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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
3      The presumed mechanism is prevention of platelet thrombus associated with vessel wall injury and
4 bin is necessary for normal propagation of a platelet thrombus at a distance from the injured vessel
5 ibodies revealed their colocalization on the platelet thrombus but not the endothelium.
6        Thus, a new mechanism is proposed for platelet thrombus clearance, via platelet oxidative frag
7 a new antithrombotic agent was developed for platelet thrombus clearance.
8 linositol 3-kinase dose dependently modulate platelet thrombus dynamics.
9                      The strong influence on platelet-thrombus encounters of red-blood-cell motion an
10  The distance, nature, and duration of close platelet-thrombus encounters were influenced by the poro
11  and PSGL-1-containing microparticles in the platelet thrombus expressing P-selectin.
12 pidly accumulates on the endothelium and the platelet thrombus following injury.
13 al importance to elucidate the mechanisms of platelet thrombus formation after vessel wall injury.
14 in disulfide isomerase (PDI) is required for platelet thrombus formation and fibrin generation after
15 by platelets, that inhibition of PDI blocked platelet thrombus formation and fibrin generation, and t
16 ng monoclonal antibody against PDI inhibited platelet thrombus formation and fibrin generation.
17 phaIIbbeta3 signaling is required for normal platelet thrombus formation and is triggered by c-Src ac
18                             Collagen-induced platelet thrombus formation at a shear rate of 5000 s(-1
19 atelets lacking supervillin exhibit enhanced platelet thrombus formation at high shear stress.
20  studied the impact of plasma fibronectin on platelet thrombus formation ex vivo in a parallel flow c
21 onhematopoietic cell DREAMs are required for platelet thrombus formation following laser-induced arte
22 nimal shear stress levels that produce acute platelet thrombus formation in mechanically stenosed art
23  that (1) platelets contain supervillin; (2) platelet thrombus formation in the PFA-100 is associated
24 iological agonists and S. aureus and reduced platelet thrombus formation in vitro.
25 es in Mh control the extent to which in vivo platelet thrombus formation is disrupted by the absence
26                                           If platelet thrombus formation is inhibited by the infusion
27 lineate the adhesive interactions supporting platelet thrombus formation on biologically relevant sur
28                  Plasma fibronectin enhances platelet thrombus formation on surfaces coated with coll
29                                      Ex vivo platelet thrombus formation on type I collagen fibrils w
30 ere was more fibrin deposited at the site of platelet thrombus formation than in wild type (WT), wher
31   To identify genetic factors that influence platelet thrombus formation under high shear stress, we
32 d confocal microscopy and exhibited enhanced platelet thrombus formation under high-shear but not low
33  agents were administered intravenously, and platelet thrombus formation was monitored by the decreas
34 platelet aggregation, platelet secretion, or platelet thrombus formation were found as measured in th
35                         PDI accumulation and platelet thrombus formation were markedly decreased afte
36 yclic flow reductions (CFRs) caused by acute platelet thrombus formation were observed in the stenose
37 f injury, neutrophil elastase secretion, and platelet thrombus formation within seconds following inj
38  IIb/IIIa receptor is important in mediating platelet thrombus formation, and the GP IIb/IIIa antagon
39       When eptifibatide was infused to block platelet thrombus formation, enhanced fibrin generation
40 phaIIbbeta3 (GPIIb-IIIa), a prerequisite for platelet thrombus formation, has been a prominent target
41  vivo in mice for both fibrin generation and platelet thrombus formation.
42 ergize to result in many-fold enhancement of platelet thrombus formation.
43 sis, promoting vasodilatation and inhibiting platelet thrombus formation.
44 n and the generation of thrombin at sites of platelet thrombus formation.
45 on ex vivo perfusion chamber and assessed as platelet-thrombus formation.
46 from VITT patients induce increased adherent platelets/thrombus formation in comparison with IgGs fro
47 connexin37 hemichannels and gap junctions in platelet thrombus function.
48 ic cleavage of VWF multimers normally limits platelet thrombus growth, and failure to cleave VWF appe
49 rotease ADAMTS13, and this reaction inhibits platelet thrombus growth.
50        We also assessed thrombin generation, platelet-thrombus interactions, and platelet accumulatio
51  beta3-null (beta3(-/-)) mice, and neither a platelet thrombus nor fibrin is generated at the vessel
52                                              Platelet thrombus on immobilized collagen was quantified
53                           Within the growing platelet thrombus, p110beta inactivation impairs the act
54 ed fibrin strands within and surrounding the platelet thrombus, reducing effects on nonactivated circ
55 +) platelets is associated with reduction in platelet thrombus size and fibrin formation.
56 marrow/low TF chimeric mice showed decreased platelet thrombus size but normal TF and fibrin levels.