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1 Abs increase thrombin generation and promote plasma clotting.
2 umor cells delayed their ability to activate plasma clotting.
3 erization during clot formation, or abrogate plasma clotting.
4  a genuine patch size threshold in quiescent plasma-clotting always occurs given enough time-whereas
5 L) plays a central role in the initiation of plasma clotting and in phagocytic clearance of injured o
6 ol plays a central role in the initiation of plasma clotting and in phagocytic clearance of injured o
7         Chlamydia-infected cells accelerated plasma clotting and increased the macrophage phagocytosi
8 nd X415-429, CHT241-252C) potently inhibited plasma clotting and prothrombinase activity with 50% inh
9                     In a factor Xa one-stage plasma clotting assay, the chimera had approximately 5 t
10  to their ability to activate factor IX in a plasma clotting assay, to hydrolyze the chromogenic subs
11 expressed in 293 fibroblasts and tested in a plasma clotting assay.
12 indistinguishable from plasma factor XI in a plasma-clotting assay and in a factor IX activation assa
13 rypsin residues 149D-163) potently inhibited plasma clotting assays and prothrombinase activity, with
14                          In kaolin-triggered plasma clotting assays containing purified phospholipid,
15 hinganine, respectively) as well as in whole plasma clotting assays.
16  R306 and was moderately resistant to APC in plasma-clotting assays and in prothrombinase assays meas
17                                     Based on plasma-clotting assays, the target zymogen for VWbp may
18 ngly up-regulates tissue factor and promotes plasma clotting by glioblastoma multiforme, but transcri
19 ypoxia up-regulate TF expression and promote plasma clotting by glioma cells, suggesting that these m
20 hogenic bacterium Bacillus subtilis, induces plasma clotting by proteolytically converting ProT into
21                   The contact pathway of the plasma clotting cascade is dispensable for normal hemost
22                Extracellular interactions of plasma clotting factor VIIa (FVIIa) with tissue factor (
23 issue factor (TF), the cellular receptor for plasma clotting factor VIIa (FVIIa).
24         Finally, the presence of VC1 delayed plasma clotting in a dose-dependent manner.
25                    Hypoxic cells accelerated plasma clotting in tilt tube assays and this effect was
26 omains of AbetaPP and APLP2 both inhibit the plasma clotting in vitro.
27 over, they are effective inhibitors of human plasma clotting in vitro.
28 lished for purified blood proteases or human plasma clotting isotropically.
29                                         In a plasma clotting system initiated with factor Xa, EPCR bl
30 titutions did profoundly impact TF-initiated plasma clotting time and the activation of factors IX an
31         HRPII attenuated the prolongation in plasma clotting time induced by heparin, suggesting that
32 h slower platelet aggregation and lengthened plasma clotting time.
33                         Sickle MPs shortened plasma-clotting time compared with control MPs, and a TF
34 red to rats in combination with heparin, and plasma clotting times (APTT) were measured to determine
35                                Studies using plasma clotting times and single stage chromogenic assay
36 sion molecule-1 mRNA, causes prolongation of plasma clotting times in both monkey and human studies.
37  and partial thromboplastin times (decreased plasma clotting times), increased levels of fibrinogen,
38 ctional assays including tail bleeding time, plasma clotting times, and tissue factor- or LPS-induced
39 r II, V, X), which corresponded to increased plasma clotting times.
40 sue factor-bearing microparticles, shortened plasma-clotting times, and increased thrombus frequency
41                Iron loading had no effect on plasma clotting, vessel wall tissue factor activity, or