ライフサイエンスコーパス: clotting time

1 s evidenced by the reduction of viscoelastic clotting time.

2 had effects on CD62 expression or activated clotting time.

3 ratory of the dilute thrombin time or ecarin clotting time.

4 basis of the diluted thrombin time or ecarin clotting time.

5 r platelet aggregation and lengthened plasma clotting time.

6 BA-T7b is more potent than TBA in prolonging clotting time.

7 ther the diluted thrombin time or the ecarin clotting time.

8 inemia, hypoalbuminemia, and prolongation of clotting times.

9 in human plasma, leading to prolongation of clotting times.

10 heparin dosing to avoid excessive activated clotting times.

11 ds [321 to 417 seconds], P = .014) activated clotting times.

12 , X), which corresponded to increased plasma clotting times.

13 us followed by boluses with target activated clotting time 200-250 s; n=1802).

14 ibrillation ablation with baseline activated clotting time (ACT) and INR values was performed.

15 ieved in the absence of changes in activated-clotting time (ACT) and template cut bleeding times, sug

16 ertainty remains about the optimal activated clotting time (ACT) for prevention of ischemic or hemorr

17 Activated clotting time (ACT) is widely used to guide unfractionat

18 The index activated clotting time (ACT) was defined as the ACT measured afte

19 blood pressure, bleeding time, and activated clotting time (ACT) were also examined.

20 tin expression, bleeding time, and activated clotting time (ACT) were quantified.

21 venous pressure, kaolin and celite activated clotting time (ACT), activated partial thromboplastin ti

22 nfractionated heparin (UFH) on the activated clotting time (ACT), and to determine whether the ACT ca

23 We correlated r-TEG values [activated clotting time (ACT), r, k, alpha, maximal amplitude (MA)

24 ial thromboplastin time (aPTT) and activated clotting time (ACT); (2) other factors influencing UFH e

25 (whole blood clotting time [WBCT], activated clotting time [ACT], and activated partial thromboplasti

26 ere divided into 25-s intervals of activated clotting times (ACTs), from <275 s to >476 s.

27 ons study (EPIC), the activated coagulation (clotting) times (ACTs) were longer in heparinized patien

28 ar interest was prolongation of the thrombin clotting time, an indicator of decreased fibrinogen or f

29 By applying a clotting time analysis based on a phenomenological mathe

30 Whole blood clotting time analysis confirmed that hemostasis was imp

31 espectively, and more than doubled activated clotting time and activated partial thromboplastin time

32 mal platelet count, plasma fibrinogen level, clotting time and fibrin crosslinking.

33 RNA-mediated knockdown of KLF2 reduced blood clotting time and flow rates.

34 ally enhanced synergistic effect that lowers clotting time and increases thrombin production at low c

35 inear relation existed between the activated clotting time and the probability of abrupt closure.

36 time, partial correction of the whole blood clotting time and thromboelastography parameters, and a

37 Despite normalization of blood clotting time and thrombus stability after r-FVIII infus

38 endent partial correction of the whole blood clotting time and, at higher doses, of the activated par

39 IgG and IgM antibodies that prolong in vitro clotting times and are associated with increased risks o

40 Whole-blood clotting times and FeCl3 carotid artery injury correctio

41 Shortening of the clotting times and lack of bleeding episodes support the

42 Studies using plasma clotting times and single stage chromogenic assays of fa

43 This resulted in improvement of clotting times and thrombin generation in hemophilic pla

44 Activated clotting times and whole blood clotting times were norma

45 sma resulted in a dose-dependent increase in clotting time, and a dose-dependent decrease in clot lys

46 ial activated thromboplastin time, activated clotting time, and thrombelastograph (TEG).

47 vated partial thromboplastin time, activated clotting time, and thromboelastography (maximum clot for

48 in cFVIII levels (1.5%-8%), a shortening of clotting times, and a reduction (> 90%) of bleeding epis

49 tor-bearing microparticles, shortened plasma-clotting times, and increased thrombus frequency in the

50 assays including tail bleeding time, plasma clotting times, and tissue factor- or LPS-induced dissem

51 Skin inflammation; thrombosis clotting times; and percentage of splenic monocytes, neu

52 rats in combination with heparin, and plasma clotting times (APTT) were measured to determine activit

53 heparin concentrations (anti-Factor Xa) and clotting times (APTT).

