK, NF-kappaB, and CX3CL1 was significantly decreased in the PD group, PDTC group, and Asp group (P &lt; 0.05).	Aspirin	144-147	mitogen-activated protein kinase 1	Homo sapiens	56-59
26635114-0	2016	Aspirin Inhibits LPS-Induced Expression of PI3K/Akt, ERK, NF-kappaB, CX3CL1, and MMPs in Human Bronchial Epithelial Cells.	Aspirin	0-7	mitogen-activated protein kinase 1	Homo sapiens	53-56
26635114-8	2016	When compared to the LPS group, expression of PI3K/Akt, ERK, NF-kappaB, and CX3CL1 was significantly decreased in the PD group, PDTC group, and Asp group (P &lt; 0.05).	Aspirin	144-147	nuclear factor kappa B subunit 1	Homo sapiens	61-70
26635114-8	2016	When compared to the LPS group, expression of PI3K/Akt, ERK, NF-kappaB, and CX3CL1 was significantly decreased in the PD group, PDTC group, and Asp group (P &lt; 0.05).	Aspirin	144-147	C-X3-C motif chemokine ligand 1	Homo sapiens	76-82
26635114-0	2016	Aspirin Inhibits LPS-Induced Expression of PI3K/Akt, ERK, NF-kappaB, CX3CL1, and MMPs in Human Bronchial Epithelial Cells.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	58-67
26635114-14	2016	Aspirin inhibited LPS-induced expression of PI3K, Akt, ERK, NF-kappaB, CX3CL1, MMP-7, and MMP-12 in human bronchial epithelial cells.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	50-53
26635114-0	2016	Aspirin Inhibits LPS-Induced Expression of PI3K/Akt, ERK, NF-kappaB, CX3CL1, and MMPs in Human Bronchial Epithelial Cells.	Aspirin	0-7	C-X3-C motif chemokine ligand 1	Homo sapiens	69-75
26635114-14	2016	Aspirin inhibited LPS-induced expression of PI3K, Akt, ERK, NF-kappaB, CX3CL1, MMP-7, and MMP-12 in human bronchial epithelial cells.	Aspirin	0-7	mitogen-activated protein kinase 1	Homo sapiens	55-58
26635114-1	2016	This study focused on the effects of aspirin on lipopolysaccharide (LPS)-induced expression of phosphoinositide 3 kinase (PI3K)/protein kinase B (Akt), extracellular signal-regulated protein kinase (ERK), nuclear factor-kappaB (NF-kappaB), CX3CL1, and MMPs in human bronchial epithelial cells.	Aspirin	37-44	mitogen-activated protein kinase 1	Homo sapiens	152-197
26635114-14	2016	Aspirin inhibited LPS-induced expression of PI3K, Akt, ERK, NF-kappaB, CX3CL1, MMP-7, and MMP-12 in human bronchial epithelial cells.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	60-69
26635114-14	2016	Aspirin inhibited LPS-induced expression of PI3K, Akt, ERK, NF-kappaB, CX3CL1, MMP-7, and MMP-12 in human bronchial epithelial cells.	Aspirin	0-7	C-X3-C motif chemokine ligand 1	Homo sapiens	71-77
26918349-10	2016	Combination of aspirin and AMPK, Akt or MEK inhibitor results in more significant inhibition of cell proliferation and induction of apoptosis than single agent.	Aspirin	15-22	mitogen-activated protein kinase kinase 7	Homo sapiens	40-43
26917098-8	2016	Acetylsalicylic acid supplementation caused a considerable increase in the expression of all active substances studied within both left and right NG and the percentage of neurons positive to particular substances fluctuated from 47.2 +- 3.6% (GAL-LI neurons in the right NG) to 67.2 +- 2.0% (cells immunoreactive to SP in the left NG).	Aspirin	0-20	tachykinin precursor 1	Homo sapiens	316-318
26918349-5	2016	Here, we show that aspirin induces the expression of MCL-1 in HepG2 and SW480 cells through AMPK-mTOR-Akt/ERK axis.	Aspirin	19-26	mechanistic target of rapamycin kinase	Homo sapiens	97-101
26918349-5	2016	Here, we show that aspirin induces the expression of MCL-1 in HepG2 and SW480 cells through AMPK-mTOR-Akt/ERK axis.	Aspirin	19-26	AKT serine/threonine kinase 1	Homo sapiens	102-105
26918349-5	2016	Here, we show that aspirin induces the expression of MCL-1 in HepG2 and SW480 cells through AMPK-mTOR-Akt/ERK axis.	Aspirin	19-26	mitogen-activated protein kinase 1	Homo sapiens	106-109
26918349-6	2016	Treatment of HepG2 and SW480 cells with aspirin leads to increased MCL-1 expression, Akt and ERK1/2 phosphorylation.	Aspirin	40-47	AKT serine/threonine kinase 1	Homo sapiens	85-88
26918349-6	2016	Treatment of HepG2 and SW480 cells with aspirin leads to increased MCL-1 expression, Akt and ERK1/2 phosphorylation.	Aspirin	40-47	mitogen-activated protein kinase 3	Homo sapiens	93-99
26918349-7	2016	Inhibition of Akt/MEK abrogates the induction of MCL-1 by aspirin.	Aspirin	58-65	AKT serine/threonine kinase 1	Homo sapiens	14-17
26918349-7	2016	Inhibition of Akt/MEK abrogates the induction of MCL-1 by aspirin.	Aspirin	58-65	mitogen-activated protein kinase kinase 7	Homo sapiens	18-21
26918349-8	2016	Aspirin activates AMPK, which in turn up-regulates mTORC2 activity, Akt, ERK1/2 phosphorylation and MCL-1 expression.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	68-71
26918349-8	2016	Aspirin activates AMPK, which in turn up-regulates mTORC2 activity, Akt, ERK1/2 phosphorylation and MCL-1 expression.	Aspirin	0-7	mitogen-activated protein kinase 3	Homo sapiens	73-79
26965534-1	2016	BACKGROUND: The PEGASUS-TIMI 54 (Prevention of Cardiovascular Events in Patients with Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis In Myocardial Infarction 54) trial studied 2 doses of ticagrelor, 90 mg twice a day (bid) and 60 mg bid, for long-term prevention of ischemic events in patients with prior myocardial infarction.	Aspirin	161-168	IKAROS family zinc finger 5	Homo sapiens	16-31
26859324-0	2016	Crystal Structure of Aspirin-Acetylated Human Cyclooxygenase-2: Insight into the Formation of Products with Reversed Stereochemistry.	Aspirin	21-28	prostaglandin-endoperoxide synthase 2	Homo sapiens	46-62
26980433-4	2016	The expression of COX2 mRNA in platelets and its influences on the effect of aspirin was also investigated.	Aspirin	77-84	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	18-22
26859324-5	2016	We determined the crystal structures of S530T murine (mu) COX-2, aspirin-acetylated human (hu) COX-2, and huCOX-2 in complex with salicylate to 1.9, 2.0, and 2.4 A, respectively.	Aspirin	65-72	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	95-100
26859324-1	2016	Aspirin and other nonsteroidal anti-inflammatory drugs target the cyclooxygenase enzymes (COX-1 and COX-2) to block the formation of prostaglandins.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	100-105
26859324-7	2016	On the basis of these structural observations, along with functional analysis of the S530T/G533V double mutant, we propose a working hypothesis for the generation of 15R-HETE by aspirin-acetylated COX-2.	Aspirin	178-185	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	197-202
26927051-3	2016	Thrombin also amplifies the response to the tissue injury, coagulation and platelet response, so the treatment of ACS is based on the combined use of both antiplatelet (such as aspirin, clopidogrel, prasugrel and ticagrelor) and antithrombotic drugs (unfractionated heparin, enoxaparin, fondaparinux and bivalirudin).	Aspirin	177-184	coagulation factor II, thrombin	Homo sapiens	0-8
26869523-0	2016	Aspirin-Triggered Resolvin D1 Inhibits TGF-beta1-Induced EndMT through Increasing the Expression of Smad7 and Is Closely Related to Oxidative Stress.	Aspirin	0-7	transforming growth factor beta 1	Homo sapiens	39-48
26869523-0	2016	Aspirin-Triggered Resolvin D1 Inhibits TGF-beta1-Induced EndMT through Increasing the Expression of Smad7 and Is Closely Related to Oxidative Stress.	Aspirin	0-7	SMAD family member 7	Homo sapiens	100-105
26503111-0	2016	Aspirin and NSAID use in association with molecular subtypes of prostate cancer defined by TMPRSS2:ERG fusion status.	Aspirin	0-7	transmembrane serine protease 2	Homo sapiens	91-98
27263286-4	2016	When compared with arsenic trioxide alone, co-treatment of arsenic trioxide with aspirin in different concentration (0, 0.1, 1.0, 2.5, 5.0 mmol/L) exhibited dual effects in intracellular ROS level, HO-1 and Nrf2 expression.	Aspirin	81-88	NFE2 like bZIP transcription factor 2	Homo sapiens	207-211
27263286-5	2016	Specifically, with the increasing of aspirin concentrations, the level of ROS induced by arsenic trioxide showed a rising trend after the first reduction, whereas, HO-1 and Nrf2 protein expression were decreased at first and then increased.	Aspirin	37-44	NFE2 like bZIP transcription factor 2	Homo sapiens	173-177
27263286-6	2016	CONCLUSION: Low concentration, less than 2.5 mmol/L, of aspirin may reduce the ROS accumulation through activating of Nrf2-HO-1 pathway, therefore decreasing the apoptotic cell death induced by arsenic trioxide.	Aspirin	56-63	NFE2 like bZIP transcription factor 2	Homo sapiens	118-122
27263286-7	2016	On the contrary, 5 mmol/L aspirin could increase the sensitivity of HepG2 to arsenic trioxide through enhancing the arsenic trioxide-induced apoptosis by ROS accumulation resulting in inhibiting the Nrf2-HO-1 pathway.	Aspirin	26-33	NFE2 like bZIP transcription factor 2	Homo sapiens	199-203
26685215-0	2016	Cyclin A2 and CDK2 as Novel Targets of Aspirin and Salicylic Acid: A Potential Role in Cancer Prevention.	Aspirin	39-46	cyclin A2	Homo sapiens	0-9
26685215-2	2016	We hypothesized that aspirin"s chemopreventive actions may involve cell-cycle regulation through modulation of the levels or activity of cyclin A2/cyclin-dependent kinase-2 (CDK2).	Aspirin	21-28	cyclin A2	Homo sapiens	137-172
26685215-3	2016	In this study, HT-29 and other diverse panel of cancer cells were used to demonstrate that both aspirin and its primary metabolite, salicylic acid, decreased cyclin A2 (CCNA2) and CDK2 protein and mRNA levels.	Aspirin	96-103	cyclin A2	Homo sapiens	158-167
26898989-0	2016	The aspirin-induced long non-coding RNA OLA1P2 blocks phosphorylated STAT3 homodimer formation.	Aspirin	4-11	signal transducer and activator of transcription 3	Homo sapiens	69-74
26685215-3	2016	In this study, HT-29 and other diverse panel of cancer cells were used to demonstrate that both aspirin and its primary metabolite, salicylic acid, decreased cyclin A2 (CCNA2) and CDK2 protein and mRNA levels.	Aspirin	96-103	cyclin A2	Homo sapiens	169-174
26685215-10	2016	These results demonstrate that aspirin and salicylic acid downregulate cyclin A2/CDK2 proteins in multiple cancer cell lines, suggesting a novel target and mechanism of action in chemoprevention.	Aspirin	31-38	cyclin A2	Homo sapiens	71-80
26685215-11	2016	IMPLICATIONS: Biochemical and structural studies indicate that the antiproliferative actions of aspirin are mediated through cyclin A2/CDK2.	Aspirin	96-103	cyclin A2	Homo sapiens	125-134
26898989-3	2016	Aspirin induces demethylation of the FOXD3 promoter and promotes expression of the FOXD3 gene.	Aspirin	0-7	forkhead box D3	Homo sapiens	37-42
26898989-3	2016	Aspirin induces demethylation of the FOXD3 promoter and promotes expression of the FOXD3 gene.	Aspirin	0-7	forkhead box D3	Homo sapiens	83-88
26898989-10	2016	CONCLUSIONS: The present study finds that the aspirin-FOXD3-OLA1P2-STAT3 axis exhibits exciting anticancer effects and provides new insights into the chemopreventive mechanisms underlying aspirin use.	Aspirin	46-53	forkhead box D3	Homo sapiens	54-59
26898989-10	2016	CONCLUSIONS: The present study finds that the aspirin-FOXD3-OLA1P2-STAT3 axis exhibits exciting anticancer effects and provides new insights into the chemopreventive mechanisms underlying aspirin use.	Aspirin	46-53	signal transducer and activator of transcription 3	Homo sapiens	67-72
26898989-10	2016	CONCLUSIONS: The present study finds that the aspirin-FOXD3-OLA1P2-STAT3 axis exhibits exciting anticancer effects and provides new insights into the chemopreventive mechanisms underlying aspirin use.	Aspirin	188-195	forkhead box D3	Homo sapiens	54-59
26898989-10	2016	CONCLUSIONS: The present study finds that the aspirin-FOXD3-OLA1P2-STAT3 axis exhibits exciting anticancer effects and provides new insights into the chemopreventive mechanisms underlying aspirin use.	Aspirin	188-195	signal transducer and activator of transcription 3	Homo sapiens	67-72
27069632-0	2016	Comparative effects of immediate-release and extended-release aspirin on basal and bradykinin-stimulated excretion of thromboxane and prostacyclin metabolites.	Aspirin	62-69	kininogen 1	Homo sapiens	83-93
27069632-8	2016	Both doses of ASA and NHP significantly reduced excretion of both thromboxane and prostacyclin metabolites following intravenous bradykinin.	Aspirin	14-17	kininogen 1	Homo sapiens	129-139
27069632-12	2016	Both forms of aspirin decrease bradykinin-stimulated thromboxane and prostacyclin production, but some stimulated prostacyclin production remains during treatment with NHP-554C.	Aspirin	14-21	kininogen 1	Homo sapiens	31-41
26709600-0	2016	Evaluation of the effect of angiotensin converting enzyme inhibitors and angiotensin receptors blockers on aspirin antiplatelet effect.	Aspirin	107-114	angiotensin I converting enzyme	Homo sapiens	28-57
26844701-12	2016	Inhibition of COX-2 with aspirin or celecoxib did not affect Caspase-3 levels but also reduced Ki-67 and beta-Catenin levels, suggesting that Caspase-3 acted via COX-2 to stimulate cell proliferation and tissue regeneration.	Aspirin	25-32	prostaglandin-endoperoxide synthase 2	Homo sapiens	14-19
26844701-12	2016	Inhibition of COX-2 with aspirin or celecoxib did not affect Caspase-3 levels but also reduced Ki-67 and beta-Catenin levels, suggesting that Caspase-3 acted via COX-2 to stimulate cell proliferation and tissue regeneration.	Aspirin	25-32	caspase 3	Homo sapiens	142-151
26612417-5	2016	The present study investigated the effect of a common COX1/2 inhibitor (Aspirin) on macrophage phenotype and tissue remodeling in a rodent model of ECM scaffold treated skeletal muscle injury.	Aspirin	72-79	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	54-60
26612417-13	2016	The COX1/2 inhibitor, Aspirin, was found to mitigate the ECM scaffold-mediated constructive remodeling response both in an in vitro co-culture system and an in vivo rat model of skeletal muscle injury.	Aspirin	22-29	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	4-10
26915040-0	2016	Mutations in PIK3CA sensitize breast cancer cells to physiologic levels of aspirin.	Aspirin	75-82	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	13-19
26915040-2	2016	Several recent studies have reported an improvement in overall survival in colorectal cancer patients who harbored mutations in the oncogene PIK3CA and received a daily aspirin regimen.	Aspirin	169-176	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	141-147
26915040-5	2016	In order to determine if mutations in PIK3CA sensitized breast cancers to aspirin treatment, we employed the use of isogenic cellular clones of the non-tumorigenic, breast epithelial cell line MCF-10A that harbored mutations in either PIK3CA or KRAS or both.	Aspirin	74-81	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	38-44
26915040-6	2016	We report that mutations in both PIK3CA and KRAS are required for the greatest aspirin sensitivity in breast cancer, and that the GSK3beta protein was hyperphosphorylated in aspirin-treated double knockin cells, but not in other clones/treatments.	Aspirin	79-86	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	33-39
26915040-6	2016	We report that mutations in both PIK3CA and KRAS are required for the greatest aspirin sensitivity in breast cancer, and that the GSK3beta protein was hyperphosphorylated in aspirin-treated double knockin cells, but not in other clones/treatments.	Aspirin	174-181	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	33-39
26915040-9	2016	Our findings provide the first evidence that mutations in PIK3CA sensitize breast cancer cells to aspirin.	Aspirin	98-105	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	58-64
26314869-4	2016	ASA usage promoted a decrease in high-sensitivity C-reactive protein (p = 0.01).	Aspirin	0-3	C-reactive protein	Homo sapiens	50-68
26711147-3	2016	Moreover, the following study showed that ASA could up-regulate the expression levels of p38 and phosphorylated p38 MAPK, suggesting ASA-induced apoptosis was associated with the p38 MAPK mediated pathway.	Aspirin	42-45	mitogen-activated protein kinase 14	Homo sapiens	89-92
26586373-5	2016	Patients" stratification based on ASA dose showed more significant reductions in P-selectin, CD40L, and MMP-9 serum levels postclopidogrel administration in patients who were on baseline 81 mg ASA, as compared to patients on 325 mg ASA.	Aspirin	34-37	CD40 ligand	Homo sapiens	93-98
26794215-6	2016	The results showed that aspirin treatment inhibited differentiation and lipid accumulation by 3T3-L1 preadipocytes, and decreased the secretion of the inflammatory adipokine MCP-1 after stimulation with tumor necrosis factor (TNF)-alpha or conditioned medium from RAW264.7 cells.	Aspirin	24-31	mast cell protease 1	Mus musculus	174-179
26794215-6	2016	The results showed that aspirin treatment inhibited differentiation and lipid accumulation by 3T3-L1 preadipocytes, and decreased the secretion of the inflammatory adipokine MCP-1 after stimulation with tumor necrosis factor (TNF)-alpha or conditioned medium from RAW264.7 cells.	Aspirin	24-31	tumor necrosis factor	Mus musculus	203-236
26794215-7	2016	In 4T1 cells, treatment with aspirin decreased cell viability and migration, possibly by suppressing MCP-1 and VEGF secretion.	Aspirin	29-36	mast cell protease 1	Mus musculus	101-106
26794215-10	2016	Aspirin treatment significantly inhibited the proliferation of 4T1 cells, and decreased the production of MCP-1 and PAI-1 in both the Ad-CM model and co-culture system.	Aspirin	0-7	mast cell protease 1	Mus musculus	106-111
26794215-11	2016	Aspirin inhibited inflammatory MCP-1 adipokine production by 3T3-L1 adipocytes and the cell growth and migration of 4T1 cells.	Aspirin	0-7	mast cell protease 1	Mus musculus	31-36
26810856-0	2016	Aspirin inhibits epithelial-to-mesenchymal transition and migration of oncogenic K-ras-expressing non-small cell lung carcinoma cells by down-regulating E-cadherin repressor Slug.	Aspirin	0-7	cadherin 1	Homo sapiens	153-163
26810856-8	2016	Aspirin inhibits EMT and decelerates the migratory potential of A549 cells by down-regulating Slug and thereby up-regulating E-cadherin.	Aspirin	0-7	cadherin 1	Homo sapiens	125-135
26711147-5	2016	In addition, ASA could led to a loss in the mitochondrial out membrane potential, up-regulate p53, phosphorylated p53 and Bax, down-regulate Bcl-2, release cytochrome c from the mitochondria to the cytoplasm, and activate caspase-9 and caspase-3 in A549 cells, which revealed that ASA could also induce apoptosis through the mitochondria mediated pathway.	Aspirin	13-16	cytochrome c, somatic	Homo sapiens	156-168
26711147-5	2016	In addition, ASA could led to a loss in the mitochondrial out membrane potential, up-regulate p53, phosphorylated p53 and Bax, down-regulate Bcl-2, release cytochrome c from the mitochondria to the cytoplasm, and activate caspase-9 and caspase-3 in A549 cells, which revealed that ASA could also induce apoptosis through the mitochondria mediated pathway.	Aspirin	13-16	caspase 3	Homo sapiens	236-245
26711147-6	2016	These results suggested that ASA played the anti-tumor role through the activation of p38 MAPK-, death receptor-, mitochondria- and caspase-dependent apoptotic pathways.	Aspirin	29-32	mitogen-activated protein kinase 14	Homo sapiens	86-89
26711147-3	2016	Moreover, the following study showed that ASA could up-regulate the expression levels of p38 and phosphorylated p38 MAPK, suggesting ASA-induced apoptosis was associated with the p38 MAPK mediated pathway.	Aspirin	42-45	mitogen-activated protein kinase 14	Homo sapiens	112-115
26711147-3	2016	Moreover, the following study showed that ASA could up-regulate the expression levels of p38 and phosphorylated p38 MAPK, suggesting ASA-induced apoptosis was associated with the p38 MAPK mediated pathway.	Aspirin	42-45	mitogen-activated protein kinase 14	Homo sapiens	112-115
26711147-3	2016	Moreover, the following study showed that ASA could up-regulate the expression levels of p38 and phosphorylated p38 MAPK, suggesting ASA-induced apoptosis was associated with the p38 MAPK mediated pathway.	Aspirin	133-136	mitogen-activated protein kinase 14	Homo sapiens	89-92
26711147-3	2016	Moreover, the following study showed that ASA could up-regulate the expression levels of p38 and phosphorylated p38 MAPK, suggesting ASA-induced apoptosis was associated with the p38 MAPK mediated pathway.	Aspirin	133-136	mitogen-activated protein kinase 14	Homo sapiens	112-115
26711147-3	2016	Moreover, the following study showed that ASA could up-regulate the expression levels of p38 and phosphorylated p38 MAPK, suggesting ASA-induced apoptosis was associated with the p38 MAPK mediated pathway.	Aspirin	133-136	mitogen-activated protein kinase 14	Homo sapiens	112-115
26711147-4	2016	Furthermore, ASA could up-regulate TNF-R1 and DR5 via activation of p38 MAPK, thereby activating caspase 8, revealing the death receptor pathway was also involved in this process.	Aspirin	13-16	mitogen-activated protein kinase 14	Homo sapiens	68-71
26711147-5	2016	In addition, ASA could led to a loss in the mitochondrial out membrane potential, up-regulate p53, phosphorylated p53 and Bax, down-regulate Bcl-2, release cytochrome c from the mitochondria to the cytoplasm, and activate caspase-9 and caspase-3 in A549 cells, which revealed that ASA could also induce apoptosis through the mitochondria mediated pathway.	Aspirin	13-16	tumor protein p53	Homo sapiens	94-97
26711147-5	2016	In addition, ASA could led to a loss in the mitochondrial out membrane potential, up-regulate p53, phosphorylated p53 and Bax, down-regulate Bcl-2, release cytochrome c from the mitochondria to the cytoplasm, and activate caspase-9 and caspase-3 in A549 cells, which revealed that ASA could also induce apoptosis through the mitochondria mediated pathway.	Aspirin	13-16	tumor protein p53	Homo sapiens	114-117
26711147-5	2016	In addition, ASA could led to a loss in the mitochondrial out membrane potential, up-regulate p53, phosphorylated p53 and Bax, down-regulate Bcl-2, release cytochrome c from the mitochondria to the cytoplasm, and activate caspase-9 and caspase-3 in A549 cells, which revealed that ASA could also induce apoptosis through the mitochondria mediated pathway.	Aspirin	13-16	BCL2 associated X, apoptosis regulator	Homo sapiens	122-125
26711147-5	2016	In addition, ASA could led to a loss in the mitochondrial out membrane potential, up-regulate p53, phosphorylated p53 and Bax, down-regulate Bcl-2, release cytochrome c from the mitochondria to the cytoplasm, and activate caspase-9 and caspase-3 in A549 cells, which revealed that ASA could also induce apoptosis through the mitochondria mediated pathway.	Aspirin	13-16	BCL2 apoptosis regulator	Homo sapiens	141-146
27534531-0	2016	Aspirin induces IL-4 production: augmented IL-4 production in aspirin-exacerbated respiratory disease.	Aspirin	0-7	interleukin 4	Homo sapiens	16-20
27534531-0	2016	Aspirin induces IL-4 production: augmented IL-4 production in aspirin-exacerbated respiratory disease.	Aspirin	0-7	interleukin 4	Homo sapiens	43-47
27534531-0	2016	Aspirin induces IL-4 production: augmented IL-4 production in aspirin-exacerbated respiratory disease.	Aspirin	62-69	interleukin 4	Homo sapiens	43-47
27534531-1	2016	Aspirin hypersensitivity is a hallmark of aspirin-exacerbated respiratory disease (AERD), a clinical syndrome characterized by the severe inflammation of the respiratory tract after ingestion of cyclooxygenase-1 inhibitors.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	195-211
27534531-1	2016	Aspirin hypersensitivity is a hallmark of aspirin-exacerbated respiratory disease (AERD), a clinical syndrome characterized by the severe inflammation of the respiratory tract after ingestion of cyclooxygenase-1 inhibitors.	Aspirin	42-49	prostaglandin-endoperoxide synthase 1	Homo sapiens	195-211
27534531-2	2016	We investigated the capacity of aspirin to induce interleukin-4 (IL-4) production in inflammatory cells relevant to AERD pathogenesis and examined the associated biochemical and molecular pathways.	Aspirin	32-39	interleukin 4	Homo sapiens	50-63
27534531-2	2016	We investigated the capacity of aspirin to induce interleukin-4 (IL-4) production in inflammatory cells relevant to AERD pathogenesis and examined the associated biochemical and molecular pathways.	Aspirin	32-39	interleukin 4	Homo sapiens	65-69
27534531-3	2016	We also compared IL-4 production in peripheral blood mononuclear cells (PBMCs) from patients with AERD vs aspirin-tolerant asthma (ATA) upon exposure to aspirin.	Aspirin	153-160	interleukin 4	Homo sapiens	17-21
27534531-4	2016	Aspirin induced IL-4 expression and activated the IL-4 promoter in a report assay.	Aspirin	0-7	interleukin 4	Homo sapiens	16-20
27534531-4	2016	Aspirin induced IL-4 expression and activated the IL-4 promoter in a report assay.	Aspirin	0-7	interleukin 4	Homo sapiens	50-54
27534531-5	2016	The capacity of aspirin to induce IL-4 expression correlated with its activity to activate mitogen-activated protein kinases, to form DNA-protein complexes on P elements in the IL-4 promoter and to synthesize nuclear factor of activated T cells, critical transcription factors for IL-4 transcription.	Aspirin	16-23	interleukin 4	Homo sapiens	34-38
27534531-5	2016	The capacity of aspirin to induce IL-4 expression correlated with its activity to activate mitogen-activated protein kinases, to form DNA-protein complexes on P elements in the IL-4 promoter and to synthesize nuclear factor of activated T cells, critical transcription factors for IL-4 transcription.	Aspirin	16-23	interleukin 4	Homo sapiens	177-181
27534531-5	2016	The capacity of aspirin to induce IL-4 expression correlated with its activity to activate mitogen-activated protein kinases, to form DNA-protein complexes on P elements in the IL-4 promoter and to synthesize nuclear factor of activated T cells, critical transcription factors for IL-4 transcription.	Aspirin	16-23	interleukin 4	Homo sapiens	177-181
27534531-6	2016	Of clinical importance, aspirin upregulated IL-4 production twice as much in PBMCs from patients with AERD compared with PBMCs from patients with ATA.	Aspirin	24-31	interleukin 4	Homo sapiens	44-48
27534531-7	2016	Our results suggest that IL-4 is an inflammatory component mediating intolerance reactions to aspirin, and thus is crucial for AERD pathogenesis.	Aspirin	94-101	interleukin 4	Homo sapiens	25-29
26728433-6	2016	Aspirin increased the activity of Metformin only in immune-competent HER2+ BC models.	Aspirin	0-7	erb-b2 receptor tyrosine kinase 2	Homo sapiens	69-73
27268661-0	2016	Mutations in PIK3CA Sensitize Breast Cancer Cells to Physiologic Levels of Aspirin.	Aspirin	75-82	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	13-19
26492523-11	2016	Aspirin, U0126, LY294002 and 5z-7-oxozeaenol attenuated the IL-1beta-induced MCP-1 expression.	Aspirin	0-7	interleukin 1 beta	Homo sapiens	60-68
26492523-12	2016	In addition, 5z-7-oxozeaenol, LY294002, U0126 and aspirin prevented the IL-1beta-induced MCP-1 secretion of pulp cells.	Aspirin	50-57	interleukin 1 beta	Mus musculus	72-80
26492523-12	2016	In addition, 5z-7-oxozeaenol, LY294002, U0126 and aspirin prevented the IL-1beta-induced MCP-1 secretion of pulp cells.	Aspirin	50-57	mast cell protease 1	Mus musculus	89-94
28107149-0	2016	Release of cyclooxygenase-2 and lipoxin A4 from blood leukocytes in aspirin-exacerbated respiratory disease.	Aspirin	68-75	prostaglandin-endoperoxide synthase 2	Homo sapiens	11-27
28107149-1	2016	BACKGROUND: The release of cyclooxygenase-2 (COX-2) and lipoxin A4 (LXA4) from blood mononuclear cells in patients with aspirin-exacerbated respiratory disease (AERD) is only partially understood.	Aspirin	120-127	prostaglandin-endoperoxide synthase 2	Homo sapiens	27-43
28107149-1	2016	BACKGROUND: The release of cyclooxygenase-2 (COX-2) and lipoxin A4 (LXA4) from blood mononuclear cells in patients with aspirin-exacerbated respiratory disease (AERD) is only partially understood.	Aspirin	120-127	prostaglandin-endoperoxide synthase 2	Homo sapiens	45-50
28119929-6	2016	Proinflammatory cytokines were decreased and the expression of NF-kappaB p65 in acinar cell nuclei was suppressed after aspirin treatment.	Aspirin	120-127	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	63-72
28119929-7	2016	Furthermore, aspirin induced the apoptosis of acinar cells by TUNEL assay, and the expression of Bax and caspase 3 was increased and the expression of Bcl-2 was decreased.	Aspirin	13-20	B cell leukemia/lymphoma 2	Mus musculus	151-156
28119929-8	2016	Intriguingly, the downregulation of critical necrosis associated proteins RIP1, RIP3, and p-MLKL was observed; what is more, we additionally found that aspirin reduced the COX level of pancreatic tissue.	Aspirin	152-159	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	74-78
26580090-1	2016	INTRODUCTION: The goal of this study was to investigate if S100B serum protein could predict secondary intracranial haemorrhagic events (SIHEs) after mild head injury (mHI) in patients taking low-dose acetylsalicylic acid (LDA), making routinely repeated head computed tomography (RRHCT) scans unnecessary.	Aspirin	201-221	S100 calcium binding protein B	Homo sapiens	59-64
26733809-6	2015	Gadolinium and acetylsalicylic acid reduced these currents, and FMRFamide, zinc (at high concentrations) and N,N,N",N"-tetrakis-(2-piridilmetil)-ethylenediamine increased them, indicating that functional ASICs are composed of the subunits ASIC1, ASIC2, and ASIC3.	Aspirin	15-35	acid sensing ion channel subunit 2	Homo sapiens	246-251
26615369-9	2016	Aspirin challenge induced the release of uLTE4, IL-6 and increased the number of CD4(+)CD45RA(-)CD45RO(+) memory T-cells only in AERD patients but failed to reduce the levels of sCD40L as observed in non-AERD subjects.	Aspirin	0-7	interleukin 6	Homo sapiens	48-52
26615369-9	2016	Aspirin challenge induced the release of uLTE4, IL-6 and increased the number of CD4(+)CD45RA(-)CD45RO(+) memory T-cells only in AERD patients but failed to reduce the levels of sCD40L as observed in non-AERD subjects.	Aspirin	0-7	CD4 molecule	Homo sapiens	81-84
26615369-10	2016	Further, IL-8 and sIL-5R-alpha levels directly correlated with the PD20ASA and the effects of aspirin on IL-6 and number of memory T-cells was more pronounced in subjects showing more strong reaction (bronchial and nasal).	Aspirin	94-101	interleukin 6	Homo sapiens	105-109
26615369-12	2016	Systemic response to oral aspirin challenge was related to an increase in serum IL-6 and the number of circulating memory T-cells in AERD patients.	Aspirin	26-33	interleukin 6	Homo sapiens	80-84
26560040-0	2016	Low E-prostanoid 2 receptor levels and deficient induction of the IL-1beta/IL-1 type I receptor/COX-2 pathway: Vicious circle in patients with aspirin-exacerbated respiratory disease.	Aspirin	143-150	interleukin 1 beta	Homo sapiens	66-74
26560040-0	2016	Low E-prostanoid 2 receptor levels and deficient induction of the IL-1beta/IL-1 type I receptor/COX-2 pathway: Vicious circle in patients with aspirin-exacerbated respiratory disease.	Aspirin	143-150	interleukin 1 receptor type 1	Homo sapiens	75-95
26560040-0	2016	Low E-prostanoid 2 receptor levels and deficient induction of the IL-1beta/IL-1 type I receptor/COX-2 pathway: Vicious circle in patients with aspirin-exacerbated respiratory disease.	Aspirin	143-150	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	96-101
26560040-1	2016	BACKGROUND: We hypothesized that the 2 reported alterations in aspirin-exacerbated respiratory disease (AERD), reduced expression/production of COX-2/prostaglandin (PG) E2 and diminished expression of E-prostanoid (EP) 2 receptor, are closely linked.	Aspirin	63-70	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	144-149
26668680-12	2016	Trend towards a lower prevalance of acetylsalicylic acid (ASA) use was present in IDH mutant PMF patients compared to wild-type counterparts (20% and 63.9%, respectively).	Aspirin	36-56	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	82-85
26668680-12	2016	Trend towards a lower prevalance of acetylsalicylic acid (ASA) use was present in IDH mutant PMF patients compared to wild-type counterparts (20% and 63.9%, respectively).	Aspirin	58-61	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	82-85
28139555-1	2016	AIM: To estimate thrombin generation test parameters in patients with coronary heart disease during coronary artery bypass surgery under extracorporeal circulation after transfusion of donor platelet concentrates during long-term therapy with acetylsalicylic acid (ASA).	Aspirin	243-263	coagulation factor II, thrombin	Homo sapiens	17-25
28139555-1	2016	AIM: To estimate thrombin generation test parameters in patients with coronary heart disease during coronary artery bypass surgery under extracorporeal circulation after transfusion of donor platelet concentrates during long-term therapy with acetylsalicylic acid (ASA).	Aspirin	265-268	coagulation factor II, thrombin	Homo sapiens	17-25
28139555-6	2016	RESULTS: During long-term ASA therapy, the patients were found to have an activated endogenous thrombin potential in the pre- and intraoperative periods, as evidenced by the high peak concentration of thrombin and the increased rate of its generation.	Aspirin	26-29	coagulation factor II, thrombin	Homo sapiens	95-103
27149936-4	2016	Of these, vitamin D-binding protein (DBP) and actin were further examined via Western blot and showed consistent results, with DBP levels significantly increased post-aspirin treatment (114.04 +- 16.69) relative to pre-treatment (66.33 +- 5.61) while actin showed the opposite trend (p &lt; 0.01 for both comparisons).	Aspirin	167-174	D-box binding PAR bZIP transcription factor	Homo sapiens	37-40
27149936-4	2016	Of these, vitamin D-binding protein (DBP) and actin were further examined via Western blot and showed consistent results, with DBP levels significantly increased post-aspirin treatment (114.04 +- 16.69) relative to pre-treatment (66.33 +- 5.61) while actin showed the opposite trend (p &lt; 0.01 for both comparisons).	Aspirin	167-174	D-box binding PAR bZIP transcription factor	Homo sapiens	127-130
27149936-7	2016	These results suggest that DBP acts in the actin scavenge system and consequently the increase in DBP levels correlated with aspirin therapy in cerebral thrombotic patients.	Aspirin	125-132	D-box binding PAR bZIP transcription factor	Homo sapiens	27-30
27149936-7	2016	These results suggest that DBP acts in the actin scavenge system and consequently the increase in DBP levels correlated with aspirin therapy in cerebral thrombotic patients.	Aspirin	125-132	D-box binding PAR bZIP transcription factor	Homo sapiens	98-101
27149936-8	2016	These findings also suggest that aspirin may prevent platelet aggregation and thrombosis through the actions of DBP and other DBP related proteins.	Aspirin	33-40	D-box binding PAR bZIP transcription factor	Homo sapiens	112-115
27149936-8	2016	These findings also suggest that aspirin may prevent platelet aggregation and thrombosis through the actions of DBP and other DBP related proteins.	Aspirin	33-40	D-box binding PAR bZIP transcription factor	Homo sapiens	126-129
26699907-0	2016	Dual effects of acetylsalicylic acid on ERK signaling and Mitf transcription lead to inhibition of melanogenesis.	Aspirin	16-36	mitogen-activated protein kinase 1	Mus musculus	40-43
26699907-7	2016	Semi-quantitative reverse transcription-polymerase chain reaction analysis showed that the inhibitory effect of ASA might be due to the inhibition of Mitf gene transcription.	Aspirin	112-115	melanogenesis associated transcription factor	Mus musculus	150-154
26699907-8	2016	Interestingly, ASA also induced ERK phosphorylation.	Aspirin	15-18	mitogen-activated protein kinase 1	Mus musculus	32-35
26699907-9	2016	Additionally, treatment with PD98059, a specific ERK phosphorylation inhibitor, abolished the anti-melanogenic effect of ASA.	Aspirin	121-124	mitogen-activated protein kinase 1	Mus musculus	49-52
26699907-10	2016	These results suggest that the depigmenting effect of ASA results from down-regulation of Mitf, which is induced by both the induction of ERK phosphorylation and the inhibition of Mitf transcription.	Aspirin	54-57	melanogenesis associated transcription factor	Mus musculus	90-94
26699907-10	2016	These results suggest that the depigmenting effect of ASA results from down-regulation of Mitf, which is induced by both the induction of ERK phosphorylation and the inhibition of Mitf transcription.	Aspirin	54-57	mitogen-activated protein kinase 1	Mus musculus	138-141
26699907-10	2016	These results suggest that the depigmenting effect of ASA results from down-regulation of Mitf, which is induced by both the induction of ERK phosphorylation and the inhibition of Mitf transcription.	Aspirin	54-57	melanogenesis associated transcription factor	Mus musculus	180-184
25970449-6	2016	Notably, lysosomal exocytosis in response to thrombin was significantly reduced if the secondary activation by ADP was inhibited by the P2Y12 antagonist cangrelor, while inhibition of thromboxane A2 formation by treatment with acetylsalicylic acid was of minor importance in this regard.	Aspirin	227-247	coagulation factor II, thrombin	Homo sapiens	45-53
26689345-5	2016	This Practice Pearl reviews the recent study Prevention of Cardiovascular Events in Patients with Prior Heart Attack Using Ticagrelor Compared With Placebo on a Background of Aspirin-Thrombolysis in Myocardial Infarction 54 (PEGASUS-TIMI 54).	Aspirin	175-182	IKAROS family zinc finger 5	Homo sapiens	225-240
27239927-3	2016	They initially received dual antiplatelet therapy: clopidogrel 75 mg + acetylsalicylic acid (ASA) 300 mg. Genetic testing was performed in all the patients to reveal the carriage of allelic variants of the genes of cytochrome P-450 isoenzymes and the efficiency of antiplatelet therapy was evaluated.	Aspirin	71-91	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	215-231
27239927-3	2016	They initially received dual antiplatelet therapy: clopidogrel 75 mg + acetylsalicylic acid (ASA) 300 mg. Genetic testing was performed in all the patients to reveal the carriage of allelic variants of the genes of cytochrome P-450 isoenzymes and the efficiency of antiplatelet therapy was evaluated.	Aspirin	93-96	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	215-231
28139555-6	2016	RESULTS: During long-term ASA therapy, the patients were found to have an activated endogenous thrombin potential in the pre- and intraoperative periods, as evidenced by the high peak concentration of thrombin and the increased rate of its generation.	Aspirin	26-29	coagulation factor II, thrombin	Homo sapiens	201-209
26394025-15	2015	Aspirin increased plasma TNFalpha more than NBS-1120-treated animals.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	25-33
26319435-5	2015	Since the parent compound aspirin, inhibits both COX-1 and COX-2, we also evaluated the effects of these compounds on COX-1 and COX-2 enzyme activities and also performed modeling of the interactions between the positional isomers of NOSH-aspirin and COX-1 and COX-2 enzymes.	Aspirin	26-33	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	59-64
26559689-1	2015	Dual antiplatelet therapy with aspirin, a platelet cyclooxygenase-1 inhibitor and P2Y12 receptor blockers, remains the major drug strategy to prevent ischemic event occurrence in patients with acute coronary syndromes and in patients undergoing coronary stenting, but there some limitations that can be overcome by targeting novel targets.	Aspirin	31-38	prostaglandin-endoperoxide synthase 1	Homo sapiens	51-67
26626190-10	2015	Aspirin efficiently reversed the upregulation of beta-catenin and P-Akt expression and the TAC- or ANG II-induced downregulation of GSK-3beta.	Aspirin	0-7	thymoma viral proto-oncogene 1	Mus musculus	68-71
26626190-10	2015	Aspirin efficiently reversed the upregulation of beta-catenin and P-Akt expression and the TAC- or ANG II-induced downregulation of GSK-3beta.	Aspirin	0-7	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	99-105
26626190-12	2015	The downregulation of beta-catenin and Akt may be the underlying signaling mechanism of the effects of aspirin.	Aspirin	103-110	thymoma viral proto-oncogene 1	Mus musculus	39-42
26342455-10	2015	The latter aspect is explicitely studied for the interaction between catalase inhibiting acetylsalicylic acid and an NO donor.	Aspirin	89-109	catalase	Homo sapiens	69-77
25471931-4	2015	The most common PIM was prescribing aspirin to patients with no history of coronary, cerebral or peripheral arterial disease or occlusive arterial events.	Aspirin	36-43	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	16-19
26522688-3	2015	We found that aspirin significantly down-regulated TfR1, while also up-regulated Fpn1 and ferritin expressions in BV-2 microglial cells in vitro.	Aspirin	14-21	solute carrier family 40 (iron-regulated transporter), member 1	Mus musculus	81-85
26522688-4	2015	We also showed that TfR1 and Fpn1 expressions were significantly higher, while ferritin contents, IL-6, TNF-alpha and hepcidin mRNA levels were lower in cells treated with aspirin plus LPS than those in cells treated with LPS only.	Aspirin	172-179	solute carrier family 40 (iron-regulated transporter), member 1	Mus musculus	29-33
26522688-4	2015	We also showed that TfR1 and Fpn1 expressions were significantly higher, while ferritin contents, IL-6, TNF-alpha and hepcidin mRNA levels were lower in cells treated with aspirin plus LPS than those in cells treated with LPS only.	Aspirin	172-179	interleukin 6	Mus musculus	98-102
26522688-4	2015	We also showed that TfR1 and Fpn1 expressions were significantly higher, while ferritin contents, IL-6, TNF-alpha and hepcidin mRNA levels were lower in cells treated with aspirin plus LPS than those in cells treated with LPS only.	Aspirin	172-179	tumor necrosis factor	Mus musculus	104-113
26319435-10	2015	All 3 positional isomers of NOSH-aspirin preferentially inhibited COX-1 over COX-2.	Aspirin	33-40	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	77-82
26536471-7	2015	By contrast, after real aspirin conditioning, placebo aspirin induced pain relief through the inhibition of all the products of cyclooxygenase, that is, PGD2, PGE2, PGF2, PGI2, thromboxane (TX)A2, without affecting ventilation and blood alkalosis.	Aspirin	54-61	prostaglandin D2 synthase	Homo sapiens	153-157
26530254-0	2015	A novel aspirin prodrug inhibits NFkappaB activity and breast cancer stem cell properties.	Aspirin	8-15	nuclear factor kappa B subunit 1	Homo sapiens	33-41
26530254-6	2015	However, ASA has also been reported to inhibit the NFkappaB pathway at very high doses.	Aspirin	9-12	nuclear factor kappa B subunit 1	Homo sapiens	51-59
26530254-7	2015	Whether ASA prodrugs can inhibit NFkappaB signaling remains relatively unexplored.	Aspirin	8-11	nuclear factor kappa B subunit 1	Homo sapiens	33-41
26530254-8	2015	METHODS: A library of ASA prodrugs was synthesized and screened for inhibition of NFkappaB activity and cancer stem-like cell (CSC) properties, an important PGE2-and NFkappaB-dependent phenotype of aggressive breast cancers.	Aspirin	22-25	nuclear factor kappa B subunit 1	Homo sapiens	82-90
26530254-8	2015	METHODS: A library of ASA prodrugs was synthesized and screened for inhibition of NFkappaB activity and cancer stem-like cell (CSC) properties, an important PGE2-and NFkappaB-dependent phenotype of aggressive breast cancers.	Aspirin	22-25	nuclear factor kappa B subunit 1	Homo sapiens	166-174
26530254-11	2015	RESULTS: While we identified multiple ASA prodrugs that are capable of inhibiting the NFkappaB pathway, several were associated with cytotoxicity.	Aspirin	38-41	nuclear factor kappa B subunit 1	Homo sapiens	86-94
26606050-11	2015	Moreover, ASA- induced gastritis resulted in increased expression of NPY (76.59 +- 3.02%) and GAL (26.45 +- 2.75%) as well as the novo-synthesis of nNOS (6.13 +- 1.11%) and LENK (4.77 +- 0.42%) in traced CCMG neurons.	Aspirin	10-13	neuropeptide Y	Sus scrofa	69-72
26606248-0	2015	Human GAPDH Is a Target of Aspirin"s Primary Metabolite Salicylic Acid and Its Derivatives.	Aspirin	27-34	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	6-11
26162710-0	2015	Early single Aspirin-triggered Lipoxin blocked morphine anti-nociception tolerance through inhibiting NALP1 inflammasome: Involvement of PI3k/Akt signaling pathway.	Aspirin	13-20	AKT serine/threonine kinase 1	Rattus norvegicus	142-145
26162710-5	2015	The administration of an exogenous analogue of lipoxin, Aspirin-triggered Lipoxin (ATL), caused a decline in Caspase-1 cleavage, inflammasome activation and mature IL-1beta production and thus attenuated the development of morphine tolerance by inhibiting upstream Akt phosphorylation.	Aspirin	56-63	interleukin 1 beta	Rattus norvegicus	164-172
26162710-5	2015	The administration of an exogenous analogue of lipoxin, Aspirin-triggered Lipoxin (ATL), caused a decline in Caspase-1 cleavage, inflammasome activation and mature IL-1beta production and thus attenuated the development of morphine tolerance by inhibiting upstream Akt phosphorylation.	Aspirin	56-63	AKT serine/threonine kinase 1	Rattus norvegicus	265-268
26099269-6	2015	Furthermore, the application of AsA, an H2O2 scavenger, significantly reduced the expression level of HsfA2 induced by SA.	Aspirin	32-35	heat shock transcription factor A2	Arabidopsis thaliana	102-107
26315555-9	2015	Further subgroup analyses showed that aspirin use could decrease risk of in situ breast tumors or hormone receptor-positive tumors and reduce risk of breast cancer in postmenopausal women.	Aspirin	38-45	nuclear receptor subfamily 4 group A member 1	Homo sapiens	98-114
26315555-10	2015	Aspirin use may not affect overall risk of breast cancer, but decrease risk of in situ breast tumors or hormone receptor-positive tumors and reduce risk of breast cancer in postmenopausal women.	Aspirin	0-7	nuclear receptor subfamily 4 group A member 1	Homo sapiens	104-120
26433033-2	2015	In our previous studies, we showed that the TNFA -308A allele is a genetic predisposition factor in a subgroup of aspirin-sensitive (ASA+) CRS patients suffering from nasal polyps (NP) in the Hungarian population.	Aspirin	114-121	tumor necrosis factor	Homo sapiens	44-48
26433033-2	2015	In our previous studies, we showed that the TNFA -308A allele is a genetic predisposition factor in a subgroup of aspirin-sensitive (ASA+) CRS patients suffering from nasal polyps (NP) in the Hungarian population.	Aspirin	133-136	tumor necrosis factor	Homo sapiens	44-48
25848131-3	2015	MATERIALS AND METHODS: Thrombin generation was measured by the Calibrated Automated Thrombogram method (0.5 pmol/L tissue factor) using human platelet-rich plasma (PRP) spiked with rivaroxaban (15, 30, or 60 ng/mL), ticagrelor (1.0 microg/mL), and acetylsalicylic acid (ASA; 100 microg/mL).	Aspirin	248-268	coagulation factor II, thrombin	Homo sapiens	23-31
25848131-3	2015	MATERIALS AND METHODS: Thrombin generation was measured by the Calibrated Automated Thrombogram method (0.5 pmol/L tissue factor) using human platelet-rich plasma (PRP) spiked with rivaroxaban (15, 30, or 60 ng/mL), ticagrelor (1.0 microg/mL), and acetylsalicylic acid (ASA; 100 microg/mL).	Aspirin	270-273	coagulation factor II, thrombin	Homo sapiens	23-31
25848131-6	2015	RESULTS: Rivaroxaban inhibited thrombin generation in a concentration-dependent manner and the effect was enhanced with ticagrelor and ticagrelor plus ASA.	Aspirin	151-154	coagulation factor II	Rattus norvegicus	31-39
26474767-11	2015	Aspirin suppressed serum levels of the pro-inflammatory cytokines on tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), and the anti-inflammatory ability was positively associated with bone morphometry.	Aspirin	0-7	tumor necrosis factor	Rattus norvegicus	69-96
26474767-11	2015	Aspirin suppressed serum levels of the pro-inflammatory cytokines on tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), and the anti-inflammatory ability was positively associated with bone morphometry.	Aspirin	0-7	tumor necrosis factor	Rattus norvegicus	98-107
26475800-3	2015	Low-dose aspirin produces a selective, complete and irreversible cyclooxygenase-1 blockade, and higher doses do not increase the antiplatelet effect.	Aspirin	9-16	prostaglandin-endoperoxide synthase 1	Homo sapiens	65-81
26475800-4	2015	Additional cyclooxygenase-2 blockade by high-dose aspirin might decrease the antithrombotic efficacy by inhibiting endothelial prostacyclin synthesis.	Aspirin	50-57	prostaglandin-endoperoxide synthase 2	Homo sapiens	11-27
26148794-3	2015	The aim of this study was to determine whether the astroglial-derived protein S100B that is released into blood can be used as a reliable negative predictive tool for intracranial bleeding in patients after MHI, when they are older than 65 years or being treated with antiplatelet drugs (low-dose aspirin, clopidogrel).	Aspirin	297-304	S100 calcium binding protein B	Homo sapiens	78-83
25239119-8	2015	Besides, the survival benefit of postdiagnosis aspirin use appeared to be confined to those patients with positive prostaglandin endoperoxide synthase 2 (PTGS2, also known as cyclooxygenase-2, COX-2) expression (HR=0.65, 95% CI 0.50 to 0.85) and with mutated PIK3CA tumours (HR=0.58, 95% CI 0.37 to 0.90).	Aspirin	47-54	prostaglandin-endoperoxide synthase 2	Homo sapiens	115-152
25857363-4	2015	HS alone and ASA + HS caused a major up-regulation of HSP70 mRNA in the first 2 h, while HSP70 protein increased gradually and was especially abundant from 2 h to 24 h. Regarding Bcl-2, all treatments rendered similar results: gene expression was down-regulated in the first 2 h, after which there was protein elevation (12-48 h after HS).	Aspirin	13-16	BCL2 apoptosis regulator	Homo sapiens	179-184
25857363-6	2015	In conclusion, 0.4 mM ASA + HS does not act as a co-inducer of HSP70 in HepG2 cells, but promotes Bcl-2 protein expression during prolonged treatment.	Aspirin	22-25	BCL2 apoptosis regulator	Homo sapiens	98-103
26188955-9	2015	Pretreatment of PRP from IS or HS subjects with 15 muM aspirin followed by 15muUnits of insulin/ml resensitized the platelets to the inhibitory effect of insulin.	Aspirin	55-62	proline rich protein HaeIII subfamily 1	Mus musculus	16-19
26597741-0	2015	Baseline placental growth factor levels for the prediction of benefit from early aspirin prophylaxis for preeclampsia prevention.	Aspirin	81-88	placental growth factor	Homo sapiens	9-32
26597741-3	2015	We hypothesized that low PlGF levels may identify women at increased risk for preeclampsia who would benefit from aspirin.	Aspirin	114-121	placental growth factor	Homo sapiens	25-29
26597741-12	2015	Further research is needed to determine whether aspirin is beneficial in women with high PlGF, and whether the paradigm linking low PlGF and preeclampsia needs to be reevaluated.	Aspirin	48-55	placental growth factor	Homo sapiens	89-93
25380191-8	2015	This review synthesizes the evidence on the COX-2-independent mechanisms of action of aspirin, salicylates, and other NSAIDs on breast cancer.	Aspirin	86-93	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	44-49
25670850-12	2015	Additionally, Zn(ASA)2 significantly increased the mRNA-expression of superoxide dismutase 1 (+73 +- 15%), glutathione peroxidase 4 (+44 +- 12%), and transforming growth factor (TGF)-beta1 (+102 +- 22%).	Aspirin	17-20	transforming growth factor, beta 1	Rattus norvegicus	150-188
25670850-14	2015	The induction of antioxidant enzymes and the anti-inflammatory cytokine TGF-beta1 may play a pivotal role in the mechanism of action of Zn(ASA)2.	Aspirin	139-142	transforming growth factor, beta 1	Rattus norvegicus	72-81
26366802-0	2015	Pharmacogenetic tests to predict the efficacy of aspirin desensitization in patients with aspirin-exacerbated respiratory diseases; HLA-DQB302.	Aspirin	49-56	major histocompatibility complex, class II, DR beta 1	Homo sapiens	132-135
26366802-0	2015	Pharmacogenetic tests to predict the efficacy of aspirin desensitization in patients with aspirin-exacerbated respiratory diseases; HLA-DQB302.	Aspirin	90-97	major histocompatibility complex, class II, DR beta 1	Homo sapiens	132-135
26366802-1	2015	This study is aimed at investigating the association of HLA-DRB1, HLA-DQA1, and HLA-DQB1 variability with the response to aspirin desensitization (AD).	Aspirin	122-129	major histocompatibility complex, class II, DR beta 1	Homo sapiens	56-64
26697360-2	2015	UDP-glucuronosyltransferases (UGT) are involved in aspirin metabolism and clearance, and variant alleles in UGT1A6 have been shown to alter salicylic acid metabolism and risk of colon neoplasia.	Aspirin	51-58	beta-1,3-glucuronyltransferase 2	Homo sapiens	0-28
25239119-8	2015	Besides, the survival benefit of postdiagnosis aspirin use appeared to be confined to those patients with positive prostaglandin endoperoxide synthase 2 (PTGS2, also known as cyclooxygenase-2, COX-2) expression (HR=0.65, 95% CI 0.50 to 0.85) and with mutated PIK3CA tumours (HR=0.58, 95% CI 0.37 to 0.90).	Aspirin	47-54	prostaglandin-endoperoxide synthase 2	Homo sapiens	154-159
26697360-2	2015	UDP-glucuronosyltransferases (UGT) are involved in aspirin metabolism and clearance, and variant alleles in UGT1A6 have been shown to alter salicylic acid metabolism and risk of colon neoplasia.	Aspirin	51-58	beta-1,3-glucuronyltransferase 2	Homo sapiens	30-33
25239119-8	2015	Besides, the survival benefit of postdiagnosis aspirin use appeared to be confined to those patients with positive prostaglandin endoperoxide synthase 2 (PTGS2, also known as cyclooxygenase-2, COX-2) expression (HR=0.65, 95% CI 0.50 to 0.85) and with mutated PIK3CA tumours (HR=0.58, 95% CI 0.37 to 0.90).	Aspirin	47-54	prostaglandin-endoperoxide synthase 2	Homo sapiens	175-191
25239119-8	2015	Besides, the survival benefit of postdiagnosis aspirin use appeared to be confined to those patients with positive prostaglandin endoperoxide synthase 2 (PTGS2, also known as cyclooxygenase-2, COX-2) expression (HR=0.65, 95% CI 0.50 to 0.85) and with mutated PIK3CA tumours (HR=0.58, 95% CI 0.37 to 0.90).	Aspirin	47-54	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	193-198
25239119-8	2015	Besides, the survival benefit of postdiagnosis aspirin use appeared to be confined to those patients with positive prostaglandin endoperoxide synthase 2 (PTGS2, also known as cyclooxygenase-2, COX-2) expression (HR=0.65, 95% CI 0.50 to 0.85) and with mutated PIK3CA tumours (HR=0.58, 95% CI 0.37 to 0.90).	Aspirin	47-54	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	259-265
25239119-11	2015	CONCLUSIONS: These findings provide further indication that postdiagnosis aspirin therapy improved CRC overall survival, especially for patients with positive PTGS2 (COX-2) expression and mutated PIK3CA tumours.	Aspirin	74-81	prostaglandin-endoperoxide synthase 2	Homo sapiens	159-164
25239119-11	2015	CONCLUSIONS: These findings provide further indication that postdiagnosis aspirin therapy improved CRC overall survival, especially for patients with positive PTGS2 (COX-2) expression and mutated PIK3CA tumours.	Aspirin	74-81	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	166-171
25239119-11	2015	CONCLUSIONS: These findings provide further indication that postdiagnosis aspirin therapy improved CRC overall survival, especially for patients with positive PTGS2 (COX-2) expression and mutated PIK3CA tumours.	Aspirin	74-81	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	196-202
25577230-2	2015	The findings of our study showed that drought stress significantly enhanced the AsA-GSH cycle by upregulating the activities of ascorbate peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), and dehydroascorbate reductase (DHAR).	Aspirin	80-83	POD1	Triticum aestivum	128-148
25577230-2	2015	The findings of our study showed that drought stress significantly enhanced the AsA-GSH cycle by upregulating the activities of ascorbate peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), and dehydroascorbate reductase (DHAR).	Aspirin	80-83	POD1	Triticum aestivum	150-153
26056043-0	2015	Metformin combined with aspirin significantly inhibit pancreatic cancer cell growth in vitro and in vivo by suppressing anti-apoptotic proteins Mcl-1 and Bcl-2.	Aspirin	24-31	BCL2 apoptosis regulator	Homo sapiens	154-159
26159746-0	2015	Reversal of IL-13-induced inflammation and Ca(2+) sensitivity by resolvin and MAG-DHA in association with ASA in human bronchi.	Aspirin	106-109	interleukin 13	Homo sapiens	12-17
26159746-5	2015	Western blot analysis revealed that the combined treatment of MAG-DHA and ASA upregulated GPR-32 expression and downregulated cytosolic TNFalpha detection, hence preventing IkappaBalpha degradation and p65-NFkappaB phosphorylation.	Aspirin	74-77	tumor necrosis factor	Homo sapiens	136-144
26159746-5	2015	Western blot analysis revealed that the combined treatment of MAG-DHA and ASA upregulated GPR-32 expression and downregulated cytosolic TNFalpha detection, hence preventing IkappaBalpha degradation and p65-NFkappaB phosphorylation.	Aspirin	74-77	NFKB inhibitor alpha	Homo sapiens	173-185
26159746-7	2015	The presence of ASA potentiated the inhibitory effects of MAG-DHA in reducing the Ca(2+) hypersensitivity triggered by IL-13 by decreasing the phosphorylation levels of the PKC-potentiated inhibitor protein-17 regulatory protein (CPI-17).	Aspirin	16-19	interleukin 13	Homo sapiens	119-124
25981167-9	2015	In the ASA model, hypothermia was decreased by oral administration of TMB, which attenuated serum histamine, OVA-specific IgE, and IL-4 levels.	Aspirin	7-10	interleukin 4	Homo sapiens	131-135
26624583-11	2015	Mean AST was significantly higher for patients taking aspirin (beta = 0.218, p = 0.049), as was mean ALT (beta = 0.264, p = 0.015).	Aspirin	54-61	solute carrier family 17 member 5	Homo sapiens	5-8
26056043-9	2015	In a PANC-1 xenograft mouse model, we demonstrated that the combination of metformin and aspirin significantly inhibited tumor growth and downregulated the protein expression of Mcl-1 and Bcl-2 in tumors.	Aspirin	89-96	B cell leukemia/lymphoma 2	Mus musculus	188-193
26201059-6	2015	Acetylation of COX-2 allows for generation of 15-(R)HETE and subsequent formation of "aspirin-triggered lipoxin" (ATL) by interaction with white cell lipoxygenases.	Aspirin	86-93	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	15-20
26209241-2	2015	In aspirin exacerbated respiratory disease (AERD), asthmatic symptoms are precipitated by ingestion of non-steroid anti-inflammatory drugs capable for pharmacologic inhibition of cyclooxygenase-1 isoenzyme.	Aspirin	3-10	prostaglandin-endoperoxide synthase 1	Homo sapiens	179-195
26085050-6	2015	For example, aspirin at antiplatelet doses might acetylate COX-2 in vascular cells, directing the activity of the enzyme into a 15-lipoxygenase which by transcellular metabolism results in the formation of 15-epi-lipoxin ( aspirin-triggered lipoxin ), an antiinflammatory mediator.	Aspirin	13-20	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	59-64
26085050-6	2015	For example, aspirin at antiplatelet doses might acetylate COX-2 in vascular cells, directing the activity of the enzyme into a 15-lipoxygenase which by transcellular metabolism results in the formation of 15-epi-lipoxin ( aspirin-triggered lipoxin ), an antiinflammatory mediator.	Aspirin	13-20	arachidonate 15-lipoxygenase	Homo sapiens	128-143
26085050-6	2015	For example, aspirin at antiplatelet doses might acetylate COX-2 in vascular cells, directing the activity of the enzyme into a 15-lipoxygenase which by transcellular metabolism results in the formation of 15-epi-lipoxin ( aspirin-triggered lipoxin ), an antiinflammatory mediator.	Aspirin	223-230	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	59-64
26085050-6	2015	For example, aspirin at antiplatelet doses might acetylate COX-2 in vascular cells, directing the activity of the enzyme into a 15-lipoxygenase which by transcellular metabolism results in the formation of 15-epi-lipoxin ( aspirin-triggered lipoxin ), an antiinflammatory mediator.	Aspirin	223-230	arachidonate 15-lipoxygenase	Homo sapiens	128-143
26056043-10	2015	Taken together, the combination of metformin and aspirin significantly inhibited pancreatic cancer cell growth in vitro and in vivo by regulating the pro- and anti-apoptotic Bcl-2 family members, supporting the continued investigation of this two drug combination as chemopreventive or chemotherapeutic agents for pancreatic cancer.	Aspirin	49-56	BCL2 apoptosis regulator	Homo sapiens	174-179
26056043-6	2015	Metformin combined with aspirin significantly inhibited the phosphorylation of mTOR and STAT3, and induced apoptosis as measured by caspase-3 and PARP cleavage.	Aspirin	24-31	mechanistic target of rapamycin kinase	Homo sapiens	79-83
26056043-6	2015	Metformin combined with aspirin significantly inhibited the phosphorylation of mTOR and STAT3, and induced apoptosis as measured by caspase-3 and PARP cleavage.	Aspirin	24-31	signal transducer and activator of transcription 3	Homo sapiens	88-93
26056043-6	2015	Metformin combined with aspirin significantly inhibited the phosphorylation of mTOR and STAT3, and induced apoptosis as measured by caspase-3 and PARP cleavage.	Aspirin	24-31	caspase 3	Homo sapiens	132-141
26056043-7	2015	Remarkably, metformin combined with aspirin significantly downregulated the anti-apoptotic proteins Mcl-1 and Bcl-2, and upregulated the pro-apoptotic proteins Bim and Puma, as well as interrupted their interactions.	Aspirin	36-43	BCL2 apoptosis regulator	Homo sapiens	110-115
26313358-5	2015	RESULTS: Mean SOST serum levels were lower in ASAS+ patients than healthy controls (49.21 +- 25.9 vs. 87.8 +- 26 pmol/L; p&lt;0.0001).	Aspirin	46-50	sclerostin	Homo sapiens	14-18
26204233-5	2015	Metabolism of RAH in mice showed that the majority of RAH is decomposed to release resveratrol and aspirin or salicylic acid either in the intestine or after absorption.	Aspirin	99-106	RAB34, member RAS oncogene family	Mus musculus	14-17
26204233-5	2015	Metabolism of RAH in mice showed that the majority of RAH is decomposed to release resveratrol and aspirin or salicylic acid either in the intestine or after absorption.	Aspirin	99-106	RAB34, member RAS oncogene family	Mus musculus	54-57
25739534-10	2015	A multivariate regression analysis revealed the serum MIG to be independently associated with the carotid IMT (max-IMT: beta=0.194, p=0.010; mean-IMT: beta=0.184, p=0.016) when controlled for age, sex, diabetes mellitus history, smoking history, body mass index, blood pressure, total cholesterol, high-density lipoprotein cholesterol, high-sensitivity C-reactive protein, and aspirin and statin medication.	Aspirin	377-384	C-X-C motif chemokine ligand 9	Homo sapiens	54-57
26345150-19	2015	In the aspirin-treated group compared to the control group, the NE had a protective effect on the stomach and caused less injury than aspirin, indicated by significant decreases in TNFalpha, iNOS, prostaglandin E2, and malondialdehyde levels, and also significant increases in glutathione, glutathione reductase, glutathione peroxidase, catalase, and superoxide dismutase.	Aspirin	7-14	tumor necrosis factor	Rattus norvegicus	181-189
26345150-19	2015	In the aspirin-treated group compared to the control group, the NE had a protective effect on the stomach and caused less injury than aspirin, indicated by significant decreases in TNFalpha, iNOS, prostaglandin E2, and malondialdehyde levels, and also significant increases in glutathione, glutathione reductase, glutathione peroxidase, catalase, and superoxide dismutase.	Aspirin	7-14	nitric oxide synthase 2	Rattus norvegicus	191-195
26345150-0	2015	The effect of aspirin nanoemulsion on TNFalpha and iNOS in gastric tissue in comparison with conventional aspirin.	Aspirin	14-21	tumor necrosis factor	Rattus norvegicus	38-46
26345150-0	2015	The effect of aspirin nanoemulsion on TNFalpha and iNOS in gastric tissue in comparison with conventional aspirin.	Aspirin	14-21	nitric oxide synthase 2	Rattus norvegicus	51-55
26345150-19	2015	In the aspirin-treated group compared to the control group, the NE had a protective effect on the stomach and caused less injury than aspirin, indicated by significant decreases in TNFalpha, iNOS, prostaglandin E2, and malondialdehyde levels, and also significant increases in glutathione, glutathione reductase, glutathione peroxidase, catalase, and superoxide dismutase.	Aspirin	7-14	catalase	Rattus norvegicus	337-345
26294325-5	2015	Of the top 10 genes (fold-change &gt; 10, P &lt; 10(-10)) regulated by metformin plus aspirin, PCDH18, CCL2, RASL11A, FAM111B and BMP5 were down-regulated &gt;= 20-fold, while NGFR, NPTX1, C7orf57, MRPL23AS1 and UNC5B were up-regulated &gt;= 10-fold.	Aspirin	86-93	protocadherin 18	Homo sapiens	95-101
26294325-5	2015	Of the top 10 genes (fold-change &gt; 10, P &lt; 10(-10)) regulated by metformin plus aspirin, PCDH18, CCL2, RASL11A, FAM111B and BMP5 were down-regulated &gt;= 20-fold, while NGFR, NPTX1, C7orf57, MRPL23AS1 and UNC5B were up-regulated &gt;= 10-fold.	Aspirin	86-93	neuronal pentraxin 1	Homo sapiens	182-187
26254051-6	2015	However, there is cross-reactivity between the NSAIDs in patients with NSAID-exacerbated cutaneous disease and NIUA, and thus only use of selective COX-2 inhibitors can replace the culprit drug if the chronic treatment is necessary, although aspirin desensitization will allow for chronic treatment with NSAIDs in some patients with NIUA.	Aspirin	242-249	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	148-153
26252649-9	2015	Only AZA+ASA group showed increased anti-inflammatory cytokines (IL-10 and TGF-beta).	Aspirin	9-12	transforming growth factor beta 1	Homo sapiens	75-83
25895638-4	2015	ATL biosynthesis requires cyclooxygenase-2 acetylation by aspirin.	Aspirin	58-65	prostaglandin-endoperoxide synthase 2	Homo sapiens	26-42
26223257-4	2015	RESULTS: Compared to baseline, at the end of Phase A, patients treated with amlodipine 5 mg + ASA 100 mg showed a statistically significant reduction of Hs-CRP (-15.0%), TNF-alpha (-21.7%), MPO (-9.7%), and sCDL40 (-15.7%), and a statistically significant increase of ADN (+15.0%).	Aspirin	94-97	tumor necrosis factor	Homo sapiens	170-179
26230583-8	2015	Recent use of aspirin and/or ibuprofen was associated with differential expression of TMC06, ST8SIA4, and STEAP3 while a summary oxidative balance score (OBS) was associated with SYCP3, HDX, and NRG4 (all up-regulated with greater oxidative balance).	Aspirin	14-21	STEAP3 metalloreductase	Homo sapiens	106-112
25990653-12	2015	ASA abrogated enzastaurin-potentiated washed-platelet aggregation and VEGF release.	Aspirin	0-3	vascular endothelial growth factor A	Homo sapiens	70-74
26223257-4	2015	RESULTS: Compared to baseline, at the end of Phase A, patients treated with amlodipine 5 mg + ASA 100 mg showed a statistically significant reduction of Hs-CRP (-15.0%), TNF-alpha (-21.7%), MPO (-9.7%), and sCDL40 (-15.7%), and a statistically significant increase of ADN (+15.0%).	Aspirin	94-97	myeloperoxidase	Homo sapiens	190-193
26223257-4	2015	RESULTS: Compared to baseline, at the end of Phase A, patients treated with amlodipine 5 mg + ASA 100 mg showed a statistically significant reduction of Hs-CRP (-15.0%), TNF-alpha (-21.7%), MPO (-9.7%), and sCDL40 (-15.7%), and a statistically significant increase of ADN (+15.0%).	Aspirin	94-97	adiponectin, C1Q and collagen domain containing	Homo sapiens	268-271
26223257-6	2015	Similarly, at the end of Phase B, amlodipine 10 mg + ASA significantly lowered Hs-CRP (-18.8%), TNF-alpha (-15.0%), MPO (-9.2%), and sCDL40 (-20.0%) and increased ADN (+11.8%), with a better effect compared to amlodipine alone.	Aspirin	53-56	tumor necrosis factor	Homo sapiens	96-105
26223257-6	2015	Similarly, at the end of Phase B, amlodipine 10 mg + ASA significantly lowered Hs-CRP (-18.8%), TNF-alpha (-15.0%), MPO (-9.2%), and sCDL40 (-20.0%) and increased ADN (+11.8%), with a better effect compared to amlodipine alone.	Aspirin	53-56	myeloperoxidase	Homo sapiens	116-119
26223257-6	2015	Similarly, at the end of Phase B, amlodipine 10 mg + ASA significantly lowered Hs-CRP (-18.8%), TNF-alpha (-15.0%), MPO (-9.2%), and sCDL40 (-20.0%) and increased ADN (+11.8%), with a better effect compared to amlodipine alone.	Aspirin	53-56	adiponectin, C1Q and collagen domain containing	Homo sapiens	163-166
26184135-0	2015	Nitric Oxide-Releasing Aspirin Suppresses NF-kappaB Signaling in Estrogen Receptor Negative Breast Cancer Cells in Vitro and in Vivo.	Aspirin	23-30	nuclear factor kappa B subunit 1	Homo sapiens	42-51
26184135-9	2015	Activation of NF-kappaB was inhibited by both isomers as demonstrated by decreases in NF-kappaB-DNA binding and luciferase activity at 24 h, However, m-NO-ASA produced transient effects at 3 h such as increased NF-kappaB-DNA-binding, increased levels of nuclear p50, even though both isomers inhibited IkappaB degradation.	Aspirin	155-158	nuclear factor kappa B subunit 1	Homo sapiens	14-23
26184135-12	2015	In xenografts, p-NO-ASA inhibited tumor growth by inhibiting proliferation (PCNA and tumor volume), inducing apoptosis (TUNEL positive cells) and reducing NF-kappaB expression.	Aspirin	20-23	nuclear factor kappa B subunit 1	Homo sapiens	155-164
26184135-9	2015	Activation of NF-kappaB was inhibited by both isomers as demonstrated by decreases in NF-kappaB-DNA binding and luciferase activity at 24 h, However, m-NO-ASA produced transient effects at 3 h such as increased NF-kappaB-DNA-binding, increased levels of nuclear p50, even though both isomers inhibited IkappaB degradation.	Aspirin	155-158	nuclear factor kappa B subunit 1	Homo sapiens	262-265
26184135-10	2015	Increase in nuclear p50 by m-NO-ASA was associated with translocation of p50 in to the nucleus as observed by immunoflouresence at 3 h. NO-ASA induced reactive oxygen species (ROS) as evidenced by overall increases in both H2DCFDA (2",7"-dichlorodihydrofluorescein) and DHE (dihydroethidium)-derived fluorescence.	Aspirin	32-35	nuclear factor kappa B subunit 1	Homo sapiens	20-23
26184135-10	2015	Increase in nuclear p50 by m-NO-ASA was associated with translocation of p50 in to the nucleus as observed by immunoflouresence at 3 h. NO-ASA induced reactive oxygen species (ROS) as evidenced by overall increases in both H2DCFDA (2",7"-dichlorodihydrofluorescein) and DHE (dihydroethidium)-derived fluorescence.	Aspirin	32-35	nuclear factor kappa B subunit 1	Homo sapiens	73-76
26184135-10	2015	Increase in nuclear p50 by m-NO-ASA was associated with translocation of p50 in to the nucleus as observed by immunoflouresence at 3 h. NO-ASA induced reactive oxygen species (ROS) as evidenced by overall increases in both H2DCFDA (2",7"-dichlorodihydrofluorescein) and DHE (dihydroethidium)-derived fluorescence.	Aspirin	139-142	nuclear factor kappa B subunit 1	Homo sapiens	20-23
26184135-10	2015	Increase in nuclear p50 by m-NO-ASA was associated with translocation of p50 in to the nucleus as observed by immunoflouresence at 3 h. NO-ASA induced reactive oxygen species (ROS) as evidenced by overall increases in both H2DCFDA (2",7"-dichlorodihydrofluorescein) and DHE (dihydroethidium)-derived fluorescence.	Aspirin	139-142	nuclear factor kappa B subunit 1	Homo sapiens	73-76
26184135-11	2015	Inhibition of ROS by N-acetyl-cysteine reversed the m-NO-ASA-mediated translocation of p50 in to the nucleus.	Aspirin	57-60	nuclear factor kappa B subunit 1	Homo sapiens	87-90
25789542-10	2015	In conclusion, aspirin medication prior to dipyrone intake preserves antiplatelet effects, circumventing the pharmacodynamic drug-drug interaction at the level of cyclooxygenase-1.	Aspirin	15-22	prostaglandin-endoperoxide synthase 1	Homo sapiens	163-179
25824964-7	2015	Aspirin counteracted TNF-alpha-mediated effects on netrin-1 synthesis by endothelial cells through COX-dependent inhibition of NF-kappaB and concomitant histone hyperacetylation.	Aspirin	0-7	tumor necrosis factor	Mus musculus	21-30
25824964-8	2015	Administration of aspirin to ApoE(-/-) mice on HFD increased blood and arterial wall levels of netrin-1 independently of its effects on platelets, accompanied by reduced plaque size and content of monocytes/macrophages, compared with untreated or clopidogrel-treated mice.	Aspirin	18-25	apolipoprotein E	Mus musculus	29-33
25824964-9	2015	In vivo blockade of netrin-1 enhanced monocyte plaque infiltration in aspirin-treated ApoE(-/-) mice.	Aspirin	70-77	apolipoprotein E	Mus musculus	86-90
25824964-11	2015	The aspirin-dependent increase of netrin-1 in ApoE(-/-) mice exerts anti-atherogenic effects by preventing arterial accumulation of monocytes.	Aspirin	4-11	apolipoprotein E	Mus musculus	46-50
25927625-6	2015	The study also focuses on the non-selective inhibitory activity of an NSAID, aspirin, against sPLA2.	Aspirin	77-84	phospholipase A2 group X	Homo sapiens	94-99
26547966-4	2015	The aim of the present study was to reveal the possible involvement of zinc-finger transcriptionfactors Egr-1 &amp; Sp-1 in the molecular mechanisms underlying gastric lesions caused by aspirin administration and stress.	Aspirin	186-193	early growth response 1	Rattus norvegicus	104-109
26068794-7	2015	The effects of ASA and BoxA were cyclooxygenase-2 independent and were not additive, consistent with both acting via inhibition of HMGB1 activity.	Aspirin	15-18	prostaglandin-endoperoxide synthase 2	Homo sapiens	33-49
25959742-0	2015	Aspirin Action in Endothelial Cells: Different Patterns of Response Between Chemokine CX3CL1/CX3CR1 and TNF-alpha/TNFR1 Signaling Pathways.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	104-113
25959742-2	2015	NF-kB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin.	Aspirin	133-140	C-X3-C motif chemokine ligand 1	Homo sapiens	76-82
25959742-9	2015	RESULTS: Aspirin significantly (p &lt;  .05) decreased CX3CL1 production, and the mean decrease in CX3CL1 production was inversely proportional to increased (p &lt; 0.05) expression of CX3CR1.	Aspirin	9-16	C-X3-C motif chemokine ligand 1	Homo sapiens	55-61
25959742-10	2015	The combined mean CX3CL1 concentrations, including all time points, equaled 782.18 +- 74.4 pg/ml in aspirin treated HUVECs compared to a total concentration of 2467.53 +- 127.5 pg/ml combined from the respective time points in the controls.	Aspirin	100-107	C-X3-C motif chemokine ligand 1	Homo sapiens	18-24
25959742-11	2015	An inhibition of TNF-alpha production in HUVECs after pretreatment with aspirin was observed.	Aspirin	72-79	tumor necrosis factor	Homo sapiens	17-26
25959742-13	2015	CONCLUSIONS: Autoregulation between CX3CL1 and CX3CR1 may explain overexpression of CX3CR1 as the compensatory effect in aspirin-treated HUVECs.	Aspirin	121-128	C-X3-C motif chemokine ligand 1	Homo sapiens	36-42
25511794-3	2015	The aim of this study was to determine the impact of alcohol on the metabolism of specific probes for CES1 (oseltamivir) and CES2 (aspirin).	Aspirin	131-138	carboxylesterase 2	Homo sapiens	125-129
25068727-3	2015	Interestingly, p-hydroxyl benzoic acid and aspirin were found potent inhibitors against CAIII with affinity constants of 9954 and 9013 M(-1) respectively.	Aspirin	43-50	carbonic anhydrase 3	Homo sapiens	88-93
25431318-8	2015	Each SNP explained less than 2.50% of the variance of plasma adiponectin, and the genetic score collectively accounted for 2.95 and 1.42% of the variability of adiponectin in women and men, respectively, after adjustment for age, body mass index, physical activity, smoking, alcohol consumption, regular use of aspirin or nonsteroidal anti-inflammatory drug and postmenopausal hormone use.	Aspirin	311-318	adiponectin, C1Q and collagen domain containing	Homo sapiens	160-171
25648873-12	2015	Soluble CD40L and sPselectin are independent markers that are reproducible over time in both plasma and sera and are reduced by 1-week of low-dose aspirin.	Aspirin	147-154	CD40 ligand	Homo sapiens	8-13
26093650-10	2015	RT-PCR demonstrated that the upregulation of NF-kappaB, MCP-1 and VCAM-1 after CA induction was reversed by aspirin treatment.	Aspirin	108-115	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	45-54
25959742-0	2015	Aspirin Action in Endothelial Cells: Different Patterns of Response Between Chemokine CX3CL1/CX3CR1 and TNF-alpha/TNFR1 Signaling Pathways.	Aspirin	0-7	C-X3-C motif chemokine ligand 1	Homo sapiens	86-92
25759104-16	2015	In conclusion, fibrinogen level was the major predictor of HPR on aspirin in this large population of high-risk vascular patients.	Aspirin	66-73	fibrinogen beta chain	Homo sapiens	15-25
26236481-7	2015	Mechanistically, NOSH-aspirin, but not aspirin, was able to reduce the production/release of interleukin-1 beta (IL-1beta) during Cg-induced paw inflammation.	Aspirin	22-29	interleukin 1 beta	Homo sapiens	93-111
26236481-7	2015	Mechanistically, NOSH-aspirin, but not aspirin, was able to reduce the production/release of interleukin-1 beta (IL-1beta) during Cg-induced paw inflammation.	Aspirin	22-29	interleukin 1 beta	Homo sapiens	113-121
26025192-8	2015	CONCLUSIONS: Our data suggest that TNF-alpha and IL-6, but not CRP, are associated with the prevalence and severity of CKD, independent from established CKD risk factors, history of cardiovascular disease, and use of antihypertensive, antidiabetic, and lipid-lowering agents and aspirin.	Aspirin	279-286	tumor necrosis factor	Homo sapiens	35-44
26025192-8	2015	CONCLUSIONS: Our data suggest that TNF-alpha and IL-6, but not CRP, are associated with the prevalence and severity of CKD, independent from established CKD risk factors, history of cardiovascular disease, and use of antihypertensive, antidiabetic, and lipid-lowering agents and aspirin.	Aspirin	279-286	interleukin 6	Homo sapiens	49-53
25974366-9	2015	Enzymes of the ascorbate-glutathione cycle (AsA-GSH cycle) showed inhibition of their activities following As(V) treatment while their activities were increased by application of NaHS.	Aspirin	44-47	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	107-112
25742316-6	2015	These effects are also observed in primary human hepatocytes and patients with dysglycaemia exhibit additional improvements in a marker of insulin resistance (proinsulin) when treated with ASA and metformin compared with either drug alone.	Aspirin	189-192	insulin	Homo sapiens	139-146
25772736-4	2015	We investigated the inhibition profiles by aspirin and its major metabolite salicylate of ethanol oxidation by recombinant human ADH1A, ADH1B1, ADH1B2, ADH1B3, ADH1C1, ADH1C2, ADH2, and ADH4, and acetaldehyde oxidation by ALDH1A1 and ALDH2, at pH 7.5 and 0.5 mM NAD(+).	Aspirin	43-50	alcohol dehydrogenase 4 (class II), pi polypeptide	Homo sapiens	176-180
25769431-7	2015	TNF-alpha-mediated up-regulation of placental fractalkine was reversed in the presence of the aspirin-derivative salicylate, which impaired activation of NF-kappaB p65 in TNF-alpha-treated explants.	Aspirin	94-101	tumor necrosis factor	Homo sapiens	0-9
25769431-7	2015	TNF-alpha-mediated up-regulation of placental fractalkine was reversed in the presence of the aspirin-derivative salicylate, which impaired activation of NF-kappaB p65 in TNF-alpha-treated explants.	Aspirin	94-101	C-X3-C motif chemokine ligand 1	Homo sapiens	46-57
25769431-7	2015	TNF-alpha-mediated up-regulation of placental fractalkine was reversed in the presence of the aspirin-derivative salicylate, which impaired activation of NF-kappaB p65 in TNF-alpha-treated explants.	Aspirin	94-101	nuclear factor kappa B subunit 1	Homo sapiens	154-163
25769431-7	2015	TNF-alpha-mediated up-regulation of placental fractalkine was reversed in the presence of the aspirin-derivative salicylate, which impaired activation of NF-kappaB p65 in TNF-alpha-treated explants.	Aspirin	94-101	tumor necrosis factor	Homo sapiens	171-180
25975240-0	2015	HLA-DRB and HLA-DQ genetic variability in patients with aspirin-exacerbated respiratory disease.	Aspirin	56-63	major histocompatibility complex, class II, DR beta 1	Homo sapiens	0-7
25772736-4	2015	We investigated the inhibition profiles by aspirin and its major metabolite salicylate of ethanol oxidation by recombinant human ADH1A, ADH1B1, ADH1B2, ADH1B3, ADH1C1, ADH1C2, ADH2, and ADH4, and acetaldehyde oxidation by ALDH1A1 and ALDH2, at pH 7.5 and 0.5 mM NAD(+).	Aspirin	43-50	alcohol dehydrogenase 4 (class II), pi polypeptide	Homo sapiens	186-190
26097892-0	2015	Aspirin Prevents Colorectal Cancer by Normalizing EGFR Expression.	Aspirin	0-7	epidermal growth factor receptor	Homo sapiens	50-54
26097892-3	2015	Here, we investigated whether aspirin can prevent CRC by normalizing EGFR expression.	Aspirin	30-37	epidermal growth factor receptor	Homo sapiens	69-73
26097892-6	2015	RESULTS: Immunohistochemistry staining results established that EGFR overexpression is an early event in colorectal tumorigenesis, which can be greatly attenuated by regular use of aspirin.	Aspirin	181-188	epidermal growth factor receptor	Homo sapiens	64-68
26097892-10	2015	CONCLUSION: Aspirin might exert its chemopreventive activity against CRC, at least partially, by normalizing EGFR expression in gastrointestinal precancerous lesions.	Aspirin	12-19	epidermal growth factor receptor	Homo sapiens	109-113
26137580-0	2015	COX-2 and EGFR: Partners in Crime Split by Aspirin.	Aspirin	43-50	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
25638779-3	2015	Aspirin (acetylsalicylate, ASA) inhibits AA oxidation by cyclooxygenase (COX)-1 and COX-2.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	84-89
25638779-3	2015	Aspirin (acetylsalicylate, ASA) inhibits AA oxidation by cyclooxygenase (COX)-1 and COX-2.	Aspirin	9-25	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	84-89
25638779-3	2015	Aspirin (acetylsalicylate, ASA) inhibits AA oxidation by cyclooxygenase (COX)-1 and COX-2.	Aspirin	27-30	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	84-89
25887212-17	2015	The NNT to achieve the minimally clinically important difference of 0.7 points ranged from 2 to 4.Compared with placebo, there was moderate quality evidence (downgraded for imprecision) that patients on an anti-TNF agent were more likely to achieve an ASAS partial remission by six months (adalimumab: RR 6.28, 95% Crl 3.13 to 12.78; etanercept: RR 4.24, 95% Crl 2.31 to 8.09; golimumab: RR 5.18, 95% Crl 1.90 to 14.79; infliximab: RR 15.41, 95% Crl 5.09 to 47.98 with a 10% to 44% absolute difference between treatment and placebo groups.	Aspirin	252-256	tumor necrosis factor	Homo sapiens	211-214
26137580-0	2015	COX-2 and EGFR: Partners in Crime Split by Aspirin.	Aspirin	43-50	epidermal growth factor receptor	Homo sapiens	10-14
25549537-0	2015	Impact of regular aspirin use on overall and cancer-specific survival in patients with colorectal cancer harboring a PIK3CA mutation.	Aspirin	18-25	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	117-123
25549537-1	2015	BACKGROUND: Recent data have suggested that regular aspirin use improves overall and cancer-specific survival in the subset of colorectal cancer (CRC) patients harboring PIK3CA mutations.	Aspirin	52-59	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	170-176
25091345-6	2015	As expected, after 4 weeks of treatment, ASA induced a significant reduction of plasma thromboxane-A2, as a consequence of cyclooxygenase-1 inhibition.	Aspirin	41-44	prostaglandin-endoperoxide synthase 1	Homo sapiens	123-139
25549537-3	2015	Our collaborative study aims to validate the association between regular aspirin use and survival in patients with PIK3CA-mutated CRC.	Aspirin	73-80	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	115-121
25814374-0	2015	Aspirin therapy inhibits NLRP1 (nucleotide-binding domain-like receptor protein 1) inflammasome gene expression in patients with peripheral artery disease.	Aspirin	0-7	NLR family pyrin domain containing 1	Homo sapiens	25-30
25727881-8	2015	RESULTS: Compared with men who were not on medication, the PSA level at the first PSA test was lower among men using 75 mg/dose aspirin (-3.9% change in PSA concentration; 95% confidence interval (CI): -5.8 to -2.1), statin (-4.6%; 95% CI: -6.2 to -2.9), metformin (-14%; 95% CI: -17 to -12) and insulin (-16%; 95% CI: -18 to -14).	Aspirin	128-135	insulin	Homo sapiens	296-303
24893560-0	2015	Low-dose aspirin for the prevention of adverse pregnancy outcomes in women with elevated alpha-fetoprotein.	Aspirin	9-16	alpha fetoprotein	Homo sapiens	89-106
25700561-2	2015	While aspirin, a cyclo-oxygenase-1 inhibitor has been the cornerstone of antithrombotic treatment for several decades, P2Y12 receptor inhibitors cangrelor, clopidogrel, prasugrel, and ticagrelor and protease-activated receptor-1 antagonist vorapaxar, have emerged as additional therapies to reduce the risk of recurrent cardiovascular events in high-risk patients.	Aspirin	6-13	prostaglandin-endoperoxide synthase 1	Homo sapiens	17-34
25700561-2	2015	While aspirin, a cyclo-oxygenase-1 inhibitor has been the cornerstone of antithrombotic treatment for several decades, P2Y12 receptor inhibitors cangrelor, clopidogrel, prasugrel, and ticagrelor and protease-activated receptor-1 antagonist vorapaxar, have emerged as additional therapies to reduce the risk of recurrent cardiovascular events in high-risk patients.	Aspirin	6-13	coagulation factor II thrombin receptor	Homo sapiens	199-228
25814374-0	2015	Aspirin therapy inhibits NLRP1 (nucleotide-binding domain-like receptor protein 1) inflammasome gene expression in patients with peripheral artery disease.	Aspirin	0-7	NLR family pyrin domain containing 1	Homo sapiens	32-81
25638730-0	2015	Aspirin inhibits expression of sFLT1 from human cytotrophoblasts induced by hypoxia, via cyclo-oxygenase 1.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	89-106
25638730-12	2015	Aspirin and sc-560 also reduced hypoxia-induced FLT1 mRNA expression and inhibited COX1 mRNA in CTBs.	Aspirin	0-7	fms related receptor tyrosine kinase 1	Homo sapiens	48-52
25927723-2	2015	UDP-glucuronosyltransferases (UGT) are involved in aspirin metabolism and clearance, and variant alleles in UGT1A6 have been shown to alter salicylic acid metabolism and risk of colon neoplasia.	Aspirin	51-58	beta-1,3-glucuronyltransferase 2	Homo sapiens	0-28
25781442-8	2015	In the conventional logistic regression analysis, the SNP rs2965667 at chromosome 12p12.3 near the MGST1 gene showed a genome-wide significant interaction with aspirin and/or NSAID use (P = 4.6 x 10(-9) for interaction).	Aspirin	160-167	microsomal glutathione S-transferase 1	Homo sapiens	99-104
25869498-4	2015	The mechanism of aspirin antiplatelet effect is due to the inhibition of cyclooxygenase-1 enzyme in platelets.	Aspirin	17-24	prostaglandin-endoperoxide synthase 1	Homo sapiens	73-89
25869498-5	2015	In some trials, almost all patients on aspirin have a very low level of serum thromboxane B2, indicating that the measured platelet reactivity in aspirin-treated patients might be due to platelet activation via other pathways, such as ADP or thrombin.	Aspirin	146-153	coagulation factor II, thrombin	Homo sapiens	242-250
25927723-2	2015	UDP-glucuronosyltransferases (UGT) are involved in aspirin metabolism and clearance, and variant alleles in UGT1A6 have been shown to alter salicylic acid metabolism and risk of colon neoplasia.	Aspirin	51-58	beta-1,3-glucuronyltransferase 2	Homo sapiens	30-33
25633316-2	2015	Blockade of the ADP receptor, P2Y12, in combination with cyclooxygenase-1 inhibition by aspirin has been among the most widely used pharmacological strategies to reduce cardiovascular event occurrence in high-risk patients.	Aspirin	88-95	prostaglandin-endoperoxide synthase 1	Homo sapiens	57-73
25325344-9	2015	However, the presence of PIA2 allele in GPIIIa gene may be associated with a better response to ASA intake in these patients, whereas other clinical and laboratory variables showed no association with this drug use.	Aspirin	96-99	integrin subunit beta 3	Homo sapiens	40-46
25861296-8	2015	Angiotensin II receptor antagonists were more often used in the group of ASA partial responders and ASA non-responders (p = 0.04).	Aspirin	73-76	angiotensinogen	Homo sapiens	0-14
25861296-8	2015	Angiotensin II receptor antagonists were more often used in the group of ASA partial responders and ASA non-responders (p = 0.04).	Aspirin	100-103	angiotensinogen	Homo sapiens	0-14
25861296-12	2015	The relationship between the effect of ASA and other medications (angiotensin II receptor blockers, fibrates, diuretics) requires further study.	Aspirin	39-42	angiotensinogen	Homo sapiens	66-80
25663486-1	2015	Aspirin-exacerbated respiratory disease (AERD) is a clinical condition which results in adverse upper and lower respiratory symptoms, particularly rhinitis, conjunctivitis, bronchospasm, and/or laryngospasm, following exposure to cyclooxygenase-1 (COX-1) inhibiting drugs, namely aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	230-246
25663486-1	2015	Aspirin-exacerbated respiratory disease (AERD) is a clinical condition which results in adverse upper and lower respiratory symptoms, particularly rhinitis, conjunctivitis, bronchospasm, and/or laryngospasm, following exposure to cyclooxygenase-1 (COX-1) inhibiting drugs, namely aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	248-253
25663486-1	2015	Aspirin-exacerbated respiratory disease (AERD) is a clinical condition which results in adverse upper and lower respiratory symptoms, particularly rhinitis, conjunctivitis, bronchospasm, and/or laryngospasm, following exposure to cyclooxygenase-1 (COX-1) inhibiting drugs, namely aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs).	Aspirin	280-287	prostaglandin-endoperoxide synthase 1	Homo sapiens	230-246
25607509-0	2015	Decreased vascular endothelial growth factor expression is associated with cell apoptosis in low-dose aspirin-induced gastric mucosal injury.	Aspirin	102-109	vascular endothelial growth factor A	Homo sapiens	10-44
25645020-4	2015	PTPL was stress regulated as it showed marked decrease in the expression when exposed to Aspirin, an antifilarial drug and Phenylarsine Oxide, PTP inhibitor.	Aspirin	89-96	lithostathine	Bos taurus	0-3
25759598-4	2015	All available NSAIDs, including acetaminophen and aspirin, are associated with potential side effects, particularly gastrointestinal and cardiovascular effects, related to their relative selectivity for COX-1 and COX-2.	Aspirin	50-57	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	213-218
25596165-5	2015	Kinetics study revealed that the modification of cytochrome c with BAMF took place at faster rates than aspirin.	Aspirin	104-111	cytochrome c, somatic	Homo sapiens	49-61
25557764-8	2015	Thus an increase in Sirt4, Nrf2, Tfam, UCP1, eNOS, HO1 and STAT3 genes could profoundly affect mitochondrial function, cholesterol homeostasis, and fatty acid oxidation, suggesting that ASA could be beneficial beyond simply its ability to inhibit cyclooxygenase.	Aspirin	186-189	sirtuin 4	Homo sapiens	20-25
25557764-8	2015	Thus an increase in Sirt4, Nrf2, Tfam, UCP1, eNOS, HO1 and STAT3 genes could profoundly affect mitochondrial function, cholesterol homeostasis, and fatty acid oxidation, suggesting that ASA could be beneficial beyond simply its ability to inhibit cyclooxygenase.	Aspirin	186-189	NFE2 like bZIP transcription factor 2	Homo sapiens	27-31
25557764-8	2015	Thus an increase in Sirt4, Nrf2, Tfam, UCP1, eNOS, HO1 and STAT3 genes could profoundly affect mitochondrial function, cholesterol homeostasis, and fatty acid oxidation, suggesting that ASA could be beneficial beyond simply its ability to inhibit cyclooxygenase.	Aspirin	186-189	transcription factor A, mitochondrial	Homo sapiens	33-37
25557764-8	2015	Thus an increase in Sirt4, Nrf2, Tfam, UCP1, eNOS, HO1 and STAT3 genes could profoundly affect mitochondrial function, cholesterol homeostasis, and fatty acid oxidation, suggesting that ASA could be beneficial beyond simply its ability to inhibit cyclooxygenase.	Aspirin	186-189	nitric oxide synthase 3	Homo sapiens	45-49
25557764-8	2015	Thus an increase in Sirt4, Nrf2, Tfam, UCP1, eNOS, HO1 and STAT3 genes could profoundly affect mitochondrial function, cholesterol homeostasis, and fatty acid oxidation, suggesting that ASA could be beneficial beyond simply its ability to inhibit cyclooxygenase.	Aspirin	186-189	signal transducer and activator of transcription 3	Homo sapiens	59-64
25762331-0	2015	Arresting amyloid with coulomb"s law: acetylation of ALS-linked SOD1 by aspirin impedes aggregation.	Aspirin	72-79	superoxide dismutase 1	Homo sapiens	64-68
25762331-2	2015	This article demonstrates that aspirin (the quintessential acylating pharmacon) can inhibit the amyloidogenesis of superoxide dismutase (SOD1) by increasing the intrinsic net negative charge of the polypeptide, i.e., by acetylation (neutralization) of multiple lysines.	Aspirin	31-38	superoxide dismutase 1	Homo sapiens	137-141
25762331-5	2015	Lysines in wild-type- and ALS-variant apo-SOD1 could also be peracetylated with aspirin after fibrillization, resulting in supercharged fibrils, with increases in formal net charge of ~2 million units.	Aspirin	80-87	superoxide dismutase 1	Homo sapiens	42-46
25600441-8	2015	RESULTS: Flow cytometry of whole blood samples from aspirin-treated patients demonstrated unchanged high platelet responsiveness towards ADP, slightly elevated responsiveness after glycoprotein VI stimulation, and decreased responsiveness after PAR1 thrombin receptor stimulation, compared to the control subjects.	Aspirin	52-59	coagulation factor II thrombin receptor	Homo sapiens	245-249
25557764-3	2015	As predicted, ASA and salicylic acid (SA) treatment resulted in generation of H2O2, which is known to be an inducer of mitochondrial gene Sirt4 and other downstream target genes of Sirt1.	Aspirin	14-17	sirtuin 4	Homo sapiens	138-143
25480980-8	2015	An aspirin-dependent reduction in 12-HHT production was responsible for delayed skin wound healing, showing that the 12-HHT/BLT2 axis also plays an important role in skin biology.	Aspirin	3-10	leukotriene B4 receptor 2	Mus musculus	124-128
25388762-0	2015	Role of p38 MAPK in enhanced human cancer cells killing by the combination of aspirin and ABT-737.	Aspirin	78-85	mitogen-activated protein kinase 14	Homo sapiens	8-11
25388762-1	2015	Regular use of aspirin after diagnosis is associated with longer survival among patients with mutated-PIK3CA colorectal cancer, but not among patients with wild-type PIK3CA cancer.	Aspirin	15-22	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	102-108
25388762-2	2015	In this study, we showed that clinically achievable concentrations of aspirin and ABT-737 in combination could induce a synergistic growth arrest in several human PIK3CA wild-type cancer cells.	Aspirin	70-77	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	163-169
25514511-2	2015	The principal pharmacological effects of aspirin are known to arise from its covalent modification of cyclooxygenase-2 (COX-2) through acetylation of Ser530, but the detailed mechanism of its biochemical action and specificity remains to be elucidated.	Aspirin	41-48	prostaglandin-endoperoxide synthase 2	Homo sapiens	102-118
25388762-5	2015	Furthermore, we showed that p38 acted as a switch between two different types of cell death (autophagy and apoptosis) induced by aspirin plus ABT-737.	Aspirin	129-136	mitogen-activated protein kinase 14	Homo sapiens	28-31
25600173-0	2015	Mapping sites of aspirin-induced acetylations in live cells by quantitative acid-cleavable activity-based protein profiling (QA-ABPP).	Aspirin	17-24	amyloid beta precursor protein	Homo sapiens	128-132
25623542-12	2015	RESULTS: Through the measurement of the glycogen level in HepG2 cell treated with TNF-alpha, it was found that aspirin and indomethacin increased glycogen levels by almost two-fold compared to amygdalin and cinnamic acid.	Aspirin	111-118	tumor necrosis factor	Homo sapiens	82-91
25514511-2	2015	The principal pharmacological effects of aspirin are known to arise from its covalent modification of cyclooxygenase-2 (COX-2) through acetylation of Ser530, but the detailed mechanism of its biochemical action and specificity remains to be elucidated.	Aspirin	41-48	prostaglandin-endoperoxide synthase 2	Homo sapiens	120-125
25514511-5	2015	The computational results confirmed that aspirin would be 10-100 times more potent against COX-1 than against COX-2, and revealed that this inhibition specificity between the two COX isoforms can be attributed mainly to the difference in kinetics rate of the covalent inhibition reaction, not the aspirin-binding step.	Aspirin	41-48	prostaglandin-endoperoxide synthase 2	Homo sapiens	110-115
25590316-1	2015	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is explained in part by overexpression of 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes (CysLTs) and driving the surge in CysLT production that occurs with aspirin ingestion.	Aspirin	12-19	arachidonate 5-lipoxygenase	Homo sapiens	101-115
25590316-13	2015	Our previous studies demonstrated that aspirin blocks trafficking of STAT6 into the nucleus and thereby prevents IL-4-mediated induction of these transcripts, thereby suggesting a modality by which aspirin desensitization could provide therapeutic benefit for AERD patients.	Aspirin	39-46	interleukin 4	Homo sapiens	113-117
25590316-13	2015	Our previous studies demonstrated that aspirin blocks trafficking of STAT6 into the nucleus and thereby prevents IL-4-mediated induction of these transcripts, thereby suggesting a modality by which aspirin desensitization could provide therapeutic benefit for AERD patients.	Aspirin	198-205	interleukin 4	Homo sapiens	113-117
25590316-1	2015	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is explained in part by overexpression of 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes (CysLTs) and driving the surge in CysLT production that occurs with aspirin ingestion.	Aspirin	288-295	arachidonate 5-lipoxygenase	Homo sapiens	101-115
25590318-1	2015	Aspirin exacerbated respiratory disease (AERD) is characterized as adult onset asthma, nasal polyps, chronic rhinosinusitis, and hypersensitivity to a cyclooxygenase-1 (COX-1) inhibitor, viz aspirin or nonsteroidal antiinflammatory drugs (NSAIDs).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	151-167
25590318-1	2015	Aspirin exacerbated respiratory disease (AERD) is characterized as adult onset asthma, nasal polyps, chronic rhinosinusitis, and hypersensitivity to a cyclooxygenase-1 (COX-1) inhibitor, viz aspirin or nonsteroidal antiinflammatory drugs (NSAIDs).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	169-174
24647791-13	2015	Aspirin and eugenol enhanced the IL-1beta-induced sICAM-1 production and ICAM-1 expression.	Aspirin	0-7	interleukin 1 beta	Homo sapiens	33-41
25590318-1	2015	Aspirin exacerbated respiratory disease (AERD) is characterized as adult onset asthma, nasal polyps, chronic rhinosinusitis, and hypersensitivity to a cyclooxygenase-1 (COX-1) inhibitor, viz aspirin or nonsteroidal antiinflammatory drugs (NSAIDs).	Aspirin	191-198	prostaglandin-endoperoxide synthase 1	Homo sapiens	151-167
25590318-1	2015	Aspirin exacerbated respiratory disease (AERD) is characterized as adult onset asthma, nasal polyps, chronic rhinosinusitis, and hypersensitivity to a cyclooxygenase-1 (COX-1) inhibitor, viz aspirin or nonsteroidal antiinflammatory drugs (NSAIDs).	Aspirin	191-198	prostaglandin-endoperoxide synthase 1	Homo sapiens	169-174
25967073-2	2015	Aspirin is a potent inhibitor of cyclooxygenase-2 (COX), which plays a critical role in the expression of immune modulators known to contribute to cerebral aneurysm formation and rupture.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	33-49
25967073-8	2015	Walls of ruptured human intracranial aneurysms have higher levels of COX-2 and microsomal prostaglandin E2 synthase 1 (mPGES-1), both of which are known to be inhibited by aspirin.	Aspirin	172-179	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	69-74
25967073-9	2015	In a pilot study, patients undergoing microsurgical clipping had attenuated expression of COX-2, mPGES-1, and macrophages in aneurysm walls after 3 months of aspirin therapy versus those that did not receive aspirin.	Aspirin	158-165	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	90-95
25967073-11	2015	Treatment with aspirin also resulted in decreased expression of COX-2 within leukocytes within aneurysms as compared to peripheral blood samples.	Aspirin	15-22	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	64-69
24743611-8	2015	However, preoperative aspirin use was associated with a significant decrease in postoperative AKI and 30-day mortality in patients with CKD undergoing cardiac surgery, in particular, the survival benefit associated with aspirin was greater in patients with CKD (vs normal kidney function): 30-day mortality was reduced by 23.3%, 58.2%, or 70.0% for patients with baseline eGFR more than or equal to 90, 30 to 59, or 15 to 30 mL/min/1.73 m2, respectively (P trend &lt; 0.001).	Aspirin	22-29	CD59 molecule (CD59 blood group)	Homo sapiens	428-433
24743611-8	2015	However, preoperative aspirin use was associated with a significant decrease in postoperative AKI and 30-day mortality in patients with CKD undergoing cardiac surgery, in particular, the survival benefit associated with aspirin was greater in patients with CKD (vs normal kidney function): 30-day mortality was reduced by 23.3%, 58.2%, or 70.0% for patients with baseline eGFR more than or equal to 90, 30 to 59, or 15 to 30 mL/min/1.73 m2, respectively (P trend &lt; 0.001).	Aspirin	220-227	CD59 molecule (CD59 blood group)	Homo sapiens	428-433
25267459-0	2015	Serum ubiquitin via CXC chemokine receptor 4 triggered cyclooxygenase-1 ubiquitination possibly involved in the pathogenesis of aspirin resistance.	Aspirin	128-135	prostaglandin-endoperoxide synthase 1	Homo sapiens	55-71
25267459-9	2015	Platelets had higher levels of ubiquitinated COX-1 showing poor response to aspirin.	Aspirin	76-83	prostaglandin-endoperoxide synthase 1	Homo sapiens	45-50
26369678-3	2015	Epidemiological, clinical, and observational studies have demonstrated that aspirin and non-steroidal antiinflammatory drugs (NSAIDs), including COX-2 inhibitors, can protect against CRC and significantly reduce its incidence.	Aspirin	76-83	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	145-150
26369686-3	2015	Individuals with two single nucleotide polymorphisms (SNPs) of cyclooxygenase-1 (COX-1), A-842G and C50T, exhibit increased sensitivity to aspirin and lower prostaglandin synthesis capacity but the polymorphism lacked statistical significance in relation to an association with bleeding peptic ulcer.	Aspirin	139-146	prostaglandin-endoperoxide synthase 1	Homo sapiens	63-79
26369686-3	2015	Individuals with two single nucleotide polymorphisms (SNPs) of cyclooxygenase-1 (COX-1), A-842G and C50T, exhibit increased sensitivity to aspirin and lower prostaglandin synthesis capacity but the polymorphism lacked statistical significance in relation to an association with bleeding peptic ulcer.	Aspirin	139-146	prostaglandin-endoperoxide synthase 1	Homo sapiens	81-86
25301295-0	2015	Spectroscopic and DFT investigation of interactions between cyclophosphamide and aspirin with lysozyme as binary and ternary systems.	Aspirin	81-88	lysozyme	Homo sapiens	94-102
26756892-6	2015	Eighty percent (118/148) taking either OTC NSAIDs or ASA were identified as having at least one PIP.	Aspirin	53-56	prolactin induced protein	Homo sapiens	96-99
25301295-1	2015	Multi-spectroscopic and density functional theory (DFT) calculations was used to study the interaction between cyclophosphamide (CYP) and aspirin (ASA) with lysozyme (LYS).	Aspirin	138-145	lysozyme	Homo sapiens	157-165
26517138-0	2015	The Implication of the Polymorphisms of COX-1, UGT1A6, and CYP2C9 among Cardiovascular Disease (CVD) Patients Treated with Aspirin.	Aspirin	123-130	prostaglandin-endoperoxide synthase 1	Homo sapiens	40-45
25301295-1	2015	Multi-spectroscopic and density functional theory (DFT) calculations was used to study the interaction between cyclophosphamide (CYP) and aspirin (ASA) with lysozyme (LYS).	Aspirin	147-150	lysozyme	Homo sapiens	157-165
26379739-6	2015	Treatment of aspirin alone significantly reduced the expressions of HO-1 (P &lt; 0.001), iNOS (P &lt; 0.001), and Bax (P &lt; 0.01) in ischemic regions.	Aspirin	13-20	nitric oxide synthase 2	Rattus norvegicus	89-93
26517138-1	2015	PURPOSE:   Enzymes potentially responsible for the pharmacokinetic variations of aspirin include cyclooxygenase-1 (COX-1), UDP-glucuronosyltransferase (UGT1A6) and P450 (CYP) (CYP2C9).	Aspirin	81-88	prostaglandin-endoperoxide synthase 1	Homo sapiens	97-113
26517138-1	2015	PURPOSE:   Enzymes potentially responsible for the pharmacokinetic variations of aspirin include cyclooxygenase-1 (COX-1), UDP-glucuronosyltransferase (UGT1A6) and P450 (CYP) (CYP2C9).	Aspirin	81-88	prostaglandin-endoperoxide synthase 1	Homo sapiens	115-120
25362654-8	2015	CONCLUSION: With the exception of a lower proportion of patients with nr-axSpA newly treated with anti-TNF agents in private practices in comparison to academic centers, adherence to ASAS treatment recommendations for TNF inhibition was equally high, and similar response rates to TNF blockers were achieved in both clinical settings.	Aspirin	183-187	tumor necrosis factor	Homo sapiens	218-221
25362654-8	2015	CONCLUSION: With the exception of a lower proportion of patients with nr-axSpA newly treated with anti-TNF agents in private practices in comparison to academic centers, adherence to ASAS treatment recommendations for TNF inhibition was equally high, and similar response rates to TNF blockers were achieved in both clinical settings.	Aspirin	183-187	tumor necrosis factor	Homo sapiens	218-221
25286881-4	2015	However, some patients continue to experience adverse ischaemic events despite treatment with aspirin and a P2Y12-receptor antagonist, because platelets can remain activated via pathways not inhibited by these agents, such as the protease-activated receptor (PAR)-1 platelet activation pathway stimulated by thrombin.	Aspirin	94-101	coagulation factor II thrombin receptor	Homo sapiens	230-265
25286881-4	2015	However, some patients continue to experience adverse ischaemic events despite treatment with aspirin and a P2Y12-receptor antagonist, because platelets can remain activated via pathways not inhibited by these agents, such as the protease-activated receptor (PAR)-1 platelet activation pathway stimulated by thrombin.	Aspirin	94-101	coagulation factor II, thrombin	Homo sapiens	308-316
25591798-8	2015	RESULTS: In Western blot analysis, COX-1 expression levels were found to be significantly reduced in mice treated with 3-(5-chlorofuran-2-yl)-5-methyl-4-phenylisoxazole (P6) in comparison to mice pretreated with aspirin (ASA), which exhibited higher levels of COX-1, thus confirming the high selectivity of P6 towards COX-1 enzyme inhibition.	Aspirin	212-219	cytochrome c oxidase I, mitochondrial	Mus musculus	35-40
25169677-10	2015	Pretreatment of LPS/IFNgamma-stimulated human microglia cells with the nonsteroidal anti-inflammatory drugs ibuprofen and aspirin, the antioxidant GSH, the H2S donor NaSH, and the anti-inflammatory cytokine IL-10, resulted in a CM with diminished ability to stimulate tau expression.	Aspirin	122-129	interferon gamma	Homo sapiens	20-28
25591798-8	2015	RESULTS: In Western blot analysis, COX-1 expression levels were found to be significantly reduced in mice treated with 3-(5-chlorofuran-2-yl)-5-methyl-4-phenylisoxazole (P6) in comparison to mice pretreated with aspirin (ASA), which exhibited higher levels of COX-1, thus confirming the high selectivity of P6 towards COX-1 enzyme inhibition.	Aspirin	221-224	cytochrome c oxidase I, mitochondrial	Mus musculus	35-40
25666703-6	2015	In contrast to native NSAIDs, their NO-releasing derivatives such as NO-ASA were found to exhibit lower gastric toxicity despite inhibiting both COX-1 and COX-2 activity in the gastric mucosa.	Aspirin	72-75	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	155-160
25734355-2	2015	Both tests are specific for aspirin action on cyclooxygenase-1.	Aspirin	28-35	prostaglandin-endoperoxide synthase 1	Homo sapiens	46-62
25666703-8	2015	Dual antiplatelet therapy with ASA and clopidogrel increases the risk of gastrointestinal bleeding in patients with acute coronary syndrome in whom concomitant treatment with a proton-pump inhibitor (PPI) was less effective owing to the interaction of clopidogrel and PPI with the same hepatic cytochrome P-450.	Aspirin	31-34	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	294-310
25624859-0	2014	Effect of common single nucleotide polymorphisms in COX-1 gene on related metabolic activity in diabetic patients treated with acetylsalicylic acid.	Aspirin	127-147	prostaglandin-endoperoxide synthase 1	Homo sapiens	52-57
25624859-1	2014	INTRODUCTION: The objective of this study was to investigate the effect of common single nucleotide genomic polymorphisms in the cyclooxygenase-1 (COX-1) gene on the thromboxane A2 (TxA2) metabolite concentrations in serum and urine, as well as on prostaglandin F2alpha (PGF2alpha) urinary excretion in the diabetic population on acetylsalicylic acid (ASA) therapy.	Aspirin	330-350	prostaglandin-endoperoxide synthase 1	Homo sapiens	129-145
25624859-1	2014	INTRODUCTION: The objective of this study was to investigate the effect of common single nucleotide genomic polymorphisms in the cyclooxygenase-1 (COX-1) gene on the thromboxane A2 (TxA2) metabolite concentrations in serum and urine, as well as on prostaglandin F2alpha (PGF2alpha) urinary excretion in the diabetic population on acetylsalicylic acid (ASA) therapy.	Aspirin	330-350	prostaglandin-endoperoxide synthase 1	Homo sapiens	147-152
25624859-1	2014	INTRODUCTION: The objective of this study was to investigate the effect of common single nucleotide genomic polymorphisms in the cyclooxygenase-1 (COX-1) gene on the thromboxane A2 (TxA2) metabolite concentrations in serum and urine, as well as on prostaglandin F2alpha (PGF2alpha) urinary excretion in the diabetic population on acetylsalicylic acid (ASA) therapy.	Aspirin	352-355	prostaglandin-endoperoxide synthase 1	Homo sapiens	129-145
25624859-1	2014	INTRODUCTION: The objective of this study was to investigate the effect of common single nucleotide genomic polymorphisms in the cyclooxygenase-1 (COX-1) gene on the thromboxane A2 (TxA2) metabolite concentrations in serum and urine, as well as on prostaglandin F2alpha (PGF2alpha) urinary excretion in the diabetic population on acetylsalicylic acid (ASA) therapy.	Aspirin	352-355	prostaglandin-endoperoxide synthase 1	Homo sapiens	147-152
25479628-6	2014	The levels of VEGF-A/C/D in Danzhi decoction group and aspirin group were significantly lower than those in mock group (P&lt;0.05), while there was no significant difference between Danzhi decoction group and aspirin group (P&gt;0.05).	Aspirin	55-62	vascular endothelial growth factor A	Homo sapiens	14-20
25106115-6	2014	In Huh7 replicon cells treated with ASA, we found decreased levels of iNOS mRNA, iNOS protein and nitrosylated protein levels at 48-72 h. ASA exposure also reduced the transactivation of the iNOS promoter in HCV replicon cells at 48 h, and this was partly due to the decrease in the affinity of transcription factor C/EBP-beta for its binding site in the iNOS promoter.	Aspirin	138-141	nitric oxide synthase 2	Homo sapiens	81-85
25106115-7	2014	siRNA silencing of iNOS decreased HCV-RNA expression (65 %) and potentiated the antiviral effect (80 %) of ASA compared with control cells.	Aspirin	107-110	nitric oxide synthase 2	Homo sapiens	19-23
25106115-8	2014	ASA reduces iNOS expression by downregulating promoter activity, mRNA and protein levels at the same time that it decreases HCV expression.	Aspirin	0-3	nitric oxide synthase 2	Homo sapiens	12-16
25106115-9	2014	These findings suggest that the antiviral activity of ASA is mediated partially through the modulation of iNOS.	Aspirin	54-57	nitric oxide synthase 2	Homo sapiens	106-110
25106115-0	2014	Downregulation of inducible nitric oxide synthase (iNOS) expression is implicated in the antiviral activity of acetylsalicylic acid in HCV-expressing cells.	Aspirin	111-131	nitric oxide synthase 2	Homo sapiens	18-49
25106115-0	2014	Downregulation of inducible nitric oxide synthase (iNOS) expression is implicated in the antiviral activity of acetylsalicylic acid in HCV-expressing cells.	Aspirin	111-131	nitric oxide synthase 2	Homo sapiens	51-55
25106115-2	2014	We evaluated the participation of inducible nitric oxide synthase (iNOS) in the regulation of HCV-RNA induced by ASA.	Aspirin	113-116	nitric oxide synthase 2	Homo sapiens	34-65
25106115-2	2014	We evaluated the participation of inducible nitric oxide synthase (iNOS) in the regulation of HCV-RNA induced by ASA.	Aspirin	113-116	nitric oxide synthase 2	Homo sapiens	67-71
25106115-6	2014	In Huh7 replicon cells treated with ASA, we found decreased levels of iNOS mRNA, iNOS protein and nitrosylated protein levels at 48-72 h. ASA exposure also reduced the transactivation of the iNOS promoter in HCV replicon cells at 48 h, and this was partly due to the decrease in the affinity of transcription factor C/EBP-beta for its binding site in the iNOS promoter.	Aspirin	36-39	nitric oxide synthase 2	Homo sapiens	70-74
25106115-6	2014	In Huh7 replicon cells treated with ASA, we found decreased levels of iNOS mRNA, iNOS protein and nitrosylated protein levels at 48-72 h. ASA exposure also reduced the transactivation of the iNOS promoter in HCV replicon cells at 48 h, and this was partly due to the decrease in the affinity of transcription factor C/EBP-beta for its binding site in the iNOS promoter.	Aspirin	36-39	nitric oxide synthase 2	Homo sapiens	81-85
25106115-6	2014	In Huh7 replicon cells treated with ASA, we found decreased levels of iNOS mRNA, iNOS protein and nitrosylated protein levels at 48-72 h. ASA exposure also reduced the transactivation of the iNOS promoter in HCV replicon cells at 48 h, and this was partly due to the decrease in the affinity of transcription factor C/EBP-beta for its binding site in the iNOS promoter.	Aspirin	36-39	nitric oxide synthase 2	Homo sapiens	81-85
25106115-6	2014	In Huh7 replicon cells treated with ASA, we found decreased levels of iNOS mRNA, iNOS protein and nitrosylated protein levels at 48-72 h. ASA exposure also reduced the transactivation of the iNOS promoter in HCV replicon cells at 48 h, and this was partly due to the decrease in the affinity of transcription factor C/EBP-beta for its binding site in the iNOS promoter.	Aspirin	36-39	nitric oxide synthase 2	Homo sapiens	81-85
25385584-2	2014	We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function.	Aspirin	150-157	prostaglandin-endoperoxide synthase 1	Homo sapiens	258-274
25106115-6	2014	In Huh7 replicon cells treated with ASA, we found decreased levels of iNOS mRNA, iNOS protein and nitrosylated protein levels at 48-72 h. ASA exposure also reduced the transactivation of the iNOS promoter in HCV replicon cells at 48 h, and this was partly due to the decrease in the affinity of transcription factor C/EBP-beta for its binding site in the iNOS promoter.	Aspirin	138-141	nitric oxide synthase 2	Homo sapiens	70-74
25106115-6	2014	In Huh7 replicon cells treated with ASA, we found decreased levels of iNOS mRNA, iNOS protein and nitrosylated protein levels at 48-72 h. ASA exposure also reduced the transactivation of the iNOS promoter in HCV replicon cells at 48 h, and this was partly due to the decrease in the affinity of transcription factor C/EBP-beta for its binding site in the iNOS promoter.	Aspirin	138-141	nitric oxide synthase 2	Homo sapiens	81-85
25106115-6	2014	In Huh7 replicon cells treated with ASA, we found decreased levels of iNOS mRNA, iNOS protein and nitrosylated protein levels at 48-72 h. ASA exposure also reduced the transactivation of the iNOS promoter in HCV replicon cells at 48 h, and this was partly due to the decrease in the affinity of transcription factor C/EBP-beta for its binding site in the iNOS promoter.	Aspirin	138-141	nitric oxide synthase 2	Homo sapiens	81-85
25173753-11	2014	Diets supplemented with low-dose aspirin reduced circulating serum and hepatic levels of PDGFB and significantly reduced progression of fibrosis in MDR2-null mice over 1 year.	Aspirin	33-40	ATP-binding cassette, sub-family B (MDR/TAP), member 4	Mus musculus	148-152
25180765-11	2014	Subgroup analysis showed that use of aspirin after diagnosis was associated with longer overall survival among patients with the variant PIK3CA gene but not for those with wild-type PIK3CA.	Aspirin	37-44	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	137-143
25338211-0	2014	Association analysis of FABP1 gene polymorphisms with aspirin-exacerbated respiratory disease in asthma.	Aspirin	54-61	fatty acid binding protein 1	Homo sapiens	24-29
25338211-1	2014	Previously, we used a proteomic approach to demonstrate that the protein level of fatty acid-binding protein 1 (FABP1) is increased in nasal polyps in patients with aspirin-exacerbated respiratory disease (AERD).	Aspirin	165-172	fatty acid binding protein 1	Homo sapiens	82-110
25338211-1	2014	Previously, we used a proteomic approach to demonstrate that the protein level of fatty acid-binding protein 1 (FABP1) is increased in nasal polyps in patients with aspirin-exacerbated respiratory disease (AERD).	Aspirin	165-172	fatty acid binding protein 1	Homo sapiens	112-117
25385584-3	2014	Although ibuprofen, naproxen, and celecoxib all had the potential to compete with the access of aspirin to the substrate binding channel of COX-1 in vitro, exposure of volunteers to a single therapeutic dose of each NSAID followed by 325 mg aspirin revealed a potent drug-drug interaction between ibuprofen and aspirin and between naproxen and aspirin but not between celecoxib and aspirin.	Aspirin	96-103	prostaglandin-endoperoxide synthase 1	Homo sapiens	140-145
25385584-2	2014	We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function.	Aspirin	150-157	prostaglandin-endoperoxide synthase 1	Homo sapiens	276-281
25385584-2	2014	We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function.	Aspirin	204-211	prostaglandin-endoperoxide synthase 1	Homo sapiens	258-274
25385584-2	2014	We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function.	Aspirin	204-211	prostaglandin-endoperoxide synthase 1	Homo sapiens	276-281
25385584-2	2014	We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function.	Aspirin	204-211	prostaglandin-endoperoxide synthase 1	Homo sapiens	258-274
25385584-2	2014	We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function.	Aspirin	204-211	prostaglandin-endoperoxide synthase 1	Homo sapiens	276-281
25385584-4	2014	The imprecision of estimates of aspirin consumption and the differential impact on the ability of aspirin to inactivate platelet COX-1 will confound head-to-head comparisons of distinct NSAIDs in ongoing clinical studies designed to measure their cardiovascular risk.	Aspirin	98-105	prostaglandin-endoperoxide synthase 1	Homo sapiens	129-134
25211369-8	2014	CONCLUSION: A triple therapy at steady state with ticagrelor plus ASA in combination with dabigatran or rivaroxaban is as effective as a combination with phenprocoumon for platelet activation and thrombin generation in vivo.	Aspirin	66-69	coagulation factor II, thrombin	Homo sapiens	196-204
25368225-3	2014	Drugs with the ability to inhibit COX-2 expression include aspirin, nonsteroidal anti-inflammatory drugs (NSAID) and selective COX-2 inhibitors.	Aspirin	59-66	prostaglandin-endoperoxide synthase 2	Homo sapiens	34-39
24506800-10	2014	When acetylsalicylic acid was combined with simvastatin treatment, the intraocular levels of Ang-2 and VEGF were significantly lower than in diabetics treated with simvastatin alone.	Aspirin	5-25	vascular endothelial growth factor A	Homo sapiens	103-107
25213262-4	2014	These clinical data support evidence that platelets contribute to the initiation and progression of venous thrombosis and aspirin inhibits thrombin formation and thrombin-mediated coagulant reactions.	Aspirin	122-129	coagulation factor II, thrombin	Homo sapiens	139-147
25213262-4	2014	These clinical data support evidence that platelets contribute to the initiation and progression of venous thrombosis and aspirin inhibits thrombin formation and thrombin-mediated coagulant reactions.	Aspirin	122-129	coagulation factor II, thrombin	Homo sapiens	162-170
24726874-0	2014	Aspirin-induced inhibition of adipogenesis was p53-dependent and associated with inactivation of pentose phosphate pathway.	Aspirin	0-7	tumor protein p53	Homo sapiens	47-50
24766194-0	2014	Aspirin inhibits proliferation and induces apoptosis of multiple myeloma cells through regulation of Bcl-2 and Bax and suppression of VEGF.	Aspirin	0-7	BCL2 apoptosis regulator	Homo sapiens	101-106
24766194-0	2014	Aspirin inhibits proliferation and induces apoptosis of multiple myeloma cells through regulation of Bcl-2 and Bax and suppression of VEGF.	Aspirin	0-7	BCL2 associated X, apoptosis regulator	Homo sapiens	111-114
24766194-0	2014	Aspirin inhibits proliferation and induces apoptosis of multiple myeloma cells through regulation of Bcl-2 and Bax and suppression of VEGF.	Aspirin	0-7	vascular endothelial growth factor A	Homo sapiens	134-138
24766194-8	2014	The myeloma cells exposed to ASA treatment displayed concentration-dependent apoptosis, which was closely associated with activation of caspases, upregulation of Bax, and downregulation of Bcl-2 and VEGF.	Aspirin	29-32	BCL2 associated X, apoptosis regulator	Homo sapiens	162-165
24766194-8	2014	The myeloma cells exposed to ASA treatment displayed concentration-dependent apoptosis, which was closely associated with activation of caspases, upregulation of Bax, and downregulation of Bcl-2 and VEGF.	Aspirin	29-32	BCL2 apoptosis regulator	Homo sapiens	189-194
24766194-8	2014	The myeloma cells exposed to ASA treatment displayed concentration-dependent apoptosis, which was closely associated with activation of caspases, upregulation of Bax, and downregulation of Bcl-2 and VEGF.	Aspirin	29-32	vascular endothelial growth factor A	Homo sapiens	199-203
25360888-13	2014	CONCLUSION: A common genetic variant in PEAR1 (rs12041331) reproducibly influenced platelet aggregation in aspirin-treated patients with coronary artery disease.	Aspirin	107-114	platelet endothelial aggregation receptor 1	Homo sapiens	40-45
24726874-3	2014	The present study aims at evaluating the possible existence of a putative p53-dependent pathway underlying the aspirin-induced inhibition of adipogenesis.	Aspirin	111-118	tumor protein p53	Homo sapiens	74-77
24726874-10	2014	It indicated that aspirin induced adipocyte differentiation through p53-p21 pathway.	Aspirin	18-25	tumor protein p53	Homo sapiens	68-71
24726874-17	2014	We demonstrated that aspirin-induced inhibition of adipogenesis was p53-dependent and associated with inactivation of PPP.	Aspirin	21-28	tumor protein p53	Homo sapiens	68-71
24726874-19	2014	Moreover, when use aspirin in therapeutic strategy, the p53 status should be considered.	Aspirin	19-26	tumor protein p53	Homo sapiens	56-59
23969075-10	2014	Patients with aspirin intolerance had higher levels of IFN-gamma (4.7+-1.4 vs. 4.1+-0.6, respectively, p=0.022).	Aspirin	14-21	interferon gamma	Homo sapiens	55-64
24952332-0	2014	Acetylsalicylic acid enhances the anti-inflammatory effect of fluoxetine through inhibition of NF-kappaB, p38-MAPK and ERK1/2 activation in lipopolysaccharide-induced BV-2 microglia cells.	Aspirin	0-20	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	95-104
24952332-5	2014	Moreover, FLX could inhibit phosphorylation of nuclear factor-kappaB (NF-kappaB) and phosphorylation of p38 mitogen-activated protein kinase (MAPK), and the combined use with ASA could enhance these effects.	Aspirin	175-178	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	47-68
25139986-6	2014	Initial activation of TLR4 results in accumulation of the cyclooxygenase-2-derived lipoxin precursor 15-hydroxyeicosatetraenoic acid (15-HETE) in esterified form within membrane phospholipids, which can be enhanced by aspirin (ASA) treatment.	Aspirin	218-225	prostaglandin-endoperoxide synthase 2	Homo sapiens	58-74
25139986-6	2014	Initial activation of TLR4 results in accumulation of the cyclooxygenase-2-derived lipoxin precursor 15-hydroxyeicosatetraenoic acid (15-HETE) in esterified form within membrane phospholipids, which can be enhanced by aspirin (ASA) treatment.	Aspirin	227-230	prostaglandin-endoperoxide synthase 2	Homo sapiens	58-74
23969075-12	2014	IFN-gamma seems to be down-regulated in the patients with CRSwNP, but could be over-expressed in the presence of aspirin intolerance.	Aspirin	113-120	interferon gamma	Homo sapiens	0-9
25012137-10	2014	Adenosine-receptor antagonism blocked the ticagrelor effect and COX2 inhibition by SC5815, or high-dose aspirin attenuated the IS-limiting effect of ticagrelor, whereas cyclooxygenase-1 inhibition or low-dose aspirin had no effect.	Aspirin	104-111	prostaglandin-endoperoxide synthase 2	Homo sapiens	64-68
24796340-10	2014	Our results suggest that a genetic decrease in COX-2 activity may be beneficial with respect to CVD risk, especially, in higher risk patients on aspirin.	Aspirin	145-152	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	47-52
24958470-7	2014	Interestingly, cyclooxygenase-2 inhibition by aspirin or celecoxib abrogated IL-1beta-mediated repression of miR-101 and IL-1beta-mediated activation of Lin28B along with their stimulatory effects on NSCLC cell proliferation and migration.	Aspirin	46-53	prostaglandin-endoperoxide synthase 2	Homo sapiens	15-31
24958470-7	2014	Interestingly, cyclooxygenase-2 inhibition by aspirin or celecoxib abrogated IL-1beta-mediated repression of miR-101 and IL-1beta-mediated activation of Lin28B along with their stimulatory effects on NSCLC cell proliferation and migration.	Aspirin	46-53	interleukin 1 beta	Homo sapiens	77-85
24958470-7	2014	Interestingly, cyclooxygenase-2 inhibition by aspirin or celecoxib abrogated IL-1beta-mediated repression of miR-101 and IL-1beta-mediated activation of Lin28B along with their stimulatory effects on NSCLC cell proliferation and migration.	Aspirin	46-53	interleukin 1 beta	Homo sapiens	121-129
24958470-7	2014	Interestingly, cyclooxygenase-2 inhibition by aspirin or celecoxib abrogated IL-1beta-mediated repression of miR-101 and IL-1beta-mediated activation of Lin28B along with their stimulatory effects on NSCLC cell proliferation and migration.	Aspirin	46-53	lin-28 homolog B	Homo sapiens	153-159
25019653-12	2014	ASP dose-dependently decreased FST-induced increase of cytokine levels, as manifested by significantly stronger effects on IL-6 and TNF-alpha levels at higher doses (25 and 50mg/kg) than the lowest dose of ASP (6 mg/kg).	Aspirin	0-3	interleukin 6	Rattus norvegicus	123-127
23677911-0	2014	Aspirin Half Maximal Inhibitory Concentration Value on Platelet Cyclooxygenase1 in Severe Type-2 Diabetes Mellitus is not Significantly Different from that of Healthy Individuals.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	64-79
25074812-6	2014	Furthermore, we demonstrate that COMMD1 acetylation is enhanced by aspirin-mediated stress, and that this acetylation is absolutely required for the protein to bind RelA under these conditions.	Aspirin	67-74	copper metabolism domain containing 1	Homo sapiens	33-39
25019653-12	2014	ASP dose-dependently decreased FST-induced increase of cytokine levels, as manifested by significantly stronger effects on IL-6 and TNF-alpha levels at higher doses (25 and 50mg/kg) than the lowest dose of ASP (6 mg/kg).	Aspirin	0-3	tumor necrosis factor	Rattus norvegicus	132-141
25123549-0	2014	Younger age, higher body mass index and lower adiponectin concentration predict higher serum thromboxane B2 level in aspirin-treated patients with type 2 diabetes: an observational study.	Aspirin	117-124	adiponectin, C1Q and collagen domain containing	Homo sapiens	46-57
25123549-13	2014	Higher BMI and lower HMW adiponectin concentration were also associated with less potent ASA effect.	Aspirin	89-92	adiponectin, C1Q and collagen domain containing	Homo sapiens	25-36
25123549-14	2014	This is the first study to demonstrate an association of lower adiponectin concentration with higher serum TXB2 level in patients treated with ASA.	Aspirin	143-146	adiponectin, C1Q and collagen domain containing	Homo sapiens	63-74
24880897-9	2014	However, treatment of inflammatory M1 macrophages with aspirin reduced secretion of the pro-inflammatory cytokines IL-1beta and IL-6, and increased secretion of the anti-inflammatory IL-10.	Aspirin	55-62	interleukin 1 beta	Homo sapiens	115-123
24930730-0	2014	Impacts of COX-1 gene polymorphisms on vascular outcomes in patients with ischemic stroke and treated with aspirin.	Aspirin	107-114	prostaglandin-endoperoxide synthase 1	Homo sapiens	11-16
24930730-1	2014	As the key point of function for aspirin to educe anti-platelet effects, cyclooxygenase-1 (COX-1) gene polymorphisms have long been suspected as a potential cause for aspirin nonresponsiveness.	Aspirin	33-40	prostaglandin-endoperoxide synthase 1	Homo sapiens	73-89
24930730-1	2014	As the key point of function for aspirin to educe anti-platelet effects, cyclooxygenase-1 (COX-1) gene polymorphisms have long been suspected as a potential cause for aspirin nonresponsiveness.	Aspirin	33-40	prostaglandin-endoperoxide synthase 1	Homo sapiens	91-96
24930730-1	2014	As the key point of function for aspirin to educe anti-platelet effects, cyclooxygenase-1 (COX-1) gene polymorphisms have long been suspected as a potential cause for aspirin nonresponsiveness.	Aspirin	167-174	prostaglandin-endoperoxide synthase 1	Homo sapiens	73-89
24930730-1	2014	As the key point of function for aspirin to educe anti-platelet effects, cyclooxygenase-1 (COX-1) gene polymorphisms have long been suspected as a potential cause for aspirin nonresponsiveness.	Aspirin	167-174	prostaglandin-endoperoxide synthase 1	Homo sapiens	91-96
24930730-3	2014	This study prospectively evaluated the impacts of COX-1 gene polymorphisms on stroke recurrence and other vascular events in a large cohort of Chinese patients with ischemic stroke and treated with aspirin.	Aspirin	198-205	prostaglandin-endoperoxide synthase 1	Homo sapiens	50-55
25126950-5	2014	Aspirin-treated human platelets were found to be phagocytosed more efficiently by macrophages, associated with attenuation in platelet proteasomal activity and upregulation of conformationally active Bax, which were consistent with enhanced platelet apoptosis.	Aspirin	0-7	BCL2 associated X, apoptosis regulator	Homo sapiens	200-203
25110431-0	2014	Aspirin inhibits cell viability and mTOR downstream signaling in gastroenteropancreatic and bronchopulmonary neuroendocrine tumor cells.	Aspirin	0-7	mechanistic target of rapamycin kinase	Homo sapiens	36-40
25110431-12	2014	Aspirin suppressed mTOR downstream signaling, evidenced by the reduced phosphorylation of the mTOR substrates 4E binding protein 1, serine/threonine kinase P70S6K and S6 ribosomal protein and inhibited glycogen synthase kinase 3 activity.	Aspirin	0-7	mechanistic target of rapamycin kinase	Homo sapiens	19-23
25110431-12	2014	Aspirin suppressed mTOR downstream signaling, evidenced by the reduced phosphorylation of the mTOR substrates 4E binding protein 1, serine/threonine kinase P70S6K and S6 ribosomal protein and inhibited glycogen synthase kinase 3 activity.	Aspirin	0-7	mechanistic target of rapamycin kinase	Homo sapiens	94-98
24880897-9	2014	However, treatment of inflammatory M1 macrophages with aspirin reduced secretion of the pro-inflammatory cytokines IL-1beta and IL-6, and increased secretion of the anti-inflammatory IL-10.	Aspirin	55-62	interleukin 6	Homo sapiens	128-132
25031079-6	2014	We report that curcumin has shown comparable binding affinity value vis-a-vis standard, the accessible surface area (ASA) of human serum albumin (uncomplexed) and its docked complex with curcumin at both binding sites was calculated and found to be close to that of warfarin and diazepam respectively.	Aspirin	117-120	albumin	Homo sapiens	131-144
24953043-1	2014	Aspirin (ASA) is a commonly used nonsteroidal anti-inflammatory drug (NSAID), which exerts its therapeutic effects through inhibition of cyclooxygenase (COX) isoform 2 (COX-2), while the inhibition of COX-1 by ASA leads to apparent side effects.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	169-174
24953043-1	2014	Aspirin (ASA) is a commonly used nonsteroidal anti-inflammatory drug (NSAID), which exerts its therapeutic effects through inhibition of cyclooxygenase (COX) isoform 2 (COX-2), while the inhibition of COX-1 by ASA leads to apparent side effects.	Aspirin	9-12	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	169-174
24953043-1	2014	Aspirin (ASA) is a commonly used nonsteroidal anti-inflammatory drug (NSAID), which exerts its therapeutic effects through inhibition of cyclooxygenase (COX) isoform 2 (COX-2), while the inhibition of COX-1 by ASA leads to apparent side effects.	Aspirin	210-213	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	169-174
24994462-5	2014	This review, according to literature availability, focuses on the relationship between human leukocyte antigens (HLA) region specifically the HLA class II genes and different asthma phenotypes/endotypes, such as allergic asthma/Th2 associated, occupational and aspirin-sensitive asthma.	Aspirin	261-268	major histocompatibility complex, class II, DR beta 1	Homo sapiens	113-116
24994462-5	2014	This review, according to literature availability, focuses on the relationship between human leukocyte antigens (HLA) region specifically the HLA class II genes and different asthma phenotypes/endotypes, such as allergic asthma/Th2 associated, occupational and aspirin-sensitive asthma.	Aspirin	261-268	major histocompatibility complex, class II, DR beta 1	Homo sapiens	142-145
24994462-6	2014	The most common HLA haplotypes in the different asthma phenotypes are HLA-DRB1in allergic asthma, HLA-DQB1in occupational asthma and HLA-DPB1 in aspirin-sensitive asthma.	Aspirin	145-152	major histocompatibility complex, class II, DR beta 1	Homo sapiens	16-19
25104439-8	2014	SOCS2 (one of three SNPs) and all STAT3, STAT5A, and STAT5B SNPs significantly interacted with use of aspirin/NSAIDs to alter breast cancer-specific mortality.	Aspirin	102-109	signal transducer and activator of transcription 3	Homo sapiens	34-39
25085874-3	2014	Therefore, we examined the association between recent (1 year) prediagnostic use of aspirin (COX1/COX2 inhibitor), lymph node involvement at breast cancer diagnosis, and breast cancer-specific mortality.	Aspirin	84-91	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	98-102
25085874-8	2014	Women with prediagnostic aspirin use were statistically significantly less likely to present with a lymph node-positive tumor than nonusers [RR = 0.89; 95% confidence interval (CI), 0.81-0.97], particularly those with larger (Pinteraction = 0.036), progesterone receptor (PR)-negative (Pinteraction &lt; 0.001) or estrogen receptor (ER)-negative (Pinteraction = 0.056) tumors.	Aspirin	25-32	estrogen receptor 1	Homo sapiens	314-331
25085874-8	2014	Women with prediagnostic aspirin use were statistically significantly less likely to present with a lymph node-positive tumor than nonusers [RR = 0.89; 95% confidence interval (CI), 0.81-0.97], particularly those with larger (Pinteraction = 0.036), progesterone receptor (PR)-negative (Pinteraction &lt; 0.001) or estrogen receptor (ER)-negative (Pinteraction = 0.056) tumors.	Aspirin	25-32	estrogen receptor 1	Homo sapiens	333-335
24908358-2	2014	Direct inhibition of cyclooxygenase-2 (COX-2) pathway is generally thought to be the main mechanism by which aspirin inhibits cancer development.	Aspirin	109-116	prostaglandin-endoperoxide synthase 2	Homo sapiens	21-37
24908358-2	2014	Direct inhibition of cyclooxygenase-2 (COX-2) pathway is generally thought to be the main mechanism by which aspirin inhibits cancer development.	Aspirin	109-116	prostaglandin-endoperoxide synthase 2	Homo sapiens	39-44
24890720-10	2014	Like eosinophils, aspirin was able to activate human mast cells directly through Ca2+ flux and PGD2 release.	Aspirin	18-25	prostaglandin D2 synthase	Homo sapiens	95-99
24836854-1	2014	Aspirin-triggered Lipoxin A4 (ATL), as a Lipoxin A4 (LXA4) epimer, is endogenously produced by aspirin-acetylated cycloxygenase-2 (COX-2) and plays a vital role in endogenous anti-inflammation via the LXA4 receptor (ALX).	Aspirin	0-7	formyl peptide receptor 2-like	Rattus norvegicus	216-219
25093007-21	2014	Taking an aspirin (ASA) regularly after being diagnosed with colon cancer is associated with less risk of dying from this cancer, especially among people who have tumors with COX-2 overexpression.16 Nonetheless, these data do not contradict the data obtained on a possible genetic predisposition, even in sporadic or non-hereditary CRC.	Aspirin	10-17	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	175-180
25093007-21	2014	Taking an aspirin (ASA) regularly after being diagnosed with colon cancer is associated with less risk of dying from this cancer, especially among people who have tumors with COX-2 overexpression.16 Nonetheless, these data do not contradict the data obtained on a possible genetic predisposition, even in sporadic or non-hereditary CRC.	Aspirin	19-22	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	175-180
25006185-10	2014	Among aspirin users, concomitant selective cox-2 inhibitor use was no longer associated with increased hazard for cardiovascular events.	Aspirin	6-13	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	43-48
24840525-5	2014	Mutations in the PIK3CA gene may be a potential predictive marker of response to aspirin after a cancer diagnosis, though pharmacological considerations suggest that platelets may be central to the antitumour efficacy of aspirin.	Aspirin	81-88	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	17-23
24890720-1	2014	Reactions to aspirin and nonsteroidal anti-inflammatory drugs in patients with aspirin-exacerbated respiratory disease (AERD) are triggered when constraints upon activated eosinophils, normally supplied by PGE2, are removed secondary to cyclooxygenase-1 inhibition.	Aspirin	13-20	prostaglandin-endoperoxide synthase 1	Homo sapiens	237-253
24890720-1	2014	Reactions to aspirin and nonsteroidal anti-inflammatory drugs in patients with aspirin-exacerbated respiratory disease (AERD) are triggered when constraints upon activated eosinophils, normally supplied by PGE2, are removed secondary to cyclooxygenase-1 inhibition.	Aspirin	79-86	prostaglandin-endoperoxide synthase 1	Homo sapiens	237-253
25197914-0	2014	Elevated total serum IgE in nonatopic patients with aspirin-exacerbated respiratory disease.	Aspirin	52-59	immunoglobulin heavy constant epsilon	Homo sapiens	21-24
25197914-1	2014	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD), also known as Samter"s triad, is characterized by asthma, recurrent nasal polyps, and by allergic-like reactions to aspirin and other nonsteroidal anti-inflammatory drugs, although it is not a true immunoglobulin E (IgE)-mediated allergy.	Aspirin	12-19	immunoglobulin heavy constant epsilon	Homo sapiens	258-274
25197914-1	2014	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD), also known as Samter"s triad, is characterized by asthma, recurrent nasal polyps, and by allergic-like reactions to aspirin and other nonsteroidal anti-inflammatory drugs, although it is not a true immunoglobulin E (IgE)-mediated allergy.	Aspirin	12-19	immunoglobulin heavy constant epsilon	Homo sapiens	276-279
24388008-0	2014	Safety risks for patients with aspirin-exacerbated respiratory disease after acute exposure to selective nonsteroidal anti-inflammatory drugs and COX-2 inhibitors: Meta-analysis of controlled clinical trials.	Aspirin	31-38	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	146-151
23792451-4	2014	Recent "molecular pathological epidemiology" (MPE) research has shown that aspirin use is associated with better prognosis and clinical outcome in PIK3CA-mutated colorectal carcinoma, suggesting somatic PIK3CA mutation as a molecular biomarker that predicts response to aspirin therapy.	Aspirin	75-82	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	147-153
24781842-7	2014	Following the addition of dipyridamole MR to aspirin, there was a significant reduction in VWF:Ag levels at 14d (p = 0.03) and 90d (p = 0.005), but not in VWF:Ag II levels (p &gt;= 0.3).	Aspirin	45-52	von Willebrand factor	Homo sapiens	91-94
24781842-8	2014	The addition of dipyridamole to aspirin led to a persistent reduction in VWF:Ag but not in VWF:Ag II levels, suggesting that dipyridamole may inhibit release of platelet-derived VWF:Ag following TIA or ischaemic stroke.	Aspirin	32-39	von Willebrand factor	Homo sapiens	73-76
23792451-4	2014	Recent "molecular pathological epidemiology" (MPE) research has shown that aspirin use is associated with better prognosis and clinical outcome in PIK3CA-mutated colorectal carcinoma, suggesting somatic PIK3CA mutation as a molecular biomarker that predicts response to aspirin therapy.	Aspirin	75-82	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	203-209
23792451-4	2014	Recent "molecular pathological epidemiology" (MPE) research has shown that aspirin use is associated with better prognosis and clinical outcome in PIK3CA-mutated colorectal carcinoma, suggesting somatic PIK3CA mutation as a molecular biomarker that predicts response to aspirin therapy.	Aspirin	270-277	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	203-209
24720773-1	2014	OBJECTIVES: To study the relationship between platelet glycoprotein IIIa gene (GP IIIa) polymorphism (Leu33Pro) and aspirin resistance in a very elderly Chinese population.	Aspirin	116-123	integrin subunit beta 3	Homo sapiens	79-86
24783984-6	2014	Special emphasis is given to the ability of aspirin to acetylate cyclooxygenases (especially COX-2) and thus to initiate a biochemical pathway leading to the generation of anti-inflammatory pro-resolving mediators synthesized from both omega-3 and omega-6 long-chain polyunsaturated fatty acids.	Aspirin	44-51	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	93-98
24896242-16	2014	ACS14, aspirin and NaHS attenuated the increase in iNOS expression caused by high glucose (25 mM).	Aspirin	7-14	nitric oxide synthase 2	Homo sapiens	51-55
24566733-0	2014	Aspirin decreases systemic exposure to clopidogrel through modulation of P-glycoprotein but does not alter its antithrombotic activity.	Aspirin	0-7	ATP binding cassette subfamily B member 1	Homo sapiens	73-87
25031568-0	2014	Association Analysis of TEC Polymorphisms with Aspirin-Exacerbated Respiratory Disease in a Korean Population.	Aspirin	47-54	tec protein tyrosine kinase	Homo sapiens	24-27
24207016-1	2014	BACKGROUND: Aspirin, a commonly used antiplatelet agent, blocks platelet thromboxane A2 (TXA2) formation from arachidonic acid (AA) by acetylating platelet cyclooxygenase-1 (COX-1).	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	156-172
25031568-3	2014	Therefore, we hypothesized that TEC polymorphisms might be involved in aspirin-exacerbated respiratory disease (AERD) pathogenesis.	Aspirin	71-78	tec protein tyrosine kinase	Homo sapiens	32-35
24987182-0	2014	Use of Aspirin in normalization of recombinant human erythropoietin-mediated hyper-reactivity of platelets in rats.	Aspirin	7-14	erythropoietin	Homo sapiens	53-67
24687028-10	2014	The benefit of aspirin was similar for tumors with strong PTGS2 expression (0.68; 0.48-0.97; P = .03), weak PTGS2 expression (0.59; 0.38-0.97; P = .02), and wild-type PIK3CA tumors (0.55; 0.40-0.75; P &lt; .001).	Aspirin	15-22	prostaglandin-endoperoxide synthase 2	Homo sapiens	58-63
24948975-8	2014	ASA resistance was found to be significantly higher in men, smokers and insulin users, besides this it was found to be significantly lower in beta blocker (BB) users, angiotensin converting enzyme inhibitor (ACEI) users with univariate analysis.	Aspirin	0-3	angiotensin I converting enzyme	Homo sapiens	167-196
24571196-6	2014	RESULTS: Both the release of NO (determined by nitrite+nitrate concentration) and the expression of endothelial-type NO synthase (eNOS) were higher in mononuclear cells from ASA sensitive as compared with those from ASA-resistant patients.	Aspirin	174-177	nitric oxide synthase 3	Homo sapiens	100-128
24571196-6	2014	RESULTS: Both the release of NO (determined by nitrite+nitrate concentration) and the expression of endothelial-type NO synthase (eNOS) were higher in mononuclear cells from ASA sensitive as compared with those from ASA-resistant patients.	Aspirin	174-177	nitric oxide synthase 3	Homo sapiens	130-134
24571196-6	2014	RESULTS: Both the release of NO (determined by nitrite+nitrate concentration) and the expression of endothelial-type NO synthase (eNOS) were higher in mononuclear cells from ASA sensitive as compared with those from ASA-resistant patients.	Aspirin	216-219	nitric oxide synthase 3	Homo sapiens	130-134
24571196-7	2014	There was a positive correlation between either the release of NO and the expression of eNOS protein in mononuclear cells with the ability of ASA to inhibit platelet activity.	Aspirin	142-145	nitric oxide synthase 3	Homo sapiens	88-92
24855830-6	2014	This study is the first to demonstrate that RGS transcripts are elevated in aspirin-resistant platelets from patients with metabolic syndrome.	Aspirin	76-83	paired like homeodomain 2	Homo sapiens	44-47
24207016-1	2014	BACKGROUND: Aspirin, a commonly used antiplatelet agent, blocks platelet thromboxane A2 (TXA2) formation from arachidonic acid (AA) by acetylating platelet cyclooxygenase-1 (COX-1).	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	174-179
24207016-3	2014	We have reported three methods that assess platelet COX-1 acetylation (inactivation) by aspirin and its direct consequences.	Aspirin	88-95	prostaglandin-endoperoxide synthase 1	Homo sapiens	52-57
24207016-8	2014	On day 7 following aspirin treatment COX-1 in the platelets was fully acetylated whereas only non-acetylated COX-1 was present in the day 0 platelets.	Aspirin	19-26	prostaglandin-endoperoxide synthase 1	Homo sapiens	37-42
24207016-13	2014	CONCLUSIONS: Only assays that clearly distinguish between acetylated and non-acetylated platelet COX-1 are useful for establishing the antiplatelet effect of aspirin.	Aspirin	158-165	prostaglandin-endoperoxide synthase 1	Homo sapiens	97-102
24315499-0	2014	Appropriate assessment of the functional consequences of platelet cyclooxygenase-1 inhibition by aspirin in vivo.	Aspirin	97-104	prostaglandin-endoperoxide synthase 1	Homo sapiens	66-82
23382539-2	2014	There is evidence that the reduction in LDL cholesterol (LDL-c) achieved with short-acting statins is superior when taken in the evening and reported improvement in BP control when aspirin and BP-lowering agents are taken in the evening.	Aspirin	181-188	component of oligomeric golgi complex 2	Homo sapiens	57-62
24748925-1	2014	Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	45-61
24748925-1	2014	Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	63-68
24748925-1	2014	Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation.	Aspirin	9-12	prostaglandin-endoperoxide synthase 1	Homo sapiens	45-61
24748925-1	2014	Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation.	Aspirin	9-12	prostaglandin-endoperoxide synthase 1	Homo sapiens	63-68
24708725-1	2014	INTRODUCTION: Recent observational studies indicate that post-diagnostic use of aspirin in breast cancer patients may protect against cancer progression perhaps by inhibiting cyclooxygenase-2 dependent mechanisms.	Aspirin	80-87	prostaglandin-endoperoxide synthase 2	Homo sapiens	175-191
24655690-0	2014	Design and rationale for the Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis in Myocardial Infarction 54 (PEGASUS-TIMI 54) trial.	Aspirin	157-164	IKAROS family zinc finger 5	Homo sapiens	207-222
24520038-0	2014	Repurposing of metformin and aspirin by targeting AMPK-mTOR and inflammation for pancreatic cancer prevention and treatment.	Aspirin	29-36	mechanistic target of rapamycin kinase	Homo sapiens	55-59
24520038-7	2014	For aspirin, the major mechanism is the anti-inflammatory action through the inhibition of COX-1/COX-2 and modulation of the NFkappaB or STAT3 pathway.	Aspirin	4-11	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	97-102
24520038-7	2014	For aspirin, the major mechanism is the anti-inflammatory action through the inhibition of COX-1/COX-2 and modulation of the NFkappaB or STAT3 pathway.	Aspirin	4-11	nuclear factor kappa B subunit 1	Homo sapiens	125-133
24594292-0	2014	Cytokines and hs-CRP levels in individuals treated with low-dose aspirin for cardiovascular prevention: a population-based study (CoLaus Study).	Aspirin	65-72	C-reactive protein	Homo sapiens	17-20
24594292-3	2014	The aim of this study was to determine the association between pro-inflammatory cytokines and hs-CRP levels and low-dose aspirin use for cardiovascular prevention in a population-based cohort (CoLaus Study).	Aspirin	121-128	C-reactive protein	Homo sapiens	97-100
24760190-1	2014	Aspirin use reduces the risk of colorectal neoplasia, at least in part, through inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2)-related pathways.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	94-131
24760190-1	2014	Aspirin use reduces the risk of colorectal neoplasia, at least in part, through inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2)-related pathways.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	133-138
24760190-1	2014	Aspirin use reduces the risk of colorectal neoplasia, at least in part, through inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2)-related pathways.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	140-156
24613833-13	2014	This can be a mechanism how aspirin prevents cancer at least in part, and a novel link between inflammatory NF-kappaB signaling and cancer.	Aspirin	28-35	nuclear factor kappa B subunit 1	Homo sapiens	108-117
24655690-9	2014	CONCLUSIONS: PEGASUS-TIMI 54 is investigating whether the addition of intensive antiplatelet therapy with ticagrelor to low-dose aspirin reduces major adverse cardiovascular events in high-risk patients with a history of myocardial infarction.	Aspirin	129-136	IKAROS family zinc finger 5	Homo sapiens	13-28
24520038-7	2014	For aspirin, the major mechanism is the anti-inflammatory action through the inhibition of COX-1/COX-2 and modulation of the NFkappaB or STAT3 pathway.	Aspirin	4-11	signal transducer and activator of transcription 3	Homo sapiens	137-142
24203353-1	2014	We aimed to investigate the association of aspirin and/or clopidogrel low response with -455G/A polymorphism of beta-fibrinogen in patients with acute coronary syndrome (ACS).	Aspirin	43-50	fibrinogen beta chain	Homo sapiens	112-127
24565956-8	2014	In an exploratory analysis, we found that among individuals with high plasma MIC-1 levels (quintiles 2-5), compared with nonuse, regular use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) was associated with a lower risk of PTGS2-positive CRC (multivariable RR = 0.60; 95% confidence interval = 0.41 to 0.88) but not PTGS2-negative CRC (multivariable RR = 1.21; 95% CI = 0.71 to 2.07).	Aspirin	144-151	prostaglandin-endoperoxide synthase 2	Homo sapiens	238-243
24834760-0	2014	Aspirin but not meloxicam attenuates early atherosclerosis in apolipoprotein E knockout mice.	Aspirin	0-7	apolipoprotein E	Mus musculus	62-78
23901798-0	2014	Effect of aspirin in prevention of adverse pregnancy outcome in women with elevated alpha-fetoprotein.	Aspirin	10-17	alpha fetoprotein	Homo sapiens	84-101
23901798-1	2014	BACKGROUND: To evaluate the effect of low-dose aspirin in prevention of adverse pregnancy outcomes (APO) in women with second trimester alpha-fetoprotein (AFP) &gt;2.5 multiple of median (MOM) and to compare aspirin effect on women with normal and abnormal uterine artery (UtA) Doppler.	Aspirin	47-54	alpha fetoprotein	Homo sapiens	136-153
23901798-1	2014	BACKGROUND: To evaluate the effect of low-dose aspirin in prevention of adverse pregnancy outcomes (APO) in women with second trimester alpha-fetoprotein (AFP) &gt;2.5 multiple of median (MOM) and to compare aspirin effect on women with normal and abnormal uterine artery (UtA) Doppler.	Aspirin	47-54	alpha fetoprotein	Homo sapiens	155-158
23901798-10	2014	CONCLUSION: Low-dose aspirin reduces APO and delivery before 34 weeks of gestation in pregnant women with unexplained elevated AFP.	Aspirin	21-28	alpha fetoprotein	Homo sapiens	127-130
24565956-8	2014	In an exploratory analysis, we found that among individuals with high plasma MIC-1 levels (quintiles 2-5), compared with nonuse, regular use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) was associated with a lower risk of PTGS2-positive CRC (multivariable RR = 0.60; 95% confidence interval = 0.41 to 0.88) but not PTGS2-negative CRC (multivariable RR = 1.21; 95% CI = 0.71 to 2.07).	Aspirin	144-151	prostaglandin-endoperoxide synthase 2	Homo sapiens	331-336
24661619-9	2014	DAPT and aspirin given only by regimen 2 and 3 reduced NICD, IL-6 and IL-1beta in the ischemic penumbral cortex.	Aspirin	9-16	interleukin 6	Rattus norvegicus	61-65
24107454-4	2014	ASA significantly increased MDA levels in both kidney and testis, whereas it significantly decreased the values of SOD, CAT, GPX, and GSH in kidney and CAT levels in testis.	Aspirin	0-3	catalase	Rattus norvegicus	120-123
24107454-4	2014	ASA significantly increased MDA levels in both kidney and testis, whereas it significantly decreased the values of SOD, CAT, GPX, and GSH in kidney and CAT levels in testis.	Aspirin	0-3	catalase	Rattus norvegicus	152-155
24661619-9	2014	DAPT and aspirin given only by regimen 2 and 3 reduced NICD, IL-6 and IL-1beta in the ischemic penumbral cortex.	Aspirin	9-16	interleukin 1 beta	Rattus norvegicus	70-78
24345330-10	2014	Our data also shown that Aspirin represses VNR-activated TGF-beta-activated kinase-1 (TAK1) activation, inhibited the interaction of TAK1/TAK-binding protein1 (TAB1), suppressed NF-kappa B activation and pro-inflammatory cytokine secretion.	Aspirin	25-32	nuclear factor kappa B subunit 1	Homo sapiens	178-188
24503478-8	2014	The cyclooxygenase activity of nanodisc-reconstituted COX-2 was reduced by aspirin acetylation and potentiated by the nonsubstrate fatty acid palmitic acid to the same extent as detergent solubilized enzyme, independent of phospholipid composition.	Aspirin	75-82	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	54-59
24624362-5	2014	Finally, mutations in PIK3CA may be the long sought biomarker for successful adjuvant therapy with aspirin in patients with CRC.	Aspirin	99-106	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	22-28
24717792-13	2014	CD4(+) IFN-gamma and CD4(+) IL-10 levels in AERD patients after 1-month aspirin desensitization treatment were similar to the healthy controls.	Aspirin	72-79	CD4 molecule	Homo sapiens	0-3
24717792-14	2014	The study confirms aspirin desensitization is effective clinically in AERD patients and suggests that IFN gamma and IL-10 expression in CD4(+) T lymphocytes may be related to the mechanism of action.	Aspirin	19-26	interferon gamma	Homo sapiens	102-111
24717792-14	2014	The study confirms aspirin desensitization is effective clinically in AERD patients and suggests that IFN gamma and IL-10 expression in CD4(+) T lymphocytes may be related to the mechanism of action.	Aspirin	19-26	CD4 molecule	Homo sapiens	136-139
24327271-4	2014	In these cohorts, the survival benefit of aspirin was shown to depend upon the level of COX-2 expression in the primary colorectal cancer.	Aspirin	42-49	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	88-93
23834376-6	2014	For carriers of the PlA2 allele, OR 0.924 (n = 2318; 95% CI 0.743, 1.151; P = 0.481) was observed for resistance to any antiplatelet drug, OR 0.862 (n = 2085; 95% CI 0.685, 1.086; P = 0.208) for resistance to aspirin and OR 1.429 (n = 233; 95% CI 0.791, 2.582; P = 0.237) for resistance to clopidogrel.	Aspirin	209-216	phospholipase A2 group IB	Homo sapiens	20-24
23834376-8	2014	PlA2 carriage was marginally associated with aspirin sensitivity using the fixed effects model when identified by the PFA-100 assay (n = 1151; OR 0.743, 95% CI 0.558, 0.989; P = 0.041) but with significant heterogeneity (I(2) = 55%; P = 0.002).	Aspirin	45-52	phospholipase A2 group IB	Homo sapiens	0-4
24327271-6	2014	Aspirin intake following colorectal cancer resection was associated with a significant improvement of survival in patients whose tumors carried mutant, but not wild-type, copies of the phosphoinositide 3-kinase (PI3KCA) gene, especially tumors that overexpressed COX-2.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	263-268
24327271-8	2014	Aspirin has also been shown to reduce the incidence of colorectal cancers bearing wild-type, but not mutant alleles of the BRAF(V600E) oncogene.	Aspirin	0-7	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	123-128
24355100-7	2014	The use of epidermal growth factor receptor-targeted therapy in advanced colon cancer patients requires knowledge of the mutation status for KRAS and BRAF genes, and knowing the mutational status of PIK3CA may predict how patients respond to aspirin to prevent colon cancer recurrence.	Aspirin	242-249	epidermal growth factor receptor	Homo sapiens	11-43
24355100-7	2014	The use of epidermal growth factor receptor-targeted therapy in advanced colon cancer patients requires knowledge of the mutation status for KRAS and BRAF genes, and knowing the mutational status of PIK3CA may predict how patients respond to aspirin to prevent colon cancer recurrence.	Aspirin	242-249	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	199-205
24474638-2	2014	Polymorphisms in genes coding GPIIb/IIIa, namely ITGA2B and ITGB3, are associated with aspirin resistance and risk for thrombotic diseases.	Aspirin	87-94	integrin subunit beta 3	Homo sapiens	60-65
24648214-7	2014	Low-dose aspirin improved HFD-induced hyperinsulinemia and hyperlipidemia, recovered PT and aPTT, inhibited upregulation of adhesion molecules and chemokines and reduced expression of PKCalpha, IKKalpha, p65, and MAPKs.	Aspirin	9-16	synaptotagmin 1	Rattus norvegicus	204-207
25272742-5	2014	Incubation of cells transfected with the above-mentioned constructs treated with aspirin was accompanied by the suppression of NF-kB, HIF1alpha, GAS, VDR, and HSF binding activity.	Aspirin	81-88	hypoxia inducible factor 1 subunit alpha	Homo sapiens	134-143
25272742-5	2014	Incubation of cells transfected with the above-mentioned constructs treated with aspirin was accompanied by the suppression of NF-kB, HIF1alpha, GAS, VDR, and HSF binding activity.	Aspirin	81-88	PAXIP1 associated glutamate rich protein 1	Homo sapiens	145-148
24568581-7	2014	A beta contact"s potential contribution to protein binding is also supposed to be inversely proportional to its ASA to follow the water exclusion hypothesis of binding hot spots.	Aspirin	112-115	amyloid beta precursor protein	Homo sapiens	0-6
24022862-2	2014	However, in some individuals TXA2 suppression by aspirin is impaired, indicating suboptimal inhibition of platelet cyclooxygenase 1 (COX-1) by aspirin.	Aspirin	143-150	prostaglandin-endoperoxide synthase 1	Homo sapiens	133-138
24605250-7	2014	Daily low-dose aspirin achieves complete and persistent inhibition of cyclooxygenase (COX)-1 in platelets (in pre-systemic circulation) while causing a limited and rapidly reversible inhibitory effect on COX-2 and/or COX-1 expressed in nucleated cells.	Aspirin	15-22	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	204-209
24022862-10	2014	CONCLUSION: The pharmacologic effect of aspirin is suboptimal in 15% of patients with SLE but in none of the control subjects, and the suboptimal response was associated with metabolic syndrome, obesity, and higher CRP concentrations.	Aspirin	40-47	C-reactive protein	Homo sapiens	215-218
24478700-9	2014	Furthermore, we revealed that aspirin enhanced extracellular signal-related kinase (ERK) but inhibited RhoA activities.	Aspirin	30-37	Eph receptor B1	Rattus norvegicus	47-82
24372992-0	2014	Aspirin in type 2 diabetes, a randomised controlled study: effect of different doses on inflammation, oxidative stress, insulin resistance and endothelial function.	Aspirin	0-7	insulin	Homo sapiens	120-127
23807310-3	2014	Aspirin and corticosteroids are known to down-regulate CRP production.	Aspirin	0-7	C-reactive protein	Homo sapiens	55-58
23807310-4	2014	In this study, we evaluated the usefulness of CRP as a biomarker for complicated diverticulitis and specifically in patients on anti-inflammatory medications: aspirin and corticosteroids.	Aspirin	159-166	C-reactive protein	Homo sapiens	46-49
23807310-9	2014	Mean CRP levels were 133.5 and 63.5 mg/ml for those with complicated and uncomplicated disease, respectively (p &lt; 0.001), and 139 and 60 mg/ml, respectively (p &lt; 0.001) in the subgroup of patients taking aspirin (n = 61).	Aspirin	210-217	C-reactive protein	Homo sapiens	5-8
23807310-12	2014	CONCLUSIONS: The CRP level distinguished between complicated and uncomplicated disease among left-sided diverticulitis patients including those taking aspirin, but not among those on corticosteroid treatment.	Aspirin	151-158	C-reactive protein	Homo sapiens	17-20
24478700-9	2014	Furthermore, we revealed that aspirin enhanced extracellular signal-related kinase (ERK) but inhibited RhoA activities.	Aspirin	30-37	Eph receptor B1	Rattus norvegicus	84-87
24478700-10	2014	In summary, we provided the first evidence that aspirin can promote oligodendrogenesis and oligodendrocyte myelination after WML, which may involve ERK and RhoA pathways.	Aspirin	48-55	Eph receptor B1	Rattus norvegicus	148-151
24259417-7	2014	Additionally, we determined the role of the aspirin-triggered 17R analog (AT-RvD1, a more chemically stable RvD1 epimeric form) in prevention of TNF-alpha-mediated salivary inflammation in mouse submandibular glands (mSMG).	Aspirin	44-51	tumor necrosis factor	Mus musculus	145-154
24535852-1	2014	Variation in the gene encoding cyclooxygenase-1 (COX-1) is involved in the process of aspirin resistance.	Aspirin	86-93	prostaglandin-endoperoxide synthase 1	Homo sapiens	31-47
24535852-1	2014	Variation in the gene encoding cyclooxygenase-1 (COX-1) is involved in the process of aspirin resistance.	Aspirin	86-93	prostaglandin-endoperoxide synthase 1	Homo sapiens	49-54
24265393-8	2014	In vivo, this selective (hem)immunoreceptor tyrosine-based activation motif signaling defect resulted in prolonged bleeding times but affected arterial thrombus formation only after concomitant treatment with acetylsalicylic acid, indicating that defective glycoprotein VI signaling in the absence of Grb2 can be compensated through thromboxane A2-induced G protein-coupled receptor signaling pathways.	Aspirin	209-229	growth factor receptor bound protein 2	Homo sapiens	301-305
24315932-8	2014	We found that ritonavir administration caused intestinal damage and its co-administration with naproxen or ASA exacerbated the severity of injury and intestinal inflammation, as assessed by measuring haematocrit, MPO, mucosal levels of PGE2 and mRNA levels of iNOS, MCP-1 and VLA-1.	Aspirin	107-110	nitric oxide synthase 2	Homo sapiens	260-264
24898335-9	2014	Fibrinogen concentration was significantly higher in women than in men among patients treated with 100 mg ASA (p&lt;0.05), but not in the other groups.	Aspirin	106-109	fibrinogen beta chain	Homo sapiens	0-10
24395886-10	2014	15-epi-lipoxin-A4 was identified in exhaled breath condensate from LAM subjects and was increased by aspirin treatment, indicative of functional COX-2 expression in the LAM airway.	Aspirin	101-108	prostaglandin-endoperoxide synthase 2	Homo sapiens	145-150
24432004-4	2014	Aspirin, a cyclooxygenase-1 inhibitor, decreases atherothrombotic associated mortality by 25%.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	11-27
24898335-10	2014	CONCLUSIONS: Significantly higher fibrinogen concentration found in aspirin treated women than men may play a role in higher ADP induced platelet aggregation.	Aspirin	68-75	fibrinogen beta chain	Homo sapiens	34-44
24282256-2	2014	Aspirin inhibits several pathways mediated by NF-kappaB, COX-2, or their targets that are important in multiple myeloma pathogenesis.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	46-55
24209633-5	2014	Furthermore, the PTP inhibitor mitigated the inhibitory effect of aspirin on COX-2 and PGE(2) upregulation and NF-kappaB activation, whereas the PKC inhibitor enhanced the inhibitory effects of aspirin on the production of COX-2 and PGE(2).	Aspirin	66-73	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	77-82
24209633-0	2014	Aspirin inhibits lipopolysaccharide-induced COX-2 expression and PGE2 production in porcine alveolar macrophages by modulating protein kinase C and protein tyrosine phosphatase activity.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	44-49
24209633-1	2014	Aspirin has been demonstrated to be effective in inhibiting COX-2 and PGE(2) in Alveolar macrophages (AMs).	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	60-65
24209633-3	2014	In the present study, we found that pretreatment with aspirin inhibited LPS-induced COX-2 and PGE(2) upregulation, IkappaBalpha degradation, NFkappaB activation and the increase of PKC activity, but elevated LPS-induced the decrease of PTP activity.	Aspirin	54-61	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	84-89
24209633-3	2014	In the present study, we found that pretreatment with aspirin inhibited LPS-induced COX-2 and PGE(2) upregulation, IkappaBalpha degradation, NFkappaB activation and the increase of PKC activity, but elevated LPS-induced the decrease of PTP activity.	Aspirin	54-61	NFKB inhibitor alpha	Homo sapiens	115-127
24209633-3	2014	In the present study, we found that pretreatment with aspirin inhibited LPS-induced COX-2 and PGE(2) upregulation, IkappaBalpha degradation, NFkappaB activation and the increase of PKC activity, but elevated LPS-induced the decrease of PTP activity.	Aspirin	54-61	nuclear factor kappa B subunit 1	Homo sapiens	141-149
24282256-2	2014	Aspirin inhibits several pathways mediated by NF-kappaB, COX-2, or their targets that are important in multiple myeloma pathogenesis.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	57-62
24282256-12	2014	This prospective study of aspirin use and multiple myeloma supports an etiologic role for aspirin-inhibited (i.e., NF-kappaB- or COX-2 mediated) pathways.	Aspirin	26-33	nuclear factor kappa B subunit 1	Homo sapiens	115-124
24282256-12	2014	This prospective study of aspirin use and multiple myeloma supports an etiologic role for aspirin-inhibited (i.e., NF-kappaB- or COX-2 mediated) pathways.	Aspirin	90-97	nuclear factor kappa B subunit 1	Homo sapiens	115-124
24282256-12	2014	This prospective study of aspirin use and multiple myeloma supports an etiologic role for aspirin-inhibited (i.e., NF-kappaB- or COX-2 mediated) pathways.	Aspirin	90-97	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	129-134
23723142-9	2014	Moreover, safety concerns related to alternative medications such as acetaminophen and selective COX-2 inhibitors may influence users of these drugs to switch to aspirin and NSAIDs.	Aspirin	162-169	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	97-102
24988246-3	2014	Polymorphisms of the CES1 gene have been reported to affect the metabolism of dabigatran etexilate, methylphenidate, oseltamivir, imidapril, and clopidogrel, whereas variants of the CES2 gene have been found to affect aspirin and irinotecan.	Aspirin	218-225	carboxylesterase 2	Homo sapiens	182-186
24243637-9	2014	Treatment of adipocyte fractions or SGBS adipocytes with metformin or acetylsalicylic acid, which target C/EBPbeta and NF-kappaB/RelA signaling, attenuated the IL-1alpha induction of 11beta-HSD1 (P&lt;=.002).	Aspirin	70-90	nuclear factor kappa B subunit 1	Homo sapiens	119-128
24243637-9	2014	Treatment of adipocyte fractions or SGBS adipocytes with metformin or acetylsalicylic acid, which target C/EBPbeta and NF-kappaB/RelA signaling, attenuated the IL-1alpha induction of 11beta-HSD1 (P&lt;=.002).	Aspirin	70-90	hydroxysteroid 11-beta dehydrogenase 1	Homo sapiens	183-194
24243637-11	2014	These molecules/signaling pathways are, therefore, potential targets for drugs, including metformin and acetylsalicylic acid, to prevent/decreased up-regulation of 11beta-HSD1 in human obese/metabolic syndrome adipose tissue.	Aspirin	104-124	hydroxysteroid 11-beta dehydrogenase 1	Homo sapiens	164-175
25612650-2	2014	The production of lipoxins is enhanced by aspirin through acetylation of cyclooxygenase-2, via a mechanism known as "aspirin-triggered lipoxin".	Aspirin	42-49	prostaglandin-endoperoxide synthase 2	Homo sapiens	73-89
25612650-2	2014	The production of lipoxins is enhanced by aspirin through acetylation of cyclooxygenase-2, via a mechanism known as "aspirin-triggered lipoxin".	Aspirin	117-124	prostaglandin-endoperoxide synthase 2	Homo sapiens	73-89
25301077-13	2014	Aspirin use was associated with lower levels of CX3CL1 (p = 0.0002) and diabetes with higher levels (p = 0.031).	Aspirin	0-7	C-X3-C motif chemokine ligand 1	Homo sapiens	48-54
24190973-8	2014	The activation of p53 through AMPK-mediated MDMX phosphorylation and inactivation was further confirmed by using cell and animal model systems with two AMPK activators, metformin and salicylate (the active form of aspirin).	Aspirin	214-221	tumor protein p53	Homo sapiens	18-21
23993980-1	2014	Aspirin is integral to the secondary prevention of cardiovascular disease and acts to impair the development of platelet-mediated atherothromboembolic events by irreversible inhibition of platelet cyclooxygenase-1 (COX-1).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	197-213
23993980-1	2014	Aspirin is integral to the secondary prevention of cardiovascular disease and acts to impair the development of platelet-mediated atherothromboembolic events by irreversible inhibition of platelet cyclooxygenase-1 (COX-1).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	215-220
24102302-9	2014	Expression of platelet-bound SDF-1 and number of CD34(+) cells were higher in patients with DCM compared with patients with ICM (p &lt; 0.001 for both) and inversely correlated with age and aspirin therapy.	Aspirin	190-197	CD34 molecule	Homo sapiens	49-53
24268424-10	2014	CONCLUSIONS: Our results suggest that the antithrombotic activities of PAR1 and/or PAR4 antagonism is influenced by shear conditions as well as by combined platelet inhibition with aspirin and a P2Y12-antagonist.	Aspirin	181-188	coagulation factor II thrombin receptor	Homo sapiens	71-75
24376548-0	2013	Platelet content of nitric oxide synthase 3 phosphorylated at Serine 1177 is associated with the functional response of platelets to aspirin.	Aspirin	133-140	nitric oxide synthase 3	Homo sapiens	20-43
23871514-10	2014	The Asp treatment significantly reduced fracture-increased echogenicity (hyperechogenicity, p&lt;0.05) in ultrasound images as well as inhibited cell death, and expression of COX-2 and BLT1.	Aspirin	4-7	leukotriene B4 receptor 1	Mus musculus	185-189
24453831-0	2013	Von Willebrand factor antigen predicts response to double dose of aspirin and clopidogrel by PFA-100 in patients undergoing primary angioplasty for ST elevation myocardial infarction.	Aspirin	66-73	von Willebrand factor	Homo sapiens	0-21
24453831-3	2013	The objective of this study was to verify the effect of double dose (DD) of aspirin and clopidogrel on HPR detected by PFA-100 and its relation to VWF and to its regulatory metalloprotease ADAMTS-13.	Aspirin	76-83	von Willebrand factor	Homo sapiens	147-150
24367646-8	2013	CONCLUSIONS: CYP4F11 and CYP2D6 SNPs may identify patients at increased risk for aspirin-induced small bowel bleeding.	Aspirin	81-88	cytochrome P450 family 4 subfamily F member 11	Homo sapiens	13-20
24367646-8	2013	CONCLUSIONS: CYP4F11 and CYP2D6 SNPs may identify patients at increased risk for aspirin-induced small bowel bleeding.	Aspirin	81-88	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	25-31
24376548-4	2013	Protein expression of nitric oxide synthase 3 (NOS3) was higher in ASA-sensitive than in ASA-resistant platelets but there were no differences in the platelet expression of nitric oxide synthase 2 (NOS2) isoform.	Aspirin	67-70	nitric oxide synthase 3	Homo sapiens	22-45
24376548-4	2013	Protein expression of nitric oxide synthase 3 (NOS3) was higher in ASA-sensitive than in ASA-resistant platelets but there were no differences in the platelet expression of nitric oxide synthase 2 (NOS2) isoform.	Aspirin	67-70	nitric oxide synthase 3	Homo sapiens	47-51
24376548-4	2013	Protein expression of nitric oxide synthase 3 (NOS3) was higher in ASA-sensitive than in ASA-resistant platelets but there were no differences in the platelet expression of nitric oxide synthase 2 (NOS2) isoform.	Aspirin	89-92	nitric oxide synthase 3	Homo sapiens	22-45
24376548-4	2013	Protein expression of nitric oxide synthase 3 (NOS3) was higher in ASA-sensitive than in ASA-resistant platelets but there were no differences in the platelet expression of nitric oxide synthase 2 (NOS2) isoform.	Aspirin	89-92	nitric oxide synthase 3	Homo sapiens	47-51
24376548-5	2013	The highest NOS3 expression in ASA-sensitive platelets was independent of the presence of T-to-C mutation at nucleotide position -786 (T(-786)   C) in the NOS3-coding gene.	Aspirin	31-34	nitric oxide synthase 3	Homo sapiens	12-16
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Aspirin	110-113	nitric oxide synthase 3	Homo sapiens	44-48
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Aspirin	110-113	nitric oxide synthase 3	Homo sapiens	90-94
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Aspirin	132-135	nitric oxide synthase 3	Homo sapiens	44-48
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Aspirin	132-135	nitric oxide synthase 3	Homo sapiens	90-94
24075938-1	2013	Nonsteroidal anti-inflammatory drugs (NSAIDs) may interfere with the anti-platelet activity of aspirin at the level of the platelet cyclooxygenase-1 (COX-1) enzyme.	Aspirin	95-102	prostaglandin-endoperoxide synthase 1	Homo sapiens	132-148
24376548-11	2013	CONCLUSIONS: Functional platelet responsiveness to ASA was associated with the platelet content of phosphorylated NOS3 at Ser(1177).	Aspirin	51-54	nitric oxide synthase 3	Homo sapiens	114-118
24075938-1	2013	Nonsteroidal anti-inflammatory drugs (NSAIDs) may interfere with the anti-platelet activity of aspirin at the level of the platelet cyclooxygenase-1 (COX-1) enzyme.	Aspirin	95-102	prostaglandin-endoperoxide synthase 1	Homo sapiens	150-155
24075938-5	2013	Docking studies suggested that NSAIDs forming hydrogen bonds with Ser530, Arg120, Tyr385 and other amino acids of the COX-1 hydrophobic channel interfere with antiplatelet activity of aspirin while non interfering NSAIDs do not form relevant hydrogen bond interactions within the aspirin binding site.	Aspirin	184-191	prostaglandin-endoperoxide synthase 1	Homo sapiens	118-123
23851581-0	2013	Regulation on RhoA in vascular smooth muscle cells under inflammatory stimulation proposes a novel mechanism mediating the multiple-beneficial action of acetylsalicylic acid.	Aspirin	153-173	ras homolog family member A	Homo sapiens	14-18
24075938-5	2013	Docking studies suggested that NSAIDs forming hydrogen bonds with Ser530, Arg120, Tyr385 and other amino acids of the COX-1 hydrophobic channel interfere with antiplatelet activity of aspirin while non interfering NSAIDs do not form relevant hydrogen bond interactions within the aspirin binding site.	Aspirin	280-287	prostaglandin-endoperoxide synthase 1	Homo sapiens	118-123
24075938-6	2013	In conclusion, docking analysis of NSAID interactions at the COX-1 active site appears useful to predict their interference with the anti-platelet activity of aspirin.	Aspirin	159-166	prostaglandin-endoperoxide synthase 1	Homo sapiens	61-66
23963688-8	2013	Association between "poor" platelet response with lower ASA dose was confirmed by conditional maximum likelihood logistic regression, which showed the independency between erythrocyte-derived parameters, as the risk factors for suboptimal platelet response to ASA, and other risk factors, like CRP or LDL-cholesterol.	Aspirin	56-59	C-reactive protein	Homo sapiens	294-297
23912646-4	2013	In this study, the release of interleukin-2 (IL-2), interleukin-4 (IL-4), and interferon-gamma (IFN-gamma) by CD4+ T lymphocytes prior to aspirin desensitization were also measured at intracellular levels, and expression of these cytokines after 1 month aspirin desensitization was evaluated.	Aspirin	254-261	interferon gamma	Homo sapiens	96-105
23912646-4	2013	In this study, the release of interleukin-2 (IL-2), interleukin-4 (IL-4), and interferon-gamma (IFN-gamma) by CD4+ T lymphocytes prior to aspirin desensitization were also measured at intracellular levels, and expression of these cytokines after 1 month aspirin desensitization was evaluated.	Aspirin	254-261	CD4 molecule	Homo sapiens	110-113
23912646-4	2013	In this study, the release of interleukin-2 (IL-2), interleukin-4 (IL-4), and interferon-gamma (IFN-gamma) by CD4+ T lymphocytes prior to aspirin desensitization were also measured at intracellular levels, and expression of these cytokines after 1 month aspirin desensitization was evaluated.	Aspirin	138-145	interferon gamma	Homo sapiens	96-105
23912646-4	2013	In this study, the release of interleukin-2 (IL-2), interleukin-4 (IL-4), and interferon-gamma (IFN-gamma) by CD4+ T lymphocytes prior to aspirin desensitization were also measured at intracellular levels, and expression of these cytokines after 1 month aspirin desensitization was evaluated.	Aspirin	254-261	interleukin 2	Homo sapiens	30-43
23851581-3	2013	This study aimed to investigate the regulatory effect of acetylsalicylic acid on RhoA in vascular smooth muscle cells (VSMCs).	Aspirin	57-77	ras homolog family member A	Homo sapiens	81-85
23851581-5	2013	RhoA overexpression was downregulated by aspirin (both 30 and 300 muM) because of enhanced degradation of RhoA protein.	Aspirin	41-48	ras homolog family member A	Homo sapiens	0-4
23851581-5	2013	RhoA overexpression was downregulated by aspirin (both 30 and 300 muM) because of enhanced degradation of RhoA protein.	Aspirin	41-48	ras homolog family member A	Homo sapiens	106-110
23851581-6	2013	The effect of LPS on increasing active RhoA level was significantly attenuated by aspirin (300 muM), which exerted no effect on RhoA translocation.	Aspirin	82-89	ras homolog family member A	Homo sapiens	39-43
23851581-7	2013	The promoted RhoA phosphorylation under LPS stimulation, coupled with RhoA protein expression, was greatly decreased by aspirin treatment.	Aspirin	120-127	ras homolog family member A	Homo sapiens	13-17
23851581-7	2013	The promoted RhoA phosphorylation under LPS stimulation, coupled with RhoA protein expression, was greatly decreased by aspirin treatment.	Aspirin	120-127	ras homolog family member A	Homo sapiens	70-74
23851581-9	2013	Our investigation indicates that the regulation of RhoA by aspirin in VSMCs under inflammatory stimulus could be a novel mechanism via which aspirin, apart from the COX-dependent action, exerted the multiple beneficial effects.	Aspirin	59-66	ras homolog family member A	Homo sapiens	51-55
23851581-9	2013	Our investigation indicates that the regulation of RhoA by aspirin in VSMCs under inflammatory stimulus could be a novel mechanism via which aspirin, apart from the COX-dependent action, exerted the multiple beneficial effects.	Aspirin	141-148	ras homolog family member A	Homo sapiens	51-55
24255997-9	2013	Some NSAIDs (such as ibuprofen) can interfere with the cardioprotective effects of aspirin by competitively binding to COX-1 enzyme, resulting in increased TXA2 production Naproxen may differ from other NSAIDs in sustaining functionally important degrees of inhibition of platelet cyclooxygenase-1 activity throughout the dosing interval.	Aspirin	83-90	prostaglandin-endoperoxide synthase 1	Homo sapiens	281-297
24166520-0	2013	Aspirin therapy for colorectal cancer with PIK3CA mutation: simply complex!	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	43-49
24062397-3	2013	Recent data have suggested that the benefit of aspirin after CRC diagnosis is limited to patients with PIK3CA-mutant cancers.	Aspirin	47-54	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	103-109
24062397-4	2013	We sought to determine the predictive utility of PIK3CA mutation for benefit from both cyclooxygenase-2 inhibition and aspirin.	Aspirin	119-126	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	49-55
24062397-8	2013	In contrast, regular aspirin use after CRC diagnosis was associated with a reduced rate of CRC recurrence in patients with PIK3CA-mutant cancers (HR, 0.11; 95% CI, 0.001 to 0.832; P = .027; (P)INTERACTION = .024) but not in patients lacking tumor PIK3CA mutation (HR, 0.92; 95% CI, 0.60 to 1.42; P = .71).	Aspirin	21-28	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	123-129
24062397-8	2013	In contrast, regular aspirin use after CRC diagnosis was associated with a reduced rate of CRC recurrence in patients with PIK3CA-mutant cancers (HR, 0.11; 95% CI, 0.001 to 0.832; P = .027; (P)INTERACTION = .024) but not in patients lacking tumor PIK3CA mutation (HR, 0.92; 95% CI, 0.60 to 1.42; P = .71).	Aspirin	21-28	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	247-253
24062397-10	2013	Our findings are concordant with recent data and support the prospective investigation of adjuvant aspirin in PIK3CA-mutant CRC.	Aspirin	99-106	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	110-116
24244288-10	2013	CONCLUSION: Our findings provide strong evidence that COX-2 and ITGA2 genetic defects might increase the risk of having aspirin insensitivity, especially for aspirin semi-resistance and in Chinese populations.	Aspirin	120-127	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	54-59
24244288-10	2013	CONCLUSION: Our findings provide strong evidence that COX-2 and ITGA2 genetic defects might increase the risk of having aspirin insensitivity, especially for aspirin semi-resistance and in Chinese populations.	Aspirin	158-165	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	54-59
24649055-0	2013	Aspirin attenuates angiotensin II-induced inflammation in bone marrow mesenchymal stem cells via the inhibition of ERK1/2 and NF-kappaB activation.	Aspirin	0-7	angiotensinogen	Homo sapiens	19-33
24649055-0	2013	Aspirin attenuates angiotensin II-induced inflammation in bone marrow mesenchymal stem cells via the inhibition of ERK1/2 and NF-kappaB activation.	Aspirin	0-7	mitogen-activated protein kinase 3	Homo sapiens	115-121
24649055-0	2013	Aspirin attenuates angiotensin II-induced inflammation in bone marrow mesenchymal stem cells via the inhibition of ERK1/2 and NF-kappaB activation.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	126-135
24649055-6	2013	In this study, we investigated the effect of aspirin on Ang II-induced inflammation in bmMSCs.	Aspirin	45-52	angiotensinogen	Homo sapiens	56-62
24649055-10	2013	The application of aspirin (0.1 mM) significantly inhibited the activation of ERK1/2 and NF-kappaB, the expression of TNF-alpha, IL-6, IL-1beta and MCP-1 genes and the secretion of TNF-alpha and IL-6.	Aspirin	19-26	mitogen-activated protein kinase 3	Homo sapiens	78-84
24649055-10	2013	The application of aspirin (0.1 mM) significantly inhibited the activation of ERK1/2 and NF-kappaB, the expression of TNF-alpha, IL-6, IL-1beta and MCP-1 genes and the secretion of TNF-alpha and IL-6.	Aspirin	19-26	nuclear factor kappa B subunit 1	Homo sapiens	89-98
24649055-10	2013	The application of aspirin (0.1 mM) significantly inhibited the activation of ERK1/2 and NF-kappaB, the expression of TNF-alpha, IL-6, IL-1beta and MCP-1 genes and the secretion of TNF-alpha and IL-6.	Aspirin	19-26	tumor necrosis factor	Homo sapiens	118-127
24649055-10	2013	The application of aspirin (0.1 mM) significantly inhibited the activation of ERK1/2 and NF-kappaB, the expression of TNF-alpha, IL-6, IL-1beta and MCP-1 genes and the secretion of TNF-alpha and IL-6.	Aspirin	19-26	interleukin 6	Homo sapiens	129-133
24649055-10	2013	The application of aspirin (0.1 mM) significantly inhibited the activation of ERK1/2 and NF-kappaB, the expression of TNF-alpha, IL-6, IL-1beta and MCP-1 genes and the secretion of TNF-alpha and IL-6.	Aspirin	19-26	interleukin 1 beta	Homo sapiens	135-143
24649055-10	2013	The application of aspirin (0.1 mM) significantly inhibited the activation of ERK1/2 and NF-kappaB, the expression of TNF-alpha, IL-6, IL-1beta and MCP-1 genes and the secretion of TNF-alpha and IL-6.	Aspirin	19-26	tumor necrosis factor	Homo sapiens	181-190
24649055-10	2013	The application of aspirin (0.1 mM) significantly inhibited the activation of ERK1/2 and NF-kappaB, the expression of TNF-alpha, IL-6, IL-1beta and MCP-1 genes and the secretion of TNF-alpha and IL-6.	Aspirin	19-26	interleukin 6	Homo sapiens	195-199
24649055-11	2013	Our findings indicated that aspirin may attenuate Ang II-induced inflammation in bmMSCs via the inhibition of ERK1/2 and NF-kappaB activation.	Aspirin	28-35	angiotensinogen	Homo sapiens	50-56
24649055-11	2013	Our findings indicated that aspirin may attenuate Ang II-induced inflammation in bmMSCs via the inhibition of ERK1/2 and NF-kappaB activation.	Aspirin	28-35	mitogen-activated protein kinase 3	Homo sapiens	110-116
24649055-11	2013	Our findings indicated that aspirin may attenuate Ang II-induced inflammation in bmMSCs via the inhibition of ERK1/2 and NF-kappaB activation.	Aspirin	28-35	nuclear factor kappa B subunit 1	Homo sapiens	121-130
23884755-5	2013	Moreover, use of low-dose aspirin for cardioprotection (a common co-treatment with the selective cyclooxygenase-2 inhibitors) further augments intestinal damage, particularly when enteric-coated aspirin is used.	Aspirin	26-33	prostaglandin-endoperoxide synthase 2	Homo sapiens	97-113
23884755-5	2013	Moreover, use of low-dose aspirin for cardioprotection (a common co-treatment with the selective cyclooxygenase-2 inhibitors) further augments intestinal damage, particularly when enteric-coated aspirin is used.	Aspirin	195-202	prostaglandin-endoperoxide synthase 2	Homo sapiens	97-113
23832067-11	2013	CONCLUSION: The variation in response to ASA may be related with an increased expression of IGF1 and IGF1R, as well as a response to clopidogrel can be affected by pharmacokinetic change related to the reverse transport pathway by increased expression of ABCC3.	Aspirin	41-44	insulin like growth factor 1	Homo sapiens	92-96
24026640-0	2013	Effects of aspirin on the ERK and PI3K/Akt signaling pathways in rats with acute pulmonary embolism.	Aspirin	11-18	Eph receptor B1	Rattus norvegicus	26-29
24026640-0	2013	Effects of aspirin on the ERK and PI3K/Akt signaling pathways in rats with acute pulmonary embolism.	Aspirin	11-18	AKT serine/threonine kinase 1	Rattus norvegicus	39-42
24026640-3	2013	The aim of this study was to examine the effects of aspirin on ERK and PI3K/Akt signaling in a rat model of APE and evaluate the prognostic values of brain natriuretic peptide (BNP), troponin (TnT) and D-Dimer.	Aspirin	52-59	Eph receptor B1	Rattus norvegicus	63-66
24026640-7	2013	The results showed that ERK and PI3K levels were decreased in the control, sham and the three aspirin groups at all time-points compared with the model group (P&lt;0.01).	Aspirin	94-101	Eph receptor B1	Rattus norvegicus	24-27
24026640-8	2013	The exception was in the medium-dose aspirin group at 24 h. The serum levels of BNP, TnT and D-Dimer were lower in the control and sham groups at all time-points compared with the model group (P&lt;0.05).	Aspirin	37-44	natriuretic peptide B	Rattus norvegicus	80-83
24026640-9	2013	Furthermore, the levels of BNP, TnT and D-Dimer levels were decreased in the aspirin-treated groups (P&lt;0.05) and markedly increased in the model group (P&lt;0.05) at 24 h compared with the levels at 6 h. Pulmonary embolism, alveolar wall necrosis and hemorrhage were observed in the model group 6, 24 and 72 h subsequent to the induction of the model.	Aspirin	77-84	natriuretic peptide B	Rattus norvegicus	27-30
23883581-0	2013	Human platelets generate phospholipid-esterified prostaglandins via cyclooxygenase-1 that are inhibited by low dose aspirin supplementation.	Aspirin	116-123	prostaglandin-endoperoxide synthase 1	Homo sapiens	68-84
24075936-6	2013	Treatment with aspirin or combined suspension of PGZ and PDL in the arthritic animals produced significant reductions in HPV and TJT, normalized BW, and significantly decreased plasma levels of TNF-alpha and IL-6.	Aspirin	15-22	tumor necrosis factor	Rattus norvegicus	194-203
24075936-6	2013	Treatment with aspirin or combined suspension of PGZ and PDL in the arthritic animals produced significant reductions in HPV and TJT, normalized BW, and significantly decreased plasma levels of TNF-alpha and IL-6.	Aspirin	15-22	interleukin 6	Rattus norvegicus	208-212
24098505-6	2013	Further mechanistic studies revealed that the actions of these phytochemicals were similar to aspirin in that they mainly inhibited COX-1 rather than COX-2, especially at low doses.	Aspirin	94-101	prostaglandin-endoperoxide synthase 2	Homo sapiens	150-155
24113271-0	2013	Aspirin-induced Bcl-2 translocation and its phosphorylation in the nucleus trigger apoptosis in breast cancer cells.	Aspirin	0-7	BCL2 apoptosis regulator	Homo sapiens	16-21
24113271-1	2013	Here, we report that B-cell lymphoma 2 (Bcl-2) is a novel target molecule of aspirin in breast cancer cells.	Aspirin	77-84	BCL2 apoptosis regulator	Homo sapiens	21-38
24113271-1	2013	Here, we report that B-cell lymphoma 2 (Bcl-2) is a novel target molecule of aspirin in breast cancer cells.	Aspirin	77-84	BCL2 apoptosis regulator	Homo sapiens	40-45
24113271-2	2013	Aspirin influenced the formation of a complex by Bcl-2 and FKBP38 and induced the nuclear translocation of Bcl-2 and its phosphorylation.	Aspirin	0-7	BCL2 apoptosis regulator	Homo sapiens	49-54
24113271-2	2013	Aspirin influenced the formation of a complex by Bcl-2 and FKBP38 and induced the nuclear translocation of Bcl-2 and its phosphorylation.	Aspirin	0-7	BCL2 apoptosis regulator	Homo sapiens	107-112
24113271-4	2013	Bcl-2 knockdown using small interfering RNA (siRNA) delayed apoptotic cell death, which correlated with increased proliferation following aspirin exposure.	Aspirin	138-145	BCL2 apoptosis regulator	Homo sapiens	0-5
24113271-5	2013	In contrast, Bcl-2 overexpression enhanced the onset of aspirin-induced apoptosis, which was also associated with a significant increase in Bcl-2 phosphorylation in the nucleus.	Aspirin	56-63	BCL2 apoptosis regulator	Homo sapiens	13-18
24113271-6	2013	Therefore, this study may provide novel insight into the molecular mechanism of aspirin, particularly its anticancer effects in Bcl-2- and estrogen receptor-positive breast cancer cells.	Aspirin	80-87	BCL2 apoptosis regulator	Homo sapiens	128-133
23955344-9	2013	With or without heme, aspirin acetylates one-half of the subunits of the native PGHS-2 dimer, the Ecat subunits.	Aspirin	22-29	prostaglandin-endoperoxide synthase 2	Homo sapiens	80-86
23955344-11	2013	Curiously, aspirin acetylates only one-quarter of the monomers of S530A/Native PGHS-2 with or without heme.	Aspirin	11-18	prostaglandin-endoperoxide synthase 2	Homo sapiens	79-85
24127927-2	2013	We undertook a prospective study to determine the influence of a 45-day course of aspirin therapy on circulating and intraplatelet levels of selected proangiogenic (vascular endothelial growth factor [VEGF]) and antiangiogenic (thrombospondin-1 [TSP-1]) proteins, and platelet protein release in women diagnosed with breast cancer who were receiving tamoxifen therapy.	Aspirin	82-89	vascular endothelial growth factor A	Homo sapiens	201-205
24127927-2	2013	We undertook a prospective study to determine the influence of a 45-day course of aspirin therapy on circulating and intraplatelet levels of selected proangiogenic (vascular endothelial growth factor [VEGF]) and antiangiogenic (thrombospondin-1 [TSP-1]) proteins, and platelet protein release in women diagnosed with breast cancer who were receiving tamoxifen therapy.	Aspirin	82-89	thrombospondin 1	Homo sapiens	246-251
24127927-3	2013	Initiation of aspirin therapy increases serum and intraplatelet levels of TSP-1 without a corresponding increase in VEGF levels.	Aspirin	14-21	thrombospondin 1	Homo sapiens	74-79
24127927-4	2013	Following aspirin therapy, VEGF levels decreased (relative to pretreatment levels) while TSP-1 returned to pretreatment levels.	Aspirin	10-17	vascular endothelial growth factor A	Homo sapiens	27-31
24127927-4	2013	Following aspirin therapy, VEGF levels decreased (relative to pretreatment levels) while TSP-1 returned to pretreatment levels.	Aspirin	10-17	thrombospondin 1	Homo sapiens	89-94
24127927-6	2013	Aspirin use also decreased thrombin receptor mediated release of TSP-1 and VEGF from platelets.	Aspirin	0-7	thrombospondin 1	Homo sapiens	65-70
24127927-6	2013	Aspirin use also decreased thrombin receptor mediated release of TSP-1 and VEGF from platelets.	Aspirin	0-7	vascular endothelial growth factor A	Homo sapiens	75-79
23806637-0	2013	Prominent role of IFN-gamma in patients with aspirin-exacerbated respiratory disease.	Aspirin	45-52	interferon gamma	Homo sapiens	18-27
23806637-5	2013	RESULTS: Gene expression analysis revealed that tissue from both aspirin-tolerant subjects and patients with AERD display a TH2 cytokine signature; however, AERD was distinguished from chronic hyperplastic eosinophilic sinusitis by the prominent expression of IFN-gamma.	Aspirin	65-72	interferon gamma	Homo sapiens	260-269
23806637-10	2013	CONCLUSIONS: High IFN-gamma levels distinguish AERD from aspirin-tolerant asthma and underlie the robust constitutive and aspirin-induced secretion of CysLTs that characterize this disorder.	Aspirin	57-64	interferon gamma	Homo sapiens	18-27
23806637-10	2013	CONCLUSIONS: High IFN-gamma levels distinguish AERD from aspirin-tolerant asthma and underlie the robust constitutive and aspirin-induced secretion of CysLTs that characterize this disorder.	Aspirin	122-129	interferon gamma	Homo sapiens	18-27
23864170-1	2013	ASAS non-responders on anti-TNF therapy show improvement in performance-based physical function.	Aspirin	0-4	tumor necrosis factor	Homo sapiens	28-31
24066944-9	2013	Ten micromoles of CRCs and Asp upregulated the expression of mothers against decapentaplegic homolog 4 (Drosophila) (SMAD4) in the TGF-beta receptor signaling pathway, and SMAD3/4 transcription activity was also increased.	Aspirin	27-30	Medea	Drosophila melanogaster	117-122
23810915-1	2013	BACKGROUND: Studies have examined whether tumor expression of PTGS2 (also known as COX-2), an enzyme inhibited by nonsteroidal anti-inflammatory drugs such as aspirin, is associated with prognosis in patients with colorectal cancer.	Aspirin	159-166	prostaglandin-endoperoxide synthase 2	Homo sapiens	62-67
23896061-2	2013	It inhibited the growth of Jurkat T-leukemia cells with an IC50 of 1.9 +- 0.2 muM whereas that of ASA was &gt;5000 muM.	Aspirin	98-101	latexin	Homo sapiens	115-118
24323374-0	2013	Interaction between vWF levels and aspirin resistance in ischemic stroke patients.	Aspirin	35-42	von Willebrand factor	Homo sapiens	20-23
24323374-1	2013	The von Willebrand factor (vWF) levels increase in acute-phase ischemic stroke because of endothelial dysfunction and thrombus formation and may reduce acetylsalicylic acid (ASA) efficiency in hemostatic cascade.	Aspirin	152-172	von Willebrand factor	Homo sapiens	4-25
24323374-1	2013	The von Willebrand factor (vWF) levels increase in acute-phase ischemic stroke because of endothelial dysfunction and thrombus formation and may reduce acetylsalicylic acid (ASA) efficiency in hemostatic cascade.	Aspirin	152-172	von Willebrand factor	Homo sapiens	27-30
24323374-1	2013	The von Willebrand factor (vWF) levels increase in acute-phase ischemic stroke because of endothelial dysfunction and thrombus formation and may reduce acetylsalicylic acid (ASA) efficiency in hemostatic cascade.	Aspirin	174-177	von Willebrand factor	Homo sapiens	4-25
24323374-1	2013	The von Willebrand factor (vWF) levels increase in acute-phase ischemic stroke because of endothelial dysfunction and thrombus formation and may reduce acetylsalicylic acid (ASA) efficiency in hemostatic cascade.	Aspirin	174-177	von Willebrand factor	Homo sapiens	27-30
24323374-2	2013	The aim of the study is to investigate the relationship between vWF levels and ASA resistance in ischemic stroke patients.	Aspirin	79-82	von Willebrand factor	Homo sapiens	64-67
24323374-6	2013	vWF levels were elevated in only ASA nonresponders and the ischemic stroke group that showed a statistically significant association with aspirin resistance (p&lt;=0.05).	Aspirin	33-36	von Willebrand factor	Homo sapiens	0-3
24323374-6	2013	vWF levels were elevated in only ASA nonresponders and the ischemic stroke group that showed a statistically significant association with aspirin resistance (p&lt;=0.05).	Aspirin	138-145	von Willebrand factor	Homo sapiens	0-3
24323374-7	2013	vWF levels increase in ASA nonresponders and ischemic stroke group in acute phase.	Aspirin	23-26	von Willebrand factor	Homo sapiens	0-3
24323374-8	2013	High vWF levels may relate to ASA resistance and recurrent strokes.	Aspirin	30-33	von Willebrand factor	Homo sapiens	5-8
24155779-5	2013	Here we investigated if aspirin attenuates EGFR-activated ovarian cancer cell growth in a COX-1 dependent manner.	Aspirin	24-31	epidermal growth factor receptor	Homo sapiens	43-47
24155779-10	2013	In particular, aspirin decreased phosphorylated Akt and Erk activated by EGF.	Aspirin	15-22	AKT serine/threonine kinase 1	Homo sapiens	48-51
24155779-10	2013	In particular, aspirin decreased phosphorylated Akt and Erk activated by EGF.	Aspirin	15-22	mitogen-activated protein kinase 1	Homo sapiens	56-59
24155779-14	2013	CONCLUSIONS: Taken together, aspirin inhibits viability of ovarian cancer cells by blocking phosphorylation of Akt and Erk activated by EGF.	Aspirin	29-36	AKT serine/threonine kinase 1	Homo sapiens	111-114
24155779-14	2013	CONCLUSIONS: Taken together, aspirin inhibits viability of ovarian cancer cells by blocking phosphorylation of Akt and Erk activated by EGF.	Aspirin	29-36	mitogen-activated protein kinase 1	Homo sapiens	119-122
23810915-1	2013	BACKGROUND: Studies have examined whether tumor expression of PTGS2 (also known as COX-2), an enzyme inhibited by nonsteroidal anti-inflammatory drugs such as aspirin, is associated with prognosis in patients with colorectal cancer.	Aspirin	159-166	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	83-88
23766266-9	2013	Moreover, cathelicidin-related antimicrobial peptide, which is the murine ortholog of LL-37, induced prostaglandin-dependent angiogenesis in vivo, which could be blocked by aspirin.	Aspirin	173-180	cathelicidin antimicrobial peptide	Homo sapiens	86-91
22609818-0	2013	Genetic polymorphisms of HO-1 and COX-1 are associated with aspirin resistance defined by light transmittance aggregation in Chinese Han patients.	Aspirin	60-67	prostaglandin-endoperoxide synthase 1	Homo sapiens	34-39
22609818-1	2013	BACKGROUND: Cyclooxygenase 1 (COX-1), COX-2, and HO-1 are involved in the process of aspirin"s effect.	Aspirin	85-92	prostaglandin-endoperoxide synthase 1	Homo sapiens	12-28
22609818-1	2013	BACKGROUND: Cyclooxygenase 1 (COX-1), COX-2, and HO-1 are involved in the process of aspirin"s effect.	Aspirin	85-92	prostaglandin-endoperoxide synthase 1	Homo sapiens	30-35
22609818-1	2013	BACKGROUND: Cyclooxygenase 1 (COX-1), COX-2, and HO-1 are involved in the process of aspirin"s effect.	Aspirin	85-92	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	38-43
23778008-0	2013	Aspirin possibly reduces cerebrovascular events in type 2 diabetic patients with higher C-reactive protein level: subanalysis from the JPAD trial.	Aspirin	0-7	C-reactive protein	Homo sapiens	88-106
23766266-0	2013	Cathelicidin LL-37 induces angiogenesis via PGE2-EP3 signaling in endothelial cells, in vivo inhibition by aspirin.	Aspirin	107-114	cathelicidin antimicrobial peptide	Homo sapiens	13-18
23778008-9	2013	PRINCIPAL CONCLUSIONS: Aspirin therapy may reduce cerebrovascular events in diabetic patients with higher CRP.	Aspirin	23-30	C-reactive protein	Homo sapiens	106-109
23778008-10	2013	Aspirin therapy could be an additional strategy as primary prevention for diabetic patients with higher CRP.	Aspirin	0-7	C-reactive protein	Homo sapiens	104-107
23799623-6	2013	MTX-mediated accumulation of the S phase marker cyclin A was also alleviated by ASA.	Aspirin	80-83	cyclin A2	Homo sapiens	48-56
23799623-8	2013	The antagonism of MTX efficacy caused by ASA was accompanied by altered expression of caspase-3, Bcl-2 and FAS but not dihydrofolate reductase (DHFR).	Aspirin	41-44	caspase 3	Homo sapiens	86-95
23799623-8	2013	The antagonism of MTX efficacy caused by ASA was accompanied by altered expression of caspase-3, Bcl-2 and FAS but not dihydrofolate reductase (DHFR).	Aspirin	41-44	BCL2 apoptosis regulator	Homo sapiens	97-102
23799623-9	2013	This suggests that the alteration of caspase-3, Bcl-2 and FAS was involved in the antagonism between ASA and MTX.	Aspirin	101-104	caspase 3	Homo sapiens	37-46
23799623-9	2013	This suggests that the alteration of caspase-3, Bcl-2 and FAS was involved in the antagonism between ASA and MTX.	Aspirin	101-104	BCL2 apoptosis regulator	Homo sapiens	48-53
23686218-8	2013	Patients treated with anti-TNF agents were more likely to display an ASAS 20 response after 12/14 weeks (RR 2.21; 95 % CI 1.91; 2.56) and 24 weeks (RR 2.68; 95 % CI 2.06; 3.48) compared with controls, which was also true for several other efficacy outcomes.	Aspirin	69-73	tumor necrosis factor	Homo sapiens	27-30
23996718-5	2013	The patient was told to use aspirin when needed analgesic and he started to use aspirin 500 mg bid.	Aspirin	80-87	BH3 interacting domain death agonist	Homo sapiens	95-98
23766266-10	2013	CONCLUSIONS: Our results identify a novel proangiogenic role of LL-37, suggesting that the axis LL-37/COX-1/PGE2 followed by EP3 signaling is amenable to therapeutic intervention in pathological angiogenesis, for instance by aspirin.	Aspirin	225-232	cathelicidin antimicrobial peptide	Homo sapiens	64-69
23766266-10	2013	CONCLUSIONS: Our results identify a novel proangiogenic role of LL-37, suggesting that the axis LL-37/COX-1/PGE2 followed by EP3 signaling is amenable to therapeutic intervention in pathological angiogenesis, for instance by aspirin.	Aspirin	225-232	prostaglandin E receptor 3	Homo sapiens	125-128
23736108-0	2013	Association analysis of tapasin polymorphisms with aspirin-exacerbated respiratory disease in asthmatics.	Aspirin	51-58	TAP binding protein	Homo sapiens	24-31
23567078-7	2013	Compared with the saline-treated MI rats, 26S and 20S in high or low dose aspirin-treated MI rats further decreased by 30% and 20%, beta5 by 30% and 12%, and beta1 by 40% and 30%, respectively, and the lost activity was correlated with the compromised cardiac functions or the decreased cell viability.	Aspirin	74-81	adaptor related protein complex 5 subunit beta 1	Rattus norvegicus	132-137
23567078-8	2013	The dose-related and selective inhibition of 26S and 20S proteasome, or the 20S proteasome subunits beta5 and beta1 by aspirin was comparable to their protein expressions in the MI rats and in the cultured cells.	Aspirin	119-126	adaptor related protein complex 5 subunit beta 1	Rattus norvegicus	100-105
23830213-0	2013	TXA2 synthesis and COX1-independent platelet reactivity in aspirin-treated patients soon after acute cerebral stroke or transient ischaemic attack.	Aspirin	59-66	prostaglandin-endoperoxide synthase 1	Homo sapiens	19-23
23830213-1	2013	INTRODUCTION: The pharmacological target of aspirin is the inhibition of cyclooxygenase-1 (COX1) and thromboxane-A2 (TX) synthesis.	Aspirin	44-51	prostaglandin-endoperoxide synthase 1	Homo sapiens	73-89
23830213-1	2013	INTRODUCTION: The pharmacological target of aspirin is the inhibition of cyclooxygenase-1 (COX1) and thromboxane-A2 (TX) synthesis.	Aspirin	44-51	prostaglandin-endoperoxide synthase 1	Homo sapiens	91-95
23830213-10	2013	Among patients with fully blocked TX, those with elevated COX1-independent platelet reactivity (mean+2SD of aspirin-treated HS) were most likely to suffer severe stroke (P&lt;0.05).	Aspirin	108-115	prostaglandin-endoperoxide synthase 1	Homo sapiens	58-62
23786234-0	2013	A mechanistic hypothesis for the aspirin-induced switch in lipid mediator production by cyclooxygenase-2.	Aspirin	33-40	prostaglandin-endoperoxide synthase 2	Homo sapiens	88-104
23786234-2	2013	For COX-2, the stereochemistry and relative abundance of generated products is influenced by Ser530 acetylation following aspirin treatment.	Aspirin	122-129	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	4-9
23786234-3	2013	The molecular bases of the high degree of stereospecificity which characterizes COX-2-catalyzed oxygenations are not yet completely understood, nor are the reasons behind the aspirin-induced shift in lipid mediator production.	Aspirin	175-182	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	80-85
23786234-5	2013	This hypothesis is supported by a computational model which accurately reproduces experimental oxygenation patterns on both native and aspirin-inhibited COX-2.	Aspirin	135-142	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	153-158
25332957-0	2013	Aspirin for colorectal cancer with PIK3CA mutations: the rising of the oldest targeted therapy?	Aspirin	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	35-41
23668350-4	2013	Furthermore, ibuprofen and aspirin were found to be preferential inhibitor of COX-1 and COX-2, respectively.	Aspirin	27-34	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	88-93
23608957-1	2013	PURPOSE: The aim of this study was to evaluate the association of PON1 genetic variants with the susceptibility to coronary artery disease (CAD) and with the clinical endpoints in aspirin and clopidogrel (dual antiplatelet therapy)-treated Han Chinese patients with CAD after percutaneous coronary intervention (PCI).	Aspirin	180-187	paraoxonase 1	Homo sapiens	66-70
23519265-7	2013	Co-treatment of HCAECs with L5 and a physiologically relevant, low concentration of aspirin (0.2 mM) attenuated the adverse effects of L5 on HCAEC survival, FGF2 expression, and FGF2 promoter methylation.	Aspirin	84-91	fibroblast growth factor 2	Homo sapiens	157-161
23519265-7	2013	Co-treatment of HCAECs with L5 and a physiologically relevant, low concentration of aspirin (0.2 mM) attenuated the adverse effects of L5 on HCAEC survival, FGF2 expression, and FGF2 promoter methylation.	Aspirin	84-91	fibroblast growth factor 2	Homo sapiens	178-182
23519265-10	2013	Furthermore, L5 impairs HCAEC function through CpG methylation of the FGF2 promoter, which is suppressed in the presence of low-concentration aspirin.	Aspirin	142-149	fibroblast growth factor 2	Homo sapiens	70-74
23736108-2	2013	TAPBP (TAP-binding protein, tapasin) is upregulated by eicosanoids, which act as potent inflammatory molecules in aspirin-related reactions.	Aspirin	114-121	TAP binding protein	Homo sapiens	0-5
23736108-2	2013	TAPBP (TAP-binding protein, tapasin) is upregulated by eicosanoids, which act as potent inflammatory molecules in aspirin-related reactions.	Aspirin	114-121	TAP binding protein	Homo sapiens	7-26
23736108-2	2013	TAPBP (TAP-binding protein, tapasin) is upregulated by eicosanoids, which act as potent inflammatory molecules in aspirin-related reactions.	Aspirin	114-121	TAP binding protein	Homo sapiens	28-35
23553791-6	2013	Systemic administration of aspirin, which significantly reduces the levels of IFN-gamma and TNF-alpha, results in blockage of MSC deficiency and tumorigenesis by inhibition of NFkappaB/SMAD7 and NFkappaB/c-FOS and c-MYC pathways in OVX mice.	Aspirin	27-34	interferon gamma	Mus musculus	78-87
23553791-6	2013	Systemic administration of aspirin, which significantly reduces the levels of IFN-gamma and TNF-alpha, results in blockage of MSC deficiency and tumorigenesis by inhibition of NFkappaB/SMAD7 and NFkappaB/c-FOS and c-MYC pathways in OVX mice.	Aspirin	27-34	tumor necrosis factor	Mus musculus	92-101
23553791-6	2013	Systemic administration of aspirin, which significantly reduces the levels of IFN-gamma and TNF-alpha, results in blockage of MSC deficiency and tumorigenesis by inhibition of NFkappaB/SMAD7 and NFkappaB/c-FOS and c-MYC pathways in OVX mice.	Aspirin	27-34	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	176-184
23553791-6	2013	Systemic administration of aspirin, which significantly reduces the levels of IFN-gamma and TNF-alpha, results in blockage of MSC deficiency and tumorigenesis by inhibition of NFkappaB/SMAD7 and NFkappaB/c-FOS and c-MYC pathways in OVX mice.	Aspirin	27-34	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	195-203
23434193-5	2013	We also highlight that formation of pro-resolving mediators can be enhanced by widely used anti-inflammatory and cardioprotective drugs (aspirin and statins) via the modification of cyclooxygenase-2 enzymatic activity.	Aspirin	137-144	prostaglandin-endoperoxide synthase 2	Homo sapiens	182-198
23800934-0	2013	Aspirin use and risk of colorectal cancer according to BRAF mutation status.	Aspirin	0-7	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	55-59
23800934-2	2013	Experimental evidence implicates a role of RAF kinases in up-regulation of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2), suggesting that BRAF-mutant colonic cells might be less sensitive to the antitumor effects of aspirin than BRAF-wild-type neoplastic cells.	Aspirin	234-241	prostaglandin-endoperoxide synthase 2	Homo sapiens	75-112
23800934-2	2013	Experimental evidence implicates a role of RAF kinases in up-regulation of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2), suggesting that BRAF-mutant colonic cells might be less sensitive to the antitumor effects of aspirin than BRAF-wild-type neoplastic cells.	Aspirin	234-241	prostaglandin-endoperoxide synthase 2	Homo sapiens	114-119
23800934-2	2013	Experimental evidence implicates a role of RAF kinases in up-regulation of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2), suggesting that BRAF-mutant colonic cells might be less sensitive to the antitumor effects of aspirin than BRAF-wild-type neoplastic cells.	Aspirin	234-241	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	156-160
23800934-8	2013	Compared with nonuse, regular aspirin use was associated with lower BRAF-wild-type cancer risk (multivariable HR, 0.73; 95% CI, 0.64 to 0.83; age-adjusted incidence rate difference [RD], -9.7; 95% CI, -12.6 to -6.7 per 100,000 person-years).	Aspirin	30-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	68-72
23800934-12	2013	The relationship between the number of aspirin tablets per week and colorectal cancer risk differed significantly by BRAF mutation status (P for heterogeneity = .005).	Aspirin	39-46	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	117-121
23800934-13	2013	CONCLUSIONS AND RELEVANCE: Regular aspirin use was associated with lower risk of BRAF-wild-type colorectal cancer but not with BRAF-mutated cancer risk.	Aspirin	35-42	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	81-85
23800934-14	2013	These findings suggest that BRAF-mutant colon tumor cells may be less sensitive to the effect of aspirin.	Aspirin	97-104	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	28-32
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	170-174
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	18-55
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	57-61
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	170-174
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	170-174
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	170-174
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	18-55
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	57-61
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	170-174
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	170-174
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	170-174
23653362-7	2013	Furthermore, we demonstrate that aspirin-induced astroglial CNTF was also functionally active and that supernatants of aspirin-treated astrocytes of wild type, but not Cntf null, mice increased myelin-associated proteins in oligodendrocytes and protected oligodendrocytes from TNF-alpha insult.	Aspirin	33-40	tumor necrosis factor	Mus musculus	277-286
23653362-7	2013	Furthermore, we demonstrate that aspirin-induced astroglial CNTF was also functionally active and that supernatants of aspirin-treated astrocytes of wild type, but not Cntf null, mice increased myelin-associated proteins in oligodendrocytes and protected oligodendrocytes from TNF-alpha insult.	Aspirin	119-126	tumor necrosis factor	Mus musculus	277-286
23649190-0	2013	Beta blockers and angiotensin-converting enzyme inhibitors" purported benefit on breast cancer survival may be explained by aspirin use.	Aspirin	124-131	angiotensin I converting enzyme	Homo sapiens	18-47
23623170-2	2013	Since activated platelets respond stronger to additional stimuli, the extent of endogenous thrombin generation may in part be responsible for the reported response variability to aspirin and clopidogrel therapy.	Aspirin	179-186	coagulation factor II, thrombin	Homo sapiens	91-99
23623170-8	2013	In the VerifyNow aspirin assay, patients without HRPR had higher peak thrombin generation than patients with HRPR (p=0.01).	Aspirin	17-24	coagulation factor II, thrombin	Homo sapiens	70-78
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	86-93	cAMP responsive element binding protein 1	Mus musculus	18-55
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	86-93	cAMP responsive element binding protein 1	Mus musculus	57-61
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	18-55
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	57-61
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	170-174
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	cAMP responsive element binding protein 1	Mus musculus	170-174
23494053-3	2013	Here we investigated the metabolism of AA via platelet 12-lipoxygenase (12-LOX) as a possible mediator of the observed transient aspirin resistance, and compared the effects of unfractionated (UFH) and low-molecular-weight (LMWH) heparin.	Aspirin	129-136	arachidonate 15-lipoxygenase	Homo sapiens	72-78
23446846-0	2013	The -308 G&gt;A SNP of TNFA is a factor predisposing to chronic rhinosinusitis associated with nasal polyposis in aspirin-sensitive Hungarian individuals: conclusions of a genetic study with multiple stratifications.	Aspirin	114-121	tumor necrosis factor	Homo sapiens	23-27
23446846-6	2013	It is concluded that genetic variants of the TNFA gene may affect the risk of CRS in a clinically well-defined group of CRSNP(+)ASA(+) patients in the Hungarian population.	Aspirin	128-131	tumor necrosis factor	Homo sapiens	45-49
24027363-1	2013	BACKGROUND: Wald and law in their landmark paper published in BMJ in 2003 hypothesized that the use of fixed dose combination of statins, beta blockers, angiotensin-converting-enzyme inhibitor (ACE) inhibitor, and aspirin (Pollypill) may decrease cardiovascular disease by &gt;80% if Pollypills are used as primary prevention.	Aspirin	214-221	angiotensin I converting enzyme	Homo sapiens	194-197
23536315-5	2013	The decrease in NET formation mediated by ASA, BAY-11-7082, and Ro 106-9920 was correlated with a significant reduction in the phosphorylation of NF-kappaB p65 subunit, indicating that the activation of this transcription factor is a relevant signaling pathway involved in the generation of DNA traps.	Aspirin	42-45	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	146-155
23611778-5	2013	We further showed that aspirin robustly enhanced Navitoclax-triggered cytosolic cytochrome c release, activation of initiator caspase-9 and effector caspase-3, and cleavage of PARP.	Aspirin	23-30	cytochrome c, somatic	Homo sapiens	80-92
23493387-8	2013	Taken together, aspirin suppressed LNCaP cell proliferation via EP3 signaling activation; EP3 downregulation contributed to prostate carcinogenesis and to progression from androgen-dependent prostate cancer to castration-resistant prostate cancer by regulating AR expression.	Aspirin	16-23	prostaglandin E receptor 3	Homo sapiens	64-67
23493387-0	2013	Prostaglandin receptor EP3 mediates growth inhibitory effect of aspirin through androgen receptor and contributes to castration resistance in prostate cancer cells.	Aspirin	64-71	prostaglandin E receptor 3	Homo sapiens	23-26
23493387-3	2013	We also found that aspirin upregulated prostaglandin receptor subtype EP3 but not EP2 or EP4.	Aspirin	19-26	prostaglandin E receptor 3	Homo sapiens	70-73
23611778-5	2013	We further showed that aspirin robustly enhanced Navitoclax-triggered cytosolic cytochrome c release, activation of initiator caspase-9 and effector caspase-3, and cleavage of PARP.	Aspirin	23-30	caspase 3	Homo sapiens	149-158
23392654-9	2013	CONCLUSION- Common genetic variation in PEAR1 may be a determinant of platelet response and cardiovascular events in patients on aspirin alone or in combination with clopidogrel.	Aspirin	129-136	platelet endothelial aggregation receptor 1	Homo sapiens	40-45
23541724-13	2013	Aspirin and ibuprofen also reversed the increased wall thickness, macroscopic damage and levels of IL-1beta, IL-6 and PGE2, and the decreased panthotenic acid levels.	Aspirin	0-7	interleukin 1 beta	Rattus norvegicus	99-107
23541724-13	2013	Aspirin and ibuprofen also reversed the increased wall thickness, macroscopic damage and levels of IL-1beta, IL-6 and PGE2, and the decreased panthotenic acid levels.	Aspirin	0-7	interleukin 6	Rattus norvegicus	109-113
23485446-6	2013	Aspirin could marginally extend the lifespan of long-live insulin-like receptor mutant daf-2(e1370) III.	Aspirin	0-7	Insulin-like receptor subunit beta;Protein kinase domain-containing protein;Receptor protein-tyrosine kinase	Caenorhabditis elegans	87-92
23639710-1	2013	Aspirin-exacerbated respiratory disease is a clinical syndrome characterized by severe, persistent asthma, hyperplastic eosinophilic sinusitis with nasal polyps, and reactions to aspirin and other nonsteroidal antiinflammatory drugs that preferentially inhibit cyclooxygenase 1.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	261-277
23639710-1	2013	Aspirin-exacerbated respiratory disease is a clinical syndrome characterized by severe, persistent asthma, hyperplastic eosinophilic sinusitis with nasal polyps, and reactions to aspirin and other nonsteroidal antiinflammatory drugs that preferentially inhibit cyclooxygenase 1.	Aspirin	179-186	prostaglandin-endoperoxide synthase 1	Homo sapiens	261-277
23441755-1	2013	BACKGROUND AND OBJECTIVE: Anomalies in the regulation of cyclooxygenase (COX)-1 and -2 have been described in nasal polyps of aspirin-induced asthma (AIA).	Aspirin	126-133	prostaglandin-endoperoxide synthase 1	Homo sapiens	57-86
23313628-4	2013	PAR-1 regulation was studied prospectively in 86 consecutive patients with stable coronary artery disease treated with aspirin and clopidogrel (67 patients) or prasugrel (19 patients) and correlated the data to ADP inducible platelet reactivity by impedance aggregometry.	Aspirin	119-126	coagulation factor II thrombin receptor	Homo sapiens	0-5
23506847-5	2013	Herein, we demonstrate that aspirin-triggered LXA4 (15 mug/kg) s.c., twice a day, reduced NF-kappaB activation and levels of proinflammatory cytokines and chemokines, as well as increased levels of anti-inflammatory IL-10 and transforming growth factor-beta.	Aspirin	28-35	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	90-99
23506847-5	2013	Herein, we demonstrate that aspirin-triggered LXA4 (15 mug/kg) s.c., twice a day, reduced NF-kappaB activation and levels of proinflammatory cytokines and chemokines, as well as increased levels of anti-inflammatory IL-10 and transforming growth factor-beta.	Aspirin	28-35	interleukin 10	Mus musculus	216-221
23483185-10	2013	The expression of VEGF-A and VEGF-C in tumor tissues inhibited by aspirin was demonstrated by immunohistochemistry, and the MVD was decreased in a dose-dependent manner (p&lt;0.05).	Aspirin	66-73	vascular endothelial growth factor C	Mus musculus	29-35
23483185-12	2013	Western blot data showed that the expression of both VEGF-A and VEGF-C was reduced after treatment with aspirin.	Aspirin	104-111	vascular endothelial growth factor C	Mus musculus	64-70
23483185-13	2013	In conclusion, the impact of aspirin-induced tumor growth delay of murine S180 sarcoma may correlate with the inhibition of angiogenesis and lymphangiogenesis by reducing VEGF-A and VEGF-C expression in tumor tissues.	Aspirin	29-36	vascular endothelial growth factor C	Mus musculus	182-188
23508960-1	2013	Aspirin is rapidly hydrolyzed within erythrocytes by a heterodimer of PAFAH1b2/PAFAH1b3 but also in plasma by an unidentified activity.	Aspirin	0-7	platelet activating factor acetylhydrolase 1b catalytic subunit 3	Homo sapiens	79-87
23266689-4	2013	The phosphorescence of thrombin was studied under physiological conditions, in acidosis (decrease of pH from 8.0 to 5.0) and on the addition of salts (magnesium sulfate and sodium chloride) and of acetylsalicylic acid, and its connection with thrombin function is discussed.	Aspirin	197-217	coagulation factor II, thrombin	Homo sapiens	23-31
23422285-0	2013	New direct and indirect methods for the detection of cyclooxygenase 1 acetylation by aspirin; the lack of aspirin resistance among healthy individuals.	Aspirin	85-92	prostaglandin-endoperoxide synthase 1	Homo sapiens	53-69
23422285-4	2013	METHODS: Two new methods were developed for the direct and indirect detection of COX-1 acetylation by aspirin in 108 healthy volunteers treated daily with 100mg enteric-coated aspirin for 7days.	Aspirin	102-109	prostaglandin-endoperoxide synthase 1	Homo sapiens	81-86
23422285-4	2013	METHODS: Two new methods were developed for the direct and indirect detection of COX-1 acetylation by aspirin in 108 healthy volunteers treated daily with 100mg enteric-coated aspirin for 7days.	Aspirin	176-183	prostaglandin-endoperoxide synthase 1	Homo sapiens	81-86
23422285-14	2013	The new methods could be used for detecting the acetylation of COX-1 by aspirin in patients on preventive aspirin therapy and for evaluating methods routinely used for such purpose.	Aspirin	72-79	prostaglandin-endoperoxide synthase 1	Homo sapiens	63-68
23422285-14	2013	The new methods could be used for detecting the acetylation of COX-1 by aspirin in patients on preventive aspirin therapy and for evaluating methods routinely used for such purpose.	Aspirin	106-113	prostaglandin-endoperoxide synthase 1	Homo sapiens	63-68
23506529-3	2013	Aspirin is a non-steroidal anti-inflammatory drug that is an irreversible inhibitor of both cyclooxygenase (COX)-1 and COX-2, It stimulates endogenous production of anti-inflammatory regulatory "braking signals", including lipoxins, which dampen the inflammatory response and reduce levels of inflammatory biomarkers, including C-reactive protein, tumor necrosis factor-alpha and interleukin (IL)--6, but not negative immunoregulatory cytokines, such as IL-4 and IL-10.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	119-124
23506529-3	2013	Aspirin is a non-steroidal anti-inflammatory drug that is an irreversible inhibitor of both cyclooxygenase (COX)-1 and COX-2, It stimulates endogenous production of anti-inflammatory regulatory "braking signals", including lipoxins, which dampen the inflammatory response and reduce levels of inflammatory biomarkers, including C-reactive protein, tumor necrosis factor-alpha and interleukin (IL)--6, but not negative immunoregulatory cytokines, such as IL-4 and IL-10.	Aspirin	0-7	interleukin 6	Homo sapiens	380-399
23506529-3	2013	Aspirin is a non-steroidal anti-inflammatory drug that is an irreversible inhibitor of both cyclooxygenase (COX)-1 and COX-2, It stimulates endogenous production of anti-inflammatory regulatory "braking signals", including lipoxins, which dampen the inflammatory response and reduce levels of inflammatory biomarkers, including C-reactive protein, tumor necrosis factor-alpha and interleukin (IL)--6, but not negative immunoregulatory cytokines, such as IL-4 and IL-10.	Aspirin	0-7	interleukin 4	Homo sapiens	454-458
23508943-7	2013	Mac-1 signaling is also target for the anti-inflammatory, pro-resolving mediators, including lipoxin A4, aspirin-triggered lipoxin A4, and resolvin E1.	Aspirin	105-112	integrin subunit beta 2	Homo sapiens	0-5
22727040-8	2013	RESULTS: After aspirin, the mean flushing scores for all symptoms decreased significantly; however, 36-53% of participants still had some degree of symptoms, even though aspirin completely blocked 11beta-PGF(2) synthesis.	Aspirin	170-177	placental growth factor	Homo sapiens	204-207
23384979-0	2013	Mechanism of the irreversible inhibition of human cyclooxygenase-1 by aspirin as predicted by QM/MM calculations.	Aspirin	70-77	prostaglandin-endoperoxide synthase 1	Homo sapiens	50-66
23384979-2	2013	Aspirin acts as an acetylating agent in which its acetyl group is covalently attached to a serine residue (S530) in the active site of the cyclooxygenase-1 enzyme.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	139-155
23384979-4	2013	In this study the putative structure of human cyclooxygenase-1 was constructed from ovine cyclooxygenase-1 by homology modeling, and the acetylsalicylic acid was docked into the arachidonic acid binding cavity of the enzyme.	Aspirin	137-157	prostaglandin-endoperoxide synthase 1	Homo sapiens	46-62
23292806-0	2013	Direct regulation of caspase-3 by the transcription factor AP-2alpha is             involved in aspirin-induced apoptosis in MDA-MB-453 breast cancer cells.	Aspirin	96-103	caspase 3	Homo sapiens	21-30
23292806-5	2013	The             present study reports that aspirin induces the apoptosis of MDA-MB-453 breast             cancer cells which was attributed to the increased expression and activation of             caspase-3.	Aspirin	43-50	caspase 3	Homo sapiens	198-207
23292806-6	2013	Moreover, AP-2alpha, a transcription factor highly expressed in MDA-MB-453             cells, was identified as a negative regulator of caspase-3 transcription and AP-2alpha             was attenuated following aspirin treatment.	Aspirin	211-218	caspase 3	Homo sapiens	136-145
23292806-7	2013	Therefore, aspirin may increase the             expression of caspase-3 by inducing the degradation of AP-2alpha, which increases             activated caspase-3 expression, thereby triggering apoptosis in MDA-MB-453 cells.	Aspirin	11-18	caspase 3	Homo sapiens	62-71
23292806-7	2013	Therefore, aspirin may increase the             expression of caspase-3 by inducing the degradation of AP-2alpha, which increases             activated caspase-3 expression, thereby triggering apoptosis in MDA-MB-453 cells.	Aspirin	11-18	caspase 3	Homo sapiens	152-161
23266689-0	2013	Acidosis, magnesium and acetylsalicylic acid: effects on thrombin.	Aspirin	24-44	coagulation factor II, thrombin	Homo sapiens	57-65
23404329-3	2013	Results             demonstrated that low doses of ASP (1 mM), CUR (10 microM) and SFN (5 microM) (ACS) combination             reduced cell viability by ~70% (P&lt;0.001), and also induced cell apoptosis by             ~51% (P&lt;0.001) accompanied by activation of caspase-3 and Poly(ADP-ribose)             polymerase (PARP) proteins.	Aspirin	51-54	caspase 3	Homo sapiens	267-276
23404329-3	2013	Results             demonstrated that low doses of ASP (1 mM), CUR (10 microM) and SFN (5 microM) (ACS) combination             reduced cell viability by ~70% (P&lt;0.001), and also induced cell apoptosis by             ~51% (P&lt;0.001) accompanied by activation of caspase-3 and Poly(ADP-ribose)             polymerase (PARP) proteins.	Aspirin	51-54	poly(ADP-ribose) polymerase 1	Homo sapiens	281-320
23404329-3	2013	Results             demonstrated that low doses of ASP (1 mM), CUR (10 microM) and SFN (5 microM) (ACS) combination             reduced cell viability by ~70% (P&lt;0.001), and also induced cell apoptosis by             ~51% (P&lt;0.001) accompanied by activation of caspase-3 and Poly(ADP-ribose)             polymerase (PARP) proteins.	Aspirin	51-54	poly(ADP-ribose) polymerase 1	Homo sapiens	322-326
23419412-1	2013	INTRODUCTION: With the arrival of the potent P2Y12 antagonists, ticagrelor and prasugrel, the need for co-treatment with aspirin in acute coronary syndromes must be re-examined.	Aspirin	121-128	purinergic receptor P2Y12	Canis lupus familiaris	45-50
23419412-5	2013	During maximal P2Y12 inhibition, aspirin provided less additional inhibition of ex vivo arachidonic acid- and collagen-induced platelet aggregation, as compared with sub-maximal P2Y12 inhibition, without additional anti-thrombotic effect in vivo.	Aspirin	33-40	purinergic receptor P2Y12	Canis lupus familiaris	15-20
23466865-4	2013	PSPLE, aspirin, cyanidin and quercetin significantly inhibited TNF-alpha-induced monocyte-endothelial cell adhesion (p &lt; 0.05).	Aspirin	7-14	tumor necrosis factor	Homo sapiens	63-72
23466865-6	2013	Significant reductions in NFkappaB expression and DNA binding by aspirin, cyanidin and quercetin were also observed in addition to decreased expression of ERK1, ERK2 and p38 MAPK (p &lt; 0.05).	Aspirin	65-72	nuclear factor kappa B subunit 1	Homo sapiens	26-34
23525414-9	2013	Expression of COX-2 (but not COX-1), mPGES-1, and macrophages was lower in the ASA group than in the control group.	Aspirin	79-82	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	14-19
23132258-0	2013	Targeting FLIP and Mcl-1 using a combination of aspirin and sorafenib sensitizes colon cancer cells to TRAIL.	Aspirin	48-55	TNF superfamily member 10	Homo sapiens	103-108
23398903-12	2013	Aspirin showed similar anti-inflammatory effects with respect to TNF-alpha during TLR-3 and TLR-7 stimulation.	Aspirin	0-7	toll like receptor 7	Homo sapiens	92-97
23398903-14	2013	Combination of Aspirin and Docosahexaenoic Acid showed augmentation in total Glutathione production during TLR-7 stimulation as well as a reduction in IL-6, TNF-alpha and Nitric Oxide.	Aspirin	15-22	toll like receptor 7	Homo sapiens	107-112
23398903-14	2013	Combination of Aspirin and Docosahexaenoic Acid showed augmentation in total Glutathione production during TLR-7 stimulation as well as a reduction in IL-6, TNF-alpha and Nitric Oxide.	Aspirin	15-22	interleukin 6	Homo sapiens	151-155
23398903-14	2013	Combination of Aspirin and Docosahexaenoic Acid showed augmentation in total Glutathione production during TLR-7 stimulation as well as a reduction in IL-6, TNF-alpha and Nitric Oxide.	Aspirin	15-22	tumor necrosis factor	Homo sapiens	157-166
26588732-7	2013	A comparison is made between umbrella sampling using regular distance restraints and HREMD with DF restraints to study aspirin binding to the protein phospholipase A2.	Aspirin	119-126	phospholipase A2 group IB	Homo sapiens	150-166
23240590-2	2013	Aspirin, a non-steroidal anti-inflammatory drug, simultaneously inhibits the aromatase activity of COX-1 and COX-2 isoforms, which is needed for prostaglandin synthesis.	Aspirin	0-7	cytochrome c oxidase I, mitochondrial	Mus musculus	99-104
22882748-2	2013	This interaction is ascribed to steric hindrance at the active site of cyclooxygenase-1 by ibuprofen, when aspirin is administered after ibuprofen.	Aspirin	107-114	prostaglandin-endoperoxide synthase 1	Homo sapiens	71-87
23064666-9	2013	Lag time, peak thrombin generation and endogenous thrombin potential were reduced at both 14 and 90 days after adding dipyridamole to aspirin (p &lt;= 0.01).	Aspirin	134-141	coagulation factor II, thrombin	Homo sapiens	50-58
23064666-12	2013	The addition of dipyridamole to aspirin led to a persistent reduction in peak and total thrombin generation ex vivo, and illustrates the diverse, potentially beneficial, newly recognised "anti-coagulant" effects of dipyridamole in ischaemic CVD.	Aspirin	32-39	coagulation factor II, thrombin	Homo sapiens	88-96
23132258-5	2013	Furthermore, combining low doses of aspirin (&lt;= 5 mm) and sorafenib (&lt;= 2.5 microm) greatly sensitized TRAIL-sensitive and TRAIL-resistant colon cancer cells to rhTRAIL, much more potently than either drug combined with rhTRAIL.	Aspirin	36-43	TNF superfamily member 10	Homo sapiens	109-114
23132258-5	2013	Furthermore, combining low doses of aspirin (&lt;= 5 mm) and sorafenib (&lt;= 2.5 microm) greatly sensitized TRAIL-sensitive and TRAIL-resistant colon cancer cells to rhTRAIL, much more potently than either drug combined with rhTRAIL.	Aspirin	36-43	TNF superfamily member 10	Homo sapiens	129-134
23306703-6	2013	Additionally, ASA, but not salicylic acid, suppressed Th17 airway inflammation, which was associated with decreased expression of acetyl-STAT3 (downstream signaling of IL-6) in the lung.	Aspirin	14-17	interleukin 6	Mus musculus	168-172
23338704-0	2013	[ASAS recommendations on the use of TNF inhibitors for patients with axial spondyloarthritis : evaluation of the 2010 update in the German-speaking area].	Aspirin	1-5	tumor necrosis factor	Homo sapiens	36-39
23338704-1	2013	The ASAS recommendations on the use of tumor necrosis factor (TNF) inhibitors for patients with axial spondyloarthritis were amended in 2010.	Aspirin	4-8	tumor necrosis factor	Homo sapiens	39-60
23338704-1	2013	The ASAS recommendations on the use of tumor necrosis factor (TNF) inhibitors for patients with axial spondyloarthritis were amended in 2010.	Aspirin	4-8	tumor necrosis factor	Homo sapiens	62-65
23306703-0	2013	Acetyl salicylic acid inhibits Th17 airway inflammation via blockade of IL-6 and IL-17 positive feedback.	Aspirin	0-21	interleukin 6	Mus musculus	72-76
23306703-5	2013	ASA inhibited the production of interleukin (IL)-17 from lung T cells as well as in vitro Th17 polarization induced by IL-6.	Aspirin	0-3	interleukin 6	Mus musculus	119-123
23306703-7	2013	Moreover, the production of IL-6 from inflammatory cells, induced by IL-17, was abolished by treatment with ASA, whereas that induced by LPS was not.	Aspirin	108-111	interleukin 6	Mus musculus	28-32
23306703-6	2013	Additionally, ASA, but not salicylic acid, suppressed Th17 airway inflammation, which was associated with decreased expression of acetyl-STAT3 (downstream signaling of IL-6) in the lung.	Aspirin	14-17	signal transducer and activator of transcription 3	Mus musculus	137-142
23306703-8	2013	Altogether, ASA, likely via its acetyl moiety, inhibits Th17 airway inflammation by blockade of IL-6 and IL-17 positive feedback.	Aspirin	12-15	interleukin 6	Mus musculus	96-100
23985963-1	2013	BACKGROUND: Aspirin"s therapeutic action is via inhibition of platelet cyclooxygenase 1 (COX-1) thromboxane A2 (TxA2) production.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	71-87
23228932-7	2013	We suggest that DHBA, generated from ASA, via its oxidation/reduction reactions mediated by Nqo1 might be involved in the production of O(2)(-.)	Aspirin	37-40	NAD(P)H quinone dehydrogenase 1	Homo sapiens	92-96
23228932-9	2013	As Sirt1 and PGC-1alpha profoundly affect mitochondrial metabolism and energy utilization, ASA may have therapeutic potential beyond its ability to inhibit cyclooxygenases.	Aspirin	91-94	PPARG coactivator 1 alpha	Homo sapiens	13-23
23200247-1	2013	The observation that the cyclooxygenase-2 (COX-2) isozyme is over-expressed in multiple types of cancer, relative to that in adjacent non-cancerous tissue, prompted this investigation to prepare a group of hybrid fluorescent conjugates wherein the COX inhibitors ibuprofen, (S)-naproxen, acetyl salicylic acid, a chlororofecoxib analog and celecoxib were coupled via a linker group to an acridone, dansyl or rhodamine B fluorophore.	Aspirin	288-309	prostaglandin-endoperoxide synthase 2	Homo sapiens	25-41
23200247-1	2013	The observation that the cyclooxygenase-2 (COX-2) isozyme is over-expressed in multiple types of cancer, relative to that in adjacent non-cancerous tissue, prompted this investigation to prepare a group of hybrid fluorescent conjugates wherein the COX inhibitors ibuprofen, (S)-naproxen, acetyl salicylic acid, a chlororofecoxib analog and celecoxib were coupled via a linker group to an acridone, dansyl or rhodamine B fluorophore.	Aspirin	288-309	prostaglandin-endoperoxide synthase 2	Homo sapiens	43-48
24107783-0	2013	MDR1 is related to intestinal epithelial injury induced by acetylsalicylic acid.	Aspirin	59-79	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
24107783-2	2013	We assessed the involvement of Multi Drug Resistance (MDR) 1 in intestinal epithelial cell injury caused by aspirin using MDR1 gene-transfected Caco2 cells.	Aspirin	108-115	ATP binding cassette subfamily B member 1	Homo sapiens	31-60
24107783-5	2013	To determine the function of MDR1 in the metabolism of aspirin, flux study was performed using (14)C-labeled aspirin.	Aspirin	55-62	ATP binding cassette subfamily B member 1	Homo sapiens	29-33
24107783-6	2013	RESULTS: The level of aspirin-induced cell injury was higher in verapamil-treated Caco2 cells than in control cells and was less serious in MDR1-transfected Caco2 cells than in control vector-transfected cells.	Aspirin	22-29	ATP binding cassette subfamily B member 1	Homo sapiens	140-144
24107783-8	2013	CONCLUSION: These data suggest that aspirin effux occurs through the MDR1 transporter and that the MDR1 transporter is involved in the pathogenesis of aspirin-induced cell injury.	Aspirin	36-43	ATP binding cassette subfamily B member 1	Homo sapiens	69-73
24107783-8	2013	CONCLUSION: These data suggest that aspirin effux occurs through the MDR1 transporter and that the MDR1 transporter is involved in the pathogenesis of aspirin-induced cell injury.	Aspirin	151-158	ATP binding cassette subfamily B member 1	Homo sapiens	99-103
23228932-0	2013	Aspirin may promote mitochondrial biogenesis via the production of hydrogen peroxide and the induction of Sirtuin1/PGC-1alpha genes.	Aspirin	0-7	PPARG coactivator 1 alpha	Homo sapiens	115-125
23228932-2	2013	We observed that treatment of cultured liver cells with ASA resulted in the induction of Sirt1, peroxisome proliferator-activated receptor-gamma co-activator-1alpha (PGC-1alpha), and NAD(P)H quinone oxidoreductase 1 (Nqo1) genes.	Aspirin	56-59	PPARG coactivator 1 alpha	Homo sapiens	96-164
23228932-2	2013	We observed that treatment of cultured liver cells with ASA resulted in the induction of Sirt1, peroxisome proliferator-activated receptor-gamma co-activator-1alpha (PGC-1alpha), and NAD(P)H quinone oxidoreductase 1 (Nqo1) genes.	Aspirin	56-59	PPARG coactivator 1 alpha	Homo sapiens	166-176
23228932-2	2013	We observed that treatment of cultured liver cells with ASA resulted in the induction of Sirt1, peroxisome proliferator-activated receptor-gamma co-activator-1alpha (PGC-1alpha), and NAD(P)H quinone oxidoreductase 1 (Nqo1) genes.	Aspirin	56-59	NAD(P)H quinone dehydrogenase 1	Homo sapiens	183-215
23228932-2	2013	We observed that treatment of cultured liver cells with ASA resulted in the induction of Sirt1, peroxisome proliferator-activated receptor-gamma co-activator-1alpha (PGC-1alpha), and NAD(P)H quinone oxidoreductase 1 (Nqo1) genes.	Aspirin	56-59	NAD(P)H quinone dehydrogenase 1	Homo sapiens	217-221
23228932-3	2013	Paraoxonase 1 (PON1) and Aryl hydrocarbon receptor (AhR) siRNA transfections inhibited the induction of gene expressions by ASA suggesting the need for the acetyl ester hydrolysis and hydroxylation to DHBA.	Aspirin	124-127	paraoxonase 1	Homo sapiens	0-13
23228932-3	2013	Paraoxonase 1 (PON1) and Aryl hydrocarbon receptor (AhR) siRNA transfections inhibited the induction of gene expressions by ASA suggesting the need for the acetyl ester hydrolysis and hydroxylation to DHBA.	Aspirin	124-127	paraoxonase 1	Homo sapiens	15-19
24469880-8	2013	CONCLUSIONS: Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA.	Aspirin	36-39	interleukin 6	Homo sapiens	194-198
24469880-8	2013	CONCLUSIONS: Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA.	Aspirin	36-39	CD40 ligand	Homo sapiens	203-208
24469880-8	2013	CONCLUSIONS: Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA.	Aspirin	80-83	interleukin 6	Homo sapiens	194-198
24469880-8	2013	CONCLUSIONS: Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA.	Aspirin	80-83	CD40 ligand	Homo sapiens	203-208
24469880-8	2013	CONCLUSIONS: Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA.	Aspirin	80-83	interleukin 6	Homo sapiens	194-198
24469880-8	2013	CONCLUSIONS: Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA.	Aspirin	80-83	CD40 ligand	Homo sapiens	203-208
23985963-1	2013	BACKGROUND: Aspirin"s therapeutic action is via inhibition of platelet cyclooxygenase 1 (COX-1) thromboxane A2 (TxA2) production.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	89-94
23038044-0	2013	Frequency, risk factors, prognosis, and genetic polymorphism of the cyclooxygenase-1 gene for aspirin resistance in elderly Chinese patients with cardiovascular disease.	Aspirin	94-101	prostaglandin-endoperoxide synthase 1	Homo sapiens	68-84
23401648-2	2013	As the protective effect of aspirin has been associated with an increased expression of COX-2, molecular imaging of COX-2, for instance, during confocal endomicroscopy could enable the identification of patients who would possibly benefit from aspirin treatment.	Aspirin	28-35	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	88-93
23401648-2	2013	As the protective effect of aspirin has been associated with an increased expression of COX-2, molecular imaging of COX-2, for instance, during confocal endomicroscopy could enable the identification of patients who would possibly benefit from aspirin treatment.	Aspirin	28-35	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	116-121
23401648-2	2013	As the protective effect of aspirin has been associated with an increased expression of COX-2, molecular imaging of COX-2, for instance, during confocal endomicroscopy could enable the identification of patients who would possibly benefit from aspirin treatment.	Aspirin	244-251	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	88-93
23401648-2	2013	As the protective effect of aspirin has been associated with an increased expression of COX-2, molecular imaging of COX-2, for instance, during confocal endomicroscopy could enable the identification of patients who would possibly benefit from aspirin treatment.	Aspirin	244-251	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	116-121
23038044-3	2013	OBJECTIVE: The frequency, risk factors, prognosis, and genetic polymorphism of the cyclooxygenase-1 (COX-1) gene for aspirin resistance have not been reported in elderly patients with CVD.	Aspirin	117-124	prostaglandin-endoperoxide synthase 1	Homo sapiens	83-99
23038044-3	2013	OBJECTIVE: The frequency, risk factors, prognosis, and genetic polymorphism of the cyclooxygenase-1 (COX-1) gene for aspirin resistance have not been reported in elderly patients with CVD.	Aspirin	117-124	prostaglandin-endoperoxide synthase 1	Homo sapiens	101-106
23038044-10	2013	The variant G-allele of COX-1 rs1330344 (-1676 A/G) significantly increased the risk of aspirin resistance defined by LTAAA + TEGAA (OR = 1.82, 95% CI 1.13- 2.92, p = 0.01).	Aspirin	88-95	prostaglandin-endoperoxide synthase 1	Homo sapiens	24-29
23038044-12	2013	The variant G-allele of COX-1 rs1330344 is significantly associated with aspirin resistance defined by LTAAA + TEGAA.	Aspirin	73-80	prostaglandin-endoperoxide synthase 1	Homo sapiens	24-29
23035985-0	2012	Quinone-induced activation of Keap1/Nrf2 signaling by aspirin prodrugs masquerading as nitric oxide.	Aspirin	54-61	kelch like ECH associated protein 1	Homo sapiens	30-35
24193355-0	2013	Clinical significance of immunoglobulin E responses to staphylococcal superantigens in patients with aspirin-exacerbated respiratory disease.	Aspirin	101-108	immunoglobulin heavy constant epsilon	Homo sapiens	25-41
24193355-1	2013	BACKGROUND: Previous studies have reported a higher prevalence of immunoglobulin E (IgE) specific for staphylococcal superantigens (SAg) in the nasal mucosa of patients with aspirin-exacerbated respiratory disease (AERD), associated with eosinophilic inflammation and leukotriene production.	Aspirin	174-181	immunoglobulin heavy constant epsilon	Homo sapiens	66-82
24193355-1	2013	BACKGROUND: Previous studies have reported a higher prevalence of immunoglobulin E (IgE) specific for staphylococcal superantigens (SAg) in the nasal mucosa of patients with aspirin-exacerbated respiratory disease (AERD), associated with eosinophilic inflammation and leukotriene production.	Aspirin	174-181	immunoglobulin heavy constant epsilon	Homo sapiens	84-87
22763923-0	2013	Association of COX-2 rs20417 with aspirin resistance.	Aspirin	34-41	prostaglandin-endoperoxide synthase 2	Homo sapiens	15-20
24860707-0	2013	Tandem mass spectrometry of nitric oxide and hydrogen sulfide releasing aspirins: a hint into activity behavior.	Aspirin	72-80	histidine triad nucleotide binding protein 1	Homo sapiens	84-88
23207797-1	2013	Patients with colorectal cancer with mutated PIK3CA, identified from two large observational cohorts, had increased cancer-specific and overall survival if they used aspirin regularly after diagnosis compared to non-users.	Aspirin	166-173	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	45-51
23207797-3	2013	Mutated PIK3CA might be a useful biomarker to select patients who would benefit from adjuvant aspirin therapy.	Aspirin	94-101	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	8-14
22994591-12	2013	The time course of plasma fibrinogen and procalcitonin levels indicate that ASA seems to reduce the activation of haemostasis and increase the resolution of inflammation.	Aspirin	76-79	fibrinogen beta chain	Homo sapiens	26-36
23301845-7	2013	To further confirm that aspirin incurs platelet apoptosis, caspase-3 activity was measured in platelets, and the result indicated that aspirin induced caspase-3 activation.	Aspirin	24-31	caspase 3	Homo sapiens	59-68
23301845-7	2013	To further confirm that aspirin incurs platelet apoptosis, caspase-3 activity was measured in platelets, and the result indicated that aspirin induced caspase-3 activation.	Aspirin	24-31	caspase 3	Homo sapiens	151-160
23301845-7	2013	To further confirm that aspirin incurs platelet apoptosis, caspase-3 activity was measured in platelets, and the result indicated that aspirin induced caspase-3 activation.	Aspirin	135-142	caspase 3	Homo sapiens	59-68
23301845-7	2013	To further confirm that aspirin incurs platelet apoptosis, caspase-3 activity was measured in platelets, and the result indicated that aspirin induced caspase-3 activation.	Aspirin	135-142	caspase 3	Homo sapiens	151-160
23301845-11	2013	Taken together, the data indicate that aspirin induces platelet apoptosis via caspase-3 activation.	Aspirin	39-46	caspase 3	Homo sapiens	78-87
23035985-0	2012	Quinone-induced activation of Keap1/Nrf2 signaling by aspirin prodrugs masquerading as nitric oxide.	Aspirin	54-61	NFE2 like bZIP transcription factor 2	Homo sapiens	36-40
23085268-0	2012	Effect of S-aspirin, a novel hydrogen-sulfide-releasing aspirin (ACS14), on atherosclerosis in apoE-deficient mice.	Aspirin	10-19	apolipoprotein E	Mus musculus	95-99
23085268-2	2012	The present study investigated the effect of a novel H(2)S-releasing aspirin, ACS14 (2-acetyloxybenzoic acid 4-(3-thioxo-3H-1,2-dithiol-5-yl)phenyl ester), on atherosclerotic plaques in fat-fed apoE(-/-) mice and the underlying mechanism with respect to CX3C chemokine receptor 1 (CX3CR1) in macrophages.	Aspirin	69-76	apolipoprotein E	Mus musculus	194-198
23228069-6	2012	Their Platelet Rich Plasma was incubated with either aspirin [2.5 micro-mole (muM) and 5 muM] or distilled water as control for three minutes after which the aggregatory response to 5 muM Adenosine Diphosphate (ADP) was measured over a period of 7 minutes.	Aspirin	53-60	latexin	Homo sapiens	78-81
23323271-6	2012	Further,we discovered that transglutaminase 2 (TGM2) is expressed at increased levels in asthma and serves asa regulator of sPLA2-X.	Aspirin	107-110	transglutaminase 2	Homo sapiens	27-45
23578461-0	2013	[Effects of aspirin on CX3CL1 and CX3CR1 in acute pulmonary embolism rats].	Aspirin	12-19	C-X3-C motif chemokine ligand 1	Rattus norvegicus	23-29
23578461-11	2013	CONCLUSION: Aspirin may improve the pathology and inhibit the expression of CX3CL1 and CX3CR1 in APE lung.	Aspirin	12-19	C-X3-C motif chemokine ligand 1	Rattus norvegicus	76-82
23600205-10	2013	CONCLUSION: Aspirin, sulindac, curcumin and PDTC could all inhibit cisplatin induced NF-kappaB activiation, which could increase cispaltin-induced chemosensativity by augments of apoptosis.	Aspirin	12-19	nuclear factor kappa B subunit 1	Homo sapiens	85-94
24281340-3	2012	At low-doses given every 24 h, aspirin is acting by a complete and persistent inhibition of cyclooxygenase (COX)-1 in platelets (in the pre-systemic circulation) while causing a limited and rapidly reversible inhibitory effect on COX-2 and/or COX-1 expressed in nucleated cells.	Aspirin	31-38	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	230-235
23027181-6	2012	RESULTS: The risk of developing breast cancer among patients taking both aspirin and an ACE inhibitor decreased as the ACE inhibitor dose increased.	Aspirin	73-80	angiotensin I converting enzyme	Homo sapiens	119-122
23027181-7	2012	Among patients receiving between 28 and 364 cumulative defined daily doses (cDDDs) of aspirin, the adjusted odds ratios (ORs) were 0.97 (0.90-1.06), 0.91 (0.82-1.03), and 0.79 (0.68-0.92) for women taking ACE inhibitors for 0-27, 28-364, and more than 365 cDDD, respectively.	Aspirin	86-93	angiotensin I converting enzyme	Homo sapiens	205-208
23027181-8	2012	Among women receiving more than 365 cDDD of aspirin, the adjusted ORs were 0.91 (0.80-1.03), 0.81 (0.70-0.94), and 0.81 (0.71-0.92) as the ACE inhibitor dose increased, respectively.	Aspirin	44-51	angiotensin I converting enzyme	Homo sapiens	139-142
22893064-3	2012	The priming action of aspirin on tumor cells was found to be dependent on an altered constitution of tumor microenvironment with respect to decline of acidosis and modulation in the expression of cell cycle and survival regulatory molecules like cyclin B1, cyclin D, bcl-2, bcl-xL, p53, and cytokines: IL-4, IL-10, IFN- gamma &amp; VEGF.	Aspirin	22-29	B cell leukemia/lymphoma 2	Mus musculus	267-272
22893064-3	2012	The priming action of aspirin on tumor cells was found to be dependent on an altered constitution of tumor microenvironment with respect to decline of acidosis and modulation in the expression of cell cycle and survival regulatory molecules like cyclin B1, cyclin D, bcl-2, bcl-xL, p53, and cytokines: IL-4, IL-10, IFN- gamma &amp; VEGF.	Aspirin	22-29	interleukin 10	Mus musculus	308-313
22893064-3	2012	The priming action of aspirin on tumor cells was found to be dependent on an altered constitution of tumor microenvironment with respect to decline of acidosis and modulation in the expression of cell cycle and survival regulatory molecules like cyclin B1, cyclin D, bcl-2, bcl-xL, p53, and cytokines: IL-4, IL-10, IFN- gamma &amp; VEGF.	Aspirin	22-29	interferon gamma	Mus musculus	315-325
23323271-6	2012	Further,we discovered that transglutaminase 2 (TGM2) is expressed at increased levels in asthma and serves asa regulator of sPLA2-X.	Aspirin	107-110	transglutaminase 2	Homo sapiens	47-51
23323271-6	2012	Further,we discovered that transglutaminase 2 (TGM2) is expressed at increased levels in asthma and serves asa regulator of sPLA2-X.	Aspirin	107-110	phospholipase A2 group X	Homo sapiens	124-129
23181222-6	2012	Several bioactive molecules such as dietary polyphenols, aspirin and its hydrolysis product salicylate, are known to stimulate PON1 transcription activation in mouse liver and HepG2 cell line.	Aspirin	57-64	paraoxonase 1	Mus musculus	127-131
22988011-6	2012	One novel strategy to improve MSC-based tissue engineering involves the reduction of IFN-gamma and TNF-alpha concentration by systemic infusion of Tregs or local application of aspirin.	Aspirin	177-184	tumor necrosis factor	Homo sapiens	99-108
22994386-9	2012	In addition, splenocytes harvested after ASA produced IL-4, IL-5, and IL-10 by re-stimulation with HWP1.	Aspirin	41-44	interleukin 10	Mus musculus	70-75
22580394-0	2012	Increase of toll-like receptor 4 but decrease of interleukin-8 mRNA expression among ischemic stroke patients under aspirin treatment.	Aspirin	116-123	C-X-C motif chemokine ligand 8	Homo sapiens	49-62
22580394-8	2012	A reduction of IL-8 expression could result from the downregulatory effects of aspirin.	Aspirin	79-86	C-X-C motif chemokine ligand 8	Homo sapiens	15-19
22174438-8	2012	The few identified experimental trials indicated that aspirin and other NSAIDs inhibit lymphangiogenesis, with a potential decrease in metastatic spread, possibly through COX-II-dependent regulation of VEGF-C expression.	Aspirin	54-61	vascular endothelial growth factor C	Homo sapiens	202-208
23033009-0	2012	beta-catenin negatively regulates expression of the prostaglandin transporter PGT in the normal intestinal epithelium and colorectal tumour cells: a role in the chemopreventive efficacy of aspirin?	Aspirin	189-196	solute carrier organic anion transporter family, member 2a1	Mus musculus	52-77
23094721-2	2012	Experimental evidence suggests that inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2) (also known as cyclooxygenase-2) by aspirin down-regulates phosphatidylinositol 3-kinase (PI3K) signaling activity.	Aspirin	132-139	prostaglandin-endoperoxide synthase 2	Homo sapiens	50-87
23094721-2	2012	Experimental evidence suggests that inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2) (also known as cyclooxygenase-2) by aspirin down-regulates phosphatidylinositol 3-kinase (PI3K) signaling activity.	Aspirin	132-139	prostaglandin-endoperoxide synthase 2	Homo sapiens	89-94
23094721-2	2012	Experimental evidence suggests that inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2) (also known as cyclooxygenase-2) by aspirin down-regulates phosphatidylinositol 3-kinase (PI3K) signaling activity.	Aspirin	132-139	prostaglandin-endoperoxide synthase 2	Homo sapiens	111-127
23094721-2	2012	Experimental evidence suggests that inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2) (also known as cyclooxygenase-2) by aspirin down-regulates phosphatidylinositol 3-kinase (PI3K) signaling activity.	Aspirin	132-139	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	155-184
23094721-3	2012	We hypothesized that the effect of aspirin on survival and prognosis in patients with cancers characterized by mutated PIK3CA (the phosphatidylinositol-4,5-bisphosphonate 3-kinase, catalytic subunit alpha polypeptide gene) might differ from the effect among those with wild-type PIK3CA cancers.	Aspirin	35-42	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	119-125
23094721-3	2012	We hypothesized that the effect of aspirin on survival and prognosis in patients with cancers characterized by mutated PIK3CA (the phosphatidylinositol-4,5-bisphosphonate 3-kinase, catalytic subunit alpha polypeptide gene) might differ from the effect among those with wild-type PIK3CA cancers.	Aspirin	35-42	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	279-285
23094721-7	2012	RESULTS: Among patients with mutated-PIK3CA colorectal cancers, regular use of aspirin after diagnosis was associated with superior colorectal cancer-specific survival (multivariate hazard ratio for cancer-related death, 0.18; 95% confidence interval [CI], 0.06 to 0.61; P&lt;0.001 by the log-rank test) and overall survival (multivariate hazard ratio for death from any cause, 0.54; 95% CI, 0.31 to 0.94; P=0.01 by the log-rank test).	Aspirin	79-86	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	37-43
23094721-9	2012	CONCLUSIONS: Regular use of aspirin after diagnosis was associated with longer survival among patients with mutated-PIK3CA colorectal cancer, but not among patients with wild-type PIK3CA cancer.	Aspirin	28-35	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	116-122
23094721-10	2012	The findings from this molecular pathological epidemiology study suggest that the PIK3CA mutation in colorectal cancer may serve as a predictive molecular biomarker for adjuvant aspirin therapy.	Aspirin	178-185	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	82-88
23033009-0	2012	beta-catenin negatively regulates expression of the prostaglandin transporter PGT in the normal intestinal epithelium and colorectal tumour cells: a role in the chemopreventive efficacy of aspirin?	Aspirin	189-196	solute carrier organic anion transporter family, member 2a1	Mus musculus	78-81
22561363-7	2012	ASA and its salicylic acid (SA) moiety both suppressed Ang II-mediated AT1R and vascular endothelial growth factor expression and the subsequent new capillary formation.	Aspirin	0-3	angiotensinogen	Homo sapiens	55-61
22917627-0	2012	Acetyl salicylic acid induces damage to intestinal epithelial cells by oxidation-related modifications of ZO-1.	Aspirin	0-21	tight junction protein 1	Homo sapiens	106-110
22917627-5	2012	We measured whether ASA induced the increase of differentiated Caco-2 permeability, the decrease of tight junction protein expression, the production of reactive oxygen species (ROS), and the expression of ROS-modified zonula occludens-1 (ZO-1) protein.	Aspirin	20-23	tight junction protein 1	Homo sapiens	219-237
22917627-5	2012	We measured whether ASA induced the increase of differentiated Caco-2 permeability, the decrease of tight junction protein expression, the production of reactive oxygen species (ROS), and the expression of ROS-modified zonula occludens-1 (ZO-1) protein.	Aspirin	20-23	tight junction protein 1	Homo sapiens	239-243
22917627-8	2012	The same concentration of ASA significantly decreased ZO-1 expression among TJ proteins as assessed by Western blot and immunocytochemistry and increased ROS production and the expression of oxidative stress-modified ZO-1 protein.	Aspirin	26-29	tight junction protein 1	Homo sapiens	54-58
22917627-8	2012	The same concentration of ASA significantly decreased ZO-1 expression among TJ proteins as assessed by Western blot and immunocytochemistry and increased ROS production and the expression of oxidative stress-modified ZO-1 protein.	Aspirin	26-29	tight junction protein 1	Homo sapiens	217-221
22917627-9	2012	However, MnTMPyP suppressed the ASA-induced increased intercellular permeability and the ASA-induced ROS-modified ZO-1 expression.	Aspirin	89-92	tight junction protein 1	Homo sapiens	114-118
22917627-10	2012	Our findings indicate that ASA-induced ROS production can specifically modify the expression of ZO-1 protein and induce increased cell permeability, which may ultimately cause small intestinal mucosal injury.	Aspirin	27-30	tight junction protein 1	Homo sapiens	96-100
22932716-16	2012	INTERPRETATION: For patients with a history of myocardial infarction, inhibition of protease-activated receptor 1 with vorapaxar reduces the risk of cardiovascular death or ischaemic events when added to standard antiplatelet treatment, including aspirin, and increases the risk of moderate or severe bleeding.	Aspirin	247-254	coagulation factor II thrombin receptor	Homo sapiens	84-113
22847161-0	2012	Potential association between ANXA4 polymorphisms and aspirin-exacerbated respiratory disease.	Aspirin	54-61	annexin A4	Homo sapiens	30-35
22521214-1	2012	INTRODUCTION: Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation.	Aspirin	14-21	prostaglandin-endoperoxide synthase 1	Homo sapiens	59-75
22521214-1	2012	INTRODUCTION: Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation.	Aspirin	14-21	prostaglandin-endoperoxide synthase 1	Homo sapiens	77-82
22521214-1	2012	INTRODUCTION: Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation.	Aspirin	23-26	prostaglandin-endoperoxide synthase 1	Homo sapiens	59-75
22521214-1	2012	INTRODUCTION: Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation.	Aspirin	23-26	prostaglandin-endoperoxide synthase 1	Homo sapiens	77-82
22883224-16	2012	Long-term antiplatelet treatment with aspirin alone seems to attenuate thrombin generation to a greater extent than with clopidogrel alone.	Aspirin	38-45	coagulation factor II, thrombin	Homo sapiens	71-79
22724630-6	2012	A 95% difference in the number of cells killed between control and TRAIL + ES surfaces was seen when aspirin treated cells were perfused over the functionalized surface for 2 h. We have demonstrated a novel biomimetic method to capture and neutralize cancer cells in flow, thus reducing the chances for the formation of secondary tumors.	Aspirin	101-108	TNF superfamily member 10	Homo sapiens	67-72
22627848-0	2012	Aspirin-intolerant asthma (AIA) assessment using the urinary biomarkers, leukotriene E4 (LTE4) and prostaglandin D2 (PGD2) metabolites.	Aspirin	0-7	prostaglandin D2 synthase	Homo sapiens	99-115
23094974-7	2012	Potential mechanisms of aspirin resistance in diabetes include elevated platelet turnover that results in an immature platelet fraction able to synthesise the uninhibited therapeutic target of aspirin, cyclooxygenase-1 (COX-1); residual thromboxane production by both COX-1-dependent and COX-1-independent pathways; up-regulation of aspirin-insensitive pathways of platelet function, such as adenosine diphosphate signalling; and increased underlying atherosclerotic disease burden that results in elevated underlying platelet hyper-reactivity.	Aspirin	24-31	prostaglandin-endoperoxide synthase 1	Homo sapiens	202-218
23094974-7	2012	Potential mechanisms of aspirin resistance in diabetes include elevated platelet turnover that results in an immature platelet fraction able to synthesise the uninhibited therapeutic target of aspirin, cyclooxygenase-1 (COX-1); residual thromboxane production by both COX-1-dependent and COX-1-independent pathways; up-regulation of aspirin-insensitive pathways of platelet function, such as adenosine diphosphate signalling; and increased underlying atherosclerotic disease burden that results in elevated underlying platelet hyper-reactivity.	Aspirin	24-31	prostaglandin-endoperoxide synthase 1	Homo sapiens	220-225
23094974-7	2012	Potential mechanisms of aspirin resistance in diabetes include elevated platelet turnover that results in an immature platelet fraction able to synthesise the uninhibited therapeutic target of aspirin, cyclooxygenase-1 (COX-1); residual thromboxane production by both COX-1-dependent and COX-1-independent pathways; up-regulation of aspirin-insensitive pathways of platelet function, such as adenosine diphosphate signalling; and increased underlying atherosclerotic disease burden that results in elevated underlying platelet hyper-reactivity.	Aspirin	24-31	prostaglandin-endoperoxide synthase 1	Homo sapiens	268-273
23094974-7	2012	Potential mechanisms of aspirin resistance in diabetes include elevated platelet turnover that results in an immature platelet fraction able to synthesise the uninhibited therapeutic target of aspirin, cyclooxygenase-1 (COX-1); residual thromboxane production by both COX-1-dependent and COX-1-independent pathways; up-regulation of aspirin-insensitive pathways of platelet function, such as adenosine diphosphate signalling; and increased underlying atherosclerotic disease burden that results in elevated underlying platelet hyper-reactivity.	Aspirin	24-31	prostaglandin-endoperoxide synthase 1	Homo sapiens	268-273
22531959-6	2012	Inhibition of NFkappaB activity in Saos2 cells by Aspirin sensitized the miR-34a overexpressing cells to cell death.	Aspirin	50-57	nuclear factor kappa B subunit 1	Homo sapiens	14-22
22795340-1	2012	INTRODUCTION: Aspirin inhibits the cyclooxygenase-1 (COX-1) mediated thromboxane A2 synthesis.	Aspirin	14-21	prostaglandin-endoperoxide synthase 1	Homo sapiens	35-51
22795340-1	2012	INTRODUCTION: Aspirin inhibits the cyclooxygenase-1 (COX-1) mediated thromboxane A2 synthesis.	Aspirin	14-21	prostaglandin-endoperoxide synthase 1	Homo sapiens	53-58
22997997-4	2012	RESULTS: Two trials showed a small but significant reduction with aspirin plus dipyridamole compared to aspirin (ARR 1.5%, P &lt; 0.05 and ARR 1.0%, P &lt; 0.05).	Aspirin	66-73	arrestin beta 1	Homo sapiens	113-118
22997997-4	2012	RESULTS: Two trials showed a small but significant reduction with aspirin plus dipyridamole compared to aspirin (ARR 1.5%, P &lt; 0.05 and ARR 1.0%, P &lt; 0.05).	Aspirin	66-73	arrestin beta 1	Homo sapiens	139-144
22997997-4	2012	RESULTS: Two trials showed a small but significant reduction with aspirin plus dipyridamole compared to aspirin (ARR 1.5%, P &lt; 0.05 and ARR 1.0%, P &lt; 0.05).	Aspirin	104-111	arrestin beta 1	Homo sapiens	113-118
22969773-9	2012	ASA correlated with AI75 (r = -0.31, p &lt;= 0.01), C-SBP (r = -0.24, p = 0.04), C-PP (r = -0.29, p = 0.01), but only showed a trend towards significance with P-SBP (r = -0.2, p = 0.09) and P-PP (r = -0.21, p = 0.08).	Aspirin	0-3	mitogen-activated protein kinase 14	Homo sapiens	52-57
22561363-9	2012	ASA and SA also suppressed NADPH oxidase (p22, p47, p67, and gp91 messenger RNA) expression.	Aspirin	0-3	CD33 molecule	Homo sapiens	52-55
22561363-10	2012	These observations suggest that ASA can inhibit Ang II-induced capillary formation in part via blocking NADPH oxidase and AT1R transcription.	Aspirin	32-35	angiotensinogen	Homo sapiens	48-54
22561363-7	2012	ASA and its salicylic acid (SA) moiety both suppressed Ang II-mediated AT1R and vascular endothelial growth factor expression and the subsequent new capillary formation.	Aspirin	0-3	vascular endothelial growth factor A	Homo sapiens	80-114
22754713-0	2012	WDR46 is a Genetic Risk Factor for Aspirin-Exacerbated Respiratory Disease in a Korean Population.	Aspirin	35-42	WD repeat domain 46	Homo sapiens	0-5
22728039-0	2012	Aspirin enhances TRAIL-induced apoptosis via regulation of ERK1/2 activation in human cervical cancer cells.	Aspirin	0-7	TNF superfamily member 10	Homo sapiens	17-22
22728039-0	2012	Aspirin enhances TRAIL-induced apoptosis via regulation of ERK1/2 activation in human cervical cancer cells.	Aspirin	0-7	mitogen-activated protein kinase 3	Homo sapiens	59-65
22728039-3	2012	Here, the effect of the non-steroidal anti-inflammatory drug aspirin on sensitization of human cervical cancer cells to TRAIL and the underlying mechanism(s) of the effect were explored.	Aspirin	61-68	TNF superfamily member 10	Homo sapiens	120-125
22728039-9	2012	These results suggest that cancer cells can be sensitized to TRAIL-induced apoptosis by pre-treatment with aspirin via suppression of ERK1/2 activation.	Aspirin	107-114	TNF superfamily member 10	Homo sapiens	61-66
22728039-9	2012	These results suggest that cancer cells can be sensitized to TRAIL-induced apoptosis by pre-treatment with aspirin via suppression of ERK1/2 activation.	Aspirin	107-114	mitogen-activated protein kinase 3	Homo sapiens	134-140
22754713-1	2012	PURPOSE: The human WD repeat-containing protein 46 (WDR46; also known as C6orf11), located at the disease-relevant centromere side of the class II major histocompatibility complex region, is hypothesized to be associated with risk of aspirin-exacerbated respiratory disease (AERD) as well as a decline in forced expiratory volume in the first second (FEV1), an important diagnostic marker of asthma.	Aspirin	234-241	WD repeat domain 46	Homo sapiens	19-50
22754713-1	2012	PURPOSE: The human WD repeat-containing protein 46 (WDR46; also known as C6orf11), located at the disease-relevant centromere side of the class II major histocompatibility complex region, is hypothesized to be associated with risk of aspirin-exacerbated respiratory disease (AERD) as well as a decline in forced expiratory volume in the first second (FEV1), an important diagnostic marker of asthma.	Aspirin	234-241	WD repeat domain 46	Homo sapiens	52-57
22754713-1	2012	PURPOSE: The human WD repeat-containing protein 46 (WDR46; also known as C6orf11), located at the disease-relevant centromere side of the class II major histocompatibility complex region, is hypothesized to be associated with risk of aspirin-exacerbated respiratory disease (AERD) as well as a decline in forced expiratory volume in the first second (FEV1), an important diagnostic marker of asthma.	Aspirin	234-241	WD repeat domain 46	Homo sapiens	73-80
22754713-7	2012	CONCLUSIONS: These findings show for the first time that WDR46 is an important genetic marker of aspirin-induced airway inflammation and may be useful for formulating new disease-management strategies.	Aspirin	97-104	WD repeat domain 46	Homo sapiens	57-62
22513397-0	2012	Decreased cyclooxygenase inhibition by aspirin in polymorphic variants of human prostaglandin H synthase-1.	Aspirin	39-46	prostaglandin-endoperoxide synthase 1	Homo sapiens	80-106
22825862-10	2012	Additionally, female patients of the ASA group also had significantly less overall (p = 0.10, OR5.3), cardiac (p = 0.021, OR 3.6) and neurologic (p = 0.042, OR 6.7) complications.	Aspirin	37-40	olfactory receptor family 5 subfamily H member 7 pseudogene	Homo sapiens	122-128
22825862-10	2012	Additionally, female patients of the ASA group also had significantly less overall (p = 0.10, OR5.3), cardiac (p = 0.021, OR 3.6) and neurologic (p = 0.042, OR 6.7) complications.	Aspirin	37-40	olfactory receptor family 2 subfamily N member 1 pseudogene	Homo sapiens	157-163
22471290-3	2012	OBJECTIVE: To characterize the kinetics and determinants of platelet cyclooxygenase-1 recovery in aspirin-treated diabetic and non-diabetic patients.	Aspirin	98-105	prostaglandin-endoperoxide synthase 1	Homo sapiens	69-85
22588264-13	2012	We speculate that the protective effect of aspirin against rupture of cerebral aneurysms may be mediated in part by inhibition of COX-2/mPGES-1.	Aspirin	43-50	prostaglandin-endoperoxide synthase 2	Homo sapiens	130-135
22513397-1	2012	OBJECTIVES: Aspirin (ASA), a major antiplatelet and cancer-preventing drug, irreversibly blocks the cyclooxygenase (COX) activity of prostaglandin H synthase-1 (PGHS-1).	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	133-159
22513397-1	2012	OBJECTIVES: Aspirin (ASA), a major antiplatelet and cancer-preventing drug, irreversibly blocks the cyclooxygenase (COX) activity of prostaglandin H synthase-1 (PGHS-1).	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	161-167
22513397-1	2012	OBJECTIVES: Aspirin (ASA), a major antiplatelet and cancer-preventing drug, irreversibly blocks the cyclooxygenase (COX) activity of prostaglandin H synthase-1 (PGHS-1).	Aspirin	21-24	prostaglandin-endoperoxide synthase 1	Homo sapiens	133-159
22513397-1	2012	OBJECTIVES: Aspirin (ASA), a major antiplatelet and cancer-preventing drug, irreversibly blocks the cyclooxygenase (COX) activity of prostaglandin H synthase-1 (PGHS-1).	Aspirin	21-24	prostaglandin-endoperoxide synthase 1	Homo sapiens	161-167
22513397-2	2012	Considerable differences in ASA effectiveness are observed between individuals, and some of this variability may be due to PGHS-1 protein variants.	Aspirin	28-31	prostaglandin-endoperoxide synthase 1	Homo sapiens	123-129
22513397-3	2012	Our overall aim is to determine which, if any, of the known variants in the mature PGHS-1 protein lead to functional alterations in COX catalysis or inhibition by ASA.	Aspirin	163-166	prostaglandin-endoperoxide synthase 1	Homo sapiens	83-89
22513397-9	2012	Computational modeling of the brief ASA pulses experienced by PGHS-1 in circulating platelets during daily ASA dosing predicted that the 60% lower ASA reactivity in R108Q yields a 15-fold increase in surviving COX activity; smaller, approximately two-fold increases in surviving COX activity were predicted for L237M and V481I.	Aspirin	36-39	prostaglandin-endoperoxide synthase 1	Homo sapiens	62-68
22513397-9	2012	Computational modeling of the brief ASA pulses experienced by PGHS-1 in circulating platelets during daily ASA dosing predicted that the 60% lower ASA reactivity in R108Q yields a 15-fold increase in surviving COX activity; smaller, approximately two-fold increases in surviving COX activity were predicted for L237M and V481I.	Aspirin	107-110	prostaglandin-endoperoxide synthase 1	Homo sapiens	62-68
22513397-9	2012	Computational modeling of the brief ASA pulses experienced by PGHS-1 in circulating platelets during daily ASA dosing predicted that the 60% lower ASA reactivity in R108Q yields a 15-fold increase in surviving COX activity; smaller, approximately two-fold increases in surviving COX activity were predicted for L237M and V481I.	Aspirin	107-110	prostaglandin-endoperoxide synthase 1	Homo sapiens	62-68
22406476-0	2012	Aspirin inhibits mTOR signaling, activates AMP-activated protein kinase, and induces autophagy in colorectal cancer cells.	Aspirin	0-7	mechanistic target of rapamycin kinase	Homo sapiens	17-21
22442156-0	2012	Cu/Zn superoxide dismutase (SOD1) induction is implicated in the antioxidative and antiviral activity of acetylsalicylic acid in HCV-expressing cells.	Aspirin	105-125	superoxide dismutase 1	Homo sapiens	28-32
22442156-8	2012	Average GPx activity was decreased, whereas a striking increase was observed in average cytosolic SOD activity at 48 and 72 h in both cells exposed to ASA, compared with untreated cells.	Aspirin	151-154	superoxide dismutase 1	Homo sapiens	98-101
22442156-10	2012	In addition, we found that inhibition of SOD1 expression reversed the effect of ASA.	Aspirin	80-83	superoxide dismutase 1	Homo sapiens	41-45
22406476-8	2012	RESULTS: Aspirin reduced mTOR signaling in CRC cells by inhibiting the mTOR effectors S6K1 and 4E-BP1.	Aspirin	9-16	mechanistic target of rapamycin kinase	Homo sapiens	25-29
22406476-8	2012	RESULTS: Aspirin reduced mTOR signaling in CRC cells by inhibiting the mTOR effectors S6K1 and 4E-BP1.	Aspirin	9-16	mechanistic target of rapamycin kinase	Homo sapiens	71-75
22713036-14	2012	As an example of crystal structure calculation involving a mixture of hydrogen bonding and dispersion interactions, we compute the equilibrium structure of two polymorphs of aspirin (2-acetoxybenzoic acid, C(9)H(8)O(4)) in the P2(1)/c monoclinic structure.	Aspirin	174-181	cyclin dependent kinase inhibitor 1A	Homo sapiens	227-232
22406476-3	2012	We investigated whether aspirin affects adenosine monophosphate-activated protein kinase (AMPK) and mTOR signaling in CRC cells.	Aspirin	24-31	mechanistic target of rapamycin kinase	Homo sapiens	100-104
22406476-10	2012	mTOR was still inhibited by aspirin in CRC cells after siRNA knockdown of AMPKalpha, indicating AMPK-dependent and AMPK-independent mechanisms of aspirin-induced inhibition of mTOR.	Aspirin	28-35	mechanistic target of rapamycin kinase	Homo sapiens	0-4
22343037-7	2012	ASA VI could decrease the levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin 6 (IL-6), but increase IL-10 content (P&lt;0.01, P&lt;0.05).	Aspirin	0-3	interleukin 6	Rattus norvegicus	80-93
22406476-10	2012	mTOR was still inhibited by aspirin in CRC cells after siRNA knockdown of AMPKalpha, indicating AMPK-dependent and AMPK-independent mechanisms of aspirin-induced inhibition of mTOR.	Aspirin	146-153	mechanistic target of rapamycin kinase	Homo sapiens	0-4
22406476-10	2012	mTOR was still inhibited by aspirin in CRC cells after siRNA knockdown of AMPKalpha, indicating AMPK-dependent and AMPK-independent mechanisms of aspirin-induced inhibition of mTOR.	Aspirin	146-153	mechanistic target of rapamycin kinase	Homo sapiens	176-180
22406476-11	2012	Aspirin induced autophagy, a feature of mTOR inhibition.	Aspirin	0-7	mechanistic target of rapamycin kinase	Homo sapiens	40-44
22406476-12	2012	Aspirin and metformin (an activator of AMPK) increased inhibition of mTOR and Akt, as well as autophagy in CRC cells.	Aspirin	0-7	mechanistic target of rapamycin kinase	Homo sapiens	69-73
22406476-12	2012	Aspirin and metformin (an activator of AMPK) increased inhibition of mTOR and Akt, as well as autophagy in CRC cells.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	78-81
22406476-14	2012	CONCLUSIONS: Aspirin is an inhibitor of mTOR and an activator of AMPK, targeting regulators of intracellular energy homeostasis and metabolism.	Aspirin	13-20	mechanistic target of rapamycin kinase	Homo sapiens	40-44
24187901-13	2012	In conclusion, consumption calcium supplement plus low-dose aspirin during pregnancy for 9 weeks in pregnant women at risk for pre-eclampsia resulted in a significant difference serum hs-CRP and increased levels of plasma TAC and total GSH as compared to the placebo group, but could not affect serum insulin levels and HOMA-IR score.	Aspirin	60-67	insulin	Homo sapiens	301-308
22507986-3	2012	We investigated whether acetylation and glycation occur at specific sites in fibrinogen and if competition between glucose and aspirin in binding to fibrinogen occurs.	Aspirin	127-134	fibrinogen beta chain	Homo sapiens	149-159
22507986-5	2012	After incubation of fibrinogen in vitro with aspirin (0.8 mM, 24 h) or glucose (100 mM, 5-10 days), we found 12 modified sites with mass spectrometric techniques.	Aspirin	45-52	fibrinogen beta chain	Homo sapiens	20-30
22449948-4	2012	In addition to RvD1, its aspirin-triggered epimer and RvD1 analogs each dose dependently and effectively activated ALX/FPR2 and GPR32 in GPCR-overexpressing beta-arrestin systems using luminescence and electric cell-substrate impedance sensing.	Aspirin	25-32	formyl peptide receptor 3	Mus musculus	115-118
22231719-3	2012	For example, fenamate NSAIDs potentiate GABA-A receptor function, indomethacin scavenges nitric oxide free radicals, and acetylsalicylic acid inhibits the translocation of NF-kappaB, all of which may contribute to their neuroprotective actions in selected experimental models of stroke.	Aspirin	121-141	nuclear factor kappa B subunit 1	Homo sapiens	172-181
22595111-8	2012	The IL-1beta-induced sVCAM-1 production was not inhibited but rather enhanced by aspirin, a cyclooxygenase (COX) inhibitor.	Aspirin	81-88	interleukin 1 beta	Homo sapiens	4-12
22159558-0	2012	SNX3-dependent regulation of epidermal growth factor receptor (EGFR) trafficking and degradation by aspirin in epidermoid carcinoma (A-431) cells.	Aspirin	100-107	epidermal growth factor receptor	Homo sapiens	29-61
22159558-0	2012	SNX3-dependent regulation of epidermal growth factor receptor (EGFR) trafficking and degradation by aspirin in epidermoid carcinoma (A-431) cells.	Aspirin	100-107	epidermal growth factor receptor	Homo sapiens	63-67
22159558-4	2012	By using an established epidermoid carcinoma cell line (A-431), which overexpresses the epidermal growth factor receptor (EGFR) and transferrin receptor (TfnR), we show that aspirin (1) reduces cell surface expression of EGFR and (2) accumulates endocytosed-EGFR and -TfnR in the early/sorting endosome (ESE).	Aspirin	174-181	epidermal growth factor receptor	Homo sapiens	88-120
22159558-4	2012	By using an established epidermoid carcinoma cell line (A-431), which overexpresses the epidermal growth factor receptor (EGFR) and transferrin receptor (TfnR), we show that aspirin (1) reduces cell surface expression of EGFR and (2) accumulates endocytosed-EGFR and -TfnR in the early/sorting endosome (ESE).	Aspirin	174-181	epidermal growth factor receptor	Homo sapiens	122-126
22159558-4	2012	By using an established epidermoid carcinoma cell line (A-431), which overexpresses the epidermal growth factor receptor (EGFR) and transferrin receptor (TfnR), we show that aspirin (1) reduces cell surface expression of EGFR and (2) accumulates endocytosed-EGFR and -TfnR in the early/sorting endosome (ESE).	Aspirin	174-181	epidermal growth factor receptor	Homo sapiens	221-225
22159558-4	2012	By using an established epidermoid carcinoma cell line (A-431), which overexpresses the epidermal growth factor receptor (EGFR) and transferrin receptor (TfnR), we show that aspirin (1) reduces cell surface expression of EGFR and (2) accumulates endocytosed-EGFR and -TfnR in the early/sorting endosome (ESE).	Aspirin	174-181	epidermal growth factor receptor	Homo sapiens	221-225
22159558-6	2012	This study sheds light on how aspirin may down-regulate surface expression of EGFR by inhibiting/delaying the exit of endocytosed-EGFR from the ESE and recycling of endocytosed-EGFR back to the cell surface.	Aspirin	30-37	epidermal growth factor receptor	Homo sapiens	78-82
22159558-6	2012	This study sheds light on how aspirin may down-regulate surface expression of EGFR by inhibiting/delaying the exit of endocytosed-EGFR from the ESE and recycling of endocytosed-EGFR back to the cell surface.	Aspirin	30-37	epidermal growth factor receptor	Homo sapiens	130-134
22159558-6	2012	This study sheds light on how aspirin may down-regulate surface expression of EGFR by inhibiting/delaying the exit of endocytosed-EGFR from the ESE and recycling of endocytosed-EGFR back to the cell surface.	Aspirin	30-37	epidermal growth factor receptor	Homo sapiens	130-134
22343037-7	2012	ASA VI could decrease the levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin 6 (IL-6), but increase IL-10 content (P&lt;0.01, P&lt;0.05).	Aspirin	0-3	tumor necrosis factor	Rattus norvegicus	36-63
22343037-7	2012	ASA VI could decrease the levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin 6 (IL-6), but increase IL-10 content (P&lt;0.01, P&lt;0.05).	Aspirin	0-3	tumor necrosis factor	Rattus norvegicus	65-74
22343037-7	2012	ASA VI could decrease the levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin 6 (IL-6), but increase IL-10 content (P&lt;0.01, P&lt;0.05).	Aspirin	0-3	interleukin 6	Rattus norvegicus	95-99
22152429-3	2012	In this study we explored the association between polymorphisms in DPCR1 and aspirin-exacerbated respiratory disease (AERD), an asthma phenotype.	Aspirin	77-84	mucin like 3	Homo sapiens	67-72
22860421-1	2012	OBJECTIVE: To investigate whether cyclooxygenase-1 (COX-1) haplotype is associated, with aspirin resistance.	Aspirin	89-96	prostaglandin-endoperoxide synthase 1	Homo sapiens	34-50
22626798-5	2012	RESULTS: A significant decrease in MT, SOD and CAT activities and GSH level and a significant increase in UI, AST, ALT, and ALP activities and LPO level were observed in aspirin treated stomach and duodenum of albino rats.	Aspirin	170-177	catalase	Rattus norvegicus	47-50
22626798-5	2012	RESULTS: A significant decrease in MT, SOD and CAT activities and GSH level and a significant increase in UI, AST, ALT, and ALP activities and LPO level were observed in aspirin treated stomach and duodenum of albino rats.	Aspirin	170-177	solute carrier family 17 member 5	Homo sapiens	110-113
22177087-4	2012	Therefore the present study was taken up to investigate the role of C3435T polymorphism (rs 1045642) of multiple drug resistance-1 (MDR-1) gene with aspirin resistance in stroke patients.	Aspirin	149-156	ATP binding cassette subfamily B member 1	Homo sapiens	104-130
22177087-4	2012	Therefore the present study was taken up to investigate the role of C3435T polymorphism (rs 1045642) of multiple drug resistance-1 (MDR-1) gene with aspirin resistance in stroke patients.	Aspirin	149-156	ATP binding cassette subfamily B member 1	Homo sapiens	132-137
22860421-1	2012	OBJECTIVE: To investigate whether cyclooxygenase-1 (COX-1) haplotype is associated, with aspirin resistance.	Aspirin	89-96	prostaglandin-endoperoxide synthase 1	Homo sapiens	52-57
22860421-7	2012	CONCLUSION: COX-1 haplotype is associated with aspirin resistance in old Chinese Han patients with cardio-cerebrovascular diseases, mutant CGCGCC-haplotype carriers of COX-1 has a significant significantly increased risk of AR.	Aspirin	47-54	prostaglandin-endoperoxide synthase 1	Homo sapiens	12-17
22860421-7	2012	CONCLUSION: COX-1 haplotype is associated with aspirin resistance in old Chinese Han patients with cardio-cerebrovascular diseases, mutant CGCGCC-haplotype carriers of COX-1 has a significant significantly increased risk of AR.	Aspirin	47-54	prostaglandin-endoperoxide synthase 1	Homo sapiens	168-173
22234683-8	2012	We conclude that the abnormal megakaryopoiesis characterizing ET accounts for a shorter-lasting antiplatelet effect of low-dose aspirin through faster renewal of platelet cyclooxygenase-1, and impaired platelet inhibition can be rescued by modulating the aspirin dosing interval rather than the dose.	Aspirin	128-135	prostaglandin-endoperoxide synthase 1	Homo sapiens	171-187
22244860-0	2012	Aspirin prevents resistin-induced endothelial dysfunction by modulating AMPK, ROS, and Akt/eNOS signaling.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	87-90
22969938-0	2012	Aspirin upregulates the expression of neuregulin 1 and survivin after focal cerebral ischemia/reperfusion in rats.	Aspirin	0-7	neuregulin 1	Rattus norvegicus	38-50
22969938-3	2012	Here, we investigated the effect of aspirin on NGR1 and survivin expression after focal cerebral ischemia/reperfusion in rats.	Aspirin	36-43	reticulon 4 receptor	Rattus norvegicus	47-51
22969938-10	2012	In conclusion, the neuroprotective effect of aspirin is at least partly mediated by the upregulation of NGR1 and survivin expression after ischemia.	Aspirin	45-52	reticulon 4 receptor	Rattus norvegicus	104-108
22468095-0	2012	Potential association of DCBLD2 polymorphisms with fall rates of FEV(1) by aspirin provocation in Korean asthmatics.	Aspirin	75-82	discoidin, CUB and LCCL domain containing 2	Homo sapiens	25-31
22238031-6	2012	The Incubation of the normal subject PRP with 5.0 muM inhibitor for 30 min followed by 0.4 muM ADP addition caused platelet aggregation in vitro, 130 muM aspirin or 400 muU insulin/ml addition was able to abrogate 0.4 muM ADP induced platelet aggregation even in the presence of 5.0 muM inhibitor.	Aspirin	154-161	latexin	Homo sapiens	50-53
22366248-9	2012	NOSH-aspirin inhibited ovine COX-1 more than ovine COX-2.	Aspirin	5-12	cytochrome c oxidase I, mitochondrial	Mus musculus	29-34
22261696-2	2012	On account of its association with aspirin exacerbated respiratory disease (AERD), the human discoidin, CUB and LCCL domain containing 2 (DCBLD2) is hypothesized to be a candidate gene for the development of nasal polyps in asthma patients.	Aspirin	35-42	discoidin, CUB and LCCL domain containing 2	Homo sapiens	138-144
21865214-12	2012	In multivariate analysis, LDL-C was the only parameter associated independently with aspirin resistance [odds ratio (OR) 1.04, 95% confidence interval (CI) 1.02-1.06; P=0.004].	Aspirin	85-92	component of oligomeric golgi complex 2	Homo sapiens	26-31
21865214-14	2012	Serum LDL-C level is closely associated with aspirin resistance in NS.	Aspirin	45-52	component of oligomeric golgi complex 2	Homo sapiens	6-11
22245433-4	2012	In this study, Asn(580) was mutated, and the mutant and wild-type COX-2 genes were expressed in COS-1 cells to determine how glycosylation affects the inhibition of COX-2 activity by aspirin, flurbiprofen, ibuprofen, celecoxib, and etoricoxib.	Aspirin	183-190	prostaglandin-endoperoxide synthase 2	Homo sapiens	165-170
22179060-5	2012	We             found that treatment with aspirin inhibited cell growth and induced apoptosis             involving both extrinsic and intrinsic pathways as measured by DNA ladder formation,             alteration in the Bax/Bcl-2 ratio, activation of the caspase activities and related             protein expressions.	Aspirin	41-48	BCL2 associated X, apoptosis regulator	Homo sapiens	220-223
22179060-5	2012	We             found that treatment with aspirin inhibited cell growth and induced apoptosis             involving both extrinsic and intrinsic pathways as measured by DNA ladder formation,             alteration in the Bax/Bcl-2 ratio, activation of the caspase activities and related             protein expressions.	Aspirin	41-48	BCL2 apoptosis regulator	Homo sapiens	224-229
22320344-0	2012	Inactivation of ovine cyclooxygenase-1 by bromoaspirin and aspirin: a quantum chemistry description.	Aspirin	47-54	prostaglandin-endoperoxide synthase 1	Homo sapiens	22-38
22209867-0	2012	Hydrogen sulfide-releasing aspirin suppresses NF-kappaB signaling in estrogen receptor negative breast cancer cells in vitro and in vivo.	Aspirin	27-34	nuclear factor kappa B subunit 1	Homo sapiens	46-55
22252409-7	2012	Decreased risks were found among women who used aspirin continuously (0.71 [0.54-0.94]) or at a low-standardized daily dose (0.72 [0.53-0.97]), who used aspirin for the prevention of cardiovascular disease (0.72 [0.57-0.97]), who used aspirin more recently, or who used selective cyclooxygenase-2 inhibitors (0.60 [0.39-0.94]).	Aspirin	48-55	prostaglandin-endoperoxide synthase 2	Homo sapiens	280-296
22306536-8	2012	Similarly to losartan, ASA, and its SA moiety suppressed Ang II-mediated AT1R transcription and fibroblast proliferation as well as expression of collagens and MMPs.	Aspirin	23-26	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	57-63
22306536-9	2012	ASA also suppressed the expression of NADPH oxidase subunits (p22(phox), p47(phox), p67(phox), NOX2 and NOX4) and ROS generation.	Aspirin	0-3	dynein cytoplasmic 1 heavy chain 1	Mus musculus	62-65
22306536-9	2012	ASA also suppressed the expression of NADPH oxidase subunits (p22(phox), p47(phox), p67(phox), NOX2 and NOX4) and ROS generation.	Aspirin	0-3	NSFL1 (p97) cofactor (p47)	Mus musculus	73-76
22306536-11	2012	These observations suggest that ASA inhibits Ang II-induced NADPH oxidase expression, NF-kappaB activation and AT1R transcription in cardiac fibroblasts, and fibroblast proliferation and collagen expression.	Aspirin	32-35	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	45-51
22792718-2	2012	The rat globin can be modified with acetylsalicylic acid on aminoacid residues K-17, K-57, K-91, K-140 in alpha subunit as well as on K-18, K-77 in beta subunit.	Aspirin	36-56	keratin 17	Rattus norvegicus	79-83
22306536-4	2012	In this study, we examined if ASA would inhibit NADPH oxidase activation, upregulation of AT1R transcription, and subsequent collagen generation in mouse cardiac fibroblasts challenged with Ang II.	Aspirin	30-33	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	190-196
22431874-0	2012	Vascular endothelial growth factor expression in nasal polyps of aspirin-intolerant patients.	Aspirin	65-72	vascular endothelial growth factor A	Homo sapiens	0-34
22431874-1	2012	OBJECTIVE: To study differences between aspirin-tolerant patients and aspirin-intolerant patients concerning vascular endothelial growth factor (VEGF) expression.	Aspirin	40-47	vascular endothelial growth factor A	Homo sapiens	109-143
22431874-1	2012	OBJECTIVE: To study differences between aspirin-tolerant patients and aspirin-intolerant patients concerning vascular endothelial growth factor (VEGF) expression.	Aspirin	40-47	vascular endothelial growth factor A	Homo sapiens	145-149
22431874-1	2012	OBJECTIVE: To study differences between aspirin-tolerant patients and aspirin-intolerant patients concerning vascular endothelial growth factor (VEGF) expression.	Aspirin	70-77	vascular endothelial growth factor A	Homo sapiens	109-143
22431874-1	2012	OBJECTIVE: To study differences between aspirin-tolerant patients and aspirin-intolerant patients concerning vascular endothelial growth factor (VEGF) expression.	Aspirin	70-77	vascular endothelial growth factor A	Homo sapiens	145-149
22431874-10	2012	RESULTS: We found higher expressed levels of VEGF and neuropilin and stronger proliferation in nasal polyps from aspirin-tolerant and aspirin-intolerant patients compared with controls.	Aspirin	113-120	vascular endothelial growth factor A	Homo sapiens	45-49
22431874-10	2012	RESULTS: We found higher expressed levels of VEGF and neuropilin and stronger proliferation in nasal polyps from aspirin-tolerant and aspirin-intolerant patients compared with controls.	Aspirin	134-141	vascular endothelial growth factor A	Homo sapiens	45-49
22431874-11	2012	In polyps from aspirin-intolerant patients, VEGF was expressed at considerably higher levels compared with those from aspirin-tolerant subjects.	Aspirin	15-22	vascular endothelial growth factor A	Homo sapiens	44-48
22431874-13	2012	CONCLUSIONS: Nasal polyps from aspirin-tolerant and aspirin-intolerant patients are characterized by strong proliferation and high levels of VEGF and neuropilin expression.	Aspirin	31-38	vascular endothelial growth factor A	Homo sapiens	141-145
22431874-13	2012	CONCLUSIONS: Nasal polyps from aspirin-tolerant and aspirin-intolerant patients are characterized by strong proliferation and high levels of VEGF and neuropilin expression.	Aspirin	52-59	vascular endothelial growth factor A	Homo sapiens	141-145
22431874-14	2012	Nasal polyps from aspirin-intolerant patients show distinctly increased VEGF levels.	Aspirin	18-25	vascular endothelial growth factor A	Homo sapiens	72-76
22252409-7	2012	Decreased risks were found among women who used aspirin continuously (0.71 [0.54-0.94]) or at a low-standardized daily dose (0.72 [0.53-0.97]), who used aspirin for the prevention of cardiovascular disease (0.72 [0.57-0.97]), who used aspirin more recently, or who used selective cyclooxygenase-2 inhibitors (0.60 [0.39-0.94]).	Aspirin	153-160	prostaglandin-endoperoxide synthase 2	Homo sapiens	280-296
22252409-7	2012	Decreased risks were found among women who used aspirin continuously (0.71 [0.54-0.94]) or at a low-standardized daily dose (0.72 [0.53-0.97]), who used aspirin for the prevention of cardiovascular disease (0.72 [0.57-0.97]), who used aspirin more recently, or who used selective cyclooxygenase-2 inhibitors (0.60 [0.39-0.94]).	Aspirin	153-160	prostaglandin-endoperoxide synthase 2	Homo sapiens	280-296
22311905-0	2012	Suboptimal inhibition of platelet cyclooxygenase-1 by aspirin in metabolic syndrome.	Aspirin	54-61	prostaglandin-endoperoxide synthase 1	Homo sapiens	34-50
22100881-0	2012	Para-NO-aspirin inhibits NF-kappaB and induces apoptosis in B-cell progenitor acute lymphoblastic leukemia.	Aspirin	8-15	nuclear factor kappa B subunit 1	Homo sapiens	25-34
22100881-4	2012	Para-NO-ASA induced cell death in the pre-B ALL cell lines in association with increased reactive oxygen species, and suppression of nuclear factor-kappaB (NF-kappaB) activity.	Aspirin	8-11	nuclear factor kappa B subunit 1	Homo sapiens	133-154
22100881-4	2012	Para-NO-ASA induced cell death in the pre-B ALL cell lines in association with increased reactive oxygen species, and suppression of nuclear factor-kappaB (NF-kappaB) activity.	Aspirin	8-11	nuclear factor kappa B subunit 1	Homo sapiens	156-165
22100881-5	2012	Chemical inhibitors of NF-kappaB similarly induced apoptosis in ALL cells, suggesting a role for suppression of NF-kappaB in para-NO-ASA-induced cell death.	Aspirin	133-136	nuclear factor kappa B subunit 1	Homo sapiens	23-32
22100881-5	2012	Chemical inhibitors of NF-kappaB similarly induced apoptosis in ALL cells, suggesting a role for suppression of NF-kappaB in para-NO-ASA-induced cell death.	Aspirin	133-136	nuclear factor kappa B subunit 1	Homo sapiens	112-121
22100881-7	2012	Our results demonstrate that para-NO-ASA potently induces apoptosis in B-lineage ALL cells via a reactive oxygen species-dependent mechanism that is associated with suppression of NF-kappaB activity.	Aspirin	37-40	nuclear factor kappa B subunit 1	Homo sapiens	180-189
22311905-1	2012	Interindividual variation in the ability of aspirin to inhibit platelet cyclooxygenase-1 (COX-1) could account for some on-treatment cardiovascular events.	Aspirin	44-51	prostaglandin-endoperoxide synthase 1	Homo sapiens	72-88
22311905-1	2012	Interindividual variation in the ability of aspirin to inhibit platelet cyclooxygenase-1 (COX-1) could account for some on-treatment cardiovascular events.	Aspirin	44-51	prostaglandin-endoperoxide synthase 1	Homo sapiens	90-95
22311905-3	2012	In a prospective, 2-week study, we evaluated the effect of aspirin (81 mg) on platelet COX-1 in 135 patients with stable coronary artery disease by measuring serum thromboxane B(2) (sTxB(2)) as an indicator of inhibition of platelet COX-1.	Aspirin	59-66	prostaglandin-endoperoxide synthase 1	Homo sapiens	87-92
22311905-11	2012	In conclusion, metabolic syndrome, which places patients at high risk for thrombotic cardiovascular events, strongly and uniquely associates with less effective inhibition of platelet COX-1 by aspirin.	Aspirin	193-200	prostaglandin-endoperoxide synthase 1	Homo sapiens	184-189
22223808-8	2012	Suppression of jasmonate signalling by phenidone or aspirin blocks the induction of JAZ/TIFY transcripts.	Aspirin	52-59	zinc finger protein 346	Homo sapiens	84-87
21670957-0	2012	Association of FANCC polymorphisms with FEV1 decline in aspirin exacerbated respiratory disease.	Aspirin	56-63	Fanconi anemia, complementation group C	Mus musculus	15-20
21670957-5	2012	However, the FEV1 decline by aspirin provocation showed significant associations with FANCC polymorphisms (P = 0.006-0.04) and a haplotype (unique to rs4647416G &gt; A, P = 0.01 under co-dominant, P = 0.006 under recessive model).	Aspirin	29-36	Fanconi anemia, complementation group C	Mus musculus	86-91
22171557-8	2012	It was found that acute doses of aspirin caused increases on the levels of NMDAR 2A (NR2A) receptors and malondialdehyde (MDA), the end product of lipid peroxidation.	Aspirin	33-40	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	75-83
22306773-13	2012	Also the up-regulation of Bcl-2, HO-1 and XIAP induced by 5mM Glu/BSO were all attenuated to a greater extent by ACS14 (20 muM) than aspirin (20 muM).	Aspirin	133-140	B cell leukemia/lymphoma 2	Mus musculus	26-31
22306773-13	2012	Also the up-regulation of Bcl-2, HO-1 and XIAP induced by 5mM Glu/BSO were all attenuated to a greater extent by ACS14 (20 muM) than aspirin (20 muM).	Aspirin	133-140	heme oxygenase 1	Mus musculus	33-37
21692746-7	2012	Intratumoral administration of aspirin was accompanied by alterations in the biophysical, biochemical and immunological composition of the tumour microenvironment with respect to pH, level of dissolved O2, glucose, lactate, nitric oxide, IFNgamma (interferon gamma), IL-4 (interleukin-4), IL-6 and IL-10, whereas the TGF-beta (tumour growth factor-beta) level was unaltered.	Aspirin	31-38	interferon gamma	Mus musculus	238-246
21692746-7	2012	Intratumoral administration of aspirin was accompanied by alterations in the biophysical, biochemical and immunological composition of the tumour microenvironment with respect to pH, level of dissolved O2, glucose, lactate, nitric oxide, IFNgamma (interferon gamma), IL-4 (interleukin-4), IL-6 and IL-10, whereas the TGF-beta (tumour growth factor-beta) level was unaltered.	Aspirin	31-38	interferon gamma	Mus musculus	248-264
21692746-7	2012	Intratumoral administration of aspirin was accompanied by alterations in the biophysical, biochemical and immunological composition of the tumour microenvironment with respect to pH, level of dissolved O2, glucose, lactate, nitric oxide, IFNgamma (interferon gamma), IL-4 (interleukin-4), IL-6 and IL-10, whereas the TGF-beta (tumour growth factor-beta) level was unaltered.	Aspirin	31-38	interleukin 6	Mus musculus	289-293
21692746-7	2012	Intratumoral administration of aspirin was accompanied by alterations in the biophysical, biochemical and immunological composition of the tumour microenvironment with respect to pH, level of dissolved O2, glucose, lactate, nitric oxide, IFNgamma (interferon gamma), IL-4 (interleukin-4), IL-6 and IL-10, whereas the TGF-beta (tumour growth factor-beta) level was unaltered.	Aspirin	31-38	interleukin 10	Mus musculus	298-303
22240749-6	2012	Pretreatment with ASA and salicylic acid prevented changes in adherence junction proteins and inhibited VEGF-induced tube formation by HUVECs in a dose-dependent manner.	Aspirin	18-21	vascular endothelial growth factor A	Homo sapiens	104-108
21692746-8	2012	Tumour cells obtained from aspirin-treated tumour-bearing mice demonstrated an altered expression of pH regulators monocarboxylate transporter-1 and V-ATPase along with alteration in the level of cell survival regulatory molecules such as survivin, vascular endothelial growth factor, heat-shock protein 70, glucose transporter-1, SOCS-5 (suppressor of cytokine signalling-5), HIF-1alpha (hypoxia-inducible factor-1alpha) and PUMA (p53 up-regulated modulator of apoptosis).	Aspirin	27-34	solute carrier family 16 (monocarboxylic acid transporters), member 1	Mus musculus	115-144
21692746-8	2012	Tumour cells obtained from aspirin-treated tumour-bearing mice demonstrated an altered expression of pH regulators monocarboxylate transporter-1 and V-ATPase along with alteration in the level of cell survival regulatory molecules such as survivin, vascular endothelial growth factor, heat-shock protein 70, glucose transporter-1, SOCS-5 (suppressor of cytokine signalling-5), HIF-1alpha (hypoxia-inducible factor-1alpha) and PUMA (p53 up-regulated modulator of apoptosis).	Aspirin	27-34	suppressor of cytokine signaling 5	Mus musculus	331-337
21692746-8	2012	Tumour cells obtained from aspirin-treated tumour-bearing mice demonstrated an altered expression of pH regulators monocarboxylate transporter-1 and V-ATPase along with alteration in the level of cell survival regulatory molecules such as survivin, vascular endothelial growth factor, heat-shock protein 70, glucose transporter-1, SOCS-5 (suppressor of cytokine signalling-5), HIF-1alpha (hypoxia-inducible factor-1alpha) and PUMA (p53 up-regulated modulator of apoptosis).	Aspirin	27-34	suppressor of cytokine signaling 5	Mus musculus	339-374
22171557-8	2012	It was found that acute doses of aspirin caused increases on the levels of NMDAR 2A (NR2A) receptors and malondialdehyde (MDA), the end product of lipid peroxidation.	Aspirin	33-40	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	85-89
22171557-11	2012	In conclusion, lipid peroxidation, caused by acute doses of aspirin may lead to excitotoxicity effects by a hippocampal NR2A-mediated mechanism.	Aspirin	60-67	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	120-124
22217332-1	2012	BACKGROUND: Since subepithelial fibrosis and protruded extracellular matrix are among the histological characteristics of polyps, the emilin/multimerin domain-containing protein 2 (EMID2) gene is speculated to be involved in the presence of nasal polyps in asthma and aspirin-hypersensitive patients.	Aspirin	268-275	collagen type XXVI alpha 1 chain	Homo sapiens	134-179
21035882-5	2012	RESULTS: Subjects (n=28) with pretreatment TXB(2) concentrations in the highest quartile ("aspirin-resistant patients") were more frequently current smokers and had elevated C-reactive protein (CRP), interleukin-6, 8-isoprostane, shorter bleeding time, and increased F1.2 production in a model of microvascular injury, when compared with the 3 remaining quartiles (all, p&lt;0.001).	Aspirin	91-98	C-reactive protein	Homo sapiens	174-192
21035882-5	2012	RESULTS: Subjects (n=28) with pretreatment TXB(2) concentrations in the highest quartile ("aspirin-resistant patients") were more frequently current smokers and had elevated C-reactive protein (CRP), interleukin-6, 8-isoprostane, shorter bleeding time, and increased F1.2 production in a model of microvascular injury, when compared with the 3 remaining quartiles (all, p&lt;0.001).	Aspirin	91-98	C-reactive protein	Homo sapiens	194-197
22217332-1	2012	BACKGROUND: Since subepithelial fibrosis and protruded extracellular matrix are among the histological characteristics of polyps, the emilin/multimerin domain-containing protein 2 (EMID2) gene is speculated to be involved in the presence of nasal polyps in asthma and aspirin-hypersensitive patients.	Aspirin	268-275	collagen type XXVI alpha 1 chain	Homo sapiens	181-186
23317278-6	2012	In addition, the combination of exemestane and aspirin exhibited a synergistic inhibition of cell proliferation, significantly arrested the cell cycle in the G0/G1 phase and produced a stronger inhibitory effect on COX-1 and Bcl-2 expression than control or individual drug treatment.	Aspirin	47-54	BCL2 apoptosis regulator	Homo sapiens	225-230
22095955-0	2012	Aspirin analogues as dual cyclooxygenase-2/5-lipoxygenase inhibitors: synthesis, nitric oxide release, molecular modeling, and biological evaluation as anti-inflammatory agents.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	26-42
22095955-0	2012	Aspirin analogues as dual cyclooxygenase-2/5-lipoxygenase inhibitors: synthesis, nitric oxide release, molecular modeling, and biological evaluation as anti-inflammatory agents.	Aspirin	0-7	arachidonate 5-lipoxygenase	Homo sapiens	43-57
23316227-10	2012	HNF-1a domain interacted most closely with resveratrol and aspirin.	Aspirin	59-66	HNF1 homeobox A	Homo sapiens	0-6
23057161-7	2012	Dendritic cell modification by aspirin, dexamethasone and VD3 were all associated with decreased production of tumour necrosis factor-alpha (TNFalpha).	Aspirin	31-38	tumor necrosis factor	Homo sapiens	141-149
23057161-9	2012	Aspirin-, dexamethasone- VD3- and butyric acid-modified DCs suppressed interferon-gamma production, proliferation and cytotoxicity in co-culture with allogeneic mononuclear cells, but inconsistent results were obtained with different allogeneic combinations.	Aspirin	0-7	interferon gamma	Homo sapiens	71-87
23042313-8	2012	In our study in patients with T2DM, platelet reactivity on ASA therapy measured with VerifyNow( ) was associated with TNF-alpha concentrations and statin therapy.	Aspirin	59-62	tumor necrosis factor	Homo sapiens	118-127
22538532-2	2012	However, a recent animal study found a vasodilating and blood pressure lowering effect of aspirin independent of COX, but mediated by inhibition of the RhoA/Rho kinase signaling pathway.	Aspirin	90-97	ras homolog family member A	Homo sapiens	152-156
22681482-0	2012	What is the relationship between effects of aspirin, statins, and C-reactive protein?	Aspirin	44-51	C-reactive protein	Homo sapiens	66-84
22724411-2	2012	Antiplatelet therapy for primary and secondary prevention of thromboembolic events is a cornerstone for the management of these patients and for many years the cyclooxygenase-1 (COX-1) inhibitor aspirin and the second generation thienopyridine clopidogrel which targets the ADP P2Y12 receptor on platelets served as the main antiplatelet agents for these indications.	Aspirin	195-202	prostaglandin-endoperoxide synthase 1	Homo sapiens	160-176
22724411-2	2012	Antiplatelet therapy for primary and secondary prevention of thromboembolic events is a cornerstone for the management of these patients and for many years the cyclooxygenase-1 (COX-1) inhibitor aspirin and the second generation thienopyridine clopidogrel which targets the ADP P2Y12 receptor on platelets served as the main antiplatelet agents for these indications.	Aspirin	195-202	prostaglandin-endoperoxide synthase 1	Homo sapiens	178-183
23101307-7	2012	In addition, a significant association was found when the (CCTTT) repetition of the NOS2A gene was present more than 14 times in patients with NP and asthma (P = .034), in patients with polyposis and intolerance to nonsteroidal anti-inflammatory drugs (P = .009), and in patients with the aspirin triad (P = .005).	Aspirin	289-296	nitric oxide synthase 2	Homo sapiens	84-89
22132000-0	2012	The IL1B-511 Polymorphism (rs16944 AA Genotype) Is Increased in Aspirin-Exacerbated Respiratory Disease in Mexican Population.	Aspirin	64-71	interleukin 1 beta	Homo sapiens	4-8
22132000-4	2012	We performed a genetic association study between IL8-251 (rs4073) and IL1B-511 (rs16944) polymorphisms in AERD, aspirin-tolerant asthma (ATA), and healthy control subjects.	Aspirin	112-119	C-X-C motif chemokine ligand 8	Homo sapiens	49-52
22132000-4	2012	We performed a genetic association study between IL8-251 (rs4073) and IL1B-511 (rs16944) polymorphisms in AERD, aspirin-tolerant asthma (ATA), and healthy control subjects.	Aspirin	112-119	interleukin 1 beta	Homo sapiens	70-74
22262978-0	2012	Interleukin-4 in the Generation of the AERD Phenotype: Implications for Molecular Mechanisms Driving Therapeutic Benefit of Aspirin Desensitization.	Aspirin	124-131	interleukin 4	Homo sapiens	0-13
22262978-1	2012	Aspirin-exacerbated respiratory disease (AERD) is explained in part by over-expression of 5-lipoxygenase, leukotriene C4 synthase (LTC(4)S) and the cysteinyl leukotriene (CysLT) receptors (CysLT1 and 2), resulting in constitutive over-production of CysLTs and the hyperresponsiveness to CysLTs that occurs with aspirin ingestion.	Aspirin	0-7	arachidonate 5-lipoxygenase	Homo sapiens	90-104
22262978-1	2012	Aspirin-exacerbated respiratory disease (AERD) is explained in part by over-expression of 5-lipoxygenase, leukotriene C4 synthase (LTC(4)S) and the cysteinyl leukotriene (CysLT) receptors (CysLT1 and 2), resulting in constitutive over-production of CysLTs and the hyperresponsiveness to CysLTs that occurs with aspirin ingestion.	Aspirin	311-318	arachidonate 5-lipoxygenase	Homo sapiens	90-104
23251150-0	2012	A molecular dynamics approach to ligand-receptor interaction in the aspirin-human serum albumin complex.	Aspirin	68-75	albumin	Homo sapiens	82-95
23251150-1	2012	In this work, we present a study of the interaction between human serum albumin (HSA) and acetylsalicylic acid (ASA, C(9)H(8)O(4)) by molecular dynamics simulations (MD).	Aspirin	90-110	albumin	Homo sapiens	66-79
23251150-1	2012	In this work, we present a study of the interaction between human serum albumin (HSA) and acetylsalicylic acid (ASA, C(9)H(8)O(4)) by molecular dynamics simulations (MD).	Aspirin	112-115	albumin	Homo sapiens	66-79
22652554-0	2012	Effect of genetic polymorphism of ALOX15 on aspirin-exacerbated respiratory disease.	Aspirin	44-51	arachidonate 15-lipoxygenase	Homo sapiens	34-40
21360558-0	2012	Effects of acetyl salycilic acid and ibuprofen in chronic liver damage induced by CCl4.	Aspirin	11-32	C-C motif chemokine ligand 4	Rattus norvegicus	82-86
22429367-10	2012	CONCLUSIONS: TEG-AA was more sensitive, specific and consistent than the P-selectin assay for detecting aspirin resistance, and the PTGS2 G765C mutation may be related to aspirin resistance.	Aspirin	171-178	prostaglandin-endoperoxide synthase 2	Homo sapiens	132-137
23166597-5	2012	Moreover, M344-mediated activation of the latent HIV LTR can be strongly inhibited by a NF-kappaB inhibitor aspirin.	Aspirin	108-115	nuclear factor kappa B subunit 1	Homo sapiens	88-97
21584653-5	2012	The neuroprotective effect of ASA was attributed to the inhibition of microglial activation because of its observed inhibitory effects on LPS-stimulated nitric oxide, tumor necrosis factor-alpha, and superoxide production by microglial cells.	Aspirin	30-33	tumor necrosis factor	Homo sapiens	167-194
21584653-6	2012	Moreover, ASA increased the production of the anti-inflammatory cytokines transforming growth factor beta-1 and interleukin-10 in neuron-glia cultures after stimulation with LPS.	Aspirin	10-13	transforming growth factor beta 1	Homo sapiens	74-107
21584653-7	2012	Mechanistic studies revealed that the neuroprotective effects of ASA were mediated through the inhibition of nicotinamide adenine dinucleotide phosphate oxidase (PHOX), a key enzyme for superoxide production in microglia.	Aspirin	65-68	dual oxidase 2	Homo sapiens	109-160
22001128-4	2012	Since safe aspirin regimens can only achieve a partial and transitory inhibition of cox-2, it may be feasible to complement the cancer-protective benefit of aspirin with other measures which decrease cox-2 expression or which limit the bioactivity of cox-2-derived PGE2.	Aspirin	11-18	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	84-89
22070887-4	2012	Based on this fact, we hypothesize that aspirin, in addition to its anti-inflammatory effect, may also specifically inhibit autoimmune response in atherosclerosis by actively increasing CD4+CD25+FOXP3+Treg cells as well as by inducing tolerogenic DCs which induce hyporesponsiveness in responder naive T cells.	Aspirin	40-47	CD4 molecule	Homo sapiens	186-189
22075236-1	2012	BACKGROUND/OBJECTIVES: ACC/AHA/SCAI recommendations include dual anti-platelet therapy (aspirin and clopidogrel) for 12 months after drug-eluting stent percutaneous coronary intervention (DES PCI).	Aspirin	88-95	suppressor of cancer cell invasion	Homo sapiens	31-35
23110215-5	2012	Aspirin induced nuclear caspase-dependent cleavage of Sp1, Sp3 and Sp4 proteins and this response was related to sequestration of zinc ions since addition of zinc sulfate blocked aspirin-mediated apoptosis and repression of Sp proteins.	Aspirin	0-7	Sp3 transcription factor	Homo sapiens	59-62
23029468-10	2012	ACS14 also obviously inhibited Asp-induced upregulation of protein expression of oxidases including XOD, p47(phox) and p67(phox).	Aspirin	31-34	NSFL1 cofactor	Rattus norvegicus	105-108
23240010-0	2012	Signal transduction pathways (MAPKs, NF-kappaB, and C/EBP) regulating COX-2 expression in nasal fibroblasts from asthma patients with aspirin intolerance.	Aspirin	134-141	CCAAT enhancer binding protein alpha	Homo sapiens	52-57
22393298-6	2012	The residual risk can be attributed to the fact that aspirin and P2Y(12) inhibitors block only the thromboxane A(2) and ADP platelet activation pathways but do not affect the other pathways that lead to thrombosis, such as the protease-activated receptor-1 pathway stimulated by thrombin, the most potent platelet agonist.	Aspirin	53-60	coagulation factor II thrombin receptor	Homo sapiens	227-256
23240010-0	2012	Signal transduction pathways (MAPKs, NF-kappaB, and C/EBP) regulating COX-2 expression in nasal fibroblasts from asthma patients with aspirin intolerance.	Aspirin	134-141	prostaglandin-endoperoxide synthase 2	Homo sapiens	70-75
23240010-1	2012	BACKGROUND: Recent studies have revealed that cyclooxygenase-2 (COX-2) expression is down-regulated in aspirin-induced asthma (AIA).	Aspirin	103-110	prostaglandin-endoperoxide synthase 2	Homo sapiens	46-62
23240010-1	2012	BACKGROUND: Recent studies have revealed that cyclooxygenase-2 (COX-2) expression is down-regulated in aspirin-induced asthma (AIA).	Aspirin	103-110	prostaglandin-endoperoxide synthase 2	Homo sapiens	64-69
23240010-3	2012	OBJECTIVE: To investigate the regulation of COX-2 expression through MAP-kinase pathway activation and nuclear factor translocation in aspirin-induced asthma (AIA).	Aspirin	135-142	prostaglandin-endoperoxide synthase 2	Homo sapiens	44-49
