PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2981130-3 1985 We compared fibrinogen binding to platelets from diabetic subjects with binding to platelets from normal subjects and determined whether aspirin (which inhibits the formation of prostaglandins and thromboxane) would inhibit the binding of fibrinogen to platelets from diabetic subjects and whether this correlated with its effects on platelet aggregation. Aspirin 137-144 fibrinogen beta chain Homo sapiens 239-249 2746495-0 1989 Aspirin acetylates fibrinogen and enhances fibrinolysis. Aspirin 0-7 fibrinogen beta chain Homo sapiens 19-29 2455569-7 1988 CP/CPK or aspirin alone reduced fibrinogen binding to 20% to 30%; however, this binding was sufficient to support full platelet aggregation. Aspirin 10-17 fibrinogen beta chain Homo sapiens 32-42 2455569-8 1988 Combined treatment with CP/CPK and aspirin abolished fibrinogen binding and aggregation. Aspirin 35-42 fibrinogen beta chain Homo sapiens 53-63 3667609-6 1987 Treatment of platelets with aspirin, incubation in the presence of creatine phosphate/creatine phosphokinase, or omission of Ca2+ and fibrinogen do not affect toxin-mediated phospholipase C activation. Aspirin 28-35 fibrinogen beta chain Homo sapiens 67-144 3010580-4 1986 The present study compares fibrinogen binding to hyperaggregable platelets from diabetic patients and to normal platelets when prostaglandin/thromboxane formation is suppressed by aspirin. Aspirin 180-187 fibrinogen beta chain Homo sapiens 27-37 3943666-6 1986 However, while aspirin (an inhibitor of thromboxane synthesis) reduced the abnormally high fibrinogen binding of platelets from nonretinopathic patients to normal control levels, it did not normalize the high fibrinogen binding of platelets from retinopathic diabetic patients. Aspirin 15-22 fibrinogen beta chain Homo sapiens 91-101 3943666-7 1986 The combination of aspirin plus apyrase (an ADP scavenger) almost suppressed fibrinogen binding and aggregation of platelets from normal or nonretinopathic diabetic subjects, whereas it had a somewhat lesser effect on binding and aggregation of platelets from retinopathic subjects. Aspirin 19-26 fibrinogen beta chain Homo sapiens 77-87 6326566-0 1984 Effect of epinephrine on fibrinogen receptor exposure by aspirin-treated platelets and platelets from concentrates in response to ADP and thrombin. Aspirin 57-64 fibrinogen beta chain Homo sapiens 25-35 6326566-3 1984 The present study extends these observations to correlate fibrinogen binding in response to various combinations of ADP, epinephrine, and thrombin with platelet aggregation and 14C-serotonin release using aspirin-treated platelets as well as platelets from stored concentrates. Aspirin 205-212 fibrinogen beta chain Homo sapiens 58-68 139704-0 1976 [Change in fibrinogen and enzymatic and nonenzymatic fibrinolytic activity of blood in patients with low-degree rheumatic heart disease under the effect of treatment with acetylsalicylic acid]. Aspirin 171-191 fibrinogen beta chain Homo sapiens 11-21 6288146-1 1982 Previous analysis of fibrinogen binding to human aspirin-treated gel-filtered platelets yielded upwardly concave Scatchard plots. Aspirin 49-56 fibrinogen beta chain Homo sapiens 21-31 7404479-1 1980 ADP causes human, aspirin-treated, gel-filtered platelets to change from their native discoid shape to spiny spheres with pseudopods, bind 125I-labeled fibrinogen, and aggregate if shaken with sufficient fibrinogen. Aspirin 18-25 fibrinogen beta chain Homo sapiens 152-162 7404479-1 1980 ADP causes human, aspirin-treated, gel-filtered platelets to change from their native discoid shape to spiny spheres with pseudopods, bind 125I-labeled fibrinogen, and aggregate if