PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33819512-1 2021 BACKGROUND: Aspirin Exacerbated Respiratory Disease (AERD) is characterized by the triad of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and intolerance to cyclooxygenase-1 (COX-1) enzyme inhibitors. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 170-186 32299908-0 2021 Identification of a homozygous recessive variant in PTGS1 resulting in a congenital aspirin-like defect in platelet function. Aspirin 84-91 prostaglandin-endoperoxide synthase 1 Homo sapiens 52-57 32299908-1 2021 We have identified a rare missense variant on chromosome 9, position 125145990 (GRCh37), in exon 8 in PTGS1 (the gene encoding cyclo-oxygenase 1, COX-1, the target of anti-thrombotic aspirin therapy). Aspirin 183-190 prostaglandin-endoperoxide synthase 1 Homo sapiens 102-107 32299908-1 2021 We have identified a rare missense variant on chromosome 9, position 125145990 (GRCh37), in exon 8 in PTGS1 (the gene encoding cyclo-oxygenase 1, COX-1, the target of anti-thrombotic aspirin therapy). Aspirin 183-190 prostaglandin-endoperoxide synthase 1 Homo sapiens 127-144 33819512-1 2021 BACKGROUND: Aspirin Exacerbated Respiratory Disease (AERD) is characterized by the triad of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and intolerance to cyclooxygenase-1 (COX-1) enzyme inhibitors. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 188-193 33336182-1 2020 Aspirin-exacerbated respiratory disease (AERD) is characterized by the triad of chronic rhinosinusitis with nasal polyposis, adult-onset asthma and non-IgE mediated reactions to aspirin and other cyclooxygenase-1 (COX-1) inhibitors. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 196-212 33657049-4 2021 Platelet aggregation induced by arachidonic acid and assessed with the use of light transmission aggregometry (LTA) was used as a direct measure of the inhibition of COX1 by aspirin. Aspirin 174-181 prostaglandin-endoperoxide synthase 1 Homo sapiens 166-170 32371071-1 2021 BACKGROUND: Aspirin Exacerbated Respiratory Disease (AERD) is characterized by asthma, chronic rhinosinusitis with nasal polyps (CRSwNP), and an intolerance to medications that inhibit cyclooxygenase-1. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 185-201 33348283-7 2021 We report that immortalized trophoblast cells express the target proteins of acetaminophen and aspirin: cyclooxygenase (COX) -1 and -2. Aspirin 95-102 prostaglandin-endoperoxide synthase 1 Homo sapiens 104-134 33336182-1 2020 Aspirin-exacerbated respiratory disease (AERD) is characterized by the triad of chronic rhinosinusitis with nasal polyposis, adult-onset asthma and non-IgE mediated reactions to aspirin and other cyclooxygenase-1 (COX-1) inhibitors. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 214-219 32596477-1 2020 Objectives: Aspirin-exacerbated respiratory disease (AERD) is a chronic respiratory condition characterized by a triad of symptoms: asthma, chronic rhinosinusitis with nasal polyposis, and a respiratory reaction to aspirin and other cyclooxygenase-1 inhibitors, also known as nonsteroidal anti-inflammatory drugs. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 233-249 32679712-1 2020 Platelet hyperactivation is involved in the established prothrombotic condition of metabolic diseases such as Type 2 Diabetes Mellitus (T2DM) and familial hypercholesterolemia (HC), justifying the therapy with aspirin, a suppressor of thromboxane synthesis through the irreversible inhibition of cyclooxygenase-1 (COX-1), to prevent cardiovascular diseases. Aspirin 210-217 prostaglandin-endoperoxide synthase 1 Homo sapiens 296-312 32679712-1 2020 Platelet hyperactivation is involved in the established prothrombotic condition of metabolic diseases such as Type 2 Diabetes Mellitus (T2DM) and familial hypercholesterolemia (HC), justifying the therapy with aspirin, a suppressor of thromboxane synthesis through the irreversible inhibition of cyclooxygenase-1 (COX-1), to prevent cardiovascular diseases. Aspirin 210-217 prostaglandin-endoperoxide synthase 1 Homo sapiens 314-319 32835720-5 2022 Aspirin at doses below 300 mg selectively and irreversibly inactivates the cyclooxygenase-1 enzyme, suppressing the production of prostaglandins and thromboxane and inhibiting inflammation and platelet aggregation. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 75-91 32654613-11 2020 Despite higher cyclooxygenase-1 inhibition, daily aspirin exposure resulted in a paradoxical attenuation of platelet inhibition in response to epinephrine and ADP over time in women but not in men. Aspirin 50-57 prostaglandin-endoperoxide synthase 1 Homo sapiens 15-31 30734682-2 2020 Common therapeutic activity of non-steroidal anti-inflammatory drugs (NSAID), such as aspirin, includes inhibition of two crucial enzymes of AA metabolism - cyclooxygenase-1 and -2 (COX-1/2), with certain risk for gastrointestinal and renal intolerance. Aspirin 86-93 prostaglandin-endoperoxide synthase 1 Homo sapiens 157-180 31915847-1 2020 PURPOSE: Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1). Aspirin 43-50 prostaglandin-endoperoxide synthase 1 Homo sapiens 73-89 31915847-1 2020 PURPOSE: Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1). Aspirin 43-50 prostaglandin-endoperoxide synthase 1 Homo sapiens 91-95 31915847-1 2020 PURPOSE: Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1). Aspirin 52-55 prostaglandin-endoperoxide synthase 1 Homo sapiens 73-89 31915847-1 2020 PURPOSE: Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1). Aspirin 52-55 prostaglandin-endoperoxide synthase 1 Homo sapiens 91-95 31693796-1 2020 BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is the triad of asthma, nasal polyposis, and sensitivity to cyclooxygenase-1 inhibitors. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 119-135 31442000-1 2019 BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is a recalcitrant inflammatory disorder defined by asthma, nasal polyposis, and sensitivity to cyclooxygenase-1 inhibitors. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 154-170 31470444-9 2020 Stopping aspirin did not affect markers of P2Y12 reactivity and had no or marginal effects on clot kinetics, but increased markers sensitive to cyclooxygenase-1 blockade. Aspirin 9-16 prostaglandin-endoperoxide synthase 1 Homo sapiens 144-160 31878351-1 2019 Given to its ability to irreversibly acetylate the platelet cyclooxygenase-1 enzyme, acetylsalicylic acid (ASA) is successfully employed for the prevention of cardiovascular disease. Aspirin 85-105 prostaglandin-endoperoxide synthase 1 Homo sapiens 60-76 31878351-1 2019 Given to its ability to irreversibly acetylate the platelet cyclooxygenase-1 enzyme, acetylsalicylic acid (ASA) is successfully employed for the prevention of cardiovascular disease. Aspirin 107-110 prostaglandin-endoperoxide synthase 1 Homo sapiens 60-76 31571629-1 2019 Background & objectives: Cytochrome P450, P2Y 12, cyclooxygenase-1 (COX1) and glycoprotein V1 (GPVI) gene polymorphisms are known to affect patient responsiveness towards aspirin and clopidogrel dual antiplatelet therapy (DAPT). Aspirin 171-178 prostaglandin-endoperoxide synthase 1 Homo sapiens 50-66 30580092-1 2019 BACKGROUND & AIMS: The antiplatelet effect of low-dose aspirin, via inhibition of cyclooxygenase-1, might contribute to its ability to reduce the risk of colorectal cancer (CRC). Aspirin 59-66 prostaglandin-endoperoxide synthase 1 Homo sapiens 86-102 31300475-4 2019 In this article, we present evidence that aspirin"s unique ability to irreversibly inhibit platelet cyclooxygenase-1 is a key mechanism by which aspirin exerts anticancer activity. Aspirin 42-49 prostaglandin-endoperoxide synthase 1 Homo sapiens 100-116 31300475-4 2019 In this article, we present evidence that aspirin"s unique ability to irreversibly inhibit platelet cyclooxygenase-1 is a key mechanism by which aspirin exerts anticancer activity. Aspirin 145-152 prostaglandin-endoperoxide synthase 1 Homo sapiens 100-116 31571629-1 2019 Background & objectives: Cytochrome P450, P2Y 12, cyclooxygenase-1 (COX1) and glycoprotein V1 (GPVI) gene polymorphisms are known to affect patient responsiveness towards aspirin and clopidogrel dual antiplatelet therapy (DAPT). Aspirin 171-178 prostaglandin-endoperoxide synthase 1 Homo sapiens 68-72 30888847-4 2019 Acetylsalicylic acid (ASA; also known as aspirin) is known to irreversibly inhibit COX-1, thereby blocking AA-mediated signaling; however, it is unclear whether ASA use alters growth factor release from freshly isolated PRP. Aspirin 0-20 prostaglandin-endoperoxide synthase 1 Homo sapiens 83-88 30654930-1 2019 Inhibition of the P2Y12 receptor by an oral P2Y12 inhibitor with loading doses along with Cyclooxygenase-1 inhibition by aspirin is considered a first-line treatment strategy in patients with the acute coronary syndrome and patients undergoing percutaneous coronary intervention (PCI). Aspirin 121-128 prostaglandin-endoperoxide synthase 1 Homo sapiens 90-106 30888847-4 2019 Acetylsalicylic acid (ASA; also known as aspirin) is known to irreversibly inhibit COX-1, thereby blocking AA-mediated signaling; however, it is unclear whether ASA use alters growth factor release from freshly isolated PRP. Aspirin 22-25 prostaglandin-endoperoxide synthase 1 Homo sapiens 83-88 30888847-4 2019 Acetylsalicylic acid (ASA; also known as aspirin) is known to irreversibly inhibit COX-1, thereby blocking AA-mediated signaling; however, it is unclear whether ASA use alters growth factor release from freshly isolated PRP. Aspirin 41-48 prostaglandin-endoperoxide synthase 1 Homo sapiens 83-88 29473449-12 2018 The effect of acetylsalicylic acid over other anti-inflammatory and anti-platelet agents is possibly attributable to its distinct mechanism of cyclooxygenase-1 inhibition. Aspirin 14-34 prostaglandin-endoperoxide synthase 1 Homo sapiens 143-159 30240925-5 2019 This pilot study aimed to elucidate the impact of hyperglycaemia on aspirin acetylation of COX-1 using a targeted mass spectrometry approach. Aspirin 68-75 prostaglandin-endoperoxide synthase 1 Homo sapiens 91-96 30240925-7 2019 Moreover, the functional aspirin-induced inhibition of COX-1 was dose-dependently impaired as glucose concentrations increased. Aspirin 25-32 prostaglandin-endoperoxide synthase 1 Homo sapiens 55-60 30240925-9 2019 These data provide new insights into the interplay between glucose and aspirin on platelet proteins and their effects on platelet COX-1. Aspirin 71-78 prostaglandin-endoperoxide synthase 1 Homo sapiens 130-135 30240925-12 2019 SIGNIFICANCE: Deciphering the mutual interplay between glucose and aspirin-mediated acetylation on platelet COX-1, might be of great interest as there is still a lack of information of the mechanism underlying this process that may contribute to the less-than expected response of platelets to aspirin, often observed in diabetes. Aspirin 67-74 prostaglandin-endoperoxide synthase 1 Homo sapiens 108-113 30240925-12 2019 SIGNIFICANCE: Deciphering the mutual interplay between glucose and aspirin-mediated acetylation on platelet COX-1, might be of great interest as there is still a lack of information of the mechanism underlying this process that may contribute to the less-than expected response of platelets to aspirin, often observed in diabetes. Aspirin 294-301 prostaglandin-endoperoxide synthase 1 Homo sapiens 108-113 30814031-2 2019 Aspirin, the most commonly used antiplatelet agent, is a cyclooxygenase-1 inhibitor and considered a mild to moderate inhibitor of platelet function. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 57-73 29781520-6 2018 A significant association with poor responsiveness to aspirin was observed for GP1BA rs2243093, PTGS1 rs1330344, PTGS2 rs689466 and TBXA2R rs1131882 polymorphisms in overall analyses. Aspirin 54-61 prostaglandin-endoperoxide synthase 1 Homo sapiens 96-101 30052978-0 2018 Studies on Prostaglandin-Endoperoxide Synthase 1: Lower Levels in Schizophrenia and After Treatment with Antipsychotic Drugs in Conjunction with Aspirin. Aspirin 145-152 prostaglandin-endoperoxide synthase 1 Homo sapiens 11-48 30052978-1 2018 Background: Antipsychotic drugs plus aspirin (acetylsalicylic acid), which targets prostaglandin-endoperoxide synthase 1 (PTGS1: COX1), improved therapeutic outcomes when treating schizophrenia. Aspirin 37-44 prostaglandin-endoperoxide synthase 1 Homo sapiens 83-120 30052978-7 2018 In CCF-STTG1 cells, a human-derived astrocytic cell line, aspirin caused a dose-dependent decrease in PTGS1 that was decreased further with the addition of risperidone. Aspirin 58-65 prostaglandin-endoperoxide synthase 1 Homo sapiens 102-107 30052978-8 2018 Conclusions: Our data suggest low levels of dorsolateral prefrontal cortex PTGS1 could be associated with the pathophysiology of schizophrenia, and improved therapeutic outcome from treating schizophrenia with antipsychotic drugs augmented with aspirin may be because such treatment lowers cortical PTGS1. Aspirin 245-252 prostaglandin-endoperoxide synthase 1 Homo sapiens 75-80 30052978-1 2018 Background: Antipsychotic drugs plus aspirin (acetylsalicylic acid), which targets prostaglandin-endoperoxide synthase 1 (PTGS1: COX1), improved therapeutic outcomes when treating schizophrenia. Aspirin 37-44 prostaglandin-endoperoxide synthase 1 Homo sapiens 122-127 30052978-8 2018 Conclusions: Our data suggest low levels of dorsolateral prefrontal cortex PTGS1 could be associated with the pathophysiology of schizophrenia, and improved therapeutic outcome from treating schizophrenia with antipsychotic drugs augmented with aspirin may be because such treatment lowers cortical PTGS1. Aspirin 245-252 prostaglandin-endoperoxide synthase 1 Homo sapiens 299-304 30052978-1 2018 Background: Antipsychotic drugs plus aspirin (acetylsalicylic acid), which targets prostaglandin-endoperoxide synthase 1 (PTGS1: COX1), improved therapeutic outcomes when treating schizophrenia. Aspirin 46-66 prostaglandin-endoperoxide synthase 1 Homo sapiens 83-120 30052978-1 2018 Background: Antipsychotic drugs plus aspirin (acetylsalicylic acid), which targets prostaglandin-endoperoxide synthase 1 (PTGS1: COX1), improved therapeutic outcomes when treating schizophrenia. Aspirin 46-66 prostaglandin-endoperoxide synthase 1 Homo sapiens 122-127 30052978-2 2018 Our microarray data showed higher levels of PTGS1 mRNA in the dorsolateral prefrontal cortex from subjects with schizophrenia of long duration of illness, suggesting aspirin plus antipsychotic drugs could have therapeutic effects by lowering PTGS1 expression in the cortex of subjects with the disorder. Aspirin 166-173 prostaglandin-endoperoxide synthase 1 Homo sapiens 44-49 30052978-2 2018 Our microarray data showed higher levels of PTGS1 mRNA in the dorsolateral prefrontal cortex from subjects with schizophrenia of long duration of illness, suggesting aspirin plus antipsychotic drugs could have therapeutic effects by lowering PTGS1 expression in the cortex of subjects with the disorder. Aspirin 166-173 prostaglandin-endoperoxide synthase 1 Homo sapiens 242-247 29316620-2 2018 Aspirin is the most commonly used non-steroid anti-inflammatory drugs (NSAIDs), and it irreversibly inhibits cyclooxygenase-1 and -2 (COX1, COX2). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 109-132 30091133-2 2018 The higher rate of ASA resistance reported in the literature may be mainly due to the cyclooxygenase-1 non-specific assays, non-compliance, and underdosing. Aspirin 19-22 prostaglandin-endoperoxide synthase 1 Homo sapiens 86-102 28859704-1 2017 BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is a disorder of nasal polyposis, asthma, and hypersensitivity respiratory reactions when on systemic cyclooxygenase 1 blockade. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 161-177 29204620-2 2017 Aspirin exerts antiplatelet effects through irreversible inhibition of cyclooxygenase-1, whereas its anticancer effects may be due to inhibition of cyclooxygenase-2 and other pathways. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 71-87 28844979-1 2017 BACKGROUND: The current standard-of-care antiplatelet therapy in cardiovascular disease patients is consisted of cyclooxygenase-1 (COX-1) inhibitor aspirin, along with a platelet receptor P2Y12 antagonist. Aspirin 148-155 prostaglandin-endoperoxide synthase 1 Homo sapiens 113-129 28859705-2 2017 Aspirin-exacerbated respiratory disease (AERD) is defined as asthma, chronic rhinosinusitis with nasal polyposis, and hypersensitivity to cyclooxygenase-1 inhibitors. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 138-154 28005558-2 2017 Oxidative stress reflected by F2-isoprostane [8-iso-prostaglandin-F2alpha (8-IsoPGF2alpha)] is a potential mechanism of failure of aspirin to adequately inhibit cyclooxygenase-1. Aspirin 131-138 prostaglandin-endoperoxide synthase 1 Homo sapiens 161-177 28668243-2 2017 Diminished PGE2 regulation in aspirin-exacerbated respiratory disease (AERD) leads to respiratory reactions on cyclooxygenase 1 inhibition. Aspirin 30-37 prostaglandin-endoperoxide synthase 1 Homo sapiens 111-127 28139830-0 2017 Low-Dose Aspirin Acetylates Cyclooxygenase-1 in Human Colorectal Mucosa: Implications for the Chemoprevention of Colorectal Cancer. Aspirin 9-16 prostaglandin-endoperoxide synthase 1 Homo sapiens 28-44 28102731-6 2017 When certain nonsteroidal anti-inflammatory drugs (NSAIDs) are taken orally, they block COX-1 acetylation by aspirin with concomitant reduction of aspirin efficacy against platelets in microfluidic assay. Aspirin 109-116 prostaglandin-endoperoxide synthase 1 Homo sapiens 88-93 28139223-2 2017 Aspirin irreversibly inhibits platelet cyclooxygenase-1 and attenuates thromboxane A2 (TXA2)-mediated platelet aggregation, but there is variable suppression of cyclooxygenase-1. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 39-55 28431615-0 2017 Association between PTGS1 polymorphisms and functional outcomes in Chinese patients with stroke during aspirin therapy: Interaction with smoking. Aspirin 103-110 prostaglandin-endoperoxide synthase 1 Homo sapiens 20-25 28431615-1 2017 PURPOSE: Prostaglandin-Endoperoxide Synthase 1 (PTGS1) and smoking may play important roles in aspirin nonresponsiveness, but the effect of their interaction on stroke outcomes remains largely unknown. Aspirin 95-102 prostaglandin-endoperoxide synthase 1 Homo sapiens 9-46 28431615-1 2017 PURPOSE: Prostaglandin-Endoperoxide Synthase 1 (PTGS1) and smoking may play important roles in aspirin nonresponsiveness, but the effect of their interaction on stroke outcomes remains largely unknown. Aspirin 95-102 prostaglandin-endoperoxide synthase 1 Homo sapiens 48-53 28431615-11 2017 CONCLUSIONS: In Chinese Han stroke patients with aspirin therapy, the adverse effect of PTGS1 polymorphisms on functional outcomes may be modulated by the smoking status. Aspirin 49-56 prostaglandin-endoperoxide synthase 1 Homo sapiens 88-93 28431615-12 2017 PTGS1 gene-smoking interaction might in part reflect the heterogeneity in the prognosis of patients treated with aspirin. Aspirin 113-120 prostaglandin-endoperoxide synthase 1 Homo sapiens 0-5 27538737-1 2017 Aspirin-exacerbated respiratory disease (AERD) refers to the combination of asthma, chronic rhinosinusitis with nasal polyposis, and acute upper and lower respiratory tract reactions to the ingestion of aspirin (acetylsalicylic acid, ASA) and other cyclooxygenase-1 inhibiting non-steroidal anti-inflammatory drugs. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 249-265 28293429-1 2017 BACKGROUND: Low-dose aspirin irreversibly inhibits platelet cyclooxygenase-1 (COX-1) and suppresses platelet aggregation. Aspirin 21-28 prostaglandin-endoperoxide synthase 1 Homo sapiens 60-76 28293429-1 2017 BACKGROUND: Low-dose aspirin irreversibly inhibits platelet cyclooxygenase-1 (COX-1) and suppresses platelet aggregation. Aspirin 21-28 prostaglandin-endoperoxide synthase 1 Homo sapiens 78-83 28293429-3 2017 Because nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly bind with COX-1, the antiplatelet effects of aspirin may be suppressed when NSAIDs are co-administered. Aspirin 110-117 prostaglandin-endoperoxide synthase 1 Homo sapiens 75-80 27538737-1 2017 Aspirin-exacerbated respiratory disease (AERD) refers to the combination of asthma, chronic rhinosinusitis with nasal polyposis, and acute upper and lower respiratory tract reactions to the ingestion of aspirin (acetylsalicylic acid, ASA) and other cyclooxygenase-1 inhibiting non-steroidal anti-inflammatory drugs. Aspirin 203-210 prostaglandin-endoperoxide synthase 1 Homo sapiens 249-265 27538737-1 2017 Aspirin-exacerbated respiratory disease (AERD) refers to the combination of asthma, chronic rhinosinusitis with nasal polyposis, and acute upper and lower respiratory tract reactions to the ingestion of aspirin (acetylsalicylic acid, ASA) and other cyclooxygenase-1 inhibiting non-steroidal anti-inflammatory drugs. Aspirin 212-232 prostaglandin-endoperoxide synthase 1 Homo sapiens 249-265 27567328-1 2017 BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is characterized by 3 clinical features: asthma, nasal polyposis, and respiratory reactions to cyclooxygenase-1 inhibitors (nonsteroidal anti-inflammatory drugs). Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 154-170 27712763-1 2016 The acute clinical symptoms that develop following the oral ingestion of aspirin, or any other inhibitor of cyclooxygenase-1, are well established in aspirin-exacerbated respiratory disease: nasal congestion, rhinorrhea, and bronchospasm. Aspirin 150-157 prostaglandin-endoperoxide synthase 1 Homo sapiens 108-124 27998883-0 2017 Unlocking Aspirin"s Chemopreventive Activity: Role of Irreversibly Inhibiting Platelet Cyclooxygenase-1. Aspirin 10-17 prostaglandin-endoperoxide synthase 1 Homo sapiens 87-103 27633788-0 2016 Aspirin inhibits the production of proangiogenic 15(S)-HETE by platelet cyclooxygenase-1. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 72-88 27633788-3 2016 Because the effective doses of aspirin are consistent with the inhibition of cyclooxygenase-1 in platelets, we used liquid chromatography with tandem mass spectrometry analyses and immunoassays of human platelet releasates coupled with angiogenesis assays to search for the mediators of these effects. Aspirin 31-38 prostaglandin-endoperoxide synthase 1 Homo sapiens 77-93 27633788-9 2016 A., Warner, T. D. Aspirin inhibits the production of proangiogenic 15(S)-HETE by platelet cyclooxygenase-1. Aspirin 18-25 prostaglandin-endoperoxide synthase 1 Homo sapiens 90-106 28286156-1 2017 BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) comprises the triad of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and intolerance to inhibitors of the cyclooxygenase-1 (COX-1) enzyme. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 178-194 28286156-1 2017 BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) comprises the triad of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and intolerance to inhibitors of the cyclooxygenase-1 (COX-1) enzyme. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 196-201 27765537-4 2016 Some non-steroidal anti-inflammatory drugs interact with aspirin pharmacodynamics by competing on the drug target, i.e. the platelet"s cyclooxygenase-1 protein. Aspirin 57-64 prostaglandin-endoperoxide synthase 1 Homo sapiens 135-151 27712764-1 2016 Aspirin-exacerbated respiratory disease (AERD) is characterized by chronic rhinosinusitis with nasal polyps, asthma, and reactions to cyclooxygenase-1-inhibiting drugs. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 134-150 27393925-3 2016 Aspirin (ASA) as a platelet-inhibiting agent through inactivation of Cyclooxygenase-1 (COX-1) is mostly used for the prevention and treatment of atherothrombotic disorders. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 69-85 27440714-11 2016 In conclusion, a variable delay in the 37 C incubation of blood samples may affect the assessment of platelet cyclooxygenase-1 inhibition by aspirin and confound the characterization of the determinants of aspirin responsiveness. Aspirin 142-149 prostaglandin-endoperoxide synthase 1 Homo sapiens 111-127 27393925-3 2016 Aspirin (ASA) as a platelet-inhibiting agent through inactivation of Cyclooxygenase-1 (COX-1) is mostly used for the prevention and treatment of atherothrombotic disorders. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 87-92 27393925-3 2016 Aspirin (ASA) as a platelet-inhibiting agent through inactivation of Cyclooxygenase-1 (COX-1) is mostly used for the prevention and treatment of atherothrombotic disorders. Aspirin 9-12 prostaglandin-endoperoxide synthase 1 Homo sapiens 69-85 27393925-3 2016 Aspirin (ASA) as a platelet-inhibiting agent through inactivation of Cyclooxygenase-1 (COX-1) is mostly used for the prevention and treatment of atherothrombotic disorders. Aspirin 9-12 prostaglandin-endoperoxide synthase 1 Homo sapiens 87-92 27393925-4 2016 ASA inhibits the COX-1 enzyme and therefore blocks platelet thromboxane A2 (TXA2) synthesis. Aspirin 0-3 prostaglandin-endoperoxide synthase 1 Homo sapiens 17-22 27103451-8 2016 Aspirin therapy significantly inhibited platelets since cyclooxygenase 1 derived thromboxane generation levels were reduced by 99%. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 56-72 27126722-1 2016 Aspirin-exacerbated respiratory disease (AERD) is an adult-onset upper and lower airway disease consisting of eosinophilic nasal polyps, asthma, and respiratory reactions to cyclooxygenase 1 (COX-1) inhibitors. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 174-190 27126722-1 2016 Aspirin-exacerbated respiratory disease (AERD) is an adult-onset upper and lower airway disease consisting of eosinophilic nasal polyps, asthma, and respiratory reactions to cyclooxygenase 1 (COX-1) inhibitors. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 192-197 27083140-6 2016 The prior glycation/carbonylation of PGHS-1 with Glu, 1,6-BPF or MGO decreased the extent of acetylation from 6.4 +- 1.1 down to 2.5 +- 0.2, 3.6 +- 0.3 and 5.2 +- 0.2 mol/mol protein, respectively, but the enzyme still remained susceptible to the subsequent inhibition of its activity with ASA. Aspirin 290-293 prostaglandin-endoperoxide synthase 1 Homo sapiens 37-43 27534531-1 2016 Aspirin hypersensitivity is a hallmark of aspirin-exacerbated respiratory disease (AERD), a clinical syndrome characterized by the severe inflammation of the respiratory tract after ingestion of cyclooxygenase-1 inhibitors. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 195-211 27083140-1 2016 Due to its ability to inhibit the blood platelet PGHS-1, acetylsalicylic acid (ASA, Aspirin( )) is widely used as a preventive agent in atherothrombotic diseases. Aspirin 57-77 prostaglandin-endoperoxide synthase 1 Homo sapiens 49-55 27083140-1 2016 Due to its ability to inhibit the blood platelet PGHS-1, acetylsalicylic acid (ASA, Aspirin( )) is widely used as a preventive agent in atherothrombotic diseases. Aspirin 79-82 prostaglandin-endoperoxide synthase 1 Homo sapiens 49-55 27083140-1 2016 Due to its ability to inhibit the blood platelet PGHS-1, acetylsalicylic acid (ASA, Aspirin( )) is widely used as a preventive agent in atherothrombotic diseases. Aspirin 84-91 prostaglandin-endoperoxide synthase 1 Homo sapiens 49-55 27083140-5 2016 When PGHS-1 was incubated with glycating/acetylating agents (glucose, Glu; 1,6-bisphosphofructose, 1,6-BPF; methylglyoxal, MGO, acetylsalicylic acid, ASA), the enzyme was modified in 13.4 +- 1.6, 5.3 +- 0.5, 10.7 +- 1.2 and 6.4 +- 1.1 mol/mol protein, respectively, and its activity was significantly reduced. Aspirin 128-148 prostaglandin-endoperoxide synthase 1 Homo sapiens 5-11 27083140-5 2016 When PGHS-1 was incubated with glycating/acetylating agents (glucose, Glu; 1,6-bisphosphofructose, 1,6-BPF; methylglyoxal, MGO, acetylsalicylic acid, ASA), the enzyme was modified in 13.4 +- 1.6, 5.3 +- 0.5, 10.7 +- 1.2 and 6.4 +- 1.1 mol/mol protein, respectively, and its activity was significantly reduced. Aspirin 150-153 prostaglandin-endoperoxide synthase 1 Homo sapiens 5-11 27129261-4 2016 The lipid is generated in nanogram amounts by platelets from endogenous arachidonate during physiological activation, with inhibition by aspirin in vitro or in vivo, implicating cyclooxygenase-1 (COX). Aspirin 137-144 prostaglandin-endoperoxide synthase 1 Homo sapiens 178-194 27534531-1 2016 Aspirin hypersensitivity is a hallmark of aspirin-exacerbated respiratory disease (AERD), a clinical syndrome characterized by the severe inflammation of the respiratory tract after ingestion of cyclooxygenase-1 inhibitors. Aspirin 42-49 prostaglandin-endoperoxide synthase 1 Homo sapiens 195-211 26559689-1 2015 Dual antiplatelet therapy with aspirin, a platelet cyclooxygenase-1 inhibitor and P2Y12 receptor blockers, remains the major drug strategy to prevent ischemic event occurrence in patients with acute coronary syndromes and in patients undergoing coronary stenting, but there some limitations that can be overcome by targeting novel targets. Aspirin 31-38 prostaglandin-endoperoxide synthase 1 Homo sapiens 51-67 26209241-2 2015 In aspirin exacerbated respiratory disease (AERD), asthmatic symptoms are precipitated by ingestion of non-steroid anti-inflammatory drugs capable for pharmacologic inhibition of cyclooxygenase-1 isoenzyme. Aspirin 3-10 prostaglandin-endoperoxide synthase 1 Homo sapiens 179-195 26475800-3 2015 Low-dose aspirin produces a selective, complete and irreversible cyclooxygenase-1 blockade, and higher doses do not increase the antiplatelet effect. Aspirin 9-16 prostaglandin-endoperoxide synthase 1 Homo sapiens 65-81 25789542-10 2015 In conclusion, aspirin medication prior to dipyrone intake preserves antiplatelet effects, circumventing the pharmacodynamic drug-drug interaction at the level of cyclooxygenase-1. Aspirin 15-22 prostaglandin-endoperoxide synthase 1 Homo sapiens 163-179 26369686-3 2015 Individuals with two single nucleotide polymorphisms (SNPs) of cyclooxygenase-1 (COX-1), A-842G and C50T, exhibit increased sensitivity to aspirin and lower prostaglandin synthesis capacity but the polymorphism lacked statistical significance in relation to an association with bleeding peptic ulcer. Aspirin 139-146 prostaglandin-endoperoxide synthase 1 Homo sapiens 63-79 25700561-2 2015 While aspirin, a cyclo-oxygenase-1 inhibitor has been the cornerstone of antithrombotic treatment for several decades, P2Y12 receptor inhibitors cangrelor, clopidogrel, prasugrel, and ticagrelor and protease-activated receptor-1 antagonist vorapaxar, have emerged as additional therapies to reduce the risk of recurrent cardiovascular events in high-risk patients. Aspirin 6-13 prostaglandin-endoperoxide synthase 1 Homo sapiens 17-34 25869498-4 2015 The mechanism of aspirin antiplatelet effect is due to the inhibition of cyclooxygenase-1 enzyme in platelets. Aspirin 17-24 prostaglandin-endoperoxide synthase 1 Homo sapiens 73-89 25590318-1 2015 Aspirin exacerbated respiratory disease (AERD) is characterized as adult onset asthma, nasal polyps, chronic rhinosinusitis, and hypersensitivity to a cyclooxygenase-1 (COX-1) inhibitor, viz aspirin or nonsteroidal antiinflammatory drugs (NSAIDs). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 151-167 25590318-1 2015 Aspirin exacerbated respiratory disease (AERD) is characterized as adult onset asthma, nasal polyps, chronic rhinosinusitis, and hypersensitivity to a cyclooxygenase-1 (COX-1) inhibitor, viz aspirin or nonsteroidal antiinflammatory drugs (NSAIDs). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 169-174 25590318-1 2015 Aspirin exacerbated respiratory disease (AERD) is characterized as adult onset asthma, nasal polyps, chronic rhinosinusitis, and hypersensitivity to a cyclooxygenase-1 (COX-1) inhibitor, viz aspirin or nonsteroidal antiinflammatory drugs (NSAIDs). Aspirin 191-198 prostaglandin-endoperoxide synthase 1 Homo sapiens 151-167 25590318-1 2015 Aspirin exacerbated respiratory disease (AERD) is characterized as adult onset asthma, nasal polyps, chronic rhinosinusitis, and hypersensitivity to a cyclooxygenase-1 (COX-1) inhibitor, viz aspirin or nonsteroidal antiinflammatory drugs (NSAIDs). Aspirin 191-198 prostaglandin-endoperoxide synthase 1 Homo sapiens 169-174 25091345-6 2015 As expected, after 4 weeks of treatment, ASA induced a significant reduction of plasma thromboxane-A2, as a consequence of cyclooxygenase-1 inhibition. Aspirin 41-44 prostaglandin-endoperoxide synthase 1 Homo sapiens 123-139 25638730-0 2015 Aspirin inhibits expression of sFLT1 from human cytotrophoblasts induced by hypoxia, via cyclo-oxygenase 1. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 89-106 25633316-2 2015 Blockade of the ADP receptor, P2Y12, in combination with cyclooxygenase-1 inhibition by aspirin has been among the most widely used pharmacological strategies to reduce cardiovascular event occurrence in high-risk patients. Aspirin 88-95 prostaglandin-endoperoxide synthase 1 Homo sapiens 57-73 25663486-1 2015 Aspirin-exacerbated respiratory disease (AERD) is a clinical condition which results in adverse upper and lower respiratory symptoms, particularly rhinitis, conjunctivitis, bronchospasm, and/or laryngospasm, following exposure to cyclooxygenase-1 (COX-1) inhibiting drugs, namely aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 230-246 25663486-1 2015 Aspirin-exacerbated respiratory disease (AERD) is a clinical condition which results in adverse upper and lower respiratory symptoms, particularly rhinitis, conjunctivitis, bronchospasm, and/or laryngospasm, following exposure to cyclooxygenase-1 (COX-1) inhibiting drugs, namely aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 248-253 25663486-1 2015 Aspirin-exacerbated respiratory disease (AERD) is a clinical condition which results in adverse upper and lower respiratory symptoms, particularly rhinitis, conjunctivitis, bronchospasm, and/or laryngospasm, following exposure to cyclooxygenase-1 (COX-1) inhibiting drugs, namely aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin 280-287 prostaglandin-endoperoxide synthase 1 Homo sapiens 230-246 25267459-0 2015 Serum ubiquitin via CXC chemokine receptor 4 triggered cyclooxygenase-1 ubiquitination possibly involved in the pathogenesis of aspirin resistance. Aspirin 128-135 prostaglandin-endoperoxide synthase 1 Homo sapiens 55-71 25267459-9 2015 Platelets had higher levels of ubiquitinated COX-1 showing poor response to aspirin. Aspirin 76-83 prostaglandin-endoperoxide synthase 1 Homo sapiens 45-50 26369686-3 2015 Individuals with two single nucleotide polymorphisms (SNPs) of cyclooxygenase-1 (COX-1), A-842G and C50T, exhibit increased sensitivity to aspirin and lower prostaglandin synthesis capacity but the polymorphism lacked statistical significance in relation to an association with bleeding peptic ulcer. Aspirin 139-146 prostaglandin-endoperoxide synthase 1 Homo sapiens 81-86 25734355-2 2015 Both tests are specific for aspirin action on cyclooxygenase-1. Aspirin 28-35 prostaglandin-endoperoxide synthase 1 Homo sapiens 46-62 26517138-0 2015 The Implication of the Polymorphisms of COX-1, UGT1A6, and CYP2C9 among Cardiovascular Disease (CVD) Patients Treated with Aspirin. Aspirin 123-130 prostaglandin-endoperoxide synthase 1 Homo sapiens 40-45 26517138-1 2015 PURPOSE: Enzymes potentially responsible for the pharmacokinetic variations of aspirin include cyclooxygenase-1 (COX-1), UDP-glucuronosyltransferase (UGT1A6) and P450 (CYP) (CYP2C9). Aspirin 81-88 prostaglandin-endoperoxide synthase 1 Homo sapiens 97-113 26517138-1 2015 PURPOSE: Enzymes potentially responsible for the pharmacokinetic variations of aspirin include cyclooxygenase-1 (COX-1), UDP-glucuronosyltransferase (UGT1A6) and P450 (CYP) (CYP2C9). Aspirin 81-88 prostaglandin-endoperoxide synthase 1 Homo sapiens 115-120 24022862-2 2014 However, in some individuals TXA2 suppression by aspirin is impaired, indicating suboptimal inhibition of platelet cyclooxygenase 1 (COX-1) by aspirin. Aspirin 143-150 prostaglandin-endoperoxide synthase 1 Homo sapiens 133-138 25385584-2 2014 We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function. Aspirin 150-157 prostaglandin-endoperoxide synthase 1 Homo sapiens 258-274 25385584-2 2014 We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function. Aspirin 150-157 prostaglandin-endoperoxide synthase 1 Homo sapiens 276-281 25385584-2 2014 We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function. Aspirin 204-211 prostaglandin-endoperoxide synthase 1 Homo sapiens 258-274 25385584-2 2014 We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function. Aspirin 204-211 prostaglandin-endoperoxide synthase 1 Homo sapiens 276-281 25385584-2 2014 We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function. Aspirin 204-211 prostaglandin-endoperoxide synthase 1 Homo sapiens 258-274 25385584-2 2014 We sought to quantitate precisely the propensity of commonly consumed NSAIDs:ibuprofen, naproxen, and celecoxib:to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function. Aspirin 204-211 prostaglandin-endoperoxide synthase 1 Homo sapiens 276-281 24930730-0 2014 Impacts of COX-1 gene polymorphisms on vascular outcomes in patients with ischemic stroke and treated with aspirin. Aspirin 107-114 prostaglandin-endoperoxide synthase 1 Homo sapiens 11-16 24930730-1 2014 As the key point of function for aspirin to educe anti-platelet effects, cyclooxygenase-1 (COX-1) gene polymorphisms have long been suspected as a potential cause for aspirin nonresponsiveness. Aspirin 33-40 prostaglandin-endoperoxide synthase 1 Homo sapiens 73-89 24930730-1 2014 As the key point of function for aspirin to educe anti-platelet effects, cyclooxygenase-1 (COX-1) gene polymorphisms have long been suspected as a potential cause for aspirin nonresponsiveness. Aspirin 33-40 prostaglandin-endoperoxide synthase 1 Homo sapiens 91-96 24930730-1 2014 As the key point of function for aspirin to educe anti-platelet effects, cyclooxygenase-1 (COX-1) gene polymorphisms have long been suspected as a potential cause for aspirin nonresponsiveness. Aspirin 167-174 prostaglandin-endoperoxide synthase 1 Homo sapiens 73-89 24930730-1 2014 As the key point of function for aspirin to educe anti-platelet effects, cyclooxygenase-1 (COX-1) gene polymorphisms have long been suspected as a potential cause for aspirin nonresponsiveness. Aspirin 167-174 prostaglandin-endoperoxide synthase 1 Homo sapiens 91-96 24930730-3 2014 This study prospectively evaluated the impacts of COX-1 gene polymorphisms on stroke recurrence and other vascular events in a large cohort of Chinese patients with ischemic stroke and treated with aspirin. Aspirin 198-205 prostaglandin-endoperoxide synthase 1 Homo sapiens 50-55 24890720-1 2014 Reactions to aspirin and nonsteroidal anti-inflammatory drugs in patients with aspirin-exacerbated respiratory disease (AERD) are triggered when constraints upon activated eosinophils, normally supplied by PGE2, are removed secondary to cyclooxygenase-1 inhibition. Aspirin 13-20 prostaglandin-endoperoxide synthase 1 Homo sapiens 237-253 24890720-1 2014 Reactions to aspirin and nonsteroidal anti-inflammatory drugs in patients with aspirin-exacerbated respiratory disease (AERD) are triggered when constraints upon activated eosinophils, normally supplied by PGE2, are removed secondary to cyclooxygenase-1 inhibition. Aspirin 79-86 prostaglandin-endoperoxide synthase 1 Homo sapiens 237-253 25624859-0 2014 Effect of common single nucleotide polymorphisms in COX-1 gene on related metabolic activity in diabetic patients treated with acetylsalicylic acid. Aspirin 127-147 prostaglandin-endoperoxide synthase 1 Homo sapiens 52-57 25624859-1 2014 INTRODUCTION: The objective of this study was to investigate the effect of common single nucleotide genomic polymorphisms in the cyclooxygenase-1 (COX-1) gene on the thromboxane A2 (TxA2) metabolite concentrations in serum and urine, as well as on prostaglandin F2alpha (PGF2alpha) urinary excretion in the diabetic population on acetylsalicylic acid (ASA) therapy. Aspirin 330-350 prostaglandin-endoperoxide synthase 1 Homo sapiens 129-145 25624859-1 2014 INTRODUCTION: The objective of this study was to investigate the effect of common single nucleotide genomic polymorphisms in the cyclooxygenase-1 (COX-1) gene on the thromboxane A2 (TxA2) metabolite concentrations in serum and urine, as well as on prostaglandin F2alpha (PGF2alpha) urinary excretion in the diabetic population on acetylsalicylic acid (ASA) therapy. Aspirin 330-350 prostaglandin-endoperoxide synthase 1 Homo sapiens 147-152 25624859-1 2014 INTRODUCTION: The objective of this study was to investigate the effect of common single nucleotide genomic polymorphisms in the cyclooxygenase-1 (COX-1) gene on the thromboxane A2 (TxA2) metabolite concentrations in serum and urine, as well as on prostaglandin F2alpha (PGF2alpha) urinary excretion in the diabetic population on acetylsalicylic acid (ASA) therapy. Aspirin 352-355 prostaglandin-endoperoxide synthase 1 Homo sapiens 129-145 25624859-1 2014 INTRODUCTION: The objective of this study was to investigate the effect of common single nucleotide genomic polymorphisms in the cyclooxygenase-1 (COX-1) gene on the thromboxane A2 (TxA2) metabolite concentrations in serum and urine, as well as on prostaglandin F2alpha (PGF2alpha) urinary excretion in the diabetic population on acetylsalicylic acid (ASA) therapy. Aspirin 352-355 prostaglandin-endoperoxide synthase 1 Homo sapiens 147-152 25385584-3 2014 Although ibuprofen, naproxen, and celecoxib all had the potential to compete with the access of aspirin to the substrate binding channel of COX-1 in vitro, exposure of volunteers to a single therapeutic dose of each NSAID followed by 325 mg aspirin revealed a potent drug-drug interaction between ibuprofen and aspirin and between naproxen and aspirin but not between celecoxib and aspirin. Aspirin 96-103 prostaglandin-endoperoxide synthase 1 Homo sapiens 140-145 25385584-4 2014 The imprecision of estimates of aspirin consumption and the differential impact on the ability of aspirin to inactivate platelet COX-1 will confound head-to-head comparisons of distinct NSAIDs in ongoing clinical studies designed to measure their cardiovascular risk. Aspirin 98-105 prostaglandin-endoperoxide synthase 1 Homo sapiens 129-134 23677911-0 2014 Aspirin Half Maximal Inhibitory Concentration Value on Platelet Cyclooxygenase1 in Severe Type-2 Diabetes Mellitus is not Significantly Different from that of Healthy Individuals. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 64-79 24207016-1 2014 BACKGROUND: Aspirin, a commonly used antiplatelet agent, blocks platelet thromboxane A2 (TXA2) formation from arachidonic acid (AA) by acetylating platelet cyclooxygenase-1 (COX-1). Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 156-172 24207016-1 2014 BACKGROUND: Aspirin, a commonly used antiplatelet agent, blocks platelet thromboxane A2 (TXA2) formation from arachidonic acid (AA) by acetylating platelet cyclooxygenase-1 (COX-1). Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 174-179 24207016-3 2014 We have reported three methods that assess platelet COX-1 acetylation (inactivation) by aspirin and its direct consequences. Aspirin 88-95 prostaglandin-endoperoxide synthase 1 Homo sapiens 52-57 24207016-8 2014 On day 7 following aspirin treatment COX-1 in the platelets was fully acetylated whereas only non-acetylated COX-1 was present in the day 0 platelets. Aspirin 19-26 prostaglandin-endoperoxide synthase 1 Homo sapiens 37-42 24207016-13 2014 CONCLUSIONS: Only assays that clearly distinguish between acetylated and non-acetylated platelet COX-1 are useful for establishing the antiplatelet effect of aspirin. Aspirin 158-165 prostaglandin-endoperoxide synthase 1 Homo sapiens 97-102 24315499-0 2014 Appropriate assessment of the functional consequences of platelet cyclooxygenase-1 inhibition by aspirin in vivo. Aspirin 97-104 prostaglandin-endoperoxide synthase 1 Homo sapiens 66-82 24748925-1 2014 Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 45-61 24748925-1 2014 Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 63-68 24748925-1 2014 Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation. Aspirin 9-12 prostaglandin-endoperoxide synthase 1 Homo sapiens 45-61 24748925-1 2014 Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation. Aspirin 9-12 prostaglandin-endoperoxide synthase 1 Homo sapiens 63-68 23384979-0 2013 Mechanism of the irreversible inhibition of human cyclooxygenase-1 by aspirin as predicted by QM/MM calculations. Aspirin 70-77 prostaglandin-endoperoxide synthase 1 Homo sapiens 50-66 24535852-1 2014 Variation in the gene encoding cyclooxygenase-1 (COX-1) is involved in the process of aspirin resistance. Aspirin 86-93 prostaglandin-endoperoxide synthase 1 Homo sapiens 31-47 24535852-1 2014 Variation in the gene encoding cyclooxygenase-1 (COX-1) is involved in the process of aspirin resistance. Aspirin 86-93 prostaglandin-endoperoxide synthase 1 Homo sapiens 49-54 24432004-4 2014 Aspirin, a cyclooxygenase-1 inhibitor, decreases atherothrombotic associated mortality by 25%. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 11-27 24255997-9 2013 Some NSAIDs (such as ibuprofen) can interfere with the cardioprotective effects of aspirin by competitively binding to COX-1 enzyme, resulting in increased TXA2 production Naproxen may differ from other NSAIDs in sustaining functionally important degrees of inhibition of platelet cyclooxygenase-1 activity throughout the dosing interval. Aspirin 83-90 prostaglandin-endoperoxide synthase 1 Homo sapiens 281-297 23883581-0 2013 Human platelets generate phospholipid-esterified prostaglandins via cyclooxygenase-1 that are inhibited by low dose aspirin supplementation. Aspirin 116-123 prostaglandin-endoperoxide synthase 1 Homo sapiens 68-84 22609818-0 2013 Genetic polymorphisms of HO-1 and COX-1 are associated with aspirin resistance defined by light transmittance aggregation in Chinese Han patients. Aspirin 60-67 prostaglandin-endoperoxide synthase 1 Homo sapiens 34-39 22609818-1 2013 BACKGROUND: Cyclooxygenase 1 (COX-1), COX-2, and HO-1 are involved in the process of aspirin"s effect. Aspirin 85-92 prostaglandin-endoperoxide synthase 1 Homo sapiens 12-28 22609818-1 2013 BACKGROUND: Cyclooxygenase 1 (COX-1), COX-2, and HO-1 are involved in the process of aspirin"s effect. Aspirin 85-92 prostaglandin-endoperoxide synthase 1 Homo sapiens 30-35 23830213-0 2013 TXA2 synthesis and COX1-independent platelet reactivity in aspirin-treated patients soon after acute cerebral stroke or transient ischaemic attack. Aspirin 59-66 prostaglandin-endoperoxide synthase 1 Homo sapiens 19-23 23830213-1 2013 INTRODUCTION: The pharmacological target of aspirin is the inhibition of cyclooxygenase-1 (COX1) and thromboxane-A2 (TX) synthesis. Aspirin 44-51 prostaglandin-endoperoxide synthase 1 Homo sapiens 73-89 23830213-1 2013 INTRODUCTION: The pharmacological target of aspirin is the inhibition of cyclooxygenase-1 (COX1) and thromboxane-A2 (TX) synthesis. Aspirin 44-51 prostaglandin-endoperoxide synthase 1 Homo sapiens 91-95 23830213-10 2013 Among patients with fully blocked TX, those with elevated COX1-independent platelet reactivity (mean+2SD of aspirin-treated HS) were most likely to suffer severe stroke (P<0.05). Aspirin 108-115 prostaglandin-endoperoxide synthase 1 Homo sapiens 58-62 23639710-1 2013 Aspirin-exacerbated respiratory disease is a clinical syndrome characterized by severe, persistent asthma, hyperplastic eosinophilic sinusitis with nasal polyps, and reactions to aspirin and other nonsteroidal antiinflammatory drugs that preferentially inhibit cyclooxygenase 1. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 261-277 23639710-1 2013 Aspirin-exacerbated respiratory disease is a clinical syndrome characterized by severe, persistent asthma, hyperplastic eosinophilic sinusitis with nasal polyps, and reactions to aspirin and other nonsteroidal antiinflammatory drugs that preferentially inhibit cyclooxygenase 1. Aspirin 179-186 prostaglandin-endoperoxide synthase 1 Homo sapiens 261-277 23441755-1 2013 BACKGROUND AND OBJECTIVE: Anomalies in the regulation of cyclooxygenase (COX)-1 and -2 have been described in nasal polyps of aspirin-induced asthma (AIA). Aspirin 126-133 prostaglandin-endoperoxide synthase 1 Homo sapiens 57-86 23993980-1 2014 Aspirin is integral to the secondary prevention of cardiovascular disease and acts to impair the development of platelet-mediated atherothromboembolic events by irreversible inhibition of platelet cyclooxygenase-1 (COX-1). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 197-213 23993980-1 2014 Aspirin is integral to the secondary prevention of cardiovascular disease and acts to impair the development of platelet-mediated atherothromboembolic events by irreversible inhibition of platelet cyclooxygenase-1 (COX-1). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 215-220 24075938-1 2013 Nonsteroidal anti-inflammatory drugs (NSAIDs) may interfere with the anti-platelet activity of aspirin at the level of the platelet cyclooxygenase-1 (COX-1) enzyme. Aspirin 95-102 prostaglandin-endoperoxide synthase 1 Homo sapiens 132-148 24075938-1 2013 Nonsteroidal anti-inflammatory drugs (NSAIDs) may interfere with the anti-platelet activity of aspirin at the level of the platelet cyclooxygenase-1 (COX-1) enzyme. Aspirin 95-102 prostaglandin-endoperoxide synthase 1 Homo sapiens 150-155 24075938-5 2013 Docking studies suggested that NSAIDs forming hydrogen bonds with Ser530, Arg120, Tyr385 and other amino acids of the COX-1 hydrophobic channel interfere with antiplatelet activity of aspirin while non interfering NSAIDs do not form relevant hydrogen bond interactions within the aspirin binding site. Aspirin 184-191 prostaglandin-endoperoxide synthase 1 Homo sapiens 118-123 24075938-5 2013 Docking studies suggested that NSAIDs forming hydrogen bonds with Ser530, Arg120, Tyr385 and other amino acids of the COX-1 hydrophobic channel interfere with antiplatelet activity of aspirin while non interfering NSAIDs do not form relevant hydrogen bond interactions within the aspirin binding site. Aspirin 280-287 prostaglandin-endoperoxide synthase 1 Homo sapiens 118-123 24075938-6 2013 In conclusion, docking analysis of NSAID interactions at the COX-1 active site appears useful to predict their interference with the anti-platelet activity of aspirin. Aspirin 159-166 prostaglandin-endoperoxide synthase 1 Homo sapiens 61-66 23422285-0 2013 New direct and indirect methods for the detection of cyclooxygenase 1 acetylation by aspirin; the lack of aspirin resistance among healthy individuals. Aspirin 85-92 prostaglandin-endoperoxide synthase 1 Homo sapiens 53-69 23422285-4 2013 METHODS: Two new methods were developed for the direct and indirect detection of COX-1 acetylation by aspirin in 108 healthy volunteers treated daily with 100mg enteric-coated aspirin for 7days. Aspirin 102-109 prostaglandin-endoperoxide synthase 1 Homo sapiens 81-86 23422285-4 2013 METHODS: Two new methods were developed for the direct and indirect detection of COX-1 acetylation by aspirin in 108 healthy volunteers treated daily with 100mg enteric-coated aspirin for 7days. Aspirin 176-183 prostaglandin-endoperoxide synthase 1 Homo sapiens 81-86 23422285-14 2013 The new methods could be used for detecting the acetylation of COX-1 by aspirin in patients on preventive aspirin therapy and for evaluating methods routinely used for such purpose. Aspirin 72-79 prostaglandin-endoperoxide synthase 1 Homo sapiens 63-68 23422285-14 2013 The new methods could be used for detecting the acetylation of COX-1 by aspirin in patients on preventive aspirin therapy and for evaluating methods routinely used for such purpose. Aspirin 106-113 prostaglandin-endoperoxide synthase 1 Homo sapiens 63-68 23384979-2 2013 Aspirin acts as an acetylating agent in which its acetyl group is covalently attached to a serine residue (S530) in the active site of the cyclooxygenase-1 enzyme. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 139-155 23384979-4 2013 In this study the putative structure of human cyclooxygenase-1 was constructed from ovine cyclooxygenase-1 by homology modeling, and the acetylsalicylic acid was docked into the arachidonic acid binding cavity of the enzyme. Aspirin 137-157 prostaglandin-endoperoxide synthase 1 Homo sapiens 46-62 23985963-1 2013 BACKGROUND: Aspirin"s therapeutic action is via inhibition of platelet cyclooxygenase 1 (COX-1) thromboxane A2 (TxA2) production. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 71-87 22882748-2 2013 This interaction is ascribed to steric hindrance at the active site of cyclooxygenase-1 by ibuprofen, when aspirin is administered after ibuprofen. Aspirin 107-114 prostaglandin-endoperoxide synthase 1 Homo sapiens 71-87 23985963-1 2013 BACKGROUND: Aspirin"s therapeutic action is via inhibition of platelet cyclooxygenase 1 (COX-1) thromboxane A2 (TxA2) production. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 89-94 23038044-0 2013 Frequency, risk factors, prognosis, and genetic polymorphism of the cyclooxygenase-1 gene for aspirin resistance in elderly Chinese patients with cardiovascular disease. Aspirin 94-101 prostaglandin-endoperoxide synthase 1 Homo sapiens 68-84 23038044-3 2013 OBJECTIVE: The frequency, risk factors, prognosis, and genetic polymorphism of the cyclooxygenase-1 (COX-1) gene for aspirin resistance have not been reported in elderly patients with CVD. Aspirin 117-124 prostaglandin-endoperoxide synthase 1 Homo sapiens 83-99 23038044-3 2013 OBJECTIVE: The frequency, risk factors, prognosis, and genetic polymorphism of the cyclooxygenase-1 (COX-1) gene for aspirin resistance have not been reported in elderly patients with CVD. Aspirin 117-124 prostaglandin-endoperoxide synthase 1 Homo sapiens 101-106 23038044-10 2013 The variant G-allele of COX-1 rs1330344 (-1676 A/G) significantly increased the risk of aspirin resistance defined by LTAAA + TEGAA (OR = 1.82, 95% CI 1.13- 2.92, p = 0.01). Aspirin 88-95 prostaglandin-endoperoxide synthase 1 Homo sapiens 24-29 23038044-12 2013 The variant G-allele of COX-1 rs1330344 is significantly associated with aspirin resistance defined by LTAAA + TEGAA. Aspirin 73-80 prostaglandin-endoperoxide synthase 1 Homo sapiens 24-29 22795340-1 2012 INTRODUCTION: Aspirin inhibits the cyclooxygenase-1 (COX-1) mediated thromboxane A2 synthesis. Aspirin 14-21 prostaglandin-endoperoxide synthase 1 Homo sapiens 35-51 23094974-7 2012 Potential mechanisms of aspirin resistance in diabetes include elevated platelet turnover that results in an immature platelet fraction able to synthesise the uninhibited therapeutic target of aspirin, cyclooxygenase-1 (COX-1); residual thromboxane production by both COX-1-dependent and COX-1-independent pathways; up-regulation of aspirin-insensitive pathways of platelet function, such as adenosine diphosphate signalling; and increased underlying atherosclerotic disease burden that results in elevated underlying platelet hyper-reactivity. Aspirin 24-31 prostaglandin-endoperoxide synthase 1 Homo sapiens 202-218 23094974-7 2012 Potential mechanisms of aspirin resistance in diabetes include elevated platelet turnover that results in an immature platelet fraction able to synthesise the uninhibited therapeutic target of aspirin, cyclooxygenase-1 (COX-1); residual thromboxane production by both COX-1-dependent and COX-1-independent pathways; up-regulation of aspirin-insensitive pathways of platelet function, such as adenosine diphosphate signalling; and increased underlying atherosclerotic disease burden that results in elevated underlying platelet hyper-reactivity. Aspirin 24-31 prostaglandin-endoperoxide synthase 1 Homo sapiens 220-225 23094974-7 2012 Potential mechanisms of aspirin resistance in diabetes include elevated platelet turnover that results in an immature platelet fraction able to synthesise the uninhibited therapeutic target of aspirin, cyclooxygenase-1 (COX-1); residual thromboxane production by both COX-1-dependent and COX-1-independent pathways; up-regulation of aspirin-insensitive pathways of platelet function, such as adenosine diphosphate signalling; and increased underlying atherosclerotic disease burden that results in elevated underlying platelet hyper-reactivity. Aspirin 24-31 prostaglandin-endoperoxide synthase 1 Homo sapiens 268-273 23094974-7 2012 Potential mechanisms of aspirin resistance in diabetes include elevated platelet turnover that results in an immature platelet fraction able to synthesise the uninhibited therapeutic target of aspirin, cyclooxygenase-1 (COX-1); residual thromboxane production by both COX-1-dependent and COX-1-independent pathways; up-regulation of aspirin-insensitive pathways of platelet function, such as adenosine diphosphate signalling; and increased underlying atherosclerotic disease burden that results in elevated underlying platelet hyper-reactivity. Aspirin 24-31 prostaglandin-endoperoxide synthase 1 Homo sapiens 268-273 22521214-1 2012 INTRODUCTION: Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation. Aspirin 14-21 prostaglandin-endoperoxide synthase 1 Homo sapiens 59-75 22521214-1 2012 INTRODUCTION: Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation. Aspirin 14-21 prostaglandin-endoperoxide synthase 1 Homo sapiens 77-82 22521214-1 2012 INTRODUCTION: Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation. Aspirin 23-26 prostaglandin-endoperoxide synthase 1 Homo sapiens 59-75 22521214-1 2012 INTRODUCTION: Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation. Aspirin 23-26 prostaglandin-endoperoxide synthase 1 Homo sapiens 77-82 22795340-1 2012 INTRODUCTION: Aspirin inhibits the cyclooxygenase-1 (COX-1) mediated thromboxane A2 synthesis. Aspirin 14-21 prostaglandin-endoperoxide synthase 1 Homo sapiens 53-58 22471290-3 2012 OBJECTIVE: To characterize the kinetics and determinants of platelet cyclooxygenase-1 recovery in aspirin-treated diabetic and non-diabetic patients. Aspirin 98-105 prostaglandin-endoperoxide synthase 1 Homo sapiens 69-85 22724411-2 2012 Antiplatelet therapy for primary and secondary prevention of thromboembolic events is a cornerstone for the management of these patients and for many years the cyclooxygenase-1 (COX-1) inhibitor aspirin and the second generation thienopyridine clopidogrel which targets the ADP P2Y12 receptor on platelets served as the main antiplatelet agents for these indications. Aspirin 195-202 prostaglandin-endoperoxide synthase 1 Homo sapiens 160-176 22234683-8 2012 We conclude that the abnormal megakaryopoiesis characterizing ET accounts for a shorter-lasting antiplatelet effect of low-dose aspirin through faster renewal of platelet cyclooxygenase-1, and impaired platelet inhibition can be rescued by modulating the aspirin dosing interval rather than the dose. Aspirin 128-135 prostaglandin-endoperoxide synthase 1 Homo sapiens 171-187 22320344-0 2012 Inactivation of ovine cyclooxygenase-1 by bromoaspirin and aspirin: a quantum chemistry description. Aspirin 47-54 prostaglandin-endoperoxide synthase 1 Homo sapiens 22-38 22311905-0 2012 Suboptimal inhibition of platelet cyclooxygenase-1 by aspirin in metabolic syndrome. Aspirin 54-61 prostaglandin-endoperoxide synthase 1 Homo sapiens 34-50 22311905-1 2012 Interindividual variation in the ability of aspirin to inhibit platelet cyclooxygenase-1 (COX-1) could account for some on-treatment cardiovascular events. Aspirin 44-51 prostaglandin-endoperoxide synthase 1 Homo sapiens 72-88 22311905-1 2012 Interindividual variation in the ability of aspirin to inhibit platelet cyclooxygenase-1 (COX-1) could account for some on-treatment cardiovascular events. Aspirin 44-51 prostaglandin-endoperoxide synthase 1 Homo sapiens 90-95 22311905-3 2012 In a prospective, 2-week study, we evaluated the effect of aspirin (81 mg) on platelet COX-1 in 135 patients with stable coronary artery disease by measuring serum thromboxane B(2) (sTxB(2)) as an indicator of inhibition of platelet COX-1. Aspirin 59-66 prostaglandin-endoperoxide synthase 1 Homo sapiens 87-92 22311905-11 2012 In conclusion, metabolic syndrome, which places patients at high risk for thrombotic cardiovascular events, strongly and uniquely associates with less effective inhibition of platelet COX-1 by aspirin. Aspirin 193-200 prostaglandin-endoperoxide synthase 1 Homo sapiens 184-189 22513397-0 2012 Decreased cyclooxygenase inhibition by aspirin in polymorphic variants of human prostaglandin H synthase-1. Aspirin 39-46 prostaglandin-endoperoxide synthase 1 Homo sapiens 80-106 22513397-1 2012 OBJECTIVES: Aspirin (ASA), a major antiplatelet and cancer-preventing drug, irreversibly blocks the cyclooxygenase (COX) activity of prostaglandin H synthase-1 (PGHS-1). Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 133-159 22513397-1 2012 OBJECTIVES: Aspirin (ASA), a major antiplatelet and cancer-preventing drug, irreversibly blocks the cyclooxygenase (COX) activity of prostaglandin H synthase-1 (PGHS-1). Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 161-167 22513397-1 2012 OBJECTIVES: Aspirin (ASA), a major antiplatelet and cancer-preventing drug, irreversibly blocks the cyclooxygenase (COX) activity of prostaglandin H synthase-1 (PGHS-1). Aspirin 21-24 prostaglandin-endoperoxide synthase 1 Homo sapiens 133-159 22513397-1 2012 OBJECTIVES: Aspirin (ASA), a major antiplatelet and cancer-preventing drug, irreversibly blocks the cyclooxygenase (COX) activity of prostaglandin H synthase-1 (PGHS-1). Aspirin 21-24 prostaglandin-endoperoxide synthase 1 Homo sapiens 161-167 22513397-2 2012 Considerable differences in ASA effectiveness are observed between individuals, and some of this variability may be due to PGHS-1 protein variants. Aspirin 28-31 prostaglandin-endoperoxide synthase 1 Homo sapiens 123-129 22513397-3 2012 Our overall aim is to determine which, if any, of the known variants in the mature PGHS-1 protein lead to functional alterations in COX catalysis or inhibition by ASA. Aspirin 163-166 prostaglandin-endoperoxide synthase 1 Homo sapiens 83-89 22513397-9 2012 Computational modeling of the brief ASA pulses experienced by PGHS-1 in circulating platelets during daily ASA dosing predicted that the 60% lower ASA reactivity in R108Q yields a 15-fold increase in surviving COX activity; smaller, approximately two-fold increases in surviving COX activity were predicted for L237M and V481I. Aspirin 36-39 prostaglandin-endoperoxide synthase 1 Homo sapiens 62-68 22513397-9 2012 Computational modeling of the brief ASA pulses experienced by PGHS-1 in circulating platelets during daily ASA dosing predicted that the 60% lower ASA reactivity in R108Q yields a 15-fold increase in surviving COX activity; smaller, approximately two-fold increases in surviving COX activity were predicted for L237M and V481I. Aspirin 107-110 prostaglandin-endoperoxide synthase 1 Homo sapiens 62-68 22513397-9 2012 Computational modeling of the brief ASA pulses experienced by PGHS-1 in circulating platelets during daily ASA dosing predicted that the 60% lower ASA reactivity in R108Q yields a 15-fold increase in surviving COX activity; smaller, approximately two-fold increases in surviving COX activity were predicted for L237M and V481I. Aspirin 107-110 prostaglandin-endoperoxide synthase 1 Homo sapiens 62-68 22860421-1 2012 OBJECTIVE: To investigate whether cyclooxygenase-1 (COX-1) haplotype is associated, with aspirin resistance. Aspirin 89-96 prostaglandin-endoperoxide synthase 1 Homo sapiens 34-50 22860421-1 2012 OBJECTIVE: To investigate whether cyclooxygenase-1 (COX-1) haplotype is associated, with aspirin resistance. Aspirin 89-96 prostaglandin-endoperoxide synthase 1 Homo sapiens 52-57 22860421-7 2012 CONCLUSION: COX-1 haplotype is associated with aspirin