22615972-8	2012	Two SNPs in TXNRD1 and four SNPs in TXNRD2 interacted with aspirin/NSAID to influence colon cancer; one SNP in TXNRD1, two SNPs in TXNRD2, and one SNP in TXNRD3 interacted with aspirin/NSAIDs to influence rectal cancer.	Aspirin	59-66	thioredoxin reductase 2	Homo sapiens	36-42
22615972-8	2012	Two SNPs in TXNRD1 and four SNPs in TXNRD2 interacted with aspirin/NSAID to influence colon cancer; one SNP in TXNRD1, two SNPs in TXNRD2, and one SNP in TXNRD3 interacted with aspirin/NSAIDs to influence rectal cancer.	Aspirin	177-184	thioredoxin reductase 2	Homo sapiens	36-42
22952917-5	2012	When stimulated with whole sperm cells, the PBMCs from patients with ASA produce less IL-3, IL-11, IL-13, ICAM-1, GCSF and more IL-2, IL-4 and IL-12p70 as compared to healthy women.	Aspirin	69-72	interleukin 13	Homo sapiens	99-104
22952917-5	2012	When stimulated with whole sperm cells, the PBMCs from patients with ASA produce less IL-3, IL-11, IL-13, ICAM-1, GCSF and more IL-2, IL-4 and IL-12p70 as compared to healthy women.	Aspirin	69-72	interleukin 2	Homo sapiens	128-132
22952917-5	2012	When stimulated with whole sperm cells, the PBMCs from patients with ASA produce less IL-3, IL-11, IL-13, ICAM-1, GCSF and more IL-2, IL-4 and IL-12p70 as compared to healthy women.	Aspirin	69-72	interleukin 4	Homo sapiens	134-138
22952917-6	2012	PBMCs from patients with ASA produce typically less IL-13, IL-7, IL-17 and MIG, and more MIP-1beta and IL-8, as compared to PBMCs from patients without ASA.	Aspirin	25-28	interleukin 13	Homo sapiens	52-57
22952917-6	2012	PBMCs from patients with ASA produce typically less IL-13, IL-7, IL-17 and MIG, and more MIP-1beta and IL-8, as compared to PBMCs from patients without ASA.	Aspirin	25-28	interleukin 7	Homo sapiens	59-63
22952917-6	2012	PBMCs from patients with ASA produce typically less IL-13, IL-7, IL-17 and MIG, and more MIP-1beta and IL-8, as compared to PBMCs from patients without ASA.	Aspirin	25-28	C-X-C motif chemokine ligand 8	Homo sapiens	103-107
22662117-11	2012	Similar effects were observed in aspirin-treated ApoE(-/-) mice.	Aspirin	33-40	apolipoprotein E	Mus musculus	49-53
22654634-3	2012	MTT spectrophotometry results showed that 20, 100, and 1000 muM aspirin doses have an inhibitory effect on growth.	Aspirin	64-71	latexin	Homo sapiens	60-63
22654634-4	2012	Cell cycle analysis revealed that aspirin doses of 100 and 1000 muM arrest the cell cycle in phase GO/G1.	Aspirin	34-41	latexin	Homo sapiens	64-67
22654634-6	2012	We highlight that treatment of osteoblast-like cells with 1000 muM aspirin increased not only the percentage of cells in apoptosis but also the percentage of necrotic cells, which was not observed in aspirin treatments at lower doses.	Aspirin	67-74	latexin	Homo sapiens	63-66
22654634-6	2012	We highlight that treatment of osteoblast-like cells with 1000 muM aspirin increased not only the percentage of cells in apoptosis but also the percentage of necrotic cells, which was not observed in aspirin treatments at lower doses.	Aspirin	200-207	latexin	Homo sapiens	63-66
22393298-6	2012	The residual risk can be attributed to the fact that aspirin and P2Y(12) inhibitors block only the thromboxane A(2) and ADP platelet activation pathways but do not affect the other pathways that lead to thrombosis, such as the protease-activated receptor-1 pathway stimulated by thrombin, the most potent platelet agonist.	Aspirin	53-60	coagulation factor II, thrombin	Homo sapiens	279-287
21995892-0	2011	Interaction of aspirin and vitamin C with bovine serum albumin.	Aspirin	15-22	albumin	Homo sapiens	49-62
21995892-4	2011	In this report, the competitive binding of vitamin C and aspirin to bovine serum albumin has been studied using constant protein concentration and various drug concentrations at pH 7.2.	Aspirin	57-64	albumin	Homo sapiens	75-88
21862721-0	2011	Aspirin reduces hypertriglyceridemia by lowering VLDL-triglyceride production in mice fed a high-fat diet.	Aspirin	0-7	CD320 antigen	Mus musculus	49-53
21862721-6	2011	This TG-lowering effect could not be explained by enhanced VLDL-TG clearance, but aspirin selectively reduced hepatic production of VLDL-TG in both APOC1 (-28%, P &lt; 0.05) and WT mice (-33%, P &lt; 0.05) without affecting VLDL-apoB production.	Aspirin	82-89	CD320 antigen	Mus musculus	132-136
21862721-6	2011	This TG-lowering effect could not be explained by enhanced VLDL-TG clearance, but aspirin selectively reduced hepatic production of VLDL-TG in both APOC1 (-28%, P &lt; 0.05) and WT mice (-33%, P &lt; 0.05) without affecting VLDL-apoB production.	Aspirin	82-89	CD320 antigen	Mus musculus	132-136
21862721-7	2011	Aspirin did not alter hepatic expression of genes involved in FA oxidation, lipogenesis, and VLDL production but decreased the incorporation of plasma-derived FA by the liver into VLDL-TG (-24%, P &lt; 0.05), which was independent of hepatic expression of genes involved in FA uptake and transport.	Aspirin	0-7	CD320 antigen	Mus musculus	180-184
21862721-8	2011	We conclude that aspirin improves hypertriglyceridemia by decreasing VLDL-TG production without affecting VLDL particle production.	Aspirin	17-24	CD320 antigen	Mus musculus	69-73
21712098-9	2011	The biosynthesis and formation of both 18S and 18R-series are enhanced with aspirin treatment and involve the utilization of dietary EPA as well as recombinant human 5-lipoxygenase and LTA(4) hydrolase in their stereospecific biosynthesis.	Aspirin	76-83	arachidonate 5-lipoxygenase	Homo sapiens	166-180
22123380-0	2011	IL-13 and IL-17A gene polymorphisms in Japanese patients with aspirin-exacerbated respiratory disease.	Aspirin	62-69	interleukin 13	Homo sapiens	0-5
21728052-2	2011	Aspirin and NSAIDs inhibit COX-2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	27-32
21728052-13	2011	The RR(95% CI) of breast cancer death for current aspirin use was similar for women with COX-2-positive and COX-2-negative tumors; 0.64 (0.43-0.96) and 0.57 (0.44-0.74), respectively.	Aspirin	50-57	prostaglandin-endoperoxide synthase 2	Homo sapiens	89-94
21728052-13	2011	The RR(95% CI) of breast cancer death for current aspirin use was similar for women with COX-2-positive and COX-2-negative tumors; 0.64 (0.43-0.96) and 0.57 (0.44-0.74), respectively.	Aspirin	50-57	prostaglandin-endoperoxide synthase 2	Homo sapiens	108-113
21728052-17	2011	If aspirin truly impacts breast cancer survival, then it is not solely via COX-2.	Aspirin	3-10	prostaglandin-endoperoxide synthase 2	Homo sapiens	75-80
21078615-0	2011	An anti-von Willebrand factor aptamer reduces platelet adhesion among patients receiving aspirin and clopidogrel in an ex vivo shear-induced arterial thrombosis.	Aspirin	89-96	von Willebrand factor	Homo sapiens	8-29
22395372-8	2012	In multivariate regression analysis, only fibrinogen level (OR=1.063, p=0.010) and pulse pressure (OR=1.197, p=0.023) were found to be independent indicators of aspirin resistance and PAI.	Aspirin	161-168	fibrinogen beta chain	Homo sapiens	42-52
22395372-9	2012	In ROC analysis, cut-off values of 50 mmHg for pulse pressure and 400 mg/dl for fibrinogen level predicted aspirin resistance with 88.9% and 74% sensitivity and 64.4% and 68% specificity, respectively.	Aspirin	107-114	fibrinogen beta chain	Homo sapiens	80-90
22395372-10	2012	CONCLUSION: Our findings suggest that measurements of fibrinogen level and pulse pressure may be used as easy and reliable methods in predicting aspirin resistance.	Aspirin	145-152	fibrinogen beta chain	Homo sapiens	54-64
21564085-8	2011	FXR(-/-) mice were more prone to develop severe gastric and intestinal injury in response to ASA and NSAIDs and showed a severe reduction in the gastrointestinal expression of cystathionine-gamma-lyase (CSE), an enzyme required for generation of hydrogen sulphide.	Aspirin	93-96	nuclear receptor subfamily 1, group H, member 4	Mus musculus	0-3
21564085-13	2011	FXR agonists protected against gastric injury caused by ASA and NSAIDs by a CSE-mediated mechanism.	Aspirin	56-59	nuclear receptor subfamily 1, group H, member 4	Mus musculus	0-3
22172261-6	2011	IVIG and aspirin treatment significantly reduced plasma TNF-alpha and hs-CRP concentrations.	Aspirin	9-16	tumor necrosis factor	Homo sapiens	56-65
22172261-8	2011	CONCLUSIONS: IVIG and aspirin treatment can improve the functions of circulating EPCs, possibly through reducing plasma concentrations of TNF-alpha and hs-CRP.	Aspirin	22-29	tumor necrosis factor	Homo sapiens	138-147
21859832-8	2011	Several single-nucleotide polymorphisms interacted significant with both NF-kappaB1 and IL6 and with aspirin/non-steroidal anti-inflammatory drugs and cigarette smoking.	Aspirin	101-108	interleukin 6	Homo sapiens	88-91
21726166-5	2011	Negative relations of CRP with both total and direct bilirubin were found after adjustment of age, body mass index, hypertension, diabetes, hypercholesterolemia, cardiovascular disease, taking aspirin, smoking, alcohol drinking and regular exercise and total bilirubin or direct bilirubin.	Aspirin	193-200	C-reactive protein	Homo sapiens	22-25
21856214-6	2011	PBZ and ASA change the affinity of each other to the binding site in serum albumin (SA).	Aspirin	8-11	albumin	Homo sapiens	69-82
21743961-8	2011	Immunoblotting experiment showed that aspirin also acetylated glucose-6-phosphate dehydrogenase and transketolase, both enzymes of pentose phosphate pathway involved in ribonucleotide biosynthesis.	Aspirin	38-45	transketolase	Homo sapiens	100-113
21856214-0	2011	A spectroscopic study of phenylbutazone and aspirin bound to serum albumin in rheumatoid diseases.	Aspirin	44-51	albumin	Homo sapiens	61-74
21728147-0	2011	Protocatechualdehyde synergizes with aspirin at the platelet cyclooxygenase-1 level.	Aspirin	37-44	prostaglandin-endoperoxide synthase 1	Homo sapiens	61-77
21728147-6	2011	Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1.	Aspirin	142-149	prostaglandin-endoperoxide synthase 1	Homo sapiens	37-53
21728147-6	2011	Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1.	Aspirin	142-149	prostaglandin-endoperoxide synthase 1	Homo sapiens	55-60
21728147-6	2011	Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1.	Aspirin	142-149	prostaglandin-endoperoxide synthase 1	Homo sapiens	202-207
21728147-6	2011	Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1.	Aspirin	142-149	prostaglandin-endoperoxide synthase 1	Homo sapiens	202-207
21728147-6	2011	Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1.	Aspirin	240-247	prostaglandin-endoperoxide synthase 1	Homo sapiens	37-53
21728147-6	2011	Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1.	Aspirin	240-247	prostaglandin-endoperoxide synthase 1	Homo sapiens	55-60
21728147-6	2011	Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1.	Aspirin	240-247	prostaglandin-endoperoxide synthase 1	Homo sapiens	202-207
21728147-6	2011	Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1.	Aspirin	240-247	prostaglandin-endoperoxide synthase 1	Homo sapiens	202-207
21728147-7	2011	Taken together, our findings suggest that the capacity of Pro and potentially other structurally similar polyphenolic compounds on promoting the binding of aspirin on platelet COX-1 might be the main mechanism of their synergism with aspirin.	Aspirin	156-163	prostaglandin-endoperoxide synthase 1	Homo sapiens	176-181
21728147-7	2011	Taken together, our findings suggest that the capacity of Pro and potentially other structurally similar polyphenolic compounds on promoting the binding of aspirin on platelet COX-1 might be the main mechanism of their synergism with aspirin.	Aspirin	234-241	prostaglandin-endoperoxide synthase 1	Homo sapiens	176-181
21856214-4	2011	Using fluorescence spectroscopy the location of binding site in serum albumin (SA) for PBZ and ASA was found.	Aspirin	95-98	albumin	Homo sapiens	64-77
21856214-10	2011	The decrease of K(aII) values suggests that the competition between PBZ and ASA in binding to serum albumin in the second class of binding sites occurs.	Aspirin	76-79	albumin	Homo sapiens	94-107
21844189-7	2011	Aspirin was hydrolyzed by HEK cells transfected with PAFAH1B2 or PAFAH1B3, and the competitive type I PAF acetylhydrolase inhibitor NaF reduced erythrocyte hydrolysis of aspirin.	Aspirin	0-7	platelet activating factor acetylhydrolase 1b catalytic subunit 3	Homo sapiens	65-73
21784135-2	2011	In the present study, we examined the neuroprotective effects of S-aspirin, a hydrogen sulfide (H(2)S)-releasing aspirin, on Abeta-induced cell toxicity.	Aspirin	65-74	histocompatibility 2, class II antigen A, beta 1	Mus musculus	125-130
21784135-2	2011	In the present study, we examined the neuroprotective effects of S-aspirin, a hydrogen sulfide (H(2)S)-releasing aspirin, on Abeta-induced cell toxicity.	Aspirin	67-74	histocompatibility 2, class II antigen A, beta 1	Mus musculus	125-130
21784135-5	2011	These data suggest that S-aspirin may protect microglial cells by inhibition of Abeta-induced inflammation and cell cycle re-entry.	Aspirin	24-33	histocompatibility 2, class II antigen A, beta 1	Mus musculus	80-85
21784135-7	2011	It was found that S-aspirin protected mitochondria from Abeta-induced loss of mitochondrial member potential.	Aspirin	20-27	histocompatibility 2, class II antigen A, beta 1	Mus musculus	56-61
21784135-9	2011	In addition, S-aspirin also prevented Abeta-induced activation of p38-mitogen activated protein kinase (MAPK).	Aspirin	15-22	histocompatibility 2, class II antigen A, beta 1	Mus musculus	38-43
21844189-5	2011	Western blotting showed that catalytic PAFAH1B2 and PAFAH1B3 subunits of the type I enzyme co-migrated with purified erythrocyte aspirin hydrolytic activity.	Aspirin	129-136	platelet activating factor acetylhydrolase 1b catalytic subunit 3	Homo sapiens	52-60
21844189-7	2011	Aspirin was hydrolyzed by HEK cells transfected with PAFAH1B2 or PAFAH1B3, and the competitive type I PAF acetylhydrolase inhibitor NaF reduced erythrocyte hydrolysis of aspirin.	Aspirin	0-7	C-X-C motif chemokine ligand 8	Homo sapiens	132-135
21844189-7	2011	Aspirin was hydrolyzed by HEK cells transfected with PAFAH1B2 or PAFAH1B3, and the competitive type I PAF acetylhydrolase inhibitor NaF reduced erythrocyte hydrolysis of aspirin.	Aspirin	170-177	platelet activating factor acetylhydrolase 1b catalytic subunit 3	Homo sapiens	65-73
21844189-7	2011	Aspirin was hydrolyzed by HEK cells transfected with PAFAH1B2 or PAFAH1B3, and the competitive type I PAF acetylhydrolase inhibitor NaF reduced erythrocyte hydrolysis of aspirin.	Aspirin	170-177	C-X-C motif chemokine ligand 8	Homo sapiens	132-135
21962096-0	2011	Variations in expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in nasal mucosa of aspirin-sensitive versus aspirin-tolerant patients with nasal polyposis.	Aspirin	118-125	TIMP metallopeptidase inhibitor 1	Homo sapiens	59-98
21361874-4	2011	The mechanism of action of different concentrations of ASA were compared in K562 (non-MDR) and Lucena (MDR) cells by analysing cell viability, apoptosis and necrosis, intracellular ROS (reactive oxygen species) formation and bcl-2, p53 and cox-2 gene expression.	Aspirin	55-58	BCL2 apoptosis regulator	Homo sapiens	225-230
21361874-8	2011	The bcl-2, p53 and cox-2 genes in both cell lines treated with ASA seem to exhibit different patterns of expression.	Aspirin	63-66	BCL2 apoptosis regulator	Homo sapiens	4-9
21361874-8	2011	The bcl-2, p53 and cox-2 genes in both cell lines treated with ASA seem to exhibit different patterns of expression.	Aspirin	63-66	tumor protein p53	Homo sapiens	11-14
21361874-4	2011	The mechanism of action of different concentrations of ASA were compared in K562 (non-MDR) and Lucena (MDR) cells by analysing cell viability, apoptosis and necrosis, intracellular ROS (reactive oxygen species) formation and bcl-2, p53 and cox-2 gene expression.	Aspirin	55-58	tumor protein p53	Homo sapiens	232-235
21361874-8	2011	The bcl-2, p53 and cox-2 genes in both cell lines treated with ASA seem to exhibit different patterns of expression.	Aspirin	63-66	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	19-24
21361874-4	2011	The mechanism of action of different concentrations of ASA were compared in K562 (non-MDR) and Lucena (MDR) cells by analysing cell viability, apoptosis and necrosis, intracellular ROS (reactive oxygen species) formation and bcl-2, p53 and cox-2 gene expression.	Aspirin	55-58	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	240-245
21900887-3	2011	Given that aspirin induces MDR1 in cancer cells and peripheral blood cells, it may induce MDR1 in intestinal epithelial cells as well, thereby affecting the absorption of clopidogrel.	Aspirin	11-18	ATP binding cassette subfamily B member 1	Homo sapiens	27-31
21900887-3	2011	Given that aspirin induces MDR1 in cancer cells and peripheral blood cells, it may induce MDR1 in intestinal epithelial cells as well, thereby affecting the absorption of clopidogrel.	Aspirin	11-18	ATP binding cassette subfamily B member 1	Homo sapiens	90-94
21900887-4	2011	In this study, aspirin treatment induced the expression of MDR1 in human epithelial colorectal (Caco-2) cells in vitro and in rat intestine in vivo, as evidenced by dose-dependent increases in gene, protein, and efflux function.	Aspirin	15-22	ATP binding cassette subfamily B member 1	Homo sapiens	59-63
21900887-5	2011	Along with the upregulation of MDR1 proteins by aspirin, clopidogrel absorption was significantly decreased in the aspirin-treated Caco-2 cells and in rat intestine.	Aspirin	48-55	ATP binding cassette subfamily B member 1	Homo sapiens	31-35
21900887-5	2011	Along with the upregulation of MDR1 proteins by aspirin, clopidogrel absorption was significantly decreased in the aspirin-treated Caco-2 cells and in rat intestine.	Aspirin	115-122	ATP binding cassette subfamily B member 1	Homo sapiens	31-35
21722632-7	2011	ASA increased the production of reactive oxygen species, reduced the cellular glutathione (GSH) pool and inhibited the activities of the mitochondrial respiratory enzyme complexes, NADH-ubiquinone oxidoreductase (complex I), cytochrome c oxidase (complex IV) and the mitochondrial matrix enzyme, aconitase.	Aspirin	0-3	cytochrome c, somatic	Homo sapiens	225-237
21720709-3	2011	Using aspirin, we found that the expression levels of AKT1 in glioma cells significantly correlated with the transcriptional activity of beta-catenin.	Aspirin	6-13	AKT serine/threonine kinase 1	Homo sapiens	54-58
21819272-5	2011	In preclinical and Phase I - II studies, inhibition of thrombin-mediated platelet activation by a PAR-1 inhibitor, in general, has added to the antithrombotic efficacy of aspirin and clopidogrel without increasing bleeding.	Aspirin	171-178	coagulation factor II, thrombin	Homo sapiens	55-63
21819272-5	2011	In preclinical and Phase I - II studies, inhibition of thrombin-mediated platelet activation by a PAR-1 inhibitor, in general, has added to the antithrombotic efficacy of aspirin and clopidogrel without increasing bleeding.	Aspirin	171-178	coagulation factor II thrombin receptor	Homo sapiens	98-103
21617849-0	2011	Aspirin reduces the apoptotic effect of etoposide via Akt activation and up-regulation of p21(cip).	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	54-57
21617849-3	2011	In the present study, we observed that aspirin caused G0/G1 phase cell cycle arrest and reduced etoposide induced caspase-3 activation in hepatocellular carcinoma G2 (HepG2) cells.	Aspirin	39-46	caspase 3	Homo sapiens	114-123
21617849-4	2011	Further investigation demonstrated that aspirin notably enhanced the activity of Akt and ERK1/2.	Aspirin	40-47	AKT serine/threonine kinase 1	Homo sapiens	81-84
21617849-4	2011	Further investigation demonstrated that aspirin notably enhanced the activity of Akt and ERK1/2.	Aspirin	40-47	mitogen-activated protein kinase 3	Homo sapiens	89-95
22039321-7	2011	Treatment with NO-ASA dose-dependently accelerated colonic healing followed by a rise in plasma NO(x) content and CBF, suppression of MPO and downregulation of COX-2, iNOS, IL-1beta and TNF-alpha mRNAs.	Aspirin	18-21	myeloperoxidase	Homo sapiens	134-137
21617849-5	2011	Blocking the activation of Akt by the PI3-K-selective inhibitor wortmannin abrogated the anti-apoptotic effect of aspirin while the MEK inhibitor U0126 did not.	Aspirin	114-121	AKT serine/threonine kinase 1	Homo sapiens	27-30
21617849-9	2011	Moreover, reduction of caspase-3 activity induced by aspirin was attenuated by silencing p21(cip) expression.	Aspirin	53-60	caspase 3	Homo sapiens	23-32
21617849-10	2011	These results indicated that the anti-apoptotic effect of aspirin was dependent on activation of Akt which inhibited cell apoptosis by up-regulating p21(cip) and blocking caspase-3 activation.	Aspirin	58-65	AKT serine/threonine kinase 1	Homo sapiens	97-100
21617849-10	2011	These results indicated that the anti-apoptotic effect of aspirin was dependent on activation of Akt which inhibited cell apoptosis by up-regulating p21(cip) and blocking caspase-3 activation.	Aspirin	58-65	caspase 3	Homo sapiens	171-180
21721879-0	2011	Antitumor effect of aspirin in glioblastoma cells by modulation of beta-catenin/T-cell factor-mediated transcriptional activity.	Aspirin	20-27	hepatocyte nuclear factor 4 alpha	Homo sapiens	67-93
21721879-4	2011	Reverse transcriptase polymerase chain reaction and Western blot analyses were used to detect the expression of multiple beta-catenin/TCF target genes following aspirin treatment.	Aspirin	161-168	hepatocyte nuclear factor 4 alpha	Homo sapiens	134-137
21721879-5	2011	RESULTS: The transcriptional activity of the beta-catenin/TCF complex was strongly inhibited by aspirin.	Aspirin	96-103	hepatocyte nuclear factor 4 alpha	Homo sapiens	58-61
21721879-8	2011	CONCLUSIONS: The results suggest that aspirin is a potent antitumor agent, and that it exerts its antineoplastic action by inhibition of the beta-catenin/TCF signaling pathway in glioma cells.	Aspirin	38-45	hepatocyte nuclear factor 4 alpha	Homo sapiens	154-157
21875809-7	2011	Conversely, MDHAR over-expressers had significantly reduced AsA levels in mature green fruits by 0.7 fold.	Aspirin	60-63	monodehydroascorbate reductase	Solanum lycopersicum	12-17
21624492-0	2011	Association of the variants in AGT gene with modified drug response in Korean aspirin-intolerant asthma patients.	Aspirin	78-85	angiotensinogen	Homo sapiens	31-34
21624492-2	2011	To carry out a case-control analysis between AGT and aspirin-induced bronchospasm following treatment with an anti-asthma drug, montelukast (MLK), 38 single nucleotide polymorphisms (SNPs) in AGT were genotyped in 56 AIA cohort.	Aspirin	53-60	angiotensinogen	Homo sapiens	45-48
22039321-7	2011	Treatment with NO-ASA dose-dependently accelerated colonic healing followed by a rise in plasma NO(x) content and CBF, suppression of MPO and downregulation of COX-2, iNOS, IL-1beta and TNF-alpha mRNAs.	Aspirin	18-21	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	160-165
22039321-7	2011	Treatment with NO-ASA dose-dependently accelerated colonic healing followed by a rise in plasma NO(x) content and CBF, suppression of MPO and downregulation of COX-2, iNOS, IL-1beta and TNF-alpha mRNAs.	Aspirin	18-21	nitric oxide synthase 2	Homo sapiens	167-171
22039321-7	2011	Treatment with NO-ASA dose-dependently accelerated colonic healing followed by a rise in plasma NO(x) content and CBF, suppression of MPO and downregulation of COX-2, iNOS, IL-1beta and TNF-alpha mRNAs.	Aspirin	18-21	interleukin 1 beta	Homo sapiens	173-181
22039321-7	2011	Treatment with NO-ASA dose-dependently accelerated colonic healing followed by a rise in plasma NO(x) content and CBF, suppression of MPO and downregulation of COX-2, iNOS, IL-1beta and TNF-alpha mRNAs.	Aspirin	18-21	tumor necrosis factor	Homo sapiens	186-195
22039321-10	2011	CONCLUSION: NO-releasing ASA, in contrast to ASA, COX-1 inhibitors, and SC-560, accelerated the healing of colitis via a mechanism involving NO mediated improvement of microcirculation and activation of sensory nerves releasing CGRP.	Aspirin	25-28	calcitonin related polypeptide alpha	Homo sapiens	228-232
21796142-0	2011	Genetic association analysis of TAP1 and TAP2 polymorphisms with aspirin exacerbated respiratory disease and its FEV1 decline.	Aspirin	65-72	transporter 1, ATP binding cassette subfamily B member	Homo sapiens	32-36
21765446-12	2011	CONCLUSION: The combination of raloxifene, aspirin and E(2) exhibits positive lipid, MCP-1 and atherosclerotic responses with minimal stimulation of breast and uterine tissues as well as platelet aggregation in a rabbit model of the menopause.	Aspirin	43-50	corticostatin-3	Oryctolagus cuniculus	85-90
21415093-6	2011	The oral administration of ASA decreased catalase (CAT), reduced glutathione (GSH), and increased lipid peroxidation (LPO) levels.	Aspirin	27-30	catalase	Rattus norvegicus	51-54
21800009-5	2011	Aspirin 75 mg BID decreased arachidonic acid (AA)-induced WBA compared to 75 mg OD (9.7 +- 4.5 vs. 12.6 +- 3.5 ohm; p = 0.003) or to 320 mg OD (11.5 +- 4.2 Ohms; p = 0.049).	Aspirin	0-7	BH3 interacting domain death agonist	Homo sapiens	14-17
21800009-13	2011	Studies of whether BID dosing of aspirin can improve clinical outcomes in such patients are of interest.	Aspirin	33-40	BH3 interacting domain death agonist	Homo sapiens	19-22
21688846-4	2011	Consequent on ASA release, the compounds were capable of inhibiting collagen-induced platelet aggregation of human platelet-rich plasma (PRP).	Aspirin	14-17	complement component 4 binding protein alpha	Homo sapiens	115-135
21688846-4	2011	Consequent on ASA release, the compounds were capable of inhibiting collagen-induced platelet aggregation of human platelet-rich plasma (PRP).	Aspirin	14-17	complement component 4 binding protein alpha	Homo sapiens	137-140
22122764-7	2011	Aspirin and non-aspirin NSAIDs inhibit COX-2, subsequent PGE(2) formation and action by transcriptional and non-transcriptional mechanisms.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	39-44
22122764-7	2011	Aspirin and non-aspirin NSAIDs inhibit COX-2, subsequent PGE(2) formation and action by transcriptional and non-transcriptional mechanisms.	Aspirin	16-23	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	39-44
22122764-9	2011	Aspirin additionally acetylates COX-2, resulting in generation of "aspirin-triggered" lipoxins (ATL), a new class of anti-inflammatory/antitumour compounds.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	32-37
22122764-9	2011	Aspirin additionally acetylates COX-2, resulting in generation of "aspirin-triggered" lipoxins (ATL), a new class of anti-inflammatory/antitumour compounds.	Aspirin	67-74	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	32-37
21529996-4	2011	RESULTS: Use of NSAIDs, particularly aspirin, was associated with a reduced odds ratio (OR) of SCC, especially tumors positive for p53 (OR 0.29; 95% confidence interval 0.11-0.79) or with PTCH loss of heterozygosity (OR 0.35; 95% confidence interval 0.13-0.96).	Aspirin	37-44	tumor protein p53	Homo sapiens	131-134
21645153-0	2011	Two novel aspirin analogues show selective cytotoxicity in primary chronic lymphocytic leukaemia cells that is associated with dual inhibition of Rel A and COX-2.	Aspirin	10-17	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	156-161
21529996-4	2011	RESULTS: Use of NSAIDs, particularly aspirin, was associated with a reduced odds ratio (OR) of SCC, especially tumors positive for p53 (OR 0.29; 95% confidence interval 0.11-0.79) or with PTCH loss of heterozygosity (OR 0.35; 95% confidence interval 0.13-0.96).	Aspirin	37-44	patched 1	Homo sapiens	188-192
21551129-5	2011	We show that c-Src activation occurs in a time- and dose-dependent manner, preceding aspirin-mediated degradation of IkappaBalpha, nuclear/nucleolar translocation of NF-kappaB/RelA and induction of apoptosis.	Aspirin	85-92	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	13-18
21696233-0	2011	Investigations with spectroscopy, zeta potential and molecular modeling of the non-cooperative behaviour between cyclophosphamide hydrochloride and aspirin upon interaction with human serum albumin: binary and ternary systems from multi-drug therapy.	Aspirin	148-155	albumin	Homo sapiens	184-197
21696233-1	2011	The interaction between cyclophosphamide hydrochloride (CYC) and aspirin (ASA) with human serum albumin (HSA) was studied by various kind of spectroscopic, zeta potential and molecular modeling under physiological conditions.	Aspirin	65-72	albumin	Homo sapiens	90-103
21505714-2	2011	Simultaneous inhibition of blood platelet cyclooxygenase-1 by aspirin and of the P2Y12 receptor by clopidogrel or prasugrel is currently recommended in this setting.	Aspirin	62-69	prostaglandin-endoperoxide synthase 1	Homo sapiens	42-58
21696233-1	2011	The interaction between cyclophosphamide hydrochloride (CYC) and aspirin (ASA) with human serum albumin (HSA) was studied by various kind of spectroscopic, zeta potential and molecular modeling under physiological conditions.	Aspirin	74-77	albumin	Homo sapiens	90-103
21551129-5	2011	We show that c-Src activation occurs in a time- and dose-dependent manner, preceding aspirin-mediated degradation of IkappaBalpha, nuclear/nucleolar translocation of NF-kappaB/RelA and induction of apoptosis.	Aspirin	85-92	NFKB inhibitor alpha	Homo sapiens	117-129
21551129-6	2011	Furthermore, inhibition of c-Src activity, by chemical inhibition or expression of a kinase dead form of the protein abrogates aspirin-mediated degradation of IkappaBalpha, nuclear translocation of RelA and apoptosis, suggesting a causal link.	Aspirin	127-134	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	27-32
21551129-6	2011	Furthermore, inhibition of c-Src activity, by chemical inhibition or expression of a kinase dead form of the protein abrogates aspirin-mediated degradation of IkappaBalpha, nuclear translocation of RelA and apoptosis, suggesting a causal link.	Aspirin	127-134	NFKB inhibitor alpha	Homo sapiens	159-171
21551129-7	2011	Expression of constitutively active c-Src mimics aspirin-induced stimulation of the NF-kappaB pathway.	Aspirin	49-56	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	36-41
21551129-7	2011	Expression of constitutively active c-Src mimics aspirin-induced stimulation of the NF-kappaB pathway.	Aspirin	49-56	nuclear factor kappa B subunit 1	Homo sapiens	84-93
21551129-9	2011	These data provide compelling evidence that c-Src is an upstream mediator of aspirin/NSAID effects on NF-kappaB signalling and apoptosis in CRC cells and have relevance to the development of future chemotherapeutic/chemopreventative agents.	Aspirin	77-84	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	44-49
21551129-9	2011	These data provide compelling evidence that c-Src is an upstream mediator of aspirin/NSAID effects on NF-kappaB signalling and apoptosis in CRC cells and have relevance to the development of future chemotherapeutic/chemopreventative agents.	Aspirin	77-84	nuclear factor kappa B subunit 1	Homo sapiens	102-111
21434767-1	2011	In this study, we evaluate the relationships between aspirin nonresponsiveness and the cyclooxygenase-1 (Cox-1) gene C50T polymorphism in stable coronary artery disease (CAD) in Tunisian patients.	Aspirin	53-60	prostaglandin-endoperoxide synthase 1	Homo sapiens	87-103
21434767-1	2011	In this study, we evaluate the relationships between aspirin nonresponsiveness and the cyclooxygenase-1 (Cox-1) gene C50T polymorphism in stable coronary artery disease (CAD) in Tunisian patients.	Aspirin	53-60	prostaglandin-endoperoxide synthase 1	Homo sapiens	105-110
21497884-11	2011	Finally, we found that CCL23 protein levels were significantly increased in NPs from patients with CRSwNP with aspirin sensitivity.	Aspirin	111-118	C-C motif chemokine ligand 23	Homo sapiens	23-28
21406194-4	2011	Here, we examined whether S-nitrosylation of the NF-kappaB, p53, and Wnt signaling proteins by NO-ASA might explain, in part, its mechanism of action in colon cancer.	Aspirin	98-101	nuclear factor kappa B subunit 1	Homo sapiens	49-58
21397936-7	2011	RESULTS: Compared with NM from control subjects, PGE(2) concentrations were significantly lower in IL-1beta-stimulated fibroblasts from patients with NPs who were tolerant to aspirin and even lower in polyps from patients with AIA.	Aspirin	175-182	interleukin 1 beta	Homo sapiens	99-107
21397936-8	2011	Similarly, IL-1beta exposure induced the expression of COX-1 and COX-2 in fibroblasts from NM of control subjects, had only moderate effects on fibroblasts from NPs of aspirin-tolerant nonasthmatic patients, and almost no effect on fibroblasts from NPs of patients with AIA.	Aspirin	168-175	interleukin 1 beta	Homo sapiens	11-19
21429568-2	2011	This study evaluates the impact of the selected polymorphisms in the COX-1 gene, the CYP5A1 gene, the P2RY1 receptor gene, and the GPIIbIIIa receptor gene on platelet response to aspirin and risk of suffering from major adverse cardiovascular and cerebrovascular events (MACCE).	Aspirin	179-186	thromboxane A synthase 1	Homo sapiens	85-91
21406194-4	2011	Here, we examined whether S-nitrosylation of the NF-kappaB, p53, and Wnt signaling proteins by NO-ASA might explain, in part, its mechanism of action in colon cancer.	Aspirin	98-101	tumor protein p53	Homo sapiens	60-63
21406194-6	2011	Using a modified biotin switch assay we demonstrated that NO-ASA S-nitrosylates the signaling proteins p53, beta-catenin, and NF-kappaB, in colon cancer cells in a time- and concentration-dependent manner.	Aspirin	61-64	tumor protein p53	Homo sapiens	103-106
21406194-6	2011	Using a modified biotin switch assay we demonstrated that NO-ASA S-nitrosylates the signaling proteins p53, beta-catenin, and NF-kappaB, in colon cancer cells in a time- and concentration-dependent manner.	Aspirin	61-64	nuclear factor kappa B subunit 1	Homo sapiens	126-135
21406194-7	2011	NO-ASA suppresses NF-kappaB binding to its cognate DNA oligonucleotide, which occurs without changes in the nuclear levels of the NF-kappaB subunits p65 and p50 and is reversed by dithiothreitol that reduces -S-NO to -SH.	Aspirin	3-6	nuclear factor kappa B subunit 1	Homo sapiens	18-27
21406194-7	2011	NO-ASA suppresses NF-kappaB binding to its cognate DNA oligonucleotide, which occurs without changes in the nuclear levels of the NF-kappaB subunits p65 and p50 and is reversed by dithiothreitol that reduces -S-NO to -SH.	Aspirin	3-6	nuclear factor kappa B subunit 1	Homo sapiens	157-160
21647198-4	2011	The risk of upper gastrointestinal bleeding with aspirin is increased with old age, male sex, ulcer history and concomitant medication with NSAIDs, cyclooxygenase 2 selective inhibitors, corticosteroids or other antithrombotic agents.	Aspirin	49-56	prostaglandin-endoperoxide synthase 2	Homo sapiens	148-164
21069571-11	2011	Both acetylsalicylic acid (IC(50) = 5.5 muM) and celecoxib (IC(50) = 7.9 nM) exhibited concentration-dependent decrease in TXB(2) production.	Aspirin	5-25	latexin	Homo sapiens	40-43
21372715-3	2011	This is further aggravated by inhibition of cyclooxygenase-1 by aspirin and other NSAIDs.	Aspirin	64-71	prostaglandin-endoperoxide synthase 1	Homo sapiens	44-60
21515838-2	2011	We hypothesized that low-dose aspirin would be beneficial in patients receiving insulin therapy, as a high-risk group.	Aspirin	30-37	insulin	Homo sapiens	80-87
21688627-4	2011	The GI protection that is associated with the use of COX-2 selective agents is largely lost when low-dose aspirin is administered concurrently for CV prophylaxis.	Aspirin	106-113	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	53-58
21219589-4	2011	ASA irreversibly inhibits cyclooxygenase-1 (COX-1) by acetylation.	Aspirin	0-3	prostaglandin-endoperoxide synthase 1	Homo sapiens	26-42
21219589-4	2011	ASA irreversibly inhibits cyclooxygenase-1 (COX-1) by acetylation.	Aspirin	0-3	prostaglandin-endoperoxide synthase 1	Homo sapiens	44-49
21514281-0	2011	Aspirin-induced AMP-activated protein kinase activation regulates the proliferation of vascular smooth muscle cells from spontaneously hypertensive rats.	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	16-44
21655062-0	2011	Effect of aspirin on the expression of hepatocyte NF-kappaB and serum TNF-alpha in streptozotocin-induced type 2 diabetic rats.	Aspirin	10-17	tumor necrosis factor	Rattus norvegicus	70-79
21655062-2	2011	We hypothesized that aspirin improves insulin resistance in type 2 diabetes by inhibiting hepatic nuclear factor kappa-beta (NF-kappaB) activation and serum tumor necrosis factor-alpha (TNF-alpha).	Aspirin	21-28	tumor necrosis factor	Rattus norvegicus	157-184
21655062-2	2011	We hypothesized that aspirin improves insulin resistance in type 2 diabetes by inhibiting hepatic nuclear factor kappa-beta (NF-kappaB) activation and serum tumor necrosis factor-alpha (TNF-alpha).	Aspirin	21-28	tumor necrosis factor	Rattus norvegicus	186-195
21655062-7	2011	The results showed administration of aspirin caused no significant lowering in fasting glucose level but significant reduction of hepatic NF-kappaB expression and serum TNF-alpha level with improved insulin resistance compared to the diabetic group.	Aspirin	37-44	tumor necrosis factor	Rattus norvegicus	169-178
21371451-6	2011	In addition, in about 50% of patients, we noticed that ASA (50 muM) significantly and time-dependently diminished thromboxane B(2) concentration in atorvastatin-treated patients.	Aspirin	55-58	latexin	Homo sapiens	63-66
21655062-9	2011	It is concluded that aspirin improves insulin resistance by inhibiting hepatic NF-kappaB activation and TNF-alpha level in streptozotocin-induced type 2 diabetic rats.	Aspirin	21-28	tumor necrosis factor	Rattus norvegicus	104-113
21514281-3	2011	Here, we investigated whether aspirin may exert therapeutic effects via AMP-activated protein kinase (AMPK) activation in vascular smooth muscle cells (VSMC) from wistar kyoto rats (WKY) and spontaneously hypertensive rats (SHR).	Aspirin	30-37	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	72-100
21514281-3	2011	Here, we investigated whether aspirin may exert therapeutic effects via AMP-activated protein kinase (AMPK) activation in vascular smooth muscle cells (VSMC) from wistar kyoto rats (WKY) and spontaneously hypertensive rats (SHR).	Aspirin	30-37	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	102-106
21514281-4	2011	Aspirin increased AMPK and acetyl-CoA carboxylase phosphorylation in a time- and dose-dependent manner in VSMCs from WKY and SHR, but with greater efficacy in SHR.	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	18-22
21514281-5	2011	In SHR, a low basal phosphorylation status of AMPK resulted in increased VSMC proliferation and aspirin-induced AMPK phosphorylation inhibited proliferation of VSMCs.	Aspirin	96-103	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	46-50
21514281-5	2011	In SHR, a low basal phosphorylation status of AMPK resulted in increased VSMC proliferation and aspirin-induced AMPK phosphorylation inhibited proliferation of VSMCs.	Aspirin	96-103	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	112-116
21514281-6	2011	Compound C, an AMPK inhibitor, and AMPK siRNA reduced the aspirin-mediated inhibition of VSMC proliferation, this effect was more pronounced in SHR than in WKY.	Aspirin	58-65	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	15-19
21514281-6	2011	Compound C, an AMPK inhibitor, and AMPK siRNA reduced the aspirin-mediated inhibition of VSMC proliferation, this effect was more pronounced in SHR than in WKY.	Aspirin	58-65	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	35-39
21514281-7	2011	In VSMCs from SHR, aspirin increased p53 and p21 expression and inhibited the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E.	Aspirin	19-26	cyclin E1	Rattus norvegicus	152-160
21514281-8	2011	These results indicate that in SHR VSMCs aspirin exerts anti-proliferative effects through the induction of AMPK phosphorylation.	Aspirin	41-48	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	108-112
21703104-0	2011	Selective cyclooxygenase-2 inhibitor cross-reactivity in aspirin-exacerbated respiratory disease.	Aspirin	57-64	prostaglandin-endoperoxide synthase 2	Homo sapiens	10-26
21076843-6	2011	The effect of aspirin on RECK status and function was evaluated using Western blotting, gelatin zymography, invasion and proliferation assays, and PhosphoELISArray analysis of Ras downstream mediators.	Aspirin	14-21	reversion inducing cysteine rich protein with kazal motifs	Homo sapiens	25-29
21076843-12	2011	Aspirin (500 muM) demonstrated myriad effects in human CCA cell lines, including growth suppression, reduced phosphorylation of Akt/Erk/c-Jun, elevation of RECK expression, inhibition of MMP-2/MMP-9 activity, and enhanced invasiveness.	Aspirin	0-7	mitogen-activated protein kinase 1	Homo sapiens	132-135
21435744-4	2011	These data support the use of acetylsalicylic acid (AAS) or aspirin, a COX-2 inhibitor, as an effective agent in colorectal cancer prevention.	Aspirin	60-67	prostaglandin-endoperoxide synthase 2	Homo sapiens	71-76
20488839-9	2011	Pretreatment of IRB and ASP showed the reduction in TBARS, elevation in GSH, SOD and catalase levels as compared with MCAO rats.	Aspirin	24-27	catalase	Rattus norvegicus	85-93
21347512-8	2011	Aspirin treatment inhibited PrP (106-126)-induced neuronal cell death in SH-SY5Y neuroblastoma cells.	Aspirin	0-7	prion protein	Homo sapiens	28-31
21347512-9	2011	In addition, the PrP (106-126)-mediated increase of p-p38, p53, cleaved-caspase-3 and decrease of Bcl-2 expressions were blocked by aspirin and the ERK inhibitor, PR98059.	Aspirin	132-139	prion protein	Homo sapiens	17-20
21347512-10	2011	Furthermore, we showed that the PrP (106-126)-mediated increase of PrPc and p-ERK1/2 were inhibited by PD98059 and aspirin.	Aspirin	115-122	prion protein	Homo sapiens	32-35
21347512-11	2011	Taken together, these results demonstrate that ERK1/2 is a key modulator of the protective effect of aspirin on PrP-106-126-mediated cellular prion protein overexpression and neurotoxicity and also suggest that aspirin may prevent neuron cell damages caused by the prion peptide.	Aspirin	101-108	prion protein	Homo sapiens	112-115
21347512-11	2011	Taken together, these results demonstrate that ERK1/2 is a key modulator of the protective effect of aspirin on PrP-106-126-mediated cellular prion protein overexpression and neurotoxicity and also suggest that aspirin may prevent neuron cell damages caused by the prion peptide.	Aspirin	211-218	prion protein	Homo sapiens	112-115
21076843-12	2011	Aspirin (500 muM) demonstrated myriad effects in human CCA cell lines, including growth suppression, reduced phosphorylation of Akt/Erk/c-Jun, elevation of RECK expression, inhibition of MMP-2/MMP-9 activity, and enhanced invasiveness.	Aspirin	0-7	reversion inducing cysteine rich protein with kazal motifs	Homo sapiens	156-160
21076843-12	2011	Aspirin (500 muM) demonstrated myriad effects in human CCA cell lines, including growth suppression, reduced phosphorylation of Akt/Erk/c-Jun, elevation of RECK expression, inhibition of MMP-2/MMP-9 activity, and enhanced invasiveness.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	128-131
21509710-9	2011	CONCLUSION: The DDAVP-induced improvement of primary haemostasis in patients with aspirin-like defect is mainly due to the marked increase of the VWF.	Aspirin	82-89	von Willebrand factor	Homo sapiens	146-149
21073332-8	2011	RESULTS: On periodontitis phase, Asp and Clo significantly reduced levels of TNF-alpha and Il-6 (P &lt;0.05), but only Asp decreased thromboxane A(2) (P &lt;0.05).	Aspirin	33-36	tumor necrosis factor	Rattus norvegicus	77-86
21073332-8	2011	RESULTS: On periodontitis phase, Asp and Clo significantly reduced levels of TNF-alpha and Il-6 (P &lt;0.05), but only Asp decreased thromboxane A(2) (P &lt;0.05).	Aspirin	33-36	interleukin 6	Rattus norvegicus	91-95
20460337-9	2011	Although the lack of response to epinephrine and aspirin treatment displayed similarities in aggregations using epinephrine, ADP, collagen, and thrombin, they differed in aggregations using AA and for ATP secretion.	Aspirin	49-56	coagulation factor II, thrombin	Homo sapiens	144-152
21457877-0	2011	Association analysis of RGS7BP gene polymorphisms with aspirin intolerance in asthmatic patients.	Aspirin	55-62	regulator of G protein signaling 7 binding protein	Homo sapiens	24-30
21457877-2	2011	OBJECTIVE: To determine the association of RGS7BP gene polymorphisms with the development of aspirin-exacerbated respiratory disease (AERD).	Aspirin	93-100	regulator of G protein signaling 7 binding protein	Homo sapiens	43-49
21457877-3	2011	METHODS: We evaluated the association of RGS7BP gene polymorphisms with response to oral aspirin challenge and with responsiveness to methacholine challenge.	Aspirin	89-96	regulator of G protein signaling 7 binding protein	Homo sapiens	41-47
21457877-5	2011	RESULTS: Logistic regression analysis of RGS7BP gene polymorphisms in patients with AERD (n = 102) and aspirin-tolerant asthma (n = 429) revealed that a haplotype of block 3 consisting of rare alleles +98092 C&gt;G, +98853 C&gt;T, and +104450 T&gt;G of the RGS7BP gene was associated with AERD.	Aspirin	103-110	regulator of G protein signaling 7 binding protein	Homo sapiens	41-47
21324923-5	2011	ASA treatment also reduced the MDSC-attracting chemokine CCL2 (C-C motif ligand 2) in the TME along with numbers of CD11b(+)Ly6G(hi)Ly6C(lo) granulocytic MDSCs in both the bone marrow and the TME.	Aspirin	0-3	integrin alpha M	Mus musculus	116-121
21116834-6	2011	After in vitro treatment with ASA, macrophages expressed low levels of MHC-II, CD80, and CD47 molecules, and showed significantly decreased phagocytosis.	Aspirin	30-33	histocompatibility-2, MHC	Mus musculus	71-77
21116834-6	2011	After in vitro treatment with ASA, macrophages expressed low levels of MHC-II, CD80, and CD47 molecules, and showed significantly decreased phagocytosis.	Aspirin	30-33	CD80 antigen	Mus musculus	79-83
20158569-8	2011	The standard anti-inflammatory drugs aspirin and indomethacin (Indo) reduced the synergistic IL-6 production by 60%.	Aspirin	37-44	interleukin 6	Homo sapiens	93-97
21562370-2	2011	Patients who develop an immunoglobulin E (IgE) hypersensitivity reaction to aspirin must abort treatment and receive alternative antithrombotic agents.	Aspirin	76-83	immunoglobulin heavy constant epsilon	Homo sapiens	24-40
21330458-14	2011	Activation of VEGF and coagulation (vWF) pathways could partially explain at a molecular level the clinical observations that bevacizumab and aspirin have a preventive effect in SOS.	Aspirin	142-149	vascular endothelial growth factor A	Homo sapiens	14-18
21330458-14	2011	Activation of VEGF and coagulation (vWF) pathways could partially explain at a molecular level the clinical observations that bevacizumab and aspirin have a preventive effect in SOS.	Aspirin	142-149	von Willebrand factor	Homo sapiens	36-39
20100067-5	2011	RESULTS AND DISCUSSION: ATR-FTIR spectra of a simple aspirin tablet formulation with varying amounts of the lubricant magnesium stearate were obtained.	Aspirin	53-60	ATR serine/threonine kinase	Homo sapiens	24-27
21301784-0	2011	Residual cyclooxygenase-1 activity and epinephrine reduce the antiplatelet effect of aspirin in patients with acute myocardial infarction.	Aspirin	85-92	prostaglandin-endoperoxide synthase 1	Homo sapiens	9-25
20158569-11	2011	Combination of statins with aspirin and/or Indo resulted in complete inhibition of the synergistic IL-6 production.	Aspirin	28-35	interleukin 6	Homo sapiens	99-103
21327631-8	2011	Treatment with IVIG and aspirin significantly decreased TNF-alpha and hs-CRP concentrations.	Aspirin	24-31	tumor necrosis factor	Homo sapiens	56-65
21327631-8	2011	Treatment with IVIG and aspirin significantly decreased TNF-alpha and hs-CRP concentrations.	Aspirin	24-31	C-reactive protein	Homo sapiens	73-76
21327631-10	2011	The results of our study indicate that the functions of circulating EPCs improved after treatment with IVIG and aspirin, which may be related to decreased concentrations of TNF-alpha and hs-CRP.	Aspirin	112-119	tumor necrosis factor	Homo sapiens	173-182
21327631-10	2011	The results of our study indicate that the functions of circulating EPCs improved after treatment with IVIG and aspirin, which may be related to decreased concentrations of TNF-alpha and hs-CRP.	Aspirin	112-119	C-reactive protein	Homo sapiens	190-193
21360823-0	2011	Nitrooxyacyl derivatives of salicylic acid: aspirin-like molecules that covalently inactivate cyclooxygenase-1.	Aspirin	44-51	prostaglandin-endoperoxide synthase 1	Homo sapiens	94-110
21360514-11	2011	CONCLUSION: Sequential administration of 220 mg naproxen twice a day and low-dose aspirin interferes with the irreversible inhibition of platelet cyclooxygenase 1 afforded by aspirin.	Aspirin	82-89	prostaglandin-endoperoxide synthase 1	Homo sapiens	146-162
21360514-11	2011	CONCLUSION: Sequential administration of 220 mg naproxen twice a day and low-dose aspirin interferes with the irreversible inhibition of platelet cyclooxygenase 1 afforded by aspirin.	Aspirin	175-182	prostaglandin-endoperoxide synthase 1	Homo sapiens	146-162
21562370-2	2011	Patients who develop an immunoglobulin E (IgE) hypersensitivity reaction to aspirin must abort treatment and receive alternative antithrombotic agents.	Aspirin	76-83	immunoglobulin heavy constant epsilon	Homo sapiens	42-45
21562370-5	2011	OBJECTIVE: We aimed to determine the efficacy and safety of a multiday outpatient aspirin desensitization protocol for patients with an IgE-mediated aspirin hypersensitivity.	Aspirin	82-89	immunoglobulin heavy constant epsilon	Homo sapiens	136-139
21562370-5	2011	OBJECTIVE: We aimed to determine the efficacy and safety of a multiday outpatient aspirin desensitization protocol for patients with an IgE-mediated aspirin hypersensitivity.	Aspirin	149-156	immunoglobulin heavy constant epsilon	Homo sapiens	136-139
20940449-0	2011	Angiostatic effects of aspirin in hypoxia-reoxygenation are linked to modulation of TGFbeta1 signaling.	Aspirin	23-30	transforming growth factor beta 1	Homo sapiens	84-92
20940449-8	2011	Treatment of HUVECs with aspirin suppressed TGFbeta1 and enhanced TGFbeta-R1 mRNA expression during HR (both P &lt; .05 vs HR alone) without a change in p53 and p21 (P-NS).	Aspirin	25-32	transforming growth factor beta 1	Homo sapiens	44-52
20940449-8	2011	Treatment of HUVECs with aspirin suppressed TGFbeta1 and enhanced TGFbeta-R1 mRNA expression during HR (both P &lt; .05 vs HR alone) without a change in p53 and p21 (P-NS).	Aspirin	25-32	transforming growth factor beta 1	Homo sapiens	44-51
20940449-9	2011	In other experiments, treatment of cells with TGFbeta1 antibody modestly decreased HR-mediated angiogenesis; however, TGFbeta1 antibody treatment significantly enhanced the inhibitory effect of aspirin on tube formation.	Aspirin	194-201	transforming growth factor beta 1	Homo sapiens	118-126
20940449-10	2011	Based on these data, we suggest that the inhibitory effect of aspirin on HR-mediated angiogenesis involves TGFbeta1-TGFbeta-R1 pathway.	Aspirin	62-69	transforming growth factor beta 1	Homo sapiens	107-115
20940449-10	2011	Based on these data, we suggest that the inhibitory effect of aspirin on HR-mediated angiogenesis involves TGFbeta1-TGFbeta-R1 pathway.	Aspirin	62-69	transforming growth factor beta 1	Homo sapiens	107-114
21062358-5	2011	It is even more recently that aspirin"s unique antiplatelet action has been recognized, with long-lasting inhibition of platelet aggregation due to irreversible inactivation of the cyclooxygenase-1 mediated production of thromboxane.	Aspirin	30-37	prostaglandin-endoperoxide synthase 1	Homo sapiens	181-197
21163909-7	2011	Acetylsalicylic acid, an irreversible inhibitor of both hPHS-1 and hPHS-2, blocked cytotoxicity and DNA oxidation in both cell lines and untransfected CHO-K1 cells lacking PHS activity were similarly resistant.	Aspirin	0-20	prostaglandin-endoperoxide synthase 1	Homo sapiens	56-62
21449675-0	2011	Association analysis of thromboxane A synthase 1 gene polymorphisms with aspirin intolerance in asthmatic patients.	Aspirin	73-80	thromboxane A synthase 1	Homo sapiens	24-48
21449675-13	2011	CONCLUSION: The rare allele of rs6962291 may play a protective role against aspirin hypersensitivity via a lower catalytic activity of the TBXAS1 gene, attributed to the increase of a nonfunctioning isoform of TBXAS1.	Aspirin	76-83	thromboxane A synthase 1	Homo sapiens	139-145
21449675-13	2011	CONCLUSION: The rare allele of rs6962291 may play a protective role against aspirin hypersensitivity via a lower catalytic activity of the TBXAS1 gene, attributed to the increase of a nonfunctioning isoform of TBXAS1.	Aspirin	76-83	thromboxane A synthase 1	Homo sapiens	210-216
21163909-7	2011	Acetylsalicylic acid, an irreversible inhibitor of both hPHS-1 and hPHS-2, blocked cytotoxicity and DNA oxidation in both cell lines and untransfected CHO-K1 cells lacking PHS activity were similarly resistant.	Aspirin	0-20	prostaglandin-endoperoxide synthase 2	Homo sapiens	67-73
21386995-9	2011	The frequency of ASA-specific IFN-gamma-secreting peripheral blood mononuclear cells, as well as the amount of IL-10 produced by ASA-specific cells, was of greater magnitude in probiotic-fed pigs compared to control animals.	Aspirin	129-132	IL10	Sus scrofa	111-116
21311822-6	2011	While serum TxB2 levels of &lt; 2 ng/ml reflect aspirin-induced inhibition of cyclo-oxygenase-1 activity with high sensitivity, VASP exhibits a wide variability upon treatment with clopidogrel or prasugrel.	Aspirin	48-55	prostaglandin-endoperoxide synthase 1	Homo sapiens	78-95
21030714-6	2011	When treated with aspirin, the patients showed a 49% reduction in the generation of CD34+/KDR+ cells, indicating that the level of circulating CD34+/KDR+ cells also relates to in vivo platelet activation.	Aspirin	18-25	CD34 molecule	Homo sapiens	84-88
21030714-6	2011	When treated with aspirin, the patients showed a 49% reduction in the generation of CD34+/KDR+ cells, indicating that the level of circulating CD34+/KDR+ cells also relates to in vivo platelet activation.	Aspirin	18-25	CD34 molecule	Homo sapiens	143-147
20824505-0	2011	Renin-angiotensin system associated with risk of upper GI mucosal injury induced by low dose aspirin: renin angiotensin system genes" polymorphism.	Aspirin	93-100	renin	Homo sapiens	0-5
20824505-0	2011	Renin-angiotensin system associated with risk of upper GI mucosal injury induced by low dose aspirin: renin angiotensin system genes" polymorphism.	Aspirin	93-100	renin	Homo sapiens	102-107
20824505-1	2011	BACKGROUND: We have previously shown that co-treatment of angiotensin type 1 receptor (AT1R) blocker (ARB) or angiotensin converting enzyme (ACE) inhibitor seem to reduce peptic ulcer among patients taking low dose aspirin.	Aspirin	215-222	angiotensin I converting enzyme	Homo sapiens	110-139
20824505-1	2011	BACKGROUND: We have previously shown that co-treatment of angiotensin type 1 receptor (AT1R) blocker (ARB) or angiotensin converting enzyme (ACE) inhibitor seem to reduce peptic ulcer among patients taking low dose aspirin.	Aspirin	215-222	angiotensin I converting enzyme	Homo sapiens	141-144
21347238-10	2011	Expression of SOCS-2 was enhanced, and TRAF6 and TNFalpha reduced, in the spleens of infected ASA-treated mice.	Aspirin	94-97	TNF receptor-associated factor 6	Mus musculus	39-44
21347238-10	2011	Expression of SOCS-2 was enhanced, and TRAF6 and TNFalpha reduced, in the spleens of infected ASA-treated mice.	Aspirin	94-97	tumor necrosis factor	Mus musculus	49-57
21081660-6	2011	We then used this GES to screen a compound library for agents that affected the GES genes in 3T3-L1 adipocytes in a way that most closely resembled the changes seen when insulin resistance was successfully reversed with aspirin and troglitazone.	Aspirin	220-227	insulin	Homo sapiens	170-177
21084063-6	2011	Treatment of rats with a single dose of aspirin (400mg/kg, orally) led to significant alterations in the levels of total nitrite and nitrate (NOx), interleukins (IL-4, 6, 10, 12), tumor necrosis factor (TNF-alpha), and interferon gamma (IFN-gamma).	Aspirin	40-47	tumor necrosis factor	Rattus norvegicus	203-212
20349206-4	2011	With RKO cells, aspirin reduced IL-6, IL-1ra, and IL-10 synthesis and enhanced IFNgamma secretion, while IL-1beta remained unchanged.	Aspirin	16-23	interleukin 6	Homo sapiens	32-36
20349206-4	2011	With RKO cells, aspirin reduced IL-6, IL-1ra, and IL-10 synthesis and enhanced IFNgamma secretion, while IL-1beta remained unchanged.	Aspirin	16-23	interferon gamma	Homo sapiens	79-87
21383917-10	2011	ABBREVIATIONS: serpin -serine protease inhibitors RCL -reactive center loop ASA -accessible surface area.	Aspirin	76-79	coagulation factor II, thrombin	Homo sapiens	23-38
20669045-0	2011	Effect of aspirin and other NSAIDs on postmenopausal breast cancer incidence by hormone receptor status: results from a prospective cohort study.	Aspirin	10-17	nuclear receptor subfamily 4 group A member 1	Homo sapiens	80-96
20669045-1	2011	Aspirin and other non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs) can inhibit aromatase activity and thus could selectively lower incidence of hormone receptor positive tumors.	Aspirin	0-7	nuclear receptor subfamily 4 group A member 1	Homo sapiens	154-170
20669045-1	2011	Aspirin and other non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs) can inhibit aromatase activity and thus could selectively lower incidence of hormone receptor positive tumors.	Aspirin	22-29	nuclear receptor subfamily 4 group A member 1	Homo sapiens	154-170
21231793-5	2011	Here we show that ASA inhibits phagocytosis and modulates expression of endosomal SNAREs, such as Vti1a, Vti1b, VAMP-3, VAMP-8 and Syn-8 (but not syn-6 and syn-16) in DC.	Aspirin	18-21	vesicle-associated membrane protein 8	Mus musculus	120-126
21226927-19	2011	The following factors correlated with the risk of ASA low response: patients with elevated hemoglobin, serum creatinine and C-reactive protein values.	Aspirin	50-53	C-reactive protein	Homo sapiens	124-142
21078384-4	2011	Preincubation with catalase, which detoxifies reactive oxygen species, or acetylsalicylic acid, an inhibitor of hPHS-1 and -2, reduced the cytotoxicity caused by DA, L-DOPA, DOPAC, and HVA in hPHS-1 and -2 cells both with and without AA.	Aspirin	74-94	prostaglandin-endoperoxide synthase 1	Homo sapiens	112-125
21078384-4	2011	Preincubation with catalase, which detoxifies reactive oxygen species, or acetylsalicylic acid, an inhibitor of hPHS-1 and -2, reduced the cytotoxicity caused by DA, L-DOPA, DOPAC, and HVA in hPHS-1 and -2 cells both with and without AA.	Aspirin	74-94	prostaglandin-endoperoxide synthase 1	Homo sapiens	192-205
21217919-1	2011	The clinical syndrome of aspirin-exacerbated respiratory disease (AERD) is a condition where inhibition of cyclooxygenase-1 (COX-1) induces attacks of upper and lower airway reactions, including rhinorrhea and varying degrees of bronchospasm and laryngospasm.	Aspirin	25-32	prostaglandin-endoperoxide synthase 1	Homo sapiens	107-123
20920611-6	2011	Aspirin (ASA) converts cyclooxygenase (COX)-2 into a form that generates new neuroprotective docosanoids from DHA; therefore, ASA might positively resolve the paradoxical effect of the concomitant presence of DHA and betaA.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	23-45
21217919-1	2011	The clinical syndrome of aspirin-exacerbated respiratory disease (AERD) is a condition where inhibition of cyclooxygenase-1 (COX-1) induces attacks of upper and lower airway reactions, including rhinorrhea and varying degrees of bronchospasm and laryngospasm.	Aspirin	25-32	prostaglandin-endoperoxide synthase 1	Homo sapiens	125-130
20920611-6	2011	Aspirin (ASA) converts cyclooxygenase (COX)-2 into a form that generates new neuroprotective docosanoids from DHA; therefore, ASA might positively resolve the paradoxical effect of the concomitant presence of DHA and betaA.	Aspirin	9-12	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	23-45
20920611-6	2011	Aspirin (ASA) converts cyclooxygenase (COX)-2 into a form that generates new neuroprotective docosanoids from DHA; therefore, ASA might positively resolve the paradoxical effect of the concomitant presence of DHA and betaA.	Aspirin	126-129	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	23-45
21548865-6	2011	This review was designed to provide an updated overview based on the experimental and clinical evidence on the involvement COX-2 derived products, lipoxins in the mechanism of gastric defense, gastroprotection and gastric adaptation to ASA.	Aspirin	236-239	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	123-128
21938206-6	2011	Both cefazolin and aspirin were found to dock in the vicinity of the predicted active sites of PON1; cefazolin bound at residues N166, S193 and Y71, while aspirin at residues N309, I310 and L311.	Aspirin	155-162	paraoxonase 1	Homo sapiens	95-99
21068203-10	2011	In addition, we observed statistically significant interaction between TGFbeta1, TGFbetaR1, and Smad3 and cigarette smoking, aspirin use, and estrogen status for both colon and rectal cancers.	Aspirin	125-132	transforming growth factor beta 1	Homo sapiens	71-79
21116822-12	2011	Furthermore, treatment with a HMG-CoA reductase inhibitor or acetylsalicylic acid showed reduced levels of IL-21, IL-23 and VCAM1 (all p &lt; 0.05), but did not influence IL-17A.	Aspirin	61-81	vascular cell adhesion molecule 1	Homo sapiens	124-129
21938206-0	2011	Homology modeling of human serum paraoxonase1 and its molecular interaction studies with aspirin and cefazolin.	Aspirin	89-96	paraoxonase 1	Homo sapiens	33-45
21938206-4	2011	Therefore, a theoretical model of HuPON1 was generated using homology modelling and precise molecular interactions of an activator aspirin and an inhibitor cefazolin with PON1 were studied using Autodock software.	Aspirin	131-138	paraoxonase 1	Homo sapiens	36-40
21938206-6	2011	Both cefazolin and aspirin were found to dock in the vicinity of the predicted active sites of PON1; cefazolin bound at residues N166, S193 and Y71, while aspirin at residues N309, I310 and L311.	Aspirin	19-26	paraoxonase 1	Homo sapiens	95-99
21166598-0	2011	The effect of aspirin on C-reactive protein in hypertensive patients.	Aspirin	14-21	C-reactive protein	Homo sapiens	25-43
21166598-2	2011	Aspirin, which has both anti-inflammatory and anti-thrombotic effects, has the potential to influence CRP release.	Aspirin	0-7	C-reactive protein	Homo sapiens	102-105
21166598-3	2011	Several studies have been reported investigating clinical effects of aspirin on CRP levels.	Aspirin	69-76	C-reactive protein	Homo sapiens	80-83
21166598-4	2011	Some studies have reported aspirin reduced CRP levels, but other studies did not.	Aspirin	27-34	C-reactive protein	Homo sapiens	43-46
21166598-5	2011	This study was designed to assess the effect of low-dose aspirin on CRP levels in controlled hypertensive patients who had low inflammatory burden.	Aspirin	57-64	C-reactive protein	Homo sapiens	68-71
21548865-9	2011	Aspirin-triggered lipoxin (ATL) synthesis, via COX-2, acts to reduce the severity of damage induced by this NSAID.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	47-52
21548865-12	2011	Suppression of COX-2 activity by selective COX-2 inhibitors such as rofecoxib or celecoxib was shown to abolish the production of ATL and to diminish the gastric tolerability of ASA and gastric adaptation developed in response to repetitive administration of this NSAID.	Aspirin	178-181	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	15-20
21548865-12	2011	Suppression of COX-2 activity by selective COX-2 inhibitors such as rofecoxib or celecoxib was shown to abolish the production of ATL and to diminish the gastric tolerability of ASA and gastric adaptation developed in response to repetitive administration of this NSAID.	Aspirin	178-181	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	43-48
22160013-1	2011	Because of the central role of platelets in cardiovascular atherothrombosis, there is a well-established therapeutic role for antiplatelet therapy that includes aspirin (a cyclooxygenase 1 [COX1] inhibitor), clopidogrel (an antagonist of the ADP P2Y(12) receptor), and the GPIIb-GPIIIa (alphaIIbbeta3) antagonists.	Aspirin	161-168	prostaglandin-endoperoxide synthase 1	Homo sapiens	172-188
20690072-7	2011	The results showed that administration with aspirin for 4 weeks or 8 weeks significantly reduced the mean escape latency, the acetylcholinesterase activity, the TNF-alpha, IL-1beta levels and increased the percentage of time spent in target quadrant.	Aspirin	44-51	tumor necrosis factor	Mus musculus	161-170
20690072-7	2011	The results showed that administration with aspirin for 4 weeks or 8 weeks significantly reduced the mean escape latency, the acetylcholinesterase activity, the TNF-alpha, IL-1beta levels and increased the percentage of time spent in target quadrant.	Aspirin	44-51	interleukin 1 beta	Mus musculus	172-180
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	mitogen-activated protein kinase 14	Homo sapiens	61-67
20886344-0	2011	Aspirin promotes apoptosis in a murine model of colorectal cancer by mechanisms involving downregulation of IL-6-STAT3 signaling pathway.	Aspirin	0-7	interleukin 6	Mus musculus	108-112
20886344-0	2011	Aspirin promotes apoptosis in a murine model of colorectal cancer by mechanisms involving downregulation of IL-6-STAT3 signaling pathway.	Aspirin	0-7	signal transducer and activator of transcription 3	Mus musculus	113-118
20886344-1	2011	BACKGROUND AND AIMS: Aspirin is associated with a reduced risk of colorectal cancer (CRC), and it showed inhibited effects on interleukin 6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) signaling pathway which is thought to play an important role in intestinal inflammation and the tumorigenesis of CRC.	Aspirin	21-28	interleukin 6	Mus musculus	126-139
20886344-1	2011	BACKGROUND AND AIMS: Aspirin is associated with a reduced risk of colorectal cancer (CRC), and it showed inhibited effects on interleukin 6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) signaling pathway which is thought to play an important role in intestinal inflammation and the tumorigenesis of CRC.	Aspirin	21-28	interleukin 6	Mus musculus	141-145
20886344-1	2011	BACKGROUND AND AIMS: Aspirin is associated with a reduced risk of colorectal cancer (CRC), and it showed inhibited effects on interleukin 6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) signaling pathway which is thought to play an important role in intestinal inflammation and the tumorigenesis of CRC.	Aspirin	21-28	signal transducer and activator of transcription 3	Mus musculus	147-197
20886344-1	2011	BACKGROUND AND AIMS: Aspirin is associated with a reduced risk of colorectal cancer (CRC), and it showed inhibited effects on interleukin 6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) signaling pathway which is thought to play an important role in intestinal inflammation and the tumorigenesis of CRC.	Aspirin	21-28	signal transducer and activator of transcription 3	Mus musculus	199-204
20886344-6	2011	The expression level of IL-6, which is an upstream molecule of STAT3 and capable of activating STAT3, was reduced in aspirin-treated mice.	Aspirin	117-124	interleukin 6	Mus musculus	24-28
20886344-6	2011	The expression level of IL-6, which is an upstream molecule of STAT3 and capable of activating STAT3, was reduced in aspirin-treated mice.	Aspirin	117-124	signal transducer and activator of transcription 3	Mus musculus	63-68
20886344-6	2011	The expression level of IL-6, which is an upstream molecule of STAT3 and capable of activating STAT3, was reduced in aspirin-treated mice.	Aspirin	117-124	signal transducer and activator of transcription 3	Mus musculus	95-100
20886344-7	2011	Furthermore, the phosphorylated form of STAT3 and the levels of STAT3"s target gene products such as Bcl-xl and Bcl-2, which are essential for cell growth and survival, were also decreased in aspirin-treated mice.	Aspirin	192-199	signal transducer and activator of transcription 3	Mus musculus	40-45
20886344-7	2011	Furthermore, the phosphorylated form of STAT3 and the levels of STAT3"s target gene products such as Bcl-xl and Bcl-2, which are essential for cell growth and survival, were also decreased in aspirin-treated mice.	Aspirin	192-199	signal transducer and activator of transcription 3	Mus musculus	64-69
20886344-7	2011	Furthermore, the phosphorylated form of STAT3 and the levels of STAT3"s target gene products such as Bcl-xl and Bcl-2, which are essential for cell growth and survival, were also decreased in aspirin-treated mice.	Aspirin	192-199	B cell leukemia/lymphoma 2	Mus musculus	112-117
20886344-8	2011	CONCLUSIONS: Our data suggested that the protective mechanisms of aspirin in CRC may be associated with its effects on induction of CRC cell apoptosis and suppression of IL-6-STAT3 signaling pathway, which implied that aspirin has a potential therapeutic activity in CRC.	Aspirin	66-73	interleukin 6	Mus musculus	170-174
20886344-8	2011	CONCLUSIONS: Our data suggested that the protective mechanisms of aspirin in CRC may be associated with its effects on induction of CRC cell apoptosis and suppression of IL-6-STAT3 signaling pathway, which implied that aspirin has a potential therapeutic activity in CRC.	Aspirin	66-73	signal transducer and activator of transcription 3	Mus musculus	175-180
20886344-8	2011	CONCLUSIONS: Our data suggested that the protective mechanisms of aspirin in CRC may be associated with its effects on induction of CRC cell apoptosis and suppression of IL-6-STAT3 signaling pathway, which implied that aspirin has a potential therapeutic activity in CRC.	Aspirin	219-226	interleukin 6	Mus musculus	170-174
20886344-8	2011	CONCLUSIONS: Our data suggested that the protective mechanisms of aspirin in CRC may be associated with its effects on induction of CRC cell apoptosis and suppression of IL-6-STAT3 signaling pathway, which implied that aspirin has a potential therapeutic activity in CRC.	Aspirin	219-226	signal transducer and activator of transcription 3	Mus musculus	175-180
21086123-0	2011	A possible association of EMID2 polymorphisms with aspirin hypersensitivity in asthma.	Aspirin	51-58	collagen type XXVI alpha 1 chain	Homo sapiens	26-31
21086123-4	2011	In this study, the allelic associations of 49 single-nucleotide polymorphisms (SNPs) of the human EMID2 gene were evaluated from 163 AIA patients and 429 aspirin-tolerant asthma (ATA) subjects as controls in a Korean population.	Aspirin	154-161	collagen type XXVI alpha 1 chain	Homo sapiens	98-103
21086123-6	2011	More interestingly, regression analysis of the decline of forced expiratory volume in one second (FEV(1)) by aspirin provocation revealed that 10 SNPs (P = 0.003-0.04) and four relevant haplotypes (P = 0.002-0.02) were significantly associated with the fall rate of FEV(1) by aspirin provocation, indicating that genetic polymorphisms of EMID2 could cause meaningful deficits in the upper and lower airways among AIA patients.	Aspirin	109-116	collagen type XXVI alpha 1 chain	Homo sapiens	338-343
21086123-7	2011	These findings provide evidence that EMID2 may be a susceptible genetic factor for aspirin hypersensitivity among asthmatics in Korean population.	Aspirin	83-90	collagen type XXVI alpha 1 chain	Homo sapiens	37-42
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	mitogen-activated protein kinase 8	Homo sapiens	173-178
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	mitogen-activated protein kinase 8	Homo sapiens	277-282
21829647-0	2011	Fatty acid binding protein 1 is related with development of aspirin-exacerbated respiratory disease.	Aspirin	60-67	fatty acid binding protein 1	Homo sapiens	0-28
21625173-1	2011	BACKGROUND/AIMS: Interindividual variation in aspirin (ASA) metabolism is attributed to concomitant use of drugs or alcohol, urine pH, ethnicity, sex, and genetic variants in UDP-glucuronosyltransferases (UGT).	Aspirin	46-53	beta-1,3-glucuronyltransferase 2	Homo sapiens	175-203
21625173-1	2011	BACKGROUND/AIMS: Interindividual variation in aspirin (ASA) metabolism is attributed to concomitant use of drugs or alcohol, urine pH, ethnicity, sex, and genetic variants in UDP-glucuronosyltransferases (UGT).	Aspirin	46-53	beta-1,3-glucuronyltransferase 2	Homo sapiens	205-208
21625173-1	2011	BACKGROUND/AIMS: Interindividual variation in aspirin (ASA) metabolism is attributed to concomitant use of drugs or alcohol, urine pH, ethnicity, sex, and genetic variants in UDP-glucuronosyltransferases (UGT).	Aspirin	55-58	beta-1,3-glucuronyltransferase 2	Homo sapiens	175-203
21625173-1	2011	BACKGROUND/AIMS: Interindividual variation in aspirin (ASA) metabolism is attributed to concomitant use of drugs or alcohol, urine pH, ethnicity, sex, and genetic variants in UDP-glucuronosyltransferases (UGT).	Aspirin	55-58	beta-1,3-glucuronyltransferase 2	Homo sapiens	205-208
21557683-6	2011	Already a 15 min exposure of platelets to glucose impaired aspirin inhibition of the platelet aggregation induced by collagen, thrombin, adenosine diphosphate (ADP), and arachidonic acid (AA).	Aspirin	59-66	coagulation factor II, thrombin	Homo sapiens	127-135
21591982-9	2011	Low-response to aspirin assessed by analyses targeting cyclooxygenase-1 activity (LTA, IA) was rare (&lt;= 8.1%).	Aspirin	16-23	prostaglandin-endoperoxide synthase 1	Homo sapiens	55-71
22022418-8	2011	P-selectin glycoprotein ligand-1 (PSGL-1) blocking antibody, which abrogates MPA formation, abolished these effects, as did the cyclooxygenase (COX)-2 selective inhibitor NS-398, aspirin and the EP1/EP2-selective antagonist AH6809.	Aspirin	179-186	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	128-150
21542252-5	2011	ATL (AT mean aspirin triggered therefore "depend on aspirin") synthesis, via COX-2, reduces the severity of damage gastrointestinal tract induced by NSAIDs.	Aspirin	13-20	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	77-82
21542252-5	2011	ATL (AT mean aspirin triggered therefore "depend on aspirin") synthesis, via COX-2, reduces the severity of damage gastrointestinal tract induced by NSAIDs.	Aspirin	52-59	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	77-82
21720139-1	2011	Aspirin irreversibly inhibits the enzyme cyclooxygenase-1 and depresses the production of thromboxane A(2), and also exerts antiplatelet effects.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	41-57
20978715-3	2011	We defined the time course and magnitude of changes of plasma eNOS and oxLDL after Aggrenox or aspirin in post-stroke patients.	Aspirin	95-102	nitric oxide synthase 3	Homo sapiens	62-66
20978715-5	2011	Both Aggrenox and aspirin similarly increased plasma eNOS activity.	Aspirin	18-25	nitric oxide synthase 3	Homo sapiens	53-57
20978715-7	2011	In the small randomised study, both aspirin and Aggrenox produced fast and sustained recovery of plasma eNOS levels, while only therapy with Aggrenox was associated with oxLDL inhibition late in the trial.	Aspirin	36-43	nitric oxide synthase 3	Homo sapiens	104-108
20674154-6	2010	NO-Aspirin and NO-naproxen reduced NF-kappaB protein levels, and activated caspase-3 enzyme in a dose- and time-dependent manner.	Aspirin	3-10	nuclear factor kappa B subunit 1	Homo sapiens	35-44
20674154-6	2010	NO-Aspirin and NO-naproxen reduced NF-kappaB protein levels, and activated caspase-3 enzyme in a dose- and time-dependent manner.	Aspirin	3-10	caspase 3	Homo sapiens	75-84
20674154-9	2010	In vivo: rats treated with NO-ASA, NONO-ASA, and NO-naproxen showed S-nitrosylation of NF-kappaB p65 in the stomach tissue, increases in plasma TNF-alpha, and reductions in mucosal PGE(2) levels.	Aspirin	30-33	nuclear factor kappa B subunit 1	Homo sapiens	87-96
20674154-9	2010	In vivo: rats treated with NO-ASA, NONO-ASA, and NO-naproxen showed S-nitrosylation of NF-kappaB p65 in the stomach tissue, increases in plasma TNF-alpha, and reductions in mucosal PGE(2) levels.	Aspirin	30-33	synaptotagmin 1	Rattus norvegicus	97-100
20674154-9	2010	In vivo: rats treated with NO-ASA, NONO-ASA, and NO-naproxen showed S-nitrosylation of NF-kappaB p65 in the stomach tissue, increases in plasma TNF-alpha, and reductions in mucosal PGE(2) levels.	Aspirin	30-33	tumor necrosis factor	Rattus norvegicus	144-153
24688156-15	2010	In the ASA+beta-glucan group, MDA and NO levels and CAT and GSH-Px activities were found to be significantly lower, while SOD activity was found to be significantly higher, in comparison with the ASA-treated group (all, P &lt; 0.001).	Aspirin	7-10	catalase	Rattus norvegicus	52-55
20640495-16	2010	Both SIM and DIP+low-dose ASA augmented Akt phosphorylation and their effect was additive.	Aspirin	26-29	AKT serine/threonine kinase 1	Rattus norvegicus	40-43
20921925-0	2010	Effect of single nucleotide polymorphisms within the interleukin-4 promoter on aspirin intolerance in asthmatics and interleukin-4 promoter activity.	Aspirin	79-86	interleukin 4	Homo sapiens	53-66
20921925-1	2010	OBJECTIVE: Aspirin affects interleukin-4 (IL-4) synthesis; however, the genetic role of IL-4 has not been evaluated in asthmatics with aspirin hypersensitivity.	Aspirin	11-18	interleukin 4	Homo sapiens	27-40
20921925-1	2010	OBJECTIVE: Aspirin affects interleukin-4 (IL-4) synthesis; however, the genetic role of IL-4 has not been evaluated in asthmatics with aspirin hypersensitivity.	Aspirin	11-18	interleukin 4	Homo sapiens	42-46
20921925-2	2010	The objective of the study was to examine the influence of single nucleotide polymorphisms (SNPs) in IL-4 gene on aspirin hypersensitivity in asthmatics at the genetic and molecular levels.	Aspirin	114-121	interleukin 4	Homo sapiens	101-105
20921925-7	2010	A reporter plasmid assay revealed that aspirin augmented IL-4 promoter transactivation with the -589T&gt;C C and -33T&gt;C C alleles, compared with that bearing the -589T&gt;C T and -33T&gt;C T alleles.	Aspirin	39-46	interleukin 4	Homo sapiens	57-61
20921925-10	2010	CONCLUSION: Aspirin may regulate IL4 expression in an allele-specific manner by altering the availability of transcription factors to the key regulatory elements in the IL4 promoter, leading to aspirin hypersensitivity.	Aspirin	12-19	interleukin 4	Homo sapiens	33-36
20921925-10	2010	CONCLUSION: Aspirin may regulate IL4 expression in an allele-specific manner by altering the availability of transcription factors to the key regulatory elements in the IL4 promoter, leading to aspirin hypersensitivity.	Aspirin	12-19	interleukin 4	Homo sapiens	169-172
20921925-10	2010	CONCLUSION: Aspirin may regulate IL4 expression in an allele-specific manner by altering the availability of transcription factors to the key regulatory elements in the IL4 promoter, leading to aspirin hypersensitivity.	Aspirin	194-201	interleukin 4	Homo sapiens	33-36
20921925-10	2010	CONCLUSION: Aspirin may regulate IL4 expression in an allele-specific manner by altering the availability of transcription factors to the key regulatory elements in the IL4 promoter, leading to aspirin hypersensitivity.	Aspirin	194-201	interleukin 4	Homo sapiens	169-172
20831471-7	2010	METHODS: We conducted an association study between 19 SNPs of the SMAP1L gene and AIA in a total of 592 Korean subjects including 163 AIA and 429 aspirin-tolerant asthma (ATA) patients.	Aspirin	146-153	small ArfGAP2	Homo sapiens	66-72
20716228-0	2010	Functional variability of the adenosine A3 receptor (ADORA3) gene polymorphism in aspirin-induced urticaria.	Aspirin	82-89	adenosine A3 receptor	Homo sapiens	30-51
20716228-0	2010	Functional variability of the adenosine A3 receptor (ADORA3) gene polymorphism in aspirin-induced urticaria.	Aspirin	82-89	adenosine A3 receptor	Homo sapiens	53-59
20716228-3	2010	OBJECTIVES: To investigate the genetic contribution of adenosine A3 receptor gene (ADORA3) polymorphisms in the pathogenesis of aspirin-induced urticaria (AIU) in a case-control association study in a Korean population.	Aspirin	128-135	adenosine A3 receptor	Homo sapiens	55-76
20716228-3	2010	OBJECTIVES: To investigate the genetic contribution of adenosine A3 receptor gene (ADORA3) polymorphisms in the pathogenesis of aspirin-induced urticaria (AIU) in a case-control association study in a Korean population.	Aspirin	128-135	adenosine A3 receptor	Homo sapiens	83-89
20716228-10	2010	CONCLUSION: These results suggest that the high-transcript haplotype, ht1 (TC), of the ADORA3 gene may contribute to the development of cutaneous hyper-reactivity to aspirin, leading to the clinical presentation of AIU.	Aspirin	166-173	adenosine A3 receptor	Homo sapiens	87-93
20967400-6	2010	Dabigatran etexilate 150 mg BID was estimated to significantly reduce the risk of any stroke compared with aspirin monotherapy by 63% (RR 0.37; 95% CI 0.20-0.69) and aspirin plus clopidogrel by 61% (RR 0.39; 95% CI 0.21-0.72).	Aspirin	107-114	BH3 interacting domain death agonist	Homo sapiens	28-31
20967400-6	2010	Dabigatran etexilate 150 mg BID was estimated to significantly reduce the risk of any stroke compared with aspirin monotherapy by 63% (RR 0.37; 95% CI 0.20-0.69) and aspirin plus clopidogrel by 61% (RR 0.39; 95% CI 0.21-0.72).	Aspirin	166-173	BH3 interacting domain death agonist	Homo sapiens	28-31
20950383-6	2010	Across the pooled study sample, change in ambulatory activity was significantly correlated with change in interleukin-6 (r = -0.32, P = 0.01) after adjustment for group, age, sex, ethnicity, aspirin and statin medication, baseline body mass index and change in body mass index.	Aspirin	191-198	interleukin 6	Homo sapiens	106-119
20831471-11	2010	CONCLUSIONS: Our findings suggest that SMAP1L might be a susceptible gene to AIA, providing a new strategy for the control of aspirin intolerance.	Aspirin	126-133	small ArfGAP2	Homo sapiens	39-45
20739877-3	2010	To evaluate the association between glycoprotein IIIa PlA1/PlA2 polymorphism and 1-year cardiovascular events occurrence in aspirin-treated patients with stable coronary artery disease.	Aspirin	124-131	phospholipase A2 group IB	Homo sapiens	59-63
21039786-1	2010	It has been proposed that aspirin (ASA) and other non-steroidal anti-inflammatory drug (NSAID)-induced urticaria (UR)/angioedema (AE) are mediated through inhibition of cyclooxygenase-1 (COX-1) enzymes.	Aspirin	26-33	prostaglandin-endoperoxide synthase 1	Homo sapiens	169-185
21039786-1	2010	It has been proposed that aspirin (ASA) and other non-steroidal anti-inflammatory drug (NSAID)-induced urticaria (UR)/angioedema (AE) are mediated through inhibition of cyclooxygenase-1 (COX-1) enzymes.	Aspirin	26-33	prostaglandin-endoperoxide synthase 1	Homo sapiens	187-192
21039786-1	2010	It has been proposed that aspirin (ASA) and other non-steroidal anti-inflammatory drug (NSAID)-induced urticaria (UR)/angioedema (AE) are mediated through inhibition of cyclooxygenase-1 (COX-1) enzymes.	Aspirin	35-38	prostaglandin-endoperoxide synthase 1	Homo sapiens	169-185
21039786-1	2010	It has been proposed that aspirin (ASA) and other non-steroidal anti-inflammatory drug (NSAID)-induced urticaria (UR)/angioedema (AE) are mediated through inhibition of cyclooxygenase-1 (COX-1) enzymes.	Aspirin	35-38	prostaglandin-endoperoxide synthase 1	Homo sapiens	187-192
21331307-0	2010	COX-2 Inhibition by Use of Rofecoxib or High Dose Aspirin Enhances ADP-Induced Platelet Aggregation in Fresh Blood.	Aspirin	50-57	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
20920644-2	2010	Conflicting evidence is available regarding whether aspirin can reduce CRP after ACS.	Aspirin	52-59	C-reactive protein	Homo sapiens	71-74
20920644-3	2010	We investigated whether the dosage and adherence to aspirin was associated with the CRP level 3 months after ACS.	Aspirin	52-59	C-reactive protein	Homo sapiens	84-87
20920644-6	2010	Logistic regression analysis was used to test whether poor adherence to aspirin and a lower aspirin dosage were associated with increased CRP levels, controlling for age, ACS type, disease co-morbidity, baseline CRP level, use of clopidogrel and statins, depressive symptoms, smoking, and adherence to other medications.	Aspirin	72-79	C-reactive protein	Homo sapiens	138-141
20920644-6	2010	Logistic regression analysis was used to test whether poor adherence to aspirin and a lower aspirin dosage were associated with increased CRP levels, controlling for age, ACS type, disease co-morbidity, baseline CRP level, use of clopidogrel and statins, depressive symptoms, smoking, and adherence to other medications.	Aspirin	92-99	C-reactive protein	Homo sapiens	138-141
20920644-7	2010	Aspirin adherence was inversely correlated with the CRP level at 3 months (Spearman"s r = -0.36, p &lt; 0.001).	Aspirin	0-7	C-reactive protein	Homo sapiens	52-55
20920644-8	2010	In the adjusted model, every 10% decrease in aspirin adherence was associated with a 1.7 increased risk (95% confidence interval 1.2 to 2.4) of a CRP level of &gt;= 3.0 mg/L at 3 months.	Aspirin	45-52	C-reactive protein	Homo sapiens	146-149
20920644-9	2010	Low-dose aspirin was associated with a 7.1 increased risk (95% confidence interval 1.5 to 33.3) of a CRP level of &gt;= 3.0 mg/L.	Aspirin	9-16	C-reactive protein	Homo sapiens	101-104
20920644-11	2010	The association between aspirin adherence and CRP level was not attenuated by controlling for other risk-reducing behaviors.	Aspirin	24-31	C-reactive protein	Homo sapiens	46-49
20920644-12	2010	In conclusion, a strong association was found between aspirin adherence and the CRP level after an ACS.	Aspirin	54-61	C-reactive protein	Homo sapiens	80-83
20934631-0	2010	Association analysis of UBE3C polymorphisms in Korean aspirin-intolerant asthmatic patients.	Aspirin	54-61	ubiquitin protein ligase E3C	Homo sapiens	24-29
20934631-5	2010	METHODS: Twenty-four nonmonomorphic genetic variants of UBE3C were genotyped in 163 patients with AIA and 429 controls with aspirin-tolerant asthma.	Aspirin	124-131	ubiquitin protein ligase E3C	Homo sapiens	56-61
20705923-6	2010	METHODS AND RESULTS: Low concentrations of aspirin induce lysine acetylation of eNOS, stimulating eNOS enzymatic activity and endothelial NO production in a cyclooxygenase-1-independent fashion.	Aspirin	43-50	prostaglandin-endoperoxide synthase 1	Homo sapiens	157-173
20705923-7	2010	Low-dose aspirin in vivo also increases bioavailable vascular NO in an eNOS-dependent and cyclooxygenase-1-independent manner.	Aspirin	9-16	nitric oxide synthase 3	Homo sapiens	71-75
20705923-0	2010	Histone deacetylase 3 antagonizes aspirin-stimulated endothelial nitric oxide production by reversing aspirin-induced lysine acetylation of endothelial nitric oxide synthase.	Aspirin	34-41	nitric oxide synthase 3	Homo sapiens	140-173
20705923-0	2010	Histone deacetylase 3 antagonizes aspirin-stimulated endothelial nitric oxide production by reversing aspirin-induced lysine acetylation of endothelial nitric oxide synthase.	Aspirin	102-109	nitric oxide synthase 3	Homo sapiens	140-173
20705923-6	2010	METHODS AND RESULTS: Low concentrations of aspirin induce lysine acetylation of eNOS, stimulating eNOS enzymatic activity and endothelial NO production in a cyclooxygenase-1-independent fashion.	Aspirin	43-50	nitric oxide synthase 3	Homo sapiens	80-84
20705923-6	2010	METHODS AND RESULTS: Low concentrations of aspirin induce lysine acetylation of eNOS, stimulating eNOS enzymatic activity and endothelial NO production in a cyclooxygenase-1-independent fashion.	Aspirin	43-50	nitric oxide synthase 3	Homo sapiens	98-102
20705923-7	2010	Low-dose aspirin in vivo also increases bioavailable vascular NO in an eNOS-dependent and cyclooxygenase-1-independent manner.	Aspirin	9-16	prostaglandin-endoperoxide synthase 1	Homo sapiens	90-106
20705923-8	2010	Low-dose aspirin promotes the binding of eNOS to calmodulin.	Aspirin	9-16	nitric oxide synthase 3	Homo sapiens	41-45
20705923-8	2010	Low-dose aspirin promotes the binding of eNOS to calmodulin.	Aspirin	9-16	calmodulin 1	Homo sapiens	49-59
20705923-9	2010	Lysine 609 in the calmodulin autoinhibitory domain of bovine eNOS mediates aspirin-stimulated binding of eNOS to calmodulin and eNOS-derived NO production.	Aspirin	75-82	calmodulin 1	Homo sapiens	18-28
20705923-9	2010	Lysine 609 in the calmodulin autoinhibitory domain of bovine eNOS mediates aspirin-stimulated binding of eNOS to calmodulin and eNOS-derived NO production.	Aspirin	75-82	nitric oxide synthase 3	Bos taurus	61-65
20705923-9	2010	Lysine 609 in the calmodulin autoinhibitory domain of bovine eNOS mediates aspirin-stimulated binding of eNOS to calmodulin and eNOS-derived NO production.	Aspirin	75-82	nitric oxide synthase 3	Bos taurus	105-109
20705923-9	2010	Lysine 609 in the calmodulin autoinhibitory domain of bovine eNOS mediates aspirin-stimulated binding of eNOS to calmodulin and eNOS-derived NO production.	Aspirin	75-82	calmodulin	Bos taurus	113-123
20705923-9	2010	Lysine 609 in the calmodulin autoinhibitory domain of bovine eNOS mediates aspirin-stimulated binding of eNOS to calmodulin and eNOS-derived NO production.	Aspirin	75-82	nitric oxide synthase 3	Bos taurus	105-109
20705923-10	2010	HDAC3 inhibits aspirin-stimulated (1) lysine acetylation of eNOS, (2) eNOS enzymatic activity, (3) eNOS-derived NO, and (4) binding of eNOS to calmodulin.	Aspirin	15-22	nitric oxide synthase 3	Homo sapiens	60-64
20705923-10	2010	HDAC3 inhibits aspirin-stimulated (1) lysine acetylation of eNOS, (2) eNOS enzymatic activity, (3) eNOS-derived NO, and (4) binding of eNOS to calmodulin.	Aspirin	15-22	nitric oxide synthase 3	Homo sapiens	70-74
20705923-10	2010	HDAC3 inhibits aspirin-stimulated (1) lysine acetylation of eNOS, (2) eNOS enzymatic activity, (3) eNOS-derived NO, and (4) binding of eNOS to calmodulin.	Aspirin	15-22	nitric oxide synthase 3	Homo sapiens	70-74
20705923-10	2010	HDAC3 inhibits aspirin-stimulated (1) lysine acetylation of eNOS, (2) eNOS enzymatic activity, (3) eNOS-derived NO, and (4) binding of eNOS to calmodulin.	Aspirin	15-22	nitric oxide synthase 3	Homo sapiens	70-74
20705923-10	2010	HDAC3 inhibits aspirin-stimulated (1) lysine acetylation of eNOS, (2) eNOS enzymatic activity, (3) eNOS-derived NO, and (4) binding of eNOS to calmodulin.	Aspirin	15-22	calmodulin 1	Homo sapiens	143-153
20705923-12	2010	CONCLUSIONS: Lysine acetylation of eNOS is a posttranslational protein modification supporting low-dose aspirin-induced vasoprotection.	Aspirin	104-111	nitric oxide synthase 3	Homo sapiens	35-39
20705923-13	2010	HDAC3, by deacetylating aspirin-acetylated eNOS, antagonizes aspirin-stimulated endothelial production of NO.	Aspirin	24-31	nitric oxide synthase 3	Homo sapiens	43-47
20705923-13	2010	HDAC3, by deacetylating aspirin-acetylated eNOS, antagonizes aspirin-stimulated endothelial production of NO.	Aspirin	61-68	nitric oxide synthase 3	Homo sapiens	43-47
20728206-8	2010	After 6 months of aspirin treatment, sputum IL-4 (P = .0007) and matrix metalloproteinase 9 (MMP-9; P = .05) decreased significantly compared with baseline.	Aspirin	18-25	interleukin 4	Homo sapiens	44-48
20728206-13	2010	In contrast, long-term treatment with aspirin involves suppression of IL-4 as well as downregulation of proinflammatory MMP-9 while T(H)1 marker FLT3-L increases.	Aspirin	38-45	interleukin 4	Homo sapiens	70-74
20920763-0	2010	Does suppression of IL-4 synthesis by aspirin explain the therapeutic benefit of aspirin desensitization treatment?	Aspirin	38-45	interleukin 4	Homo sapiens	20-24
20624109-0	2010	High-dose fibrinogen concentrate for haemostatic therapy of a major trauma patient with recent clopidogrel and aspirin intake.	Aspirin	111-118	fibrinogen beta chain	Homo sapiens	10-20
20723029-0	2010	High on-aspirin platelet reactivity as measured with aggregation-based, cyclooxygenase-1 inhibition sensitive platelet function tests is associated with the occurrence of atherothrombotic events.	Aspirin	8-15	prostaglandin-endoperoxide synthase 1	Homo sapiens	72-88
20664853-3	2010	Although this new group of 1,1-diaryl-2-(4-hydroxyaminosulfonylphenyl)alk-1-enes exhibited weak inhibition of the constitutive cyclooxygenase-1 (COX-1) and inducible COX-2 isozymes, in vivo studies showed anti-inflammatory potencies that were generally intermediate between that of the reference drugs aspirin and ibuprofen.	Aspirin	302-309	prostaglandin-endoperoxide synthase 1	Homo sapiens	127-143
20664853-3	2010	Although this new group of 1,1-diaryl-2-(4-hydroxyaminosulfonylphenyl)alk-1-enes exhibited weak inhibition of the constitutive cyclooxygenase-1 (COX-1) and inducible COX-2 isozymes, in vivo studies showed anti-inflammatory potencies that were generally intermediate between that of the reference drugs aspirin and ibuprofen.	Aspirin	302-309	prostaglandin-endoperoxide synthase 1	Homo sapiens	145-150
20862244-7	2010	Finally, connectivity map analysis for AnxA1 and peptide Ac2-26 indicated striking similarities with known anti-inflammatory therapeutics, glucocorticoids and aspirin-like compounds, as well as with histone deacetylase inhibitors.	Aspirin	159-166	adenylate cyclase 2	Homo sapiens	57-60
20337611-3	2010	OBJECTIVE: To evaluate the therapeutic or adverse effects of acetyl salicylic acid (ASA) on the expression of Th1-type and Th17-type inflammation induced by airway exposure to LPS-containing allergens.	Aspirin	61-82	negative elongation factor complex member C/D, Th1l	Mus musculus	110-113
20697066-8	2010	Use of aspirin is proven to lower risk of colorectal cancer, and recent evidence suggests that aspirin use in patients with colorectal cancer improves cancer-specific and overall survival, especially in patients with tumors that express cyclooxygenase-2 (COX-2).	Aspirin	95-102	prostaglandin-endoperoxide synthase 2	Homo sapiens	237-253
20697066-8	2010	Use of aspirin is proven to lower risk of colorectal cancer, and recent evidence suggests that aspirin use in patients with colorectal cancer improves cancer-specific and overall survival, especially in patients with tumors that express cyclooxygenase-2 (COX-2).	Aspirin	95-102	prostaglandin-endoperoxide synthase 2	Homo sapiens	255-260
20337611-3	2010	OBJECTIVE: To evaluate the therapeutic or adverse effects of acetyl salicylic acid (ASA) on the expression of Th1-type and Th17-type inflammation induced by airway exposure to LPS-containing allergens.	Aspirin	84-87	negative elongation factor complex member C/D, Th1l	Mus musculus	110-113
20337611-6	2010	RESULTS: Lung infiltration of eosinophils was enhanced in OVA/LPS-sensitized mice by ASA treatment, which was accompanied by the enhanced production of eotaxin.	Aspirin	85-88	chemokine (C-C motif) ligand 11	Mus musculus	152-159
20337611-8	2010	Lung inflammation induced by LPS-containing allergen was markedly reduced in IL-13-deficient mice in the context of ASA treatment, but not without ASA.	Aspirin	116-119	interleukin 13	Mus musculus	77-82
20665602-6	2010	The expression of GRP78 was induced in endothelial cells after exposure to hydrogen peroxide for 12 h. The overexpression of GRP78 was inhibited by nimesulide and aspirin, but not by piroxicam.	Aspirin	163-170	heat shock protein family A (Hsp70) member 5	Homo sapiens	18-23
20665602-6	2010	The expression of GRP78 was induced in endothelial cells after exposure to hydrogen peroxide for 12 h. The overexpression of GRP78 was inhibited by nimesulide and aspirin, but not by piroxicam.	Aspirin	163-170	heat shock protein family A (Hsp70) member 5	Homo sapiens	125-130
20665602-5	2010	The results showed that after the endothelial cells were incubated with 250 muM of hydrogen peroxide for 12 h, apoptosis increased, which was antagonized by the cyclooxygenase-2 inhibitor nimesulide or the nonselective cyclooxygenase inhibitor aspirin, but not by the cyclooxygenase-1 inhibitor piroxicam.	Aspirin	244-251	prostaglandin-endoperoxide synthase 2	Homo sapiens	161-177
22396856-9	2010	This depends on the allosteric effects of ASA on cyclooxygenase-2 and following production - from DHA - of specific lipid mediators (resolvins, protectins, and electrophilic oxo-derivatives).	Aspirin	42-45	prostaglandin-endoperoxide synthase 2	Homo sapiens	49-65
20864907-11	2010	Following appropriate discussions, acetylsalicylic acid (ASA) can soon be restarted acutely after bleeding; long-term PPI co-therapy is imperative in patients having bled on nonsteroidal anti-inflammatory drugs if still needed (preferably with a cyclooxygenase-2, if appropriate) or ASA (not clopidogrel alone).	Aspirin	57-60	prostaglandin-endoperoxide synthase 2	Homo sapiens	246-262
20550971-17	2010	Elevated POD#5 uTxB2 and pre-operative CRP were correlated with thrombosis in aspirin treated subjects.	Aspirin	78-85	C-reactive protein	Homo sapiens	39-42
20713906-0	2010	Letter by Violi et al regarding article, "Association of cyclooxygenase-1-dependent and -independent platelet function assays with adverse clinical outcomes in aspirin-treated patients presenting for cardiac catheterization".	Aspirin	160-167	prostaglandin-endoperoxide synthase 1	Homo sapiens	57-73
20359903-5	2010	Aspirin being a COX-2 inhibitor has been shown to reduce the chance of metastasis in adenocarcinoma but not squamous carcinoma.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	16-21
20653671-3	2010	WHAT THIS PAPER ADDS: The data presented in this manuscript clearly show that the endocannabinoid 2-arrachidonyl glycerol can activate platelet activity, but that the effects are mediated through an aspirin-sensitive pathway that is not affected by cannabinoid receptor antagonists or FAAH inhibition, but is abolished by MAGL inhibition.	Aspirin	199-206	fatty acid amide hydrolase	Homo sapiens	285-289
20397022-1	2010	PURPOSE: To investigate the effect of cyclooxygenase-2 (Cox-2) inhibitor aspirin (acetylsalicylic acid, ASA) and proteasome inhibitor bortezomib in the proliferation and apoptosis of colorectal cancer cell lines.	Aspirin	73-80	prostaglandin-endoperoxide synthase 2	Homo sapiens	38-54
20397022-1	2010	PURPOSE: To investigate the effect of cyclooxygenase-2 (Cox-2) inhibitor aspirin (acetylsalicylic acid, ASA) and proteasome inhibitor bortezomib in the proliferation and apoptosis of colorectal cancer cell lines.	Aspirin	73-80	prostaglandin-endoperoxide synthase 2	Homo sapiens	56-61
20397022-1	2010	PURPOSE: To investigate the effect of cyclooxygenase-2 (Cox-2) inhibitor aspirin (acetylsalicylic acid, ASA) and proteasome inhibitor bortezomib in the proliferation and apoptosis of colorectal cancer cell lines.	Aspirin	82-102	prostaglandin-endoperoxide synthase 2	Homo sapiens	56-61
20397022-6	2010	In the first two cell lines ASA inhibitory effects are Cox-2 independent because HCT116 cells do not express the enzyme while in HT-29 cells, Cox-2 has no activity as shown by a Cox activity assay.	Aspirin	28-31	prostaglandin-endoperoxide synthase 2	Homo sapiens	55-60
20397022-7	2010	In CaCo2 cells that express enzymatically active Cox-2 this activity is inhibited by ASA.	Aspirin	85-88	prostaglandin-endoperoxide synthase 2	Homo sapiens	49-54
20397022-8	2010	ASA is also able to suppress the increase in Cox-2 activity induced by bortezomib in these cells.	Aspirin	0-3	prostaglandin-endoperoxide synthase 2	Homo sapiens	45-50
20587336-6	2010	Our findings provide further evidence that polymorphisms in PTGER3 might play a significant role in aspirin hypersensitivity among Korean asthmatics.	Aspirin	100-107	prostaglandin E receptor 3	Homo sapiens	60-66
20514442-5	2010	We report that treatment of the DNA MMR competent/p53 mutant colorectal cancer cell line SW480 with 1 mM aspirin for 48 h caused changes in mRNA expression of several key genes involved in DNA damage signalling pathways, including a significant down-regulation in transcription of the genes ATR, BRCA1 and MAPK12.	Aspirin	105-112	tumor protein p53	Homo sapiens	50-53
20514442-5	2010	We report that treatment of the DNA MMR competent/p53 mutant colorectal cancer cell line SW480 with 1 mM aspirin for 48 h caused changes in mRNA expression of several key genes involved in DNA damage signalling pathways, including a significant down-regulation in transcription of the genes ATR, BRCA1 and MAPK12.	Aspirin	105-112	ATR serine/threonine kinase	Homo sapiens	291-294
20188076-5	2010	Protein levels of Hsp70, the product of HSPA1A, and fos were increased in p-NO-ASA-treated Jurkat T and HT-29 colon cancer cells in a dose-dependent manner.	Aspirin	79-82	heat shock protein family A (Hsp70) member 1A	Homo sapiens	40-46
20513247-0	2010	Positive association between aspirin-intolerant asthma and genetic polymorphisms of FSIP1: a case-case study.	Aspirin	29-36	fibrous sheath interacting protein 1	Homo sapiens	84-89
20513247-11	2010	Our findings suggest that FSIP1 gene might be a susceptibility gene for aspirin intolerance in asthmatics.	Aspirin	72-79	fibrous sheath interacting protein 1	Homo sapiens	26-31
19424877-0	2010	Aspirin inhibits ErbB2 to induce apoptosis in cervical cancer cells.	Aspirin	0-7	erb-b2 receptor tyrosine kinase 2	Homo sapiens	17-22
20404564-0	2010	The effects of the histone deacetylase inhibitor romidepsin (FK228) are enhanced by aspirin (ASA) in COX-1 positive ovarian cancer cells through augmentation of p21.	Aspirin	84-91	prostaglandin-endoperoxide synthase 1	Homo sapiens	101-106
20404564-0	2010	The effects of the histone deacetylase inhibitor romidepsin (FK228) are enhanced by aspirin (ASA) in COX-1 positive ovarian cancer cells through augmentation of p21.	Aspirin	93-96	prostaglandin-endoperoxide synthase 1	Homo sapiens	101-106
20404564-6	2010	ASA is a relatively selective inhibitor of cyclooxygenase-1 (COX-1) and has anti-proliferative effects in ovarian cancer cells.	Aspirin	0-3	prostaglandin-endoperoxide synthase 1	Homo sapiens	43-59
20404564-6	2010	ASA is a relatively selective inhibitor of cyclooxygenase-1 (COX-1) and has anti-proliferative effects in ovarian cancer cells.	Aspirin	0-3	prostaglandin-endoperoxide synthase 1	Homo sapiens	61-66
20404564-8	2010	The growth inhibitory effects of FK228 were enhanced by ASA in COX-1 positive ovarian cancer cells.	Aspirin	56-59	prostaglandin-endoperoxide synthase 1	Homo sapiens	63-68
20404564-11	2010	In the COX-1 positive cells, p21 expression was augmented by the addition of ASA to FK228 treatment.	Aspirin	77-80	prostaglandin-endoperoxide synthase 1	Homo sapiens	7-12
20404564-12	2010	Furthermore, COX-1 siRNA attenuated the effects of combined ASA and FK228 on the levels of p21 expression and the amount of growth inhibition.	Aspirin	60-63	prostaglandin-endoperoxide synthase 1	Homo sapiens	13-18
20404564-14	2010	However, a significant delay in p21 protein degradation in the presence of ASA and FK228 in COX-1 positive cells was associated with inhibition of proteasome activity.	Aspirin	75-78	prostaglandin-endoperoxide synthase 1	Homo sapiens	92-97
20819511-6	2010	Activation of p38 mitogen activated protein kinase and NF-kappaB, the expression of intercellular adhesion molecule-1 and monocyte chemotactic protein-1, which were only mildly affected by aspirin or pravastatin alone, were significantly attenuated by their combination.	Aspirin	189-196	mitogen-activated protein kinase 14	Homo sapiens	14-17
20819511-6	2010	Activation of p38 mitogen activated protein kinase and NF-kappaB, the expression of intercellular adhesion molecule-1 and monocyte chemotactic protein-1, which were only mildly affected by aspirin or pravastatin alone, were significantly attenuated by their combination.	Aspirin	189-196	nuclear factor kappa B subunit 1	Homo sapiens	55-64
19424877-4	2010	In the present study, we investigated whether aspirin had therapeutic value in cervical cancer and examined the effects of aspirin on the amplification and expression of ErbB2.	Aspirin	123-130	erb-b2 receptor tyrosine kinase 2	Homo sapiens	170-175
19424877-7	2010	Western blot and immunocytochemical staining showed that aspirin induced a dose- and time-dependent reduction of ErbB2 expression that was due to proteosome-mediated degradation of this protein.	Aspirin	57-64	erb-b2 receptor tyrosine kinase 2	Homo sapiens	113-118
19424877-8	2010	To further investigate the underlying mechanism by which aspirin exerts its apoptosis effects, we studied the ErbB2 downstream cell survival signaling pathways and the expression of anti-apoptosis gene Bcl-2.	Aspirin	57-64	erb-b2 receptor tyrosine kinase 2	Homo sapiens	110-115
19424877-8	2010	To further investigate the underlying mechanism by which aspirin exerts its apoptosis effects, we studied the ErbB2 downstream cell survival signaling pathways and the expression of anti-apoptosis gene Bcl-2.	Aspirin	57-64	BCL2 apoptosis regulator	Homo sapiens	202-207
19424877-9	2010	We found that aspirin inhibited the activation of extracellular signal-regulated kinase (ERK) and AKT.	Aspirin	14-21	mitogen-activated protein kinase 1	Homo sapiens	50-87
19424877-9	2010	We found that aspirin inhibited the activation of extracellular signal-regulated kinase (ERK) and AKT.	Aspirin	14-21	mitogen-activated protein kinase 1	Homo sapiens	89-92
19424877-9	2010	We found that aspirin inhibited the activation of extracellular signal-regulated kinase (ERK) and AKT.	Aspirin	14-21	AKT serine/threonine kinase 1	Homo sapiens	98-101
19424877-11	2010	These data reveal that aspirin significantly induces apoptosis and inhibits proliferation, which maybe via inhibiting ErbB2 downstream cell survival signaling pathways.	Aspirin	23-30	erb-b2 receptor tyrosine kinase 2	Homo sapiens	118-123
20180823-6	2010	HF patients on low-dose aspirin had significantly lower 11-dehydro-TXB(2) (P &lt; 0.0001), sCD40L (P = 0.007) and 2,3-dinor-6-keto-PGF(1alpha) (P = 0.005) than HF patients not treated with aspirin.	Aspirin	24-31	placental growth factor	Homo sapiens	131-134
20194532-0	2010	Asymmetric acetylation of the cyclooxygenase-2 homodimer by aspirin and its effects on the oxygenation of arachidonic, eicosapentaenoic, and docosahexaenoic acids.	Aspirin	60-67	prostaglandin-endoperoxide synthase 2	Homo sapiens	30-46
20194532-3	2010	Here we report that aspirin maximally acetylates one monomer of human (hu) PGHS-2.	Aspirin	20-27	prostaglandin-endoperoxide synthase 2	Homo sapiens	75-81
20194532-6	2010	The 18R- and 17R-resolvins putatively involved in resolution of inflammation are reportedly formed via aspirin-acetylated PGHS-2 from eicosapentaenoic acid and docosahexaenoic acid, respectively, so we also characterized the oxygenation of these omega-3 fatty acids by aspirin-treated huPGHS-2.	Aspirin	103-110	prostaglandin-endoperoxide synthase 2	Homo sapiens	122-128
20194532-6	2010	The 18R- and 17R-resolvins putatively involved in resolution of inflammation are reportedly formed via aspirin-acetylated PGHS-2 from eicosapentaenoic acid and docosahexaenoic acid, respectively, so we also characterized the oxygenation of these omega-3 fatty acids by aspirin-treated huPGHS-2.	Aspirin	269-276	prostaglandin-endoperoxide synthase 2	Homo sapiens	122-128
27713316-2	2010	Aspirin and several small molecule NSAIDs are known to inhibit the enzymes cyclooxygenase-1 (COX-1) and -2 (COX-2).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	75-91
27713316-2	2010	Aspirin and several small molecule NSAIDs are known to inhibit the enzymes cyclooxygenase-1 (COX-1) and -2 (COX-2).	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	108-113
20427397-10	2010	The protective effect of aspirin was mainly observed in patients in whom COX-2 initial expression was low (RR for recurrence in patients taking aspirin with low COX-2 expression: 0.59; 95% CI 0.39 to 0.90; p=0.02).	Aspirin	25-32	prostaglandin-endoperoxide synthase 2	Homo sapiens	73-78
20427397-10	2010	The protective effect of aspirin was mainly observed in patients in whom COX-2 initial expression was low (RR for recurrence in patients taking aspirin with low COX-2 expression: 0.59; 95% CI 0.39 to 0.90; p=0.02).	Aspirin	25-32	prostaglandin-endoperoxide synthase 2	Homo sapiens	161-166
20427397-10	2010	The protective effect of aspirin was mainly observed in patients in whom COX-2 initial expression was low (RR for recurrence in patients taking aspirin with low COX-2 expression: 0.59; 95% CI 0.39 to 0.90; p=0.02).	Aspirin	144-151	prostaglandin-endoperoxide synthase 2	Homo sapiens	161-166
20436486-4	2010	Modulation of COX-2 activity by aspirin increased the rate of EFOX production and their intracellular levels.	Aspirin	32-39	prostaglandin-endoperoxide synthase 2	Homo sapiens	14-19
20352155-5	2010	Serum and urinary thromboxane metabolites were measured several times to evaluate cyclooxygenase-1 inhibition by aspirin.	Aspirin	113-120	prostaglandin-endoperoxide synthase 1	Homo sapiens	82-98
20096260-7	2010	Aspirin, quercetin, and simvastatin are compounds reported to increase PON1 expression.	Aspirin	0-7	paraoxonase 1	Homo sapiens	71-75
20631409-12	2010	The thrombolytic actions of lipophilic ACE-Is (e.g., quinapril and perindopril) were prevented by pretreatment with either bradykinin B(2) receptor antagonists (e.g., icatibant) or with endothelial COX-2 inhibitors (e.g., rofecoxib, celecoxib and high dose aspirin).	Aspirin	257-264	kininogen 1	Homo sapiens	123-133
20133435-9	2010	Furthermore, the increased P-selectin surface expression was obviously reduced in platelets from mice treated with aspirin/hypergravity compared with those from mice treated with hypergravity alone.	Aspirin	115-122	selectin, platelet	Mus musculus	27-37
20586862-2	2010	Two single nucleotide polymorphisms (SNP) of cyclooxygenase-1 (COX-1), A-842G and C50T, exhibited increased sensitivity to aspirin and had lower prostaglandin synthesis capacity, lacking statistical significance in the association with bleeding peptic ulcer.	Aspirin	123-130	prostaglandin-endoperoxide synthase 1	Homo sapiens	45-61
20586862-2	2010	Two single nucleotide polymorphisms (SNP) of cyclooxygenase-1 (COX-1), A-842G and C50T, exhibited increased sensitivity to aspirin and had lower prostaglandin synthesis capacity, lacking statistical significance in the association with bleeding peptic ulcer.	Aspirin	123-130	prostaglandin-endoperoxide synthase 1	Homo sapiens	63-68
20586862-7	2010	In a recent investigation, carriage of the IL-1beta-511 T allele was significantly associated with peptic ulcer among low-dose aspirin users.	Aspirin	127-134	interleukin 1 beta	Homo sapiens	43-51
20631416-2	2010	The elucidation by John Vane of the mechanism of action of aspirin in 1971 was followed twenty years later by the discovery of a second cyclooxygenase enzyme, COX-2 and the rapid development of selective inhibitors of this enzyme.	Aspirin	59-66	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	159-164
20631416-3	2010	The COX-2 inhibitors are potent anti-inflammatory drugs without the damaging side effects on the stomach mucosa of the non-selective aspirin-like inhibitors.	Aspirin	133-140	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	4-9
20631417-4	2010	This theory, which is now generally accepted, states that asthma attacks precipitated by aspirin and other NSAIDs have no allergic background; instead, they occur due to the inhibition of cyclooxygenase-1 in sensitive patients.	Aspirin	89-96	prostaglandin-endoperoxide synthase 1	Homo sapiens	188-204
20223228-0	2010	Combination of aspirin with telmisartan suppresses the augmented TGFbeta/smad signaling during the development of streptozotocin-induced type I diabetic nephropathy.	Aspirin	15-22	transforming growth factor beta 1	Homo sapiens	65-72
20629307-11	2010	Interestingly, compared with the rats in the OB group, the serum concentrations of TNF-alpha and CRP decreased significantly in the rats in the OB-AS group, to which high dose aspirin was given (P &lt; 0.05).	Aspirin	176-183	tumor necrosis factor	Rattus norvegicus	83-92
20223228-8	2010	Treatment of aspirin significantly prevented the progression of nephropathy and inhibited the augmented COX-2, NFkappaB (p65 levels), TNFalpha, and TGFbeta-smad expression.	Aspirin	13-20	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	104-109
20223228-8	2010	Treatment of aspirin significantly prevented the progression of nephropathy and inhibited the augmented COX-2, NFkappaB (p65 levels), TNFalpha, and TGFbeta-smad expression.	Aspirin	13-20	nuclear factor kappa B subunit 1	Homo sapiens	111-119
20223228-8	2010	Treatment of aspirin significantly prevented the progression of nephropathy and inhibited the augmented COX-2, NFkappaB (p65 levels), TNFalpha, and TGFbeta-smad expression.	Aspirin	13-20	tumor necrosis factor	Homo sapiens	134-142
20223228-8	2010	Treatment of aspirin significantly prevented the progression of nephropathy and inhibited the augmented COX-2, NFkappaB (p65 levels), TNFalpha, and TGFbeta-smad expression.	Aspirin	13-20	transforming growth factor beta 1	Homo sapiens	148-155
20223228-10	2010	This is the first report which shows that aspirin in combination with telmisartan is more proficient in the treatment of diabetic nephropathy than any single drug therapy and involves the change in expression of inflammatory markers and TGFbeta-smad signaling.	Aspirin	42-49	transforming growth factor beta 1	Homo sapiens	237-244
20079805-11	2010	The activity of the inducible isoform (iNOS) was inhibited by the three types of treatment (-31.8% for ASA, -29.1% for VOO and -56.0% for ASA plus VOO).	Aspirin	103-106	nitric oxide synthase 2	Rattus norvegicus	39-43
20233223-2	2010	Here, we have assessed the role played by NO, formed by inducible NOS (iNOS), in the inflammation induced by aspirin in the gut, by modulating HIF-1 activity.	Aspirin	109-116	nitric oxide synthase 2	Rattus norvegicus	71-75
20233223-3	2010	EXPERIMENTAL APPROACH: The role of iNOS-derived NO on leucocyte-endothelial interactions induced by aspirin was evaluated by intravital microscopy in mesenteric venules of rats pretreated with selective iNOS inhibitors, 1400W or l-N6-(1-iminoethyl)-lysine.	Aspirin	100-107	nitric oxide synthase 2	Rattus norvegicus	35-39
20233223-8	2010	iNOS expression and iNOS-derived NO synthesis were observed in leucocytes of the mesentery of aspirin-treated rats.	Aspirin	94-101	nitric oxide synthase 2	Rattus norvegicus	0-4
20233223-8	2010	iNOS expression and iNOS-derived NO synthesis were observed in leucocytes of the mesentery of aspirin-treated rats.	Aspirin	94-101	nitric oxide synthase 2	Rattus norvegicus	20-24
20233223-9	2010	Blockade of iNOS activity in aspirin-treated rats: (i) did not modify leucocyte infiltration at 6 h, but reduced the number of polymorphonuclear leucocyte and increased that of macrophages at 24 h; (ii) increased HIF-1alpha immunostaining in macrophages of the mesentery; and (iii) prevented the decrease in CD36 immunostaining induced by aspirin in these cells.	Aspirin	29-36	nitric oxide synthase 2	Rattus norvegicus	12-16
20233223-9	2010	Blockade of iNOS activity in aspirin-treated rats: (i) did not modify leucocyte infiltration at 6 h, but reduced the number of polymorphonuclear leucocyte and increased that of macrophages at 24 h; (ii) increased HIF-1alpha immunostaining in macrophages of the mesentery; and (iii) prevented the decrease in CD36 immunostaining induced by aspirin in these cells.	Aspirin	339-346	nitric oxide synthase 2	Rattus norvegicus	12-16
20144559-6	2010	The prevalence of aspirin non-responders for WBA-AA, TXB(2), PFA-100((R)), CPA and Coll1:5 was 13.1%, 8.2%, 14.8%, 9.7% and 16.4% respectively.	Aspirin	18-25	carboxypeptidase A1	Homo sapiens	75-78
20116423-0	2010	Aspirin induces apoptosis in YD-8 human oral squamous carcinoma cells through activation of caspases, down-regulation of Mcl-1, and inactivation of ERK-1/2 and AKT.	Aspirin	0-7	mitogen-activated protein kinase 3	Homo sapiens	148-155
20116423-0	2010	Aspirin induces apoptosis in YD-8 human oral squamous carcinoma cells through activation of caspases, down-regulation of Mcl-1, and inactivation of ERK-1/2 and AKT.	Aspirin	0-7	AKT serine/threonine kinase 1	Homo sapiens	160-163
20116423-5	2010	Data of Western blot further demonstrated that aspirin treatment caused activation of caspases, down-regulation of Mcl-1 protein, dephosphorylation of ERK-1/2 and AKT, and also IkappaB-alpha proteolysis-dependent NF-kappaB activation in YD-8 cells.	Aspirin	47-54	mitogen-activated protein kinase 3	Homo sapiens	151-158
20116423-5	2010	Data of Western blot further demonstrated that aspirin treatment caused activation of caspases, down-regulation of Mcl-1 protein, dephosphorylation of ERK-1/2 and AKT, and also IkappaB-alpha proteolysis-dependent NF-kappaB activation in YD-8 cells.	Aspirin	47-54	AKT serine/threonine kinase 1	Homo sapiens	163-166
20116423-5	2010	Data of Western blot further demonstrated that aspirin treatment caused activation of caspases, down-regulation of Mcl-1 protein, dephosphorylation of ERK-1/2 and AKT, and also IkappaB-alpha proteolysis-dependent NF-kappaB activation in YD-8 cells.	Aspirin	47-54	NFKB inhibitor alpha	Homo sapiens	177-190
20116423-5	2010	Data of Western blot further demonstrated that aspirin treatment caused activation of caspases, down-regulation of Mcl-1 protein, dephosphorylation of ERK-1/2 and AKT, and also IkappaB-alpha proteolysis-dependent NF-kappaB activation in YD-8 cells.	Aspirin	47-54	nuclear factor kappa B subunit 1	Homo sapiens	213-222
20116423-8	2010	These findings collectively suggest that aspirin induces apoptosis in YD-8 cells and the induction may be correlated to activation of caspases, caspase-dependent Mcl-1 proteolysis, inactivation of ERK-1/2 and AKT, and activation of NF-kappaB.	Aspirin	41-48	mitogen-activated protein kinase 3	Homo sapiens	197-204
20116423-8	2010	These findings collectively suggest that aspirin induces apoptosis in YD-8 cells and the induction may be correlated to activation of caspases, caspase-dependent Mcl-1 proteolysis, inactivation of ERK-1/2 and AKT, and activation of NF-kappaB.	Aspirin	41-48	AKT serine/threonine kinase 1	Homo sapiens	209-212
20116423-8	2010	These findings collectively suggest that aspirin induces apoptosis in YD-8 cells and the induction may be correlated to activation of caspases, caspase-dependent Mcl-1 proteolysis, inactivation of ERK-1/2 and AKT, and activation of NF-kappaB.	Aspirin	41-48	nuclear factor kappa B subunit 1	Homo sapiens	232-241
20358028-0	2010	IL-13 Gene Polymorphisms are Associated With Rhinosinusitis and Eosinophilic Inflammation in Aspirin Intolerant Asthma.	Aspirin	93-100	interleukin 13	Homo sapiens	0-5
19932480-6	2010	Aspirin and SC-560, a cyclooxygenase-1 inhibitor, suppressed the ristocetin-induced sCD40L release from platelets in parallel with TXA(2) production.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	22-38
20233223-2	2010	Here, we have assessed the role played by NO, formed by inducible NOS (iNOS), in the inflammation induced by aspirin in the gut, by modulating HIF-1 activity.	Aspirin	109-116	nitric oxide synthase 2	Rattus norvegicus	56-69
20339548-0	2010	Role of TGF-beta1 and MAP kinases in the antiproliferative effect of aspirin in human vascular smooth muscle cells.	Aspirin	69-76	transforming growth factor beta 1	Homo sapiens	8-17
20339548-7	2010	ASA (2 mM) induced TGF-beta1 secretion; however it was unable to induce Smad activation.	Aspirin	0-3	transforming growth factor beta 1	Homo sapiens	19-28
20339548-8	2010	ASA increased p38(MAPK) phosphorylation in a TGF-beta1-independent manner.	Aspirin	0-3	mitogen-activated protein kinase 14	Homo sapiens	14-17
20339548-8	2010	ASA increased p38(MAPK) phosphorylation in a TGF-beta1-independent manner.	Aspirin	0-3	transforming growth factor beta 1	Homo sapiens	45-54
20339548-10	2010	Pre-surgical serum levels of TGF-beta1 in patients who took at antiplatelet doses ASA were assessed by ELISA and remained unchanged.	Aspirin	82-85	transforming growth factor beta 1	Homo sapiens	29-38
20339548-11	2010	CONCLUSIONS/SIGNIFICANCE: In vitro antiproliferative effects of aspirin (at antiinflammatory concentration) on human VSMC obtained from bypass patients are mediated by TGF-beta1 and p38(MAPK).	Aspirin	64-71	transforming growth factor beta 1	Homo sapiens	168-177
20339548-11	2010	CONCLUSIONS/SIGNIFICANCE: In vitro antiproliferative effects of aspirin (at antiinflammatory concentration) on human VSMC obtained from bypass patients are mediated by TGF-beta1 and p38(MAPK).	Aspirin	64-71	mitogen-activated protein kinase 14	Homo sapiens	182-185
20339548-12	2010	Pre-surgical serum levels of TGF- beta1 from bypass patients who took aspirin at antiplatelet doses did not change.	Aspirin	70-77	transforming growth factor beta 1	Homo sapiens	29-39
20079805-11	2010	The activity of the inducible isoform (iNOS) was inhibited by the three types of treatment (-31.8% for ASA, -29.1% for VOO and -56.0% for ASA plus VOO).	Aspirin	138-141	nitric oxide synthase 2	Rattus norvegicus	39-43
20005558-0	2010	The effect of the long term aspirin administration on the progress of atherosclerosis in apoE-/- LDLR-/- double knockout mouse.	Aspirin	28-35	apolipoprotein E	Mus musculus	89-93
20233202-0	2010	Aspirin-triggered lipoxin in patients treated with aspirin and selective vs. nonselective COX-2 inhibitors.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	90-95
20233202-2	2010	We tested the hypothesis that the co-administration of aspirin with either the selective COX-2 inhibitor celecoxib or the nonselective COX inhibitor ibuprofen reduces ATL biosynthesis.	Aspirin	55-62	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	89-94
19908241-7	2010	In Western blot, combined TGZ and ASA also could downregulate Cdk2, E2F-1, cyclin B1, cyclin D3 protein, and the ratio of phospho-Rb/Rb.	Aspirin	34-37	cyclin D3	Homo sapiens	86-95
19633925-5	2010	In addition, the combination treatment of COX-2 siRNA and acidum acetil salicylicum (aspirin) has a synergistic effect.	Aspirin	85-92	prostaglandin-endoperoxide synthase 2	Homo sapiens	42-47
20005558-2	2010	Aspirin was given to homozygous, apoE(-/-) and LDLR(-/-) double deficient mice for 12 weeks.	Aspirin	0-7	apolipoprotein E	Mus musculus	33-37
20005558-15	2010	CONCLUSION: Our results suggest that endothelial dysfunction with low dose aspirin improved, reduced progression of atherosclerosis in apoE(-/-) and LDLR(-/-) double deficient mice and provides a pathophysiological basis for the beneficial effects of aspirin in atherosclerosis, and low doses appeared to be more efficient than high doses.	Aspirin	75-82	apolipoprotein E	Mus musculus	135-139
20065114-0	2010	NCX 4040, a nitric oxide-donating aspirin, exerts anti-inflammatory effects through inhibition of I kappa B-alpha degradation in human monocytes.	Aspirin	34-41	NFKB inhibitor alpha	Homo sapiens	98-113
20124488-5	2010	The odds ratios between SMAD7 and colon cancer among individuals reporting recent aspirin/nonsteroidal anti-inflammatory drug use was 0.60 (95% CI, 0.43-0.85) for the CC genotype of the rs4939827 polymorphism and 1.69 (95% CI, 1.20-2.38) for the TT genotype of the rs1295371 polymorphism.	Aspirin	82-89	SMAD family member 7	Homo sapiens	24-29
20137092-3	2010	We investigated the effect of ASA to regulate the expressions and activities of these molecules in THP-1 macrophages.	Aspirin	30-33	GLI family zinc finger 2	Homo sapiens	99-104
20137092-8	2010	These data suggest that acetyl salicylic acid may alleviate symptoms of atherosclerosis by two potential mechanisms: maintaining the plaque stability via inhibiting activities of inflammatory molecules MMP-9 and NF-kappaB, and increasing the cholesterol efflux through inducing expressions of ABCA1 and SR-BI.	Aspirin	24-45	nuclear factor kappa B subunit 1	Homo sapiens	212-221
19887674-0	2010	The contribution of cyclooxygenase-1 and -2 to persistent thromboxane biosynthesis in aspirin-treated essential thrombocythemia: implications for antiplatelet therapy.	Aspirin	86-93	prostaglandin-endoperoxide synthase 1	Homo sapiens	20-43
19887674-1	2010	We tested whether cyclooxygenase 2 (COX-2) expression and unacetylated COX-1 in newly formed platelets might contribute to persistent thromboxane (TX) biosynthesis in aspirin-treated essential thrombocythemia (ET).	Aspirin	167-174	prostaglandin-endoperoxide synthase 2	Homo sapiens	18-34
19887674-1	2010	We tested whether cyclooxygenase 2 (COX-2) expression and unacetylated COX-1 in newly formed platelets might contribute to persistent thromboxane (TX) biosynthesis in aspirin-treated essential thrombocythemia (ET).	Aspirin	167-174	prostaglandin-endoperoxide synthase 2	Homo sapiens	36-41
19887674-10	2010	Accelerated platelet regeneration in most aspirin-treated ET patients may explain aspirin-persistent TXA(2) biosynthesis through enhanced COX-2 activity and faster renewal of unacetylated COX-1.	Aspirin	42-49	prostaglandin-endoperoxide synthase 2	Homo sapiens	138-143
19887674-10	2010	Accelerated platelet regeneration in most aspirin-treated ET patients may explain aspirin-persistent TXA(2) biosynthesis through enhanced COX-2 activity and faster renewal of unacetylated COX-1.	Aspirin	82-89	prostaglandin-endoperoxide synthase 2	Homo sapiens	138-143
19936928-0	2010	Aspirin induces apoptosis in human leukemia cells independently  of NF-kappaB and MAPKs through alteration of the Mcl-1/Noxa  balance.	Aspirin	0-7	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	120-124
19936928-7	2010	We studied the regulation of Bcl-2 family members in aspirin-induced apoptosis.	Aspirin	53-60	BCL2 apoptosis regulator	Homo sapiens	29-34
19936928-8	2010	Aspirin increased the mRNA levels of some pro-apoptotic members, such as BIM, NOXA, BMF or PUMA, but their protein levels did not change.	Aspirin	0-7	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	78-82
19936928-12	2010	Furthermore, in CLL cells aspirin induced an increase in the protein levels of Noxa.	Aspirin	26-33	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	79-83
19936928-13	2010	Knockdown of Noxa or Puma significantly attenuated aspirin-induced apoptosis.	Aspirin	51-58	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	13-17
19936928-14	2010	These results indicate that aspirin induces apoptosis through alteration of the Mcl-1/ Noxa balance.	Aspirin	28-35	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	87-91
19880272-0	2010	Aspirin inhibits MMP-9 mRNA expression and release via the PPARalpha/gamma and COX-2/mPGES-1-mediated pathways in macrophages derived from THP-1 cells.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	79-84
19880272-4	2010	Additionally, the COX-2 mRNA expression, mPGES-1 mRNA and protein expression in macrophages were all decreased after incubation with aspirin for 24h and the PGE(2) release was also decreased.	Aspirin	133-140	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	18-23
19880272-7	2010	It might be concluded that aspirin could inhibit the MMP-9 gene expression and release through the PPARalpha/gamma and COX-2/mPGES-1-mediated pathways and the two pathways might be partly overlapped and even be interrelated.	Aspirin	27-34	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	119-124
19922491-8	2010	Both 2HBZ and ASA induced caspase-3 activation in the cells, which confirmed that their cytotoxic effects were the result of apoptotic cell death.	Aspirin	14-17	caspase 3	Homo sapiens	26-35
19997773-0	2010	Aspirin inhibits fractalkine expression in atherosclerotic plaques and reduces atherosclerosis in ApoE gene knockout mice.	Aspirin	0-7	apolipoprotein E	Mus musculus	98-102
20033269-0	2010	Fractalkine as an important target of aspirin in the prevention of atherogenesis : Editorial to: "Aspirin inhibits fractalkine expression in atherosclerotic plaques and reduces atherosclerosis in ApoE gene knockout mice" by H. Liu et al.	Aspirin	38-45	apolipoprotein E	Mus musculus	196-200
20033269-0	2010	Fractalkine as an important target of aspirin in the prevention of atherogenesis : Editorial to: "Aspirin inhibits fractalkine expression in atherosclerotic plaques and reduces atherosclerosis in ApoE gene knockout mice" by H. Liu et al.	Aspirin	98-105	apolipoprotein E	Mus musculus	196-200
19998405-4	2010	We investigated whether acetylation of Lys-residues by sulfosuccinimidyl acetate (SNA) or aspirin (ASA) would alter the crosslinking activity of TGM2.	Aspirin	90-97	transglutaminase 2	Homo sapiens	145-149
20169081-5	2010	Supporting a role for PGE(2) we observed that acetylsalicylic acid impaired the ability of MSC to inhibit the production of inflammatory cytokines and to stimulate the production of IL-10 by LPS-stimulated M. Moreover, we found that MSC constitutively produce PGE2 at levels able to inhibit the production of TNF-alpha and IL-6 by activated M. MSC also inhibited the up-regulation of CD86 and MHC class II in LPS-stimulated M impairing their ability to activate antigen-specific T CD4+ cells.	Aspirin	46-66	interleukin 10	Mus musculus	182-187
20169081-5	2010	Supporting a role for PGE(2) we observed that acetylsalicylic acid impaired the ability of MSC to inhibit the production of inflammatory cytokines and to stimulate the production of IL-10 by LPS-stimulated M. Moreover, we found that MSC constitutively produce PGE2 at levels able to inhibit the production of TNF-alpha and IL-6 by activated M. MSC also inhibited the up-regulation of CD86 and MHC class II in LPS-stimulated M impairing their ability to activate antigen-specific T CD4+ cells.	Aspirin	46-66	tumor necrosis factor	Mus musculus	309-318
20169081-5	2010	Supporting a role for PGE(2) we observed that acetylsalicylic acid impaired the ability of MSC to inhibit the production of inflammatory cytokines and to stimulate the production of IL-10 by LPS-stimulated M. Moreover, we found that MSC constitutively produce PGE2 at levels able to inhibit the production of TNF-alpha and IL-6 by activated M. MSC also inhibited the up-regulation of CD86 and MHC class II in LPS-stimulated M impairing their ability to activate antigen-specific T CD4+ cells.	Aspirin	46-66	interleukin 6	Mus musculus	323-327
20169081-5	2010	Supporting a role for PGE(2) we observed that acetylsalicylic acid impaired the ability of MSC to inhibit the production of inflammatory cytokines and to stimulate the production of IL-10 by LPS-stimulated M. Moreover, we found that MSC constitutively produce PGE2 at levels able to inhibit the production of TNF-alpha and IL-6 by activated M. MSC also inhibited the up-regulation of CD86 and MHC class II in LPS-stimulated M impairing their ability to activate antigen-specific T CD4+ cells.	Aspirin	46-66	CD86 antigen	Mus musculus	384-388
20043115-6	2010	RT-PCR quantitative analysis showed that aspirin treatment reduced significantly (P&lt;0.01) the AOM-triggered increase in mRNA levels of soluble inflammatory mediators (TNFalpha and IL-1beta) and metalloproteinases (MMP3 and MMP7).	Aspirin	41-48	tumor necrosis factor	Rattus norvegicus	170-178
20043115-6	2010	RT-PCR quantitative analysis showed that aspirin treatment reduced significantly (P&lt;0.01) the AOM-triggered increase in mRNA levels of soluble inflammatory mediators (TNFalpha and IL-1beta) and metalloproteinases (MMP3 and MMP7).	Aspirin	41-48	interleukin 1 beta	Rattus norvegicus	183-191
19998405-4	2010	We investigated whether acetylation of Lys-residues by sulfosuccinimidyl acetate (SNA) or aspirin (ASA) would alter the crosslinking activity of TGM2.	Aspirin	99-102	transglutaminase 2	Homo sapiens	145-149
19184424-0	2010	Chronic aspirin use suppresses CDH1 methylation in human gastric mucosa.	Aspirin	8-15	cadherin 1	Homo sapiens	31-35
19942655-5	2010	The addition of acetylsalicylic acid had significantly suppressive effect on the IL-6 production by lipopolysaccharide-stimulated patients" peripheral blood mononuclear cells.	Aspirin	16-36	interleukin 6	Homo sapiens	81-85
19788892-6	2010	Analysis of serum cytokines of aspirin-induced rats showed a moderate decrease in interleukin-10 (IL-10) with considerable increase of interleukin-6 (IL-6) and interferon-gamma (INF-gamma) when compared with control.	Aspirin	31-38	interleukin 6	Rattus norvegicus	135-148
19788892-6	2010	Analysis of serum cytokines of aspirin-induced rats showed a moderate decrease in interleukin-10 (IL-10) with considerable increase of interleukin-6 (IL-6) and interferon-gamma (INF-gamma) when compared with control.	Aspirin	31-38	interleukin 6	Rattus norvegicus	150-154
19966835-10	2010	Aspirin inhibits GSK-3beta activation and suppresses the expression of its downstream gene products (cyclin D1 and Bcl-2), which are implicated in proliferation, survival and chemoresistance of pancreatic cancer.	Aspirin	0-7	BCL2 apoptosis regulator	Homo sapiens	115-120
20648923-9	2010	Furthermore, compared to ASA and to diclofenac (Diclo, CAS 15307-79-6), the COX-1 and COX-2 mRNA expressions were influenced differently by STW 33-I and fraction E. ASA and Diclo inhibited both the COX-1 and COX-2 mRNA expressions, whereas STW 33-I and its fraction E increased the COX-1 mRNA expression.	Aspirin	165-168	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	86-91
20648923-9	2010	Furthermore, compared to ASA and to diclofenac (Diclo, CAS 15307-79-6), the COX-1 and COX-2 mRNA expressions were influenced differently by STW 33-I and fraction E. ASA and Diclo inhibited both the COX-1 and COX-2 mRNA expressions, whereas STW 33-I and its fraction E increased the COX-1 mRNA expression.	Aspirin	165-168	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	208-213
19621391-6	2010	Our in vitro data using EOC cell line showed that inhibition of COX-2 by aspirin, selective inhibitor NS398 and gene silencing by COX-2 specific siRNA impaired phosphorylation of AKT resulting decreased downstream signaling leading to cell growth inhibition and induction of apoptosis.	Aspirin	73-80	thymoma viral proto-oncogene 1	Mus musculus	179-182
19621391-7	2010	Finally, treatment of MDAH2774 cell line xenografts with aspirin resulted in growth inhibition of tumors in NUDE mice via down-regulation of COX-2 and AKT activity.	Aspirin	57-64	thymoma viral proto-oncogene 1	Mus musculus	151-154
20370474-7	2010	BP was significantly reduced after aspirin at bedtime and to a larger extent in women (-8.0/-5.6 mmHg in SBP/DBP) than men (5.5/3.4 mmHg, respectively; p &lt; 0.009 between men and women).	Aspirin	35-42	D-box binding PAR bZIP transcription factor	Homo sapiens	109-112
19184424-4	2010	We investigated the methylation status of CDH1 in noncancerous gastric mucosa in chronic aspirin user, and assessed its effect on methylation-associated carcinogenesis.	Aspirin	89-96	cadherin 1	Homo sapiens	42-46
19184424-8	2010	CDH1 methylation more frequently occurred in H. pylori-infection-positive subjects (P &lt; 0.0001), while chronic aspirin users had a significantly lower risk of CDH1 methylation [nonuser versus user 36.1% versus 10.8%; odds ratio (OR) = 0.21, 95% confidence interval (CI) = 0.07-0.63, P = 0.005].	Aspirin	114-121	cadherin 1	Homo sapiens	162-166
19184424-9	2010	Logistic regression analysis showed that chronic aspirin use was the independent factor for lower risk of CDH1 methylation (adjusted OR = 0.21, 95%CI = 0.07-0.66, P = 0.008).	Aspirin	49-56	cadherin 1	Homo sapiens	106-110
19184424-10	2010	Chronic aspirin use was associated with lower risk of CDH1 methylation in H. pylori-positive subjects (nonuser versus user 49.5% versus 19.0%; OR = 0.24, 95%CI = 0.08-0.76, P = 0.01).	Aspirin	8-15	cadherin 1	Homo sapiens	54-58
19184424-13	2010	Our data suggest that chronic aspirin use is associated with reduced risk of CDH1 methylation in human gastric mucosa.	Aspirin	30-37	cadherin 1	Homo sapiens	77-81
21088444-7	2010	In cells transfected with a specific peroxisome proliferator-activated receptor (PPAR)-alpha small interfering RNA, the induction of ABCA1 expression and apoA-I-mediated 3H-cholesterol efflux by aspirin were substantially suppressed.	Aspirin	195-202	peroxisome proliferator activated receptor alpha	Mus musculus	81-92
19741170-5	2010	Aspirin caused gastric injury that peaked 6 h after dosing and returned to normality at 24 h. iNOS mRNA expression occurs in the corpus in parallel with damage.	Aspirin	0-7	nitric oxide synthase 2	Homo sapiens	94-98
19741170-7	2010	Aspirin induced HIF-1alpha stabilization and TFF2 mRNA up-regulation in the mucosa, but these effects were diminished when iNOS activity was inhibited.	Aspirin	0-7	hypoxia inducible factor 1 subunit alpha	Homo sapiens	16-26
19741170-7	2010	Aspirin induced HIF-1alpha stabilization and TFF2 mRNA up-regulation in the mucosa, but these effects were diminished when iNOS activity was inhibited.	Aspirin	0-7	trefoil factor 2	Homo sapiens	45-49
19741170-7	2010	Aspirin induced HIF-1alpha stabilization and TFF2 mRNA up-regulation in the mucosa, but these effects were diminished when iNOS activity was inhibited.	Aspirin	0-7	nitric oxide synthase 2	Homo sapiens	123-127
20005575-4	2010	We evaluated whether peripheral blood leukocytes from women with a history of preterm birth produce elevated amounts of TNFalpha upon stimulation with pathogens associated with preterm birth and if pre-treatment with aspirin, an anti-inflammatory medication, decreases the ex vivo production of this cytokine.	Aspirin	217-224	tumor necrosis factor	Homo sapiens	120-128
20005575-6	2010	In women who consumed aspirin each day for one week, TNFalpha production was increased in leukocytes from control women stimulated with Escherichia coli and U. urealyticum, but was reduced or unchanged in leukocytes from women with preterm birth.	Aspirin	22-29	tumor necrosis factor	Homo sapiens	53-61
21088444-8	2010	CONCLUSIONS: The data demonstrate that low-dose aspirin increases ABCA1 expression via a PPAR-alpha-dependent mechanism and increases apoA-I-mediated cholesterol efflux.	Aspirin	48-55	peroxisome proliferator activated receptor alpha	Mus musculus	89-99
20062920-5	2010	The expression of glyceraldehyde 3-phosphate dehydrogenase was increased in the ASA-resistant platelets (1751.1 + or - 220.6 vs. 4273.3 + or - 971.7, 95% confidence interval [CI] 1815.11 to 4061.2, p=0.001).	Aspirin	80-83	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	18-58
19996015-11	2009	This study suggests that multiple mechanisms, including but not confined to inadequate inhibition of COX-1, are responsible for poor clinical outcomes in aspirin-treated patients, and therefore the term aspirin resistance is inappropriate.	Aspirin	154-161	prostaglandin-endoperoxide synthase 1	Homo sapiens	101-106
20137501-12	2009	Co-incubation with aspirin markedly inhibited SA-beta-gal activity dose-dependently.	Aspirin	19-26	SH3 domain binding protein 5	Homo sapiens	46-53
20137501-16	2009	CONCLUSION: The anti-senescent effects of aspirin are fulfilled by increasing NO production via the up-regulation of NOS activity and preventing caveolin-1 expression, caveolin-1/eNOS interaction and ADMA accumulation.	Aspirin	42-49	caveolin 1	Homo sapiens	145-155
20137501-16	2009	CONCLUSION: The anti-senescent effects of aspirin are fulfilled by increasing NO production via the up-regulation of NOS activity and preventing caveolin-1 expression, caveolin-1/eNOS interaction and ADMA accumulation.	Aspirin	42-49	caveolin 1	Homo sapiens	168-178
19962464-11	2009	This was confirmed in vitro by incubating washed aspirin-free and aspirin (1 muM)-treated platelets from normal subjects with 1 to 20 microM atorvastatin.	Aspirin	66-73	latexin	Homo sapiens	77-80
20608787-11	2010	ASA attenuated the endotoxin-induced platelet plug formation (measured by PFA-100) significantly better than NCX 4016 and placebo (p &lt; 0.004), while there was no difference in soluble P-selectin or VWF-levels.	Aspirin	0-3	von Willebrand factor	Homo sapiens	201-204
19487018-1	2010	INTRODUCTION: The aim of this study was to further characterize the effect of the antiplatelet agents, aspirin and eptifibatide, on the surface expression of CD40L and CD62P on platelets from patients with stable coronary artery disease.	Aspirin	103-110	CD40 ligand	Homo sapiens	158-163
19487018-5	2010	Platelet activation by adenosine diphosphate (ADP) or thrombin agonist peptide (TRAP) increased CD62P and CD40L surface density in the presence of aspirin by 1.9 - 2.8 -fold.	Aspirin	147-154	coagulation factor II, thrombin	Homo sapiens	54-62
19487018-5	2010	Platelet activation by adenosine diphosphate (ADP) or thrombin agonist peptide (TRAP) increased CD62P and CD40L surface density in the presence of aspirin by 1.9 - 2.8 -fold.	Aspirin	147-154	CD40 ligand	Homo sapiens	106-111
19996015-0	2009	Association of cyclooxygenase-1-dependent and -independent platelet function assays with adverse clinical outcomes in aspirin-treated patients presenting for cardiac catheterization.	Aspirin	118-125	prostaglandin-endoperoxide synthase 1	Homo sapiens	15-31
19996015-1	2009	BACKGROUND: Poor clinical outcome in aspirin-treated patients has been termed aspirin resistance and may result from inadequate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin.	Aspirin	37-44	prostaglandin-endoperoxide synthase 1	Homo sapiens	151-167
19996015-1	2009	BACKGROUND: Poor clinical outcome in aspirin-treated patients has been termed aspirin resistance and may result from inadequate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin.	Aspirin	37-44	prostaglandin-endoperoxide synthase 1	Homo sapiens	169-174
19996015-1	2009	BACKGROUND: Poor clinical outcome in aspirin-treated patients has been termed aspirin resistance and may result from inadequate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin.	Aspirin	78-85	prostaglandin-endoperoxide synthase 1	Homo sapiens	151-167
19996015-1	2009	BACKGROUND: Poor clinical outcome in aspirin-treated patients has been termed aspirin resistance and may result from inadequate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin.	Aspirin	78-85	prostaglandin-endoperoxide synthase 1	Homo sapiens	151-167
19996015-2	2009	The objectives of this study were to determine prospectively whether COX-1-dependent and other platelet function assays correlate with clinical outcomes in aspirin-treated patients.	Aspirin	156-163	prostaglandin-endoperoxide synthase 1	Homo sapiens	69-74
19996015-10	2009	CONCLUSIONS: In this prospective study of 700 aspirin-treated patients presenting for angiographic evaluation of coronary artery disease, residual platelet COX-1 function measured by serum thromboxane B(2) and COX-1-independent platelet function measured by PFA-100 collagen-ADP CT, but not indirect COX-1-dependent assays (arachidonic acid-stimulated platelet markers, shortened PFA-100 collagen-epinephrine CT), correlate with subsequent major adverse cardiovascular events.	Aspirin	46-53	prostaglandin-endoperoxide synthase 1	Homo sapiens	156-161
19822838-8	2009	Low-dose aspirin (325 mg/d) is beneficial in stabilizing CRP levels, which may be abrogated by folate.	Aspirin	9-16	C-reactive protein	Homo sapiens	57-60
19785994-4	2009	We demonstrated that the presence of aspirin at concentrations (0.25-2mM) compatible with amounts in plasma during chronic anti-inflammatory therapy resulted in a significant inhibition of DNA cleavage induced by both peroxynitrite and SIN-1.	Aspirin	37-44	MAPK associated protein 1	Homo sapiens	236-241
19785994-5	2009	Moreover, the consumption of oxygen caused by 250 microM SIN-1 was found to be decreased in the presence of aspirin, indicating that aspirin might affect the auto-oxidation of SIN-1.	Aspirin	108-115	MAPK associated protein 1	Homo sapiens	57-62
19785994-5	2009	Moreover, the consumption of oxygen caused by 250 microM SIN-1 was found to be decreased in the presence of aspirin, indicating that aspirin might affect the auto-oxidation of SIN-1.	Aspirin	108-115	MAPK associated protein 1	Homo sapiens	176-181
19785994-5	2009	Moreover, the consumption of oxygen caused by 250 microM SIN-1 was found to be decreased in the presence of aspirin, indicating that aspirin might affect the auto-oxidation of SIN-1.	Aspirin	133-140	MAPK associated protein 1	Homo sapiens	57-62
19785994-5	2009	Moreover, the consumption of oxygen caused by 250 microM SIN-1 was found to be decreased in the presence of aspirin, indicating that aspirin might affect the auto-oxidation of SIN-1.	Aspirin	133-140	MAPK associated protein 1	Homo sapiens	176-181
19706045-8	2009	Stimulating the Wnt/beta-catenin pathway by both Wnt 3a and GSK-3beta inhibitors (LiCl and SB 216763), blocked aspirin-induced apoptosis and protected mitochondrial function, as demonstrated by decreased cytochrome c release and caspase-3 activity.	Aspirin	111-118	caspase 3	Homo sapiens	229-238
19048181-9	2009	An important consideration affecting the use of aspirin in diabetic patients is its interaction with ACE-inhibitors.	Aspirin	48-55	angiotensin I converting enzyme	Homo sapiens	101-104
19706045-9	2009	Aspirin initially caused a time-dependent decrease in COX-2 expression but subsequently, and unexpectedly, elevated the latter.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	54-59
19706045-7	2009	RESULTS: In these MSCs, aspirin induced morphological changes characteristic of apoptosis, cytochrome c release from mitochondria, and caspase-3 activation.	Aspirin	24-31	cytochrome c, somatic	Homo sapiens	91-103
19706045-7	2009	RESULTS: In these MSCs, aspirin induced morphological changes characteristic of apoptosis, cytochrome c release from mitochondria, and caspase-3 activation.	Aspirin	24-31	caspase 3	Homo sapiens	135-144
19706045-10	2009	Stimulation of COX-2 expression by aspirin was further enhanced following stimulation of the Wnt/beta-catenin pathway.	Aspirin	35-42	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	15-20
19706045-8	2009	Stimulating the Wnt/beta-catenin pathway by both Wnt 3a and GSK-3beta inhibitors (LiCl and SB 216763), blocked aspirin-induced apoptosis and protected mitochondrial function, as demonstrated by decreased cytochrome c release and caspase-3 activity.	Aspirin	111-118	cytochrome c, somatic	Homo sapiens	204-216
19706045-11	2009	Application of the COX-2 inhibitor NS-398 suppressed elevated COX-2 expression and promoted aspirin-induced apoptosis.	Aspirin	92-99	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	19-24
19706045-12	2009	CONCLUSION: These results demonstrate that the Wnt/beta-catenin pathway is a key modulator of aspirin-induced apoptosis in MSCs by regulation of mitochrondrial/caspase-3 function.	Aspirin	94-101	caspase 3	Homo sapiens	160-169
19903376-6	2009	KEY FINDINGS: The blood levels of hs-CRP, TNF-alpha, IL-6 and TXB2 were significantly decreased after 2 weeks of treatment with 300 mg/day of aspirin.	Aspirin	142-149	tumor necrosis factor	Homo sapiens	42-51
19890703-4	2009	Residual risk can be attributed, at least in part, to the fact that thrombosis continues in the presence of current treatments because aspirin and P2Y(12) ADP receptor antagonists each block only one of multiple platelet activation pathways, and thus do not impact other platelet activation pathways, such as the one triggered by interaction of thrombin with protease-activated receptor (PAR)-1, thereby exposing patients to continued accumulation of thrombotic events.	Aspirin	135-142	coagulation factor II, thrombin	Homo sapiens	345-353
19890703-4	2009	Residual risk can be attributed, at least in part, to the fact that thrombosis continues in the presence of current treatments because aspirin and P2Y(12) ADP receptor antagonists each block only one of multiple platelet activation pathways, and thus do not impact other platelet activation pathways, such as the one triggered by interaction of thrombin with protease-activated receptor (PAR)-1, thereby exposing patients to continued accumulation of thrombotic events.	Aspirin	135-142	coagulation factor II thrombin receptor	Homo sapiens	359-394
19576865-3	2009	The p- and m-NO-ASA isomers strongly inhibited cell growth and beta-catenin/TCF transcriptional activity compared to ASA; the IC50s for growth inhibition were 57+/-4, 193+/-10 and &gt;5000microM, and for transcriptional inhibition they were 12+/-1.8, 75+/-6.5 and &gt;5000microM for p-, m-NO-ASA and ASA, respectively.	Aspirin	16-19	hepatocyte nuclear factor 4 alpha	Homo sapiens	76-79
19576865-5	2009	COX-2 expression was induced by p-NO-ASA, protein kinase C inhibitors reversed this induction.	Aspirin	37-40	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
19730809-0	2009	Aspirin attenuates insulin resistance in muscle of diet-induced obese rats by inhibiting inducible nitric oxide synthase production and S-nitrosylation of IRbeta/IRS-1 and Akt.	Aspirin	0-7	insulin	Homo sapiens	19-26
19730809-0	2009	Aspirin attenuates insulin resistance in muscle of diet-induced obese rats by inhibiting inducible nitric oxide synthase production and S-nitrosylation of IRbeta/IRS-1 and Akt.	Aspirin	0-7	nitric oxide synthase 2	Rattus norvegicus	89-120
19730809-0	2009	Aspirin attenuates insulin resistance in muscle of diet-induced obese rats by inhibiting inducible nitric oxide synthase production and S-nitrosylation of IRbeta/IRS-1 and Akt.	Aspirin	0-7	insulin receptor substrate 1	Rattus norvegicus	162-167
19730809-0	2009	Aspirin attenuates insulin resistance in muscle of diet-induced obese rats by inhibiting inducible nitric oxide synthase production and S-nitrosylation of IRbeta/IRS-1 and Akt.	Aspirin	0-7	AKT serine/threonine kinase 1	Rattus norvegicus	172-175
19730809-1	2009	AIM/HYPOTHESIS: High-dose aspirin treatment improves fasting and postprandial hyperglycaemia in patients with type 2 diabetes, as well as in animal models of insulin resistance associated with obesity and sepsis.	Aspirin	26-33	insulin	Homo sapiens	158-165
19730809-2	2009	In this study, we investigated the effects of aspirin treatment on inducible nitric oxide synthase (iNOS)-mediated insulin resistance and on S-nitrosylation of insulin receptor (IR)-beta, IRS-1 and protein kinase B (Akt) in the muscle of diet-induced obese rats and also in iNos (also known as Nos2)-/- mice on high fat diet.	Aspirin	46-53	nitric oxide synthase 2	Rattus norvegicus	67-98
19730809-2	2009	In this study, we investigated the effects of aspirin treatment on inducible nitric oxide synthase (iNOS)-mediated insulin resistance and on S-nitrosylation of insulin receptor (IR)-beta, IRS-1 and protein kinase B (Akt) in the muscle of diet-induced obese rats and also in iNos (also known as Nos2)-/- mice on high fat diet.	Aspirin	46-53	nitric oxide synthase 2	Rattus norvegicus	100-104
19730809-2	2009	In this study, we investigated the effects of aspirin treatment on inducible nitric oxide synthase (iNOS)-mediated insulin resistance and on S-nitrosylation of insulin receptor (IR)-beta, IRS-1 and protein kinase B (Akt) in the muscle of diet-induced obese rats and also in iNos (also known as Nos2)-/- mice on high fat diet.	Aspirin	46-53	insulin	Homo sapiens	115-122
19730809-6	2009	These alterations were reversed by aspirin treatment, in parallel with an improvement in insulin signalling and sensitivity, as measured by insulin tolerance test and glucose clamp.	Aspirin	35-42	insulin	Homo sapiens	89-96
19730809-6	2009	These alterations were reversed by aspirin treatment, in parallel with an improvement in insulin signalling and sensitivity, as measured by insulin tolerance test and glucose clamp.	Aspirin	35-42	insulin	Homo sapiens	140-147
19730809-7	2009	Conversely, while aspirin reversed the increased phosphorylation of IkappaB kinase beta and c-Jun amino-terminal kinase, as well as IRS-1 serine phosphorylation in diet-induced obese rats and iNos -/- mice on high-fat diet, these alterations were not associated with the improvement of insulin action induced by this drug.	Aspirin	18-25	inhibitor of nuclear factor kappa B kinase subunit beta	Rattus norvegicus	68-87
19730809-7	2009	Conversely, while aspirin reversed the increased phosphorylation of IkappaB kinase beta and c-Jun amino-terminal kinase, as well as IRS-1 serine phosphorylation in diet-induced obese rats and iNos -/- mice on high-fat diet, these alterations were not associated with the improvement of insulin action induced by this drug.	Aspirin	18-25	nitric oxide synthase 2	Rattus norvegicus	192-196
19730809-7	2009	Conversely, while aspirin reversed the increased phosphorylation of IkappaB kinase beta and c-Jun amino-terminal kinase, as well as IRS-1 serine phosphorylation in diet-induced obese rats and iNos -/- mice on high-fat diet, these alterations were not associated with the improvement of insulin action induced by this drug.	Aspirin	18-25	insulin	Homo sapiens	286-293
19730809-8	2009	CONCLUSIONS/INTERPRETATION: Our data demonstrate that aspirin treatment not only reduces iNOS protein levels, but also S-nitrosylation of IRbeta, IRS-1 and Akt.	Aspirin	54-61	nitric oxide synthase 2	Rattus norvegicus	89-93
19730809-8	2009	CONCLUSIONS/INTERPRETATION: Our data demonstrate that aspirin treatment not only reduces iNOS protein levels, but also S-nitrosylation of IRbeta, IRS-1 and Akt.	Aspirin	54-61	insulin receptor substrate 1	Rattus norvegicus	146-151
19730809-8	2009	CONCLUSIONS/INTERPRETATION: Our data demonstrate that aspirin treatment not only reduces iNOS protein levels, but also S-nitrosylation of IRbeta, IRS-1 and Akt.	Aspirin	54-61	AKT serine/threonine kinase 1	Rattus norvegicus	156-159
19730809-9	2009	These changes are associated with improved insulin resistance and signalling, suggesting a novel mechanism of insulin sensitisation evoked by aspirin treatment.	Aspirin	142-149	insulin	Homo sapiens	43-50
19805643-0	2009	Time-dependent effects of low-dose aspirin on plasma renin activity, aldosterone, cortisol, and catecholamines.	Aspirin	35-42	renin	Homo sapiens	53-58
19805643-3	2009	We investigated the effect of 100 mg of aspirin administered at bedtime compared with administration on awakening on plasma renin activity and aldosterone levels over 24 hours and excretion of cortisol and catecholamines in 24-hour urine samples.	Aspirin	40-47	renin	Homo sapiens	124-129
19805643-7	2009	Aspirin intake at bedtime compared with on awakening reduced average (24-hour) plasma renin activity by 0.08 microg/L per hour (95% CI: 0.03 to 0.13 microg/L per hour; P=0.003) without affecting aldosterone levels (95% CI: -0.01 to 0.01 nmol/L; P=0.93).	Aspirin	0-7	renin	Homo sapiens	86-91
19805643-9	2009	In conclusion, aspirin taken at bedtime compared with on awakening significantly diminished 24-hour plasma renin activity and excretion of cortisol, dopamine, and norepinephrine in 24-hour urine.	Aspirin	15-22	renin	Homo sapiens	107-112
19903376-6	2009	KEY FINDINGS: The blood levels of hs-CRP, TNF-alpha, IL-6 and TXB2 were significantly decreased after 2 weeks of treatment with 300 mg/day of aspirin.	Aspirin	142-149	interleukin 6	Homo sapiens	53-57
19903376-8	2009	The blood level of IL-6 in the 300 mg/day aspirin group was significantly lower than that in the other two groups after 2 weeks of therapy.	Aspirin	42-49	interleukin 6	Homo sapiens	19-23
19755647-3	2009	Aspirin inhibits COX-2 activity and lowers the risk for colorectal adenomas and cancer.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	17-22
20224667-11	2009	CONCLUSIONS: The +82466C&gt;T polymorphism and haplotype 1 of the PPARG gene may be linked to increased risk for aspirin hypersensitivity in asthma.	Aspirin	113-120	peroxisome proliferator activated receptor gamma	Homo sapiens	66-71
19755647-10	2009	These results support the hypothesis that COX-2 plays a role in the etiology of colon cancer and may be a target for aspirin chemoprevention and warrant further investigation in other colorectal adenoma and cancer populations.	Aspirin	117-124	prostaglandin-endoperoxide synthase 2	Homo sapiens	42-47
19483113-3	2009	OBJECTIVES: Because aspirin-triggered 15-epi-lipoxin A(4) (15-epi-LXA(4)) modulates Mac-1 expression, we investigated the impact of 15-epi-LXA(4) on MPO suppression of neutrophil apoptosis and MPO-mediated neutrophil-dependent acute lung injury.	Aspirin	20-27	integrin subunit beta 2	Homo sapiens	84-89
19486029-3	2009	OBJECTIVE: To study the in vitro effects of aspirin on the concurrent release of histamine, leukotriene C4 (LTC4) and IL-4 from human basophils and to also evaluate changes in surface activation markers (CD63, CD69 and CD203c) expressed by these cells.	Aspirin	44-51	interleukin 4	Homo sapiens	118-122
19814664-7	2009	Aspirin may be another promising drug, but trials have shown a higher rate of HF admissions with aspirin, suggesting that aspirin may attenuate the angiotensin-converting enzyme inhibitor effect on cardiac function.	Aspirin	0-7	angiotensin I converting enzyme	Homo sapiens	148-177
19814664-7	2009	Aspirin may be another promising drug, but trials have shown a higher rate of HF admissions with aspirin, suggesting that aspirin may attenuate the angiotensin-converting enzyme inhibitor effect on cardiac function.	Aspirin	97-104	angiotensin I converting enzyme	Homo sapiens	148-177
19814664-7	2009	Aspirin may be another promising drug, but trials have shown a higher rate of HF admissions with aspirin, suggesting that aspirin may attenuate the angiotensin-converting enzyme inhibitor effect on cardiac function.	Aspirin	122-129	angiotensin I converting enzyme	Homo sapiens	148-177
19767079-0	2009	Associations of functional NLRP3 polymorphisms with susceptibility to food-induced anaphylaxis and aspirin-induced asthma.	Aspirin	99-106	NLR family pyrin domain containing 3	Homo sapiens	27-32
19767079-3	2009	OBJECTIVE: We sought to examine whether NLRP3 polymorphisms are associated with susceptibility to food allergy, food-induced anaphylaxis, and aspirin-induced asthma (AIA).	Aspirin	142-149	NLR family pyrin domain containing 3	Homo sapiens	40-45
19767084-3	2009	OBJECTIVE: We hypothesized that aspirin desensitization blocks IL-4-induced expression of these LT activities through inhibition of signal transducer and activator of transcription 6 (STAT6)-mediated transcription.	Aspirin	32-39	interleukin 4	Homo sapiens	63-67
19767084-8	2009	RESULTS: Upregulation of LT receptor mRNA by IL-4 was negated by aspirin and ketorolac but not by sodium salicylate.	Aspirin	65-72	interleukin 4	Homo sapiens	45-49
19767084-10	2009	Aspirin and ketorolac decreased the IL-4-inducible expression of nuclear STAT6 observed in mobility shift assays and Western hybridization.	Aspirin	0-7	interleukin 4	Homo sapiens	36-40
19767084-12	2009	Assuming that normal monocytes behave like monocytes from patients with aspirin-exacerbated respiratory disease, inhibition of IL-4-STAT6 might explain a mechanism in aspirin desensitization daily treatment, resulting in downregulation of production and responsiveness to cysteinyl leukotrienes.	Aspirin	72-79	interleukin 4	Homo sapiens	127-137
19767084-12	2009	Assuming that normal monocytes behave like monocytes from patients with aspirin-exacerbated respiratory disease, inhibition of IL-4-STAT6 might explain a mechanism in aspirin desensitization daily treatment, resulting in downregulation of production and responsiveness to cysteinyl leukotrienes.	Aspirin	167-174	interleukin 4	Homo sapiens	127-137
19563267-2	2009	The common anti-inflammatory drugs (such as aspirin, ibuprofen and naproxen) all act by blocking the action of both the COX-1 and COX-2 enzymes.	Aspirin	44-51	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	130-135
19820387-6	2009	Aspirin decreased Bcl-xl proteinum expression, and the effect was related with its concentration (P &lt; 0.05).	Aspirin	0-7	BCL2 like 1	Homo sapiens	18-24
19820387-7	2009	CONCLUSIONS: : Aspirin has a distinct depressant effect on human Ishikawa adenocarcinoma endometrium cell growth, and its effect may be realized by lowering Bcl-xl proteinum expression.	Aspirin	15-22	BCL2 like 1	Homo sapiens	157-163
19786240-10	2009	ERK 1/2 activation was significantly increased post-PTA in both the aspirin/clopidogrel and aspirin/placebo groups (P &lt; .001).	Aspirin	68-75	mitogen-activated protein kinase 3	Homo sapiens	0-7
19786240-10	2009	ERK 1/2 activation was significantly increased post-PTA in both the aspirin/clopidogrel and aspirin/placebo groups (P &lt; .001).	Aspirin	92-99	mitogen-activated protein kinase 3	Homo sapiens	0-7
19595669-0	2009	Aspirin induces apoptosis through the blockade of IL-6-STAT3 signaling pathway in human glioblastoma A172 cells.	Aspirin	0-7	interleukin 6	Homo sapiens	50-54
19595669-0	2009	Aspirin induces apoptosis through the blockade of IL-6-STAT3 signaling pathway in human glioblastoma A172 cells.	Aspirin	0-7	signal transducer and activator of transcription 3	Homo sapiens	55-60
19595669-5	2009	Moreover, the expression of STAT3 target genes such as Cyclin D1, XIAP, and Bcl-2 that are essential for cell growth and survival was apparently attenuated after aspirin treatment.	Aspirin	162-169	signal transducer and activator of transcription 3	Homo sapiens	28-33
19595669-5	2009	Moreover, the expression of STAT3 target genes such as Cyclin D1, XIAP, and Bcl-2 that are essential for cell growth and survival was apparently attenuated after aspirin treatment.	Aspirin	162-169	BCL2 apoptosis regulator	Homo sapiens	76-81
19595669-6	2009	We also showed that the expression and secretion of interleukin-6 (IL-6), leading to STAT3 phosphorylation, was inhibited by aspirin.	Aspirin	125-132	interleukin 6	Homo sapiens	52-65
19595669-6	2009	We also showed that the expression and secretion of interleukin-6 (IL-6), leading to STAT3 phosphorylation, was inhibited by aspirin.	Aspirin	125-132	interleukin 6	Homo sapiens	67-71
19595669-6	2009	We also showed that the expression and secretion of interleukin-6 (IL-6), leading to STAT3 phosphorylation, was inhibited by aspirin.	Aspirin	125-132	signal transducer and activator of transcription 3	Homo sapiens	85-90
19595669-7	2009	When administered exogenous IL-6 to aspirin-treated A172 cells, the phosphorylation of STAT3 and cellular apoptosis were restrained compared to aspirin only-treated cells.	Aspirin	36-43	interleukin 6	Homo sapiens	28-32
19595669-7	2009	When administered exogenous IL-6 to aspirin-treated A172 cells, the phosphorylation of STAT3 and cellular apoptosis were restrained compared to aspirin only-treated cells.	Aspirin	36-43	signal transducer and activator of transcription 3	Homo sapiens	87-92
19595669-7	2009	When administered exogenous IL-6 to aspirin-treated A172 cells, the phosphorylation of STAT3 and cellular apoptosis were restrained compared to aspirin only-treated cells.	Aspirin	144-151	interleukin 6	Homo sapiens	28-32
19595669-7	2009	When administered exogenous IL-6 to aspirin-treated A172 cells, the phosphorylation of STAT3 and cellular apoptosis were restrained compared to aspirin only-treated cells.	Aspirin	144-151	signal transducer and activator of transcription 3	Homo sapiens	87-92
19595669-8	2009	Taken together, our results indicate that aspirin causes apoptosis via down-regulation of IL-6-dependent STAT3 signaling, suggesting that aspirin could be therapeutically useful for a potential anti-glioblastoma therapeutic approach.	Aspirin	42-49	interleukin 6	Homo sapiens	90-94
19595669-8	2009	Taken together, our results indicate that aspirin causes apoptosis via down-regulation of IL-6-dependent STAT3 signaling, suggesting that aspirin could be therapeutically useful for a potential anti-glioblastoma therapeutic approach.	Aspirin	42-49	signal transducer and activator of transcription 3	Homo sapiens	105-110
19595669-8	2009	Taken together, our results indicate that aspirin causes apoptosis via down-regulation of IL-6-dependent STAT3 signaling, suggesting that aspirin could be therapeutically useful for a potential anti-glioblastoma therapeutic approach.	Aspirin	138-145	interleukin 6	Homo sapiens	90-94
19595669-8	2009	Taken together, our results indicate that aspirin causes apoptosis via down-regulation of IL-6-dependent STAT3 signaling, suggesting that aspirin could be therapeutically useful for a potential anti-glioblastoma therapeutic approach.	Aspirin	138-145	signal transducer and activator of transcription 3	Homo sapiens	105-110
19540194-5	2009	C18-DOM increased the expression of anti-atherogenic molecule namely heme oxygenase-1 in endothelial cells and all these data showed that C18-DOM is exhibiting aspirin-like effects.	Aspirin	160-167	Bardet-Biedl syndrome 9	Homo sapiens	0-7
19540194-5	2009	C18-DOM increased the expression of anti-atherogenic molecule namely heme oxygenase-1 in endothelial cells and all these data showed that C18-DOM is exhibiting aspirin-like effects.	Aspirin	160-167	Bardet-Biedl syndrome 9	Homo sapiens	138-145
19268942-5	2009	In human THP-1-derived macrophages, induction of SR-BI protein by aspirin was abrogated by concomitant pharmacological inhibition of nuclear factor-kappa B (NF-kappaB).	Aspirin	66-73	GLI family zinc finger 2	Homo sapiens	9-14
19268942-5	2009	In human THP-1-derived macrophages, induction of SR-BI protein by aspirin was abrogated by concomitant pharmacological inhibition of nuclear factor-kappa B (NF-kappaB).	Aspirin	66-73	nuclear factor kappa B subunit 1	Homo sapiens	157-166
19268942-8	2009	CONCLUSIONS: We suggest that aspirin treatment might lead to enhanced expression of SR-BI in human plaque macrophages and that this effect is dependent on the presence of NF-kappaB.	Aspirin	29-36	nuclear factor kappa B subunit 1	Homo sapiens	171-180
19483113-9	2009	CONCLUSIONS: These results demonstrate that aspirin-triggered 15-epi-LXA(4) enhances resolution of inflammation by overriding the powerful antiapoptosis signal from MPO, thereby demonstrating a hitherto unrecognized mechanism by which aspirin promotes resolution of inflammation.	Aspirin	44-51	myeloperoxidase	Homo sapiens	165-168
19483113-9	2009	CONCLUSIONS: These results demonstrate that aspirin-triggered 15-epi-LXA(4) enhances resolution of inflammation by overriding the powerful antiapoptosis signal from MPO, thereby demonstrating a hitherto unrecognized mechanism by which aspirin promotes resolution of inflammation.	Aspirin	235-242	myeloperoxidase	Homo sapiens	165-168
19542225-6	2009	Both HepG2 and LS180 cells treated with NO-aspirin 2 showed an increase in glutathione S-transferase-P1 (GST-P1), glutamate-cysteine ligase (GCL), and NAD(P)H:quinone oxidoreductase-1 (NQO1) expression.	Aspirin	43-50	NAD(P)H quinone dehydrogenase 1	Homo sapiens	151-183
19542225-6	2009	Both HepG2 and LS180 cells treated with NO-aspirin 2 showed an increase in glutathione S-transferase-P1 (GST-P1), glutamate-cysteine ligase (GCL), and NAD(P)H:quinone oxidoreductase-1 (NQO1) expression.	Aspirin	43-50	NAD(P)H quinone dehydrogenase 1	Homo sapiens	185-189
19082925-6	2009	Compared with control group, the differences of the treatment group and aspirin group of rats are significant (P &lt; 0.05) for prothrombin time and thrombin time, and very significant (P &lt; 0.01) for activated partial thromboplastin time.	Aspirin	72-79	coagulation factor II	Rattus norvegicus	131-139
19407805-1	2009	BACKGROUND: Aspirin has been found to prevent angiotensin II-induced hypertension and to induce nitric oxide (NO) release from vascular endothelium.	Aspirin	12-19	angiotensinogen	Homo sapiens	46-60
19680014-3	2009	Inhibition of cyclooxygenase (COX)-1 and COX-2 by aspirin or its related compounds, nonsteroidal antiinflammatory drugs (NSAIDs), has been associated with both adverse and beneficial effects in the gastrointestinal (GI) tract.	Aspirin	50-57	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	41-46
19680014-11	2009	Inhibition of COX-2 by NSAIDs, coxibs, or aspirin seems to provide beneficial effects to the GI tract.	Aspirin	42-49	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	14-19
19671906-10	2009	Among 459 participants with colorectal cancers that were accessible for immunohistochemical assessment, the effect of aspirin differed significantly according to cyclooxygenase 2 (COX-2) expression (P for interaction = .04).	Aspirin	118-125	prostaglandin-endoperoxide synthase 2	Homo sapiens	162-178
19671906-10	2009	Among 459 participants with colorectal cancers that were accessible for immunohistochemical assessment, the effect of aspirin differed significantly according to cyclooxygenase 2 (COX-2) expression (P for interaction = .04).	Aspirin	118-125	prostaglandin-endoperoxide synthase 2	Homo sapiens	180-185
19671906-11	2009	Regular aspirin use after diagnosis was associated with a lower risk of colorectal cancer-specific mortality among participants in whom primary tumors overexpressed COX-2 (multivariate HR, 0.39; 95% CI, 0.20-0.76), whereas aspirin use was not associated with lower risk among those with primary tumors with weak or absent expression (multivariate HR, 1.22; 95% CI, 0.36-4.18).	Aspirin	8-15	prostaglandin-endoperoxide synthase 2	Homo sapiens	165-170
19671906-12	2009	CONCLUSION: Regular aspirin use after the diagnosis of colorectal cancer is associated with lower risk of colorectal cancer-specific and overall mortality, especially among individuals with tumors that overexpress COX-2.	Aspirin	20-27	prostaglandin-endoperoxide synthase 2	Homo sapiens	214-219
19375439-7	2009	In contrast, aspirin reduced both LPS- and IL-1beta induced fever, whereas diazepam had little effect on these fever states.	Aspirin	13-20	interleukin 1 beta	Rattus norvegicus	43-51
19222424-3	2009	The goal of this study was to investigate a gene-gene interaction between IL-10 and TGF-beta1 polymorphisms in Korean asthmatics with aspirin hypersensitivity.	Aspirin	134-141	transforming growth factor beta 1	Homo sapiens	84-93
19462226-0	2009	Aspirin inhibits MMP-2 and MMP-9 expression and activity through PPARalpha/gamma and TIMP-1-mediated mechanisms in cultured mouse celiac macrophages.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Mus musculus	65-74
19462226-0	2009	Aspirin inhibits MMP-2 and MMP-9 expression and activity through PPARalpha/gamma and TIMP-1-mediated mechanisms in cultured mouse celiac macrophages.	Aspirin	0-7	tissue inhibitor of metalloproteinase 1	Mus musculus	85-91
19462226-4	2009	The results showed that MMP-2/9 mRNA expression and release were significantly decreased after cultured mouse celiac macrophages were treated with aspirin 12.5-50 microg/ml for 24 h, while the TIMP-1 mRNA expression and release, and peroxisome proliferator-activated receptor (PPAR) alpha/gamma mRNA expression were increased after the same treatment.	Aspirin	147-154	tissue inhibitor of metalloproteinase 1	Mus musculus	193-199
19462226-4	2009	The results showed that MMP-2/9 mRNA expression and release were significantly decreased after cultured mouse celiac macrophages were treated with aspirin 12.5-50 microg/ml for 24 h, while the TIMP-1 mRNA expression and release, and peroxisome proliferator-activated receptor (PPAR) alpha/gamma mRNA expression were increased after the same treatment.	Aspirin	147-154	peroxisome proliferator activated receptor alpha	Mus musculus	233-288
19462226-5	2009	Moreover the aspirin-induced down-regulation of MMP-2/9 mRNA expression and reduction of MMP-9 release were notably alleviated after pretreatment with specific inhibitors of PPARalpha/gamma.	Aspirin	13-20	peroxisome proliferator activated receptor alpha	Mus musculus	174-183
19462226-6	2009	These results suggested that aspirin could inhibit the expression and release of MMP-2/9 by up-regulation of PPARalpha/gamma gene expression, and also inhibit the activity of MMP-2/9 by induction of TIMP-1 expression, which might be good for the stabilization of atherosclerotic plaques and the prevention of cardio-cerebrovascular events.	Aspirin	29-36	peroxisome proliferator activated receptor alpha	Mus musculus	109-118
19462226-6	2009	These results suggested that aspirin could inhibit the expression and release of MMP-2/9 by up-regulation of PPARalpha/gamma gene expression, and also inhibit the activity of MMP-2/9 by induction of TIMP-1 expression, which might be good for the stabilization of atherosclerotic plaques and the prevention of cardio-cerebrovascular events.	Aspirin	29-36	tissue inhibitor of metalloproteinase 1	Mus musculus	199-205
18846318-2	2009	Treatment of Platelet Rich Plasma (PRP) with the dialyzed supernatant from the leucocyte suspension incubated with 80 microM aspirin resulted in parallel syntheses of NO and IFN-alpha as determined by methemoglobin assay and enzyme linked immunosorbent assay respectively.	Aspirin	125-132	proline rich protein HaeIII subfamily 1	Mus musculus	13-33
18846318-2	2009	Treatment of Platelet Rich Plasma (PRP) with the dialyzed supernatant from the leucocyte suspension incubated with 80 microM aspirin resulted in parallel syntheses of NO and IFN-alpha as determined by methemoglobin assay and enzyme linked immunosorbent assay respectively.	Aspirin	125-132	proline rich protein HaeIII subfamily 1	Mus musculus	35-38
19579086-0	2009	Diabetes mellitus is associated with increased ex vivo-platelet aggregation and decreased response to aspirin - antithrombotic potential of ACE-inhibitors and AT1-antagonists.	Aspirin	102-109	angiotensin I converting enzyme	Homo sapiens	140-143
19652893-9	2009	These results suggest that some of the variability in the reported incidence of "aspirin resistance" is unrelated to aspirin intake but related to inherent limitations of some assays to detect aspirin mediated effects or to underlying platelet reactivity variability independent of aspirin-mediated cyclooxygenase-1 inhibition.	Aspirin	81-88	prostaglandin-endoperoxide synthase 1	Homo sapiens	299-315
19465478-0	2009	Binding modes of aromatic ligands to mammalian heme peroxidases with associated functional implications: crystal structures of lactoperoxidase complexes with acetylsalicylic acid, salicylhydroxamic acid, and benzylhydroxamic acid.	Aspirin	158-178	lactoperoxidase	Homo sapiens	127-142
19306941-4	2009	In this evidence-based review, we have endeavored to answer 12 commonly encountered questions in clinical practice that deal with the following: extent of the problem of NSAID/aspirin-induced gastroduodenal damage and its impact on public health; role of proton pump inhibitors (PPIs) in the primary prevention, healing, and secondary prevention of NSAID/aspirin-induced gastroduodenal ulceration as assessed by using endoscopic end points; role of PPIs in the prevention of adverse clinical outcomes related to NSAID/aspirin use; whether PPIs are effective in NSAID-induced dyspepsia; comparison of PPI co-therapy with selective cyclooxygenase-2 inhibitors for risk reduction of adverse clinical outcomes; role of PPIs in preventing rebleeding from aspirin +/- clopidogrel therapy in high-risk patients; identifying high-risk patients who can benefit from PPI co-therapy; the role of other gastroprotective agents for prevention of NSAID/aspirin-induced gastroduodenal damage; and the cost-effectiveness of and limitations to the use of PPIs for prevention of gastroduodenal damage related to the use of NSAIDs or aspirin.	Aspirin	176-183	prostaglandin-endoperoxide synthase 2	Homo sapiens	630-646
19377066-2	2009	The aim of the present study was to determine the mechanism by which aspirin acutely increases the activity of NO synthase type 3 (NOS-3), the predominant NOS isoform expressed by platelets, and specifically whether this occurs through an increase in its acetylation.	Aspirin	69-76	nitric oxide synthase 3	Homo sapiens	111-136
19377066-8	2009	At all concentrations tested, aspirin increased the activity of NOS-3 from platelets.	Aspirin	30-37	nitric oxide synthase 3	Homo sapiens	64-69
19377066-10	2009	Serine phosphorylation of NOS-3 in platelets was decreased, and this was especially marked for serine-1177 phosphorylation, whereas acetylation of NOS-3 was increased, by aspirin incubation.	Aspirin	171-178	nitric oxide synthase 3	Homo sapiens	26-31
19377066-10	2009	Serine phosphorylation of NOS-3 in platelets was decreased, and this was especially marked for serine-1177 phosphorylation, whereas acetylation of NOS-3 was increased, by aspirin incubation.	Aspirin	171-178	nitric oxide synthase 3	Homo sapiens	147-152
19377066-11	2009	HeLa cells transfected with NOS-3 exhibited an increase in NO biosynthesis following aspirin exposure, and this was associated with acetylation of the enzyme on both serine-765 and serine-771.	Aspirin	85-92	nitric oxide synthase 3	Homo sapiens	28-33
19377066-12	2009	CONCLUSION: Aspirin acetylates NOS-3 acutely in platelets, and this causes an increase in its activity as well as a decrease in its phosphorylation.	Aspirin	12-19	nitric oxide synthase 3	Homo sapiens	31-36
19377066-13	2009	It is also possible that aspirin indirectly affects NOS-3 activity by acetylating other substrates within the platelet, but this remains to be determined.	Aspirin	25-32	nitric oxide synthase 3	Homo sapiens	52-57
19493461-0	2009	Aspirin inhibits tumor necrosis factor-alpha-stimulated fractalkine expression in human umbilical vein endothelial cells.	Aspirin	0-7	C-X3-C motif chemokine ligand 1	Homo sapiens	56-67
21475861-9	2009	In a recent study using protein-specific anti-acetyl lysine antibodies and immunological methods, we demonstrated the ability of aspirin to acetylate the tumor suppressor protein p53.	Aspirin	129-136	tumor protein p53	Homo sapiens	179-182
19404617-4	2009	Aspirin has been shown to attenuate the adrenocorticotropic hormone (ACTH) and cortisol response to physiological challenge suggesting its potential to act as an augmenting agent in depression.	Aspirin	0-7	proopiomelanocortin	Homo sapiens	40-67
19404617-4	2009	Aspirin has been shown to attenuate the adrenocorticotropic hormone (ACTH) and cortisol response to physiological challenge suggesting its potential to act as an augmenting agent in depression.	Aspirin	0-7	proopiomelanocortin	Homo sapiens	69-73
19534809-11	2009	Both of these markers were increased upon COX-2 suppression by aspirin pretreatment prior to DCA exposure.	Aspirin	63-70	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	42-47
19409619-0	2009	Effect of aspirin treatment on TNFalpha production by women with a history of preterm birth.	Aspirin	10-17	tumor necrosis factor	Homo sapiens	31-39
19409619-2	2009	The objectives of this study were (1) to determine if there is a similar differential responsiveness for peripheral blood mononuclear leukocytes (PBML) and (2) to determine if treatment with aspirin influences LPS-stimulated TNFalpha production in these patients.	Aspirin	191-198	tumor necrosis factor	Homo sapiens	225-233
19409619-7	2009	Aspirin treatment enhanced LPS-stimulated TNFalpha production by PBML from controls but not cases.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	42-50
19409619-9	2009	Aspirin increases TNFalpha production by PBML in control women but not in women with a history of preterm birth.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	18-26
19446280-1	2009	Low-dose aspirin (100 mg/day) was recently found to increase serum levels of alpha-1 protease inhibitor (A1-PI).	Aspirin	9-16	serpin family A member 1	Homo sapiens	77-103
19446280-1	2009	Low-dose aspirin (100 mg/day) was recently found to increase serum levels of alpha-1 protease inhibitor (A1-PI).	Aspirin	9-16	serpin family A member 1	Homo sapiens	105-110
19446280-4	2009	The previously described increase of A1-PI levels by low-dose aspirin was most likely caused by multiple endoscopies within a few days, which caused a systemic stress response.	Aspirin	62-69	serpin family A member 1	Homo sapiens	37-42
19401417-10	2009	The two drugs were instead concordant in reducing the upregulation of genes of the TGF-beta pathway (55% for sorbinil and 40% for aspirin) and apoptosis (74 and 42%, respectively).	Aspirin	130-137	transforming growth factor, beta 1	Rattus norvegicus	83-91
19046748-3	2009	A secondary aim was to replicate the interaction of PTGS2 rs20417 (-765G to C) with aspirin use on coronary heart disease risk observed in the Atherosclerosis Risk in Communities Study (ARIC).	Aspirin	84-91	prostaglandin-endoperoxide synthase 2	Homo sapiens	52-57
19046748-10	2009	CONCLUSIONS: Study results suggest that variation in TBXAS1 and PTGIS may influence MI risk, and carriers of rs20417C allele might derive greater benefits from aspirin use in primary prevention.	Aspirin	160-167	thromboxane A synthase 1	Homo sapiens	53-59
19601807-5	2009	Metabolites of 15-LOX-1 and 2 are anti-tumorigenic; similarly, 15-epi-LXA(4) synthesized during COX-2 acetylation by low doses of aspirin too possesses anti-tumorigenic effects.	Aspirin	130-137	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	96-101
19601807-6	2009	Acetylating nonsteroidal anti-inflammatory drugs (NSAIDs), like aspirin, switches COX-2 from forming PGE(2) (promoting tumorigenesis) to 15-epi-LXA(4) (antitumorigenesis).	Aspirin	64-71	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	82-87
19618315-0	2009	Thrombin formation and platelet activation at the site of vascular injury in patients with coronary artery disease treated with clopidogrel combined with aspirin.	Aspirin	154-161	coagulation factor II, thrombin	Homo sapiens	0-8
19618315-6	2009	RESULTS: Total amounts of thrombin markers produced at the site of injury were similar before and after addition of clopidogrel, whereas platelet release of sCD40L and P-selectin was lower during treatment with aspirin + clopidogrel by 33.8% and 27.8% (p &lt; 0.001), respectively.	Aspirin	211-218	coagulation factor II, thrombin	Homo sapiens	26-34
19155536-7	2009	For regular users of aspirin, the progression rate was significantly slower than that for non-regular users (regular users progressed 0.80 mL/min/1.73 m(2) per year slower than non-regular users; 95% CI 0.1, 1.5).	Aspirin	21-28	CD59 molecule (CD59 blood group)	Homo sapiens	142-147
19493461-10	2009	Aspirin inhibited fractalkine expression in a dose-dependent manner at mRNA and protein levels.	Aspirin	0-7	C-X3-C motif chemokine ligand 1	Homo sapiens	18-29
19493461-15	2009	Aspirin decreased COX-2 expression in a dose-dependent manner at mRNA and protein levels.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	18-23
19493461-16	2009	CONCLUSIONS: TNF-alpha-stimulated fractalkine expression is suppressed by aspirin in a dose-dependent manner through the nuclear factor-kappa B p65 pathway.	Aspirin	74-81	tumor necrosis factor	Homo sapiens	13-22
19493461-16	2009	CONCLUSIONS: TNF-alpha-stimulated fractalkine expression is suppressed by aspirin in a dose-dependent manner through the nuclear factor-kappa B p65 pathway.	Aspirin	74-81	C-X3-C motif chemokine ligand 1	Homo sapiens	34-45
19048345-4	2009	Specificity of AST was determined using a non-phosphorylable mutant sensor containing an alanine substitution (ASA).	Aspirin	111-114	solute carrier family 17 member 5	Homo sapiens	15-18
19466516-0	2009	The effect of preoperative aspirin administration on postoperative level of von Willebrand factor in off-pump coronary artery bypass surgery.	Aspirin	27-34	von Willebrand factor	Homo sapiens	76-97
19466516-8	2009	Preoperative use of aspirin before OPCAB could suppress the postoperative increase in von Willebrand factor, a possible indicator of endothelial damage, only in the early postoperative phase.	Aspirin	20-27	von Willebrand factor	Homo sapiens	86-107
19048345-5	2009	RESULTS: The PI-3K inhibitor LY294002 and Akt kinase inhibitor perifosine led to temporal- and dose-dependent increases in complemented FL activities in 293T human kidney cancer cells stably expressing AST (293T/AST) but not in 293T/ASA cells.	Aspirin	233-236	AKT serine/threonine kinase 1	Homo sapiens	42-45
19215971-2	2009	We investigated whether 75 mg of daily non-enteric coated aspirin would completely inhibit the platelet cyclooxygenase-1 activity to a comparable extent in healthy individuals and stable CAD patients.	Aspirin	58-65	prostaglandin-endoperoxide synthase 1	Homo sapiens	104-120
19673332-1	2009	OBJECTIVE: To investigate the inhibitory effect of arsenic trioxide, aspirin and their combination on the growth of human gastric adenocarcinoma SGC-7901 graft in nude mice.	Aspirin	69-76	sarcoglycan beta	Homo sapiens	145-148
19048345-5	2009	RESULTS: The PI-3K inhibitor LY294002 and Akt kinase inhibitor perifosine led to temporal- and dose-dependent increases in complemented FL activities in 293T human kidney cancer cells stably expressing AST (293T/AST) but not in 293T/ASA cells.	Aspirin	233-236	solute carrier family 17 member 5	Homo sapiens	202-205
19048345-6	2009	Inhibition of endogenous Akt phosphorylation and kinase activities by perifosine also correlated with increase in complemented FL activities in 293T/AST cells but not in 293T/ASA cells.	Aspirin	175-178	AKT serine/threonine kinase 1	Homo sapiens	25-28
18775097-5	2009	ASA and HT-AC had a greater effect in whole blood than in PRP when ADP or collagen was used as inducer.	Aspirin	0-3	complement component 4 binding protein alpha	Homo sapiens	58-61
18775097-6	2009	ASA and HT-AC had a greater effect in PRP+leucocytes than in PRP alone.	Aspirin	0-3	complement component 4 binding protein alpha	Homo sapiens	38-41
18775097-6	2009	ASA and HT-AC had a greater effect in PRP+leucocytes than in PRP alone.	Aspirin	0-3	complement component 4 binding protein alpha	Homo sapiens	61-64
19250144-0	2009	Association of TNF-alpha promoter polymorphisms with aspirin-induced urticaria.	Aspirin	53-60	tumor necrosis factor	Homo sapiens	15-24
18946735-4	2009	The reduction of dopamine transporter (DAT)-positive signals and PPAR gamma expression, and accumulation of activated microglial cells were significantly and dose-dependently attenuated by four injections of a nonsteroidal anti-inflammatory drug and a PPAR gamma ligand, ibuprofen (10 or 20 mg/kg x 4, s.c.) given 30 min prior to each METH injection, but not by either a low or high dose of aspirin.	Aspirin	391-398	peroxisome proliferator activated receptor gamma	Homo sapiens	252-262
19023563-10	2009	In conclusion, MCT1-mediated transport of (14)C-BT in Caco-2 cells is modulated by either acute or chronic exposure to some pharmacological agents and drugs of abuse (acetaldehyde, acetylsalicylic acid, indomethacin, caffeine, theophylline and the drugs of abuse tetrahydrocannabinol and MDMA).	Aspirin	181-201	solute carrier family 16 member 1	Homo sapiens	15-19
19345795-5	2009	Aspirin inhibited IL-1beta-induced PGF(2alpha), but not IL-8 production.	Aspirin	0-7	interleukin 1 beta	Homo sapiens	18-26
19122175-7	2009	The finding that LSS-dependent reduction of TNF-alpha generation and HO-1 induction were abrogated by the selective inhibitor of COX-2 NS-398, the nonselective COX inhibitor aspirin, or the specific prostacyclin receptor (IP) antagonist RO3244794 illuminates the central role played by LSS-induced COX-2-dependent prostacyclin in restraining endothelial inflammation.	Aspirin	174-181	tumor necrosis factor	Homo sapiens	44-53
19212664-0	2009	Aspirin inhibits camptothecin-induced p21CIP1 levels and potentiates apoptosis in human breast cancer cells.	Aspirin	0-7	cyclin dependent kinase inhibitor 1A	Homo sapiens	38-45
19212664-2	2009	We hypothesized that the anticancer effects of aspirin may involve acetylation of the tumor suppressor protein p53, a known regulator of apoptosis.	Aspirin	47-54	tumor protein p53	Homo sapiens	111-114
19212664-3	2009	In the present study, we determined if aspirin at the physiologically achievable concentration of 100 microM acetylates p53 and modulates the expression of p21CIP1, a protein involved in cell cycle arrest, and Bax, a pro-apoptotic protein.	Aspirin	39-46	tumor protein p53	Homo sapiens	120-123
19212664-3	2009	In the present study, we determined if aspirin at the physiologically achievable concentration of 100 microM acetylates p53 and modulates the expression of p21CIP1, a protein involved in cell cycle arrest, and Bax, a pro-apoptotic protein.	Aspirin	39-46	cyclin dependent kinase inhibitor 1A	Homo sapiens	156-163
19212664-3	2009	In the present study, we determined if aspirin at the physiologically achievable concentration of 100 microM acetylates p53 and modulates the expression of p21CIP1, a protein involved in cell cycle arrest, and Bax, a pro-apoptotic protein.	Aspirin	39-46	BCL2 associated X, apoptosis regulator	Homo sapiens	210-213
19212664-4	2009	Using MDA-MB-231 human breast cancer cells, we demonstrate that aspirin at 100 microM concentration markedly acetylated the p53 protein, which was primarily localized to the nucleus.	Aspirin	64-71	tumor protein p53	Homo sapiens	124-127
19212664-5	2009	Aspirin induced p21CIP1 protein levels in a transient fashion in contrast to the sustained induction of Bax.	Aspirin	0-7	cyclin dependent kinase inhibitor 1A	Homo sapiens	16-23
19212664-7	2009	Remarkably, when cells were co-treated with aspirin and CPT, p21CIP1 levels were drastically downregulated, and this phenomenon was observed in many cancer cell lines.	Aspirin	44-51	cyclin dependent kinase inhibitor 1A	Homo sapiens	61-68
19212664-8	2009	Incubation of recombinant p21 with cytoplasmic extracts from aspirin-treated cells caused its degradation suggesting the involvement of proteases in the disappearance of p21CIP1.	Aspirin	61-68	cyclin dependent kinase inhibitor 1A	Homo sapiens	26-29
19212664-8	2009	Incubation of recombinant p21 with cytoplasmic extracts from aspirin-treated cells caused its degradation suggesting the involvement of proteases in the disappearance of p21CIP1.	Aspirin	61-68	cyclin dependent kinase inhibitor 1A	Homo sapiens	170-177
19212664-10	2009	Our observation that aspirin has the ability to inhibit p21CIP1 after its initial induction has important implications in chemotherapy, and suggests its potential use to increase the efficacy of anticancer agents.	Aspirin	21-28	cyclin dependent kinase inhibitor 1A	Homo sapiens	56-63
19146957-10	2009	The different effects of ASA on CD4(+)CD25(+)Foxp3(+) Treg cells and CD4(+)CD25(-) T cells may potentially make hosts susceptible to tolerance induction which would be beneficial for tolerance induction in patients with autoimmune diseases or allo-grafts.	Aspirin	25-28	CD4 molecule	Homo sapiens	32-35
19248197-6	2009	COX-1 and -2 mRNA levels were significantly increased in the EA group as compared to the control and ASA groups, and NO levels were also significantly increased in the EA group as compared to the ASA group.	Aspirin	101-104	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	0-12
19575683-3	2009	The ingestion of aspirin and other cyclooxygenase-1 (COX-1) inhibitors induces exacerbations of airway disease that may be life-threatening.	Aspirin	17-24	prostaglandin-endoperoxide synthase 1	Homo sapiens	53-58
19236238-3	2009	Conversely, NSAIDs including aspirin inhibit COX-2 and, therefore, have anti-neoplastic properties.	Aspirin	29-36	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	45-50
18992263-3	2009	Insulin-related genes were associated with CIMP-positive and MSI tumors, with the strongest associations among aspirin users.	Aspirin	111-118	insulin	Homo sapiens	0-7
19026633-3	2009	Furthermore, we demonstrated that the non-steroidal anti-inflammatory drug, sulindac sulfide, the cyclooxygenase-2 (COX-2) selective inhibitor, celecoxib, and the nitric oxide-donating aspirin derivative, NO-ASA, blocked Wnt/beta-catenin signaling in PC-3 and DU145 cells.	Aspirin	185-192	prostaglandin-endoperoxide synthase 2	Homo sapiens	116-121
19026633-3	2009	Furthermore, we demonstrated that the non-steroidal anti-inflammatory drug, sulindac sulfide, the cyclooxygenase-2 (COX-2) selective inhibitor, celecoxib, and the nitric oxide-donating aspirin derivative, NO-ASA, blocked Wnt/beta-catenin signaling in PC-3 and DU145 cells.	Aspirin	208-211	prostaglandin-endoperoxide synthase 2	Homo sapiens	98-114
19299662-3	2009	Indeed, a new class of selective inhibitors of the cyclooxygenase-2 isozyme was introduced, about ten years ago, and these so-called coxibs quickly became regarded as preferable, in certain clinical contexts, to avoid side effects associated with the use of aspirin and previously developed NSAIDs.	Aspirin	258-265	prostaglandin-endoperoxide synthase 2	Homo sapiens	51-67
18474393-8	2009	Similarly, peak thrombin levels were reduced in patients treated with warfarin (-18%+/-7%, p=0.049) and aspirin/warfarin (-19%+/-5%, p=0.029), whereas an increase (12%+/-4%, p=0.029) occurred during aspirin treatment alone.	Aspirin	104-111	coagulation factor II, thrombin	Homo sapiens	16-24
18474393-8	2009	Similarly, peak thrombin levels were reduced in patients treated with warfarin (-18%+/-7%, p=0.049) and aspirin/warfarin (-19%+/-5%, p=0.029), whereas an increase (12%+/-4%, p=0.029) occurred during aspirin treatment alone.	Aspirin	199-206	coagulation factor II, thrombin	Homo sapiens	16-24
18805632-8	2009	When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA.	Aspirin	113-116	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	5-10
18805632-8	2009	When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA.	Aspirin	113-116	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	59-64
18805632-8	2009	When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA.	Aspirin	113-116	cyclin dependent kinase inhibitor 1A	Homo sapiens	84-87
18805632-8	2009	When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA.	Aspirin	113-116	cyclin dependent kinase inhibitor 1A	Homo sapiens	88-93
18805632-8	2009	When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA.	Aspirin	250-253	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	5-10
18805632-8	2009	When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA.	Aspirin	250-253	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	59-64
18805632-8	2009	When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA.	Aspirin	250-253	cyclin dependent kinase inhibitor 1A	Homo sapiens	84-87
18805632-8	2009	When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA.	Aspirin	250-253	cyclin dependent kinase inhibitor 1A	Homo sapiens	88-93
18983829-0	2009	Human carboxylesterases HCE1 and HCE2: ontogenic expression, inter-individual variability and differential hydrolysis of oseltamivir, aspirin, deltamethrin and permethrin.	Aspirin	134-141	carboxylesterase 2	Homo sapiens	33-37
18992263-7	2009	Most associations varied by recent aspirin/NSAID use: IL6 rs1800796 and rs1800795 polymorphisms were associated inversely with tumor mutations in the presence of aspirin/NSAIDs; POMC significantly reduced risk of Ki-ras-mutated tumors when aspirin/NSAIDs were not used; the TCF7L2 rs7903146 was associated with reduced risk of Ki-ras-mutated tumors in the presence of aspirin and increased risk in the absence of aspirin.	Aspirin	35-42	interleukin 6	Homo sapiens	54-57
18992263-7	2009	Most associations varied by recent aspirin/NSAID use: IL6 rs1800796 and rs1800795 polymorphisms were associated inversely with tumor mutations in the presence of aspirin/NSAIDs; POMC significantly reduced risk of Ki-ras-mutated tumors when aspirin/NSAIDs were not used; the TCF7L2 rs7903146 was associated with reduced risk of Ki-ras-mutated tumors in the presence of aspirin and increased risk in the absence of aspirin.	Aspirin	35-42	proopiomelanocortin	Homo sapiens	178-182
18992263-7	2009	Most associations varied by recent aspirin/NSAID use: IL6 rs1800796 and rs1800795 polymorphisms were associated inversely with tumor mutations in the presence of aspirin/NSAIDs; POMC significantly reduced risk of Ki-ras-mutated tumors when aspirin/NSAIDs were not used; the TCF7L2 rs7903146 was associated with reduced risk of Ki-ras-mutated tumors in the presence of aspirin and increased risk in the absence of aspirin.	Aspirin	162-169	interleukin 6	Homo sapiens	54-57
18992263-7	2009	Most associations varied by recent aspirin/NSAID use: IL6 rs1800796 and rs1800795 polymorphisms were associated inversely with tumor mutations in the presence of aspirin/NSAIDs; POMC significantly reduced risk of Ki-ras-mutated tumors when aspirin/NSAIDs were not used; the TCF7L2 rs7903146 was associated with reduced risk of Ki-ras-mutated tumors in the presence of aspirin and increased risk in the absence of aspirin.	Aspirin	162-169	interleukin 6	Homo sapiens	54-57
18992263-7	2009	Most associations varied by recent aspirin/NSAID use: IL6 rs1800796 and rs1800795 polymorphisms were associated inversely with tumor mutations in the presence of aspirin/NSAIDs; POMC significantly reduced risk of Ki-ras-mutated tumors when aspirin/NSAIDs were not used; the TCF7L2 rs7903146 was associated with reduced risk of Ki-ras-mutated tumors in the presence of aspirin and increased risk in the absence of aspirin.	Aspirin	162-169	interleukin 6	Homo sapiens	54-57
18992263-7	2009	Most associations varied by recent aspirin/NSAID use: IL6 rs1800796 and rs1800795 polymorphisms were associated inversely with tumor mutations in the presence of aspirin/NSAIDs; POMC significantly reduced risk of Ki-ras-mutated tumors when aspirin/NSAIDs were not used; the TCF7L2 rs7903146 was associated with reduced risk of Ki-ras-mutated tumors in the presence of aspirin and increased risk in the absence of aspirin.	Aspirin	162-169	interleukin 6	Homo sapiens	54-57
19575683-5	2009	Patients with aspirin sensitivity are often able to tolerate selective COX-2 inhibitors.	Aspirin	14-21	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	71-76
19345936-5	2009	Herein, we tested a variety of Cox-1/Cox-2 non-selective NSAIDs, namely ibuprofen, tylenol, aspirin and naproxen and report that they blunt IgM and IgG synthesis in stimulated human peripheral blood mononuclear cells (PBMC).	Aspirin	92-99	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	37-42
19641312-9	2009	CONCLUSION: Triflusal modulates additional mechanisms to those of aspirin [pro-inflammatory (IL-6) and chemokine (MIP-1 and MCP-1) pathways] that could participate in the ischemic damage process following human acute stroke.	Aspirin	66-73	interleukin 6	Homo sapiens	93-97
19295242-7	2009	CONCLUSIONS: The main finding of this study is that COX-2 appears to be differentially regulated in aspirin-sensitive patients.	Aspirin	100-107	prostaglandin-endoperoxide synthase 2	Homo sapiens	52-57
19390185-6	2009	More subjects with the PTGS1 17PP versus PL genotype had incomplete ex-vivo inhibition of platelet aggregation by aspirin (57 vs. 20%; p = 0.04).	Aspirin	114-121	prostaglandin-endoperoxide synthase 1	Homo sapiens	23-28
19390185-8	2009	Similarly, nonlinear mapping showed a direct relationship between the PTGS1 17P allele and decreased aspirin response.	Aspirin	101-108	prostaglandin-endoperoxide synthase 1	Homo sapiens	70-75
19390185-10	2009	CONCLUSIONS: Our data suggest that the PTGS1 P17L genotype contributes to response to aspirin as assessed by ex-vivo platelet aggregation.	Aspirin	86-93	prostaglandin-endoperoxide synthase 1	Homo sapiens	39-44
19390185-11	2009	Our data further suggest that the association between PTGS1 genotype and aspirin response might vary by ethnicity.	Aspirin	73-80	prostaglandin-endoperoxide synthase 1	Homo sapiens	54-59
19641312-4	2009	RESULTS: An increase in IL-6 level was found in the aspirin group when compared to the triflusal group at the third and seventh day (p &lt; 0.05).	Aspirin	52-59	interleukin 6	Homo sapiens	24-28
19938885-0	2009	Low-dose aspirin reduces gastro-protective properties of COX-2 selective inhibitors.	Aspirin	9-16	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	57-62
19938885-2	2009	With this case we emphasize that the potential of the stomach-protecting properties of COX-2 selective inhibitors may be reduced in patients who are simultaneously taking aspirin.	Aspirin	171-178	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	87-92
19938885-3	2009	We also review several pathogenic mechanisms that have been advanced by animal studies to explain the finding that a COX-2 selective inhibitor plus low-dose aspirin leads to an ulcer rate near that of a dual COX-1/COX-2 inhibitor alone.	Aspirin	157-164	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	214-219
19114773-7	2009	COX-2 inhibition still seems preferred option, as the effects observed with aspirin (the only chemopreventive agent with some apparent future) are more profound only in tumors and cells expressing COX-2.	Aspirin	76-83	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
19114773-7	2009	COX-2 inhibition still seems preferred option, as the effects observed with aspirin (the only chemopreventive agent with some apparent future) are more profound only in tumors and cells expressing COX-2.	Aspirin	76-83	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	197-202
19114773-10	2009	By inhibiting COX-2 or other tumorigenic targets, NSAIDs, especially aspirin or new aspirin derivates, may prevent colon cancer in selected populations.	Aspirin	69-76	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	14-19
19114773-10	2009	By inhibiting COX-2 or other tumorigenic targets, NSAIDs, especially aspirin or new aspirin derivates, may prevent colon cancer in selected populations.	Aspirin	84-91	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	14-19
21701610-10	2009	Acetylsalicylic acid appears to diminish the benefit of COX-2s over tNSAIDs.	Aspirin	0-20	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	56-61
19940340-4	2009	The Ca(2+)-induced solvent accessible surface area (ASA) changes of calmodulin (CaM) and S100 proteins were employed to monitor and optimize HDX protocol efficiency.	Aspirin	52-55	calmodulin 1	Homo sapiens	68-78
19940340-4	2009	The Ca(2+)-induced solvent accessible surface area (ASA) changes of calmodulin (CaM) and S100 proteins were employed to monitor and optimize HDX protocol efficiency.	Aspirin	52-55	calmodulin 1	Homo sapiens	80-83
19940340-4	2009	The Ca(2+)-induced solvent accessible surface area (ASA) changes of calmodulin (CaM) and S100 proteins were employed to monitor and optimize HDX protocol efficiency.	Aspirin	52-55	S100 calcium binding protein B	Homo sapiens	89-93
19390185-0	2009	Influence of cyclooxygenase-1 genotype on ex vivo aspirin response in patients at risk for stroke.	Aspirin	50-57	prostaglandin-endoperoxide synthase 1	Homo sapiens	13-29
19390185-1	2009	BACKGROUND: We sought to determine whether cyclooxygenase-1 (PTGS1) genotype is associated with the ability of aspirin to inhibit platelet aggregation in patients at risk for stroke.	Aspirin	111-118	prostaglandin-endoperoxide synthase 1	Homo sapiens	43-59
19390185-1	2009	BACKGROUND: We sought to determine whether cyclooxygenase-1 (PTGS1) genotype is associated with the ability of aspirin to inhibit platelet aggregation in patients at risk for stroke.	Aspirin	111-118	prostaglandin-endoperoxide synthase 1	Homo sapiens	61-66
19390185-4	2009	The association between PTGS1 A-707G and P17L genotypes and aspirin response, as assessed by ex vivo studies and 11-dhTxB(2) concentrations, was evaluated by statistical testing and nonlinear mapping.	Aspirin	60-67	prostaglandin-endoperoxide synthase 1	Homo sapiens	24-29
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	Aspirin	45-52	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	220-226
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	Aspirin	45-52	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	231-237
19295242-0	2009	Aspirin-induced COX-2 overexpression in monocytes of aspirin-intolerant patients.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	16-21
19295242-0	2009	Aspirin-induced COX-2 overexpression in monocytes of aspirin-intolerant patients.	Aspirin	53-60	prostaglandin-endoperoxide synthase 2	Homo sapiens	16-21
19295242-1	2009	BACKGROUND: We hypothesize that alternate regulation of cyclooxygenase-2 (COX-2) may predispose patients to aspirin-induced exacerbations.Therefore, we want to examine the dynamics of COX-2 up-regulation in whole blood monocytes in the presence and absence of aspirin.	Aspirin	108-115	prostaglandin-endoperoxide synthase 2	Homo sapiens	56-72
19295242-1	2009	BACKGROUND: We hypothesize that alternate regulation of cyclooxygenase-2 (COX-2) may predispose patients to aspirin-induced exacerbations.Therefore, we want to examine the dynamics of COX-2 up-regulation in whole blood monocytes in the presence and absence of aspirin.	Aspirin	108-115	prostaglandin-endoperoxide synthase 2	Homo sapiens	74-79
19295242-1	2009	BACKGROUND: We hypothesize that alternate regulation of cyclooxygenase-2 (COX-2) may predispose patients to aspirin-induced exacerbations.Therefore, we want to examine the dynamics of COX-2 up-regulation in whole blood monocytes in the presence and absence of aspirin.	Aspirin	108-115	prostaglandin-endoperoxide synthase 2	Homo sapiens	184-189
19295242-1	2009	BACKGROUND: We hypothesize that alternate regulation of cyclooxygenase-2 (COX-2) may predispose patients to aspirin-induced exacerbations.Therefore, we want to examine the dynamics of COX-2 up-regulation in whole blood monocytes in the presence and absence of aspirin.	Aspirin	260-267	prostaglandin-endoperoxide synthase 2	Homo sapiens	56-72
19295242-1	2009	BACKGROUND: We hypothesize that alternate regulation of cyclooxygenase-2 (COX-2) may predispose patients to aspirin-induced exacerbations.Therefore, we want to examine the dynamics of COX-2 up-regulation in whole blood monocytes in the presence and absence of aspirin.	Aspirin	260-267	prostaglandin-endoperoxide synthase 2	Homo sapiens	74-79
19295242-4	2009	RESULTS: We found significantly higher COX-2 expression levels after stimulation with LPS and aspirin (mean 78.8, range 44.9-92.3; p = 0.0002) in comparison to LPS alone (mean 65.9%, range 33.6-82.6) in AI patients.	Aspirin	94-101	prostaglandin-endoperoxide synthase 2	Homo sapiens	39-44
19295242-8	2009	What is really new is the observation that aspirin and LPS increase COX-2 expression on blood monocytes of AI asthmatics, a finding in contrast with the lack of an effect of the same stimuli on COX-2 expression on monocytes from healthy subjects.	Aspirin	43-50	prostaglandin-endoperoxide synthase 2	Homo sapiens	68-73
19214674-9	2009	CONCLUSIONS: PPI was superior to H2-receptor antagonist for prevention of peptic ulcer, and cotreatment with AT1 receptor blocker or ACE inhibitor seemed to reduce peptic ulcer among patients taking low-dose aspirin.	Aspirin	208-215	angiotensin I converting enzyme	Homo sapiens	133-136
19129740-2	2009	To assess whether this finding related to modifications of fibrinogen clotting property by ASA, purified fibrinogen was incubated with ASA and/or salicylic acid (SA).	Aspirin	91-94	fibrinogen beta chain	Homo sapiens	59-69
19129740-2	2009	To assess whether this finding related to modifications of fibrinogen clotting property by ASA, purified fibrinogen was incubated with ASA and/or salicylic acid (SA).	Aspirin	135-138	fibrinogen beta chain	Homo sapiens	105-115
19448967-2	2009	This study aimed to examine effects of corpus atrophy and the genotypes of genes related to peptic ulcer, including IL-1beta, on risk of aspirin ulcer.	Aspirin	137-144	interleukin 1 beta	Homo sapiens	116-124
19266372-1	2009	An increasing literature mostly based on retrospective surveys has been consistently documenting a correlation between physical abuse in childhood (CPA) and substance abuse in adulthood (ASA).	Aspirin	187-190	carboxypeptidase A1	Homo sapiens	148-151
19266372-4	2009	CPA is but one of numerous stressors and factors contributing to ASA.	Aspirin	65-68	carboxypeptidase A1	Homo sapiens	0-3
18695943-1	2009	BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) may be prothrombotic, may worsen hypertension or congestive heart failure and obstruct access to the binding site of aspirin to cyclooxygenase-1 and thereby interfere with aspirin"s mechanism of action in reducing death and recurrent myocardial infarction (MI).	Aspirin	176-183	prostaglandin-endoperoxide synthase 1	Homo sapiens	187-203
18695943-1	2009	BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) may be prothrombotic, may worsen hypertension or congestive heart failure and obstruct access to the binding site of aspirin to cyclooxygenase-1 and thereby interfere with aspirin"s mechanism of action in reducing death and recurrent myocardial infarction (MI).	Aspirin	231-238	prostaglandin-endoperoxide synthase 1	Homo sapiens	187-203
19064331-8	2009	Only 53% of patients met modified New York criteria and only 23% met ASAS criteria for starting TNF antagonist therapy.	Aspirin	69-73	tumor necrosis factor	Homo sapiens	96-99
19114962-7	2009	The CYP5A1*9 mutant was significantly more prevalent among stroke patients with history of previous cerebrovascular attacks (p<0.01); and among those who failed secondary Aspirin prophylaxis even after adjusting for the common risk factors for cardiovascular disease (OR 1.49, 95% CI 1.06-2.11).	Aspirin	171-178	thromboxane A synthase 1	Homo sapiens	4-10
20069077-5	2009	There was a significant difference at Week 6 in model-adjusted CD40-ligand levels in favor of clopidogrel plus aspirin compared with placebo plus aspirin in both the intent-to-treat population (difference between least-squares means = -186.5; 95% confidence interval, -342.3 to -30.8; P = 0.02) and the per-protocol population (P = 0.05).	Aspirin	111-118	CD40 ligand	Homo sapiens	63-74
18971601-0	2009	Aspirin inhibits MMP-2 and MMP-9 expressions and activities through upregulation of PPARalpha/gamma and TIMP gene expressions in ox-LDL-stimulated macrophages derived from human monocytes.	Aspirin	0-7	TIMP metallopeptidase inhibitor 1	Homo sapiens	104-108
18971601-7	2009	Interestingly, expression of nuclear factor (NF)- kappaB was also decreased by aspirin.	Aspirin	79-86	nuclear factor kappa B subunit 1	Homo sapiens	29-56
18971601-8	2009	RT-PCR study also indicated that aspirin could upregulate the expression of tissue inhibitors of metalloproteinases (TIMP)-1 and TIMP-2.	Aspirin	33-40	TIMP metallopeptidase inhibitor 1	Homo sapiens	76-124
18971601-10	2009	These results demonstrate that aspirin could inhibit MMP-2 and MMP-9 expression through upregulation of PPARalpha/gamma expression in ox-LDL-stimulated macrophages, and could potentially inhibit MMP-2 and MMP-9 activity by induction of TIMP-1 and TIMP-2 expression.	Aspirin	31-38	TIMP metallopeptidase inhibitor 1	Homo sapiens	236-242
19114962-3	2009	In addition, we compared the CYP5A1 allelic prevalence in 71 patients with stroke recurrence despite Aspirin use, in comparison with patients who have not experienced recurrent stroke while taking Aspirin.	Aspirin	101-108	thromboxane A synthase 1	Homo sapiens	29-35
19009911-6	2008	CONCLUSIONS: CAT activity and MEL level decreased in the liver tissues of rats with BDL after administration of either melatonin alone or with ASA.	Aspirin	143-146	catalase	Rattus norvegicus	13-16
18797182-4	2008	The LTB(4)/BLT1 pathway appears to play an important role in the pathogenesis of severe persistent asthma, aspirin- and exercise-induced asthma, allergic rhinitis, and atopic dermatitis together with other mediators including cysteinyl leukotrienes, cytokines, and chemokines.	Aspirin	107-114	leukotriene B4 receptor 1	Mus musculus	11-15
19075637-5	2008	Platelet inhibition by Aspirin results from the irreversible inhibition of cyclooxygenase-1 enzyme and prevention of thromboxane A2, a potent aggregatory agent, formation.	Aspirin	23-30	prostaglandin-endoperoxide synthase 1	Homo sapiens	75-91
18482463-7	2008	Aspirin up-regulated mRNA and protein expression of COX-2 and HB-EGF, but not of TGF alpha; APE reduced aspirin-induced mRNA and protein over-expression of COX-2 and HB-EGF; aspirin significantly increased gastric MDA and this effect was counteracted by APE pre-treatment.	Aspirin	0-7	heparin-binding EGF-like growth factor	Rattus norvegicus	62-68
18482463-7	2008	Aspirin up-regulated mRNA and protein expression of COX-2 and HB-EGF, but not of TGF alpha; APE reduced aspirin-induced mRNA and protein over-expression of COX-2 and HB-EGF; aspirin significantly increased gastric MDA and this effect was counteracted by APE pre-treatment.	Aspirin	0-7	heparin-binding EGF-like growth factor	Rattus norvegicus	166-172
18482463-7	2008	Aspirin up-regulated mRNA and protein expression of COX-2 and HB-EGF, but not of TGF alpha; APE reduced aspirin-induced mRNA and protein over-expression of COX-2 and HB-EGF; aspirin significantly increased gastric MDA and this effect was counteracted by APE pre-treatment.	Aspirin	104-111	heparin-binding EGF-like growth factor	Rattus norvegicus	166-172
18784348-3	2008	Acetylsalicylic acid (ASA) can reduce this flush, presumably by decreasing prostaglandin D(2) (PGD(2)) release from macrophages.	Aspirin	0-20	prostaglandin D2 synthase	Homo sapiens	95-101
18982014-0	2008	Low-dose acetylsalicylic acid inhibits the secretion of interleukin-6 from white adipose tissue.	Aspirin	9-29	interleukin 6	Mus musculus	56-69
18982014-4	2008	DESIGN: The effect of acetylsalicylic acid (ASA), an inhibitor of COX, on IL-6 was assessed in human subjects and mice.	Aspirin	22-42	interleukin 6	Homo sapiens	74-78
18982014-4	2008	DESIGN: The effect of acetylsalicylic acid (ASA), an inhibitor of COX, on IL-6 was assessed in human subjects and mice.	Aspirin	44-47	interleukin 6	Homo sapiens	74-78
18982014-6	2008	METHODS AND RESULTS: In obese humans, low-dose ASA (150 mg day(-1) for 10 days) inhibited systemic IL-6 and reduced IL-6 release from SC WAT ex vivo (0.2 mM).	Aspirin	47-50	interleukin 6	Homo sapiens	99-103
18982014-6	2008	METHODS AND RESULTS: In obese humans, low-dose ASA (150 mg day(-1) for 10 days) inhibited systemic IL-6 and reduced IL-6 release from SC WAT ex vivo (0.2 mM).	Aspirin	47-50	interleukin 6	Homo sapiens	116-120
18982014-7	2008	Similarly, in mice, ASA (0.2 and 2.0 mg kg(-1)) suppressed SC WAT 6-keto-PGF(1alpha) (a stable metabolite of prostacyclin) and IL-6 release.	Aspirin	20-23	interleukin 6	Mus musculus	127-131
18982014-9	2008	Both ASA (5 mM) and NS-398 (COX-2 selective inhibitor &lt;or=1 microM), but not SC-560 (COX-1 selective inhibitor &lt;or=1 microM), attenuated IL-6 release from murine WAT in vitro and abolished its depot differences.	Aspirin	5-8	interleukin 6	Mus musculus	143-147
18982014-11	2008	CONCLUSIONS: In adipose tissue, constitutive COX-2-coupled prostacyclin triggers the release of basal IL-6, which in obese subjects is significantly dampened by ASA ingestion, thus offering a novel, modifiable pathway to regulate the potentially pathological component of this cytokine.	Aspirin	161-164	interleukin 6	Mus musculus	102-106
19138248-0	2008	Association between a TGFbeta1 promoter polymorphism and the phenotype of aspirin-intolerant chronic urticaria in a Korean population.	Aspirin	74-81	transforming growth factor beta 1	Homo sapiens	22-30
19138248-3	2008	OBJECTIVE: We examined the association of a TGFbeta1 genetic polymorphism with aspirin-intolerant chronic urticaria (AICU) and aspirin-tolerant chronic urticaria (ATCU) in a Korean population.	Aspirin	79-86	transforming growth factor beta 1	Homo sapiens	44-52
19002051-0	2008	Aspirin "responsiveness", "nonresponsiveness" or "resistance": a putative role for von Willebrand factor?	Aspirin	0-7	von Willebrand factor	Homo sapiens	83-104
19260592-11	2008	CONCLUSIONS: Aspirin use among diabetic patients in Tel Aviv is relatively high and similar to that in other western countries.	Aspirin	13-20	ETS variant transcription factor 6	Homo sapiens	52-55
18784348-3	2008	Acetylsalicylic acid (ASA) can reduce this flush, presumably by decreasing prostaglandin D(2) (PGD(2)) release from macrophages.	Aspirin	22-25	prostaglandin D2 synthase	Homo sapiens	95-101
18848489-6	2008	After 6 months of anti-TNF treatment, patients with NY criteria (NY+) met the updated ASAS outcome more often than NY- (70% versus 58%) (chi-square: 0.041): reduction of BASDAI of 2.86+/-2.18 (NY+) versus 2.48+/-2.39 (NY-) (NS).	Aspirin	86-90	tumor necrosis factor	Homo sapiens	23-26
18848489-8	2008	ASAS outcome was met in 45%/60%/69%/88% of patients with 0/1/2/&gt;/=3 parameters to guide physician"s opinion from SFR: raised ESR or CRP was present in 66%, active enthesitis or arthritis in 49%, coxitis in 13%, active or relapsing uveitis in 11%, inflammation of sacro-iliac or spine on MRI in 12%, and worsening of articular damage in 5%.	Aspirin	0-4	C-reactive protein	Homo sapiens	135-138
19260323-8	2008	CONCLUSION: Patients with ACI cotreated with puerarin and aspirin improved the neurological function, decreased the levels of serum vWF and sTM, indicating puerarin with aspirin had the protective effects on the damaged vascular endothelial cells.	Aspirin	170-177	von Willebrand factor	Homo sapiens	132-135
19260323-6	2008	After 14 days treatment, the level of serum vWF and NIHSS score were obviously decreased in patients treated with puerarin and aspirin, not in basic treated patients.	Aspirin	127-134	von Willebrand factor	Homo sapiens	44-47
19260323-8	2008	CONCLUSION: Patients with ACI cotreated with puerarin and aspirin improved the neurological function, decreased the levels of serum vWF and sTM, indicating puerarin with aspirin had the protective effects on the damaged vascular endothelial cells.	Aspirin	58-65	von Willebrand factor	Homo sapiens	132-135
19100419-11	2008	Compared with patients in the ASA-sensitive group, patients in the ASA-resistant group showed significantly higher total cholesterol, low-density lipoprotein cholesterol, triglyceride, C-reactive protein, and fibrinogen levels and lower GFRs (44 +/- 21 mL/min vs 63 +/- 26 mL/min, P = .03).	Aspirin	67-70	C-reactive protein	Homo sapiens	185-203
19100419-11	2008	Compared with patients in the ASA-sensitive group, patients in the ASA-resistant group showed significantly higher total cholesterol, low-density lipoprotein cholesterol, triglyceride, C-reactive protein, and fibrinogen levels and lower GFRs (44 +/- 21 mL/min vs 63 +/- 26 mL/min, P = .03).	Aspirin	67-70	fibrinogen beta chain	Homo sapiens	209-219
18625344-7	2008	In addition, the aspirin nano-emulsion further reduced the auricular levels of IL-1alpha (-37%) and TNFalpha (-69%) compared to the aspirin suspension preparation (p&lt;0.05).	Aspirin	17-24	tumor necrosis factor	Mus musculus	100-108
18789901-7	2008	Acetylcholine, bradykinin and sodium nitroprusside all caused dose-dependent vasodilatation in the presence and absence of aspirin and the "nitric oxide clamp" (P&lt; or =0.005 for all).	Aspirin	123-130	kininogen 1	Homo sapiens	15-25
19014523-8	2008	Treatment with the putative chemopreventive agent aspirin, which decreased Nuclear factor-kappaB activity, also decreased MUC2 transcription.	Aspirin	50-57	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	122-126
18727619-0	2008	Association of angiotensin I-converting enzyme gene polymorphisms with aspirin intolerance in asthmatics.	Aspirin	71-78	angiotensin I converting enzyme	Homo sapiens	15-46
18727619-10	2008	CONCLUSION: The -262 A&gt;T polymorphism in the promoter of the ACE gene is associated with AIA, and the rare allele of -262 A&gt;T may confer aspirin hypersensitivity via the down-regulation of ACE expression.	Aspirin	143-150	angiotensin I converting enzyme	Homo sapiens	64-67
18727619-10	2008	CONCLUSION: The -262 A&gt;T polymorphism in the promoter of the ACE gene is associated with AIA, and the rare allele of -262 A&gt;T may confer aspirin hypersensitivity via the down-regulation of ACE expression.	Aspirin	143-150	angiotensin I converting enzyme	Homo sapiens	195-198
18753249-2	2008	Clinical data show that mixed COX-1/COX-2 inhibitors such as aspirin, but not COX-2 selective inhibitors such as rofecoxib, induce bronchoconstriction and asthma in sensitive individuals.	Aspirin	61-68	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	36-41
18753249-8	2008	Cells cultured from aspirin-sensitive or control human donors contained similar levels of COX-1 and COX-2 immunoreactivity.	Aspirin	20-27	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	100-105
18519978-0	2008	Induction of paraoxonase 1 and apolipoprotein A-I gene expression by aspirin.	Aspirin	69-76	paraoxonase 1	Mus musculus	13-26
18678619-6	2008	SUL, IND, and ASA (5 mM) suppressed PPARdelta and 14-3-3 proteins in a manner parallel to PARP cleavage.	Aspirin	14-17	poly(ADP-ribose) polymerase 1	Homo sapiens	90-94
18838564-5	2008	Increasing age, female sex, history of peripheral artery disease, current smoking, and oral hypoglycemic or angiotensin-converting enzyme inhibitor therapy were independently associated with higher urinary concentrations of 11-dehydro thromboxane B(2), whereas aspirin dose &gt; or =150 mg/d, history of treatment with nonsteroidal antiinflammatory drugs, history of hypercholesterolemia, and statin treatment were associated with lower concentrations.	Aspirin	261-268	angiotensin I converting enzyme	Homo sapiens	108-137
18519978-4	2008	Mice treated with aspirin also showed a 2-fold increase in plasma PON1 activity and a significant induction of both PON1 and apoA-I gene expression in the liver.	Aspirin	18-25	paraoxonase 1	Mus musculus	66-70
18519978-4	2008	Mice treated with aspirin also showed a 2-fold increase in plasma PON1 activity and a significant induction of both PON1 and apoA-I gene expression in the liver.	Aspirin	18-25	paraoxonase 1	Mus musculus	116-120
18519978-6	2008	Accordingly, aspirin treatment of AhR(-/-) animals failed to induce PON1 gene expression.	Aspirin	13-20	aryl-hydrocarbon receptor	Mus musculus	34-37
18519978-7	2008	We previously suggested that aspirin might be hydrolyzed by serum PON1, which could account for its short plasma half-life of 10 min.	Aspirin	29-36	paraoxonase 1	Mus musculus	66-70
18519978-8	2008	Taken together with the current studies, we suggest that the antiatherosclerotic effects of aspirin might be mediated by its hydrolytic product salicylate and that the induction of PON1 and apoA-I might be important in the cardioprotective effects of aspirin.	Aspirin	251-258	paraoxonase 1	Mus musculus	181-185
18794027-0	2008	Renal effects of aspirin are clearly dose-dependent and are of clinical importance from a dose of 160 mg. BACKGROUND: High doses of aspirin counteract the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors.	Aspirin	17-24	angiotensin I converting enzyme	Homo sapiens	177-206
18922348-7	2008	The HLA-A*24, HLA-Cw*12, and HLA-DRB1*04 alleles were determined to be significantly higher in the NP patients with asthma and ASA triad (P &lt; 0.05).	Aspirin	127-130	major histocompatibility complex, class I, A	Homo sapiens	4-9
18922348-7	2008	The HLA-A*24, HLA-Cw*12, and HLA-DRB1*04 alleles were determined to be significantly higher in the NP patients with asthma and ASA triad (P &lt; 0.05).	Aspirin	127-130	major histocompatibility complex, class II, DR beta 1	Homo sapiens	4-7
18922348-7	2008	The HLA-A*24, HLA-Cw*12, and HLA-DRB1*04 alleles were determined to be significantly higher in the NP patients with asthma and ASA triad (P &lt; 0.05).	Aspirin	127-130	major histocompatibility complex, class II, DR beta 1	Homo sapiens	29-37
18667601-0	2008	Aspirin induces gastric epithelial barrier dysfunction by activating p38 MAPK via claudin-7.	Aspirin	0-7	mitogen-activated protein kinase 14	Homo sapiens	69-72
18667601-5	2008	Both aspirin-mediated permeability and phosphorylation of p38 MAPK were significantly attenuated by SB-203580 (a p38 MAPK inhibitor) but not by U-0126 (a MEK1 inhibitor) or SP-600125 (a JNK inhibitor).	Aspirin	5-12	mitogen-activated protein kinase 14	Homo sapiens	58-61
18667601-5	2008	Both aspirin-mediated permeability and phosphorylation of p38 MAPK were significantly attenuated by SB-203580 (a p38 MAPK inhibitor) but not by U-0126 (a MEK1 inhibitor) or SP-600125 (a JNK inhibitor).	Aspirin	5-12	mitogen-activated protein kinase 14	Homo sapiens	113-116
18667601-5	2008	Both aspirin-mediated permeability and phosphorylation of p38 MAPK were significantly attenuated by SB-203580 (a p38 MAPK inhibitor) but not by U-0126 (a MEK1 inhibitor) or SP-600125 (a JNK inhibitor).	Aspirin	5-12	mitogen-activated protein kinase 8	Homo sapiens	186-189
18544566-0	2008	NO-donating aspirin inhibits angiogenesis by suppressing VEGF expression in HT-29 human colon cancer mouse xenografts.	Aspirin	12-19	vascular endothelial growth factor A	Homo sapiens	57-61
18544566-7	2008	The expression of vascular endothelial growth factor (VEGF) was significantly reduced in response to NO-ASA, with the p- isomer being more potent than the m-.	Aspirin	104-107	vascular endothelial growth factor A	Homo sapiens	18-52
18544566-7	2008	The expression of vascular endothelial growth factor (VEGF) was significantly reduced in response to NO-ASA, with the p- isomer being more potent than the m-.	Aspirin	104-107	vascular endothelial growth factor A	Homo sapiens	54-58
18544566-8	2008	NO-ASA altered the spatial distribution of VGEF expression, with 16.7% of the vehicle-treated xenografts displaying diminished VEGF in the inner region of the area between necrosis and the outer perimeter of the tumor, compared with those treated with m- (58.3%) or p-NO-ASA (75%, P &lt; 0.01 for both versus control).	Aspirin	3-6	vascular endothelial growth factor A	Homo sapiens	127-131
18794027-0	2008	Renal effects of aspirin are clearly dose-dependent and are of clinical importance from a dose of 160 mg. BACKGROUND: High doses of aspirin counteract the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors.	Aspirin	17-24	angiotensin I converting enzyme	Homo sapiens	208-211
18794027-0	2008	Renal effects of aspirin are clearly dose-dependent and are of clinical importance from a dose of 160 mg. BACKGROUND: High doses of aspirin counteract the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors.	Aspirin	132-139	angiotensin I converting enzyme	Homo sapiens	177-206
18794027-0	2008	Renal effects of aspirin are clearly dose-dependent and are of clinical importance from a dose of 160 mg. BACKGROUND: High doses of aspirin counteract the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors.	Aspirin	132-139	angiotensin I converting enzyme	Homo sapiens	208-211
18794027-2	2008	AIM: To study renal effects of different doses of aspirin in elderly healthy volunteers who had an activated renin-angiotensin system.	Aspirin	50-57	renin	Homo sapiens	109-114
18702823-1	2008	BACKGROUND: Epidemiologic and laboratory investigations suggest that aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) have chemopreventive effects against colon cancer perhaps due at least in part to their activity against cyclooxygenase-2 (COX-2), the rate-limiting enzyme of the prostaglandin cascade.	Aspirin	69-76	prostaglandin-endoperoxide synthase 2	Homo sapiens	238-254
18702823-1	2008	BACKGROUND: Epidemiologic and laboratory investigations suggest that aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) have chemopreventive effects against colon cancer perhaps due at least in part to their activity against cyclooxygenase-2 (COX-2), the rate-limiting enzyme of the prostaglandin cascade.	Aspirin	69-76	prostaglandin-endoperoxide synthase 2	Homo sapiens	256-261
18511696-9	2008	The PEAR1 SNP explained up to 6.9% of the locus specific genetic variance in blacks and up to 2.5% of the genetic variance in whites after ASA.	Aspirin	139-142	platelet endothelial aggregation receptor 1	Homo sapiens	4-9
18660649-3	2008	All NSAIDs and aspirin inhibit active sites of cyclooxygenase-1 and cyclooxygenase-2.	Aspirin	15-22	prostaglandin-endoperoxide synthase 1	Homo sapiens	47-63
18660649-3	2008	All NSAIDs and aspirin inhibit active sites of cyclooxygenase-1 and cyclooxygenase-2.	Aspirin	15-22	prostaglandin-endoperoxide synthase 2	Homo sapiens	68-84
18034847-6	2008	RESULTS: Use of aspirin resulted in a CRP reduction of 1.23 +/- 1.02 mg/l (mean +/- s.e.m.	Aspirin	16-23	C-reactive protein	Homo sapiens	38-41
18034847-8	2008	Aspirin reduced IL-6 with 0.7 +/- 0.5 pg/ml, whereas use of placebo resulted in a mean increase of 0.2 +/- 0.8 pg/ml (P = 0.302).	Aspirin	0-7	interleukin 6	Homo sapiens	16-20
18511696-10	2008	CONCLUSIONS: PEAR1 appears to play an important role in agonist-induced platelet aggregation and in the response to ASA in both whites and blacks.	Aspirin	116-119	platelet endothelial aggregation receptor 1	Homo sapiens	13-18
18671842-16	2008	CONCLUSION: Here we show that furoxan-aspirin, B8, significantly reduces TNFalpha release from both monocytes and macrophages and suggest that inhibition of NF-kappaB activation is a likely mechanism for the effect.	Aspirin	38-45	tumor necrosis factor	Homo sapiens	73-81
18812631-8	2008	Aspirin-triggered lipoxin synthesis, via COX-2, acts to reduce the severity of damage induced by this drug.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	41-46
18671842-0	2008	A novel hybrid aspirin-NO-releasing compound inhibits TNFalpha release from LPS-activated human monocytes and macrophages.	Aspirin	15-22	tumor necrosis factor	Homo sapiens	54-62
18671842-16	2008	CONCLUSION: Here we show that furoxan-aspirin, B8, significantly reduces TNFalpha release from both monocytes and macrophages and suggest that inhibition of NF-kappaB activation is a likely mechanism for the effect.	Aspirin	38-45	nuclear factor kappa B subunit 1	Homo sapiens	157-166
18585504-0	2008	An assessment of the joint associations of aspirin and statin use with C-reactive protein concentration.	Aspirin	43-50	C-reactive protein	Homo sapiens	71-89
18636671-0	2008	Mechanisms underlying aspirin-mediated growth inhibition and apoptosis induction of cyclooxygenase-2 negative colon cancer cell line SW480.	Aspirin	22-29	prostaglandin-endoperoxide synthase 2	Homo sapiens	84-100
18636671-10	2008	After treatment with aspirin, SW480 cells displayed typically morphological features of apoptosis and necrosis under TEM, and increased the Bcl-2 expression in cells, but the expression of Bax was down regulated.	Aspirin	21-28	BCL2 apoptosis regulator	Homo sapiens	140-145
18636671-10	2008	After treatment with aspirin, SW480 cells displayed typically morphological features of apoptosis and necrosis under TEM, and increased the Bcl-2 expression in cells, but the expression of Bax was down regulated.	Aspirin	21-28	BCL2 associated X, apoptosis regulator	Homo sapiens	189-192
18480058-0	2008	The ATP-gated P2X1 receptor plays a pivotal role in activation of aspirin-treated platelets by thrombin and epinephrine.	Aspirin	66-73	coagulation factor II, thrombin	Homo sapiens	95-103
18480058-3	2008	The results show that epinephrine acted via alpha(2A)-adrenergic receptors to provoke aggregation, secretion, and Ca(2+) mobilization in aspirin-treated platelets pre-stimulated with subthreshold concentrations of thrombin.	Aspirin	137-144	coagulation factor II, thrombin	Homo sapiens	214-222
18480058-10	2008	Thus, in aspirin-treated platelets, PAR4, but not PAR1, interacts synergistically with alpha(2A)-adrenergic receptors, and the PI3-kinase/Akt pathway is involved in this cross-talk.	Aspirin	9-16	AKT serine/threonine kinase 1	Homo sapiens	138-141
18585504-1	2008	BACKGROUND: The use of aspirin alone and statins alone has been shown to reduce markers of inflammation, including C-reactive protein (CRP); however, their combination has been poorly studied.	Aspirin	23-30	C-reactive protein	Homo sapiens	115-133
18585504-1	2008	BACKGROUND: The use of aspirin alone and statins alone has been shown to reduce markers of inflammation, including C-reactive protein (CRP); however, their combination has been poorly studied.	Aspirin	23-30	C-reactive protein	Homo sapiens	135-138
18585504-2	2008	METHODS: In a cross-sectional analysis of black and white adults &gt; or =45 years old from the REGARDS cohort, the associations of aspirin and statin use with CRP were examined.	Aspirin	132-139	C-reactive protein	Homo sapiens	160-163
18585504-5	2008	RESULTS: Estimated mean CRP was 2.78 mg/L for subjects taking neither drug, 2.73 mg/L with aspirin only, 2.29 mg/L with statins only, and 2.03 mg/L for subjects taking both agents.	Aspirin	91-98	C-reactive protein	Homo sapiens	24-27
18585504-8	2008	In addition, among statin users, the use of aspirin for &gt;5 years compared with &lt; or =5 years was associated with apparent significantly lower CRP concentrations (P = .01).	Aspirin	44-51	C-reactive protein	Homo sapiens	148-151
18585504-9	2008	CONCLUSIONS: The combined use of aspirin and statins was associated with a synergistically lower CRP concentration, especially among participants taking aspirin for &gt;5 years.	Aspirin	33-40	C-reactive protein	Homo sapiens	97-100
18585504-9	2008	CONCLUSIONS: The combined use of aspirin and statins was associated with a synergistically lower CRP concentration, especially among participants taking aspirin for &gt;5 years.	Aspirin	153-160	C-reactive protein	Homo sapiens	97-100
18785396-8	2008	HIV-positive patients with CD4 counts &gt;200 cells/microl were more likely to be ASA 1 or 2 (OR 3.88).	Aspirin	82-85	CD4 molecule	Homo sapiens	27-30
18673140-3	2008	Aspirin and salicylic acid (SA) are allosteric inhibitors of ET-1 binding to ET(A) receptors.	Aspirin	0-7	endothelin 1	Rattus norvegicus	61-65
18462455-0	2008	Involvement of 15-lipoxygenase and prostaglandin EP receptors in aspirin-triggered 15-hydroxyeicosatetraenoic acid generation in aspirin-sensitive asthmatics.	Aspirin	65-72	arachidonate 15-lipoxygenase	Homo sapiens	15-30
18462455-0	2008	Involvement of 15-lipoxygenase and prostaglandin EP receptors in aspirin-triggered 15-hydroxyeicosatetraenoic acid generation in aspirin-sensitive asthmatics.	Aspirin	129-136	arachidonate 15-lipoxygenase	Homo sapiens	15-30
18575740-7	2008	To gain insight into the mechanism underlying the synergistic action of HDIs and aspirin, we employed the deacetylated metabolite of aspirin, salicylic acid, and the cyclooxygenase-1- and -2-selective inhibitors, SC-560 and NS-398, respectively.	Aspirin	81-88	prostaglandin-endoperoxide synthase 1	Homo sapiens	166-190
18785396-9	2008	Of HIV-positive patients with CD4 counts &lt;200 cells/microl, significantly more were classified as ASA 1 or 2 than ASA 3 or 4 (p &lt; 0.0001).	Aspirin	101-104	CD4 molecule	Homo sapiens	30-33
18281372-8	2008	The in vitro study demonstrated that TNFalpha significantly increased CD40L expression, an effect weakly influenced by aspirin but significantly reduced by AACOCF3, an inhibitor of PLA(2), apocynin, an inhibitor of NADPH oxidase, or staurosporine, an inhibitor of PKC.	Aspirin	119-126	tumor necrosis factor	Homo sapiens	37-45
18612540-0	2008	The C50T polymorphism of the cyclooxygenase-1 gene and the risk of thrombotic events during low-dose therapy with acetyl salicylic acid.	Aspirin	114-135	prostaglandin-endoperoxide synthase 1	Homo sapiens	29-45
18612540-1	2008	Aspirin prevents thrombotic events by inhibiting platelet cyclooxygenase-1 (COX-1), thus reducing thromboxane A2 formation and platelet aggregation.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	58-74
18612540-1	2008	Aspirin prevents thrombotic events by inhibiting platelet cyclooxygenase-1 (COX-1), thus reducing thromboxane A2 formation and platelet aggregation.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	76-81
18612540-2	2008	The C50T polymorphism of COX-1 is associated with an impaired inhibition of both thromboxane production and in-vitro platelet aggregation by aspirin.	Aspirin	141-148	prostaglandin-endoperoxide synthase 1	Homo sapiens	25-30
18612540-11	2008	In prior laboratory studies the COX-1 C50T polymorphism was associated with an impaired inhibitory effect of aspirin on thromboxane production and platelet function.	Aspirin	109-116	prostaglandin-endoperoxide synthase 1	Homo sapiens	32-37
18281372-8	2008	The in vitro study demonstrated that TNFalpha significantly increased CD40L expression, an effect weakly influenced by aspirin but significantly reduced by AACOCF3, an inhibitor of PLA(2), apocynin, an inhibitor of NADPH oxidase, or staurosporine, an inhibitor of PKC.	Aspirin	119-126	CD40 ligand	Homo sapiens	70-75
18483385-0	2008	Aspirin sensitizes cancer cells to TRAIL-induced apoptosis by reducing survivin levels.	Aspirin	0-7	TNF superfamily member 10	Homo sapiens	35-40
18319729-7	2008	The stroke aspirin-resistant group had higher levels of IL-6 than the stroke aspirin-sensitive group (2.4+/-1 versus 1.8+/-0.9 ng/mL, P=0.037).	Aspirin	11-18	interleukin 6	Homo sapiens	56-60
18319729-9	2008	These analyses showed that IL-6 was independently associated with stroke severity as the outcome (B=3.738, P=0.036), and aspirin resistance was independently associated with IL-6 (B=0.765, P=0.005) as the outcome.	Aspirin	121-128	interleukin 6	Homo sapiens	174-178
18335236-3	2008	It is known that ASA serves as an apoptotic agent on cancer cells through the inhibition of the COX-2 enzyme.	Aspirin	17-20	cytochrome c oxidase subunit 2	Arabidopsis thaliana	96-101
18483373-7	2008	In univariate analysis, aspirin use attenuated the tamoxifen-associated increase in VEGF in the platelet releasate and decreased serum levels of VEGF (P = 0.03).	Aspirin	24-31	vascular endothelial growth factor A	Homo sapiens	84-88
18483373-7	2008	In univariate analysis, aspirin use attenuated the tamoxifen-associated increase in VEGF in the platelet releasate and decreased serum levels of VEGF (P = 0.03).	Aspirin	24-31	vascular endothelial growth factor A	Homo sapiens	145-149
18483385-10	2008	CONCLUSIONS: Aspirin sensitizes transformed breast epithelial cells to TRAIL-based therapies in vitro and in vivo by a novel mechanism involving survivin depletion.	Aspirin	13-20	TNF superfamily member 10	Homo sapiens	71-76
18483385-2	2008	We examined whether the nonsteroidal anti-inflammatory drug aspirin sensitized cancer cells to TRAIL agonists in vitro and in vivo and investigated the underlying mechanism.	Aspirin	60-67	TNF superfamily member 10	Homo sapiens	95-100
18483385-3	2008	EXPERIMENTAL DESIGN: The effects of aspirin on sensitivity to TRAIL agonists and expression of apoptosis regulators was determined in human breast cancer cell lines and xenograft tumors.	Aspirin	36-43	TNF superfamily member 10	Homo sapiens	62-67
18483385-4	2008	The specific role of survivin depletion in the TRAIL-sensitizing effects of aspirin was determined by silencing survivin.	Aspirin	76-83	TNF superfamily member 10	Homo sapiens	47-52
18483385-5	2008	RESULTS: Aspirin sensitized human breast cancer cells, but not untransformed human mammary epithelial cells, to TRAIL-induced caspase activation and apoptosis by a cyclooxygenase-2-independent mechanism.	Aspirin	9-16	TNF superfamily member 10	Homo sapiens	112-117
18483385-5	2008	RESULTS: Aspirin sensitized human breast cancer cells, but not untransformed human mammary epithelial cells, to TRAIL-induced caspase activation and apoptosis by a cyclooxygenase-2-independent mechanism.	Aspirin	9-16	prostaglandin-endoperoxide synthase 2	Homo sapiens	164-180
18483385-6	2008	Aspirin also sensitized breast cancer cells to apoptosis induced by a human agonistic TRAIL receptor-2 monoclonal antibody (lexatumumab).	Aspirin	0-7	TNF superfamily member 10	Homo sapiens	86-91
18483385-8	2008	Silencing survivin with small interfering RNAs sensitized breast cancer cells to TRAIL-induced apoptosis, underscoring the functional role of survivin depletion in the TRAIL-sensitizing actions of aspirin.	Aspirin	197-204	TNF superfamily member 10	Homo sapiens	81-86
18483385-8	2008	Silencing survivin with small interfering RNAs sensitized breast cancer cells to TRAIL-induced apoptosis, underscoring the functional role of survivin depletion in the TRAIL-sensitizing actions of aspirin.	Aspirin	197-204	TNF superfamily member 10	Homo sapiens	168-173
18411340-5	2008	In this study, we show that LX and aspirin (ASA)-triggered LX (ATL) inhibit innate immune signaling by inducing suppressor of cytokine signaling (SOCS) 2-dependent ubiquitinylation and proteasome-mediated degradation of TNF receptor-associated factor (TRAF) 2 and TRAF6, which are adaptor molecules that couple TNF and interleukin-1 receptor/Toll-like receptor family members to intracellular signaling events.	Aspirin	35-42	tumor necrosis factor	Homo sapiens	220-223
18411340-5	2008	In this study, we show that LX and aspirin (ASA)-triggered LX (ATL) inhibit innate immune signaling by inducing suppressor of cytokine signaling (SOCS) 2-dependent ubiquitinylation and proteasome-mediated degradation of TNF receptor-associated factor (TRAF) 2 and TRAF6, which are adaptor molecules that couple TNF and interleukin-1 receptor/Toll-like receptor family members to intracellular signaling events.	Aspirin	44-47	tumor necrosis factor	Homo sapiens	220-223
18393288-0	2008	Acetylsalicylic acid inhibits hepatitis C virus RNA and protein expression through cyclooxygenase 2 signaling pathways.	Aspirin	0-20	prostaglandin-endoperoxide synthase 2	Homo sapiens	83-99
18355801-0	2008	Aspirin inhibits human bradykinin B2 receptor ligand binding function.	Aspirin	0-7	kininogen 1	Homo sapiens	23-33
18355801-2	2008	The effect of aspirin on bradykinin binding to cell-surface receptor and on signal transduction were studied in CHO-K1 cells, stably expressing the human B2 receptor.	Aspirin	14-21	kininogen 1	Homo sapiens	25-35
18355801-5	2008	Aspirin reduces the apparent affinity of the receptor for [3H]-bradykinin by accelerating the dissociation rate of [3H]-bradykinin-receptor complexes.	Aspirin	0-7	kininogen 1	Homo sapiens	63-73
18355801-5	2008	Aspirin reduces the apparent affinity of the receptor for [3H]-bradykinin by accelerating the dissociation rate of [3H]-bradykinin-receptor complexes.	Aspirin	0-7	kininogen 1	Homo sapiens	120-130
18355801-6	2008	In addition, aspirin reduces the capacity of unlabeled bradykinin or the B2 receptor antagonist icatibant to destabilize pre-formed [3H]-bradykinin-receptor complexes.	Aspirin	13-20	kininogen 1	Homo sapiens	55-65
18355801-6	2008	In addition, aspirin reduces the capacity of unlabeled bradykinin or the B2 receptor antagonist icatibant to destabilize pre-formed [3H]-bradykinin-receptor complexes.	Aspirin	13-20	kininogen 1	Homo sapiens	137-147
18435972-7	2008	After the 2 aspirin doses, men and women had near complete suppression of platelet aggregation to arachidonic acid in whole blood and in platelet-rich plasma (PRP), the direct cyclo-oxygenase-1 pathway affected by aspirin.	Aspirin	12-19	prostaglandin-endoperoxide synthase 1	Homo sapiens	176-193
18435972-7	2008	After the 2 aspirin doses, men and women had near complete suppression of platelet aggregation to arachidonic acid in whole blood and in platelet-rich plasma (PRP), the direct cyclo-oxygenase-1 pathway affected by aspirin.	Aspirin	214-221	prostaglandin-endoperoxide synthase 1	Homo sapiens	176-193
18393288-7	2008	However, we found that HCV-induced cyclooxygenase 2 (COX-2) messenger RNA and protein levels and activity and these effects were down-regulated by ASA, possibly by a nuclear factor kappa B-independent mechanism.	Aspirin	147-150	prostaglandin-endoperoxide synthase 2	Homo sapiens	35-51
18393288-7	2008	However, we found that HCV-induced cyclooxygenase 2 (COX-2) messenger RNA and protein levels and activity and these effects were down-regulated by ASA, possibly by a nuclear factor kappa B-independent mechanism.	Aspirin	147-150	prostaglandin-endoperoxide synthase 2	Homo sapiens	53-58
18393288-8	2008	We also observed that the ASA-dependent inhibition of viral replication was due in part to inhibition of COX-2 and activation of p38 and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 (MEK1/2) mitogen-activated protein kinases (MAPKs).	Aspirin	26-29	prostaglandin-endoperoxide synthase 2	Homo sapiens	105-110
18393288-8	2008	We also observed that the ASA-dependent inhibition of viral replication was due in part to inhibition of COX-2 and activation of p38 and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 (MEK1/2) mitogen-activated protein kinases (MAPKs).	Aspirin	26-29	mitogen-activated protein kinase 14	Homo sapiens	129-132
18393288-9	2008	Inhibition of these kinases by SB203580 and U0126, respectively, and by short interfering RNA silencing of p38 and MEK1 MAPK prevented the antiviral effect of ASA.	Aspirin	159-162	mitogen-activated protein kinase 14	Homo sapiens	107-110
18393288-10	2008	Taken together, our findings suggest that the anti-HCV effect of ASA in the Huh7 replicon cells is due to its inhibitory effect on COX-2 expression, which is mediated in part by the activation of MEK1/2/p38 MAPK.	Aspirin	65-68	prostaglandin-endoperoxide synthase 2	Homo sapiens	131-136
18393288-10	2008	Taken together, our findings suggest that the anti-HCV effect of ASA in the Huh7 replicon cells is due to its inhibitory effect on COX-2 expression, which is mediated in part by the activation of MEK1/2/p38 MAPK.	Aspirin	65-68	mitogen-activated protein kinase 14	Homo sapiens	203-206
18221358-1	2008	BACKGROUND: Permanent inactivation of cyclooxygenase-1 and inhibition of platelet thromboxane A(2) (TxA(2)) constitute the main mechanisms underlying the prevention of vascular disease by aspirin.	Aspirin	188-195	prostaglandin-endoperoxide synthase 1	Homo sapiens	38-54
18414055-3	2008	We found that combination treatment with 1,25D and non-specific COX inhibitors acetyl salicylic acid (ASA) or indomethacin can robustly potentiate differentiation of other types of human leukemia cells, i.e., U937, THP-1, and that ASA +/- 1,25D is effective in primary AML cultures.	Aspirin	79-100	GLI family zinc finger 2	Homo sapiens	215-220
18414055-3	2008	We found that combination treatment with 1,25D and non-specific COX inhibitors acetyl salicylic acid (ASA) or indomethacin can robustly potentiate differentiation of other types of human leukemia cells, i.e., U937, THP-1, and that ASA +/- 1,25D is effective in primary AML cultures.	Aspirin	102-105	GLI family zinc finger 2	Homo sapiens	215-220
18187132-1	2008	To assess the effects of acetylsalicylic acid (ASA) on glutamate and interleukin-6 (IL-6) release in the striatum of rats suffering from cerebral ischemia, we used the microdialysis technique with probes implanted 2 h prior to stroke onset.	Aspirin	47-50	interleukin 6	Rattus norvegicus	69-82
18187132-1	2008	To assess the effects of acetylsalicylic acid (ASA) on glutamate and interleukin-6 (IL-6) release in the striatum of rats suffering from cerebral ischemia, we used the microdialysis technique with probes implanted 2 h prior to stroke onset.	Aspirin	47-50	interleukin 6	Rattus norvegicus	84-88
18187132-7	2008	Pooled post-ischemic microdialysate concentrations of IL-6 in temporary MCAO were significantly higher after ASA treatment (215+/-81 pg/mL, p=0.0297) than in saline-treated rats (80+/-13 pg/mL).	Aspirin	109-112	interleukin 6	Rattus norvegicus	54-58
18187132-10	2008	These results suggest that the neuroprotective effect of ASA is reflected by glutamate attenuation and IL-6 induction even if given after stroke onset, but only if reperfusion is achieved.	Aspirin	57-60	interleukin 6	Rattus norvegicus	103-107
18373616-3	2008	Aspirin, non-steroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase 2 (Cox-2) inhibitors have been shown to decrease the incidence of colorectal cancer.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	78-83
18059344-2	2008	Modulation of the NF-kappaB pathway has been implicated as a key effector of the antitumour effect of aspirin, but the effects of non-aspirin NSAIDs on this pathway have yet to be fully defined.	Aspirin	102-109	nuclear factor kappa B subunit 1	Homo sapiens	18-27
18180914-11	2008	The OR (odds ratio) for ASA was 0.73 [95% confidence interval (CI) 0.63-0.85], for beta-blockers, 0.72 (0.63-0.83), for lipid-lowering drugs, 0.75 (0.65-0.86) and for ACE inhibitors, 0.76 (0.67-0.86).	Aspirin	24-27	angiotensin I converting enzyme	Homo sapiens	167-170
18058818-1	2008	Our previous study showed that aspirin induced apoptosis of esophageal cancer cells in vitro by inhibiting the pathway of NF-kappaB downstream regulation of cyclooxygenase-2.	Aspirin	31-38	prostaglandin-endoperoxide synthase 2	Homo sapiens	157-173
18356686-8	2008	The combination of aspirin with propranolol, single aspirin, and single propranolol all attenuated the acute response in plasma VWF:Ag levels to psychosocial stress.	Aspirin	19-26	von Willebrand factor	Homo sapiens	128-131
18280093-11	2008	Multivariate analysis showed being ASA IIIA or IIIB is an independent predictor of survival, after adjusting for age, coronary artery disease, hyperlipidemia, COPD, and preoperative albumin levels.	Aspirin	35-38	albumin	Homo sapiens	182-189
18308578-9	2008	Both aspirin and enoxaparin normalized brain concentrations of PGE and TNF-alpha and elevated thrombin inhibitors, the latter effect being more pronounced for enoxaparin.	Aspirin	5-12	tumor necrosis factor	Mus musculus	71-80
18308578-9	2008	Both aspirin and enoxaparin normalized brain concentrations of PGE and TNF-alpha and elevated thrombin inhibitors, the latter effect being more pronounced for enoxaparin.	Aspirin	5-12	coagulation factor II	Mus musculus	94-102
18308505-13	2008	Adjusting for diabetes, hyperlipidemia, hypertension, coronary artery disease, aspirin or other anti-inflammatory uses, and statin therapy, 4(th) quartile CRP was independently associated with disease progression (OR 1.8, 95% CI; 1.03-2.99, P &lt; .05).	Aspirin	79-86	C-reactive protein	Homo sapiens	155-158
18193074-0	2008	ATL-1, an analogue of aspirin-triggered lipoxin A4, is a potent inhibitor of several steps in angiogenesis induced by vascular endothelial growth factor.	Aspirin	22-29	atlastin GTPase 1	Homo sapiens	0-5
18193074-0	2008	ATL-1, an analogue of aspirin-triggered lipoxin A4, is a potent inhibitor of several steps in angiogenesis induced by vascular endothelial growth factor.	Aspirin	22-29	vascular endothelial growth factor A	Homo sapiens	118-152
18193074-2	2008	We have demonstrated that ATL-1, a synthetic analogue of aspirin-triggered lipoxin A(4), inhibits VEGF-induced endothelial cell (EC) migration.	Aspirin	57-64	atlastin GTPase 1	Homo sapiens	26-31
18193074-2	2008	We have demonstrated that ATL-1, a synthetic analogue of aspirin-triggered lipoxin A(4), inhibits VEGF-induced endothelial cell (EC) migration.	Aspirin	57-64	vascular endothelial growth factor A	Homo sapiens	98-102
18356686-8	2008	The combination of aspirin with propranolol, single aspirin, and single propranolol all attenuated the acute response in plasma VWF:Ag levels to psychosocial stress.	Aspirin	52-59	von Willebrand factor	Homo sapiens	128-131
17644113-3	2008	The aim of this study was to investigate the effect of DC and ASA on NF-kappaB signaling, and determine its role in programmed cell death in a human gastric carcinoma cell line.	Aspirin	62-65	nuclear factor kappa B subunit 1	Homo sapiens	69-78
17644113-8	2008	Although, ASA itself had no effect on the NF-kappaB pathway, nor did it reduce DC-induced NF-kappaB translocation, it did prevent DC-induced caspase-3, -6 and -9 activation, poly (ADP-ribose) polymerase and lamin A processing, DNA degradation, and PKC signaling, all indices of apoptosis.	Aspirin	10-13	poly(ADP-ribose) polymerase 1	Homo sapiens	141-202
18302581-3	2008	This study hypothesizes that thrombin production during OPCAB stimulates this acquired ASA-R.	Aspirin	87-90	coagulation factor II, thrombin	Homo sapiens	29-37
18256393-1	2008	BACKGROUND: Intensified multifactorial intervention - with tight glucose regulation and the use of renin-angiotensin system blockers, aspirin, and lipid-lowering agents - has been shown to reduce the risk of nonfatal cardiovascular disease among patients with type 2 diabetes mellitus and microalbuminuria.	Aspirin	134-141	renin	Homo sapiens	99-104
18038215-1	2008	Aspirin exerts anti-thrombotic action by acetylating and inactivating cyclooxygenase-1, preventing the production of thromboxane A2 in platelets.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	70-86
18215612-11	2008	CONCLUSIONS: For patients with MI complicated by AF, the combination of aspirin and an oral direct thrombin inhibitor seems beneficial.	Aspirin	72-79	coagulation factor II, thrombin	Homo sapiens	99-107
17881186-0	2008	Aspirin, but not propranolol, attenuates the acute stress-induced increase in circulating levels of interleukin-6: a randomized, double-blind, placebo-controlled study.	Aspirin	0-7	interleukin 6	Homo sapiens	100-113
17881186-2	2008	We investigated the effect of aspirin and propranolol on the responsiveness of plasma IL-6 levels to acute psychosocial stress.	Aspirin	30-37	interleukin 6	Homo sapiens	86-90
17881186-6	2008	The change in IL-6 from pre-stress to 105 min post-stress differed between subjects with aspirin medication and those without (p =0.033; eta p2=0.059).	Aspirin	89-96	interleukin 6	Homo sapiens	14-18
17881186-7	2008	IL-6 levels increased less from pre-stress to 105 min post-stress (p &lt;0.027) and were lower (p =0.010) at 105 min post-stress in subjects with aspirin than in subjects without aspirin.	Aspirin	146-153	interleukin 6	Homo sapiens	0-4
17881186-7	2008	IL-6 levels increased less from pre-stress to 105 min post-stress (p &lt;0.027) and were lower (p =0.010) at 105 min post-stress in subjects with aspirin than in subjects without aspirin.	Aspirin	179-186	interleukin 6	Homo sapiens	0-4
17881186-11	2008	Aspirin but not propranolol attenuated the stress-induced increase in plasma IL-6 levels.	Aspirin	0-7	interleukin 6	Homo sapiens	77-81
18053020-1	2008	BACKGROUND AND AIMS: Aspirin, a cyclo-oxygenase (COX)-1 and COX-2 inhibitor, is the antiplatelet drug of choice to prevent serious vascular events.	Aspirin	21-28	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	60-65
18001701-5	2008	The effects of a 6-month treatment with aspirin 100 mg/day on VEGF levels of 20 hypertensive patients were also studied.	Aspirin	40-47	vascular endothelial growth factor A	Homo sapiens	62-66
18001701-8	2008	Aspirin treated hypertensives showed a significant reduction of sP-selectin (-26%, p&lt;0.01) and VEGF (-33%, p&lt;0.01) levels.	Aspirin	0-7	vascular endothelial growth factor A	Homo sapiens	98-102
18001701-10	2008	CONCLUSIONS: In vivo activation of platelets in hypertensive patients is responsible for enhanced circulating VEGF levels, which are significantly lowered by aspirin treatment.	Aspirin	158-165	vascular endothelial growth factor A	Homo sapiens	110-114
18092833-4	2008	In this review, the effects of several drugs such as AZT (anti-AIDS), cis-Pt (antitumor), aspirin (anti-inflammatory), and vitamin C (antioxidant) on the stability and conformation of RNase A in vitro are compared.	Aspirin	90-97	ribonuclease pancreatic	Bos taurus	184-191
18203887-8	2008	Cotreatment in HT-29 and 22Rv1 cells with EPA and acetyl salicylic acid, an inhibitor of cyclooxygenase activity, activated the PPRE reporter at levels similar to EPA alone, suggesting that EPA itself is a ligand of PPARgamma.	Aspirin	50-71	peroxisome proliferator activated receptor gamma	Homo sapiens	216-225
18174252-0	2008	NO-donating aspirin inhibits the activation of NF-kappaB in human cancer cell lines and Min mice.	Aspirin	12-19	nuclear factor kappa B subunit 1	Homo sapiens	47-56
18174252-6	2008	The effect of NO-ASA on NF-kappaB binding to DNA was significantly correlated with its effect on cell growth (P &lt; 0.05) indicating that the growth inhibitory effect of NO-ASA may be mediated by its effect on NF-kappaB.	Aspirin	17-20	nuclear factor kappa B subunit 1	Homo sapiens	24-33
18174252-6	2008	The effect of NO-ASA on NF-kappaB binding to DNA was significantly correlated with its effect on cell growth (P &lt; 0.05) indicating that the growth inhibitory effect of NO-ASA may be mediated by its effect on NF-kappaB.	Aspirin	17-20	nuclear factor kappa B subunit 1	Homo sapiens	211-220
18174252-6	2008	The effect of NO-ASA on NF-kappaB binding to DNA was significantly correlated with its effect on cell growth (P &lt; 0.05) indicating that the growth inhibitory effect of NO-ASA may be mediated by its effect on NF-kappaB.	Aspirin	174-177	nuclear factor kappa B subunit 1	Homo sapiens	24-33
18174252-6	2008	The effect of NO-ASA on NF-kappaB binding to DNA was significantly correlated with its effect on cell growth (P &lt; 0.05) indicating that the growth inhibitory effect of NO-ASA may be mediated by its effect on NF-kappaB.	Aspirin	174-177	nuclear factor kappa B subunit 1	Homo sapiens	211-220
18174252-7	2008	Compared with control, NO-ASA decreased NF-kappaB activation in intestinal epithelial cells of APC(min+/-) mice by 38.4% (P &lt; 0.01).	Aspirin	26-29	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	40-49
19126992-0	2008	Relation of platelet aggregation and fibrinogen levels to advancing age in aspirin- and thienopyridine-treated patients.	Aspirin	75-82	fibrinogen beta chain	Homo sapiens	37-47
18239256-10	2008	RESULTS: Patients with effective ASA inhibition had significantly lower plasma fibrinogen level (p&lt;0.05) and red blood cell aggregation values both in the heterogenous and the selected populations (p&lt;0.01).	Aspirin	33-36	fibrinogen beta chain	Homo sapiens	79-89
18239256-14	2008	Thus, increased plasma fibrinogen level may play an important role in the in vitro and in vivo platelet resistance to ASA.	Aspirin	118-121	fibrinogen beta chain	Homo sapiens	23-33
18196976-0	2008	NCX-4016, a nitro-derivative of aspirin, inhibits EGFR and STAT3 signaling and modulates Bcl-2 proteins in cisplatin-resistant human ovarian cancer cells and xenografts.	Aspirin	32-39	epidermal growth factor receptor	Homo sapiens	50-54
18196976-0	2008	NCX-4016, a nitro-derivative of aspirin, inhibits EGFR and STAT3 signaling and modulates Bcl-2 proteins in cisplatin-resistant human ovarian cancer cells and xenografts.	Aspirin	32-39	signal transducer and activator of transcription 3	Homo sapiens	59-64
17495879-7	2008	However, aspirin utilization appeared to modify the relationship between the PTGS2 G-765C polymorphism and CHD risk (interaction P=0.072).	Aspirin	9-16	prostaglandin-endoperoxide synthase 2	Homo sapiens	77-82
19126992-7	2008	In aspirin-treated patients also fibrinogen levels increased with aging (p&lt;0.001).	Aspirin	3-10	fibrinogen beta chain	Homo sapiens	33-43
18209566-5	2008	The results showed that aspirin significantly suppressed COX-2 and ICAM-1 expression induced by ox-LDL and also inhibited IkappaB phosphorylation in human umbilical vein endothelial cells (HUVECs).	Aspirin	24-31	prostaglandin-endoperoxide synthase 2	Homo sapiens	57-62
18197933-6	2008	Both aspirin (5-20 mmol/L) and Nimesulide (0.1-0.8 mmol/L) inhibited EC-9706 cell line proliferation and suppressed its COX-2 mRNA expression dose-dependently.	Aspirin	5-12	prostaglandin-endoperoxide synthase 2	Homo sapiens	120-125
18197933-7	2008	However, only aspirin (5-20 mmol/L) could inhibit proliferation in the EC-109 cell line and suppress COX-2 mRNA expression.	Aspirin	14-21	prostaglandin-endoperoxide synthase 2	Homo sapiens	101-106
18343248-0	2008	A case-control study of the association between polymorphisms of the endothelial nitric oxide synthase and glycoprotein IIIa genes and upper gastrointestinal bleeding in users of low-dose aspirin.	Aspirin	188-195	nitric oxide synthase 3	Homo sapiens	69-102
18343248-10	2008	CONCLUSION: In this small, selected population of individuals taking low-dose aspirin for secondary prevention, carriage of the "a" allele of the eNOS gene was associated with a decreased risk for upper GI bleeding.	Aspirin	78-85	nitric oxide synthase 3	Homo sapiens	146-150
18090373-9	2008	The COX-1 and COX-2 inhibitor aspirin (10(-6)-10(-5) mol/L) and the COX-2 inhibitor nimesulide (10(-6) mol/L) induced leftward shifts of the concentration-response curve for vasopressin in gastroepiploic artery.	Aspirin	30-37	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	14-19
18090373-9	2008	The COX-1 and COX-2 inhibitor aspirin (10(-6)-10(-5) mol/L) and the COX-2 inhibitor nimesulide (10(-6) mol/L) induced leftward shifts of the concentration-response curve for vasopressin in gastroepiploic artery.	Aspirin	30-37	arginine vasopressin	Homo sapiens	174-185
18090373-12	2008	CONCLUSION: The results provide functional evidence that aspirin at high concentrations and the COX-2 selective inhibitor nimesulide potentiate the contractile response of gastroepiploic artery to vasopressin, thus suggesting the release of relaxant prostaglandins by the peptide.	Aspirin	57-64	arginine vasopressin	Homo sapiens	197-208
18090373-14	2008	The amplifying effect of aspirin on vasopressin-induced contraction may contribute to early graft failure when the gastroepiploic artery is used as a coronary artery bypass graft.	Aspirin	25-32	arginine vasopressin	Homo sapiens	36-47
19055028-1	2008	Aspirin (acetylsalicylic acid, ASA) treatment resulted in a significant decrease in the amount of the sulfur-rich Gomori-positive material present in the cytoplasm of periventricular glia.	Aspirin	0-7	anti-sarcolemmal autoantibodies	Mus musculus	31-34
18209566-6	2008	Moreover, aspirin reduced the level of p38 MAPK phosphorylation.	Aspirin	10-17	mitogen-activated protein kinase 14	Homo sapiens	39-42
18209566-7	2008	Our findings suggest that aspirin can decrease inflammatory responses induced by ox-LDL, and the mechanism might be associated with NF-kappaB activation pathway and inhibition of p38 MAPK phosphorylation.	Aspirin	26-33	mitogen-activated protein kinase 14	Homo sapiens	179-182
17584993-15	2008	Thus, PGE2 is released during the clinical reactions to aspirin through an alternative COX-2 pathway.	Aspirin	56-63	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	87-92
17944992-1	2008	BACKGROUND: Anti-inflammatory analgesics, including ibuprofen and naproxen, are known to interfere with the antiplatelet effect of aspirin, presumably as a result of a drug-drug interaction at the level of platelet cyclooxygenase-1 (COX-1).	Aspirin	131-138	prostaglandin-endoperoxide synthase 1	Homo sapiens	215-231
17944992-1	2008	BACKGROUND: Anti-inflammatory analgesics, including ibuprofen and naproxen, are known to interfere with the antiplatelet effect of aspirin, presumably as a result of a drug-drug interaction at the level of platelet cyclooxygenase-1 (COX-1).	Aspirin	131-138	prostaglandin-endoperoxide synthase 1	Homo sapiens	233-238
17944992-8	2008	Moreover, MAA attenuated the effect of aspirin on COX activity of platelet microsomes, suggesting a competition with aspirin at the COX-1 enzyme.	Aspirin	117-124	prostaglandin-endoperoxide synthase 1	Homo sapiens	132-137
17944992-9	2008	This was confirmed by docking studies, which revealed that MAA forms a strong hydrogen bond with serine 530 within the COX-1, thereby preventing enzyme acetylation by aspirin.	Aspirin	167-174	prostaglandin-endoperoxide synthase 1	Homo sapiens	119-124
19266085-10	2008	Therefore, we conclude that aspirin-induced calpain mediates an antitumor effect via caspase-3 in cervical cancer cells.	Aspirin	28-35	caspase 3	Homo sapiens	85-94
18528523-3	2008	In particular, a study of the chemopreventive effect of two isomers of NO-aspirin on intestinal neoplasia in Min mice showed that, compared to wild-type controls, PPARdelta is overexpressed in the intestinal mucosa of Min mice; PPARdelta responds to m- and p-NO-ASA proportionally to their antitumor effect (p- &gt; m-).	Aspirin	74-81	peroxisome proliferator activator receptor delta	Mus musculus	163-172
18528523-3	2008	In particular, a study of the chemopreventive effect of two isomers of NO-aspirin on intestinal neoplasia in Min mice showed that, compared to wild-type controls, PPARdelta is overexpressed in the intestinal mucosa of Min mice; PPARdelta responds to m- and p-NO-ASA proportionally to their antitumor effect (p- &gt; m-).	Aspirin	262-265	peroxisome proliferator activator receptor delta	Mus musculus	163-172
18528523-4	2008	This effect is accompanied by the induction of epithelial cell death, which correlates with the antineoplastic effect of NO-aspirin; and NO-aspirin"s effect on PPARdelta is specific (no changes in PPARalpha or PPARgamma).	Aspirin	140-147	peroxisome proliferator activator receptor delta	Mus musculus	160-169
17934975-1	2008	OBJECTIVE: To assess the prevalence of a lacking aspirin effect on cyclooxygenase-1 (COX-1) ("aspirin resistance") in patients with symptomatic, stable coronary heart disease (CHD) using test methods directly reflecting inhibition of COX-1.	Aspirin	49-56	prostaglandin-endoperoxide synthase 1	Homo sapiens	67-83
17934975-1	2008	OBJECTIVE: To assess the prevalence of a lacking aspirin effect on cyclooxygenase-1 (COX-1) ("aspirin resistance") in patients with symptomatic, stable coronary heart disease (CHD) using test methods directly reflecting inhibition of COX-1.	Aspirin	49-56	prostaglandin-endoperoxide synthase 1	Homo sapiens	85-90
17934975-1	2008	OBJECTIVE: To assess the prevalence of a lacking aspirin effect on cyclooxygenase-1 (COX-1) ("aspirin resistance") in patients with symptomatic, stable coronary heart disease (CHD) using test methods directly reflecting inhibition of COX-1.	Aspirin	94-101	prostaglandin-endoperoxide synthase 1	Homo sapiens	67-83
17934975-1	2008	OBJECTIVE: To assess the prevalence of a lacking aspirin effect on cyclooxygenase-1 (COX-1) ("aspirin resistance") in patients with symptomatic, stable coronary heart disease (CHD) using test methods directly reflecting inhibition of COX-1.	Aspirin	94-101	prostaglandin-endoperoxide synthase 1	Homo sapiens	85-90
17934975-10	2008	CONCLUSION: Repeated AA-induced platelet aggregometry showed that COX-1 could be blocked by low-dose aspirin in all 289 tested patients, suggesting that aspirin resistance is rare in patients with stable CHD.	Aspirin	101-108	prostaglandin-endoperoxide synthase 1	Homo sapiens	66-71
18217153-0	2008	Effect of chronic treatment with acetylsalicylic acid and clopidogrel on atheroprogression and atherothrombosis in ApoE-deficient mice in vivo.	Aspirin	33-53	apolipoprotein E	Mus musculus	115-119
17584993-16	2008	The clinical implications of this finding are in line with current observations of good tolerance of the selective COX-2 inhibitors in aspirin-sensitive patients.	Aspirin	135-142	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	115-120
18156036-10	2007	Data support the conclusion that COX-2 inhibitors are preferable to non-selective NSAIDs in patients with chronic pain and cardiovascular risk needing low-dose aspirin, but relative risks and benefits should be assessed individually for each patient.	Aspirin	160-167	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	33-38
18064329-9	2007	Evolutionary, this mechanism may prevent COX-2-dependent thromboxane synthesis in the platelet, which would potentiate the likelihood of thrombosis; pharmacologically, this mechanism would prevent an aspirin-insensitive pathway of thromboxane formation.	Aspirin	200-207	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	41-46
18160362-0	2007	[Use of aspirin in patients taking angiotensin converting enzyme inhibitors].	Aspirin	8-15	angiotensin I converting enzyme	Homo sapiens	35-64
18160362-5	2007	Theoretically, aspirin, which inhibits cyclooxygenase enzyme, may reduce bradykinin mediated prostaglandin synthesis and blunt the beneficial effects of ACE inhibitors, when used together.	Aspirin	15-22	kininogen 1	Homo sapiens	73-83
18160362-5	2007	Theoretically, aspirin, which inhibits cyclooxygenase enzyme, may reduce bradykinin mediated prostaglandin synthesis and blunt the beneficial effects of ACE inhibitors, when used together.	Aspirin	15-22	angiotensin I converting enzyme	Homo sapiens	153-156
18160362-7	2007	In this article, we reviewed the possible interaction between aspirin and ACE inhibitors in light of literature findings.	Aspirin	62-69	angiotensin I converting enzyme	Homo sapiens	74-77
17848598-5	2007	We observed that ASA promoted TRAIL-induced apoptotic death in both LNCaP and its derived cells (C4, C4-2, and C4-2B).	Aspirin	17-20	TNF superfamily member 10	Homo sapiens	30-35
17848598-6	2007	These enhancements of TRAIL"s effect were related to the decrease in survivin protein expression by pretreatment with ASA.	Aspirin	118-121	TNF superfamily member 10	Homo sapiens	22-27
17848598-11	2007	Taken together, our studies suggested that ASA-promoted TRAIL cytotoxicity is mediated by down-regulating survivin, and the down-regulation of survivin is due to inhibition of E2F-1 binding activity to the survivin promoter region.	Aspirin	43-46	TNF superfamily member 10	Homo sapiens	56-61
18167181-0	2007	Aspirin inhibits the proliferation of tobacco-related esophageal squamous carcinomas cell lines through cyclooxygenase 2 pathway.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	104-120
18167181-4	2007	Whether aspirin can inhibit the proliferation of the ESCC cell lines pretreated with EE, and regulate the mRNA expression levels of COX-2 are also examined.	Aspirin	8-15	prostaglandin-endoperoxide synthase 2	Homo sapiens	132-137
18167181-14	2007	However, the cell growth inhibition of aspirin was correlated with the down-regulation of COX-2 gene.	Aspirin	39-46	prostaglandin-endoperoxide synthase 2	Homo sapiens	90-95
17694420-6	2007	Both IL6 polymorphisms were associated with significant interaction with current use of aspirin/NSAIDs to alter risk of colon cancer: individuals with a C allele in either polymorphism who were current users of aspirin/NSAIDs had the lowest colon cancer risk.	Aspirin	88-95	interleukin 6	Homo sapiens	5-8
17694420-6	2007	Both IL6 polymorphisms were associated with significant interaction with current use of aspirin/NSAIDs to alter risk of colon cancer: individuals with a C allele in either polymorphism who were current users of aspirin/NSAIDs had the lowest colon cancer risk.	Aspirin	211-218	interleukin 6	Homo sapiens	5-8
17694420-7	2007	CRC risk also was associated with an interaction between VDR and IL6 genotypes that was modified by current use of aspirin/NSAIDs.	Aspirin	115-122	interleukin 6	Homo sapiens	65-68
17848598-0	2007	Aspirin enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in hormone-refractory prostate cancer cells through survivin down-regulation.	Aspirin	0-7	TNF superfamily member 10	Homo sapiens	17-72
17848598-3	2007	In this study, we examined whether acetylsalicylic acid (ASA), so-called aspirin, enhances TRAIL-induced apoptosis in androgen-dependent LNCaP and androgen-independent LNCaP-derived prostate cancer cells.	Aspirin	35-55	TNF superfamily member 10	Homo sapiens	91-96
17848598-3	2007	In this study, we examined whether acetylsalicylic acid (ASA), so-called aspirin, enhances TRAIL-induced apoptosis in androgen-dependent LNCaP and androgen-independent LNCaP-derived prostate cancer cells.	Aspirin	57-60	TNF superfamily member 10	Homo sapiens	91-96
17848598-3	2007	In this study, we examined whether acetylsalicylic acid (ASA), so-called aspirin, enhances TRAIL-induced apoptosis in androgen-dependent LNCaP and androgen-independent LNCaP-derived prostate cancer cells.	Aspirin	73-80	TNF superfamily member 10	Homo sapiens	91-96
18064330-12	2007	In conclusion, adding clopidogrel to aspirin treatment inhibited platelet activation by both ADP, thrombin and collagen in vitro, but did not influence the prothrombotic responses to exercise.	Aspirin	37-44	coagulation factor II, thrombin	Homo sapiens	98-106
17892525-7	2007	CONCLUSION: The increase in gastrointestinal hospitalization attributable to aspirin differed with the non-steroidal anti-inflammatory drug used, and seemed higher with cyclo-oxygenase-2 inhibitors than with non-selective non-steroidal anti-inflammatory drugs.	Aspirin	77-84	prostaglandin-endoperoxide synthase 2	Homo sapiens	169-186
17876871-10	2007	CONCLUSION: These results suggest that the effect of ULDA on platelet activity in portal hypertensive rats, could act through a COX 2 pathway more than the COX 1, predominant for aspirin at higher doses.	Aspirin	179-186	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	156-161
17978563-0	2007	Copper-aspirin complex inhibits cyclooxygenase-2 more selectively than aspirin.	Aspirin	7-14	prostaglandin-endoperoxide synthase 2	Homo sapiens	32-48
17978563-7	2007	The selective inhibition index on COX-2, IC(50) (COX-1)/IC(50) (COX-2), of Cu-Asp was 3.33+/-0.89, while that of Asp was 0.42+/-0.12.	Aspirin	78-81	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	34-39
17978563-7	2007	The selective inhibition index on COX-2, IC(50) (COX-1)/IC(50) (COX-2), of Cu-Asp was 3.33+/-0.89, while that of Asp was 0.42+/-0.12.	Aspirin	78-81	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	64-69
17978563-8	2007	The results suggest that, unlike Asp, Cu-Asp is a relatively selective inhibitor of COX-2 in the present models; the selectivity of Cu-Asp is about seven-fold greater than that of Asp.	Aspirin	41-44	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	84-89
18201436-8	2007	Aspirin desensitization differentially affects interferon (IFN) gamma expression.	Aspirin	0-7	interferon gamma	Homo sapiens	47-69
18201436-10	2007	Aspirin desensitization in an aspirin-sensitive patient with asthma resulted in an increase in IFN-gamma expression by CD4(+) lymphocytes and a decrease in IFN-gamma expression by CD8(+) lymphocytes, the significance of which needs additional investigation.	Aspirin	0-7	interferon gamma	Homo sapiens	95-104
18201436-10	2007	Aspirin desensitization in an aspirin-sensitive patient with asthma resulted in an increase in IFN-gamma expression by CD4(+) lymphocytes and a decrease in IFN-gamma expression by CD8(+) lymphocytes, the significance of which needs additional investigation.	Aspirin	0-7	interferon gamma	Homo sapiens	156-165
18201436-10	2007	Aspirin desensitization in an aspirin-sensitive patient with asthma resulted in an increase in IFN-gamma expression by CD4(+) lymphocytes and a decrease in IFN-gamma expression by CD8(+) lymphocytes, the significance of which needs additional investigation.	Aspirin	30-37	interferon gamma	Homo sapiens	95-104
18201436-10	2007	Aspirin desensitization in an aspirin-sensitive patient with asthma resulted in an increase in IFN-gamma expression by CD4(+) lymphocytes and a decrease in IFN-gamma expression by CD8(+) lymphocytes, the significance of which needs additional investigation.	Aspirin	30-37	interferon gamma	Homo sapiens	156-165
17640058-3	2007	Prostaglandin H synthase 1 (PTGS1) and PTGS2 are key enzymes in prostaglandin synthesis and are inhibited by aspirin, whilst interleukin-10 (IL-10) is an important antiinflammatory cytokine.	Aspirin	109-116	prostaglandin-endoperoxide synthase 1	Homo sapiens	0-26
17640058-3	2007	Prostaglandin H synthase 1 (PTGS1) and PTGS2 are key enzymes in prostaglandin synthesis and are inhibited by aspirin, whilst interleukin-10 (IL-10) is an important antiinflammatory cytokine.	Aspirin	109-116	prostaglandin-endoperoxide synthase 1	Homo sapiens	28-33
17640058-3	2007	Prostaglandin H synthase 1 (PTGS1) and PTGS2 are key enzymes in prostaglandin synthesis and are inhibited by aspirin, whilst interleukin-10 (IL-10) is an important antiinflammatory cytokine.	Aspirin	109-116	prostaglandin-endoperoxide synthase 2	Homo sapiens	39-44
17641958-0	2007	Differential contribution of the CysLTR1 gene in patients with aspirin hypersensitivity.	Aspirin	63-70	cysteinyl leukotriene receptor 1	Homo sapiens	33-40
17641958-3	2007	As in vivo functional study, changes of peripheral mRNA level of CysLTR1 were measured by real-time PCR before and after aspirin challenge.	Aspirin	121-128	cysteinyl leukotriene receptor 1	Homo sapiens	65-72
17641958-6	2007	The CysLTR1 mRNA levels increased significantly after aspirin challenge in AIA patients (P = 0.013).	Aspirin	54-61	cysteinyl leukotriene receptor 1	Homo sapiens	4-11
17641958-7	2007	In conclusion, the CysLTR1 polymorphism may contribute to develop to the AIA phenotype and be used as a genetic marker for differentiating two major aspirin hypersensitivity phenotypes.	Aspirin	149-156	cysteinyl leukotriene receptor 1	Homo sapiens	19-26
17993938-9	2007	Odds ratio for death was 1.76 (95% CI, 1.14-2.72) for pre-injury ASA-PS 2, and 2.25 (95% CI, 1.36-3.71) for ASA-PS 3-4 compared with for ASA-PS 1 and adjusted for ISS, RTS, and age.	Aspirin	65-68	taste 2 receptor member 64 pseudogene	Homo sapiens	69-73
17510082-7	2007	Moreover, aspirin induced cell death mainly in cells expressing p53.	Aspirin	10-17	tumor protein p53	Homo sapiens	64-67
17510082-6	2007	Aspirin and sulindac sulfide induced a G1 arrest within 48 h. While all cell lines responded in a comparable way to sulindac sulfide, the aspirin-induced G1 arrest was dependent on p21Waf1/Cip1--as cells lacking the cyclin-dependent kinase inhibitor failed to show this arrest--and on ataxia-telangiectasia-mutated kinase (ATM)--as the inhibitor caffeine abrogated the checkpoint.	Aspirin	0-7	cyclin dependent kinase inhibitor 1A	Homo sapiens	189-193
17510082-6	2007	Aspirin and sulindac sulfide induced a G1 arrest within 48 h. While all cell lines responded in a comparable way to sulindac sulfide, the aspirin-induced G1 arrest was dependent on p21Waf1/Cip1--as cells lacking the cyclin-dependent kinase inhibitor failed to show this arrest--and on ataxia-telangiectasia-mutated kinase (ATM)--as the inhibitor caffeine abrogated the checkpoint.	Aspirin	138-145	cyclin dependent kinase inhibitor 1A	Homo sapiens	189-193
17510082-8	2007	Aspirin induced the phosphorylation of p53 at residue Ser15 within 8 h in a caffeine-dependent manner, and also caused the activation of checkpoint kinase 2 and the cleavage of caspase 7.	Aspirin	0-7	tumor protein p53	Homo sapiens	39-42
17510082-9	2007	Our results suggest that aspirin induces a G1 arrest and apoptosis by activating p53 and p21Waf1/Cip1 in an ATM-dependent way.	Aspirin	25-32	tumor protein p53	Homo sapiens	81-84
17510082-9	2007	Our results suggest that aspirin induces a G1 arrest and apoptosis by activating p53 and p21Waf1/Cip1 in an ATM-dependent way.	Aspirin	25-32	cyclin dependent kinase inhibitor 1A	Homo sapiens	97-101
18034968-11	2007	Several studies have indicated that selective COX-2 inhibitors can be safely administered in patients with aspirin-exacerbated respiratory disease and NSAID-induced cutaneous reactions, although their use has been curtailed by their cardiovascular side effects.	Aspirin	107-114	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	46-51
17719296-0	2007	Effects of recombinant human erythropoietin on antiplatelet action of aspirin and clopidogrel in healthy subjects: results of a double-blind, placebo-controlled randomized trial.	Aspirin	70-77	erythropoietin	Homo sapiens	29-43
17719296-8	2007	Recombinant human erythropoietin at a dose of 400 U/kg significantly blunted the post-aspirin increase in bleeding time when compared with placebo (P = .03) but did not alter post-clopidogrel bleeding times nor PFA closure times.	Aspirin	86-93	erythropoietin	Homo sapiens	18-32
17979514-4	2007	Aspirin response phenotypes can be categorized as directly or indirectly related to cyclooxygenase-1 (COX-1) activity, with phenotypic variation indirectly related to COX-1 being much more prominent.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	84-100
17979514-4	2007	Aspirin response phenotypes can be categorized as directly or indirectly related to cyclooxygenase-1 (COX-1) activity, with phenotypic variation indirectly related to COX-1 being much more prominent.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	102-107
17979514-4	2007	Aspirin response phenotypes can be categorized as directly or indirectly related to cyclooxygenase-1 (COX-1) activity, with phenotypic variation indirectly related to COX-1 being much more prominent.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	167-172
17924829-0	2007	CysLTR1 promoter polymorphism and requirement for leukotriene receptor antagonist in aspirin-intolerant asthma patients.	Aspirin	85-92	cysteinyl leukotriene receptor 1	Homo sapiens	0-7
17526656-9	2007	In addition, NO-aspirin downregulated inducible NO synthase (iNOS; 0.37-fold, P &lt; 0.01) and cyclooxygenase-2 (COX-2; 0.61-fold, P &lt; 0.05) gene expression compared with the vehicle group after 48 h of reperfusion.	Aspirin	16-23	nitric oxide synthase 2	Rattus norvegicus	38-59
17526656-9	2007	In addition, NO-aspirin downregulated inducible NO synthase (iNOS; 0.37-fold, P &lt; 0.01) and cyclooxygenase-2 (COX-2; 0.61-fold, P &lt; 0.05) gene expression compared with the vehicle group after 48 h of reperfusion.	Aspirin	16-23	nitric oxide synthase 2	Rattus norvegicus	61-65
17867925-2	2007	Aspirin exhibits its antiplatelet action by irreversibly inhibiting platelet cyclooxygenase-1 enzyme, thus preventing the production of thromboxane A2 (TXA2).	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	77-93
17867925-7	2007	Possible causes of aspirin resistance include poor compliance, inadequate dose, drug interactions, genetic polymorphisms of cyclooxygenase-1, increased platelet turnover and upregulation of non-platelet pathways of thromboxane production.	Aspirin	19-26	prostaglandin-endoperoxide synthase 1	Homo sapiens	124-140
17869645-6	2007	Both BAY- and ASA-allogeneic DC and autologous alloantigen pulsed DC were weaker stimulators of T cells (by MLR) compared with controls, and there was reduced IL-2 and IFN-gamma production by T cells stimulated with BAY-DC or ASA-DC (by ELISPOT) (more marked results were always observed with ASA-treated DC).	Aspirin	14-17	interleukin 2	Homo sapiens	159-163
17869645-6	2007	Both BAY- and ASA-allogeneic DC and autologous alloantigen pulsed DC were weaker stimulators of T cells (by MLR) compared with controls, and there was reduced IL-2 and IFN-gamma production by T cells stimulated with BAY-DC or ASA-DC (by ELISPOT) (more marked results were always observed with ASA-treated DC).	Aspirin	14-17	interferon gamma	Homo sapiens	168-177
17700214-1	2007	Aspirin has the potential to influence C-reactive protein (CRP) levels, an inflammatory marker, by its anti-inflammatory activity.	Aspirin	0-7	C-reactive protein	Homo sapiens	39-57
17700214-1	2007	Aspirin has the potential to influence C-reactive protein (CRP) levels, an inflammatory marker, by its anti-inflammatory activity.	Aspirin	0-7	C-reactive protein	Homo sapiens	59-62
17611980-0	2007	The effect of low-dose aspirin on the decreased risk of development of dyspepsia and gastrointestinal ulcers associated to cyclooxygenase-2 selective inhibitors.	Aspirin	23-30	prostaglandin-endoperoxide synthase 2	Homo sapiens	123-139
17654043-3	2007	Twenty day treatment with 3 g of l-arginine and 75 mg of acetylsalicylic acid daily resulted in a decrease of the level of lipid peroxidation products and augmentation of alpha-1-antitrypsin activity.	Aspirin	57-77	serpin family A member 1	Homo sapiens	171-190
17665043-7	2007	Further, we found that the expression of Snail, an important transcription factor in EMT, was increased in this process, which is inhibited by the nuclear factor kappa B (NFkappaB) inhibitor aspirin while not affected by the reactive oxygen species (ROS) scavenger N-acetyl cysteine.	Aspirin	191-198	snail family transcriptional repressor 1	Homo sapiens	41-46
17665043-7	2007	Further, we found that the expression of Snail, an important transcription factor in EMT, was increased in this process, which is inhibited by the nuclear factor kappa B (NFkappaB) inhibitor aspirin while not affected by the reactive oxygen species (ROS) scavenger N-acetyl cysteine.	Aspirin	191-198	nuclear factor kappa B subunit 1	Homo sapiens	147-169
17665043-7	2007	Further, we found that the expression of Snail, an important transcription factor in EMT, was increased in this process, which is inhibited by the nuclear factor kappa B (NFkappaB) inhibitor aspirin while not affected by the reactive oxygen species (ROS) scavenger N-acetyl cysteine.	Aspirin	191-198	nuclear factor kappa B subunit 1	Homo sapiens	171-179
17611980-1	2007	OBJECTIVE: To evaluate the risk of gastrointestinal (GI) symptoms and ulcers associated to the use of low-dose aspirin (ASA) among patients with rheumatoid arthritis (RA) and osteoarthritis (OA) treated with cyclooxygenase-2 (COX-2) drugs, to clarify the controversy in the literature.	Aspirin	111-118	prostaglandin-endoperoxide synthase 2	Homo sapiens	208-224
17611980-1	2007	OBJECTIVE: To evaluate the risk of gastrointestinal (GI) symptoms and ulcers associated to the use of low-dose aspirin (ASA) among patients with rheumatoid arthritis (RA) and osteoarthritis (OA) treated with cyclooxygenase-2 (COX-2) drugs, to clarify the controversy in the literature.	Aspirin	111-118	prostaglandin-endoperoxide synthase 2	Homo sapiens	226-231
17611980-1	2007	OBJECTIVE: To evaluate the risk of gastrointestinal (GI) symptoms and ulcers associated to the use of low-dose aspirin (ASA) among patients with rheumatoid arthritis (RA) and osteoarthritis (OA) treated with cyclooxygenase-2 (COX-2) drugs, to clarify the controversy in the literature.	Aspirin	120-123	prostaglandin-endoperoxide synthase 2	Homo sapiens	208-224
17611980-1	2007	OBJECTIVE: To evaluate the risk of gastrointestinal (GI) symptoms and ulcers associated to the use of low-dose aspirin (ASA) among patients with rheumatoid arthritis (RA) and osteoarthritis (OA) treated with cyclooxygenase-2 (COX-2) drugs, to clarify the controversy in the literature.	Aspirin	120-123	prostaglandin-endoperoxide synthase 2	Homo sapiens	226-231
17609236-13	2007	However, approximately 4% of patients with a history of aspirin-induced skin reactions may experience a cutaneous reaction following a challenge to a COX-2 selective NSAID.	Aspirin	56-63	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	150-155
17609236-7	2007	The primary mechanism is believed to be inhibition of the cyclooxygenase 1 (COX-1) enzyme; as such, patients with aspirin sensitivity often display cross-reactions to nonselective NSAIDs that inhibit the COX-1 enzyme.	Aspirin	114-121	prostaglandin-endoperoxide synthase 1	Homo sapiens	58-74
17609236-7	2007	The primary mechanism is believed to be inhibition of the cyclooxygenase 1 (COX-1) enzyme; as such, patients with aspirin sensitivity often display cross-reactions to nonselective NSAIDs that inhibit the COX-1 enzyme.	Aspirin	114-121	prostaglandin-endoperoxide synthase 1	Homo sapiens	76-81
17609236-7	2007	The primary mechanism is believed to be inhibition of the cyclooxygenase 1 (COX-1) enzyme; as such, patients with aspirin sensitivity often display cross-reactions to nonselective NSAIDs that inhibit the COX-1 enzyme.	Aspirin	114-121	prostaglandin-endoperoxide synthase 1	Homo sapiens	204-209
17663920-2	2007	OBJECTIVE: Our aim was to determine tolerance of Celecoxib, a selective inhibitor of cyclooxygenase-2 (Cox-2), by oral challenge test in patients who showed skin reactions (diffuse erythema or urticaria/angioedema) after taking ASA and/or NSAIDs.	Aspirin	228-231	prostaglandin-endoperoxide synthase 2	Homo sapiens	103-108
17609236-14	2007	Since acetaminophen is a weak inhibitor of the COX-1 enzyme, patients with aspirin-induced asthma should not take more than 1000 mg of acetaminophen in a single dose.	Aspirin	75-82	prostaglandin-endoperoxide synthase 1	Homo sapiens	47-52
17609236-12	2007	COX-2 selective NSAIDs, especially in patients with aspirin-induced asthma, have not been found to cross-react.	Aspirin	52-59	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
17609236-15	2007	CONCLUSIONS: Management of patients with aspirin/NSAID sensitivity includes avoidance of aspirin/nonselective NSAIDs, use of COX-2 selective NSAIDs, acetaminophen in doses less than 1000 mg, and desensitization.	Aspirin	41-48	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	125-130
17556027-10	2007	The co-administration of acetylsalicylic acid appears to reduce the GI safety of COX-2s in subgroup analyses.	Aspirin	25-45	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	81-86
17556027-12	2007	The co-administration of acetylsalicylic acid might reduce the safety advantage of COX-2s over that of nonselective NSAIDs.	Aspirin	25-45	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	83-88
17555340-4	2007	The expression of one isotype of the fibrinogen gamma chain and three isotypes of haptoglobin was increased in ASA-resistant patients.	Aspirin	111-114	fibrinogen gamma chain	Homo sapiens	37-59
17606122-12	2007	Change in eGFR was positively associated with preoperative aspirin use (P = .006) and preoperative eGFR (P &lt; .001), while a negative association was observed for captured particle counts &gt;60 microm (P = .015).	Aspirin	59-66	epidermal growth factor receptor	Homo sapiens	10-14
17555340-4	2007	The expression of one isotype of the fibrinogen gamma chain and three isotypes of haptoglobin was increased in ASA-resistant patients.	Aspirin	111-114	haptoglobin	Homo sapiens	82-93
17555340-6	2007	In vitro incubation of vitamin D binding protein (DBP) with blood from healthy volunteers reduced the inhibitory effect of ASA on thromboxane A2 production.	Aspirin	123-126	D-box binding PAR bZIP transcription factor	Homo sapiens	50-53
17555340-7	2007	DBP may be a new regulator of the inhibitory effect of ASA on platelets.	Aspirin	55-58	D-box binding PAR bZIP transcription factor	Homo sapiens	0-3
17508966-13	2007	In ASA patients there was a significant positive correlation between the COX-1 AS index and the percentage of aspirin-triggered increase in 15-HETE generation (r = 0.51; P &lt; 0.03).	Aspirin	3-6	prostaglandin-endoperoxide synthase 1	Homo sapiens	73-78
17562955-1	2007	BACKGROUND: The antiplatelet effect of aspirin is attributed to platelet cyclooxygenase-1 inhibition.	Aspirin	39-46	prostaglandin-endoperoxide synthase 1	Homo sapiens	73-89
17508965-0	2007	PGE suppresses excessive anti-IgE induced cysteinyl leucotrienes production in mast cells of patients with aspirin exacerbated respiratory disease.	Aspirin	107-114	immunoglobulin heavy constant epsilon	Homo sapiens	30-33
17508966-0	2007	Alternative splicing of cyclooxygenase-1 gene: altered expression in leucocytes from patients with bronchial asthma and association with aspirin-induced 15-HETE release.	Aspirin	137-144	prostaglandin-endoperoxide synthase 1	Homo sapiens	24-40
17508966-13	2007	In ASA patients there was a significant positive correlation between the COX-1 AS index and the percentage of aspirin-triggered increase in 15-HETE generation (r = 0.51; P &lt; 0.03).	Aspirin	110-117	prostaglandin-endoperoxide synthase 1	Homo sapiens	73-78
17508966-2	2007	In a subpopulation of aspirin-sensitive asthmatics (ASA) inhibition of COX-1 by nonsteroidal anti-inflammatory drugs results in activation of inflammatory cells and development of symptoms.	Aspirin	22-29	prostaglandin-endoperoxide synthase 1	Homo sapiens	71-76
17508966-2	2007	In a subpopulation of aspirin-sensitive asthmatics (ASA) inhibition of COX-1 by nonsteroidal anti-inflammatory drugs results in activation of inflammatory cells and development of symptoms.	Aspirin	52-55	prostaglandin-endoperoxide synthase 1	Homo sapiens	71-76
17508966-14	2007	CONCLUSIONS: Alternatively spliced variants of COX-1 mRNA are differently expressed in patients with bronchial asthma and may be associated with aspirin-triggered 15-HETE generation.	Aspirin	145-152	prostaglandin-endoperoxide synthase 1	Homo sapiens	47-52
17508966-4	2007	We aimed to assess the expression of spliced variants of COX-1 mRNA in PBLs from patients with asthma and in healthy subjects (HS) referring the expression to patients characteristics (including ASA-sensitivity) and to aspirin-triggered 15-hydroxyeicosatetraenoic acid (15-HETE) generation.	Aspirin	195-198	prostaglandin-endoperoxide synthase 1	Homo sapiens	57-62
17508966-4	2007	We aimed to assess the expression of spliced variants of COX-1 mRNA in PBLs from patients with asthma and in healthy subjects (HS) referring the expression to patients characteristics (including ASA-sensitivity) and to aspirin-triggered 15-hydroxyeicosatetraenoic acid (15-HETE) generation.	Aspirin	219-226	prostaglandin-endoperoxide synthase 1	Homo sapiens	57-62
17545608-8	2007	More interestingly, aspirin, a nonsteroidal anti-inflammatory drug that preferentially inhibits COX-1, compromises PPARdelta function and cell growth by inhibiting extracellular signal-regulated kinases 1/2, members of the mitogen-activated protein kinase family.	Aspirin	20-27	mitogen-activated protein kinase 3	Homo sapiens	164-206
17485238-3	2007	In addition, it has been recognized that the TGF-beta1 pathway is involved in the vascular mechanism of action of some current clinical drugs, such as acetylsalicylic acid, thiazolidinediones and statins.	Aspirin	151-171	transforming growth factor beta 1	Homo sapiens	45-54
17550447-0	2007	Abnormal nuclear factor (NF)-kappaB signal pathway and aspirin inhibits tumor necrosis factor alpha-induced NF-kappaB activation in keloid fibroblasts.	Aspirin	55-62	tumor necrosis factor	Homo sapiens	72-99
17550447-3	2007	OBJECTIVE: To examine the effect of aspirin on the tumor necrosis factor (TNF)-alpha-induced NF-kappaB activation in keloid fibroblasts.	Aspirin	36-43	tumor necrosis factor	Homo sapiens	51-84
17550447-9	2007	Aspirin pretreatment can inhibit TNF-alpha-induced activation of NF-kappaB in a dose-dependent manner by preventing the phosphorylation and degradation of IkappaBalpha and nuclear translocation of NF-kappaB.	Aspirin	0-7	tumor necrosis factor	Homo sapiens	33-42
17550447-9	2007	Aspirin pretreatment can inhibit TNF-alpha-induced activation of NF-kappaB in a dose-dependent manner by preventing the phosphorylation and degradation of IkappaBalpha and nuclear translocation of NF-kappaB.	Aspirin	0-7	NFKB inhibitor alpha	Homo sapiens	155-167
17559347-0	2007	Frequency of genetic polymorphisms of COX1, GPIIIa and P2Y1 in a Chinese population and association with attenuated response to aspirin.	Aspirin	128-135	prostaglandin-endoperoxide synthase 1	Homo sapiens	38-42
16945375-7	2007	Pre-incubation of the cells with aspirin (100 microM) entirely prevented the nicotinic acid effects on PGD2 secretion.	Aspirin	33-40	prostaglandin D2 synthase	Homo sapiens	103-107
17633905-8	2007	Aspirin also has an intriguing interaction with CRP in that the magnitude of relative risk reduction attributable to aspirin in primary prevention appears to be greatest among those with elevated CRP and declines proportionately in direct relation to CRP levels.	Aspirin	0-7	C-reactive protein	Homo sapiens	48-51
17633905-8	2007	Aspirin also has an intriguing interaction with CRP in that the magnitude of relative risk reduction attributable to aspirin in primary prevention appears to be greatest among those with elevated CRP and declines proportionately in direct relation to CRP levels.	Aspirin	0-7	C-reactive protein	Homo sapiens	196-199
17633905-8	2007	Aspirin also has an intriguing interaction with CRP in that the magnitude of relative risk reduction attributable to aspirin in primary prevention appears to be greatest among those with elevated CRP and declines proportionately in direct relation to CRP levels.	Aspirin	0-7	C-reactive protein	Homo sapiens	196-199
17633905-8	2007	Aspirin also has an intriguing interaction with CRP in that the magnitude of relative risk reduction attributable to aspirin in primary prevention appears to be greatest among those with elevated CRP and declines proportionately in direct relation to CRP levels.	Aspirin	117-124	C-reactive protein	Homo sapiens	48-51
17633905-8	2007	Aspirin also has an intriguing interaction with CRP in that the magnitude of relative risk reduction attributable to aspirin in primary prevention appears to be greatest among those with elevated CRP and declines proportionately in direct relation to CRP levels.	Aspirin	117-124	C-reactive protein	Homo sapiens	196-199
17633905-8	2007	Aspirin also has an intriguing interaction with CRP in that the magnitude of relative risk reduction attributable to aspirin in primary prevention appears to be greatest among those with elevated CRP and declines proportionately in direct relation to CRP levels.	Aspirin	117-124	C-reactive protein	Homo sapiens	196-199
17605878-6	2007	The results showed that compared with the normal control group, the contents of TXB(2) and GMP-140 in plasma markedly increased in all of PC groups and aspirin group, and the contents of 6-Keto-PGF1alpha in plasma decreased.	Aspirin	152-159	selectin P	Rattus norvegicus	91-98
17605878-8	2007	Compared with the aspirin group, the contents of TXB(2) and GMP-140 in plasma reduced in all of PC groups and the contents of 6-Keto-PGF1alpha in plasma increased which was obvious in PC 400 mg/(kg x d) group.	Aspirin	18-25	selectin P	Rattus norvegicus	60-67
17522398-0	2007	Aspirin and the risk of colorectal cancer in relation to the expression of COX-2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	75-80
17522398-2	2007	METHODS: We estimated cyclooxygenase-2 (COX-2) expression by immunohistochemical assay of sections from paraffin-embedded colorectal-cancer specimens from two large cohorts of participants who provided data on aspirin use from a questionnaire every 2 years.	Aspirin	210-217	prostaglandin-endoperoxide synthase 2	Homo sapiens	40-45
17522398-3	2007	We applied Cox regression to a competing-risks analysis to compare the effects of aspirin use on the relative risk of colorectal cancer in relation to the expression of COX-2 in the tumor.	Aspirin	82-89	prostaglandin-endoperoxide synthase 2	Homo sapiens	169-174
17522398-6	2007	The effect of aspirin use differed significantly in relation to COX-2 expression (P for heterogeneity=0.02).	Aspirin	14-21	prostaglandin-endoperoxide synthase 2	Homo sapiens	64-69
17522398-7	2007	Regular aspirin use conferred a significant reduction in the risk of colorectal cancers that overexpressed COX-2 (multivariate relative risk, 0.64; 95% confidence interval [CI], 0.52 to 0.78), whereas regular aspirin use had no influence on tumors with weak or absent expression of COX-2 (multivariate relative risk, 0.96; 95% CI, 0.73 to 1.26).	Aspirin	8-15	prostaglandin-endoperoxide synthase 2	Homo sapiens	107-112
17522398-8	2007	The age-standardized incidence rate for cancers that overexpressed COX-2 was 37 per 100,000 person-years among regular aspirin users, as compared with 56 per 100,000 person-years among those who did not use aspirin regularly; in contrast, the rate for cancers with weak or absent COX-2 expression was 27 per 100,000 person-years among regular aspirin users, as compared with 28 per 100,000 person-years among nonregular aspirin users.	Aspirin	119-126	prostaglandin-endoperoxide synthase 2	Homo sapiens	67-72
17522398-9	2007	CONCLUSIONS: Regular use of aspirin appears to reduce the risk of colorectal cancers that overexpress COX-2 but not the risk of colorectal cancers with weak or absent expression of COX-2.	Aspirin	28-35	prostaglandin-endoperoxide synthase 2	Homo sapiens	102-107
17552415-4	2007	In patients with CVD the use of acetylsalicylic acid and often, depending on the specific disease, a beta-blocker or an angiotensin converting enzyme (ACE) inhibitor are recommended.	Aspirin	32-52	angiotensin I converting enzyme	Homo sapiens	120-149
17552415-4	2007	In patients with CVD the use of acetylsalicylic acid and often, depending on the specific disease, a beta-blocker or an angiotensin converting enzyme (ACE) inhibitor are recommended.	Aspirin	32-52	angiotensin I converting enzyme	Homo sapiens	151-154
17589567-11	2007	Intake of ibuprofen or aspirin also produced significant risk reductions (OR=0.40, 95% CI=0.23-0.73 and OR=0.53, 95% CI=0.34-0.82, respectively), whereas acetaminophen, an analgesic with negligible COX-2 activity, had no effect on the risk (OR=1.36, 95% CI=0.53-3.37).	Aspirin	23-30	prostaglandin-endoperoxide synthase 2	Homo sapiens	198-203
19075973-6	2007	The common anti-inflammatory drugs (like aspirin, ibuprofen, and naproxen) all act by blocking the action of both the COX-1 and COX-2 enzymes.	Aspirin	41-48	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	128-133
17549314-0	2007	Lack of aspirin-induced decrease in thrombin formation in subjects resistant to aspirin.	Aspirin	8-15	coagulation factor II, thrombin	Homo sapiens	36-44
17470694-0	2007	Heritability of platelet responsiveness to aspirin in activation pathways directly and indirectly related to cyclooxygenase-1.	Aspirin	43-50	prostaglandin-endoperoxide synthase 1	Homo sapiens	109-125
17470694-4	2007	Ex vivo platelet function was determined before and after ingestion of ASA (81 mg/d for 2 weeks) with the use of a panel of measures that assessed platelet activation in pathways directly and indirectly related to cyclooxygenase-1, the enzyme inhibited by ASA.	Aspirin	256-259	prostaglandin-endoperoxide synthase 1	Homo sapiens	214-230
17559347-0	2007	Frequency of genetic polymorphisms of COX1, GPIIIa and P2Y1 in a Chinese population and association with attenuated response to aspirin.	Aspirin	128-135	integrin subunit beta 3	Homo sapiens	44-50
17516296-0	2007	TNF-alpha -308G&gt;A polymorphism modulates cytokine serum concentrations and macrovascular complications in diabetic patients on aspirin.	Aspirin	130-137	tumor necrosis factor	Homo sapiens	0-9
17485013-5	2007	RESULTS: The COX-1 and COX-2 inhibitor aspirin at high concentrations (10(-6) to 10(-5) mol/L) and the COX-2 inhibitor nimesulide (10(-6) mol/L) potentiated the contractile responses of the arterial rings to sympathetic neurogenic stimulation and norepinephrine.	Aspirin	39-46	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	23-28
17485013-9	2007	Aspirin at high concentrations and the COX-2 selective inhibitor nimesulide potentiated the contractile response of gastroepiploic artery to adrenergic stimulation by inhibiting COX-2-derived PGI(2).	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	178-183
17132819-0	2007	Aspirin activates the NF-kappaB signalling pathway and induces apoptosis in intestinal neoplasia in two in vivo models of human colorectal cancer.	Aspirin	0-7	nuclear factor kappa B subunit 1	Homo sapiens	22-31
17132819-1	2007	Substantial evidence indicates that aspirin has antitumour activity against large bowel cancer and modulation of the NF-kappaB (NF-kappaB) signalling pathway has been identified as a key mechanism in this effect.	Aspirin	36-43	nuclear factor kappa B subunit 1	Homo sapiens	128-137
17132819-2	2007	However, studies examining how aspirin affects the NF-kappaB pathway to promote apoptosis have been restricted to in vitro analysis in tissue culture systems and have produced contrasting results.	Aspirin	31-38	nuclear factor kappa B subunit 1	Homo sapiens	51-60
17132819-3	2007	Here, we employed two animal models of human colorectal cancer to determine aspirin effects on the NF-kappaB pathway in colorectal neoplasia in vivo, and the relationship of such effects to the induction of apoptosis.	Aspirin	76-83	nuclear factor kappa B subunit 1	Homo sapiens	99-108
17132819-4	2007	We demonstrate that aspirin induces phosphorylation and degradation of cytoplasmic IkappaBalpha in xenografted HT-29 tumours and in adenomas from APC(Min+/-) mice.	Aspirin	20-27	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	83-95
17132819-8	2007	These in vivo findings further establish that aspirin induces activation of the NF-kappaB pathway in neoplastic epithelial cells and provide further support that this effect is important for the antitumour activity of the agent.	Aspirin	46-53	nuclear factor kappa B subunit 1	Homo sapiens	80-89
17390393-9	2007	Treatment with the PGE(2) synthesis inhibitor acetylsalicylic acid (AAS) in vivo reduced parasitemia and enhanced LPS-stimulated production of TNF by macrophages, but the effect was less in infected mice than in normal mice.	Aspirin	46-66	tumor necrosis factor	Mus musculus	143-146
17516296-10	2007	CONCLUSION: TNF-alpha -308G&gt;A polymorphism modulates cytokine serum concentrations and macrovascular complications in diabetic patients on aspirin.	Aspirin	142-149	tumor necrosis factor	Homo sapiens	12-21
17516296-11	2007	Diabetic carriers of the TNF-alpha -308A allele might benefit more from a prophylaxis with low dose aspirin than non-carriers.	Aspirin	100-107	tumor necrosis factor	Homo sapiens	25-34
17615799-4	2007	Acetylsalicylic acid (ASA) has been attributed with reducing levels of the transcription factor nuclear factor kappaB (NF-kappaB), C-reactive protein, and soluble CD40 ligand, although the evidence relating to the latter two markers is conflicting.	Aspirin	0-20	C-reactive protein	Homo sapiens	131-149
17615799-4	2007	Acetylsalicylic acid (ASA) has been attributed with reducing levels of the transcription factor nuclear factor kappaB (NF-kappaB), C-reactive protein, and soluble CD40 ligand, although the evidence relating to the latter two markers is conflicting.	Aspirin	22-25	C-reactive protein	Homo sapiens	131-149
17320862-3	2007	Aspirin, at 10, 30 and 100 mg/kg doses, increased IL-1beta levels in exudates, however, only the highest dose lead to a significant increase when compared to control, whereas a significant increase in TNF-alpha level was observed at all doses tested.	Aspirin	0-7	interleukin 1 beta	Rattus norvegicus	50-58
17306251-6	2007	We previously demonstrated that treatment of mast cells with heat shock or acetylsalicylic acid results in an increase of TNF-alpha and IL-6 release.	Aspirin	75-95	tumor necrosis factor	Homo sapiens	122-131
17325651-8	2007	CONCLUSIONS AND IMPLICATIONS: Aspirin"s gastric toxicity in combination with a coxib can be dissociated from its ability to inhibit COX-1 and appears to be dependent, in part, on its ability to attenuate the stomach"s surface hydrophobic barrier.	Aspirin	30-37	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	132-137
17306251-6	2007	We previously demonstrated that treatment of mast cells with heat shock or acetylsalicylic acid results in an increase of TNF-alpha and IL-6 release.	Aspirin	75-95	interleukin 6	Homo sapiens	136-140
16793048-4	2007	We hypothesized that aspirin would be effectively hydrolyzed by PON 1 and many of its anti-atherogenic effects, at least in part, could be accounted for by its antioxidant product, salicylic acid.	Aspirin	21-28	paraoxonase 1	Homo sapiens	64-69
16793048-5	2007	In this study, we determined the ability of human plasma and PON 1-rich HDL to hydrolyze acetyl ester of salicylic acid (aspirin).	Aspirin	121-128	paraoxonase 1	Homo sapiens	61-66
17320862-3	2007	Aspirin, at 10, 30 and 100 mg/kg doses, increased IL-1beta levels in exudates, however, only the highest dose lead to a significant increase when compared to control, whereas a significant increase in TNF-alpha level was observed at all doses tested.	Aspirin	0-7	tumor necrosis factor	Rattus norvegicus	201-210
17416766-11	2007	IL6 genotype and haplotype significantly modified the association between aspirin and breast cancer, with the greatest effect modification being among women not recently exposed to hormones [P interaction = 0.06 (for non-Hispanic white) and 0.04 (for Hispanic/Native American) and SNP rs1800796 or -572G&gt;C].	Aspirin	74-81	interleukin 6	Homo sapiens	0-3
17416766-12	2007	These data suggest that IL6 is associated with breast cancer risk and modifies the association between estrogen and aspirin and breast cancer risk.	Aspirin	116-123	interleukin 6	Homo sapiens	24-27
17148593-4	2007	Aspirin can reduce thrombin generation with the subsequent attenuation of thrombin-mediated coagulant reactions such as factor XIII activation.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	19-27
17342322-0	2007	Failure of apoptosis and activation on NFkappaB by celecoxib and aspirin in lung cancer cell lines.	Aspirin	65-72	nuclear factor kappa B subunit 1	Homo sapiens	39-47
17342322-3	2007	We investigated the effects of celecoxib and aspirin in the induction of apoptosis and in the ability to activate NFkappaB in three non-small cell lung cancer cell lines.	Aspirin	45-52	nuclear factor kappa B subunit 1	Homo sapiens	114-122
17342322-7	2007	Similarly, aspirin at both concentrations did not induce any apoptotic response, but activated NFkappaB in a dose-dependent manner.	Aspirin	11-18	nuclear factor kappa B subunit 1	Homo sapiens	95-103
17148593-4	2007	Aspirin can reduce thrombin generation with the subsequent attenuation of thrombin-mediated coagulant reactions such as factor XIII activation.	Aspirin	0-7	coagulation factor II, thrombin	Homo sapiens	74-82
17339623-8	2007	Colorectal adenoma incidence was also reduced with non-ASA NSAID use in cohort studies (relative risk, 0.64 [CI, 0.48 to 0.85]) and case-control studies (relative risk, 0.54 [CI, 0.4 to 0.74]) and by COX-2 inhibitors in randomized, controlled trials (relative risk, 0.72 [CI, 0.68 to 0.77]).	Aspirin	55-58	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	200-205
17355113-9	2007	It is also known that some drugs act directly in the inhibition of NF-kappaB, thus producing regulation of apoptosis; some examples are aspirin and corticosteroids.	Aspirin	136-143	nuclear factor kappa B subunit 1	Homo sapiens	67-76
17444284-2	2007	Aims of this study were to detect EPO resistance in patients with DM and/or CRF and to prove, that acetylsalicylic acid (ASA) is able to improve the haemopoietic status by decreasing neocytolysis.	Aspirin	99-119	erythropoietin	Homo sapiens	34-37
17444284-2	2007	Aims of this study were to detect EPO resistance in patients with DM and/or CRF and to prove, that acetylsalicylic acid (ASA) is able to improve the haemopoietic status by decreasing neocytolysis.	Aspirin	121-124	erythropoietin	Homo sapiens	34-37
17444284-7	2007	Single dose of ASA induced a fast increase in serum EPO level, a concomitant rise of the Rtc number and rate, red blood cell count, haematocrit and haemoglobin p &lt; 0.01 for each).	Aspirin	15-18	erythropoietin	Homo sapiens	52-55
17444284-10	2007	In these patients, ASA treatment increases serum EPO level.	Aspirin	19-22	erythropoietin	Homo sapiens	49-52
16943252-0	2006	Antiplatelet agents aspirin and clopidogrel are hydrolyzed by distinct carboxylesterases, and clopidogrel is transesterificated in the presence of ethyl alcohol.	Aspirin	20-27	carboxylesterase 1	Homo sapiens	71-88
17308107-4	2007	Here, we investigate the upstream molecular mechanisms responsible for nucleolar targeting of RelA and show that aspirin activates the p38 mitogen-activated protein kinase (MAPK) pathway in colorectal cancer cells.	Aspirin	113-120	RELA proto-oncogene, NF-kB subunit	Homo sapiens	94-98
17308107-5	2007	We also show that aspirin causes rapid, ubiquitin-dependent degradation of cyclin D1, a known p38 target.	Aspirin	18-25	cyclin D1	Homo sapiens	75-84
17308107-6	2007	Aspirin-induced p38 activation preceded cyclin D1 degradation, which was then followed by activation of the NF-kappaB pathway, suggesting a causative link.	Aspirin	0-7	cyclin D1	Homo sapiens	40-49
17308107-7	2007	Indeed, chemical p38 inhibition (PD169316) and small interfering RNA directed against p38 blocked aspirin-induced cyclin D1 degradation, nucleolar translocation of RelA, and apoptosis.	Aspirin	98-105	cyclin D1	Homo sapiens	114-123
17308107-7	2007	Indeed, chemical p38 inhibition (PD169316) and small interfering RNA directed against p38 blocked aspirin-induced cyclin D1 degradation, nucleolar translocation of RelA, and apoptosis.	Aspirin	98-105	RELA proto-oncogene, NF-kB subunit	Homo sapiens	164-168
17308107-8	2007	Furthermore, chemical inhibition of the cyclin D1/cyclin-dependent kinase 4 (CDK4) kinase complex, used as a surrogate for cyclin D1 degradation, caused nucleolar translocation of RelA, repression of kappaB-driven transcription, and apoptosis, thereby reproducing the effects of aspirin.	Aspirin	279-286	cyclin D1	Homo sapiens	40-75
17308107-8	2007	Furthermore, chemical inhibition of the cyclin D1/cyclin-dependent kinase 4 (CDK4) kinase complex, used as a surrogate for cyclin D1 degradation, caused nucleolar translocation of RelA, repression of kappaB-driven transcription, and apoptosis, thereby reproducing the effects of aspirin.	Aspirin	279-286	cyclin dependent kinase 4	Homo sapiens	77-81
17308107-8	2007	Furthermore, chemical inhibition of the cyclin D1/cyclin-dependent kinase 4 (CDK4) kinase complex, used as a surrogate for cyclin D1 degradation, caused nucleolar translocation of RelA, repression of kappaB-driven transcription, and apoptosis, thereby reproducing the effects of aspirin.	Aspirin	279-286	cyclin D1	Homo sapiens	40-49
17308107-9	2007	In addition, we found that aspirin and the CDK4 inhibitor induced nucleolar translocation of RelA and apoptosis through a common mechanism involving the NH(2)-terminal nucleolar localization signal.	Aspirin	27-34	RELA proto-oncogene, NF-kB subunit	Homo sapiens	93-97
17308107-10	2007	Collectively, these data suggest that aspirin causes inhibition of cyclin D1/CDK4 through the p38 MAPK pathway.	Aspirin	38-45	cyclin D1	Homo sapiens	67-76
17308107-10	2007	Collectively, these data suggest that aspirin causes inhibition of cyclin D1/CDK4 through the p38 MAPK pathway.	Aspirin	38-45	cyclin dependent kinase 4	Homo sapiens	77-81
16914369-0	2007	Effects of aspirin and clopidogrel on plasma brain natriuretic peptide in patients with heart failure receiving ACE inhibitors.	Aspirin	11-18	natriuretic peptide B	Homo sapiens	45-70
16914369-3	2007	AIM: To investigate the effect of aspirin and clopidogrel on brain natriuretic peptide (BNP) levels in HF patients treated with ACE inhibitors.	Aspirin	34-41	natriuretic peptide B	Homo sapiens	61-86
16914369-3	2007	AIM: To investigate the effect of aspirin and clopidogrel on brain natriuretic peptide (BNP) levels in HF patients treated with ACE inhibitors.	Aspirin	34-41	natriuretic peptide B	Homo sapiens	88-91
16914369-8	2007	BNP levels increased in the aspirin group from day 0 to day 14 (107+/-103 to 144+/-149 pg/ml, p=0.04) whereas clopidogrel had no effect (104+/-107 and 97+/-99 pg/ml respectively, p=0.61).	Aspirin	28-35	natriuretic peptide B	Homo sapiens	0-3
16914369-9	2007	CONCLUSION: This study demonstrates an adverse effect of aspirin 325 mg/day on BNP plasma levels in HF patients treated with ACE inhibitors.	Aspirin	57-64	natriuretic peptide B	Homo sapiens	79-82
17073578-9	2006	Kinetic studies determined the type of inhibition of SULT1A1 for three agents (meclofenamate, nimesulide, aspirin) to be non-competitive or partial non-competitive versus both substrate (p-nitrophenol) and cofactor (PAPS).	Aspirin	106-113	sulfotransferase family 1A member 1	Homo sapiens	53-60
17073578-11	2006	The inhibition of SULT1A1 by meclofenamate, nimesulide, salicylate and aspirin may be clinically relevant based on ratio of inhibition constant to predicted in vivo inhibitor concentration ([I]/IC(50) &gt; 1).	Aspirin	71-78	sulfotransferase family 1A member 1	Homo sapiens	18-25
16818512-9	2006	NO-indomethacin at 40 and 80 ppm and NO-aspirin at 3,000 ppm significantly inhibited the colon tumors" (P &lt; 0.01 to P &lt; 0.001) total cyclooxygenase (COX), including COX-2 activity (52-75% inhibition) and formation of prostaglandin E2 (PGE2), PGF2alpha, and 6-keto-PGF1alpha, and TxB2 from arachidonic acid (53-77% inhibition).	Aspirin	40-47	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	171-176
16440541-4	2006	RESULTS: The mean +/- SD values of the semiquantitatively evaluated immunoexpression of ICAM-1, VCAM-1, and VLA-4 were significantly increased in patients with aspirin hypersensitivity compared with aspirin-tolerant patients (1.7 +/- 0.8 vs 0.9 +/- 0.8, P &lt; .003; 1.8 +/- 0.8 vs 0.8 +/- 0.8, P &lt; .001; and 2.2 +/- 0.7 vs 1.3 +/- 0.7, P &lt; .001, respectively), whereas the mean +/- SD values of the expression of lymphocyte function-associated antigen 1 did not differ significantly (2.4 +/- 0.5 vs 2.2 +/- 0.9; P = .57).	Aspirin	160-167	integrin subunit alpha L	Homo sapiens	420-460
16776633-5	2006	The effectiveness of ASA-mediated inhibition of platelet cyclooxygenase-1 was verified by determination of plasma thromboxane B(2) and urine 11-dehydro-thromboxane B(2), accepted as reference assays for monitoring of ASA-mediated platelet cyclooxygenase-1 inhibition.	Aspirin	21-24	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	57-73