shaken with sufficient fibrinogen. Aspirin 18-25 fibrinogen beta chain Homo sapiens 204-214 24203353-1 2014 We aimed to investigate the association of aspirin and/or clopidogrel low response with -455G/A polymorphism of beta-fibrinogen in patients with acute coronary syndrome (ACS). Aspirin 43-50 fibrinogen beta chain Homo sapiens 112-127 33307284-1 2021 Acetylsalicylic acid (ASA) and type 2 diabetes mellitus (T2DM) affect fibrin clot properties through fibrinogen acetylation or glycation. Aspirin 0-20 fibrinogen beta chain Homo sapiens 101-111 33307284-1 2021 Acetylsalicylic acid (ASA) and type 2 diabetes mellitus (T2DM) affect fibrin clot properties through fibrinogen acetylation or glycation. Aspirin 22-25 fibrinogen beta chain Homo sapiens 101-111 33307284-2 2021 We aimed to identify glycation and acetylation sites on fibrinogen in plasma fibrin clot of T2DM patients with respect to effects of ASA and fibrin clot properties. Aspirin 133-136 fibrinogen beta chain Homo sapiens 56-66 31356179-15 2019 The PIA1 allele may be a potential factor for aspirin resistance with elevated fibrinogen concentration. Aspirin 46-53 fibrinogen beta chain Homo sapiens 79-89 1215973-4 1975 125I-fibrinogen half-life was 2.1 days under aspirin and 1.9 days under combined aspirin/heparin therapy. Aspirin 45-52 fibrinogen beta chain Homo sapiens 5-15 1215973-4 1975 125I-fibrinogen half-life was 2.1 days under aspirin and 1.9 days under combined aspirin/heparin therapy. Aspirin 81-88 fibrinogen beta chain Homo sapiens 5-15 25759104-16 2015 In conclusion, fibrinogen level was the major predictor of HPR on aspirin in this large population of high-risk vascular patients. Aspirin 66-73 fibrinogen beta chain Homo sapiens 15-25 19100419-11 2008 Compared with patients in the ASA-sensitive group, patients in the ASA-resistant group showed significantly higher total cholesterol, low-density lipoprotein cholesterol, triglyceride, C-reactive protein, and fibrinogen levels and lower GFRs (44 +/- 21 mL/min vs 63 +/- 26 mL/min, P = .03). Aspirin 67-70 fibrinogen beta chain Homo sapiens 209-219 24898335-9 2014 Fibrinogen concentration was significantly higher in women than in men among patients treated with 100 mg ASA (p<0.05), but not in the other groups. Aspirin 106-109 fibrinogen beta chain Homo sapiens 0-10 24898335-10 2014 CONCLUSIONS: Significantly higher fibrinogen concentration found in aspirin treated women than men may play a role in higher ADP induced platelet aggregation. Aspirin 68-75 fibrinogen beta chain Homo sapiens 34-44 22994591-12 2013 The time course of plasma fibrinogen and procalcitonin levels indicate that ASA seems to reduce the activation of haemostasis and increase the resolution of inflammation. Aspirin 76-79 fibrinogen beta chain Homo sapiens 26-36 22507986-3 2012 We investigated whether acetylation and glycation occur at specific sites in fibrinogen and if competition between glucose and aspirin in binding to fibrinogen occurs. Aspirin 127-134 fibrinogen beta chain Homo sapiens 149-159 22507986-5 2012 After incubation of fibrinogen in vitro with aspirin (0.8 mM, 24 h) or glucose (100 mM, 5-10 days), we found 12 modified sites with mass spectrometric techniques. Aspirin 45-52 fibrinogen beta chain Homo sapiens 20-30 22395372-8 2012 In multivariate regression analysis, only fibrinogen level (OR=1.063, p=0.010) and pulse pressure (OR=1.197, p=0.023) were found to be independent indicators of aspirin resistance and PAI. Aspirin 161-168 fibrinogen beta chain Homo sapiens 42-52 22395372-9 2012 In ROC analysis, cut-off values of 50 mmHg for pulse pressure and 400 mg/dl for fibrinogen level predicted aspirin resistance with 88.9% and 74% sensitivity and 64.4% and 