PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 27133131-8 2016 Thrombin elevated ~900 lipids >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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 25208590-11 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 24155779-8 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 24155779-11 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 22320344-1 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 61-68 mitochondrially encoded cytochrome c oxidase I Homo sapiens 241-246 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 19110389-4 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 < 0.001). Aspirin 95-102 mitochondrially encoded cytochrome c oxidase I Homo sapiens 25-30 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 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 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 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 < 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 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 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 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 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 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 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 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 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 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 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 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 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 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 I Homo sapiens 64-69 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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