16776633-5	2006	The effectiveness of ASA-mediated inhibition of platelet cyclooxygenase-1 was verified by determination of plasma thromboxane B(2) and urine 11-dehydro-thromboxane B(2), accepted as reference assays for monitoring of ASA-mediated platelet cyclooxygenase-1 inhibition.	Aspirin	21-24	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	239-255
16776633-5	2006	The effectiveness of ASA-mediated inhibition of platelet cyclooxygenase-1 was verified by determination of plasma thromboxane B(2) and urine 11-dehydro-thromboxane B(2), accepted as reference assays for monitoring of ASA-mediated platelet cyclooxygenase-1 inhibition.	Aspirin	217-220	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	57-73
17357503-4	2006	QRT-PCR showed that the target gene cyclin D1 mRNA expression was gradually decreased with the dosage of aspirin.	Aspirin	105-112	cyclin D1	Homo sapiens	36-45
17097036-12	2006	CONCLUSION: The mechanism of atherosclerosis suppression by aspirin in cholesterol-fed rabbits is related to the inhibition of COX-2 expression together with the reduced inflammation followed by, but not related to the hypolipidemic effects.	Aspirin	60-67	prostaglandin G/H synthase 2	Oryctolagus cuniculus	127-132
17259670-7	2006	In contrast, aspirin reduced carrageenan-induced paw edema equally in WT and hepatocyte-specific RXRalpha-deficient mice.	Aspirin	13-20	retinoid X receptor alpha	Mus musculus	97-105
16815474-2	2006	The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST).	Aspirin	71-74	glucose-6-phosphate dehydrogenase	Rattus norvegicus	194-227
16815474-2	2006	The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST).	Aspirin	71-74	glucose-6-phosphate dehydrogenase	Rattus norvegicus	229-234
16305586-1	2005	BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid.	Aspirin	15-35	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	54-85
16305586-1	2005	BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid.	Aspirin	15-35	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	87-93
16815474-9	2006	Increased ASA-induced G6PDH activity was recorded in both diabetic and nondiabetic rats.	Aspirin	10-13	glucose-6-phosphate dehydrogenase	Rattus norvegicus	22-27
16305586-1	2005	BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid.	Aspirin	231-251	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	54-85
16305586-1	2005	BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid.	Aspirin	231-251	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	87-93
16815474-10	2006	While both glycation due to diabetic hyperglycemia and ASA-mediated acetylation had very similar effects on the activities of all studied enzymes but G6PDH, we conclude that non-enzymatic modification by either glucose or ASA may be a common mechanism of the observed convergence.	Aspirin	55-58	glucose-6-phosphate dehydrogenase	Rattus norvegicus	150-155
16305586-2	2005	The objective of this study was to assess whether polymorphisms in UGT1A6 and CYP2C9 genes are related to the prevalence of upper gastrointestinal symptoms in cardiovascular patients using acetylsalicylic acid for secondary prevention of ischaemic heart disease.	Aspirin	189-209	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	67-73
16698007-0	2006	The effect of aspirin and vitamins C and E on HbA1c assays.	Aspirin	14-21	hemoglobin subunit alpha 1	Homo sapiens	46-50
16698007-9	2006	ASA induces a modest, not clinically relevant, increase in HbA1c levels with one of the methods.	Aspirin	0-3	hemoglobin subunit alpha 1	Homo sapiens	59-63
16880202-7	2006	Finally, we have shown that aspirin treatment caused changes in the mitochondrial membrane potential, release of cytochrome c from mitochondria, and activation of caspase-9 and -3, which could be because of the proteasomal dysfunction.	Aspirin	28-35	caspase 9	Mus musculus	163-179
16858988-7	2005	The majority of patients had ASA PS 1 and 2.	Aspirin	29-32	taste 2 receptor member 62 pseudogene	Homo sapiens	33-43
16829143-6	2006	On treatment with aspirin, which inhibited the cell-cell contact and network-like structure formation, there was no down regulation of MMPs and cells continued to produce MMP-2 and MMP-9.	Aspirin	18-25	matrix metallopeptidase 2	Homo sapiens	171-176
16104558-0	2005	[Critical events in the operating room among 1,440,776 patients with ASA PS 1 for elective surgery].	Aspirin	69-72	presenilin 1	Homo sapiens	73-77
16104558-5	2005	Among these, 1,440,776 patients with ASA PS 1 for elective surgery were analyzed.	Aspirin	37-40	presenilin 1	Homo sapiens	41-45
15851630-6	2005	Moreover, angiotensin II selectively increased cardiac cyclooxygenase-2 but not cyclooxygenase-1 expression, which was totally prevented by acetylsalicylic acid treatment.	Aspirin	140-160	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	55-71
16977569-12	2006	Heterozygous JAK2 V617F mutation with slightly increased kinase activity is enough for the induction of spontaneous megakaryopoiesis and erythropoiesis, and an increase of hypersensitive platelets is the cause of aspirin-sensitive, platelet-mediated microvascular ischemic and thrombotic complications in ET and early PV mimicking ET.	Aspirin	213-220	Janus kinase 2	Homo sapiens	13-17
15898979-0	2005	Association of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.	Aspirin	79-100	thromboxane A2 receptor	Homo sapiens	15-38
15898979-3	2005	This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA).	Aspirin	103-124	thromboxane A2 receptor	Homo sapiens	61-67
15898979-3	2005	This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA).	Aspirin	126-129	thromboxane A2 receptor	Homo sapiens	61-67
15898979-8	2005	CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T&gt;C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.	Aspirin	121-124	thromboxane A2 receptor	Homo sapiens	59-65
16797247-1	2006	BACKGROUND AND AIMS: Variant genotypes of uridine diphosphate glucuronsyltransferase isoenzyme 1A6 (UGT1A6) associated with decreased metabolic activity have been associated with an enhanced protective effect of aspirin on the development of colorectal adenomas.	Aspirin	212-219	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	42-98
15850829-7	2005	In ET patients receiving aspirin, the increments in f-MLP-induced PMN-CD11b and in PMN-platelet aggregates were significantly lower versus ET subjects not treated with aspirin.	Aspirin	25-32	cysteine and glycine rich protein 3	Homo sapiens	54-57
15850829-7	2005	In ET patients receiving aspirin, the increments in f-MLP-induced PMN-CD11b and in PMN-platelet aggregates were significantly lower versus ET subjects not treated with aspirin.	Aspirin	168-175	cysteine and glycine rich protein 3	Homo sapiens	54-57
16797247-1	2006	BACKGROUND AND AIMS: Variant genotypes of uridine diphosphate glucuronsyltransferase isoenzyme 1A6 (UGT1A6) associated with decreased metabolic activity have been associated with an enhanced protective effect of aspirin on the development of colorectal adenomas.	Aspirin	212-219	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	100-106
15931578-1	2005	Previous investigations have shown that calcitonin gene-related peptide (CGRP) protects gastric mucosa against injury induced by acetylsalicylic acid (ASA) and that rutaecarpine activates vanilloid receptors to evoke CGRP release.	Aspirin	129-149	calcitonin-related polypeptide alpha	Rattus norvegicus	40-71
16816107-6	2006	In in vivo studies low-dose aspirin treatment (6 mg/kg.day) induced SR-BI expression in wild-type and PPAR-alpha knockout mice, respectively, whereas the opposite effect was observed upon high-dose aspirin treatment (60 mg/kg.day) in these animals.	Aspirin	28-35	scavenger receptor class B, member 1	Mus musculus	68-73
15931578-1	2005	Previous investigations have shown that calcitonin gene-related peptide (CGRP) protects gastric mucosa against injury induced by acetylsalicylic acid (ASA) and that rutaecarpine activates vanilloid receptors to evoke CGRP release.	Aspirin	129-149	calcitonin-related polypeptide alpha	Rattus norvegicus	73-77
15931578-1	2005	Previous investigations have shown that calcitonin gene-related peptide (CGRP) protects gastric mucosa against injury induced by acetylsalicylic acid (ASA) and that rutaecarpine activates vanilloid receptors to evoke CGRP release.	Aspirin	151-154	calcitonin-related polypeptide alpha	Rattus norvegicus	40-71
15931578-1	2005	Previous investigations have shown that calcitonin gene-related peptide (CGRP) protects gastric mucosa against injury induced by acetylsalicylic acid (ASA) and that rutaecarpine activates vanilloid receptors to evoke CGRP release.	Aspirin	151-154	calcitonin-related polypeptide alpha	Rattus norvegicus	73-77
16816107-7	2006	We could show that COX-independent effects of aspirin were able to enhance expression of SR-BI in macrophages in a post-transcriptional, PPAR-alpha independent way, suggesting a novel pharmacologic effect of aspirin.	Aspirin	46-53	cytochrome c oxidase subunit 8A	Homo sapiens	19-22
16816107-7	2006	We could show that COX-independent effects of aspirin were able to enhance expression of SR-BI in macrophages in a post-transcriptional, PPAR-alpha independent way, suggesting a novel pharmacologic effect of aspirin.	Aspirin	208-215	cytochrome c oxidase subunit 8A	Homo sapiens	19-22
15814734-8	2005	COX-2-derived products increased levels of the proresolving lipid mediators lipoxin A4 (LXA4) and, in the presence of aspirin, 15-epi-LXA4.	Aspirin	118-125	prostaglandin-endoperoxide synthase 2	Mus musculus	0-5
16600694-5	2006	The results showed that (i) aspirin, fenofibrate and clofibrate decrease significantly the MCP-1 expression and secretion in human endothelial cells; (ii) the high glucose up-regulated expression of MCP-1 in endothelial cells was significantly reduced by inhibitors of NF-kB and reactive oxygen species; (iii) all drugs notably decrease the level of the reactive oxygen species and activation of NF-kB and AP-1.	Aspirin	28-35	jun proto-oncogene	Mus musculus	406-410
15755648-8	2005	A molecular modeling (docking) study indicated that the SO(2)NHCOCH(3) substituent present in N-acetyl-2-carboxy-4-(2,4-fluorophenyl)benzenesulfonamide, like the acetoxy substituent in aspirin, is suitably positioned to acetylate the Ser(530) hydroxyl group in the COX-2 primary binding site.	Aspirin	185-192	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	265-270
16886565-2	2006	The aim of the study was to investigate the influence of NSAIDs on nitric oxide synthesis and releasing to bloodstream Acetylsalicic acid (ASA) and diclofenac as COX-1 and COX-2 inhibitors and nimesulide as selective COX-2 inhibitor were used in study.	Aspirin	139-142	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	217-222
15546949-7	2005	Src family tyrosine kinase inhibitors also inhibited platelet aggregation and decreased the PAC-1 binding caused by costimulation of G(i) and G(z) signaling pathways in aspirin-treated platelets.	Aspirin	169-176	dual specificity phosphatase 2	Homo sapiens	92-97
15769457-10	2005	The PGE(2) receptors implicated in CD36 modulation by ASA are the EP2/EP4 subtypes.	Aspirin	54-57	prostaglandin E receptor 2	Homo sapiens	66-69
16673274-3	2006	Inhibition of platelet cyclooxygenase-1 by aspirin is followed by relief of microvascular disturbances; correction of shortened platelet survival; correction of increased plasma beta-TG, PF4, and TM levels; and correction of increased TXB2 excretion to normal.	Aspirin	43-50	pro-platelet basic protein	Homo sapiens	178-185
16601836-10	2006	Aspirin treatment reduced PGI-M already at the lowest dosage (by approximately 25%), but PGI-M excretion and platelet aggregability were not correlated.	Aspirin	0-7	glucose-6-phosphate isomerase	Homo sapiens	26-29
16310244-7	2006	The data also showed that NF-kappaB activation and its associated gene expressions, such as COX-2, iNOS, VCAM-1 and ICAM-1, were all suppressed by the low dose aspirin supplementation through the inhibition of phosphorylation and degradation of IkappaBalpha via the NIK/IKK pathway.	Aspirin	160-167	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	92-97
16310244-7	2006	The data also showed that NF-kappaB activation and its associated gene expressions, such as COX-2, iNOS, VCAM-1 and ICAM-1, were all suppressed by the low dose aspirin supplementation through the inhibition of phosphorylation and degradation of IkappaBalpha via the NIK/IKK pathway.	Aspirin	160-167	vascular cell adhesion molecule 1	Rattus norvegicus	105-111
16310244-8	2006	Our molecular exploration further revealed that aspirin"s suppressive action of NF-kappaB was mediated by its ability to inhibit the nuclear translocation of cytosolic thioredoxin and redox factor-1.	Aspirin	48-55	apurinic/apyrimidinic endodeoxyribonuclease 1	Rattus norvegicus	184-198
16943621-0	2006	Aspirin interaction with ribonuclease A.	Aspirin	0-7	ribonuclease A family member 1, pancreatic	Homo sapiens	25-39
16804302-0	2006	Oral but not parenteral aspirin upregulates COX-2 expression in rat stomachs.	Aspirin	24-31	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	44-49
16804302-6	2006	ASA induced both damage and COX-2 expression in the stomach when given p.o.	Aspirin	0-3	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	28-33
16179345-5	2005	As quantified by fluorescence-activated cell sorting analysis in whole blood, aspirin, but not its metabolite salicylic acid, induced dose-dependent shedding of human and murine GPIbalpha and GPV from the platelet surface, whereas other glycoproteins remained unaffected by this treatment.	Aspirin	78-85	glycoprotein 1b, alpha polypeptide	Mus musculus	178-187
16179345-8	2005	Shed fragments of GPIbalpha and GPV were elevated in the plasma of aspirin-injected mice compared with animals injected with control buffer.	Aspirin	67-74	glycoprotein 1b, alpha polypeptide	Mus musculus	18-27
16179345-9	2005	These data demonstrate that aspirin at high concentrations induces shedding of GPIbalpha and GPV by an ADAM17-dependent mechanism and that this process can occur in vivo.	Aspirin	28-35	glycoprotein 1b, alpha polypeptide	Mus musculus	79-88
16216591-0	2005	Aspirin inhibits thrombin action on endothelial cells via up-regulation of aminopeptidase N/CD13 expression.	Aspirin	0-7	alanyl aminopeptidase, membrane	Homo sapiens	75-91
16216591-0	2005	Aspirin inhibits thrombin action on endothelial cells via up-regulation of aminopeptidase N/CD13 expression.	Aspirin	0-7	alanyl aminopeptidase, membrane	Homo sapiens	92-96
17595529-8	2007	COX-2, evaluated with mRNA and protein expression, was significantly augmented in aspirin group compared with others.	Aspirin	82-89	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-5
16216591-2	2005	METHODS AND RESULTS: Using enhanced subtraction hybridization analysis, we found in human umbilical vein endothelial cells (HUVECs) that aspirin up-regulates the expression of aminopeptidase N (APN/CD13) mRNA and its surface protein levels in a dose-dependent manner.	Aspirin	137-144	alanyl aminopeptidase, membrane	Homo sapiens	176-192
16216591-2	2005	METHODS AND RESULTS: Using enhanced subtraction hybridization analysis, we found in human umbilical vein endothelial cells (HUVECs) that aspirin up-regulates the expression of aminopeptidase N (APN/CD13) mRNA and its surface protein levels in a dose-dependent manner.	Aspirin	137-144	alanyl aminopeptidase, membrane	Homo sapiens	194-197
16216591-2	2005	METHODS AND RESULTS: Using enhanced subtraction hybridization analysis, we found in human umbilical vein endothelial cells (HUVECs) that aspirin up-regulates the expression of aminopeptidase N (APN/CD13) mRNA and its surface protein levels in a dose-dependent manner.	Aspirin	137-144	alanyl aminopeptidase, membrane	Homo sapiens	198-202
16216591-3	2005	Enzymatic activity of APN/CD13 on HUVECs was increased approximately 1.5-fold by 1 mmol L(-1) of aspirin, and treatment with bestatin, an inhibitor for APN/CD13 metalloprotease activity, attenuated the enhanced activities of APN/CD13.	Aspirin	97-104	alanyl aminopeptidase, membrane	Homo sapiens	22-25
16216591-3	2005	Enzymatic activity of APN/CD13 on HUVECs was increased approximately 1.5-fold by 1 mmol L(-1) of aspirin, and treatment with bestatin, an inhibitor for APN/CD13 metalloprotease activity, attenuated the enhanced activities of APN/CD13.	Aspirin	97-104	alanyl aminopeptidase, membrane	Homo sapiens	26-30
16216591-3	2005	Enzymatic activity of APN/CD13 on HUVECs was increased approximately 1.5-fold by 1 mmol L(-1) of aspirin, and treatment with bestatin, an inhibitor for APN/CD13 metalloprotease activity, attenuated the enhanced activities of APN/CD13.	Aspirin	97-104	alanyl aminopeptidase, membrane	Homo sapiens	152-155
18332613-0	2007	Reverse effect of aspirin: is the prothrombotic effect after aspirin discontinuation mediated by cyclooxygenase 2 inhibition?	Aspirin	18-25	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	97-113
16216591-3	2005	Enzymatic activity of APN/CD13 on HUVECs was increased approximately 1.5-fold by 1 mmol L(-1) of aspirin, and treatment with bestatin, an inhibitor for APN/CD13 metalloprotease activity, attenuated the enhanced activities of APN/CD13.	Aspirin	97-104	alanyl aminopeptidase, membrane	Homo sapiens	152-155
18332613-2	2007	OBJECTIVES: We hypothesized that infinitesimal concentrations of aspirin could persist in plasma after its discontinuation, thereby inducing a prothrombotic effect that could be due to a modification in the mechanism of action of aspirin via the cyclooxygenase 1 (COX-1) and COX-2 pathways.	Aspirin	65-72	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	246-262
18332613-2	2007	OBJECTIVES: We hypothesized that infinitesimal concentrations of aspirin could persist in plasma after its discontinuation, thereby inducing a prothrombotic effect that could be due to a modification in the mechanism of action of aspirin via the cyclooxygenase 1 (COX-1) and COX-2 pathways.	Aspirin	65-72	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	264-269
16216591-6	2005	CONCLUSIONS: Aspirin may exert its anti-atherothrombotic effects in part via the inhibition of thrombin action by up-regulating APN/CD13 on endothelial cells.	Aspirin	13-20	alanyl aminopeptidase, membrane	Homo sapiens	128-131
18332613-2	2007	OBJECTIVES: We hypothesized that infinitesimal concentrations of aspirin could persist in plasma after its discontinuation, thereby inducing a prothrombotic effect that could be due to a modification in the mechanism of action of aspirin via the cyclooxygenase 1 (COX-1) and COX-2 pathways.	Aspirin	65-72	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	275-280
18332613-2	2007	OBJECTIVES: We hypothesized that infinitesimal concentrations of aspirin could persist in plasma after its discontinuation, thereby inducing a prothrombotic effect that could be due to a modification in the mechanism of action of aspirin via the cyclooxygenase 1 (COX-1) and COX-2 pathways.	Aspirin	230-237	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	246-262
16216591-6	2005	CONCLUSIONS: Aspirin may exert its anti-atherothrombotic effects in part via the inhibition of thrombin action by up-regulating APN/CD13 on endothelial cells.	Aspirin	13-20	alanyl aminopeptidase, membrane	Homo sapiens	132-136
18332613-2	2007	OBJECTIVES: We hypothesized that infinitesimal concentrations of aspirin could persist in plasma after its discontinuation, thereby inducing a prothrombotic effect that could be due to a modification in the mechanism of action of aspirin via the cyclooxygenase 1 (COX-1) and COX-2 pathways.	Aspirin	230-237	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	264-269
18332613-2	2007	OBJECTIVES: We hypothesized that infinitesimal concentrations of aspirin could persist in plasma after its discontinuation, thereby inducing a prothrombotic effect that could be due to a modification in the mechanism of action of aspirin via the cyclooxygenase 1 (COX-1) and COX-2 pathways.	Aspirin	230-237	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	275-280
16279562-6	2005	RESULTS: When compared with AERD patients who received no controller medications, the combined use of LTMDs, inhaled corticosteroids, and long-acting beta2-agonists led to a statistically significant change in aspirin challenge outcomes (P = .009), mainly shifting the reaction from a classic upper and lower respiratory tract reaction to naso-ocular reactions only.	Aspirin	210-217	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	150-155
17219690-4	2006	Unlike immature dendritic cells, aspirin DCs are resistant to the effects of maturational stimuli, as determined by low levels of CD40, CD80, CD83 and CD86 expression.	Aspirin	33-40	CD40 molecule	Homo sapiens	130-134
17219690-4	2006	Unlike immature dendritic cells, aspirin DCs are resistant to the effects of maturational stimuli, as determined by low levels of CD40, CD80, CD83 and CD86 expression.	Aspirin	33-40	CD86 molecule	Homo sapiens	151-155
17221106-1	2006	The daily use of aspirin in patients with type 2 diabetes mellitus (DM2) reduces significantly cardiovascular events (CVE).	Aspirin	17-24	immunoglobulin heavy diversity 1-14 (non-functional)	Homo sapiens	68-71
17221106-2	2006	In the absence of contraindications, American Diabetes Association (ADA) recommends the use of aspirin to all DM2 patients older than 40 years of age.	Aspirin	95-102	immunoglobulin heavy diversity 1-14 (non-functional)	Homo sapiens	110-113
17221106-10	2006	Strategies to enhance the use of aspirin should be developed to reduce the morbidity and mortality from cardiovascular diseases in patients with DM2.	Aspirin	33-40	immunoglobulin heavy diversity 1-14 (non-functional)	Homo sapiens	145-148
16943252-8	2006	Consistent with the tissue distribution of two carboxylesterases human carboxylesterase (HCE) 1 and HCE2, recombinant HCE1 hydrolyzed clopidogrel, whereas recombinant HCE2 hydrolyzed aspirin.	Aspirin	183-190	carboxylesterase 1	Homo sapiens	118-122
17074929-3	2006	Activation of IRF3 by viral infection in vivo greatly enhances bile acid- and aspirin-induced hepatotoxicity.	Aspirin	78-85	interferon regulatory factor 3	Homo sapiens	14-18
17097036-10	2006	The expression of COX-2 and macrophage in plaque of the aspirin treated group were decreased compared with that in untreated cholesterol-fed group.	Aspirin	56-63	prostaglandin G/H synthase 2	Oryctolagus cuniculus	18-23
17085674-2	2006	Functional polymorphisms of UGT1A6 (T181A and R184S) and CYP2C9 (R144C and I359L) have been reported to modify the protective effect of aspirin on colorectal adenoma risk.	Aspirin	136-143	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	28-34
17085674-7	2006	When patients were stratified by genotype and aspirin intervention, those with variant UGT1A6 alleles were at reduced recurrence risk irrespective of whether they received aspirin or placebo (RR, 0.62; 95% CI, 0.42-0.92 and RR, 0.63; 95% CI, 0.44-0.91, respectively).	Aspirin	46-53	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	87-93
17047198-0	2006	Ornithine decarboxylase polymorphism modification of response to aspirin treatment for colorectal adenoma prevention.	Aspirin	65-72	ornithine decarboxylase 1	Homo sapiens	0-23
17047198-1	2006	BACKGROUND: Previous research suggests that the G315A single-nucleotide polymorphism in the ornithine decarboxylase (ODC) gene may be a genetic marker for risk of colorectal neoplasia and may also modify the association of aspirin use with risk.	Aspirin	223-230	ornithine decarboxylase 1	Homo sapiens	92-115
17047198-1	2006	BACKGROUND: Previous research suggests that the G315A single-nucleotide polymorphism in the ornithine decarboxylase (ODC) gene may be a genetic marker for risk of colorectal neoplasia and may also modify the association of aspirin use with risk.	Aspirin	223-230	ornithine decarboxylase 1	Homo sapiens	117-120
17047198-11	2006	CONCLUSION: ODC genotype may modify the response to aspirin treatment for colorectal adenoma prevention.	Aspirin	52-59	ornithine decarboxylase 1	Homo sapiens	12-15
16869801-3	2006	We demonstrate that in aspirin-treated human DCs, there is reduced expression of CD1a, HLA-DR and CD86, up-regulation of ILT-3 expression and marginal increases in PDL-1.	Aspirin	23-30	CD1a molecule	Homo sapiens	81-85
16869801-3	2006	We demonstrate that in aspirin-treated human DCs, there is reduced expression of CD1a, HLA-DR and CD86, up-regulation of ILT-3 expression and marginal increases in PDL-1.	Aspirin	23-30	CD86 molecule	Homo sapiens	98-102
16861926-0	2006	Nitrogen oxide-releasing aspirin induces histone H2AX phosphorylation, ATM activation and apoptosis preferentially in S-phase cells: involvement of reactive oxygen species.	Aspirin	25-32	H2A.X variant histone	Homo sapiens	49-53
16861926-4	2006	We observed that even brief (1 h) treatment of human B-lymphoblastoid TK6 cells with &gt;or=5 microM NO-ASA led to DNA damage revealed by the alkaline and neutral comet assays, histone H2AX phosphorylation on Ser 139, and ATM phosphorylation on Ser 1981, a marker of activation of this kinase.	Aspirin	104-107	H2A.X variant histone	Homo sapiens	185-189
16861926-8	2006	The induction of phosphorylation of H2AX on Ser 139 by NO-ASA was markedly attenuated in the presence of N-acetyl-L-cysteine, a scavenger of reactive oxygen species (ROS).	Aspirin	58-61	H2A.X variant histone	Homo sapiens	36-40
16895542-10	2006	Western blot analysis demonstrated that the protein level of phosphorylated beta-catenin increased, whereas that of cyclin D1 decreased, after treatment of MSC with aspirin.	Aspirin	165-172	cyclin D1	Homo sapiens	116-125
16476694-0	2006	Pharmacodynamics, pharmacokinetics, and safety of the oral reversible P2Y12 antagonist AZD6140 with aspirin in patients with atherosclerosis: a double-blind comparison to clopidogrel with aspirin.	Aspirin	100-107	purinergic receptor P2Y12	Homo sapiens	70-75
16460959-15	2006	It could be stressed that aspirin, unlike other non-selective and selective COX-2 inhibitors increases the risk of the abdominal wall defects, which are observed more often in growth-retarded fetuses.	Aspirin	26-33	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	76-81
16262603-0	2006	Induction of spermidine/spermine N1-acetyltransferase (SSAT) by aspirin in Caco-2 colon cancer cells.	Aspirin	64-71	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	13-53
16262603-0	2006	Induction of spermidine/spermine N1-acetyltransferase (SSAT) by aspirin in Caco-2 colon cancer cells.	Aspirin	64-71	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	55-59
16262603-3	2006	In the present study, we show that a variety of NSAIDs, including aspirin, sulindac, ibuprofen and indomethacin, can induce SSAT gene expression in Caco-2 cells.	Aspirin	66-73	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	124-128
16262603-4	2006	Aspirin, at physiological concentrations, can induce SSAT mRNA via transcriptional initiation mechanisms.	Aspirin	0-7	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	53-57
16262603-8	2006	Aspirin treatment led to the activation of NF-kappaB signalling and increased binding at these NF-kappaB sites in the SSAT promoter, hence providing a potential mechanism for the induction of SSAT by aspirin in these cells.	Aspirin	0-7	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	118-122
16262603-8	2006	Aspirin treatment led to the activation of NF-kappaB signalling and increased binding at these NF-kappaB sites in the SSAT promoter, hence providing a potential mechanism for the induction of SSAT by aspirin in these cells.	Aspirin	0-7	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	192-196
16262603-8	2006	Aspirin treatment led to the activation of NF-kappaB signalling and increased binding at these NF-kappaB sites in the SSAT promoter, hence providing a potential mechanism for the induction of SSAT by aspirin in these cells.	Aspirin	200-207	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	118-122
16262603-8	2006	Aspirin treatment led to the activation of NF-kappaB signalling and increased binding at these NF-kappaB sites in the SSAT promoter, hence providing a potential mechanism for the induction of SSAT by aspirin in these cells.	Aspirin	200-207	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	192-196
16262603-9	2006	Aspirin-induced SSAT ultimately leads to a decrease in cellular polyamine content, which has been associated with decreased carcinogenesis.	Aspirin	0-7	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	16-20
16262603-10	2006	These results suggest that activation of SSAT by aspirin and different NSAIDs may be a common property of NSAIDs that plays an important role in their chemopreventive actions in colorectal cancer.	Aspirin	49-56	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	41-45
16444599-3	2006	Non-steroidal anti-inflammatory drugs (NSAIDS), piroxicam, aspirin, ibuprofen, naproxen and celecoxib all specifically inhibited tNOX activity of HeLa (human cervical carcinoma) and BT-20 (human mammary carcinoma) cells (IC(50) in the nanomolar range) without effect on ECTO-NOX activities of non-cancer MCF-10A mammary epithelial cells.	Aspirin	59-66	tripartite motif containing 33	Homo sapiens	270-274
16395490-4	2005	42 (75%) of the women had another IVF-attempt after this haemostaseological evaluation and received low molecular weight heparin and/ or acetylsalicylic acid in the case of positivity for APC-resistance, lupus anticoagulant or antibodies against annexin V, cardiolipin or beta(2)-glycoprotein-1.	Aspirin	137-157	APC regulator of WNT signaling pathway	Homo sapiens	188-191
15976387-9	2005	Additionally, increased expression of the oxidative phosphorylation enzyme COX IV was observed in mitochondrial fractions exposed to ASA at concentrations &gt;5 mM.	Aspirin	133-136	cytochrome c oxidase subunit 4I1	Homo sapiens	75-81
15782500-11	2005	Meanwhile, aspirin, clopidogrel, and their combination also decreased serum CRP (P &lt; 0.05-0.01), without affecting lipid levels.	Aspirin	11-18	C-reactive protein	Oryctolagus cuniculus	76-79
15782500-12	2005	There was a trend, not significantly, to lower serum C-reactive protein in group B compared with group A or group C. CONCLUSIONS: Aspirin and clopidogrel inhibit neointimal proliferation and prevent the development of atherosclerosis with equivalent effects.	Aspirin	130-137	C-reactive protein	Oryctolagus cuniculus	53-71
15358635-8	2005	On the other hand, aspirin and NS398 significantly decreased MIF protein and mRNA expression, and completely blocked bile acid-induced MIF synthesis in the presence or absence of prostaglandin E(2).	Aspirin	19-26	macrophage migration inhibitory factor	Homo sapiens	61-64
15358635-8	2005	On the other hand, aspirin and NS398 significantly decreased MIF protein and mRNA expression, and completely blocked bile acid-induced MIF synthesis in the presence or absence of prostaglandin E(2).	Aspirin	19-26	macrophage migration inhibitory factor	Homo sapiens	135-138
15358635-10	2005	Whereas bile acids induce MIF expression in ESCC cells, aspirin and NS398 significantly inhibit MIF expression, even in the presence of bile acids, via a COX-independent mechanism.	Aspirin	56-63	macrophage migration inhibitory factor	Homo sapiens	96-99
15297470-6	2004	Although all treatments, including celecoxib, were effective in reducing gastric PGE2 synthesis, administering arthritic rats with ASA resulted in a significant increase in gastric content of aspirin-triggered lipoxin (ATL), a COX-2-derived lipid mediator that regulates proinflammatory responses at the neutrophils/endothelial interface.	Aspirin	131-134	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	227-232
15371279-13	2004	We postulate that NOS and COX-2 act together to contribute to retinal cell death in diabetes and to the development of diabetic retinopathy and that inhibition of retinopathy by aminoguanidine or aspirin is due at least in part to inhibition of this NO/COX-2 axis.	Aspirin	196-203	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	253-258
15482377-1	2004	Recent in vitro studies, clinical trials and epidemiological studies have suggested possible interactions between aspirin and other cyclo-oxygenase (COX) inhibitors, such as ibuprofen of the COX-2 inhibitors celecoxib and rofecoxib.	Aspirin	114-121	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	191-196
15447849-0	2004	[Aspirin inhibits proliferation and expression of p44/42 MAPK phosphorylation in vascular endothelial cells].	Aspirin	1-8	interferon induced protein 44	Homo sapiens	50-53
15447849-7	2004	The expression of phosphorylated p44/42 MAPK protein was significantly inhibited by aspirin.	Aspirin	84-91	interferon induced protein 44	Homo sapiens	33-36
16039999-3	2005	Incubation with aspirin inhibited senescence-associated beta-galactosidase activity and increased telomerase activity.	Aspirin	16-23	galactosidase beta 1	Homo sapiens	56-74
15379229-0	2004	ASA--Advanced Source Analysis of continuous and event-related EEG/MEG signals.	Aspirin	0-3	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	66-69
15236176-6	2004	Aspirin/HCl, in comparison to saline or HCl alone, induced a 4-6-fold increase in gastric mucosal prostaglandin E(2) concentration in the cyclooxygenase-1 knockout mice, whereas it decreased prostaglandin E(2) levels in wild-type and cyclooxygenase-2 knockout mice.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Mus musculus	234-250
15236176-7	2004	This paradoxical aspirin-induced increase in gastric prostaglandin E(2) in cyclooxygenase-1 knockout mice seemed to correspond to an increase in cyclooxygenase-2 messenger RNA and protein expression.	Aspirin	17-24	prostaglandin-endoperoxide synthase 2	Mus musculus	145-161
15236176-11	2004	Aspirin seems to paradoxically increase the gastric mucosal prostaglandin E(2) concentration in cyclooxygenase-1 knockout mice, possibly by the induction of cyclooxygenase-2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Mus musculus	157-173
16364202-0	2005	Inhibitory effect of acetylsalicylic acid on matrix metalloproteinase - 2 activity in human endothelial cells exposed to high glucose.	Aspirin	21-41	matrix metallopeptidase 2	Homo sapiens	45-73
16151033-8	2005	In contrast, therapy with C+ASA resulted in a significant inhibition of platelet activity assessed by ADP- (P=0.00001) and collagen-induced (P=0.02) aggregation; closure time prolongation (P=0.03), and reduction of platelet activation units with Ultegra (P=0.00001); expression of PECAM-1 (P=0.01), and GP IIb/IIIa activity with PAC-1 (P=0.02) when compared with ASA group.	Aspirin	28-31	platelet and endothelial cell adhesion molecule 1	Homo sapiens	281-288
15988014-4	2005	We demonstrate that the RelA component of NF-kappaB is sequestered in the nucleolus in response to the proapoptotic NF-kappaB stimuli aspirin, serum withdrawal, and UV-C radiation.	Aspirin	134-141	RELA proto-oncogene, NF-kB subunit	Homo sapiens	24-28
14746947-9	2004	CONCLUSION: These limited data give some support to the potential favourable effect of early treatment with ASA in pregnant women at risk of PIH and IUGR.	Aspirin	108-111	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	141-144
15345481-5	2005	Inhibition of COX-2 by acetyl salicylic acid (1 mM), NS-398 (5 microM), or celecoxib (3 microM) abolished the increase in cAMP and markedly reduced alpha(2C)-AR induction in response to serum stimulation.	Aspirin	23-44	adrenoceptor alpha 2C	Homo sapiens	148-160
14965321-4	2004	COX enzymes are clinically important because they are inhibited by aspirin and numerous other non-steroidal anti-inflammatory drugs.	Aspirin	67-74	cytochrome c oxidase subunit 8A	Homo sapiens	0-3
14965321-7	2004	During the past forty years systematic advances in our understanding of the structure, regulation and function of COX isoenzymes have enabled the design and synthesis of COX-2 selective inhibitors as agents intended to lessen the gastrointestinal irritation of aspirin and non-selective NSAIDs.	Aspirin	261-268	cytochrome c oxidase subunit 8A	Homo sapiens	114-117
16125378-0	2005	Anti-inflammatory circuitry: lipoxin, aspirin-triggered lipoxins and their receptor ALX.	Aspirin	38-45	hematopoietic SH2 domain containing	Homo sapiens	84-87
18970138-1	2005	PLS-1, a variant of the partial least-squares algorithm was used for the solid-phase spectrofluorimetric determination of acetylsalicylic acid (ASA) and caffeine (CF) in pharmaceutical formulations.	Aspirin	122-142	plastin 1	Homo sapiens	0-5
15489888-1	2004	Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin have been shown to suppress transcription factor NF-kappaB, which controls the expression of genes such as cyclooxygenase (COX)-2 and cyclin D1, leading to inhibition of proliferation of tumor cells.	Aspirin	54-61	cyclin D1	Homo sapiens	196-205
18970138-1	2005	PLS-1, a variant of the partial least-squares algorithm was used for the solid-phase spectrofluorimetric determination of acetylsalicylic acid (ASA) and caffeine (CF) in pharmaceutical formulations.	Aspirin	144-147	plastin 1	Homo sapiens	0-5
18970138-7	2005	The final PLS-1 models were used for the determination of ASA and CF in pharmaceutical formulations.	Aspirin	58-61	plastin 1	Homo sapiens	10-15
12960371-2	2003	Selective COX-2 inhibitors block ATL formation and exacerbate mucosal injury in rats treated with aspirin.	Aspirin	98-105	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	10-15
12913786-9	2003	P2Y(12) antagonists in combination with anticoagulants (thrombin inhibitors, factor Xa inhibitors) act synergistically in inhibiting thrombus formation (similar to aspirin) ex vivo.	Aspirin	164-171	purinergic receptor P2Y12	Homo sapiens	0-7
15581743-8	2004	Aspirin and nonsteroidal anti-inflammatory drugs inhibit gallbladder mucin secretion and prevent gallstone formation in animal models.	Aspirin	0-7	LOC100508689	Homo sapiens	69-74
15326064-5	2004	When ATL synthesis was inhibited by pretreatment with a selective cyclooxygenase-2 inhibitor (celecoxib) or a 5-lipoxygenase inhibitor (zileuton), the aspirin-induced increase in BP was significantly augmented.	Aspirin	151-158	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	66-82
12709408-1	2003	In addition to inhibiting formation of prothrombotic eicosanoids, aspirin causes the acetylation of cyclooxygenase (COX)-2.	Aspirin	66-73	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	100-122
12709408-2	2003	The acetylated COX-2 remains active, and upon cell activation, initiates the generation of 15R-HETE, a lipid substrate for 5-lipoxygenase (LOX) leading to the formation of 15-epi-LXA4 (also termed "aspirin-triggered lipoxin," or ATL).	Aspirin	198-205	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	15-20
12813129-10	2003	Unexpectedly, GSK-3beta was also phosphorylated upon aspirin treatment in six colorectal cancer cell lines.	Aspirin	53-60	glycogen synthase kinase 3 beta	Homo sapiens	14-23
15199473-4	2003	Aspirin and salicylate at therapeutic concentrations inhibit COX-2 protein expression through interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2 promoter/enhancer.	Aspirin	0-7	CCAAT enhancer binding protein beta	Homo sapiens	123-158
15199473-4	2003	Aspirin and salicylate at therapeutic concentrations inhibit COX-2 protein expression through interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2 promoter/enhancer.	Aspirin	0-7	CCAAT enhancer binding protein beta	Homo sapiens	160-169
15199473-7	2003	These recent studies provide new insight into the pharmacological actions of aspirin and salicylate preparations and implicate C/EBPbeta as a potential target for therapy of inflammation and tissue injury.	Aspirin	77-84	CCAAT enhancer binding protein beta	Homo sapiens	127-136
15817699-9	2005	These observations provide insight into the association between hypertension and acute coronary syndrome and a possible mechanism by which Ang-converting enzyme inhibitor and aspirin may reduce the risk for heart attacks.	Aspirin	175-182	angiogenin	Homo sapiens	139-142
15988014-8	2005	Furthermore, we show that the retention of RelA in the nucleoplasm inhibits this decrease in NF-kappaB-driven transcription and blocks apoptosis induced by aspirin and UV-C radiation.	Aspirin	156-163	RELA proto-oncogene, NF-kB subunit	Homo sapiens	43-47
15481331-5	2004	Accordingly, the role of caspases in aspirin-induced apoptosis was also evaluated.	Aspirin	37-44	caspase 8	Homo sapiens	25-33
15778399-9	2005	Moreover, aspirin-triggered lipoxin A(4) analog evoked release of the antiphlogistic cytokine TGF-beta.	Aspirin	10-17	transforming growth factor, beta 1	Mus musculus	94-102
15481331-8	2004	We conclude that physiologically relevant concentrations of aspirin induces apoptosis in human gastric cells through a caspase-mediated mechanism.	Aspirin	60-67	caspase 8	Homo sapiens	119-126
15763433-7	2005	This observation suggests a possible COX-mediated anti-inflammatory effect of low-dose aspirin, which should be further confirmed by intervention studies.	Aspirin	87-94	cytochrome c oxidase subunit 8A	Homo sapiens	37-40
15236338-8	2004	On two-dimensional Western blots, human anti-sperm antibodies (ASA) and rabbit anti-P36 antibodies recognized five to six isoforms of P36, all 36/37 kDa in size, with a pI between 5.1 and 5.7.	Aspirin	63-66	5'-nucleotidase, cytosolic IIIA	Homo sapiens	134-137
15770010-1	2005	Genetic variation in the uridine diphosphate glucuronosyltransferase 1A6 (UGT1A6) enzyme is associated with impaired metabolism of aspirin.	Aspirin	131-138	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	25-72
15770010-1	2005	Genetic variation in the uridine diphosphate glucuronosyltransferase 1A6 (UGT1A6) enzyme is associated with impaired metabolism of aspirin.	Aspirin	131-138	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	74-80
14665439-0	2004	Aspirin, but not NO-releasing aspirin (NCX-4016), interacts with selective COX-2 inhibitors to aggravate gastric damage and inflammation.	Aspirin	0-7	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	75-80
15770010-8	2005	Thus, functional polymorphisms in the UGT1A6 enzyme statistically significantly modify the effect of aspirin on colorectal neoplasia, and certain subsets of the population, defined by genotype, may obtain differential benefit from aspirin chemoprevention.	Aspirin	101-108	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	38-44
15770010-8	2005	Thus, functional polymorphisms in the UGT1A6 enzyme statistically significantly modify the effect of aspirin on colorectal neoplasia, and certain subsets of the population, defined by genotype, may obtain differential benefit from aspirin chemoprevention.	Aspirin	231-238	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	38-44
14665439-1	2004	Aceylation of cyclooxygenase (COX)-2 by aspirin can trigger the formation of 15(R)-epilipoxin A4, or aspirin-triggered lipoxin (ATL).	Aspirin	40-47	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	14-36
14665439-1	2004	Aceylation of cyclooxygenase (COX)-2 by aspirin can trigger the formation of 15(R)-epilipoxin A4, or aspirin-triggered lipoxin (ATL).	Aspirin	101-108	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	14-36
14665439-3	2004	Selective COX-2 inhibitors block ATL synthesis and exacerbate aspirin-induced gastric damage.	Aspirin	62-69	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	10-15
12943528-11	2004	Aspirin treatment stimulated caspase-3 activity.	Aspirin	0-7	caspase 3	Rattus norvegicus	29-38
15726594-3	2005	Despite these in vitro and ex vivo findings, we observed two patients develop acute HIT while receiving both clopidogrel and aspirin: both patients" sera tested strongly positive in a heparin-dependent washed platelet activation assay (100% serotonin release) and PF4/heparin-enzyme-immunoassay (2.594 and 2.190 absorbance units).	Aspirin	125-132	platelet factor 4	Homo sapiens	264-267
15579484-0	2005	Activation of the caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric cancer.	Aspirin	52-59	caspase 8	Homo sapiens	18-27
15579484-7	2005	We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release.	Aspirin	15-22	caspase 8	Homo sapiens	33-42
15579484-10	2005	In conclusion, our results identify a role of caspase-8/Bid and activation of Bax as a novel mechanism for aspirin-induced apoptosis in gastric cancer.	Aspirin	107-114	caspase 8	Homo sapiens	46-55
15784113-0	2005	The human leucocyte antigen-DRB1*1302-DQB1*0609-DPB1*0201 haplotype may be a strong genetic marker for aspirin-induced urticaria.	Aspirin	103-110	major histocompatibility complex, class II, DP beta 1	Homo sapiens	48-52
15784113-7	2005	In haplotype analysis, the HLA-DRB1(*)1302-DQB1(*)0609-DPB1(*)0201 was significantly higher in the aspirin-induced urticaria (8.0%) than in the aspirin-intolerant asthma (0.7%, P=0.0014) and normal controls (2.0%, P=0.0006).	Aspirin	99-106	major histocompatibility complex, class II, DP beta 1	Homo sapiens	55-59
15784113-8	2005	CONCLUSION: These findings suggest that the HLA-DRB1(*)1302-DQB1(*)0609-DPB1(*)0201 may be a strong genetic marker to determine the aspirin-induced urticaria phenotype.	Aspirin	132-139	major histocompatibility complex, class II, DP beta 1	Homo sapiens	72-76
14566053-5	2003	The IC50 values for Beta-catenin/TCF-4-signaling inhibition by NO-ASA were: o-, 2.6 +/- 0.4; m-, 15 +/- 5; p-, 1.1 +/- 0.1 microM; and for ASA, &gt;5,000 microM.	Aspirin	66-69	transcription factor 4	Homo sapiens	33-38
14566053-5	2003	The IC50 values for Beta-catenin/TCF-4-signaling inhibition by NO-ASA were: o-, 2.6 +/- 0.4; m-, 15 +/- 5; p-, 1.1 +/- 0.1 microM; and for ASA, &gt;5,000 microM.	Aspirin	139-142	transcription factor 4	Homo sapiens	33-38
14566053-7	2003	NO-ASA disrupted the association of Beta-catenin and TCF-4 in the nucleus, whereas ASA did not affect it.	Aspirin	3-6	transcription factor 4	Homo sapiens	53-58
14511359-13	2003	Inhibited the activation of p42/p44 mitogen-activated protein kinase (MAPK) by PD98059, a specific inhibitor of extracellular regulatory kinase (ERK), significantly decreased cell viability and enhanced the expression of p53 induced by ASA.	Aspirin	236-239	interferon induced protein 44	Homo sapiens	32-35
12927657-2	2003	This study determined whether aspirin, which reverses platelet aggregation, or amiloride, a vasodilator, significantly reversed this rCBF hypoperfusion.	Aspirin	30-37	CCAAT/enhancer binding protein zeta	Rattus norvegicus	133-137
15735566-7	2005	In vitro studies on CagA and VacA positive Hp subjected to culture medium containing aspirin showed a dose dependent reduction in bacterial growth with complete bacteria killing occurring at 500 microg/ml of aspirin.	Aspirin	85-92	S100 calcium binding protein A8	Homo sapiens	20-24
15735566-7	2005	In vitro studies on CagA and VacA positive Hp subjected to culture medium containing aspirin showed a dose dependent reduction in bacterial growth with complete bacteria killing occurring at 500 microg/ml of aspirin.	Aspirin	208-215	S100 calcium binding protein A8	Homo sapiens	20-24
12890715-12	2003	(6) Reversal of antiadhesive activities of aspirin by celecoxib was associated with increased expression of LFA-1 on PMN and E-selectin on HUVEC.	Aspirin	43-50	integrin subunit alpha L	Homo sapiens	108-113
12879250-11	2003	The inhibition of PNF by AsA was associated with decreased intra-islet levels of inflammation-related molecules (IL-1, TNF-alpha, iNOS, COX-2) and chemokines (MCP-1 and MIP-3alpha).	Aspirin	25-28	cytochrome c oxidase II, mitochondrial	Mus musculus	136-141
12637254-0	2003	Gastritis increases resistance to aspirin-induced mucosal injury via COX-2-mediated lipoxin synthesis.	Aspirin	34-41	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	69-74
15505105-0	2004	Anti-glycoprotein VI treatment severely compromises hemostasis in mice with reduced alpha2beta1 levels or concomitant aspirin therapy.	Aspirin	118-125	glycoprotein 6 (platelet)	Mus musculus	5-20
15505105-8	2004	Conversely, inhibition of TxA2 production by aspirin severely compromised hemostasis in anti-GP VI-treated or GP VI/Fc receptor gamma-chain-deficient but not control mice.	Aspirin	45-52	glycoprotein 6 (platelet)	Mus musculus	93-98
12637254-2	2003	Acetylation of COX-2 by aspirin has been shown to result in the generation of 15(R)-epi-lipoxin A4, which exerts protective effects in the stomach.	Aspirin	24-31	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	15-20
12637254-14	2003	These results support the notion that aspirin-triggered lipoxin synthesis via COX-2 makes an important contribution to mucosal defense in both the normal and inflamed stomach.	Aspirin	38-45	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	78-83
12807437-7	2003	Ascorbic acid alone or in combination with acetylsalicylic acid did not inhibit cyclooxygenase-2 (COX-2) protein synthesis but inhibited COX-2 enzyme activity.	Aspirin	43-63	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	137-142
12810952-6	2003	We show that individuals homozygous for the minor ODC A-allele who reported using aspirin are approximately 0.10 times as likely to have an adenoma recurrence as non-aspirin users homozygous for the major G-allele.	Aspirin	82-89	ornithine decarboxylase 1	Homo sapiens	50-53
12810952-6	2003	We show that individuals homozygous for the minor ODC A-allele who reported using aspirin are approximately 0.10 times as likely to have an adenoma recurrence as non-aspirin users homozygous for the major G-allele.	Aspirin	166-173	ornithine decarboxylase 1	Homo sapiens	50-53
14592556-4	2003	Pretreatment with COX-1 and COX-3 inhibitors (aspirin at a low dose of 1 mg kg(-1), SC 560 and acetaminophen, 0.3-3 mg kg(-1)) slightly augmented thrombolysis by ACE-I, while COX-2 inhibitors (nimesulide and coxibs at doses &lt;1 mg kg(-1) and aspirin at a high dose of 50 mg kg(-1)) or a kinin B2 receptor antagonist (icatibant) abolished it.	Aspirin	46-53	cytochrome c oxidase III, mitochondrial	Rattus norvegicus	28-33
14592556-4	2003	Pretreatment with COX-1 and COX-3 inhibitors (aspirin at a low dose of 1 mg kg(-1), SC 560 and acetaminophen, 0.3-3 mg kg(-1)) slightly augmented thrombolysis by ACE-I, while COX-2 inhibitors (nimesulide and coxibs at doses &lt;1 mg kg(-1) and aspirin at a high dose of 50 mg kg(-1)) or a kinin B2 receptor antagonist (icatibant) abolished it.	Aspirin	46-53	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	175-180
14592556-4	2003	Pretreatment with COX-1 and COX-3 inhibitors (aspirin at a low dose of 1 mg kg(-1), SC 560 and acetaminophen, 0.3-3 mg kg(-1)) slightly augmented thrombolysis by ACE-I, while COX-2 inhibitors (nimesulide and coxibs at doses &lt;1 mg kg(-1) and aspirin at a high dose of 50 mg kg(-1)) or a kinin B2 receptor antagonist (icatibant) abolished it.	Aspirin	244-251	cytochrome c oxidase III, mitochondrial	Rattus norvegicus	28-33
12624303-0	2003	Aspirin inhibits p44/42 mitogen-activated protein kinase and is protective against hypoxia/reoxygenation neuronal damage.	Aspirin	0-7	mitogen activated protein kinase 3	Rattus norvegicus	17-20
12624303-11	2003	ASA strongly inhibited this ERK1/2 activation.	Aspirin	0-3	mitogen activated protein kinase 3	Rattus norvegicus	28-34
12535861-2	2003	To examine the contribution of the histamine-forming enzyme, histidine decarboxylase, to drug-induced gastric lesions, we compared the effects of aspirin, indomethacin and dexamethasone on histidine decarboxylase activity in mice.	Aspirin	146-153	histidine decarboxylase	Mus musculus	189-212
12538492-7	2003	In HCT116+chr3 cells, treatment with 1 mM of aspirin increased expression of the hMLH1 and hPMS2 proteins by 2.5-fold and 2-fold, respectively, and increased expression of the hMSH2 and hMSH6 proteins by 2-3-fold.	Aspirin	45-52	mutS homolog 2	Homo sapiens	176-181
15485683-0	2004	Aspirin inhibits ox-LDL-mediated LOX-1 expression and metalloproteinase-1 in human coronary endothelial cells.	Aspirin	0-7	oxidized low density lipoprotein receptor 1	Homo sapiens	33-38
15485683-4	2004	We hypothesized that aspirin may interfere with LOX-1 expression and subsequent MMP activation.	Aspirin	21-28	oxidized low density lipoprotein receptor 1	Homo sapiens	48-53
15485683-6	2004	Aspirin, in a dose- and time-dependent fashion, reduced ox-LDL-mediated LOX-1 expression (P&lt;0.01).	Aspirin	0-7	oxidized low density lipoprotein receptor 1	Homo sapiens	72-77
15485683-11	2004	CONCLUSION: These observations suggest that aspirin inhibits ox-LDL-mediated LOX-1 expression and interferes with the effects of ox-LDL in intracellular signaling (p38MAPK activation) and subsequent MMP-1 activity.	Aspirin	44-51	oxidized low density lipoprotein receptor 1	Homo sapiens	77-82
15508788-3	2004	In presented work the influence of acetylsalicylic acid, metoprolol, simvastatin, isosorbide mononitrate and molsidomine on total activity of adenosine deaminase and its isoenzymes--ADA1 and ADA2 in vivo was studied.	Aspirin	35-55	transcriptional adaptor 2A	Homo sapiens	191-195
15120641-6	2004	Aspirin and rofecoxib (non-selective and selective COX-2 inhibitor, respectively) each abolished fibronectin-associated induction of MMP-2 and induced dose-dependent reductions in cellular invasiveness.	Aspirin	0-7	matrix metallopeptidase 2	Homo sapiens	133-138
15045137-10	2004	The agonist-dependent CTGF secretion was significantly inhibited by aspirin.	Aspirin	68-75	cellular communication network factor 2	Homo sapiens	22-26
15045137-12	2004	Aspirin treatment prevents CTGF release, suggesting that clinical benefits of this drug may involve the inhibition of CTGF secretion.	Aspirin	0-7	cellular communication network factor 2	Homo sapiens	27-31
15045137-12	2004	Aspirin treatment prevents CTGF release, suggesting that clinical benefits of this drug may involve the inhibition of CTGF secretion.	Aspirin	0-7	cellular communication network factor 2	Homo sapiens	118-122
15007363-0	2004	HLA association in aspirin-intolerant asthma: DPB1*0301 as a strong marker in a Korean population.	Aspirin	19-26	major histocompatibility complex, class II, DP beta 1	Homo sapiens	46-50
14975458-7	2004	In contrast, the combination of nimesulide and aspirin inhibited PGI-M excretion to a greater extent than aspirin (p = 0.001).	Aspirin	47-54	glucose-6-phosphate isomerase	Homo sapiens	65-68
15183041-8	2004	(3) Aspirin intake reduced platelet degranulation and PAC-1 expression only for AYPGKF costimulation with collagen.	Aspirin	4-11	dual specificity phosphatase 2	Homo sapiens	54-59
14642793-12	2003	(3) Classic non-steroidal anti-inflammatory drugs such as aspirin prolonged ulcer healing under diabetic conditions due to suppression of endogenous prostaglandins and the fall in the microcirculation at the ulcer margin and these effects were mimicked by selective, so called "safe" COX-2 inhibitor, rofecoxib, suggesting that both COX isoforms are important sources of prostaglandins that are essential in the ulcer healing in diabetes.	Aspirin	58-65	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	284-289
14614633-2	2003	Blockage of mucin release with aspirin inhibits the formation of primary gallstones in animal models.	Aspirin	31-38	LOC100508689	Homo sapiens	12-17
12774850-6	2003	In contrast, we identified polyamine biosynthesis as a cellular target of aspirin, since the treatment of HT-29 Glc(-/+) cells with aspirin reduced the flux of L-ornithine through ornithine decarboxylase, an effect that could not be explained by an acute action of the drug on the ornithine decarboxylase catalytic activity.	Aspirin	74-81	ornithine decarboxylase 1	Homo sapiens	180-203
12774850-6	2003	In contrast, we identified polyamine biosynthesis as a cellular target of aspirin, since the treatment of HT-29 Glc(-/+) cells with aspirin reduced the flux of L-ornithine through ornithine decarboxylase, an effect that could not be explained by an acute action of the drug on the ornithine decarboxylase catalytic activity.	Aspirin	74-81	ornithine decarboxylase 1	Homo sapiens	281-304
12774850-6	2003	In contrast, we identified polyamine biosynthesis as a cellular target of aspirin, since the treatment of HT-29 Glc(-/+) cells with aspirin reduced the flux of L-ornithine through ornithine decarboxylase, an effect that could not be explained by an acute action of the drug on the ornithine decarboxylase catalytic activity.	Aspirin	132-139	ornithine decarboxylase 1	Homo sapiens	180-203
12774850-6	2003	In contrast, we identified polyamine biosynthesis as a cellular target of aspirin, since the treatment of HT-29 Glc(-/+) cells with aspirin reduced the flux of L-ornithine through ornithine decarboxylase, an effect that could not be explained by an acute action of the drug on the ornithine decarboxylase catalytic activity.	Aspirin	132-139	ornithine decarboxylase 1	Homo sapiens	281-304
12774850-7	2003	Since polyamine biosynthesis is strictly necessary for HT-29 cell growth, our data suggest that reduced flux through ornithine decarboxylase may participate in the antiproliferative activity of aspirin towards colonic tumoral cells.	Aspirin	194-201	ornithine decarboxylase 1	Homo sapiens	117-140
12781799-5	2003	Aspirin treatment of erythromelalgia in thrombocythemia patients resulted in the disappearance of the erythromelalgic, thrombotic signs and symptoms, correction of the shortened platelet survival times, and a significant reduction of the increased levels of beta-TG, PF4, TM and urinary TxB2 excretion to normal.	Aspirin	0-7	pro-platelet basic protein	Homo sapiens	258-265
12781799-5	2003	Aspirin treatment of erythromelalgia in thrombocythemia patients resulted in the disappearance of the erythromelalgic, thrombotic signs and symptoms, correction of the shortened platelet survival times, and a significant reduction of the increased levels of beta-TG, PF4, TM and urinary TxB2 excretion to normal.	Aspirin	0-7	platelet factor 4	Homo sapiens	267-270
12684272-8	2003	Aspirin induced the activation of p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinases.	Aspirin	0-7	mitogen-activated protein kinase 14	Mus musculus	34-37
12591106-11	2003	One tablet of aspirin moderately inhibited expression of most surface platelet receptors measured, and such inhibition reached significance (p&lt;0.05) for PAC-1, CD31, CD41, CD42, CD62p, and CD151.	Aspirin	14-21	dual specificity phosphatase 2	Homo sapiens	156-161
12591106-11	2003	One tablet of aspirin moderately inhibited expression of most surface platelet receptors measured, and such inhibition reached significance (p&lt;0.05) for PAC-1, CD31, CD41, CD42, CD62p, and CD151.	Aspirin	14-21	platelet and endothelial cell adhesion molecule 1	Homo sapiens	163-167
12852480-5	2003	Hence, the developmental toxicity seen in rats after exposure to aspirin may be due to the irreversible inhibition of COX-1 and/or COX-2.	Aspirin	65-72	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	131-136
12852480-20	2003	Such a finding is consistent with the concept that reversible inhibition of COX-1 and/or COX-2 by other NSAIDs would produce weaker developmental toxicity signals than aspirin.	Aspirin	168-175	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	89-94
12852481-2	2003	Aspirin (acetylsalicylic acid [ASA]), an irreversible cyclooxygenase 1 and 2 inhibitor, induces developmental anomalies when administered to Wistar rats on gestational day (GD) 9, 10, or 11 (Kimmel CA, Wilson JG, Schumacher HJ.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	54-76
12852481-2	2003	Aspirin (acetylsalicylic acid [ASA]), an irreversible cyclooxygenase 1 and 2 inhibitor, induces developmental anomalies when administered to Wistar rats on gestational day (GD) 9, 10, or 11 (Kimmel CA, Wilson JG, Schumacher HJ.	Aspirin	9-29	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	54-76
12852481-2	2003	Aspirin (acetylsalicylic acid [ASA]), an irreversible cyclooxygenase 1 and 2 inhibitor, induces developmental anomalies when administered to Wistar rats on gestational day (GD) 9, 10, or 11 (Kimmel CA, Wilson JG, Schumacher HJ.	Aspirin	31-34	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	54-76
12852483-2	2003	Aspirin, an NSAID that irreversibly inhibits cyclooxygenase 1 (COX-1) and COX-2, induces DH, VSD, and MD when administered as one dose during the sensitive periods of development in rats.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	45-61
12852483-2	2003	Aspirin, an NSAID that irreversibly inhibits cyclooxygenase 1 (COX-1) and COX-2, induces DH, VSD, and MD when administered as one dose during the sensitive periods of development in rats.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	63-68
12852483-2	2003	Aspirin, an NSAID that irreversibly inhibits cyclooxygenase 1 (COX-1) and COX-2, induces DH, VSD, and MD when administered as one dose during the sensitive periods of development in rats.	Aspirin	0-7	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	74-79
12852484-8	2003	One CA isoform, CA-4, demonstrated developmentally regulated embryonic mRNA expression that coincided with ASA sensitivity ASA exposure failed to induce upregulation of any of these mRNAs.	Aspirin	107-110	carbonic anhydrase 4	Rattus norvegicus	16-20
12852484-8	2003	One CA isoform, CA-4, demonstrated developmentally regulated embryonic mRNA expression that coincided with ASA sensitivity ASA exposure failed to induce upregulation of any of these mRNAs.	Aspirin	123-126	carbonic anhydrase 4	Rattus norvegicus	16-20
12679220-9	2003	In contrast, high doses of ASA (25 mg/kg), which are used as antirheumatic therapy, abrogate both COX-2 activity and late PC, suggesting that nonselective doses of NSAIDs should be used with caution in patients with atherosclerotic cardiovascular disease because they may deprive the heart of its innate defensive response.	Aspirin	27-30	prostaglandin G/H synthase 2	Oryctolagus cuniculus	98-103
12679222-0	2003	Improved endothelial function by the thromboxane A2 receptor antagonist S 18886 in patients with coronary artery disease treated with aspirin.	Aspirin	134-141	thromboxane A2 receptor	Homo sapiens	37-60
12695747-0	2003	Aspirin inhibits surface glycoprotein IIb/IIIa, P-selectin, CD63, and CD107a receptor expression on human platelets.	Aspirin	0-7	lysosomal associated membrane protein 1	Homo sapiens	70-76
12695747-7	2003	Dose-dependent inhibition of GPIIb/IIIa, P-selectin, CD63, and CD107a receptor expression was observed in the aspirin-treated whole-blood samples.	Aspirin	110-117	lysosomal associated membrane protein 1	Homo sapiens	63-69
12615789-0	2003	Inhibitory effects of glycoprotein IIb/IIIa antagonists and aspirin on the release of soluble CD40 ligand during platelet stimulation.	Aspirin	60-67	CD40 molecule	Homo sapiens	94-98
12781040-12	2003	Aspirin could down-regulate the strong expression of cyclooxygenase-2 in the tissue of gastric adenocarcinomas of nude mice.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Mus musculus	53-69
12781040-13	2003	CONCLUSION: A combination of octreotide and aspirin significantly inhibited proliferation of gastric cancer through mediation of somatostatin receptors and suppression of cyclooxygenase-2.	Aspirin	44-51	prostaglandin-endoperoxide synthase 2	Mus musculus	171-187
12624303-14	2003	CONCLUSIONS: Inhibition of the sustained activation of ERK1/2 may partially contribute to neuroprotection achieved by ASA against H/R injury.	Aspirin	118-121	mitogen activated protein kinase 3	Rattus norvegicus	55-61
12852484-10	2003	Correlation of COX-1 and CA-4 expression with ASA sensitivity suggested that embryonic COX-1 and possibly CA4 are much more likely candidates for mediators of ASA developmental toxicity.	Aspirin	46-49	carbonic anhydrase 4	Rattus norvegicus	25-29
12852484-10	2003	Correlation of COX-1 and CA-4 expression with ASA sensitivity suggested that embryonic COX-1 and possibly CA4 are much more likely candidates for mediators of ASA developmental toxicity.	Aspirin	159-162	carbonic anhydrase 4	Rattus norvegicus	106-109
12605343-0	2003	Aspirin and diabetes: inhibition of amylin aggregation by nonsteroidal anti-inflammatory drugs.	Aspirin	0-7	islet amyloid polypeptide	Homo sapiens	36-42
12605343-6	2003	Using circular dichroism and Congo red absorption techniques we found that clinically relevant doses of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDS) prevented and also reversed the beta-sheet conformation of human amylin.	Aspirin	104-111	islet amyloid polypeptide	Homo sapiens	233-239
12480553-9	2003	CONCLUSIONS: Most patients with Gilbert"s syndrome, in addition to their reduced B-UGT enzyme activity, may have abnormalities in the glucuronidation of aspirin or coumarin- and dopamine-derivatives, due to this combination of UGT1A1*28 and UGT1A6*2 genotypes.	Aspirin	153-160	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	241-247
12404234-3	2002	We determined whether aspirin-triggered lipoxin (LX) production via COX-2 diminishes aspirin-induced damage in the rat stomach.	Aspirin	22-29	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	68-73
12404234-3	2002	We determined whether aspirin-triggered lipoxin (LX) production via COX-2 diminishes aspirin-induced damage in the rat stomach.	Aspirin	85-92	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	68-73
12404234-9	2002	Aspirin rapidly up-regulated COX-2 expression in the stomach and caused a significant increase in gastric 15(R)-epi-LXA4 production, which was abolished by celecoxib.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	29-34
12404234-11	2002	CONCLUSIONS: Aspirin administration results in elevated production of 15(R)-epi-LXA4 via COX-2.	Aspirin	13-20	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	89-94
12404234-13	2002	Co-administration of aspirin and a selective COX-2 inhibitor results in substantially more severe gastric injury than is produced with either agent alone.	Aspirin	21-28	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	45-50
12417048-8	2002	However, expression in HCC of mRNAs for intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, both of which are considered to play key roles in attachment of cancer cells to the endothelium, was significantly suppressed by ASP.	Aspirin	242-245	vascular cell adhesion molecule 1	Rattus norvegicus	78-111
12147297-6	2002	ASA decreased while methylprednisolone increased C1q secretion from human peritoneal macrophages in vitro, which correlated well with the percentage of CD14 positive cells after treatment.	Aspirin	0-3	CD14 molecule	Homo sapiens	152-156
11981761-0	2002	Aspirin and NS-398 inhibit hepatocyte growth factor-induced invasiveness of human hepatoma cells.	Aspirin	0-7	hepatocyte growth factor	Homo sapiens	27-51
11981761-7	2002	In conclusion, our results suggest that aspirin and NS-398 inhibit HGF-induced invasiveness of HepG2 human hepatoma cells through ERK1/2.	Aspirin	40-47	hepatocyte growth factor	Homo sapiens	67-70
11964481-7	2002	This interplay may help explain the adverse cardiovascular effects associated with selective COX-2 inhibitors, which, unlike aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), inhibit PGI2 but not TxA2.	Aspirin	125-132	cytochrome c oxidase II, mitochondrial	Mus musculus	93-98
11906968-7	2002	Pretreatment with aspirin, or with drugs that selectively inhibit cyclo-oxygenase-2 (celecoxib, meloxicam and DuP-697), resulted in a concentration-dependent exacerbation of the myocardial dysfunction and damage.	Aspirin	18-25	prostaglandin G/H synthase 2	Oryctolagus cuniculus	66-83
11701434-5	2001	This effect was seen within 12 h and was maximal by 36 h. Aspirin blocked the induction of UCP-2 by EPA, indicating involvement of the prostaglandin pathway.	Aspirin	58-65	uncoupling protein 2	Homo sapiens	91-96
11701434-6	2001	Hepatocytes treated with arachidonic acid, the immediate precursor to the prostaglandins, also exhibited an aspirin-inhibitable increase in UCP-2 levels, further supporting the involvement of prostaglandins in regulating hepatic UCP-2.	Aspirin	108-115	uncoupling protein 2	Homo sapiens	140-145
11701434-6	2001	Hepatocytes treated with arachidonic acid, the immediate precursor to the prostaglandins, also exhibited an aspirin-inhibitable increase in UCP-2 levels, further supporting the involvement of prostaglandins in regulating hepatic UCP-2.	Aspirin	108-115	uncoupling protein 2	Homo sapiens	229-234
11680515-12	2001	Aspirin therapy reduced regional cerebral blood flow (rCBF) from 82.8m +/- 4.7 to 62.5 +/- 6.6 (n = 30; p = 0.0005).	Aspirin	0-7	CCAAT/enhancer binding protein zeta	Rattus norvegicus	54-58
11680515-14	2001	In a separate series of experiments, all agents able to reverse aspirin antagonism of thrombolysis demonstrated an improvement in rCBF, suggesting a common mechanism for this diverse group of agents in reversing aspirin"s antagonism of thrombolysis.	Aspirin	64-71	CCAAT/enhancer binding protein zeta	Rattus norvegicus	130-134
11680515-14	2001	In a separate series of experiments, all agents able to reverse aspirin antagonism of thrombolysis demonstrated an improvement in rCBF, suggesting a common mechanism for this diverse group of agents in reversing aspirin"s antagonism of thrombolysis.	Aspirin	212-219	CCAAT/enhancer binding protein zeta	Rattus norvegicus	130-134
11560562-7	2001	ABC or T with ASA alone resulted in nearly the same magnitude of reduction in FIB and platelet aggregation.	Aspirin	14-17	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	0-3
11467994-0	2001	Serum interleukin-5 in aspirin-induced asthma.	Aspirin	23-30	interleukin 5	Homo sapiens	6-19
11467994-2	2001	In patients with aspirin-induced asthma (AIA) bronchial biopsies revealed eosinophil infiltration and a marked increase in IL-5 positive cells.	Aspirin	17-24	interleukin 5	Homo sapiens	123-127
11467994-8	2001	CONCLUSION: Overexpression of IL-5 reported in the airways of aspirin-sensitive patients with asthma was not reflected in their blood.	Aspirin	62-69	interleukin 5	Homo sapiens	30-34
12404234-0	2002	Cyclooxygenase-2-derived lipoxin A4 increases gastric resistance to aspirin-induced damage.	Aspirin	68-75	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	0-16
12404234-2	2002	Acetylation of COX-2 by aspirin can result in production of an antiinflammatory substance, 15(R)-epi-LXA4.	Aspirin	24-31	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	15-20
12124433-0	2002	Aspirin provides cyclin-dependent kinase 5-dependent protection against subsequent hypoxia/reoxygenation damage in culture.	Aspirin	0-7	cyclin-dependent kinase 5	Rattus norvegicus	17-42
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	0-7	mitogen activated protein kinase 3	Rattus norvegicus	184-187
12538492-8	2003	For SW480 cells, treatment with 1 and 5 mM of aspirin increased expression of the hMLH1 and hPMS2 proteins by 2-4-fold and 3-5-fold, respectively, and increased expression of the hMSH2 and hMSH6 proteins by 3-7-fold.	Aspirin	46-53	mutS homolog 2	Homo sapiens	179-184
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	0-7	mitogen activated protein kinase 3	Rattus norvegicus	225-236
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	9-29	mitogen activated protein kinase 3	Rattus norvegicus	184-187
12904124-6	2003	Despite these risks, the benefits of GPI therapy in addition to conventional treatment, such as aspirin and heparin, should be considered for these high-risk patients.	Aspirin	96-103	glucose-6-phosphate isomerase	Homo sapiens	37-40
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	9-29	mitogen activated protein kinase 3	Rattus norvegicus	225-236
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	31-34	mitogen activated protein kinase 3	Rattus norvegicus	184-187
12124433-1	2002	Aspirin [acetylsalicylic acid (ASA)] is an anti-inflammatory drug that protects against cellular injury by inhibiting cyclooxygenases (COX), inducible nitric oxide synthase (iNOS) and p44/42 mitogen-activated protein kinase (p44/42 MAPK), or by preventing translocation of nuclear factor kappaB (NF-kappaB).	Aspirin	31-34	mitogen activated protein kinase 3	Rattus norvegicus	225-236
12124433-7	2002	Hypoxia/reoxygenation alone reduced both the protein amount and activity of Cdk5, and this reduction was inhibited by pre-treatment with ASA.	Aspirin	137-140	cyclin-dependent kinase 5	Rattus norvegicus	76-80
12124433-8	2002	Moreover, the protein amount of a neuronal Cdk5 activator, p35, recovered after reoxygenation only in ASA-treated samples.	Aspirin	102-105	cyclin-dependent kinase 5	Rattus norvegicus	43-47
12124433-9	2002	The prevention of the loss in Cdk5 activity during reoxygenation was crucial for ASA-induced protection, because co-administration of Cdk5 inhibitors at the onset ofreoxygenation abolished the protection.	Aspirin	81-84	cyclin-dependent kinase 5	Rattus norvegicus	30-34
12124433-9	2002	The prevention of the loss in Cdk5 activity during reoxygenation was crucial for ASA-induced protection, because co-administration of Cdk5 inhibitors at the onset ofreoxygenation abolished the protection.	Aspirin	81-84	cyclin-dependent kinase 5	Rattus norvegicus	134-138
12527134-11	2003	In particular, these data suggest that LOX activation during inflammatory processes or during cyclo-oxygenase inhibition (e.g. by aspirin) is a potential intrinsic source of VR1 activation in inner ear ganglia.	Aspirin	130-137	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	174-177
12124433-10	2002	In conclusion, pre-treatment with ASA induces tolerance against hypoxia/reoxygenation damage in spinal cord cultures by restoring Cdk5 and p35 protein expression.	Aspirin	34-37	cyclin-dependent kinase 5	Rattus norvegicus	130-134
27264763-5	2002	Aspirin treatment of erythromelalgia in thrombocythemia patients resulted in disappearance of the erythromelalgic, thrombotic signs and symptoms, correction of the shortened platelet survival times, and significant reduction of the increased levels of ss-TG, PF IV, thrombomodulin and urinary T x B2 excretion to normal.	Aspirin	0-7	testis-specific transcript, Y-linked 13B	Homo sapiens	259-264
14586772-4	2003	Aspirin-induced asthma (AIA) is a typical drug-induced phenotype due to aspirin or nonsteroidal antiinflammatory drugs, and these drugs are metabolized by CYP2C9 and UGT1A6, which are regulated by PXR.	Aspirin	0-7	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	166-172
12044784-10	2002	Acetylsalicylic acid was found to inhibit gelatinolytic activity both in control and adenocarcinoma tissues, preferentially the active forms of gelatinases MMP-2 and MMP-9.	Aspirin	0-20	matrix metallopeptidase 2	Homo sapiens	156-161
14586772-4	2003	Aspirin-induced asthma (AIA) is a typical drug-induced phenotype due to aspirin or nonsteroidal antiinflammatory drugs, and these drugs are metabolized by CYP2C9 and UGT1A6, which are regulated by PXR.	Aspirin	72-79	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	166-172
12848984-5	2002	Heparin and aspirin are the drugs of choice for APS-related miscarriage, although it is not clear whether combination of both drugs is necessary for all women.	Aspirin	12-19	SH2B adaptor protein 2	Homo sapiens	48-51
12194922-0	2002	Effect of aspirin treatment on serum concentrations of lipoprotein(a) in patients with atherosclerotic diseases.	Aspirin	10-17	lipoprotein(a)	Homo sapiens	55-69
12194922-2	2002	We previously reported that aspirin reduced Lp(a) production by cultured hepatocytes via the reduction of apolipoprotein(a) [apo(a)] gene transcription.	Aspirin	28-35	lipoprotein(a)	Homo sapiens	44-49
12194922-2	2002	We previously reported that aspirin reduced Lp(a) production by cultured hepatocytes via the reduction of apolipoprotein(a) [apo(a)] gene transcription.	Aspirin	28-35	lipoprotein(a)	Homo sapiens	106-123
12194922-2	2002	We previously reported that aspirin reduced Lp(a) production by cultured hepatocytes via the reduction of apolipoprotein(a) [apo(a)] gene transcription.	Aspirin	28-35	lipoprotein(a)	Homo sapiens	125-131
12194922-3	2002	METHODS: We evaluated both the effect of aspirin treatment (81 mg/day) on serum Lp(a) concentrations and the correlation between the degree of reduction in serum Lp(a) and the type of apo(a) isoform in 70 patients with coronary artery disease or cerebral infarction.	Aspirin	41-48	lipoprotein(a)	Homo sapiens	80-85
12194922-4	2002	RESULTS: Aspirin lowered serum Lp(a) concentrations to approximately 80% of the baseline values in patients with high Lp(a) concentrations (&gt;300 mg/L).	Aspirin	9-16	lipoprotein(a)	Homo sapiens	31-36
12194922-4	2002	RESULTS: Aspirin lowered serum Lp(a) concentrations to approximately 80% of the baseline values in patients with high Lp(a) concentrations (&gt;300 mg/L).	Aspirin	9-16	lipoprotein(a)	Homo sapiens	118-123
12194922-8	2002	These findings suggest that aspirin decreases serum Lp(a) concentrations via a decrease in apo(a) gene transcription more effectively in patients with high transcriptional activity of this gene.	Aspirin	28-35	lipoprotein(a)	Homo sapiens	52-57
12194922-8	2002	These findings suggest that aspirin decreases serum Lp(a) concentrations via a decrease in apo(a) gene transcription more effectively in patients with high transcriptional activity of this gene.	Aspirin	28-35	lipoprotein(a)	Homo sapiens	91-97
12413588-7	2002	Platelets from aspirin-resistant patients bound PAC-1 significantly more (p=0.03) than the aspirin-sensitive patients and controls when activated with 10 micro M ADP.	Aspirin	15-22	dual specificity phosphatase 2	Homo sapiens	48-53
11877318-18	2002	In contrast, phenanthroline and apyrase significantly enhanced the anti-aggregatory effects of aspirin against thrombin-, PAR1AP- and TRAP-induced aggregation suggesting the involvement of ADP- and MMP-2-dependent pathways.	Aspirin	95-102	matrix metallopeptidase 2	Homo sapiens	198-203
11687510-0	2001	Aspirin-triggered lipoxin A4 and lipoxin A4 up-regulate transcriptional corepressor NAB1 in human neutrophils.	Aspirin	0-7	NGFI-A binding protein 1	Homo sapiens	84-88
11745453-1	2001	The epidemiologic evidence and rodent studies suggest strongly that nonselective inhibitors of cyclooxygenase (COX) enzymes such as aspirin, inhibiting both COX-1 and COX-2 isoforms, reduce the incidence of and mortality from intestinal tumors.	Aspirin	132-139	cytochrome c oxidase II, mitochondrial	Mus musculus	167-172
11728532-9	2001	RESULTS: In a drug free group, digestion of a single tablet of aspirin resulted in a significantly (p&lt;0.05) diminished expression of PECAM-1, GP IIb, fibrinogen binding with PAC-1 antibody, GP Ib, P-selectin, and CD151.	Aspirin	63-70	platelet and endothelial cell adhesion molecule 1	Homo sapiens	136-143
11728532-9	2001	RESULTS: In a drug free group, digestion of a single tablet of aspirin resulted in a significantly (p&lt;0.05) diminished expression of PECAM-1, GP IIb, fibrinogen binding with PAC-1 antibody, GP Ib, P-selectin, and CD151.	Aspirin	63-70	dual specificity phosphatase 2	Homo sapiens	177-182
11705451-3	2001	The homogenates of bovine platelets and polymorphonuclear leukocytes were used as COX-1, 12-LOX, and 5-LOX enzyme sources; the homogenate of aspirin-pretreated lipopolysaccharide-induced RAW 264.7 cells was used for the COX-2 enzyme source.	Aspirin	141-148	cytochrome c oxidase II, mitochondrial	Mus musculus	220-225
11278846-5	2001	These findings indicate that contrary to the current view that salicylate acts via inhibition of nuclear factor kappaB the pharmacological actions of aspirin and salicylates are mediated by inhibiting CCAAT/enhancer-binding protein beta binding and transactivation.	Aspirin	150-157	CCAAT enhancer binding protein beta	Homo sapiens	201-236
11453099-0	2001	Delay in oral mucosal ulcer healing by aspirin is linked to the disturbances in p38 mitogen-activated protein kinase activation.	Aspirin	39-46	mitogen activated protein kinase 14	Rattus norvegicus	80-116
11453099-2	2001	In this study, we investigated the effect of a specific inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), SB 203580, on the rate of buccal mucosal ulcer healing and the apoptotic processes in rats subjected to intragastric administration of aspirin.	Aspirin	253-260	mitogen activated protein kinase 14	Rattus norvegicus	69-105
11453099-2	2001	In this study, we investigated the effect of a specific inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), SB 203580, on the rate of buccal mucosal ulcer healing and the apoptotic processes in rats subjected to intragastric administration of aspirin.	Aspirin	253-260	mitogen activated protein kinase 14	Rattus norvegicus	107-115
11453099-8	2001	CONCLUSIONS: The results of our findings link the delay in buccal mucosal ulcer healing caused by aspirin ingestion to the disturbances in the p38 MAPK activation.	Aspirin	98-105	mitogen activated protein kinase 14	Rattus norvegicus	143-146
11322923-6	2001	Wogonin inhibited COX-2 activity directly (IC(50) = 46 microM) from the homogenate of aspirin-pretreated RAW cells, as determined by measuring [(14)C]PGE(2) formation from [(14)C]arachidonic acid.	Aspirin	86-93	prostaglandin-endoperoxide synthase 2	Mus musculus	18-23
11325819-0	2001	CYP2C9 and UGT1A6 genotypes modulate the protective effect of aspirin on colon adenoma risk.	Aspirin	62-69	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	11-17
11325819-3	2001	NSAIDs, particularly aspirin, are glucuronidated by UGT1A6 and some classes of NSAIDs are also metabolized by cytochrome P450 (CYP) 2C9.	Aspirin	21-28	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	52-58
11141472-1	2001	Aspirin-triggered lipoxin A(4) (ATL, 15-epi-LXA(4)) and leukotriene D(4) (LTD(4)) possess opposing vascular actions mediated via receptors distinct from the LXA(4) receptor (ALX) that is involved in leukocyte trafficking.	Aspirin	0-7	hematopoietic SH2 domain containing	Homo sapiens	174-177
11141472-8	2001	These results indicate that ATL and LTD(4) bind and compete with equal affinity at CysLT(1), providing a molecular basis for aspirin-triggered LXs serving as a local damper of both vascular CysLT(1) signals as well as ALX receptor-regulated polymorphonuclear leukocyte traffic.	Aspirin	125-132	hematopoietic SH2 domain containing	Homo sapiens	218-221
11765447-5	2001	IL-5 levels were higher in polips with allergic and aspirin idiocracy background compared with inflammatory polips.	Aspirin	52-59	interleukin 5	Homo sapiens	0-4
11195467-3	2000	The NSAIDs used in this study include acetylsalicylic acid (ASA) that is anti-inflammatory with COX-1 and COX-2 inhibition and N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS398) that is a specific COX-2 inhibitor.	Aspirin	38-58	cytochrome c oxidase II, mitochondrial	Mus musculus	106-111
11195467-3	2000	The NSAIDs used in this study include acetylsalicylic acid (ASA) that is anti-inflammatory with COX-1 and COX-2 inhibition and N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS398) that is a specific COX-2 inhibitor.	Aspirin	60-63	cytochrome c oxidase II, mitochondrial	Mus musculus	106-111
11195467-3	2000	The NSAIDs used in this study include acetylsalicylic acid (ASA) that is anti-inflammatory with COX-1 and COX-2 inhibition and N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS398) that is a specific COX-2 inhibitor.	Aspirin	60-63	cytochrome c oxidase II, mitochondrial	Mus musculus	209-214
10970676-9	2000	Pretreatment of the mice with aspirin, an irreversible inhibitor of COX1 and COX2, prevented the hypophagic response to IL-1, 16 h, but not 40 h later.	Aspirin	30-37	cytochrome c oxidase II, mitochondrial	Mus musculus	77-81
10970676-9	2000	Pretreatment of the mice with aspirin, an irreversible inhibitor of COX1 and COX2, prevented the hypophagic response to IL-1, 16 h, but not 40 h later.	Aspirin	30-37	interleukin 1 complex	Mus musculus	120-124
10859212-6	2000	Caspase 3 protein was activated, and the number of apoptotic cells increased in mucosa after one aspirin dose.	Aspirin	97-104	caspase 3	Rattus norvegicus	0-9
10692466-2	2000	The two isoforms of cyclooxygenase, COX-1 and COX-2, are acetylated by aspirin at Ser-530 and Ser-516, respectively, in the cyclooxygenase active site.	Aspirin	71-78	cytochrome c oxidase II, mitochondrial	Mus musculus	46-51
10692466-6	2000	Site-directed mutagenesis of Val-434, Arg-513, and Val-523 in mouse COX-2 to their COX-1 equivalents resulted in abrogation of 11- and 15-HETE production after aspirin treatment, confirming the hypothesis that these residues are the major isoform selectivity determinants regulating HETE production.	Aspirin	160-167	cytochrome c oxidase II, mitochondrial	Mus musculus	68-73
10648469-0	2000	NO-aspirin protects from T cell-mediated liver injury by inhibiting caspase-dependent processing of Th1-like cytokines.	Aspirin	3-10	caspase 1	Mus musculus	68-75
10648469-7	2000	At a dose of 100 mg/kg, NO-aspirin caused a 40%-80% reduction of interleukin (IL)-1beta, IL-12, IL-18, interferon (IFN)-gamma, and tumor necrosis factor alpha production without affecting cytokine messenger RNA expression.	Aspirin	27-34	interleukin 18	Mus musculus	96-101
10648469-8	2000	NO-aspirin prevented Fas, Fas ligand, and IL-2 receptor up-regulation on spleen lymphocytes and Fas ligand on hepatocytes and caused the S-nitrosylation/inhibition of IL-1beta-converting enzyme-like cysteine proteases (caspases) involved in the processing and maturation of IL-1beta and IL-18.	Aspirin	3-10	interleukin 18	Mus musculus	287-292
10339595-1	1999	The antiinflammatory action of aspirin generally has been attributed to direct inhibition of cyclooxygenases (COX-1 and COX-2), but additional mechanisms are likely at work.	Aspirin	31-38	cytochrome c oxidase II, mitochondrial	Mus musculus	120-125
11775855-5	1999	Compared with LPS-stimulated group, both NF-kappa B activity and TNF-alpha concentration were significantly lowered in DEX- or ASA-treated groups (P &lt; 0.01).	Aspirin	127-130	tumor necrosis factor	Sus scrofa	65-74
11775855-6	1999	CONCLUSIONS: LPS might activate NF-kappa B in the PIMs, and induce the increase of transcription and expression of TNF-alpha gene; Both DEX and ASA could inhibit the activation of NF-kappa B and reduce the release of TNF-alpha.	Aspirin	144-147	tumor necrosis factor	Sus scrofa	115-124
11775855-6	1999	CONCLUSIONS: LPS might activate NF-kappa B in the PIMs, and induce the increase of transcription and expression of TNF-alpha gene; Both DEX and ASA could inhibit the activation of NF-kappa B and reduce the release of TNF-alpha.	Aspirin	144-147	tumor necrosis factor	Sus scrofa	217-226
10220459-7	1999	In mice pretreated with aspirin (10 and 30 mg/kg), followed by challenge with lipopolysaccharide, COX-2 mRNA expression in peritoneal macrophages was markedly suppressed.	Aspirin	24-31	cytochrome c oxidase II, mitochondrial	Mus musculus	98-103
11829001-0	2002	Aspirin gets a tentative nod.	Aspirin	0-7	atrophin 1	Homo sapiens	25-28
11390449-6	2001	Nuclear extracts of purified, aspirin-treated DC revealed a decreased NF-kappaB DNA-binding activity, whereas Ab supershift analysis indicated that aspirin targeted primarily NF-kappaB p50.	Aspirin	148-155	CD40 antigen	Mus musculus	185-188
11390449-7	2001	Unexpectedly, aspirin promoted the generation of CD11c+ DC, due to apparent suppression of granulocyte development.	Aspirin	14-21	integrin alpha X	Mus musculus	49-54
10476618-7	1999	The incidence of proteinuric PIH was significantly lower in patients given low-dose aspirin than in the control group (p &lt; 0.05).	Aspirin	84-91	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	29-32
11276157-1	2001	Low-dose aspirin gets the nod.	Aspirin	9-16	atrophin 1	Homo sapiens	26-29
12070535-6	2002	In animal models, neutralization of circulating TFPI activity results in restoration of intravascular thrombus formation previously abolished by aspirin.	Aspirin	145-152	tissue factor pathway inhibitor	Homo sapiens	48-52
10476618-12	1999	Low-dose aspirin may offer a degree of protection from proteinuric PIH in these high-risk women.	Aspirin	9-16	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	67-70
11313997-0	2001	The nonsteroidal anti-inflammatory drugs aspirin and indomethacin attenuate beta-catenin/TCF-4 signaling.	Aspirin	41-48	transcription factor 4	Homo sapiens	89-94
11886462-3	2002	Aspirin prophylaxis begun for suspected rheumatic fever led to compartment syndromes of all four extremities, which resolved with high-dose FVIII and surgical decompression.	Aspirin	0-7	coagulation factor VIII	Homo sapiens	140-145
9808189-6	1998	ASA was found to inhibit secretion of the IL-12 heterodimer as well as p40 monomer by human monocytic cells.	Aspirin	0-3	interleukin 9	Homo sapiens	71-74
11402053-6	2001	Despite this difference, aspirin-treated COX-2 oxygenates 2-AG to afford 15-hydroxyeicosatetraenoic acid glycerol ester in a reaction analogous to the C-15 oxygenation of arachidonic acid observed with acetylated COX-2.	Aspirin	25-32	cytochrome c oxidase II, mitochondrial	Mus musculus	41-46
11180504-12	2001	In conclusion, the inhibition of either COX-1/COX-2 by acetylsalicylic acid or preferentially COX-2 by meloxicam provided a clear neuroprotection against MPTP-toxicity on the striatal and nigral levels.	Aspirin	55-75	cytochrome c oxidase II, mitochondrial	Mus musculus	46-51
11306048-0	2001	Effects of 3-methylcholanthrene and aspirin co-administration on ALDH3A1 in HepG2 cells.	Aspirin	36-43	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	65-72
9808189-8	1998	Analysis of the regulation of the p40 gene promoter revealed that ASA inhibited NF-kappaB activation and binding to the p40-kappaB site in the p40 promoter, leading to transcriptional repression of the p40 gene.	Aspirin	66-69	interleukin 9	Homo sapiens	34-37
11306048-7	2001	When cells were firstly exposed to 3MC (2.5 and 5.0 microM) and then to aspirin (0.25 mM), the induced ALDH3A1 activity was further enhanced in a statistically significant way (P&lt;0.05).	Aspirin	72-79	aldehyde dehydrogenase 3 family member A1	Homo sapiens	103-110
11306048-8	2001	On the contrary, when aspirin application was preceded 3MC exposuring a statistically significant decrease in ALDH3A1 inducibility was observed, as compared with the application of 3MC alone.	Aspirin	22-29	aldehyde dehydrogenase 3 family member A1	Homo sapiens	110-117
11402053-6	2001	Despite this difference, aspirin-treated COX-2 oxygenates 2-AG to afford 15-hydroxyeicosatetraenoic acid glycerol ester in a reaction analogous to the C-15 oxygenation of arachidonic acid observed with acetylated COX-2.	Aspirin	25-32	cytochrome c oxidase II, mitochondrial	Mus musculus	213-218
9808189-8	1998	Analysis of the regulation of the p40 gene promoter revealed that ASA inhibited NF-kappaB activation and binding to the p40-kappaB site in the p40 promoter, leading to transcriptional repression of the p40 gene.	Aspirin	66-69	interleukin 9	Homo sapiens	120-123
11401513-0	2001	Aspirin inhibits matrix metalloproteinase-2 activity, increases E-cadherin production, and inhibits in vitro invasion of tumor cells.	Aspirin	0-7	matrix metallopeptidase 2	Homo sapiens	17-43
11401513-6	2001	Gelatin-based zymography assay showed that aspirin inhibited MMP-2 activity of SK-Hep-1 cancer cells.	Aspirin	43-50	matrix metallopeptidase 2	Homo sapiens	61-66
11401513-11	2001	These results indicate that aspirin can modulate both MMP-2 and E-cadherin production and therein may possess antimetastatic effect.	Aspirin	28-35	matrix metallopeptidase 2	Homo sapiens	54-59
11195467-7	2000	ASA (294 mg/kg diet) and NS398 also inhibited the expression of COX-2.	Aspirin	0-3	cytochrome c oxidase II, mitochondrial	Mus musculus	64-69
11195467-9	2000	Expression of cyclin B2 was decreased and expression of Fas-L and BAD were increased in lung tissues treated with both NS398 and ASA.	Aspirin	129-132	Fas ligand (TNF superfamily, member 6)	Mus musculus	56-61
11034327-6	2000	Therefore, aspirin-induced apoptosis involves caspase activation through cytochrome c release.	Aspirin	11-18	caspase 8	Homo sapiens	46-53
9808189-8	1998	Analysis of the regulation of the p40 gene promoter revealed that ASA inhibited NF-kappaB activation and binding to the p40-kappaB site in the p40 promoter, leading to transcriptional repression of the p40 gene.	Aspirin	66-69	interleukin 9	Homo sapiens	120-123
9808189-8	1998	Analysis of the regulation of the p40 gene promoter revealed that ASA inhibited NF-kappaB activation and binding to the p40-kappaB site in the p40 promoter, leading to transcriptional repression of the p40 gene.	Aspirin	66-69	interleukin 9	Homo sapiens	120-123
9780130-8	1998	After a therapeutic dose of aspirin, plasma concentrations of salicylic acid are within the range for TPMT inhibition.	Aspirin	28-35	thiopurine S-methyltransferase	Homo sapiens	102-106
10964669-6	2000	A combination of aspirin with B-NOD could be formulated in which the individual concentrations of aspirin and B-NOD may be useful in the long-term treatment of coronary artery disease and in clinical situations in which long-term release of NO may be beneficial.	Aspirin	17-24	atrophin 1	Homo sapiens	112-115
10964669-6	2000	A combination of aspirin with B-NOD could be formulated in which the individual concentrations of aspirin and B-NOD may be useful in the long-term treatment of coronary artery disease and in clinical situations in which long-term release of NO may be beneficial.	Aspirin	98-105	atrophin 1	Homo sapiens	32-35
11247918-5	2001	In addition, the level of PGE2 augmented by IL-1alpha was due to the increase of cyclooxygenase (COX) activity, which was inhibited by progesterone and 17beta-estradiol as well as by indomethacin and a specific COX-2 inhibitor, NS-398, but not by the well-known COX-1 inhibitor, aspirin.	Aspirin	279-286	interleukin-1 alpha	Oryctolagus cuniculus	44-53
9760036-5	1998	In contrast, at 3 h after carrageenin injection, cyclooxygenase 2 inhibitors significantly inhibited all inflammatory parameters however suppression with piroxicam and aspirin was greater, and more pronounced than at 6 h. NS-398 and nimesulide dosing did not reduce thromboxane B2 production from platelets isolated from rats with carrageenin-induced pleurisy, demonstrating that at the doses used, cyclooxygenase 2 inhibitors did not inhibit cyclooxygenase 1, as platelets contain only this isoform.	Aspirin	168-175	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	49-65
11248289-5	2001	Aspirin (ASA) treatment of platelets allowed reversible primary aggregation but inhibited irreversible complete aggregation, suggesting that MDC- and TARC-induced full platelet aggregation is dependent on cyclooxygenase metabolites of arachidonic acid.	Aspirin	0-7	C-C motif chemokine ligand 22	Homo sapiens	141-144
11248289-5	2001	Aspirin (ASA) treatment of platelets allowed reversible primary aggregation but inhibited irreversible complete aggregation, suggesting that MDC- and TARC-induced full platelet aggregation is dependent on cyclooxygenase metabolites of arachidonic acid.	Aspirin	0-7	C-C motif chemokine ligand 17	Homo sapiens	150-154
11248289-5	2001	Aspirin (ASA) treatment of platelets allowed reversible primary aggregation but inhibited irreversible complete aggregation, suggesting that MDC- and TARC-induced full platelet aggregation is dependent on cyclooxygenase metabolites of arachidonic acid.	Aspirin	9-12	C-C motif chemokine ligand 22	Homo sapiens	141-144
11248289-5	2001	Aspirin (ASA) treatment of platelets allowed reversible primary aggregation but inhibited irreversible complete aggregation, suggesting that MDC- and TARC-induced full platelet aggregation is dependent on cyclooxygenase metabolites of arachidonic acid.	Aspirin	9-12	C-C motif chemokine ligand 17	Homo sapiens	150-154
11205285-5	2000	RESULTS: aspirin, at plasma attainable levels, induced NF-IL6 DNA-binding activity, and increased MDR1 mRNA expression (by up to 140%), as well as the expression of P-gp, in Molt-4 cells.	Aspirin	9-16	CCAAT enhancer binding protein beta	Homo sapiens	55-61
10891429-8	2000	Further, second-wave aggregation induced by MDC in platelet-rich plasma was inhibited by aspirin, ADP scavenger creatine phosphate/creative phosphokinase (CP/CPK), and ARL-66096, an antagonist of the ADP P2T(AC) receptor involved in adenylyl cyclase inhibition.	Aspirin	89-96	C-C motif chemokine ligand 22	Homo sapiens	44-47
10891429-10	2000	SDF-1-induced aggregation was inhibited by aspirin, but it was only slightly affected by CP/CPK, ARL-66096, or A3P5PS.	Aspirin	43-50	C-X-C motif chemokine ligand 12	Homo sapiens	0-5
10807421-8	2000	CONCLUSION: Growth factors, including HGF, EGF and IGF-I, reversed the aspirin-induced inhibition of wound repair through their cytoprotective effects on gastric epithelial cells.	Aspirin	71-78	pro-epidermal growth factor	Oryctolagus cuniculus	43-46
10639009-3	1999	The purpose of this study was: 1) to determine the effect of gastric injury by ethanol and aspirin on the expression of leptin in gastric mucosa and 2) to investigate whether exogenous leptin affects the integrity of gastric mucosa exposed to noxious agents such as ethanol or aspirin.	Aspirin	91-98	leptin	Rattus norvegicus	120-126
10639009-13	1999	The exposure of gastric mucosa to noxious agents such as ethanol and aspirin was associated with markedly increased expression for gastric leptin at mRNA and protein level.	Aspirin	69-76	leptin	Rattus norvegicus	139-145
10639009-15	1999	The pretreatment with exogenous leptin reduced dose-dependently these ethanol or aspirin-induced gastric lesions.	Aspirin	81-88	leptin	Rattus norvegicus	32-38
10567380-0	1999	Aspirin reduces apolipoprotein(a) (apo(a)) production in human hepatocytes by suppression of apo(a) gene transcription.	Aspirin	0-7	lipoprotein(a)	Homo sapiens	16-33
10567380-0	1999	Aspirin reduces apolipoprotein(a) (apo(a)) production in human hepatocytes by suppression of apo(a) gene transcription.	Aspirin	0-7	lipoprotein(a)	Homo sapiens	35-41
10567380-0	1999	Aspirin reduces apolipoprotein(a) (apo(a)) production in human hepatocytes by suppression of apo(a) gene transcription.	Aspirin	0-7	lipoprotein(a)	Homo sapiens	93-99
10567380-2	1999	Our preliminary observations suggest that, in some patients with coronary heart disease with high serum Lp(a) levels, administration of aspirin reduced Lp(a) levels.	Aspirin	136-143	lipoprotein(a)	Homo sapiens	104-109
10567380-2	1999	Our preliminary observations suggest that, in some patients with coronary heart disease with high serum Lp(a) levels, administration of aspirin reduced Lp(a) levels.	Aspirin	136-143	lipoprotein(a)	Homo sapiens	152-157
10567380-3	1999	Therefore, we aimed to analyze the effects of aspirin on the production of apo(a), the expression of apolipoprotein(a) (apo(a)) mRNA and the transcriptional activity of apo(a) gene promoter.	Aspirin	46-53	lipoprotein(a)	Homo sapiens	75-81
10567380-4	1999	Aspirin (5 mM) reduced the apo(a) levels in culture medium of human hepatocytes and suppressed apo(a) mRNA expression to 73% and 85% of the controls, respectively.	Aspirin	0-7	lipoprotein(a)	Homo sapiens	27-33
10567380-4	1999	Aspirin (5 mM) reduced the apo(a) levels in culture medium of human hepatocytes and suppressed apo(a) mRNA expression to 73% and 85% of the controls, respectively.	Aspirin	0-7	lipoprotein(a)	Homo sapiens	95-101
10567380-5	1999	Aspirin also reduced the transcriptional activity of apo(a) gene transfected into HepG2 hepatoma cells in a dose-dependent manner, with a maximal effect at 5 mM (44.3 +/- 1.5% of the control).	Aspirin	0-7	lipoprotein(a)	Homo sapiens	53-59
10567380-7	1999	Deletion analysis of apo(a) gene promoter showed that promoter region extending from -30 to +138 is critical for the effect of aspirin.	Aspirin	127-134	lipoprotein(a)	Homo sapiens	21-27
10567380-8	1999	Furthermore, enhanced production, mRNA expression, and gene transcription of apo(a) by interleukin-6 were also inhibited by aspirin.	Aspirin	124-131	lipoprotein(a)	Homo sapiens	77-83
10553090-0	1999	Salicylic acid and aspirin inhibit the activity of RSK2 kinase and repress RSK2-dependent transcription of cyclic AMP response element binding protein- and NF-kappa B-responsive genes.	Aspirin	19-26	ribosomal protein S6 kinase A3	Homo sapiens	51-55
10553090-0	1999	Salicylic acid and aspirin inhibit the activity of RSK2 kinase and repress RSK2-dependent transcription of cyclic AMP response element binding protein- and NF-kappa B-responsive genes.	Aspirin	19-26	ribosomal protein S6 kinase A3	Homo sapiens	75-79
10564079-2	1999	ATL biosynthesis is initiated by ASA acetylation of cyclooxygenase (COX)-2 and was originally identified during the interaction of leukocytes with either endothelial or epithelial cells.	Aspirin	33-36	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	52-74
10564079-11	1999	Taken together and considering that ASA is hydrolyzed on its first pass through the portal circulation, these data indicate that, during ASA"s consumption, liver tissue generates biologically relevant amounts of ATL by COX-2-independent mechanisms.	Aspirin	36-39	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	219-224
10952521-3	2000	Experiments using model probes coated with -CH3 and -COOH terminated SAMs have been performed on the two aspirin crystal planes (001) and (100).	Aspirin	105-112	methionine adenosyltransferase 1A	Homo sapiens	69-73
10903918-2	2000	In RAW 264.7 macrophages, lipopolysaccharide (LPS)-induced COX-2-dependent synthesis of prostaglandin E(2) (PGE(2)) was suppressed by aspirin (IC(50) of 5.	Aspirin	134-141	cytochrome c oxidase II, mitochondrial	Mus musculus	59-64
10912743-3	2000	This study assessed the effects of chronic treatment with low doses of aspirin (100 mg/day) on clinic and ambulatory systolic (SBP) and diastolic (DBP) BP in hypertensives on chronic, stable antihypertensive therapy.	Aspirin	71-78	selenium binding protein 1	Homo sapiens	127-130
10567380-9	1999	These results demonstrate that aspirin reduces apo(a) production from hepatocytes via reduction of the transcriptional activity of apo(a) gene with suppression of apo(a) mRNA expression.	Aspirin	31-38	lipoprotein(a)	Homo sapiens	47-53
10567380-9	1999	These results demonstrate that aspirin reduces apo(a) production from hepatocytes via reduction of the transcriptional activity of apo(a) gene with suppression of apo(a) mRNA expression.	Aspirin	31-38	lipoprotein(a)	Homo sapiens	131-137
10567380-9	1999	These results demonstrate that aspirin reduces apo(a) production from hepatocytes via reduction of the transcriptional activity of apo(a) gene with suppression of apo(a) mRNA expression.	Aspirin	31-38	lipoprotein(a)	Homo sapiens	131-137
10567380-10	1999	The suppression of apo(a) production by aspirin may at least in part play a role in the anti-atherogenic effect of aspirin in vascular disorders.	Aspirin	40-47	lipoprotein(a)	Homo sapiens	19-25
10567380-10	1999	The suppression of apo(a) production by aspirin may at least in part play a role in the anti-atherogenic effect of aspirin in vascular disorders.	Aspirin	115-122	lipoprotein(a)	Homo sapiens	19-25
10593167-8	1999	After the administration of low-dose aspirin (40 mg/day) for about 1 month, the TX/PGI ratio decreased to around the normal level.	Aspirin	37-44	glucose-6-phosphate isomerase	Homo sapiens	83-86
10543283-7	1999	Marked increases were observed in the numbers of interleukin (IL)-5 mRNA+ cells (p=0.004) in aspirin-sensitive patients, whereas lower numbers of IL-4 mRNA+ cells were observed, with a trend for a difference from controls (p=0.07).	Aspirin	93-100	interleukin 5	Homo sapiens	49-67
10419767-0	1999	Sites of action for future therapy: an adenosine-dependent mechanism by which aspirin retains its antiinflammatory activity in cyclooxygenase-2 and NFkappaB knockout mice.	Aspirin	78-85	prostaglandin-endoperoxide synthase 2	Mus musculus	127-143
10419767-5	1999	Indeed, aspirin retained its antiinflammatory properties even in COX-2 knockouts.	Aspirin	8-15	cytochrome c oxidase II, mitochondrial	Mus musculus	65-70
10422768-12	1999	Leptin was also effective to attenuate aspirin-induced damage and the accompanying fall in the GBF, whereas CCK-8 dose dependently worsened aspirin damage and failed to influence GBF.	Aspirin	39-46	leptin	Rattus norvegicus	0-6
10207634-3	1999	This study was designed to determine whether treatment with 81 mg of aspirin per day for 3 months would alter two putative surrogate end point biomarkers of chemoprevention of colorectal cancer [i.e., mucosal prostaglandin E2 (PGE2) formation and transforming growth factor alpha (TGF-alpha) expression] in normal-appearing rectal mucosa from individuals with a history of adenomatous polyps.	Aspirin	69-76	transforming growth factor alpha	Homo sapiens	281-290
10207634-6	1999	The extent of TGF-alpha staining in rectal crypts was also reduced significantly (P = 0.039) by daily aspirin.	Aspirin	102-109	transforming growth factor alpha	Homo sapiens	14-23
10207634-8	1999	Thus, 81 mg of aspirin daily significantly reduced rectal mucosal PGE2 formation and TGF-alpha expression in patients with a history of adenomatous polyps.	Aspirin	15-22	transforming growth factor alpha	Homo sapiens	85-94
9850065-3	1998	COX-2-specific inhibitors are less toxic than ASA.	Aspirin	46-49	cytochrome c oxidase II, mitochondrial	Mus musculus	0-5
9736731-6	1998	These results suggest that aspirin/sulindac induces a genetic selection for microsatellite stability in a subset of MMR-deficient cells and may provide an effective prophylactic therapy for hereditary nonpolyposis colorectal cancer kindreds where alteration of the hMSH2 and hMLH1 genes are associated with the majority of cancer susceptibility cases.	Aspirin	27-34	mutS homolog 2	Homo sapiens	265-270
9596581-0	1998	Aspirin-like molecules that covalently inactivate cyclooxygenase-2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	50-66
9596581-1	1998	Many of aspirin"s therapeutic effects arise from its acetylation of cyclooxygenase-2 (COX-2), whereas its antithrombotic and ulcerogenic effects result from its acetylation of COX-1.	Aspirin	8-15	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	68-84
9596581-1	1998	Many of aspirin"s therapeutic effects arise from its acetylation of cyclooxygenase-2 (COX-2), whereas its antithrombotic and ulcerogenic effects result from its acetylation of COX-1.	Aspirin	8-15	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	86-91
9596581-2	1998	Here, aspirin-like molecules were designed that preferentially acetylate and irreversibly inactivate COX-2.	Aspirin	6-13	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	101-106
9663836-0	1997	Aspirin causes rapid up-regulation of cyclo-oxygenase-2 expression in the stomach of rats.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	38-55
9663836-8	1997	Aspirin caused a significant increase in COX-2 mRNA expression and a marked increase in COX-2 immunoreactivity, particularly in the superficial mucosa.	Aspirin	0-7	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	41-46
9663836-8	1997	Aspirin caused a significant increase in COX-2 mRNA expression and a marked increase in COX-2 immunoreactivity, particularly in the superficial mucosa.	Aspirin	0-7	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	88-93
9663836-10	1997	Pre-treatment with prostaglandin E2 prevented the induction of COX-2 by aspirin.	Aspirin	72-79	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	63-68
9663836-13	1997	CONCLUSIONS: These results demonstrate a rapid up-regulation of COX-2 expression in response to aspirin, possibly representing a compensatory response to inhibition of gastric prostaglandin synthesis.	Aspirin	96-103	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	64-69
9640079-2	1997	Aspirin therapy will reduce platelet activation both by its negative effect on platelet aggregation (SPA) and by inhibition of granule release which liberates such mediators as platelet factor 4 (PF4) and plasminogen activator inhibitor 1 (PAI-1).	Aspirin	0-7	surfactant protein A1	Homo sapiens	101-104
9640079-2	1997	Aspirin therapy will reduce platelet activation both by its negative effect on platelet aggregation (SPA) and by inhibition of granule release which liberates such mediators as platelet factor 4 (PF4) and plasminogen activator inhibitor 1 (PAI-1).	Aspirin	0-7	platelet factor 4	Homo sapiens	196-199
9640079-12	1997	Aspirin did not satisfactorily reduce the level of PF4, although it strongly inhibited SPA.	Aspirin	0-7	surfactant protein A1	Homo sapiens	87-90
10528118-6	1999	COX-2 selective inhibitors induced the seizure at earlier onset and more severe mortality within the first hour than indomethacin and aspirin.	Aspirin	134-141	prostaglandin-endoperoxide synthase 2	Mus musculus	0-5
9760036-5	1998	In contrast, at 3 h after carrageenin injection, cyclooxygenase 2 inhibitors significantly inhibited all inflammatory parameters however suppression with piroxicam and aspirin was greater, and more pronounced than at 6 h. NS-398 and nimesulide dosing did not reduce thromboxane B2 production from platelets isolated from rats with carrageenin-induced pleurisy, demonstrating that at the doses used, cyclooxygenase 2 inhibitors did not inhibit cyclooxygenase 1, as platelets contain only this isoform.	Aspirin	168-175	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	399-415
9386173-10	1997	In a different study, subjects were given oral aspirin (75 mg or 1 g) 2 hours before the study.	Aspirin	47-54	olfactory receptor family 1 subfamily G member 1	Homo sapiens	62-71
9760036-5	1998	In contrast, at 3 h after carrageenin injection, cyclooxygenase 2 inhibitors significantly inhibited all inflammatory parameters however suppression with piroxicam and aspirin was greater, and more pronounced than at 6 h. NS-398 and nimesulide dosing did not reduce thromboxane B2 production from platelets isolated from rats with carrageenin-induced pleurisy, demonstrating that at the doses used, cyclooxygenase 2 inhibitors did not inhibit cyclooxygenase 1, as platelets contain only this isoform.	Aspirin	168-175	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	443-459
9726391-0	1998	Activation of genes for spasmolytic peptide, transforming growth factor alpha and for cyclooxygenase (COX)-1 and COX-2 during gastric adaptation to aspirin damage in rats.	Aspirin	148-155	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	113-118
10521370-5	1999	Acetylsalicylic acid pretreatment (300 micromol/L, 30 minutes) significantly reduced the HDL-induced PGI(2) release, suggesting that both preexisting and induced Cox-2 activities were involved in the HDL effect.	Aspirin	0-20	prostaglandin G/H synthase 2	Oryctolagus cuniculus	162-167
9726391-12	1998	This adaptation to ASA was accompanied by approximately a 90% reduction in prostaglandin E2 biosynthesis, by a significant rise in BrdU uptake by glandular cells predominantly in the neck region of gastric glands and by expression of SP (SP/beta-actin ratio; 0.96 +/- 0.08 in ASA-adapted mucosa vs. 0.38 +/- 0.05 in the control mucosa) and TGF alpha (TGF alpha/beta-actin ratio: 0.97 +/- 0.07 in ASA-adapted mucosa vs. 0.77 +/- 0.06 in the control mucosa).	Aspirin	19-22	actin, beta	Rattus norvegicus	241-251
9726391-12	1998	This adaptation to ASA was accompanied by approximately a 90% reduction in prostaglandin E2 biosynthesis, by a significant rise in BrdU uptake by glandular cells predominantly in the neck region of gastric glands and by expression of SP (SP/beta-actin ratio; 0.96 +/- 0.08 in ASA-adapted mucosa vs. 0.38 +/- 0.05 in the control mucosa) and TGF alpha (TGF alpha/beta-actin ratio: 0.97 +/- 0.07 in ASA-adapted mucosa vs. 0.77 +/- 0.06 in the control mucosa).	Aspirin	19-22	actin, beta	Rattus norvegicus	361-371
9726391-14	1998	CONCLUSIONS: (i) Gastric adaptation to aspirin injury involves enhanced cell proliferation which appears to be mediated by increased expression of SP and TGF alpha, and (ii) rapid upregulation of COX-2 expression following single and repeated ASA insults may represent a compensatory response to suppression of prostaglandin generation by this NSAID.	Aspirin	39-46	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	196-201
9052515-13	1997	Aspirin significantly increased TGF-alpha levels in the gastric body and duodenum after one week.	Aspirin	0-7	transforming growth factor alpha	Homo sapiens	32-41
9726391-14	1998	CONCLUSIONS: (i) Gastric adaptation to aspirin injury involves enhanced cell proliferation which appears to be mediated by increased expression of SP and TGF alpha, and (ii) rapid upregulation of COX-2 expression following single and repeated ASA insults may represent a compensatory response to suppression of prostaglandin generation by this NSAID.	Aspirin	243-246	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	196-201
9052515-14	1997	The rise in antral TGF-alpha appeared delayed and blunted by the aspirin treatment compared to control.	Aspirin	65-72	transforming growth factor alpha	Homo sapiens	19-28
10364014-6	1999	A 297-bp fragment of the cagA gene was detected in 96% of the isolates from the NSAID and ASA users and 100% from the non-NSAID users (p = 1.0).	Aspirin	90-93	S100 calcium binding protein A8	Homo sapiens	25-29
10364014-12	1999	A variable region of the cagA gene was more frequently detected in isolates from patients not taking NSAIDs or ASA, suggesting that this gene may be modified by NSAID- or ASA-related factors or that certain strains may be selected for in patients taking these medications.	Aspirin	111-114	S100 calcium binding protein A8	Homo sapiens	25-29
9808873-11	1998	Differences in BTG levels between aspirin-treated and aspirin-untreated patients became significant at 48 hours after thrombolysis in both groups.	Aspirin	34-41	pro-platelet basic protein	Homo sapiens	15-18
10364014-12	1999	A variable region of the cagA gene was more frequently detected in isolates from patients not taking NSAIDs or ASA, suggesting that this gene may be modified by NSAID- or ASA-related factors or that certain strains may be selected for in patients taking these medications.	Aspirin	171-174	S100 calcium binding protein A8	Homo sapiens	25-29
9052515-22	1997	Further studies of mucosal levels of TGF-alpha in response to aspirin-induced injury in humans appear warranted.	Aspirin	62-69	transforming growth factor alpha	Homo sapiens	37-46
9808873-11	1998	Differences in BTG levels between aspirin-treated and aspirin-untreated patients became significant at 48 hours after thrombolysis in both groups.	Aspirin	54-61	pro-platelet basic protein	Homo sapiens	15-18
9023270-6	1997	When calcium ionophore A23187 was used to mobilize endogenous AA, acetylsalicylic acid and indomethacin equipotently inhibited both PGHS-1 and PGHS-2 isozymes.	Aspirin	66-86	prostaglandin-endoperoxide synthase 2	Mus musculus	143-149
8941724-5	1996	We now report that aspirin inhibits the IL-1beta-induced sPLA2 activity in rat mesangial cells in a dose-dependent manner.	Aspirin	19-26	phospholipase A2 group IIA	Rattus norvegicus	57-62
8941724-6	1996	The IC50 value of aspirin for sPLA2 inhibition was 6.5 mM.	Aspirin	18-25	phospholipase A2 group IIA	Rattus norvegicus	30-35
10096266-1	1999	BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and indomethacin (INN, indometacin) inhibit both the constitutive (COX-1) and inducible (COX-2) isoforms of cyclooxygenase.	Aspirin	66-73	cytochrome c oxidase subunit I	Cricetulus griseus	153-158
9706843-0	1998	Effect of acetaldehyde and acetylsalicylic acid on HbA1c chromatography in the FPLC method with Mono S cation exchanger.	Aspirin	27-47	hemoglobin subunit alpha 1	Homo sapiens	51-55
8941724-7	1996	This decrease in sPLA2 activity was not due to direct inhibition of enzymatic activity but rather to the fact that aspirin inhibits the expression of IL-1beta-induced sPLA2 protein and mRNA.	Aspirin	115-122	phospholipase A2 group IIA	Rattus norvegicus	17-22
8941724-7	1996	This decrease in sPLA2 activity was not due to direct inhibition of enzymatic activity but rather to the fact that aspirin inhibits the expression of IL-1beta-induced sPLA2 protein and mRNA.	Aspirin	115-122	phospholipase A2 group IIA	Rattus norvegicus	167-172
8941724-8	1996	Furthermore, by electrophoretic mobility shift analysis we demonstrate reduced DNA binding of the nuclear factor kappaB, an essential component of the IL-1beta-dependent upregulation of sPLA2 gene transcription, after treatment of the cells with aspirin.	Aspirin	246-253	phospholipase A2 group IIA	Rattus norvegicus	186-191
8941724-9	1996	The study described in this report indicates that the inhibition of sPLA2 expression as induced by pro-inflammatory cytokines potentially represents an additional mechanism of action for aspirin.	Aspirin	187-194	phospholipase A2 group IIA	Rattus norvegicus	68-73
10092995-4	1999	Aspirin inhibited nitric oxide release from IL-1 beta-stimulated BVSMCs in a dose-dependent manner.	Aspirin	0-7	interleukin 1 beta	Bos taurus	44-53
9627095-10	1998	Aspirin, but not NCX-4016, markedly suppressed systemic COX-1 and COX-2 activity, and colonic prostaglandin synthesis.	Aspirin	0-7	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	66-71
8883266-5	1996	Treatment of erythromelalgia with aspirin resulted in disappearance of erythromelalgic signs and symptoms, which was paralleled by a significant decrease of beta-TG and TM levels.	Aspirin	34-41	pro-platelet basic protein	Homo sapiens	157-164
9334204-0	1997	Inhibition of ultraviolet B-induced activator protein-1 (AP-1) activity by aspirin in AP-1-luciferase transgenic mice.	Aspirin	75-82	jun proto-oncogene	Mus musculus	57-61
10203577-13	1999	In addition, aspirin and indomethacin, but not CyA, induced Hsp70 expression in HUVECs that correlated with induction of HSF-1 activity.	Aspirin	13-20	heat shock transcription factor 1	Homo sapiens	121-126
9334204-0	1997	Inhibition of ultraviolet B-induced activator protein-1 (AP-1) activity by aspirin in AP-1-luciferase transgenic mice.	Aspirin	75-82	jun proto-oncogene	Mus musculus	86-90
9334204-7	1997	The topical pretreatment of mouse skin with aspirin markedly blocked the UVB-induced AP-1 transactivation in vivo.	Aspirin	44-51	jun proto-oncogene	Mus musculus	85-89
9361993-2	1997	Glucose suppressed the aspirin-induced histidine decarboxylase activity without changing serum gastrin.	Aspirin	23-30	histidine decarboxylase	Rattus norvegicus	39-62
9822550-3	1998	Compound 70 selectively inactivates COX-2 by acetylating the same serine residue that aspirin acetylates.	Aspirin	86-93	prostaglandin-endoperoxide synthase 2	Mus musculus	36-41
9822550-12	1998	That COX-2 inhibition by aspirin resulted from the acetylation of Ser516 was confirmed by tryptic digestion and peptide mapping of COX-2 labeled with [1-14C-acetyl]salicyclic acid.	Aspirin	25-32	prostaglandin-endoperoxide synthase 2	Mus musculus	5-10
9822550-12	1998	That COX-2 inhibition by aspirin resulted from the acetylation of Ser516 was confirmed by tryptic digestion and peptide mapping of COX-2 labeled with [1-14C-acetyl]salicyclic acid.	Aspirin	25-32	prostaglandin-endoperoxide synthase 2	Mus musculus	131-136
9196254-10	1997	The cytotoxic activity of splenic natural killer cells against YAC-1 cells was reduced by 60% (P = .002); treatment with acetylsalicylic acid (254 mg/kg of diet) reduced the NNK-induced natural killer cell cytotoxicity inhibition by 50% (P = .02), whereas the administration of the specific cyclooxygenase-2 inhibitor NS-398 (7 mg/kg of diet) resulted in an almost complete recovery (approximately 95%, P = .04) of natural killer cell activity.	Aspirin	121-141	prostaglandin-endoperoxide synthase 2	Mus musculus	291-307
9769277-1	1998	We determined the effect of a long acting beta2-agonist, salmeterol, on aspirin-induced asthma (AIA) attacks and urinary release of eicosanoids in a double-blind, placebo-controlled, crossover study in 10 asthmatics sensitive to aspirin.	Aspirin	72-79	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	42-47
10639270-8	1997	Using the Cox model, adjusting for variables significantly associated with outcome, aspirin use remained a significant predictor of 14-day outcome (p = 0.04) but not of 12-week outcome (p = 0.06).	Aspirin	84-91	cytochrome c oxidase subunit 8A	Homo sapiens	10-13
9556499-5	1998	During pregnancy induced hypertension (PIH) and in occlusive disorders, aspirin provides relief through inhibition of cyclooxygenase, an enzyme required for the metabolism of arachidonic acid to produce prostaglandins and prostacyclins in platelets and in endothelial cells.	Aspirin	72-79	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	39-42
8910005-0	1996	Aspirin changes the secretion rate and amino acid composition of human small intestinal mucin in subjects with ileal conduits.	Aspirin	0-7	LOC100508689	Homo sapiens	88-93
9443604-3	1998	Histofluorescence staining for PGHS activity in intact cells demonstrated that quiescent 3T3 cells expressed only PGHS-1 activity and serum-activated 3T3 cells pretreated with aspirin expressed only PGHS-2 activity.	Aspirin	176-183	prostaglandin-endoperoxide synthase 2	Mus musculus	199-205
8910005-2	1996	Aspirin (600 mg per day, administered orally) increased the daily mucin output by 37-104% in subjects by days 3 or 4, but thereafter the mucin output declined to below the baseline level by day 10.	Aspirin	0-7	LOC100508689	Homo sapiens	66-71
8910005-2	1996	Aspirin (600 mg per day, administered orally) increased the daily mucin output by 37-104% in subjects by days 3 or 4, but thereafter the mucin output declined to below the baseline level by day 10.	Aspirin	0-7	LOC100508689	Homo sapiens	137-142
10328851-2	1998	To assess the changes in cytoskeleton induced by thrombin and PMA, suspensions of aspirin-treated,32P-prelabeled, washed pig platelets in Hepes buffer containing ADP scavengers were activated with thrombin, and with PMA, an activator of protein kinase C. The cytoskeletal fraction was prepared by adding Triton extraction buffer.	Aspirin	82-89	coagulation factor II, thrombin	Sus scrofa	197-205
8910005-5	1996	One possible explanation, consistent with the compositional analyses, is that the N- and C-terminal regions of the mucin subunits have been cleaved off and lost during aspirin administration.	Aspirin	168-175	LOC100508689	Homo sapiens	115-120
10608053-11	1998	Patients treated with aspirin showed lower levels of BTG only from the 48th hour after thrombolysis in both groups.	Aspirin	22-29	pro-platelet basic protein	Homo sapiens	53-56
8910005-6	1996	The observed changes in mucin secretion may have implications for the mechanism of the toxic effects of aspirin on the small intestine by altering the barrier properties of the mucus layer.	Aspirin	104-111	LOC100508689	Homo sapiens	24-29
10608053-20	1998	Treatment with aspirin reduced beta-thromboglobulin plasma levels only at 48th hour in both groups.	Aspirin	15-22	pro-platelet basic protein	Homo sapiens	31-51
8768288-4	1996	The authors recorded therefore an increase of prostaglandin metabolites and PF4 even in patients who were treated with ASA before the invasive examination.	Aspirin	119-122	platelet factor 4	Homo sapiens	76-79
8868511-7	1996	Additionally, in five YSMI patients the influence of prolonged aspirin administration (0.3g daily for more than 30 days) on the Fraxiparine mobilsable pool of PF4 and beta-thromboglobulin (beta-TG) concentration in the plasma was determined after injection of 180 IC anti-Xa U/kg b.w.	Aspirin	63-70	platelet factor 4	Homo sapiens	159-162
9372649-0	1997	Expression of interleukin-5 and granulocyte-macrophage colony-stimulating factor in aspirin-sensitive and non-aspirin-sensitive asthmatic airways.	Aspirin	84-91	interleukin 5	Homo sapiens	14-27
9372649-5	1997	ASA airways demonstrated a significant 2-fold increase in the total number of submucosal inflammatory cells expressing IL-5 (p = 0.03) and approximate 4- and 2-fold increases in the numbers of mast cells expressing IL-5 and GM-CSF (p = 0.02 and p = 0.04, respectively).	Aspirin	0-3	interleukin 5	Homo sapiens	119-123
9372649-5	1997	ASA airways demonstrated a significant 2-fold increase in the total number of submucosal inflammatory cells expressing IL-5 (p = 0.03) and approximate 4- and 2-fold increases in the numbers of mast cells expressing IL-5 and GM-CSF (p = 0.02 and p = 0.04, respectively).	Aspirin	0-3	interleukin 5	Homo sapiens	215-219
9372649-7	1997	These results suggest a central role for the mast cell and eosinophil in regulation of the inflammatory cell infiltrate of ASA airways by secretion of the hemopoietic cytokines IL-5 and GM-CSF.	Aspirin	123-126	interleukin 5	Homo sapiens	177-181
8868511-7	1996	Additionally, in five YSMI patients the influence of prolonged aspirin administration (0.3g daily for more than 30 days) on the Fraxiparine mobilsable pool of PF4 and beta-thromboglobulin (beta-TG) concentration in the plasma was determined after injection of 180 IC anti-Xa U/kg b.w.	Aspirin	63-70	pro-platelet basic protein	Homo sapiens	167-187
8549662-7	1996	Parallel to their effect on cell cycle, ASA and indomethacin also reduced the levels of p34cdc2 and p33cdk2, two cyclin-dependent kinases that are important for cell cycle progression.	Aspirin	40-43	cyclin dependent kinase 2	Homo sapiens	100-107
9360028-6	1997	A small (approximately 2 mmHg in the 24h mean of SBP), but statistically significant, BP reduction was found when 500 mg/day ASA was given to healthy volunteers at Time 2.	Aspirin	125-128	selenium binding protein 1	Homo sapiens	49-52
7608559-6	1995	The initial PGD2 burst in activated MMC-34 cells is prevented by aspirin pretreatment, suggesting that constitutive PGS-1 present in mast cells before activation is responsible for the early PGD2 production in response to activation.	Aspirin	65-72	phosphatidylglycerophosphate synthase 1	Mus musculus	116-121
9244238-8	1997	In contrast, luminal stenosis was only 11+/-12% and 6+/-3% in pigs given high and low doses, respectively, of rTFPI for 24 hours compared with 46+/-22% in pigs given heparin for 24 hours and 40+/-19% in those given both heparin and aspirin (P&lt;.0002).	Aspirin	232-239	tissue factor pathway inhibitor	Rattus norvegicus	110-115
7872783-4	1995	Based on these differences between PGHS-1 and PGHS-2, we reasoned that a salicylate ester containing an acyl group somewhat larger than the acetyl group of aspirin might be a selective inhibitor of PGHS-2.	Aspirin	156-163	prostaglandin-endoperoxide synthase 2	Mus musculus	198-204
9259112-9	1997	According to the Cox"s proportional hazards model, the estimated risk ratio (ASA group vs. nicametate group) was 0.538, with a 95% confidence interval of 0.284-1.019.	Aspirin	77-80	cytochrome c oxidase subunit 8A	Homo sapiens	17-20
9152412-7	1997	After the macrophages were treated with aspirin to inactivate existing COX-1 and COX-2, however, treatment with 12-0-tetradecanoylphorbol 13-acetate increased PGE2 production.	Aspirin	40-47	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	81-86
7525421-5	1994	Gastric adaptation to aspirin was accompanied by a significant rise in gastric blood flow, reduction in both blood neutrophilia and mucosal neutrophil infiltration, and a remarkable increase in mucosal cell regeneration and mucosal content of epidermal growth factor.	Aspirin	22-29	epidermal growth factor like 1	Rattus norvegicus	243-266
9092536-0	1997	Inhibition of activator protein 1 activity and neoplastic transformation by aspirin.	Aspirin	76-83	jun proto-oncogene	Mus musculus	14-33
9092536-5	1997	Aspirin and aspirin-like salicylates inhibited the activation of AP-1 in the same dose range as seen for the inhibition of tumor promoter-induced transformation.	Aspirin	0-7	jun proto-oncogene	Mus musculus	65-69
9092536-5	1997	Aspirin and aspirin-like salicylates inhibited the activation of AP-1 in the same dose range as seen for the inhibition of tumor promoter-induced transformation.	Aspirin	12-19	jun proto-oncogene	Mus musculus	65-69
7946179-10	1994	Addition of aspirin to nitrendipine produced a significant decrease and flattening of the beta-TG curve, whereas the combination of aspirin and isradipine was accompanied by a partial increase in plasma beta-TG levels.	Aspirin	12-19	pro-platelet basic protein	Homo sapiens	90-97
9092536-8	1997	The inhibition effects on the activation of AP-1 activity by aspirin and aspirin-like salicylates may further explain the anti-carcinogenesis mechanism of action of these drugs.	Aspirin	61-68	jun proto-oncogene	Mus musculus	44-48
9092536-8	1997	The inhibition effects on the activation of AP-1 activity by aspirin and aspirin-like salicylates may further explain the anti-carcinogenesis mechanism of action of these drugs.	Aspirin	73-80	jun proto-oncogene	Mus musculus	44-48
7946179-10	1994	Addition of aspirin to nitrendipine produced a significant decrease and flattening of the beta-TG curve, whereas the combination of aspirin and isradipine was accompanied by a partial increase in plasma beta-TG levels.	Aspirin	132-139	pro-platelet basic protein	Homo sapiens	203-210
8205303-9	1994	Aspirin added to nitrendipine led to a further significant decrease in beta-TG levels whereas its addition to isradipine was accompanied by a partial increase in plasma beta-TG.	Aspirin	0-7	pro-platelet basic protein	Homo sapiens	71-78
9226224-8	1997	However, on the basis of its physiology and pathophysiology, low-dose aspirin has been recommended in pregnancies at risk to prevent or, at least, to delay the occurrence of PE-E.	Aspirin	70-77	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	174-178
8970343-5	1996	Fifteen minutes after aspirin instillation, there was a statistically significant rise in peptido-leukotrienes, IL-5, and eosinophil number in AIA, but not in ATA, but not in ATA patients.	Aspirin	22-29	interleukin 5	Homo sapiens	112-116
8265610-4	1993	Aspirin, indomethacin, and ibuprofen were more potent inhibitors of COX-1 than COX-2 in all models used.	Aspirin	0-7	cytochrome c oxidase subunit II	Ovis aries	79-84
8840947-9	1996	In this case-controlled retrospective series of renal transplant patients with documented CsA-TMA, the triple-drug combination of isradipine, aspirin, and pentoxifylline allowed for the successful reinstitution of CsA or conversion to FK506 in the setting of TMA, and resulted in increased transplant survival compared with previous reports.	Aspirin	142-149	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	214-217
8153084-4	1993	Amnion cells treated with IL-1 beta recovered rapidly from aspirin pretreatment suggesting an action on fatty acid cyclooxygenase (COX).	Aspirin	59-66	cytochrome c oxidase subunit 8A	Homo sapiens	131-134
8724348-7	1996	Soluble CR1 inhibited ASA- and C-mediated neutrophil aggregation by 46% and sperm phagocytosis by 57%.	Aspirin	22-25	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	8-11
8454631-2	1993	Aspirin completely inhibited bis-oxygenation of arachidonate by PGH synthase-1; in contrast, aspirin-treated PGH synthase-2 metabolized arachidonate primarily to 15-hydroxyeicosatetraenoic acid (15-HETE) instead of PGH2.	Aspirin	93-100	prostaglandin-endoperoxide synthase 2	Mus musculus	109-123
8466742-9	1993	Aspirin added to nitrendipine produced a significant decrease in beta-TG levels whereas isradipine plus aspirin was accompanied by a partial increase in beta-TG.	Aspirin	0-7	pro-platelet basic protein	Homo sapiens	65-72
21544484-4	1996	Aspirin increased HLA-DR alpha steady-state mRNA levels and HLA-DR alpha gene transcription rate.	Aspirin	0-7	major histocompatibility complex, class II, DR alpha	Homo sapiens	18-30
21544484-4	1996	Aspirin increased HLA-DR alpha steady-state mRNA levels and HLA-DR alpha gene transcription rate.	Aspirin	0-7	major histocompatibility complex, class II, DR alpha	Homo sapiens	60-72
8466742-9	1993	Aspirin added to nitrendipine produced a significant decrease in beta-TG levels whereas isradipine plus aspirin was accompanied by a partial increase in beta-TG.	Aspirin	104-111	pro-platelet basic protein	Homo sapiens	153-160
1341072-4	1992	We have identified the following biological roles for TGF alpha in the stomach, using a variety of primate and rodent models: inhibition of acid secretion; stimulation of mucous cell growth; protection against ethanol- and aspirin-induced injury.	Aspirin	223-230	transforming growth factor alpha	Homo sapiens	54-63
1285867-2	1992	Data from our studies and from a number of prospective controlled trials have suggested that aspirin in doses of 60-150 md/day during the second and third trimester reduces the risk of PIH and improves maternal and neonatal outcomes.	Aspirin	93-100	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	185-188
1285867-4	1992	However, meta-analysis of existing trials suggests that low dose aspirin reduces the risk of PIH and severe low birth weight.	Aspirin	65-72	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	93-96
1285867-8	1992	On the basis of these findings and pending the results of ongoing large-scale randomized multicenter trials, we suggest that daily low dose aspirin (1 to 2 mg/kg/day) be recommended only for select women at high risk for developing PIH and its associated complications.	Aspirin	140-147	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	232-235
1632294-0	1992	Platelet PGI2-receptor behaviour change after treatment with acetylsalicylic acid in healthy volunteers.	Aspirin	61-81	prostaglandin I2 receptor	Homo sapiens	9-22
1632294-1	1992	After treatment of human platelet membrane fractions with different concentrations of acetylsalicylic acid (ASA) the Iloprost binding capacity (Bmax) and also the dissociation constant (Kd) of the high-affinity PGI2-receptor increased significantly (p less than 0.01, low-affinity receptor only an increase of Bmax, p less than 0.01), whereas only a significant (p less than 0.05) increase of the Kd of the high-affinity receptor was observed for intact platelets.	Aspirin	86-106	prostaglandin I2 receptor	Homo sapiens	211-224
1632294-1	1992	After treatment of human platelet membrane fractions with different concentrations of acetylsalicylic acid (ASA) the Iloprost binding capacity (Bmax) and also the dissociation constant (Kd) of the high-affinity PGI2-receptor increased significantly (p less than 0.01, low-affinity receptor only an increase of Bmax, p less than 0.01), whereas only a significant (p less than 0.05) increase of the Kd of the high-affinity receptor was observed for intact platelets.	Aspirin	108-111	prostaglandin I2 receptor	Homo sapiens	211-224
1830520-5	1991	This was significantly reduced by pretreatment with low-dose aspirin (1 mg/kg/day), by high-dose aspirin (20 mg/kg/day) plus dipyridamole, and especially by thrombin inhibition with hirudin.	Aspirin	61-68	coagulation factor II, thrombin	Sus scrofa	157-165
8631786-7	1996	The phosphorylation of Vav in response to thrombin was maximal within 15 s and was unaffected by aspirin, inhibitors of aggregation, or the presence of the ADP scavenger, apyrase.	Aspirin	97-104	vav guanine nucleotide exchange factor 1	Homo sapiens	23-26
8527516-14	1995	These findings strongly implicate the CD11b/CD18 glycoprotein complex (CR3) in the adhesive events involved in ASA- and C-mediated immune destruction of motile sperm by neutrophils.	Aspirin	111-114	teratocarcinoma-derived growth factor 1 pseudogene 3	Homo sapiens	71-74
1829118-2	1991	Previous clinical trials with small numbers of patients have suggested that aspirin in doses of 60 to 150 mg/d during the second and third trimesters reduces the risk of PIH and improves maternal and neonatal outcomes.	Aspirin	76-83	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	170-173
8549027-11	1995	Children also taking enzyme-inducing antiepileptic drugs require a larger valproic acid dose/kg, whereas the coadministration of aspirin (acetylsalicylic acid) may decrease the clearance of unbound drug (CLu/F), and thus require a decrease in the daily dose of valproic acid.	Aspirin	129-136	clusterin	Homo sapiens	204-207
8549027-11	1995	Children also taking enzyme-inducing antiepileptic drugs require a larger valproic acid dose/kg, whereas the coadministration of aspirin (acetylsalicylic acid) may decrease the clearance of unbound drug (CLu/F), and thus require a decrease in the daily dose of valproic acid.	Aspirin	138-158	clusterin	Homo sapiens	204-207
1829118-3	1991	OBJECTIVE: --We performed a meta-analysis of the six published controlled trials to estimate more precisely (1) the magnitude of protection of aspirin from PIH; (2) the effect of aspirin on severe low-birth-weight infants, cesarean section, and perinatal mortality; and (3) the risk of adverse effects.	Aspirin	143-150	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	156-159
1829118-6	1991	RESULTS: --Among 394 subjects from six trials, the RR of PIH among women who took aspirin was 0.35 (95% confidence interval [CI], 0.22 to 0.55) and the number needed to be treated was 4.4, meaning that between four and five high-risk women would need to be treated with aspirin to prevent one case of PIH.	Aspirin	82-89	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	57-60
7587793-2	1995	Previous studies have demonstrated that aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) can both inhibit gallbladder mucin secretion and prevent gallstone formation in animal models of cholesterol gallstone disease.	Aspirin	40-47	LOC100508689	Homo sapiens	132-137
1829118-6	1991	RESULTS: --Among 394 subjects from six trials, the RR of PIH among women who took aspirin was 0.35 (95% confidence interval [CI], 0.22 to 0.55) and the number needed to be treated was 4.4, meaning that between four and five high-risk women would need to be treated with aspirin to prevent one case of PIH.	Aspirin	82-89	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	301-304
7560666-11	1995	A clinical history of aspirin sensitivity was strongly correlated with nonallergic CHS/NP, as well as the nonallergic CHS/NP profile of cytokines, including IFN-gamma.	Aspirin	22-29	lysosomal trafficking regulator	Homo sapiens	83-89
1829118-6	1991	RESULTS: --Among 394 subjects from six trials, the RR of PIH among women who took aspirin was 0.35 (95% confidence interval [CI], 0.22 to 0.55) and the number needed to be treated was 4.4, meaning that between four and five high-risk women would need to be treated with aspirin to prevent one case of PIH.	Aspirin	270-277	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	57-60
7560666-16	1995	Aspirin sensitivity is strongly correlated with nonallergic CHS/NP and production of the nonallergic CHS/NP profile of cytokines, including IFN-gamma.	Aspirin	0-7	lysosomal trafficking regulator	Homo sapiens	60-66
7560666-16	1995	Aspirin sensitivity is strongly correlated with nonallergic CHS/NP and production of the nonallergic CHS/NP profile of cytokines, including IFN-gamma.	Aspirin	0-7	lysosomal trafficking regulator	Homo sapiens	101-107
1829118-9	1991	CONCLUSION: --This meta-analysis suggests that low-dose aspirin reduces the risks of PIH and severe low birth weight, with no observed risk of maternal or neonatal adverse effects.	Aspirin	56-63	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	85-88
1829277-0	1991	Stimulation of plasmin activity by aspirin.	Aspirin	35-42	plasminogen	Homo sapiens	15-22
7475134-4	1995	Coronary vascular resistance before and after ischemia were lower in the aspirin plus L-arginine group (0.19 +/- 0.03 dynes.sec/cm5, p = 0.001, and 0.23 +/- 0.04 dynes.sec/cm5, p = 0.01, respectively) compared with those of the control group (0.24 +/- 0.02 and 0.28 +/- 0.07 dynes.sec/cm5, respectively).	Aspirin	73-80	Cardiac mass QTL 5	Rattus norvegicus	128-131
7475134-4	1995	Coronary vascular resistance before and after ischemia were lower in the aspirin plus L-arginine group (0.19 +/- 0.03 dynes.sec/cm5, p = 0.001, and 0.23 +/- 0.04 dynes.sec/cm5, p = 0.01, respectively) compared with those of the control group (0.24 +/- 0.02 and 0.28 +/- 0.07 dynes.sec/cm5, respectively).	Aspirin	73-80	Cardiac mass QTL 5	Rattus norvegicus	172-175
7475134-4	1995	Coronary vascular resistance before and after ischemia were lower in the aspirin plus L-arginine group (0.19 +/- 0.03 dynes.sec/cm5, p = 0.001, and 0.23 +/- 0.04 dynes.sec/cm5, p = 0.01, respectively) compared with those of the control group (0.24 +/- 0.02 and 0.28 +/- 0.07 dynes.sec/cm5, respectively).	Aspirin	73-80	Cardiac mass QTL 5	Rattus norvegicus	172-175
1829277-1	1991	This study demonstrates an enhancing effect of aspirin on the amidolytic activity of plasmin.	Aspirin	47-54	plasminogen	Homo sapiens	85-92
1829277-2	1991	The stimulation of plasmin by aspirin was concentration-dependent and was attained at aspirin concentrations above 2 x 10(-4) M. Aspirin produced a small, reproducible and statistically significant stimulation of the chromogenic activity of plasmin upon H-D-Valyl-L-Leucyl-L-Lysine-p-nitroanilide (S-2251) or pyro-Glu-Gly-Arg-p-nitroanilide (S-2444).	Aspirin	30-37	plasminogen	Homo sapiens	19-26
1829277-2	1991	The stimulation of plasmin by aspirin was concentration-dependent and was attained at aspirin concentrations above 2 x 10(-4) M. Aspirin produced a small, reproducible and statistically significant stimulation of the chromogenic activity of plasmin upon H-D-Valyl-L-Leucyl-L-Lysine-p-nitroanilide (S-2251) or pyro-Glu-Gly-Arg-p-nitroanilide (S-2444).	Aspirin	30-37	plasminogen	Homo sapiens	241-248
1829277-2	1991	The stimulation of plasmin by aspirin was concentration-dependent and was attained at aspirin concentrations above 2 x 10(-4) M. Aspirin produced a small, reproducible and statistically significant stimulation of the chromogenic activity of plasmin upon H-D-Valyl-L-Leucyl-L-Lysine-p-nitroanilide (S-2251) or pyro-Glu-Gly-Arg-p-nitroanilide (S-2444).	Aspirin	86-93	plasminogen	Homo sapiens	19-26
1829277-2	1991	The stimulation of plasmin by aspirin was concentration-dependent and was attained at aspirin concentrations above 2 x 10(-4) M. Aspirin produced a small, reproducible and statistically significant stimulation of the chromogenic activity of plasmin upon H-D-Valyl-L-Leucyl-L-Lysine-p-nitroanilide (S-2251) or pyro-Glu-Gly-Arg-p-nitroanilide (S-2444).	Aspirin	129-136	plasminogen	Homo sapiens	19-26
1829277-2	1991	The stimulation of plasmin by aspirin was concentration-dependent and was attained at aspirin concentrations above 2 x 10(-4) M. Aspirin produced a small, reproducible and statistically significant stimulation of the chromogenic activity of plasmin upon H-D-Valyl-L-Leucyl-L-Lysine-p-nitroanilide (S-2251) or pyro-Glu-Gly-Arg-p-nitroanilide (S-2444).	Aspirin	129-136	plasminogen	Homo sapiens	241-248
1829277-3	1991	Kinetic analysis demonstrated a slight decrease in the affinity of plasmin for substrate S-2251 in the presence of aspirin, reflected by a change of the Km from 3.2 x 10(-4) M to 3.8 x 10(-4) M, and an increase of the Vm.	Aspirin	115-122	plasminogen	Homo sapiens	67-74
1829277-6	1991	The effect of AHA suggests a specific involvement of lysine binding sites (LBS) on plasmin in the interaction of the enzyme with aspirin.	Aspirin	129-136	plasminogen	Homo sapiens	83-90
1829277-7	1991	Transient acidification of plasmin abolished its response to aspirin, to AHA and to their combination.	Aspirin	61-68	plasminogen	Homo sapiens	27-34
1829277-10	1991	It is conceivable that in addition to the antithrombotic effect of aspirin ascribed to its interaction with the platelets, aspirin also directly stimulates plasmin activity.	Aspirin	123-130	plasminogen	Homo sapiens	156-163
2147914-2	1990	Ticlopidine and aspirin/dipyridamole, but not xanthinol nicotinate, improved platelet aggregation, reduced beta-thromboglobulin, platelet factor IV and fibrinopeptide A concentrations, and increased antithrombin III concentrations and red blood cell filterability.	Aspirin	16-23	pro-platelet basic protein	Homo sapiens	107-127
2139442-0	1990	Increased plasma beta-thromboglobulin in patients with coronary artery vein graft occlusion: response to low dose aspirin.	Aspirin	114-121	pro-platelet basic protein	Homo sapiens	17-37
2139442-3	1990	Serial beta-thromboglobulin levels were measured in 105 patients randomized to receive aspirin (324 mg/day) or placebo beginning within 1 h after surgery.	Aspirin	87-94	pro-platelet basic protein	Homo sapiens	7-27
2139442-9	1990	The reduction in beta-thromboglobulin concentration from the preoperative level to 12 months postoperatively was greater in the aspirin-treated group (p less than 0.001).	Aspirin	128-135	pro-platelet basic protein	Homo sapiens	17-37
2139442-10	1990	Multivariate logistic regression analysis demonstrated a significant association between preoperative beta-thromboglobulin concentration and graft occlusion (p less than 0.02), and aspirin treatment was effective in preventing occlusion when adjusted for the preoperative beta-thromboglobulin level (p less than 0.005).	Aspirin	181-188	pro-platelet basic protein	Homo sapiens	272-292
34942378-6	2022	Inhibition of COX-1 with aspirin, as expected, completely abolished production of TxA2 and PGD/E2, but also significantly inhibited the release of 11-HETE (89 +- 3%) and 9-HODE (74 +- 6%), and reduced 15-HETE and 13-HODE by ~33 %.	Aspirin	25-32	phosphoglycerate dehydrogenase	Homo sapiens	91-94
34641628-5	2021	6.5 times stronger than that of SNT-MLT (43.3% and 6.7% enzyme inhibition, equivalent to the activity of acetylsalicylic acid in conc.	Aspirin	105-125	MALT1 paracaspase	Homo sapiens	36-39
34730204-0	2021	Comparison between use of direct oral anticoagulants and aspirin for risk of thromboembolism complications in patients undergoing total knee and hip arthroplasty: a systematic review and meta-analysis.	Aspirin	57-64	hedgehog interacting protein	Homo sapiens	145-148
34692356-0	2021	Aspirin Compared With Other Anticoagulants for Use as Venous Thromboembolism Prophylaxis in Elective Orthopaedic Hip and Knee Operations: A Narrative Literature Review.	Aspirin	0-7	hedgehog interacting protein	Homo sapiens	113-116
34576324-8	2021	Furthermore, preincubation with either apamin plus TRAM-34 or paxillin significantly attenuated aspirin vasodilation (p < 0.05).	Aspirin	96-103	paxillin	Rattus norvegicus	62-70
34589424-5	2021	Here, we aimed to (1) compare the effects of aspirin and clopidogrel on pancreatic cancer prevention, (2) characterize the effects of clopidogrel (platelet P2RY12 inhibitor) on cancer-associated thrombosis and cancer growth in vivo, (3) determine the effect of P2RY12 across different digestive-tract cancers in vitro, and (4) analyze the expression pattern of P2RY12 in two different cancer types affecting the digestive system.	Aspirin	45-52	purinergic receptor P2Y12	Homo sapiens	361-367
34572022-3	2021	Among them, lipoxins (LXA4) and aspirin-triggered lipoxin A4 (AT-LXA4) mediate beneficial responses through the activation of N-formyl peptide receptor-2 (FPR2).	Aspirin	32-39	formyl peptide receptor 2	Rattus norvegicus	126-153
8771423-8	1996	However, increased TGF-alpha expression after ASA was noted, particularly in hyperplastic surface epithelium.	Aspirin	46-49	transforming growth factor alpha	Homo sapiens	19-28
8771423-11	1996	Healthy subjects on prolonged ASA treatment gradually develop parameters of chronic reactive gastritis accompanied by increased TGF-alpha expression in gastric surface epithelial cells, especially in hyperplastic areas.	Aspirin	30-33	transforming growth factor alpha	Homo sapiens	128-137
34572022-3	2021	Among them, lipoxins (LXA4) and aspirin-triggered lipoxin A4 (AT-LXA4) mediate beneficial responses through the activation of N-formyl peptide receptor-2 (FPR2).	Aspirin	32-39	formyl peptide receptor 2	Rattus norvegicus	155-159
34157031-6	2021	Notably, KNL and KNM doses stimulated the rate of enzyme activities of APX, GR and DHAR, involved in the AsA-GSH cycle thereby efficiently regulates the level of AsA and GSH in Trigonella grown under Cd stress.	Aspirin	105-108	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	71-74
8726470-4	1996	In this study, it was demonstrated that among four fusion inhibitors, aspirin, doxorubicin, HMBA and TPA, three of the inhibitors, except for TPA, inhibited myogenin gene expression.	Aspirin	70-77	myogenin	Homo sapiens	157-165
34157031-6	2021	Notably, KNL and KNM doses stimulated the rate of enzyme activities of APX, GR and DHAR, involved in the AsA-GSH cycle thereby efficiently regulates the level of AsA and GSH in Trigonella grown under Cd stress.	Aspirin	162-165	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	71-74
8591993-8	1996	Induction of hsp27 and alpha B crystallin in adrenal glands of heat-stressed (42 degrees C for 15 min) rats was also enhanced by prior injection of aspirin, another inhibitor of cyclooxygenase.	Aspirin	148-155	heat shock protein family B (small) member 1	Rattus norvegicus	13-18
34202960-8	2021	RESULTS: Clopidogrel vs. aspirin monotherapy was associated with better endothelial function (RHI: 2.11 +- 0.77% vs. 1.87 +- 0.72%, p = 0.045), lower platelet reactivity (130 +- 64 vs. 214 +- 50 P2Y12 reaction unit (PRU), p < 0.001) and prolonged reaction time (TEG R: 5.5 +- 1.2 vs. 5.1 +- 1.1 min, p = 0.037).	Aspirin	25-32	purinergic receptor P2Y12	Homo sapiens	195-200
8591993-8	1996	Induction of hsp27 and alpha B crystallin in adrenal glands of heat-stressed (42 degrees C for 15 min) rats was also enhanced by prior injection of aspirin, another inhibitor of cyclooxygenase.	Aspirin	148-155	crystallin, alpha B	Rattus norvegicus	23-41
8658372-7	1996	RESULTS: A decrease in both absolute mast cell numbers staining with mast cell tryptase (AA1) and the percentage of mast cells co-immunostaining with 5-lipoxygenase was seen in the ASA patients after lysine aspirin challenge compared with the non-ASA control group.	Aspirin	181-184	AA1	Homo sapiens	89-92
34071189-10	2021	Furthermore, miR-126, Let-7e and miR-223 expressions in the clopidogrel group were significantly higher than in the ASA group (p = 0.014; p = 0.013; p = 0.028, respectively).	Aspirin	116-119	microRNA let-7e	Homo sapiens	22-28
8537043-6	1995	As adaptation to ASA developed, however, the areas of gastric lesions were reduced by more than 80% and there was a noticeable decrease in deep necrosis, a partial restoration of gastric blood flow, an approximately four-fold increase in EGF expression (but not in TGF alpha) and its receptors, and an appreciable increase in mucosal cell proliferation compared with vehicle treated rats.	Aspirin	17-20	epidermal growth factor like 1	Rattus norvegicus	238-241
7564880-5	1995	However, indomethacin, diclofenac, phenylbutazone, mefenamic acid, naproxen, piroxicam, aspirin and W-7 inhibit, in a concentration-dependent way, the calmodulin-stimulated activity of phosphodiesterase.	Aspirin	88-95	calmodulin 1	Rattus norvegicus	151-161
8537043-7	1995	Increases in the mucosal expression of EGF receptors and the luminal content of EGF were also found in ASA adapted animals.	Aspirin	103-106	epidermal growth factor like 1	Rattus norvegicus	39-42
34071189-10	2021	Furthermore, miR-126, Let-7e and miR-223 expressions in the clopidogrel group were significantly higher than in the ASA group (p = 0.014; p = 0.013; p = 0.028, respectively).	Aspirin	116-119	microRNA 223	Homo sapiens	33-40
8537043-7	1995	Increases in the mucosal expression of EGF receptors and the luminal content of EGF were also found in ASA adapted animals.	Aspirin	103-106	epidermal growth factor like 1	Rattus norvegicus	80-83
8537043-10	1995	Gastric adaptation to ASA enhances the mucosal resistance to injury by strong irritants probably as a result of the restoration of the gastric blood flow and increased cell proliferation that may result from increased mucosal expression of EGF and its receptors.	Aspirin	22-25	epidermal growth factor like 1	Rattus norvegicus	240-243
7825862-11	1994	Aspirin irreversibly inhibits PGHS-1, preventing this isozyme from forming PGH2 or any other oxygenated product; in contrast, aspirin treatment of PGHS-2 causes this enzyme to form 15-hydroxy-5c,8c,11c,13t-eicosatetraenoic acid (15-HETE) instead of PGH2.	Aspirin	126-133	prostaglandin-endoperoxide synthase 2	Mus musculus	147-153
34776464-0	2021	P2Y12 Inhibitors Exacerbate Low-dose Aspirin-induced Small Bowel Injury in Dual Antiplatelet Therapy.	Aspirin	37-44	purinergic receptor P2Y12	Homo sapiens	0-5
35619249-7	2022	RESULTS: The search identified 4 randomized clinical trials comparing P2Y12 inhibitors with aspirin for secondary stroke prevention that collectively enrolled 24508 patients (12253 received P2Y12 inhibitor and 12255 received aspirin).	Aspirin	92-99	purinergic receptor P2Y12	Homo sapiens	190-195
7942522-1	1994	Coumadin Aspirin Reinfarction (CARS) Pilot Study Group.	Aspirin	9-16	cysteinyl-tRNA synthetase 1	Homo sapiens	31-35
35619249-7	2022	RESULTS: The search identified 4 randomized clinical trials comparing P2Y12 inhibitors with aspirin for secondary stroke prevention that collectively enrolled 24508 patients (12253 received P2Y12 inhibitor and 12255 received aspirin).	Aspirin	225-232	purinergic receptor P2Y12	Homo sapiens	70-75
8166943-1	1994	PROBLEM: Effectiveness of early administered low-dose aspirin in prevention of pregnancy-induced hypertension (PIH) and fetal growth retardation in twin pregnancies was investigated in a randomized placebo controlled, double-blind trial in 47 twin pregnancies.	Aspirin	54-61	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	111-114
35546632-7	2022	Remarkably, the anti-inflammatory drug aspirin strongly attenuates HFD-induced diabetes and AD pathologies in neuronal C/EBPbeta Tg mice.	Aspirin	39-46	CCAAT/enhancer binding protein (C/EBP), alpha	Mus musculus	119-128
8166943-10	1994	CONCLUSION: Low-dose aspirin reduces the incidence of PIH and has a beneficial effect on fetal growth in twin pregnancies.	Aspirin	21-28	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	54-57
35335908-8	2022	ASA significantly decreased the expression levels of miRNA155, NLRP3, and IL1B, and produced a significant decrease in caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex with a reduction in the process of neuroinflammation and neuronal damage.	Aspirin	0-3	caspase 8	Homo sapiens	119-128
21043721-5	1994	While 50% of the secretion of beta-TG persisted in spite of aspirin treatment, secretion of (14)C-serotonin was completely abolished.	Aspirin	60-67	pro-platelet basic protein	Homo sapiens	30-37
21043721-7	1994	Platelet secretion of beta-TG and (14)C-serotonin induced by a high dose of collagen was significantly reduced by aspirin, while a low dose of collagen induced a cyclooxygenase-independent secretion of beta-TG and (14)C-serotonin.	Aspirin	114-121	pro-platelet basic protein	Homo sapiens	22-29
35181471-2	2022	We sought to evaluate the contribution of ASA to the risk of CS in PFO patients based on studies published so far by means of a systematic review and metanalysis.	Aspirin	42-45	citrate synthase	Homo sapiens	61-63
8215400-15	1993	Mitogen-inducible activity in RS2 cells was inhibited by aspirin, indicating that PGHS-2, like PGHS-1, can be inactivated by this drug.	Aspirin	57-64	prostaglandin-endoperoxide synthase 2	Mus musculus	82-88
8103026-7	1993	The aspirin-induced increase in PMN adherence to HUVEC was significantly reduced by monoclonal antibodies against CD18, CD11b, CD11a, and intercellular adhesion molecule 1.	Aspirin	4-11	integrin subunit alpha L	Homo sapiens	127-132
8103026-9	1993	CONCLUSIONS: These studies indicate that aspirin promotes neutrophil adherence to endothelium via CD11a/CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule 1; the adhesion response is partially mediated by leukotriene B4.	Aspirin	41-48	integrin subunit alpha L	Homo sapiens	98-103
35181471-3	2022	A literature search, based on PubMed, Google Scholar and EMBASE databases, was performed to locate articles, published English language between 2000 and 2021, analysing the relationship between ASA and CS.	Aspirin	194-197	citrate synthase	Homo sapiens	202-204
35181471-10	2022	PFO Patients with ASA were at higher risk of CS compared to those without (odd ratio: 3.38, 95% CI: 2.72-5.51, p<0.001, I2=4.3%,).	Aspirin	18-21	citrate synthase	Homo sapiens	45-47
35115097-1	2022	BACKGROUND: The use of apixaban instead of vitamin K antagonists (VKA) as well as dropping aspirin results in less bleeding and comparable ischemic events in patients with atrial fibrillation and acute coronary syndrome and/or percutaneous coronary intervention treated with a P2Y12 inhibitor.	Aspirin	91-98	purinergic receptor P2Y12	Homo sapiens	277-282
8342880-7	1993	In conclusion low-dose ASA inhibits collagen-induced release of both beta-TG and PDGF in PRP and TxB2-synthesis in PRP and serum.	Aspirin	23-26	pro-platelet basic protein	Homo sapiens	69-76
35197754-9	2022	The linsitinib and aspirin as the IGF1-R antagonists inhibited colon cancer resistance against regorafenib, stem-cell like colon cancer cells growth, decreased expression of CD133, CD44, CD24, and also increased CDX2, PTEN gene expression.	Aspirin	19-26	prominin 1	Homo sapiens	174-179
8335847-7	1993	CONCLUSION: We have shown, however, that there is a significant decrease in the incidence of DPB1*0401 in both aspirin-tolerant and aspirin-intolerant subjects with asthma in both populations studied.	Aspirin	111-118	major histocompatibility complex, class II, DP beta 1	Homo sapiens	93-97
8335847-7	1993	CONCLUSION: We have shown, however, that there is a significant decrease in the incidence of DPB1*0401 in both aspirin-tolerant and aspirin-intolerant subjects with asthma in both populations studied.	Aspirin	132-139	major histocompatibility complex, class II, DP beta 1	Homo sapiens	93-97
35164195-0	2022	Development and Validation of a Novel HPLC Method to Analyse Metabolic Reaction Products Catalysed by the CYP3A2 Isoform: In Vitro Inhibition of CYP3A2 Enzyme Activity by Aspirin (Drugs Often Used Together in COVID-19 Treatment).	Aspirin	171-178	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	106-112
8105522-0	1993	N-acetyl-beta-D-glucosaminidase (NAG) and alanine aminopeptidase (AAP) excretion after acute administration of acetaminophen, salsalate and aspirin in rats.	Aspirin	140-147	O-GlcNAcase	Rattus norvegicus	0-31
35164195-0	2022	Development and Validation of a Novel HPLC Method to Analyse Metabolic Reaction Products Catalysed by the CYP3A2 Isoform: In Vitro Inhibition of CYP3A2 Enzyme Activity by Aspirin (Drugs Often Used Together in COVID-19 Treatment).	Aspirin	171-178	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	145-151
35164195-3	2022	Thus, the purpose of this study was to use High-Performance Liquid Chromatography (HPLC) to evaluate the in vitro inhibition of CYP3A2 enzyme activity using aspirin in rat liver microsomes (RLMs).	Aspirin	157-164	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	128-134
35164195-7	2022	The results showed that aspirin competitively inhibits 6beta-hydroxylation (CYP3A2 activity) with an inhibition constant (Ki) = 95.46 microM and the concentration of the inhibitor causing 50% inhibition of original enzyme activity (IC50) = 190.92 microM.	Aspirin	24-31	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	76-82
2529003-4	1989	In contrast, aspirin reduced the increments induced by venous occlusion as follows: t-PA:Ag by 45% (P = .001); t-PA activity (euglobulin lysis time, ELT) by 43% (P = .006); and t-PA activity (alpha 2-plasmin inhibitor-plasmin complexes, PIPC) by 41% (P = .003).	Aspirin	13-20	plasminogen	Homo sapiens	200-207
8094168-2	1993	Meta-analysis of data from several controlled trials has shown that low-dose aspirin reduces the risk of pregnancy-induced hypertension (PIH) and intrauterine growth retardation (IUGR) in women at high risk of these disorders.	Aspirin	77-84	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	137-140
8094168-10	1993	Our study gives little support to the notion that low-dose aspirin is beneficial in women at moderate risk of PIH or IUGR.	Aspirin	59-66	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	110-113
2529003-4	1989	In contrast, aspirin reduced the increments induced by venous occlusion as follows: t-PA:Ag by 45% (P = .001); t-PA activity (euglobulin lysis time, ELT) by 43% (P = .006); and t-PA activity (alpha 2-plasmin inhibitor-plasmin complexes, PIPC) by 41% (P = .003).	Aspirin	13-20	plasminogen	Homo sapiens	218-225
2561117-2	1989	Both aspirin and paracetamol inhibit Na+K+ ATPase and Mg2+ ATPase in a dose dependent manner.	Aspirin	5-12	dynein axonemal heavy chain 8	Homo sapiens	43-49
1506726-3	1992	Recent evidence suggested that aspirin in low doses was effective in reducing the incidence of PIH, by selective inhibition of platelet-derived TXA2 biosynthesis.	Aspirin	31-38	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	95-98
2561117-2	1989	Both aspirin and paracetamol inhibit Na+K+ ATPase and Mg2+ ATPase in a dose dependent manner.	Aspirin	5-12	mucin 7, secreted	Homo sapiens	54-57
2561117-2	1989	Both aspirin and paracetamol inhibit Na+K+ ATPase and Mg2+ ATPase in a dose dependent manner.	Aspirin	5-12	dynein axonemal heavy chain 8	Homo sapiens	59-65
2481709-9	1989	These effects on platelet function were absent in platelets exposed to acetylsalicylic acid and prevented by indomethacin, the prostaglandin H2 (PGH2)/thromboxane A2 (TXA2) receptor antagonist, daltroban, and the functional antagonist, iloprost.	Aspirin	71-91	thromboxane A2 receptor	Homo sapiens	151-181
1412183-4	1992	In the ASA group TAT levels were increased at 9 months, whereas no significant changes in fibrinogen, FPA or D-dimer from baseline were noted.	Aspirin	7-10	tyrosine aminotransferase	Homo sapiens	17-20
7858871-10	1994	Aspirin, 100 microM, indomethacin, 100 nM to 10 microM, piroxicam, 1 to 100 microM, and sodium meclofenamate, 10 nM, all potentiated cell-associated IL-1-like activity in LPS- stimulated macrophages.	Aspirin	0-7	interleukin 1 complex	Mus musculus	149-153
8038151-9	1994	N-(Carboxyheptyl)maleimide is the most potent covalent inactivator of PGHS yet described with an inhibitory potency 3-5 orders of magnitude greater than aspirin.	Aspirin	153-160	prostaglandin-endoperoxide synthase 2	Mus musculus	70-74
8017762-10	1994	Aspirin irreversibly inhibits PGHS-1, preventing this isozyme from forming any product; in contrast, aspirin treatment of PGHS-2 causes this enzyme to form 15-hydroxy-5c,8c,11c,13t-eicosatetraenoic acid (15-HETE) instead of PGH2.	Aspirin	101-108	prostaglandin-endoperoxide synthase 2	Mus musculus	122-128
8148359-10	1994	The plasma levels of FPA and beta-TG were slightly lower in nonsmokers and after aspirin ingestion.	Aspirin	81-88	pro-platelet basic protein	Homo sapiens	29-36
8287681-6	1994	A recessive gene, asa, implicated in the control of autoimmune response, is located within the predicted region for Camkg.	Aspirin	18-21	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	116-121
8509363-1	1993	The 5,6-epoxyeicosatrienoic acid (5,6-EET), a renal vasodilator metabolite of arachidonic acid via cytochrome P450 (P450) requires cyclooxygenase for expression of its vasoactivity as the responses are inhibited by indomethacin and other aspirin-like drugs.	Aspirin	238-245	cytochrome P-450	Oryctolagus cuniculus	99-145
8480641-5	1993	In 5 patients with prolonged rest angina who received aspirin, plasma TAT levels (ng/ml) were significantly decreased (4.52 +/- 1.18 at baseline, 2.50 +/- 0.65 at 1 hour and 2.16 +/- 0.42 at 24 hours after aspirin administration, p &lt; 0.01) with a significant decrease in plasma 11-dehydro-TXB2 levels.	Aspirin	54-61	tyrosine aminotransferase	Homo sapiens	70-73
8480641-5	1993	In 5 patients with prolonged rest angina who received aspirin, plasma TAT levels (ng/ml) were significantly decreased (4.52 +/- 1.18 at baseline, 2.50 +/- 0.65 at 1 hour and 2.16 +/- 0.42 at 24 hours after aspirin administration, p &lt; 0.01) with a significant decrease in plasma 11-dehydro-TXB2 levels.	Aspirin	206-213	tyrosine aminotransferase	Homo sapiens	70-73
8480641-6	1993	However, the reduction in TAT after aspirin administration was slight in patients without prolonged rest angina (n = 4).	Aspirin	36-43	tyrosine aminotransferase	Homo sapiens	26-29
1840245-3	1991	A similar aspirin-induced increase, as seen in urinary dolichol concentration, was also observed in the urinary excretion of two lysosomal enzymes--beta-hexosaminidase and beta-glucuronidase.	Aspirin	10-17	O-GlcNAcase	Homo sapiens	148-167
1840245-3	1991	A similar aspirin-induced increase, as seen in urinary dolichol concentration, was also observed in the urinary excretion of two lysosomal enzymes--beta-hexosaminidase and beta-glucuronidase.	Aspirin	10-17	glucuronidase beta	Homo sapiens	172-190
2813856-0	1989	Close arterial infusion of calcitonin gene-related peptide into the rat stomach inhibits aspirin- and ethanol-induced hemorrhagic damage.	Aspirin	89-96	calcitonin-related polypeptide alpha	Rattus norvegicus	27-58
1804603-3	1991	The results have shown that 8% of the pregnant women in the aspirin treatment group had developed PIH, which was substantially lower than that in the control group (24%) (P less than 0.05).	Aspirin	60-67	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	98-101
1804603-6	1991	It was presumed that low dose aspirin may have prophylactic effect on PIH.	Aspirin	30-37	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	70-73
2813856-2	1989	The present study, therefore, examined whether rat alpha-CGRP, administered via different routes, is able to protect against mucosal injury induced by gastric perfusion with 25% ethanol or acidified aspirin (25 mM, pH 1.5) in urethane-anesthetized rats.	Aspirin	199-206	calcitonin-related polypeptide alpha	Rattus norvegicus	57-61
1835913-3	1991	We also studied the effects of low-dose aspirin (81 mg/day) on the plasma level of heparin-releasable PF4 in the CAD patients.	Aspirin	40-47	platelet factor 4	Homo sapiens	102-105
2813856-3	1989	Close arterial infusion of CGRP (15 pmol/min) to the stomach, via a catheter placed in the abdominal aorta proximal to the celiac artery, significantly reduced gross mucosal damage caused by ethanol and aspirin whereas mean arterial blood pressure (BP) was not altered.	Aspirin	203-210	calcitonin-related polypeptide alpha	Rattus norvegicus	27-31
2813856-6	1989	Intragastric administration of CGRP (260 nM) significantly inhibited aspirin-induced mucosal damage but did not influence damage in response to ethanol.	Aspirin	69-76	calcitonin-related polypeptide alpha	Rattus norvegicus	31-35
2813856-8	1989	These data indicate that only close arterial administration of CGRP to the rat stomach, at doses devoid of a systemic hypotensive effect, is able to protect against both ethanol- and aspirin-induced mucosal damage.	Aspirin	183-190	calcitonin-related polypeptide alpha	Rattus norvegicus	63-67
2548436-1	1989	Modifications of serum levels of iron transferrin and copper ceruloplasmin after acute inflammation by carrageenan and treatment with acetyl salicylic acid [ASA] or Cu(II)2(acetylsalicylate)4 [Cu(II)2(AS)4] were studied in the rat by EPR spectroscopy.	Aspirin	134-155	ceruloplasmin	Rattus norvegicus	61-74
33775806-7	2021	The results from molecular docking showed that 22 compounds adopted the same orientation as aspirin and had an excellent stability in the active site pocket of PTGS2.	Aspirin	92-99	prostaglandin-endoperoxide synthase 2	Mus musculus	160-165
2548436-1	1989	Modifications of serum levels of iron transferrin and copper ceruloplasmin after acute inflammation by carrageenan and treatment with acetyl salicylic acid [ASA] or Cu(II)2(acetylsalicylate)4 [Cu(II)2(AS)4] were studied in the rat by EPR spectroscopy.	Aspirin	157-160	ceruloplasmin	Rattus norvegicus	61-74
33589277-1	2021	BACKGROUND: Uncertainty remains surrounding the use of aspirin as a sole chemoprophylactic agent to reduce the risk of venous thromboembolism (deep vein thrombosis or pulmonary embolism) and bleeding after primary total hip arthroplasty.	Aspirin	55-62	hedgehog interacting protein	Homo sapiens	220-223
2791406-8	1989	On the contrary, aspirin with ticlopidine reduced TXB2 as well as beta TG and PF4.	Aspirin	17-24	pro-platelet basic protein	Homo sapiens	66-73
33589277-13	2021	Sole use of aspirin for venous thromboembolism prophylaxis after total hip arthroplasty should be considered in the appropriate patient.	Aspirin	12-19	hedgehog interacting protein	Homo sapiens	71-74
34876147-9	2021	The platelet reactivity index (PRI) level in the VASP test was also markedly lower in the group given aspirin and ticagrelor (P <  0.001).	Aspirin	102-109	vasodilator stimulated phosphoprotein	Homo sapiens	49-53
34864618-0	2021	Genome-Wide association between EYA1 and Aspirin-induced peptic ulceration.	Aspirin	41-48	EYA transcriptional coactivator and phosphatase 1	Homo sapiens	32-36
34864618-12	2021	INTERPRETATION: Genetic variation in an intron of the EYA1 gene increases the risk of endoscopically confirmed aspirin-induced PUD.	Aspirin	111-118	EYA transcriptional coactivator and phosphatase 1	Homo sapiens	54-58
34915778-7	2021	Nevertheless, after a brief period of dual antiplatelet therapy, patients at high bleeding risk may benefit from discontinuation of aspirin if a P2Y12 inhibitor is used, hence reducing the bleeding risk with no rebound in thrombotic events.	Aspirin	132-139	purinergic receptor P2Y12	Homo sapiens	145-150
34857988-9	2021	Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin.	Aspirin	304-311	prostaglandin-endoperoxide synthase 2	Mus musculus	59-75
34857988-9	2021	Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin.	Aspirin	304-311	prostaglandin-endoperoxide synthase 2	Mus musculus	77-81
34857988-9	2021	Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin.	Aspirin	304-311	yes-associated protein 1	Mus musculus	147-171
34857988-9	2021	Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin.	Aspirin	304-311	yes-associated protein 1	Mus musculus	173-177
34857988-9	2021	Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin.	Aspirin	304-311	high mobility group box 1	Mus musculus	194-219
34857988-9	2021	Immunohistochemical analyses and western blots showed that cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), and the active form of Yes-associated protein 1 (YAP1), and cytosolic high mobility group box 1 (HMGB1) were strongly expressed at colorectal tumor sites and clearly suppressed by aspirin.	Aspirin	304-311	high mobility group box 1	Mus musculus	221-226
34857988-11	2021	The present results suggest that the ingestion of aspirin suppressed carcinogenesis caused by inflammation through decreases in COX2 and ROS levels, resulting in reductions in DNA damage and oncogenic YAP1.	Aspirin	50-57	prostaglandin-endoperoxide synthase 2	Mus musculus	128-132
34857988-11	2021	The present results suggest that the ingestion of aspirin suppressed carcinogenesis caused by inflammation through decreases in COX2 and ROS levels, resulting in reductions in DNA damage and oncogenic YAP1.	Aspirin	50-57	yes-associated protein 1	Mus musculus	201-205
34479029-2	2021	The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro.	Aspirin	48-55	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	106-134
34479029-2	2021	The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro.	Aspirin	48-55	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	136-140
34769120-4	2021	The present study was designed to determine, for the first time, the changes in pituitary adenylate cyclase-activating polypeptide (PACAP), substance P (SP) and galanin (GAL) expression in porcine jejunum after long-term treatment with aspirin, indomethacin and naproxen.	Aspirin	236-243	galanin and GMAP prepropeptide	Sus scrofa	170-173
34901735-7	2021	We found that antiplatelet medication acetylsalicylic acid (ASA) led to reduced chemokine (CC motif) ligand 5 (CCL5) and chemokine (CXC motif) ligand 4 (CXCL4) release from platelets, while leukocyte chemotaxis was not affected.	Aspirin	38-58	platelet factor 4	Homo sapiens	153-158
34901735-7	2021	We found that antiplatelet medication acetylsalicylic acid (ASA) led to reduced chemokine (CC motif) ligand 5 (CCL5) and chemokine (CXC motif) ligand 4 (CXCL4) release from platelets, while leukocyte chemotaxis was not affected.	Aspirin	60-63	platelet factor 4	Homo sapiens	153-158
34705291-6	2022	In independent cohorts of healthy volunteers and patients with diabetes we validated aspirin"s effects on five genes: EIF2S3, CHRNB1, EPAS1, SLC9A3R2, and HLA-DRA.	Aspirin	85-92	major histocompatibility complex, class II, DR alpha	Homo sapiens	155-162
34502520-5	2021	We observed that acetylsalicylic acid (ASA) decreased the area of the thrombus while increasing the PECAM-1/thrombus ratio in healthy mice and humans in a dose-dependent manner.	Aspirin	17-37	platelet/endothelial cell adhesion molecule 1	Mus musculus	100-107
34502520-5	2021	We observed that acetylsalicylic acid (ASA) decreased the area of the thrombus while increasing the PECAM-1/thrombus ratio in healthy mice and humans in a dose-dependent manner.	Aspirin	39-42	platelet/endothelial cell adhesion molecule 1	Mus musculus	100-107
34502520-6	2021	In LPS-treated mice, the PECAM-1/thrombus ratio decreased as the dose of ASA increased in both thrombosis models, but the direction of change in the thrombus area was inconsistent.	Aspirin	73-76	platelet/endothelial cell adhesion molecule 1	Mus musculus	25-32
34384631-14	2021	It is recommended to start non-steroidal anti-inflammatory drugs (NSAIDs) or aspirin as soon as possible during the aura phase, not to treat the aura, but to avoid or to diminish the headache phase.	Aspirin	77-84	aurora kinase A	Homo sapiens	116-120
34540977-0	2021	Aspirin-induced long-term tumor remission in hepatocellular carcinoma with adenomatous polyposis coli stop-gain mutation: A case report.	Aspirin	0-7	APC regulator of WNT signaling pathway	Homo sapiens	75-101
34540977-8	2021	Aspirin has been reported to suppress the Wnt pathway by inducing beta-catenin phosphorylation through the activation of glycogen synthase kinase 3 beta via cyclooxygenase-2 pathway inhibition.	Aspirin	0-7	glycogen synthase kinase 3 beta	Homo sapiens	121-152
34483913-13	2021	In vitro, aspirin decreased the activation of NF-kappaB signaling of DCs, as well as impeded MHCII and co-stimulatory molecules (CD80, CD86, and CD40) expression on DCs.	Aspirin	10-17	CD40 antigen	Mus musculus	145-149
34429873-6	2021	Additionally, high expression of the hydroxyprostaglandin dehydrogenase gene, HPGD encoding prostaglandin-degrading enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH) and low expression of the proteoglycan 2 gene, PRG2 encoding constituent of the eosinophil granule in sputum cells might serve as a predictor of good response to aspirin therapy.	Aspirin	333-340	proteoglycan 2, pro eosinophil major basic protein	Homo sapiens	218-222
34144387-4	2021	The ASAS-perSpA is a cross-sectional study that recruited consecutive patients with SpA (as diagnosed by their rheumatologist) from 68 centers worldwide and collected patient and disease data.	Aspirin	4-8	surfactant protein A1	Homo sapiens	84-87
34327200-9	2021	Moreover, we found that although glycolipid metabolism indicators can be corrected, the CXCL2 elevation and BMSC dysfunctions cannot be fully rescued by diet correction and anti-inflammatory aspirin treatment, indicating the long-lasting deleterious effects of HFD on serum CXCL2 levels and BMSC functions.	Aspirin	191-198	C-X-C motif chemokine ligand 2	Rattus norvegicus	274-279
34319045-12	2021	RESULTS: ASA bound specifically to SW480 cells via interaction between the aptamer and nucleolin because the nucleolin was highly expressed in SW480 cells.	Aspirin	9-12	nucleolin	Homo sapiens	87-96
34319045-12	2021	RESULTS: ASA bound specifically to SW480 cells via interaction between the aptamer and nucleolin because the nucleolin was highly expressed in SW480 cells.	Aspirin	9-12	nucleolin	Homo sapiens	109-118
34121855-5	2021	Combination of aspirin and ginkgolide injection could better reduce brain water content, reduce apoptosis rate of cortical cells P < 0.05, reduce expression levels of caspase-3, Bax and p-REK1/2 proteins in ischemic brain tissue P < 0.05, and increase expression level of Bcl-2 protein than aspirin and ginkgolide injection alone P < 0.05).	Aspirin	15-22	caspase 3	Rattus norvegicus	167-176
34122428-8	2021	At these concentrations, we found that both COX-inhibitors could induce intrinsic apoptosis of CD19.CAR-T cells showing a significant reduction in the ratio of JC-10 red to JC-10 green CAR-T cells from 6.46 +- 7.03 (mean +- SD) to 1.76 +- 0.67 by celecoxib and to 4.41 +- 0.32 by aspirin, respectively.	Aspirin	280-287	CD19 molecule	Homo sapiens	95-99
35453025-5	2022	Moreover, the expression levels of ASA-GSH synthesis genes, APX, GR, and GST were significantly increased by 171.5%, 465.2%, and 256.8% in roots, respectively, whereas GSH, DHAR, or MDHAR were significantly decreased by 48.5%, 54.3%, or 60.0% in roots under MT + Cd stress.	Aspirin	35-38	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	60-63
35258157-10	2022	Overexpression of SlDHAR in fruit increased AsA content, but did not affect the cell wall thickness or fruit firmness and softening.	Aspirin	44-47	dehydroascorbate reductase 1	Solanum lycopersicum	18-24
35585040-5	2022	Mass spectrum analysis and biochemical results revealed that HDAC6 inhibitor or aspirin treatment promoted MIF acetylation on the K78 residue.	Aspirin	80-87	macrophage migration inhibitory factor	Homo sapiens	107-110
35237927-4	2022	Aspirin-free P2Y12 inhibitor monotherapy is now being evaluated in several prospective studies as a novel strategy of antiplatelet therapy after PCI.	Aspirin	0-7	purinergic receptor P2Y12	Homo sapiens	13-18
35392432-0	2022	Aspirin Suppressed PD-L1 Expression through Suppressing KAT5 and Subsequently Inhibited PD-1 and PD-L1 Signaling to Attenuate OC Development.	Aspirin	0-7	K(lysine) acetyltransferase 5	Mus musculus	56-60
35392432-12	2022	Analysis on molecular mechanisms revealed that KAT5 bonded to the promoter region of PD-L1 and upregulated its expression via enhancing histone H3 lysine 27 acetylation (H3K27ac), whereas ASP downregulated KAT5 expression and blocked this phenomenon.	Aspirin	188-191	K(lysine) acetyltransferase 5	Mus musculus	206-210
35392432-14	2022	Hence, we proposed that ASP decreased expression of PD-L1 protein via inhibiting the epigenetic regulation by KAT5 and suppressed the PD-1/PD-L1 signaling to attenuate tumor growth.	Aspirin	24-27	K(lysine) acetyltransferase 5	Mus musculus	110-114
1398237-1	1992	Aspirin, which inhibits mucin secretion in the gastrointestinal tract prevents gall stone formation in animals and may reduce gall stone recurrence in man.	Aspirin	0-7	LOC100508689	Homo sapiens	24-29
1398237-2	1992	This study examines the effect of aspirin on mucin synthesis in human gall bladder explants.	Aspirin	34-41	LOC100508689	Homo sapiens	45-50
1398237-10	1992	This study provides a method for measuring human gall bladder mucin synthesis and shows its irreversible inhibition by acetylsalicylic acid and diclofenac at concentrations compatible with a therapeutic dose.	Aspirin	119-139	LOC100508689	Homo sapiens	62-67
1427067-1	1992	The experience in the United States with aspirin sensitivity associated with rhinosinusitis and asthma is generally in agreement with the European perspective offered by Drs.	Aspirin	41-48	sushi repeat containing protein X-linked	Homo sapiens	170-173
1383635-7	1992	At 10(-12) mol/site, intradermally injected PACAP and VIP caused a maximum increase in skin blood flow at 15 min of 379 +/- 96 and 307 +/- 121% (% increase above basal +/- SEM), respectively, and these responses were not significantly affected by oral aspirin (600 mg) taken 1.5 h beforehand.	Aspirin	252-259	adenylate cyclase activating polypeptide 1	Homo sapiens	44-49
1950781-0	1991	Effect of calcitonin gene-related peptide (CGRP) on aspirin- and ethanol-induced injury in the rat stomach.	Aspirin	52-59	calcitonin-related polypeptide alpha	Rattus norvegicus	10-41
1950781-0	1991	Effect of calcitonin gene-related peptide (CGRP) on aspirin- and ethanol-induced injury in the rat stomach.	Aspirin	52-59	calcitonin-related polypeptide alpha	Rattus norvegicus	43-47
2277204-4	1990	Recently, antiplatelet treatment such as low-dose aspirin therapy has been effective in preventing the development of PIH and preeclampsia.	Aspirin	50-57	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	118-121
2231997-3	1990	In vitro, aspirin clearly decreased the activity of gastric alcohol dehydrogenase in human subjects and in rat models, but not that of hepatic alcohol dehydrogenase in rats.	Aspirin	10-17	alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide	Homo sapiens	52-81
2231997-5	1990	Thus, aspirin may increase the bioavailability of ingested ethanol in humans, possibly by reducing ethanol oxidation by gastric alcohol dehydrogenase.	Aspirin	6-13	alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide	Homo sapiens	120-149
1705427-1	1990	In anesthetized rabbits with pulmonary embolized thrombi the interactions of saruplase (recombinant unglycosylated single-chain urokinase-type plasminogen activator, CAS 99149-95-8) with acetylsalicylic acid (ASA), glyceryl trinitrate (nitroglycerin, GTN), heparin, and the antifibrinolytics tranexamic acid and aprotinin have been studied.	Aspirin	187-207	urokinase-type plasminogen activator	Oryctolagus cuniculus	128-164
2107595-8	1990	Thus, during the last 5 days of ASA treatment the median excretion of Tx-M was depressed (p less than 0.001) to 148 (range 48-428) pg/mg creatinine, while that of PGI-M was decreased (p less than 0.01) to 313 (range 42-2658) pg/mg creatinine.	Aspirin	32-35	glucose-6-phosphate isomerase	Homo sapiens	163-166
34809447-12	2022	In the community-based Bruneck study (n=338), plasma S100A8/A9 was inversely associated with platelet reactivity-an effect abrogated by aspirin.	Aspirin	136-143	S100 calcium binding protein A8	Homo sapiens	53-62
34873128-9	2021	Administration of aspirin-triggered (AT) resolvin D1 (AT-RvD1) and AT lipoxin A4 (AT-LXA4), which are agonistic to ALX/FPR2, immediately after reperfusion improved lung function, reduced inflammatory cytokine levels, attenuated lung edema, and decreased neutrophil infiltration 3 h after reperfusion.	Aspirin	18-25	formyl peptide receptor 2	Rattus norvegicus	119-123
34795536-10	2021	Conclusion: A remarkable reduction in early-onset preeclampsia was observed with early initiation of low-dose aspirin in those screened positive for maternal characteristics and serum PAPP-A/PLGF.	Aspirin	110-117	pappalysin 1	Homo sapiens	184-190
2791406-8	1989	On the contrary, aspirin with ticlopidine reduced TXB2 as well as beta TG and PF4.	Aspirin	17-24	platelet factor 4	Homo sapiens	78-81
34790277-7	2021	Furthermore, the number of GSI-B4, OPN, and MMP-3 cells decreased in the ASA group compared to the control group.	Aspirin	73-76	secreted phosphoprotein 1	Rattus norvegicus	35-38
35269388-0	2022	ASA Status, NPPA/NPPB Haplotype and Coronary Artery Disease Have an Impact on BNP/NT-proBNP Plasma Levels.	Aspirin	0-3	natriuretic peptide B	Homo sapiens	78-81
3286527-3	1988	In this case report we present the outcome of the combination of plasma exchange, dipyridamole and aspirin in the management of a TTP-like syndrome that complicated the post-operative course of liver transplantation.	Aspirin	99-106	ZFP36 ring finger protein	Homo sapiens	130-133
35075676-10	2022	Although ASA did not affect anti-CD3/CD28-mediated proliferation, it significantly reduced CSM2 and CSM1-mediated T-cell proliferation.	Aspirin	9-12	CD28 molecule	Homo sapiens	37-41
2891837-1	1987	Histamine H2 receptor antagonists have been reported to protect the gastric mucosa of animals and humans against aspirin-induced damage.	Aspirin	113-120	histamine receptor H2	Homo sapiens	0-21
34303997-4	2021	Correspondingly, the CS-PS NPs can also be used as a drug carrier for aspirin, which presents very good drug loading and release behavior in PBS (pH = 7.4).	Aspirin	70-77	citrate synthase	Homo sapiens	21-23
2894763-11	1988	Partial protections against aspirin-induced or other NSAID-induced gastric mucosal damage has been demonstrated, at least in some studies, by sucralfate, prostaglandins, omeprazole and histamine (H2)-receptor antagonists.	Aspirin	28-35	histamine receptor H2	Homo sapiens	185-208
34604694-9	2021	Conclusion  The VN assays can differentiate the early potent anti-alphaIIbbeta3 effects of RUC-4 from delayed effects of P2Y12 antagonists in the presence of aspirin.	Aspirin	158-165	purinergic receptor P2Y12	Homo sapiens	121-126
2960124-4	1987	Administration to the patients of ASA, at the dose that does not affect prostacyclin production, determined a decrease of beta-TG in 77% of the patients.	Aspirin	34-37	pro-platelet basic protein	Homo sapiens	122-129
3053882-5	1988	Intragastric instillation of EGF can prevent gastric ulcerations induced by aspirin as well as cysteamine in rats.	Aspirin	76-83	epidermal growth factor like 1	Rattus norvegicus	29-32
34824680-4	2021	For example, a contemporary metanalysis of trials that assessed P2Y12 inhibitor monotherapy versus prolonged (>= 12 months) dual antiplatelet therapy (which includes aspirin) after percutaneous coronary intervention reported a lower risk of major bleeding and no increase in stent thrombosis, all-cause mortality, myocardial infarction (MI), or stroke in the P2Y12 monotherapy group.	Aspirin	166-173	purinergic receptor P2Y12	Homo sapiens	359-364
2856654-1	1988	Intracisternal or intracerebroventricular injection of TRH (0.1-10 micrograms) in rats stimulated the secretion of gastric acid and pepsin secretion, increased gastric mucosal blood flow and gastric contractility and emptying, induced gastric hemorrhagic lesions and aggravated experimental ulcers elicited by aspirin, serotonin or indomethacin.	Aspirin	310-317	thyrotropin releasing hormone	Rattus norvegicus	55-58
34414020-14	2021	In addition, the mRNA levels of CDKN1A, BAX, FOXF1, PUMA, and RRAD in EOC cells were significantly increased by the aspirin treatment.	Aspirin	116-123	BCL2 binding component 3	Homo sapiens	52-56
34144111-1	2021	BACKGROUND: Eosinophilic asthma and nasal polyposis are hallmarks of aspirin-exacerbated respiratory disease (AERD), and IL-5 inhibition has been shown to provide therapeutic benefit.	Aspirin	69-76	interleukin 5	Homo sapiens	121-125
2954264-6	1987	Therapy with ASA caused a significant decrease in the plasma levels of beta-TG (median: 30.4----26.6 ng/ml, p less than 0.001) and PF 4 (2.95----2.2 ng/ml, p less than 0.01).	Aspirin	13-16	pro-platelet basic protein	Homo sapiens	71-78
35570383-1	2022	P2Y12 inhibitors, including aspirin, are key components of dual-antiplatelet therapy (DAPT), which is the optimal therapeutic strategy for preventing arterial thrombosis in patients with acute coronary syndromes (ACS) who underwent stent implantation.	Aspirin	28-35	purinergic receptor P2Y12	Homo sapiens	0-5
35629166-8	2022	Our research showed that patients can receive treatment with warfarin and aspirin with a personalized dosage and LVAD complications can be predicted by reference to their genotype polymorphisms in VKORC1, ITGB3 and UGT1A6 genes.	Aspirin	74-81	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	215-221
2954264-6	1987	Therapy with ASA caused a significant decrease in the plasma levels of beta-TG (median: 30.4----26.6 ng/ml, p less than 0.001) and PF 4 (2.95----2.2 ng/ml, p less than 0.01).	Aspirin	13-16	platelet factor 4	Homo sapiens	131-135
3100533-5	1987	However, IP3 and Ca2+-induced PAC1 binding were abolished by indomethacin or aspirin, which had no effect on PAC1 binding caused by Gpp(NH)p, phorbol ester, or diacylglycerol.	Aspirin	77-84	dual specificity phosphatase 2	Homo sapiens	30-34
35418991-7	2022	Aspirin-intolerant patients displayed significantly elevated IL-5 and CCL17 levels in nasal secretions corresponding to a more pronounced eosinophilic type 2 inflammation.	Aspirin	0-7	interleukin 5	Homo sapiens	61-65
35418991-7	2022	Aspirin-intolerant patients displayed significantly elevated IL-5 and CCL17 levels in nasal secretions corresponding to a more pronounced eosinophilic type 2 inflammation.	Aspirin	0-7	C-C motif chemokine ligand 17	Homo sapiens	70-75
3098249-0	1986	Effect of acetylsalicylic acid on gastric mucin viscosity, permeability to hydrogen ion, and susceptibility to pepsin.	Aspirin	10-30	LOC100508689	Homo sapiens	42-47
35371873-3	2022	Aspirin may have a synergistic effect with PD-1 inhibitors via inhibition of prostaglandin E2 (PGE2) production, which can reverse the ability of tumor cells to evade the immune system.	Aspirin	0-7	programmed cell death 1	Homo sapiens	43-47
3098249-5	1986	Viscosity measurements showed a drop in mucin viscosity following preincubation with aspirin.	Aspirin	85-92	LOC100508689	Homo sapiens	40-45
3098249-7	1986	Permeability studies revealed that preincubation with 2.0 X 10(-5) M aspirin increased the permeability of mucin to hydrogen ion by 10%, while an 18% increase was obtained with 4.0 X 10(-5) M aspirin.	Aspirin	69-76	LOC100508689	Homo sapiens	107-112
2472829-1	1989	The inhibition of hepatic microsomal cytochrome P450 and cytochrome b5 levels by poly(rI.rC) and aspirin in vitro was studied in male Swiss mice.	Aspirin	97-104	cytochrome b5 type A (microsomal)	Mus musculus	57-70
2472829-3	1989	Aspirin (200 mg/kg) decreased the level of cytochrome P450 and cytochrome b5 to 45 and 23%, respectively.	Aspirin	0-7	cytochrome b5 type A (microsomal)	Mus musculus	63-76
3098249-7	1986	Permeability studies revealed that preincubation with 2.0 X 10(-5) M aspirin increased the permeability of mucin to hydrogen ion by 10%, while an 18% increase was obtained with 4.0 X 10(-5) M aspirin.	Aspirin	192-199	LOC100508689	Homo sapiens	107-112
3160472-4	1985	Administration of aspirin (ASA) was more effective than flunarizine in inducing a decrease in beta-TG and PF4 plasma levels in migraineurs.	Aspirin	18-25	pro-platelet basic protein	Homo sapiens	94-101
3230331-0	1988	Effect of indomethacin, aspirin, and acetaminophen on in vitro antiviral and antiproliferative activities of recombinant human interferon-alpha 2a.	Aspirin	24-31	interferon alpha 2	Homo sapiens	127-146
2892555-12	1987	Aspirin (600 mg orally) significantly inhibited the distant flare response to SP, NKA and CGRP, but not that caused by NKB or histamine; the local erythema induced by CGRP was unaffected by aspirin.	Aspirin	0-7	histocompatibility minor 13	Homo sapiens	78-80
3160472-4	1985	Administration of aspirin (ASA) was more effective than flunarizine in inducing a decrease in beta-TG and PF4 plasma levels in migraineurs.	Aspirin	18-25	platelet factor 4	Homo sapiens	106-109
3535158-3	1986	Aspirin was able to reduce the postoperative increase in circulating platelet aggregates, platelet factor 4 and beta-thromboglobulin observed in control group.	Aspirin	0-7	pro-platelet basic protein	Homo sapiens	112-132
3160472-4	1985	Administration of aspirin (ASA) was more effective than flunarizine in inducing a decrease in beta-TG and PF4 plasma levels in migraineurs.	Aspirin	27-30	pro-platelet basic protein	Homo sapiens	94-101
3160472-4	1985	Administration of aspirin (ASA) was more effective than flunarizine in inducing a decrease in beta-TG and PF4 plasma levels in migraineurs.	Aspirin	27-30	platelet factor 4	Homo sapiens	106-109
2858204-7	1985	Indomethacin (Id) and Aspirin reduced significantly PGE2 synthesis and GRF-induced GH release.	Aspirin	22-29	growth hormone releasing hormone	Rattus norvegicus	71-74
3161220-10	1985	Moreover, beta-TG levels in patients on chronic ASA therapy at the time of stroke did not differ from those in patients of the same diagnostic categories not taking aspirin.	Aspirin	48-51	pro-platelet basic protein	Homo sapiens	10-17
6370554-10	1984	Whereas aspirin, 325 mg, reduced PGI-M excretion a mean 29%, excretion increased 48% and 100% after CGS 13080, 100 mg and 200 mg. Aspirin, 20 mg, did not alter prostacyclin biosynthesis.	Aspirin	8-15	glucose-6-phosphate isomerase	Homo sapiens	33-36
6230778-8	1984	Administration of aspirin to the patients affected by common and classic migraine caused a decrease in plasma beta-TG and PF4 concentration.	Aspirin	18-25	pro-platelet basic protein	Homo sapiens	110-117
6230778-8	1984	Administration of aspirin to the patients affected by common and classic migraine caused a decrease in plasma beta-TG and PF4 concentration.	Aspirin	18-25	platelet factor 4	Homo sapiens	122-125
6202020-6	1984	Moreover, the significant reduction in PF4 release in vitro after aspirin suggests that GAGs-induced PF4 release is related to a cyclooxygenase-dependent activation process.	Aspirin	66-73	platelet factor 4	Homo sapiens	39-42
6202020-6	1984	Moreover, the significant reduction in PF4 release in vitro after aspirin suggests that GAGs-induced PF4 release is related to a cyclooxygenase-dependent activation process.	Aspirin	66-73	platelet factor 4	Homo sapiens	101-104
6215739-6	1982	Aspirin given to six patients at a dose sufficient to eliminate the secondary phase of ADP-induced platelet aggregation reduced mean beta TG and the mean beta TG: whole blood platelet count ratio but did not alter mean FpA and B beta 1-42.	Aspirin	0-7	pro-platelet basic protein	Homo sapiens	133-140
6215739-6	1982	Aspirin given to six patients at a dose sufficient to eliminate the secondary phase of ADP-induced platelet aggregation reduced mean beta TG and the mean beta TG: whole blood platelet count ratio but did not alter mean FpA and B beta 1-42.	Aspirin	0-7	pro-platelet basic protein	Homo sapiens	154-161
6176160-6	1982	Significant reductions in circulating platelet aggregates and beta-thromboglobulin levels were achieved in 10 patients by dipyridamole and aspirin therapy.	Aspirin	139-146	pro-platelet basic protein	Homo sapiens	62-82
7037068-5	1982	Aggregation and release of 14C-serotonin and PF4 were inhibited by the metabolic inhibitors 2-deoxyglucose (16.7 mM) and antimycin-A (8.3 micrograms/ml), by the membrane-active drugs mepacrine (10 microM) and chlorpromazine (0.025 mM), by PGI2 (5.34 nM), which elevates intracellular c-AMP, by indomethacin (10 microM) or aspirin (100 microM).	Aspirin	322-329	platelet factor 4	Homo sapiens	45-48
162473-4	1979	This increased aggregatability (not hyperglycemia determined) is reversed by a few days of insulin treatment or by dipyrimadole (alone or with synergistic acetyl salicylic acid): (2) Beta-thromboglobulin is released from platelets and is increased in venesected blood from diabetics after a standardized procedure (no prostaglandin E1 in anticoagulant) with final radioimmunoassay.	Aspirin	155-176	pro-platelet basic protein	Homo sapiens	183-203
820705-4	1976	The free fraction of thyroid hormones remained constant during treatment but a significant decrease of TSH concentration (30%) was noted after TRH injection on Acetylsalicylic Acid treatment whereas no changes were noted for PRL.	Aspirin	160-180	thyrotropin releasing hormone	Homo sapiens	143-146
1085402-1	1976	Analgesic nephropathy is part of a wider clinical syndrome associated with the abuse of APC compounds, that is, a minimum total intake of 2 kg of aspirin or phenacetin.	Aspirin	146-153	APC regulator of WNT signaling pathway	Homo sapiens	88-91
34011436-8	2021	The adjusted hazard for the Bleeding Academic Research Consortium (BARC) type 2 to 5 bleeding was significantly lower in P2Y12 inhibitor monotherapy than in conventional DAPT (IPTW-adjusted HR, 0.341; 95% CI, 0.190 to 0.614; p < 0.001) and in aspirin monotherapy (IPTW-adjusted HR, 0.359; 95% CI, 0.182 to 0.708; p = 0.003).	Aspirin	243-250	purinergic receptor P2Y12	Homo sapiens	121-126
33993103-6	2021	To verify our method, we detected ADEs with alanine aminotransferase (ALT) elevation in patients receiving aspirin, clopidogrel and ticlopidine.	Aspirin	107-114	glutamic--pyruvic transaminase	Homo sapiens	44-68
33844134-5	2021	An original aspirin-containing CAIX inhibitor AcAs has been developed.	Aspirin	12-19	carbonic anhydrase 9	Homo sapiens	31-35
33844134-6	2021	RESULTS: Based on the downregulation of CAIX level, both in vitro and in vivo, AcAs can overcome the acquired resistance and more effectively attenuate myocardial ischemia and hypoxia injury than that of aspirin.	Aspirin	204-211	carbonic anhydrase 9	Homo sapiens	40-44
33844134-7	2021	CAIX inhibitor is believed to recover the extracellular pH value so as to ensure the stable effect of aspirin.	Aspirin	102-109	carbonic anhydrase 9	Homo sapiens	0-4
33174669-3	2021	Inhibition of the SARS CoV-2 RBD / ACE2 PPI is currently being evaluated asa target for therapeutic and/or prophylactic intervention.	Aspirin	73-76	angiotensin converting enzyme 2	Homo sapiens	35-39
33461308-1	2021	Background: In the AUGUSTUS trial, apixaban resulted in less bleeding and fewer hospitalizations than vitamin K antagonists (VKA), and aspirin caused more bleeding than placebo in patients with atrial fibrillation and acute coronary syndrome or percutaneous coronary intervention treated with a P2Y12 inhibitor.	Aspirin	135-142	purinergic receptor P2Y12	Homo sapiens	295-300
33758122-6	2021	Another recently published VORA-PRATIC (Vorapaxar in Patients with Prior Myocardial Infarction Treated with prasugrel and ticagrelor) study showed that among post-MI patients treated with potent P2Y12 inhibitors (prasugrel or ticagrelor), vorapaxar reduced platelet-driven global thrombogenicity, an effect that persisted, albeit attenuated, in the absence of aspirin.	Aspirin	360-367	purinergic receptor P2Y12	Homo sapiens	195-200
33669632-3	2021	High-mobility group box 1 (HMGB1) is a type of exosomal cargo, and the antiplatelet drugs aspirin and dipyridamole interfered with its incorporation into the exosomes.	Aspirin	90-97	high mobility group box 1	Mus musculus	0-25
33669632-3	2021	High-mobility group box 1 (HMGB1) is a type of exosomal cargo, and the antiplatelet drugs aspirin and dipyridamole interfered with its incorporation into the exosomes.	Aspirin	90-97	high mobility group box 1	Mus musculus	27-32
33574709-9	2021	Specifically, we found that aspirin and salicylic acid increase the expression of REDD1 protein, that is known for its suppressive function towards mTORC1.	Aspirin	28-35	CREB regulated transcription coactivator 1	Mus musculus	148-154
33574709-10	2021	Unexpectedly, we observed that siRNA knockdown of REDD1 expression facilitated aspirin-mediated suppression of mTORC1 downstream substrate 4E-BP1 phosphorylation in the MDA-MB-468 cell line.	Aspirin	79-86	CREB regulated transcription coactivator 1	Mus musculus	111-117
33491760-14	2021	In conclusion, the present study indicated that aspirin partially inhibited cholangiocarcinoma cell proliferation and tumor growth by inducing G0/G1 phase cell cycle arrest, potentially through the miR-340-5p/cyclin D1 axis.	Aspirin	48-55	cyclin D1	Homo sapiens	209-218
33285683-1	2020	BACKGROUND: The purpose of this meta-analysis is to compare the efficacy and safety of aspirin and rivaroxaban in the prevention of venous thromboembolism (VTE) following either total knee arthroplasty or total hip arthroplasty.	Aspirin	87-94	hedgehog interacting protein	Homo sapiens	211-214
33040197-1	2020	INTRODUCTION: Acetylsalicylic acid (aspirin) is a commonly prescribed medication, especially in the age group of individuals who undergo elective total hip arthroplasty (THA).	Aspirin	14-34	hedgehog interacting protein	Homo sapiens	152-155
33040197-1	2020	INTRODUCTION: Acetylsalicylic acid (aspirin) is a commonly prescribed medication, especially in the age group of individuals who undergo elective total hip arthroplasty (THA).	Aspirin	36-43	hedgehog interacting protein	Homo sapiens	152-155
33447595-7	2020	Results: Treatment with ASA significantly inhibited the proliferation, invasion, and migration capabilities, and caused a significant decrease in angiogenin and PIGF secretion in both CM and UM.	Aspirin	24-27	angiogenin	Homo sapiens	146-156
33298861-7	2020	Aspirin also improved tumor control by immunogenic chemotherapeutics, and this effect was lost in T cell-deficient mice, as well as upon knockdown of an essential autophagy gene (Atg5) in cancer cells.	Aspirin	0-7	autophagy related 5	Mus musculus	179-183
33082288-5	2020	Treating cultured CSCs or 4T1 tumor-bearing mice with the nonsteroidal anti-inflammatory drug aspirin restored SMAR1 expression and ABCG2 repression and enhanced tumor sensitivity to doxorubicin.	Aspirin	94-101	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	132-137
3111564-6	1987	While the release of PGl2 could be inhibited by pretreatment of the cells with 100 microM acetylsalicylic acid (ASA), the induction of tissue factor activity remained unaffected by ASA.	Aspirin	90-110	succinate dehydrogenase complex assembly factor 2	Homo sapiens	21-25
3111564-6	1987	While the release of PGl2 could be inhibited by pretreatment of the cells with 100 microM acetylsalicylic acid (ASA), the induction of tissue factor activity remained unaffected by ASA.	Aspirin	112-115	succinate dehydrogenase complex assembly factor 2	Homo sapiens	21-25
2437338-3	1987	In the first patient, although aspirin prevented both in vitro heparin-induced platelet aggregation (70% without and 7.5% with aspirin) and 14C serotonin release (48% without and 0% with aspirin), intraoperative administration of heparin resulted in an increase in plasma levels of platelet factor 4 from 8 to 260 ng/ml and beta-thromboglobulin levels from 29 to 39 ng/ml.	Aspirin	31-38	pro-platelet basic protein	Homo sapiens	324-344
3088727-3	1986	The aspirin substitutes acetaminophen and ibuprofen were studied as aldose reductase inhibitors and were found to be effective in reducing sorbitol accumulation in lenses exposed to high glucose stress.	Aspirin	4-11	aldo-keto reductase family 1 member B1	Oryctolagus cuniculus	68-84
2867260-0	1986	Low-dose aspirin prevents pregnancy-induced hypertension and pre-eclampsia in angiotensin-sensitive primigravidae.	Aspirin	9-16	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	26-56
2867260-1	1986	The possibility of preventing pregnancy-induced hypertension (PIH) and pre-eclampsia in primigravidae by suppressing production of thromboxane A2 with low-dose aspirin was investigated in a randomised, placebo-controlled, double-blind trial.	Aspirin	160-167	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	62-65
2867260-6	1986	Low-dose aspirin may restore prostacyclin/thromboxane imbalance, previously suggested as an important aetiological factor in PIH and pre-eclampsia.	Aspirin	9-16	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	125-128
2934863-4	1985	Both prior to and after ASA ingestion ADP removal by creatine phosphate/creatine phosphokinase (CP/CPK) resulted in a reduced, reversible platelet aggregation induced by PAF alone or in combination with the other agonists.	Aspirin	24-27	phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha	Homo sapiens	99-102
2934863-5	1985	The ADP-removal and ASA-ingestion also strongly inhibited the beta-TG release.	Aspirin	20-23	pro-platelet basic protein	Homo sapiens	62-69
6633508-5	1983	Concentrations required to inhibit TPMT by 50% ranged from 20 microM for 3,4-dimethoxy-5-hydroxybenzoic acid to 2.1 mM for acetylsalicylic acid.	Aspirin	123-143	thiopurine S-methyltransferase	Homo sapiens	35-39
6587820-8	1983	Both dihydroxybenzene sulfonate and acetylsalicylate protected human erythrocytes from hemolysis at concentrations from 10(-3) to 10(-5) M. The removal of erythrocyte sialic acid using neuraminidase to reduce surface negative charge led to unequivocal interference with aggregation (MAI technique of CHIEN et al., J. Gen.	Aspirin	36-52	neuraminidase 1	Homo sapiens	185-198
6184841-0	1982	Effect of aspirin on platelet 5-hydroxytryptamine and beta-thromboglobulin plasma levels in patients with myeloproliferative diseases.	Aspirin	10-17	pro-platelet basic protein	Homo sapiens	54-74
7281165-1	1981	Urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) has been studied in rats submitted to potentially nephrotoxic drugs (acetylsalicylic acid, gentamicin).	Aspirin	128-148	O-GlcNAcase	Rattus norvegicus	54-57
7009654-5	1981	Aspirin treatment led to an increase in mean arterial pressure (P &lt; 0.001) and mean pulmonary arterial pressure (P &lt; 0.005), but cardiac index, urine flow, platelets, leukocytes, fibrin degradation products, and cathepsin D levels remained similar to untreated controls.	Aspirin	0-7	cathepsin D	Canis lupus familiaris	218-229
7390731-3	1980	Acetylsalicylic acid at blood levelsof about 1 mM produced a significant lowering of the beta-hexosaminidase concentration in tears.	Aspirin	0-20	O-GlcNAcase	Homo sapiens	89-108
7353335-5	1980	During continued aspirin administration, no change was observed in elimination half-life (t 1/2 beta) of total serum DPH but there was a trend toward reduced t 1/2 beta in saliva.	Aspirin	17-24	interleukin 1 receptor like 1	Homo sapiens	158-168
311157-2	1978	An elevated NAG level was particularly common in patients receiving gold or aspirin therapy.	Aspirin	76-83	O-GlcNAcase	Homo sapiens	12-15
949546-14	1976	In contrast, the ingestion of aspirin by mouth inhibited the release of serotonin, beta-glucuronidase, and K+ by thrombin.	Aspirin	30-37	glucuronidase beta	Homo sapiens	83-101
1085402-5	1976	In the APC mixture, aspirin appears to be the major nephrotoxic agent while phenacetin and paracetamol play a secondary and synergistic role in the nephrotoxicity.	Aspirin	20-27	APC regulator of WNT signaling pathway	Homo sapiens	7-10
4846730-1	1974	Callaway of papers MM1 and MM11 at the 86th meeting of the ASA.	Aspirin	59-62	prefoldin subunit 5	Homo sapiens	19-22
6401084-3	1984	In the subjects showing substantial temporary hearing loss induced by the aspirin, (1) forward masking declined at about a normal rate as the masker-to-signal interval was increased, (2) the temporal-integration functions were flatter than normal, and (3) detection of a temporal gap was worse than normal at low sound-pressure levels (SPLs) but was essentially normal at levels above about 60 dB SPL.	Aspirin	74-81	sphingosine-1-phosphate lyase 1	Homo sapiens	336-339
6197783-7	1983	In many patients with ischemic or obstructive cerebro-vascular diseases treated with anti-platelet drugs such as Aspirin, Dipyridamole, Bencyclane or Ticlopidine, a significant fall in plasma concentration of beta-TG was chronologically demonstrated.	Aspirin	113-120	pro-platelet basic protein	Homo sapiens	209-216
6859071-9	1983	The retardant aspirin effect in diabetic cataracts is linked to inhibition of tissue aldose reductase and lens protein glycosylation.	Aspirin	14-21	aldo-keto reductase family 1 member B1	Oryctolagus cuniculus	85-101
6342005-5	1983	ASA or naloxone pretreatments significantly lowered the captopril hypotensive effect, thus suggesting an involvement of prostaglandin and opioid systems in blood pressure elevation in "non renin dependent" hypertension.	Aspirin	0-3	renin	Rattus norvegicus	189-194
6174402-3	1981	Death from anaphylactic shock in BALB/c mice mediated by active systemic anaphylaxis (ASA) or heterologous passive systemic anaphylaxis (PSA) was completely prevented in one of five cases by NSP given 5000 micrograms/animal i.v..	Aspirin	86-89	reticulon 1	Mus musculus	191-194
7030877-1	1981	This study compares the effect of epidermal growth factor and prostaglandins (PGE2 or PGI2), applied topically to gastric mucosa, on gastric secretion and formation of ASA-induced gastric ulcerations in rats.	Aspirin	168-171	epidermal growth factor like 1	Rattus norvegicus	34-57
7030877-2	1981	Epidermal growth factor given topically in non-antisecretory doses prevented dose-dependently the formation of ASA-induced ulcers without affecting prostaglandin generation but with a significant rise in DNA synthesis in the oxyntic mucosa.	Aspirin	111-114	epidermal growth factor like 1	Rattus norvegicus	0-23
33031402-0	2020	Increased expression of serine palmitoyl transferase and ORMDL3 polymorphism are associated with eosinophilic inflammation and airflow limitation in aspirin-exacerbated respiratory disease.	Aspirin	149-156	ORMDL sphingolipid biosynthesis regulator 3	Homo sapiens	57-63
6894078-2	1981	The ultrastructural alterations in the small-intestinal mucosa of mice given aspirin for five weeks were observed by light microscopy and scanning (SEM) and transmission (TEM) electron microscopy.	Aspirin	77-84	tenomodulin	Mus musculus	171-174
113475-7	1979	The mean PRB decreased from 22.1 +/- 9.2 to 9.6 +/- 8.6 (p less than 0.001) after aspirin ingestion.	Aspirin	82-89	RB transcriptional corepressor 1	Homo sapiens	9-12
32921373-3	2020	Aspirin-free strategies consisting of P2Y12 inhibitor monotherapy following percutaneous coronary intervention (PCI) have now been tested in several large randomized controlled trials.	Aspirin	0-7	purinergic receptor P2Y12	Homo sapiens	38-43
113475-8	1979	Subjects whose bleeding time was prolonged greater than 2.4 min had a significantly higher mean PRB before aspirin and a significantly greater mean decrease in PRB after aspirin than those whose bleeding time was prolonged less than or equal to 2.4 min.	Aspirin	170-177	RB transcriptional corepressor 1	Homo sapiens	160-163
32887656-6	2020	We used age-stratified Cox proportional hazards regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations of aspirin use with risk of ER+, ER-, and TN breast cancer, adjusted for established breast cancer risk factors.	Aspirin	153-160	epiregulin	Homo sapiens	178-180
32887656-6	2020	We used age-stratified Cox proportional hazards regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations of aspirin use with risk of ER+, ER-, and TN breast cancer, adjusted for established breast cancer risk factors.	Aspirin	153-160	epiregulin	Homo sapiens	183-185
32887656-10	2020	Aspirin may represent a potential opportunity for chemoprevention of ER- and TN breast cancer.	Aspirin	0-7	epiregulin	Homo sapiens	69-71
115671-7	1979	In contrast, aspirin inhibited the TSH response to TRH in intact rats, when pituitary TSH content decreased significantly.	Aspirin	13-20	thyrotropin releasing hormone	Rattus norvegicus	51-54
32861238-7	2020	ASA-positive seminal fluid exhibited significant increases in the mean migration distance (2.6 +- 1.4 cm vs. 1.54 +- 1.1 cm, respectively; p< 0.001) and sperm concentration (174 +- 121.0 x 103/mL vs. 101 +- 93.7 x 103/mL, respectively; p= 0.033) after treatment with SPA compared to pre-treated samples.	Aspirin	0-3	surfactant protein A1	Homo sapiens	267-270
115671-11	1979	In addition, there is a dissociation between the action of indomethacin and the action of aspirin in the TSH response to TRH.	Aspirin	90-97	thyrotropin releasing hormone	Rattus norvegicus	121-124
32854760-0	2020	Aspirin mediates histone methylation that inhibits inflammation-related stemness gene expression to diminish cancer stemness via COX-independent manner.	Aspirin	0-7	cytochrome c oxidase subunit 8A	Homo sapiens	129-132
930725-3	1977	The gastric mucosa on stimulation by ulcerogenic aspirin, on the other hand, responds immediately to the insult by rapid shedding of its adherent mucin, then, within 5 minutes by an almost complete shut-down of respiration and biosynthesis, not only of glycoproteins but also of proteins and nucleic acids.	Aspirin	49-56	LOC100508689	Homo sapiens	146-151
32854760-9	2020	In regards to the underlying molecular mechanism of action, aspirin reduces histone demethylase (KDM6A/B) expression that mediates histone methylation and suppresses gene expression via a COX-independent manner.	Aspirin	60-67	cytochrome c oxidase subunit 8A	Homo sapiens	188-191
32551860-0	2020	The Safety and Efficacy of Aspirin Discontinuation on a Background of a P2Y12 Inhibitor in Patients after Percutaneous Coronary Intervention: A Systematic Review and Meta-Analysis.	Aspirin	27-34	purinergic receptor P2Y12	Homo sapiens	72-77
32551860-1	2020	Background: Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor has been shown to reduce the risk of MACE compared to aspirin alone after PCI or ACS but with increased risk of bleeding.	Aspirin	134-141	purinergic receptor P2Y12	Homo sapiens	64-69
32551860-3	2020	Methods: A meta-analysis was conducted from randomized trials (2001-2020) that studied discontinuation of aspirin 1-3 months after PCI with continued P2Y12 inhibitor monotherapy compared to traditional DAPT.	Aspirin	106-113	purinergic receptor P2Y12	Homo sapiens	150-155
32551860-11	2020	Conclusions: Discontinuation of aspirin with continued P2Y12 inhibitor monotherapy reduces risk of bleeding when stopped 1-3 months after PCI.	Aspirin	32-39	purinergic receptor P2Y12	Homo sapiens	55-60
4853047-0	1974	Lowering of kininogen in rat blood by adrenaline and its inhibition by sympatholytic agents, heparin and aspirin.	Aspirin	105-112	kininogen 2-like 1	Rattus norvegicus	12-21
31542850-1	2020	INTRODUCTION: Despite the use of the new generation P2Y12 inhibitors (Ticagrelor and Prasugrel) with aspirin is the recommended therapy in acute NSTE-ACS patients, their current use in clinical practice remains quite low and might be related, among several variables, with increased comorbidity burden.	Aspirin	101-108	purinergic receptor P2Y12	Homo sapiens	52-57
34016116-14	2021	CONCLUSION: An acceptable and usable decision aid was developed to support decisions about aspirin use to prevent colorectal cancer.	Aspirin	91-98	activation induced cytidine deaminase	Homo sapiens	46-49
32661222-0	2020	Aspirin attenuates YAP and beta-catenin expression by promoting beta-TrCP to overcome docetaxel and vinorelbine resistance in triple-negative breast cancer.	Aspirin	0-7	Yes1 associated transcriptional regulator	Homo sapiens	19-22
33987897-0	2021	Influence of daily aspirin therapy on ACE2 expression and function - implications for SARS-CoV2 and patients with aspirin-exacerbated respiratory disease.	Aspirin	19-26	angiotensin converting enzyme 2	Homo sapiens	38-42
32661222-4	2020	Interestingly, aspirin not only significantly inhibited the growth of TNBC cells, but also attenuated YAP and beta-catenin expression by upregulating the E3 ubiquitin ligase beta-TrCP to abolished docetaxel and vinorelbine resistance.	Aspirin	15-22	Yes1 associated transcriptional regulator	Homo sapiens	102-105
33987897-0	2021	Influence of daily aspirin therapy on ACE2 expression and function - implications for SARS-CoV2 and patients with aspirin-exacerbated respiratory disease.	Aspirin	114-121	angiotensin converting enzyme 2	Homo sapiens	38-42
32169518-8	2020	Furthermore, the levels of HMGB1 of subjects with URSA could be reduced by administrating low doses of aspirin (ASPL).	Aspirin	103-110	high mobility group box 1	Homo sapiens	27-32
33705573-9	2021	Other features including non-steroidal anti-inflammatory drugs and/or aspirin use (OR 1.19; 95% CI 1.00 to 1.42), smoking (OR 1.14; 95% CI 0.96 to 1.35) or obesity (OR 1.10; 95% CI 0.92 to 1.33) were not significantly associated with Barrett"s oesophagus.	Aspirin	70-77	olfactory receptor family 7 subfamily E member 87 pseudogene	Homo sapiens	83-90
32313942-10	2020	Strikingly, aspirin suppressed ESCC growth by inhibiting HBXIP and HMGA2.	Aspirin	12-19	late endosomal/lysosomal adaptor, MAPK and MTOR activator 5	Homo sapiens	57-62
32351866-8	2020	The transcripts corresponding to AsA-GSH pathway enzymes SOD, APX, GR, DHAR, and MDHAR were up-regulated by 8- to 12-fold under combined drought and heat.	Aspirin	33-36	dehydroascorbate reductase 1	Solanum lycopersicum	71-75
32677810-4	2020	Previously, we showed that aspirin-induced gastric injury is associated with reduction in glutamate release by inhibition of cystine-glutamate transporter (xCT) activity.	Aspirin	27-34	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	156-159
33631404-0	2021	The aberrant expression of CD69 on peripheral T-helper cells in diet-induced inflammation is ameliorated by low-dose aspirin and metformin treatment.	Aspirin	117-124	CD69 molecule	Homo sapiens	27-31
32713065-4	2021	We aimed to investigate whether statins and chronic ASA intake are associated with lower risk of PEP.	Aspirin	52-55	prolyl endopeptidase	Homo sapiens	97-100
31637734-0	2020	Aspirin promotes tenogenic differentiation of tendon stem cells and facilitates tendinopathy healing through regulating the GDF7/Smad1/5 signaling pathway.	Aspirin	0-7	SMAD family member 1	Homo sapiens	129-134
31637734-14	2020	In addition, aspirin increased the expression of TNC, TNMD, and Scx and biomechanical properties of the injured tendon.	Aspirin	13-20	scleraxis bHLH transcription factor	Homo sapiens	64-67
31637734-15	2020	In conclusion, aspirin promoted TSC tenogenesis and tendinopathy healing through GDF7/Smad1/5 signaling, and this provided new treatment evidence of aspirin for tendinopathy and tendon injuries.	Aspirin	15-22	SMAD family member 1	Homo sapiens	86-93
32323648-10	2020	ASA VI also induced a significant decrease in bone volume and density and an increase in trabecular spacing and RANKL (receptor activator of nuclear factor kappa-B ligand) expression at the compression side.	Aspirin	0-3	TNF superfamily member 11	Rattus norvegicus	112-117
32323648-10	2020	ASA VI also induced a significant decrease in bone volume and density and an increase in trabecular spacing and RANKL (receptor activator of nuclear factor kappa-B ligand) expression at the compression side.	Aspirin	0-3	TNF superfamily member 11	Rattus norvegicus	119-170
33847681-1	2021	BACKGROUND: In this analysis, we aimed to compare the efficacy and safety of dual therapy (DT) with a non-vitamin K oral anticoagulant (NOAC) and an adenosine diphosphate receptor antagonist (P2Y12 inhibitor) vs triple therapy (TT) with aspirin, a P2Y12 inhibitor and a vitamin K antagonist for the treatment of diabetes mellitus (DM) patients with co-existing atrial fibrillation (AF) following percutaneous coronary intervention (PCI).	Aspirin	237-244	purinergic receptor P2Y12	Homo sapiens	192-197
32186937-5	2020	Results: The developed methods demonstrated limits of detection ranging from 0.67 to 1.09 mug/ml-1 for CPS and 0.49 to 0.71 mug.ml-1 for ASP.	Aspirin	137-140	interleukin 17F	Homo sapiens	128-132
33592258-0	2021	Aspirin eugenol ester ameliorates paraquat-induced oxidative damage through ROS/p38-MAPK-mediated mitochondrial apoptosis pathway.	Aspirin	0-7	mitogen activated protein kinase 14	Rattus norvegicus	80-88
32521895-8	2020	The expression levels of TCF4 and LEF1, key molecules of the Wnt/beta-catenin signaling pathway, were lowered in HCC cells treated with 4 mM ASP, and the nuclear translocation of beta-catenin was weakened.	Aspirin	141-144	transcription factor 4	Homo sapiens	25-29
32521895-8	2020	The expression levels of TCF4 and LEF1, key molecules of the Wnt/beta-catenin signaling pathway, were lowered in HCC cells treated with 4 mM ASP, and the nuclear translocation of beta-catenin was weakened.	Aspirin	141-144	lymphoid enhancer binding factor 1	Homo sapiens	34-38
33917483-6	2021	Mechanistically, activation of AMPK by aspirin results in decreased expression of the urea cycle enzyme carbamoyl-phosphate synthase 1 (CPS1) in HCC cells and xenografts.	Aspirin	39-46	carbamoyl-phosphate synthase 1	Homo sapiens	104-134
32099910-8	2020	The proliferation assay showed FUT8 partial knockdown by transfection of siRNA significantly suppressed the proliferation of Ishikawa cells, concomitant with the upregulation in the gene expressions associated with the interesting pathways associated with de-ubiquitination, aspirin trigger, mesenchymal-epithelial transition (MET) et al.	Aspirin	275-282	fucosyltransferase 8	Homo sapiens	31-35
34050956-11	2021	CONCLUSIONS: Among rivaroxaban, enoxaparin, and aspirin used for thromboprophylaxis in knee and hip arthroplasty or revision, aspirin had significantly decreased odds of bleeding complications compared to enoxaparin.	Aspirin	126-133	hedgehog interacting protein	Homo sapiens	96-99
33917483-6	2021	Mechanistically, activation of AMPK by aspirin results in decreased expression of the urea cycle enzyme carbamoyl-phosphate synthase 1 (CPS1) in HCC cells and xenografts.	Aspirin	39-46	carbamoyl-phosphate synthase 1	Homo sapiens	136-140
31557387-10	2020	Increased VWF activity, decreased physical status according to American Society of Anesthesiologists (ASA) classification (ASA class >2), and increased duration of surgery were associated with decreased FVIII clearance.	Aspirin	102-105	coagulation factor VIII	Homo sapiens	203-208
33879541-7	2021	During the COVID-19 pandemic, low-dose aspirin is used effectively in secondary prevention of atherosclerotic cardiovascular disease, prevention of venous thromboembolism after total hip or knee replacement, prevention of pre-eclampsia and postdischarge treatment for multisystem inflammatory syndrome in children.	Aspirin	39-46	hedgehog interacting protein	Homo sapiens	183-186
31905343-6	2020	The combined treatment of aspirin and cisplatin suppressed the expression of the anti-apoptotic protein Bcl-2 and the EMT-related proteins, up-regulated the levels of the cleaved PARP and Bax, and blocked the PI3K/AKT and RAF-MEK-ERK signaling pathway.	Aspirin	26-33	collagen type XI alpha 2 chain	Homo sapiens	179-183
31905343-6	2020	The combined treatment of aspirin and cisplatin suppressed the expression of the anti-apoptotic protein Bcl-2 and the EMT-related proteins, up-regulated the levels of the cleaved PARP and Bax, and blocked the PI3K/AKT and RAF-MEK-ERK signaling pathway.	Aspirin	26-33	zinc fingers and homeoboxes 2	Homo sapiens	222-225
34042199-1	2021	BACKGROUND: The RE-DUAL PCI trial demonstrated that in patients with nonvalvular atrial fibrillation (AF) undergoing percutaneous coronary intervention (PCI), dual therapy with dabigatran and a P2Y12 inhibitor, either clopidogrel or ticagrelor, reduced the risk of bleeding without an increased risk of thromboembolic events as compared to triple therapy with warfarin in addition to a P2Y12 inhibitor and aspirin.	Aspirin	406-413	purinergic receptor P2Y12	Homo sapiens	194-199
34016116-0	2021	Development and user-testing of a brief decision aid for aspirin as a preventive approach alongside colorectal cancer screening.	Aspirin	57-64	activation induced cytidine deaminase	Homo sapiens	49-52
33555916-8	2021	Dual antiplatelet therapy with aspirin and a P2Y12 inhibitor should be given to all patients during the peri-PCI period (during inpatient stay, until time of discharge, up to 1 week after PCI, at the discretion of the treating physician), after which the default strategy is to stop aspirin and continue treatment with a P2Y12 inhibitor, preferably clopidogrel, in combination with a non-vitamin K antagonist oral anticoagulant (ie, double therapy).	Aspirin	283-290	purinergic receptor P2Y12	Homo sapiens	45-50
34016116-4	2021	A decision aid to support people to consider aspirin therapy alongside participation in the NHS bowel cancer screening programme may have an additional impact on colorectal cancer prevention.	Aspirin	45-52	activation induced cytidine deaminase	Homo sapiens	11-14
34016116-5	2021	This study aims to develop and user-test a brief decision aid about aspirin to enable informed decision-making for colorectal screening-eligible members of the public.	Aspirin	68-75	activation induced cytidine deaminase	Homo sapiens	58-61
34016116-6	2021	METHODS: We undertook a qualitative study to develop an aspirin decision aid leaflet to support bowel screening responders in deciding whether to take aspirin to reduce their risk of colorectal cancer.	Aspirin	56-63	activation induced cytidine deaminase	Homo sapiens	73-76
34016116-6	2021	METHODS: We undertook a qualitative study to develop an aspirin decision aid leaflet to support bowel screening responders in deciding whether to take aspirin to reduce their risk of colorectal cancer.	Aspirin	151-158	activation induced cytidine deaminase	Homo sapiens	73-76
33979377-11	2021	Our results indicated that <= 1-month aspirin may be enough in P2Y12 inhibitor monotherapy strategy for ACS patients undergoing PCI.	Aspirin	38-45	purinergic receptor P2Y12	Homo sapiens	63-68
34003664-0	2021	Early P2Y12 Receptor Monotherapy Following Drug-Eluting Stenting: Is It Time to Give Up Aspirin?	Aspirin	88-95	purinergic receptor P2Y12	Homo sapiens	6-11
33618601-3	2021	Beyond its numerous functions in plants, SA has great pharmaceutical importance since it acts as an intermediate for the synthesis of various drugs and dyes e.g. aspirin.	Aspirin	162-169	acyl-CoA synthetase medium chain family member 3	Homo sapiens	41-43
33824459-11	2022	Aspirin alleviates breast cancer via targeting PD-L1 and HBXIP.	Aspirin	0-7	late endosomal/lysosomal adaptor, MAPK and MTOR activator 5	Homo sapiens	57-62
33918289-6	2021	In this study, we have used cytotoxicity and molecular docking studies to show that NCX4040, a nitric oxide donor related to aspirin, inhibited the functions of ATPase which resulted in significant reversal of resistance to both adriamycin and topotecan in P-gp- and BCRP-expressing human cancer cell lines, respectively.	Aspirin	125-132	dynein axonemal heavy chain 8	Homo sapiens	161-167
33706989-5	2021	ASA is an essential member of the duo that makes up dual antiplatelet therapy (a P2Y12 inhibitor plus ASA) and also dual pathway inhibition (vascular dose rivaroxaban plus ASA), and data for both approaches are growing.	Aspirin	0-3	uridine phosphorylase 1	Homo sapiens	49-51
33706989-5	2021	ASA is an essential member of the duo that makes up dual antiplatelet therapy (a P2Y12 inhibitor plus ASA) and also dual pathway inhibition (vascular dose rivaroxaban plus ASA), and data for both approaches are growing.	Aspirin	0-3	purinergic receptor P2Y12	Homo sapiens	81-86
33318029-7	2021	Of these, aspirin decreased MCM6, RRM2 and ARFIP2 expression and MR analysis showed that a standard deviation increase in mRNA/protein expression was associated with increased CRC risk (OR:1.08, 95% CI:1.03-1.13, OR:3.33, 95% CI:2.46-4.50 and OR:1.15, 95% CI:1.02-1.29, respectively).	Aspirin	10-17	ADP ribosylation factor interacting protein 2	Homo sapiens	43-49
33318029-8	2021	CONCLUSIONS: MCM6 and RRM2 are involved in DNA repair whereby reduced expression may lead to increased DNA aberrations and ultimately cancer cell death, whereas ARFIP2 is involved in actin cytoskeletal regulation indicating a possible role in aspirin"s reduction of metastasis.	Aspirin	243-250	ADP ribosylation factor interacting protein 2	Homo sapiens	161-167
33574709-0	2021	siRNA Knockdown of REDD1 Facilitates Aspirin-Mediated Dephosphorylation of mTORC1 Target 4E-BP1 in MDA-MB-468 Human Breast Cancer Cell Line.	Aspirin	37-44	CREB regulated transcription coactivator 1	Mus musculus	75-81
33574709-2	2021	Inhibition of mTORC1 (mechanistic target of rapamycin complex 1) activity upon aspirin treatment has been reported in breast cancer cells harboring PI3KCA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) mutation and is considered to account for anticancer action.	Aspirin	79-86	CREB regulated transcription coactivator 1	Mus musculus	14-20
33574709-6	2021	Knockdown by siRNA approach was applied to assess the role of REDD1/DDIT4 (DNA damage-inducible transcript 4) in mTORC1 inhibition by aspirin.	Aspirin	134-141	CREB regulated transcription coactivator 1	Mus musculus	113-119
33574709-7	2021	Results: We show a decline in phosphorylation of mTORC1 downstream substrate 4E-BP1 (eukaryotic translation initiation factor 4E-binding protein 1) in response to treatment with aspirin and its metabolite salicylic acid in MDA-MB-468, MCF-7, MDA-MB-231, and MCF10A cell lines.	Aspirin	178-185	CREB regulated transcription coactivator 1	Mus musculus	49-55
33162063-3	2021	We explored the risk of PH associated with standard antiplatelet therapy (sAP: acetylsalicylic acid, and/or clopidogrel) in the context of aneurysmal subarachnoid hemorrhage (aSAH).	Aspirin	79-99	phenylalanine hydroxylase	Homo sapiens	24-26
33488022-0	2021	P2Y12 Inhibitor Monotherapy after Percutaneous Coronary Intervention: Is It Safe to Abandon Aspirin?	Aspirin	92-99	purinergic receptor P2Y12	Homo sapiens	0-5
33488022-7	2021	An early aspirin-free strategy with P2Y12 inhibitor monotherapy seems feasible in some of the patients after PCI.	Aspirin	9-16	purinergic receptor P2Y12	Homo sapiens	36-41
32971322-0	2021	Aspirin rescues Wnt-driven stem-like phenotype in human intestinal organoids and increases the Wnt antagonist Dickkopf-1.	Aspirin	0-7	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	110-120
32971322-7	2021	RESULTS: Aspirin rescues the Wnt-driven cystic organoid phenotype by promoting budding in mouse and human Apc deficient organoids, which is paralleled by decreased stem cell marker expression.	Aspirin	9-16	APC regulator of WNT signaling pathway	Homo sapiens	106-109
32971322-10	2021	Aspirin increases expression of the Wnt antagonist Dickkopf-1 (DKK-1) in CRC cells and organoids derived from FAP patients which contributes to EMT and CSC inhibition.	Aspirin	0-7	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	51-61
32971322-10	2021	Aspirin increases expression of the Wnt antagonist Dickkopf-1 (DKK-1) in CRC cells and organoids derived from FAP patients which contributes to EMT and CSC inhibition.	Aspirin	0-7	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	63-68
32971322-11	2021	CONCLUSIONS: We provide evidence of phenotypic biomarkers of response to aspirin with an increased epithelial and reduced stem-like state mediated by an increase in DKK-1 This highlights a novel mechanism of aspirin-mediated Wnt inhibition and potential phenotypic and molecular biomarkers for trials.	Aspirin	73-80	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	165-170
32971322-11	2021	CONCLUSIONS: We provide evidence of phenotypic biomarkers of response to aspirin with an increased epithelial and reduced stem-like state mediated by an increase in DKK-1 This highlights a novel mechanism of aspirin-mediated Wnt inhibition and potential phenotypic and molecular biomarkers for trials.	Aspirin	208-215	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	165-170
33287104-9	2020	ASA also showed a significant increase of five ATP-binding cassette (ABC) transporters (giABC, giABCP, giMDRP, giMRPL and giMDRAP1).	Aspirin	0-3	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	69-72
33287104-11	2020	Taken together, these results suggest an important role of HSPs and ABC drug transporters in contributing to stress tolerance and protecting cells from ASA-induced stress.	Aspirin	152-155	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	68-71
32853794-6	2020	ASA alone or in combination with ticagrelor(a P2Y12 blocker) affected platelet aggregation associated with profound inhibition of TXB2 generation.	Aspirin	0-3	purinergic receptor P2Y12	Homo sapiens	46-51
32574107-5	2020	The redness at the inoculation site of bacillus Calmette-Guerin, a specific feature of Kawasaki disease, is reproduced by activation of the STING pathway, which is inhibited upstream by aspirin, intravenous immunoglobulins, and Vitamin-D.	Aspirin	186-193	stimulator of interferon response cGAMP interactor 1	Homo sapiens	140-145
32574107-8	2020	Aspirin and dipyridamole, besides their anti-platelet activity, also reduce tissue factor procoagulant activity, and aspirin inhibits the STING pathway upstream of STING.	Aspirin	117-124	stimulator of interferon response cGAMP interactor 1	Mus musculus	138-143
32574107-8	2020	Aspirin and dipyridamole, besides their anti-platelet activity, also reduce tissue factor procoagulant activity, and aspirin inhibits the STING pathway upstream of STING.	Aspirin	117-124	stimulator of interferon response cGAMP interactor 1	Homo sapiens	164-169
33329515-2	2020	In the current study, we found that both aspirin and 5-aminoimidazole-4-carboxamide-1-beta-riboside (AICAR) siginificantly attenuated virus replication by inhibiting BEFV-induced autophagy via suppressing the BEFV-activated PI3K/Akt/NF-kappaB and Src/JNK pathways as well as inducing reversion of the BEFV-suppressed PI3K-Akt-mTORC1 pathway.	Aspirin	41-48	CREB regulated transcription coactivator 1	Mus musculus	326-332
33100875-9	2020	ASA VI also activated PPAR-gamma signaling pathway in LPS-treated microglia.	Aspirin	0-3	peroxisome proliferator activated receptor gamma	Mus musculus	22-32
33100875-10	2020	The anti-inflammatory effects of ASA VI in microglia were blocked by treating PPAR-gamma antagonist (GW9662).	Aspirin	33-36	peroxisome proliferator activated receptor gamma	Mus musculus	78-88
33100875-11	2020	These results showed that ASA VI promote the transition of microglia cells from proinflammatory to anti-inflammatory by regulating PPAR-gamma pathway.	Aspirin	26-29	peroxisome proliferator activated receptor gamma	Mus musculus	131-141
33047719-4	2020	RESULTS: CMTM5 gene expression in HAPR (High on aspirin platelet reactivity) group was 1.72 times compared with No-HAPR group, which was significantly higher than No-HAPR group.	Aspirin	48-55	CKLF like MARVEL transmembrane domain containing 5	Homo sapiens	9-14
33116404-0	2020	Novel Molecular Mechanism of Aspirin and Celecoxib Targeting Mammalian Neuraminidase-1 Impedes Epidermal Growth Factor Receptor Signaling Axis and Induces Apoptosis in Pancreatic Cancer Cells.	Aspirin	29-36	neuraminidase 1	Homo sapiens	71-86
33116404-5	2020	Aim: Here, we propose that aspirin and celecoxib exert their anti-cancer effects by targeting and inhibiting mammalian neuraminidase-1 (Neu-1).	Aspirin	27-34	neuraminidase 1	Homo sapiens	119-134
33116404-5	2020	Aim: Here, we propose that aspirin and celecoxib exert their anti-cancer effects by targeting and inhibiting mammalian neuraminidase-1 (Neu-1).	Aspirin	27-34	neuraminidase 1	Homo sapiens	136-141
33116404-12	2020	Results: For the first time, aspirin and celecoxib were shown to significantly inhibit Neu-1 sialidase activity in a dose- and time-dependent manner following stimulation with EGF.	Aspirin	29-36	neuraminidase 1	Homo sapiens	87-92
33116404-13	2020	Aspirin blocked Neu-1 desialylation of alpha-2,3-sialic acid expression following 30 min stimulation with EGF.	Aspirin	0-7	neuraminidase 1	Homo sapiens	16-21
33116404-17	2020	Conclusion: These findings signify a novel multimodality mechanism(s) of action for aspirin and celecoxib, specifically targeting and inhibiting Neu-1 activity, regulating EGF-induced growth receptor activation and inducing apoptosis and necrosis in a dose- and time-dependent manner.	Aspirin	84-91	neuraminidase 1	Homo sapiens	145-150
33116404-18	2020	Repurposing aspirin and celecoxib as anti-cancer agents may also upend other critical targets involved in multistage tumorigenesis regulated by mammalian neuraminidase-1.	Aspirin	12-19	neuraminidase 1	Homo sapiens	154-169
32581009-8	2020	However, aspirin users were more likely to have low FoxP3, a T regulatory cell marker (OR: 5.60, 95% CI: 1.16-27.07), and statin users were more likely to have low CD68, a macrophage marker (OR: 1.63, 95% CI: 0.81-3.27).	Aspirin	9-16	forkhead box P3	Homo sapiens	52-57
32945920-1	2021	BACKGROUND: A decreased antiplatelet prophylaxis (low response, LR/high on-treatment platelet reactivity, HPR) with acetylsalicylic acid (ASA) is associated with an increased risk of thromboembolic events.	Aspirin	116-136	haptoglobin-related protein	Homo sapiens	106-109
32945920-1	2021	BACKGROUND: A decreased antiplatelet prophylaxis (low response, LR/high on-treatment platelet reactivity, HPR) with acetylsalicylic acid (ASA) is associated with an increased risk of thromboembolic events.	Aspirin	138-141	haptoglobin-related protein	Homo sapiens	106-109
32772110-7	2020	DAPT with low-dose ASA and ticagrelor [odds ratio (OR) 2.53, 95% credible interval (CrI) 1.35-4.72; I2 = 55; low certainty] or clopidogrel (OR 1.56, 95% CrI 1.02-2.39; I2 = 55; very low certainty) improved saphenous vein graft patency when compared to low-dose ASA monotherapy.	Aspirin	19-22	EP300 interacting inhibitor of differentiation 1	Homo sapiens	65-90
32487324-7	2020	Yet Aspirin and Clopidogrel each comparably lowered CK-MB, AST, MMP-2, MMP-9, and the lipid peroxidation product malondialdehyde (MDA) in the hyperlipidemic animals exposed to AMI.	Aspirin	4-11	matrix metallopeptidase 9	Mus musculus	71-76
32627038-9	2020	In addition, aspirin upregulated the levels of caspase-cleaved cytokeratin 18, increased the proportion of early apoptotic cells, decreased the levels of clusterin and heat shock protein 70 (HSP 70), upregulated the levels of miRNA-137 and inhibited epidermal growth factor receptor (EGFR) activation.	Aspirin	13-20	keratin 18	Mus musculus	63-77
32545774-3	2020	We found that the human H4 glioma cell-killing effects of aspirin involved mitochondria-mediated apoptosis accompanied by endoplasmic reticulum (ER) stress, Noxa upregulation, Mcl-1 downregulation, Bax mitochondrial distribution and oligomerization, and caspase 3/caspase 8/caspase 9 activation.	Aspirin	58-65	caspase 8	Homo sapiens	264-273
32053214-11	2020	The treatment of DPCs with 0.05 mM ASA showed increased alkaline phosphatase activity (p &lt; 0.001), mineralisation (p &lt; 0.05), and increased the expression of the osteo/odontogenic genes, DMP1 and DSPP (p &lt; 0.05).	Aspirin	35-38	dentin sialophosphoprotein	Homo sapiens	202-206
32053214-12	2020	Low concentration (0.05mM) ASA reduced inflammatory cytokines IL-6 (p &lt; 0.001), CCL21 (P &lt; 0.05) and MMP-9 (p &lt; 0.05) in an ex vivo pulpitis model.	Aspirin	27-30	C-C motif chemokine ligand 21	Homo sapiens	83-88
32199912-0	2020	IL-5Ralpha marks nasal polyp IgG4- and IgE-expressing cells in aspirin-exacerbated respiratory disease.	Aspirin	63-70	interleukin 5 receptor subunit alpha	Homo sapiens	0-10
31665395-3	2020	Unexpectedly, after 13 days of treatment, VerifyNow showed a P2Y12 reaction unit (PRU) value of 216, approximately >5 times the mean PRU of other patients on aspirin and ticagrelor.	Aspirin	158-165	purinergic receptor P2Y12	Homo sapiens	61-66
32323728-0	2020	Aspirin inhibits endometrial fibrosis by suppressing the TGF-beta1-Smad2/Smad3 pathway in intrauterine adhesions.	Aspirin	0-7	SMAD family member 2	Homo sapiens	67-72
32323728-0	2020	Aspirin inhibits endometrial fibrosis by suppressing the TGF-beta1-Smad2/Smad3 pathway in intrauterine adhesions.	Aspirin	0-7	SMAD family member 3	Homo sapiens	73-78
32323728-7	2020	However, whether aspirin can inhibit endometrial fibrosis through the TGF-beta1-Smad2/Smad3 pathway to prevent postoperative re-adhesion remains to be elucidated.	Aspirin	17-24	SMAD family member 2	Homo sapiens	80-85
32323728-7	2020	However, whether aspirin can inhibit endometrial fibrosis through the TGF-beta1-Smad2/Smad3 pathway to prevent postoperative re-adhesion remains to be elucidated.	Aspirin	17-24	SMAD family member 3	Homo sapiens	86-91
32323728-8	2020	The results of the present study suggested that aspirin inhibits endometrial fibrosis by suppressing the TGF-beta1-Smad2/Smad3 pathway, which may provide new hypotheses for the mechanism of action of aspirin in the treatment of IUAs.	Aspirin	48-55	SMAD family member 2	Homo sapiens	115-120
32323728-8	2020	The results of the present study suggested that aspirin inhibits endometrial fibrosis by suppressing the TGF-beta1-Smad2/Smad3 pathway, which may provide new hypotheses for the mechanism of action of aspirin in the treatment of IUAs.	Aspirin	48-55	SMAD family member 3	Homo sapiens	121-126
32323728-8	2020	The results of the present study suggested that aspirin inhibits endometrial fibrosis by suppressing the TGF-beta1-Smad2/Smad3 pathway, which may provide new hypotheses for the mechanism of action of aspirin in the treatment of IUAs.	Aspirin	200-207	SMAD family member 2	Homo sapiens	115-120
32323728-8	2020	The results of the present study suggested that aspirin inhibits endometrial fibrosis by suppressing the TGF-beta1-Smad2/Smad3 pathway, which may provide new hypotheses for the mechanism of action of aspirin in the treatment of IUAs.	Aspirin	200-207	SMAD family member 3	Homo sapiens	121-126
32205444-4	2020	We also show that aspirin-triggered 15-epi-lipoxin A4 (15-epi-LXA4) and 17-epi-resolvin D1 (17-epi-RvD1) through the receptor ALX/FPR2 antagonize cues from CpG DNA, preserve C5aR expression, restore impaired phagocytosis, and redirect human PMNs to apoptosis.	Aspirin	18-25	hematopoietic SH2 domain containing	Homo sapiens	126-129
32251451-6	2020	Although the number of metastases in the lungs remained unchanged in ASA-treated mice, infiltration of inflammatory cells was increased concomitantly with higher G-CSF and serotonin concentrations in the lungs.	Aspirin	69-72	colony stimulating factor 3 (granulocyte)	Mus musculus	162-167
32258142-0	2020	Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPARdelta-AMPK-PGC-1alpha Pathway in Dyslipidemic Conditions.	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	106-110
32258142-3	2020	The protein levels of biomarkers (PPARdelta, AMPK, and PGC-1alpha) involved in oxidative phosphorylation in both the vascular endothelial and liver cells were elevated by the aspirin in hyperlipidemic condition.	Aspirin	175-182	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	45-49
32218705-3	2020	We noted an increase of cell viability and proliferation with or without Abeta1-42 peptide presence in aspirin treated cells.	Aspirin	103-110	AA1	Homo sapiens	73-79
32218705-5	2020	Also, aspirin diminished necrosis process (LDH levels), pro-inflammatory mediators (IL-beta and TNF-alpha) and NF-KB protein expression, increasing anti-inflammatory PPAR-gamma protein expression, preventing Abeta1-42 toxic effects.	Aspirin	6-13	AA1	Homo sapiens	208-214
32218705-6	2020	Aspirin inhibited COX-2 and iNOS without changes in COX-1 expression, increasing anti-oxidant protein (Cu/Zn-SOD and Mn-SOD) expression in presence or absence of Abeta1-42.	Aspirin	0-7	superoxide dismutase 2	Homo sapiens	117-123
32011647-0	2020	Clinical Effectiveness and Safety of Aspirin for Venous Thromboembolism Prophylaxis After Total Hip and Knee Replacement: A Systematic Review and Meta-analysis of Randomized Clinical Trials.	Aspirin	37-44	hedgehog interacting protein	Homo sapiens	96-99
32000660-11	2020	After treatment with aspirin, as phosphorylation of PI3K and Protein kinase B (PKB, Akt) was decreased, Raptor expression was also decreased.	Aspirin	21-28	regulatory associated protein of MTOR complex 1	Homo sapiens	104-110
32000660-12	2020	CONCLUSION: Aspirin can regulate the proliferation, apoptosis and autophagy of CRC cells through the PI3K/Akt/Raptor pathway, affecting PIK3CA-mutant CRC.	Aspirin	12-19	regulatory associated protein of MTOR complex 1	Homo sapiens	110-116
31852420-0	2020	Low-Dose Aspirin Treatment Attenuates Male Rat Salt-Sensitive Hypertension via Platelet Cyclooxygenase 1 and Complement Cascade Pathway.	Aspirin	9-16	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	88-104
31852420-7	2020	These effects were related to the ability of aspirin to prevent the adhesion of leukocytes to endothelial cells via inhibition of the platelet cyclooxygenase 1 but not the cyclooxygenase 2 pathway.	Aspirin	45-52	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	143-159
31852420-7	2020	These effects were related to the ability of aspirin to prevent the adhesion of leukocytes to endothelial cells via inhibition of the platelet cyclooxygenase 1 but not the cyclooxygenase 2 pathway.	Aspirin	45-52	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	172-188
31905343-8	2020	The combination of aspirin and cisplatin effectively attenuated the translocation of NF-kappaB p65/p50 from the cytoplasm to the nucleus, and abrogated the binding of NF-kappaB p65/p50 to the COX-2 promoter, thereby down-regulating COX-2 expression and PGE2 synthesis.	Aspirin	19-26	RELA proto-oncogene, NF-kB subunit	Homo sapiens	85-98
31905343-8	2020	The combination of aspirin and cisplatin effectively attenuated the translocation of NF-kappaB p65/p50 from the cytoplasm to the nucleus, and abrogated the binding of NF-kappaB p65/p50 to the COX-2 promoter, thereby down-regulating COX-2 expression and PGE2 synthesis.	Aspirin	19-26	RELA proto-oncogene, NF-kB subunit	Homo sapiens	167-180
32025207-0	2020	Compound C enhances the anticancer effect of aspirin in HER-2-positive breast cancer by regulating lipid metabolism in an AMPK-independent pathway.	Aspirin	45-52	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	122-126
32025207-5	2020	Aspirin exhibited anticancer effects in HER-2-positive breast cancer by inhibiting cell growth and inducing apoptosis through the activation of AMP-activated protein kinase (AMPK).	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	144-172
32025207-5	2020	Aspirin exhibited anticancer effects in HER-2-positive breast cancer by inhibiting cell growth and inducing apoptosis through the activation of AMP-activated protein kinase (AMPK).	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	174-178
31796122-0	2019	Acetylsalicylic acid rescues the immunomodulation of inflamed gingiva-derived mesenchymal stem cells via upregulating FasL in mice.	Aspirin	0-20	Fas ligand (TNF superfamily, member 6)	Mus musculus	118-122
31796122-8	2019	Mechanistically, ASA was capable of upregulating the expression of Fas ligand (FasL) in iGMSCs, leading to an improvement in iGMSC-mediated T cell apoptosis and therapeutic efficacy in the treatment in colitis mice.	Aspirin	17-20	Fas ligand (TNF superfamily, member 6)	Mus musculus	67-77
31796122-8	2019	Mechanistically, ASA was capable of upregulating the expression of Fas ligand (FasL) in iGMSCs, leading to an improvement in iGMSC-mediated T cell apoptosis and therapeutic efficacy in the treatment in colitis mice.	Aspirin	17-20	Fas ligand (TNF superfamily, member 6)	Mus musculus	79-83
31796122-9	2019	CONCLUSIONS: This study indicates that the deficient immunomodulatory function of iGMSCs could be rescued by ASA pretreatment via upregulating of FasL in mice.	Aspirin	109-112	Fas ligand (TNF superfamily, member 6)	Mus musculus	146-150
31729456-5	2019	A search for the underlying mechanism revealed that aspirin pre-treatment abrogates p300 binding both at TATA-box and initiator (INR) regions of mTOR promoter of CSCs, thereby impeding RNA polymerase II binding at those sites and repressing mTOR gene transcription.	Aspirin	52-59	E1A binding protein p300	Homo sapiens	84-88
31781346-11	2019	Histological analysis showed that aspirin treatment prevented the loss of COL2 and decreased MMP-3 and MMP-13, inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), IL-1beta, and TNF-alpha expression in the IVD tissues.	Aspirin	34-41	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	141-157
31781346-11	2019	Histological analysis showed that aspirin treatment prevented the loss of COL2 and decreased MMP-3 and MMP-13, inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), IL-1beta, and TNF-alpha expression in the IVD tissues.	Aspirin	34-41	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	159-164
31801720-9	2019	A total of 10 220 differentially expressed genes were identified from the TCGA database, and among them 4 genes (CDC25C, TPX2, CDC20, PLK1) were found to be the potential targets for aspirin.	Aspirin	183-190	thioesterase superfamily member 4	Homo sapiens	99-105
31525775-7	2019	Results: 2.5% of women and 12.1% of men were likely to have a net benefit from aspirin treatment for 5 years if 1 CVD event was assumed to be equivalent in severity to 1 major bleed, increasing to 21.4% of women and 40.7% of men if 1 CVD event was assumed to be equivalent to 2 major bleeds.	Aspirin	79-86	ATP synthase inhibitory factor subunit 1	Homo sapiens	109-113
31525775-7	2019	Results: 2.5% of women and 12.1% of men were likely to have a net benefit from aspirin treatment for 5 years if 1 CVD event was assumed to be equivalent in severity to 1 major bleed, increasing to 21.4% of women and 40.7% of men if 1 CVD event was assumed to be equivalent to 2 major bleeds.	Aspirin	79-86	ATP synthase inhibitory factor subunit 1	Homo sapiens	229-233
31185432-4	2019	All pharmaceuticals except acetylsalicylic acid and sulfathiazole were found in PS1, PS2, and PS3 samples, whereas acetylsalicylic acid, carbamazepine, sulfamethazine, and sulfamethoxazole were found in PS4, most of the pharmaceuticals were not present in PS5.	Aspirin	27-47	taste 2 receptor member 62 pseudogene	Homo sapiens	80-83
31243598-2	2019	In vitro and in vivo analysis showed that aspirin induced compromised Bcl-XL level and subsequent ATP depletion.	Aspirin	42-49	BCL2-like 1	Mus musculus	70-76
31243598-8	2019	Collectively, aspirin inhibits tumors growth in mice and induces oncosis in which the compromised Bcl-XL and intracellular ATP depletion play a dominant role, which provides insights into the therapeutic strategy of aspirin in oncology.	Aspirin	14-21	BCL2-like 1	Mus musculus	98-104
31243598-8	2019	Collectively, aspirin inhibits tumors growth in mice and induces oncosis in which the compromised Bcl-XL and intracellular ATP depletion play a dominant role, which provides insights into the therapeutic strategy of aspirin in oncology.	Aspirin	216-223	BCL2-like 1	Mus musculus	98-104
31469551-0	2019	Arg-513 and Leu-531 Are Key Residues Governing Time-Dependent Inhibition of Cyclooxygenase-2 by Aspirin and Celebrex.	Aspirin	96-103	prostaglandin-endoperoxide synthase 2	Mus musculus	76-92
31488302-0	2019	Do We Have Good Reasons to Pay Bleeding Penalty With Lifelong Aspirin After LAAO?	Aspirin	62-69	interleukin 4 induced 1	Homo sapiens	76-80
31488303-0	2019	Reply: Do We Have Good Reasons to Pay Bleeding Penalty With Lifelong Aspirin After LAAO?	Aspirin	69-76	interleukin 4 induced 1	Homo sapiens	83-87
31488304-0	2019	Reply: Do We Have Good Reasons to Pay Bleeding Penalty With Lifelong Aspirin After LAAO?	Aspirin	69-76	interleukin 4 induced 1	Homo sapiens	83-87
31301530-9	2019	Moreover, components of the AsA-GSH cycle i.e. enzymes (ascorbate peroxidase, monodehydroascorbate reducatse, dehydroascorbate reducatse and glutathione reductase) and metabolites (ascorbate and glutathione) were declined by the Cd.	Aspirin	28-31	peroxidase	Solanum lycopersicum	66-76
31301530-9	2019	Moreover, components of the AsA-GSH cycle i.e. enzymes (ascorbate peroxidase, monodehydroascorbate reducatse, dehydroascorbate reducatse and glutathione reductase) and metabolites (ascorbate and glutathione) were declined by the Cd.	Aspirin	28-31	glutathione reductase	Solanum lycopersicum	141-162
31174954-12	2019	CONCLUSIONS: High plasma level of HbA1c is involved in enhanced platelet aggregability in acute atherothrombotic stroke patients, and prestroke administration of aspirin may be beneficial to clinical outcomes.	Aspirin	162-169	hemoglobin subunit alpha 1	Homo sapiens	34-38
33071517-0	2019	Erratum to "Aspirin for venous thromboembolism prophylaxis after hip or knee arthroplasty: An updated meta-analysis of randomized controlled trials": [J. Orthop.	Aspirin	12-19	hedgehog interacting protein	Homo sapiens	65-68
31278071-0	2019	Aspirin targets P4HA2 through inhibiting NF-kappaB and LMCD1-AS1/let-7g to inhibit tumour growth and collagen deposition in hepatocellular carcinoma.	Aspirin	0-7	prostaglandin D2 receptor	Homo sapiens	61-64
31278071-6	2019	A mouse xenograft model, cell viability assay, colony formation assay, and immunohistochemistry analysis were used to evaluate the anti-fibrosis effect of aspirin through targeting the NF-kappaB/P4HA2 axis and LMCD1-AS1/let-7g/P4HA2 axis in vitro and in vivo.	Aspirin	155-162	procollagen-proline, 2-oxoglutarate 4-dioxygenase (proline 4-hydroxylase), alpha II polypeptide	Mus musculus	195-200
31278071-6	2019	A mouse xenograft model, cell viability assay, colony formation assay, and immunohistochemistry analysis were used to evaluate the anti-fibrosis effect of aspirin through targeting the NF-kappaB/P4HA2 axis and LMCD1-AS1/let-7g/P4HA2 axis in vitro and in vivo.	Aspirin	155-162	procollagen-proline, 2-oxoglutarate 4-dioxygenase (proline 4-hydroxylase), alpha II polypeptide	Mus musculus	227-232
31278071-8	2019	FINDINGS: In xenograft mice, aspirin was capable of targeting P4HA2 to decrease collagen deposition, resulting in the inhibition of liver tumour growth.	Aspirin	29-36	procollagen-proline, 2-oxoglutarate 4-dioxygenase (proline 4-hydroxylase), alpha II polypeptide	Mus musculus	62-67
30187283-0	2019	Low-Dose Aspirin Upregulates Tyrosine Hydroxylase and Increases Dopamine Production in Dopaminergic Neurons: Implications for Parkinson"s Disease.	Aspirin	9-16	tyrosine hydroxylase	Mus musculus	29-49
30187283-4	2019	At low doses, aspirin increased the expression of TH and the production of DA in mouse MN9D dopaminergic neuronal cells.	Aspirin	14-21	tyrosine hydroxylase	Mus musculus	50-52
30187283-5	2019	Accordingly, oral administration of aspirin increased the expression of TH in the nigra and upregulated the level of DA in striatum of normal C57/BL6 mice and aged A53T alpha-syn transgenic mice.	Aspirin	36-43	tyrosine hydroxylase	Mus musculus	72-74
31090331-4	2019	Through the study of network pharmacology,12 components of aspirin and Trichosanthis Fructus,including hydroxygenkwanin,quercetin and adenosine,were found to show the anti-platelet aggregation and anti-thrombosis mechanisms through9 common protein targets,such as SRC,RAC1,MAPK14,MAPK1,AKT1,and 14 common signaling pathways,such as VEGF signaling pathway.	Aspirin	59-66	Rac family small GTPase 1	Rattus norvegicus	268-272
31090331-4	2019	Through the study of network pharmacology,12 components of aspirin and Trichosanthis Fructus,including hydroxygenkwanin,quercetin and adenosine,were found to show the anti-platelet aggregation and anti-thrombosis mechanisms through9 common protein targets,such as SRC,RAC1,MAPK14,MAPK1,AKT1,and 14 common signaling pathways,such as VEGF signaling pathway.	Aspirin	59-66	mitogen activated protein kinase 14	Rattus norvegicus	273-279
31090331-4	2019	Through the study of network pharmacology,12 components of aspirin and Trichosanthis Fructus,including hydroxygenkwanin,quercetin and adenosine,were found to show the anti-platelet aggregation and anti-thrombosis mechanisms through9 common protein targets,such as SRC,RAC1,MAPK14,MAPK1,AKT1,and 14 common signaling pathways,such as VEGF signaling pathway.	Aspirin	59-66	mitogen activated protein kinase 1	Rattus norvegicus	273-278
30604228-13	2019	CONCLUSION: Aspirin attenuates podocyte injury in DN, which may be through COX-2-mediated dysregulation of LDLr pathway.	Aspirin	12-19	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	75-80
30389521-4	2019	Here we present novel studies, at solution as well as fibrillar states of a nonapeptide covering the 264-272 region of NPM1: this small fragment is the most amyloidogenic stretch of the entire protein and its conformational and aggregation properties were investigated through Circular Dichroism, Fluorescence spectroscopies, amyloid seeding assay (ASA), isothermal titration calorimetry (ITC) and electrospray ionization (ESI) mass analyses.	Aspirin	349-352	nucleophosmin 1	Homo sapiens	119-123
30701538-0	2019	Aspirin inhibits cancer stem cells properties and growth of glioblastoma multiforme through Rb1 pathway modulation.	Aspirin	0-7	RB transcriptional corepressor 1	Homo sapiens	92-95
30701538-2	2019	In addition, aspirin-induced Cox-dependent and -independent antitumor effects have also been described.	Aspirin	13-20	cytochrome c oxidase subunit 8A	Homo sapiens	29-32
29672839-7	2019	Inhibition of cyclooxygenase 1 by aspirin, supplementation of PGI2 by beraprost, and inhibition of PGIS S-nitrosylation by N-acetyl-cysteine improved GTN-induced nitrate cross-tolerance in rats.	Aspirin	34-41	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	14-30
30156911-8	2019	Our results demonstrate the efficacy of low-dose aspirin in treating a vast array of cardiovascular parameters and suggest modulation of adaptive immunity as a novel mechanism underlying adverse cardiovascular profiles associated with COX-2 inhibitors.	Aspirin	49-56	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	235-240
31424405-7	2019	This review delineates such functions of aspirin and analyzes underlying mechanisms that involve peroxisome proliferator-activated receptor alpha (PPARalpha)-mediated transcription of transcription factor EB (TFEB), the master regulator of lysosomal biogenesis.	Aspirin	41-48	transcription factor EB	Homo sapiens	209-213
30575713-1	2018	Addressing the optimal management approach for patients who are receiving single or dual antiplatelet therapy is a common and sometimes challenging clinical problem, especially for patients with coronary stents who are receiving dual antiplatelet therapy with acetylsalicylic acid (ASA) combined with a P2Y12 inhibitor.	Aspirin	282-285	purinergic receptor P2Y12	Homo sapiens	303-308
30546409-6	2018	At the same time, cilostazol combined with aspirin could effectively reduce the levels of serum inflammatory factors MMP-2 and MMP-9 in patients, except for nitric oxide (NO), and the differences were statistically significant (P&lt;0.05).	Aspirin	43-50	matrix metallopeptidase 2	Homo sapiens	117-122
30482850-4	2018	Aspirin reduced the development of EAE driven by myelin basic protein (MBP)-specific T cells and the associated perivascular cuffing, inflammation, and demyelination.	Aspirin	0-7	myelin basic protein	Mus musculus	49-69
30482850-4	2018	Aspirin reduced the development of EAE driven by myelin basic protein (MBP)-specific T cells and the associated perivascular cuffing, inflammation, and demyelination.	Aspirin	0-7	myelin basic protein	Mus musculus	71-74
30082425-2	2018	We analysed population response to online promotion of an educational tool built by the Ask About Aspirin campaign in the USA to inform people about aspirin as a preventive aid.	Aspirin	149-156	activation induced cytidine deaminase	Homo sapiens	173-176
29629844-8	2018	Western blotting analysis indicated that aspirin decreased expression of vascular cell adhesion molecule-1 (VCAM-1), at both protein and mRNA levels, and these correlated with the reduction of NF-kappaB p65 phosphorylation.	Aspirin	41-48	RELA proto-oncogene, NF-kB subunit	Homo sapiens	193-206
29386221-8	2018	Remarkably, acetylsalicylic acid (aspirin) was predicted to be a tamoxifen sensitizer using a drug repositioning approach and was shown to reverse resistance by targeting PDE4D/cAMP/ER stress axis.	Aspirin	12-32	epiregulin	Homo sapiens	182-184
29386221-8	2018	Remarkably, acetylsalicylic acid (aspirin) was predicted to be a tamoxifen sensitizer using a drug repositioning approach and was shown to reverse resistance by targeting PDE4D/cAMP/ER stress axis.	Aspirin	34-41	epiregulin	Homo sapiens	182-184
29679301-2	2018	The advent of non-vitamin K antagonist oral anticoagulants (NOACs) increased treatment options, while there is cumulative evidence that dual combination of a NOAC and a P2Y12 receptor antagonist attenuates risk of bleeding, compared to traditional triple therapy, consisting of a vitamin K antagonist (VKA), aspirin, and a P2Y12 receptor antagonist, without significantly compromising efficacy.	Aspirin	308-315	purinergic receptor P2Y12	Homo sapiens	169-174
29443445-1	2018	Essentials Strong P2Y12 blockade may cause platelet inhibition that is only minimally enhanced by aspirin.	Aspirin	98-105	purinergic receptor P2Y12	Homo sapiens	18-23
29443445-5	2018	SUMMARY: Background Recent studies have shown that the thromboxane A2 -dependent pathway is dependent on the ADP-P2Y12 pathway, and that strong P2Y12 receptor blockade alone causes inhibition of platelet aggregation that is minimally enhanced by aspirin.	Aspirin	246-253	purinergic receptor P2Y12	Homo sapiens	144-149
29157985-7	2018	Given the prominent role of COX-1 inhibition in aspirin-sensitive asthma, these data implicate preformed mediators stored in granules as the initial drivers of these adverse reactions.	Aspirin	48-55	cytochrome c oxidase subunit I	Cavia porcellus	28-33
29447787-1	2018	BACKGROUND AND RATIONALE: Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor reduces thrombotic events in patients undergoing percutaneous coronary intervention (PCI), but these benefits come at the expense of increased risk of bleeding when compared with aspirin monotherapy.	Aspirin	273-280	purinergic receptor P2Y12	Homo sapiens	78-83
29344879-5	2018	In the aspirin group, the changes from baseline to end point in the IIEF-EF, SEP-2, and SEP-3 scores were 7.2, 36.6, and 46.6%, respectively.	Aspirin	7-14	septin 6	Homo sapiens	77-82
29456855-7	2018	The five-year relative survival for stage III CRC was 101% [95% confidence interval (CI)=76-126] in the 18 patients with DM2 treated with metformin and ASA, 55% (95% CI=31-78) in the 23 without DM2 treated with ASA, 55% (95% CI=45-65) in the 150 without DM2 not taking ASA, and 29% (95% CI=13-45) in the 43 with DM2 treated with metformin, however not with ASA.	Aspirin	152-155	immunoglobulin heavy diversity 1-14 (non-functional)	Homo sapiens	121-124
29328467-4	2018	In the present study, we report a new link between aspirin, metformin, TGF-beta1 and murine breast cancer inhibition.	Aspirin	51-58	transforming growth factor, beta 1	Mus musculus	71-80
29328467-5	2018	Specifically, we showed that aspirin and metformin enhanced 4T1 cell apoptosis by inducing secretion of TGF-beta1, whereas estradiol weakened the effect.	Aspirin	29-36	transforming growth factor, beta 1	Mus musculus	104-113
29475508-10	2018	High-dose aspirin, but not low-dose aspirin, also significantly decreased IL-2 expression, although the decrease was not as marked as that seen with cyclosporine alone or in combination with aspirin.	Aspirin	10-17	interleukin 2	Canis lupus familiaris	74-78
29471853-15	2018	Interestingly, aspirin (ASA) suppressed the HBXIP/HOXB13 axis by decreasing HBXIP expression, overcoming TAM resistance in vitro and in vivo.	Aspirin	15-22	late endosomal/lysosomal adaptor, MAPK and MTOR activator 5	Homo sapiens	44-49
29471853-15	2018	Interestingly, aspirin (ASA) suppressed the HBXIP/HOXB13 axis by decreasing HBXIP expression, overcoming TAM resistance in vitro and in vivo.	Aspirin	15-22	late endosomal/lysosomal adaptor, MAPK and MTOR activator 5	Homo sapiens	76-81
29471853-15	2018	Interestingly, aspirin (ASA) suppressed the HBXIP/HOXB13 axis by decreasing HBXIP expression, overcoming TAM resistance in vitro and in vivo.	Aspirin	24-27	late endosomal/lysosomal adaptor, MAPK and MTOR activator 5	Homo sapiens	44-49
29471853-15	2018	Interestingly, aspirin (ASA) suppressed the HBXIP/HOXB13 axis by decreasing HBXIP expression, overcoming TAM resistance in vitro and in vivo.	Aspirin	24-27	late endosomal/lysosomal adaptor, MAPK and MTOR activator 5	Homo sapiens	76-81
29471853-17	2018	Therapeutically, ASA can serve as a potential candidate for reversing TAM resistance by inhibiting HBXIP expression.	Aspirin	17-20	late endosomal/lysosomal adaptor, MAPK and MTOR activator 5	Homo sapiens	99-104
29399134-0	2018	Increased expression of tight junction protein occludin is associated with the protective effect of mosapride against aspirin-induced gastric injury.	Aspirin	118-125	occludin	Rattus norvegicus	47-55
29375570-0	2017	From Human Megakaryocytes to Platelets: Effects of Aspirin on High-Mobility Group Box 1/Receptor for Advanced Glycation End Products Axis.	Aspirin	51-58	high mobility group box 1	Homo sapiens	62-87
29375570-4	2017	Aspirin "in vivo" and "in vitro" not only reduces HMGB1 and receptor for advanced glycation end products expression on MKs and PLTs but also drives the movement of HMGB1 from MKs into PLTs and PLT-derived MV.	Aspirin	0-7	high mobility group box 1	Homo sapiens	50-55
29375570-4	2017	Aspirin "in vivo" and "in vitro" not only reduces HMGB1 and receptor for advanced glycation end products expression on MKs and PLTs but also drives the movement of HMGB1 from MKs into PLTs and PLT-derived MV.	Aspirin	0-7	high mobility group box 1	Homo sapiens	164-169
29195233-5	2018	We show herein that, ASA-BMMSCs treatment reduced inflammatory infiltration and alveolar bone loss in periodontitis rats, reflected by immunohistochemistry staining of OPG/RANK-L and Micro-CT. Levels of TNF-alpha and IL-17 decreased while IL-10 increased after the treatment of ASA-BMMSCs in periodontitis rats.	Aspirin	21-24	TNF superfamily member 11	Rattus norvegicus	172-178
28709878-9	2018	CONCLUSIONS: The instability of the TBXA2R transcript and the lack of effect on platelet aggregation might suggest a protective role for the TBXA2R TT genotype against atherothrombosis and its complications in high-risk aspirin-treated patients.	Aspirin	220-227	thromboxane A2 receptor	Homo sapiens	141-147
28781013-8	2017	IPTW-weighted Cox regression revealed a powerful inverse association between aspirin use and moderate to severe CAV (adjusted hazard ratio 0.13; 95% confidence interval 0.03-0.59), which was directionally consistent for CAV of any severity (adjusted hazard ratio 0.50; 95% confidence interval 0.23-1.08).	Aspirin	77-84	cytochrome c oxidase subunit 8A	Homo sapiens	14-17
29172284-5	2017	Consistent with its effect on the cell cycle, aspirin also reduced the expressionof cyclin D1 and cyclin-dependent kinase 4 (Cdk-4), which are important for G0/G1 cell cycle progression.	Aspirin	46-53	cyclin D1	Homo sapiens	84-93
29172284-5	2017	Consistent with its effect on the cell cycle, aspirin also reduced the expressionof cyclin D1 and cyclin-dependent kinase 4 (Cdk-4), which are important for G0/G1 cell cycle progression.	Aspirin	46-53	cyclin dependent kinase 4	Homo sapiens	98-123
29172284-5	2017	Consistent with its effect on the cell cycle, aspirin also reduced the expressionof cyclin D1 and cyclin-dependent kinase 4 (Cdk-4), which are important for G0/G1 cell cycle progression.	Aspirin	46-53	cyclin dependent kinase 4	Homo sapiens	125-130
28387464-12	2017	In conclusion, JK-1 was proved to be an acid-sensitive H2 S donor and could attenuate ASP-related gastric lesions through reconstruction of endogenous gastric defence.	Aspirin	86-89	reticulophagy regulator 1	Homo sapiens	15-19
28849118-6	2017	Western blotting demonstrated K-Ras-p110alpha interaction was required for the effects of aspirin-induced inhibition on cell growth and cell cycle transition via cell cycle regulators, including cyclin D1 and cyclin-dependent kinase 2 (CDK2).	Aspirin	90-97	cyclin D1	Homo sapiens	195-204
28849118-6	2017	Western blotting demonstrated K-Ras-p110alpha interaction was required for the effects of aspirin-induced inhibition on cell growth and cell cycle transition via cell cycle regulators, including cyclin D1 and cyclin-dependent kinase 2 (CDK2).	Aspirin	90-97	cyclin dependent kinase 2	Homo sapiens	209-234
28849118-6	2017	Western blotting demonstrated K-Ras-p110alpha interaction was required for the effects of aspirin-induced inhibition on cell growth and cell cycle transition via cell cycle regulators, including cyclin D1 and cyclin-dependent kinase 2 (CDK2).	Aspirin	90-97	cyclin dependent kinase 2	Homo sapiens	236-240
28975318-0	2017	In PCI-treated ACS, switching from aspirin + a newer P2Y12 blocker to aspirin + clopidogrel reduced adverse events.	Aspirin	35-42	purinergic receptor P2Y12	Homo sapiens	53-58
28520566-2	2017	We encountered a patient with a diagnosis of longstanding Janus kinase-2 gene-negative ET on aspirin therapy presenting for labor epidural.	Aspirin	93-100	Janus kinase 2	Homo sapiens	58-72
28668706-8	2017	Molecular dynamic simulations also showed that interaction of catalase with curcumin resulted in changes in accessible surface area (ASA) and pKa, two effective parameters of glycation, in potential glycation lysine residues.	Aspirin	133-136	catalase	Bos taurus	62-70
28912509-4	2017	We found that ASA could downregulate the expressions of iNOS and TNF-alpha both in mouse peritoneum macrophages and RAW264.7 cells induced by LPS via the IkappaK/IkappaB/NF-kappaB pathway and a COX2/PGE2/EP2/NF-kappaB feedback loop, without affecting the expressions of FIZZ/YM-1/ARG1 induced by IL-4.	Aspirin	14-17	cytochrome c oxidase II, mitochondrial	Mus musculus	194-198
28912509-4	2017	We found that ASA could downregulate the expressions of iNOS and TNF-alpha both in mouse peritoneum macrophages and RAW264.7 cells induced by LPS via the IkappaK/IkappaB/NF-kappaB pathway and a COX2/PGE2/EP2/NF-kappaB feedback loop, without affecting the expressions of FIZZ/YM-1/ARG1 induced by IL-4.	Aspirin	14-17	arginase, liver	Mus musculus	280-284
28713783-9	2017	Furthermore, pre-administration of aspirin in mice intravenously injected with SlaA attenuated the transcriptional abundance of ICAM1 and VCAM1 in the aorta.	Aspirin	35-42	intercellular adhesion molecule 1	Mus musculus	128-133
28346830-7	2017	A combination of DHA and ASA efficiently enhanced heterodimer formations of PPARalpha and RXRalpha and increased the expression of neurotrophic factors PSD-95, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF), while inhibiting NFkappaB and COX2.	Aspirin	25-28	discs large MAGUK scaffold protein 4	Homo sapiens	152-158
28346830-8	2017	These findings suggest that a combination of DHA and ASA could significantly improve the expression of PSD-95, BDNF, and GDNF by promoting heterodimerization of PPARalpha and RXRalpha, thus supplying a new therapeutic method for PD.	Aspirin	53-56	discs large MAGUK scaffold protein 4	Homo sapiens	103-109
28359761-0	2017	Aspirin suppresses the abnormal lipid metabolism in liver cancer cells via disrupting an NFkappaB-ACSL1 signaling.	Aspirin	0-7	acyl-CoA synthetase long chain family member 1	Homo sapiens	98-103
28359761-5	2017	In this study, we report that aspirin can suppress the abnormal lipid metabolism of HCC cells through inhibiting acyl-CoA synthetase long-chain family member 1 (ACSL1), a lipid metabolism-related enzyme.	Aspirin	30-37	acyl-CoA synthetase long chain family member 1	Homo sapiens	113-159
28359761-5	2017	In this study, we report that aspirin can suppress the abnormal lipid metabolism of HCC cells through inhibiting acyl-CoA synthetase long-chain family member 1 (ACSL1), a lipid metabolism-related enzyme.	Aspirin	30-37	acyl-CoA synthetase long chain family member 1	Homo sapiens	161-166
28359761-8	2017	Strikingly, we identified that aspirin was able to down-regulate ACSL1 at the levels of mRNA and protein.	Aspirin	31-38	acyl-CoA synthetase long chain family member 1	Homo sapiens	65-70
28359761-12	2017	Thus, we conclude that aspirin suppresses the abnormal lipid metabolism in HCC cells via disrupting an NFkappaB-ACSL1 signaling.	Aspirin	23-30	acyl-CoA synthetase long chain family member 1	Homo sapiens	112-117
28216620-12	2017	Our results suggest that an autophagy- and p38/ROS-dependent pathway mediates the anti-cardiac fibrosis effect of ASA in CFs.	Aspirin	114-117	mitogen-activated protein kinase 14	Mus musculus	43-46
28327594-5	2017	Aspirin dissociated bound hexokinase II (HK-II) from mitochondria.	Aspirin	0-7	hexokinase 2	Homo sapiens	26-39
28327594-5	2017	Aspirin dissociated bound hexokinase II (HK-II) from mitochondria.	Aspirin	0-7	hexokinase 2	Homo sapiens	41-46
28327594-6	2017	Further, aspirin promoted the closure of recombinant human VDAC1, reconstituted in planar lipid bilayer.	Aspirin	9-16	voltage dependent anion channel 1	Homo sapiens	59-64
28327594-7	2017	Taken together, these results imply that VDAC1 serves as a novel target for aspirin.	Aspirin	76-83	voltage dependent anion channel 1	Homo sapiens	41-46
28327594-8	2017	Modulation of VDAC1 is possibly associated with the cell death and anticancer effects of aspirin.	Aspirin	89-96	voltage dependent anion channel 1	Homo sapiens	14-19
26232640-3	2017	In conjunction with previous findings that link agonism of GPR35 with significant reduction in nociceptive pain, GPR35 has emerged as a potential effector of regulation of mechanical sensitivity and analgesia of the Ret tyrosine kinase, and as a receptor involved in the transmission of anti-inflammatory effects of aspirin- potentially through affecting leucocyte rolling, adhesion and extravasation.	Aspirin	316-323	G protein-coupled receptor 35	Homo sapiens	113-118
28168001-11	2017	Rats treated with TRCQT alone or in combination with aspirin showed decreased apoptosis by a reduction in the number of TUNEL positive cells, which inhibited the expression of activated caspase-3 (P = 0.038) and Bax (P = 0.004; P = 0.003).	Aspirin	53-60	caspase 3	Rattus norvegicus	186-195
28103874-8	2017	For ASA, IC50 were 0.50 mug/mL (COX-1) and 5.14 mug/mL (COX-2).	Aspirin	4-7	cytochrome c oxidase subunit II	Equus caballus	56-61
28770228-1	2017	BACKGROUND: High on-aspirin treatment platelets reactivity (HPR) is a significant problem in long-term secondary prevention of cardiovascular events.	Aspirin	20-27	haptoglobin-related protein	Homo sapiens	60-63
28770228-8	2017	Arachidonic acid-induced aggregation of platelets from aspirin-HPR patients did not lead to increased release of MMP-2, MMP-9, and TIMP-4.	Aspirin	55-62	haptoglobin-related protein	Homo sapiens	63-66
28362883-2	2017	The aspirin and P2Y 12 response unit (ARU and PRU, respectively) assays detect the effect of aspirin and P2Y 12 inhibitors in the cardiac population.	Aspirin	4-11	purinergic receptor P2Y12	Homo sapiens	105-111
27740874-6	2016	Expert commentary: Ongoing studies are now investigating the plausibility of removing aspirin therapy in the setting of potent P2Y12 receptor blockade via ticagrelor monotherapy or replacing aspirin with an oral anticoagulant.	Aspirin	86-93	purinergic receptor P2Y12	Homo sapiens	127-132
27825819-15	2016	ASA caused hemorrhagic gastric mucosal damage and significantly decreased GBF, H2S production, CO content, mRNA or protein expression for CSE, 3-MST, HO-2 and increased mRNA and/or protein expression for CBS, HO-1, Nrf-2, HIF-1alpha, iNOS, IL-1beta, COX-2 in gastric mucosa and COHb concentration in blood.	Aspirin	0-3	cystathionine gamma-lyase	Rattus norvegicus	138-141
27825819-15	2016	ASA caused hemorrhagic gastric mucosal damage and significantly decreased GBF, H2S production, CO content, mRNA or protein expression for CSE, 3-MST, HO-2 and increased mRNA and/or protein expression for CBS, HO-1, Nrf-2, HIF-1alpha, iNOS, IL-1beta, COX-2 in gastric mucosa and COHb concentration in blood.	Aspirin	0-3	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	250-255
27698862-11	2016	The immunohistochemistry and western blot analysis data from the models revealed that the expression of p-mTOR, HIF-1alpha and VEGF-A was decreased, while the expression of ULK1 and LC3A was increased following treatment with aspirin and everolimus.	Aspirin	226-233	unc-51 like kinase 1	Mus musculus	173-177
27698862-14	2016	Alternatively, aspirin may induce autophagy by inhibiting the mTOR signaling target and then increasing ULK1 and LC3A.	Aspirin	15-22	unc-51 like kinase 1	Mus musculus	104-108
27262845-3	2016	Four of the most important HSPs including HspB1 (Hsp27), Hsp60, Hsp70, and Hsp90 were induced by aspirin pretreatment and were suppressed by BAPTA-AM.	Aspirin	97-104	heat shock protein family B (small) member 1	Gallus gallus	42-47
27262845-3	2016	Four of the most important HSPs including HspB1 (Hsp27), Hsp60, Hsp70, and Hsp90 were induced by aspirin pretreatment and were suppressed by BAPTA-AM.	Aspirin	97-104	heat shock protein family B (small) member 1	Gallus gallus	49-54
27262845-3	2016	Four of the most important HSPs including HspB1 (Hsp27), Hsp60, Hsp70, and Hsp90 were induced by aspirin pretreatment and were suppressed by BAPTA-AM.	Aspirin	97-104	heat shock protein family D (Hsp60) member 1	Gallus gallus	57-62
27262845-6	2016	Comparing to other HSPs, HspB1 presented the largest increase after aspirin treatments, 86-fold higher than the baseline (the level before HS).	Aspirin	68-75	heat shock protein family B (small) member 1	Gallus gallus	25-30
27262845-7	2016	These findings suggested that multiple HSPs participated in aspirin"s anti-heat stress function but HspB1 may contribute the most.	Aspirin	60-67	heat shock protein family B (small) member 1	Gallus gallus	100-105
27430169-5	2016	The mRNA expression of osteoclastic marker genes, including cathepsin K, TRAP, matrix metalloproteinase 9 and calcitonin receptor, were suppressed by aspirin as identified using reverse transcription-quantitative polymerase chain reaction analysis.	Aspirin	150-157	cathepsin K	Mus musculus	60-71
27430169-5	2016	The mRNA expression of osteoclastic marker genes, including cathepsin K, TRAP, matrix metalloproteinase 9 and calcitonin receptor, were suppressed by aspirin as identified using reverse transcription-quantitative polymerase chain reaction analysis.	Aspirin	150-157	matrix metallopeptidase 9	Mus musculus	79-129
27125773-4	2016	However, an analysis of ASA dose-effect relationships for doses of 50 - 500 mg (PO and IV) shows that doses of ASA up to 100 mg daily produce only a small or moderate inhibition in collagen/epinephrine-induced platelet aggregation and have no significant effect on the important platelet factors, PF3 and PF4.	Aspirin	111-114	platelet factor 4	Homo sapiens	305-308
27125773-5	2016	Doses of ASA 300 - 500 mg, on the other hand, inhibit platelet aggregation almost completely and, in addition, produce a 50 - 70% inhibition in PF3 and PF4 lasting at least 24 hours.	Aspirin	9-12	platelet factor 4	Homo sapiens	152-155
26910344-4	2016	ELISA analysis, revealed that HspB1 expression induced by ASA averaged 45.62-fold higher than that of the control.	Aspirin	58-61	heat shock protein family B (small) member 1	Gallus gallus	30-35
26910344-6	2016	ASA pre-treatment induced a level of HspB1 presumed to be sufficient to protect myocardial cells from acute heat stress in the extracorporal model, although more detailed mechanisms will require further investigation.	Aspirin	0-3	heat shock protein family B (small) member 1	Gallus gallus	37-42
26995378-1	2016	Dual antiplatelet therapy (DAPT), the combination of aspirin and a P2Y12 inhibitor, given for 12 months remains the standard of care after presentation with acute coronary syndrome (ACS) because it has been shown to be associated with a significant reduction in ischemic events compared with aspirin monotherapy.	Aspirin	292-299	purinergic receptor P2Y12	Homo sapiens	67-72
27073629-1	2016	The present study was performed to determine whether aspirin, a cyclooxygenase (COX) inhibitor, has an effect on the expression of connexin 43 (Cx43) in C6 glioma cells.	Aspirin	53-60	gap junction protein alpha 1	Homo sapiens	131-142
27073629-1	2016	The present study was performed to determine whether aspirin, a cyclooxygenase (COX) inhibitor, has an effect on the expression of connexin 43 (Cx43) in C6 glioma cells.	Aspirin	53-60	gap junction protein alpha 1	Homo sapiens	144-148
27073629-2	2016	Using an in vitro glioma invasion model, the expression of Cx43 protein in C6 cells was significantly increased following aspirin treatment at a dose of 8 mmol/l for 30, 60 and 120 min via western blot analysis.	Aspirin	122-129	gap junction protein alpha 1	Homo sapiens	59-63
27073629-3	2016	The peak value of the Cx43 expression was observed in C6 cells after 120 min of aspirin treatment, which was significantly reduced by prostaglandin E2 (PGE2).	Aspirin	80-87	gap junction protein alpha 1	Homo sapiens	22-26
27073629-5	2016	This led to the conclusion that the aspirin-induced glioma invasion decrease may be associated with the increased expression of Cx43 protein and formation of GJIC.	Aspirin	36-43	gap junction protein alpha 1	Homo sapiens	128-132
26843365-1	2016	AIMS: The objective of the present substudy was to examine whether aspirin poor/high responsiveness (APR/AHR) is associated with increased rates of major adverse cardiovascular events (MACE) and serious bleeding after primary percutaneous coronary intervention (PPCI).	Aspirin	67-74	aryl hydrocarbon receptor	Homo sapiens	105-108
26918349-0	2016	AMPK-mediated up-regulation of mTORC2 and MCL-1 compromises the anti-cancer effects of aspirin.	Aspirin	87-94	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	0-4
26918349-0	2016	AMPK-mediated up-regulation of mTORC2 and MCL-1 compromises the anti-cancer effects of aspirin.	Aspirin	87-94	CREB regulated transcription coactivator 2	Mus musculus	31-37
26918349-2	2016	Besides cyclooxygenase, AMPK is another target of the nonsteroid anti-inflammatory agent aspirin.	Aspirin	89-96	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	24-28
26918349-5	2016	Here, we show that aspirin induces the expression of MCL-1 in HepG2 and SW480 cells through AMPK-mTOR-Akt/ERK axis.	Aspirin	19-26	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	92-96
26918349-8	2016	Aspirin activates AMPK, which in turn up-regulates mTORC2 activity, Akt, ERK1/2 phosphorylation and MCL-1 expression.	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	18-22
26918349-8	2016	Aspirin activates AMPK, which in turn up-regulates mTORC2 activity, Akt, ERK1/2 phosphorylation and MCL-1 expression.	Aspirin	0-7	CREB regulated transcription coactivator 2	Mus musculus	51-57
26936616-6	2016	For the purpose of analysis, ASA PS was dichotomized to ASA PS 1 and 2 vs. ASA PS &gt;2.	Aspirin	29-32	taste 2 receptor member 62 pseudogene	Homo sapiens	60-70
26936616-8	2016	RESULTS: There was a 6.1 % (95 % CI: 5.1-7.1 %) absolute increase in the fraction of ASA PS 1&amp;2 classifications after the transition from paper (54.9 %) to AIMS (61.0 %); p &lt; 0.001.	Aspirin	85-88	taste 2 receptor member 62 pseudogene	Homo sapiens	89-93
26506219-4	2016	RESULTS: Ten muM aspirin significantly inhibited Ang II-induced increase in cardiomyocyte size, the mRNA, and protein levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and beta-myosin heavy chain (beta-MHC) (P &lt; 0.05).	Aspirin	17-24	myosin, heavy polypeptide 7, cardiac muscle, beta	Mus musculus	199-222
26506219-4	2016	RESULTS: Ten muM aspirin significantly inhibited Ang II-induced increase in cardiomyocyte size, the mRNA, and protein levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and beta-myosin heavy chain (beta-MHC) (P &lt; 0.05).	Aspirin	17-24	myosin, heavy polypeptide 7, cardiac muscle, beta	Mus musculus	224-232
26506219-5	2016	Meantime, consistent with the result in vitro, the increase in HW/BW ratio, the mRNA, and protein levels of ANP, BNP, and beta-MHC could be reduced by aspirin in vivo (P &lt; 0.05).	Aspirin	151-158	myosin, heavy polypeptide 7, cardiac muscle, beta	Mus musculus	122-130
26506219-7	2016	Moreover, aspirin blunted the increase inCa(2+) and inhibited the calcineurin activity and NFAT dephosphorylation caused by Ang II (P &lt; 0.05).	Aspirin	10-17	angiogenin, ribonuclease, RNase A family, 5	Mus musculus	124-127
26663880-11	2016	RESULTS: Clopidogrel plus aspirin and clopidogrel plus placebo reduced beta-TG by a GMR of 0.51 (0.42-0.63) and 0.54 (0.46-0.64) at 2 h. Ticagrelor plus aspirin and ticagrelor plus placebo decreased beta-TG by a GMR of 0.38 (0.26-0.57) and 0.47 (0.31-0.72).	Aspirin	26-33	pro-platelet basic protein	Homo sapiens	71-78
26663880-11	2016	RESULTS: Clopidogrel plus aspirin and clopidogrel plus placebo reduced beta-TG by a GMR of 0.51 (0.42-0.63) and 0.54 (0.46-0.64) at 2 h. Ticagrelor plus aspirin and ticagrelor plus placebo decreased beta-TG by a GMR of 0.38 (0.26-0.57) and 0.47 (0.31-0.72).	Aspirin	26-33	colony stimulating factor 2 receptor subunit alpha	Homo sapiens	84-87
26663880-12	2016	Ticagrelor plus aspirin and ticagrelor plus placebo reduced f1.2 by a GMR of 0.58 (0.45-0.75) and 0.55 (0.38-0.80); clopidogrel did not.	Aspirin	16-23	colony stimulating factor 2 receptor subunit alpha	Homo sapiens	70-73
26639039-4	2016	HPR on clopidogrel and aspirin was defined after PCI as P2Y12 reaction units (PRU) &gt;208 and aspirin reaction units &gt;550, respectively.	Aspirin	23-30	purinergic receptor P2Y12	Homo sapiens	56-61
26051534-5	2016	Cell surface expression of the EP2 receptor protein was lower in fibroblasts from subjects with AERD than in fibroblasts from healthy control subjects and aspirin-tolerant subjects (P &lt; 0.01 for both).	Aspirin	155-162	prostaglandin E receptor 2	Homo sapiens	31-34
31605753-0	2020	Poor control of asthma symptoms with interleukin-5 inhibitors in four patients with aspirin-exacerbated respiratory disease.	Aspirin	84-91	interleukin 5	Homo sapiens	37-50
31912715-4	2019	Decreased ischemic events have been reported while comparing oral rivaroxaban and apixaban with aspirin to improve the therapeutic outcome in several clinical trials, including Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects with Acute Coronary Syndrome-Thrombolysis in Myocardial Infarction 51, Apixaban for Prevention of Acute Ischemic and Safety Events, and GEMINI-ACS-1 phase II clinical trials.	Aspirin	96-103	acyl-CoA synthetase long chain family member 1	Homo sapiens	411-416
31838976-3	2019	Methods and Results To evaluate potential pathways linking COMT with CVD, and COMT effect modification of aspirin in prevention, we examined COMT association with CVD risk and subclinical measures, coronary artery calcium, and carotid intima-media thickness in MESA (Multi-Ethnic Study of Atherosclerosis).	Aspirin	106-113	catechol-O-methyltransferase	Homo sapiens	78-82
31838976-3	2019	Methods and Results To evaluate potential pathways linking COMT with CVD, and COMT effect modification of aspirin in prevention, we examined COMT association with CVD risk and subclinical measures, coronary artery calcium, and carotid intima-media thickness in MESA (Multi-Ethnic Study of Atherosclerosis).	Aspirin	106-113	catechol-O-methyltransferase	Homo sapiens	78-82
31838976-8	2019	Adjusted hazard ratios for COMT rs4818 CVD association were 0.79 (95% CI, 0.65-0.95; P=0.02) among individuals who used aspirin <3 days per week and 0.89 (95% CI, 0.71-1.13; P=0.34) among more frequent users (Pinteraction=0.39).	Aspirin	120-127	catechol-O-methyltransferase	Homo sapiens	27-31
31805984-11	2019	RESULTS: Aspirin had no influence on the surface phenotype, proliferation, or apoptosis of DCs, though aspirin significantly inhibited osteoclast differentiation in RANKL-stimulated DCs.	Aspirin	103-110	TNF superfamily member 11	Rattus norvegicus	165-170
31805984-14	2019	CONCLUSIONS: Aspirin inhibited RANKL-induced OC differentiation in DCs via the NF-kappaB pathway, downregulating expression of NFATc1.	Aspirin	13-20	TNF superfamily member 11	Rattus norvegicus	31-36
31555339-4	2019	Aspirin, niacin, estrogens, and statins, which act on different molecular pathways, may be prescribed to patients with mild or modest elevations of Lp(a) levels.	Aspirin	0-7	lipoprotein(a)	Homo sapiens	148-153
31685067-2	2019	Identification of the signs and symptoms of aspirin misuse are important in light of prevalent non-prescribed medicine/over-the-counter medication (NPM/OTC) misuse.	Aspirin	44-51	nucleophosmin 1	Homo sapiens	148-151
30187283-7	2019	While investigating mechanisms, we found the presence of cAMP response element (CRE) in the promoter of TH gene and the rapid induction of cAMP response element binding (CREB) activation by aspirin in dopaminergic neuronal cells.	Aspirin	190-197	tyrosine hydroxylase	Mus musculus	104-106
30187283-9	2019	The abrogation of aspirin-induced expression of TH by siRNA knockdown of CREB and the recruitment of CREB to the TH gene promoter by aspirin suggest that aspirin stimulates the transcription of TH in dopaminergic neurons via CREB.	Aspirin	18-25	tyrosine hydroxylase	Mus musculus	48-50
30187283-9	2019	The abrogation of aspirin-induced expression of TH by siRNA knockdown of CREB and the recruitment of CREB to the TH gene promoter by aspirin suggest that aspirin stimulates the transcription of TH in dopaminergic neurons via CREB.	Aspirin	133-140	tyrosine hydroxylase	Mus musculus	113-115
30187283-9	2019	The abrogation of aspirin-induced expression of TH by siRNA knockdown of CREB and the recruitment of CREB to the TH gene promoter by aspirin suggest that aspirin stimulates the transcription of TH in dopaminergic neurons via CREB.	Aspirin	133-140	tyrosine hydroxylase	Mus musculus	113-115
30187283-9	2019	The abrogation of aspirin-induced expression of TH by siRNA knockdown of CREB and the recruitment of CREB to the TH gene promoter by aspirin suggest that aspirin stimulates the transcription of TH in dopaminergic neurons via CREB.	Aspirin	133-140	tyrosine hydroxylase	Mus musculus	113-115
30187283-9	2019	The abrogation of aspirin-induced expression of TH by siRNA knockdown of CREB and the recruitment of CREB to the TH gene promoter by aspirin suggest that aspirin stimulates the transcription of TH in dopaminergic neurons via CREB.	Aspirin	133-140	tyrosine hydroxylase	Mus musculus	113-115
31138859-10	2019	For adult rat groups, aspirin significantly inhibited the production of 6-keto PGF1a, PGE2, and TXB2; however, it neither changed the ICP, AUC, or ICP/ MAP ratios nor altered the protein expression of eNOS, nNOS, COX-1, and COX-2.	Aspirin	22-29	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	213-218
31138859-10	2019	For adult rat groups, aspirin significantly inhibited the production of 6-keto PGF1a, PGE2, and TXB2; however, it neither changed the ICP, AUC, or ICP/ MAP ratios nor altered the protein expression of eNOS, nNOS, COX-1, and COX-2.	Aspirin	22-29	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	224-229
30883047-1	2019	BACKGROUND: Ticagrelor is an oral P2Y12 inhibitor that is used with aspirin to reduce the risk of ischemic events among patients with acute coronary syndromes or previous myocardial infarction.	Aspirin	68-75	purinergic receptor P2Y12	Homo sapiens	34-39
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	62-69	cyclin D1	Homo sapiens	96-105
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	182-189	cyclin D1	Homo sapiens	96-105
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	182-189	cyclin D1	Homo sapiens	96-105
30720135-8	2019	Taken together and in light of our previous findings that the aspirin-like analogues can affect cyclin D1 expression and nuclear factor-kappaB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation.	Aspirin	182-189	cyclin D1	Homo sapiens	96-105
30895761-12	2019	CONCLUSIONS: Our study evaluated patients with ACS or stable coronary artery disease undergoing PCI and treated with mono-antiplatelet therapy with P2Y12 inhibitors due to aspirin intolerance shows a 25% incidence of POCE at one year.	Aspirin	172-179	purinergic receptor P2Y12	Homo sapiens	148-153
30756509-0	2019	Aspirin ameliorates lung cancer by targeting the miR-98/WNT1 axis.	Aspirin	0-7	microRNA 98	Homo sapiens	49-55
30756509-7	2019	The levels of miR-98 and WNT1 were tested through immunoblotting and quantitative real-time PCR analysis in lung cancer cells under aspirin treatment.	Aspirin	132-139	microRNA 98	Homo sapiens	14-20
30756509-13	2019	After treatment with aspirin the expression of miR-98 was induced and then its target gene, WNT1, was depressed in the cells.	Aspirin	21-28	microRNA 98	Homo sapiens	47-53
30756509-14	2019	CONCLUSION: Aspirin targets the miR-98/WNT1 axis to ameliorate lung cancer development.	Aspirin	12-19	microRNA 98	Homo sapiens	32-38
31745500-1	2019	Ever since evidence about the increased risk of stent thrombosis with drug eluting stents (DES) surfaced in 2005, the Food and Drug Administration (FDA) has recommended the use of dual antiplatelet therapy (aspirin with P2Y12 inhibitor) following DES placement.	Aspirin	207-214	purinergic receptor P2Y12	Homo sapiens	220-225
29890239-0	2019	A trial of type 12 purinergic (P2Y12) receptor inhibition with prasugrel identifies a potentially distinct endotype of patients with aspirin-exacerbated respiratory disease.	Aspirin	133-140	purinergic receptor P2Y12	Homo sapiens	31-36
29890239-12	2019	In a small subset of patients with AERD who had greater baseline platelet activation and milder upper respiratory symptoms during aspirin-induced reactions, P2Y12 receptor antagonism with prasugrel completely inhibited all aspirin-induced reaction symptoms, suggesting a contribution from P2Y12 receptor signaling in this subset.	Aspirin	130-137	purinergic receptor P2Y12	Homo sapiens	157-162
29890239-12	2019	In a small subset of patients with AERD who had greater baseline platelet activation and milder upper respiratory symptoms during aspirin-induced reactions, P2Y12 receptor antagonism with prasugrel completely inhibited all aspirin-induced reaction symptoms, suggesting a contribution from P2Y12 receptor signaling in this subset.	Aspirin	223-230	purinergic receptor P2Y12	Homo sapiens	157-162
29461906-10	2019	The results obtained using the P-selectin P2Y12 Test in 102 patients taking aspirin and clopidogrel were similar to the more traditional approaches in that a wide scatter of results was obtained.	Aspirin	76-83	purinergic receptor P2Y12	Homo sapiens	42-47
30120100-6	2018	Compared with non-SP cells, the miR-491 expression was significantly decreased in SP cells, which was significantly reversed by ASA (P&lt;0.05).	Aspirin	128-131	microRNA 491	Homo sapiens	32-39
30120100-8	2018	In the presence of Doxo, miR-491 inhibitor reduced the inhibitory effect of ASA on the cell viability of SP cells, which was significantly reversed by knockdown of ABCG2 (P&lt;0.05).Conclusion: ASA enhanced the sensitivity of SP cells to Doxo via regulating the miR-491/ABCG2 signaling pathway.	Aspirin	76-79	microRNA 491	Homo sapiens	25-32
30120100-8	2018	In the presence of Doxo, miR-491 inhibitor reduced the inhibitory effect of ASA on the cell viability of SP cells, which was significantly reversed by knockdown of ABCG2 (P&lt;0.05).Conclusion: ASA enhanced the sensitivity of SP cells to Doxo via regulating the miR-491/ABCG2 signaling pathway.	Aspirin	76-79	microRNA 491	Homo sapiens	262-269
30120100-8	2018	In the presence of Doxo, miR-491 inhibitor reduced the inhibitory effect of ASA on the cell viability of SP cells, which was significantly reversed by knockdown of ABCG2 (P&lt;0.05).Conclusion: ASA enhanced the sensitivity of SP cells to Doxo via regulating the miR-491/ABCG2 signaling pathway.	Aspirin	194-197	microRNA 491	Homo sapiens	25-32
30120100-8	2018	In the presence of Doxo, miR-491 inhibitor reduced the inhibitory effect of ASA on the cell viability of SP cells, which was significantly reversed by knockdown of ABCG2 (P&lt;0.05).Conclusion: ASA enhanced the sensitivity of SP cells to Doxo via regulating the miR-491/ABCG2 signaling pathway.	Aspirin	194-197	microRNA 491	Homo sapiens	262-269
30498334-9	2018	Treatment with aspirin + new P2Y12 inhibitors reduced all-cause deaths (OR: 0.91, 95% credibility interval: 0.84-0.98) and cardiac death risk (OR: 0.86, 95% credibility interval: 0.79-0.93).	Aspirin	15-22	purinergic receptor P2Y12	Homo sapiens	29-34
30302017-12	2018	We recommend the use of aspirin chemothromboprophylaxis, the posterior approach and spinal anaesthetic in total hip replacement due to the apparent causal effect on reduced mortality.	Aspirin	24-31	hedgehog interacting protein	Homo sapiens	112-115
30057104-15	2018	Combining high-dose PPI with aspirin had the strongest effect compared with low-dose PPI without aspirin (TR 1 59, 1 14-2 23, p=0 0068).	Aspirin	29-36	taste 1 receptor member 1	Homo sapiens	106-110
29872488-0	2018	Aspirin induces autophagy via inhibition of the acetyltransferase EP300.	Aspirin	0-7	E1A binding protein p300	Homo sapiens	66-71
28442495-7	2018	Aspirin blocked IkappaB phosphorylation, p65 nuclear translocation, CDX2 promoter activation and CDX2 expression induced by acid and bile salts in NES-B cells.	Aspirin	0-7	RELA proto-oncogene, NF-kB subunit	Homo sapiens	41-44
29552221-4	2018	Previous studies have implicated prostaglandin-independent signaling pathways and certain associated proteins, including SOX7, in aspirin-induced CRC suppression.	Aspirin	130-137	SRY-box transcription factor 7	Homo sapiens	121-125
29196297-5	2018	The cytotoxicity of sorafenib and aspirin was blocked by inhibition of the AMPK or ERK pathways through shRNA or via pharmacologic inhibitors of RAF (LY3009120), MEK (trametinib), or AMPK (compound C).	Aspirin	34-41	midkine	Mus musculus	162-165
29115440-7	2018	Endoplasmic reticulum (ER) stress was suppressed by aspirin treatment through the downregulation of protein kinase R-like endoplasmic reticulum kinase, eukaryotic translation initiation factor 2 subunit 1 and C/EBP homologous protein expression levels in cerebrovascular endothelial cells.	Aspirin	52-59	eukaryotic translation initiation factor 2, subunit 1 alpha	Mus musculus	152-214
29185103-3	2017	Aspirin alone increases 15-epi-lipoxin A4, but when combined with statins, cyclooxygenase-2 is completely blocked.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Mus musculus	75-91
29285098-6	2017	It was also observed that aspirin has a suppressive effect on the activation of nuclear factor (NF)-kappaB and inhibits the phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases 1/2, p38 and c-Jun N-terminal kinase.	Aspirin	26-33	mitogen-activated protein kinase 3	Mus musculus	196-238
29285098-6	2017	It was also observed that aspirin has a suppressive effect on the activation of nuclear factor (NF)-kappaB and inhibits the phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases 1/2, p38 and c-Jun N-terminal kinase.	Aspirin	26-33	mitogen-activated protein kinase 14	Mus musculus	240-243
29285098-7	2017	Furthermore, subsequent to inhibition of the MAPK pathway by specific inhibitors (PD98059, SB203580 and SP600125), the expression of MMP-9 was reduced, indicating that the inhibitory effect of aspirin on MMP-9 in TNF-alpha-treated RAW264.7 cells may be, at least in part, through suppression of NF-kappaB activation and the MAPK pathway.	Aspirin	193-200	matrix metallopeptidase 9	Mus musculus	133-138
29285098-7	2017	Furthermore, subsequent to inhibition of the MAPK pathway by specific inhibitors (PD98059, SB203580 and SP600125), the expression of MMP-9 was reduced, indicating that the inhibitory effect of aspirin on MMP-9 in TNF-alpha-treated RAW264.7 cells may be, at least in part, through suppression of NF-kappaB activation and the MAPK pathway.	Aspirin	193-200	matrix metallopeptidase 9	Mus musculus	204-209
28844193-9	2017	CONCLUSIONS: Among patients with atrial fibrillation who had undergone PCI, the risk of bleeding was lower among those who received dual therapy with dabigatran and a P2Y12 inhibitor than among those who received triple therapy with warfarin, a P2Y12 inhibitor, and aspirin.	Aspirin	266-273	purinergic receptor P2Y12	Homo sapiens	167-172
28687354-0	2017	Aspirin disrupts the mTOR-Raptor complex and potentiates the anti-cancer activities of sorafenib via mTORC1 inhibition.	Aspirin	0-7	CREB regulated transcription coactivator 1	Mus musculus	101-107
28687354-3	2017	In this study, we revealed the mechanism underlying the effects of aspirin on AMPK-mTOR signaling, and described a mechanism-based rationale for the use of aspirin in cancer therapy.	Aspirin	67-74	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	78-82
28687354-3	2017	In this study, we revealed the mechanism underlying the effects of aspirin on AMPK-mTOR signaling, and described a mechanism-based rationale for the use of aspirin in cancer therapy.	Aspirin	156-163	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	78-82
28687354-4	2017	We found that aspirin inhibited mTORC1 signaling through AMPK-dependent and -independent manners.	Aspirin	14-21	CREB regulated transcription coactivator 1	Mus musculus	32-38
28687354-4	2017	We found that aspirin inhibited mTORC1 signaling through AMPK-dependent and -independent manners.	Aspirin	14-21	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	57-61
28687354-5	2017	Aspirin inhibited the AMPK-TSC pathway, thus resulting in the suppression of mTORC1 activity.	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	22-26
28687354-5	2017	Aspirin inhibited the AMPK-TSC pathway, thus resulting in the suppression of mTORC1 activity.	Aspirin	0-7	CREB regulated transcription coactivator 1	Mus musculus	77-83
28687354-7	2017	Additionally, the combination of aspirin and sorafenib showed synergetic effects via inhibiting mTORC1 signaling and the PI3K/AKT, MAPK/ERK pathways.	Aspirin	33-40	CREB regulated transcription coactivator 1	Mus musculus	96-102
28950987-3	2017	RESULTS: HPV+ CeCa cells expressed significantly higher levels of CD73 in the membrane (p&lt;0.01) than HPV- CeCa cells and this expression was associated with the production of larger amounts of Ado (&gt;400muM) compared to HPV-CeCa cells (&lt;200muM) in the presence of AMP, as well asa stronger inhibition of (&gt;50%) proliferation, activation, and cytotoxic activity of CD8+ T cells via interaction with A2A adenosine receptor.	Aspirin	285-288	5'-nucleotidase ecto	Homo sapiens	66-70
29552073-10	2017	The study revealed that aspirin desensitization can improve the quality of life of patients with AERD, lessen their symptoms and medication requirements, lower their levels of IL5, and improve some pulmonary function tests such as FEV1.	Aspirin	24-31	interleukin 5	Homo sapiens	176-179
28915899-4	2017	In this study, we focused our attention on the genetic variability of the TAS2R16 gene, encoding for one of the bitter taste receptors that selectively binds to salicin, a natural antipyretic that resembles aspirin.	Aspirin	207-214	taste 2 receptor member 16	Homo sapiens	74-81
28900541-8	2017	Mechanistic studies demonstrated that combining sorafenib and aspirin yielded significant synergistically anti-tumor effects by simultaneously silencing ACSL4 and the induction of GADD45B expression in HCC cells both in vitro and in the orthotopic HCC xenograft mouse model.	Aspirin	62-69	acyl-CoA synthetase long-chain family member 4	Mus musculus	153-158
28900541-8	2017	Mechanistic studies demonstrated that combining sorafenib and aspirin yielded significant synergistically anti-tumor effects by simultaneously silencing ACSL4 and the induction of GADD45B expression in HCC cells both in vitro and in the orthotopic HCC xenograft mouse model.	Aspirin	62-69	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	180-187
29207652-9	2017	On ear edema model the anti-inflammation activity of 10 nmol/kg IQCA-TAVV equaled that of 1.1mmol/kg aspirin.	Aspirin	101-108	IQ motif containing with AAA domain	Mus musculus	64-68
28830373-2	2017	Several pharmaco-epidemiology cohort studies have shown protective effects of aspirin on diseases using various statistical methods, with the Cox regression model being the most commonly used approach.	Aspirin	78-85	cytochrome c oxidase subunit 8A	Homo sapiens	142-145
28745576-5	2017	Prevalences of aspirin and clopidogrel high on-treatment platelet reactivity (HPR; local cutoffs: 300 AU*min for aspirin and 600 AU*min for clopidogrel) were 11.5% and 19.8% respectively.	Aspirin	15-22	haptoglobin-related protein	Homo sapiens	78-81
28717171-0	2017	The aspirin metabolite salicylate inhibits lysine acetyltransferases and MUC1 induced epithelial to mesenchymal transition.	Aspirin	4-11	mucin 1, cell surface associated	Homo sapiens	73-77
28453742-11	2017	Rolipram and acetylsalicylic acid showed noninterpretable results in hAT.	Aspirin	13-33	transmembrane serine protease 11D	Homo sapiens	69-72
28385176-13	2017	In conclusion, this meta-analysis shows that in patients with ACS, adding P2Y12 inhibitors to aspirin and other standard treatments reduces ischemic events and all-cause mortality.	Aspirin	94-101	purinergic receptor P2Y12	Homo sapiens	74-79
28415819-0	2017	Aspirin regulation of c-myc and cyclinD1 proteins to overcome tamoxifen resistance in estrogen receptor-positive breast cancer cells.	Aspirin	0-7	cyclin D1	Homo sapiens	32-40
28415819-4	2017	Aspirin combined with tamoxifen can down regulate cyclinD1 and block cell cycle in G0/G1 phase.	Aspirin	0-7	cyclin D1	Homo sapiens	50-58
28415819-6	2017	When knocking down c-myc in MCF-7/TAM, cells become more sensitive to tamoxifen, cell cycle is blocked as well, indicating that aspirin can regulate c-myc and cyclinD1 proteins to overcome tamoxifen resistance.	Aspirin	128-135	cyclin D1	Homo sapiens	159-167
27862978-0	2017	ABCC3 Polymorphisms and mRNA Expression Influence the Concentration of a Carboxylic Acid Metabolite in Patients on Clopidogrel and Aspirin Therapy.	Aspirin	131-138	ATP binding cassette subfamily C member 3	Homo sapiens	0-5
28060522-0	2017	Aspirin and (or) omega-3 polyunsaturated fatty acids protect against corticohippocampal neurodegeneration and downregulate lipoxin A4 production and formyl peptide receptor-like 1 expression in pentylenetetrazole-kindled rats.	Aspirin	0-7	formyl peptide receptor 2	Rattus norvegicus	149-179
28327594-2	2017	Here we showed that silencing of VDAC1 protected HeLa cells from aspirin-induced cell death.	Aspirin	65-72	voltage dependent anion channel 1	Homo sapiens	33-38
28327594-3	2017	Compared to the wild type cells, VDAC1 knocked down cells showed lesser change of mitochondrial membrane potential (Deltapsim), upon aspirin treatment.	Aspirin	133-140	voltage dependent anion channel 1	Homo sapiens	33-38
28327594-4	2017	Aspirin augmented ATP and ionomycin-induced mitochondrial Ca2+ uptake which was abolished in VDAC1 knocked down cells.	Aspirin	0-7	voltage dependent anion channel 1	Homo sapiens	93-98
28154202-6	2017	Additionally, microarray analysis of 151 colorectal cancer cell lines identified important cell-cycle regulatory genes that are downstream targets of PIK3 and were also dysregulated by aspirin treatment (PCNA and RB1).	Aspirin	185-192	RB transcriptional corepressor 1	Homo sapiens	213-216
28057599-0	2017	Aspirin plus sorafenib potentiates cisplatin cytotoxicity in resistant head and neck cancer cells through xCT inhibition.	Aspirin	0-7	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	106-109
28057599-5	2017	The combination of aspirin and sorafenib induced xCT inhibition, GSH depletion, and ROS accumulation in cancer cells.	Aspirin	19-26	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	49-52
28057599-6	2017	Genetic and pharmacological inhibition of xCT potentiated the cytotoxic effects of aspirin plus sorafenib; this effect was diminished by xCT overexpression.	Aspirin	83-90	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	42-45
28057599-6	2017	Genetic and pharmacological inhibition of xCT potentiated the cytotoxic effects of aspirin plus sorafenib; this effect was diminished by xCT overexpression.	Aspirin	83-90	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	137-140
28057599-7	2017	Low-dose aspirin plus sorafenib enhanced the cytotoxicity of cisplatin in resistant HNC cells through xCT inhibition and oxidant and DNA damage.	Aspirin	9-16	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	102-105
27986411-0	2017	Interleukin 16 and CCL17/thymus and activation-regulated chemokine in patients with aspirin-exacerbated respiratory disease.	Aspirin	84-91	interleukin 16	Homo sapiens	0-14
27986411-0	2017	Interleukin 16 and CCL17/thymus and activation-regulated chemokine in patients with aspirin-exacerbated respiratory disease.	Aspirin	84-91	C-C motif chemokine ligand 17	Homo sapiens	19-24
28184261-5	2017	After this period, it is generally recommended that the P2Y12 inhibitor be stopped for the amount of time necessary for platelet function recovery (clopidogrel 5-7 days, prasugrel 7-10 days, ticagrelor 3-5 days), and that aspirin be continued during the perioperative period.	Aspirin	222-229	purinergic receptor P2Y12	Homo sapiens	56-61
28362883-2	2017	The aspirin and P2Y 12 response unit (ARU and PRU, respectively) assays detect the effect of aspirin and P2Y 12 inhibitors in the cardiac population.	Aspirin	93-100	purinergic receptor P2Y12	Homo sapiens	16-22
27999284-5	2016	These findings provide evidence that aspirin down regulates hepcidin by inhibiting IL6/JAK2/STAT3 and P65 (nuclear factor-kappaB) pathways in the cells under inflammatory conditions, and imply that an aspirin-induced reduction in TfR1 and an increase in ferritin are not associated with IRP1 and NO.	Aspirin	201-208	transferrin receptor	Mus musculus	230-234
27913448-7	2016	In addition, consumption of certain anti-inflammatory drugs, including aspirin, can significantly reduce cancer risk, suggesting that common nonsteroidal anti-inflammatory drugs (NSAID) and more specific COX2 inhibitors can be used in cancer prevention.	Aspirin	71-78	cox2	Nicotiana tabacum	204-208
27816726-9	2016	AST-IV did not appear to interfere with the anti-inflammatory activity of Asp since COX-2 level in model gastritis rats treated with Asp plus AST-IV was equally suppressed as in model gastritis rats treated with Asp alone.	Aspirin	133-136	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	84-89
27816726-9	2016	AST-IV did not appear to interfere with the anti-inflammatory activity of Asp since COX-2 level in model gastritis rats treated with Asp plus AST-IV was equally suppressed as in model gastritis rats treated with Asp alone.	Aspirin	133-136	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	84-89
26516174-2	2016	Based on the demonstration that P2Y12R antagonists inhibit thromboxane A2 (TxA2) production (target of ASA), it was surmised that ACS patients might be treated with P2Y12R antagonists only.	Aspirin	103-106	purinergic receptor P2Y12	Homo sapiens	32-38
26516174-2	2016	Based on the demonstration that P2Y12R antagonists inhibit thromboxane A2 (TxA2) production (target of ASA), it was surmised that ACS patients might be treated with P2Y12R antagonists only.	Aspirin	103-106	purinergic receptor P2Y12	Homo sapiens	165-171
26645266-1	2016	OBJECTIVE: The aim of this study was to investigate the protective effects of aspirin (AS) and vitamin C (VC) against cardiac damage induced by chronic corn syrup (CS) consumption via a mechanism involving sirtuin-1 (ST-1), hypoxia-inducible factor-1alpha (HIF-1alpha), and the caspase-3 pathway in rats.	Aspirin	78-85	caspase 3	Rattus norvegicus	278-287
27586412-1	2016	P2Y12 receptor antagonists, concurrently administered with aspirin in what has come to be commonly called dual antiplatelet therapy, are a mainstay of treatment for patients with acute coronary syndromes.	Aspirin	59-66	purinergic receptor P2Y12	Homo sapiens	0-5
27430429-3	2016	In the current study, the addition of NF-kappaB inhibitors (Bay11-7082, Z-LLF-CHO and aspirin) was observed to induce the EBV lytic genes BZLF1, BRLF1 and BMRF1 in EBV-positive gastric cancer (GC) cells.	Aspirin	86-93	BMRF1	Human gammaherpesvirus 4	155-160
27175028-5	2016	In JAK2(V617F)-mutated patients, low-dose aspirin was associated with a reduced incidence of venous thrombosis with no effect on the risk of bleeding.	Aspirin	42-49	Janus kinase 2	Homo sapiens	3-13
27175028-6	2016	Coexistence of JAK2(V617F)-mutation and cardiovascular risk factors increased the risk of thrombosis, even after adjusting for treatment with low-dose aspirin (incidence rate ratio: 9.8; 95% confidence interval: 2.3-42.3; P=0.02).	Aspirin	151-158	Janus kinase 2	Homo sapiens	15-19
27230877-7	2016	The DS BR-DIM or fertility drugs (e.g., Met + Asa) that are used to enhance maternal metabolism to support fertility can also chronically slow embryo growth and block development in an AMPK-dependent manner.	Aspirin	46-49	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	185-189
27054838-1	2016	OBJECTIVE: The objective of the study is to evaluate low-dose aspirin (LDA) for pre-eclampsia prevention in twin gestations with elevated maternal serum human chorionic gonadotropin (hCG).	Aspirin	62-69	chorionic gonadotropin subunit beta 5	Homo sapiens	183-186
27289074-10	2016	At day 4 after STEMI, HPR-aspirin was found in 26% patients and HPR-P2Y12i in 7%.	Aspirin	26-33	haptoglobin-related protein	Homo sapiens	22-25
27289074-12	2016	Diabetes and age were predictors of HPR-aspirin.	Aspirin	40-47	haptoglobin-related protein	Homo sapiens	36-39
27289074-13	2016	HPR-aspirin was persistent 75days later in 36% patients.	Aspirin	4-11	haptoglobin-related protein	Homo sapiens	0-3
27289074-15	2016	HPR-aspirin and HPR on both aspirin and P2Y12i were significantly associated with MACCE.	Aspirin	4-11	haptoglobin-related protein	Homo sapiens	0-3
27289074-16	2016	CONCLUSION: HPR-aspirin is frequent just after STEMI and associated with MACCE especially when associated with HPR-P2Y12i.	Aspirin	16-23	haptoglobin-related protein	Homo sapiens	12-15
27289074-16	2016	CONCLUSION: HPR-aspirin is frequent just after STEMI and associated with MACCE especially when associated with HPR-P2Y12i.	Aspirin	16-23	haptoglobin-related protein	Homo sapiens	111-114
27412561-0	2016	miR-145 mediated the role of aspirin in resisting VSMCs proliferation and anti-inflammation through CD40.	Aspirin	29-36	CD40 molecule	Homo sapiens	100-104
27412561-2	2016	This study was designed to investigate whether miR-145 is involved in the regulation of vascular smooth muscle cells" (VSMCs) proliferation and to determine the anti-inflammatory effects of ASA via its regulation of CD40 to provide a new theoretical basis for the pharmacological effect of aspirin.	Aspirin	190-193	CD40 molecule	Homo sapiens	216-220
27412561-11	2016	CONCLUSION: miR-145 is involved in the anti-proliferation and anti-inflammation effects of aspirin on VSMCs by inhibiting the expression of CD40.	Aspirin	91-98	CD40 molecule	Homo sapiens	140-144
26562035-8	2016	CONCLUSIONS: The results of our study demonstrate that 15% of normal donors and 38% of patients taking aspirin only would be classified as having a therapeutic response to P2Y12 inhibition using current guidelines.	Aspirin	103-110	purinergic receptor P2Y12	Homo sapiens	172-177
26988274-8	2016	Concomitant use of NSAIDs was associated with an increased risk of schizophrenia relapse (HRR = 1.21; 95%-CI = 1.11-1.31), particularly associated with acetylsalicylic acid and diclofenac.	Aspirin	152-172	nuclear receptor subfamily 1 group H member 4	Homo sapiens	90-97
27161407-16	2016	DHI strengthened the inhibition activity of ASA on both COX-1 and COX-2, which showed that DHI alleviated ASA induced gastric mucosal damage but not antagonized anti-COX effect of ASA.	Aspirin	44-47	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	66-71
27161407-16	2016	DHI strengthened the inhibition activity of ASA on both COX-1 and COX-2, which showed that DHI alleviated ASA induced gastric mucosal damage but not antagonized anti-COX effect of ASA.	Aspirin	106-109	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	66-71
27161407-16	2016	DHI strengthened the inhibition activity of ASA on both COX-1 and COX-2, which showed that DHI alleviated ASA induced gastric mucosal damage but not antagonized anti-COX effect of ASA.	Aspirin	106-109	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	66-71
27216891-7	2016	Interestingly, we found that in vivo injection of aspirin rescued the periodontitis of rats through inhibiting inflammation and upregulating GCN5 expression.	Aspirin	50-57	lysine acetyltransferase 2A	Rattus norvegicus	141-145
27216891-9	2016	In conclusion, GCN5 plays a protective role in periodontitis through acetylation of DKK1 and applying drugs targeting GCN5, such as aspirin, could be a new approach for periodontitis treatment.	Aspirin	132-139	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	84-88
27002150-7	2016	Intriguingly, salicylate/aspirin prevents the phosphorylation of AMPKalpha at Ser-485, blocks cAMP-PKA negative regulation of AMPK, and improves metformin resistance.	Aspirin	25-32	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	65-69
