PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28830373-2 2017 Several pharmaco-epidemiology cohort studies have shown protective effects of aspirin on diseases using various statistical methods, with the Cox regression model being the most commonly used approach. Aspirin 78-85 cytochrome c oxidase subunit 8A Homo sapiens 142-145 32854760-0 2020 Aspirin mediates histone methylation that inhibits inflammation-related stemness gene expression to diminish cancer stemness via COX-independent manner. Aspirin 0-7 cytochrome c oxidase subunit 8A Homo sapiens 129-132 32854760-9 2020 In regards to the underlying molecular mechanism of action, aspirin reduces histone demethylase (KDM6A/B) expression that mediates histone methylation and suppresses gene expression via a COX-independent manner. Aspirin 60-67 cytochrome c oxidase subunit 8A Homo sapiens 188-191 31002173-8 2019 Aspirin significantly reduced the stroke recurrence in patients with lacunar stroke analyzed with multivariate stepwise analysis using model of Cox proportional hazards with backward elimination (HR = 0.67, 95% CI 0.45-0.99). Aspirin 0-7 cytochrome c oxidase subunit 8A Homo sapiens 144-147 30701538-2 2019 In addition, aspirin-induced Cox-dependent and -independent antitumor effects have also been described. Aspirin 13-20 cytochrome c oxidase subunit 8A Homo sapiens 29-32 28781013-8 2017 IPTW-weighted Cox regression revealed a powerful inverse association between aspirin use and moderate to severe CAV (adjusted hazard ratio 0.13; 95% confidence interval 0.03-0.59), which was directionally consistent for CAV of any severity (adjusted hazard ratio 0.50; 95% confidence interval 0.23-1.08). Aspirin 77-84 cytochrome c oxidase subunit 8A Homo sapiens 14-17 25604474-1 2015 With the aim to design new biologically active bioinorganic drugs of aspirin, whose mode of action is based on the inhibition of the cyclooxygenase(COX) enzymes, derivatives of Zeise"s salt were synthesized in this structure-activity relationship study. Aspirin 69-76 cytochrome c oxidase subunit 8A Homo sapiens 148-151 25604474-2 2015 Surprisingly, not only these Zeise-aspirin compounds but also Zeise"s salt itself showed high inhibitory potency against COX enzymes in in vitro assays. Aspirin 35-42 cytochrome c oxidase subunit 8A Homo sapiens 121-124 23895681-7 2013 Furtermore, other results suggest that the chemopreventive and therapeutic effects of aspirin are also mediated through COX-independent mechanisms. Aspirin 86-93 cytochrome c oxidase subunit 8A Homo sapiens 120-123 18180620-0 2008 Effects of aspirin and propranolol on the acute psychological stress response in factor VIII coagulant activity: a randomized, double-blind, placebo-controlled experimental study. Aspirin 11-18 cytochrome c oxidase subunit 8A Homo sapiens 88-92 23038044-9 2013 Additionally, Cox proportional hazards regression modeling demonstrated that aspirin resistance and cerebrovascular disease were associated with major adverse long-term outcomes (HR for aspirin resistance = 2.31, 95% CI 1.11-4.81, p = 0.026). Aspirin 77-84 cytochrome c oxidase subunit 8A Homo sapiens 14-17 23038044-9 2013 Additionally, Cox proportional hazards regression modeling demonstrated that aspirin resistance and cerebrovascular disease were associated with major adverse long-term outcomes (HR for aspirin resistance = 2.31, 95% CI 1.11-4.81, p = 0.026). Aspirin 186-193 cytochrome c oxidase subunit 8A Homo sapiens 14-17 22452804-13 2012 In addition, Cox proportional hazard regression modeling demonstrated that aspirin resistance or semiresponders (HR = 3.050, 95% CI: 1.464-6.354, p = 0.003) and diabetes (HR = 2.055, 95% CI: 1.060-3.981, p = 0.033) were associated with major adverse long-term outcomes. Aspirin 75-82 cytochrome c oxidase subunit 8A Homo sapiens 13-16 21215580-11 2011 Among all covariates included in the Cox models (including predictors of mortality such as American Society of Anesthesiologists [ASA] score), the psoas area was the most significant. Aspirin 130-133 cytochrome c oxidase subunit 8A Homo sapiens 37-40 20397022-6 2010 In the first two cell lines ASA inhibitory effects are Cox-2 independent because HCT116 cells do not express the enzyme while in HT-29 cells, Cox-2 has no activity as shown by a Cox activity assay. Aspirin 