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1 ularization (26% versus 53%) or receive dual anti-platelets (40% versus 68%) than those without kidne
2 ystemic platelet depletion, produced with an anti-platelet Ab, on blood and tissue levels of 5-HT, an
3 erghei infection can enhance the activity of anti-platelet Abs as indicated by a significantly (p < 0
4 f aggregation was blocked using a monoclonal anti-platelet activating factor receptor (PafR) antibody
5 ceae) roots showed potential oestrogenic and anti-platelet activities.
6 onents exhibited significant oestrogenic and anti-platelet activities; demonstrating for the first ti
7                          This broad-spectrum anti-platelet activity is also present in excretory and
8 system in MCF-7 breast cancer cell-line; the anti-platelet activity was evaluated using the anti-plat
9                               Because of its anti-platelet activity, aspirin is a non-disease factor
10 s can be avoided and long-term medication of anti-platelet agent is not needed.
11 sk factors (such as anti-hypertensive drugs, anti-platelet agents and statins) seem to have little or
12 gement of patients taking anticoagulants and anti-platelet agents has been examined, and it appears t
13                   The effect of conventional anti-platelet agents is limited in secondary stroke prev
14 t treatments for arterial thrombosis include anti-platelet agents such as aspirin, thienopyridines an
15   Other approaches, perhaps involving potent anti-platelet agents, should be considered for patients
16 lammatory agents, anti-thrombotic agents and anti-platelet agents.
17 onstrated with the synthesis of Satigrel, an anti-platelet aggregating agent.
18 c peptide exhibiting both FXa inhibition and anti-platelet aggregation activities, with a low bleedin
19  was identified with both FXa inhibition and anti-platelet aggregation activities.
20          Just OSP exhibited a dose-dependent anti-platelet aggregation activity [inductor (IC(50,) mg
21                                       A high anti-platelet aggregation activity for FPJO-CRL2051 was
22 rdioprotective phytochemicals with potential anti-platelet aggregation activity, although this benefi
23 ti-platelet activity was evaluated using the anti-platelet aggregation assay.
24 ninogen has the properties of anti-adhesion, anti-platelet aggregation, and anti-thrombosis, whereas
25            Numerous studies demonstrate that anti-platelet alloantibodies can induce significant plat
26                In fact, for nearly 50 years, anti-platelet alloantibodies were considered to be the s
27 n explain platelet removal in the absence of anti-platelet alloantibodies, many patients experience p
28 latelet clearance in the complete absence of anti-platelet alloantibodies.
29 ol from vessel walls and local anti-oxidant, anti-platelet and anti-inflammatory actions.
30                                 Use of acute anti-platelet and anti-thrombin therapy within the first
31                                  Through its anti-platelet and anti-thrombotic activities, abciximab
32 ular Dysfunction and Post-PCI Ischemia Among Anti-Platelet and Anti-Thrombotic Agents-Thrombolysis In
33 rted to have a variety of anti-inflammatory, anti-platelet, and anti-carcinogenic effects.
34       Thus, Notch pathway can be a potential anti-platelet/anti-thrombotic therapeutic target.
35    Blocking FcgammaRIV binding to pathogenic anti-platelet antibodies is sufficient to protect mice f
36                                  Most of the anti-platelet antibody ( approximately 85%) could be ads
37                                          The anti-platelet antibody hindered megakaryocyte differenti
38                            Affinity-purified anti-platelet antibody reacted with a recombinant GPIIIa
39 pleted from the systemic circulation with an anti-platelet antibody, blood-retinal barrier breakdown
40 muR is required for the pathogenicity of IgM anti-platelet autoantibodies but is not sufficient to ex
41 ivirus, exacerbates the pathogenicity of IgM anti-platelet, but not anti-erythrocyte autoantibodies.
42  and are inhibited by both anticoagulant and anti-platelet compounds.
43 on of Rap1b, which was largely unaffected by anti-platelet-derived growth factor (PDGF) antibodies.
44 duction was partly abrogated by neutralizing anti-platelet-derived growth factor (PDGF) antibodies.
45                                Monitoring of anti-platelet-derived growth factor receptor (PDGF-R) an
46  anti-vascular endothelial growth factor and anti-platelet-derived growth factor signaling.
47  evaluated the use of a mouse/human chimeric anti-platelet-derived growth factor-beta receptor antibo
48 suggesting that the ITS force map can report anti-platelet drug efficacy.
49 ion which is sensitive to treatment with the anti-platelet drug tirofiban, suggesting that the ITS fo
50 e-lowering drugs, a mast cell stabilizer, an anti-platelet drug, or fenofibrate slow AAA growth.
51 amongst patient groups based on the usage of anti-platelet drugs on discharge.
