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1 el wall injury, before the appearance of the platelet thrombus.
2 ose of WE tested (0.011 mg/kg bolus) reduced platelet thrombus accumulation by 80% and was at least a
4 bin is necessary for normal propagation of a platelet thrombus at a distance from the injured vessel
9 The distance, nature, and duration of close platelet-thrombus encounters were influenced by the poro
12 al importance to elucidate the mechanisms of platelet thrombus formation after vessel wall injury.
13 in disulfide isomerase (PDI) is required for platelet thrombus formation and fibrin generation after
14 by platelets, that inhibition of PDI blocked platelet thrombus formation and fibrin generation, and t
16 phaIIbbeta3 signaling is required for normal platelet thrombus formation and is triggered by c-Src ac
19 studied the impact of plasma fibronectin on platelet thrombus formation ex vivo in a parallel flow c
20 onhematopoietic cell DREAMs are required for platelet thrombus formation following laser-induced arte
21 nimal shear stress levels that produce acute platelet thrombus formation in mechanically stenosed art
22 that (1) platelets contain supervillin; (2) platelet thrombus formation in the PFA-100 is associated
24 es in Mh control the extent to which in vivo platelet thrombus formation is disrupted by the absence
26 lineate the adhesive interactions supporting platelet thrombus formation on biologically relevant sur
29 ere was more fibrin deposited at the site of platelet thrombus formation than in wild type (WT), wher
30 To identify genetic factors that influence platelet thrombus formation under high shear stress, we
31 d confocal microscopy and exhibited enhanced platelet thrombus formation under high-shear but not low
32 agents were administered intravenously, and platelet thrombus formation was monitored by the decreas
33 platelet aggregation, platelet secretion, or platelet thrombus formation were found as measured in th
35 yclic flow reductions (CFRs) caused by acute platelet thrombus formation were observed in the stenose
36 IIb/IIIa receptor is important in mediating platelet thrombus formation, and the GP IIb/IIIa antagon
38 phaIIbbeta3 (GPIIb-IIIa), a prerequisite for platelet thrombus formation, has been a prominent target
45 ic cleavage of VWF multimers normally limits platelet thrombus growth, and failure to cleave VWF appe
48 beta3-null (beta3(-/-)) mice, and neither a platelet thrombus nor fibrin is generated at the vessel
50 ed fibrin strands within and surrounding the platelet thrombus, reducing effects on nonactivated circ
52 marrow/low TF chimeric mice showed decreased platelet thrombus size but normal TF and fibrin levels.
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