PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10870801-0 2000 A low dose of aspirin (75 mg/day) lowers thrombin generation to a similar extent as a high dose of aspirin (300 mg/day). Aspirin 14-21 coagulation factor II, thrombin Homo sapiens 41-49 10870801-1 2000 This randomized, double-blind, parallel-group study was performed to assess the effect of 1-week treatment with 75 and 300 mg aspirin on thrombin generation. Aspirin 126-133 coagulation factor II, thrombin Homo sapiens 137-145 10870801-5 2000 At the site of microvascular injury, 75 mg aspirin led to a marked, about 60%, reduction in the total amount of thrombin generated (P = 0.04). Aspirin 43-50 coagulation factor II, thrombin Homo sapiens 112-120 10870801-7 2000 We conclude that the thrombin-lowering action of aspirin in the range between 75 and 300 mg daily given for 7 days is not dose dependent. Aspirin 49-56 coagulation factor II, thrombin Homo sapiens 21-29 10527411-0 1999 Orally administered acetylsalicylic acid decreases protein incorporation into the cytoskeleton of thrombin-stimulated platelets. Aspirin 20-40 coagulation factor II, thrombin Homo sapiens 98-106 11096641-1 1999 Inhibition of thrombin and platelets during percutaneous coronary intervention (PCI), using a combination of unfractionated heparin and aspirin, is designed primarily to minimize the rare but devastating potential acute thrombotic complications of the procedure. Aspirin 136-143 coagulation factor II, thrombin Homo sapiens 14-22 12749780-6 2000 Also in subjects without cardiovascular risk factors, it is predictable that early and continuous administration of low-dose aspirin, by inhibiting platelet aggregation and thrombin formation, particularly in morning hours, may represent an effective therapy for the prevention of myocardial infarction and morning sudden cardiac death. Aspirin 125-132 coagulation factor II, thrombin Homo sapiens 173-181 10494034-8 1999 All antithrombotics, be it anticoagulants (e.g. OAC, all heparins or hirudin) or antiplatelet drugs (aspirin, GPIIb/IIIa blockers) diminish thrombin generation. Aspirin 101-108 coagulation factor II, thrombin Homo sapiens 140-148 10385763-13 1999 CONCLUSION: Addition of abciximab to heparin plus aspirin during PCI was associated with a significant decrease in thrombin generation and a borderline decrease in thrombin activity. Aspirin 50-57 coagulation factor II, thrombin Homo sapiens 115-123 12567448-2 1999 METHODS: Using rosette forming assay to observe the effect of ASA on the binding of platelets to neutrophil and radioimmunoassay to observe the effect of ASA on the thrombin-induced expression of GMP-140 on the surface of human platelets. Aspirin 154-157 coagulation factor II, thrombin Homo sapiens 165-173 12567448-6 1999 At high concentration, ASA significantly inhibited thrombin (0.5 U/ml) stimulated platelets binding to neutrophils and expressing GMP-140 on their surface. Aspirin 23-26 coagulation factor II, thrombin Homo sapiens 51-59 12567448-7 1999 When the final concentration of ASA was 500,5000 micrograms/ml, the ratio of thrombin-stimulated platelets binding neutrophils was (34.7 +/- 3.8)%, (21.2 +/- 3.6)% respectively (n = 20, P < 0.01); the number of molecular of GMP-140 expressing on the surface of platelet was (1.02 +/- 0.24) x 10(3), (0.68 +/- 0.18) x 10(3) per platelet respectively (n = 9, P < 0.001). Aspirin 32-35 coagulation factor II, thrombin Homo sapiens 77-85 10385763-13 1999 CONCLUSION: Addition of abciximab to heparin plus aspirin during PCI was associated with a significant decrease in thrombin generation and a borderline decrease in thrombin activity. Aspirin 50-57 coagulation factor II, thrombin Homo sapiens 164-172 8662657-1 1996 The presence of prostaglandin (PG) H2 in the supernatant of human umbilical vein endothelial cells (HUVEC) stimulated by thrombin restores the capacity of aspirin-treated platelets to generate thromboxane (TX) B2. Aspirin 155-162 coagulation factor II, thrombin Homo sapiens 121-129 9915793-11 1999 Heterologous TP phosphorylation was observed in aspirin-treated platelets exposed to thrombin, high concentrations of collagen, and the calcium ionophore A 23187. Aspirin 48-55 coagulation factor II, thrombin Homo sapiens 85-93 10725977-2 1999 The effect of orally administered acetylsalicylic acid to healthy volunteers on incorporation of contractile protein and beta 3 integrin into the cytoskeletal core of thrombin-stimulated platelets was studied. Aspirin 34-54 coagulation factor II, thrombin Homo sapiens 167-175 10725977-5 1999 In conclusion, we have shown that acetylsalicylic acid, besides the known inhibitory effect on thromboxane synthesis, promotes changes in the cytoskeletal organization of thrombin-stimulated platelets that could limit thrombus formation. Aspirin 34-54 coagulation factor II, thrombin Homo sapiens 171-179 9851736-5 1998 The in vitro and in vivo anti-platelet studies show that these phenolic esters inhibited (1) arachidonate-triggered human platelet aggregation and (2) thrombin-stimulated rat serum thromboxane A2 production by platelets in the clotting process almost as effectively as aspirin. Aspirin 269-276 coagulation factor II, thrombin Homo sapiens 151-159 9840028-0 1998 Influence of low- and high-dose aspirin treatment on thrombin generation in whole blood. Aspirin 32-39 coagulation factor II, thrombin Homo sapiens 53-61 9840028-1 1998 The effects of two doses of aspirin (75 and 500 mg/day during 1 week) on thrombin generation was investigated in healthy volunteers. Aspirin 28-35 coagulation factor II, thrombin Homo sapiens 73-81 9840028-3 1998 High dose aspirin (500 mg daily) attenuated thrombin generation, whereas low-dose treatment (75 mg daily) failed to attenuate thrombin formation significantly. Aspirin 10-17 coagulation factor II, thrombin Homo sapiens 44-52 9840028-5 1998 Our results show that aspirin suppresses thrombin formation in whole blood in a dose-dependent fashion and that the "antithrombin" effects of aspirin require higher doses than the antiaggregating effects. Aspirin 22-29 coagulation factor II, thrombin Homo sapiens 41-49 9798988-8 1998 When platelets were pretreated with aspirin, thrombin-induced secretion of storage granule and lysosomal contents was slightly inhibited, but secretion was inhibited by ethanol to the same extent as the untreated platelets, indicating that this inhibition was independent of thromboxane A2. Aspirin 36-43 coagulation factor II, thrombin Homo sapiens 45-53 10751796-4 1998 We investigated whether aspirin alone can prevent platelet and thrombin activity induced by catheterization in ten consecutive patients (nine males, mean 50 +/- 8 years) undergoing elective left cardiac catheterization after at least 5 days of oral aspirin (75-300 mg/d). Aspirin 24-31 coagulation factor II, thrombin Homo sapiens 63-71 9356662-0 1997 Platelet aggregation in response to collagen and thrombin reliably detects the ingestion of low-dose aspirin. Aspirin 101-108 coagulation factor II, thrombin Homo sapiens 49-57 9356662-5 1997 Assessment of collagen-induced platelet aggregation relative to platelet responses of the same subject elicited either by thrombin or by a combination of collagen and thrombin does substantially improve the reliability of functional assays of aspirin. Aspirin 243-250 coagulation factor II, thrombin Homo sapiens 167-175 10193729-2 1999 BACKGROUND: Aspirin inhibits thrombin formation, but its performance is blunted in hypercholesterolemia. Aspirin 12-19 coagulation factor II, thrombin Homo sapiens 29-37 10193729-9 1999 RESULTS: Two-week treatment with aspirin had no effect on thrombin markers in vivo, while ex vivo it depressed the total amount of thrombin formed, though not the reaction rate. Aspirin 33-40 coagulation factor II, thrombin Homo sapiens 131-139 9723822-0 1998 The effect of aspirin on thrombin stimulated platelet adhesion receptor expression and the role of neutrophils. Aspirin 14-21 coagulation factor II, thrombin Homo sapiens 25-33 9723822-3 1998 The aim of the study was to determine the effects of aspirin on thrombin-induced platelet expression of the alpha-granule membrane protein, P-selectin, and the platelet surface glycoprotein required for aggregation, GPIIb-IIIa, and to assess whether this was enhanced by the presence of neutrophils. Aspirin 53-60 coagulation factor II, thrombin Homo sapiens 64-72 9723822-9 1998 CONCLUSIONS: These results confirm that thrombin-induced platelet alpha-granule release, with consequent P-selectin expression, and platelet GPIIb-IIIa expression, are not affected by aspirin inhibition of cyclo-oxygenase and suggest that the anti-thrombotic efficacy of aspirin in vivo may partly depend on other mechanisms. Aspirin 271-278 coagulation factor II, thrombin Homo sapiens 40-48 9577163-6 1998 Although aspirin and heparin have been the conventionally used agents for inhibiting thrombin and platelet function, newer agents such as hirudin or hirulog and inhibitors of the platelet glycoprotein IIb-IIIa receptors are becoming available, and their clinical application will increase in the future. Aspirin 9-16 coagulation factor II, thrombin Homo sapiens 85-93 9551715-4 1998 Triflusal, in the presence of neutrophils, showed a greater antiplatelet potency than acetylsalicylic acid to inhibit thrombin-induced platelet activation. Aspirin 86-106 coagulation factor II, thrombin Homo sapiens 118-126 9062962-0 1997 Aspirin delays thrombin generation in vitro through interaction with platelet phospholipids. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 15-23 9372101-6 1996 A new aspirin derivative is currently being developed that appears to stimulate platelet nitric oxide release, inhibit thrombin-induced platelet aggregation, and lower gastric toxicity. Aspirin 6-13 coagulation factor II, thrombin Homo sapiens 119-127 8870177-0 1996 Is platelet phospholipid-dependent thrombin generation altered by acute myocardial infarction or aspirin? Aspirin 97-104 coagulation factor II, thrombin Homo sapiens 35-43 8696958-0 1996 Inhibition of thrombin generation by aspirin is blunted in hypercholesterolemia. Aspirin 37-44 coagulation factor II, thrombin Homo sapiens 14-22 8696958-1 1996 Recent evidence indicates that aspirin inhibits thrombin generation in clotting blood. Aspirin 31-38 coagulation factor II, thrombin Homo sapiens 48-56 8696958-4 1996 The effects of aspirin on thrombin generation were evaluated in (1) 46 healthy volunteers, 2 hours after ingestion of a single, 500-mg dose and (2) 28 survivors of myocardial infarction who took 300 mg aspirin/d for 2 weeks. Aspirin 15-22 coagulation factor II, thrombin Homo sapiens 26-34 8696958-7 1996 Aspirin depressed thrombin generation in the group of subjects with serum cholesterol < 6.2 mmol/L and LDL cholesterol < 4.0 mmol/L but not in the group with high blood cholesterol levels. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 18-26 8696958-9 1996 There was a significant correlation between total serum cholesterol or LDL cholesterol and total amount of thrombin generated after aspirin treatment. Aspirin 132-139 coagulation factor II, thrombin Homo sapiens 107-115 8865538-9 1996 Responses of aspirin-pretreated platelets to thrombin, SFLLRN, U46619 and PAF were also inhibited by probenecid, indicating that prevention of TXA2 formation does not account for all the inhibitory effects. Aspirin 13-20 coagulation factor II, thrombin Homo sapiens 45-53 8662657-7 1996 Aspirin-treated or untreated cells were incubated in the absence or presence of SC58125 and stimulated by thrombin, the ionophore A23187, or exogenous arachidonic acid. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 106-114 8735820-4 1996 NCX 4215 and NCX 4016 in a dose-dependent way inhibited also thrombin-induced aggregation of platelets pretreated with acetylsalicylic acid. Aspirin 119-139 coagulation factor II, thrombin Homo sapiens 61-69 8621413-1 1996 Prostaglandin I2 (PGI2) and sodium nitroprusside (SNP) induce a rapid decay of the thrombin-promoted increase of [Ca2+]i in aspirin-treated platelets incubated in the absence of external Ca2+. Aspirin 124-131 coagulation factor II, thrombin Homo sapiens 83-91 8629598-0 1996 Effects of aspirin on status of thrombin generation in atrial fibrillation. Aspirin 11-18 coagulation factor II, thrombin Homo sapiens 32-40 7529817-7 1995 Actually, the higher doses of aspirin promoted platelet thrombus formation by thrombin even in the absence of protamine. Aspirin 30-37 coagulation factor II, thrombin Homo sapiens 78-86 8578530-0 1995 Thrombin generation in myocardial infarction and hypercholesterolemia: effects of aspirin. Aspirin 82-89 coagulation factor II, thrombin Homo sapiens 0-8 8578530-8 1995 Recent evidence indicates that antithrombotic effects of aspirin might be explained, partly at least, by its inhibition of thrombin formation. Aspirin 57-64 coagulation factor II, thrombin Homo sapiens 123-131 7641602-2 1995 This remarkable efficacy is rather unexpected, as aspirin selectively inhibits platelet aggregation mediated through activation of the arachidonic-thromboxane pathway, but not platelet aggregation induced by adenosine diphosphate (ADP), collagen and low levels of thrombin. Aspirin 50-57 coagulation factor II, thrombin Homo sapiens 264-272 7529817-5 1995 Reported here is the effect of aspirin on the platelet thrombi produced by thrombin in this manner. Aspirin 31-38 coagulation factor II, thrombin Homo sapiens 75-83 7529817-6 1995 Aspirin was found to inhibit platelet thrombosis by thrombin in low doses (optimum dose 2.5 mg/kg body weight), but at higher doses the aspirin was less effective. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 52-60 21043667-8 1996 Pretreatment of platelets with acetylsalicylic acid (ASA) before gel-filtration moderately inhibited thrombin-induced dense and alpha-granule release in GFP at a concentration range of 0.01-0.03 U/ml. Aspirin 31-51 coagulation factor II, thrombin Homo sapiens 101-109 21043667-8 1996 Pretreatment of platelets with acetylsalicylic acid (ASA) before gel-filtration moderately inhibited thrombin-induced dense and alpha-granule release in GFP at a concentration range of 0.01-0.03 U/ml. Aspirin 53-56 coagulation factor II, thrombin Homo sapiens 101-109 8746200-2 1995 This reocclusion is thought to be due to in situ platelet activation mediated by thromboxane (Tx) A2 and thrombin; hence, aspirin and thrombin inhibitors are often used in patients with acute myocardial infarction. Aspirin 122-129 coagulation factor II, thrombin Homo sapiens 105-113 8675638-2 1995 NCX 4215 was approximately seven times more potent than aspirin as an inhibitor of thrombin-induced human platelet aggregation in vitro, but did not inhibit platelet thromboxane synthesis or gastric prostaglandin synthesis. Aspirin 56-63 coagulation factor II, thrombin Homo sapiens 83-91 7490920-4 1995 Although aspirin, heparin, and warfarin sodium have been the conventionally used agents for inhibiting thrombin and platelet function, newer agents such as hirudin and inhibitors of the platelet glycoprotein IIb-IIIa receptor are becoming available, and their clinical application will increase in the future. Aspirin 9-16 coagulation factor II, thrombin Homo sapiens 103-111 7491348-0 1995 [High levels of cholesterol and lipoprotein (A) in serum decreases the inhibitory effect of aspirin on generation of thrombin]. Aspirin 92-99 coagulation factor II, thrombin Homo sapiens 117-125 7491348-2 1995 Recently, we have found that aspirin decreases not only platelet aggregation but also thrombin generation. Aspirin 29-36 coagulation factor II, thrombin Homo sapiens 86-94 7491348-4 1995 Therefore we decided to examine influence of a single dose of aspirin (500 mg) on thrombin generation in healthy volunteers. Aspirin 62-69 coagulation factor II, thrombin Homo sapiens 82-90 7491348-6 1995 Aspirin reduced thrombin generation in persons with normal serum level of lipids. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 16-24 7491348-8 1995 While the mechanism by which aspirin affects thrombin generation remains to be elucidated, our data indicate that hypercholesterolemic subjects might benefit less than others from preventive aspirin treatment. Aspirin 29-36 coagulation factor II, thrombin Homo sapiens 45-53 7895367-5 1995 Aspirin facilitated the inhibitory effect of neutrophils on platelet activation by thrombin, ADP, or epinephrine. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 83-91 21043735-4 1995 There are now at least two systems of platelet activation under intensive study: (a) agonist (e.g. ADP and thrombin) induced platelet activation when fibrinogen is the ligand; this process occurs at low shear forces and is aspirin sensitive; (b) secondly, in marked contrast, at high shear forces, shear itself activates the platelets and von Willebrand"s factor (vWf) is the ligand, and this process is aspirin insensitive. Aspirin 223-230 coagulation factor II, thrombin Homo sapiens 107-115 21043735-4 1995 There are now at least two systems of platelet activation under intensive study: (a) agonist (e.g. ADP and thrombin) induced platelet activation when fibrinogen is the ligand; this process occurs at low shear forces and is aspirin sensitive; (b) secondly, in marked contrast, at high shear forces, shear itself activates the platelets and von Willebrand"s factor (vWf) is the ligand, and this process is aspirin insensitive. Aspirin 404-411 coagulation factor II, thrombin Homo sapiens 107-115 7740476-0 1994 Inhibition of thrombin generation by aspirin. Aspirin 37-44 coagulation factor II, thrombin Homo sapiens 14-22 7980423-2 1994 In aspirin-treated platelets the thrombin-induced increase of cytosolic Ca2+ ([Ca2+]i) associated with the release from the intracellular stores is followed by a decrease to the baseline which is largely dependent on the re-uptake into the stores. Aspirin 3-10 coagulation factor II, thrombin Homo sapiens 33-41 10603518-1 1994 Background: Current strategies in the treatment of patients with acute coronary syndromes include antiplatelet agents and thrombin antagonists, most commonly aspirin and heparin, respectively. Aspirin 158-165 coagulation factor II, thrombin Homo sapiens 122-130 7974380-5 1994 It is also demonstrated that intake of 500 mg of aspirin significantly delays and inhibits thrombin generation in non-anticoagulated, thromboplastin triggered whole blood, whereas it has no effect on the coagulation in citrated plasma. Aspirin 49-56 coagulation factor II, thrombin Homo sapiens 91-99 7974380-6 1994 The effect of aspirin intake on thrombin generation in blood is roughly equal to that of 0.03 U/ml of unfractionated heparin. Aspirin 14-21 coagulation factor II, thrombin Homo sapiens 32-40 8313551-6 1994 Whole blood platelet aggregation levels in response to 0.050 and 0.075 U of thrombin at baseline were 10.8 +/- 1.0 and 11.9 +/- 1.0 omega; aggregation was inhibited after 7 days of treatment with verapamil to 6.5 +/- 1.1 and 7.8 +/- 0.9 omega (P < .05 versus baseline) and after 7 days of treatment with verapamil and aspirin to 6.1 +/- 1.1 and 7.2 +/- 1.0 omega (P < .05), respectively. Aspirin 321-328 coagulation factor II, thrombin Homo sapiens 76-84 8043909-6 1994 These methods permitted to demonstrate that, aspirin, contrary to several other antiplatelet drugs, delay the process of thrombin formation. Aspirin 45-52 coagulation factor II, thrombin Homo sapiens 121-129 8043909-7 1994 Continuous dampening of thrombin formation by aspirin might be one of the mechanisms responsible for its prophylactic and therapeutic efficacy. Aspirin 46-53 coagulation factor II, thrombin Homo sapiens 24-32 1391958-6 1992 Two hours after the ingestion of 500 mg of aspirin, thrombin formation became significantly impaired both in vitro and ex vivo. Aspirin 43-50 coagulation factor II, thrombin Homo sapiens 52-60 7690778-8 1993 The neutrophil downregulatory effect on thrombin-induced platelet reactivity was