52  quantified the inhibition efficiency of two anti-platelet drugs providing a proof-of-concept demonst
53                       MeB blocked the direct anti-platelet effect of the NO donors in the absence of
54 nce PGI2), release contributes to the marked anti-platelet effects observed after the in vivo adminis
55  DISPERSE (Dose confIrmation Study assessing anti-Platelet Effects of AZD6140 vs. clopidogRel in non-
56          Microvascular growth was studied by anti-platelet endothelial cell adhesion molecule (PECAM)
57      Retinas from eyes injected with labeled anti-platelet endothelial cell adhesion molecule 1 (PECA
58 blished methods, such as a function blocking anti-platelet endothelial cell adhesion molecule 1 antib
59 tibody (MoAb; 50% +/- 18% inhibition) and by anti-platelet endothelial cell adhesion molecule-1 (PECA
60 s sinus thrombosis with thrombocytopenia and anti-platelet factor 4 (anti-PF4) antibodies in individu
61 otic disorder associated with development of anti-platelet factor 4 (anti-PF4)/heparin autoantibodies
62                            VITT is caused by anti-platelet factor 4 (PF4) antibodies activating plate
63                          Platelet-activating anti-platelet factor 4 (PF4)/heparin antibodies and anti
64  the performance of 3 immunoassays detecting anti-platelet factor 4 (PF4)/heparin antibodies, derived
65 penia (HIT) is caused by platelet-activating anti-platelet factor 4 (PF4)/heparin antibodies.
66   Both patients tested strongly positive for anti-platelet factor 4 (PF4)/heparin immunoglobulin (Ig)
67                Kanack and colleagues analyze anti-platelet factor 4 antibodies from 5 patients with v
68  results (including the results of tests for anti-platelet factor 4 antibodies where available), and
69 osis in association with platelet-activating anti-platelet factor 4 antibodies.
70 in antibodies show several similarities with anti-platelet factor 4-heparin antibodies and are a pote
71                                 An ELISA for anti-platelet factor 4/heparin antibodies was performed
72 SA for a panel of 8 autoantibodies including anti-platelet factor 4/polyanion (anti-PF4/P), anti-phos
73                                              Anti-platelet factor-4 (PF4) antibodies were observed in
74   Thus HIV-1-ITP patients have high-affinity anti-platelet GPIIIa against a major antigenic determina
75            High-affinity (Kd = 1 x 10(-9) M) anti-platelet GPIIIa has been isolated from serum immune
76 uential immunoabsorption with anti-CSPG4 and anti-platelet growth factor receptor alpha mAb to charac
77  platelet clearance is described in which an anti-platelet IgG causes platelet fragmentation via the
78                                              Anti-platelet integrin GPIIIa49-66 antibody (Ab) induces
79 viduals (n=565) from the Pharmacogenomics of Anti-Platelet Intervention (PAPI) Study and conducted a
80 hat contain platelet membrane components and anti-platelet membrane GPIIIa49-66 IgG antibodies.
81 ables: use of aspirin/NSAIDs/anti-coagulants/anti-platelets, pathologic diagnoses (including differen
82                (Patterns of Non-Adherence to Anti-Platelet Regimen in Stented Patients [PARIS]; NCT00
83 d in the PARIS (Patterns of Non-Adherence to Anti-Platelet Regimen in Stented Patients) registry, sep
84     PARIS (Patterns of Non-Adherence to Dual Anti-Platelet Regimen in Stented Patients) was a prospec
85  pathway may explain why anti-alpha-thrombin/anti-platelet regimens fail to completely abrogate throm
86 al PARIS study (Patterns of Non-Adherence to Anti-Platelet Regimens in Stented Patients Registry), 42
87      The PARIS (patterns of non-adherence to anti-platelet regimens in stented patients) registry is
88 PARIS registry (Patterns of Non-Adherence to Anti-Platelet Regimens in Stented Patients) were categor
89  similar results, showing a benefit of using anti-platelets (Relative risk 0.90, 95% CI 0.84 to 0.97)
90 he recovery from thrombocytopenia induced by anti-platelet serum.
91                          The SWAP (SWitching Anti Platelet) study was a phase 2, multicenter, randomi
92 esent initial work in developing cargo-free, anti-platelet therapeutics specifically for conditions o
93 sivation and aid in the development of novel anti-platelet therapeutics.
94 ts an important target in the development of anti-platelet therapeutics.
95 ERS: A Clinical Study Comparing Two Forms of Anti-platelet Therapy After Stent Implantation) study ra
96 ERS: A Clinical Study Comparing Two Forms of Anti-Platelet Therapy After Stent Implantation), an all-
97 ERS: A Clinical Study Comparing Two Forms of Anti-platelet Therapy After Stent Implantation; NCT01813
98 ic cross-talk has important implications for anti-platelet therapy because it suggests a novel approa
99 ular benefit from potent anti-thrombotic and anti-platelet therapy or early invasive treatment strate
100                                         Dual anti-platelet therapy represents standard care for treat
101                           Those who received anti-platelet therapy were associated with elevated risk
102                           Assessment of Dual Anti-platelet Therapy With Drug-Eluting Stents (ADAPT-DE
103 on, 93% of the atherosclerosis patients took anti-platelet therapy.
104                                              Anti-platelet treatment without inhibiting CD40L release
105                                              Anti-Platelet Trialists' Collaboration (APTC) events occ
106 n groups in serious ocular adverse events or Anti-Platelet Trialists' Collaboration arterial thromboe
107  endophthalmitis, and the total incidence of Anti-Platelet Trialists' Collaboration events was 4.7%.
108                The total 2-year incidence of Anti-Platelet Trialists' Collaboration events was 6.7%.
109                             The incidence of Anti-Platelet Trialists' Collaboration-defined arterial
110                                          One Anti-Platelet Trialists' Collaboration-defined event of

 
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