ライフサイエンスコーパス: clotting time

1 had effects on CD62 expression or activated clotting time.

2 ific assays diluted thrombin time and ecarin clotting time.

3 samples resulted in a seven-fold increase in clotting time.

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

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

6 s evidenced by the reduction of viscoelastic clotting time.

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

8 r platelet aggregation and lengthened plasma clotting time.

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

10 inemia, hypoalbuminemia, and prolongation of clotting times.

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

12 heparin dosing to avoid excessive activated clotting times.

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

14 ples to LPS significantly (P < 0.05) reduced clotting times.

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

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

17 S) variables, with normal ranges indicated: clotting time (38-79 s), clot formation time (34-159 s),

18 n time (34-159 s), amplitude at 10 min after clotting time (43-65 mm), maximum clot firmness (50-72 m

19 -75; p=0.01); mean amplitude at 10 min after clotting time 45.1 mm (SD 7.0) versus 33.9 mm (SD 8.6; p

20 d cases and moderate to severe cases: median clotting time 56 s (range 42-81; IQR 48-64) versus 69 s

21 owed good blood-clotting ability by reducing clotting time (6 min relative to the control).

22 had a linear correlation with the activated clotting time (ACT) (Pearson's r = 0.86, P < 0.0001).

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

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

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

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

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

28 Activated clotting time (ACT) was measured before sheath removal.

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

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

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

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

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

34 plastin time (aPTT) as well as the activated clotting time (ACT).

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

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

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

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

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

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

41 Whole blood clotting time analysis confirmed that hemostasis was imp

42 is connected to an inline pressure sensor a clotting time analysis is applied, allowing for the accu

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

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

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

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

47 R(2) values for both clotting time and percent rise from baseline were > 0.98

48 ns did profoundly impact TF-initiated plasma clotting time and the activation of factors IX and X by

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

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

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

52 131 patients (72.5%) with an elevated ecarin clotting time and was similar for upper and lower GI ble

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

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

55 Clotting times and coagulation factor assays were compar

56 Clotting times and coagulation factor assays were not di

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

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

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

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

61 Activated clotting times and whole blood clotting times were norma

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

63 tration and diluted thrombin time and ecarin clotting time, and a non-linear relationship with activa

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

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

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

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

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

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

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

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

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

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

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

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

76 Over 4 years, we replaced the activated clotting time assay with the anti-Xa heparin activity as

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

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

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

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

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

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

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

84 PS) and their removal from plasma lengthened clotting times by more than three-fold.

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

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

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

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

89 nalyses showed moderate correlations between clotting times (CTs) (r = 0.63-0.67; p < 0.001, respecti

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

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

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

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

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

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

96 ensor exhibited no variation in the measured clotting time, even when flexed to a 35 mm bend radius.

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

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

99 The activated clotting time followed a similar anticoagulant response

100 patients received heparin with an activated clotting time goal of >350 seconds.

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

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

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

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

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

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

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

108 Furthermore, this device detects a prolonged clotting time in clinical blood samples drawn from pedia

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

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

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

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

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

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

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

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

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

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

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

120 0low mice had sixfold and fourfold prolonged clotting times in prothrombin time and activated partial

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

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

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

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

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

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

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

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

129 ere also recorded: amplitude at 10 min after clotting time (normal range 7-23 mm) and maximum clot fi

130 The clotting time obtained with beta-thrombin was increased

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

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

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

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

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

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

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

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

139 DMB prolonged clotting time of normal plasma.

140 Activated clotting times of 200-240 s were maintained using intrav

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

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

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

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

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

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

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

148 Secondary outcomes were reduction in clotting times over 1 hour, hemolysis, reduced platelet

149 uiring RBC transfusion (p = 0.01), activated clotting time (p = 0.001), and antithrombin levels (p =

150 ness (p=0.024) and amplitude at 10 min after clotting time (p=0.090) were lowest on days 4-6 of illne

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

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

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

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

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

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

157 bleeding decreased from 69% using activated clotting time to 51% (p = 0.03).

158 ne oxygenation changed from hourly activated clotting time to anti-Xa heparin activity assay every 6

159 tudy describes the transition from activated clotting time to anti-Xa heparin activity assay monitori

160 rporeal membrane oxygenation using activated clotting times to anti-Xa heparin activity assays.

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

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

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

164 than other commonly used parameters such as clotting time, TPH or Thrombin Production Rate (TPR).

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

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

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

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

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

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

171 s metabolites, the median APD when extending clotting time was 9.08%.

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

173 Rotational thromboelastometry clotting time was not significantly prolonged.

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

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

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

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

178 y was based on correction of the whole blood clotting time (WBCT) at multiple timepoints over 24 h.

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

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

181 mes were half that of the manual whole blood clotting time (WBCT, legacy method) and exhibited a sens

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

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

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

185 of heparin to achieve therapeutic activated clotting times were also noted.

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

187 PoC coagulometer baseline clotting times were half that of the manual whole blood

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

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

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

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

192 -initiated and diluted Russell's viper venom clotting time, which could be partly rescued by excess p

193 lation factors enable correction of in vitro clotting time with Factor V-, VIII-, IX- and XI-deficien

194 APIX caused dose-related prolongations of clotting time with minimal impact on other ROTEM paramet

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

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