enhanced by aspirin treatment. Aspirin 93-100 coagulation factor II, thrombin Homo sapiens 40-48 8480641-0 1993 Effects of aspirin DL-lysine on thrombin generation in unstable angina pectoris. Aspirin 11-18 coagulation factor II, thrombin Homo sapiens 32-40 8480641-8 1993 These results suggest that aspirin rapidly reduces thrombin generation through inhibition of platelet activity in patients with unstable angina with prolonged rest angina. Aspirin 27-34 coagulation factor II, thrombin Homo sapiens 51-59 21043850-0 1993 Release of Choline Metabolites from Human Platelets: Evidence for Activation of Phospholipase D and of Phosphatidylcholine-specific Phospholipase C. In aspirin-treated platelets labelled by preincubation with [(3)H]-choline, enhanced release of both [(3)H]-choline and [(3)H]-choline phosphate resulted from stimulation by collagen or thrombin. Aspirin 152-159 coagulation factor II, thrombin Homo sapiens 335-343 8329564-6 1993 Thrombin overcomes the aspirin inhibition indication that the platelet surface charge reduction is associated with platelet activation. Aspirin 23-30 coagulation factor II, thrombin Homo sapiens 0-8 1309058-3 1992 Although heparin and aspirin may attenuate ongoing thrombin and thromboxane generation, respectively, a relatively high percentage (10-20%) of patients treated with heparin and aspirin still have complications associated with thrombolysis. Aspirin 21-28 coagulation factor II, thrombin Homo sapiens 51-59 1309058-5 1992 Therefore, careful consideration must be given to small molecule, active-site thrombin inhibitors which may prove to be more effective than heparin and to fibrinogen receptor antagonists which block aggregation to all known platelet agonists and have a much broader spectrum of activity than aspirin. Aspirin 292-299 coagulation factor II, thrombin Homo sapiens 78-86 1391958-9 1992 Thus, aspirin, contrary to other antiplatelet drugs, depresses thrombin formation in clotting blood, a phenomenon that might be of clinical relevance. Aspirin 6-13 coagulation factor II, thrombin Homo sapiens 63-71 1511739-4 1992 These inhibitors also blocked the platelet aggregation and protein-tyrosine phosphorylation induced with thrombin in aspirin-treated platelets. Aspirin 117-124 coagulation factor II, thrombin Homo sapiens 105-113 1868238-3 1991 Aspirin-treated platelets alone (58 x 10(6)) were fully aggregated by thrombin at 0.05 U/mL or more. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 70-78 1537105-0 1992 High-dose aspirin inhibits shear-induced platelet reaction involving thrombin generation. Aspirin 10-17 coagulation factor II, thrombin Homo sapiens 69-77 1729878-8 1992 Thrombin antagonism and platelet inhibition, primarily with heparin and aspirin, respectively, form the mainstay of conjunctive therapy. Aspirin 72-79 coagulation factor II, thrombin Homo sapiens 0-8 1811279-3 1991 At the stable period, low-dose aspirin inhibited platelet aggregation induced by ADP, collagen, or arachidonic acid, and suppressed the increase in intracellular Ca2+ concentration [( Ca2+]i) induced by thrombin significantly. Aspirin 31-38 coagulation factor II, thrombin Homo sapiens 203-211 1896957-5 1991 Aspirin and indomethacin inhibited the formation of the fluorochrome only when platelets were stimulated by thrombin. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 108-116 1913263-7 1991 Two hours after ingestion of 500 mg aspirin, this difference increased up to 150 sec, although the individual responses varied markedly (P = 0.08), while the generation of thrombin became strongly depressed in both groups. Aspirin 36-43 coagulation factor II, thrombin Homo sapiens 172-180 2035557-3 1991 In women taking aspirin, values of thrombin-induced platelet malondialdehyde production were approximately 10% of those determined in the placebo group, indicating marked suppression of thromboxane A2 synthesis. Aspirin 16-23 coagulation factor II, thrombin Homo sapiens 35-43 2303480-7 1990 Therefore, as it appears to be true for thrombin, platelet response upon binding of anti-p24/CD9 is primarily mediated by the activation of phospholipase C. When platelets pretreated with aspirin (200 microM) and apyrase (1 mg/ml) were subsequently exposed to anti-p24/CD9, aggregation still occurred. Aspirin 188-195 coagulation factor II, thrombin Homo sapiens 40-48 1674588-2 1991 12-HPETE but not 12-hydroxy-5,8,10,14-eicosatetraenoic acid blocks the U46619- and the thrombin-triggered aggregation of aspirin-treated platelets, dose dependently. Aspirin 121-128 coagulation factor II, thrombin Homo sapiens 87-95 2145839-1 1990 Administration of aspirin (81 mg/day for 2-3 weeks) in nine healthy volunteers (out of an initial ten subjects, only nine qualified) resulted in a greater than 95% decrease of thromboxane B2 production by thrombin-stimulated platelets. Aspirin 18-25 coagulation factor II, thrombin Homo sapiens 205-213 2190817-1 1990 alpha-Thrombin, gamma-thrombin, and platelet-activating factor each stimulated the mobilization of intracellular Ca2+ stores in aspirin-treated human platelets. Aspirin 128-135 coagulation factor II, thrombin Homo sapiens 6-14 2190817-1 1990 alpha-Thrombin, gamma-thrombin, and platelet-activating factor each stimulated the mobilization of intracellular Ca2+ stores in aspirin-treated human platelets. Aspirin 128-135 coagulation factor II, thrombin Homo sapiens 22-30 35600474-5 2022 ASA plus rivaroxaban treatment resulted in a significantly decreased thrombin peak in PRP for two triggers, namely, low concentration of tissue factor (TF) and thrombin, compared to ASA monotherapy. Aspirin 0-3 coagulation factor II, thrombin Homo sapiens 69-77 35600474-11 2022 In conclusion, the data of this pilot study indicate an inhibitory effect of rivaroxaban on the thrombin propagation phase of CD36-sensitive platelet thrombin formation in patients with PAD treated with ASA plus rivaroxaban combination therapy, which is associated with decreased PAR-1 but not thrombin-mediated platelet activation. Aspirin 203-206 coagulation factor II, thrombin Homo sapiens 96-104 2107565-7 1990 Aspirin treated platelets aggregated with thrombin demonstrated no thromboxane B2 production and no glutathione disulfide generation. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 42-50 34730556-2 2021 In the present study, the antithrombotic effect of ASA in patients with CAD was assessed in platelet-rich plasma (PRP) using integral tests of the hemostasis study: the T-TAS system (Total Thrombus-formation Analysis System) and the thrombin generation test (TGT). Aspirin 51-54 coagulation factor II, thrombin Homo sapiens 233-241 35600474-11 2022 In conclusion, the data of this pilot study indicate an inhibitory effect of rivaroxaban on the thrombin propagation phase of CD36-sensitive platelet thrombin formation in patients with PAD treated with ASA plus rivaroxaban combination therapy, which is associated with decreased PAR-1 but not thrombin-mediated platelet activation. Aspirin 203-206 coagulation factor II, thrombin Homo sapiens 150-158 35600474-5 2022 ASA plus rivaroxaban treatment resulted in a significantly decreased thrombin peak in PRP for two triggers, namely, low concentration of tissue factor (TF) and thrombin, compared to ASA monotherapy. Aspirin 0-3 coagulation factor II, thrombin Homo sapiens 160-168 35600474-5 2022 ASA plus rivaroxaban treatment resulted in a significantly decreased thrombin peak in PRP for two triggers, namely, low concentration of tissue factor (TF) and thrombin, compared to ASA monotherapy. Aspirin 182-185 coagulation factor II, thrombin Homo sapiens 69-77 35600474-6 2022 TF-controlled thrombin generation was additionally characterized by a significantly prolonged lag time in PRP and platelet-free plasma during ASA plus rivaroxaban combination therapy. Aspirin 142-145 coagulation factor II, thrombin Homo sapiens 14-22 35600474-7 2022 In comparison, ASA plus clopidogrel treatment presented a significant reduction of the thrombin peak in PRP, which was less pronounced than during subsequent ASA plus rivaroxaban therapy. Aspirin 15-18 coagulation factor II, thrombin Homo sapiens 87-95 2529923-0 1989 Effect of aspirin on platelet-von Willebrand factor surface expression on thrombin and ADP-stimulated platelets. Aspirin 10-17 coagulation factor II, thrombin Homo sapiens 74-82 2529923-4 1989 We studied native and ASA-treated platelets for their ability to mobilize and to express platelet-vWF in response to adenosine diphosphate (ADP) or thrombin. Aspirin 22-25 coagulation factor II, thrombin Homo sapiens 148-156 2529923-6 1989 ASA-treated platelets responded identically to native platelets to low (0.01 U/mL) and high (1.0 U/mL) concentrations of thrombin, while the ADP-induced increase in ASA-treated platelets was only 50% to 60% of that for control platelets. Aspirin 0-3 coagulation factor II, thrombin Homo sapiens 121-129 3176082-6 1988 Aspirin treatment reduced baseline [Cai2+] as well as thrombin- and collagen-induced [Cai2+] changes. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 54-62 2494147-0 1989 Effect of scavengers of active oxygen species and pretreatment with acetyl-salicylic acid on the injury to cultured endothelial cells by thrombin-stimulated platelets. Aspirin 68-89 coagulation factor II, thrombin Homo sapiens 137-145 2730914-1 1989 Removal of extracellular sodium decreased calcium mobilization from intracellular stores induced by thrombin in aspirin-treated human platelets. Aspirin 112-119 coagulation factor II, thrombin Homo sapiens 100-108 2842885-2 1988 Using a new method in which thrombin-induced platelet aggregation was measured in the presence of endothelial cells, we showed that aspirin-treated endothelial cells inhibited platelet aggregating activity of thrombin in an incubation time- and cell number-dependent manner. Aspirin 132-139 coagulation factor II, thrombin Homo sapiens 28-36 2842885-2 1988 Using a new method in which thrombin-induced platelet aggregation was measured in the presence of endothelial cells, we showed that aspirin-treated endothelial cells inhibited platelet aggregating activity of thrombin in an incubation time- and cell number-dependent manner. Aspirin 132-139 coagulation factor II, thrombin Homo sapiens 209-217 3115070-3 1987 Aspirin-treated platelets aggregated in response to PAF-acether and to 0.25 U/ml thrombin as much as control platelets in absence of detectable thromboxane A2, and were less responsive to 0.05-0.1 U/ml. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 81-89 3115070-4 1987 Thrombin-induced aggregation of aspirin-treated platelets was unaffected by the PAF-acether antagonists BN 52021, CV-3988 and Ro 19-3704. Aspirin 32-39 coagulation factor II, thrombin Homo sapiens 0-8 3108319-4 1987 When the prelabeled platelets were suspended together with aspirin-treated lymphocytes and stimulated with ionophore, thrombin, or collagen, a 6KPGF1 alpha peak was detected and enhanced by 1-BI. Aspirin 59-66 coagulation factor II, thrombin Homo sapiens 118-126 3617010-6 1987 The calcium response to thrombin was inhibited to a lesser extent by aspirin, and aspirin did not prevent potentiation by epinephrine. Aspirin 69-76 coagulation factor II, thrombin Homo sapiens 24-32 2959114-0 1987 Antipain or leupeptin in combination with aspirin or indomethacin synergistically inhibit human platelet activation by thrombin and trypsin. Aspirin 42-49 coagulation factor II, thrombin Homo sapiens 119-127 3788962-4 1986 The results indicate that thrombin-induced platelet serotonin release, following aspirin ingestion, was subnormal in most hypothyroid patients. Aspirin 81-88 coagulation factor II, thrombin Homo sapiens 26-34 3085729-6 1986 Prior treatment of the platelets with 100 microM acetylsalicylate to block the cyclooxygenase-dependent pathway caused minor reduction in dense-body secretion induced by TPA or thrombin or the combination of both, but otherwise the relative results were comparable to the untreated platelets. Aspirin 49-65 coagulation factor II, thrombin Homo sapiens 177-185 3797446-1 1986 In vitro salicylates /aspirin, salicylic acid, salicylamide and gentisic acid/ inhibited formation of 12-lipoxygenase products in intact human washed platelets which were stimulated with thrombin or arachidonic acid. Aspirin 22-29 coagulation factor II, thrombin Homo sapiens 187-195 3931099-0 1985 Effect of aspirin on serum thrombin time and bleeding time. Aspirin 10-17 coagulation factor II, thrombin Homo sapiens 27-35 3010580-5 1986 It was found that pre-treatment with aspirin reduced collagen or thrombin-induced binding to platelets from non-retinopathic diabetics to the values seen in controls. Aspirin 37-44 coagulation factor II, thrombin Homo sapiens 65-73 3010580-7 1986 The combination of aspirin with apyrase (an ADP scavenger) almost completely inhibited binding and aggregation of platelets from normal controls or non-retinopathic diabetics exposed to collagen or thrombin, whereas it only partially affected binding and aggregation of platelets from retinopathics. Aspirin 19-26 coagulation factor II, thrombin Homo sapiens 198-206 3959543-9 1986 Treatment of the platelets with acetylsalicylic acid prior to the experiment depressed the detachment effect of thrombin-stimulated platelets, but did not alter the effect on the release of 51Cr into the ambient fluid. Aspirin 32-52 coagulation factor II, thrombin Homo sapiens 112-120 3954674-7 1986 After stimulation with thrombin or collagen, the hyperaggregable platelets from FH patients were shown to bind significantly more fibrinogen than control platelets even when PG/Tx formation was suppressed (aspirin) and secreted ADP was scavenged (apyrase). Aspirin 206-213 coagulation factor II, thrombin Homo sapiens 23-31 3931686-12 1985 The culture media from endothelial cells inhibited thrombin-induced platelet aggregation, an effect blocked by aspirin. Aspirin 111-118 coagulation factor II, thrombin Homo sapiens 51-59 3931099-4 1985 These data indicate that inhibition of cyclooxygenase product formation by aspirin may alter the third stage of coagulation, specifically, endogenous thrombin activity. Aspirin 75-82 coagulation factor II, thrombin Homo sapiens 150-158 6897511-3 1982 Moreover, malondialdehyde levels in human PRP after addition of thrombin were inhibited at the same degree by parsalmide, ASA and indometacin. Aspirin 122-125 coagulation factor II, thrombin Homo sapiens 64-72 6407547-3 1983 Binding to aspirin-treated platelets was normal in response to U-46619, reduced by 60%-70% in response to ADP, collagen, and thrombin, and absent in response to arachidonic acid. Aspirin 11-18 coagulation factor II, thrombin Homo sapiens 125-133 6401733-5 1983 When aspirin-treated platelets were prelabeled with [14C]- or [3H]arachidonate, the specific activity of phospholipid-bound arachidonate pools remained constant after thrombin stimulation. Aspirin 5-12 coagulation factor II, thrombin Homo sapiens 167-175 6326566-2 1984 Recently epinephrine was reported to induce maximal aggregation of aspirin-treated platelets when combined with ADP or thrombin, and to increase fibrinogen binding of non-aspirin treated platelets stimulated with low doses of ADP. Aspirin 67-74 coagulation factor II, thrombin Homo sapiens 119-127 6405453-2 1983 We further compared the effects of acetylsalicylic acid, indomethacin, naproxen sodium and diclofenac sodium on platelet TxA2 production in response to thrombin-induced aggregation during spontaneous clotting, and on prostacyclin (PGI2) production by umbilical arteries in a superfusion system by measuring the 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) concentration in the superfusate. Aspirin 35-55 coagulation factor II, thrombin Homo sapiens 152-160 7048597-5 1982 Platelets isolated from donors who ingested aspirin were incapable of thromboxane synthesis (less than 5 pmol/ml) but remained normally responsive to thrombin-induced activation. Aspirin 44-51 coagulation factor II, thrombin Homo sapiens 150-158 7048597-8 1982 Furthermore, the fact that cardiac perfusion was preserved during a thrombin challenge of platelets from aspirin-treated donors establishes a fundamental role for the products of cyclooxygenase activity (e.g., thromboxanes) in the genesis of this form of myocardial ischemia. Aspirin 105-112 coagulation factor II, thrombin Homo sapiens 68-76 7284687-7 1981 Aspirin was nearly as effective as CCI 17810 against collagen, and adrenaline but about 10 times less active against arachidonic acid; it did not inhibit the primary response to ADP and was only a weak inhibitor of thrombin-induced aggregation. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 215-223 7280120-5 1981 Results of the study demonstrate that aspirin-treated SPD platelets, which cannot form thromboxane or undergo the release reaction on stimulation by arachidonate, can still undergo irreversible aggregation in response to thrombin and ADP if treated first with epinephrine. Aspirin 38-45 coagulation factor II, thrombin Homo sapiens 221-229 7258182-4 1981 Stimulation of "myeloproliferative" platelets with thrombin after blocking the prostaglandin pathway with aspirin resulted in reduced aggregation, indicating either a deficiency of the storage pool of adenine nucleotides in the platelets or an abnormality of a membrane receptor for thrombin. Aspirin 106-113 coagulation factor II, thrombin Homo sapiens 51-59 212713-4 1978 Aspirin (10(-4) M) inhibited contraction induced by thrombin at concentration of 0.1 and 0.02 UI/ml (p less than 0.01 at each concentration). Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 52-60 376548-2 1979 Aspirin treatment of cultured endothelial cells from the umbilical vein increased the adherence of 51Cr-platelets when thrombin was present. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 119-127 376548-9 1979 The increase in thrombin-induced platelet adherence to 1 mM aspirin-treated monolayers was reversed 2 h after removal of the aspirin solution. Aspirin 60-67 coagulation factor II, thrombin Homo sapiens 16-24 376548-9 1979 The increase in thrombin-induced platelet adherence to 1 mM aspirin-treated monolayers was reversed 2 h after removal of the aspirin solution. Aspirin 125-132 coagulation factor II, thrombin Homo sapiens 16-24 94874-1 1979 In thrombin-induced DIC, acetylsalicylic acid (ASA) prevents the strong initial fall in platelet count and the obturation of the microvasculature of the lung with platelet aggregates. Aspirin 25-45 coagulation factor II, thrombin Homo sapiens 3-11 94874-1 1979 In thrombin-induced DIC, acetylsalicylic acid (ASA) prevents the strong initial fall in platelet count and the obturation of the microvasculature of the lung with platelet aggregates. Aspirin 47-50 coagulation factor II, thrombin Homo sapiens 3-11 701483-0 1978 Effect of aspirin on thrombin-induced adherence of platelets to cultured cells from the blood vessel wall. Aspirin 10-17 coagulation factor II, thrombin Homo sapiens 21-29 701483-6 1978 Platelet adherence induced by thrombin was enhanced significantly by treatment of the endothelial monolayer with 1-2 mM aspirin. Aspirin 120-127 coagulation factor II, thrombin Homo sapiens 30-38 701483-8 1978 An aspirin concentration of 0.1 mM was sufficient to block thrombin-induced malonaldehyde production in platelets but it did not interfere with the inhibitory effect of the endothelium against platelet adherence. Aspirin 3-10 coagulation factor II, thrombin Homo sapiens 59-67 6776148-4 1980 To ascertain whether aspirin-treated endothelial cells produce PGI(2) from endoperoxides released by stimulated platelets, [(3)H]arachidonic acid-prelabeled platelets were reacted in aggregometer cuvettes with the calcium ionophore A 23187, thrombin, or collagen in the presence of aspirin-treated endothelial cell suspensions. Aspirin 21-28 coagulation factor II, thrombin Homo sapiens 241-249 6995153-2 1980 Treatment of the endothelium with high