28-31 cytochrome c oxidase subunit 8A Homo sapiens 55-58 18180620-2 2008 We investigated whether aspirin and propranolol affect the responsiveness of plasma clotting factor VIII activity levels to acute psychosocial stress. Aspirin 24-31 cytochrome c oxidase subunit 8A Homo sapiens 100-104 18180620-7 2008 The clotting factor VIII activity level decreased from prestress to immediately poststress in the aspirin/propranolol group relative to the placebo group (P = 0.048) and the aspirin group (P < 0.06). Aspirin 98-105 cytochrome c oxidase subunit 8A Homo sapiens 20-24 18180620-7 2008 The clotting factor VIII activity level decreased from prestress to immediately poststress in the aspirin/propranolol group relative to the placebo group (P = 0.048) and the aspirin group (P < 0.06). Aspirin 174-181 cytochrome c oxidase subunit 8A Homo sapiens 20-24 18180620-8 2008 Between 45 min and 105 min poststress, clotting factor VIII levels increased in the aspirin/propranolol group relative to the placebo group (P = 0.007) and the aspirin group (P = 0.039). Aspirin 84-91 cytochrome c oxidase subunit 8A Homo sapiens 55-59 18180620-8 2008 Between 45 min and 105 min poststress, clotting factor VIII levels increased in the aspirin/propranolol group relative to the placebo group (P = 0.007) and the aspirin group (P = 0.039). Aspirin 160-167 cytochrome c oxidase subunit 8A Homo sapiens 55-59 18180620-10 2008 Propranolol in combination with aspirin diminished the acute response in clotting factor VIII activity to psychosocial stress compared with placebo medication and aspirin alone. Aspirin 32-39 cytochrome c oxidase subunit 8A Homo sapiens 89-93 18180620-10 2008 Propranolol in combination with aspirin diminished the acute response in clotting factor VIII activity to psychosocial stress compared with placebo medication and aspirin alone. Aspirin 163-170 cytochrome c oxidase subunit 8A Homo sapiens 89-93 18180620-11 2008 The effect of single aspirin on the acute clotting factor VIII stress response was indistinguishable from a placebo effect. Aspirin 21-28 cytochrome c oxidase subunit 8A Homo sapiens 58-62 14965321-4 2004 COX enzymes are clinically important because they are inhibited by aspirin and numerous other non-steroidal anti-inflammatory drugs. Aspirin 67-74 cytochrome c oxidase subunit 8A Homo sapiens 0-3 16816107-7 2006 We could show that COX-independent effects of aspirin were able to enhance expression of SR-BI in macrophages in a post-transcriptional, PPAR-alpha independent way, suggesting a novel pharmacologic effect of aspirin. Aspirin 46-53 cytochrome c oxidase subunit 8A Homo sapiens 19-22 16816107-7 2006 We could show that COX-independent effects of aspirin were able to enhance expression of SR-BI in macrophages in a post-transcriptional, PPAR-alpha independent way, suggesting a novel pharmacologic effect of aspirin. Aspirin 208-215 cytochrome c oxidase subunit 8A Homo sapiens 19-22 15763433-7 2005 This observation suggests a possible COX-mediated anti-inflammatory effect of low-dose aspirin, which should be further confirmed by intervention studies. Aspirin 87-94 cytochrome c oxidase subunit 8A Homo sapiens 37-40 14965321-7 2004 During the past forty years systematic advances in our understanding of the structure, regulation and function of COX isoenzymes have enabled the design and synthesis of COX-2 selective inhibitors as agents intended to lessen the gastrointestinal irritation of aspirin and non-selective NSAIDs. Aspirin 261-268 cytochrome c oxidase subunit 8A Homo sapiens 114-117 10639270-8 1997 Using the Cox model, adjusting for variables significantly associated with outcome, aspirin use remained a significant predictor of 14-day outcome (p = 0.04) but not of 12-week outcome (p = 0.06). Aspirin 84-91 cytochrome c oxidase subunit 8A Homo sapiens 10-13 9259112-9 1997 According to the Cox"s proportional hazards model, the estimated risk ratio (ASA group vs. nicametate group) was 0.538, with a 95% confidence interval of 0.284-1.019. Aspirin 77-80 cytochrome c oxidase subunit 8A Homo sapiens 17-20 8153084-4 1993 Amnion cells treated with IL-1 beta recovered rapidly from aspirin pretreatment suggesting an action on fatty acid cyclooxygenase (COX). Aspirin 59-66 cytochrome c oxidase subunit 8A Homo sapiens 131-134