54 cordingly, the dilute-thrombin or the ecarin clotting times are best suited for dabigatran and the pr

55 d cells, KLF2 overexpression increased blood clotting time as well as flow rates under basal and infl

56 , FVIII neutralization resulted in prolonged clotting times as measured by thromboelastography and pr

57 we found significantly reduced bleeding and clotting times, as well as increased in vivo thrombosis,

58 In a modified cephalin clotting time assay, in vivo administration of Factor IX

59 nticoagulation was to maintain the activated clotting time at 200 seconds.

60 given intravenously to maintain an activated clotting time at 270 to 300 s.

61 (pharmacologic concentrations) corrected the clotting time at all TF concentrations tested (0-100 pM)

62 thrombin time and 81 with an elevated ecarin clotting time at baseline, the median maximum percentage

63 eding during a routine operation, had normal clotting times, but markedly reduced prothrombin consump

64 hrombin-thrombomodulin complex, prolongs the clotting time by generating pharmacological quantities o

65 rs and corrected the prolongation of ex vivo clotting times by such inhibitors.

66 Variation due to clotting time caused changes in energy metabolites, whic

67 Sickle MPs shortened plasma-clotting time compared with control MPs, and a TF antibo

68 A minimum target activated clotting time could not be identified; rather, the highe

69 elets activated with SFLLRN or collagen, the clotting time decreased to 100 +/- 10 sec.

70 d levels of liver function enzymes and blood clotting times, decreased levels of platelets, multifoca

71 cation in liver transplantation is increased clotting times due to inhibition of protein synthesis re

72 irements to maintain a therapeutic activated clotting time during RFA was reduced by 50% in patients

73 ersal of diluted thrombin time (dTT), ecarin clotting time (ECT), activated partial thromboplastin ti

74 However, rennet clotting time, ethanol stability and foaming ability wer

75 pulmonary embolism model and showed shorter clotting times ex vivo.

76 a proteins, decreased platelet count, slower clotting times, fibrin deposits in tissue sections, and

77 The activated clotting time followed a similar anticoagulant response

78 entional anticoagulation protocol (activated clotting time >250 s) in 10 procedures (group 1), with a

79 Anticoagulation (activated clotting time >250 s) was maintained after dual transsep

80 ith an aggressive anticoagulation (activated clotting time >320 s) in 13 procedures (group 3).

81 superfused with heparinized blood (activated clotting time >350 seconds) at 37 degrees C.

82 antagonist and heparin to maintain activated clotting time>350 seconds; (2) submerged loading of the

83 inant placental bikunin(1-170) prolonged the clotting time in an activated partial thromboplastin tim

84 displayed a dose-dependent reduction of the clotting time in buffer, with a 20 microM aptamer achiev

85 Whole blood clotting time in FIX-deficient mice was corrected throug

86 cus vesiculosus, decreases bleeding time and clotting time in hemophilia, possibly through inhibition

87 gs, and applying this system to measuring of clotting time in small volumes of whole blood and plasma

88 y anti-TF antibody also has no effect on the clotting time in the absence of exogenous TF.

89 IIa, soluble tissue factor, and calcium, the clotting time in the absence of platelets was >5 min.

90 n its COX-mediated metabolites in shortening clotting time in vitro.

91 eved was sufficient to correct the prolonged clotting times in a mouse model of haemophilia B, and re

92 dogs demonstrated approximately twice normal clotting times in a platelet factor 3 availability assay

93 lecule-1 mRNA, causes prolongation of plasma clotting times in both monkey and human studies.

94 X-deficient plasma, as well as FXa-initiated clotting times in FX-deficient plasma.

95 the ability of TFPI to prolong TF-initiated clotting times in FXI- or FIX-deficient plasma, as well

96 ence of added APC without affecting baseline clotting times in the absence of APC, showing that certa

97 rtial thromboplastin times (decreased plasma clotting times), increased levels of fibrinogen, and inc

98 HRPII attenuated the prolongation in plasma clotting time induced by heparin, suggesting that HRPII

99 y alveolar macrophages, resulting in reduced clotting times, intravascular thrombin formation, and ac

100 The prolonged clotting time is correlated with delays in platelet acti

101 This shortening of the clotting time is equivalent to about a 5-fold increase i

102 ry angioplasty, as measured by the activated clotting time, is related to the risk of abrupt vessel c

103 Because polyphosphate did not alter thrombin clotting times, it appeared to exert all its procoagulan

104 The clotting time obtained with beta-thrombin was increased

105 eparinization was maintained at an activated clotting time of 150-180 secs.

