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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                      The strong influence on platelet-thrombus encounters of red-blood-cell motion an
9  The distance, nature, and duration of close platelet-thrombus encounters were influenced by the poro
10  and PSGL-1-containing microparticles in the platelet thrombus expressing P-selectin.
11 pidly accumulates on the endothelium and the platelet thrombus following injury.
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
15 ng monoclonal antibody against PDI inhibited platelet thrombus formation and fibrin generation.
16 phaIIbbeta3 signaling is required for normal platelet thrombus formation and is triggered by c-Src ac
17                             Collagen-induced platelet thrombus formation at a shear rate of 5000 s(-1
18 atelets lacking supervillin exhibit enhanced platelet thrombus formation at high shear stress.
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
23 iological agonists and S. aureus and reduced platelet thrombus formation in vitro.
24 es in Mh control the extent to which in vivo platelet thrombus formation is disrupted by the absence
25                                           If platelet thrombus formation is inhibited by the infusion
26 lineate the adhesive interactions supporting platelet thrombus formation on biologically relevant sur
27                  Plasma fibronectin enhances platelet thrombus formation on surfaces coated with coll
28                                      Ex vivo platelet thrombus formation on type I collagen fibrils w
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
34                         PDI accumulation and platelet thrombus formation were markedly decreased afte
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
37       When eptifibatide was infused to block platelet thrombus formation, enhanced fibrin generation
38 phaIIbbeta3 (GPIIb-IIIa), a prerequisite for platelet thrombus formation, has been a prominent target
39  vivo in mice for both fibrin generation and platelet thrombus formation.
40 ergize to result in many-fold enhancement of platelet thrombus formation.
41 sis, promoting vasodilatation and inhibiting platelet thrombus formation.
42 n and the generation of thrombin at sites of platelet thrombus formation.
43 on ex vivo perfusion chamber and assessed as platelet-thrombus formation.
44 connexin37 hemichannels and gap junctions in platelet thrombus function.
45 ic cleavage of VWF multimers normally limits platelet thrombus growth, and failure to cleave VWF appe
46 rotease ADAMTS13, and this reaction inhibits platelet thrombus growth.
47        We also assessed thrombin generation, platelet-thrombus interactions, and platelet accumulatio
48  beta3-null (beta3(-/-)) mice, and neither a platelet thrombus nor fibrin is generated at the vessel
49                           Within the growing platelet thrombus, p110beta inactivation impairs the act
50 ed fibrin strands within and surrounding the platelet thrombus, reducing effects on nonactivated circ
51 +) platelets is associated with reduction in platelet thrombus size and fibrin formation.
52 marrow/low TF chimeric mice showed decreased platelet thrombus size but normal TF and fibrin levels.

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