68% specificity, respectively. Aspirin 107-114 fibrinogen beta chain Homo sapiens 80-90 22395372-10 2012 CONCLUSION: Our findings suggest that measurements of fibrinogen level and pulse pressure may be used as easy and reliable methods in predicting aspirin resistance. Aspirin 145-152 fibrinogen beta chain Homo sapiens 54-64 20624109-0 2010 High-dose fibrinogen concentrate for haemostatic therapy of a major trauma patient with recent clopidogrel and aspirin intake. Aspirin 111-118 fibrinogen beta chain Homo sapiens 10-20 19129740-2 2009 To assess whether this finding related to modifications of fibrinogen clotting property by ASA, purified fibrinogen was incubated with ASA and/or salicylic acid (SA). Aspirin 91-94 fibrinogen beta chain Homo sapiens 59-69 19129740-2 2009 To assess whether this finding related to modifications of fibrinogen clotting property by ASA, purified fibrinogen was incubated with ASA and/or salicylic acid (SA). Aspirin 135-138 fibrinogen beta chain Homo sapiens 105-115 16930084-8 2006 RESULTS: Compared with aspirin-resistant patients, patients who demonstrated effective aspirin inhibition had a significantly lower plasma fibrinogen level (3.3 g/L vs 3.8 g/L; p < 0.05) and significantly lower RBC aggregation values (24.3 vs 28.2; p < 0.01). Aspirin 87-94 fibrinogen beta chain Homo sapiens 139-149 19126992-0 2008 Relation of platelet aggregation and fibrinogen levels to advancing age in aspirin- and thienopyridine-treated patients. Aspirin 75-82 fibrinogen beta chain Homo sapiens 37-47 19126992-7 2008 In aspirin-treated patients also fibrinogen levels increased with aging (p<0.001). Aspirin 3-10 fibrinogen beta chain Homo sapiens 33-43 18239256-10 2008 RESULTS: Patients with effective ASA inhibition had significantly lower plasma fibrinogen level (p<0.05) and red blood cell aggregation values both in the heterogenous and the selected populations (p<0.01). Aspirin 33-36 fibrinogen beta chain Homo sapiens 79-89 18239256-14 2008 Thus, increased plasma fibrinogen level may play an important role in the in vitro and in vivo platelet resistance to ASA. Aspirin 118-121 fibrinogen beta chain Homo sapiens 23-33 16756193-11 2006 Flowcytometry for P-selectin expression and fibrinogen binding to platelets can be used to monitor antiplatelet therapy with aspirin following acute myocardial infarction. Aspirin 125-132 fibrinogen beta chain Homo sapiens 44-54 15049721-4 2004 Increased platelet thromboxane production as well as activation of platelet receptors for fibrinogen and or adenosine diphosphate (ADP) are often present, and can be treated with aspirin (acetylsalicylic acid) and/or receptor blockers. Aspirin 179-186 fibrinogen beta chain Homo sapiens 90-100 16181986-2 2005 The present study was performed to extend the dose-response curve for effects of ASA on fibrinogen clotting properties and to examine the variability of these effects during a 24-h dose interval. Aspirin 81-84 fibrinogen beta chain Homo sapiens 88-98 15049721-4 2004 Increased platelet thromboxane production as well as activation of platelet receptors for fibrinogen and or adenosine diphosphate (ADP) are often present, and can be treated with aspirin (acetylsalicylic acid) and/or receptor blockers. Aspirin 188-208 fibrinogen beta chain Homo sapiens 90-100 11723016-5 2001 In the Pl(A1A1) homozygotes, aspirin ingestion resulted in reductions in the velocity of thrombin B-chain formation (by 32.1%; P=0.007), prothrombin consumption (by 30.4%; P=0.018), factor Va generation (by 28.9%; P=0.014), fibrinogen removal (by 41.2%; P=0.001), and factor XIII activation (by 22.6%; P=0.026). Aspirin 29-36 fibrinogen beta chain Homo sapiens 224-234 14593356-13 2003 CONCLUSION: Short term use of ticlopidine in patients