ライフサイエンスコーパス: clot formation

1 nd neonatal porcine islets prolonged time to clot formation.

2 nitiating a process that ultimately leads to clot formation.

3 and were found to be efficacious in reducing clot formation.

4 fibrin polymerization that lead to insoluble clot formation.

5 B, a process that does not occur until after clot formation.

6 can actively contribute to the processes of clot formation.

7 oagulant effect, after the initial stages of clot formation.

8 Addition of glucose to the medium prevents clot formation.

9 y recruit adjacent erythrocytes to assist in clot formation.

10 gen is a critical protein for hemostasis and clot formation.

11 nce have been reported and are attributed to clot formation.

12 riances in the ability to tolerate excessive clot formation.

13 Ia (also known as thrombin) to prevent blood clot formation.

14 lex, plays a procoagulant role during fibrin clot formation.

15 ture, which may then lead to abnormal fibrin clot formation.

16 elet membranes provide a platform to amplify clot formation.

17 ed blood, an agent that could affect in vivo clot formation.

18 a multicausal disease involving intravenous clot formation.

19 of fibrinogen was shown to accelerate fibrin clot formation.

20 ss-links the gamma-chains of fibrin early in clot formation.

21 20 fM results in pronounced acceleration of clot formation.

22 pair of enzymes is sufficient to yield rapid clot formation.

23 inogen to non-nitrating oxidants decelerates clot formation.

24 a high propensity for cell adhesion and bulk clot formation.

25 prostaglandin E(2), that are released during clot formation.

26 the inhibition of thrombin-catalyzed fibrin clot formation.

27 caused a dose-dependent increase in time to clot formation (3.6-fold increase at the 300 micrograms/

28 At the point of clot formation, 80% of the fibrinogen is depleted from t

29 XO inactivation resulted in clot formation after reperfusion in all animals, whereas

30 We found significantly greater clot formation after uremic serum exposure, which was su

31 uences: increased initial velocity of fibrin clot formation, altered fibrin clot architecture, increa

32 ovide an effective strategy to enhance blood clot formation and act as a rapid pan-hemostatic agent f

33 Sheets could be an unanticipated factor in clot formation and adhesion in vivo, and are a unique ma

34 complexes are not observed until well after clot formation and are never equivalent to ELISA-TAT val

35 itional studies to investigate the effect of clot formation and blood fractionation on DNA availabili

36 The rate of fibrin clot formation and clot architecture was restored upon d

37 e for fibrin crosslinking during whole blood clot formation and consolidation and establish FXIIIa ac

38 RU-505 restored Abeta-induced altered fibrin clot formation and degradation in vitro and inhibited ve

39 AD samples, and intravital brain imaging of clot formation and dissolution revealed abnormal thrombo

40 interventions aimed at reducing peritumoral clot formation and enhancing NK cell function in the per

41 de-nitrite system, significantly accelerates clot formation and factor XIII cross-linking, whereas ex

42 strate of mMCP-7, this tryptase can regulate clot formation and fibrinogen/integrin-dependent cellula

43 ma levels of D-dimers, reflective of in vivo clot formation and fibrinolysis.

44 nt role in the balance between intravascular clot formation and fibrinolytic potential.

45 ore detailed view of thrombin generation and clot formation and have been studied in hemophilia for a

46 than 150,000/microl) can lead to inadequate clot formation and increased risk of bleeding, while thr

47 oduced cell-derived microparticles on fibrin clot formation and its properties.

48 atelets or microorganisms initially promotes clot formation and stability; subsequent degradation of

49 eliberately low blood pressure to facilitate clot formation and stabilization.

50 times faster than native Met-alpha2AP during clot formation and that clot lysis rates are slowed in d

51 s, the implications for our understanding of clot formation and therapeutic intervention may be of ma

52 m that stems from the known vicious cycle of clot formation and tumor growth.

53 e von Willebrand factor, a key step in blood clot formation and wound healing.

54 ted against arterial thrombosis (obstructive clot formation) and stroke.

55 functions for thrombin in addition to fibrin clot formation, and identify a previously unrecognized r

56 Thrombosis, or blood clot formation, and its sequelae remain a leading cause

57 re involved in cell signaling, inflammation, clot formation, and other crucial biological processes.

58 rform this cleavage function to impede blood clot formation around the worms in vivo.

59 of lateral aggregation, leading to abnormal clot formation, as shown by an impaired increase in turb

60 loss after tail-clip assay, and reinstalled clot formation, as tested by in vivo imaging of laser-in

61 ns/enzymes in the interstitial spaces during clot formation, as well as the design of fibrinolytic dr

62 P2Y(1)(2) inhibitors to limit human platelet clot formation at doses recommended by the American Coll

63 tion cascade plays a critical role in fibrin clot formation at extravascular sites, the expression an

64 ets and for vascular collagens to facilitate clot formation at sites of injury.

65 LigBCen2R binding to FgalphaCC reduced clot formation but did not affect plasminogen and tissue

66 nated heparin not only prolongs the onset of clot formation but has a significant effect on its fract

67 Here, we show that clot formation by TF indirectly enhances tumor cell surv

68 ides reversed inhibition of thrombin-induced clot formation by UFH.

