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1 ystemic platelet depletion, produced with an anti-platelet Ab, on blood and tissue levels of 5-HT, an
2 erghei infection can enhance the activity of anti-platelet Abs as indicated by a significantly (p < 0
3 f aggregation was blocked using a monoclonal anti-platelet activating factor receptor (PafR) antibody
5 onents exhibited significant oestrogenic and anti-platelet activities; demonstrating for the first ti
7 system in MCF-7 breast cancer cell-line; the anti-platelet activity was evaluated using the anti-plat
9 gement of patients taking anticoagulants and anti-platelet agents has been examined, and it appears t
10 t treatments for arterial thrombosis include anti-platelet agents such as aspirin, thienopyridines an
11 Other approaches, perhaps involving potent anti-platelet agents, should be considered for patients
12 c peptide exhibiting both FXa inhibition and anti-platelet aggregation activities, with a low bleedin
15 ninogen has the properties of anti-adhesion, anti-platelet aggregation, and anti-thrombosis, whereas
18 n explain platelet removal in the absence of anti-platelet alloantibodies, many patients experience p
23 ular Dysfunction and Post-PCI Ischemia Among Anti-Platelet and Anti-Thrombotic Agents-Thrombolysis In
25 Blocking FcgammaRIV binding to pathogenic anti-platelet antibodies is sufficient to protect mice f
29 pleted from the systemic circulation with an anti-platelet antibody, blood-retinal barrier breakdown
30 muR is required for the pathogenicity of IgM anti-platelet autoantibodies but is not sufficient to ex
31 ivirus, exacerbates the pathogenicity of IgM anti-platelet, but not anti-erythrocyte autoantibodies.
33 on of Rap1b, which was largely unaffected by anti-platelet-derived growth factor (PDGF) antibodies.
34 duction was partly abrogated by neutralizing anti-platelet-derived growth factor (PDGF) antibodies.
37 evaluated the use of a mouse/human chimeric anti-platelet-derived growth factor-beta receptor antibo
39 ion which is sensitive to treatment with the anti-platelet drug tirofiban, suggesting that the ITS fo
41 nce PGI2), release contributes to the marked anti-platelet effects observed after the in vivo adminis
42 DISPERSE (Dose confIrmation Study assessing anti-Platelet Effects of AZD6140 vs. clopidogRel in non-
45 blished methods, such as a function blocking anti-platelet endothelial cell adhesion molecule 1 antib
46 tibody (MoAb; 50% +/- 18% inhibition) and by anti-platelet endothelial cell adhesion molecule-1 (PECA
47 otic disorder associated with development of anti-platelet factor 4 (anti-PF4)/heparin autoantibodies
48 Both patients tested strongly positive for anti-platelet factor 4 (PF4)/heparin immunoglobulin (Ig)
49 in antibodies show several similarities with anti-platelet factor 4-heparin antibodies and are a pote
51 Thus HIV-1-ITP patients have high-affinity anti-platelet GPIIIa against a major antigenic determina
53 platelet clearance is described in which an anti-platelet IgG causes platelet fragmentation via the
55 viduals (n=565) from the Pharmacogenomics of Anti-Platelet Intervention (PAPI) Study and conducted a
58 d in the PARIS (Patterns of Non-Adherence to Anti-Platelet Regimen in Stented Patients) registry, sep
59 pathway may explain why anti-alpha-thrombin/anti-platelet regimens fail to completely abrogate throm
60 al PARIS study (Patterns of Non-Adherence to Anti-Platelet Regimens in Stented Patients Registry), 42
62 similar results, showing a benefit of using anti-platelets (Relative risk 0.90, 95% CI 0.84 to 0.97)
66 ic cross-talk has important implications for anti-platelet therapy because it suggests a novel approa
67 ular benefit from potent anti-thrombotic and anti-platelet therapy or early invasive treatment strate
71 n groups in serious ocular adverse events or Anti-Platelet Trialists' Collaboration arterial thromboe
72 endophthalmitis, and the total incidence of Anti-Platelet Trialists' Collaboration events was 4.7%.
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