with NSTEACS treated with aspirin and unfractionated heparin was associated with lower levels of TAT and fibrinogen (relative to control group) on day 14. Aspirin 80-87 fibrinogen beta chain Homo sapiens 159-169 11728532-9 2001 RESULTS: In a drug free group, digestion of a single tablet of aspirin resulted in a significantly (p<0.05) diminished expression of PECAM-1, GP IIb, fibrinogen binding with PAC-1 antibody, GP Ib, P-selectin, and CD151. Aspirin 63-70 fibrinogen beta chain Homo sapiens 153-163 11672762-5 2001 Platelet fibrinogen binding and P-selectin expression were significantly lower in patients treated with ticlopidine but not with aspirin than in those not treated with any antiplatelet agent, and were lowest in those treated with both ticlopidine and aspirin. Aspirin 129-136 fibrinogen beta chain Homo sapiens 9-19 11672762-5 2001 Platelet fibrinogen binding and P-selectin expression were significantly lower in patients treated with ticlopidine but not with aspirin than in those not treated with any antiplatelet agent, and were lowest in those treated with both ticlopidine and aspirin. Aspirin 251-258 fibrinogen beta chain Homo sapiens 9-19 11721406-5 1999 Further study indicated that HI117 and SJ9A4-induced Fg binding was reduced by pretreatment of platelets with sphingosine, aspirin, apyrase, and/or PGI2. Aspirin 123-130 fibrinogen beta chain Homo sapiens 53-55 11246553-6 2001 In blood from subjects given aspirin for 5 days, abciximab-induced inhibition of the capacity to bind fibrinogen in response to 1 microM ADP was greater when the daily dose had been 325 mg compared with 81 mg (% inhibition: no aspirin 53 +/- 6; 81 mg daily 62 +/- 5; 325 mg daily 69 +/- 6). Aspirin 29-36 fibrinogen beta chain Homo sapiens 102-112 11145946-11 2001 The superiority of abciximab over aspirin in accelerating fibrinolysis of forming and preformed PRCs is related to its ability to modulate the interactions of fibrinogen and fibrin with platelets. Aspirin 34-41 fibrinogen beta chain Homo sapiens 159-169 11460511-0 2001 Modified clotting properties of fibrinogen in the presence of acetylsalicylic acid in a purified system. Aspirin 62-82 fibrinogen beta chain Homo sapiens 32-42 11460511-1 2001 To assess how treatment with acetylsalicylic acid (ASA) alters the fibrin network structure, clotting was initiated in purified fibrinogen incubated with ASA by adding thrombin. Aspirin 29-49 fibrinogen beta chain Homo sapiens 128-138 8883279-2 1996 Smoking was positively associated with fibrinogen, also after adjustment for other lifestyle factors, age, use of anticoagulants and aspirin like drugs, body mass index, and history of myocardial infarction. Aspirin 133-140 fibrinogen beta chain Homo sapiens 39-49 10193737-10 1999 CONCLUSIONS: Among these apparently healthy U.S. male physicians, fibrinogen is associated with increased risk of future MI independent of other coronary risk factors, atherogenic factors such as lipids and antithrombotics such as aspirin. Aspirin 231-238 fibrinogen beta chain Homo sapiens 66-76 8880021-3 1996 Acetylsalicylic acid, however, also acetylates fibrinogen. Aspirin 0-20 fibrinogen beta chain Homo sapiens 47-57 8880021-11 1996 In conclusion, the protective effect of acetylsalicylic acid may be ascribed to its effect not only on platelets but also on fibrinogen. Aspirin 40-60 fibrinogen beta chain Homo sapiens 125-135 10608044-0 1998 Prothrombotic Consequences of the Oxidation of Fibrinogen and their Inhibition by Aspirin. Aspirin 82-89 fibrinogen beta chain Homo sapiens 47-57 10608044-2 1998 Aspirin can nonenzymatically acetylate fibrinogen"s lysine residues, the functional groups most susceptible to oxidative modification. Aspirin 0-7 fibrinogen beta