concentrations of aspirin to block PGI2 formation was associated with increased platelet adherence in a system employing thrombin and 51Cr-labeled platelets. Aspirin 57-64 coagulation factor II, thrombin Homo sapiens 160-168 7403340-2 1980 Concentrations of ADP, thrombin and arachidonate that caused reversible stimulation of aspirin platelets produced irreversible aggregation when the aspirin samples had been pretreated with epinephrine. Aspirin 87-94 coagulation factor II, thrombin Homo sapiens 23-31 7403340-2 1980 Concentrations of ADP, thrombin and arachidonate that caused reversible stimulation of aspirin platelets produced irreversible aggregation when the aspirin samples had been pretreated with epinephrine. Aspirin 148-155 coagulation factor II, thrombin Homo sapiens 23-31 205238-7 1978 Thrombin decreased the cyclic AMP content of patients" platelets and also that of control platelets pretreated with aspirin. Aspirin 116-123 coagulation factor II, thrombin Homo sapiens 0-8 190267-7 1977 Thrombin treatment of platelets also blocks the acetylation of cyclo-oxygenase by aspirin since the hydrolyzed arachidonic acid competes with aspirin for the active site on cyclo-oxygenase. Aspirin 82-89 coagulation factor II, thrombin Homo sapiens 0-8 196696-2 1977 Platelets pre-incubated with acetylsalicylic acid showed only a decrease of cyclic AMP upon addition of thrombin. Aspirin 29-49 coagulation factor II, thrombin Homo sapiens 104-112 190267-7 1977 Thrombin treatment of platelets also blocks the acetylation of cyclo-oxygenase by aspirin since the hydrolyzed arachidonic acid competes with aspirin for the active site on cyclo-oxygenase. Aspirin 142-149 coagulation factor II, thrombin Homo sapiens 0-8 949546-13 1976 Pretreatment of platelets with aspirin in vitro inhibited thrombin-induced release of serotonin but had no effect on the loss of K+ or beta-glucuronidase. Aspirin 31-38 coagulation factor II, thrombin Homo sapiens 58-66 949546-14 1976 In contrast, the ingestion of aspirin by mouth inhibited the release of serotonin, beta-glucuronidase, and K+ by thrombin. Aspirin 30-37 coagulation factor II, thrombin Homo sapiens 113-121 4644711-0 1972 The effect of acetylsalicylic acid on the peripheral and pulmonary vascular responses to thrombin. Aspirin 14-34 coagulation factor II, thrombin Homo sapiens 89-97 1262333-3 1976 Further, added aspirin, a known inhibitor of the burst in O2 consumption caused by thrombin, also blunted the stimulatory effect of arachidonate on O2 consumption, and eicosatetraynoate, a known inhibitor of arachidonate oxygenation, blunted the burst in O2 consumption initiated by both thrombin and arachidonate. Aspirin 15-22 coagulation factor II, thrombin Homo sapiens 83-91 1262333-3 1976 Further, added aspirin, a known inhibitor of the burst in O2 consumption caused by thrombin, also blunted the stimulatory effect of arachidonate on O2 consumption, and eicosatetraynoate, a known inhibitor of arachidonate oxygenation, blunted the burst in O2 consumption initiated by both thrombin and arachidonate. Aspirin 15-22 coagulation factor II, thrombin Homo sapiens 288-296 1260021-3 1976 Acetylsalicylate blocked the formation of malonyldialdehyde completely and partially inhibited the O2 burst induced by thrombin. Aspirin 0-16 coagulation factor II, thrombin Homo sapiens 119-127 178701-2 1976 These effects resemble those produced by ADP, epinephrine, collagen, and thrombin in association with the platelet release reaction but are less effectively inhibited by aspirin. Aspirin 171-178 coagulation factor II, thrombin Homo sapiens 73-81 1168851-1 1975 Acetylsalicylic acid was shown both in vivo and in vitro to prevent the platelet lipid peroxidation normally induced by the aggregating agents thrombin and epinephrine, and the sulfhydryl inhibitor N-ethylmaleimide. Aspirin 0-20 coagulation factor II, thrombin Homo sapiens 143-151 1115776-6 1975 Prostaglandin E1 (0.03 mM) and acetylsalicylic acid (0.8 mM) had little effect on basal respiration, but inhibited the thrombin-stimulated burst of oxygen consumption. Aspirin 31-51 coagulation factor II, thrombin Homo sapiens 119-127 5055976-0 1972 Effect of defibrinogenation and acetylsalicylic acid on the circulatory response to thrombin. Aspirin 32-52 coagulation factor II, thrombin Homo sapiens 84-92 32761372-0 2021 ImpaCt of aspirin regimen on THrombin generation in diabEtic patients with acute coronary syndrome: CARTHaGE-ACS trial. Aspirin 10-17 coagulation factor II, thrombin Homo sapiens 29-37 4106764-0 1971 Effect of steroids, acetylsalicylic acid and bishydroxycoumarin on prothrombin time. Aspirin 20-40 coagulation factor II, thrombin Homo sapiens 67-78 5531310-2 1970 Addition of ASA in vitro to human platelet-rich plasma also inhibited platelet aggregation by thrombin, ADP and collagen. Aspirin 12-15 coagulation factor II, thrombin Homo sapiens 94-102 30888847-16 2019 Although ASA had no effect on TBN-mediated release of VEGF and TGF-beta1 from LR-PRP, ASA did partially block TBN-mediated release of PDGF-AB, although the mechanism remains unclear. Aspirin 86-89 coagulation factor II, thrombin Homo sapiens 110-113 31453830-8 2020 Our results suggest that, in the setting of durable LVADs, aspirin minimally modulates the biochemical pathway of platelet-mediated thrombin generation. Aspirin 59-66 coagulation factor II, thrombin Homo sapiens 132-140 31764002-7 2020 The mechanism by which a thrombin-like enzyme VLCV (thrombin-like enzyme)-induced platelet aggregation was explored in presence of ticlopidin, clopidogrel and aspirin. Aspirin 159-166 coagulation factor II, thrombin Homo sapiens 25-33 31764002-7 2020 The mechanism by which a thrombin-like enzyme VLCV (thrombin-like enzyme)-induced platelet aggregation was explored in presence of ticlopidin, clopidogrel and aspirin. Aspirin 159-166 coagulation factor II, thrombin Homo sapiens 52-60 30888847-5 2019 PURPOSE:: To assess the effects of low-dose ASA use on activation of growth factor release from freshly isolated human PRP via AA and thrombin (TBN). Aspirin 44-47 coagulation factor II, thrombin Homo sapiens 134-142 30888847-5 2019 PURPOSE:: To assess the effects of low-dose ASA use on activation of growth factor release from freshly isolated human PRP via AA and thrombin (TBN). Aspirin 44-47 coagulation factor II, thrombin Homo sapiens 144-147 32532481-7 2020 RESULTS: After THA, there was a significantly lower risk of VTE associated with the use of direct thrombin inhibitors (0.44%; odds ratio [OR], 0.69; 95% confidence interval [95% CI], 0.55-0.87; P = .002) and factor Xa inhibitors (0.37%; OR, 0.63; 95% CI, 0.47-0.85; P = .003) compared with aspirin (0.63%). Aspirin 290-297 coagulation factor II, thrombin Homo sapiens 98-106 32009527-4 2020 Methods and Results The effects of ASA on CD40L-treated human platelets, in response to suboptimal concentrations of collagen or thrombin, were assessed at levels of aggregation, thromboxane A2 secretion, and phosphorylation of p38 mitogen-activated protein kinase, nuclear factor kappa B, transforming growth factor-beta-activated kinase 1, and myosin light chain. Aspirin 35-38 coagulation factor II, thrombin Homo sapiens 129-137 32009527-5 2020 sCD40L significantly elevated thromboxane A2 secretion in platelets in response to suboptimal doses of collagen and thrombin, which was reversed by ASA. Aspirin 148-151 coagulation factor II, thrombin Homo sapiens 116-124 32009527-7 2020 sCD40L potentiated platelet aggregation, an effect completely reversed and partially reduced by ASA in response to a suboptimal dose of collagen and thrombin, respectively. Aspirin 96-99 coagulation factor II, thrombin Homo sapiens 149-157 30888847-18 2019 CLINICAL RELEVANCE:: Reduction in growth factor release attributed to daily use of low-dose ASA or other COX inhibitors can be mitigated when PRP samples are activated with TBN. Aspirin 92-95 coagulation factor II, thrombin Homo sapiens 173-176 30332694-5 2018 Despite the use of antiplatelet therapies, including aspirin and P2Y12-receptor antagonists, some patients with artery disease continue to experience recurrent cardiovascular ischaemic events due to excessive thrombin generation beyond the acute period. Aspirin 53-60 coagulation factor II, thrombin Homo sapiens 209-217 29227173-6 2019 The aim of this study was to assess the level of AA-, ADP- and thrombin-mediated platelet reactivity in patients on aspirin before, during, and after major vascular surgery, which represents a model of on/off vascular inflammation. Aspirin 116-123 coagulation factor II, thrombin Homo sapiens 63-71 28128747-1 2017 To evaluate the parameters of the thrombin generation test (TGT) in coronary artery disease (CAD) patients on prolonged aspirin therapy during on-pump coronary artery bypass grafting (CABG) after donor platelet concentrate transfusion. Aspirin 120-127 coagulation factor II, thrombin Homo sapiens 34-42 29084693-8 2017 Prothrombin time was significantly decreased by mixing (10 microg) of ASM (16.67+-1.15 sec), ASH (12.33+-0.57 sec), ASC (15.33+-0.57 sec) and ASA (9.0+-1.0 sec) to that of vehicle (20.0+-1.0 sec). Aspirin 142-145 coagulation factor II, thrombin Homo sapiens 0-11 30615391-2 2017 The effect of anti-thrombocyte substances on thrombin-induced increasing of the level of cytoplasmic Ca in thrombocytes was analyzed on example of acetylsalicylic acid. Aspirin 147-167 coagulation factor II, thrombin Homo sapiens 45-53 30615391-4 2017 It is established that in the given test acetylsalicylic acid inhibits thrombin-induced increasing of cytoplasmic Ca at 0.125-5.0 mk/mol concentrations. Aspirin 41-61 coagulation factor II, thrombin Homo sapiens 71-79 29131082-2 2018 We previously described that aspirin has effects beyond inhibition of platelet aggregation, as it inhibited thrombin-mediated release of sphingosine-1-phosphate (S1P) from human platelets. Aspirin 29-36 coagulation factor II, thrombin Homo sapiens 108-116 28128747-6 2017 Activation of the endogenous thrombin potential was observed in patients on prolonged aspirin therapy in the pre- and intraoperative periods, as confirmed by high peak thrombin and increased velocity index. Aspirin 86-93 coagulation factor II, thrombin Homo sapiens 29-37 28128747-6 2017 Activation of the endogenous thrombin potential was observed in patients on prolonged aspirin therapy in the pre- and intraoperative periods, as confirmed by high peak thrombin and increased velocity index. Aspirin 86-93 coagulation factor II, thrombin Homo sapiens 168-176 27399131-8 2016 CONCLUSION: Ticagrelor and apixaban with or without ASA inhibit platelet activation and thrombin formation in vivo in healthy subjects. Aspirin 52-55 coagulation factor II, thrombin Homo sapiens 88-96 30303352-5 2017 Results: It was shown that the antiplatelet effect of aspirin in the preoperative period was manifest as inhibition of the initial stage of blood coagulation accompanied by increased thrombin potential, the total gain of anticoagulant and fibrinolytic activity of the blood. Aspirin 54-61 coagulation factor II, thrombin Homo sapiens 183-191 27713620-8 2016 Aspirin (5.6-560 microM) and cilostazol (5-10 microM) significantly inhibited thrombin-induced increases in [Ca2+]i in a concentration-dependent manner. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 78-86 27713620-12 2016 The combination of aspirin and sodium valproate synergistically inhibited thrombin-induced [Ca2+]i. Aspirin 19-26 coagulation factor II, thrombin Homo sapiens 74-82 27133131-8 2016 Thrombin elevated ~900 lipids >2-fold with 86% newly appearing and 45% inhibited by aspirin supplementation, indicating COX-1 is required for major activation-dependent lipidomic fluxes. Aspirin 87-94 coagulation factor II, thrombin Homo sapiens 0-8 26873936-5 2016 Aspirin consumption significantly blocked thrombin- and collagen-induced increases in exosome cargo levels of chemokines and HMGB1, without altering total exosome secretion or GPVI cargo. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 42-50 26927051-3 2016 Thrombin also amplifies the response to the tissue injury, coagulation and platelet response, so the treatment of ACS is based on the combined use of both antiplatelet (such as aspirin, clopidogrel, prasugrel and ticagrelor) and antithrombotic drugs (unfractionated heparin, enoxaparin, fondaparinux and bivalirudin). Aspirin 177-184 coagulation factor II, thrombin Homo sapiens 0-8 27018926-12 2016 After RIC during aspirin treatment, changes in thrombin generation were inconsistent; increased peak (p=0.04) and time to peak (p<0.001) and a decrease in lag-time (p<0.001). Aspirin 17-24 coagulation factor II, thrombin Homo sapiens 47-55 28139555-1 2016 AIM: To estimate thrombin generation test parameters in patients with coronary heart disease during coronary artery bypass surgery under extracorporeal circulation after transfusion of donor platelet concentrates during long-term therapy with acetylsalicylic acid (ASA). Aspirin 243-263 coagulation factor II, thrombin Homo sapiens 17-25 25970449-6 2016 Notably, lysosomal exocytosis in response to thrombin was significantly reduced if the secondary activation by ADP was inhibited by the P2Y12 antagonist cangrelor, while inhibition of thromboxane A2 formation by treatment with acetylsalicylic acid was of minor importance in this regard. Aspirin 227-247 coagulation factor II, thrombin Homo sapiens 45-53 28139555-1 2016 AIM: To estimate thrombin generation test parameters in patients with coronary heart disease during coronary artery bypass surgery under extracorporeal circulation after transfusion of donor platelet concentrates during long-term therapy with acetylsalicylic acid (ASA). Aspirin 265-268 coagulation factor II, thrombin Homo sapiens 17-25 28139555-6 2016 RESULTS: During long-term ASA therapy, the patients were found to have an activated endogenous thrombin potential in the pre- and intraoperative periods, as evidenced by the high peak concentration of thrombin and the increased rate of its generation. Aspirin 26-29 coagulation factor II, thrombin Homo sapiens 95-103 28139555-6 2016 RESULTS: During long-term ASA therapy, the patients were found to have an activated endogenous thrombin potential in the pre- and intraoperative periods, as evidenced by the high peak concentration of thrombin and the increased rate of its generation. Aspirin 26-29 coagulation factor II, thrombin Homo sapiens 201-209 22393298-6 2012 The residual risk can be attributed to the fact that aspirin and P2Y(12) inhibitors block only the thromboxane A(2) and ADP platelet activation pathways but do not affect the other pathways that lead to thrombosis, such as the protease-activated receptor-1 pathway stimulated by thrombin, the most potent platelet agonist. Aspirin 53-60 coagulation factor II, thrombin Homo sapiens 279-287 25211369-8 2014 CONCLUSION: A triple therapy at steady state with ticagrelor plus ASA in combination with dabigatran or rivaroxaban is as effective as a combination with phenprocoumon for platelet activation and thrombin generation in vivo. Aspirin 66-69 coagulation factor II, thrombin Homo sapiens 196-204 25213262-4 2014 These clinical data support evidence that platelets contribute to the initiation and progression of venous thrombosis and aspirin inhibits thrombin formation and thrombin-mediated coagulant reactions. Aspirin 122-129 coagulation factor II, thrombin Homo sapiens 139-147 25213262-4 2014 These clinical data support evidence that platelets contribute to the initiation and progression of venous thrombosis and aspirin inhibits thrombin formation and thrombin-mediated coagulant reactions. Aspirin 122-129 coagulation factor II, thrombin Homo sapiens 162-170 23266689-0 2013 Acidosis, magnesium and acetylsalicylic acid: effects on thrombin. Aspirin 24-44 coagulation factor II, thrombin Homo sapiens 57-65 23266689-4 2013 The phosphorescence of thrombin was studied under physiological conditions, in acidosis (decrease of pH from 8.0 to 5.0) and on the addition of salts (magnesium sulfate and sodium chloride) and of acetylsalicylic acid, and its connection with thrombin function is discussed. Aspirin 197-217 coagulation factor II, thrombin Homo sapiens 23-31 23064666-9 2013 Lag time, peak thrombin generation and endogenous thrombin potential were reduced at both 14 and 90 days after adding dipyridamole to aspirin (p <= 0.01). Aspirin 134-141 coagulation factor II, thrombin Homo sapiens 50-58 23064666-12 2013 The addition of dipyridamole to aspirin led to a persistent reduction in peak and total thrombin generation ex vivo, and illustrates the diverse, potentially beneficial, newly recognised "anti-coagulant" effects of dipyridamole in ischaemic CVD. Aspirin 32-39 coagulation factor II, thrombin Homo sapiens 88-96 22883224-16 2012 Long-term antiplatelet treatment with aspirin alone seems to attenuate thrombin generation to a greater extent than with clopidogrel alone. Aspirin 38-45 coagulation factor II, thrombin Homo sapiens 71-79 25848131-3 2015 MATERIALS AND METHODS: Thrombin generation was measured by the Calibrated Automated Thrombogram method (0.5 pmol/L tissue factor) using human platelet-rich plasma (PRP) spiked with rivaroxaban (15, 30, or 60 ng/mL), ticagrelor (1.0 microg/mL), and acetylsalicylic acid (ASA; 100 microg/mL). Aspirin 248-268 coagulation factor II, thrombin Homo sapiens 23-31 25848131-3 2015 MATERIALS AND METHODS: Thrombin generation was measured by the Calibrated Automated Thrombogram method (0.5 pmol/L tissue factor) using human platelet-rich plasma (PRP) spiked with rivaroxaban (15, 30, or 60 ng/mL), ticagrelor (1.0 microg/mL), and acetylsalicylic acid (ASA; 100 microg/mL). Aspirin 270-273 coagulation factor II, thrombin Homo sapiens 23-31 25869498-5 2015 In some trials, almost all patients on aspirin have a very low level of serum thromboxane B2, indicating that the measured platelet reactivity in aspirin-treated patients might be due to platelet activation via other pathways, such as ADP or thrombin. Aspirin 146-153 coagulation factor II, thrombin Homo sapiens 242-250 25286881-4 2015 However, some patients continue to experience adverse ischaemic events despite treatment with aspirin and a P2Y12-receptor antagonist, because platelets can remain activated via pathways not inhibited by these agents, such as the protease-activated receptor (PAR)-1 platelet activation pathway stimulated by thrombin. Aspirin 94-101 coagulation factor II, thrombin Homo sapiens 308-316 23623170-2 2013 Since activated platelets respond stronger to additional stimuli, the extent of endogenous thrombin generation may in part be responsible for the reported response variability to aspirin and clopidogrel therapy. Aspirin 179-186 coagulation factor II, thrombin Homo sapiens 91-99 23623170-8 2013 In the VerifyNow aspirin assay, patients without HRPR had higher peak thrombin generation than patients with HRPR (p=0.01). Aspirin 17-24 coagulation factor II, thrombin Homo sapiens 70-78 20460337-9 2011 Although the lack of response to epinephrine and aspirin treatment displayed similarities in aggregations using epinephrine, ADP, collagen, and thrombin, they differed in aggregations using AA and for ATP secretion. Aspirin 49-56 coagulation factor II, thrombin Homo sapiens 144-152 21819272-5 2011 In preclinical and Phase I - II studies, inhibition of thrombin-mediated platelet activation by a PAR-1 inhibitor, in general, has added to the antithrombotic efficacy of aspirin and clopidogrel without increasing bleeding. Aspirin 171-178 coagulation factor II, thrombin Homo sapiens 55-63 21383917-10 2011 ABBREVIATIONS: serpin -serine protease inhibitors RCL -reactive center loop ASA -accessible surface area. Aspirin 76-79 coagulation factor II, thrombin Homo sapiens 23-38 21557683-6 2011 Already a 15 min exposure of platelets to glucose impaired aspirin inhibition of the platelet aggregation induced by collagen, thrombin, adenosine diphosphate (ADP), and arachidonic acid (AA). Aspirin 