27417614-3	2016	Antepartum low-dose aspirin prophylaxis, costing USD $10-24 can cut the incidence of PE-E in half.	Aspirin	20-27	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	85-89
27417614-4	2016	Antepartum low molecular weight heparin combined with low-dose aspirin prophylaxis can cut the incidence of early onset PE-E and fetuses that are small for their gestational age in half.	Aspirin	63-70	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	120-124
26910344-0	2016	In vitro evaluation of aspirin-induced HspB1 against heat stress damage in chicken myocardial cells.	Aspirin	23-30	heat shock protein family B (small) member 1	Gallus gallus	39-44
26910344-1	2016	To understand the potential association of heat stress resistance with HspB1 induction by aspirin (ASA) in chicken myocardial cells, variations of HspB1 expression and heat stressed-induced damage of myocardial cells after ASA administration were studied in primary cultured myocardial cells.	Aspirin	90-97	heat shock protein family B (small) member 1	Gallus gallus	71-76
26910344-1	2016	To understand the potential association of heat stress resistance with HspB1 induction by aspirin (ASA) in chicken myocardial cells, variations of HspB1 expression and heat stressed-induced damage of myocardial cells after ASA administration were studied in primary cultured myocardial cells.	Aspirin	99-102	heat shock protein family B (small) member 1	Gallus gallus	71-76
26873936-5	2016	Aspirin consumption significantly blocked thrombin- and collagen-induced increases in exosome cargo levels of chemokines and HMGB1, without altering total exosome secretion or GPVI cargo.	Aspirin	0-7	high mobility group box 1	Homo sapiens	125-130
26873936-7	2016	The plasma platelet-derived exosome number is lower and its chemokine and HMGB1 levels higher after age 65 yr. Aspirin consumption significantly suppressed cargo protein levels of plasma platelet-derived exosomes without altering total levels of exosomes.	Aspirin	111-118	high mobility group box 1	Homo sapiens	74-79
26596838-7	2016	Aspirin also acetylated recombinant p53 (rp53) in vitro suggesting that it occurs through a non-enzymatic chemical reaction.	Aspirin	0-7	retinol dehydrogenase 12	Homo sapiens	41-45
26596838-8	2016	Mass spectrometry analysis and immunoblotting identified 10 acetylated lysines on rp53, and molecular modeling showed that all lysines targeted by aspirin are surface exposed.	Aspirin	147-154	retinol dehydrogenase 12	Homo sapiens	82-86
26704566-4	2016	In order to investigate the link between polyamine catabolism and the effects of aspirin we used a "Tet off" system that induced the activity of spermidine/spermine N (1)-acetyltransferase (SSAT) in human prostate cancer cells (LNCap).	Aspirin	81-88	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	190-194
26704566-5	2016	Treatment with aspirin was found to decrease induced SSAT activity in these cells.	Aspirin	15-22	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	53-57
26704566-6	2016	A negative correlation was observed between increased polyamine catabolism via increased SSAT activity and the sensitivity to aspirin.	Aspirin	126-133	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	89-93
26704566-9	2016	The results indicate that SSAT and its related polyamine metabolism may play a key role in sensitivity of cancer cells to aspirin and possibly other NSAIDs and this may have implications for the development of novel chemopreventative agents.	Aspirin	122-129	spermidine/spermine N1-acetyltransferase 1	Homo sapiens	26-30
27055402-7	2016	Consistent with LEF1 being a downstream effector of Wnt signaling, aspirin, but not I3C, downregulated protein levels of the Wnt co-receptor LDL receptor-related protein-6 and beta-catenin and upregulated the beta-catenin destruction complex component Axin.	Aspirin	67-74	lymphoid enhancer binding factor 1	Homo sapiens	16-20
26743169-9	2016	CONCLUSIONS: Synergistic inhibition of both P2Y1 and P2Y12 adenosine diphosphate receptors by GLS-409 immediately attenuates platelet-mediated thrombosis and effectively blocks agonist-stimulated platelet aggregation irrespective of concomitant aspirin therapy.	Aspirin	245-252	purinergic receptor P2Y12	Homo sapiens	53-58
26497333-6	2016	Furthermore, Zn(ASA)2 significantly increased the myocardial mRNA-expression of superoxide dismutase-1, glutathione peroxidase-4 and decreased the level of Na(+)/K(+)/ATPase.	Aspirin	16-19	glutathione peroxidase 4	Rattus norvegicus	104-128
26685215-0	2016	Cyclin A2 and CDK2 as Novel Targets of Aspirin and Salicylic Acid: A Potential Role in Cancer Prevention.	Aspirin	39-46	cyclin dependent kinase 2	Homo sapiens	14-18
26685215-2	2016	We hypothesized that aspirin"s chemopreventive actions may involve cell-cycle regulation through modulation of the levels or activity of cyclin A2/cyclin-dependent kinase-2 (CDK2).	Aspirin	21-28	cyclin dependent kinase 2	Homo sapiens	174-178
26685215-3	2016	In this study, HT-29 and other diverse panel of cancer cells were used to demonstrate that both aspirin and its primary metabolite, salicylic acid, decreased cyclin A2 (CCNA2) and CDK2 protein and mRNA levels.	Aspirin	96-103	cyclin dependent kinase 2	Homo sapiens	180-184
26685215-10	2016	These results demonstrate that aspirin and salicylic acid downregulate cyclin A2/CDK2 proteins in multiple cancer cell lines, suggesting a novel target and mechanism of action in chemoprevention.	Aspirin	31-38	cyclin dependent kinase 2	Homo sapiens	81-85
26685215-11	2016	IMPLICATIONS: Biochemical and structural studies indicate that the antiproliferative actions of aspirin are mediated through cyclin A2/CDK2.	Aspirin	96-103	cyclin dependent kinase 2	Homo sapiens	135-139
26915040-6	2016	We report that mutations in both PIK3CA and KRAS are required for the greatest aspirin sensitivity in breast cancer, and that the GSK3beta protein was hyperphosphorylated in aspirin-treated double knockin cells, but not in other clones/treatments.	Aspirin	174-181	glycogen synthase kinase 3 beta	Homo sapiens	130-138
26679648-1	2015	OBJECTIVE: To elucidate the correlation between the single nucleotide polymorphism of CKLF-like MARVEL transmembrane member 5 (CMTM5) gene rs723840 and the occurrence of high on aspirin platelet reactivity (HAPR).	Aspirin	178-185	CKLF like MARVEL transmembrane domain containing 5	Homo sapiens	86-125
26679648-1	2015	OBJECTIVE: To elucidate the correlation between the single nucleotide polymorphism of CKLF-like MARVEL transmembrane member 5 (CMTM5) gene rs723840 and the occurrence of high on aspirin platelet reactivity (HAPR).	Aspirin	178-185	CKLF like MARVEL transmembrane domain containing 5	Homo sapiens	127-132
26679648-10	2015	CONCLUSION: Our study finds a significant correlation between CMTM5 gene rs723840 polymorphism and high on aspirin platelet reactivity.	Aspirin	107-114	CKLF like MARVEL transmembrane domain containing 5	Homo sapiens	62-67
26626190-9	2015	Aspirin also normalized the upregulated hypertrophic biomarkers, beta-myosin heavy chain (beta-MHC), atrial natriuretic peptide (ANP), and b-type natriuretic peptide (BNP).	Aspirin	0-7	myosin, heavy polypeptide 7, cardiac muscle, beta	Mus musculus	65-88
26626190-9	2015	Aspirin also normalized the upregulated hypertrophic biomarkers, beta-myosin heavy chain (beta-MHC), atrial natriuretic peptide (ANP), and b-type natriuretic peptide (BNP).	Aspirin	0-7	myosin, heavy polypeptide 7, cardiac muscle, beta	Mus musculus	90-98
26606050-11	2015	Moreover, ASA- induced gastritis resulted in increased expression of NPY (76.59 +- 3.02%) and GAL (26.45 +- 2.75%) as well as the novo-synthesis of nNOS (6.13 +- 1.11%) and LENK (4.77 +- 0.42%) in traced CCMG neurons.	Aspirin	10-13	galanin and GMAP prepropeptide	Sus scrofa	94-97
26366802-1	2015	This study is aimed at investigating the association of HLA-DRB1, HLA-DQA1, and HLA-DQB1 variability with the response to aspirin desensitization (AD).	Aspirin	122-129	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	66-74
26398390-9	2015	ASA resistant patients had higher concentrations of brain natriuretic peptide (BNP), high-sensitivity C-reactive protein (hs-CRP), leukocytes (WBC) and platelets (PLT) but lower concentrations of hemoglobin (HGB).	Aspirin	0-3	natriuretic peptide B	Homo sapiens	52-77
26398390-9	2015	ASA resistant patients had higher concentrations of brain natriuretic peptide (BNP), high-sensitivity C-reactive protein (hs-CRP), leukocytes (WBC) and platelets (PLT) but lower concentrations of hemoglobin (HGB).	Aspirin	0-3	natriuretic peptide B	Homo sapiens	79-82
26125438-4	2015	The functional significance of secreted Ac-APE1/Ref-1 was studied by induction of intracellular hyperacetylation through co-treatment with acetylsalicylic acid and TSA in MDA-MB-231 cells.	Aspirin	139-159	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	43-47
26125438-4	2015	The functional significance of secreted Ac-APE1/Ref-1 was studied by induction of intracellular hyperacetylation through co-treatment with acetylsalicylic acid and TSA in MDA-MB-231 cells.	Aspirin	139-159	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	48-53
26237513-0	2015	Soluble CD40 Ligand in Aspirin-Treated Patients Undergoing Cardiac Catheterization.	Aspirin	23-30	CD40 molecule	Homo sapiens	8-12
25648873-0	2015	Reproducibility over time and effect of low-dose aspirin on soluble P-selectin and soluble CD40 ligand.	Aspirin	49-56	CD40 molecule	Homo sapiens	91-95
26093650-9	2015	Aspirin-treated rats exhibited a significant decrease in degradation of internal elastic lamina (IEL), medial layer thinning, CA size and macrophages infiltration with reduced expression of MMP-2 and 9 compared with rats in the CA group.	Aspirin	0-7	matrix metallopeptidase 2	Rattus norvegicus	190-195
26093650-10	2015	RT-PCR demonstrated that the upregulation of NF-kappaB, MCP-1 and VCAM-1 after CA induction was reversed by aspirin treatment.	Aspirin	108-115	vascular cell adhesion molecule 1	Rattus norvegicus	66-72
25936230-10	2015	Aspirin had a preventive effect against all adverse events in anti-PF4/H antibody-positive patients, but not in antibody-negative patients.	Aspirin	0-7	platelet factor 4	Homo sapiens	67-70
25936230-12	2015	CONCLUSIONS: Aspirin prevention of thrombosis and death in patients undergoing HD might require consideration of the anti-PF4/H antibody status.	Aspirin	13-20	platelet factor 4	Homo sapiens	122-125
26101955-0	2015	Aspirin"s Active Metabolite Salicylic Acid Targets High Mobility Group Box 1 to Modulate Inflammatory Responses.	Aspirin	0-7	high mobility group box 1	Homo sapiens	51-76
26111687-8	2015	CONCLUSION: In high-risk pregnancies, early aspirin intervention starting before 16 weeks of gestation can prevent PIH, preeclampsia, IUGR, and preterm birth and help to increase the birth weight.	Aspirin	44-51	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	115-118
25975240-0	2015	HLA-DRB and HLA-DQ genetic variability in patients with aspirin-exacerbated respiratory disease.	Aspirin	56-63	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	0-3
25860557-7	2015	As for the OPR to aspirin, a weak statistical significance was observed in rs5445 (GNB3) (P = 0.049) and rs5758 (TBXA2R) (P = 0.045).	Aspirin	18-25	thromboxane A2 receptor	Homo sapiens	113-119
24903239-16	2015	Aspirin pretreatment improved glucose tolerance in annexin7 (-/-) mice.	Aspirin	0-7	annexin A7	Mus musculus	51-59
25604474-1	2015	With the aim to design new biologically active bioinorganic drugs of aspirin, whose mode of action is based on the inhibition of the cyclooxygenase(COX) enzymes, derivatives of Zeise"s salt were synthesized in this structure-activity relationship study.	Aspirin	69-76	cytochrome c oxidase subunit 8A	Homo sapiens	148-151
25604474-2	2015	Surprisingly, not only these Zeise-aspirin compounds but also Zeise"s salt itself showed high inhibitory potency against COX enzymes in in vitro assays.	Aspirin	35-42	cytochrome c oxidase subunit 8A	Homo sapiens	121-124
25557764-1	2015	In our previous findings, we have demonstrated that aspirin/acetyl salicylic acid (ASA) might induce sirtuins via aryl hydrocarbon receptor (Ah receptor).	Aspirin	52-59	aryl hydrocarbon receptor	Homo sapiens	114-139
25557764-1	2015	In our previous findings, we have demonstrated that aspirin/acetyl salicylic acid (ASA) might induce sirtuins via aryl hydrocarbon receptor (Ah receptor).	Aspirin	52-59	aryl hydrocarbon receptor	Homo sapiens	141-152
25557764-1	2015	In our previous findings, we have demonstrated that aspirin/acetyl salicylic acid (ASA) might induce sirtuins via aryl hydrocarbon receptor (Ah receptor).	Aspirin	60-81	aryl hydrocarbon receptor	Homo sapiens	114-139
25557764-1	2015	In our previous findings, we have demonstrated that aspirin/acetyl salicylic acid (ASA) might induce sirtuins via aryl hydrocarbon receptor (Ah receptor).	Aspirin	60-81	aryl hydrocarbon receptor	Homo sapiens	141-152
25557764-1	2015	In our previous findings, we have demonstrated that aspirin/acetyl salicylic acid (ASA) might induce sirtuins via aryl hydrocarbon receptor (Ah receptor).	Aspirin	83-86	aryl hydrocarbon receptor	Homo sapiens	114-139
25557764-1	2015	In our previous findings, we have demonstrated that aspirin/acetyl salicylic acid (ASA) might induce sirtuins via aryl hydrocarbon receptor (Ah receptor).	Aspirin	83-86	aryl hydrocarbon receptor	Homo sapiens	141-152
25387004-0	2015	Epithelial MUC1 promotes cell migration, reduces apoptosis and affects levels of mucosal modulators during acetylsalicylic acid (aspirin)-induced gastropathy.	Aspirin	107-127	mucin 1, transmembrane	Mus musculus	11-15
25387004-0	2015	Epithelial MUC1 promotes cell migration, reduces apoptosis and affects levels of mucosal modulators during acetylsalicylic acid (aspirin)-induced gastropathy.	Aspirin	129-136	mucin 1, transmembrane	Mus musculus	11-15
25387004-3	2015	In the present study, we showed that acetylsalicylic acid (ASA; aspirin) up-regulated MUC1/Muc1 expression in the gastric mucosa of humans and wild-type (WT) mice.	Aspirin	37-57	mucin 1, cell surface associated	Homo sapiens	86-90
25387004-3	2015	In the present study, we showed that acetylsalicylic acid (ASA; aspirin) up-regulated MUC1/Muc1 expression in the gastric mucosa of humans and wild-type (WT) mice.	Aspirin	37-57	mucin 1, cell surface associated	Homo sapiens	91-95
25387004-3	2015	In the present study, we showed that acetylsalicylic acid (ASA; aspirin) up-regulated MUC1/Muc1 expression in the gastric mucosa of humans and wild-type (WT) mice.	Aspirin	59-62	mucin 1, cell surface associated	Homo sapiens	86-90
25387004-3	2015	In the present study, we showed that acetylsalicylic acid (ASA; aspirin) up-regulated MUC1/Muc1 expression in the gastric mucosa of humans and wild-type (WT) mice.	Aspirin	59-62	mucin 1, cell surface associated	Homo sapiens	91-95
25387004-3	2015	In the present study, we showed that acetylsalicylic acid (ASA; aspirin) up-regulated MUC1/Muc1 expression in the gastric mucosa of humans and wild-type (WT) mice.	Aspirin	64-71	mucin 1, cell surface associated	Homo sapiens	86-90
25387004-3	2015	In the present study, we showed that acetylsalicylic acid (ASA; aspirin) up-regulated MUC1/Muc1 expression in the gastric mucosa of humans and wild-type (WT) mice.	Aspirin	64-71	mucin 1, cell surface associated	Homo sapiens	91-95
25116182-0	2015	Aspirin-responsive, migraine-like transient cerebral and ocular ischemic attacks and erythromelalgia in JAK2-positive essential thrombocythemia and polycythemia vera.	Aspirin	0-7	Janus kinase 2	Homo sapiens	104-108
25394850-4	2015	Mechanistically, ASA treatment upregulates the telomerase reverse transcriptase (TERT)/Wnt/beta-catenin cascade, leading to improvement of SHED-mediated bone regeneration, and also upregulates TERT/FASL signaling, leading to improvement of SHED-mediated T-cell apoptosis and ameliorating disease phenotypes in dextran sodium sulfate-induced colitis mice.	Aspirin	17-20	Fas ligand (TNF superfamily, member 6)	Mus musculus	198-202
26457728-2	2015	Medical professionals and students often use the mnemonic "MONA" (morphine, oxygen, nitroglycerin and aspirin) to recall treatments for ACS; however, this list of therapies is outdated.	Aspirin	102-109	GRB2 related adaptor protein 2	Homo sapiens	59-63
25674544-2	2015	Noteworthy, PCI patients require a dual antiplatelet therapy (DAPT), with aspirine and a thienopiridine (clopidogrel, prasugrel, ticagrelor), because of the high risk of stent thrombosis (ST), myocardial infarction (MI) and death, especially within the first month.	Aspirin	74-82	serpin family A member 5	Homo sapiens	12-15
24824502-9	2014	Salicylate (the major in vivo metabolite of aspirin) activates AMPK, and this could be responsible for at least some of the anticancer and anti-inflammatory effects of aspirin.	Aspirin	44-51	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	63-67
24824502-9	2014	Salicylate (the major in vivo metabolite of aspirin) activates AMPK, and this could be responsible for at least some of the anticancer and anti-inflammatory effects of aspirin.	Aspirin	168-175	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	63-67
25123696-1	2014	Current percutaneous coronary intervention (PCI) guidelines recommend the use of a P2Y12 inhibitor with aspirin and an injectable anticoagulant.	Aspirin	104-111	purinergic receptor P2Y12	Homo sapiens	83-88
24952332-0	2014	Acetylsalicylic acid enhances the anti-inflammatory effect of fluoxetine through inhibition of NF-kappaB, p38-MAPK and ERK1/2 activation in lipopolysaccharide-induced BV-2 microglia cells.	Aspirin	0-20	mitogen-activated protein kinase 14	Mus musculus	106-109
24952332-0	2014	Acetylsalicylic acid enhances the anti-inflammatory effect of fluoxetine through inhibition of NF-kappaB, p38-MAPK and ERK1/2 activation in lipopolysaccharide-induced BV-2 microglia cells.	Aspirin	0-20	mitogen-activated protein kinase 3	Mus musculus	119-125
24952332-6	2014	Notably, the adjunctive agent ASA could also inhibit phosphorylation of extracellular-regulated kinase 1/2 (ERK1/2).	Aspirin	30-33	mitogen-activated protein kinase 3	Mus musculus	108-114
25035343-0	2014	Polymorphisms in catechol-O-methyltransferase modify treatment effects of aspirin on risk of cardiovascular disease.	Aspirin	74-81	catechol-O-methyltransferase	Homo sapiens	17-45
25074812-6	2014	Furthermore, we demonstrate that COMMD1 acetylation is enhanced by aspirin-mediated stress, and that this acetylation is absolutely required for the protein to bind RelA under these conditions.	Aspirin	67-74	RELA proto-oncogene, NF-kB subunit	Homo sapiens	165-169
25104439-8	2014	SOCS2 (one of three SNPs) and all STAT3, STAT5A, and STAT5B SNPs significantly interacted with use of aspirin/NSAIDs to alter breast cancer-specific mortality.	Aspirin	102-109	signal transducer and activator of transcription 5B	Homo sapiens	53-59
25085874-8	2014	Women with prediagnostic aspirin use were statistically significantly less likely to present with a lymph node-positive tumor than nonusers [RR = 0.89; 95% confidence interval (CI), 0.81-0.97], particularly those with larger (Pinteraction = 0.036), progesterone receptor (PR)-negative (Pinteraction &lt; 0.001) or estrogen receptor (ER)-negative (Pinteraction = 0.056) tumors.	Aspirin	25-32	progesterone receptor	Homo sapiens	249-270
25085874-8	2014	Women with prediagnostic aspirin use were statistically significantly less likely to present with a lymph node-positive tumor than nonusers [RR = 0.89; 95% confidence interval (CI), 0.81-0.97], particularly those with larger (Pinteraction = 0.036), progesterone receptor (PR)-negative (Pinteraction &lt; 0.001) or estrogen receptor (ER)-negative (Pinteraction = 0.056) tumors.	Aspirin	25-32	progesterone receptor	Homo sapiens	272-274
24265116-0	2014	Acetylsalicylic acid inhibits IL-18-induced cardiac fibroblast migration through the induction of RECK.	Aspirin	0-20	interleukin 18	Mus musculus	30-35
24265116-0	2014	Acetylsalicylic acid inhibits IL-18-induced cardiac fibroblast migration through the induction of RECK.	Aspirin	0-20	reversion-inducing-cysteine-rich protein with kazal motifs	Mus musculus	98-102
24265116-5	2014	Further, therapeutic concentrations of ASA inhibited IL-18-induced H(2)O(2) generation, MMP9 activation, RECK suppression, and CF migration.	Aspirin	39-42	interleukin 18	Mus musculus	53-58
24265116-5	2014	Further, therapeutic concentrations of ASA inhibited IL-18-induced H(2)O(2) generation, MMP9 activation, RECK suppression, and CF migration.	Aspirin	39-42	matrix metallopeptidase 9	Mus musculus	88-92
24265116-5	2014	Further, therapeutic concentrations of ASA inhibited IL-18-induced H(2)O(2) generation, MMP9 activation, RECK suppression, and CF migration.	Aspirin	39-42	reversion-inducing-cysteine-rich protein with kazal motifs	Mus musculus	105-109
24265116-6	2014	The salicylic acid moiety of ASA similarly attenuated IL-18-induced CF migration.	Aspirin	29-32	interleukin 18	Mus musculus	54-59
24673112-9	2014	ASA treatment was associated with higher urinary excretion of 15-epi-LXA4 (7 70 +- 1 48 vs. 2 06 +- 0 30 mug/day, P &lt; 0 05) in mild-to-moderate CHF patients and lower BNP levels in both groups.	Aspirin	0-3	natriuretic peptide B	Homo sapiens	170-173
24768597-2	2014	In this study we have demonstrated for the first time that inhibitors of SPP, such as L685,458, (Z-LL)2 ketone, aspirin, ibuprofen and DAPT, significantly reduced HSV-1 replication in tissue culture.	Aspirin	112-119	histocompatibility minor 13	Homo sapiens	73-76
24855830-5	2014	Although there were no clinical differences between the two groups, transcripts of RGS2, RGS10, and RGS18 were significantly higher in aspirin-resistant patients than in aspirin-sensitive patients.	Aspirin	135-142	regulator of G protein signaling 2	Homo sapiens	83-87
24855830-5	2014	Although there were no clinical differences between the two groups, transcripts of RGS2, RGS10, and RGS18 were significantly higher in aspirin-resistant patients than in aspirin-sensitive patients.	Aspirin	135-142	regulator of G protein signaling 10	Homo sapiens	89-94
24855830-5	2014	Although there were no clinical differences between the two groups, transcripts of RGS2, RGS10, and RGS18 were significantly higher in aspirin-resistant patients than in aspirin-sensitive patients.	Aspirin	135-142	regulator of G protein signaling 18	Homo sapiens	100-105
24855830-5	2014	Although there were no clinical differences between the two groups, transcripts of RGS2, RGS10, and RGS18 were significantly higher in aspirin-resistant patients than in aspirin-sensitive patients.	Aspirin	170-177	regulator of G protein signaling 2	Homo sapiens	83-87
24855830-5	2014	Although there were no clinical differences between the two groups, transcripts of RGS2, RGS10, and RGS18 were significantly higher in aspirin-resistant patients than in aspirin-sensitive patients.	Aspirin	170-177	regulator of G protein signaling 10	Homo sapiens	89-94
24855830-5	2014	Although there were no clinical differences between the two groups, transcripts of RGS2, RGS10, and RGS18 were significantly higher in aspirin-resistant patients than in aspirin-sensitive patients.	Aspirin	170-177	regulator of G protein signaling 18	Homo sapiens	100-105
24613833-0	2014	Aspirin augments the expression of Adenomatous Polyposis Coli protein by suppression of IKKbeta.	Aspirin	0-7	APC regulator of WNT signaling pathway	Homo sapiens	35-61
24529662-2	2014	In combination with aspirin, these new P2Y12 inhibitors are now the first line treatments for patients with acute coronary syndrome.	Aspirin	20-27	purinergic receptor P2Y12	Homo sapiens	39-44
24850385-5	2014	AMPK is activated by two widely used clinical drugs, metformin and aspirin, and also by many natural products of plants that are either derived from traditional medicines or are promoted as "nutraceuticals."	Aspirin	67-74	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	0-4
24209633-3	2014	In the present study, we found that pretreatment with aspirin inhibited LPS-induced COX-2 and PGE(2) upregulation, IkappaBalpha degradation, NFkappaB activation and the increase of PKC activity, but elevated LPS-induced the decrease of PTP activity.	Aspirin	54-61	protein tyrosine phosphatase receptor type U	Homo sapiens	236-239
24988246-3	2014	Polymorphisms of the CES1 gene have been reported to affect the metabolism of dabigatran etexilate, methylphenidate, oseltamivir, imidapril, and clopidogrel, whereas variants of the CES2 gene have been found to affect aspirin and irinotecan.	Aspirin	218-225	carboxylesterase 1	Homo sapiens	21-25
24243637-9	2014	Treatment of adipocyte fractions or SGBS adipocytes with metformin or acetylsalicylic acid, which target C/EBPbeta and NF-kappaB/RelA signaling, attenuated the IL-1alpha induction of 11beta-HSD1 (P&lt;=.002).	Aspirin	70-90	CCAAT enhancer binding protein beta	Homo sapiens	105-114
24243637-9	2014	Treatment of adipocyte fractions or SGBS adipocytes with metformin or acetylsalicylic acid, which target C/EBPbeta and NF-kappaB/RelA signaling, attenuated the IL-1alpha induction of 11beta-HSD1 (P&lt;=.002).	Aspirin	70-90	RELA proto-oncogene, NF-kB subunit	Homo sapiens	129-133
24433129-0	2014	Beta-thromboglobulin as a marker of perioperative myocardial infarction in patients undergoing coronary artery bypass grafting following aspirin discontinuation.	Aspirin	137-144	pro-platelet basic protein	Homo sapiens	0-20
23872723-2	2013	The present study was to evaluate auraptene as a potential anti-inflammatory agent and investigate the mechanism of auraptene against prostaglandins E2 (PGE2) and cyclooxygenase-2 (COX-2) on lipopolysaccharide (LPS)-stimulated RAW 264.7 cells by comparing it with aspirin as a positive control group.	Aspirin	264-271	prostaglandin-endoperoxide synthase 2	Mus musculus	181-186
23792301-0	2013	Aspirin-triggered 15-epi-lipoxin A4 predicts cyclooxygenase-2 in the lungs of LPS-treated mice but not in the circulation: implications for a clinical test.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Mus musculus	45-61
23792301-3	2013	When acetylated by aspirin, however, COX-2 (but not COX-1) can form 15(R)-HETE, which is metabolized to aspirin-triggered lipoxin (ATL), 15-epi-lipoxin A4.	Aspirin	19-26	cytochrome c oxidase II, mitochondrial	Mus musculus	37-42
23792301-3	2013	When acetylated by aspirin, however, COX-2 (but not COX-1) can form 15(R)-HETE, which is metabolized to aspirin-triggered lipoxin (ATL), 15-epi-lipoxin A4.	Aspirin	104-111	cytochrome c oxidase II, mitochondrial	Mus musculus	37-42
23792301-11	2013	Thus, in mice in which COX-2 has been induced by LPS treatment, aspirin triggers detectable 15-epi-lipoxin A4 in lung tissue, but not in plasma.	Aspirin	64-71	cytochrome c oxidase II, mitochondrial	Mus musculus	23-28
24066944-9	2013	Ten micromoles of CRCs and Asp upregulated the expression of mothers against decapentaplegic homolog 4 (Drosophila) (SMAD4) in the TGF-beta receptor signaling pathway, and SMAD3/4 transcription activity was also increased.	Aspirin	27-30	SMAD family member 4	Homo sapiens	61-102
24066944-9	2013	Ten micromoles of CRCs and Asp upregulated the expression of mothers against decapentaplegic homolog 4 (Drosophila) (SMAD4) in the TGF-beta receptor signaling pathway, and SMAD3/4 transcription activity was also increased.	Aspirin	27-30	glass bottom boat	Drosophila melanogaster	131-139
24187844-9	2013	The results showed that ACS has obviously penetration of the negatively charged drug aspirin, and certain penetration of neutral drug issorbide mononitrate, but inhibition of positively charged terazosin.	Aspirin	85-92	acyl-CoA synthetase short chain family member 2	Homo sapiens	24-27
23649702-3	2013	In human, monkey, and dog plasma, aspirin was hydrolyzed by their major hydrolases, paraoxonase (PON), butyrylcholinesterase (BChE), and albumin.	Aspirin	34-41	butyrylcholinesterase	Canis lupus familiaris	103-124
23649702-3	2013	In human, monkey, and dog plasma, aspirin was hydrolyzed by their major hydrolases, paraoxonase (PON), butyrylcholinesterase (BChE), and albumin.	Aspirin	34-41	butyrylcholinesterase	Canis lupus familiaris	126-130
23522855-1	2013	INTRODUCTION: Aspirin inhibits both the cyclooxygenase (COX)-1-dependent production of thromboxane A2 (TXA2) in platelets and COX-2-dependent production of anti-aggregatory prostaglandin I2 (PGI2) in vessel walls, resulting in "aspirin dilemma."	Aspirin	14-21	cytochrome c oxidase subunit I	Cavia porcellus	40-62
23522855-1	2013	INTRODUCTION: Aspirin inhibits both the cyclooxygenase (COX)-1-dependent production of thromboxane A2 (TXA2) in platelets and COX-2-dependent production of anti-aggregatory prostaglandin I2 (PGI2) in vessel walls, resulting in "aspirin dilemma."	Aspirin	14-21	cytochrome c oxidase subunit II	Cavia porcellus	126-131
23653362-0	2013	Up-regulation of ciliary neurotrophic factor in astrocytes by aspirin: implications for remyelination in multiple sclerosis.	Aspirin	62-69	ciliary neurotrophic factor	Mus musculus	17-44
23653362-3	2013	Interestingly, aspirin increased mRNA and protein expression of CNTF in primary mouse and human astrocytes in a dose- and time-dependent manner.	Aspirin	15-22	ciliary neurotrophic factor	Mus musculus	64-68
23653362-5	2013	H-89, an inhibitor of PKA, abrogated aspirin-induced expression of CNTF.	Aspirin	37-44	ciliary neurotrophic factor	Mus musculus	67-71
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	143-147
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	245-249
23805255-0	2013	Elevation of Eosinophil-Derived Neurotoxin in Plasma of the Subjects with Aspirin-Exacerbated Respiratory Disease: A Possible Peripheral Blood Protein Biomarker.	Aspirin	74-81	ribonuclease A family member 2	Homo sapiens	13-42
23703473-0	2013	Aspirin enhances IFN-alpha-induced growth inhibition and apoptosis of hepatocellular carcinoma via JAK1/STAT1 pathway.	Aspirin	0-7	Janus kinase 1	Mus musculus	99-103
23703473-5	2013	Further study revealed that aspirin-prompted phosphorylation of STAT1 was activated through phosphorylation of JAK1.	Aspirin	28-35	Janus kinase 1	Mus musculus	111-115
23454623-0	2013	Aspirin insensitive thrombophilia: transcript profiling of blood identifies platelet abnormalities and HLA restriction.	Aspirin	0-7	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	103-106
33316184-2	2020	The safety and efficacy of aspirin discontinuation on a background of a P2Y12 inhibitor in patients after percutaneous coronary intervention: a systematic review and meta-analysis.	Aspirin	27-34	purinergic receptor P2Y12	Homo sapiens	72-77
23220496-0	2013	Association of single nucleotide polymorphisms on Interleukin 17 receptor A (IL17RA) gene with aspirin hypersensitivity in asthmatics.	Aspirin	95-102	interleukin 17 receptor A	Homo sapiens	50-75
23220496-0	2013	Association of single nucleotide polymorphisms on Interleukin 17 receptor A (IL17RA) gene with aspirin hypersensitivity in asthmatics.	Aspirin	95-102	interleukin 17 receptor A	Homo sapiens	77-83
23220496-1	2013	AIM: To investigate the association of single nucleotide polymorphisms (SNP) on IL17RA gene with Aspirin Exacerbated Respiratory Disease (AERD) and the functional effect of these variants on expression of IL17RA gene products.	Aspirin	97-104	interleukin 17 receptor A	Homo sapiens	80-86
23220496-2	2013	MATERIAL &amp; METHODS: 15 SNPs of IL17RA gene were analyzed in 825 normal controls and 143 subjects with AERD and 411 with aspirin-tolerant asthma (ATA) and functionally characterized using measurement of protein and m-RNA expression.	Aspirin	124-131	interleukin 17 receptor A	Homo sapiens	35-41
33302757-0	2020	When Less Becomes More: Insights on the Pharmacodynamic Effects of Aspirin Withdrawal in Patients With Potent Platelet P2Y12 Inhibition Induced by Ticagrelor.	Aspirin	67-74	purinergic receptor P2Y12	Homo sapiens	119-124
23102217-5	2012	Indeed, AMPK is activated by the drugs metformin and salicylate, the latter being the major breakdown product of aspirin.	Aspirin	113-120	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	8-12
22707158-8	2012	The treatment of the MI mice with low-dose aspirin effectively inhibits the ischaemia-induced prostanoid generation and FasL expression in the myocardium, leading to the reduction in cardiac apoptosis following cardiac ischaemia.	Aspirin	43-50	Fas ligand (TNF superfamily, member 6)	Mus musculus	120-124
33376036-0	2021	Aspirin Use for Venous Thromboembolism Prevention Is Safe and Effective in Overweight and Obese Patients Undergoing Revision Total Hip and Knee Arthroplasty.	Aspirin	0-7	hedgehog interacting protein	Homo sapiens	131-134
33125972-8	2020	RT-qPCR analysis show that Asp-Sr/beta-TCP, beta-TCP group and Sr/beta-TCP group showed increased BMP2, Smad1, OPG than the OVX group(p < 0.05), while Asp-Sr/beta-TCP exhibited decreased TNF-alpha IFN-gamma and RANKL than the OVX group(p < 0.05).	Aspirin	27-30	bone morphogenetic protein 2	Rattus norvegicus	98-102
33125972-8	2020	RT-qPCR analysis show that Asp-Sr/beta-TCP, beta-TCP group and Sr/beta-TCP group showed increased BMP2, Smad1, OPG than the OVX group(p < 0.05), while Asp-Sr/beta-TCP exhibited decreased TNF-alpha IFN-gamma and RANKL than the OVX group(p < 0.05).	Aspirin	27-30	TNF superfamily member 11	Rattus norvegicus	211-216
33313269-0	2020	Aspirin alleviates denervation-induced muscle atrophy via regulating the Sirt1/PGC-1alpha axis and STAT3 signaling.	Aspirin	0-7	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	79-89
22251166-0	2012	Contribution of the OBSCN nonsynonymous variants to aspirin exacerbated respiratory disease susceptibility in Korean population.	Aspirin	52-59	obscurin, cytoskeletal calmodulin and titin-interacting RhoGEF	Mus musculus	20-25
33313269-12	2020	Mitochondrial vacuolation and autophagy were inhibited, as evidenced by reduced level of autophagy related proteins PINK1, BNIP3, LC3B and Atg7 in mice treated with aspirin compared with mice treated with saline.	Aspirin	165-172	BCL2/adenovirus E1B interacting protein 3	Mus musculus	123-128
22251166-8	2012	Although further functional evaluation is required, our findings suggest that OBSCN polymorphisms, in particular, highly conserved nonsynonymous Leu2116Phe variant, might contribute to aspirin hypersensitivity in asthmatics.	Aspirin	185-192	obscurin, cytoskeletal calmodulin and titin-interacting RhoGEF	Mus musculus	78-83
33313269-12	2020	Mitochondrial vacuolation and autophagy were inhibited, as evidenced by reduced level of autophagy related proteins PINK1, BNIP3, LC3B and Atg7 in mice treated with aspirin compared with mice treated with saline.	Aspirin	165-172	microtubule-associated protein 1 light chain 3 beta	Mus musculus	130-134
33313269-13	2020	In addition, aspirin treatment inhibited the slow-to-fast twitch muscle fiber conversion, which were related with triggering the expression of Sirt1 and PGC-1alpha.	Aspirin	13-20	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	153-163
22406476-9	2012	Aspirin changed nucleotide ratios and activated AMPK in CRC cells.	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	48-52
22406476-12	2012	Aspirin and metformin (an activator of AMPK) increased inhibition of mTOR and Akt, as well as autophagy in CRC cells.	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	39-43
33313269-15	2020	Conclusions: This is the first study to find that aspirin can alleviate denervation-induced muscle atrophy and inhibit the type I-to-type II muscle fiber conversion and mitophagy possibly through regulating the STAT3 inflammatory signaling pathway and Sirt1/PGC-1alpha signal axis.	Aspirin	50-57	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	258-268
22406476-14	2012	CONCLUSIONS: Aspirin is an inhibitor of mTOR and an activator of AMPK, targeting regulators of intracellular energy homeostasis and metabolism.	Aspirin	13-20	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	65-69
31783142-13	2020	CONCLUSION: Our results reveal that "aspirin resistance" is frequently found in T2DM, and is strongly related to insulin resistance and severity of CAD, but weakly related to HbA1c and not at all to inflammatory parameters.	Aspirin	37-44	hemoglobin subunit alpha 1	Homo sapiens	175-179
32994805-8	2020	In addition, celecoxib alone or in combination with aspirin inhibited the migration and invasion of NSCLC cells by inhibiting MMP-9 and MMP-2 activity levels.	Aspirin	52-59	matrix metallopeptidase 2	Homo sapiens	136-141
32295429-9	2020	Furthermore, aspirin increased the immunoexpression of cyclooxygenase (COX) 2 and nuclear factor kappa-B (NF-kappaB).	Aspirin	13-20	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	55-77
22570283-12	2012	Lowered SPINK5 expression might be a contributing factor leading to CRS, and appears to be characteristic for patients suffering from aspirin intolerance and from allergies.	Aspirin	134-141	serine peptidase inhibitor Kazal type 5	Homo sapiens	8-14
32779497-8	2020	Considering patient safety, the results support a strategy of DAPT for 1 to 3 months followed by aspirin-free P2Y12 inhibitor monotherapy.	Aspirin	97-104	purinergic receptor P2Y12	Homo sapiens	110-115
22217881-0	2012	Aspirin inhibits the production of reactive oxygen species by downregulating Nox4 and inducible nitric oxide synthase in human endothelial cells exposed to oxidized low-density lipoprotein.	Aspirin	0-7	NADPH oxidase 4	Homo sapiens	77-81
22217881-3	2012	The results showed that aspirin attenuated reactive oxygen species generation induced by ox-LDL and downregulated Nox4 and inducible nitric oxide synthase expression.	Aspirin	24-31	NADPH oxidase 4	Homo sapiens	114-118
22217881-4	2012	Redox-sensitive transcription factor nuclear factor kappa B was inactivated by aspirin, significantly preventing nuclear factor kappa B p65 subunit translocation into the nucleus.	Aspirin	79-86	RELA proto-oncogene, NF-kB subunit	Homo sapiens	136-139
32774705-9	2020	Moreover, the phosphorylation of HSP90beta (S254) and GSK3beta (Y216) may be a crucial factor in the aspirin-mediated regulation of apoptosis according to protein-protein interaction analysis.	Aspirin	101-108	glycogen synthase kinase 3 alpha	Mus musculus	54-62
22217881-6	2012	Aspirin ameliorated oxidative stress by downregulating Nox4 and inducible nitric oxide synthase and improved endothelial cell function by increasing endothelial nitric oxide synthase expression.	Aspirin	0-7	NADPH oxidase 4	Homo sapiens	55-59
22306536-9	2012	ASA also suppressed the expression of NADPH oxidase subunits (p22(phox), p47(phox), p67(phox), NOX2 and NOX4) and ROS generation.	Aspirin	0-3	cytochrome b-245, beta polypeptide	Mus musculus	95-99
22306536-9	2012	ASA also suppressed the expression of NADPH oxidase subunits (p22(phox), p47(phox), p67(phox), NOX2 and NOX4) and ROS generation.	Aspirin	0-3	NADPH oxidase 4	Mus musculus	104-108
22306773-13	2012	Also the up-regulation of Bcl-2, HO-1 and XIAP induced by 5mM Glu/BSO were all attenuated to a greater extent by ACS14 (20 muM) than aspirin (20 muM).	Aspirin	133-140	X-linked inhibitor of apoptosis	Mus musculus	42-46
32172203-0	2020	Aspirin enhances regulatory functional activities of monocytes and downregulates CD16 and CD40 expression in myocardial infarction autoinflammatory disease.	Aspirin	0-7	CD40 molecule	Homo sapiens	90-94
21692746-6	2012	Tumour cells of aspirin-treated mice were found arrested in G0/G1 phase of the cell cycle and showed nuclear localization of cyclin B1.	Aspirin	16-23	cyclin B1	Mus musculus	125-134
21692746-7	2012	Intratumoral administration of aspirin was accompanied by alterations in the biophysical, biochemical and immunological composition of the tumour microenvironment with respect to pH, level of dissolved O2, glucose, lactate, nitric oxide, IFNgamma (interferon gamma), IL-4 (interleukin-4), IL-6 and IL-10, whereas the TGF-beta (tumour growth factor-beta) level was unaltered.	Aspirin	31-38	transforming growth factor, beta 1	Mus musculus	317-325
32172203-2	2020	In this study, we have tried to evaluate the aspirin (acetylsalicylic acid, ASA) treatment effect on the CD16-expressed MOs and activation-associated CD40 in MI.	Aspirin	45-52	CD40 molecule	Homo sapiens	150-154
32172203-2	2020	In this study, we have tried to evaluate the aspirin (acetylsalicylic acid, ASA) treatment effect on the CD16-expressed MOs and activation-associated CD40 in MI.	Aspirin	54-74	CD40 molecule	Homo sapiens	150-154
32172203-2	2020	In this study, we have tried to evaluate the aspirin (acetylsalicylic acid, ASA) treatment effect on the CD16-expressed MOs and activation-associated CD40 in MI.	Aspirin	76-79	CD40 molecule	Homo sapiens	150-154
32172203-9	2020	Furthermore, the expression levels of CD16 and CD40 were significantly downregulated in ASA-treated MOs.	Aspirin	88-91	CD40 molecule	Homo sapiens	47-51
32245119-0	2020	Neurochemical Plasticity of nNOS-, VIP- and CART-Immunoreactive Neurons Following Prolonged Acetylsalicylic Acid Supplementation in the Porcine Jejunum.	Aspirin	92-112	nitric oxide synthase 1	Homo sapiens	28-32
32245119-5	2020	Therefore, the goal of the present study was to determine the influence of prolonged ASA supplementation on the immunolocalization of neuronal nitric oxide synthase (nNOS), vasoactive intestinal peptide (VIP) and cocaine- and amphetamine- regulated transcript peptide (CART) in the porcine jejunum.	Aspirin	85-88	nitric oxide synthase 1	Homo sapiens	134-164
22391069-5	2012	In further analysis, although significant signals disappeared after corrections for multiple testing, two HLA-DRA polymorphisms  (rs9268644C&gt;A, rs3129878A&gt;C) were found to be potential markers for nasal polyp development in aspirin-tolerant asthma (p = 0.005 and 0.007, respectively) compared with the aspirin-exacerbated respiratory disease (p &gt; 0.05) subgroup.	Aspirin	230-237	major histocompatibility complex, class II, DR alpha	Homo sapiens	106-113
22391069-5	2012	In further analysis, although significant signals disappeared after corrections for multiple testing, two HLA-DRA polymorphisms  (rs9268644C&gt;A, rs3129878A&gt;C) were found to be potential markers for nasal polyp development in aspirin-tolerant asthma (p = 0.005 and 0.007, respectively) compared with the aspirin-exacerbated respiratory disease (p &gt; 0.05) subgroup.	Aspirin	308-315	major histocompatibility complex, class II, DR alpha	Homo sapiens	106-113
32245119-5	2020	Therefore, the goal of the present study was to determine the influence of prolonged ASA supplementation on the immunolocalization of neuronal nitric oxide synthase (nNOS), vasoactive intestinal peptide (VIP) and cocaine- and amphetamine- regulated transcript peptide (CART) in the porcine jejunum.	Aspirin	85-88	nitric oxide synthase 1	Homo sapiens	166-170
21360558-8	2012	ASA and IBP prevented translocation of NFkappaB to the nucleus and, interestingly, ASA induced MMP-2 and MMP-13 whereas IBP induced MMP-2, MMP-9 and MMP-13.	Aspirin	0-3	matrix metallopeptidase 2	Rattus norvegicus	132-137
32258142-8	2020	The elevated levels of macrophage antigen, angiotensin II type1 receptor, and lipid accumulation were decreased in both the liver and aorta tissues in the aspirin-treated group.	Aspirin	155-162	angiotensin II receptor type 1	Homo sapiens	43-72
21360558-8	2012	ASA and IBP prevented translocation of NFkappaB to the nucleus and, interestingly, ASA induced MMP-2 and MMP-13 whereas IBP induced MMP-2, MMP-9 and MMP-13.	Aspirin	83-86	matrix metallopeptidase 2	Rattus norvegicus	95-100
32258142-9	2020	In conclusion, aspirin can systemically and simultaneously ameliorate NAFLD and atherosclerosis by inhibiting lipid biosynthesis and inflammation and by elevating catabolic metabolism through the activation of the PPARdelta-AMPK-PGC-1alpha pathway.	Aspirin	15-22	protein kinase AMP-activated catalytic subunit alpha 1	Sus scrofa	224-228
21564085-9	2011	CSE expression was reduced by  50% in wild-type mice challenged with ASA.	Aspirin	69-72	cystathionase (cystathionine gamma-lyase)	Mus musculus	0-3
32077309-0	2021	Steroids Inhibit Eosinophil Accumulation and Downregulate Hematopoietic Chemotaxic Prostaglandin D2 Receptor in Aspirin-Exacerbated Respiratory Disease.	Aspirin	112-119	prostaglandin D2 receptor	Homo sapiens	83-108
21564085-13	2011	FXR agonists protected against gastric injury caused by ASA and NSAIDs by a CSE-mediated mechanism.	Aspirin	56-59	cystathionase (cystathionine gamma-lyase)	Mus musculus	76-79
22171135-0	2011	SOX7 is involved in aspirin-mediated growth inhibition of human colorectal cancer cells.	Aspirin	20-27	SRY-box transcription factor 7	Homo sapiens	0-4
22171135-1	2011	AIM: To confirm the role of sex-determining region Y-box 7 (Sox7) in aspirin-mediated growth inhibition of COX-independent human colorectal cancer cells.	Aspirin	69-76	SRY-box transcription factor 7	Homo sapiens	28-58
32071459-11	2020	RESULTS: MTT assay showed that 1-100 mumol/L aspirin or meloxicam significantly promoted the proliferation of hDPC in a concentration dependent manner (P&lt;0.05).	Aspirin	45-52	decapping mRNA 2	Homo sapiens	110-114
22171135-1	2011	AIM: To confirm the role of sex-determining region Y-box 7 (Sox7) in aspirin-mediated growth inhibition of COX-independent human colorectal cancer cells.	Aspirin	69-76	SRY-box transcription factor 7	Homo sapiens	60-64
22171135-6	2011	RESULTS: SOX7 was upregulated by aspirin and was involved in aspirin-mediated growth inhibition of SW480 human colorectal cancer cells.	Aspirin	33-40	SRY-box transcription factor 7	Homo sapiens	9-13
22171135-6	2011	RESULTS: SOX7 was upregulated by aspirin and was involved in aspirin-mediated growth inhibition of SW480 human colorectal cancer cells.	Aspirin	61-68	SRY-box transcription factor 7	Homo sapiens	9-13
32181097-9	2020	This systematic review would suggest that the early or first-aid administration of aspirin to adults with non-traumatic chest pain improves survival as compared with late or in-hospital administration.	Aspirin	83-90	activation induced cytidine deaminase	Homo sapiens	61-64
22171135-7	2011	The p38MAPK pathway played a role in aspirin-induced SOX7 expression, during which the AP1 transcription factors c-Jun and c-Fos upregulated SOX7 promoter activities.	Aspirin	37-44	SRY-box transcription factor 7	Homo sapiens	53-57
22171135-7	2011	The p38MAPK pathway played a role in aspirin-induced SOX7 expression, during which the AP1 transcription factors c-Jun and c-Fos upregulated SOX7 promoter activities.	Aspirin	37-44	SRY-box transcription factor 7	Homo sapiens	141-145
22171135-8	2011	RESULTS: SOX7 is upregulated by aspirin and is involved in aspirin-mediated growth inhibition of human colorectal cancer SW480 cells.	Aspirin	32-39	SRY-box transcription factor 7	Homo sapiens	9-13
22171135-8	2011	RESULTS: SOX7 is upregulated by aspirin and is involved in aspirin-mediated growth inhibition of human colorectal cancer SW480 cells.	Aspirin	59-66	SRY-box transcription factor 7	Homo sapiens	9-13
21784135-4	2011	Western blotting analysis showed that S-aspirin suppressed the protein expression levels of cyclooxygenase-2 and growth arrest DNA damage (GADD).	Aspirin	38-47	prostaglandin-endoperoxide synthase 2	Mus musculus	92-108
32000660-0	2020	Aspirin has a better effect on PIK3CA mutant colorectal cancer cells by PI3K/Akt/Raptor pathway.	Aspirin	0-7	regulatory associated protein of MTOR complex 1	Homo sapiens	81-87
21784135-9	2011	In addition, S-aspirin also prevented Abeta-induced activation of p38-mitogen activated protein kinase (MAPK).	Aspirin	15-22	mitogen-activated protein kinase 14	Mus musculus	66-69
21784135-10	2011	In conclusion, our results suggest that S-aspirin may protect microglial injury via inhibition of inflammation, prevention of mitochondria function, and stimulation of cell growth via stimulating p38-MAPK pathway.	Aspirin	40-49	mitogen-activated protein kinase 14	Mus musculus	196-199
31805177-11	2019	Although the mechanisms underlying this enhancement of sensitization are still controversial, our study suggests that modification of cytokine production due to impairment of the intestinal barrier function and inhibition of cyclooxygenase-1 activity by aspirin may be involved.	Aspirin	254-261	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	225-241
31805984-0	2019	Aspirin inhibits RANKL-induced osteoclast differentiation in dendritic cells by suppressing NF-kappaB and NFATc1 activation.	Aspirin	0-7	TNF superfamily member 11	Rattus norvegicus	17-22
31557056-9	2019	CONCLUSIONS: An antithrombotic regimen consisting of apixaban and a P2Y12 inhibitor without aspirin provides superior safety and similar efficacy in patients with atrial fibrillation who have ACS, whether managed medically or with PCI, and those undergoing elective PCI compared with regimens that include vitamin K antagonists, aspirin, or both.	Aspirin	329-336	purinergic receptor P2Y12	Homo sapiens	68-73
21985141-2	2011	Variation in COX-2 expression could be a mechanism for variable response to aspirin.	Aspirin	76-83	cytochrome c oxidase subunit II	Canis lupus familiaris	13-18
21985141-14	2011	Variability in platelet COX-2 expression should be explored as a potential mechanism for, or marker of, variable aspirin responsiveness.	Aspirin	113-120	cytochrome c oxidase subunit II	Canis lupus familiaris	24-29
31625710-0	2019	Aspirin reduces the incidence of postmenopausal osteoporosis in rats through OPG-RANKL-RANK signaling pathway.	Aspirin	0-7	TNF superfamily member 11	Rattus norvegicus	81-86
21867913-2	2011	We report an aspirin-triggered DHA metabolome that biosynthesizes a potent product in inflammatory exudates and human leukocytes, namely aspirin-triggered Neuroprotectin D1/Protectin D1 [AT-(NPD1/PD1)].	Aspirin	13-20	programmed cell death 1	Homo sapiens	192-195
21867913-2	2011	We report an aspirin-triggered DHA metabolome that biosynthesizes a potent product in inflammatory exudates and human leukocytes, namely aspirin-triggered Neuroprotectin D1/Protectin D1 [AT-(NPD1/PD1)].	Aspirin	137-144	programmed cell death 1	Homo sapiens	192-195
21645153-0	2011	Two novel aspirin analogues show selective cytotoxicity in primary chronic lymphocytic leukaemia cells that is associated with dual inhibition of Rel A and COX-2.	Aspirin	10-17	RELA proto-oncogene, NF-kB subunit	Homo sapiens	146-151
21592450-8	2011	Aspirin increased the risk of hemorrhagic stroke (RR 1.36; 95% CI, 1.01-1.82), major bleeding (RR 1.66; 95% CI, 1.41-1.95), and gastrointestinal bleeding (RR 1.37; 95% CI, 1.15-1.62).	Aspirin	0-7	ribonucleotide reductase catalytic subunit M1	Homo sapiens	50-54
21592450-8	2011	Aspirin increased the risk of hemorrhagic stroke (RR 1.36; 95% CI, 1.01-1.82), major bleeding (RR 1.66; 95% CI, 1.41-1.95), and gastrointestinal bleeding (RR 1.37; 95% CI, 1.15-1.62).	Aspirin	0-7	ribonucleotide reductase catalytic subunit M1	Homo sapiens	95-99
21592450-8	2011	Aspirin increased the risk of hemorrhagic stroke (RR 1.36; 95% CI, 1.01-1.82), major bleeding (RR 1.66; 95% CI, 1.41-1.95), and gastrointestinal bleeding (RR 1.37; 95% CI, 1.15-1.62).	Aspirin	0-7	ribonucleotide reductase catalytic subunit M1	Homo sapiens	95-99
21221715-6	2011	HPR on aspirin (HPR(Aspirin)) defined as an ARU value &gt;=550.	Aspirin	7-14	haptoglobin-related protein	Homo sapiens	0-3
21221715-6	2011	HPR on aspirin (HPR(Aspirin)) defined as an ARU value &gt;=550.	Aspirin	7-14	haptoglobin-related protein	Homo sapiens	16-28
21554368-10	2011	P2Y12 is the same receptor targeted by ticlopidine and clopidogrel, platelet inhibitors used in lieu of aspirin in people at risk for cardiovascular disease; thus, spontaneous bleeding is not expected unless there are other contributing factors.	Aspirin	104-111	purinergic receptor P2Y12	Homo sapiens	0-5
21461252-0	2011	Role of Toll-like Receptor 3 Variants in Aspirin-Exacerbated Respiratory Disease.	Aspirin	41-48	toll like receptor 3	Homo sapiens	8-28
21461252-1	2011	PURPOSE: Although the mechanism of virus-induced, aspirin-exacerbated respiratory disease (AERD) is not known fully, direct activation of viral components through Toll-like receptor 3 (TLR3) has been suggested.	Aspirin	50-57	toll like receptor 3	Homo sapiens	185-189
21324923-4	2011	In mouse models of glioma, treatment with the COX-2 inhibitors acetylsalicylic acid (ASA) or celecoxib inhibited systemic PGE2 production and delayed glioma development.	Aspirin	63-83	cytochrome c oxidase II, mitochondrial	Mus musculus	46-51
21324923-4	2011	In mouse models of glioma, treatment with the COX-2 inhibitors acetylsalicylic acid (ASA) or celecoxib inhibited systemic PGE2 production and delayed glioma development.	Aspirin	85-88	cytochrome c oxidase II, mitochondrial	Mus musculus	46-51
21324923-5	2011	ASA treatment also reduced the MDSC-attracting chemokine CCL2 (C-C motif ligand 2) in the TME along with numbers of CD11b(+)Ly6G(hi)Ly6C(lo) granulocytic MDSCs in both the bone marrow and the TME.	Aspirin	0-3	lymphocyte antigen 6 complex, locus G	Mus musculus	124-128
21324923-7	2011	Conversely, these mice or ASA-treated wild-type mice displayed enhanced expression of CXCL10 (C-X-C motif chemokine 10) and infiltration of cytotoxic T lymphocytes (CTL) in the TME, consistent with a relief of MDSC-mediated immunosuppression.	Aspirin	26-29	chemokine (C-X-C motif) ligand 10	Mus musculus	86-92
21324923-7	2011	Conversely, these mice or ASA-treated wild-type mice displayed enhanced expression of CXCL10 (C-X-C motif chemokine 10) and infiltration of cytotoxic T lymphocytes (CTL) in the TME, consistent with a relief of MDSC-mediated immunosuppression.	Aspirin	26-29	chemokine (C-X-C motif) ligand 10	Mus musculus	94-118
20966167-6	2011	Clopidogrel, the most widely used drug that inhibits P2Y12, is effective both in monotherapy and in combination with acetylsalicylic acid.	Aspirin	117-137	purinergic receptor P2Y12	Homo sapiens	53-58
21231793-0	2011	Aspirin regulates SNARE protein expression and phagocytosis in dendritic cells.	Aspirin	0-7	vesicle transport through interaction with t-SNAREs 1B	Mus musculus	18-23
21231793-5	2011	Here we show that ASA inhibits phagocytosis and modulates expression of endosomal SNAREs, such as Vti1a, Vti1b, VAMP-3, VAMP-8 and Syn-8 (but not syn-6 and syn-16) in DC.	Aspirin	18-21	vesicle transport through interaction with t-SNAREs 1B	Mus musculus	105-110
21231793-6	2011	We further show that the phagocytic inhibitory effect of ASA is dependent on the expression of Vti1a and Vti1b.	Aspirin	57-60	vesicle transport through interaction with t-SNAREs 1B	Mus musculus	105-110
21231793-8	2011	Our results suggest that ASA modulates phagocytosis in part through the control of endosomal SNARE protein expression and localization in DC.	Aspirin	25-28	vesicle transport through interaction with t-SNAREs 1B	Mus musculus	93-98
20690072-7	2011	The results showed that administration with aspirin for 4 weeks or 8 weeks significantly reduced the mean escape latency, the acetylcholinesterase activity, the TNF-alpha, IL-1beta levels and increased the percentage of time spent in target quadrant.	Aspirin	44-51	acetylcholinesterase	Mus musculus	126-146
20886344-7	2011	Furthermore, the phosphorylated form of STAT3 and the levels of STAT3"s target gene products such as Bcl-xl and Bcl-2, which are essential for cell growth and survival, were also decreased in aspirin-treated mice.	Aspirin	192-199	BCL2-like 1	Mus musculus	101-107
21660742-2	2011	The detailed AFM imaging of the circular DNA after incubation with -various concentrations of vincristine and aspirin have been demonstrated.	Aspirin	110-117	afamin	Homo sapiens	13-16
20640495-3	2010	Dipyridamole (DIP) augments the IS-limiting effects of statins by blocking the cellular reuptake of adenosine; whereas aspirin (ASA) attenuates the effect by inhibiting COX2.	Aspirin	119-126	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	169-173
20640495-3	2010	Dipyridamole (DIP) augments the IS-limiting effects of statins by blocking the cellular reuptake of adenosine; whereas aspirin (ASA) attenuates the effect by inhibiting COX2.	Aspirin	128-131	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	169-173
20640495-17	2010	Both SIM and DIP+low-dose ASA augmented eNOS, ERK 1/2 and CREB phosphorylation.	Aspirin	26-29	mitogen activated protein kinase 3	Rattus norvegicus	46-53
21061537-3	2010	Therefore, high risk patients for peptic ulcers should be prevented with antisecretory drugs, such as PPI or histamine H2-receptor antagonists, because ulcer bleedings in patients with treatment of low-dose aspirin can be serious.	Aspirin	207-214	histamine receptor H2	Homo sapiens	109-130
20835687-5	2010	The luciferase activity in the stable clone was enhanced by the recombinant Wnt-3A (rWnt-3A; 100-400 ng/mL) and GSK3beta inhibitor (2"Z,3"E)-6-bromoindirubin-3"-oxime (BIO; 5 microM) but was inhibited by aspirin (5 mM).	Aspirin	204-211	Wnt family member 3A	Homo sapiens	76-82
20835687-5	2010	The luciferase activity in the stable clone was enhanced by the recombinant Wnt-3A (rWnt-3A; 100-400 ng/mL) and GSK3beta inhibitor (2"Z,3"E)-6-bromoindirubin-3"-oxime (BIO; 5 microM) but was inhibited by aspirin (5 mM).	Aspirin	204-211	glycogen synthase kinase 3 beta	Homo sapiens	112-120
21089263-2	2010	Aspirin may be a better bet.	Aspirin	0-7	delta/notch like EGF repeat containing	Homo sapiens	17-20
20842562-6	2010	To achieve Lp(a) reduction, one evidence-based approach is to initiate therapy with low-dose aspirin and extended-release niacin, titrated from 0.5 g up to 2 g over several weeks.	Aspirin	93-100	lipoprotein(a)	Homo sapiens	11-16
20597033-2	2010	Antiplatelet therapy includes the administration of aspirin and clopidogrel, either alone or in combination, which act through the inhibition of thromboxane A2 generation and blockade of the Gi-coupled P2Y12 purinergic receptor, respectively.	Aspirin	52-59	purinergic receptor P2Y12	Homo sapiens	202-207
20514442-5	2010	We report that treatment of the DNA MMR competent/p53 mutant colorectal cancer cell line SW480 with 1 mM aspirin for 48 h caused changes in mRNA expression of several key genes involved in DNA damage signalling pathways, including a significant down-regulation in transcription of the genes ATR, BRCA1 and MAPK12.	Aspirin	105-112	mitogen-activated protein kinase 12	Homo sapiens	306-312
20514442-8	2010	Although a correlation was not seen between transcript and protein levels of ATR, BRCA1 and GADD45alpha, an increase in XRCC3 encoded protein expression upon aspirin treatment in SW480 cells was observed by immunoblotting, immunofluorescence and immunohistochemical analysis.	Aspirin	158-165	growth arrest and DNA damage inducible alpha	Homo sapiens	92-103
20350286-12	2010	CONCLUSION: COX 2 inhibition induced a pro-thrombotic effect that was antagonized by aspirin at 1 mg/kg or 100 mg/kg.	Aspirin	85-92	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	12-17
20586862-4	2010	There are some genetic polymorphisms for aspirin resistance, such as platelet membrane glycoproteins, thromboxane A2 (TXA2) receptor, platelet activating factor acetylhydrolase and coagulation factor XIII; however, data on the frequency of gastrointestinal (GI) events in these variants are lacking.	Aspirin	41-48	thromboxane A2 receptor	Homo sapiens	102-132
20144559-6	2010	The prevalence of aspirin non-responders for WBA-AA, TXB(2), PFA-100((R)), CPA and Coll1:5 was 13.1%, 8.2%, 14.8%, 9.7% and 16.4% respectively.	Aspirin	18-25	semaphorin 3A	Homo sapiens	83-88
19752399-0	2010	Identification and absolute configuration of dihydroxy-arachidonic acids formed by oxygenation of 5S-HETE by native and aspirin-acetylated COX-2.	Aspirin	120-127	cytochrome c oxidase II, mitochondrial	Mus musculus	139-144
19752399-2	2010	Acetylation of COX-2 by aspirin abrogates prostaglandin synthesis and triggers formation of 15R-HETE as the sole product of oxygenation of arachidonic acid.	Aspirin	24-31	cytochrome c oxidase II, mitochondrial	Mus musculus	15-20
19752399-3	2010	Here, we investigated the formation of by-products of the transformation of 5S-HETE by native COX-2 and by aspirin-acetylated COX-2 using HPLC-ultraviolet, GC-MS, and LC-MS analysis.	Aspirin	107-114	cytochrome c oxidase II, mitochondrial	Mus musculus	126-131
19965971-9	2010	Patients who received heparin and aspirin had significantly higher live birth rate (RR 1.301; 95% CI 1.040, 1.629) than aspirin alone, with the number needed to achieve one live birth being 5.6.	Aspirin	34-41	ribonucleotide reductase catalytic subunit M1	Homo sapiens	84-88
26581884-2	2016	Addition of a potent P2Y12 inhibitor to aspirin is the standard therapy for non-ST-segment elevation acute coronary syndrome (NSTE-ACS) patients undergoing percutaneous coronary intervention (PCI).	Aspirin	40-47	purinergic receptor P2Y12	Homo sapiens	21-26
26546721-8	2015	In contrast to current antiplatelet strategies, the glycoprotein IIb/IIIa (GPIIb/IIIa) antagonist RGDS peptide only prevented cancer cells-induced platelet aggregation, but not platelet adhesion and secretion; whereas the cyclooxygenase inhibitor aspirin and the adenosine diphosphate (ADP) scavenger apyrase affected neither platelet aggregation nor platelet secretion.	Aspirin	247-254	ral guanine nucleotide dissociation stimulator	Homo sapiens	98-102
26527225-11	2015	Regarding safety, medium-dose aspirin (100-300 mg daily) and aspirin/clopidogrel combination showed an increased risk of MB compared with warfarin (RR 1.17 and 1.15, respectively), as per dabigatran 150 mg and rivaroxaban in older elderly (RR 1.17 and 1.12, respectively).	Aspirin	30-37	ribonucleotide reductase catalytic subunit M1	Homo sapiens	240-244
26527225-11	2015	Regarding safety, medium-dose aspirin (100-300 mg daily) and aspirin/clopidogrel combination showed an increased risk of MB compared with warfarin (RR 1.17 and 1.15, respectively), as per dabigatran 150 mg and rivaroxaban in older elderly (RR 1.17 and 1.12, respectively).	Aspirin	61-68	ribonucleotide reductase catalytic subunit M1	Homo sapiens	148-152
26527225-11	2015	Regarding safety, medium-dose aspirin (100-300 mg daily) and aspirin/clopidogrel combination showed an increased risk of MB compared with warfarin (RR 1.17 and 1.15, respectively), as per dabigatran 150 mg and rivaroxaban in older elderly (RR 1.17 and 1.12, respectively).	Aspirin	61-68	ribonucleotide reductase catalytic subunit M1	Homo sapiens	240-244
26522688-3	2015	We found that aspirin significantly down-regulated TfR1, while also up-regulated Fpn1 and ferritin expressions in BV-2 microglial cells in vitro.	Aspirin	14-21	transferrin receptor	Mus musculus	51-55
26522688-4	2015	We also showed that TfR1 and Fpn1 expressions were significantly higher, while ferritin contents, IL-6, TNF-alpha and hepcidin mRNA levels were lower in cells treated with aspirin plus LPS than those in cells treated with LPS only.	Aspirin	172-179	transferrin receptor	Mus musculus	20-24
26522688-6	2015	Our findings also suggested that hepcidin might play a dominant role in the control of TfR1 expression by aspirin in the cells treated with LPS.	Aspirin	106-113	transferrin receptor	Mus musculus	87-91
25670850-12	2015	Additionally, Zn(ASA)2 significantly increased the mRNA-expression of superoxide dismutase 1 (+73 +- 15%), glutathione peroxidase 4 (+44 +- 12%), and transforming growth factor (TGF)-beta1 (+102 +- 22%).	Aspirin	17-20	glutathione peroxidase 4	Rattus norvegicus	107-131
26094902-9	2015	It was certified that the increase in the amount of NO release, the decrease in the luciferase promoter activity and the expression of cyclin D1 and c-myc in HCT116 cells were affected by aspirin and ISMN in a synergistic manner.	Aspirin	188-195	cyclin D1	Homo sapiens	135-144
25891179-4	2015	Compared with treatment by sCT or ASA alone, combined treatment (sCT+ASA) increased BMD, improved femur bone strength, normalized trabecular network architecture and morphology, and increased mRNA and protein expression of OPG, while reducing the expression of RANKL.	Aspirin	69-72	TNF superfamily member 11	Rattus norvegicus	261-266
26230583-8	2015	Recent use of aspirin and/or ibuprofen was associated with differential expression of TMC06, ST8SIA4, and STEAP3 while a summary oxidative balance score (OBS) was associated with SYCP3, HDX, and NRG4 (all up-regulated with greater oxidative balance).	Aspirin	14-21	ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 4	Homo sapiens	93-100
26230583-8	2015	Recent use of aspirin and/or ibuprofen was associated with differential expression of TMC06, ST8SIA4, and STEAP3 while a summary oxidative balance score (OBS) was associated with SYCP3, HDX, and NRG4 (all up-regulated with greater oxidative balance).	Aspirin	14-21	neuregulin 4	Homo sapiens	195-199
25824964-0	2015	Aspirin-induced histone acetylation in endothelial cells enhances synthesis of the secreted isoform of netrin-1 thus inhibiting monocyte vascular infiltration.	Aspirin	0-7	netrin 1	Mus musculus	103-111
25824964-2	2015	We investigated the effect of aspirin, which is widely used in cardiovascular prophylaxis, on the synthesis of different isoforms of netrin-1 by endothelial cells under pro-inflammatory conditions, and defined the net effect of aspirin-dependent systemic modulation of netrin-1 on atherosclerosis progression.	Aspirin	30-37	netrin 1	Mus musculus	133-141
25824964-7	2015	Aspirin counteracted TNF-alpha-mediated effects on netrin-1 synthesis by endothelial cells through COX-dependent inhibition of NF-kappaB and concomitant histone hyperacetylation.	Aspirin	0-7	netrin 1	Mus musculus	51-59
25824964-8	2015	Administration of aspirin to ApoE(-/-) mice on HFD increased blood and arterial wall levels of netrin-1 independently of its effects on platelets, accompanied by reduced plaque size and content of monocytes/macrophages, compared with untreated or clopidogrel-treated mice.	Aspirin	18-25	netrin 1	Mus musculus	95-103
25824964-9	2015	In vivo blockade of netrin-1 enhanced monocyte plaque infiltration in aspirin-treated ApoE(-/-) mice.	Aspirin	70-77	netrin 1	Mus musculus	20-28
25824964-10	2015	CONCLUSIONS AND IMPLICATIONS: Aspirin counteracts down-regulation of secreted netrin-1 induced by pro-inflammatory stimuli in endothelial cells.	Aspirin	30-37	netrin 1	Mus musculus	78-86
25824964-11	2015	The aspirin-dependent increase of netrin-1 in ApoE(-/-) mice exerts anti-atherogenic effects by preventing arterial accumulation of monocytes.	Aspirin	4-11	netrin 1	Mus musculus	34-42
26101955-10	2015	Identification of HMGB1 as a pharmacological target of SA/aspirin provides new insights into the mechanisms of action of one of the world"s longest and most used natural and synthetic drugs.	Aspirin	58-65	high mobility group box 1	Homo sapiens	18-23
26068794-0	2015	Aspirin delays mesothelioma growth by inhibiting HMGB1-mediated tumor progression.	Aspirin	0-7	high mobility group box 1	Homo sapiens	49-54
26068794-3	2015	We hypothesized that ASA may exert anticancer properties in MM by abrogating the carcinogenic effects of HMGB1.	Aspirin	21-24	high mobility group box 1	Homo sapiens	105-110
26068794-4	2015	Using HMGB1-secreting and -non-secreting human MM cell lines, we determined whether aspirin inhibited the hallmarks of HMGB1-induced MM cell growth in vitro and in vivo.	Aspirin	84-91	high mobility group box 1	Homo sapiens	119-124
26068794-5	2015	Our data demonstrated that ASA and its metabolite, salicylic acid (SA), inhibit motility, migration, invasion and anchorage-independent colony formation of MM cells via a novel HMGB1-mediated mechanism.	Aspirin	27-30	high mobility group box 1	Homo sapiens	177-182
26068794-7	2015	The effects of ASA and BoxA were cyclooxygenase-2 independent and were not additive, consistent with both acting via inhibition of HMGB1 activity.	Aspirin	15-18	high mobility group box 1	Homo sapiens	131-136
26068794-8	2015	Our findings provide a rationale for the well documented, yet poorly understood antitumorigenic activity of aspirin, which we show proceeds via HMGB1 inhibition.	Aspirin	108-115	high mobility group box 1	Homo sapiens	144-149
19966835-10	2010	Aspirin inhibits GSK-3beta activation and suppresses the expression of its downstream gene products (cyclin D1 and Bcl-2), which are implicated in proliferation, survival and chemoresistance of pancreatic cancer.	Aspirin	0-7	glycogen synthase kinase 3 beta	Homo sapiens	17-26
19966835-10	2010	Aspirin inhibits GSK-3beta activation and suppresses the expression of its downstream gene products (cyclin D1 and Bcl-2), which are implicated in proliferation, survival and chemoresistance of pancreatic cancer.	Aspirin	0-7	cyclin D1	Homo sapiens	101-110
19966835-12	2010	CONCLUSION: Our results suggest that aspirin inhibits the proliferation of gemcitabine-resistant pancreatic cancer cells and augments the antisurvival effect of gemcitabine, probably by suppressing the activity of GSK-3beta and its downstream gene products.	Aspirin	37-44	glycogen synthase kinase 3 beta	Homo sapiens	214-223
25904552-5	2015	LTC4 upregulated the expressions of ICAM-1 and VCAM-1 in an aspirin-sensitive and TP receptor-dependent manner.	Aspirin	60-67	intercellular adhesion molecule 1	Mus musculus	36-42
31781346-6	2019	We found that aspirin preserved the extracellular matrix (ECM) content of collagen type II (COL2) and aggrecan while inhibiting the expression of matrix-degenerating enzymes, including matrix metalloproteinase 3 and 13 (MMP-3 and MMP-13) and A disintegrin and metalloproteinase with thrombospondin motifs 4 and 5 (ADAMTS-4, ADAMTS-5).	Aspirin	14-21	ADAM metallopeptidase with thrombospondin type 1 motif, 4	Rattus norvegicus	314-322
25769431-7	2015	TNF-alpha-mediated up-regulation of placental fractalkine was reversed in the presence of the aspirin-derivative salicylate, which impaired activation of NF-kappaB p65 in TNF-alpha-treated explants.	Aspirin	94-101	RELA proto-oncogene, NF-kB subunit	Homo sapiens	164-167
20035517-2	2010	We report a Janus kinase 2-homozygous patient with BCS who thrombosed a transjugular intrahepatic portosystemic shunt (TIPS) despite treatment with warfarin (international normalized ratio = 3.0), aspirin, and clopidogrel.	Aspirin	197-204	Janus kinase 2	Homo sapiens	12-26
30646422-1	2019	OBJECTIVE:  To assess the effect of aspirin use in low-risk pregnancy on: (1) pregnancy-associated plasma protein-A (PAPP-A) and placental-like growth factor (PLGF); (2) urinary albumin-to-creatinine ratio (ACR) and blood pressure; (3) fetal growth parameters; and (4) placental histopathology.	Aspirin	36-43	pappalysin 1	Homo sapiens	78-115
20095973-4	2009	The preclinical rationale for combination chemoprevention with DFMO and the NSAID sulindac, was strengthened by the observation that a SNP (single nucleotide polymorphism) in the ODC promoter was prognostic for adenoma recurrence in patients with prior sporadic colon polyps and predicted reduced risk of adenoma in those patients taking aspirin.	Aspirin	338-345	ornithine decarboxylase 1	Homo sapiens	179-182
30646422-1	2019	OBJECTIVE:  To assess the effect of aspirin use in low-risk pregnancy on: (1) pregnancy-associated plasma protein-A (PAPP-A) and placental-like growth factor (PLGF); (2) urinary albumin-to-creatinine ratio (ACR) and blood pressure; (3) fetal growth parameters; and (4) placental histopathology.	Aspirin	36-43	pappalysin 1	Homo sapiens	117-123
25778862-0	2015	Association of P2RY12 polymorphisms with eosinophil and platelet activation in patients with aspirin-exacerbated respiratory disease.	Aspirin	93-100	purinergic receptor P2Y12	Homo sapiens	15-21
25887212-17	2015	The NNT to achieve the minimally clinically important difference of 0.7 points ranged from 2 to 4.Compared with placebo, there was moderate quality evidence (downgraded for imprecision) that patients on an anti-TNF agent were more likely to achieve an ASAS partial remission by six months (adalimumab: RR 6.28, 95% Crl 3.13 to 12.78; etanercept: RR 4.24, 95% Crl 2.31 to 8.09; golimumab: RR 5.18, 95% Crl 1.90 to 14.79; infliximab: RR 15.41, 95% Crl 5.09 to 47.98 with a 10% to 44% absolute difference between treatment and placebo groups.	Aspirin	252-256	interleukin 27 receptor subunit alpha	Homo sapiens	401-406
31106412-9	2019	Omega-3 fatty acids only, aspirin only, or omega-3 fatty acids plus aspirin also inhibited the protein expressions of COX-2 and iNOS in LPS-stimulated RAW264.7 cells.	Aspirin	26-33	cytochrome c oxidase II, mitochondrial	Mus musculus	118-123
31106412-9	2019	Omega-3 fatty acids only, aspirin only, or omega-3 fatty acids plus aspirin also inhibited the protein expressions of COX-2 and iNOS in LPS-stimulated RAW264.7 cells.	Aspirin	68-75	cytochrome c oxidase II, mitochondrial	Mus musculus	118-123
31106412-10	2019	In addition, omega-3 combined with ASA also inhibited the RANKL-induced gene expressions of MMPs in dose-dependent manners.	Aspirin	35-38	TNF superfamily member 11	Rattus norvegicus	58-63
31106412-10	2019	In addition, omega-3 combined with ASA also inhibited the RANKL-induced gene expressions of MMPs in dose-dependent manners.	Aspirin	35-38	matrix metallopeptidase 2	Rattus norvegicus	92-96
20214591-4	2009	Among the enzymes involved in aspirin biodisposition a major role is played by the enzymes UDP-glucuronosyltransferase UGT1A6, cytochrome P450 CYP2C9 and the xenobiotic/medium chain fatty acid:CoA ligase ACSM2, although other UGTs and ACSMs enzymes may significantly contribute to aspirin metabolism.	Aspirin	30-37	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	119-125
20214591-4	2009	Among the enzymes involved in aspirin biodisposition a major role is played by the enzymes UDP-glucuronosyltransferase UGT1A6, cytochrome P450 CYP2C9 and the xenobiotic/medium chain fatty acid:CoA ligase ACSM2, although other UGTs and ACSMs enzymes may significantly contribute to aspirin metabolism.	Aspirin	281-288	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	119-125
31418171-3	2019	Here we show that diflunisal, an aspirin-like nonsteroidal anti-inflammatory drug (NSAID) that has been in clinical use for decades, specifically inhibits in vitro and in vivo the chemotactic activity of HMGB1 at nanomolar concentrations, at least in part by binding directly to both HMGB1 and CXCL12 and disrupting their heterocomplex.	Aspirin	33-40	high mobility group box 1	Homo sapiens	204-209
20214591-7	2009	Major polymorphisms related to aspirin biodisposition are rs2070959, rs1105879 and rs6759892 for the UGT1A6 gene, rs1133607 for the ACSM2 gene, and rs1799853, rs1057910, rs28371686, rs9332131 and rs28371685 for the CYP2C9 gene.	Aspirin	31-38	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	101-107
19608566-3	2009	By inhibiting vasoconstriction, the use of low-dose aspirin in the first trimester could influence placentation and therefore prevent or delay development of hypertensive pregnancy complications, such as pregnancy-induced hypertension (PIH) and pre-eclampsia (PE).	Aspirin	52-59	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	236-239
19595669-5	2009	Moreover, the expression of STAT3 target genes such as Cyclin D1, XIAP, and Bcl-2 that are essential for cell growth and survival was apparently attenuated after aspirin treatment.	Aspirin	162-169	cyclin D1	Homo sapiens	55-64
31267433-4	2019	A low response to aspirin and clopidogrel was defined in terms of aspirin reaction units > 550 and P2Y12 reaction units >= 230, respectively, by VerifyNow assay.	Aspirin	18-25	purinergic receptor P2Y12	Homo sapiens	99-104
19407805-7	2009	A significant ambulatory BP reduction was, however, observed in the subjects who received aspirin at bedtime (decrease of 6/3 mm Hg in the 24-h mean of systolic (SBP)/diastolic BP (DBP), respectively; P &lt; 0.001), without changes in heart rate (HR) from baseline.	Aspirin	90-97	selenium binding protein 1	Homo sapiens	162-165
19407805-8	2009	BP was homogeneously controlled along the 24 h after bedtime aspirin administration (6/4 mm Hg reduction in activity mean of SBP/DBP; 6/3 mm Hg reduction in sleep-time mean, respectively).	Aspirin	61-68	selenium binding protein 1	Homo sapiens	125-128
31565672-5	2019	In addition, we also showed that exposure to 4-mM aspirin led to an inhibition of intracellular ATP and lactate synthesis in vascular ECs, and a down-regulation of the phosphorylation level of NF-kappaB p65 was observed.	Aspirin	50-57	RELA proto-oncogene, NF-kB subunit	Homo sapiens	203-206
19341823-10	2009	ASA inhibited the expression of CD1a and prevented downregulation of CD14, NCX 4016 stimulated the differentiation of CD1a+CD14+ and CD1a(-)CD14+ cells, whereas NCX 4040 decreased the proportion of CD1a+CD14(-) and increased the frequency of CD1a+CD14+ cells, compared to control.	Aspirin	0-3	CD1a molecule	Homo sapiens	32-36
19341823-10	2009	ASA inhibited the expression of CD1a and prevented downregulation of CD14, NCX 4016 stimulated the differentiation of CD1a+CD14+ and CD1a(-)CD14+ cells, whereas NCX 4040 decreased the proportion of CD1a+CD14(-) and increased the frequency of CD1a+CD14+ cells, compared to control.	Aspirin	0-3	CD14 molecule	Homo sapiens	69-73
19341823-11	2009	Maturation, both in ASA and NO-ASA treated MoDC was characterized by decreased allostimulatory activity, lower expression of CD83, HLA-DR, costimulatory molecules and CD54 and decreased production of IL-10 and IL-12 p40.	Aspirin	20-23	interleukin 9	Homo sapiens	216-219
19341823-11	2009	Maturation, both in ASA and NO-ASA treated MoDC was characterized by decreased allostimulatory activity, lower expression of CD83, HLA-DR, costimulatory molecules and CD54 and decreased production of IL-10 and IL-12 p40.	Aspirin	31-34	interleukin 9	Homo sapiens	216-219
32123852-8	2019	However, the suppressive effect of aspirin on DOX-induced p53 accumulation was significantly decreased in COX2 knockout mouse embryonic fibroblasts.	Aspirin	35-42	prostaglandin-endoperoxide synthase 2	Mus musculus	106-110
32123852-9	2019	Additionally, treatment of senescent fibroblasts with aspirin or celecoxib, a COX2 specific inhibitor, reduced cell viability and decreased the levels of Bcl-xL protein.	Aspirin	54-61	prostaglandin-endoperoxide synthase 2	Mus musculus	78-82
18775538-8	2009	CONCLUSIONS: In the Women"s Health Study, carriers of an apolipoprotein(a) variant had elevated Lp(a), doubled cardiovascular risk, and appeared to benefit more from aspirin than non-carriers.	Aspirin	166-173	lipoprotein(a)	Homo sapiens	57-74
32123852-9	2019	Additionally, treatment of senescent fibroblasts with aspirin or celecoxib, a COX2 specific inhibitor, reduced cell viability and decreased the levels of Bcl-xL protein.	Aspirin	54-61	BCL2-like 1	Mus musculus	154-160
31265948-4	2019	In this study, aspirin reversed the epithelial-mesenchymal transition (EMT) by promoting miR-203 expression in cells, and, remarkably, it repressed exosomal LMP1 (exo-LMP1) secretion from EBV-positive cells.	Aspirin	15-22	microRNA 203a	Homo sapiens	89-96
19249429-0	2009	Assessment of P2Y(12) inhibition with the point-of-care device VerifyNow P2Y12 in patients treated with prasugrel or clopidogrel coadministered with aspirin.	Aspirin	149-156	purinergic receptor P2Y12	Homo sapiens	73-78
19146957-10	2009	The different effects of ASA on CD4(+)CD25(+)Foxp3(+) Treg cells and CD4(+)CD25(-) T cells may potentially make hosts susceptible to tolerance induction which would be beneficial for tolerance induction in patients with autoimmune diseases or allo-grafts.	Aspirin	25-28	forkhead box P3	Homo sapiens	45-50
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	Aspirin	45-52	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	185-191
19031027-8	2009	It has been possible to demonstrate that in aspirin treated, human DCs there is inhibition of the nuclear factor K-B (NFKB) signalling pathway, modified cytokine production, reduced expression of co-stimulatory molecules (CD40, CD80, and CD86) and increased expression of immunoglobulin-like transcript-3 (ILT3).	Aspirin	44-51	CD40 molecule	Homo sapiens	222-226
31265948-9	2019	The study revealed that aspirin is a promising drug for NPC therapy via its targeting of exo-LMP1 transfer and the regulatory effect of LMP1 on miR-203 expression.	Aspirin	24-31	microRNA 203a	Homo sapiens	144-151
31265948-11	2019	Our study also provides a rationale for the use of exo-LMP1 or exosomal miR-203 (exo-miR203) in EBV-targeted therapy by aspirin in invasive NPC.	Aspirin	120-127	microRNA 203a	Homo sapiens	72-79
19031027-8	2009	It has been possible to demonstrate that in aspirin treated, human DCs there is inhibition of the nuclear factor K-B (NFKB) signalling pathway, modified cytokine production, reduced expression of co-stimulatory molecules (CD40, CD80, and CD86) and increased expression of immunoglobulin-like transcript-3 (ILT3).	Aspirin	44-51	CD80 molecule	Homo sapiens	228-232
19031027-8	2009	It has been possible to demonstrate that in aspirin treated, human DCs there is inhibition of the nuclear factor K-B (NFKB) signalling pathway, modified cytokine production, reduced expression of co-stimulatory molecules (CD40, CD80, and CD86) and increased expression of immunoglobulin-like transcript-3 (ILT3).	Aspirin	44-51	CD86 molecule	Homo sapiens	238-242
31568119-4	2019	The purpose of this study was to explore the preliminary impact of a preset telephone alarm on medication adherence in adults prescribed ASA for 35 days after knee or hip arthroplasty.	Aspirin	137-140	hedgehog interacting protein	Homo sapiens	167-170
19262071-0	2009	Effect of genetic polymorphisms in UDP-glucuronosyltransferase 1A6 (UGT1A6) on acetylsalicylic acid metabolism in healthy female volunteers.	Aspirin	79-99	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	35-66
19262071-0	2009	Effect of genetic polymorphisms in UDP-glucuronosyltransferase 1A6 (UGT1A6) on acetylsalicylic acid metabolism in healthy female volunteers.	Aspirin	79-99	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	68-74
19262071-1	2009	OBJECTIVE: To compare plasma concentrations of acetylsalicylic acid (ASA) and its metabolites between genetic polymorphisms in the gene encoding for UDP-glucuronosyltransferase 1A6 (UGT1A6), an enzyme involved in ASA metabolism.	Aspirin	47-67	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	149-180
31002173-8	2019	Aspirin significantly reduced the stroke recurrence in patients with lacunar stroke analyzed with multivariate stepwise analysis using model of Cox proportional hazards with backward elimination (HR = 0.67, 95% CI 0.45-0.99).	Aspirin	0-7	cytochrome c oxidase subunit 8A	Homo sapiens	144-147
19262071-1	2009	OBJECTIVE: To compare plasma concentrations of acetylsalicylic acid (ASA) and its metabolites between genetic polymorphisms in the gene encoding for UDP-glucuronosyltransferase 1A6 (UGT1A6), an enzyme involved in ASA metabolism.	Aspirin	47-67	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	182-188
19262071-1	2009	OBJECTIVE: To compare plasma concentrations of acetylsalicylic acid (ASA) and its metabolites between genetic polymorphisms in the gene encoding for UDP-glucuronosyltransferase 1A6 (UGT1A6), an enzyme involved in ASA metabolism.	Aspirin	69-72	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	149-180
19262071-1	2009	OBJECTIVE: To compare plasma concentrations of acetylsalicylic acid (ASA) and its metabolites between genetic polymorphisms in the gene encoding for UDP-glucuronosyltransferase 1A6 (UGT1A6), an enzyme involved in ASA metabolism.	Aspirin	69-72	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	182-188
19262071-1	2009	OBJECTIVE: To compare plasma concentrations of acetylsalicylic acid (ASA) and its metabolites between genetic polymorphisms in the gene encoding for UDP-glucuronosyltransferase 1A6 (UGT1A6), an enzyme involved in ASA metabolism.	Aspirin	213-216	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	149-180
19262071-1	2009	OBJECTIVE: To compare plasma concentrations of acetylsalicylic acid (ASA) and its metabolites between genetic polymorphisms in the gene encoding for UDP-glucuronosyltransferase 1A6 (UGT1A6), an enzyme involved in ASA metabolism.	Aspirin	213-216	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	182-188
19262071-7	2009	CONCLUSION: In females receiving ASA, the presence of the UGT1A6*2 compared to the UGT1A6*1 homozygote genotype is associated with lower plasma levels of SA, indicating faster pharmacokinetics.	Aspirin	33-36	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	58-64
19262071-7	2009	CONCLUSION: In females receiving ASA, the presence of the UGT1A6*2 compared to the UGT1A6*1 homozygote genotype is associated with lower plasma levels of SA, indicating faster pharmacokinetics.	Aspirin	33-36	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	83-89
25860199-0	2015	[Direct inhibition of TRPV1 by acetylsalicylic acid : New effect of an old drug].	Aspirin	31-51	transient receptor potential cation channel subfamily V member 1	Homo sapiens	22-27
31098750-13	2019	However, aspirin treatment was associated with significantly increased risks of any bleeding (RR 1.63; 95% CI: 1.31-2.03; P &lt; 0.01), major bleeding (RR 1.41; 95% CI: 1.26-1.57; P &lt; 0.01), and GI bleeding (RR 1.85; 95% CI: 1.38-2.48; P &lt; 0.01) compared with placebo.	Aspirin	9-16	ribonucleotide reductase catalytic subunit M1	Homo sapiens	94-98
25781442-10	2015	In case-only interaction analysis, the SNP rs16973225 at chromosome 15q25.2 near the IL16 gene showed a genome-wide significant interaction with use of aspirin and/or NSAIDs (P = 8.2 x 10(-9) for interaction).	Aspirin	152-159	interleukin 16	Homo sapiens	85-89
31098750-13	2019	However, aspirin treatment was associated with significantly increased risks of any bleeding (RR 1.63; 95% CI: 1.31-2.03; P &lt; 0.01), major bleeding (RR 1.41; 95% CI: 1.26-1.57; P &lt; 0.01), and GI bleeding (RR 1.85; 95% CI: 1.38-2.48; P &lt; 0.01) compared with placebo.	Aspirin	9-16	ribonucleotide reductase catalytic subunit M1	Homo sapiens	152-156
31098750-13	2019	However, aspirin treatment was associated with significantly increased risks of any bleeding (RR 1.63; 95% CI: 1.31-2.03; P &lt; 0.01), major bleeding (RR 1.41; 95% CI: 1.26-1.57; P &lt; 0.01), and GI bleeding (RR 1.85; 95% CI: 1.38-2.48; P &lt; 0.01) compared with placebo.	Aspirin	9-16	ribonucleotide reductase catalytic subunit M1	Homo sapiens	152-156
29335863-7	2019	Aspirin combined NXT and the adjusted-dose warfarin was equally effective in elderly patients with non-valvular AF in prevention of ischemic stroke.	Aspirin	0-7	nuclear transport factor 2 like export factor 1	Homo sapiens	17-20
30604228-0	2019	Aspirin attenuates podocyte injury in diabetic rats through overriding cyclooxygenase-2-mediated dysregulation of LDL receptor pathway.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	71-87
30604228-12	2019	However, when COX-2 expression was inhibited by aspirin, these changes in the DM rats were significantly attenuated.	Aspirin	48-55	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	14-19
30017554-10	2019	CONCLUSIONS: MC-intrinsic COX-1 amplifies IL-33-induced activation in the setting of innate type 2 immunity and might help explain the phenomenon of therapeutic desensitization to aspirin by nonselective COX inhibitors in patients with AERD.	Aspirin	180-187	interleukin 33	Homo sapiens	42-47
28974130-9	2019	In the subgroup that received aspirin before 11 weeks (110 cases), irrespective of the dosage, the uterine blood flow is significantly improved (average uterine PI 1.7 compared with 2.22, p &lt; .05, (0.24-0.7) 95% CI) and the PAPP-A levels are higher (1.2 compared with 0.82, p &gt; .05, [(-0.65) - 0.02] 95% CI).	Aspirin	30-37	pappalysin 1	Homo sapiens	227-233
30215226-6	2019	RESULTS: In Col/EPI, 73.2% (365/499), 72.6% (390/537), and 55.3% (3,442/6,228) patients showed prolonged CTs for aspirin, clopidogrel, and NSAIDs, respectively.	Aspirin	113-120	tissue factor pathway inhibitor	Homo sapiens	16-19
29439623-8	2018	Additionally, aspirin also reversed T0070907-induced changes in the levels of thromboxane B2, vascular endothelial growth factor, soluble fms-like tyrosine kinase, and matrix metalloproteinase 2 in both maternal blood and placental tissue.	Aspirin	14-21	matrix metallopeptidase 2	Rattus norvegicus	168-194
29439623-9	2018	The increased messenger RNA and protein levels of Cox1 and Cox2 induced by T0070907 were markedly reduced by aspirin treatment.	Aspirin	109-116	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	59-63
30120100-0	2018	Aspirin enhances the sensitivity of hepatocellular carcinoma side population cells to doxorubicin via miR-491/ABCG2.	Aspirin	0-7	microRNA 491	Homo sapiens	102-109
30120100-1	2018	Objective: To explore whether aspirin (ASA) enhances the sensitivity of hepatocellular carcinoma (HCC) side population (SP) cells to doxorubicin (Doxo) via miR-491/ATP-binding cassette sub-family G member 2 (ABCG2).Methods: Non-SP and SP cells were isolated from MHCC-97L cell line using flow cytometry analysis and fluorescence-activated cell sorting.	Aspirin	30-37	microRNA 491	Homo sapiens	156-163
30120100-1	2018	Objective: To explore whether aspirin (ASA) enhances the sensitivity of hepatocellular carcinoma (HCC) side population (SP) cells to doxorubicin (Doxo) via miR-491/ATP-binding cassette sub-family G member 2 (ABCG2).Methods: Non-SP and SP cells were isolated from MHCC-97L cell line using flow cytometry analysis and fluorescence-activated cell sorting.	Aspirin	39-42	microRNA 491	Homo sapiens	156-163
30389909-10	2018	Notably, aspirin attenuates E2-induced cancer stem-like traits through decreasing both H19 and ERbeta expression.	Aspirin	9-16	estrogen receptor 2	Homo sapiens	95-101
31198543-13	2019	Higher CTRP1 levels were associated with slower renal progression (hazard ratio 0.992, 95% confidence interval 0.986-0.998; P = 0.001) in a model adjusted for obesity, aspirin, albuminuria and renal function.	Aspirin	168-175	C1q and TNF related 1	Homo sapiens	7-12
25743752-0	2015	Aspirin regulates hepatocellular lipid metabolism by activating AMPK signaling pathway.	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	64-68
30021726-2	2018	Potential anticancer effects of ASA may be mediated by its ability to suppress prostaglandin E2 (PGE2) production and activate 5"-adenosine monophosphate-activated protein kinase (AMPK).	Aspirin	32-35	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	180-184
25743752-3	2015	We presently investigated aspirin"s promotion of AMP-activated protein kinase (AMPK) pathway activation in human hepatoma HepG2 cells by examining AMPK expression, the promotion of AMPK activation.	Aspirin	26-33	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	49-77
25743752-3	2015	We presently investigated aspirin"s promotion of AMP-activated protein kinase (AMPK) pathway activation in human hepatoma HepG2 cells by examining AMPK expression, the promotion of AMPK activation.	Aspirin	26-33	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	79-83
25743752-3	2015	We presently investigated aspirin"s promotion of AMP-activated protein kinase (AMPK) pathway activation in human hepatoma HepG2 cells by examining AMPK expression, the promotion of AMPK activation.	Aspirin	26-33	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	147-151
25743752-3	2015	We presently investigated aspirin"s promotion of AMP-activated protein kinase (AMPK) pathway activation in human hepatoma HepG2 cells by examining AMPK expression, the promotion of AMPK activation.	Aspirin	26-33	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	147-151
25743752-4	2015	Then we investigated the influence of aspirin-promoted AMPK signaling on fatty acid oxidation in HepG2 cells.	Aspirin	38-45	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	55-59
25743752-5	2015	The results demonstrated that aspirin treatment did not regulate the expression of AMPK and its downstream target, Acetyl-Coenzyme A Carboxylase (ACC), but activated the AMPK signaling pathway by promoting the phosphorylation of AMPK and ACC.	Aspirin	30-37	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	170-174
25743752-5	2015	The results demonstrated that aspirin treatment did not regulate the expression of AMPK and its downstream target, Acetyl-Coenzyme A Carboxylase (ACC), but activated the AMPK signaling pathway by promoting the phosphorylation of AMPK and ACC.	Aspirin	30-37	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	170-174
26379740-7	2015	Furthermore, paeonol, a representative component of Moutan cortex, and aspirin which is known to have platelet aggregation-inhibiting activity (COX-1 inhibitor) also showed similar effects.	Aspirin	71-78	cytochrome c oxidase subunit I	Cavia porcellus	144-149
18840621-4	2008	Simvastatin, aspirin, metoprolol, and isosorbide mononitrate significantly decreased plasma total adenosine activity (by 50%, 34%, 29%, and 19%, respectively; P &lt; .05 to P &lt; .001) mainly by decreasing the activity of ADA(2).	Aspirin	13-20	transcriptional adaptor 2A	Homo sapiens	223-229
30021726-5	2018	ASA-mediated inhibition of cell migration and pigmentation was rescued by exogenous PGE2 or Compound C, which inhibits AMPK activation.	Aspirin	0-3	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	119-123
18930406-6	2008	However, the hydroxymethyl compounds 10a-b and the parent NONO-coxibs 12a-b exhibited good AI activities (ED(50)=76.7-111.6 micromol/kg po range) that were greater than that exhibited by the reference drugs aspirin (ED(50)=710 micromol/kg po) and ibuprofen (ED(50)=327 micromol/kg po), but less than that of celecoxib (ED(50)=30.9mumol/kg po).	Aspirin	207-214	non-POU domain containing octamer binding	Homo sapiens	58-62
30021726-9	2018	ASA-treated mice bearing sensitive and resistant tumors exhibited both decreased PGE2 in plasma and tumors and increased phosphorylated AMPK in tumors.	Aspirin	0-3	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	136-140
18667601-0	2008	Aspirin induces gastric epithelial barrier dysfunction by activating p38 MAPK via claudin-7.	Aspirin	0-7	claudin 7	Homo sapiens	82-91
30021726-10	2018	We conclude that ASA inhibits colony formation, cell motility, and pigmentation through suppression of PGE2 and activation of AMPK and reduces growth of some melanoma tumors in vivo This preclinical model could be used for further tumor and biomarker studies to support future melanoma chemoprevention trials in humans.	Aspirin	17-20	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	126-130
18667601-6	2008	Aspirin significantly decreased the quantity of claudin-7 protein produced by MKN28 cells but not the quantity of claudin-3, claudin-4, ZO-1, or occludin.	Aspirin	0-7	claudin 7	Homo sapiens	48-57
25524333-1	2014	BACKGROUND: After percutaneous coronary intervention (PCI) for non-ST-segment elevation myocardial infarction (NSTEMI), treatment with a P2Y12 antagonist with aspirin is recommended for 1 year.	Aspirin	159-166	purinergic receptor P2Y12	Homo sapiens	137-142
18667601-7	2008	The aspirin-induced decrease in claudin-7 protein was completely abolished by SB-203580 pretreatment.	Aspirin	4-11	claudin 7	Homo sapiens	32-41
18667601-8	2008	These results demonstrate, for the first time, that claudin-7 protein is important in aspirin-induced gastric barrier loss and that p38 MAPK activity mediates this epithelial barrier dysfunction.	Aspirin	86-93	claudin 7	Homo sapiens	52-61
29805889-0	2014	Association Between the P2RY12 Receptor Gene Polymorphism and Aspirin Resistance in Patients with Coronary Artery Disease.	Aspirin	62-69	purinergic receptor P2Y12	Homo sapiens	24-30
30280037-9	2018	Analysis using the cBio portal indicated that aspirin might have effects on multiple tumor suppressors, such as TP53, PTEN, and RB1 and that TP53 might play a central role in aspirin-associated genes.	Aspirin	46-53	RB transcriptional corepressor 1	Homo sapiens	128-131
29805889-4	2014	Aim: We investigated the association of P2RY12 gene polymorphisms with aspirin resistance in patients with coronary artery disease (CAD).	Aspirin	71-78	purinergic receptor P2Y12	Homo sapiens	40-46
29779133-8	2018	The findings also indicate that aspirin may induce HSP60 and HSP47 expression in renal cells.	Aspirin	32-39	heat shock protein family D (Hsp60) member 1	Gallus gallus	51-56
25106115-6	2014	In Huh7 replicon cells treated with ASA, we found decreased levels of iNOS mRNA, iNOS protein and nitrosylated protein levels at 48-72 h. ASA exposure also reduced the transactivation of the iNOS promoter in HCV replicon cells at 48 h, and this was partly due to the decrease in the affinity of transcription factor C/EBP-beta for its binding site in the iNOS promoter.	Aspirin	36-39	CCAAT enhancer binding protein beta	Homo sapiens	316-326
29779133-9	2018	Finally, the expression patterns of HSP60 and HSP47 indicated that they may play a renoprotective role, as their expression was higher in the aspirin-treated groups.	Aspirin	142-149	heat shock protein family D (Hsp60) member 1	Gallus gallus	36-41
24506800-10	2014	When acetylsalicylic acid was combined with simvastatin treatment, the intraocular levels of Ang-2 and VEGF were significantly lower than in diabetics treated with simvastatin alone.	Aspirin	5-25	angiopoietin 2	Homo sapiens	93-98
29779133-10	2018	In conclusion, the present findings show that heat stress causes renal damage in poultry and that aspirin may play a protective role against this damage via pathways that involve HSP60 and HSP47.	Aspirin	98-105	heat shock protein family D (Hsp60) member 1	Gallus gallus	179-184
25035343-3	2014	It further aimed to evaluate whether aspirin, a commonly used CVD prevention agent, modified the potential association of COMT with incident CVD.	Aspirin	37-44	catechol-O-methyltransferase	Homo sapiens	122-126
30214631-0	2018	Aspirin cooperates with p300 to activate the acetylation of H3K9 and promote FasL-mediated apoptosis of cancer stem-like cells in colorectal cancer.	Aspirin	0-7	E1A binding protein p300	Homo sapiens	24-28
25035343-4	2014	APPROACH AND RESULTS: We examined COMT polymorphism rs4680 (MAF [minor allele frequency], 0.47), encoding a nonsynonymous methionine-to-valine substitution, in the Women"s Genome Health Study (WGHS), a large population-based cohort of women with randomized allocation to aspirin or vitamin E when compared with placebo and 10-year follow-up.	Aspirin	271-278	catechol-O-methyltransferase	Homo sapiens	34-38
25035343-10	2014	CONCLUSIONS: Common COMT polymorphisms were associated with incident CVD, and this association was modified by randomized allocation to aspirin or vitamin E.	Aspirin	136-143	catechol-O-methyltransferase	Homo sapiens	20-24
24994462-6	2014	The most common HLA haplotypes in the different asthma phenotypes are HLA-DRB1in allergic asthma, HLA-DQB1in occupational asthma and HLA-DPB1 in aspirin-sensitive asthma.	Aspirin	145-152	major histocompatibility complex, class II, DP beta 1	Homo sapiens	133-141
30214631-9	2018	Furthermore, aspirin directly interacts with p300 in the nucleus, promotes H3K9 acetylation, activates FasL expression, and induces apoptosis in colorectal CSCs.	Aspirin	13-20	E1A binding protein p300	Homo sapiens	45-49
30214631-12	2018	Conclusions: Taken together, we revealed a unique epigenetic and cox-independent pathway (p300-AcH3K9-FasL axis) by which aspirin eliminates colorectal CSCs.	Aspirin	122-129	E1A binding protein p300	Homo sapiens	90-94
30034291-8	2018	In the coculture of both cells, aspirin inhibited secretion of MCP-1, IL-6, and TGF-beta.	Aspirin	32-39	transforming growth factor, beta 1	Mus musculus	80-88
25079372-2	2014	We found that accumulation of the threonine pathway intermediate beta-aspartate semialdehyde (ASA), substrate of homoserine dehydrogenase (Hom6), attenuates the GAAC transcriptional response by accelerating degradation of Gcn4, already an exceedingly unstable protein, in cells starved for isoleucine and valine.	Aspirin	94-97	homoserine dehydrogenase	Saccharomyces cerevisiae S288C	139-143
30034291-9	2018	Furthermore, aspirin significantly decreased the M2 macrophage marker CD206, but increased M1 marker CD11c expression.	Aspirin	13-20	integrin alpha X	Mus musculus	101-106
25079372-2	2014	We found that accumulation of the threonine pathway intermediate beta-aspartate semialdehyde (ASA), substrate of homoserine dehydrogenase (Hom6), attenuates the GAAC transcriptional response by accelerating degradation of Gcn4, already an exceedingly unstable protein, in cells starved for isoleucine and valine.	Aspirin	94-97	amino acid starvation-responsive transcription factor GCN4	Saccharomyces cerevisiae S288C	222-226
25079372-3	2014	The reduction in Gcn4 abundance on ASA accumulation requires Cdk8/Srb10 and Pho85, cyclin-dependent kinases (CDKs) known to mediate rapid turnover of Gcn4 by the proteasome via phosphorylation of the Gcn4 activation domain under nonstarvation conditions.	Aspirin	35-38	amino acid starvation-responsive transcription factor GCN4	Saccharomyces cerevisiae S288C	17-21
29781520-6	2018	A significant association with poor responsiveness to aspirin was observed for GP1BA rs2243093, PTGS1 rs1330344, PTGS2 rs689466 and TBXA2R rs1131882 polymorphisms in overall analyses.	Aspirin	54-61	thromboxane A2 receptor	Homo sapiens	132-138
25079372-3	2014	The reduction in Gcn4 abundance on ASA accumulation requires Cdk8/Srb10 and Pho85, cyclin-dependent kinases (CDKs) known to mediate rapid turnover of Gcn4 by the proteasome via phosphorylation of the Gcn4 activation domain under nonstarvation conditions.	Aspirin	35-38	amino acid starvation-responsive transcription factor GCN4	Saccharomyces cerevisiae S288C	150-154
25079372-3	2014	The reduction in Gcn4 abundance on ASA accumulation requires Cdk8/Srb10 and Pho85, cyclin-dependent kinases (CDKs) known to mediate rapid turnover of Gcn4 by the proteasome via phosphorylation of the Gcn4 activation domain under nonstarvation conditions.	Aspirin	35-38	amino acid starvation-responsive transcription factor GCN4	Saccharomyces cerevisiae S288C	150-154
29781520-7	2018	Further subgroup analyses demonstrated that ITGA2 rs1126643, PTGS1 rs1330344, PTGS2 rs20417, PTGS2 rs689466 and TBXA2R rs1131882 polymorphisms were significantly associated with poor responsiveness to aspirin in Asians, whereas only GP1BA rs2243093 polymorphism was significantly correlated with this phenomenon in Caucasians.	Aspirin	201-208	integrin subunit alpha 2	Homo sapiens	44-49
25079372-5	2014	These and other findings suggest that the two CDKs target different populations of Gcn4 on ASA accumulation, with Srb10 clearing mostly inactive Gcn4 molecules at the promoter that are enriched for sumoylation of the activation domain, and Pho85 clearing molecules unbound to the UAS that include both fully functional and inactive Gcn4 species.	Aspirin	91-94	amino acid starvation-responsive transcription factor GCN4	Saccharomyces cerevisiae S288C	83-87
24837419-5	2014	Aspirin and the nonsteroid anti-inflammatory drug (NSAID) ketoprofen, at clinically relevant doses, have been proposed to inhibit amyloid formation by amylin and thus may hold promise for treatment of islet amyloidosis.	Aspirin	0-7	islet amyloid polypeptide	Homo sapiens	151-157
29781520-8	2018	In conclusion, our findings indicate that GP1BA rs2243093, ITGA2 rs1126643, PTGS1 rs1330344, PTGS2 rs20417, PTGS2 rs689466 and TBXA2R rs1131882 polymorphisms may serve as genetic biomarkers of poor responsiveness to aspirin in certain ethnic groups.	Aspirin	216-223	thromboxane A2 receptor	Homo sapiens	127-133
29381509-9	2018	Moreover, the ratio of apoptotic neurons in the anterior horn and the levels of the apoptosis-related proteins caspase-3, cleaved caspase-3, and Bax were significantly decreased in the aspirin group compared with the vehicle group.	Aspirin	185-192	caspase 3	Rattus norvegicus	111-120
29381509-9	2018	Moreover, the ratio of apoptotic neurons in the anterior horn and the levels of the apoptosis-related proteins caspase-3, cleaved caspase-3, and Bax were significantly decreased in the aspirin group compared with the vehicle group.	Aspirin	185-192	caspase 3	Rattus norvegicus	130-139
29397336-11	2018	CONCLUSION: Artesunate markedly ameliorated aspirin induced gastric injury in rats by targeting oxidative stress and COX-2 dependent as well as COX-2 independent proinflammatory signaling pathways and could have a therapeutic potential in gastric ulcer disease.	Aspirin	44-51	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	117-122
29397336-11	2018	CONCLUSION: Artesunate markedly ameliorated aspirin induced gastric injury in rats by targeting oxidative stress and COX-2 dependent as well as COX-2 independent proinflammatory signaling pathways and could have a therapeutic potential in gastric ulcer disease.	Aspirin	44-51	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	144-149
30415260-12	2018	RESULTS: Aspirin induced morphological apoptosis in rat TSCs via the mitochondrial/caspase-3 pathway and induced cellular apoptosis in the Achilles tendon.	Aspirin	9-16	caspase 3	Rattus norvegicus	83-92
30415260-14	2018	Aspirin administration led to a dose-dependent increase in COX-2 expression.	Aspirin	0-7	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	59-64
30415260-16	2018	CONCLUSION: The Wnt/beta-catenin pathway plays a vital role in aspirin-induced apoptosis by regulating mitochondrial/caspase-3 function.	Aspirin	63-70	caspase 3	Rattus norvegicus	117-126
29518782-0	2018	Aspirin Reduces Cardiac Interstitial Fibrosis by Inhibiting Erk1/2-Serpine2 and P-Akt Signalling Pathways.	Aspirin	0-7	mitogen-activated protein kinase 3	Mus musculus	60-66
29518782-0	2018	Aspirin Reduces Cardiac Interstitial Fibrosis by Inhibiting Erk1/2-Serpine2 and P-Akt Signalling Pathways.	Aspirin	0-7	serine (or cysteine) peptidase inhibitor, clade E, member 2	Mus musculus	67-75
29518782-9	2018	The enhanced phosphorylation of Erk1/2 caused by TAC (p-Erk1, 1.49+-0.19-fold; p-Erk2, 1.96+-0.68-fold) was suppressed by aspirin (p-Erk1, 1.04+-0.15-fold; p-Erk2, 0.87+-0.06-fold).	Aspirin	122-129	mitogen-activated protein kinase 3	Mus musculus	32-38
29518782-9	2018	The enhanced phosphorylation of Erk1/2 caused by TAC (p-Erk1, 1.49+-0.19-fold; p-Erk2, 1.96+-0.68-fold) was suppressed by aspirin (p-Erk1, 1.04+-0.15-fold; p-Erk2, 0.87+-0.06-fold).	Aspirin	122-129	mitogen-activated protein kinase 3	Mus musculus	32-36
29518782-9	2018	The enhanced phosphorylation of Erk1/2 caused by TAC (p-Erk1, 1.49+-0.19-fold; p-Erk2, 1.96+-0.68-fold) was suppressed by aspirin (p-Erk1, 1.04+-0.15-fold; p-Erk2, 0.87+-0.06-fold).	Aspirin	122-129	mitogen-activated protein kinase 3	Mus musculus	56-60
29518782-10	2018	SerpinE2 levels were suppressed via the Erk1/2 signalling pathway following treatment with aspirin (1.36+-0.12-fold for TAC; 1.06+-0.07-fold for aspirin+TAC).	Aspirin	91-98	serine (or cysteine) peptidase inhibitor, clade E, member 2	Mus musculus	0-8
29518782-10	2018	SerpinE2 levels were suppressed via the Erk1/2 signalling pathway following treatment with aspirin (1.36+-0.12-fold for TAC; 1.06+-0.07-fold for aspirin+TAC).	Aspirin	91-98	mitogen-activated protein kinase 3	Mus musculus	40-46
29518782-10	2018	SerpinE2 levels were suppressed via the Erk1/2 signalling pathway following treatment with aspirin (1.36+-0.12-fold for TAC; 1.06+-0.07-fold for aspirin+TAC).	Aspirin	145-152	serine (or cysteine) peptidase inhibitor, clade E, member 2	Mus musculus	0-8
29518782-10	2018	SerpinE2 levels were suppressed via the Erk1/2 signalling pathway following treatment with aspirin (1.36+-0.12-fold for TAC; 1.06+-0.07-fold for aspirin+TAC).	Aspirin	145-152	mitogen-activated protein kinase 3	Mus musculus	40-46
29518782-12	2018	CONCLUSIONS: Our study reveals a novel mechanism by which aspirin alleviates pressure overload-induced cardiac interstitial fibrosis in TAC mice by suppressing the p-Erk1/2 and p-Akt/beta-catenin signalling pathways.	Aspirin	58-65	mitogen-activated protein kinase 3	Mus musculus	166-172
29345592-2	2018	On top of aspirin, P2Y12- inhibitors are successfully used to treat and prevent these events for a duration of one year after an acute coronary episode or 6 months after drug-eluting stent implantation.	Aspirin	10-17	purinergic receptor P2Y12	Homo sapiens	19-24
29129512-2	2018	The thieno[3,2-c]pyridine class of therapeutic agents, of which clopidogrel is the most commonly used, target the P2Y12 receptor, and are often used in combination with acetylsalicylic acid (ASA).	Aspirin	191-194	purinergic receptor P2Y12	Homo sapiens	114-119
29343628-13	2018	Indeed, some existing drugs such as metformin and aspirin, which were derived from traditional herbal remedies, appear to work, in part, by activating AMPK.	Aspirin	50-57	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	151-155
28987816-1	2018	To understand the potential mechanisms involved in the beneficial effects of aspirin (ASA) in mood disorders, Alzheimer"s (AD) and Parkinson"s disease (PD), we investigated the effects of ASA on the expression of iron transport proteins transferrin receptor 1 (TfR1), ferroportin 1 (Fpn1), and iron storage protein ferritin light chain (Ft-L) in interleukin-6 (IL-6)-treated PC-12 cells.	Aspirin	188-191	transferrin receptor	Rattus norvegicus	237-259
24781569-16	2014	CONCLUSIONS: Our study revealed that ASA physical status class is associated with increased SICU length of stay, mechanical ventilation, vasopressor treatment duration, NOD, readmission to ICU, and surgery risk is associated with NOD.	Aspirin	37-40	atrophin 1	Homo sapiens	169-172
28439613-12	2017	Only one patient taking aspirin as a sole agent had a delayed injury on D-CTH (1.1%, 95% CI 0-4.2%).	Aspirin	24-31	V-set and immunoglobulin domain containing 2	Homo sapiens	74-77
24781569-16	2014	CONCLUSIONS: Our study revealed that ASA physical status class is associated with increased SICU length of stay, mechanical ventilation, vasopressor treatment duration, NOD, readmission to ICU, and surgery risk is associated with NOD.	Aspirin	37-40	atrophin 1	Homo sapiens	230-233
24687028-3	2014	OBJECTIVE: To demonstrate that survival benefit associated with low-dose aspirin use after a diagnosis of colorectal cancer might depend on HLA class I antigen expression.	Aspirin	73-80	MHC class I polypeptide-related sequence A	Homo sapiens	140-159
24687028-9	2014	RESULTS: The overall survival benefit associated with aspirin use after a diagnosis of colon cancer had an adjusted rate ratio (RR) of 0.53 (95% CI, 0.38-0.74; P &lt; .001) when tumors expressed HLA class I antigen compared with an RR of 1.03 (0.66-1.61; P = .91) when HLA antigen expression was lost.	Aspirin	54-61	MHC class I polypeptide-related sequence A	Homo sapiens	195-214
24687028-12	2014	CONCLUSIONS AND RELEVANCE: Contrary to the original hypothesis, aspirin use after colon cancer diagnosis was associated with improved survival if tumors expressed HLA class I antigen.	Aspirin	64-71	MHC class I polypeptide-related sequence A	Homo sapiens	163-182
24687028-14	2014	HLA class I antigen might serve as a predictive biomarker for adjuvant aspirin therapy in colon cancer.	Aspirin	71-78	MHC class I polypeptide-related sequence A	Homo sapiens	0-19
24495935-0	2014	Acetylsalicylic acid enhances tachyphylaxis of repetitive capsaicin responses in TRPV1-GFP expressing HEK293 cells.	Aspirin	0-20	transient receptor potential cation channel subfamily V member 1	Homo sapiens	81-86
18503633-12	2008	Treatments exerted no effect on vascular Cox-1 mRNA whereas Cox-2 mRNA was moderately reduced by aspirin and triflusal (placebo 100% +/- 9%, aspirin 70% +/- 2% and triflusal 70% +/- 2%; P &lt; 0.05).	Aspirin	97-104	cytochrome c oxidase subunit II	Oryctolagus cuniculus	60-65
18503633-12	2008	Treatments exerted no effect on vascular Cox-1 mRNA whereas Cox-2 mRNA was moderately reduced by aspirin and triflusal (placebo 100% +/- 9%, aspirin 70% +/- 2% and triflusal 70% +/- 2%; P &lt; 0.05).	Aspirin	141-148	cytochrome c oxidase subunit II	Oryctolagus cuniculus	60-65
18503633-13	2008	Cox-2 protein levels were slightly higher in the triflusal versus aspirin group (placebo 100% +/- 6%, aspirin 35% +/- 10% and triflusal 61% +/- 9%; P &lt; 0.005 versus placebo).	Aspirin	66-73	cytochrome c oxidase subunit II	Oryctolagus cuniculus	0-5
18503633-13	2008	Cox-2 protein levels were slightly higher in the triflusal versus aspirin group (placebo 100% +/- 6%, aspirin 35% +/- 10% and triflusal 61% +/- 9%; P &lt; 0.005 versus placebo).	Aspirin	102-109	cytochrome c oxidase subunit II	Oryctolagus cuniculus	0-5
24495935-2	2014	ASA also inhibits capsaicin- and heat-induced responses in cultured dorsal root ganglia (DRG) neurons, suggesting TRPV1 (transient receptor potential channel of the vanilloid receptor family, subtype 1) to be an additional target of ASA.	Aspirin	0-3	transient receptor potential cation channel subfamily V member 1	Homo sapiens	114-119
29285098-0	2017	Aspirin suppresses TNF-alpha-induced MMP-9 expression via NF-kappaB and MAPK signaling pathways in RAW264.7 cells.	Aspirin	0-7	matrix metallopeptidase 9	Mus musculus	37-42
24495935-2	2014	ASA also inhibits capsaicin- and heat-induced responses in cultured dorsal root ganglia (DRG) neurons, suggesting TRPV1 (transient receptor potential channel of the vanilloid receptor family, subtype 1) to be an additional target of ASA.	Aspirin	233-236	transient receptor potential cation channel subfamily V member 1	Homo sapiens	114-119
24495935-3	2014	We now studied the effect of ASA on heterologously expressed rat TRPV1 using calcium microfluorimetry.	Aspirin	29-32	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	65-70
29285098-3	2017	The present study aimed to investigate the pharmacological effects of aspirin on tumor necrosis factor-alpha (TNF-alpha)-induced MMP-9 expression and the underlying molecular mechanisms in murine macrophage RAW264.7 cells.	Aspirin	70-77	matrix metallopeptidase 9	Mus musculus	129-134
24495935-7	2014	These data suggest that ASA increases the tachyphylaxis of rTRPV1 channel activation.	Aspirin	24-27	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	59-65
29285098-4	2017	Western blot analysis indicated that the protein level of MMP-9 was reduced by aspirin in a dose-dependent manner.	Aspirin	79-86	matrix metallopeptidase 9	Mus musculus	58-63
29285098-5	2017	In addition, downregulation of MMP-9 mRNA and activity were detected in aspirin-treated cells using quantitative polymerase chain reaction and a gelatin zymography assay separately.	Aspirin	72-79	matrix metallopeptidase 9	Mus musculus	31-36
29218104-6	2017	We further analyzed the expression of cyclins and found that the level of cyclin D1 was significantly reduced after aspirin treatment, while there was no obvious effect on the levels of cyclin A2 and cyclin E1.	Aspirin	116-123	cyclin D1	Homo sapiens	74-83
24587951-0	2014	Polymorphisms of ATF6B Are Potentially Associated With FEV1 Decline by Aspirin Provocation in Asthmatics.	Aspirin	71-78	activating transcription factor 6 beta	Homo sapiens	17-22
24587951-3	2014	The aim of this study is to investigate the associations of ATF6B genetic variants with aspirin-exacerbated respiratory disease (AERD) and its major phenotype, % decline of FEV1 by aspirin provocation.	Aspirin	88-95	activating transcription factor 6 beta	Homo sapiens	60-65
24587951-3	2014	The aim of this study is to investigate the associations of ATF6B genetic variants with aspirin-exacerbated respiratory disease (AERD) and its major phenotype, % decline of FEV1 by aspirin provocation.	Aspirin	181-188	activating transcription factor 6 beta	Homo sapiens	60-65
24587951-4	2014	METHODS: Four common single nucleotide polymorphisms (SNPs) of ATF6B were genotyped and statistically analyzed in 93 AERD patients and 96 aspirin-tolerant asthma (ATA) as controls.	Aspirin	138-145	activating transcription factor 6 beta	Homo sapiens	63-68
24587951-6	2014	CONCLUSIONS: Although further functional and replication studies are needed, our preliminary findings suggest that ATF6B may be related to obstructive phenotypes in response to aspirin exposure in adult asthmatics.	Aspirin	177-184	activating transcription factor 6 beta	Homo sapiens	115-120
24555545-2	2014	Thus, functional alterations of the RAB1A gene may contribute to aspirin intolerance in asthmatic sufferers.	Aspirin	65-72	RAB1A, member RAS oncogene family	Homo sapiens	36-41
24555545-3	2014	To investigate the relationship between single-nucleotide polymorphisms (SNPs) in the RAB1A gene and aspirin-exacerbated respiratory disease (AERD), asthmatics (n=1197) were categorized into AERD and aspirin-tolerant asthma (ATA).	Aspirin	101-108	RAB1A, member RAS oncogene family	Homo sapiens	86-91
24555545-3	2014	To investigate the relationship between single-nucleotide polymorphisms (SNPs) in the RAB1A gene and aspirin-exacerbated respiratory disease (AERD), asthmatics (n=1197) were categorized into AERD and aspirin-tolerant asthma (ATA).	Aspirin	200-207	RAB1A, member RAS oncogene family	Homo sapiens	86-91
24309957-0	2014	Impact of aspirin dosing on the effects of P2Y12 inhibition in patients with acute coronary syndromes.	Aspirin	10-17	purinergic receptor P2Y12	Homo sapiens	43-48
24309957-3	2014	In the Platelet Inhibition and Patients Outcome (PLATO) study, higher doses of aspirin appeared to neutralise the additional benefit of the potent P2Y12 inhibitor ticagrelor compared to clopidogrel (Circulation 124: 544-554, 2011).	Aspirin	79-86	purinergic receptor P2Y12	Homo sapiens	147-152
24209633-5	2014	Furthermore, the PTP inhibitor mitigated the inhibitory effect of aspirin on COX-2 and PGE(2) upregulation and NF-kappaB activation, whereas the PKC inhibitor enhanced the inhibitory effects of aspirin on the production of COX-2 and PGE(2).	Aspirin	66-73	protein tyrosine phosphatase receptor type U	Homo sapiens	17-20
24190973-8	2014	The activation of p53 through AMPK-mediated MDMX phosphorylation and inactivation was further confirmed by using cell and animal model systems with two AMPK activators, metformin and salicylate (the active form of aspirin).	Aspirin	214-221	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	30-34
24433129-7	2014	Postoperatively, after administration of 4-6 doses of aspirin, beta-TG increased by 16.7% and 8-iso-PGF2alpha increased by 17.2% 5-7 days after surgery (p = 0.005 and p &lt; 0.001, respectively).	Aspirin	54-61	pro-platelet basic protein	Homo sapiens	63-70
23871514-10	2014	The Asp treatment significantly reduced fracture-increased echogenicity (hyperechogenicity, p&lt;0.05) in ultrasound images as well as inhibited cell death, and expression of COX-2 and BLT1.	Aspirin	4-7	prostaglandin-endoperoxide synthase 2	Mus musculus	175-180
18260128-5	2008	We found that treatment with ASA and APT102 in combination (ASA + APT102), but not either drug alone, significantly decreased breast cancer and melanoma bone metastases in mice with fewer bleeding complications than observed with alphaIIb beta3 inhibition.	Aspirin	29-32	calcium channel, voltage-dependent, beta 3 subunit	Mus musculus	239-244
18506123-21	2008	The favorable clinical outcomes with aspirin and clopidogrel have validated COX-1 and P2Y12 receptors as targets for new drug development.	Aspirin	37-44	purinergic receptor P2Y12	Homo sapiens	86-91
18335236-6	2008	ASA treatment of Arabidopsis cells induces typical PCD-linked morphological and biochemical changes, namely cell shrinkage, nuclear DNA degradation, loss of mitochondrial membrane potential, cytochrome c release from mitochondria and induction of caspase-like activity.	Aspirin	0-3	Cytochrome c	Arabidopsis thaliana	191-203
18414055-6	2008	Transfection of small interfering (si) RNA to Raf1 decreased differentiation of U937 cells induced by a combination of ASA or indomethacin with 1,25D.	Aspirin	119-122	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	46-50
18497555-5	2008	Aspirin resistance was defined as a closure time of less than 186 seconds with Col/Epi cartridges despite regular aspirin therapy.	Aspirin	0-7	tissue factor pathway inhibitor	Homo sapiens	83-86
18991696-8	2008	Pharmacogenetic studies on aspirin hypersensitivity have identified distinct types of predictors, such as HLA genotypes, a polymorphism in the promoter of the FcepsilonRIalpha gene, and variants in genes of enzymes from the arachidonic acid pathway.	Aspirin	27-34	Fc epsilon receptor Ia	Homo sapiens	159-175
19090241-6	2007	Both selective COX-2 inhibitor (celecoxib) and non-selective COX-2 inhibitor (aspirin) decreased the rigidity of parkinsonian rats p<0.05 but rigidity recovery after administration the selective COX-2 inhibitor was more than non-selective COX-2 inhibitor.	Aspirin	78-85	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	61-66
19090241-6	2007	Both selective COX-2 inhibitor (celecoxib) and non-selective COX-2 inhibitor (aspirin) decreased the rigidity of parkinsonian rats p<0.05 but rigidity recovery after administration the selective COX-2 inhibitor was more than non-selective COX-2 inhibitor.	Aspirin	78-85	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	61-66
19090241-6	2007	Both selective COX-2 inhibitor (celecoxib) and non-selective COX-2 inhibitor (aspirin) decreased the rigidity of parkinsonian rats p<0.05 but rigidity recovery after administration the selective COX-2 inhibitor was more than non-selective COX-2 inhibitor.	Aspirin	78-85	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	61-66
17957565-5	2007	Large differences were demonstrated in both aspirin and clopidogrel groups in response to therapy as assessed by both the area under the curve at 15 minutes and %CIn.	Aspirin	44-51	pyridoxal phosphatase	Homo sapiens	162-165
17957565-7	2007	CONCLUSION: Modified TEG, employing AUC15 and %CIn, is a promising tool for assessing responses to aspirin and clopidogrel.	Aspirin	99-106	pyridoxal phosphatase	Homo sapiens	47-50
17538005-4	2007	In this study, we investigated the effect of aspirin and pravastatin on LOX-1 expression on plate-lets.	Aspirin	45-52	oxidized low density lipoprotein receptor 1	Homo sapiens	72-77
17538005-10	2007	In other experiments, treatment with aspirin (1-10 mM) and pravastatin (1-5 microM) reduced platelet LOX-1 expression, with a synergistic effect of the combination of aspirin and pravastatin.	Aspirin	37-44	oxidized low density lipoprotein receptor 1	Homo sapiens	101-106
17538005-10	2007	In other experiments, treatment with aspirin (1-10 mM) and pravastatin (1-5 microM) reduced platelet LOX-1 expression, with a synergistic effect of the combination of aspirin and pravastatin.	Aspirin	167-174	oxidized low density lipoprotein receptor 1	Homo sapiens	101-106
17538005-15	2007	Furthermore, aspirin and pravastatin inhibit LOX-1 expression on platelets in part by favorably affecting ROS and NO release from activated platelets.	Aspirin	13-20	oxidized low density lipoprotein receptor 1	Homo sapiens	45-50
17845920-0	2007	Effect of aspirin on lipoprotein(a) in patients with ischemic stroke.	Aspirin	10-17	lipoprotein(a)	Homo sapiens	21-32
17622933-0	2007	UGT1A6 polymorphism and salicylic acid glucuronidation following aspirin.	Aspirin	65-72	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	0-6
17489881-9	2007	The TFPI level in aspirin-resistant patients (119.5 +/- 13.5 ng/mL) was significantly higher than that in aspirin-sensitive patients (107.8 +/- 18.9 ng/mL; P &lt; 0.05).	Aspirin	18-25	tissue factor pathway inhibitor	Homo sapiens	4-8
17489881-9	2007	The TFPI level in aspirin-resistant patients (119.5 +/- 13.5 ng/mL) was significantly higher than that in aspirin-sensitive patients (107.8 +/- 18.9 ng/mL; P &lt; 0.05).	Aspirin	106-113	tissue factor pathway inhibitor	Homo sapiens	4-8
29218104-10	2017	The results suggested that aspirin inhibited the proliferation of MSCs and caused cell-cycle arrest in the G0/G1 phase through downregulation of cyclin D1, which could be related to the increased expression of miRNA145.	Aspirin	27-34	cyclin D1	Homo sapiens	145-154
28844979-2	2017	Recently, the triple antiplatelet therapy with aspirin, a P2Y12 receptor antagonist and a protease activated receptor-1 (PAR-1) antagonist, has been suggested for the secondary prevention of atherothrombotic events, however presented an increased risk of bleeding.	Aspirin	47-54	purinergic receptor P2Y12	Homo sapiens	58-63
28988629-6	2017	Compound 3k was selected asa new drug candidate of selective and orally active non-peptide SSTR2 agonists for treatment of Type 2 diabetes with low in vivo PLsis potential.	Aspirin	25-28	somatostatin receptor 2	Rattus norvegicus	91-96
29045972-9	2017	Mechanically, ASA treatment increased FasL expression of Fas/FasL death pathway in GMSCs to induce T cells apoptosis.	Aspirin	14-17	Fas ligand (TNF superfamily, member 6)	Mus musculus	38-42
29045972-9	2017	Mechanically, ASA treatment increased FasL expression of Fas/FasL death pathway in GMSCs to induce T cells apoptosis.	Aspirin	14-17	Fas ligand (TNF superfamily, member 6)	Mus musculus	61-65
28632940-9	2017	In population studies, the I4399M variant has been correlated with elevated plasma Lp(a) levels and higher coronary heart disease risk, and carriers of the SNP had increased cardiovascular benefit from aspirin therapy.	Aspirin	202-209	lipoprotein(a)	Homo sapiens	83-88
24249731-3	2013	In the presence of aspirin, acetylated cyclooxygenase-2 loses the activity required to synthesize PGs but maintains the oxygenase activity to produce 15R-HETE from arachidonate.	Aspirin	19-26	prostaglandin-endoperoxide synthase 2	Mus musculus	39-55
28457985-6	2017	Besides, the relative expression of HLA-DQA1 was significantly lower in low on-aspirin platelet reactivity (LAPR) patients, when compared with HAPR and high normal (HN) group (p=0.028).	Aspirin	79-86	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	36-44
23751937-7	2013	A proposed hypothetical mechanism for the interaction between ticagrelor and higher aspirin dose is linked to the level of P2Y12 inhibition and the potential prothrombotic effects of high-dose aspirin through the suppression of prostacyclin.	Aspirin	84-91	purinergic receptor P2Y12	Homo sapiens	123-128
28636992-5	2017	Similar ASA-induced effects in-vitro were seen in human melanoma and nasopharyngeal carcinoma cells positive or negative in PAF-R.	Aspirin	8-11	platelet activating factor receptor	Homo sapiens	124-129
28508119-6	2017	Our general approach in patients with elevated Lp(a) levels is to aggressively manage other modifiable cardiovascular risk factors including lifestyle modification, consideration of aspirin therapy, and LDL-C lowering.	Aspirin	182-189	lipoprotein(a)	Homo sapiens	47-52
24018490-10	2013	Among proteins differentially expressed in Huh7-HCV cells, we found proteins related to cell proliferation (MTMR6, FAM22, HDGF and HCF-1) after 24 h of ASA treatment; and upregulation of angiostatin, PI4KA and STAT-1 after 48 h of treatment.	Aspirin	152-155	myotubularin related protein 6	Homo sapiens	108-113
24018490-10	2013	Among proteins differentially expressed in Huh7-HCV cells, we found proteins related to cell proliferation (MTMR6, FAM22, HDGF and HCF-1) after 24 h of ASA treatment; and upregulation of angiostatin, PI4KA and STAT-1 after 48 h of treatment.	Aspirin	152-155	heparin binding growth factor	Homo sapiens	122-126
24018490-10	2013	Among proteins differentially expressed in Huh7-HCV cells, we found proteins related to cell proliferation (MTMR6, FAM22, HDGF and HCF-1) after 24 h of ASA treatment; and upregulation of angiostatin, PI4KA and STAT-1 after 48 h of treatment.	Aspirin	152-155	phosphatidylinositol 4-kinase alpha	Homo sapiens	200-205
24018490-11	2013	Finally, at 72 h of ASA exposure, we identified overexpression of adenylsuccinate synthase, 2"-3"-di-deoxyadenosine, ubiquitin-protein-ligase E6A, adenylosuccinate-lyase and nibrin (NBN).	Aspirin	20-23	adenylosuccinate lyase	Homo sapiens	147-169
23792825-5	2013	Glutathione reductase (GR, EC 1.6.4.2) and tripeptide glutathione (GSH, gamma-Glutamyl-Cysteinyl-Glycine) are two major components of ascorbate-glutathione (AsA-GSH) pathway which play significant role in protecting cells against ROS and its reaction products-accrued potential anomalies.	Aspirin	157-160	glutathione-disulfide reductase	Homo sapiens	0-21
28528204-6	2017	Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1.	Aspirin	10-17	C-C motif chemokine receptor 1	Homo sapiens	181-185
23792825-5	2013	Glutathione reductase (GR, EC 1.6.4.2) and tripeptide glutathione (GSH, gamma-Glutamyl-Cysteinyl-Glycine) are two major components of ascorbate-glutathione (AsA-GSH) pathway which play significant role in protecting cells against ROS and its reaction products-accrued potential anomalies.	Aspirin	157-160	glutathione-disulfide reductase	Homo sapiens	23-25
28618904-4	2017	The aim of this article is to provide an overview of the evidence from randomized clinical trials with a focus on the best association between aspirin and a P2Y12 inhibitor such as clopidogrel, prasugrel or ticagrelor, on the selection of the appropriate agent based on the revascularization strategy and on the optimal duration of such an intensive treatment.	Aspirin	143-150	purinergic receptor P2Y12	Homo sapiens	157-162
23794731-10	2013	CONCLUSIONS: This study suggests that Abcc4 in the stomach facilitates the oral absorption of dasatinib, and it possibly plays a similar role for other orally administered substrates, such as acetylsalicylic acid.	Aspirin	192-212	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	38-43
28232079-2	2017	METHODS: The activity of rhodanese, 3-mercaptopyruvate sulfurtransferase (MPST) and gamma-cystathionase (CSE), functioning as antioxidant proteins and capable of producing H2S, was investigated in mouse liver and brain after intraperitoneal once a day administration of sodium nitroprusside (5 mg/kg body weight) or acetylsalicylic acid (500 mg/kg body weight) continued for 5 days.	Aspirin	316-336	cystathionase (cystathionine gamma-lyase)	Mus musculus	84-103
28232079-2	2017	METHODS: The activity of rhodanese, 3-mercaptopyruvate sulfurtransferase (MPST) and gamma-cystathionase (CSE), functioning as antioxidant proteins and capable of producing H2S, was investigated in mouse liver and brain after intraperitoneal once a day administration of sodium nitroprusside (5 mg/kg body weight) or acetylsalicylic acid (500 mg/kg body weight) continued for 5 days.	Aspirin	316-336	cystathionase (cystathionine gamma-lyase)	Mus musculus	105-108
28264838-7	2017	To target the metabolic phenotype induced by loss of BRCA1, a drug-repurposing approach was used and aspirin was identified as an agent that counteracted the increase in HK2 and the increase in glycolysis induced by BRCA1 impairment.	Aspirin	101-108	hexokinase 2	Homo sapiens	170-173
23894577-6	2013	We found that acetaminophen (relative risk [RR] 1.01, 95% confidence interval [CI] 0.88-1.17) and aspirin (RR 1.02, 95% CI 0.91-1.14) were not associated with bladder cancer risk.	Aspirin	98-105	ribonucleotide reductase catalytic subunit M1	Homo sapiens	107-111
24073359-2	2013	The continuous administration of low-dose aspirin to TH-MYCN mice (a model of pediatric neuroblastoma) delays tumor outgrowth and decreases tumor-promoting inflammation by inhibiting regulatory cells of the innate immune system as well as immunosuppressive mediators such as transforming growth factor beta (TGFbeta) and thromboxane A2.	Aspirin	42-49	transforming growth factor, beta 1	Mus musculus	308-315
23800934-2	2013	Experimental evidence implicates a role of RAF kinases in up-regulation of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2), suggesting that BRAF-mutant colonic cells might be less sensitive to the antitumor effects of aspirin than BRAF-wild-type neoplastic cells.	Aspirin	234-241	zinc fingers and homeoboxes 2	Homo sapiens	43-46
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	245-249
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	389-393
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	143-147
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	245-249
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	245-249
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	389-393
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	143-147
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	245-249
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	245-249
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	ciliary neurotrophic factor	Mus musculus	389-393
23653362-7	2013	Furthermore, we demonstrate that aspirin-induced astroglial CNTF was also functionally active and that supernatants of aspirin-treated astrocytes of wild type, but not Cntf null, mice increased myelin-associated proteins in oligodendrocytes and protected oligodendrocytes from TNF-alpha insult.	Aspirin	33-40	ciliary neurotrophic factor	Mus musculus	60-64
23762376-0	2013	HSP-72 accelerated expression in mononuclear cells induced in vivo by acetyl salicylic acid can be reproduced in vitro when combined with H2O2.	Aspirin	70-91	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	0-6
23803522-13	2013	PDTC, asa strong NF-kappaB inhibitor, may inhibit NF-kappaB activity and further significantly decreased expressions of alpha-SMA, integrin alpha5 and fibronectin which were important part of ECM, leading to drastically attenuated pulmonary fibrosis.	Aspirin	6-9	integrin subunit alpha 5	Rattus norvegicus	131-146
23392055-3	2013	METHODS: The single-nucleotide polymorphisms in HSPA1B-179C&gt;T and 1267A&gt;G gene were examined in patients with AERD and those with aspirin-tolerant asthma (ATA).	Aspirin	136-143	heat shock protein family A (Hsp70) member 1B	Homo sapiens	48-54
23470716-0	2013	A genetic effect of IL-5 receptor alpha polymorphism in patients with aspirin-exacerbated respiratory disease.	Aspirin	70-77	interleukin 5	Homo sapiens	20-24
23666308-1	2013	The novel oral P2Y12 inhibitors (prasugrel and ticagrelor) have been incorporated into the recently updated acute coronary syndrome (ACS) guidelines, as an adjunct antiplatelet treatment to aspirin.	Aspirin	190-197	purinergic receptor P2Y12	Homo sapiens	15-20
23240590-2	2013	Aspirin, a non-steroidal anti-inflammatory drug, simultaneously inhibits the aromatase activity of COX-1 and COX-2 isoforms, which is needed for prostaglandin synthesis.	Aspirin	0-7	cytochrome c oxidase II, mitochondrial	Mus musculus	109-114
22121102-6	2013	The following statistically significant interactions were observed: TYK2 with aspirin/NSAID use; STAT1, STAT4, and TYK2 with estrogen status; and JAK2, STAT2, STAT4, STAT5A, STAT5B, and STAT6 with smoking status and colon cancer risk; JAK2, STAT6, and TYK2 with aspirin/NSAID use; JAK1 with estrogen status; STAT2 with cigarette smoking and rectal cancer.	Aspirin	78-85	tyrosine kinase 2	Homo sapiens	68-72
23228932-3	2013	Paraoxonase 1 (PON1) and Aryl hydrocarbon receptor (AhR) siRNA transfections inhibited the induction of gene expressions by ASA suggesting the need for the acetyl ester hydrolysis and hydroxylation to DHBA.	Aspirin	124-127	aryl hydrocarbon receptor	Homo sapiens	25-50
23228932-3	2013	Paraoxonase 1 (PON1) and Aryl hydrocarbon receptor (AhR) siRNA transfections inhibited the induction of gene expressions by ASA suggesting the need for the acetyl ester hydrolysis and hydroxylation to DHBA.	Aspirin	124-127	aryl hydrocarbon receptor	Homo sapiens	52-55
23218405-0	2013	Ginkgo biloba extract and aspirin synergistically attenuate activated platelet-induced ROS production and LOX-1 expression in human coronary artery endothelial cells.	Aspirin	26-33	oxidized low density lipoprotein receptor 1	Homo sapiens	106-111
23218405-1	2013	AIM: In the present study, we investigated whether the therapeutic dosages of Ginkgo biloba extract (EGb) and Aspirin (ASP) might synergistically suppress oxidative stress through regulating the expressions of LOX-1 and phosphorylated p38MAPK (p-p38MAPK) in human coronary artery endothelial cells (HCAECs) ex vivo.	Aspirin	110-117	oxidized low density lipoprotein receptor 1	Homo sapiens	210-215
23218405-1	2013	AIM: In the present study, we investigated whether the therapeutic dosages of Ginkgo biloba extract (EGb) and Aspirin (ASP) might synergistically suppress oxidative stress through regulating the expressions of LOX-1 and phosphorylated p38MAPK (p-p38MAPK) in human coronary artery endothelial cells (HCAECs) ex vivo.	Aspirin	119-122	oxidized low density lipoprotein receptor 1	Homo sapiens	210-215
23218405-11	2013	It appears that the synergistic effect of EGb and ASP may correlate with the inhibition of ROS production, LOX-1 expression and p38MAPK phosphorylation.	Aspirin	50-53	oxidized low density lipoprotein receptor 1	Homo sapiens	107-112
23895681-7	2013	Furtermore, other results suggest that the chemopreventive and therapeutic effects of aspirin are also mediated through COX-independent mechanisms.	Aspirin	86-93	cytochrome c oxidase subunit 8A	Homo sapiens	120-123
23600205-6	2013	RESULTS: When SiHa cells were pretreated with aspirin, sulindac, curcumin or PDTC, Western blot showed that the expression of P65 was inhibited upon cisplatin stimulus (P &lt; 0.05).	Aspirin	46-53	RELA proto-oncogene, NF-kB subunit	Homo sapiens	126-129
22893064-3	2012	The priming action of aspirin on tumor cells was found to be dependent on an altered constitution of tumor microenvironment with respect to decline of acidosis and modulation in the expression of cell cycle and survival regulatory molecules like cyclin B1, cyclin D, bcl-2, bcl-xL, p53, and cytokines: IL-4, IL-10, IFN- gamma &amp; VEGF.	Aspirin	22-29	cyclin B1	Mus musculus	246-255
22893064-3	2012	The priming action of aspirin on tumor cells was found to be dependent on an altered constitution of tumor microenvironment with respect to decline of acidosis and modulation in the expression of cell cycle and survival regulatory molecules like cyclin B1, cyclin D, bcl-2, bcl-xL, p53, and cytokines: IL-4, IL-10, IFN- gamma &amp; VEGF.	Aspirin	22-29	BCL2-like 1	Mus musculus	274-280
22893265-13	2012	Meanwhile, among those taking LMWH vs aspirin, the frequency rates of ERIS were 1.1% (2 of 180) vs 0 (0); 0.6% (1 of 180) vs 1.2% (2 of 173) for SICH;and 2.2% (4 of 180) vs 2.9% (5 of 173) for symptomatic and asymptomatic cerebral hemorrhage, respectively; they showed nonsignificant trends.	Aspirin	38-45	stimulator of interferon response cGAMP interactor 1	Homo sapiens	70-74
21474293-2	2012	We hypothesized that minocycline induced MMP-2 and MMP-9 inhibition can be enhanced by aspirin (through its COX and tPA inhibitory action) and this combination can reduce cardiovascular dysfunction of diabetes.	Aspirin	87-94	matrix metallopeptidase 2	Rattus norvegicus	41-46
21474293-16	2012	Present study revealed that aspirin potentate minocycline induced MMP-2 and MMP-9 inhibition to ameliorate cardiovascular dysfunction of diabetes and this combination can be an approach for the treatment.	Aspirin	28-35	matrix metallopeptidase 2	Rattus norvegicus	66-71
22452804-13	2012	In addition, Cox proportional hazard regression modeling demonstrated that aspirin resistance or semiresponders (HR = 3.050, 95% CI: 1.464-6.354, p = 0.003) and diabetes (HR = 2.055, 95% CI: 1.060-3.981, p = 0.033) were associated with major adverse long-term outcomes.	Aspirin	75-82	cytochrome c oxidase subunit 8A	Homo sapiens	13-16
23687524-0	2012	Histamine H2 receptor antagonists for decreasing gastrointestinal harms in adults using acetylsalicylic acid: systematic review and meta-analysis.	Aspirin	88-108	histamine receptor H2	Homo sapiens	0-21
22561363-10	2012	These observations suggest that ASA can inhibit Ang II-induced capillary formation in part via blocking NADPH oxidase and AT1R transcription.	Aspirin	32-35	angiotensin II receptor type 1	Homo sapiens	122-126
22561363-11	2012	Because SA moiety had similar effect as ASA on AT1R expression, we suggest that the effect of ASA on new capillary formation is mediated by its SA moiety.	Aspirin	94-97	angiotensin II receptor type 1	Homo sapiens	47-51
22526472-0	2012	Aspirin metabolites are GPR35 agonists.	Aspirin	0-7	G protein-coupled receptor 35	Homo sapiens	24-29
22526472-2	2012	Here, we report the agonist activity of several aspirin metabolites at GPR35, a poorly characterized orphan G protein-coupled receptor.	Aspirin	48-55	G protein-coupled receptor 35	Homo sapiens	71-76
22526472-3	2012	2,3,5-Trihydroxybenzoic acid, an aspirin catabolite, was found to be the most potent GPR35 agonist among aspirin metabolites.	Aspirin	33-40	G protein-coupled receptor 35	Homo sapiens	85-90
22526472-5	2012	These results suggest that the GPR35 agonist activity of certain aspirin metabolites may contribute to the clinical features of aspirin.	Aspirin	65-72	G protein-coupled receptor 35	Homo sapiens	31-36
22526472-5	2012	These results suggest that the GPR35 agonist activity of certain aspirin metabolites may contribute to the clinical features of aspirin.	Aspirin	128-135	G protein-coupled receptor 35	Homo sapiens	31-36
22560621-4	2012	OBJECTIVES: To estimate the incremental cost-effectiveness of using genetic test results for 2 LPA variants to derive modified Framingham Risk Score estimates and to use these estimates to identify patients likely to benefit from aspirin use according to USPSTF guidelines for aspirin use in the primary prevention of CVD.	Aspirin	230-237	lipoprotein(a)	Homo sapiens	95-98
22560621-8	2012	RESULTS: Recommending aspirin to patients whose CVD risk surpassed the risk threshold when LPA information was included in their risk assessment would prevent an estimated 65 CVD events over 10 years.	Aspirin	22-29	lipoprotein(a)	Homo sapiens	91-94
22560621-10	2012	CONCLUSIONS: LPA genotyping in the context of the aspirin use guidelines for primary prevention of CVD could be cost-effective.	Aspirin	50-57	lipoprotein(a)	Homo sapiens	13-16
28087411-7	2017	The preventive effects of aspirin was associated with the inhibition of nuclear factor-kappaB (NF-kappaB)-dependent MIR155HG (miR-155 host gene) expression.	Aspirin	26-33	MIR155 host gene	Homo sapiens	126-143
27940576-0	2017	Aspirin Suppresses Growth in PI3K-Mutant Breast Cancer by Activating AMPK and Inhibiting mTORC1 Signaling.	Aspirin	0-7	CREB regulated transcription coactivator 1	Mus musculus	89-95
28278500-9	2017	In addition, aspirin treatment caused a strong decrease in nuclear factor-kappa B (NF-kappaB) activation, inhibitor of kappaB (IkappaB)-alpha phosphorylation together with translocation of NF-kappaB p65 to nucleus and IkappaB kinase (IKK)- beta activation.	Aspirin	13-20	RELA proto-oncogene, NF-kB subunit	Homo sapiens	199-202
29179207-9	2017	RESULTS: Aspirin attenuated colonosphere formation and decreased the ALDH1 positive cell population of colorectal cancer cells.	Aspirin	9-16	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	69-74
29179207-11	2017	Consistently, aspirin decreased the protein expression of stemness-related transcription factors, including c-Myc, OCT4 and NANOG.	Aspirin	14-21	POU domain, class 5, transcription factor 1, related sequence 1	Mus musculus	115-119
28055284-0	2017	Aspirin attenuates monocrotaline-induced pulmonary arterial hypertension in rats by suppressing the ERK/MAPK pathway.	Aspirin	0-7	mitogen activated protein kinase 3	Rattus norvegicus	104-108
28055284-11	2017	Treatment with ASA significantly inhibited the increased p-ERK1/2 and restored the impaired endothelial nitric oxide synthase (eNOS) in MCT-treated rats.	Aspirin	15-18	mitogen activated protein kinase 3	Rattus norvegicus	59-65
28055284-12	2017	This study demonstrated that ASA distinctively attenuates MCT-induced PAH by inhibition of the ERK1/2 signaling pathway.	Aspirin	29-32	mitogen activated protein kinase 3	Rattus norvegicus	95-101
27959713-1	2016	BACKGROUND: In patients with atrial fibrillation undergoing percutaneous coronary intervention (PCI) with placement of stents, standard anticoagulation with a vitamin K antagonist plus dual antiplatelet therapy (DAPT) with a P2Y12 inhibitor and aspirin reduces the risk of thrombosis and stroke but increases the risk of bleeding.	Aspirin	245-252	purinergic receptor P2Y12	Homo sapiens	225-230
27999284-1	2016	Aspirin down regulates transferrin receptor 1 (TfR1) and up regulates ferroportin 1 (Fpn1) and ferritin expression in BV-2 microglial cells treated without lipopolysaccharides (LPS), as well as down regulates hepcidin and interleukin 6 (IL-6) in cells treated with LPS.	Aspirin	0-7	transferrin receptor	Mus musculus	23-45
27999284-1	2016	Aspirin down regulates transferrin receptor 1 (TfR1) and up regulates ferroportin 1 (Fpn1) and ferritin expression in BV-2 microglial cells treated without lipopolysaccharides (LPS), as well as down regulates hepcidin and interleukin 6 (IL-6) in cells treated with LPS.	Aspirin	0-7	transferrin receptor	Mus musculus	47-51
27999284-5	2016	These findings provide evidence that aspirin down regulates hepcidin by inhibiting IL6/JAK2/STAT3 and P65 (nuclear factor-kappaB) pathways in the cells under inflammatory conditions, and imply that an aspirin-induced reduction in TfR1 and an increase in ferritin are not associated with IRP1 and NO.	Aspirin	37-44	transferrin receptor	Mus musculus	230-234
27824864-10	2016	The risk of GIB associated with NSAIDs/aspirin use increased with greater alcohol consumption (multivariable RR 1.37; 95% CI, 0.85-2.19 for 1-14g/day of alcohol, RR 1.75; 95% CI, 1.07-2.88 for &gt;= 15g/day compared to nondrinkers).	Aspirin	39-46	ribonucleotide reductase catalytic subunit M1	Homo sapiens	109-113
27824864-10	2016	The risk of GIB associated with NSAIDs/aspirin use increased with greater alcohol consumption (multivariable RR 1.37; 95% CI, 0.85-2.19 for 1-14g/day of alcohol, RR 1.75; 95% CI, 1.07-2.88 for &gt;= 15g/day compared to nondrinkers).	Aspirin	39-46	ribonucleotide reductase catalytic subunit M1	Homo sapiens	162-166
27641736-8	2016	The TBXA2R rs1131882 CC genotype, which was found more frequently in the aspirin-insensitive group (81.8% vs 62.4%) than in the sensitive group, was identified as a risk factor for aspirin resistance (odds ratio=2.712, 95% CI: 1.080-6.810) with a higher level of AA-induced platelet aggregation.	Aspirin	73-80	thromboxane A2 receptor	Homo sapiens	4-10
27641736-8	2016	The TBXA2R rs1131882 CC genotype, which was found more frequently in the aspirin-insensitive group (81.8% vs 62.4%) than in the sensitive group, was identified as a risk factor for aspirin resistance (odds ratio=2.712, 95% CI: 1.080-6.810) with a higher level of AA-induced platelet aggregation.	Aspirin	181-188	thromboxane A2 receptor	Homo sapiens	4-10
27678446-8	2016	Of note, the Lp(a) level did not respond to atorvastatin but did decrease 15% after aspirin 325 mg was added although his Lp(a) levels were variable, and it is not clear that this was cause and effect.	Aspirin	84-91	lipoprotein(a)	Homo sapiens	13-18
27378565-7	2016	Noteworthy, salicylic acid, a metabolite of aspirin, has been recently found to inhibit HMGB1.	Aspirin	44-51	high mobility group box 1	Homo sapiens	88-93
27391154-2	2016	We investigated the roles of transcriptional factor activator protein 2alpha (AP-2alpha) in the beneficial effects of aspirin in the growth and vulnerability of atherosclerotic plaque.	Aspirin	118-125	transcription factor AP-2, alpha	Mus musculus	78-87
27391154-4	2016	In vivo lentivirus-mediated RNA interference of AP-2alpha reversed the inhibitory effects of aspirin on atherosclerosis in Apoe-/- mice.	Aspirin	93-100	transcription factor AP-2, alpha	Mus musculus	48-57
27391154-5	2016	Mechanically, aspirin increased AP-2alpha phosphorylation and its activity, upregulated IkBalpha mRNA and protein levels, and reduced oxidative stress in cultured vascular smooth muscle cells.	Aspirin	14-21	transcription factor AP-2, alpha	Mus musculus	32-41
27391154-6	2016	Furthermore, deficiency of AP-2alpha completely abolished aspirin-induced upregulation of IkBalpha levels and inhibition of oxidative stress in Apoe-/- mice.	Aspirin	58-65	transcription factor AP-2, alpha	Mus musculus	27-36
27391154-8	2016	CONCLUSION: Aspirin activates AP-2alpha to upregulate IkBalpha gene expression, resulting in attenuations of plaque development and instability in atherosclerosis.	Aspirin	12-19	transcription factor AP-2, alpha	Mus musculus	30-39
27423939-4	2016	More recently, aspirin dosing has been thoroughly studied in the CAD population with concomitant therapy (such as P2Y12 inhibitors); however, patients in these studies were not randomized to aspirin dose.	Aspirin	15-22	purinergic receptor P2Y12	Homo sapiens	114-119
27296993-11	2016	Aspirin decreases aneurysm rupture in human and mice, in part through cyclooxygenase-2 pathways.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Mus musculus	70-86
27230877-1	2016	PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development.	Aspirin	72-79	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	159-187
22932114-20	2012	Aspirin could prevent bone loss by decreasing COX-2 expression in OVX rats.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	46-51
22159558-2	2012	Aspirin had been reported to down-regulate surface expression of CD40, CD80, CD86, and MHCII in myeloid dendritic cells (DC), which played essential roles in regulating the immune system.	Aspirin	0-7	CD40 molecule	Homo sapiens	65-69
27230877-1	2016	PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development.	Aspirin	268-275	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	159-187
22159558-2	2012	Aspirin had been reported to down-regulate surface expression of CD40, CD80, CD86, and MHCII in myeloid dendritic cells (DC), which played essential roles in regulating the immune system.	Aspirin	0-7	CD80 molecule	Homo sapiens	71-75
22159558-2	2012	Aspirin had been reported to down-regulate surface expression of CD40, CD80, CD86, and MHCII in myeloid dendritic cells (DC), which played essential roles in regulating the immune system.	Aspirin	0-7	CD86 molecule	Homo sapiens	77-81
27230877-1	2016	PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development.	Aspirin	277-280	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	159-187
22159558-4	2012	By using an established epidermoid carcinoma cell line (A-431), which overexpresses the epidermal growth factor receptor (EGFR) and transferrin receptor (TfnR), we show that aspirin (1) reduces cell surface expression of EGFR and (2) accumulates endocytosed-EGFR and -TfnR in the early/sorting endosome (ESE).	Aspirin	174-181	transferrin receptor	Homo sapiens	132-152
27230877-3	2016	RESULT(S): Met, Asa, BR-DIM, or hyperosmotic sorbitol stress induces rapid ~50-85 % Rex1 and/or Oct4 protein loss in two-cell embryos.	Aspirin	16-19	RNA exonuclease 1 homolog	Homo sapiens	84-88
22159558-4	2012	By using an established epidermoid carcinoma cell line (A-431), which overexpresses the epidermal growth factor receptor (EGFR) and transferrin receptor (TfnR), we show that aspirin (1) reduces cell surface expression of EGFR and (2) accumulates endocytosed-EGFR and -TfnR in the early/sorting endosome (ESE).	Aspirin	174-181	transferrin receptor	Homo sapiens	154-158
22159558-4	2012	By using an established epidermoid carcinoma cell line (A-431), which overexpresses the epidermal growth factor receptor (EGFR) and transferrin receptor (TfnR), we show that aspirin (1) reduces cell surface expression of EGFR and (2) accumulates endocytosed-EGFR and -TfnR in the early/sorting endosome (ESE).	Aspirin	174-181	transferrin receptor	Homo sapiens	268-272
27230877-6	2016	CONCLUSION: These experimental designs here showed that Met-, Asa-, BR-DIM-, or sorbitol stress-induced rapid potency loss in two-cell embryos is AMPK dependent as suggested by inhibition of Rex1 and/or Oct4 protein loss with an AMPK inhibitor.	Aspirin	62-65	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	146-150
22159558-5	2012	Further elucidation of the mechanism suggests that aspirin enhances recruitment of SNX3 and SNX5 to membranes and consistently, both SNX3 and SNX5 play essential roles in the aspirin-mediated accumulation of endocytosed-TfnR at the ESE.	Aspirin	51-58	sorting nexin 5	Homo sapiens	92-96
22159558-5	2012	Further elucidation of the mechanism suggests that aspirin enhances recruitment of SNX3 and SNX5 to membranes and consistently, both SNX3 and SNX5 play essential roles in the aspirin-mediated accumulation of endocytosed-TfnR at the ESE.	Aspirin	51-58	transferrin receptor	Homo sapiens	220-224
27230877-6	2016	CONCLUSION: These experimental designs here showed that Met-, Asa-, BR-DIM-, or sorbitol stress-induced rapid potency loss in two-cell embryos is AMPK dependent as suggested by inhibition of Rex1 and/or Oct4 protein loss with an AMPK inhibitor.	Aspirin	62-65	RNA exonuclease 1 homolog	Homo sapiens	191-195
22159558-5	2012	Further elucidation of the mechanism suggests that aspirin enhances recruitment of SNX3 and SNX5 to membranes and consistently, both SNX3 and SNX5 play essential roles in the aspirin-mediated accumulation of endocytosed-TfnR at the ESE.	Aspirin	175-182	sorting nexin 5	Homo sapiens	92-96
22159558-5	2012	Further elucidation of the mechanism suggests that aspirin enhances recruitment of SNX3 and SNX5 to membranes and consistently, both SNX3 and SNX5 play essential roles in the aspirin-mediated accumulation of endocytosed-TfnR at the ESE.	Aspirin	175-182	sorting nexin 5	Homo sapiens	142-146
22159558-5	2012	Further elucidation of the mechanism suggests that aspirin enhances recruitment of SNX3 and SNX5 to membranes and consistently, both SNX3 and SNX5 play essential roles in the aspirin-mediated accumulation of endocytosed-TfnR at the ESE.	Aspirin	175-182	transferrin receptor	Homo sapiens	220-224
27230877-6	2016	CONCLUSION: These experimental designs here showed that Met-, Asa-, BR-DIM-, or sorbitol stress-induced rapid potency loss in two-cell embryos is AMPK dependent as suggested by inhibition of Rex1 and/or Oct4 protein loss with an AMPK inhibitor.	Aspirin	62-65	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	229-233
27289074-2	2016	We aimed to assess high platelet reactivity on aspirin (HPR-aspirin) and its association with P2Y12i (HPR-P2Y12i) during the acute phase of STEMI.	Aspirin	47-54	haptoglobin-related protein	Homo sapiens	56-59
22690022-0	2012	Stereocontrolled total synthesis of neuroprotectin D1 / protectin D1 and its aspirin-triggered stereoisomer.	Aspirin	77-84	leiomodin 1	Homo sapiens	51-68
26525539-6	2016	RESULTS: Basal autophagy in the gastric mucosa was inhibited by ASA as demonstrated by increased levels of p62 and ubiquitinated proteins and total LC3 and a reduced LC3-II/LC3-I ratio.	Aspirin	64-67	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	107-110
22690022-4	2012	The same strategy, was also employed for the total synthesis of aspirin-triggered neuroprotectin D1 / protectin D1 having the 17(R)-stereochemistry.	Aspirin	64-71	leiomodin 1	Homo sapiens	97-114
26525539-6	2016	RESULTS: Basal autophagy in the gastric mucosa was inhibited by ASA as demonstrated by increased levels of p62 and ubiquitinated proteins and total LC3 and a reduced LC3-II/LC3-I ratio.	Aspirin	64-67	annexin A3	Rattus norvegicus	148-151
21692746-8	2012	Tumour cells obtained from aspirin-treated tumour-bearing mice demonstrated an altered expression of pH regulators monocarboxylate transporter-1 and V-ATPase along with alteration in the level of cell survival regulatory molecules such as survivin, vascular endothelial growth factor, heat-shock protein 70, glucose transporter-1, SOCS-5 (suppressor of cytokine signalling-5), HIF-1alpha (hypoxia-inducible factor-1alpha) and PUMA (p53 up-regulated modulator of apoptosis).	Aspirin	27-34	ATPase, H+ transporting, lysosomal V0 subunit D2	Mus musculus	149-157
26525539-6	2016	RESULTS: Basal autophagy in the gastric mucosa was inhibited by ASA as demonstrated by increased levels of p62 and ubiquitinated proteins and total LC3 and a reduced LC3-II/LC3-I ratio.	Aspirin	64-67	annexin A3	Rattus norvegicus	166-169
21692746-8	2012	Tumour cells obtained from aspirin-treated tumour-bearing mice demonstrated an altered expression of pH regulators monocarboxylate transporter-1 and V-ATPase along with alteration in the level of cell survival regulatory molecules such as survivin, vascular endothelial growth factor, heat-shock protein 70, glucose transporter-1, SOCS-5 (suppressor of cytokine signalling-5), HIF-1alpha (hypoxia-inducible factor-1alpha) and PUMA (p53 up-regulated modulator of apoptosis).	Aspirin	27-34	baculoviral IAP repeat-containing 5	Mus musculus	239-247
26525539-6	2016	RESULTS: Basal autophagy in the gastric mucosa was inhibited by ASA as demonstrated by increased levels of p62 and ubiquitinated proteins and total LC3 and a reduced LC3-II/LC3-I ratio.	Aspirin	64-67	annexin A3	Rattus norvegicus	166-169
26525539-7	2016	Similarly, ASA increased p62 and decreased LC3-II accumulation and the number of EmGFP/LC3B puncta in AGS cells.	Aspirin	11-14	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	25-28
26525539-7	2016	Similarly, ASA increased p62 and decreased LC3-II accumulation and the number of EmGFP/LC3B puncta in AGS cells.	Aspirin	11-14	annexin A3	Rattus norvegicus	43-46
26968189-1	2016	BACKGROUND/AIMS: Healthcare-associated pneumonia (HCAP) was proposed asa new pneumonia category in 2005, and treatment recommendations includebroad-spectrum antibiotics directed at multidrug-resistant (MDR) pathogens.However, this concept continues to be controversial, and microbiological data arelacking for HCAP patients in the intensive care unit (ICU).	Aspirin	69-72	structural maintenance of chromosomes 3	Homo sapiens	17-48
22038552-7	2012	RESULTS: While gastric acid secretion did not differ significantly between aspirin-takers and controls, gastric mucus secretion, in terms of mucin output, was significantly increased in aspirin-takers compared to controls (4.1 (SD 4.8) vs. 2.3 (1.4) mg hexose/10 min, P &lt; 0.05).	Aspirin	186-193	LOC100508689	Homo sapiens	141-146
22038552-8	2012	Consequently, the acid/mucin ratio was significantly decreased in aspirin-takers compared to controls (1.2 (1.0) vs. 1.7 (1.4), P &lt; 0.05).	Aspirin	66-73	LOC100508689	Homo sapiens	23-28
23057161-6	2012	In contrast, treatment of immature dendritic cells with aspirin, dexamethasone, 1alpha,25-dihydroxyvitamin D3 (VD3) or butyric acid was associated with diminished expression of CD1a, CD1c, CD40, CD80 and CD83.	Aspirin	56-63	CD1a molecule	Homo sapiens	177-181
23057161-6	2012	In contrast, treatment of immature dendritic cells with aspirin, dexamethasone, 1alpha,25-dihydroxyvitamin D3 (VD3) or butyric acid was associated with diminished expression of CD1a, CD1c, CD40, CD80 and CD83.	Aspirin	56-63	CD1c molecule	Homo sapiens	183-187
23057161-6	2012	In contrast, treatment of immature dendritic cells with aspirin, dexamethasone, 1alpha,25-dihydroxyvitamin D3 (VD3) or butyric acid was associated with diminished expression of CD1a, CD1c, CD40, CD80 and CD83.	Aspirin	56-63	CD40 molecule	Homo sapiens	189-193
26968189-1	2016	BACKGROUND/AIMS: Healthcare-associated pneumonia (HCAP) was proposed asa new pneumonia category in 2005, and treatment recommendations includebroad-spectrum antibiotics directed at multidrug-resistant (MDR) pathogens.However, this concept continues to be controversial, and microbiological data arelacking for HCAP patients in the intensive care unit (ICU).	Aspirin	69-72	structural maintenance of chromosomes 3	Homo sapiens	50-54
23057161-6	2012	In contrast, treatment of immature dendritic cells with aspirin, dexamethasone, 1alpha,25-dihydroxyvitamin D3 (VD3) or butyric acid was associated with diminished expression of CD1a, CD1c, CD40, CD80 and CD83.	Aspirin	56-63	CD80 molecule	Homo sapiens	195-199
26721257-0	2016	Uptake and Documentation of the Use of an Encounter Decision Aid in Usual Practice: A Retrospective Analysis of the Use of the Statin/Aspirin Choice Decision Aid.	Aspirin	134-141	activation induced cytidine deaminase	Homo sapiens	158-161
22045867-4	2012	We hypothesised that inhibition of MMP-2 and MMP-9 by minocycline can be potentiated by aspirin through inhibition of cyclooxygenase-2 and tissue plasminogen activator, resulting in amelioration of clinical cerebral ischaemia in diabetes.	Aspirin	88-95	matrix metallopeptidase 2	Rattus norvegicus	35-40
22045867-4	2012	We hypothesised that inhibition of MMP-2 and MMP-9 by minocycline can be potentiated by aspirin through inhibition of cyclooxygenase-2 and tissue plasminogen activator, resulting in amelioration of clinical cerebral ischaemia in diabetes.	Aspirin	88-95	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	118-134
22045867-9	2012	Our data indicate that combination of aspirin and minocycline therapy protects from the consequences of cerebral ischaemia in animal models of diabetes and is associated with inhibition of MMP-2 and MMP-9.	Aspirin	38-45	matrix metallopeptidase 2	Rattus norvegicus	189-194
26918349-14	2016	These data demonstrate that AMPK-mediated up-regulation of mTORC2 and MCL-1 may compromise the anticancer effects of aspirin.	Aspirin	117-124	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	28-32
22197650-23	2012	Activation of p38 &amp; ERK MAP kinases was prevented in aspirin group (p &lt; 0.05, CI -1.796--0.014).	Aspirin	57-64	mitogen activated protein kinase 14	Rattus norvegicus	14-17
26918349-14	2016	These data demonstrate that AMPK-mediated up-regulation of mTORC2 and MCL-1 may compromise the anticancer effects of aspirin.	Aspirin	117-124	CREB regulated transcription coactivator 2	Mus musculus	59-65
22197650-26	2012	CONCLUSIONS: Our data demonstrated that low dose aspirin reduced the incidence of duodenoesophageal reflux induced histological changes in the esophagus by preventing activation of proliferative &amp; anti-apoptotic MAP kinases such as p38 &amp; ER as well as protease activity.	Aspirin	49-56	mitogen activated protein kinase 14	Rattus norvegicus	236-239
26898989-0	2016	The aspirin-induced long non-coding RNA OLA1P2 blocks phosphorylated STAT3 homodimer formation.	Aspirin	4-11	OLA1 pseudogene 2	Homo sapiens	40-46
22070887-4	2012	Based on this fact, we hypothesize that aspirin, in addition to its anti-inflammatory effect, may also specifically inhibit autoimmune response in atherosclerosis by actively increasing CD4+CD25+FOXP3+Treg cells as well as by inducing tolerogenic DCs which induce hyporesponsiveness in responder naive T cells.	Aspirin	40-47	forkhead box P3	Homo sapiens	195-200
26898989-2	2016	RESULTS: We identify an aspirin-induced upregulated lncRNA, OLA1P2, in human colorectal cancer.	Aspirin	24-31	OLA1 pseudogene 2	Homo sapiens	60-66
26898989-8	2016	Regular use of aspirin dramatically decreases the number of metastatic nodules of cancer cells in immunodeficient mouse lungs, and OLA1P2 silencing markedly weakens the anti-metastatic activity of aspirin in the lungs.	Aspirin	197-204	OLA1 pseudogene 2	Homo sapiens	131-137
26898989-10	2016	CONCLUSIONS: The present study finds that the aspirin-FOXD3-OLA1P2-STAT3 axis exhibits exciting anticancer effects and provides new insights into the chemopreventive mechanisms underlying aspirin use.	Aspirin	46-53	OLA1 pseudogene 2	Homo sapiens	60-66
21833043-8	2011	Aspirin treatment reduced the basal superoxide production and blunted the oxidative and hypertensive effect of angiotensin II in wild type and cyclo-oxygenase-1 deficient mice whereas it lost completely its antioxidative property in angiotensin II-treated aortic smooth muscle cells isolated from cyclo-oxygenase-2 deficient mice.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Mus musculus	297-314
26898989-10	2016	CONCLUSIONS: The present study finds that the aspirin-FOXD3-OLA1P2-STAT3 axis exhibits exciting anticancer effects and provides new insights into the chemopreventive mechanisms underlying aspirin use.	Aspirin	188-195	OLA1 pseudogene 2	Homo sapiens	60-66
21721879-6	2011	Increasing the concentration of aspirin resulted in decreased expression of c-myc, cyclin D1, and fra-1 mRNA and protein in U87 and A172 cells in a dose-dependent manner.	Aspirin	32-39	cyclin D1	Homo sapiens	83-92
26506219-4	2016	RESULTS: Ten muM aspirin significantly inhibited Ang II-induced increase in cardiomyocyte size, the mRNA, and protein levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and beta-myosin heavy chain (beta-MHC) (P &lt; 0.05).	Aspirin	17-24	angiogenin, ribonuclease, RNase A family, 5	Mus musculus	49-52
21875809-6	2011	Mature green and red ripe fruit from DHAR over-expressing lines had a 1.6 fold increase in AsA content in plants grown under relatively low light conditions (150 mumol m(-2) s(-1)).	Aspirin	91-94	dehydroascorbate reductase 1	Solanum lycopersicum	37-41
26711147-4	2016	Furthermore, ASA could up-regulate TNF-R1 and DR5 via activation of p38 MAPK, thereby activating caspase 8, revealing the death receptor pathway was also involved in this process.	Aspirin	13-16	caspase 8	Homo sapiens	97-106
21726122-2	2011	The adhesion molecule CD58 gene may play a crucial role in aspirin-exacerbated respiratory disease (AERD) pathogenesis by mediating the biological functions of asthma-inducing mechanisms including T helper cells, proinflammatory cytokines, and natural killer T cells.	Aspirin	59-66	CD58 molecule	Homo sapiens	22-26
25345915-10	2015	Use of non-aspirin NSAIDs was associated with increased risk of NHL (POR = 1.41, 95% CI 1.01-1.97) amongst females only.	Aspirin	11-18	ADP ribosylation factor interacting protein 2	Homo sapiens	69-76
21726122-3	2011	OBJECTIVE: This study aimed to investigate the association of CD58 variations with aspirin-induced bronchospasm in Korean asthma patients.	Aspirin	83-90	CD58 molecule	Homo sapiens	62-66
21742097-6	2011	Aspirin was associated with hemorrhagic stroke (RR 1.35, 95% CI 1.01-1.81, P = .04) and major bleeding (RR 1.62, 95% CI 1.31-2.00, P &lt; .001).	Aspirin	0-7	ribonucleotide reductase catalytic subunit M1	Homo sapiens	48-52
21742097-6	2011	Aspirin was associated with hemorrhagic stroke (RR 1.35, 95% CI 1.01-1.81, P = .04) and major bleeding (RR 1.62, 95% CI 1.31-2.00, P &lt; .001).	Aspirin	0-7	ribonucleotide reductase catalytic subunit M1	Homo sapiens	104-108
17319904-0	2007	Reticulated platelets and uninhibited COX-1 and COX-2 decrease the antiplatelet effects of aspirin.	Aspirin	91-98	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	38-43
17319904-9	2007	Stimulated P-selectin and integrin alpha(IIb)beta(3) expression were also higher in the upper tertile both before and after aspirin.	Aspirin	124-131	selectin P	Homo sapiens	11-21
16442186-7	2007	Urinary 11-dehydro-TXB(2) was significantly reduced by aspirin, but not by rofecoxib, consistently with a COX-1-mediated TXA(2) biosynthesis.	Aspirin	55-62	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	106-111
26641551-8	2015	RESULTS: A small-scale screen revealed that the nonsteroidal anti-inflammatory drugs (NSAIDs), glafenine, ibuprofen, and acetylsalicylic acid dissolved in 0.2% dimethyl sulfoxide (DMSO), partially rescued the trafficking defect in some SLC4A11 mutants, expressed in HEK293 cells.	Aspirin	121-141	solute carrier family 4, sodium bicarbonate transporter-like, member 11	Mus musculus	236-243
26527225-11	2015	Regarding safety, medium-dose aspirin (100-300 mg daily) and aspirin/clopidogrel combination showed an increased risk of MB compared with warfarin (RR 1.17 and 1.15, respectively), as per dabigatran 150 mg and rivaroxaban in older elderly (RR 1.17 and 1.12, respectively).	Aspirin	30-37	ribonucleotide reductase catalytic subunit M1	Homo sapiens	148-152
21866633-2	2011	METHODS: 3beta-2-acetoxy-benzoyl-diosgenin ester (ABDE) was synthesized by acylation of aspirin through two-step of reaction.	Aspirin	88-95	olfactory receptor family 52 subfamily A member 5	Mus musculus	9-16
26162710-0	2015	Early single Aspirin-triggered Lipoxin blocked morphine anti-nociception tolerance through inhibiting NALP1 inflammasome: Involvement of PI3k/Akt signaling pathway.	Aspirin	13-20	NLR family, pyrin domain containing 1A	Rattus norvegicus	102-107
21076843-12	2011	Aspirin (500 muM) demonstrated myriad effects in human CCA cell lines, including growth suppression, reduced phosphorylation of Akt/Erk/c-Jun, elevation of RECK expression, inhibition of MMP-2/MMP-9 activity, and enhanced invasiveness.	Aspirin	0-7	matrix metallopeptidase 2	Homo sapiens	187-192
25962903-13	2015	This EP2 control of mast cell-mediated bronchoconstriction is presumably exaggerated in patients with aspirin-exacerbated respiratory disease.	Aspirin	102-109	prostaglandin E receptor 2	Homo sapiens	5-8
21215580-11	2011	Among all covariates included in the Cox models (including predictors of mortality such as American Society of Anesthesiologists [ASA] score), the psoas area was the most significant.	Aspirin	130-133	cytochrome c oxidase subunit 8A	Homo sapiens	37-40
26856059-3	2015	It was shown that acetylsalicylic acid and its principal metabolite, salicylic acid, can be purified from the endogenous admixtures present in the biological materials by column chromatography on silica gel L 40/100 mcm.	Aspirin	18-38	ubiquitin A-52 residue ribosomal protein fusion product 1	Homo sapiens	207-219
21070398-0	2011	Association of thromboxane A2 receptor (TBXA2R) gene polymorphism in patients with aspirin-intolerant acute urticaria.	Aspirin	83-90	thromboxane A2 receptor	Homo sapiens	15-38
21070398-0	2011	Association of thromboxane A2 receptor (TBXA2R) gene polymorphism in patients with aspirin-intolerant acute urticaria.	Aspirin	83-90	thromboxane A2 receptor	Homo sapiens	40-46
21070398-3	2011	This study evaluated the association between genetic TBXA2R variants and the development of acetyl salicylic acid (ASA)-intolerant acute urticaria (AIAU).	Aspirin	92-113	thromboxane A2 receptor	Homo sapiens	53-59
21070398-3	2011	This study evaluated the association between genetic TBXA2R variants and the development of acetyl salicylic acid (ASA)-intolerant acute urticaria (AIAU).	Aspirin	115-118	thromboxane A2 receptor	Homo sapiens	53-59
20824505-1	2011	BACKGROUND: We have previously shown that co-treatment of angiotensin type 1 receptor (AT1R) blocker (ARB) or angiotensin converting enzyme (ACE) inhibitor seem to reduce peptic ulcer among patients taking low dose aspirin.	Aspirin	215-222	angiotensin II receptor type 1	Homo sapiens	58-85
20824505-1	2011	BACKGROUND: We have previously shown that co-treatment of angiotensin type 1 receptor (AT1R) blocker (ARB) or angiotensin converting enzyme (ACE) inhibitor seem to reduce peptic ulcer among patients taking low dose aspirin.	Aspirin	215-222	angiotensin II receptor type 1	Homo sapiens	87-91
26519141-2	2015	It has been recently shown that the host immune system has fundamental effects on the fate of transplanted mesenchymal stem cells during bone repair, where the topical administration of aspirin is capable of improving calvarial bone repair in rodents by inhibiting tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) production.	Aspirin	186-193	tumor necrosis factor	Sus scrofa	265-292
21189314-0	2011	What is the best dose of aspirin in association with P2Y12 antagonists?	Aspirin	25-32	purinergic receptor P2Y12	Homo sapiens	53-58
21084063-7	2011	Notably, collagen deposition in glandular tissue and localization of cyclooxygenase 1, 2, and epidermal growth factor were considerably affected in aspirin-treated rats.	Aspirin	148-155	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	69-85
26519141-2	2015	It has been recently shown that the host immune system has fundamental effects on the fate of transplanted mesenchymal stem cells during bone repair, where the topical administration of aspirin is capable of improving calvarial bone repair in rodents by inhibiting tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) production.	Aspirin	186-193	tumor necrosis factor	Sus scrofa	294-303
26519141-2	2015	It has been recently shown that the host immune system has fundamental effects on the fate of transplanted mesenchymal stem cells during bone repair, where the topical administration of aspirin is capable of improving calvarial bone repair in rodents by inhibiting tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) production.	Aspirin	186-193	interferon gamma	Sus scrofa	309-325
21415533-1	2011	Low-dose aspirin acts by irreversibly acetylating internal cyclooxygenase-1 (COX-1) on platelets, thereby suppressing platelet aggregation.	Aspirin	9-16	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	59-75
26519141-2	2015	It has been recently shown that the host immune system has fundamental effects on the fate of transplanted mesenchymal stem cells during bone repair, where the topical administration of aspirin is capable of improving calvarial bone repair in rodents by inhibiting tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) production.	Aspirin	186-193	interferon gamma	Sus scrofa	327-336
21415533-1	2011	Low-dose aspirin acts by irreversibly acetylating internal cyclooxygenase-1 (COX-1) on platelets, thereby suppressing platelet aggregation.	Aspirin	9-16	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	77-82
21415533-2	2011	Because nonsteroidal anti-inflammatory drugs (NSAIDs) also inhibit COX-1, the antiplatelet effects of aspirin may be suppressed when it is co-administered with NSAIDs.	Aspirin	102-109	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	67-72
26519141-9	2015	Aspirin-BMSC treatment has significantly decreased the concentration of TNF-alpha and IFN-gamma (p &lt; 0.05).	Aspirin	0-7	tumor necrosis factor	Sus scrofa	72-81
21415533-11	2011	Accordingly, if co-administration with NSAIDs is necessary with low-dose aspirin, a selective COX-2 inhibitor, such as etodolac, should be used.	Aspirin	73-80	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	94-99
26519141-9	2015	Aspirin-BMSC treatment has significantly decreased the concentration of TNF-alpha and IFN-gamma (p &lt; 0.05).	Aspirin	0-7	interferon gamma	Sus scrofa	86-95
26342029-3	2015	We now demonstrate that patients with AERD have markedly increased epithelial expression of the alarmin-like cytokine IL-33 in nasal polyps, as compared with polyps from aspirin-tolerant control subjects.	Aspirin	170-177	interleukin 33	Homo sapiens	118-123
20798393-1	2010	The ornithine decarboxylase-1 (ODC1) polymorphism at position +316 affects binding by transcriptional activators and repressors and modulates the risk of metachronous colorectal adenomas, particularly in association with aspirin use.	Aspirin	221-228	ornithine decarboxylase 1	Homo sapiens	4-29
20798393-1	2010	The ornithine decarboxylase-1 (ODC1) polymorphism at position +316 affects binding by transcriptional activators and repressors and modulates the risk of metachronous colorectal adenomas, particularly in association with aspirin use.	Aspirin	221-228	ornithine decarboxylase 1	Homo sapiens	31-35
20705923-0	2010	Histone deacetylase 3 antagonizes aspirin-stimulated endothelial nitric oxide production by reversing aspirin-induced lysine acetylation of endothelial nitric oxide synthase.	Aspirin	34-41	histone deacetylase 3	Homo sapiens	0-21
20705923-0	2010	Histone deacetylase 3 antagonizes aspirin-stimulated endothelial nitric oxide production by reversing aspirin-induced lysine acetylation of endothelial nitric oxide synthase.	Aspirin	102-109	histone deacetylase 3	Homo sapiens	0-21
19880966-8	2010	RESULTS: After 3 and 5 months of treatment, enalapril and aspirin were able to significantly delay progression of mPanINs in LsL-Kras(G12D); Pdx1-Cre mice.	Aspirin	58-65	pancreatic and duodenal homeobox 1	Mus musculus	141-145
19880966-9	2010	Furthermore, development of invasive pancreatic cancer in LsL-Kras(G12D); LsL-Trp53(R172H); Pdx1-Cre transgenic mice was partially inhibited by enalapril and aspirin.	Aspirin	158-165	pancreatic and duodenal homeobox 1	Mus musculus	92-96
19908241-7	2010	In Western blot, combined TGZ and ASA also could downregulate Cdk2, E2F-1, cyclin B1, cyclin D3 protein, and the ratio of phospho-Rb/Rb.	Aspirin	34-37	cyclin dependent kinase 2	Homo sapiens	62-66
20094648-2	2010	Aspirin and clopidogrel, the two most widely prescribed anti-platelet drugs, are metabolized to active compounds that covalently and irreversibly modify their respective therapeutic targets (COX1 and P2Y12).	Aspirin	0-7	purinergic receptor P2Y12	Homo sapiens	200-205
19621391-6	2010	Our in vitro data using EOC cell line showed that inhibition of COX-2 by aspirin, selective inhibitor NS398 and gene silencing by COX-2 specific siRNA impaired phosphorylation of AKT resulting decreased downstream signaling leading to cell growth inhibition and induction of apoptosis.	Aspirin	73-80	prostaglandin-endoperoxide synthase 2	Mus musculus	64-69
19621391-7	2010	Finally, treatment of MDAH2774 cell line xenografts with aspirin resulted in growth inhibition of tumors in NUDE mice via down-regulation of COX-2 and AKT activity.	Aspirin	57-64	prostaglandin-endoperoxide synthase 2	Mus musculus	141-146
20370474-6	2010	With ASA on awakening, ambulatory BP was unchanged in men and slightly but significantly elevated in women (1.7/1.4 mmHg in the 48 h SBP/DBP means, respectively; p &lt; 0.023).	Aspirin	5-8	selenium binding protein 1	Homo sapiens	133-136
20370474-7	2010	BP was significantly reduced after aspirin at bedtime and to a larger extent in women (-8.0/-5.6 mmHg in SBP/DBP) than men (5.5/3.4 mmHg, respectively; p &lt; 0.009 between men and women).	Aspirin	35-42	selenium binding protein 1	Homo sapiens	105-108
21053780-7	2010	IL-5 and eosinophil cationic protein (ECP) levels showed a decreasing trend in patients with NP and an increasing trend in patients with associated aspirin sensitivity.	Aspirin	148-155	interleukin 5	Homo sapiens	0-4
19706045-8	2009	Stimulating the Wnt/beta-catenin pathway by both Wnt 3a and GSK-3beta inhibitors (LiCl and SB 216763), blocked aspirin-induced apoptosis and protected mitochondrial function, as demonstrated by decreased cytochrome c release and caspase-3 activity.	Aspirin	111-118	Wnt family member 3A	Homo sapiens	49-55
19706045-8	2009	Stimulating the Wnt/beta-catenin pathway by both Wnt 3a and GSK-3beta inhibitors (LiCl and SB 216763), blocked aspirin-induced apoptosis and protected mitochondrial function, as demonstrated by decreased cytochrome c release and caspase-3 activity.	Aspirin	111-118	glycogen synthase kinase 3 beta	Homo sapiens	60-69
20040278-2	2009	After many years of a "monopoly" of aspirin, ADP receptor P2Y12 inhibitors were introduced with a significant improvement in clinical outcome.	Aspirin	36-43	purinergic receptor P2Y12	Homo sapiens	58-63
19882081-1	2009	The P2Y12 receptor has proven to be a key target in the prevention of complications associated with atherosclerotic vascular disease especially in the context of acute coronary syndrome and percutaneous coronary intervention in addition to aspirin.	Aspirin	240-247	purinergic receptor P2Y12	Homo sapiens	4-9
17334511-10	2007	In conclusion, a GPIbalpha-blocking antibody, as well as P2Y(1) and P2Y(12) receptor antagonists, alone or in combination, reduce in contrast to aspirin human plaque-induced platelet thrombus formation under arterial flow.	Aspirin	145-152	purinergic receptor P2Y1	Homo sapiens	57-63
17259075-1	2007	Aspirin (ASA) inhibits cycloxygenase-1 and modifies cycloxygenase-2 (COX2) by acetylation at Ser(530), leading to a shift from production of PGH(2), the precursor of prostaglandin, to 15-R-HETE which is converted by 5-lipoxygenase to 15-epi-lipoxin A(4) (15-epi-LXA4), a potent anti-inflammatory mediator.	Aspirin	0-7	arachidonate 5-lipoxygenase	Rattus norvegicus	216-230
17259075-1	2007	Aspirin (ASA) inhibits cycloxygenase-1 and modifies cycloxygenase-2 (COX2) by acetylation at Ser(530), leading to a shift from production of PGH(2), the precursor of prostaglandin, to 15-R-HETE which is converted by 5-lipoxygenase to 15-epi-lipoxin A(4) (15-epi-LXA4), a potent anti-inflammatory mediator.	Aspirin	9-12	arachidonate 5-lipoxygenase	Rattus norvegicus	216-230
17264949-3	2007	It was the aim of the present study to assess whether the response to aspirin and clopidogrel may be influenced by the 807 C/T polymorphism of the glycoprotein Ia (GpIa) gene in patients with non-ST elevation acute coronary syndrome (NSTE ACS).	Aspirin	70-77	multimerin 1	Homo sapiens	147-162
17264949-3	2007	It was the aim of the present study to assess whether the response to aspirin and clopidogrel may be influenced by the 807 C/T polymorphism of the glycoprotein Ia (GpIa) gene in patients with non-ST elevation acute coronary syndrome (NSTE ACS).	Aspirin	70-77	multimerin 1	Homo sapiens	164-168
17264949-3	2007	It was the aim of the present study to assess whether the response to aspirin and clopidogrel may be influenced by the 807 C/T polymorphism of the glycoprotein Ia (GpIa) gene in patients with non-ST elevation acute coronary syndrome (NSTE ACS).	Aspirin	70-77	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	239-242
17328244-7	2007	Aspirin and phenylbutazone also dose-dependently attenuated CD4+ T cell proliferation stimulated by concanavalin A (Con A) and CD8+ CTLL-2 cell proliferation induced by interleukin (IL)-2.	Aspirin	0-7	interleukin 2	Mus musculus	169-187
17467777-7	2007	Sample storage at room temperature increased baseline activity of platelets already after 2 h. After ARA stimulation, the proportion of CD62p-positive platelets was considerably lower in aspirin-treated patients than in controls (median [lower-upper quartile]: 4% [3-6] vs. 50% [29-68], p&lt;0.001).	Aspirin	187-194	selectin P	Homo sapiens	136-141
17219690-5	2006	Aspirin DCs were demonstrated to express high levels of the co-inhibitor of T-cell activation ILT-3.	Aspirin	0-7	leukocyte immunoglobulin like receptor B4	Homo sapiens	94-99
17107286-1	2006	Clinical trials have demonstrated the superior clinical efficacy of dual antiplatelet therapy with a thienopyridine (a P2Y(12) receptor blocker) and aspirin (COX-1 inhibitor) in patients undergoing stenting as well as patients with acute coronary syndromes.	Aspirin	149-156	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	158-163
17202761-6	2006	In the profiling of an in vivo single dose, benzbromarone and aspirin were located in the same cluster of the three PPARalpha agonists.	Aspirin	62-69	peroxisome proliferator activated receptor alpha	Rattus norvegicus	116-125
17202761-7	2006	The clustering of in vitro data revealed that benzbromarone, three NSAIDs (aspirin, indomethacin and diclofenac sodium) and valproic acid belonged to the same cluster of PPARalpha agonists, supporting the reports that benzbromarone,valproic acid and some NSAIDs were reported to be PPARalpha agonists.	Aspirin	75-82	peroxisome proliferator activated receptor alpha	Rattus norvegicus	170-179
16963239-6	2006	RESULTS: Oral administration of ASA caused acute gastric erosions and an increase in myeloperoxidase activity.	Aspirin	32-35	myeloperoxidase	Rattus norvegicus	85-100
17085674-2	2006	Functional polymorphisms of UGT1A6 (T181A and R184S) and CYP2C9 (R144C and I359L) have been reported to modify the protective effect of aspirin on colorectal adenoma risk.	Aspirin	136-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
17080027-0	2006	PI3Kgamma inhibition: towards an "aspirin of the 21st century"?	Aspirin	34-41	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	0-9
17147060-5	2006	Significant decrease was also observed in the level of reduced glutathione (GSH), superoxide dismutase (SOD), glutathione-s-transferase and catalase activities for aspirin and nimesulide group while Celecoxib caused an increase in glutathione reductase (GR).	Aspirin	164-171	glutathione-disulfide reductase	Rattus norvegicus	231-252
17147060-5	2006	Significant decrease was also observed in the level of reduced glutathione (GSH), superoxide dismutase (SOD), glutathione-s-transferase and catalase activities for aspirin and nimesulide group while Celecoxib caused an increase in glutathione reductase (GR).	Aspirin	164-171	glutathione-disulfide reductase	Rattus norvegicus	254-256
17147060-6	2006	Aspirin and nimesulide exhibited an increase in the brush border membrane (BBM) bound enzyme activities like sucrase, lactase, maltase and alkaline phosphatase in the small intestine while celecoxib showed decrease in lactase, maltase and alkaline phosphatase.	Aspirin	0-7	lactase	Rattus norvegicus	118-125
17147060-6	2006	Aspirin and nimesulide exhibited an increase in the brush border membrane (BBM) bound enzyme activities like sucrase, lactase, maltase and alkaline phosphatase in the small intestine while celecoxib showed decrease in lactase, maltase and alkaline phosphatase.	Aspirin	0-7	lactase	Rattus norvegicus	218-225
17080224-7	2006	In the aspirin group we found significantly lower levels of TNFa and MCP-1 after one year; 1.00 versus 1.16 pg/ml (p &lt; 0.001) and 245 versus 261 pg/ml (p &lt; 0.001), respectively.	Aspirin	7-14	C-C motif chemokine ligand 2	Homo sapiens	69-74
16878161-0	2006	Effect of aspirin on the Wnt/beta-catenin pathway is mediated via protein phosphatase 2A.	Aspirin	10-17	catenin beta 1	Homo sapiens	29-41
16878161-3	2006	We studied the effects of aspirin on the oncogenic Wnt/beta-catenin pathway activity in colorectal cancer cell lines and observed that aspirin dose-dependently decreased the activity of this pathway, as judged by TCF-driven luciferase activity, reduced Wnt target gene expression and increased phosphorylation of beta-catenin by immunoblotting.	Aspirin	135-142	catenin beta 1	Homo sapiens	55-67
16878161-3	2006	We studied the effects of aspirin on the oncogenic Wnt/beta-catenin pathway activity in colorectal cancer cell lines and observed that aspirin dose-dependently decreased the activity of this pathway, as judged by TCF-driven luciferase activity, reduced Wnt target gene expression and increased phosphorylation of beta-catenin by immunoblotting.	Aspirin	135-142	catenin beta 1	Homo sapiens	313-325
16878161-5	2006	Importantly, aspirin treatment caused increased phosphorylation of protein phosphatase 2A (PP2A), an event associated with inhibition of PP2A enzymatic activity, which was confirmed by a reduction in enzymatic PP2A activity.	Aspirin	13-20	protein phosphatase 2 phosphatase activator	Homo sapiens	91-95
16878161-5	2006	Importantly, aspirin treatment caused increased phosphorylation of protein phosphatase 2A (PP2A), an event associated with inhibition of PP2A enzymatic activity, which was confirmed by a reduction in enzymatic PP2A activity.	Aspirin	13-20	protein phosphatase 2 phosphatase activator	Homo sapiens	137-141
16878161-5	2006	Importantly, aspirin treatment caused increased phosphorylation of protein phosphatase 2A (PP2A), an event associated with inhibition of PP2A enzymatic activity, which was confirmed by a reduction in enzymatic PP2A activity.	Aspirin	13-20	protein phosphatase 2 phosphatase activator	Homo sapiens	137-141
16878161-6	2006	Moreover, this inhibition of PP2A enzymatic activity was essential for the effects of aspirin on the Wnt/beta-catenin pathway as shown by transient transfection with PP2A constructs.	Aspirin	86-93	protein phosphatase 2 phosphatase activator	Homo sapiens	29-33
16878161-6	2006	Moreover, this inhibition of PP2A enzymatic activity was essential for the effects of aspirin on the Wnt/beta-catenin pathway as shown by transient transfection with PP2A constructs.	Aspirin	86-93	catenin beta 1	Homo sapiens	105-117
16878161-6	2006	Moreover, this inhibition of PP2A enzymatic activity was essential for the effects of aspirin on the Wnt/beta-catenin pathway as shown by transient transfection with PP2A constructs.	Aspirin	86-93	protein phosphatase 2 phosphatase activator	Homo sapiens	166-170
16878161-7	2006	The findings in this article provide a molecular explanation for the efficacy of aspirin in chemoprevention of colorectal cancer and shows biochemical evidence that PP2A is an important regulator of Wnt/beta-catenin pathway activity in these cells.	Aspirin	81-88	protein phosphatase 2 phosphatase activator	Homo sapiens	165-169
16894002-6	2006	Patients with ACS as the admission diagnosis more frequently received cardiac catheterization (during 2000-2001, 39% versus 17%, p &lt; 0.001), percutaneous coronary intervention (19% versus 4%, p &lt; 0.001), and evidence-based therapy; during 1998-2001, opportunities to give ASA or BB on admission were fulfilled for 88% versus 73% (p &lt; 0.001), and on discharge, for 87% versus 74% (p &lt; 0.005).	Aspirin	278-281	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	14-17
16869801-0	2006	Aspirin-treated human DCs up-regulate ILT-3 and induce hyporesponsiveness and regulatory activity in responder T cells.	Aspirin	0-7	leukocyte immunoglobulin like receptor B4	Homo sapiens	38-43
16869801-3	2006	We demonstrate that in aspirin-treated human DCs, there is reduced expression of CD1a, HLA-DR and CD86, up-regulation of ILT-3 expression and marginal increases in PDL-1.	Aspirin	23-30	leukocyte immunoglobulin like receptor B4	Homo sapiens	121-126
16869801-3	2006	We demonstrate that in aspirin-treated human DCs, there is reduced expression of CD1a, HLA-DR and CD86, up-regulation of ILT-3 expression and marginal increases in PDL-1.	Aspirin	23-30	CD274 molecule	Homo sapiens	164-169
16869801-4	2006	Aspirin-treated DCs are partially resistant to phenotypic changes following maturational stimuli, such as lipopolysaccharide (LPS) or TNFalpha, IL-1alpha and PGE2.	Aspirin	0-7	interleukin 1 alpha	Homo sapiens	144-153
16865277-8	2006	Our findings indicate that although gastric cancer does not seem to harbour mutations which render the cancer cells constitutively susceptible to gefitinib, the co-administration of ASA can strengthen RTK inhibitor activity in adenocarcinoma cells by EGFR activation.	Aspirin	182-185	ret proto-oncogene	Homo sapiens	201-204
17078596-4	2006	RESULTS: Several ex vivo studies show that some non-selective NSAIDs can block the active site of Cox1 thus preventing aspirin from exerting its platelet anti-aggregating cardio-preventive action.	Aspirin	119-126	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	98-102
17870554-4	2006	RESULTS: Several ex vivo studies show that some non-selective NSAIDs can block the active site of Cox1 thus preventing aspirin from exerting its platelet anti-aggregating cardio-preventive action.	Aspirin	119-126	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	98-102
26219912-0	2015	Aspirin Targets SIRT1 and AMPK to Induce Senescence of Colorectal Carcinoma Cells.	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	26-30
16861926-0	2006	Nitrogen oxide-releasing aspirin induces histone H2AX phosphorylation, ATM activation and apoptosis preferentially in S-phase cells: involvement of reactive oxygen species.	Aspirin	25-32	ATM serine/threonine kinase	Homo sapiens	71-74
16861926-4	2006	We observed that even brief (1 h) treatment of human B-lymphoblastoid TK6 cells with &gt;or=5 microM NO-ASA led to DNA damage revealed by the alkaline and neutral comet assays, histone H2AX phosphorylation on Ser 139, and ATM phosphorylation on Ser 1981, a marker of activation of this kinase.	Aspirin	104-107	ATM serine/threonine kinase	Homo sapiens	222-225
16895542-3	2006	However, the effect of aspirin, an assistant medication used extensively in the treatment of cardiovascular diseases, on MSC is not clear.	Aspirin	23-30	musculin	Homo sapiens	121-124
16895542-5	2006	In the present study, we investigated the effect of aspirin on the growth of MSC in vitro and the underlying mechanism of its action.	Aspirin	52-59	musculin	Homo sapiens	77-80
16895542-7	2006	The 3-(4,5-dimethyl-2 thiazoyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay revealed that 1, 5 and 10 mmol/L aspirin inhibited the growth of MSC by 18, 37 and 62%, respectively.	Aspirin	113-120	musculin	Homo sapiens	145-148
16895542-8	2006	DNA synthesis of MSC was inhibited by 25, 57 and 90% following treatment with 1, 5 and 10 mmol/L aspirin, respectively, as determined by the tritiated thymidine incorporation assay.	Aspirin	97-104	musculin	Homo sapiens	17-20
16895542-10	2006	Western blot analysis demonstrated that the protein level of phosphorylated beta-catenin increased, whereas that of cyclin D1 decreased, after treatment of MSC with aspirin.	Aspirin	165-172	catenin beta 1	Homo sapiens	76-88
16895542-10	2006	Western blot analysis demonstrated that the protein level of phosphorylated beta-catenin increased, whereas that of cyclin D1 decreased, after treatment of MSC with aspirin.	Aspirin	165-172	musculin	Homo sapiens	156-159
16895542-13	2006	These observations indicate that aspirin inhibits MSC proliferation and that the downregulation of the wnt/beta-catenin signal pathway may be involved in the growth inhibition of MSC by aspirin.	Aspirin	33-40	musculin	Homo sapiens	50-53
16895542-13	2006	These observations indicate that aspirin inhibits MSC proliferation and that the downregulation of the wnt/beta-catenin signal pathway may be involved in the growth inhibition of MSC by aspirin.	Aspirin	33-40	musculin	Homo sapiens	179-182
26219912-5	2015	In this study, we investigated the effects of aspirin on TIS of human colorectal carcinoma (CRC) cells and show that it occurs via sirtuin 1 (SIRT1) and AMP-activated protein kinase (AMPK), two key regulators of cellular metabolism.	Aspirin	46-53	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	153-181
26219912-5	2015	In this study, we investigated the effects of aspirin on TIS of human colorectal carcinoma (CRC) cells and show that it occurs via sirtuin 1 (SIRT1) and AMP-activated protein kinase (AMPK), two key regulators of cellular metabolism.	Aspirin	46-53	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	183-187
26219912-6	2015	Aspirin increased the senescence of CRC cells, increased the protein levels of SIRT1, phospho-AMPK (T172), and phospho-acetyl CoA carboxylase (S79), and reduced the cellular level of ATP.	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	94-98
26219912-7	2015	Small-interfering RNA-mediated downregulation or pharmacological inhibition of SIRT1 or AMPK significantly attenuated the aspirin-induced cellular senescence in CRC cells.	Aspirin	122-129	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	88-92
16895542-13	2006	These observations indicate that aspirin inhibits MSC proliferation and that the downregulation of the wnt/beta-catenin signal pathway may be involved in the growth inhibition of MSC by aspirin.	Aspirin	186-193	catenin beta 1	Homo sapiens	107-119
16895542-13	2006	These observations indicate that aspirin inhibits MSC proliferation and that the downregulation of the wnt/beta-catenin signal pathway may be involved in the growth inhibition of MSC by aspirin.	Aspirin	186-193	musculin	Homo sapiens	179-182
26219912-9	2015	Remarkably, SIRT1 knockdown abrogated the aspirin-induced activation of AMPK, and vice versa.	Aspirin	42-49	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	72-76
26219912-11	2015	Collectively, these novel findings suggest that aspirin could provide anticancer effects by inducing senescence in human CRC cells through the reciprocal regulation of SIRT1-AMPK pathways.	Aspirin	48-55	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	174-178
26056043-6	2015	Metformin combined with aspirin significantly inhibited the phosphorylation of mTOR and STAT3, and induced apoptosis as measured by caspase-3 and PARP cleavage.	Aspirin	24-31	collagen type XI alpha 2 chain	Homo sapiens	146-150
16792175-9	2006	In aspirin-sensitive polyps the number of eosinophils was significantly higher than in the other patient groups and they had significantly higher eotaxin, eotaxin-2, and -3 protein levels than non-allergic and significantly higher amounts of eotaxin-3 compared with allergic patients.	Aspirin	3-10	C-C motif chemokine ligand 24	Homo sapiens	155-172
26056043-7	2015	Remarkably, metformin combined with aspirin significantly downregulated the anti-apoptotic proteins Mcl-1 and Bcl-2, and upregulated the pro-apoptotic proteins Bim and Puma, as well as interrupted their interactions.	Aspirin	36-43	myeloid cell leukemia sequence 1	Mus musculus	100-105
26056043-9	2015	In a PANC-1 xenograft mouse model, we demonstrated that the combination of metformin and aspirin significantly inhibited tumor growth and downregulated the protein expression of Mcl-1 and Bcl-2 in tumors.	Aspirin	89-96	myeloid cell leukemia sequence 1	Mus musculus	178-183
26313358-4	2015	DKK-1 and SOST serum levels were assessed at baseline and were compared between the subgroup of patients fulfilling ASAS criteria for SpA (n = 486; 68.6%) and 80 healthy controls.	Aspirin	116-120	surfactant protein A1	Homo sapiens	134-137
16756193-11	2006	Flowcytometry for P-selectin expression and fibrinogen binding to platelets can be used to monitor antiplatelet therapy with aspirin following acute myocardial infarction.	Aspirin	125-132	selectin P	Homo sapiens	18-28
26294325-5	2015	Of the top 10 genes (fold-change &gt; 10, P &lt; 10(-10)) regulated by metformin plus aspirin, PCDH18, CCL2, RASL11A, FAM111B and BMP5 were down-regulated &gt;= 20-fold, while NGFR, NPTX1, C7orf57, MRPL23AS1 and UNC5B were up-regulated &gt;= 10-fold.	Aspirin	86-93	bone morphogenetic protein 5	Homo sapiens	130-134
26294325-5	2015	Of the top 10 genes (fold-change &gt; 10, P &lt; 10(-10)) regulated by metformin plus aspirin, PCDH18, CCL2, RASL11A, FAM111B and BMP5 were down-regulated &gt;= 20-fold, while NGFR, NPTX1, C7orf57, MRPL23AS1 and UNC5B were up-regulated &gt;= 10-fold.	Aspirin	86-93	MRPL23 antisense RNA 1	Homo sapiens	198-207
16771000-1	2006	INTRODUCTION: Aspirin is administered to patients with acute coronary syndromes (ACSs), but prehospital providers do not administer aspirin to all patients with chest pain that could be secondary to an ACS.	Aspirin	14-21	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	81-84
25777663-3	2015	The landmark CURE trial showed that the addition of a P2Y12 antagonist, clopidogrel, to aspirin was beneficial in the treatment of acute coronary syndromes.	Aspirin	88-95	purinergic receptor P2Y12	Homo sapiens	54-59
16488805-4	2006	Potential causes of aspirin resistance include inadequate dose, drug interactions, genetic polymorphisms of COX-1 and other genes involved in thromboxane biosynthesis, upregulation of non-platelet sources of thromboxane biosynthesis, and increased platelet turnover.	Aspirin	20-27	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	108-113
16458133-9	2006	With collagen as the agonist, platelets from PlA1/A2 donors were markedly and significantly less inhibited by ASA (p = 0.005).	Aspirin	110-113	POU class 2 homeobox 3	Homo sapiens	45-52
25859006-5	2015	Treatment of MT-COMP mice with aspirin or resveratrol from birth to P28 decreased mutant COMP intracellular retention and chondrocyte cell death, and restored chondrocyte proliferation.	Aspirin	31-38	cartilage oligomeric matrix protein	Mus musculus	16-20
16433794-1	2006	BACKGROUND: We have reported that in patients with chronic idiopathic urticaria (CIU) who reacted adversely to aspirin, the frequency of the (-444)C allele of the leukotriene C(4) synthase gene (LTC4S) was higher than in patients who tolerated aspirin well.	Aspirin	111-118	leukotriene C4 synthase	Homo sapiens	163-188
16433794-1	2006	BACKGROUND: We have reported that in patients with chronic idiopathic urticaria (CIU) who reacted adversely to aspirin, the frequency of the (-444)C allele of the leukotriene C(4) synthase gene (LTC4S) was higher than in patients who tolerated aspirin well.	Aspirin	111-118	leukotriene C4 synthase	Homo sapiens	195-200
25859006-5	2015	Treatment of MT-COMP mice with aspirin or resveratrol from birth to P28 decreased mutant COMP intracellular retention and chondrocyte cell death, and restored chondrocyte proliferation.	Aspirin	31-38	cartilage oligomeric matrix protein	Mus musculus	89-93
16433794-1	2006	BACKGROUND: We have reported that in patients with chronic idiopathic urticaria (CIU) who reacted adversely to aspirin, the frequency of the (-444)C allele of the leukotriene C(4) synthase gene (LTC4S) was higher than in patients who tolerated aspirin well.	Aspirin	244-251	leukotriene C4 synthase	Homo sapiens	163-188
16433794-1	2006	BACKGROUND: We have reported that in patients with chronic idiopathic urticaria (CIU) who reacted adversely to aspirin, the frequency of the (-444)C allele of the leukotriene C(4) synthase gene (LTC4S) was higher than in patients who tolerated aspirin well.	Aspirin	244-251	leukotriene C4 synthase	Homo sapiens	195-200
16433794-9	2006	In family 2, urticaria following aspirin ingestion was present only with variant LTC4S genotype.	Aspirin	33-40	leukotriene C4 synthase	Homo sapiens	81-86
26147767-0	2015	PPI versus Histamine H2 Receptor Antagonists for Prevention of Upper Gastrointestinal Injury Associated with Low-Dose Aspirin: Systematic Review and Meta-analysis.	Aspirin	118-125	histamine receptor H2	Homo sapiens	11-32
26135128-13	2015	CONCLUSION: Rebamipide administration in aspirin-induced SII mice could improve the intestinal barrier structure and promote the regeneration of small intestinal epithelial injury through up-regulating COX-2 expression and the accumulation of beta-catenin.	Aspirin	41-48	cytochrome c oxidase II, mitochondrial	Mus musculus	202-207
16472047-8	2006	High-dose aspirin inhibits cyclooxygenase and IkappaB kinase-beta and reduces fasting plasma glucose concentration, although there has not, as yet, been a large-scale trial to examine the effect of aspirin on the risk of developing diabetes.	Aspirin	10-17	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	46-65
15976387-1	2005	This study was undertaken to determine whether the Bcl-2 family proteins and Smac are regulators of aspirin-mediated apoptosis in a gastric mucosal cell line known as AGS cells.	Aspirin	100-107	diablo IAP-binding mitochondrial protein	Homo sapiens	77-81
15976387-6	2005	In contrast, expression of Smac was significantly decreased in mitochondrial fractions of ASA-treated cells.	Aspirin	90-93	diablo IAP-binding mitochondrial protein	Homo sapiens	27-31
25956131-0	2015	Acetyl salicylic acid protected against heat stress damage in chicken myocardial cells and may associate with induced Hsp27 expression.	Aspirin	0-21	heat shock protein family B (small) member 1	Gallus gallus	118-123
25956131-5	2015	Hsp27 expression was induced under all experimental conditions but was one-fold higher in the ASA-pretreated animals (0.3138 +- 0.0340 ng/mL) than in untreated animals (0.1437 +- 0.0476 ng/mL) 1 h after heat stress exposure, and such an increase was sustained over the length of the experiment.	Aspirin	94-97	heat shock protein family B (small) member 1	Gallus gallus	0-5
16150050-1	2005	BACKGROUND: Aspirin (acetylsalicylic acid) irreversibly inhibits platelet cyclooxygenase (COX)-1, the enzyme that converts arachidonic acid (AA) to the potent platelet agonist thromboxane (TX) A2.	Aspirin	12-19	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	74-96
18603541-10	2009	In conclusion, the prothrombotic effects described in recent observational studies are likely produced by a direct effect of aspirin, whose putative mechanism involving COX 2 inhibition remains poorly understood.	Aspirin	125-132	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	169-174
16150050-1	2005	BACKGROUND: Aspirin (acetylsalicylic acid) irreversibly inhibits platelet cyclooxygenase (COX)-1, the enzyme that converts arachidonic acid (AA) to the potent platelet agonist thromboxane (TX) A2.	Aspirin	21-41	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	74-96
25956131-6	2015	Our findings indicate that pretreatment with ASA protects chicken myocardial cells from acute heat stress in vivo with almost no obvious side effects, and this protection may involve an enhancement of Hsp27 expression.	Aspirin	45-48	heat shock protein family B (small) member 1	Gallus gallus	201-206
16150050-3	2005	AIMS: To evaluate the hypothesis that incomplete suppression of platelet COX as a consequence of variation in the COX-1 gene may affect aspirin response and thus contribute to aspirin resistance.	Aspirin	136-143	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	114-119
19486029-6	2009	RESULTS: Aspirin-induced expression of CD63, CD69 and CD203c yielded 30%, 80% and 70% sensitivity, respectively, but with poor specificity.	Aspirin	9-16	CD69 molecule	Homo sapiens	45-49
16150050-3	2005	AIMS: To evaluate the hypothesis that incomplete suppression of platelet COX as a consequence of variation in the COX-1 gene may affect aspirin response and thus contribute to aspirin resistance.	Aspirin	176-183	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	114-119
26426591-8	2015	While cyclooxygenase-1 protein decreased with the three drugs tested but not with L-NAME (p &lt; 0.05), the cyclooxygenase-2 protein decreased only with aspirin and parecoxib (p &lt; 0.05).	Aspirin	153-160	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	108-124
16150050-8	2005	RESULTS: COX-1 haplotype was significantly associated with aspirin response determined by AA-induced platelet aggregation (P = 0.004; 4 d.f.).	Aspirin	59-66	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	9-14
16150050-11	2005	Heterogeneity in the way patients respond to aspirin may in part reflect variation in COX-1 genotype.	Aspirin	45-52	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	86-91
16151033-8	2005	In contrast, therapy with C+ASA resulted in a significant inhibition of platelet activity assessed by ADP- (P=0.00001) and collagen-induced (P=0.02) aggregation; closure time prolongation (P=0.03), and reduction of platelet activation units with Ultegra (P=0.00001); expression of PECAM-1 (P=0.01), and GP IIb/IIIa activity with PAC-1 (P=0.02) when compared with ASA group.	Aspirin	28-31	ADCYAP receptor type I	Homo sapiens	329-334
16190133-3	2005	On the other hand, aspirin blocks both COX-1 and COX-2 enzymes without decreasing PGI2 but blocks TXA2 synthesis that explains its beneficial action in the prevention of coronary heart disease (CHD).	Aspirin	19-26	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	39-44
16190133-4	2005	The inhibitory action of aspirin on COX-1 and COX-2 enzymes enhances the tissue concentrations of dihomo-gamma-linolenic acid (DGLA), arachidonic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA).	Aspirin	25-32	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	36-41
19275326-8	2009	Thus asa, "morning," was easier in asau or asazu than in all of asap, asapdo, asaf, or asafte, despite the fact that the /f/ in the latter two is a possible realization of fu, with devoiced [u].	Aspirin	5-8	microtubule associated protein 9	Homo sapiens	64-68
18983829-0	2009	Human carboxylesterases HCE1 and HCE2: ontogenic expression, inter-individual variability and differential hydrolysis of oseltamivir, aspirin, deltamethrin and permethrin.	Aspirin	134-141	carboxylesterase 1	Homo sapiens	24-28
15817699-6	2005	Furthermore, Ang II and the AT(2) agonist increased prostaglandin E(2) (PGE(2)), which in turn mediated the increase in MMP-1, as shown by the inhibition of MMP-1 by indomethacin or aspirin.	Aspirin	182-189	matrix metallopeptidase 1	Homo sapiens	120-125
25772736-4	2015	We investigated the inhibition profiles by aspirin and its major metabolite salicylate of ethanol oxidation by recombinant human ADH1A, ADH1B1, ADH1B2, ADH1B3, ADH1C1, ADH1C2, ADH2, and ADH4, and acetaldehyde oxidation by ALDH1A1 and ALDH2, at pH 7.5 and 0.5 mM NAD(+).	Aspirin	43-50	aldehyde dehydrogenase 2 family member	Homo sapiens	234-239
15817699-6	2005	Furthermore, Ang II and the AT(2) agonist increased prostaglandin E(2) (PGE(2)), which in turn mediated the increase in MMP-1, as shown by the inhibition of MMP-1 by indomethacin or aspirin.	Aspirin	182-189	matrix metallopeptidase 1	Homo sapiens	157-162
25834652-3	2015	The aim of this study was to investigate the effectiveness of Ankaferd blood clotter (ABC) as a new topical herbal blood clotter to decrease mediastinal bleeding in emergent beating heart CABG patients who medicated with clopidogrel and acetyl salisilic acite (ASA) prior to CABG surgery.	Aspirin	261-264	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	62-84
15990700-2	2005	In contrast, aspirin blocks both COX-1 and COX-2 enzymes that, in turn, increases intracellular concentrations of dihomo-gamma-linolenic acid (DGLA), arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and reduced formation of eicosanoids.	Aspirin	13-20	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	33-38
15770215-8	2005	Here, we set out to determine the p53 and hMLH1 dependency of the effects of aspirin on NFkappaB signalling and apoptosis in CRC.	Aspirin	77-84	mutL homolog 1	Homo sapiens	42-47
19910682-5	2009	The cyclooxygenase inhibitor aspirin decreased erythrocyte PS exposure in infected annexin-A7(-/-) mice and abolished the differences of parasitemia and survival between the genotypes.	Aspirin	29-36	annexin A7	Mus musculus	83-93
19207549-0	2009	Influence of aspirin and cigarette smoke extract on the expression of cyclin D1 and effects of cell cycle in esophageal squamous cell carcinoma cell line.	Aspirin	13-20	cyclin D1	Homo sapiens	70-79
19207549-6	2009	However, aspirin can inhibit the cell growth and suppress the protein level of cyclin D(1) after CSE affected the EC109 cell line in a dose-dependent manner (P &lt; 0.01).	Aspirin	9-16	cyclin D1	Homo sapiens	79-90
25834652-3	2015	The aim of this study was to investigate the effectiveness of Ankaferd blood clotter (ABC) as a new topical herbal blood clotter to decrease mediastinal bleeding in emergent beating heart CABG patients who medicated with clopidogrel and acetyl salisilic acite (ASA) prior to CABG surgery.	Aspirin	261-264	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	86-89
19207549-8	2009	Aspirin can inhibit the cell growth and suppress the protein level of cyclin D(1) after CSE affected EC109 cell line.	Aspirin	0-7	cyclin D1	Homo sapiens	70-81
25834652-18	2015	To provide cardiac tamponade because of excessive mediastinal bleeding and requirement of blood transfusion after emergent CABG patients who previously administered clopidogrel and ASA, we propose local use of ABC solution as a potent coagulant agent.	Aspirin	181-184	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	210-213
25743752-8	2015	Thus, we confirmed in this study that aspirin promoted lipid oxidation by upregulating the AMPK signaling pathway.	Aspirin	38-45	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	91-95
20008209-3	2009	After many years of a "monopoly" of aspirin, ADP receptor P2Y12 inhibitors were introduced with a significant improvement in clinical outcome.	Aspirin	36-43	purinergic receptor P2Y12	Homo sapiens	58-63
18971601-0	2009	Aspirin inhibits MMP-2 and MMP-9 expressions and activities through upregulation of PPARalpha/gamma and TIMP gene expressions in ox-LDL-stimulated macrophages derived from human monocytes.	Aspirin	0-7	matrix metallopeptidase 2	Homo sapiens	17-22
18971601-3	2009	Following treatment of cells with aspirin, MMP-2 and MMP-9 expression and release were significantly reduced.	Aspirin	34-41	matrix metallopeptidase 2	Homo sapiens	43-48
18971601-10	2009	These results demonstrate that aspirin could inhibit MMP-2 and MMP-9 expression through upregulation of PPARalpha/gamma expression in ox-LDL-stimulated macrophages, and could potentially inhibit MMP-2 and MMP-9 activity by induction of TIMP-1 and TIMP-2 expression.	Aspirin	31-38	matrix metallopeptidase 2	Homo sapiens	53-58
15757620-2	2005	Aspirin resistance was significantly associated with genetic variation in the platelet surface adenosine 5-diphosphate receptor gene P2Y1.	Aspirin	0-7	purinergic receptor P2Y1	Homo sapiens	133-137
15579484-7	2005	We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release.	Aspirin	15-22	caspase 9	Homo sapiens	44-53
18971601-10	2009	These results demonstrate that aspirin could inhibit MMP-2 and MMP-9 expression through upregulation of PPARalpha/gamma expression in ox-LDL-stimulated macrophages, and could potentially inhibit MMP-2 and MMP-9 activity by induction of TIMP-1 and TIMP-2 expression.	Aspirin	31-38	matrix metallopeptidase 2	Homo sapiens	195-200
25342594-7	2015	Either Aspirin or LUT gavages alone or combined produce a significant decrease in colon polyp number and size, significantly decreasing CEA, COX-2, and oxidative stress and increasing antioxidant markers.	Aspirin	7-14	CEA cell adhesion molecule 20	Rattus norvegicus	136-139
18982014-11	2008	CONCLUSIONS: In adipose tissue, constitutive COX-2-coupled prostacyclin triggers the release of basal IL-6, which in obese subjects is significantly dampened by ASA ingestion, thus offering a novel, modifiable pathway to regulate the potentially pathological component of this cytokine.	Aspirin	161-164	cytochrome c oxidase II, mitochondrial	Mus musculus	45-50
18547651-6	2008	The activation of NF-kappaB was followed by increased mRNA expression of TNF-alpha and IL-1beta peaking at about 20 h. In the presence of microglia, aspirin significantly inhibited neuro-2a cell death induced by PrP106-126.	Aspirin	149-156	prion protein	Mus musculus	212-215
15871445-1	2005	Intolerance reactions to acetyl salicylic acid (ASA) and nonsteroidal anti-inflammatory drugs (NSAIDs) are common and caused by inhibition of COX-1 enzyme.	Aspirin	25-46	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	142-147
15871445-1	2005	Intolerance reactions to acetyl salicylic acid (ASA) and nonsteroidal anti-inflammatory drugs (NSAIDs) are common and caused by inhibition of COX-1 enzyme.	Aspirin	48-51	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	142-147
18673140-3	2008	Aspirin and salicylic acid (SA) are allosteric inhibitors of ET-1 binding to ET(A) receptors.	Aspirin	0-7	endothelin receptor type A	Rattus norvegicus	77-82
25342594-7	2015	Either Aspirin or LUT gavages alone or combined produce a significant decrease in colon polyp number and size, significantly decreasing CEA, COX-2, and oxidative stress and increasing antioxidant markers.	Aspirin	7-14	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	141-146
15626589-4	2005	The administration of aspirin 50 mg daily for 5 consecutive days to colorectal cancer patients caused a cumulative inhibition of platelet cyclooxygenase (COX)-1 activity either ex vivo, as assessed by the measurement of serum TXB(2) levels, or in vivo, as assessed by urinary 11-dehydro-TXB(2) excretion.	Aspirin	22-29	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	138-160
15626589-6	2005	Permanent inactivation of platelet COX-1 by low-dose aspirin might restore anti-tumor reactivity.	Aspirin	53-60	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	35-40
25464488-0	2015	Aspirin-triggered 15-epi-lipoxin A4 signals through FPR2/ALX in vascular smooth muscle cells and protects against intimal hyperplasia after carotid ligation.	Aspirin	0-7	hematopoietic SH2 domain containing	Homo sapiens	57-60
15613743-13	2004	ASA and rofecoxib, that significantly suppressed the mucosal prostaglandin (PG) E(2) generation in ulcer area, delayed significantly the rate of ulcer healing and decreased the GBF at ulcer margin, while elevating plasma IL-1beta, TNF-alpha and IL-10 concentrations in non-diabetic rats and these alterations were significantly augmented in diabetic animals.	Aspirin	0-3	interleukin 10	Rattus norvegicus	245-250
15613743-14	2004	In contrast to ASA, the treatment with NO-ASA failed to influence both, the ulcer healing and GBF at ulcer margin and significantly attenuated the plasma levels of IL-1beta, TNF-alpha and IL-10 as compared to those recorded in ASA- or rofecoxib-treated animals.	Aspirin	42-45	interleukin 10	Rattus norvegicus	188-193
15613743-14	2004	In contrast to ASA, the treatment with NO-ASA failed to influence both, the ulcer healing and GBF at ulcer margin and significantly attenuated the plasma levels of IL-1beta, TNF-alpha and IL-10 as compared to those recorded in ASA- or rofecoxib-treated animals.	Aspirin	42-45	interleukin 10	Rattus norvegicus	188-193
15658056-2	2004	The role of aspirin, as an irreversible COX-1 inhibitor and antiplatelet agent, is well elucidated and established.	Aspirin	12-19	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	40-45
18374541-6	2008	This is a general effect for NSAIDs because sulindac sulfide, aspirin and indomethacin also inhibited the binding of c-Raf to Ras.	Aspirin	62-69	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	117-122
25744739-6	2015	Treatment with aspirin and new P2Y12 receptor blockers has further reduced the rate of cardiovascular death, myocardial infarction or stroke after ACS compared with aspirin and clopidogrel.	Aspirin	165-172	purinergic receptor P2Y12	Homo sapiens	31-36
26224244-1	2015	INTRODUCTION: Clopidogrel, prasugrel, and ticagrelor are the currently available oral P2Y12 inhibitors for the treatment of ST-segment elevation myocardial infarction (STEMI), in association with aspirin.	Aspirin	196-203	purinergic receptor P2Y12	Homo sapiens	86-91
15505105-9	2004	CONCLUSIONS: Anti-GP VI therapy may result in defective hemostasis in patients with reduced alpha2beta1 levels or concomitant aspirin therapy.	Aspirin	126-133	glycoprotein VI platelet	Homo sapiens	18-23
15485683-4	2004	We hypothesized that aspirin may interfere with LOX-1 expression and subsequent MMP activation.	Aspirin	21-28	matrix metallopeptidase 1	Homo sapiens	80-83
15485683-11	2004	CONCLUSION: These observations suggest that aspirin inhibits ox-LDL-mediated LOX-1 expression and interferes with the effects of ox-LDL in intracellular signaling (p38MAPK activation) and subsequent MMP-1 activity.	Aspirin	44-51	matrix metallopeptidase 1	Homo sapiens	199-204
26466642-5	2015	Preconditioning with aspirin but not rapamycin tended to reduce the number of mouse bone marrow-derived immature DCs expressing CD40 and major histocompatibility complex class II molecules upon LPS stimulation.	Aspirin	21-28	CD40 antigen	Mus musculus	128-132
15576013-7	2004	It is plausible that the COX-2 inhibition is associated with altered homeostasis that is compensated with the cardioprotection effect of COX-1 inhibition that patients receive either through the less COX-2 selectivity of other NSAIDs or through co-administration of low dose aspirin.	Aspirin	275-282	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	137-142
15358033-2	2004	BACKGROUND: NCX-4016 is an aspirin derivative containing a nitric oxide-releasing moiety that prevents platelet activation and modulates tissue factor (TF) expression and cytokine release from lipopolysaccharide (LPS)-stimulated monocytes.	Aspirin	27-34	coagulation factor III, tissue factor	Homo sapiens	137-150
15358033-2	2004	BACKGROUND: NCX-4016 is an aspirin derivative containing a nitric oxide-releasing moiety that prevents platelet activation and modulates tissue factor (TF) expression and cytokine release from lipopolysaccharide (LPS)-stimulated monocytes.	Aspirin	27-34	coagulation factor III, tissue factor	Homo sapiens	152-154
15136050-0	2004	Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-alpha stimulated human umbilical vein endothelial cells.	Aspirin	0-7	C-C motif chemokine ligand 2	Homo sapiens	17-51
15136050-6	2004	In this study, we found that aspirin inhibited TNF-alpha (10 ng/ml)-induced MCP-1 and IL-8 expression at the RNA and protein levels in human umbilical vein endothelial cells (HUVECs), monocyte adhesion and transmigration, and that its inhibitory effects were not due to decreased HUVEC viability as assessed by MTT test.	Aspirin	29-36	C-C motif chemokine ligand 2	Homo sapiens	76-81
15136050-7	2004	Aspirin at the dose as low as 10 microg/ml significantly inhibited the release of TNF-stimulated MCP-1 by 29.1% (P = 0.008) and IL-8 by 26.9% (P = 0.0146) as compared to TNF-stimulated release.	Aspirin	0-7	C-C motif chemokine ligand 2	Homo sapiens	97-102
15136050-11	2004	These results in our study suggest that aspirin inhibits TNF-alpha stimulated MCP-1 and IL-8 release in HUVECs, for its additional therapeutic effects of aspirin in causing atherosclerosis.	Aspirin	40-47	C-C motif chemokine ligand 2	Homo sapiens	78-83
15140133-6	2004	A lack of shape change was also observed in aspirin-treated P2Y(1)- and G(alphaq)-deficient mouse platelets and in delta-storage pool-deficient platelets from Fawn Hooded rats.	Aspirin	44-51	purinergic receptor P2Y, G-protein coupled 1	Mus musculus	60-73
15140133-7	2004	In contrast, when the second ADP receptor P2Y(12) was inhibited with AR-C69931MX, aspirin-treated platelets were still able to change shape and displayed only a moderate decrease in aggregation and secretion.	Aspirin	82-89	purinergic receptor P2Y12	Rattus norvegicus	42-49
15140134-3	2004	Alpha granule release was measured by determining P-selectin surface expression in aspirin-treated washed platelets.	Aspirin	83-90	selectin P	Homo sapiens	50-60
15156148-5	2004	Developmental exposure to the COX inhibitor aspirin results in mild impairment of sexual behavior.	Aspirin	44-51	coproporphyrinogen oxidase	Rattus norvegicus	30-33
15309216-1	2004	This study was conducted to assess the feasibility of COX1 NSAID substitution for aspirin for preventative therapy related to circulating anticoagulants, as manifest by inhibition of platelet aggregation.	Aspirin	82-89	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	54-58
15095932-4	2004	DATA SYNTHESIS: For the patient with ST-segment elevation (STE) ACS, nonenteric-coated aspirin should be initiated immediately, if possible before arrival at the emergency department.	Aspirin	87-94	sulfotransferase family 1E member 1	Homo sapiens	59-62
14975457-2	2004	Aspirin and older agents in this class are nonselective inhibitors of both COX-1 and COX-2.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	75-80
14975457-4	2004	Among the NSAID, only aspirin has been proven to significantly reduce cardiovascular risk, primarily through inhibition of COX-1-mediated platelet aggregation.	Aspirin	22-29	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	123-128
14637166-5	2003	HO-1 mRNA was significantly elevated by either ASA or vitamin C in gastric epithelial cells, combination of both substances further increased expression.	Aspirin	47-50	heme oxygenase 1	Homo sapiens	0-4
14637166-6	2003	HO-1 protein and enzyme activity rose in cells exposed to vitamin C alone or combined with ASA, but not after stimulation with ASA alone.	Aspirin	91-94	heme oxygenase 1	Homo sapiens	0-4
14637166-6	2003	HO-1 protein and enzyme activity rose in cells exposed to vitamin C alone or combined with ASA, but not after stimulation with ASA alone.	Aspirin	127-130	heme oxygenase 1	Homo sapiens	0-4
14637166-7	2003	In contrast to endothelia, in which ASA simultaneously induces HO-1 mRNA and protein expression, gastric epithelial cells require vitamin C to translate HO-1 mRNA into active protein, which then may exert gastroprotection by its antioxidant and vasodilative properties.	Aspirin	36-39	heme oxygenase 1	Homo sapiens	63-67
12816731-0	2003	Bronchial mast cells are the dominating LTC4S-expressing cells in aspirin-tolerant asthma.	Aspirin	66-73	leukotriene C4 synthase	Homo sapiens	40-45
12816731-2	2003	Multicolor immunohistofluorescence examination of bronchial cryosections from 30 treated, untreated, or bronchial antigen-provoked aspirin-tolerant individuals with asthma and nine control subjects revealed that the dominating LTC4S-expressing cells were mast cells (&gt; 80%), and not eosinophils.	Aspirin	131-138	leukotriene C4 synthase	Homo sapiens	227-232
12816731-7	2003	Thus, mucosal mast cells, and not eosinophils, were the dominating LTC4S-containing cells in both untreated and treated aspirin-tolerant asthma.	Aspirin	120-127	leukotriene C4 synthase	Homo sapiens	67-72
14597584-5	2003	Thrombin and TXA2 also synergized with P2Y12 in the absence of anticoagulation, because combined treatment of aspirin or C921-78 (a factor Xa inhibitor) with CT50547 or 2-MeSAMP (a P2Y12 antagonist) inhibited the thrombotic process, whereas all treatments failed to inhibit thrombosis when used individually.	Aspirin	110-117	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	39-44
14597584-6	2003	Synergism was also observed ex vivo when P2Y12-deficient (P2Y12-/-) mice were administered aspirin or coagulation inhibitors (C921-78 and bivalirudin).	Aspirin	91-98	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	41-46
14597584-8	2003	CONCLUSIONS: Our study indicates that (1) thrombin inhibitors and aspirin have a demonstrable synergy of antithrombotic activity with P2Y12 antagonism and (2) the in vitro analysis of the antithrombotic activity of P2Y12 antagonists is affected by the anticoagulant used for blood collection.	Aspirin	66-73	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	134-139
14597584-8	2003	CONCLUSIONS: Our study indicates that (1) thrombin inhibitors and aspirin have a demonstrable synergy of antithrombotic activity with P2Y12 antagonism and (2) the in vitro analysis of the antithrombotic activity of P2Y12 antagonists is affected by the anticoagulant used for blood collection.	Aspirin	66-73	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	215-220
14597584-9	2003	This suggests that the antithrombotic potential of P2Y12 antagonists in vitro may be overestimated in anticoagulated samples of blood and best achieved in vivo by the inclusion of aspirin and/or a thrombin inhibitor.	Aspirin	180-187	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	51-56
14597948-4	2003	Results and conclusions The therapy with aspirin plus clopidogrel attenuated agonist-induced platelet aggregation and P-selectin surface exposure (P &lt;.05 vs aspirin monotherapy).	Aspirin	41-48	selectin P	Homo sapiens	118-128
14532966-8	2003	Furthermore, aspirin inhibited migration of PC-3 cells, suggesting an effect on the uPA-uPAR signaling complex.	Aspirin	13-20	plasminogen activator, urokinase receptor	Homo sapiens	88-92
14532966-10	2003	Altogether, our data suggests that aspirin inhibits the formation of uPA-uPAR-FN-alpha3beta1 and uPA-uPAR-VN-alphavbeta3 complexes, resulting in the suppression of cell adhesion and cell motility of the highly invasive prostate cancer cells PC-3.	Aspirin	35-42	plasminogen activator, urokinase receptor	Homo sapiens	73-77
14532966-10	2003	Altogether, our data suggests that aspirin inhibits the formation of uPA-uPAR-FN-alpha3beta1 and uPA-uPAR-VN-alphavbeta3 complexes, resulting in the suppression of cell adhesion and cell motility of the highly invasive prostate cancer cells PC-3.	Aspirin	35-42	plasminogen activator, urokinase receptor	Homo sapiens	101-105
14592549-1	2003	Inhibition of platelet cyclooxygenase (COX)-1 is involved in aspirin cardioprotection observed in clinical trials, but, in some patients, aspirin is unable to protect from thrombotic complications.	Aspirin	61-68	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	23-45
14592549-2	2003	An incomplete suppression of platelet thromboxane (TX) A2 biosynthesis has been assumed to participate in the phenomenon of aspirin resistance, as a consequence of the following possible mechanisms: (i) COX-2 expression in newly formed platelets; (ii) pharmacodynamic interactions between aspirin and coadministered nonsteroidal antiinflammatory drugs (e.g. ibuprofen); (iii) expression of variant isoforms of COX-1 with reduced sensitivity to irreversible inactivation at Ser529.	Aspirin	124-131	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	410-415
14592549-4	2003	Thus, in a subset of patients with unstable angina treated with low-dose aspirin, to almost completely block platelet COX-1 activity, enhanced TXA2 biosynthesis in vivo has been demonstrated, presumably through an increased generation of COX-2-dependent PGH2 in plaque monocytes/macrophages or activated vascular cells.	Aspirin	73-80	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	118-123
12945880-8	2003	These data suggest reduced release of circulating TF by combined anti-platelet therapy with ticlopidine and aspirin after coronary artery stenting, which may-contribute to the lower incidence of subacute stent thrombosis previously observed.	Aspirin	108-115	coagulation factor III, tissue factor	Homo sapiens	50-52
12813129-0	2003	Reduction of beta-catenin/T-cell transcription factor signaling by aspirin and indomethacin is caused by an increased stabilization of phosphorylated beta-catenin.	Aspirin	67-74	catenin beta 1	Homo sapiens	13-25
12813129-0	2003	Reduction of beta-catenin/T-cell transcription factor signaling by aspirin and indomethacin is caused by an increased stabilization of phosphorylated beta-catenin.	Aspirin	67-74	catenin beta 1	Homo sapiens	150-162
12813129-4	2003	Previously, we have shown that the nonsteroidal anti-inflammatory drugs (NSAIDs) aspirin and indomethacin down-regulate beta-catenin/TCF signaling in colorectal cancer cells.	Aspirin	81-88	catenin beta 1	Homo sapiens	120-132
12813129-8	2003	The aspirin-induced beta-catenin phosphorylation in colon cancer cells preceded down-regulation of beta-catenin/TCF signaling, suggesting a causal relationship.	Aspirin	4-11	catenin beta 1	Homo sapiens	20-32
12813129-8	2003	The aspirin-induced beta-catenin phosphorylation in colon cancer cells preceded down-regulation of beta-catenin/TCF signaling, suggesting a causal relationship.	Aspirin	4-11	catenin beta 1	Homo sapiens	99-111
18413818-0	2008	Ornithine decarboxylase G316A genotype is prognostic for colorectal adenoma recurrence and predicts efficacy of aspirin chemoprevention.	Aspirin	112-119	ornithine decarboxylase 1	Homo sapiens	0-23
18413818-3	2008	We investigated the influence of ODC G316A on the chemopreventive activity of aspirin in colorectal adenoma (CRA) recurrence.	Aspirin	78-85	ornithine decarboxylase 1	Homo sapiens	33-36
18413818-4	2008	EXPERIMENTAL DESIGN: We genotyped ODC G316A in 546 individuals in the United Kingdom Colorectal Adenoma Prevention trial of aspirin for CRA recurrence prevention and pooled our findings with data from two other randomized intervention trials.	Aspirin	124-131	ornithine decarboxylase 1	Homo sapiens	34-37
18413818-5	2008	RESULTS: The United Kingdom Colorectal Adenoma Prevention participants with homozygous ODC 316AA genotype were at reduced CRA recurrence risk [relative risk (RR), 0.43; 95% confidence interval (95% CI), 0.16-1.15], particularly if also exposed to aspirin (RR, 0.24; 95% CI, 0.03-1.71).	Aspirin	247-254	ornithine decarboxylase 1	Homo sapiens	87-90
18413818-7	2008	Following stratification by genotype and aspirin exposure, individuals with homozygous wild-type or heterozygous genotypes derived modest benefit from aspirin (RR, 0.85; 95% CI, 0.72-1.01), whereas in those with both ODC 316AA genotype and aspirin exposure recurrence risk was halved (RR, 0.52; 95% CI, 0.29-0.91).	Aspirin	151-158	ornithine decarboxylase 1	Homo sapiens	217-220
18413818-7	2008	Following stratification by genotype and aspirin exposure, individuals with homozygous wild-type or heterozygous genotypes derived modest benefit from aspirin (RR, 0.85; 95% CI, 0.72-1.01), whereas in those with both ODC 316AA genotype and aspirin exposure recurrence risk was halved (RR, 0.52; 95% CI, 0.29-0.91).	Aspirin	151-158	ornithine decarboxylase 1	Homo sapiens	217-220
18413818-8	2008	CONCLUSION: The ODC G316A genotype is prognostic for CRA recurrence and predictive of an enhanced response to aspirin in preventing recurrence.	Aspirin	110-117	ornithine decarboxylase 1	Homo sapiens	16-19
17995973-3	2008	* The majority of patients with vascular disease receive acetylsalicylic acid as an anti-aggregatory agent, which has also been shown to induce a variable response; however, the role of P2Y(12) ADP receptor polymorphisms in the platelet response to acetylsalicylic acid in patients with vascular disease has not yet been studied.	Aspirin	249-269	purinergic receptor P2Y12	Homo sapiens	186-193
18082496-6	2008	In contrast, when compared with the ASA group, therapy with C + ASA resulted in significant inhibition of platelet activity assessed by adenosine diphosphate aggregation (P = .0001); closure time prolongation (P = .0003) and reduction of platelet activation units with Ultegra (P = .0001); and expression of platelet/endothelial cell adhesion molecule 1 (P = .002), glycoprotein IIb/IIIa antigen (P = .0002), and activity (P = .0001).	Aspirin	64-67	platelet and endothelial cell adhesion molecule 1	Homo sapiens	308-353
17521312-0	2007	EAACI/GA2LEN guideline: aspirin provocation tests for diagnosis of aspirin hypersensitivity.	Aspirin	24-31	electron transfer flavoprotein subunit alpha	Homo sapiens	6-9
17521312-0	2007	EAACI/GA2LEN guideline: aspirin provocation tests for diagnosis of aspirin hypersensitivity.	Aspirin	67-74	electron transfer flavoprotein subunit alpha	Homo sapiens	6-9
17526656-9	2007	In addition, NO-aspirin downregulated inducible NO synthase (iNOS; 0.37-fold, P &lt; 0.01) and cyclooxygenase-2 (COX-2; 0.61-fold, P &lt; 0.05) gene expression compared with the vehicle group after 48 h of reperfusion.	Aspirin	16-23	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	95-111
17526656-9	2007	In addition, NO-aspirin downregulated inducible NO synthase (iNOS; 0.37-fold, P &lt; 0.01) and cyclooxygenase-2 (COX-2; 0.61-fold, P &lt; 0.05) gene expression compared with the vehicle group after 48 h of reperfusion.	Aspirin	16-23	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	113-118
17503164-3	2007	Here, based on the ASA, we have defined a new factor, the surface stability factor (SSF).	Aspirin	19-22	peter pan homolog	Homo sapiens	84-87
17622933-7	2007	Further, UGT1A6 *1/*1 individuals excreted a lower percentage of aspirin and its metabolites in the first 12 h and a greater percentage after 12 h than UGT1A6 *2/*2 individuals.	Aspirin	65-72	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	9-15
26517138-0	2015	The Implication of the Polymorphisms of COX-1, UGT1A6, and CYP2C9 among Cardiovascular Disease (CVD) Patients Treated with Aspirin.	Aspirin	123-130	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	47-53
17426257-10	2007	Aspirin did not prevent complication in JAK2 (617V&gt;F)-positive patients and appeared to worsen outcome in JAK2 (617V&gt;F)-negative patients.	Aspirin	0-7	Janus kinase 2	Homo sapiens	109-113
26517138-1	2015	PURPOSE:   Enzymes potentially responsible for the pharmacokinetic variations of aspirin include cyclooxygenase-1 (COX-1), UDP-glucuronosyltransferase (UGT1A6) and P450 (CYP) (CYP2C9).	Aspirin	81-88	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	152-158
12778080-0	2003	Age-related difference in susceptibility of Apc(Min/+) mice towards the chemopreventive efficacy of dietary aspirin and curcumin.	Aspirin	108-115	APC, WNT signaling pathway regulator	Mus musculus	44-47
26517138-10	2015	CONCLUSION: Screening of patients with defective genetic variants of UGT1A6 and CYP2C9*3 helps in identifying patients at risk of aspirin induced gastritis.	Aspirin	130-137	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	69-75
12778080-1	2003	The nonsteroidal anti-inflammatory drug aspirin and the spice curcumin retard adenoma formation when administered long-term to Apc(Min/+) mice, a model of human familial adenomatous polyposis coli.	Aspirin	40-47	APC, WNT signaling pathway regulator	Mus musculus	127-130
24433337-3	2015	Recent data also suggest that P2Y12 antagonists can affect the response to aspirin.	Aspirin	75-82	purinergic receptor P2Y12	Homo sapiens	30-35
12778080-3	2003	When aspirin is administered to Apc(Min/+) mice only postweaning, but not before, it is inefficacious, while curcumin given postweaning is active.	Aspirin	5-12	APC, WNT signaling pathway regulator	Mus musculus	32-35
17966595-11	2007	Independent predictors of beta-thromboglobulin were a male gender and aspirin use cessation (beta = 0.46; p = 0.01).	Aspirin	70-77	pro-platelet basic protein	Homo sapiens	26-46
17545350-1	2007	OBJECTIVE: To determine the efficacy of a computerised decision aid in patients with atrial fibrillation making decisions on whether to take warfarin or aspirin therapy.	Aspirin	153-160	activation induced cytidine deaminase	Homo sapiens	64-67
25350775-2	2015	However, higher on-treatment platelet reactivity was associated with lower plasma miR-223 in patients with coronary artery disease (CAD) on dual antiplatelet therapy (DAPT) including clopidogrel and aspirin.	Aspirin	199-206	microRNA 223	Homo sapiens	82-89
17535415-15	2007	COX-2 expression decreased after dietary aspirin or aspirin and PEITC treatment.	Aspirin	41-48	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-5
17535415-15	2007	COX-2 expression decreased after dietary aspirin or aspirin and PEITC treatment.	Aspirin	52-59	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-5
17496729-7	2007	In the haplotype analysis of each gene, the frequency of PTGIR ht3[G-G-C-C], which includes 1915T&gt;C, differed significantly between the aspirin-intolerant asthma patients and aspirin-tolerant asthma patients (P=0.015).	Aspirin	139-146	prostaglandin I2 receptor	Homo sapiens	57-62
17496729-7	2007	In the haplotype analysis of each gene, the frequency of PTGIR ht3[G-G-C-C], which includes 1915T&gt;C, differed significantly between the aspirin-intolerant asthma patients and aspirin-tolerant asthma patients (P=0.015).	Aspirin	178-185	prostaglandin I2 receptor	Homo sapiens	57-62
12778080-4	2003	Here the hypothesis was tested that dietary aspirin (0.05%) or curcumin (0.2%) prevent or delay adenoma formation in offsprings when administered to Apc(Min/+) mothers and up to the end of weaning, but not afterwards.	Aspirin	44-51	APC, WNT signaling pathway regulator	Mus musculus	149-152
12778080-8	2003	These results show that aspirin exerts chemopreventive activity in the Apc(Min/+) mouse during tumour initiation/early promotion, while curcumin is efficacious when given at a later stage of carcinogenic progression.	Aspirin	24-31	APC, WNT signaling pathway regulator	Mus musculus	71-74
12591106-11	2003	One tablet of aspirin moderately inhibited expression of most surface platelet receptors measured, and such inhibition reached significance (p&lt;0.05) for PAC-1, CD31, CD41, CD42, CD62p, and CD151.	Aspirin	14-21	selectin P	Homo sapiens	181-186
12515107-5	2002	Is the recent publication of PEP trial showing a significant decrease of pulmonary embolism mortality (0.6 versus 0.3%, p = 0.03) able to reinforce aspirin use in venous thrombosis prophylaxis?	Aspirin	148-155	progestagen associated endometrial protein	Homo sapiens	29-32
12569976-0	2002	Uncoupled regulation of leukotriene C4 synthase in platelets from aspirin-intolerant asthmatics and healthy volunteers after aspirin treatment.	Aspirin	125-132	leukotriene C4 synthase	Homo sapiens	24-47
12569976-4	2002	METHODS: The effect of arachidonic acid or platelet agonists on LTC4 synthase activity was investigated in platelets obtained from healthy volunteers, aspirin-intolerant asthmatics or aspirin-tolerant asthmatics after in vivo treatment or in vitro pre-incubation with aspirin.	Aspirin	151-158	leukotriene C4 synthase	Homo sapiens	64-77
12569976-4	2002	METHODS: The effect of arachidonic acid or platelet agonists on LTC4 synthase activity was investigated in platelets obtained from healthy volunteers, aspirin-intolerant asthmatics or aspirin-tolerant asthmatics after in vivo treatment or in vitro pre-incubation with aspirin.	Aspirin	184-191	leukotriene C4 synthase	Homo sapiens	64-77
12569976-4	2002	METHODS: The effect of arachidonic acid or platelet agonists on LTC4 synthase activity was investigated in platelets obtained from healthy volunteers, aspirin-intolerant asthmatics or aspirin-tolerant asthmatics after in vivo treatment or in vitro pre-incubation with aspirin.	Aspirin	184-191	leukotriene C4 synthase	Homo sapiens	64-77
12569976-7	2002	Arachidonic acid-induced inhibition of LTC4 synthase activity was totally abolished in platelets collected from peripheral blood already 30 min after aspirin ingestion but was fully restored in platelets collected 3 to 7 days after the administration of aspirin.	Aspirin	150-157	leukotriene C4 synthase	Homo sapiens	39-52
12569976-7	2002	Arachidonic acid-induced inhibition of LTC4 synthase activity was totally abolished in platelets collected from peripheral blood already 30 min after aspirin ingestion but was fully restored in platelets collected 3 to 7 days after the administration of aspirin.	Aspirin	254-261	leukotriene C4 synthase	Homo sapiens	39-52
12569976-10	2002	Similarly, LTC4 synthase activity in platelets from AIA and aspirin-tolerant asthmatics (ATA) was reduced by approximately 50% after pre-treatment with arachidonic acid in vitro.	Aspirin	60-67	leukotriene C4 synthase	Homo sapiens	11-24
12067934-7	2002	RESULTS: Performance of coronary angiography and percutaneous coronary interventions (PCI) during the hospital stay were independent predictors of prescription of aspirin at discharge (odds ratio (OR) 1.29 and 1.89, p = 0.053 and p &lt; 0.0001, respectively).	Aspirin	163-170	olfactory receptor family 4 subfamily F member 16	Homo sapiens	185-211
12131538-7	2002	The simultaneous treatment with aspirin prevented the increase in SBP, in plasma glucose levels and in aortic O2- production, and attenuated the rise in insulin levels as well as insulin resistance in the glucose-fed rats.	Aspirin	32-39	spermine binding protein	Rattus norvegicus	66-69
12131538-8	2002	Positive correlations between aortic O2- production and SBP, as well as between insulin resistance and SBP or between O2- production and insulin resistance, were found in control, glucose-fed and aspirin-treated, glucose-fed rats.	Aspirin	196-203	spermine binding protein	Rattus norvegicus	56-59
12131538-8	2002	Positive correlations between aortic O2- production and SBP, as well as between insulin resistance and SBP or between O2- production and insulin resistance, were found in control, glucose-fed and aspirin-treated, glucose-fed rats.	Aspirin	196-203	spermine binding protein	Rattus norvegicus	80-106
12063521-0	2002	Leukotriene C4 synthase promoter polymorphism in Japanese patients with aspirin-induced asthma.	Aspirin	72-79	leukotriene C4 synthase	Homo sapiens	0-23
12063521-1	2002	BACKGROUND: The A to C transversion in the promoter region of the gene encoding leukotriene C4 synthase (LTC4S) is proposed to be associated with the development of aspirin-induced asthma (AIA).	Aspirin	165-172	leukotriene C4 synthase	Homo sapiens	80-103
12063521-1	2002	BACKGROUND: The A to C transversion in the promoter region of the gene encoding leukotriene C4 synthase (LTC4S) is proposed to be associated with the development of aspirin-induced asthma (AIA).	Aspirin	165-172	leukotriene C4 synthase	Homo sapiens	105-110
12063521-3	2002	METHODS: Genotyping of LTC4S gene promoter was performed on 60 patients with AIA, 100 patients with aspirin-tolerant asthma (ATA), and 110 control subjects.	Aspirin	100-107	leukotriene C4 synthase	Homo sapiens	23-28
11941383-2	2002	It is widely recognized that in some adult patients with asthma, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase (COX)-1 exacerbate the condition.	Aspirin	65-72	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	142-164
11941383-12	2002	To prevent life-threatening reactions, patients with AIA should avoid aspirin and other analgesics that inhibit COX-1.	Aspirin	70-77	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	112-117
11801685-0	2002	Aspirin and salicylates inhibit the IL-4- and IL-13-induced activation of STAT6.	Aspirin	0-7	signal transducer and activator of transcription 6	Homo sapiens	74-79
11801685-5	2002	We found that treatment of cell lines and primary cells with aspirin and salicylates, but not acetaminophen, inhibited the activation of STAT6 by IL-4 and IL-13.	Aspirin	61-68	signal transducer and activator of transcription 6	Homo sapiens	137-142
11801685-9	2002	Because STAT6 activation by IL-4 and IL-13 participates in the development of allergic diseases, our results provide a mechanism to explain the beneficial effects of aspirin and salicylate treatment of these diseases.	Aspirin	166-173	signal transducer and activator of transcription 6	Homo sapiens	8-13
11792343-1	2002	Aspirin, nonselective nonsteroidal anti-inflammatory drugs (NSAIDs), and specific cyclooxygenase-2 (COX-2) inhibitors each have distinctive effects on COX-1-mediated thromboxane biosynthesis, the major determinant of platelet aggregation.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	151-156
11700329-3	2002	Whereas the inhibition of nuclear factor-kappaB by aspirin and sodium salicylate can be partly accounted for by their binding to IkappaB kinase-beta, the broad range of transcriptional targets of NSAID suggests that the products of COX activity might affect one or more among the early steps in the TCR-signaling cascade.	Aspirin	51-58	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	129-148
11700329-3	2002	Whereas the inhibition of nuclear factor-kappaB by aspirin and sodium salicylate can be partly accounted for by their binding to IkappaB kinase-beta, the broad range of transcriptional targets of NSAID suggests that the products of COX activity might affect one or more among the early steps in the TCR-signaling cascade.	Aspirin	51-58	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	299-302
12112002-6	2002	And, NSAIDs aspirin and diclofenase dose dependently inhibited LPS/IFN-gamma-induced HO-1 protein accompanied by suppression of PGE(2) (not NO) production.	Aspirin	12-19	interferon regulatory factor 6	Homo sapiens	63-66
12112002-6	2002	And, NSAIDs aspirin and diclofenase dose dependently inhibited LPS/IFN-gamma-induced HO-1 protein accompanied by suppression of PGE(2) (not NO) production.	Aspirin	12-19	heme oxygenase 1	Homo sapiens	85-89
11717412-1	2001	Both nonsteroidal anti-inflammatory drugs, such as ibuprofen, and the prototypical selective cyclooxygenase (Cox)-2 inhibitors DuP-697 and NS-398 block the inhibition of Cox-1 by aspirin in vitro.	Aspirin	179-186	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	170-175
11585736-0	2001	Suppression of intestinal and mammary neoplasia by lifetime administration of aspirin in Apc(Min/+) and Apc(Min/+), Msh2(-/-) mice.	Aspirin	78-85	APC, WNT signaling pathway regulator	Mus musculus	89-92
11585736-6	2001	Finally, we analyzed (Apc(Min/+), Msh2(-/-)) mice and found that lifetime aspirin exposure significantly delayed the onset of both intestinal and mammary neoplasia.	Aspirin	74-81	APC, WNT signaling pathway regulator	Mus musculus	22-25
11585736-7	2001	Thus embryonic and perinatal exposure to aspirin suppresses neoplasia specifically associated with the loss of Apc function, opening a potential window of opportunity for nonsteroidal anti-inflammatory drug intervention.	Aspirin	41-48	APC, WNT signaling pathway regulator	Mus musculus	111-114
11543770-1	2001	The aim of this study was to investigate the facilitatory effects of subanalgesic or low doses of different drugs (acetylsalicylic acid, ibuprofen and morphine) on the antinociceptive responses induced by the endogenous opioid peptides, enkephalins, protected from their catabolism by the dual enkephalin-degrading enzymes inhibitor RB101.	Aspirin	115-135	proenkephalin	Rattus norvegicus	237-247
11577463-2	2001	During the century after that, aspirin has been found to show its anti-inflammatory, analgesic and anti-pyretic activities by reducing prostaglandins biosynthesis through inhibition of cyclooxygenase (COX); and then COX was found to be constituted of two isoforms, constitutive COX-1 and inducible COX-2.	Aspirin	31-38	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	278-283
29805889-13	2014	Conclusion: We found an association of H2 haplotype in P2RY12 gene with aspirin resistance in patients with CAD.	Aspirin	72-79	purinergic receptor P2Y12	Homo sapiens	55-61
25106115-6	2014	In Huh7 replicon cells treated with ASA, we found decreased levels of iNOS mRNA, iNOS protein and nitrosylated protein levels at 48-72 h. ASA exposure also reduced the transactivation of the iNOS promoter in HCV replicon cells at 48 h, and this was partly due to the decrease in the affinity of transcription factor C/EBP-beta for its binding site in the iNOS promoter.	Aspirin	138-141	CCAAT enhancer binding protein beta	Homo sapiens	316-326
24372313-10	2014	Systemic administration of aspirin and clopidogrel induced a significant decrease ( p &lt; 0.05) in the expression of CXCL4.	Aspirin	27-34	platelet factor 4	Rattus norvegicus	118-123
24836463-10	2014	The addition of the oral administration of cilostazol either alone or with aspirin administration may be beneficial for subsequent cerebral ischemic damage in terms of reducing infarct volume, improving rCBF during ischemia, inhibiting the apoptotic pathway, and reducing oxidative stress.	Aspirin	75-82	CCAAT/enhancer binding protein zeta	Rattus norvegicus	203-207
24730450-0	2014	Aspirin treatment improved mesenchymal stem cell immunomodulatory properties via the 15d-PGJ2/PPARgamma/TGF-beta1 pathway.	Aspirin	0-7	peroxisome proliferator activated receptor gamma	Mus musculus	94-103
24730450-0	2014	Aspirin treatment improved mesenchymal stem cell immunomodulatory properties via the 15d-PGJ2/PPARgamma/TGF-beta1 pathway.	Aspirin	0-7	transforming growth factor, beta 1	Mus musculus	104-113
24730450-3	2014	In the present study, we show that aspirin (acetylsalicylic acid, ASA)-treated BMMSCs have significantly improved immunomodulatory function, as indicated by upregulation of regulatory T cells (Tregs) and downregulation of Th17 cells via the 15d-PGJ2/PPARgamma/TGF-beta1 pathway.	Aspirin	35-42	peroxisome proliferator activated receptor gamma	Mus musculus	250-259
24730450-3	2014	In the present study, we show that aspirin (acetylsalicylic acid, ASA)-treated BMMSCs have significantly improved immunomodulatory function, as indicated by upregulation of regulatory T cells (Tregs) and downregulation of Th17 cells via the 15d-PGJ2/PPARgamma/TGF-beta1 pathway.	Aspirin	35-42	transforming growth factor, beta 1	Mus musculus	260-269
24730450-3	2014	In the present study, we show that aspirin (acetylsalicylic acid, ASA)-treated BMMSCs have significantly improved immunomodulatory function, as indicated by upregulation of regulatory T cells (Tregs) and downregulation of Th17 cells via the 15d-PGJ2/PPARgamma/TGF-beta1 pathway.	Aspirin	44-64	peroxisome proliferator activated receptor gamma	Mus musculus	250-259
24730450-3	2014	In the present study, we show that aspirin (acetylsalicylic acid, ASA)-treated BMMSCs have significantly improved immunomodulatory function, as indicated by upregulation of regulatory T cells (Tregs) and downregulation of Th17 cells via the 15d-PGJ2/PPARgamma/TGF-beta1 pathway.	Aspirin	44-64	transforming growth factor, beta 1	Mus musculus	260-269
24730450-3	2014	In the present study, we show that aspirin (acetylsalicylic acid, ASA)-treated BMMSCs have significantly improved immunomodulatory function, as indicated by upregulation of regulatory T cells (Tregs) and downregulation of Th17 cells via the 15d-PGJ2/PPARgamma/TGF-beta1 pathway.	Aspirin	66-69	peroxisome proliferator activated receptor gamma	Mus musculus	250-259
24730450-3	2014	In the present study, we show that aspirin (acetylsalicylic acid, ASA)-treated BMMSCs have significantly improved immunomodulatory function, as indicated by upregulation of regulatory T cells (Tregs) and downregulation of Th17 cells via the 15d-PGJ2/PPARgamma/TGF-beta1 pathway.	Aspirin	66-69	transforming growth factor, beta 1	Mus musculus	260-269
25123549-1	2014	BACKGROUND: Evidence from the literature suggests diminished acetylsalicylic acid (ASA) treatment efficacy in type 2 diabetes (DM2).	Aspirin	61-81	immunoglobulin heavy diversity 1-14 (non-functional)	Homo sapiens	127-130
25123549-1	2014	BACKGROUND: Evidence from the literature suggests diminished acetylsalicylic acid (ASA) treatment efficacy in type 2 diabetes (DM2).	Aspirin	83-86	immunoglobulin heavy diversity 1-14 (non-functional)	Homo sapiens	127-130
25123549-2	2014	High on-aspirin platelet reactivity (HAPR) in DM2 has been linked to poor glycemic and lipid control.	Aspirin	8-15	immunoglobulin heavy diversity 1-14 (non-functional)	Homo sapiens	46-49
25123549-4	2014	The aim of this study was to assess the relationship between laboratory response to ASA and metabolic control, insulin resistance and adipokines in DM2.	Aspirin	84-87	immunoglobulin heavy diversity 1-14 (non-functional)	Homo sapiens	148-151
25123549-12	2014	Younger DM2 patients may therefore require total daily ASA doses higher than 75 mg, preferably as a twice-daily regimen, to achieve full therapeutic effect.	Aspirin	55-58	immunoglobulin heavy diversity 1-14 (non-functional)	Homo sapiens	8-11
25037197-0	2014	Circulating dickkopf-1 in diabetes mellitus: association with platelet activation and effects of improved metabolic control and low-dose aspirin.	Aspirin	137-144	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	12-22
25037197-5	2014	DKK-1 levels were significantly lower in diabetic patients receiving compared with those not on aspirin treatment (P=0.008); in the latter, DKK-1 was significantly correlated with 11-dehydro-thromboxane B2, ADMA, and CD40L (rho=0.303.	Aspirin	96-103	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	0-5
25037197-5	2014	DKK-1 levels were significantly lower in diabetic patients receiving compared with those not on aspirin treatment (P=0.008); in the latter, DKK-1 was significantly correlated with 11-dehydro-thromboxane B2, ADMA, and CD40L (rho=0.303.	Aspirin	96-103	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	140-145
25037197-10	2014	Plasma DKK-1 levels are reduced with improvement of glycemic control and low-dose aspirin treatment.	Aspirin	82-89	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	7-12
25029546-3	2014	We studied two genotypic and allelic frequencies of rs2427827 (-344C/T) and rs2251746 (-66T/C) gene polymorphisms of FcepsilonRIalpha in 20 patients with AICU, 52 subjects with airway hypersensitivity without aspirin intolerance, and 50 controls in a Chinese population.	Aspirin	209-216	Fc epsilon receptor Ia	Homo sapiens	117-133
25061736-5	2014	We also used aspirin as an inhibitor of the Wnt signaling pathway in the treatment of hepG2 cells transfected with the pReceiver-M29/thy-1 expression vector to make detailed observations of apoptosis in hepG2 cells as well as the differential expression of beta-catenin, cyclinD1, and thy-1.	Aspirin	13-20	cyclin D1	Homo sapiens	271-279
24418973-11	2014	ASA and ketorolac both decreased the activity of MMP-2, MMP-9, and uPA.	Aspirin	0-3	matrix metallopeptidase 9	Mus musculus	56-61
11274933-2	2001	To address this issue, a Cardiac Hospital Atherosclerosis Management Program (CHAMP) focused on initiation of aspirin, cholesterol-lowering medication (hydroxymethylglutaryl coenzyme A [HMG CoA] reductase inhibitor titrated to achieve low-density lipoprotein [LDL] cholesterol &lt; or =100 mg/dl), beta blocker, and angiotensin-converting enzyme (ACE) inhibitor therapy in conjunction with diet and exercise counseling before hospital discharge in patients with established coronary artery disease.	Aspirin	110-117	Mov10 like RISC complex RNA helicase 1	Homo sapiens	78-83
11274933-4	2001	In the pre- and post-CHAMP patient groups, aspirin use at discharge improved from 68% to 92% (p &lt;0.01), beta blocker use improved from 12% to 62% (p &lt;0.01), ACE inhibitor use increased from 6% to 58% (p &lt;0.01), and statin use increased from 6% to 86% (p &lt;0.01).	Aspirin	43-50	Mov10 like RISC complex RNA helicase 1	Homo sapiens	21-26
11330422-4	2001	The increases in thiobarbituric acid-reactive substances and tissue-associated myeloperoxidase activity 3 hr after aspirin administration were significantly inhibited by pretreatment with polaprezinc.	Aspirin	115-122	myeloperoxidase	Rattus norvegicus	79-94
11383931-3	2001	Pharmacological COX-1 inhibition was performed with the prescription of acetylsalicylic acid (ASA) at a low dose, and COX-2 selective inhibition was performed with celecoxib.	Aspirin	72-92	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	16-21
24665827-7	2014	RESULTS: (1) PF4/H antibody-positive patients suffered a significantly higher incidence of thrombosis than those who were antibody-negative; (2) PF4/H antibody-positive patients who survived a thrombosis manifested a significantly longer bleeding time and decreased maximum percentage of platelet aggregation inhibition; (3) aspirin and clopidogrel decreased the incidence of thrombosis in PF4/H antibody-positive patients by inhibiting platelet activation.	Aspirin	325-332	platelet factor 4	Homo sapiens	145-148
11383931-3	2001	Pharmacological COX-1 inhibition was performed with the prescription of acetylsalicylic acid (ASA) at a low dose, and COX-2 selective inhibition was performed with celecoxib.	Aspirin	94-97	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	16-21
24665827-7	2014	RESULTS: (1) PF4/H antibody-positive patients suffered a significantly higher incidence of thrombosis than those who were antibody-negative; (2) PF4/H antibody-positive patients who survived a thrombosis manifested a significantly longer bleeding time and decreased maximum percentage of platelet aggregation inhibition; (3) aspirin and clopidogrel decreased the incidence of thrombosis in PF4/H antibody-positive patients by inhibiting platelet activation.	Aspirin	325-332	platelet factor 4	Homo sapiens	13-18
24923427-8	2014	Protein expression of ERalpha, COX-2, Cyclin A, and Bcl-xL were reduced in celecoxib-treated tumor samples, whereas only Bcl-xL expression was suppressed in those treated with aspirin.	Aspirin	176-183	BCL2-like 1	Mus musculus	121-127
11337927-2	2001	The purpose of this study is to elucidate efficacy and safety of a combined approach using a bolus injection of low dose of mutant tissue plasminogen activator (mt-PA) with heparin and aspirin to ensure definite antithrombin and antiplatelet efficacy, followed by back-up percutaneous transluminal coronary angioplasty(PTCA).	Aspirin	185-192	serpin family C member 1	Homo sapiens	212-224
24666617-3	2014	This study was designed to define the impact of dual antiplatelet therapy (dAPT) on clinical outcomes among aspirin-resistant patients who underwent coronary artery surgery.	Aspirin	108-115	apontic	Drosophila melanogaster	75-79
11226331-4	2001	Here, we show that a NO-releasing aspirin derivative (NCX-4016) reduces the degree of restenosis after balloon angioplasty in low-density lipoprotein receptor-deficient mice and this effect is associated with reduced vascular smooth muscle cell (VSMC) proliferation and macrophage deposition at the site of injury.	Aspirin	34-41	T cell leukemia, homeobox 2	Mus musculus	54-57
11173047-2	2001	Aspirin, conventional nonsteroidal anti-inflammatory drugs (NSAIDs), and COX-2-specific inhibitors exhibit different patterns of inhibition of COX-1-mediated thromboxane biosynthesis and COX-2-mediated prostacyclin biosynthesis.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	143-148
11251618-0	2001	COX-1 sparing drugs in aspirin-sensitive asthma.	Aspirin	23-30	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	0-5
11964666-9	2001	The gene coding for LTC4 synthase exists in two common alleles, one of which appears to be associated with a severe, steroid-dependent type of aspirin-induced asthma.	Aspirin	143-150	leukotriene C4 synthase	Homo sapiens	20-33
11281181-5	2001	Gastric LPO and MPO activity that were increased significantly by ASA were decreased after treatment with omeprazole, famotidine, and melatonin.	Aspirin	66-69	myeloperoxidase	Rattus norvegicus	16-19
17018963-12	2000	All aspirinlike drugs have until quite recently been mixed blockers of cyclooxigenases (COX 1 and COX 2) with aspirin itself being the most outstanding COX 1 blocker.	Aspirin	4-11	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	152-157
17018963-12	2000	All aspirinlike drugs have until quite recently been mixed blockers of cyclooxigenases (COX 1 and COX 2) with aspirin itself being the most outstanding COX 1 blocker.	Aspirin	4-11	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	88-93
11034940-4	2000	METHODS AND RESULTS: Using washed platelets from normal donors and tyrphostin-A47 and aspirin as tyrosine kinase and COX-1 inhibitors, respectively, we found that tyrphostin-A47 downregulated (1) the thrombin-activated conformational change of alpha(IIb)beta(3), (2) actin polymerization and cytoskeletal reorganization, and (3) the quantity of tyrosine-phospho-rylated proteins associated with the reorganized cytoskeleton.	Aspirin	86-93	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	117-122
11031220-8	2000	At a comparable level of resting CBF ( approximately 15% below baseline), the RHR was reduced more in the control (-56+/-9%), heparin-treated (-49+/-9%), and aspirin-treated (-61+/-12) groups (P:&lt;0.05) than in the GP IIb/IIIa inhibitor-treated group (-26+/-6%).	Aspirin	158-165	integrin alpha-IIb	Sus scrofa	217-223
11078056-5	2000	In contrast, aspirin-like nonselective NSAIDs such as sulindac and indomethacin inhibit not only the enzymatic action of the highly inducible, proinflammatory COX-2 but the constitutively expressed, cytoprotective COX-1 as well.	Aspirin	13-20	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	214-219
10887308-3	2000	A single nucleotide polymorphism consisting of an adenine (A) to cytosine (C) transversion -444 nucleotides upstream of the ATG translation start site in the LTC(4)S gene has been associated with a relative risk of 3.89 for the aspirin-intolerant phenotype in Polish patients.	Aspirin	228-235	leukotriene C4 synthase	Homo sapiens	158-165
10887308-8	2000	The LTC(4)S genotype distribution was consistent with the Hardy-Weinberg equilibrium in patients with aspirin-tolerant asthma and unaffected control subjects but not in patients with aspirin-intolerant asthma; however, the distributions were not significantly different among the phenotype groups.	Aspirin	102-109	leukotriene C4 synthase	Homo sapiens	4-11
10844112-0	2000	Prevention of pulmonary thromboembolism by NCX 4016, a nitric oxide-releasing aspirin.	Aspirin	78-85	T cell leukemia, homeobox 2	Mus musculus	43-46
10844112-1	2000	We studied the antithrombotic activity of 2-acetoxybenzoate 2-[1-nitroxy-methyl]-phenyl ester (NCX 4016), a novel nitric oxide (NO)-releasing aspirin derivative, in vivo in different animal models of platelet-dependent and independent pulmonary thromboembolism and compared it with that of aspirin.	Aspirin	142-149	T cell leukemia, homeobox 2	Mus musculus	95-98
10811855-3	2000	Platelet COX-1 inhibition by chronic administration of low-dose aspirin before LPS did not alter the symptomatic and febrile responses to LPS, but the increment in urinary PGI-M and Tx-M were both partially depressed.	Aspirin	64-71	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	9-14
10807421-8	2000	CONCLUSION: Growth factors, including HGF, EGF and IGF-I, reversed the aspirin-induced inhibition of wound repair through their cytoprotective effects on gastric epithelial cells.	Aspirin	71-78	insulin-like growth factor I	Oryctolagus cuniculus	51-56
10818443-6	2000	This contrasts with activation of the LXA4 receptor by an aspirin-triggered lipoxin A4 mimetic that before leukotriene B4 gave an inverse relationship with rapidly increasing PSDP levels, and inhibition of both PLD activity and superoxide generation.	Aspirin	58-65	formyl peptide receptor 2	Homo sapiens	38-51
10634286-3	2000	This study was undertaken to determine whether EMT-Ps are able to retain information regarding the use of aspirin in AMI after a standard didactic session.	Aspirin	106-113	IL2 inducible T cell kinase	Homo sapiens	47-50
10634286-14	2000	CONCLUSION: These results suggest that EMT-Ps can retain information regarding the out-of-hospital use of aspirin for AMI after a standard didactic session.	Aspirin	106-113	IL2 inducible T cell kinase	Homo sapiens	39-42
10583440-9	1999	Aspirin pretreatment, on the other hand, prolonged bleeding time (P &lt; 0.001) and decreased P-selectin expression of platelets in wound blood (P = 0.03).	Aspirin	0-7	selectin P	Homo sapiens	94-104
24692722-7	2014	The probable polar and non-polar interactions of possible S100A8 inhibitors (aspirin, celecoxib, dexamethasone and diclofenac) were examined by performing molecular docking and binding free energy calculations.	Aspirin	77-84	S100 calcium binding protein A8	Homo sapiens	58-64
10591082-8	1999	Immunohistochemical studies of mucosal biopsies from the bronchi of aspirin-intolerant asthmatics show that LTC4S is overrepresented in individuals with this phenotype, and this finding correlates with overproduction of cysteinyl leukotrienes and lysine-aspirin bronchial hyperreactivity.	Aspirin	68-75	leukotriene C4 synthase	Homo sapiens	108-113
10591082-8	1999	Immunohistochemical studies of mucosal biopsies from the bronchi of aspirin-intolerant asthmatics show that LTC4S is overrepresented in individuals with this phenotype, and this finding correlates with overproduction of cysteinyl leukotrienes and lysine-aspirin bronchial hyperreactivity.	Aspirin	254-261	leukotriene C4 synthase	Homo sapiens	108-113
24692722-12	2014	We identified S100A8 as a prospective biomarker for kidney cancer and in silico analysis showed that aspirin, celecoxib, dexamethasone and diclofenac binds to S100A8 and may inhibit downstream signaling in kidney cancer.	Aspirin	101-108	S100 calcium binding protein A8	Homo sapiens	14-20
24692722-12	2014	We identified S100A8 as a prospective biomarker for kidney cancer and in silico analysis showed that aspirin, celecoxib, dexamethasone and diclofenac binds to S100A8 and may inhibit downstream signaling in kidney cancer.	Aspirin	101-108	S100 calcium binding protein A8	Homo sapiens	159-165
24606818-14	2014	Treatment with a combination of minocycline and aspirin decreased percentage infarct volume, arrhythmias, mortality and collagen level when compared with vehicle-treated diabetic controls and showed reduced levels of MMP-2 and MMP-9.	Aspirin	48-55	matrix metallopeptidase 2	Rattus norvegicus	217-222
24408984-8	2014	CONCLUSIONS: The early morphologic involvement of the GCL+IPL and INL+OPL layers in ARM eyes, as revealed by the ASA, could be related to early anatomic changes described in the inner retina of ARM eyes.	Aspirin	113-116	pleckstrin homology like domain family A member 2	Homo sapiens	58-61
24102302-9	2014	Expression of platelet-bound SDF-1 and number of CD34(+) cells were higher in patients with DCM compared with patients with ICM (p &lt; 0.001 for both) and inversely correlated with age and aspirin therapy.	Aspirin	190-197	C-X-C motif chemokine ligand 12	Homo sapiens	29-34
24268424-10	2014	CONCLUSIONS: Our results suggest that the antithrombotic activities of PAR1 and/or PAR4 antagonism is influenced by shear conditions as well as by combined platelet inhibition with aspirin and a P2Y12-antagonist.	Aspirin	181-188	Prader Willi/Angelman region RNA 4	Homo sapiens	83-87
24244288-10	2013	CONCLUSION: Our findings provide strong evidence that COX-2 and ITGA2 genetic defects might increase the risk of having aspirin insensitivity, especially for aspirin semi-resistance and in Chinese populations.	Aspirin	120-127	integrin subunit alpha 2	Homo sapiens	64-69
24244288-10	2013	CONCLUSION: Our findings provide strong evidence that COX-2 and ITGA2 genetic defects might increase the risk of having aspirin insensitivity, especially for aspirin semi-resistance and in Chinese populations.	Aspirin	158-165	integrin subunit alpha 2	Homo sapiens	64-69
10521382-4	1999	Hence, we hypothesized that aspirin, which inhibits LPS-induced, nuclear factor kappaB-dependent TF expression in vitro and platelet activation in vivo, may suppress LPS-induced coagulation in humans.	Aspirin	28-35	coagulation factor III, tissue factor	Homo sapiens	97-99
23832067-11	2013	CONCLUSION: The variation in response to ASA may be related with an increased expression of IGF1 and IGF1R, as well as a response to clopidogrel can be affected by pharmacokinetic change related to the reverse transport pathway by increased expression of ABCC3.	Aspirin	41-44	ATP binding cassette subfamily C member 3	Homo sapiens	255-260
22649123-3	2013	We aimed to assess the prevalence of the combined use of aspirin, statin, and BP-lowering agents in patients with established cardiovascular diseases or type 2 diabetes mellitus (DM2) in the period 1996-2009.	Aspirin	57-64	immunoglobulin heavy diversity 1-14 (non-functional)	Homo sapiens	179-182
11245096-5	1999	In the presence of aspirin (Asp 1 mmol.L-1)-treated EEC 1 x 10(9) cells.L-1, the aggregation of Asp (1 mmol.L-1) and methylene blue (10 mumol.L-1)-treated platelets in response to thrombin 500 U.L-1 and platelet activating factor (PAF 1 nmol.L-1) was markedly inhibited and was reversible, which was very similar to that in apyrase-treated platelets.	Aspirin	19-26	PAF1 homolog, Paf1/RNA polymerase II complex component	Bos taurus	231-236
10458713-9	1999	MCSF, IL-6, and CRP were all reduced after 6 weeks of aspirin treatment (P&lt;0.05).	Aspirin	54-61	colony stimulating factor 1	Homo sapiens	0-4
23831034-8	2013	RESULTS: A set of 60 coexpressed genes named the "aspirin response signature" (ARS) was associated with PFS in HV1 (r = -0.31, p = 0.03), HV2 (r = -0.34, Bonferroni p = 0.03), and OPC (p = 0.046).	Aspirin	50-57	hydrogen voltage gated channel 1	Homo sapiens	111-114
10404093-8	1999	We also observed a reduction of MSI phenotype after aspirin or sulindac treatment in a hMLH1-defective gastric cancer cell line SNU-1, which lacks COX-2 expression.	Aspirin	52-59	mutL homolog 1	Homo sapiens	87-92
23884248-2	2013	Different aspirin dosing regimens have been suggested to impact outcomes when used in combination with adenosine diphosphate (ADP) P2Y12 receptor antagonists.	Aspirin	10-17	purinergic receptor P2Y12	Homo sapiens	131-136
10066433-5	1999	In contrast to GPVI-mediated platelet activation, most of these phenomena induced by GPIa/IIa activation were markedly suppressed by acetylsalicylic acid (ASA) or cytochalasin D.	Aspirin	133-153	glycoprotein VI platelet	Homo sapiens	15-19
10066433-5	1999	In contrast to GPVI-mediated platelet activation, most of these phenomena induced by GPIa/IIa activation were markedly suppressed by acetylsalicylic acid (ASA) or cytochalasin D.	Aspirin	133-153	multimerin 1	Homo sapiens	85-89
23648742-6	2013	We found that low doses of aspirin suppressed ERR in allergen-sensitized rats, as well as the expressions of RANKL, pro-inflammatory cytokines, and LTB4.	Aspirin	27-34	TNF superfamily member 11	Rattus norvegicus	109-114
10066433-5	1999	In contrast to GPVI-mediated platelet activation, most of these phenomena induced by GPIa/IIa activation were markedly suppressed by acetylsalicylic acid (ASA) or cytochalasin D.	Aspirin	155-158	glycoprotein VI platelet	Homo sapiens	15-19
10066433-5	1999	In contrast to GPVI-mediated platelet activation, most of these phenomena induced by GPIa/IIa activation were markedly suppressed by acetylsalicylic acid (ASA) or cytochalasin D.	Aspirin	155-158	multimerin 1	Homo sapiens	85-89
10320091-7	1999	In every tissue a significant increase of pLT after aspirin challenge was observed.	Aspirin	52-59	N-acylethanolamine acid amidase	Homo sapiens	42-45
23553791-6	2013	Systemic administration of aspirin, which significantly reduces the levels of IFN-gamma and TNF-alpha, results in blockage of MSC deficiency and tumorigenesis by inhibition of NFkappaB/SMAD7 and NFkappaB/c-FOS and c-MYC pathways in OVX mice.	Aspirin	27-34	SMAD family member 7	Mus musculus	185-190
23762376-4	2013	RESULTS: Peripheral blood mononuclear cells from rats challenged with acetyl salicylic acid presented a faster kinetics of expression of HSP-72 messenger RNA and protein in response to in vitro heat shock.	Aspirin	70-91	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	137-143
23762376-6	2013	CONCLUSIONS: Administration of acetyl salicylic acid to rats alters HSP-72 expression mechanism in a way that it becomes more efficient in response to in vitro heat shock.	Aspirin	31-52	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	68-74
23741443-11	2013	CONCLUSIONS: Aspirin minimized the pro-metastasis effect of sorafenib by up-regulating the tumor suppressor HTATIP2; this mechanism is mediated through inhibition of COX2.	Aspirin	13-20	cytochrome c oxidase II, mitochondrial	Mus musculus	166-170
10937986-2	1999	AIMS AND METHODS: The WASH study is a prospective, randomised, open-label, blinded-end-point pilot study comparing the outcome of management without anti-thrombotic therapy compared to treatment with aspirin or warfarin in three parallel arms in patients with chronic heart failure due to left ventricular systolic dysfunction.	Aspirin	200-207	WASP family homolog 6, pseudogene	Homo sapiens	22-26
10092995-6	1999	Furthermore, aspirin and the blockade of NO generation by BVSMCs reduced the production of tumour necrosis factor alpha (TNF-alpha) by these cells.	Aspirin	13-20	tumor necrosis factor	Bos taurus	121-130
10092995-8	1999	The inhibition of iNOS expression by aspirin was further associated with a reduced ability of BVSMCs to produce TNF-alpha.	Aspirin	37-44	tumor necrosis factor	Bos taurus	112-121
23611778-5	2013	We further showed that aspirin robustly enhanced Navitoclax-triggered cytosolic cytochrome c release, activation of initiator caspase-9 and effector caspase-3, and cleavage of PARP.	Aspirin	23-30	collagen type XI alpha 2 chain	Homo sapiens	176-180
24093982-5	2013	Platelet P2Y12 receptor inhibitors are an important group of antiplatelet compounds that can be combined with aspirin in the management of ACS.	Aspirin	110-117	purinergic receptor P2Y12	Homo sapiens	9-14
9817203-0	1998	The anti-inflammatory agents aspirin and salicylate inhibit the activity of I(kappa)B kinase-beta.	Aspirin	29-36	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	76-97
9817203-5	1998	Here we demonstrate that the anti-inflammatory agents aspirin and sodium salicylate specifically inhibit IKK-beta activity in vitro and in vivo.	Aspirin	54-61	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	105-113
9817203-6	1998	The mechanism of aspirin and sodium salicylate inhibition is due to binding of these agents to IKK-beta to reduce ATP binding.	Aspirin	17-24	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	95-103
9817203-7	1998	Our results indicate that the anti-inflammatory properties of aspirin and salicylate are mediated in part by their specific inhibition of IKK-beta, thereby preventing activation by NF-kappaB of genes involved in the pathogenesis of the inflammatory response.	Aspirin	62-69	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	138-146
24334852-7	2013	Aspirin (100 microM added to the glands 1 hr prior to the experiment) significantly increased  pHi/min to similar values in both genotypes.	Aspirin	0-7	glucose-6-phosphate isomerase 1	Mus musculus	95-98
9650830-6	1998	Four of them suppressed interleukin-1alpha production to a basal level and showed different mode of antipyretic action from that of aspirin in interleukin-1alpha-injected mice.	Aspirin	132-139	interleukin 1 alpha	Mus musculus	143-161
23038044-9	2013	Additionally, Cox proportional hazards regression modeling demonstrated that aspirin resistance and cerebrovascular disease were associated with major adverse long-term outcomes (HR for aspirin resistance = 2.31, 95% CI 1.11-4.81, p = 0.026).	Aspirin	77-84	cytochrome c oxidase subunit 8A	Homo sapiens	14-17
23038044-9	2013	Additionally, Cox proportional hazards regression modeling demonstrated that aspirin resistance and cerebrovascular disease were associated with major adverse long-term outcomes (HR for aspirin resistance = 2.31, 95% CI 1.11-4.81, p = 0.026).	Aspirin	186-193	cytochrome c oxidase subunit 8A	Homo sapiens	14-17
23777967-3	2013	The recently observed benefit of an alternative P2Y12 receptor antagonist (ticragelor) on survival as compared with clopidogrel suggests that the toxicity of the clopidogrel/aspirin combination likely results from an "off-target" effect.	Aspirin	174-181	purinergic receptor P2Y12	Homo sapiens	48-53
9545330-1	1998	Prostaglandin endoperoxide H synthases-1 and -2 (PGHS-1 and -2) are the major targets of nonsteroidal anti-inflammatory drugs like aspirin and ibuprofen.	Aspirin	131-138	prostaglandin-endoperoxide synthase 1	Mus musculus	49-62
23126503-0	2012	Comparative binding effects of aspirin and anti-inflammatory Cu complex in the active site of LOX-1.	Aspirin	31-38	oxidized low density lipoprotein receptor 1	Homo sapiens	94-99
17016059-2	2007	BACKGROUND: The anti-inflammatory actions of acetylsalicylic acid (ASA)/non-steroidal anti-inflammatory drugs (NSAIDs) are thought to be due to inhibition of COX-2, whereas the side effects such as gastric damage and aspirin-induced asthma are mediated through inhibition of COX-1.	Aspirin	45-65	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	275-280
17016059-2	2007	BACKGROUND: The anti-inflammatory actions of acetylsalicylic acid (ASA)/non-steroidal anti-inflammatory drugs (NSAIDs) are thought to be due to inhibition of COX-2, whereas the side effects such as gastric damage and aspirin-induced asthma are mediated through inhibition of COX-1.	Aspirin	67-70	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	275-280
23126503-3	2012	In silico docking experiments in LOX-1 showed that aspirin does only weakly bind to LOX-1, while the complex binds with high affinity.	Aspirin	51-58	oxidized low density lipoprotein receptor 1	Homo sapiens	33-38
23126503-3	2012	In silico docking experiments in LOX-1 showed that aspirin does only weakly bind to LOX-1, while the complex binds with high affinity.	Aspirin	51-58	oxidized low density lipoprotein receptor 1	Homo sapiens	84-89
22574824-12	2012	CONCLUSIONS: Polymorphisms in P2RY1 and P2RY12 are associated with on-aspirin platelet reactivity in patients with CAD.	Aspirin	70-77	purinergic receptor P2Y12	Homo sapiens	40-46
17174877-6	2006	CASE REPORT: We present a case of recurrent acute in-stent thrombosis in a patient with mild antithrombin III (AT) deficiency despite the combined administration of clopidogrel and aspirin.	Aspirin	181-188	serpin family C member 1	Homo sapiens	93-109
22745359-7	2012	In addition, our gelatinase zymography and fluorescence data confirmed that the cardol-cardanol mixture, salicylic acid, and aspirin, all of which lack key functional groups present in anacardic acid, are much weaker MMP-2/MMP-9 inhibitors.	Aspirin	125-132	matrix metallopeptidase 9	Mus musculus	223-228
17030227-1	2006	Aspirin and other nonsteroidal anti-inflammatory drugs that inhibit COX-1 induce unique nonallergic reactions, consisting of attacks of rhinitis and asthma.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	68-73
17030227-4	2006	This review focuses on a description of patients with aspirin-exacerbated respiratory disease, methods available to diagnose their condition, the unique ability of all nonsteroidal anti-inflammatory drugs that inhibit COX-1 to cross-react with aspirin, an update on pathogenesis, and current thoughts about treatment.	Aspirin	54-61	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	218-223
17030227-4	2006	This review focuses on a description of patients with aspirin-exacerbated respiratory disease, methods available to diagnose their condition, the unique ability of all nonsteroidal anti-inflammatory drugs that inhibit COX-1 to cross-react with aspirin, an update on pathogenesis, and current thoughts about treatment.	Aspirin	244-251	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	218-223
16952320-8	2006	RESULTS: Aspirin significantly decreased growth rate in a dose-dependent manner, alone and as a combined treatment with IL-1 with a maximum reduction in growth rate at 300 mg/ml (P &lt; 0.05).	Aspirin	9-16	interleukin 1 alpha	Homo sapiens	120-124
22893213-6	2012	In this study, we show that lipopolysaccharide (LPS) provokes upregulation of galectin-3 expression on both gene and protein level in monocyte-like THP-1 cells, which can be inhibited by dexamethasone, but not with non-steroidal anti-inflammatory drugs aspirin and indomethacin.	Aspirin	253-260	galectin 3	Homo sapiens	78-88
16859832-5	2006	COX-1 and COX-2 inhibition by traditional NSAIDs (for example, aspirin) although chemopreventive have some side effects due to the role of COX-1 in maintaining the integrity of the gastric mucosa.	Aspirin	63-70	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	139-144
22531959-6	2012	Inhibition of NFkappaB activity in Saos2 cells by Aspirin sensitized the miR-34a overexpressing cells to cell death.	Aspirin	50-57	microRNA 34a	Homo sapiens	73-80
16890573-9	2006	CONCLUSIONS: Heterogeneity in the suppression of platelet COX-1 activity by aspirin occurred in CHD patients.	Aspirin	76-83	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	58-63
22561363-3	2012	We examined if ASA would inhibit AT1R transcription, which requires NADPH oxidase, and thereby new capillary formation.	Aspirin	15-18	angiotensin II receptor type 1	Homo sapiens	33-37
16890573-10	2006	The measurement of the serum TXB2 level seems to be an appropriate biomarker to identify patients who have an inadequate inhibition of platelet COX-1 activity by aspirin.	Aspirin	162-169	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	144-149
22561363-7	2012	ASA and its salicylic acid (SA) moiety both suppressed Ang II-mediated AT1R and vascular endothelial growth factor expression and the subsequent new capillary formation.	Aspirin	0-3	angiotensin II receptor type 1	Homo sapiens	71-75
22406476-3	2012	We investigated whether aspirin affects adenosine monophosphate-activated protein kinase (AMPK) and mTOR signaling in CRC cells.	Aspirin	24-31	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	40-88
22406476-3	2012	We investigated whether aspirin affects adenosine monophosphate-activated protein kinase (AMPK) and mTOR signaling in CRC cells.	Aspirin	24-31	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	90-94
16733498-3	2006	In addition, LCPUFAs form precursors to anti-inflammatory products such as resolvins, lipoxins, and aspirin-triggered 15 epimer LXs (ATLs), nitric oxide, prostaglandin E1 and prostacyclin (PGI2) that suppress inflammatory process and enhance healing of tissue injury with little or no loss of function.	Aspirin	100-107	small nucleolar RNA, H/ACA box 73A	Homo sapiens	168-187
22570283-4	2012	STUDY DESIGN: SPINK5 single-nucleotide polymorphisms (SNPs) and SPINK5 expression levels were correlated with CRS without (CRSsNP) and with nasal polyps (CRSwNP), aspirin intolerance, asthma, and allergies.	Aspirin	163-170	serine peptidase inhibitor Kazal type 5	Homo sapiens	14-20
22570283-10	2012	It was noted that in individuals with CRSwNP, aspirin intolerance, and allergies, SPINK5 expression was lowered.	Aspirin	46-53	serine peptidase inhibitor Kazal type 5	Homo sapiens	82-88
22517326-3	2012	At concentrations reached in plasma after administration of salsalate or of aspirin at high doses, salicylate activates adenosine monophosphate-activated protein kinase (AMPK), a central regulator of cell growth and metabolism.	Aspirin	76-83	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	120-168
16810615-9	2006	Results of the first phase III trial (PT1) that compared anagrelide/aspirin with hydroxyurea/aspirin have sparked an intense discussion, given that the combination of anagrelide and aspirin causes more bleeding complications in the gastrointestinal tract.	Aspirin	68-75	zinc finger protein 77	Homo sapiens	38-41
16810615-9	2006	Results of the first phase III trial (PT1) that compared anagrelide/aspirin with hydroxyurea/aspirin have sparked an intense discussion, given that the combination of anagrelide and aspirin causes more bleeding complications in the gastrointestinal tract.	Aspirin	93-100	zinc finger protein 77	Homo sapiens	38-41
16810615-9	2006	Results of the first phase III trial (PT1) that compared anagrelide/aspirin with hydroxyurea/aspirin have sparked an intense discussion, given that the combination of anagrelide and aspirin causes more bleeding complications in the gastrointestinal tract.	Aspirin	93-100	zinc finger protein 77	Homo sapiens	38-41
16600694-0	2006	Aspirin and PPAR-alpha activators inhibit monocyte chemoattractant protein-1 expression induced by high glucose concentration in human endothelial cells.	Aspirin	0-7	C-C motif chemokine ligand 2	Homo sapiens	42-76
22517326-3	2012	At concentrations reached in plasma after administration of salsalate or of aspirin at high doses, salicylate activates adenosine monophosphate-activated protein kinase (AMPK), a central regulator of cell growth and metabolism.	Aspirin	76-83	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	170-174
22517326-6	2012	Our results suggest that AMPK activation could explain some beneficial effects of salsalate and aspirin in humans.	Aspirin	96-103	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	25-29
22294275-0	2012	Association study between TRIM26 polymorphisms and risk of aspirin-exacerbated             respiratory disease.	Aspirin	59-66	tripartite motif containing 26	Homo sapiens	26-32
16397127-2	2006	In 17 subjects with TLR4 polymorphisms versus 17 wild type (untreated with aspirin, matched for age, sex, and cardiovascular risk factors), intima-media thickness in the common carotid arteries was significantly lower.	Aspirin	75-82	toll like receptor 4	Homo sapiens	20-24
16141240-0	2006	NO-donating aspirin isomers downregulate peroxisome proliferator-activated receptor (PPAR)delta expression in APC(min/+) mice proportionally to their tumor inhibitory effect: Implications for the role of PPARdelta in carcinogenesis.	Aspirin	12-19	APC, WNT signaling pathway regulator	Mus musculus	114-117
16141240-4	2006	We studied histochemically the effect of the meta and para positional isomers of NO-ASA on PPARdelta expression in Min (multiple intestinal neoplasia) and wild-type mice, and on cell proliferation and apoptosis.	Aspirin	84-87	APC, WNT signaling pathway regulator	Mus musculus	115-118
22294275-3	2012	Thus, we hypothesized that TRIM26 polymorphisms             may affect aspirin-induced bronchospasm and explored whether the gene can be a             marker for diagnosis of AERD.	Aspirin	71-78	tripartite motif containing 26	Homo sapiens	27-33
22201025-0	2012	Genetic variations in KIFC1 and the risk of aspirin exacerbated respiratory disease in a Korean population: an association analysis.	Aspirin	44-51	kinesin family member C1	Homo sapiens	22-27
16461132-4	2006	METHODS: By using specific antibodies, immunohistochemistry, and image analysis, we measured the expression of EP(1-4) in nasal biopsies from patients with aspirin-sensitive (n = 12) and nonaspirin-sensitive (n = 10) polypoid rhinosinusitis and normal controls (n = 9).	Aspirin	156-163	prostaglandin E receptor 1	Homo sapiens	111-117
16493486-0	2006	Polymorphisms of COX-1 and GPVI associate with the antiplatelet effect of aspirin in coronary artery disease patients.	Aspirin	74-81	glycoprotein VI platelet	Homo sapiens	27-31
21846594-9	2012	Continued surveillance of MPN-related mortality rates in the population is needed in view of recent attempts (including the use of aspirin) to control cardiovascular complications of MPN.	Aspirin	131-138	serine protease 27	Homo sapiens	26-29
16493486-12	2006	Aspirin non-response detected by PFA-100 associated with C13254T polymorphism of GP VI and female gender (P = 0.012 and P = 0.019, respectively).	Aspirin	0-7	glycoprotein VI platelet	Homo sapiens	81-86
16489670-9	2006	The gastric contents of MPO and pro-inflammatory cytokines were all increased after the administration of aspirin and reduced to nearly normal levels by ATL-146e.	Aspirin	106-113	myeloperoxidase	Rattus norvegicus	24-27
21846594-9	2012	Continued surveillance of MPN-related mortality rates in the population is needed in view of recent attempts (including the use of aspirin) to control cardiovascular complications of MPN.	Aspirin	131-138	serine protease 27	Homo sapiens	183-186
22244860-0	2012	Aspirin prevents resistin-induced endothelial dysfunction by modulating AMPK, ROS, and Akt/eNOS signaling.	Aspirin	0-7	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	72-76
22276844-8	2012	Besides inhibiting platelet function, antiplatelet therapy with aspirin may also decrease the plasma concentration of Lp(a) and modulate its influence on platelets.	Aspirin	64-71	lipoprotein(a)	Homo sapiens	118-123
16546864-0	2006	Restoration by aspirin of impaired plasma maspin level in human breast cancer.	Aspirin	15-22	serpin family B member 5	Homo sapiens	42-48
16546864-2	2006	We investigated the effect of aspirin induced increase of plasma nitric oxide (NO) on plasma maspin production in breast cancer patients.	Aspirin	30-37	serpin family B member 5	Homo sapiens	93-99
16546864-9	2006	These results indicated that the ingestion of aspirin might be beneficial for breast cancer through increased maspin production.	Aspirin	46-53	serpin family B member 5	Homo sapiens	110-116
22101342-0	2012	Thromboxane A2 receptor +795T&gt;C and chemoattractant receptor-homologous molecule expressed on Th2 cells -466T&gt;C gene polymorphisms in patients with aspirin-exacerbated respiratory disease.	Aspirin	154-161	thromboxane A2 receptor	Homo sapiens	0-23
16340184-0	2006	Dipyridamole decreases protease-activated receptor and annexin-v binding on platelets of post stroke patients with aspirin nonresponsiveness.	Aspirin	115-122	annexin A5	Homo sapiens	55-64
17357503-0	2006	Down-regulation of beta-catenin nuclear localization by aspirin correlates with growth inhibition of Jurkat cell line.	Aspirin	56-63	catenin beta 1	Homo sapiens	19-31
17357503-3	2006	Jurkat cells treated with 3 mmol/L of aspirin could significantly decrease nuclear localization of beta-catenin, and at 5 mmol/L of aspirin, the nuclear localization of beta-catenin was undetectable.	Aspirin	38-45	catenin beta 1	Homo sapiens	99-111
22101342-1	2012	It is well known that aspirin-exacerbated respiratory disease (AERD) is more common in women than in men, however, whether gene polymorphisms of the thromboxane A2 receptor (TBXA2R) and chemoattractant receptor-homologous molecules expressed on Th2 cells (CRTH2) are associated with the susceptibility of AERD remains unknown.	Aspirin	22-29	thromboxane A2 receptor	Homo sapiens	149-172
17357503-3	2006	Jurkat cells treated with 3 mmol/L of aspirin could significantly decrease nuclear localization of beta-catenin, and at 5 mmol/L of aspirin, the nuclear localization of beta-catenin was undetectable.	Aspirin	38-45	catenin beta 1	Homo sapiens	169-181
22101342-1	2012	It is well known that aspirin-exacerbated respiratory disease (AERD) is more common in women than in men, however, whether gene polymorphisms of the thromboxane A2 receptor (TBXA2R) and chemoattractant receptor-homologous molecules expressed on Th2 cells (CRTH2) are associated with the susceptibility of AERD remains unknown.	Aspirin	22-29	thromboxane A2 receptor	Homo sapiens	174-180
17357503-3	2006	Jurkat cells treated with 3 mmol/L of aspirin could significantly decrease nuclear localization of beta-catenin, and at 5 mmol/L of aspirin, the nuclear localization of beta-catenin was undetectable.	Aspirin	132-139	catenin beta 1	Homo sapiens	169-181
22030088-2	2012	Genetic variants in the UGT1A6 enzyme are associated with delayed aspirin metabolism and greater chemopreventive efficacy.	Aspirin	66-73	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	24-30
17357503-6	2006	We are led to conclude that aspirin acts through beta-catenin-independent mechanisms.	Aspirin	28-35	catenin beta 1	Homo sapiens	49-61
17357503-7	2006	The effects of aspirin include down-regulation of beta-catenin nuclear localization and G0/G1 cell cycle arrest, which might serve as a means of growth inhibition in aspirin-treated human Jurkat cell line.	Aspirin	15-22	catenin beta 1	Homo sapiens	50-62
22030088-9	2012	However, among those with a variant UGT1A6 genotype on aspirin, the RR of adenoma was 1.60 (95% CI, 0.81-3.15) after withdrawal of 200-mg twice daily and 1.98 (95% CI, 1.06-3.70) after withdrawal of 400-mg twice daily celecoxib compared with withdrawal of placebo.	Aspirin	55-62	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	36-42
17357503-7	2006	The effects of aspirin include down-regulation of beta-catenin nuclear localization and G0/G1 cell cycle arrest, which might serve as a means of growth inhibition in aspirin-treated human Jurkat cell line.	Aspirin	166-173	catenin beta 1	Homo sapiens	50-62
22030088-12	2012	However, discontinuing celecoxib among aspirin-using individuals who initially developed adenoma despite a UGT1A6 variant genotype resulted in rapid reemergence of disease.	Aspirin	39-46	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	107-113
16199534-7	2005	Biochemical analysis revealed that ASA inhibited NF-kappaB activity, which is known to regulate BCL-2 gene expression, by dephosphorylating IkappaB-alpha and inhibiting IKKbeta activity but not by affecting the HER-2/neu phosphatidylinositol 3-kinase-Akt signal pathway.	Aspirin	35-38	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	169-176
23101307-8	2012	The PTGDR diplotype CCCT/CCCC (-613CC, -549CC, -441CC and -197TC) was more frequent in patients with NP (P = .043), NP with asthma (P = .013), and the aspirin triad (P = .041).	Aspirin	151-158	prostaglandin D2 receptor	Homo sapiens	4-9
16305586-1	2005	BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid.	Aspirin	15-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-118
16305586-1	2005	BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid.	Aspirin	15-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
23029468-7	2012	ACS14 abrogated Asp-induced upregulation of COX-2 expression, but had no effect on the reduced PGE(2) level.	Aspirin	16-19	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	44-49
16305586-1	2005	BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid.	Aspirin	231-251	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
16305586-2	2005	The objective of this study was to assess whether polymorphisms in UGT1A6 and CYP2C9 genes are related to the prevalence of upper gastrointestinal symptoms in cardiovascular patients using acetylsalicylic acid for secondary prevention of ischaemic heart disease.	Aspirin	189-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
21930798-0	2011	Variants downstream of the ornithine decarboxylase gene influence risk of colorectal adenoma and aspirin chemoprevention.	Aspirin	97-104	ornithine decarboxylase 1	Homo sapiens	27-50
16273283-8	2005	The increases of thiobarbituric acid-reactive substances (TBA-RS) and myeloperoxidase (MPO) activity 3 h after aspirin administration were significantly inhibited by pretreatment with TMG.	Aspirin	111-118	myeloperoxidase	Rattus norvegicus	70-85
16273283-8	2005	The increases of thiobarbituric acid-reactive substances (TBA-RS) and myeloperoxidase (MPO) activity 3 h after aspirin administration were significantly inhibited by pretreatment with TMG.	Aspirin	111-118	myeloperoxidase	Rattus norvegicus	87-90
16273283-9	2005	The gastric concentration of cytokine-induced neutrophil chemoattractants-1 (CINC-1) increased after aspirin administration, and the increase was also inhibited by pretreatment with TMG.	Aspirin	101-108	C-X-C motif chemokine ligand 1	Rattus norvegicus	29-75
16273283-9	2005	The gastric concentration of cytokine-induced neutrophil chemoattractants-1 (CINC-1) increased after aspirin administration, and the increase was also inhibited by pretreatment with TMG.	Aspirin	101-108	C-X-C motif chemokine ligand 1	Rattus norvegicus	77-83
21930798-1	2011	Increased mucosal polyamine levels and ornithine decarboxylase (ODC) activity are associated with an increased risk of colorectal neoplasia and aspirin treatment reduces risk.	Aspirin	144-151	ornithine decarboxylase 1	Homo sapiens	39-62
21930798-1	2011	Increased mucosal polyamine levels and ornithine decarboxylase (ODC) activity are associated with an increased risk of colorectal neoplasia and aspirin treatment reduces risk.	Aspirin	144-151	ornithine decarboxylase 1	Homo sapiens	64-67
16144976-2	2005	Aspirin exerts its antithrombotic activity by irreversibly inactivating platelet cyclooxygenase (COX)-1.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	81-103
16144976-9	2005	In conclusion, our data show that NCX 4016 acts as a direct and irreversible inhibitor of COX-1 and that the presence of a spacer and NO-donating moiety in the molecule slows the kinetics of COX-1 inhibition by NCX 4016, compared with aspirin.	Aspirin	235-242	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	191-196
21930798-2	2011	Previous studies suggest that a single-nucleotide polymorphism (SNP) in the promoter of the ODC gene (rs2302615) may be associated with adenoma risk and/or response to aspirin chemoprevention.	Aspirin	168-175	ornithine decarboxylase 1	Homo sapiens	92-95
21930798-11	2011	Our findings suggest that common genetic variants located downstream (3") of the ODC gene influence risk of colorectal adenoma and may also impact the efficacy of aspirin chemoprevention.	Aspirin	163-170	ornithine decarboxylase 1	Homo sapiens	81-84
9547339-7	1998	Cyclooxygenase (COX) II is emerging as an important component in wound healing and proliferation in intestinal epithelia and when acetylated by acetylsalicylic acid (aspirin) initiates the biosynthesis of a LXA4 receptor ligand.	Aspirin	144-164	formyl peptide receptor 2	Homo sapiens	207-220
26598271-12	2011	The other is phospholipase A2, which is known as a receptor of acetylsalicylic acid or aspirin.	Aspirin	63-83	calcium-independent phospholipase A2 VIA	Drosophila melanogaster	13-29
9547339-7	1998	Cyclooxygenase (COX) II is emerging as an important component in wound healing and proliferation in intestinal epithelia and when acetylated by acetylsalicylic acid (aspirin) initiates the biosynthesis of a LXA4 receptor ligand.	Aspirin	166-173	formyl peptide receptor 2	Homo sapiens	207-220
9466979-10	1998	Bronchial responsiveness to lysine-aspirin correlated exclusively with LTC4 synthase+ cell counts (rho = -0.63, P = 0.049, n = 10).	Aspirin	35-42	leukotriene C4 synthase	Homo sapiens	71-84
16359516-2	2005	The mechanism accounting for such a reduced sensitivity might involve an impaired interaction of aspirin with cyclooxygenase-1 (COX)-1.	Aspirin	97-104	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	110-134
26598271-12	2011	The other is phospholipase A2, which is known as a receptor of acetylsalicylic acid or aspirin.	Aspirin	87-94	calcium-independent phospholipase A2 VIA	Drosophila melanogaster	13-29
16282376-9	2005	NO-ASA disrupted adherens junctions by inducing cleavage of beta- and gamma-catenin, resulting in cell detachment.	Aspirin	3-6	catenin beta 1	Homo sapiens	60-83
21966608-0	2011	Polymorphisms of Aspirin-Metabolizing Enzymes CYP2C9, NAT2 and UGT1A6 in Aspirin-Intolerant Urticaria.	Aspirin	17-24	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	63-69
16042570-5	2005	General COX (COX-1 and -2) inhibition by traditional NSAIDs (non-steroidal anti-inflammatory drugs), such as aspirin, although chemopreventive, has some side effects, as do some conventional COX-2-selective NSAIDs.	Aspirin	109-116	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	13-25
9696137-10	1998	Patients receiving aspirin had lower median CD63 values (13.1%) when compared to those patients who were not (18.0%, P = 0.023).	Aspirin	19-26	CD63 molecule	Homo sapiens	44-48
21966608-0	2011	Polymorphisms of Aspirin-Metabolizing Enzymes CYP2C9, NAT2 and UGT1A6 in Aspirin-Intolerant Urticaria.	Aspirin	73-80	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	63-69
9372649-0	1997	Expression of interleukin-5 and granulocyte-macrophage colony-stimulating factor in aspirin-sensitive and non-aspirin-sensitive asthmatic airways.	Aspirin	84-91	colony stimulating factor 2	Homo sapiens	32-80
9372649-5	1997	ASA airways demonstrated a significant 2-fold increase in the total number of submucosal inflammatory cells expressing IL-5 (p = 0.03) and approximate 4- and 2-fold increases in the numbers of mast cells expressing IL-5 and GM-CSF (p = 0.02 and p = 0.04, respectively).	Aspirin	0-3	colony stimulating factor 2	Homo sapiens	224-230
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	0-21	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	46-77
9372649-7	1997	These results suggest a central role for the mast cell and eosinophil in regulation of the inflammatory cell infiltrate of ASA airways by secretion of the hemopoietic cytokines IL-5 and GM-CSF.	Aspirin	123-126	colony stimulating factor 2	Homo sapiens	186-192
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	0-21	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	79-85
16034127-0	2005	Involvement of the Rho-kinase/myosin light chain kinase pathway on human monocyte chemotaxis induced by ATL-1, an aspirin-triggered lipoxin A4 synthetic analog.	Aspirin	114-121	myosin light chain kinase	Homo sapiens	30-55
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	23-26	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	46-77
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	23-26	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	79-85
21812912-0	2011	Antiplatelet effects of aspirin vary with level of P2Y12 receptor blockade supplied by either ticagrelor or prasugrel.	Aspirin	24-31	purinergic receptor P2Y12	Homo sapiens	51-56
15978611-5	2005	High glucose treatment also activated IKKbeta, and pretreatment with aspirin, a pharmacological inhibitor of IKKbeta, prevented both glucose-induced IKKbeta activation and the effect of high glucose to impair insulin-mediated NO production.	Aspirin	69-76	inhibitor of nuclear factor kappa B kinase subunit beta	Bos taurus	38-45
15978611-5	2005	High glucose treatment also activated IKKbeta, and pretreatment with aspirin, a pharmacological inhibitor of IKKbeta, prevented both glucose-induced IKKbeta activation and the effect of high glucose to impair insulin-mediated NO production.	Aspirin	69-76	inhibitor of nuclear factor kappa B kinase subunit beta	Bos taurus	109-116
15978611-5	2005	High glucose treatment also activated IKKbeta, and pretreatment with aspirin, a pharmacological inhibitor of IKKbeta, prevented both glucose-induced IKKbeta activation and the effect of high glucose to impair insulin-mediated NO production.	Aspirin	69-76	inhibitor of nuclear factor kappa B kinase subunit beta	Bos taurus	109-116
15978611-5	2005	High glucose treatment also activated IKKbeta, and pretreatment with aspirin, a pharmacological inhibitor of IKKbeta, prevented both glucose-induced IKKbeta activation and the effect of high glucose to impair insulin-mediated NO production.	Aspirin	69-76	insulin	Bos taurus	209-216
16152823-6	2005	ET and CD62p in the CSDP group lowered significantly, while SOD raised significantly (P &lt; 0.05), CD62p in the ASP group lowered significantly (P &lt; 0.05).	Aspirin	113-116	selectin P	Homo sapiens	100-105
9383683-7	1997	The increase in NO production in response to IL-1 alpha and TNF-alpha was further stimulated by aspirin and inhibited by exogenous addition of PGE2, suggesting that PGE2 produced by the cytokines, in turn, negatively modulates NO production.	Aspirin	96-103	interleukin 1 alpha	Mus musculus	45-55
9487340-5	1997	METHODS: The expression of COX-1 and COX-2 isoenzymes has been studied in the bronchial mucosa of 10 normal and 18 asthmatic subjects, 11 of whom had aspirin-sensitive asthma (ASA) and seven had non-aspirin-sensitive asthma (NASA) RESULTS: There was a significant fourfold and 14-fold increase, respectively, in the epithelial and submucosal cellular expression of COX-2, but not of COX-1, in asthmatic patients.	Aspirin	150-157	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	27-32
23556096-13	2011	While para-NO-ASA action involved inhibition of beta-catenin/Lef-1 signaling, meta-NO-ASA did not show any impact on this signaling pathway.	Aspirin	14-17	lymphoid enhancer binding factor 1	Mus musculus	61-66
9361371-6	1997	All three aspirin preparations reduced the extent of the platelet responses to most agonists: platelet aggregation induced by collagen, ristocetin and arachidonate and 14C-5HT release induced by collagen, streptokinase, and various combinations of ADP, adrenaline and PAF.	Aspirin	10-17	PCNA clamp associated factor	Homo sapiens	268-271
9475035-14	1997	Older nonsteroidal antiinflammatory drugs like aspirin and indomethacin are non selective inhibitors of COX activity and therefore, in addition to inhibiting COX-2 activity, inhibit the formation of eicosanoids by COX-1.	Aspirin	47-54	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	214-219
15806396-0	2005	Functional promoter polymorphism in the TBX21 gene associated with aspirin-induced asthma.	Aspirin	67-74	T-box transcription factor 21	Homo sapiens	40-45
15990752-10	2005	The Pl A1,A1 allele of glycoprotein IIIa was present in 36 subjects (83.7.%) and the Pl A1,A2 allele was present in 7 subjects (16.2.%) in the aspirin-resistant patients group.	Aspirin	143-150	POU class 2 homeobox 3	Homo sapiens	85-90
15990752-11	2005	The Pl A1,A1 allele of glycoprotein IIIa was present in 37 subjects (72.5%) and the Pl A1,A2 allele was present in 14 subjects (27.5%) in the aspirin-sensitive patients group ( P = .195).	Aspirin	142-149	POU class 2 homeobox 3	Homo sapiens	4-9
15990752-11	2005	The Pl A1,A1 allele of glycoprotein IIIa was present in 37 subjects (72.5%) and the Pl A1,A2 allele was present in 14 subjects (27.5%) in the aspirin-sensitive patients group ( P = .195).	Aspirin	142-149	POU class 2 homeobox 3	Homo sapiens	84-89
9263656-2	1997	The standard antiplatelet and antithrombin agents used today in patients with acute coronary syndromes are aspirin and heparin.	Aspirin	107-114	serpin family C member 1	Homo sapiens	30-42
15769457-10	2005	The PGE(2) receptors implicated in CD36 modulation by ASA are the EP2/EP4 subtypes.	Aspirin	54-57	prostaglandin E receptor 4	Homo sapiens	70-73
21457221-2	2011	The present study specifically addresses the pharmacological interactions between selective COX-2 inhibitors and ASA and the possible consequences for the thrombotic risk during long-term treatment.	Aspirin	113-116	cytochrome c oxidase subunit II	Oryctolagus cuniculus	92-97
9174558-16	1997	Aspirin was associated with a significant excess of 5 (SD 1) transfused or fatal extracranial bleeds per 1000; in the absence of heparin the excess was 2 (SD 1) and was not significant.	Aspirin	0-7	CUP2Q35	Homo sapiens	55-59
21457221-12	2011	CONCLUSIONS: COX-2 inhibition by rofecoxib attenuates the antithrombotic and anti-atherosclerotic effects of ASA during long-term treatment in cholesterol-fed rabbits.	Aspirin	109-112	cytochrome c oxidase subunit II	Oryctolagus cuniculus	13-18
21796142-0	2011	Genetic association analysis of TAP1 and TAP2 polymorphisms with aspirin exacerbated respiratory disease and its FEV1 decline.	Aspirin	65-72	transporter 2, ATP binding cassette subfamily B member	Homo sapiens	41-45
9154324-3	1997	COX-1 is expressed constitutively and is known to be the site of action of aspirin and other nonsteroidal anti-inflammatory drugs.	Aspirin	75-82	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	0-5
21796142-4	2011	Interestingly, regression analysis revealed that polymorphisms and haplotypes of TAP2 were associated with FEV1 decline by aspirin provocation (P=0.002-0.04), with about twofold decline rate of FEV1 in most of minor homozygotes compared with major homozygotes.	Aspirin	123-130	transporter 2, ATP binding cassette subfamily B member	Homo sapiens	81-85
21640159-8	2011	However, in these rats adjunctive aspirin treatment significantly improved the depressive behaviors and downregulated the COX-2 level and PGE(2) concentration in the hippocampus.	Aspirin	34-41	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	122-127
9130576-0	1997	Profound overexpression of leukotriene C4 synthase in bronchial biopsies from aspirin-intolerant asthmatic patients.	Aspirin	78-85	leukotriene C4 synthase	Homo sapiens	27-50
9175172-3	1997	The IC50S of aspirin, indomethacin and tenoxicam for human COX-1 were 0.41 +/- 0.07 microgram/ml, 0.008 +/- 0.003 microgram/ml, and 7.94 +/- 3.28 micrograms/ml, respectively, and for human COX-20.64 +/- 0.16 microgram/ml, 0.09 +/- 0.05 microgram/ml, and 10.61 +/- 1.50 micrograms/ml, for aspirin, indomethacin, and tenoxicam.	Aspirin	13-20	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	59-64
9175172-3	1997	The IC50S of aspirin, indomethacin and tenoxicam for human COX-1 were 0.41 +/- 0.07 microgram/ml, 0.008 +/- 0.003 microgram/ml, and 7.94 +/- 3.28 micrograms/ml, respectively, and for human COX-20.64 +/- 0.16 microgram/ml, 0.09 +/- 0.05 microgram/ml, and 10.61 +/- 1.50 micrograms/ml, for aspirin, indomethacin, and tenoxicam.	Aspirin	288-295	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	59-64
21640159-9	2011	Thus, our results suggest that aspirin can be served as an effective adjunctive agent in the treatment resistant depression mediated by inhibition of the COX-2 level and PGE(2) concentration.	Aspirin	31-38	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	154-159
9263351-3	1997	Aspirin is an approximately 150- to 200-fold more potent inhibitor of the (constitutive) isoform of the platelet enzyme (COX-1) than the (inducible) isoform (COX-2) which is expressed by cytokines, inflammatory stimuli, and some growth factors.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	121-126
9263351-4	1997	This explains the different dosage requirements of aspirin as an antithrombotic (COX-1) and an anti-inflammatory drug (COX-2), respectively.	Aspirin	51-58	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	81-86
9263351-14	1997	In this case, inhibition of COX-1 by aspirin will also reduce the amount of precursors for vascular prostacyclin synthesis, provided, for example, from adhering platelets.	Aspirin	37-44	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	28-33
8972019-0	1996	Acetylsalicylic acid and sodium salicylate inhibit LPS-induced NF-kappa B/c-Rel nuclear translocation, and synthesis of tissue factor (TF) and tumor necrosis factor alfa (TNF-alpha) in human monocytes.	Aspirin	0-20	coagulation factor III, tissue factor	Homo sapiens	120-133
8972019-0	1996	Acetylsalicylic acid and sodium salicylate inhibit LPS-induced NF-kappa B/c-Rel nuclear translocation, and synthesis of tissue factor (TF) and tumor necrosis factor alfa (TNF-alpha) in human monocytes.	Aspirin	0-20	coagulation factor III, tissue factor	Homo sapiens	135-137
21551129-4	2011	Here, we demonstrate that aspirin activates the c-Src tyrosine kinase pathway in CRC cells.	Aspirin	26-33	C-terminal Src kinase	Homo sapiens	48-69
21551129-6	2011	Furthermore, inhibition of c-Src activity, by chemical inhibition or expression of a kinase dead form of the protein abrogates aspirin-mediated degradation of IkappaBalpha, nuclear translocation of RelA and apoptosis, suggesting a causal link.	Aspirin	127-134	RELA proto-oncogene, NF-kB subunit	Homo sapiens	198-202
21479357-0	2011	Association analysis of DTD1 gene variations with aspirin-intolerance in asthmatics.	Aspirin	50-57	D-aminoacyl-tRNA deacylase 1	Homo sapiens	24-28
8843948-7	1996	In addition to SA, induction of IS10a occurred to varying degrees upon treatment with acetylsalicylic acid, benzoic acid, 2,4-dichlorophenoxyacetic acid, methyl jasmonate, and hydrogen peroxide, whereas treatment with other compounds had no effect.	Aspirin	86-106	scopoletin glucosyltransferase-like	Nicotiana tabacum	32-37
21479342-5	2011	Clopidogrel, the most widely used drug that inhibits P2Y12, is effective both in monotherapy and in combination with acetylsalicylic acid (ASA).	Aspirin	117-137	purinergic receptor P2Y12	Homo sapiens	53-58
9594142-1	1996	The number of alpha-granule membrane protein 140 (GMP-140) molecules was detected by using specific monoclonal antibodies (125I-SZ-51) against GMP-140 in three groups of patients with unstable angina treated with aspirin 50 mg (n = 27), 150 mg (n = 26) and 300 mg (n = 30) a day before and 7 days after treatment.	Aspirin	213-220	selectin P	Homo sapiens	14-48
9594142-1	1996	The number of alpha-granule membrane protein 140 (GMP-140) molecules was detected by using specific monoclonal antibodies (125I-SZ-51) against GMP-140 in three groups of patients with unstable angina treated with aspirin 50 mg (n = 27), 150 mg (n = 26) and 300 mg (n = 30) a day before and 7 days after treatment.	Aspirin	213-220	selectin P	Homo sapiens	50-57
9594142-3	1996	The results indicated that the number of GMP-140 molecules decreased significantly and the number of platelets increased significantly after treatment with aspirin.	Aspirin	156-163	selectin P	Homo sapiens	41-48
9594142-5	1996	When 300 mg of aspirin was used, the number of GMP-140 molecules was lower than that in a control group of healthy subjects (P &lt; 0.005) and the number of platelets reached that of the control group (P &gt; 0.05).	Aspirin	15-22	selectin P	Homo sapiens	47-54
21479342-5	2011	Clopidogrel, the most widely used drug that inhibits P2Y12, is effective both in monotherapy and in combination with acetylsalicylic acid (ASA).	Aspirin	139-142	purinergic receptor P2Y12	Homo sapiens	53-58
21386995-9	2011	The frequency of ASA-specific IFN-gamma-secreting peripheral blood mononuclear cells, as well as the amount of IL-10 produced by ASA-specific cells, was of greater magnitude in probiotic-fed pigs compared to control animals.	Aspirin	17-20	interferon gamma	Sus scrofa	30-39
21270415-8	2011	Compared with current users of low-dose ASA, those who discontinued treatment 31-180 days before the index date had a significantly increased overall risk of IS/TIA (RR 1.40; 95% CI 1.03-1.92).	Aspirin	40-43	ribonucleotide reductase catalytic subunit M1	Homo sapiens	166-170
8885505-4	1996	In the CIS more than 3/4 of children aged 1-18 years had been given aspirin for fever.	Aspirin	68-75	cytokine inducible SH2 containing protein	Homo sapiens	7-10
8724348-8	1996	Motile sperm incubated with C-fixing ASA- sera showed a time-dependent increase in the binding of C3 fragments as detected by flow cytometry using anti-iC3b neoantigen, anti-C3c, and anti-C3d monoclonal antibodies (mAbs).	Aspirin	37-40	endogenous retrovirus group K member 13	Homo sapiens	188-191
8724348-9	1996	A negative correlation (r2 = -0.930; p &lt; 0.001) was found between the increase in sperm-associated C3d fluorescence and the percentage motile sperm in the presence of ASA- sera.	Aspirin	170-173	endogenous retrovirus group K member 13	Homo sapiens	102-105
21084063-6	2011	Treatment of rats with a single dose of aspirin (400mg/kg, orally) led to significant alterations in the levels of total nitrite and nitrate (NOx), interleukins (IL-4, 6, 10, 12), tumor necrosis factor (TNF-alpha), and interferon gamma (IFN-gamma).	Aspirin	40-47	interleukin 4	Rattus norvegicus	162-166
21084063-6	2011	Treatment of rats with a single dose of aspirin (400mg/kg, orally) led to significant alterations in the levels of total nitrite and nitrate (NOx), interleukins (IL-4, 6, 10, 12), tumor necrosis factor (TNF-alpha), and interferon gamma (IFN-gamma).	Aspirin	40-47	tumor necrosis factor-like	Rattus norvegicus	180-201