106 enous administration of PN2KPI prolonged the clotting time of both human and murine plasma, and PN2KP

107 e serine residue (FXII-S544A), shortened the clotting time of FXII-deficient plasma and enhanced thro

108 ically modified PAEC significantly prolonged clotting time of human blood (115.0 +/- 16.1 min, p < 0.

109 Murine factor XI shortens the clotting time of human factor XI deficient plasma in an

110 binds tightly to factor IXa and prolongs the clotting time of human plasma.

111 nd 3 null mice significantly shorten the RVV clotting time of normal plasma in a dose-dependent fashi

112 mboplastin time and the factor Xa- one-stage clotting time of normal plasma was markedly enhanced by

113 DMB prolonged clotting time of normal plasma.

114 rical data from the synthetic plasma suggest clotting times of 3-5 min, which are similar to that obs

115 heparin was administered with goal-activated clotting times of 300 to 400 seconds for all LV procedur

116 dose dependently prolonged factor Xa-1-stage clotting times of normal plasma in the presence of added

117 lactosylceramide, dose-dependently prolonged clotting times of normal plasma in the presence, but not

118 ated sheep showed no difference in activated clotting time or platelet count but exhibited less fibri

119 peptide did not influence significantly the clotting time or thrombin-antithrombin III complex (TAT)

120 human complement, had little or no effect on clotting times or prothrombin consumption of normal or C

121 ining the venom clotting test with the quick clotting time (prothrombin time), it was possible to dia

122 time, partial thromboplastin time, activated clotting time, R+K, alpha, or maximum amplitude between

123 Expression of the variants shortened clotting times, reduced blood loss after tail-clip assay

124 ted, based on determination of the activated clotting time, the activated partial thromboplastin time

125 , different hemolysis levels, differences in clotting times, the number of freeze-thaw cycles, and di

126 hromboplastin time to 122% +/- 4%, activated clotting time to 124% +/- 3%, and R + K to 119% +/- 3% (

127 ial thromboplastin time and prothrombin time clotting times to baseline at 60 mins.

128 ARC19499 restored thromboelastography clotting times to baseline levels and corrected bleeding

129 nd doxycycline treatment returned thrombosis clotting times to that of control mice (P=0.69).

130 sion to the endothelial surface and prolongs clotting time under inflammatory states.

131 roban) into blood samples and to measure the clotting time using the activated partial thromboplastin

132 anticoagulation to an intermediate activated clotting time value of 186 seconds.

133 sal with RB007 returned the median activated clotting time value to 144 seconds.

134 Median activated clotting time values rose from 151 to 236 seconds after

135 the presence of unstimulated platelets, the clotting time was 200 +/- 20 sec.

136 n were normal; however, when the whole blood clotting time was measured at 25 degrees C in plastic tu

137 Rotational thromboelastometry clotting time was not significantly prolonged.

138 to a factor VIIInull background, whole blood clotting time was partially corrected, equivalent to a 3

139 intraprocedural heparin, the mean activated clotting time was significantly lower in patients who he

140 human fIIa(MZ), significant prolongation of clotting times was observed for fII(MZ) plasma.

141 edly accelerated clotting (53.3% decrease in clotting time) was observed in carotid artery preparatio

142 months and normalization of the whole blood clotting time (WBCT) for about a month.

143 in HemA mice, and fully corrects whole blood clotting time (WBCT) in HemA dogs immediately after dosi

144 Coagulation tests (whole blood clotting time [WBCT], activated clotting time [ACT], and

145 ial activated thromboplastin time, activated clotting time were consistently prolonged by acidosis (a

146 t gender, Cr, weight, and the peak activated clotting time were not associated with bleeding.

147 the rates of release of fibrinopeptides and clotting times were delayed compared with control.

148 in patients in whom intraprocedure activated clotting times were measured were identified from a popu

149 Activated clotting times and whole blood clotting times were normalized, activated partial thromb

150 Higher activated clotting times were not associated with an increased lik

151 in double-knockout mice revealed that native clotting times were shortened and thrombin-antithrombin

152 activated partial thromboplastin time [APTT] clotting times with and without APC) of the treated fact

153 compatibility of PAEC, as shown by increased clotting time (WT: 84.3 +/- 11.3 min, p < 0.001; GTKO.hC