chain Homo sapiens 39-49 10608044-5 1998 Exposure of fibrinogen to aspirin led to acetylation of lysine residues and inhibition of oxidation. Aspirin 26-33 fibrinogen beta chain Homo sapiens 12-22 10608044-10 1998 These data show that oxidized fibrinogen manifests prothrombotic effects that can be prevented by acetylation and suggest that inhibition of fibrinogen oxidation may be an additional antithrombotic benefit of aspirin therapy. Aspirin 209-216 fibrinogen beta chain Homo sapiens 30-40 10608044-10 1998 These data show that oxidized fibrinogen manifests prothrombotic effects that can be prevented by acetylation and suggest that inhibition of fibrinogen oxidation may be an additional antithrombotic benefit of aspirin therapy. Aspirin 209-216 fibrinogen beta chain Homo sapiens 141-151 8091447-5 1994 In patients receiving aspirin, the platelet aggregability induced by 2 micrograms/mL collagen and 5 and 10 mumol/L adenosine diphosphate decreased compared with aggregability before medication (P < .005), but the reductions had no significant correlation with the plasma fibrinogen concentration. Aspirin 22-29 fibrinogen beta chain Homo sapiens 274-284 7585737-5 1995 ASL and ASA were positively associated with age, fasting blood sugar levels and plasma fibrinogen levels, and these associations were statistically significant. Aspirin 8-11 fibrinogen beta chain Homo sapiens 87-97 21043735-4 1995 There are now at least two systems of platelet activation under intensive study: (a) agonist (e.g. ADP and thrombin) induced platelet activation when fibrinogen is the ligand; this process occurs at low shear forces and is aspirin sensitive; (b) secondly, in marked contrast, at high shear forces, shear itself activates the platelets and von Willebrand"s factor (vWf) is the ligand, and this process is aspirin insensitive. Aspirin 223-230 fibrinogen beta chain Homo sapiens 150-160 21043735-4 1995 There are now at least two systems of platelet activation under intensive study: (a) agonist (e.g. ADP and thrombin) induced platelet activation when fibrinogen is the ligand; this process occurs at low shear forces and is aspirin sensitive; (b) secondly, in marked contrast, at high shear forces, shear itself activates the platelets and von Willebrand"s factor (vWf) is the ligand, and this process is aspirin insensitive. Aspirin 404-411 fibrinogen beta chain Homo sapiens 150-160 7533066-16 1994 These findings suggest that platelet fibrinogen binding and the release of platelet alpha-granule and lysosomal contents, in response to stimulation with physiological agonists, can continue in patients despite aspirin therapy. Aspirin 211-218 fibrinogen beta chain Homo sapiens 37-47 8121125-5 1993 Fibrinogen level increased from 3.34 +/- 0.15 to 3.95 +/- 0.18 g/l, p < 0.001, and from 3.36 +/- 0.17 to 3.94 +/- 0.17 g/l p = 0.003 in aspirin and heparin groups, respectively. Aspirin 139-146 fibrinogen beta chain Homo sapiens 0-10 1899346-2 1991 The present study explored the direct association of membrane-bound fibrinogen with the Triton X-100 (Sigma Chemical Co, St Louis, MO) insoluble cytoskeleton of aspirin-treated, gel-filtered platelets, activated but not aggregated with 20 mumol/L adenosine diphosphate (ADP) or 150 mU/mL human thrombin (THR) when bound fibrinogen had become resistant to dissociation by EDTA. Aspirin 161-168 fibrinogen beta chain Homo sapiens 68-78 2024888-3 1991 Aspirin-insensitive pathways, mediated by protein kinase C and myosin light-chain kinase, lead to a change of platelet shape, with an attendant striking increase in their surface (pseudopods) followed by exposure of receptors for fibrinogen and vWf on GPIIb-IIIa. Aspirin 0-7 fibrinogen beta chain Homo sapiens 230-240