20922562-0	2011	KIF3A, a cilia structural gene on chromosome 5q31, and its polymorphisms show an association with aspirin hypersensitivity in asthma.	Aspirin	98-105	kinesin family member 3A	Homo sapiens	0-5
8835129-5	1996	RESULTS: In the absence of aspirin, CD62P expression induced by AA and COL was greater in ASA+ patients compared with control subjects (P &lt; 0.001) while CD62P expression with PAF, AA and COL was reduced in ASA- when compared with ASA+ and control subjects (P &lt; 0.001).	Aspirin	90-93	selectin P	Homo sapiens	36-41
8835129-5	1996	RESULTS: In the absence of aspirin, CD62P expression induced by AA and COL was greater in ASA+ patients compared with control subjects (P &lt; 0.001) while CD62P expression with PAF, AA and COL was reduced in ASA- when compared with ASA+ and control subjects (P &lt; 0.001).	Aspirin	209-212	selectin P	Homo sapiens	36-41
8835129-5	1996	RESULTS: In the absence of aspirin, CD62P expression induced by AA and COL was greater in ASA+ patients compared with control subjects (P &lt; 0.001) while CD62P expression with PAF, AA and COL was reduced in ASA- when compared with ASA+ and control subjects (P &lt; 0.001).	Aspirin	90-94	selectin P	Homo sapiens	36-41
8835129-6	1996	CD63 expression with PAF and AA was reduced in both ASA+ and ASA- patients compared with control subjects (P &lt; 0.001).	Aspirin	52-56	CD63 molecule	Homo sapiens	0-4
8835129-6	1996	CD63 expression with PAF and AA was reduced in both ASA+ and ASA- patients compared with control subjects (P &lt; 0.001).	Aspirin	52-56	PCNA clamp associated factor	Homo sapiens	21-24
8835129-6	1996	CD63 expression with PAF and AA was reduced in both ASA+ and ASA- patients compared with control subjects (P &lt; 0.001).	Aspirin	52-55	CD63 molecule	Homo sapiens	0-4
8835129-6	1996	CD63 expression with PAF and AA was reduced in both ASA+ and ASA- patients compared with control subjects (P &lt; 0.001).	Aspirin	52-55	PCNA clamp associated factor	Homo sapiens	21-24
8835129-7	1996	Aspirin inhibited the expression of both CD62P and CD63 after agonist stimulation.	Aspirin	0-7	selectin P	Homo sapiens	41-46
8835129-7	1996	Aspirin inhibited the expression of both CD62P and CD63 after agonist stimulation.	Aspirin	0-7	CD63 molecule	Homo sapiens	51-55
8835129-8	1996	Greater inhibition of CD62P expression was observed in ASA+ compared with ASA- patients (P &lt; 0.001) and normal subjects (P &lt; 0.05) while greater inhibition of CD63 expression was observed in normal subjects compared with both ASA+ and ASA- patients (P &lt; 0.05).	Aspirin	55-59	selectin P	Homo sapiens	22-27
20922562-2	2011	RESULTS: A treatment with aspirin in the human bronchial epithelial cells increased the mRNA expression level of KIF3A compared to that of the untreated control (P &lt;= 0.01), and nasal polyp epithelia from aspirin-intolerant asthma (AIA) patients also showed a higher expression of KIF3A protein than aspirin-tolerant asthma controls.	Aspirin	26-33	kinesin family member 3A	Homo sapiens	113-118
20922562-2	2011	RESULTS: A treatment with aspirin in the human bronchial epithelial cells increased the mRNA expression level of KIF3A compared to that of the untreated control (P &lt;= 0.01), and nasal polyp epithelia from aspirin-intolerant asthma (AIA) patients also showed a higher expression of KIF3A protein than aspirin-tolerant asthma controls.	Aspirin	26-33	kinesin family member 3A	Homo sapiens	284-289
20922562-2	2011	RESULTS: A treatment with aspirin in the human bronchial epithelial cells increased the mRNA expression level of KIF3A compared to that of the untreated control (P &lt;= 0.01), and nasal polyp epithelia from aspirin-intolerant asthma (AIA) patients also showed a higher expression of KIF3A protein than aspirin-tolerant asthma controls.	Aspirin	208-215	kinesin family member 3A	Homo sapiens	113-118
20922562-3	2011	Further logistic analyses revealed that most polymorphisms of KIF3A were significantly associated with AIA (P = 0.0004-0.02; P(corr) = 0.004-0.04) and the decline of forced expiratory volume at 1 s (FEV(1))% by aspirin provocation (P = 0.004-0.04; P(corr) = 0.03).	Aspirin	211-218	kinesin family member 3A	Homo sapiens	62-67
8835129-8	1996	Greater inhibition of CD62P expression was observed in ASA+ compared with ASA- patients (P &lt; 0.001) and normal subjects (P &lt; 0.05) while greater inhibition of CD63 expression was observed in normal subjects compared with both ASA+ and ASA- patients (P &lt; 0.05).	Aspirin	55-58	selectin P	Homo sapiens	22-27
20922562-4	2011	DISCUSSION: Our findings suggest that the KIF3A gene and/or its polymorphisms might have a susceptibility effect on AIA, providing a new step toward controlling aspirin intolerance in asthmatics.	Aspirin	161-168	kinesin family member 3A	Homo sapiens	42-47
8835129-8	1996	Greater inhibition of CD62P expression was observed in ASA+ compared with ASA- patients (P &lt; 0.001) and normal subjects (P &lt; 0.05) while greater inhibition of CD63 expression was observed in normal subjects compared with both ASA+ and ASA- patients (P &lt; 0.05).	Aspirin	232-236	selectin P	Homo sapiens	22-27
8835129-8	1996	Greater inhibition of CD62P expression was observed in ASA+ compared with ASA- patients (P &lt; 0.001) and normal subjects (P &lt; 0.05) while greater inhibition of CD63 expression was observed in normal subjects compared with both ASA+ and ASA- patients (P &lt; 0.05).	Aspirin	74-77	selectin P	Homo sapiens	22-27
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	nuclear factor of activated T cells 5	Homo sapiens	69-74
8835129-9	1996	In ASA+ patients and normal subjects, stimulation with PAF and COL resulted in only one platelet population while in contrast with 1 mM AA two populations were observed.	Aspirin	3-6	PCNA clamp associated factor	Homo sapiens	55-58
8835129-10	1996	CONCLUSIONS: Enhanced AA- and collagen-induced platelet CD62P expression in ASA+ patients compared with normal subjects and greater inhibition by aspirin of CD62P expression in ASA+ may be relevant to the pathogenesis of this syndrome.	Aspirin	76-80	selectin P	Homo sapiens	56-61
8835129-10	1996	CONCLUSIONS: Enhanced AA- and collagen-induced platelet CD62P expression in ASA+ patients compared with normal subjects and greater inhibition by aspirin of CD62P expression in ASA+ may be relevant to the pathogenesis of this syndrome.	Aspirin	146-153	selectin P	Homo sapiens	157-162
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	nuclear factor of activated T cells 5	Homo sapiens	180-185
8835129-10	1996	CONCLUSIONS: Enhanced AA- and collagen-induced platelet CD62P expression in ASA+ patients compared with normal subjects and greater inhibition by aspirin of CD62P expression in ASA+ may be relevant to the pathogenesis of this syndrome.	Aspirin	177-181	selectin P	Homo sapiens	157-162
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	nuclear factor of activated T cells 5	Homo sapiens	180-185
8835129-11	1996	Reduced expression of CD62P and CD63 in platelets of ASA- patients following stimulation with PAF and AA may also have implications for the role of platelets and these mediators in the pathogenesis of other forms of asthma.	Aspirin	53-56	selectin P	Homo sapiens	22-27
8835129-11	1996	Reduced expression of CD62P and CD63 in platelets of ASA- patients following stimulation with PAF and AA may also have implications for the role of platelets and these mediators in the pathogenesis of other forms of asthma.	Aspirin	53-56	CD63 molecule	Homo sapiens	32-36
21905501-1	2011	BACKGROUND AND OBJECTIVE: Lymphocyte-oriented kinase deficiency encoded by the serine/threonine kinase 10 (STK10) gene correlates with the intracellular adhesion molecule 1 (ICAM-1)/lymphocyte function associated antigen 1 (LFA-1) complex in aspirin hypersensitivity.	Aspirin	242-249	integrin subunit alpha L	Homo sapiens	182-222
8835129-11	1996	Reduced expression of CD62P and CD63 in platelets of ASA- patients following stimulation with PAF and AA may also have implications for the role of platelets and these mediators in the pathogenesis of other forms of asthma.	Aspirin	53-56	PCNA clamp associated factor	Homo sapiens	94-97
8573071-4	1996	Exposure of 5-[14C]hydroxytryptamine-labelled platelets to cathepsin G, in the presence of acetylsalicylic acid and phosphocreatine/creatine kinase, induced platelet aggregation and degranulation in a concentration-dependent manner (0.1-3.0 microM).	Aspirin	91-111	cathepsin G	Homo sapiens	59-70
21043596-4	1996	In an experimental model in vitro that resembles vessel wall/platelet/PMN interaction in vivo, we found that aspirin (100 muM), a COX inhibitor, but not L-NMMA (100 muM) and a NO-synthase inhibitor, reversed the inhibitory effect of arterial wall on P-selectin mediated platelet/PMN adhesion.	Aspirin	109-116	selectin P	Homo sapiens	250-260
15776109-3	2005	We created hypomorphic PGHS1 (PGHS1(Neo/Neo)) mice, in which the substantial but tissue-dependent variability in the inhibition of PGHS1-derived eicosanoids achieved by low-dose aspirin treatment is mimicked, to assess the relative impact of this strategy on hemostatic and reproductive function.	Aspirin	178-185	prostaglandin-endoperoxide synthase 1	Mus musculus	23-28
15776109-8	2005	PGHS1(Neo/Neo) mice provide a model of low-dose aspirin therapy that elucidates how prevention or delay of preeclampsia might be achieved without compromising reproductive function.	Aspirin	48-55	prostaglandin-endoperoxide synthase 1	Mus musculus	0-5
21905501-1	2011	BACKGROUND AND OBJECTIVE: Lymphocyte-oriented kinase deficiency encoded by the serine/threonine kinase 10 (STK10) gene correlates with the intracellular adhesion molecule 1 (ICAM-1)/lymphocyte function associated antigen 1 (LFA-1) complex in aspirin hypersensitivity.	Aspirin	242-249	integrin subunit alpha L	Homo sapiens	224-229
21219209-3	2011	The objective of present study was to inhibit MMP-2 and MMP-9 by combination of minocycline and aspirin to treat diabetic nephropathy.	Aspirin	96-103	matrix metallopeptidase 2	Rattus norvegicus	46-51
15567157-0	2005	NO-donating aspirin inhibits the growth of leukemic Jurkat cells and modulates beta-catenin expression.	Aspirin	12-19	catenin beta 1	Homo sapiens	79-91
15567157-4	2005	The para isomer of NO-ASA degraded beta-catenin in a dose- and time-dependent manner coinciding with increasing expression of activated caspase-3.	Aspirin	22-25	catenin beta 1	Homo sapiens	35-47
15567157-5	2005	The caspase inhibitor ZVAD blocked beta-catenin cleavage by p-NO-ASA and partially reversed cell growth inhibition by p-NO-ASA but not that by ASA.	Aspirin	65-68	catenin beta 1	Homo sapiens	35-47
8584072-1	1995	Acetylsalicylic acid (ASS) is one of the best examined substances used in secondary prevention after TIA and stroke.	Aspirin	0-20	argininosuccinate synthase 1	Homo sapiens	22-25
20881612-0	2010	Antiangiogenic and antimitotic effects of aspirin in hypoxia-reoxygenation modulation of the LOX-1-NADPH oxidase axis as a potential mechanism.	Aspirin	42-49	oxidized low density lipoprotein receptor 1	Homo sapiens	93-98
15892673-4	2005	Non-selective cyclooxygenase-1 (COX-1) inhibitors used in periodontal research include compounds such as aspirin, flurbiprofen, ibuprofen, naproxen and piroxicam.	Aspirin	105-112	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	32-37
20881612-9	2010	Aspirin had no effect on endothelial nitric oxide synthase and canceled the transcriptional activation of the LOX-1 and p47(phox) subunit of NADPH oxidase.	Aspirin	0-7	oxidized low density lipoprotein receptor 1	Homo sapiens	110-115
15464695-0	2004	Association of aspirin use with vitamin B12 deficiency (results of the BACH study).	Aspirin	15-22	acyl-CoA thioesterase 7	Homo sapiens	71-75
7627706-11	1995	The complete inhibition of mox-LDL-induced platelet aggregation by aspirin could contribute to its beneficial effect in cardiovascular disease.	Aspirin	67-74	monooxygenase DBH like 1	Homo sapiens	27-30
20881612-10	2010	Based on these data, we hypothesize that aspirin preserves the integrity of adherens junctions and thus blunts angiogenic response to HR through downregulation of LOX-1 and the LOX-1-mediated p47(phox) component of NADPH oxidase transcription, thus preventing NADPH oxidase assembly and function.	Aspirin	41-48	oxidized low density lipoprotein receptor 1	Homo sapiens	163-168
20881612-10	2010	Based on these data, we hypothesize that aspirin preserves the integrity of adherens junctions and thus blunts angiogenic response to HR through downregulation of LOX-1 and the LOX-1-mediated p47(phox) component of NADPH oxidase transcription, thus preventing NADPH oxidase assembly and function.	Aspirin	41-48	oxidized low density lipoprotein receptor 1	Homo sapiens	177-182
20805751-2	2010	In humans, aspirin blocks the androgen response to human chorionic gonadotropin (hCG), and, because hCG-stimulated androgen production in utero is crucial for normal testicular descent, exposure to COX inhibitors at vulnerable times during gestation may impair testicular descent.	Aspirin	11-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
7543841-6	1995	High dose aprotinin is also effective in procedures known to possess a high risk for excessive blood loss, such as repeat CABG or heart valve replacement surgery, cardiac surgery in patients with infective endocarditis, or in patients receiving aspirin (acetylsalicylic acid) before surgery.	Aspirin	245-252	pancreatic trypsin inhibitor	Bos taurus	10-19
7543841-6	1995	High dose aprotinin is also effective in procedures known to possess a high risk for excessive blood loss, such as repeat CABG or heart valve replacement surgery, cardiac surgery in patients with infective endocarditis, or in patients receiving aspirin (acetylsalicylic acid) before surgery.	Aspirin	254-274	pancreatic trypsin inhibitor	Bos taurus	10-19
15261941-8	2004	On multivariate analysis, aspirin use was a determinant of pP-sel (p = 0.03) and sP-sel (p = 0.01), but the use of other drugs or other co-morbidity (e.g., diabetes, smoking) did not influence either P-selectin value.	Aspirin	26-33	selectin P	Homo sapiens	200-210
15236176-3	2004	RESULTS: The gastric mucosa of cyclooxygenase-1 knockout mice was more severely injured by both HCl alone and aspirin/HCl than that of wild-type and cyclooxygenase-2 knockout mice.	Aspirin	110-117	prostaglandin-endoperoxide synthase 1	Mus musculus	31-47
15236176-4	2004	HCl alone and aspirin/HCl also induced a more profound decrease in surface hydrophobicity in cyclooxygenase-1 knockout mice than in wild-type mice, whereas this surface property was unaffected in cyclooxygenase-2 knockout mice.	Aspirin	14-21	prostaglandin-endoperoxide synthase 1	Mus musculus	93-109
15236176-5	2004	The gastric injury induced by aspirin/HCl in cyclooxygenase-1 knockout mice could be prevented if the animals were treated with phosphatidylcholine-associated aspirin.	Aspirin	30-37	prostaglandin-endoperoxide synthase 1	Mus musculus	45-61
20709806-8	2010	Importantly, receptors for aspirin-triggered lipoxin and resolvin E1 (ALX and ChemR23, respectively) were identified in human VSMCs.	Aspirin	27-34	hematopoietic SH2 domain containing	Homo sapiens	70-73
15236176-5	2004	The gastric injury induced by aspirin/HCl in cyclooxygenase-1 knockout mice could be prevented if the animals were treated with phosphatidylcholine-associated aspirin.	Aspirin	159-166	prostaglandin-endoperoxide synthase 1	Mus musculus	45-61
15236176-6	2004	Aspirin/HCl, in comparison to saline or HCl alone, induced a 4-6-fold increase in gastric mucosal prostaglandin E(2) concentration in the cyclooxygenase-1 knockout mice, whereas it decreased prostaglandin E(2) levels in wild-type and cyclooxygenase-2 knockout mice.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Mus musculus	138-154
15236176-7	2004	This paradoxical aspirin-induced increase in gastric prostaglandin E(2) in cyclooxygenase-1 knockout mice seemed to correspond to an increase in cyclooxygenase-2 messenger RNA and protein expression.	Aspirin	17-24	prostaglandin-endoperoxide synthase 1	Mus musculus	75-91
15236176-11	2004	Aspirin seems to paradoxically increase the gastric mucosal prostaglandin E(2) concentration in cyclooxygenase-1 knockout mice, possibly by the induction of cyclooxygenase-2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Mus musculus	96-112
15155956-8	2004	However, CD62p expression was significantly suppressed by aspirin treatment (P=0.024) and more substantially suppressed by clopidogrel (P&lt;0.0001) on day 90.	Aspirin	58-65	selectin P	Homo sapiens	9-14
7597660-11	1995	Incubation with aspirin but not with PAF caused an increase in oxygen-free radical production in aspirin-intolerant patients whereas in aspirin-tolerant patients PAF, rather than aspirin, was the more potent stimulus for oxygen-free radical production.	Aspirin	16-23	PCNA clamp associated factor	Homo sapiens	162-165
7534663-4	1995	Induction of VCAM-1 and E-selectin surface expression by TNF was dose-dependently reduced by aspirin over the same range, while induction of intercellular adhesion molecule-1 (ICAM-1) was hardly affected.	Aspirin	93-100	selectin E	Homo sapiens	24-34
7534663-6	1995	As a functional consequence, adhesion of U937 monocytes to TNF-stimulated HUVECs was markedly reduced by aspirin due to suppression of VCAM-1 and E-selectin upregulation.	Aspirin	105-112	selectin E	Homo sapiens	146-156
7534663-8	1995	CONCLUSIONS: Our data suggest that aspirin inhibits NF-kappa B mobilization, induction of VCAM-1 and E-selectin, and subsequent monocyte adhesion in endothelial cells stimulated by TNF, thereby providing an additional mechanism for therapeutic effects of aspirin.	Aspirin	35-42	selectin E	Homo sapiens	101-111
20705923-10	2010	HDAC3 inhibits aspirin-stimulated (1) lysine acetylation of eNOS, (2) eNOS enzymatic activity, (3) eNOS-derived NO, and (4) binding of eNOS to calmodulin.	Aspirin	15-22	histone deacetylase 3	Homo sapiens	0-5
15041603-0	2004	Acetylsalicylic acid, diclofenac, and lornoxicam, but not rofecoxib, affect platelet CD 62 expression.	Aspirin	0-20	selectin P	Homo sapiens	85-90
20705923-13	2010	HDAC3, by deacetylating aspirin-acetylated eNOS, antagonizes aspirin-stimulated endothelial production of NO.	Aspirin	24-31	histone deacetylase 3	Homo sapiens	0-5
15041603-6	2004	Aspirin, diclofenac, and lornoxicam had a significant effect on arachidonic acid and collagen-induced CD 62 P expression in platelets, whereas rofecoxib did not show this effect.	Aspirin	0-7	selectin P	Homo sapiens	102-109
20705923-13	2010	HDAC3, by deacetylating aspirin-acetylated eNOS, antagonizes aspirin-stimulated endothelial production of NO.	Aspirin	61-68	histone deacetylase 3	Homo sapiens	0-5
15066917-7	2004	We observed a significant interaction between IRS1 genotype and aspirin/NSAIDs use and risk of colorectal cancer.	Aspirin	64-71	insulin receptor substrate 1	Homo sapiens	46-50
20728206-13	2010	In contrast, long-term treatment with aspirin involves suppression of IL-4 as well as downregulation of proinflammatory MMP-9 while T(H)1 marker FLT3-L increases.	Aspirin	38-45	fms related receptor tyrosine kinase 3 ligand	Homo sapiens	145-151
15066917-13	2004	In addition, the observed interactions for aspirin/NSAIDs and IRS1 and VDR genotypes suggest that mechanisms other than COX-2 inhibition may be contributing to the protective effect of aspirin and NSAIDs on colorectal cancer risk.	Aspirin	43-50	insulin receptor substrate 1	Homo sapiens	62-66
15066917-13	2004	In addition, the observed interactions for aspirin/NSAIDs and IRS1 and VDR genotypes suggest that mechanisms other than COX-2 inhibition may be contributing to the protective effect of aspirin and NSAIDs on colorectal cancer risk.	Aspirin	185-192	insulin receptor substrate 1	Homo sapiens	62-66
7878664-12	1995	The reduction in phenytoin teratogenicity by the dual PHS/LPO inhibitor ETYA was considerably greater than that previously reported for acetylsalicylic acid, which inhibits only PHS.	Aspirin	136-156	pterin 4 alpha carbinolamine dehydratase/dimerization cofactor of hepatocyte nuclear factor 1 alpha (TCF1) 1	Mus musculus	54-57
7878664-12	1995	The reduction in phenytoin teratogenicity by the dual PHS/LPO inhibitor ETYA was considerably greater than that previously reported for acetylsalicylic acid, which inhibits only PHS.	Aspirin	136-156	pterin 4 alpha carbinolamine dehydratase/dimerization cofactor of hepatocyte nuclear factor 1 alpha (TCF1) 1	Mus musculus	178-181
20647328-10	2010	Collectively, these results identify a novel GLI1-to-CDK2 pathway in esophageal carcinogenesis, which is a bona fide target for effective combinatorial chemoprevention with Urso and Aspirin.	Aspirin	182-189	cyclin dependent kinase 2	Homo sapiens	53-57
7825862-11	1994	Aspirin irreversibly inhibits PGHS-1, preventing this isozyme from forming PGH2 or any other oxygenated product; in contrast, aspirin treatment of PGHS-2 causes this enzyme to form 15-hydroxy-5c,8c,11c,13t-eicosatetraenoic acid (15-HETE) instead of PGH2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Mus musculus	30-36
8017762-10	1994	Aspirin irreversibly inhibits PGHS-1, preventing this isozyme from forming any product; in contrast, aspirin treatment of PGHS-2 causes this enzyme to form 15-hydroxy-5c,8c,11c,13t-eicosatetraenoic acid (15-HETE) instead of PGH2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Mus musculus	30-36
15020512-8	2004	11-dehydro-TxB2 excretion with and without aspirin was related to MCSF concentrations (p &lt; 0.01), and the percentage reduction of MCSF by aspirin was related to the reduction of 11-dehydro-TxB2 (p &lt; 0.05) and the reduction of the ischaemic burden compared with placebo (p &lt; 0.05).	Aspirin	43-50	colony stimulating factor 1	Homo sapiens	66-70
15020512-8	2004	11-dehydro-TxB2 excretion with and without aspirin was related to MCSF concentrations (p &lt; 0.01), and the percentage reduction of MCSF by aspirin was related to the reduction of 11-dehydro-TxB2 (p &lt; 0.05) and the reduction of the ischaemic burden compared with placebo (p &lt; 0.05).	Aspirin	141-148	colony stimulating factor 1	Homo sapiens	133-137
20659762-6	2010	RESULTS: Subjects taking aspirin at the time of study entry had a lower numbers of CD133+/34+ cells compared to those not previously exposed (0.01% vs. 0.05% of MNCs, P&lt;0.03).	Aspirin	25-32	prominin 1	Homo sapiens	83-88
15100686-13	2004	In patients who reacted to aspirin, frequency of (-444)C allele of LTC4S was significantly higher than in patients who did not react.	Aspirin	27-34	leukotriene C4 synthase	Homo sapiens	67-72
8051610-2	1994	After 1-4 h intragastric irrigation of the stomach with AVP (1-100 ng kg-1) plus 20 mM acidified ASA solution, a significant (P &lt; 0.05) inhibition in gastric mucosal lesions and acid back-diffusion produced by acidified ASA solution was observed.	Aspirin	223-226	arginine vasopressin	Canis lupus familiaris	56-59
8051610-0	1994	Protective effects of arginine-vasopressin on aspirin-induced gastric mucosal damage in anaesthetized dogs.	Aspirin	46-53	arginine vasopressin	Canis lupus familiaris	22-42
8051610-4	1994	Furthermore, a correlation (r = 0.883; P &lt; 0.01) between AVP-induced inhibition in ASA-provoked reduction in gastric PGE2 secretion and in mucus production was found.	Aspirin	86-89	arginine vasopressin	Canis lupus familiaris	60-63
8051610-6	1994	Thus, intragastric AVP protects gastric mucosa against ASA-induced damage without producing cardiovascular side effects.	Aspirin	55-58	arginine vasopressin	Canis lupus familiaris	19-22
8051610-7	1994	The inhibitory effects of AVP (100 ng kg-1) on acidified ASA-induced reduction in PGE2 and mucus secretion, as well as on ASA-induced enhancement in acid back-diffusion and erosion production were dose-dependently reversed by a specific V1 antagonist, 1-(beta-mercapto-beta,beta-cyclopenta-methylene-propionic acid), 2-(o-methyl)tyrosine-Arg8-vasopressin.	Aspirin	57-60	arginine vasopressin	Canis lupus familiaris	26-29
20597903-0	2010	Association of SLC6A12 variants with aspirin-intolerant asthma in a Korean population.	Aspirin	37-44	solute carrier family 6 member 12	Homo sapiens	15-22
7511345-8	1994	Moreover, iloprost, a stable analogue of prostacyclin, reversed the aspirin inhibitory effects on fibrinolytic activity by restoring t-PA vascular release after venous stasis.	Aspirin	68-75	plasminogen activator, tissue type	Rattus norvegicus	133-137
14685013-5	2004	These data predict that TF/VIIa inhibition, in the presence of chronic aspirin therapy in patients with cardiovascular risk factors, will be a safe therapy for thrombotic disorders.	Aspirin	71-78	coagulation factor III, tissue factor	Homo sapiens	24-26
20597903-4	2010	Eight single nucleotide polymorphisms (SNPs) in SLC6A12 were genotyped in 163 aspirin-intolerant asthma (AIA) and 429 aspirin-tolerant asthma (ATA) patients of Korean ethnicity.	Aspirin	78-85	solute carrier family 6 member 12	Homo sapiens	48-55
15061569-14	2004	ASA inhibits COX-1 and converts COX-2 into an ASA-triggered lipid mediator-generating system that produces an array of novel endogenous local autacoids from dietary omega-3 PUFA.	Aspirin	0-3	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	13-18
20597903-4	2010	Eight single nucleotide polymorphisms (SNPs) in SLC6A12 were genotyped in 163 aspirin-intolerant asthma (AIA) and 429 aspirin-tolerant asthma (ATA) patients of Korean ethnicity.	Aspirin	118-125	solute carrier family 6 member 12	Homo sapiens	48-55
20597903-7	2010	In addition, SNPs of SLC6A12 were significantly associated with the fall rate of FEV(1) by aspirin provocation suggesting that SLC6A12 could affect reversibility of lung function abnormalities in AIA patients.	Aspirin	91-98	solute carrier family 6 member 12	Homo sapiens	21-28
15068834-4	2004	We evaluated aspirin"s effects on proliferating cell nuclear antigen (PCNA) immunohistochemistry and epithelial mucin histochemistry using the lectin, Amaranthus caudatus agglutinin (ACA) in crypt sections from rectal biopsies.	Aspirin	13-20	proliferating cell nuclear antigen	Homo sapiens	70-74
20597903-7	2010	In addition, SNPs of SLC6A12 were significantly associated with the fall rate of FEV(1) by aspirin provocation suggesting that SLC6A12 could affect reversibility of lung function abnormalities in AIA patients.	Aspirin	91-98	solute carrier family 6 member 12	Homo sapiens	127-134
12943528-12	2004	Overexpression of eNOS, VEGF and its receptor Flk-1 occurred early after azoxymethane administration in rat colonic tissue, even before morphological changes associated with tumour generation were observed, and aspirin prevented the overexpression of both eNOS and VEGF receptor Flk-1.	Aspirin	211-218	vascular endothelial growth factor A	Rattus norvegicus	265-269
20397022-6	2010	In the first two cell lines ASA inhibitory effects are Cox-2 independent because HCT116 cells do not express the enzyme while in HT-29 cells, Cox-2 has no activity as shown by a Cox activity assay.	Aspirin	28-31	cytochrome c oxidase subunit 8A	Homo sapiens	55-58
12943528-12	2004	Overexpression of eNOS, VEGF and its receptor Flk-1 occurred early after azoxymethane administration in rat colonic tissue, even before morphological changes associated with tumour generation were observed, and aspirin prevented the overexpression of both eNOS and VEGF receptor Flk-1.	Aspirin	211-218	kinase insert domain receptor	Rattus norvegicus	279-284
8236145-9	1993	Aggregation and secretion induced by MAbs plus beta 2 GPI did not require exogenous fibrinogen and were variably inhibited in the presence of acetyl salicylic acid, apyrase or Ca2+, depending on the concentrations used for the two proteins.	Aspirin	142-163	apolipoprotein H	Homo sapiens	47-57
20214971-3	2010	A recent promising finding is that chronic treatment with high-dose salicylate (the active ingredient of aspirin) for several weeks enhances expression of the outer hair cell (OHC) motor protein (prestin), resulting in strengthened OHC electromotility and enhanced distortion product otoacoustic emissions (DPOAE).	Aspirin	105-112	solute carrier family 26 member 5	Rattus norvegicus	196-203
8358552-4	1993	Cell-free supernatants, sonicates or rapid filtrates of PAF-stimulated PMN suspensions did not induce platelet adhesion to endothelial cells, but the PMN sonicates induced platelet adhesion when endothelial cells were pretreated with both aspirin and NG-nitro-L-arginine (L-NOARG).	Aspirin	239-246	PCNA clamp associated factor	Homo sapiens	56-59
8506551-4	1993	The plasminogen activator inhibitor-1 levels were significantly elevated in patients not receiving antiplatelet medication compared with control subjects (P &lt; .01), whereas they were in the normal range and significantly lower in patients receiving ticlopidine or aspirin than in patients not receiving antiplatelet medication (P &lt; .01).	Aspirin	267-274	serpin family E member 1	Homo sapiens	4-37
8481398-6	1993	Our investigations of the reactions of cyanate and aspirin with bovine gamma II-crystallins show that the cysteinyl residues are also carbamylated and acetylated at pH 7.4.	Aspirin	51-58	G protein subunit gamma 7	Bos taurus	71-79
8378861-8	1993	In the CHDM, allergic or pseudoallergic reactions were observed in 0.23% of patients exposed to minor analgesics (including ASA preparations on a daily dose up to 1.0 g and pyrazolones, mainly metamizole, propyphenazone) and in 0.81% of patients exposed to NSAIDs (including the pyrazolone oxyphenbutazone).	Aspirin	124-127	CHDM	Homo sapiens	7-11
8385368-0	1993	Effects of acetyl salicylic acid and cilostazol administration on serum thrombomodulin concentration in diabetic patients.	Aspirin	11-32	thrombomodulin	Homo sapiens	72-86
1463470-2	1992	Escherichia coli dihydrodipicolinate synthase (DHDPS) (EC 4.2.1.52), the first enzyme unique to lysine biosynthesis, catalyses the condensation of pyruvate and aspartate beta-semialdehyde (ASA) by a ping-pong mechanism.	Aspirin	189-192	dihydrodipicolinate synthase	Escherichia coli	17-45
1463470-2	1992	Escherichia coli dihydrodipicolinate synthase (DHDPS) (EC 4.2.1.52), the first enzyme unique to lysine biosynthesis, catalyses the condensation of pyruvate and aspartate beta-semialdehyde (ASA) by a ping-pong mechanism.	Aspirin	189-192	dihydrodipicolinate synthase	Escherichia coli	47-52
1280469-2	1992	Both the cyclooxygenase inhibitors acetylsalicylic acid and indomethacin enhanced PAI-1 induction.	Aspirin	35-55	serpin family E member 2	Rattus norvegicus	82-87
1643209-7	1992	It is proposed that the increased LPS-induced TF activity and TNF production following aspirin intake may be due to suppressed PGE2 formation.	Aspirin	87-94	coagulation factor III, tissue factor	Homo sapiens	46-48
1868238-11	1991	These data demonstrate that EDRF/NO formation from L-arginine by human EC plays an important role as an aspirin-insensitive fluid-phase inhibitor of human platelet reactivity.	Aspirin	104-111	alpha hemoglobin stabilizing protein	Homo sapiens	28-32
1657632-4	1991	PAF also decreased forced expiratory volume in one second (FEV1) by 16% (p less than 0.01), which was markedly attenuated by acetylsalicylic acid.	Aspirin	125-145	PCNA clamp associated factor	Homo sapiens	0-3
2024888-3	1991	Aspirin-insensitive pathways, mediated by protein kinase C and myosin light-chain kinase, lead to a change of platelet shape, with an attendant striking increase in their surface (pseudopods) followed by exposure of receptors for fibrinogen and vWf on GPIIb-IIIa.	Aspirin	0-7	myosin light chain kinase	Homo sapiens	63-88
2123794-6	1990	PMNL depleted from COx by acetyl salicylic acid (ASA) recovered to synthesize PGE2 following exposure to GM-CSF.	Aspirin	49-52	colony stimulating factor 2	Homo sapiens	105-111
2230220-7	1990	The material produced by epidermal cells was identical to synthetic paf because: 1) the aggregation of aspirin-treated and ADP-insensitive washed rabbit platelets it induced was inhibited by BN 52021, an antagonist of the paf putative receptor; 2) the factor was inactivated by phospholipase A2 but was insensitive to lipase from Rhizopus arrhizus; 3) it exhibited the same retention time as synthetic paf during standard and reverse-phase (RP) high-pressure liquid chromatography (HPLC) elution.	Aspirin	103-110	phospholipase A2	Oryctolagus cuniculus	278-294
12941295-2	2003	In this report, we studied the changes in Mcl-1 protein and mRNA expression induced by staurosporine and aspirin.	Aspirin	105-112	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	42-47
12941295-14	2003	Mcl-1 disappearance might be necessary but not sufficient for the induction of apoptosis by staurosporine and aspirin.	Aspirin	110-117	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	0-5
12960371-1	2003	In addition to inhibiting cyclooxygenase (COX)-1-derived prostanoid biosynthesis, aspirin acetylates COX-2, enabling the conversion of arachidonic acid to 15(R)-epi lipoxin A4, or aspirin-triggered lipoxin (ATL).	Aspirin	82-89	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	26-48
13678940-0	2003	Resistance in vitro to low-dose aspirin is associated with platelet PlA1 (GP IIIa) polymorphism but not with C807T(GP Ia/IIa) and C-5T Kozak (GP Ibalpha) polymorphisms.	Aspirin	32-39	POU class 2 homeobox 3	Homo sapiens	68-72
13678940-7	2003	Aspirin-resistant patients were significantly more often Pl(A1/A1) (86.2%; n = 25) than sensitive patients (59.4%; n = 41; p = 0.01).	Aspirin	0-7	POU class 2 homeobox 3	Homo sapiens	57-65
13678940-11	2003	CONCLUSIONS: Platelets homozygous for the Pl(A1) allele appear to be less sensitive to inhibitory action of low-dose aspirin.	Aspirin	117-124	POU class 2 homeobox 3	Homo sapiens	42-47
12927812-0	2003	Heme oxygenase-1 induction may explain the antioxidant profile of aspirin.	Aspirin	66-73	heme oxygenase 1	Homo sapiens	0-16
12927812-2	2003	In cultured endothelial cells derived from human umbilical vein, aspirin (30-300 microM) increased heme oxygenase-1 (HO-1) protein levels in a concentration-dependent fashion up to fivefold over basal levels.	Aspirin	65-72	heme oxygenase 1	Homo sapiens	99-115
12927812-2	2003	In cultured endothelial cells derived from human umbilical vein, aspirin (30-300 microM) increased heme oxygenase-1 (HO-1) protein levels in a concentration-dependent fashion up to fivefold over basal levels.	Aspirin	65-72	heme oxygenase 1	Homo sapiens	117-121
12927812-6	2003	The nitric oxide (NO) synthase blocker L-NAME prevented aspirin-dependent HO-1 induction.	Aspirin	56-63	heme oxygenase 1	Homo sapiens	74-78
12927812-7	2003	These findings demonstrate that aspirin targets HO-1, presumably via NO-dependent pathways.	Aspirin	32-39	heme oxygenase 1	Homo sapiens	48-52
12927812-8	2003	Induction of HO-1 expression and activity may be a novel mechanism by which aspirin prevents cellular injury under inflammatory conditions and in cardiovascular disease.	Aspirin	76-83	heme oxygenase 1	Homo sapiens	13-17
14504662-8	2003	Administration of 100% EtOH was accompanied by a pronounced upregulation of HSP70, which was reduced by ASA, but enhanced by NO-ASA application.	Aspirin	104-107	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	76-81
14504662-8	2003	Administration of 100% EtOH was accompanied by a pronounced upregulation of HSP70, which was reduced by ASA, but enhanced by NO-ASA application.	Aspirin	128-131	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	76-81
14504662-10	2003	In contrast to ASA, NO-ASA attenuated gastric mucosal lesions and significantly upregulated HSP70 expression despite blockade of sensory nerves.	Aspirin	23-26	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	92-97
14504662-12	2003	CONCLUSIONS: NO-ASA protects gastric mucosa even after blockade of sensory nerves due to the upregulation of HSP70 expression and attenuation of the oxidative injury resulting from strong upregulation of genes for antioxidant enzymes.	Aspirin	16-19	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	109-114
12709408-0	2003	Relative contribution of acetylated cyclo-oxygenase (COX)-2 and 5-lipooxygenase (LOX) in regulating gastric mucosal integrity and adaptation to aspirin.	Aspirin	144-151	arachidonate 5-lipoxygenase	Rattus norvegicus	81-84
12709408-2	2003	The acetylated COX-2 remains active, and upon cell activation, initiates the generation of 15R-HETE, a lipid substrate for 5-lipoxygenase (LOX) leading to the formation of 15-epi-LXA4 (also termed "aspirin-triggered lipoxin," or ATL).	Aspirin	198-205	arachidonate 5-lipoxygenase	Rattus norvegicus	123-137
12709408-2	2003	The acetylated COX-2 remains active, and upon cell activation, initiates the generation of 15R-HETE, a lipid substrate for 5-lipoxygenase (LOX) leading to the formation of 15-epi-LXA4 (also termed "aspirin-triggered lipoxin," or ATL).	Aspirin	198-205	arachidonate 5-lipoxygenase	Rattus norvegicus	139-142
12870263-2	2003	The biological effects induced by aspirin and indomethacin on T98G cells, in which the expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were confirmed by RT-PCR and immunostaining, were investigated by studying cell proliferation and apoptosis assays.	Aspirin	34-41	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	119-124
14524272-8	2003	The inhibition of COX-1, but not COX-2, was shown to precipitate post-challenge symptoms precipitated by aspirin.	Aspirin	105-112	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	18-23
12671717-10	2003	Much lesser inhibitory effect on ODC activity was observed in aspirin-treated cells.	Aspirin	62-69	ornithine decarboxylase 1	Rattus norvegicus	33-36
12671717-12	2003	Our study revealed that celecoxib and aspirin share the ability to inhibit ODC activity and alter the pattern of immediate-early gene expression.	Aspirin	38-45	ornithine decarboxylase 1	Rattus norvegicus	75-78
12695747-0	2003	Aspirin inhibits surface glycoprotein IIb/IIIa, P-selectin, CD63, and CD107a receptor expression on human platelets.	Aspirin	0-7	selectin P	Homo sapiens	48-58
12695747-0	2003	Aspirin inhibits surface glycoprotein IIb/IIIa, P-selectin, CD63, and CD107a receptor expression on human platelets.	Aspirin	0-7	CD63 molecule	Homo sapiens	60-64
12695747-7	2003	Dose-dependent inhibition of GPIIb/IIIa, P-selectin, CD63, and CD107a receptor expression was observed in the aspirin-treated whole-blood samples.	Aspirin	110-117	selectin P	Homo sapiens	41-51
12695747-7	2003	Dose-dependent inhibition of GPIIb/IIIa, P-selectin, CD63, and CD107a receptor expression was observed in the aspirin-treated whole-blood samples.	Aspirin	110-117	CD63 molecule	Homo sapiens	53-57
12668894-2	2003	Constitutively-expressed cyclooxygenase (COX-1) inhibition is likely to be responsible for the cross-reactions and side effects associated with these drugs, as well as the anaphylactoid reactions sometimes seen in aspirin-sensitive respiratory disease.	Aspirin	214-221	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	41-46
12668895-7	2003	Desensitization to aspirin will result in cross-desensitization to all NSATDs that inhibit COX-1.	Aspirin	19-26	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	91-96
12668895-10	2003	Because low-dose ASA exerts a cardioprotective effect by irreversible inhibition of COX-1, AERD patients who are at risk for coronary artery disease should be considered for aspirin desensitization.	Aspirin	17-20	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	84-89
12637702-9	2003	CONCLUSIONS: CD63 expression reflecting the release of platelet lysosomes is consistently increased after stroke and incompletely suppressed by treatment with aspirin, clopidogrel, or both.	Aspirin	159-166	CD63 molecule	Homo sapiens	13-17
14586741-7	2003	Chronic aspirin treatment in diabetic rats significantly attenuated mesangial expansion, and effectively suppressed CTGF induction, as well as inhibiting the upregulation of TGF-beta1 and fibronectin expression.	Aspirin	8-15	cellular communication network factor 2	Rattus norvegicus	116-120
14586741-7	2003	Chronic aspirin treatment in diabetic rats significantly attenuated mesangial expansion, and effectively suppressed CTGF induction, as well as inhibiting the upregulation of TGF-beta1 and fibronectin expression.	Aspirin	8-15	fibronectin 1	Rattus norvegicus	188-199
14586741-8	2003	In cultured mesangial cells, aspirin treatment abolished high glucose-stimulated CTGF upregulation.	Aspirin	29-36	cellular communication network factor 2	Rattus norvegicus	81-85
12574066-2	2003	COX-1 and -2 are of particular interest because they are the major targets of nonsteroidal antiinflammatory drugs (NSAIDs) including aspirin, ibuprofen, and the new COX-2-selective inhibitors.	Aspirin	133-140	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	0-12
12542208-6	2002	PAF activity correlated with tissue eosinophilia and polyps obtained from patients with aspirin-sensitive asthma contained relatively large amounts of PAF, with enriched infiltration of eosinophils.	Aspirin	88-95	PCNA clamp associated factor	Homo sapiens	0-3
12542208-6	2002	PAF activity correlated with tissue eosinophilia and polyps obtained from patients with aspirin-sensitive asthma contained relatively large amounts of PAF, with enriched infiltration of eosinophils.	Aspirin	88-95	PCNA clamp associated factor	Homo sapiens	151-154
12429575-10	2002	Aspirin, indomethacin and nimesulide inhibited COX-1 activity, without altering LO activity.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	47-52
12429575-12	2002	NO-aspirin, like aspirin inhibited COX-1 activity in blood from both groups.	Aspirin	3-10	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	35-40
12429575-12	2002	NO-aspirin, like aspirin inhibited COX-1 activity in blood from both groups.	Aspirin	17-24	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	35-40
12368230-0	2002	Aspirin (ASA) regulates 5-lipoxygenase activity and peroxisome proliferator-activated receptor alpha-mediated CINC-1 release in rat liver cells: novel actions of lipoxin A4 (LXA4) and ASA-triggered 15-epi-LXA4.	Aspirin	0-7	arachidonate 5-lipoxygenase	Rattus norvegicus	24-38
12368230-0	2002	Aspirin (ASA) regulates 5-lipoxygenase activity and peroxisome proliferator-activated receptor alpha-mediated CINC-1 release in rat liver cells: novel actions of lipoxin A4 (LXA4) and ASA-triggered 15-epi-LXA4.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Rattus norvegicus	52-100
12368230-0	2002	Aspirin (ASA) regulates 5-lipoxygenase activity and peroxisome proliferator-activated receptor alpha-mediated CINC-1 release in rat liver cells: novel actions of lipoxin A4 (LXA4) and ASA-triggered 15-epi-LXA4.	Aspirin	0-7	C-X-C motif chemokine ligand 1	Rattus norvegicus	110-116
12368230-0	2002	Aspirin (ASA) regulates 5-lipoxygenase activity and peroxisome proliferator-activated receptor alpha-mediated CINC-1 release in rat liver cells: novel actions of lipoxin A4 (LXA4) and ASA-triggered 15-epi-LXA4.	Aspirin	9-12	arachidonate 5-lipoxygenase	Rattus norvegicus	24-38
12368230-0	2002	Aspirin (ASA) regulates 5-lipoxygenase activity and peroxisome proliferator-activated receptor alpha-mediated CINC-1 release in rat liver cells: novel actions of lipoxin A4 (LXA4) and ASA-triggered 15-epi-LXA4.	Aspirin	9-12	peroxisome proliferator activated receptor alpha	Rattus norvegicus	52-100
12368230-0	2002	Aspirin (ASA) regulates 5-lipoxygenase activity and peroxisome proliferator-activated receptor alpha-mediated CINC-1 release in rat liver cells: novel actions of lipoxin A4 (LXA4) and ASA-triggered 15-epi-LXA4.	Aspirin	9-12	C-X-C motif chemokine ligand 1	Rattus norvegicus	110-116
12368230-0	2002	Aspirin (ASA) regulates 5-lipoxygenase activity and peroxisome proliferator-activated receptor alpha-mediated CINC-1 release in rat liver cells: novel actions of lipoxin A4 (LXA4) and ASA-triggered 15-epi-LXA4.	Aspirin	184-187	peroxisome proliferator activated receptor alpha	Rattus norvegicus	52-100
12368230-2	2002	In the current investigation, we examined the effects of ASA on COX and 5-lipoxygenase (5-LO) pathways and its impact on peroxisome proliferator-activated receptor alpha (PPARalpha) and cytokine-induced neutrophil chemoattractant-1 (CINC-1) levels in rat liver cells.	Aspirin	57-60	arachidonate 5-lipoxygenase	Rattus norvegicus	72-86
12368230-2	2002	In the current investigation, we examined the effects of ASA on COX and 5-lipoxygenase (5-LO) pathways and its impact on peroxisome proliferator-activated receptor alpha (PPARalpha) and cytokine-induced neutrophil chemoattractant-1 (CINC-1) levels in rat liver cells.	Aspirin	57-60	C-X-C motif chemokine ligand 1	Rattus norvegicus	186-231
12368230-4	2002	In hepatocytes, ASA significantly inhibited PPARalpha protein expression and CINC-1 secretion, effects that were also observed in hepatocytes exposed to the selective PPARalpha agonist Wy-14643.	Aspirin	16-19	peroxisome proliferator activated receptor alpha	Rattus norvegicus	44-53
12368230-4	2002	In hepatocytes, ASA significantly inhibited PPARalpha protein expression and CINC-1 secretion, effects that were also observed in hepatocytes exposed to the selective PPARalpha agonist Wy-14643.	Aspirin	16-19	C-X-C motif chemokine ligand 1	Rattus norvegicus	77-83
12368230-4	2002	In hepatocytes, ASA significantly inhibited PPARalpha protein expression and CINC-1 secretion, effects that were also observed in hepatocytes exposed to the selective PPARalpha agonist Wy-14643.	Aspirin	16-19	peroxisome proliferator activated receptor alpha	Rattus norvegicus	167-176
12368230-6	2002	Interestingly, the endogenous antiinflammatory eicosanoids LXA4 and ASA-triggered 15-epi-LXA4, in addition to inhibiting macrophage 5-LO activity to a similar extent as PGE2, significantly reduced PPARalpha and CINC-1 levels in hepatocytes.	Aspirin	68-71	peroxisome proliferator activated receptor alpha	Rattus norvegicus	197-206
12368230-6	2002	Interestingly, the endogenous antiinflammatory eicosanoids LXA4 and ASA-triggered 15-epi-LXA4, in addition to inhibiting macrophage 5-LO activity to a similar extent as PGE2, significantly reduced PPARalpha and CINC-1 levels in hepatocytes.	Aspirin	68-71	C-X-C motif chemokine ligand 1	Rattus norvegicus	211-217
12368230-7	2002	Taken together and because arachidonic acid-derived products, PPARalpha levels, and CINC-1 secretion are involved in the extent and duration of an inflammatory response, these findings provide additional molecular mechanisms for the pharmacological properties of ASA.	Aspirin	263-266	peroxisome proliferator activated receptor alpha	Rattus norvegicus	62-71
12368230-7	2002	Taken together and because arachidonic acid-derived products, PPARalpha levels, and CINC-1 secretion are involved in the extent and duration of an inflammatory response, these findings provide additional molecular mechanisms for the pharmacological properties of ASA.	Aspirin	263-266	C-X-C motif chemokine ligand 1	Rattus norvegicus	84-90
12428662-1	2002	OBJECTIVE: To evaluate in vivo activity in dogs of meloxicam or aspirin, previously shown in vitro to be a selective cyclooxygenase-2 (COX-2) inhibitor (COX-1 sparing drug), or a nonselective COX inhibitor, respectively.	Aspirin	64-71	prostaglandin-endoperoxide synthase 2	Canis lupus familiaris	117-133
12428662-1	2002	OBJECTIVE: To evaluate in vivo activity in dogs of meloxicam or aspirin, previously shown in vitro to be a selective cyclooxygenase-2 (COX-2) inhibitor (COX-1 sparing drug), or a nonselective COX inhibitor, respectively.	Aspirin	64-71	prostaglandin-endoperoxide synthase 2	Canis lupus familiaris	135-140
20421472-1	2010	Lipoxins (Lxs) and aspirin-triggered epi-Lxs (15-epi-LxA(4)) act through the ALX/FPRL1 receptor to block leukocyte trafficking, dampen cytokine/chemokine synthesis, and enhance phagocytic clearance of apoptotic leukocytes-key requisites for inflammatory resolution.	Aspirin	19-26	hematopoietic SH2 domain containing	Homo sapiens	77-80
12368905-2	2002	Here, we report that inhibition of PMN infiltration by ASA and DEX is a property shared by aspirin-triggered lipoxins (ATL) and the glucocorticoid-induced annexin 1 (ANXA1)-derived peptides that are both generated in vivo and act at the lipoxin A(4) receptor (ALXR/FPRL1) to halt PMN diapedesis.	Aspirin	55-58	formyl peptide receptor 2	Homo sapiens	260-264
12368905-2	2002	Here, we report that inhibition of PMN infiltration by ASA and DEX is a property shared by aspirin-triggered lipoxins (ATL) and the glucocorticoid-induced annexin 1 (ANXA1)-derived peptides that are both generated in vivo and act at the lipoxin A(4) receptor (ALXR/FPRL1) to halt PMN diapedesis.	Aspirin	55-58	formyl peptide receptor 2	Homo sapiens	265-270
20421472-6	2010	Elevating 15-epi-LxA(4) in early resolvers using aspirin increased blister leukocyte ALX but reduced cytokines/chemokines as well as polymorphonuclear leukocyte and macrophage numbers.	Aspirin	49-56	hematopoietic SH2 domain containing	Homo sapiens	85-88
12208460-11	2002	The results indicate that a specific enzyme present in human plasma, probably human butyrylcholinesterase, catalyses aspirin release from isosorbide diaspirinate.	Aspirin	117-124	butyrylcholinesterase	Homo sapiens	84-105
12147297-4	2002	We investigated the effects of anti-inflammatory drugs (methylprednisolone and acetylsalicylic acid (ASA)) on C1q secretion in human peritoneal macrophages in vitro.	Aspirin	79-99	complement C1q A chain	Homo sapiens	110-113
12147297-4	2002	We investigated the effects of anti-inflammatory drugs (methylprednisolone and acetylsalicylic acid (ASA)) on C1q secretion in human peritoneal macrophages in vitro.	Aspirin	101-104	complement C1q A chain	Homo sapiens	110-113
20185595-10	2010	Detecting an interaction between acetylsalicylic acid and PF4-H-ABs regarding sudden death and mortality, we found that the association between PF4-H-ABs and outcomes was restricted to patients with acetylsalicylic acid use, most likely because of indication bias.	Aspirin	33-53	platelet factor 4	Homo sapiens	144-147
12209639-3	2002	To test the role of BCR signaling competence on the induction of tolerance-mediated receptor editing, we crossed the 3-83 Tg mice with mice deficient in CD45, a protein tyrosine phosphatase that functions asa positive regulator of the BCR signaling.	Aspirin	205-208	protein tyrosine phosphatase, receptor type, C	Mus musculus	153-157
20185595-10	2010	Detecting an interaction between acetylsalicylic acid and PF4-H-ABs regarding sudden death and mortality, we found that the association between PF4-H-ABs and outcomes was restricted to patients with acetylsalicylic acid use, most likely because of indication bias.	Aspirin	199-219	platelet factor 4	Homo sapiens	58-61
20185595-10	2010	Detecting an interaction between acetylsalicylic acid and PF4-H-ABs regarding sudden death and mortality, we found that the association between PF4-H-ABs and outcomes was restricted to patients with acetylsalicylic acid use, most likely because of indication bias.	Aspirin	199-219	platelet factor 4	Homo sapiens	144-147
20185595-11	2010	CONCLUSIONS: In hemodialysis patients who have type 2 diabetes and are treated with acetylsalicylic acid, PF4-H-ABs are associated with sudden and all-cause death.	Aspirin	84-104	platelet factor 4	Homo sapiens	106-109
20223228-8	2010	Treatment of aspirin significantly prevented the progression of nephropathy and inhibited the augmented COX-2, NFkappaB (p65 levels), TNFalpha, and TGFbeta-smad expression.	Aspirin	13-20	RELA proto-oncogene, NF-kB subunit	Homo sapiens	121-124
11891303-4	2002	Moreover, we demonstrate that such BPI expression is transcriptionally regulated by analogs of endogenously occurring anti-inflammatory eicosanoids (aspirin-triggered lipoxins, ATLa).	Aspirin	149-156	bactericidal permeability increasing protein	Homo sapiens	35-38
19752399-5	2010	5S,15R-diHETE was the only product formed by aspirin-acetylated COX-2.	Aspirin	45-52	cytochrome c oxidase II, mitochondrial	Mus musculus	64-69
11855867-4	2002	Focus formation of PDGF-B-chain-transformed mouse fibroblasts was suppressed by treatment with acetylsalicylic acid (ASA) and salicylic acid, which are known inhibitors of NF-kappaB activation, but other nonsteroidal anti-inflammatory drugs that do not have an effect on NF-kappaB activity did not affect focus formation in these cells.	Aspirin	95-115	platelet derived growth factor, B polypeptide	Mus musculus	19-25
20174466-5	2010	Participants taking ASA alone had reduced urine Tx-M/PGI-M compared to no ASA or NSAID; however, participants taking NSAIDs plus ASA did not have reduced urine Tx-M/PGI-M ratio compared to NSAIDs alone.	Aspirin	20-23	glucose-6-phosphate isomerase	Homo sapiens	53-56
11855867-4	2002	Focus formation of PDGF-B-chain-transformed mouse fibroblasts was suppressed by treatment with acetylsalicylic acid (ASA) and salicylic acid, which are known inhibitors of NF-kappaB activation, but other nonsteroidal anti-inflammatory drugs that do not have an effect on NF-kappaB activity did not affect focus formation in these cells.	Aspirin	117-120	platelet derived growth factor, B polypeptide	Mus musculus	19-25
11855867-6	2002	Therefore, the transcription factor NF-kappaB plays a vital role in PDGF-B chain transformation of mouse fibroblast cells, and the NF-kappaB activity is sensitive to treatment with ASA.	Aspirin	181-184	platelet derived growth factor, B polypeptide	Mus musculus	68-74
20407607-0	2010	Attenuation of diabetic retinopathy by enhanced inhibition of MMP-2 and MMP-9 using aspirin and minocycline in streptozotocin-diabetic rats.	Aspirin	84-91	matrix metallopeptidase 2	Rattus norvegicus	62-67
11916084-6	2002	By contrast, tyrosine phosphorylation of Pyk2 was only partially reduced by aspirin and RGDS, and was not affected by either calcium chelation or PKC inhibition, suggesting that activation of this kinase does not require phospholipase-mediated signalling.	Aspirin	76-83	protein tyrosine kinase 2 beta	Homo sapiens	41-45
11433179-0	2001	NCX4016 (NO-aspirin) inhibits thromboxane biosynthesis and tissue factor expression and activity in human monocytes.	Aspirin	12-19	coagulation factor III, tissue factor	Homo sapiens	59-72
11433179-3	2001	MATERIAL AND METHODS: The effects of NCX4016 and ASA on the release of thromboxane (TX) B2 and tissue factor expression and activity were compared using adherent human monocytes.	Aspirin	49-52	coagulation factor III, tissue factor	Homo sapiens	95-108
11419884-6	2001	RESULTS: Trough platelet COX-1-derived serum Tx B2 concentrations decreased by 100% with daily aspirin and by 90%, 84% and 78% with 325, 81 and 40 mg aspirin every-third-day (p &lt; 0.001).	Aspirin	95-102	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	25-30
11419884-6	2001	RESULTS: Trough platelet COX-1-derived serum Tx B2 concentrations decreased by 100% with daily aspirin and by 90%, 84% and 78% with 325, 81 and 40 mg aspirin every-third-day (p &lt; 0.001).	Aspirin	150-157	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	25-30
11419884-8	2001	CONCLUSIONS: Low doses of aspirin that markedly inhibit platelet COX-1 activity, as manifested by a profound decline in platelet-derived serum Tx B2 concentrations, have no detectable effect on serum CRP levels in healthy men and women.	Aspirin	26-33	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	65-70
20407607-2	2010	We hypothesized that minocycline induced MMP-2 and MMP-9 inhibition can be enhanced by aspirin, a non-selective COX and tPA inhibitor and this combination can reduce progression of diabetic retinopathy.	Aspirin	87-94	matrix metallopeptidase 2	Rattus norvegicus	41-46
11380325-10	2001	The increases in thiobarbituric acid-reactive substances and myeloperoxidase activity after aspirin administration were both significantly inhibited by pre-treatment with pioglitazone (10 mg/kg).	Aspirin	92-99	myeloperoxidase	Rattus norvegicus	61-76
19909736-5	2010	ASA VI also raised the activities of mitochondrial enzymes (succinate dehydrogenase (SDH), isocitrate dehydrogenase (ICDH), malate dehydrogenase (MDH) and alpha-ketoglutarate dehydrogenase (alpha-KGDH)) and those of adenosine triphosphate (ATP) content, but lowered Ca(2+) level.	Aspirin	0-3	oxoglutarate dehydrogenase	Rattus norvegicus	155-188
11251623-1	2001	In a subset of patients with asthma, aspirin and several other non-steroidal anti-inflammatory drugs (NSAID) that inhibit simultaneously cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) precipitate dangerous asthmatic attacks.	Aspirin	37-44	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	155-160
11251623-2	2001	We tested the hypothesis that in patients with aspirin-induced asthma the attacks are triggered by inhibition of COX-1 and not COX-2.	Aspirin	47-54	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	113-118
11251623-8	2001	NSAID that inhibit COX-1, but not COX-2, trigger asthmatic attacks in patients with asthma and aspirin intolerance.	Aspirin	95-102	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	19-24
11313997-0	2001	The nonsteroidal anti-inflammatory drugs aspirin and indomethacin attenuate beta-catenin/TCF-4 signaling.	Aspirin	41-48	catenin beta 1	Homo sapiens	76-88
11313997-4	2001	We therefore investigated beta-catenin/TCF signaling in response to aspirin or indomethacin, respectively, in four CRC cell lines (SW948, SW480, HCT116, LoVo).	Aspirin	68-75	catenin beta 1	Homo sapiens	26-38
11313997-5	2001	Both, aspirin and indomethacin inhibited transcription of a beta-catenin/TCF-responsive reporter gene in a dose dependent manner.	Aspirin	6-13	catenin beta 1	Homo sapiens	60-72
11313997-10	2001	These results strongly suggest that aspirin and indomethacin attenuate the transcription of beta-catenin/TCF-responsive genes, by modulating TCF activity without disrupting beta-catenin/TCF complex formation.	Aspirin	36-43	catenin beta 1	Homo sapiens	92-104
1981242-5	1990	High concentrations of indomethacin, aspirin, and 12 other nonsteroidal antiinflammatory drugs (NSAID) inhibited IL-1 activity, or production or both.	Aspirin	37-44	interleukin 1 alpha	Homo sapiens	113-117
20036315-0	2010	Aspirin-triggered lipoxin induces CB1-dependent catalepsy in mice.	Aspirin	0-7	cannabinoid receptor 1 (brain)	Mus musculus	34-37
11552047-8	2001	Aspirin is a more potent inhibitor of Cox-1 than of Cox-2, unlike other non-steroidal anti-inflammatory drugs (NSAIDs), which have limited selectivity.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	38-43
2385209-2	1990	Acetylsalicylic acid (ASS) is increasingly used in the prevention of cardiovascular diseases.	Aspirin	0-20	argininosuccinate synthase 1	Homo sapiens	22-25
20036315-2	2010	Aspirin, a non-selective COX inhibitor, acetylates COX-2 with generation of a lipoxygenase (LOX) substrate, whose end product is the 15-epi-lipoxin A(4) (15-epi-LXA(4)), an aspirin-triggered lipoxin.	Aspirin	0-7	prostaglandin-endoperoxide synthase 2	Mus musculus	51-56
20036315-2	2010	Aspirin, a non-selective COX inhibitor, acetylates COX-2 with generation of a lipoxygenase (LOX) substrate, whose end product is the 15-epi-lipoxin A(4) (15-epi-LXA(4)), an aspirin-triggered lipoxin.	Aspirin	173-180	prostaglandin-endoperoxide synthase 2	Mus musculus	51-56
19997773-0	2010	Aspirin inhibits fractalkine expression in atherosclerotic plaques and reduces atherosclerosis in ApoE gene knockout mice.	Aspirin	0-7	chemokine (C-X3-C motif) ligand 1	Mus musculus	17-28
11152927-8	2000	Aspirin diminished P-selectin expression in sodium arachidonate-stimulated platelets (from 77.7 +/- 11.8% to 40.2 +/- 3.6%, P&lt;0.0001) in non-aspirinated and platelets from aspirin-treated donors, respectively.	Aspirin	0-7	selectin P	Homo sapiens	19-29
19997773-1	2010	OBJECTIVE: To determine the fractalkine expression in the aorta of ApoE (-/-) mice and the effect of high-dose aspirin intervention on fractalkine expression and atherosclerotic lesion formation.	Aspirin	111-118	chemokine (C-X3-C motif) ligand 1	Mus musculus	135-146
11152927-9	2000	Abciximab (3, 4, and 5 microg/ml) added to platelets from aspirin-treated donors decreased P-selectin expression in platelets stimulated with sodium arachidonate from 40.2 +/- 8.6% to 25.6 +/- 11.5% (P=0.027), to 20.5 +/- 3.5% (P&lt;0.0001), and to 22.5 +/- 1.8% (P&lt;0.0001).	Aspirin	58-65	selectin P	Homo sapiens	91-101
2142859-5	1990	The ANP-induced relaxation was not modified by pretreatment with 5 x 10(-7) M propranolol, 5 x 10(-7) M atropine, 10(-6) M cimetidine, 5 x 10(-5) M aspirin, or 10(-5) M ouabain.	Aspirin	148-155	natriuretic peptide A	Bos taurus	4-7
11211927-7	2000	Using the mean of the results for PGE2 and TXB2 inhibition, the COX-1/COX-2 ratios of the IC50 values for aspirin and NS-398 are &lt; 0.1 and &gt; 130, respectively.	Aspirin	106-113	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	64-69
19997773-6	2010	Both RT-PCR analysis and immunohistochemical analysis showed that fractalkine expression was the strongest in the high-fat diet group and was significantly decreased by aspirin treatment.	Aspirin	169-176	chemokine (C-X3-C motif) ligand 1	Mus musculus	66-77
11034327-4	2000	The apoptotic effect of aspirin was analyzed in different cell lines (Jurkat, MOLT-4, Raji and HL-60) showing induction of mitochondrial cytochrome c release and caspases 9, 3 and 8 processing.	Aspirin	24-31	caspase 9	Homo sapiens	162-181
19997773-8	2010	CONCLUSIONS: The results of our study indicate that high dose aspirin can improve the atherosclerotic lesion and suppress the fractalkine expression in murine aorta.	Aspirin	62-69	chemokine (C-X3-C motif) ligand 1	Mus musculus	126-137
20033269-0	2010	Fractalkine as an important target of aspirin in the prevention of atherogenesis : Editorial to: "Aspirin inhibits fractalkine expression in atherosclerotic plaques and reduces atherosclerosis in ApoE gene knockout mice" by H. Liu et al.	Aspirin	38-45	chemokine (C-X3-C motif) ligand 1	Mus musculus	0-11
2114514-7	1990	Moreover, PGE2 production was potently induced by PMA and slightly by EGF in the cyclooxygenase-inactivated cells by acetyl salicylate pretreatment, which also suggests that both agents might induce the synthesis of cyclooxygenase in cultured porcine thyroid cells, although we did not measure its activity.	Aspirin	117-134	epidermal growth factor	Homo sapiens	70-73
20033269-0	2010	Fractalkine as an important target of aspirin in the prevention of atherogenesis : Editorial to: "Aspirin inhibits fractalkine expression in atherosclerotic plaques and reduces atherosclerosis in ApoE gene knockout mice" by H. Liu et al.	Aspirin	38-45	chemokine (C-X3-C motif) ligand 1	Mus musculus	115-126
20033269-0	2010	Fractalkine as an important target of aspirin in the prevention of atherogenesis : Editorial to: "Aspirin inhibits fractalkine expression in atherosclerotic plaques and reduces atherosclerosis in ApoE gene knockout mice" by H. Liu et al.	Aspirin	98-105	chemokine (C-X3-C motif) ligand 1	Mus musculus	0-11
11798822-2	2000	METHODS: The polymorphisms of CYP1A1 and CYP2E1 gene were analyzed in 158 PD patients and 150 unrelated healthy controls with PCR-RFLP and ASA techniques.	Aspirin	139-142	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	30-36
20033269-0	2010	Fractalkine as an important target of aspirin in the prevention of atherogenesis : Editorial to: "Aspirin inhibits fractalkine expression in atherosclerotic plaques and reduces atherosclerosis in ApoE gene knockout mice" by H. Liu et al.	Aspirin	98-105	chemokine (C-X3-C motif) ligand 1	Mus musculus	115-126
20127554-3	2010	This conference report highlights selected presentations on aspirin-triggered lipoxins for inflammation, hepatocyte nuclear factor HNF4alpha as a target for intestinal inflammation, P2Y nucleotide receptor antagonism for inflammatory diseases, antioxidant approaches for hearing loss prevention, targeting protein kinase CK2 in neuronal injury, the role of AATF (apoptosis antagonizing transcription factor)-mediated neuroprotection in Alzheimer"s disease, and lessons from bioactive proteins from plants.	Aspirin	60-67	apoptosis antagonizing transcription factor	Homo sapiens	357-361
10704169-7	2000	Pl(A1,A2) platelets were more sensitive to inhibition of aggregation by pharmacologically relevant concentrations of aspirin and abciximab.	Aspirin	117-124	POU class 2 homeobox 3	Homo sapiens	0-5
2157034-6	1990	The non-steroidal anti-inflammatory drugs, phenylbutazone, salicylic acid, aspirin, sodium salicylate in addition to D-penicillamine and dimethylsulfoxide caused dose-dependent inhibition of the cytochrome-c reduction when the cells were stimulated by PMA.	Aspirin	75-82	cytochrome c, somatic	Equus caballus	195-207
10741635-8	2000	CD62 expression as a marker of platelet granular secretion was reduced to 66% by clopidogrel (P &lt; .01) and to 41% by the combination of clopidogrel and aspirin; aspirin alone had no effect.	Aspirin	155-162	selectin P	Homo sapiens	0-4
10741635-8	2000	CD62 expression as a marker of platelet granular secretion was reduced to 66% by clopidogrel (P &lt; .01) and to 41% by the combination of clopidogrel and aspirin; aspirin alone had no effect.	Aspirin	164-171	selectin P	Homo sapiens	0-4
34979192-0	2022	Aspirin ameliorates the cognition impairment in mice following benzo(a)pyrene treatment via down-regulating BDNF IV methylation.	Aspirin	0-7	brain derived neurotrophic factor	Mus musculus	108-112
34979192-10	2022	Aspirin co-treatment rescued DNMTs activation and BDNF IV hypermethylation, and mitigated the recession in BDNF mRNA and protein induced by B(a)P treatment.	Aspirin	0-7	brain derived neurotrophic factor	Mus musculus	50-54
34979192-10	2022	Aspirin co-treatment rescued DNMTs activation and BDNF IV hypermethylation, and mitigated the recession in BDNF mRNA and protein induced by B(a)P treatment.	Aspirin	0-7	brain derived neurotrophic factor	Mus musculus	107-111
20127554-3	2010	This conference report highlights selected presentations on aspirin-triggered lipoxins for inflammation, hepatocyte nuclear factor HNF4alpha as a target for intestinal inflammation, P2Y nucleotide receptor antagonism for inflammatory diseases, antioxidant approaches for hearing loss prevention, targeting protein kinase CK2 in neuronal injury, the role of AATF (apoptosis antagonizing transcription factor)-mediated neuroprotection in Alzheimer"s disease, and lessons from bioactive proteins from plants.	Aspirin	60-67	apoptosis antagonizing transcription factor	Homo sapiens	363-406
20062937-10	2010	High-dose ASA counterbalances the lack of COX 2 with an antithrombotic effect.	Aspirin	10-13	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	42-47
10624490-0	1999	Leukotriene C4 synthase: a candidate gene for the aspirin-intolerant asthmatic phenotype.	Aspirin	50-57	leukotriene C4 synthase	Homo sapiens	0-23
10624490-5	1999	More specifically, profound overexpression of LTC4S in aspirin-induced asthma seems to be a principal determinant of the respiratory reactions to aspirin, and a single-nucleotide polymorphism in the 5" regulatory region associates significantly with the aspirin-intolerant phenotype in Polish patients.	Aspirin	55-62	leukotriene C4 synthase	Homo sapiens	46-51
20062937-12	2010	COX 2 inhibition produced by residual ASA is the probable cause of ischaemic accidents and drug-eluting stents thrombosis a few days after ASA withdrawal.	Aspirin	38-41	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-5
10624490-5	1999	More specifically, profound overexpression of LTC4S in aspirin-induced asthma seems to be a principal determinant of the respiratory reactions to aspirin, and a single-nucleotide polymorphism in the 5" regulatory region associates significantly with the aspirin-intolerant phenotype in Polish patients.	Aspirin	146-153	leukotriene C4 synthase	Homo sapiens	46-51
10624490-5	1999	More specifically, profound overexpression of LTC4S in aspirin-induced asthma seems to be a principal determinant of the respiratory reactions to aspirin, and a single-nucleotide polymorphism in the 5" regulatory region associates significantly with the aspirin-intolerant phenotype in Polish patients.	Aspirin	146-153	leukotriene C4 synthase	Homo sapiens	46-51
34979192-12	2022	These findings reveal a critical role of BDNF IV methylation in the neurotoxicity of B(a)P, and demonstrate a promising prevention of aspirin against B(a)P-induced cognitive impairment via inhibiting BDNF IV hypermethylation.	Aspirin	134-141	brain derived neurotrophic factor	Mus musculus	41-45
10624490-6	1999	This data strongly support LTC4S as a candidate gene in this phenotype of asthma, and further characterization of LTC4S in terms of enzymatic function and gene regulation will likely contribute to the understanding of the gene as one potentially responsible for the allergic inflammation underlying aspirin-intolerance.	Aspirin	299-306	leukotriene C4 synthase	Homo sapiens	27-32
34935423-9	2021	Computer-assisted analyses of molecules with potential to bind bradykinin receptor B2 (BKRB2), suggested a potential role for aspirin as a BK antagonist.	Aspirin	126-133	bradykinin receptor B2	Homo sapiens	63-85
20062937-12	2010	COX 2 inhibition produced by residual ASA is the probable cause of ischaemic accidents and drug-eluting stents thrombosis a few days after ASA withdrawal.	Aspirin	139-142	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-5
10624490-6	1999	This data strongly support LTC4S as a candidate gene in this phenotype of asthma, and further characterization of LTC4S in terms of enzymatic function and gene regulation will likely contribute to the understanding of the gene as one potentially responsible for the allergic inflammation underlying aspirin-intolerance.	Aspirin	299-306	leukotriene C4 synthase	Homo sapiens	114-119
34868050-9	2021	At the genital tract, ASA use correlated with a decreased of activated CD4+T cells (CD4+CCR5+CD161+ (p=0.02) and CD4+CCR5+CD95+ (p=0.001)).	Aspirin	22-25	Fas cell surface death receptor	Homo sapiens	122-126
19542225-4	2009	These effects were further characterized as being mediated through transcriptional regulation: NO-aspirin 2 inhibited binding of ligand (TCDD)-activated aryl hydrocarbon receptor to the CYP1A1 enhancer sequence; additionally, NO-aspirin 2 suppressed carcinogen-induced expression of CYP1A heterogeneous nuclear RNA.	Aspirin	98-105	aryl hydrocarbon receptor	Homo sapiens	153-178
10480951-4	1999	Recently, we demonstrated that both aspirin and sodium salicylate, but not indomethacin, inhibited the activity of an IkappaB kinase beta (IKKbeta) that is required to activate the nuclear factor-kappaB (NF-kappaB) pathway.	Aspirin	36-43	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	118-137
10480951-4	1999	Recently, we demonstrated that both aspirin and sodium salicylate, but not indomethacin, inhibited the activity of an IkappaB kinase beta (IKKbeta) that is required to activate the nuclear factor-kappaB (NF-kappaB) pathway.	Aspirin	36-43	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	139-146
10480951-6	1999	Similar to our previous results with aspirin, this inhibition is due to sulindac-mediated decreases in IKKbeta kinase activity.	Aspirin	37-44	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	103-110
19542225-4	2009	These effects were further characterized as being mediated through transcriptional regulation: NO-aspirin 2 inhibited binding of ligand (TCDD)-activated aryl hydrocarbon receptor to the CYP1A1 enhancer sequence; additionally, NO-aspirin 2 suppressed carcinogen-induced expression of CYP1A heterogeneous nuclear RNA.	Aspirin	229-236	aryl hydrocarbon receptor	Homo sapiens	153-178
34748282-4	2022	Given that we have identified several non-steroidal anti-inflammatory drugs (NSAIDs) including Aspirin potently induce the degradation of AXL, we questioned whether NSAIDs could counteract the AXL-mediated neoplastic phenotypes.	Aspirin	95-102	AXL receptor tyrosine kinase	Homo sapiens	138-141
19542225-6	2009	Both HepG2 and LS180 cells treated with NO-aspirin 2 showed an increase in glutathione S-transferase-P1 (GST-P1), glutamate-cysteine ligase (GCL), and NAD(P)H:quinone oxidoreductase-1 (NQO1) expression.	Aspirin	43-50	glutamate-cysteine ligase catalytic subunit	Homo sapiens	114-139
10479672-9	1999	Fluindione in combination with aspirin inhibited TF-induced thrombus formation in a comparable manner.	Aspirin	31-38	coagulation factor III, tissue factor	Homo sapiens	49-51
10479672-14	1999	Aspirin enhances the antithrombotic effectiveness of fluindione, because combined treatment interrupts both TF- and collagen-induced thrombus formation.	Aspirin	0-7	coagulation factor III, tissue factor	Homo sapiens	108-110
34748282-7	2022	Our findings suggest that the combination of inhibitors and NSAIDs, especially Aspirin, could be a simple but efficient modality to treat melanoma in which AXL is a key factor for drug-resistance, metastasis, and relapse.	Aspirin	79-86	AXL receptor tyrosine kinase	Homo sapiens	156-159
19542225-6	2009	Both HepG2 and LS180 cells treated with NO-aspirin 2 showed an increase in glutathione S-transferase-P1 (GST-P1), glutamate-cysteine ligase (GCL), and NAD(P)H:quinone oxidoreductase-1 (NQO1) expression.	Aspirin	43-50	glutamate-cysteine ligase catalytic subunit	Homo sapiens	141-144
10496355-4	1999	The effect of aspirin on Annexin V binding was inhibited by the caspase inhibitor Z-VAD.fmk, indicating the involvement of caspases in the apoptotic action of aspirin.	Aspirin	14-21	annexin A5	Homo sapiens	25-34
19462226-0	2009	Aspirin inhibits MMP-2 and MMP-9 expression and activity through PPARalpha/gamma and TIMP-1-mediated mechanisms in cultured mouse celiac macrophages.	Aspirin	0-7	matrix metallopeptidase 9	Mus musculus	27-32
10496355-4	1999	The effect of aspirin on Annexin V binding was inhibited by the caspase inhibitor Z-VAD.fmk, indicating the involvement of caspases in the apoptotic action of aspirin.	Aspirin	159-166	annexin A5	Homo sapiens	25-34
19462226-3	2009	The purpose of present study was to investigate the inhibitory effects of aspirin on MMP-2 and MMP-9 expression and activity in cultured mouse celiac macrophages, and to determine the possible mechanisms.	Aspirin	74-81	matrix metallopeptidase 9	Mus musculus	95-100
12567448-2	1999	METHODS: Using rosette forming assay to observe the effect of ASA on the binding of platelets to neutrophil and radioimmunoassay to observe the effect of ASA on the thrombin-induced expression of GMP-140 on the surface of human platelets.	Aspirin	154-157	selectin P	Homo sapiens	196-203
12567448-6	1999	At high concentration, ASA significantly inhibited thrombin (0.5 U/ml) stimulated platelets binding to neutrophils and expressing GMP-140 on their surface.	Aspirin	23-26	selectin P	Homo sapiens	130-137
19462226-5	2009	Moreover the aspirin-induced down-regulation of MMP-2/9 mRNA expression and reduction of MMP-9 release were notably alleviated after pretreatment with specific inhibitors of PPARalpha/gamma.	Aspirin	13-20	matrix metallopeptidase 9	Mus musculus	89-94
12567448-7	1999	When the final concentration of ASA was 500,5000 micrograms/ml, the ratio of thrombin-stimulated platelets binding neutrophils was (34.7 +/- 3.8)%, (21.2 +/- 3.6)% respectively (n = 20, P &lt; 0.01); the number of molecular of GMP-140 expressing on the surface of platelet was (1.02 +/- 0.24) x 10(3), (0.68 +/- 0.18) x 10(3) per platelet respectively (n = 9, P &lt; 0.001).	Aspirin	32-35	selectin P	Homo sapiens	227-234
12567448-8	1999	CONCLUSIONS: It contributes to the antithrombosis of ASA that inhibiting platelet-neutrophil adhesion by down expression of GMP-140 on the surface of human platelets.	Aspirin	53-56	selectin P	Homo sapiens	124-131
19597002-7	2009	However, aspirin(low) triggered 15-epi-lipoxin A(4) synthesis and up-regulated its receptor (FPRL1, ALX).	Aspirin	9-16	hematopoietic SH2 domain containing	Homo sapiens	100-103
10418796-8	1999	Patients with acute coronary syndromes (on aspirin) had significantly increased P-selectin expression in response to ADP compared with healthy subjects (on aspirin), but no difference in ADP-induced fibrinogen binding was observed.	Aspirin	43-50	selectin P	Homo sapiens	80-90
10418796-8	1999	Patients with acute coronary syndromes (on aspirin) had significantly increased P-selectin expression in response to ADP compared with healthy subjects (on aspirin), but no difference in ADP-induced fibrinogen binding was observed.	Aspirin	156-163	selectin P	Homo sapiens	80-90
10419767-1	1999	The antiinflammatory action of aspirin is generally attributed to inhibition of cyclooxygenases 1 and 2, but additional mechanisms are at work.	Aspirin	31-38	prostaglandin-endoperoxide synthase 1	Mus musculus	80-103
34294337-2	2021	In this system, methotrexate (MTX) loaded CaCO3 (CaCO3/MTX) and aspirin (Asp) are co-entrapped in the hydrogels of alginate (Alg) and sodium carboxymethyl cellulose (CMC) crosslinked with Ca2+.	Aspirin	64-71	metaxin 1	Homo sapiens	30-33
34638901-6	2021	A non-cytotoxic acetylsalicylic acid treatment decreased HFF-induced ALDH1bright C91/PL cells, downregulated mesenchymal and stemness genes in cocultured cells, and delayed lymphoma growth in immunosuppressed mice, thus hindering the supportive activity of HFF on CSCs.	Aspirin	16-36	aldehyde dehydrogenase 1 family member A1	Homo sapiens	69-74
19652892-7	2009	For comparison, aspirin and clopidogrel induced only 2.0- to 2.6 -fold changes in other tests (VASP assay, Cone and Platelet Analyzer and PFA-100).	Aspirin	16-23	vasodilator stimulated phosphoprotein	Homo sapiens	95-99
34471538-8	2021	We genotyped aspirin-treated patients with T-ARMS-PCR for missense rs5918 (PlA1/A1) polymorphism of the ITGB3 gene.	Aspirin	13-20	POU class 2 homeobox 3	Homo sapiens	75-82
34414020-8	2021	The expression and acetylation levels of p53 in EOC cells treated with aspirin were determined using western blotting, and p53 acetylation levels were examined in tumors harvested from the transplanted mice.	Aspirin	71-78	transformation related protein 53, pseudogene	Mus musculus	41-44
10380911-0	1999	Aspirin-induced increases in soluble IL-1 receptor type II concentrations in vitro and in vivo.	Aspirin	0-7	interleukin 1 alpha	Homo sapiens	37-41
19433014-7	2009	In perhaps the most significant pharmacogenomic study with aspirin to date, a large primary prevention trial showed that the apolipoprotein A genotype was associated with risk of stroke and other cardiovascular events in women and that aspirin eliminated this risk.	Aspirin	59-66	lipoprotein(a)	Homo sapiens	125-141
10380911-8	1999	Thus, low-dose aspirin therapy may prevent inflammation by increasing soluble receptor secretion, thereby preventing IL-1 from binding target cells.	Aspirin	15-22	interleukin 1 alpha	Homo sapiens	117-121
10334197-7	1999	However, there was a significant aspirin x RS interaction, which suggests that aspirin could prevent the small intestine tumour-enhancing effects of RS in this Apc-driven tumorigenesis model.	Aspirin	79-86	APC, WNT signaling pathway regulator	Mus musculus	160-163
34414020-13	2021	Aspirin did not affect p53 protein expression but increased the p53 acetylation level in a concentration-dependent manner.	Aspirin	0-7	transformation related protein 53, pseudogene	Mus musculus	64-67
34414020-16	2021	These antitumor effects of aspirin might be mediated by p53 acetylation and subsequent activation of p53 target genes.	Aspirin	27-34	transformation related protein 53, pseudogene	Mus musculus	56-59
34414020-16	2021	These antitumor effects of aspirin might be mediated by p53 acetylation and subsequent activation of p53 target genes.	Aspirin	27-34	transformation related protein 53, pseudogene	Mus musculus	101-104
34307673-0	2021	Effects of Aspirin on Myocardial Ischemia-Reperfusion Injury in Rats through STAT3 Signaling Pathway.	Aspirin	11-18	signal transducer and activator of transcription 3	Rattus norvegicus	77-82
34307673-1	2021	Objective: To investigate the role and mechanism of aspirin in myocardial injury induced by myocardial ischemia-reperfusion in rats through STAT3 signaling pathway.	Aspirin	52-59	signal transducer and activator of transcription 3	Rattus norvegicus	140-145
19298588-0	2009	Soluble CD40 ligand and endothelial dysfunction in aspirin-treated polycythaemia vera patients.	Aspirin	51-58	CD40 molecule	Homo sapiens	8-12
34307673-10	2021	The results of PCR showed that compared with the MI/R group, the mRNA expression of Bax in the aspirin group was significantly decreased, while that of Bcl-2 was significantly increased (p < 0.05).	Aspirin	95-102	BCL2 associated X, apoptosis regulator	Rattus norvegicus	84-87
34307673-11	2021	Western blot analysis showed that compared with the MI/R group, aspirin pretreatment significantly increased the expression levels of p-STAT3 and p-JAK2 (p < 0.05).	Aspirin	64-71	signal transducer and activator of transcription 3	Rattus norvegicus	136-141
34307673-12	2021	Conclusion: The mechanism of aspirin preconditioning to protect the heart from MI/R injury appears to be related to JAK2/STAT3 and related to the activation of the signaling pathway.	Aspirin	29-36	signal transducer and activator of transcription 3	Rattus norvegicus	121-126
35600474-5	2022	ASA plus rivaroxaban treatment resulted in a significantly decreased thrombin peak in PRP for two triggers, namely, low concentration of tissue factor (TF) and thrombin, compared to ASA monotherapy.	Aspirin	0-3	coagulation factor III, tissue factor	Homo sapiens	137-150
35600474-5	2022	ASA plus rivaroxaban treatment resulted in a significantly decreased thrombin peak in PRP for two triggers, namely, low concentration of tissue factor (TF) and thrombin, compared to ASA monotherapy.	Aspirin	182-185	coagulation factor III, tissue factor	Homo sapiens	137-150
35629166-8	2022	Our research showed that patients can receive treatment with warfarin and aspirin with a personalized dosage and LVAD complications can be predicted by reference to their genotype polymorphisms in VKORC1, ITGB3 and UGT1A6 genes.	Aspirin	74-81	vitamin K epoxide reductase complex subunit 1	Homo sapiens	197-203
35434898-8	2022	RESULTS: Aspirin delayed time to metastasis in MDA-MB-231/LN/2-4/H2N xenografts and decreased growth of HER2+ /TNBC primary tumours.	Aspirin	9-16	erb-b2 receptor tyrosine kinase 2	Mus musculus	104-108
35498027-7	2022	Results: Tanshinone IIA reduced the serum levels of C-reactive protein (CRP), interleukin (IL)-1beta, IL-6, and P-selectin in KD patients; such inhibitory effect was more significant compared to aspirin and IVIG.	Aspirin	195-202	selectin P	Homo sapiens	112-122
35000048-0	2022	COX-1, COX-2 and CYP2C19 variations may be related to cardiovascular events due to acetylsalicylic acid resistance.	Aspirin	83-103	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	0-5
35371873-4	2022	This appears to be strongest in cancers that express PI3 kinase (PI3K) signaling activity, which aspirin downregulates.	Aspirin	97-104	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	53-63
35022893-7	2022	Effect modification by BMI and parity showed current aspirin use to only be associated with larger non-dense area among women with a BMI >= 30 (beta = 28.2, 95% CI: 10.8, 45.7), and with lower percent density among parous women (beta = -3.3, 95% CI: -6.4, -0.3).	Aspirin	53-60	glycoprotein A33	Homo sapiens	229-240
2620689-9	1989	These relaxations were mainly mediated by EDRF, because inhibition of vascular prostacyclin synthesis with aspirin did not inhibit the relaxations significantly, but the relaxations were abolished by the aforementioned EDRF inhibitors.	Aspirin	107-114	alpha hemoglobin stabilizing protein	Homo sapiens	42-46
2808538-3	1989	When indomethacin or acetylsalicylic acid, an inhibitor of prostaglandin production, was added to FS-4 cells, cell growth stimulated by EGF or TNF was increased, suggesting that prostaglandins induced by these mitogens antagonize their growth stimulatory actions.	Aspirin	21-41	epidermal growth factor	Homo sapiens	136-139
2491756-0	1989	Blood-brain barrier breakdown in cold-injured brain is linked to a biphasic stimulation of ornithine decarboxylase activity and polyamine synthesis: both are coordinately inhibited by verapamil, dexamethasone, and aspirin.	Aspirin	214-221	ornithine decarboxylase 1	Rattus norvegicus	91-114
2855314-4	1988	The contraction phase was inhibited in a concentration-dependent manner by indomethacin and acetylsalicylate, demonstrating that this activity of neurotensin was dependent on prostaglandin synthesis.	Aspirin	92-108	neurotensin/neuromedin N	Cavia porcellus	146-157
10436863-16	1999	LTC4S is profoundly overexpressed in the aspirin-induced asthmatic phenotype and correlates with overproduction of cysteinyl LTs and bronchial hyperreactivity to lysine aspirin.	Aspirin	41-48	leukotriene C4 synthase	Homo sapiens	0-5
18989778-3	2009	Simultaneous exposure to ASA and EtOH increased EtOH-induced caspase-3 activity and decreased cell viability, indicating synergetic damaging action.	Aspirin	25-28	caspase 3	Rattus norvegicus	61-70
19144570-5	2009	Aspirin-induced stimulation was accompanied by increased Ser-505 phosphorylation of cytosolic phospholipase A(2), which occurred independently of extracellular signal-regulated protein kinase-1/2 and p38 mitogen-activated protein kinase pathways.	Aspirin	0-7	mitogen activated protein kinase 14	Rattus norvegicus	200-203
19132198-2	2009	We correlated ASA responsiveness with haplotypes of seven candidate genes, selected for their documented role in platelet function, namely, the genes for integrins alpha2beta1and alphaIIbbeta3 (ITGA2, ITGA2B, and ITGB3), platelet glycoproteins Ibalpha and VI (GPIBA and GP6), the purinergic receptor P2Y1 (P2RY1), and prostaglandin H synthase 1 (PTGS1 = COX1).	Aspirin	14-17	integrin subunit alpha 2	Homo sapiens	194-199
19513289-2	2008	This study investigated the effects of combining cilostazol with aspirin on the expressions of P-selectin and PAC-1 on activated platelets in acute ischemic stroke.	Aspirin	65-72	dual specificity phosphatase 2	Homo sapiens	110-115
19513289-7	2008	RESULTS: After 5 days the extent of PAC-1 expression on activated platelets was significantly lower for combined aspirin and cilostazol treatment (61.0+/-19.3%, p=0.008; mean+/-standard deviation) than the baseline level (70.9+/-12.9%), but did not differ between aspirin alone (66.0 +/-19.0%) and baseline (70.1+/-15.7%).	Aspirin	113-120	dual specificity phosphatase 2	Homo sapiens	36-41
19513289-10	2008	CONCLUSIONS: This study found that the combined regimen of aspirin and cilostazol exerts the beneficial effect of reducing PAC-1 activity on activated platelets in acute ischemic stroke.	Aspirin	59-66	dual specificity phosphatase 2	Homo sapiens	123-128
19038077-45	2008	Limited information suggests that, in women with elevated hCG in the second trimester and/or abnormal uterine artery Doppler (at 22-24 weeks), low-dose aspirin (60-81 mg daily) is associated with higher birthweight and lower incidence of gestational hypertension with proteinuria.	Aspirin	152-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
18534315-3	2008	His postoperative management included the examination of his peripheral blood as well as bone marrow, which confirmed that the cause of his elevated platelet count was due to JAK2 V617F mutation that is treated by hydroxyurea and aspirin after being discharged from the hospital.	Aspirin	230-237	Janus kinase 2	Homo sapiens	175-179
18566520-4	2008	In addition, basic fibroblast growth factor-stimulated vasculogenesis (140% of vessels as compared to control) was partially reversed by t-resveratrol (35% of inhibition) and treatments with cyclooxygenase inhibitors (acetylsalicylic acid and indomethacin) as well a protein-kinase C (PKC) activator (phorbol-12,13-dibutyrate) decreased the vessel number to 60%, 50%, and 44%, respectively.	Aspirin	218-238	fibroblast growth factor 2	Gallus gallus	13-43
10097187-5	1999	The best-characterized of these mutants (vtc1) contains approximately 25% of wild-type AsA and is defective in AsA biosynthesis.	Aspirin	87-90	Glucose-1-phosphate adenylyltransferase family protein	Arabidopsis thaliana	41-45
10097187-5	1999	The best-characterized of these mutants (vtc1) contains approximately 25% of wild-type AsA and is defective in AsA biosynthesis.	Aspirin	111-114	Glucose-1-phosphate adenylyltransferase family protein	Arabidopsis thaliana	41-45
18380576-9	2008	Cyclooxygenase-2 expression remained unchanged in pyloric mucosa; in duodenal mucosa, aspirin significantly increased COX-2 expression, compared with effects of deracoxib and carprofen.	Aspirin	86-93	cytochrome c oxidase subunit II	Canis lupus familiaris	118-123
9949237-2	1999	METHODS: CYP1A1 rare genotypes MspI C and VV were detected with the methods of PCR-RFLP and ASA in a case-control study including 59 cases of lung cancer, 59 hospital controls and 73 healthy controls.	Aspirin	92-95	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	9-15
17554594-10	2008	Furthermore, expression of PAC-1 was significantly increased in patients with aspirin nonresponse as compared to aspirin responders (P = 0.003 and P = 0.0006 respectively).	Aspirin	78-85	dual specificity phosphatase 2	Homo sapiens	27-32
10028935-13	1999	In contrast, short-term administration of a high antiinflammatory dose of aspirin severely blunts myocardial reactive hyperemia through a mechanism that is independent of both cyclooxygenase and nitric oxide metabolic pathways.	Aspirin	74-81	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	176-190
17554594-10	2008	Furthermore, expression of PAC-1 was significantly increased in patients with aspirin nonresponse as compared to aspirin responders (P = 0.003 and P = 0.0006 respectively).	Aspirin	113-120	dual specificity phosphatase 2	Homo sapiens	27-32
18175938-6	2008	ASA (2 mM) inhibited alpha-MSH-enhanced melanin synthesis in melanoma more strongly than other well-known anti-melanogenic agents such as arbutin (2 mM) and kojic acid (200 microM).	Aspirin	0-3	pro-opiomelanocortin-alpha	Mus musculus	21-30
10709674-3	1999	As discussed above, all six potential chemopreventive agents, aspirin, 2-CPR, DFMO, 4-HPR, piroxicam, and 9-cis-retinoic acid, decreased the level of AOM-induced ACF.	Aspirin	62-69	ACF	Homo sapiens	162-165
10709674-5	1999	Hence, aspirin and 2-CPR would appear to be false positive in the ACF assay.	Aspirin	7-14	ACF	Homo sapiens	66-69
10709674-7	1999	The false positive result for aspirin could be due to the lower sensitivity of the AOM-induced colon cancer assay compared to the ACF assay.	Aspirin	30-37	ACF	Homo sapiens	130-133
10709674-8	1999	However, aspirin [table: see text] significantly reduced the yield of ACF at a dose (600 mg/kg diet) one-third the dose (1800 mg/kg diet) that did not reproducibly reduce the yield of colon tumors.	Aspirin	9-16	ACF	Homo sapiens	70-73
18180620-0	2008	Effects of aspirin and propranolol on the acute psychological stress response in factor VIII coagulant activity: a randomized, double-blind, placebo-controlled experimental study.	Aspirin	11-18	cytochrome c oxidase subunit 8A	Homo sapiens	88-92
9824663-9	1998	The increase in PAI-1 release by this mechanism was suppressed by a cyclooxygenase inhibitor, aspirin, whereas the inhibitor did not affect TNF-alpha-induced increase in PAI-1 release.	Aspirin	94-101	serpin family E member 1	Homo sapiens	16-21
18180620-2	2008	We investigated whether aspirin and propranolol affect the responsiveness of plasma clotting factor VIII activity levels to acute psychosocial stress.	Aspirin	24-31	cytochrome c oxidase subunit 8A	Homo sapiens	100-104
18180620-7	2008	The clotting factor VIII activity level decreased from prestress to immediately poststress in the aspirin/propranolol group relative to the placebo group (P = 0.048) and the aspirin group (P &lt; 0.06).	Aspirin	98-105	cytochrome c oxidase subunit 8A	Homo sapiens	20-24
9779851-1	1998	OBJECTIVE: To determine if acetylsalicylic acid (ASA) suppresses the stimulatory effects of transforming growth factor-beta (TGF-beta) and insulin-like growth factor-1 (IGF-1) on glycosaminoglycan (GAG) synthesis by cultured bovine articular chondrocytes (BAC), and whether such a suppression can be counteracted by the addition of misoprostol, a prostaglandin (PG) E1 analog.	Aspirin	27-47	insulin like growth factor 1	Bos taurus	139-167
18180620-7	2008	The clotting factor VIII activity level decreased from prestress to immediately poststress in the aspirin/propranolol group relative to the placebo group (P = 0.048) and the aspirin group (P &lt; 0.06).	Aspirin	174-181	cytochrome c oxidase subunit 8A	Homo sapiens	20-24
9779851-1	1998	OBJECTIVE: To determine if acetylsalicylic acid (ASA) suppresses the stimulatory effects of transforming growth factor-beta (TGF-beta) and insulin-like growth factor-1 (IGF-1) on glycosaminoglycan (GAG) synthesis by cultured bovine articular chondrocytes (BAC), and whether such a suppression can be counteracted by the addition of misoprostol, a prostaglandin (PG) E1 analog.	Aspirin	27-47	insulin like growth factor 1	Bos taurus	169-174
9779851-1	1998	OBJECTIVE: To determine if acetylsalicylic acid (ASA) suppresses the stimulatory effects of transforming growth factor-beta (TGF-beta) and insulin-like growth factor-1 (IGF-1) on glycosaminoglycan (GAG) synthesis by cultured bovine articular chondrocytes (BAC), and whether such a suppression can be counteracted by the addition of misoprostol, a prostaglandin (PG) E1 analog.	Aspirin	49-52	insulin like growth factor 1	Bos taurus	139-167
18180620-8	2008	Between 45 min and 105 min poststress, clotting factor VIII levels increased in the aspirin/propranolol group relative to the placebo group (P = 0.007) and the aspirin group (P = 0.039).	Aspirin	84-91	cytochrome c oxidase subunit 8A	Homo sapiens	55-59
9779851-1	1998	OBJECTIVE: To determine if acetylsalicylic acid (ASA) suppresses the stimulatory effects of transforming growth factor-beta (TGF-beta) and insulin-like growth factor-1 (IGF-1) on glycosaminoglycan (GAG) synthesis by cultured bovine articular chondrocytes (BAC), and whether such a suppression can be counteracted by the addition of misoprostol, a prostaglandin (PG) E1 analog.	Aspirin	49-52	insulin like growth factor 1	Bos taurus	169-174
18180620-8	2008	Between 45 min and 105 min poststress, clotting factor VIII levels increased in the aspirin/propranolol group relative to the placebo group (P = 0.007) and the aspirin group (P = 0.039).	Aspirin	160-167	cytochrome c oxidase subunit 8A	Homo sapiens	55-59
18180620-10	2008	Propranolol in combination with aspirin diminished the acute response in clotting factor VIII activity to psychosocial stress compared with placebo medication and aspirin alone.	Aspirin	32-39	cytochrome c oxidase subunit 8A	Homo sapiens	89-93
18180620-10	2008	Propranolol in combination with aspirin diminished the acute response in clotting factor VIII activity to psychosocial stress compared with placebo medication and aspirin alone.	Aspirin	163-170	cytochrome c oxidase subunit 8A	Homo sapiens	89-93
18180620-11	2008	The effect of single aspirin on the acute clotting factor VIII stress response was indistinguishable from a placebo effect.	Aspirin	21-28	cytochrome c oxidase subunit 8A	Homo sapiens	58-62
18231737-6	2007	Platelet GP I a T allele was significantly associated with aspirin resistance as revealed by multiple logistic regression (OR=3.76, 95% CI: 2.87-9.58).	Aspirin	59-66	glucose-6-phosphate isomerase	Homo sapiens	9-13
18231737-7	2007	The results suggest that inherited platelet GP I a variations may have an important impact on aspirin resistance and the presence of GP I a T allele may be a marker of genetic susceptibility to aspirin resistance.	Aspirin	94-101	glucose-6-phosphate isomerase	Homo sapiens	44-48
18231737-7	2007	The results suggest that inherited platelet GP I a variations may have an important impact on aspirin resistance and the presence of GP I a T allele may be a marker of genetic susceptibility to aspirin resistance.	Aspirin	194-201	glucose-6-phosphate isomerase	Homo sapiens	133-137
17510082-8	2007	Aspirin induced the phosphorylation of p53 at residue Ser15 within 8 h in a caffeine-dependent manner, and also caused the activation of checkpoint kinase 2 and the cleavage of caspase 7.	Aspirin	0-7	checkpoint kinase 2	Homo sapiens	137-156
17531573-3	2007	This study examined the correlation between measurements of aspirin resistance and the level of inhibition of the thienopyridine-specific P2Y12 platelet receptor and CK-MB release after PCI.	Aspirin	60-67	purinergic receptor P2Y12	Homo sapiens	138-143
17615799-4	2007	Acetylsalicylic acid (ASA) has been attributed with reducing levels of the transcription factor nuclear factor kappaB (NF-kappaB), C-reactive protein, and soluble CD40 ligand, although the evidence relating to the latter two markers is conflicting.	Aspirin	0-20	CD40 molecule	Homo sapiens	163-167
17615799-4	2007	Acetylsalicylic acid (ASA) has been attributed with reducing levels of the transcription factor nuclear factor kappaB (NF-kappaB), C-reactive protein, and soluble CD40 ligand, although the evidence relating to the latter two markers is conflicting.	Aspirin	22-25	CD40 molecule	Homo sapiens	163-167
17346695-12	2007	Whereas, TRPV1 agonists, capsaicin and piperine, inhibited gastric lesions induced by ethanol, 1% ammonia, and aspirin, but had less of an effect on 0.6 M HCl-induced gastric lesions.	Aspirin	111-118	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	9-14
16473396-4	2007	When acting alone, both C-reactive protein and ASA inhibited collagen-dependent platelet aggregation and reduced the expressions of two platelet surface membrane activation markers: P-selectin and activated GPIIbIIIa complex.	Aspirin	47-50	selectin P	Homo sapiens	182-192
9922982-0	1998	Effect of roxatidine bismuth citrate (MX1) against acetylsalicylic acid- and indomethacin-induced gastric mucosal damage in rats.	Aspirin	51-71	MX dynamin like GTPase 1	Rattus norvegicus	38-41
9922982-7	1998	The results of the present study suggest that MX1 has a gastroprotective effect against ASA- and indomethacin-induced ulcers which might be due both to its H2-blocking and mucus-stimulating activity.	Aspirin	88-91	MX dynamin like GTPase 1	Rattus norvegicus	46-49
9736731-2	1998	In this study, we show that microsatellite instability (MSI) in colorectal cancer cells deficient for a subset of the human mismatch repair (MMR) genes (hMLH1, hMSH2, and hMSH6), is markedly reduced during exposure to aspirin or sulindac [or Clinoril, which is chemically related to indomethacin (Indocin)].	Aspirin	218-225	mutL homolog 1	Homo sapiens	153-158
9736731-2	1998	In this study, we show that microsatellite instability (MSI) in colorectal cancer cells deficient for a subset of the human mismatch repair (MMR) genes (hMLH1, hMSH2, and hMSH6), is markedly reduced during exposure to aspirin or sulindac [or Clinoril, which is chemically related to indomethacin (Indocin)].	Aspirin	218-225	mutS homolog 6	Homo sapiens	171-176
9736731-6	1998	These results suggest that aspirin/sulindac induces a genetic selection for microsatellite stability in a subset of MMR-deficient cells and may provide an effective prophylactic therapy for hereditary nonpolyposis colorectal cancer kindreds where alteration of the hMSH2 and hMLH1 genes are associated with the majority of cancer susceptibility cases.	Aspirin	27-34	mutL homolog 1	Homo sapiens	275-280
9781832-13	1998	Similar results were seen in CAST, a double-blind trial of aspirin vs. placebo in patients with suspected ischaemic stroke treated within 48 hours.	Aspirin	59-66	calpastatin	Homo sapiens	29-33
9781832-14	1998	A meta-analysis of the results of IST, CAST and MAST-I showed a statistically significant effect of early aspirin treatment.	Aspirin	106-113	calpastatin	Homo sapiens	39-43
9706142-3	1998	METHODS: We administered aspirin to the Min/+ mouse, an animal with a germline mutation in Apc, a gene that is essential for normal epithelial cell growth and differentiation.	Aspirin	25-32	APC, WNT signaling pathway regulator	Mus musculus	91-94
9706142-9	1998	CONCLUSIONS: These data confirm a role for aspirin in suppression of Apc-associated intestinal carcinogenesis.	Aspirin	43-50	APC, WNT signaling pathway regulator	Mus musculus	69-72
9661890-8	1998	Confirmation that cells were undergoing necrosis in response to aspirin was evident from the presence of cells that bound annexin V and accumulated propidium iodide in the absence of a population that bound annexin alone.	Aspirin	64-71	annexin A5	Homo sapiens	122-131
9630216-5	1998	Treatment of endothelial cells with aspirin or a COX-1 antisense oligonucleotide inhibits COX-1 activity/expression and suppresses tube formation.	Aspirin	36-43	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	90-95
9608925-7	1998	Aspirin may interfere with free radicals and inhibit TF formation.	Aspirin	0-7	coagulation factor III, tissue factor	Homo sapiens	53-55
9440807-9	1998	Second, the effect of iodide on class I RNA levels and on enhancer A complex formation with Mod-1 and the p50/p65 heterodimer is inhibited by agents that block the inositol phosphate, Ca++, phospholipase A2, arachidonate signal transduction pathway: acetylsalicylate, indomethacin, and 5,8,11,14-eicosatetraynoic acid.	Aspirin	250-266	phospholipase A2 group IB	Rattus norvegicus	190-206
9640079-2	1997	Aspirin therapy will reduce platelet activation both by its negative effect on platelet aggregation (SPA) and by inhibition of granule release which liberates such mediators as platelet factor 4 (PF4) and plasminogen activator inhibitor 1 (PAI-1).	Aspirin	0-7	serpin family E member 1	Homo sapiens	205-238
9640079-2	1997	Aspirin therapy will reduce platelet activation both by its negative effect on platelet aggregation (SPA) and by inhibition of granule release which liberates such mediators as platelet factor 4 (PF4) and plasminogen activator inhibitor 1 (PAI-1).	Aspirin	0-7	serpin family E member 1	Homo sapiens	240-245
9640079-11	1997	Lower activities of PAI-1, in patients treated with aspirin, can be ascribed to its reduced release from platelets.	Aspirin	52-59	serpin family E member 1	Homo sapiens	20-25
9393345-0	1997	Leukotriene C4 synthase promoter polymorphism and risk of aspirin-induced asthma.	Aspirin	58-65	leukotriene C4 synthase	Homo sapiens	0-23
9067546-7	1997	GST pi levels were raised (1.9-3.6 x) in stomach by ibuprofen, ASA, and sulindac, and in small intestine by indomethacin, piroxicam, ASA, and sulindac.	Aspirin	63-66	glutathione S-transferase kappa 1	Homo sapiens	0-3
9067546-7	1997	GST pi levels were raised (1.9-3.6 x) in stomach by ibuprofen, ASA, and sulindac, and in small intestine by indomethacin, piroxicam, ASA, and sulindac.	Aspirin	133-136	glutathione S-transferase kappa 1	Homo sapiens	0-3
9048556-1	1997	Dihydrodipicolinate synthase (DHDPS) catalyzes the formation of dihydrodipicolinate from pyruvate and L-aspartate beta-semialdehyde (ASA).	Aspirin	133-136	dihydrodipicolinate synthase	Escherichia coli	0-28
9023270-4	1997	When exogenous AA was used, acetylsalicylic acid was a 5- to 10-fold more potent inhibitor of PGHS-1, whereas indomethacin was a 4- to 5-fold more potent inhibitor of PGHS-2.	Aspirin	28-48	prostaglandin-endoperoxide synthase 1	Mus musculus	94-100
9023270-6	1997	When calcium ionophore A23187 was used to mobilize endogenous AA, acetylsalicylic acid and indomethacin equipotently inhibited both PGHS-1 and PGHS-2 isozymes.	Aspirin	66-86	prostaglandin-endoperoxide synthase 1	Mus musculus	132-138
8662657-3	1996	HUVEC treated with aspirin lost their capacity to generate PGs but recovery occurred after 3- or 6-h induction of Cox-2 with phorbol ester or IL-1alpha.	Aspirin	19-26	interleukin 1 alpha	Homo sapiens	142-151
8662657-4	1996	Enzyme activity of the newly synthesized Cox-2 in aspirin-treated cells, evaluated after immunoprecipitation, was similar to untreated cells but after 18 h of cell stimulation only 50-60% recovery of Cox-1 was observed.	Aspirin	50-57	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	200-205
8662657-9	1996	However, in acetylsalicylic acid-treated cells, after 6-h stimulation with IL-1alpha, newly synthesized Cox-2 produced less TXB2 than 6-keto-PGF1alpha compared to untreated cells.	Aspirin	12-32	interleukin 1 alpha	Homo sapiens	75-84
8600164-6	1996	Inhibition of cyclooxygenase by acetylsalicylic acid augmented the growth response of fibroblasts to all: SP, FGF, and EGF.	Aspirin	32-52	epidermal growth factor	Homo sapiens	119-122
8839134-0	1996	Aspirin-interleukin-3 interrelationships in patients with anti-phospholipid syndrome.	Aspirin	0-7	interleukin 3	Homo sapiens	8-21
7587805-2	1995	Oral administration of acidified aspirin (200 mg/kg) resulted in linear hemorrhagic erosions and an increase in myeloperoxidase activity, an index of neutrophil infiltration, in the gastric mucosa.	Aspirin	33-40	myeloperoxidase	Rattus norvegicus	112-127
7587805-3	1995	Aspirin-induced gastric damage and the increase in myeloperoxidase activity were significantly inhibited by the injection of anti-CD11a, anti-CD11b, anti-intercellular adhesion molecule-1 monoclonal antibodies, and the combination of superoxide dismutase and catalase, which are scavengers of active oxygen species.	Aspirin	0-7	myeloperoxidase	Rattus norvegicus	51-66
7872783-1	1995	Aspirin causes a time-dependent inhibition of prostaglandin endoperoxide H synthases (PGHS)-1 and -2 by acetylating active site serines present in both isozymes.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Mus musculus	46-100
8774994-4	1995	Myeloperoxidase (MPO) activity in the gastric mucosa, an index of neutrophil infiltration, significantly increased 3 h after aspirin administration.	Aspirin	125-132	myeloperoxidase	Rattus norvegicus	0-15
8774994-4	1995	Myeloperoxidase (MPO) activity in the gastric mucosa, an index of neutrophil infiltration, significantly increased 3 h after aspirin administration.	Aspirin	125-132	myeloperoxidase	Rattus norvegicus	17-20
7896048-10	1994	A 2-fold reduction in the ED50 of A-1C occurred when it was coadministered with aspirin to mice; also, the toxicity reduced slightly, increasing the therapeutic index by a factor of 2.2.	Aspirin	80-87	B cell leukemia/lymphoma 2 related protein A1c	Mus musculus	34-38
8107285-5	1994	Even though addition of CV3988 (specific PAF inhibitor) with ASA and CP/CPK had no further effect on collagen-induced whole blood aggregation, collagen-induced whole blood aggregation was significantly reduced in whole blood pretreated with CV3988 or ASA alone; but not with CP/CPK alone.	Aspirin	61-64	PCNA clamp associated factor	Homo sapiens	41-44
8107285-9	1994	ASA pretreatment of leukocytes significantly reduced the collagen-induced PAF synthesis.	Aspirin	0-3	PCNA clamp associated factor	Homo sapiens	74-77
8107285-10	1994	Thus, PAF seemed to affect collagen-induced whole blood aggregation and ASA seemed to inhibit PAF synthesis.	Aspirin	72-75	PCNA clamp associated factor	Homo sapiens	94-97
8241105-7	1993	In the c7E3-Fab group, reperfusion was obtained within 25 +/- 8 minutes (P &lt; .01 versus aspirin group) and was associated with a delayed reocclusion of 63 +/- 63 minutes (P &lt; .05 versus aspirin group).	Aspirin	91-98	FA complementation group B	Homo sapiens	12-15
8241105-7	1993	In the c7E3-Fab group, reperfusion was obtained within 25 +/- 8 minutes (P &lt; .01 versus aspirin group) and was associated with a delayed reocclusion of 63 +/- 63 minutes (P &lt; .05 versus aspirin group).	Aspirin	192-199	FA complementation group B	Homo sapiens	12-15
8400294-10	1993	Aspirin and an adenosine diphosphate scavenger system had only a slight but not significant effect on changes in antibody binding induced by cathepsin G.	Aspirin	0-7	cathepsin G	Homo sapiens	141-152
8215400-15	1993	Mitogen-inducible activity in RS2 cells was inhibited by aspirin, indicating that PGHS-2, like PGHS-1, can be inactivated by this drug.	Aspirin	57-64	prostaglandin-endoperoxide synthase 1	Mus musculus	95-101
7688561-7	1993	Restimulation of the ASA+ activated T cells by triggering TCR-CD3 or CD2 induced proliferation and apoptosis in a fraction of the cells.	Aspirin	21-24	CD2 molecule	Homo sapiens	69-72
1643209-1	1992	To determine how aspirin intake might influence lipopolysaccharide (LPS)-induced tissue factor (TF) activity and tumour necrosis factor (TNF) in human blood monocytes, we collected blood before and at various times after intake of 300 mg aspirin in 25 healthy volunteers.	Aspirin	17-24	coagulation factor III, tissue factor	Homo sapiens	81-94
1643209-1	1992	To determine how aspirin intake might influence lipopolysaccharide (LPS)-induced tissue factor (TF) activity and tumour necrosis factor (TNF) in human blood monocytes, we collected blood before and at various times after intake of 300 mg aspirin in 25 healthy volunteers.	Aspirin	17-24	coagulation factor III, tissue factor	Homo sapiens	96-98
1643209-4	1992	The rise in TF activity was maximal within 1 h after aspirin intake and no further rise was observed 3, 4 or 24 h after aspirin intake.	Aspirin	53-60	coagulation factor III, tissue factor	Homo sapiens	12-14
1643209-5	1992	In contrast, TF activity induced by incubating whole blood in the absence of LPS fell rapidly after the intake of aspirin.	Aspirin	114-121	coagulation factor III, tissue factor	Homo sapiens	13-15
1318427-5	1992	However, the pretreatment of HUVEC with a combination of aspirin and L-NG-monomethyl arginine (LNMMA) as an inhibitor of EDRF completely abolished the HUVEC-mediated decrease in PRP aggregation, [TXA2] and [Ca++]i induced by ET, and also abolished the enhancement of [cGMP]i and [cAMP]i in platelets.	Aspirin	57-64	alpha hemoglobin stabilizing protein	Homo sapiens	121-125
21554579-7	1992	Indomethacin and aspirin also caused a 50% decrease in NAT activity.	Aspirin	17-24	aralkylamine N-acetyltransferase	Gallus gallus	55-58
1565180-5	1992	NSAIDs such as aspirin, indomethacin, meclofenamate and others may promote POD by blocking this prostaglandin pathway while promoting the cytochrome P450 monooxygenase pathway which may produce vasodilator, diuretic and natriuretic paracrine hormones.	Aspirin	15-22	cytochrome P450, family 2, subfamily j, polypeptide 3	Rattus norvegicus	138-167
1746447-7	1991	Although antiplatelet and antithrombin agents such as aspirin and heparin help to decrease rethrombosis, these agents are far from ideal.	Aspirin	54-61	serpin family C member 1	Homo sapiens	26-38
1820025-4	1991	We report the use of ASA to detect and characterize the mutation in the murine beta-globin gene, Hbb-b1d-m1, and find that the codon for beta 145 tyrosine (TAC) has been replaced by the codon for cysteine (TGC).	Aspirin	21-24	hemoglobin, beta adult major chain	Mus musculus	97-103
1804603-7	1991	The mechanism of aspirin may be the inhibition of TXA2 and Fn synthesis and decreased consumption of AT-III.	Aspirin	17-24	serpin family C member 1	Homo sapiens	101-107
1805857-3	1991	All 19 (100%) of the ASA-positive sera contained immunoglobulin (Ig)G ASA of the IgG1 and IgG3 subclasses.	Aspirin	21-24	immunoglobulin heavy constant gamma 3 (G3m marker)	Homo sapiens	90-94
1805857-4	1991	A 1:1 correlation was observed between the presence of IgG1 and IgG3 ASA.	Aspirin	69-72	immunoglobulin heavy constant gamma 3 (G3m marker)	Homo sapiens	64-68
1805857-6	1991	The ability of the IgG1 and IgG3 ASA-positive sera to deposit complement (C) on sperm was demonstrated by the concomitant binding to antibody-laden sperm of polyclonal antibodies to the membrane attack complex (C5b-9) of C. Both C-fixing and non-C-fixing ASA-positive sera were found to possess IgG1 and IgG3 antisperm antibodies.	Aspirin	33-36	immunoglobulin heavy constant gamma 3 (G3m marker)	Homo sapiens	28-32
1805857-6	1991	The ability of the IgG1 and IgG3 ASA-positive sera to deposit complement (C) on sperm was demonstrated by the concomitant binding to antibody-laden sperm of polyclonal antibodies to the membrane attack complex (C5b-9) of C. Both C-fixing and non-C-fixing ASA-positive sera were found to possess IgG1 and IgG3 antisperm antibodies.	Aspirin	33-36	immunoglobulin heavy constant gamma 3 (G3m marker)	Homo sapiens	304-308
1805857-6	1991	The ability of the IgG1 and IgG3 ASA-positive sera to deposit complement (C) on sperm was demonstrated by the concomitant binding to antibody-laden sperm of polyclonal antibodies to the membrane attack complex (C5b-9) of C. Both C-fixing and non-C-fixing ASA-positive sera were found to possess IgG1 and IgG3 antisperm antibodies.	Aspirin	255-258	immunoglobulin heavy constant gamma 3 (G3m marker)	Homo sapiens	28-32
1779407-3	1991	However, the number of EGF binding sites was increased 12 h after aspirin administration.	Aspirin	66-73	epidermal growth factor	Rattus norvegicus	23-26
1900943-0	1991	Aspirin inhibits interleukin 1-induced prostaglandin H synthase expression in cultured endothelial cells.	Aspirin	0-7	interleukin 1 alpha	Homo sapiens	17-30
1900943-3	1991	Pretreatment with aspirin at low concentrations (0.1-1 micrograms/ml) inhibited more than 60% of the enzyme mass and also the cyclooxygenase activity in IL-1-induced cells with only minimal effects on the basal level of the synthase enzyme in cells without IL-1.	Aspirin	18-25	interleukin 1 alpha	Homo sapiens	153-157
1900943-3	1991	Pretreatment with aspirin at low concentrations (0.1-1 micrograms/ml) inhibited more than 60% of the enzyme mass and also the cyclooxygenase activity in IL-1-induced cells with only minimal effects on the basal level of the synthase enzyme in cells without IL-1.	Aspirin	18-25	interleukin 1 alpha	Homo sapiens	257-261
1900943-5	1991	Similarly low levels of aspirin inhibited the increased L-[35S]methionine incorporation into PGH synthase that was induced by IL-1 and also suppressed expression of the 2.7-kilobase PGH synthase mRNA.	Aspirin	24-31	interleukin 1 alpha	Homo sapiens	126-130
1699986-0	1990	Basophil histamine release by platelet-activating factor in aspirin-sensitive subjects with asthma.	Aspirin	60-67	PCNA clamp associated factor	Homo sapiens	30-56
1699986-1	1990	Histamine release induced by platelet-activating factor (PAF) from leukocytes of aspirin-sensitive subjects with asthma was higher than that from normal control subjects, despite the similarity of anti-IgE-induced histamine release.	Aspirin	81-88	PCNA clamp associated factor	Homo sapiens	29-55
1699986-1	1990	Histamine release induced by platelet-activating factor (PAF) from leukocytes of aspirin-sensitive subjects with asthma was higher than that from normal control subjects, despite the similarity of anti-IgE-induced histamine release.	Aspirin	81-88	PCNA clamp associated factor	Homo sapiens	57-60
1699986-2	1990	Moreover, basophils of some aspirin-sensitive subjects with asthma released histamine by PAF stimulation in the absence of cytochalasin B that affects histamine release and is required in PAF-induced histamine release from leukocytes of atopic subjects with asthma and normal control subjects.	Aspirin	28-35	PCNA clamp associated factor	Homo sapiens	89-92
1699986-2	1990	Moreover, basophils of some aspirin-sensitive subjects with asthma released histamine by PAF stimulation in the absence of cytochalasin B that affects histamine release and is required in PAF-induced histamine release from leukocytes of atopic subjects with asthma and normal control subjects.	Aspirin	28-35	PCNA clamp associated factor	Homo sapiens	188-191
1699986-5	1990	The results in the present study indicate the pathophysiologic significance of PAF-induced histamine release and that activation of basophils by PAF may be relevant to the pathogenesis in some aspirin-sensitive subjects with asthma.	Aspirin	193-200	PCNA clamp associated factor	Homo sapiens	145-148
2105090-5	1990	The recovery of PGI2 synthesis after aspirin was faster in IL-1-treated EC than in control cells.	Aspirin	37-44	interleukin 1 alpha	Homo sapiens	59-63
2295516-1	1990	Recent reports indicate that cyclooxygenase inhibitors such as aspirin may facilitate the release of interleukin-2 from thymic T cells.	Aspirin	63-70	interleukin 2	Rattus norvegicus	101-114
2367981-2	1990	It was shown that platelets of asthmatics with the atopic and aspirin-sensitive disease forms are more sensitive to the stimulating action of platelet activating factor (PAF) in aggregation response and intracellular Ca2+ influx induction than platelets of patients suffering mostly from the recurrent bronchopulmonary infections with atopic component (so-called "mixed" asthma) and more activated than platelets of healthy donors.	Aspirin	62-69	PCNA clamp associated factor	Homo sapiens	142-168
2367981-2	1990	It was shown that platelets of asthmatics with the atopic and aspirin-sensitive disease forms are more sensitive to the stimulating action of platelet activating factor (PAF) in aggregation response and intracellular Ca2+ influx induction than platelets of patients suffering mostly from the recurrent bronchopulmonary infections with atopic component (so-called "mixed" asthma) and more activated than platelets of healthy donors.	Aspirin	62-69	PCNA clamp associated factor	Homo sapiens	170-173
2367981-7	1990	It may be concluded that platelets of atopic and aspirin asthmatics are more active, their "hyper-reaction" to PAF is expressed by higher aggregability and the lower PAF concentration threshold.	Aspirin	49-56	PCNA clamp associated factor	Homo sapiens	111-114
2367981-7	1990	It may be concluded that platelets of atopic and aspirin asthmatics are more active, their "hyper-reaction" to PAF is expressed by higher aggregability and the lower PAF concentration threshold.	Aspirin	49-56	PCNA clamp associated factor	Homo sapiens	166-169
3922403-0	1985	Glucose-6-phosphate dehydrogenase from Saccharomyces cerevisiae: characterization of a reactive lysine residue labeled with acetylsalicylic acid.	Aspirin	124-144	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	0-33
3922403-1	1985	Glucose-6-phosphate dehydrogenase from Saccharomyces cerevisiae (bakers" yeast) reacts with acetylsalicylic acid, and this is accompanied by inactivation and modification of essentially one lysine residue per subunit.	Aspirin	92-112	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	0-33
33764864-14	2021	ASA (OR 1.9), preinjury residence (OR 1.4) and age (OR 1.1) had statistical influence on survival, but not delay to surgery.	Aspirin	0-3	olfactory receptor family 10 subfamily R member 3 pseudogene	Homo sapiens	5-11
34699386-8	2021	The GPR32 agonist aspirin-triggered resolvin D1 (AT-RvD1) regulated leukocyte responses, including enhancing macrophage phagocytosis and intracellular signaling in hGPR32mycTgxFpr2-/-xApoe-/- transgenic mice but not in the Fpr2-/-xApoe-/- non-transgenic littermates.	Aspirin	18-25	G protein-coupled receptor 32	Homo sapiens	4-9
34699386-8	2021	The GPR32 agonist aspirin-triggered resolvin D1 (AT-RvD1) regulated leukocyte responses, including enhancing macrophage phagocytosis and intracellular signaling in hGPR32mycTgxFpr2-/-xApoe-/- transgenic mice but not in the Fpr2-/-xApoe-/- non-transgenic littermates.	Aspirin	18-25	G protein-coupled receptor 32	Homo sapiens	164-180
34904537-2	2021	Objectives were to (i) develop pregnancy-specific 95% reference intervals for a range of laboratory based platelet function tests (PFTs); (ii) select an optimal and acceptable PFT that reflected aspirin"s COX-1 inhibition in women with confirmed aspirin adherence in pregnancy; and (iii) identify genomic variants that may influence pregnant women"s platelet response to aspirin.The study included two independent cohorts of pregnant women.	Aspirin	195-202	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	205-210
17127481-3	2006	Inhibition of platelet cyclooxygenase (COX 1) by aspirin is followed by relief of microvascular disturbances, correction of shortened platelet survival, and return of plasma levels of beta-tg, PF4, TM levels and TxB2 excretion to normal.	Aspirin	49-56	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	39-44
34895290-4	2021	In this trial, we will evaluate whether the addition of prednisolone to standard intravenous immunoglobulin (IVIG) plus aspirin therapy can reduce the occurrence of CAL in Chinese patients with KD.	Aspirin	120-127	filamin binding LIM protein 1	Homo sapiens	165-168
17139367-0	2006	Effect of antiplatelet agents clopidogrel, aspirin, and cilostazol on circulating tissue factor procoagulant activity in patients with peripheral arterial disease.	Aspirin	43-50	coagulation factor III, tissue factor	Homo sapiens	82-95
34872933-5	2021	Consumption of atorvastatin, aspirin, and glyceryl trinitrate was found to be higher in the CAD groups compared with the control group.	Aspirin	29-36	aconitate decarboxylase 1	Homo sapiens	92-95
34775204-10	2021	Many of the synthesized agents show enhanced COX-1/2 properties than aspirin with better selectivity index towards COX-2 relative to COX-1.	Aspirin	69-76	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	45-52
34707700-9	2021	Moreover, the results indicated that the effects of aspirin treatment on PE might be mediated via the AKT/mTOR signaling pathway.	Aspirin	52-59	mechanistic target of rapamycin kinase	Mus musculus	106-110
17139367-8	2006	TF-PCA levels declined following treatment with clopidogrel alone, and with combinations of clopidogrel with aspirin or cilostazol, with the lowest levels being with the triple-drug combination.	Aspirin	109-116	coagulation factor III, tissue factor	Homo sapiens	0-2
34741613-10	2021	In experiment 2, aspirin tended to increase serum LBP (P = 0.06), but had no effect on concentrations of IL-6, haptoglobin, SAA, or AST (P >= 0.25).	Aspirin	17-24	lipopolysaccharide binding protein	Bos taurus	50-53
16936242-10	2006	The LPS- and IL-1alpha- but not GM-CSF-mediated antiapoptotic effect was markedly reduced in PMNs from donors who had ingested ASA.	Aspirin	127-130	interleukin 1 alpha	Mus musculus	13-22
34689954-0	2021	Effects of dietary aspirin on high-LET radiation-induced prostaglandin E2 levels and gastrointestinal tumorigenesis in Apc1638N/+ mice.	Aspirin	19-26	APC, WNT signaling pathway regulator	Mus musculus	119-122
16815474-0	2006	Antioxidative enzyme and glutathione S-transferase activities in diabetic rats exposed to long-term ASA treatment.	Aspirin	100-103	hematopoietic prostaglandin D synthase	Rattus norvegicus	25-50
34769120-4	2021	The present study was designed to determine, for the first time, the changes in pituitary adenylate cyclase-activating polypeptide (PACAP), substance P (SP) and galanin (GAL) expression in porcine jejunum after long-term treatment with aspirin, indomethacin and naproxen.	Aspirin	236-243	adenylate cyclase activating polypeptide 1	Sus scrofa	132-137
16815474-2	2006	The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST).	Aspirin	71-74	hematopoietic prostaglandin D synthase	Rattus norvegicus	240-265
16815474-2	2006	The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST).	Aspirin	71-74	hematopoietic prostaglandin D synthase	Rattus norvegicus	267-270
16880202-5	2006	Aspirin exposure also resulted in an increase in the half-life of pd1EGFP, a model substrate of proteasome, as well as various intracellular substrates like Bax, IkappaB-alpha, p53, and p27(kip1).	Aspirin	0-7	transformation related protein 53, pseudogene	Mus musculus	177-180
34769074-7	2021	The measurement of thromboxane B2 (TxB2) in serum (a stable metabolic product of TxA2) is the only test that measures the effect of aspirin on the activity of COX-1 in platelets.	Aspirin	132-139	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	159-164
34705291-6	2022	In independent cohorts of healthy volunteers and patients with diabetes we validated aspirin"s effects on five genes: EIF2S3, CHRNB1, EPAS1, SLC9A3R2, and HLA-DRA.	Aspirin	85-92	cholinergic receptor nicotinic beta 1 subunit	Homo sapiens	126-132
16893520-0	2006	Aspirin upregulates expression of urokinase type plasminogen activator receptor (uPAR) gene in human colon cancer cells through AP1.	Aspirin	0-7	plasminogen activator, urokinase receptor	Homo sapiens	34-79
34705291-6	2022	In independent cohorts of healthy volunteers and patients with diabetes we validated aspirin"s effects on five genes: EIF2S3, CHRNB1, EPAS1, SLC9A3R2, and HLA-DRA.	Aspirin	85-92	endothelial PAS domain protein 1	Homo sapiens	134-139
34705291-6	2022	In independent cohorts of healthy volunteers and patients with diabetes we validated aspirin"s effects on five genes: EIF2S3, CHRNB1, EPAS1, SLC9A3R2, and HLA-DRA.	Aspirin	85-92	SLC9A3 regulator 2	Homo sapiens	141-149
16893520-0	2006	Aspirin upregulates expression of urokinase type plasminogen activator receptor (uPAR) gene in human colon cancer cells through AP1.	Aspirin	0-7	plasminogen activator, urokinase receptor	Homo sapiens	81-85
34575088-8	2021	AGE 232 resulted in a decrease in the number of neutrophils attached to the human umbilical vein endothelial cells (HUVECs) and lower inhibition of COX-1 in response to bleeding and damage to blood vessels, a major side effect of ASA.	Aspirin	230-233	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	148-153
16893520-1	2006	In this study, the effects of acetylsalicylic acid (aspirin) on the expression of uPAR and the mechanism by which it regulates expression of uPAR was examined in two different colon cancer cell lines HCT116 and GEO, respectively.	Aspirin	30-50	plasminogen activator, urokinase receptor	Homo sapiens	82-86
16893520-1	2006	In this study, the effects of acetylsalicylic acid (aspirin) on the expression of uPAR and the mechanism by which it regulates expression of uPAR was examined in two different colon cancer cell lines HCT116 and GEO, respectively.	Aspirin	52-59	plasminogen activator, urokinase receptor	Homo sapiens	82-86
16893520-2	2006	The study shows that under physiological concentration, aspirin upregulates steady-state level expression of uPAR mRNA as well as expression of uPAR protein.	Aspirin	56-63	plasminogen activator, urokinase receptor	Homo sapiens	109-113
16893520-2	2006	The study shows that under physiological concentration, aspirin upregulates steady-state level expression of uPAR mRNA as well as expression of uPAR protein.	Aspirin	56-63	plasminogen activator, urokinase receptor	Homo sapiens	144-148
16893520-3	2006	Using a transient transfection assay, a region corresponding to -1 to -398 region of uPAR promoter has been identified which shows maximum responsiveness to aspirin treatment and found that this region is sufficient for the aspirin-induced up-regulation of uPAR.	Aspirin	157-164	plasminogen activator, urokinase receptor	Homo sapiens	85-89
34688318-1	2021	This study analyzed the correlation between the Notch3 mutation and stroke by testing an effective nanoparticle-loaded aspirin in stroke therapy.	Aspirin	119-126	notch receptor 3	Homo sapiens	48-54
16893520-3	2006	Using a transient transfection assay, a region corresponding to -1 to -398 region of uPAR promoter has been identified which shows maximum responsiveness to aspirin treatment and found that this region is sufficient for the aspirin-induced up-regulation of uPAR.	Aspirin	157-164	plasminogen activator, urokinase receptor	Homo sapiens	257-261
16893520-3	2006	Using a transient transfection assay, a region corresponding to -1 to -398 region of uPAR promoter has been identified which shows maximum responsiveness to aspirin treatment and found that this region is sufficient for the aspirin-induced up-regulation of uPAR.	Aspirin	224-231	plasminogen activator, urokinase receptor	Homo sapiens	85-89
16893520-3	2006	Using a transient transfection assay, a region corresponding to -1 to -398 region of uPAR promoter has been identified which shows maximum responsiveness to aspirin treatment and found that this region is sufficient for the aspirin-induced up-regulation of uPAR.	Aspirin	224-231	plasminogen activator, urokinase receptor	Homo sapiens	257-261
34435480-0	2021	Expression of NLR and IL-1beta and their predictive efficacy value in acute myocardial infarction patients treated with aspirin combined with clopidogrel.	Aspirin	120-127	interleukin 1 alpha	Homo sapiens	22-30
16893520-5	2006	Using gel mobility shift assays, it is found that the distal AP1 region between -171 and -186 is responsible for the aspirin-induced up-regulation of uPAR.	Aspirin	117-124	plasminogen activator, urokinase receptor	Homo sapiens	150-154
34540977-8	2021	Aspirin has been reported to suppress the Wnt pathway by inducing beta-catenin phosphorylation through the activation of glycogen synthase kinase 3 beta via cyclooxygenase-2 pathway inhibition.	Aspirin	0-7	catenin beta 1	Homo sapiens	66-78
16893520-10	2006	Thus, an AP1 mediated pathway for aspirin induced up-regulation of uPAR has been identified.	Aspirin	34-41	plasminogen activator, urokinase receptor	Homo sapiens	67-71
34428217-5	2021	Experiments demonstrate for the first time that plasma concentrations of Acetylsalicylic acid significantly increased TLR ligand-triggered IL-1beta, IL-10, and IL-6 production in a dose-dependent manner.	Aspirin	73-93	interleukin 1 alpha	Homo sapiens	139-147
17063752-18	2006	Although the LTC4S polymorphism has previously been associated with aspirin-sensitive asthma, this is the first demonstration that the polymorphism is associated with CHES and this is independent of aspirin sensitivity.	Aspirin	68-75	leukotriene C4 synthase	Homo sapiens	13-18
34428217-8	2021	Low PGE2 levels were at least involved in the enhanced IL-1beta production by Acetylsalicylic acid.	Aspirin	78-98	interleukin 1 alpha	Homo sapiens	55-63
34428833-9	2021	Through blocking cyclooxygenase-1 activity and thus inhibiting platelet TxA2 synthesis and granule secretion with aspirin, we found that THC did not further decrease the inhibitory effects of aspirin on thrombosis formation.	Aspirin	114-121	prostaglandin-endoperoxide synthase 1	Mus musculus	17-33
16816107-7	2006	We could show that COX-independent effects of aspirin were able to enhance expression of SR-BI in macrophages in a post-transcriptional, PPAR-alpha independent way, suggesting a novel pharmacologic effect of aspirin.	Aspirin	46-53	peroxisome proliferator activated receptor alpha	Homo sapiens	137-147
34429873-6	2021	Additionally, high expression of the hydroxyprostaglandin dehydrogenase gene, HPGD encoding prostaglandin-degrading enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH) and low expression of the proteoglycan 2 gene, PRG2 encoding constituent of the eosinophil granule in sputum cells might serve as a predictor of good response to aspirin therapy.	Aspirin	333-340	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	78-82
16583357-2	2006	In the bronchi of patients with aspirin-intolerant asthma, we previously linked cys-LT over-production and aspirin hyper-reactivity with elevated immunoexpression in eosinophils of the terminal enzyme for cys-LT production, LTC4 synthase.	Aspirin	32-39	leukotriene C4 synthase	Homo sapiens	224-237
34121855-5	2021	Combination of aspirin and ginkgolide injection could better reduce brain water content, reduce apoptosis rate of cortical cells P < 0.05, reduce expression levels of caspase-3, Bax and p-REK1/2 proteins in ischemic brain tissue P < 0.05, and increase expression level of Bcl-2 protein than aspirin and ginkgolide injection alone P < 0.05).	Aspirin	15-22	BCL2 associated X, apoptosis regulator	Rattus norvegicus	178-181
34122428-4	2021	Celecoxib, a selective COX-2 inhibitor, and aspirin, a non-selective COX-1 and COX-2 inhibitor, are being used as anti-inflammatory, analgesic and anti-pyretic drugs.	Aspirin	44-51	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	69-74
16583357-5	2006	In the mucosa of polyps from aspirin-intolerant asthmatic patients, cells immunopositive for LTC4 synthase were four-fold more numerous than in aspirin-tolerant asthmatic patients (p=0.04).	Aspirin	29-36	leukotriene C4 synthase	Homo sapiens	93-106
35535453-6	2022	In both cell lines, treatment of miR-302/367-transfected cells with aspirin upregulated expression of some main pluripotency factors such as OCT4, SOX2, NANOG, and KLF4, and downregulated expression of some invasion and angiogenesis markers at gene and protein levels.	Aspirin	68-75	POU class 5 homeobox 1	Homo sapiens	141-145
16583357-5	2006	In the mucosa of polyps from aspirin-intolerant asthmatic patients, cells immunopositive for LTC4 synthase were four-fold more numerous than in aspirin-tolerant asthmatic patients (p=0.04).	Aspirin	144-151	leukotriene C4 synthase	Homo sapiens	93-106
35535453-8	2022	Both miR-302/367 and aspirin upregulated the expression of FOXD3 protein which is a known inducer of OCT4 and NANOG.	Aspirin	21-28	POU class 5 homeobox 1	Homo sapiens	101-105
16583357-8	2006	Co-localisation confirmed that five-fold higher eosinophil counts (p=0.007) accounted for the increased LTC4 synthase expression in polyps from aspirin-intolerant asthmatic patients, with no alterations in mast cells or macrophages.	Aspirin	144-151	leukotriene C4 synthase	Homo sapiens	104-117
35521358-6	2022	Daily administration of aspirin (ASA, 150 mg/kg body weight) for 3 successive days induced a significant increase in gastric juice volume, pepsin activity, serum transaminases, alkaline phosphatase, urea, creatinine, tumor necrosis factor-alpha, myeloperoxidase, and tissue malondialdehyde levels.	Aspirin	24-31	myeloperoxidase	Rattus norvegicus	246-261
16583357-10	2006	Our results indicate that a marked over-representation of LTC4 synthase in mucosal eosinophils is closely linked to aspirin intolerance in the nasal airway, as in the bronchial airways.	Aspirin	116-123	leukotriene C4 synthase	Homo sapiens	58-71
35521358-6	2022	Daily administration of aspirin (ASA, 150 mg/kg body weight) for 3 successive days induced a significant increase in gastric juice volume, pepsin activity, serum transaminases, alkaline phosphatase, urea, creatinine, tumor necrosis factor-alpha, myeloperoxidase, and tissue malondialdehyde levels.	Aspirin	33-36	myeloperoxidase	Rattus norvegicus	246-261
16909598-6	2006	In addition, PCNA levels in both HT-29 cell and SW480 cells were reduced by aspirin and celecoxib.	Aspirin	76-83	proliferating cell nuclear antigen	Homo sapiens	13-17
16491398-6	2006	However, aspirin, which was found to stimulate NO synthesis to normal ranges, normalized maspin production in these cells in breast cancer.	Aspirin	9-16	serpin family B member 5	Homo sapiens	89-95
35482455-5	2022	Platelet-induced tumor cell PD-L1 upregulation was reduced by anti-platelet agents, such as aspirin and ticagrelor.	Aspirin	92-99	CD274 molecule	Homo sapiens	28-33
35268679-10	2022	Similarly, we found that 4-MU decreased body temperature, serum histamine, and IL4 secretion in OVA-challenged ASA model mice.	Aspirin	111-114	interleukin 4	Mus musculus	79-82
35075676-10	2022	Although ASA did not affect anti-CD3/CD28-mediated proliferation, it significantly reduced CSM2 and CSM1-mediated T-cell proliferation.	Aspirin	9-12	desmin	Homo sapiens	91-95
35075676-10	2022	Although ASA did not affect anti-CD3/CD28-mediated proliferation, it significantly reduced CSM2 and CSM1-mediated T-cell proliferation.	Aspirin	9-12	desmin	Homo sapiens	100-104
35075676-11	2022	Supernatants of LPS-stimulated CSM2 but not of CSM1 macrophages could overcome the inhibition by ASA.	Aspirin	97-100	desmin	Homo sapiens	31-35
16491398-8	2006	Restoration of NO production by aspirin can be useful for the restoration of maspin production in breast cancer.	Aspirin	32-39	serpin family B member 5	Homo sapiens	77-83
35111059-12	2021	Posttreatment with aspirin also reduced hyperoxia-induced increases in the numbers of lung macrophages, intracellular ROS levels, and the expression of TNF-alpha, IL-1beta, and IL-4; it also increased CC10, SPC and Nrp-1 levels compared with hyperoxia exposure alone.	Aspirin	19-26	interleukin 1 alpha	Mus musculus	163-171
35111059-12	2021	Posttreatment with aspirin also reduced hyperoxia-induced increases in the numbers of lung macrophages, intracellular ROS levels, and the expression of TNF-alpha, IL-1beta, and IL-4; it also increased CC10, SPC and Nrp-1 levels compared with hyperoxia exposure alone.	Aspirin	19-26	interleukin 4	Mus musculus	177-181
17784643-0	2006	Ultracytochemical demonstration of soluble guanylate cyclase activation in rat aorta by NCX4016, a NO-releasing aspirin derivative.	Aspirin	112-119	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	35-60
2503540-0	1989	Recombinant plasminogen activator inhibitor-1 reverses the bleeding tendency associated with the combined administration of tissue-type plasminogen activator and aspirin in rabbits.	Aspirin	162-169	serpin family E member 1	Homo sapiens	12-45
2758765-3	1989	To obtain further information about this event we have compared the affects of aspirin on platelet aggregation and secretion induced by PAF and collagen.	Aspirin	79-86	PCNA clamp associated factor	Homo sapiens	136-139
2758765-7	1989	Aspirin inhibited the magnitude of both platelet aggregation and secretion induced by PAF and collagen, but the degree of inhibition was much greater for collagen.	Aspirin	0-7	PCNA clamp associated factor	Homo sapiens	86-89
2758765-11	1989	Inconsistencies reported in previous studies of the effect of aspirin on PAF-induced platelet aggregation may be explained, in part, by the doses of PAF used and the method of inactivating cyclo-oxygenase (in vitro compared with in vivo).	Aspirin	62-69	PCNA clamp associated factor	Homo sapiens	73-76
2758765-11	1989	Inconsistencies reported in previous studies of the effect of aspirin on PAF-induced platelet aggregation may be explained, in part, by the doses of PAF used and the method of inactivating cyclo-oxygenase (in vitro compared with in vivo).	Aspirin	62-69	PCNA clamp associated factor	Homo sapiens	149-152
3416553-2	1988	Aspirin inhibits platelet aggregation but its antiaggregate effects can be overcome by the synergistic action of sodium arachidonate (AA) plus platelet activating factor (PAF).	Aspirin	0-7	PCNA clamp associated factor	Homo sapiens	171-174
17784643-1	2006	Biochemical studies demonstrate that the NO-releasing-aspirin derivative (NCX4016) stimulates soluble guanylate cyclase (sGC) activity and increases cyclic GMP (cGMP) in human platelet and monocytes by releasing NO.	Aspirin	54-61	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	94-119
17784643-1	2006	Biochemical studies demonstrate that the NO-releasing-aspirin derivative (NCX4016) stimulates soluble guanylate cyclase (sGC) activity and increases cyclic GMP (cGMP) in human platelet and monocytes by releasing NO.	Aspirin	54-61	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	121-124
16600694-5	2006	The results showed that (i) aspirin, fenofibrate and clofibrate decrease significantly the MCP-1 expression and secretion in human endothelial cells; (ii) the high glucose up-regulated expression of MCP-1 in endothelial cells was significantly reduced by inhibitors of NF-kB and reactive oxygen species; (iii) all drugs notably decrease the level of the reactive oxygen species and activation of NF-kB and AP-1.	Aspirin	28-35	C-C motif chemokine ligand 2	Homo sapiens	91-96
16600694-6	2006	Together, the findings indicate that in endothelial cells aspirin and PPAR-alpha activators reduce the high glucose-increased expression of MCP-1 by a mechanism that includes the inhibition of reactive oxygen species, and decrease of AP-1 and NF-kB activation.	Aspirin	58-65	C-C motif chemokine ligand 2	Homo sapiens	140-145
16338111-4	2006	In addition, results have shown that administration of aspirin increases lipid peroxidation status, xanthine oxidase (XO), myeloperoxidase and decrease in selenium-glutathione peroxidase activities in the gastric mucosa, resulting in mucosal damage at both cellular and subcellular level.	Aspirin	55-62	myeloperoxidase	Rattus norvegicus	123-138
16267095-4	2006	In these cell lines, NO-ASA induced the activity and expression of NAD(P)H:quinone oxireductase (NQO) and glutathione S-transferase (GST).	Aspirin	24-27	hematopoietic prostaglandin D synthase	Mus musculus	106-131
16386371-0	2006	Acetylsalicylic acid decreases tau phosphorylation at serine 422.	Aspirin	0-20	microtubule associated protein tau	Homo sapiens	31-34
16386371-3	2006	In this work, we have found that in the presence of acetylsalicylic acid, at a concentration like that used for anti-inflammatory treatments, tau phosphorylation at serine 422 decreases.	Aspirin	52-72	microtubule associated protein tau	Homo sapiens	142-145
16519515-1	2006	The two cyclooxygenase enzymes, COX-1 and COX-2, are responsible for the committed step in prostaglandin biosynthesis and are the targets of the nonsteroidal antiinflammatory drugs aspirin and ibuprofen and the COX-2 selective inhibitors, Celebrex, Vioxx, and Bextra.	Aspirin	181-188	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	32-37
16516312-5	2006	We confirmed the repressive effect of aspirin on GFAP transcription by GFAP promoter-driven reporter assay and found that one NF-kappaB binding site conserved in the mouse and human GFAP gene promoters is critical for this effect.	Aspirin	38-45	glial fibrillary acidic protein	Mus musculus	49-53
16516312-5	2006	We confirmed the repressive effect of aspirin on GFAP transcription by GFAP promoter-driven reporter assay and found that one NF-kappaB binding site conserved in the mouse and human GFAP gene promoters is critical for this effect.	Aspirin	38-45	glial fibrillary acidic protein	Mus musculus	71-75
16310244-7	2006	The data also showed that NF-kappaB activation and its associated gene expressions, such as COX-2, iNOS, VCAM-1 and ICAM-1, were all suppressed by the low dose aspirin supplementation through the inhibition of phosphorylation and degradation of IkappaBalpha via the NIK/IKK pathway.	Aspirin	160-167	NFKB inhibitor alpha	Rattus norvegicus	245-257
16293803-0	2006	Complement C3a and C4a increased in plasma of patients with aspirin-induced asthma.	Aspirin	60-67	complement C4A (Rodgers blood group)	Homo sapiens	19-22
16293803-10	2006	Moreover, C3a and C4a levels and the ratios of C3a/C3 and C4a/C4 were correlated with the changes of FEV(1) values after aspirin challenge.	Aspirin	121-128	complement C4A (Rodgers blood group)	Homo sapiens	18-21
16293803-10	2006	Moreover, C3a and C4a levels and the ratios of C3a/C3 and C4a/C4 were correlated with the changes of FEV(1) values after aspirin challenge.	Aspirin	121-128	complement C4A (Rodgers blood group)	Homo sapiens	58-61
16469680-10	2006	Selective COX-2 inhibition with nimesulide and COX-1 inhibition with low-dose aspirin appear to be well-tolerated in the short-term.	Aspirin	78-85	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	47-52
16505607-5	2006	Leukotriene C4 synthase has been established as a key genetic determinant of aspirin-induced asthma, but recent studies have demonstrated that several single nucleotide polymorphisms in the promoters of prostaglandin E2 receptor subtype 2, CYSLTR1 and CYSLTR2 and T-box expressed in T cells (TBX21) could increase risk for the condition.	Aspirin	77-84	leukotriene C4 synthase	Homo sapiens	0-23
16376882-3	2006	Ovarian cancer cells pretreated with general aspirin derivative acetylsalicylic acid and specific Cox-2 inhibitor (NS-398) before stimulation with LPA, FasL cell surface presentation was significantly blocked, so was the apoptosis of activated lymphocytes mediated by increasing FasL on the ovarian cancer cell surface.	Aspirin	45-52	Fas ligand	Homo sapiens	152-156
16376882-3	2006	Ovarian cancer cells pretreated with general aspirin derivative acetylsalicylic acid and specific Cox-2 inhibitor (NS-398) before stimulation with LPA, FasL cell surface presentation was significantly blocked, so was the apoptosis of activated lymphocytes mediated by increasing FasL on the ovarian cancer cell surface.	Aspirin	45-52	Fas ligand	Homo sapiens	279-283
16376882-3	2006	Ovarian cancer cells pretreated with general aspirin derivative acetylsalicylic acid and specific Cox-2 inhibitor (NS-398) before stimulation with LPA, FasL cell surface presentation was significantly blocked, so was the apoptosis of activated lymphocytes mediated by increasing FasL on the ovarian cancer cell surface.	Aspirin	64-84	Fas ligand	Homo sapiens	152-156
16842204-5	2006	It is now clear that inhibition of COX1 accounts for the unwanted side effects of aspirin-like drugs such as gastric irritation and renal damage.	Aspirin	82-89	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	35-39
16785823-4	2006	The development of low-dose aspirin as an antiplatelet agent has been instrumental in characterizing the role of platelet COX-1 in atherothrombosis.	Aspirin	28-35	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	122-127
16179345-1	2005	Aspirin is effective in the therapy of cardiovascular diseases, because it causes acetylation of cyclooxygenase 1 (COX-1) leading to irreversible inhibition of platelets.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Mus musculus	97-113
16179345-1	2005	Aspirin is effective in the therapy of cardiovascular diseases, because it causes acetylation of cyclooxygenase 1 (COX-1) leading to irreversible inhibition of platelets.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Mus musculus	115-120
16215864-10	2005	On the other hand, using aspirin/NSAIDs appeared to increase IGFBP-3 levels significantly among pre-menopausal Hispanic women.	Aspirin	25-32	insulin like growth factor binding protein 3	Homo sapiens	61-68
16310056-1	2005	BACKGROUND: Although animal studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, may protect against cutaneous squamous cell carcinoma (SCC) and actinic keratoses (AKs), possible effects on keratinocytic cancers in humans are unknown.	Aspirin	106-113	serpin family B member 3	Homo sapiens	170-173
16304252-14	2005	CONCLUSION: This study shows that eotaxin-2 is differentially secreted in patients with asthma according to aspirin intolerance, and that secretion is not time-dependent in response to the APT in AIA and ATA patients.	Aspirin	108-115	C-C motif chemokine ligand 24	Homo sapiens	34-43
15901601-0	2005	Novel lipid mediator aspirin-triggered lipoxin A4 induces heme oxygenase-1 in endothelial cells.	Aspirin	21-28	heme oxygenase 1	Homo sapiens	58-74
15901601-2	2005	Recently, it was reported that aspirin induces heme oxygenase-1 (HO-1) expression on endothelial cells (EC) in a COX-independent manner, what confers protection against prooxidant insults.	Aspirin	31-38	heme oxygenase 1	Homo sapiens	47-63
15901601-2	2005	Recently, it was reported that aspirin induces heme oxygenase-1 (HO-1) expression on endothelial cells (EC) in a COX-independent manner, what confers protection against prooxidant insults.	Aspirin	31-38	heme oxygenase 1	Homo sapiens	65-69
15901601-4	2005	In this study, we investigated whether an aspirin-triggered lipoxin A(4) stable analog, 15-epi-16-(para-fluoro)-phenoxy-lipoxin A(4) (ATL-1) was able to induce endothelial HO-1.	Aspirin	42-49	heme oxygenase 1	Homo sapiens	172-176
15871650-0	2005	Value for money in disease management of acute coronary syndrome--the price of aspirin to reduce the costs of ACS.	Aspirin	79-86	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	110-113
15886804-7	2005	Tyrosine phosphorylation of p27 and p31 in response to collagen, but not thrombin, is prevented by aspirin and the TXA(2) receptor antagonist SQ29548, indicating that the effect of collagen strongly relies on TXA(2) signaling.	Aspirin	99-106	interferon alpha inducible protein 27	Homo sapiens	28-31
15886804-7	2005	Tyrosine phosphorylation of p27 and p31 in response to collagen, but not thrombin, is prevented by aspirin and the TXA(2) receptor antagonist SQ29548, indicating that the effect of collagen strongly relies on TXA(2) signaling.	Aspirin	99-106	proteasome 26S subunit, non-ATPase 8	Homo sapiens	36-39
15837265-8	2005	Moreover, the rapid recovery of platelet COX-1 activity and function supports the occurrence of a pharmacodynamic interaction between naproxen and aspirin.	Aspirin	147-154	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	41-46
15837265-9	2005	CONCLUSIONS: Naproxen interfered with the inhibitory effect of aspirin on platelet COX-1 activity and function.	Aspirin	63-70	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	83-88
15837265-10	2005	This pharmacodynamic interaction might undermine the sustained inhibition of platelet COX-1 that is necessary for aspirin"s cardioprotective effects.	Aspirin	114-121	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	86-91
15849372-9	2005	The paper focuses on the association between Pl(A1/A2) polymorphism and sensitivity (or resistance) to aspirin and the inhibitory efficacy of GPIIb-IIIa antagonists.	Aspirin	103-110	POU class 2 homeobox 3	Homo sapiens	45-53
15498669-7	2004	Structure-activity data acquired indicate that a (Z)-olefin having cis C-1 4-acetoxyphenyl (phenyl) and C-2 4-methylsulfonylphenyl substituents, and a C-1 phenyl substituent in conjunction with either a C-2 hydrogen or short alkyl substituent provides a novel template to design acyclic olefinic COX-2 inhibitors that, like aspirin, have the potential to acetylate COX-2.	Aspirin	324-331	heterogeneous nuclear ribonucleoprotein C	Homo sapiens	151-154
15345513-2	2004	We evaluated whether one of these new compounds, consisting of aspirin coupled to an NO-releasing moiety (NCX 4016), would protect limbs from supervening arterial occlusion.	Aspirin	63-70	T cell leukemia, homeobox 2	Mus musculus	106-109
15345513-10	2004	Vascular endothelial growth factor-A expression was reduced by aspirin, with this effect being blunted by NCX 4016.	Aspirin	63-70	T cell leukemia, homeobox 2	Mus musculus	106-109
15546508-3	2004	ASA and indomethacin triggered apoptosis in cells of all three lines through release of cytosolic cytochrome c, activation of caspase-9 and-3, and cleavage of poly(ADP-ribose) polymerase (PARP), but NS398 induced minimal apoptosis only in Ishikawa cells.	Aspirin	0-3	caspase 9	Homo sapiens	126-141
15646027-3	2004	Aspirin increased PPARdelta mRNA levels in Jurkat cells, but decreased the activity of both PPARdelta and PPARalpha/gamma, assayed using the luciferase reporter constructs DRE and ACO, respectively.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Homo sapiens	106-115
15326064-5	2004	When ATL synthesis was inhibited by pretreatment with a selective cyclooxygenase-2 inhibitor (celecoxib) or a 5-lipoxygenase inhibitor (zileuton), the aspirin-induced increase in BP was significantly augmented.	Aspirin	151-158	arachidonate 5-lipoxygenase	Rattus norvegicus	110-124
15326064-8	2004	Moreover, immunodepletion of neutrophils, a major source of 5-lipoxygenase, resulted in a significant reduction of ATL formation and augmented aspirin"s pressor effects.	Aspirin	143-150	arachidonate 5-lipoxygenase	Rattus norvegicus	60-74
15175008-1	2004	Arylsulphatases B (ASB) and A (ASA) are subject to a unique post-translational modification that is required for their function.	Aspirin	31-34	arylsulfatase B	Homo sapiens	0-17
15175008-1	2004	Arylsulphatases B (ASB) and A (ASA) are subject to a unique post-translational modification that is required for their function.	Aspirin	31-34	arylsulfatase B	Homo sapiens	19-22
15290664-2	2004	The cytochrome P-450 (CYP) 2C9 (CYP2C9) enzyme is involved in the metabolism of several drugs, including possibly aspirin, and such carcinogens as smoking-related polycyclic aromatic hydrocarbons.	Aspirin	114-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-30
15290664-2	2004	The cytochrome P-450 (CYP) 2C9 (CYP2C9) enzyme is involved in the metabolism of several drugs, including possibly aspirin, and such carcinogens as smoking-related polycyclic aromatic hydrocarbons.	Aspirin	114-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
15370100-5	2004	Aspirin inhibited CD62P expression and GPIIb/IIIa activation induced by collagen, but not thrombin.	Aspirin	0-7	selectin P	Homo sapiens	18-23
15198222-6	2004	RESULTS: Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas NS398, carprofen, tolfenamic acid, nimesulide, and etodolac had more than 5 times greater preference for inhibiting COX-2 than COX-1.	Aspirin	9-16	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	119-122
15131571-2	2004	LTC(4) synthase is a key enzyme in the cys-LT biosynthetic pathway, and studies in small populations have suggested that a promoter polymorphism (A(-444)C) in the gene might be associated with asthma severity and aspirin intolerance.	Aspirin	213-220	leukotriene C4 synthase	Homo sapiens	0-15
15131571-10	2004	CONCLUSIONS: Our data confirm that, independent of transcriptional activity, the C(-444) allele in the LTC(4) synthase gene is weakly associated with the asthma phenotype, but it is not related to disease severity or aspirin intolerance.	Aspirin	217-224	leukotriene C4 synthase	Homo sapiens	103-118
14697260-0	2004	NO-donating aspirin inhibits intestinal carcinogenesis in Min (APC(Min/+)) mice.	Aspirin	12-19	APC, WNT signaling pathway regulator	Mus musculus	63-74
15500197-1	2004	It was the aim of this clinical study to demonstrate the efficacy of 1000 mg acetylsalicylic acid (ASA, CAS 50-78-2) in combination with 60 mg pseudoephedrine (PSE, CAS 90-82-4), compared with placebo, in the symptomatic treatment of nasal congestion associated with the common cold.	Aspirin	77-97	BCAR1 scaffold protein, Cas family member	Homo sapiens	104-107
12943528-0	2004	Aspirin inhibits endothelial nitric oxide synthase (eNOS) and Flk-1 (vascular endothelial growth factor receptor-2) prior to rat colon tumour development.	Aspirin	0-7	kinase insert domain receptor	Rattus norvegicus	62-67
12943528-0	2004	Aspirin inhibits endothelial nitric oxide synthase (eNOS) and Flk-1 (vascular endothelial growth factor receptor-2) prior to rat colon tumour development.	Aspirin	0-7	kinase insert domain receptor	Rattus norvegicus	69-114
12943528-9	2004	Aspirin treatment reduced Flk-1 expression in both control and azoxymethane-treated rats.	Aspirin	0-7	kinase insert domain receptor	Rattus norvegicus	26-31
12943528-12	2004	Overexpression of eNOS, VEGF and its receptor Flk-1 occurred early after azoxymethane administration in rat colonic tissue, even before morphological changes associated with tumour generation were observed, and aspirin prevented the overexpression of both eNOS and VEGF receptor Flk-1.	Aspirin	211-218	vascular endothelial growth factor A	Rattus norvegicus	24-28
14753751-6	2003	Additionally, aspirin effectively prevents caspase-3 and caspase-9 (cysteinyl aspartate-specific proteases) activation by H2O2.	Aspirin	14-21	caspase 9	Homo sapiens	57-66
14623265-7	2003	NC-4016 and aspirin inhibited platelet COX-1 comparably while NO-donors were ineffective.	Aspirin	12-19	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	39-44
14640056-2	2003	The mechanisms by which acetylsalicylic acid and other NSAIDs, including COX-2 inhibitors, exert this effect include: inhibition of COX-2, induction of apoptosis and induction of the P21 protein that controls the development of crypt cells.	Aspirin	24-44	H3 histone pseudogene 16	Homo sapiens	183-186
14616128-0	2003	RANTES, eotaxin and eotaxin-2 expression and production in patients with aspirin triad.	Aspirin	73-80	C-C motif chemokine ligand 24	Homo sapiens	20-29
14566053-0	2003	Nitric oxide-donating aspirin inhibits beta-catenin/T cell factor (TCF) signaling in SW480 colon cancer cells by disrupting the nuclear beta-catenin-TCF association.	Aspirin	22-29	catenin beta 1	Homo sapiens	39-51
14566053-0	2003	Nitric oxide-donating aspirin inhibits beta-catenin/T cell factor (TCF) signaling in SW480 colon cancer cells by disrupting the nuclear beta-catenin-TCF association.	Aspirin	22-29	catenin beta 1	Homo sapiens	136-148
14566053-2	2003	We studied the ortho, meta, and para (o-, m-, and p-) positional isomers of NO-donating aspirin (NO-ASA), a chemopreventive agent against colon cancer, for their effect on Beta-catenin/T cell factor (TCF) signaling.	Aspirin	88-95	catenin beta 1	Homo sapiens	172-184
14566053-3	2003	In human SW480 colon carcinoma cells, cell-growth inhibition by NO-ASA [IC50 values for p-, o-, and m- were 48.1 +/- 4.3 (mean +/-SEM), 60.4 +/- 2.1, and 900 +/-50 microM, respectively] was accompanied by significant inhibition of Beta-catenin signaling.	Aspirin	67-70	catenin beta 1	Homo sapiens	231-243
14566053-5	2003	The IC50 values for Beta-catenin/TCF-4-signaling inhibition by NO-ASA were: o-, 2.6 +/- 0.4; m-, 15 +/- 5; p-, 1.1 +/- 0.1 microM; and for ASA, &gt;5,000 microM.	Aspirin	66-69	catenin beta 1	Homo sapiens	20-32
14566053-5	2003	The IC50 values for Beta-catenin/TCF-4-signaling inhibition by NO-ASA were: o-, 2.6 +/- 0.4; m-, 15 +/- 5; p-, 1.1 +/- 0.1 microM; and for ASA, &gt;5,000 microM.	Aspirin	139-142	catenin beta 1	Homo sapiens	20-32
14566053-7	2003	NO-ASA disrupted the association of Beta-catenin and TCF-4 in the nucleus, whereas ASA did not affect it.	Aspirin	3-6	catenin beta 1	Homo sapiens	36-48
14511359-10	2003	In the meanwhile, phosphorylation of p53 at serine 15, accumulation of p53 and increased the expression of its downstream target genes, p21 and Bax induced by ASA.	Aspirin	159-162	H3 histone pseudogene 16	Homo sapiens	136-139
14511359-13	2003	Inhibited the activation of p42/p44 mitogen-activated protein kinase (MAPK) by PD98059, a specific inhibitor of extracellular regulatory kinase (ERK), significantly decreased cell viability and enhanced the expression of p53 induced by ASA.	Aspirin	236-239	cyclin dependent kinase 20	Homo sapiens	28-31
14511359-17	2003	Furthermore, the apoptotic effect was enhanced by blocking the activation of p42/p44 MAPK in response to treatment with ASA, thus indicating a negative role for p42/p44 MAPK.	Aspirin	120-123	cyclin dependent kinase 20	Homo sapiens	77-80
14511359-17	2003	Furthermore, the apoptotic effect was enhanced by blocking the activation of p42/p44 MAPK in response to treatment with ASA, thus indicating a negative role for p42/p44 MAPK.	Aspirin	120-123	cyclin dependent kinase 20	Homo sapiens	161-164
12800193-0	2003	Expression profiling of CC531 colon carcinoma cells reveals similar regulation of beta-catenin target genes by both butyrate and aspirin.	Aspirin	129-136	catenin beta 1	Rattus norvegicus	82-94
12874188-11	2003	CONCLUSIONS: Platelet aspirin resistance involves an impairment of both in vivo and in vitro inhibition of platelet functions and is probably due to a disturbed inhibition of platelet COX-1 by aspirin.	Aspirin	22-29	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	184-189
12874188-11	2003	CONCLUSIONS: Platelet aspirin resistance involves an impairment of both in vivo and in vitro inhibition of platelet functions and is probably due to a disturbed inhibition of platelet COX-1 by aspirin.	Aspirin	193-200	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	184-189
12887308-3	2003	BPI expression was markedly up-regulated by exposure of epithelia to lipoxins, endogenous anti-inflammatory eicosanoids that are generated in vivo in the context of aspirin treatment (aspirin-triggered lipoxins).	Aspirin	165-172	bactericidal permeability increasing protein	Homo sapiens	0-3
12887308-3	2003	BPI expression was markedly up-regulated by exposure of epithelia to lipoxins, endogenous anti-inflammatory eicosanoids that are generated in vivo in the context of aspirin treatment (aspirin-triggered lipoxins).	Aspirin	184-191	bactericidal permeability increasing protein	Homo sapiens	0-3
12890715-12	2003	(6) Reversal of antiadhesive activities of aspirin by celecoxib was associated with increased expression of LFA-1 on PMN and E-selectin on HUVEC.	Aspirin	43-50	selectin E	Homo sapiens	125-135
12890715-14	2003	(7) The present results support the notion that inhibition of ATL formation is mechanistically linked to the reversal of the antiadhesive activity of aspirin caused by selective COX-1 inhibitors and suggests that the LTB(4)/ATL balance modulates pro- and antiadhesive activity of nonsteroidal anti-inflammatory drugs at the leukocyte-endothelial cell interface.	Aspirin	150-157	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	178-183
12965185-4	2003	Administration of D in rats pretreated with alpha-tocopherol (alphaT) or acetylsalicylic acid (ASA) decreased the activities of GPx, GR and MDA levels, while the GSH level was increased compared with rats treated with D alone.	Aspirin	73-93	glutathione-disulfide reductase	Rattus norvegicus	133-135
12965185-4	2003	Administration of D in rats pretreated with alpha-tocopherol (alphaT) or acetylsalicylic acid (ASA) decreased the activities of GPx, GR and MDA levels, while the GSH level was increased compared with rats treated with D alone.	Aspirin	95-98	glutathione-disulfide reductase	Rattus norvegicus	133-135
12879250-11	2003	The inhibition of PNF by AsA was associated with decreased intra-islet levels of inflammation-related molecules (IL-1, TNF-alpha, iNOS, COX-2) and chemokines (MCP-1 and MIP-3alpha).	Aspirin	25-28	chemokine (C-C motif) ligand 20	Mus musculus	169-179
12897207-9	2003	The data suggest that more aggressive strategies of P2Y12 antagonism will be antithrombotic without the requirement of aspirin cotherapy and may provide benefits even to the aspirin-nonresponder population.	Aspirin	119-126	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	52-57
12897207-9	2003	The data suggest that more aggressive strategies of P2Y12 antagonism will be antithrombotic without the requirement of aspirin cotherapy and may provide benefits even to the aspirin-nonresponder population.	Aspirin	174-181	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	52-57
12714600-0	2003	Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in tumor necrosis factor-treated cells through targeting multiple serine kinases.	Aspirin	0-7	insulin receptor substrate 1	Homo sapiens	43-71
12714600-3	2003	In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha.	Aspirin	42-49	insulin receptor substrate 1	Homo sapiens	102-130
12714600-3	2003	In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha.	Aspirin	42-49	insulin receptor substrate 1	Homo sapiens	132-137
12714600-3	2003	In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha.	Aspirin	51-71	insulin receptor substrate 1	Homo sapiens	102-130
12714600-3	2003	In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha.	Aspirin	51-71	insulin receptor substrate 1	Homo sapiens	132-137
12714600-8	2003	Interestingly, aspirin treatment inhibited the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha.	Aspirin	15-22	insulin receptor substrate 1	Homo sapiens	66-71
12851613-12	2003	Although aspirin time dependently decreased the percent of P-selectin positive platelets (P =.02), treatment with roxifiban resulted in the phasic changes with the early inhibition (P =.01) and then 2-fold activation (P =.0001) starting at week 12 of the therapy.	Aspirin	9-16	selectin P	Homo sapiens	59-69
12527817-3	2003	One of these, triacetylsalicylhydroxamic acid (TriAcSHA) was more effective than aspirin and O-acetylsalicylhydroxamic acid in inactivating both COX-1 and COX-2.	Aspirin	81-88	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	145-150
12527817-4	2003	Preincubation of COX-1 with inhibitor for 5 min yielded IC(50) values of 18 microM for TriAcSHA and 60 microM for acetylsalicylic acid.	Aspirin	114-134	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	17-22
12527817-6	2003	As with aspirin, mutation of the serine 530 of COX-1 to alanine abolished the activity of the TriAcSHA.	Aspirin	8-15	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	47-52
12535860-2	2003	Here, we report that treatment of coronary artery patients with 100 mg/day of aspirin does not attenuate thrombin generation, but reduces free thrombin by favouring the formation of thrombin/antithrombin (TAT) complexes.	Aspirin	78-85	serpin family C member 1	Homo sapiens	191-203
12538492-7	2003	In HCT116+chr3 cells, treatment with 1 mM of aspirin increased expression of the hMLH1 and hPMS2 proteins by 2.5-fold and 2-fold, respectively, and increased expression of the hMSH2 and hMSH6 proteins by 2-3-fold.	Aspirin	45-52	mutL homolog 1	Homo sapiens	81-86
12538492-7	2003	In HCT116+chr3 cells, treatment with 1 mM of aspirin increased expression of the hMLH1 and hPMS2 proteins by 2.5-fold and 2-fold, respectively, and increased expression of the hMSH2 and hMSH6 proteins by 2-3-fold.	Aspirin	45-52	PMS1 homolog 2, mismatch repair system component	Homo sapiens	91-96
12538492-7	2003	In HCT116+chr3 cells, treatment with 1 mM of aspirin increased expression of the hMLH1 and hPMS2 proteins by 2.5-fold and 2-fold, respectively, and increased expression of the hMSH2 and hMSH6 proteins by 2-3-fold.	Aspirin	45-52	mutS homolog 6	Homo sapiens	186-191
12538492-8	2003	For SW480 cells, treatment with 1 and 5 mM of aspirin increased expression of the hMLH1 and hPMS2 proteins by 2-4-fold and 3-5-fold, respectively, and increased expression of the hMSH2 and hMSH6 proteins by 3-7-fold.	Aspirin	46-53	mutL homolog 1	Homo sapiens	82-87
12538492-8	2003	For SW480 cells, treatment with 1 and 5 mM of aspirin increased expression of the hMLH1 and hPMS2 proteins by 2-4-fold and 3-5-fold, respectively, and increased expression of the hMSH2 and hMSH6 proteins by 3-7-fold.	Aspirin	46-53	PMS1 homolog 2, mismatch repair system component	Homo sapiens	92-97
12538492-8	2003	For SW480 cells, treatment with 1 and 5 mM of aspirin increased expression of the hMLH1 and hPMS2 proteins by 2-4-fold and 3-5-fold, respectively, and increased expression of the hMSH2 and hMSH6 proteins by 3-7-fold.	Aspirin	46-53	mutS homolog 6	Homo sapiens	189-194
14586772-4	2003	Aspirin-induced asthma (AIA) is a typical drug-induced phenotype due to aspirin or nonsteroidal antiinflammatory drugs, and these drugs are metabolized by CYP2C9 and UGT1A6, which are regulated by PXR.	Aspirin	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
12891293-12	2003	CONCLUSION: Compared with controls the use of ticlopidine in patients with NSTEACS treated with aspirin and UFH was associated with less pronounced lowering of PAI activity and lower level of D-dimer.	Aspirin	96-103	serpin family E member 1	Homo sapiens	160-163
12714834-2	2002	In this study, we showed that the combination regimen of clopidogrel with aspirin could downregulate the P-selectin expression on platelets and the plasma concentration of C-reactive protein (CRP) in acute stage of atherosclerotic ischemic stroke.	Aspirin	74-81	selectin P	Homo sapiens	105-115
12714834-5	2002	RESULTS: The combined regimen of clopidogrel and aspirin significantly reduced platelet P-selectin expression (93.6 +/- 16.6, p &lt; 0.01) and plasma concentration of CRP (1.2 +/- 1.5 mg/dl, p &lt; 0.01) after 7 days of stroke onset compared with the values (P-selectin; 115.5 +/- 20.7, CRP; 2.5 +/- 2.8 mg/dl) of initial 24 hr.	Aspirin	49-56	selectin P	Homo sapiens	88-98
12714834-5	2002	RESULTS: The combined regimen of clopidogrel and aspirin significantly reduced platelet P-selectin expression (93.6 +/- 16.6, p &lt; 0.01) and plasma concentration of CRP (1.2 +/- 1.5 mg/dl, p &lt; 0.01) after 7 days of stroke onset compared with the values (P-selectin; 115.5 +/- 20.7, CRP; 2.5 +/- 2.8 mg/dl) of initial 24 hr.	Aspirin	49-56	selectin P	Homo sapiens	259-269
12586130-7	2002	Evaluating both aspirin groups together (n=129), the levels of soluble P-selectin were significantly higher in non-responders as compared to responders (p=0.012).	Aspirin	16-23	selectin P	Homo sapiens	71-81
12204495-7	2002	CONCLUSIONS: Troponin T release occurs after successful intervention in 74% of the patients undergoing elective PCI after 48 h even after pretreatment with aspirin and clopidogrel.	Aspirin	156-163	troponin T1, slow skeletal type	Homo sapiens	13-23
12195225-9	2002	So, even minimal aspirin doses inhibit the activity of COX-1, which shunts the already abnormal metabolism of arachidonic acid.	Aspirin	17-24	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	55-60
12396127-5	2002	Aspirin, a COX inhibitor, was not effective.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	11-14
11994707-3	2002	OBJECTIVE: The aim of these studies was to investigate Cox-1 and Cox-2 regulation in NPs of aspirin-tolerant human patients compared with that seen in nasal mucosa (NM).	Aspirin	92-99	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	55-60
11994707-8	2002	CONCLUSION: These data showing an abnormal regulation of Cox-1 and Cox-2 in NPs from aspirin-tolerant patients reinforce the concept that prostanoid metabolism might be important in the pathogenesis of inflammatory nasal diseases and suggest a potential role for this alteration in the formation of NPs.	Aspirin	85-92	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	57-62
11877318-18	2002	In contrast, phenanthroline and apyrase significantly enhanced the anti-aggregatory effects of aspirin against thrombin-, PAR1AP- and TRAP-induced aggregation suggesting the involvement of ADP- and MMP-2-dependent pathways.	Aspirin	95-102	WD and tetratricopeptide repeats 1	Homo sapiens	189-193
11747987-7	2002	Accordingly, PKC epsilon is activated and translocates from the membrane fraction to the cytoskeleton fraction in aspirin-treated cells.	Aspirin	114-121	protein kinase C epsilon	Homo sapiens	13-24
12086293-4	2002	The gastrointestinal toxicity of nonselective NSAIDs and aspirin derives from the inhibition of the cyclooxygenase (COX) enzyme, COX-1, which synthesizes gastroprotective prostaglandins, while the anti-inflammatory and pain-relieving effects are largely derived from inhibition of COX-2-derived prostaglandins.	Aspirin	57-64	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	129-134
12214159-4	2002	Aspirin plus clopidogrel significantly inhibited platelet aggregation, fibrinogen receptor activation and release of P-selectin and prolonged in vitro bleeding time (p &lt; 0.01).	Aspirin	0-7	selectin P	Homo sapiens	117-127
11871134-13	2002	In patients with high risk for coronary heart diseases, hsCRP-guided therapy is possible by using aspirin, stains, and antibiotics for prevention of ACS.	Aspirin	98-105	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	149-152
11720731-0	2001	Antinociceptive profiles of aspirin and acetaminophen in formalin, substance P and glutamate pain models.	Aspirin	28-35	tachykinin 1	Mus musculus	67-78
11717412-3	2001	Here, we have evaluated the relative potential of ibuprofen and various coxibs to interfere with the inactivation of Cox-1 by aspirin by using purified enzyme and calcium ionophore-activated human platelets.	Aspirin	126-133	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	117-122
11717412-4	2001	The irreversible inactivation of Cox-1 by aspirin can be antagonized by ibuprofen and coxibs, albeit with widely different potencies.	Aspirin	42-49	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	33-38
11717412-7	2001	The EC(50) value for the antagonism against 10 microM aspirin for each drug is approximately 10- to 40-fold lower than the corresponding IC(50) value for inhibition of platelet Cox-1 activity, consistent with the much weaker initial binding of aspirin to Cox-1 as compared with arachidonic acid.	Aspirin	54-61	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	177-182
11717412-7	2001	The EC(50) value for the antagonism against 10 microM aspirin for each drug is approximately 10- to 40-fold lower than the corresponding IC(50) value for inhibition of platelet Cox-1 activity, consistent with the much weaker initial binding of aspirin to Cox-1 as compared with arachidonic acid.	Aspirin	54-61	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	255-260
11717412-7	2001	The EC(50) value for the antagonism against 10 microM aspirin for each drug is approximately 10- to 40-fold lower than the corresponding IC(50) value for inhibition of platelet Cox-1 activity, consistent with the much weaker initial binding of aspirin to Cox-1 as compared with arachidonic acid.	Aspirin	244-251	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	177-182
11717412-7	2001	The EC(50) value for the antagonism against 10 microM aspirin for each drug is approximately 10- to 40-fold lower than the corresponding IC(50) value for inhibition of platelet Cox-1 activity, consistent with the much weaker initial binding of aspirin to Cox-1 as compared with arachidonic acid.	Aspirin	244-251	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	255-260
11717412-8	2001	These results show that a low affinity for Cox-1 and a high degree of Cox-2 selectivity confers a low potential to block aspirin inhibition of platelet Cox-1, consistent with the results of clinical studies.	Aspirin	121-128	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	43-48
11717412-8	2001	These results show that a low affinity for Cox-1 and a high degree of Cox-2 selectivity confers a low potential to block aspirin inhibition of platelet Cox-1, consistent with the results of clinical studies.	Aspirin	121-128	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	152-157
11764219-4	2001	We investigated the possible effects of 3 different nonsteroidal antiinflammatory drugs (NSAID; aceclofenac, piroxicam, aspirin) on IL-1Ra and NO production in human articular chondrocytes.	Aspirin	120-127	interleukin 1 receptor antagonist	Homo sapiens	132-138
11750884-6	2001	Aspirin, an inhibitor of cyclooxygenase 1 and 2, had no effect on LPL activity in 3T3-L1 adipocytes, did not affect body composition when fed to growing mice, and failed to influence the effects of CLA on LPL activity in 3T3-L1 cells or body composition in mice.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Mus musculus	25-47
11728532-9	2001	RESULTS: In a drug free group, digestion of a single tablet of aspirin resulted in a significantly (p&lt;0.05) diminished expression of PECAM-1, GP IIb, fibrinogen binding with PAC-1 antibody, GP Ib, P-selectin, and CD151.	Aspirin	63-70	selectin P	Homo sapiens	200-210
11672759-2	2001	ASA inhibits thromboxane A(2) (TXA(2)) production by blocking the constitutive cyclooxygenase (COX)-1 enzyme, but only to a small degree the inducible COX-2.	Aspirin	0-3	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	79-101
11672762-5	2001	Platelet fibrinogen binding and P-selectin expression were significantly lower in patients treated with ticlopidine but not with aspirin than in those not treated with any antiplatelet agent, and were lowest in those treated with both ticlopidine and aspirin.	Aspirin	129-136	selectin P	Homo sapiens	32-42
11672762-5	2001	Platelet fibrinogen binding and P-selectin expression were significantly lower in patients treated with ticlopidine but not with aspirin than in those not treated with any antiplatelet agent, and were lowest in those treated with both ticlopidine and aspirin.	Aspirin	251-258	selectin P	Homo sapiens	32-42
11588175-8	2001	This paper shows (1) that ASIC mRNAs are present in many small sensory neurons along with substance P and isolectin B4 and that, in case of inflammation, ASIC1a appears in some larger Abeta fibers, (2) that NSAIDs prevent the large increase of ASIC expression in sensory neurons induced by inflammation, and (3) that NSAIDs such as aspirin, diclofenac, and flurbiprofen directly inhibit ASIC currents on sensory neurons and when cloned ASICs are heterologously expressed.	Aspirin	332-339	acid sensing ion channel subunit 1	Homo sapiens	26-30
11588175-8	2001	This paper shows (1) that ASIC mRNAs are present in many small sensory neurons along with substance P and isolectin B4 and that, in case of inflammation, ASIC1a appears in some larger Abeta fibers, (2) that NSAIDs prevent the large increase of ASIC expression in sensory neurons induced by inflammation, and (3) that NSAIDs such as aspirin, diclofenac, and flurbiprofen directly inhibit ASIC currents on sensory neurons and when cloned ASICs are heterologously expressed.	Aspirin	332-339	acid sensing ion channel subunit 1	Homo sapiens	154-158
11588175-8	2001	This paper shows (1) that ASIC mRNAs are present in many small sensory neurons along with substance P and isolectin B4 and that, in case of inflammation, ASIC1a appears in some larger Abeta fibers, (2) that NSAIDs prevent the large increase of ASIC expression in sensory neurons induced by inflammation, and (3) that NSAIDs such as aspirin, diclofenac, and flurbiprofen directly inhibit ASIC currents on sensory neurons and when cloned ASICs are heterologously expressed.	Aspirin	332-339	acid sensing ion channel subunit 1	Homo sapiens	154-158
11435113-2	2001	The crystal structures of two human arylsulfatases, ASA and ASB, along with ASA mutants and their complexes led to different proposals for the catalytic mechanism in the hydrolysis of sulfate esters.	Aspirin	76-79	arylsulfatase B	Homo sapiens	60-63
11325819-0	2001	CYP2C9 and UGT1A6 genotypes modulate the protective effect of aspirin on colon adenoma risk.	Aspirin	62-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11325819-3	2001	NSAIDs, particularly aspirin, are glucuronidated by UGT1A6 and some classes of NSAIDs are also metabolized by cytochrome P450 (CYP) 2C9.	Aspirin	21-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-135
11325819-8	2001	However, this association was absent in aspirin users who carried the CYP2C9 variant alleles (OR, 0.88; 95% CI, 0.51-1.53) or who were homozygous wild-type UGT1A6 (OR, 0.86; 95% CI, 0.50-1.50).	Aspirin	40-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
11326011-2	2001	A 423- to 551-bp Acanthamoeba-specific amplimer ASA.S1 obtained with primers JDP1 and JDP2 was the most reliable for purposes i and ii.	Aspirin	48-51	Jun dimerization protein 2	Homo sapiens	86-90
11235048-4	2001	New evidence suggests that aspirin sensitivity may be linked to the COX-1 pathway, and COX-2 inhibitors, as a result of their selectivity, may be beneficial in patients with aspirin-induced asthma.	Aspirin	27-34	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	68-73
11145657-4	2001	The role of L-selectin down-regulation in reducing T cell adhesion in this system was supported by the fact that aspirin inhibited T cell adhesion also on plastic-immobilized L-selectin ligand or when alpha(4) integrin-mediated adhesion to endothelium was blocked by specific mAbs.	Aspirin	113-120	selectin L	Homo sapiens	12-22
11145657-4	2001	The role of L-selectin down-regulation in reducing T cell adhesion in this system was supported by the fact that aspirin inhibited T cell adhesion also on plastic-immobilized L-selectin ligand or when alpha(4) integrin-mediated adhesion to endothelium was blocked by specific mAbs.	Aspirin	113-120	selectin L	Homo sapiens	175-185
11145657-7	2001	Finally, the infusion of aspirin into healthy volunteers induced down-regulation of L-selectin on circulating T cells.	Aspirin	25-32	selectin L	Homo sapiens	84-94
11166001-4	2001	The antithrombotic effect of aspirin  does not appear to be dose related over a wide range of daily doses (30 to 1,300  mg), an observation consistent with saturability of platelet COX-1 inhibition by  aspirin at very low doses.	Aspirin	202-209	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	181-186
11141472-1	2001	Aspirin-triggered lipoxin A(4) (ATL, 15-epi-LXA(4)) and leukotriene D(4) (LTD(4)) possess opposing vascular actions mediated via receptors distinct from the LXA(4) receptor (ALX) that is involved in leukocyte trafficking.	Aspirin	0-7	formyl peptide receptor 2	Homo sapiens	157-172
11211927-4	2000	To measure COX-2 activity, cells were transiently pre-treated with aspirin to irreversibly inhibit constitutive COX-1, treated with lipopolysaccharide (LPS) to induce COX-2 and then stimulated with AA.	Aspirin	67-74	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	112-117
11244692-8	2000	With regard to antiaggregants, IST and CAST were done using Aspirin, showing a drop in early recurrences and increase in recoveries, so that aspirin has been recommended for use during the first 48 hours.	Aspirin	60-67	calpastatin	Homo sapiens	39-43
11244692-8	2000	With regard to antiaggregants, IST and CAST were done using Aspirin, showing a drop in early recurrences and increase in recoveries, so that aspirin has been recommended for use during the first 48 hours.	Aspirin	141-148	calpastatin	Homo sapiens	39-43
11054089-0	2000	Relationship between bleeding time, aspirin and the PlA1/A2 polymorphism of platelet glycoprotein IIIa.	Aspirin	36-43	POU class 2 homeobox 3	Homo sapiens	52-56
11054089-6	2000	Thus, BT both at baseline and after aspirin depends on the PlA1/A2 polymorphism of glycoprotein IIIa.	Aspirin	36-43	POU class 2 homeobox 3	Homo sapiens	59-63
10987587-6	2000	Clopidogrel with or without aspirin significantly suppressed expression of platelet activation markers CD 62p, CD 63 and PAC-1 after stimulation with ADP or thrombin (p &lt; 0.001).	Aspirin	28-35	selectin P	Homo sapiens	103-109
10987587-6	2000	Clopidogrel with or without aspirin significantly suppressed expression of platelet activation markers CD 62p, CD 63 and PAC-1 after stimulation with ADP or thrombin (p &lt; 0.001).	Aspirin	28-35	CD63 molecule	Homo sapiens	111-116
10987587-6	2000	Clopidogrel with or without aspirin significantly suppressed expression of platelet activation markers CD 62p, CD 63 and PAC-1 after stimulation with ADP or thrombin (p &lt; 0.001).	Aspirin	28-35	ADCYAP receptor type I	Homo sapiens	121-126
10942685-1	2000	OBJECTIVES: the preventive effect of acetylsalicylic acid in cardiovascular disease may be due to inhibition of platelet aggregation mediated by COX-1, but may in addition be due to anti-inflammatory effects by inhibition of COX-2.	Aspirin	37-57	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	145-150
10977131-10	2000	After incubation with LPS plus acetylsalicylic acid, positive staining was observed for both COX-1-ir and COX-2-ir.	Aspirin	31-51	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	93-98
10744623-3	2000	Nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin and indomethacin that block COX-1 and -2 have been shown to have beneficial effects for tumor patients.	Aspirin	51-58	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	87-99
11014724-5	2000	It remains to be seen whether the new antithrombin agents reduce the rate of periprocedural complications if used in combination with aspirin and new antiplatelet therapies.	Aspirin	134-141	serpin family C member 1	Homo sapiens	38-50
11078261-0	2000	Effect of aspirin and ticlopidine on plasma tissue factor levels in stable and unstable angina pectoris.	Aspirin	10-17	coagulation factor III, tissue factor	Homo sapiens	44-57
10381057-12	1999	Among all NSAID tested, meloxicam and aspirin were the least potent inhibitors of COX-1 (IC50 = 36.6 microM and 3.57 microM, respectively).	Aspirin	38-45	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	82-87
10381057-16	1999	Aspirin and piroxicam were about 8 times more active against COX-1 than COX-2, indomethacin was 7 times more active, and diclofenac was an equipotent inhibitor of COX-1 and COX-2.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	61-66
10381057-16	1999	Aspirin and piroxicam were about 8 times more active against COX-1 than COX-2, indomethacin was 7 times more active, and diclofenac was an equipotent inhibitor of COX-1 and COX-2.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	163-168
10416217-7	1999	The rank order of cytotoxicity observed in hMIC was phenylbutazone &gt; mefenamic acid &gt; aspirin &gt; paracetamol.	Aspirin	92-99	mannosidase alpha class 1C member 1	Homo sapiens	43-47
10725977-4	1999	Acetylsalicylic acid intake resulted in decreased incorporation of myosin and actin (32% and 20%, respectively), and a decrease (36%) in the association of beta 3 integrin with the cytoskeletal elements was evident.	Aspirin	0-20	myosin heavy chain 14	Homo sapiens	67-73
9831331-5	1998	The lowest COX-2 selectivities, which means the highest COX-1 selectivities, were observed in indomethacin, aspirin, and oxaprozin.	Aspirin	108-115	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	56-61
9748494-0	1998	Butyrylcholinesterase-catalysed hydrolysis of aspirin, a negatively charged ester, and aspirin-related neutral esters.	Aspirin	46-53	butyrylcholinesterase	Homo sapiens	0-21
9748494-0	1998	Butyrylcholinesterase-catalysed hydrolysis of aspirin, a negatively charged ester, and aspirin-related neutral esters.	Aspirin	87-94	butyrylcholinesterase	Homo sapiens	0-21
9748494-1	1998	Although aspirin (acetylsalicylic acid) is negatively charged, it is hydrolysed by butyrylcholinesterase (BuChE).	Aspirin	9-16	butyrylcholinesterase	Homo sapiens	83-104
9748494-1	1998	Although aspirin (acetylsalicylic acid) is negatively charged, it is hydrolysed by butyrylcholinesterase (BuChE).	Aspirin	9-16	butyrylcholinesterase	Homo sapiens	106-111
9748494-1	1998	Although aspirin (acetylsalicylic acid) is negatively charged, it is hydrolysed by butyrylcholinesterase (BuChE).	Aspirin	18-38	butyrylcholinesterase	Homo sapiens	83-104
9748494-1	1998	Although aspirin (acetylsalicylic acid) is negatively charged, it is hydrolysed by butyrylcholinesterase (BuChE).	Aspirin	18-38	butyrylcholinesterase	Homo sapiens	106-111
9748494-3	1998	The presence of Ca2+ or Mg2+ (&lt;100 mM) in buffer did not change the Km, but accelerated the rate of hydrolysis of aspirin by wild-type or D70G mutant BuChE by 5-fold.	Aspirin	117-124	butyrylcholinesterase	Homo sapiens	153-158
9748494-11	1998	Molecular modelling of aspirin binding to BuChE indicated perpendicular interactions between the aromatic rings of W82 and aspirin.	Aspirin	23-30	butyrylcholinesterase	Homo sapiens	42-47
9748494-11	1998	Molecular modelling of aspirin binding to BuChE indicated perpendicular interactions between the aromatic rings of W82 and aspirin.	Aspirin	123-130	butyrylcholinesterase	Homo sapiens	42-47
9723822-8	1998	A reduction in P-selectin and GPIIb-IIIa receptor density on non-activated platelets co-incubated with unstimulated neutrophils was associated with NO release from neutrophils, but this was not enhanced by the addition of aspirin.	Aspirin	222-229	selectin P	Homo sapiens	15-25
9250401-0	1997	Potentiation of heat stress-induced hsp70 expression in vivo by aspirin.	Aspirin	64-71	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	36-41
9250401-2	1997	We investigated the influence of aspirin on hsp70 expression in intact rats subjected to heat stress.	Aspirin	33-40	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	44-49
9250401-5	1997	Comparison of hsp70 expression in the treatment groups revealed that in all tissues examined, aspirin-plus-heat treatment resulted in 3-4 fold higher levels of hsp70 mRNA relative to those seen with heat treatment alone.	Aspirin	94-101	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	14-19
9250401-5	1997	Comparison of hsp70 expression in the treatment groups revealed that in all tissues examined, aspirin-plus-heat treatment resulted in 3-4 fold higher levels of hsp70 mRNA relative to those seen with heat treatment alone.	Aspirin	94-101	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	160-165
9250401-7	1997	In keeping with the mRNA expression, Hsp70 protein levels were also elevated in aspirin-plus-heat treated animals.	Aspirin	80-87	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	37-42
9250401-11	1997	This increased hyperthermic response to heat stress probably accounts for the potentiation of hsp70 expression observed in aspirin-plus-heat treated rats.	Aspirin	123-130	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	94-99
9159600-8	1997	As a consequence, lipid therapy and aspirin use have increased greatly among middle aged and older US citizens, especially those with CAD.	Aspirin	36-43	aconitate decarboxylase 1	Homo sapiens	134-137
9476567-3	1997	Aspirin and heparin have been used as therapeutic mainstays for acute coronary syndromes, acting as antiplatelet and antithrombin agents, respectively.	Aspirin	0-7	serpin family C member 1	Homo sapiens	117-129
8641009-4	1996	Thus, we hypothesized that the best concomitant antithrombotic therapy (recombinant [r]-hirudin, heparin, or aspirin) will maximally accelerate thrombolysis by r-tissue-type plasminogen activator (rTPA) and reduce residual thrombus.	Aspirin	109-116	plasminogen activator, tissue type	Rattus norvegicus	197-201
8839134-11	1996	The in vitro studies revealed that only low dose aspirin (10 mg/microliters) stimulated IL-3 production while higher doses of the drug failed to induce the cytokine generation.	Aspirin	49-56	interleukin 3	Homo sapiens	88-92
8839134-14	1996	Low dose aspirin is capable of stimulating IL-3 production in vitro most probably through an elevation of leukotriene production, which may explain its beneficial activity in preventing the manifestations of APS.	Aspirin	9-16	interleukin 3	Homo sapiens	43-47
8835129-1	1996	BACKGROUND: Activation of platelets and expression of adhesion molecules (e.g. CD62P and CD63) which mediate interactions between platelets and other cells may be important in the pathogenesis of aspirin-sensitive asthma.	Aspirin	196-203	selectin P	Homo sapiens	79-84
8835129-1	1996	BACKGROUND: Activation of platelets and expression of adhesion molecules (e.g. CD62P and CD63) which mediate interactions between platelets and other cells may be important in the pathogenesis of aspirin-sensitive asthma.	Aspirin	196-203	CD63 molecule	Homo sapiens	89-93
8835129-2	1996	OBJECTIVE: To determine the expression of CD62P and CD63 on platelets from aspirin-sensitive asthmatic (ASA+), aspirin-tolerant asthmatic (ASA-) and normal subjects and to assess the modulatory effect of aspirin on platelet CD62P and CD63 expression following stimulation with either platelet-activating factor (PAF), arachidonic acid (AA) or collagen (COL).	Aspirin	75-82	selectin P	Homo sapiens	42-47
8835129-2	1996	OBJECTIVE: To determine the expression of CD62P and CD63 on platelets from aspirin-sensitive asthmatic (ASA+), aspirin-tolerant asthmatic (ASA-) and normal subjects and to assess the modulatory effect of aspirin on platelet CD62P and CD63 expression following stimulation with either platelet-activating factor (PAF), arachidonic acid (AA) or collagen (COL).	Aspirin	75-82	CD63 molecule	Homo sapiens	52-56
8835129-2	1996	OBJECTIVE: To determine the expression of CD62P and CD63 on platelets from aspirin-sensitive asthmatic (ASA+), aspirin-tolerant asthmatic (ASA-) and normal subjects and to assess the modulatory effect of aspirin on platelet CD62P and CD63 expression following stimulation with either platelet-activating factor (PAF), arachidonic acid (AA) or collagen (COL).	Aspirin	111-118	selectin P	Homo sapiens	42-47
8835129-2	1996	OBJECTIVE: To determine the expression of CD62P and CD63 on platelets from aspirin-sensitive asthmatic (ASA+), aspirin-tolerant asthmatic (ASA-) and normal subjects and to assess the modulatory effect of aspirin on platelet CD62P and CD63 expression following stimulation with either platelet-activating factor (PAF), arachidonic acid (AA) or collagen (COL).	Aspirin	111-118	selectin P	Homo sapiens	42-47
8549662-7	1996	Parallel to their effect on cell cycle, ASA and indomethacin also reduced the levels of p34cdc2 and p33cdk2, two cyclin-dependent kinases that are important for cell cycle progression.	Aspirin	40-43	cyclin dependent kinase 1	Homo sapiens	88-95
8548426-2	1996	We assessed platelet activation by using flow cytometry to measure platelet surface expression of P-selectin and glycoprotein IIb/IIIa in 20 patients with AMI and 20 with UA, all of whom were treated with aspirin.	Aspirin	205-212	selectin P	Homo sapiens	98-108
8713785-7	1996	Stimulated monocyte TF expression was directly proportional to the platelet count and was reduced by platelet protective anticoagulants and by ingestion of aspirin.	Aspirin	156-163	coagulation factor III, tissue factor	Homo sapiens	20-22
7641350-11	1995	The results of TIMI 7 lend support to the use of an antithrombin agent with aspirin in patients with unstable angina.	Aspirin	76-83	serpin family C member 1	Homo sapiens	52-64
7762021-7	1995	When aspirin (20 mg/kg) was administered 18 hours before embolism and subsequent lysis with TPA (0.3 mg/kg bolus; 3 mg/kg per hour IV), the pretreatment significantly antagonized the rate and extent of TPA-induced clot lysis by up to 70%.	Aspirin	5-12	tissue-type plasminogen activator	Oryctolagus cuniculus	92-95
7762021-7	1995	When aspirin (20 mg/kg) was administered 18 hours before embolism and subsequent lysis with TPA (0.3 mg/kg bolus; 3 mg/kg per hour IV), the pretreatment significantly antagonized the rate and extent of TPA-induced clot lysis by up to 70%.	Aspirin	5-12	tissue-type plasminogen activator	Oryctolagus cuniculus	202-205
7762021-10	1995	CONCLUSIONS: We conclude that aspirin reduces the effects of TPA in embolic stroke models.	Aspirin	30-37	tissue-type plasminogen activator	Oryctolagus cuniculus	61-64
7607578-0	1995	Circadian variations of plasminogen activator activity, tissue-type plasminogen activator antigen, plasminogen activator inhibition and plasmin inhibition in rat aorta, heart and brain are influenced by endotoxin or aspirin or endotoxin plus aspirin.	Aspirin	216-223	plasminogen activator, tissue type	Rattus norvegicus	56-89
7872783-4	1995	Based on these differences between PGHS-1 and PGHS-2, we reasoned that a salicylate ester containing an acyl group somewhat larger than the acetyl group of aspirin might be a selective inhibitor of PGHS-2.	Aspirin	156-163	prostaglandin-endoperoxide synthase 1	Mus musculus	35-41
7805229-9	1995	In conditional logistic regression analyses, the odds ratios of carotid atherosclerosis were, for PAI-1, for example, 1.22, 1.54, and 1.60 in the second, third, and fourth quartiles compared with the first quartile (P &lt; .0001, test of linear trend, adjusting for age, systolic blood pressure, total cholesterol, acetylsalicylic acid use, and time of blood draw).	Aspirin	315-335	serpin family E member 1	Homo sapiens	98-103
8572925-0	1995	Aspirin-like drugs can protect human T lymphocytes against benzoquinone cytotoxicity: evidence for a NAD(P)H:quinone reductase-dependent mechanism.	Aspirin	0-7	crystallin zeta	Homo sapiens	101-126
7804312-6	1994	Furthermore, it was found that low dose aspirin most probably affect positively APLS via inducing an increased production of IL-3 by monocytes.	Aspirin	40-47	interleukin 3	Homo sapiens	125-129
8037708-9	1994	These findings indicate that CINC/gro is produced in pituitary gland and also suggests the possibility that CINC/gro may play some role asa modulator of anterior pituitary function, especially in the cross-talk mechanism between the immune and neuroendocrine systems.	Aspirin	136-139	C-X-C motif chemokine ligand 1	Rattus norvegicus	34-37
8037708-9	1994	These findings indicate that CINC/gro is produced in pituitary gland and also suggests the possibility that CINC/gro may play some role asa modulator of anterior pituitary function, especially in the cross-talk mechanism between the immune and neuroendocrine systems.	Aspirin	136-139	C-X-C motif chemokine ligand 1	Rattus norvegicus	113-116
7945519-2	1994	Acetylsalicylic acid (ASA, CAS 50-78-2) and ibuprofen (IB) are commonly used over-the-counter drugs for short-term treatment of pain of different origin.	Aspirin	0-20	BCAR1 scaffold protein, Cas family member	Homo sapiens	27-30
8273807-3	1994	Epidermal growth factor (EGF), on the other hand, has been shown to be gastroprotective, stimulating DNA synthesis, and preventing ASA-induced gastric ulceration.	Aspirin	131-134	epidermal growth factor	Homo sapiens	0-23
8273807-3	1994	Epidermal growth factor (EGF), on the other hand, has been shown to be gastroprotective, stimulating DNA synthesis, and preventing ASA-induced gastric ulceration.	Aspirin	131-134	epidermal growth factor	Homo sapiens	25-28
8454631-2	1993	Aspirin completely inhibited bis-oxygenation of arachidonate by PGH synthase-1; in contrast, aspirin-treated PGH synthase-2 metabolized arachidonate primarily to 15-hydroxyeicosatetraenoic acid (15-HETE) instead of PGH2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Mus musculus	64-78
8381725-7	1993	Thrombocytopenia induced by t-PA, but not by SK, was partially prevented by aspirin.	Aspirin	76-83	tissue-type plasminogen activator	Oryctolagus cuniculus	28-32
8490954-6	1993	Treatment of muscles with cyclo-oxygenase inhibitors, indomethacin (1 x 10(-5) M) or acetyl salicylic acid (2 x 10(-4) M), abolished the prolongation of action potential duration elicited by IL-1.	Aspirin	85-106	interleukin 1 alpha	Homo sapiens	191-195
7680369-8	1993	Expression on platelets of P-selectin induced by plasma from one patient was independent of whether the donor had taken aspirin.	Aspirin	120-127	selectin P	Homo sapiens	27-37
8430224-0	1993	Acetylsalicylic acid inhibits anticardiolipin antibody-induced platelet-activating factor (PAF) synthesis.	Aspirin	0-20	PCNA clamp associated factor	Homo sapiens	63-89
8430224-0	1993	Acetylsalicylic acid inhibits anticardiolipin antibody-induced platelet-activating factor (PAF) synthesis.	Aspirin	0-20	PCNA clamp associated factor	Homo sapiens	91-94
8430224-3	1993	Since acetylsalicylic acid (ASA) is an accepted therapeutic alternative in these patients, we sought to determine if ASA would attenuate endothelial cell PAF production resulting from ACA exposure.	Aspirin	117-120	PCNA clamp associated factor	Homo sapiens	154-157
8430224-6	1993	ASA consistently decreased ACA-induced PAF synthesis (No ASA, 9573 +/- 443 vs 1mmol/L ASA, 4829 +/- 838 dpm/ml; p = 0.016) and the observed reduction was dose-dependent over a range of ASA concentrations (0.1, 1, 10 and 100 mmol/L; ANOVA, p = .00015).	Aspirin	0-3	PCNA clamp associated factor	Homo sapiens	39-42
8430224-7	1993	Reduced PAF synthesis was also observed in cultures exposed to ASA and incubated with antibody-negative serum.	Aspirin	63-66	PCNA clamp associated factor	Homo sapiens	8-11
8430224-8	1993	These observations suggest that in ACA-positive women, the antithrombotic effects of ASA may relate in part, to reduced endothelial cell PAF synthesis.	Aspirin	85-88	PCNA clamp associated factor	Homo sapiens	137-140
8111770-0	1993	Effect of single oral dose of aspirin on human platelet functions and plasma plasminogen activator inhibitor-1.	Aspirin	30-37	serpin family E member 1	Homo sapiens	77-110
8111770-3	1993	Aspirin demonstrated a rapid onset of action (at 2 h after ingestion) in specifically inhibiting ex vivo AA-mediated functions including (a) fibrinogen binding to gel-purified platelets, (b) platelet aggregation, and (c) platelet PAI-1 release.	Aspirin	0-7	serpin family E member 1	Homo sapiens	230-235
8111770-7	1993	In conclusion, a single oral dose of aspirin has long-acting effects on AA-induced platelet activation and reduces plasma levels of PAI-1 as well.	Aspirin	37-44	serpin family E member 1	Homo sapiens	132-137
8121125-3	1993	Initial PAI activity was lower in the aspirin group presumably due to later admissions of these patients during the day.	Aspirin	38-45	serpin family E member 1	Homo sapiens	8-11
8121125-4	1993	By day 3 activity of PAI increased from 13.5 +/- 2.0 to 18.2 +/- 1.93 U/ml, p = 0.018, and from 17.8 +/- 1.83 to 20.2 +/- 2.44 U/ml, ns, in heparin- and aspirin-treated patients, respectively.	Aspirin	153-160	serpin family E member 1	Homo sapiens	21-24
21043888-6	1993	Having obtained evidence that cathepsin G can function in the presence of plasma, we measured its ability to hydrolyze phosphatidylinositol 4,5-bisphosphate (PtdIns4,5-P2) and generate phosphatidic acid (PtdA) in aspirin-treated platelets.	Aspirin	213-220	cathepsin G	Homo sapiens	30-41
1306782-2	1992	The correlation of severe arrhythmia and administration of aspirin with platelet GMP-140 in AMI were studied respectively.	Aspirin	59-66	selectin P	Homo sapiens	81-88
1540486-0	1992	The effects of varying doses of aspirin on human platelet activation induced by PAF, collagen and arachidonic acid.	Aspirin	32-39	PCNA clamp associated factor	Homo sapiens	80-83
1540486-2	1992	The effect of increasing doses of orally administered aspirin (30-900 mg) on platelet aggregation and ATP release induced by arachidonic acid (AA), collagen and platelet activating factor (PAF) was assessed in 12 normal volunteers.	Aspirin	54-61	PCNA clamp associated factor	Homo sapiens	189-192
1540486-7	1992	The mean maximum degrees of inhibition of platelet aggregation induced by aspirin for AA, collagen and PAF were 100%, 48% and 21% of baseline, respectively.	Aspirin	74-81	PCNA clamp associated factor	Homo sapiens	103-106
1540486-9	1992	The minimum cumulative doses of aspirin producing these effects were 240, 240 and 90 mg for AA, collagen and PAF respectively.	Aspirin	32-39	PCNA clamp associated factor	Homo sapiens	109-112
1540486-13	1992	However, prior to aspirin ingestion, PAF produced a greater maximum response in platelets from females (P less than 0.02) while following aspirin ingestion PAF-induced activation was inhibited to a greater degree in females (P less than 0.02).	Aspirin	138-145	PCNA clamp associated factor	Homo sapiens	156-159
1905593-8	1991	Equipotent doses of Bat-PA and t-PA both resulted in approximate 2.5-fold increases in the template bleeding times of aspirin-pretreated rabbits.	Aspirin	118-125	tissue-type plasminogen activator	Oryctolagus cuniculus	22-26
1782413-4	1991	This paper reviews the mechanisms and possible pathogenetic implication of two related compounds, LT and PAF in acute mucosal injury by topical irritants such as ethanol, aspirin, bile salts and by stress.	Aspirin	171-178	PCNA clamp associated factor	Homo sapiens	105-108
2043486-6	1991	With ASA-treated normal PRP, the patient"s IgG failed to induce aggregation itself, but enhanced ADP- or STA2-induced aggregation.	Aspirin	5-8	WD and tetratricopeptide repeats 1	Homo sapiens	97-101
2147914-2	1990	Ticlopidine and aspirin/dipyridamole, but not xanthinol nicotinate, improved platelet aggregation, reduced beta-thromboglobulin, platelet factor IV and fibrinopeptide A concentrations, and increased antithrombin III concentrations and red blood cell filterability.	Aspirin	16-23	serpin family C member 1	Homo sapiens	199-215
2115784-1	1990	Platelet aggregation induced by threshold concentrations of agonists such as collagen, PAF or epinephrine was inhibited in vitro by 100 microM aspirin but was restored by stimulating platelets with high concentrations of collagen, PAF or by a combination of epinephrine and PAF.	Aspirin	143-150	PCNA clamp associated factor	Homo sapiens	87-90
2115784-2	1990	Incubating aspirin-treated platelets with 50-100 microM vitamin E or vitamin E acetate inhibited platelet aggregation by high concentrations of collagen and PAF and by the combination of epinephrine and PAF; platelet thromboxane A2 formation was less than 10% in samples incubated with 100 microM aspirin.	Aspirin	11-18	PCNA clamp associated factor	Homo sapiens	157-160
2115784-2	1990	Incubating aspirin-treated platelets with 50-100 microM vitamin E or vitamin E acetate inhibited platelet aggregation by high concentrations of collagen and PAF and by the combination of epinephrine and PAF; platelet thromboxane A2 formation was less than 10% in samples incubated with 100 microM aspirin.	Aspirin	11-18	PCNA clamp associated factor	Homo sapiens	203-206
2371491-0	1990	Acetylsalicylic acid inhibits platelet PAI-1 antigen release without affecting circulating PAI-1 antigen in plasma.	Aspirin	0-20	serpin family E member 1	Homo sapiens	39-44
2371491-3	1990	It is presently unknown to what extent the treatment with acetylsalicylic acid (ASA) inhibits platelet PAI-1 release and if release inhibition has an effect on plasma PAI-1 levels.	Aspirin	58-78	serpin family E member 1	Homo sapiens	103-108
2371491-3	1990	It is presently unknown to what extent the treatment with acetylsalicylic acid (ASA) inhibits platelet PAI-1 release and if release inhibition has an effect on plasma PAI-1 levels.	Aspirin	80-83	serpin family E member 1	Homo sapiens	103-108
2371491-4	1990	We therefore investigated by a double-blind placebo-controlled crossover study the effects of oral ASA (500 mg/day for 3 days) on platelet PAI-1 release and on plasma PAI-1 levels of healthy male volunteers.	Aspirin	99-102	serpin family E member 1	Homo sapiens	139-144
2371491-5	1990	The PAI-1 release from platelets stimulated by arachidonic acid and collagen was significantly reduced by ASA: from average values of 88 and 80% to 14 and 17%, respectively (p less than 0.01).	Aspirin	106-109	serpin family E member 1	Homo sapiens	4-9
34742142-3	2021	Our aim was to explore whether serum thromboxane B2 (sTXB2) and soluble P-selectin can be used to identify patients who are at risk of increased platelet reactivity while on aspirin.	Aspirin	174-181	selectin P	Homo sapiens	72-82
34822026-4	2022	Furthermore, we describe other potential benefits related to aspirin-triggered lipoxins and resolvins while illustrating how NSAIDs interfere with COX-1, COX-2, SARS-CoV-2/ SARS-CoV-2 ORF protein-dependent activation of caspases and their subsequent mitochondrial dysfunction, endoplasmic reticulum stress, apoptosis and necroptosis which were associated with COVID-19 complications.	Aspirin	61-68	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	147-152
34203378-0	2021	Aspirin-Triggered Resolvin D1 Reduces Proliferation and the Neutrophil to Lymphocyte Ratio in a Mutant KRAS-Driven Lung Adenocarcinoma Model.	Aspirin	0-7	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	103-107
34071189-10	2021	Furthermore, miR-126, Let-7e and miR-223 expressions in the clopidogrel group were significantly higher than in the ASA group (p = 0.014; p = 0.013; p = 0.028, respectively).	Aspirin	116-119	microRNA 126	Homo sapiens	13-20
35592422-4	2022	Objective: The objective of the study was to investigate the correlation between aspirin use and STA-MCA bypass efficacy, including patency, postoperative neoangiogenesis, and follow-up outcomes.	Aspirin	81-88	GCY	Homo sapiens	97-100
35301267-0	2022	Geographical prevalence of family history in patients with axial spondyloarthritis and its association with HLA-B27 in the ASAS-PerSpA study.	Aspirin	123-127	major histocompatibility complex, class I, B	Homo sapiens	108-115
35197754-9	2022	The linsitinib and aspirin as the IGF1-R antagonists inhibited colon cancer resistance against regorafenib, stem-cell like colon cancer cells growth, decreased expression of CD133, CD44, CD24, and also increased CDX2, PTEN gene expression.	Aspirin	19-26	phosphatase and tensin homolog	Homo sapiens	218-222
35127290-6	2022	Results: SA-beta-gal staining, PCR, and western blot revealed that aspirin could alleviate the cellular expression of senescence-related indicators of BM-MSCs, including a decrease of SA-beta-gal-positive cells and staining intensity, and downregulation of p16, p21, and p53 expression after aspirin treatment.	Aspirin	67-74	H3 histone pseudogene 16	Homo sapiens	262-265
35198081-2	2022	We have evaluated the possibility of CEST MRI of orthotopic breast tumor xenografts with unlabeled aspirin"s conversion to salicylic acid (SA) through various enzymatic activities, most notably inhibition of cyclooxygenase (COX)-1/-2 enzymes.	Aspirin	99-106	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	208-230
34983353-2	2022	By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies.	Aspirin	87-107	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	41-46
34983353-2	2022	By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies.	Aspirin	109-116	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	41-46
2529003-6	1989	Aspirin had no effect on the increment in PAI-1:Ag induced by venous occlusion, but similar to the effect on t-PA:Ag, aspirin induced a 51% inhibition of the increment in t-PA-PAI-1 complex formation.	Aspirin	118-125	serpin family E member 1	Homo sapiens	176-181
2692315-1	1989	Acetylsalicylic acid (ASS) is increasingly used in the prevention of cardiovascular diseases.	Aspirin	0-20	argininosuccinate synthase 1	Homo sapiens	22-25
2576532-0	1989	Liver gamma-glutamyl transpeptidase activity following chronic treatment with acetylsalicylic acid in rats.	Aspirin	78-98	gamma-glutamyltransferase 1	Rattus norvegicus	6-35
2576532-2	1989	Chronic administration of a high dose of ASA (200 mg/kg body weight) resulted in a significant increase in liver plasma membrane gamma-glutamyl transpeptidase activity, cholesterol, and phospholipid levels.	Aspirin	41-44	gamma-glutamyltransferase 1	Rattus norvegicus	129-158
3122357-5	1987	Sodium arachidonate (NaAA)-induced PA was inhibited by 125 mg ASA in all tested methods; since inhibition of ADP-induced PA was not observed in NWB or CWB and the impedance methods failed to show a second wave of ADP-induced PA the significance of the second wave appears doubtful.	Aspirin	62-65	N-acylethanolamine acid amidase	Homo sapiens	21-25
3552746-5	1987	However, the fertilization rate in couples with ASA to sperm head (ASA-H) of at least one isotype in female serum (n = 6) was significantly less than in those without ASA-H (n = 34; 34% versus 74%, P less than 0.01).	Aspirin	48-51	N-acylsphingosine amidohydrolase 1	Homo sapiens	67-72
3582495-2	1987	Whether added to ACD-PRP or ingested by the blood donors, aspirin suppressed the synergic effect of clonidine plus PAF-acether in plasma but failed to block the potentiated aggregation of adrenaline plus PAF-acether.	Aspirin	58-65	PCNA clamp associated factor	Homo sapiens	115-118
3612479-0	1987	[Analysis of traces of organic solvents in microgranules of acetylsalicylic acid coated with HP55].	Aspirin	60-80	DNA polymerase gamma 2, accessory subunit	Homo sapiens	93-97
3612482-0	1987	[Fabrication and coating of microgranules of acetylsalicylic acid: use of HP55].	Aspirin	45-65	DNA polymerase gamma 2, accessory subunit	Homo sapiens	74-78
3576518-1	1987	32P-labelled human platelets loaded with quin 2 and pretreated with aspirin were stimulated with 1-100 nM platelet activating factor (PAF-acether or 1-0-alkyl-2-acetyl-sn-glycero-3-phosphocholine) in a medium containing the ADP-scavenging system creatine phosphate/creatine phosphokinase.	Aspirin	68-75	PCNA clamp associated factor	Homo sapiens	134-137
3100335-4	1987	Aspirin pre-treatment studies and the use of [acetyl-14C]aspirin showed that IL-1 increased PGE2 production through the induction of cyclo-oxygenase.	Aspirin	0-7	interleukin 1 alpha	Homo sapiens	77-81
3443144-1	1987	Plasma aspirin esterase activity and cholinesterase activity were reduced in patients with aspirin sensitive asthma and aspirin sensitive urticaria compared to asthmatic and dermatological controls.	Aspirin	91-98	butyrylcholinesterase	Homo sapiens	37-51
3098249-1	1986	The effect of acetylsalicylic acid (aspirin) on peptic degradation of gastric mucin, its viscosity and the ability to retard the diffusion of hydrogen ion was investigated.	Aspirin	36-43	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	70-83
3715801-5	1986	Ex vivo, dipyridamole, aspirin and the combination of these drugs inhibited the platelet aggregation induced by PAF and AA.	Aspirin	23-30	PCNA clamp associated factor	Homo sapiens	112-115
3706054-2	1986	Inhibition of the cyclo-oxygenase pathway by aspirin prevented the amplification of primary platelet aggregation induced by threshold concentrations of PAF.	Aspirin	45-52	PCNA clamp associated factor	Homo sapiens	152-155
3706054-4	1986	Aspirin also prevented the synergism between PAF and ADP when subthreshold concentrations of both compounds were combined.	Aspirin	0-7	PCNA clamp associated factor	Homo sapiens	45-48
3484709-3	1986	In metiamide-treated tissues, 20 mM SAN caused an immediate fall in potential difference and an increase in resistance; 2 mM SAN and 20 mM ASA produced similar qualitative electrical changes, but only those induced by ASA were reversible.	Aspirin	218-221	N-alpha-acetyltransferase 50, NatE catalytic subunit	Homo sapiens	36-39
3484709-3	1986	In metiamide-treated tissues, 20 mM SAN caused an immediate fall in potential difference and an increase in resistance; 2 mM SAN and 20 mM ASA produced similar qualitative electrical changes, but only those induced by ASA were reversible.	Aspirin	218-221	N-alpha-acetyltransferase 50, NatE catalytic subunit	Homo sapiens	125-128
3923145-0	1985	Amplification of primary response of human platelets to platelet-activating factor: aspirin-sensitive and aspirin-insensitive pathways.	Aspirin	84-91	PCNA clamp associated factor	Homo sapiens	56-82
3923145-0	1985	Amplification of primary response of human platelets to platelet-activating factor: aspirin-sensitive and aspirin-insensitive pathways.	Aspirin	106-113	PCNA clamp associated factor	Homo sapiens	56-82
3923145-1	1985	The irreversible human platelet aggregation induced by threshold concentrations of platelet-activating factor (PAF) in citrated plasma was reversed by aspirin (100 mumol/L, with 10 minutes" preincubation).	Aspirin	151-158	PCNA clamp associated factor	Homo sapiens	83-109
3923145-1	1985	The irreversible human platelet aggregation induced by threshold concentrations of platelet-activating factor (PAF) in citrated plasma was reversed by aspirin (100 mumol/L, with 10 minutes" preincubation).	Aspirin	151-158	PCNA clamp associated factor	Homo sapiens	111-114
3923145-3	1985	The inhibitory effect of aspirin could be overcome by using 10 times higher PAF concentrations or, even more effectively, by combining threshold concentrations of both PAF and one of the other agonists studied (ADP, epinephrine, and U-46619, a stable endoperoxide analog, but not serotonin).	Aspirin	25-32	PCNA clamp associated factor	Homo sapiens	76-79
3923145-3	1985	The inhibitory effect of aspirin could be overcome by using 10 times higher PAF concentrations or, even more effectively, by combining threshold concentrations of both PAF and one of the other agonists studied (ADP, epinephrine, and U-46619, a stable endoperoxide analog, but not serotonin).	Aspirin	25-32	PCNA clamp associated factor	Homo sapiens	168-171
3923145-5	1985	It is concluded that the aspirin-sensitive pathway is sufficient but not necessary to amplify the primary response of human platelets to PAF.	Aspirin	25-32	PCNA clamp associated factor	Homo sapiens	137-140
3927505-0	1985	Human platelet aggregation and release reaction induced by platelet activating factor (PAF-acether)--effects of acetylsalicylic acid and external ionized calcium.	Aspirin	112-132	PCNA clamp associated factor	Homo sapiens	87-90
3927505-4	1985	ASA completely inhibited the platelet secretion induced by low concentrations of PAF-acether, but caused only partial inhibition when platelets were exposed to high concentrations of PAF-acether.	Aspirin	0-3	PCNA clamp associated factor	Homo sapiens	81-84
3927505-4	1985	ASA completely inhibited the platelet secretion induced by low concentrations of PAF-acether, but caused only partial inhibition when platelets were exposed to high concentrations of PAF-acether.	Aspirin	0-3	PCNA clamp associated factor	Homo sapiens	183-186
6636041-4	1983	After administration of aspirin (acetylsalicylic acid), however, AT-III levels increased presumably due to inhibition of coagulation activities.	Aspirin	24-31	serpin family C member 1	Homo sapiens	65-71
6636041-4	1983	After administration of aspirin (acetylsalicylic acid), however, AT-III levels increased presumably due to inhibition of coagulation activities.	Aspirin	33-53	serpin family C member 1	Homo sapiens	65-71
6408754-4	1983	The specific effect of PAF, however, seems to be limited to induce reversible aggregation since second wave of aggregation and serotonin release were suppressed by a combination of acetylsalicylic acid and an ADP scavenging system.	Aspirin	181-201	PCNA clamp associated factor	Homo sapiens	23-26
6825260-4	1983	Use of cholinesterase inhibitor in sample tubes for determination of acetylsalicylic acid and salicylic acid is recommended.	Aspirin	69-89	butyrylcholinesterase	Homo sapiens	7-21
6286928-9	1982	Pretreatment of mice with 100 mg/kg of aspirin, orally, produced a 53% reduction in the elevation of serum ACE produced by carbon tetrachloride.	Aspirin	39-46	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	107-110
7297912-3	1981	Aspirin (at pH 2) and soluble aspirin (pH 4.4) applied topically reduced buccal PD, but this fall was abolished by buffering to pH 7.	Aspirin	30-37	prolyl 4-hydroxylase, transmembrane	Homo sapiens	39-43
314697-3	1979	The permeability coefficient for unionized acetylsalicylic acid increased from 0.27 to 0.43 mumoles, h-1, cm-2, mM-1 when its luminal concentration was increased above 3 mM.	Aspirin	43-63	H1.5 linker histone, cluster member	Homo sapiens	101-104
14773113-0	1950	[Comparison of the effect of serums of various species on acetylcholine and on acetylsalicylic acid (pseudocholinesterase and aspirin-esterase)].	Aspirin	79-99	butyrylcholinesterase	Homo sapiens	101-121
34000466-2	2021	Here, we report that aspirin attenuates the glycolysis and proliferation of hepatoma cells through modulating the levels of lysine 2-hydroxyisobutyrylation (Khib) of enolase 1 (ENO1).	Aspirin	21-28	enolase 1	Homo sapiens	166-175
34000466-2	2021	Here, we report that aspirin attenuates the glycolysis and proliferation of hepatoma cells through modulating the levels of lysine 2-hydroxyisobutyrylation (Khib) of enolase 1 (ENO1).	Aspirin	21-28	enolase 1	Homo sapiens	177-181
34000466-4	2021	Moreover, 4 mM aspirin reduced the activities of ENO1, a key enzyme of glycolysis, and decreased the levels of ENO1 Khib in the cells.	Aspirin	15-22	enolase 1	Homo sapiens	49-53
34000466-4	2021	Moreover, 4 mM aspirin reduced the activities of ENO1, a key enzyme of glycolysis, and decreased the levels of ENO1 Khib in the cells.	Aspirin	15-22	enolase 1	Homo sapiens	111-115
34000466-10	2021	Functionally, ENO1, but not ENO1 mutant (K281R), could rescue the aspirin-induced inhibition of proliferation of liver cancer cells in vitro, suggesting that ENO1K281 is involved in the aspirin-mediated inhibition of liver cancer.	Aspirin	66-73	enolase 1	Homo sapiens	14-18
34000466-10	2021	Functionally, ENO1, but not ENO1 mutant (K281R), could rescue the aspirin-induced inhibition of proliferation of liver cancer cells in vitro, suggesting that ENO1K281 is involved in the aspirin-mediated inhibition of liver cancer.	Aspirin	186-193	enolase 1	Homo sapiens	14-18
33741381-8	2021	Asp-X3-CH3 did not cause significant loss of COX-1 expression in gastric mucosal cells, whereas Asp-X3 and Aspirin both caused significant loss of COX-1 expression as demonstrated by western blot, consistent with their effects on the content of PGE2 in these cells as determined by ELISA assay.	Aspirin	107-114	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	147-152
34039715-10	2021	CONCLUSIONS: Among adult patients with ischaemic-onset MMD undergoing STA-MCA bypass procedures, aspirin might increase the bypass patency rate, without increasing the bleeding risk.	Aspirin	97-104	GCY	Homo sapiens	70-73
33974468-5	2021	RESULTS: The expressions of PR, PRA, and PRB protein were significantly increased in the eutopic endometrium after low-dose aspirin treatment, and the level of PRB mRNA was also increased while the ratio of PRA/PRB mRNA was decreased in the eutopic endometrium.	Aspirin	124-131	progesterone receptor	Rattus norvegicus	28-30
33964802-6	2021	Referring to the anti-inflammatory effects, the most active compound was 6i, which was more active than IND and aspirin (ASP) in term of denaturation effect, on bovine serum albumin (BSA), as indirect assay to predict the anti-inflammatory effect.	Aspirin	112-119	assembly factor for spindle microtubules	Homo sapiens	121-124
32299908-1	2021	We have identified a rare missense variant on chromosome 9, position 125145990 (GRCh37), in exon 8 in PTGS1 (the gene encoding cyclo-oxygenase 1, COX-1, the target of anti-thrombotic aspirin therapy).	Aspirin	183-190	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	146-151
33917483-4	2021	Here, we report that aspirin markedly induces CREB/ATF1 phosphorylation in HCC cells, which compromises aspirin"s anti-HCC effect.	Aspirin	21-28	activating transcription factor 1	Homo sapiens	51-55
33917483-4	2021	Here, we report that aspirin markedly induces CREB/ATF1 phosphorylation in HCC cells, which compromises aspirin"s anti-HCC effect.	Aspirin	104-111	activating transcription factor 1	Homo sapiens	51-55
33917483-5	2021	Inhibition of AMP-activated protein kinase (AMPK) abrogates the induction of CREB/ATF1 phosphorylation by aspirin.	Aspirin	106-113	activating transcription factor 1	Homo sapiens	82-86
33917483-7	2021	Treatment with aspirin or CPS1 knockdown stimulates soluble adenylyl cyclase expression, thereby increasing cyclic AMP (cAMP) synthesis and stimulating PKA-CREB/ATF1 signaling.	Aspirin	15-22	activating transcription factor 1	Homo sapiens	161-165
33917483-8	2021	Importantly, abrogation of aspirin-induced CREB/ATF1 phosphorylation could sensitize HCC to aspirin.	Aspirin	27-34	activating transcription factor 1	Homo sapiens	48-52
33917483-8	2021	Importantly, abrogation of aspirin-induced CREB/ATF1 phosphorylation could sensitize HCC to aspirin.	Aspirin	92-99	activating transcription factor 1	Homo sapiens	48-52
32973115-12	2021	Assessment of platelet surface P-selectin revealed: aspirin test 528 [317, 834], >500 54.8%; clopidogrel test 429 [303, 656], >860 11.3%.	Aspirin	52-59	selectin P	Homo sapiens	31-41
33637594-8	2021	CD38highCD117high MCs are distinct from circulating MC progenitors and are enriched for proliferation, which is markedly increased in CRSwNP patients with aspirin-exacerbated respiratory disease, a severe disease subset characterized by increased MC burden and elevated MC activation.	Aspirin	155-162	CD38 molecule	Homo sapiens	0-4
33222458-11	2021	Moreover, XST+ASA+CLP group also had lower levels of NOX2, inducible nitric oxide synthase (iNOS), interleukin (IL)-6, and p-STAT3/STAT3.	Aspirin	14-17	signal transducer and activator of transcription 3	Rattus norvegicus	125-130
33222458-11	2021	Moreover, XST+ASA+CLP group also had lower levels of NOX2, inducible nitric oxide synthase (iNOS), interleukin (IL)-6, and p-STAT3/STAT3.	Aspirin	14-17	signal transducer and activator of transcription 3	Rattus norvegicus	131-136
33222458-12	2021	CONCLUSIONS: These results demonstrate that a combination of XST, ASA, and CLP effectively protected rats against middle cerebral artery occlusion/reperfusion (MCAO/R) injury by suppressing the NOX2/IL-6/ STAT3 pathway.	Aspirin	66-69	signal transducer and activator of transcription 3	Rattus norvegicus	205-210
33455983-5	2021	Genetic testing found that both cytochrome P450 2C19 (CYP2C19) (G681A) and glycoprotein Ia (GPIa) (C807T, G873A) were hybrid mutant types, demonstrating that the patient was possibly resistant to clopidogrel and aspirin simultaneously.	Aspirin	212-219	multimerin 1	Homo sapiens	75-90
33455983-5	2021	Genetic testing found that both cytochrome P450 2C19 (CYP2C19) (G681A) and glycoprotein Ia (GPIa) (C807T, G873A) were hybrid mutant types, demonstrating that the patient was possibly resistant to clopidogrel and aspirin simultaneously.	Aspirin	212-219	multimerin 1	Homo sapiens	92-96
33610409-2	2021	The purpose of this study was to determine the safety of ASA for venous thromboembolism (VTE) prophylaxis after total joint arthroplasty in patients with prior history of gastrointestinal (GI) issues.	Aspirin	57-60	G protein subunit alpha i1	Homo sapiens	189-191
33610409-11	2021	In logistic regression analysis, ASA was associated with a protective effect against GI bleed (OR = 0.09, 95% CI 0.01-0.40, P = .003).	Aspirin	33-36	G protein subunit alpha i1	Homo sapiens	85-87
33610409-12	2021	CONCLUSION: ASA is safe for VTE prophylaxis after total joint arthroplasty in patients with history of GI issues and is not associated with an increased risk of postoperative GI bleeds.	Aspirin	12-15	G protein subunit alpha i1	Homo sapiens	103-105
33230059-11	2021	CONCLUSION: Proton pump inhibitor was superior to histamine-2 receptor antagonist in the prevention of gastroduodenal mucosal breaks in high-risk users of low-dose aspirin, and smoking was an independent risk factor for developing gastroduodenal mucosal breaks.	Aspirin	164-171	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	12-23
33285161-10	2021	The administration of LTD4 to Ptges-/- mice, which display enhanced LTC4 synthesis similar to aspirin exacerbated respiratory disease (AERD), completely blocked the physiologic response to subsequent lysine-aspirin inhalation challenges, as well as increases in IL-33, type 2 cytokines, and biochemical markers of mast cell and platelet activation.	Aspirin	207-214	prostaglandin E synthase	Mus musculus	30-35
33125972-5	2020	MTT, ARS results show that the cell mineralization and viability of Asp-Sr/beta-TCP group is significantly higher than Control group, beta-TCP group and Sr/beta-TCP group.	Aspirin	68-71	SRP receptor subunit beta	Rattus norvegicus	72-79
33125972-7	2020	X-ray images, Micro-CT and Histological analysis evaluation show that, group Asp-Sr/beta-TCP presented the strongest effect on bone regeneration and bone mineralization, when compared with beta-TCP group and Sr/beta-TCP group.	Aspirin	77-80	SRP receptor subunit beta	Rattus norvegicus	81-88
33125972-8	2020	RT-qPCR analysis show that Asp-Sr/beta-TCP, beta-TCP group and Sr/beta-TCP group showed increased BMP2, Smad1, OPG than the OVX group(p < 0.05), while Asp-Sr/beta-TCP exhibited decreased TNF-alpha IFN-gamma and RANKL than the OVX group(p < 0.05).	Aspirin	27-30	SRP receptor subunit beta	Rattus norvegicus	31-38
33125972-8	2020	RT-qPCR analysis show that Asp-Sr/beta-TCP, beta-TCP group and Sr/beta-TCP group showed increased BMP2, Smad1, OPG than the OVX group(p < 0.05), while Asp-Sr/beta-TCP exhibited decreased TNF-alpha IFN-gamma and RANKL than the OVX group(p < 0.05).	Aspirin	27-30	TNF receptor superfamily member 11B	Rattus norvegicus	111-114
33125972-8	2020	RT-qPCR analysis show that Asp-Sr/beta-TCP, beta-TCP group and Sr/beta-TCP group showed increased BMP2, Smad1, OPG than the OVX group(p < 0.05), while Asp-Sr/beta-TCP exhibited decreased TNF-alpha IFN-gamma and RANKL than the OVX group(p < 0.05).	Aspirin	27-30	interferon gamma	Rattus norvegicus	197-206
33184378-5	2020	In both in vivo and in vitro models, SA and ASA triggered endoplasmic reticulum (ER) stress, which culminates with the upregulation of the pro-apoptotic transcription factor C/EBP homologous protein (CHOP).	Aspirin	44-47	DNA-damage inducible transcript 3	Mus musculus	174-198
33184378-5	2020	In both in vivo and in vitro models, SA and ASA triggered endoplasmic reticulum (ER) stress, which culminates with the upregulation of the pro-apoptotic transcription factor C/EBP homologous protein (CHOP).	Aspirin	44-47	DNA-damage inducible transcript 3	Mus musculus	200-204
33184378-6	2020	These effects are initiated by ASA/SA-triggered Akt/mTOR/AMPK-dependent activation of nitric oxide synthase 3 (eNOS), which increases nitric oxide and reactive oxygen species production inducing ER stress response.	Aspirin	31-34	mechanistic target of rapamycin kinase	Mus musculus	52-56
33313269-12	2020	Mitochondrial vacuolation and autophagy were inhibited, as evidenced by reduced level of autophagy related proteins PINK1, BNIP3, LC3B and Atg7 in mice treated with aspirin compared with mice treated with saline.	Aspirin	165-172	PTEN induced putative kinase 1	Mus musculus	116-121
33049446-5	2020	Under salt stress, the SlSOS1/2 and SlNHX1 genes were highly expressed, and the accumulation of Na+ was lower in the transgenic seedlings than in WT, however, ROS accumulated to a greater degree in the former, and the ROS-scavenging-related enzyme activities and AsA content were lower in the transgenic seedlings than WT.	Aspirin	263-266	plasmalemma Na+/H+ antiporter	Solanum lycopersicum	23-31
32896555-0	2020	Aspirin restores endothelial function by mitigating 17beta-estradiol-induced alpha-SMA accumulation and autophagy inhibition via Vps15 scaffold regulation of Beclin-1 phosphorylation.	Aspirin	0-7	beclin 1, autophagy related	Mus musculus	158-166
32896555-7	2020	Aspirin promoted Beclin1 phosphorylation in autophagy initiation complexes and enhanced autophagy.	Aspirin	0-7	beclin 1, autophagy related	Mus musculus	17-24
32299015-1	2020	Aspirin-exacerbated respiratory disease (AERD) classically presents with severe asthma, nasal polyposis, and respiratory exacerbations in response to cyclooxygenase (COX)-1 inhibition.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	150-172
32302241-0	2020	Is aspirin a substrate of MDR1/P-glycoprotein?	Aspirin	3-10	ATP-binding cassette, sub-family B (MDR/TAP), member 1	Sus scrofa	26-30
32302241-3	2020	We observed significantly lower cellular uptake of acetyl salicylic acid in MDR1 transfected LLC-PK1 cells compared to LLC-PK1 wild-type (WT) cells, however, the in vitro efflux of acetyl salicylic acid in MDR1 transfected LLC-PK1 cells was not inhibited by known inhibitors under various conditions.	Aspirin	51-72	ATP-binding cassette, sub-family B (MDR/TAP), member 1	Sus scrofa	76-80
32302241-3	2020	We observed significantly lower cellular uptake of acetyl salicylic acid in MDR1 transfected LLC-PK1 cells compared to LLC-PK1 wild-type (WT) cells, however, the in vitro efflux of acetyl salicylic acid in MDR1 transfected LLC-PK1 cells was not inhibited by known inhibitors under various conditions.	Aspirin	51-72	ATP-binding cassette, sub-family B (MDR/TAP), member 1	Sus scrofa	206-210
32302241-3	2020	We observed significantly lower cellular uptake of acetyl salicylic acid in MDR1 transfected LLC-PK1 cells compared to LLC-PK1 wild-type (WT) cells, however, the in vitro efflux of acetyl salicylic acid in MDR1 transfected LLC-PK1 cells was not inhibited by known inhibitors under various conditions.	Aspirin	181-202	ATP-binding cassette, sub-family B (MDR/TAP), member 1	Sus scrofa	76-80
32302241-3	2020	We observed significantly lower cellular uptake of acetyl salicylic acid in MDR1 transfected LLC-PK1 cells compared to LLC-PK1 wild-type (WT) cells, however, the in vitro efflux of acetyl salicylic acid in MDR1 transfected LLC-PK1 cells was not inhibited by known inhibitors under various conditions.	Aspirin	181-202	ATP-binding cassette, sub-family B (MDR/TAP), member 1	Sus scrofa	206-210
32994805-7	2020	Further research showed that the anti-tumor effect of celecoxib combined with aspirin was mainly produced by activating caspase-9/caspase-3, arresting cell cycle and inhibiting the ERK-MAPK signaling pathway.	Aspirin	78-85	caspase 9	Homo sapiens	120-129
32842685-0	2020	Identification of the Effects of Aspirin and Sulindac Sulfide on the Inhibition of HMGA2-Mediated Oncogenic Capacities in Colorectal Cancer.	Aspirin	33-40	high mobility group AT-hook 2	Homo sapiens	83-88
32842685-5	2020	In this study, we identified aspirin and sulindac sulfide as novel potential inhibitors of HMGA2 using a genome-wide mRNA signature-based approach.	Aspirin	29-36	high mobility group AT-hook 2	Homo sapiens	91-96
32842685-6	2020	In addition, aspirin and sulindac sulfide induced cytotoxicity of CRC cells stably expressing HMGA2 by inhibiting cell proliferation and migration.	Aspirin	13-20	high mobility group AT-hook 2	Homo sapiens	94-99
32842685-8	2020	Collectively, this is the first study to report that aspirin and sulindac sulfide are novel potential inhibitors of HMGA2, which can induce cytotoxicity of CRC cells stably expressing HMGA2 by inhibiting cell proliferation and migration through influencing inflammatory-response genes, the majority of which are involved in GPCR signaling.	Aspirin	53-60	high mobility group AT-hook 2	Homo sapiens	116-121
32842685-8	2020	Collectively, this is the first study to report that aspirin and sulindac sulfide are novel potential inhibitors of HMGA2, which can induce cytotoxicity of CRC cells stably expressing HMGA2 by inhibiting cell proliferation and migration through influencing inflammatory-response genes, the majority of which are involved in GPCR signaling.	Aspirin	53-60	high mobility group AT-hook 2	Homo sapiens	184-189
32842685-8	2020	Collectively, this is the first study to report that aspirin and sulindac sulfide are novel potential inhibitors of HMGA2, which can induce cytotoxicity of CRC cells stably expressing HMGA2 by inhibiting cell proliferation and migration through influencing inflammatory-response genes, the majority of which are involved in GPCR signaling.	Aspirin	53-60	C-X-C motif chemokine receptor 6	Homo sapiens	324-328
32629916-6	2020	The results revealed that aspirin inhibited macrophage chemoattractant protein (MCP-1), interleukin (IL-6), IL-1beta, and plasminogen activator inhibitor (PAI-1) production in 3T3-L1 adipocytes stimulated by tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS).	Aspirin	26-33	interleukin 1 alpha	Mus musculus	108-116
32629916-6	2020	The results revealed that aspirin inhibited macrophage chemoattractant protein (MCP-1), interleukin (IL-6), IL-1beta, and plasminogen activator inhibitor (PAI-1) production in 3T3-L1 adipocytes stimulated by tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS).	Aspirin	26-33	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	155-160
32239624-6	2020	The combination of osimertinib and aspirin induced strong anti-proliferative and proapoptotic effects in osimertinib-resistant NSCLC cells through inhibition of Akt/FoxO3a signaling component phosphorylation and increased Bim expression.	Aspirin	35-42	BCL2 like 11	Homo sapiens	222-225
32239624-7	2020	Furthermore, Bim knockdown by siRNA significantly attenuated osimertinib resensitization by aspirin.	Aspirin	92-99	BCL2 like 11	Homo sapiens	13-16
32239624-11	2020	In summary, aspirin synergistically enhances the antitumor activity of osimertinib in osimertinib-resistant lung cancer cells through promoting Bim-dependent apoptosis.	Aspirin	12-19	BCL2 like 11	Homo sapiens	144-147
32058295-0	2020	Regular aspirin intake and prognosis of TxN2-3M0 nasopharyngeal carcinoma: A cohort study based on propensity score matching.	Aspirin	8-15	thioredoxin 2	Homo sapiens	40-44
32258142-9	2020	In conclusion, aspirin can systemically and simultaneously ameliorate NAFLD and atherosclerosis by inhibiting lipid biosynthesis and inflammation and by elevating catabolic metabolism through the activation of the PPARdelta-AMPK-PGC-1alpha pathway.	Aspirin	15-22	PPARG coactivator 1 alpha	Sus scrofa	229-239
31653513-7	2020	CONCLUSION: Besides markedly lowering LDL-c levels, our results suggest that HC patients benefit from anti-PCSK9 mAb treatment also for reducing platelet reactivity and increasing platelet sensitivity to the inhibitory effects of aspirin.	Aspirin	230-237	proprotein convertase subtilisin/kexin type 9	Homo sapiens	107-112
31815277-9	2020	Chromatin immunoprecipitation assays using acetyl-H3K56 or acetyl-H3K122 antibody revealed that aspirin blocked the TGFbeta2-induced acetylation of H3K56 and H3K122 at the promoter regions of ACTA2 and COL1A.	Aspirin	96-103	actin alpha 2, smooth muscle	Homo sapiens	192-197
32238706-8	2020	Administration of non-steroidal anti-inflammatory drugs, namely aspirin and etodolac, to inhibit prostanoid synthesis suppressed the biased expression of Th1- and Th2-cytokines as well as molecular markers of Th1 and Th2 cells in the diet-restricted thymus, without affecting the reduction of thymus size.	Aspirin	64-71	heart and neural crest derivatives expressed 2	Mus musculus	163-166
32238706-8	2020	Administration of non-steroidal anti-inflammatory drugs, namely aspirin and etodolac, to inhibit prostanoid synthesis suppressed the biased expression of Th1- and Th2-cytokines as well as molecular markers of Th1 and Th2 cells in the diet-restricted thymus, without affecting the reduction of thymus size.	Aspirin	64-71	heart and neural crest derivatives expressed 2	Mus musculus	217-220
31746356-11	2020	Based on the present results, it is suggested that 2,3-DHBA and 2,5-DHBA may contribute to the chemopreventive properties of aspirin, possibly through the inhibition of CDKs.	Aspirin	125-132	cyclin dependent kinase 1	Homo sapiens	169-173
31805984-0	2019	Aspirin inhibits RANKL-induced osteoclast differentiation in dendritic cells by suppressing NF-kappaB and NFATc1 activation.	Aspirin	0-7	nuclear factor of activated T-cells 1	Rattus norvegicus	106-112
31625710-0	2019	Aspirin reduces the incidence of postmenopausal osteoporosis in rats through OPG-RANKL-RANK signaling pathway.	Aspirin	0-7	TNF receptor superfamily member 11B	Rattus norvegicus	77-80
31824307-0	2019	Wnt/beta-Catenin Pathway-Regulated Fibromodulin Expression Is Crucial for Breast Cancer Metastasis and Inhibited by Aspirin.	Aspirin	116-123	catenin beta 1	Homo sapiens	4-16
31824307-4	2019	Aspirin inhibits BCCMI by attenuating Wnt/beta-catenin signaling and suppressing FMOD expression via inhibiting deacetylation of beta-catenin by histone deacetylase 6 (HDAC6) leading to beta-catenin phosphorylation and cytoplasmic degradation.	Aspirin	0-7	catenin beta 1	Homo sapiens	42-54
31824307-4	2019	Aspirin inhibits BCCMI by attenuating Wnt/beta-catenin signaling and suppressing FMOD expression via inhibiting deacetylation of beta-catenin by histone deacetylase 6 (HDAC6) leading to beta-catenin phosphorylation and cytoplasmic degradation.	Aspirin	0-7	catenin beta 1	Homo sapiens	129-141
31824307-4	2019	Aspirin inhibits BCCMI by attenuating Wnt/beta-catenin signaling and suppressing FMOD expression via inhibiting deacetylation of beta-catenin by histone deacetylase 6 (HDAC6) leading to beta-catenin phosphorylation and cytoplasmic degradation.	Aspirin	0-7	catenin beta 1	Homo sapiens	129-141
31824307-6	2019	Our findings identify a critical role of FMOD in cancer metastasis, reveal a mechanism regulating FMOD transcription and impacting tumor metastasis, uncover action targets and mechanism for the anticancer activity of Aspirin, and expand the understanding of the Wnt/beta-catenin pathway and tumor metastasis, which are valuable for development of cancer therapeutics.	Aspirin	217-224	catenin beta 1	Homo sapiens	266-278
31228190-0	2019	Genetic variation at the coronary artery disease risk locus GUCY1A3 modifies cardiovascular disease prevention effects of aspirin.	Aspirin	122-129	guanylate cyclase 1 soluble subunit alpha 1	Homo sapiens	60-67
31228190-1	2019	AIMS: Efficacy of aspirin in primary prevention of cardiovascular disease (CVD) may be influenced by a common allele in guanylate cyclase GUCY1A3, which has been shown to modify platelet function and increase CVD risk.	Aspirin	18-25	guanylate cyclase 1 soluble subunit alpha 1	Homo sapiens	138-145
31228190-2	2019	METHODS AND RESULTS: We investigated whether homozygotes of the GUCY1A3 rs7692387 risk (G) allele benefited from aspirin in two long-term, randomized placebo-controlled trials of aspirin in primary CVD prevention: the Women"s Genome Health Study (WGHS, N = 23 294) and a myocardial infarction (MI, N = 550) and stroke (N = 382) case-control set from the Physician"s Health Study (PHS, N = 22 071).	Aspirin	113-120	guanylate cyclase 1 soluble subunit alpha 1	Homo sapiens	64-71
31228190-7	2019	CONCLUSION: In two randomized placebo-controlled trials in the setting of primary prevention, aspirin reduced the incidence of CVD events in individuals homozygous for the GUCY1A3 risk (G) allele, whereas heterozygote individuals had more events when taking aspirin.	Aspirin	94-101	guanylate cyclase 1 soluble subunit alpha 1	Homo sapiens	172-179
31543315-1	2019	BACKGROUND: About one third of all patients with proximal femur fractures take oral anticoagulation like aspirin (ASS), direct platelet aggregation inhibitors like Clopidogrel and Ticagrelor (PAI), vitamin-K-antagonists like Warfarin (VKA) and direct oral anticoagulants like Rivaroxaban, Dabigatran and Apixaban (DOAC).	Aspirin	105-112	serpin family E member 1	Homo sapiens	192-195
31801720-11	2019	Western blotting showed that aspirin could down-regulate the expression levels of several pivotal proteins that regulated cell cycle and cell division, including CDC25C, TPX2, CDC20 and PLK1.	Aspirin	29-36	cell division cycle 25C	Homo sapiens	162-168
31801720-12	2019	CONCLUSIONS: CDC25C, TPX2, CDC20 and PLK1 may be potential targets for aspirin to inhibit the proliferation of human breast cancer cells, by affecting the progress of cell cycle and cell division.	Aspirin	71-78	cell division cycle 25C	Homo sapiens	13-19
31663307-0	2019	Aspirin inhibits proliferation and promotes apoptosis of hepatocellular carcinoma cells via wnt/beta-catenin signaling pathway.	Aspirin	0-7	catenin beta 1	Homo sapiens	96-108
30920641-2	2019	OBJECTIVES: To examine the association between aspirin and NSAID (nonaspirin) use and the risk of BCC and SCC in a large cohort specifically designed for skin cancer outcomes.	Aspirin	47-54	serpin family B member 3	Homo sapiens	106-109
30920641-4	2019	We used Cox proportional hazards models to estimate the hazard ratios (HRs) between self-reported aspirin and NSAID use 1 year prior to study baseline and the first histologically confirmed BCC or SCC for high-risk (history of skin cancer excisions or more than five actinic lesions treated) and average-to-low-risk participants (no history of skin cancer excision and at most five actinic lesions treated).	Aspirin	98-105	serpin family B member 3	Homo sapiens	197-200
30920641-7	2019	Aspirin use was associated with reduced risk of SCC (HR 0 77, 95% confidence interval 0 64-0 93) only among infrequent (less than weekly) users and was not associated with BCC.	Aspirin	0-7	serpin family B member 3	Homo sapiens	48-51
31220426-11	2019	RESULTS: Overall Mo from control subjects exposed to ASA showed increased secretion of IL-1RA, IL-8, MCP-1, and TNF-alpha and Mo from stroke patients showed greater release of IL-1RA and MCP-1.	Aspirin	53-56	interleukin 1 receptor antagonist	Homo sapiens	87-93
31220426-11	2019	RESULTS: Overall Mo from control subjects exposed to ASA showed increased secretion of IL-1RA, IL-8, MCP-1, and TNF-alpha and Mo from stroke patients showed greater release of IL-1RA and MCP-1.	Aspirin	53-56	C-C motif chemokine ligand 2	Homo sapiens	101-106
31220426-13	2019	In addition, in co-cultures independent of Mo origin, ASA reduced IL-6, IL-8, MCP-1, and TNF-alpha.	Aspirin	54-57	C-C motif chemokine ligand 2	Homo sapiens	78-83
32123852-7	2019	Moreover, aspirin reduced p53 and p21 accumulation in DOX-treated human and mouse fibroblasts.	Aspirin	10-17	H3 histone pseudogene 16	Homo sapiens	34-37
32123852-8	2019	However, the suppressive effect of aspirin on DOX-induced p53 accumulation was significantly decreased in COX2 knockout mouse embryonic fibroblasts.	Aspirin	35-42	transformation related protein 53, pseudogene	Mus musculus	58-61
30907747-0	2019	Aspirin blocks formation of metastatic intravascular niches by inhibiting platelet-derived COX-1/thromboxane A2.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Mus musculus	91-96
30907747-5	2019	Here, we have shown that aspirin dramatically reduced lung metastasis through inhibition of COX-1 while the cancer cells remained intravascular and that inhibition of platelet COX-1 alone was sufficient to impair metastasis.	Aspirin	25-32	prostaglandin-endoperoxide synthase 1	Mus musculus	92-97
30017554-10	2019	CONCLUSIONS: MC-intrinsic COX-1 amplifies IL-33-induced activation in the setting of innate type 2 immunity and might help explain the phenomenon of therapeutic desensitization to aspirin by nonselective COX inhibitors in patients with AERD.	Aspirin	180-187	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	26-31
30677414-7	2019	Irreversible inactivation of platelet cyclooxygenase 1 by acetylsalicylic acid did not reduce BjV-induced platelet aggregation.	Aspirin	58-78	prostaglandin-endoperoxide synthase 1	Mus musculus	38-54
30737317-9	2019	Nonsteroidal anti-inflammatory drugs (e.g. aspirin, ibuprofen, and naproxen) block PG synthesis by inhibiting COX-1 and COX-2.	Aspirin	43-50	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	110-115
31530979-8	2019	Furthermore, the results seem to imply that ASA and KET have certain potential to induce Foxp3 expression in CD25+CD8+ and CD25+CD4+ T cells, respectively.	Aspirin	44-47	forkhead box P3	Mus musculus	89-94
29985735-4	2019	All cyclo-oxygenase (COX-1)-dependent tests and some COX-1-independent tests (PFA-CEPI, LTA-ADP) demonstrated significant reductions in platelet reactivity with all ASA doses.	Aspirin	165-168	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	21-26
29985735-4	2019	All cyclo-oxygenase (COX-1)-dependent tests and some COX-1-independent tests (PFA-CEPI, LTA-ADP) demonstrated significant reductions in platelet reactivity with all ASA doses.	Aspirin	165-168	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	53-58
30556891-6	2018	RESULTS: In 12Z cells, aspirin and other NSAIDs enhanced MRP4 mRNA and protein expression; these treatments also induced PPARa expression.	Aspirin	23-30	peroxisome proliferator activated receptor alpha	Homo sapiens	121-126
30556891-7	2018	Aspirin and diclofenac-induced increases in MRP4 expression were not observed in cells where PPARa was knocked down using siRNA.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Homo sapiens	93-98
29611728-5	2018	First, we investigated the cytotoxic effect of aspirin on the intestinal epithelial cell line in rats at a high concentration, and found that aspirin significantly decreased heat shock protein 70 expression, increased reactive oxygen species production, and increased epithelial cell apoptosis.	Aspirin	142-149	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	174-195
30560156-1	2018	This data article associated with the manuscript "A high glucose levels is associated with decreased aspirin-mediated acetylation of platelet cyclooxygenase (COX)-1 at serine 529: a pilot study" (Finamore et al., 2018) refers to the shotgun proteomics approach carried out on platelet protein extracts from diabetic patients and healthy controls.	Aspirin	101-108	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	142-164
30389909-10	2018	Notably, aspirin attenuates E2-induced cancer stem-like traits through decreasing both H19 and ERbeta expression.	Aspirin	9-16	H19 imprinted maternally expressed transcript	Homo sapiens	87-90
30392338-0	2018	[Aspirin inhibits cell stemness of esophageal cancer by downregulation of chemokine CCL2].	Aspirin	1-8	C-C motif chemokine ligand 2	Homo sapiens	84-88
30392338-8	2018	When chemokine CCL2 was knocked down, the levels of Nanog gene in M2+ shCCL2-KYSE450+ ASA group and M2+ shCCL2-KYSE450 group were decreased to 1.22+-0.11 and 1.17+-0.08, respectively, and there was no statistically significant difference between them (P=0.69).	Aspirin	86-89	C-C motif chemokine ligand 2	Homo sapiens	15-19
30392338-9	2018	Flow cytometry analyses showed that the expression levels of CD90 in control and ASA cells were (2.93+-0.52)% and (1.30+-0.17)%, respectively, and the difference was statistically significant (P&lt;0.05).	Aspirin	81-84	Thy-1 cell surface antigen	Homo sapiens	61-65
30392338-11	2018	Conclusions: Tumor-associated macrophages enhances the stemness of esophageal cancer cells, whereas aspirin attenuates the stemness by suppressing the expression of CCL2.	Aspirin	100-107	C-C motif chemokine ligand 2	Homo sapiens	165-169
30416852-1	2018	The current work studied the chemopreventive efficacy of orally administered chitosan coated solid-lipid nanoparticle (c-SLN) encapsulated aspirin (ASP), curcumin (CUR) and free sulforaphane (SFN), ACS-cSLN, in the LSL-Kras G12D/+; Pdx-1 Cre/+ transgenic mouse model of pancreatic ductal adenocarcinoma (PDAC).	Aspirin	139-146	sarcolipin	Mus musculus	121-124
29897665-3	2018	Given that altered AA metabolism is associated with aspirin-exacerbated respiratory disease (AERD), we hypothesized that expression of the CB2R gene CNR2 is increased in AERD.	Aspirin	52-59	cannabinoid receptor 2	Homo sapiens	149-153
30280037-9	2018	Analysis using the cBio portal indicated that aspirin might have effects on multiple tumor suppressors, such as TP53, PTEN, and RB1 and that TP53 might play a central role in aspirin-associated genes.	Aspirin	46-53	phosphatase and tensin homolog	Homo sapiens	118-122
30214631-0	2018	Aspirin cooperates with p300 to activate the acetylation of H3K9 and promote FasL-mediated apoptosis of cancer stem-like cells in colorectal cancer.	Aspirin	0-7	Fas ligand	Homo sapiens	77-81
30214631-9	2018	Furthermore, aspirin directly interacts with p300 in the nucleus, promotes H3K9 acetylation, activates FasL expression, and induces apoptosis in colorectal CSCs.	Aspirin	13-20	Fas ligand	Homo sapiens	103-107
30214631-12	2018	Conclusions: Taken together, we revealed a unique epigenetic and cox-independent pathway (p300-AcH3K9-FasL axis) by which aspirin eliminates colorectal CSCs.	Aspirin	122-129	Fas ligand	Homo sapiens	102-106
29885857-3	2018	Gentisic acid (GA) is a minor catabolite of aspirin; yet humans carrying CYP2C9-variants incapable to catabolize aspirin to GA do not benefit from aspirin in prevention against colonic adenoma.	Aspirin	113-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
29885857-3	2018	Gentisic acid (GA) is a minor catabolite of aspirin; yet humans carrying CYP2C9-variants incapable to catabolize aspirin to GA do not benefit from aspirin in prevention against colonic adenoma.	Aspirin	113-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
29922884-0	2018	Comment on "Targeting AMPK, mTOR and beta-Catenin by Combined Metformin and Aspirin Therapy in HCC: An Appraisal in Egyptian HCC Patients".	Aspirin	76-83	catenin beta 1	Homo sapiens	37-49
29792865-7	2018	Such aspirin-induced changes of ABT-737 resistance was accompanied by a host of biochemical events like protein phosphatase 2A (PP2A) activation, AKT dephosphorylation, Mcl-1/FLICE inhibiting protein (FLIP)/XIAP downregulation, and Bax mitochondrial redistribution.	Aspirin	5-12	protein phosphatase 2 phosphatase activator	Homo sapiens	112-126
29792865-7	2018	Such aspirin-induced changes of ABT-737 resistance was accompanied by a host of biochemical events like protein phosphatase 2A (PP2A) activation, AKT dephosphorylation, Mcl-1/FLICE inhibiting protein (FLIP)/XIAP downregulation, and Bax mitochondrial redistribution.	Aspirin	5-12	protein phosphatase 2 phosphatase activator	Homo sapiens	128-132
29792865-7	2018	Such aspirin-induced changes of ABT-737 resistance was accompanied by a host of biochemical events like protein phosphatase 2A (PP2A) activation, AKT dephosphorylation, Mcl-1/FLICE inhibiting protein (FLIP)/XIAP downregulation, and Bax mitochondrial redistribution.	Aspirin	5-12	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	169-174
29792865-10	2018	Since PP2A, Akt, and Mcl-1 play critical roles in RCC malignancy and treatment resistance, our present study showed that aspirin, an alternative adjuvant agent, had recalled ABT-737 sensitivity in the RCC cells through processes involving the PP2A/Akt/Mcl-1 axis.	Aspirin	121-128	protein phosphatase 2 phosphatase activator	Homo sapiens	6-10
30034291-7	2018	Treatment with aspirin inhibited 4T1 cell growth and migration and MCP-1, PAI-1, and IL-6 production.	Aspirin	15-22	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	74-79
30069194-7	2018	In addition to the well-researched antiplatelet effect, other properties of ASA have been discovered, such as the non-COX-1 dependent improvement of endothelial function or the hypotensive effect after evening administration.	Aspirin	76-79	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	118-123
29656179-0	2018	Novel reno-protective mechanism of Aspirin involves H2AK119 monoubiquitination and Set7 in preventing type 1 diabetic nephropathy.	Aspirin	35-42	KMT5A pseudogene 1	Homo sapiens	83-87
29656179-8	2018	RESULTS: Aspirin administration, reduced the protein expression of Mysm1, increased the protein expression of H2AK119-Ub and thereby reduced the Set7 protein expression in glomeruli isolated from diabetic animals and prevented renal fibrosis.	Aspirin	9-16	KMT5A pseudogene 1	Homo sapiens	145-149
29656179-9	2018	CONCLUSIONS: In conclusion, our results are clearly indicating that, aspirin prevents renal fibrosis in diabetic animals through decreasing the expression of Mysm1, increasing the expression of H2AK119-Ub and thereby decreasing the protein expression of Set7, which is a novel mechanism.	Aspirin	69-76	KMT5A pseudogene 1	Homo sapiens	254-258
30046765-9	2018	In aspirin-treated volunteers, an inverse relationship between miR-21 and MRP4 platelet expression was found after aspirin treatment.	Aspirin	115-122	microRNA 21	Homo sapiens	63-69
30046765-11	2018	Conclusion: The results reported in this study provide information that aspirin induces the modulation of platelet miR-21 expression levels and this modulation can be responsible for MRP4 enhancement in circulating platelets.	Aspirin	72-79	microRNA 21	Homo sapiens	115-121
29381509-9	2018	Moreover, the ratio of apoptotic neurons in the anterior horn and the levels of the apoptosis-related proteins caspase-3, cleaved caspase-3, and Bax were significantly decreased in the aspirin group compared with the vehicle group.	Aspirin	185-192	BCL2 associated X, apoptosis regulator	Rattus norvegicus	145-148
29381509-10	2018	Immunofluorescence staining was used to detect the colocalization of NeuN and HO-1, and the results showed that aspirin significantly increased expression of the HO-1 protein in neurons.	Aspirin	112-119	RNA binding fox-1 homolog 3	Rattus norvegicus	69-73
29541457-6	2018	On the other hand, the levels of phosphorylated-HSP27 induced by ristocetin in the platelets from a patient of the anti-platelet group taking ASA were significantly lower than those from a patient of the control group.	Aspirin	142-145	heat shock protein family B (small) member 1	Homo sapiens	48-53
29492489-1	2018	[(Prop-2-ynyl)-2-acetoxybenzoate]dicobalthexacarbonyl (Co-ASS), an organometallic derivative of the irreversible cyclooxygenase-1/2 (COX-1/2) inhibitor acetylsalicylic acid (ASS), demonstrated high growth-inhibitory potential against various tumor cell lines and inhibition of both COX isoenzymes.	Aspirin	152-172	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	133-140
29511271-0	2018	Publisher Correction: Aspirin metabolite sodium salicylate selectively inhibits transcriptional activity of ATF6alpha and downstream target genes.	Aspirin	22-29	activating transcription factor 6	Homo sapiens	108-117
29219948-7	2018	In summary, ASA VI promotes angiogenesis of HUVECs in vitro via up-regulating the HIF-1alpha/VEGF pathway, and efficiently enhances the vascularization in regenerated tissue and facilitates wound healing in vivo.	Aspirin	12-15	vascular endothelial growth factor A	Rattus norvegicus	93-97
29349624-2	2018	RESULTS: Compared to the untreated control or individual drug, the combinations of aspirin and vitamin D3 significantly decreased the rates of cell proliferation by CCK-8 assay, and caused higher rates of cell apoptosis in both CAL-27 and SCC-15 cells by Annexin V-FITC apoptosis assay and flow cytometry.	Aspirin	83-90	annexin A5	Homo sapiens	255-264
30052978-1	2018	Background: Antipsychotic drugs plus aspirin (acetylsalicylic acid), which targets prostaglandin-endoperoxide synthase 1 (PTGS1: COX1), improved therapeutic outcomes when treating schizophrenia.	Aspirin	37-44	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	129-133
30052978-1	2018	Background: Antipsychotic drugs plus aspirin (acetylsalicylic acid), which targets prostaglandin-endoperoxide synthase 1 (PTGS1: COX1), improved therapeutic outcomes when treating schizophrenia.	Aspirin	46-66	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	129-133
29520141-4	2018	In vivo IQCA-TAVV targeted arterial thrombus, dose dependently inhibited arterial thrombosis with a 1 nmol/kg of minimal effective dose, and the activity was1670 folds of that of aspirin.	Aspirin	179-186	IQ motif containing with AAA domain 1	Homo sapiens	8-12
29094287-0	2018	Targeting AMPK, mTOR and beta-Catenin by Combined Metformin and Aspirin Therapy in HCC: An Appraisal in Egyptian HCC Patients.	Aspirin	64-71	catenin beta 1	Homo sapiens	25-37
29094287-3	2018	OBJECTIVE: The current work aimed to investigate the possibility of targeting AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), and beta-catenin proteins through combined metformin/aspirin treatment in the HepG2 cell line, and to explore such molecular targets in Egyptian HCC patients.	Aspirin	206-213	catenin beta 1	Homo sapiens	157-169
29094287-8	2018	Additionally, metformin/aspirin combined treatment enhanced cell-cell membrane localization of beta-catenin expression in HepG2 cells, which might inhibit the metastatic potential of HepG2 cells.	Aspirin	24-31	catenin beta 1	Homo sapiens	95-107
29094287-10	2018	CONCLUSIONS: Targeting AMPK, mTOR and beta-catenin by combined metformin/aspirin treatment could be a promising therapeutic strategy for Egyptian HCC patients, and possibly other HCC patients.	Aspirin	73-80	catenin beta 1	Homo sapiens	38-50
29496171-6	2018	RESULTS: Compared with the model group, the level of CECs density and the expressions of albumen and mRNA of ICAM-1 were significantly decreased in the aspirin,resveratrol,total flavones of hawthorn and resveratrol combined with total flavones of hawthorn groups (P &lt; .05).	Aspirin	152-159	ICAM-1	Oryctolagus cuniculus	109-115
29336282-1	2018	Aspirin-exacerbated respiratory disease (AERD) is characterized by chronic eosinophilic nasal polyps, asthma, and airway reactions upon cyclooxygenase (COX) 1 inhibition.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	136-158
30415260-0	2018	High Concentration of Aspirin Induces Apoptosis in Rat Tendon Stem Cells via Inhibition of the Wnt/beta-Catenin Pathway.	Aspirin	22-29	Wnt family member 2	Rattus norvegicus	95-98
30415260-0	2018	High Concentration of Aspirin Induces Apoptosis in Rat Tendon Stem Cells via Inhibition of the Wnt/beta-Catenin Pathway.	Aspirin	22-29	catenin beta 1	Rattus norvegicus	99-111
30415260-6	2018	The aim of our study was to determine whether aspirin induces apoptosis in rat TSCs via the Wnt/beta-catenin pathway.	Aspirin	46-53	Wnt family member 2	Rattus norvegicus	92-95
30415260-6	2018	The aim of our study was to determine whether aspirin induces apoptosis in rat TSCs via the Wnt/beta-catenin pathway.	Aspirin	46-53	catenin beta 1	Rattus norvegicus	96-108
30415260-9	2018	Next, we used western blotting to determine the effect of aspirin on the Wnt/beta-catenin pathway.	Aspirin	58-65	Wnt family member 2	Rattus norvegicus	73-76
30415260-9	2018	Next, we used western blotting to determine the effect of aspirin on the Wnt/beta-catenin pathway.	Aspirin	58-65	catenin beta 1	Rattus norvegicus	77-89
30415260-11	2018	Finally, we used flow cytometry, fluorescence, and western blotting to investigate the aspirin-induced apoptosis of TSCs via the Wnt/beta-catenin pathway.	Aspirin	87-94	Wnt family member 2	Rattus norvegicus	129-132
30415260-11	2018	Finally, we used flow cytometry, fluorescence, and western blotting to investigate the aspirin-induced apoptosis of TSCs via the Wnt/beta-catenin pathway.	Aspirin	87-94	catenin beta 1	Rattus norvegicus	133-145
30415260-16	2018	CONCLUSION: The Wnt/beta-catenin pathway plays a vital role in aspirin-induced apoptosis by regulating mitochondrial/caspase-3 function.	Aspirin	63-70	Wnt family member 2	Rattus norvegicus	16-19
30415260-16	2018	CONCLUSION: The Wnt/beta-catenin pathway plays a vital role in aspirin-induced apoptosis by regulating mitochondrial/caspase-3 function.	Aspirin	63-70	catenin beta 1	Rattus norvegicus	20-32
29284385-8	2018	In human AAA, only a few number of studies focused on anti-platelet therapy mostly using acetylsalicylic acid (aspirin, ASA), a COX1 inhibitor.	Aspirin	89-109	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	128-132
29284385-8	2018	In human AAA, only a few number of studies focused on anti-platelet therapy mostly using acetylsalicylic acid (aspirin, ASA), a COX1 inhibitor.	Aspirin	111-118	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	128-132
29284385-8	2018	In human AAA, only a few number of studies focused on anti-platelet therapy mostly using acetylsalicylic acid (aspirin, ASA), a COX1 inhibitor.	Aspirin	120-123	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	128-132
29195233-5	2018	We show herein that, ASA-BMMSCs treatment reduced inflammatory infiltration and alveolar bone loss in periodontitis rats, reflected by immunohistochemistry staining of OPG/RANK-L and Micro-CT. Levels of TNF-alpha and IL-17 decreased while IL-10 increased after the treatment of ASA-BMMSCs in periodontitis rats.	Aspirin	21-24	TNF receptor superfamily member 11B	Rattus norvegicus	168-171
28987816-0	2018	Aspirin increases ferroportin 1 expression by inhibiting hepcidin via the JAK/STAT3 pathway in interleukin 6-treated PC-12 cells.	Aspirin	0-7	signal transducer and activator of transcription 3	Rattus norvegicus	78-83
29200971-0	2017	vWF/ADAMTS13 is associated with on-aspirin residual platelet reactivity and clinical outcome in patients with stable coronary artery disease.	Aspirin	35-42	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	4-12
29200971-16	2017	Conclusion: These results indicate that ADAMTS13 is of importance for RPR, and that it in combination with vWF also is associated with clinical endpoints in stable CAD patients on aspirin.	Aspirin	180-187	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	40-48
29218104-7	2017	Because we showed that the expression of miRNA145 was significantly increased after aspirin treatment, we further transfected MSCs with an miRNA145 mimic or miRNA145 inhibitor.	Aspirin	84-91	microRNA 145	Homo sapiens	41-49
29218104-9	2017	Transfection with miRNA145 inhibitor abolished the downregulation of cyclin D induced by aspirin.	Aspirin	89-96	microRNA 145	Homo sapiens	18-26
29218104-10	2017	The results suggested that aspirin inhibited the proliferation of MSCs and caused cell-cycle arrest in the G0/G1 phase through downregulation of cyclin D1, which could be related to the increased expression of miRNA145.	Aspirin	27-34	microRNA 145	Homo sapiens	210-218
28378909-1	2017	The influence of platelet turnover on cyclooxygenase (COX-1) inhibition by low-dose aspirin remains largely uncharacterized due to limited feasibility of studying aspirin pharmacodynamics in bone marrow precursors.	Aspirin	84-91	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	54-59
28378909-2	2017	We developed an in silico compartmental model describing the aspirin effects on COX-1 activity in a population of megakaryocytes (MK) and in peripheral platelets.	Aspirin	61-68	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	80-85
28378909-5	2017	In conclusion, the in silico model accurately describes COX-1 inactivation by low-dose aspirin in MK and platelets in different clinical settings, and might help personalize aspirin regimens in conditions of altered megakaryopoiesis.	Aspirin	87-94	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	56-61
28378909-5	2017	In conclusion, the in silico model accurately describes COX-1 inactivation by low-dose aspirin in MK and platelets in different clinical settings, and might help personalize aspirin regimens in conditions of altered megakaryopoiesis.	Aspirin	174-181	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	56-61
29142602-5	2017	In addition, the GC MKN45 cell line was treated with apatinib (a tyrosine kinase inhibitor) and aspirin (an activator of the transcription factor, PPARalpha) to investigate the effects of these compounds on tumorigenesis.	Aspirin	96-103	peroxisome proliferator activated receptor alpha	Homo sapiens	147-156
29045972-5	2017	RESULTS: The proliferation of GMSCs and the expressions of CD105, CD146 in GMSCs were increased after ASA treatment.	Aspirin	102-105	endoglin	Mus musculus	59-64
28569920-5	2017	Under arterial flow, GPVI-Fc inhibited plaque-induced platelet aggregation by 57 %, and significantly increased platelet inhibition by ASA (28 %) and ticagrelor (47 %) to about 81 % each.	Aspirin	135-138	glycoprotein VI platelet	Homo sapiens	21-25
28569920-9	2017	We conclude that GPVI-Fc added on top of single or dual antiplatelet therapy with ASA and/or a P2Y12 antagonist is likely to improve anti-atherothrombotic protection without increasing bleeding risk.	Aspirin	82-85	glycoprotein VI platelet	Homo sapiens	17-21
28528204-6	2017	Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1.	Aspirin	10-17	colony stimulating factor 2	Homo sapiens	251-255
28060561-11	2017	Correspondingly, aspirin treatment significantly accelerated the decrease of orthodontic force-induced secretion of TNF-alpha and IFN-gamma in serum and the expression of TNF-alpha and IFN-gamma in periodontal ligament during relapse.	Aspirin	17-24	interferon gamma	Rattus norvegicus	130-139
28060561-11	2017	Correspondingly, aspirin treatment significantly accelerated the decrease of orthodontic force-induced secretion of TNF-alpha and IFN-gamma in serum and the expression of TNF-alpha and IFN-gamma in periodontal ligament during relapse.	Aspirin	17-24	interferon gamma	Rattus norvegicus	185-194
28276730-7	2017	In the thromboelastometry, a significant decrease of the A10, A20 and MCF parameters were observed in the EXTEM/FIBTEM tests after they were modified by the addition of a synthetic IIbIIIa receptor antagonist alone or in combination with ASA.	Aspirin	238-241	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	57-60
28184026-0	2017	Identification of TMEM208 and PQLC2 as reference genes for normalizing mRNA expression in colorectal cancer treated with aspirin.	Aspirin	121-128	transmembrane protein 208	Homo sapiens	18-25
28184026-6	2017	We have showed that three traditional internal reference genes, beta-actin, GAPDH and alpha-tubulin, are not suitable for studying gene transcription in colon cancer cells treated with aspirin, and we have identified and validated TMEM208 and PQLC2 as the ideal internal reference genes for detecting the molecular targets of aspirin in colon cancer in vitro and in vivo.	Aspirin	326-333	transmembrane protein 208	Homo sapiens	231-238
28446712-0	2017	Aspirin inhibits the SHH/GLI1 signaling pathway and sensitizes malignant glioma cells to temozolomide therapy.	Aspirin	0-7	sonic hedgehog signaling molecule	Homo sapiens	21-24
28446712-2	2017	Here we investigated the aspirin"s antineoplastic molecular route by targeting SHH/GLI1 pathway and examined the feasibility of aspirin combined with TMZ therapy.	Aspirin	25-32	sonic hedgehog signaling molecule	Homo sapiens	79-82
28446712-3	2017	Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) revealed that the activity of the SHH/GLI1 pathway was strongly inhibited by aspirin.	Aspirin	153-160	sonic hedgehog signaling molecule	Homo sapiens	110-113
28446712-4	2017	Aspirin acted as the glioma growth-inhibitory and pro-apoptosis roles by inhibiting the SHH/GLI1 pathway and reprogramming the epithelial to mesenchymal transition (EMT).	Aspirin	0-7	sonic hedgehog signaling molecule	Homo sapiens	88-91
28446712-8	2017	Collectively, aspirin has a therapeutic potential for SHH/GLI1 targeted therapy against glioma cells.	Aspirin	14-21	sonic hedgehog signaling molecule	Homo sapiens	54-57
28232079-2	2017	METHODS: The activity of rhodanese, 3-mercaptopyruvate sulfurtransferase (MPST) and gamma-cystathionase (CSE), functioning as antioxidant proteins and capable of producing H2S, was investigated in mouse liver and brain after intraperitoneal once a day administration of sodium nitroprusside (5 mg/kg body weight) or acetylsalicylic acid (500 mg/kg body weight) continued for 5 days.	Aspirin	316-336	mercaptopyruvate sulfurtransferase	Mus musculus	36-72
28232079-2	2017	METHODS: The activity of rhodanese, 3-mercaptopyruvate sulfurtransferase (MPST) and gamma-cystathionase (CSE), functioning as antioxidant proteins and capable of producing H2S, was investigated in mouse liver and brain after intraperitoneal once a day administration of sodium nitroprusside (5 mg/kg body weight) or acetylsalicylic acid (500 mg/kg body weight) continued for 5 days.	Aspirin	316-336	mercaptopyruvate sulfurtransferase	Mus musculus	74-78
28232079-2	2017	METHODS: The activity of rhodanese, 3-mercaptopyruvate sulfurtransferase (MPST) and gamma-cystathionase (CSE), functioning as antioxidant proteins and capable of producing H2S, was investigated in mouse liver and brain after intraperitoneal once a day administration of sodium nitroprusside (5 mg/kg body weight) or acetylsalicylic acid (500 mg/kg body weight) continued for 5 days.	Aspirin	316-336	histocompatibility 2, S region (C4, Slp, Bf, C2)	Mus musculus	172-175
28278500-0	2017	Aspirin Inhibits IKK-beta-mediated Prostate Cancer Cell Invasion by Targeting Matrix Metalloproteinase-9 and Urokinase-Type Plasminogen Activator.	Aspirin	0-7	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	17-25
28278500-8	2017	Our data further showed that aspirin was able to inhibit both urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) expression in the cells.	Aspirin	29-36	serpin family E member 1	Homo sapiens	109-142
28278500-8	2017	Our data further showed that aspirin was able to inhibit both urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) expression in the cells.	Aspirin	29-36	serpin family E member 1	Homo sapiens	144-149
28278500-9	2017	In addition, aspirin treatment caused a strong decrease in nuclear factor-kappa B (NF-kappaB) activation, inhibitor of kappaB (IkappaB)-alpha phosphorylation together with translocation of NF-kappaB p65 to nucleus and IkappaB kinase (IKK)- beta activation.	Aspirin	13-20	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	218-244
28278500-10	2017	Moreover, the inhibitory effects of aspirin on cell invasion were reversed by IKK-beta overexpression, while the IKK inhibitor sensitizes the anti-invasive effect of aspirin in prostate cancer cells.	Aspirin	36-43	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	78-86
28278500-11	2017	CONCLUSION: The present research concluded that aspirin suppressed prostate cancer cell invasion by reducing MMP-9 activity and uPA expression through decreasing of IKK-beta-mediated NF-kappaB activation, indicating that the ability of aspirin to inhibit cell invasion might be useful in the chemoprevention of metastatic prostate cancer.	Aspirin	48-55	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	165-173
28278500-11	2017	CONCLUSION: The present research concluded that aspirin suppressed prostate cancer cell invasion by reducing MMP-9 activity and uPA expression through decreasing of IKK-beta-mediated NF-kappaB activation, indicating that the ability of aspirin to inhibit cell invasion might be useful in the chemoprevention of metastatic prostate cancer.	Aspirin	236-243	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	165-173
27892731-12	2017	Secondly, current data raise important and clinically relevant questions about, how AA stimulation induces clotting in individuals in whom aspirin is effective at its COX-1 target.	Aspirin	139-146	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	167-172
27999284-0	2016	Aspirin down Regulates Hepcidin by Inhibiting NF-kappaB and IL6/JAK2/STAT3 Pathways in BV-2 Microglial Cells Treated with Lipopolysaccharide.	Aspirin	0-7	Janus kinase 2	Mus musculus	64-68
27999284-4	2016	We demonstrated that aspirin inhibited hepcidin mRNA as well as NO production in cells treated with LPS, but not in cells without LPS, suppresses IL-6, JAK2, STAT3, and P65 (nuclear factor-kappaB) phosphorylation and has no effect on IRP1 in cells treated with or without LPS.	Aspirin	21-28	Janus kinase 2	Mus musculus	152-156
27999284-4	2016	We demonstrated that aspirin inhibited hepcidin mRNA as well as NO production in cells treated with LPS, but not in cells without LPS, suppresses IL-6, JAK2, STAT3, and P65 (nuclear factor-kappaB) phosphorylation and has no effect on IRP1 in cells treated with or without LPS.	Aspirin	21-28	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	169-172
27999284-5	2016	These findings provide evidence that aspirin down regulates hepcidin by inhibiting IL6/JAK2/STAT3 and P65 (nuclear factor-kappaB) pathways in the cells under inflammatory conditions, and imply that an aspirin-induced reduction in TfR1 and an increase in ferritin are not associated with IRP1 and NO.	Aspirin	37-44	Janus kinase 2	Mus musculus	87-91
27999284-5	2016	These findings provide evidence that aspirin down regulates hepcidin by inhibiting IL6/JAK2/STAT3 and P65 (nuclear factor-kappaB) pathways in the cells under inflammatory conditions, and imply that an aspirin-induced reduction in TfR1 and an increase in ferritin are not associated with IRP1 and NO.	Aspirin	37-44	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	102-105
27825819-21	2016	In contrast to H2S, CO ameliorates hypoxia, regulates Nrf-2 expression but similarly to H2S acts on sGC-dependent manner to restore gastric microcirculation and exhibit anti-inflammatory activity in gastric mucosa compromised by ASA.	Aspirin	229-232	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	100-103
27554763-7	2016	We find that the interaction of activated platelets with lung adenocarcinoma cells upregulates COX-2 expression and PGE2 biosynthesis, and inhibition of platelet COX-1 by aspirin inhibits PGE2 production by the platelet-tumor cell aggregates.	Aspirin	171-178	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	162-167
27554763-9	2016	This supports a hypothesis that the remarkable prevention of metastasis from adenocarcinomas, and particularly from colon adenocarcinomas, by low-dose aspirin results from its effect on platelet COX-1 combined with inhibition of PGE2 biosynthesis in metastasizing tumor cells.	Aspirin	151-158	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	195-200
27712766-1	2016	Aspirin-exacerbated respiratory disease (AERD) involves overexpression of proinflammatory mediators, including 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes.	Aspirin	0-7	leukotriene C4 synthase	Homo sapiens	130-153
27712766-1	2016	Aspirin-exacerbated respiratory disease (AERD) involves overexpression of proinflammatory mediators, including 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes.	Aspirin	0-7	leukotriene C4 synthase	Homo sapiens	155-160
27712767-1	2016	Aspirin-exacerbated respiratory disease (AERD) is a clinical syndrome characterized by severe persistent asthma, hyperplastic eosinophilic sinusitis with nasal polyps, and an intolerance to aspirin and other NSAIDs that preferentially inhibit COX-1.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	243-248
27899979-0	2016	Aspirin inhibits the proliferation and migration of gastric cancer cells in p53-knockout mice.	Aspirin	0-7	transformation related protein 53, pseudogene	Mus musculus	76-79
27899979-1	2016	The aim of the present study was to investigate the effect of aspirin on the cell proliferation and migration of gastric cancer cells in p53-knockout mice.	Aspirin	62-69	transformation related protein 53, pseudogene	Mus musculus	137-140
27488919-10	2016	We show that although all of the aspirin conjugates act through the COX-TXAS pathway by inhibiting COX-1, the parent fatty acids do not act via this pathway.	Aspirin	33-40	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	99-104
27557515-3	2016	We found that therapeutic dosages of aspirin prevented IL-6 from inducing the down-regulation of p53 expression and the acquisition of the epithelial mesenchymal transition (EMT) phenotypic changes in the cell lines.	Aspirin	37-44	transformation related protein 53, pseudogene	Mus musculus	97-100
27557515-8	2016	It is worth noting that aspirin down-regulated ribosome biogenesis, stabilized p53 and up-regulated E-cadherin expression in unstimulated control cells also.	Aspirin	24-31	transformation related protein 53, pseudogene	Mus musculus	79-82
27557515-9	2016	In conclusion, these data showed that therapeutic dosages of aspirin increase the p53-mediated tumor-suppressor activity of the cells thus being in this way able to reduce the risk of cancer onset, either or not linked to chronic inflammatory processes.	Aspirin	61-68	transformation related protein 53, pseudogene	Mus musculus	82-85
27262381-5	2016	Our results revealed that 100mg/kg ASA significantly reduced interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha levels in the E groups; however, the IL-10 level was considerably increased.	Aspirin	35-38	interleukin 10	Rattus norvegicus	155-160
27566955-0	2016	Systems Pharmacogenomics Finds RUNX1 Is an Aspirin-Responsive Transcription Factor Linked to Cardiovascular Disease and Colon Cancer.	Aspirin	43-50	RUNX family transcription factor 1	Homo sapiens	31-36
27566955-1	2016	Aspirin prevents cardiovascular disease and colon cancer; however aspirin"s inhibition of platelet COX-1 only partially explains its diverse effects.	Aspirin	66-73	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	99-104
27566955-4	2016	Megakaryocytic cells exposed to aspirin and its metabolite (salicylic acid, a weak COX-1 inhibitor) showed up regulation in the RUNX1 P1 isoform and MYL9, which is transcriptionally regulated by RUNX1.	Aspirin	32-39	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	83-88
27566955-4	2016	Megakaryocytic cells exposed to aspirin and its metabolite (salicylic acid, a weak COX-1 inhibitor) showed up regulation in the RUNX1 P1 isoform and MYL9, which is transcriptionally regulated by RUNX1.	Aspirin	32-39	RUNX family transcription factor 1	Homo sapiens	128-133
27566955-4	2016	Megakaryocytic cells exposed to aspirin and its metabolite (salicylic acid, a weak COX-1 inhibitor) showed up regulation in the RUNX1 P1 isoform and MYL9, which is transcriptionally regulated by RUNX1.	Aspirin	32-39	RUNX family transcription factor 1	Homo sapiens	195-200
27566955-5	2016	In human subjects, RUNX1 P1 expression in blood and RUNX1-regulated platelet proteins, including MYL9, were aspirin-responsive and associated with platelet function.	Aspirin	108-115	RUNX family transcription factor 1	Homo sapiens	19-24
27566955-5	2016	In human subjects, RUNX1 P1 expression in blood and RUNX1-regulated platelet proteins, including MYL9, were aspirin-responsive and associated with platelet function.	Aspirin	108-115	RUNX family transcription factor 1	Homo sapiens	52-57
27566955-8	2016	We show that RUNX1 P1 expression is associated with colon cancer free survival suggesting a role for RUNX1 in aspirin"s protective effect in colon cancer.	Aspirin	110-117	RUNX family transcription factor 1	Homo sapiens	13-18
27566955-8	2016	We show that RUNX1 P1 expression is associated with colon cancer free survival suggesting a role for RUNX1 in aspirin"s protective effect in colon cancer.	Aspirin	110-117	RUNX family transcription factor 1	Homo sapiens	101-106
27566955-9	2016	Our studies reveal an effect of aspirin on RUNX1 and gene expression that may additionally explain aspirin"s effects in cardiovascular disease and cancer.	Aspirin	32-39	RUNX family transcription factor 1	Homo sapiens	43-48
27566955-9	2016	Our studies reveal an effect of aspirin on RUNX1 and gene expression that may additionally explain aspirin"s effects in cardiovascular disease and cancer.	Aspirin	99-106	RUNX family transcription factor 1	Homo sapiens	43-48
27318652-0	2016	Interaction between COX-1 and COX-2 Variants Associated with Aspirin Resistance in Chinese Stroke Patients.	Aspirin	61-68	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	20-25
27230877-3	2016	RESULT(S): Met, Asa, BR-DIM, or hyperosmotic sorbitol stress induces rapid ~50-85 % Rex1 and/or Oct4 protein loss in two-cell embryos.	Aspirin	16-19	POU class 5 homeobox 1	Homo sapiens	96-100
27230877-6	2016	CONCLUSION: These experimental designs here showed that Met-, Asa-, BR-DIM-, or sorbitol stress-induced rapid potency loss in two-cell embryos is AMPK dependent as suggested by inhibition of Rex1 and/or Oct4 protein loss with an AMPK inhibitor.	Aspirin	62-65	POU class 5 homeobox 1	Homo sapiens	203-207
25252038-6	2016	RESULTS: At univariate analysis, C2238/ANP-minor allele carrier status and treatment with beta-blocker, aspirin and statin were associated with risk of re-ACS.	Aspirin	104-111	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	155-158
27489545-1	2016	In subjects with non-steroidal anti-inflammatory drugs (NSAIDs)- exacerbated respiratory disease (NERD) symptoms are triggered by acetyl salicylic acid (ASA) and other strong COX-1 inhibitors, and in some cases by weak COX-1 or by selective COX-2 inhibitors.	Aspirin	153-156	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	219-224
26059811-4	2016	Together, our data show that aspirin can directly target oligodendroglial lineage cells and promote their differentiation through inhibition of Wnt/beta-catenin signaling pathway.	Aspirin	29-36	catenin beta 1	Rattus norvegicus	148-160
27074574-7	2016	In conclusion, targeting platelet COX-1 with low-dose aspirin exerts an antimetastatic action by averting the stem cell mimicry of cancer cells associated with enhanced proaggregatory effects induced by platelet-tumor cell interactions.	Aspirin	54-61	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	34-39
26691435-0	2016	Thymic stromal lymphopoietin controls prostaglandin D2 generation in patients with aspirin-exacerbated respiratory disease.	Aspirin	83-90	thymic stromal lymphopoietin	Homo sapiens	0-28
26691435-10	2016	Levels of the cleaved active form of TSLP were increased in nasal polyps from patients with AERD relative to those in aspirin-tolerant control subjects.	Aspirin	118-125	thymic stromal lymphopoietin	Homo sapiens	37-41
26635114-0	2016	Aspirin Inhibits LPS-Induced Expression of PI3K/Akt, ERK, NF-kappaB, CX3CL1, and MMPs in Human Bronchial Epithelial Cells.	Aspirin	0-7	matrix metallopeptidase 7	Homo sapiens	81-85
26635114-1	2016	This study focused on the effects of aspirin on lipopolysaccharide (LPS)-induced expression of phosphoinositide 3 kinase (PI3K)/protein kinase B (Akt), extracellular signal-regulated protein kinase (ERK), nuclear factor-kappaB (NF-kappaB), CX3CL1, and MMPs in human bronchial epithelial cells.	Aspirin	37-44	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	95-120
26891941-0	2016	Association of TRPM3 Polymorphism (rs10780946) and Aspirin-Exacerbated Respiratory Disease (AERD).	Aspirin	51-58	transient receptor potential cation channel subfamily M member 3	Homo sapiens	15-20
26918349-9	2016	MCL-1 knockdown sensitizes cancer cells to aspirin-induced apoptosis.	Aspirin	43-50	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	0-5
26918349-11	2016	Moreover, sorafenib blocks aspirin-induced MCL-1 up-regulation.	Aspirin	27-34	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	43-48
26918349-14	2016	These data demonstrate that AMPK-mediated up-regulation of mTORC2 and MCL-1 may compromise the anticancer effects of aspirin.	Aspirin	117-124	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	70-75
26859324-1	2016	Aspirin and other nonsteroidal anti-inflammatory drugs target the cyclooxygenase enzymes (COX-1 and COX-2) to block the formation of prostaglandins.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	90-95
25579384-9	2016	Otherwise, the non-steroidal anti-inflammatory drugs nimesulide, acetylsalicylic acid, ibuprofen, and diclofenac sodium decreased the extracellular glutamate and glutamine levels, downregulated GS and AChE activities, and restored ACh levels in Pro-treated astrocytes.	Aspirin	65-85	acetylcholinesterase	Rattus norvegicus	201-205
26456703-1	2016	AIMS: The aim of the study was to analyze the interaction between celecoxib and low dose aspirin for COX-1 binding and its consequences on the aspirin-mediated antiplatelet effects.	Aspirin	89-96	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	101-106
26456703-2	2016	METHODS: We investigated ex vivo the interaction between celecoxib and aspirin for COX-1 binding and measured the resulting antiplatelet effects.	Aspirin	71-78	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	83-88
26314861-0	2016	Aspirin and salicylic acid decrease c-Myc expression in cancer cells: a potential role in chemoprevention.	Aspirin	0-7	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	36-41
26314861-2	2016	We hypothesized that aspirin"s anti-cancer effect may occur through downregulation of c-Myc gene expression.	Aspirin	21-28	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	86-91
26314861-3	2016	Here, we demonstrate that aspirin and its primary metabolite, salicylic acid, decrease the c-Myc protein levels in human HCT-116 colon and in few other cancer cell lines.	Aspirin	26-33	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	91-96
26314861-9	2016	High-performance liquid chromatography (HPLC) analysis showed that aspirin taken up by cells was rapidly metabolized to salicylic acid, suggesting that aspirin"s inhibitory effect on c-Myc may occur through formation of salicylic acid.	Aspirin	67-74	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	183-188
26314861-9	2016	High-performance liquid chromatography (HPLC) analysis showed that aspirin taken up by cells was rapidly metabolized to salicylic acid, suggesting that aspirin"s inhibitory effect on c-Myc may occur through formation of salicylic acid.	Aspirin	152-159	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	183-188
26314861-11	2016	Inhibition of c-Myc may represent an important pathway by which aspirin exerts its anti-cancer effect and decrease the occurrence of cancer in epithelial tissues.	Aspirin	64-71	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	14-19
26711147-4	2016	Furthermore, ASA could up-regulate TNF-R1 and DR5 via activation of p38 MAPK, thereby activating caspase 8, revealing the death receptor pathway was also involved in this process.	Aspirin	13-16	TNF receptor superfamily member 1A	Homo sapiens	35-41
26711147-4	2016	Furthermore, ASA could up-regulate TNF-R1 and DR5 via activation of p38 MAPK, thereby activating caspase 8, revealing the death receptor pathway was also involved in this process.	Aspirin	13-16	TNF receptor superfamily member 10b	Homo sapiens	46-49
28119929-5	2016	We found that aspirin reduced serum amylase and lipase levels, decreased the MPO activity, and alleviated the histopathological manifestations of pancreas and pancreatitis-associated lung injury.	Aspirin	14-21	lipase, endothelial	Mus musculus	48-54
28119929-6	2016	Proinflammatory cytokines were decreased and the expression of NF-kappaB p65 in acinar cell nuclei was suppressed after aspirin treatment.	Aspirin	120-127	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	73-76
25994118-4	2016	In this study, as insulin treated with aspirin at 37 C, a significant level of acetylation was observed by flourescamine and o-phthalaldehyde assay.	Aspirin	39-46	insulin	Bos taurus	18-25
26733809-6	2015	Gadolinium and acetylsalicylic acid reduced these currents, and FMRFamide, zinc (at high concentrations) and N,N,N",N"-tetrakis-(2-piridilmetil)-ethylenediamine increased them, indicating that functional ASICs are composed of the subunits ASIC1, ASIC2, and ASIC3.	Aspirin	15-35	acid sensing ion channel subunit 1	Homo sapiens	239-244
26733809-6	2015	Gadolinium and acetylsalicylic acid reduced these currents, and FMRFamide, zinc (at high concentrations) and N,N,N",N"-tetrakis-(2-piridilmetil)-ethylenediamine increased them, indicating that functional ASICs are composed of the subunits ASIC1, ASIC2, and ASIC3.	Aspirin	15-35	acid sensing ion channel subunit 3	Homo sapiens	257-262
26658843-4	2015	Thus, the aim of this study was conducted to compare the treatment efficacy, degree of anemia and inflammation, and changes in serum hepcidin in children who received a combination of high-dose aspirin and IVIG in the acute stage of KD, and those who received IVIG alone.	Aspirin	194-201	hepcidin antimicrobial peptide	Homo sapiens	133-141
26511379-0	2015	NCX 4040, a nitric oxide-donating aspirin derivative, inhibits Prevotella intermedia lipopolysaccharide-induced production of proinflammatory mediators in murine macrophages.	Aspirin	34-41	T cell leukemia, homeobox 2	Mus musculus	0-3
26511379-1	2015	In this study, the effects and underlying mechanisms of NCX 4040, a nitric oxide (NO)-donating aspirin derivative, on the production of proinflammatory mediators were examined using murine macrophages exposed to lipopolysaccharide (LPS) from Prevotella intermedia, a pathogen implicated in the etiology of periodontal disease.	Aspirin	95-102	T cell leukemia, homeobox 2	Mus musculus	56-59
26511379-3	2015	Notably, NCX 4040 was much more effective than the parental compound aspirin in reducing LPS-induced production of inflammatory mediators.	Aspirin	69-76	T cell leukemia, homeobox 2	Mus musculus	9-12
25407017-3	2015	Using HepG2 cells, we evaluated (a) the inhibition of TCDD-mediated induction of CYP1A1 exerted by resveratrol-aspirin derivatives using the EROD assay, and (b) CYP1A1 mRNA in vitro.	Aspirin	111-118	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	81-87
26319435-5	2015	Since the parent compound aspirin, inhibits both COX-1 and COX-2, we also evaluated the effects of these compounds on COX-1 and COX-2 enzyme activities and also performed modeling of the interactions between the positional isomers of NOSH-aspirin and COX-1 and COX-2 enzymes.	Aspirin	26-33	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	49-54
26504148-7	2015	CONCLUSIONS: Together, these results suggest that linoleic acid-derived oxylipids may contribute to the non-COX1 mediated variability in response to aspirin.	Aspirin	149-156	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	108-112
26385700-1	2015	BET 1: Which form of aspirin is the fastest to inhibit platelet aggregation in emergency department patients with non-ST segment elevation myocardial infarction?	Aspirin	21-28	Bet1 golgi vesicular membrane trafficking protein	Homo sapiens	0-5
26358341-3	2015	OBJECTIVE: To investigate the expression profiles of EP receptors, including EP1, EP2, EP3, and EP4 receptors in different Chinese patients with CRS with aspirin tolerance.	Aspirin	154-161	prostaglandin E receptor 4	Homo sapiens	96-99
26056043-0	2015	Metformin combined with aspirin significantly inhibit pancreatic cancer cell growth in vitro and in vivo by suppressing anti-apoptotic proteins Mcl-1 and Bcl-2.	Aspirin	24-31	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	144-149
26056043-5	2015	Compared to the untreated control or individual drug, the combination of metformin and aspirin significantly inhibited cell migration and colony formation of both PANC-1 and BxPC-3 cells.	Aspirin	87-94	pancreas protein 1	Mus musculus	163-169
26056043-9	2015	In a PANC-1 xenograft mouse model, we demonstrated that the combination of metformin and aspirin significantly inhibited tumor growth and downregulated the protein expression of Mcl-1 and Bcl-2 in tumors.	Aspirin	89-96	pancreas protein 1	Mus musculus	5-11
26345150-19	2015	In the aspirin-treated group compared to the control group, the NE had a protective effect on the stomach and caused less injury than aspirin, indicated by significant decreases in TNFalpha, iNOS, prostaglandin E2, and malondialdehyde levels, and also significant increases in glutathione, glutathione reductase, glutathione peroxidase, catalase, and superoxide dismutase.	Aspirin	7-14	glutathione-disulfide reductase	Rattus norvegicus	290-311
26294325-5	2015	Of the top 10 genes (fold-change &gt; 10, P &lt; 10(-10)) regulated by metformin plus aspirin, PCDH18, CCL2, RASL11A, FAM111B and BMP5 were down-regulated &gt;= 20-fold, while NGFR, NPTX1, C7orf57, MRPL23AS1 and UNC5B were up-regulated &gt;= 10-fold.	Aspirin	86-93	C-C motif chemokine ligand 2	Homo sapiens	103-107
26294325-5	2015	Of the top 10 genes (fold-change &gt; 10, P &lt; 10(-10)) regulated by metformin plus aspirin, PCDH18, CCL2, RASL11A, FAM111B and BMP5 were down-regulated &gt;= 20-fold, while NGFR, NPTX1, C7orf57, MRPL23AS1 and UNC5B were up-regulated &gt;= 10-fold.	Aspirin	86-93	RAS like family 11 member A	Homo sapiens	109-116
26294325-5	2015	Of the top 10 genes (fold-change &gt; 10, P &lt; 10(-10)) regulated by metformin plus aspirin, PCDH18, CCL2, RASL11A, FAM111B and BMP5 were down-regulated &gt;= 20-fold, while NGFR, NPTX1, C7orf57, MRPL23AS1 and UNC5B were up-regulated &gt;= 10-fold.	Aspirin	86-93	FAM111 trypsin like peptidase B	Homo sapiens	118-125
26294325-5	2015	Of the top 10 genes (fold-change &gt; 10, P &lt; 10(-10)) regulated by metformin plus aspirin, PCDH18, CCL2, RASL11A, FAM111B and BMP5 were down-regulated &gt;= 20-fold, while NGFR, NPTX1, C7orf57, MRPL23AS1 and UNC5B were up-regulated &gt;= 10-fold.	Aspirin	86-93	nerve growth factor receptor	Homo sapiens	176-180
25772736-4	2015	We investigated the inhibition profiles by aspirin and its major metabolite salicylate of ethanol oxidation by recombinant human ADH1A, ADH1B1, ADH1B2, ADH1B3, ADH1C1, ADH1C2, ADH2, and ADH4, and acetaldehyde oxidation by ALDH1A1 and ALDH2, at pH 7.5 and 0.5 mM NAD(+).	Aspirin	43-50	alcohol dehydrogenase 1A (class I), alpha polypeptide	Homo sapiens	129-134
25772736-4	2015	We investigated the inhibition profiles by aspirin and its major metabolite salicylate of ethanol oxidation by recombinant human ADH1A, ADH1B1, ADH1B2, ADH1B3, ADH1C1, ADH1C2, ADH2, and ADH4, and acetaldehyde oxidation by ALDH1A1 and ALDH2, at pH 7.5 and 0.5 mM NAD(+).	Aspirin	43-50	aldehyde dehydrogenase 1 family member A1	Homo sapiens	222-229
25838094-8	2015	The high-periostin group was older at onset of asthma (P = 0.04), had a higher prevalence of aspirin intolerance (P = 0.04) or concomitant nasal disorders (P = 0.03-0.001), higher peripheral eosinophil counts (P &lt; 0.001), and lower pulmonary function (P = 0.02-0.07).	Aspirin	93-100	periostin	Homo sapiens	9-18
25953941-3	2015	It was found, that patients with high levels of ASA &gt;150 mg/l, or average 100-150 mg/l, had statistically significant (p=0,001) high content of Ig A and Ig G relative to the control group.	Aspirin	48-51	immunoglobulin heavy variable 4-38-2-like	Homo sapiens	147-151
25638730-12	2015	Aspirin and sc-560 also reduced hypoxia-induced FLT1 mRNA expression and inhibited COX1 mRNA in CTBs.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	83-87
25638730-15	2015	Sc-560 recapitulated the effects of aspirin on sFLT1 expression and release in CTBs suggesting that the aspirin effect may be mediated via inhibition of COX1.	Aspirin	36-43	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	153-157
25638730-15	2015	Sc-560 recapitulated the effects of aspirin on sFLT1 expression and release in CTBs suggesting that the aspirin effect may be mediated via inhibition of COX1.	Aspirin	104-111	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	153-157
26054192-8	2015	After pretreatment with EA and moxibustion, the relative expression levels of miRNA 290 and miRNA 494 were significantly higher in the EA, moxibustion and Aspirin pretreatment groups than in the model group (P &lt; 0.01), while cortical AQP 4 expression levels were significantly lower in the EA, moxibustion and Aspirin pretreatment groups than in the model group (P &lt; 0.	Aspirin	155-162	aquaporin 4	Rattus norvegicus	237-242
25592153-0	2015	Dipeptidyl-peptidase 10 as a genetic biomarker for the aspirin-exacerbated respiratory disease phenotype.	Aspirin	55-62	dipeptidyl peptidase like 10	Homo sapiens	0-23
25592153-5	2015	METHODS: A case-control association study of DPP10 gene polymorphisms was performed in 3 groups of patients: 274 with AERD, 272 with aspirin-tolerant asthma, and 99 normal healthy controls.	Aspirin	133-140	dipeptidyl peptidase like 10	Homo sapiens	45-50
25592153-9	2015	The DPP10 level was significantly higher in sera from patients with AERD compared with patients with aspirin-tolerant asthma and control subjects (P = .021 and P &lt; .001, respectively).	Aspirin	101-108	dipeptidyl peptidase like 10	Homo sapiens	4-9
25660936-0	2015	Reply: Triple therapy for atrial fibrillation and ACS with or without PCI: don"t drop aspirin just yet.	Aspirin	86-93	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	50-53
25464488-0	2015	Aspirin-triggered 15-epi-lipoxin A4 signals through FPR2/ALX in vascular smooth muscle cells and protects against intimal hyperplasia after carotid ligation.	Aspirin	0-7	formyl peptide receptor 2	Homo sapiens	52-56
25514511-5	2015	The computational results confirmed that aspirin would be 10-100 times more potent against COX-1 than against COX-2, and revealed that this inhibition specificity between the two COX isoforms can be attributed mainly to the difference in kinetics rate of the covalent inhibition reaction, not the aspirin-binding step.	Aspirin	41-48	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	91-96
25562554-5	2015	In urticaria or angioedema induced by multiple NSAIDs, patients without underlying disease develop urticaria or angioedema 30-90 minutes after ingestion of COX-1-inhibiting NSAIDs including aspirin.	Aspirin	190-197	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	156-161
25590316-1	2015	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is explained in part by overexpression of 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes (CysLTs) and driving the surge in CysLT production that occurs with aspirin ingestion.	Aspirin	12-19	leukotriene C4 synthase	Homo sapiens	120-143
25590316-1	2015	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is explained in part by overexpression of 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes (CysLTs) and driving the surge in CysLT production that occurs with aspirin ingestion.	Aspirin	12-19	leukotriene C4 synthase	Homo sapiens	145-150
25590316-1	2015	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is explained in part by overexpression of 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes (CysLTs) and driving the surge in CysLT production that occurs with aspirin ingestion.	Aspirin	288-295	leukotriene C4 synthase	Homo sapiens	120-143
25590316-1	2015	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is explained in part by overexpression of 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes (CysLTs) and driving the surge in CysLT production that occurs with aspirin ingestion.	Aspirin	288-295	leukotriene C4 synthase	Homo sapiens	145-150
25590316-13	2015	Our previous studies demonstrated that aspirin blocks trafficking of STAT6 into the nucleus and thereby prevents IL-4-mediated induction of these transcripts, thereby suggesting a modality by which aspirin desensitization could provide therapeutic benefit for AERD patients.	Aspirin	39-46	signal transducer and activator of transcription 6	Homo sapiens	69-74
25314608-0	2015	Acetylsalicylic acid mitigates erythropoietin-associated blood pressure increase in nonuremic rats.	Aspirin	0-20	erythropoietin	Rattus norvegicus	31-45
25307725-0	2015	Competition between low-dose aspirin and other NSAIDs for COX-1 binding and its clinical consequences for the drugs" antiplatelet effects.	Aspirin	29-36	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	58-63
25307725-3	2015	AREAS COVERED: The competition between the low-dose aspirin and other NSAIDs for binding to COX-1 is described, including the recent findings on the differences in the interaction of NSAIDs with the individual COX-1 subunits, and the clinical consequences of this drug-drug interaction.	Aspirin	52-59	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	92-97
25307725-3	2015	AREAS COVERED: The competition between the low-dose aspirin and other NSAIDs for binding to COX-1 is described, including the recent findings on the differences in the interaction of NSAIDs with the individual COX-1 subunits, and the clinical consequences of this drug-drug interaction.	Aspirin	52-59	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	210-215
26517138-0	2015	The Implication of the Polymorphisms of COX-1, UGT1A6, and CYP2C9 among Cardiovascular Disease (CVD) Patients Treated with Aspirin.	Aspirin	123-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
26517138-1	2015	PURPOSE:   Enzymes potentially responsible for the pharmacokinetic variations of aspirin include cyclooxygenase-1 (COX-1), UDP-glucuronosyltransferase (UGT1A6) and P450 (CYP) (CYP2C9).	Aspirin	81-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
26517138-10	2015	CONCLUSION: Screening of patients with defective genetic variants of UGT1A6 and CYP2C9*3 helps in identifying patients at risk of aspirin induced gastritis.	Aspirin	130-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
25666703-6	2015	In contrast to native NSAIDs, their NO-releasing derivatives such as NO-ASA were found to exhibit lower gastric toxicity despite inhibiting both COX-1 and COX-2 activity in the gastric mucosa.	Aspirin	72-75	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	145-150
25521733-1	2014	BACKGROUND AND AIM: In our previous study, the SLCO1B1 521TT genotype and the SLCO1B1*1b haplotype were significantly associated with the risk of peptic ulcer in patients taking low-dose aspirin (LDA).	Aspirin	187-194	solute carrier organic anion transporter family member 1B1	Homo sapiens	47-54
25521733-1	2014	BACKGROUND AND AIM: In our previous study, the SLCO1B1 521TT genotype and the SLCO1B1*1b haplotype were significantly associated with the risk of peptic ulcer in patients taking low-dose aspirin (LDA).	Aspirin	187-194	solute carrier organic anion transporter family member 1B1	Homo sapiens	78-85
25521733-9	2014	CONCLUSION: The CHST2 2082 T allele as well as SLCO1B1*1b haplotype may identify patients at increased risk for aspirin-induced peptic ulcer or ulcer bleeding.	Aspirin	112-119	carbohydrate sulfotransferase 2	Homo sapiens	16-21
25521733-9	2014	CONCLUSION: The CHST2 2082 T allele as well as SLCO1B1*1b haplotype may identify patients at increased risk for aspirin-induced peptic ulcer or ulcer bleeding.	Aspirin	112-119	solute carrier organic anion transporter family member 1B1	Homo sapiens	47-54
25634391-1	2014	BACKGROUND: Clopidogrel has been the only available antiplatelet drug used along with aspirin in patients of ACS.	Aspirin	86-93	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	109-112
24726874-10	2014	It indicated that aspirin induced adipocyte differentiation through p53-p21 pathway.	Aspirin	18-25	H3 histone pseudogene 16	Homo sapiens	72-75
25061736-5	2014	We also used aspirin as an inhibitor of the Wnt signaling pathway in the treatment of hepG2 cells transfected with the pReceiver-M29/thy-1 expression vector to make detailed observations of apoptosis in hepG2 cells as well as the differential expression of beta-catenin, cyclinD1, and thy-1.	Aspirin	13-20	Thy-1 cell surface antigen	Homo sapiens	133-138
25061736-5	2014	We also used aspirin as an inhibitor of the Wnt signaling pathway in the treatment of hepG2 cells transfected with the pReceiver-M29/thy-1 expression vector to make detailed observations of apoptosis in hepG2 cells as well as the differential expression of beta-catenin, cyclinD1, and thy-1.	Aspirin	13-20	catenin beta 1	Homo sapiens	257-269
25061736-5	2014	We also used aspirin as an inhibitor of the Wnt signaling pathway in the treatment of hepG2 cells transfected with the pReceiver-M29/thy-1 expression vector to make detailed observations of apoptosis in hepG2 cells as well as the differential expression of beta-catenin, cyclinD1, and thy-1.	Aspirin	13-20	Thy-1 cell surface antigen	Homo sapiens	285-290
24418973-11	2014	ASA and ketorolac both decreased the activity of MMP-2, MMP-9, and uPA.	Aspirin	0-3	plasminogen activator, urokinase	Mus musculus	67-70
24923427-8	2014	Protein expression of ERalpha, COX-2, Cyclin A, and Bcl-xL were reduced in celecoxib-treated tumor samples, whereas only Bcl-xL expression was suppressed in those treated with aspirin.	Aspirin	176-183	estrogen receptor 1 (alpha)	Mus musculus	22-29
24661619-0	2014	Perioperative aspirin improves neurological outcome after focal brain ischemia possibly via inhibition of Notch 1 in rat.	Aspirin	14-21	notch receptor 1	Rattus norvegicus	106-113
24661619-13	2014	Inhibition of Notch activation and neuroinflammation may contribute to the neuroprotection of aspirin.	Aspirin	94-101	notch receptor 1	Rattus norvegicus	14-19
24345330-9	2014	We corroborated that treatment of Aspirin significantly diminishes VNR-repressed SIRT1, LKB1 and AMPK phosphorylation and VNR-promoted NADPH oxidase activation, however, those findings were vanished by SIRT1 and AMPK siRNAs.	Aspirin	34-41	serine/threonine kinase 11	Homo sapiens	88-92
24345330-10	2014	Our data also shown that Aspirin represses VNR-activated TGF-beta-activated kinase-1 (TAK1) activation, inhibited the interaction of TAK1/TAK-binding protein1 (TAB1), suppressed NF-kappa B activation and pro-inflammatory cytokine secretion.	Aspirin	25-32	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	57-84
24345330-10	2014	Our data also shown that Aspirin represses VNR-activated TGF-beta-activated kinase-1 (TAK1) activation, inhibited the interaction of TAK1/TAK-binding protein1 (TAB1), suppressed NF-kappa B activation and pro-inflammatory cytokine secretion.	Aspirin	25-32	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	86-90
24345330-10	2014	Our data also shown that Aspirin represses VNR-activated TGF-beta-activated kinase-1 (TAK1) activation, inhibited the interaction of TAK1/TAK-binding protein1 (TAB1), suppressed NF-kappa B activation and pro-inflammatory cytokine secretion.	Aspirin	25-32	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	133-137
24401839-7	2014	Taken together, these findings identify a previously unrecognized role of TERT in improving the immunomodulatory capacity of BMMSCs, suggesting that aspirin treatment is a practical approach to significantly reduce cell dosage in BMMSC-based immunotherapies.	Aspirin	149-156	telomerase reverse transcriptase	Mus musculus	74-78
24435454-0	2014	Could empirical low-dose-aspirin administration during IVF cycle affect both the oocytes and embryos quality via COX 1-2 activity inhibition?	Aspirin	25-32	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	113-118
24393660-10	2014	Intake of aspirin caused a significant rise in LPS-induced TF activity that was almost abolished by histamine at 0.033 muM.	Aspirin	10-17	coagulation factor III, tissue factor	Homo sapiens	59-61
24315932-8	2014	We found that ritonavir administration caused intestinal damage and its co-administration with naproxen or ASA exacerbated the severity of injury and intestinal inflammation, as assessed by measuring haematocrit, MPO, mucosal levels of PGE2 and mRNA levels of iNOS, MCP-1 and VLA-1.	Aspirin	107-110	C-C motif chemokine ligand 2	Homo sapiens	266-271
24315932-8	2014	We found that ritonavir administration caused intestinal damage and its co-administration with naproxen or ASA exacerbated the severity of injury and intestinal inflammation, as assessed by measuring haematocrit, MPO, mucosal levels of PGE2 and mRNA levels of iNOS, MCP-1 and VLA-1.	Aspirin	107-110	integrin subunit alpha 1	Homo sapiens	276-281
25243161-0	2014	Impact of blood type, functional polymorphism (T-1676C) of the COX-1 gene promoter and clinical factors on the development of peptic ulcer during cardiovascular prophylaxis with low-dose aspirin.	Aspirin	187-194	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	63-68
25243161-1	2014	AIMS: To investigate the impact of blood type, functional polymorphism (T-1676C) of the COX-1 gene promoter, and clinical factors on the development of peptic ulcer during cardiovascular prophylaxis with low-dose aspirin.	Aspirin	213-220	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	88-93
25243161-2	2014	METHODS: In a case-control study including 111 low-dose aspirin users with peptic ulcers and 109 controls (asymptomatic aspirin users), the polymorphism (T-1676C) of the COX-1 gene promoter was genotyped, and blood type, H pylori status, and clinical factors were assessed.	Aspirin	56-63	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	170-175
25243161-2	2014	METHODS: In a case-control study including 111 low-dose aspirin users with peptic ulcers and 109 controls (asymptomatic aspirin users), the polymorphism (T-1676C) of the COX-1 gene promoter was genotyped, and blood type, H pylori status, and clinical factors were assessed.	Aspirin	120-127	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	170-175
25295267-0	2014	Comparison of proton pump inhibitor and histamine-2 receptor antagonist in the prevention of recurrent peptic ulcers/erosions in long-term low-dose aspirin users: a retrospective cohort study.	Aspirin	148-155	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	14-25
25295267-1	2014	BACKGROUND: Proton pump inhibitor and histamine-2 receptor antagonist can prevent aspirin-related ulcers/erosions but few studies compare the efficacy of these two agents.	Aspirin	82-89	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	12-23
23782140-13	2014	In contrast, antisecretory drugs such as a proton pump inhibitor and histamine H2 receptor antagonists markedly suppressed the gastric bleeding and lesion responses to ASA plus clopidogrel under histamine-stimulated acid secretion, but had no effect on the responses to acidified ASA plus clopidogrel.	Aspirin	168-171	histamine receptor H 2	Rattus norvegicus	69-90
23782140-13	2014	In contrast, antisecretory drugs such as a proton pump inhibitor and histamine H2 receptor antagonists markedly suppressed the gastric bleeding and lesion responses to ASA plus clopidogrel under histamine-stimulated acid secretion, but had no effect on the responses to acidified ASA plus clopidogrel.	Aspirin	280-283	histamine receptor H 2	Rattus norvegicus	69-90
25531811-5	2014	In monocytes, we found no changes in basal or lipopolysaccharide (LPS)-stimulated PGE2 synthesis, but the response to EP4 receptor activation with respect to inhibition of LPS-induced tumor necrosis factor-alpha release was reduced in AERD patients, especially in the presence of aspirin (acetylsalicylic acid).	Aspirin	280-287	prostaglandin E receptor 4	Homo sapiens	118-121
25531811-5	2014	In monocytes, we found no changes in basal or lipopolysaccharide (LPS)-stimulated PGE2 synthesis, but the response to EP4 receptor activation with respect to inhibition of LPS-induced tumor necrosis factor-alpha release was reduced in AERD patients, especially in the presence of aspirin (acetylsalicylic acid).	Aspirin	289-309	prostaglandin E receptor 4	Homo sapiens	118-121
24255997-9	2013	Some NSAIDs (such as ibuprofen) can interfere with the cardioprotective effects of aspirin by competitively binding to COX-1 enzyme, resulting in increased TXA2 production Naproxen may differ from other NSAIDs in sustaining functionally important degrees of inhibition of platelet cyclooxygenase-1 activity throughout the dosing interval.	Aspirin	83-90	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	119-124
24244288-0	2013	The association of four common polymorphisms from four candidate genes (COX-1, COX-2, ITGA2B, ITGA2) with aspirin insensitivity: a meta-analysis.	Aspirin	106-113	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	72-77
24649055-10	2013	The application of aspirin (0.1 mM) significantly inhibited the activation of ERK1/2 and NF-kappaB, the expression of TNF-alpha, IL-6, IL-1beta and MCP-1 genes and the secretion of TNF-alpha and IL-6.	Aspirin	19-26	C-C motif chemokine ligand 2	Homo sapiens	148-153
24098505-6	2013	Further mechanistic studies revealed that the actions of these phytochemicals were similar to aspirin in that they mainly inhibited COX-1 rather than COX-2, especially at low doses.	Aspirin	94-101	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	132-137
23625286-8	2013	CONCLUSIONS: 15-PGDH levels vary across the population in a stable and reproducible manner, and are resistant to alteration by aspirin.	Aspirin	127-134	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	13-20
23766266-10	2013	CONCLUSIONS: Our results identify a novel proangiogenic role of LL-37, suggesting that the axis LL-37/COX-1/PGE2 followed by EP3 signaling is amenable to therapeutic intervention in pathological angiogenesis, for instance by aspirin.	Aspirin	225-232	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	102-107
23935747-3	2013	The aim of the present study was to investigate whether aspirin inhibits the activation of telomerase and hTERT in unstable carotid plaques.	Aspirin	56-63	telomerase reverse transcriptase	Homo sapiens	106-111
23935747-8	2013	In addition, aspirin was demonstrated to inhibit the mRNA and protein expression of hTERT through the suppression of hTERT transcriptional activity; however, it had no inhibitory effect on the telomerase activity of the circulating PMNs.	Aspirin	13-20	telomerase reverse transcriptase	Homo sapiens	84-89
23935747-8	2013	In addition, aspirin was demonstrated to inhibit the mRNA and protein expression of hTERT through the suppression of hTERT transcriptional activity; however, it had no inhibitory effect on the telomerase activity of the circulating PMNs.	Aspirin	13-20	telomerase reverse transcriptase	Homo sapiens	117-122
23935747-11	2013	Aspirin was demonstrated to inhibit the activation of telomerase via an hTERT-dependent manner in the PMN cells of unstable carotid plaques, and thus hTERT may be considered as a target in the treatment of cerebrovascular diseases.	Aspirin	0-7	telomerase reverse transcriptase	Homo sapiens	72-77
23935747-11	2013	Aspirin was demonstrated to inhibit the activation of telomerase via an hTERT-dependent manner in the PMN cells of unstable carotid plaques, and thus hTERT may be considered as a target in the treatment of cerebrovascular diseases.	Aspirin	0-7	telomerase reverse transcriptase	Homo sapiens	150-155
23870238-3	2013	The ASA classification includes 6 grades: ASAP1, a normal healthy person; ASAP2, mild systemic disease; ASAP3, severe systemic disease; ASAP4, severe systemic disease that is a constant threat to life; ASAP5, a critically ill patient who is not expected to survive without the operation; and ASAP6, declared brain-dead patient whose organs are being removed for donor purposes.	Aspirin	4-7	ArfGAP with SH3 domain, ankyrin repeat and PH domain 2	Homo sapiens	74-79
23870238-3	2013	The ASA classification includes 6 grades: ASAP1, a normal healthy person; ASAP2, mild systemic disease; ASAP3, severe systemic disease; ASAP4, severe systemic disease that is a constant threat to life; ASAP5, a critically ill patient who is not expected to survive without the operation; and ASAP6, declared brain-dead patient whose organs are being removed for donor purposes.	Aspirin	4-7	ArfGAP with SH3 domain, ankyrin repeat and PH domain 3	Homo sapiens	104-109
23553791-6	2013	Systemic administration of aspirin, which significantly reduces the levels of IFN-gamma and TNF-alpha, results in blockage of MSC deficiency and tumorigenesis by inhibition of NFkappaB/SMAD7 and NFkappaB/c-FOS and c-MYC pathways in OVX mice.	Aspirin	27-34	FBJ osteosarcoma oncogene	Mus musculus	204-209
23579966-9	2013	Inhibition of platelet aggregation by aspirin in vitro has been associated with polymorphisms in the cyclo-oxygenase (COX)-1 gene.	Aspirin	38-45	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	101-124