resistance in old Chinese Han patients with cardio-cerebrovascular diseases, mutant CGCGCC-haplotype carriers of COX-1 has a significant significantly increased risk of AR. Aspirin 47-54 prostaglandin-endoperoxide synthase 1 Homo sapiens 12-17 22860421-7 2012 CONCLUSION: COX-1 haplotype is associated with aspirin resistance in old Chinese Han patients with cardio-cerebrovascular diseases, mutant CGCGCC-haplotype carriers of COX-1 has a significant significantly increased risk of AR. Aspirin 47-54 prostaglandin-endoperoxide synthase 1 Homo sapiens 168-173 22724411-2 2012 Antiplatelet therapy for primary and secondary prevention of thromboembolic events is a cornerstone for the management of these patients and for many years the cyclooxygenase-1 (COX-1) inhibitor aspirin and the second generation thienopyridine clopidogrel which targets the ADP P2Y12 receptor on platelets served as the main antiplatelet agents for these indications. Aspirin 195-202 prostaglandin-endoperoxide synthase 1 Homo sapiens 178-183 21505714-2 2011 Simultaneous inhibition of blood platelet cyclooxygenase-1 by aspirin and of the P2Y12 receptor by clopidogrel or prasugrel is currently recommended in this setting. Aspirin 62-69 prostaglandin-endoperoxide synthase 1 Homo sapiens 42-58 21728147-0 2011 Protocatechualdehyde synergizes with aspirin at the platelet cyclooxygenase-1 level. Aspirin 37-44 prostaglandin-endoperoxide synthase 1 Homo sapiens 61-77 21728147-6 2011 Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1. Aspirin 142-149 prostaglandin-endoperoxide synthase 1 Homo sapiens 37-53 21728147-6 2011 Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1. Aspirin 142-149 prostaglandin-endoperoxide synthase 1 Homo sapiens 55-60 21728147-6 2011 Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1. Aspirin 142-149 prostaglandin-endoperoxide synthase 1 Homo sapiens 202-207 21728147-6 2011 Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1. Aspirin 142-149 prostaglandin-endoperoxide synthase 1 Homo sapiens 202-207 21728147-6 2011 Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1. Aspirin 240-247 prostaglandin-endoperoxide synthase 1 Homo sapiens 37-53 21728147-6 2011 Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1. Aspirin 240-247 prostaglandin-endoperoxide synthase 1 Homo sapiens 55-60 21728147-6 2011 Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1. Aspirin 240-247 prostaglandin-endoperoxide synthase 1 Homo sapiens 202-207 21728147-6 2011 Pro formed a stable complex into the cyclooxygenase-1 (COX-1) channel by in silico docking and significantly promoted the platelet-associated aspirin clearance, suggesting that the Pro interaction with COX-1 was favorable to the binding of aspirin with COX-1. Aspirin 240-247 prostaglandin-endoperoxide synthase 1 Homo sapiens 202-207 21728147-7 2011 Taken together, our findings suggest that the capacity of Pro and potentially other structurally similar polyphenolic compounds on promoting the binding of aspirin on platelet COX-1 might be the main mechanism of their synergism with aspirin. Aspirin 156-163 prostaglandin-endoperoxide synthase 1 Homo sapiens 176-181 21728147-7 2011 Taken together, our findings suggest that the capacity of Pro and potentially other structurally similar polyphenolic compounds on promoting the binding of aspirin on platelet COX-1 might be the main mechanism of their synergism with aspirin. Aspirin 234-241 prostaglandin-endoperoxide synthase 1 Homo sapiens 176-181 21301784-0 2011 Residual cyclooxygenase-1 activity and epinephrine reduce the antiplatelet effect of aspirin in patients with acute myocardial infarction. Aspirin 85-92 prostaglandin-endoperoxide synthase 1 Homo sapiens 9-25 21434767-1 2011 In this study, we evaluate the relationships between aspirin nonresponsiveness and the cyclooxygenase-1 (Cox-1) gene C50T polymorphism in stable coronary artery disease (CAD) in Tunisian patients. Aspirin 53-60 prostaglandin-endoperoxide synthase 1 Homo sapiens 87-103 21434767-1 2011 In this study, we evaluate the relationships between aspirin nonresponsiveness and the cyclooxygenase-1 (Cox-1) gene C50T polymorphism in stable coronary artery disease (CAD) in Tunisian patients. Aspirin 53-60 prostaglandin-endoperoxide synthase 1 Homo sapiens 105-110 21372715-3 2011 This is further aggravated by inhibition of cyclooxygenase-1 by aspirin and other NSAIDs. Aspirin 64-71 prostaglandin-endoperoxide synthase 1 Homo sapiens 44-60 21219589-4 2011 ASA irreversibly inhibits cyclooxygenase-1 (COX-1) by acetylation. Aspirin 0-3 prostaglandin-endoperoxide synthase 1 Homo sapiens 26-42 21219589-4 2011 ASA irreversibly inhibits cyclooxygenase-1 (COX-1) by acetylation. Aspirin 0-3 prostaglandin-endoperoxide synthase 1 Homo sapiens 44-49 21360514-11 2011 CONCLUSION: Sequential administration of 220 mg naproxen twice a day and low-dose aspirin interferes with the irreversible inhibition of platelet cyclooxygenase 1 afforded by aspirin. Aspirin 82-89 prostaglandin-endoperoxide synthase 1 Homo sapiens 146-162 21360823-0 2011 Nitrooxyacyl derivatives of salicylic acid: aspirin-like molecules that covalently inactivate cyclooxygenase-1. Aspirin 44-51 prostaglandin-endoperoxide synthase 1 Homo sapiens 94-110 21360514-11 2011 CONCLUSION: Sequential administration of 220 mg naproxen twice a day and low-dose aspirin interferes with the irreversible inhibition of platelet cyclooxygenase 1 afforded by aspirin. Aspirin 175-182 prostaglandin-endoperoxide synthase 1 Homo sapiens 146-162 21163909-7 2011 Acetylsalicylic acid, an irreversible inhibitor of both hPHS-1 and hPHS-2, blocked cytotoxicity and DNA oxidation in both cell lines and untransfected CHO-K1 cells lacking PHS activity were similarly resistant. Aspirin 0-20 prostaglandin-endoperoxide synthase 1 Homo sapiens 56-62 21062358-5 2011 It is even more recently that aspirin"s unique antiplatelet action has been recognized, with long-lasting inhibition of platelet aggregation due to irreversible inactivation of the cyclooxygenase-1 mediated production of thromboxane. Aspirin 30-37 prostaglandin-endoperoxide synthase 1 Homo sapiens 181-197 21311822-6 2011 While serum TxB2 levels of < 2 ng/ml reflect aspirin-induced inhibition of cyclo-oxygenase-1 activity with high sensitivity, VASP exhibits a wide variability upon treatment with clopidogrel or prasugrel. Aspirin 48-55 prostaglandin-endoperoxide synthase 1 Homo sapiens 78-95 21078384-4 2011 Preincubation with catalase, which detoxifies reactive oxygen species, or acetylsalicylic acid, an inhibitor of hPHS-1 and -2, reduced the cytotoxicity caused by DA, L-DOPA, DOPAC, and HVA in hPHS-1 and -2 cells both with and without AA. Aspirin 74-94 prostaglandin-endoperoxide synthase 1 Homo sapiens 112-125 21078384-4 2011 Preincubation with catalase, which detoxifies reactive oxygen species, or acetylsalicylic acid, an inhibitor of hPHS-1 and -2, reduced the cytotoxicity caused by DA, L-DOPA, DOPAC, and HVA in hPHS-1 and -2 cells both with and without AA. Aspirin 74-94 prostaglandin-endoperoxide synthase 1 Homo sapiens 192-205 21591982-9 2011 Low-response to aspirin assessed by analyses targeting cyclooxygenase-1 activity (LTA, IA) was rare (<= 8.1%). Aspirin 16-23 prostaglandin-endoperoxide synthase 1 Homo sapiens 55-71 22160013-1 2011 Because of the central role of platelets in cardiovascular atherothrombosis, there is a well-established therapeutic role for antiplatelet therapy that includes aspirin (a cyclooxygenase 1 [COX1] inhibitor), clopidogrel (an antagonist of the ADP P2Y(12) receptor), and the GPIIb-GPIIIa (alphaIIbbeta3) antagonists. Aspirin 161-168 prostaglandin-endoperoxide synthase 1 Homo sapiens 172-188 21217919-1 2011 The clinical syndrome of aspirin-exacerbated respiratory disease (AERD) is a condition where inhibition of cyclooxygenase-1 (COX-1) induces attacks of upper and lower airway reactions, including rhinorrhea and varying degrees of bronchospasm and laryngospasm. Aspirin 25-32 prostaglandin-endoperoxide synthase 1 Homo sapiens 107-123 21217919-1 2011 The clinical syndrome of aspirin-exacerbated respiratory disease (AERD) is a condition where inhibition of cyclooxygenase-1 (COX-1) induces attacks of upper and lower airway reactions, including rhinorrhea and varying degrees of bronchospasm and laryngospasm. Aspirin 25-32 prostaglandin-endoperoxide synthase 1 Homo sapiens 125-130 20664853-3 2010 Although this new group of 1,1-diaryl-2-(4-hydroxyaminosulfonylphenyl)alk-1-enes exhibited weak inhibition of the constitutive cyclooxygenase-1 (COX-1) and inducible COX-2 isozymes, in vivo studies showed anti-inflammatory potencies that were generally intermediate between that of the reference drugs aspirin and ibuprofen. Aspirin 302-309 prostaglandin-endoperoxide synthase 1 Homo sapiens 127-143 21720139-1 2011 Aspirin irreversibly inhibits the enzyme cyclooxygenase-1 and depresses the production of thromboxane A(2), and also exerts antiplatelet effects. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 41-57 21039786-1 2010 It has been proposed that aspirin (ASA) and other non-steroidal anti-inflammatory drug (NSAID)-induced urticaria (UR)/angioedema (AE) are mediated through inhibition of cyclooxygenase-1 (COX-1) enzymes. Aspirin 26-33 prostaglandin-endoperoxide synthase 1 Homo sapiens 169-185 21039786-1 2010 It has been proposed that aspirin (ASA) and other non-steroidal anti-inflammatory drug (NSAID)-induced urticaria (UR)/angioedema (AE) are mediated through inhibition of cyclooxygenase-1 (COX-1) enzymes. Aspirin 26-33 prostaglandin-endoperoxide synthase 1 Homo sapiens 187-192 21039786-1 2010 It has been proposed that aspirin (ASA) and other non-steroidal anti-inflammatory drug (NSAID)-induced urticaria (UR)/angioedema (AE) are mediated through inhibition of cyclooxygenase-1 (COX-1) enzymes. Aspirin 35-38 prostaglandin-endoperoxide synthase 1 Homo sapiens 169-185 21039786-1 2010 It has been proposed that aspirin (ASA) and other non-steroidal anti-inflammatory drug (NSAID)-induced urticaria (UR)/angioedema (AE) are mediated through inhibition of cyclooxygenase-1 (COX-1) enzymes. Aspirin 35-38 prostaglandin-endoperoxide synthase 1 Homo sapiens 187-192 20705923-6 2010 METHODS AND RESULTS: Low concentrations of aspirin induce lysine acetylation of eNOS, stimulating eNOS enzymatic activity and endothelial NO production in a cyclooxygenase-1-independent fashion. Aspirin 43-50 prostaglandin-endoperoxide synthase 1 Homo sapiens 157-173 20705923-7 2010 Low-dose aspirin in vivo also increases bioavailable vascular NO in an eNOS-dependent and cyclooxygenase-1-independent manner. Aspirin 9-16 prostaglandin-endoperoxide synthase 1 Homo sapiens 90-106 20723029-0 2010 High on-aspirin platelet reactivity as measured with aggregation-based, cyclooxygenase-1 inhibition sensitive platelet function tests is associated with the occurrence of atherothrombotic events. Aspirin 8-15 prostaglandin-endoperoxide synthase 1 Homo sapiens 72-88 20664853-3 2010 Although this new group of 1,1-diaryl-2-(4-hydroxyaminosulfonylphenyl)alk-1-enes exhibited weak inhibition of the constitutive cyclooxygenase-1 (COX-1) and inducible COX-2 isozymes, in vivo studies showed anti-inflammatory potencies that were generally intermediate between that of the reference drugs aspirin and ibuprofen. Aspirin 302-309 prostaglandin-endoperoxide synthase 1 Homo sapiens 145-150 20352155-5 2010 Serum and urinary thromboxane metabolites were measured several times to evaluate cyclooxygenase-1 inhibition by aspirin. Aspirin 113-120 prostaglandin-endoperoxide synthase 1 Homo sapiens 82-98 20713906-0 2010 Letter by Violi et al regarding article, "Association of cyclooxygenase-1-dependent and -independent platelet function assays with adverse clinical outcomes in aspirin-treated patients presenting for cardiac catheterization". Aspirin 160-167 prostaglandin-endoperoxide synthase 1 Homo sapiens 57-73 20404564-0 2010 The effects of the histone deacetylase inhibitor romidepsin (FK228) are enhanced by aspirin (ASA) in COX-1 positive ovarian cancer cells through augmentation of p21. Aspirin 84-91 prostaglandin-endoperoxide synthase 1 Homo sapiens 101-106 20404564-0 2010 The effects of the histone deacetylase inhibitor romidepsin (FK228) are enhanced by aspirin (ASA) in COX-1 positive ovarian cancer cells through augmentation of p21. Aspirin 93-96 prostaglandin-endoperoxide synthase 1 Homo sapiens 101-106 20404564-6 2010 ASA is a relatively selective inhibitor of cyclooxygenase-1 (COX-1) and has anti-proliferative effects in ovarian cancer cells. Aspirin 0-3 prostaglandin-endoperoxide synthase 1 Homo sapiens 43-59 20404564-6 2010 ASA is a relatively selective inhibitor of cyclooxygenase-1 (COX-1) and has anti-proliferative effects in ovarian cancer cells. Aspirin 0-3 prostaglandin-endoperoxide synthase 1 Homo sapiens 61-66 20404564-8 2010 The growth inhibitory effects of FK228 were enhanced by ASA in COX-1 positive ovarian cancer cells. Aspirin 56-59 prostaglandin-endoperoxide synthase 1 Homo sapiens 63-68 20404564-11 2010 In the COX-1 positive cells, p21 expression was augmented by the addition of ASA to FK228 treatment. Aspirin 77-80 prostaglandin-endoperoxide synthase 1 Homo sapiens 7-12 20404564-12 2010 Furthermore, COX-1 siRNA attenuated the effects of combined ASA and FK228 on the levels of p21 expression and the amount of growth inhibition. Aspirin 60-63 prostaglandin-endoperoxide synthase 1 Homo sapiens 13-18 20404564-14 2010 However, a significant delay in p21 protein degradation in the presence of ASA and FK228 in COX-1 positive cells was associated with inhibition of proteasome activity. Aspirin 75-78 prostaglandin-endoperoxide synthase 1 Homo sapiens 92-97 20631417-4 2010 This theory, which is now generally accepted, states that asthma attacks precipitated by aspirin and other NSAIDs have no allergic background; instead, they occur due to the inhibition of cyclooxygenase-1 in sensitive patients. Aspirin 89-96 prostaglandin-endoperoxide synthase 1 Homo sapiens 188-204 27713316-2 2010 Aspirin and several small molecule NSAIDs are known to inhibit the enzymes cyclooxygenase-1 (COX-1) and -2 (COX-2). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 75-91 20586862-2 2010 Two single nucleotide polymorphisms (SNP) of cyclooxygenase-1 (COX-1), A-842G and C50T, exhibited increased sensitivity to aspirin and had lower prostaglandin synthesis capacity, lacking statistical significance in the association with bleeding peptic ulcer. Aspirin 123-130 prostaglandin-endoperoxide synthase 1 Homo sapiens 45-61 20586862-2 2010 Two single nucleotide polymorphisms (SNP) of cyclooxygenase-1 (COX-1), A-842G and C50T, exhibited increased sensitivity to aspirin and had lower prostaglandin synthesis capacity, lacking statistical significance in the association with bleeding peptic ulcer. Aspirin 123-130 prostaglandin-endoperoxide synthase 1 Homo sapiens 63-68 19996015-11 2009 This study suggests that multiple mechanisms, including but not confined to inadequate inhibition of COX-1, are responsible for poor clinical outcomes in aspirin-treated patients, and therefore the term aspirin resistance is inappropriate. Aspirin 154-161 prostaglandin-endoperoxide synthase 1 Homo sapiens 101-106 19932480-6 2010 Aspirin and SC-560, a cyclooxygenase-1 inhibitor, suppressed the ristocetin-induced sCD40L release from platelets in parallel with TXA(2) production. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 22-38 19887674-0 2010 The contribution of cyclooxygenase-1 and -2 to persistent thromboxane biosynthesis in aspirin-treated essential thrombocythemia: implications for antiplatelet therapy. Aspirin 86-93 prostaglandin-endoperoxide synthase 1 Homo sapiens 20-43 19996015-0 2009 Association of cyclooxygenase-1-dependent and -independent platelet function assays with adverse clinical outcomes in aspirin-treated patients presenting for cardiac catheterization. Aspirin 118-125 prostaglandin-endoperoxide synthase 1 Homo sapiens 15-31 19996015-1 2009 BACKGROUND: Poor clinical outcome in aspirin-treated patients has been termed aspirin resistance and may result from inadequate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin. Aspirin 37-44 prostaglandin-endoperoxide synthase 1 Homo sapiens 151-167 19996015-1 2009 BACKGROUND: Poor clinical outcome in aspirin-treated patients has been termed aspirin resistance and may result from inadequate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin. Aspirin 37-44 prostaglandin-endoperoxide synthase 1 Homo sapiens 169-174 19996015-1 2009 BACKGROUND: Poor clinical outcome in aspirin-treated patients has been termed aspirin resistance and may result from inadequate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin. Aspirin 78-85 prostaglandin-endoperoxide synthase 1 Homo sapiens 151-167 19996015-1 2009 BACKGROUND: Poor clinical outcome in aspirin-treated patients has been termed aspirin resistance and may result from inadequate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin. Aspirin 78-85 prostaglandin-endoperoxide synthase 1 Homo sapiens 151-167 19215971-2 2009 We investigated whether 75 mg of daily non-enteric coated aspirin would completely inhibit the platelet cyclooxygenase-1 activity to a comparable extent in healthy individuals and stable CAD patients. Aspirin 58-65 prostaglandin-endoperoxide synthase 1 Homo sapiens 104-120 19996015-2 2009 The objectives of this study were to determine prospectively whether COX-1-dependent and other platelet function assays correlate with clinical outcomes in aspirin-treated patients. Aspirin 156-163 prostaglandin-endoperoxide synthase 1 Homo sapiens 69-74 19996015-10 2009 CONCLUSIONS: In this prospective study of 700 aspirin-treated patients presenting for angiographic evaluation of coronary artery disease, residual platelet COX-1 function measured by serum thromboxane B(2) and COX-1-independent platelet function measured by PFA-100 collagen-ADP CT, but not indirect COX-1-dependent assays (arachidonic acid-stimulated platelet markers, shortened PFA-100 collagen-epinephrine CT), correlate with subsequent major adverse cardiovascular events. Aspirin 46-53 prostaglandin-endoperoxide synthase 1 Homo sapiens 156-161 19652893-9 2009 These results suggest that some of the variability in the reported incidence of "aspirin resistance" is unrelated to aspirin intake but related to inherent limitations of some assays to detect aspirin mediated effects or to underlying platelet reactivity variability independent of aspirin-mediated cyclooxygenase-1 inhibition. Aspirin 81-88 prostaglandin-endoperoxide synthase 1 Homo sapiens 299-315 19390185-0 2009 Influence of cyclooxygenase-1 genotype on ex vivo aspirin response in patients at risk for stroke. Aspirin 50-57 prostaglandin-endoperoxide synthase 1 Homo sapiens 13-29 19575683-3 2009 The ingestion of aspirin and other cyclooxygenase-1 (COX-1) inhibitors induces exacerbations of airway disease that may be life-threatening. Aspirin 17-24 prostaglandin-endoperoxide synthase 1 Homo sapiens 53-58 19390185-6 2009 More subjects with the PTGS1 17PP versus PL genotype had incomplete ex-vivo inhibition of platelet aggregation by aspirin (57 vs. 20%; p = 0.04). Aspirin 114-121 prostaglandin-endoperoxide synthase 1 Homo sapiens 23-28 19390185-8 2009 Similarly, nonlinear mapping showed a direct relationship between the PTGS1 17P allele and decreased aspirin response. Aspirin 101-108 prostaglandin-endoperoxide synthase 1 Homo sapiens 70-75 19390185-1 2009 BACKGROUND: We sought to determine whether cyclooxygenase-1 (PTGS1) genotype is associated with the ability of aspirin to inhibit platelet aggregation in patients at risk for stroke. Aspirin 111-118 prostaglandin-endoperoxide synthase 1 Homo sapiens 43-59 19390185-10 2009 CONCLUSIONS: Our data suggest that the PTGS1 P17L genotype contributes to response to aspirin as assessed by ex-vivo platelet aggregation. Aspirin 86-93 prostaglandin-endoperoxide synthase 1 Homo sapiens 39-44 19390185-11 2009 Our data further suggest that the association between PTGS1 genotype and aspirin response might vary by ethnicity. Aspirin 73-80 prostaglandin-endoperoxide synthase 1 Homo sapiens 54-59 19390185-1 2009 BACKGROUND: We sought to determine whether cyclooxygenase-1 (PTGS1) genotype is associated with the ability of aspirin to inhibit platelet aggregation in patients at risk for stroke. Aspirin 111-118 prostaglandin-endoperoxide synthase 1 Homo sapiens 61-66 19390185-4 2009 The association between PTGS1 A-707G and P17L genotypes and aspirin response, as assessed by ex vivo studies and 11-dhTxB(2) concentrations, was evaluated by statistical testing and nonlinear mapping. Aspirin 60-67 prostaglandin-endoperoxide synthase 1 Homo sapiens 24-29 18038215-1 2008 Aspirin exerts anti-thrombotic action by acetylating and inactivating cyclooxygenase-1, preventing the production of thromboxane A2 in platelets. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 70-86 18695943-1 2009 BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) may be prothrombotic, may worsen hypertension or congestive heart failure and obstruct access to the binding site of aspirin to cyclooxygenase-1 and thereby interfere with aspirin"s mechanism of action in reducing death and recurrent myocardial infarction (MI). Aspirin 176-183 prostaglandin-endoperoxide synthase 1 Homo sapiens 187-203 18695943-1 2009 BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) may be prothrombotic, may worsen hypertension or congestive heart failure and obstruct access to the binding site of aspirin to cyclooxygenase-1 and thereby interfere with aspirin"s mechanism of action in reducing death and recurrent myocardial infarction (MI). Aspirin 231-238 prostaglandin-endoperoxide synthase 1 Homo sapiens 187-203 19075637-5 2008 Platelet inhibition by Aspirin results from the irreversible inhibition of cyclooxygenase-1 enzyme and prevention of thromboxane A2, a potent aggregatory agent, formation. Aspirin 23-30 prostaglandin-endoperoxide synthase 1 Homo sapiens 75-91 18660649-3 2008 All NSAIDs and aspirin inhibit active sites of cyclooxygenase-1 and cyclooxygenase-2. Aspirin 15-22 prostaglandin-endoperoxide synthase 1 Homo sapiens 47-63 18575740-7 2008 To gain insight into the mechanism underlying the synergistic action of HDIs and aspirin, we employed the deacetylated metabolite of aspirin, salicylic acid, and the cyclooxygenase-1- and -2-selective inhibitors, SC-560 and NS-398, respectively. Aspirin 81-88 prostaglandin-endoperoxide synthase 1 Homo sapiens 166-190 18435972-7 2008 After the 2 aspirin doses, men and women had near complete suppression of platelet aggregation to arachidonic acid in whole blood and in platelet-rich plasma (PRP), the direct cyclo-oxygenase-1 pathway affected by aspirin. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 176-193 18435972-7 2008 After the 2 aspirin doses, men and women had near complete suppression of platelet aggregation to arachidonic acid in whole blood and in platelet-rich plasma (PRP), the direct cyclo-oxygenase-1 pathway affected by aspirin. Aspirin 214-221 prostaglandin-endoperoxide synthase 1 Homo sapiens 176-193 18221358-1 2008 BACKGROUND: Permanent inactivation of cyclooxygenase-1 and inhibition of platelet thromboxane A(2) (TxA(2)) constitute the main mechanisms underlying the prevention of vascular disease by aspirin. Aspirin 188-195 prostaglandin-endoperoxide synthase 1 Homo sapiens 38-54 18612540-0 2008 The C50T polymorphism of the cyclooxygenase-1 gene and the risk of thrombotic events during low-dose therapy with acetyl salicylic acid. Aspirin 114-135 prostaglandin-endoperoxide synthase 1 Homo sapiens 29-45 18612540-1 2008 Aspirin prevents thrombotic events by inhibiting platelet cyclooxygenase-1 (COX-1), thus reducing thromboxane A2 formation and platelet aggregation. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 58-74 18612540-1 2008 Aspirin prevents thrombotic events by inhibiting platelet cyclooxygenase-1 (COX-1), thus reducing thromboxane A2 formation and platelet aggregation. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 76-81 18612540-2 2008 The C50T polymorphism of COX-1 is associated with an impaired inhibition of both thromboxane production and in-vitro platelet aggregation by aspirin. Aspirin 141-148 prostaglandin-endoperoxide synthase 1 Homo sapiens 25-30 18612540-11 2008 In prior laboratory studies the COX-1 C50T polymorphism was associated with an impaired inhibitory effect of aspirin on thromboxane production and platelet function. Aspirin 109-116 prostaglandin-endoperoxide synthase 1 Homo sapiens 32-37 17934975-1 2008 OBJECTIVE: To assess the prevalence of a lacking aspirin effect on cyclooxygenase-1 (COX-1) ("aspirin resistance") in patients with symptomatic, stable coronary heart disease (CHD) using test methods directly reflecting inhibition of COX-1. Aspirin 49-56 prostaglandin-endoperoxide synthase 1 Homo sapiens 67-83 17944992-1 2008 BACKGROUND: Anti-inflammatory analgesics, including ibuprofen and naproxen, are known to interfere with the antiplatelet effect of aspirin, presumably as a result of a drug-drug interaction at the level of platelet cyclooxygenase-1 (COX-1). Aspirin 131-138 prostaglandin-endoperoxide synthase 1 Homo sapiens 215-231 17944992-1 2008 BACKGROUND: Anti-inflammatory analgesics, including ibuprofen and naproxen, are known to interfere with the antiplatelet effect of aspirin, presumably as a result of a drug-drug interaction at the level of platelet cyclooxygenase-1 (COX-1). Aspirin 131-138 prostaglandin-endoperoxide synthase 1 Homo sapiens 233-238 17944992-8 2008 Moreover, MAA attenuated the effect of aspirin on COX activity of platelet microsomes, suggesting a competition with aspirin at the COX-1 enzyme. Aspirin 117-124 prostaglandin-endoperoxide synthase 1 Homo sapiens 132-137 17944992-9 2008 This was confirmed by docking studies, which revealed that MAA forms a strong hydrogen bond with serine 530 within the COX-1, thereby preventing enzyme acetylation by aspirin. Aspirin 167-174 prostaglandin-endoperoxide synthase 1 Homo sapiens 119-124 17934975-1 2008 OBJECTIVE: To assess the prevalence of a lacking aspirin effect on cyclooxygenase-1 (COX-1) ("aspirin resistance") in patients with symptomatic, stable coronary heart disease (CHD) using test methods directly reflecting inhibition of COX-1. Aspirin 49-56 prostaglandin-endoperoxide synthase 1 Homo sapiens 85-90 17934975-1 2008 OBJECTIVE: To assess the prevalence of a lacking aspirin effect on cyclooxygenase-1 (COX-1) ("aspirin resistance") in patients with symptomatic, stable coronary heart disease (CHD) using test methods directly reflecting inhibition of COX-1. Aspirin 94-101 prostaglandin-endoperoxide synthase 1 Homo sapiens 67-83 17934975-1 2008 OBJECTIVE: To assess the prevalence of a lacking aspirin effect on cyclooxygenase-1 (COX-1) ("aspirin resistance") in patients with symptomatic, stable coronary heart disease (CHD) using test methods directly reflecting inhibition of COX-1. Aspirin 94-101 prostaglandin-endoperoxide synthase 1 Homo sapiens 85-90 17934975-10 2008 CONCLUSION: Repeated AA-induced platelet aggregometry showed that COX-1 could be blocked by low-dose aspirin in all 289 tested patients, suggesting that aspirin resistance is rare in patients with stable CHD. Aspirin 101-108 prostaglandin-endoperoxide synthase 1 Homo sapiens 66-71 17979514-4 2007 Aspirin response phenotypes can be categorized as directly or indirectly related to cyclooxygenase-1 (COX-1) activity, with phenotypic variation indirectly related to COX-1 being much more prominent. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 84-100 17640058-3 2007 Prostaglandin H synthase 1 (PTGS1) and PTGS2 are key enzymes in prostaglandin synthesis and are inhibited by aspirin, whilst interleukin-10 (IL-10) is an important antiinflammatory cytokine. Aspirin 109-116 prostaglandin-endoperoxide synthase 1 Homo sapiens 0-26 17640058-3 2007 Prostaglandin H synthase 1 (PTGS1) and PTGS2 are key enzymes in prostaglandin synthesis and are inhibited by aspirin, whilst interleukin-10 (IL-10) is an important antiinflammatory cytokine. Aspirin 109-116 prostaglandin-endoperoxide synthase 1 Homo sapiens 28-33 17979514-4 2007 Aspirin response phenotypes can be categorized as directly or indirectly related to cyclooxygenase-1 (COX-1) activity, with phenotypic variation indirectly related to COX-1 being much more prominent. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 102-107 17979514-4 2007 Aspirin response phenotypes can be categorized as directly or indirectly related to cyclooxygenase-1 (COX-1) activity, with phenotypic variation indirectly related to COX-1 being much more prominent. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 167-172 17429206-3 2007 The antiplatelet effect of cyclooxygenase-1 inhibitors lasts less than 4 h. Skin and colonic bleeding times are prolonged for 3 and 5 days after aspirin and ticlopidine withdrawal respectively. Aspirin 145-152 prostaglandin-endoperoxide synthase 1 Homo sapiens 27-43 17609236-14 2007 Since acetaminophen is a weak inhibitor of the COX-1 enzyme, patients with aspirin-induced asthma should not take more than 1000 mg of acetaminophen in a single dose. Aspirin 75-82 prostaglandin-endoperoxide synthase 1 Homo sapiens 47-52 17508966-0 2007 Alternative splicing of cyclooxygenase-1 gene: altered expression in leucocytes from patients with bronchial asthma and association with aspirin-induced 15-HETE release. Aspirin 137-144 prostaglandin-endoperoxide synthase 1 Homo sapiens 24-40 17508966-2 2007 In a subpopulation of aspirin-sensitive asthmatics (ASA) inhibition of COX-1 by nonsteroidal anti-inflammatory drugs results in activation of inflammatory cells and development of symptoms. Aspirin 22-29 prostaglandin-endoperoxide synthase 1 Homo sapiens 71-76 17508966-2 2007 In a subpopulation of aspirin-sensitive asthmatics (ASA) inhibition of COX-1 by nonsteroidal anti-inflammatory drugs results in activation of inflammatory cells and development of symptoms. Aspirin 52-55 prostaglandin-endoperoxide synthase 1 Homo sapiens 71-76 17508966-4 2007 We aimed to assess the expression of spliced variants of COX-1 mRNA in PBLs from patients with asthma and in healthy subjects (HS) referring the expression to patients characteristics (including ASA-sensitivity) and to aspirin-triggered 15-hydroxyeicosatetraenoic acid (15-HETE) generation. Aspirin 195-198 prostaglandin-endoperoxide synthase 1 Homo sapiens 57-62 17508966-4 2007 We aimed to assess the expression of spliced variants of COX-1 mRNA in PBLs from patients with asthma and in healthy subjects (HS) referring the expression to patients characteristics (including ASA-sensitivity) and to aspirin-triggered 15-hydroxyeicosatetraenoic acid (15-HETE) generation. Aspirin 219-226 prostaglandin-endoperoxide synthase 1 Homo sapiens 57-62 17559347-0 2007 Frequency of genetic polymorphisms of COX1, GPIIIa and P2Y1 in a Chinese population and association with attenuated response to aspirin. Aspirin 128-135 prostaglandin-endoperoxide synthase 1 Homo sapiens 38-42 17242290-0 2007 Letter by Kronish et al regarding article, "Residual arachidonic acid-induced platelet activation via an adenosine diphosphate-dependent but cyclooxygenase-1- and cyclooxygenase-2-independent pathway: a 700-patient study of aspirin resistance". Aspirin 224-231 prostaglandin-endoperoxide synthase 1 Homo sapiens 141-157 17867925-2 2007 Aspirin exhibits its antiplatelet action by irreversibly inhibiting platelet cyclooxygenase-1 enzyme, thus preventing the production of thromboxane A2 (TXA2). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 77-93 17867925-7 2007 Possible causes of aspirin resistance include poor compliance, inadequate dose, drug interactions, genetic polymorphisms of cyclooxygenase-1, increased platelet turnover and upregulation of non-platelet pathways of thromboxane production. Aspirin 19-26 prostaglandin-endoperoxide synthase 1 Homo sapiens 124-140 17609236-7 2007 The primary mechanism is believed to be inhibition of the cyclooxygenase 1 (COX-1) enzyme; as such, patients with aspirin sensitivity often display cross-reactions to nonselective NSAIDs that inhibit the COX-1 enzyme. Aspirin 114-121 prostaglandin-endoperoxide synthase 1 Homo sapiens 58-74 17609236-7 2007 The primary mechanism is believed to be inhibition of the cyclooxygenase 1 (COX-1) enzyme; as such, patients with aspirin sensitivity often display cross-reactions to nonselective NSAIDs that inhibit the COX-1 enzyme. Aspirin 114-121 prostaglandin-endoperoxide synthase 1 Homo sapiens 76-81 17609236-7 2007 The primary mechanism is believed to be inhibition of the cyclooxygenase 1 (COX-1) enzyme; as such, patients with aspirin sensitivity often display cross-reactions to nonselective NSAIDs that inhibit the COX-1 enzyme. Aspirin 114-121 prostaglandin-endoperoxide synthase 1 Homo sapiens 204-209 17562955-1 2007 BACKGROUND: The antiplatelet effect of aspirin is attributed to platelet cyclooxygenase-1 inhibition. Aspirin 39-46 prostaglandin-endoperoxide synthase 1 Homo sapiens 73-89 17508966-13 2007 In ASA patients there was a significant positive correlation between the COX-1 AS index and the percentage of aspirin-triggered increase in 15-HETE generation (r = 0.51; P < 0.03). Aspirin 3-6 prostaglandin-endoperoxide synthase 1 Homo sapiens 73-78 17508966-13 2007 In ASA patients there was a significant positive correlation between the COX-1 AS index and the percentage of aspirin-triggered increase in 15-HETE generation (r = 0.51; P < 0.03). Aspirin 110-117 prostaglandin-endoperoxide synthase 1 Homo sapiens 73-78 17508966-14 2007 CONCLUSIONS: Alternatively spliced variants of COX-1 mRNA are differently expressed in patients with bronchial asthma and may be associated with aspirin-triggered 15-HETE generation. Aspirin 145-152 prostaglandin-endoperoxide synthase 1 Homo sapiens 47-52 17470694-0 2007 Heritability of platelet responsiveness to aspirin in activation pathways directly and indirectly related to cyclooxygenase-1. Aspirin 43-50 prostaglandin-endoperoxide synthase 1 Homo sapiens 109-125 17470694-4 2007 Ex vivo platelet function was determined before and after ingestion of ASA (81 mg/d for 2 weeks) with the use of a panel of measures that assessed platelet activation in pathways directly and indirectly related to cyclooxygenase-1, the enzyme inhibited by ASA. Aspirin 256-259 prostaglandin-endoperoxide synthase 1 Homo sapiens 214-230 17340471-1 2007 Aspirin irreversibly inhibits platelet cyclooxygenase-1 (COX-1). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 39-55 17340471-1 2007 Aspirin irreversibly inhibits platelet cyclooxygenase-1 (COX-1). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 57-62 17340471-3 2007 Aspirin resistance has to be defined by its inability to inhibit COX-1. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 65-70 17241655-2 2007 Possible causes of aspirin resistance include poor compliance, drug interaction, inadequate aspirin dose, increase turnover of platelets, genetic polymorphisms of cyclo-oxygenase-1, and upregulation of alternate (non-platelet) pathways of thromboxane production. Aspirin 19-26 prostaglandin-endoperoxide synthase 1 Homo sapiens 163-180 18024618-6 2007 True "aspirin resistance" implies that cyclooxygenase-1 is less sensitive to inactivation by aspirin. Aspirin 6-13 prostaglandin-endoperoxide synthase 1 Homo sapiens 39-55 18024618-6 2007 True "aspirin resistance" implies that cyclooxygenase-1 is less sensitive to inactivation by aspirin. Aspirin 93-100 prostaglandin-endoperoxide synthase 1 Homo sapiens 39-55 16937749-2 2006 OBJECTIVE: To classify patients with a history of aspirin-induced urticaria as cross-reactors or single-drug reactors by oral challenges with another strong COX-1 inhibitor, namely, ketoprofen. Aspirin 50-57 prostaglandin-endoperoxide synthase 1 Homo sapiens 157-162 16977569-2 2006 These are all reversible by inhibition of platelet cyclooxygenase 1 with aspirin, and are therefore indicative of platelet activation and platelet-mediated thrombotic processes. Aspirin 73-80 prostaglandin-endoperoxide synthase 1 Homo sapiens 51-67 17008981-2 2006 Aspirin irreversibly inhibits the cyclooxygenase-1 (COX-1) enzyme, whereas non-steroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit the COX-1 enzyme. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 34-50 17008981-2 2006 Aspirin irreversibly inhibits the cyclooxygenase-1 (COX-1) enzyme, whereas non-steroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit the COX-1 enzyme. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 52-57 16706971-3 2006 RESULTS: Subjects taking 81 mg of aspirin (n = 50) and controls (n = 38) were evaluated for platelet aggregation and platelet cyclooxygenase-1 (COX-1) activity by measuring collagen-induced thromboxane B2 production. Aspirin 34-41 prostaglandin-endoperoxide synthase 1 Homo sapiens 144-149 16890573-0 2006 Heterogeneity in the suppression of platelet cyclooxygenase-1 activity by aspirin in coronary heart disease. Aspirin 74-81 prostaglandin-endoperoxide synthase 1 Homo sapiens 45-61 16785341-9 2006 CONCLUSIONS: There is a residual arachidonic acid-induced platelet activation in aspirin-treated patients that (1) is caused by underdosing and/or noncompliance in only approximately 2% of patients and (2) in the remaining patients, occurs via a cyclooxygenase-1 and cyclooxygenase-2 independent pathway, in direct proportion to the degree of baseline platelet activation, and is mediated in part by adenosine diphosphate-induced platelet activation. Aspirin 81-88 prostaglandin-endoperoxide synthase 1 Homo sapiens 246-262 16706971-10 2006 CONCLUSIONS: Aspirin resistance expressed as unsuppressed platelet COX-1 activity is a rare condition in an out-patient population. Aspirin 13-20 prostaglandin-endoperoxide synthase 1 Homo sapiens 67-72 16675319-4 2006 In addition, NSAIDs, particularly ibuprofen, may interfere with the antithrombotic benefits of aspirin through competitive interaction with platelet cyclooxygenase-1 (COX-1). Aspirin 95-102 prostaglandin-endoperoxide synthase 1 Homo sapiens 149-165 16675319-4 2006 In addition, NSAIDs, particularly ibuprofen, may interfere with the antithrombotic benefits of aspirin through competitive interaction with platelet cyclooxygenase-1 (COX-1). Aspirin 95-102 prostaglandin-endoperoxide synthase 1 Homo sapiens 167-172 16673274-3 2006 Inhibition of platelet cyclooxygenase-1 by aspirin is followed by relief of microvascular disturbances; correction of shortened platelet survival; correction of increased plasma beta-TG, PF4, and TM levels; and correction of increased TXB2 excretion to normal. Aspirin 43-50 prostaglandin-endoperoxide synthase 1 Homo sapiens 23-39 16484611-0 2006 De novo synthesis of cyclooxygenase-1 counteracts the suppression of platelet thromboxane biosynthesis by aspirin. Aspirin 106-113 prostaglandin-endoperoxide synthase 1 Homo sapiens 21-37 16484611-1 2006 Aspirin affords cardioprotection through the acetylation of serine529 in human cyclooxygenase-1 (COX-1) of anucleated platelets, inducing a permanent defect in thromboxane A2 (TXA2)-dependent platelet function. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 79-95 16484611-1 2006 Aspirin affords cardioprotection through the acetylation of serine529 in human cyclooxygenase-1 (COX-1) of anucleated platelets, inducing a permanent defect in thromboxane A2 (TXA2)-dependent platelet function. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 97-102 16484611-2 2006 However, heterogeneity of COX-1 suppression by aspirin has been detected in cardiovascular disease and may contribute to failure to prevent clinical events. Aspirin 47-54 prostaglandin-endoperoxide synthase 1 Homo sapiens 26-31 16551714-8 2006 However, after aspirin therapy, the percent aggregation to arachidonic acid (the direct COX-1 pathway) decreased more in women than in men (P<.001) and demonstrated near total suppression of residual platelet reactivity in both men and women. Aspirin 15-22 prostaglandin-endoperoxide synthase 1 Homo sapiens 88-93 16551714-12 2006 However, most women achieved total suppression of aggregation in the direct COX-1 pathway, the putative mechanism for aspirin"s cardioprotection. Aspirin 118-125 prostaglandin-endoperoxide synthase 1 Homo sapiens 76-81 16609625-3 2006 The major side effect of aspirin is related to its ability to suppress prostaglandin (PG) synthesis by constitutive cyclooxygenase-1 (COX-1). Aspirin 25-32 prostaglandin-endoperoxide synthase 1 Homo sapiens 116-132 16447059-9 2006 Prostaglandin-endoperoxide synthase 1 (also known as cyclooxygenase 1) inhibitors (acetylsalicylic acid and indomethacin) did not alter the rate of hexose uptake and SCLC2A4 subcellular distribution in L6 myotubes. Aspirin 83-103 prostaglandin-endoperoxide synthase 1 Homo sapiens 0-37 16609625-3 2006 The major side effect of aspirin is related to its ability to suppress prostaglandin (PG) synthesis by constitutive cyclooxygenase-1 (COX-1). Aspirin 25-32 prostaglandin-endoperoxide synthase 1 Homo sapiens 134-139 15972451-6 2005 Rate of onset and recovery following aspirin withdrawal was consistent with cyclooxygenase 1 (COX-1) inhibition. Aspirin 37-44 prostaglandin-endoperoxide synthase 1 Homo sapiens 76-92 20477089-1 2006 Aspirin and other nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase-1 participate in unique pseudoallergic reactions, in which biochemical inhibitions rather than immunoglobulin E antibody direct the cascade of mediators and ultimate reactions. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 68-84 15972451-6 2005 Rate of onset and recovery following aspirin withdrawal was consistent with cyclooxygenase 1 (COX-1) inhibition. Aspirin 37-44 prostaglandin-endoperoxide synthase 1 Homo sapiens 94-99 15972451-9 2005 Comparisons of platelet COX-1 or -2 expression and urinary 11-dehydro-thromboxane B2 excretion suggested that aspirin was less able to block platelet activation in vivo in hypercholesterolemia. Aspirin 110-117 prostaglandin-endoperoxide synthase 1 Homo sapiens 24-29 16150050-0 2005 Cyclooxygenase-1 haplotype modulates platelet response to aspirin. Aspirin 58-65 prostaglandin-endoperoxide synthase 1 Homo sapiens 0-16 15967068-1 2005 In some patients with chronic idiopathic urticaria (CIU), aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase 1 (COX-1) precipitate wheals and swelling. Aspirin 58-65 prostaglandin-endoperoxide synthase 1 Homo sapiens 135-151 15967068-1 2005 In some patients with chronic idiopathic urticaria (CIU), aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase 1 (COX-1) precipitate wheals and swelling. Aspirin 58-65 prostaglandin-endoperoxide synthase 1 Homo sapiens 153-158 15967068-3 2005 Skin reactions triggered by aspirin are associated with the inhibition of cyclooxygenase, specifically COX-1, but not COX-2, and are characterized by overproduction of cysteinyl leukotrienes (cys-LTs). Aspirin 28-35 prostaglandin-endoperoxide synthase 1 Homo sapiens 103-108 15346640-1 2004 The antiplatelet effect of aspirin is mostly explained by the irreversible cyclooxygenase-1 inhibition resulting in the suppression of thromboxane A2 synthesis. Aspirin 27-34 prostaglandin-endoperoxide synthase 1 Homo sapiens 75-91 15921208-1 2005 BACKGROUND: Cyclooxygenase 1 (Cox-1) plays a key role in arachidonic acid metabolism and in the pathophysiology and immunology of nasal polyposis in patients suffering from aspirin intolerance. Aspirin 173-180 prostaglandin-endoperoxide synthase 1 Homo sapiens 12-28 15921208-1 2005 BACKGROUND: Cyclooxygenase 1 (Cox-1) plays a key role in arachidonic acid metabolism and in the pathophysiology and immunology of nasal polyposis in patients suffering from aspirin intolerance. Aspirin 173-180 prostaglandin-endoperoxide synthase 1 Homo sapiens 30-35 15892673-4 2005 Non-selective cyclooxygenase-1 (COX-1) inhibitors used in periodontal research include compounds such as aspirin, flurbiprofen, ibuprofen, naproxen and piroxicam. Aspirin 105-112 prostaglandin-endoperoxide synthase 1 Homo sapiens 14-30 15613671-7 2004 Aspirin sensitivity is most often manifested as rhinitis and asthma or urticaria/angioedema induced by cross-reacting nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase 1. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 168-184 15521369-3 2004 Reactions to aspirin and NSAIDs in patients with AERD are largely due to inhibition of COX-1. Aspirin 13-20 prostaglandin-endoperoxide synthase 1 Homo sapiens 87-92 15337874-2 2004 Aspirin irreversibly binds cyclooxygenase-1, thereby reducing platelet aggregation for the lifetime of each platelet. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 27-43 14680616-1 2004 Aspirin-exacerbated respiratory disease (AERD) is an adult-onset condition that manifests as asthma, rhinosinusitis/nasal polyps, and sensitivity to aspirin and other cyclooxygenase-1 (COX-1)-inhibitor nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 167-183 14769263-1 2004 Aspirin exacerbated respiratory disease (AERD) is an adult onset condition manifested as asthma, rhinosinusitis/nasal polyps, and sensitivity to aspirin and other cyclooxygenase-1 (Cox-1)-inhibitor nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 163-179 14769263-1 2004 Aspirin exacerbated respiratory disease (AERD) is an adult onset condition manifested as asthma, rhinosinusitis/nasal polyps, and sensitivity to aspirin and other cyclooxygenase-1 (Cox-1)-inhibitor nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 181-186 14680616-1 2004 Aspirin-exacerbated respiratory disease (AERD) is an adult-onset condition that manifests as asthma, rhinosinusitis/nasal polyps, and sensitivity to aspirin and other cyclooxygenase-1 (COX-1)-inhibitor nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 185-190 15199473-1 2003 Aspirin acetylates serine-530 of cyclooxygenase-1 (COX-1), thereby blocking thromboxane A (2) synthesis in platelets and reducing platelet aggregation. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 33-49 12870263-2 2003 The biological effects induced by aspirin and indomethacin on T98G cells, in which the expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were confirmed by RT-PCR and immunostaining, were investigated by studying cell proliferation and apoptosis assays. Aspirin 34-41 prostaglandin-endoperoxide synthase 1 Homo sapiens 101-117 15199473-1 2003 Aspirin acetylates serine-530 of cyclooxygenase-1 (COX-1), thereby blocking thromboxane A (2) synthesis in platelets and reducing platelet aggregation. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 51-56 12668895-6 2003 Cross-reactions between aspirin and other drugs are dependent upon inhibition of the cyclooxygenase-1 isoenzyme. Aspirin 24-31 prostaglandin-endoperoxide synthase 1 Homo sapiens 85-101 12767724-1 2003 Anti-thrombotic therapy with aspirin, which at low doses acts as a selective inhibitor of platelet cyclooxygenase 1 (COX-1) activity, is well established. Aspirin 29-36 prostaglandin-endoperoxide synthase 1 Homo sapiens 99-115 12767724-1 2003 Anti-thrombotic therapy with aspirin, which at low doses acts as a selective inhibitor of platelet cyclooxygenase 1 (COX-1) activity, is well established. Aspirin 29-36 prostaglandin-endoperoxide synthase 1 Homo sapiens 117-122 12767724-2 2003 However, a major limitation of aspirin treatment is its gastrointestinal toxicity, which is thought to be linked to the suppression of COX-1-mediated production of cytoprotective prostaglandins. Aspirin 31-38 prostaglandin-endoperoxide synthase 1 Homo sapiens 135-140 12612897-10 2003 CONCLUSIONS: In this study, we have proven the concept that addition of an NO-donating moiety to aspirin results in a new chemical entity that maintains cyclooxygenase-1 and platelet inhibitory activity while nearly avoiding gastrointestinal damage. Aspirin 97-104 prostaglandin-endoperoxide synthase 1 Homo sapiens 153-169 12545150-0 2003 Genetic variation in cyclooxygenase 1: effects on response to aspirin. Aspirin 62-69 prostaglandin-endoperoxide synthase 1 Homo sapiens 21-37 12591106-12 2003 We conclude that a single dose of aspirin affects major platelet receptors, presumably directly or indirectly through the inhibition of prostanoids via platelet cyclooxygenase-1 blockade. Aspirin 34-41 prostaglandin-endoperoxide synthase 1 Homo sapiens 161-177 12545150-9 2003 CONCLUSIONS: The discovery of a functional single-nucleotide polymorphism in the cyclooxygenase 1 locus may ultimately improve the safe and effective use of acetylsalicylic acid by better tailoring of dosage with an individual"s genetic variation. Aspirin 157-177 prostaglandin-endoperoxide synthase 1 Homo sapiens 81-97 12871563-0 2003 Aspirin resistance is not a common biochemical phenotype explained by unblocked cyclooxygenase-1 activity. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 80-96 15041270-0 2003 Mutations within the cyclooxygenase-1 gene in aspirin non-responders with recurrence of stroke. Aspirin 46-53 prostaglandin-endoperoxide synthase 1 Homo sapiens 21-37 15041270-1 2003 INTRODUCTION: Aspirin is a common antiplatelet drug used in the prevention of ischemic stroke due to its inhibitory effect on platelet cyclooxygenase-1 (Cox-1). Aspirin 14-21 prostaglandin-endoperoxide synthase 1 Homo sapiens 135-151 15041270-1 2003 INTRODUCTION: Aspirin is a common antiplatelet drug used in the prevention of ischemic stroke due to its inhibitory effect on platelet cyclooxygenase-1 (Cox-1). Aspirin 14-21 prostaglandin-endoperoxide synthase 1 Homo sapiens 153-158 15041270-3 2003 In this study, we have searched for variants of the Cox-1 gene that could possibly result in an unblocked and thus, aspirin-resistant Cox-1 enzyme and phenotype. Aspirin 116-123 prostaglandin-endoperoxide synthase 1 Homo sapiens 52-57 15041270-3 2003 In this study, we have searched for variants of the Cox-1 gene that could possibly result in an unblocked and thus, aspirin-resistant Cox-1 enzyme and phenotype. Aspirin 116-123 prostaglandin-endoperoxide synthase 1 Homo sapiens 134-139 15041270-4 2003 MATERIALS AND METHODS: The Cox-1 gene was sequenced in 68 patients with recurrent ischemic stroke despite taking aspirin. Aspirin 113-120 prostaglandin-endoperoxide synthase 1 Homo sapiens 27-32 14561202-4 2002 In this distinct clinical syndrome, aspirin and most other nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase-1 precipitate rhinitis and asthma attacks. Aspirin 36-43 prostaglandin-endoperoxide synthase 1 Homo sapiens 109-125 12705063-3 2003 More than 100 years after aspirin, an inhibitor of cyclooxygenase-1 and -2, was first used for the treatment of rheumatic diseases, analogues were developed for the same and other inclinations that now are available for clinical use. Aspirin 26-33 prostaglandin-endoperoxide synthase 1 Homo sapiens 51-74 12398900-6 2002 This finding indicates that specific PGHS-2 inhibitors are similar to ibuprofen in their ability to compete with aspirin, an irreversible time-dependent inhibitor of PGHS-1 often used for prevention of spontaneous thrombosis. Aspirin 113-120 prostaglandin-endoperoxide synthase 1 Homo sapiens 166-172 12225961-5 2002 The nonselective cyclooxygenase inhibitors indomethacin and meclofenamate and the preferential cyclooxygenase-1 inhibitor aspirin augmented NO-induced relaxation specifically in newborns, whereas the selective cycloxygenase-2 inhibitor NS-398 had no effect. Aspirin 122-129 prostaglandin-endoperoxide synthase 1 Homo sapiens 95-111 12167656-2 2002 Acetylation of Ser-530 of PGHS-1 by aspirin abolishes all oxygenase activity and transforms the peroxide-induced tyrosyl radical from a functional 33-35-gauss (G) wide doublet/wide singlet to a 26-G narrow singlet unable to oxidize AA. Aspirin 36-43 prostaglandin-endoperoxide synthase 1 Homo sapiens 26-32 11827357-5 2001 Aspirin, a selective platelet cyclo-oxygenase-1 inhibitor still remains the most extensively studied antiplatelet agent, even though there is growing evidence that many other compounds could be valuable either in association, or alternatives in antithrombotic therapy. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 30-47 12734579-1 2001 In platelets, PGHS-1-dependant formation of thromboxane A(2) is an important modulator of platelet function and a target for pharmacological inhibition of platelet function by aspirin. Aspirin 176-183 prostaglandin-endoperoxide synthase 1 Homo sapiens 14-20 11717412-0 2001 A high level of cyclooxygenase-2 inhibitor selectivity is associated with a reduced interference of platelet cyclooxygenase-1 inactivation by aspirin. Aspirin 142-149 prostaglandin-endoperoxide synthase 1 Homo sapiens 109-125 11190906-1 2001 Aspirin"s antithrombotic effect is mediated predominately by inhibition of platelet cyclooxygenase-1, leading to a decline in serum thromboxane A2 concentrations. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 84-100 11405554-1 2001 BACKGROUND: The preventive effect of low-dose aspirin in cardiovascular disease is generally attributed to its antiplatelet action caused by differential inhibition of platelet cyclooxygenase-1. Aspirin 46-53 prostaglandin-endoperoxide synthase 1 Homo sapiens 177-193 11447381-11 2001 From the standpoint of the mechanisms involved in aspirin-induced respiratory reactions, this study strongly supports inhibition of cyclooxygenase-1 as the essential initiator of these types of reactions. Aspirin 50-57 prostaglandin-endoperoxide synthase 1 Homo sapiens 132-148 11251623-1 2001 In a subset of patients with asthma, aspirin and several other non-steroidal anti-inflammatory drugs (NSAID) that inhibit simultaneously cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) precipitate dangerous asthmatic attacks. Aspirin 37-44 prostaglandin-endoperoxide synthase 1 Homo sapiens 137-153 10988074-1 2000 Prostaglandin H synthase-1 and -2 (PGHS-1 and -2) catalyze the committed step in prostaglandin synthesis and are targets for nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin. Aspirin 176-183 prostaglandin-endoperoxide synthase 1 Homo sapiens 35-48 10477832-0 1999 PGHS-2 inhibitors, NS-398 and DuP-697, attenuate the inhibition of PGHS-1 by aspirin and indomethacin without altering its activity. Aspirin 77-84 prostaglandin-endoperoxide synthase 1 Homo sapiens 67-73 10781899-1 2000 OBJECTIVE: Because the prostaglandin endoperoxide H synthase-1 (PGHS-1)-dependent formation of thromboxane A(2) is an important modulator of platelet function, this pathway represents a pharmacologic target for the inhibition of platelet function by aspirin. Aspirin 250-257 prostaglandin-endoperoxide synthase 1 Homo sapiens 23-62 10781899-1 2000 OBJECTIVE: Because the prostaglandin endoperoxide H synthase-1 (PGHS-1)-dependent formation of thromboxane A(2) is an important modulator of platelet function, this pathway represents a pharmacologic target for the inhibition of platelet function by aspirin. Aspirin 250-257 prostaglandin-endoperoxide synthase 1 Homo sapiens 64-70 10841038-4 2000 When these cells were pretreated with aspirin to inactivate their PGHS-1 and then activated by serum and phorbol ester (TPA) for 6 h, the cells expressed PGHS-2 activity alone. Aspirin 38-45 prostaglandin-endoperoxide synthase 1 Homo sapiens 66-72 10966456-2 2000 PGHS-1 and 2 are of particular interest because they are the major targets of nonsteroidal anti-inflammatory drugs (NSAIDs) including aspirin, ibuprofen, and the new COX-2 inhibitors. Aspirin 134-141 prostaglandin-endoperoxide synthase 1 Homo sapiens 0-12 10477832-3 1999 In the present study we have tested the effects of DuP-697 and NS-398 on the activity of PGHS-1 and further explored the interactions between these agents and the inhibition of PGHS-1 by aspirin, indomethacin and ibuprofen. Aspirin 187-194 prostaglandin-endoperoxide synthase 1 Homo sapiens 177-183 10477832-5 1999 The results show that DuP-697 and NS-398, at concentrations ranges which do not inhibit PGHS-1 activity, significantly attenuated the inhibition of PGHS-1 that was caused by aspirin and indomethacin. Aspirin 174-181 prostaglandin-endoperoxide synthase 1 Homo sapiens 148-154 10477832-8 1999 These results suggest that PGHS-2 inhibitors DuP-697 and NS-398 possibly interact with PGHS-1 at a site different from the enzyme"s catalytic site, thus causing attenuation of PGHS-1 inhibition by aspirin and indomethacin without altering PGHS-1 basal activity or the ibuprofen-induced inhibition. Aspirin 197-204 prostaglandin-endoperoxide synthase 1 Homo sapiens 87-93 10477832-8 1999 These results suggest that PGHS-2 inhibitors DuP-697 and NS-398 possibly interact with PGHS-1 at a site different from the enzyme"s catalytic site, thus causing attenuation of PGHS-1 inhibition by aspirin and indomethacin without altering PGHS-1 basal activity or the ibuprofen-induced inhibition. Aspirin 197-204 prostaglandin-endoperoxide synthase 1 Homo sapiens 176-182 10477832-8 1999 These results suggest that PGHS-2 inhibitors DuP-697 and NS-398 possibly interact with PGHS-1 at a site different from the enzyme"s catalytic site, thus causing attenuation of PGHS-1 inhibition by aspirin and indomethacin without altering PGHS-1 basal activity or the ibuprofen-induced inhibition. Aspirin 197-204 prostaglandin-endoperoxide synthase 1 Homo sapiens 176-182 10400832-1 1999 In some patients with asthma, aspirin (ASA) and all nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase enzymes (cyclooxygenase-1 and -2) precipitate asthmatic attacks and naso-ocular reactions. Aspirin 30-37 prostaglandin-endoperoxide synthase 1 Homo sapiens 126-149 8114674-7 1994 Recombinant hPGHS-1 and hPGHS-2 both produced 15- and 11-hydroxyeicosatetraenoic acid (HETE) from arachidonic acid, with 15-HETE production by hPGHS-2 being stimulated 5-fold by preincubation with aspirin. Aspirin 197-204 prostaglandin-endoperoxide synthase 1 Homo sapiens 12-19 10400832-1 1999 In some patients with asthma, aspirin (ASA) and all nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase enzymes (cyclooxygenase-1 and -2) precipitate asthmatic attacks and naso-ocular reactions. Aspirin 39-42 prostaglandin-endoperoxide synthase 1 Homo sapiens 126-149 10206978-6 1999 This shift in product profile was accentuated if cyclooxygenase-1 was permanently inactivated with aspirin before cyclooxygenase-2 induction. Aspirin 99-106 prostaglandin-endoperoxide synthase 1 Homo sapiens 49-65 9916892-7 1998 It is unabated, however, in the presence of substances inhibiting cyclooxygenase-1 and/or cyclooxygenase-2 (e.g., acetyl salicylic acid, SC 58125, L 745337), but is decreased by approx. Aspirin 114-135 prostaglandin-endoperoxide synthase 1 Homo sapiens 66-82 7493972-9 1995 Aspirin is an acid NSAID that inhibits PGHS-1 through a unique covalent acetylation of the enzyme and also showed a reduced rate of inactivation of the mutated enzyme. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 39-45 7554708-8 1995 The daily administration of low-dose aspirin (40 mg), a selective inhibitor of platelet PGHS-1, caused a cumulative inhibition of urinary 11-dehydro-TXB2 and whole blood TXB2 production that recovered with a timecourse consistent with platelet turnover. Aspirin 37-44 prostaglandin-endoperoxide synthase 1 Homo sapiens 88-94 7996488-2 1994 Heparinized human whole blood samples were incubated with lipopolysaccharide (LPS, 0.1-50 micrograms/ml) for 0 to 24 hr at 37 degrees C. The contribution of platelet PGHS-1 was suppressed by either pretreating the subjects with aspirin (300 mg 48 hr before sampling) or adding aspirin (10 micrograms/ml) in vitro at time 0. Aspirin 228-235 prostaglandin-endoperoxide synthase 1 Homo sapiens 166-172 7996488-2 1994 Heparinized human whole blood samples were incubated with lipopolysaccharide (LPS, 0.1-50 micrograms/ml) for 0 to 24 hr at 37 degrees C. The contribution of platelet PGHS-1 was suppressed by either pretreating the subjects with aspirin (300 mg 48 hr before sampling) or adding aspirin (10 micrograms/ml) in vitro at time 0. Aspirin 277-284 prostaglandin-endoperoxide synthase 1 Homo sapiens 166-172 8175750-1 1994 Aspirin (acetylsalicylate) treatment of human (h) prostaglandin endoperoxide H synthase (PGHS)-1 expressed in cos-1 cells caused a time-dependent inactivation of oxygenase activity. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 50-96 8175750-1 1994 Aspirin (acetylsalicylate) treatment of human (h) prostaglandin endoperoxide H synthase (PGHS)-1 expressed in cos-1 cells caused a time-dependent inactivation of oxygenase activity. Aspirin 9-25 prostaglandin-endoperoxide synthase 1 Homo sapiens 50-96 8175750-8 1994 This indicates that Ser-516 is the site of aspirin acetylation of hPGHS-2; this residue is homologous to the "active site" serine of PGHS-1. Aspirin 43-50 prostaglandin-endoperoxide synthase 1 Homo sapiens 133-139 9515564-1 1998 Aspirin and conventional nonsteroidal anti-inflammatory drugs are nonselective inhibitors of cyclooxygenase-1 (COX-1) and COX-2 enzymes. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 93-109 9515564-1 1998 Aspirin and conventional nonsteroidal anti-inflammatory drugs are nonselective inhibitors of cyclooxygenase-1 (COX-1) and COX-2 enzymes. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 111-116 9351505-8 1997 The contribution of PGHS-1 was suppressed by pretreatment of the volunteers with aspirin (500 mg; 48 h before venepuncture). Aspirin 81-88 prostaglandin-endoperoxide synthase 1 Homo sapiens 20-26 9048568-7 1997 Acetylation of PGHS-1 by ASA, in contrast, inhibited both lipoxygenase and cyclooxygenase activity. Aspirin 25-28 prostaglandin-endoperoxide synthase 1 Homo sapiens 15-21 8648609-4 1996 Most of the aspirin-like maleimides inactivated the cyclooxygenase activity of purified ovine PGHS-1 in a time- and concentration-dependent manner similar to that of aspirin. Aspirin 12-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 94-100 34820927-1 2022 Aspirin-exacerbated respiratory disease (AERD) is a clinical syndrome characterized by asthma, chronic rhinosinusitis with nasal polyposis (CRSwNP), and acute respiratory symptoms following exposure to aspirin and other cyclooxygenase-1 inhibiting nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 220-236 34429873-1 2021 Introduction: Aspirin-exacerbated respiratory disease (AERD) is a phenotype of asthma characterized by eosinophilic inflammation in the airways, mast cell activation, cysteinyl leukotriene overproduction, and acute respiratory reactions on exposure to cyclooxygenase-1 inhibitors. Aspirin 14-21 prostaglandin-endoperoxide synthase 1 Homo sapiens 252-268 34364538-1 2021 Aspirin-exacerbated respiratory disease (AERD) is a condition composed of chronic rhinosinusitis with nasal polyposis and asthma that is defined by respiratory hypersensitivity reactions to the cyclooxygenase 1-inhibitory effects of nonsteroidal anti-inflammatory drugs. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 194-210 34942378-6 2022 Inhibition of COX-1 with aspirin, as expected, completely abolished production of TxA2 and PGD/E2, but also significantly inhibited the release of 11-HETE (89 +- 3%) and 9-HODE (74 +- 6%), and reduced 15-HETE and 13-HODE by ~33 %. Aspirin 25-32 prostaglandin-endoperoxide synthase 1 Homo sapiens 14-19 34705291-1 2022 Aspirin has known effects beyond inhibiting platelet cyclooxygenase-1 (COX1) that have been incompletely characterized. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 53-69 34705291-1 2022 Aspirin has known effects beyond inhibiting platelet cyclooxygenase-1 (COX1) that have been incompletely characterized. Aspirin 0-7 prostaglandin-endoperoxide synthase 1 Homo sapiens 71-75 34983353-2 2022 By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies. Aspirin 87-107 prostaglandin-endoperoxide synthase 1 Homo sapiens 17-39 34983353-2 2022 By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies. Aspirin 109-116 prostaglandin-endoperoxide synthase 1 Homo sapiens 17-39