69 duction of VCAM-1 is dependent on tumor cell-clot formation, decreasing upon induction of tissue fact

70 creased tumor cell survival without altering clot formation, demonstrating that the recruitment of fu

71 r repair may explain why control of clinical clot formation does not lead to full control of intimal

72 for advanced numerical simulations of blood clot formation during flow in blood vessels.

73 As clot formation ensues, platelets interact with polymeriz

74 es present during the early stages of fibrin-clot formation from the beginning of polymerization to t

75 Ib compared with that of uPA-T, and prevents clot formation in a microfluidic system.

76 ease, we examined its relationship to fibrin clot formation in AD.

77 tor VIIa to initiate thrombin generation and clot formation in blood from healthy donors, blood from

78 nted inhibition of FVIIa/TF/FXa and improved clot formation in hemophilia blood and plasma.

79 ding can be directly assessed by visualizing clot formation in microvessels, and correlations can be

80 concentrations < or = 5.5 nmol/L, prevented clot formation in normal plasma, whereas under similar c

81 utes in 10 of 11 rats tested) with defective clot formation in the WF strain.

82 60-18[29] inhibits thrombin-catalyzed fibrin clot formation in vitro.

83 olonged bleeding times in vivo and defective clot formation in WF rats.

84 h platelets or PCPS vesicles added to induce clot formation indicated that, even in the presence of h

85 Intravascular clot formation is an important factor in a number of car

86 Blood clot formation is crucial to maintain normal physiologic

87 telet, once thought to be solely involved in clot formation, is now known to be a key mediator in var

88 FVIII, which is not biologically active for clot formation, is sufficient for accelerating proteolyt

89 show that the ARFOE-OCE is sensitive to the clot formation kinetics and can differentiate the elasti

90 oagulation metrics, including reaction time, clot formation kinetics and maximum shear modulus.

91 illation is discussed, including left atrial clot formation, maintenance of sinus rhythm after cardio

92 In addition, local fibrin clot formation may be implicated in host defense against

93 nding of events leading to platelet-mediated clot formation may provide insight into new therapeutic

94 measured effects of hematocrit in 2 in vivo clot formation models.

95 able clot formation without inhibiting early clot formation, offering a new potential target for anti

96 deficiency results in significantly delayed clot formation only at sufficiently low TF concentration

97 uggesting an influence either on intraatrial clot formation or embolization.

98 n of arterial occlusion by the inhibition of clot formation or even atherosclerotic disease process i

99 assembly, suggesting that, in events such as clot formation or injury, reversible Abeta assembly coul

100 rinogen, affect fibrin polymerization during clot formation, or abrogate plasma clotting.

101 vity, leading to differential enhancement in clot formation over protection from blood loss in hemoph

102 n factors to perform its key roles in fibrin clot formation, platelet aggregation, and wound healing.

103 Bacteria present during clot formation produce a visibly disorganized microstruc

104 on in several ways, that is, by facilitating clot formation, production of antimicrobial proteins, an

105 omboelastography was used to measure time to clot formation (r-time) in both rhesus and human blood,

106 mboelastography (TEG) demonstrated increased clot formation rate, associated with portal vein platele

107 o-drugs activated selectively at the site of clot formation represents a new approach to prevent thro

108 ient in CD40L showed markedly delayed fibrin clot formation, suggesting a role for the ligand in bloo

109 Blood-clot formation that results in the complete occlusion of

110 tting time, and thromboelastography (maximum clot formation time [R+K], clotting rapidity [alpha], an

111 In a model of arterial photochemical injury, clot formation time was shortened in CRPtg mice; mean ti

112 gnificantly increased coagulation, decreased clot formation time, and increased maximum clot firmness

113 relationship is found between the incipient clot formation time, T(GP), and the activated partial th

114 ponse is characterized by a progression from clot formation, to an inflammatory phase, to a repair ph

115 ly 78% of its normal level and hence improve clot formation under dilution.

116 uencies using 4 set-points and the effect of clot formation using a chemical trigger.

117 Thrombin-stimulated clot formation was completely inhibited by heparin.

118 Clot formation was delayed from 11.1 to 15.7 minutes, wh

119 Clot formation was initiated in whole blood with 5 pM Tf

120 levated APC concentrations (>5.5 nmol/L), no clot formation was observed in either plasma from normal

121 increase in peritumoral fibrin and platelet clot formation was observed in surgically stressed mice,

122 s captured by thrombin-AR-modified cells and clot formation was visualized.

123 To assess the importance of clot formation, we inhibited coagulation with hirudin, a

124 Fibrinopeptide release and insoluble clot formation were only marginally influenced by additi

125 erexpression is associated with pathological clot formation whereas its absence does not cause severe

126 metabolic processing, and increase in fibrin clot formation, with significant upregulation of fibrino

127 aggregation, thrombin activation, and fibrin clot formation within (and downstream of) NETs in vivo.

128 lipid signaling pathways involved in stable clot formation without inhibiting early clot formation,