23611778-0	2013	Aspirin overcomes Navitoclax-resistance in hepatocellular carcinoma cells through suppression of Mcl-1.	Aspirin	0-7	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	97-102
23611778-4	2013	Here, we reported that aspirin markedly suppressed Mcl-1 expression, and significantly enhanced Navitoclax-mediated cell viability inhibition and apoptosis induction in HCC cells.	Aspirin	23-30	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	51-56
23611778-5	2013	We further showed that aspirin robustly enhanced Navitoclax-triggered cytosolic cytochrome c release, activation of initiator caspase-9 and effector caspase-3, and cleavage of PARP.	Aspirin	23-30	caspase 9	Homo sapiens	126-135
23611778-7	2013	Taken together, our study suggests that aspirin can be used to enhance Navitoclax-mediated anticancer activity via suppression of Mcl-1.	Aspirin	40-47	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	130-135
23535745-1	2013	We report the development and demonstration of an assay that distinguishes the pharmacological effects of two widely used antiplatelet therapies, aspirin (COX-1 inhibitor) and clopidogrel (P2Y12 inhibitor).	Aspirin	146-153	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	155-160
23238666-1	2013	Inhibition of platelet function by aspirin results from irreversible inhibition of platelet cyclooxygenase (COX)-1.	Aspirin	35-42	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	92-114
23755755-6	2013	Aspirin alone inhibited profoundly and persistently platelet COX-1 activity and AA-induced platelet aggregation throughout 24-h dosing interval which was affected by the co-administration of floctafenine.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	61-66
22890587-3	2013	ASA"s cardioprotective antiplatelet effect is entirely COX-1 dependent.	Aspirin	0-3	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	55-60
22890587-15	2013	CONCLUSIONS: COX-1 affinity determines the interaction between NSAIDs and ASA on thrombocyte adhesion and aggregation.	Aspirin	74-77	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	13-18
23525414-9	2013	Expression of COX-2 (but not COX-1), mPGES-1, and macrophages was lower in the ASA group than in the control group.	Aspirin	79-82	prostaglandin E synthase	Mus musculus	37-44
23230963-0	2013	Aspirin-/TMZ-coloaded microspheres exert synergistic antiglioma efficacy via inhibition of beta-catenin transactivation.	Aspirin	0-7	catenin beta 1	Homo sapiens	91-103
23230963-4	2013	RESULTS: Aspirin microsphere treatment induced slight apoptosis and modestly inhibited proliferation of LN229 and U87 cells in vitro and in vivo through inhibition of beta-catenin transactivation.	Aspirin	9-16	catenin beta 1	Homo sapiens	167-179
23230963-8	2013	Furthermore, aspirin/TMZ microsphere intratumoral injection downregulated the expression of beta-catenin, TCF4, pAKT, pSTAT3, and PCNA and delayed tumor growth in nude mice harboring subcutaneous LN229 xenografts.	Aspirin	13-20	transcription factor 4	Mus musculus	106-110
23230963-9	2013	CONCLUSIONS: Aspirin sensitized TMZ chemotherapy efficacy through inhibition of beta-catenin transactivation; furthermore, the coloaded microspheres achieved a sustained release action to reduce the TMZ dosage, offering the potential for improved treatment of glioblastomas.	Aspirin	13-20	catenin beta 1	Homo sapiens	80-92
23132258-0	2013	Targeting FLIP and Mcl-1 using a combination of aspirin and sorafenib sensitizes colon cancer cells to TRAIL.	Aspirin	48-55	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	19-24
23132258-6	2013	The increase in rhTRAIL sensitivity was due to inhibition of FLIP and Mcl-1 protein expression following aspirin and sorafenib co-treatment, as confirmed by knock-down studies.	Aspirin	105-112	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	70-75
23132258-9	2013	These results underscore the potential of combining low doses of aspirin with sorafenib to inhibit proliferation and target the anti-apoptotic proteins FLIP and Mcl-1 in colon cancer cells.	Aspirin	65-72	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	161-166
22948171-2	2013	A possible antigen for ASA is the human cysteine-rich secretory protein 2 (CRISP-2), a sperm surface protein important in sperm-oocyte interaction.	Aspirin	23-26	cysteine rich secretory protein 2	Homo sapiens	40-73
22948171-2	2013	A possible antigen for ASA is the human cysteine-rich secretory protein 2 (CRISP-2), a sperm surface protein important in sperm-oocyte interaction.	Aspirin	23-26	cysteine rich secretory protein 2	Homo sapiens	75-82
22948171-7	2013	Interestingly, affinity-purified ASA from MAR+ patients" sera reacted against both Ves v 5 and CRISP-2, leading to sperm immobilization.	Aspirin	33-36	cysteine rich secretory protein 2	Homo sapiens	95-102
22948171-8	2013	Immunofluorescence analysis showed that ASA bound to the sperm surface, including the head part where CRISP-2 is localized.	Aspirin	40-43	cysteine rich secretory protein 2	Homo sapiens	102-109
23278865-0	2013	Cyclooxygenase expression and platelet function in healthy dogs receiving low-dose aspirin.	Aspirin	83-90	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	0-14
23278865-2	2013	HYPOTHESIS/OBJECTIVES: That low-dose aspirin would inhibit platelet function, decrease thromboxane synthesis, and alter platelet cyclooxygenase (COX) expression.	Aspirin	37-44	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	129-143
23278865-2	2013	HYPOTHESIS/OBJECTIVES: That low-dose aspirin would inhibit platelet function, decrease thromboxane synthesis, and alter platelet cyclooxygenase (COX) expression.	Aspirin	37-44	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	145-148
23278865-12	2013	CONCLUSIONS AND CLINICAL IMPORTANCE: Low-dose aspirin consistently inhibits platelet function in approximately one-third of healthy dogs, despite decreased thromboxane synthesis and increased platelet COX expression in most dogs.	Aspirin	46-53	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	201-204
22784989-13	2013	Aspirin exerted a negative effect on allergic skin inflammation by indirect regulation on DNMT1 via Tip60.	Aspirin	0-7	DNA methyltransferase 1	Rattus norvegicus	90-95
22784989-13	2013	Aspirin exerted a negative effect on allergic skin inflammation by indirect regulation on DNMT1 via Tip60.	Aspirin	0-7	lysine acetyltransferase 5	Rattus norvegicus	100-105
23063682-7	2012	The protein activity was measured by kynurenine concentration and the assay was validated by dose-responsive inhibition of IDO-1 antagonists including 1-methyltryptaphan, indomethacin and acetylsalicylic acid.	Aspirin	188-208	indoleamine 2,3-dioxygenase 1	Homo sapiens	123-128
22918213-8	2012	Further significant increases in periostin expression were noted in patients with chronic rhinosinusitis with nasal polyps and in those with aspirin-induced asthma.	Aspirin	141-148	periostin	Homo sapiens	33-42
22918213-10	2012	CONCLUSIONS: Production of pendrin and periostin is upregulated in allergic rhinitis, chronic rhinosinusitis with nasal polyps, and aspirin-induced asthma.	Aspirin	132-139	periostin	Homo sapiens	39-48
22862794-9	2012	The CD62P-positive platelet value of blood from volunteers who had taken aspirin was decreased, and platelet activation was inhibited as well.	Aspirin	73-80	selectin P	Homo sapiens	4-9
23282385-1	2012	: Aspirin (ASA) hypersensitivity comprises types I to III (Cox-1 mediated) and types IV and V (IgE antibody mediated).	Aspirin	2-9	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	59-64
23282385-1	2012	: Aspirin (ASA) hypersensitivity comprises types I to III (Cox-1 mediated) and types IV and V (IgE antibody mediated).	Aspirin	11-14	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	59-64
22574824-1	2012	INTRODUCTION: Association of P2RY1 and P2RY12 polymorphisms with on-aspirin platelet reactivity was investigated.	Aspirin	68-75	purinergic receptor P2Y1	Homo sapiens	29-34
22574824-12	2012	CONCLUSIONS: Polymorphisms in P2RY1 and P2RY12 are associated with on-aspirin platelet reactivity in patients with CAD.	Aspirin	70-77	purinergic receptor P2Y1	Homo sapiens	30-35
23019409-0	2012	Inhibition of pancreatic intraepithelial neoplasia progression to carcinoma by nitric oxide-releasing aspirin in p48(Cre/+)-LSL-Kras(G12D/+) mice.	Aspirin	102-109	interferon regulatory factor 9	Mus musculus	113-116
23019409-0	2012	Inhibition of pancreatic intraepithelial neoplasia progression to carcinoma by nitric oxide-releasing aspirin in p48(Cre/+)-LSL-Kras(G12D/+) mice.	Aspirin	102-109	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	128-132
22540218-0	2012	Aspirin twice a day keeps new COX-1 at bay.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	30-35
22343037-7	2012	ASA VI could decrease the levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin 6 (IL-6), but increase IL-10 content (P&lt;0.01, P&lt;0.05).	Aspirin	0-3	interleukin 10	Rattus norvegicus	115-120
22491884-6	2012	If ASS intake is interrupted for more than 48 h, aspirin desensitization should be resumed to prevent renewed intolerance reactions.	Aspirin	49-56	argininosuccinate synthase 1	Homo sapiens	3-6
22380734-0	2012	Potential association of DDR1 genetic variant with FEV1 decline by aspirin provocation in asthmatics.	Aspirin	67-74	discoidin domain receptor tyrosine kinase 1	Homo sapiens	25-29
22380734-3	2012	OBJECTIVE: To investigate the potential genetic associations between DDR1 and aspirin-exacerbated respiratory disease (AERD), this study conducted association studies of DDR1 single nucleotide polymorphisms (SNPs) with AERD and the obstructive symptom of forced expiratory volume in 1 s (FEV(1)) decline after aspirin provocation.	Aspirin	78-85	discoidin domain receptor tyrosine kinase 1	Homo sapiens	69-73
22380734-3	2012	OBJECTIVE: To investigate the potential genetic associations between DDR1 and aspirin-exacerbated respiratory disease (AERD), this study conducted association studies of DDR1 single nucleotide polymorphisms (SNPs) with AERD and the obstructive symptom of forced expiratory volume in 1 s (FEV(1)) decline after aspirin provocation.	Aspirin	310-317	discoidin domain receptor tyrosine kinase 1	Homo sapiens	170-174
22380734-7	2012	In the results of logistic analyses using age, sex, smoking status, and atopy as covariates, DDR1 rs1264320 in the intronic region showed a potent association signal with FEV(1) decline by aspirin provocation in asthmatics of this study even after corrections for multiple testing (p = .003 and corrected p = .01).	Aspirin	189-196	discoidin domain receptor tyrosine kinase 1	Homo sapiens	93-97
22380734-10	2012	CONCLUSION: Despite the need for further functional evaluations and replications, we conclude that DDR1 polymorphisms are not likely to contribute to predispositions of AERD, but may be potentially associated with FEV(1) decline by aspirin provocation in asthmatics.	Aspirin	232-239	discoidin domain receptor tyrosine kinase 1	Homo sapiens	99-103
22262921-8	2012	This was supported by the finding that in cocultures of a human colon adenocarcinoma cell line (HT-29) and platelets enhanced TXA(2) generation was almost completely inhibited by pretreatment of platelets with aspirin, a preferential inhibitor of COX-1.	Aspirin	210-217	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	247-252
22320344-1	2012	The resulting noncovalent bonding of the salicylic acid to ovine COX-1 after bromoaspirin and aspirin acetylation by Ser530 is investigated within the scope of density functional theory considering a 6.5 A radius binding pocket.	Aspirin	82-89	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	65-70
22320344-4	2012	We demonstrate that the binding energies of bromoaspirin and aspirin to COX-1 are very close when second-order quantum refinements of the structural data are performed, which points to an explanation on why the IC(50) values for the 126 muM COX-1 activity of both bromoaspirin and aspirin are practically the same.	Aspirin	49-56	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	72-77
22320344-4	2012	We demonstrate that the binding energies of bromoaspirin and aspirin to COX-1 are very close when second-order quantum refinements of the structural data are performed, which points to an explanation on why the IC(50) values for the 126 muM COX-1 activity of both bromoaspirin and aspirin are practically the same.	Aspirin	49-56	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	241-246
23317278-6	2012	In addition, the combination of exemestane and aspirin exhibited a synergistic inhibition of cell proliferation, significantly arrested the cell cycle in the G0/G1 phase and produced a stronger inhibitory effect on COX-1 and Bcl-2 expression than control or individual drug treatment.	Aspirin	47-54	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	215-220
22918738-2	2012	Aspirin acts by irreversibly inhibiting COX-1 and therefore blocking the synthesis of proaggregatory thromboxane A (2) (TxA(2)).	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	40-45
22942727-2	2012	Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression.	Aspirin	49-69	C-C motif chemokine ligand 2	Homo sapiens	191-221
22942727-2	2012	Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression.	Aspirin	49-69	C-C motif chemokine ligand 2	Homo sapiens	223-228
22942727-2	2012	Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression.	Aspirin	103-106	C-C motif chemokine ligand 2	Homo sapiens	191-221
22942727-2	2012	Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression.	Aspirin	103-106	C-C motif chemokine ligand 2	Homo sapiens	223-228
22942727-3	2012	We hypothesized that early treatment with ASA + ER-DP will reduce levels of MCP-1 also in patients with ischemic stroke.	Aspirin	42-45	C-C motif chemokine ligand 2	Homo sapiens	76-81
22942727-8	2012	Comparisons within MCP-1 baseline quartiles indicated that patients in the highest quartile (&gt;217-973 pg/mL) showed improved outcome at 90 days if treated with ASA + ER-DP in comparison to treatment with ASA alone (p = 0.004).	Aspirin	163-166	C-C motif chemokine ligand 2	Homo sapiens	19-24
22150675-5	2012	We aimed to compare the effects of aspirin and prodrugs of aspirin (1-5) on human platelet aggregation stimulated by ADP and collagen and associated receptor expression (GPIIb/IIIa and P-selectin) in platelet-rich plasma (PRP) and washed platelets (WP).	Aspirin	59-66	selectin P	Homo sapiens	185-195
23110215-4	2012	Moreover, we also showed by RNA interference that beta-catenin, an important target of aspirin in some studies, is an Sp-regulated gene.	Aspirin	87-94	catenin beta 1	Homo sapiens	50-62
23029468-10	2012	ACS14 also obviously inhibited Asp-induced upregulation of protein expression of oxidases including XOD, p47(phox) and p67(phox).	Aspirin	31-34	methionyl aminopeptidase 2	Rattus norvegicus	119-122
22662201-3	2012	Expression of PPARalpha receptor and PPARalpha ligands-biosynthetic (NAPE-PLD) and -degrading (FAAH and NAAA) enzymes were analyzed in untreated active and 5-ASA/glucocorticoids/immunomodulators-treated quiescent UC patients compared to healthy human colonic tissue by RT-PCR and immunohistochemical analyses.	Aspirin	158-161	peroxisome proliferator activated receptor alpha	Homo sapiens	14-23
22662201-3	2012	Expression of PPARalpha receptor and PPARalpha ligands-biosynthetic (NAPE-PLD) and -degrading (FAAH and NAAA) enzymes were analyzed in untreated active and 5-ASA/glucocorticoids/immunomodulators-treated quiescent UC patients compared to healthy human colonic tissue by RT-PCR and immunohistochemical analyses.	Aspirin	158-161	peroxisome proliferator activated receptor alpha	Homo sapiens	37-46
22021865-4	2011	In multivariable-adjusted logistic regression analyses, ASA class III-IV (OR 6.1, 95% CI:1.6-22.8) and higher Deyo-Charlson comorbidity score (OR 1.2, 95% CI:1.0-1.4) were significantly associated with odds of 90-day cardiac event post-THA in patients with no known previous cardiac event.	Aspirin	56-59	olfactory receptor family 2 subfamily I member 1 pseudogene	Homo sapiens	74-80
22021865-7	2011	In TKA patients with no previous cardiac history, age &gt;65 years (OR 4.1, 95% CI:1.2-14.0) and in TKA patients with known cardiac disease, ASA class III-IV (OR 3.2, 95% CI:1.8-5.7) was significantly associated with odds of 90-day cardiac events.	Aspirin	141-144	olfactory receptor family 7 subfamily E member 55 pseudogene	Homo sapiens	159-165
22128216-0	2011	Heat shock protein 70-dependent protective effect of polaprezinc on acetylsalicylic acid-induced apoptosis of rat intestinal epithelial cells.	Aspirin	68-88	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	0-21
22128216-13	2011	We conclude that polaprezinc-increased Heat shock protein 70 expression might be an important mechanism by which polaprezinc suppresses acetylsalicylic acid-induced small intestinal apoptosis, a hallmark of acetylsalicylic acid-induced enteropathy.	Aspirin	136-156	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	39-60
22128216-13	2011	We conclude that polaprezinc-increased Heat shock protein 70 expression might be an important mechanism by which polaprezinc suppresses acetylsalicylic acid-induced small intestinal apoptosis, a hallmark of acetylsalicylic acid-induced enteropathy.	Aspirin	207-227	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	39-60
21844189-7	2011	Aspirin was hydrolyzed by HEK cells transfected with PAFAH1B2 or PAFAH1B3, and the competitive type I PAF acetylhydrolase inhibitor NaF reduced erythrocyte hydrolysis of aspirin.	Aspirin	0-7	platelet activating factor acetylhydrolase 1b catalytic subunit 2	Homo sapiens	53-61
21844189-7	2011	Aspirin was hydrolyzed by HEK cells transfected with PAFAH1B2 or PAFAH1B3, and the competitive type I PAF acetylhydrolase inhibitor NaF reduced erythrocyte hydrolysis of aspirin.	Aspirin	0-7	PCNA clamp associated factor	Homo sapiens	53-56
21844189-7	2011	Aspirin was hydrolyzed by HEK cells transfected with PAFAH1B2 or PAFAH1B3, and the competitive type I PAF acetylhydrolase inhibitor NaF reduced erythrocyte hydrolysis of aspirin.	Aspirin	170-177	platelet activating factor acetylhydrolase 1b catalytic subunit 2	Homo sapiens	53-61
21844189-7	2011	Aspirin was hydrolyzed by HEK cells transfected with PAFAH1B2 or PAFAH1B3, and the competitive type I PAF acetylhydrolase inhibitor NaF reduced erythrocyte hydrolysis of aspirin.	Aspirin	170-177	PCNA clamp associated factor	Homo sapiens	53-56
21966608-0	2011	Polymorphisms of Aspirin-Metabolizing Enzymes CYP2C9, NAT2 and UGT1A6 in Aspirin-Intolerant Urticaria.	Aspirin	17-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
21966608-0	2011	Polymorphisms of Aspirin-Metabolizing Enzymes CYP2C9, NAT2 and UGT1A6 in Aspirin-Intolerant Urticaria.	Aspirin	73-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	0-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-106
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	0-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	23-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-106
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	23-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
21077940-8	2011	Aspirin, NDGA, and preconditioned apocynin suppressed ox-LDL-induced intracellular ROS production and LOX-1 expression, while allopurinol and rotenone failed to do so.	Aspirin	0-7	oxidized low density lipoprotein receptor 1	Rattus norvegicus	102-107
21720709-3	2011	Using aspirin, we found that the expression levels of AKT1 in glioma cells significantly correlated with the transcriptional activity of beta-catenin.	Aspirin	6-13	catenin beta 1	Homo sapiens	137-149
21816313-1	2011	OBJECTIVES: In this study we investigate: 1) the role of multidrug resistance protein-4 (MRP4), an organic anion unidirectional transporter, in modulating aspirin action on human platelet cyclooxygenase (COX)-1; and 2) whether the impairment of aspirin-COX-1 interaction, found in coronary artery bypass grafting (CABG) patients, could be dependent on MRP4-mediated transport.	Aspirin	155-162	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	188-210
21816313-1	2011	OBJECTIVES: In this study we investigate: 1) the role of multidrug resistance protein-4 (MRP4), an organic anion unidirectional transporter, in modulating aspirin action on human platelet cyclooxygenase (COX)-1; and 2) whether the impairment of aspirin-COX-1 interaction, found in coronary artery bypass grafting (CABG) patients, could be dependent on MRP4-mediated transport.	Aspirin	155-162	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	253-258
21816313-8	2011	Platelets from CABG patients showed a high expression of MRP4 whose in vitro inhibition enhanced aspirin effect on COX-1 (349 +- 141 pg/108 cells vs. 1,670 +- 646 pg/108 cells TxB2-production).	Aspirin	97-104	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	115-120
22122764-10	2011	COX-1 inhibition might also contribute to antitumour effects of aspirin, for example at low-dose aspirin.	Aspirin	64-71	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	0-5
22122764-10	2011	COX-1 inhibition might also contribute to antitumour effects of aspirin, for example at low-dose aspirin.	Aspirin	97-104	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	0-5
21529996-4	2011	RESULTS: Use of NSAIDs, particularly aspirin, was associated with a reduced odds ratio (OR) of SCC, especially tumors positive for p53 (OR 0.29; 95% confidence interval 0.11-0.79) or with PTCH loss of heterozygosity (OR 0.35; 95% confidence interval 0.13-0.96).	Aspirin	37-44	serpin family B member 3	Homo sapiens	95-98
21529996-8	2011	CONCLUSIONS: This study supports the hypothesis that NSAIDs, aspirin in particular, may reduce risk of SCC and may affect specific molecular subtypes of SCC.	Aspirin	61-68	serpin family B member 3	Homo sapiens	103-106
21529996-8	2011	CONCLUSIONS: This study supports the hypothesis that NSAIDs, aspirin in particular, may reduce risk of SCC and may affect specific molecular subtypes of SCC.	Aspirin	61-68	serpin family B member 3	Homo sapiens	153-156
21514281-7	2011	In VSMCs from SHR, aspirin increased p53 and p21 expression and inhibited the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E.	Aspirin	19-26	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	37-40
21228223-8	2011	Our results suggest a late PGE(2)-mediated phosphoregulation of LTC(4)S during microbial exposure, which may contribute to resolution of inflammation, with implications for aspirin hypersensitivity.	Aspirin	173-180	leukotriene C4 synthase	Homo sapiens	64-71
21251196-7	2011	Acetylsalicylic acid (ASA) and two structurally unrelated reversible cyclooxygenase inhibitors diclofenac and ibuprofen suppressed S1P release.	Aspirin	0-20	sphingosine-1-phosphate receptor 1	Mus musculus	131-134
21251196-7	2011	Acetylsalicylic acid (ASA) and two structurally unrelated reversible cyclooxygenase inhibitors diclofenac and ibuprofen suppressed S1P release.	Aspirin	22-25	sphingosine-1-phosphate receptor 1	Mus musculus	131-134
21251196-8	2011	Oral ASA (500-mg single dose or 100 mg over 3 days) attenuated S1P release from platelets in healthy human volunteers ex vivo.	Aspirin	5-8	sphingosine-1-phosphate receptor 1	Mus musculus	63-66
21528774-5	2011	RESULTS: The results showed that treatment with aspirin caused a marked decrease in pancreatic lipase and amylase compared with that of the control group.	Aspirin	48-55	pancreatic lipase	Rattus norvegicus	84-101
21528774-6	2011	This decrease in aspirin treated group was accompanied by significant increase in the intestinal amylase, lipase, alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) compared with the control group.	Aspirin	17-24	lipase G, endothelial type	Rattus norvegicus	106-112
21528774-7	2011	On the other hand, gum combined with aspirin caused a significant increase in pancreatic and intestinal lipase, amylase accompanied with significant increase in intestinal ALP and LDH compared with that of the control group.	Aspirin	37-44	lipase G, endothelial type	Rattus norvegicus	104-110
20940449-8	2011	Treatment of HUVECs with aspirin suppressed TGFbeta1 and enhanced TGFbeta-R1 mRNA expression during HR (both P &lt; .05 vs HR alone) without a change in p53 and p21 (P-NS).	Aspirin	25-32	H3 histone pseudogene 16	Homo sapiens	161-164
21319963-4	2011	The vast majority of atherothrombotic events in patients treated with aspirin result from mechanisms that are dependent on residual (non-COX-1-dependent) platelet reactivity.	Aspirin	70-77	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	137-142
21084063-6	2011	Treatment of rats with a single dose of aspirin (400mg/kg, orally) led to significant alterations in the levels of total nitrite and nitrate (NOx), interleukins (IL-4, 6, 10, 12), tumor necrosis factor (TNF-alpha), and interferon gamma (IFN-gamma).	Aspirin	40-47	interferon gamma	Rattus norvegicus	219-246
21226927-7	2011	ALR was treated by increasing the dose to 300 mg in a first step or to 500 mg ASA when the first modification did not take effect sufficiently.	Aspirin	78-81	growth factor, augmenter of liver regeneration	Homo sapiens	0-3
21226927-10	2011	For ALR, with a dose adjustment of 300 mg ASA daily, 94.6% of ALR were effectively treated and the residual 5.4% by administration of daily dosages of 500 mg ASA.	Aspirin	42-45	growth factor, augmenter of liver regeneration	Homo sapiens	4-7
21226927-10	2011	For ALR, with a dose adjustment of 300 mg ASA daily, 94.6% of ALR were effectively treated and the residual 5.4% by administration of daily dosages of 500 mg ASA.	Aspirin	42-45	growth factor, augmenter of liver regeneration	Homo sapiens	62-65
21226927-10	2011	For ALR, with a dose adjustment of 300 mg ASA daily, 94.6% of ALR were effectively treated and the residual 5.4% by administration of daily dosages of 500 mg ASA.	Aspirin	158-161	growth factor, augmenter of liver regeneration	Homo sapiens	4-7
21755814-2	2011	A simple analytical method using liquid chromatography-tandem mass spectrometry (LC-MS/MS) in atmospheric chemical ionization mode (APCI) for the simultaneous estimation of acetylsalicylic acid (ASA, CAS 50-78-2) and its active metabolite salicylic acid (SA, CAS 69-72-7) in human plasma has been developed and validated.	Aspirin	173-193	BCAR1 scaffold protein, Cas family member	Homo sapiens	259-262
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	30-36
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	TNF receptor superfamily member 1A	Homo sapiens	191-199
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	TNF receptor superfamily member 1A	Homo sapiens	287-295
21284493-7	2011	High residual platelet response in platelet function tests only partially dependent on COX-1 may reveal a condition of persistent platelet reactivity in a subset of aspirin-treated patients characterizing them as a subgroup at higher vascular risk.	Aspirin	165-172	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	87-92
20881612-9	2010	Aspirin had no effect on endothelial nitric oxide synthase and canceled the transcriptional activation of the LOX-1 and p47(phox) subunit of NADPH oxidase.	Aspirin	0-7	pleckstrin	Homo sapiens	120-154
20881612-10	2010	Based on these data, we hypothesize that aspirin preserves the integrity of adherens junctions and thus blunts angiogenic response to HR through downregulation of LOX-1 and the LOX-1-mediated p47(phox) component of NADPH oxidase transcription, thus preventing NADPH oxidase assembly and function.	Aspirin	41-48	pleckstrin	Homo sapiens	192-195
20930165-6	2010	In the Evaluation of Vascular Care in Alzheimer"s Disease (EVA) trial (conducted in our center), 4.6% of patients in the group receiving a multicomponent treatment that included aspirin had an ICH (3/65; 95% confidence interval [CI], 1.0 to 12.9) versus 0% in the control group (0/58; 95% CI, 0 to 6.2).	Aspirin	178-185	caspase 5	Homo sapiens	193-202
20739877-3	2010	To evaluate the association between glycoprotein IIIa PlA1/PlA2 polymorphism and 1-year cardiovascular events occurrence in aspirin-treated patients with stable coronary artery disease.	Aspirin	124-131	POU class 2 homeobox 3	Homo sapiens	54-58
20670296-0	2010	Acetyl salicylic acid (aspirin) improves synthesis of maspin and lowers incidence of metastasis in breast cancer patients [corrected].	Aspirin	0-21	serpin family B member 5	Homo sapiens	54-60
20670296-0	2010	Acetyl salicylic acid (aspirin) improves synthesis of maspin and lowers incidence of metastasis in breast cancer patients [corrected].	Aspirin	23-30	serpin family B member 5	Homo sapiens	54-60
20670296-2	2010	Ingestion of acetylsalicylic acid (aspirin) by breast cancer patients has been reported to restore the systemic synthesis of maspin through the stimulation of systemic nitric oxide production.	Aspirin	13-33	serpin family B member 5	Homo sapiens	125-131
20670296-2	2010	Ingestion of acetylsalicylic acid (aspirin) by breast cancer patients has been reported to restore the systemic synthesis of maspin through the stimulation of systemic nitric oxide production.	Aspirin	35-42	serpin family B member 5	Homo sapiens	125-131
20337611-0	2010	Conversion of Th17-type into Th2-type inflammation by acetyl salicylic acid via the adenosine and uric acid pathway in the lung.	Aspirin	54-75	heart and neural crest derivatives expressed 2	Mus musculus	29-32
20337611-11	2010	CONCLUSION: These findings suggest that ASA changes Th17-type into Th2-type inflammation mainly via the adenosine and uric acid metabolic pathway in the lung.	Aspirin	40-43	heart and neural crest derivatives expressed 2	Mus musculus	67-70
20823666-8	2010	Either SZ-21 or aspirin can inhibit the ADP-induced expression of P-selectin and GPIIb/IIIa.	Aspirin	16-23	selectin P	Homo sapiens	66-76
20564267-3	2010	A total of 6, 9 and 21 significant features with a false discovery rate of &lt;0.05 were identified by INCA upon comparing EDTA- versus EDTA-ASA-plasma, EDTA-plasma versus serum and EDTA-ASA-plasma versus serum, respectively.	Aspirin	141-144	caspase recruitment domain family member 17	Homo sapiens	103-107
20564267-3	2010	A total of 6, 9 and 21 significant features with a false discovery rate of &lt;0.05 were identified by INCA upon comparing EDTA- versus EDTA-ASA-plasma, EDTA-plasma versus serum and EDTA-ASA-plasma versus serum, respectively.	Aspirin	187-190	caspase recruitment domain family member 17	Homo sapiens	103-107
20135645-8	2010	CONCLUSION: These findings support an effect of aspirin use on PSA, particularly among never smokers.	Aspirin	48-55	kallikrein related peptidase 3	Homo sapiens	63-66
20421472-1	2010	Lipoxins (Lxs) and aspirin-triggered epi-Lxs (15-epi-LxA(4)) act through the ALX/FPRL1 receptor to block leukocyte trafficking, dampen cytokine/chemokine synthesis, and enhance phagocytic clearance of apoptotic leukocytes-key requisites for inflammatory resolution.	Aspirin	19-26	formyl peptide receptor 2	Homo sapiens	81-86
19880966-2	2010	Recent evidence suggests that aspirin and inhibitors of angiotensin-I converting enzyme (ACE inhibitors) have potential chemopreventive properties.	Aspirin	30-37	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	89-92
20443220-9	2010	Plasma gastrin levels were raised in subjects given melatonin or tryptophan plus ASA, but not in those with ASA alone.	Aspirin	81-84	gastrin	Homo sapiens	7-14
20443220-9	2010	Plasma gastrin levels were raised in subjects given melatonin or tryptophan plus ASA, but not in those with ASA alone.	Aspirin	108-111	gastrin	Homo sapiens	7-14
20543887-2	2010	Irreversible inhibition of platelet COX-1-derived TXA(2) with low-dose aspirin affords protection against primary and secondary vascular thrombotic events, underscoring the central role of TXA(2) as a platelet agonist in cardiovascular disease.	Aspirin	71-78	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	36-41
19940233-10	2010	Concomitant proton-pump inhibitor therapy may prevent advanced effects of low-dose aspirin.	Aspirin	83-90	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	12-23
20407607-2	2010	We hypothesized that minocycline induced MMP-2 and MMP-9 inhibition can be enhanced by aspirin, a non-selective COX and tPA inhibitor and this combination can reduce progression of diabetic retinopathy.	Aspirin	87-94	coproporphyrinogen oxidase	Rattus norvegicus	112-115
19887674-1	2010	We tested whether cyclooxygenase 2 (COX-2) expression and unacetylated COX-1 in newly formed platelets might contribute to persistent thromboxane (TX) biosynthesis in aspirin-treated essential thrombocythemia (ET).	Aspirin	167-174	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	71-76
19887674-10	2010	Accelerated platelet regeneration in most aspirin-treated ET patients may explain aspirin-persistent TXA(2) biosynthesis through enhanced COX-2 activity and faster renewal of unacetylated COX-1.	Aspirin	42-49	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	188-193
19887674-10	2010	Accelerated platelet regeneration in most aspirin-treated ET patients may explain aspirin-persistent TXA(2) biosynthesis through enhanced COX-2 activity and faster renewal of unacetylated COX-1.	Aspirin	82-89	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	188-193
19936928-0	2010	Aspirin induces apoptosis in human leukemia cells independently  of NF-kappaB and MAPKs through alteration of the Mcl-1/Noxa  balance.	Aspirin	0-7	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	114-119
19936928-9	2010	In contrast, aspirin decreased the protein levels of Mcl-1.	Aspirin	13-20	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	53-58
19936928-14	2010	These results indicate that aspirin induces apoptosis through alteration of the Mcl-1/ Noxa balance.	Aspirin	28-35	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	80-85
19880272-0	2010	Aspirin inhibits MMP-9 mRNA expression and release via the PPARalpha/gamma and COX-2/mPGES-1-mediated pathways in macrophages derived from THP-1 cells.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Homo sapiens	59-68
19880272-0	2010	Aspirin inhibits MMP-9 mRNA expression and release via the PPARalpha/gamma and COX-2/mPGES-1-mediated pathways in macrophages derived from THP-1 cells.	Aspirin	0-7	prostaglandin E synthase	Mus musculus	85-92
19880272-3	2010	The results indicated that after the macrophages were incubated with aspirin for 24h, the MMP-9 mRNA expression and release were decreased, while the PPAR alpha/gamma mRNA and protein expression was increased, respectively, and PPAR alpha/gamma agonists could also decrease MMP-9 mRNA expression and release.	Aspirin	69-76	peroxisome proliferator activated receptor alpha	Homo sapiens	150-160
19880272-3	2010	The results indicated that after the macrophages were incubated with aspirin for 24h, the MMP-9 mRNA expression and release were decreased, while the PPAR alpha/gamma mRNA and protein expression was increased, respectively, and PPAR alpha/gamma agonists could also decrease MMP-9 mRNA expression and release.	Aspirin	69-76	peroxisome proliferator activated receptor alpha	Homo sapiens	228-238
19880272-4	2010	Additionally, the COX-2 mRNA expression, mPGES-1 mRNA and protein expression in macrophages were all decreased after incubation with aspirin for 24h and the PGE(2) release was also decreased.	Aspirin	133-140	prostaglandin E synthase	Mus musculus	41-48
19880272-7	2010	It might be concluded that aspirin could inhibit the MMP-9 gene expression and release through the PPARalpha/gamma and COX-2/mPGES-1-mediated pathways and the two pathways might be partly overlapped and even be interrelated.	Aspirin	27-34	peroxisome proliferator activated receptor alpha	Homo sapiens	99-108
19880272-7	2010	It might be concluded that aspirin could inhibit the MMP-9 gene expression and release through the PPARalpha/gamma and COX-2/mPGES-1-mediated pathways and the two pathways might be partly overlapped and even be interrelated.	Aspirin	27-34	prostaglandin E synthase	Mus musculus	125-132
20444018-8	2010	In contrast, aspirin, flunixin meglumine, and PTPBS reduced tumor necrosis factor-alpha (TNFalpha) mRNA concentration.	Aspirin	13-20	tumor necrosis factor	Bos taurus	89-97
19955429-0	2010	Coxibs interfere with the action of aspirin by binding tightly to one monomer of cyclooxygenase-1.	Aspirin	36-43	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	81-97
19955429-2	2010	COX-1 and COX-2 are both targets of nonselective nonsteroidal antiinflammatory drugs (nsNSAIDs) including aspirin whereas COX-2 activity is preferentially blocked by COX-2 inhibitors called coxibs.	Aspirin	106-113	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	0-5
19955429-2	2010	COX-1 and COX-2 are both targets of nonselective nonsteroidal antiinflammatory drugs (nsNSAIDs) including aspirin whereas COX-2 activity is preferentially blocked by COX-2 inhibitors called coxibs.	Aspirin	106-113	prostaglandin-endoperoxide synthase 2	Canis lupus familiaris	10-15
19955429-5	2010	Although celecoxib binding to one monomer of COX-1 does not affect the normal catalytic processing of AA by the second, partner subunit, celecoxib does interfere with the inhibition of COX-1 by aspirin in vitro.	Aspirin	194-201	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	185-190
20858219-4	2010	Low-dose aspirin, behaving as a preferential inhibitor of platelet COX-1, allowed to enlighten the role exerted by this isoenzyme in many mammalian cell types.	Aspirin	9-16	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	67-72
21062249-6	2010	The causes of aspirin resistance are numerous but potential mechanisms include lack of patient adherence, non COX-1 mediated thromboxane A2 synthesis, increased activity of alternate platelet activation pathways, interference of aspirin action by other drugs and probably pharmacogenetic factors.	Aspirin	14-21	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	110-115
21067313-1	2010	Antiplatelet therapy for the management of patients with cardiovascular risks often includes a combination therapy of aspirin and clopidogrel, acting through inhibition of thromboxane generation and blockade of G(i)-coupled P2Y12 receptor, respectively.	Aspirin	118-125	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	224-229
20062920-4	2010	The expression of two gelsolin precursor isotypes and one F-acting capping protein isotype was decreased in ASA-resistant platelets (p&lt;0.05).	Aspirin	108-111	gelsolin	Homo sapiens	22-30
19706045-10	2009	Stimulation of COX-2 expression by aspirin was further enhanced following stimulation of the Wnt/beta-catenin pathway.	Aspirin	35-42	catenin beta 1	Homo sapiens	97-109
19706045-12	2009	CONCLUSION: These results demonstrate that the Wnt/beta-catenin pathway is a key modulator of aspirin-induced apoptosis in MSCs by regulation of mitochrondrial/caspase-3 function.	Aspirin	94-101	catenin beta 1	Homo sapiens	51-63
19957887-3	2009	In hot plate method, SN1 not only produced analgesia in mice but also potentiated the analgesic action of pentazocine and aspirin.	Aspirin	122-129	solute carrier family 38, member 3	Mus musculus	21-24
19427737-5	2009	Acetyl salicylic acid (Aspirin) is effective in lowering PAI-1 levels and platelets aggregation; as such we decided to treat patients affected by CSCR with low dose Aspirin.	Aspirin	0-21	serpin family E member 1	Homo sapiens	57-62
19427737-5	2009	Acetyl salicylic acid (Aspirin) is effective in lowering PAI-1 levels and platelets aggregation; as such we decided to treat patients affected by CSCR with low dose Aspirin.	Aspirin	23-30	serpin family E member 1	Homo sapiens	57-62
19542225-3	2009	In HepG2 human hepatoma cells and in LS180 colonic adenocarcinoma cells, NO-aspirin 2 inhibited 2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD)-induced cytochrome P450 (CYP) enzyme activity and CYP1A1 and CYP1A2 mRNA expression.	Aspirin	76-83	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	188-194
19542225-3	2009	In HepG2 human hepatoma cells and in LS180 colonic adenocarcinoma cells, NO-aspirin 2 inhibited 2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD)-induced cytochrome P450 (CYP) enzyme activity and CYP1A1 and CYP1A2 mRNA expression.	Aspirin	76-83	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	199-205
19542225-4	2009	These effects were further characterized as being mediated through transcriptional regulation: NO-aspirin 2 inhibited binding of ligand (TCDD)-activated aryl hydrocarbon receptor to the CYP1A1 enhancer sequence; additionally, NO-aspirin 2 suppressed carcinogen-induced expression of CYP1A heterogeneous nuclear RNA.	Aspirin	98-105	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	186-192
19542225-4	2009	These effects were further characterized as being mediated through transcriptional regulation: NO-aspirin 2 inhibited binding of ligand (TCDD)-activated aryl hydrocarbon receptor to the CYP1A1 enhancer sequence; additionally, NO-aspirin 2 suppressed carcinogen-induced expression of CYP1A heterogeneous nuclear RNA.	Aspirin	229-236	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	186-192
19542225-6	2009	Both HepG2 and LS180 cells treated with NO-aspirin 2 showed an increase in glutathione S-transferase-P1 (GST-P1), glutamate-cysteine ligase (GCL), and NAD(P)H:quinone oxidoreductase-1 (NQO1) expression.	Aspirin	43-50	glutathione S-transferase pi 1	Homo sapiens	75-103
19542225-6	2009	Both HepG2 and LS180 cells treated with NO-aspirin 2 showed an increase in glutathione S-transferase-P1 (GST-P1), glutamate-cysteine ligase (GCL), and NAD(P)H:quinone oxidoreductase-1 (NQO1) expression.	Aspirin	43-50	glutathione S-transferase pi 1	Homo sapiens	105-111
19597002-7	2009	However, aspirin(low) triggered 15-epi-lipoxin A(4) synthesis and up-regulated its receptor (FPRL1, ALX).	Aspirin	9-16	formyl peptide receptor 2	Homo sapiens	93-98
19652885-0	2009	Interactions of gallic acid, resveratrol, quercetin and aspirin at the platelet cyclooxygenase-1 level.	Aspirin	56-63	prostaglandin-endoperoxide synthase 1	Mus musculus	80-96
19652885-10	2009	Gallic acid interactions with other polyphenols or aspirin at the level of platelet COX-1 might partly explain the complex, and possibly contrasting, effects of wine and other components of the Mediterranean diet on platelets and on the pharmacologic effect of low-dose aspirin.	Aspirin	51-58	prostaglandin-endoperoxide synthase 1	Mus musculus	84-89
19652885-10	2009	Gallic acid interactions with other polyphenols or aspirin at the level of platelet COX-1 might partly explain the complex, and possibly contrasting, effects of wine and other components of the Mediterranean diet on platelets and on the pharmacologic effect of low-dose aspirin.	Aspirin	270-277	prostaglandin-endoperoxide synthase 1	Mus musculus	84-89
19465478-1	2009	The binding and structural studies of bovine lactoperoxidase with three aromatic ligands, acetylsalicylic acid (ASA), salicylhydoxamic acid (SHA), and benzylhydroxamic acid (BHA) show that all the three compounds bind to lactoperoxidase at the substrate binding site on the distal heme side.	Aspirin	90-110	lactoperoxidase	Bos taurus	45-60
19297212-10	2009	Aspirin and placebo treatment were associated with elevated P-selectin expression, platelet-monocyte aggregation and reduced CD42b expression (p&lt;0.05, Wilcoxon signed-rank test) post-exercise.	Aspirin	0-7	selectin P	Homo sapiens	60-70
19297212-11	2009	No difference was seen in spontaneous platelet aggregation whilst soluble P-selectin was reduced post-exercise with combination treatment with aspirin and cilostazol (p&lt;0.05, Wilcoxon signed-rank test).	Aspirin	143-150	selectin P	Homo sapiens	74-84
19276616-2	2009	A 21-day pre- and post-ischemic treatment with KGK (10 - 300 mg/kg) and aspirin (5 mg/kg) improved the spatial memory impairment and neuronal death in the hippocampal CA1 region induced by repeated cerebral ischemia.	Aspirin	72-79	carbonic anhydrase 1	Rattus norvegicus	167-170
19146957-0	2009	The significantly enhanced frequency of functional CD4+CD25+Foxp3+ T regulatory cells in therapeutic dose aspirin-treated mice.	Aspirin	106-113	forkhead box P3	Mus musculus	60-65
19146957-3	2009	However, the effect of ASA on CD4(+)CD25(+)Foxp3(+) Treg cells has yet to be determined.	Aspirin	23-26	forkhead box P3	Mus musculus	43-48
19146957-4	2009	The frequency, phenotype and immunosuppressive function of CD4(+)CD25(+)Foxp3(+) Treg cells were detected in BALB/c mice treated with low or high doses of ASA for 4 weeks.	Aspirin	155-158	forkhead box P3	Mus musculus	72-77
19146957-5	2009	ASA significantly decreased the percentage and number of CD4(+) T cells in the periphery, while ASA remarkably increased the percentage of CD4(+)CD25(+)Foxp3(+) Treg cells in CD4(+)T cells.	Aspirin	96-99	forkhead box P3	Mus musculus	152-157
19155731-8	2009	Medications associated with PPD are reviewed and the patient"s use of mesalamine and balsalazide for ulcerative colitis are deemed potential triggers, given their relative similarity to aspirin, a known trigger of PPD.	Aspirin	186-193	cellular communication network factor 6	Homo sapiens	214-217
19001529-9	2009	Mean log (FABP4) level showed lower values in subjects taking aspirin, and higher values in subjects taking statin and anti-hypertensive drugs.	Aspirin	62-69	fatty acid binding protein 4	Homo sapiens	10-15
19152549-8	2009	As expected, acetylsalicylic acid appeared to be COX-1-selective and ibuprofen effectively inhibited both COX-1 and COX-2.	Aspirin	13-33	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	49-54
19345936-5	2009	Herein, we tested a variety of Cox-1/Cox-2 non-selective NSAIDs, namely ibuprofen, tylenol, aspirin and naproxen and report that they blunt IgM and IgG synthesis in stimulated human peripheral blood mononuclear cells (PBMC).	Aspirin	92-99	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	31-36
19641312-9	2009	CONCLUSION: Triflusal modulates additional mechanisms to those of aspirin [pro-inflammatory (IL-6) and chemokine (MIP-1 and MCP-1) pathways] that could participate in the ischemic damage process following human acute stroke.	Aspirin	66-73	transportin 1	Homo sapiens	114-119
19641312-9	2009	CONCLUSION: Triflusal modulates additional mechanisms to those of aspirin [pro-inflammatory (IL-6) and chemokine (MIP-1 and MCP-1) pathways] that could participate in the ischemic damage process following human acute stroke.	Aspirin	66-73	C-C motif chemokine ligand 2	Homo sapiens	124-129
19729693-9	2009	Response to aspirin and clopidogrel was assessed by interaction with collagen (2microg/ml) and Adenosine diphosphate (ADP) (10micro/ml) respectively.	Aspirin	12-19	WD and tetratricopeptide repeats 1	Homo sapiens	95-122
19075637-13	2008	Recent investigations of Aspirin drug response have unraveled genetic variations in the cox-1 gene that are associated with the occurrence of Aspirin sensitivity or lack of protections against cardiovascular accidents.	Aspirin	25-32	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	88-93
19075637-13	2008	Recent investigations of Aspirin drug response have unraveled genetic variations in the cox-1 gene that are associated with the occurrence of Aspirin sensitivity or lack of protections against cardiovascular accidents.	Aspirin	142-149	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	88-93
19075637-14	2008	Screening for cox-1 gene variants will identify susceptible patients and reduce undesirable side-effects associated with Aspirin.	Aspirin	121-128	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	14-19
19513289-2	2008	This study investigated the effects of combining cilostazol with aspirin on the expressions of P-selectin and PAC-1 on activated platelets in acute ischemic stroke.	Aspirin	65-72	selectin P	Homo sapiens	95-105
18625344-4	2008	Nano-emulsion preparations of aspirin prepared with a Microfluidizer Processor were evaluated in the croton-oil-induced ear edema CD-1 mouse model using ear lobe thickness and the accumulation of specific in situ cytokines as biomarkers of inflammation.	Aspirin	30-37	CD1 antigen complex	Mus musculus	130-134
18625344-7	2008	In addition, the aspirin nano-emulsion further reduced the auricular levels of IL-1alpha (-37%) and TNFalpha (-69%) compared to the aspirin suspension preparation (p&lt;0.05).	Aspirin	17-24	interleukin 1 alpha	Mus musculus	79-88
18625344-9	2008	In conclusion, these studies indicate that a nano-emulsion preparation of aspirin significantly improved the anti-inflammatory properties of an aspirin suspension in a CD-1 mouse model of induced inflammation.	Aspirin	74-81	CD1 antigen complex	Mus musculus	168-172
18625344-9	2008	In conclusion, these studies indicate that a nano-emulsion preparation of aspirin significantly improved the anti-inflammatory properties of an aspirin suspension in a CD-1 mouse model of induced inflammation.	Aspirin	144-151	CD1 antigen complex	Mus musculus	168-172
18684223-8	2008	Treatment with aspirin was associated with a fall in total cholesterol, LDL-C and VLDL-C, and a significant rise in serum HDL-C. Aspirin treatment also restored endothelial function and beta(2)-adrenoceptor activity.	Aspirin	15-22	adrenoceptor beta 2	Rattus norvegicus	186-206
18684223-8	2008	Treatment with aspirin was associated with a fall in total cholesterol, LDL-C and VLDL-C, and a significant rise in serum HDL-C. Aspirin treatment also restored endothelial function and beta(2)-adrenoceptor activity.	Aspirin	129-136	adrenoceptor beta 2	Rattus norvegicus	186-206
18684223-11	2008	Aspirin improves endothelial function and beta(2)-adrenoceptor activity during experimentally induced hypercholesterolaemia in rats, possibly due to an antioxidant effect.	Aspirin	0-7	adrenoceptor beta 2	Rattus norvegicus	42-62
19145733-0	2008	Low-dose aspirin reduces the gene expression of gastrokine-1 in the antral mucosa of healthy subjects.	Aspirin	9-16	gastrokine 1	Homo sapiens	48-60
19145733-3	2008	AIM: To study the gastric mucosal expression of GKN1 during acute low-dose ASA consumption.	Aspirin	75-78	gastrokine 1	Homo sapiens	48-52
19145733-12	2008	CONCLUSION: Our data demonstrated that low-dose ASA downregulates GKN1 expression specifically in antral mucosa.	Aspirin	48-51	gastrokine 1	Homo sapiens	66-70
18411340-0	2008	Native and aspirin-triggered lipoxins control innate immunity by inducing proteasomal degradation of TRAF6.	Aspirin	11-18	TNF receptor associated factor 6	Homo sapiens	101-106
18411340-5	2008	In this study, we show that LX and aspirin (ASA)-triggered LX (ATL) inhibit innate immune signaling by inducing suppressor of cytokine signaling (SOCS) 2-dependent ubiquitinylation and proteasome-mediated degradation of TNF receptor-associated factor (TRAF) 2 and TRAF6, which are adaptor molecules that couple TNF and interleukin-1 receptor/Toll-like receptor family members to intracellular signaling events.	Aspirin	35-42	TNF receptor associated factor 6	Homo sapiens	264-269
18411340-5	2008	In this study, we show that LX and aspirin (ASA)-triggered LX (ATL) inhibit innate immune signaling by inducing suppressor of cytokine signaling (SOCS) 2-dependent ubiquitinylation and proteasome-mediated degradation of TNF receptor-associated factor (TRAF) 2 and TRAF6, which are adaptor molecules that couple TNF and interleukin-1 receptor/Toll-like receptor family members to intracellular signaling events.	Aspirin	44-47	TNF receptor associated factor 6	Homo sapiens	264-269
18411340-9	2008	Proteasomal degradation of TRAF6 is a central mechanism underlying LX-driven immune counterregulation, and a hitherto unappreciated mechanism of action of ASA.	Aspirin	155-158	TNF receptor associated factor 6	Homo sapiens	27-32
18355801-8	2008	Aspirin effect on B2 receptor binding properties is not accompanied by alteration of the cell-surface organization of the receptor in dimers and monomers.	Aspirin	0-7	bradykinin receptor B2	Homo sapiens	18-29
18355801-9	2008	Aspirin does not influence the receptor ability to transduce bradykinin binding into activation of G-proteins and phospholipase C. These results suggest that aspirin is an allosteric inhibitor of the B2 receptor, a property that may be involved in its therapeutic actions.	Aspirin	158-165	bradykinin receptor B2	Homo sapiens	200-211
18393288-8	2008	We also observed that the ASA-dependent inhibition of viral replication was due in part to inhibition of COX-2 and activation of p38 and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 (MEK1/2) mitogen-activated protein kinases (MAPKs).	Aspirin	26-29	mitogen-activated protein kinase kinase 1	Homo sapiens	220-226
18393288-10	2008	Taken together, our findings suggest that the anti-HCV effect of ASA in the Huh7 replicon cells is due to its inhibitory effect on COX-2 expression, which is mediated in part by the activation of MEK1/2/p38 MAPK.	Aspirin	65-68	mitogen-activated protein kinase kinase 1	Homo sapiens	196-202
18391768-7	2008	The gene most characteristic of the ASA phenotype was periostin (POSTN), which was upregulated relative to controls.	Aspirin	36-39	periostin	Homo sapiens	54-63
18391768-7	2008	The gene most characteristic of the ASA phenotype was periostin (POSTN), which was upregulated relative to controls.	Aspirin	36-39	periostin	Homo sapiens	65-70
18222077-0	2008	Differential modulation of PPARalpha and gamma target gene expression in the liver and kidney of rats treated with aspirin.	Aspirin	115-122	peroxisome proliferator activated receptor alpha	Rattus norvegicus	27-36
18059035-6	2008	However, recent aspirin/NSAID use significantly interacted with both LEP polymorphisms.	Aspirin	16-23	leptin	Homo sapiens	69-72
18393143-18	2008	The favorable clinical outcomes with aspirin and clopidogrel have validated cyclooxygenase (COX)-1 and P2Y (12) receptors as targets for new drug development.	Aspirin	37-44	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	76-98
18053020-1	2008	BACKGROUND AND AIMS: Aspirin, a cyclo-oxygenase (COX)-1 and COX-2 inhibitor, is the antiplatelet drug of choice to prevent serious vascular events.	Aspirin	21-28	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	32-55
18175938-0	2008	Down-regulation of tyrosinase expression by acetylsalicylic acid in murine B16 melanoma.	Aspirin	44-64	tyrosinase	Mus musculus	19-29
18175938-8	2008	To clarify the target of ASA action in melanogenesis, we performed Western blotting for tyrosinase, which is a key melanogenic enzyme.	Aspirin	25-28	tyrosinase	Mus musculus	88-98
18175938-9	2008	ASA inhibited tyrosinase expression in a dose-dependent manner.	Aspirin	0-3	tyrosinase	Mus musculus	14-24
18175938-10	2008	Therefore, the depigmenting effect of ASA might be due to inhibition of tyrosinase expression or enhancement of tyrosinase degradation.	Aspirin	38-41	tyrosinase	Mus musculus	72-82
18175938-10	2008	Therefore, the depigmenting effect of ASA might be due to inhibition of tyrosinase expression or enhancement of tyrosinase degradation.	Aspirin	38-41	tyrosinase	Mus musculus	112-122
17584993-14	2008	This different response might indicate COX-1-dependent prostaglandin E2 control of inflammatory cells in aspirin-induced asthma.	Aspirin	105-112	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	39-44
17631383-3	2008	Our objective was to examine whether platelet responsiveness to in vitro aspirin treatment could be affected by cyclooxygenase (COX)-1/2 protein levels in platelets or single-nucleotide polymorphisms (SNPs), which could possibly change specific activity of enzymes and/or aspirin susceptibility.	Aspirin	73-80	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	112-134
18231737-1	2007	To explore the correlation between the C807T polymorphism of platelet membrane glycoprotein I a (GP I a) gene and aspirin resistance in Chinese people, 200 patients with high-risk of atherosclerosis took aspirin (100 mg/d) for 7 days.	Aspirin	114-121	multimerin 1	Homo sapiens	97-103
18231737-1	2007	To explore the correlation between the C807T polymorphism of platelet membrane glycoprotein I a (GP I a) gene and aspirin resistance in Chinese people, 200 patients with high-risk of atherosclerosis took aspirin (100 mg/d) for 7 days.	Aspirin	204-211	multimerin 1	Homo sapiens	97-103
18045204-8	2007	Aspirin, which is a well known salicylic acid-based drug, was also found to inhibit AKR1C1 activity.	Aspirin	0-7	aldo-keto reductase family 1 member C1	Homo sapiens	84-90
18045204-9	2007	This is the first report to show aspirin (IC(50)=21 microM) and its metabolite salicylic acid (IC(50)=7.8 microM) as inhibitors of AKR1C1.	Aspirin	33-40	aldo-keto reductase family 1 member C1	Homo sapiens	131-137
17510082-6	2007	Aspirin and sulindac sulfide induced a G1 arrest within 48 h. While all cell lines responded in a comparable way to sulindac sulfide, the aspirin-induced G1 arrest was dependent on p21Waf1/Cip1--as cells lacking the cyclin-dependent kinase inhibitor failed to show this arrest--and on ataxia-telangiectasia-mutated kinase (ATM)--as the inhibitor caffeine abrogated the checkpoint.	Aspirin	138-145	ATM serine/threonine kinase	Homo sapiens	285-321
17510082-6	2007	Aspirin and sulindac sulfide induced a G1 arrest within 48 h. While all cell lines responded in a comparable way to sulindac sulfide, the aspirin-induced G1 arrest was dependent on p21Waf1/Cip1--as cells lacking the cyclin-dependent kinase inhibitor failed to show this arrest--and on ataxia-telangiectasia-mutated kinase (ATM)--as the inhibitor caffeine abrogated the checkpoint.	Aspirin	138-145	ATM serine/threonine kinase	Homo sapiens	323-326
17510082-8	2007	Aspirin induced the phosphorylation of p53 at residue Ser15 within 8 h in a caffeine-dependent manner, and also caused the activation of checkpoint kinase 2 and the cleavage of caspase 7.	Aspirin	0-7	caspase 7	Homo sapiens	177-186
17510082-9	2007	Our results suggest that aspirin induces a G1 arrest and apoptosis by activating p53 and p21Waf1/Cip1 in an ATM-dependent way.	Aspirin	25-32	ATM serine/threonine kinase	Homo sapiens	108-111
17545608-8	2007	More interestingly, aspirin, a nonsteroidal anti-inflammatory drug that preferentially inhibits COX-1, compromises PPARdelta function and cell growth by inhibiting extracellular signal-regulated kinases 1/2, members of the mitogen-activated protein kinase family.	Aspirin	20-27	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	96-101
17296320-1	2007	OBJECTIVES: Platelet monocyte aggregates (PMA) and monocyte chemoattractant protein-1 (MCP-1) play a significant role in atherosclerotic disease but the effect of aspirin and their role in peripheral arterial disease (PAD) requires further investigation.	Aspirin	163-170	C-C motif chemokine ligand 2	Homo sapiens	87-92
17543677-8	2007	CONCLUSIONS: Flow cytometric measurement of CD62p expression on platelets after incubation with ARA proved to be a practicable tool to monitor aspirin-induced inhibition of platelet COX.	Aspirin	143-150	selectin P	Homo sapiens	44-49
17559347-0	2007	Frequency of genetic polymorphisms of COX1, GPIIIa and P2Y1 in a Chinese population and association with attenuated response to aspirin.	Aspirin	128-135	purinergic receptor P2Y1	Homo sapiens	55-59
17559347-8	2007	As a comparison reference group, 6 out of 24 subjects in the prospective aspirin trial had the P2Y1 CT893/AG1622 genotype that displays a low frequency (&lt;7%) in the Chinese population.	Aspirin	73-80	purinergic receptor P2Y1	Homo sapiens	95-99
17559347-12	2007	After aspirin treatment, the net decrease in arachidonic acid-induced platelet aggregation was significantly larger in the P2Y1 CT893/AG1622 genotype panel (83.4 +/- 3.7%, net reduction by aspirin expressed as percentage of baseline) compared with CC893/GG1622 (68.2 +/- 13.5%), CC893/AG1622 (68.9 +/- 9.6%) and CC893/AA1622 (65.1 +/- 9.1%) genotypic groups (p = 0.012, 0.025 and 0.004, respectively; statistical power = 77%).	Aspirin	6-13	purinergic receptor P2Y1	Homo sapiens	123-127
17559347-12	2007	After aspirin treatment, the net decrease in arachidonic acid-induced platelet aggregation was significantly larger in the P2Y1 CT893/AG1622 genotype panel (83.4 +/- 3.7%, net reduction by aspirin expressed as percentage of baseline) compared with CC893/GG1622 (68.2 +/- 13.5%), CC893/AG1622 (68.9 +/- 9.6%) and CC893/AA1622 (65.1 +/- 9.1%) genotypic groups (p = 0.012, 0.025 and 0.004, respectively; statistical power = 77%).	Aspirin	189-196	purinergic receptor P2Y1	Homo sapiens	123-127
17559347-16	2007	Importantly, the presence of the P2Y1 893CC genotype appears to confer an attenuated antiplatelet effect during aspirin treatment in healthy Chinese volunteers.	Aspirin	112-119	purinergic receptor P2Y1	Homo sapiens	33-37
17589617-5	2007	Consequently, the use of the thrombolytic recombinant tissue-plasminogen activator (rTPA) associated with aspirin was the treatment of choice, and complete dissolution of the thrombus was achieved without adverse effects.	Aspirin	106-113	plasminogen activator, tissue type	Rattus norvegicus	84-88
17580408-0	2007	Aspirin is lifesaving for cancer patients with ACS.	Aspirin	0-7	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	47-50
17518513-6	2007	However, a similar interaction was not observed with other commonly used drugs, including lower doses of aspirin, which target preferentially COX-1.	Aspirin	105-112	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	142-147
17068302-7	2006	At 2 years, 56% of the patients treated with IAT and 42% of the patients treated with aspirin achieved functional independence (mRS, 0 to 2; P=0.037).	Aspirin	86-93	sterile alpha motif domain containing 11	Mus musculus	128-131
16880202-5	2006	Aspirin exposure also resulted in an increase in the half-life of pd1EGFP, a model substrate of proteasome, as well as various intracellular substrates like Bax, IkappaB-alpha, p53, and p27(kip1).	Aspirin	0-7	BCL2-associated X protein	Mus musculus	157-160
16880202-5	2006	Aspirin exposure also resulted in an increase in the half-life of pd1EGFP, a model substrate of proteasome, as well as various intracellular substrates like Bax, IkappaB-alpha, p53, and p27(kip1).	Aspirin	0-7	cyclin-dependent kinase inhibitor 1B	Mus musculus	186-189
16880202-5	2006	Aspirin exposure also resulted in an increase in the half-life of pd1EGFP, a model substrate of proteasome, as well as various intracellular substrates like Bax, IkappaB-alpha, p53, and p27(kip1).	Aspirin	0-7	cyclin-dependent kinase inhibitor 1B	Mus musculus	190-194
16893520-0	2006	Aspirin upregulates expression of urokinase type plasminogen activator receptor (uPAR) gene in human colon cancer cells through AP1.	Aspirin	0-7	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	128-131
16893520-5	2006	Using gel mobility shift assays, it is found that the distal AP1 region between -171 and -186 is responsible for the aspirin-induced up-regulation of uPAR.	Aspirin	117-124	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	61-64
16893520-10	2006	Thus, an AP1 mediated pathway for aspirin induced up-regulation of uPAR has been identified.	Aspirin	34-41	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	9-12
17026894-10	2006	Compared with the patients treated with clopidogrel and ASA in the CURE study, we also found a three times greater risk of major bleeding in period 2.	Aspirin	56-59	period circadian regulator 2	Homo sapiens	141-149
16829143-6	2006	On treatment with aspirin, which inhibited the cell-cell contact and network-like structure formation, there was no down regulation of MMPs and cells continued to produce MMP-2 and MMP-9.	Aspirin	18-25	matrix metallopeptidase 9	Homo sapiens	181-186
16816107-4	2006	In contrast, using 5 mmol/l of aspirin, SR-BI expression and function were significantly decreased.	Aspirin	31-38	scavenger receptor class B member 1	Homo sapiens	40-45
16816107-7	2006	We could show that COX-independent effects of aspirin were able to enhance expression of SR-BI in macrophages in a post-transcriptional, PPAR-alpha independent way, suggesting a novel pharmacologic effect of aspirin.	Aspirin	46-53	scavenger receptor class B member 1	Homo sapiens	89-94
16816107-7	2006	We could show that COX-independent effects of aspirin were able to enhance expression of SR-BI in macrophages in a post-transcriptional, PPAR-alpha independent way, suggesting a novel pharmacologic effect of aspirin.	Aspirin	208-215	scavenger receptor class B member 1	Homo sapiens	89-94
16600694-2	2006	Since accelerated atherosclerosis is the main complication of diabetes and both diseases encompass an inflammatory reaction, we hypothesized that the anti-inflammatory drugs, aspirin and peroxisome proliferator-activated receptor (PPAR-alpha) activators (fenofibrate and clofibrate), could have an effect on the high glucose-induced MCP-1 expression in endothelial cells.	Aspirin	175-182	chemokine (C-C motif) ligand 2	Mus musculus	333-338
16600694-5	2006	The results showed that (i) aspirin, fenofibrate and clofibrate decrease significantly the MCP-1 expression and secretion in human endothelial cells; (ii) the high glucose up-regulated expression of MCP-1 in endothelial cells was significantly reduced by inhibitors of NF-kB and reactive oxygen species; (iii) all drugs notably decrease the level of the reactive oxygen species and activation of NF-kB and AP-1.	Aspirin	28-35	chemokine (C-C motif) ligand 2	Mus musculus	199-204
16635206-9	2006	About 30% of ASA recognized apo lactate dehydrogenase (LDHC4) as a cognate antigen, 30% voltage-dependent anion channel (VDAC2).	Aspirin	13-16	lactate dehydrogenase C	Mus musculus	55-60
16267095-5	2006	Compared with untreated Min mice, NO-ASA increased in the liver the activity (nmol/min/mg; mean+/-SEM for all) of NQO (85+/-6 versus 128+/-11, P&lt;0.05) and GST (2560+/-233 versus 4254+/-608, P&lt;0.005) and also in the intestine but not in the kidney; the expression of NQO1 and GST P1-1 was also increased.	Aspirin	37-40	NAD(P)H dehydrogenase, quinone 1	Mus musculus	272-276
16267095-8	2006	NO-ASA induced concentration-dependently the translocation of Nrf2 into the nucleus as documented by immunofluorescence and immunoblotting; this paralleled the induction of NQO1 and GST P1-1.	Aspirin	3-6	NAD(P)H dehydrogenase, quinone 1	Mus musculus	173-177
16267095-9	2006	Thus NO-ASA induces phase II enzymes, at least in part, through the action of NO that it releases and by modulating the Keap1-Nrf2 pathway; this effect may be part of its mechanism of action against colon and other cancers.	Aspirin	8-11	kelch-like ECH-associated protein 1	Mus musculus	120-125
16649551-0	2006	ACEA (arachidonyl-2-chloroethylamide), the selective cannabinoid CB1 receptor agonist, protects against aspirin-induced gastric ulceration.	Aspirin	104-111	cannabinoid receptor 1	Rattus norvegicus	65-68
16497833-0	2006	Reversal to cisplatin sensitivity in recurrent human ovarian cancer cells by NCX-4016, a nitro derivative of aspirin.	Aspirin	109-116	T cell leukemia homeobox 2	Homo sapiens	77-80
16497833-5	2006	We used NCX-4016 [2-(acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester], a derivative of aspirin containing a nitro group that releases nitric oxide in a sustained fashion for several hours in cells and in vivo, and we studied its cytotoxic efficacy against human ovarian cancer cells (HOCCs).	Aspirin	93-100	T cell leukemia homeobox 2	Homo sapiens	8-11
16516312-0	2006	Aspirin-induced blockade of NF-kappaB activity restrains up-regulation of glial fibrillary acidic protein in human astroglial cells.	Aspirin	0-7	glial fibrillary acidic protein	Homo sapiens	74-105
16516312-3	2006	Aspirin, widely used to prevent NF-kappaB activity, reduced the levels of GFAP mRNA and protein in human astroglial cells including human glioblastoma A172 cells and primary human brain astrocyte cells (HBAs).	Aspirin	0-7	glial fibrillary acidic protein	Homo sapiens	74-78
16516312-4	2006	Furthermore, aspirin inhibited the effects of hypoxic injury on the up-regulation of GFAP expression in HBAs.	Aspirin	13-20	glial fibrillary acidic protein	Homo sapiens	85-89
16516312-5	2006	We confirmed the repressive effect of aspirin on GFAP transcription by GFAP promoter-driven reporter assay and found that one NF-kappaB binding site conserved in the mouse and human GFAP gene promoters is critical for this effect.	Aspirin	38-45	glial fibrillary acidic protein	Homo sapiens	71-75
16310244-7	2006	The data also showed that NF-kappaB activation and its associated gene expressions, such as COX-2, iNOS, VCAM-1 and ICAM-1, were all suppressed by the low dose aspirin supplementation through the inhibition of phosphorylation and degradation of IkappaBalpha via the NIK/IKK pathway.	Aspirin	160-167	intercellular adhesion molecule 1	Rattus norvegicus	116-122
16293803-0	2006	Complement C3a and C4a increased in plasma of patients with aspirin-induced asthma.	Aspirin	60-67	complement C3	Homo sapiens	11-14
16293803-10	2006	Moreover, C3a and C4a levels and the ratios of C3a/C3 and C4a/C4 were correlated with the changes of FEV(1) values after aspirin challenge.	Aspirin	121-128	complement C3	Homo sapiens	10-13
16293803-10	2006	Moreover, C3a and C4a levels and the ratios of C3a/C3 and C4a/C4 were correlated with the changes of FEV(1) values after aspirin challenge.	Aspirin	121-128	complement C3	Homo sapiens	47-50
16393293-1	2006	BACKGROUND: In animal studies, aspirin and non-aspirin non-steroidal anti-inflammatory drugs contribute to gastroduodenal damage via cyclo-oxygenase inhibition and consecutive leucotriene formation (COX-LOX eicosanoid shunt).	Aspirin	31-38	lysyl oxidase	Homo sapiens	203-206
16393293-1	2006	BACKGROUND: In animal studies, aspirin and non-aspirin non-steroidal anti-inflammatory drugs contribute to gastroduodenal damage via cyclo-oxygenase inhibition and consecutive leucotriene formation (COX-LOX eicosanoid shunt).	Aspirin	47-54	lysyl oxidase	Homo sapiens	203-206
15970796-0	2005	Association analysis of cysteinyl-leukotriene receptor 2 (CYSLTR2) polymorphisms with aspirin intolerance in asthmatics.	Aspirin	86-93	cysteinyl leukotriene receptor 2	Homo sapiens	24-56
15970796-0	2005	Association analysis of cysteinyl-leukotriene receptor 2 (CYSLTR2) polymorphisms with aspirin intolerance in asthmatics.	Aspirin	86-93	cysteinyl leukotriene receptor 2	Homo sapiens	58-65
15970796-1	2005	OBJECTIVES AND METHODS: The cysteinyl leukotriene receptor 2 (CYSLTR2) gene on chromosome 13q14.12-q21.1 encodes a receptor for CYSLTs, potent biological mediators in the pathogenesis of asthma, particularly that associated with aspirin intolerance (AIA).	Aspirin	229-236	cysteinyl leukotriene receptor 2	Homo sapiens	28-60
15970796-1	2005	OBJECTIVES AND METHODS: The cysteinyl leukotriene receptor 2 (CYSLTR2) gene on chromosome 13q14.12-q21.1 encodes a receptor for CYSLTs, potent biological mediators in the pathogenesis of asthma, particularly that associated with aspirin intolerance (AIA).	Aspirin	229-236	cysteinyl leukotriene receptor 2	Homo sapiens	62-69
15970796-2	2005	In an effort to discover additional polymorphism(s), the variant(s) of which have been implicated in asthma and aspirin intolerance, we scrutinized genetic polymorphisms of the CYSLTR2 gene, and evaluated this locus as a potential candidate for asthma.	Aspirin	112-119	cysteinyl leukotriene receptor 2	Homo sapiens	177-184
15970796-10	2005	CONCLUSION: CYSLTR2 polymorphisms are associated with aspirin intolerance in asthmatics.	Aspirin	54-61	cysteinyl leukotriene receptor 2	Homo sapiens	12-19
15935075-3	2005	We show here that aspirin exerts at least some of its effects through PKCzeta, decreasing the NMDA-induced activation, cleavage and nuclear translocation of this molecule.	Aspirin	18-25	protein kinase C zeta	Homo sapiens	70-77
15935075-4	2005	Aspirin (acetylsalicylic acid) directly inhibited the protein kinase activity of PKCzeta, whereas salicylic acid did not.	Aspirin	0-7	protein kinase C zeta	Homo sapiens	81-88
15935075-4	2005	Aspirin (acetylsalicylic acid) directly inhibited the protein kinase activity of PKCzeta, whereas salicylic acid did not.	Aspirin	9-29	protein kinase C zeta	Homo sapiens	81-88
15935075-5	2005	This direct effect of aspirin on purified human PKCzeta is consistent with PKCzeta inhibition preventing the NMDA-induced death of cortical neurones.	Aspirin	22-29	protein kinase C zeta	Homo sapiens	48-55
15935075-5	2005	This direct effect of aspirin on purified human PKCzeta is consistent with PKCzeta inhibition preventing the NMDA-induced death of cortical neurones.	Aspirin	22-29	protein kinase C zeta	Homo sapiens	75-82
15935075-8	2005	Aspirin protects cells against NMDA-induced apoptosis by means of a novel mechanism targeting PKCzeta, a key molecule in inflammatory responses and neurodegeneration.	Aspirin	0-7	protein kinase C zeta	Homo sapiens	94-101
15755483-1	2005	Besides aspirin several new drugs for inhibition of platelet aggregation and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibition are used in secondary stroke prevention.	Aspirin	8-15	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	Mus musculus	77-134
15696087-4	2005	OBJECTIVE: To compare expression of cysLT 1 and cysLT 2 on leukocytes, mucus glands, and epithelium in 32 patients with chronic polypoid rhinosinusitis (21 aspirin-sensitive, 11 aspirin-tolerant) and 9 normal controls.	Aspirin	156-163	cysteinyl leukotriene receptor 2	Homo sapiens	48-55
15696087-6	2005	RESULTS: The percentages of mucosal CD45 + leukocytes expressing cysLT 1 were significantly ( P &lt; .0001) elevated in the aspirin-sensitive but not the aspirin-tolerant patients compared with the controls.	Aspirin	124-131	protein tyrosine phosphatase receptor type C	Homo sapiens	36-40
15696087-8	2005	On epithelial and glandular cells, expression of cysLT 2 significantly exceeded that of cysLT 1 in both the patients with rhinosinusitis and the controls ( P &lt; or = .004), although there was no significant difference in the expression of either receptor in the patients with rhinosinusitis (aspirin-sensitive or aspirin-tolerant) and the controls.	Aspirin	294-301	cysteinyl leukotriene receptor 2	Homo sapiens	49-56
15696087-8	2005	On epithelial and glandular cells, expression of cysLT 2 significantly exceeded that of cysLT 1 in both the patients with rhinosinusitis and the controls ( P &lt; or = .004), although there was no significant difference in the expression of either receptor in the patients with rhinosinusitis (aspirin-sensitive or aspirin-tolerant) and the controls.	Aspirin	315-322	cysteinyl leukotriene receptor 2	Homo sapiens	49-56
15624282-7	2004	Administration of GpIIb/IIIa in addition to thrombolytics, aspirin and heparin was associated with a significant reduction in the combined criteria by 17% (95% CI: 10% - 23%) and a significant excess of major bleeding by 69% (95% CI: 38% - 109%).	Aspirin	59-66	integrin subunit alpha 2b	Homo sapiens	18-23
15643090-9	2004	In consistency with the changes of Ad-ETR1 mRNA, ethylene or ASA treatment had marked effects on the kiwifruit ethylene production and fruit softening (Fig.	Aspirin	61-64	Signal transduction histidine kinase, hybrid-type, ethylene sensor	Arabidopsis thaliana	38-42
15345513-10	2004	Vascular endothelial growth factor-A expression was reduced by aspirin, with this effect being blunted by NCX 4016.	Aspirin	63-70	vascular endothelial growth factor A	Mus musculus	0-36
15646027-2	2004	Here we analyze the role of PPARdelta in aspirin-induced apoptosis of Jurkat cells, which, together with other lymphoid cell lines, express PPARdelta mRNA.	Aspirin	41-48	peroxisome proliferator activated receptor delta	Homo sapiens	28-37
15646027-2	2004	Here we analyze the role of PPARdelta in aspirin-induced apoptosis of Jurkat cells, which, together with other lymphoid cell lines, express PPARdelta mRNA.	Aspirin	41-48	peroxisome proliferator activated receptor delta	Homo sapiens	140-149
15646027-3	2004	Aspirin increased PPARdelta mRNA levels in Jurkat cells, but decreased the activity of both PPARdelta and PPARalpha/gamma, assayed using the luciferase reporter constructs DRE and ACO, respectively.	Aspirin	0-7	peroxisome proliferator activated receptor delta	Homo sapiens	18-27
15646027-3	2004	Aspirin increased PPARdelta mRNA levels in Jurkat cells, but decreased the activity of both PPARdelta and PPARalpha/gamma, assayed using the luciferase reporter constructs DRE and ACO, respectively.	Aspirin	0-7	peroxisome proliferator activated receptor delta	Homo sapiens	92-101
15365123-11	2004	There was a trend toward higher risk of recurrent stroke or death as F1.2 levels increased in aspirin (RR: 1.30, 95% CI: 0.57 to 2.94, p = 0.53) and warfarin treated patients (RR: 1.68, 95% CI: 0.48 to 5.94, p = 0.42).	Aspirin	94-101	coagulation factor XII	Homo sapiens	69-73
15337432-0	2004	Acetylsalicylic acid as a potential regulator of prolidase-convertible pro-drugs in control and neoplastic cells.	Aspirin	0-20	peptidase D	Homo sapiens	49-58
15337432-2	2004	In order to limit the action of prolidase on the pro-drug in normal cells, prolidase inhibitor, acetylsalicylic acid (ASA), was tested in fibroblasts (showing average prolidase activity for normal cells) and in MDA-MB 231 breast cancer cells (showing elevated activity of the enzyme).	Aspirin	96-116	peptidase D	Homo sapiens	75-84
15337432-2	2004	In order to limit the action of prolidase on the pro-drug in normal cells, prolidase inhibitor, acetylsalicylic acid (ASA), was tested in fibroblasts (showing average prolidase activity for normal cells) and in MDA-MB 231 breast cancer cells (showing elevated activity of the enzyme).	Aspirin	96-116	peptidase D	Homo sapiens	75-84
15326075-0	2004	Nitroaspirins and morpholinosydnonimine but not aspirin inhibit the formation of superoxide and the expression of gp91phox induced by endotoxin and cytokines in pig pulmonary artery vascular smooth muscle cells and endothelial cells.	Aspirin	5-12	cytochrome b-245 beta chain	Homo sapiens	114-122
15370100-5	2004	Aspirin inhibited CD62P expression and GPIIb/IIIa activation induced by collagen, but not thrombin.	Aspirin	0-7	integrin subunit alpha 2b	Homo sapiens	39-44
15240674-1	2004	The 2-(acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester (NCX-4016) is a NO-releasing derivative of aspirin.	Aspirin	4-29	T cell leukemia homeobox 2	Homo sapiens	62-65
15240674-1	2004	The 2-(acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester (NCX-4016) is a NO-releasing derivative of aspirin.	Aspirin	104-111	T cell leukemia homeobox 2	Homo sapiens	62-65
15240674-3	2004	Exposure of lymphocytes and monocytes to aspirin, 2-(acetyloxy)benzoic acid 3-(hydroxymethyl)phenyl ester (NCX-4017), a non-NO-releasing analog of NCX-4016, and cyclooxygenase inhibitors, reduced PG formation, but has no effect on cytokine/chemokine release.	Aspirin	41-48	T cell leukemia homeobox 2	Homo sapiens	107-110
15240674-3	2004	Exposure of lymphocytes and monocytes to aspirin, 2-(acetyloxy)benzoic acid 3-(hydroxymethyl)phenyl ester (NCX-4017), a non-NO-releasing analog of NCX-4016, and cyclooxygenase inhibitors, reduced PG formation, but has no effect on cytokine/chemokine release.	Aspirin	41-48	T cell leukemia homeobox 2	Homo sapiens	147-150
15304745-7	2004	The treatment of the mature adipocytes with exogenous PGD2, 15-deoxy-delta12,14-PGJ2 and PGE2, in the presence of aspirin, enhanced the adipogenesis.	Aspirin	114-121	prostaglandin D2 synthase (brain)	Mus musculus	54-58
14976132-10	2004	Furthermore, they point towards a role for Rac1 in the action of aspirin in colon cancer.	Aspirin	65-72	Rac family small GTPase 1	Homo sapiens	43-47
14762100-1	2004	2-(Acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester (NCX-4016) is a nitric oxide (NO)-releasing derivative of aspirin that inhibits cyclooxygenase (COX) activity and releases NO.	Aspirin	115-122	T cell leukemia homeobox 2	Homo sapiens	58-61
15173663-6	2004	RESULTS: In cells treated with acetylsalicylic acid, a concomitant decrease in prolidase activity, prolidase phosphorylation (at the threonine residue), and collagen biosynthesis were observed.	Aspirin	31-51	peptidase D	Homo sapiens	79-88
15173663-6	2004	RESULTS: In cells treated with acetylsalicylic acid, a concomitant decrease in prolidase activity, prolidase phosphorylation (at the threonine residue), and collagen biosynthesis were observed.	Aspirin	31-51	peptidase D	Homo sapiens	99-108
15173663-10	2004	CONCLUSIONS: The inhibitory effect of acetylsalicylic acid on collagen biosynthesis in fibroblasts is coupled to the inhibition of prolidase phosphorylation (but not expression) and down-regulation of the intracellular signal transmitted by the b1-integrin receptor.	Aspirin	38-58	peptidase D	Homo sapiens	131-140
15085057-4	2004	Especially the additional value of GP IIb/IIIa inhibition on top of an aggressive antithrombotic therapy (including aspirin, heparins, and clopidogrel) requires further clarification.	Aspirin	116-123	integrin subunit alpha 2b	Homo sapiens	35-41
12943528-0	2004	Aspirin inhibits endothelial nitric oxide synthase (eNOS) and Flk-1 (vascular endothelial growth factor receptor-2) prior to rat colon tumour development.	Aspirin	0-7	nitric oxide synthase 3	Rattus norvegicus	52-56
12943528-5	2004	Aspirin treatment (10 mg/kg of body weight per day) reduced eNOS expression, but failed to modify the expression of VEGF in the colonic tissue of azoxymethane-treated rats.	Aspirin	0-7	nitric oxide synthase 3	Rattus norvegicus	60-64
12943528-12	2004	Overexpression of eNOS, VEGF and its receptor Flk-1 occurred early after azoxymethane administration in rat colonic tissue, even before morphological changes associated with tumour generation were observed, and aspirin prevented the overexpression of both eNOS and VEGF receptor Flk-1.	Aspirin	211-218	nitric oxide synthase 3	Rattus norvegicus	18-22
12943528-12	2004	Overexpression of eNOS, VEGF and its receptor Flk-1 occurred early after azoxymethane administration in rat colonic tissue, even before morphological changes associated with tumour generation were observed, and aspirin prevented the overexpression of both eNOS and VEGF receptor Flk-1.	Aspirin	211-218	nitric oxide synthase 3	Rattus norvegicus	256-260
14753751-4	2003	Our studies reveal that a commonly used non-steroid anti-inflammatory drug, acetylsalicylic acid (aspirin) prevents H2O2-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	76-96	NFKB inhibitor beta	Homo sapiens	251-262
14753751-4	2003	Our studies reveal that a commonly used non-steroid anti-inflammatory drug, acetylsalicylic acid (aspirin) prevents H2O2-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	98-105	NFKB inhibitor beta	Homo sapiens	251-262
14616128-0	2003	RANTES, eotaxin and eotaxin-2 expression and production in patients with aspirin triad.	Aspirin	73-80	C-C motif chemokine ligand 5	Homo sapiens	0-6
14511359-0	2003	Activation of p53 signalling in acetylsalicylic acid-induced apoptosis in OC2 human oral cancer cells.	Aspirin	32-52	one cut homeobox 2	Homo sapiens	74-77
14511359-2	2003	The aim of this study was to investigate the possible existence of a putative p53-dependent pathway underlying the ASA-induced apoptosis in OC2 cells, a human oral cancer cell line.	Aspirin	115-118	one cut homeobox 2	Homo sapiens	140-143
12829521-8	2003	Correspondingly, aspirin enhanced NO synthase activity (citrulline formation) and intracellular cyclic GMP accumulation in endothelial cells.	Aspirin	17-24	5'-nucleotidase, cytosolic II	Homo sapiens	103-106
12829521-10	2003	CONCLUSIONS: Our data suggest that endothelial NO synthase is a site of action of aspirin and that the NO/cyclic GMP system assumes a crucial function in mediating the cytoprotective action of aspirin.	Aspirin	193-200	5'-nucleotidase, cytosolic II	Homo sapiens	113-116
12890715-3	2003	(2) In the present study, we have examined the role of acetylated COX-2 and 5-LOX in modulating antiadhesive effects of aspirin on adhesion of PMN to endotoxin (LPS)-primed human umbilical endothelial cells (HUVEC).	Aspirin	120-127	lysyl oxidase	Homo sapiens	78-81
12832097-0	2003	Inhibition of cytosolic phospholipase A2 mRNA expression: a novel mechanism for acetylsalicylic acid-mediated growth inhibition and apoptosis in colon cancer cells.	Aspirin	80-100	phospholipase A2 group IVA	Homo sapiens	14-40
12832097-6	2003	RT-PCR analysis revealed that treatment of ASA induced a concentration-dependent downregulation of cytosolic phospholipase A2 (cPLA2) mRNA expression in SW480 cells and also in two other colorectal cancer cell lines, Colo320 and HT-29 cells.	Aspirin	43-46	phospholipase A2 group IVA	Homo sapiens	99-125
12832097-6	2003	RT-PCR analysis revealed that treatment of ASA induced a concentration-dependent downregulation of cytosolic phospholipase A2 (cPLA2) mRNA expression in SW480 cells and also in two other colorectal cancer cell lines, Colo320 and HT-29 cells.	Aspirin	43-46	phospholipase A2 group IVA	Homo sapiens	127-132
12832097-8	2003	Our results indicate that the ASA-induced downregulation of cytosolic phospholipase A2 mRNA expression might be a novel mechanism for ASA-mediated growth inhibition and apoptosis in colon cancer cells.	Aspirin	30-33	phospholipase A2 group IVA	Homo sapiens	60-86
12832097-8	2003	Our results indicate that the ASA-induced downregulation of cytosolic phospholipase A2 mRNA expression might be a novel mechanism for ASA-mediated growth inhibition and apoptosis in colon cancer cells.	Aspirin	134-137	phospholipase A2 group IVA	Homo sapiens	60-86
12714600-8	2003	Interestingly, aspirin treatment inhibited the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha.	Aspirin	15-22	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	121-126
12865403-2	2003	A new study reveals that salicylic acid, the major metabolite of aspirin, acts at the level of transcription to downregulate the production of fibrinogen, fibronectin, and alpha-hemolysin - virulence factors necessary for bacterial replication in host tissues and, now, potential therapeutic targets.	Aspirin	65-72	fibronectin 1	Canis lupus familiaris	155-166
14592546-5	2003	The antipyretic action of aspirin may be mediated by inhibition of COX-3 in hypothalamic endothelial cells or by inhibition of COX-1 localised close to sensory receptors of peripheral vagal afferents.	Aspirin	26-33	cytochrome c oxidase III, mitochondrial	Mus musculus	67-72
12473561-0	2002	NCX-4016 (NO-aspirin) inhibits lipopolysaccharide-induced tissue factor expression in vivo: role of nitric oxide.	Aspirin	13-20	coagulation factor III, tissue factor	Rattus norvegicus	58-71
11877318-18	2002	In contrast, phenanthroline and apyrase significantly enhanced the anti-aggregatory effects of aspirin against thrombin-, PAR1AP- and TRAP-induced aggregation suggesting the involvement of ADP- and MMP-2-dependent pathways.	Aspirin	95-102	TRAP	Homo sapiens	134-138
16206787-10	2002	RESULTS: Ketoprofen, aspirin, and etodolac were COX-1 selective.	Aspirin	21-28	cytochrome c oxidase subunit I	Canis lupus familiaris	48-53
12489254-7	2002	Ecabet sodium (CAS 86408-72-2) and cimetidine (CAS 51481-61-9) significantly inhibited ASA-induced gastric lesions in RF rats, whereas sucralfate (CAS 54182-58-0) tended to inhibit it.	Aspirin	87-90	BCAR1 scaffold protein, Cas family member	Rattus norvegicus	15-18
12489254-7	2002	Ecabet sodium (CAS 86408-72-2) and cimetidine (CAS 51481-61-9) significantly inhibited ASA-induced gastric lesions in RF rats, whereas sucralfate (CAS 54182-58-0) tended to inhibit it.	Aspirin	87-90	BCAR1 scaffold protein, Cas family member	Rattus norvegicus	47-50
12489254-7	2002	Ecabet sodium (CAS 86408-72-2) and cimetidine (CAS 51481-61-9) significantly inhibited ASA-induced gastric lesions in RF rats, whereas sucralfate (CAS 54182-58-0) tended to inhibit it.	Aspirin	87-90	BCAR1 scaffold protein, Cas family member	Rattus norvegicus	47-50
11796443-11	2002	In the ASA group, aspirin-induced IAR was associated with a fall in urinary 11-dhTXB(2)/creatinine, increased the levels of sputum LTC(4)-LTD(4) and ECP and urinary LTE(4)/creatinine.	Aspirin	7-10	ribonuclease A family member 3	Homo sapiens	149-152
11796443-11	2002	In the ASA group, aspirin-induced IAR was associated with a fall in urinary 11-dhTXB(2)/creatinine, increased the levels of sputum LTC(4)-LTD(4) and ECP and urinary LTE(4)/creatinine.	Aspirin	18-25	ribonuclease A family member 3	Homo sapiens	149-152
11781283-7	2002	Aspirin prevents 2952 colorectal cancers and saves 5301 life-years at an ICER of $47,249 per life-year saved compared with no intervention.	Aspirin	0-7	cAMP responsive element modulator	Homo sapiens	73-77
11781283-9	2002	Varying the annual aspirin-related costs between $50 and $200 results in ICER changes between $4617 and $57,080, with the 2 strategies breaking even at $70.	Aspirin	19-26	cAMP responsive element modulator	Homo sapiens	73-77
11781283-10	2002	Applying aspirin chemoprevention plus colonoscopy screening concomitantly yields an ICER of $227,607 per life-year saved compared with screening colonoscopy alone.	Aspirin	9-16	cAMP responsive element modulator	Homo sapiens	84-88
11728532-9	2001	RESULTS: In a drug free group, digestion of a single tablet of aspirin resulted in a significantly (p&lt;0.05) diminished expression of PECAM-1, GP IIb, fibrinogen binding with PAC-1 antibody, GP Ib, P-selectin, and CD151.	Aspirin	63-70	integrin subunit alpha 2b	Homo sapiens	145-151
11728532-9	2001	RESULTS: In a drug free group, digestion of a single tablet of aspirin resulted in a significantly (p&lt;0.05) diminished expression of PECAM-1, GP IIb, fibrinogen binding with PAC-1 antibody, GP Ib, P-selectin, and CD151.	Aspirin	63-70	CD151 molecule (Raph blood group)	Homo sapiens	216-221
11600135-8	2001	Cigarette smoking, use of aspirin and/or NSAIDs, use of vitamin/mineral supplements, and consumption of caffeine were associated with both Ki-ras+ and Ki-ras- tumors; the associations were not confounded by dietary intake or other lifestyle factors.	Aspirin	26-33	KRAS proto-oncogene, GTPase	Homo sapiens	139-145
11816721-4	2001	MAP4-RPPGF administration had a sustained antiplatelet effect, preventing gamma-thrombin-induced (12.5 nM) platelet activation for 4 h. Its antiplatelet effect summated with that of aspirin and/or clopidogrel.	Aspirin	182-189	microtubule associated protein 4	Canis lupus familiaris	0-4
11322917-3	2001	Patients with objective evidence of ischemia, especially elevated myocardial enzymes, as well as patients on chronic aspirin therapy at the time of their ACS, appear to derive the greatest benefit from the addition of a GP IIb/IIIa antagonist.	Aspirin	117-124	integrin subunit alpha 2b	Homo sapiens	220-226
11164230-4	2001	The ASA values for the chains A and B in 1AGA and 1CAR indicate that there are not much interchain interactions and the chains in both the molecules interact equally with the solvent.	Aspirin	4-7	bridging integrator 1	Homo sapiens	23-51
11846053-7	2001	Aspirin, at therapeutic concentrations, also decreased LPS-induced IL-12 and IL-10 production.	Aspirin	0-7	interleukin 10	Homo sapiens	77-82
11192938-2	2000	Here, we review our findings indicating that inflammatory exudates from mice treated with omega-3 PUFA and aspirin (ASA) generate a novel array of bioactive lipid signals.	Aspirin	116-119	pumilio RNA binding family member 3	Homo sapiens	98-102
10862819-5	2000	In both treatments, the acetylsalicylic acid prevented delta-aminolevulinic dehydratase and porphobilinogen deaminase inactivation in diabetic mice and blocked the accumulation of lipoperoxidative aldehydes.	Aspirin	24-44	hydroxymethylbilane synthase	Mus musculus	92-117
10671506-7	2000	Remarkably, aspirin-treated COX-2 formed 15R-HETE with removal of the pro-S hydrogen at C-13 (3-9% retention of pro-S tritium label), the same stereoselectivity as in the formation of prostaglandins by native cyclooxygenase.	Aspirin	12-19	homeobox C13	Homo sapiens	88-92
10731377-6	2000	Several clinical trials in the past few years have documented the beneficial value of GP IIb/IIIa inhibitors in patients treated with aspirin and heparin, with a significant reduction in the cumulative end-point of death and/or myocardial infarction at 48-96 hours (odds ratio--OR 0.81, 95% confidence interval--CI 0.71-0.92, p &lt; 0.01).	Aspirin	134-141	integrin subunit alpha 2b	Homo sapiens	86-92
10938881-1	2000	Since results of recent clinical trial, performed in patients suffering from acute coronary syndromes, suggested that aspirin improved the efficacy of an anti-GP-IIb/IIIa therapy, this work was set to study the mechanism underlying such a mechanism of aspirin.	Aspirin	118-125	integrin subunit alpha 2b	Homo sapiens	159-165
10938881-10	2000	Therefore, our study shows that aspirin pretreatment promotes a "thrombolytic" activity of GP-IIb/IIIa inhibitors and, in particular, of SR121566, a potent and selective member of this new class of compounds.	Aspirin	32-39	integrin subunit alpha 2b	Homo sapiens	91-97
9923894-7	1999	The GPIIb-IIIa blockers are taking the clinician and patient out of the era of aspirin monotherapy when platelet inhibition is required.	Aspirin	79-86	integrin subunit alpha 2b	Homo sapiens	4-9
27093739-2	1999	GOT and GPT activities were increased in plasma but decreased significantly in liver and kidney in aspirin treated animals.	Aspirin	99-106	glutamic--pyruvic transaminase	Rattus norvegicus	8-11
10065898-0	1999	In vivo antithrombotic effects of a nitric oxide-releasing aspirin derivative, NCX-4016.	Aspirin	59-66	T cell leukemia homeobox 2	Homo sapiens	79-82
9703216-7	1998	Acetyl salicylic acid was effective in preventing both hemoglobin glycation and ALA-D inactivation by glucose.	Aspirin	0-21	aminolevulinate dehydratase	Homo sapiens	80-85
9726391-12	1998	This adaptation to ASA was accompanied by approximately a 90% reduction in prostaglandin E2 biosynthesis, by a significant rise in BrdU uptake by glandular cells predominantly in the neck region of gastric glands and by expression of SP (SP/beta-actin ratio; 0.96 +/- 0.08 in ASA-adapted mucosa vs. 0.38 +/- 0.05 in the control mucosa) and TGF alpha (TGF alpha/beta-actin ratio: 0.97 +/- 0.07 in ASA-adapted mucosa vs. 0.77 +/- 0.06 in the control mucosa).	Aspirin	19-22	transforming growth factor alpha	Rattus norvegicus	340-349
9726391-12	1998	This adaptation to ASA was accompanied by approximately a 90% reduction in prostaglandin E2 biosynthesis, by a significant rise in BrdU uptake by glandular cells predominantly in the neck region of gastric glands and by expression of SP (SP/beta-actin ratio; 0.96 +/- 0.08 in ASA-adapted mucosa vs. 0.38 +/- 0.05 in the control mucosa) and TGF alpha (TGF alpha/beta-actin ratio: 0.97 +/- 0.07 in ASA-adapted mucosa vs. 0.77 +/- 0.06 in the control mucosa).	Aspirin	19-22	transforming growth factor alpha	Rattus norvegicus	351-360
9726391-14	1998	CONCLUSIONS: (i) Gastric adaptation to aspirin injury involves enhanced cell proliferation which appears to be mediated by increased expression of SP and TGF alpha, and (ii) rapid upregulation of COX-2 expression following single and repeated ASA insults may represent a compensatory response to suppression of prostaglandin generation by this NSAID.	Aspirin	39-46	transforming growth factor alpha	Rattus norvegicus	154-163
9723822-8	1998	A reduction in P-selectin and GPIIb-IIIa receptor density on non-activated platelets co-incubated with unstimulated neutrophils was associated with NO release from neutrophils, but this was not enhanced by the addition of aspirin.	Aspirin	222-229	integrin subunit alpha 2b	Homo sapiens	30-35
9744535-8	1998	The combination of ASA and A-79715 was the most effective preventive intervention and reduced lung tumor multiplicity by 87% and lung tumor incidence by 24%, demonstrating that inhibition of both 5-lipoxygenase and cyclooxygenase is more effective than inhibition of either pathway alone.	Aspirin	19-22	arachidonate 5-lipoxygenase	Mus musculus	196-210
9579743-2	1998	The effect of the NSAIDs indomethacin, indoprofen, diclofenac and acetylsalicylic acid on the increase in guanosine 3":5"-cyclic monophosphate (cyclic GMP) induced by nitric oxide-donor agents was tested in human whole platelets and in platelet crude homogenate.	Aspirin	66-86	5'-nucleotidase, cytosolic II	Homo sapiens	151-154
9579743-10	1998	Indomethacin (10 microM), indoprofen (30 microM), diclofenac (100 microM) and acetylsalicylic acid (1000 microM) showed a comparable efficacy in inhibiting platelet thromboxane B2 (TXB2) production, suggesting that the inhibitory effect of indomethacin and indoprofen on the increase in cyclic GMP induced by both NO-donors was not mediated by inhibition of cyclooxygenase.	Aspirin	78-98	5'-nucleotidase, cytosolic II	Homo sapiens	294-297
9484990-8	1998	Aspirin (15 mg/kg) administered 30 minutes before injury attenuated 111In-platelet deposition at 4 hours by 67%, with an associated decrease in bound Xa/Va and thrombin activity at 15 minutes and 4 hours.	Aspirin	0-7	prothrombin	Oryctolagus cuniculus	160-168
10235667-1	1997	ACP and ALP activities in plasma were increased in aspirin treated groups for a period of seven days.	Aspirin	51-58	PDZ and LIM domain 3	Rattus norvegicus	8-11
10235667-3	1997	ACP and ALP activities in liver and kidney were decreased significantly in aspirin treated animals.	Aspirin	75-82	PDZ and LIM domain 3	Rattus norvegicus	8-11
9085161-3	1997	Mucin production recovered 7 h after the administration of 50 mg/kg acidified aspirin.	Aspirin	78-85	solute carrier family 13 member 2	Rattus norvegicus	0-5
9085161-4	1997	Doses of acidified aspirin higher than 100 mg/kg decreased mucin content in the surface and deep corpus mucosal layers and no recovery was seen 7 h after the administration.	Aspirin	19-26	solute carrier family 13 member 2	Rattus norvegicus	59-64
8997168-4	1996	Patients treated with IVIG-and-aspirin had by the fourth day developed a highly-significant increase in T cells, CD4 T cells and CD8 T cells and a decrease in B cells.	Aspirin	31-38	CD8a molecule	Homo sapiens	129-132
8574434-0	1995	The value of C1 esterase inhibitor in patients with aspirin-sensitive urticaria.	Aspirin	52-59	serpin family G member 1	Homo sapiens	13-34
8574434-1	1995	The aim of the study was to evaluate the concentration and activity of C1 esterase inhibitor (C1 INH) in patients with aspirin-sensitive urticaria.	Aspirin	119-126	serpin family G member 1	Homo sapiens	71-92
8574434-1	1995	The aim of the study was to evaluate the concentration and activity of C1 esterase inhibitor (C1 INH) in patients with aspirin-sensitive urticaria.	Aspirin	119-126	serpin family G member 1	Homo sapiens	94-100
7608559-6	1995	The initial PGD2 burst in activated MMC-34 cells is prevented by aspirin pretreatment, suggesting that constitutive PGS-1 present in mast cells before activation is responsible for the early PGD2 production in response to activation.	Aspirin	65-72	prostaglandin D2 synthase (brain)	Mus musculus	12-16
7608559-6	1995	The initial PGD2 burst in activated MMC-34 cells is prevented by aspirin pretreatment, suggesting that constitutive PGS-1 present in mast cells before activation is responsible for the early PGD2 production in response to activation.	Aspirin	65-72	prostaglandin D2 synthase (brain)	Mus musculus	191-195
7537680-6	1995	Endogenous CCK released by intraduodenal instillation of oleate prevented the formation of acute gastric lesions induced by both ethanol and aspirin and the protective effects were abolished by pretreatment with loxiglumide.	Aspirin	141-148	cholecystokinin	Rattus norvegicus	11-14
8572925-4	1995	We had previously found that aspirin-like drugs (ALD) induce AP-1 in human T lymphocytes.	Aspirin	29-36	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	61-65
7899465-13	1995	PGE2 significantly inhibited the secretin- and CCK-stimulated pancreatic secretion which was further suppressed by the concomitant ASA infusion.	Aspirin	131-134	cholecystokinin	Rattus norvegicus	47-50
7899465-15	1995	The data indicate that ASA inhibits both secretin- and CCK-stimulated pancreatic secretion by a mechanism independent of prostaglandin biosynthesis inhibition.	Aspirin	23-26	cholecystokinin	Rattus norvegicus	55-58
7988664-4	1994	Other studies suggest that various anti-inflammatory drugs, including acetylsalicyclic acid, auranofin and dexamethasone, can also facilitate HSP expression in macrophages.	Aspirin	70-91	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	142-145
8049200-9	1994	This reduction in thrombin-induced responses was also observed with aspirin-treated platelets, which cannot form thromboxane A2.	Aspirin	68-75	prothrombin	Oryctolagus cuniculus	18-26
7961243-4	1994	PAF-induced vaso- and bronchoconstriction were unaffected by the non-redox 5-lipoxygenase inhibitor ZM-230,487 but were markedly attenuated by inhibition of cyclooxygenase with acetylsalicylic acid or thromboxane-receptor antagonism with BM-13177.	Aspirin	177-197	PCNA clamp associated factor	Rattus norvegicus	0-3
21043859-1	1993	Increases in [cyclic-3",5"-GMP] in aspirin-treated platelet-rich plasma and washed platelet preparations resulted from stimulation by all excitatory agonists tested, and by other agents which induced aggregate formation.	Aspirin	35-42	5'-nucleotidase, cytosolic II	Homo sapiens	27-30
1281834-1	1992	This study was designed to determine whether transforming growth factor alpha (TGF alpha) protects rat gastric mucosa against ethanol- and aspirin-induced injury.	Aspirin	139-146	transforming growth factor alpha	Rattus norvegicus	45-77
1281834-1	1992	This study was designed to determine whether transforming growth factor alpha (TGF alpha) protects rat gastric mucosa against ethanol- and aspirin-induced injury.	Aspirin	139-146	transforming growth factor alpha	Rattus norvegicus	79-88
1476271-9	1992	Prostaglandin E2 production increased in the stenotic kidney when the stenosis was more than 70%; aspirin inhibited prostaglandin synthesis and suppressed the stimulation of renin release.	Aspirin	98-105	renin	Canis lupus familiaris	174-179
1326692-2	1992	The active serum component consists of lipids bound to an isoform of serum albumin that we have named active serum albumin (ASA).	Aspirin	124-127	albumin	Rattus norvegicus	69-82
1326692-2	1992	The active serum component consists of lipids bound to an isoform of serum albumin that we have named active serum albumin (ASA).	Aspirin	124-127	albumin	Rattus norvegicus	109-122
1326692-5	1992	Preincubation of ASA with monospecific antibodies to serum albumin suppressed its ability to induce neurite retraction in a dose dependent fashion.	Aspirin	17-20	albumin	Rattus norvegicus	53-66
1326692-7	1992	The Ins1,4,5P3 increase was also blocked, in a titratable fashion, when ASA was preincubated with monospecific antibodies to serum albumin.	Aspirin	72-75	albumin	Rattus norvegicus	125-138
2033129-4	1991	Eosinophil cationic protein levels were significantly increased in the serum of patients with atopic dermatitis (p less than or equal to 0.005) and patients with a history of pseudoallergic reactions to acetylsalicylic acid (p less than or equal to 0.01).	Aspirin	203-223	ribonuclease A family member 3	Homo sapiens	0-27
1903353-6	1991	PRP from rats given aspirin and warfarin also aggregated normally with ADP or collagen addition.	Aspirin	20-27	proline rich protein 2-like 1	Rattus norvegicus	0-3
1671747-4	1991	Pretreatment with aspirin significantly attenuated the effects of interleukin-1 beta on both the vasopressin and oxytocin levels.	Aspirin	18-25	oxytocin/neurophysin I prepropeptide	Homo sapiens	113-121
1899904-5	1991	The recovery of PHS activity of cells in which the existing PHS was inhibited by aspirin was enhanced by TPA treatment.	Aspirin	81-88	pterin-4 alpha-carbinolamine dehydratase 1	Rattus norvegicus	16-19
1899904-5	1991	The recovery of PHS activity of cells in which the existing PHS was inhibited by aspirin was enhanced by TPA treatment.	Aspirin	81-88	pterin-4 alpha-carbinolamine dehydratase 1	Rattus norvegicus	60-63
2354361-5	1990	Moreover, the antipyretic effects of sodium salicylate suggest that aspirin-like drugs may induce the release of alpha-melanocyte-stimulating hormone which, in turn, attenuates the PGE1-evoked fever.	Aspirin	68-75	proopiomelanocortin	Rattus norvegicus	113-149
2190817-1	1990	alpha-Thrombin, gamma-thrombin, and platelet-activating factor each stimulated the mobilization of intracellular Ca2+ stores in aspirin-treated human platelets.	Aspirin	128-135	carbonic anhydrase 2	Homo sapiens	113-116
34666508-11	2022	Our study suggests that CYP2C19 genotypes and clinical risk factors can be integrated by ABCD-GENE score to estimate the efficacy of clopidogrel-aspirin therapy.	Aspirin	145-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
34604175-6	2021	To compare the effect of programmed acetylation at specific lysine residues to non-specific acetylation, we produced acetylated TrxR1 using aspirin as a model non-enzymatic acetyl donor.	Aspirin	140-147	thioredoxin reductase 1	Homo sapiens	128-133
34604175-7	2021	Mass spectrometry confirmed aspirin-induced acetylation at multiple lysine residues in TrxR1.	Aspirin	28-35	thioredoxin reductase 1	Homo sapiens	87-92
34576080-4	2021	Remarkably, the percentage of CNS-infiltrated CD4+ T cells, the major drivers of neuroinflammation, was decreased to 40.98 +- 3.28% in ASA-treated mice compared to 56.11 +- 1.46% in control animals at the disease maximum as revealed by flow cytometry.	Aspirin	135-138	CD4 antigen	Mus musculus	46-49
34632302-4	2021	Objective: Since aspirin is a widely available pain reliever that shows promise beyond its known pain-relieving capacity, we examined whether aspirin could upregulate the IL-1Ra in the brain.	Aspirin	142-149	interleukin 1 receptor antagonist	Mus musculus	171-177
34632302-7	2021	Results: Aspirin increased the expression of IL-1Ra mRNA and protein in primary mouse astrocytes and mouse BV-2 microglial cells.	Aspirin	9-16	interleukin 1 receptor antagonist	Mus musculus	45-51
34632302-8	2021	While investigating the mechanism, we found that the IL-1Ra gene promoter harbors peroxisome proliferator response element (PPRE) and that aspirin upregulated IL-1Ra in astrocytes isolated from peroxisome proliferator-activated receptor-beta knockout (PPARbeta-/-), but not PPARalpha-/-, mice.	Aspirin	139-146	interleukin 1 receptor antagonist	Mus musculus	159-165
34632302-9	2021	Moreover, we observed that aspirin bound to tyrosine 314 residue of PPARalpha to stimulate IL-1Ra and that aspirin treatment also increased the recruitment of PPARalpha to the IL-1Ra promoter.	Aspirin	27-34	interleukin 1 receptor antagonist	Mus musculus	91-97
34632302-9	2021	Moreover, we observed that aspirin bound to tyrosine 314 residue of PPARalpha to stimulate IL-1Ra and that aspirin treatment also increased the recruitment of PPARalpha to the IL-1Ra promoter.	Aspirin	107-114	interleukin 1 receptor antagonist	Mus musculus	176-182
34632302-10	2021	Accordingly, aspirin increased IL-1Ra in vivo in the brain of wild type and PPARbeta-/-, but not in PPARalpha-/- mice.	Aspirin	13-20	interleukin 1 receptor antagonist	Mus musculus	31-37
34193316-0	2021	Effects of polymorphic cytochrome P450 2A6 genotypes on chemoprevention against colorectal tumors in single Japanese cohort using daily low-dose aspirin: insights into future personalized treatments.	Aspirin	145-152	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	23-42
34193316-4	2021	RESULTS: The chemopreventive effects of daily aspirin were found to be inversely dependent on the predicted enzyme activity of the CYP2A6 phenotype (based on normal genotypes (CYP2A6*1/*1,*7,*9) and impaired genotypes (CYP2A6*4,*7,*9/*4,*7,*9 and CYP2A6*1/*4)) among a nonsmoker Japanese cohort without familial adenomatous polyposis.	Aspirin	46-53	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	131-137
34193316-4	2021	RESULTS: The chemopreventive effects of daily aspirin were found to be inversely dependent on the predicted enzyme activity of the CYP2A6 phenotype (based on normal genotypes (CYP2A6*1/*1,*7,*9) and impaired genotypes (CYP2A6*4,*7,*9/*4,*7,*9 and CYP2A6*1/*4)) among a nonsmoker Japanese cohort without familial adenomatous polyposis.	Aspirin	46-53	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	176-182
34193316-4	2021	RESULTS: The chemopreventive effects of daily aspirin were found to be inversely dependent on the predicted enzyme activity of the CYP2A6 phenotype (based on normal genotypes (CYP2A6*1/*1,*7,*9) and impaired genotypes (CYP2A6*4,*7,*9/*4,*7,*9 and CYP2A6*1/*4)) among a nonsmoker Japanese cohort without familial adenomatous polyposis.	Aspirin	46-53	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	219-225
34193316-4	2021	RESULTS: The chemopreventive effects of daily aspirin were found to be inversely dependent on the predicted enzyme activity of the CYP2A6 phenotype (based on normal genotypes (CYP2A6*1/*1,*7,*9) and impaired genotypes (CYP2A6*4,*7,*9/*4,*7,*9 and CYP2A6*1/*4)) among a nonsmoker Japanese cohort without familial adenomatous polyposis.	Aspirin	46-53	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	247-253
34193316-5	2021	CONCLUSIONS: The CYP2A6 wild-type allele could be a candidate biomarker for reduced chemopreventive effects of daily aspirin in a population with wide-ranging CYP2A6 phenotypes with a high frequency of impaired activities resulting from variations and whole-gene deletions.	Aspirin	117-124	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	17-23
34193316-5	2021	CONCLUSIONS: The CYP2A6 wild-type allele could be a candidate biomarker for reduced chemopreventive effects of daily aspirin in a population with wide-ranging CYP2A6 phenotypes with a high frequency of impaired activities resulting from variations and whole-gene deletions.	Aspirin	117-124	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	159-165
34193316-6	2021	The CYP2A6 genotypes could be applicable to future personalized treatments for colorectal tumor chemoprevention with daily aspirin.	Aspirin	123-130	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	4-10
34078519-0	2021	MiR-877-5p targets PDK-1 to promote aspirin-induced apoptosis in gastric mucosal cells.	Aspirin	36-43	pyruvate dehydrogenase kinase 1	Homo sapiens	19-24
34078519-12	2021	PDK1 inhibited the apoptosis of GES-1 cells treated by aspirin.	Aspirin	55-62	pyruvate dehydrogenase kinase 1	Homo sapiens	0-4
34078519-14	2021	Downregulation of miR-877-5p reduced the apoptosis by targeting PDK1 in GES-1 cells treated by aspirin, indicating that miR-877-5p may be a potential therapeutic target for gastric mucosal injury caused by aspirin.	Aspirin	95-102	pyruvate dehydrogenase kinase 1	Homo sapiens	64-68
34078519-14	2021	Downregulation of miR-877-5p reduced the apoptosis by targeting PDK1 in GES-1 cells treated by aspirin, indicating that miR-877-5p may be a potential therapeutic target for gastric mucosal injury caused by aspirin.	Aspirin	206-213	pyruvate dehydrogenase kinase 1	Homo sapiens	64-68
35280552-6	2022	Our results showed that the ability of Solanum lycopersicum plants to effectively synchronize the actions of antioxidant enzymes associated in reactive oxygen species (ROS) scavenging - notably superoxidase dismutase (SOD), ascorbate peroxidase (APX), and glutathione reductase (GR) - with good maintenance of the AsA/DHA ratio, that could be connected to FA stress tolerance.	Aspirin	314-317	superoxide dismutase [Cu-Zn], chloroplastic	Solanum lycopersicum	218-221
35335908-0	2022	Acetylsalicylic Acid Suppresses Alcoholism-Induced Cognitive Impairment Associated with Atorvastatin Intake by Targeting Cerebral miRNA155 and NLRP3: In Vivo, and In Silico Study.	Aspirin	0-20	microRNA 155	Homo sapiens	130-138
35335908-8	2022	ASA significantly decreased the expression levels of miRNA155, NLRP3, and IL1B, and produced a significant decrease in caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex with a reduction in the process of neuroinflammation and neuronal damage.	Aspirin	0-3	microRNA 155	Homo sapiens	53-61
35335908-11	2022	Taken together, the present study highlights the protective pharmacological effect of ASA to attenuate the deleterious effect of alcohol intake and long term ATOR therapy on the cognitive function via targeting miRNA155 and NLRP3 proteins.	Aspirin	86-89	microRNA 155	Homo sapiens	211-219
35197754-0	2022	Linsitinib and aspirin as the IGF1-R antagonists, inhibit regorafenib-resistant chemotherapy in colon cancer.	Aspirin	15-22	insulin like growth factor 1 receptor	Homo sapiens	30-36
35197754-4	2022	Therefore, it is thought that inhibiting IGF-1R by Linsitinib and Aspirin, the resistance of colorectal cancer cells to Regorafenib can be reduced.	Aspirin	66-73	insulin like growth factor 1 receptor	Homo sapiens	41-47
35197754-9	2022	The linsitinib and aspirin as the IGF1-R antagonists inhibited colon cancer resistance against regorafenib, stem-cell like colon cancer cells growth, decreased expression of CD133, CD44, CD24, and also increased CDX2, PTEN gene expression.	Aspirin	19-26	insulin like growth factor 1 receptor	Homo sapiens	34-40
35197754-9	2022	The linsitinib and aspirin as the IGF1-R antagonists inhibited colon cancer resistance against regorafenib, stem-cell like colon cancer cells growth, decreased expression of CD133, CD44, CD24, and also increased CDX2, PTEN gene expression.	Aspirin	19-26	CD44 molecule (Indian blood group)	Homo sapiens	181-185
35197754-9	2022	The linsitinib and aspirin as the IGF1-R antagonists inhibited colon cancer resistance against regorafenib, stem-cell like colon cancer cells growth, decreased expression of CD133, CD44, CD24, and also increased CDX2, PTEN gene expression.	Aspirin	19-26	caudal type homeobox 2	Homo sapiens	212-216
35275501-3	2022	We found 101 (46.12%) patients to be aspirin-resistant, and PAg-ADP% was the most prominent risk factor of aspirin resistance.	Aspirin	37-44	phosphoprotein membrane anchor with glycosphingolipid microdomains 1	Homo sapiens	60-63
35275501-3	2022	We found 101 (46.12%) patients to be aspirin-resistant, and PAg-ADP% was the most prominent risk factor of aspirin resistance.	Aspirin	107-114	phosphoprotein membrane anchor with glycosphingolipid microdomains 1	Homo sapiens	60-63
2529003-4	1989	In contrast, aspirin reduced the increments induced by venous occlusion as follows: t-PA:Ag by 45% (P = .001); t-PA activity (euglobulin lysis time, ELT) by 43% (P = .006); and t-PA activity (alpha 2-plasmin inhibitor-plasmin complexes, PIPC) by 41% (P = .003).	Aspirin	13-20	chromosome 20 open reading frame 181	Homo sapiens	84-88
2529003-4	1989	In contrast, aspirin reduced the increments induced by venous occlusion as follows: t-PA:Ag by 45% (P = .001); t-PA activity (euglobulin lysis time, ELT) by 43% (P = .006); and t-PA activity (alpha 2-plasmin inhibitor-plasmin complexes, PIPC) by 41% (P = .003).	Aspirin	13-20	chromosome 20 open reading frame 181	Homo sapiens	111-115
2529003-4	1989	In contrast, aspirin reduced the increments induced by venous occlusion as follows: t-PA:Ag by 45% (P = .001); t-PA activity (euglobulin lysis time, ELT) by 43% (P = .006); and t-PA activity (alpha 2-plasmin inhibitor-plasmin complexes, PIPC) by 41% (P = .003).	Aspirin	13-20	chromosome 20 open reading frame 181	Homo sapiens	111-115
2529003-6	1989	Aspirin had no effect on the increment in PAI-1:Ag induced by venous occlusion, but similar to the effect on t-PA:Ag, aspirin induced a 51% inhibition of the increment in t-PA-PAI-1 complex formation.	Aspirin	118-125	chromosome 20 open reading frame 181	Homo sapiens	171-175
2529003-8	1989	Aspirin inhibits the t-PA activity induced by venous occlusion primarily by inhibiting the release of t-PA antigen.	Aspirin	0-7	chromosome 20 open reading frame 181	Homo sapiens	21-25
2529003-8	1989	Aspirin inhibits the t-PA activity induced by venous occlusion primarily by inhibiting the release of t-PA antigen.	Aspirin	0-7	chromosome 20 open reading frame 181	Homo sapiens	102-106
2510359-1	1989	Three murine monoclonal antibodies (anti-CD9: ALB6, anti-CD41: VI-PL3 and PL2-49/GPIIb - final concentration: 7.5 micrograms/mL) are shown to elicit after a lag time aggregation of washed platelets and a calcium signal (as detected by light emitted by loaded aequorin), which is only partially inhibited by aspirin.	Aspirin	307-314	integrin subunit alpha 2b	Homo sapiens	57-61
2498384-9	1989	Aspirin and sodium salicylate were, respectively, 0.05% and 0.20% as active as unlabeled T4 as inhibitors of [125I]T4 binding to TTR, but these compounds had only 3-4 x 10(-6)% of the activity of T4 for TBG binding.	Aspirin	0-7	serpin family A member 7	Homo sapiens	203-206
2778854-7	1989	On the other hand, the inoculation of P-4-OVA conjugate with FCA produced positive reaction in all of PCA, ASA and PHA tests.	Aspirin	107-110	exosome component 10	Mus musculus	38-41
2657281-4	1989	ZAC reduces acid and peptic secretion, increases mucus secretion, protects mucosa from disruption by aspirin and reverses the reduction of blood flow caused by noradrenaline.	Aspirin	101-108	PLAG1 like zinc finger 1	Homo sapiens	0-3
3287674-3	1988	Bovine aortic endothelial cells (EC) were grown to confluence on microcarrier beads, pretreated with aspirin (1 mmol/l), and their addition to the platelet cuvette also caused a dose-dependent inhibition of aggregation induced by PAF, thrombin and A23187.	Aspirin	101-108	coagulation factor II, thrombin	Bos taurus	235-243
2966775-7	1988	Ibuprofen and aspirin also had an effect comparable to indomethacin on SpA-gamma-IFN production.	Aspirin	14-21	surfactant protein A2	Homo sapiens	71-74
2820018-0	1987	Inhibition by aspirin of the stimulated PGI2 synthesis after administration of kallikrein to hypertensive patients (new aspects of chemical pathogeny concerning the messenger systems: A and C).	Aspirin	14-21	kallikrein related peptidase 4	Homo sapiens	79-89
2820018-7	1987	We may conclude that administration of kallikrein can stimulate PGI2 synthesis, which, in turn, can be blocked by relatively high (= nocive) doses of aspirin.	Aspirin	150-157	kallikrein related peptidase 4	Homo sapiens	39-49
3563890-9	1987	Thus although FN coating of PTFE grafts significantly increases their affinity for platelets, this effect can be effectively abolished by pretreatment with aspirin and dipyridamole.	Aspirin	156-163	fibronectin 1	Canis lupus familiaris	14-16
2880593-8	1987	cEH activity was also induced in the kidney but only about 2-fold by fenofibrate, tiadenol and acetylsalicylic acid.	Aspirin	95-115	epoxide hydrolase 2	Rattus norvegicus	0-3
2433307-4	1987	In contrast, patients treated with ASA plus IVGG had by day 4 a highly significant decrease in HLA-Dr+ Leu 3+ helper T cells (P less than 0.001), an increase in Leu 2+ suppressor/cytotoxic T cells (P less than 0.01), and a decrease in spontaneous IgG (P less than 0.01) and IgM synthesis (P less than 0.001).	Aspirin	35-38	CD8a molecule	Homo sapiens	161-166
3660339-4	1987	In contrast, oral administration of large amounts of aspirin in one subject or in vitro incubation of PRP with TXA2 -endoperoxide receptor blocker SQ 29,548 (20-100 nM) significantly inhibited SPA.	Aspirin	53-60	surfactant protein A2	Homo sapiens	193-196
3481699-7	1987	The rate of inhibition of mucin sulfation was proportional to concentrations of aspirin up to 3 X 10(-4) M and of sucralfate up to 1 X 10(-4) M, at which concentrations about 50% reduction in sulfotransferase activity was obtained.	Aspirin	80-87	solute carrier family 13 member 2	Rattus norvegicus	26-31
3628476-3	1987	Clofibrate, tiadenol and acetylsalicylic acid caused a 8-, 13- and 4.5-fold induction of cEH and a 13-, 19- and 5-fold induction of peroxisomal beta-oxidation activity, respectively.	Aspirin	25-45	epoxide hydrolase 2	Rattus norvegicus	89-92
3103170-0	1986	Differential effects of aspirin and dexamethasone on phospholipase A2 and C activities and arachidonic acid release from endothelial cells in response to bradykinin and leukotriene D4.	Aspirin	24-31	kininogen 1	Bos taurus	154-164
3103170-4	1986	Aspirin blocked bradykinin-stimulated production of arachidonic acid but left the response to LTD4 unaffected.	Aspirin	0-7	kininogen 1	Bos taurus	16-26
3926022-0	1985	Duration of the effect of aspirin on the synthesis of thromboxane by density subpopulations of rabbit platelets stimulated with thrombin.	Aspirin	26-33	prothrombin	Oryctolagus cuniculus	128-136
6239255-2	1984	An IgM anti-aspirin antibody which agglutinated erythrocytes of the patient and of ABO compatible donors in the presence of aspirin was isolated in the serum.	Aspirin	12-19	ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase	Homo sapiens	83-86
6333271-4	1984	The ASA also demonstrated CSF activity for both granulocyte and macrophage colonies when assayed on normal mouse and human bone marrow cells.	Aspirin	4-7	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	26-29
6333271-6	1984	Serological cross-reactivity between human CSF I and HL-60 ASA was detectable by immune precipitation and neutralization of biological activity with rabbit anti-CSF I antibodies.	Aspirin	59-62	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	43-46
6333271-6	1984	Serological cross-reactivity between human CSF I and HL-60 ASA was detectable by immune precipitation and neutralization of biological activity with rabbit anti-CSF I antibodies.	Aspirin	59-62	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	161-164
6403485-4	1983	The cyclooxygenase inhibitors, indomethacin and aspirin, however, both resulted in significant inhibition, causing a shift in the C3a dose-response curve to higher concentrations.	Aspirin	48-55	complement C3	Homo sapiens	130-133
6844741-3	1983	0.05 M CaCl2 given to dams as tap water on days 8 through 20 of gestation inhibited ASA-induced hypocalcemic effect in maternal plasma.	Aspirin	84-87	SEC14-like lipid binding 2	Rattus norvegicus	30-33
6844741-4	1983	Tap water of 0.002-0.05 M CaCl2, Ca(OH)2 and Ca-lactate on days 8 through 20 of gestation alleviated malformations elicited by the administration of ASA (500 mg/kg s.c.) on the 11th day of gestation resulting in a decrease in the fetotoxicity in rats.	Aspirin	149-152	SEC14-like lipid binding 2	Rattus norvegicus	0-3
7135345-4	1982	Furthermore, when exposure to PAF-acether was associated to inactivation of platelet cyclooxygenase with aspirin, aggregation to thrombin persisted, validating the claim that thrombin induces aggregation by a third pathway unrelated to ADP and to thromboxane A2.	Aspirin	105-112	prothrombin	Oryctolagus cuniculus	175-183
6979585-1	1982	Expression of H-2Kk and H-2Dk molecules was studied by indirect immunofluorescence on vaccinia virus-infected Ls cells (derived from the L929 cell line), using D-23b and ASA-21 monospecific alloantisera, respectively directed against the H-2.23 and H-2.32 private specificities of the H-2k haplotype.	Aspirin	170-173	relaxin 2	Homo sapiens	14-17
7297912-3	1981	Aspirin (at pH 2) and soluble aspirin (pH 4.4) applied topically reduced buccal PD, but this fall was abolished by buffering to pH 7.	Aspirin	0-7	polyhomeotic homolog 2	Homo sapiens	12-16
7355969-6	1980	During steady-state conditions, the influx of acetylsalicylic acid into the fetal compartment will equal the efflux, or Cp X (M - F) = Cf X F. Combining these two equations yields the following description of placental clearance: Cp = Ctot x F/M.	Aspirin	46-66	EBP cholestenol delta-isomerase	Homo sapiens	120-124
200138-1	1977	In female rats aspirin-induced gastrin mucosal damage was increased and glycoprotein synthesis decreased by fasting and by insulin administration.	Aspirin	15-22	gastrin	Rattus norvegicus	31-38
4453620-0	1974	Inhibition by indomethacin and aspirin of 15-hydroxyprostaglandin dehydrogenase in vitro.	Aspirin	31-38	carbonyl reductase 1	Homo sapiens	42-79
4176225-1	1968	Acetylsalicylic acid (ASA, aspirin) and sodium salicylate inhibit platelet aggregation induced by collagen, antigen-antibody complexes, gamma globulin-coated particles or thrombin.	Aspirin	0-20	prothrombin	Oryctolagus cuniculus	171-179
4176225-1	1968	Acetylsalicylic acid (ASA, aspirin) and sodium salicylate inhibit platelet aggregation induced by collagen, antigen-antibody complexes, gamma globulin-coated particles or thrombin.	Aspirin	22-25	prothrombin	Oryctolagus cuniculus	171-179
4176225-1	1968	Acetylsalicylic acid (ASA, aspirin) and sodium salicylate inhibit platelet aggregation induced by collagen, antigen-antibody complexes, gamma globulin-coated particles or thrombin.	Aspirin	27-34	prothrombin	Oryctolagus cuniculus	171-179
33743316-7	2021	Besides, aspirin administration decreased the microvessels density and the VEGF expression in rosacea-like skin.	Aspirin	9-16	vascular endothelial growth factor A	Mus musculus	75-79
34033814-0	2021	Inhibiting Wnt production by downregulating prostaglandins to prevent colon tumor formation by aspirin.	Aspirin	95-102	wingless-type MMTV integration site family, member 6	Mus musculus	11-14
34033814-7	2021	In addition, the transcriptomic and proteomic analyses both indicated that aspirin has an inhibitory effect on the Wnt pathway.	Aspirin	75-82	wingless-type MMTV integration site family, member 6	Mus musculus	115-118
34033814-8	2021	The in vitro results further indicated that aspirin inhibits WNT6 production, possibly by suppressing its transcription factor NR4A2, which in turn is regulated by prostaglandin E2, thereby ultimately inhibiting the Wnt pathway.	Aspirin	44-51	wingless-type MMTV integration site family, member 6	Mus musculus	61-65
34033814-8	2021	The in vitro results further indicated that aspirin inhibits WNT6 production, possibly by suppressing its transcription factor NR4A2, which in turn is regulated by prostaglandin E2, thereby ultimately inhibiting the Wnt pathway.	Aspirin	44-51	nuclear receptor subfamily 4, group A, member 2	Mus musculus	127-132
34033814-8	2021	The in vitro results further indicated that aspirin inhibits WNT6 production, possibly by suppressing its transcription factor NR4A2, which in turn is regulated by prostaglandin E2, thereby ultimately inhibiting the Wnt pathway.	Aspirin	44-51	wingless-type MMTV integration site family, member 6	Mus musculus	216-219
33974468-0	2021	Low-dose aspirin can downregulate progesterone resistance and increase the expression of LIF in endometriosis during the implantation window.	Aspirin	9-16	LIF, interleukin 6 family cytokine	Rattus norvegicus	89-92
33974468-5	2021	RESULTS: The expressions of PR, PRA, and PRB protein were significantly increased in the eutopic endometrium after low-dose aspirin treatment, and the level of PRB mRNA was also increased while the ratio of PRA/PRB mRNA was decreased in the eutopic endometrium.	Aspirin	124-131	RB transcriptional corepressor 1	Rattus norvegicus	41-44
33974468-5	2021	RESULTS: The expressions of PR, PRA, and PRB protein were significantly increased in the eutopic endometrium after low-dose aspirin treatment, and the level of PRB mRNA was also increased while the ratio of PRA/PRB mRNA was decreased in the eutopic endometrium.	Aspirin	124-131	RB transcriptional corepressor 1	Rattus norvegicus	160-163
33974468-5	2021	RESULTS: The expressions of PR, PRA, and PRB protein were significantly increased in the eutopic endometrium after low-dose aspirin treatment, and the level of PRB mRNA was also increased while the ratio of PRA/PRB mRNA was decreased in the eutopic endometrium.	Aspirin	124-131	RB transcriptional corepressor 1	Rattus norvegicus	160-163
33974468-8	2021	CONCLUSIONS: The results suggest that the low-dose aspirin treatment could downregulate progesterone resistance and increase the expression of LIF of endometriosis rats during the implantation window, which could improve endometrial receptivity and enhance the pregnant rate of endometriosis.	Aspirin	51-58	LIF, interleukin 6 family cytokine	Rattus norvegicus	143-146
33865015-0	2021	Aspirin facilitates trophoblast invasion and epithelial-mesenchymal transition by regulating the miR-200-ZEB1 axis in preeclampsia.	Aspirin	0-7	zinc finger E-box binding homeobox 1	Homo sapiens	105-109
33865015-9	2021	For the first time, aspirin was shown to fully reverse miR-200-mediated trophoblast biology and act through the network signaling of TGF-beta1/ZEB1/miR-200.	Aspirin	20-27	zinc finger E-box binding homeobox 1	Homo sapiens	143-147
33917483-0	2021	Blockade of AMPK-Mediated cAMP-PKA-CREB/ATF1 Signaling Synergizes with Aspirin to Inhibit Hepatocellular Carcinoma.	Aspirin	71-78	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	12-16
33917483-4	2021	Here, we report that aspirin markedly induces CREB/ATF1 phosphorylation in HCC cells, which compromises aspirin"s anti-HCC effect.	Aspirin	21-28	cAMP responsive element binding protein 1	Homo sapiens	46-50
33917483-4	2021	Here, we report that aspirin markedly induces CREB/ATF1 phosphorylation in HCC cells, which compromises aspirin"s anti-HCC effect.	Aspirin	104-111	cAMP responsive element binding protein 1	Homo sapiens	46-50
33917483-5	2021	Inhibition of AMP-activated protein kinase (AMPK) abrogates the induction of CREB/ATF1 phosphorylation by aspirin.	Aspirin	106-113	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	14-42
33917483-5	2021	Inhibition of AMP-activated protein kinase (AMPK) abrogates the induction of CREB/ATF1 phosphorylation by aspirin.	Aspirin	106-113	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	44-48
33917483-5	2021	Inhibition of AMP-activated protein kinase (AMPK) abrogates the induction of CREB/ATF1 phosphorylation by aspirin.	Aspirin	106-113	cAMP responsive element binding protein 1	Homo sapiens	77-81
33917483-6	2021	Mechanistically, activation of AMPK by aspirin results in decreased expression of the urea cycle enzyme carbamoyl-phosphate synthase 1 (CPS1) in HCC cells and xenografts.	Aspirin	39-46	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	31-35
33917483-7	2021	Treatment with aspirin or CPS1 knockdown stimulates soluble adenylyl cyclase expression, thereby increasing cyclic AMP (cAMP) synthesis and stimulating PKA-CREB/ATF1 signaling.	Aspirin	15-22	cAMP responsive element binding protein 1	Homo sapiens	156-160
33917483-8	2021	Importantly, abrogation of aspirin-induced CREB/ATF1 phosphorylation could sensitize HCC to aspirin.	Aspirin	27-34	cAMP responsive element binding protein 1	Homo sapiens	43-47
33917483-8	2021	Importantly, abrogation of aspirin-induced CREB/ATF1 phosphorylation could sensitize HCC to aspirin.	Aspirin	92-99	cAMP responsive element binding protein 1	Homo sapiens	43-47
33398741-7	2021	Moreover, aspirin and krill oil combination revealed considerable mitigation of silica-induced upregulated expression of the inflammatory and fibrotic mediators: nuclear factor kappa-B, transforming growth factor-beta1, and matrix metalloproteinase-9.	Aspirin	10-17	matrix metallopeptidase 9	Rattus norvegicus	224-250
33280009-9	2021	Plasmatic MMP-9 was significantly increased in COVID-19 patients.Platelet and neutrophil activation markers, but less so NETs, normalized after recovery.In vitro, plasma from COVID-19 patients triggered platelet and neutrophil activation and NET formation, the latter blocked by therapeutic dose low-molecular weight heparin, but not by aspirin or dypiridamole.	Aspirin	337-344	matrix metallopeptidase 9	Homo sapiens	10-15
33619996-5	2021	Aspirin was used to increase eNOS expression in the acute angle group, while N(G)-nitro-L-arginine methyl ester (L-name) was used to decrease eNOS expression in the obtuse angle group.	Aspirin	0-7	nitric oxide synthase 3	Rattus norvegicus	29-33
33222458-0	2021	Xuesaitong injection (lyophilized) combined with aspirin and clopidogrel protect against focal cerebral ischemic/reperfusion injury in rats by suppressing oxidative stress and inflammation and regulating the NOX2/IL-6/STAT3 pathway.	Aspirin	49-56	cytochrome b-245 beta chain	Rattus norvegicus	208-212
33222458-11	2021	Moreover, XST+ASA+CLP group also had lower levels of NOX2, inducible nitric oxide synthase (iNOS), interleukin (IL)-6, and p-STAT3/STAT3.	Aspirin	14-17	cytochrome b-245 beta chain	Rattus norvegicus	53-57
33222458-12	2021	CONCLUSIONS: These results demonstrate that a combination of XST, ASA, and CLP effectively protected rats against middle cerebral artery occlusion/reperfusion (MCAO/R) injury by suppressing the NOX2/IL-6/ STAT3 pathway.	Aspirin	66-69	cytochrome b-245 beta chain	Rattus norvegicus	194-198
32669062-10	2021	There were higher concentrations of elastin in AAA wall among patients taking both of aspirin and statins (1.21 [0.77-3.02] vs 0.78 (0.49-1.05) ng/ml, p = 0.044) than in patients who did not take both of these drugs.	Aspirin	86-93	elastin	Homo sapiens	36-43
33455983-5	2021	Genetic testing found that both cytochrome P450 2C19 (CYP2C19) (G681A) and glycoprotein Ia (GPIa) (C807T, G873A) were hybrid mutant types, demonstrating that the patient was possibly resistant to clopidogrel and aspirin simultaneously.	Aspirin	212-219	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-52
33455983-5	2021	Genetic testing found that both cytochrome P450 2C19 (CYP2C19) (G681A) and glycoprotein Ia (GPIa) (C807T, G873A) were hybrid mutant types, demonstrating that the patient was possibly resistant to clopidogrel and aspirin simultaneously.	Aspirin	212-219	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
33493277-5	2021	Aspirin attenuated the role of sFlt-1 in oxidative stress and endothelial dysfunction and reduced apoptosis of trophoblasts by inactivating the NF-kappaB signaling pathway in HTR-8/SVneo trophoblast cells.	Aspirin	0-7	FMS-like tyrosine kinase 1	Mus musculus	31-37
33493277-6	2021	Blood pressure, urine protein, swelling of the villous vessels and mitochondrial parameters were noted to be much better after aspirin administrated to sFlt-1 treated pregnant mice.	Aspirin	127-134	FMS-like tyrosine kinase 1	Mus musculus	152-158
33493277-7	2021	In conclusion, aspirin reverses the endothelial dysfunction and oxidative stress caused by sFlt-1 and thus reduces apoptosis of preeclamptic trophoblasts by inactivating NF-kappaB signaling pathway.	Aspirin	15-22	FMS-like tyrosine kinase 1	Mus musculus	91-97
33378943-0	2021	Long-term aspirin intervention can inhibit TIGIT, regulating T cells to reverse damage to intestines.	Aspirin	10-17	T cell immunoreceptor with Ig and ITIM domains	Mus musculus	43-48
33378943-7	2021	The results showed that long-term aspirin intervention could reverse damage to the intestines, an effect related to the drug"s significant inhibitory effect on TIGIT.	Aspirin	34-41	T cell immunoreceptor with Ig and ITIM domains	Mus musculus	160-165
33378943-9	2021	In summary, we demonstrated that long-term aspirin intervention could inhibit TIGIT, regulating T cells to reverse damage to the intestines.	Aspirin	43-50	T cell immunoreceptor with Ig and ITIM domains	Mus musculus	78-83
33378943-10	2021	Furthermore, aspirin is a potential therapy for diseases related to an increase in TIGIT.	Aspirin	13-20	T cell immunoreceptor with Ig and ITIM domains	Mus musculus	83-88
33411687-7	2020	IPA was higher at all time points except at baseline in patients with ticagrelor/aspirin compared with those with clopidogrel/aspirin in both carriers and non-carriers of CYP2C19 lose-of-function alleles (all p<0.05).	Aspirin	126-133	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	171-178
33125972-5	2020	MTT, ARS results show that the cell mineralization and viability of Asp-Sr/beta-TCP group is significantly higher than Control group, beta-TCP group and Sr/beta-TCP group.	Aspirin	68-71	secreted Ly6/Plaur domain containing 1	Mus musculus	5-8
33125972-8	2020	RT-qPCR analysis show that Asp-Sr/beta-TCP, beta-TCP group and Sr/beta-TCP group showed increased BMP2, Smad1, OPG than the OVX group(p < 0.05), while Asp-Sr/beta-TCP exhibited decreased TNF-alpha IFN-gamma and RANKL than the OVX group(p < 0.05).	Aspirin	27-30	SMAD family member 1	Rattus norvegicus	104-109
33114368-7	2020	Higher plasma BDNF levels were observed in asthma patients with aspirin sensitivity and aspirin-exacerbated respiratory disease.	Aspirin	64-71	brain derived neurotrophic factor	Homo sapiens	14-18
33114368-7	2020	Higher plasma BDNF levels were observed in asthma patients with aspirin sensitivity and aspirin-exacerbated respiratory disease.	Aspirin	88-95	brain derived neurotrophic factor	Homo sapiens	14-18
33114368-8	2020	These results suggest that plasma BDNF may serve as a potential peripheral biomarker for asthma, particularly asthma with aspirin sensitivity.	Aspirin	122-129	brain derived neurotrophic factor	Homo sapiens	34-38
32992455-8	2020	Therefore, we believe that AsA blocks the cell cycle via an ROS-dependent Akt/Cyclin D1/Rb signaling pathway, which consequently leads to the observed antitumor effect both in vitro and in vivo.	Aspirin	27-30	cyclin D1	Mus musculus	78-90
33014509-9	2020	Following surgery, her symptoms resolved, and she remains on aspirin and ultrasound surveillance.	Aspirin	61-68	Src homology 2 domain containing E	Homo sapiens	46-49
32994805-8	2020	In addition, celecoxib alone or in combination with aspirin inhibited the migration and invasion of NSCLC cells by inhibiting MMP-9 and MMP-2 activity levels.	Aspirin	52-59	matrix metallopeptidase 9	Homo sapiens	126-131
32878589-0	2021	Safety and efficacy of low-dose aspirin in ischemic stroke patients with different G6PD conditions.	Aspirin	32-39	glucose-6-phosphate dehydrogenase	Homo sapiens	83-87
32634649-8	2020	Furthermore, treatment with 75 mg of aspirin resulted in higher negative pregnancy rates in patients with MTHFR A1298C genotypes.	Aspirin	37-44	methylenetetrahydrofolate reductase	Homo sapiens	106-111
33229758-0	2020	Aspirin-Triggered Lipoxin Protects Lipopolysaccharide-Induced Acute Kidney Injury via the TLR4/MyD88/NF-kappaB Pathway.	Aspirin	0-7	myeloid differentiation primary response gene 88	Mus musculus	95-100
32802112-11	2020	In addition, ELISA showed that the expression of VEGF, bFGF, and CD62P in serum of the HYW group was significantly decreased than the control group (P < 0.05), and the expression of VEGF and bFGF in serum of the aspirin group was significantly decreased than the control group (P < 0.05).	Aspirin	212-219	vascular endothelial growth factor A	Mus musculus	49-53
32802112-11	2020	In addition, ELISA showed that the expression of VEGF, bFGF, and CD62P in serum of the HYW group was significantly decreased than the control group (P < 0.05), and the expression of VEGF and bFGF in serum of the aspirin group was significantly decreased than the control group (P < 0.05).	Aspirin	212-219	vascular endothelial growth factor A	Mus musculus	182-186
32568642-2	2020	The CHANCE trial (Clopidogrel in High-Risk Patients With Acute Nondisabling Cerebrovascular Events) found a significant interaction between loss-of-function allele status for the CYP2C19 gene and the effect of dual antiplatelet therapy with aspirin and clopidogrel on the rate of early recurrent stroke following acute transient ischemic attack/minor stroke.	Aspirin	241-248	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	179-186
32629916-6	2020	The results revealed that aspirin inhibited macrophage chemoattractant protein (MCP-1), interleukin (IL-6), IL-1beta, and plasminogen activator inhibitor (PAI-1) production in 3T3-L1 adipocytes stimulated by tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS).	Aspirin	26-33	chemokine (C-C motif) ligand 2	Mus musculus	80-85
32172203-0	2020	Aspirin enhances regulatory functional activities of monocytes and downregulates CD16 and CD40 expression in myocardial infarction autoinflammatory disease.	Aspirin	0-7	Fc gamma receptor IIIa	Homo sapiens	81-85
32172203-2	2020	In this study, we have tried to evaluate the aspirin (acetylsalicylic acid, ASA) treatment effect on the CD16-expressed MOs and activation-associated CD40 in MI.	Aspirin	45-52	Fc gamma receptor IIIa	Homo sapiens	105-109
32172203-2	2020	In this study, we have tried to evaluate the aspirin (acetylsalicylic acid, ASA) treatment effect on the CD16-expressed MOs and activation-associated CD40 in MI.	Aspirin	54-74	Fc gamma receptor IIIa	Homo sapiens	105-109
32172203-2	2020	In this study, we have tried to evaluate the aspirin (acetylsalicylic acid, ASA) treatment effect on the CD16-expressed MOs and activation-associated CD40 in MI.	Aspirin	76-79	Fc gamma receptor IIIa	Homo sapiens	105-109
32172203-9	2020	Furthermore, the expression levels of CD16 and CD40 were significantly downregulated in ASA-treated MOs.	Aspirin	88-91	Fc gamma receptor IIIa	Homo sapiens	38-42
32172203-10	2020	CONCLUSIONS: We show for the first time that ASA immunomodulates the functional activities of MOs during MI and promotes their switching toward a classical phenotype, exhibiting low CD16 expression levels and thereby anti-inflammatory properties.	Aspirin	45-48	Fc gamma receptor IIIa	Homo sapiens	182-186
32258142-9	2020	In conclusion, aspirin can systemically and simultaneously ameliorate NAFLD and atherosclerosis by inhibiting lipid biosynthesis and inflammation and by elevating catabolic metabolism through the activation of the PPARdelta-AMPK-PGC-1alpha pathway.	Aspirin	15-22	peroxisome proliferator activated receptor delta	Homo sapiens	214-223
31837556-3	2020	Salinity stress enhanced the AsA-GSH cycle-related enzymes, glutathione reductase (GR), ascorbate peroxidase (APX), and dehydroascorbate reductase (DHAR), and monodehydroascorbate reductase (MDHAR).	Aspirin	29-32	glutathione S-transferase DHAR2-like	Capsicum annuum	148-152
31837556-3	2020	Salinity stress enhanced the AsA-GSH cycle-related enzymes, glutathione reductase (GR), ascorbate peroxidase (APX), and dehydroascorbate reductase (DHAR), and monodehydroascorbate reductase (MDHAR).	Aspirin	29-32	monodehydroascorbate reductase	Capsicum annuum	159-189
31837556-3	2020	Salinity stress enhanced the AsA-GSH cycle-related enzymes, glutathione reductase (GR), ascorbate peroxidase (APX), and dehydroascorbate reductase (DHAR), and monodehydroascorbate reductase (MDHAR).	Aspirin	29-32	monodehydroascorbate reductase	Capsicum annuum	191-196
31815277-0	2020	Aspirin Inhibits TGFbeta2-Induced Epithelial to Mesenchymal Transition of Lens Epithelial Cells: Selective acetylation of K56 and K122 in histone H3.	Aspirin	0-7	transforming growth factor beta 2	Homo sapiens	17-25
31815277-3	2020	In this study, we tested the efficacy of aspirin in inhibiting the TGFb2-mediated EMT of human LECs, LECs in human lens capsular bags, and lensectomized mice.	Aspirin	41-48	transforming growth factor beta 2	Homo sapiens	67-72
31815277-5	2020	Aspirin also halted the EMT response of TGFbeta2 when introduced after EMT initiation.	Aspirin	0-7	transforming growth factor beta 2	Homo sapiens	40-48
31815277-9	2020	Chromatin immunoprecipitation assays using acetyl-H3K56 or acetyl-H3K122 antibody revealed that aspirin blocked the TGFbeta2-induced acetylation of H3K56 and H3K122 at the promoter regions of ACTA2 and COL1A.	Aspirin	96-103	transforming growth factor beta 2	Homo sapiens	116-124
31815277-11	2020	Taken together, our results showed that aspirin inhibits TGFbeta2-mediated EMT of LECs, possibly from epigenetic downregulation of EMT-related genes.	Aspirin	40-47	transforming growth factor beta 2	Homo sapiens	57-65
31653347-12	2020	Our finding suggests possibly relevant alterations to alpha2-antiplasmin function at high glycemia and during aspirin use.	Aspirin	110-117	serpin family F member 2	Homo sapiens	54-72
31824307-0	2019	Wnt/beta-Catenin Pathway-Regulated Fibromodulin Expression Is Crucial for Breast Cancer Metastasis and Inhibited by Aspirin.	Aspirin	116-123	fibromodulin	Homo sapiens	35-47
31824307-4	2019	Aspirin inhibits BCCMI by attenuating Wnt/beta-catenin signaling and suppressing FMOD expression via inhibiting deacetylation of beta-catenin by histone deacetylase 6 (HDAC6) leading to beta-catenin phosphorylation and cytoplasmic degradation.	Aspirin	0-7	fibromodulin	Homo sapiens	81-85
31824307-6	2019	Our findings identify a critical role of FMOD in cancer metastasis, reveal a mechanism regulating FMOD transcription and impacting tumor metastasis, uncover action targets and mechanism for the anticancer activity of Aspirin, and expand the understanding of the Wnt/beta-catenin pathway and tumor metastasis, which are valuable for development of cancer therapeutics.	Aspirin	217-224	fibromodulin	Homo sapiens	41-45
31781346-6	2019	We found that aspirin preserved the extracellular matrix (ECM) content of collagen type II (COL2) and aggrecan while inhibiting the expression of matrix-degenerating enzymes, including matrix metalloproteinase 3 and 13 (MMP-3 and MMP-13) and A disintegrin and metalloproteinase with thrombospondin motifs 4 and 5 (ADAMTS-4, ADAMTS-5).	Aspirin	14-21	matrix metallopeptidase 3	Rattus norvegicus	185-218
31781346-6	2019	We found that aspirin preserved the extracellular matrix (ECM) content of collagen type II (COL2) and aggrecan while inhibiting the expression of matrix-degenerating enzymes, including matrix metalloproteinase 3 and 13 (MMP-3 and MMP-13) and A disintegrin and metalloproteinase with thrombospondin motifs 4 and 5 (ADAMTS-4, ADAMTS-5).	Aspirin	14-21	matrix metallopeptidase 3	Rattus norvegicus	220-225
31781346-6	2019	We found that aspirin preserved the extracellular matrix (ECM) content of collagen type II (COL2) and aggrecan while inhibiting the expression of matrix-degenerating enzymes, including matrix metalloproteinase 3 and 13 (MMP-3 and MMP-13) and A disintegrin and metalloproteinase with thrombospondin motifs 4 and 5 (ADAMTS-4, ADAMTS-5).	Aspirin	14-21	matrix metallopeptidase 13	Rattus norvegicus	230-236
31781346-11	2019	Histological analysis showed that aspirin treatment prevented the loss of COL2 and decreased MMP-3 and MMP-13, inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), IL-1beta, and TNF-alpha expression in the IVD tissues.	Aspirin	34-41	matrix metallopeptidase 3	Rattus norvegicus	93-98
31781346-11	2019	Histological analysis showed that aspirin treatment prevented the loss of COL2 and decreased MMP-3 and MMP-13, inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), IL-1beta, and TNF-alpha expression in the IVD tissues.	Aspirin	34-41	matrix metallopeptidase 13	Rattus norvegicus	103-109
31526123-12	2019	In patients with complex AAA, 4 strokes occurred among rivaroxaban-assigned patients and 4 strokes among aspirin-assigned patients.	Aspirin	105-112	AAA1	Homo sapiens	25-28
31801720-9	2019	A total of 10 220 differentially expressed genes were identified from the TCGA database, and among them 4 genes (CDC25C, TPX2, CDC20, PLK1) were found to be the potential targets for aspirin.	Aspirin	183-190	TPX2 microtubule nucleation factor	Homo sapiens	121-125
31801720-9	2019	A total of 10 220 differentially expressed genes were identified from the TCGA database, and among them 4 genes (CDC25C, TPX2, CDC20, PLK1) were found to be the potential targets for aspirin.	Aspirin	183-190	cell division cycle 20	Homo sapiens	127-132
31801720-9	2019	A total of 10 220 differentially expressed genes were identified from the TCGA database, and among them 4 genes (CDC25C, TPX2, CDC20, PLK1) were found to be the potential targets for aspirin.	Aspirin	183-190	polo like kinase 1	Homo sapiens	134-138
31801720-11	2019	Western blotting showed that aspirin could down-regulate the expression levels of several pivotal proteins that regulated cell cycle and cell division, including CDC25C, TPX2, CDC20 and PLK1.	Aspirin	29-36	TPX2 microtubule nucleation factor	Homo sapiens	170-174
31801720-11	2019	Western blotting showed that aspirin could down-regulate the expression levels of several pivotal proteins that regulated cell cycle and cell division, including CDC25C, TPX2, CDC20 and PLK1.	Aspirin	29-36	cell division cycle 20	Homo sapiens	176-181
31801720-11	2019	Western blotting showed that aspirin could down-regulate the expression levels of several pivotal proteins that regulated cell cycle and cell division, including CDC25C, TPX2, CDC20 and PLK1.	Aspirin	29-36	polo like kinase 1	Homo sapiens	186-190
31801720-12	2019	CONCLUSIONS: CDC25C, TPX2, CDC20 and PLK1 may be potential targets for aspirin to inhibit the proliferation of human breast cancer cells, by affecting the progress of cell cycle and cell division.	Aspirin	71-78	TPX2 microtubule nucleation factor	Homo sapiens	21-25
31801720-12	2019	CONCLUSIONS: CDC25C, TPX2, CDC20 and PLK1 may be potential targets for aspirin to inhibit the proliferation of human breast cancer cells, by affecting the progress of cell cycle and cell division.	Aspirin	71-78	cell division cycle 20	Homo sapiens	27-32
31801720-12	2019	CONCLUSIONS: CDC25C, TPX2, CDC20 and PLK1 may be potential targets for aspirin to inhibit the proliferation of human breast cancer cells, by affecting the progress of cell cycle and cell division.	Aspirin	71-78	polo like kinase 1	Homo sapiens	37-41
31262687-1	2019	BACKGROUND: Studies suggest regular aspirin use decreases breast cancer (BRCA) risk, with high doses exerting an "anti-cancer" effect.	Aspirin	36-43	BRCA1 DNA repair associated	Homo sapiens	73-77
31262687-11	2019	CONCLUSION: High-dose aspirin after diagnosis may confer BRCA treatment benefits.	Aspirin	22-29	BRCA1 DNA repair associated	Homo sapiens	57-61
31530062-0	2019	Serum level of stem cell factor and its soluble receptor in aspirin-exacerbated respiratory disease.	Aspirin	60-67	KIT ligand	Homo sapiens	15-31
31530062-1	2019	Aim: Stem cell factor (SCF) may be associated with inflammatory processes leading to aspirin-induced asthma.	Aspirin	85-92	KIT ligand	Homo sapiens	5-21
31530062-1	2019	Aim: Stem cell factor (SCF) may be associated with inflammatory processes leading to aspirin-induced asthma.	Aspirin	85-92	KIT ligand	Homo sapiens	23-26
31530062-2	2019	This study evaluated the relationship between serum level of SCF and its soluble receptor with aspirin-induced asthma.	Aspirin	95-102	KIT ligand	Homo sapiens	61-64
31530062-9	2019	Conclusion: Our findings suggest that SCF and C-kit receptors have a direct effect on the severity of aspirin-induced asthma.	Aspirin	102-109	KIT ligand	Homo sapiens	38-41
31565672-0	2019	Aspirin, a Potential GLUT1 Inhibitor in a Vascular Endothelial Cell Line.	Aspirin	0-7	solute carrier family 2 member 1	Homo sapiens	21-26
31565672-3	2019	Herein, we demonstrate that glucose transporter 1 (GLUT1), a main glucose transporter in ECs, can be down-regulated by aspirin.	Aspirin	119-126	solute carrier family 2 member 1	Homo sapiens	28-49
31565672-3	2019	Herein, we demonstrate that glucose transporter 1 (GLUT1), a main glucose transporter in ECs, can be down-regulated by aspirin.	Aspirin	119-126	solute carrier family 2 member 1	Homo sapiens	51-56
31565672-4	2019	Exposure to 4-mM aspirin significantly decreased GLUT1 at the mRNA and protein level, resulting in impaired glucose uptake capacity in vascular ECs.	Aspirin	17-24	solute carrier family 2 member 1	Homo sapiens	49-54
31565672-6	2019	Taken together, these findings indicate 4-mM aspirin inhibits glucose uptake and glucose metabolism of vascular ECs through down-regulating GLUT1 expression and suggest that GLUT1 has potential to be a target for aspirin in vascular ECs.	Aspirin	45-52	solute carrier family 2 member 1	Homo sapiens	140-145
31565672-6	2019	Taken together, these findings indicate 4-mM aspirin inhibits glucose uptake and glucose metabolism of vascular ECs through down-regulating GLUT1 expression and suggest that GLUT1 has potential to be a target for aspirin in vascular ECs.	Aspirin	45-52	solute carrier family 2 member 1	Homo sapiens	174-179
31565672-6	2019	Taken together, these findings indicate 4-mM aspirin inhibits glucose uptake and glucose metabolism of vascular ECs through down-regulating GLUT1 expression and suggest that GLUT1 has potential to be a target for aspirin in vascular ECs.	Aspirin	213-220	solute carrier family 2 member 1	Homo sapiens	174-179
31265948-4	2019	In this study, aspirin reversed the epithelial-mesenchymal transition (EMT) by promoting miR-203 expression in cells, and, remarkably, it repressed exosomal LMP1 (exo-LMP1) secretion from EBV-positive cells.	Aspirin	15-22	PDZ and LIM domain 7	Homo sapiens	157-161
31265948-4	2019	In this study, aspirin reversed the epithelial-mesenchymal transition (EMT) by promoting miR-203 expression in cells, and, remarkably, it repressed exosomal LMP1 (exo-LMP1) secretion from EBV-positive cells.	Aspirin	15-22	PDZ and LIM domain 7	Homo sapiens	167-171
31265948-9	2019	The study revealed that aspirin is a promising drug for NPC therapy via its targeting of exo-LMP1 transfer and the regulatory effect of LMP1 on miR-203 expression.	Aspirin	24-31	PDZ and LIM domain 7	Homo sapiens	93-97
31265948-9	2019	The study revealed that aspirin is a promising drug for NPC therapy via its targeting of exo-LMP1 transfer and the regulatory effect of LMP1 on miR-203 expression.	Aspirin	24-31	PDZ and LIM domain 7	Homo sapiens	136-140
31060007-2	2019	Because they both are the substrates of carboxylesterase 2 (CES2), aspirin attenuated the metabolic activation of and platelet response to vicagrel in mice treated with the two drugs concomitantly.	Aspirin	67-74	carboxylesterase 2H	Mus musculus	40-58
31060007-2	2019	Because they both are the substrates of carboxylesterase 2 (CES2), aspirin attenuated the metabolic activation of and platelet response to vicagrel in mice treated with the two drugs concomitantly.	Aspirin	67-74	carboxylesterase 2H	Mus musculus	60-64
31140860-6	2019	While there are several mechanisms for the maintenance of Tregs under immune insults, aspirin increases the level of interleukin-11 (IL-11), an immunomodulatory cytokine, and IL-11 alone is sufficient to protect Tregs.	Aspirin	86-93	interleukin 11	Mus musculus	117-131
31140860-6	2019	While there are several mechanisms for the maintenance of Tregs under immune insults, aspirin increases the level of interleukin-11 (IL-11), an immunomodulatory cytokine, and IL-11 alone is sufficient to protect Tregs.	Aspirin	86-93	interleukin 11	Mus musculus	133-138
31140860-7	2019	Being a multifunctional molecule, aspirin stimulates the activation of cAMP-response element-binding (CREB) to promote the recruitment of CREB to the IL-11 gene promoter and stimulate the transcription of IL-11 in splenocytes.	Aspirin	34-41	interleukin 11	Mus musculus	150-155
31140860-7	2019	Being a multifunctional molecule, aspirin stimulates the activation of cAMP-response element-binding (CREB) to promote the recruitment of CREB to the IL-11 gene promoter and stimulate the transcription of IL-11 in splenocytes.	Aspirin	34-41	interleukin 11	Mus musculus	205-210
31140860-8	2019	Therefore, it appears that low-dose aspirin protects EAE via CREB-mediated stimulation of IL-11-Treg pathway and that aspirin may have therapeutic importance in MS.	Aspirin	36-43	interleukin 11	Mus musculus	90-95
31090213-9	2019	In this paper, we found that aspirin attenuates cancer cell proliferation and induces CRC cells apoptosis by down-regulating the expression of TIGIT, which provides new evidence for the application of aspirin in cancer treatment.	Aspirin	29-36	T cell immunoreceptor with Ig and ITIM domains	Homo sapiens	143-148
31090213-9	2019	In this paper, we found that aspirin attenuates cancer cell proliferation and induces CRC cells apoptosis by down-regulating the expression of TIGIT, which provides new evidence for the application of aspirin in cancer treatment.	Aspirin	201-208	T cell immunoreceptor with Ig and ITIM domains	Homo sapiens	143-148
30878837-9	2019	The activities of APX and GR were increased concomitantly with the ratios of AsA/DHA and GSH/GSSG.	Aspirin	77-80	cytosolic ascorbate peroxidase 2	Solanum lycopersicum	18-21
30771281-0	2019	Nox2-mediated platelet activation by glycoprotein (GP) VI: Effect of rivaroxaban alone and in combination with aspirin.	Aspirin	111-118	cytochrome b-245 beta chain	Homo sapiens	0-4
30952372-5	2019	RESULTS: ASA accelerates in vitro and in vivo odontogenic differentiation of SCAPs associated with down-regulation of runt-related nuclear factor 2 and up-regulation of specificity protein 7, nuclear factor I C, and dentin phosphoprotein.	Aspirin	9-12	transcription termination factor 2	Homo sapiens	139-147
30952372-8	2019	LY294402 and small interfering RNA for AKT also suppressed the ASA-induced expression of runt-related nuclear factor 2 and enhanced ASA-induced expression of specificity protein 7, nuclear factor I C, and dentin phosphoprotein in SCAPs.	Aspirin	63-66	transcription termination factor 2	Homo sapiens	110-118
30061570-1	2019	The effect of dual antiplatelet therapy, clopidogrel combined with aspirin, was influenced by CYP2C19 gene mutation and heterogeneity of population.	Aspirin	67-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	94-101
30017554-0	2019	COX-1 mediates IL-33-induced extracellular signal-regulated kinase activation in mast cells: Implications for aspirin sensitivity.	Aspirin	110-117	interleukin 33	Mus musculus	15-20
30017554-4	2019	METHODS: We used an ex vivo model of mouse bone marrow-derived mast cells and an IL-33-dependent in vivo model of aspirin-exacerbated respiratory disease (AERD).	Aspirin	114-121	interleukin 33	Mus musculus	81-86
31530979-8	2019	Furthermore, the results seem to imply that ASA and KET have certain potential to induce Foxp3 expression in CD25+CD8+ and CD25+CD4+ T cells, respectively.	Aspirin	44-47	interleukin 2 receptor, alpha chain	Mus musculus	109-113
31530979-8	2019	Furthermore, the results seem to imply that ASA and KET have certain potential to induce Foxp3 expression in CD25+CD8+ and CD25+CD4+ T cells, respectively.	Aspirin	44-47	CD8a molecule	Homo sapiens	114-117
31530979-8	2019	Furthermore, the results seem to imply that ASA and KET have certain potential to induce Foxp3 expression in CD25+CD8+ and CD25+CD4+ T cells, respectively.	Aspirin	44-47	interleukin 2 receptor, alpha chain	Mus musculus	123-127
31530979-8	2019	Furthermore, the results seem to imply that ASA and KET have certain potential to induce Foxp3 expression in CD25+CD8+ and CD25+CD4+ T cells, respectively.	Aspirin	44-47	CD4 antigen	Mus musculus	128-131
30377203-8	2018	However, recent aspirin use was associated with lower ovarian cancer risk for high [OR 0.54; 95% confidence interval (CI), 0.37-0.78], but not low (OR 1.50; 95% CI, 0.97-2.31), CD163 density (P heterogeneity &lt; 0.001).	Aspirin	16-23	CD163 molecule	Homo sapiens	177-182
30556891-3	2018	Recently, it was demonstrated that aspirin induces platelet MRP4 over-expression, through genomic modulation in megakaryocytes.	Aspirin	35-42	ATP binding cassette subfamily C member 4	Homo sapiens	60-64
30556891-6	2018	RESULTS: In 12Z cells, aspirin and other NSAIDs enhanced MRP4 mRNA and protein expression; these treatments also induced PPARa expression.	Aspirin	23-30	ATP binding cassette subfamily C member 4	Homo sapiens	57-61
30556891-7	2018	Aspirin and diclofenac-induced increases in MRP4 expression were not observed in cells where PPARa was knocked down using siRNA.	Aspirin	0-7	ATP binding cassette subfamily C member 4	Homo sapiens	44-48
29520080-13	2018	Among patients with minor stroke or TIA taking clopidogrel-aspirin treatment, CYP2C19 LOF carrier state was associated with higher risk of new stroke in those with eGFR &lt; 75 ml/min/1.73 m2.	Aspirin	59-66	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	78-85
29691782-10	2018	Adherence to aspirin had an ICER of US$25/QALY in the non-diabetic population, while it saved US$297 per patient over a 5-year period in the type II diabetes population.	Aspirin	13-20	cAMP responsive element modulator	Homo sapiens	28-32
29439623-3	2018	In this study, we aimed to investigate whether aspirin could attenuate PPARgamma inhibitor (T0070907)-induced preeclampsia and its impact on expression of PPARgamma.	Aspirin	47-54	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	71-80
29439623-3	2018	In this study, we aimed to investigate whether aspirin could attenuate PPARgamma inhibitor (T0070907)-induced preeclampsia and its impact on expression of PPARgamma.	Aspirin	47-54	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	155-164
29439623-10	2018	Importantly, T0070907 repressed both transcriptional and translational levels of PPARgamma, which were reversed by aspirin.	Aspirin	115-122	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	81-90
29439623-11	2018	In conclusion, this study suggests that aspirin prevented the occurrence of preeclampsia, which is possibly through enhancing both transcriptional and translational levels of PPARgamma.	Aspirin	40-47	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	175-184
30486577-11	2018	Flow cytometry and Western blot assay results indicated that aspirin could reduce the expression of ALDH1, SOX2, octamer-binding transcription factor 4 (OCT4) and NANOG in 4T1 cells.	Aspirin	61-68	SRY (sex determining region Y)-box 2	Mus musculus	107-111
30486577-11	2018	Flow cytometry and Western blot assay results indicated that aspirin could reduce the expression of ALDH1, SOX2, octamer-binding transcription factor 4 (OCT4) and NANOG in 4T1 cells.	Aspirin	61-68	POU domain, class 5, transcription factor 1	Mus musculus	113-151
30486577-11	2018	Flow cytometry and Western blot assay results indicated that aspirin could reduce the expression of ALDH1, SOX2, octamer-binding transcription factor 4 (OCT4) and NANOG in 4T1 cells.	Aspirin	61-68	POU domain, class 5, transcription factor 1	Mus musculus	153-157
30392338-6	2018	The expression levels of Nanog gene in control and ASA groups were 1.00 and 0.50+-0.10, respectively, and the difference was statistically significant (P&lt;0.05).	Aspirin	51-54	Nanog homeobox	Homo sapiens	25-30
30392338-7	2018	Moreover, the expression of Nanog gene in cells of KYSE-450+ M2 group and M2+ KYSE-450+ ASA group was 1.74+-0.13 and 1.43+-0.05, showing statistically significant difference (P&lt;0.05).	Aspirin	88-91	Nanog homeobox	Homo sapiens	28-33
30392338-8	2018	When chemokine CCL2 was knocked down, the levels of Nanog gene in M2+ shCCL2-KYSE450+ ASA group and M2+ shCCL2-KYSE450 group were decreased to 1.22+-0.11 and 1.17+-0.08, respectively, and there was no statistically significant difference between them (P=0.69).	Aspirin	86-89	Nanog homeobox	Homo sapiens	52-57
29922884-0	2018	Comment on "Targeting AMPK, mTOR and beta-Catenin by Combined Metformin and Aspirin Therapy in HCC: An Appraisal in Egyptian HCC Patients".	Aspirin	76-83	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	22-26
29967008-3	2018	Transcription factor EB (TFEB) is known as a master regulator of lysosomal biogenesis and, here, we reveal that aspirin, one of the most widely used medications in the world, upregulates TFEB and increases lysosomal biogenesis in brain cells.	Aspirin	112-119	transcription factor EB	Mus musculus	0-23
29967008-3	2018	Transcription factor EB (TFEB) is known as a master regulator of lysosomal biogenesis and, here, we reveal that aspirin, one of the most widely used medications in the world, upregulates TFEB and increases lysosomal biogenesis in brain cells.	Aspirin	112-119	transcription factor EB	Mus musculus	25-29
29967008-3	2018	Transcription factor EB (TFEB) is known as a master regulator of lysosomal biogenesis and, here, we reveal that aspirin, one of the most widely used medications in the world, upregulates TFEB and increases lysosomal biogenesis in brain cells.	Aspirin	112-119	transcription factor EB	Mus musculus	187-191
29967008-4	2018	Interestingly, aspirin induced the activation of peroxisome proliferator-activated receptor alpha (PPARalpha) and stimulated the transcription of Tfeb via PPARalpha.	Aspirin	15-22	transcription factor EB	Mus musculus	146-150
29967008-7	2018	Aspirin, one of the most widely used medications in the world, activates peroxisome proliferator-activated receptor alpha (PPARalpha) to upregulate transcription factor EB and increase lysosomal biogenesis in brain cells.	Aspirin	0-7	transcription factor EB	Mus musculus	148-171
29792865-7	2018	Such aspirin-induced changes of ABT-737 resistance was accompanied by a host of biochemical events like protein phosphatase 2A (PP2A) activation, AKT dephosphorylation, Mcl-1/FLICE inhibiting protein (FLIP)/XIAP downregulation, and Bax mitochondrial redistribution.	Aspirin	5-12	X-linked inhibitor of apoptosis	Homo sapiens	207-211
29980196-8	2018	In mouse primary microglia, recombinant SAA but not S. pneumoniae stimulated TNFalpha, IL-1beta, IL-6 and CCL-2 expression, and this response was completely blocked by the pro-resolving Fpr2 agonist aspirin-triggered resolvin D1 (AT-RvD1).	Aspirin	199-206	serum amyloid A cluster	Mus musculus	40-43
29980196-8	2018	In mouse primary microglia, recombinant SAA but not S. pneumoniae stimulated TNFalpha, IL-1beta, IL-6 and CCL-2 expression, and this response was completely blocked by the pro-resolving Fpr2 agonist aspirin-triggered resolvin D1 (AT-RvD1).	Aspirin	199-206	formyl peptide receptor 2	Mus musculus	186-190
30047573-9	2018	In the ASA arm, there was a 35% and 28% decrease in the proportion of genital T cells that were CD4+CCR5+ (p = 0.017) and Th17 (p = 0.04) respectively.	Aspirin	7-10	C-C motif chemokine receptor 5	Homo sapiens	100-104
29766772-2	2018	Anticoagulant treatment with rivaroxaban, an oral factor Xa inhibitor, may result in a lower risk of recurrent stroke than aspirin.	Aspirin	123-130	coagulation factor X	Homo sapiens	50-59
29525076-1	2018	BACKGROUND: The New Approach Rivaroxaban Inhibition of Factor Xa in a Global Trial vs. ASA to Prevent Embolism in Embolic Stroke of Undetermined Source (NAVIGATE-ESUS) trial is a randomized phase-III trial comparing rivaroxaban versus aspirin in patients with recent ESUS.	Aspirin	235-242	coagulation factor X	Homo sapiens	55-64
29901608-0	2018	Efficacy and safety of CYP2C19 genotype in stroke or transient ischemic attack patients treated with clopidogrel monotherapy or clopidogrel plus aspirin: Protocol for a systemic review and meta-analysis.	Aspirin	145-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
29901608-1	2018	BACKGROUND: The relationship of CYP2C19 genotype and clinical efficacy in stroke or transient ischemic attack (TIA) patients treated with clopidogrel monotherapy or clopidogrel plus aspirin remains unknown.	Aspirin	182-189	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
29656179-8	2018	RESULTS: Aspirin administration, reduced the protein expression of Mysm1, increased the protein expression of H2AK119-Ub and thereby reduced the Set7 protein expression in glomeruli isolated from diabetic animals and prevented renal fibrosis.	Aspirin	9-16	Myb like, SWIRM and MPN domains 1	Homo sapiens	67-72
29656179-9	2018	CONCLUSIONS: In conclusion, our results are clearly indicating that, aspirin prevents renal fibrosis in diabetic animals through decreasing the expression of Mysm1, increasing the expression of H2AK119-Ub and thereby decreasing the protein expression of Set7, which is a novel mechanism.	Aspirin	69-76	Myb like, SWIRM and MPN domains 1	Homo sapiens	158-163
29781520-6	2018	A significant association with poor responsiveness to aspirin was observed for GP1BA rs2243093, PTGS1 rs1330344, PTGS2 rs689466 and TBXA2R rs1131882 polymorphisms in overall analyses.	Aspirin	54-61	glycoprotein Ib platelet subunit alpha	Homo sapiens	79-84
29781520-8	2018	In conclusion, our findings indicate that GP1BA rs2243093, ITGA2 rs1126643, PTGS1 rs1330344, PTGS2 rs20417, PTGS2 rs689466 and TBXA2R rs1131882 polymorphisms may serve as genetic biomarkers of poor responsiveness to aspirin in certain ethnic groups.	Aspirin	216-223	glycoprotein Ib platelet subunit alpha	Homo sapiens	42-47
30046765-9	2018	In aspirin-treated volunteers, an inverse relationship between miR-21 and MRP4 platelet expression was found after aspirin treatment.	Aspirin	3-10	ATP binding cassette subfamily C member 4	Homo sapiens	74-78
30046765-9	2018	In aspirin-treated volunteers, an inverse relationship between miR-21 and MRP4 platelet expression was found after aspirin treatment.	Aspirin	115-122	ATP binding cassette subfamily C member 4	Homo sapiens	74-78
30046765-11	2018	Conclusion: The results reported in this study provide information that aspirin induces the modulation of platelet miR-21 expression levels and this modulation can be responsible for MRP4 enhancement in circulating platelets.	Aspirin	72-79	ATP binding cassette subfamily C member 4	Homo sapiens	183-187
29381509-10	2018	Immunofluorescence staining was used to detect the colocalization of NeuN and HO-1, and the results showed that aspirin significantly increased expression of the HO-1 protein in neurons.	Aspirin	112-119	heme oxygenase 1	Rattus norvegicus	78-82
29381509-10	2018	Immunofluorescence staining was used to detect the colocalization of NeuN and HO-1, and the results showed that aspirin significantly increased expression of the HO-1 protein in neurons.	Aspirin	112-119	heme oxygenase 1	Rattus norvegicus	162-166
29381509-12	2018	In conclusion, aspirin induces neuroprotective effects by inhibiting astrocyte activation and apoptosis after SCI through the activation of the Nrf2/HO-1 signaling pathway.	Aspirin	15-22	heme oxygenase 1	Rattus norvegicus	149-153
29471042-9	2018	The expression of HDAC9 was increased in a does-dependent manner when aspirin was introduced during BMSCs adipogenic differentiation.	Aspirin	70-77	histone deacetylase 9	Homo sapiens	18-23
29471042-10	2018	Docking study showed that high affinity of HDAC9 to aspirin was existed, suggesting that HDAC9 may has an important role in the process of aspirin-induced suppression of adipogenesis.	Aspirin	52-59	histone deacetylase 9	Homo sapiens	43-48
29471042-10	2018	Docking study showed that high affinity of HDAC9 to aspirin was existed, suggesting that HDAC9 may has an important role in the process of aspirin-induced suppression of adipogenesis.	Aspirin	52-59	histone deacetylase 9	Homo sapiens	89-94
29471042-10	2018	Docking study showed that high affinity of HDAC9 to aspirin was existed, suggesting that HDAC9 may has an important role in the process of aspirin-induced suppression of adipogenesis.	Aspirin	139-146	histone deacetylase 9	Homo sapiens	43-48
29471042-10	2018	Docking study showed that high affinity of HDAC9 to aspirin was existed, suggesting that HDAC9 may has an important role in the process of aspirin-induced suppression of adipogenesis.	Aspirin	139-146	histone deacetylase 9	Homo sapiens	89-94
29050464-5	2018	RESULTS: In MEA analysis, adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP)-induced platelet aggregations were lower in the CPD and the TCG groups; arachidonic acid (AA)-induced platelet aggregation was lower in the ASA group, whereas collagen (COL)-induced platelet aggregations were comparable among four groups.	Aspirin	242-245	TRAP	Homo sapiens	58-94
29050464-5	2018	RESULTS: In MEA analysis, adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP)-induced platelet aggregations were lower in the CPD and the TCG groups; arachidonic acid (AA)-induced platelet aggregation was lower in the ASA group, whereas collagen (COL)-induced platelet aggregations were comparable among four groups.	Aspirin	242-245	TRAP	Homo sapiens	96-100
29408091-0	2018	Aspirin induces Beclin-1-dependent autophagy of human hepatocellular carcinoma cell.	Aspirin	0-7	beclin 1	Homo sapiens	16-24
29408091-4	2018	Results showed that aspirin increased LC3II/LC3I ratio, decreased p62 expression, and enhanced autophagic flux (autophagosome and autolysosome puncta) in Hep3B, HepG2, or SMMC-7721 cells, reflecting the autophagy of HCC cells.	Aspirin	20-27	nucleoporin 62	Homo sapiens	66-69
29408091-5	2018	The autophagic effects of aspirin depended on Beclin-1 expression.	Aspirin	26-33	beclin 1	Homo sapiens	46-54
29408091-6	2018	Aspirin disrupted the interaction between Bcl-2 and Beclin-1.	Aspirin	0-7	beclin 1	Homo sapiens	52-60
29219948-7	2018	In summary, ASA VI promotes angiogenesis of HUVECs in vitro via up-regulating the HIF-1alpha/VEGF pathway, and efficiently enhances the vascularization in regenerated tissue and facilitates wound healing in vivo.	Aspirin	12-15	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	82-92
29407631-9	2018	CONCLUSIONS: For Chinese patients with ACS treated with aspirin and clopidogrel, genetic mutations in rs822441/rs822442 in PEAR1 correlated significantly with platelet activity after adjusting for CYP2C19 *2/*3 alleles.	Aspirin	56-63	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	197-204
29094287-0	2018	Targeting AMPK, mTOR and beta-Catenin by Combined Metformin and Aspirin Therapy in HCC: An Appraisal in Egyptian HCC Patients.	Aspirin	64-71	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	10-14
29094287-3	2018	OBJECTIVE: The current work aimed to investigate the possibility of targeting AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), and beta-catenin proteins through combined metformin/aspirin treatment in the HepG2 cell line, and to explore such molecular targets in Egyptian HCC patients.	Aspirin	206-213	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	78-106
29094287-3	2018	OBJECTIVE: The current work aimed to investigate the possibility of targeting AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), and beta-catenin proteins through combined metformin/aspirin treatment in the HepG2 cell line, and to explore such molecular targets in Egyptian HCC patients.	Aspirin	206-213	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	108-112
29094287-10	2018	CONCLUSIONS: Targeting AMPK, mTOR and beta-catenin by combined metformin/aspirin treatment could be a promising therapeutic strategy for Egyptian HCC patients, and possibly other HCC patients.	Aspirin	73-80	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	23-27
29329538-4	2018	METHODS: We measured peripheral blood gene expression levels of ITGA2B, which is upregulated by aspirin and correlates with platelet reactivity on aspirin, and a 5 gene validated smoking gene expression score (sGES) where higher expression correlates with smoking status, in participants from the previously reported PREDICT trial (NCT 00500617).	Aspirin	96-103	integrin subunit alpha 2b	Homo sapiens	64-70
29518782-12	2018	CONCLUSIONS: Our study reveals a novel mechanism by which aspirin alleviates pressure overload-induced cardiac interstitial fibrosis in TAC mice by suppressing the p-Erk1/2 and p-Akt/beta-catenin signalling pathways.	Aspirin	58-65	catenin (cadherin associated protein), beta 1	Mus musculus	183-195
28847510-4	2017	The activity of the mutated ALK2 was suppressed by pharmacological AMPK activators such as metformin and aspirin, while their actions were blocked by the dominant negative mutant of AMPK and mimicked by the constitutively active mutant of AMPK.	Aspirin	105-112	activin A receptor type 1	Homo sapiens	28-32
28847510-4	2017	The activity of the mutated ALK2 was suppressed by pharmacological AMPK activators such as metformin and aspirin, while their actions were blocked by the dominant negative mutant of AMPK and mimicked by the constitutively active mutant of AMPK.	Aspirin	105-112	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	67-71
28703660-8	2017	Conclusion Treatment with low-dose aspirin, enoxaparin and folic acid was the most effective therapy in women with RM who carried a C677T MTHFR mutation.	Aspirin	35-42	methylenetetrahydrofolate reductase	Homo sapiens	138-143
29018906-7	2017	The Amor criteria showed the highest sensitivity (98.2%) while the ASAS criteria for the axial SpA had highest specificity (100%).	Aspirin	67-71	surfactant protein A2	Homo sapiens	95-98
29018906-8	2017	The sensitivity and specificity of the remaining criteria were: 93.8 and 63.8% for ESSG, 95.6 and 62.7% for Garmisch-Partenkirchen, 91.2 and 75.3% for ASAS criteria for peripheral SpA, respectively.	Aspirin	151-155	surfactant protein A2	Homo sapiens	180-183
28866366-1	2017	Interleukin-8 (CXCL8) was originally described asa chemokine whose main function is the attraction of a polymorphonuclear inflammatory leukocyte infiltrate acting on CXCR1/2.	Aspirin	47-50	C-X-C motif chemokine receptor 1	Homo sapiens	166-171
28939077-9	2017	In overall, we present the first descriptive portrait of somatic alterations underlying the genome of tobacco/nut chewing HPV-negative early tongue cancer, and identify MMP10 asa potential prognostic biomarker to stratify those likely to develop metastases.	Aspirin	175-178	matrix metallopeptidase 10	Homo sapiens	169-174
28932294-0	2017	Aspirin-Induced Gastric Lesions Alters EGFR and PECAM-1 Immunoreactivity in Wistar Rats: Modulatory Action of Flavonoid Fraction of Musa Paradisiaca.	Aspirin	0-7	epidermal growth factor receptor	Rattus norvegicus	39-43
28932294-15	2017	CONCLUSION: The efficacy of Musa paradisiaca in attenuating the damaging effects of aspirin on the gastric mucosa was observed as there was a significantly increased reactivity for EGFR and PECAM-1 in the gastric corpus in a dose-dependent manner.	Aspirin	84-91	epidermal growth factor receptor	Rattus norvegicus	181-185
28636992-0	2017	Acetylsalicylic acid inhibits the growth of melanoma tumors via SOX2-dependent-PAF-R-independent signaling pathway.	Aspirin	0-20	SRY (sex determining region Y)-box 2	Mus musculus	64-68
28636992-0	2017	Acetylsalicylic acid inhibits the growth of melanoma tumors via SOX2-dependent-PAF-R-independent signaling pathway.	Aspirin	0-20	platelet-activating factor receptor	Mus musculus	79-84
28636992-4	2017	The current studies using stably PAF-R-positive (B16-PAFR) and negative (B16-MSCV) murine melanoma cells and PAF-R-expressing and deficient mice, demonstrate that ASA inhibits the in-vitro and in-vivo growth of highly aggressive B16F10 melanoma via bypassing tumoral or stromal PAF-R signaling.	Aspirin	163-166	platelet-activating factor receptor	Mus musculus	33-38
28636992-4	2017	The current studies using stably PAF-R-positive (B16-PAFR) and negative (B16-MSCV) murine melanoma cells and PAF-R-expressing and deficient mice, demonstrate that ASA inhibits the in-vitro and in-vivo growth of highly aggressive B16F10 melanoma via bypassing tumoral or stromal PAF-R signaling.	Aspirin	163-166	platelet-activating factor receptor	Mus musculus	109-114
28636992-4	2017	The current studies using stably PAF-R-positive (B16-PAFR) and negative (B16-MSCV) murine melanoma cells and PAF-R-expressing and deficient mice, demonstrate that ASA inhibits the in-vitro and in-vivo growth of highly aggressive B16F10 melanoma via bypassing tumoral or stromal PAF-R signaling.	Aspirin	163-166	platelet-activating factor receptor	Mus musculus	109-114
28636992-7	2017	Importantly, PCR array and qRT-PCR analysis of B16-tumors revealed significant downregulation of sry-related high-mobility-box-2 (SOX2) oncogene by ASA treatment.	Aspirin	148-151	SRY (sex determining region Y)-box 2	Mus musculus	97-128
28636992-7	2017	Importantly, PCR array and qRT-PCR analysis of B16-tumors revealed significant downregulation of sry-related high-mobility-box-2 (SOX2) oncogene by ASA treatment.	Aspirin	148-151	SRY (sex determining region Y)-box 2	Mus musculus	130-134
28636992-9	2017	Moreover, PGF2alpha-receptor antagonist, AL8810 mimics ASA-induced decreased melanoma cells survival which was significantly blocked by PGF2alpha and FGF-1.	Aspirin	55-58	prostaglandin F receptor	Mus musculus	10-28
28636992-10	2017	These findings indicate that ASA inhibits the growth of aggressive melanoma via SOX2-dependent-PAF-R-indepedent pathway.	Aspirin	29-32	SRY (sex determining region Y)-box 2	Mus musculus	80-84
28636992-10	2017	These findings indicate that ASA inhibits the growth of aggressive melanoma via SOX2-dependent-PAF-R-indepedent pathway.	Aspirin	29-32	platelet-activating factor receptor	Mus musculus	95-100
28528204-5	2017	Remarkably, aspirin strongly reduced the pro-inflammatory IL-1beta and TNF-alpha production, while it increased the anti-inflammatory IL-10 level in LPS-challenged cells.	Aspirin	12-19	interleukin 10	Homo sapiens	134-139
28528204-6	2017	Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1.	Aspirin	10-17	interleukin 10	Homo sapiens	245-249
28528204-6	2017	Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1.	Aspirin	10-17	C-X-C motif chemokine ligand 1	Homo sapiens	257-262
28528204-6	2017	Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1.	Aspirin	10-17	C-C motif chemokine ligand 5	Homo sapiens	264-268
28060561-0	2017	Aspirin Blocks Orthodontic Relapse via Inhibition of CD4+ T Lymphocytes.	Aspirin	0-7	Cd4 molecule	Rattus norvegicus	53-56
28060561-8	2017	The effects of aspirin on CD4+ T and Th1 cells were also analyzed in vitro.	Aspirin	15-22	Cd4 molecule	Rattus norvegicus	26-29
28060561-12	2017	Furthermore, aspirin treatment in vitro significantly repressed the differentiation of CD4+ T and Th1 cells.	Aspirin	13-20	Cd4 molecule	Rattus norvegicus	87-90
28507597-0	2017	Low adherence to national guidelines for proton-pump inhibitor prescription in patients receiving combination aspirin and anticoagulation.	Aspirin	110-117	ATPase H+/K+ transporting subunit alpha	Homo sapiens	41-52
28507597-2	2017	Therefore, multisociety guidelines recommend prophylactic proton-pump inhibitors (PPIs) for patients receiving aspirin and anticoagulation.	Aspirin	111-118	ATPase H+/K+ transporting subunit alpha	Homo sapiens	58-69
28184026-0	2017	Identification of TMEM208 and PQLC2 as reference genes for normalizing mRNA expression in colorectal cancer treated with aspirin.	Aspirin	121-128	solute carrier family 66 member 1	Homo sapiens	30-35
28446712-0	2017	Aspirin inhibits the SHH/GLI1 signaling pathway and sensitizes malignant glioma cells to temozolomide therapy.	Aspirin	0-7	GLI family zinc finger 1	Homo sapiens	25-29
28446712-2	2017	Here we investigated the aspirin"s antineoplastic molecular route by targeting SHH/GLI1 pathway and examined the feasibility of aspirin combined with TMZ therapy.	Aspirin	25-32	GLI family zinc finger 1	Homo sapiens	83-87
28446712-3	2017	Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) revealed that the activity of the SHH/GLI1 pathway was strongly inhibited by aspirin.	Aspirin	153-160	GLI family zinc finger 1	Homo sapiens	114-118
28446712-4	2017	Aspirin acted as the glioma growth-inhibitory and pro-apoptosis roles by inhibiting the SHH/GLI1 pathway and reprogramming the epithelial to mesenchymal transition (EMT).	Aspirin	0-7	GLI family zinc finger 1	Homo sapiens	92-96
28446712-5	2017	The immunofluorescence assay showed aspirin could prevent the nuclear translocation of GLI1 to inhibit its transcriptional regulation.	Aspirin	36-43	GLI family zinc finger 1	Homo sapiens	87-91
28446712-7	2017	Furthermore, aspirin combined with TMZ enhanced chemosensitivity and GLI1-induced chemoprotection was partly blocked by aspirin in vitro and in vivo.	Aspirin	13-20	GLI family zinc finger 1	Homo sapiens	69-73
28446712-7	2017	Furthermore, aspirin combined with TMZ enhanced chemosensitivity and GLI1-induced chemoprotection was partly blocked by aspirin in vitro and in vivo.	Aspirin	120-127	GLI family zinc finger 1	Homo sapiens	69-73
28446712-8	2017	Collectively, aspirin has a therapeutic potential for SHH/GLI1 targeted therapy against glioma cells.	Aspirin	14-21	GLI family zinc finger 1	Homo sapiens	58-62
28264838-7	2017	To target the metabolic phenotype induced by loss of BRCA1, a drug-repurposing approach was used and aspirin was identified as an agent that counteracted the increase in HK2 and the increase in glycolysis induced by BRCA1 impairment.	Aspirin	101-108	BRCA1 DNA repair associated	Homo sapiens	53-58
28264838-8	2017	Evidence from this study indicates that the tumor suppressor functions of BRCA1 extend beyond DNA repair to include metabolic endpoints and identifies aspirin as an ovarian cancer chemopreventive agent capable of reversing the metabolic derangements caused by loss of BRCA1.	Aspirin	151-158	BRCA1 DNA repair associated	Homo sapiens	74-79
28264838-8	2017	Evidence from this study indicates that the tumor suppressor functions of BRCA1 extend beyond DNA repair to include metabolic endpoints and identifies aspirin as an ovarian cancer chemopreventive agent capable of reversing the metabolic derangements caused by loss of BRCA1.	Aspirin	151-158	BRCA1 DNA repair associated	Homo sapiens	268-273
27533953-10	2017	Basophil activation (quantified by upregulation of CD203c in response to aspirin) was higher in cases at W6-8 than in controls (P = 0.0002).	Aspirin	73-80	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	51-57
28087411-0	2017	Aspirin prevents TNF-alpha-induced endothelial cell dysfunction by regulating the NF-kappaB-dependent miR-155/eNOS pathway: Role of a miR-155/eNOS axis in preeclampsia.	Aspirin	0-7	microRNA 155	Homo sapiens	102-109
28087411-0	2017	Aspirin prevents TNF-alpha-induced endothelial cell dysfunction by regulating the NF-kappaB-dependent miR-155/eNOS pathway: Role of a miR-155/eNOS axis in preeclampsia.	Aspirin	0-7	microRNA 155	Homo sapiens	134-141
28087411-5	2017	Aspirin prevented the TNF-alpha-mediated increase in miR-155 biogenesis and decreases in eNOS expression and NO/cGMP production in cultured human umbilical vein endothelial cells (HUVECs).	Aspirin	0-7	microRNA 155	Homo sapiens	53-60
28087411-7	2017	The preventive effects of aspirin was associated with the inhibition of nuclear factor-kappaB (NF-kappaB)-dependent MIR155HG (miR-155 host gene) expression.	Aspirin	26-33	microRNA 155	Homo sapiens	116-122
28087411-8	2017	Aspirin recovered the TNF-alpha-mediated decrease in wild-type, but not mutant, eNOS 3"-untranslated region reporter activity, whose effect was blocked by miR-155 mimic.	Aspirin	0-7	microRNA 155	Homo sapiens	155-162
28087411-9	2017	Moreover, aspirin prevented TNF-alpha-mediated endothelial cell dysfunction associated with impaired vasorelaxation, angiogenesis, and trophoblast invasion, and the preventive effects were blocked by miR-155 mimic or an eNOS inhibitor.	Aspirin	10-17	microRNA 155	Homo sapiens	200-207
28087411-10	2017	Aspirin rescued TNF-alpha-mediated eNOS downregulation coupled with endothelial dysfunction by inhibiting NF-kappaB-dependent transcriptional miR-155 biogenesis.	Aspirin	0-7	microRNA 155	Homo sapiens	142-149
28137499-0	2017	Association of interleukin-25 levels with development of aspirin induced respiratory diseases.	Aspirin	57-64	interleukin 25	Homo sapiens	15-29
28137499-8	2017	After the aspirin challenge, the IL-25 levels were markedly decreased in the ATA group (p = 0.024), while not changed in the AERD group.	Aspirin	10-17	interleukin 25	Homo sapiens	33-38
28137499-9	2017	The post-challenge IL-25 levels of all asthmatic subjects were significantly correlated with aspirin challenge - induced declines in FEV1 (r = 0.357, p = 0.011), but not with basal and post challenge LTC4 and PGD2 levels.	Aspirin	93-100	interleukin 25	Homo sapiens	19-24
28137499-10	2017	CONCLUSIONS: IL-25 is associated with bronchospasm after aspirin challenge, possibly via mechanisms other than altered LTC4 and PGD2 production.	Aspirin	57-64	interleukin 25	Homo sapiens	13-18
28125730-0	2017	The Influence of BRAF and KRAS Mutation Status on the Association between Aspirin Use and Survival after Colon Cancer Diagnosis.	Aspirin	74-81	KRAS proto-oncogene, GTPase	Homo sapiens	26-30
28125730-3	2017	The aim of this study was to investigate the influence of BRAF and KRAS mutation status on the association between aspirin use and overall survival after colon cancer diagnosis.	Aspirin	115-122	KRAS proto-oncogene, GTPase	Homo sapiens	67-71
28278500-0	2017	Aspirin Inhibits IKK-beta-mediated Prostate Cancer Cell Invasion by Targeting Matrix Metalloproteinase-9 and Urokinase-Type Plasminogen Activator.	Aspirin	0-7	matrix metallopeptidase 9	Homo sapiens	78-104
28278500-7	2017	Aspirin treatment significantly resulted in reduction of matrix metalloproteinase-9 (MMP-9) and upregulation of tissue inhibitors of metalloproteinase-1 (TIMP-1) activity, which are the proteolytic enzymes contributing to the degradation of extracellular matrix and basement membrane in cell invasion and metastasis.	Aspirin	0-7	matrix metallopeptidase 9	Homo sapiens	57-83
28278500-7	2017	Aspirin treatment significantly resulted in reduction of matrix metalloproteinase-9 (MMP-9) and upregulation of tissue inhibitors of metalloproteinase-1 (TIMP-1) activity, which are the proteolytic enzymes contributing to the degradation of extracellular matrix and basement membrane in cell invasion and metastasis.	Aspirin	0-7	matrix metallopeptidase 9	Homo sapiens	85-90
28278500-11	2017	CONCLUSION: The present research concluded that aspirin suppressed prostate cancer cell invasion by reducing MMP-9 activity and uPA expression through decreasing of IKK-beta-mediated NF-kappaB activation, indicating that the ability of aspirin to inhibit cell invasion might be useful in the chemoprevention of metastatic prostate cancer.	Aspirin	48-55	matrix metallopeptidase 9	Homo sapiens	109-114
27999284-0	2016	Aspirin down Regulates Hepcidin by Inhibiting NF-kappaB and IL6/JAK2/STAT3 Pathways in BV-2 Microglial Cells Treated with Lipopolysaccharide.	Aspirin	0-7	hepcidin antimicrobial peptide	Mus musculus	23-31
27999284-1	2016	Aspirin down regulates transferrin receptor 1 (TfR1) and up regulates ferroportin 1 (Fpn1) and ferritin expression in BV-2 microglial cells treated without lipopolysaccharides (LPS), as well as down regulates hepcidin and interleukin 6 (IL-6) in cells treated with LPS.	Aspirin	0-7	hepcidin antimicrobial peptide	Mus musculus	209-217
27999284-4	2016	We demonstrated that aspirin inhibited hepcidin mRNA as well as NO production in cells treated with LPS, but not in cells without LPS, suppresses IL-6, JAK2, STAT3, and P65 (nuclear factor-kappaB) phosphorylation and has no effect on IRP1 in cells treated with or without LPS.	Aspirin	21-28	hepcidin antimicrobial peptide	Mus musculus	39-47
27999284-4	2016	We demonstrated that aspirin inhibited hepcidin mRNA as well as NO production in cells treated with LPS, but not in cells without LPS, suppresses IL-6, JAK2, STAT3, and P65 (nuclear factor-kappaB) phosphorylation and has no effect on IRP1 in cells treated with or without LPS.	Aspirin	21-28	aconitase 1	Mus musculus	234-238
27999284-5	2016	These findings provide evidence that aspirin down regulates hepcidin by inhibiting IL6/JAK2/STAT3 and P65 (nuclear factor-kappaB) pathways in the cells under inflammatory conditions, and imply that an aspirin-induced reduction in TfR1 and an increase in ferritin are not associated with IRP1 and NO.	Aspirin	37-44	hepcidin antimicrobial peptide	Mus musculus	60-68
27999284-5	2016	These findings provide evidence that aspirin down regulates hepcidin by inhibiting IL6/JAK2/STAT3 and P65 (nuclear factor-kappaB) pathways in the cells under inflammatory conditions, and imply that an aspirin-induced reduction in TfR1 and an increase in ferritin are not associated with IRP1 and NO.	Aspirin	37-44	aconitase 1	Mus musculus	287-291
27999284-5	2016	These findings provide evidence that aspirin down regulates hepcidin by inhibiting IL6/JAK2/STAT3 and P65 (nuclear factor-kappaB) pathways in the cells under inflammatory conditions, and imply that an aspirin-induced reduction in TfR1 and an increase in ferritin are not associated with IRP1 and NO.	Aspirin	201-208	hepcidin antimicrobial peptide	Mus musculus	60-68
27683757-0	2016	Enhanced platelet MRP4 expression and correlation with platelet function in patients under chronic aspirin treatment.	Aspirin	99-106	ATP binding cassette subfamily C member 4	Homo sapiens	18-22
27683757-1	2016	Platelet multidrug resistance protein4 (MRP4)-overexpression has a role in reducing aspirin action.	Aspirin	84-91	ATP binding cassette subfamily C member 4	Homo sapiens	9-38
27683757-1	2016	Platelet multidrug resistance protein4 (MRP4)-overexpression has a role in reducing aspirin action.	Aspirin	84-91	ATP binding cassette subfamily C member 4	Homo sapiens	40-44
27683757-2	2016	Aspirin in vivo treatment enhances platelet MRP4 expression and MRP4 mediated transport inhibition reduces platelet function and delays thrombus formation.	Aspirin	0-7	ATP binding cassette subfamily C member 4	Homo sapiens	44-48
27683757-3	2016	The aim of our work was to verify whether MRP4 expression is enhanced in platelets obtained from patients under chronic aspirin treatment and whether it correlates with residual platelet reactivity.	Aspirin	120-127	ATP binding cassette subfamily C member 4	Homo sapiens	42-46
27683757-6	2016	Platelets obtained from ASA&gt;2 months patients that present high levels of platelet MRP4, have higher serum TxB2 levels and collagen-induced platelet aggregation compared to patient with low levels of MRP4 in platelets.	Aspirin	24-27	ATP binding cassette subfamily C member 4	Homo sapiens	86-90
27683757-6	2016	Platelets obtained from ASA&gt;2 months patients that present high levels of platelet MRP4, have higher serum TxB2 levels and collagen-induced platelet aggregation compared to patient with low levels of MRP4 in platelets.	Aspirin	24-27	ATP binding cassette subfamily C member 4	Homo sapiens	203-207
27683757-8	2016	We can assert that, in patients under chronic aspirin treatment, platelets that present high MRP4 levels have an increase of residual platelet reactivity, which is due in part to incomplete COX-1 inhibition, and in part to COX-1-independent mechanism.	Aspirin	46-53	ATP binding cassette subfamily C member 4	Homo sapiens	93-97
27348236-1	2016	CONCLUSION: The study suggests that cancerous inhibitor of protein phosphatase 2A (CIP2A) expression and eosinophilia associate with chronic rhinosinusitis with nasal polyps with aspirin exacerbated respiratory disease (CRSwNP + AERD).	Aspirin	179-186	cellular inhibitor of PP2A	Homo sapiens	36-81
27348236-1	2016	CONCLUSION: The study suggests that cancerous inhibitor of protein phosphatase 2A (CIP2A) expression and eosinophilia associate with chronic rhinosinusitis with nasal polyps with aspirin exacerbated respiratory disease (CRSwNP + AERD).	Aspirin	179-186	cellular inhibitor of PP2A	Homo sapiens	83-88
27641736-9	2016	Due to the combined effects of PLA2G7 rs1051931 and rs7756935, carriers of the AA-CC haplotype had a higher level of ADP-induced platelet aggregation, and were at considerably higher risk of aspirin resistance than noncarriers (odds ratio=8.233, 95% CI: 1.590-42.638).	Aspirin	191-198	phospholipase A2 group VII	Homo sapiens	31-37
27504605-5	2016	We observed a statistically significant association between elevated TNFR-2 levels and colorectal cancer risk in the placebo arm (RRhighestvs.lowesttertile=1.77; 95% CI=1.02-3.06; Ptrend=0.02), but not in the aspirin arm (Ptrend=0.72).	Aspirin	209-216	TNF receptor superfamily member 1B	Homo sapiens	69-75
28011952-11	2016	which in our previous studies significantly reduced the ethanol and aspirin-induced gastric damage, significantly decreased the number of WRS-induced gastric lesions while raising the GBF and significantly increasing the activity of SOD and GSH (P &lt; 0.05).	Aspirin	68-75	superoxide dismutase 2	Rattus norvegicus	233-236
27672332-12	2016	Other significant risk factors for advanced CRN were age (OR 1.050; 95% CI 1.003-1.009; P=0.036) and body mass index (OR 1.205; 95% CI 1.067-1.361; P=0.003), whereas aspirin use (OR 0.414; 95% CI 0.173-0.990; P=0.047) was a preventive factor.	Aspirin	166-173	crooked neck pre-mRNA splicing factor 1	Homo sapiens	44-47
27391154-7	2016	Clinically, conventional doses of aspirin increased AP-2alpha phosphorylation and IkBalpha protein expression in humans subjects.	Aspirin	34-41	transcription factor AP-2 alpha	Homo sapiens	52-61
27296993-13	2016	15-Hydroxyprostaglandin dehydrogenase activation in females reduces the incidence of rupture and eliminates the sex-differential response to aspirin.	Aspirin	141-148	carbonyl reductase 1	Homo sapiens	0-37
27356773-0	2016	Aspirin inhibits glucose-6-phosphate dehydrogenase activity in HCT 116 cells through acetylation: Identification of aspirin-acetylated sites.	Aspirin	0-7	glucose-6-phosphate dehydrogenase	Homo sapiens	17-50
27356773-0	2016	Aspirin inhibits glucose-6-phosphate dehydrogenase activity in HCT 116 cells through acetylation: Identification of aspirin-acetylated sites.	Aspirin	116-123	glucose-6-phosphate dehydrogenase	Homo sapiens	17-50
27356773-3	2016	Our previous study demonstrated that exposure of HCT 116 human colorectal cancer cells to aspirin caused acetylation of G6PD, and this was associated with a decrease in its enzyme activity.	Aspirin	90-97	glucose-6-phosphate dehydrogenase	Homo sapiens	120-124
27356773-4	2016	In the present study, this observation was expanded to HT-29 colorectal cancer cells, in order to compare aspirin-mediated acetylation of G6PD and its activity between HCT 116 and HT-29 cells.	Aspirin	106-113	glucose-6-phosphate dehydrogenase	Homo sapiens	138-142
27356773-5	2016	In addition, the present study aimed to determine the acetylation targets of aspirin on recombinant G6PD to provide an insight into the mechanisms of inhibition.	Aspirin	77-84	glucose-6-phosphate dehydrogenase	Homo sapiens	100-104
27356773-7	2016	Mass spectrometry analysis of aspirin-acetylated G6PD (isoform a) revealed that aspirin acetylated a total of 14 lysine residues, which were dispersed throughout the length of the G6PD protein.	Aspirin	30-37	glucose-6-phosphate dehydrogenase	Homo sapiens	49-53
27356773-7	2016	Mass spectrometry analysis of aspirin-acetylated G6PD (isoform a) revealed that aspirin acetylated a total of 14 lysine residues, which were dispersed throughout the length of the G6PD protein.	Aspirin	80-87	glucose-6-phosphate dehydrogenase	Homo sapiens	49-53
27356773-7	2016	Mass spectrometry analysis of aspirin-acetylated G6PD (isoform a) revealed that aspirin acetylated a total of 14 lysine residues, which were dispersed throughout the length of the G6PD protein.	Aspirin	80-87	glucose-6-phosphate dehydrogenase	Homo sapiens	180-184
27356773-9	2016	Acetylation of G6PD at several sites, including K235 (K205 in isoform b), may mediate inhibition of G6PD activity, which may contribute to the ability of aspirin to exert anticancer effects through decreased synthesis of ribose sugars and NADPH.	Aspirin	154-161	glucose-6-phosphate dehydrogenase	Homo sapiens	15-19
27356773-9	2016	Acetylation of G6PD at several sites, including K235 (K205 in isoform b), may mediate inhibition of G6PD activity, which may contribute to the ability of aspirin to exert anticancer effects through decreased synthesis of ribose sugars and NADPH.	Aspirin	154-161	glucose-6-phosphate dehydrogenase	Homo sapiens	100-104
26525539-8	2016	ASA activated the PI3K/Akt-GSK3-mTOR pathway, which phosphorylates ULK1 to prevent autophagy initiation, changes that were inhibited by the PI3K-inhibitor wortmannin.	Aspirin	0-3	mechanistic target of rapamycin kinase	Rattus norvegicus	32-36
26556638-2	2016	We therefore investigated whether in vivo and thrombin receptor activating peptide (TRAP)-stimulated platelet activation and monocyte-platelet aggregate (MPA) levels can serve as independent risk markers for adverse outcomes in aspirin-treated patients presenting for cardiac catheterization.	Aspirin	228-235	TRAP	Homo sapiens	84-88
26773298-8	2016	In the aspirin/clopidogrel group, the PL24 -AUC10 was higher in poor metabolizers (PMs) with cytochrome P450 2C19(CYP2C19) polymorphisms (152 +- 112, 95% CI 103.4-200.6) than in the non-PM group (87 +- 74, 95% CI 73.8-100.2).	Aspirin	7-14	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-113
26773298-8	2016	In the aspirin/clopidogrel group, the PL24 -AUC10 was higher in poor metabolizers (PMs) with cytochrome P450 2C19(CYP2C19) polymorphisms (152 +- 112, 95% CI 103.4-200.6) than in the non-PM group (87 +- 74, 95% CI 73.8-100.2).	Aspirin	7-14	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	114-121
26917098-8	2016	Acetylsalicylic acid supplementation caused a considerable increase in the expression of all active substances studied within both left and right NG and the percentage of neurons positive to particular substances fluctuated from 47.2 +- 3.6% (GAL-LI neurons in the right NG) to 67.2 +- 2.0% (cells immunoreactive to SP in the left NG).	Aspirin	0-20	galanin and GMAP prepropeptide	Homo sapiens	243-246
28119929-5	2016	We found that aspirin reduced serum amylase and lipase levels, decreased the MPO activity, and alleviated the histopathological manifestations of pancreas and pancreatitis-associated lung injury.	Aspirin	14-21	myeloperoxidase	Mus musculus	77-80
28119929-7	2016	Furthermore, aspirin induced the apoptosis of acinar cells by TUNEL assay, and the expression of Bax and caspase 3 was increased and the expression of Bcl-2 was decreased.	Aspirin	13-20	BCL2-associated X protein	Mus musculus	97-100
28119929-7	2016	Furthermore, aspirin induced the apoptosis of acinar cells by TUNEL assay, and the expression of Bax and caspase 3 was increased and the expression of Bcl-2 was decreased.	Aspirin	13-20	caspase 3	Mus musculus	105-114
28119929-8	2016	Intriguingly, the downregulation of critical necrosis associated proteins RIP1, RIP3, and p-MLKL was observed; what is more, we additionally found that aspirin reduced the COX level of pancreatic tissue.	Aspirin	152-159	receptor-interacting serine-threonine kinase 3	Mus musculus	80-84
28119929-8	2016	Intriguingly, the downregulation of critical necrosis associated proteins RIP1, RIP3, and p-MLKL was observed; what is more, we additionally found that aspirin reduced the COX level of pancreatic tissue.	Aspirin	152-159	mixed lineage kinase domain-like	Mus musculus	92-96
26162710-5	2015	The administration of an exogenous analogue of lipoxin, Aspirin-triggered Lipoxin (ATL), caused a decline in Caspase-1 cleavage, inflammasome activation and mature IL-1beta production and thus attenuated the development of morphine tolerance by inhibiting upstream Akt phosphorylation.	Aspirin	56-63	caspase 1	Rattus norvegicus	109-118
26342029-0	2015	Aspirin-Exacerbated Respiratory Disease Involves a Cysteinyl Leukotriene-Driven IL-33-Mediated Mast Cell Activation Pathway.	Aspirin	0-7	interleukin 33	Mus musculus	80-85
26219912-0	2015	Aspirin Targets SIRT1 and AMPK to Induce Senescence of Colorectal Carcinoma Cells.	Aspirin	0-7	sirtuin 1	Homo sapiens	16-21
26219912-5	2015	In this study, we investigated the effects of aspirin on TIS of human colorectal carcinoma (CRC) cells and show that it occurs via sirtuin 1 (SIRT1) and AMP-activated protein kinase (AMPK), two key regulators of cellular metabolism.	Aspirin	46-53	sirtuin 1	Homo sapiens	131-140
26219912-5	2015	In this study, we investigated the effects of aspirin on TIS of human colorectal carcinoma (CRC) cells and show that it occurs via sirtuin 1 (SIRT1) and AMP-activated protein kinase (AMPK), two key regulators of cellular metabolism.	Aspirin	46-53	sirtuin 1	Homo sapiens	142-147
26219912-6	2015	Aspirin increased the senescence of CRC cells, increased the protein levels of SIRT1, phospho-AMPK (T172), and phospho-acetyl CoA carboxylase (S79), and reduced the cellular level of ATP.	Aspirin	0-7	sirtuin 1	Homo sapiens	79-84
26219912-7	2015	Small-interfering RNA-mediated downregulation or pharmacological inhibition of SIRT1 or AMPK significantly attenuated the aspirin-induced cellular senescence in CRC cells.	Aspirin	122-129	sirtuin 1	Homo sapiens	79-84
26219912-9	2015	Remarkably, SIRT1 knockdown abrogated the aspirin-induced activation of AMPK, and vice versa.	Aspirin	42-49	sirtuin 1	Homo sapiens	12-17
26219912-10	2015	During the progression of aspirin-induced cellular senescence in CRC cells, SIRT1 showed increased deacetylase activity at a relatively early time point but was characterized by decreased activity with increased cytoplasmic localization at a later time point.	Aspirin	26-33	sirtuin 1	Homo sapiens	76-81
26219912-11	2015	Collectively, these novel findings suggest that aspirin could provide anticancer effects by inducing senescence in human CRC cells through the reciprocal regulation of SIRT1-AMPK pathways.	Aspirin	48-55	sirtuin 1	Homo sapiens	168-173
25995130-0	2015	Cost-Effectiveness of Proton Pump Inhibitor Co-Therapy in Patients Taking Aspirin for Secondary Prevention of Ischemic Stroke.	Aspirin	74-81	ATPase H+/K+ transporting subunit alpha	Homo sapiens	22-33
26395086-13	2015	CONCLUSIONS: If patients with suspected axial SpA have either (1) IBP according to Calin/ASAS definition plus alternating buttock pain, or (2) IBP according to Calin definition plus awakening at night, or (3) dactylitis or 4) IBD, the probability of finding a positive MRI-SI increases significantly.	Aspirin	89-93	surfactant protein A2	Homo sapiens	46-49
25577230-2	2015	The findings of our study showed that drought stress significantly enhanced the AsA-GSH cycle by upregulating the activities of ascorbate peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), and dehydroascorbate reductase (DHAR).	Aspirin	80-83	probable glutathione S-transferase DHAR1, cytosolic	Triticum aestivum	188-214
25577230-2	2015	The findings of our study showed that drought stress significantly enhanced the AsA-GSH cycle by upregulating the activities of ascorbate peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), and dehydroascorbate reductase (DHAR).	Aspirin	80-83	probable glutathione S-transferase DHAR1, cytosolic	Triticum aestivum	217-221
26294325-5	2015	Of the top 10 genes (fold-change &gt; 10, P &lt; 10(-10)) regulated by metformin plus aspirin, PCDH18, CCL2, RASL11A, FAM111B and BMP5 were down-regulated &gt;= 20-fold, while NGFR, NPTX1, C7orf57, MRPL23AS1 and UNC5B were up-regulated &gt;= 10-fold.	Aspirin	86-93	chromosome 7 open reading frame 57	Homo sapiens	189-196
26294325-5	2015	Of the top 10 genes (fold-change &gt; 10, P &lt; 10(-10)) regulated by metformin plus aspirin, PCDH18, CCL2, RASL11A, FAM111B and BMP5 were down-regulated &gt;= 20-fold, while NGFR, NPTX1, C7orf57, MRPL23AS1 and UNC5B were up-regulated &gt;= 10-fold.	Aspirin	86-93	unc-5 netrin receptor B	Homo sapiens	212-217
26135128-0	2015	Rebamipide Promotes the Regeneration of Aspirin-Induced Small-Intestine Mucosal Injury through Accumulation of beta-Catenin.	Aspirin	40-47	catenin (cadherin associated protein), beta 1	Mus musculus	111-123
26135128-13	2015	CONCLUSION: Rebamipide administration in aspirin-induced SII mice could improve the intestinal barrier structure and promote the regeneration of small intestinal epithelial injury through up-regulating COX-2 expression and the accumulation of beta-catenin.	Aspirin	41-48	catenin (cadherin associated protein), beta 1	Mus musculus	243-255
26019129-7	2015	CONCLUSIONS: There were significant differences in recurrent stroke by CYP2C19 genotype-inferred metabolizer status in white subcortical stroke patients receiving dual antiplatelet therapy with aspirin and clopidogrel, consistent with cardiovascular studies on CYP2C19 and clopidogrel; however, the bleeding risk that led to early termination of the antiplatelet arm of the SPS3 trial does not appear to be explained by CYP2C19 genotype.	Aspirin	194-201	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
25824885-0	2015	Simvastatin combined with aspirin increases the survival time of heart allograft by activating CD4(+)CD25(+) Treg cells and enhancing vascular endothelial cell protection.	Aspirin	26-33	Cd4 molecule	Rattus norvegicus	95-98
25793910-3	2015	The solution properties of ASA-inulins were investigated using dye solubilization, surface tension, and dynamic light scattering, and all three techniques confirmed that the molecules aggregated in solution above a critical concentration (critical aggregation concentration, CAC).	Aspirin	27-30	carbonic anhydrase 2	Homo sapiens	275-278
25793910-5	2015	The hydrodynamic diameter of ASA-inulins above the CAC was determined from dynamic light scattering studies and was shown to increase with alkenyl chain length, from 4 nm for the octenyl derivative to 55 nm for the hexadecenyl derivative.	Aspirin	29-32	carbonic anhydrase 2	Homo sapiens	51-54
24647791-13	2015	Aspirin and eugenol enhanced the IL-1beta-induced sICAM-1 production and ICAM-1 expression.	Aspirin	0-7	intercellular adhesion molecule 1	Homo sapiens	51-57
25278289-6	2014	Interestingly, the racial difference in PAR4-mediated platelet aggregation persisted in platelets treated ex vivo with aspirin and 2MeSAMP (2-methylthioadenosine 5"-monophosphate triethylammonium salt hydrate), suggesting that the racial difference is independent of secondary feedback.	Aspirin	119-126	F2R like thrombin or trypsin receptor 3	Homo sapiens	40-44
25483761-8	2014	Predictors of readmission for RNx included higher ASA score (OR: 1.77, p = 0.03), and the presence of any complications during the index hospitalization (OR: 2.21, p = 0.03).	Aspirin	50-53	T cell leukemia homeobox 3	Homo sapiens	30-33
25549592-12	2014	There was an increase in CCL5 levels in patients receiving Acetylsalicylic Acid (ASA) therapy (p=0.046).	Aspirin	59-79	C-C motif chemokine ligand 5	Homo sapiens	25-29
25549592-12	2014	There was an increase in CCL5 levels in patients receiving Acetylsalicylic Acid (ASA) therapy (p=0.046).	Aspirin	81-84	C-C motif chemokine ligand 5	Homo sapiens	25-29
24818590-11	2014	CONCLUSION: The addition of prednisolone to heparin and low dose aspirin might be beneficial in patients with unexplained recurrent miscarriage, and this effect might be due to a suppressive effect of steroids on the peripheral CD16 NK cells concentration.	Aspirin	65-72	Fc gamma receptor IIIa	Homo sapiens	228-232
24880897-0	2014	Low dose aspirin is associated with plasma chemerin levels and may reduce adipose tissue inflammation.	Aspirin	9-16	retinoic acid receptor responder 2	Homo sapiens	43-51
24880897-5	2014	Mean plasma chemerin levels were similar in controls and CAD patients but significantly higher in CAD patients not taking low dose aspirin.	Aspirin	131-138	retinoic acid receptor responder 2	Homo sapiens	12-20
24880897-6	2014	To investigate the mechanism of chemerin reduction by aspirin, we analyzed chemerin expression in hepatocytes and adipocytes treated with aspirin in the presence and absence of inflammatory cytokines.	Aspirin	54-61	retinoic acid receptor responder 2	Homo sapiens	32-40
24880897-6	2014	To investigate the mechanism of chemerin reduction by aspirin, we analyzed chemerin expression in hepatocytes and adipocytes treated with aspirin in the presence and absence of inflammatory cytokines.	Aspirin	138-145	retinoic acid receptor responder 2	Homo sapiens	75-83
24880897-9	2014	However, treatment of inflammatory M1 macrophages with aspirin reduced secretion of the pro-inflammatory cytokines IL-1beta and IL-6, and increased secretion of the anti-inflammatory IL-10.	Aspirin	55-62	interleukin 10	Homo sapiens	183-188
24880897-10	2014	In summary, we show that plasma chemerin levels are associated with markers of inflammation and that they are significantly higher in CAD patients not treated with low dose aspirin.	Aspirin	173-180	retinoic acid receptor responder 2	Homo sapiens	32-40
24880897-11	2014	In addition, we show that low dose aspirin treatment reduces pro-inflammatory cytokine secretion by macrophages, which may lead to reduced chemerin secretion by adipocytes and may be a reason for the lower chemerin levels in the circulation of CAD patients on low dose aspirin.	Aspirin	35-42	retinoic acid receptor responder 2	Homo sapiens	139-147
24880897-11	2014	In addition, we show that low dose aspirin treatment reduces pro-inflammatory cytokine secretion by macrophages, which may lead to reduced chemerin secretion by adipocytes and may be a reason for the lower chemerin levels in the circulation of CAD patients on low dose aspirin.	Aspirin	35-42	retinoic acid receptor responder 2	Homo sapiens	206-214
25055737-6	2014	Incubation of PRP from AMI with dermcidin antibody restored the sensitivity of the platelets to the aspirin effect.	Aspirin	100-107	dermcidin	Homo sapiens	32-41
25055737-7	2014	Incubation of AMI PRP pretreated with 15 muM aspirin, a stimulator of the NO synthesis, resulted in the increased production of NO in the platelets that removed the bound dermcidin by 40% from the high affinity binding sites of AMI platelets.	Aspirin	45-52	dermcidin	Homo sapiens	171-180
25037196-10	2014	CONCLUSIONS: Circulating MRP-8/14 is associated with TX-dependent platelet activation in ACS, even during low-dose aspirin treatment, suggesting a contribution of residual TX to MRP-8/14 shedding, which may further amplify platelet activation.	Aspirin	115-122	ATP binding cassette subfamily C member 11	Homo sapiens	25-30
25029546-9	2014	Although the mean fluorescence intensity of CD203c expression and the percentage of histamine release were significantly up-regulated by aspirin, they were not affected by anti-IgE antibodies.	Aspirin	137-144	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	44-50
24418973-11	2014	ASA and ketorolac both decreased the activity of MMP-2, MMP-9, and uPA.	Aspirin	0-3	matrix metallopeptidase 2	Mus musculus	49-54
24418943-3	2014	To evaluate an impact of CYP2C19 G681A and CYP4F2 G1347A polymorphisms and clinical factors on dual antiplatelet effect of clopidogrel and aspirin.	Aspirin	139-146	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
24699240-9	2014	While 8-hydroxy-2-deoxyguanosine and malondialdehyde levels were significantly decreased, NR2B and nAChRalpha7 expressions were significantly increased in the aspirin+ascorbic acid group as compared to the control group (p &lt; 0.05).	Aspirin	159-166	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	90-94
24606818-4	2014	Further, we hypothesized that minocycline induced MMP-2 and MMP-9 inhibition will be potentiated by aspirin and the combination of both drugs will prevent worsening of MI in diabetic patients.	Aspirin	100-107	matrix metallopeptidase 9	Homo sapiens	60-65
24606818-14	2014	Treatment with a combination of minocycline and aspirin decreased percentage infarct volume, arrhythmias, mortality and collagen level when compared with vehicle-treated diabetic controls and showed reduced levels of MMP-2 and MMP-9.	Aspirin	48-55	matrix metallopeptidase 9	Rattus norvegicus	227-232
24565956-8	2014	In an exploratory analysis, we found that among individuals with high plasma MIC-1 levels (quintiles 2-5), compared with nonuse, regular use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) was associated with a lower risk of PTGS2-positive CRC (multivariable RR = 0.60; 95% confidence interval = 0.41 to 0.88) but not PTGS2-negative CRC (multivariable RR = 1.21; 95% CI = 0.71 to 2.07).	Aspirin	144-151	growth differentiation factor 15	Homo sapiens	77-82
24565956-11	2014	Aspirin/NSAID use appeared to lower risk of PTGS2-positive cancers, particularly among individuals with high levels of circulating MIC-1.	Aspirin	0-7	growth differentiation factor 15	Homo sapiens	131-136
24345330-0	2014	Aspirin attenuates vinorelbine-induced endothelial inflammation via modulating SIRT1/AMPK axis.	Aspirin	0-7	sirtuin 1	Homo sapiens	79-84
24345330-0	2014	Aspirin attenuates vinorelbine-induced endothelial inflammation via modulating SIRT1/AMPK axis.	Aspirin	0-7	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	85-89
24345330-9	2014	We corroborated that treatment of Aspirin significantly diminishes VNR-repressed SIRT1, LKB1 and AMPK phosphorylation and VNR-promoted NADPH oxidase activation, however, those findings were vanished by SIRT1 and AMPK siRNAs.	Aspirin	34-41	sirtuin 1	Homo sapiens	81-86
24345330-9	2014	We corroborated that treatment of Aspirin significantly diminishes VNR-repressed SIRT1, LKB1 and AMPK phosphorylation and VNR-promoted NADPH oxidase activation, however, those findings were vanished by SIRT1 and AMPK siRNAs.	Aspirin	34-41	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	97-101
24345330-9	2014	We corroborated that treatment of Aspirin significantly diminishes VNR-repressed SIRT1, LKB1 and AMPK phosphorylation and VNR-promoted NADPH oxidase activation, however, those findings were vanished by SIRT1 and AMPK siRNAs.	Aspirin	34-41	sirtuin 1	Homo sapiens	202-207
24345330-9	2014	We corroborated that treatment of Aspirin significantly diminishes VNR-repressed SIRT1, LKB1 and AMPK phosphorylation and VNR-promoted NADPH oxidase activation, however, those findings were vanished by SIRT1 and AMPK siRNAs.	Aspirin	34-41	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	212-216
24717792-14	2014	The study confirms aspirin desensitization is effective clinically in AERD patients and suggests that IFN gamma and IL-10 expression in CD4(+) T lymphocytes may be related to the mechanism of action.	Aspirin	19-26	interleukin 10	Homo sapiens	116-121
24642922-9	2014	Emerging evidence hints that CAC may also promote long-term adherence to aspirin, exercise, diet, and statin therapy.	Aspirin	73-80	carbonic anhydrase 2	Homo sapiens	29-32
24474638-2	2014	Polymorphisms in genes coding GPIIb/IIIa, namely ITGA2B and ITGB3, are associated with aspirin resistance and risk for thrombotic diseases.	Aspirin	87-94	integrin subunit alpha 2b	Homo sapiens	30-35
24474638-2	2014	Polymorphisms in genes coding GPIIb/IIIa, namely ITGA2B and ITGB3, are associated with aspirin resistance and risk for thrombotic diseases.	Aspirin	87-94	integrin subunit alpha 2b	Homo sapiens	49-55
25272742-5	2014	Incubation of cells transfected with the above-mentioned constructs treated with aspirin was accompanied by the suppression of NF-kB, HIF1alpha, GAS, VDR, and HSF binding activity.	Aspirin	81-88	vitamin D receptor	Homo sapiens	150-153
25272742-6	2014	The findings revealed for NF-kB, NFAT, and STAT1 confirm the published data concerning the mechanisms of aspirin action.	Aspirin	105-112	signal transducer and activator of transcription 1	Homo sapiens	43-48
24408984-8	2014	CONCLUSIONS: The early morphologic involvement of the GCL+IPL and INL+OPL layers in ARM eyes, as revealed by the ASA, could be related to early anatomic changes described in the inner retina of ARM eyes.	Aspirin	113-116	germ cell-less 2, spermatogenesis associated	Homo sapiens	54-57
24478700-9	2014	Furthermore, we revealed that aspirin enhanced extracellular signal-related kinase (ERK) but inhibited RhoA activities.	Aspirin	30-37	ras homolog family member A	Rattus norvegicus	103-107
24478700-10	2014	In summary, we provided the first evidence that aspirin can promote oligodendrogenesis and oligodendrocyte myelination after WML, which may involve ERK and RhoA pathways.	Aspirin	48-55	ras homolog family member A	Rattus norvegicus	156-160
24881732-1	2014	OBJECTIVE: The Japanese health insurance system approved the use of proton pump inhibitors (PPIs) for the prevention of peptic ulcers in patients using low-dose aspirin (LDA) and/or non-steroidal anti-inflammatory drugs (NSAIDs).	Aspirin	161-168	ATPase H+/K+ transporting subunit alpha	Homo sapiens	68-79
24153330-0	2013	Aspirin augments IgE-mediated histamine release from human peripheral basophils via Syk kinase activation.	Aspirin	0-7	spleen associated tyrosine kinase	Homo sapiens	84-87
24153330-9	2013	When the IgE receptor signaling pathway was activated, aspirin increased the phosphorylation of Syk.	Aspirin	55-62	spleen associated tyrosine kinase	Homo sapiens	96-99
24153330-11	2013	CONCLUSIONS: Aspirin enhanced histamine release from basophils via increased Syk kinase activation, and that the augmentation of histamine release by NSAIDs or FAs may be one possible cause of worsening symptoms in patients with chronic urticaria and FDEIA.	Aspirin	13-20	spleen associated tyrosine kinase	Homo sapiens	77-80
24064546-0	2013	Overexpression of S100A9 in human glioma and in-vitro inhibition by aspirin.	Aspirin	68-75	S100 calcium binding protein A9	Homo sapiens	18-24
24064546-10	2013	Aspirin treatment inhibited cell proliferation and caused early apoptosis in glioma, coupled with reduced S100A9 levels.	Aspirin	0-7	S100 calcium binding protein A9	Homo sapiens	106-112
24064546-13	2013	Aspirin may be a novel candidate for targeted prevention of S100A9 overexpression in glioma cells.	Aspirin	0-7	S100 calcium binding protein A9	Homo sapiens	60-66
23832067-11	2013	CONCLUSION: The variation in response to ASA may be related with an increased expression of IGF1 and IGF1R, as well as a response to clopidogrel can be affected by pharmacokinetic change related to the reverse transport pathway by increased expression of ABCC3.	Aspirin	41-44	insulin like growth factor 1 receptor	Homo sapiens	101-106
24183037-6	2013	The proportion of patients with the PLAA above 20% value was significantly lower in the combination group than those in the aspirin alone group (32.1% vs 62.1%, P&lt;0.05).	Aspirin	124-131	phospholipase A2 activating protein	Homo sapiens	36-40
24183037-7	2013	PLAA of two groups one and two days after taking aspirin or plus clopidogrel were (24.2+-31.9)% vs. (49.6+-32.6)% and (13.8+-27.2)% vs. (37.6+-37.4)%, respectively (P&lt;0.05).	Aspirin	49-56	phospholipase A2 activating protein	Homo sapiens	0-4
23876149-3	2013	The clean biochemical approach revealed that proteoliposomes comprising purified NPT1 as the only protein source transport various organic anions such as urate, p-aminohippuric acid (PAH), and acetylsalicylic acid (aspirin) in a membrane potential (Deltapsi)-driven and Cl(-) -dependent manner.	Aspirin	215-222	solute carrier family 17 member 1	Homo sapiens	81-85
23870238-3	2013	The ASA classification includes 6 grades: ASAP1, a normal healthy person; ASAP2, mild systemic disease; ASAP3, severe systemic disease; ASAP4, severe systemic disease that is a constant threat to life; ASAP5, a critically ill patient who is not expected to survive without the operation; and ASAP6, declared brain-dead patient whose organs are being removed for donor purposes.	Aspirin	4-7	ArfGAP with SH3 domain, ankyrin repeat and PH domain 1	Homo sapiens	42-47
23741443-0	2013	Aspirin minimized the pro-metastasis effect of sorafenib and improved survival by up-regulating HTATIP2 in hepatocellular carcinoma.	Aspirin	0-7	HIV-1 Tat interactive protein 2	Mus musculus	96-103
23741443-7	2013	The molecular mechanism of HTATIP2 regulation by aspirin was explored.	Aspirin	49-56	HIV-1 Tat interactive protein 2	Mus musculus	27-34
23741443-8	2013	RESULTS: Aspirin suppressed the pro-invasion and pro-metastasis effects of sorafenib in HCC and up-regulated HTATIP2 expression.	Aspirin	9-16	HIV-1 Tat interactive protein 2	Mus musculus	109-116
23741443-9	2013	Aspirin did not inhibit the proliferation of HCC cells, but it decreased the invasiveness of HCC with lower expression of HTATIP2 and increased expression of a set of markers, indicating a mesenchymal-to-epithelial transition in tumor cells.	Aspirin	0-7	HIV-1 Tat interactive protein 2	Mus musculus	122-129
23741443-11	2013	CONCLUSIONS: Aspirin minimized the pro-metastasis effect of sorafenib by up-regulating the tumor suppressor HTATIP2; this mechanism is mediated through inhibition of COX2.	Aspirin	13-20	HIV-1 Tat interactive protein 2	Mus musculus	108-115
23543480-10	2013	Hypertension, peripheral arteriopathy and use of low-dose aspirin or diuretics were positive predictors of baseline NGAL, while treatment with calcium channel blockers and statins were negative predictors.	Aspirin	58-65	lipocalin 2	Homo sapiens	116-120
23638194-9	2013	We explored whether this observation was related to the metabolic shift toward the production of 5-lipoxygenase derivatives, and although we did not observe an increase in LTB4 production in infected RAW cells and mice infected, we did find an increase in 15-epi-LXA4 (an ASA-triggered lipoxin).	Aspirin	272-275	arachidonate 5-lipoxygenase	Mus musculus	97-111
23357179-0	2013	Preeclampsia-like symptoms induced in mice by fetoplacental expression of STOX1 are reversed by aspirin treatment.	Aspirin	96-103	storkhead box 1	Mus musculus	74-79
23237781-12	2013	The finding that SNP variations in the human GLYAT gene influence the kinetic properties of the enzyme may explain some of the inter-individual variation in glycine conjugation capacity, which is relevant to the metabolism of xenobiotics such as aspirin and the industrial solvent xylene, and to the treatment of some metabolic disorders.	Aspirin	246-253	glycine-N-acyltransferase	Homo sapiens	45-50
23230963-8	2013	Furthermore, aspirin/TMZ microsphere intratumoral injection downregulated the expression of beta-catenin, TCF4, pAKT, pSTAT3, and PCNA and delayed tumor growth in nude mice harboring subcutaneous LN229 xenografts.	Aspirin	13-20	catenin (cadherin associated protein), beta 1	Mus musculus	92-104
23230963-8	2013	Furthermore, aspirin/TMZ microsphere intratumoral injection downregulated the expression of beta-catenin, TCF4, pAKT, pSTAT3, and PCNA and delayed tumor growth in nude mice harboring subcutaneous LN229 xenografts.	Aspirin	13-20	proliferating cell nuclear antigen	Mus musculus	130-134
23306703-7	2013	Moreover, the production of IL-6 from inflammatory cells, induced by IL-17, was abolished by treatment with ASA, whereas that induced by LPS was not.	Aspirin	108-111	interleukin 17A	Mus musculus	69-74
23306703-8	2013	Altogether, ASA, likely via its acetyl moiety, inhibits Th17 airway inflammation by blockade of IL-6 and IL-17 positive feedback.	Aspirin	12-15	interleukin 17A	Mus musculus	105-110
23277876-0	2013	Association Analysis Between FILIP1 Polymorphisms and Aspirin Hypersensitivity in Korean Asthmatics.	Aspirin	54-61	filamin A interacting protein 1	Homo sapiens	29-35
22881598-0	2013	Activation of the bile acid receptor GPBAR1 protects against gastrointestinal injury caused by non-steroidal anti-inflammatory drugs and aspirin in mice.	Aspirin	137-144	G protein-coupled bile acid receptor 1	Mus musculus	37-43
22881598-7	2013	Mice lacking GPBAR1 were more sensitive to gastric and intestinal injury caused by ASA and NSAIDs and exhibited a markedly reduced expression of cystathionine-gamma-liase (CSE), cystathionine-beta-synthase (CBS) and endothelial NOS enzymes required for generation of H(2)S and NO, in the stomach.	Aspirin	83-86	G protein-coupled bile acid receptor 1	Mus musculus	13-19
23126503-5	2012	When aspirin was added in the solution containing LOX and the complex [Cu(tpp)(pmt)](2), the former was shown to hinder the binding of the Cu complex significantly.	Aspirin	5-12	lysyl oxidase	Homo sapiens	50-53
23126503-6	2012	This may be interpreted as the copper complex aiding the transfer of aspirin through an acid-base reaction at the LOX enzyme which subsequently blocks its binding.	Aspirin	69-76	lysyl oxidase	Homo sapiens	114-117
23085268-2	2012	The present study investigated the effect of a novel H(2)S-releasing aspirin, ACS14 (2-acetyloxybenzoic acid 4-(3-thioxo-3H-1,2-dithiol-5-yl)phenyl ester), on atherosclerotic plaques in fat-fed apoE(-/-) mice and the underlying mechanism with respect to CX3C chemokine receptor 1 (CX3CR1) in macrophages.	Aspirin	69-76	chemokine (C-X3-C motif) receptor 1	Mus musculus	254-279
23085268-2	2012	The present study investigated the effect of a novel H(2)S-releasing aspirin, ACS14 (2-acetyloxybenzoic acid 4-(3-thioxo-3H-1,2-dithiol-5-yl)phenyl ester), on atherosclerotic plaques in fat-fed apoE(-/-) mice and the underlying mechanism with respect to CX3C chemokine receptor 1 (CX3CR1) in macrophages.	Aspirin	69-76	chemokine (C-X3-C motif) receptor 1	Mus musculus	281-287
22918213-3	2012	This study investigated the expression of pendrin and periostin in sinonasal tissue of patients with allergic rhinitis, chronic rhinosinusitis, and aspirin-induced asthma.	Aspirin	148-155	solute carrier family 26 member 4	Homo sapiens	42-49
22918213-10	2012	CONCLUSIONS: Production of pendrin and periostin is upregulated in allergic rhinitis, chronic rhinosinusitis with nasal polyps, and aspirin-induced asthma.	Aspirin	132-139	solute carrier family 26 member 4	Homo sapiens	27-34
22996069-8	2012	5,7-Dihydroxy-4-methylcoumarins, in particular those containing a lipophilic side chain at C-3, reached the activity of acetylsalicylic acid on AA-induced aggregation.	Aspirin	120-140	complement C3	Homo sapiens	91-94
23033009-0	2012	beta-catenin negatively regulates expression of the prostaglandin transporter PGT in the normal intestinal epithelium and colorectal tumour cells: a role in the chemopreventive efficacy of aspirin?	Aspirin	189-196	catenin (cadherin associated protein), beta 1	Mus musculus	0-12
22745359-7	2012	In addition, our gelatinase zymography and fluorescence data confirmed that the cardol-cardanol mixture, salicylic acid, and aspirin, all of which lack key functional groups present in anacardic acid, are much weaker MMP-2/MMP-9 inhibitors.	Aspirin	125-132	matrix metallopeptidase 2	Mus musculus	217-222
22753481-6	2012	Treatment with aspirin and clopidogrel during the chronic phase of the disease diminished the number of intrahepatic HBV-specific CD8(+) T cells and HBV-nonspecific inflammatory cells, the severity of liver fibrosis, and the development of HCC.	Aspirin	15-22	CD8a molecule	Homo sapiens	130-133
22542748-0	2012	Ability of rabeprazole to prevent gastric mucosal damage from clopidogrel and low doses of aspirin depends on CYP2C19 genotype.	Aspirin	91-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	110-117
22150675-5	2012	We aimed to compare the effects of aspirin and prodrugs of aspirin (1-5) on human platelet aggregation stimulated by ADP and collagen and associated receptor expression (GPIIb/IIIa and P-selectin) in platelet-rich plasma (PRP) and washed platelets (WP).	Aspirin	59-66	integrin subunit alpha 2b	Homo sapiens	170-175
23110215-5	2012	Aspirin induced nuclear caspase-dependent cleavage of Sp1, Sp3 and Sp4 proteins and this response was related to sequestration of zinc ions since addition of zinc sulfate blocked aspirin-mediated apoptosis and repression of Sp proteins.	Aspirin	0-7	Sp4 transcription factor	Homo sapiens	67-70
23110215-5	2012	Aspirin induced nuclear caspase-dependent cleavage of Sp1, Sp3 and Sp4 proteins and this response was related to sequestration of zinc ions since addition of zinc sulfate blocked aspirin-mediated apoptosis and repression of Sp proteins.	Aspirin	179-186	Sp4 transcription factor	Homo sapiens	67-70
23050414-11	2012	In all scoring systems, except of the MPM for cancer patients and TRIOS, the PDR values correlated significantly with the preoperative ASA group assessment.	Aspirin	135-138	PDR	Homo sapiens	77-80
22448321-2	2012	A stress-induced protein identified to be dermcidin isoform 2 of Mr. 11 kDa from blood plasma of hypertensive persons when injected (0.1 muM) in rabbits increased the systolic pressure by 77% and diastolic pressure by 45% over the controls within 2 h. Ingestion of acetyl salicylic acid (150 mg/70 kg) by these subjects reduced systolic (130 mm Hg) and diastolic pressures (80 mm Hg) with reduction of plasma dermcidin level to normal ranges (9 nM).	Aspirin	265-286	dermcidin	Homo sapiens	42-51
22448321-4	2012	Aspirin was found to reduce hypertension by reduction of plasma dermcidin level, neutralized the effect of cyclooxygenase, and restored the pancreatic insulin synthesis through NO synthesis.	Aspirin	0-7	dermcidin	Homo sapiens	64-73
21862721-5	2011	Aspirin treatment reduced hepatic NF-kappaB activity in HFD-fed APOC1 and WT mice, and in addition, aspirin decreased plasma TG levels (-32%, P &lt; 0.05) in hypertriglyceridemic APOC1 mice.	Aspirin	0-7	apolipoprotein C-I	Mus musculus	64-69
21862721-5	2011	Aspirin treatment reduced hepatic NF-kappaB activity in HFD-fed APOC1 and WT mice, and in addition, aspirin decreased plasma TG levels (-32%, P &lt; 0.05) in hypertriglyceridemic APOC1 mice.	Aspirin	0-7	apolipoprotein C-I	Mus musculus	179-184
21862721-5	2011	Aspirin treatment reduced hepatic NF-kappaB activity in HFD-fed APOC1 and WT mice, and in addition, aspirin decreased plasma TG levels (-32%, P &lt; 0.05) in hypertriglyceridemic APOC1 mice.	Aspirin	100-107	apolipoprotein C-I	Mus musculus	64-69
21862721-5	2011	Aspirin treatment reduced hepatic NF-kappaB activity in HFD-fed APOC1 and WT mice, and in addition, aspirin decreased plasma TG levels (-32%, P &lt; 0.05) in hypertriglyceridemic APOC1 mice.	Aspirin	100-107	apolipoprotein C-I	Mus musculus	179-184
21862721-6	2011	This TG-lowering effect could not be explained by enhanced VLDL-TG clearance, but aspirin selectively reduced hepatic production of VLDL-TG in both APOC1 (-28%, P &lt; 0.05) and WT mice (-33%, P &lt; 0.05) without affecting VLDL-apoB production.	Aspirin	82-89	apolipoprotein C-I	Mus musculus	148-153
21855977-0	2011	Polymorphisms of the CYP2C19 gene in Japanese patients with aspirin-exacerbated respiratory disease.	Aspirin	60-67	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
21966608-0	2011	Polymorphisms of Aspirin-Metabolizing Enzymes CYP2C9, NAT2 and UGT1A6 in Aspirin-Intolerant Urticaria.	Aspirin	17-24	N-acetyltransferase 2	Homo sapiens	54-58
21966608-0	2011	Polymorphisms of Aspirin-Metabolizing Enzymes CYP2C9, NAT2 and UGT1A6 in Aspirin-Intolerant Urticaria.	Aspirin	73-80	N-acetyltransferase 2	Homo sapiens	54-58
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	0-21	N-acetyltransferase 2	Homo sapiens	121-143
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	0-21	N-acetyltransferase 2	Homo sapiens	145-149
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	23-26	N-acetyltransferase 2	Homo sapiens	121-143
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	23-26	N-acetyltransferase 2	Homo sapiens	145-149
21962096-0	2011	Variations in expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in nasal mucosa of aspirin-sensitive versus aspirin-tolerant patients with nasal polyposis.	Aspirin	118-125	matrix metallopeptidase 9	Homo sapiens	28-54
21962096-0	2011	Variations in expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in nasal mucosa of aspirin-sensitive versus aspirin-tolerant patients with nasal polyposis.	Aspirin	143-150	matrix metallopeptidase 9	Homo sapiens	28-54
21980231-12	2011	Proton pump inhibitor and rebamipide prevented low-dose acetylsalicylic acid-induced gastrointestinal complications compared with the placebo group.	Aspirin	56-76	ATPase H+/K+ transporting subunit alpha	Homo sapiens	0-11
21816313-0	2011	Aspirin extrusion from human platelets through multidrug resistance protein-4-mediated transport: evidence of a reduced drug action in patients after coronary artery bypass grafting.	Aspirin	0-7	ATP binding cassette subfamily C member 4	Homo sapiens	47-77
21816313-1	2011	OBJECTIVES: In this study we investigate: 1) the role of multidrug resistance protein-4 (MRP4), an organic anion unidirectional transporter, in modulating aspirin action on human platelet cyclooxygenase (COX)-1; and 2) whether the impairment of aspirin-COX-1 interaction, found in coronary artery bypass grafting (CABG) patients, could be dependent on MRP4-mediated transport.	Aspirin	155-162	ATP binding cassette subfamily C member 4	Homo sapiens	57-87
21816313-1	2011	OBJECTIVES: In this study we investigate: 1) the role of multidrug resistance protein-4 (MRP4), an organic anion unidirectional transporter, in modulating aspirin action on human platelet cyclooxygenase (COX)-1; and 2) whether the impairment of aspirin-COX-1 interaction, found in coronary artery bypass grafting (CABG) patients, could be dependent on MRP4-mediated transport.	Aspirin	155-162	ATP binding cassette subfamily C member 4	Homo sapiens	89-93
21816313-1	2011	OBJECTIVES: In this study we investigate: 1) the role of multidrug resistance protein-4 (MRP4), an organic anion unidirectional transporter, in modulating aspirin action on human platelet cyclooxygenase (COX)-1; and 2) whether the impairment of aspirin-COX-1 interaction, found in coronary artery bypass grafting (CABG) patients, could be dependent on MRP4-mediated transport.	Aspirin	155-162	ATP binding cassette subfamily C member 4	Homo sapiens	352-356
21816313-1	2011	OBJECTIVES: In this study we investigate: 1) the role of multidrug resistance protein-4 (MRP4), an organic anion unidirectional transporter, in modulating aspirin action on human platelet cyclooxygenase (COX)-1; and 2) whether the impairment of aspirin-COX-1 interaction, found in coronary artery bypass grafting (CABG) patients, could be dependent on MRP4-mediated transport.	Aspirin	245-252	ATP binding cassette subfamily C member 4	Homo sapiens	57-87
21816313-1	2011	OBJECTIVES: In this study we investigate: 1) the role of multidrug resistance protein-4 (MRP4), an organic anion unidirectional transporter, in modulating aspirin action on human platelet cyclooxygenase (COX)-1; and 2) whether the impairment of aspirin-COX-1 interaction, found in coronary artery bypass grafting (CABG) patients, could be dependent on MRP4-mediated transport.	Aspirin	245-252	ATP binding cassette subfamily C member 4	Homo sapiens	89-93
21816313-3	2011	Aspirin is an organic anion and could be a substrate for MRP4.	Aspirin	0-7	ATP binding cassette subfamily C member 4	Homo sapiens	57-61
21816313-6	2011	RESULTS: Inhibition of MRP4-mediated transport by dipyridamole or Mk-571 increases aspirin entrapment and its in vitro effect on COX-1 activity (142.7 +- 34.6 pg/10(8) cells vs. 343.7 +- 169.3 pg/108 cells TxB2-production).	Aspirin	83-90	ATP binding cassette subfamily C member 4	Homo sapiens	23-27
21816313-7	2011	Platelets derived from megakaryocytes transfected with MRP4 small interfering ribonucleic acid have a higher aspirin entrapment and drug COX-1 activity.	Aspirin	109-116	ATP binding cassette subfamily C member 4	Homo sapiens	55-59
21816313-8	2011	Platelets from CABG patients showed a high expression of MRP4 whose in vitro inhibition enhanced aspirin effect on COX-1 (349 +- 141 pg/108 cells vs. 1,670 +- 646 pg/108 cells TxB2-production).	Aspirin	97-104	ATP binding cassette subfamily C member 4	Homo sapiens	57-61
21615437-0	2011	Cost-effectiveness analysis: cardiovascular benefits of proton pump inhibitor co-therapy in patients using aspirin for secondary prevention.	Aspirin	107-114	ATPase H+/K+ transporting subunit alpha	Homo sapiens	56-67
21615437-2	2011	Proton pump inhibitor (PPI) co-therapy may reduce ASA-related dyspepsia, enhancing ASA adherence and improving CV outcomes.	Aspirin	50-53	ATPase H+/K+ transporting subunit alpha	Homo sapiens	0-11
21615437-2	2011	Proton pump inhibitor (PPI) co-therapy may reduce ASA-related dyspepsia, enhancing ASA adherence and improving CV outcomes.	Aspirin	83-86	ATPase H+/K+ transporting subunit alpha	Homo sapiens	0-11
21615437-10	2011	ASA plus PPI was also more costly than ASA alone, with an ICER of $19000 per life-year saved.	Aspirin	0-3	cAMP responsive element modulator	Homo sapiens	58-62
21615437-12	2011	CONCLUSIONS: Proton pump inhibitor co-therapy has the potential to impact not only GI, but also CV outcomes in patients with CV disease using ASA and such co-therapy is likely to be cost-effective.	Aspirin	142-145	ATPase H+/K+ transporting subunit alpha	Homo sapiens	13-24
21562004-0	2011	Proton pump inhibitor use and risk of adverse cardiovascular events in aspirin treated patients with first time myocardial infarction: nationwide propensity score matched study.	Aspirin	71-78	ATPase H+/K+ transporting subunit alpha	Homo sapiens	0-11
21562004-1	2011	OBJECTIVE: To examine the effect of proton pump inhibitors on adverse cardiovascular events in aspirin treated patients with first time myocardial infarction.	Aspirin	95-102	ATPase H+/K+ transporting subunit alpha	Homo sapiens	36-47
21562004-10	2011	Conclusion In aspirin treated patients with first time myocardial infarction, treatment with proton pump inhibitors was associated with an increased risk of adverse cardiovascular events.	Aspirin	14-21	ATPase H+/K+ transporting subunit alpha	Homo sapiens	93-104
21514281-7	2011	In VSMCs from SHR, aspirin increased p53 and p21 expression and inhibited the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E.	Aspirin	19-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-48
21116834-6	2011	After in vitro treatment with ASA, macrophages expressed low levels of MHC-II, CD80, and CD47 molecules, and showed significantly decreased phagocytosis.	Aspirin	30-33	CD47 antigen (Rh-related antigen, integrin-associated signal transducer)	Mus musculus	89-93
21473831-5	2011	To the A1-3 groups aspirin 50, 100 and 200 mumol/L were added respectively.	Aspirin	19-26	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	7-11
21473831-15	2011	As expression of HO-1 is increased in aspirin groups, it may be considered as a protective factor against anti oxidative damage in AEC II cell culture.	Aspirin	38-45	heme oxygenase 1	Rattus norvegicus	17-21
21311765-8	2011	CONCLUSION: Discordant results from MTHFR studies and randomised trials could be explained by aspirin reducing or negating the anti-platelet effect of lowering homocysteine.	Aspirin	94-101	methylenetetrahydrofolate reductase	Homo sapiens	36-41
21097689-1	2011	PURPOSE: Nitric oxide-donating acetylsalicylic acid (NO-ASA) has been shown to possess an antineoplastic effect in Wnt-/beta-catenin-active cancers.	Aspirin	31-51	catenin (cadherin associated protein), beta 1	Mus musculus	120-132
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	TNF receptor associated factor 2	Homo sapiens	80-85
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	NFAT activating protein with ITAM motif 1	Homo sapiens	138-143
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	nuclear factor of activated T cells 1	Homo sapiens	148-153
22199996-6	2011	Aspirin/NSAID interacted with MAP3K7 (colon cancer) and with MAPK14, NFAT5, and TRAF2 (rectal cancer); smoking cigarettes interacted with NFAM1 and NFAT2 (colon cancer) and MAPK8, NFAT5, and TNFRSF1A (rectal cancer); BMI interacted with NFAM1 and NFAT5 (colon cancer) and with MAPK8 and TNFRSF1A (rectal cancer).	Aspirin	0-7	NFAT activating protein with ITAM motif 1	Homo sapiens	237-242
21905501-1	2011	BACKGROUND AND OBJECTIVE: Lymphocyte-oriented kinase deficiency encoded by the serine/threonine kinase 10 (STK10) gene correlates with the intracellular adhesion molecule 1 (ICAM-1)/lymphocyte function associated antigen 1 (LFA-1) complex in aspirin hypersensitivity.	Aspirin	242-249	serine/threonine kinase 10	Homo sapiens	26-52
21905501-1	2011	BACKGROUND AND OBJECTIVE: Lymphocyte-oriented kinase deficiency encoded by the serine/threonine kinase 10 (STK10) gene correlates with the intracellular adhesion molecule 1 (ICAM-1)/lymphocyte function associated antigen 1 (LFA-1) complex in aspirin hypersensitivity.	Aspirin	242-249	serine/threonine kinase 10	Homo sapiens	79-105
21905501-1	2011	BACKGROUND AND OBJECTIVE: Lymphocyte-oriented kinase deficiency encoded by the serine/threonine kinase 10 (STK10) gene correlates with the intracellular adhesion molecule 1 (ICAM-1)/lymphocyte function associated antigen 1 (LFA-1) complex in aspirin hypersensitivity.	Aspirin	242-249	serine/threonine kinase 10	Homo sapiens	107-112
21905501-1	2011	BACKGROUND AND OBJECTIVE: Lymphocyte-oriented kinase deficiency encoded by the serine/threonine kinase 10 (STK10) gene correlates with the intracellular adhesion molecule 1 (ICAM-1)/lymphocyte function associated antigen 1 (LFA-1) complex in aspirin hypersensitivity.	Aspirin	242-249	intercellular adhesion molecule 1	Homo sapiens	139-172
21905501-1	2011	BACKGROUND AND OBJECTIVE: Lymphocyte-oriented kinase deficiency encoded by the serine/threonine kinase 10 (STK10) gene correlates with the intracellular adhesion molecule 1 (ICAM-1)/lymphocyte function associated antigen 1 (LFA-1) complex in aspirin hypersensitivity.	Aspirin	242-249	intercellular adhesion molecule 1	Homo sapiens	174-180
21878077-14	2011	These results indicates that variations of GP IIb/IIIa content affect platelet aggregating activity within first hours of ACS upon ASA treatment.	Aspirin	131-134	integrin subunit alpha 2b	Homo sapiens	43-49
21329420-5	2011	In healthy volunteers positive associations were observed between GP IIb-IIIa number and the level of ADP-induced aggregation when this relationship was analysed in untreated platelet-rich plasma (PRP) as well as upon in vitro addition of aspirin or non-saturating concentrations of GP IIb-IIIa blockers.	Aspirin	239-246	integrin subunit alpha 2b	Homo sapiens	66-72
21329420-5	2011	In healthy volunteers positive associations were observed between GP IIb-IIIa number and the level of ADP-induced aggregation when this relationship was analysed in untreated platelet-rich plasma (PRP) as well as upon in vitro addition of aspirin or non-saturating concentrations of GP IIb-IIIa blockers.	Aspirin	239-246	integrin subunit alpha 2b	Homo sapiens	283-289
21219209-3	2011	The objective of present study was to inhibit MMP-2 and MMP-9 by combination of minocycline and aspirin to treat diabetic nephropathy.	Aspirin	96-103	matrix metallopeptidase 9	Rattus norvegicus	56-61
20964555-8	2010	Aspirin, when combined with all doses of ethanol, increased ADA activity, which is crucial for purine metabolism.	Aspirin	0-7	adenosine deaminase	Rattus norvegicus	60-63
20925583-1	2010	In humans, the glycine N-acyltransferase enzyme (GLYAT) is thought to be important in the detoxification of endogenous and xenobiotic compounds which contain a carboxylic acid group, such as benzoic, isovaleric, or acetylsalicylic acids.	Aspirin	215-236	glycine-N-acyltransferase	Homo sapiens	15-47
20925583-1	2010	In humans, the glycine N-acyltransferase enzyme (GLYAT) is thought to be important in the detoxification of endogenous and xenobiotic compounds which contain a carboxylic acid group, such as benzoic, isovaleric, or acetylsalicylic acids.	Aspirin	215-236	glycine-N-acyltransferase	Homo sapiens	49-54
21072201-5	2010	Among 11 candidate genes, multivariate logistic analyses showed that SNPs of CEP68 gene showed the most significant association with aspirin intolerance (P values of co-dominant for CEP68, 6.0x10(-5) to 4.0x10(-5)).	Aspirin	133-140	centrosomal protein 68	Homo sapiens	77-82
21072201-5	2010	Among 11 candidate genes, multivariate logistic analyses showed that SNPs of CEP68 gene showed the most significant association with aspirin intolerance (P values of co-dominant for CEP68, 6.0x10(-5) to 4.0x10(-5)).	Aspirin	133-140	centrosomal protein 68	Homo sapiens	182-187
21072201-7	2010	Moreover, the nonsynonymous CEP68 rs7572857G&gt;A variant that replaces glycine with serine showed a higher decline of forced expiratory volume in 1s (FEV(1)) by aspirin provocation than other variants (P = 3.0x10(-5)).	Aspirin	162-169	centrosomal protein 68	Homo sapiens	28-33
21072201-8	2010	Our findings imply that CEP68 could be a susceptible gene for aspirin intolerance in asthmatics, suggesting that the nonsynonymous Gly74Ser could affect the polarity of the protein structure.	Aspirin	62-69	centrosomal protein 68	Homo sapiens	24-29
20709806-8	2010	Importantly, receptors for aspirin-triggered lipoxin and resolvin E1 (ALX and ChemR23, respectively) were identified in human VSMCs.	Aspirin	27-34	chemerin chemokine-like receptor 1	Homo sapiens	78-85
20728206-8	2010	After 6 months of aspirin treatment, sputum IL-4 (P = .0007) and matrix metalloproteinase 9 (MMP-9; P = .05) decreased significantly compared with baseline.	Aspirin	18-25	matrix metallopeptidase 9	Homo sapiens	65-91
20728206-8	2010	After 6 months of aspirin treatment, sputum IL-4 (P = .0007) and matrix metalloproteinase 9 (MMP-9; P = .05) decreased significantly compared with baseline.	Aspirin	18-25	matrix metallopeptidase 9	Homo sapiens	93-98
20728206-13	2010	In contrast, long-term treatment with aspirin involves suppression of IL-4 as well as downregulation of proinflammatory MMP-9 while T(H)1 marker FLT3-L increases.	Aspirin	38-45	matrix metallopeptidase 9	Homo sapiens	120-125
20862244-7	2010	Finally, connectivity map analysis for AnxA1 and peptide Ac2-26 indicated striking similarities with known anti-inflammatory therapeutics, glucocorticoids and aspirin-like compounds, as well as with histone deacetylase inhibitors.	Aspirin	159-166	annexin A1	Homo sapiens	39-44
20647328-10	2010	Collectively, these results identify a novel GLI1-to-CDK2 pathway in esophageal carcinogenesis, which is a bona fide target for effective combinatorial chemoprevention with Urso and Aspirin.	Aspirin	182-189	GLI family zinc finger 1	Homo sapiens	45-49
20823666-8	2010	Either SZ-21 or aspirin can inhibit the ADP-induced expression of P-selectin and GPIIb/IIIa.	Aspirin	16-23	integrin subunit alpha 2b	Homo sapiens	81-86
20471983-7	2010	Prestin STAS significantly deviates from the related bacterial ASA proteins, especially in the N-terminal region, which-although previously considered merely as a generic linker between the domain and the last transmembrane helix-is indeed fully part of the domain.	Aspirin	63-66	solute carrier family 26 member 5	Homo sapiens	0-7
20153751-0	2010	The antinociceptive effect of acetylsalicylic acid is differently affected by a CB1 agonist or antagonist and involves the serotonergic system in rats.	Aspirin	30-50	cannabinoid receptor 1	Rattus norvegicus	80-83
20005558-2	2010	Aspirin was given to homozygous, apoE(-/-) and LDLR(-/-) double deficient mice for 12 weeks.	Aspirin	0-7	low density lipoprotein receptor	Mus musculus	47-51
20005558-15	2010	CONCLUSION: Our results suggest that endothelial dysfunction with low dose aspirin improved, reduced progression of atherosclerosis in apoE(-/-) and LDLR(-/-) double deficient mice and provides a pathophysiological basis for the beneficial effects of aspirin in atherosclerosis, and low doses appeared to be more efficient than high doses.	Aspirin	75-82	low density lipoprotein receptor	Mus musculus	149-153
20026598-6	2010	Interestingly, the administration of aspirin (an inhibitor of Tsp-1) to the pregnant heterozygote mothers led to a reduction in Tsp-1 levels and a substantial rescue of the embryonic lethality.	Aspirin	37-44	thrombospondin 1	Mus musculus	62-67
20026598-6	2010	Interestingly, the administration of aspirin (an inhibitor of Tsp-1) to the pregnant heterozygote mothers led to a reduction in Tsp-1 levels and a substantial rescue of the embryonic lethality.	Aspirin	37-44	thrombospondin 1	Mus musculus	128-133
20065114-0	2010	NCX 4040, a nitric oxide-donating aspirin, exerts anti-inflammatory effects through inhibition of I kappa B-alpha degradation in human monocytes.	Aspirin	34-41	T cell leukemia homeobox 2	Homo sapiens	0-3
20407607-0	2010	Attenuation of diabetic retinopathy by enhanced inhibition of MMP-2 and MMP-9 using aspirin and minocycline in streptozotocin-diabetic rats.	Aspirin	84-91	matrix metallopeptidase 9	Rattus norvegicus	72-77
20407607-2	2010	We hypothesized that minocycline induced MMP-2 and MMP-9 inhibition can be enhanced by aspirin, a non-selective COX and tPA inhibitor and this combination can reduce progression of diabetic retinopathy.	Aspirin	87-94	matrix metallopeptidase 9	Rattus norvegicus	51-56
20036315-2	2010	Aspirin, a non-selective COX inhibitor, acetylates COX-2 with generation of a lipoxygenase (LOX) substrate, whose end product is the 15-epi-lipoxin A(4) (15-epi-LXA(4)), an aspirin-triggered lipoxin.	Aspirin	0-7	cytochrome c oxidase subunit 4I1	Mus musculus	25-28
20137092-4	2010	Our results showed that ASA inhibited MMP-9 mRNA expression, and caused the decrease in the MMP-9 activities from the cell culture supernatants.	Aspirin	24-27	matrix metallopeptidase 9	Homo sapiens	38-43
20137092-4	2010	Our results showed that ASA inhibited MMP-9 mRNA expression, and caused the decrease in the MMP-9 activities from the cell culture supernatants.	Aspirin	24-27	matrix metallopeptidase 9	Homo sapiens	92-97
20137092-6	2010	On the contrary, acetyl salicylic acid induced the expressions of ABCA1 and SR-BI, two molecules known to reduce the progression of atherosclerosis, at both mRNA and protein levels.	Aspirin	17-38	ATP binding cassette subfamily A member 1	Homo sapiens	66-71
20137092-6	2010	On the contrary, acetyl salicylic acid induced the expressions of ABCA1 and SR-BI, two molecules known to reduce the progression of atherosclerosis, at both mRNA and protein levels.	Aspirin	17-38	scavenger receptor class B member 1	Homo sapiens	76-81
20137092-8	2010	These data suggest that acetyl salicylic acid may alleviate symptoms of atherosclerosis by two potential mechanisms: maintaining the plaque stability via inhibiting activities of inflammatory molecules MMP-9 and NF-kappaB, and increasing the cholesterol efflux through inducing expressions of ABCA1 and SR-BI.	Aspirin	24-45	matrix metallopeptidase 9	Homo sapiens	202-207
20137092-8	2010	These data suggest that acetyl salicylic acid may alleviate symptoms of atherosclerosis by two potential mechanisms: maintaining the plaque stability via inhibiting activities of inflammatory molecules MMP-9 and NF-kappaB, and increasing the cholesterol efflux through inducing expressions of ABCA1 and SR-BI.	Aspirin	24-45	ATP binding cassette subfamily A member 1	Homo sapiens	293-298
20137092-8	2010	These data suggest that acetyl salicylic acid may alleviate symptoms of atherosclerosis by two potential mechanisms: maintaining the plaque stability via inhibiting activities of inflammatory molecules MMP-9 and NF-kappaB, and increasing the cholesterol efflux through inducing expressions of ABCA1 and SR-BI.	Aspirin	24-45	scavenger receptor class B member 1	Homo sapiens	303-308
19880272-0	2010	Aspirin inhibits MMP-9 mRNA expression and release via the PPARalpha/gamma and COX-2/mPGES-1-mediated pathways in macrophages derived from THP-1 cells.	Aspirin	0-7	matrix metallopeptidase 9	Homo sapiens	17-22
19880272-1	2010	In present study, we investigated the effects of aspirin on matrix metalloproteinase (MMP)-9 mRNA expression and release and its possible mechanisms in macrophages derived from THP-1 cells.	Aspirin	49-56	matrix metallopeptidase 9	Homo sapiens	60-92
19880272-3	2010	The results indicated that after the macrophages were incubated with aspirin for 24h, the MMP-9 mRNA expression and release were decreased, while the PPAR alpha/gamma mRNA and protein expression was increased, respectively, and PPAR alpha/gamma agonists could also decrease MMP-9 mRNA expression and release.	Aspirin	69-76	matrix metallopeptidase 9	Homo sapiens	90-95
19880272-3	2010	The results indicated that after the macrophages were incubated with aspirin for 24h, the MMP-9 mRNA expression and release were decreased, while the PPAR alpha/gamma mRNA and protein expression was increased, respectively, and PPAR alpha/gamma agonists could also decrease MMP-9 mRNA expression and release.	Aspirin	69-76	matrix metallopeptidase 9	Homo sapiens	274-279
19880272-7	2010	It might be concluded that aspirin could inhibit the MMP-9 gene expression and release through the PPARalpha/gamma and COX-2/mPGES-1-mediated pathways and the two pathways might be partly overlapped and even be interrelated.	Aspirin	27-34	matrix metallopeptidase 9	Homo sapiens	53-58
20523081-8	2010	Individual TSPO density values correlated significantly and negatively with both SCI-SAS-A and ASA-27 total scores.	Aspirin	95-98	translocator protein	Homo sapiens	11-15
21088444-7	2010	In cells transfected with a specific peroxisome proliferator-activated receptor (PPAR)-alpha small interfering RNA, the induction of ABCA1 expression and apoA-I-mediated 3H-cholesterol efflux by aspirin were substantially suppressed.	Aspirin	195-202	ATP-binding cassette, sub-family A (ABC1), member 1	Mus musculus	133-138
21088444-7	2010	In cells transfected with a specific peroxisome proliferator-activated receptor (PPAR)-alpha small interfering RNA, the induction of ABCA1 expression and apoA-I-mediated 3H-cholesterol efflux by aspirin were substantially suppressed.	Aspirin	195-202	apolipoprotein A-I	Mus musculus	154-160
21088444-8	2010	CONCLUSIONS: The data demonstrate that low-dose aspirin increases ABCA1 expression via a PPAR-alpha-dependent mechanism and increases apoA-I-mediated cholesterol efflux.	Aspirin	48-55	ATP-binding cassette, sub-family A (ABC1), member 1	Mus musculus	66-71
21088444-8	2010	CONCLUSIONS: The data demonstrate that low-dose aspirin increases ABCA1 expression via a PPAR-alpha-dependent mechanism and increases apoA-I-mediated cholesterol efflux.	Aspirin	48-55	apolipoprotein A-I	Mus musculus	134-140
20062920-8	2010	The protein expression of the chloride intracellular channel isotype 1 was increased in ASA-resistant platelets (21.3 + or - 3.8 vs. 48.8 + or - 6.0, CI 29.5 to 45.95, p=0.03) while the expression of two HSP60 and two HSP71 isotypes was decreased.	Aspirin	88-91	heat shock protein family D (Hsp60) member 1	Homo sapiens	204-209
20062920-8	2010	The protein expression of the chloride intracellular channel isotype 1 was increased in ASA-resistant platelets (21.3 + or - 3.8 vs. 48.8 + or - 6.0, CI 29.5 to 45.95, p=0.03) while the expression of two HSP60 and two HSP71 isotypes was decreased.	Aspirin	88-91	heat shock protein family A (Hsp70) member 8	Homo sapiens	218-223
19462226-0	2009	Aspirin inhibits MMP-2 and MMP-9 expression and activity through PPARalpha/gamma and TIMP-1-mediated mechanisms in cultured mouse celiac macrophages.	Aspirin	0-7	matrix metallopeptidase 2	Mus musculus	17-22
19462226-3	2009	The purpose of present study was to investigate the inhibitory effects of aspirin on MMP-2 and MMP-9 expression and activity in cultured mouse celiac macrophages, and to determine the possible mechanisms.	Aspirin	74-81	matrix metallopeptidase 2	Mus musculus	85-90
19462226-4	2009	The results showed that MMP-2/9 mRNA expression and release were significantly decreased after cultured mouse celiac macrophages were treated with aspirin 12.5-50 microg/ml for 24 h, while the TIMP-1 mRNA expression and release, and peroxisome proliferator-activated receptor (PPAR) alpha/gamma mRNA expression were increased after the same treatment.	Aspirin	147-154	matrix metallopeptidase 2	Mus musculus	24-31
19462226-5	2009	Moreover the aspirin-induced down-regulation of MMP-2/9 mRNA expression and reduction of MMP-9 release were notably alleviated after pretreatment with specific inhibitors of PPARalpha/gamma.	Aspirin	13-20	matrix metallopeptidase 2	Mus musculus	48-55
19462226-6	2009	These results suggested that aspirin could inhibit the expression and release of MMP-2/9 by up-regulation of PPARalpha/gamma gene expression, and also inhibit the activity of MMP-2/9 by induction of TIMP-1 expression, which might be good for the stabilization of atherosclerotic plaques and the prevention of cardio-cerebrovascular events.	Aspirin	29-36	matrix metallopeptidase 2	Mus musculus	81-86
19462226-6	2009	These results suggested that aspirin could inhibit the expression and release of MMP-2/9 by up-regulation of PPARalpha/gamma gene expression, and also inhibit the activity of MMP-2/9 by induction of TIMP-1 expression, which might be good for the stabilization of atherosclerotic plaques and the prevention of cardio-cerebrovascular events.	Aspirin	29-36	matrix metallopeptidase 2	Mus musculus	175-180
18846318-0	2009	The role of leucocytes in the acetyl salicylic acid (aspirin) induced nitric oxide synthesis in the production of interferon-alpha, a potent inhibitor of platelet aggregation and a thrombolytic agent.	Aspirin	30-51	interferon alpha	Mus musculus	114-130
18846318-0	2009	The role of leucocytes in the acetyl salicylic acid (aspirin) induced nitric oxide synthesis in the production of interferon-alpha, a potent inhibitor of platelet aggregation and a thrombolytic agent.	Aspirin	53-60	interferon alpha	Mus musculus	114-130
18846318-1	2009	The role of aspirin-induced NO synthesis in the production of interferon-alpha (IFN-alpha) in leucocytes and the effect of IFN-alpha on platelet aggregation was studied.	Aspirin	12-19	interferon alpha	Mus musculus	62-78
18846318-1	2009	The role of aspirin-induced NO synthesis in the production of interferon-alpha (IFN-alpha) in leucocytes and the effect of IFN-alpha on platelet aggregation was studied.	Aspirin	12-19	interferon alpha	Mus musculus	80-89
18846318-2	2009	Treatment of Platelet Rich Plasma (PRP) with the dialyzed supernatant from the leucocyte suspension incubated with 80 microM aspirin resulted in parallel syntheses of NO and IFN-alpha as determined by methemoglobin assay and enzyme linked immunosorbent assay respectively.	Aspirin	125-132	interferon alpha	Mus musculus	174-183
19573120-2	2009	Anti-inflammatory interventions such as aspirin and statins (anti-IFRx) might be a novel approach to the treatment of obesity and Type 2 diabetes mellitus (T2DM).	Aspirin	40-47	mohawk homeobox	Homo sapiens	66-70
19034473-8	2009	ECP levels in nasal secretions were higher in patients with asthma or aspirin intolerance than in patients without asthma or aspirin intolerance, while no significant differences were found between allergic and non-allergic patients.	Aspirin	70-77	ribonuclease A family member 3	Homo sapiens	0-3
19034473-8	2009	ECP levels in nasal secretions were higher in patients with asthma or aspirin intolerance than in patients without asthma or aspirin intolerance, while no significant differences were found between allergic and non-allergic patients.	Aspirin	125-132	ribonuclease A family member 3	Homo sapiens	0-3
19034473-13	2009	The results of this study provide evidence that ECP levels in nasal secretions of patients with NP correlate with the presence of asthma or aspirin intolerance and severity of NP determined by CT scores.	Aspirin	140-147	ribonuclease A family member 3	Homo sapiens	48-51
19376786-9	2009	CONCLUSION: In this large cohort, multicentre STEMI registry in-cath-lab use of GP IIb/IIIa inhibitors and clopidogrel alone or in combination was associated with the reduction of 1 year all-cause mortality in the setting of primary PCI in comparison with aspirin only.	Aspirin	256-263	integrin subunit alpha 2b	Homo sapiens	80-86
19429918-0	2009	Genetic variation of CYP2C19 affects both pharmacokinetic and pharmacodynamic responses to clopidogrel but not prasugrel in aspirin-treated patients with coronary artery disease.	Aspirin	124-131	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
19297212-10	2009	Aspirin and placebo treatment were associated with elevated P-selectin expression, platelet-monocyte aggregation and reduced CD42b expression (p&lt;0.05, Wilcoxon signed-rank test) post-exercise.	Aspirin	0-7	glycoprotein Ib platelet subunit alpha	Homo sapiens	125-130
19250145-0	2009	Variable number of tandem repeats polymorphism of platelet glycoprotein Ib alpha in Chinese people and CC genotype with aspirin sensitivity in patients with cerebral infarction.	Aspirin	120-127	glycoprotein Ib platelet subunit alpha	Homo sapiens	59-80
19250145-1	2009	BACKGROUND AND OBJECTIVE: To study the prevalence of variable number of tandem repeats (VNTR) polymorphism in platelet membrane glycoprotein (GP) Ib alpha in a Chinese Han population and to determine the relationship between VNTR polymorphisms and aspirin resistance.	Aspirin	248-255	glycoprotein Ib platelet subunit alpha	Homo sapiens	142-154
19250145-9	2009	The CC genotype of the VTNR polymorphism in GPIb appears to be more sensitive to the inhibitory action of low-dose aspirin.	Aspirin	115-122	integrin subunit alpha V	Homo sapiens	23-27
18946735-4	2009	The reduction of dopamine transporter (DAT)-positive signals and PPAR gamma expression, and accumulation of activated microglial cells were significantly and dose-dependently attenuated by four injections of a nonsteroidal anti-inflammatory drug and a PPAR gamma ligand, ibuprofen (10 or 20 mg/kg x 4, s.c.) given 30 min prior to each METH injection, but not by either a low or high dose of aspirin.	Aspirin	391-398	solute carrier family 6 member 3	Homo sapiens	17-37
18946735-4	2009	The reduction of dopamine transporter (DAT)-positive signals and PPAR gamma expression, and accumulation of activated microglial cells were significantly and dose-dependently attenuated by four injections of a nonsteroidal anti-inflammatory drug and a PPAR gamma ligand, ibuprofen (10 or 20 mg/kg x 4, s.c.) given 30 min prior to each METH injection, but not by either a low or high dose of aspirin.	Aspirin	391-398	solute carrier family 6 member 3	Homo sapiens	39-42
19146957-0	2009	The significantly enhanced frequency of functional CD4+CD25+Foxp3+ T regulatory cells in therapeutic dose aspirin-treated mice.	Aspirin	106-113	CD4 antigen	Mus musculus	51-54
19146957-0	2009	The significantly enhanced frequency of functional CD4+CD25+Foxp3+ T regulatory cells in therapeutic dose aspirin-treated mice.	Aspirin	106-113	interleukin 2 receptor, alpha chain	Mus musculus	55-59
19146957-3	2009	However, the effect of ASA on CD4(+)CD25(+)Foxp3(+) Treg cells has yet to be determined.	Aspirin	23-26	interleukin 2 receptor, alpha chain	Mus musculus	36-40
19146957-4	2009	The frequency, phenotype and immunosuppressive function of CD4(+)CD25(+)Foxp3(+) Treg cells were detected in BALB/c mice treated with low or high doses of ASA for 4 weeks.	Aspirin	155-158	CD4 antigen	Mus musculus	59-62
19146957-4	2009	The frequency, phenotype and immunosuppressive function of CD4(+)CD25(+)Foxp3(+) Treg cells were detected in BALB/c mice treated with low or high doses of ASA for 4 weeks.	Aspirin	155-158	interleukin 2 receptor, alpha chain	Mus musculus	65-69
19146957-5	2009	ASA significantly decreased the percentage and number of CD4(+) T cells in the periphery, while ASA remarkably increased the percentage of CD4(+)CD25(+)Foxp3(+) Treg cells in CD4(+)T cells.	Aspirin	0-3	CD4 antigen	Mus musculus	57-60
19146957-5	2009	ASA significantly decreased the percentage and number of CD4(+) T cells in the periphery, while ASA remarkably increased the percentage of CD4(+)CD25(+)Foxp3(+) Treg cells in CD4(+)T cells.	Aspirin	96-99	CD4 antigen	Mus musculus	139-142
19146957-5	2009	ASA significantly decreased the percentage and number of CD4(+) T cells in the periphery, while ASA remarkably increased the percentage of CD4(+)CD25(+)Foxp3(+) Treg cells in CD4(+)T cells.	Aspirin	96-99	interleukin 2 receptor, alpha chain	Mus musculus	145-149
19146957-5	2009	ASA significantly decreased the percentage and number of CD4(+) T cells in the periphery, while ASA remarkably increased the percentage of CD4(+)CD25(+)Foxp3(+) Treg cells in CD4(+)T cells.	Aspirin	96-99	CD4 antigen	Mus musculus	139-142
19146957-6	2009	The total cell numbers of thymocytes were significantly decreased in ASA-treated mice, but the number of CD4(+) CD25(+)Fxop3(+) cells and its ratio in CD4(+)CD8(-) thymocytes were markedly enhanced in the thymi of ASA-treated mice.	Aspirin	214-217	CD4 antigen	Mus musculus	105-108
19146957-6	2009	The total cell numbers of thymocytes were significantly decreased in ASA-treated mice, but the number of CD4(+) CD25(+)Fxop3(+) cells and its ratio in CD4(+)CD8(-) thymocytes were markedly enhanced in the thymi of ASA-treated mice.	Aspirin	214-217	interleukin 2 receptor, alpha chain	Mus musculus	112-116
19067400-7	2009	Maternal cigarette smoking and aspirin use each increased the risk of AB-L, but not TLD; while decongestants and possibly antihypertensive medications increased the risk of TLD, but not AB-L.	Aspirin	31-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-74
19260323-8	2008	CONCLUSION: Patients with ACI cotreated with puerarin and aspirin improved the neurological function, decreased the levels of serum vWF and sTM, indicating puerarin with aspirin had the protective effects on the damaged vascular endothelial cells.	Aspirin	170-177	sulfotransferase family 1A member 3	Homo sapiens	140-143
18855583-12	2008	and aspirin induce brain-derived neurotrophic factor (BDNF) protein expression and this protein has a crucial role in neuronal survival.	Aspirin	4-11	brain derived neurotrophic factor	Homo sapiens	19-52
18855583-12	2008	and aspirin induce brain-derived neurotrophic factor (BDNF) protein expression and this protein has a crucial role in neuronal survival.	Aspirin	4-11	brain derived neurotrophic factor	Homo sapiens	54-58
18519978-0	2008	Induction of paraoxonase 1 and apolipoprotein A-I gene expression by aspirin.	Aspirin	69-76	apolipoprotein A-I	Mus musculus	31-49
18519978-3	2008	To determine the mechanisms by which aspirin might inhibit atherosclerosis, we incubated HEPG2 cells and rat primary hepatocytes with aspirin or salicylic acid and noted an increase in paraoxonase 1(PON1) activity in the medium, together with an induction of PON1 and apolipoprotein A-I (apoA-I) gene expression.	Aspirin	37-44	paraoxonase 1	Rattus norvegicus	185-198
18519978-3	2008	To determine the mechanisms by which aspirin might inhibit atherosclerosis, we incubated HEPG2 cells and rat primary hepatocytes with aspirin or salicylic acid and noted an increase in paraoxonase 1(PON1) activity in the medium, together with an induction of PON1 and apolipoprotein A-I (apoA-I) gene expression.	Aspirin	37-44	paraoxonase 1	Rattus norvegicus	199-203
18519978-3	2008	To determine the mechanisms by which aspirin might inhibit atherosclerosis, we incubated HEPG2 cells and rat primary hepatocytes with aspirin or salicylic acid and noted an increase in paraoxonase 1(PON1) activity in the medium, together with an induction of PON1 and apolipoprotein A-I (apoA-I) gene expression.	Aspirin	134-141	paraoxonase 1	Rattus norvegicus	185-198
18519978-4	2008	Mice treated with aspirin also showed a 2-fold increase in plasma PON1 activity and a significant induction of both PON1 and apoA-I gene expression in the liver.	Aspirin	18-25	apolipoprotein A-I	Mus musculus	125-131
18411340-5	2008	In this study, we show that LX and aspirin (ASA)-triggered LX (ATL) inhibit innate immune signaling by inducing suppressor of cytokine signaling (SOCS) 2-dependent ubiquitinylation and proteasome-mediated degradation of TNF receptor-associated factor (TRAF) 2 and TRAF6, which are adaptor molecules that couple TNF and interleukin-1 receptor/Toll-like receptor family members to intracellular signaling events.	Aspirin	35-42	suppressor of cytokine signaling 2	Homo sapiens	112-153
18411340-5	2008	In this study, we show that LX and aspirin (ASA)-triggered LX (ATL) inhibit innate immune signaling by inducing suppressor of cytokine signaling (SOCS) 2-dependent ubiquitinylation and proteasome-mediated degradation of TNF receptor-associated factor (TRAF) 2 and TRAF6, which are adaptor molecules that couple TNF and interleukin-1 receptor/Toll-like receptor family members to intracellular signaling events.	Aspirin	35-42	TNF receptor associated factor 2	Homo sapiens	220-259
18411340-5	2008	In this study, we show that LX and aspirin (ASA)-triggered LX (ATL) inhibit innate immune signaling by inducing suppressor of cytokine signaling (SOCS) 2-dependent ubiquitinylation and proteasome-mediated degradation of TNF receptor-associated factor (TRAF) 2 and TRAF6, which are adaptor molecules that couple TNF and interleukin-1 receptor/Toll-like receptor family members to intracellular signaling events.	Aspirin	44-47	suppressor of cytokine signaling 2	Homo sapiens	112-153
18411340-5	2008	In this study, we show that LX and aspirin (ASA)-triggered LX (ATL) inhibit innate immune signaling by inducing suppressor of cytokine signaling (SOCS) 2-dependent ubiquitinylation and proteasome-mediated degradation of TNF receptor-associated factor (TRAF) 2 and TRAF6, which are adaptor molecules that couple TNF and interleukin-1 receptor/Toll-like receptor family members to intracellular signaling events.	Aspirin	44-47	TNF receptor associated factor 2	Homo sapiens	220-259
18393288-4	2008	We incubated Huh7 replicon cells with 2-8 mM ASA for different times and measured HCV-RNA and protein levels by northern blot, real-time polymerase chain reaction, and western analysis, respectively.	Aspirin	45-48	MIR7-3 host gene	Homo sapiens	13-17
18393288-10	2008	Taken together, our findings suggest that the anti-HCV effect of ASA in the Huh7 replicon cells is due to its inhibitory effect on COX-2 expression, which is mediated in part by the activation of MEK1/2/p38 MAPK.	Aspirin	65-68	MIR7-3 host gene	Homo sapiens	76-80
18054208-9	2008	Individual TSPO density values were significantly and negatively correlated with both SCI-SAS-A and ASA-27 total scores, but not with HAM-D total score or HAM-D anxiety/somatization factor score.	Aspirin	100-103	translocator protein	Homo sapiens	11-15
18222077-3	2008	There was no effect on liver mRNA-PPARalpha, while mRNA-PPARgamma was down-regulated, probably as a result of enzymatic inhibition of cyclooxygenases (COXs) by aspirin which has been shown to decrease the levels of PGJ2 and its metabolites, known as strong endogenous ligands for PPARgamma.	Aspirin	160-167	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	56-65
18313079-9	2008	At 5 weeks after salt loading, macrophage accumulation and matrix metalloproteinase-9 activity at the stroke-negative area in cerebral cortex of SHRSP were significantly reduced by treatment with aspirin.	Aspirin	196-203	matrix metallopeptidase 9	Rattus norvegicus	59-85
18209566-5	2008	The results showed that aspirin significantly suppressed COX-2 and ICAM-1 expression induced by ox-LDL and also inhibited IkappaB phosphorylation in human umbilical vein endothelial cells (HUVECs).	Aspirin	24-31	intercellular adhesion molecule 1	Homo sapiens	67-73
18159608-0	2007	Association of beta 2-adrenergic receptor polymorphism with the phenotype of aspirin-intolerant acute urticaria.	Aspirin	77-84	adrenoceptor beta 2	Homo sapiens	15-41
17555340-0	2007	Relationship between vitamin D binding protein and aspirin resistance in coronary ischemic patients: a proteomic study.	Aspirin	51-58	GC vitamin D binding protein	Homo sapiens	21-46
17555340-5	2007	Three vitamin D binding protein isotypes were increased in ASA-resistant patients.	Aspirin	59-62	GC vitamin D binding protein	Homo sapiens	6-31
17555340-6	2007	In vitro incubation of vitamin D binding protein (DBP) with blood from healthy volunteers reduced the inhibitory effect of ASA on thromboxane A2 production.	Aspirin	123-126	GC vitamin D binding protein	Homo sapiens	23-48
17336029-4	2007	Aspirin co-treatment suppressed effectively the genotoxicity of MMC in a dose-dependent manner and the sex ratio at a dose of aspirin 10mg/bottle elevated from 0.01 (without aspirin) to 0.65 at sc z(1) w(+(TE)) mei-9(a) mei-41(D5)/-C(1)DX, y f [mei-9 mei-41, Rec(-) male.Rec(+) female] consists of DNA repair-deficient (Rec(-)) males and -proficient (Rec(+)) females.	Aspirin	0-7	recombination-defective	Drosophila melanogaster	259-262
17336029-4	2007	Aspirin co-treatment suppressed effectively the genotoxicity of MMC in a dose-dependent manner and the sex ratio at a dose of aspirin 10mg/bottle elevated from 0.01 (without aspirin) to 0.65 at sc z(1) w(+(TE)) mei-9(a) mei-41(D5)/-C(1)DX, y f [mei-9 mei-41, Rec(-) male.Rec(+) female] consists of DNA repair-deficient (Rec(-)) males and -proficient (Rec(+)) females.	Aspirin	0-7	recombination-defective	Drosophila melanogaster	271-274
17336029-4	2007	Aspirin co-treatment suppressed effectively the genotoxicity of MMC in a dose-dependent manner and the sex ratio at a dose of aspirin 10mg/bottle elevated from 0.01 (without aspirin) to 0.65 at sc z(1) w(+(TE)) mei-9(a) mei-41(D5)/-C(1)DX, y f [mei-9 mei-41, Rec(-) male.Rec(+) female] consists of DNA repair-deficient (Rec(-)) males and -proficient (Rec(+)) females.	Aspirin	0-7	recombination-defective	Drosophila melanogaster	271-274
17336029-4	2007	Aspirin co-treatment suppressed effectively the genotoxicity of MMC in a dose-dependent manner and the sex ratio at a dose of aspirin 10mg/bottle elevated from 0.01 (without aspirin) to 0.65 at sc z(1) w(+(TE)) mei-9(a) mei-41(D5)/-C(1)DX, y f [mei-9 mei-41, Rec(-) male.Rec(+) female] consists of DNA repair-deficient (Rec(-)) males and -proficient (Rec(+)) females.	Aspirin	0-7	recombination-defective	Drosophila melanogaster	271-274
17336029-4	2007	Aspirin co-treatment suppressed effectively the genotoxicity of MMC in a dose-dependent manner and the sex ratio at a dose of aspirin 10mg/bottle elevated from 0.01 (without aspirin) to 0.65 at sc z(1) w(+(TE)) mei-9(a) mei-41(D5)/-C(1)DX, y f [mei-9 mei-41, Rec(-) male.Rec(+) female] consists of DNA repair-deficient (Rec(-)) males and -proficient (Rec(+)) females.	Aspirin	126-133	recombination-defective	Drosophila melanogaster	259-262
17336029-4	2007	Aspirin co-treatment suppressed effectively the genotoxicity of MMC in a dose-dependent manner and the sex ratio at a dose of aspirin 10mg/bottle elevated from 0.01 (without aspirin) to 0.65 at sc z(1) w(+(TE)) mei-9(a) mei-41(D5)/-C(1)DX, y f [mei-9 mei-41, Rec(-) male.Rec(+) female] consists of DNA repair-deficient (Rec(-)) males and -proficient (Rec(+)) females.	Aspirin	126-133	recombination-defective	Drosophila melanogaster	271-274
17336029-4	2007	Aspirin co-treatment suppressed effectively the genotoxicity of MMC in a dose-dependent manner and the sex ratio at a dose of aspirin 10mg/bottle elevated from 0.01 (without aspirin) to 0.65 at sc z(1) w(+(TE)) mei-9(a) mei-41(D5)/-C(1)DX, y f [mei-9 mei-41, Rec(-) male.Rec(+) female] consists of DNA repair-deficient (Rec(-)) males and -proficient (Rec(+)) females.	Aspirin	126-133	recombination-defective	Drosophila melanogaster	271-274
17336029-4	2007	Aspirin co-treatment suppressed effectively the genotoxicity of MMC in a dose-dependent manner and the sex ratio at a dose of aspirin 10mg/bottle elevated from 0.01 (without aspirin) to 0.65 at sc z(1) w(+(TE)) mei-9(a) mei-41(D5)/-C(1)DX, y f [mei-9 mei-41, Rec(-) male.Rec(+) female] consists of DNA repair-deficient (Rec(-)) males and -proficient (Rec(+)) females.	Aspirin	126-133	recombination-defective	Drosophila melanogaster	271-274
17336029-5	2007	The antigenotoxic effect of aspirin on [mei-41, Rec(-) male.Rec(+) female] was similar to that on [mei-9, Rec(-) male.Rec(+) female].	Aspirin	28-35	recombination-defective	Drosophila melanogaster	48-51
17545608-8	2007	More interestingly, aspirin, a nonsteroidal anti-inflammatory drug that preferentially inhibits COX-1, compromises PPARdelta function and cell growth by inhibiting extracellular signal-regulated kinases 1/2, members of the mitogen-activated protein kinase family.	Aspirin	20-27	peroxisome proliferator activated receptor delta	Homo sapiens	115-124
17106444-0	2007	Marked prevention of ischemic brain injury by Neu2000, an NMDA antagonist and antioxidant derived from aspirin and sulfasalazine.	Aspirin	103-110	neuralized E3 ubiquitin protein ligase 1	Homo sapiens	46-49
17580012-7	2007	CONCLUSIONS: Use of GPIIb/IIIa inhibitors reduces the risk of adverse cardiac events in NSTEACS patients pre-treated with aspirin and thienopyridines but increases the risk of severe bleeding and thrombocytopenia.	Aspirin	122-129	integrin subunit alpha 2b	Homo sapiens	20-25
17589617-5	2007	Consequently, the use of the thrombolytic recombinant tissue-plasminogen activator (rTPA) associated with aspirin was the treatment of choice, and complete dissolution of the thrombus was achieved without adverse effects.	Aspirin	106-113	chromosome 20 open reading frame 181	Homo sapiens	54-82
2968288-0	1988	Inhibition by corticosteroids of epidermal growth factor-induced recovery of cyclooxygenase after aspirin inactivation.	Aspirin	98-105	epidermal growth factor	Homo sapiens	33-56
2891837-0	1987	Prevention of aspirin-induced gastric mucosal injury by histamine H2 receptor antagonists: a crossover endoscopic and intragastric pH study in the dog.	Aspirin	14-21	histamine receptor H2	Canis lupus familiaris	56-77
3320388-1	1987	Because prosthetic neointima produces much less prostacyclin (PGI2) than arterial intima and may be more susceptible to cyclooxygenase inhibition, aspirin treatment might enhance surface thrombogenesis.	Aspirin	147-154	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	120-134
3111273-7	1987	Both aspirin and 3.4 M NaCl induced ODC activity 6 h later.	Aspirin	5-12	ornithine decarboxylase 1	Rattus norvegicus	36-39
3090104-5	1986	Production of 12-hydroxyeicosatetraenoic acid (12-HETE) was demonstrated biochemically in aspirin-treated platelet/arachidonate/mononuclear cell preparations that generated high levels of TFa.	Aspirin	90-97	coagulation factor III, tissue factor	Homo sapiens	188-191
3295745-7	1986	LIF production of lymphocytes was inhibited by INDO, ASA, PhB, CHINOIN 127 and CHINOIN 105.	Aspirin	53-56	LIF interleukin 6 family cytokine	Homo sapiens	0-3
3751624-1	1986	Aspirin and indomethacin decreased the hydrolysis of microsomal phospholipids by exogenous soluble phospholipase A2 and increased lipid peroxidation in rat liver microsomes.	Aspirin	0-7	phospholipase A2 group IB	Rattus norvegicus	99-115
2414631-0	1985	Acetylsalicylic acid, paracetamol and morphine inhibit behavioral responses to intrathecally administered substance P or capsaicin.	Aspirin	0-20	tachykinin 1	Mus musculus	106-117
2968288-3	1988	Aspirin-treated cells recovered within 2 h by a process that was blocked by cycloheximide but not by actinomycin D, and that required a serum component identified as epidermal growth factor (EGF).	Aspirin	0-7	epidermal growth factor	Homo sapiens	166-189
2968288-3	1988	Aspirin-treated cells recovered within 2 h by a process that was blocked by cycloheximide but not by actinomycin D, and that required a serum component identified as epidermal growth factor (EGF).	Aspirin	0-7	epidermal growth factor	Homo sapiens	191-194
2968288-9	1988	The results suggest that cyclooxygenase recovery in aspirin-inactivated vascular smooth muscle cells is mediated by an EGF-dependent translational control that is inhibited by corticosteroids.	Aspirin	52-59	epidermal growth factor	Homo sapiens	119-122
3335267-1	1988	A prospective study was conducted with a man displaying 57.5 +/- 13.4% tail tip-directed ASAs to relate results of in vitro tests with attempts to conceive.	Aspirin	89-93	TOR signaling pathway regulator	Homo sapiens	76-79
2891837-8	1987	These results indicate that acid inhibition is an important component of the mechanisms whereby histamine H2 receptor antagonists protect the gastric mucosa from aspirin-induced damage in the dog.	Aspirin	162-169	histamine receptor H2	Canis lupus familiaris	96-117
3677282-1	1987	The in vitro effect of procainamide on plasma cholinesterase (PCHE) activity in the plasma of ten normal ASA physical status I patients was studied using a kinetic method.	Aspirin	105-108	butyrylcholinesterase	Homo sapiens	46-60
2961218-4	1987	At low PAF concentrations aggregation and BTG release were blocked by apyrase (a scavenger of ADP), by ASA (an inhibitor of cyclooxygenase) and by BM 13177 (a thromboxane receptor antagonist).	Aspirin	103-106	PCNA clamp associated factor	Homo sapiens	7-10
2961218-5	1987	Higher concentrations of PAF overcame the effect of apyrase, but only induced reversible aggregation and minor release in the presence of ASA or BM 13177.	Aspirin	138-141	PCNA clamp associated factor	Homo sapiens	25-28
3477825-8	1987	In addition, the positive uterine inotropism evoked by histamine in the ME region of preparations isolated at the 16th day of pregnancy, was significantly reduced by an antagonist of phospholipase A2 (mepacrine, 10(-4) M) as well as by acetylsalicylic acid (ASA at 10(-4) M), an inhibitor of cyclooxygenase.	Aspirin	258-261	phospholipase A2 group IB	Rattus norvegicus	183-199
3877078-7	1985	IL-1 induction of endothelial adhesivity was concentration dependent (maximum, 10 U/ml), time dependent (peak, 4-6 h), and reversible, was blocked by cycloheximide (10 micrograms/ml) or actinomycin D (5 micrograms/ml) but not by acetylsalicylic acid (100 microM), and occurred without detectable endothelial cell damage.	Aspirin	229-249	interleukin 1 alpha	Homo sapiens	0-4
2934863-3	1985	Upon oral intake of aspirin (ASA) the PAF-induced irreversible aggregation as well as the synergistic irreversible aggregation became reversible.	Aspirin	20-27	PCNA clamp associated factor	Homo sapiens	38-41
2934863-3	1985	Upon oral intake of aspirin (ASA) the PAF-induced irreversible aggregation as well as the synergistic irreversible aggregation became reversible.	Aspirin	29-32	PCNA clamp associated factor	Homo sapiens	38-41
6482089-9	1984	Other anti-inflammatory agents including aspirin, sodium salicylate, phenylbutazone and prednisolone were found to be poorly or scarcely inhibitory for both cathepsins B and H.	Aspirin	41-48	cathepsin B	Rattus norvegicus	157-175
6241781-0	1984	Suppressive effect of acetylsalicylic acid on erythropoietin-responsive cells in mice.	Aspirin	22-42	erythropoietin	Mus musculus	46-60
6241781-5	1984	Administration of ASA prior to administration of erythropoietin (Epo) into post-hypoxic polycythemic mice depresses the incorporation of 59Fe into erythrocytes.	Aspirin	18-21	erythropoietin	Mus musculus	65-68
6241781-7	1984	When ASA is given 24 hr after injection of Epo, suppression is less marked.	Aspirin	5-8	erythropoietin	Mus musculus	43-46
6858789-0	1983	Study of platelet aggregation induced by platelet activating factor (PAF) after administration of ticlopidine or aspirin.	Aspirin	113-120	PCNA clamp associated factor	Homo sapiens	69-72
6858789-4	1983	The 23 subjects receiving aspirin showed a diminution of platelet aggregation induced by PAF due to inhibition of ADP release.	Aspirin	26-33	PCNA clamp associated factor	Homo sapiens	89-92
6401999-7	1983	3 Low dose aspirin had comparable effects on NaAA-induced release to dazoxiben, but in contrast to dazoxiben, the effectiveness of low-dose aspirin in inhibiting NaAA induced release reaction was related to its effectiveness in inhibiting MDA generation.	Aspirin	11-18	N-acylethanolamine acid amidase	Homo sapiens	45-49
6401999-7	1983	3 Low dose aspirin had comparable effects on NaAA-induced release to dazoxiben, but in contrast to dazoxiben, the effectiveness of low-dose aspirin in inhibiting NaAA induced release reaction was related to its effectiveness in inhibiting MDA generation.	Aspirin	140-147	N-acylethanolamine acid amidase	Homo sapiens	162-166
6401999-9	1983	5 A combination of dazoxiben and low dose aspirin had a greater effect on platelet behaviour in response to NaAA, ADP, and adrenaline than either drug alone.	Aspirin	42-49	N-acylethanolamine acid amidase	Homo sapiens	108-112
6795686-5	1981	Aspirin or indomethacin, blockers of cyclooxygenase, inhibited chemiluminescence but failed to block the metabolic response to arachidonic acid.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	37-51
7202949-4	1981	The motilin-induced contractions were not influenced by atropine, chlorpheniramine, cimetidine, phentolamine, propranolol, cinanserin, 1-sar-8-ala-angiotensin II, or aspirin.	Aspirin	166-173	promotilin	Oryctolagus cuniculus	4-11
6109202-0	1980	Topical aspirin for wasp stings.	Aspirin	8-15	WASP actin nucleation promoting factor	Homo sapiens	20-24
482278-0	1979	The effect of aspirin on erythropoietin formation in the rat.	Aspirin	14-21	erythropoietin	Rattus norvegicus	25-39
758857-2	1979	Animals treated preoperatively and for three days postoperatively with either aspirin (600 mgm BID) or low molecular weight dextran (500 cc/day) had statistically significant increased graft patency as compared to controls during the treatment interval.	Aspirin	78-85	BH3 interacting domain death agonist	Bos taurus	95-98
15305-3	1977	Aspirin significantly increased gastric-mucosal clearance of aminopyrine (mucosal blood flow), outputs of Na+, Ca++, Mg++, hemoglobin, and plasma transferrin-Cr51 into the pouch contents, and disappearance of H+ from lumen to mucosa.	Aspirin	0-7	inhibitor of carbonic anhydrase	Canis lupus familiaris	146-157
34039715-2	2021	In this study, we aimed to assess whether aspirin improves STA-MCA bypass patency and is safe in patients with MMD.	Aspirin	42-49	GCY	Homo sapiens	59-62
34039715-8	2021	The STA-MCA bypass patency rate in the aspirin group was higher than that in the non-aspirin group (98.7% vs 89.7%; HR 1.57; 95% CI 1.106 to 2.235; p=0.012).	Aspirin	39-46	GCY	Homo sapiens	4-7
33957022-7	2021	Results: All nine patients showed ASA stenosis in the area of T-OPLL.	Aspirin	34-37	OPLL	Homo sapiens	64-68
33957022-10	2021	Conclusions: This is the first study to report detection of ASA stenosis in patients with T-OPLL.	Aspirin	60-63	OPLL	Homo sapiens	92-96
3798362-0	1986	Teratogenic effects on the CD-1 mouse embryo exposed to concurrent doses of ethanol and aspirin.	Aspirin	88-95	CD1 antigen complex	Mus musculus	27-31
3798362-14	1986	These results indicate an additive effect of aspirin and ethanol on the developing CD-1 mouse fetus.	Aspirin	45-52	CD1 antigen complex	Mus musculus	83-87
3539408-2	1986	Since, at times, chronic urticaria may appear histologically similar to a mild cell-mediated immune response, the release of the T cell-derived lymphokine leucocyte inhibitory factor (LIF), in response to incubation with these additives and with acetylsalicylic acid (ASA), was measured in vitro using cells from normal controls, from patients with chronic urticaria with or without clinically associated additive sensitivity and from patients with asthma with or without associated ASA sensitivity.	Aspirin	246-266	LIF interleukin 6 family cytokine	Homo sapiens	184-187
3539408-2	1986	Since, at times, chronic urticaria may appear histologically similar to a mild cell-mediated immune response, the release of the T cell-derived lymphokine leucocyte inhibitory factor (LIF), in response to incubation with these additives and with acetylsalicylic acid (ASA), was measured in vitro using cells from normal controls, from patients with chronic urticaria with or without clinically associated additive sensitivity and from patients with asthma with or without associated ASA sensitivity.	Aspirin	268-271	LIF interleukin 6 family cytokine	Homo sapiens	184-187
3539408-2	1986	Since, at times, chronic urticaria may appear histologically similar to a mild cell-mediated immune response, the release of the T cell-derived lymphokine leucocyte inhibitory factor (LIF), in response to incubation with these additives and with acetylsalicylic acid (ASA), was measured in vitro using cells from normal controls, from patients with chronic urticaria with or without clinically associated additive sensitivity and from patients with asthma with or without associated ASA sensitivity.	Aspirin	483-486	LIF interleukin 6 family cytokine	Homo sapiens	184-187
3539408-4	1986	In addition, tartrazine caused LIF release from mononuclear cells of ASA-sensitive asthmatics.	Aspirin	69-72	LIF interleukin 6 family cytokine	Homo sapiens	31-34
3759743-5	1986	Pretreatment with either indomethacin or aspirin potentiated the Pa response to ACh while eliminating the ACh-associated decrease in Rus/Rds.	Aspirin	41-48	peripherin 2	Canis lupus familiaris	137-140
3095926-0	1986	Acetylation of antithrombin III by aspirin.	Aspirin	35-42	serpin family C member 1	Homo sapiens	15-31
3095926-2	1986	Since aspirin (acetylsalicylic acid) is known to acetylate numerous biologic macromolecules, the effect of aspirin on antithrombin III was investigated.	Aspirin	107-114	serpin family C member 1	Homo sapiens	118-134
3095926-3	1986	It was found that antithrombin III is irreversibly inactivated by treatment with aspirin.	Aspirin	81-88	serpin family C member 1	Homo sapiens	18-34
3095926-8	1986	Amino group analysis of aspirin-treated antithrombin III using trinitrobenzenesulfonic acid revealed that one to two primary amino groups are lost relative to the untreated antithrombin III.	Aspirin	24-31	serpin family C member 1	Homo sapiens	40-56
3095926-8	1986	Amino group analysis of aspirin-treated antithrombin III using trinitrobenzenesulfonic acid revealed that one to two primary amino groups are lost relative to the untreated antithrombin III.	Aspirin	24-31	serpin family C member 1	Homo sapiens	173-189
3095926-9	1986	It is concluded that the reaction of aspirin with antithrombin III results in specific acetylation of lysine residues.	Aspirin	37-44	serpin family C member 1	Homo sapiens	50-66
3709328-7	1986	In contrast, indomethacin (5 mg/kg) and aspirin (200 mg/kg) as cyclooxygenase inhibitors or quinacrine (100 mg/kg) as a phospholipase A2 inhibitor significantly decreased both the pH and acid neutralizing capacity.	Aspirin	40-47	phospholipase A2 group IB	Rattus norvegicus	120-136
3920919-4	1985	In rings of femoral and pulmonary vein contracted with norepinephrine, arachidonic acid produced a concentration-dependent increase in tension that was eliminated by removal of the endothelium or by treatment with the inhibitors of cyclooxygenase (indomethacin, meclofenamate, or acetylsalicyclic acid).	Aspirin	280-301	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	232-246
3922878-4	1985	Both Fc gamma fragments and p23 were able to induce the release of PGE from splenic adherent macrophages and, in the former case, the release was inhibited by either IM or aspirin.	Aspirin	172-179	prostaglandin E synthase 3	Homo sapiens	28-31
7138896-3	1982	Under optimal pH, phospholipase A2 activity was not affected by aspirin but was inhibited by indomethacin.	Aspirin	64-71	phospholipase A2 group IB	Rattus norvegicus	18-34
6954880-4	1982	Prostaglandins E1, E2 and F2 alpha increased the vascular tone of the renal arterial strips, and generated marked oscillations in their contractions which were inhibited by aspirin or indomethacin.	Aspirin	173-180	small nucleolar RNA, H/ACA box 73A	Homo sapiens	15-34
33782564-0	2021	Aspirin reduces the incidence of metastasis in a pre-clinical study of Braf mutant serrated colorectal neoplasia.	Aspirin	0-7	Braf transforming gene	Mus musculus	71-75
33782564-2	2021	The effect of aspirin on the ~20% of colorectal cancers arising via BRAF mutation is yet to be established.	Aspirin	14-21	Braf transforming gene	Mus musculus	68-72
33782564-9	2021	CONCLUSIONS: Aspirin reduces the incidence of metastatic Braf mutant carcinoma, although this is not due to a reduction in primary disease.	Aspirin	13-20	Braf transforming gene	Mus musculus	57-61
33959001-10	2021	Results: Atorvastatin and aspirin combination increased the release of IL-1RA from stroke Mo.	Aspirin	26-33	interleukin 1 receptor antagonist	Homo sapiens	71-77
33959001-11	2021	In MSCs, atorvastatin and aspirin combination reduced the release of pro-inflammatory cytokines such as IL-6, IL-8, MCP-1 and IFN-gamma.	Aspirin	26-33	C-C motif chemokine ligand 2	Homo sapiens	116-121
33872443-8	2021	MIS-C patients (50%) received enoxaparin thromboprophylaxis (in addition to aspirin) with significant improvement in their inflammatory and ROTEM parameters upon outpatient follow up; none developed symptomatic thrombosis.	Aspirin	76-83	anti-Mullerian hormone	Homo sapiens	0-3
33824459-11	2022	Aspirin alleviates breast cancer via targeting PD-L1 and HBXIP.	Aspirin	0-7	CD274 molecule	Homo sapiens	47-52
33917483-12	2021	Targeting the PKA-CREB/ATF1 axis may be a strategy to improve the therapeutic effects of aspirin on HCC.	Aspirin	89-96	activating transcription factor 1	Homo sapiens	23-27
33918289-6	2021	In this study, we have used cytotoxicity and molecular docking studies to show that NCX4040, a nitric oxide donor related to aspirin, inhibited the functions of ATPase which resulted in significant reversal of resistance to both adriamycin and topotecan in P-gp- and BCRP-expressing human cancer cell lines, respectively.	Aspirin	125-132	phosphoglycolate phosphatase	Homo sapiens	257-261
7305554-3	1981	In the isolated dog coronary arterial strips, acetylsalicylic acid (10-4 M) produced the contractions of them, which were significantly inhibited by calcium-free solution, diltiazem, nifedipine, phospholipase A2, arachidonate and prostaglandin E1.	Aspirin	46-66	phospholipase A2 group IB	Canis lupus familiaris	195-211
7250148-3	1981	Aspirin exerts an effect which is less pronounced and involves the enhancement of the C-6 hydroxylation.	Aspirin	0-7	complement C6	Rattus norvegicus	86-89
216717-0	1979	Measurement of antithrombin III in healthy subjects studied before and after taking aspirin and dipyridamole.	Aspirin	84-91	serpin family C member 1	Homo sapiens	15-31
146611-1	1978	Acetyl-salicylic acid has been found to inhibit the aggregation of erythrocytes and thrombocytes stimulated by proteolytic enzymes (fibrinolysin and trypsin) and phospholipase A.	Aspirin	0-21	phospholipase A and acyltransferase 1	Homo sapiens	162-177
826460-1	1976	A saline extract of polyurethane (SPU) induces enzymatic conversion of arachidonic acid (either exogenous or released through the action of exogenous phospholipase-A) by activating a hitherto undiscovered labile enzyme, synthetase-alpha which is not blocked by aspirin.	Aspirin	261-268	phospholipase A and acyltransferase 1	Homo sapiens	150-165
34029712-3	2021	Symptoms due to increased baseline and/or episodic release of PGD2 can be prevented with aspirin, an inhibitor of cyclooxygenase (COX)1 and COX2.	Aspirin	89-96	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	114-135
33444716-17	2021	CONCLUSION: Our studies implicated that NXT could restore HI injury and inhibit thrombosis through COX2-VEGF/NFkappaB signaling, which is consistent with the molecular target of aspirin.	Aspirin	178-185	cytochrome c oxidase II, mitochondrial	Danio rerio	99-103
33444716-17	2021	CONCLUSION: Our studies implicated that NXT could restore HI injury and inhibit thrombosis through COX2-VEGF/NFkappaB signaling, which is consistent with the molecular target of aspirin.	Aspirin	178-185	vascular endothelial growth factor Aa	Danio rerio	104-108
33714797-8	2021	Atrial fibrillation was more commonly reported in TACI (39.3 %) and less common in POCI (8.1 %) (p < 0.001).Comparing TACI vs Non TACI Stroke Subtypes demonstrated major differences in cumulative survival,among the cases with no previous aspirin treatment, after 3 years (51.9 % vs 88.8 %).The increased risk of mortality at 12 months is consistently observed for the presence of a previous atrial fibrillation (OR 3.01 95 %CI 1.69-5.39), TACI subtype (OR 10.4 95 %CI 4.83-22.6) and NIHSS over 10 (OR 9.33 95 % CI 4,49-19.4).	Aspirin	238-245	TNF receptor superfamily member 13B	Homo sapiens	118-122
33714797-8	2021	Atrial fibrillation was more commonly reported in TACI (39.3 %) and less common in POCI (8.1 %) (p < 0.001).Comparing TACI vs Non TACI Stroke Subtypes demonstrated major differences in cumulative survival,among the cases with no previous aspirin treatment, after 3 years (51.9 % vs 88.8 %).The increased risk of mortality at 12 months is consistently observed for the presence of a previous atrial fibrillation (OR 3.01 95 %CI 1.69-5.39), TACI subtype (OR 10.4 95 %CI 4.83-22.6) and NIHSS over 10 (OR 9.33 95 % CI 4,49-19.4).	Aspirin	238-245	TNF receptor superfamily member 13B	Homo sapiens	118-122
33714797-8	2021	Atrial fibrillation was more commonly reported in TACI (39.3 %) and less common in POCI (8.1 %) (p < 0.001).Comparing TACI vs Non TACI Stroke Subtypes demonstrated major differences in cumulative survival,among the cases with no previous aspirin treatment, after 3 years (51.9 % vs 88.8 %).The increased risk of mortality at 12 months is consistently observed for the presence of a previous atrial fibrillation (OR 3.01 95 %CI 1.69-5.39), TACI subtype (OR 10.4 95 %CI 4.83-22.6) and NIHSS over 10 (OR 9.33 95 % CI 4,49-19.4).	Aspirin	238-245	TNF receptor superfamily member 13B	Homo sapiens	118-122
33714797-12	2021	Severity of disease at diagnosis, represented by TACI subtype is clearly associated to decreased survival among patients with no record of previous aspirin therapy.	Aspirin	148-155	TNF receptor superfamily member 13B	Homo sapiens	49-53
33318029-7	2021	Of these, aspirin decreased MCM6, RRM2 and ARFIP2 expression and MR analysis showed that a standard deviation increase in mRNA/protein expression was associated with increased CRC risk (OR:1.08, 95% CI:1.03-1.13, OR:3.33, 95% CI:2.46-4.50 and OR:1.15, 95% CI:1.02-1.29, respectively).	Aspirin	10-17	ribonucleotide reductase regulatory subunit M2	Homo sapiens	34-38
33318029-8	2021	CONCLUSIONS: MCM6 and RRM2 are involved in DNA repair whereby reduced expression may lead to increased DNA aberrations and ultimately cancer cell death, whereas ARFIP2 is involved in actin cytoskeletal regulation indicating a possible role in aspirin"s reduction of metastasis.	Aspirin	243-250	ribonucleotide reductase regulatory subunit M2	Homo sapiens	22-26
33634725-2	2021	This is due to the ability to block GPVI while having minimal effects on hemostasis, making it a more attractive target over current dual-antiplatelet therapy (DAPT) with acetyl salicylic acid and P2Y12 inhibitors where bleeding can be a problem.	Aspirin	171-192	glycoprotein VI platelet	Homo sapiens	36-40
33574709-0	2021	siRNA Knockdown of REDD1 Facilitates Aspirin-Mediated Dephosphorylation of mTORC1 Target 4E-BP1 in MDA-MB-468 Human Breast Cancer Cell Line.	Aspirin	37-44	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	89-95
33574709-7	2021	Results: We show a decline in phosphorylation of mTORC1 downstream substrate 4E-BP1 (eukaryotic translation initiation factor 4E-binding protein 1) in response to treatment with aspirin and its metabolite salicylic acid in MDA-MB-468, MCF-7, MDA-MB-231, and MCF10A cell lines.	Aspirin	178-185	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	77-83
33574709-7	2021	Results: We show a decline in phosphorylation of mTORC1 downstream substrate 4E-BP1 (eukaryotic translation initiation factor 4E-binding protein 1) in response to treatment with aspirin and its metabolite salicylic acid in MDA-MB-468, MCF-7, MDA-MB-231, and MCF10A cell lines.	Aspirin	178-185	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	85-146
33441016-0	2021	Low miR-19b-1-5p Expression Is Related to Aspirin Resistance and Major Adverse Cardio- Cerebrovascular Events in Patients With Acute Coronary Syndrome.	Aspirin	42-49	microRNA 19b-1	Homo sapiens	4-13
33441016-3	2021	We investigated whether miR-19b-1-5p could be utilized as a biomarker for aspirin resistance and future major adverse cardio-cerebrovascular (MACCE) events in patients with ACS.	Aspirin	74-81	microRNA 19b-1	Homo sapiens	24-33
33441016-8	2021	Low miR-19b-1-5p expression was found to be related to aspirin resistance as could be observed from sustained platelet aggregation in the presence of aspirin (-Log-miR-19b-1-5p, [unstandardized beta, 44.50; 95% CI, 2.20-86.80; P<0.05]), even after adjusting for age, sex, ethnicity, and prior history of stroke.	Aspirin	55-62	microRNA 19b-1	Homo sapiens	4-13
33441016-8	2021	Low miR-19b-1-5p expression was found to be related to aspirin resistance as could be observed from sustained platelet aggregation in the presence of aspirin (-Log-miR-19b-1-5p, [unstandardized beta, 44.50; 95% CI, 2.20-86.80; P<0.05]), even after adjusting for age, sex, ethnicity, and prior history of stroke.	Aspirin	150-157	microRNA 19b-1	Homo sapiens	4-13
33441016-11	2021	Conclusions Lower miR-19b-1-5p expression was found to be associated with sustained platelet aggregation on aspirin, and a higher risk of MACCE in patients with ACS.	Aspirin	108-115	microRNA 19b-1	Homo sapiens	18-27
33441016-12	2021	Therefore, miR-19b-1-5p could be a suitable marker for aspirin resistance and might predict recurrence of MACCE in patients with ACS.	Aspirin	55-62	microRNA 19b-1	Homo sapiens	11-20
33467191-6	2021	In aspirin sensitive patients, the levels of COX1.2, COX1.3, COX1.4 and COX1.5 isoforms were higher compared to aspirin-tolerant patients.	Aspirin	3-10	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	45-49
33467191-6	2021	In aspirin sensitive patients, the levels of COX1.2, COX1.3, COX1.4 and COX1.5 isoforms were higher compared to aspirin-tolerant patients.	Aspirin	112-119	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	45-49
32988222-12	2021	Consistently and importantly, aspirin abolishes the enhancing effects of PCSK9 on platelet activation and in vivo thrombosis.	Aspirin	30-37	proprotein convertase subtilisin/kexin type 9	Homo sapiens	73-78
32988222-15	2021	PCSK9 inhibitors or aspirin abolish the enhancing effects of PCSK9, supporting the use of aspirin in patients with high plasma PCSK9 levels in addition to PCSK9 inhibitors to prevent thrombotic complications.	Aspirin	20-27	proprotein convertase subtilisin/kexin type 9	Homo sapiens	61-66
32988222-15	2021	PCSK9 inhibitors or aspirin abolish the enhancing effects of PCSK9, supporting the use of aspirin in patients with high plasma PCSK9 levels in addition to PCSK9 inhibitors to prevent thrombotic complications.	Aspirin	20-27	proprotein convertase subtilisin/kexin type 9	Homo sapiens	61-66
32988222-15	2021	PCSK9 inhibitors or aspirin abolish the enhancing effects of PCSK9, supporting the use of aspirin in patients with high plasma PCSK9 levels in addition to PCSK9 inhibitors to prevent thrombotic complications.	Aspirin	20-27	proprotein convertase subtilisin/kexin type 9	Homo sapiens	61-66
32988222-15	2021	PCSK9 inhibitors or aspirin abolish the enhancing effects of PCSK9, supporting the use of aspirin in patients with high plasma PCSK9 levels in addition to PCSK9 inhibitors to prevent thrombotic complications.	Aspirin	90-97	proprotein convertase subtilisin/kexin type 9	Homo sapiens	0-5
32988222-15	2021	PCSK9 inhibitors or aspirin abolish the enhancing effects of PCSK9, supporting the use of aspirin in patients with high plasma PCSK9 levels in addition to PCSK9 inhibitors to prevent thrombotic complications.	Aspirin	90-97	proprotein convertase subtilisin/kexin type 9	Homo sapiens	61-66
32988222-15	2021	PCSK9 inhibitors or aspirin abolish the enhancing effects of PCSK9, supporting the use of aspirin in patients with high plasma PCSK9 levels in addition to PCSK9 inhibitors to prevent thrombotic complications.	Aspirin	90-97	proprotein convertase subtilisin/kexin type 9	Homo sapiens	61-66
32988222-15	2021	PCSK9 inhibitors or aspirin abolish the enhancing effects of PCSK9, supporting the use of aspirin in patients with high plasma PCSK9 levels in addition to PCSK9 inhibitors to prevent thrombotic complications.	Aspirin	90-97	proprotein convertase subtilisin/kexin type 9	Homo sapiens	61-66
33105321-0	2021	Chronic application of low-dose aspirin affects multiple parameters of three blood cellular types and antithrombin activity: A 1: 1: 1 Propensity Score Matching Analysis.	Aspirin	32-39	serpin family C member 1	Homo sapiens	102-114
33105321-6	2021	A dose-dependent relationship was observed between aspirin and decreased HPR incidence (PAA < 0.001, PADP < 0.01, respectively), decreased monocyte ratio (P = 0.052), increased antithrombin activity (P < 0.001), and increased platelet distribution width (P < 0.05).	Aspirin	51-58	serpin family C member 1	Homo sapiens	177-189
33105321-8	2021	Our finding demonstrated that aspirin exerts its antithrombotic effects at least by antiplatelet function, enhancing antithrombin activity and suppressing monocytes in vivo.	Aspirin	30-37	serpin family C member 1	Homo sapiens	117-129
33184378-6	2020	These effects are initiated by ASA/SA-triggered Akt/mTOR/AMPK-dependent activation of nitric oxide synthase 3 (eNOS), which increases nitric oxide and reactive oxygen species production inducing ER stress response.	Aspirin	31-34	nitric oxide synthase 3, endothelial cell	Mus musculus	111-115
33115436-15	2020	Peaks in TnT were less frequent in aspirin-treated patients.	Aspirin	35-42	troponin T1, slow skeletal type	Homo sapiens	9-12
33116404-12	2020	Results: For the first time, aspirin and celecoxib were shown to significantly inhibit Neu-1 sialidase activity in a dose- and time-dependent manner following stimulation with EGF.	Aspirin	29-36	epidermal growth factor	Homo sapiens	176-179
33116404-13	2020	Aspirin blocked Neu-1 desialylation of alpha-2,3-sialic acid expression following 30 min stimulation with EGF.	Aspirin	0-7	epidermal growth factor	Homo sapiens	106-109
33116404-15	2020	Aspirin inhibited phosphorylation of the EGFR in EGF-stimulated cells.	Aspirin	0-7	epidermal growth factor	Homo sapiens	41-44
33116404-17	2020	Conclusion: These findings signify a novel multimodality mechanism(s) of action for aspirin and celecoxib, specifically targeting and inhibiting Neu-1 activity, regulating EGF-induced growth receptor activation and inducing apoptosis and necrosis in a dose- and time-dependent manner.	Aspirin	84-91	epidermal growth factor	Homo sapiens	172-175
33920786-0	2021	ZINC40099027 Promotes Gastric Mucosal Repair in Ongoing Aspirin-Associated Gastric Injury by Activating Focal Adhesion Kinase.	Aspirin	56-63	PTK2 protein tyrosine kinase 2	Mus musculus	104-125
33920786-12	2021	These results suggest that ZN27 ameliorates ongoing aspirin-associated gastric mucosal injury by a pathway involving FAK activation.	Aspirin	52-59	PTK2 protein tyrosine kinase 2	Mus musculus	117-120
33618245-4	2021	OBSERVATIONS: This paper reviews randomized controlled trials that showed that celecoxib, a selective COX-2 inhibitor, or low-dose aspirin, which inhibits COX-1 and inhibits/acetylates COX-2, reduced bipolar symptoms in patients on mood stabilizers.	Aspirin	131-138	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	155-160
33756460-1	2021	BACKGROUND: Acetylsalicylic acid hypersensitivity (ASAH) limits therapeutic options in patients with acute coronary syndrome (ACS), who benefit from dual antiplatelet therapy (DAPT), especially when undergoing stent implantation.	Aspirin	12-32	N-acylsphingosine amidohydrolase 1	Homo sapiens	51-55
33574709-10	2021	Unexpectedly, we observed that siRNA knockdown of REDD1 expression facilitated aspirin-mediated suppression of mTORC1 downstream substrate 4E-BP1 phosphorylation in the MDA-MB-468 cell line.	Aspirin	79-86	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	139-145
33574709-11	2021	REDD1 downregulation slightly encouraged reduction in 4E-BP1 phosphorylation by aspirin in MCF-7 cells but did not elicit a reproducible effect in the MDA-MB-231 cell line.	Aspirin	80-87	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	54-60
33370633-7	2021	The severity of dyspepsia assessment (SODA) results showed that patients in PNS + ASA group exhibited relieved dyspeptic symptoms as compared with those in ASA group, which might be associated with enhanced secretion of gastrin and motilin.	Aspirin	82-85	gastrin	Homo sapiens	220-227
31744370-8	2020	We observed a marked elevation in TF concentration at 10.00 a.m. only in aspirin-resistant patients and a significant increase in TFPI concentration at 10 a.m. only in aspirin-sensitive patients.	Aspirin	73-80	coagulation factor III, tissue factor	Homo sapiens	34-36
33101034-9	2020	Results: Plasma H19 was significantly up-regulated in patients with aspirin resistance (p=0.0203), and the H19 levels were positively associated with urine 11dhTXB2/creatinine (R=0.04364, p=0.0106) and positively associated with the level of 8-iso-PGF2alpha (R=0.04561, p=0.0089).	Aspirin	68-75	H19 imprinted maternally expressed transcript	Homo sapiens	16-19
33101034-10	2020	The ROC curves indicated that H19 can sensitively and specifically diagnose aspirin resistance (area under the curve, 0.8005; 95% CI, 0.7301-0.8710; p < 0.0001; specificity, 75.86207%; sensitivity, 73.84615%.).	Aspirin	76-83	H19 imprinted maternally expressed transcript	Homo sapiens	30-33
33101034-11	2020	H19 is an independent risk factor for aspirin resistance (OR=1.129, p=0.0321), and aspirin resistance and H19 are closely related with ischemic stroke recurrence.	Aspirin	38-45	H19 imprinted maternally expressed transcript	Homo sapiens	0-3
33101034-12	2020	Conclusions: H19 is closely associated with aspirin resistance, and H19 probably induces aspirin resistance through increasing the production of 8-iso-prostaglandin-2alpha.	Aspirin	44-51	H19 imprinted maternally expressed transcript	Homo sapiens	13-16
33101034-12	2020	Conclusions: H19 is closely associated with aspirin resistance, and H19 probably induces aspirin resistance through increasing the production of 8-iso-prostaglandin-2alpha.	Aspirin	89-96	H19 imprinted maternally expressed transcript	Homo sapiens	68-71
33101034-13	2020	Besides which, H19 may serve as a serological marker for diagnosing aspirin resistance with high specificity and sensitivity, and the test of H19 could give clues to the recurrence of ischemic stroke.	Aspirin	68-75	H19 imprinted maternally expressed transcript	Homo sapiens	15-18
32933639-11	2020	Compared with the low-dose ginsenoside Rb1 group, the aspirin group and the high-dose ginsenoside Rb1 group had significant reductions in the levels of TNF-alpha, IL-6, and IL-1beta (P<0.05); the high-dose ginsenoside Rb1 group had significant increases in the expression levels of P-PI3K/PI3K and P-AKT/AKT (P<0.05).	Aspirin	54-61	interleukin 1 alpha	Mus musculus	173-181
32847114-6	2020	We initially characterized resveratrol-aspirin derivatives as products that can inhibit cytochrome P450 Family 1 Subfamily A Member 1 (CYP1A1) activity, DNA methyltransferase (DNMT) activity, and cyclooxygenase (COX) activity.	Aspirin	39-46	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	88-133
32847114-6	2020	We initially characterized resveratrol-aspirin derivatives as products that can inhibit cytochrome P450 Family 1 Subfamily A Member 1 (CYP1A1) activity, DNA methyltransferase (DNMT) activity, and cyclooxygenase (COX) activity.	Aspirin	39-46	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	135-141
31420920-0	2020	Aspirin for the prevention and treatment of pre-eclampsia: A matter of COX-1 and/or COX-2 inhibition?	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	71-76
32627038-9	2020	In addition, aspirin upregulated the levels of caspase-cleaved cytokeratin 18, increased the proportion of early apoptotic cells, decreased the levels of clusterin and heat shock protein 70 (HSP 70), upregulated the levels of miRNA-137 and inhibited epidermal growth factor receptor (EGFR) activation.	Aspirin	13-20	epidermal growth factor receptor	Mus musculus	250-282
32627038-9	2020	In addition, aspirin upregulated the levels of caspase-cleaved cytokeratin 18, increased the proportion of early apoptotic cells, decreased the levels of clusterin and heat shock protein 70 (HSP 70), upregulated the levels of miRNA-137 and inhibited epidermal growth factor receptor (EGFR) activation.	Aspirin	13-20	epidermal growth factor receptor	Mus musculus	284-288
32627038-10	2020	In addition, we observed that aspirin suppressed cell proliferation partially through the miRNA-137/EGFR pathway.	Aspirin	30-37	epidermal growth factor receptor	Mus musculus	100-104
32488348-14	2020	CONCLUSION: Our results propose a promising antidepressant effect for ASA VI possibly through the downregulation of IDO expression and normalization of the aberrant glutamate transmission.	Aspirin	70-73	indoleamine 2,3-dioxygenase 1	Mus musculus	116-119
32545774-3	2020	We found that the human H4 glioma cell-killing effects of aspirin involved mitochondria-mediated apoptosis accompanied by endoplasmic reticulum (ER) stress, Noxa upregulation, Mcl-1 downregulation, Bax mitochondrial distribution and oligomerization, and caspase 3/caspase 8/caspase 9 activation.	Aspirin	58-65	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	176-181
33170486-10	2021	Moreover, these results suggest that the definition of > 95% inhibition of serum TxB2 to indicate the level of platelet COX-1 inhibition needed for clinical efficacy may be overestimated and should be re-considered in future translational research investigations that attempt to link the clinical efficacy of ASA with a laboratory measurement cutoff.	Aspirin	309-312	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	120-125