59-66 coagulation factor II, thrombin Homo sapiens 127-135 18474393-8 2009 Similarly, peak thrombin levels were reduced in patients treated with warfarin (-18%+/-7%, p=0.049) and aspirin/warfarin (-19%+/-5%, p=0.029), whereas an increase (12%+/-4%, p=0.029) occurred during aspirin treatment alone. Aspirin 104-111 coagulation factor II, thrombin Homo sapiens 16-24 19618315-0 2009 Thrombin formation and platelet activation at the site of vascular injury in patients with coronary artery disease treated with clopidogrel combined with aspirin. Aspirin 154-161 coagulation factor II, thrombin Homo sapiens 0-8 19618315-6 2009 RESULTS: Total amounts of thrombin markers produced at the site of injury were similar before and after addition of clopidogrel, whereas platelet release of sCD40L and P-selectin was lower during treatment with aspirin + clopidogrel by 33.8% and 27.8% (p < 0.001), respectively. Aspirin 211-218 coagulation factor II, thrombin Homo sapiens 26-34 19487018-5 2010 Platelet activation by adenosine diphosphate (ADP) or thrombin agonist peptide (TRAP) increased CD62P and CD40L surface density in the presence of aspirin by 1.9 - 2.8 -fold. Aspirin 147-154 coagulation factor II, thrombin Homo sapiens 54-62 19890703-4 2009 Residual risk can be attributed, at least in part, to the fact that thrombosis continues in the presence of current treatments because aspirin and P2Y(12) ADP receptor antagonists each block only one of multiple platelet activation pathways, and thus do not impact other platelet activation pathways, such as the one triggered by interaction of thrombin with protease-activated receptor (PAR)-1, thereby exposing patients to continued accumulation of thrombotic events. Aspirin 135-142 coagulation factor II, thrombin Homo sapiens 345-353 18474393-8 2009 Similarly, peak thrombin levels were reduced in patients treated with warfarin (-18%+/-7%, p=0.049) and aspirin/warfarin (-19%+/-5%, p=0.029), whereas an increase (12%+/-4%, p=0.029) occurred during aspirin treatment alone. Aspirin 199-206 coagulation factor II, thrombin Homo sapiens 16-24 18480058-0 2008 The ATP-gated P2X1 receptor plays a pivotal role in activation of aspirin-treated platelets by thrombin and epinephrine. Aspirin 66-73 coagulation factor II, thrombin Homo sapiens 95-103 18480058-3 2008 The results show that epinephrine acted via alpha(2A)-adrenergic receptors to provoke aggregation, secretion, and Ca(2+) mobilization in aspirin-treated platelets pre-stimulated with subthreshold concentrations of thrombin. Aspirin 137-144 coagulation factor II, thrombin Homo sapiens 214-222 18215612-11 2008 CONCLUSIONS: For patients with MI complicated by AF, the combination of aspirin and an oral direct thrombin inhibitor seems beneficial. Aspirin 72-79 coagulation factor II, thrombin Homo sapiens 99-107 18302581-3 2008 This study hypothesizes that thrombin production during OPCAB stimulates this acquired ASA-R. Aspirin 87-90 coagulation factor II, thrombin Homo sapiens 29-37 17549314-0 2007 Lack of aspirin-induced decrease in thrombin formation in subjects resistant to aspirin. Aspirin 8-15 coagulation factor II, thrombin Homo sapiens 36-44 18064330-12 2007 In conclusion, adding clopidogrel to aspirin treatment inhibited platelet activation by both ADP, thrombin and collagen in vitro, but did not influence the prothrombotic responses to exercise. Aspirin 37-44 coagulation factor II, thrombin Homo sapiens 98-106 17917621-3 2007 UFH was combined with aspirin to suppress thrombin propagation and fibrin formation in patients presenting with acute coronary syndromes (ACS) or patients undergoing percutaneous coronary intervention (PCI). Aspirin 22-29 coagulation factor II, thrombin Homo sapiens 42-50 17314111-2 2007 In the ESTEEM trial, the oral direct thrombin inhibitor ximelagatran reduced the risk of new ischaemic events when compared with placebo in aspirin treated post myocardial infarction patients. Aspirin 140-147 coagulation factor II, thrombin Homo sapiens 37-45 19839181-9 2007 Statins reduce inflammation, modify the composition of atheromatous plaque and promote stabilisation, while acetylsalicylic acid reduces the formation of thrombin, exerts an anti-thrombotic action, reduces endothelial dysfunction and the proliferation of vascular smooth muscle cells, and, like statins, has an anti-inflammatory effect. Aspirin 108-128 coagulation factor II, thrombin Homo sapiens 154-162 17148593-4 2007 Aspirin can reduce thrombin generation with the subsequent attenuation of thrombin-mediated coagulant reactions such as factor XIII activation. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 19-27 17148593-4 2007 Aspirin can reduce thrombin generation with the subsequent attenuation of thrombin-mediated coagulant reactions such as factor XIII activation. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 74-82 17642204-0 2007 [The thrombin generation is associated with the PIA1/A2 beta3, integrin polymorphism in aspirin-treated patients with coronary artery disease: a role of statins]. Aspirin 88-95 coagulation factor II, thrombin Homo sapiens 5-13 17642204-14 2007 CONCLUSIONS: In a model of microvascular injury the PIA1/A2 polymorphism influenced thrombin formation but not platelet activation in CAD patients treated with low-dose aspirin. Aspirin 169-176 coagulation factor II, thrombin Homo sapiens 84-92 17532367-9 2007 RESULTS AND CONCLUSIONS: Aggrastat, AN51, and aspirin all suppressed thrombin formation. Aspirin 46-53 coagulation factor II, thrombin Homo sapiens 69-77 16675000-5 2007 RESULTS: Aspirin-depressed thrombin generation in A1 homozygotes (p=0.04), but not in A2 carriers. Aspirin 9-16 coagulation factor II, thrombin Homo sapiens 27-35 16961610-0 2006 Recombinant factor VIIa reverses the inhibitory effect of aspirin or aspirin plus clopidogrel on in vitro thrombin generation. Aspirin 58-65 coagulation factor II, thrombin Homo sapiens 106-114 17016788-2 2006 DISCUSSION: Hyphemas can occur after blunt trauma, intraocular surgery, spontaneously and in association with the use of substances that alter platelet or thrombin function (aspirin, ethanol). Aspirin 174-181 coagulation factor II, thrombin Homo sapiens 155-163 16961610-0 2006 Recombinant factor VIIa reverses the inhibitory effect of aspirin or aspirin plus clopidogrel on in vitro thrombin generation. Aspirin 69-76 coagulation factor II, thrombin Homo sapiens 106-114 16961610-3 2006 This study investigated: (a) whether a regimen of aspirin or clopidogrel plus aspirin significantly inhibited platelet thrombin generation (TG); and (b) the reversal of this inhibition by recombinant activated factor VII (rFVIIa). Aspirin 50-57 coagulation factor II, thrombin Homo sapiens 119-127 16961610-3 2006 This study investigated: (a) whether a regimen of aspirin or clopidogrel plus aspirin significantly inhibited platelet thrombin generation (TG); and (b) the reversal of this inhibition by recombinant activated factor VII (rFVIIa). Aspirin 78-85 coagulation factor II, thrombin Homo sapiens 119-127 16368345-12 2006 Preserved aspirin sensitivity in the aprotinin group may explain the observed reduction in thrombotic events and might be related to the suppression of perioperative and transmyocardial thrombin formation. Aspirin 10-17 coagulation factor II, thrombin Homo sapiens 186-194 16469512-4 2006 Thrombin-induced intracellular ROS production was inhibited by NAD(P)H oxidase inhibitors (DPI and apocynin), cyclooxygenase inhibitor (acetylsalicylic acid), and superoxide scavengers (tiron and MnTMPyP). Aspirin 136-157 coagulation factor II, thrombin Homo sapiens 0-8 15650548-6 2005 When 0.4 IU/ml thrombin was used in samples provided by 10 healthy individuals treated with acetysalicylic acid, Ks levels were increased during versus before therapy. Aspirin 92-111 coagulation factor II, thrombin Homo sapiens 15-23 16216591-0 2005 Aspirin inhibits thrombin action on endothelial cells via up-regulation of aminopeptidase N/CD13 expression. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 17-25 16216591-4 2005 Since activated thrombin receptor is reported to be inactivated by APN/CD13 in vitro, protective actions of aspirin on HUVECs by thrombin stimulation were examined, resulting in the suppression of endothelin-1 and reactive oxygen species productions in HUVECs. Aspirin 108-115 coagulation factor II, thrombin Homo sapiens 129-137 16216591-6 2005 CONCLUSIONS: Aspirin may exert its anti-atherothrombotic effects in part via the inhibition of thrombin action by up-regulating APN/CD13 on endothelial cells. Aspirin 13-20 coagulation factor II, thrombin Homo sapiens 95-103 16015412-2 2005 Aspirin also inhibits thrombin generation (TG) in platelet-rich plasma (PRP) activated by sodium arachidonate (AA). Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 22-30 16399303-0 2006 Endothelial injury and acquired aspirin resistance as promoters of regional thrombin formation and early vein graft failure after coronary artery bypass grafting. Aspirin 32-39 coagulation factor II, thrombin Homo sapiens 76-84 15894964-3 2005 We investigated whether (a) cigarette smoking is linked to increased cytokine production, which may mediate platelet activation and thrombin generation in chronic coronary artery disease (CAD), and (b) aspirin treatment inhibits smoking-related changes on cytokines, platelets, and thrombin. Aspirin 202-209 coagulation factor II, thrombin Homo sapiens 132-140 15894964-3 2005 We investigated whether (a) cigarette smoking is linked to increased cytokine production, which may mediate platelet activation and thrombin generation in chronic coronary artery disease (CAD), and (b) aspirin treatment inhibits smoking-related changes on cytokines, platelets, and thrombin. Aspirin 202-209 coagulation factor II, thrombin Homo sapiens 282-290 15650548-7 2005 Since almost no thrombin generation was found in the samples with the higher dose of exogenous thrombin, we considered that modifications in fibrinogen clotting property by acetysalicylic acid rendered the fibrin network more permeable. Aspirin 173-192 coagulation factor II, thrombin Homo sapiens 95-103 13678873-12 2003 INTERPRETATION: Oral direct thrombin inhibition with ximelagatran and acetylsalicylic acid is more effective than acetylsalicylic acid alone in preventing major cardiovascular events during 6 months of treatment in patients who have had a recent myocardial infarction. Aspirin 70-90 coagulation factor II, thrombin Homo sapiens 28-36 15020512-10 2004 Aspirin may prevent transient coronary flow reductions through platelet, thrombin, and cytokine inhibition. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 73-81 15213852-12 2004 Pretreatment with aspirin inhibits ERK2 activation induced by 0.1 U/ml thrombin, but has no effect at high concentrations of thrombin. Aspirin 18-25 coagulation factor II, thrombin Homo sapiens 71-79 14607210-7 2003 The ESTEEM study showed that the oral thrombin inhibitor ximelagatran plus aspirin was more effective than aspirin alone in the prophylaxis of major cardiovascular events following MI. Aspirin 75-82 coagulation factor II, thrombin Homo sapiens 38-46 14607210-7 2003 The ESTEEM study showed that the oral thrombin inhibitor ximelagatran plus aspirin was more effective than aspirin alone in the prophylaxis of major cardiovascular events following MI. Aspirin 107-114 coagulation factor II, thrombin Homo sapiens 38-46 13678873-12 2003 INTERPRETATION: Oral direct thrombin inhibition with ximelagatran and acetylsalicylic acid is more effective than acetylsalicylic acid alone in preventing major cardiovascular events during 6 months of treatment in patients who have had a recent myocardial infarction. Aspirin 114-134 coagulation factor II, thrombin Homo sapiens 28-36 12535860-0 2003 Anti-thrombin action of low-dose acetylsalicylic acid. Aspirin 33-53 coagulation factor II, thrombin Homo sapiens 5-13 12652502-12 2003 In patients with false aneurysms and failed compression therapy under full-dose aspirin, clopidogrel, and heparin, selective thrombin injection is highly effective and safe. Aspirin 80-87 coagulation factor II, thrombin Homo sapiens 125-133 12883841-23 2003 CONCLUSION: In patients with FA taking aspirin and clopidogrel, selective thrombin injection is more effective than manual compression. Aspirin 39-46 coagulation factor II, thrombin Homo sapiens 74-82 14592550-7 2003 Moreover, platelet-neutrophil adhesion induced by thrombin, fMPL or LPS was inhibited by the inhibitor of cyclooxygenase (aspirin), by TXA2 synthase inhibitor (camonagrel), by PAF receptor antagonist (WEB 2170), by the inhibitor of FLAP (MK 886) and by cysLTs receptors antagonist (MK 571). Aspirin 122-129 coagulation factor II, thrombin Homo sapiens 50-58 12730088-8 2003 Naproxen and aspirin significantly suppressed thrombin generation. Aspirin 13-20 coagulation factor II, thrombin Homo sapiens 46-54 12535860-2 2003 Here, we report that treatment of coronary artery patients with 100 mg/day of aspirin does not attenuate thrombin generation, but reduces free thrombin by favouring the formation of thrombin/antithrombin (TAT) complexes. Aspirin 78-85 coagulation factor II, thrombin Homo sapiens 143-151 12535860-2 2003 Here, we report that treatment of coronary artery patients with 100 mg/day of aspirin does not attenuate thrombin generation, but reduces free thrombin by favouring the formation of thrombin/antithrombin (TAT) complexes. Aspirin 78-85 coagulation factor II, thrombin Homo sapiens 143-151 12386502-4 2002 The older standbys of aspirin, heparins, nitrates, beta-blockers, and thrombolytic therapy have given way to vastly improved interventional capabilities (with improved adjunctive pharmacotherapy), low molecular weight heparins, glycoprotein IIb/IIIa antagonists, safer theinopyridines, thrombin inhibitors, and newer generation fibrinolytics. Aspirin 22-29 coagulation factor II, thrombin Homo sapiens 286-294 12515735-2 2003 Given that acetylation of fibrinogen by aspirin can alter its clotting properties and the presence of fibrin stimulates thrombin-mediated activation of FXIII, we have tested the hypothesis that treatment with aspirin differentially modulates the influence of the FXIII Val34Leu polymorphism on its activation in vivo. Aspirin 209-216 coagulation factor II, thrombin Homo sapiens 120-128 12515735-5 2003 Although the Leu34-positive and -negative subjects were similar with respect to aspirin-related impairment of thrombin generation, aspirin led to a more pronounced inhibition of the activation of FXIII in the Leu34 carriers as compared with the Val34 homozygotes. Aspirin 80-87 coagulation factor II, thrombin Homo sapiens 110-118 12529741-3 2002 Even in the presence of aspirin, the platelets from various individuals showed highly different thrombin-induced Ca(2+) responses. Aspirin 24-31 coagulation factor II, thrombin Homo sapiens 96-104 11687759-1 2001 Aspirin depresses thrombin generation, probably through a mechanism independent of the cyclooxygenase inhibition, but rather related to acetylation of the platelet membrane macromolecules. Aspirin 0-7 coagulation factor II, thrombin Homo sapiens 18-26 11877318-18 2002 In contrast, phenanthroline and apyrase significantly enhanced the anti-aggregatory effects of aspirin against thrombin-, PAR1AP- and TRAP-induced aggregation suggesting the involvement of ADP- and MMP-2-dependent pathways. Aspirin 95-102 coagulation factor II, thrombin Homo sapiens 111-119 11874470-2 2002 Fluorescence ratio imaging indicates that immobilized, aspirin-treated platelets, loaded with Fura-2, respond to inositol 1,4,5-trisphosphate- (InsP3)-generating agonists such as thrombin by high-frequency, irregular rises in cytosolic [Ca2+]i with spikes that vary in peak level and peak-to-peak interval. Aspirin 55-62 coagulation factor II, thrombin Homo sapiens 179-187 11723016-5 2001 In the Pl(A1A1) homozygotes, aspirin ingestion resulted in reductions in the velocity of thrombin B-chain formation (by 32.1%; P=0.007), prothrombin consumption (by 30.4%; P=0.018), factor Va generation (by 28.9%; P=0.014), fibrinogen removal (by 41.2%; P=0.001), and factor XIII activation (by 22.6%; P=0.026). Aspirin 29-36 coagulation factor II, thrombin Homo sapiens 89-97 11246536-0 2001 Treatment with simvastatin and low-dose aspirin depresses thrombin generation in patients with coronary heart disease and borderline-high cholesterol levels. Aspirin 40-47 coagulation factor II, thrombin Homo sapiens 58-66 11322862-3 2001 At present there is only limited clinical use of some parenteral preparations of thrombin inhibitors in acute situations, especially when the common antithrombotic drugs heparin, warfarin and aspirin are ineffective or associated with side effects. Aspirin 192-199 coagulation factor II, thrombin Homo sapiens 81-89 11171808-0 2001 Platelet glycoprotein IIIa pl(a) polymorphism and effects of aspirin on thrombin generation. Aspirin 61-68 coagulation factor II, thrombin Homo sapiens 72-80 11246536-2 2001 We assessed the effects of low-dose aspirin (75 mg daily) on thrombin generation in patients with coronary heart disease and average blood cholesterol levels. Aspirin 36-43 coagulation factor II, thrombin Homo sapiens 61-69 11246536-4 2001 Seven-day treatment with low-dose aspirin decreased thrombin generation ex vivo only in patients with total cholesterol < or = 5.2 mmol/L. Aspirin 34-41 coagulation factor II, thrombin Homo sapiens 52-60 11246536-6 2001 In these patients, already taking low-dose aspirin, additional three-month simvastatin treatment resulted in a reduction of thrombin generation. Aspirin 43-50 coagulation factor II, thrombin Homo sapiens 124-132 11246536-7 2001 This demonstrates that low-dose aspirin depresses thrombin generation only in subjects with desirable blood cholesterol levels, while in others, with borderline-high cholesterol, thrombin formation is being reduced following the addition of simvastatin. Aspirin 32-39 coagulation factor II, thrombin Homo sapiens 50-58 11460511-1 2001 To assess how treatment with acetylsalicylic acid (ASA) alters the fibrin network structure, clotting was initiated in purified fibrinogen incubated with ASA by adding thrombin. Aspirin 29-49 coagulation factor II, thrombin Homo sapiens 168-176 11460511-1 2001 To assess how treatment with acetylsalicylic acid (ASA) alters the fibrin network structure, clotting was initiated in purified fibrinogen incubated with ASA by adding thrombin. Aspirin 51-54 coagulation factor II, thrombin Homo sapiens 168-176 11460511-1 2001 To assess how treatment with acetylsalicylic acid (ASA) alters the fibrin network structure, clotting was initiated in purified fibrinogen incubated with ASA by adding thrombin. Aspirin 154-157 coagulation factor II, thrombin Homo sapiens 168-176 10987587-6 2000 Clopidogrel with or without aspirin significantly suppressed expression of platelet activation markers CD 62p, CD 63 and PAC-1 after stimulation with ADP or thrombin (p < 0.001). Aspirin 28-35 coagulation factor II, thrombin Homo sapiens 157-165 10987587-10 2000 Clopidogrel in combination with aspirin showed synergistic inhibitory effects after stimulation with collagen and thrombin compared with monotherapies. Aspirin 32-39 coagulation factor II, thrombin Homo sapiens 114-122 11154121-0 2000 Effect of sodium arachidonate on thrombin generation through platelet activation--inhibitory effect of aspirin. Aspirin 103-110 coagulation factor II, thrombin Homo sapiens 33-41 11034940-4 2000 METHODS AND RESULTS: Using washed platelets from normal donors and tyrphostin-A47 and aspirin as tyrosine kinase and COX-1 inhibitors, respectively, we found that tyrphostin-A47 downregulated (1) the thrombin-activated conformational change of alpha(IIb)beta(3), (2) actin polymerization and cytoskeletal reorganization, and (3) the quantity of tyrosine-phospho-rylated proteins associated with the reorganized cytoskeleton. Aspirin 86-93 coagulation factor II, thrombin Homo sapiens 200-208