33484117-4	2021	For example, the importance of cyclooxygenase (COX)-1-derived TXA2 from activated platelets in contributing to primary hemostasis and atherothrombosis is demonstrated in animal and human models by the bleeding complications and cardioprotective effects associated with low-dose aspirin, a selective inhibitor of platelet COX-1.	Aspirin	278-285	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	31-53
33373378-1	2020	INTRODUCTION: Reduced antiplatelet activity of aspirin (ALR) or clopidogrel (CLR) is associated with an increased risk of thromboembolic events.	Aspirin	47-54	growth factor, augmenter of liver regeneration	Homo sapiens	56-59
33293599-4	2020	The exposure of platelets to Aspirin [an inhibitor of cyclooxygenase (COX)-1] reduced the generation of TXA2 and prevented the morphological and functional changes induced by platelets in CASMC.	Aspirin	29-36	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	54-76
33284715-6	2021	In humans, rs465566 KAR gene polymorphism associates with altered in vitro platelet responses suggesting enhanced aspirin effect.	Aspirin	114-121	KAR	Homo sapiens	20-23
33125972-8	2020	RT-qPCR analysis show that Asp-Sr/beta-TCP, beta-TCP group and Sr/beta-TCP group showed increased BMP2, Smad1, OPG than the OVX group(p < 0.05), while Asp-Sr/beta-TCP exhibited decreased TNF-alpha IFN-gamma and RANKL than the OVX group(p < 0.05).	Aspirin	151-154	SRP receptor subunit beta	Rattus norvegicus	31-38
33172886-9	2021	CONCLUSIONS: Prescribing low-dose or no aspirin in the acute-phase of KD might be associated with a decreased incidence of CAL.	Aspirin	40-47	filamin binding LIM protein 1	Homo sapiens	123-126
32956986-11	2020	CONCLUSION: Concurrent aspirin use with osimertinib in EGFR-mutant NSCLC patients was associated with improved survival, regardless of lines of therapy, CNS metastatic status, EGFR mutation type, age, gender, TP53, and PD-L1 status.	Aspirin	23-30	CD274 molecule	Homo sapiens	219-224
33082288-5	2020	Treating cultured CSCs or 4T1 tumor-bearing mice with the nonsteroidal anti-inflammatory drug aspirin restored SMAR1 expression and ABCG2 repression and enhanced tumor sensitivity to doxorubicin.	Aspirin	94-101	BTG3 associated nuclear protein	Mus musculus	111-116
33101034-0	2020	Long Non-Coding RNA H19 Positively Associates With Aspirin Resistance in the Patients of Cerebral Ischemic Stroke.	Aspirin	51-58	H19 imprinted maternally expressed transcript	Homo sapiens	20-23
33101034-5	2020	Since the relationship between H19 and aspirin resistance have never been reported, herein, we aimed to evaluate the H19 expression in aspirin-resistant ischemic stroke patients and subsequently, ascertain the ability of H19 to diagnose aspirin resistance.	Aspirin	135-142	H19 imprinted maternally expressed transcript	Homo sapiens	117-120
33101034-5	2020	Since the relationship between H19 and aspirin resistance have never been reported, herein, we aimed to evaluate the H19 expression in aspirin-resistant ischemic stroke patients and subsequently, ascertain the ability of H19 to diagnose aspirin resistance.	Aspirin	135-142	H19 imprinted maternally expressed transcript	Homo sapiens	117-120
33101034-5	2020	Since the relationship between H19 and aspirin resistance have never been reported, herein, we aimed to evaluate the H19 expression in aspirin-resistant ischemic stroke patients and subsequently, ascertain the ability of H19 to diagnose aspirin resistance.	Aspirin	135-142	H19 imprinted maternally expressed transcript	Homo sapiens	117-120
33101034-5	2020	Since the relationship between H19 and aspirin resistance have never been reported, herein, we aimed to evaluate the H19 expression in aspirin-resistant ischemic stroke patients and subsequently, ascertain the ability of H19 to diagnose aspirin resistance.	Aspirin	135-142	H19 imprinted maternally expressed transcript	Homo sapiens	117-120
32968106-5	2020	CYP2C9 accounts for nearly 75% of salicylic acid hydroxylation in HLMs at concentrations reached after usual aspirin doses.	Aspirin	109-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
32935167-0	2020	Adsorption of acetylsalicylic acid on the aluminum nitride nanotube in both gas and solvent medium: a DFT study.	Aspirin	14-34	gastrin	Homo sapiens	76-79
32815992-17	2020	Aspirin increased SAA (P = 0.04) and tended to increase LBP (P = 0.09) in serum, but did not affect any other serum inflammatory marker (P >= 0.19).	Aspirin	0-7	lipopolysaccharide binding protein	Bos taurus	56-59
32535107-1	2020	The most recognized mechanism of aspirin(acetylsalicylic acid, ASA) action, at therapeutic dosing, is the inhibition of prostanoid biosynthesis through the acetylation of cyclooxygenase(COX)-isozymes (COX-1 at serine-529 and COX-2 at serine-516).	Aspirin	33-40	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	201-206
32535107-1	2020	The most recognized mechanism of aspirin(acetylsalicylic acid, ASA) action, at therapeutic dosing, is the inhibition of prostanoid biosynthesis through the acetylation of cyclooxygenase(COX)-isozymes (COX-1 at serine-529 and COX-2 at serine-516).	Aspirin	41-61	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	201-206
32535107-1	2020	The most recognized mechanism of aspirin(acetylsalicylic acid, ASA) action, at therapeutic dosing, is the inhibition of prostanoid biosynthesis through the acetylation of cyclooxygenase(COX)-isozymes (COX-1 at serine-529 and COX-2 at serine-516).	Aspirin	63-66	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	201-206
32661222-0	2020	Aspirin attenuates YAP and beta-catenin expression by promoting beta-TrCP to overcome docetaxel and vinorelbine resistance in triple-negative breast cancer.	Aspirin	0-7	catenin beta 1	Homo sapiens	27-39
32661222-0	2020	Aspirin attenuates YAP and beta-catenin expression by promoting beta-TrCP to overcome docetaxel and vinorelbine resistance in triple-negative breast cancer.	Aspirin	0-7	beta-transducin repeat containing E3 ubiquitin protein ligase	Homo sapiens	64-73
32661222-4	2020	Interestingly, aspirin not only significantly inhibited the growth of TNBC cells, but also attenuated YAP and beta-catenin expression by upregulating the E3 ubiquitin ligase beta-TrCP to abolished docetaxel and vinorelbine resistance.	Aspirin	15-22	catenin beta 1	Homo sapiens	110-122
32661222-4	2020	Interestingly, aspirin not only significantly inhibited the growth of TNBC cells, but also attenuated YAP and beta-catenin expression by upregulating the E3 ubiquitin ligase beta-TrCP to abolished docetaxel and vinorelbine resistance.	Aspirin	15-22	beta-transducin repeat containing E3 ubiquitin protein ligase	Homo sapiens	174-183
32545774-3	2020	We found that the human H4 glioma cell-killing effects of aspirin involved mitochondria-mediated apoptosis accompanied by endoplasmic reticulum (ER) stress, Noxa upregulation, Mcl-1 downregulation, Bax mitochondrial distribution and oligomerization, and caspase 3/caspase 8/caspase 9 activation.	Aspirin	58-65	caspase 9	Homo sapiens	274-283
32545774-4	2020	Genetic silencing of Noxa or Bax attenuated aspirin-induced viability loss and apoptosis, while silencing Mcl-1 augmented the effects of aspirin.	Aspirin	137-144	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	106-111
31550962-0	2020	Aspirin, low molecular weight heparin, or both in preventing pregnancy complications in women with recurrent pregnancy loss and factor V Leiden mutation.	Aspirin	0-7	coagulation factor V	Homo sapiens	128-143
32297484-0	2020	Aspirin-targeted PD-L1 in lung cancer growth inhibition.	Aspirin	0-7	CD274 molecule	Homo sapiens	17-22
32297484-3	2020	This study aimed to clarify the role of PD-L1 in aspirin-suppressed lung cancer.	Aspirin	49-56	CD274 molecule	Homo sapiens	40-45
32297484-5	2020	The role of aspirin in the modulation of PD-L1 expression was analyzed by western blot or RT-PCR assays.	Aspirin	12-19	CD274 molecule	Homo sapiens	41-46
32297484-6	2020	In lung cancer cells, the influence of aspirin on PD-L1 promoter activity was detected using a luciferase reporter assay.	Aspirin	39-46	CD274 molecule	Homo sapiens	50-55
32297484-8	2020	The function of PD-L1 in aspirin-mediated growth inhibition of lung cancer was examined using a cell viability assay.	Aspirin	25-32	CD274 molecule	Homo sapiens	16-21
32297484-10	2020	Aspirin was able to markedly decrease the expression of PD-L1 at the mRNA and protein levels in lung cancer cells.	Aspirin	0-7	CD274 molecule	Homo sapiens	56-61
32297484-11	2020	For the mechanism study, we found that the promoter of PD-L1 was inactivated by aspirin via TAZ transcriptional coactivator in the cells.	Aspirin	80-87	CD274 molecule	Homo sapiens	55-60
32297484-12	2020	With regard to the functional investigation, aspirin was capable of resisting cell proliferation and PD-L1 overexpression abolished aspirin-depressed cell proliferation in lung cancer.	Aspirin	132-139	CD274 molecule	Homo sapiens	101-106
32297484-13	2020	CONCLUSIONS: Aspirin suppressed the growth of lung cancer cells via targeting the TAZ/PD-L1 axis.	Aspirin	13-20	CD274 molecule	Homo sapiens	86-91
32478188-7	2020	Immunohistochemical analysis of the dorsal root ganglia indicated that ASA reduced the expression of ASIC3 during OA progression.	Aspirin	71-74	acid sensing ion channel subunit 3	Homo sapiens	101-106
32478188-9	2020	Significance: These findings suggest that ASA may have the ability to attenuate secondary hyperalgesia through suppression of ASIC3 and/or TNF-alpha expression.	Aspirin	42-45	acid sensing ion channel subunit 3	Homo sapiens	126-131
32131611-7	2020	In a randomized trial of patients with psoriasis, 2 weeks of 81 mg low-dose aspirin, a COX-1 inhibitor, reduced serum thromboxane (Tx) B2 and reduced brachial vein endothelial proinflammatory transcript expression >70% compared with the no-treatment group (P<0.01).	Aspirin	76-83	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	87-92
32131611-10	2020	Low-dose aspirin improved endothelial cell health in psoriasis via platelet COX-1 inhibition.	Aspirin	9-16	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	76-81
32205146-7	2020	As expected, serum periostin is particularly elevated in comorbidities associated with the eosinophilic/type 2 subtype of severe asthma, including eosinophilic chronic rhinosinusitis, aspirin-exacerbated respiratory diseases, allergic bronchopulmonary aspergillosis, and eosinophilic granulomatosis with polyangiitis.	Aspirin	184-191	periostin	Homo sapiens	19-28
32205444-4	2020	We also show that aspirin-triggered 15-epi-lipoxin A4 (15-epi-LXA4) and 17-epi-resolvin D1 (17-epi-RvD1) through the receptor ALX/FPR2 antagonize cues from CpG DNA, preserve C5aR expression, restore impaired phagocytosis, and redirect human PMNs to apoptosis.	Aspirin	18-25	formyl peptide receptor 2	Homo sapiens	130-134
32014718-2	2020	To further evaluate the modulation of T-helper 1 (Th1) and T-helper 2 (Th2) cytokines using short-term low-dose aspirin in combination with metformin.	Aspirin	112-119	heart and neural crest derivatives expressed 2	Mus musculus	71-74
32014718-15	2020	Furthermore low-dose aspirin treatment showed the modest attenuation of the selected Th2 cytokines, IL-10 and IL-13 when compared to low-dose aspirin with metformin (P < 0.01).	Aspirin	21-28	heart and neural crest derivatives expressed 2	Mus musculus	85-88
32014718-17	2020	The short-term treatment using low-dose aspirin combined with metformin may provide therapeutic benefits in preventing complications associated with dysregulated Th2 cell responses.	Aspirin	40-47	heart and neural crest derivatives expressed 2	Mus musculus	162-165
31797405-0	2020	PPARalpha serves as a new receptor of aspirin for neuroprotection.	Aspirin	38-45	peroxisome proliferator activated receptor alpha	Homo sapiens	0-9
31797405-3	2020	Recently, we have established that peroxisome proliferator-activated receptor alpha (PPARalpha) acts as a novel receptor of aspirin.	Aspirin	124-131	peroxisome proliferator activated receptor alpha	Homo sapiens	35-83
31797405-3	2020	Recently, we have established that peroxisome proliferator-activated receptor alpha (PPARalpha) acts as a novel receptor of aspirin.	Aspirin	124-131	peroxisome proliferator activated receptor alpha	Homo sapiens	85-94
31797405-4	2020	Activation of PPARalpha by aspirin stimulated a series of downstream signaling pathways that could potentially ameliorate different Alzheimer"s disease (AD)-related pathologies.	Aspirin	27-34	peroxisome proliferator activated receptor alpha	Homo sapiens	14-23
31797405-5	2020	In this mini-review, we have discussed how aspirin-PPARalpha interaction plays a pivotal role in the amelioration of AD pathology via the stimulation of neurotrophic factors, upregulation of plasticity-associated genes, and removal of plaque burden in hippocampal neurons.	Aspirin	43-50	peroxisome proliferator activated receptor alpha	Homo sapiens	51-60
32218705-6	2020	Aspirin inhibited COX-2 and iNOS without changes in COX-1 expression, increasing anti-oxidant protein (Cu/Zn-SOD and Mn-SOD) expression in presence or absence of Abeta1-42.	Aspirin	0-7	inositol-3-phosphate synthase 1	Homo sapiens	28-32
32000660-10	2020	After 48 h of treatment with aspirin, the phosphorylation of eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1) and ribosomal protein S6 kinase B1 (S6K1) was reduced, cell proliferation has been inhibited.	Aspirin	29-36	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	102-122
32000660-10	2020	After 48 h of treatment with aspirin, the phosphorylation of eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1) and ribosomal protein S6 kinase B1 (S6K1) was reduced, cell proliferation has been inhibited.	Aspirin	29-36	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	124-130
32000660-10	2020	After 48 h of treatment with aspirin, the phosphorylation of eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1) and ribosomal protein S6 kinase B1 (S6K1) was reduced, cell proliferation has been inhibited.	Aspirin	29-36	ribosomal protein S6 kinase B1	Homo sapiens	136-166
32000660-10	2020	After 48 h of treatment with aspirin, the phosphorylation of eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1) and ribosomal protein S6 kinase B1 (S6K1) was reduced, cell proliferation has been inhibited.	Aspirin	29-36	ribosomal protein S6 kinase B1	Homo sapiens	168-172
31622780-9	2020	STATEMENT OF SIGNIFICANCE: We developed an adaptive in vivo sensing device whereby a drug, aspirin, can be released upon the detection of a proinflammatory cytokine, interferon-gamma (IFN-gamma), in real time with a sensitivity of 10 pg mL-1.	Aspirin	91-98	L1 cell adhesion molecule	Mus musculus	237-241
31622780-10	2020	Moreover, the aspirin triggered by IFN-gamma depressed inflammation in the rat model and was delivered indirectly through blood and cerebrospinal fluid or directly to the inflammation tissue or organ without adverse gastrointestinal effects observed in the liver and kidney.	Aspirin	14-21	interferon gamma	Rattus norvegicus	35-44
31326260-0	2020	A genetic variant near TSLP is associated with chronic rhinosinusitis with nasal polyps and aspirin-exacerbated respiratory disease in Japanese populations.	Aspirin	92-99	thymic stromal lymphopoietin	Homo sapiens	23-27
32025207-9	2020	Aspirin exhibits anticancer effects in HER-2-positive breast cancer by regulating lipid metabolism mediated by c-myc, and Compound C strengthens these effects in an AMPK-independent manner.	Aspirin	0-7	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	111-116
30734682-2	2020	Common therapeutic activity of non-steroidal anti-inflammatory drugs (NSAID), such as aspirin, includes inhibition of two crucial enzymes of AA metabolism - cyclooxygenase-1 and -2 (COX-1/2), with certain risk for gastrointestinal and renal intolerance.	Aspirin	86-93	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	182-189
31982834-0	2020	The relationship of a Prothrombin G20210A mutation or a factor V Leiden mutation and on-aspirin platelet (re-)activity.	Aspirin	88-95	coagulation factor V	Homo sapiens	56-71
31730866-6	2019	However, the combined therapy (10 mg/kg BW tofacitinib and 100 mg/kg BW aspirin) significantly decreased the levels of TNF-alpha, IL-6, serum amyloid A, HOMA-IR, blood glucose level and SOC-3 gene expression but significantly (P &lt; 0.05) improved glucose homoestasis, insulin secretion, HOMA-beta and GLUT-4 gene expression when compared to diabetic untreated rat.	Aspirin	72-79	solute carrier family 2 member 4	Rattus norvegicus	303-309
32266380-3	2020	We performed a multicenter, double-blind trial to investigate the efficacy of three aspirin regimens in optimizing platelet COX-1 inhibition while preserving COX-2-dependent vascular thromboresistance.	Aspirin	84-91	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	124-129
32239624-0	2020	Aspirin sensitizes osimertinib-resistant NSCLC cells in vitro and in vivo via Bim-dependent apoptosis induction.	Aspirin	0-7	BCL2 like 11	Homo sapiens	78-81
32546966-10	2020	Tmx treatment of MDA-MB-231-TmxR cells in combination with ASA, Met and OP markedly reduced the ALDH1A1 by 134-fold compared to the same treatment for the parental cell line.	Aspirin	59-62	aldehyde dehydrogenase 1 family member A1	Homo sapiens	96-103
32313942-10	2020	Strikingly, aspirin suppressed ESCC growth by inhibiting HBXIP and HMGA2.	Aspirin	12-19	high mobility group AT-hook 2	Homo sapiens	67-72
32685898-7	2020	Results: Platelet reactivity was higher in women compared with men when activated with protease activating receptor 1-activating peptide SFLLRN (PAR1-AP) and adenosine 5"-phosphate (ADP), independent of age, basal activation status, estimated glomerular filtration rate < 60, platelet count, statin use, the use of P2Y12 inhibitors, or the use of aspirin.	Aspirin	347-354	Prader Willi/Angelman region RNA 1	Homo sapiens	145-149
32239559-0	2020	Dual modulation of formyl peptide receptor 2 by aspirin-triggered lipoxin contributes to its anti-inflammatory activity.	Aspirin	48-55	formyl peptide receptor 2	Homo sapiens	19-44
31637734-0	2020	Aspirin promotes tenogenic differentiation of tendon stem cells and facilitates tendinopathy healing through regulating the GDF7/Smad1/5 signaling pathway.	Aspirin	0-7	growth differentiation factor 7	Homo sapiens	124-128
31637734-12	2020	RNA sequencing showed that growth differentiation factor 6 (GDF6), GDF7, and GDF11 were upregulated in induction medium with the aspirin group compared with the induction medium group.	Aspirin	129-136	growth differentiation factor 7	Homo sapiens	67-71
31637734-15	2020	In conclusion, aspirin promoted TSC tenogenesis and tendinopathy healing through GDF7/Smad1/5 signaling, and this provided new treatment evidence of aspirin for tendinopathy and tendon injuries.	Aspirin	15-22	growth differentiation factor 7	Homo sapiens	81-85
31867296-1	2019	Objective: To investigate the distribution of the single nucleotide polymorphism (SNP) of LTC4S A-444C in children with Kawasaki disease in northern China and determine whether LTC4S A-444C SNP is associated with aspirin-induced urticaria (AIU).	Aspirin	213-220	leukotriene C4 synthase	Homo sapiens	177-182
31727004-0	2019	Increased risk of aspirin-induced gastric mucosal erosion in elderly Chinese men harboring SLCO1B1*1b/*1b while using aspirin and an ACEI or ARB concomitantly.	Aspirin	18-25	solute carrier organic anion transporter family member 1B1	Homo sapiens	91-98
31727004-3	2019	This study aimed to evaluate the relationship between SLCO1B1 polymorphisms, which can affect ACEI and ARB transport, and gastric mucosal erosion in elderly male Chinese patients with cardiovascular disease who use aspirin.	Aspirin	215-222	solute carrier organic anion transporter family member 1B1	Homo sapiens	54-61
31727004-6	2019	After adjustment for significant factors, SLCO1B1*1b/*1b (OR, 2.64; 95% CI, 1.59-4.17; p &lt; 0.05) was found to be associated with gastric mucosal erosion in aspirin users.	Aspirin	159-166	solute carrier organic anion transporter family member 1B1	Homo sapiens	42-49
31727004-7	2019	CONCLUSIONS: The presence of the SLCO1B1*1b/*1b diplotype may be a risk factor for aspirin-induced gastric mucosal erosion in elderly Chinese men taking aspirin and an ACEI or ARB concomitantly.	Aspirin	83-90	solute carrier organic anion transporter family member 1B1	Homo sapiens	33-40
31727004-7	2019	CONCLUSIONS: The presence of the SLCO1B1*1b/*1b diplotype may be a risk factor for aspirin-induced gastric mucosal erosion in elderly Chinese men taking aspirin and an ACEI or ARB concomitantly.	Aspirin	153-160	solute carrier organic anion transporter family member 1B1	Homo sapiens	33-40
31446057-2	2019	In our current study, we investigated the oxidative stress mediated cell death mechanism of a NSAID derivative NCX4040 (a nitric oxide (NO) releasing form of aspirin) in castration-resistant prostate cancer (CRPC) PC3 cell line.	Aspirin	158-165	BTG anti-proliferation factor 2	Homo sapiens	214-217
31801720-9	2019	A total of 10 220 differentially expressed genes were identified from the TCGA database, and among them 4 genes (CDC25C, TPX2, CDC20, PLK1) were found to be the potential targets for aspirin.	Aspirin	183-190	cell division cycle 25C	Homo sapiens	113-119
31185432-4	2019	All pharmaceuticals except acetylsalicylic acid and sulfathiazole were found in PS1, PS2, and PS3 samples, whereas acetylsalicylic acid, carbamazepine, sulfamethazine, and sulfamethoxazole were found in PS4, most of the pharmaceuticals were not present in PS5.	Aspirin	27-47	taste 2 receptor member 6 pseudogene	Homo sapiens	94-97
31273781-0	2019	Aspirin up-regulates suppressor of cytokine signaling 3 in glial cells via PPARalpha.	Aspirin	0-7	suppressor of cytokine signaling 3	Mus musculus	21-55
31273781-5	2019	This study underlines the importance of aspirin in upregulating SOCS3 in astrocytes and microglia.	Aspirin	40-47	suppressor of cytokine signaling 3	Mus musculus	64-69
31273781-6	2019	Aspirin increased the expression of Socs3 mRNA and protein in mouse astrocytes and BV-2 microglial cells in both a time- and dose-dependent manner.	Aspirin	0-7	suppressor of cytokine signaling 3	Mus musculus	36-41
31273781-7	2019	While investigating the mechanism, we found that Socs3 gene promoter harbors peroxisome proliferator response element and that aspirin up-regulated SOCS3 in astrocytes isolated from PPARbeta (-/-), but not PPARalpha (-/-), mice.	Aspirin	127-134	suppressor of cytokine signaling 3	Mus musculus	148-153
31273781-8	2019	Accordingly, aspirin increased SOCS3 in vivo in the cortex of wild type and PPARbeta (-/-), but not PPARalpha (-/-), mice.	Aspirin	13-20	suppressor of cytokine signaling 3	Mus musculus	31-36
31273781-9	2019	Similarly, aspirin treatment increased astroglial and microglial SOCS3 in the cortex of FAD5X, but not FAD5X/PPARalpha (-/-), mice.	Aspirin	11-18	suppressor of cytokine signaling 3	Mus musculus	65-70
31273781-10	2019	Finally, recruitment of PPARalpha by aspirin to the proximal, but not distal, peroxisome proliferator response element of the Socs3 promoter suggests that aspirin increases the transcription of Socs3 gene via PPARalpha.	Aspirin	37-44	suppressor of cytokine signaling 3	Mus musculus	126-131
31273781-10	2019	Finally, recruitment of PPARalpha by aspirin to the proximal, but not distal, peroxisome proliferator response element of the Socs3 promoter suggests that aspirin increases the transcription of Socs3 gene via PPARalpha.	Aspirin	37-44	suppressor of cytokine signaling 3	Mus musculus	194-199
31273781-10	2019	Finally, recruitment of PPARalpha by aspirin to the proximal, but not distal, peroxisome proliferator response element of the Socs3 promoter suggests that aspirin increases the transcription of Socs3 gene via PPARalpha.	Aspirin	155-162	suppressor of cytokine signaling 3	Mus musculus	126-131
31273781-10	2019	Finally, recruitment of PPARalpha by aspirin to the proximal, but not distal, peroxisome proliferator response element of the Socs3 promoter suggests that aspirin increases the transcription of Socs3 gene via PPARalpha.	Aspirin	155-162	suppressor of cytokine signaling 3	Mus musculus	194-199
31273781-11	2019	This study describes a novel property of aspirin in elevating SOCS3 in glial cells via PPARalpha and suggests that aspirin may be further considered for therapeutic application in neuroinflammatory and neurodegenerative disorders.	Aspirin	41-48	suppressor of cytokine signaling 3	Mus musculus	62-67
31322841-11	2019	Seven clusters were identified among patients where the highest NMDE Cystatin-2 levels clustered with asthma, tissue eosinophilia, and aspirin-exacerbated respiratory disease (AERD).	Aspirin	135-142	cystatin SA	Homo sapiens	69-79
31278071-0	2019	Aspirin targets P4HA2 through inhibiting NF-kappaB and LMCD1-AS1/let-7g to inhibit tumour growth and collagen deposition in hepatocellular carcinoma.	Aspirin	0-7	LIM and cysteine rich domains 1	Homo sapiens	55-60
31278071-0	2019	Aspirin targets P4HA2 through inhibiting NF-kappaB and LMCD1-AS1/let-7g to inhibit tumour growth and collagen deposition in hepatocellular carcinoma.	Aspirin	0-7	microRNA let-7g	Homo sapiens	65-71
31278071-6	2019	A mouse xenograft model, cell viability assay, colony formation assay, and immunohistochemistry analysis were used to evaluate the anti-fibrosis effect of aspirin through targeting the NF-kappaB/P4HA2 axis and LMCD1-AS1/let-7g/P4HA2 axis in vitro and in vivo.	Aspirin	155-162	LIM and cysteine-rich domains 1	Mus musculus	210-215
31278071-6	2019	A mouse xenograft model, cell viability assay, colony formation assay, and immunohistochemistry analysis were used to evaluate the anti-fibrosis effect of aspirin through targeting the NF-kappaB/P4HA2 axis and LMCD1-AS1/let-7g/P4HA2 axis in vitro and in vivo.	Aspirin	155-162	microRNA let7g	Mus musculus	220-226
30187283-5	2019	Accordingly, oral administration of aspirin increased the expression of TH in the nigra and upregulated the level of DA in striatum of normal C57/BL6 mice and aged A53T alpha-syn transgenic mice.	Aspirin	36-43	synuclein, alpha	Mus musculus	169-178
31193169-9	2019	In addition, bone-related protein OCN and RUNX2, and Smad2/3 phosphorylation was upregulated after ASA VI treatment in ADSCs.	Aspirin	99-102	SMAD family member 2	Rattus norvegicus	53-60
30388256-13	2019	Regular use of NSAIDs and aspirin may be more strongly associated with risk reduction of MSI-high CRC without KRAS or BRAF mutation.	Aspirin	26-33	B-Raf proto-oncogene, serine/threonine kinase	Rattus norvegicus	118-122
29512148-5	2019	Aspirin permanently inhibits platelet COX-1, underlying its anti-thrombotic and anti-cancer action.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	38-43
31939218-5	2019	In most organometallic ASA derivatives, the original ability for COX-1/2 acetylation persists, yet the acetylation sites are modified in comparison to that triggered by ASA itself.	Aspirin	23-26	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	65-70
31090331-4	2019	Through the study of network pharmacology,12 components of aspirin and Trichosanthis Fructus,including hydroxygenkwanin,quercetin and adenosine,were found to show the anti-platelet aggregation and anti-thrombosis mechanisms through9 common protein targets,such as SRC,RAC1,MAPK14,MAPK1,AKT1,and 14 common signaling pathways,such as VEGF signaling pathway.	Aspirin	59-66	vascular endothelial growth factor A	Rattus norvegicus	332-336
31090331-5	2019	After the intervention with Trichosanthis Fructus pellets combined with aspirin pellets,the vascular endothslia growth factor(VEGF) signaling pathway can be activated to inhibit platelet aggregation and improve vascular endothelial function,and show the anti-platelet aggregation and anti-thrombosis mechanisms,which verify the results of the network pharmacology,and explain the anti-platelet aggregation and anti-thrombotic mechanisms of the combination of Trichosanthis Fructus pellets with aspirin pellets.	Aspirin	72-79	vascular endothelial growth factor A	Rattus norvegicus	126-130
31090331-5	2019	After the intervention with Trichosanthis Fructus pellets combined with aspirin pellets,the vascular endothslia growth factor(VEGF) signaling pathway can be activated to inhibit platelet aggregation and improve vascular endothelial function,and show the anti-platelet aggregation and anti-thrombosis mechanisms,which verify the results of the network pharmacology,and explain the anti-platelet aggregation and anti-thrombotic mechanisms of the combination of Trichosanthis Fructus pellets with aspirin pellets.	Aspirin	494-501	vascular endothelial growth factor A	Rattus norvegicus	126-130
30737317-11	2019	Inhibition of COX-1 by low-dose aspirin prevents thrombosis.	Aspirin	32-39	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	14-19
30701538-1	2019	Several clinical studies indicated that the daily use of aspirin or acetylsalicylic acid reduces the cancer risk via cyclooxygenases (Cox-1 and Cox-2) inhibition.	Aspirin	57-64	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	134-139
30701538-1	2019	Several clinical studies indicated that the daily use of aspirin or acetylsalicylic acid reduces the cancer risk via cyclooxygenases (Cox-1 and Cox-2) inhibition.	Aspirin	68-88	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	134-139
31424405-0	2019	PPARalpha Between Aspirin and Plaque Clearance.	Aspirin	18-25	peroxisome proliferator activated receptor alpha	Homo sapiens	0-9
31424405-7	2019	This review delineates such functions of aspirin and analyzes underlying mechanisms that involve peroxisome proliferator-activated receptor alpha (PPARalpha)-mediated transcription of transcription factor EB (TFEB), the master regulator of lysosomal biogenesis.	Aspirin	41-48	peroxisome proliferator activated receptor alpha	Homo sapiens	147-156
30537987-11	2018	AMPK activation by aspirin and metformin effectively abrogated the statin-induced aberrant upregulation of HMGCR and sensitized these resistant cells to fluvastatin.	Aspirin	19-26	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	107-112
30482850-5	2018	The effects of aspirin required the presence of CD25+FoxP3+ Tregs Aspirin increased the amounts of Foxp3 and interleukin-4 (IL-4) in T cells and suppressed the differentiation of naive T cells into T helper 17 (TH17) and TH1 cells.	Aspirin	15-22	forkhead box P3	Mus musculus	99-104
30482850-5	2018	The effects of aspirin required the presence of CD25+FoxP3+ Tregs Aspirin increased the amounts of Foxp3 and interleukin-4 (IL-4) in T cells and suppressed the differentiation of naive T cells into T helper 17 (TH17) and TH1 cells.	Aspirin	15-22	interleukin 4	Mus musculus	109-122
30482850-5	2018	The effects of aspirin required the presence of CD25+FoxP3+ Tregs Aspirin increased the amounts of Foxp3 and interleukin-4 (IL-4) in T cells and suppressed the differentiation of naive T cells into T helper 17 (TH17) and TH1 cells.	Aspirin	15-22	interleukin 4	Mus musculus	124-128
30482850-5	2018	The effects of aspirin required the presence of CD25+FoxP3+ Tregs Aspirin increased the amounts of Foxp3 and interleukin-4 (IL-4) in T cells and suppressed the differentiation of naive T cells into T helper 17 (TH17) and TH1 cells.	Aspirin	66-73	forkhead box P3	Mus musculus	53-58
30482850-5	2018	The effects of aspirin required the presence of CD25+FoxP3+ Tregs Aspirin increased the amounts of Foxp3 and interleukin-4 (IL-4) in T cells and suppressed the differentiation of naive T cells into T helper 17 (TH17) and TH1 cells.	Aspirin	66-73	forkhead box P3	Mus musculus	99-104
30482850-5	2018	The effects of aspirin required the presence of CD25+FoxP3+ Tregs Aspirin increased the amounts of Foxp3 and interleukin-4 (IL-4) in T cells and suppressed the differentiation of naive T cells into T helper 17 (TH17) and TH1 cells.	Aspirin	66-73	interleukin 4	Mus musculus	109-122
30482850-5	2018	The effects of aspirin required the presence of CD25+FoxP3+ Tregs Aspirin increased the amounts of Foxp3 and interleukin-4 (IL-4) in T cells and suppressed the differentiation of naive T cells into T helper 17 (TH17) and TH1 cells.	Aspirin	66-73	interleukin 4	Mus musculus	124-128
30126026-0	2018	Epithelial folliculin enhances airway inflammation in aspirin-exacerbated respiratory disease.	Aspirin	54-61	folliculin	Homo sapiens	11-21
30392302-7	2018	Conclusions: Clavien-Dindo score is feasible to be applied in management of patients with LPD.ASA score, texture of pancreas, and intraoperative blood transfusion were independently associated with postoperative complications.	Aspirin	94-97	acyl-CoA synthetase bubblegum family member 1	Homo sapiens	90-93
30370665-0	2018	Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in growth hormone treated animals.	Aspirin	0-7	insulin receptor substrate 1	Homo sapiens	43-71
30370665-6	2018	Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in growth hormone treated animals.	Aspirin	0-7	insulin receptor substrate 1	Homo sapiens	43-71
30015780-11	2018	MiR-26b was found significantly down-regulated in patients on ASA treatment as compared to control group (P &lt; 0.005) and this was validated by RealTime PCR.	Aspirin	62-65	microRNA 26b	Homo sapiens	0-7
30015780-14	2018	CONCLUSION: We found that miR-26b is down-regulated in platelets in patients on chronic ASA treatment.	Aspirin	88-91	microRNA 26b	Homo sapiens	26-33
30015780-16	2018	Thus, miR-26b seems to be involved in MRP4 modulation and may contribute to ASA resistance.	Aspirin	76-79	microRNA 26b	Homo sapiens	6-13
29857294-12	2018	The higher expression of VEGFA in aspirin + PNS group verified the predicted potential protective targets of PNS.	Aspirin	34-41	vascular endothelial growth factor A	Rattus norvegicus	25-30
29857294-13	2018	CONCLUSIONS: PNS may have protective function for aspirin-induced gastrointestinal injury through increasing VEGFA expression.	Aspirin	50-57	vascular endothelial growth factor A	Rattus norvegicus	109-114
29052493-0	2018	Impaired liver cytochrome P450 2C11 activity after dual antiplatelet therapy with aspirin and clopidogrel in rats.	Aspirin	82-89	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	15-35
29052493-8	2018	After two-week DAPT with ASA and CLP in rats, the activities of aspirin esterase and rCyp2c11, enzymes mediating rat metabolism of ASA and CLP, respectively, in prepared rat liver microsomes were measured followed by further determination of rCyp2c11 mRNA expressions.	Aspirin	131-134	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	85-93
30154452-8	2018	Finally, several anti-inflammatory drugs, including resveratrol, aspirin, vitamin E and ursolic acid, significantly increased the levels of the HIPK2 mRNA and protein by modulating promoter activity and the 3"-UTR stability of the HIPK2 gene.	Aspirin	65-72	homeodomain interacting protein kinase 2	Mus musculus	144-149
30154452-8	2018	Finally, several anti-inflammatory drugs, including resveratrol, aspirin, vitamin E and ursolic acid, significantly increased the levels of the HIPK2 mRNA and protein by modulating promoter activity and the 3"-UTR stability of the HIPK2 gene.	Aspirin	65-72	homeodomain interacting protein kinase 2	Mus musculus	231-236
29942487-0	2018	Aspirin inhibited the metastasis of colon cancer cells by inhibiting the expression of toll-like receptor 4.	Aspirin	0-7	toll like receptor 4	Homo sapiens	87-107
28948649-0	2018	Association of GPIa and COX-2 gene polymorphism with aspirin resistance.	Aspirin	53-60	multimerin 1	Homo sapiens	15-19
28948649-1	2018	OBJECTIVE: This study aimed to explore the association between GPIa, COX-2 gene polymorphisms and aspirin resistance in the ischemic stroke patients from the southern part of Jiangsu province.	Aspirin	98-105	multimerin 1	Homo sapiens	63-67
31972198-5	2020	The findings obtained by RT-PCR and western blotting indicated that KF could suppress aspirin-induced NF-kappaB activation via stabilization of IkappaB-alpha and thereby induced the downregulation of COX-2 and iNOS.	Aspirin	86-93	cox2	Saccharina sculpera	200-205
31792942-4	2020	Surprisingly, we found a very low PAC-1 binding capacity in MPN patients; however, the expression of PAC-1 was almost completely recovered with aspirin intake.	Aspirin	144-151	ADCYAP receptor type I	Homo sapiens	101-106
32521895-1	2020	PURPOSE: To explore the effects of aspirin (ASP) on the proliferation and apoptosis of HepG2 hepatocellular carcinoma (HCC) cells via the Wnt/beta-catenin signaling pathway.	Aspirin	35-42	catenin beta 1	Homo sapiens	142-154
32521895-1	2020	PURPOSE: To explore the effects of aspirin (ASP) on the proliferation and apoptosis of HepG2 hepatocellular carcinoma (HCC) cells via the Wnt/beta-catenin signaling pathway.	Aspirin	44-47	catenin beta 1	Homo sapiens	142-154
32521895-8	2020	The expression levels of TCF4 and LEF1, key molecules of the Wnt/beta-catenin signaling pathway, were lowered in HCC cells treated with 4 mM ASP, and the nuclear translocation of beta-catenin was weakened.	Aspirin	141-144	catenin beta 1	Homo sapiens	65-77
32521895-8	2020	The expression levels of TCF4 and LEF1, key molecules of the Wnt/beta-catenin signaling pathway, were lowered in HCC cells treated with 4 mM ASP, and the nuclear translocation of beta-catenin was weakened.	Aspirin	141-144	catenin beta 1	Homo sapiens	179-191
32521895-9	2020	The beta-catenin activator exerted a negative influence on the anticancer effect of ASP.	Aspirin	84-87	catenin beta 1	Homo sapiens	4-16
32521895-10	2020	CONCLUSIONS: ASP inhibits the proliferation and promotes the apoptosis of HCC cells through the Wnt/beta-catenin signaling pathway.	Aspirin	13-16	catenin beta 1	Homo sapiens	100-112
31608617-11	2020	The group co-administered with DHEA and aspirin showed significant increases in SOD, GST, CAT, GSH, Progesterone, Ca2+ ATPase, Na+ ATPase, H+ ATPase and significant reduction (p<0.05) in malondialdehyde, VEGF, TNF-alpha and estrogen as compared with the DHEA group.	Aspirin	40-47	hematopoietic prostaglandin D synthase	Rattus norvegicus	85-88
31608617-11	2020	The group co-administered with DHEA and aspirin showed significant increases in SOD, GST, CAT, GSH, Progesterone, Ca2+ ATPase, Na+ ATPase, H+ ATPase and significant reduction (p<0.05) in malondialdehyde, VEGF, TNF-alpha and estrogen as compared with the DHEA group.	Aspirin	40-47	vascular endothelial growth factor A	Rattus norvegicus	204-208
31608617-12	2020	The histopathological analysis showed reductions in cystic fibrosis, atretic ovaries, increased expression of Bcl-2 and E- Cadherin and reduced Bax expression in the group that received Aspirin and DHEA.	Aspirin	186-193	cadherin 1	Rattus norvegicus	120-131
31608617-12	2020	The histopathological analysis showed reductions in cystic fibrosis, atretic ovaries, increased expression of Bcl-2 and E- Cadherin and reduced Bax expression in the group that received Aspirin and DHEA.	Aspirin	186-193	BCL2 associated X, apoptosis regulator	Rattus norvegicus	144-147
31963688-0	2020	Aspirin Enhances the Protection of Hsp90 from Heat-Stressed Injury in Cardiac Microvascular Endothelial Cells Through PI3K-Akt and PKM2 Pathways.	Aspirin	0-7	heat shock protein 90 alpha family class A member 1	Homo sapiens	35-40
31963688-0	2020	Aspirin Enhances the Protection of Hsp90 from Heat-Stressed Injury in Cardiac Microvascular Endothelial Cells Through PI3K-Akt and PKM2 Pathways.	Aspirin	0-7	pyruvate kinase M1/2	Homo sapiens	131-135
31963688-9	2020	ASA treatment of CMVECs induced a significant expression of Hsp90, which promoted both Akt and PKM2 signals, which are beneficial for relieving HS damage and maintaining the function of CMVECs.	Aspirin	0-3	heat shock protein 90 alpha family class A member 1	Homo sapiens	60-65
31963688-9	2020	ASA treatment of CMVECs induced a significant expression of Hsp90, which promoted both Akt and PKM2 signals, which are beneficial for relieving HS damage and maintaining the function of CMVECs.	Aspirin	0-3	pyruvate kinase M1/2	Homo sapiens	95-99
31963688-11	2020	To the best of our knowledge, this is the first study to show that HS damages CMVECs and the protection mechanism of Hsp90 on it, and that ASA provides a new potential strategy for regulating cardiac microcirculation preventing HS-induced heart failure.	Aspirin	139-142	heat shock protein 90 alpha family class A member 1	Homo sapiens	117-122
31622780-6	2020	Moreover, the released aspirin triggered by the immunoregulatory cytokine IFN-gamma is able to inhibit inflammation in a rat model, and the release of aspirin can be quantitatively controlled.	Aspirin	23-30	interferon gamma	Rattus norvegicus	74-83
31622780-6	2020	Moreover, the released aspirin triggered by the immunoregulatory cytokine IFN-gamma is able to inhibit inflammation in a rat model, and the release of aspirin can be quantitatively controlled.	Aspirin	151-158	interferon gamma	Rattus norvegicus	74-83
31805984-12	2019	DC osteoclast differentiation was modulated by aspirin via the nuclear factor kappa B (NF-kappaB)/nuclear factor of activated T cell, cytoplasmic 1 (NFATc1) signaling pathway.	Aspirin	47-54	nuclear factor of activated T-cells 1	Rattus norvegicus	149-155
31805984-14	2019	CONCLUSIONS: Aspirin inhibited RANKL-induced OC differentiation in DCs via the NF-kappaB pathway, downregulating expression of NFATc1.	Aspirin	13-20	nuclear factor of activated T-cells 1	Rattus norvegicus	127-133
31511539-1	2019	The aim of this study was to investigate the association among the PlA1/A2 gene polymorphism, laboratory aspirin resistance and adverse clinical outcomes in coronary artery disease (CAD) patients who were on aspirin maintainance therapy.	Aspirin	105-112	POU class 2 homeobox 3	Homo sapiens	67-71
31511539-1	2019	The aim of this study was to investigate the association among the PlA1/A2 gene polymorphism, laboratory aspirin resistance and adverse clinical outcomes in coronary artery disease (CAD) patients who were on aspirin maintainance therapy.	Aspirin	208-215	POU class 2 homeobox 3	Homo sapiens	67-71
28403626-10	2019	In patients with ACS treated with aspirin and clopidogrel, residual platelet aggregation was significantly reduced 20 min after intravenous bolus of 1 mg/kg pegnivacogin (100% versus 43.21+-8.23%, p=0.020).	Aspirin	34-41	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	17-20
31248980-6	2019	We found that the specific deletion of COX-1 in platelets, which recapitulated the human pharmacodynamics of low-dose aspirin, that is, suppression of platelet thromboxane (TX)A2 production associated with substantial sparing of the systemic production of prostacyclin, resulted in milder symptoms of colitis, in the acute phase, and almost complete recovery from the disease after DSS withdrawal.	Aspirin	118-125	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	39-44
31248980-11	2019	Through the generation of a mouse with specific deletion of cyclooxygenase-1 in megakaryocytes/platelets, which recapitulates the human pharmacodynamics of low-dose aspirin, we demonstrate the important role of platelet-derived thromboxane A2 in the development of experimental colitis and fibrosis, thus providing the rationale to investigate the potential efficacy of low-dose aspirin in limiting the inflammation and tissue damage associated with IBD.	Aspirin	165-172	prostaglandin-endoperoxide synthase 1	Mus musculus	60-76
31248980-11	2019	Through the generation of a mouse with specific deletion of cyclooxygenase-1 in megakaryocytes/platelets, which recapitulates the human pharmacodynamics of low-dose aspirin, we demonstrate the important role of platelet-derived thromboxane A2 in the development of experimental colitis and fibrosis, thus providing the rationale to investigate the potential efficacy of low-dose aspirin in limiting the inflammation and tissue damage associated with IBD.	Aspirin	379-386	prostaglandin-endoperoxide synthase 1	Mus musculus	60-76
31243131-7	2019	Furthermore, acetylsalicylic acid (ASA), a potent inhibitor of the NF-kappaB activator kinase IkappaB kinase beta (IKK-beta), did not significantly diminish reactivation in a primary CD4+ T central memory (TCM) cell latency model.	Aspirin	13-33	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	94-113
31243131-7	2019	Furthermore, acetylsalicylic acid (ASA), a potent inhibitor of the NF-kappaB activator kinase IkappaB kinase beta (IKK-beta), did not significantly diminish reactivation in a primary CD4+ T central memory (TCM) cell latency model.	Aspirin	13-33	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	115-123
31243131-7	2019	Furthermore, acetylsalicylic acid (ASA), a potent inhibitor of the NF-kappaB activator kinase IkappaB kinase beta (IKK-beta), did not significantly diminish reactivation in a primary CD4+ T central memory (TCM) cell latency model.	Aspirin	35-38	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	94-113
31243131-7	2019	Furthermore, acetylsalicylic acid (ASA), a potent inhibitor of the NF-kappaB activator kinase IkappaB kinase beta (IKK-beta), did not significantly diminish reactivation in a primary CD4+ T central memory (TCM) cell latency model.	Aspirin	35-38	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	115-123
31103824-9	2019	In the uterus, quercetin supplement to aspirin prevented the expression of VEGF and sFlt-1 mRNA.	Aspirin	39-46	vascular endothelial growth factor A	Rattus norvegicus	75-79
30768153-3	2019	This study sought to investigate whether homozygous GUCY1A3 (rs7692387) risk allele carriers display higher on-aspirin platelet reactivity and risk of ischaemic events early after coronary intervention.	Aspirin	111-118	guanylate cyclase 1 soluble subunit alpha 1	Homo sapiens	52-59
30768153-4	2019	METHODS AND RESULTS: The association of GUCY1A3 genotype and on-aspirin platelet reactivity was analysed in the genetics substudy of the ISAR-ASPI registry (n = 1678) using impedance aggregometry.	Aspirin	64-71	guanylate cyclase 1 soluble subunit alpha 1	Homo sapiens	40-47
30768153-6	2019	Homozygous GUCY1A3 risk allele carriers (GG) displayed increased on-aspirin platelet reactivity compared with non-risk allele (AA/AG) carriers [150 (interquartile range 91-209) vs. 134 (85-194) AU min, P &lt; 0.01].	Aspirin	68-75	guanylate cyclase 1 soluble subunit alpha 1	Homo sapiens	11-18
30768153-10	2019	CONCLUSION: We conclude that homozygous GUCY1A3 risk allele carriers are at increased risk of cardiovascular death or stent thrombosis within 30 days after coronary stenting, likely due to higher on-aspirin platelet reactivity.	Aspirin	199-206	guanylate cyclase 1 soluble subunit alpha 1	Homo sapiens	40-47
30585827-11	2019	Better hospital performance on SEP-1 was associated with higher rates of timely head CT interpretation for stroke patients (rho = 0.16; p < 0.001), more frequent aspirin administration for patients with chest pain or heart attacks (rho = 0.24; p < 0.001) and shorter median time to electrocardiogram for patients with chest pain (rho = -0.12; p < 0.001).	Aspirin	162-169	septin 1	Homo sapiens	31-36
31307465-8	2019	Inhibition of cyclooxygenase by ASA attenuated LPS-mediated P-selectin expression demonstrating that TLR4 signaling in platelets is partially dependent on TxA2 pathway.	Aspirin	32-35	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	14-28
30684314-0	2019	Co-expression of the aryl hydrocarbon receptor and estrogen receptor in the developing teeth of rat offspring after rat mothers" exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin and the protective action of alpha-tocopherol and acetylsalicylic acid.	Aspirin	227-247	estrogen receptor 1	Rattus norvegicus	51-68
30684314-8	2019	In the TCDD+E and TCDD+ASA groups, there was a weak or negative ER expression and slightly stronger expression of AhR than in the TCDD group.	Aspirin	23-26	estrogen receptor 1	Rattus norvegicus	64-66
31384532-0	2019	Aspirin alleviates endothelial gap junction dysfunction through inhibition of NLRP3 inflammasome activation in LPS-induced vascular injury.	Aspirin	0-7	NLR family, pyrin domain containing 3	Mus musculus	78-83
31384532-3	2019	We hypothesized that low-dose aspirin could ameliorate endothelial injury by inhibiting the activation of NLRP3 inflammasomes and ultimately prevent cardiovascular diseases.	Aspirin	30-37	NLR family, pyrin domain containing 3	Mus musculus	106-111
31384532-7	2019	We found that aspirin could inhibit NLRP3 inflammasome formation and activation in vitro in dose-dependent manner and has correlation between the NLRP3 inflammasome and the ROS/TXNIP pathway.	Aspirin	14-21	NLR family, pyrin domain containing 3	Mus musculus	36-41
31384532-7	2019	We found that aspirin could inhibit NLRP3 inflammasome formation and activation in vitro in dose-dependent manner and has correlation between the NLRP3 inflammasome and the ROS/TXNIP pathway.	Aspirin	14-21	NLR family, pyrin domain containing 3	Mus musculus	146-151
31384532-8	2019	We also found that low-concentration aspirin could inhibit the formation and activation of NLRP3 inflammasome and restore the expression of the endothelial tight junction protein zonula occludens-1/2 (ZO1/2).	Aspirin	37-44	NLR family, pyrin domain containing 3	Mus musculus	91-96
31384532-9	2019	We assume that aspirin can ameliorate the endothelial layer dysfunction by suppressing the activation of NLRP3 inflammasome.	Aspirin	15-22	NLR family, pyrin domain containing 3	Mus musculus	105-110
31571629-1	2019	Background & objectives: Cytochrome P450, P2Y 12, cyclooxygenase-1 (COX1) and glycoprotein V1 (GPVI) gene polymorphisms are known to affect patient responsiveness towards aspirin and clopidogrel dual antiplatelet therapy (DAPT).	Aspirin	171-178	glycoprotein VI platelet	Homo sapiens	95-99
31090213-0	2019	Use of aspirin in the prevention of colorectal cancer through TIGIT-CD155 pathway.	Aspirin	7-14	PVR cell adhesion molecule	Homo sapiens	68-73
30836126-10	2019	We report that the throughput efficiency of using ASA to automatically annotate images of Iba1 microglia is more than five times greater than that of manual stereology counts of the same sections.	Aspirin	50-53	induction of brown adipocytes 1	Mus musculus	90-94
30694883-1	2019	BACKGROUND: We previously found differences in the minor allele frequency (MAF) of single-nucleotide polymorphisms (SNPs) in transmembrane protein 196 (TMEM196) between 995 patients with aspirin-tolerant asthma (ATA) and 141 asthmatic patients with NSAID-exacerbated respiratory disease (NERD).	Aspirin	187-194	transmembrane protein 196	Homo sapiens	152-159
30913329-2	2019	Here, two cyclometalated IrIII complexes Ir2 and Ir3 formed by conjugation of Ir1 with two antiphlogistics (aspirin and salicylic acid) have been designed.	Aspirin	108-115	nischarin	Homo sapiens	78-81
30759486-0	2019	Aspirin-Dependent Effects on Purinergic P2Y1 Receptor Expression.	Aspirin	0-7	purinergic receptor P2Y1	Homo sapiens	40-44
30759486-3	2019	We hypothesized that recovery of ADP-induced platelet activation could be attributed to increased P2Y1 expression induced by chronic aspirin exposure.	Aspirin	133-140	purinergic receptor P2Y1	Homo sapiens	98-102
30759486-5	2019	DAMI cells treated with aspirin or WY14643 (PPARalpha agonist) had a significant up-regulation of P2Y1 mRNA, which was shown to be a PPARalpha-dependent process.	Aspirin	24-31	peroxisome proliferator activated receptor alpha	Homo sapiens	44-53
30759486-5	2019	DAMI cells treated with aspirin or WY14643 (PPARalpha agonist) had a significant up-regulation of P2Y1 mRNA, which was shown to be a PPARalpha-dependent process.	Aspirin	24-31	purinergic receptor P2Y1	Homo sapiens	98-102
30759486-5	2019	DAMI cells treated with aspirin or WY14643 (PPARalpha agonist) had a significant up-regulation of P2Y1 mRNA, which was shown to be a PPARalpha-dependent process.	Aspirin	24-31	peroxisome proliferator activated receptor alpha	Homo sapiens	133-142
30759486-6	2019	In human megakaryocytic progenitors, in the presence of aspirin or WY14643, P2Y1 mRNA expression was higher than in mock culture.	Aspirin	56-63	purinergic receptor P2Y1	Homo sapiens	76-80
30759486-7	2019	P2Y1 expression increased in platelets obtained from HVs treated with aspirin for 8 weeks.	Aspirin	70-77	purinergic receptor P2Y1	Homo sapiens	0-4
30759486-8	2019	Platelets obtained from patients who were on aspirin for more than 2 months had increased P2Y1 expression and ADP-induced aggregation compared with patients on aspirin treatment for less than a month.	Aspirin	45-52	purinergic receptor P2Y1	Homo sapiens	90-94
30759486-9	2019	Overall, our results suggest that aspirin induces genomic changes in megakaryocytes leading to P2Y1 up-regulation and that PPARalpha is the nuclear receptor involved in this regulation.	Aspirin	34-41	purinergic receptor P2Y1	Homo sapiens	95-99
30885738-8	2019	Additionally, significant increases in antioxidant enzymes and heat shock protein 70 localization in gastric tissue were evident following BV treatment after ASA exposure.	Aspirin	158-161	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	63-84
31008410-9	2019	Finally, we evaluated this protocol to detect the inhibition of PDMPs generation, washed platelets were incubated with acetylsalicylic acid (10 muM) and an inhibition of 7.7-fold in PDMPs generation for activation of TLR4 was found.	Aspirin	119-139	toll like receptor 4	Homo sapiens	217-221
30923029-0	2019	Omission of aspirin after ACS or stenting in patients with oral anticoagulation - why have the goalposts moved?	Aspirin	12-19	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	26-29
30720135-5	2019	The present authors proposed that aspirin, diaspirin and analogues, and diflunisal (a salicylic acid derivative) may rapidly perturb EGF and EGF receptor (EGFR) internalisation.	Aspirin	34-41	epidermal growth factor	Homo sapiens	133-136
30720135-9	2019	These findings may also have implications in understanding the inhibitory effect of aspirin and salicylates on wound healing, given the critical role of EGF in the response to tissue trauma.	Aspirin	84-91	epidermal growth factor	Homo sapiens	153-156
31013226-0	2019	The Effect of Aspirin as an Irreversible COX1 Inhibitor in Preventing Non-Valvular Atrial Fibrillation After Coronary Bypass Surgery.	Aspirin	14-21	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	41-45
31013226-1	2019	BACKGROUND: We investigated whether the use of aspirin (irreversible COX1 inhibitor) in the preoperative period may prevent non-valvular atrial fibrillation, which is the most common rhythm problem in the postoperative period.	Aspirin	47-54	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	69-73
30799039-3	2019	Here we report that acetylation inhibits cGAS activation and that the enforced acetylation of cGAS by aspirin robustly suppresses self-DNA-induced autoimmunity.	Aspirin	102-109	cyclic GMP-AMP synthase	Homo sapiens	94-98
30799039-6	2019	Importantly, we show that aspirin can directly acetylate cGAS and efficiently inhibit cGAS-mediated immune responses.	Aspirin	26-33	cyclic GMP-AMP synthase	Homo sapiens	57-61
30799039-6	2019	Importantly, we show that aspirin can directly acetylate cGAS and efficiently inhibit cGAS-mediated immune responses.	Aspirin	26-33	cyclic GMP-AMP synthase	Homo sapiens	86-90
30240925-0	2019	A high glucose level is associated with decreased aspirin-mediated acetylation of platelet cyclooxygenase (COX)-1 at serine 529: A pilot study.	Aspirin	50-57	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	91-113
29890239-1	2019	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is characterized by asthma, recurrent nasal polyposis, and respiratory reactions on ingestion of COX-1 inhibitors.	Aspirin	12-19	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	156-161
30406348-2	2019	Non-selective non-steroidal anti-inflammatory drugs (NSAIDs) are known to interfere with the antiplatelet effect of aspirin through competitive binding with COX-1.	Aspirin	116-123	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	157-162
30612679-6	2019	In conclusion, both HP and aspirin, as physiological and pharmacological inductors of HSP70, respectively, attenuate the carbohydrate-related disturbances in diabetic rats, with almost tendency to normalisation to the control values for most of the estimated parameters.	Aspirin	27-34	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	86-91
29461906-5	2019	The P-selectin Aspirin Test revealed substantial inhibition of platelet function in all but three of 96 patients receiving aspirin with clopidogrel and in none of 51 patients receiving aspirin and prasugrel.	Aspirin	123-130	selectin P	Homo sapiens	4-14
29461906-10	2019	The results obtained using the P-selectin P2Y12 Test in 102 patients taking aspirin and clopidogrel were similar to the more traditional approaches in that a wide scatter of results was obtained.	Aspirin	76-83	selectin P	Homo sapiens	31-41
28503981-5	2018	We found that aspirin plus prasugrel or aspirin plus ticagrelor inhibited platelet responses to multiple agonists and reduced P-selectin expression.	Aspirin	14-21	selectin P	Homo sapiens	126-136
28503981-5	2018	We found that aspirin plus prasugrel or aspirin plus ticagrelor inhibited platelet responses to multiple agonists and reduced P-selectin expression.	Aspirin	40-47	selectin P	Homo sapiens	126-136
29490275-6	2018	Accordingly, the pro-autophagic activity of aspirin and salicylate on the nematode Caenorhabditis elegans is lost when the expression of the EP300 ortholog cpb-1 is reduced.	Aspirin	44-51	Cytoplasmic polyadenylation element-binding protein 1	Caenorhabditis elegans	156-161
29282304-4	2018	Endogenously generated cysLTs induced eosinophilia and expanded group 2 innate lymphoid cells (ILC2s) in aspirin-exacerbated respiratory disease-like Ptges-/- mice.	Aspirin	105-112	prostaglandin E synthase	Mus musculus	150-155
29282304-9	2018	Pharmacological blockade of CysLT2R prior to inhalation challenge of Ptges-/- mice with aspirin blocked IL-33-dependent mast cell activation, mediator release, and changes in lung function.	Aspirin	88-95	prostaglandin E synthase	Mus musculus	69-74
29375570-5	2017	These findings suggest that consumption of low doses of aspirin reduces the risk of atherosclerosis complications as well as reducing PLT aggregation by the inhibition of COX-1.	Aspirin	56-63	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	171-176
29079505-7	2018	Finally, small molecule inhibitors of IKK-activity, including Aspirin, inhibited the accumulation of activated IKK proteins in the AIS.	Aspirin	62-69	component of inhibitor of nuclear factor kappa B kinase complex	Rattus norvegicus	38-41
29079505-7	2018	Finally, small molecule inhibitors of IKK-activity, including Aspirin, inhibited the accumulation of activated IKK proteins in the AIS.	Aspirin	62-69	component of inhibitor of nuclear factor kappa B kinase complex	Rattus norvegicus	111-114
29635252-10	2018	CONCLUSIONS: Our findings suggest that PEAR1, P2Y12, and UGT2A1 genetic variants may be potential biomarkers that can be used to guide clinical applications of clopidogrel and aspirin in Chinese patients.	Aspirin	176-183	UDP glucuronosyltransferase family 2 member A1 complex locus	Homo sapiens	57-63
29195233-5	2018	We show herein that, ASA-BMMSCs treatment reduced inflammatory infiltration and alveolar bone loss in periodontitis rats, reflected by immunohistochemistry staining of OPG/RANK-L and Micro-CT. Levels of TNF-alpha and IL-17 decreased while IL-10 increased after the treatment of ASA-BMMSCs in periodontitis rats.	Aspirin	21-24	interleukin 17A	Rattus norvegicus	217-222
29195233-5	2018	We show herein that, ASA-BMMSCs treatment reduced inflammatory infiltration and alveolar bone loss in periodontitis rats, reflected by immunohistochemistry staining of OPG/RANK-L and Micro-CT. Levels of TNF-alpha and IL-17 decreased while IL-10 increased after the treatment of ASA-BMMSCs in periodontitis rats.	Aspirin	21-24	interleukin 10	Rattus norvegicus	239-244
29075787-8	2017	Immunoblotting experiments showed that aspirin acetylated CDK1, and pre-incubation with salicylic acid and its derivatives prevented aspirin-mediated CDK1 acetylation, which supported the data obtained from molecular docking studies.	Aspirin	39-46	cyclin dependent kinase 1	Homo sapiens	58-62
29075787-8	2017	Immunoblotting experiments showed that aspirin acetylated CDK1, and pre-incubation with salicylic acid and its derivatives prevented aspirin-mediated CDK1 acetylation, which supported the data obtained from molecular docking studies.	Aspirin	133-140	cyclin dependent kinase 1	Homo sapiens	150-154
29142602-11	2017	Treatment of MKN45 cells with aspirin reduced the levels of phosphorylated AKT by activating PPARalpha, whereas treatment with apatinib inhibited the phosphorylation of vascular endothelial growth factor receptor 2 and phosphoinositide-3 kinase in MKN45 cells.	Aspirin	30-37	peroxisome proliferator activated receptor alpha	Homo sapiens	93-102
28082531-13	2017	However, aspirin reduced pulmonary neutrophilia and tissue damaging neutrophil proteases (Matrix Metalloproteinase (MMP)-8/-9), reduced BAL concentrations of tumour necrosis factor alpha and reduced systemic and pulmonary TXB2.	Aspirin	9-16	matrix metallopeptidase 8	Homo sapiens	90-122
28975318-0	2017	In PCI-treated ACS, switching from aspirin + a newer P2Y12 blocker to aspirin + clopidogrel reduced adverse events.	Aspirin	35-42	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	15-18
28975318-0	2017	In PCI-treated ACS, switching from aspirin + a newer P2Y12 blocker to aspirin + clopidogrel reduced adverse events.	Aspirin	70-77	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	15-18
28912509-4	2017	We found that ASA could downregulate the expressions of iNOS and TNF-alpha both in mouse peritoneum macrophages and RAW264.7 cells induced by LPS via the IkappaK/IkappaB/NF-kappaB pathway and a COX2/PGE2/EP2/NF-kappaB feedback loop, without affecting the expressions of FIZZ/YM-1/ARG1 induced by IL-4.	Aspirin	14-17	interleukin 4	Mus musculus	296-300
28835710-0	2017	Aspirin metabolite sodium salicylate selectively inhibits transcriptional activity of ATF6alpha and downstream target genes.	Aspirin	0-7	activating transcription factor 6	Homo sapiens	86-95
28835710-2	2017	In this work we describe ATF6alpha as a newly target of the aspirin metabolite sodium salicylate (NaSal).	Aspirin	60-67	activating transcription factor 6	Homo sapiens	25-34
28139830-2	2017	We aimed to compare the effects of low-dose aspirin (100 mg/day for 7 days) given to 40 individuals undergoing CRC screening on the extent of cyclooxygenase (COX)-1 acetylation at serine-529 (AceCOX-1), in blood platelets vs. colorectal mucosa, at 7 (group 1) and 24 h (group 2) after dosing.	Aspirin	44-51	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	142-164
28139830-6	2017	These findings demonstrate that low-dose aspirin produces long-lasting acetylation of COX-1 and downregulation of p-S6 in human colorectal mucosa, an effect that may interfere with early colorectal carcinogenesis.	Aspirin	41-48	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	86-91
28713783-9	2017	Furthermore, pre-administration of aspirin in mice intravenously injected with SlaA attenuated the transcriptional abundance of ICAM1 and VCAM1 in the aorta.	Aspirin	35-42	vascular cell adhesion molecule 1	Mus musculus	138-143
29798643-7	2017	The ASA in all directions was significantly decreased in the DDH group when compared with the values in the control group ( P&lt;0.05).	Aspirin	4-7	aldo-keto reductase family 1 member C1	Homo sapiens	61-64
28346830-7	2017	A combination of DHA and ASA efficiently enhanced heterodimer formations of PPARalpha and RXRalpha and increased the expression of neurotrophic factors PSD-95, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF), while inhibiting NFkappaB and COX2.	Aspirin	25-28	peroxisome proliferator activated receptor alpha	Homo sapiens	76-85
28346830-8	2017	These findings suggest that a combination of DHA and ASA could significantly improve the expression of PSD-95, BDNF, and GDNF by promoting heterodimerization of PPARalpha and RXRalpha, thus supplying a new therapeutic method for PD.	Aspirin	53-56	peroxisome proliferator activated receptor alpha	Homo sapiens	161-170
28406723-0	2017	Aspirin Use and Colorectal Cancer Survival According to Tumor CD274 (Programmed Cell Death 1 Ligand 1) Expression Status.	Aspirin	0-7	CD274 molecule	Homo sapiens	62-67
28406723-0	2017	Aspirin Use and Colorectal Cancer Survival According to Tumor CD274 (Programmed Cell Death 1 Ligand 1) Expression Status.	Aspirin	0-7	CD274 molecule	Homo sapiens	69-101
28406723-3	2017	We hypothesized that the survival benefit associated with aspirin might be stronger in colorectal carcinoma with a lower CD274 (PDCD1 ligand 1, PD-L1) expression level that resulted in lower signaling of the immune checkpoint pathway.	Aspirin	58-65	CD274 molecule	Homo sapiens	121-126
28406723-3	2017	We hypothesized that the survival benefit associated with aspirin might be stronger in colorectal carcinoma with a lower CD274 (PDCD1 ligand 1, PD-L1) expression level that resulted in lower signaling of the immune checkpoint pathway.	Aspirin	58-65	CD274 molecule	Homo sapiens	128-142
28406723-3	2017	We hypothesized that the survival benefit associated with aspirin might be stronger in colorectal carcinoma with a lower CD274 (PDCD1 ligand 1, PD-L1) expression level that resulted in lower signaling of the immune checkpoint pathway.	Aspirin	58-65	CD274 molecule	Homo sapiens	144-149
28406723-6	2017	Results The association of postdiagnosis aspirin use with colorectal cancer-specific survival differed by CD274 expression status ( Pinteraction &lt; .001); compared with aspirin nonusers; multivariable-adjusted hazard ratios for regular aspirin users were 0.16 (95% CI, 0.06 to 0.41) in patients with low CD274 and 1.01 (95% CI, 0.61 to 1.67) in patients with high CD274.	Aspirin	41-48	CD274 molecule	Homo sapiens	106-111
28406723-6	2017	Results The association of postdiagnosis aspirin use with colorectal cancer-specific survival differed by CD274 expression status ( Pinteraction &lt; .001); compared with aspirin nonusers; multivariable-adjusted hazard ratios for regular aspirin users were 0.16 (95% CI, 0.06 to 0.41) in patients with low CD274 and 1.01 (95% CI, 0.61 to 1.67) in patients with high CD274.	Aspirin	41-48	CD274 molecule	Homo sapiens	306-311
28406723-6	2017	Results The association of postdiagnosis aspirin use with colorectal cancer-specific survival differed by CD274 expression status ( Pinteraction &lt; .001); compared with aspirin nonusers; multivariable-adjusted hazard ratios for regular aspirin users were 0.16 (95% CI, 0.06 to 0.41) in patients with low CD274 and 1.01 (95% CI, 0.61 to 1.67) in patients with high CD274.	Aspirin	41-48	CD274 molecule	Homo sapiens	306-311
27942866-9	2017	Vitamin E, levamisole, ASA, and ASA plus vitamin E inhibited AhR and COX-2 expression in embryos after 7 days and decreased AhR and COX-2 expression in embryos after 13 days.	Aspirin	23-26	aryl hydrocarbon receptor 1 alpha	Gallus gallus	61-64
27942866-9	2017	Vitamin E, levamisole, ASA, and ASA plus vitamin E inhibited AhR and COX-2 expression in embryos after 7 days and decreased AhR and COX-2 expression in embryos after 13 days.	Aspirin	23-26	aryl hydrocarbon receptor 1 alpha	Gallus gallus	124-127
27942866-9	2017	Vitamin E, levamisole, ASA, and ASA plus vitamin E inhibited AhR and COX-2 expression in embryos after 7 days and decreased AhR and COX-2 expression in embryos after 13 days.	Aspirin	32-35	aryl hydrocarbon receptor 1 alpha	Gallus gallus	61-64
27942866-9	2017	Vitamin E, levamisole, ASA, and ASA plus vitamin E inhibited AhR and COX-2 expression in embryos after 7 days and decreased AhR and COX-2 expression in embryos after 13 days.	Aspirin	32-35	aryl hydrocarbon receptor 1 alpha	Gallus gallus	124-127
28338108-10	2017	CONCLUSION: Patients with non-variceal UGIB caused by the use of NSAIDs or low-dose aspirin are more frequent carriers of the VKORC1 -1639 G&gt;A AA genotype, as compared to those without UGIB.	Aspirin	84-91	vitamin K epoxide reductase complex subunit 1	Homo sapiens	126-132
28168001-11	2017	Rats treated with TRCQT alone or in combination with aspirin showed decreased apoptosis by a reduction in the number of TUNEL positive cells, which inhibited the expression of activated caspase-3 (P = 0.038) and Bax (P = 0.004; P = 0.003).	Aspirin	53-60	BCL2 associated X, apoptosis regulator	Rattus norvegicus	212-215
28068952-0	2017	Interaction among COX-2, P2Y1 and GPIIIa gene variants is associated with aspirin resistance and early neurological deterioration in Chinese stroke patients.	Aspirin	74-81	purinergic receptor P2Y1	Homo sapiens	25-29
28052796-0	2017	Genetic variants of the gasdermin B gene associated with the development of aspirin-exacerbated respiratory diseases.	Aspirin	76-83	gasdermin B	Homo sapiens	24-35
28052796-8	2017	Our findings indicated that genetic variations of GSDMB may be associated with the development of AERD and aspirin-induced bronchospasm.	Aspirin	107-114	gasdermin B	Homo sapiens	50-55
29552640-7	2017	Evidence also suggests that HPGD (15-PDGH) expression levels in normal colon and the germline rs6983267 polymorphism that relates to tumor CTNNB1 (beta-catenin)/WNT signaling status may predict the efficacy of aspirin for cancer chemoprevention.	Aspirin	210-217	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	28-32
29552640-7	2017	Evidence also suggests that HPGD (15-PDGH) expression levels in normal colon and the germline rs6983267 polymorphism that relates to tumor CTNNB1 (beta-catenin)/WNT signaling status may predict the efficacy of aspirin for cancer chemoprevention.	Aspirin	210-217	catenin beta 1	Homo sapiens	139-145
29552640-7	2017	Evidence also suggests that HPGD (15-PDGH) expression levels in normal colon and the germline rs6983267 polymorphism that relates to tumor CTNNB1 (beta-catenin)/WNT signaling status may predict the efficacy of aspirin for cancer chemoprevention.	Aspirin	210-217	catenin beta 1	Homo sapiens	147-159
27683033-0	2016	A novel co-drug of aspirin and ursolic acid interrupts adhesion, invasion and migration of cancer cells to vascular endothelium via regulating EMT and EGFR-mediated signaling pathways: multiple targets for cancer metastasis prevention and treatment.	Aspirin	19-26	IL2 inducible T cell kinase	Homo sapiens	143-146
27573422-0	2016	Aspirin-triggered resolvin D1 inhibits TGF-beta1-induced EMT through the inhibition of the mTOR pathway by reducing the expression of PKM2 and is closely linked to oxidative stress.	Aspirin	0-7	pyruvate kinase M1/2	Homo sapiens	134-138
27545856-8	2016	Immunologic testing showed significantly elevated levels of serum wasp immunoglobulin E. Therapy with aspirin and atorvastatin was started.	Aspirin	102-109	WASP actin nucleation promoting factor	Homo sapiens	66-70
27698862-0	2016	Aspirin may inhibit angiogenesis and induce autophagy by inhibiting mTOR signaling pathway in murine hepatocarcinoma and sarcoma models.	Aspirin	0-7	mechanistic target of rapamycin kinase	Mus musculus	68-72
27698862-11	2016	The immunohistochemistry and western blot analysis data from the models revealed that the expression of p-mTOR, HIF-1alpha and VEGF-A was decreased, while the expression of ULK1 and LC3A was increased following treatment with aspirin and everolimus.	Aspirin	226-233	mechanistic target of rapamycin kinase	Mus musculus	106-110
27698862-11	2016	The immunohistochemistry and western blot analysis data from the models revealed that the expression of p-mTOR, HIF-1alpha and VEGF-A was decreased, while the expression of ULK1 and LC3A was increased following treatment with aspirin and everolimus.	Aspirin	226-233	hypoxia inducible factor 1, alpha subunit	Mus musculus	112-122
27698862-13	2016	The inhibitory action of aspirin and everolimus on tumor angiogenesis may be through inhibiting the expression of p-mTOR, HIF-1alpha and VEGF-A.	Aspirin	25-32	mechanistic target of rapamycin kinase	Mus musculus	116-120
27698862-13	2016	The inhibitory action of aspirin and everolimus on tumor angiogenesis may be through inhibiting the expression of p-mTOR, HIF-1alpha and VEGF-A.	Aspirin	25-32	hypoxia inducible factor 1, alpha subunit	Mus musculus	122-132
27698862-14	2016	Alternatively, aspirin may induce autophagy by inhibiting the mTOR signaling target and then increasing ULK1 and LC3A.	Aspirin	15-22	mechanistic target of rapamycin kinase	Mus musculus	62-66
27698862-14	2016	Alternatively, aspirin may induce autophagy by inhibiting the mTOR signaling target and then increasing ULK1 and LC3A.	Aspirin	15-22	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	113-117
30894990-7	2016	Results: Lower concentrations of aspirin (1muMu and 10muM) promoted cell growth and increased ALP levels and Runx-2 expression, while higher concentrations (100muMu and 1000muMu) inhibited cell growth (P &lt; 0.05), and lost their effect on ALP activity after 3 days, while even showing an inhibitory effect on the expression of Runx-2.	Aspirin	33-40	runt related transcription factor 2	Mus musculus	109-115
30894990-7	2016	Results: Lower concentrations of aspirin (1muMu and 10muM) promoted cell growth and increased ALP levels and Runx-2 expression, while higher concentrations (100muMu and 1000muMu) inhibited cell growth (P &lt; 0.05), and lost their effect on ALP activity after 3 days, while even showing an inhibitory effect on the expression of Runx-2.	Aspirin	33-40	runt related transcription factor 2	Mus musculus	329-335
27515206-2	2016	Aspirin (ASA), increasingly accepted as predominantly a cyclooxygenase (COX)-1 inhibitor, is a prodrug for salicylic acid (SA) which has no such activity.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	56-78
27515206-2	2016	Aspirin (ASA), increasingly accepted as predominantly a cyclooxygenase (COX)-1 inhibitor, is a prodrug for salicylic acid (SA) which has no such activity.	Aspirin	9-12	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	56-78
27515206-5	2016	Very low doses of ASA will, on repeat dosing, produce near maximal platelet COX-1 inhibition.	Aspirin	18-21	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	76-81
27430169-0	2016	Aspirin inhibits osteoclastogenesis by suppressing the activation of NF-kappaB and MAPKs in RANKL-induced RAW264.7 cells.	Aspirin	0-7	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	92-97
27430169-3	2016	The effects of aspirin on receptor-activator of nuclear factor kappaB (NF-kappaB) ligand (RANKL)-induced osteoclasts were investigated in RAW264.7 cells in the current study.	Aspirin	15-22	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	90-95
27430169-4	2016	Using tartrate-resistant acid phosphatase (TRAP) staining, it was observed that aspirin inhibited the differentiation of RANKL-induced RAW264.7 cells.	Aspirin	80-87	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	121-126
27430169-6	2016	The immunofluorescence assay indicated that aspirin markedly inhibited NF-kappaB p65 translocation to the nucleus in RANKL-induced RAW264.7 cells.	Aspirin	44-51	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	81-84
27430169-6	2016	The immunofluorescence assay indicated that aspirin markedly inhibited NF-kappaB p65 translocation to the nucleus in RANKL-induced RAW264.7 cells.	Aspirin	44-51	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	117-122
27430169-8	2016	Taken together, these data identified that aspirin inhibits osteoclastogenesis by suppressing the activation of NF-kappaB and MAPKs in RANKL-induced RAW264.7 cells, implying that aspirin may possess therapeutic potential for use in the prevention and treatment of osteoporosis.	Aspirin	43-50	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	135-140
27430169-8	2016	Taken together, these data identified that aspirin inhibits osteoclastogenesis by suppressing the activation of NF-kappaB and MAPKs in RANKL-induced RAW264.7 cells, implying that aspirin may possess therapeutic potential for use in the prevention and treatment of osteoporosis.	Aspirin	179-186	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	135-140
27548237-3	2016	A decision analysis model was constructed comparing three P2Y12 inhibitors in addition to aspirin in patients with NSTE-ACS.	Aspirin	90-97	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	120-123
27208743-5	2016	The multivariate logistic regression analysis showed that ADAMTS13 activity (p=0.031) d-Dimer (p=0.015) and cystatin C (p=0.001) remained associated with retinopathy after adjustment for age, diabetes duration, use of statin, use of ACEi or angiotensin antagonist, use of acetylsalicylic acid and glomerular filtration rate.	Aspirin	272-292	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	58-66
26915678-0	2016	Nonsteroidal anti-inflammatory-induced inhibition of signal transducer and activator of transcription 6 (STAT-6) phosphorylation in aspirin-exacerbated respiratory disease.	Aspirin	132-139	signal transducer and activator of transcription 6	Homo sapiens	53-103
26915678-0	2016	Nonsteroidal anti-inflammatory-induced inhibition of signal transducer and activator of transcription 6 (STAT-6) phosphorylation in aspirin-exacerbated respiratory disease.	Aspirin	132-139	signal transducer and activator of transcription 6	Homo sapiens	105-111
27393450-4	2016	We conducted this study to investigate whether previously studied polymorphisms in COX-1, GPIIIa, GPIa and P2RYI genes could be the cause of aspirin resistance in our population.	Aspirin	141-148	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	83-88
27393450-4	2016	We conducted this study to investigate whether previously studied polymorphisms in COX-1, GPIIIa, GPIa and P2RYI genes could be the cause of aspirin resistance in our population.	Aspirin	141-148	multimerin 1	Homo sapiens	98-102
27154726-5	2016	Moreover, aspirin-triggered lipoxin A4 activation of neutrophil Fpr2/3 regulated neutrophil-platelet aggregate formation in the brain and inhibited the reactivity of the cerebral microvasculature.	Aspirin	10-17	formyl peptide receptor 2	Homo sapiens	64-68
27154726-8	2016	Furthermore, aspirin treatment significantly reduced cerebral leukocyte recruitment and increased endogenous levels of aspirin-triggered lipoxin A4, effects again mediated by Fpr2/3.	Aspirin	13-20	formyl peptide receptor 2	Homo sapiens	175-181
27154726-8	2016	Furthermore, aspirin treatment significantly reduced cerebral leukocyte recruitment and increased endogenous levels of aspirin-triggered lipoxin A4, effects again mediated by Fpr2/3.	Aspirin	119-126	formyl peptide receptor 2	Homo sapiens	175-181
26601827-3	2016	In this study, we aimed to investigate the relationships between SNPs of the COX-1, IL-1beta, IL-1RN, and TNF genes and aspirin-induced peptic ulcers, as pilot research in a Korean population.	Aspirin	120-127	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	77-82
26601827-3	2016	In this study, we aimed to investigate the relationships between SNPs of the COX-1, IL-1beta, IL-1RN, and TNF genes and aspirin-induced peptic ulcers, as pilot research in a Korean population.	Aspirin	120-127	interleukin 1 receptor antagonist	Homo sapiens	94-100
26635114-10	2016	RT-qPCR: When compared to the LPS group, expression of MMP-7 and MMP-12 was significantly decreased in Asp group (P &lt; 0.05).	Aspirin	103-106	matrix metallopeptidase 7	Homo sapiens	55-60
26635114-14	2016	Aspirin inhibited LPS-induced expression of PI3K, Akt, ERK, NF-kappaB, CX3CL1, MMP-7, and MMP-12 in human bronchial epithelial cells.	Aspirin	0-7	matrix metallopeptidase 7	Homo sapiens	79-84
26918349-0	2016	AMPK-mediated up-regulation of mTORC2 and MCL-1 compromises the anti-cancer effects of aspirin.	Aspirin	87-94	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	42-47
26918349-5	2016	Here, we show that aspirin induces the expression of MCL-1 in HepG2 and SW480 cells through AMPK-mTOR-Akt/ERK axis.	Aspirin	19-26	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	53-58
26918349-6	2016	Treatment of HepG2 and SW480 cells with aspirin leads to increased MCL-1 expression, Akt and ERK1/2 phosphorylation.	Aspirin	40-47	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	67-72
26918349-7	2016	Inhibition of Akt/MEK abrogates the induction of MCL-1 by aspirin.	Aspirin	58-65	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	49-54
26918349-8	2016	Aspirin activates AMPK, which in turn up-regulates mTORC2 activity, Akt, ERK1/2 phosphorylation and MCL-1 expression.	Aspirin	0-7	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	100-105
27263286-4	2016	When compared with arsenic trioxide alone, co-treatment of arsenic trioxide with aspirin in different concentration (0, 0.1, 1.0, 2.5, 5.0 mmol/L) exhibited dual effects in intracellular ROS level, HO-1 and Nrf2 expression.	Aspirin	81-88	heme oxygenase 1	Homo sapiens	198-202
27263286-5	2016	Specifically, with the increasing of aspirin concentrations, the level of ROS induced by arsenic trioxide showed a rising trend after the first reduction, whereas, HO-1 and Nrf2 protein expression were decreased at first and then increased.	Aspirin	37-44	heme oxygenase 1	Homo sapiens	164-168
27263286-6	2016	CONCLUSION: Low concentration, less than 2.5 mmol/L, of aspirin may reduce the ROS accumulation through activating of Nrf2-HO-1 pathway, therefore decreasing the apoptotic cell death induced by arsenic trioxide.	Aspirin	56-63	heme oxygenase 1	Homo sapiens	123-127
27263286-7	2016	On the contrary, 5 mmol/L aspirin could increase the sensitivity of HepG2 to arsenic trioxide through enhancing the arsenic trioxide-induced apoptosis by ROS accumulation resulting in inhibiting the Nrf2-HO-1 pathway.	Aspirin	26-33	heme oxygenase 1	Homo sapiens	204-208
26844701-12	2016	Inhibition of COX-2 with aspirin or celecoxib did not affect Caspase-3 levels but also reduced Ki-67 and beta-Catenin levels, suggesting that Caspase-3 acted via COX-2 to stimulate cell proliferation and tissue regeneration.	Aspirin	25-32	catenin beta 1	Homo sapiens	105-117
26506219-4	2016	RESULTS: Ten muM aspirin significantly inhibited Ang II-induced increase in cardiomyocyte size, the mRNA, and protein levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and beta-myosin heavy chain (beta-MHC) (P &lt; 0.05).	Aspirin	17-24	natriuretic peptide type A	Mus musculus	128-154
26506219-4	2016	RESULTS: Ten muM aspirin significantly inhibited Ang II-induced increase in cardiomyocyte size, the mRNA, and protein levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and beta-myosin heavy chain (beta-MHC) (P &lt; 0.05).	Aspirin	17-24	natriuretic peptide type B	Mus musculus	162-187
26506219-4	2016	RESULTS: Ten muM aspirin significantly inhibited Ang II-induced increase in cardiomyocyte size, the mRNA, and protein levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and beta-myosin heavy chain (beta-MHC) (P &lt; 0.05).	Aspirin	17-24	natriuretic peptide type B	Mus musculus	189-192
26506219-5	2016	Meantime, consistent with the result in vitro, the increase in HW/BW ratio, the mRNA, and protein levels of ANP, BNP, and beta-MHC could be reduced by aspirin in vivo (P &lt; 0.05).	Aspirin	151-158	natriuretic peptide type B	Mus musculus	113-116
26276129-9	2016	The MPO levels decreased statistically significantly in the group administered ASA.	Aspirin	79-82	myeloperoxidase	Rattus norvegicus	4-7
26194538-1	2016	BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is characterized by respiratory reactions on ingestion of COX-1 inhibitors and cysteinyl leukotriene overproduction.	Aspirin	12-19	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	117-122
26194538-2	2016	The hypersensitivity reaction is induced by low doses of aspirin that inhibit COX-1 in platelets.	Aspirin	57-64	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	78-83
26644261-13	2016	The pharmacodynamic response to aspirin was impaired in patients with moderate/severe CKD (92; interquartile range [IQR], 282 ng mL(-1) ) as compared to patients with normal/mildly reduced renal function (36; IQR, 100 ng mL(-1) ; difference in medians, 57; CI, 5-110 ng mL(-1) ; P = 0.013).	Aspirin	32-39	L1 cell adhesion molecule	Mus musculus	129-135
26644261-13	2016	The pharmacodynamic response to aspirin was impaired in patients with moderate/severe CKD (92; interquartile range [IQR], 282 ng mL(-1) ) as compared to patients with normal/mildly reduced renal function (36; IQR, 100 ng mL(-1) ; difference in medians, 57; CI, 5-110 ng mL(-1) ; P = 0.013).	Aspirin	32-39	L1 cell adhesion molecule	Mus musculus	221-227
26644261-13	2016	The pharmacodynamic response to aspirin was impaired in patients with moderate/severe CKD (92; interquartile range [IQR], 282 ng mL(-1) ) as compared to patients with normal/mildly reduced renal function (36; IQR, 100 ng mL(-1) ; difference in medians, 57; CI, 5-110 ng mL(-1) ; P = 0.013).	Aspirin	32-39	L1 cell adhesion molecule	Mus musculus	221-227
26711147-5	2016	In addition, ASA could led to a loss in the mitochondrial out membrane potential, up-regulate p53, phosphorylated p53 and Bax, down-regulate Bcl-2, release cytochrome c from the mitochondria to the cytoplasm, and activate caspase-9 and caspase-3 in A549 cells, which revealed that ASA could also induce apoptosis through the mitochondria mediated pathway.	Aspirin	13-16	caspase 9	Homo sapiens	222-231
26519680-0	2016	Low miR-19b-1-5p expression in isolated platelets after aspirin use is related to aspirin insensitivity.	Aspirin	56-63	microRNA 19b-1	Homo sapiens	4-13
26519680-0	2016	Low miR-19b-1-5p expression in isolated platelets after aspirin use is related to aspirin insensitivity.	Aspirin	82-89	microRNA 19b-1	Homo sapiens	4-13
26492523-11	2016	Aspirin, U0126, LY294002 and 5z-7-oxozeaenol attenuated the IL-1beta-induced MCP-1 expression.	Aspirin	0-7	C-C motif chemokine ligand 2	Homo sapiens	77-82
26759534-0	2015	Neutralization by Acetyl Salicylic Acid of the Testosterone induced Impaired Maspin Synthesis Stimulated by Estriol in Neutrophils through Nitric Oxide Synthesis.	Aspirin	18-39	serpin family B member 5	Homo sapiens	77-83
26759534-9	2015	Incubation of 25microM aspirin that stimulated NO synthesis restored the inhibition of maspin synthesis by testosterone by 79.1%.	Aspirin	23-30	serpin family B member 5	Homo sapiens	87-93
26319435-10	2015	All 3 positional isomers of NOSH-aspirin preferentially inhibited COX-1 over COX-2.	Aspirin	33-40	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	66-71
26105589-0	2015	Proton pump inhibitors are associated with lower gastrointestinal tract bleeding in low-dose aspirin users with ischaemic heart disease.	Aspirin	93-100	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	0-11
26105589-8	2015	CONCLUSIONS: In low-dose aspirin users, concomitant use of proton pump inhibitors increased lower gastrointestinal bleeding risk, independent from effects on upper gastrointestinal bleeding.	Aspirin	25-32	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	59-70
26094902-9	2015	It was certified that the increase in the amount of NO release, the decrease in the luciferase promoter activity and the expression of cyclin D1 and c-myc in HCT116 cells were affected by aspirin and ISMN in a synergistic manner.	Aspirin	188-195	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	149-154
26201059-7	2015	In the cardiovascular system, aspirin also acetylates eNOS with subsequent upregulation of NO formation and enhanced expression of the antioxidans heme-oxygenase-1.	Aspirin	30-37	heme oxygenase 1	Homo sapiens	147-163
26085050-2	2015	In ACS, aspirin at antiplatelet doses exhibits anti-inflammatory effects as seen from the decrease in inflammation markers such as CRP, M-CSF, MCP-1 and others.	Aspirin	8-15	colony stimulating factor 1	Homo sapiens	136-141
26085050-2	2015	In ACS, aspirin at antiplatelet doses exhibits anti-inflammatory effects as seen from the decrease in inflammation markers such as CRP, M-CSF, MCP-1 and others.	Aspirin	8-15	C-C motif chemokine ligand 2	Homo sapiens	143-148
25891179-4	2015	Compared with treatment by sCT or ASA alone, combined treatment (sCT+ASA) increased BMD, improved femur bone strength, normalized trabecular network architecture and morphology, and increased mRNA and protein expression of OPG, while reducing the expression of RANKL.	Aspirin	69-72	TNF receptor superfamily member 11B	Rattus norvegicus	223-226
26139061-1	2015	Inactivation of platelet cyclooxygenase (COX)-1 by low-dose aspirin leads to long-lasting suppression of thromboxane (TX) A2 production and TXA2-mediated platelet activation and aggregation.	Aspirin	60-67	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	25-47
26139061-2	2015	This effect is necessary and sufficient to explain aspirin"s unique (among other COX-1 inhibitors) effectiveness in preventing atherothrombosis, as well as its shared (with other antiplatelet agents) bleeding liability.	Aspirin	51-58	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	81-86
25867761-8	2015	The tumor growth-inhibitory and reprogramming roles of ASA could be mediated through inhibition of TGF-beta/SMAD4 signaling pathway that is associated with growth, motility, invasion, and metastasis in advanced BCs.	Aspirin	55-58	SMAD family member 4	Mus musculus	108-113
25959742-0	2015	Aspirin Action in Endothelial Cells: Different Patterns of Response Between Chemokine CX3CL1/CX3CR1 and TNF-alpha/TNFR1 Signaling Pathways.	Aspirin	0-7	TNF receptor superfamily member 1A	Homo sapiens	114-119
25904552-5	2015	LTC4 upregulated the expressions of ICAM-1 and VCAM-1 in an aspirin-sensitive and TP receptor-dependent manner.	Aspirin	60-67	vascular cell adhesion molecule 1	Mus musculus	47-53
25638779-3	2015	Aspirin (acetylsalicylate, ASA) inhibits AA oxidation by cyclooxygenase (COX)-1 and COX-2.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	57-79
25638779-3	2015	Aspirin (acetylsalicylate, ASA) inhibits AA oxidation by cyclooxygenase (COX)-1 and COX-2.	Aspirin	9-25	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	57-79
25638779-3	2015	Aspirin (acetylsalicylate, ASA) inhibits AA oxidation by cyclooxygenase (COX)-1 and COX-2.	Aspirin	27-30	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	57-79
25966060-5	2015	Expressions of integrin beta3 and LIF in the endometrium of mice in the TCM treatment group were significantly increased compared to aspirin-treated and control mice, and those of aspirin-treated mice were increased compared to the control group.	Aspirin	133-140	leukemia inhibitory factor	Mus musculus	34-37
25727881-8	2015	RESULTS: Compared with men who were not on medication, the PSA level at the first PSA test was lower among men using 75 mg/dose aspirin (-3.9% change in PSA concentration; 95% confidence interval (CI): -5.8 to -2.1), statin (-4.6%; 95% CI: -6.2 to -2.9), metformin (-14%; 95% CI: -17 to -12) and insulin (-16%; 95% CI: -18 to -14).	Aspirin	128-135	kallikrein related peptidase 3	Homo sapiens	59-62
25727881-8	2015	RESULTS: Compared with men who were not on medication, the PSA level at the first PSA test was lower among men using 75 mg/dose aspirin (-3.9% change in PSA concentration; 95% confidence interval (CI): -5.8 to -2.1), statin (-4.6%; 95% CI: -6.2 to -2.9), metformin (-14%; 95% CI: -17 to -12) and insulin (-16%; 95% CI: -18 to -14).	Aspirin	128-135	kallikrein related peptidase 3	Homo sapiens	82-85
25727881-8	2015	RESULTS: Compared with men who were not on medication, the PSA level at the first PSA test was lower among men using 75 mg/dose aspirin (-3.9% change in PSA concentration; 95% confidence interval (CI): -5.8 to -2.1), statin (-4.6%; 95% CI: -6.2 to -2.9), metformin (-14%; 95% CI: -17 to -12) and insulin (-16%; 95% CI: -18 to -14).	Aspirin	128-135	kallikrein related peptidase 3	Homo sapiens	82-85
26054192-10	2015	The effects of both EA and moxibustion groups were significantly superior to those of Aspirin pretreatment group in up-regulating expression of miRNA 290 and miRNA 494 and down-regulating expression of AQP 4 (P &lt; 0.01, P &lt; 0.05).	Aspirin	86-93	aquaporin 4	Rattus norvegicus	202-207
25817250-5	2015	In conditions involving down regulated GSH homeostasis, GGC serves asa crucialrate-limiting substrate for GSH synthetase, the main enzyme responsible for condensing glycine with GGC to form the final thiol tripeptide, GSH.	Aspirin	67-70	glutathione synthetase	Homo sapiens	106-120
25759598-4	2015	All available NSAIDs, including acetaminophen and aspirin, are associated with potential side effects, particularly gastrointestinal and cardiovascular effects, related to their relative selectivity for COX-1 and COX-2.	Aspirin	50-57	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	203-208
25615803-5	2015	For promazine and amoxicillin, they resulted in the change of binding force distribution of myoglobin/antibody (i.e., from unimodal distribution to bimodal distribution) and the increase of binding probability; for aspirin, it only resulted in the change of the binding force distribution, and for sodium penicillin, it resulted in the increase of the average binding force and the binding probability.	Aspirin	215-222	myoglobin	Homo sapiens	92-101
25557764-8	2015	Thus an increase in Sirt4, Nrf2, Tfam, UCP1, eNOS, HO1 and STAT3 genes could profoundly affect mitochondrial function, cholesterol homeostasis, and fatty acid oxidation, suggesting that ASA could be beneficial beyond simply its ability to inhibit cyclooxygenase.	Aspirin	186-189	uncoupling protein 1	Homo sapiens	39-43
25557764-8	2015	Thus an increase in Sirt4, Nrf2, Tfam, UCP1, eNOS, HO1 and STAT3 genes could profoundly affect mitochondrial function, cholesterol homeostasis, and fatty acid oxidation, suggesting that ASA could be beneficial beyond simply its ability to inhibit cyclooxygenase.	Aspirin	186-189	heme oxygenase 1	Homo sapiens	51-54
25638171-1	2015	BACKGROUND: Dobesilate (2,5-dihydroxyphenyl sulfonate, DHPS) was recently identified as the most potent member of a family of fibroblast growth factor (FGF) inhibitors headed by gentisic acid, one of the main catabolites of aspirin.	Aspirin	224-231	deoxyhypusine synthase	Rattus norvegicus	55-59
26379739-6	2015	Treatment of aspirin alone significantly reduced the expressions of HO-1 (P &lt; 0.001), iNOS (P &lt; 0.001), and Bax (P &lt; 0.01) in ischemic regions.	Aspirin	13-20	BCL2 associated X, apoptosis regulator	Rattus norvegicus	114-117
30192051-4	2018	Indeed, salicylic acid and acetylsalicylic acid extend lifespan in worms by activating AMPK and the forkhead transcription factor DAF-16/FOXO.	Aspirin	27-47	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	130-136
30414472-5	2018	Next, we classified the mutation of 4 aspirin DPTs in SCLC (IKBKB, NFKBIA, PTGS2 and TP53) using cBio Portal.	Aspirin	38-45	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	60-65
30414472-6	2018	Further, we identified top 50 overexpressed genes of SCLC by Oncomine, and the interconnected genes with the 4 aspirin DPTs in SCLC (IKBKB, NFKBIA, PTGS2 and TP53) by STRING.	Aspirin	111-118	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	133-138
29969574-13	2018	Aspirin also obviously downregulated the mRNA expressions of IL-6, IL-1beta, and MCP-1 and assuaged the activation of TLR4, MyD88, NF-kappaBp65, and TLR2 in the placental tissue.	Aspirin	0-7	MYD88, innate immune signal transduction adaptor	Rattus norvegicus	124-129
29969574-14	2018	Our results indicated that aspirin could assuage preeclampsia-like phenotypes, and this improvement effect is possibly the result of the suppression of pro-inflammatory cytokines via the TLR4, MyD88, NF-kappaBp65, and TLR2 signaling pathway.	Aspirin	27-34	MYD88, innate immune signal transduction adaptor	Rattus norvegicus	193-198
29621646-3	2018	Modified glassy carbon electrode of N-CQD/Cu2O/GCE is developed and is used for the sensor studies of aspirin.	Aspirin	102-109	guanylate cyclase 2E, pseudogene	Homo sapiens	47-50
29792865-10	2018	Since PP2A, Akt, and Mcl-1 play critical roles in RCC malignancy and treatment resistance, our present study showed that aspirin, an alternative adjuvant agent, had recalled ABT-737 sensitivity in the RCC cells through processes involving the PP2A/Akt/Mcl-1 axis.	Aspirin	121-128	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	21-26
29792865-10	2018	Since PP2A, Akt, and Mcl-1 play critical roles in RCC malignancy and treatment resistance, our present study showed that aspirin, an alternative adjuvant agent, had recalled ABT-737 sensitivity in the RCC cells through processes involving the PP2A/Akt/Mcl-1 axis.	Aspirin	121-128	protein phosphatase 2 phosphatase activator	Homo sapiens	243-247
29792865-10	2018	Since PP2A, Akt, and Mcl-1 play critical roles in RCC malignancy and treatment resistance, our present study showed that aspirin, an alternative adjuvant agent, had recalled ABT-737 sensitivity in the RCC cells through processes involving the PP2A/Akt/Mcl-1 axis.	Aspirin	121-128	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	252-257
29574792-6	2018	We provide evidence in vitro that atorvastatin reduced residual TXB2 generation by increasing the extent of acetylation of platelet COX-1 by aspirin.	Aspirin	141-148	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	132-137
29880847-3	2018	However, the pharmacodynamics of low-dose aspirin is impaired in ET, reflecting accelerated renewal of platelet cyclooxygenase (COX)-1.	Aspirin	42-49	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	112-134
29805582-0	2018	Effects of aspirin on proliferation, invasion and apoptosis of Hep-2 cells via the PTEN/AKT/NF-kappaB/survivin signaling pathway.	Aspirin	11-18	phosphatase and tensin homolog	Homo sapiens	83-87
29805582-7	2018	Hep-2 cells treated with aspirin exhibited a significant upregulation of phosphatase and tensin homolog (PTEN) and decreased levels of phosphorylated protein kinase B (AKT).	Aspirin	25-32	phosphatase and tensin homolog	Homo sapiens	105-109
29805582-10	2018	These results indicated that the molecular mechanism underlying the antitumor effects of aspirin may be associated with the inhibition of tumor invasion and induction of apoptosis by regulating the activity of the PTEN/AKT/NF-kappaB/survivin signaling pathway.	Aspirin	89-96	phosphatase and tensin homolog	Homo sapiens	214-218
30046765-2	2018	Aspirin enhances platelet MRP4 expression with a PPARalpha-dependent mechanism and reduces miR-21 expression that, in turn, downregulates PPARalpha expression.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Homo sapiens	49-58
30046765-2	2018	Aspirin enhances platelet MRP4 expression with a PPARalpha-dependent mechanism and reduces miR-21 expression that, in turn, downregulates PPARalpha expression.	Aspirin	0-7	microRNA 21	Homo sapiens	91-97
30046765-2	2018	Aspirin enhances platelet MRP4 expression with a PPARalpha-dependent mechanism and reduces miR-21 expression that, in turn, downregulates PPARalpha expression.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Homo sapiens	138-147
30046765-3	2018	Objective: The aim of our study was to verify the relationship between miR-21 and MRP4-PPARalpha levels induced by aspirin treatment.	Aspirin	115-122	microRNA 21	Homo sapiens	71-77
30046765-3	2018	Objective: The aim of our study was to verify the relationship between miR-21 and MRP4-PPARalpha levels induced by aspirin treatment.	Aspirin	115-122	peroxisome proliferator activated receptor alpha	Homo sapiens	87-96
30046765-4	2018	Methods: We evaluated the changes in MRP4-PPARalpha, mRNA, MRP4 protein, and miR-21 expression induced by aspirin in: (i) in vitro-treated megakaryoblastic cell line (DAMI), (ii) primary megakaryocytes cultures and derived platelets, (iii) healthy volunteers" platelets treated with aspirin, and (iv) aspirinated patients (aspirin-treated patients) and in a control population (control).	Aspirin	106-113	microRNA 21	Homo sapiens	77-83
30046765-5	2018	Results: We observed an aspirin-induced reverse relationship between the expression of miR-21 and PPARalpha-MRP4.	Aspirin	24-31	microRNA 21	Homo sapiens	87-93
30046765-5	2018	Results: We observed an aspirin-induced reverse relationship between the expression of miR-21 and PPARalpha-MRP4.	Aspirin	24-31	peroxisome proliferator activated receptor alpha	Homo sapiens	98-107
30046765-6	2018	In DAMI cells the miR-21 mimic transfection reduces PPARalpha and MRP4 expression, even if cells were treated with aspirin after transfection.	Aspirin	115-122	microRNA 21	Homo sapiens	18-24
30046765-8	2018	In human megakaryocytes, aspirin treatment lead to a miR-21 downregulation and a MRP4 upregulation and this trend is confirmed in derived platelets.	Aspirin	25-32	microRNA 21	Homo sapiens	53-59
30046765-9	2018	In aspirin-treated volunteers, an inverse relationship between miR-21 and MRP4 platelet expression was found after aspirin treatment.	Aspirin	3-10	microRNA 21	Homo sapiens	63-69
29028441-3	2018	We estimated the effect of physiological (heat stress: 45 min at 41 +- 0.5  C) and pharmacological (aspirin treatment) induction of HSP70 on several parameters of oxidative state in the pancreas and liver of diabetic rats.	Aspirin	100-107	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	132-137
29028441-7	2018	Pre-treatment of HP-diabetic animals with aspirin led to an additional increase of PARP and HSP70.	Aspirin	42-49	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	92-97
29028441-8	2018	Both HP and aspirin, as physiological and pharmacological inductors of HSP70, respectively, enhanced the antioxidative defense mechanisms of the liver and pancreas in diabetic rats.	Aspirin	12-19	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	71-76
29316620-2	2018	Aspirin is the most commonly used non-steroid anti-inflammatory drugs (NSAIDs), and it irreversibly inhibits cyclooxygenase-1 and -2 (COX1, COX2).	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	134-138
30564469-12	2018	Tom"s medical history includes hypertension that is adequately controlled with lisinopril (20 mg/day), coronary artery disease (on daily aspirin 81 mg) with left ventricular ejection fraction (LVEF) of &gt; 50%, which is within the normal range (50%-75%), benign prostatic hyperplasia for which he is treated with finasteride, and hyperlipidemia that is treated with atorvastatin.	Aspirin	137-144	pre-mRNA processing factor 6	Homo sapiens	0-3
28987816-4	2018	The data imply that ASA increases Fpn1 expression by inhibiting hepcidin expression via the IL-6/JAK/STAT3 pathway and show that the reduced content of Ft-L is due to the increased Fpn1 and subsequent iron release in the cells.	Aspirin	20-23	signal transducer and activator of transcription 3	Rattus norvegicus	101-106
29045972-2	2017	METHODS: Flow cytometry analysis were used to analyze the role of ASA in the expression of stem cells surface markers CD146, CD105, CD90, CD34 and CD45 in GMSCs,and the GMSCs proliferation was analyzed by 5-bromo-2-deoxyuridine (BrdU) staining and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.	Aspirin	66-69	endoglin	Mus musculus	125-130
29045972-2	2017	METHODS: Flow cytometry analysis were used to analyze the role of ASA in the expression of stem cells surface markers CD146, CD105, CD90, CD34 and CD45 in GMSCs,and the GMSCs proliferation was analyzed by 5-bromo-2-deoxyuridine (BrdU) staining and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.	Aspirin	66-69	CD34 antigen	Mus musculus	138-142
29045972-2	2017	METHODS: Flow cytometry analysis were used to analyze the role of ASA in the expression of stem cells surface markers CD146, CD105, CD90, CD34 and CD45 in GMSCs,and the GMSCs proliferation was analyzed by 5-bromo-2-deoxyuridine (BrdU) staining and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.	Aspirin	66-69	protein tyrosine phosphatase, receptor type, C	Mus musculus	147-151
29035123-6	2017	RESULTS: There is a genetic association between polymorphisms of genes involved in the synthesis of proteins related to arachidonic acid metabolism (LTC4S, ALOX5), antigen presentation (HLA), inflammation (IL5, IL17), and aspirin metabolism (CYP2C19).	Aspirin	222-229	leukotriene C4 synthase	Homo sapiens	149-154
28910305-11	2017	The results suggest that aspirin increase metabolism and regulate germline signalling to activate downstream DAF-12 and DAF-16 to extend lifespan.	Aspirin	25-32	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	120-126
28900541-0	2017	Simultaneous silencing of ACSL4 and induction of GADD45B in hepatocellular carcinoma cells amplifies the synergistic therapeutic effect of aspirin and sorafenib.	Aspirin	139-146	growth arrest and DNA damage inducible beta	Homo sapiens	49-56
28900541-10	2017	In conclusion, sorafenib and aspirin provide synergistic therapeutic effects on HCC cells that are achieved through simultaneous silencing of ACSL4 and induction of GADD45B expression.	Aspirin	29-36	growth arrest and DNA damage inducible beta	Homo sapiens	165-172
28679740-2	2017	We showed that in murine models of ovarian cancer, a P2Y12 inhibitor (ticagrelor) reduced tumor growth by 60% compared with aspirin and by 75% compared with placebo.	Aspirin	124-131	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	53-58
28346830-0	2017	Synergetic Neuroprotective Effect of Docosahexaenoic Acid and Aspirin in SH-Y5Y by Inhibiting miR-21 and Activating RXRalpha and PPARalpha.	Aspirin	62-69	microRNA 21	Homo sapiens	94-100
28346830-0	2017	Synergetic Neuroprotective Effect of Docosahexaenoic Acid and Aspirin in SH-Y5Y by Inhibiting miR-21 and Activating RXRalpha and PPARalpha.	Aspirin	62-69	peroxisome proliferator activated receptor alpha	Homo sapiens	129-138
28346830-5	2017	DHA and ASA could activate RXRalpha and PPARalpha, respectively.	Aspirin	8-11	peroxisome proliferator activated receptor alpha	Homo sapiens	40-49
28415819-0	2017	Aspirin regulation of c-myc and cyclinD1 proteins to overcome tamoxifen resistance in estrogen receptor-positive breast cancer cells.	Aspirin	0-7	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	22-27
28415819-6	2017	When knocking down c-myc in MCF-7/TAM, cells become more sensitive to tamoxifen, cell cycle is blocked as well, indicating that aspirin can regulate c-myc and cyclinD1 proteins to overcome tamoxifen resistance.	Aspirin	128-135	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	19-24
28415819-6	2017	When knocking down c-myc in MCF-7/TAM, cells become more sensitive to tamoxifen, cell cycle is blocked as well, indicating that aspirin can regulate c-myc and cyclinD1 proteins to overcome tamoxifen resistance.	Aspirin	128-135	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	149-154
28540312-4	2017	We present a case in which a patient successfully underwent a 3-month course of rivaroxaban in addition to his dual antiplatelet regimen of aspirin and ticagrelor for his STE-ACS and LV thrombus with resultant complete dissolution.	Aspirin	140-147	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	175-178
28154202-6	2017	Additionally, microarray analysis of 151 colorectal cancer cell lines identified important cell-cycle regulatory genes that are downstream targets of PIK3 and were also dysregulated by aspirin treatment (PCNA and RB1).	Aspirin	185-192	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	150-154
28344655-0	2017	Interactions among COX-2, GPIIIa and P2Y1 variants are associated with aspirin responsiveness and adverse events in patients with ischemic stroke.	Aspirin	71-78	purinergic receptor P2Y1	Homo sapiens	37-41
28181214-17	2017	Primary outcomes Aspirin versus placeboMore women who received aspirin experienced adequate pain relief compared with women who received placebo over four to eight hours after administration (risk ratio (RR) 2.03, 95% confidence intervals (CI) 1.69 to 2.42; 13 RCTs, 1001 women; low-quality evidence).	Aspirin	63-70	ribonucleotide reductase regulatory subunit M2	Homo sapiens	192-209
27903583-0	2017	Aspirin therapy reduces the ability of platelets to promote colon and pancreatic cancer cell proliferation: Implications for the oncoprotein c-MYC.	Aspirin	0-7	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	141-146
27903583-7	2017	The ability of platelets to upregulate c-MYC and cancer cell proliferation was reversed by an antiplatelet concentration of aspirin.	Aspirin	124-131	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	39-44
27903583-8	2017	In conclusion, we show for the first time that inhibition of platelets by aspirin can affect their ability to induce cancer cell proliferation through the modulation of the c-MYC oncoprotein.	Aspirin	74-81	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	173-178
27992364-3	2017	Meanwhile, miR-30eoverexpression inPC9G cells resulted in reduced cell proliferation and migration,reversing drug resistance to gefitinib.Conversely,miR-30e silencing in PC9 cells increased proliferation as well as migration, and conferred resistance to gefitinib.Moreover, HOXA1, which was identified asa new miR-30etarget, plays important roles in regulating cell fate, early developmental patterns and organogenesis.Importantly, miR-30ealso inhibited PC9G growth in vivo.	Aspirin	302-305	microRNA 30e	Homo sapiens	11-18
27992364-3	2017	Meanwhile, miR-30eoverexpression inPC9G cells resulted in reduced cell proliferation and migration,reversing drug resistance to gefitinib.Conversely,miR-30e silencing in PC9 cells increased proliferation as well as migration, and conferred resistance to gefitinib.Moreover, HOXA1, which was identified asa new miR-30etarget, plays important roles in regulating cell fate, early developmental patterns and organogenesis.Importantly, miR-30ealso inhibited PC9G growth in vivo.	Aspirin	302-305	proprotein convertase subtilisin/kexin type 9	Homo sapiens	35-38
28630872-9	2017	The control group was characterized by higher PAI-1 following ASA treatment and sICAM-1 both at baseline and after ASA, but no differences in MDA and 6-keto-PGF-1 alpha and platelet aggregation were noted.	Aspirin	62-65	serpin family E member 1	Homo sapiens	46-51
27405497-9	2017	Clinical data on aspirin, an irreversible inhibitor of both COX-1 and COX-2, are mainly experimental and hypothetical at this stage, but may be promising in depressed patients with concomitant inflammatory conditions.	Aspirin	17-24	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	60-65
28630782-5	2017	RESULTS: The aspirin P-selectin test demonstrated that platelet expression was lower in 494 patients taking aspirin than in 162 patients not: mean 210 (SD 188) versus 570 (435), difference 360.3 (95% CI 312.2-408.4) (2p &lt; 0.001).	Aspirin	13-20	selectin P	Homo sapiens	21-31
28630782-9	2017	CONCLUSIONS: Aspirin and clopidogrel suppress stimulated platelet P-selectin, although one-quarter of patients on clopidogrel have high on-treatment platelet reactivity.	Aspirin	13-20	selectin P	Homo sapiens	66-76
27683757-8	2016	We can assert that, in patients under chronic aspirin treatment, platelets that present high MRP4 levels have an increase of residual platelet reactivity, which is due in part to incomplete COX-1 inhibition, and in part to COX-1-independent mechanism.	Aspirin	46-53	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	190-195
27683757-8	2016	We can assert that, in patients under chronic aspirin treatment, platelets that present high MRP4 levels have an increase of residual platelet reactivity, which is due in part to incomplete COX-1 inhibition, and in part to COX-1-independent mechanism.	Aspirin	46-53	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	223-228
30551280-1	2016	Aspirin-exacerbated respiratory disease (AERD) is characterized by the triad of asthma, eosinophilic nasal polyposis and a hypersensitivity to all medications that inhibit the cyclo- oxygenase (COX) -1 enzyme.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	176-201
27430429-3	2016	In the current study, the addition of NF-kappaB inhibitors (Bay11-7082, Z-LLF-CHO and aspirin) was observed to induce the EBV lytic genes BZLF1, BRLF1 and BMRF1 in EBV-positive gastric cancer (GC) cells.	Aspirin	86-93	protein Zta	Human gammaherpesvirus 4	138-143
27412561-0	2016	miR-145 mediated the role of aspirin in resisting VSMCs proliferation and anti-inflammation through CD40.	Aspirin	29-36	microRNA 145	Homo sapiens	0-7
27412561-9	2016	The protective effects of ASA in VSMCs were reversed by a pretreatment with a miR-145 inhibitor.	Aspirin	26-29	microRNA 145	Homo sapiens	78-85
27412561-10	2016	We also found that the expression of miR-145 in peripheral blood mononuclear cells in ischemic stroke patients was significantly increased after a 10-day treatment with aspirin.	Aspirin	169-176	microRNA 145	Homo sapiens	37-44
27412561-11	2016	CONCLUSION: miR-145 is involved in the anti-proliferation and anti-inflammation effects of aspirin on VSMCs by inhibiting the expression of CD40.	Aspirin	91-98	microRNA 145	Homo sapiens	12-19
27118470-9	2016	Similarly, the rise in P-selectin (17%; IQR: -5.0/39.7; P = 0.03 vs. baseline) observed in untreated participants was abolished by all treatments, with aspirin 300 mg exerting the strongest effect (-30.7%; IQR: -58.4/-0.03; P = 0.007 vs. untreated).	Aspirin	152-159	selectin P	Homo sapiens	23-33
27032071-11	2016	Additionally, MDA levels in coelomic fluid were negatively correlated with dietary AsA levels, while antioxidant capacities (SOD, GSH-Px and CAT) were positively correlated with dietary AsA levels.	Aspirin	186-189	superoxide dismutase [Mn], mitochondrial	Cucumis sativus	125-128
26969214-0	2016	Aspirin induces Nrf2-mediated transcriptional activation of haem oxygenase-1 in protection of human melanocytes from H2 O2 -induced oxidative stress.	Aspirin	0-7	heme oxygenase 1	Homo sapiens	60-76
26969214-9	2016	Furthermore, we found ASA dramatically induced NRF2 nuclear translocation, enhanced ARE-luciferase activity, increased both p- NRF2 and total NRF2 levels, and induced the expression of haem oxygenase-1 (HO-1) in human melanocytes.	Aspirin	22-25	heme oxygenase 1	Homo sapiens	185-201
26969214-9	2016	Furthermore, we found ASA dramatically induced NRF2 nuclear translocation, enhanced ARE-luciferase activity, increased both p- NRF2 and total NRF2 levels, and induced the expression of haem oxygenase-1 (HO-1) in human melanocytes.	Aspirin	22-25	heme oxygenase 1	Homo sapiens	203-207
26969214-10	2016	In addition, knockdown of Nrf2 expression or pharmacological inhibition of HO-1 abrogated the protective action of ASA on melanocytes against H2 O2 -induced cytotoxicity and apoptosis.	Aspirin	115-118	heme oxygenase 1	Homo sapiens	75-79
26969214-11	2016	These results suggest that ASA protects human melanocytes against H2 O2 -induced oxidative stress via Nrf2-driven transcriptional activation of HO-1.	Aspirin	27-30	heme oxygenase 1	Homo sapiens	144-148
27347106-11	2016	In conclusion, aspirin can inhibit the growth of ovarian cancer of p53S rats due to its upregulation of the expression of caspase-3 protein and downregulation of the expression of bcl-2 protein.	Aspirin	15-22	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	67-70
27147748-5	2016	Expression of BART miRNAs and lncRNAs correlated with NF-kappaB activity in EBV-infected epithelial cells, while treatment of EBV-harboring NPC C666-1 cells with aspirin (acetylsalicylic acid [ASA]) and the IkappaB kinase inhibitor PS-1145 inhibited NF-kappaB activity, resulting in downregulation of BART expression.	Aspirin	162-169	ADP ribosylation factor like GTPase 2 binding protein	Homo sapiens	14-18
26491233-2	2015	We found that multidrug resistance protein-4 (MRP4) overexpression has a role in reducing aspirin action in patients after bypass surgery and, very recently, we found that aspirin enhances platelet MRP4 levels through peroxisome proliferator activated receptor-alpha (PPARalpha).	Aspirin	90-97	peroxisome proliferator activated receptor alpha	Homo sapiens	218-266
26491233-2	2015	We found that multidrug resistance protein-4 (MRP4) overexpression has a role in reducing aspirin action in patients after bypass surgery and, very recently, we found that aspirin enhances platelet MRP4 levels through peroxisome proliferator activated receptor-alpha (PPARalpha).	Aspirin	90-97	peroxisome proliferator activated receptor alpha	Homo sapiens	268-277
26491233-2	2015	We found that multidrug resistance protein-4 (MRP4) overexpression has a role in reducing aspirin action in patients after bypass surgery and, very recently, we found that aspirin enhances platelet MRP4 levels through peroxisome proliferator activated receptor-alpha (PPARalpha).	Aspirin	172-179	peroxisome proliferator activated receptor alpha	Homo sapiens	218-266
26491233-2	2015	We found that multidrug resistance protein-4 (MRP4) overexpression has a role in reducing aspirin action in patients after bypass surgery and, very recently, we found that aspirin enhances platelet MRP4 levels through peroxisome proliferator activated receptor-alpha (PPARalpha).	Aspirin	172-179	peroxisome proliferator activated receptor alpha	Homo sapiens	268-277
26422851-0	2015	The effects of aspirin, flurbiprofen, and NO-donating acetylsalicylic acid (NCX 4016) on mice models of endotoxic and septic shock.	Aspirin	54-74	T cell leukemia, homeobox 2	Mus musculus	76-79
26422851-2	2015	The aim of this study was to investigate the effects of aspirin, flurbiprofen, and NO-donating acetylsalicylic acid (NCX 4016) on cecal ligation and puncture (CLP) and endotoxin-induced septic shock (LPS) models in mice.	Aspirin	95-115	T cell leukemia, homeobox 2	Mus musculus	117-120
24902864-3	2014	Aspirin enhances MRP4-mRNA levels in rat liver and drug administration transcriptionally regulates MRP4 gene expression through peroxisome proliferator-activated receptor-alpha (PPARalpha).	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Rattus norvegicus	128-176
24902864-3	2014	Aspirin enhances MRP4-mRNA levels in rat liver and drug administration transcriptionally regulates MRP4 gene expression through peroxisome proliferator-activated receptor-alpha (PPARalpha).	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Rattus norvegicus	178-187
24902864-5	2014	RESULTS: In DAMI cells, aspirin and WY14643 treatment induced a significant increase in MRP4 and PPARalpha expression.	Aspirin	24-31	peroxisome proliferator activated receptor alpha	Homo sapiens	97-106
24902864-6	2014	In human MKs grown in the presence of either aspirin or WY14643, MRP4 and PPARalpha-mRNA were higher than in control cultures and derived platelets showed an enhancement in MRP4 protein expression.	Aspirin	45-52	peroxisome proliferator activated receptor alpha	Homo sapiens	74-83
25129612-7	2014	Significantly higher alpha smooth muscle actin mRNA and protein expression were measured after Zn (ASA)2 and Zn-treatment in comparison with the untreated and ASA-groups while the expression of matrix-metalloproteinase-9 was significantly higher in these groups compared to Zn (ASA)2.	Aspirin	99-102	actin gamma 2, smooth muscle	Rattus norvegicus	21-46
25129612-7	2014	Significantly higher alpha smooth muscle actin mRNA and protein expression were measured after Zn (ASA)2 and Zn-treatment in comparison with the untreated and ASA-groups while the expression of matrix-metalloproteinase-9 was significantly higher in these groups compared to Zn (ASA)2.	Aspirin	159-162	actin gamma 2, smooth muscle	Rattus norvegicus	21-46
25129612-7	2014	Significantly higher alpha smooth muscle actin mRNA and protein expression were measured after Zn (ASA)2 and Zn-treatment in comparison with the untreated and ASA-groups while the expression of matrix-metalloproteinase-9 was significantly higher in these groups compared to Zn (ASA)2.	Aspirin	159-162	actin gamma 2, smooth muscle	Rattus norvegicus	21-46
25173753-11	2014	Diets supplemented with low-dose aspirin reduced circulating serum and hepatic levels of PDGFB and significantly reduced progression of fibrosis in MDR2-null mice over 1 year.	Aspirin	33-40	platelet derived growth factor, B polypeptide	Mus musculus	89-94
25330142-8	2014	CONCLUSION: Our study showed that the GMP-140 serum level and PAG were increased after ASD and VSD occlusion, and patients may have a trend of decreased GMP-140 serum levels after the ASD or VSD occlusion surgeries after the treatment with aspirin.	Aspirin	240-247	selectin P	Homo sapiens	38-45
25330142-8	2014	CONCLUSION: Our study showed that the GMP-140 serum level and PAG were increased after ASD and VSD occlusion, and patients may have a trend of decreased GMP-140 serum levels after the ASD or VSD occlusion surgeries after the treatment with aspirin.	Aspirin	240-247	selectin P	Homo sapiens	153-160
25208590-11	2014	Low-dose aspirin taken at bedtime compared with intake on awakening reduces COX-1-dependent platelet reactivity during morning hours in healthy subjects.	Aspirin	9-16	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	76-81
25440788-7	2014	Finally, the combination of aspirin, clopidogrel, and low-dose rivaroxaban has recently been approved by the European Medicines Agency (but not the Food and Drug Administration) for secondary prevention after ACS.	Aspirin	28-35	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	209-212
25439353-3	2014	COX-1-inhibiting nonsteroidal anti-inflammatory drugs, including aspirin, aggravate the preexisting upper and lower respiratory disease, sometimes in a life-threatening manner.	Aspirin	65-72	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	0-5
25030064-7	2014	Moreover, administration of low-dose aspirin caused a significant reduction in total B cells in peripheral blood of healthy human volunteers, coincidentally with reduced TxA2 production and downregulation of JAK/STAT5 signaling.	Aspirin	37-44	signal transducer and activator of transcription 5A	Homo sapiens	212-217
25030064-8	2014	Taken together, our results demonstrate that COX-1-derived TxA2 plays a critical role in the stage transition of early B-cell development through regulation of JAK/STAT5 signaling and indicate a potential immune-suppressive effect of low-dose aspirin in humans.	Aspirin	243-250	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	45-50
25030064-8	2014	Taken together, our results demonstrate that COX-1-derived TxA2 plays a critical role in the stage transition of early B-cell development through regulation of JAK/STAT5 signaling and indicate a potential immune-suppressive effect of low-dose aspirin in humans.	Aspirin	243-250	signal transducer and activator of transcription 5A	Homo sapiens	164-169
25139986-6	2014	Initial activation of TLR4 results in accumulation of the cyclooxygenase-2-derived lipoxin precursor 15-hydroxyeicosatetraenoic acid (15-HETE) in esterified form within membrane phospholipids, which can be enhanced by aspirin (ASA) treatment.	Aspirin	218-225	toll like receptor 4	Homo sapiens	22-26
25139986-6	2014	Initial activation of TLR4 results in accumulation of the cyclooxygenase-2-derived lipoxin precursor 15-hydroxyeicosatetraenoic acid (15-HETE) in esterified form within membrane phospholipids, which can be enhanced by aspirin (ASA) treatment.	Aspirin	227-230	toll like receptor 4	Homo sapiens	22-26
25037608-0	2014	Association of serum periostin with aspirin-exacerbated respiratory disease.	Aspirin	36-43	periostin	Homo sapiens	21-30
25037608-2	2014	OBJECTIVE: To investigate the clinical implications of serum periostin levels in patients with aspirin-exacerbated respiratory disease (AERD) based on its overlapping TH2-mediated pathogenesis with the eosinophilic asthma.	Aspirin	95-102	periostin	Homo sapiens	61-70
25110431-8	2014	RESULTS: Treatment with aspirin suppressed the viability/proliferation of BON1, NCI-H727 and GOT1 cells in a time- and dose-dependent manner.	Aspirin	24-31	glutamic-oxaloacetic transaminase 1	Homo sapiens	93-97
25110431-12	2014	Aspirin suppressed mTOR downstream signaling, evidenced by the reduced phosphorylation of the mTOR substrates 4E binding protein 1, serine/threonine kinase P70S6K and S6 ribosomal protein and inhibited glycogen synthase kinase 3 activity.	Aspirin	0-7	ribosomal protein S6 kinase B1	Homo sapiens	156-162
24953043-0	2014	A computational prospect to aspirin side effects: aspirin and COX-1 interaction analysis based on non-synonymous SNPs.	Aspirin	28-35	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	62-67
24953043-1	2014	Aspirin (ASA) is a commonly used nonsteroidal anti-inflammatory drug (NSAID), which exerts its therapeutic effects through inhibition of cyclooxygenase (COX) isoform 2 (COX-2), while the inhibition of COX-1 by ASA leads to apparent side effects.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	201-206
24953043-1	2014	Aspirin (ASA) is a commonly used nonsteroidal anti-inflammatory drug (NSAID), which exerts its therapeutic effects through inhibition of cyclooxygenase (COX) isoform 2 (COX-2), while the inhibition of COX-1 by ASA leads to apparent side effects.	Aspirin	9-12	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	201-206
27147748-5	2016	Expression of BART miRNAs and lncRNAs correlated with NF-kappaB activity in EBV-infected epithelial cells, while treatment of EBV-harboring NPC C666-1 cells with aspirin (acetylsalicylic acid [ASA]) and the IkappaB kinase inhibitor PS-1145 inhibited NF-kappaB activity, resulting in downregulation of BART expression.	Aspirin	162-169	ADP ribosylation factor like GTPase 2 binding protein	Homo sapiens	301-305
27147748-5	2016	Expression of BART miRNAs and lncRNAs correlated with NF-kappaB activity in EBV-infected epithelial cells, while treatment of EBV-harboring NPC C666-1 cells with aspirin (acetylsalicylic acid [ASA]) and the IkappaB kinase inhibitor PS-1145 inhibited NF-kappaB activity, resulting in downregulation of BART expression.	Aspirin	193-196	ADP ribosylation factor like GTPase 2 binding protein	Homo sapiens	14-18
27133131-8	2016	Thrombin elevated ~900 lipids &gt;2-fold with 86% newly appearing and 45% inhibited by aspirin supplementation, indicating COX-1 is required for major activation-dependent lipidomic fluxes.	Aspirin	87-94	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	123-128
26596838-6	2016	In both cell lines, aspirin induced p21(CIP1).	Aspirin	20-27	H3 histone pseudogene 16	Homo sapiens	36-39
27055402-7	2016	Consistent with LEF1 being a downstream effector of Wnt signaling, aspirin, but not I3C, downregulated protein levels of the Wnt co-receptor LDL receptor-related protein-6 and beta-catenin and upregulated the beta-catenin destruction complex component Axin.	Aspirin	67-74	catenin beta 1	Homo sapiens	176-188
27055402-7	2016	Consistent with LEF1 being a downstream effector of Wnt signaling, aspirin, but not I3C, downregulated protein levels of the Wnt co-receptor LDL receptor-related protein-6 and beta-catenin and upregulated the beta-catenin destruction complex component Axin.	Aspirin	67-74	catenin beta 1	Homo sapiens	209-221
26743169-9	2016	CONCLUSIONS: Synergistic inhibition of both P2Y1 and P2Y12 adenosine diphosphate receptors by GLS-409 immediately attenuates platelet-mediated thrombosis and effectively blocks agonist-stimulated platelet aggregation irrespective of concomitant aspirin therapy.	Aspirin	245-252	purinergic receptor P2Y1	Homo sapiens	44-48
26470782-6	2016	Platelet COX-1 suppression by low-dose aspirin and the kinetics of its recovery after drug withdrawal were similar in patients and control subjects and were unaffected by glucose variability.	Aspirin	39-46	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	9-14
27001784-1	2016	The purpose of the research is to give the effectiveness and safety of ticagrelor in combination with acetylsalicylic acid as preoperative treatment of primary stenting in patients with ACS.	Aspirin	102-122	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	186-189
26586373-5	2016	Patients" stratification based on ASA dose showed more significant reductions in P-selectin, CD40L, and MMP-9 serum levels postclopidogrel administration in patients who were on baseline 81 mg ASA, as compared to patients on 325 mg ASA.	Aspirin	34-37	selectin P	Homo sapiens	81-91
26794215-10	2016	Aspirin treatment significantly inhibited the proliferation of 4T1 cells, and decreased the production of MCP-1 and PAI-1 in both the Ad-CM model and co-culture system.	Aspirin	0-7	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	116-121
26626190-2	2015	The vascular properties of low-dose acetyl salicylic acid (aspirin) provide cardiovascular benefits through the irreversible inhibition of platelet cyclooxygenase 1; however, the possible anti-hypertrophic properties and potential mechanism of aspirin have not been investigated in detail.	Aspirin	36-57	prostaglandin-endoperoxide synthase 1	Mus musculus	148-164
26626190-2	2015	The vascular properties of low-dose acetyl salicylic acid (aspirin) provide cardiovascular benefits through the irreversible inhibition of platelet cyclooxygenase 1; however, the possible anti-hypertrophic properties and potential mechanism of aspirin have not been investigated in detail.	Aspirin	59-66	prostaglandin-endoperoxide synthase 1	Mus musculus	148-164
26626190-9	2015	Aspirin also normalized the upregulated hypertrophic biomarkers, beta-myosin heavy chain (beta-MHC), atrial natriuretic peptide (ANP), and b-type natriuretic peptide (BNP).	Aspirin	0-7	natriuretic peptide type A	Mus musculus	101-127
26626190-9	2015	Aspirin also normalized the upregulated hypertrophic biomarkers, beta-myosin heavy chain (beta-MHC), atrial natriuretic peptide (ANP), and b-type natriuretic peptide (BNP).	Aspirin	0-7	natriuretic peptide type B	Mus musculus	139-165
26626190-9	2015	Aspirin also normalized the upregulated hypertrophic biomarkers, beta-myosin heavy chain (beta-MHC), atrial natriuretic peptide (ANP), and b-type natriuretic peptide (BNP).	Aspirin	0-7	natriuretic peptide type B	Mus musculus	167-170
26626190-10	2015	Aspirin efficiently reversed the upregulation of beta-catenin and P-Akt expression and the TAC- or ANG II-induced downregulation of GSK-3beta.	Aspirin	0-7	glycogen synthase kinase 3 beta	Mus musculus	132-141
26245672-2	2015	Low-dose aspirin, that induces a permanent inactivation of platelet cyclooxygenase (COX)-1, thus inhibiting TXA2 biosynthesis, should be theoretically considered the drug of choice.	Aspirin	9-16	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	68-90
26245672-5	2015	Among the proposed mechanisms, the variable turnover rate of the drug target (platelet COX-1) appears to represent the most convincing determinant of the inter-individual variability in aspirin response.	Aspirin	186-193	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	87-92
26474767-11	2015	Aspirin suppressed serum levels of the pro-inflammatory cytokines on tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), and the anti-inflammatory ability was positively associated with bone morphometry.	Aspirin	0-7	interferon gamma	Rattus norvegicus	113-129
26474767-11	2015	Aspirin suppressed serum levels of the pro-inflammatory cytokines on tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), and the anti-inflammatory ability was positively associated with bone morphometry.	Aspirin	0-7	interferon gamma	Rattus norvegicus	131-140
26134597-11	2015	Aspirin, but not PGE2, attenuated the increased mortality in mPGES-1 KO mice (P &lt; .05).	Aspirin	0-7	prostaglandin E synthase	Mus musculus	61-68
26159746-5	2015	Western blot analysis revealed that the combined treatment of MAG-DHA and ASA upregulated GPR-32 expression and downregulated cytosolic TNFalpha detection, hence preventing IkappaBalpha degradation and p65-NFkappaB phosphorylation.	Aspirin	74-77	G protein-coupled receptor 32	Homo sapiens	90-96
26159746-5	2015	Western blot analysis revealed that the combined treatment of MAG-DHA and ASA upregulated GPR-32 expression and downregulated cytosolic TNFalpha detection, hence preventing IkappaBalpha degradation and p65-NFkappaB phosphorylation.	Aspirin	74-77	golgi reassembly stacking protein 1	Homo sapiens	202-205
26159746-7	2015	The presence of ASA potentiated the inhibitory effects of MAG-DHA in reducing the Ca(2+) hypersensitivity triggered by IL-13 by decreasing the phosphorylation levels of the PKC-potentiated inhibitor protein-17 regulatory protein (CPI-17).	Aspirin	16-19	protein phosphatase 1 regulatory inhibitor subunit 14A	Homo sapiens	230-236
26237513-6	2015	Dual antiplatelet therapy with aspirin and clopidogrel was associated with significantly lower levels of sCD40L and lower platelet surface expressions of P-selectin and activated GPIIb/IIIa compared to aspirin monotherapy (all p&lt;=0.01).	Aspirin	31-38	selectin P	Homo sapiens	154-164
25648873-0	2015	Reproducibility over time and effect of low-dose aspirin on soluble P-selectin and soluble CD40 ligand.	Aspirin	49-56	selectin P	Homo sapiens	68-78
26093650-10	2015	RT-PCR demonstrated that the upregulation of NF-kappaB, MCP-1 and VCAM-1 after CA induction was reversed by aspirin treatment.	Aspirin	108-115	C-C motif chemokine ligand 2	Rattus norvegicus	56-61
25978737-3	2015	In this study, we engineered original cysteine positional variants of a Fab fragment, with less than 20% of ASA, and evaluated their thiol reactivities through conjugation with various kinds of payloads.	Aspirin	108-111	FA complementation group B	Homo sapiens	72-75
26149041-1	2015	The current standard care for acute coronary syndromes is dual antiplatelet therapy combining the COX1 inhibitor aspirin with a drug targeting the P2Y12 receptor, together with anticoagulation during and after early revascularization by percutaneous intervention.	Aspirin	113-120	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	98-102
28275397-2	2015	The aim of this study was to investigate the association between the -444A/C polymorphism of LTC4S gene and asthma, asthma phenotypes (aspirin intolerant/tolerant asthma) and different characteristics of the patients.	Aspirin	135-142	leukotriene C4 synthase	Homo sapiens	93-98
28275397-8	2015	CONCLUSION: The results show that LTC4S -444A/C SNP is not associated with susceptibility to asthma in Romanian patients, but could influence asthma phenotype, namely aspirin intolerant asthma.	Aspirin	167-174	leukotriene C4 synthase	Homo sapiens	34-39
25860557-7	2015	As for the OPR to aspirin, a weak statistical significance was observed in rs5445 (GNB3) (P = 0.049) and rs5758 (TBXA2R) (P = 0.045).	Aspirin	18-25	G protein subunit beta 3	Homo sapiens	83-87
25521453-2	2015	To investigate whether the use of aspirin and other NSAIDS reduces the risk of squamous cell carcinoma (SCC), we conducted a systematic review on the basis of published epidemiologic studies and calculated summary estimates for aspirin, nonaspirin NSAIDS, and any NSAIDS use.	Aspirin	34-41	serpin family B member 3	Homo sapiens	104-107
25521453-5	2015	There was significant heterogeneity between studies regarding SCC risk estimates for aspirin use and any NSAIDS use.	Aspirin	85-92	serpin family B member 3	Homo sapiens	62-65
25604474-4	2015	It was demonstrated by LC-ESI tandem-mass spectrometry that Zeise"s salt platinates the essential amino acids Tyr385 (active site of the enzyme) and Ser516 (will be acetylated by aspirin) of COX-1, thereby strongly impairing the function of the enzyme.	Aspirin	179-186	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	191-196
25116182-6	2015	Aspirin relieves the peripheral, cerebral and ocular ischemic disturbances by irreversible inhibition of platelet cyclo-oxygenase (COX-1) activity and aggregation ex vivo.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	131-136
25590316-13	2015	Our previous studies demonstrated that aspirin blocks trafficking of STAT6 into the nucleus and thereby prevents IL-4-mediated induction of these transcripts, thereby suggesting a modality by which aspirin desensitization could provide therapeutic benefit for AERD patients.	Aspirin	198-205	signal transducer and activator of transcription 6	Homo sapiens	69-74
26699137-10	2015	The effect of efavirenz on annexin-V-binding was further significantly blunted by p38 kinase inhibitor SB203580 (2 microM) and casein kinase 1alpha inhibitor D4476 (10 microM), but not by cyclooxygenase inhibitor aspirin (50 microM).	Aspirin	213-220	annexin A5	Homo sapiens	27-36
25967073-8	2015	Walls of ruptured human intracranial aneurysms have higher levels of COX-2 and microsomal prostaglandin E2 synthase 1 (mPGES-1), both of which are known to be inhibited by aspirin.	Aspirin	172-179	prostaglandin E synthase	Mus musculus	119-126
25967073-9	2015	In a pilot study, patients undergoing microsurgical clipping had attenuated expression of COX-2, mPGES-1, and macrophages in aneurysm walls after 3 months of aspirin therapy versus those that did not receive aspirin.	Aspirin	158-165	prostaglandin E synthase	Mus musculus	97-104
25936612-1	2015	Aspirin-exacerbated respiratory disease is a clinical entity comprising chronic rhinosinusitis with nasal polyposis, asthma and intolerance to COX-1 inhibiting drugs.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	143-148
25125468-4	2015	Previously, we found that treatment with the pro-resolving mediator aspirin-triggered lipoxin A4 (ATL), improved cognition, reduced Abeta levels, and enhanced microglia phagocytic activity in Tg2576 transgenic AD mice.	Aspirin	68-75	amyloid beta (A4) precursor protein	Mus musculus	132-137
25394850-4	2015	Mechanistically, ASA treatment upregulates the telomerase reverse transcriptase (TERT)/Wnt/beta-catenin cascade, leading to improvement of SHED-mediated bone regeneration, and also upregulates TERT/FASL signaling, leading to improvement of SHED-mediated T-cell apoptosis and ameliorating disease phenotypes in dextran sodium sulfate-induced colitis mice.	Aspirin	17-20	telomerase reverse transcriptase	Mus musculus	47-79
25394850-4	2015	Mechanistically, ASA treatment upregulates the telomerase reverse transcriptase (TERT)/Wnt/beta-catenin cascade, leading to improvement of SHED-mediated bone regeneration, and also upregulates TERT/FASL signaling, leading to improvement of SHED-mediated T-cell apoptosis and ameliorating disease phenotypes in dextran sodium sulfate-induced colitis mice.	Aspirin	17-20	telomerase reverse transcriptase	Mus musculus	81-85
25394850-4	2015	Mechanistically, ASA treatment upregulates the telomerase reverse transcriptase (TERT)/Wnt/beta-catenin cascade, leading to improvement of SHED-mediated bone regeneration, and also upregulates TERT/FASL signaling, leading to improvement of SHED-mediated T-cell apoptosis and ameliorating disease phenotypes in dextran sodium sulfate-induced colitis mice.	Aspirin	17-20	telomerase reverse transcriptase	Mus musculus	193-197
25450028-2	2015	Complexes 1 and 3 are also obtained when aspirin (aspH) is used.	Aspirin	41-48	aspartate beta-hydroxylase	Homo sapiens	50-54
25544832-8	2014	GBP patients were 43 [10] years old, 78% female, BMI 45 [7] kg/m(2), 73% ASA physical status of 2.	Aspirin	73-76	transmembrane protein 132A	Homo sapiens	0-3
25208590-9	2014	However, the morning increase in COX-1-dependent platelet activity was reduced by intake of aspirin at bedtime compared with on awakening (mean difference VerifyNow: -23 Aspirin Reaction Units [CI -50 to 4]; STxB2: -1.7 ng/ml [CI -2.7 to -0.8]).	Aspirin	92-99	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	33-38
25208590-9	2014	However, the morning increase in COX-1-dependent platelet activity was reduced by intake of aspirin at bedtime compared with on awakening (mean difference VerifyNow: -23 Aspirin Reaction Units [CI -50 to 4]; STxB2: -1.7 ng/ml [CI -2.7 to -0.8]).	Aspirin	170-177	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	33-38
25093998-0	2014	Effects of aspirin &amp; simvastatin and aspirin, simvastatin, &amp; lipoic acid on heme oxygenase-1 in healthy human subjects.	Aspirin	41-48	heme oxygenase 1	Homo sapiens	84-100
25104439-0	2014	Genetic variation in the JAK/STAT/SOCS signaling pathway influences breast cancer-specific mortality through interaction with cigarette smoking and use of aspirin/NSAIDs: the Breast Cancer Health Disparities Study.	Aspirin	155-162	cytokine inducible SH2 containing protein	Homo sapiens	34-38
25104439-8	2014	SOCS2 (one of three SNPs) and all STAT3, STAT5A, and STAT5B SNPs significantly interacted with use of aspirin/NSAIDs to alter breast cancer-specific mortality.	Aspirin	102-109	signal transducer and activator of transcription 5A	Homo sapiens	41-47
25085874-3	2014	Therefore, we examined the association between recent (1 year) prediagnostic use of aspirin (COX1/COX2 inhibitor), lymph node involvement at breast cancer diagnosis, and breast cancer-specific mortality.	Aspirin	84-91	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	93-97
25056814-3	2014	Polymorphisms rs4794067 and rs16947078 of TBX21 were found to be associated with acetylsalicylic acid-induced and allergic asthma, respectively.	Aspirin	81-101	T-box transcription factor 21	Homo sapiens	42-47
24942808-1	2014	BACKGROUND: Even though the acetylation of platelet cyclooxygenase (COX)-1 at serine-529 is the direct mechanism of action of low-dose aspirin, its antiplatelet effect has been characterized using indirect indexes of COX-1 activity.	Aspirin	135-142	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	52-74
24942808-1	2014	BACKGROUND: Even though the acetylation of platelet cyclooxygenase (COX)-1 at serine-529 is the direct mechanism of action of low-dose aspirin, its antiplatelet effect has been characterized using indirect indexes of COX-1 activity.	Aspirin	135-142	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	217-222
24942808-4	2014	RESULTS: Acetylation of platelet COX-1 was measurable before detection of aspirin levels in the systemic circulation and increased in a cumulative fashion upon repeated dosing.	Aspirin	74-81	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	33-38
24942808-8	2014	CONCLUSIONS: The demonstrated feasibility of quantifying the extent and duration of platelet COX-1 acetylation will allow characterizing the genetic, pharmacokinetic and pharmacodynamic determinants of the inter-individual variability in the antiplatelet response to low-dose aspirin as well as identifying extra-platelet sites of drug action.	Aspirin	276-283	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	93-98
24908358-4	2014	To address this inconsistency, we hypothesize that antiplatelet effect of aspirin via inhibition of COX-1 may be one of potential mechanisms to inhibit carcinogenesis.	Aspirin	74-81	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	100-105
24836854-0	2014	Aspirin-triggered Lipoxin A4 attenuates mechanical allodynia in association with inhibiting spinal JAK2/STAT3 signaling in neuropathic pain in rats.	Aspirin	0-7	signal transducer and activator of transcription 3	Rattus norvegicus	104-109
24889212-7	2014	RESULTS: We found indications that aspirin interacted with rs6983267 close to MYC (encoding a transcription factor involved in cell cycle progression, apoptosis and cellular transformation) and NSAIDs interacted with rs3024505 and rs1800872 in or close to IL10 (encoding IL-10) in preventing CRC.	Aspirin	35-42	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	78-81
24682773-8	2014	Aspirin desensitization uses the repetitive application of aspirin to induce a tolerance to NSAIDs, especially COX-1 inhibitors.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	111-116
24682773-8	2014	Aspirin desensitization uses the repetitive application of aspirin to induce a tolerance to NSAIDs, especially COX-1 inhibitors.	Aspirin	59-66	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	111-116
25023354-4	2014	Low-dose aspirin acts as an antiplatelet agent by causing an irreversible inactivation of platelet COX-1 activity and the synthesis of thromboxane A2.	Aspirin	9-16	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	99-104
24613833-0	2014	Aspirin augments the expression of Adenomatous Polyposis Coli protein by suppression of IKKbeta.	Aspirin	0-7	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	88-95
24613833-9	2014	Previous reports indicated that aspirin specifically inhibits IKKbeta activity, and constitutively active form of IKKbeta accelerates APC loss.	Aspirin	32-39	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	62-69
24613833-10	2014	We found that aspirin suppressed the expression of IKKbeta, and the deletion of IKKbeta by siRNA increases the expression of APC in HEK294 cells.	Aspirin	14-21	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	51-58
24613833-12	2014	Taken together, these results reveal that aspirin up-regulates the expression of APC via the suppression of IKKbeta.	Aspirin	42-49	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	108-115
24520038-7	2014	For aspirin, the major mechanism is the anti-inflammatory action through the inhibition of COX-1/COX-2 and modulation of the NFkappaB or STAT3 pathway.	Aspirin	4-11	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	91-96
24648214-7	2014	Low-dose aspirin improved HFD-induced hyperinsulinemia and hyperlipidemia, recovered PT and aPTT, inhibited upregulation of adhesion molecules and chemokines and reduced expression of PKCalpha, IKKalpha, p65, and MAPKs.	Aspirin	9-16	component of inhibitor of nuclear factor kappa B kinase complex	Rattus norvegicus	194-202
24205990-4	2014	Most commonly-used anti-platelet drugs such as aspirin block the cyclooxygenase (COX)-1 pathway of platelet activation, similar to the action of antioxidants with respect to neutralising hydrogen peroxide (H2 O2 ), with a similar effect on thromboxane production via the COX-1 pathway.	Aspirin	47-54	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	65-87
24205990-4	2014	Most commonly-used anti-platelet drugs such as aspirin block the cyclooxygenase (COX)-1 pathway of platelet activation, similar to the action of antioxidants with respect to neutralising hydrogen peroxide (H2 O2 ), with a similar effect on thromboxane production via the COX-1 pathway.	Aspirin	47-54	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	271-276
25293617-2	2014	The proven benefits of aspirin in preventing further thrombotic events in patients with prior ACS or stroke make it difficult to withdraw this therapy.	Aspirin	23-30	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	94-97
24243637-9	2014	Treatment of adipocyte fractions or SGBS adipocytes with metformin or acetylsalicylic acid, which target C/EBPbeta and NF-kappaB/RelA signaling, attenuated the IL-1alpha induction of 11beta-HSD1 (P&lt;=.002).	Aspirin	70-90	interleukin 1 alpha	Homo sapiens	160-169
24317174-1	2013	BACKGROUND: Regular aspirin use reduces the risk for colorectal cancer (CRC), possibly through inhibition of WNT/cadherin-associated protein beta1 (CTNNB1 or beta-catenin) signaling.	Aspirin	20-27	catenin beta 1	Homo sapiens	148-154
24317174-1	2013	BACKGROUND: Regular aspirin use reduces the risk for colorectal cancer (CRC), possibly through inhibition of WNT/cadherin-associated protein beta1 (CTNNB1 or beta-catenin) signaling.	Aspirin	20-27	catenin beta 1	Homo sapiens	158-170
24317174-9	2013	Moreover, among individuals with protective T allele, the effect of regular aspirin use was limited to those with positive nuclear CTNNB1 expression.	Aspirin	76-83	catenin beta 1	Homo sapiens	131-137
24317174-10	2013	In a functional analysis, in vitro treatment of LS174T cells (a cell line heterozygous for rs6983267) with aspirin was statistically significantly associated with higher G/T allelic ratio of TCF7L2 immunoprecipitated DNA (P = .03).	Aspirin	107-114	transcription factor 7 like 2	Homo sapiens	191-197
24317174-11	2013	CONCLUSIONS: Our results support an influence of aspirin on WNT/CTNNB1 signaling and suggest that aspirin chemoprevention may be tailored according to rs6983267 genotype.	Aspirin	49-56	catenin beta 1	Homo sapiens	64-70
24211213-10	2013	Comparison of the myosin ATPase activated by the various mutant actins at the same concentration of F-actin showed that the extent of activation correlates well with the solvent-accessible surface areas (ASA) of the replaced amino acid molecule.	Aspirin	204-207	myosin heavy chain 14	Homo sapiens	18-24
23386708-5	2013	METHODS AND RESULTS: In vitro platelet activation resulted in the transfer of miR-126 from the platelet to the plasma compartment, which was prevented by aspirin.	Aspirin	154-161	microRNA 126	Homo sapiens	78-85
23386708-7	2013	The administration of aspirin resulted both in platelet inhibition and concomitantly reduced circulating levels of platelet-derived microRNAs including miR-126.	Aspirin	22-29	microRNA 126	Homo sapiens	152-159
23386708-9	2013	Consequently, in patho-physiological conditions associated with platelet activation, such as diabetes type 2, the administration of aspirin may lead to reduced levels of circulating miR-126.	Aspirin	132-139	microRNA 126	Homo sapiens	182-189
23838032-1	2013	AIMS: Aspirin achieves its antithrombotic effect through inactivation of cyclo-oxygenase (COX)-1, thereby preventing generation of thromboxane (TX)A2 from arachidonic acid (AA).	Aspirin	6-13	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	73-96
23838032-2	2013	The reported prevalence of aspirin "resistance" varies significantly and is usually based on platelet function tests (PFTs) that use AA-induced platelet reactivity as a surrogate measure of the effect of aspirin, rather than specific assessment of its effect on its therapeutic target (ie, COX-1 inhibition).	Aspirin	27-34	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	290-295
23838032-9	2013	However, serum [TXB2] was consistently low, thereby confirming adequate inhibition of COX-1 by aspirin.	Aspirin	95-102	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	86-91
23838032-11	2013	CONCLUSION: This study demonstrates that although COX-1 activity is adequately and consistently suppressed by aspirin in stroke patients, this effect is not reliably indicated by whole-blood clotting in response to AA.	Aspirin	110-117	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	50-55
23896061-0	2013	Hydrogen sulfide-releasing aspirin inhibits the growth of leukemic Jurkat cells and modulates beta-catenin expression.	Aspirin	27-34	catenin beta 1	Homo sapiens	94-106
23668350-4	2013	Furthermore, ibuprofen and aspirin were found to be preferential inhibitor of COX-1 and COX-2, respectively.	Aspirin	27-34	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	78-83
23649702-10	2013	It is postulated that calcium and magnesium bind to BChE and thereby change the conformation of the enzyme to a more appropriate position for aspirin hydrolysis.	Aspirin	142-149	butyrylcholinesterase	Homo sapiens	52-56
22351525-9	2013	TERT-CLPTM1L rs2853668 interacted significantly with aspirin/NSAID use, where those with the AA genotype had a much lower risk of colon cancer when using aspirin/NSAIDs than those with the other genotypes.	Aspirin	53-60	telomerase reverse transcriptase	Homo sapiens	0-4
22351525-9	2013	TERT-CLPTM1L rs2853668 interacted significantly with aspirin/NSAID use, where those with the AA genotype had a much lower risk of colon cancer when using aspirin/NSAIDs than those with the other genotypes.	Aspirin	53-60	CLPTM1 like	Homo sapiens	5-12
22351525-9	2013	TERT-CLPTM1L rs2853668 interacted significantly with aspirin/NSAID use, where those with the AA genotype had a much lower risk of colon cancer when using aspirin/NSAIDs than those with the other genotypes.	Aspirin	154-161	telomerase reverse transcriptase	Homo sapiens	0-4
22351525-9	2013	TERT-CLPTM1L rs2853668 interacted significantly with aspirin/NSAID use, where those with the AA genotype had a much lower risk of colon cancer when using aspirin/NSAIDs than those with the other genotypes.	Aspirin	154-161	CLPTM1 like	Homo sapiens	5-12
23549485-0	2013	Soluble P-selectin level correlates with acetylsalicylic acid but not with clopidogrel response in patients with stable coronary artery disease after a percutaneous coronary intervention.	Aspirin	41-61	selectin P	Homo sapiens	8-18
23493387-2	2013	Here, we first confirmed that aspirin downregulated androgen receptor (AR) and prostate-specific antigen in prostate cancer cells.	Aspirin	30-37	kallikrein related peptidase 3	Homo sapiens	79-104
23494120-4	2013	In Helicobacter pylori-negative patients with normal gastric histology taking aspirin or NSAIDs, we found elevated gastric PAI-1 mRNA abundance compared with controls; the increase in patients on aspirin was independent of whether they were also taking proton pump inhibitors.	Aspirin	78-85	serpin family E member 1	Homo sapiens	123-128
23494120-4	2013	In Helicobacter pylori-negative patients with normal gastric histology taking aspirin or NSAIDs, we found elevated gastric PAI-1 mRNA abundance compared with controls; the increase in patients on aspirin was independent of whether they were also taking proton pump inhibitors.	Aspirin	196-203	serpin family E member 1	Homo sapiens	123-128
23494120-11	2013	Thus, PAI-1 expression is increased in gastric epithelial cells in response to mucosal irritants such as aspirin and NSAIDs probably via an indirect mechanism, and PAI-1 acts as a local autoregulator to minimize mucosal damage.	Aspirin	105-112	serpin family E member 1	Homo sapiens	6-11
23349014-7	2013	Treatment with low-dose aspirin to mice homozygous for the TH-MYCN transgene significantly reduced the tumor burden (P &lt; 0.01), the presence of tumor-associated cells of the innate immune system (P &lt; 0.01), as well as the intratumoral expression of transforming growth factor-beta, thromboxane A2 (P &lt; 0.05) and prostaglandin D2 (P &lt; 0.01).	Aspirin	24-31	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	62-66
23349014-8	2013	In conclusion, tumor-associated inflammation appears as a potential therapeutic target in NB and low-dose aspirin reduces tumor burden in the TH-MYCN transgenic mouse model of NB, hence warranting further studies on aspirin in high-risk NB.	Aspirin	106-113	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	145-149
23283029-3	2013	Hypothetically considering its antiaggregating and anti-inflammatory effects, aspirin might also be beneficial for the primary prevention of ACS in patients with pneumonia.	Aspirin	78-85	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	141-144
23283029-10	2013	RESULTS: The chi-test showed that the rates of ACS at 1 month were 1.1% (n=1) in the aspirin group and 10.6% (n=10) in the control group (relative risk, 0.103; 95% confidence interval 0.005-0.746; P=0.015).	Aspirin	85-92	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	47-50
23283029-11	2013	Aspirin therapy was associated with a 9% absolute reduction in the risk for ACS.	Aspirin	0-7	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	76-79
23283029-13	2013	CONCLUSION: This randomized open-label study shows that acetyl salicylic acid is beneficial in the reduction of ACS and cardiovascular mortality among patients with pneumonia.	Aspirin	56-77	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	112-115
23485446-0	2013	Aspirin extends the lifespan of Caenorhabditis elegans via AMPK and DAF-16/FOXO in dietary restriction pathway.	Aspirin	0-7	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	68-74
23485446-4	2013	The extension of lifespan by aspirin requires DAF-16/FOXO, AMPK, and LKB1, but not SIR-2.1.	Aspirin	29-36	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	46-52
23485446-7	2013	Taken together, aspirin might act through a dietary restriction-like mechanism, via increasing the AMP:ATP ratio and activating LKB1, subsequently activating AMPK, which stimulates DAF-16 to induce downstream effects through a DAF-16 translocation independent manner.	Aspirin	16-23	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	181-187
23485446-7	2013	Taken together, aspirin might act through a dietary restriction-like mechanism, via increasing the AMP:ATP ratio and activating LKB1, subsequently activating AMPK, which stimulates DAF-16 to induce downstream effects through a DAF-16 translocation independent manner.	Aspirin	16-23	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	227-233
23524841-10	2013	CONCLUSIONS: In patients with chronic stable coronary disease, all clinically relevant daily doses of aspirin tested, from 81 to 1300 mg, produce similar and statistically significant increases in HO-1 and decreases in ADMA.	Aspirin	102-109	heme oxygenase 1	Homo sapiens	197-201
23169598-2	2013	Among these genes, periostin is known to be overexpressed in nasal polyps obtained from aspirin-sensitive patients.	Aspirin	88-95	periostin	Homo sapiens	19-28
23404329-3	2013	Results             demonstrated that low doses of ASP (1 mM), CUR (10 microM) and SFN (5 microM) (ACS) combination             reduced cell viability by ~70% (P&lt;0.001), and also induced cell apoptosis by             ~51% (P&lt;0.001) accompanied by activation of caspase-3 and Poly(ADP-ribose)             polymerase (PARP) proteins.	Aspirin	51-54	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	99-102
24953043-2	2014	In the present study, the relationship between COX-1 non-synonymous single nucleotide polymorphisms (nsSNPs) and aspirin related side effects was investigated.	Aspirin	113-120	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	47-52
24953043-3	2014	The functional impacts of 37 nsSNPs on aspirin inhibition potency of COX-1 with COX-1/aspirin molecular docking were computationally analyzed, and each SNP was scored based on DOCK Amber score.	Aspirin	39-46	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	69-74
24953043-3	2014	The functional impacts of 37 nsSNPs on aspirin inhibition potency of COX-1 with COX-1/aspirin molecular docking were computationally analyzed, and each SNP was scored based on DOCK Amber score.	Aspirin	39-46	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	80-85
24953043-3	2014	The functional impacts of 37 nsSNPs on aspirin inhibition potency of COX-1 with COX-1/aspirin molecular docking were computationally analyzed, and each SNP was scored based on DOCK Amber score.	Aspirin	86-93	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	69-74
24953043-9	2014	Our data represent a computational sub-population pattern for aspirin COX-1 related side effects, and provide basis for further research on COX-1/ASA interaction.	Aspirin	62-69	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	70-75
24953043-9	2014	Our data represent a computational sub-population pattern for aspirin COX-1 related side effects, and provide basis for further research on COX-1/ASA interaction.	Aspirin	146-149	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	140-145
24861258-8	2014	RESULTS: Platelet aggregation increased by 109+-150 (arachidonic acid) and 47+-155 (collagen) aggregation units per minute from 1 to 24 h after aspirin intake (p-values &lt;0.0001) with corresponding increases in thromboxane B2 (5.6+-5.1 ng/ml, p&lt;0.0001) and soluble P-selectin (6.2+-15.5 ng/ml, p&lt;0.0001).	Aspirin	144-151	selectin P	Homo sapiens	270-280
25079372-3	2014	The reduction in Gcn4 abundance on ASA accumulation requires Cdk8/Srb10 and Pho85, cyclin-dependent kinases (CDKs) known to mediate rapid turnover of Gcn4 by the proteasome via phosphorylation of the Gcn4 activation domain under nonstarvation conditions.	Aspirin	35-38	cyclin-dependent serine/threonine protein kinase SSN3	Saccharomyces cerevisiae S288C	61-65
25079372-3	2014	The reduction in Gcn4 abundance on ASA accumulation requires Cdk8/Srb10 and Pho85, cyclin-dependent kinases (CDKs) known to mediate rapid turnover of Gcn4 by the proteasome via phosphorylation of the Gcn4 activation domain under nonstarvation conditions.	Aspirin	35-38	cyclin-dependent serine/threonine protein kinase SSN3	Saccharomyces cerevisiae S288C	66-71
25079372-3	2014	The reduction in Gcn4 abundance on ASA accumulation requires Cdk8/Srb10 and Pho85, cyclin-dependent kinases (CDKs) known to mediate rapid turnover of Gcn4 by the proteasome via phosphorylation of the Gcn4 activation domain under nonstarvation conditions.	Aspirin	35-38	cyclin-dependent serine/threonine protein kinase SSN3	Saccharomyces cerevisiae S288C	109-113
25079372-5	2014	These and other findings suggest that the two CDKs target different populations of Gcn4 on ASA accumulation, with Srb10 clearing mostly inactive Gcn4 molecules at the promoter that are enriched for sumoylation of the activation domain, and Pho85 clearing molecules unbound to the UAS that include both fully functional and inactive Gcn4 species.	Aspirin	91-94	cyclin-dependent serine/threonine protein kinase SSN3	Saccharomyces cerevisiae S288C	46-50
25075522-9	2014	The combination of LPS and ASA selectively altered the CYP 3A4, CYP 2E1 and CYP 1A1 catalytic activities.	Aspirin	27-30	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	64-71
25075522-9	2014	The combination of LPS and ASA selectively altered the CYP 3A4, CYP 2E1 and CYP 1A1 catalytic activities.	Aspirin	27-30	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	76-83
24759558-4	2014	Here, we integrate the available evidence on periostin expression and its roles in otolaryngological diseases, including allergic rhinitis, chronic rhinosinusitis with nasal polyps, aspirin-induced asthma, organized hematoma, eosinophilic otitis media, and IgG4-related disease.	Aspirin	182-189	periostin	Homo sapiens	45-54
24692216-0	2014	Aspirin and probenecid inhibit organic anion transporter 3-mediated renal uptake of cilostazol and probenecid induces metabolism of cilostazol in the rat.	Aspirin	0-7	solute carrier family 22 member 8	Rattus norvegicus	31-58
24692216-11	2014	Benzylpenicillin, aspirin, and cyclo-trans-4-l-hydroxyprolyl-l-serine (JBP485) reduced cilostazol uptake in kidney slices and human organic anion transporter 3 (hOAT3)-human embryonic kidney 293 (HEK293) cells, whereas p-aminohippuric acid did not.	Aspirin	18-25	solute carrier family 22 member 8	Homo sapiens	132-159
24692216-15	2014	Aspirin inhibits OAT3-mediated uptake of cilostazol and does not influence cilostazol metabolism.	Aspirin	0-7	solute carrier family 22 member 8	Rattus norvegicus	17-21
24748969-8	2014	As platelets lack a nucleus, regular aspirin use may exert long-lasting effects on irreversible inhibition of cyclooxygenase (COX)-1 and, subsequently, the secretion of alpha-granules, which contributes to the maintenance of the EMT state of CTCs.	Aspirin	37-44	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	110-132
24748969-9	2014	Thus, we hypothesized that the inhibition of platelet-induced EMT of CTCs through the COX-1 signaling pathway may contribute to the intriguing antimetastatic potential of aspirin.	Aspirin	171-178	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	86-91
24760190-3	2014	We hypothesized that the effect of aspirin may be antagonized by low 15-PGDH expression in the normal colon.	Aspirin	35-42	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	69-76
24760190-7	2014	Compared with nonuse, regular aspirin use was associated with lower risk of colorectal cancer that developed within a background of colonic mucosa with high 15-PGDH expression [multivariable HR, 0.49; 95% confidence interval (CI), 0.34 to 0.71], but not with low 15-PGDH expression (multivariable HR, 0.90; 95% CI, 0.63 to 1.27) (P for heterogeneity = 0.018).	Aspirin	30-37	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	157-164
24760190-7	2014	Compared with nonuse, regular aspirin use was associated with lower risk of colorectal cancer that developed within a background of colonic mucosa with high 15-PGDH expression [multivariable HR, 0.49; 95% confidence interval (CI), 0.34 to 0.71], but not with low 15-PGDH expression (multivariable HR, 0.90; 95% CI, 0.63 to 1.27) (P for heterogeneity = 0.018).	Aspirin	30-37	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	263-270
24760190-8	2014	Regular aspirin use was associated with lower incidence of colorectal cancers arising in association with high 15-PGDH expression, but not with low 15-PGDH expression in normal colon mucosa.	Aspirin	8-15	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	111-118
24760190-9	2014	This suggests that 15-PGDH expression level in normal colon mucosa may serve as a biomarker that may predict stronger benefit from aspirin chemoprevention.	Aspirin	131-138	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	19-26
24503782-2	2014	Previously, it has been reported that COX inhibitors, such as aspirin, reduce the incidence of human colorectal cancer; therefore, it is widely believed that COX-2 is a potential therapeutic and chemoprevention target for several types of human cancer.	Aspirin	62-69	prostaglandin-endoperoxide synthase 2	Canis lupus familiaris	158-163
24120690-0	2014	Plasma apolipoprotein H levels are different between aspirin induced respiratory diseases and aspirin tolerant asthma.	Aspirin	53-60	apolipoprotein H	Homo sapiens	7-23
24120690-0	2014	Plasma apolipoprotein H levels are different between aspirin induced respiratory diseases and aspirin tolerant asthma.	Aspirin	94-101	apolipoprotein H	Homo sapiens	7-23
24589018-5	2014	After 2 weeks of drinking, we detected the gastric mucosal damage together with MPO, MDA and 8-OHdG in rat aspirin induced gastric injury model.	Aspirin	107-114	myeloperoxidase	Rattus norvegicus	80-83
24587639-8	2014	The oxidative stress levels of MDA and MPO in the gastric tissues increased significantly in the aspirin-treated group compared with the HRW group (2.43 +- 0.145 vs 1.79 +- 0.116 nmol/mg prot, P &lt; 0.05 and 2.53 +- 0.238 vs 1.40 +- 0.208 U/g tissue, P &lt; 0.05, respectively).	Aspirin	97-104	myeloperoxidase	Rattus norvegicus	39-42
24605250-7	2014	Daily low-dose aspirin achieves complete and persistent inhibition of cyclooxygenase (COX)-1 in platelets (in pre-systemic circulation) while causing a limited and rapidly reversible inhibitory effect on COX-2 and/or COX-1 expressed in nucleated cells.	Aspirin	15-22	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	70-92
24605250-7	2014	Daily low-dose aspirin achieves complete and persistent inhibition of cyclooxygenase (COX)-1 in platelets (in pre-systemic circulation) while causing a limited and rapidly reversible inhibitory effect on COX-2 and/or COX-1 expressed in nucleated cells.	Aspirin	15-22	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	217-222
25258626-8	2014	Factors affecting the utilization of DPP-4 inhibitors included age (P = 0.049) and concomitant use of beta blockers (P = 0.045) and aspirin (P = 0.008).	Aspirin	132-139	dipeptidyl peptidase 4	Homo sapiens	37-42
24190973-8	2014	The activation of p53 through AMPK-mediated MDMX phosphorylation and inactivation was further confirmed by using cell and animal model systems with two AMPK activators, metformin and salicylate (the active form of aspirin).	Aspirin	214-221	MDM4 regulator of p53	Homo sapiens	44-48
25139652-4	2014	It has been shown that NSAIDs with high COX-1 affinity like ibuprofen and naproxen cause a pharmacodynamic interaction with the inhibition of thromboxane synthesis by acetylsalicylic acid.	Aspirin	167-187	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	40-45
23216649-0	2014	The membrane expression of P-selectin, but not monocyte-platelet aggregates, is influenced by variability in response to aspirin in patients with coronary artery disease.	Aspirin	121-128	selectin P	Homo sapiens	27-37
24433232-0	2014	A platelet P-selectin test predicts adverse cardiovascular events in patients with acute coronary syndromes treated with aspirin and clopidogrel.	Aspirin	121-128	selectin P	Homo sapiens	11-21
24453831-3	2013	The objective of this study was to verify the effect of double dose (DD) of aspirin and clopidogrel on HPR detected by PFA-100 and its relation to VWF and to its regulatory metalloprotease ADAMTS-13.	Aspirin	76-83	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	189-198
23989613-0	2013	Aspirin prolongs survival and reduces the number of Foxp3+ regulatory T cells in a genetically engineered mouse model of pancreatic cancer.	Aspirin	0-7	forkhead box P3	Mus musculus	52-57
23989613-12	2013	Furthermore, we found that administration of aspirin in combination with gemcitabine reduced the number of Foxp3(+) regulatory T cells significantly.	Aspirin	45-52	forkhead box P3	Mus musculus	107-112
24155779-0	2013	Aspirin Blocks EGF-stimulated Cell Viability in a COX-1 Dependent Manner in Ovarian Cancer Cells.	Aspirin	0-7	epidermal growth factor	Homo sapiens	15-18
24155779-0	2013	Aspirin Blocks EGF-stimulated Cell Viability in a COX-1 Dependent Manner in Ovarian Cancer Cells.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	50-55
24155779-3	2013	Because aspirin is a rather selective inhibitor of COX-1, the ability of aspirin to reduce the risk of ovarian cancer may be dependent on the level of COX-1 expression in those cells.	Aspirin	8-15	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	51-56
24155779-3	2013	Because aspirin is a rather selective inhibitor of COX-1, the ability of aspirin to reduce the risk of ovarian cancer may be dependent on the level of COX-1 expression in those cells.	Aspirin	8-15	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	151-156
24155779-3	2013	Because aspirin is a rather selective inhibitor of COX-1, the ability of aspirin to reduce the risk of ovarian cancer may be dependent on the level of COX-1 expression in those cells.	Aspirin	73-80	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	51-56
24155779-3	2013	Because aspirin is a rather selective inhibitor of COX-1, the ability of aspirin to reduce the risk of ovarian cancer may be dependent on the level of COX-1 expression in those cells.	Aspirin	73-80	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	151-156
24155779-5	2013	Here we investigated if aspirin attenuates EGFR-activated ovarian cancer cell growth in a COX-1 dependent manner.	Aspirin	24-31	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	90-95
24155779-6	2013	METHODS: Cell viability assays and Western blot analyses were used to determine the effect of aspirin on EGF-stimulated cell proliferation.	Aspirin	94-101	epidermal growth factor	Homo sapiens	105-108
24155779-8	2013	RESULTS: Aspirin inhibited cell viability induced by EGF in a dose dependent manner in COX-1 positive ovarian cancer cells.	Aspirin	9-16	epidermal growth factor	Homo sapiens	53-56
24155779-8	2013	RESULTS: Aspirin inhibited cell viability induced by EGF in a dose dependent manner in COX-1 positive ovarian cancer cells.	Aspirin	9-16	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	87-92
24155779-10	2013	In particular, aspirin decreased phosphorylated Akt and Erk activated by EGF.	Aspirin	15-22	epidermal growth factor	Homo sapiens	73-76
24155779-11	2013	COX-1 silencing in COX-1 positive cells attenuated the inhibitory effect of aspirin on EGF-stimulated cell viability.	Aspirin	76-83	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	0-5
24155779-11	2013	COX-1 silencing in COX-1 positive cells attenuated the inhibitory effect of aspirin on EGF-stimulated cell viability.	Aspirin	76-83	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	19-24
24155779-11	2013	COX-1 silencing in COX-1 positive cells attenuated the inhibitory effect of aspirin on EGF-stimulated cell viability.	Aspirin	76-83	epidermal growth factor	Homo sapiens	87-90
24155779-14	2013	CONCLUSIONS: Taken together, aspirin inhibits viability of ovarian cancer cells by blocking phosphorylation of Akt and Erk activated by EGF.	Aspirin	29-36	epidermal growth factor	Homo sapiens	136-139
24018490-11	2013	Finally, at 72 h of ASA exposure, we identified overexpression of adenylsuccinate synthase, 2"-3"-di-deoxyadenosine, ubiquitin-protein-ligase E6A, adenylosuccinate-lyase and nibrin (NBN).	Aspirin	20-23	nibrin	Homo sapiens	174-180
24018490-11	2013	Finally, at 72 h of ASA exposure, we identified overexpression of adenylsuccinate synthase, 2"-3"-di-deoxyadenosine, ubiquitin-protein-ligase E6A, adenylosuccinate-lyase and nibrin (NBN).	Aspirin	20-23	nibrin	Homo sapiens	182-185
22609818-0	2013	Genetic polymorphisms of HO-1 and COX-1 are associated with aspirin resistance defined by light transmittance aggregation in Chinese Han patients.	Aspirin	60-67	heme oxygenase 1	Homo sapiens	25-29
22609818-1	2013	BACKGROUND: Cyclooxygenase 1 (COX-1), COX-2, and HO-1 are involved in the process of aspirin"s effect.	Aspirin	85-92	heme oxygenase 1	Homo sapiens	49-53
23799623-10	2013	Exogenously added folic acid reversed the MTX-mediated DHFR inhibition following either MTX or MTX + ASA treatments.	Aspirin	101-104	dihydrofolate reductase	Homo sapiens	55-59
23804278-1	2013	Platelet P2Y12-ADP and COX-1 receptor inhibition with oral clopidogrel (CLO) and low-dose aspirin (ASA), respectively, attenuates reflex-mediated cutaneous vasodilation, but little is known about how these medications affect local vasodilatory signaling.	Aspirin	90-97	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	23-28
23804278-1	2013	Platelet P2Y12-ADP and COX-1 receptor inhibition with oral clopidogrel (CLO) and low-dose aspirin (ASA), respectively, attenuates reflex-mediated cutaneous vasodilation, but little is known about how these medications affect local vasodilatory signaling.	Aspirin	99-102	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	23-28
23976826-8	2013	The discussed information thus provides insight to the predicted active site and ASA values of Dopamine N-acetyl transferase model in Tribolium castaneum.	Aspirin	81-84	dopamine N acetyltransferase	Tribolium castaneum	104-124
23475158-3	2013	The inhibition rate of reversine and aspirin on cervical cancer cell lines" (HeLa and U14) was determined by MTT method, cell cycle of HeLa and U14 cells was analyzed by FACS, mitochondrial membrane potential of HeLa and U14 was detected using a JC-1 kit.	Aspirin	37-44	small nucleolar RNA, C/D box 14A	Homo sapiens	86-89
24073359-0	2013	Neuroblastoma-related inflammation: May small doses of aspirin be suitable for small cancer patients?	Aspirin	55-62	Rho guanine nucleotide exchange factor (GEF) 16	Mus musculus	0-13
24073359-2	2013	The continuous administration of low-dose aspirin to TH-MYCN mice (a model of pediatric neuroblastoma) delays tumor outgrowth and decreases tumor-promoting inflammation by inhibiting regulatory cells of the innate immune system as well as immunosuppressive mediators such as transforming growth factor beta (TGFbeta) and thromboxane A2.	Aspirin	42-49	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	56-60
23664562-0	2013	Effective, selective and specific inhibition of COX-1 may overcome the "aspirin paradox".	Aspirin	72-79	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	48-53
23474908-12	2013	Hence, 12 months of ACS treatment using ticagrelor/ASA instead of clopidogrel/ASA may offer a cost-effective therapeutic option, even when the generic price for clopidogrel is employed.	Aspirin	51-54	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	20-23
23803522-13	2013	PDTC, asa strong NF-kappaB inhibitor, may inhibit NF-kappaB activity and further significantly decreased expressions of alpha-SMA, integrin alpha5 and fibronectin which were important part of ECM, leading to drastically attenuated pulmonary fibrosis.	Aspirin	6-9	actin gamma 2, smooth muscle	Rattus norvegicus	120-129
23803522-13	2013	PDTC, asa strong NF-kappaB inhibitor, may inhibit NF-kappaB activity and further significantly decreased expressions of alpha-SMA, integrin alpha5 and fibronectin which were important part of ECM, leading to drastically attenuated pulmonary fibrosis.	Aspirin	6-9	fibronectin 1	Rattus norvegicus	151-162
23508960-0	2013	Aspirin hydrolysis in plasma is a variable function of butyrylcholinesterase and platelet-activating factor acetylhydrolase 1b2 (PAFAH1b2).	Aspirin	0-7	butyrylcholinesterase	Homo sapiens	55-76
23508960-0	2013	Aspirin hydrolysis in plasma is a variable function of butyrylcholinesterase and platelet-activating factor acetylhydrolase 1b2 (PAFAH1b2).	Aspirin	0-7	platelet activating factor acetylhydrolase 1b catalytic subunit 2	Homo sapiens	81-127
23508960-0	2013	Aspirin hydrolysis in plasma is a variable function of butyrylcholinesterase and platelet-activating factor acetylhydrolase 1b2 (PAFAH1b2).	Aspirin	0-7	platelet activating factor acetylhydrolase 1b catalytic subunit 2	Homo sapiens	129-137
23508960-1	2013	Aspirin is rapidly hydrolyzed within erythrocytes by a heterodimer of PAFAH1b2/PAFAH1b3 but also in plasma by an unidentified activity.	Aspirin	0-7	platelet activating factor acetylhydrolase 1b catalytic subunit 2	Homo sapiens	70-78
23508960-5	2013	A genome-wide association study of 2054 GeneBank subjects identified a single locus immediately adjacent to the BCHE (butyrylcholinesterase) gene associated with plasma aspirin hydrolytic activity (lead SNP, rs6445035; p = 9.1 x 10(-17)).	Aspirin	169-176	butyrylcholinesterase	Homo sapiens	112-116
23508960-5	2013	A genome-wide association study of 2054 GeneBank subjects identified a single locus immediately adjacent to the BCHE (butyrylcholinesterase) gene associated with plasma aspirin hydrolytic activity (lead SNP, rs6445035; p = 9.1 x 10(-17)).	Aspirin	169-176	butyrylcholinesterase	Homo sapiens	118-139
23508960-6	2013	However, its penetrance was low, and plasma from an individual with an inactivating mutation in BCHE still effectively hydrolyzed aspirin.	Aspirin	130-137	butyrylcholinesterase	Homo sapiens	96-100
23508960-9	2013	Inhibitors showed that both butyrylcholinesterase (BChE) and PAFAH1b2 contribute to aspirin hydrolysis in plasma, with variation primarily reflecting non-genetic variation of BChE activity.	Aspirin	84-91	butyrylcholinesterase	Homo sapiens	28-49
23508960-9	2013	Inhibitors showed that both butyrylcholinesterase (BChE) and PAFAH1b2 contribute to aspirin hydrolysis in plasma, with variation primarily reflecting non-genetic variation of BChE activity.	Aspirin	84-91	butyrylcholinesterase	Homo sapiens	51-55
23508960-9	2013	Inhibitors showed that both butyrylcholinesterase (BChE) and PAFAH1b2 contribute to aspirin hydrolysis in plasma, with variation primarily reflecting non-genetic variation of BChE activity.	Aspirin	84-91	platelet activating factor acetylhydrolase 1b catalytic subunit 2	Homo sapiens	61-69
23508960-9	2013	Inhibitors showed that both butyrylcholinesterase (BChE) and PAFAH1b2 contribute to aspirin hydrolysis in plasma, with variation primarily reflecting non-genetic variation of BChE activity.	Aspirin	84-91	butyrylcholinesterase	Homo sapiens	175-179
23508960-10	2013	Therefore, aspirin is hydrolyzed in plasma by two enzymes, BChE and a new extracellular form of platelet-activating factor acetylhydrolase, PAFAH1b2.	Aspirin	11-18	butyrylcholinesterase	Homo sapiens	59-63
23508960-10	2013	Therefore, aspirin is hydrolyzed in plasma by two enzymes, BChE and a new extracellular form of platelet-activating factor acetylhydrolase, PAFAH1b2.	Aspirin	11-18	platelet activating factor acetylhydrolase 1b catalytic subunit 2	Homo sapiens	140-148
23508960-11	2013	Hydrolytic effectiveness varies widely primarily from non-genetic variation of BChE activity that affects aspirin bioavailability in blood and the ability of aspirin to inhibit platelet aggregation.	Aspirin	106-113	butyrylcholinesterase	Homo sapiens	79-83
23629578-9	2013	Aspirin is an anti-thrombotic agent because of its ability to inhibit the COX-1 enzyme that produces the pro-aggregatory thromboxane.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	74-79
23506529-3	2013	Aspirin is a non-steroidal anti-inflammatory drug that is an irreversible inhibitor of both cyclooxygenase (COX)-1 and COX-2, It stimulates endogenous production of anti-inflammatory regulatory "braking signals", including lipoxins, which dampen the inflammatory response and reduce levels of inflammatory biomarkers, including C-reactive protein, tumor necrosis factor-alpha and interleukin (IL)--6, but not negative immunoregulatory cytokines, such as IL-4 and IL-10.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	92-114
22866967-6	2013	Aspirin fails to improve stress resistance or lifespan in nematodes lacking DAF-16, implying that it acts through this FOXO transcription factor.	Aspirin	0-7	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	76-82
23240590-13	2013	The expression of vWF and VEGF protein was increased in the female aspirin-treated group.	Aspirin	67-74	Von Willebrand factor	Mus musculus	18-21
24329513-4	2013	BChE is responsible for detoxification reactions, and the compounds such as cocaine, succinylcholine, and acetylsalicylic acid are degraded in the body.	Aspirin	106-126	butyrylcholinesterase	Homo sapiens	0-4
24281340-3	2012	At low-doses given every 24 h, aspirin is acting by a complete and persistent inhibition of cyclooxygenase (COX)-1 in platelets (in the pre-systemic circulation) while causing a limited and rapidly reversible inhibitory effect on COX-2 and/or COX-1 expressed in nucleated cells.	Aspirin	31-38	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	92-114
23441445-2	2012	We report the first known case of ASA desensitization in a 41-year-old woman with inherited thrombophilia, who had homozygosity (4G/4G polymorphism) of the plasminogen activator inhibitor-1 (PAI-1) gene and first trimester recurrent miscarriage, and had previously presented with anaphylaxis to ASA.	Aspirin	34-37	serpin family E member 1	Homo sapiens	156-189
23441445-2	2012	We report the first known case of ASA desensitization in a 41-year-old woman with inherited thrombophilia, who had homozygosity (4G/4G polymorphism) of the plasminogen activator inhibitor-1 (PAI-1) gene and first trimester recurrent miscarriage, and had previously presented with anaphylaxis to ASA.	Aspirin	34-37	serpin family E member 1	Homo sapiens	191-196
23441445-2	2012	We report the first known case of ASA desensitization in a 41-year-old woman with inherited thrombophilia, who had homozygosity (4G/4G polymorphism) of the plasminogen activator inhibitor-1 (PAI-1) gene and first trimester recurrent miscarriage, and had previously presented with anaphylaxis to ASA.	Aspirin	295-298	serpin family E member 1	Homo sapiens	156-189
23441445-2	2012	We report the first known case of ASA desensitization in a 41-year-old woman with inherited thrombophilia, who had homozygosity (4G/4G polymorphism) of the plasminogen activator inhibitor-1 (PAI-1) gene and first trimester recurrent miscarriage, and had previously presented with anaphylaxis to ASA.	Aspirin	295-298	serpin family E member 1	Homo sapiens	191-196
22524621-4	2012	To investigate whether GTF2H4 genetic variants could be a causative factor for AERD development and FEV(1) decline by aspirin provocation, five common single-nucleotide polymorphisms (SNPs) were genotyped in 93 patients with AERD and 96 aspirin-tolerant asthma (ATA) controls.	Aspirin	118-125	general transcription factor IIH subunit 4	Homo sapiens	23-29
22893064-3	2012	The priming action of aspirin on tumor cells was found to be dependent on an altered constitution of tumor microenvironment with respect to decline of acidosis and modulation in the expression of cell cycle and survival regulatory molecules like cyclin B1, cyclin D, bcl-2, bcl-xL, p53, and cytokines: IL-4, IL-10, IFN- gamma &amp; VEGF.	Aspirin	22-29	transformation related protein 53, pseudogene	Mus musculus	282-285
22893064-3	2012	The priming action of aspirin on tumor cells was found to be dependent on an altered constitution of tumor microenvironment with respect to decline of acidosis and modulation in the expression of cell cycle and survival regulatory molecules like cyclin B1, cyclin D, bcl-2, bcl-xL, p53, and cytokines: IL-4, IL-10, IFN- gamma &amp; VEGF.	Aspirin	22-29	interleukin 4	Mus musculus	302-306
23083110-3	2012	Aspirin (acetylsalicylic acid) monotherapy improves patient outcomes by irreversibly inhibiting the cyclooxygenase (COX)-1 enzyme in the arachidonic acid pathway.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	100-122
23083110-3	2012	Aspirin (acetylsalicylic acid) monotherapy improves patient outcomes by irreversibly inhibiting the cyclooxygenase (COX)-1 enzyme in the arachidonic acid pathway.	Aspirin	9-29	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	100-122
22765917-6	2012	Hippocampal neuronal loss five weeks after SE was also attenuated in the CA1, CA3 and hilus following aspirin administration.	Aspirin	102-109	carbonic anhydrase 1	Rattus norvegicus	73-76
22884858-8	2012	CONCLUSIONS: This meta-analysis suggested that the -444A/C polymorphism in the LTC4S gene would be a risk factor for asthma in Caucasians and aspirin-tolerant populations.	Aspirin	142-149	leukotriene C4 synthase	Homo sapiens	79-84
22561363-9	2012	ASA and SA also suppressed NADPH oxidase (p22, p47, p67, and gp91 messenger RNA) expression.	Aspirin	0-3	calcineurin like EF-hand protein 1	Homo sapiens	42-45
22561363-9	2012	ASA and SA also suppressed NADPH oxidase (p22, p47, p67, and gp91 messenger RNA) expression.	Aspirin	0-3	inhibitor of growth family member 1	Homo sapiens	47-50
22695889-0	2012	Genetic variability of prostaglandin E2 receptor subtype EP4 gene in aspirin-intolerant chronic urticaria.	Aspirin	69-76	prostaglandin E receptor 4	Homo sapiens	23-60
22695889-3	2012	Considering the association of PTGER4 in mast cells, urticaria- and aspirin-related disease, we hypothesized the genetic variability of PTGER4 may be associated with aspirin-intolerant chronic urticaria (AICU).	Aspirin	68-75	prostaglandin E receptor 4	Homo sapiens	31-37
22695889-3	2012	Considering the association of PTGER4 in mast cells, urticaria- and aspirin-related disease, we hypothesized the genetic variability of PTGER4 may be associated with aspirin-intolerant chronic urticaria (AICU).	Aspirin	68-75	prostaglandin E receptor 4	Homo sapiens	136-142
22695889-7	2012	Furthermore, the effect of aspirin was performed for PTGER4 mRNA expression using real-time PCR, and PGE2 production was checked in HMC-1 cells using ELISA.	Aspirin	27-34	prostaglandin E receptor 4	Homo sapiens	53-59
22658594-1	2012	Epidemiology studies and clinical trials have suggested that the use of non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin, can significantly reduce the incidence of and mortality associated with many cancers, and upregulation of the COX2-PGE(2) pathway in tumor microenvironments might drive several aspects of cancer progression.	Aspirin	130-137	cytochrome c oxidase II, mitochondrial	Danio rerio	249-253
22828690-0	2012	Aspirin-inspired analgesia: old drug, new mechanism, Sans Cox?	Aspirin	0-7	USH1 protein network component sans	Homo sapiens	53-57
22825862-6	2012	In detail, the myocardial event rate was lower in the ASA arm: 0.7 versus 4.4 %; p = 0.012, OR 6.1 (95 %CI [1.4;27.45].	Aspirin	54-57	olfactory receptor family 2 subfamily I member 1 pseudogene	Homo sapiens	92-98
22159558-5	2012	Further elucidation of the mechanism suggests that aspirin enhances recruitment of SNX3 and SNX5 to membranes and consistently, both SNX3 and SNX5 play essential roles in the aspirin-mediated accumulation of endocytosed-TfnR at the ESE.	Aspirin	51-58	sorting nexin 3	Homo sapiens	83-87
22159558-5	2012	Further elucidation of the mechanism suggests that aspirin enhances recruitment of SNX3 and SNX5 to membranes and consistently, both SNX3 and SNX5 play essential roles in the aspirin-mediated accumulation of endocytosed-TfnR at the ESE.	Aspirin	175-182	sorting nexin 3	Homo sapiens	83-87
22159558-5	2012	Further elucidation of the mechanism suggests that aspirin enhances recruitment of SNX3 and SNX5 to membranes and consistently, both SNX3 and SNX5 play essential roles in the aspirin-mediated accumulation of endocytosed-TfnR at the ESE.	Aspirin	175-182	sorting nexin 3	Homo sapiens	133-137
22373734-5	2012	Also, hypersensitivity of aspirin owing to its inhibitory action against COX-1 is a significant concern clinically.	Aspirin	26-33	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	73-78
21395960-9	2012	RESULTS: Aspirin was negatively associated with high PSA velocity in model 1 (odds ratio (95% confidence interval): 0.24 (0.06, 0.94), P-value = 0.04) and model 2 (odds ratio = 0.22 (0.08, 0.59), P-value = 0.003), whereas smoking was positively associated with high PSA velocity in model 1 (1.03 (0.92, 1.13), P-value = 0.01).	Aspirin	9-16	kallikrein related peptidase 3	Homo sapiens	53-56
21395960-9	2012	RESULTS: Aspirin was negatively associated with high PSA velocity in model 1 (odds ratio (95% confidence interval): 0.24 (0.06, 0.94), P-value = 0.04) and model 2 (odds ratio = 0.22 (0.08, 0.59), P-value = 0.003), whereas smoking was positively associated with high PSA velocity in model 1 (1.03 (0.92, 1.13), P-value = 0.01).	Aspirin	9-16	kallikrein related peptidase 3	Homo sapiens	266-269
22377711-0	2012	Association analysis of formyl peptide receptor 2 (FPR2) polymorphisms and aspirin exacerbated respiratory diseases.	Aspirin	75-82	formyl peptide receptor 2	Homo sapiens	51-55
22377711-10	2012	The decline of FEV(1) after aspirin challenge was significantly lower in the subjects with GG homozygotes of FPR2 -4209T&gt;G than those with the other genotypes (P=0.0002).	Aspirin	28-35	formyl peptide receptor 2	Homo sapiens	109-113
22294277-0	2012	Time-dependent changes in non-COX-1-dependent platelet  function with daily aspirin therapy.	Aspirin	76-83	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	30-35
22294277-1	2012	To develop an integrated metric of non-COX-1-dependent platelet function (NCDPF) to measure the temporal response to aspirin in healthy volunteers and diabetics.	Aspirin	117-124	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	39-44
22320344-4	2012	We demonstrate that the binding energies of bromoaspirin and aspirin to COX-1 are very close when second-order quantum refinements of the structural data are performed, which points to an explanation on why the IC(50) values for the 126 muM COX-1 activity of both bromoaspirin and aspirin are practically the same.	Aspirin	61-68	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	72-77
22320344-4	2012	We demonstrate that the binding energies of bromoaspirin and aspirin to COX-1 are very close when second-order quantum refinements of the structural data are performed, which points to an explanation on why the IC(50) values for the 126 muM COX-1 activity of both bromoaspirin and aspirin are practically the same.	Aspirin	61-68	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	241-246
22306536-4	2012	In this study, we examined if ASA would inhibit NADPH oxidase activation, upregulation of AT1R transcription, and subsequent collagen generation in mouse cardiac fibroblasts challenged with Ang II.	Aspirin	30-33	angiotensin II, type I receptor-associated protein	Mus musculus	90-94
22088425-0	2012	Association of SLCO1B1 1b with peptic ulcer amongst Japanese patients taking low-dose aspirin.	Aspirin	86-93	solute carrier organic anion transporter family member 1B1	Homo sapiens	15-22
22088425-8	2012	CONCLUSIONS: SLCO1B1 1b haplotype may identify patients at increased risk for aspirin-induced peptic ulcer.	Aspirin	78-85	solute carrier organic anion transporter family member 1B1	Homo sapiens	13-20
21692746-8	2012	Tumour cells obtained from aspirin-treated tumour-bearing mice demonstrated an altered expression of pH regulators monocarboxylate transporter-1 and V-ATPase along with alteration in the level of cell survival regulatory molecules such as survivin, vascular endothelial growth factor, heat-shock protein 70, glucose transporter-1, SOCS-5 (suppressor of cytokine signalling-5), HIF-1alpha (hypoxia-inducible factor-1alpha) and PUMA (p53 up-regulated modulator of apoptosis).	Aspirin	27-34	hypoxia inducible factor 1, alpha subunit	Mus musculus	377-387
21692746-8	2012	Tumour cells obtained from aspirin-treated tumour-bearing mice demonstrated an altered expression of pH regulators monocarboxylate transporter-1 and V-ATPase along with alteration in the level of cell survival regulatory molecules such as survivin, vascular endothelial growth factor, heat-shock protein 70, glucose transporter-1, SOCS-5 (suppressor of cytokine signalling-5), HIF-1alpha (hypoxia-inducible factor-1alpha) and PUMA (p53 up-regulated modulator of apoptosis).	Aspirin	27-34	hypoxia inducible factor 1, alpha subunit	Mus musculus	389-420
21956205-6	2012	Finally, based upon the well known but poorly understood preventive effect of aspirin on colorectal cancer incidence and mortality, we report downregulation of miR-21 upon administration of aspirin.	Aspirin	78-85	microRNA 21	Homo sapiens	160-166
21956205-6	2012	Finally, based upon the well known but poorly understood preventive effect of aspirin on colorectal cancer incidence and mortality, we report downregulation of miR-21 upon administration of aspirin.	Aspirin	190-197	microRNA 21	Homo sapiens	160-166
22696303-2	2012	BChE is a non specific enzyme that hydrolyzes different choline esters (succinylcholine, mivacurium) and many other drugs such as aspirin, cocaine and procaine.	Aspirin	130-137	butyrylcholinesterase	Homo sapiens	0-4
23057161-6	2012	In contrast, treatment of immature dendritic cells with aspirin, dexamethasone, 1alpha,25-dihydroxyvitamin D3 (VD3) or butyric acid was associated with diminished expression of CD1a, CD1c, CD40, CD80 and CD83.	Aspirin	56-63	CD83 molecule	Homo sapiens	204-208
22045867-4	2012	We hypothesised that inhibition of MMP-2 and MMP-9 by minocycline can be potentiated by aspirin through inhibition of cyclooxygenase-2 and tissue plasminogen activator, resulting in amelioration of clinical cerebral ischaemia in diabetes.	Aspirin	88-95	plasminogen activator, tissue type	Rattus norvegicus	139-167
22262978-1	2012	Aspirin-exacerbated respiratory disease (AERD) is explained in part by over-expression of 5-lipoxygenase, leukotriene C4 synthase (LTC(4)S) and the cysteinyl leukotriene (CysLT) receptors (CysLT1 and 2), resulting in constitutive over-production of CysLTs and the hyperresponsiveness to CysLTs that occurs with aspirin ingestion.	Aspirin	0-7	leukotriene C4 synthase	Homo sapiens	106-129
22262978-1	2012	Aspirin-exacerbated respiratory disease (AERD) is explained in part by over-expression of 5-lipoxygenase, leukotriene C4 synthase (LTC(4)S) and the cysteinyl leukotriene (CysLT) receptors (CysLT1 and 2), resulting in constitutive over-production of CysLTs and the hyperresponsiveness to CysLTs that occurs with aspirin ingestion.	Aspirin	0-7	leukotriene C4 synthase	Homo sapiens	131-138
22952917-5	2012	When stimulated with whole sperm cells, the PBMCs from patients with ASA produce less IL-3, IL-11, IL-13, ICAM-1, GCSF and more IL-2, IL-4 and IL-12p70 as compared to healthy women.	Aspirin	69-72	interleukin 3	Homo sapiens	86-90
22952917-5	2012	When stimulated with whole sperm cells, the PBMCs from patients with ASA produce less IL-3, IL-11, IL-13, ICAM-1, GCSF and more IL-2, IL-4 and IL-12p70 as compared to healthy women.	Aspirin	69-72	interleukin 11	Homo sapiens	92-97
22952917-5	2012	When stimulated with whole sperm cells, the PBMCs from patients with ASA produce less IL-3, IL-11, IL-13, ICAM-1, GCSF and more IL-2, IL-4 and IL-12p70 as compared to healthy women.	Aspirin	69-72	colony stimulating factor 3	Homo sapiens	114-118
22952917-6	2012	PBMCs from patients with ASA produce typically less IL-13, IL-7, IL-17 and MIG, and more MIP-1beta and IL-8, as compared to PBMCs from patients without ASA.	Aspirin	25-28	C-C motif chemokine ligand 4	Homo sapiens	89-98
21833043-8	2011	Aspirin treatment reduced the basal superoxide production and blunted the oxidative and hypertensive effect of angiotensin II in wild type and cyclo-oxygenase-1 deficient mice whereas it lost completely its antioxidative property in angiotensin II-treated aortic smooth muscle cells isolated from cyclo-oxygenase-2 deficient mice.	Aspirin	0-7	prostaglandin-endoperoxide synthase 1	Mus musculus	143-160
21844189-0	2011	Intracellular erythrocyte platelet-activating factor acetylhydrolase I inactivates aspirin in blood.	Aspirin	83-90	PCNA clamp associated factor	Homo sapiens	26-52
21844189-5	2011	Western blotting showed that catalytic PAFAH1B2 and PAFAH1B3 subunits of the type I enzyme co-migrated with purified erythrocyte aspirin hydrolytic activity.	Aspirin	129-136	platelet activating factor acetylhydrolase 1b catalytic subunit 2	Homo sapiens	39-47
21844189-6	2011	Recombinant PAFAH1B2, but not its family member plasma PAF acetylhydrolase, hydrolyzed aspirin, and PAF competitively inhibited aspirin hydrolysis by purified or recombinant erythrocyte enzymes.	Aspirin	87-94	platelet activating factor acetylhydrolase 1b catalytic subunit 2	Homo sapiens	12-20
21844189-6	2011	Recombinant PAFAH1B2, but not its family member plasma PAF acetylhydrolase, hydrolyzed aspirin, and PAF competitively inhibited aspirin hydrolysis by purified or recombinant erythrocyte enzymes.	Aspirin	87-94	PCNA clamp associated factor	Homo sapiens	12-15
21844189-6	2011	Recombinant PAFAH1B2, but not its family member plasma PAF acetylhydrolase, hydrolyzed aspirin, and PAF competitively inhibited aspirin hydrolysis by purified or recombinant erythrocyte enzymes.	Aspirin	128-135	platelet activating factor acetylhydrolase 1b catalytic subunit 2	Homo sapiens	12-20
21844189-6	2011	Recombinant PAFAH1B2, but not its family member plasma PAF acetylhydrolase, hydrolyzed aspirin, and PAF competitively inhibited aspirin hydrolysis by purified or recombinant erythrocyte enzymes.	Aspirin	128-135	PCNA clamp associated factor	Homo sapiens	12-15
21617849-0	2011	Aspirin reduces the apoptotic effect of etoposide via Akt activation and up-regulation of p21(cip).	Aspirin	0-7	H3 histone pseudogene 16	Homo sapiens	90-93
21617849-7	2011	Our data showed that the protein expression and ser146 phosphorylation levels of p21(cip) were significantly increased after treatment with aspirin, whereas p53 or p27 showed no change.	Aspirin	140-147	H3 histone pseudogene 16	Homo sapiens	81-84
21617849-9	2011	Moreover, reduction of caspase-3 activity induced by aspirin was attenuated by silencing p21(cip) expression.	Aspirin	53-60	H3 histone pseudogene 16	Homo sapiens	89-92
21617849-10	2011	These results indicated that the anti-apoptotic effect of aspirin was dependent on activation of Akt which inhibited cell apoptosis by up-regulating p21(cip) and blocking caspase-3 activation.	Aspirin	58-65	H3 histone pseudogene 16	Homo sapiens	149-152
21721879-4	2011	Reverse transcriptase polymerase chain reaction and Western blot analyses were used to detect the expression of multiple beta-catenin/TCF target genes following aspirin treatment.	Aspirin	161-168	catenin beta 1	Homo sapiens	121-133
21721879-5	2011	RESULTS: The transcriptional activity of the beta-catenin/TCF complex was strongly inhibited by aspirin.	Aspirin	96-103	catenin beta 1	Homo sapiens	45-57
21721879-6	2011	Increasing the concentration of aspirin resulted in decreased expression of c-myc, cyclin D1, and fra-1 mRNA and protein in U87 and A172 cells in a dose-dependent manner.	Aspirin	32-39	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	76-81
21721879-6	2011	Increasing the concentration of aspirin resulted in decreased expression of c-myc, cyclin D1, and fra-1 mRNA and protein in U87 and A172 cells in a dose-dependent manner.	Aspirin	32-39	FOS like 1, AP-1 transcription factor subunit	Homo sapiens	98-103
21721879-8	2011	CONCLUSIONS: The results suggest that aspirin is a potent antitumor agent, and that it exerts its antineoplastic action by inhibition of the beta-catenin/TCF signaling pathway in glioma cells.	Aspirin	38-45	catenin beta 1	Homo sapiens	141-153
21911156-8	2011	The myeloperoxidase activity and the serum level of APP were elevated among MMF- and aspirin-treated animals.	Aspirin	85-92	myeloperoxidase	Rattus norvegicus	4-19
21816313-10	2011	Aspirin effect on COX-1 is little-related to MRP4-mediated aspirin transport in HV, but in CABG patients with MRP4 over-expression, its pharmacological inhibition enhances aspirin action in an efficient way.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	18-23
21429568-2	2011	This study evaluates the impact of the selected polymorphisms in the COX-1 gene, the CYP5A1 gene, the P2RY1 receptor gene, and the GPIIbIIIa receptor gene on platelet response to aspirin and risk of suffering from major adverse cardiovascular and cerebrovascular events (MACCE).	Aspirin	179-186	purinergic receptor P2Y1	Homo sapiens	102-107
21429568-9	2011	CONCLUSION: The 1622A/G mutation of the P2RY1 gene could contribute to inadequate platelet response to aspirin and is associated with an increased risk of suffering from MACCE.	Aspirin	103-110	purinergic receptor P2Y1	Homo sapiens	40-45
21063876-6	2011	In conclusion, although aspirin suppressed platelet activity and even surface P-selectin expression, higher doses worsened endothelial-mediated arterial dilation.	Aspirin	24-31	selectin P	Homo sapiens	78-88
21331560-0	2011	Role of expression of prostaglandin synthases 1 and 2 and leukotriene C4 synthase in aspirin-intolerant asthma: a theoretical study.	Aspirin	85-92	leukotriene C4 synthase	Homo sapiens	58-81
21331560-1	2011	Altered expressions of the key enzymes in arachidonic acid (AA) metabolism, prostaglandin synthase 1 and 2 and cysteinyl leukotriene C(4) synthase, are of importance in understanding aspirin-induced asthma.	Aspirin	183-190	leukotriene C4 synthase	Homo sapiens	121-146
21360823-3	2011	Further studies using COX-1 expressed in human HEK293T cells showed that this inhibition mechanism is similar to that of aspirin; namely, the products are able to covalently bind to the Ser 530 residue present in the active cleft of the enzyme.	Aspirin	121-128	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	22-27
21159364-4	2011	It is the aim of this study to investigate i) the effect of immunomodulatory treatment on endothelial cell tissue factor (TF) expression and function, ii) the regulation of the observed TF activity, and iii) the modulating effect of low molecular weight heparin and aspirin on TF activity in vitro.	Aspirin	266-273	coagulation factor III, tissue factor	Homo sapiens	186-188
21159364-4	2011	It is the aim of this study to investigate i) the effect of immunomodulatory treatment on endothelial cell tissue factor (TF) expression and function, ii) the regulation of the observed TF activity, and iii) the modulating effect of low molecular weight heparin and aspirin on TF activity in vitro.	Aspirin	266-273	coagulation factor III, tissue factor	Homo sapiens	186-188
21319963-1	2011	At antiplatelet doses of 75-325 mg/day, aspirin irreversibly inhibits the platelet cyclooxygenase (COX)-1-dependent thromboxane A(2) (TXA(2)) formation.	Aspirin	40-47	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	83-105
20349206-4	2011	With RKO cells, aspirin reduced IL-6, IL-1ra, and IL-10 synthesis and enhanced IFNgamma secretion, while IL-1beta remained unchanged.	Aspirin	16-23	interleukin 1 receptor antagonist	Homo sapiens	38-44
20427204-9	2011	COL-MEA and ADP-MEA discriminated between preoperative ASA and clopidogrel intake (ASA: sensitivity = 86.3%, and specificity = 89.3%; clopidogrel: sensitivity = 87.5%, and specificity = 95.1%).	Aspirin	55-58	WD and tetratricopeptide repeats 1	Homo sapiens	12-19
21035850-0	2010	Treatment with low-dose aspirin increased the level LIF and integrin beta3 expression in mice during the implantation window.	Aspirin	24-31	leukemia inhibitory factor	Mus musculus	52-55
20539104-3	2010	Selective NSAIDs act on COX-1 (eg, aspirin) or COX-2 (eg, celecoxib) isoenzymes, respectively.	Aspirin	35-42	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	24-29
20609405-2	2010	If you imagine yourself as a castaway on an island you might pick water, glucose, penicillin, and ethanol in combination with aspirin.	Aspirin	126-133	protein interacting with PRKCA 1	Homo sapiens	61-65
20188076-1	2010	NO-donating aspirin (NO-ASA, para isomer) has been reported to exhibit strong growth inhibitory effect in Jurkat T-acute lymphoblastic leukemia (T-ALL) cells mediated in part by beta-catenin degradation and caspase activation, but the mechanism(s) still remains unclear.	Aspirin	12-19	catenin beta 1	Homo sapiens	178-190
20188076-1	2010	NO-donating aspirin (NO-ASA, para isomer) has been reported to exhibit strong growth inhibitory effect in Jurkat T-acute lymphoblastic leukemia (T-ALL) cells mediated in part by beta-catenin degradation and caspase activation, but the mechanism(s) still remains unclear.	Aspirin	24-27	catenin beta 1	Homo sapiens	178-190
20135645-0	2010	Effect of aspirin, other NSAIDs, and statins on PSA and PSA velocity.	Aspirin	10-17	kallikrein related peptidase 3	Homo sapiens	48-51
20135645-0	2010	Effect of aspirin, other NSAIDs, and statins on PSA and PSA velocity.	Aspirin	10-17	kallikrein related peptidase 3	Homo sapiens	56-59
20135645-4	2010	RESULTS: Baseline PSA levels were significantly lower in aspirin users compared to non-users (5.17 ng/ml vs. 7.58 ng/ml, P = 0.001).	Aspirin	57-64	kallikrein related peptidase 3	Homo sapiens	18-21
20135645-7	2010	Aspirin, statin, or other NSAID use at baseline demonstrated a non-significant negative association with PSA velocity.	Aspirin	0-7	kallikrein related peptidase 3	Homo sapiens	105-108
20138334-9	2010	HPR patients with inadequate aspirin inhibition were significantly more often homozygous PlA1/A1 (65.4% vs. 47.7%, p=0.015).	Aspirin	29-36	POU class 2 homeobox 3	Homo sapiens	89-96
20138334-11	2010	CONCLUSION: In CAD patients receiving daily low dose of aspirin, there is a significant and independent association between the expression of GPIIIa PlA1 allele and the occurrence of persistent HPR detected with PFA-100.	Aspirin	56-63	POU class 2 homeobox 3	Homo sapiens	149-153
19880966-9	2010	Furthermore, development of invasive pancreatic cancer in LsL-Kras(G12D); LsL-Trp53(R172H); Pdx1-Cre transgenic mice was partially inhibited by enalapril and aspirin.	Aspirin	158-165	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	62-66
19880966-9	2010	Furthermore, development of invasive pancreatic cancer in LsL-Kras(G12D); LsL-Trp53(R172H); Pdx1-Cre transgenic mice was partially inhibited by enalapril and aspirin.	Aspirin	158-165	transformation related protein 53	Mus musculus	78-83
19880966-11	2010	Using real-time PCR we found a significant downregulation of the target genes VEGF and RelA demonstrating our ability to achieve effective pharmacological levels of aspirin and enalapril during pancreatic cancer formation in vivo.	Aspirin	165-172	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	87-91
19796209-0	2010	Genetic variability in CRTH2 polymorphism increases eotaxin-2 levels in patients with aspirin exacerbated respiratory disease.	Aspirin	86-93	C-C motif chemokine ligand 24	Homo sapiens	52-61
19908241-7	2010	In Western blot, combined TGZ and ASA also could downregulate Cdk2, E2F-1, cyclin B1, cyclin D3 protein, and the ratio of phospho-Rb/Rb.	Aspirin	34-37	E2F transcription factor 1	Homo sapiens	68-73
19908241-7	2010	In Western blot, combined TGZ and ASA also could downregulate Cdk2, E2F-1, cyclin B1, cyclin D3 protein, and the ratio of phospho-Rb/Rb.	Aspirin	34-37	cyclin B1	Homo sapiens	75-84
20094648-2	2010	Aspirin and clopidogrel, the two most widely prescribed anti-platelet drugs, are metabolized to active compounds that covalently and irreversibly modify their respective therapeutic targets (COX1 and P2Y12).	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	191-195
19955429-10	2010	Our studies predict that the cardioprotective effect of low-dose aspirin on COX-1 may be blunted when taken with coxibs.	Aspirin	65-72	prostaglandin-endoperoxide synthase 1	Canis lupus familiaris	76-81
20648923-2	2010	In addition to reducing inflammation and pain, acetylsalicylic acid (ASA, CAS 50-78-2), like other synthetic non-steroidal anti-inflammatory drugs (NSAIDs), has been shown to exert anti-proliferative effects and to induce apoptosis in a variety of cell lines, e.g., colon, stomach, and prostate cancer cells.	Aspirin	47-67	BCAR1 scaffold protein, Cas family member	Homo sapiens	74-77
20648923-2	2010	In addition to reducing inflammation and pain, acetylsalicylic acid (ASA, CAS 50-78-2), like other synthetic non-steroidal anti-inflammatory drugs (NSAIDs), has been shown to exert anti-proliferative effects and to induce apoptosis in a variety of cell lines, e.g., colon, stomach, and prostate cancer cells.	Aspirin	69-72	BCAR1 scaffold protein, Cas family member	Homo sapiens	74-77
20446806-1	2010	A preliminary investigation was conducted into the influence of aspirin on the luminol-enhanced chemiluminescence of platelets stimulated with platelet-activating factor (PAF).	Aspirin	64-71	PCNA clamp associated factor	Homo sapiens	143-169
20446806-1	2010	A preliminary investigation was conducted into the influence of aspirin on the luminol-enhanced chemiluminescence of platelets stimulated with platelet-activating factor (PAF).	Aspirin	64-71	PCNA clamp associated factor	Homo sapiens	171-174
19487018-1	2010	INTRODUCTION: The aim of this study was to further characterize the effect of the antiplatelet agents, aspirin and eptifibatide, on the surface expression of CD40L and CD62P on platelets from patients with stable coronary artery disease.	Aspirin	103-110	selectin P	Homo sapiens	168-173
19487018-5	2010	Platelet activation by adenosine diphosphate (ADP) or thrombin agonist peptide (TRAP) increased CD62P and CD40L surface density in the presence of aspirin by 1.9 - 2.8 -fold.	Aspirin	147-154	selectin P	Homo sapiens	96-101
19706045-0	2009	Aspirin induces apoptosis in mesenchymal stem cells requiring Wnt/beta-catenin pathway.	Aspirin	0-7	catenin beta 1	Homo sapiens	66-78
19706045-8	2009	Stimulating the Wnt/beta-catenin pathway by both Wnt 3a and GSK-3beta inhibitors (LiCl and SB 216763), blocked aspirin-induced apoptosis and protected mitochondrial function, as demonstrated by decreased cytochrome c release and caspase-3 activity.	Aspirin	111-118	catenin beta 1	Homo sapiens	20-32
19808249-0	2009	Native and aspirin-triggered lipoxins control innate immunity by inducing proteasomal degradation of TRAF6.	Aspirin	11-18	TNF receptor associated factor 6	Homo sapiens	101-106
19486029-6	2009	RESULTS: Aspirin-induced expression of CD63, CD69 and CD203c yielded 30%, 80% and 70% sensitivity, respectively, but with poor specificity.	Aspirin	9-16	CD63 molecule	Homo sapiens	39-43
19767084-0	2009	Modulation by aspirin of nuclear phospho-signal transducer and activator of transcription 6 expression: Possible role in therapeutic benefit associated with aspirin desensitization.	Aspirin	14-21	signal transducer and activator of transcription 6	Homo sapiens	41-91
19767084-0	2009	Modulation by aspirin of nuclear phospho-signal transducer and activator of transcription 6 expression: Possible role in therapeutic benefit associated with aspirin desensitization.	Aspirin	157-164	signal transducer and activator of transcription 6	Homo sapiens	41-91
19767084-1	2009	BACKGROUND: Aspirin-exacerbated respiratory disease is characterized by asthma, nasal polyps, and intolerance to aspirin with overexpression of leukotriene (LT) C(4) synthase and cysteinyl leukotriene receptors.	Aspirin	12-19	leukotriene C4 synthase	Homo sapiens	144-174
19767084-3	2009	OBJECTIVE: We hypothesized that aspirin desensitization blocks IL-4-induced expression of these LT activities through inhibition of signal transducer and activator of transcription 6 (STAT6)-mediated transcription.	Aspirin	32-39	signal transducer and activator of transcription 6	Homo sapiens	132-182
19767084-3	2009	OBJECTIVE: We hypothesized that aspirin desensitization blocks IL-4-induced expression of these LT activities through inhibition of signal transducer and activator of transcription 6 (STAT6)-mediated transcription.	Aspirin	32-39	signal transducer and activator of transcription 6	Homo sapiens	184-189
19767084-10	2009	Aspirin and ketorolac decreased the IL-4-inducible expression of nuclear STAT6 observed in mobility shift assays and Western hybridization.	Aspirin	0-7	signal transducer and activator of transcription 6	Homo sapiens	73-78
19767084-11	2009	CONCLUSION: The LT receptor and synthase promoters have STAT6-binding sites that are engaged by IL-4-induced nuclear extracts and inhibited by aspirin.	Aspirin	143-150	signal transducer and activator of transcription 6	Homo sapiens	56-61
19695356-4	2009	In this review, we highlight the relevant trial evidence for antiplatelet therapy (aspirin, P2Y(12) inhibitors, and small molecule glycoprotein IIb/IIIa inhibitors) in NSTE ACS in relation to age, taking into consideration the risks and benefits, dose, concomitant therapy, and duration of use.	Aspirin	83-90	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	173-176
19563267-2	2009	The common anti-inflammatory drugs (such as aspirin, ibuprofen and naproxen) all act by blocking the action of both the COX-1 and COX-2 enzymes.	Aspirin	44-51	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	120-125
23292525-2	2013	Since the human class II, major histocompatibility complex,             transactivator (CIITA) is a positive regulator of class II, major histocompatibility             complex gene transcription, the CIITA gene is thought to be involved in the presence             of nasal polyps in asthma and aspirin hypersensitive patients.	Aspirin	296-303	class II major histocompatibility complex transactivator	Homo sapiens	88-93
23292525-2	2013	Since the human class II, major histocompatibility complex,             transactivator (CIITA) is a positive regulator of class II, major histocompatibility             complex gene transcription, the CIITA gene is thought to be involved in the presence             of nasal polyps in asthma and aspirin hypersensitive patients.	Aspirin	296-303	class II major histocompatibility complex transactivator	Homo sapiens	201-206
23245937-1	2013	INTRODUCTION: Previous work suggests that the extent of platelet inhibition by P2Y(1) receptor antagonism may be underappreciated, particularly in the context of dual antiplatelet therapy with aspirin and clopidogrel.	Aspirin	193-200	purinergic receptor P2Y1	Homo sapiens	79-94
24009859-5	2013	In special, a nonsteroid anti-inflammatory drug aspirin, a COX-1 inhibitor, inhibited COX-1 activity by 11.3% at the same concentration (50 muM) as EGCG that inhibited COX-1 activity to 96.9% as compared with that of control.	Aspirin	48-55	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	59-64
24009859-5	2013	In special, a nonsteroid anti-inflammatory drug aspirin, a COX-1 inhibitor, inhibited COX-1 activity by 11.3% at the same concentration (50 muM) as EGCG that inhibited COX-1 activity to 96.9% as compared with that of control.	Aspirin	48-55	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	86-91
24009859-5	2013	In special, a nonsteroid anti-inflammatory drug aspirin, a COX-1 inhibitor, inhibited COX-1 activity by 11.3% at the same concentration (50 muM) as EGCG that inhibited COX-1 activity to 96.9% as compared with that of control.	Aspirin	48-55	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	86-91
24009859-6	2013	This suggests that EGCG has a stronger effect than that of aspirin on inhibition of COX-1 activity.	Aspirin	59-66	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	84-89
22893199-3	2013	In fact, at low-doses, aspirin acts mainly by an irreversible inactivation of platelet cyclooxygenase (COX)-1 in the presystemic circulation, which translates into a long-lasting inhibition of platelet function.	Aspirin	23-30	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	87-109
22893199-7	2013	COX-independent mechanisms of aspirin, such as the inhibition of NF-kB signaling and Wnt/beta-catenin signaling and the acetylation of extra-COX proteins, have been suggested to play a role in its chemopreventive effects.	Aspirin	30-37	catenin beta 1	Homo sapiens	89-101
22893200-8	2013	In this context, the use of low-dose aspirin (which mainly acts by inhibiting platelet COX-1-dependent TXA(2)) may have a place for chemoprevention of CRCs (see also                  Chap.	Aspirin	37-44	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	87-92
23126516-9	2013	SFN/ASA-treated wounds showed a significantly higher (p &lt; 0.001) expression of matrix metalloproteinase-1, resulting in reduced collagen deposition and less scarring.	Aspirin	4-7	stratifin	Homo sapiens	0-3
23126516-9	2013	SFN/ASA-treated wounds showed a significantly higher (p &lt; 0.001) expression of matrix metalloproteinase-1, resulting in reduced collagen deposition and less scarring.	Aspirin	4-7	matrix metallopeptidase 1	Homo sapiens	82-108
24281340-3	2012	At low-doses given every 24 h, aspirin is acting by a complete and persistent inhibition of cyclooxygenase (COX)-1 in platelets (in the pre-systemic circulation) while causing a limited and rapidly reversible inhibitory effect on COX-2 and/or COX-1 expressed in nucleated cells.	Aspirin	31-38	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	243-248
24281340-5	2012	COX-independent mechanisms of aspirin, such as the inhibition of Wnt/ b-catenin and NF-kB signaling and the acetylation of extra-COX proteins, have been suggested to play a role in its chemo-preventive effects, but their relevance remains to be demonstrated in vivo at clinical doses.	Aspirin	30-37	catenin beta 1	Homo sapiens	70-79
22994386-9	2012	In addition, splenocytes harvested after ASA produced IL-4, IL-5, and IL-10 by re-stimulation with HWP1.	Aspirin	41-44	interleukin 4	Mus musculus	54-58
22994386-9	2012	In addition, splenocytes harvested after ASA produced IL-4, IL-5, and IL-10 by re-stimulation with HWP1.	Aspirin	41-44	interleukin 5	Mus musculus	60-64
19644598-3	2009	Acetyl salicylic acid achieves a reduction of thromboxane A2 formation by inhibition of COX-1.	Aspirin	0-21	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	88-93
19414551-5	2009	Our results demonstrate an increased level of expression of the adhesion molecule E-selectin, but not of intracellular adhesion molecule 1, vascular adhesion molecule 1, or vascular adhesion protein 1, in H. pylori-induced gastritis but not in gastritis induced by acetylsalicylic acid or pouchitis.	Aspirin	265-285	selectin E	Homo sapiens	82-92
19241108-6	2009	Survival for T2N0M0 SCC patients was significantly improved with aspirin (71) compared with placebo (167) or no tablet (134) (P = 0.0004).	Aspirin	65-72	serpin family B member 3	Homo sapiens	20-23
19423536-5	2009	Among cases, but not controls, average MLH1 expression tended to be higher with current alcohol consumption, regular aspirin use, and higher total intakes of calcium, vitamin D, and folate.	Aspirin	117-124	mutL homolog 1	Homo sapiens	39-43
19255811-9	2009	RESULTS: In the base case, testing and treating patients with CYP2C9*2 and/or CYP2C9*3 with aspirin rather than warfarin was best (8.97 QALYs).	Aspirin	92-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
19350112-1	2009	COX-1 polymorphism C50T, in complete linkage disequilibrium with the other polymorphism A-842G, has been depicted as a determinant of pharmacological response to aspirin treatment.	Aspirin	162-169	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	0-5
19028575-4	2009	The developed models were applied to calculate the dose-dependence of aspirin and celecoxib action on COX- 1 in vitro and in vivo conditions.	Aspirin	70-77	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	102-108
19028575-5	2009	The mechanism of the enhancement of aspirin efficiency in platelet as compared to its action on purified COX-1 was elucidated.	Aspirin	36-43	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	105-110
19028575-7	2009	Simulation of the combined effect of two NSAIDs, aspirin and celecoxib, on COX-1 allowed us to reveal the mechanism underlying the suppression of aspirin-mediated COX-1 inhibition by celecoxib.	Aspirin	49-56	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	75-80
19028575-7	2009	Simulation of the combined effect of two NSAIDs, aspirin and celecoxib, on COX-1 allowed us to reveal the mechanism underlying the suppression of aspirin-mediated COX-1 inhibition by celecoxib.	Aspirin	49-56	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	163-168
19028575-7	2009	Simulation of the combined effect of two NSAIDs, aspirin and celecoxib, on COX-1 allowed us to reveal the mechanism underlying the suppression of aspirin-mediated COX-1 inhibition by celecoxib.	Aspirin	146-153	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	75-80
19028575-7	2009	Simulation of the combined effect of two NSAIDs, aspirin and celecoxib, on COX-1 allowed us to reveal the mechanism underlying the suppression of aspirin-mediated COX-1 inhibition by celecoxib.	Aspirin	146-153	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	163-168
18514659-3	2009	However, TXA(2) formation remains elevated in patients with cardiovascular disease on doses of aspirin that fully suppress platelet COX-1, suggesting other tissue sources for TXA(2) formation.	Aspirin	95-102	prostaglandin-endoperoxide synthase 1	Mus musculus	132-137
18851958-0	2009	Acetylsalicylic acid and salicylic acid decrease tumor cell viability and glucose metabolism modulating 6-phosphofructo-1-kinase structure and activity.	Aspirin	0-20	phosphofructokinase, muscle	Homo sapiens	104-128
19938885-3	2009	We also review several pathogenic mechanisms that have been advanced by animal studies to explain the finding that a COX-2 selective inhibitor plus low-dose aspirin leads to an ulcer rate near that of a dual COX-1/COX-2 inhibitor alone.	Aspirin	157-164	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	208-213
18413191-0	2009	Inhibition of platelet GPIIb-IIIa and P-selectin expression by aspirin is impaired by stress hyperglycemia.	Aspirin	63-70	selectin P	Homo sapiens	38-48
18413191-6	2009	In vitro, ASA significantly inhibited both GPIIb-IIIa expression (36.5%) and P-selectin expression (81%; P&lt;.005).	Aspirin	10-13	selectin P	Homo sapiens	77-87
18413191-7	2009	However, increased blood glucose (200 mg/dl) significantly impaired the inhibitory effect of ASA (84% for GPIIb-IIIa, P&lt;.005; 48% for P-selectin, P=NS).	Aspirin	93-96	selectin P	Homo sapiens	137-147
18413191-9	2009	A statistically significant interaction between glucose concentration and ASA dose was found (P&lt;.001 for GPIIb-IIIa and P=.004 for P-selectin).	Aspirin	74-77	selectin P	Homo sapiens	134-144
18413191-10	2009	In vitro, concentration-dependent stress hyperglycemia significantly impaired the inhibitory effects of aspirin on human platelet GPIIb-IIIa and P-selectin expression.	Aspirin	104-111	selectin P	Homo sapiens	145-155
19297549-4	2009	Salicylic acid on the other hand, as well as acetyl salicylic acid, suppresses LIN6 expression, supporting the fact that LIN6 is an inducible compound of the defence/stress response pathway that is antagonistically regulated by jasmonates and salicylates.	Aspirin	45-66	acid invertase	Solanum lycopersicum	79-83
19297549-4	2009	Salicylic acid on the other hand, as well as acetyl salicylic acid, suppresses LIN6 expression, supporting the fact that LIN6 is an inducible compound of the defence/stress response pathway that is antagonistically regulated by jasmonates and salicylates.	Aspirin	45-66	acid invertase	Solanum lycopersicum	121-125
19862937-0	2009	The A-444C polymorphism in the leukotriene C4 synthase gene is associated with aspirin-induced urticaria.	Aspirin	79-86	leukotriene C4 synthase	Homo sapiens	31-54
19862937-3	2009	Previous studies have suggested a role for the A-444C polymorphism on the leukotriene C4 synthase gene (LTC4S) in aspirin-induced urticaria (AIU), but the results are controversial.	Aspirin	114-121	leukotriene C4 synthase	Homo sapiens	74-97
19862937-3	2009	Previous studies have suggested a role for the A-444C polymorphism on the leukotriene C4 synthase gene (LTC4S) in aspirin-induced urticaria (AIU), but the results are controversial.	Aspirin	114-121	leukotriene C4 synthase	Homo sapiens	104-109
18971601-0	2009	Aspirin inhibits MMP-2 and MMP-9 expressions and activities through upregulation of PPARalpha/gamma and TIMP gene expressions in ox-LDL-stimulated macrophages derived from human monocytes.	Aspirin	0-7	peroxisome proliferator activated receptor alpha	Homo sapiens	84-93
18971601-6	2009	RT-PCR and ELISA assays showed that inhibition of MMP-9 levels by aspirin was notably alleviated by PPAR antagonists.	Aspirin	66-73	peroxisome proliferator activated receptor alpha	Homo sapiens	100-104
18971601-10	2009	These results demonstrate that aspirin could inhibit MMP-2 and MMP-9 expression through upregulation of PPARalpha/gamma expression in ox-LDL-stimulated macrophages, and could potentially inhibit MMP-2 and MMP-9 activity by induction of TIMP-1 and TIMP-2 expression.	Aspirin	31-38	peroxisome proliferator activated receptor alpha	Homo sapiens	104-113
19069170-1	2008	Aspirin inhibits platelet activation through the permanent inactivation of the cyclooxygenase (COX) activity of prostaglandin H synthase-1 (referred to as COX-1), and consequently inhibits the biosynthesis of thromboxane A2 (TXA2), a platelet agonist.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	155-160
22727736-2	2012	The effects of clopidogrel and aspirin (ASA) on equine platelet CD62P expression were investigated.	Aspirin	40-43	selectin P	Equus caballus	64-69
23199511-3	2012	At low-doses, aspirin acts mainly by an irreversible inactivation of platelet cyclooxygenase (COX)-1 activity.	Aspirin	14-21	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	78-100
22561694-6	2012	In addition, the increased transcription of MCP-1 was detectable at later maturation phase of adipogenesis, which was prevented by co-incubation with aspirin.	Aspirin	150-157	C-C motif chemokine ligand 2	Homo sapiens	44-49
22561694-7	2012	Although 15d-PGJ(2) was more potent than Delta(12)-PGJ(2), both PGJ(2) derivatives series had similar effects to rescue dose-dependently the expression of the MCP-1 gene attenuated by aspirin.	Aspirin	184-191	C-C motif chemokine ligand 2	Homo sapiens	159-164
22588264-13	2012	We speculate that the protective effect of aspirin against rupture of cerebral aneurysms may be mediated in part by inhibition of COX-2/mPGES-1.	Aspirin	43-50	prostaglandin E synthase	Mus musculus	136-143
22406476-5	2012	Phosphorylation of AMPK was measured; the effects of loss of AMPKalpha on the aspirin-induced effects of mTOR were determined using small interfering RNA (siRNA) in CRC cells and in AMPK(alpha1/alpha2-/-) mouse embryonic fibroblasts.	Aspirin	78-85	mechanistic target of rapamycin kinase	Mus musculus	105-109
22406476-8	2012	RESULTS: Aspirin reduced mTOR signaling in CRC cells by inhibiting the mTOR effectors S6K1 and 4E-BP1.	Aspirin	9-16	ribosomal protein S6 kinase B1	Homo sapiens	86-101
22406476-13	2012	Rectal mucosal samples from patients given aspirin had reduced phosphorylation of S6K1 and S6.	Aspirin	43-50	ribosomal protein S6 kinase B1	Homo sapiens	82-86
22494617-4	2012	Glucose-aspirin was sevenfold more water soluble than aspirin and it was about 8- to 9-fold more active in inhibiting cell growth than aspirin in their anti-cancer cell culture activity on breast (SKBR3), pancreatic (PANC-1), and prostate (PC3) cell lines, whereas the activity was similar on a benign non-cancerous cell line (WI 38).	Aspirin	8-15	proprotein convertase subtilisin/kexin type 1	Homo sapiens	240-243
21950486-5	2012	KEY RESULTS: Compared with ASA, ASA + M strongly inhibited ADP-induced peak platelet aggregation (88%), late aggregation (84%), P-selectin expression (85%) and alpha(IIb) beta(3) activation (62%) (28%, 65%, 70% and 51% inhibition, respectively, for ASA/C vs. ASA).	Aspirin	32-35	selectin P	Homo sapiens	128-138
21950486-5	2012	KEY RESULTS: Compared with ASA, ASA + M strongly inhibited ADP-induced peak platelet aggregation (88%), late aggregation (84%), P-selectin expression (85%) and alpha(IIb) beta(3) activation (62%) (28%, 65%, 70% and 51% inhibition, respectively, for ASA/C vs. ASA).	Aspirin	32-35	selectin P	Homo sapiens	128-138
21950486-5	2012	KEY RESULTS: Compared with ASA, ASA + M strongly inhibited ADP-induced peak platelet aggregation (88%), late aggregation (84%), P-selectin expression (85%) and alpha(IIb) beta(3) activation (62%) (28%, 65%, 70% and 51% inhibition, respectively, for ASA/C vs. ASA).	Aspirin	32-35	selectin P	Homo sapiens	128-138
22159558-0	2012	SNX3-dependent regulation of epidermal growth factor receptor (EGFR) trafficking and degradation by aspirin in epidermoid carcinoma (A-431) cells.	Aspirin	100-107	sorting nexin 3	Homo sapiens	0-4
22570750-7	2012	The increases in MPO levels induced by diclofenac and aspirin were significantly higher in 1-year-old than 7-week-old rats (p&lt;0.05).	Aspirin	54-61	myeloperoxidase	Rattus norvegicus	17-20
22306536-8	2012	Similarly to losartan, ASA, and its SA moiety suppressed Ang II-mediated AT1R transcription and fibroblast proliferation as well as expression of collagens and MMPs.	Aspirin	23-26	angiotensin II, type I receptor-associated protein	Mus musculus	73-77
22306536-9	2012	ASA also suppressed the expression of NADPH oxidase subunits (p22(phox), p47(phox), p67(phox), NOX2 and NOX4) and ROS generation.	Aspirin	0-3	methionine aminopeptidase 2	Mus musculus	84-87
22306536-11	2012	These observations suggest that ASA inhibits Ang II-induced NADPH oxidase expression, NF-kappaB activation and AT1R transcription in cardiac fibroblasts, and fibroblast proliferation and collagen expression.	Aspirin	32-35	angiotensin II, type I receptor-associated protein	Mus musculus	111-115
22306536-12	2012	The critical role of NADPH oxidase activity in stimulation of AT1R transcription became apparent in experiments where ASA also inhibited AT1R transcription in cardiac fibroblasts challenged with H2O2.	Aspirin	118-121	angiotensin II, type I receptor-associated protein	Mus musculus	62-66
22306536-12	2012	The critical role of NADPH oxidase activity in stimulation of AT1R transcription became apparent in experiments where ASA also inhibited AT1R transcription in cardiac fibroblasts challenged with H2O2.	Aspirin	118-121	angiotensin II, type I receptor-associated protein	Mus musculus	137-141
22306536-13	2012	Since SA had similar effect as ASA on AT1R expression, we suggest that ASA"s effect is mediated by its SA moiety.	Aspirin	31-34	angiotensin II, type I receptor-associated protein	Mus musculus	38-42
22306536-13	2012	Since SA had similar effect as ASA on AT1R expression, we suggest that ASA"s effect is mediated by its SA moiety.	Aspirin	71-74	angiotensin II, type I receptor-associated protein	Mus musculus	38-42
21692746-7	2012	Intratumoral administration of aspirin was accompanied by alterations in the biophysical, biochemical and immunological composition of the tumour microenvironment with respect to pH, level of dissolved O2, glucose, lactate, nitric oxide, IFNgamma (interferon gamma), IL-4 (interleukin-4), IL-6 and IL-10, whereas the TGF-beta (tumour growth factor-beta) level was unaltered.	Aspirin	31-38	interleukin 4	Mus musculus	267-271
21692746-7	2012	Intratumoral administration of aspirin was accompanied by alterations in the biophysical, biochemical and immunological composition of the tumour microenvironment with respect to pH, level of dissolved O2, glucose, lactate, nitric oxide, IFNgamma (interferon gamma), IL-4 (interleukin-4), IL-6 and IL-10, whereas the TGF-beta (tumour growth factor-beta) level was unaltered.	Aspirin	31-38	interleukin 4	Mus musculus	273-286
23050049-9	2012	Use of aspirin/NSAIDs interacted significantly with TERT rs10069690 and rs2242652 to alter TL.	Aspirin	7-14	telomerase reverse transcriptase	Homo sapiens	52-56
22429367-4	2012	Aspirin resistance was assessed by thrombo elastography (TEG, with arachidonic acid [AA] or adenosine diphosphate as inducers), serum/urinary 11-dehydrothromboxane B2 (11-DH-TXB2) assay, platelet function analyser-100 assay and P-selectin assay.	Aspirin	0-7	selectin P	Homo sapiens	228-238
22429367-8	2012	TEG-AA was more sensitive, specific and consistent than P-selectin in detecting aspirin resistance.	Aspirin	80-87	selectin P	Homo sapiens	56-66
22615972-8	2012	Two SNPs in TXNRD1 and four SNPs in TXNRD2 interacted with aspirin/NSAID to influence colon cancer; one SNP in TXNRD1, two SNPs in TXNRD2, and one SNP in TXNRD3 interacted with aspirin/NSAIDs to influence rectal cancer.	Aspirin	59-66	thioredoxin reductase 3	Homo sapiens	154-160
18797154-8	2008	(5) Evaluation of the association between C metabolism and the single nucleotide polymorphisms of glutathione S-transferase P (GSTP) 1-1 showed a lower urinary C excretion and a significantly lower C level in 24-h urine (p&lt;0.05) after AsA loading, and a significantly lower urinary C excretion between 0 and 3 h after DAsA loading (p&lt;0.05) for the GA heterozygotes than for the AA homozygotes.	Aspirin	238-241	glutathione S-transferase pi 1	Homo sapiens	98-136
18480058-0	2008	The ATP-gated P2X1 receptor plays a pivotal role in activation of aspirin-treated platelets by thrombin and epinephrine.	Aspirin	66-73	purinergic receptor P2X 1	Homo sapiens	14-27
18355801-0	2008	Aspirin inhibits human bradykinin B2 receptor ligand binding function.	Aspirin	0-7	bradykinin receptor B2	Homo sapiens	34-45
18355801-4	2008	We found that the widely used analgesic, anti-thrombotic, and anti-inflammatory drug aspirin alters the B2 receptor ligand binding properties.	Aspirin	85-92	bradykinin receptor B2	Homo sapiens	104-115
18355801-6	2008	In addition, aspirin reduces the capacity of unlabeled bradykinin or the B2 receptor antagonist icatibant to destabilize pre-formed [3H]-bradykinin-receptor complexes.	Aspirin	13-20	bradykinin receptor B2	Homo sapiens	73-84
18360096-7	2008	In addition, aspirin induced the increasing transport of fluorescine isothiocyanate-labeled dextrans with localized disruption and decreased expression of ZO-1 protein on rat gastric mucosal cell line RGM-1.	Aspirin	13-20	tight junction protein 1	Rattus norvegicus	155-159
18078964-0	2008	The aspirin metabolite salicylate enhances neuronal excitation in rat hippocampal CA1 area through reducing GABAergic inhibition.	Aspirin	4-11	carbonic anhydrase 1	Rattus norvegicus	82-85
17630652-15	2008	CONCLUSIONS: Tight relationships between aggregation and cytometric quantification of platelet markers in whole blood, in particular CD62P, allow to predict aggregation response to ADP from flow data in patients treated with aspirin alone or with aspirin plus clopidogrel.	Aspirin	225-232	selectin P	Homo sapiens	133-138
17630652-15	2008	CONCLUSIONS: Tight relationships between aggregation and cytometric quantification of platelet markers in whole blood, in particular CD62P, allow to predict aggregation response to ADP from flow data in patients treated with aspirin alone or with aspirin plus clopidogrel.	Aspirin	247-254	selectin P	Homo sapiens	133-138
21788065-7	2011	In healthy individuals the resting platelet expression of CD62P, plasma level of soluble CD62P and percentage of circulating monocyte-platelet aggregates were lower after the aspirin intake period (P=0.009; P=0.04; P=0.004, respectively).	Aspirin	175-182	selectin P	Homo sapiens	58-63
21788065-7	2011	In healthy individuals the resting platelet expression of CD62P, plasma level of soluble CD62P and percentage of circulating monocyte-platelet aggregates were lower after the aspirin intake period (P=0.009; P=0.04; P=0.004, respectively).	Aspirin	175-182	selectin P	Homo sapiens	89-94
21984018-1	2011	Metalcarbonyl complexes with ligands derived from acetylsalicylic acid demonstrated high cytotoxic potential against various tumor cell lines and strong inhibition of the cyclooxygenase enzymes COX-1 and 2.	Aspirin	50-70	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	194-205
21459117-4	2011	In addition, long term potentiation (LTP) in the CA1 region of the hippocampus, a cellular correlate of learning and memory, was also impaired in ASA(-/-) mice.	Aspirin	146-149	carbonic anhydrase 1	Mus musculus	49-52
21945907-5	2011	The linearity range was found to be 1-5, 10-50 and 2-10 mug mL-1 for ramipril, aspirin and atorvastatin calcium, respectively.	Aspirin	79-86	L1 cell adhesion molecule	Mus musculus	60-64
21415093-7	2011	Although myeloperoxidase (MPO) activity was increased by ASA, it was found to be lower in the ASA plus SC group.	Aspirin	57-60	myeloperoxidase	Rattus norvegicus	9-24
21415093-7	2011	Although myeloperoxidase (MPO) activity was increased by ASA, it was found to be lower in the ASA plus SC group.	Aspirin	57-60	myeloperoxidase	Rattus norvegicus	26-29
21415093-7	2011	Although myeloperoxidase (MPO) activity was increased by ASA, it was found to be lower in the ASA plus SC group.	Aspirin	94-97	myeloperoxidase	Rattus norvegicus	9-24
21631613-0	2011	Leukotriene C4 synthase: the engine of aspirin intolerance?	Aspirin	39-46	leukotriene C4 synthase	Homo sapiens	0-23
21700086-1	2011	OBJECTIVES: The aim of this study was to assess the association between genetic variants of the insulin receptor substrate (IRS)-1 gene, platelet function, and long-term outcomes in patients with type 2 diabetes mellitus (DM) and stable coronary artery disease while on aspirin and clopidogrel therapy.	Aspirin	270-277	insulin receptor substrate 1	Homo sapiens	96-130
21406194-6	2011	Using a modified biotin switch assay we demonstrated that NO-ASA S-nitrosylates the signaling proteins p53, beta-catenin, and NF-kappaB, in colon cancer cells in a time- and concentration-dependent manner.	Aspirin	61-64	catenin beta 1	Homo sapiens	108-120
21396389-7	2011	In addition, aspirin treatment, which has been postulated to attenuate cytokine formation and the activation of the Nalp3 inflammasome after APAP, had no effect on release of DAMPs, hepatic neutrophil accumulation or liver injury.	Aspirin	13-20	NLR family, pyrin domain containing 3	Mus musculus	116-121
21324923-5	2011	ASA treatment also reduced the MDSC-attracting chemokine CCL2 (C-C motif ligand 2) in the TME along with numbers of CD11b(+)Ly6G(hi)Ly6C(lo) granulocytic MDSCs in both the bone marrow and the TME.	Aspirin	0-3	lymphocyte antigen 6 complex, locus C1	Mus musculus	132-136
21544164-4	2011	We utilize a threedimensional residue measure of solvent exposure, accessible surface area (ASA), which shows that major segments of gp120 and gp41 known structures are solvent exposed across clades.	Aspirin	92-95	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	133-138
20506261-8	2011	Aspirin, NSAID and paracetamol use were associated with reduced serum PSA concentrations amongst controls.	Aspirin	0-7	kallikrein related peptidase 3	Homo sapiens	70-73
20506261-10	2011	Our conclusions are unlikely to be influenced by PSA detection bias because the inverse associations of aspirin, NSAID and paracetamol use with serum PSA would have attenuated (not generated) the observed positive associations.	Aspirin	104-111	kallikrein related peptidase 3	Homo sapiens	150-153
21231793-5	2011	Here we show that ASA inhibits phagocytosis and modulates expression of endosomal SNAREs, such as Vti1a, Vti1b, VAMP-3, VAMP-8 and Syn-8 (but not syn-6 and syn-16) in DC.	Aspirin	18-21	syntaxin 16	Mus musculus	156-162
21116822-12	2011	Furthermore, treatment with a HMG-CoA reductase inhibitor or acetylsalicylic acid showed reduced levels of IL-21, IL-23 and VCAM1 (all p &lt; 0.05), but did not influence IL-17A.	Aspirin	61-81	interleukin 23 subunit alpha	Homo sapiens	114-119
21205744-6	2011	In agreement with our in vivo results, both S-ibuprofen and aspirin were found to decrease total levels of beta-catenin while increasing its phosphorylation.	Aspirin	60-67	catenin beta 1	Homo sapiens	107-119
21346370-0	2011	Possible association of SLC22A2 polymorphisms with aspirin-intolerant asthma.	Aspirin	51-58	solute carrier family 22 member 2	Homo sapiens	24-31
21346370-2	2011	Solute carrier family 22, member 2 (SLC22A2), also known as organic cation transporter 2 (OCT2), is predominantly expressed in the luminal membrane of airway epithelial cells and has been shown to mediate the transport of prostaglandins on the cyclooxygenase pathway which is regulated by aspirin blockage.	Aspirin	289-296	solute carrier family 22 member 2	Homo sapiens	0-34
21346370-2	2011	Solute carrier family 22, member 2 (SLC22A2), also known as organic cation transporter 2 (OCT2), is predominantly expressed in the luminal membrane of airway epithelial cells and has been shown to mediate the transport of prostaglandins on the cyclooxygenase pathway which is regulated by aspirin blockage.	Aspirin	289-296	solute carrier family 22 member 2	Homo sapiens	36-43
21346370-2	2011	Solute carrier family 22, member 2 (SLC22A2), also known as organic cation transporter 2 (OCT2), is predominantly expressed in the luminal membrane of airway epithelial cells and has been shown to mediate the transport of prostaglandins on the cyclooxygenase pathway which is regulated by aspirin blockage.	Aspirin	289-296	solute carrier family 22 member 2	Homo sapiens	60-88
21346370-2	2011	Solute carrier family 22, member 2 (SLC22A2), also known as organic cation transporter 2 (OCT2), is predominantly expressed in the luminal membrane of airway epithelial cells and has been shown to mediate the transport of prostaglandins on the cyclooxygenase pathway which is regulated by aspirin blockage.	Aspirin	289-296	solute carrier family 22 member 2	Homo sapiens	90-94
21346370-4	2011	METHODS: To investigate the associations between AIA and genetic polymorphisms of the SLC22A2 gene, 18 variants were genotyped in 163 AIA subjects and 429 aspirin-tolerant asthma (ATA) controls.	Aspirin	155-162	solute carrier family 22 member 2	Homo sapiens	86-93
21346370-8	2011	In addition, a polymorphism in intron 4 (rs3912161) and a haplotype (SLC22A2-ht3) showed significantly stronger association signals with the FEV(1) fall rate induced by aspirin provocation in AIA subjects compared with ATA controls (p = 0.004, P(corr) = 0.05).	Aspirin	169-176	solute carrier family 22 member 2	Homo sapiens	69-76
21346370-9	2011	CONCLUSION: Our findings suggest that SLC22A2 could be a susceptibility gene for aspirin intolerance in asthmatics.	Aspirin	81-88	solute carrier family 22 member 2	Homo sapiens	38-45
22022418-8	2011	P-selectin glycoprotein ligand-1 (PSGL-1) blocking antibody, which abrogates MPA formation, abolished these effects, as did the cyclooxygenase (COX)-2 selective inhibitor NS-398, aspirin and the EP1/EP2-selective antagonist AH6809.	Aspirin	179-186	selectin P ligand	Homo sapiens	0-32
22022418-8	2011	P-selectin glycoprotein ligand-1 (PSGL-1) blocking antibody, which abrogates MPA formation, abolished these effects, as did the cyclooxygenase (COX)-2 selective inhibitor NS-398, aspirin and the EP1/EP2-selective antagonist AH6809.	Aspirin	179-186	selectin P ligand	Homo sapiens	34-40
21071691-11	2010	In this respect, the EP4 agonist synergized with acetylsalicylic acid.	Aspirin	49-69	prostaglandin E receptor 4	Homo sapiens	21-24
20640495-17	2010	Both SIM and DIP+low-dose ASA augmented eNOS, ERK 1/2 and CREB phosphorylation.	Aspirin	26-29	cAMP responsive element binding protein 1	Rattus norvegicus	58-62
21035850-5	2010	The mechanism of this increased implantation rate is unclear, and in this study we hypothesised that the expression of integrin beta3 or LIF may be altered, during implantation window, by treatment with low-dose aspirin.	Aspirin	212-219	leukemia inhibitory factor	Mus musculus	137-140
21035850-8	2010	We found the expression of LIF or integrin beta3 was significantly increased in the endometrium of mice that were treated with low dose of aspirin by immuno-fluorescence.	Aspirin	139-146	leukemia inhibitory factor	Mus musculus	27-30
21035850-9	2010	In addition, the mRNA level of LIF or integrin beta3 on the endometrium of aspirin treated mice was also significantly increased compared to untreated mice.	Aspirin	75-82	leukemia inhibitory factor	Mus musculus	31-34
21035850-10	2010	We conclude that low dose aspirin alters the expression of endometrial LIF and integrin beta3 and that these changes may increase endometrial receptivity.	Aspirin	26-33	leukemia inhibitory factor	Mus musculus	71-74
21061542-7	2010	In conclusions, the assessment for genotype of COX-1 gene promoter polymorphism, especially rs1330344, may be useful for detecting the high risk group of developing NSAID/aspirin-induced ulcer diseases.	Aspirin	171-178	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	47-52
20886180-7	2010	Plaque macrophages synthesise PGH2/PGG2 via COX-2; these potent prostanoids can trigger platelet activation and aggregation despite COX-1 inhibition by aspirin.	Aspirin	152-159	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	132-137
20670296-7	2010	Daily ingestion of aspirin by participants resulted in an increase in maspin levels from 0.95 +- 0.04 to 4.63 +- 0.05 nM after 24 h. These levels were maintained for 3 years.	Aspirin	19-26	serpin family B member 5	Homo sapiens	70-76
20452758-2	2010	The aim of this study was to determine levels of MCP-3, RANTES, eotaxin, Il-5 and Il-3 in aspirin intolerant asthmatics (AIA) after nasal lysine-aspirin (Lys-ASA) challenge.	Aspirin	90-97	interleukin 3	Homo sapiens	82-86
21265493-0	2010	Proton pump inhibitors in patients treated with aspirin and clopidogrel after acute coronary syndrome.	Aspirin	48-55	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	0-11
21265493-2	2010	Numerous drugs are known to inhibit P-450 isoenzymes, including proton pump inhibitors (PPIs), which are often associated with aspirin and clopidogrel to prevent adverse gastrointestinal effects.	Aspirin	127-134	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	64-75
20857806-10	2010	Multivariate analysis revealed independent correlation of consuming low-dose aspirin (standardized coefficient beta = 11.701, P = 0.004), diabetes (beta = 2.921, P = 0.027), cigarette smoking (beta = 2.910, P = 0.037) and nausea (beta = 3.620, P = 0.015) with organic dyspepsia.	Aspirin	77-84	eukaryotic translation elongation factor 1 beta 2 pseudogene 2	Homo sapiens	230-238
20404564-0	2010	The effects of the histone deacetylase inhibitor romidepsin (FK228) are enhanced by aspirin (ASA) in COX-1 positive ovarian cancer cells through augmentation of p21.	Aspirin	84-91	H3 histone pseudogene 16	Homo sapiens	161-164
20404564-0	2010	The effects of the histone deacetylase inhibitor romidepsin (FK228) are enhanced by aspirin (ASA) in COX-1 positive ovarian cancer cells through augmentation of p21.	Aspirin	93-96	H3 histone pseudogene 16	Homo sapiens	161-164
20404564-11	2010	In the COX-1 positive cells, p21 expression was augmented by the addition of ASA to FK228 treatment.	Aspirin	77-80	H3 histone pseudogene 16	Homo sapiens	29-32
20404564-12	2010	Furthermore, COX-1 siRNA attenuated the effects of combined ASA and FK228 on the levels of p21 expression and the amount of growth inhibition.	Aspirin	60-63	H3 histone pseudogene 16	Homo sapiens	91-94
20404564-13	2010	The additional increase in p21 by ASA in FK228-treated cells was not observed at the promoter or transcriptional levels.	Aspirin	34-37	H3 histone pseudogene 16	Homo sapiens	27-30
20404564-14	2010	However, a significant delay in p21 protein degradation in the presence of ASA and FK228 in COX-1 positive cells was associated with inhibition of proteasome activity.	Aspirin	75-78	H3 histone pseudogene 16	Homo sapiens	32-35
20819511-6	2010	Activation of p38 mitogen activated protein kinase and NF-kappaB, the expression of intercellular adhesion molecule-1 and monocyte chemotactic protein-1, which were only mildly affected by aspirin or pravastatin alone, were significantly attenuated by their combination.	Aspirin	189-196	C-C motif chemokine ligand 2	Homo sapiens	122-152
20445534-0	2010	CYP2C9*3 Loss-of-Function Allele Is Associated With Acute Upper Gastrointestinal Bleeding Related to the Use of NSAIDs Other Than Aspirin.	Aspirin	130-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20445534-1	2010	Nonsteroidal anti-inflammatory drugs (NSAIDs), other than aspirin, are to some extent metabolized by cytochrome P450 2C9 (CYP2C9).	Aspirin	58-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-120
20445534-1	2010	Nonsteroidal anti-inflammatory drugs (NSAIDs), other than aspirin, are to some extent metabolized by cytochrome P450 2C9 (CYP2C9).	Aspirin	58-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
20445534-5	2010	In the aspirin group, 12 patients (9.2%) had the CYP2C9 359Leu allele as compared with 19 (33.3%) in the non-ASP group (odds ratio (OR) = 5.0; 95% confidence interval 2.2-11.1, P &lt; 0.0001).	Aspirin	7-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
27713316-2	2010	Aspirin and several small molecule NSAIDs are known to inhibit the enzymes cyclooxygenase-1 (COX-1) and -2 (COX-2).	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	93-106
19880966-8	2010	RESULTS: After 3 and 5 months of treatment, enalapril and aspirin were able to significantly delay progression of mPanINs in LsL-Kras(G12D); Pdx1-Cre mice.	Aspirin	58-65	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	129-133
20586862-5	2010	Carrying the CYP2C9 variants is reported a significantly increased risk of non-aspirin NSAID-related GI bleeding.	Aspirin	79-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
20116423-0	2010	Aspirin induces apoptosis in YD-8 human oral squamous carcinoma cells through activation of caspases, down-regulation of Mcl-1, and inactivation of ERK-1/2 and AKT.	Aspirin	0-7	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	121-126
20116423-5	2010	Data of Western blot further demonstrated that aspirin treatment caused activation of caspases, down-regulation of Mcl-1 protein, dephosphorylation of ERK-1/2 and AKT, and also IkappaB-alpha proteolysis-dependent NF-kappaB activation in YD-8 cells.	Aspirin	47-54	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	115-120
20116423-8	2010	These findings collectively suggest that aspirin induces apoptosis in YD-8 cells and the induction may be correlated to activation of caspases, caspase-dependent Mcl-1 proteolysis, inactivation of ERK-1/2 and AKT, and activation of NF-kappaB.	Aspirin	41-48	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	162-167
20223389-10	2010	Patients who received aspirin were more likely to be white (60% vs 54%, P = .0009) or have an ACS diagnosis (82% vs 50%, P &lt; .0001).	Aspirin	22-29	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	94-97
20223389-13	2010	CONCLUSION: For patients with undifferentiated chest pain, overall race, sex, and age differences were explained by higher rates of aspirin administered to older men with non-ACS chest pain.	Aspirin	132-139	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	175-178
19788892-6	2010	Analysis of serum cytokines of aspirin-induced rats showed a moderate decrease in interleukin-10 (IL-10) with considerable increase of interleukin-6 (IL-6) and interferon-gamma (INF-gamma) when compared with control.	Aspirin	31-38	interleukin 10	Rattus norvegicus	82-96
19788892-6	2010	Analysis of serum cytokines of aspirin-induced rats showed a moderate decrease in interleukin-10 (IL-10) with considerable increase of interleukin-6 (IL-6) and interferon-gamma (INF-gamma) when compared with control.	Aspirin	31-38	interleukin 10	Rattus norvegicus	98-103
19788892-6	2010	Analysis of serum cytokines of aspirin-induced rats showed a moderate decrease in interleukin-10 (IL-10) with considerable increase of interleukin-6 (IL-6) and interferon-gamma (INF-gamma) when compared with control.	Aspirin	31-38	interferon gamma	Rattus norvegicus	160-187
20648923-9	2010	Furthermore, compared to ASA and to diclofenac (Diclo, CAS 15307-79-6), the COX-1 and COX-2 mRNA expressions were influenced differently by STW 33-I and fraction E. ASA and Diclo inhibited both the COX-1 and COX-2 mRNA expressions, whereas STW 33-I and its fraction E increased the COX-1 mRNA expression.	Aspirin	165-168	BCAR1 scaffold protein, Cas family member	Homo sapiens	55-58
20648923-9	2010	Furthermore, compared to ASA and to diclofenac (Diclo, CAS 15307-79-6), the COX-1 and COX-2 mRNA expressions were influenced differently by STW 33-I and fraction E. ASA and Diclo inhibited both the COX-1 and COX-2 mRNA expressions, whereas STW 33-I and its fraction E increased the COX-1 mRNA expression.	Aspirin	165-168	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	76-81
20648923-9	2010	Furthermore, compared to ASA and to diclofenac (Diclo, CAS 15307-79-6), the COX-1 and COX-2 mRNA expressions were influenced differently by STW 33-I and fraction E. ASA and Diclo inhibited both the COX-1 and COX-2 mRNA expressions, whereas STW 33-I and its fraction E increased the COX-1 mRNA expression.	Aspirin	165-168	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	198-203
20648923-9	2010	Furthermore, compared to ASA and to diclofenac (Diclo, CAS 15307-79-6), the COX-1 and COX-2 mRNA expressions were influenced differently by STW 33-I and fraction E. ASA and Diclo inhibited both the COX-1 and COX-2 mRNA expressions, whereas STW 33-I and its fraction E increased the COX-1 mRNA expression.	Aspirin	165-168	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	198-203
22282685-3	2010	Aspirin is a non-steroidal anti-inflammatory drug that exerts its anti-platelet action through the irreversible acetylation of platelet cyclooxygenase (COX)-1, blocking thromboxane A2 production.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	136-158
19884005-3	2009	AI structure-activity studies showed that the C-4 (14a) and C-5 (14b) salicylate regioisomers were 1.4- and 1.6-fold more potent than aspirin, and the C-5 N-acetyl-2-carboxybenzenesulfonamide regioisomer (22b) was 1.3- and 2.8-fold more potent than ibuprofen and aspirin, respectively.	Aspirin	134-141	complement C4A (Rodgers blood group)	Homo sapiens	46-49
19884005-3	2009	AI structure-activity studies showed that the C-4 (14a) and C-5 (14b) salicylate regioisomers were 1.4- and 1.6-fold more potent than aspirin, and the C-5 N-acetyl-2-carboxybenzenesulfonamide regioisomer (22b) was 1.3- and 2.8-fold more potent than ibuprofen and aspirin, respectively.	Aspirin	134-141	complement C5	Homo sapiens	60-63
19884005-3	2009	AI structure-activity studies showed that the C-4 (14a) and C-5 (14b) salicylate regioisomers were 1.4- and 1.6-fold more potent than aspirin, and the C-5 N-acetyl-2-carboxybenzenesulfonamide regioisomer (22b) was 1.3- and 2.8-fold more potent than ibuprofen and aspirin, respectively.	Aspirin	263-270	complement C4A (Rodgers blood group)	Homo sapiens	46-49
19884005-3	2009	AI structure-activity studies showed that the C-4 (14a) and C-5 (14b) salicylate regioisomers were 1.4- and 1.6-fold more potent than aspirin, and the C-5 N-acetyl-2-carboxybenzenesulfonamide regioisomer (22b) was 1.3- and 2.8-fold more potent than ibuprofen and aspirin, respectively.	Aspirin	263-270	complement C5	Homo sapiens	60-63
19884005-3	2009	AI structure-activity studies showed that the C-4 (14a) and C-5 (14b) salicylate regioisomers were 1.4- and 1.6-fold more potent than aspirin, and the C-5 N-acetyl-2-carboxybenzenesulfonamide regioisomer (22b) was 1.3- and 2.8-fold more potent than ibuprofen and aspirin, respectively.	Aspirin	263-270	complement C5	Homo sapiens	151-154
20641589-17	2004	BChE also inactivates some drugs, e.g., aspirin, amitriptyline, and bambuterol (1, 6).	Aspirin	40-47	butyrylcholinesterase	Homo sapiens	0-4
20641640-17	2004	BChE also inactivates some drugs, e.g., aspirin, amitriptyline, and bambuterol.	Aspirin	40-47	butyrylcholinesterase	Homo sapiens	0-4
19890703-2	2009	DISCUSSION: The key role of platelet-mediated thrombosis in the pathogenesis of NSTE ACS is confirmed by the proven clinical benefits of antiplatelet agents (aspirin and a P2Y(12) adenosine diphosphate [ADP] receptor antagonist) in this setting.	Aspirin	158-165	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	85-88
20306635-9	2009	Treatment with thalidomide showed a significant benefit compared to aspirin (RR 2.43; 95% CI 1.28 to 4.59).	Aspirin	68-75	ribonucleotide reductase regulatory subunit M2	Homo sapiens	77-81
19576865-3	2009	The p- and m-NO-ASA isomers strongly inhibited cell growth and beta-catenin/TCF transcriptional activity compared to ASA; the IC50s for growth inhibition were 57+/-4, 193+/-10 and &gt;5000microM, and for transcriptional inhibition they were 12+/-1.8, 75+/-6.5 and &gt;5000microM for p-, m-NO-ASA and ASA, respectively.	Aspirin	16-19	catenin beta 1	Homo sapiens	63-75
19576865-4	2009	p-NO-ASA reduced the expression of Wnt/beta-catenin downstream target gene cyclin D1, and total cellular beta-catenin levels.	Aspirin	5-8	catenin beta 1	Homo sapiens	39-51
19576865-4	2009	p-NO-ASA reduced the expression of Wnt/beta-catenin downstream target gene cyclin D1, and total cellular beta-catenin levels.	Aspirin	5-8	catenin beta 1	Homo sapiens	105-117
20214591-4	2009	Among the enzymes involved in aspirin biodisposition a major role is played by the enzymes UDP-glucuronosyltransferase UGT1A6, cytochrome P450 CYP2C9 and the xenobiotic/medium chain fatty acid:CoA ligase ACSM2, although other UGTs and ACSMs enzymes may significantly contribute to aspirin metabolism.	Aspirin	30-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
20214591-4	2009	Among the enzymes involved in aspirin biodisposition a major role is played by the enzymes UDP-glucuronosyltransferase UGT1A6, cytochrome P450 CYP2C9 and the xenobiotic/medium chain fatty acid:CoA ligase ACSM2, although other UGTs and ACSMs enzymes may significantly contribute to aspirin metabolism.	Aspirin	30-37	acyl-CoA synthetase medium chain family member 2A	Homo sapiens	204-209
20214591-4	2009	Among the enzymes involved in aspirin biodisposition a major role is played by the enzymes UDP-glucuronosyltransferase UGT1A6, cytochrome P450 CYP2C9 and the xenobiotic/medium chain fatty acid:CoA ligase ACSM2, although other UGTs and ACSMs enzymes may significantly contribute to aspirin metabolism.	Aspirin	281-288	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
20214591-4	2009	Among the enzymes involved in aspirin biodisposition a major role is played by the enzymes UDP-glucuronosyltransferase UGT1A6, cytochrome P450 CYP2C9 and the xenobiotic/medium chain fatty acid:CoA ligase ACSM2, although other UGTs and ACSMs enzymes may significantly contribute to aspirin metabolism.	Aspirin	281-288	acyl-CoA synthetase medium chain family member 2A	Homo sapiens	204-209
20214591-7	2009	Major polymorphisms related to aspirin biodisposition are rs2070959, rs1105879 and rs6759892 for the UGT1A6 gene, rs1133607 for the ACSM2 gene, and rs1799853, rs1057910, rs28371686, rs9332131 and rs28371685 for the CYP2C9 gene.	Aspirin	31-38	acyl-CoA synthetase medium chain family member 2A	Homo sapiens	132-137
20214591-7	2009	Major polymorphisms related to aspirin biodisposition are rs2070959, rs1105879 and rs6759892 for the UGT1A6 gene, rs1133607 for the ACSM2 gene, and rs1799853, rs1057910, rs28371686, rs9332131 and rs28371685 for the CYP2C9 gene.	Aspirin	31-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	215-221
19711064-6	2009	However, there is some evidence that selective COX-2 inhibition and COX-1 inhibition (with low-dose aspirin) appear to be well-tolerated in the short term.	Aspirin	100-107	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	68-73
19540194-5	2009	C18-DOM increased the expression of anti-atherogenic molecule namely heme oxygenase-1 in endothelial cells and all these data showed that C18-DOM is exhibiting aspirin-like effects.	Aspirin	160-167	heme oxygenase 1	Homo sapiens	69-85
19680014-3	2009	Inhibition of cyclooxygenase (COX)-1 and COX-2 by aspirin or its related compounds, nonsteroidal antiinflammatory drugs (NSAIDs), has been associated with both adverse and beneficial effects in the gastrointestinal (GI) tract.	Aspirin	50-57	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	14-36
19341823-11	2009	Maturation, both in ASA and NO-ASA treated MoDC was characterized by decreased allostimulatory activity, lower expression of CD83, HLA-DR, costimulatory molecules and CD54 and decreased production of IL-10 and IL-12 p40.	Aspirin	20-23	CD83 molecule	Homo sapiens	125-129
19341823-11	2009	Maturation, both in ASA and NO-ASA treated MoDC was characterized by decreased allostimulatory activity, lower expression of CD83, HLA-DR, costimulatory molecules and CD54 and decreased production of IL-10 and IL-12 p40.	Aspirin	31-34	CD83 molecule	Homo sapiens	125-129
19618315-6	2009	RESULTS: Total amounts of thrombin markers produced at the site of injury were similar before and after addition of clopidogrel, whereas platelet release of sCD40L and P-selectin was lower during treatment with aspirin + clopidogrel by 33.8% and 27.8% (p &lt; 0.001), respectively.	Aspirin	211-218	selectin P	Homo sapiens	168-178
19618315-9	2009	CONCLUSION: Our study shows that clopidogrel combined with aspirin does not reduce thrombin formation following vascular injury, but attenuates platelet sCD40L and P-selectin release.	Aspirin	59-66	selectin P	Homo sapiens	164-174
19440925-0	2009	Measurement of platelet P-selectin for remote testing of platelet function during treatment with clopidogrel and/or aspirin.	Aspirin	116-123	selectin P	Homo sapiens	24-34
19440925-2	2009	Here we have established methods to assess the effects of clopidogrel and aspirin on platelets based on measurements of platelet P-selectin.	Aspirin	74-81	selectin P	Homo sapiens	129-139
19440925-12	2009	Aspirin markedly inhibited P-selectin expression induced by AA/Epi.	Aspirin	0-7	selectin P	Homo sapiens	27-37
19440925-17	2009	It is concluded that measurements of P-selectin performed on fixed blood samples following platelet stimulation in whole blood in a remote setting can be used effectively to monitor the effects of clopidogrel and aspirin.	Aspirin	213-220	selectin P	Homo sapiens	37-47
19346231-0	2009	COX-1 sensitivity and thromboxane A2 production in type 1 and type 2 diabetic patients under chronic aspirin treatment.	Aspirin	101-108	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	0-5
19346231-9	2009	CONCLUSION: COX-1 sensitivity and TxB(2) production is similarly reduced in both T1DM and T2DM patients under chronic aspirin treatment.	Aspirin	118-125	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	12-17
19255811-9	2009	RESULTS: In the base case, testing and treating patients with CYP2C9*2 and/or CYP2C9*3 with aspirin rather than warfarin was best (8.97 QALYs).	Aspirin	92-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
19286210-8	2009	In contrast, prostate specific antigen was significantly lower in aspirin users (7.3 vs 8.0 ng/ml, p = 0.01).	Aspirin	66-73	kallikrein related peptidase 3	Homo sapiens	13-38
19286210-9	2009	The association between prostate specific antigen and aspirin was significant in men with latent prostate cancer (6.1 vs 7.3 ng/ml, p &lt;0.01), marginal in patients with high grade prostatic intraepithelial neoplasia (5.0 vs 5.9 ng/ml, p = 0.09) and nonsignificant in those with a negative biopsy (5.6 vs 5.7 ng/ml, p = 0.64).	Aspirin	54-61	kallikrein related peptidase 3	Homo sapiens	24-49
19286210-10	2009	The strongest prostate specific antigen-aspirin association was in men with cancer and a prostate volume of 60 ml or more (7.3 vs 12.7 ng/ml, p &lt;0.01).	Aspirin	40-47	kallikrein related peptidase 3	Homo sapiens	14-39
19286210-11	2009	CONCLUSIONS: Prostate specific antigen was significantly lower in aspirin users with latent cancer.	Aspirin	66-73	kallikrein related peptidase 3	Homo sapiens	13-38
19210906-1	2009	NSAIDs-including aspirin (ASA)-that inhibit cyclooxygenase (COX)-1 induce nonallergic hypersensitivity reactions consisting of attacks of rhinitis and asthma.	Aspirin	17-24	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	44-66
19210906-1	2009	NSAIDs-including aspirin (ASA)-that inhibit cyclooxygenase (COX)-1 induce nonallergic hypersensitivity reactions consisting of attacks of rhinitis and asthma.	Aspirin	26-29	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	44-66
19146957-9	2009	ASA significantly enhanced the frequency of functional CD4(+)CD25(+)Foxp3(+) Treg cells in mice in a therapeutic dose range.	Aspirin	0-3	forkhead box P3	Mus musculus	68-73
19036898-2	2009	Low-dose aspirin therapy is widely prescribed to inhibit COX-1 in platelets for atherothrombotic prevention.	Aspirin	9-16	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	57-62
19110389-2	2009	Aspirin irreversibly inhibits cyclooxygenase (COX) 1 involved in the platelet production of thromboxane (TX) A(2), an inducer of vasoconstriction and a platelet activating agent.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	30-52
19110389-4	2009	For clarity"s sake a real aspirin resistance would be the absence of COX1 inhibition due to intrinsic platelet factors (which has never been reported).	Aspirin	26-33	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	69-73
19187636-15	2009	In CT scans of ASA detection, the mean CT values in the aorta at the arch and at T11 were 360 and 358 HU, respectively, whereas in CT scans without ASA detection, the CT values in the aorta at the arch and at T11 were lower (P &lt; 0.05), 297 and 317 HU, respectively.	Aspirin	15-18	CD2 molecule	Homo sapiens	81-84
19187636-15	2009	In CT scans of ASA detection, the mean CT values in the aorta at the arch and at T11 were 360 and 358 HU, respectively, whereas in CT scans without ASA detection, the CT values in the aorta at the arch and at T11 were lower (P &lt; 0.05), 297 and 317 HU, respectively.	Aspirin	15-18	CD2 molecule	Homo sapiens	209-212
19026633-3	2009	Furthermore, we demonstrated that the non-steroidal anti-inflammatory drug, sulindac sulfide, the cyclooxygenase-2 (COX-2) selective inhibitor, celecoxib, and the nitric oxide-donating aspirin derivative, NO-ASA, blocked Wnt/beta-catenin signaling in PC-3 and DU145 cells.	Aspirin	185-192	catenin beta 1	Homo sapiens	225-237
19092646-6	2009	Both HO-1 and ferritin have been identified as targets of, and inducible by, aspirin and, in the case of HO-1, aspirin-triggered lipoxins.	Aspirin	77-84	heme oxygenase 1	Homo sapiens	5-9
19092646-6	2009	Both HO-1 and ferritin have been identified as targets of, and inducible by, aspirin and, in the case of HO-1, aspirin-triggered lipoxins.	Aspirin	111-118	heme oxygenase 1	Homo sapiens	5-9
19092646-6	2009	Both HO-1 and ferritin have been identified as targets of, and inducible by, aspirin and, in the case of HO-1, aspirin-triggered lipoxins.	Aspirin	111-118	heme oxygenase 1	Homo sapiens	105-109
19183882-3	2009	Recently, however, salicylate the active metabolite of aspirin showed COX-independent anti-inflammatory effects through induction of HO-1.	Aspirin	55-62	heme oxygenase 1	Homo sapiens	133-137
18851958-3	2009	The present work aims at evaluating whether ASA could directly decrease cell glycolysis through inhibition of the major regulatory enzyme within this pathway, 6-phosphofructo-1-kinase (PFK).	Aspirin	44-47	phosphofructokinase, muscle	Homo sapiens	159-183
18851958-3	2009	The present work aims at evaluating whether ASA could directly decrease cell glycolysis through inhibition of the major regulatory enzyme within this pathway, 6-phosphofructo-1-kinase (PFK).	Aspirin	44-47	phosphofructokinase, muscle	Homo sapiens	185-188
18851958-4	2009	We show that ASA and SA inhibit purified PFK in a dose-dependent manner, and that this inhibition occurs due to the modulation of the enzyme quaternary structure.	Aspirin	13-16	phosphofructokinase, muscle	Homo sapiens	41-44
18851958-6	2009	The inhibitory effects of ASA and SA on PFK are fully reversible and can be prevented or reverted by the binding of the enzyme to the actin filaments.	Aspirin	26-29	phosphofructokinase, muscle	Homo sapiens	40-43
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	Aspirin	45-52	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	102-124
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	Aspirin	45-52	multimerin 1	Homo sapiens	161-166
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	Aspirin	45-52	purinergic receptor P2Y1	Homo sapiens	195-201
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	Aspirin	45-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
19031027-8	2009	It has been possible to demonstrate that in aspirin treated, human DCs there is inhibition of the nuclear factor K-B (NFKB) signalling pathway, modified cytokine production, reduced expression of co-stimulatory molecules (CD40, CD80, and CD86) and increased expression of immunoglobulin-like transcript-3 (ILT3).	Aspirin	44-51	leukocyte immunoglobulin like receptor B4	Homo sapiens	272-304
19031027-8	2009	It has been possible to demonstrate that in aspirin treated, human DCs there is inhibition of the nuclear factor K-B (NFKB) signalling pathway, modified cytokine production, reduced expression of co-stimulatory molecules (CD40, CD80, and CD86) and increased expression of immunoglobulin-like transcript-3 (ILT3).	Aspirin	44-51	leukocyte immunoglobulin like receptor B4	Homo sapiens	306-310
18773975-3	2008	The reduction of growth factors such as transforming growth factor-alpha (TGF)-alpha and vascular endothelial cell growth factor (VEGF) by aspirin was determined by immunohistochemistry method.	Aspirin	139-146	vascular endothelial growth factor A	Rattus norvegicus	130-134
18773975-4	2008	Administration of CAA produced significant protection against aspirin induced gastric toxicity by showing significant increase in PGE2, TGF-alpha, VEGF expression and accompanied by a significant inhibition of nitric oxide and regulating the levels of cytokines in rats.	Aspirin	62-69	vascular endothelial growth factor A	Rattus norvegicus	147-151
18753249-0	2008	COX-1, and not COX-2 activity, regulates airway function: relevance to aspirin-sensitive asthma.	Aspirin	71-78	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	0-5
18753249-2	2008	Clinical data show that mixed COX-1/COX-2 inhibitors such as aspirin, but not COX-2 selective inhibitors such as rofecoxib, induce bronchoconstriction and asthma in sensitive individuals.	Aspirin	61-68	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	30-35
18753249-8	2008	Cells cultured from aspirin-sensitive or control human donors contained similar levels of COX-1 and COX-2 immunoreactivity.	Aspirin	20-27	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	90-95
18753249-9	2008	COX activity in cells from aspirin-sensitive or tolerant patients was inhibited by aspirin, SC560, which blocks COX-1 selectively, but not by rofecoxib, which is a selective inhibitor of COX-2.	Aspirin	27-34	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	112-117
18753249-9	2008	COX activity in cells from aspirin-sensitive or tolerant patients was inhibited by aspirin, SC560, which blocks COX-1 selectively, but not by rofecoxib, which is a selective inhibitor of COX-2.	Aspirin	83-90	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	112-117
18753249-10	2008	These observations show that despite the presence of COX-2, COX-1 is functionally predominant in the airways and explains clinical observations relating to drug specificity in patients with aspirin-sensitive asthma.	Aspirin	190-197	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	60-65
18586686-7	2008	No additive interactions with body mass index or weight gain were present, but there was some evidence of interaction between PPARA variants and aspirin use, defined as use at least once per week for 6 months or longer.	Aspirin	145-152	peroxisome proliferator activated receptor alpha	Homo sapiens	126-131
18855644-4	2008	Aspirin works by irreversibly acetylating the cyclooxygenase (COX-1) enzyme, thus suppressing the production of thromboxane A(2) (TxA(2)) and inhibiting platelet activation and aggregation.	Aspirin	0-7	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	62-67
18558473-5	2008	When increased CIMT or carotid plaque was detected, physicians were more likely to prescribe aspirin and lipid-lowering therapy (P &lt; .001).	Aspirin	93-100	CIMT	Homo sapiens	15-19
18495783-2	2008	Human neutrophils express the pleiotropic receptor formyl peptide receptor-like 1/lipoxin A4 (LXA(4)) receptor that binds a variety of ligands, including the acute-phase reactant serum amyloid A (SAA), the anti-inflammatory lipids LXA(4) and aspirin-triggered 15-epi-LXA(4) (ATL), and the glucocorticoid-inducible protein annexin 1.	Aspirin	242-249	formyl peptide receptor 2	Homo sapiens	51-81
18495783-2	2008	Human neutrophils express the pleiotropic receptor formyl peptide receptor-like 1/lipoxin A4 (LXA(4)) receptor that binds a variety of ligands, including the acute-phase reactant serum amyloid A (SAA), the anti-inflammatory lipids LXA(4) and aspirin-triggered 15-epi-LXA(4) (ATL), and the glucocorticoid-inducible protein annexin 1.	Aspirin	242-249	formyl peptide receptor 2	Homo sapiens	94-110
18295304-7	2008	CONCLUSION: Our data demonstrate that the inter-individual variability of platelet sensitivity to aspirin is due to a reduced efficacy of aspirin on platelet COX-1 despite ascertained patient compliance.	Aspirin	98-105	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	158-163
18295304-7	2008	CONCLUSION: Our data demonstrate that the inter-individual variability of platelet sensitivity to aspirin is due to a reduced efficacy of aspirin on platelet COX-1 despite ascertained patient compliance.	Aspirin	138-145	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	158-163
18341815-6	2007	CD62p decreasing level post various aspirin were also similar among groups [IA: (10.9 +/- 18.6)%, OA1: (9.0 +/- 11.8)%, OA2: (7.1 +/- 15.7)%, all P &gt; 0.05].	Aspirin	36-43	selectin P	Homo sapiens	0-5
17978563-7	2007	The selective inhibition index on COX-2, IC(50) (COX-1)/IC(50) (COX-2), of Cu-Asp was 3.33+/-0.89, while that of Asp was 0.42+/-0.12.	Aspirin	78-81	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	49-54
17598014-8	2007	The P-selectin expression on ADP-activated platelets was increased (p &lt; 0.01) in aspirin treated ASA-resistant CAD patients as compared to ASA-sensitive group or aspirin-treated healthy subjects.	Aspirin	165-172	selectin P	Homo sapiens	4-14
19075973-6	2007	The common anti-inflammatory drugs (like aspirin, ibuprofen, and naproxen) all act by blocking the action of both the COX-1 and COX-2 enzymes.	Aspirin	41-48	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	118-123
17549313-0	2007	Gallic acid, a dietary polyphenolic component, blunts the inhibition of platelet COX-1 by aspirin: preliminary in-vitro findings.	Aspirin	90-97	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	81-86
17372821-9	2007	The gastric contents of myeloperoxidase and pro-inflammatory cytokines were all increased after aspirin administration and significantly reduced by cilostazol treatment.	Aspirin	96-103	myeloperoxidase	Rattus norvegicus	24-39
17306251-15	2007	We conclude that heat shock and acetylsalicylic acid induce the production and release of heat shock proteins from mast cells, which in turn stimulate leukotriene synthesis through activation of TLR4.	Aspirin	32-52	toll like receptor 4	Homo sapiens	195-199
17414229-5	2007	Prasugrel plus ASA resulted in additive inhibition of collagen- and TRAP-induced platelet aggregation.	Aspirin	15-18	TRAP	Homo sapiens	68-72
16991207-2	2006	Effects of four nonsteroidal anti-inflammatory drugs including aspirin, paracetamol, sodium salicylate and phenacetin on prolidase (PLD) activity in erythrocytes were investigated.	Aspirin	63-70	peptidase D	Homo sapiens	132-135
16816107-2	2006	In this study we investigated the influence of aspirin and other NSAIDs on SR-BI expression and function in cultured human macrophages as well as in different mouse strains.	Aspirin	47-54	scavenger receptor class B member 1	Homo sapiens	75-80
16816107-3	2006	Incubation of human macrophages with 0.5 mmol/l aspirin resulted in increased SR-BI protein expression and increased uptake of HDL-associated [3H]cholesteryl oleate without changes of SR-BI mRNA levels.	Aspirin	48-55	scavenger receptor class B member 1	Homo sapiens	78-83
16815697-10	2006	The skin PGD2 and PGF(2 alpha) of ASA 10 min were almost same to those of ASA 6 h. In the normal skin of COX-1-deficient mice, skin PGD2 level was lower than that of wild-type mice, although PGE2, PGI2 and PGF(2 alpha) levels were almost equal to those of wild type.	Aspirin	34-37	prostaglandin D2 synthase (brain)	Mus musculus	132-136
16547586-0	2006	The role of PKCzeta in NMDA-induced retinal ganglion cell death: prevention by aspirin.	Aspirin	79-86	protein kinase C zeta	Homo sapiens	12-19
16547586-4	2006	PKCzeta regulates the NF-kappaB pathway in cellular responses to various stresses and we have shown that aspirin inhibits purified human PKCzeta.	Aspirin	105-112	protein kinase C zeta	Homo sapiens	0-7
16547586-4	2006	PKCzeta regulates the NF-kappaB pathway in cellular responses to various stresses and we have shown that aspirin inhibits purified human PKCzeta.	Aspirin	105-112	protein kinase C zeta	Homo sapiens	137-144
16547586-9	2006	We also found that pretreatment with aspirin or the coinjection of NMDA with a specific PKCzeta inhibitor counteracted the effects of NMDA.	Aspirin	37-44	protein kinase C zeta	Homo sapiens	88-95
16440541-4	2006	RESULTS: The mean +/- SD values of the semiquantitatively evaluated immunoexpression of ICAM-1, VCAM-1, and VLA-4 were significantly increased in patients with aspirin hypersensitivity compared with aspirin-tolerant patients (1.7 +/- 0.8 vs 0.9 +/- 0.8, P &lt; .003; 1.8 +/- 0.8 vs 0.8 +/- 0.8, P &lt; .001; and 2.2 +/- 0.7 vs 1.3 +/- 0.7, P &lt; .001, respectively), whereas the mean +/- SD values of the expression of lymphocyte function-associated antigen 1 did not differ significantly (2.4 +/- 0.5 vs 2.2 +/- 0.9; P = .57).	Aspirin	160-167	intercellular adhesion molecule 1	Homo sapiens	88-94
16440541-4	2006	RESULTS: The mean +/- SD values of the semiquantitatively evaluated immunoexpression of ICAM-1, VCAM-1, and VLA-4 were significantly increased in patients with aspirin hypersensitivity compared with aspirin-tolerant patients (1.7 +/- 0.8 vs 0.9 +/- 0.8, P &lt; .003; 1.8 +/- 0.8 vs 0.8 +/- 0.8, P &lt; .001; and 2.2 +/- 0.7 vs 1.3 +/- 0.7, P &lt; .001, respectively), whereas the mean +/- SD values of the expression of lymphocyte function-associated antigen 1 did not differ significantly (2.4 +/- 0.5 vs 2.2 +/- 0.9; P = .57).	Aspirin	199-206	intercellular adhesion molecule 1	Homo sapiens	88-94
16440541-6	2006	CONCLUSIONS: In nasal polyps of aspirin-hypersensitive patients, up-regulation of the adhesion molecules ICAM-1 and VCAM-1 and the integrin VLA-4 may play an important role in the development of chronic eosinophilic inflammation.	Aspirin	32-39	intercellular adhesion molecule 1	Homo sapiens	105-111
16326168-0	2006	Stabilization of advanced atherosclerosis in low-density lipoprotein receptor-deficient mice by aspirin.	Aspirin	96-103	low density lipoprotein receptor	Mus musculus	45-77
16326168-7	2006	At the end of the study, LDLR(-/-) mice that had received aspirin had suppressed biosynthesis of thromboxane B2, the major products of COX-1 activity, reduced monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1 levels compared with controls.	Aspirin	58-65	low density lipoprotein receptor	Mus musculus	25-29
16326168-7	2006	At the end of the study, LDLR(-/-) mice that had received aspirin had suppressed biosynthesis of thromboxane B2, the major products of COX-1 activity, reduced monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1 levels compared with controls.	Aspirin	58-65	chemokine (C-C motif) ligand 2	Mus musculus	159-193
16169935-9	2006	Only the dual inhibitor of p38 and JNK and the use of combined siRNA silencing of p38 and cJun abrogated the ability of NO-aspirin to block cell growth.	Aspirin	123-130	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	90-94
16306357-7	2005	The diabetic rat retina showed increased expression of the transcription factor CCAAT/enhancer-binding protein-beta, one of the known targets of low-intermediate concentrations of aspirin.	Aspirin	180-187	CCAAT/enhancer binding protein beta	Rattus norvegicus	80-115
16261369-2	2005	We prepared copper(II) aspirinate [Cu2(asp)4] from Cu(II) and aspirin, which has been in use for many years as an antipyretic, an analgesic, and an anti-inflammatory agent.	Aspirin	23-30	coiled-coil domain containing 47	Mus musculus	35-44
16144976-1	2005	Benzoic acid, 2-(acetyl-oxy)-3-[(nitrooxy)methyl]phenyl ester (NCX 4016), a new drug made by an aspirin molecule linked, through a spacer, to a nitric oxide (NO)-donating moiety, is now under clinical testing for the treatment of atherothrombotic conditions.	Aspirin	96-103	T cell leukemia homeobox 2	Homo sapiens	63-66
16144976-6	2005	All the NCX 4016 derivatives containing acetylsalicylic acid inhibited the activity of oCOX-1 and oCOX-2, whereas the deacetylated metabolites and the nitric oxide-donating moiety were inactive.	Aspirin	40-60	T cell leukemia homeobox 2	Homo sapiens	8-11
16144976-8	2005	Reversible COX inhibitors (indomethacin) or salicylic acid incubated with the enzyme before NCX 4016 prevent the irreversible inhibition of oCOX-1 by NCX 4016 as well as by aspirin.	Aspirin	173-180	T cell leukemia homeobox 2	Homo sapiens	92-95
16144976-9	2005	In conclusion, our data show that NCX 4016 acts as a direct and irreversible inhibitor of COX-1 and that the presence of a spacer and NO-donating moiety in the molecule slows the kinetics of COX-1 inhibition by NCX 4016, compared with aspirin.	Aspirin	235-242	T cell leukemia homeobox 2	Homo sapiens	34-37
16144976-9	2005	In conclusion, our data show that NCX 4016 acts as a direct and irreversible inhibitor of COX-1 and that the presence of a spacer and NO-donating moiety in the molecule slows the kinetics of COX-1 inhibition by NCX 4016, compared with aspirin.	Aspirin	235-242	T cell leukemia homeobox 2	Homo sapiens	211-214
16862684-6	2005	PMI occurred more frequently in male, underlying disease of hypertension, diabetes mellitus, ischemic heart disease, ASA class &gt;2, under general anesthesia and during operation.	Aspirin	117-120	transmembrane protein 11	Homo sapiens	0-3
15813808-0	2005	Association of stem cell factor expression in nasal polyp epithelial cells with aspirin sensitivity and asthma.	Aspirin	80-87	KIT ligand	Homo sapiens	15-31
15813808-7	2005	The SCF/beta-actin mRNA ratios were significantly higher in ASA-hypersensitive (AH) asthmatics (median 0.97, range: 0.8-1.5) when compared with ASA-tolerant (AT) patients (median 0.5, range: 0.1-0.7; P &lt; 0.001).	Aspirin	60-63	KIT ligand	Homo sapiens	4-7
15813808-7	2005	The SCF/beta-actin mRNA ratios were significantly higher in ASA-hypersensitive (AH) asthmatics (median 0.97, range: 0.8-1.5) when compared with ASA-tolerant (AT) patients (median 0.5, range: 0.1-0.7; P &lt; 0.001).	Aspirin	60-63	POTE ankyrin domain family member F	Homo sapiens	8-18
15850829-7	2005	In ET patients receiving aspirin, the increments in f-MLP-induced PMN-CD11b and in PMN-platelet aggregates were significantly lower versus ET subjects not treated with aspirin.	Aspirin	25-32	integrin subunit alpha M	Homo sapiens	70-75
15794069-14	2005	Associated acetylsalicylic acid intolerance seems to enhance the amount of RANTES in NPs and might explain in part the more severe clinical course in those patients.	Aspirin	11-31	C-C motif chemokine ligand 5	Homo sapiens	75-81
15813672-8	2005	In a mechanism possibly unrelated to its effect on platelet reactivity to aggregating stimuli, the presence of the PL(A2) allele might influence the antiaggregatory effect of platelet inhibitory drugs such as aspirin (acetylsalicylic acid), clopidogrel, and GPIIb/IIIa antagonists.	Aspirin	209-216	phospholipase A2 group IIA	Homo sapiens	115-120
15813672-8	2005	In a mechanism possibly unrelated to its effect on platelet reactivity to aggregating stimuli, the presence of the PL(A2) allele might influence the antiaggregatory effect of platelet inhibitory drugs such as aspirin (acetylsalicylic acid), clopidogrel, and GPIIb/IIIa antagonists.	Aspirin	218-238	phospholipase A2 group IIA	Homo sapiens	115-120
16123543-5	2005	When eligible patients were extrapolated to the Australian population, for every 1,000 cases, 46 (95% CI 17-69) could have been saved from death or dependency with stroke unit management, 6 (95% CI 1-11) by using aspirin, 11 (95% CI 5-17) or 10 (95% CI 3-16) by using tPA at 3 and 6 h, respectively.	Aspirin	213-220	chromosome 20 open reading frame 181	Homo sapiens	268-271
15203109-7	2004	RESULTS: The treatment with ASA produced an important attenuation in the induction of cyclin E and cyclin D1 provoked by DAB.	Aspirin	28-31	proliferating cell nuclear antigen	Mus musculus	86-92
15203109-7	2004	RESULTS: The treatment with ASA produced an important attenuation in the induction of cyclin E and cyclin D1 provoked by DAB.	Aspirin	28-31	cyclin D1	Mus musculus	99-108
15203109-9	2004	The administration of ASA to DAB treated animals induced Cdk2 (29%).	Aspirin	22-25	cyclin-dependent kinase 2	Mus musculus	57-61
15203109-11	2004	CONCLUSION: The deregulation of cyclin/CDK expression and the up-regulation of p21 and p27 with the administration of ASA, post-treatment of the carcinogen administration, would block the pass through out to the G0/G1 check point to permit the cells to repair their DNA and HO-1 protected the liver from reactive oxygen species produced from DAB.	Aspirin	118-121	proliferating cell nuclear antigen	Mus musculus	32-38
15203109-11	2004	CONCLUSION: The deregulation of cyclin/CDK expression and the up-regulation of p21 and p27 with the administration of ASA, post-treatment of the carcinogen administration, would block the pass through out to the G0/G1 check point to permit the cells to repair their DNA and HO-1 protected the liver from reactive oxygen species produced from DAB.	Aspirin	118-121	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	79-82
15203109-11	2004	CONCLUSION: The deregulation of cyclin/CDK expression and the up-regulation of p21 and p27 with the administration of ASA, post-treatment of the carcinogen administration, would block the pass through out to the G0/G1 check point to permit the cells to repair their DNA and HO-1 protected the liver from reactive oxygen species produced from DAB.	Aspirin	118-121	cyclin-dependent kinase inhibitor 1B	Mus musculus	87-90
15337432-2	2004	In order to limit the action of prolidase on the pro-drug in normal cells, prolidase inhibitor, acetylsalicylic acid (ASA), was tested in fibroblasts (showing average prolidase activity for normal cells) and in MDA-MB 231 breast cancer cells (showing elevated activity of the enzyme).	Aspirin	118-121	peptidase D	Homo sapiens	75-84
15337432-2	2004	In order to limit the action of prolidase on the pro-drug in normal cells, prolidase inhibitor, acetylsalicylic acid (ASA), was tested in fibroblasts (showing average prolidase activity for normal cells) and in MDA-MB 231 breast cancer cells (showing elevated activity of the enzyme).	Aspirin	118-121	peptidase D	Homo sapiens	75-84
15337432-6	2004	It suggests that ASA may serve as an inhibitor of prolidase-convertible pro-drugs in normal cells.	Aspirin	17-20	peptidase D	Homo sapiens	50-59
15007033-6	2004	Only clonidine treatment totally prevented the development of insulin resistance, and high-dose aspirin, known to prevent insulin resistance by inhibition of the activity of IkappaB kinase-beta, decreased the degree of insulin resistance by almost 70%.	Aspirin	96-103	insulin	Canis lupus familiaris	122-129
15007033-6	2004	Only clonidine treatment totally prevented the development of insulin resistance, and high-dose aspirin, known to prevent insulin resistance by inhibition of the activity of IkappaB kinase-beta, decreased the degree of insulin resistance by almost 70%.	Aspirin	96-103	insulin	Canis lupus familiaris	122-129
15099277-5	2004	In the warfarin-alone group as compared with the aspirin-alone group significantly lower levels of F1 + 2 and D-dimer (P &lt; 0.001 for both), but significantly higher levels of sTF (P = 0.007) were found after 6 weeks.	Aspirin	49-56	coagulation factor XII	Homo sapiens	99-105
18429969-6	2008	The PlA1/A2 variant was significantly associated with aspirin resistance when measured in healthy subjects [odds ratio (OR) 2.36, 95% confidence interval (CI) 1.24, 4.49; P = 0.009].	Aspirin	54-61	POU class 2 homeobox 3	Homo sapiens	4-11
18429969-8	2008	Moreover, the observed effect of PlA1/A2 genotype varied depending on the methodology used for determining aspirin sensitivity/resistance.	Aspirin	107-114	POU class 2 homeobox 3	Homo sapiens	33-37
18429969-10	2008	CONCLUSIONS: Our data support a genetic association between the PlA1/A2 molecular variant and aspirin resistance in healthy subjects, with the effect diminishing in the presence of cardiovascular disease.	Aspirin	94-101	POU class 2 homeobox 3	Homo sapiens	64-71
18581076-2	2008	From the laboratory point of view, resistance to aspirin is the inability to achieve the expected inhibition of platelet cyclooxygenase-(COX-)1 with prevention of platelet thromboxane (TX) A2 formation.	Aspirin	49-56	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	121-143
18506123-21	2008	The favorable clinical outcomes with aspirin and clopidogrel have validated COX-1 and P2Y12 receptors as targets for new drug development.	Aspirin	37-44	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	76-81
18414668-5	2008	Expression of IL-32 in influenza A virus infected A549 human lung epithelial cells was blocked by either selective COX-2 inhibitor NS398 or Aspirin, a known anti-inflammatory drug, indicating IL-32 was induced through COX-2 in the inflammatory cascade.	Aspirin	140-147	interleukin 32	Homo sapiens	14-19
18414668-5	2008	Expression of IL-32 in influenza A virus infected A549 human lung epithelial cells was blocked by either selective COX-2 inhibitor NS398 or Aspirin, a known anti-inflammatory drug, indicating IL-32 was induced through COX-2 in the inflammatory cascade.	Aspirin	140-147	interleukin 32	Homo sapiens	192-197
18398040-4	2008	We did, however, observe a statistically significant interaction between the rs7903146 TCF7L2 polymorphism and recent use of aspirin/nonsteroidal anti-inflammatory drugs (NSAID; P = 0.001).	Aspirin	125-132	transcription factor 7 like 2	Homo sapiens	87-93
18398040-7	2008	These data suggest that colon cancer risk associated with the rs7903146 TCF7L2 polymorphism is modified by use of aspirin/NSAIDs.	Aspirin	114-121	transcription factor 7 like 2	Homo sapiens	72-78
18397691-3	2008	Apart from aspirin, which irreversibly inactivates COX-1, high-dose naproxen causes sustained COX-1 inhibition throughout the dose interval in some individuals.	Aspirin	11-18	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	51-56
18253906-11	2008	Hypertension (OR 1.1) and aspirin use (OR 1.1) did not increase the risk of postpolypectomy bleeding.	Aspirin	26-33	olfactory receptor family 4 subfamily F member 16	Homo sapiens	39-45
18086495-10	2008	Positive aspirin challenge was associated with a significant increase in eotaxin 2 serum concentration.	Aspirin	9-16	C-C motif chemokine ligand 24	Homo sapiens	73-82
18000161-6	2008	The results show that ASA therapy causes a decrease in the glucose level and AGE and HbA1c formation, improves the lipid profile, HDL functionality, and the antioxidant capacity, induces serum HSP70, and overall decreases mortality of diabetic rats in comparison with the group without treatment.	Aspirin	22-25	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	193-198
17984087-2	2008	Selective inhibition of COX-2 over COX-1 results in preferential decrease in prostacyclin production over thromboxane A2 production, thus leading to less gastric effects than those seen with nonselective COX inhibitors such as acetylsalicylic acid (aspirin).	Aspirin	227-247	mitochondrial Cytochrome c oxidase subunit I	Drosophila melanogaster	35-40
17984087-2	2008	Selective inhibition of COX-2 over COX-1 results in preferential decrease in prostacyclin production over thromboxane A2 production, thus leading to less gastric effects than those seen with nonselective COX inhibitors such as acetylsalicylic acid (aspirin).	Aspirin	249-256	mitochondrial Cytochrome c oxidase subunit I	Drosophila melanogaster	35-40
18090373-9	2008	The COX-1 and COX-2 inhibitor aspirin (10(-6)-10(-5) mol/L) and the COX-2 inhibitor nimesulide (10(-6) mol/L) induced leftward shifts of the concentration-response curve for vasopressin in gastroepiploic artery.	Aspirin	30-37	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	4-9
17848598-10	2007	Data from electrophoretic mobility shift assay and chromatin immunoprecipitation analyses revealed that ASA inhibited the transcription factor E2F-1 binding activity to the survivin promoter region, which is known to regulate survivin gene transcription.	Aspirin	104-107	E2F transcription factor 1	Homo sapiens	143-148
17848598-11	2007	Taken together, our studies suggested that ASA-promoted TRAIL cytotoxicity is mediated by down-regulating survivin, and the down-regulation of survivin is due to inhibition of E2F-1 binding activity to the survivin promoter region.	Aspirin	43-46	E2F transcription factor 1	Homo sapiens	176-181
17641958-1	2007	In this study, we compared the roles of CysLT receptor type 1 (CysLTR1) and leukotriene C4 synthase (LTC4S) gene polymorphisms in two major aspirin-related allergic diseases, aspirin-intolerant asthma (AIA) and aspirin-induced chronic urticaria/angioedema (AICU).	Aspirin	140-147	leukotriene C4 synthase	Homo sapiens	101-106
17156785-8	2007	In contrast, clopidogrel, aspirin or atorvastatin treated rabbits showed a significant reduction in progression of atherosclerosis and decreased the levels of P-selection, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in serum and vascular wall.	Aspirin	26-33	ICAM-1	Oryctolagus cuniculus	207-213
17156785-8	2007	In contrast, clopidogrel, aspirin or atorvastatin treated rabbits showed a significant reduction in progression of atherosclerosis and decreased the levels of P-selection, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in serum and vascular wall.	Aspirin	26-33	vascular cell adhesion protein 1	Oryctolagus cuniculus	216-244
17156785-8	2007	In contrast, clopidogrel, aspirin or atorvastatin treated rabbits showed a significant reduction in progression of atherosclerosis and decreased the levels of P-selection, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in serum and vascular wall.	Aspirin	26-33	vascular cell adhesion protein 1	Oryctolagus cuniculus	246-252
17510082-0	2007	Aspirin blocks proliferation in colon cells by inducing a G1 arrest and apoptosis through activation of the checkpoint kinase ATM.	Aspirin	0-7	ATM serine/threonine kinase	Homo sapiens	126-129
17510082-6	2007	Aspirin and sulindac sulfide induced a G1 arrest within 48 h. While all cell lines responded in a comparable way to sulindac sulfide, the aspirin-induced G1 arrest was dependent on p21Waf1/Cip1--as cells lacking the cyclin-dependent kinase inhibitor failed to show this arrest--and on ataxia-telangiectasia-mutated kinase (ATM)--as the inhibitor caffeine abrogated the checkpoint.	Aspirin	0-7	ATM serine/threonine kinase	Homo sapiens	285-321
17510082-6	2007	Aspirin and sulindac sulfide induced a G1 arrest within 48 h. While all cell lines responded in a comparable way to sulindac sulfide, the aspirin-induced G1 arrest was dependent on p21Waf1/Cip1--as cells lacking the cyclin-dependent kinase inhibitor failed to show this arrest--and on ataxia-telangiectasia-mutated kinase (ATM)--as the inhibitor caffeine abrogated the checkpoint.	Aspirin	0-7	ATM serine/threonine kinase	Homo sapiens	323-326
17697815-0	2007	Effects of triple antiplatelet therapy (aspirin, clopidogrel, and cilostazol) on platelet aggregation and P-selectin expression in patients undergoing coronary artery stent implantation.	Aspirin	40-47	selectin P	Homo sapiens	106-116
17493929-7	2007	In patients without aspirin, a significant increase in P-selectin expression was observed on day 1 after intervention in RF ablation compared with cryoablation (80 +/- 26 vs. 63 +/- 16 arbitrary units; P = 0.048).	Aspirin	20-27	selectin P	Homo sapiens	55-65
17549408-8	2007	Animals of the aspirin/DFMO group exhibited an inactivation of ornithine decarboxylase, a key enzyme in polyamine biosynthesis, and a two-fold reduction in the prostaglandin E2 content of the colonic mucosa (p&lt;0.01).	Aspirin	15-22	ornithine decarboxylase 1	Rattus norvegicus	63-86
17598014-8	2007	The P-selectin expression on ADP-activated platelets was increased (p &lt; 0.01) in aspirin treated ASA-resistant CAD patients as compared to ASA-sensitive group or aspirin-treated healthy subjects.	Aspirin	84-91	selectin P	Homo sapiens	4-14
17598014-8	2007	The P-selectin expression on ADP-activated platelets was increased (p &lt; 0.01) in aspirin treated ASA-resistant CAD patients as compared to ASA-sensitive group or aspirin-treated healthy subjects.	Aspirin	100-103	selectin P	Homo sapiens	4-14
17598014-8	2007	The P-selectin expression on ADP-activated platelets was increased (p &lt; 0.01) in aspirin treated ASA-resistant CAD patients as compared to ASA-sensitive group or aspirin-treated healthy subjects.	Aspirin	142-145	selectin P	Homo sapiens	4-14
17284450-4	2007	Exposure of cells to acetyl salicylic acid resulted in strong activation of eIF2alpha stress-activated protein kinase R-like endoplasmic reticulum kinase (PERK).	Aspirin	21-42	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	103-153
17284450-4	2007	Exposure of cells to acetyl salicylic acid resulted in strong activation of eIF2alpha stress-activated protein kinase R-like endoplasmic reticulum kinase (PERK).	Aspirin	21-42	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	155-159
15031457-8	2004	RESULTS: Aspirin, a low-cost intervention applicable to a large number of stroke patients (9153 first-ever cases), resulted in modest health benefits (946 DALYs saved) and a mean ICER (based on incidence costs) of US 1421 dollars per DALY saved.	Aspirin	9-16	cAMP responsive element modulator	Homo sapiens	179-183
15066917-10	2004	We also observed a significant interaction between aspirin/NSAIDs use and the VDR gene.	Aspirin	51-58	vitamin D receptor	Homo sapiens	78-81
15066917-11	2004	Having the SS or BB VDR genotypes reduced risk of colorectal cancer among non-aspirin/NSAID users; however, aspirin/NSAIDs reduced risk for all VDR genotypes.	Aspirin	78-85	vitamin D receptor	Homo sapiens	20-23
15066917-11	2004	Having the SS or BB VDR genotypes reduced risk of colorectal cancer among non-aspirin/NSAID users; however, aspirin/NSAIDs reduced risk for all VDR genotypes.	Aspirin	108-115	vitamin D receptor	Homo sapiens	144-147
15066917-13	2004	In addition, the observed interactions for aspirin/NSAIDs and IRS1 and VDR genotypes suggest that mechanisms other than COX-2 inhibition may be contributing to the protective effect of aspirin and NSAIDs on colorectal cancer risk.	Aspirin	185-192	vitamin D receptor	Homo sapiens	71-74
12941295-10	2003	Moreover, the translational factor eIF2alpha was transiently phosphorylated and therefore inhibited very soon after aspirin treatment.	Aspirin	116-123	eukaryotic translation initiation factor 2A	Homo sapiens	35-44
12960371-3	2003	In the present study, we have examined whether inhibition of COX-2 activity in healthy volunteers taking aspirin exacerbates gastric mucosal injury and if such an effect would be prevented by NCX-4016, a NO-releasing derivative of aspirin.	Aspirin	231-238	T cell leukemia homeobox 2	Homo sapiens	192-195
12960371-6	2003	The mean mucosal injury score was 5.8 +/- 1.8 in subjects treated with aspirin and 2.4 +/- 0.7 (P &lt; 0.01 vs. aspirin) in subjects treated with NCX-4016.	Aspirin	112-119	T cell leukemia homeobox 2	Homo sapiens	146-149
14582459-1	2003	NCX-4016 is a nitric oxide-aspirin conjugate non-steroidal anti-inflammatory drug that is under investigation by NicOx for the potential treatment of cardiovascular disorders and colon cancer.	Aspirin	27-34	T cell leukemia homeobox 2	Homo sapiens	0-3
12954156-8	2003	We found that the expression of the activated GPIIb/IIIa complex was significantly reduced in those diabetic cardiac patients who were taking aspirin (P&lt;.05).	Aspirin	142-149	integrin subunit alpha 2b	Homo sapiens	46-51
12787065-8	2003	Two NF-kappa B inhibitors, aspirin (10 mM) and MG-132 (0.1 microM), blocked basal apoE and apoJ secretion as well as LPS-induced apoJ secretion.	Aspirin	27-34	clusterin	Rattus norvegicus	129-133
12846439-3	2003	NCX-4016 consists of the parent molecule (aspirin) linked to a "spacer" via an ester linkage, which is in turn connected to a nitric oxide-releasing moiety.	Aspirin	42-49	T cell leukemia homeobox 2	Homo sapiens	0-3
12846439-4	2003	Both aspirin and nitric oxide moieties of NCX-4016 contribute to its effectiveness, the latter occurring via both cyclic guanosyl monophosphate-dependent and -independent mechanisms.	Aspirin	5-12	T cell leukemia homeobox 2	Homo sapiens	42-45
12846439-5	2003	In vitro studies have shown that NCX-4016 inhibits platelet aggregation induced by aspirin-sensitive (arachidonic acid) and aspirin-insensitive (thrombin) agonist.	Aspirin	83-90	T cell leukemia homeobox 2	Homo sapiens	33-36
12695747-7	2003	Dose-dependent inhibition of GPIIb/IIIa, P-selectin, CD63, and CD107a receptor expression was observed in the aspirin-treated whole-blood samples.	Aspirin	110-117	integrin subunit alpha 2b	Homo sapiens	29-34
12615789-7	2003	Platelets from aspirin-treated individuals were partially protected from sCD40L release, but only when the agonist was collagen, an affect augmented by the addition of GP IIb/IIIa antagonists.	Aspirin	15-22	integrin subunit alpha 2b	Homo sapiens	168-174
12621388-5	2003	Up-regulation of MAC-1 on monocytes after stimulation with thrombin receptor-activating peptide and adenosine diphosphate was significantly lower in patients treated with clopidogrel and aspirin.	Aspirin	187-194	integrin subunit alpha M	Homo sapiens	17-22
12621391-6	2003	RESULTS: Both 7-day and 14-day aspirin intake increased the activity of CYP2C19 significantly, as indicated by 4-hydroxymephenytoin urinary recovery (P &lt;.001).	Aspirin	31-38	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
12621391-7	2003	Induction of low-dose aspirin on CYP2C19 was time-dependent.	Aspirin	22-29	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
12621391-11	2003	Both 7-day and 14-day low-dose aspirin induced the in vivo activities of CYP2C19 but did not affect the activities of CYP1A2, CYP2D6, and CYP2E1.	Aspirin	31-38	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-80
12621391-13	2003	When low-dose aspirin is used in combination with drugs that are substrates of CYP2C19, doses of the latter should be adjusted to ensure their efficacy.	Aspirin	14-21	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	79-86
14728074-12	2003	CONCLUSION: The GP IIb/IIIa receptor antagonist abciximab, when used with aspirin and heparin, has demonstrated efficacy in reducing the short- and long-term risk of ischemic complications in patients with ischemic heart disease undergoing percutaneous coronary intervention, when used with aspirin and heparin.	Aspirin	74-81	integrin subunit alpha 2b	Homo sapiens	16-22
14728074-12	2003	CONCLUSION: The GP IIb/IIIa receptor antagonist abciximab, when used with aspirin and heparin, has demonstrated efficacy in reducing the short- and long-term risk of ischemic complications in patients with ischemic heart disease undergoing percutaneous coronary intervention, when used with aspirin and heparin.	Aspirin	291-298	integrin subunit alpha 2b	Homo sapiens	16-22
12749745-12	2003	CONCLUSION: The GP IIb/IIIa receptor antagonist abciximab, when used with aspirin and heparin, has demonstrated efficacy in reducing the short- and long-term risk of ischaemic complications in patients with ischaemic heart disease undergoing percutaneous coronary intervention, when used with aspirin and heparin.	Aspirin	74-81	integrin subunit alpha 2b	Homo sapiens	16-22
12749745-12	2003	CONCLUSION: The GP IIb/IIIa receptor antagonist abciximab, when used with aspirin and heparin, has demonstrated efficacy in reducing the short- and long-term risk of ischaemic complications in patients with ischaemic heart disease undergoing percutaneous coronary intervention, when used with aspirin and heparin.	Aspirin	293-300	integrin subunit alpha 2b	Homo sapiens	16-22
12480553-9	2003	CONCLUSIONS: Most patients with Gilbert"s syndrome, in addition to their reduced B-UGT enzyme activity, may have abnormalities in the glucuronidation of aspirin or coumarin- and dopamine-derivatives, due to this combination of UGT1A1*28 and UGT1A6*2 genotypes.	Aspirin	153-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	227-233
12534448-2	2002	The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils.	Aspirin	46-53	intercellular adhesion molecule 1	Homo sapiens	213-246
12534448-2	2002	The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils.	Aspirin	46-53	intercellular adhesion molecule 1	Homo sapiens	248-254
12534448-7	2002	Plasma levels of both IL-6 and ICAM-1 were reduced in patients taking aspirin.	Aspirin	70-77	intercellular adhesion molecule 1	Homo sapiens	31-37
12421891-7	2002	The percentage of CD45+ leukocytes expressing the CysLT1 receptor was also higher in the aspirin-sensitive subjects (25 percent of CD45+ leukocytes [range, 4 to 50] vs. 5 percent of CD45+ leukocytes [range, 2 to 11]; P&lt;0.001); the percentage of CD45+ leukocytes expressing the LTB4 receptor did not differ significantly between these two groups.	Aspirin	89-96	protein tyrosine phosphatase receptor type C	Homo sapiens	18-22
12421891-7	2002	The percentage of CD45+ leukocytes expressing the CysLT1 receptor was also higher in the aspirin-sensitive subjects (25 percent of CD45+ leukocytes [range, 4 to 50] vs. 5 percent of CD45+ leukocytes [range, 2 to 11]; P&lt;0.001); the percentage of CD45+ leukocytes expressing the LTB4 receptor did not differ significantly between these two groups.	Aspirin	89-96	protein tyrosine phosphatase receptor type C	Homo sapiens	131-135
12421891-7	2002	The percentage of CD45+ leukocytes expressing the CysLT1 receptor was also higher in the aspirin-sensitive subjects (25 percent of CD45+ leukocytes [range, 4 to 50] vs. 5 percent of CD45+ leukocytes [range, 2 to 11]; P&lt;0.001); the percentage of CD45+ leukocytes expressing the LTB4 receptor did not differ significantly between these two groups.	Aspirin	89-96	protein tyrosine phosphatase receptor type C	Homo sapiens	131-135
12421891-7	2002	The percentage of CD45+ leukocytes expressing the CysLT1 receptor was also higher in the aspirin-sensitive subjects (25 percent of CD45+ leukocytes [range, 4 to 50] vs. 5 percent of CD45+ leukocytes [range, 2 to 11]; P&lt;0.001); the percentage of CD45+ leukocytes expressing the LTB4 receptor did not differ significantly between these two groups.	Aspirin	89-96	protein tyrosine phosphatase receptor type C	Homo sapiens	131-135
12428662-1	2002	OBJECTIVE: To evaluate in vivo activity in dogs of meloxicam or aspirin, previously shown in vitro to be a selective cyclooxygenase-2 (COX-2) inhibitor (COX-1 sparing drug), or a nonselective COX inhibitor, respectively.	Aspirin	64-71	cytochrome c oxidase subunit I	Canis lupus familiaris	153-158
12428662-9	2002	Suppression of concentrations of PGE2 in the gastric mucosa and TXB2 in blood by aspirin administration is consistent with activity against COX-1.	Aspirin	81-88	cytochrome c oxidase subunit I	Canis lupus familiaris	140-145
12368905-2	2002	Here, we report that inhibition of PMN infiltration by ASA and DEX is a property shared by aspirin-triggered lipoxins (ATL) and the glucocorticoid-induced annexin 1 (ANXA1)-derived peptides that are both generated in vivo and act at the lipoxin A(4) receptor (ALXR/FPRL1) to halt PMN diapedesis.	Aspirin	55-58	annexin A1	Homo sapiens	166-171
12207011-1	2002	We investigated the effect of a nitric oxide (NO)-releasing derivative of aspirin (NCX-4016) on a mitochondria-dependent model of apoptosis in human umbilical endothelial cells (HUVEC).	Aspirin	74-81	T cell leukemia homeobox 2	Homo sapiens	83-86
12417048-8	2002	However, expression in HCC of mRNAs for intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, both of which are considered to play key roles in attachment of cancer cells to the endothelium, was significantly suppressed by ASP.	Aspirin	242-245	intercellular adhesion molecule 1	Rattus norvegicus	40-73
12208806-4	2002	METHODS AND RESULTS: In LDL receptor-deficient mice fed a high fat diet compared with control mice, low-dose aspirin induced a significant decrease in circulating levels and vascular formation of soluble intercellular molecule-1, monocyte chemoattractant protein-1, tumor necrosis factor-alpha, interleukin-12p 40, without affecting lipid levels.	Aspirin	109-116	low density lipoprotein receptor	Mus musculus	24-36
12208806-4	2002	METHODS AND RESULTS: In LDL receptor-deficient mice fed a high fat diet compared with control mice, low-dose aspirin induced a significant decrease in circulating levels and vascular formation of soluble intercellular molecule-1, monocyte chemoattractant protein-1, tumor necrosis factor-alpha, interleukin-12p 40, without affecting lipid levels.	Aspirin	109-116	chemokine (C-C motif) ligand 2	Mus musculus	204-293
11821258-8	2002	High-dose aspirin, etanercept, and high-dose meloxicam each reduced retinal ICAM-1 expression.	Aspirin	10-17	intercellular adhesion molecule 1	Rattus norvegicus	76-82
11583738-5	2001	Further, although aspirin treatment improved the efficacy of all GPIIb/IIIa antagonists, it did not alter the differences between Classes I and II antagonists.	Aspirin	18-25	integrin subunit alpha 2b	Homo sapiens	65-70
11567665-3	2001	Furthermore, the inhibitory effect of aspirin on GP IIb/IIIa blocker-induced platelet aggregation is discussed as a clinically relevant finding.	Aspirin	38-45	integrin subunit alpha 2b	Homo sapiens	49-55
11532860-12	2001	Our results suggest that one of the major pathways which mediates the anti-tumour response of aspirin and indomethacin in gastric cancer cells is through up-regulation of bax and bak and activation of caspase-3.	Aspirin	94-101	BCL2 antagonist/killer 1	Homo sapiens	179-182
11476469-5	2001	RESULTS: In AIA, aspirin induced an immediate reaction associated with increased urinary LTE4/Cr and sputum ECP and a fall in urinary 11-dhTXB2/Cr.	Aspirin	17-24	ribonuclease A family member 3	Homo sapiens	108-111
11476469-6	2001	Pranlukast inhibited the bronchial reaction and an increase in sputum ECP after threshold dosed of ASA, but failed to change aspirin-induced LT production in sputum and urine.	Aspirin	99-102	ribonuclease A family member 3	Homo sapiens	70-73
11380325-0	2001	Pioglitazone, a specific PPAR-gamma ligand, inhibits aspirin-induced gastric mucosal injury in rats.	Aspirin	53-60	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	25-35
11887863-0	2001	Aspirin protected the nitric oxide/cyclic GMP generating system in human peritoneum.	Aspirin	0-7	5'-nucleotidase, cytosolic II	Homo sapiens	42-45
11195467-9	2000	Expression of cyclin B2 was decreased and expression of Fas-L and BAD were increased in lung tissues treated with both NS398 and ASA.	Aspirin	129-132	cyclin B2	Mus musculus	14-23
11022121-0	2000	A short course of oral aspirin increases IL-18-induced interferon-gamma production in whole blood cultures.	Aspirin	23-30	interleukin 18	Homo sapiens	41-46
11022121-2	2000	Four days after cessation of a 3-day regimen of 650 mg of oral aspirin, there was a 70% increase in interferon-gamma (IFN-gamma) production, stimulated by a combination of interleukin-18 (IL-18) plus lipopolysaccharide (p &lt; 0.05).	Aspirin	63-70	interleukin 18	Homo sapiens	172-186
11022121-2	2000	Four days after cessation of a 3-day regimen of 650 mg of oral aspirin, there was a 70% increase in interferon-gamma (IFN-gamma) production, stimulated by a combination of interleukin-18 (IL-18) plus lipopolysaccharide (p &lt; 0.05).	Aspirin	63-70	interleukin 18	Homo sapiens	188-193
10903927-3	2000	Similarly, NO-aspirin (10-100 microM) was found to induce tolerance to its own cyclic GMP stimulatory action and to that of GTN.	Aspirin	14-21	5'-nucleotidase, cytosolic II	Homo sapiens	86-89
10903927-6	2000	Prolonged treatment with NO-aspirin causes down-regulation of the cellular cyclic GMP response, suggesting that tolerance may occur during therapy with NO-aspirin.	Aspirin	28-35	5'-nucleotidase, cytosolic II	Homo sapiens	82-85
10903927-6	2000	Prolonged treatment with NO-aspirin causes down-regulation of the cellular cyclic GMP response, suggesting that tolerance may occur during therapy with NO-aspirin.	Aspirin	155-162	5'-nucleotidase, cytosolic II	Homo sapiens	82-85
10968413-10	2000	We describe here that NCX 4016 (65 mg/kg/day) increased prostacyclin and thromboxane A2 production in the infarcted heart muscle, overcoming the inhibitory effects of ASA.	Aspirin	167-170	T cell leukemia homeobox 2	Homo sapiens	22-25
10896240-4	2000	The median ratio for TF-/beta-actin mRNA increased from 1.5 +/- 0.44 in the presence of LPS-alone, to 2.5 +/- 0.51 when 5 mM aspirin was added.	Aspirin	125-132	POTE ankyrin domain family member F	Homo sapiens	25-35
10741635-7	2000	Fibrinogen binding to the platelet GPIIb/IIIa receptor was reduced for aspirin to 69% (difference not significant), to 63% for clopidogrel (difference not significant), and to 63% for the clopidogrel plus aspirin combination (P &lt; .01).	Aspirin	71-78	integrin subunit alpha 2b	Homo sapiens	35-40
10741635-7	2000	Fibrinogen binding to the platelet GPIIb/IIIa receptor was reduced for aspirin to 69% (difference not significant), to 63% for clopidogrel (difference not significant), and to 63% for the clopidogrel plus aspirin combination (P &lt; .01).	Aspirin	205-212	integrin subunit alpha 2b	Homo sapiens	35-40
10741635-9	2000	In vitro, with pretreatment with aspirin and clopidogrel, inhibitory effects of the GPIIb/IIIa inhibitors on fibrinogen binding were additive to changes observed with aspirin or clopidogrel alone.	Aspirin	33-40	integrin subunit alpha 2b	Homo sapiens	84-89
10741635-11	2000	Aspirin and clopidogrel reinforced effects of the GPIIb/IIIa inhibitors on adenosine diphosphate (5 micromol/L)-induced aggregation in an additive manner, a supra-additive effect was observed with collagen (2 microg x mL(-1))-induced aggregation.	Aspirin	0-7	integrin subunit alpha 2b	Homo sapiens	50-55
10741635-12	2000	CONCLUSION: The augmentation of the antiaggregatory effects of GPIIb/IIIa inhibitors by aspirin and clopidogrel and the lack of antisecretory effects of GPIIb/IIIa inhibitors may favor their combination with clopidogrel.	Aspirin	88-95	integrin subunit alpha 2b	Homo sapiens	63-68
10547619-1	1999	Aspirin (acetylsalicylic acid) was used to determine the inhibition of arylamine N-acetyltransferase (NAT) activity and DNA adduct formation in a human bladder tumour cell line (T24).	Aspirin	0-7	bromodomain containing 2	Homo sapiens	102-105
10547619-6	1999	The results demonstrated that NAT activity and 2-aminofluorene-DNA adduct formation in human bladder tumour cells were inhibited by acetylsalicylic acid in a dose-dependent manner.	Aspirin	132-152	bromodomain containing 2	Homo sapiens	30-33
10477259-6	1999	These results not only demonstrate that aspirin and its metabolite salicylate may have pro-inflammatory as well as anti-inflammatory effects but also raise the possibility that new cellular targets may be identified for modulating the Janus kinase-STAT signalling pathway.	Aspirin	40-47	signal transducer and activator of transcription 1	Mus musculus	248-252
10532207-3	1999	Because cross-linking of the activated platelet receptor glycoprotein (GP) IIb-IIIa by plasma fibrinogen represents the final common pathway to coronary thrombus formation, several GP IIb-IIIa inhibitors have been developed as a potentially more effective antithrombotic therapy than agents currently used for this purpose, namely aspirin and heparin.	Aspirin	331-338	integrin subunit alpha 2b	Homo sapiens	181-187
10422768-12	1999	Leptin was also effective to attenuate aspirin-induced damage and the accompanying fall in the GBF, whereas CCK-8 dose dependently worsened aspirin damage and failed to influence GBF.	Aspirin	140-147	cholecystokinin	Rattus norvegicus	108-111
10203355-14	1999	It can be concluded that (1) iNOS can be induced without active NF-kappaB; (2) Dex, acetylsalicylic acid, and PDTC inhibit only p65; and (3) JAK2 is involved in iNOS induction, and the contribution of JAK2 to nitrite production is greater than that of NF-kappaB.	Aspirin	84-104	Janus kinase 2	Rattus norvegicus	141-145
10203355-14	1999	It can be concluded that (1) iNOS can be induced without active NF-kappaB; (2) Dex, acetylsalicylic acid, and PDTC inhibit only p65; and (3) JAK2 is involved in iNOS induction, and the contribution of JAK2 to nitrite production is greater than that of NF-kappaB.	Aspirin	84-104	Janus kinase 2	Rattus norvegicus	201-205
10092995-2	1999	MATERIALS AND METHODS: The aim of the present study was to examine whether anti-inflammatory doses of acetylsalicylic acid (aspirin) could regulate iNOS protein expression in bovine vascular smooth muscle cells (BVSMCs) in culture.	Aspirin	102-122	nitric oxide synthase 2	Bos taurus	148-152
10092995-2	1999	MATERIALS AND METHODS: The aim of the present study was to examine whether anti-inflammatory doses of acetylsalicylic acid (aspirin) could regulate iNOS protein expression in bovine vascular smooth muscle cells (BVSMCs) in culture.	Aspirin	124-131	nitric oxide synthase 2	Bos taurus	148-152
9706142-8	1998	Finally, aspirin produced a decrease in intracellular beta-catenin levels, suggesting that modulation of this protein is associated with tumor prevention.	Aspirin	9-16	catenin (cadherin associated protein), beta 1	Mus musculus	54-66
9488677-8	1998	The potencies of the ligands for ASAs increase in the following order: mannobiose (Manalpha1-3Man) &lt; mannotriose (Manalpha1-6Manalpha1-3Man) approximately mannopentaose &lt;&lt; Man9-oligosaccharide.	Aspirin	33-37	mannosidase alpha class 1A member 1	Homo sapiens	181-185
9557826-1	1998	Using flow cytometry, we studied the expression of the CD16 antigen by lymphocytes present in human semen samples from three groups of patients: 60 fertile men attending for vasectomy, 60 sterile patients without antisperm antibodies (ASA) and 18 immunological sterile patients with ASA in their ejaculate.	Aspirin	283-286	Fc gamma receptor IIIa	Homo sapiens	55-59
9557826-5	1998	However, a significant increase in the number of CD16+ lymphocytes was observed in the ejaculate of sterile patients with ASA as compared to the other groups.	Aspirin	122-125	Fc gamma receptor IIIa	Homo sapiens	49-53
9440807-9	1998	Second, the effect of iodide on class I RNA levels and on enhancer A complex formation with Mod-1 and the p50/p65 heterodimer is inhibited by agents that block the inositol phosphate, Ca++, phospholipase A2, arachidonate signal transduction pathway: acetylsalicylate, indomethacin, and 5,8,11,14-eicosatetraynoic acid.	Aspirin	250-266	malic enzyme 1	Rattus norvegicus	92-97
9540854-11	1997	Aspirin and ibuprofen were shown to inactivate GAP-DH very rapidly in-vitro.	Aspirin	0-7	LOC786101	Bos taurus	47-53
9435549-3	1997	As NO can inhibit neutrophil adherence, it is possible that such a derivative of aspirin (NCX-4016) would exert inhibitory effects on neutrophil adherence and therefore be capable of protecting the stomach against shock-induced gastric damage.	Aspirin	81-88	T cell leukemia homeobox 2	Homo sapiens	90-93
9640079-0	1997	[Evaluation of platelet function and tissue plasminogen activator activity in ischemic heart disease depending on concurrence with hyperlipoproteinemia and aspirin therapy].	Aspirin	156-163	chromosome 20 open reading frame 181	Homo sapiens	37-65
9085161-0	1997	Recovery of mucin content in surface layer of rat gastric mucosa after HCl-aspirin-induced mucosal damage.	Aspirin	75-82	solute carrier family 13 member 2	Rattus norvegicus	12-17
9085161-1	1997	Quantitative changes in mucin (mucus glycoprotein) in different layers of rat gastric mucosa after mucosal damage induced by acidified acetylsalicylic acid (HCl-aspirin; 0.15N HCl, 20-200 mg acetylsalicylic acid/kg body weight) were studied.	Aspirin	135-155	solute carrier family 13 member 2	Rattus norvegicus	24-29
9085161-2	1997	More than 50 mg/kg HCl-aspirin led to a significant increase in macroscopic gastric injury (expressed as ulcer index) at 3 h, compared with control (no aspirin) and there was a significant recovery at 7 h. Three h after dosing with 50 mg/kg acidified aspirin, there was superficial mucosal damage and decreased mucin content in the surface mucosal layer.	Aspirin	23-30	solute carrier family 13 member 2	Rattus norvegicus	311-316
9150301-11	1997	The Fos results reveal clear differences in the way that BA (aspirin) and L-54 (ibuprofen + caffeine + paracetamol) affected transmission of the noxious signal.	Aspirin	61-68	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	4-7
9057644-7	1997	LPS-induced PGE2 and thromboxane B2 (TXB2) production in aspirin-treated neutrophils was significantly inhibited by IL-10, IL-4, and NS-398.	Aspirin	57-64	interleukin 10	Homo sapiens	116-121
9054746-10	1997	SPA was significantly inhibited by the cyclooxygenase enzyme inhibitors aspirin and indomethacin: by SQ29548, a thromboxane (Tx) A2 receptor antagonist; by diphenyliodonium an inhibitor of flavoprotein-dependent enzymes: and by arachidonyl trifluoromethyl ketone, a selective inhibitor of cytosolic phospholipase A2.	Aspirin	72-79	phospholipase A2 group IVA	Homo sapiens	289-315
9815674-0	1997	Effect of aspirin on prostaglandin E2 and leukotriene B4 production in human colonic mucosa from cancer patients.	Aspirin	10-17	cystatin 12, pseudogene	Homo sapiens	35-56
9028737-6	1997	Peptide nucleic acid (PNA) clamping was used to improve the K-ras ASA assay.	Aspirin	66-69	KRAS proto-oncogene, GTPase	Homo sapiens	60-65
9112701-4	1996	Prolidase activity was measured in cultured human skin fibroblasts, treated with some non-steroid antiinflammatory drugs (acetyl-salicylic acid, sodium salicylate, phenylbutazone, indometacin).	Aspirin	122-143	peptidase D	Homo sapiens	0-9
8950792-1	1996	We studied in vitro the antiplatelet activity of a new nitroderivative chemically related to acetylsalicylic acid: 2 acetoxybenzoate 2-[1-nitroxy-methyl]-phenyl ester (NCX 4016), in order to identify any effects due to the release of nitric oxide and the blockade of cyclo-oxygenase.	Aspirin	93-113	T cell leukemia homeobox 2	Homo sapiens	168-171
8921427-0	1996	Induction of cytokines and ICAM-1 by proinflammatory cytokines in primary rheumatoid synovial fibroblasts and inhibition by N-acetyl-L-cysteine and aspirin.	Aspirin	148-155	intercellular adhesion molecule 1	Homo sapiens	27-33
12226423-7	1996	Inhibition of JA biosynthesis by aspirin blocked the heat-induced Pin2 gene expression in tomato wild-type leaves.	Aspirin	33-40	auxin efflux carrier component 2	Solanum lycopersicum	66-70
8927481-7	1996	PAR to food additives occurs frequently in patients suffering from urticaria, asthma and may be accompanied by history of aspirin or NSAI pseudoallergic reactions.	Aspirin	122-129	jumping translocation breakpoint	Homo sapiens	0-3
8613050-0	1996	Increased gastroduodenal concentrations of transforming growth factor alpha in adaptation to aspirin in monkeys and rats.	Aspirin	93-100	transforming growth factor alpha	Rattus norvegicus	43-75
8613050-3	1996	The aim of this study was to determine whether gastroduodenal tissue levels of TGF-alpha and EGF protein were altered during adaptation to aspirin-induced injury in monkeys and rats in vivo.	Aspirin	139-146	transforming growth factor alpha	Rattus norvegicus	79-88
8613050-7	1996	RESULTS: Long-term administration of aspirin caused a significant increase in gastric and duodenal tissue levels of TGF-alpha in monkeys and rats; the increased levels of TGF-alpha significantly correlated with the decrease in aspirin-induced injury.	Aspirin	37-44	transforming growth factor alpha	Rattus norvegicus	116-125
8613050-7	1996	RESULTS: Long-term administration of aspirin caused a significant increase in gastric and duodenal tissue levels of TGF-alpha in monkeys and rats; the increased levels of TGF-alpha significantly correlated with the decrease in aspirin-induced injury.	Aspirin	37-44	transforming growth factor alpha	Rattus norvegicus	171-180
8613050-7	1996	RESULTS: Long-term administration of aspirin caused a significant increase in gastric and duodenal tissue levels of TGF-alpha in monkeys and rats; the increased levels of TGF-alpha significantly correlated with the decrease in aspirin-induced injury.	Aspirin	227-234	transforming growth factor alpha	Rattus norvegicus	171-180
8613050-10	1996	CONCLUSIONS: Adaptation of the gastric mucosa to the damaging effect of aspirin is associated with a significant and specific increase in TGF-alpha protein in the gastroduodenum.	Aspirin	72-79	transforming growth factor alpha	Rattus norvegicus	138-147
8784790-9	1996	In contrast to LPS, platelet-activating factor (PAF) induced immediate TX release and bronchoconstriction that was prevented by acetyl salicylic acid, but not by CGP-28238.	Aspirin	128-149	PCNA clamp associated factor	Rattus norvegicus	20-46
8784790-9	1996	In contrast to LPS, platelet-activating factor (PAF) induced immediate TX release and bronchoconstriction that was prevented by acetyl salicylic acid, but not by CGP-28238.	Aspirin	128-149	PCNA clamp associated factor	Rattus norvegicus	48-51
8611656-0	1996	Glycation-induced inactivation of malate dehydrogenase protection by aspirin and a lens molecular chaperone, alpha-crystallin.	Aspirin	69-76	malic enzyme 1	Homo sapiens	34-54
8735820-1	1996	The antiplatelet activity of two new nitrocompounds, chemically related to acetylsalicylic acid (NCX 4215 and NCX 4016), was studied in vitro to verify the hypothetical dual action of these drugs.	Aspirin	75-95	T cell leukemia homeobox 2	Homo sapiens	97-100
8735820-4	1996	NCX 4215 and NCX 4016 in a dose-dependent way inhibited also thrombin-induced aggregation of platelets pretreated with acetylsalicylic acid.	Aspirin	119-139	T cell leukemia homeobox 2	Homo sapiens	0-3
8735820-4	1996	NCX 4215 and NCX 4016 in a dose-dependent way inhibited also thrombin-induced aggregation of platelets pretreated with acetylsalicylic acid.	Aspirin	119-139	T cell leukemia homeobox 2	Homo sapiens	13-16
8527516-13	1995	Only the combination of mAbs directed to the beta 2-integrin, CD11b (D12/SHCL-3), or CD18 (MHM23) subunits maximally inhibited ASA- and C-mediated sperm adhesion to neutrophils (by 70%) or sperm phagocytosis (by 75%), as well as neutrophil aggregation (by 96%).	Aspirin	127-130	integrin subunit alpha M	Homo sapiens	62-67
8527516-14	1995	These findings strongly implicate the CD11b/CD18 glycoprotein complex (CR3) in the adhesive events involved in ASA- and C-mediated immune destruction of motile sperm by neutrophils.	Aspirin	111-114	integrin subunit alpha M	Homo sapiens	38-43
7587805-3	1995	Aspirin-induced gastric damage and the increase in myeloperoxidase activity were significantly inhibited by the injection of anti-CD11a, anti-CD11b, anti-intercellular adhesion molecule-1 monoclonal antibodies, and the combination of superoxide dismutase and catalase, which are scavengers of active oxygen species.	Aspirin	0-7	intercellular adhesion molecule 1	Rattus norvegicus	154-187
7587805-4	1995	These results suggest that neutrophil-endothelial adhesive interactions, which occur via CD11a/ CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule-1, and oxygen-derived free radicals produced by neutrophils are implicated in the production of aspirin-induced gastric mucosal injury.	Aspirin	273-280	intercellular adhesion molecule 1	Rattus norvegicus	145-178
7574023-8	1995	Inhibitions obtained with chemicals or drugs glucuronidated by either UGT1 or UGT2 families (1-naphtol, 4-hydroxybiphenyl, carvacrol, n-propylgallate, ketoprofen, chloramphenicol, acetylsalicylic acid) indicated that at least two UGT isoforms are involved in propofol glucuronidation.	Aspirin	180-200	UDP-glucose glycoprotein glucosyltransferase 2	Homo sapiens	78-82
17351530-4	2007	CASES: We report an unusual presentation of manganese intoxication due to administration of a combination of acetylsalicylic acid and ephedrine HCl, potassium permanganate, and vinegar melted in tap water and administered parenterally as a psychostimulant substance in 2 cases who developed symptoms resembling parkinsonism.	Aspirin	109-129	nuclear RNA export factor 1	Homo sapiens	195-198
17334511-10	2007	In conclusion, a GPIbalpha-blocking antibody, as well as P2Y(1) and P2Y(12) receptor antagonists, alone or in combination, reduce in contrast to aspirin human plaque-induced platelet thrombus formation under arterial flow.	Aspirin	145-152	glycoprotein Ib platelet subunit alpha	Homo sapiens	17-26
17334512-0	2007	Prevention by NCX 4016, a nitric oxide-donating aspirin, but not by aspirin, of the acute endothelial dysfunction induced by exercise in patients with intermittent claudication.	Aspirin	48-55	T cell leukemia homeobox 2	Homo sapiens	14-17
17137604-3	2007	The participation of PGE2 was confirmed by the use of indomethacin (indo) and of acetyl salicylic acid (ASA), cyclooxygenase inhibitors, which inhibited pilocarpine-induced mucin release.	Aspirin	81-102	solute carrier family 13 member 2	Rattus norvegicus	173-178
17137604-3	2007	The participation of PGE2 was confirmed by the use of indomethacin (indo) and of acetyl salicylic acid (ASA), cyclooxygenase inhibitors, which inhibited pilocarpine-induced mucin release.	Aspirin	104-107	solute carrier family 13 member 2	Rattus norvegicus	173-178
17239863-5	2007	ICAM-1 and VCAM-1 expression stimulated by IL-1beta was reduced by the treatment with aspirin, whereas the expression of E-selectin was unaffected.	Aspirin	86-93	intercellular adhesion molecule 1	Homo sapiens	0-6
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	83-90	intercellular adhesion molecule 1	Homo sapiens	118-124
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	191-198	intercellular adhesion molecule 1	Homo sapiens	118-124
17239863-6	2007	Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.	Aspirin	191-198	intercellular adhesion molecule 1	Homo sapiens	327-333
17274829-2	2007	Anti-inflammatory drug acetyl salicylic acid elevates CDK-5 and reduces ischemia - reperfusion injury in cultured neurons.	Aspirin	23-44	cyclin-dependent kinase 5	Mus musculus	54-59
17191118-0	2007	The role of PKCzeta in amikacin-induced apoptosis in the cochlea: prevention by aspirin.	Aspirin	80-87	protein kinase C zeta	Homo sapiens	12-19
17191118-8	2007	Prior treatment with aspirin prevented PKCzeta cleavage and nuclear translocation.	Aspirin	21-28	protein kinase C zeta	Homo sapiens	39-46
17184645-0	2007	Dose-related efficacy of aspirin after coronary surgery in patients With Pl(A2) polymorphism (NCT00262275).	Aspirin	25-32	phospholipase A2 group IIA	Homo sapiens	73-78
17184645-9	2007	The interaction coefficient describes a higher aggregation of 19% (95% confidence interval: 2 to 36; p = 0.03) and less inhibition with an EC50 of -2.07 (-4.19 to 0.04; p = 0.06) in patients who were both Pl(A2) positive and receiving low-dose aspirin.	Aspirin	244-251	phospholipase A2 group IIA	Homo sapiens	205-210
17184645-11	2007	The impaired response of persons with the Pl(A2) polymorphism to aspirin may be dose related, with significant improvement observed in patients using medium- rather than low-dose aspirin.	Aspirin	65-72	phospholipase A2 group IIA	Homo sapiens	42-47
17184645-11	2007	The impaired response of persons with the Pl(A2) polymorphism to aspirin may be dose related, with significant improvement observed in patients using medium- rather than low-dose aspirin.	Aspirin	179-186	phospholipase A2 group IIA	Homo sapiens	42-47
17630485-0	2007	The BC genotype of the VNTR polymorphism of platelet glycoprotein Ibalpha is overrepresented in patients with recurrent stroke regardless of aspirin therapy.	Aspirin	141-148	glycoprotein Ib platelet subunit alpha	Homo sapiens	53-73
17630485-8	2007	CONCLUSION: The BC genotype of the VNTR polymorphism of GP Ibalpha is an independent predictor of recurrent events in stroke patients treated with aspirin.	Aspirin	147-154	glycoprotein Ib platelet subunit alpha	Homo sapiens	56-66
17432927-13	2007	These findings and data from our previous studies suggest that patients with a Pl(A2) allele homozygosity may benefit from antiplatelet therapy based on clopidogrel rather than aspirin.	Aspirin	177-184	phospholipase A2 group IIA	Homo sapiens	79-84
17219690-6	2006	Aspirin DCs themselves produce less IL-10 and more IL-12 than immature DCs, but no specific cytokine is necessary for their tolerogenic capacity.	Aspirin	0-7	interleukin 10	Homo sapiens	36-41
17432196-5	2006	A clinical trial of the GP IIb/IIIa inhibitor abciximab, which is a more potent antiplatelet agent than aspirin, had recently been conducted, although it was stopped because of the concern on the safety.	Aspirin	104-111	integrin subunit alpha 2b	Homo sapiens	24-30
16991207-3	2006	Aspirin enhanced PLD activity whereas the other three had inhibiting effects.	Aspirin	0-7	peptidase D	Homo sapiens	17-20
16887052-6	2006	Compared with ALI group, the level of NF-KappaB activity and the expression of ICAM-1 and P-selectin were obviously down regulated, and also the pathological lesion and inflammatory response of lung were improved in LMWH and ASA groups.	Aspirin	225-228	intercellular adhesion molecule 1	Rattus norvegicus	79-85
16961726-0	2006	Pharmacologic profile and therapeutic potential of NCX 4016, a nitric oxide-releasing aspirin, for cardiovascular disorders.	Aspirin	86-93	T cell leukemia homeobox 2	Homo sapiens	51-54
16961726-1	2006	NCX 4016, 2-(acetyloxy)benzoic acid 3-[(nitrooxy)methyl]phenyl ester, is a new molecule in which a nitric oxide (NO)-releasing moiety is covalently linked to aspirin.	Aspirin	10-35	T cell leukemia homeobox 2	Homo sapiens	0-3
16961726-1	2006	NCX 4016, 2-(acetyloxy)benzoic acid 3-[(nitrooxy)methyl]phenyl ester, is a new molecule in which a nitric oxide (NO)-releasing moiety is covalently linked to aspirin.	Aspirin	158-165	T cell leukemia homeobox 2	Homo sapiens	0-3
16792175-9	2006	In aspirin-sensitive polyps the number of eosinophils was significantly higher than in the other patient groups and they had significantly higher eotaxin, eotaxin-2, and -3 protein levels than non-allergic and significantly higher amounts of eotaxin-3 compared with allergic patients.	Aspirin	3-10	C-C motif chemokine ligand 26	Homo sapiens	242-251
16415877-0	2006	Anti-inflammatory actions of lipoxin A4 and aspirin-triggered lipoxin are SOCS-2 dependent.	Aspirin	44-51	suppressor of cytokine signaling 2	Mus musculus	74-80
16415877-8	2006	We also show that SOCS-2 is a crucial intracellular mediator of the anti-inflammatory actions of aspirin-induced lipoxins in vivo.	Aspirin	97-104	suppressor of cytokine signaling 2	Mus musculus	18-24
21783632-9	2005	An addition of acetylsalicylic acid, known, non-specific inhibitor of prolidase to the cells treated with 100muM NiCl(II), significantly reduced both collagen biosynthesis and prolidase activity.	Aspirin	15-35	peptidase D	Homo sapiens	70-79
21783632-9	2005	An addition of acetylsalicylic acid, known, non-specific inhibitor of prolidase to the cells treated with 100muM NiCl(II), significantly reduced both collagen biosynthesis and prolidase activity.	Aspirin	15-35	peptidase D	Homo sapiens	176-185
21783632-10	2005	It suggests that acetylsalicylic acid prevents nickel-induced increase in collagen biosynthesis through inhibition of prolidase activity in human fibroblasts.	Aspirin	17-37	peptidase D	Homo sapiens	118-127
16230075-12	2005	CONCLUSIONS: These data establish a physiologic role for H(2)S in regulating the gastric microcirculation and identify CSE as a novel target for ASA/NSAIDs.	Aspirin	145-148	cystathionine gamma-lyase	Homo sapiens	119-122
16151033-8	2005	In contrast, therapy with C+ASA resulted in a significant inhibition of platelet activity assessed by ADP- (P=0.00001) and collagen-induced (P=0.02) aggregation; closure time prolongation (P=0.03), and reduction of platelet activation units with Ultegra (P=0.00001); expression of PECAM-1 (P=0.01), and GP IIb/IIIa activity with PAC-1 (P=0.02) when compared with ASA group.	Aspirin	28-31	integrin subunit alpha 2b	Homo sapiens	303-309
16030091-5	2005	There was a significant interaction between the IL-10-592 C/A polymorphism and aspirin use (Pinteraction = 0.03).	Aspirin	79-86	interleukin 10	Homo sapiens	48-53
16030091-6	2005	Carriers of the variant IL-10-592 (A) allele, who produce less of the anti-inflammatory cytokine interleukin-10, had a statistically significant 50% reduced risk of colorectal cancer when taking regular aspirin (odds ratio, 0.5; 95% confidence interval, 0.25-0.97), whereas risk was not reduced in carriers of the A allele who did not use aspirin, or among aspirin users with the CC genotype.	Aspirin	203-210	interleukin 10	Homo sapiens	24-29
16030091-6	2005	Carriers of the variant IL-10-592 (A) allele, who produce less of the anti-inflammatory cytokine interleukin-10, had a statistically significant 50% reduced risk of colorectal cancer when taking regular aspirin (odds ratio, 0.5; 95% confidence interval, 0.25-0.97), whereas risk was not reduced in carriers of the A allele who did not use aspirin, or among aspirin users with the CC genotype.	Aspirin	203-210	interleukin 10	Homo sapiens	97-111
16030091-6	2005	Carriers of the variant IL-10-592 (A) allele, who produce less of the anti-inflammatory cytokine interleukin-10, had a statistically significant 50% reduced risk of colorectal cancer when taking regular aspirin (odds ratio, 0.5; 95% confidence interval, 0.25-0.97), whereas risk was not reduced in carriers of the A allele who did not use aspirin, or among aspirin users with the CC genotype.	Aspirin	339-346	interleukin 10	Homo sapiens	24-29
16030091-6	2005	Carriers of the variant IL-10-592 (A) allele, who produce less of the anti-inflammatory cytokine interleukin-10, had a statistically significant 50% reduced risk of colorectal cancer when taking regular aspirin (odds ratio, 0.5; 95% confidence interval, 0.25-0.97), whereas risk was not reduced in carriers of the A allele who did not use aspirin, or among aspirin users with the CC genotype.	Aspirin	339-346	interleukin 10	Homo sapiens	97-111
16030091-6	2005	Carriers of the variant IL-10-592 (A) allele, who produce less of the anti-inflammatory cytokine interleukin-10, had a statistically significant 50% reduced risk of colorectal cancer when taking regular aspirin (odds ratio, 0.5; 95% confidence interval, 0.25-0.97), whereas risk was not reduced in carriers of the A allele who did not use aspirin, or among aspirin users with the CC genotype.	Aspirin	339-346	interleukin 10	Homo sapiens	24-29
16030091-6	2005	Carriers of the variant IL-10-592 (A) allele, who produce less of the anti-inflammatory cytokine interleukin-10, had a statistically significant 50% reduced risk of colorectal cancer when taking regular aspirin (odds ratio, 0.5; 95% confidence interval, 0.25-0.97), whereas risk was not reduced in carriers of the A allele who did not use aspirin, or among aspirin users with the CC genotype.	Aspirin	339-346	interleukin 10	Homo sapiens	97-111
16030091-7	2005	It is possible that carriers of the mutant IL-10-592 allele are more likely to derive anti-inflammatory and chemopreventive benefits from aspirin in the presence of a lower production of their own endogenous anti-inflammatory interleukin-10.	Aspirin	138-145	interleukin 10	Homo sapiens	43-48
15710755-5	2005	PAF-AH activity was lower in women than in men and was affected by the intake of lipid-lowering drugs (-12%; P&lt;0.001), aspirin (-6%; P&lt;0.001), beta-blockers (-6%; P&lt;0.001), and digitalis (+7%; P&lt;0.001).	Aspirin	122-129	phospholipase A2 group VII	Homo sapiens	0-6
15710755-8	2005	In individuals not taking lipid-lowering drugs and after adjustment for use of aspirin, beta-blocker, and digitalis, the odds ratio for CAD associated with increasing PAF-AH activity was 1.39 (95% CI 1.26 to 1.54, P&lt;0.001), a finding that was robust against further adjustments.	Aspirin	79-86	phospholipase A2 group VII	Homo sapiens	167-173
15784113-0	2005	The human leucocyte antigen-DRB1*1302-DQB1*0609-DPB1*0201 haplotype may be a strong genetic marker for aspirin-induced urticaria.	Aspirin	103-110	major histocompatibility complex, class II, DQ beta 1	Homo sapiens	38-42
15784113-7	2005	In haplotype analysis, the HLA-DRB1(*)1302-DQB1(*)0609-DPB1(*)0201 was significantly higher in the aspirin-induced urticaria (8.0%) than in the aspirin-intolerant asthma (0.7%, P=0.0014) and normal controls (2.0%, P=0.0006).	Aspirin	99-106	major histocompatibility complex, class II, DQ beta 1	Homo sapiens	43-47
15784113-8	2005	CONCLUSION: These findings suggest that the HLA-DRB1(*)1302-DQB1(*)0609-DPB1(*)0201 may be a strong genetic marker to determine the aspirin-induced urticaria phenotype.	Aspirin	132-139	major histocompatibility complex, class II, DQ beta 1	Homo sapiens	60-64
15823962-5	2005	The structure of the complex clearly shows that aspirin is literally embedded in the hydrophobic environment of PLA2.	Aspirin	48-55	phospholipase A2 group IIA	Homo sapiens	112-116
15823962-7	2005	Thus, the structure of the complex clearly shows that aspirin occupies a favourable place in the specific binding site of PLA2.	Aspirin	54-61	phospholipase A2 group IIA	Homo sapiens	122-126
15823962-8	2005	The binding studies have shown that acetyl salicylate (aspirin) binds to PLA2 enzyme specifically with a dissociation constant of 6.4 x 10(-6) M. The structural details and binding data suggest that the inhibition of PLA2 by aspirin is of pharmacological	Aspirin	36-53	phospholipase A2 group IIA	Homo sapiens	73-77
15823962-8	2005	The binding studies have shown that acetyl salicylate (aspirin) binds to PLA2 enzyme specifically with a dissociation constant of 6.4 x 10(-6) M. The structural details and binding data suggest that the inhibition of PLA2 by aspirin is of pharmacological	Aspirin	36-53	phospholipase A2 group IIA	Homo sapiens	217-221
15823962-8	2005	The binding studies have shown that acetyl salicylate (aspirin) binds to PLA2 enzyme specifically with a dissociation constant of 6.4 x 10(-6) M. The structural details and binding data suggest that the inhibition of PLA2 by aspirin is of pharmacological	Aspirin	55-62	phospholipase A2 group IIA	Homo sapiens	73-77
15823962-8	2005	The binding studies have shown that acetyl salicylate (aspirin) binds to PLA2 enzyme specifically with a dissociation constant of 6.4 x 10(-6) M. The structural details and binding data suggest that the inhibition of PLA2 by aspirin is of pharmacological	Aspirin	55-62	phospholipase A2 group IIA	Homo sapiens	217-221
15823962-8	2005	The binding studies have shown that acetyl salicylate (aspirin) binds to PLA2 enzyme specifically with a dissociation constant of 6.4 x 10(-6) M. The structural details and binding data suggest that the inhibition of PLA2 by aspirin is of pharmacological	Aspirin	225-232	phospholipase A2 group IIA	Homo sapiens	73-77
15823962-8	2005	The binding studies have shown that acetyl salicylate (aspirin) binds to PLA2 enzyme specifically with a dissociation constant of 6.4 x 10(-6) M. The structural details and binding data suggest that the inhibition of PLA2 by aspirin is of pharmacological	Aspirin	225-232	phospholipase A2 group IIA	Homo sapiens	217-221
15457395-11	2004	In case of pre-interventional application of the GP IIb/IIIa receptor inhibitor 22.3 % of patients revealed normal (TIMI-3) flow of the IRA before PCI, compared to 14.9 % TIMI-3 flow with 5000 IE Heparin/500 mg aspirin alone (p &lt; 0.05).	Aspirin	211-218	integrin subunit alpha 2b	Homo sapiens	49-55
15358033-0	2004	Co-administration of nitric oxide-aspirin (NCX-4016) and aspirin prevents platelet and monocyte activation and protects against gastric damage induced by aspirin in humans.	Aspirin	34-41	T cell leukemia homeobox 2	Homo sapiens	43-46
15358033-2	2004	BACKGROUND: NCX-4016 is an aspirin derivative containing a nitric oxide-releasing moiety that prevents platelet activation and modulates tissue factor (TF) expression and cytokine release from lipopolysaccharide (LPS)-stimulated monocytes.	Aspirin	27-34	T cell leukemia homeobox 2	Homo sapiens	12-15
15358033-8	2004	NCX-4016 was not associated with gastric damage, and significantly reduced gastric injury when co-administered with aspirin, although both drugs reduced gastric PGE2 production to the same extent.	Aspirin	116-123	T cell leukemia homeobox 2	Homo sapiens	0-3
15265945-0	2004	A stable aspirin-triggered lipoxin A4 analog blocks phosphorylation of leukocyte-specific protein 1 in human neutrophils.	Aspirin	9-16	lymphocyte specific protein 1	Homo sapiens	71-99
15158979-0	2004	The healing effect of TGF-alpha on gastric ulcer induced by acetylsalicylic acid in rats.	Aspirin	60-80	transforming growth factor alpha	Rattus norvegicus	22-31
14762100-0	2004	Cooperation between aspirin-triggered lipoxin and nitric oxide (NO) mediates antiadhesive properties of 2-(Acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester (NCX-4016) (NO-aspirin) on neutrophil-endothelial cell adherence.	Aspirin	20-27	T cell leukemia homeobox 2	Homo sapiens	162-165
14762100-0	2004	Cooperation between aspirin-triggered lipoxin and nitric oxide (NO) mediates antiadhesive properties of 2-(Acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester (NCX-4016) (NO-aspirin) on neutrophil-endothelial cell adherence.	Aspirin	104-129	T cell leukemia homeobox 2	Homo sapiens	162-165
14762100-0	2004	Cooperation between aspirin-triggered lipoxin and nitric oxide (NO) mediates antiadhesive properties of 2-(Acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester (NCX-4016) (NO-aspirin) on neutrophil-endothelial cell adherence.	Aspirin	176-183	T cell leukemia homeobox 2	Homo sapiens	162-165
14762100-1	2004	2-(Acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester (NCX-4016) is a nitric oxide (NO)-releasing derivative of aspirin that inhibits cyclooxygenase (COX) activity and releases NO.	Aspirin	0-25	T cell leukemia homeobox 2	Homo sapiens	58-61
15173663-0	2004	Acetylsalicylic acid-dependent inhibition of collagen biosynthesis and beta1-integrin signaling in cultured fibroblasts.	Aspirin	0-20	integrin subunit beta 1	Homo sapiens	71-85
15508788-3	2004	In presented work the influence of acetylsalicylic acid, metoprolol, simvastatin, isosorbide mononitrate and molsidomine on total activity of adenosine deaminase and its isoenzymes--ADA1 and ADA2 in vivo was studied.	Aspirin	35-55	adenosine deaminase	Homo sapiens	142-161
15036249-5	2004	Our studies reveal that acetylsalicylic acid (aspirin) prevents TNFalpha- and IL-1-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	24-44	NFKB inhibitor beta	Homo sapiens	213-224
15036249-5	2004	Our studies reveal that acetylsalicylic acid (aspirin) prevents TNFalpha- and IL-1-induced NF-kappaB activation in a dose-dependent manner through inhibition of phosphorylation and degradation of IkappaBalpha and IkappaBbeta.	Aspirin	46-53	NFKB inhibitor beta	Homo sapiens	213-224
14563672-1	2004	Aspirin that has been chemically combined with a nitric oxide (NO) donor (NCX-4016) has been shown to inhibit cyclooxygenase and prostaglandin generation while maintaining the inhibitory effects of aspirin.	Aspirin	0-7	T cell leukemia homeobox 2	Homo sapiens	74-77
14563672-1	2004	Aspirin that has been chemically combined with a nitric oxide (NO) donor (NCX-4016) has been shown to inhibit cyclooxygenase and prostaglandin generation while maintaining the inhibitory effects of aspirin.	Aspirin	198-205	T cell leukemia homeobox 2	Homo sapiens	74-77
14762891-1	2004	NCX4016 [2-acetoxybenzoic acid 3"-(nitrooxymethyl)phenyl ester] is a recently developed nitrooxy-derivative of aspirin with improved antiinflammatory, analgesic, and antithrombotic activity as well as increased gastrointestinal safety.	Aspirin	111-118	T cell leukemia homeobox 2	Homo sapiens	0-3
14699495-1	2004	BACKGROUND AND AIMS: Aspirin exerts antitumor effect partly through blocking tumor promoter-induced activator protein-1 (AP-1) activation.	Aspirin	21-28	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	100-119
14699495-1	2004	BACKGROUND AND AIMS: Aspirin exerts antitumor effect partly through blocking tumor promoter-induced activator protein-1 (AP-1) activation.	Aspirin	21-28	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	121-125
14691786-7	2004	During period 2, 1,941 of 7,236 (26.8%) patients with possible ACS received aspirin (chi(2) p&lt;0.0001; odds ratio [OR]=2.06; 95% confidence interval [CI]=1.86-2.29).	Aspirin	76-83	period circadian regulator 2	Homo sapiens	7-15
15580388-0	2004	The role of transforming growth factor alpha formulation on aspirin-induced ulcer healing and oxidant stress in the gastric mucosa.	Aspirin	60-67	transforming growth factor alpha	Rattus norvegicus	12-44
15580388-13	2004	CONCLUSION: These findings suggest that TGF-alpha accelerates the healing process after aspirin-induced gastric injury, and a relationship was observed between this application and the oxidative reactions.	Aspirin	88-95	transforming growth factor alpha	Rattus norvegicus	40-49
14532966-9	2003	Finally, aspirin suppressed adhesion of PC-3 cells to fibronectin (FN), which binds to an alpha3beta1 integrin receptor, and to vitronectin (VN), which binds to alphavbeta3 integrin receptor.	Aspirin	9-16	vitronectin	Homo sapiens	128-139
14532966-9	2003	Finally, aspirin suppressed adhesion of PC-3 cells to fibronectin (FN), which binds to an alpha3beta1 integrin receptor, and to vitronectin (VN), which binds to alphavbeta3 integrin receptor.	Aspirin	9-16	vitronectin	Homo sapiens	141-143
12910692-7	2003	Immunohistochemistry and immunoblotting indicated that aspirin effectively decreased COX-2 and c-fos expression in SGC-7901 cell.	Aspirin	55-62	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	95-100
12795646-10	2003	Acetylsalicylic acid and omeprazole significantly increased the expression of CYPs 2A6, 2E1 and 3A4, respectively.	Aspirin	0-20	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	78-99
12738997-0	2003	NCX 4016, a nitric oxide-releasing aspirin derivative, exhibits a significant antiproliferative effect and alters cell cycle progression in human colon adenocarcinoma cell lines.	Aspirin	35-42	T cell leukemia homeobox 2	Homo sapiens	0-3
12738997-2	2003	We assessed the cytotoxic activity of a new aspirin derivative, NCX 4016, after different exposure schedules, in three human colon adenocarcinoma cell lines.	Aspirin	44-51	T cell leukemia homeobox 2	Homo sapiens	64-67
12738997-9	2003	Our results indicate that NCX 4016 has an in vitro cytostatic activity superior to that of its parental aspirin compound, which makes it a potentially important tumor preventive agent.	Aspirin	104-111	T cell leukemia homeobox 2	Homo sapiens	26-29
12787065-8	2003	Two NF-kappa B inhibitors, aspirin (10 mM) and MG-132 (0.1 microM), blocked basal apoE and apoJ secretion as well as LPS-induced apoJ secretion.	Aspirin	27-34	clusterin	Rattus norvegicus	91-95
12787905-0	2003	Spin-lattice relaxation of 13CH3 groups in 13C-enriched aspirin after proton saturation.	Aspirin	56-63	spindlin 1	Homo sapiens	0-4
12787905-1	2003	We studied the spin-lattice relaxation of the 13C magnetisation, M(C), in 13C-enriched single crystal of aspirin (only methyl carbons enriched to 99%) at the carbon resonance frequency of 54.5 MHz.	Aspirin	105-112	spindlin 1	Homo sapiens	15-19
12894587-4	2003	Inhibitors of the NF kappa B signaling pathway, which is activated by LMP-1, including I kappa B super-repressor and aspirin reduce or cancel induction of MMP-9, COX-2 and invasiveness of LMP-1-expressing cells.	Aspirin	117-124	PDZ and LIM domain 7	Homo sapiens	70-75
12894587-4	2003	Inhibitors of the NF kappa B signaling pathway, which is activated by LMP-1, including I kappa B super-repressor and aspirin reduce or cancel induction of MMP-9, COX-2 and invasiveness of LMP-1-expressing cells.	Aspirin	117-124	matrix metallopeptidase 9	Homo sapiens	155-160
12894587-4	2003	Inhibitors of the NF kappa B signaling pathway, which is activated by LMP-1, including I kappa B super-repressor and aspirin reduce or cancel induction of MMP-9, COX-2 and invasiveness of LMP-1-expressing cells.	Aspirin	117-124	PDZ and LIM domain 7	Homo sapiens	188-193
12774850-5	2003	The aspirin effects were apparently unrelated to prostaglandin biosynthesis inhibition, since although these cells were found to express high levels of cyclooxygenase 1 (COX-1) and low levels of COX-2 proteins, they did not produce any measurable net amounts of prostaglandins, based on both utilization of radiolabelled arachidonic acid and the radioimmunoassay of prostaglandins E2 and F2 alpha.	Aspirin	4-11	cystatin 12, pseudogene	Homo sapiens	381-396
12846439-5	2003	In vitro studies have shown that NCX-4016 inhibits platelet aggregation induced by aspirin-sensitive (arachidonic acid) and aspirin-insensitive (thrombin) agonist.	Aspirin	124-131	T cell leukemia homeobox 2	Homo sapiens	33-36
12846439-9	2003	Indeed, a 7-day course of NCX-4016 results in 90% reduction of gastric damage caused by equimolar doses of aspirin.	Aspirin	107-114	T cell leukemia homeobox 2	Homo sapiens	26-29
14618072-1	2003	GP IIb/IIIa antagonists are qualitatively different from classical antiplatelet agents, such as aspirin or clopidogrel.	Aspirin	96-103	integrin subunit alpha 2b	Homo sapiens	0-6
12684272-0	2003	Stress-responsive JNK mitogen-activated protein kinase mediates aspirin-induced suppression of B16 melanoma cellular proliferation.	Aspirin	64-71	mitogen-activated protein kinase 8	Mus musculus	18-21
12684272-8	2003	Aspirin induced the activation of p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinases.	Aspirin	0-7	mitogen-activated protein kinase 8	Mus musculus	42-65
12684272-8	2003	Aspirin induced the activation of p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinases.	Aspirin	0-7	mitogen-activated protein kinase 8	Mus musculus	67-70
12684272-10	2003	Inhibition of JNK, but not p38, decreased the suppressive effect of aspirin upon the proliferation of B16 cells.	Aspirin	68-75	mitogen-activated protein kinase 8	Mus musculus	14-17
12612897-0	2003	Gastrointestinal safety of NO-aspirin (NCX-4016) in healthy human volunteers: a proof of concept endoscopic study.	Aspirin	30-37	T cell leukemia homeobox 2	Homo sapiens	39-42
12612897-1	2003	BACKGROUND AND AIMS: NCX-4016 is a nitric oxide-releasing derivative of aspirin with antiplatelet activity.	Aspirin	72-79	T cell leukemia homeobox 2	Homo sapiens	21-24
12591106-11	2003	One tablet of aspirin moderately inhibited expression of most surface platelet receptors measured, and such inhibition reached significance (p&lt;0.05) for PAC-1, CD31, CD41, CD42, CD62p, and CD151.	Aspirin	14-21	integrin subunit alpha 2b	Homo sapiens	169-173
12591106-11	2003	One tablet of aspirin moderately inhibited expression of most surface platelet receptors measured, and such inhibition reached significance (p&lt;0.05) for PAC-1, CD31, CD41, CD42, CD62p, and CD151.	Aspirin	14-21	CD151 molecule (Raph blood group)	Homo sapiens	192-197
12124433-8	2002	Moreover, the protein amount of a neuronal Cdk5 activator, p35, recovered after reoxygenation only in ASA-treated samples.	Aspirin	102-105	cyclin-dependent kinase 5 regulatory subunit 1	Rattus norvegicus	59-62
12124433-10	2002	In conclusion, pre-treatment with ASA induces tolerance against hypoxia/reoxygenation damage in spinal cord cultures by restoring Cdk5 and p35 protein expression.	Aspirin	34-37	cyclin-dependent kinase 5 regulatory subunit 1	Rattus norvegicus	139-142
12044784-10	2002	Acetylsalicylic acid was found to inhibit gelatinolytic activity both in control and adenocarcinoma tissues, preferentially the active forms of gelatinases MMP-2 and MMP-9.	Aspirin	0-20	matrix metallopeptidase 9	Homo sapiens	166-171
12481162-0	2002	Nitric oxide releasing aspirin protects the gastric mucosa against stress and promotes healing of stress-induced gastric mucosal damage: role of heat shock protein 70.	Aspirin	23-30	heat shock protein family A (Hsp70) member 4	Homo sapiens	145-166
12481162-13	2002	HSP70 mRNA was significantly upregulated by WRS, and this was significantly attenuated by ASA, but not by NO-ASA.	Aspirin	90-93	heat shock protein family A (Hsp70) member 4	Homo sapiens	0-5
12481162-15	2002	CONCLUSION: NO-ASA exhibits mucosal protective and healing effects against WRS-induced gastric lesions due to the release of NO, which induces gastric hyperemia, and the attenuation of lipid peroxidation and counteracts the inhibition of HSP70 expression induced by native ASA.	Aspirin	15-18	heat shock protein family A (Hsp70) member 4	Homo sapiens	238-243
11844897-3	2002	The percentage of patients with a 2-hour headache response after the first dose for all 3 attacks (the primary end point) was 33.4% with zolmitriptan and 32.9% with acetylsalicylic acid plus metoclopramide [odds ratio 1.06, 95% confidence interval (CI) 0.77-1.47; p = 0.7228].	Aspirin	165-185	paired box 5	Homo sapiens	84-89
11585736-0	2001	Suppression of intestinal and mammary neoplasia by lifetime administration of aspirin in Apc(Min/+) and Apc(Min/+), Msh2(-/-) mice.	Aspirin	78-85	mutS homolog 2	Mus musculus	116-120
11585736-6	2001	Finally, we analyzed (Apc(Min/+), Msh2(-/-)) mice and found that lifetime aspirin exposure significantly delayed the onset of both intestinal and mammary neoplasia.	Aspirin	74-81	mutS homolog 2	Mus musculus	34-38
11447266-3	2001	2-(Acetyloxy) benzoic acid 3-(nitrooxymethyl) phenyl ester (NCX-1000) is a chemical entity obtained by adding an NO-releasing moiety to ursodeoxycholic acid (UDCA), a compound that is selectively metabolized by hepatocytes.	Aspirin	0-26	T cell leukemia homeobox 2	Homo sapiens	60-63
11386043-2	2001	Patients receiving anti-GP IIb-IIIa therapy have a lower risk of death or myocardial infarction than those receiving the classic anti-agregant, aspirin, alone.	Aspirin	144-151	integrin subunit alpha 2b	Homo sapiens	24-30
11273998-3	2001	METHODS AND RESULTS: For dose-finding, the effect of aspirin (1, 2, 5, and 10 mmol/L) on the tumor necrosis factor-alpha-induced upregulation of intercellular adhesion molecule-1 was analyzed in monocultures of human coronary endothelial cells (HCAEC) and the SMCs of the human coronary media (HCMSMC).	Aspirin	53-60	intercellular adhesion molecule 1	Homo sapiens	145-178
11273998-4	2001	In cytoflow and Northern blot experiments, the expression of intercellular adhesion molecule-1 was slightly reduced after incubation with 5 mmol/L aspirin, and strong inhibition was found after incubation with 10 mmol/L.	Aspirin	147-154	intercellular adhesion molecule 1	Homo sapiens	61-94
11238189-8	2001	DNA synthesis of the cell line (Panc-1) with an activating point mutation in codon 12 of the ki-ras gene was significantly stimulated by NNK when cells were maintained in complete medium and this response was inhibited by the beta-blocker ICI118,551, the COX-inhibitor aspirin, or the 5-lipox-inhibitor MK-886.	Aspirin	269-276	KRAS proto-oncogene, GTPase	Homo sapiens	93-99
11226331-4	2001	Here, we show that a NO-releasing aspirin derivative (NCX-4016) reduces the degree of restenosis after balloon angioplasty in low-density lipoprotein receptor-deficient mice and this effect is associated with reduced vascular smooth muscle cell (VSMC) proliferation and macrophage deposition at the site of injury.	Aspirin	34-41	low density lipoprotein receptor	Mus musculus	126-158
11097175-0	2000	Amidation of salicyluric acid and gentisuric acid: a possible role for peptidylglycine alpha-amidating monooxygenase in the metabolism of aspirin.	Aspirin	138-145	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	71-116
11097175-2	2000	Two known metabolites of aspirin, salicyluric acid and gentisuric acid, are also substrates for PAM, leading to the formation of salicylamide and gentisamide.	Aspirin	25-32	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	96-99
7671259-2	1995	In the present report we describe that in human erythroleukemic cells, aspirin (400 microM), when administered during or immediately after a hyperthermic treatment, causes an increase in the amount of HSP70 synthesized and prolongs HSP70 synthesis for a period of several hours.	Aspirin	71-78	heat shock protein family A (Hsp70) member 4	Homo sapiens	201-206
7671259-2	1995	In the present report we describe that in human erythroleukemic cells, aspirin (400 microM), when administered during or immediately after a hyperthermic treatment, causes an increase in the amount of HSP70 synthesized and prolongs HSP70 synthesis for a period of several hours.	Aspirin	71-78	heat shock protein family A (Hsp70) member 4	Homo sapiens	232-237
7671259-4	1995	In the presence of aspirin, the heat shock transcription factor is maintained in the activated DNA-binding state for a period twice as long as control, an effect which results in enhanced and prolonged HSP70 mRNA transcription.	Aspirin	19-26	heat shock protein family A (Hsp70) member 4	Homo sapiens	202-207
7671259-7	1995	On the other hand, the ability of aspirin to enhance HSP70 synthesis suggests that nonsteroidal anti-inflammatory drugs could potentiate the cytoprotective role of HSPs in pathological states, including fever, inflammation, and ischemia.	Aspirin	34-41	heat shock protein family A (Hsp70) member 4	Homo sapiens	53-58
8774994-1	1995	Recent studies have indicated that aspirin promotes neutrophil adherence to endothelium via CD11/CD18-dependent interactions with intercellular adhesion molecule 1, which subsequently leads to neutrophil-mediated cell injury.	Aspirin	35-42	intercellular adhesion molecule 1	Rattus norvegicus	130-163
7899465-2	1995	We studied the effect of aspirin (ASA) on secretin- and cholecystokinin (CCK)- or meal-stimulated pancreatic secretion.	Aspirin	25-32	cholecystokinin	Rattus norvegicus	73-76
7899465-2	1995	We studied the effect of aspirin (ASA) on secretin- and cholecystokinin (CCK)- or meal-stimulated pancreatic secretion.	Aspirin	34-37	cholecystokinin	Rattus norvegicus	56-71
7899465-2	1995	We studied the effect of aspirin (ASA) on secretin- and cholecystokinin (CCK)- or meal-stimulated pancreatic secretion.	Aspirin	34-37	cholecystokinin	Rattus norvegicus	73-76
7899465-11	1995	ASA, but not SA inhibited the secretin- and CCK-stimulated pancreatic secretion including volume, bicarbonate, and protein in a dose-dependent manner without affecting basal pancreatic secretion.	Aspirin	0-3	cholecystokinin	Rattus norvegicus	44-47
8171410-0	1994	Effect of aspirin and clopidogrel on platelet-dependent tissue factor expression in endothelial cells.	Aspirin	10-17	coagulation factor III, tissue factor	Rattus norvegicus	56-69
8103026-6	1993	Incubation of neutrophils with aspirin increased surface expression of CD11b and CD18 on neutrophils.	Aspirin	31-38	integrin subunit alpha M	Homo sapiens	71-76
8103026-7	1993	The aspirin-induced increase in PMN adherence to HUVEC was significantly reduced by monoclonal antibodies against CD18, CD11b, CD11a, and intercellular adhesion molecule 1.	Aspirin	4-11	integrin subunit alpha M	Homo sapiens	120-125
8103026-7	1993	The aspirin-induced increase in PMN adherence to HUVEC was significantly reduced by monoclonal antibodies against CD18, CD11b, CD11a, and intercellular adhesion molecule 1.	Aspirin	4-11	intercellular adhesion molecule 1	Homo sapiens	138-171
8103026-8	1993	Aspirin-induced neutrophil adhesion was diminished by treatment with either a lipoxygenase inhibitor or a leukotriene B4 (LTB4) receptor antagonist.	Aspirin	0-7	leukotriene B4 receptor	Homo sapiens	106-136
8103026-9	1993	CONCLUSIONS: These studies indicate that aspirin promotes neutrophil adherence to endothelium via CD11a/CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule 1; the adhesion response is partially mediated by leukotriene B4.	Aspirin	41-48	integrin subunit alpha M	Homo sapiens	114-119
8510013-0	1993	The gastrin/cholecystokinin-B receptor antagonist L-365,260 reduces basal acid secretion and prevents gastrointestinal damage induced by aspirin, ethanol and cysteamine in the rat.	Aspirin	137-144	gastrin	Rattus norvegicus	4-11
8469685-4	1993	The significant increase in TXB2 concentrations in plasma and bronchoalveolar lavage (BAL) after ET-1 challenge (15-fold and 4-fold, respectively) have been reduced or abolished by ASA as well as HOE 944 and not altered by BM 13177.	Aspirin	181-184	endothelin-1	Cavia porcellus	97-101
8443857-7	1993	Aspirin and indomethacin potentiated the responses to ET-1 at very low PCO2 more than at normal PCO2, but attenuated the responses to low concentration of ET-1 at high PCO2.	Aspirin	0-7	endothelin-1	Cavia porcellus	54-58
8443857-7	1993	Aspirin and indomethacin potentiated the responses to ET-1 at very low PCO2 more than at normal PCO2, but attenuated the responses to low concentration of ET-1 at high PCO2.	Aspirin	0-7	endothelin-1	Cavia porcellus	155-159
1602386-11	1992	The glucocorticoid-receptor antagonist, RU 38486, also potentiated aspirin-induced gastric damage and reduced the gastroprotective efficacy of IL-1 without modifying its effect on gastric fluid volume.	Aspirin	67-74	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	4-27
1891476-0	1991	Thrombopoietin production in mice treated with acetylsalicylic acid.	Aspirin	47-67	thrombopoietin	Mus musculus	0-14
1891476-8	1991	The results support the hypothesis that platelet production in ASA-treated mice is elevated by release and action of thrombopoietin.	Aspirin	63-66	thrombopoietin	Mus musculus	117-131
2358373-1	1990	Male and female juvenile as well as adult rats were treated with acetylsalicylic acid in order to examine the effect of the drug on over-all activity and activity distribution of phosphoenolpyruvate carboxykinase (PEPCK) in the liver acinus.	Aspirin	65-85	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	214-219
2358373-2	1990	Upon administration of acetylsalicylic acid PEPCK activity increased in juvenile males and adult females, but was reduced in juvenile females and adult males.	Aspirin	23-43	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	44-49
33590615-8	2021	In platelets, the opening of the channel Kca 1.1 led to a reduced sensitivity to agonists with blunted aggregation in response to ADP, with an inhibitory capacity additive to that of aspirin.	Aspirin	183-190	potassium calcium-activated channel subfamily M alpha 1	Homo sapiens	41-48
33795788-4	2021	In order to optimize antiplatelet therapy for these patients and avoid the waste of medical resources, it is important to identify the subgroups that genuinely benefit from DAPT with clopidogrel plus aspirin through CYP2C19 genotyping.	Aspirin	200-207	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	216-223
33772362-14	2022	CONCLUSION: ASA-induced RBBB is associated with a higher volume of infused ethanol and higher maximum CK release.	Aspirin	12-15	cytidine/uridine monophosphate kinase 1	Homo sapiens	102-104
33785950-12	2021	The decrease in ASA and subsequent decrease in regulatory T cell population was due to the strong negative correlation between regulatory T cells and IL-10 (r = -0.817, p = 0.004).	Aspirin	16-19	interleukin 10	Homo sapiens	150-155
34875953-0	2022	Combined apocyanin and aspirin treatment activates the PI3K/Nrf2/HO-1 signaling pathway and ameliorates preeclampsia symptoms in rats.	Aspirin	23-30	heme oxygenase 1	Rattus norvegicus	65-69
34875953-9	2022	Meanwhile, compared with single-dose apocyanin or aspirin, the combined treatment significantly corrected abnormal pregnancy outcomes, decreased sFlt-1 and PlGF, and alleviated oxidative stress both in blood and placental tissues.	Aspirin	50-57	placental growth factor	Rattus norvegicus	156-160
34875953-10	2022	Moreover, the combined treatment upregulated PI3K, Akt, Nrf2, and HO-1 protein levels in the placental tissues from PE rats.Conclusion: Overall, our results suggested that combined treatment of apocyanin and aspirin ameliorates the PE symptoms compared with single-dose apocyanin or aspirin in a PE rat model.	Aspirin	208-215	heme oxygenase 1	Rattus norvegicus	66-70
34875953-10	2022	Moreover, the combined treatment upregulated PI3K, Akt, Nrf2, and HO-1 protein levels in the placental tissues from PE rats.Conclusion: Overall, our results suggested that combined treatment of apocyanin and aspirin ameliorates the PE symptoms compared with single-dose apocyanin or aspirin in a PE rat model.	Aspirin	283-290	heme oxygenase 1	Rattus norvegicus	66-70
34495376-2	2021	Recent studies with the direct factor Xa inhibitor rivaroxaban in combination with low-dose aspirin demonstrated a significant reduction of major cardiovascular events, especially in individuals with type 2 diabetes and proven cardiovascular disease.	Aspirin	92-99	coagulation factor X	Homo sapiens	31-40
34851561-3	2021	The aim was to investigate the association between presence of the CYP2C19*2 allele and ISR within one-year after PCI in patients prescribed dual antiplatelet therapy with aspirin and clopidogrel.	Aspirin	172-179	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
34901735-7	2021	We found that antiplatelet medication acetylsalicylic acid (ASA) led to reduced chemokine (CC motif) ligand 5 (CCL5) and chemokine (CXC motif) ligand 4 (CXCL4) release from platelets, while leukocyte chemotaxis was not affected.	Aspirin	38-58	C-C motif chemokine ligand 5	Homo sapiens	111-115
34901735-7	2021	We found that antiplatelet medication acetylsalicylic acid (ASA) led to reduced chemokine (CC motif) ligand 5 (CCL5) and chemokine (CXC motif) ligand 4 (CXCL4) release from platelets, while leukocyte chemotaxis was not affected.	Aspirin	60-63	C-C motif chemokine ligand 5	Homo sapiens	111-115
34631738-8	2021	The odds of smoking, statins, aspirin and beta-blocker use were decreased in MCi in reference to CC (all p < 0.05), 29 (74.35%) patients with unresolved symptoms underwent repeat colonoscopies with biopsies.	Aspirin	30-37	multiciliate differentiation and DNA synthesis associated cell cycle protein	Homo sapiens	77-80
34688318-7	2021	However, in the Notch3 mutation mouse model, cerebral infarction and hemorrhage often occurred after being treated with aspirin.	Aspirin	120-127	notch 3	Mus musculus	16-22
34428217-5	2021	Experiments demonstrate for the first time that plasma concentrations of Acetylsalicylic acid significantly increased TLR ligand-triggered IL-1beta, IL-10, and IL-6 production in a dose-dependent manner.	Aspirin	73-93	interleukin 10	Homo sapiens	149-154
34575604-4	2021	A quantitative PCR (qPCR) validation study of PTGDR2 that encodes for CRTH2 receptor, expressed in cells involved in T2 inflammation, was developed in a cohort of 361 independent subjects: 94 non-asthmatic non-atopic controls, 187 asthmatic patients (including 82 with chronic rhinosinusitis with nasal polyposis (CRSwNP) and 24 with aspirin-exacerbated respiratory disease (AERD)), 52 with allergic rhinitis, and 28 with CRSwNP without asthma.	Aspirin	334-341	prostaglandin D2 receptor 2	Homo sapiens	46-52
34429873-6	2021	Additionally, high expression of the hydroxyprostaglandin dehydrogenase gene, HPGD encoding prostaglandin-degrading enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH) and low expression of the proteoglycan 2 gene, PRG2 encoding constituent of the eosinophil granule in sputum cells might serve as a predictor of good response to aspirin therapy.	Aspirin	333-340	carbonyl reductase 1	Homo sapiens	123-160
34429873-6	2021	Additionally, high expression of the hydroxyprostaglandin dehydrogenase gene, HPGD encoding prostaglandin-degrading enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH) and low expression of the proteoglycan 2 gene, PRG2 encoding constituent of the eosinophil granule in sputum cells might serve as a predictor of good response to aspirin therapy.	Aspirin	333-340	carbonyl reductase 1	Homo sapiens	162-169
35535453-6	2022	In both cell lines, treatment of miR-302/367-transfected cells with aspirin upregulated expression of some main pluripotency factors such as OCT4, SOX2, NANOG, and KLF4, and downregulated expression of some invasion and angiogenesis markers at gene and protein levels.	Aspirin	68-75	SRY-box transcription factor 2	Homo sapiens	147-151
35535453-6	2022	In both cell lines, treatment of miR-302/367-transfected cells with aspirin upregulated expression of some main pluripotency factors such as OCT4, SOX2, NANOG, and KLF4, and downregulated expression of some invasion and angiogenesis markers at gene and protein levels.	Aspirin	68-75	Nanog homeobox	Homo sapiens	153-158
35535453-6	2022	In both cell lines, treatment of miR-302/367-transfected cells with aspirin upregulated expression of some main pluripotency factors such as OCT4, SOX2, NANOG, and KLF4, and downregulated expression of some invasion and angiogenesis markers at gene and protein levels.	Aspirin	68-75	Kruppel like factor 4	Homo sapiens	164-168
35535453-8	2022	Both miR-302/367 and aspirin upregulated the expression of FOXD3 protein which is a known inducer of OCT4 and NANOG.	Aspirin	21-28	Nanog homeobox	Homo sapiens	110-115
35506370-8	2022	TDO inhibition and increased free Trp availability by salicylate may underpin the antidepressant effect of aspirin and distinguish it from other nonsteroidal antiinflammatory drugs.	Aspirin	107-114	tryptophan 2,3-dioxygenase	Homo sapiens	0-3
35392432-8	2022	ASP treatment also caused downregulated PD-L1 and Ki-67 levels in mice tumors.	Aspirin	0-3	antigen identified by monoclonal antibody Ki 67	Mus musculus	50-55
35111059-12	2021	Posttreatment with aspirin also reduced hyperoxia-induced increases in the numbers of lung macrophages, intracellular ROS levels, and the expression of TNF-alpha, IL-1beta, and IL-4; it also increased CC10, SPC and Nrp-1 levels compared with hyperoxia exposure alone.	Aspirin	19-26	secretoglobin, family 1A, member 1 (uteroglobin)	Mus musculus	201-205
11064108-7	2000	The increases in plasma PAF correlated well with the ASA-associated decreases in body temperature, suggesting that PAF plays an important role in ASA in W/W(v) mice.	Aspirin	53-56	patchy fur	Mus musculus	24-27
11064108-7	2000	The increases in plasma PAF correlated well with the ASA-associated decreases in body temperature, suggesting that PAF plays an important role in ASA in W/W(v) mice.	Aspirin	53-56	patchy fur	Mus musculus	115-118
11064108-7	2000	The increases in plasma PAF correlated well with the ASA-associated decreases in body temperature, suggesting that PAF plays an important role in ASA in W/W(v) mice.	Aspirin	146-149	patchy fur	Mus musculus	24-27
11064108-7	2000	The increases in plasma PAF correlated well with the ASA-associated decreases in body temperature, suggesting that PAF plays an important role in ASA in W/W(v) mice.	Aspirin	146-149	patchy fur	Mus musculus	115-118
11046058-3	2000	Here, we tested the hypothesis that NCX-4016, a NO-aspirin derivative, inhibits proinflammatory cytokine release from endotoxin (LPS)-challenged monocytes.	Aspirin	51-58	T cell leukemia homeobox 2	Homo sapiens	36-39
10860637-4	2000	The relaxing effect of A II was also mediated through the release of cyclo-oxygenase products of arachidonic acid, as evidenced by the inhibition of the response by lysine acetylsalicylic acid (ASA) pretreatment.	Aspirin	194-197	arginase type II	Mus musculus	23-27
10811139-0	2000	Aspirin inhibits tumor cell invasiveness induced by Epstein-Barr virus latent membrane protein 1 through suppression of matrix metalloproteinase-9 expression.	Aspirin	0-7	PDZ and LIM domain 7	Homo sapiens	71-96
10811139-9	2000	Treatment with aspirin or sodium salicylate inhibited invasiveness of the LMP1-expressing C33A cells (P &lt; 0.03) and suppressed both the LMP1-induced MMP-9 expression in zymographic analyses and LMP1-induced MMP-9 promoter activity in CAT reporter assays (P &lt; 0.01).	Aspirin	15-22	PDZ and LIM domain 7	Homo sapiens	74-78
10811139-9	2000	Treatment with aspirin or sodium salicylate inhibited invasiveness of the LMP1-expressing C33A cells (P &lt; 0.03) and suppressed both the LMP1-induced MMP-9 expression in zymographic analyses and LMP1-induced MMP-9 promoter activity in CAT reporter assays (P &lt; 0.01).	Aspirin	15-22	PDZ and LIM domain 7	Homo sapiens	139-143
10811139-9	2000	Treatment with aspirin or sodium salicylate inhibited invasiveness of the LMP1-expressing C33A cells (P &lt; 0.03) and suppressed both the LMP1-induced MMP-9 expression in zymographic analyses and LMP1-induced MMP-9 promoter activity in CAT reporter assays (P &lt; 0.01).	Aspirin	15-22	matrix metallopeptidase 9	Homo sapiens	152-157
10811139-9	2000	Treatment with aspirin or sodium salicylate inhibited invasiveness of the LMP1-expressing C33A cells (P &lt; 0.03) and suppressed both the LMP1-induced MMP-9 expression in zymographic analyses and LMP1-induced MMP-9 promoter activity in CAT reporter assays (P &lt; 0.01).	Aspirin	15-22	PDZ and LIM domain 7	Homo sapiens	139-143
10811139-9	2000	Treatment with aspirin or sodium salicylate inhibited invasiveness of the LMP1-expressing C33A cells (P &lt; 0.03) and suppressed both the LMP1-induced MMP-9 expression in zymographic analyses and LMP1-induced MMP-9 promoter activity in CAT reporter assays (P &lt; 0.01).	Aspirin	15-22	matrix metallopeptidase 9	Homo sapiens	210-215
10811139-17	2000	These results suggest that aspirin may be able to suppress invasion and metastasis of EBV-associated tumors that express LMP1 by suppression of MMP-9.	Aspirin	27-34	PDZ and LIM domain 7	Homo sapiens	121-125
10811139-17	2000	These results suggest that aspirin may be able to suppress invasion and metastasis of EBV-associated tumors that express LMP1 by suppression of MMP-9.	Aspirin	27-34	matrix metallopeptidase 9	Homo sapiens	144-149
10793178-7	2000	GP IIb/IIIa inhibitors have been shown to improve angiographic Thrombolysis in Myocardial Infarction (TIMI) 3 flow rates when used as reperfusion therapy given with heparin and aspirin as compared with heparin and aspirin alone.	Aspirin	177-184	integrin subunit alpha 2b	Homo sapiens	0-6
10793178-7	2000	GP IIb/IIIa inhibitors have been shown to improve angiographic Thrombolysis in Myocardial Infarction (TIMI) 3 flow rates when used as reperfusion therapy given with heparin and aspirin as compared with heparin and aspirin alone.	Aspirin	214-221	integrin subunit alpha 2b	Homo sapiens	0-6
2546284-3	1989	These effects were also observed with aspirin-treated platelets stimulated with thrombin.	Aspirin	38-45	prothrombin	Oryctolagus cuniculus	80-88
10807421-8	2000	CONCLUSION: Growth factors, including HGF, EGF and IGF-I, reversed the aspirin-induced inhibition of wound repair through their cytoprotective effects on gastric epithelial cells.	Aspirin	71-78	hepatocyte growth factor	Oryctolagus cuniculus	38-41
10818443-6	2000	This contrasts with activation of the LXA4 receptor by an aspirin-triggered lipoxin A4 mimetic that before leukotriene B4 gave an inverse relationship with rapidly increasing PSDP levels, and inhibition of both PLD activity and superoxide generation.	Aspirin	58-65	phospholipid phosphatase 6	Homo sapiens	175-179
10556149-2	1999	In blood-free perfused and ventilated rat lungs, PAF increased lung weight by 0.59 +/- 0.18 g. The cyclooxygenase inhibitor aspirin (500 microM) blocked this response by one-third, and the quinolines quinine (330 microM), quinidine (100 microM), and chloroquine (100 microM) by two-thirds.	Aspirin	124-131	PCNA clamp associated factor	Rattus norvegicus	49-52
10556149-4	1999	In combination with aspirin, quinine or quinidine completely prevented PAF-induced weight gain and the concomitant increase of the capillary filtration coefficient (K(f,c)).	Aspirin	20-27	PCNA clamp associated factor	Rattus norvegicus	71-74
10502232-2	1999	Studies in patients scheduled for percutaneous coronary intervention and those with unstable angina or non-Q-wave myocardial infarction have shown that a combination of intravenous GP IIb-IIIa inhibitors with aspirin and heparin is associated with a reduction in death or myocardial infarction compared with therapy with aspirin and heparin alone.	Aspirin	321-328	integrin subunit alpha 2b	Homo sapiens	181-187
10501189-9	1999	The results of our experiments provide a further understanding of the effects of estrogen and aspirin on astroglial cells exposed to A beta and LPS.	Aspirin	94-101	amyloid beta precursor protein	Rattus norvegicus	133-139
10581998-6	1999	Among antiplatelet agents, the logic combination of aspirin and ticlopidine or clopidogrel is already challenging the anti-GP IIb/IIIa orally active compounds.	Aspirin	52-59	integrin subunit alpha 2b	Homo sapiens	123-129
10096266-1	1999	BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and indomethacin (INN, indometacin) inhibit both the constitutive (COX-1) and inducible (COX-2) isoforms of cyclooxygenase.	Aspirin	66-73	cytochrome c oxidase subunit II	Cricetulus griseus	175-180
10092995-5	1999	In addition, aspirin significantly inhibited iNOS protein expression in BVSMCs and reduced the translocation of the nuclear factor-kappa B (NF-kappa B).	Aspirin	13-20	nitric oxide synthase 2	Bos taurus	45-49
10092995-7	1999	CONCLUSION: High doses of aspirin inhibited iNOS protein expression in BVSMCs and decreased NF-kappa B mobilization.	Aspirin	26-33	nitric oxide synthase 2	Bos taurus	44-48
10092995-8	1999	The inhibition of iNOS expression by aspirin was further associated with a reduced ability of BVSMCs to produce TNF-alpha.	Aspirin	37-44	nitric oxide synthase 2	Bos taurus	18-22
10203577-13	1999	In addition, aspirin and indomethacin, but not CyA, induced Hsp70 expression in HUVECs that correlated with induction of HSF-1 activity.	Aspirin	13-20	heat shock protein family A (Hsp70) member 4	Homo sapiens	60-65
10203577-14	1999	CONCLUSION: Our results show that the tested agents (except indomethacin) are inhibitors of the T cell-mediated immune response, as expected, that aspirin is an effective suppressor of adhesion molecule expression, and that all three agents can induce Hsp60 in HUVECs.	Aspirin	147-154	heat shock protein family D (Hsp60) member 1	Homo sapiens	252-257
9925295-1	1998	Antagonists of the glycoprotein GPIIb/IIIa are a promising class of antithrombotic agents offering potential advantages over present antiplatelet agents (i.e., aspirin and ticlopidine).	Aspirin	160-167	integrin subunit alpha 2b	Homo sapiens	32-37
9851747-0	1998	The first commercial bottle of aspirin: March 6, 1899.	Aspirin	31-38	membrane associated ring-CH-type finger 6	Homo sapiens	40-47
3142075-6	1988	Inhibition of the effects of thrombin and PAF was also observed with aspirin-treated platelets.	Aspirin	69-76	prothrombin	Oryctolagus cuniculus	29-37
3517511-4	1986	Since the recovery of prostacyclin production in aspirin treated cells was stimulated by interleukin-2, our results suggest that the stimulatory effect of interleukin-2 on prostacyclin synthesis is at least partially mediated by the de novo synthesis of cyclooxygenase.	Aspirin	49-56	interleukin 2	Bos taurus	89-102
3517511-4	1986	Since the recovery of prostacyclin production in aspirin treated cells was stimulated by interleukin-2, our results suggest that the stimulatory effect of interleukin-2 on prostacyclin synthesis is at least partially mediated by the de novo synthesis of cyclooxygenase.	Aspirin	49-56	interleukin 2	Bos taurus	155-168
3707547-1	1986	The present study has utilized the iodinatable cross-linking agent N-hydroxysuccinimidyl-4-azidosalicylic acid (ASA) to examine the specific interaction between the proline-rich glycoprotein (PRG) of human parotid saliva and Streptococcus sanguis G9B.	Aspirin	112-115	proline rich protein BstNI subfamily 3	Homo sapiens	165-190
3707547-6	1986	1% of the 125I-ASA-PRG was cross-linked to the bacterial surface.	Aspirin	15-18	proline rich protein BstNI subfamily 3	Homo sapiens	19-22
2869642-6	1986	When vagal stimulations were performed after the rats had been pretreated with aspirin or indomethacin, more somatostatin than gastrin was detected in the perfusate independently of the perfusate pH.	Aspirin	79-86	gastrin	Rattus norvegicus	127-134
3766258-9	1986	Treatment for one week with a diet containing clofibrate (0.25%), tiadenol (0.5%) or acetylsalicylic acid (1%) caused a 8, 13 and 5 fold increase in cytosolic epoxide hydrolase activity respectively in the liver which parallelled the induction of peroxisomal beta-oxidation activity (13, 19 and 5 fold, respectively).	Aspirin	85-105	epoxide hydrolase 2	Rattus norvegicus	149-176
2420162-5	1985	This study shows that progressive structural changes in the ASA molecule can shift the pharmacological profile from a cyclooxygenase inhibitor (ASA) to an inactive compound (ABA) to a PDE inhibitor (3-MP) and back again to a cyclooxygenase inhibitor (3-HMP).	Aspirin	60-63	inner membrane mitochondrial protein	Homo sapiens	253-256
6430802-1	1984	3-Hydroperoxy-3-methylphthalide (3-HMP), a structural analog of acetylsalicylic acid (ASA), was found to have some antiinflammatory properties which are distinct from those of ASA.	Aspirin	64-84	inner membrane mitochondrial protein	Homo sapiens	35-38
6430802-1	1984	3-Hydroperoxy-3-methylphthalide (3-HMP), a structural analog of acetylsalicylic acid (ASA), was found to have some antiinflammatory properties which are distinct from those of ASA.	Aspirin	86-89	inner membrane mitochondrial protein	Homo sapiens	35-38
6430802-3	1984	3-HMP inhibits prostaglandin and thromboxane production from exogenous [14C]arachidonic acid by human platelet lysates in vitro and does so at lower concentrations than ASA (3-HMP IC50 = 10 microM; ASA IC50 = 50 microM).	Aspirin	198-201	inner membrane mitochondrial protein	Homo sapiens	2-5
6711391-4	1984	Incubation of PLC1 in Tyrode"s buffer or acetylsalicylic acid (ASA), but not salicylate, resulted in a time-dependent loss of PAF activity.	Aspirin	41-61	phospholipase C beta 1	Rattus norvegicus	14-18
6711391-4	1984	Incubation of PLC1 in Tyrode"s buffer or acetylsalicylic acid (ASA), but not salicylate, resulted in a time-dependent loss of PAF activity.	Aspirin	41-61	PCNA clamp associated factor	Rattus norvegicus	126-129
6711391-4	1984	Incubation of PLC1 in Tyrode"s buffer or acetylsalicylic acid (ASA), but not salicylate, resulted in a time-dependent loss of PAF activity.	Aspirin	63-66	phospholipase C beta 1	Rattus norvegicus	14-18
6711391-4	1984	Incubation of PLC1 in Tyrode"s buffer or acetylsalicylic acid (ASA), but not salicylate, resulted in a time-dependent loss of PAF activity.	Aspirin	63-66	PCNA clamp associated factor	Rattus norvegicus	126-129
6711391-9	1984	These studies suggest that ASA regulates PAF availability unrelated to its effect on cyclooxygenase and that MC membrane products directly inhibit PAF activity from rat PLC.	Aspirin	27-30	PCNA clamp associated factor	Rattus norvegicus	41-44
6442910-4	1984	Rats treated in vivo with different doses of acetylsalicylic acid or of tranylcypromine, two cyclo-oxygenase inhibitors, abolished the aggregation differences between arterial and venous PRP.	Aspirin	45-65	proline rich protein 2-like 1	Rattus norvegicus	187-190
6315014-2	1983	The non-steroidal anti-inflammatory drugs indomethacin and aspirin inhibited PGE2 synthesis by RBL-1 cells, which had been stimulated with the calcium ionophore A-23187, in a dose-dependent manner with an IC50 of 0.7 and 7.8 microM respectively.	Aspirin	59-66	RB transcriptional corepressor like 1	Rattus norvegicus	95-100
6821701-3	1983	Thus, in these experiments we examined the effect of aspirin (a weak inhibitor of thrombin-mediated platelet aggregation) under conditions in which thrombin was a major factor in the initiation and growth of the thrombi.	Aspirin	53-60	prothrombin	Oryctolagus cuniculus	82-90
6821701-7	1983	The tendency to inhibit thrombus formation appeared to be unrelated to an effect on platelets but was associated with prolongation of the one-stage prothrombin time and increased whole blood fibrinolytic activity; doses of aspirin that inhibited platelet  aggregation in response to sodium arachidonate or collagen, and PGI2 formation by the vessel wall, did not have a significant effect on the amount of thrombus present at 5 days.	Aspirin	223-230	prothrombin	Oryctolagus cuniculus	148-159
6403485-5	1983	When the antihistamine, pyrilamine, was included with either indomethacin or aspirin, the C3a response was inhibited further, although pyrilamine alone had no effect.	Aspirin	77-84	complement C3	Homo sapiens	90-93
99321-1	1978	Salicylic acid, 1,10- and 1,7-phenanthroline prevented inhibition by aspirin of platelet aggregation and of generation of thromboxane A2 due to arachidonic acid, to the ionophore A21387, to thrombin and to collagen.	Aspirin	69-76	prothrombin	Oryctolagus cuniculus	190-198
191476-3	1977	Enhanced accumulation of cyclic GMP produced by arachidonic or collagen was prevented by prior exposure of platelets to aspirin or indomethacin.	Aspirin	120-127	5'-nucleotidase, cytosolic II	Homo sapiens	32-35
4362746-2	1974	Collagen increased and aspirin decreased the cyclic [(3)H]GMP concentration in platelets.	Aspirin	23-30	5'-nucleotidase, cytosolic II	Homo sapiens	58-61
5432368-5	1970	Further studies disclosed that both salicylate and gentisate competitively inhibited the G-6-PD from the ASA-sensitive patient resulting in a marked change in the K(m) for NADP.	Aspirin	105-108	glucose-6-phosphate dehydrogenase	Homo sapiens	89-95
5432368-10	1970	In this connection, gentisate seems to play a major role in ASA-induced hemolysis for it is both a G-6-PD inhibitor and an "oxidant."	Aspirin	60-63	glucose-6-phosphate dehydrogenase	Homo sapiens	99-105
5929266-0	1966	Influence of the ABO blood group and salivary ABH secretor status on the cell-removing effect of aspirin on human gastric mucosa.	Aspirin	97-104	ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase	Homo sapiens	17-32
9869155-2	1998	Despite this, the preferential use of aspirin has been supported by an American cost-effectiveness analysis (JAMA 1995; 273: 965).	Aspirin	38-45	F11 receptor	Homo sapiens	109-113
5929266-0	1966	Influence of the ABO blood group and salivary ABH secretor status on the cell-removing effect of aspirin on human gastric mucosa.	Aspirin	97-104	alkB homolog 1, histone H2A dioxygenase	Homo sapiens	46-49
33964545-7	2021	Acetylsalicylic acid resistance was an independent predictor of poor 90 days outcome (OR for modified Rankin scale (mRS) <= 2: 0.10 95% CI: 0.02 - 0.69) whereas Clopidogrel resistance was an independent predictor of good outcome (OR for mRS <= 2: 7.09 95%CI: 1.33 - 37.72).	Aspirin	0-20	sterile alpha motif domain containing 11	Mus musculus	116-119
33964545-7	2021	Acetylsalicylic acid resistance was an independent predictor of poor 90 days outcome (OR for modified Rankin scale (mRS) <= 2: 0.10 95% CI: 0.02 - 0.69) whereas Clopidogrel resistance was an independent predictor of good outcome (OR for mRS <= 2: 7.09 95%CI: 1.33 - 37.72).	Aspirin	0-20	sterile alpha motif domain containing 11	Mus musculus	237-240
9784604-11	1998	(B) Neutrophil stimulation (PMN group/ASA group) evoked a rapid increase in DeltaPAP and MPO activity, while the changes in vascular permeability were rather moderate, but still significant.	Aspirin	38-41	myeloperoxidase	Oryctolagus cuniculus	89-92
33917483-12	2021	Targeting the PKA-CREB/ATF1 axis may be a strategy to improve the therapeutic effects of aspirin on HCC.	Aspirin	89-96	cAMP responsive element binding protein 1	Homo sapiens	18-22
33574709-0	2021	siRNA Knockdown of REDD1 Facilitates Aspirin-Mediated Dephosphorylation of mTORC1 Target 4E-BP1 in MDA-MB-468 Human Breast Cancer Cell Line.	Aspirin	37-44	DNA damage inducible transcript 4	Homo sapiens	19-24
33574709-6	2021	Knockdown by siRNA approach was applied to assess the role of REDD1/DDIT4 (DNA damage-inducible transcript 4) in mTORC1 inhibition by aspirin.	Aspirin	134-141	DNA damage inducible transcript 4	Homo sapiens	62-67
33574709-6	2021	Knockdown by siRNA approach was applied to assess the role of REDD1/DDIT4 (DNA damage-inducible transcript 4) in mTORC1 inhibition by aspirin.	Aspirin	134-141	DNA damage inducible transcript 4	Homo sapiens	68-73
9809499-9	1998	As PGE2 promotes TH2 and inhibits THI type cytokine generation, we hypothesize that the decreased use of aspirin may be a factor in facilitating allergic sensitization and asthma by augmenting the relative TH1/TH2 cytokine imbalance in genetically predisposed children.	Aspirin	105-112	negative elongation factor complex member C/D	Homo sapiens	206-209
33574709-9	2021	Specifically, we found that aspirin and salicylic acid increase the expression of REDD1 protein, that is known for its suppressive function towards mTORC1.	Aspirin	28-35	DNA damage inducible transcript 4	Homo sapiens	82-87
33493277-0	2021	Aspirin reduces sFlt-1 mediated apoptosis of trophoblast cells in preeclampsia.	Aspirin	0-7	FMS-like tyrosine kinase 1	Mus musculus	16-22
33493277-3	2021	The aim of this study was to to reveal the underlying mechanism of aspirin in reducing sFlt-1 mediated apoptosis of trophoblast cells in preeclampsia.	Aspirin	67-74	FMS-like tyrosine kinase 1	Mus musculus	87-93
9641298-6	1998	The area of macroscopic damage was significantly reduced only in rats where hSP (200 micromol/L) was given in conjunction with ASA (P &lt; 0.05).	Aspirin	127-130	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	76-79
33493277-4	2021	Serum sFlt-1 and sEng profiles and placental oxidative stresslevels were significantly decreased in preeclampsia patients treated with aspirin compared with untreated patients without it, while serum PLGF and placental SOD profiles were increased in preeclampsia patients with aspirin.	Aspirin	135-142	FMS-like tyrosine kinase 1	Mus musculus	6-12
33467191-6	2021	In aspirin sensitive patients, the levels of COX1.2, COX1.3, COX1.4 and COX1.5 isoforms were higher compared to aspirin-tolerant patients.	Aspirin	3-10	cytochrome c oxidase assembly factor COX14	Homo sapiens	61-67
9413930-4	1998	ASA induced apoptosis in HT-29 colon adenocarcinoma cells at concentrations &gt; or =1 mM as established by: (a) morphological changes consistent with apoptosis in cells examined by fluorescence microscopy and semi-thin cell sections, and (b) DNA strand breaks: 45% of the cells were TdT-mediated dUTP nick end labeling (TUNEL) positive at 3 mM at 72 hr, and 70% were positive by the comet assay.	Aspirin	0-3	DNA nucleotidylexotransferase	Homo sapiens	284-287
9872509-16	1998	Addition to L-NAME of L-arginine, but not D-arginine, restored the protective and hyperemic effects of CCK-8 and duodenal oleate against gastric lesions induced by ethanol or acidified ASA.	Aspirin	185-188	cholecystokinin	Rattus norvegicus	103-106
33321293-3	2021	In this study, we designed a fully synthetic poly (ethylene) glycol (PEG)-based hydrogel to release the specialized pro-resolving lipid mediator aspirin-triggered resolvin-D1 (AT-RvD1) and recombinant human interleukin 10 (IL-10).	Aspirin	145-152	interleukin 10	Homo sapiens	207-221
33321293-3	2021	In this study, we designed a fully synthetic poly (ethylene) glycol (PEG)-based hydrogel to release the specialized pro-resolving lipid mediator aspirin-triggered resolvin-D1 (AT-RvD1) and recombinant human interleukin 10 (IL-10).	Aspirin	145-152	interleukin 10	Homo sapiens	223-228
33287104-0	2020	Antigiardial Activity of Acetylsalicylic Acid Is Associated with Overexpression of HSP70 and Membrane Transporters.	Aspirin	25-45	heat shock protein family A (Hsp70) member 4	Homo sapiens	83-88
33287104-8	2020	Using mass spectrometry and real-time quantitative reverse transcription (qRT-PCR), we identified that ASA induced the overexpression of heat shock protein 70 (HSP70).	Aspirin	103-106	heat shock protein family A (Hsp70) member 4	Homo sapiens	137-158
33287104-8	2020	Using mass spectrometry and real-time quantitative reverse transcription (qRT-PCR), we identified that ASA induced the overexpression of heat shock protein 70 (HSP70).	Aspirin	103-106	heat shock protein family A (Hsp70) member 4	Homo sapiens	160-165
9431267-0	1997	Reduced skin hyperemia during tap water iontophoresis after intake of acetylsalicylic acid.	Aspirin	70-90	nuclear RNA export factor 1	Homo sapiens	30-33
9480585-8	1997	GP IIb/IIIa-antagonists (antibodies, synthetic antagonists) significantly improve the clinical effects of aspirin.	Aspirin	106-113	integrin subunit alpha 2b	Homo sapiens	0-6
32930782-12	2020	Adequate adherence with aspirin results in an increase in ATL and IL-10 with reduced IL-8 plasma concentration.	Aspirin	24-31	interleukin 10	Homo sapiens	66-71
33247982-0	2021	Risks of adverse events for users of proton-pump inhibitors plus aspirin or clopidogrel in patients with aspirin-related ulcer bleeding.	Aspirin	105-112	ATPase H+/K+ transporting subunit alpha	Homo sapiens	37-48
9180245-7	1997	Treatment with aspirin inhibited NF-kappaB nuclear translocation and binding and was associated with reduction of ICAM-1 expression, SMC proliferation and neointimal thickening following balloon injury.	Aspirin	15-22	intercellular adhesion molecule 1	Rattus norvegicus	114-120
33121452-0	2020	Effectiveness and safety of high dose clopidogrel plus aspirin in ischemic stroke patients with the single CYP2C19 loss-of-function allele: a randomized trial.	Aspirin	55-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	107-114
33121452-11	2020	CONCLUSIONS: In patients with ischaemic stroke who had a single CYP2C19 loss-of-function allele and moderate to severe cerebral stenosis, fewer vascular events occurred within 3 months with high dose of clopidogrel and aspirin than with normal dose of clopidogrel and aspirin.	Aspirin	219-226	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
33121452-11	2020	CONCLUSIONS: In patients with ischaemic stroke who had a single CYP2C19 loss-of-function allele and moderate to severe cerebral stenosis, fewer vascular events occurred within 3 months with high dose of clopidogrel and aspirin than with normal dose of clopidogrel and aspirin.	Aspirin	268-275	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
32738656-6	2020	Such electrospun PLGA@ASA nanofiber coatings could promote proliferation and osteogenic differentiation of bone mesenchymal stem cells (BMSCs) as well as inhibit M1 polarization and RANKL-induced osteoclast differentiation of macrophages in vitro.	Aspirin	22-25	TNF superfamily member 11	Homo sapiens	182-187
8996217-1	1997	In Swiss 3T3 fibroblasts, aspirin inhibited proliferation induced by the complete mitogenic factors platelet-derived growth factor (PDGF) and bombesin.	Aspirin	26-33	gastrin releasing peptide	Homo sapiens	142-150
8996217-2	1997	Aspirin decreased the maximum mitogenic effect of bombesin without modifying the concentration necessary to obtain half maximal DNA synthesis stimulation.	Aspirin	0-7	gastrin releasing peptide	Homo sapiens	50-58
8996217-9	1997	The inhibitory effects of aspirin on PDGF or bombesin-stimulated DNA synthesis were counteracted by 280 nM prostaglandin E2.	Aspirin	26-33	gastrin releasing peptide	Homo sapiens	45-53
8972019-0	1996	Acetylsalicylic acid and sodium salicylate inhibit LPS-induced NF-kappa B/c-Rel nuclear translocation, and synthesis of tissue factor (TF) and tumor necrosis factor alfa (TNF-alpha) in human monocytes.	Aspirin	0-20	REL proto-oncogene, NF-kB subunit	Homo sapiens	74-79
32651213-8	2020	There was a significant interaction between expression level of RP11-89N17 and regular use of aspirin only on CRC risk (P-GxE=3.23x10-5).	Aspirin	94-101	pre-mRNA processing factor 31	Homo sapiens	64-68
8537043-5	1995	The first dose of ASA produced numerous gastric lesions and deep histological necrosis accompanied by a fall in the gastric blood flow, negligible expression of epidermal growth factor (EGF) and transforming growth factor alpha (TGF alpha) or their receptors, and no evidence of mucosal proliferation.	Aspirin	18-21	transforming growth factor alpha	Rattus norvegicus	229-238
8537043-6	1995	As adaptation to ASA developed, however, the areas of gastric lesions were reduced by more than 80% and there was a noticeable decrease in deep necrosis, a partial restoration of gastric blood flow, an approximately four-fold increase in EGF expression (but not in TGF alpha) and its receptors, and an appreciable increase in mucosal cell proliferation compared with vehicle treated rats.	Aspirin	17-20	transforming growth factor alpha	Rattus norvegicus	265-274
32755422-4	2020	AREAS COVERED: The COMPASS trial demonstrated that in patients with stable atherosclerotic disease, very low-dose rivaroxaban, a direct factor Xa inhibitor, when combined with aspirin, reduced the rate of recurrent ischemic events, at the cost of increased bleeding.	Aspirin	176-183	coagulation factor X	Homo sapiens	136-145
32847114-6	2020	We initially characterized resveratrol-aspirin derivatives as products that can inhibit cytochrome P450 Family 1 Subfamily A Member 1 (CYP1A1) activity, DNA methyltransferase (DNMT) activity, and cyclooxygenase (COX) activity.	Aspirin	39-46	DNA methyltransferase 1	Homo sapiens	153-174
32847114-6	2020	We initially characterized resveratrol-aspirin derivatives as products that can inhibit cytochrome P450 Family 1 Subfamily A Member 1 (CYP1A1) activity, DNA methyltransferase (DNMT) activity, and cyclooxygenase (COX) activity.	Aspirin	39-46	DNA methyltransferase 1	Homo sapiens	176-180
32487324-7	2020	Yet Aspirin and Clopidogrel each comparably lowered CK-MB, AST, MMP-2, MMP-9, and the lipid peroxidation product malondialdehyde (MDA) in the hyperlipidemic animals exposed to AMI.	Aspirin	4-11	matrix metallopeptidase 2	Mus musculus	64-69
7491221-1	1995	OBJECTIVE: Varying observations have been made concerning the use of aspirin (ASA) and/or intravenous immunoglobulin (IVIG) in the prevention of coronary artery aneurysm (CAA) in children with Kawasaki disease.	Aspirin	69-76	teashirt zinc finger homeobox 1	Homo sapiens	171-174
7491221-9	1995	CONCLUSION: The incidence of CAA both at 30 and 60 days was significantly lower in low-IVIG than in ASA and in high-IVIG than in low-IVIG groups.	Aspirin	100-103	teashirt zinc finger homeobox 1	Homo sapiens	29-32
8719538-0	1995	Aspirin and acetaminophen reduced both Fos expression in rat lumbar spinal cord and inflammatory signs produced by carrageenin inflammation.	Aspirin	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8719538-1	1995	This study, performed in freely moving rats, evaluates the effects of the two most prescribed analgesics, aspirin and acetaminophen, on carrageenin inflammation and the associated c-Fos expression in the rat lumbar spinal cord.	Aspirin	106-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
8719538-8	1995	There was a tendency for both aspirin and acetaminophen to have a more pronounced effect on the number of Fos-LI neurones located in deeper laminae, these differential effects being significant for 75 mg/kg of aspirin (P &lt; 0.01) and 150 mg/kg of acetaminophen (P &lt; 0.01).	Aspirin	30-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
32049589-0	2020	Aspirin Causes Lipid Accumulation and Damage to Cell Membrane by Regulating DCI1/OLE1 in Saccharomyces cerevisiae.	Aspirin	0-7	putative dodecenoyl-CoA isomerase DCI1	Saccharomyces cerevisiae S288C	76-80
32049589-0	2020	Aspirin Causes Lipid Accumulation and Damage to Cell Membrane by Regulating DCI1/OLE1 in Saccharomyces cerevisiae.	Aspirin	0-7	stearoyl-CoA 9-desaturase	Saccharomyces cerevisiae S288C	81-85
32049589-7	2020	These effects of aspirin were attributed to the alterations of the expression of DCI1 and OLE1.	Aspirin	17-24	putative dodecenoyl-CoA isomerase DCI1	Saccharomyces cerevisiae S288C	81-85
8719538-8	1995	There was a tendency for both aspirin and acetaminophen to have a more pronounced effect on the number of Fos-LI neurones located in deeper laminae, these differential effects being significant for 75 mg/kg of aspirin (P &lt; 0.01) and 150 mg/kg of acetaminophen (P &lt; 0.01).	Aspirin	210-217	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
32049589-7	2020	These effects of aspirin were attributed to the alterations of the expression of DCI1 and OLE1.	Aspirin	17-24	stearoyl-CoA 9-desaturase	Saccharomyces cerevisiae S288C	90-94
8719538-10	1995	Furthermore there was a positive correlation between the effects of aspirin and acetaminophen on the number of Fos-LI neurones and the inflammatory signs which developed after carrageenin.	Aspirin	68-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
32049589-8	2020	Similarly, aspirin was able to cause lipid accumulation and damage to the cell membrane by interfering with the expression of OLE1 in Candida albicans.	Aspirin	11-18	stearoyl-CoA 9-desaturase	Saccharomyces cerevisiae S288C	126-130
32627038-8	2020	Moreover, aspirin induced G0/G1 cell cycle arrest and modulated the levels of cell cycle-related molecules such as cyclin E, cyclin D1, and cyclin-dependent kinase 2 (Cdk2).	Aspirin	10-17	cyclin D1	Mus musculus	125-134
32627038-8	2020	Moreover, aspirin induced G0/G1 cell cycle arrest and modulated the levels of cell cycle-related molecules such as cyclin E, cyclin D1, and cyclin-dependent kinase 2 (Cdk2).	Aspirin	10-17	cyclin-dependent kinase 2	Mus musculus	140-165
32627038-8	2020	Moreover, aspirin induced G0/G1 cell cycle arrest and modulated the levels of cell cycle-related molecules such as cyclin E, cyclin D1, and cyclin-dependent kinase 2 (Cdk2).	Aspirin	10-17	cyclin-dependent kinase 2	Mus musculus	167-171
32750030-10	2020	Aspirin also increased the LC3II/LC3I ratio, decreased p62 expression, and enhanced autophagic flux (autophagosome and autolysosome puncta) in the HCAECs.	Aspirin	0-7	nucleoporin 62	Homo sapiens	55-58
32750030-11	2020	p-NF-kappaB and p-p38 mitogen-activated protein kinase inhibition, sVCAM-1 and sICAM-1 secretion, and eNOS activity promotion by aspirin treatment were found to be dependent on Beclin-1.	Aspirin	129-136	beclin 1	Homo sapiens	177-185
32750030-12	2020	These results suggested that aspirin can protect ECs from ox-LDL-, Ang-II-, and HG-induced injury by activating autophagy in a Beclin-1-dependent manner.	Aspirin	29-36	beclin 1	Homo sapiens	127-135
32053214-12	2020	Low concentration (0.05mM) ASA reduced inflammatory cytokines IL-6 (p &lt; 0.001), CCL21 (P &lt; 0.05) and MMP-9 (p &lt; 0.05) in an ex vivo pulpitis model.	Aspirin	27-30	matrix metallopeptidase 9	Homo sapiens	107-112
8575983-5	1995	CAP37 expression by neutrophils undergoing ASA- and C-dependent sperm phagocytosis was increased as measured by flow cytometry.	Aspirin	43-46	azurocidin 1	Homo sapiens	0-5
32365457-6	2020	Moreover, our study including bioinformatic approaches revealed that aspirin increased the expression levels of glutaminolysis-related genes with upregulation of activating transcription factor 4 (ATF4) in PIK3CA-mutated CRC cells.	Aspirin	69-76	activating transcription factor 4	Homo sapiens	162-195
32365457-6	2020	Moreover, our study including bioinformatic approaches revealed that aspirin increased the expression levels of glutaminolysis-related genes with upregulation of activating transcription factor 4 (ATF4) in PIK3CA-mutated CRC cells.	Aspirin	69-76	activating transcription factor 4	Homo sapiens	197-201
32258142-0	2020	Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPARdelta-AMPK-PGC-1alpha Pathway in Dyslipidemic Conditions.	Aspirin	0-7	peroxisome proliferator activated receptor delta	Homo sapiens	96-105
32258142-3	2020	The protein levels of biomarkers (PPARdelta, AMPK, and PGC-1alpha) involved in oxidative phosphorylation in both the vascular endothelial and liver cells were elevated by the aspirin in hyperlipidemic condition.	Aspirin	175-182	peroxisome proliferator activated receptor delta	Homo sapiens	34-43
7480082-4	1995	Acetylsalicylic acid (556 microM) and the PAF antagonist WEB 2086 (10 microM) significantly attenuated PAF-induced eicosanoid formation.	Aspirin	0-20	PCNA clamp associated factor	Rattus norvegicus	103-106
32258142-4	2020	Also in the stimulation pathway of oxidative phosphorylation by aspirin, PPARdelta was a superior regulator than AMPK and PGC-1alpha in HepG2 cells.	Aspirin	64-71	peroxisome proliferator activated receptor delta	Homo sapiens	73-82
8547213-10	1995	In contrast, only additive effects of SIN-1 and iloprost were observed when platelet aggregation was measured in aspirin-treated PRP stimulated by ADP, TRAP, or collagen.	Aspirin	113-120	TRAP	Homo sapiens	152-156
32376540-7	2020	CONCLUSIONS: For stable angina patients with complicated left main coronary artery lesions and intermediate metabolizer CYP2C19 gene, aspirin combined with ticagrelor antiplatelet therapy after PCI is effective, the effect of ticagrelor is better than clopidogrel on MACE, and ticagrelor does not seem to increase the risk of bleeding.	Aspirin	134-141	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	120-127
7599351-4	1995	Significant and marked elevation of basal Cai levels was observed in platelets from the diabetic subjects when no aspirin was used during platelet isolation.	Aspirin	114-121	carbonic anhydrase 1	Homo sapiens	42-45
32000660-9	2020	The expression level of MAP1LC3 (LC3) in cells increases with the concentration of aspirin demonstrates that aspirin can induce autophagy in CRC cells.	Aspirin	83-90	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	28-31
32000660-9	2020	The expression level of MAP1LC3 (LC3) in cells increases with the concentration of aspirin demonstrates that aspirin can induce autophagy in CRC cells.	Aspirin	109-116	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	28-31
31910903-11	2020	Circulating miR-197 was lower in those cardiovascular disease during therapy with aspirin (p = 0.039) or prasugrel (p = 0.0083).	Aspirin	82-89	microRNA 197	Homo sapiens	12-19
8068732-5	1994	All venom PLA2s induced platelet activation that was accompanied by the liberation of arachidonic acid and was abolished by aspirin.	Aspirin	124-131	phospholipase A2 group IIA	Homo sapiens	10-15
7524120-4	1994	On the other hand, pretreatment with indomethacin and aspirin, inhibitors of cyclooxygenase, inhibited bradykinin-induced oxidation of DCFH.	Aspirin	54-61	kininogen 1	Bos taurus	103-113
31131755-0	2020	Association of CYP2C19 and HSP70 genes polymorphism with aspirin-exacerbated respiratory disease in Kurdistan province.	Aspirin	57-64	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
31131755-0	2020	Association of CYP2C19 and HSP70 genes polymorphism with aspirin-exacerbated respiratory disease in Kurdistan province.	Aspirin	57-64	heat shock protein family A (Hsp70) member 4	Homo sapiens	27-32
31131755-2	2020	Recently, polymorphism in CYP2C19 and HSP genes has been observed in aspirin-exacerbated respiratory disease (AERD).	Aspirin	69-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
32018223-0	2020	Aspirin modulates STOX1 expression and reverses STOX1-induced insufficient proliferation and migration of trophoblast cells.	Aspirin	0-7	storkhead box 1	Homo sapiens	18-23
32018223-0	2020	Aspirin modulates STOX1 expression and reverses STOX1-induced insufficient proliferation and migration of trophoblast cells.	Aspirin	0-7	storkhead box 1	Homo sapiens	48-53
7513960-4	1994	The number of ICAM-1-stained blood vessels in the mucosa increased significantly after 30 min of treatment with intragastric aspirin (30 mM; 25.2 +/- 7.2/mm2, P &lt; 0.01) and indomethacin (20 mg/kg; 20.7 +/- 4.4/mm2, P &lt; 0.01) before any appreciable mucosal damage was evident.	Aspirin	125-132	intercellular adhesion molecule 1	Rattus norvegicus	14-20
32018223-4	2020	The aim of the present study was to explore the underlying mechanism, and the relationship between STOX1 and aspirin in preeclampsia.	Aspirin	109-116	storkhead box 1	Homo sapiens	99-104
32018223-11	2020	Furthermore, we found that aspirin modulated the expression level of STOX1 and reversed proliferation and migration of STOX1-induced insufficient trophoblast cells.	Aspirin	27-34	storkhead box 1	Homo sapiens	69-74
32018223-11	2020	Furthermore, we found that aspirin modulated the expression level of STOX1 and reversed proliferation and migration of STOX1-induced insufficient trophoblast cells.	Aspirin	27-34	storkhead box 1	Homo sapiens	119-124
8065795-0	1994	Chronic treatments with aspirin or acetaminophen reduce both the development of polyarthritis and Fos-like immunoreactivity in rat lumbar spinal cord.	Aspirin	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
8065795-2	1994	The aim of this study was to evaluate the suitability of the Fos-LI technique to gauge the effects of the two most prescribed analgesics, aspirin and acetaminophen (paracetamol), on spinal cord neurons of polyarthritic rats.	Aspirin	138-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
8065795-9	1994	(3) In contrast, when the same chronic treatment was applied during the development of AIA, i.e., 1 week after inoculation, the number of Fos-LI nuclei was significantly decreased (about 50%) in aspirin- and acetaminophen-treated groups as compared to vehicle-treated groups.	Aspirin	195-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
8103026-9	1993	CONCLUSIONS: These studies indicate that aspirin promotes neutrophil adherence to endothelium via CD11a/CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule 1; the adhesion response is partially mediated by leukotriene B4.	Aspirin	41-48	intercellular adhesion molecule 1	Homo sapiens	153-186
32018223-12	2020	CONCLUSION: The present study suggested that inhibition of the expression of STOX1 could promote the effects of aspirin in the treatment of preeclampsia.	Aspirin	112-119	storkhead box 1	Homo sapiens	77-82
31889962-0	2019	Expression of COX-1, COX-2, 5-LOX and CysLT 2  in nasal polyps and bronchial tissue of patients with aspirin exacerbated airway disease.	Aspirin	101-108	cysteinyl leukotriene receptor 2	Homo sapiens	38-45
8361960-3	1993	Twenty minutes later these ASA-pretreated groups were given intraarterial secretin (18 CU/kg) and cholecystokinin (CCK) (18 micrograms/kg).	Aspirin	27-30	cholecystokinin	Rattus norvegicus	98-113
8361960-3	1993	Twenty minutes later these ASA-pretreated groups were given intraarterial secretin (18 CU/kg) and cholecystokinin (CCK) (18 micrograms/kg).	Aspirin	27-30	cholecystokinin	Rattus norvegicus	115-118
8361960-9	1993	At lower ASA dosages, the bicarbonate and protein concentrations and outputs of secretin-CCK-stimulated rats were higher than the basal values and the levels of rats without hormonal stimulation.	Aspirin	9-12	cholecystokinin	Rattus norvegicus	89-92
8361960-12	1993	Among the various hypotheses that may explain this phenomenon, an antagonizing effect of ASA on secretin-CCK action should be the first to be considered.	Aspirin	89-92	cholecystokinin	Rattus norvegicus	105-108
8401339-1	1993	The aim of the study was to evaluate concentration and activity of C1 esterase inhibitor (C1 INH) in patients with aspirin-sensitive urticaria.	Aspirin	115-122	serpin family G member 1	Homo sapiens	67-88
8401339-1	1993	The aim of the study was to evaluate concentration and activity of C1 esterase inhibitor (C1 INH) in patients with aspirin-sensitive urticaria.	Aspirin	115-122	serpin family G member 1	Homo sapiens	90-96
1281834-5	1992	Intraperitoneal administration of TGF alpha at a dose of 10 micrograms/kg, which does not significantly inhibit gastric acid secretion, decreased aspirin-induced macroscopic damage by &gt; 80%.	Aspirin	146-153	transforming growth factor alpha	Rattus norvegicus	34-43
1451229-2	1992	She had been treated with prophylactic, subcutaneous heparin and aspirin throughout her pregnancy.	Aspirin	65-72	Src homology 2 domain containing E	Homo sapiens	0-3
1650039-4	1991	We therefore tested whether aspirin and dipyridamole alone or together can affect PDGF-A chain mRNA levels in cultured human saphenous vein ECs and SMCs.	Aspirin	28-35	platelet derived growth factor subunit A	Homo sapiens	82-88
2024888-3	1991	Aspirin-insensitive pathways, mediated by protein kinase C and myosin light-chain kinase, lead to a change of platelet shape, with an attendant striking increase in their surface (pseudopods) followed by exposure of receptors for fibrinogen and vWf on GPIIb-IIIa.	Aspirin	0-7	integrin subunit alpha 2b	Homo sapiens	252-257
1987704-17	1991	In the second series of 13 dogs given aspirin, 8 dogs have required an appreciably lower dose of injected insulin to maintain fasting blood glucose at acceptable levels.	Aspirin	38-45	insulin	Canis lupus familiaris	106-113
1701376-0	1990	Alterations in rat intestinal mucin patterns following luminal infusion of acetylsalicylic acid and prostaglandin derivatives.	Aspirin	75-95	solute carrier family 13 member 2	Rattus norvegicus	30-35
1701376-2	1990	In this study, rats were treated with acetylsalicylic acid (ASA) or prostaglandins (PG), and their effects on the synthesis and secretion of small intestinal mucin were examined.	Aspirin	38-58	solute carrier family 13 member 2	Rattus norvegicus	158-163
1701376-2	1990	In this study, rats were treated with acetylsalicylic acid (ASA) or prostaglandins (PG), and their effects on the synthesis and secretion of small intestinal mucin were examined.	Aspirin	60-63	solute carrier family 13 member 2	Rattus norvegicus	158-163
2277866-1	1990	The present investigation reports the effect of chronic oral administration of mancozeb, a fungicide, on hepatic microsomal carboxylesterases/amidases or B-esterases responsible for hydrolytic metabolism of aspirin (acetylsalicylic acid or ASA) at pH 5.5 and 7.4, 2-acetylaminofluorene (AAF), acetanilide and p-nitrophenylacetate (NPA) and cholinesterase in rat.	Aspirin	207-214	butyrylcholinesterase	Rattus norvegicus	340-354
2303480-7	1990	Therefore, as it appears to be true for thrombin, platelet response upon binding of anti-p24/CD9 is primarily mediated by the activation of phospholipase C. When platelets pretreated with aspirin (200 microM) and apyrase (1 mg/ml) were subsequently exposed to anti-p24/CD9, aggregation still occurred.	Aspirin	188-195	CD9 molecule	Homo sapiens	93-96
2392949-1	1990	The influence of the POMC-system on the effects of morphine during learning are studied using physical (adrenalectomy, stress) and drug impacts (morphine, methamizol, acetysal) on the functional activity of the system.	Aspirin	167-175	proopiomelanocortin	Rattus norvegicus	21-25
34864310-6	2022	Aspirin quickly interrupted the STIM1-Orai1 interaction, whereas Sulindac mainly suppressed STIM1 translocation.	Aspirin	0-7	ORAI calcium release-activated calcium modulator 1	Homo sapiens	38-43
31402456-8	2019	RESULTS: All-cause mortality was elevated among aspirin users who had methylated promotor of BRCA1 (HR, 1.67; 95% CI, 1.26-2.22), but not among those with unmethylated promoter of BRCA1 (HR, 0.99; 95% CI, 0.67-1.45; P for interaction &lt;=.05).	Aspirin	48-55	BRCA1 DNA repair associated	Homo sapiens	93-98
31402456-8	2019	RESULTS: All-cause mortality was elevated among aspirin users who had methylated promotor of BRCA1 (HR, 1.67; 95% CI, 1.26-2.22), but not among those with unmethylated promoter of BRCA1 (HR, 0.99; 95% CI, 0.67-1.45; P for interaction &lt;=.05).	Aspirin	48-55	BRCA1 DNA repair associated	Homo sapiens	180-185
34816883-8	2021	The comparison between the two groups, on the first day, showed more PCNA+ cells in the livers of the animals that received ASA (p=0.047), and on the seventh day the number was lower in the experimental group (p=0.007).	Aspirin	124-127	proliferating cell nuclear antigen	Rattus norvegicus	69-73
31402456-9	2019	Decreased breast cancer-specific mortality was observed among aspirin users who had unmethylated promotor of BRCA1 and PR and global hypermethylation of LINE-1 (HR, 0.60, 0.78, and 0.63, respectively; P for interaction &lt;=.05), although the 95% CIs included the null.	Aspirin	62-69	BRCA1 DNA repair associated	Homo sapiens	109-114
31402456-10	2019	CONCLUSIONS: The current study suggests that the LINE-1 global methylation and promoter methylation of BRCA1 and PR in tumor may interact with aspirin use to influence mortality after breast cancer.	Aspirin	143-150	BRCA1 DNA repair associated	Homo sapiens	103-108
34868050-8	2021	In the blood, the level of ASA was inversely correlated with the following: the proportion of Th17 expressing HLA-DR (p=0.04), the proportion of effector CD4+ T cells expressing CCR5 (p=0.03) and the proportion of CD8+Tc17 expressing CCR5 (p=0.04).	Aspirin	27-30	C-C motif chemokine receptor 5	Homo sapiens	178-182
31557405-0	2019	Aspirin inhibits adipogenesis of tendon stem cells and lipids accumulation in rat injury tendon through regulating PTEN/PI3K/AKT signalling.	Aspirin	0-7	phosphatase and tensin homolog	Rattus norvegicus	115-119
31557405-15	2019	In conclusion, by down-regulating PTEN/PI3K/AKT signalling, aspirin inhibited adipogenesis of TSCs and fatty infiltration in injury tendon, promoted biomechanical properties and decreased rupture risk of injury tendon.	Aspirin	60-67	phosphatase and tensin homolog	Rattus norvegicus	34-38
31243598-4	2019	Overexpression of Bax/Bad significantly promoted aspirin-induced oncosis.	Aspirin	49-56	BCL2-associated X protein	Mus musculus	18-21
30771281-7	2019	In platelets co-incubated with ASA, rivaroxaban amplified the ASA antiplatelet effect, which was achieved with 30 ng/ml and prevalently attributable to Nox2 inhibition and impaired isoprostane biosynthesis.	Aspirin	62-65	cytochrome b-245 beta chain	Homo sapiens	152-156
34868050-8	2021	In the blood, the level of ASA was inversely correlated with the following: the proportion of Th17 expressing HLA-DR (p=0.04), the proportion of effector CD4+ T cells expressing CCR5 (p=0.03) and the proportion of CD8+Tc17 expressing CCR5 (p=0.04).	Aspirin	27-30	CD8a molecule	Homo sapiens	214-217
34868050-8	2021	In the blood, the level of ASA was inversely correlated with the following: the proportion of Th17 expressing HLA-DR (p=0.04), the proportion of effector CD4+ T cells expressing CCR5 (p=0.03) and the proportion of CD8+Tc17 expressing CCR5 (p=0.04).	Aspirin	27-30	C-C motif chemokine receptor 5	Homo sapiens	234-238
30388256-13	2019	Regular use of NSAIDs and aspirin may be more strongly associated with risk reduction of MSI-high CRC without KRAS or BRAF mutation.	Aspirin	26-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	110-114
34868050-9	2021	At the genital tract, ASA use correlated with a decreased of activated CD4+T cells (CD4+CCR5+CD161+ (p=0.02) and CD4+CCR5+CD95+ (p=0.001)).	Aspirin	22-25	C-C motif chemokine receptor 5	Homo sapiens	88-92
31014052-3	2019	Western blot was used to detect the expressions of microtubule-associated protein light chain 3 (LC3), p62 and cysteinyl aspartate specific proteinase 3 (caspase-3) after treatment with aspirin, metformin and 3-Methyladenine (3-MA).	Aspirin	186-193	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	97-100
34868050-9	2021	At the genital tract, ASA use correlated with a decreased of activated CD4+T cells (CD4+CCR5+CD161+ (p=0.02) and CD4+CCR5+CD95+ (p=0.001)).	Aspirin	22-25	C-C motif chemokine receptor 5	Homo sapiens	117-121
31014052-7	2019	Moreover, treatment with metformin increased the protein expression of LC3II/I ratio, and decreased the expression of p62, while treatment with aspirin decreased the expression of LC3II/I ratio and increased the expression of p62.	Aspirin	144-151	nucleoporin 62	Homo sapiens	226-229
30585832-9	2019	In contrast, acetylsalicylic acid treatment resulted in enhanced plasma levels of tumor necrosis factor-alpha (+53%; p = 0.02), interleukin-6 (+91%; p = 0.03), and interleukin-8 (+42%; p = 0.02) upon the second challenge, whereas plasma levels of the key antiinflammatory cytokine interleukin-10 were attenuated (-40%; p = 0.003).	Aspirin	13-33	interleukin 10	Homo sapiens	281-295
30585832-11	2019	Ex vivo exposure of platelets to acetylsalicylic acid increased production of tumor necrosis factor-alpha (+66%) and decreased production of interleukin-10 (-23%) by monocytes of sepsis patients.	Aspirin	33-53	interleukin 10	Homo sapiens	141-155
30347416-6	2019	RESULTS: In comparison with period 1 (n = 16, 25% of patients), patients in period 2 (n = 75, 50% of patients) included a significantly greater percentage of patients with a high ASA score (3/4; p = 0.001).	Aspirin	179-182	period circadian regulator 2	Homo sapiens	76-84
30378182-9	2019	ASA CM also increased the deposition of extracellular matrix (ECM) proteins, including collagen, elastin, and sGAG.	Aspirin	0-3	elastin	Homo sapiens	97-104
30772975-3	2019	Loss-of-function allele carriers of CYP2C19 were included and randomly divided into loading dose group (first dose of 300 mg clopidogrel) and standard dose group (first dose of 75 mg clopidogrel), 100 mg aspirin was gave at the same time, followed by aspirin 100 mg/d plus clopidogrel 75 mg/d maintaining for 20 days.	Aspirin	204-211	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
30772975-3	2019	Loss-of-function allele carriers of CYP2C19 were included and randomly divided into loading dose group (first dose of 300 mg clopidogrel) and standard dose group (first dose of 75 mg clopidogrel), 100 mg aspirin was gave at the same time, followed by aspirin 100 mg/d plus clopidogrel 75 mg/d maintaining for 20 days.	Aspirin	251-258	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
29925918-0	2019	Aspirin inhibits the proliferation of hepatoma cells through controlling GLUT1-mediated glucose metabolism.	Aspirin	0-7	solute carrier family 2 member 1	Homo sapiens	73-78
29925918-2	2019	In this study, we report that aspirin modulates glucose uptake through downregulating glucose transporter 1 (GLUT1), leading to the inhibition of hepatoma cell proliferation.	Aspirin	30-37	solute carrier family 2 member 1	Homo sapiens	86-107
29925918-2	2019	In this study, we report that aspirin modulates glucose uptake through downregulating glucose transporter 1 (GLUT1), leading to the inhibition of hepatoma cell proliferation.	Aspirin	30-37	solute carrier family 2 member 1	Homo sapiens	109-114
29925918-4	2019	Interestingly, we identified that GLUT1 and HIF1alpha could be decreased by aspirin.	Aspirin	76-83	solute carrier family 2 member 1	Homo sapiens	34-39
29925918-7	2019	CoCl2-activated HIF1alpha expression could slightly rescue the GLUT1 expression inhibited by aspirin or PDTC, suggesting that aspirin depressed GLUT1 through targeting NF-kappaB or NF-kappaB/HIF1alpha signaling.	Aspirin	93-100	solute carrier family 2 member 1	Homo sapiens	63-68
29925918-7	2019	CoCl2-activated HIF1alpha expression could slightly rescue the GLUT1 expression inhibited by aspirin or PDTC, suggesting that aspirin depressed GLUT1 through targeting NF-kappaB or NF-kappaB/HIF1alpha signaling.	Aspirin	126-133	solute carrier family 2 member 1	Homo sapiens	63-68
29925918-7	2019	CoCl2-activated HIF1alpha expression could slightly rescue the GLUT1 expression inhibited by aspirin or PDTC, suggesting that aspirin depressed GLUT1 through targeting NF-kappaB or NF-kappaB/HIF1alpha signaling.	Aspirin	126-133	solute carrier family 2 member 1	Homo sapiens	144-149
29925918-10	2019	Functionally, overexpression of GLUT1 blocked the PDTC-induced or aspirin-induced inhibition of glucose metabolism in HepG2 cells.	Aspirin	66-73	solute carrier family 2 member 1	Homo sapiens	32-37
29925918-11	2019	Conversely, aspirin failed to work when GLUT1 was stably knocked down in the cells.	Aspirin	12-19	solute carrier family 2 member 1	Homo sapiens	40-45
29925918-12	2019	Administration of aspirin could depress the growth of hepatoma cells through controlling GLUT1 in vitro and in vivo.	Aspirin	18-25	solute carrier family 2 member 1	Homo sapiens	89-94
30546409-6	2018	At the same time, cilostazol combined with aspirin could effectively reduce the levels of serum inflammatory factors MMP-2 and MMP-9 in patients, except for nitric oxide (NO), and the differences were statistically significant (P&lt;0.05).	Aspirin	43-50	matrix metallopeptidase 9	Homo sapiens	127-132
30482850-0	2018	Aspirin ameliorates experimental autoimmune encephalomyelitis through interleukin-11-mediated protection of regulatory T cells.	Aspirin	0-7	interleukin 11	Mus musculus	70-84
30482850-5	2018	The effects of aspirin required the presence of CD25+FoxP3+ Tregs Aspirin increased the amounts of Foxp3 and interleukin-4 (IL-4) in T cells and suppressed the differentiation of naive T cells into T helper 17 (TH17) and TH1 cells.	Aspirin	15-22	interleukin 2 receptor, alpha chain	Mus musculus	48-52
30482850-5	2018	The effects of aspirin required the presence of CD25+FoxP3+ Tregs Aspirin increased the amounts of Foxp3 and interleukin-4 (IL-4) in T cells and suppressed the differentiation of naive T cells into T helper 17 (TH17) and TH1 cells.	Aspirin	66-73	interleukin 2 receptor, alpha chain	Mus musculus	48-52
30482850-6	2018	Aspirin also increased the transcription of Il11 mediated by the transcription factor CREB, which was necessary for the generation of Tregs Neutralization of IL-11 negated the effects of aspirin on Treg development and exacerbated EAE.	Aspirin	0-7	interleukin 11	Mus musculus	44-48
30482850-6	2018	Aspirin also increased the transcription of Il11 mediated by the transcription factor CREB, which was necessary for the generation of Tregs Neutralization of IL-11 negated the effects of aspirin on Treg development and exacerbated EAE.	Aspirin	0-7	interleukin 11	Mus musculus	158-163
30482850-6	2018	Aspirin also increased the transcription of Il11 mediated by the transcription factor CREB, which was necessary for the generation of Tregs Neutralization of IL-11 negated the effects of aspirin on Treg development and exacerbated EAE.	Aspirin	187-194	interleukin 11	Mus musculus	44-48
30482850-6	2018	Aspirin also increased the transcription of Il11 mediated by the transcription factor CREB, which was necessary for the generation of Tregs Neutralization of IL-11 negated the effects of aspirin on Treg development and exacerbated EAE.	Aspirin	187-194	interleukin 11	Mus musculus	158-163
30358688-2	2018	Relevant evidence indicated that aspirin and vicagrel are the drug substrate for carboxylesterase 2.	Aspirin	33-40	carboxylesterase 2H	Mus musculus	81-99
30350844-6	2018	Policosanol + aspirin decreased significantly the mRS score mean from the first interim check-up.	Aspirin	14-21	sterile alpha motif domain containing 11	Mus musculus	50-53
30350844-8	2018	More over, policosanol + aspirin (80.3%) treatment achieved significant results (mRS &lt;= 1), whereas the placebo + aspirin did not (8.5%).	Aspirin	25-32	sterile alpha motif domain containing 11	Mus musculus	81-84
29793021-8	2018	Acetylsalicylic acid (ASA) blocked the enhancement of thrombus formation by TPO in both WT and p110alpha KO mice.	Aspirin	0-20	thrombopoietin	Mus musculus	76-79
29793021-8	2018	Acetylsalicylic acid (ASA) blocked the enhancement of thrombus formation by TPO in both WT and p110alpha KO mice.	Aspirin	22-25	thrombopoietin	Mus musculus	76-79
30015780-4	2018	In the present study, we assessed the role of platelet miRNAs in modulating MRP4 function in response to ASA.	Aspirin	105-108	ATP binding cassette subfamily C member 4	Homo sapiens	76-80
30015780-5	2018	METHODS: MRP4 mRNA expression has been analyzed by RealTime PCR in platelets from patients on chronic ASA treatment versus a control group.	Aspirin	102-105	ATP binding cassette subfamily C member 4	Homo sapiens	9-13
30015780-10	2018	RESULTS: We observed a higher MRP4 mRNA expression in platelets of patients under ASA treatment compared to the control group (p&lt;0.005).	Aspirin	82-85	ATP binding cassette subfamily C member 4	Homo sapiens	30-34
30128710-0	2018	Aspirin plus clopidogrel may reduce the risk of early neurologic deterioration in ischemic stroke patients carrying CYP2C19*2 reduced-function alleles.	Aspirin	0-7	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
30128710-11	2018	Stratified analyses revealed that clopidogrel plus aspirin could be more effective in reducing END than aspirin alone for carriers of CYP2C19*2 reduced-function alleles (18.8 vs. 34.9%, P = 0.006).	Aspirin	51-58	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	134-141
30128710-13	2018	CONCLUSIONS: Dual therapy with clopidogrel and aspirin may be adequate for prevention of END in carriers of CYP2C19 reduced-function alleles, but not for noncarriers.	Aspirin	47-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	108-115
29804161-0	2018	Dual therapy with clopidogrel and aspirin prevents early neurological deterioration in ischemic stroke patients carrying CYP2C19*2 reduced-function alleles.	Aspirin	34-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	121-128
29804161-13	2018	Dual therapy with clopidogrel and aspirin may be adequate for patients carrying CYP2C19*2 reduced-function alleles.	Aspirin	34-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	80-87
34784372-5	2021	Aspirin-triggered resolvin D1 (AT-RvD1) is a pro-resolving mediator of inflammation that acts through N-formyl peptide receptor 2 (FPR2).	Aspirin	0-7	formyl peptide receptor 2	Mus musculus	131-135
34790277-0	2021	Aspirin Exerts Neuroprotective Effects by Reversing Lipopolysaccharide-Induced Secondary Brain Injury and Inhibiting Matrix Metalloproteinase-3 Gene Expression.	Aspirin	0-7	matrix metallopeptidase 3	Rattus norvegicus	117-143
29936693-0	2018	Clustering of ABCB1 and CYP2C19 Genetic Variants Predicts Risk of Major Bleeding and Thrombotic Events in Elderly Patients with Acute Coronary Syndrome Receiving Dual Antiplatelet Therapy with Aspirin and Clopidogrel.	Aspirin	193-200	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
29936693-2	2018	The aim of this pilot prospective study was to evaluate 12-month cardiovascular outcomes in elderly patients with acute coronary syndrome (ACS) receiving dual antiplatelet therapy (aspirin and clopidogrel) according to the clustering of CYP2C19 and ABCB1 genetic variants.	Aspirin	181-188	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	237-244
34790277-7	2021	Furthermore, the number of GSI-B4, OPN, and MMP-3 cells decreased in the ASA group compared to the control group.	Aspirin	73-76	matrix metallopeptidase 3	Rattus norvegicus	44-49
34790277-13	2021	In the ASA group, the MMP-3 expression was also considerably decreased (p < 0.05).	Aspirin	7-10	matrix metallopeptidase 3	Rattus norvegicus	22-27
34638442-3	2021	However, prognostic data on aspirin use after a colorectal cancer diagnosis in relation to KRAS mutational status is limited.	Aspirin	28-35	KRAS proto-oncogene, GTPase	Homo sapiens	91-95
34638442-7	2021	We observed a significant 10-year overall survival benefit in patients with aspirin use and combined wild-type PIK3CA and mutated-KRAS tumors (HR = 0.38; 95% CI = 0.17-0.87; p = 0.02), but not in patients without aspirin use.	Aspirin	76-83	KRAS proto-oncogene, GTPase	Homo sapiens	130-134
34638442-8	2021	Our data indicate a benefit of aspirin usage particularly for patients with combined wild-type PIK3CA and mutated-KRAS tumor characteristics.	Aspirin	31-38	KRAS proto-oncogene, GTPase	Homo sapiens	114-118
30018744-9	2018	In addition, we also found survivin-independent effects of ASA on the cell cycle that were mediated through inhibition of cyclin A, cyclin dependent kinase 2 (CDK2) and phospho-CDK2.	Aspirin	59-62	cyclin dependent kinase 2	Rattus norvegicus	132-157
30018744-9	2018	In addition, we also found survivin-independent effects of ASA on the cell cycle that were mediated through inhibition of cyclin A, cyclin dependent kinase 2 (CDK2) and phospho-CDK2.	Aspirin	59-62	cyclin dependent kinase 2	Rattus norvegicus	159-163
30018744-9	2018	In addition, we also found survivin-independent effects of ASA on the cell cycle that were mediated through inhibition of cyclin A, cyclin dependent kinase 2 (CDK2) and phospho-CDK2.	Aspirin	59-62	cyclin dependent kinase 2	Rattus norvegicus	177-181
29743380-1	2018	BACKGROUND: Patients with reduced-function CYP2C19 genotypes on dual antiplatelet therapy (DAPT) with aspirin and clopidogrel show higher clinical risk for acute myocardial infarction (AMI).	Aspirin	102-109	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
29381509-0	2018	Aspirin suppresses neuronal apoptosis, reduces tissue inflammation, and restrains astrocyte activation by activating the Nrf2/HO-1 signaling pathway.	Aspirin	0-7	heme oxygenase 1	Rattus norvegicus	126-130
29381509-2	2018	Aspirin has been shown to exert several pharmacological effects by inducing the expression of the heme oxygenase-1 (HO-1) protein.	Aspirin	0-7	heme oxygenase 1	Rattus norvegicus	98-114
29381509-2	2018	Aspirin has been shown to exert several pharmacological effects by inducing the expression of the heme oxygenase-1 (HO-1) protein.	Aspirin	0-7	heme oxygenase 1	Rattus norvegicus	116-120
34126182-0	2021	Inhibition of desmoglein-1 by aspirin leads to synthetic lethality of keratinocytes in Shuanghuanglian-induced cutaneous eruption response.	Aspirin	30-37	desmoglein 1	Homo sapiens	14-26
34126182-5	2021	Western boltting was used to detect the effects of ASA on desmoglein-1 (DSG1) expression; we found that DSG1 expression was down-regulated in vivo and in vitro.	Aspirin	51-54	desmoglein 1	Homo sapiens	58-70
34126182-5	2021	Western boltting was used to detect the effects of ASA on desmoglein-1 (DSG1) expression; we found that DSG1 expression was down-regulated in vivo and in vitro.	Aspirin	51-54	desmoglein 1 alpha	Mus musculus	72-76
34126182-5	2021	Western boltting was used to detect the effects of ASA on desmoglein-1 (DSG1) expression; we found that DSG1 expression was down-regulated in vivo and in vitro.	Aspirin	51-54	desmoglein 1 alpha	Mus musculus	104-108
29381509-7	2018	The expression of Nrf2, quinine oxidoreductase 1, and HO-1 proteins was increased in aspirin-treated animals after SCI compared with the vehicle group.	Aspirin	85-92	heme oxygenase 1	Rattus norvegicus	54-58
29386221-8	2018	Remarkably, acetylsalicylic acid (aspirin) was predicted to be a tamoxifen sensitizer using a drug repositioning approach and was shown to reverse resistance by targeting PDE4D/cAMP/ER stress axis.	Aspirin	12-32	phosphodiesterase 4D	Homo sapiens	171-176
29386221-8	2018	Remarkably, acetylsalicylic acid (aspirin) was predicted to be a tamoxifen sensitizer using a drug repositioning approach and was shown to reverse resistance by targeting PDE4D/cAMP/ER stress axis.	Aspirin	34-41	phosphodiesterase 4D	Homo sapiens	171-176
34126182-7	2021	These results demonstrate that DSG1 deficiency is a potential cause of cutaneous eruptions caused by the combination of SHL and ASA, and neochlorogenic acid and rutin are the main allergenic components.	Aspirin	128-131	desmoglein 1	Homo sapiens	31-35
29642568-0	2018	Irradiation-Induced Cardiac Connexin-43 and miR-21 Responses Are Hampered by Treatment with Atorvastatin and Aspirin.	Aspirin	109-116	microRNA 21	Rattus norvegicus	44-50
29642568-8	2018	Furthermore, treatment with aspirin, atorvastatin, and sildenafil completely prevented an increase of miR-21 in the LV while having partial effect in the RV post irradiation.	Aspirin	28-35	microRNA 21	Rattus norvegicus	102-108
34471538-3	2021	Studies reported the genetic polymorphisms of CYP2C19*2, CYP2C19*17, and ITGB3 cause an alteration of the pharmacodynamic and pharmacokinetic profile of aspirin and clopidogrel.	Aspirin	153-160	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-53
29642568-11	2018	Treatment with aspirin and atorvastatin interfered with irradiation-induced compensatory changes in myocardial Cx43 protein and miR-21 by preventing their elevation, possibly via amelioration of oxidative stress and inflammation.	Aspirin	15-22	microRNA 21	Rattus norvegicus	128-134
34471538-3	2021	Studies reported the genetic polymorphisms of CYP2C19*2, CYP2C19*17, and ITGB3 cause an alteration of the pharmacodynamic and pharmacokinetic profile of aspirin and clopidogrel.	Aspirin	153-160	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
29344879-5	2018	In the aspirin group, the changes from baseline to end point in the IIEF-EF, SEP-2, and SEP-3 scores were 7.2, 36.6, and 46.6%, respectively.	Aspirin	7-14	septin 3	Homo sapiens	88-93
29448294-9	2018	A reduction of platelet aggregation and secretion were observed in aspirin-treated patients with HARPR.This study supports the role of MRP4 on modulating platelet function which occurs through cAMP-independent mechanisms.	Aspirin	67-74	ATP binding cassette subfamily C member 4	Homo sapiens	135-139
29448294-10	2018	Moreover, inhibition of MRP4 induced by cilostazol enhances aspirin-induced antiplatelet effects and reduces HARPR.	Aspirin	60-67	ATP binding cassette subfamily C member 4	Homo sapiens	24-28
34632302-11	2021	Similarly, aspirin treatment also increased astroglial and microglial IL-1Ra in the cortex of 5xFAD, but not 5xFAD/PPARalpha-/- mice.	Aspirin	11-18	interleukin 1 receptor antagonist	Mus musculus	70-76
34632302-12	2021	Conclusion: Aspirin may reduce the severity of different neurological conditions by upregulating IL-1Ra and reducing the inflammation.	Aspirin	12-19	interleukin 1 receptor antagonist	Mus musculus	97-103
34414020-14	2021	In addition, the mRNA levels of CDKN1A, BAX, FOXF1, PUMA, and RRAD in EOC cells were significantly increased by the aspirin treatment.	Aspirin	116-123	forkhead box F1	Homo sapiens	45-50
29471853-15	2018	Interestingly, aspirin (ASA) suppressed the HBXIP/HOXB13 axis by decreasing HBXIP expression, overcoming TAM resistance in vitro and in vivo.	Aspirin	15-22	homeobox B13	Homo sapiens	50-56
34414020-14	2021	In addition, the mRNA levels of CDKN1A, BAX, FOXF1, PUMA, and RRAD in EOC cells were significantly increased by the aspirin treatment.	Aspirin	116-123	RRAD, Ras related glycolysis inhibitor and calcium channel regulator	Homo sapiens	62-66
29471853-15	2018	Interestingly, aspirin (ASA) suppressed the HBXIP/HOXB13 axis by decreasing HBXIP expression, overcoming TAM resistance in vitro and in vivo.	Aspirin	24-27	homeobox B13	Homo sapiens	50-56
29258006-5	2018	Haplotypes of 11-dehydro TxB2 increasing alleles for both PPARGC1B and CNTN4 were significantly associated with 11-dehydro TxB2, explaining 5.2% and 4.5% of the variation in the whole cohort, and 8.8% and 7.9% in participants not taking aspirin, respectively.	Aspirin	237-244	contactin 4	Homo sapiens	71-76
34307673-11	2021	Western blot analysis showed that compared with the MI/R group, aspirin pretreatment significantly increased the expression levels of p-STAT3 and p-JAK2 (p < 0.05).	Aspirin	64-71	Janus kinase 2	Rattus norvegicus	148-152
34307673-12	2021	Conclusion: The mechanism of aspirin preconditioning to protect the heart from MI/R injury appears to be related to JAK2/STAT3 and related to the activation of the signaling pathway.	Aspirin	29-36	Janus kinase 2	Rattus norvegicus	116-120
29258006-10	2018	If specific protection of PPARGC1B and CNTN4 variant carriers by aspirin is confirmed by additional studies, PPARGC1B and CNTN4 genotyping could potentially assist in clinical decision making regarding the use of aspirin in primary prevention.	Aspirin	65-72	contactin 4	Homo sapiens	39-44
29282304-9	2018	Pharmacological blockade of CysLT2R prior to inhalation challenge of Ptges-/- mice with aspirin blocked IL-33-dependent mast cell activation, mediator release, and changes in lung function.	Aspirin	88-95	cysteinyl leukotriene receptor 2	Mus musculus	28-35
29282304-9	2018	Pharmacological blockade of CysLT2R prior to inhalation challenge of Ptges-/- mice with aspirin blocked IL-33-dependent mast cell activation, mediator release, and changes in lung function.	Aspirin	88-95	interleukin 33	Mus musculus	104-109
29282304-10	2018	Thus, CysLT2R signaling, IL-33-dependent ILC2 expansion, and IL-33-driven mast cell activation are necessary for induction of type 2 immunopathology and aspirin sensitivity.	Aspirin	153-160	cysteinyl leukotriene receptor 2	Mus musculus	6-13
29282304-10	2018	Thus, CysLT2R signaling, IL-33-dependent ILC2 expansion, and IL-33-driven mast cell activation are necessary for induction of type 2 immunopathology and aspirin sensitivity.	Aspirin	153-160	interleukin 33	Mus musculus	25-30
29282304-10	2018	Thus, CysLT2R signaling, IL-33-dependent ILC2 expansion, and IL-33-driven mast cell activation are necessary for induction of type 2 immunopathology and aspirin sensitivity.	Aspirin	153-160	interleukin 33	Mus musculus	61-66
34261702-8	2021	Blocking CTLA4 and IL1B with the specific mAbs significantly suppressed tumor progression and metastasis in the mouse models resistant to anti-PD1 therapy, and the therapeutic efficacy was optimized by blocking cyclooxygenases with aspirin.	Aspirin	232-239	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	9-14
29534838-0	2018	Cortactin expression in nasal polyps of Aspirin-Exacerbated Respiratory Disease (AERD) patients.	Aspirin	40-47	cortactin	Homo sapiens	0-9
35000048-0	2022	COX-1, COX-2 and CYP2C19 variations may be related to cardiovascular events due to acetylsalicylic acid resistance.	Aspirin	83-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
29977412-9	2018	Strawberries and aspirin, alone and in combination, significantly suppressed squamous epithelial cell proliferation (PCNA).	Aspirin	17-24	proliferating cell nuclear antigen	Rattus norvegicus	117-121
35183904-1	2022	BACKGROUND AND AIMS: The platelet inhibitor aspirin reduces inflammation and atherosclerosis in both apolipoprotein E deficient (apoE-/-) mice and low-density lipoprotein receptor deficient (Ldlr-/-) mice.	Aspirin	44-51	low density lipoprotein receptor	Mus musculus	147-179
35183904-1	2022	BACKGROUND AND AIMS: The platelet inhibitor aspirin reduces inflammation and atherosclerosis in both apolipoprotein E deficient (apoE-/-) mice and low-density lipoprotein receptor deficient (Ldlr-/-) mice.	Aspirin	44-51	low density lipoprotein receptor	Mus musculus	191-195
35108049-5	2022	Inhibition of AT-SPM biosynthesis or knockout of the AT-SPM receptor Alx/Fpr2 reversed the immunomodulatory actions of aspirin on macrophages and CD8+ T cells and abrogated its protective effects during I-CRC.	Aspirin	119-126	formyl peptide receptor 2	Mus musculus	73-77
2529003-0	1989	Inhibition of tissue plasminogen activator activity by aspirin in vivo and its relationship to levels of tissue plasminogen activator inhibitor antigen, plasminogen activator and their complexes.	Aspirin	55-62	chromosome 20 open reading frame 181	Homo sapiens	14-42
2529003-0	1989	Inhibition of tissue plasminogen activator activity by aspirin in vivo and its relationship to levels of tissue plasminogen activator inhibitor antigen, plasminogen activator and their complexes.	Aspirin	55-62	chromosome 20 open reading frame 181	Homo sapiens	105-133
2529003-2	1989	The current study was performed to confirm the original observation and determine the mechanism by which aspirin suppresses the incremental t-PA activity induced by venous occlusion.	Aspirin	105-112	chromosome 20 open reading frame 181	Homo sapiens	140-144
2504679-2	1989	In this paper we have assessed the effects of acetylsalicylic acid (aspirin), thymosin alpha and thymosin fraction 5 (TF5), a partially purified calf thymic preparation, on production of IFN-gamma in vitro.	Aspirin	46-66	interferon gamma	Bos taurus	187-196
2504679-2	1989	In this paper we have assessed the effects of acetylsalicylic acid (aspirin), thymosin alpha and thymosin fraction 5 (TF5), a partially purified calf thymic preparation, on production of IFN-gamma in vitro.	Aspirin	68-75	interferon gamma	Bos taurus	187-196
2499551-6	1989	ASA administration strongly increased BLG absorption, not prevented by DSCG pretreatment.	Aspirin	0-3	beta-lactoglobulin	Bos taurus	38-41
2573217-2	1989	Preparations of the phenothiazine (aminazine, tizercine) and pyrazolone (amidopyrine, analginum) series and non-steroid anti-inflammatory drugs (acetylsalicylic acid, sodium salicylate) exert a significant effect on the glucocorticoid-receptor interplay.	Aspirin	145-165	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	220-243
3191032-4	1988	Such platelet inhibitors as acetylsalicylic acid, prostaglandin E1 and cytochalasin B reduced the capacity of platelets to bind ligand, and by kinetic experiments involving enzymatic digestion of radiolabelled bound HRGP the ligand revealed to remain surface bound rather than being taken up to inner parts of the cell.	Aspirin	28-48	histidine rich glycoprotein	Homo sapiens	216-220
3171983-8	1988	In the sodium-restricted animals (plasma renin activity, 18-24 ng of angiotensin l/ml/hr) ASA decreased PGE2 excretion but SA did not.	Aspirin	90-93	renin	Canis lupus familiaris	41-46
20144114-4	1987	The results of this study are as follows: The drugs, phenylbutazone, indomethacin and acetyl-salicylic acid, are effective, when they are administered at the initial phase of inflammation, while in the chronic phase the effects of them are variable, though significant in patients whose PSP clearance rate is below 45 per cent.	Aspirin	86-107	microseminoprotein beta	Homo sapiens	287-290
3010025-0	1986	Studies on the use of a novel affinity matrix, sepharose amine-succinyl-amine haloperidol hemisuccinate, ASA-HHS, for purification of canine dopamine (D2) receptor.	Aspirin	105-108	dopamine receptor D2	Canis lupus familiaris	141-163
3963535-1	1986	The influence of three saline cathartics and tap water on the adsorption characteristics of activated charcoal for aspirin was studied with adsorption isotherms.	Aspirin	115-122	nuclear RNA export factor 1	Homo sapiens	45-48
3918199-2	1985	LCAT was assayed using an endogenous (S/N) and an artificial (ASA) substrate to differentiate between altered plasma substrate composition (which would influence the S/N method) and enzyme quantity (measured by the exogenous ASA method).	Aspirin	62-65	lecithin-cholesterol acyltransferase	Homo sapiens	0-4
3918199-2	1985	LCAT was assayed using an endogenous (S/N) and an artificial (ASA) substrate to differentiate between altered plasma substrate composition (which would influence the S/N method) and enzyme quantity (measured by the exogenous ASA method).	Aspirin	225-228	lecithin-cholesterol acyltransferase	Homo sapiens	0-4
3918199-7	1985	Longitudinal analyses showed that during the first 21 days of TPN nine patients showed a further fall in ASA LCAT and a rise in free cholesterol, thereafter ASA LCAT activity rose and free cholesterol fell despite continuation of TPN.	Aspirin	105-108	lecithin-cholesterol acyltransferase	Homo sapiens	109-113
6466389-0	1984	Effects of aspirin and salicylic acid on lecithin-cholesterol acyltransferase and cholesterol content in rat serum.	Aspirin	11-18	lecithin-cholesterol acyltransferase	Homo sapiens	41-77
6546237-9	1984	In the cholesterol-fed prairie dog, blockage of mucin release with aspirin inhibits gallstone formation.	Aspirin	67-74	mucin	Canis lupus familiaris	48-53
7041954-2	1982	However, when the animals were pre-treated with aspirin (10 mg/kg), there was a marked change in the ratio of radioactive counts between control and treated segments, consistent with platelet deposition on the walls of thrombin-treated segments.	Aspirin	48-55	prothrombin	Oryctolagus cuniculus	219-227
6281811-4	1982	Similarly, aspirin (30 micrograms/ml) and flufenamate (1 microgram/ml) showed a strong inhibition of the contraction of parenchymal strips to LTB4; these results suggested that cyclooxygenase products mediate the action of LTB4.	Aspirin	11-18	prostaglandin reductase 1	Cavia porcellus	142-146
6281811-4	1982	Similarly, aspirin (30 micrograms/ml) and flufenamate (1 microgram/ml) showed a strong inhibition of the contraction of parenchymal strips to LTB4; these results suggested that cyclooxygenase products mediate the action of LTB4.	Aspirin	11-18	prostaglandin reductase 1	Cavia porcellus	223-227
6894770-5	1981	Endotoxin-induced hypoglycemia and elevations in serum acid phosphatase and beta-glucuronidase activities, lysosomal enzymes, were all significantly (P less than .01) attenuated by pretreatment with aspirin (15 mg/kg) 30 min before endotoxin.	Aspirin	199-206	glucuronidase, beta	Rattus norvegicus	76-94
7466399-3	1981	Aspirin given to prairie dogs inhibited mucin hypersecretion and gel accumulation and prevented gallstone formation without influencing the cholesterol content of supersaturated bile.	Aspirin	0-7	mucin	Canis lupus familiaris	40-45
7198795-8	1981	In the gastric or jejunal acute ulceration model, sulfomucin production is decreased by aspirin and markedly enhanced by Prostaglandin E1, providing additional evidence for the cytoprotective role of the mucin blanket.	Aspirin	88-95	solute carrier family 13 member 2	Rattus norvegicus	55-60
7229910-1	1980	The acidic compounds, such as phenoxyacetic acids, substituted benzoic acids, or acetylsalicylic acid, were found to bind to bovine serum albumin (BSA).	Aspirin	81-101	albumin	Rattus norvegicus	132-145
7205544-4	1980	In the acute exudative stage of this inflammation, a single oral administration of dexamethasone, indomethacin, phenylbutazone or aspirin all exerted potent anti-exudative effect, while in the chronic proliferative stage, only dexamethasone was effective in inhibiting the exudation of the labeled albumin.	Aspirin	130-137	albumin	Rattus norvegicus	298-305
26360-2	1978	In Wistar rats and humans the results indicate that the daily iron loss under ASA is significantly higher (almost by the factor 2) than that under benorilate.	Aspirin	78-81	transcription termination factor 2	Homo sapiens	121-129
589365-0	1977	Glucagon and secretin in aspirin-induced erosive gastritis.	Aspirin	25-32	secretin	Homo sapiens	13-21
17672-1	1977	Acetylsalicylic acid, salicylic acid and indomethacin were equally effective in inhibiting aggregation of plasma-free rabbit platelets induced by carrageenan and by thrombin.	Aspirin	0-20	prothrombin	Oryctolagus cuniculus	165-173
4514302-1	1973	Incubation of HbS (or HbA) with aspirin leads to incorporation of acetyl groups into the protein.	Aspirin	32-39	keratin 90, pseudogene	Homo sapiens	22-25
33964863-6	2021	Especially, the possible role of MRP4 in the excretion of xenobiotic and antiplatelet drugs such as aspirin is discussed, thus imparting platelet aspirin tolerance and correlating the protein with the ineffectiveness of aspirin antiplatelet therapy.	Aspirin	100-107	ATP binding cassette subfamily C member 4	Homo sapiens	33-37
33964863-6	2021	Especially, the possible role of MRP4 in the excretion of xenobiotic and antiplatelet drugs such as aspirin is discussed, thus imparting platelet aspirin tolerance and correlating the protein with the ineffectiveness of aspirin antiplatelet therapy.	Aspirin	146-153	ATP binding cassette subfamily C member 4	Homo sapiens	33-37
33964863-6	2021	Especially, the possible role of MRP4 in the excretion of xenobiotic and antiplatelet drugs such as aspirin is discussed, thus imparting platelet aspirin tolerance and correlating the protein with the ineffectiveness of aspirin antiplatelet therapy.	Aspirin	146-153	ATP binding cassette subfamily C member 4	Homo sapiens	33-37
32803738-7	2021	In aspirin-treated patients with high levels of MRP4, reduced SNP inhibition was found compared to those with low levels of MRP4.	Aspirin	3-10	ATP binding cassette subfamily C member 4	Homo sapiens	48-52
32803738-7	2021	In aspirin-treated patients with high levels of MRP4, reduced SNP inhibition was found compared to those with low levels of MRP4.	Aspirin	3-10	ATP binding cassette subfamily C member 4	Homo sapiens	124-128
33574709-10	2021	Unexpectedly, we observed that siRNA knockdown of REDD1 expression facilitated aspirin-mediated suppression of mTORC1 downstream substrate 4E-BP1 phosphorylation in the MDA-MB-468 cell line.	Aspirin	79-86	DNA damage inducible transcript 4	Homo sapiens	50-55
33574709-11	2021	REDD1 downregulation slightly encouraged reduction in 4E-BP1 phosphorylation by aspirin in MCF-7 cells but did not elicit a reproducible effect in the MDA-MB-231 cell line.	Aspirin	80-87	DNA damage inducible transcript 4	Homo sapiens	0-5
33574709-13	2021	Conclusion: The current findings suggest that REDD1 downregulation might improve the anticancer activity of aspirin in a subset of breast tumors.	Aspirin	108-115	DNA damage inducible transcript 4	Homo sapiens	46-51
33359561-6	2021	Inflammation, enhanced by these lipid oxidation products, plays a key role in the up-regulation of PCSK6 activity as demonstrated by cell pretreatment with NS-398, with epigallocatechin gallate or with acetylsalicylic acid, all with anti-inflammatory effects.	Aspirin	202-222	proprotein convertase subtilisin/kexin type 6	Homo sapiens	99-104
33370633-7	2021	The severity of dyspepsia assessment (SODA) results showed that patients in PNS + ASA group exhibited relieved dyspeptic symptoms as compared with those in ASA group, which might be associated with enhanced secretion of gastrin and motilin.	Aspirin	82-85	motilin	Homo sapiens	232-239
33430037-11	2021	Aspirin use was associated with increases of M1 macrophages, plasma cells, CD8+ T cells, and reduction of M2 macrophages in the resected tumor.	Aspirin	0-7	CD8a molecule	Homo sapiens	75-78
33386711-0	2021	Low-dose Btk inhibitors: an "aspirin" of tomorrow?	Aspirin	29-36	Bruton tyrosine kinase	Homo sapiens	9-12
33298861-1	2020	Salicylate, the active derivative of aspirin (acetylsalicylate), recapitulates the mode of action of caloric restriction inasmuch as it stimulates autophagy through the inhibition of the acetyltransferase activity of EP300.	Aspirin	37-44	E1A binding protein p300	Mus musculus	217-222
33298861-1	2020	Salicylate, the active derivative of aspirin (acetylsalicylate), recapitulates the mode of action of caloric restriction inasmuch as it stimulates autophagy through the inhibition of the acetyltransferase activity of EP300.	Aspirin	46-62	E1A binding protein p300	Mus musculus	217-222
33170592-4	2020	Platelets from ASA-sensitive patients showed higher expression of the proapoptotic proteins Bak and Bax than those from ASA-resistant patients, although only Bak protein remained different when the results were adjusted by age.	Aspirin	15-18	BCL2 antagonist/killer 1	Homo sapiens	92-95
33170592-4	2020	Platelets from ASA-sensitive patients showed higher expression of the proapoptotic proteins Bak and Bax than those from ASA-resistant patients, although only Bak protein remained different when the results were adjusted by age.	Aspirin	15-18	BCL2 antagonist/killer 1	Homo sapiens	158-161
33111589-5	2021	Results revealed that platelet-like particles (PLPs) derived from ASA-exposed Meg-01 cells, showed higher content of pro-apoptotic proteins Bax and Bak than PLPs from non-ASA incubated Meg-01 cells.	Aspirin	66-69	BCL2 antagonist/killer 1	Homo sapiens	148-151
33111589-6	2021	It was accompanied of reduced cytochrome C oxidase activity and higher mitochondrial content of PTEN-induced putative kinase-1 in PLPs from ASA-incubated Meg-01 cells.	Aspirin	140-143	PTEN induced kinase 1	Homo sapiens	96-126
32980046-12	2020	Aspirin had no effect on STBEV uptake or cellular gene expression on its own, however it down regulated ICAM-1 protein expression in combination with preeclamptic STBEV exposure.	Aspirin	0-7	intercellular adhesion molecule 1	Homo sapiens	104-110
32815915-6	2020	alpha2-Antiplasmin incubation with ASA did not affect its affinity to fibrin.	Aspirin	35-38	serpin family F member 2	Homo sapiens	0-18
32815915-7	2020	alpha2-Antiplasmin incubation with ASA and glucose resulted in 4.2-fold increased affinity to fibrin compared with alpha2-antiplasmin incubated with 50 mmol/l glucose (P < 0.001).	Aspirin	35-38	serpin family F member 2	Homo sapiens	0-18
32815992-17	2020	Aspirin increased SAA (P = 0.04) and tended to increase LBP (P = 0.09) in serum, but did not affect any other serum inflammatory marker (P >= 0.19).	Aspirin	0-7	serum amyloid A protein	Bos taurus	18-21
32854760-8	2020	In addition, our results showed that aspirin inhibits inflammation-related stemness gene expression (especially ICAM3) identified by a high-throughput siRNA platform.	Aspirin	37-44	intercellular adhesion molecule 3	Homo sapiens	112-117
32798401-9	2020	CCK-8 showed that the proliferation activity of U266 cells could be inhibited by aspirin, which showed a time-and dose-dependent manner; at the same time, the expression level of Blimp1 in U266 cells were decreased with the increasing of aspirin concentration, while the expression level of ATF4 and CHOP was increased with the increasing of aspirin concentration.	Aspirin	81-88	activating transcription factor 4	Homo sapiens	291-295
32798401-10	2020	CONCLUSIONS: Blimp1 may display the anti-apoptosis of myeloma cells through interfering with ATF4/CHOP signaling pathway; low dose of aspirin may play anti-myeloma effect by inhibiting the expression of Blimp1 in myeloma cells.	Aspirin	134-141	activating transcription factor 4	Homo sapiens	93-97
32523458-6	2020	In the COMPASS study, the association of aspirin with the factor Xa inhibitor, rivaroxaban, in a dose of one-fourth of the dose used in atrial fibrillation, decreased by more than 20% the incidence of CV events in patients with multi-district ATS.	Aspirin	41-48	coagulation factor X	Homo sapiens	58-67
32169518-8	2020	Furthermore, the levels of HMGB1 of subjects with URSA could be reduced by administrating low doses of aspirin (ASPL).	Aspirin	103-110	ASPSCR1 tether for SLC2A4, UBX domain containing	Homo sapiens	112-116
32546966-9	2020	Tmx treatment of MDA-MB-231 cells in combination with ASA, Met and OP markedly reduced the CD44/CD24 ratio by 6.5-fold compared to the untreated control group.	Aspirin	54-57	CD44 molecule (Indian blood group)	Homo sapiens	91-95
32351866-8	2020	The transcripts corresponding to AsA-GSH pathway enzymes SOD, APX, GR, DHAR, and MDHAR were up-regulated by 8- to 12-fold under combined drought and heat.	Aspirin	33-36	cytosolic ascorbate peroxidase 2	Solanum lycopersicum	62-65
32070879-0	2020	Aspirin exerts anti-tumor effect through inhibiting Blimp1 and activating ATF4/CHOP pathway in multiple myeloma.	Aspirin	0-7	activating transcription factor 4	Homo sapiens	74-78
31637734-12	2020	RNA sequencing showed that growth differentiation factor 6 (GDF6), GDF7, and GDF11 were upregulated in induction medium with the aspirin group compared with the induction medium group.	Aspirin	129-136	growth differentiation factor 6	Homo sapiens	27-58
31637734-12	2020	RNA sequencing showed that growth differentiation factor 6 (GDF6), GDF7, and GDF11 were upregulated in induction medium with the aspirin group compared with the induction medium group.	Aspirin	129-136	growth differentiation factor 6	Homo sapiens	60-64
31637734-12	2020	RNA sequencing showed that growth differentiation factor 6 (GDF6), GDF7, and GDF11 were upregulated in induction medium with the aspirin group compared with the induction medium group.	Aspirin	129-136	growth differentiation factor 11	Homo sapiens	77-82
31637734-14	2020	In addition, aspirin increased the expression of TNC, TNMD, and Scx and biomechanical properties of the injured tendon.	Aspirin	13-20	tenascin C	Homo sapiens	49-52
32252624-2	2020	AsA biosynthesis has been well studied in plants, and MIOX is a critical enzyme in plants AsA biosynthesis pathway.	Aspirin	90-93	myo-inositol oxygenase	Solanum lycopersicum	54-58
32252624-3	2020	However, Myo-inositol oxygenase (MIOX) gene family members and their involvement in AsA biosynthesis and response to abiotic stress remain unclear.	Aspirin	84-87	myo-inositol oxygenase	Solanum lycopersicum	9-31
32252624-3	2020	However, Myo-inositol oxygenase (MIOX) gene family members and their involvement in AsA biosynthesis and response to abiotic stress remain unclear.	Aspirin	84-87	myo-inositol oxygenase	Solanum lycopersicum	33-37
32052858-5	2020	PARTICIPANTS: Older (>=65 y) CLC residents with LLE/AD, admitted for 7 days or longer in fiscal years 2009 to 2015, who had a history of coronary artery disease and/or stroke/transient ischemic attack, and used aspirin within the first week of CLC admission (n = 13 844).	Aspirin	211-218	Charcot-Leyden crystal galectin	Homo sapiens	29-32
32244293-5	2020	Hence, we hypothesized that Aspirin could act as a substrate for esterase activity, and the product salicylic acid (SA), an inhibitor of CAII.	Aspirin	28-35	carbonic anhydrase 2	Homo sapiens	137-141
32244293-6	2020	Here, we present the crystal structure of CAII in complex with SA, a product of CAII crystals pre-soaked with Aspirin, to 1.35A resolution.	Aspirin	110-117	carbonic anhydrase 2	Homo sapiens	42-46
32244293-7	2020	In addition, we provide kinetic data to support the observation that CAII converts Aspirin to its deacetylated form, SA.	Aspirin	83-90	carbonic anhydrase 2	Homo sapiens	69-73
32244293-8	2020	This data may also explain the short half-life of Aspirin, with CAII so abundant in blood, and that Aspirin could act as a suicide inhibitor of CAII.	Aspirin	50-57	carbonic anhydrase 2	Homo sapiens	64-68
32244293-8	2020	This data may also explain the short half-life of Aspirin, with CAII so abundant in blood, and that Aspirin could act as a suicide inhibitor of CAII.	Aspirin	50-57	carbonic anhydrase 2	Homo sapiens	144-148
32244293-8	2020	This data may also explain the short half-life of Aspirin, with CAII so abundant in blood, and that Aspirin could act as a suicide inhibitor of CAII.	Aspirin	100-107	carbonic anhydrase 2	Homo sapiens	144-148
31918208-1	2020	Tumor cell-induced platelet aggregation (TCIPA) is the core mechanism potentiating high viability for circulatory tumor cells,which is the rate-limiting factor for metastasis.Additionally,as supported by the successful application of aspirin,the pro-malignant effects during tumor-platelets interaction can be largely neutralized by pharmacological deactivation of platelets.Caulis Spatholobi is widely used as an anti-coagulation herb in traditional Chinese medicine,indicating its potential against TCIPA.In our study,three fractions of Caulis Spatholobi extracts were firstly prepared.In colorectal cancer(CRC) model,the anti-metastatic potential was evaluated both in vitro and in vivo followed by the detection of their platlet regulatory effects.Results showed that all three extracts significantly suppressed the invasion and metastasis of CRC.Mechanistically,by blocking platelet-derived PDGF-B releasing,they reversed the enhanced epithelial mesenchymal transition during MC38-platelets interation.Further,ethyl acetate fraction shows the most promising efficacy for the future application in treatment.Overall,our study have for the first time proved CaulisSpatholobi extracts,especially the ethyl acetate fraction,as a potent TCIPA inhibitor during metastatic progression,which provided a novel candidate for pharmacologically blockage of metastasis in CRC.	Aspirin	234-241	platelet derived growth factor subunit B	Homo sapiens	896-902
32027271-19	2020	After aspirin stimulation of different concentrations for 48 hours, the expression level of Blimp1 in U266 cells decreased with increasing of drug concentration, while the expression levels of ATF4 and CHOP increased with increasing of drug concentration.	Aspirin	6-13	activating transcription factor 4	Homo sapiens	193-197
32027271-21	2020	Aspirin can inhibit the proliferation activity of myeloma cells by down-regulating Blimp1 expression in myeloma cells and up-regulating ATF4 and CHOP expression, therefore plays an anti-tumor rote.	Aspirin	0-7	activating transcription factor 4	Homo sapiens	136-140
31726963-9	2020	Our study suggests that BMI significantly influences the correlation between CYP2C19 genotype and efficacy of clopidogrel-aspirin therapy.	Aspirin	122-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-84
29757761-12	2019	Main mechanisms include medication nonadherence, interaction with proton pump inhibitors, esterase-mediated ASA inactivation, post-coronary artery bypass grafting (CABG) MRP-4-mediated ASA consumption, cyclooxygenase-1 (COX-1) polymorphisms, high platelet turnover-associated regeneration of platelet COX-1, and the documented platelet ability of de novo COX-1 synthesis in response to thrombin and fibrinogen.	Aspirin	185-188	ATP binding cassette subfamily C member 4	Homo sapiens	170-175
30974489-10	2019	Amongst smokers, clopidogrel plus aspirin might decrease the recurrence rate of stroke in non-carriers of *2 and *3 alleles of CYP2C19 compared with aspirin alone.	Aspirin	34-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	127-134
30684314-0	2019	Co-expression of the aryl hydrocarbon receptor and estrogen receptor in the developing teeth of rat offspring after rat mothers" exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin and the protective action of alpha-tocopherol and acetylsalicylic acid.	Aspirin	227-247	aryl hydrocarbon receptor	Rattus norvegicus	21-46
30684314-8	2019	In the TCDD+E and TCDD+ASA groups, there was a weak or negative ER expression and slightly stronger expression of AhR than in the TCDD group.	Aspirin	23-26	aryl hydrocarbon receptor	Rattus norvegicus	114-117
30684314-11	2019	The increase in AhR in TCDD+E and TCDD+ASA groups indicate a preventive action of antioxidant and antiinflammatory pharmaceutics, which may limit negative effects of TCDD.	Aspirin	39-42	aryl hydrocarbon receptor	Rattus norvegicus	16-19
31090213-0	2019	Use of aspirin in the prevention of colorectal cancer through TIGIT-CD155 pathway.	Aspirin	7-14	T cell immunoreceptor with Ig and ITIM domains	Homo sapiens	62-67
31090213-8	2019	We found that the expression of TIGIT decreased with an increase in the concentration of aspirin and that the suppression of TIGIT can affect the effect of aspirin on cell proliferation.	Aspirin	89-96	T cell immunoreceptor with Ig and ITIM domains	Homo sapiens	32-37
31090213-8	2019	We found that the expression of TIGIT decreased with an increase in the concentration of aspirin and that the suppression of TIGIT can affect the effect of aspirin on cell proliferation.	Aspirin	156-163	T cell immunoreceptor with Ig and ITIM domains	Homo sapiens	32-37
31090213-8	2019	We found that the expression of TIGIT decreased with an increase in the concentration of aspirin and that the suppression of TIGIT can affect the effect of aspirin on cell proliferation.	Aspirin	156-163	T cell immunoreceptor with Ig and ITIM domains	Homo sapiens	125-130
31171523-13	2019	CONCLUSION: Patients with minor stroke or transient ischaemic attack who are treated with ticagrelor plus aspirin have a lower proportion of high platelet reactivity than those who are treated with clopidogrel plus aspirin, particularly for those who are carriers of the CYP2C19 loss-of-function allele.	Aspirin	106-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	271-278
31138859-10	2019	For adult rat groups, aspirin significantly inhibited the production of 6-keto PGF1a, PGE2, and TXB2; however, it neither changed the ICP, AUC, or ICP/ MAP ratios nor altered the protein expression of eNOS, nNOS, COX-1, and COX-2.	Aspirin	22-29	nitric oxide synthase 3	Rattus norvegicus	201-205
31138859-10	2019	For adult rat groups, aspirin significantly inhibited the production of 6-keto PGF1a, PGE2, and TXB2; however, it neither changed the ICP, AUC, or ICP/ MAP ratios nor altered the protein expression of eNOS, nNOS, COX-1, and COX-2.	Aspirin	22-29	nitric oxide synthase 1	Rattus norvegicus	207-211
30944655-5	2019	In the present study, it was demonstrated that the expression of several positive regulators of EMT and Wnt signaling was repressed by aspirin treatment in SW480 tumor cells, and that this reduction was due to alterations in the localization of zinc finger E-box binding homeobox 1 and Snail family transcriptional repressor 2.	Aspirin	135-142	zinc finger E-box binding homeobox 1	Homo sapiens	245-281
30944655-5	2019	In the present study, it was demonstrated that the expression of several positive regulators of EMT and Wnt signaling was repressed by aspirin treatment in SW480 tumor cells, and that this reduction was due to alterations in the localization of zinc finger E-box binding homeobox 1 and Snail family transcriptional repressor 2.	Aspirin	135-142	snail family transcriptional repressor 2	Homo sapiens	286-326
30583998-8	2019	Patients treated with aspirin were significantly more common in the UGT1A1*28/*28 homozygous group than in the other groups (7/23 (30.4%) compared to 22/269 (8.2%), p = 0.001).	Aspirin	22-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
30961940-1	2019	BACKGROUND: We hypothesized that the peculiar mixed interleukin-4 (IL-4/Th2) and interferon gamma INF-gamma (INF-gamma/Th1) inflammatory milieu found in the airways of patients with aspirin-exacerbated respiratory disease (AERD) is responsible for the altered regulation of the IL-1beta/IL-1RI-/EP2/COX-2 autocrine loop also found in these patients.	Aspirin	182-189	negative elongation factor complex member C/D	Homo sapiens	109-122
29663427-0	2019	Surfactant protein D alleviates eosinophil-mediated airway inflammation and remodeling in patients with aspirin-exacerbated respiratory disease.	Aspirin	104-111	surfactant protein D	Homo sapiens	0-20
29663427-2	2019	However, the role of SPD in the pathogenesis of aspirin-exacerbated respiratory disease (AERD) is still unclear.	Aspirin	48-55	surfactant protein D	Homo sapiens	21-24
29663427-3	2019	METHODS: The serum SPD level was measured in patients with AERD (n = 336), those with aspirin-tolerant asthma (ATA, n = 442), and healthy controls (HC, n = 104).	Aspirin	86-93	surfactant protein D	Homo sapiens	19-22
29663427-8	2019	RESULTS: The serum SPD level was significantly lower (P &lt; .001) in AERD compared with ATA patients, and negatively correlated with fall in FEV1 (%) after lysine-aspirin bronchoprovocation test and/or the urinary LTE4 level.	Aspirin	164-171	surfactant protein D	Homo sapiens	19-22
29871742-6	2018	ADA had a moderate positive correlation with leucocyte and band neutrophil counts, haptoglobin, salivary alpha-amylase and ASA score, and a low positive correlation with C-reactive protein.	Aspirin	123-126	adenosine deaminase	Canis lupus familiaris	0-3
30046765-1	2018	Background: A mechanism involved in high on-aspirin treatment residual platelet reactivity is platelet multidrug resistance protein 4 (MRP4) overexpression.	Aspirin	44-51	ATP binding cassette subfamily C member 4	Homo sapiens	103-133
30046765-1	2018	Background: A mechanism involved in high on-aspirin treatment residual platelet reactivity is platelet multidrug resistance protein 4 (MRP4) overexpression.	Aspirin	44-51	ATP binding cassette subfamily C member 4	Homo sapiens	135-139
30046765-2	2018	Aspirin enhances platelet MRP4 expression with a PPARalpha-dependent mechanism and reduces miR-21 expression that, in turn, downregulates PPARalpha expression.	Aspirin	0-7	ATP binding cassette subfamily C member 4	Homo sapiens	26-30
30046765-3	2018	Objective: The aim of our study was to verify the relationship between miR-21 and MRP4-PPARalpha levels induced by aspirin treatment.	Aspirin	115-122	ATP binding cassette subfamily C member 4	Homo sapiens	82-86
30046765-4	2018	Methods: We evaluated the changes in MRP4-PPARalpha, mRNA, MRP4 protein, and miR-21 expression induced by aspirin in: (i) in vitro-treated megakaryoblastic cell line (DAMI), (ii) primary megakaryocytes cultures and derived platelets, (iii) healthy volunteers" platelets treated with aspirin, and (iv) aspirinated patients (aspirin-treated patients) and in a control population (control).	Aspirin	106-113	ATP binding cassette subfamily C member 4	Homo sapiens	37-41
30046765-5	2018	Results: We observed an aspirin-induced reverse relationship between the expression of miR-21 and PPARalpha-MRP4.	Aspirin	24-31	ATP binding cassette subfamily C member 4	Homo sapiens	108-112
30046765-8	2018	In human megakaryocytes, aspirin treatment lead to a miR-21 downregulation and a MRP4 upregulation and this trend is confirmed in derived platelets.	Aspirin	25-32	ATP binding cassette subfamily C member 4	Homo sapiens	81-85
28406726-10	2018	Pretreatment of platelets with acetylsalicylic acid did not change the effect of ADP but inhibited the effect of TRAP.	Aspirin	31-51	TRAP	Homo sapiens	113-117
29605975-1	2018	Proton pump inhibitors (PPIs) potently inhibit gastric acid secretion and are widely used for treatment of acid-related diseases including gastroesophageal reflux disease and secondary prevention of aspirin/NSAID-induced ulcers.	Aspirin	199-206	ATPase H+/K+ transporting subunit alpha	Homo sapiens	0-11
28442495-0	2018	Aspirin prevents NF-kappaB activation and CDX2 expression stimulated by acid and bile salts in oesophageal squamous cells of patients with Barrett"s oesophagus.	Aspirin	0-7	caudal type homeobox 2	Homo sapiens	42-46
28442495-2	2018	CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) signalling, which can be inhibited by aspirin.	Aspirin	197-204	caudal type homeobox 2	Homo sapiens	0-4
28442495-3	2018	We explored mechanisms underlying differences between NES-B and NES-G cells in CDX2 expression and effects of aspirin on that CDX2 expression.	Aspirin	110-117	caudal type homeobox 2	Homo sapiens	126-130
28442495-7	2018	Aspirin blocked IkappaB phosphorylation, p65 nuclear translocation, CDX2 promoter activation and CDX2 expression induced by acid and bile salts in NES-B cells.	Aspirin	0-7	caudal type homeobox 2	Homo sapiens	68-72
28442495-7	2018	Aspirin blocked IkappaB phosphorylation, p65 nuclear translocation, CDX2 promoter activation and CDX2 expression induced by acid and bile salts in NES-B cells.	Aspirin	0-7	caudal type homeobox 2	Homo sapiens	97-101
28442495-8	2018	CONCLUSIONS: Differences between NES-B and NES-G cells in NF-kappaB activation by acid and bile salts can account for their differences in CDX2 expression, and their CDX2 expression can be blocked by aspirin.	Aspirin	200-207	caudal type homeobox 2	Homo sapiens	166-170
29315961-13	2018	An optimized protocol of heparin before TP, double TP, and intravenous aspirin in non-ARP resulted in a significantly lowered CE incidence and severity.	Aspirin	71-78	arginine-glutamic acid dipeptide repeats	Homo sapiens	86-89
29448294-2	2018	Platelet function and thrombus formation are impaired in MRP4 knockout mice models, and, among aspirin-treated patients, high on-aspirin residual platelet reactivity (HARPR) positively correlates with MRP4 levels.	Aspirin	95-102	ATP binding cassette subfamily C member 4	Homo sapiens	201-205
29448294-2	2018	Platelet function and thrombus formation are impaired in MRP4 knockout mice models, and, among aspirin-treated patients, high on-aspirin residual platelet reactivity (HARPR) positively correlates with MRP4 levels.	Aspirin	129-136	ATP binding cassette subfamily C member 4	Homo sapiens	201-205
29468963-7	2018	It is important to note that some classical drugs available on the pharmaceutical market, such as acetylsalicylic acid, were also described more recently as NF-kappaB pathway modulators as IKKbeta inhibitors.	Aspirin	98-118	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	189-196
30317710-7	2018	Patients with AAA were significantly more medicated with acetylsalicylic acid and had more aortic thrombi (P=0,031 and P=0,002, respectively).	Aspirin	57-77	AAA1	Homo sapiens	14-17
29246216-0	2017	Association analysis of ILVBL gene polymorphisms with aspirin-exacerbated respiratory disease in asthma.	Aspirin	54-61	ilvB acetolactate synthase like	Homo sapiens	24-29
29246216-1	2017	BACKGROUND: We previously reported that the ILVBL gene on chromosome 19p13.1 was associated with the risk for aspirin-exacerbated respiratory disease (AERD) and the percent decline of forced expired volume in one second (FEV1) after an oral aspirin challenge test.	Aspirin	110-117	ilvB acetolactate synthase like	Homo sapiens	44-49
29246216-1	2017	BACKGROUND: We previously reported that the ILVBL gene on chromosome 19p13.1 was associated with the risk for aspirin-exacerbated respiratory disease (AERD) and the percent decline of forced expired volume in one second (FEV1) after an oral aspirin challenge test.	Aspirin	241-248	ilvB acetolactate synthase like	Homo sapiens	44-49
28899503-10	2017	RESULTS: Under non-inflammatory conditions P. tremula E and ASA increased cellular proteins (P) IL-8 and IL-10; S. virgaurea E modulated IL-1alpha, IL-10, IL-15 and Groalpha (P).	Aspirin	60-63	C-X-C motif chemokine ligand 1	Homo sapiens	165-173
28900541-7	2017	Using Hep3B and HuH7 HCC cells, it was demonstrated that sorafenib and aspirin acted synergistically to induce apoptosis.	Aspirin	71-78	MIR7-3 host gene	Homo sapiens	16-20
28724214-8	2017	The co-exposure of alpha-pinene with aspirin on cells significantly increased the survival of cells and the level of GSH, and decreased the levels of MDA and total SOD and the activity of Mn-SOD.	Aspirin	37-44	superoxide dismutase 2	Rattus norvegicus	164-167
28724214-8	2017	The co-exposure of alpha-pinene with aspirin on cells significantly increased the survival of cells and the level of GSH, and decreased the levels of MDA and total SOD and the activity of Mn-SOD.	Aspirin	37-44	superoxide dismutase 2	Rattus norvegicus	188-194
28346830-0	2017	Synergetic Neuroprotective Effect of Docosahexaenoic Acid and Aspirin in SH-Y5Y by Inhibiting miR-21 and Activating RXRalpha and PPARalpha.	Aspirin	62-69	retinoid X receptor alpha	Homo sapiens	116-124
28346830-5	2017	DHA and ASA could activate RXRalpha and PPARalpha, respectively.	Aspirin	8-11	retinoid X receptor alpha	Homo sapiens	27-35
28487961-0	2017	Influence of aspirin on the CX3CL1/CX3CR1 signaling pathway in acute pulmonary embolism.	Aspirin	13-20	C-X3-C motif chemokine receptor 1	Rattus norvegicus	35-41
28487961-1	2017	The present study aimed to explore the influence of aspirin on the CX3CL1/CX3CR1 signaling pathway in acute pulmonary embolism (APE) in rats.	Aspirin	52-59	C-X3-C motif chemokine receptor 1	Rattus norvegicus	74-80
28487961-7	2017	Aspirin significantly decreased pulmonary artery pressure, improve pathological changes in the embolism, and decreased the expression of CX3CL1/CX3CR1 and CX3CL1/NF-kappaB.	Aspirin	0-7	C-X3-C motif chemokine receptor 1	Rattus norvegicus	144-150
28487961-10	2017	In conclusion, aspirin improved pathological changes in rats with APE via the CX3CL1/CX3CR1 signaling pathway.	Aspirin	15-22	C-X3-C motif chemokine receptor 1	Rattus norvegicus	85-91
27762101-3	2017	The preliminary in vitro trials revealed that compounds with urea as the linker were not active, and the presence of aspirin elevated the potency of 6k against tumor cells, wound healing, and the protein expression of cyclic D1 and MMP9.	Aspirin	117-124	matrix metallopeptidase 9	Homo sapiens	232-236
28289237-8	2017	CONCLUSIONS: In patients with minor stroke or high-risk transient ischemic attack, clopidogrel-aspirin when compared with aspirin alone reduced stroke recurrence only in noncarriers of CYP2C19 loss-of-function allele and normal GA levels.	Aspirin	95-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	185-192
27992364-3	2017	Meanwhile, miR-30eoverexpression inPC9G cells resulted in reduced cell proliferation and migration,reversing drug resistance to gefitinib.Conversely,miR-30e silencing in PC9 cells increased proliferation as well as migration, and conferred resistance to gefitinib.Moreover, HOXA1, which was identified asa new miR-30etarget, plays important roles in regulating cell fate, early developmental patterns and organogenesis.Importantly, miR-30ealso inhibited PC9G growth in vivo.	Aspirin	302-305	membrane associated ring-CH-type finger 8	Homo sapiens	11-14
27992364-3	2017	Meanwhile, miR-30eoverexpression inPC9G cells resulted in reduced cell proliferation and migration,reversing drug resistance to gefitinib.Conversely,miR-30e silencing in PC9 cells increased proliferation as well as migration, and conferred resistance to gefitinib.Moreover, HOXA1, which was identified asa new miR-30etarget, plays important roles in regulating cell fate, early developmental patterns and organogenesis.Importantly, miR-30ealso inhibited PC9G growth in vivo.	Aspirin	302-305	membrane associated ring-CH-type finger 8	Homo sapiens	149-152
27992364-3	2017	Meanwhile, miR-30eoverexpression inPC9G cells resulted in reduced cell proliferation and migration,reversing drug resistance to gefitinib.Conversely,miR-30e silencing in PC9 cells increased proliferation as well as migration, and conferred resistance to gefitinib.Moreover, HOXA1, which was identified asa new miR-30etarget, plays important roles in regulating cell fate, early developmental patterns and organogenesis.Importantly, miR-30ealso inhibited PC9G growth in vivo.	Aspirin	302-305	membrane associated ring-CH-type finger 8	Homo sapiens	149-152
27999284-5	2016	These findings provide evidence that aspirin down regulates hepcidin by inhibiting IL6/JAK2/STAT3 and P65 (nuclear factor-kappaB) pathways in the cells under inflammatory conditions, and imply that an aspirin-induced reduction in TfR1 and an increase in ferritin are not associated with IRP1 and NO.	Aspirin	201-208	aconitase 1	Mus musculus	287-291
27208561-0	2016	Aspirin resistance may be identified by miR-92a in plasma combined with platelet distribution width.	Aspirin	0-7	membrane associated ring-CH-type finger 8	Homo sapiens	40-43
27208561-2	2016	This study aimed to investigate the value of circulating miR-92a and platelet size as biomarkers of the individual response to aspirin therapy.	Aspirin	127-134	membrane associated ring-CH-type finger 8	Homo sapiens	57-60
27208561-7	2016	RESULTS: When defining aspirin resistance as an ASPItest &gt;=30U, the optimal cut-off values for discrimination of aspirin responders and aspirin resistant patients were found to be PDW&gt;11.8fL and a relative expression level of miR-92a&gt;4.5.	Aspirin	23-30	membrane associated ring-CH-type finger 8	Homo sapiens	232-235
27208561-8	2016	Using these cut-off values we could define a PDW/miR-92a-score with a specificity of 97.5% and a sensitivity of 80.0% in relation to detect aspirin resistance.	Aspirin	140-147	membrane associated ring-CH-type finger 8	Homo sapiens	49-52
27208561-10	2016	CONCLUSION: Aspirin resistance can potentially be identified by miR-92a levels in plasma combined with PDW.	Aspirin	12-19	membrane associated ring-CH-type finger 8	Homo sapiens	64-67
26645266-0	2016	Protective effects of aspirin and vitamin C against corn syrup consumption-induced cardiac damage through sirtuin-1 and HIF-1alpha pathway.	Aspirin	22-29	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	120-130
26645266-1	2016	OBJECTIVE: The aim of this study was to investigate the protective effects of aspirin (AS) and vitamin C (VC) against cardiac damage induced by chronic corn syrup (CS) consumption via a mechanism involving sirtuin-1 (ST-1), hypoxia-inducible factor-1alpha (HIF-1alpha), and the caspase-3 pathway in rats.	Aspirin	78-85	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	257-267
27430429-3	2016	In the current study, the addition of NF-kappaB inhibitors (Bay11-7082, Z-LLF-CHO and aspirin) was observed to induce the EBV lytic genes BZLF1, BRLF1 and BMRF1 in EBV-positive gastric cancer (GC) cells.	Aspirin	86-93	BRLF1	Human gammaherpesvirus 4	145-150
27348249-13	2016	CONCLUSIONS AND RELEVANCE: Among patients with minor ischemic stroke or transient ischemic attack, the use of clopidogrel plus aspirin compared with aspirin alone reduced the risk of a new stroke only in the subgroup of patients who were not carriers of the CYP2C19 loss-of-function alleles.	Aspirin	127-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	258-265
27032071-11	2016	Additionally, MDA levels in coelomic fluid were negatively correlated with dietary AsA levels, while antioxidant capacities (SOD, GSH-Px and CAT) were positively correlated with dietary AsA levels.	Aspirin	186-189	catalase isozyme 1	Cucumis sativus	130-144
27347106-0	2016	Aspirin inhibits growth of ovarian cancer by upregulating caspase-3 and downregulating bcl-2.	Aspirin	0-7	caspase 3	Mus musculus	58-67
27347106-10	2016	The relative expression level of caspase-3, bcl-2 protein of the 3 mmol/l aspirin group was significantly improved and reduced, respectively.	Aspirin	74-81	caspase 3	Mus musculus	33-42
27347106-11	2016	In conclusion, aspirin can inhibit the growth of ovarian cancer of p53S rats due to its upregulation of the expression of caspase-3 protein and downregulation of the expression of bcl-2 protein.	Aspirin	15-22	caspase 3	Mus musculus	122-131
27216891-8	2016	Furthermore, aspirin treatment of PDLSCs upregulated GCN5 expression and increased osteogenic differentiation of PDLSCs.	Aspirin	13-20	lysine acetyltransferase 2A	Homo sapiens	53-57
27216891-9	2016	In conclusion, GCN5 plays a protective role in periodontitis through acetylation of DKK1 and applying drugs targeting GCN5, such as aspirin, could be a new approach for periodontitis treatment.	Aspirin	132-139	lysine acetyltransferase 2A	Homo sapiens	15-19
27216891-9	2016	In conclusion, GCN5 plays a protective role in periodontitis through acetylation of DKK1 and applying drugs targeting GCN5, such as aspirin, could be a new approach for periodontitis treatment.	Aspirin	132-139	lysine acetyltransferase 2A	Homo sapiens	118-122
27006152-6	2016	A total 89 patients were included in the analysis; 13 patients (15%) had ASA of non-LAD SPA.	Aspirin	73-76	surfactant protein A2	Homo sapiens	88-91
27006152-7	2016	These patients were more likely to have a history of failed ASA, more than one SPA treated, more ethanol dose injected, longer procedures, and higher contrast use compared with those who had ASA of LAD-SPA.	Aspirin	191-194	surfactant protein A2	Homo sapiens	202-205
27006152-9	2016	In conclusion, in a cohort of patients undergoing ASA, 15% had ablation of SPA culprit that did not originate from the LAD.	Aspirin	50-53	surfactant protein A2	Homo sapiens	75-78
27006152-11	2016	Systematic screening for the ideal culprit SPA with nonselective coronary injection of echo contrast should be used to avoid incomplete or failed ASA.	Aspirin	146-149	surfactant protein A2	Homo sapiens	43-46
27055402-7	2016	Consistent with LEF1 being a downstream effector of Wnt signaling, aspirin, but not I3C, downregulated protein levels of the Wnt co-receptor LDL receptor-related protein-6 and beta-catenin and upregulated the beta-catenin destruction complex component Axin.	Aspirin	67-74	axin 1	Homo sapiens	252-256
26743169-8	2016	Finally, in vitro treatment with GLS-409 showed effects similar to that of cangrelor and the combination of cangrelor with the selective P2Y1 inhibitor MRS 2179 on agonist-stimulated platelet aggregation in human platelet-rich plasma and whole blood before and 2 hours after aspirin intake.	Aspirin	275-282	glutaminase 2	Rattus norvegicus	33-36
26743169-9	2016	CONCLUSIONS: Synergistic inhibition of both P2Y1 and P2Y12 adenosine diphosphate receptors by GLS-409 immediately attenuates platelet-mediated thrombosis and effectively blocks agonist-stimulated platelet aggregation irrespective of concomitant aspirin therapy.	Aspirin	245-252	glutaminase 2	Rattus norvegicus	94-97
26915040-6	2016	We report that mutations in both PIK3CA and KRAS are required for the greatest aspirin sensitivity in breast cancer, and that the GSK3beta protein was hyperphosphorylated in aspirin-treated double knockin cells, but not in other clones/treatments.	Aspirin	79-86	KRAS proto-oncogene, GTPase	Homo sapiens	44-48
26915040-6	2016	We report that mutations in both PIK3CA and KRAS are required for the greatest aspirin sensitivity in breast cancer, and that the GSK3beta protein was hyperphosphorylated in aspirin-treated double knockin cells, but not in other clones/treatments.	Aspirin	174-181	KRAS proto-oncogene, GTPase	Homo sapiens	44-48
26586373-5	2016	Patients" stratification based on ASA dose showed more significant reductions in P-selectin, CD40L, and MMP-9 serum levels postclopidogrel administration in patients who were on baseline 81 mg ASA, as compared to patients on 325 mg ASA.	Aspirin	34-37	matrix metallopeptidase 9	Homo sapiens	104-109
26586373-5	2016	Patients" stratification based on ASA dose showed more significant reductions in P-selectin, CD40L, and MMP-9 serum levels postclopidogrel administration in patients who were on baseline 81 mg ASA, as compared to patients on 325 mg ASA.	Aspirin	193-196	matrix metallopeptidase 9	Homo sapiens	104-109
26586373-5	2016	Patients" stratification based on ASA dose showed more significant reductions in P-selectin, CD40L, and MMP-9 serum levels postclopidogrel administration in patients who were on baseline 81 mg ASA, as compared to patients on 325 mg ASA.	Aspirin	193-196	matrix metallopeptidase 9	Homo sapiens	104-109
26794215-7	2016	In 4T1 cells, treatment with aspirin decreased cell viability and migration, possibly by suppressing MCP-1 and VEGF secretion.	Aspirin	29-36	vascular endothelial growth factor A	Mus musculus	111-115
26828987-8	2016	Additionally, it was found that patients who have clopidogrel and/or aspirin resistance also have CYP2C19*1/*2 or CYPC19*2/*2 genotype.	Aspirin	69-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	98-105
26739449-1	2016	BACKGROUND: The aim of this study was to investigate the association between serum concentrations of the brain-derived neurotrophic factor (BDNF), platelet reactivity and inflammatory markers, as well as its association with BDNF encoding gene variants in type 2 diabetic patients (T2DM) during acetylsalicylic acid (ASA) therapy.	Aspirin	295-315	brain derived neurotrophic factor	Homo sapiens	105-138
27533057-0	2016	Proton pump inhibitor use by aspirin-treated coronary artery disease patients is not associated with increased risk of cardiovascular events.	Aspirin	29-36	ATPase H+/K+ transporting subunit alpha	Homo sapiens	0-11
27533057-1	2016	AIMS: Daily low-dose aspirin is recommended for prevention of cardiovascular events in patients with coronary artery disease (CAD), and proton pump inhibitors (PPIs) are recommended to prevent or treat aspirin-associated gastrointestinal injury.	Aspirin	202-209	ATPase H+/K+ transporting subunit alpha	Homo sapiens	136-147
26626190-10	2015	Aspirin efficiently reversed the upregulation of beta-catenin and P-Akt expression and the TAC- or ANG II-induced downregulation of GSK-3beta.	Aspirin	0-7	catenin (cadherin associated protein), beta 1	Mus musculus	49-61
26626190-12	2015	The downregulation of beta-catenin and Akt may be the underlying signaling mechanism of the effects of aspirin.	Aspirin	103-110	catenin (cadherin associated protein), beta 1	Mus musculus	22-34
26264906-0	2015	Association of CYP2C19, CYP3A5 and GPIIb/IIIa gene polymorphisms with Aspirin and Clopidogrel Resistance in a cohort of Indian patients with Coronary Artery Disease.	Aspirin	70-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
26264906-0	2015	Association of CYP2C19, CYP3A5 and GPIIb/IIIa gene polymorphisms with Aspirin and Clopidogrel Resistance in a cohort of Indian patients with Coronary Artery Disease.	Aspirin	70-77	integrin subunit alpha 2b	Homo sapiens	35-40
26606050-11	2015	Moreover, ASA- induced gastritis resulted in increased expression of NPY (76.59 +- 3.02%) and GAL (26.45 +- 2.75%) as well as the novo-synthesis of nNOS (6.13 +- 1.11%) and LENK (4.77 +- 0.42%) in traced CCMG neurons.	Aspirin	10-13	nitric oxide synthase 1	Sus scrofa	148-152
26606050-12	2015	Additionally, a network of CART-, CGRP-, SP-, VIP-, LENK-, nNOS- immunoreactive (IR) nerve fibers encircling the FB-positive perikarya were observed in both intact and ASA-treated animals.	Aspirin	168-171	nitric oxide synthase 1	Sus scrofa	59-63
26290157-9	2015	There was an increased risk of delayed PPB in patients on clopidogrel + aspirin and/or NSAIDs (OR = 3.4, 95% CI 1.3-8.8, P = 0.01, I(2)  = 0).	Aspirin	72-79	histatin 1	Homo sapiens	39-42
26366802-1	2015	This study is aimed at investigating the association of HLA-DRB1, HLA-DQA1, and HLA-DQB1 variability with the response to aspirin desensitization (AD).	Aspirin	122-129	major histocompatibility complex, class II, DQ beta 1	Homo sapiens	80-88
26539867-8	2015	We have shown: 1) the 145Met GP Iba allele prevalence in patients with atherotrombotic stroke development due to macroangiopathy; 2) the pre-mRNA transform into the mature mRNA in activated platelets and this process may be stopped by the antiplatelet therapy by acetylsalicylic acid.	Aspirin	263-283	glycoprotein Ib platelet subunit alpha	Homo sapiens	29-35
26237513-6	2015	Dual antiplatelet therapy with aspirin and clopidogrel was associated with significantly lower levels of sCD40L and lower platelet surface expressions of P-selectin and activated GPIIb/IIIa compared to aspirin monotherapy (all p&lt;=0.01).	Aspirin	31-38	integrin subunit alpha 2b	Homo sapiens	179-184
26018088-11	2015	Our study has thus revealed that EP2 in neutrophils and tumor-associated fibroblasts promotes colon tumorigenesis by amplifying inflammation and shaping tumor microenvironment, and suggests that EP2 antagonists are promising candidates of aspirin-alternative for chemoprevention of colorectal cancer.	Aspirin	239-246	prostaglandin E receptor 2 (subtype EP2)	Mus musculus	33-36
26018088-11	2015	Our study has thus revealed that EP2 in neutrophils and tumor-associated fibroblasts promotes colon tumorigenesis by amplifying inflammation and shaping tumor microenvironment, and suggests that EP2 antagonists are promising candidates of aspirin-alternative for chemoprevention of colorectal cancer.	Aspirin	239-246	prostaglandin E receptor 2 (subtype EP2)	Mus musculus	195-198
25503556-8	2015	We observed a strong correlation between RAGE and disease severity, recurrence, undergone operations, asthma and aspirin exacerbated respiratory disease (AERD).	Aspirin	113-120	advanced glycosylation end-product specific receptor	Homo sapiens	41-45
25954113-0	2015	Proton pump inhibitors in prevention of low-dose aspirin-associated upper gastrointestinal injuries.	Aspirin	49-56	ATPase H+/K+ transporting subunit alpha	Homo sapiens	0-11
25954113-1	2015	AIM: To determine the preventive effect and safety of proton pump inhibitors (PPIs) in low-dose aspirin (LDA)-associated gastrointestinal (GI) ulcers and bleeding.	Aspirin	96-103	ATPase H+/K+ transporting subunit alpha	Homo sapiens	54-65
25557764-3	2015	As predicted, ASA and salicylic acid (SA) treatment resulted in generation of H2O2, which is known to be an inducer of mitochondrial gene Sirt4 and other downstream target genes of Sirt1.	Aspirin	14-17	sirtuin 1	Homo sapiens	181-186
25394850-4	2015	Mechanistically, ASA treatment upregulates the telomerase reverse transcriptase (TERT)/Wnt/beta-catenin cascade, leading to improvement of SHED-mediated bone regeneration, and also upregulates TERT/FASL signaling, leading to improvement of SHED-mediated T-cell apoptosis and ameliorating disease phenotypes in dextran sodium sulfate-induced colitis mice.	Aspirin	17-20	catenin (cadherin associated protein), beta 1	Mus musculus	91-103
25109257-5	2014	Similar to aspirin, we found that an early response to the analogues was a reduction in levels of cyclin D1 and stimulation of the NF-kappaB pathway.	Aspirin	11-18	cyclin D1	Mus musculus	98-107
25104439-8	2014	SOCS2 (one of three SNPs) and all STAT3, STAT5A, and STAT5B SNPs significantly interacted with use of aspirin/NSAIDs to alter breast cancer-specific mortality.	Aspirin	102-109	suppressor of cytokine signaling 2	Homo sapiens	0-5
25093045-0	2014	Acetylsalicylic acid, aging and coronary artery disease are associated with ABCA1 DNA methylation in men.	Aspirin	0-20	ATP binding cassette subfamily A member 1	Homo sapiens	76-81
24836854-0	2014	Aspirin-triggered Lipoxin A4 attenuates mechanical allodynia in association with inhibiting spinal JAK2/STAT3 signaling in neuropathic pain in rats.	Aspirin	0-7	Janus kinase 2	Rattus norvegicus	99-103
25055737-0	2014	Dermcidin isoform-2 induced nullification of the effect of acetyl salicylic acid in platelet aggregation in acute myocardial infarction.	Aspirin	59-80	dermcidin	Homo sapiens	0-9
25055737-5	2014	When normal PRP was incubated with 0.4 muM dermcidin, the platelets became resistant to the inhibitory effect of aspirin similar to that in the case of AMI.	Aspirin	113-120	dermcidin	Homo sapiens	43-52
25037196-6	2014	In ACS patients, plasma MRP-8/14 and urinary 11-dehydro-TXB2 levels were linearly correlated (r=0.651, P&lt;0.001) but significantly higher than those in IHD patients (P=0.012, P=0.044) only among subjects not receiving aspirin.	Aspirin	220-227	ATP binding cassette subfamily C member 11	Homo sapiens	24-29
25037196-7	2014	In aspirin-treated ACS patients, MRP-8/14 and 11-dehydro-TXB2 were lower versus those not receiving aspirin (P&lt;0.001) and still significantly correlated (r=0.528, P&lt;0.001).	Aspirin	3-10	ATP binding cassette subfamily C member 11	Homo sapiens	33-38
25037196-8	2014	Higher 11-dehydro-TXB2 significantly predicted higher MRP-8/14 in both all ACS patients and ACS receiving aspirin (P&lt;0.001, adj R(2)=0.463 and adj R(2)=0.497) after multivariable adjustment.	Aspirin	106-113	ATP binding cassette subfamily C member 11	Homo sapiens	54-59
24889212-7	2014	RESULTS: We found indications that aspirin interacted with rs6983267 close to MYC (encoding a transcription factor involved in cell cycle progression, apoptosis and cellular transformation) and NSAIDs interacted with rs3024505 and rs1800872 in or close to IL10 (encoding IL-10) in preventing CRC.	Aspirin	35-42	interleukin 10	Homo sapiens	256-260
24889212-7	2014	RESULTS: We found indications that aspirin interacted with rs6983267 close to MYC (encoding a transcription factor involved in cell cycle progression, apoptosis and cellular transformation) and NSAIDs interacted with rs3024505 and rs1800872 in or close to IL10 (encoding IL-10) in preventing CRC.	Aspirin	35-42	interleukin 10	Homo sapiens	271-276
24571196-4	2014	The aim was to analyse the relationship between platelet response to ASA and both NO generation and vitamin-D-binding protein content in mononuclear cells.	Aspirin	69-72	GC vitamin D binding protein	Homo sapiens	100-125
24571196-8	2014	DBP content in mononuclear cells was higher in ASA resistant than in ASA sensitive.	Aspirin	47-50	GC vitamin D binding protein	Homo sapiens	0-3
24571196-8	2014	DBP content in mononuclear cells was higher in ASA resistant than in ASA sensitive.	Aspirin	69-72	GC vitamin D binding protein	Homo sapiens	0-3
24571196-9	2014	The level of DBP content in mononuclear cells was negatively associated with the ability of ASA to inhibit platelets.	Aspirin	92-95	GC vitamin D binding protein	Homo sapiens	13-16
24520038-0	2014	Repurposing of metformin and aspirin by targeting AMPK-mTOR and inflammation for pancreatic cancer prevention and treatment.	Aspirin	29-36	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	50-54
24632840-11	2014	In line with the ex vivo findings, sFlt-1-induced BP elevation could be prevented in vivo by oral treatment with either a high-dose of the COX inhibitor aspirin (N = 7) or with picotamide (N = 9), a dual thromboxane A2 synthase inhibitor and receptor antagonist.	Aspirin	153-160	FMS-like tyrosine kinase 1	Mus musculus	35-41
24618698-4	2014	A recent genome-wide association study identified the gene encoding the centrosomal protein of 68 KDa (CEP68) as the major locus associated with aspirin intolerance susceptibility in asthmatics.	Aspirin	145-152	centrosomal protein 68	Homo sapiens	72-101
24618698-4	2014	A recent genome-wide association study identified the gene encoding the centrosomal protein of 68 KDa (CEP68) as the major locus associated with aspirin intolerance susceptibility in asthmatics.	Aspirin	145-152	centrosomal protein 68	Homo sapiens	103-108
24609741-2	2014	Thus, GP IIb-IIIa inhibitors could favour endogenous thrombolysis by reducing thrombus growth and preventing thrombus re-formation through competitive inhibition with fibrinogen and, due to their mechanism of action, are likely to have a more profound antiplatelet effect with more rapid onset than conventional antiplatelet agents, such as aspirin or clopidogrel.	Aspirin	341-348	integrin subunit alpha 2b	Homo sapiens	6-12
24452610-8	2014	However, in Rivaroxaban in Combination With Aspirin Alone or With Aspirin and a Thienopyridine in Patients With Acute Coronary Syndromes (ATLAS ACS 2 TIMI 51), fatal bleeding or fatal ICH did not increase with low-dose rivaroxaban added to low-dose acetylsalicylic acid-based standard care compared with standard care alone.	Aspirin	44-51	acyl-CoA synthetase long chain family member 5	Homo sapiens	144-149
24648214-7	2014	Low-dose aspirin improved HFD-induced hyperinsulinemia and hyperlipidemia, recovered PT and aPTT, inhibited upregulation of adhesion molecules and chemokines and reduced expression of PKCalpha, IKKalpha, p65, and MAPKs.	Aspirin	9-16	protein kinase C, alpha	Rattus norvegicus	184-192
24683408-5	2014	A PLAA level above 20% was defined as aspirin resistance.	Aspirin	38-45	phospholipase A2 activating protein	Homo sapiens	2-6
24624912-7	2014	The G allele of CCR3 -520T&gt;G was associated with persistent bronchial hypersensitivity to aspirin.	Aspirin	93-100	C-C motif chemokine receptor 3	Homo sapiens	16-20
24428436-10	2014	Treatment with ASA normalised the raised mRNA expressions of nNOS in diabetic penile tissues.	Aspirin	15-18	nitric oxide synthase 1	Rattus norvegicus	61-65
24088578-1	2014	AIM: Carriers of the reduced-function CYP2C19 allele receiving dual antiplatelet therapy (DAPT) with aspirin and clopidogrel exhibit diminished platelet inhibition and an increased risk of events.	Aspirin	101-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
24026640-9	2013	Furthermore, the levels of BNP, TnT and D-Dimer levels were decreased in the aspirin-treated groups (P&lt;0.05) and markedly increased in the model group (P&lt;0.05) at 24 h compared with the levels at 6 h. Pulmonary embolism, alveolar wall necrosis and hemorrhage were observed in the model group 6, 24 and 72 h subsequent to the induction of the model.	Aspirin	77-84	troponin T3, fast skeletal type	Rattus norvegicus	32-35
24113271-2	2013	Aspirin influenced the formation of a complex by Bcl-2 and FKBP38 and induced the nuclear translocation of Bcl-2 and its phosphorylation.	Aspirin	0-7	FKBP prolyl isomerase 8	Homo sapiens	59-65
23688555-8	2013	Response to aspirin was significantly associated with GPIba C-5T polymorphism (P&lt;0.05).	Aspirin	12-19	glycoprotein Ib platelet subunit alpha	Homo sapiens	54-59
23688555-10	2013	CONCLUSION: A considerable fraction of the Jordanian population is resistant to the antiplatelet effect of aspirin, which might be related to GPIba C-5T polymorphism.	Aspirin	107-114	glycoprotein Ib platelet subunit alpha	Homo sapiens	142-147
23880611-0	2013	Upregulation of CD11b on eosinophils in aspirin induced asthma.	Aspirin	40-47	integrin subunit alpha M	Homo sapiens	16-21
23880611-4	2013	CD11b and CD16 expressions on the peripheral-blood granulocytes after administration of aspirin and different concentrations of PGE2 in vitro were examined using flowcytometry.	Aspirin	88-95	integrin subunit alpha M	Homo sapiens	0-5
23880611-4	2013	CD11b and CD16 expressions on the peripheral-blood granulocytes after administration of aspirin and different concentrations of PGE2 in vitro were examined using flowcytometry.	Aspirin	88-95	Fc gamma receptor IIIa	Homo sapiens	10-14
23880611-5	2013	RESULTS: Aspirin induced a significant increase in CD11b expression on eosinophils (CD16 negative granulocytes) in 19 AIA patients and one non-AIA patient.	Aspirin	9-16	integrin subunit alpha M	Homo sapiens	51-56
23880611-5	2013	RESULTS: Aspirin induced a significant increase in CD11b expression on eosinophils (CD16 negative granulocytes) in 19 AIA patients and one non-AIA patient.	Aspirin	9-16	Fc gamma receptor IIIa	Homo sapiens	84-88
23880611-6	2013	Increase in CD11b expression on eosinophils by aspirin administration was suppressed by PGE2 in a dose-dependent manner.	Aspirin	47-54	integrin subunit alpha M	Homo sapiens	12-17
23880611-9	2013	In addition, PGE2 may be involved in regulation of CD11b expression on eosinophils by aspirin administration.	Aspirin	86-93	integrin subunit alpha M	Homo sapiens	51-56
23809370-0	2013	NSAID, aspirin delays gastric ulcer healing with reduced accumulation of CXCR4(+)VEGFR1(+) cells to the ulcer granulation tissues.	Aspirin	7-14	chemokine (C-X-C motif) receptor 4	Mus musculus	73-78
23809370-0	2013	NSAID, aspirin delays gastric ulcer healing with reduced accumulation of CXCR4(+)VEGFR1(+) cells to the ulcer granulation tissues.	Aspirin	7-14	FMS-like tyrosine kinase 1	Mus musculus	81-87
23799623-4	2013	In the present study, we revealed that the treatment with a combination of MTX and ASA resulted in antagonism of the cytotoxic effect as demonstrated by SRB and colony formation assays.	Aspirin	83-86	chaperonin containing TCP1 subunit 4	Homo sapiens	153-156
23615159-1	2013	Edoxaban is an oral factor Xa (FXa) inhibitor in clinical development for stroke prevention in patients with atrial fibrillation, an elderly population that frequently receives aspirin (ASA) and/or nonsteroidal anti-inflammatory drugs for concurrent illnesses.	Aspirin	177-184	coagulation factor X	Homo sapiens	31-34
23615159-1	2013	Edoxaban is an oral factor Xa (FXa) inhibitor in clinical development for stroke prevention in patients with atrial fibrillation, an elderly population that frequently receives aspirin (ASA) and/or nonsteroidal anti-inflammatory drugs for concurrent illnesses.	Aspirin	186-189	coagulation factor X	Homo sapiens	31-34
23733341-5	2013	Such LXA4-based circuit could be activated by aspirin (30-100 mg/kg), which triggered formation of 15-epi-LXA4 in wild-type mice, yet it was effective in Fpr2/3(-/-) mice.	Aspirin	46-53	formyl peptide receptor 2	Mus musculus	154-158
23703473-0	2013	Aspirin enhances IFN-alpha-induced growth inhibition and apoptosis of hepatocellular carcinoma via JAK1/STAT1 pathway.	Aspirin	0-7	interferon alpha	Mus musculus	17-26
23703473-0	2013	Aspirin enhances IFN-alpha-induced growth inhibition and apoptosis of hepatocellular carcinoma via JAK1/STAT1 pathway.	Aspirin	0-7	signal transducer and activator of transcription 1	Mus musculus	104-109
23703473-2	2013	In this study we want to investigate whether aspirin can improve the antitumor efficiency of IFN-alpha on hepatocellular carcinoma (HCC) through the activation of STAT1.	Aspirin	45-52	interferon alpha	Mus musculus	93-102
23703473-2	2013	In this study we want to investigate whether aspirin can improve the antitumor efficiency of IFN-alpha on hepatocellular carcinoma (HCC) through the activation of STAT1.	Aspirin	45-52	signal transducer and activator of transcription 1	Mus musculus	163-168
23703473-3	2013	We found that aspirin not only significantly enhanced IFN-alpha-induced antiproliferation and apoptosis of HCC in vitro study but also enhanced tumor growth inhibition in nude mice.	Aspirin	14-21	interferon alpha	Mus musculus	54-63
23703473-4	2013	Although IFN-alpha alone resulted in significant phosphorylation of both STAT1 and STAT3, aspirin only prompted the IFN-alpha-induced phosphorylation of STAT1.	Aspirin	90-97	interferon alpha	Mus musculus	116-125
23703473-4	2013	Although IFN-alpha alone resulted in significant phosphorylation of both STAT1 and STAT3, aspirin only prompted the IFN-alpha-induced phosphorylation of STAT1.	Aspirin	90-97	signal transducer and activator of transcription 1	Mus musculus	153-158
23703473-5	2013	Further study revealed that aspirin-prompted phosphorylation of STAT1 was activated through phosphorylation of JAK1.	Aspirin	28-35	signal transducer and activator of transcription 1	Mus musculus	64-69
23703473-7	2013	Taken together, our findings suggest a novel strategy of using aspirin to overcome tumor resistance and enhance the effectiveness of IFN-alpha in HCC treatment through activating STAT1 gene, and have potential implications for improving future IFN-alpha protein and gene therapy.	Aspirin	63-70	interferon alpha	Mus musculus	133-142
23703473-7	2013	Taken together, our findings suggest a novel strategy of using aspirin to overcome tumor resistance and enhance the effectiveness of IFN-alpha in HCC treatment through activating STAT1 gene, and have potential implications for improving future IFN-alpha protein and gene therapy.	Aspirin	63-70	signal transducer and activator of transcription 1	Mus musculus	179-184
23703473-7	2013	Taken together, our findings suggest a novel strategy of using aspirin to overcome tumor resistance and enhance the effectiveness of IFN-alpha in HCC treatment through activating STAT1 gene, and have potential implications for improving future IFN-alpha protein and gene therapy.	Aspirin	63-70	interferon alpha	Mus musculus	244-253
23552127-10	2013	CONCLUSION: This retrospective analysis of the SMILE-4 study confirmed the good efficacy of zofenopril and ASA in the prevention of long-term cardiovascular outcomes also in the subgroup of patients with hypertension.	Aspirin	107-110	transmembrane O-mannosyltransferase targeting cadherins 3	Homo sapiens	47-52
23441755-0	2013	Low prostaglandin E2 and cyclooxygenase expression in nasal mucosa fibroblasts of aspirin-intolerant asthmatics.	Aspirin	82-89	cystatin 12, pseudogene	Homo sapiens	18-39
23306703-0	2013	Acetyl salicylic acid inhibits Th17 airway inflammation via blockade of IL-6 and IL-17 positive feedback.	Aspirin	0-21	interleukin 17A	Mus musculus	81-86
23306703-5	2013	ASA inhibited the production of interleukin (IL)-17 from lung T cells as well as in vitro Th17 polarization induced by IL-6.	Aspirin	0-3	interleukin 17A	Mus musculus	32-51
23228932-5	2013	As predicted, ASA and SA treatment resulted in the production of H(2)O(2), a known inducer of Sirt1 and confirmed in the current studies.	Aspirin	14-17	sirtuin 1	Homo sapiens	94-99
23228932-9	2013	As Sirt1 and PGC-1alpha profoundly affect mitochondrial metabolism and energy utilization, ASA may have therapeutic potential beyond its ability to inhibit cyclooxygenases.	Aspirin	91-94	sirtuin 1	Homo sapiens	3-8
23578461-10	2013	At 4 h and 72 h post-embolization, the CX3CL1 and CX3CR1-positive cell counts of the control, sham and aspirin groups were significantly less than those of the model group (P &lt; 0.05).	Aspirin	103-110	C-X3-C motif chemokine receptor 1	Homo sapiens	50-56
23578461-11	2013	CONCLUSION: Aspirin may improve the pathology and inhibit the expression of CX3CL1 and CX3CR1 in APE lung.	Aspirin	12-19	C-X3-C motif chemokine receptor 1	Rattus norvegicus	87-93
23667899-2	2012	The KLK locus has been implicated asa high susceptibility risk loci in numerous cancer studies through the last decade.	Aspirin	34-37	kallikrein related peptidase 4	Homo sapiens	4-7
22961402-0	2012	CD55 polymorphisms and risk of aspirin-exacerbated respiratory disease.	Aspirin	31-38	CD55 molecule (Cromer blood group)	Homo sapiens	0-4
22427378-2	2012	The aim of the study was to determine whether in T2DM patients aspirin enhances platelet isoprostanes, which are eicosanoids with proaggregating properties derived from arachidonic acid oxidation by platelet NOX2, the catalytic subunit of reduced NAD phosphate oxidase.	Aspirin	63-70	cytochrome b-245 beta chain	Homo sapiens	208-212
22427378-5	2012	Higher platelet recruitment, platelet isoprostane, and NOX2 activation was found in diabetic versus nondiabetic patients and in aspirin-treated diabetic patients versus nontreated patients (P &lt; 0.001).	Aspirin	128-135	cytochrome b-245 beta chain	Homo sapiens	55-59
22449948-4	2012	In addition to RvD1, its aspirin-triggered epimer and RvD1 analogs each dose dependently and effectively activated ALX/FPR2 and GPR32 in GPCR-overexpressing beta-arrestin systems using luminescence and electric cell-substrate impedance sensing.	Aspirin	25-32	formyl peptide receptor 2	Mus musculus	119-123
22449948-4	2012	In addition to RvD1, its aspirin-triggered epimer and RvD1 analogs each dose dependently and effectively activated ALX/FPR2 and GPR32 in GPCR-overexpressing beta-arrestin systems using luminescence and electric cell-substrate impedance sensing.	Aspirin	25-32	G protein-coupled bile acid receptor 1	Mus musculus	137-141
22626798-5	2012	RESULTS: A significant decrease in MT, SOD and CAT activities and GSH level and a significant increase in UI, AST, ALT, and ALP activities and LPO level were observed in aspirin treated stomach and duodenum of albino rats.	Aspirin	170-177	PDZ and LIM domain 3	Rattus norvegicus	124-127
21756248-4	2012	Aspirin (30 muM) significantly attenuated the elevation of RhoA, while indomethacin and salicylate had no similar effect.	Aspirin	0-7	ras homolog family member A	Rattus norvegicus	59-63
21756248-6	2012	8-Br-PET-cGMP solely enhanced the RhoA expression that was abrogated by preincubation with aspirin.	Aspirin	91-98	ras homolog family member A	Rattus norvegicus	34-38
21756248-7	2012	Degradation analysis indicated that aspirin enhanced the protein degradation rate of RhoA and GDP-bound RhoA seemed to be more susceptible to aspirin-enhanced degradation compared with the GTP-bound form.	Aspirin	36-43	ras homolog family member A	Rattus norvegicus	85-89
21756248-7	2012	Degradation analysis indicated that aspirin enhanced the protein degradation rate of RhoA and GDP-bound RhoA seemed to be more susceptible to aspirin-enhanced degradation compared with the GTP-bound form.	Aspirin	36-43	ras homolog family member A	Rattus norvegicus	104-108
21756248-7	2012	Degradation analysis indicated that aspirin enhanced the protein degradation rate of RhoA and GDP-bound RhoA seemed to be more susceptible to aspirin-enhanced degradation compared with the GTP-bound form.	Aspirin	142-149	ras homolog family member A	Rattus norvegicus	85-89
21756248-7	2012	Degradation analysis indicated that aspirin enhanced the protein degradation rate of RhoA and GDP-bound RhoA seemed to be more susceptible to aspirin-enhanced degradation compared with the GTP-bound form.	Aspirin	142-149	ras homolog family member A	Rattus norvegicus	104-108
21756248-8	2012	Our results indicate that aspirin attenuates the LPS-induced overexpression of RhoA both by inhibiting new synthesis and accelerating protein degradation, which may help elucidate the multiple beneficial effects of aspirin.	Aspirin	26-33	ras homolog family member A	Rattus norvegicus	79-83
21756248-8	2012	Our results indicate that aspirin attenuates the LPS-induced overexpression of RhoA both by inhibiting new synthesis and accelerating protein degradation, which may help elucidate the multiple beneficial effects of aspirin.	Aspirin	215-222	ras homolog family member A	Rattus norvegicus	79-83
22792718-3	2012	The human globin can be modified with acetylsalicylic acid on aminoacid residues K-17, K-41, K-57 and K-91 in alpha subunit as well as on K-18, K-96 and K- 133 in beta subunit.	Aspirin	38-58	keratin 17	Homo sapiens	81-85
22792718-4	2012	We identified of acetetylated lysines K-17 and K-57 in alpha subunit of human hemoglobin after incubation whole blood with 0.1 mg/mL acetylsalicylic acid during 3 h.	Aspirin	133-153	keratin 17	Homo sapiens	38-42
21360558-8	2012	ASA and IBP prevented translocation of NFkappaB to the nucleus and, interestingly, ASA induced MMP-2 and MMP-13 whereas IBP induced MMP-2, MMP-9 and MMP-13.	Aspirin	0-3	matrix metallopeptidase 13	Rattus norvegicus	105-111
21360558-8	2012	ASA and IBP prevented translocation of NFkappaB to the nucleus and, interestingly, ASA induced MMP-2 and MMP-13 whereas IBP induced MMP-2, MMP-9 and MMP-13.	Aspirin	0-3	matrix metallopeptidase 9	Rattus norvegicus	139-144
21360558-8	2012	ASA and IBP prevented translocation of NFkappaB to the nucleus and, interestingly, ASA induced MMP-2 and MMP-13 whereas IBP induced MMP-2, MMP-9 and MMP-13.	Aspirin	0-3	matrix metallopeptidase 13	Rattus norvegicus	149-155
21360558-8	2012	ASA and IBP prevented translocation of NFkappaB to the nucleus and, interestingly, ASA induced MMP-2 and MMP-13 whereas IBP induced MMP-2, MMP-9 and MMP-13.	Aspirin	83-86	matrix metallopeptidase 13	Rattus norvegicus	105-111
22615972-8	2012	Two SNPs in TXNRD1 and four SNPs in TXNRD2 interacted with aspirin/NSAID to influence colon cancer; one SNP in TXNRD1, two SNPs in TXNRD2, and one SNP in TXNRD3 interacted with aspirin/NSAIDs to influence rectal cancer.	Aspirin	59-66	thioredoxin reductase 1	Homo sapiens	12-18
22171135-7	2011	The p38MAPK pathway played a role in aspirin-induced SOX7 expression, during which the AP1 transcription factors c-Jun and c-Fos upregulated SOX7 promoter activities.	Aspirin	37-44	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	87-90
22171135-7	2011	The p38MAPK pathway played a role in aspirin-induced SOX7 expression, during which the AP1 transcription factors c-Jun and c-Fos upregulated SOX7 promoter activities.	Aspirin	37-44	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-118
22171135-7	2011	The p38MAPK pathway played a role in aspirin-induced SOX7 expression, during which the AP1 transcription factors c-Jun and c-Fos upregulated SOX7 promoter activities.	Aspirin	37-44	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	123-128
21692767-0	2011	A functional promoter polymorphism of the human IL18 gene is associated with aspirin-induced urticaria.	Aspirin	77-84	interleukin 18	Homo sapiens	48-52
21692767-7	2011	RESULTS: A significant association was detected between both AIU in general and the aspirin-intolerant acute urticaria (AIAU) phenotype and the IL18 promoter polymorphism -607A/C.	Aspirin	84-91	interleukin 18	Homo sapiens	144-148
21692767-11	2011	CONCLUSIONS: The high transcript haplotype ht1 [CG] of the IL18 gene may contribute to the development of acute cutaneous inflammation sensitive to aspirin, leading to the clinical presentation of AIAU.	Aspirin	148-155	interleukin 18	Homo sapiens	59-63
21743961-8	2011	Immunoblotting experiment showed that aspirin also acetylated glucose-6-phosphate dehydrogenase and transketolase, both enzymes of pentose phosphate pathway involved in ribonucleotide biosynthesis.	Aspirin	38-45	glucose-6-phosphate dehydrogenase	Homo sapiens	62-95
21985141-13	2011	After aspirin exposure, COX-1 expression increased despite impairment of platelet function, while COX-2 expression varied markedly among dogs.	Aspirin	6-13	cytochrome c oxidase subunit I	Canis lupus familiaris	24-29
21429049-0	2011	Over-expression of the LTC4 synthase gene in mice reproduces human aspirin-induced asthma.	Aspirin	67-74	leukotriene C4 synthase	Mus musculus	23-36
21429049-1	2011	BACKGROUND: The pathogenesis of aspirin-induced asthma (AIA) is presumed to involve the aspirin/non-steroidal anti-inflammatory drug (NSAID)-induced abnormal metabolism of arachidonic acid, resulting in an increase in 5-lipoxygenase (5-LO) metabolites, particularly leukotriene C(4) (LTC(4) ).	Aspirin	32-39	arachidonate 5-lipoxygenase	Mus musculus	218-232
21429049-1	2011	BACKGROUND: The pathogenesis of aspirin-induced asthma (AIA) is presumed to involve the aspirin/non-steroidal anti-inflammatory drug (NSAID)-induced abnormal metabolism of arachidonic acid, resulting in an increase in 5-lipoxygenase (5-LO) metabolites, particularly leukotriene C(4) (LTC(4) ).	Aspirin	88-95	arachidonate 5-lipoxygenase	Mus musculus	218-232
21324923-5	2011	ASA treatment also reduced the MDSC-attracting chemokine CCL2 (C-C motif ligand 2) in the TME along with numbers of CD11b(+)Ly6G(hi)Ly6C(lo) granulocytic MDSCs in both the bone marrow and the TME.	Aspirin	0-3	chemokine (C-C motif) ligand 2	Mus musculus	57-61
21324923-5	2011	ASA treatment also reduced the MDSC-attracting chemokine CCL2 (C-C motif ligand 2) in the TME along with numbers of CD11b(+)Ly6G(hi)Ly6C(lo) granulocytic MDSCs in both the bone marrow and the TME.	Aspirin	0-3	chemokine (C-C motif) ligand 2	Mus musculus	63-81
21347238-10	2011	Expression of SOCS-2 was enhanced, and TRAF6 and TNFalpha reduced, in the spleens of infected ASA-treated mice.	Aspirin	94-97	suppressor of cytokine signaling 2	Mus musculus	14-20
21231793-5	2011	Here we show that ASA inhibits phagocytosis and modulates expression of endosomal SNAREs, such as Vti1a, Vti1b, VAMP-3, VAMP-8 and Syn-8 (but not syn-6 and syn-16) in DC.	Aspirin	18-21	vesicle transport through interaction with t-SNAREs 1A	Mus musculus	98-103
21231793-5	2011	Here we show that ASA inhibits phagocytosis and modulates expression of endosomal SNAREs, such as Vti1a, Vti1b, VAMP-3, VAMP-8 and Syn-8 (but not syn-6 and syn-16) in DC.	Aspirin	18-21	vesicle-associated membrane protein 3	Mus musculus	112-118
21231793-6	2011	We further show that the phagocytic inhibitory effect of ASA is dependent on the expression of Vti1a and Vti1b.	Aspirin	57-60	vesicle transport through interaction with t-SNAREs 1A	Mus musculus	95-100
21168205-0	2011	Effects of calcium, magnesium, low-dose aspirin and low-molecular-weight heparin on the release of PP13 from placental explants.	Aspirin	40-47	galectin 13	Homo sapiens	99-103
21097689-1	2011	PURPOSE: Nitric oxide-donating acetylsalicylic acid (NO-ASA) has been shown to possess an antineoplastic effect in Wnt-/beta-catenin-active cancers.	Aspirin	56-59	catenin (cadherin associated protein), beta 1	Mus musculus	120-132
21097689-4	2011	Interference of NO-ASA with Wnt/beta-catenin signaling was analyzed through immunoblots of different pathway members.	Aspirin	19-22	catenin (cadherin associated protein), beta 1	Mus musculus	32-44
21116822-12	2011	Furthermore, treatment with a HMG-CoA reductase inhibitor or acetylsalicylic acid showed reduced levels of IL-21, IL-23 and VCAM1 (all p &lt; 0.05), but did not influence IL-17A.	Aspirin	61-81	interleukin 21	Homo sapiens	107-112
20961724-7	2011	The in vitro experiments showed that buserelin alone increased (P &lt; 0.01) and antide and buserelin plus acetylsalicylic acid decreased (P &lt; 0.01) testosterone and PGF(2alpha) production and COX1 activity, whereas antide and compound 48/80 counteracted buserelin effects.	Aspirin	107-127	cytochrome c oxidase subunit I	Vicugna pacos	196-200
21829036-0	2011	Arg16Gly beta2-adrenergic receptor gene polymorphism in Japanese patients with aspirin-exacerbated respiratory disease.	Aspirin	79-86	adrenoceptor beta 2	Homo sapiens	9-34
22312933-6	2011	RESULTS: NPDCs from aspirin-sensitive patients contained more eosinophils (14% vs 9%, P &lt; .05) and released 2.4-fold more ECP (P &lt; .01) at baseline.	Aspirin	20-27	ribonuclease A family member 3	Homo sapiens	125-128
21494357-9	2011	In MAP2, only the co-treatment of ginkgolide A and aspirin showed increasing effect.	Aspirin	51-58	microtubule associated protein 2	Homo sapiens	3-7
21035850-0	2010	Treatment with low-dose aspirin increased the level LIF and integrin beta3 expression in mice during the implantation window.	Aspirin	24-31	integrin beta 3	Mus musculus	60-74
21035850-5	2010	The mechanism of this increased implantation rate is unclear, and in this study we hypothesised that the expression of integrin beta3 or LIF may be altered, during implantation window, by treatment with low-dose aspirin.	Aspirin	212-219	integrin beta 3	Mus musculus	119-133
21035850-8	2010	We found the expression of LIF or integrin beta3 was significantly increased in the endometrium of mice that were treated with low dose of aspirin by immuno-fluorescence.	Aspirin	139-146	integrin beta 3	Mus musculus	34-48
21035850-9	2010	In addition, the mRNA level of LIF or integrin beta3 on the endometrium of aspirin treated mice was also significantly increased compared to untreated mice.	Aspirin	75-82	integrin beta 3	Mus musculus	38-52
21035850-10	2010	We conclude that low dose aspirin alters the expression of endometrial LIF and integrin beta3 and that these changes may increase endometrial receptivity.	Aspirin	26-33	integrin beta 3	Mus musculus	79-93
21061539-0	2010	[Role of proton pump inhibitor in the management of low dose aspirin related ulcerations].	Aspirin	61-68	ATPase H+/K+ transporting subunit alpha	Homo sapiens	9-20
21061539-6	2010	Herein, we focus on the role of proton pump inhibitor (PPI) in the strategy to prevent and to treat aspirin-induced peptic ulcerations and their complications, based on the scientific evidence.	Aspirin	100-107	ATPase H+/K+ transporting subunit alpha	Homo sapiens	32-43
20953352-2	2010	The first issue of the new journal, "Aging &amp; Disease" comprises articles that discuss the current knowledge pertaining to changes in reelin signaling in normal &amp; pathological forms of aging, memory and neurogenesis in Aging &amp; Alzheimer"s disease, the efficacy of a non-steroidal anti-inflammatory drug aspirin in combination with docosahexaenoic acid for reducing the risk for Alzheimer"s disease, and the usefulness of stem cell transplantation for improving memory in aging and Alzheimer"s disease.	Aspirin	314-321	reelin	Homo sapiens	137-143
20566650-3	2010	Here, we show that proteoliposomes containing purified SLC17A1 transport various organic anions such as p-aminohippuric acid and acetylsalicylic acid (aspirin) in an inside positive membrane potential (Deltapsi)-dependent manner.	Aspirin	129-149	solute carrier family 17 member 1	Homo sapiens	55-62
20566650-3	2010	Here, we show that proteoliposomes containing purified SLC17A1 transport various organic anions such as p-aminohippuric acid and acetylsalicylic acid (aspirin) in an inside positive membrane potential (Deltapsi)-dependent manner.	Aspirin	151-158	solute carrier family 17 member 1	Homo sapiens	55-62
20653671-3	2010	WHAT THIS PAPER ADDS: The data presented in this manuscript clearly show that the endocannabinoid 2-arrachidonyl glycerol can activate platelet activity, but that the effects are mediated through an aspirin-sensitive pathway that is not affected by cannabinoid receptor antagonists or FAAH inhibition, but is abolished by MAGL inhibition.	Aspirin	199-206	monoglyceride lipase	Homo sapiens	322-326
20514442-5	2010	We report that treatment of the DNA MMR competent/p53 mutant colorectal cancer cell line SW480 with 1 mM aspirin for 48 h caused changes in mRNA expression of several key genes involved in DNA damage signalling pathways, including a significant down-regulation in transcription of the genes ATR, BRCA1 and MAPK12.	Aspirin	105-112	BRCA1 DNA repair associated	Homo sapiens	296-301
20514442-8	2010	Although a correlation was not seen between transcript and protein levels of ATR, BRCA1 and GADD45alpha, an increase in XRCC3 encoded protein expression upon aspirin treatment in SW480 cells was observed by immunoblotting, immunofluorescence and immunohistochemical analysis.	Aspirin	158-165	BRCA1 DNA repair associated	Homo sapiens	82-87
20514442-8	2010	Although a correlation was not seen between transcript and protein levels of ATR, BRCA1 and GADD45alpha, an increase in XRCC3 encoded protein expression upon aspirin treatment in SW480 cells was observed by immunoblotting, immunofluorescence and immunohistochemical analysis.	Aspirin	158-165	X-ray repair cross complementing 3	Homo sapiens	120-125
20514442-9	2010	This is the first report of XRCC3 gene transcription and encoded protein expression being susceptible to exposure to the non-steroidal anti-inflammatory drug, aspirin.	Aspirin	159-166	X-ray repair cross complementing 3	Homo sapiens	28-33
20188076-5	2010	Protein levels of Hsp70, the product of HSPA1A, and fos were increased in p-NO-ASA-treated Jurkat T and HT-29 colon cancer cells in a dose-dependent manner.	Aspirin	79-82	heat shock protein family A (Hsp70) member 4	Homo sapiens	18-23
20188076-5	2010	Protein levels of Hsp70, the product of HSPA1A, and fos were increased in p-NO-ASA-treated Jurkat T and HT-29 colon cancer cells in a dose-dependent manner.	Aspirin	79-82	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	52-55
20819511-6	2010	Activation of p38 mitogen activated protein kinase and NF-kappaB, the expression of intercellular adhesion molecule-1 and monocyte chemotactic protein-1, which were only mildly affected by aspirin or pravastatin alone, were significantly attenuated by their combination.	Aspirin	189-196	intercellular adhesion molecule 1	Homo sapiens	84-117
20022477-0	2010	Association of the CCR3 gene polymorphism with aspirin exacerbated respiratory disease.	Aspirin	47-54	C-C motif chemokine receptor 3	Homo sapiens	19-23
20022477-3	2010	OBJECTIVES: The main objective of this study is to investigate the association between CCR3 gene polymorphisms and aspirin hypersensitivity, including AERD and AICU.	Aspirin	115-122	C-C motif chemokine receptor 3	Homo sapiens	87-91
20022477-4	2010	METHODS: CCR3 mRNA expression was measured after an aspirin provocation test by real-time PCR.	Aspirin	52-59	C-C motif chemokine receptor 3	Homo sapiens	9-13
20022477-6	2010	RESULTS: CCR3 mRNA expression was significantly increased after aspirin provocation in AERD patients (P=0.002) but not in AICU patients.	Aspirin	64-71	C-C motif chemokine receptor 3	Homo sapiens	9-13
20022477-9	2010	CONCLUSION: This result suggests that the CCR3 genetic polymorphisms may contribute to the development of the AERD phenotype and may be used as a genetic marker for differentiating between the two major aspirin hypersensitivity phenotypes.	Aspirin	203-210	C-C motif chemokine receptor 3	Homo sapiens	42-46
20521434-0	2010	AAA- a further step towards a moratorium for aspirin in the primary prevention.	Aspirin	45-52	AAA1	Homo sapiens	0-3
20233223-9	2010	Blockade of iNOS activity in aspirin-treated rats: (i) did not modify leucocyte infiltration at 6 h, but reduced the number of polymorphonuclear leucocyte and increased that of macrophages at 24 h; (ii) increased HIF-1alpha immunostaining in macrophages of the mesentery; and (iii) prevented the decrease in CD36 immunostaining induced by aspirin in these cells.	Aspirin	29-36	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	213-223
20233223-10	2010	CONCLUSIONS AND IMPLICATIONS: NO, associated with acute gut inflammation induced by aspirin, diminished HIF-1alpha stabilization in macrophages.	Aspirin	84-91	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	104-114
20012515-6	2010	Less than half of the patients with CAC were receiving aspirin or statin medications prior to PET/CT imaging.	Aspirin	55-62	carbonic anhydrase 2	Homo sapiens	36-39
19896470-0	2010	Inhibition of soluble epoxide hydrolase enhances the anti-inflammatory effects of aspirin and 5-lipoxygenase activation protein inhibitor in a murine model.	Aspirin	82-89	epoxide hydrolase 2, cytoplasmic	Mus musculus	14-39
19896470-9	2010	These data illustrate that inhibition of sEH by both pharmacological intervention and gene knockout enhances the anti-inflammatory effects of aspirin and MK886, suggesting the possibility of modulating multiple branches to achieve better therapeutic effects.	Aspirin	142-149	epoxide hydrolase 2, cytoplasmic	Mus musculus	41-44
20043115-6	2010	RT-PCR quantitative analysis showed that aspirin treatment reduced significantly (P&lt;0.01) the AOM-triggered increase in mRNA levels of soluble inflammatory mediators (TNFalpha and IL-1beta) and metalloproteinases (MMP3 and MMP7).	Aspirin	41-48	matrix metallopeptidase 3	Rattus norvegicus	217-221
20043115-6	2010	RT-PCR quantitative analysis showed that aspirin treatment reduced significantly (P&lt;0.01) the AOM-triggered increase in mRNA levels of soluble inflammatory mediators (TNFalpha and IL-1beta) and metalloproteinases (MMP3 and MMP7).	Aspirin	41-48	matrix metallopeptidase 7	Rattus norvegicus	226-230
20608787-2	2010	A nitroderivate of ASA, 2-(acetyloxy)benzoic acid 3-(nitrooxymethyl)-phenyl ester (NCX 4016) was synthesized, which additionally acts through nitric oxide release.	Aspirin	19-22	T cell leukemia homeobox 2	Homo sapiens	83-86
20848331-9	2009	Certain polymorphisms (eg, CYP2C19) may prevent this conversion and lead to failure of clopidogrel to prevent major cardiovascular events.In patients with well-controlled or treated cardiovascular risk factors, aspirin plus extended-release dipyridamole and clopidogrel may provide similar results in preventing recurrent stroke, but aspirin plus extended-release dipyridamole may be associated with a slightly higher risk of major hemorrhage.	Aspirin	211-218	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
20848331-9	2009	Certain polymorphisms (eg, CYP2C19) may prevent this conversion and lead to failure of clopidogrel to prevent major cardiovascular events.In patients with well-controlled or treated cardiovascular risk factors, aspirin plus extended-release dipyridamole and clopidogrel may provide similar results in preventing recurrent stroke, but aspirin plus extended-release dipyridamole may be associated with a slightly higher risk of major hemorrhage.	Aspirin	334-341	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
20067114-5	2009	RESULTS: The LD50 (iv) in mice of RIP was 25.2 mg/kg in ASA, guinea pigs of the higher and lower RIP group all appeared stong allergic responses and most of them died quickly.	Aspirin	56-59	receptor interacting serine/threonine kinase 1	Rattus norvegicus	34-37
19840403-11	2009	CONCLUSION: The sequence variants of CysLTR2 may affect its transcription and the stability of its mRNA, resulting in altered expression of CysLTR2 protein, which in turn causes some asthmatics to be susceptible to aspirin hypersensitivity.	Aspirin	215-222	cysteinyl leukotriene receptor 2	Homo sapiens	37-44
19840403-11	2009	CONCLUSION: The sequence variants of CysLTR2 may affect its transcription and the stability of its mRNA, resulting in altered expression of CysLTR2 protein, which in turn causes some asthmatics to be susceptible to aspirin hypersensitivity.	Aspirin	215-222	cysteinyl leukotriene receptor 2	Homo sapiens	140-147
19595669-5	2009	Moreover, the expression of STAT3 target genes such as Cyclin D1, XIAP, and Bcl-2 that are essential for cell growth and survival was apparently attenuated after aspirin treatment.	Aspirin	162-169	X-linked inhibitor of apoptosis	Homo sapiens	66-70
19268942-0	2009	Influence of aspirin on SR-BI expression in human carotid plaques.	Aspirin	13-20	scavenger receptor class B member 1	Homo sapiens	24-29
19268942-1	2009	BACKGROUND: We recently showed that aspirin promotes scavenger receptor class-B type I (SR-BI) protein expression in vitro in primary human macrophages and in vivo in resident peritoneal macrophages of mice.	Aspirin	36-43	scavenger receptor class B member 1	Homo sapiens	53-86
19268942-1	2009	BACKGROUND: We recently showed that aspirin promotes scavenger receptor class-B type I (SR-BI) protein expression in vitro in primary human macrophages and in vivo in resident peritoneal macrophages of mice.	Aspirin	36-43	scavenger receptor class B member 1	Homo sapiens	88-93
19268942-4	2009	However, aspirin increased the expression of SR-BI protein in the analyzed specimens.	Aspirin	9-16	scavenger receptor class B member 1	Homo sapiens	45-50
19268942-5	2009	In human THP-1-derived macrophages, induction of SR-BI protein by aspirin was abrogated by concomitant pharmacological inhibition of nuclear factor-kappa B (NF-kappaB).	Aspirin	66-73	scavenger receptor class B member 1	Homo sapiens	49-54
19268942-8	2009	CONCLUSIONS: We suggest that aspirin treatment might lead to enhanced expression of SR-BI in human plaque macrophages and that this effect is dependent on the presence of NF-kappaB.	Aspirin	29-36	scavenger receptor class B member 1	Homo sapiens	84-89
19341823-6	2009	As we found that ASA at 4-8 mM, NCX 4016 at 400-800 microM and NCX 4040 at 4-8 microM stimulated apoptosis of monocytes and immature MoDC, sub-apoptotic concentrations of ASA (2 mM), NCX 4016 (200 microM) and NCX 4040 (2 microM) were used in experiments.	Aspirin	171-174	T cell leukemia homeobox 2	Homo sapiens	32-35
19341823-6	2009	As we found that ASA at 4-8 mM, NCX 4016 at 400-800 microM and NCX 4040 at 4-8 microM stimulated apoptosis of monocytes and immature MoDC, sub-apoptotic concentrations of ASA (2 mM), NCX 4016 (200 microM) and NCX 4040 (2 microM) were used in experiments.	Aspirin	171-174	T cell leukemia homeobox 2	Homo sapiens	63-66
19341823-6	2009	As we found that ASA at 4-8 mM, NCX 4016 at 400-800 microM and NCX 4040 at 4-8 microM stimulated apoptosis of monocytes and immature MoDC, sub-apoptotic concentrations of ASA (2 mM), NCX 4016 (200 microM) and NCX 4040 (2 microM) were used in experiments.	Aspirin	171-174	T cell leukemia homeobox 2	Homo sapiens	63-66
19341823-6	2009	As we found that ASA at 4-8 mM, NCX 4016 at 400-800 microM and NCX 4040 at 4-8 microM stimulated apoptosis of monocytes and immature MoDC, sub-apoptotic concentrations of ASA (2 mM), NCX 4016 (200 microM) and NCX 4040 (2 microM) were used in experiments.	Aspirin	171-174	T cell leukemia homeobox 2	Homo sapiens	63-66
19341823-9	2009	ASA and NCX 4016 decreased production of IL-10, whereas NCX 4040 had the opposite effect.	Aspirin	0-3	interleukin 10	Homo sapiens	41-46
19341823-10	2009	ASA inhibited the expression of CD1a and prevented downregulation of CD14, NCX 4016 stimulated the differentiation of CD1a+CD14+ and CD1a(-)CD14+ cells, whereas NCX 4040 decreased the proportion of CD1a+CD14(-) and increased the frequency of CD1a+CD14+ cells, compared to control.	Aspirin	0-3	T cell leukemia homeobox 2	Homo sapiens	75-78
19341823-10	2009	ASA inhibited the expression of CD1a and prevented downregulation of CD14, NCX 4016 stimulated the differentiation of CD1a+CD14+ and CD1a(-)CD14+ cells, whereas NCX 4040 decreased the proportion of CD1a+CD14(-) and increased the frequency of CD1a+CD14+ cells, compared to control.	Aspirin	0-3	T cell leukemia homeobox 2	Homo sapiens	161-164
19341823-11	2009	Maturation, both in ASA and NO-ASA treated MoDC was characterized by decreased allostimulatory activity, lower expression of CD83, HLA-DR, costimulatory molecules and CD54 and decreased production of IL-10 and IL-12 p40.	Aspirin	20-23	intercellular adhesion molecule 1	Homo sapiens	167-171
19341823-11	2009	Maturation, both in ASA and NO-ASA treated MoDC was characterized by decreased allostimulatory activity, lower expression of CD83, HLA-DR, costimulatory molecules and CD54 and decreased production of IL-10 and IL-12 p40.	Aspirin	20-23	interleukin 10	Homo sapiens	200-205
19341823-11	2009	Maturation, both in ASA and NO-ASA treated MoDC was characterized by decreased allostimulatory activity, lower expression of CD83, HLA-DR, costimulatory molecules and CD54 and decreased production of IL-10 and IL-12 p40.	Aspirin	31-34	intercellular adhesion molecule 1	Homo sapiens	167-171
19341823-11	2009	Maturation, both in ASA and NO-ASA treated MoDC was characterized by decreased allostimulatory activity, lower expression of CD83, HLA-DR, costimulatory molecules and CD54 and decreased production of IL-10 and IL-12 p40.	Aspirin	31-34	interleukin 10	Homo sapiens	200-205
19146957-8	2009	CD4(+)CD25(+) Treg cells in ASA-treated mice exhibited unimpaired immunosuppressive function on CD4(+)CD25(-) T effector cells.	Aspirin	28-31	CD4 antigen	Mus musculus	0-3
19146957-8	2009	CD4(+)CD25(+) Treg cells in ASA-treated mice exhibited unimpaired immunosuppressive function on CD4(+)CD25(-) T effector cells.	Aspirin	28-31	interleukin 2 receptor, alpha chain	Mus musculus	6-10
19146957-9	2009	ASA significantly enhanced the frequency of functional CD4(+)CD25(+)Foxp3(+) Treg cells in mice in a therapeutic dose range.	Aspirin	0-3	CD4 antigen	Mus musculus	55-58
19146957-9	2009	ASA significantly enhanced the frequency of functional CD4(+)CD25(+)Foxp3(+) Treg cells in mice in a therapeutic dose range.	Aspirin	0-3	interleukin 2 receptor, alpha chain	Mus musculus	61-65
19146957-10	2009	The different effects of ASA on CD4(+)CD25(+)Foxp3(+) Treg cells and CD4(+)CD25(-) T cells may potentially make hosts susceptible to tolerance induction which would be beneficial for tolerance induction in patients with autoimmune diseases or allo-grafts.	Aspirin	25-28	interferon stimulated exonuclease gene 20	Homo sapiens	38-42
19178400-0	2009	Histamine N-methyltransferase 939A>G polymorphism affects mRNA stability in patients with acetylsalicylic acid-intolerant chronic urticaria.	Aspirin	90-110	histamine N-methyltransferase	Homo sapiens	0-29
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	Aspirin	45-52	glycoprotein Ib platelet subunit alpha	Homo sapiens	133-159
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	Aspirin	45-52	integrin subunit alpha 2b	Homo sapiens	172-178
18773975-4	2008	Administration of CAA produced significant protection against aspirin induced gastric toxicity by showing significant increase in PGE2, TGF-alpha, VEGF expression and accompanied by a significant inhibition of nitric oxide and regulating the levels of cytokines in rats.	Aspirin	62-69	transforming growth factor alpha	Rattus norvegicus	136-145
19260323-8	2008	CONCLUSION: Patients with ACI cotreated with puerarin and aspirin improved the neurological function, decreased the levels of serum vWF and sTM, indicating puerarin with aspirin had the protective effects on the damaged vascular endothelial cells.	Aspirin	58-65	sulfotransferase family 1A member 3	Homo sapiens	140-143
18678619-6	2008	SUL, IND, and ASA (5 mM) suppressed PPARdelta and 14-3-3 proteins in a manner parallel to PARP cleavage.	Aspirin	14-17	peroxisome proliferator activated receptor delta	Homo sapiens	36-45
18495783-2	2008	Human neutrophils express the pleiotropic receptor formyl peptide receptor-like 1/lipoxin A4 (LXA(4)) receptor that binds a variety of ligands, including the acute-phase reactant serum amyloid A (SAA), the anti-inflammatory lipids LXA(4) and aspirin-triggered 15-epi-LXA(4) (ATL), and the glucocorticoid-inducible protein annexin 1.	Aspirin	242-249	serum amyloid A1 cluster	Homo sapiens	179-194
18495783-2	2008	Human neutrophils express the pleiotropic receptor formyl peptide receptor-like 1/lipoxin A4 (LXA(4)) receptor that binds a variety of ligands, including the acute-phase reactant serum amyloid A (SAA), the anti-inflammatory lipids LXA(4) and aspirin-triggered 15-epi-LXA(4) (ATL), and the glucocorticoid-inducible protein annexin 1.	Aspirin	242-249	serum amyloid A1 cluster	Homo sapiens	196-199
18472019-0	2008	NCX 4040, an NO-donating acetylsalicylic acid derivative: efficacy and mechanisms of action in cancer cells.	Aspirin	25-45	T cell leukemia homeobox 2	Homo sapiens	0-3
18472019-4	2008	In the present paper, we report the results obtained from in in vitro experimental systems aimed to evaluate the activity and mechanisms of action of the novel NO-releasing aspirin derivative, NCX 4040.	Aspirin	173-180	T cell leukemia homeobox 2	Homo sapiens	193-196
18492771-0	2008	The nitric oxide-donating derivative of acetylsalicylic acid, NCX 4016, stimulates glucose transport and glucose transporters translocation in 3T3-L1 adipocytes.	Aspirin	40-60	T cell leukemia homeobox 2	Homo sapiens	62-65
18492771-1	2008	NCX 4016 is a nitric oxide (NO)-donating derivative of acetylsalicylic acid.	Aspirin	55-75	T cell leukemia homeobox 2	Homo sapiens	0-3
18751381-6	2008	Aspirin induced IL-10 expression in the macrophages, MCF-7 and tamoxifen-pretreated MCF-7 cells.	Aspirin	0-7	interleukin 10	Homo sapiens	16-21
18751381-7	2008	Aspirin-pretreated macrophages potently induced IL-10 expression in the MCF-7 cells.	Aspirin	0-7	interleukin 10	Homo sapiens	48-53
17978344-5	2008	In the present study, ESP immunoreacted on Western blots with 4 (27%) of 15 antisperm antibody (ASA)-positive serum samples from infertile male patients and 2 (40%) of 5 ASA-positive female sera.	Aspirin	96-99	sperm equatorial segment protein 1	Homo sapiens	22-25
17978344-5	2008	In the present study, ESP immunoreacted on Western blots with 4 (27%) of 15 antisperm antibody (ASA)-positive serum samples from infertile male patients and 2 (40%) of 5 ASA-positive female sera.	Aspirin	170-173	sperm equatorial segment protein 1	Homo sapiens	22-25
18458661-3	2008	We conducted a meta-analysis to determine the efficacy and safety of adding a Gp IIb/IIIa inhibitor to clopidogrel, aspirin, and heparin before PCI.	Aspirin	116-123	integrin subunit alpha 2b	Homo sapiens	78-84
18484795-2	2008	Intravenous GP IIb/IIIa antagonists abciximab, tirofiban and eptifibatide have demonstrated efficacy in acute coronary syndromes when combined with heparin, aspirin, clopidogrel and percutanous coronary interventions.	Aspirin	157-164	integrin subunit alpha 2b	Homo sapiens	12-18
18201436-10	2007	Aspirin desensitization in an aspirin-sensitive patient with asthma resulted in an increase in IFN-gamma expression by CD4(+) lymphocytes and a decrease in IFN-gamma expression by CD8(+) lymphocytes, the significance of which needs additional investigation.	Aspirin	0-7	CD8a molecule	Homo sapiens	180-183
18201436-10	2007	Aspirin desensitization in an aspirin-sensitive patient with asthma resulted in an increase in IFN-gamma expression by CD4(+) lymphocytes and a decrease in IFN-gamma expression by CD8(+) lymphocytes, the significance of which needs additional investigation.	Aspirin	30-37	CD8a molecule	Homo sapiens	180-183
17760507-1	2007	We recently reported that NCX-4016, a derivative of aspirin containing a nitro moiety that releases nitric oxide (NO) in a sustained fashion in biologic systems, is a potent cytotoxic agent inhibiting the proliferation of cisplatin-resistant human ovarian cancer cells.	Aspirin	52-59	T cell leukemia homeobox 2	Homo sapiens	26-29
17156785-8	2007	In contrast, clopidogrel, aspirin or atorvastatin treated rabbits showed a significant reduction in progression of atherosclerosis and decreased the levels of P-selection, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in serum and vascular wall.	Aspirin	26-33	C-C motif chemokine 2	Oryctolagus cuniculus	258-288
17156785-8	2007	In contrast, clopidogrel, aspirin or atorvastatin treated rabbits showed a significant reduction in progression of atherosclerosis and decreased the levels of P-selection, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in serum and vascular wall.	Aspirin	26-33	C-C motif chemokine 2	Oryctolagus cuniculus	290-295
17468226-7	2007	The largest of these so-called ASA (ATP Synthase-Associated) subunits, ASA1, is shown to be an extrinsic protein.	Aspirin	31-34	uncharacterized protein	Chlamydomonas reinhardtii	71-75
17284450-4	2007	Exposure of cells to acetyl salicylic acid resulted in strong activation of eIF2alpha stress-activated protein kinase R-like endoplasmic reticulum kinase (PERK).	Aspirin	21-42	eukaryotic translation initiation factor 2A	Homo sapiens	76-85
20722142-11	2007	RESULTS: EFFECTIVENESS FOR CHEMOPREVENTION: Regular use of ASA appears to be effective at reducing the incidence of CRA.	Aspirin	59-62	myotubularin related protein 11	Homo sapiens	116-119
28857200-0	2017	By inhibiting PFKFB3, aspirin overcomes sorafenib resistance in hepatocellular carcinoma.	Aspirin	22-29	6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3	Mus musculus	14-20
28857200-5	2017	High glycolysis and PFKFB3 overexpression occupied a dominant position in sorafenib resistance, and can be targeted and overcome by aspirin.	Aspirin	132-139	6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3	Mus musculus	20-26
28847510-8	2017	Our studies provide novel insight into potential approaches to treatment of FOP, since several AMPK activators (e.g. metformin, berberine, and aspirin) are already in clinical use for the treatment of diabetes and metabolic syndromes.	Aspirin	143-150	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	95-99
28843992-1	2017	The discovery of druggable oncogenic drivers (i.e. EGFR and ALK), along with the introduction of comprehensive tumor genotyping techniques into the daily clinical practice define non-small-cell lung cancer (NSCLC) asa group of heterogeneous diseases, requiring a context-personalized clinico-therapeutical approach.	Aspirin	214-217	ALK receptor tyrosine kinase	Homo sapiens	60-63
29042428-12	2017	The susceptibility of an individual to aspirin may differ according to the level of 15-PGDH.	Aspirin	39-46	carbonyl reductase 1	Homo sapiens	84-91
28927796-5	2017	This work further demonstrates the versatility of scaffold-hopping asa method to develop structurally diverse, potent inhibitors of LSD1.	Aspirin	67-70	lysine demethylase 1A	Homo sapiens	132-136
28849118-0	2017	Aspirin inhibits the proliferation of human uterine leiomyoma cells by downregulation of K-Ras-p110alpha interaction.	Aspirin	0-7	KRAS proto-oncogene, GTPase	Homo sapiens	89-94
28849118-5	2017	Further studies revealed that aspirin blocked the interaction between K-Ras and p110alpha by co-immunoprecipitation and immunofluorescence.	Aspirin	30-37	KRAS proto-oncogene, GTPase	Homo sapiens	70-75
28849118-6	2017	Western blotting demonstrated K-Ras-p110alpha interaction was required for the effects of aspirin-induced inhibition on cell growth and cell cycle transition via cell cycle regulators, including cyclin D1 and cyclin-dependent kinase 2 (CDK2).	Aspirin	90-97	KRAS proto-oncogene, GTPase	Homo sapiens	30-35
28849118-8	2017	Taken together, these results suggest that aspirin inhibited human uterine leiomyoma cell growth by regulating K-Ras-p110alpha interaction.	Aspirin	43-50	KRAS proto-oncogene, GTPase	Homo sapiens	111-116
28849118-9	2017	Aspirin which targeting on interaction between K-Ras and p110alpha may serve as a new therapeutic drug for uterine leiomyoma treatment.	Aspirin	0-7	KRAS proto-oncogene, GTPase	Homo sapiens	47-52
29156815-0	2017	The effect of aspirin on circulating netrin-1 levels in humans is dependent on the inflammatory status of the vascular endothelium.	Aspirin	14-21	netrin 1	Homo sapiens	37-45
29156815-1	2017	In atherosclerotic animal models, the cyclo-oxygenase (COX)-inhibitor aspirin counteracts downregulation of endothelial-derived netrin-1, thus reducing arterial inflammation.	Aspirin	70-77	netrin 1	Homo sapiens	128-136
29156815-2	2017	We here explored the effect of aspirin on netrin-1 in healthy subjects undergoing influenza immunisation, which is an established experimental model of inflammation-related endothelial dysfunction.	Aspirin	31-38	netrin 1	Homo sapiens	42-50
29156815-4	2017	Aspirin counteracted vaccine-induced endothelial activation and reduction of netrin-1 in a dose-dependent manner (-3.06% and -17.03% from baseline at a dose of 300mg and 75mg respectively; p=0.0465 and p&gt;0.05 vs untreated).	Aspirin	0-7	netrin 1	Homo sapiens	77-85
29156815-7	2017	In a separate population of 40 healthy unimmunised volunteers, 28-day treatment with aspirin 300mg reduced netrin-1 (-18.76% from baseline; p=0.0012) without affecting endothelial markers or hs-CRP; as expected, aspirin suppressed TXB2 and PGE2.	Aspirin	85-92	netrin 1	Homo sapiens	107-115
29156815-9	2017	In conclusion, aspirin counteracts downregulation of netrin-1 following endothelial dysfunction due to its anti-inflammatory effect on the activated endothelium.	Aspirin	15-22	netrin 1	Homo sapiens	53-61
29156815-10	2017	However, inhibition of COX-dependent prostanoids negatively modulates netrin-1 synthesis in healthy subjects, and this could give rise to aspirin-dependent reduction in netrin-1 under steady state conditions.	Aspirin	138-145	netrin 1	Homo sapiens	70-78
29156815-10	2017	However, inhibition of COX-dependent prostanoids negatively modulates netrin-1 synthesis in healthy subjects, and this could give rise to aspirin-dependent reduction in netrin-1 under steady state conditions.	Aspirin	138-145	netrin 1	Homo sapiens	169-177
28912509-4	2017	We found that ASA could downregulate the expressions of iNOS and TNF-alpha both in mouse peritoneum macrophages and RAW264.7 cells induced by LPS via the IkappaK/IkappaB/NF-kappaB pathway and a COX2/PGE2/EP2/NF-kappaB feedback loop, without affecting the expressions of FIZZ/YM-1/ARG1 induced by IL-4.	Aspirin	14-17	prostaglandin E receptor 2 (subtype EP2)	Mus musculus	204-207
28912509-4	2017	We found that ASA could downregulate the expressions of iNOS and TNF-alpha both in mouse peritoneum macrophages and RAW264.7 cells induced by LPS via the IkappaK/IkappaB/NF-kappaB pathway and a COX2/PGE2/EP2/NF-kappaB feedback loop, without affecting the expressions of FIZZ/YM-1/ARG1 induced by IL-4.	Aspirin	14-17	chitinase-like 3	Mus musculus	270-279
28633086-5	2017	The GSH-AsA related genes including APX, MDHAR, and DHAR were commonly upregulated by melatonin and correlated to the antioxidant enzyme activity as well as the content of GSH and AsA, indicating that the increase of GSH and AsA was attributed to the expression of these genes.	Aspirin	8-11	probable glutathione S-transferase DHAR1, cytosolic	Triticum aestivum	42-46
28633086-5	2017	The GSH-AsA related genes including APX, MDHAR, and DHAR were commonly upregulated by melatonin and correlated to the antioxidant enzyme activity as well as the content of GSH and AsA, indicating that the increase of GSH and AsA was attributed to the expression of these genes.	Aspirin	180-183	probable glutathione S-transferase DHAR1, cytosolic	Triticum aestivum	42-46
28633086-5	2017	The GSH-AsA related genes including APX, MDHAR, and DHAR were commonly upregulated by melatonin and correlated to the antioxidant enzyme activity as well as the content of GSH and AsA, indicating that the increase of GSH and AsA was attributed to the expression of these genes.	Aspirin	180-183	probable glutathione S-transferase DHAR1, cytosolic	Triticum aestivum	42-46
29088823-0	2017	Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells.	Aspirin	54-61	beclin 1	Homo sapiens	0-8
29088823-3	2017	In this study, we demonstrated that aspirin induced autophagosome formation in colorectal cancer cells, but autophagic degradation was blocked through aspirin-mediated Beclin 1 acetylation.	Aspirin	151-158	beclin 1	Homo sapiens	168-176
29088823-5	2017	Collectively, our findings indicate the dual roles of aspirin on autophagy, and demonstrate a new mechanism by which Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells.	Aspirin	171-178	beclin 1	Homo sapiens	117-125
28713400-11	2017	Taken together, our results revealed a possible physiological role of AdBiL in the activation of the key enzymes of AsA-GSH cycle, PPP and down-regulation of GSNO reductase, thereby reducing oxidative and nitrosative stress in plants.	Aspirin	116-119	E3 ubiquitin ligase AdBiL	Solanum lycopersicum	70-75
28346830-7	2017	A combination of DHA and ASA efficiently enhanced heterodimer formations of PPARalpha and RXRalpha and increased the expression of neurotrophic factors PSD-95, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF), while inhibiting NFkappaB and COX2.	Aspirin	25-28	retinoid X receptor alpha	Homo sapiens	90-98
28346830-7	2017	A combination of DHA and ASA efficiently enhanced heterodimer formations of PPARalpha and RXRalpha and increased the expression of neurotrophic factors PSD-95, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF), while inhibiting NFkappaB and COX2.	Aspirin	25-28	brain derived neurotrophic factor	Homo sapiens	160-193
28346830-7	2017	A combination of DHA and ASA efficiently enhanced heterodimer formations of PPARalpha and RXRalpha and increased the expression of neurotrophic factors PSD-95, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF), while inhibiting NFkappaB and COX2.	Aspirin	25-28	brain derived neurotrophic factor	Homo sapiens	195-199
28346830-8	2017	These findings suggest that a combination of DHA and ASA could significantly improve the expression of PSD-95, BDNF, and GDNF by promoting heterodimerization of PPARalpha and RXRalpha, thus supplying a new therapeutic method for PD.	Aspirin	53-56	brain derived neurotrophic factor	Homo sapiens	111-115
28346830-8	2017	These findings suggest that a combination of DHA and ASA could significantly improve the expression of PSD-95, BDNF, and GDNF by promoting heterodimerization of PPARalpha and RXRalpha, thus supplying a new therapeutic method for PD.	Aspirin	53-56	retinoid X receptor alpha	Homo sapiens	175-183
28625251-6	2017	In those experiments, it was also confirmed that aspirin had antagonistic and reverse effects on various biological functions of DCD.	Aspirin	49-56	dermcidin	Homo sapiens	129-132
27809364-11	2017	Multivariable analysis showed that the risks for PPB were as follows: heparin bridging therapy (OR 6.34, P = 0.0002); low-dose aspirin (LDA) continuation (OR 5.30, P = 0.0079); and lesion size (OR 1.06, P &lt; 0.0001).	Aspirin	127-134	histatin 1	Homo sapiens	49-52
28195948-1	2017	The SMILE-4 study showed that in patients with left ventricular dysfunction (LVD) after acute myocardial infarction, early treatment with zofenopril plus acetyl salicylic acid is associated with an improved 1-year survival, free from death or hospitalization for cardiovascular (CV) causes, as compared to ramipril plus acetyl salicylic acid.	Aspirin	154-175	transmembrane O-mannosyltransferase targeting cadherins 3	Homo sapiens	4-9
28195948-1	2017	The SMILE-4 study showed that in patients with left ventricular dysfunction (LVD) after acute myocardial infarction, early treatment with zofenopril plus acetyl salicylic acid is associated with an improved 1-year survival, free from death or hospitalization for cardiovascular (CV) causes, as compared to ramipril plus acetyl salicylic acid.	Aspirin	320-341	transmembrane O-mannosyltransferase targeting cadherins 3	Homo sapiens	4-9
28216620-8	2017	In addition, ASA significantly inhibited CF apoptosis, and decreased the levels of apoptosis markers (cleaved caspase 3 and Parp1), which might serve as a side effect of anti-fibrotic effect of ASA.	Aspirin	13-16	poly (ADP-ribose) polymerase family, member 1	Mus musculus	124-129
28216620-8	2017	In addition, ASA significantly inhibited CF apoptosis, and decreased the levels of apoptosis markers (cleaved caspase 3 and Parp1), which might serve as a side effect of anti-fibrotic effect of ASA.	Aspirin	194-197	poly (ADP-ribose) polymerase family, member 1	Mus musculus	124-129
28381198-2	2017	This study aimed to evaluate whether the combination of ticagrelor and aspirin was superior to that of clopidogrel and aspirin in reducing the 90-day high on-treatment platelet reactivity for acute minor stroke or transient ischemic attack, especially for carriers of cytochrome P450 2C19 loss-of-function allele.	Aspirin	71-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	268-288
28103874-8	2017	For ASA, IC50 were 0.50 mug/mL (COX-1) and 5.14 mug/mL (COX-2).	Aspirin	4-7	cytochrome c oxidase subunit I	Equus caballus	32-37
27270429-3	2017	Notably, humans with genetic deficiency of either 6PGD or another oxidative PPP enzyme, glucose-6-phosphate dehydrogenase, exhibit non-immune hemolytic anemia upon exposure to aspirin and various antimalarial drugs.	Aspirin	176-183	glucose-6-phosphate dehydrogenase	Homo sapiens	88-121
28049513-9	2017	Chronic treatment with analgesics increased the CSD-evoked expression of Fos in the TNC and amygdala [18 +- 10.2 Fos-immunoreactive (IR) neurons per slide in the amygdala of rats treated with aspirin, 11 +- 5.4 IR neurons per slide in rats treated with acetaminophen, and 4 +- 3.7 IR neurons per slide in saline-treated control rats, P &lt; 0.001].	Aspirin	192-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
29090039-0	2017	Platelet Carbonic Anhydrase II, a Forgotten Enzyme, May Be Responsible for Aspirin Resistance.	Aspirin	75-82	carbonic anhydrase 2	Homo sapiens	9-30
29090039-8	2017	RESULTS: The LC/MS analysis of platelet proteome between groups revealed that out of all identified proteins, the only discriminatory protein, affecting aspirin responsiveness, is platelet carbonic anhydrase II (CA II).	Aspirin	153-160	carbonic anhydrase 2	Homo sapiens	189-210
29090039-8	2017	RESULTS: The LC/MS analysis of platelet proteome between groups revealed that out of all identified proteins, the only discriminatory protein, affecting aspirin responsiveness, is platelet carbonic anhydrase II (CA II).	Aspirin	153-160	carbonic anhydrase 2	Homo sapiens	212-217
28514405-13	2017	In the patients who failed to achieve ASAS partial remission, the baseline and final serum concentrations of IL-17A were higher than in those who achieved the remission.	Aspirin	38-42	interleukin 17A	Homo sapiens	109-115
27825819-15	2016	ASA caused hemorrhagic gastric mucosal damage and significantly decreased GBF, H2S production, CO content, mRNA or protein expression for CSE, 3-MST, HO-2 and increased mRNA and/or protein expression for CBS, HO-1, Nrf-2, HIF-1alpha, iNOS, IL-1beta, COX-2 in gastric mucosa and COHb concentration in blood.	Aspirin	0-3	heme oxygenase 1	Rattus norvegicus	209-213
27825819-15	2016	ASA caused hemorrhagic gastric mucosal damage and significantly decreased GBF, H2S production, CO content, mRNA or protein expression for CSE, 3-MST, HO-2 and increased mRNA and/or protein expression for CBS, HO-1, Nrf-2, HIF-1alpha, iNOS, IL-1beta, COX-2 in gastric mucosa and COHb concentration in blood.	Aspirin	0-3	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	222-232
27698862-11	2016	The immunohistochemistry and western blot analysis data from the models revealed that the expression of p-mTOR, HIF-1alpha and VEGF-A was decreased, while the expression of ULK1 and LC3A was increased following treatment with aspirin and everolimus.	Aspirin	226-233	vascular endothelial growth factor A	Mus musculus	127-133
27698862-13	2016	The inhibitory action of aspirin and everolimus on tumor angiogenesis may be through inhibiting the expression of p-mTOR, HIF-1alpha and VEGF-A.	Aspirin	25-32	vascular endothelial growth factor A	Mus musculus	137-143
27430169-4	2016	Using tartrate-resistant acid phosphatase (TRAP) staining, it was observed that aspirin inhibited the differentiation of RANKL-induced RAW264.7 cells.	Aspirin	80-87	acid phosphatase 5, tartrate resistant	Mus musculus	6-41
27430169-4	2016	Using tartrate-resistant acid phosphatase (TRAP) staining, it was observed that aspirin inhibited the differentiation of RANKL-induced RAW264.7 cells.	Aspirin	80-87	acid phosphatase 5, tartrate resistant	Mus musculus	43-47
27430169-5	2016	The mRNA expression of osteoclastic marker genes, including cathepsin K, TRAP, matrix metalloproteinase 9 and calcitonin receptor, were suppressed by aspirin as identified using reverse transcription-quantitative polymerase chain reaction analysis.	Aspirin	150-157	acid phosphatase 5, tartrate resistant	Mus musculus	73-77
27301936-0	2016	PPM1A Methylation Is Associated With Vascular Recurrence in Aspirin-Treated Patients.	Aspirin	60-67	protein phosphatase, Mg2+/Mn2+ dependent 1A	Homo sapiens	0-5
27301936-8	2016	Joint analysis identified an epigenome-wide association for cg04985020 (PPM1A; P=1.78x10(-07)), with vascular recurrence in patients treated with aspirin.	Aspirin	146-153	protein phosphatase, Mg2+/Mn2+ dependent 1A	Homo sapiens	72-77
27301936-9	2016	CONCLUSIONS: The pattern of differential methylation in PPM1A is associated with vascular recurrence in aspirin-treated stroke patients.	Aspirin	104-111	protein phosphatase, Mg2+/Mn2+ dependent 1A	Homo sapiens	56-61
27064683-9	2016	Interestingly, aspirin, a non-specific cyclooxygenase (COX) inhibitor, partially blocked PAF-induced sudden death, whereas NS-398, a specific COX-2 inhibitor, completely protected mice from the lethal effects of PAF.	Aspirin	15-22	patchy fur	Mus musculus	89-92
26635114-10	2016	RT-qPCR: When compared to the LPS group, expression of MMP-7 and MMP-12 was significantly decreased in Asp group (P &lt; 0.05).	Aspirin	103-106	matrix metallopeptidase 12	Homo sapiens	65-71
26635114-14	2016	Aspirin inhibited LPS-induced expression of PI3K, Akt, ERK, NF-kappaB, CX3CL1, MMP-7, and MMP-12 in human bronchial epithelial cells.	Aspirin	0-7	matrix metallopeptidase 12	Homo sapiens	90-96
26810856-0	2016	Aspirin inhibits epithelial-to-mesenchymal transition and migration of oncogenic K-ras-expressing non-small cell lung carcinoma cells by down-regulating E-cadherin repressor Slug.	Aspirin	0-7	KRAS proto-oncogene, GTPase	Homo sapiens	81-86
26810856-0	2016	Aspirin inhibits epithelial-to-mesenchymal transition and migration of oncogenic K-ras-expressing non-small cell lung carcinoma cells by down-regulating E-cadherin repressor Slug.	Aspirin	0-7	snail family transcriptional repressor 2	Homo sapiens	174-178
26810856-8	2016	Aspirin inhibits EMT and decelerates the migratory potential of A549 cells by down-regulating Slug and thereby up-regulating E-cadherin.	Aspirin	0-7	snail family transcriptional repressor 2	Homo sapiens	94-98
26810856-9	2016	Aspirin impedes activation and nuclear translocation of p65NFkappaB, essential for this transcription factor being available for SLUG promoter binding.	Aspirin	0-7	snail family transcriptional repressor 2	Homo sapiens	129-133
26810856-11	2016	CONCLUSIONS: Cumulatively, these results signify a crucial role of the anti-inflammatory agent aspirin as a novel negative regulator of epithelial-to-mesenchymal transition thereby suggesting its candidature as a promising tool for deterring metastasis of highly invasive K-ras-expressing NSCLC cells.	Aspirin	95-102	KRAS proto-oncogene, GTPase	Homo sapiens	272-277
26739449-1	2016	BACKGROUND: The aim of this study was to investigate the association between serum concentrations of the brain-derived neurotrophic factor (BDNF), platelet reactivity and inflammatory markers, as well as its association with BDNF encoding gene variants in type 2 diabetic patients (T2DM) during acetylsalicylic acid (ASA) therapy.	Aspirin	317-320	brain derived neurotrophic factor	Homo sapiens	105-138
27149936-0	2016	Vitamin D-Binding Protein Acts in the Actin Scavenge System and Can Have Increased Expression During Aspirin Therapy.	Aspirin	101-108	GC vitamin D binding protein	Homo sapiens	0-25
27149936-4	2016	Of these, vitamin D-binding protein (DBP) and actin were further examined via Western blot and showed consistent results, with DBP levels significantly increased post-aspirin treatment (114.04 +- 16.69) relative to pre-treatment (66.33 +- 5.61) while actin showed the opposite trend (p &lt; 0.01 for both comparisons).	Aspirin	167-174	GC vitamin D binding protein	Homo sapiens	10-35
26141932-1	2016	Platelet Multidrug Resistance Protein 4 (MRP4)-overexpression has a role in reducing aspirin action in patients after by-pass surgery.	Aspirin	85-92	ATP binding cassette subfamily C member 4	Homo sapiens	9-39
26141932-1	2016	Platelet Multidrug Resistance Protein 4 (MRP4)-overexpression has a role in reducing aspirin action in patients after by-pass surgery.	Aspirin	85-92	ATP binding cassette subfamily C member 4	Homo sapiens	41-45
26141932-2	2016	Aspirin induces platelet MRP4 over-expression, through megakaryocytes genomic modulation.	Aspirin	0-7	ATP binding cassette subfamily C member 4	Homo sapiens	25-29
26694373-7	2015	Activities of AsA-GSH cycle enzymes such as ascorbate peroxidase (APX), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR) and glutathione reductase (GR) increased after Spd pretreatment in LT affected seedlings.	Aspirin	14-17	L-ascorbate peroxidase, cytosolic	Vigna radiata	66-69
26694373-7	2015	Activities of AsA-GSH cycle enzymes such as ascorbate peroxidase (APX), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR) and glutathione reductase (GR) increased after Spd pretreatment in LT affected seedlings.	Aspirin	14-17	monodehydroascorbate reductase	Vigna radiata	72-102
26694373-7	2015	Activities of AsA-GSH cycle enzymes such as ascorbate peroxidase (APX), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR) and glutathione reductase (GR) increased after Spd pretreatment in LT affected seedlings.	Aspirin	14-17	monodehydroascorbate reductase	Vigna radiata	104-109
25604769-1	2015	BACKGROUND AND OBJECTIVES: The aim of this study was, first, to investigate the effect of omega 3 (omega3) fatty acids plus low-dose aspirin with closed debridement in the treatment of patients with periodontitis and type 2 diabetes mellitus (DM), and second, to estimate the expression of monocyte chemoattractant protein-3 (MCP-3) in response to the supposed modulatory therapy.	Aspirin	133-140	C-C motif chemokine ligand 7	Homo sapiens	290-324
25604769-1	2015	BACKGROUND AND OBJECTIVES: The aim of this study was, first, to investigate the effect of omega 3 (omega3) fatty acids plus low-dose aspirin with closed debridement in the treatment of patients with periodontitis and type 2 diabetes mellitus (DM), and second, to estimate the expression of monocyte chemoattractant protein-3 (MCP-3) in response to the supposed modulatory therapy.	Aspirin	133-140	C-C motif chemokine ligand 7	Homo sapiens	326-331
26522688-4	2015	We also showed that TfR1 and Fpn1 expressions were significantly higher, while ferritin contents, IL-6, TNF-alpha and hepcidin mRNA levels were lower in cells treated with aspirin plus LPS than those in cells treated with LPS only.	Aspirin	172-179	hepcidin antimicrobial peptide	Mus musculus	118-126
26522688-6	2015	Our findings also suggested that hepcidin might play a dominant role in the control of TfR1 expression by aspirin in the cells treated with LPS.	Aspirin	106-113	hepcidin antimicrobial peptide	Mus musculus	33-41
25857363-3	2015	We also evaluated the effects of 0.4 mM aspirin (ASA) as a potential pharmacological co-inducer of HSP, both alone and in a combination with HS (ASA + HS).	Aspirin	49-52	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	99-102
25857363-4	2015	HS alone and ASA + HS caused a major up-regulation of HSP70 mRNA in the first 2 h, while HSP70 protein increased gradually and was especially abundant from 2 h to 24 h. Regarding Bcl-2, all treatments rendered similar results: gene expression was down-regulated in the first 2 h, after which there was protein elevation (12-48 h after HS).	Aspirin	13-16	heat shock protein family A (Hsp70) member 4	Homo sapiens	54-59
26252649-9	2015	Only AZA+ASA group showed increased anti-inflammatory cytokines (IL-10 and TGF-beta).	Aspirin	9-12	interleukin 10	Homo sapiens	65-70
26230583-8	2015	Recent use of aspirin and/or ibuprofen was associated with differential expression of TMC06, ST8SIA4, and STEAP3 while a summary oxidative balance score (OBS) was associated with SYCP3, HDX, and NRG4 (all up-regulated with greater oxidative balance).	Aspirin	14-21	synaptonemal complex protein 3	Homo sapiens	179-184
25824964-3	2015	EXPERIMENTAL APPROACH: Netrin-1 synthesis was studied in vitro using human endothelial cells stimulated with TNF-alpha, with or without aspirin treatment.	Aspirin	136-143	netrin 1	Homo sapiens	23-31
25959742-0	2015	Aspirin Action in Endothelial Cells: Different Patterns of Response Between Chemokine CX3CL1/CX3CR1 and TNF-alpha/TNFR1 Signaling Pathways.	Aspirin	0-7	C-X3-C motif chemokine receptor 1	Homo sapiens	93-99
25959742-2	2015	NF-kB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin.	Aspirin	133-140	C-X3-C motif chemokine receptor 1	Homo sapiens	83-89
25959742-13	2015	CONCLUSIONS: Autoregulation between CX3CL1 and CX3CR1 may explain overexpression of CX3CR1 as the compensatory effect in aspirin-treated HUVECs.	Aspirin	121-128	C-X3-C motif chemokine receptor 1	Homo sapiens	47-53
25959742-13	2015	CONCLUSIONS: Autoregulation between CX3CL1 and CX3CR1 may explain overexpression of CX3CR1 as the compensatory effect in aspirin-treated HUVECs.	Aspirin	121-128	C-X3-C motif chemokine receptor 1	Homo sapiens	84-90
25959742-14	2015	Inhibition of CX3CR1 could prevent thrombotic complications in the early period after discontinuation of aspirin.	Aspirin	105-112	C-X3-C motif chemokine receptor 1	Homo sapiens	14-20
26028921-2	2015	We investigated the role of serum specific IgE to thyroid peroxidase (TPO) in patients with aspirin intolerant acute urticaria (AIAU) and aspirin intolerant chronic urticaria (AICU).	Aspirin	92-99	thyroid peroxidase	Homo sapiens	70-73
25966060-5	2015	Expressions of integrin beta3 and LIF in the endometrium of mice in the TCM treatment group were significantly increased compared to aspirin-treated and control mice, and those of aspirin-treated mice were increased compared to the control group.	Aspirin	133-140	integrin beta 3	Mus musculus	15-29
25091345-7	2015	By contrast, ASA significantly increased the plasma and urine 8-iso-PGF2alpha, a well-known prothrombotic molecule, parallel to an increase of plasma NOX2 levels.	Aspirin	13-16	cytochrome b-245 beta chain	Homo sapiens	150-154
25817250-5	2015	In conditions involving down regulated GSH homeostasis, GGC serves asa crucialrate-limiting substrate for GSH synthetase, the main enzyme responsible for condensing glycine with GGC to form the final thiol tripeptide, GSH.	Aspirin	67-70	gamma-glutamylcyclotransferase	Homo sapiens	56-59
25546326-6	2015	Aspirin desensitization was reported to decrease the levels of CD4+ T cell-derived cytokines, including INF-gamma and IL-10, in line with the newly defined role of INF-gamma in AERD.	Aspirin	0-7	interleukin 10	Homo sapiens	118-123
28210674-4	2015	METHODS: IL33 expression was evaluated in mice and human biopsy specimens infected with H pylori and in mice after dosing with aspirin.	Aspirin	127-134	interleukin 33	Mus musculus	9-13
23728159-0	2015	Exploring PLATO-USA paradox and CURRENT-OASIS 7 trials reveals the benefit of higher aspirin dose.	Aspirin	85-92	cAMP responsive element binding protein 3 like 1	Homo sapiens	40-45
25267459-0	2015	Serum ubiquitin via CXC chemokine receptor 4 triggered cyclooxygenase-1 ubiquitination possibly involved in the pathogenesis of aspirin resistance.	Aspirin	128-135	C-X-C motif chemokine receptor 4	Homo sapiens	20-44
25267459-8	2015	In vitro, we found that extracellular Ub, via the CXC chemokine receptor 4 (CXCR4) pathway, facilitated COX-1 to be ubiquitined and prevented aspirin to acetylate its target.	Aspirin	142-149	C-X-C motif chemokine receptor 4	Homo sapiens	50-74
25267459-8	2015	In vitro, we found that extracellular Ub, via the CXC chemokine receptor 4 (CXCR4) pathway, facilitated COX-1 to be ubiquitined and prevented aspirin to acetylate its target.	Aspirin	142-149	C-X-C motif chemokine receptor 4	Homo sapiens	76-81
26379739-6	2015	Treatment of aspirin alone significantly reduced the expressions of HO-1 (P &lt; 0.001), iNOS (P &lt; 0.001), and Bax (P &lt; 0.01) in ischemic regions.	Aspirin	13-20	heme oxygenase 1	Rattus norvegicus	68-72
26491233-0	2015	Multidrug Resistance Protein-4 Influences Aspirin Toxicity in Human Cell Line.	Aspirin	42-49	ATP binding cassette subfamily C member 4	Homo sapiens	0-30
26491233-2	2015	We found that multidrug resistance protein-4 (MRP4) overexpression has a role in reducing aspirin action in patients after bypass surgery and, very recently, we found that aspirin enhances platelet MRP4 levels through peroxisome proliferator activated receptor-alpha (PPARalpha).	Aspirin	90-97	ATP binding cassette subfamily C member 4	Homo sapiens	14-44
26491233-2	2015	We found that multidrug resistance protein-4 (MRP4) overexpression has a role in reducing aspirin action in patients after bypass surgery and, very recently, we found that aspirin enhances platelet MRP4 levels through peroxisome proliferator activated receptor-alpha (PPARalpha).	Aspirin	90-97	ATP binding cassette subfamily C member 4	Homo sapiens	46-50
26491233-2	2015	We found that multidrug resistance protein-4 (MRP4) overexpression has a role in reducing aspirin action in patients after bypass surgery and, very recently, we found that aspirin enhances platelet MRP4 levels through peroxisome proliferator activated receptor-alpha (PPARalpha).	Aspirin	172-179	ATP binding cassette subfamily C member 4	Homo sapiens	14-44
26491233-2	2015	We found that multidrug resistance protein-4 (MRP4) overexpression has a role in reducing aspirin action in patients after bypass surgery and, very recently, we found that aspirin enhances platelet MRP4 levels through peroxisome proliferator activated receptor-alpha (PPARalpha).	Aspirin	172-179	ATP binding cassette subfamily C member 4	Homo sapiens	46-50
26491233-2	2015	We found that multidrug resistance protein-4 (MRP4) overexpression has a role in reducing aspirin action in patients after bypass surgery and, very recently, we found that aspirin enhances platelet MRP4 levels through peroxisome proliferator activated receptor-alpha (PPARalpha).	Aspirin	172-179	ATP binding cassette subfamily C member 4	Homo sapiens	198-202
26491233-3	2015	In the present paper, we verified whether exposure of human embryonic kidney-293 cells (Hek-293) to aspirin modifies MRP4 gene expression and its correlation with drug elimination and cell toxicity.	Aspirin	100-107	ATP binding cassette subfamily C member 4	Homo sapiens	117-121
26491233-5	2015	Furthermore, aspirin effects, induced at low dose, already enhance MRP4 gene expression.	Aspirin	13-20	ATP binding cassette subfamily C member 4	Homo sapiens	67-71
24902864-0	2014	Aspirin influences megakaryocytic gene expression leading to up-regulation of multidrug resistance protein-4 in human platelets.	Aspirin	0-7	ATP binding cassette subfamily C member 4	Homo sapiens	78-108
24902864-1	2014	AIM: The aim of the study was to investigate whether human megakaryocytic cells have an adaptive response to aspirin treatment, leading to an enhancement of multidrug resistance protein-4 (MRP4) expression in circulating platelets responsible for a reduced aspirin action.	Aspirin	109-116	ATP binding cassette subfamily C member 4	Homo sapiens	157-187
24902864-1	2014	AIM: The aim of the study was to investigate whether human megakaryocytic cells have an adaptive response to aspirin treatment, leading to an enhancement of multidrug resistance protein-4 (MRP4) expression in circulating platelets responsible for a reduced aspirin action.	Aspirin	109-116	ATP binding cassette subfamily C member 4	Homo sapiens	189-193
24902864-1	2014	AIM: The aim of the study was to investigate whether human megakaryocytic cells have an adaptive response to aspirin treatment, leading to an enhancement of multidrug resistance protein-4 (MRP4) expression in circulating platelets responsible for a reduced aspirin action.	Aspirin	257-264	ATP binding cassette subfamily C member 4	Homo sapiens	189-193
24902864-2	2014	We recently found that platelet MRP4 overexpression has a role in reducing aspirin action in patients after by-pass surgery.	Aspirin	75-82	ATP binding cassette subfamily C member 4	Homo sapiens	32-36
24902864-3	2014	Aspirin enhances MRP4-mRNA levels in rat liver and drug administration transcriptionally regulates MRP4 gene expression through peroxisome proliferator-activated receptor-alpha (PPARalpha).	Aspirin	0-7	ATP binding cassette subfamily C member 4	Rattus norvegicus	17-21
24902864-3	2014	Aspirin enhances MRP4-mRNA levels in rat liver and drug administration transcriptionally regulates MRP4 gene expression through peroxisome proliferator-activated receptor-alpha (PPARalpha).	Aspirin	0-7	ATP binding cassette subfamily C member 4	Rattus norvegicus	99-103
24902864-4	2014	METHODS: The effects induced by aspirin or PPARalpha agonist (WY14643) on MRP4 modulation were evaluated in vitro in a human megakaryoblastic DAMI cell line, in megakaryocytes (MKs) and in platelets obtained from human haematopoietic progenitor cell (HPC) cultures, and in vivo platelets obtained from aspirin treated healthy volunteers (HV).	Aspirin	32-39	ATP binding cassette subfamily C member 4	Homo sapiens	74-78
24902864-5	2014	RESULTS: In DAMI cells, aspirin and WY14643 treatment induced a significant increase in MRP4 and PPARalpha expression.	Aspirin	24-31	ATP binding cassette subfamily C member 4	Homo sapiens	88-92
24902864-6	2014	In human MKs grown in the presence of either aspirin or WY14643, MRP4 and PPARalpha-mRNA were higher than in control cultures and derived platelets showed an enhancement in MRP4 protein expression.	Aspirin	45-52	ATP binding cassette subfamily C member 4	Homo sapiens	65-69
24902864-6	2014	In human MKs grown in the presence of either aspirin or WY14643, MRP4 and PPARalpha-mRNA were higher than in control cultures and derived platelets showed an enhancement in MRP4 protein expression.	Aspirin	45-52	ATP binding cassette subfamily C member 4	Homo sapiens	173-177
24902864-7	2014	The ability of aspirin to modulate MRP4 expression in MKs and to transfer it to platelets was also confirmed in vivo.	Aspirin	15-22	ATP binding cassette subfamily C member 4	Homo sapiens	35-39
24902864-8	2014	In fact, we found the highest MRP4 mRNA and protein expression in platelets obtained from HV after 15 days" aspirin treatment.	Aspirin	108-115	ATP binding cassette subfamily C member 4	Homo sapiens	30-34
25444678-5	2014	Pharmacological modulation of AA metabolism by aspirin induced hepatic generation of leukotrienes (LTs) and lipoxins (LXs), thereby increasing hepatic expression of the bile salt export pump Abcb11.	Aspirin	47-54	ATP binding cassette subfamily B member 11	Homo sapiens	191-197
25143486-6	2014	ASA treatment increased levels of ASA-triggered lipoxin (ATL; 15-epi-lipoxin A4), and blocking the lipoxin A4 receptor (ALX) with a peptide antagonist (Boc2) or using ALX knockouts (Fpr2/3(-/-)) reversed this protection.	Aspirin	0-3	formyl peptide receptor 2	Mus musculus	182-186
25017950-5	2014	While the rigid C8 spacer impedes any ordering, ASA capped C15 tends to form ordered hydrogels over extended regions of the phase diagram that resemble mesh phases and L(alpha)/L(3) polymorphism.	Aspirin	48-51	placenta associated 8	Homo sapiens	59-62
24607918-9	2014	PE prevention by aspirin was most effective when the risk was determined by low PP13 alone, less effective for combining low PP13 with RFs, and ineffective when determined by RFs alone.	Aspirin	17-24	galectin 13	Homo sapiens	80-84
24607918-10	2014	CONCLUSION: When PE risk is determined by low first trimester PP13 or by combined low PP13 and RFs, prevention with aspirin is warranted.	Aspirin	116-123	galectin 13	Homo sapiens	86-90
25079372-3	2014	The reduction in Gcn4 abundance on ASA accumulation requires Cdk8/Srb10 and Pho85, cyclin-dependent kinases (CDKs) known to mediate rapid turnover of Gcn4 by the proteasome via phosphorylation of the Gcn4 activation domain under nonstarvation conditions.	Aspirin	35-38	cyclin-dependent serine/threonine-protein kinase PHO85	Saccharomyces cerevisiae S288C	76-81
24945997-10	2014	Such aspirin use was associated with lower risk of all-cause mortality (HR=0.53, 95% CI=0.45-0.63, P&lt;0.001) and breast cancer-specific mortality (HR=0.42, 95% CI=0.31-0.55, P&lt;0.001) after adjusting for age, socioeconomic status, TNM stage, tumour grade, oestrogen receptor status, surgery, radiotherapy, chemotherapy, adjuvant endocrine therapy and aspirin use prediagnosis.	Aspirin	5-12	teneurin transmembrane protein 1	Homo sapiens	235-238
25093045-7	2014	Furthermore, we showed that acetylsalicylic acid therapy is associated with 3.6% lower ABCA1 DNA methylation levels (P = 0.006), independent of aging and CAD status of patients.	Aspirin	28-48	ATP binding cassette subfamily A member 1	Homo sapiens	87-92
24760190-0	2014	Aspirin and the risk of colorectal cancer in relation to the expression of 15-hydroxyprostaglandin dehydrogenase (HPGD).	Aspirin	0-7	carbonyl reductase 1	Homo sapiens	75-112
24760190-0	2014	Aspirin and the risk of colorectal cancer in relation to the expression of 15-hydroxyprostaglandin dehydrogenase (HPGD).	Aspirin	0-7	carbonyl reductase 1	Homo sapiens	114-118
24520038-8	2014	In addition, aspirin may activate AMPK, and both agents may affect Notch, Wnt/beta-catenin, and other signaling pathways.	Aspirin	13-20	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	34-38
23881471-0	2014	Aspirin use is associated with lower prostate cancer risk in male carriers of BRCA mutations.	Aspirin	0-7	BRCA1 DNA repair associated	Homo sapiens	78-82
24094975-1	2013	AIM: This study aimed to evaluate the effect of P/E-selectin blockage on antisperm antibody (ASA) development and histopathological alterations in experimental orchitis.	Aspirin	93-96	selectin E	Rattus norvegicus	50-60
24094975-24	2013	CONCLUSION: P/E-selectin blockage may reduce ASA production after orchitis when combined with antimicrobial treatment.	Aspirin	45-48	selectin E	Rattus norvegicus	14-24
24018490-10	2013	Among proteins differentially expressed in Huh7-HCV cells, we found proteins related to cell proliferation (MTMR6, FAM22, HDGF and HCF-1) after 24 h of ASA treatment; and upregulation of angiostatin, PI4KA and STAT-1 after 48 h of treatment.	Aspirin	152-155	MIR7-3 host gene	Homo sapiens	43-47
24018490-10	2013	Among proteins differentially expressed in Huh7-HCV cells, we found proteins related to cell proliferation (MTMR6, FAM22, HDGF and HCF-1) after 24 h of ASA treatment; and upregulation of angiostatin, PI4KA and STAT-1 after 48 h of treatment.	Aspirin	152-155	host cell factor C1	Homo sapiens	131-136
24018490-10	2013	Among proteins differentially expressed in Huh7-HCV cells, we found proteins related to cell proliferation (MTMR6, FAM22, HDGF and HCF-1) after 24 h of ASA treatment; and upregulation of angiostatin, PI4KA and STAT-1 after 48 h of treatment.	Aspirin	152-155	signal transducer and activator of transcription 1	Homo sapiens	210-216
24018490-13	2013	We found that ASA induces different protein patterns in Huh7-HCV cells promoting activation of proteins involved in cell progression, repair of double strand breaks, proliferation, inhibition of apoptosis and growth stimulation at the same time that it decreased HCV expression.	Aspirin	14-17	MIR7-3 host gene	Homo sapiens	56-60
23876149-3	2013	The clean biochemical approach revealed that proteoliposomes comprising purified NPT1 as the only protein source transport various organic anions such as urate, p-aminohippuric acid (PAH), and acetylsalicylic acid (aspirin) in a membrane potential (Deltapsi)-driven and Cl(-) -dependent manner.	Aspirin	193-213	solute carrier family 17 member 1	Homo sapiens	81-85
24013153-6	2013	Meanwhile, co-administration of piracetam with acetylsalicylic acid was accompanied by an expressed antiamnetic potential - the reduction of early markers of proteins degradation (aldehydephenylhydrazones, APH) by 21,7% (p&lt;0,05) and late markers of proteins degradation (ketonephenylhydrazones, KPH) by 23,8% (p&lt;0,001) was noted.	Aspirin	47-67	acylaminoacyl-peptide hydrolase	Rattus norvegicus	206-209
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	CREB binding protein	Mus musculus	283-303
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	CREB binding protein	Mus musculus	283-303
23653362-6	2013	The activation of cAMP-response element-binding protein (CREB), but not NF-kappaB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB.	Aspirin	113-120	CREB binding protein	Mus musculus	283-303
23483185-0	2013	Impact of acetylsalicylic acid on tumor angiogenesis and lymphangiogenesis through inhibition of VEGF signaling in a murine sarcoma model.	Aspirin	10-30	vascular endothelial growth factor A	Mus musculus	97-101
23483185-10	2013	The expression of VEGF-A and VEGF-C in tumor tissues inhibited by aspirin was demonstrated by immunohistochemistry, and the MVD was decreased in a dose-dependent manner (p&lt;0.05).	Aspirin	66-73	vascular endothelial growth factor A	Mus musculus	18-24
23483185-12	2013	Western blot data showed that the expression of both VEGF-A and VEGF-C was reduced after treatment with aspirin.	Aspirin	104-111	vascular endothelial growth factor A	Mus musculus	53-59
23483185-13	2013	In conclusion, the impact of aspirin-induced tumor growth delay of murine S180 sarcoma may correlate with the inhibition of angiogenesis and lymphangiogenesis by reducing VEGF-A and VEGF-C expression in tumor tissues.	Aspirin	29-36	vascular endothelial growth factor A	Mus musculus	171-177
23506529-3	2013	Aspirin is a non-steroidal anti-inflammatory drug that is an irreversible inhibitor of both cyclooxygenase (COX)-1 and COX-2, It stimulates endogenous production of anti-inflammatory regulatory "braking signals", including lipoxins, which dampen the inflammatory response and reduce levels of inflammatory biomarkers, including C-reactive protein, tumor necrosis factor-alpha and interleukin (IL)--6, but not negative immunoregulatory cytokines, such as IL-4 and IL-10.	Aspirin	0-7	interleukin 10	Homo sapiens	463-468
23292806-0	2013	Direct regulation of caspase-3 by the transcription factor AP-2alpha is             involved in aspirin-induced apoptosis in MDA-MB-453 breast cancer cells.	Aspirin	96-103	transcription factor AP-2 alpha	Homo sapiens	59-68
23292806-6	2013	Moreover, AP-2alpha, a transcription factor highly expressed in MDA-MB-453             cells, was identified as a negative regulator of caspase-3 transcription and AP-2alpha             was attenuated following aspirin treatment.	Aspirin	211-218	transcription factor AP-2 alpha	Homo sapiens	10-19
23292806-6	2013	Moreover, AP-2alpha, a transcription factor highly expressed in MDA-MB-453             cells, was identified as a negative regulator of caspase-3 transcription and AP-2alpha             was attenuated following aspirin treatment.	Aspirin	211-218	transcription factor AP-2 alpha	Homo sapiens	164-173
23292806-7	2013	Therefore, aspirin may increase the             expression of caspase-3 by inducing the degradation of AP-2alpha, which increases             activated caspase-3 expression, thereby triggering apoptosis in MDA-MB-453 cells.	Aspirin	11-18	transcription factor AP-2 alpha	Homo sapiens	103-112
23240590-11	2013	In the female aspirin-treated group, MPO activity and the number of F4/80-positive macrophages was higher than in the control group.	Aspirin	14-21	myeloperoxidase	Mus musculus	37-40
23240590-13	2013	The expression of vWF and VEGF protein was increased in the female aspirin-treated group.	Aspirin	67-74	vascular endothelial growth factor A	Mus musculus	26-30
23228932-0	2013	Aspirin may promote mitochondrial biogenesis via the production of hydrogen peroxide and the induction of Sirtuin1/PGC-1alpha genes.	Aspirin	0-7	sirtuin 1	Homo sapiens	106-114
23228932-2	2013	We observed that treatment of cultured liver cells with ASA resulted in the induction of Sirt1, peroxisome proliferator-activated receptor-gamma co-activator-1alpha (PGC-1alpha), and NAD(P)H quinone oxidoreductase 1 (Nqo1) genes.	Aspirin	56-59	sirtuin 1	Homo sapiens	89-94
22881598-8	2013	Treating GPBAR1(+/+) mice with two GPBAR1 agonists, ciprofloxacin and betulinic acid, rescued mice from gastric injury caused by ASA and NSAIDs.	Aspirin	129-132	G protein-coupled bile acid receptor 1	Mus musculus	9-15
22881598-8	2013	Treating GPBAR1(+/+) mice with two GPBAR1 agonists, ciprofloxacin and betulinic acid, rescued mice from gastric injury caused by ASA and NSAIDs.	Aspirin	129-132	G protein-coupled bile acid receptor 1	Mus musculus	35-41
22881598-13	2013	GPBAR1 agonists protect against gastrointestinal injury caused by ASA and NSAIDs by a COX-independent mechanism.	Aspirin	66-69	G protein-coupled bile acid receptor 1	Mus musculus	0-6
22893064-3	2012	The priming action of aspirin on tumor cells was found to be dependent on an altered constitution of tumor microenvironment with respect to decline of acidosis and modulation in the expression of cell cycle and survival regulatory molecules like cyclin B1, cyclin D, bcl-2, bcl-xL, p53, and cytokines: IL-4, IL-10, IFN- gamma &amp; VEGF.	Aspirin	22-29	vascular endothelial growth factor A	Mus musculus	332-336
21474293-2	2012	We hypothesized that minocycline induced MMP-2 and MMP-9 inhibition can be enhanced by aspirin (through its COX and tPA inhibitory action) and this combination can reduce cardiovascular dysfunction of diabetes.	Aspirin	87-94	matrix metallopeptidase 9	Rattus norvegicus	51-56
21474293-16	2012	Present study revealed that aspirin potentate minocycline induced MMP-2 and MMP-9 inhibition to ameliorate cardiovascular dysfunction of diabetes and this combination can be an approach for the treatment.	Aspirin	28-35	matrix metallopeptidase 9	Rattus norvegicus	76-81
23158034-6	2012	RESULTS: There were significant increases in the prescribing of statins (OR 1.78; 95% CI 1.66-1.91) and aspirin (OR 1.47, 95% CI 1.50-1.59) in Period 2 as compared with Period 1.	Aspirin	104-111	period circadian regulator 2	Homo sapiens	143-151
23047410-3	2012	We report a case of a 78-year-old, ASA IV patient suffering from acute cholecystitis and concomitant (62 mm) AAA.	Aspirin	35-38	AAA1	Homo sapiens	109-112
22765917-6	2012	Hippocampal neuronal loss five weeks after SE was also attenuated in the CA1, CA3 and hilus following aspirin administration.	Aspirin	102-109	carbonic anhydrase 3	Rattus norvegicus	78-81
22337717-6	2012	MRP4 is a versatile transporter, and various additional functions have been proposed, notably lipid mediator release and a role in aspirin resistance.	Aspirin	131-138	ATP binding cassette subfamily C member 4	Homo sapiens	0-4
21756248-0	2012	Acetylsalicylic acid regulates overexpressed small GTPase RhoA in vascular smooth muscle cells through prevention of new synthesis and enhancement of protein degradation.	Aspirin	0-20	ras homolog family member A	Rattus norvegicus	58-62
21756248-2	2012	In the present study, we aimed at investigating the effect of aspirin on RhoA expression under a stress state in rat VSMCs (vascular smooth muscle cells) and the underlying mechanisms.	Aspirin	62-69	ras homolog family member A	Rattus norvegicus	73-77
22045867-9	2012	Our data indicate that combination of aspirin and minocycline therapy protects from the consequences of cerebral ischaemia in animal models of diabetes and is associated with inhibition of MMP-2 and MMP-9.	Aspirin	38-45	matrix metallopeptidase 9	Rattus norvegicus	199-204
22697009-0	2012	A possible association between ZNRD1 and aspirin-induced airway bronchoconstriction in a Korean population.	Aspirin	41-48	RNA polymerase I subunit H	Homo sapiens	31-36
22697009-7	2012	CONCLUSIONS: These preliminary findings suggest a possible relationship between ZNRD1 and aspirin-induced respiratory dysfunctions in a Korean population and provide essential information on the etiology of AERD.	Aspirin	90-97	RNA polymerase I subunit H	Homo sapiens	80-85
21584653-6	2012	Moreover, ASA increased the production of the anti-inflammatory cytokines transforming growth factor beta-1 and interleukin-10 in neuron-glia cultures after stimulation with LPS.	Aspirin	10-13	interleukin 10	Homo sapiens	112-126
22952917-5	2012	When stimulated with whole sperm cells, the PBMCs from patients with ASA produce less IL-3, IL-11, IL-13, ICAM-1, GCSF and more IL-2, IL-4 and IL-12p70 as compared to healthy women.	Aspirin	69-72	intercellular adhesion molecule 1	Homo sapiens	106-112
22952917-6	2012	PBMCs from patients with ASA produce typically less IL-13, IL-7, IL-17 and MIG, and more MIP-1beta and IL-8, as compared to PBMCs from patients without ASA.	Aspirin	25-28	interleukin 17A	Homo sapiens	65-70
22654612-0	2012	Galectin-10 is released in the nasal lavage fluid of patients with aspirin-sensitive respiratory disease.	Aspirin	67-74	Charcot-Leyden crystal galectin	Homo sapiens	0-11
22654612-1	2012	The aim of this work was to determine the presence of galectin-10 in nasal lavage fluid (NLF) of patients with aspirin-sensitive respiratory disease (ASRD) before and after challenge with L-ASA (aspirin) by ELISA.	Aspirin	111-118	Charcot-Leyden crystal galectin	Homo sapiens	54-65
22654612-1	2012	The aim of this work was to determine the presence of galectin-10 in nasal lavage fluid (NLF) of patients with aspirin-sensitive respiratory disease (ASRD) before and after challenge with L-ASA (aspirin) by ELISA.	Aspirin	195-202	Charcot-Leyden crystal galectin	Homo sapiens	54-65
22123380-0	2011	IL-13 and IL-17A gene polymorphisms in Japanese patients with aspirin-exacerbated respiratory disease.	Aspirin	62-69	interleukin 17A	Homo sapiens	10-16
22123389-0	2011	Association of interleukin 10 promoter polymorphism at -819 T&gt;C with aspirin-induced urticaria in a Korean population.	Aspirin	72-79	interleukin 10	Homo sapiens	15-29
21743961-9	2011	In vitro assays of these enzymes revealed that aspirin did not affect pyruvate kinase and lactate dehydrogenase activity; however, it decreased glucose 6 phosphate dehydrogenase activity.	Aspirin	47-54	glucose-6-phosphate dehydrogenase	Homo sapiens	144-177
21743961-11	2011	Selective inhibition of glucose-6-phosphate dehydrogenase may represent an important mechanism by which aspirin may exert its anti-cancer effects through inhibition of ribonucleotide synthesis.	Aspirin	104-111	glucose-6-phosphate dehydrogenase	Homo sapiens	24-57
21803431-0	2011	Differential effect of clopidogrel and aspirin on the release of BDNF from platelets.	Aspirin	39-46	brain derived neurotrophic factor	Homo sapiens	65-69
21816313-9	2011	CONCLUSIONS: Aspirin is a substrate for MRP4 and can be extruded from platelet through its transportation.	Aspirin	13-20	ATP binding cassette subfamily C member 4	Homo sapiens	40-44
21816313-10	2011	Aspirin effect on COX-1 is little-related to MRP4-mediated aspirin transport in HV, but in CABG patients with MRP4 over-expression, its pharmacological inhibition enhances aspirin action in an efficient way.	Aspirin	59-66	ATP binding cassette subfamily C member 4	Homo sapiens	45-49
21816313-10	2011	Aspirin effect on COX-1 is little-related to MRP4-mediated aspirin transport in HV, but in CABG patients with MRP4 over-expression, its pharmacological inhibition enhances aspirin action in an efficient way.	Aspirin	172-179	ATP binding cassette subfamily C member 4	Homo sapiens	45-49
21816313-10	2011	Aspirin effect on COX-1 is little-related to MRP4-mediated aspirin transport in HV, but in CABG patients with MRP4 over-expression, its pharmacological inhibition enhances aspirin action in an efficient way.	Aspirin	172-179	ATP binding cassette subfamily C member 4	Homo sapiens	110-114
21205219-9	2011	Aspirin administration to CCT diet-fed animals (CCT + Asp) reverted all the studied biochemical and histological changes towards normality.	Aspirin	0-7	FLVCR heme transporter 2	Rattus norvegicus	26-29
21205219-9	2011	Aspirin administration to CCT diet-fed animals (CCT + Asp) reverted all the studied biochemical and histological changes towards normality.	Aspirin	0-7	FLVCR heme transporter 2	Rattus norvegicus	48-51
21076843-12	2011	Aspirin (500 muM) demonstrated myriad effects in human CCA cell lines, including growth suppression, reduced phosphorylation of Akt/Erk/c-Jun, elevation of RECK expression, inhibition of MMP-2/MMP-9 activity, and enhanced invasiveness.	Aspirin	0-7	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	136-141
21076843-12	2011	Aspirin (500 muM) demonstrated myriad effects in human CCA cell lines, including growth suppression, reduced phosphorylation of Akt/Erk/c-Jun, elevation of RECK expression, inhibition of MMP-2/MMP-9 activity, and enhanced invasiveness.	Aspirin	0-7	matrix metallopeptidase 9	Homo sapiens	193-198
21030714-6	2011	When treated with aspirin, the patients showed a 49% reduction in the generation of CD34+/KDR+ cells, indicating that the level of circulating CD34+/KDR+ cells also relates to in vivo platelet activation.	Aspirin	18-25	kinase insert domain receptor	Homo sapiens	90-93
21030714-6	2011	When treated with aspirin, the patients showed a 49% reduction in the generation of CD34+/KDR+ cells, indicating that the level of circulating CD34+/KDR+ cells also relates to in vivo platelet activation.	Aspirin	18-25	kinase insert domain receptor	Homo sapiens	149-152
20349206-4	2011	With RKO cells, aspirin reduced IL-6, IL-1ra, and IL-10 synthesis and enhanced IFNgamma secretion, while IL-1beta remained unchanged.	Aspirin	16-23	interleukin 10	Homo sapiens	50-55
21329420-8	2011	Positive correlation of the level of ADP-induced aggregation and GP IIb-IIIa content was detected in patients with ACS within the first hour upon admission to the hospital when they had already received aspirin, but not clopidogrel.	Aspirin	203-210	integrin subunit alpha 2b	Homo sapiens	65-71
20860846-0	2010	Association of CACNG6 polymorphisms with aspirin-intolerance asthmatics in a Korean population.	Aspirin	41-48	calcium voltage-gated channel auxiliary subunit gamma 6	Homo sapiens	15-21
20860846-5	2010	METHODS: To study the associations between AIA and polymorphisms in CACNG6 gene, eight variants were genotyped in 102 AIA cases and 429 aspirin-tolerant asthma (ATA) controls.	Aspirin	136-143	calcium voltage-gated channel auxiliary subunit gamma 6	Homo sapiens	68-74
20602614-0	2010	Association analysis of N-acetyl transferase-2 polymorphisms with aspirin intolerance among asthmatics.	Aspirin	66-73	N-acetyltransferase 2	Homo sapiens	24-46
20602614-2	2010	Thus, functional alterations of the NAT gene may contribute to the risk of aspirin-intolerant asthma.	Aspirin	75-82	bromodomain containing 2	Homo sapiens	36-39
20602614-7	2010	The logistic regression analysis demonstrated that NAT2 -9246G&gt;C and haplotype 2 (TCACGG) were significantly associated with the risk of aspirin-intolerant asthma.	Aspirin	140-147	N-acetyltransferase 2	Homo sapiens	51-55
20602614-9	2010	CONCLUSION: In a large genetic epidemiology study of aspirin-intolerant asthma in a Korean population, genetic polymorphisms of NAT2 were found to be related to a risk of aspirin hypersensitivity among asthmatics.	Aspirin	53-60	N-acetyltransferase 2	Homo sapiens	128-132
20602614-9	2010	CONCLUSION: In a large genetic epidemiology study of aspirin-intolerant asthma in a Korean population, genetic polymorphisms of NAT2 were found to be related to a risk of aspirin hypersensitivity among asthmatics.	Aspirin	171-178	N-acetyltransferase 2	Homo sapiens	128-132
20299485-8	2010	On the contrary, pretreatment with the NO donor NCX 4016, alone or in combination with aspirin, suppressed platelet activation induced by acute hyperglycemia (NCX 4016 +10.5 +/- 8.3 s; NCX 4016 plus aspirin: +12.0 +/- 10.7 s, P &lt; 0.05 vs. placebo for both).	Aspirin	87-94	T cell leukemia homeobox 2	Homo sapiens	48-51
20299485-8	2010	On the contrary, pretreatment with the NO donor NCX 4016, alone or in combination with aspirin, suppressed platelet activation induced by acute hyperglycemia (NCX 4016 +10.5 +/- 8.3 s; NCX 4016 plus aspirin: +12.0 +/- 10.7 s, P &lt; 0.05 vs. placebo for both).	Aspirin	199-206	T cell leukemia homeobox 2	Homo sapiens	48-51
19880966-11	2010	Using real-time PCR we found a significant downregulation of the target genes VEGF and RelA demonstrating our ability to achieve effective pharmacological levels of aspirin and enalapril during pancreatic cancer formation in vivo.	Aspirin	165-172	vascular endothelial growth factor A	Mus musculus	78-82
20347141-5	2010	Hence these cells were used to investigate the effect of varying concentrations of vitamin C, acetylsalicylic acid (ASA), Trolox) and heparin on cell fusion and PP13 and beta-hCG levels.	Aspirin	116-119	galectin 13	Homo sapiens	161-165
20233223-0	2010	Nitric oxide, derived from inducible nitric oxide synthase, decreases hypoxia inducible factor-1alpha in macrophages during aspirin-induced mesenteric inflammation.	Aspirin	124-131	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	70-101
20377702-7	2010	In homozygous T(4) transgenic seedlings, DHAR overexpression was increased up to 1.5 to 5.4 fold, which enhanced foliar ascorbic acid levels 2- to 4.25-fold and ratio of AsA/DHA about 3- to 16-fold relative to wild type.	Aspirin	170-173	dehydroascorbate reductase	Arabidopsis thaliana	41-45
20135061-4	2010	It was the objective of this study to assess the potential influence of alpha2A-AR and beta2-AR gene polymorphisms on platelet reactivity after dual antiplatelet therapy with aspirin and clopidogrel in ACS.	Aspirin	175-182	adrenoceptor alpha 2A	Homo sapiens	72-82
20135061-4	2010	It was the objective of this study to assess the potential influence of alpha2A-AR and beta2-AR gene polymorphisms on platelet reactivity after dual antiplatelet therapy with aspirin and clopidogrel in ACS.	Aspirin	175-182	adrenoceptor beta 2	Homo sapiens	87-95
20215502-2	2010	We showed that glucocorticoids and chemopreventive modified nonsteroidal anti-inflammatory drugs, such as nitric oxide-donating aspirin (NO-ASA) and phospho-aspirin, induced ANXA1 in cultured human colon and pancreatic cancer cells.	Aspirin	128-135	annexin A1	Homo sapiens	174-179
20215502-2	2010	We showed that glucocorticoids and chemopreventive modified nonsteroidal anti-inflammatory drugs, such as nitric oxide-donating aspirin (NO-ASA) and phospho-aspirin, induced ANXA1 in cultured human colon and pancreatic cancer cells.	Aspirin	140-143	annexin A1	Homo sapiens	174-179
20215502-2	2010	We showed that glucocorticoids and chemopreventive modified nonsteroidal anti-inflammatory drugs, such as nitric oxide-donating aspirin (NO-ASA) and phospho-aspirin, induced ANXA1 in cultured human colon and pancreatic cancer cells.	Aspirin	157-164	annexin A1	Homo sapiens	174-179
19796209-0	2010	Genetic variability in CRTH2 polymorphism increases eotaxin-2 levels in patients with aspirin exacerbated respiratory disease.	Aspirin	86-93	prostaglandin D2 receptor 2	Homo sapiens	23-28
19796209-3	2010	Considering the fact that eosinophil infiltration is prominent in the upper and lower airways of aspirin exacerbated respiratory disease (AERD) compared to aspirin-tolerant asthma (ATA) patients, we hypothesized that activation of eosinophils via dysregulation of the CRTH2 gene may play an important role and be an important marker for AERD.	Aspirin	97-104	prostaglandin D2 receptor 2	Homo sapiens	268-273
20140805-5	2010	The activity of AFF1 (50 mg kg(-1)) was higher than that of the standard anti-inflammatory drug, aspirin (100 mg kg(-1)).	Aspirin	97-104	AF4/FMR2 family, member 1	Rattus norvegicus	16-20
21088444-0	2010	Aspirin increases apolipoprotein-A-I-mediated cholesterol efflux via enhancing expression of ATP-binding cassette transporter A1.	Aspirin	0-7	apolipoprotein A-I	Mus musculus	18-36
21088444-0	2010	Aspirin increases apolipoprotein-A-I-mediated cholesterol efflux via enhancing expression of ATP-binding cassette transporter A1.	Aspirin	0-7	ATP-binding cassette, sub-family A (ABC1), member 1	Mus musculus	93-128
21088444-5	2010	RESULTS: 0.5 mmol/l aspirin increased apoA-I-mediated cholesterol efflux and increased the expression of ABCA1.	Aspirin	20-27	apolipoprotein A-I	Mus musculus	38-44
21088444-5	2010	RESULTS: 0.5 mmol/l aspirin increased apoA-I-mediated cholesterol efflux and increased the expression of ABCA1.	Aspirin	20-27	ATP-binding cassette, sub-family A (ABC1), member 1	Mus musculus	105-110
21088444-6	2010	By increasing the dose of aspirin higher than 0.5 mmol/l, ABCA1 expression and function were significantly decreased.	Aspirin	26-33	ATP-binding cassette, sub-family A (ABC1), member 1	Mus musculus	58-63
20438395-0	2010	Validation of a procedure to assess ASA-response in patients with decreased, initial TRAP induced aggregation.	Aspirin	36-39	TRAP	Homo sapiens	85-89
20438395-3	2010	However, assessing the platelet function is highly affected by pre-analytical and analytical conditions and often reduced aggregation by TRAP induced aggregation (TRAP-test) is seen, rendering the samples difficult for interpretation of the ASPI-test and the responder status to ASA.	Aspirin	279-282	TRAP	Homo sapiens	137-141
20438395-3	2010	However, assessing the platelet function is highly affected by pre-analytical and analytical conditions and often reduced aggregation by TRAP induced aggregation (TRAP-test) is seen, rendering the samples difficult for interpretation of the ASPI-test and the responder status to ASA.	Aspirin	279-282	TRAP	Homo sapiens	163-167
20438395-8	2010	Normalisation of the ASPI-test result using the TRAP-test result may provide a method to judge on the ASA response status in patients with decreased initial "general platelet activatability".	Aspirin	102-105	TRAP	Homo sapiens	48-52
21053780-7	2010	IL-5 and eosinophil cationic protein (ECP) levels showed a decreasing trend in patients with NP and an increasing trend in patients with associated aspirin sensitivity.	Aspirin	148-155	ribonuclease A family member 3	Homo sapiens	9-36
21053780-7	2010	IL-5 and eosinophil cationic protein (ECP) levels showed a decreasing trend in patients with NP and an increasing trend in patients with associated aspirin sensitivity.	Aspirin	148-155	ribonuclease A family member 3	Homo sapiens	38-41
19958602-6	2009	RESULTS: The frequency of -1562CT genotype of MMP-9 was significantly high in NP patients with aspirin-induced asthma (p = 0.014).	Aspirin	95-102	matrix metallopeptidase 9	Homo sapiens	46-51
19958602-9	2009	CONCLUSION: In this study, MMP-9 -1562CT genotype was associated with susceptibility to NP in aspirin-induced asthmatic patients.	Aspirin	94-101	matrix metallopeptidase 9	Homo sapiens	27-32
19486029-6	2009	RESULTS: Aspirin-induced expression of CD63, CD69 and CD203c yielded 30%, 80% and 70% sensitivity, respectively, but with poor specificity.	Aspirin	9-16	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	54-60
19222424-3	2009	The goal of this study was to investigate a gene-gene interaction between IL-10 and TGF-beta1 polymorphisms in Korean asthmatics with aspirin hypersensitivity.	Aspirin	134-141	interleukin 10	Homo sapiens	74-79
18849138-0	2009	Acetylsalicylic acid regulates MMP-2 activity and inhibits colorectal invasion of murine B16F0 melanoma cells in C57BL/6J mice: effects of prostaglandin F(2)alpha.	Aspirin	0-20	matrix metallopeptidase 2	Mus musculus	31-36
18849138-5	2009	Gelatin-based zymography assays showed that acetylsalicylic acid inhibited the MMP-2 activity of B16F0 melanoma cells.	Aspirin	44-64	matrix metallopeptidase 2	Mus musculus	79-84
18849138-7	2009	Acetylsalicylic acid can inhibit PGF(2)alpha synthesis and PGF(2)alpha is a key stimulator of MMP-2 production.	Aspirin	0-20	matrix metallopeptidase 2	Mus musculus	94-99
19522741-0	2009	Aspirin reduces the prothrombotic activity of C-reactive protein.	Aspirin	0-7	C-reactive protein, pentraxin-related	Mus musculus	46-64
19376786-7	2009	Propensity-adjusted survival analysis showed significant reduction of mortality for combination therapy with GP IIb/IIIa inhibitors and clopidogrel, clopidogrel alone, and GP IIb/IIIa inhibitors alone over aspirin alone.	Aspirin	206-213	integrin subunit alpha 2b	Homo sapiens	109-115
19376786-7	2009	Propensity-adjusted survival analysis showed significant reduction of mortality for combination therapy with GP IIb/IIIa inhibitors and clopidogrel, clopidogrel alone, and GP IIb/IIIa inhibitors alone over aspirin alone.	Aspirin	206-213	integrin subunit alpha 2b	Homo sapiens	172-178
19428338-8	2009	The suppression of anti-adipogenic PGE(2) by COX inhibitors such as aspirin and NS-398 partially blocked the effect of IL-17A on adipocyte differentiation in hBM-MSCs.	Aspirin	68-75	interleukin 17A	Homo sapiens	119-125
19226274-0	2009	Chemokine CC-ligand 5 production and eosinophil activation into the upper airways of aspirin-sensitive patients.	Aspirin	85-92	C-C motif chemokine ligand 5	Homo sapiens	0-21
19226274-2	2009	OBJECTIVE: We have investigated chemokine CC-ligand 5 (CCL5) production and its association with eosinophil activation in the upper airways of aspirin-sensitive patients both in vivo and in vitro.	Aspirin	143-150	C-C motif chemokine ligand 5	Homo sapiens	32-53
19226274-2	2009	OBJECTIVE: We have investigated chemokine CC-ligand 5 (CCL5) production and its association with eosinophil activation in the upper airways of aspirin-sensitive patients both in vivo and in vitro.	Aspirin	143-150	C-C motif chemokine ligand 5	Homo sapiens	55-59
19226274-8	2009	Similarly, the concentrations of both eosinophil cationic protein (ECP) and cysteinil leukotriene (cys-LTs) were increased significantly in the aspirin-sensitive but not in the tolerant patients.	Aspirin	144-151	ribonuclease A family member 3	Homo sapiens	38-65
19226274-8	2009	Similarly, the concentrations of both eosinophil cationic protein (ECP) and cysteinil leukotriene (cys-LTs) were increased significantly in the aspirin-sensitive but not in the tolerant patients.	Aspirin	144-151	ribonuclease A family member 3	Homo sapiens	67-70
19226274-10	2009	On incubation with aspirin, nasal tissue derived from aspirin-sensitive but not that derived from tolerant subjects released increased CCL5 levels in culture.	Aspirin	19-26	C-C motif chemokine ligand 5	Homo sapiens	135-139
19226274-10	2009	On incubation with aspirin, nasal tissue derived from aspirin-sensitive but not that derived from tolerant subjects released increased CCL5 levels in culture.	Aspirin	54-61	C-C motif chemokine ligand 5	Homo sapiens	135-139
19226274-12	2009	CONCLUSION: Altogether, these findings suggest that CCL5 is released in aspirin-sensitive asthma/rhinosinusitis.	Aspirin	72-79	C-C motif chemokine ligand 5	Homo sapiens	52-56
18474393-9	2009	F1+2 levels decreased by 64% and 58% in the warfarin and aspirin/warfarin groups, respectively (p=0.001 for both).	Aspirin	57-64	coagulation factor XII	Homo sapiens	0-4
19494523-9	2009	RESULTS: The highest sensitivity and specificity of CD63 were 33.3 and 79.2%, respectively, and of CD203c were 16.7 and 100%, respectively, for ASA.	Aspirin	144-147	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	99-105
18413191-0	2009	Inhibition of platelet GPIIb-IIIa and P-selectin expression by aspirin is impaired by stress hyperglycemia.	Aspirin	63-70	integrin subunit alpha 2b	Homo sapiens	23-28
18413191-6	2009	In vitro, ASA significantly inhibited both GPIIb-IIIa expression (36.5%) and P-selectin expression (81%; P&lt;.005).	Aspirin	10-13	integrin subunit alpha 2b	Homo sapiens	43-48
18413191-7	2009	However, increased blood glucose (200 mg/dl) significantly impaired the inhibitory effect of ASA (84% for GPIIb-IIIa, P&lt;.005; 48% for P-selectin, P=NS).	Aspirin	93-96	integrin subunit alpha 2b	Homo sapiens	106-111
18413191-9	2009	A statistically significant interaction between glucose concentration and ASA dose was found (P&lt;.001 for GPIIb-IIIa and P=.004 for P-selectin).	Aspirin	74-77	integrin subunit alpha 2b	Homo sapiens	108-113
18413191-10	2009	In vitro, concentration-dependent stress hyperglycemia significantly impaired the inhibitory effects of aspirin on human platelet GPIIb-IIIa and P-selectin expression.	Aspirin	104-111	integrin subunit alpha 2b	Homo sapiens	130-135
18971601-0	2009	Aspirin inhibits MMP-2 and MMP-9 expressions and activities through upregulation of PPARalpha/gamma and TIMP gene expressions in ox-LDL-stimulated macrophages derived from human monocytes.	Aspirin	0-7	matrix metallopeptidase 9	Homo sapiens	27-32
18971601-3	2009	Following treatment of cells with aspirin, MMP-2 and MMP-9 expression and release were significantly reduced.	Aspirin	34-41	matrix metallopeptidase 9	Homo sapiens	53-58
18971601-6	2009	RT-PCR and ELISA assays showed that inhibition of MMP-9 levels by aspirin was notably alleviated by PPAR antagonists.	Aspirin	66-73	matrix metallopeptidase 9	Homo sapiens	50-55
18971601-8	2009	RT-PCR study also indicated that aspirin could upregulate the expression of tissue inhibitors of metalloproteinases (TIMP)-1 and TIMP-2.	Aspirin	33-40	TIMP metallopeptidase inhibitor 2	Homo sapiens	129-135
18971601-10	2009	These results demonstrate that aspirin could inhibit MMP-2 and MMP-9 expression through upregulation of PPARalpha/gamma expression in ox-LDL-stimulated macrophages, and could potentially inhibit MMP-2 and MMP-9 activity by induction of TIMP-1 and TIMP-2 expression.	Aspirin	31-38	matrix metallopeptidase 9	Homo sapiens	63-68
18971601-10	2009	These results demonstrate that aspirin could inhibit MMP-2 and MMP-9 expression through upregulation of PPARalpha/gamma expression in ox-LDL-stimulated macrophages, and could potentially inhibit MMP-2 and MMP-9 activity by induction of TIMP-1 and TIMP-2 expression.	Aspirin	31-38	matrix metallopeptidase 9	Homo sapiens	205-210
18971601-10	2009	These results demonstrate that aspirin could inhibit MMP-2 and MMP-9 expression through upregulation of PPARalpha/gamma expression in ox-LDL-stimulated macrophages, and could potentially inhibit MMP-2 and MMP-9 activity by induction of TIMP-1 and TIMP-2 expression.	Aspirin	31-38	TIMP metallopeptidase inhibitor 2	Homo sapiens	247-253
19132198-2	2009	We correlated ASA responsiveness with haplotypes of seven candidate genes, selected for their documented role in platelet function, namely, the genes for integrins alpha2beta1and alphaIIbbeta3 (ITGA2, ITGA2B, and ITGB3), platelet glycoproteins Ibalpha and VI (GPIBA and GP6), the purinergic receptor P2Y1 (P2RY1), and prostaglandin H synthase 1 (PTGS1 = COX1).	Aspirin	14-17	integrin subunit alpha 2b	Homo sapiens	201-207
18358478-11	2008	CONCLUSIONS: The pro-thrombotic phenotype of CRPtg mice was suppressed by aspirin/heparin, revealing CRP"s influence on neointimal growth after trans-femoral arterial wire-injury.	Aspirin	74-81	C-reactive protein, pentraxin-related	Mus musculus	45-48
18485921-1	2008	Properties of the NO-ASA family of NO-donating NSAIDs (NO-NSAIDs), notably NCX 4016 (mNO-ASA) and NCX 4040 (pNO-ASA), reported in more than one hundred publications, have included positive preclinical data in cancer chemoprevention and therapy.	Aspirin	21-24	T cell leukemia homeobox 2	Homo sapiens	75-78
18485921-1	2008	Properties of the NO-ASA family of NO-donating NSAIDs (NO-NSAIDs), notably NCX 4016 (mNO-ASA) and NCX 4040 (pNO-ASA), reported in more than one hundred publications, have included positive preclinical data in cancer chemoprevention and therapy.	Aspirin	21-24	T cell leukemia homeobox 2	Homo sapiens	98-101
18489507-10	2008	CONCLUSIONS: The use of GPIIb/IIIa inhibitors upstream in high-risk NSTE-ACS patients (TIMI score &gt; or = 3) pretreated with aspirin and clopidogrel is cost-effective, particularly in the younger age groups.	Aspirin	127-134	integrin subunit alpha 2b	Homo sapiens	24-29
18560754-0	2008	Prestin up-regulation in chronic salicylate (aspirin) administration: an implication of functional dependence of prestin expression.	Aspirin	45-52	solute carrier family 26 member 5	Homo sapiens	0-7
18480058-5	2008	Furthermore, platelets pre-exposed to the PAR4-activating peptide AYPGKF, but not to the PAR1-activating peptide SFLLRN, were aggregated by epinephrine, whereas both AYPGKF and SFLLRN synergized with epinephrine in the absence of aspirin.	Aspirin	230-237	F2R like thrombin or trypsin receptor 3	Homo sapiens	42-46
18480058-10	2008	Thus, in aspirin-treated platelets, PAR4, but not PAR1, interacts synergistically with alpha(2A)-adrenergic receptors, and the PI3-kinase/Akt pathway is involved in this cross-talk.	Aspirin	9-16	F2R like thrombin or trypsin receptor 3	Homo sapiens	36-40
18480058-12	2008	These results suggest a new mechanism that has ATP as a key element and circumvents the action of aspirin on epinephrine-facilitated PAR4-mediated platelet activation.	Aspirin	98-105	F2R like thrombin or trypsin receptor 3	Homo sapiens	133-137
18712091-7	2008	The level of residual aggregation in the presence of aspirin also correlated with GP IIb-IIIa content and increased in subjects with high receptor content.	Aspirin	53-60	integrin subunit alpha 2b	Homo sapiens	82-88
18712091-12	2008	High GP IIb-IIIa content is associated with increased platelet aggregation activity and decreased efficacy of aggregation inhibition by aspirin.	Aspirin	136-143	integrin subunit alpha 2b	Homo sapiens	5-11
18302761-3	2008	The antitumor efficacy and mechanism of NCX-4040, a nitric oxide-releasing aspirin derivative, against ovarian cancer is studied.	Aspirin	75-82	T cell leukemia homeobox 2	Homo sapiens	40-43
17941953-0	2008	Galectin-10 mRNA is overexpressed in peripheral blood of aspirin-induced asthma.	Aspirin	57-64	Charcot-Leyden crystal galectin	Homo sapiens	0-11
17941953-12	2008	Employing two molecular biological methods, we demonstrate that galectin-10 mRNA is overexpressed in AIA, suggesting a novel candidate gene and a potentially innovative pathway for mucosal inflammation in aspirin intolerance.	Aspirin	205-212	Charcot-Leyden crystal galectin	Homo sapiens	64-75
18196976-0	2008	NCX-4016, a nitro-derivative of aspirin, inhibits EGFR and STAT3 signaling and modulates Bcl-2 proteins in cisplatin-resistant human ovarian cancer cells and xenografts.	Aspirin	32-39	T cell leukemia homeobox 2	Homo sapiens	0-3
18196976-1	2008	We have previously reported the inhibitory effect of NCX-4016, a nitro derivative of aspirin, on the proliferation of cisplatin-resistant human ovarian cancer cells, in vitro (Bratasz et al., Proc Natl Acad Sci USA 2006; 103:3914-9).	Aspirin	85-92	T cell leukemia homeobox 2	Homo sapiens	53-56
18417193-0	2008	Enhancing effect of the (145)Met-allele of GPIb alpha on platelet sensitivity to aspirin under high-shear conditions.	Aspirin	81-88	glycoprotein Ib platelet subunit alpha	Homo sapiens	43-53
17694420-7	2007	CRC risk also was associated with an interaction between VDR and IL6 genotypes that was modified by current use of aspirin/NSAIDs.	Aspirin	115-122	vitamin D receptor	Homo sapiens	57-60
17971198-0	2007	Study of molecular mechanisms of pro-apoptotic activity of NCX 4040, a novel nitric oxide-releasing aspirin, in colon cancer cell lines.	Aspirin	100-107	T cell leukemia homeobox 2	Homo sapiens	59-62
17971198-2	2007	In the present study, we investigated the mechanisms underlying the cytotoxicity of NCX 4040, a novel NO-aspirin with promising antineoplastic action, in in vitro human colon cancer models.	Aspirin	105-112	T cell leukemia homeobox 2	Homo sapiens	84-87
17927648-3	2007	In rats, subcutaneous administration of NTG (10 mg/kg) increases significantly the number of nNOS-immunoreactive neurons in the TNC after 4 hours, which could be attenuated by acetyl-salicylate (Aspirin), a nonselective COX-inhibitor.	Aspirin	176-193	nitric oxide synthase 1	Rattus norvegicus	93-97
17927648-3	2007	In rats, subcutaneous administration of NTG (10 mg/kg) increases significantly the number of nNOS-immunoreactive neurons in the TNC after 4 hours, which could be attenuated by acetyl-salicylate (Aspirin), a nonselective COX-inhibitor.	Aspirin	195-202	nitric oxide synthase 1	Rattus norvegicus	93-97
17650080-13	2007	Patients with elevated postoperative cTnI had significantly increased AA-mediated platelet aggregation and a higher incidence of non-response to aspirin compared with patients who did not.	Aspirin	145-152	troponin I3, cardiac type	Homo sapiens	37-41
17903525-0	2007	Nitric oxide-donating aspirin (NCX 4016) inhibits neointimal thickening in a pig model of saphenous vein-carotid artery interposition grafting: a comparison with aspirin and morpholinosydnonimine (SIN-1).	Aspirin	22-29	T cell leukemia homeobox 2	Homo sapiens	31-34
17903525-3	2007	A drug class that fulfills this pharmacologic criterion is nitric oxide-donating aspirin (NCX 4016).	Aspirin	81-88	T cell leukemia homeobox 2	Homo sapiens	90-93
17903525-4	2007	METHODS: The effect of administration of the aspirin-nitric oxide adduct, NCX 4016, compared with those of aspirin alone and the nitric oxide donor, morpholinosydnonimine, alone (once daily for 1 month) on thickening of saphenous vein-carotid artery interposition grafts was investigated.	Aspirin	45-52	T cell leukemia homeobox 2	Homo sapiens	74-77
17903525-6	2007	Aspirin alone (60 mg x kg(-1) x d(-1)) and morpholinosydnonimine alone (1 mg x kg(-1) x d(-1)), also inhibited neointimal thickness and neointimal area, although they were less potent than NCX 4016.	Aspirin	0-7	T cell leukemia homeobox 2	Homo sapiens	189-192
17847705-0	2007	Kinetic, thermodynamic and statistical studies on the inhibition of adenosine deaminase by aspirin and diclofenac.	Aspirin	91-98	adenosine deaminase	Homo sapiens	68-87
17847705-1	2007	The kinetic and thermodynamic effects of aspirin and diclofenac on the activity of adenosine deaminase (ADA) were studied in 50 mM phosphate buffer pH = 7.5 at 27 and 37 degrees C, using UV-Vis spectrophotometry and isothermal titration calorimetry (ITC).	Aspirin	41-48	adenosine deaminase	Homo sapiens	83-102
17847705-1	2007	The kinetic and thermodynamic effects of aspirin and diclofenac on the activity of adenosine deaminase (ADA) were studied in 50 mM phosphate buffer pH = 7.5 at 27 and 37 degrees C, using UV-Vis spectrophotometry and isothermal titration calorimetry (ITC).	Aspirin	41-48	adenosine deaminase	Homo sapiens	104-107
17706514-2	2007	The child was affected by a right hemiparesis because of a hypoxic-ischemic disorder that occurred in the first hours of life and was heterozygous for the methylenetetrahydrofolate reductase gene mutation 677C-T. Intravenous heparin and aspirin were initiated on postoperative day 7.	Aspirin	237-244	methylenetetrahydrofolate reductase	Homo sapiens	155-190
17579083-0	2007	Aspirin-triggered lipoxins override the apoptosis-delaying action of serum amyloid A in human neutrophils: a novel mechanism for resolution of inflammation.	Aspirin	0-7	serum amyloid A1 cluster	Homo sapiens	69-84
17579083-6	2007	Furthermore, aspirin-triggered 15-epi-lipoxin A(4) (15-epi-LXA(4)) and its stable analog 15-epi-16-p-fluorophenoxy-LXA(4), which binds to the same receptor as SAA, effectively overrode the antiapoptosis signal from SAA even when neutrophils were treated with 15-epi-LXA(4) at either 1 or 4 h postculture with SAA.	Aspirin	13-20	serum amyloid A1 cluster	Homo sapiens	159-162
17579083-6	2007	Furthermore, aspirin-triggered 15-epi-lipoxin A(4) (15-epi-LXA(4)) and its stable analog 15-epi-16-p-fluorophenoxy-LXA(4), which binds to the same receptor as SAA, effectively overrode the antiapoptosis signal from SAA even when neutrophils were treated with 15-epi-LXA(4) at either 1 or 4 h postculture with SAA.	Aspirin	13-20	serum amyloid A1 cluster	Homo sapiens	215-218
17579083-6	2007	Furthermore, aspirin-triggered 15-epi-lipoxin A(4) (15-epi-LXA(4)) and its stable analog 15-epi-16-p-fluorophenoxy-LXA(4), which binds to the same receptor as SAA, effectively overrode the antiapoptosis signal from SAA even when neutrophils were treated with 15-epi-LXA(4) at either 1 or 4 h postculture with SAA.	Aspirin	13-20	serum amyloid A1 cluster	Homo sapiens	215-218
17428820-7	2007	The preventive effect of acetylsalicylic acid on glycation of methemoglobin and consequently, Hb-AGE formation also has been included.	Aspirin	25-45	hemoglobin subunit gamma 2	Homo sapiens	62-75
17535415-16	2007	PCNA expression was significantly reduced in the aspirin and PEITC group.	Aspirin	49-56	proliferating cell nuclear antigen	Rattus norvegicus	0-4