ライフサイエンスコーパス: thromboplastin

1 ood following activation of coagulation with thromboplastin.

2 ated and varied significantly with different thromboplastins.

3 in shear rates and an immediate change after thromboplastin activation.

4 use models of pulmonary thrombosis caused by thromboplastin and ischemia-reperfusion (I/R), scFv/uPA-

5 associated with prolongation of the partial thromboplastin and prothrombin times and hyperfibrinolys

6 Prolongation of the partial thromboplastin and prothrombin times was only observed w

7 0 minutes of arrival for analysis of partial thromboplastin and prothrombin times, prothrombin fragme

8 mortality, and had similar activated partial thromboplastin and tail vein bleeding times.

9 ombin times were determined by using several thromboplastins, and INRs were calculated for the patien

10 thrombin assay indicated a level of 51% with thromboplastin as an activator.

11 d type FIX (wt-FIX) in the activated partial thromboplastin assay.

12 Individual thromboplastins differed in sensitivity to the presence

13 g warfarin, INRs obtained by using different thromboplastins greatly varied and often overestimated t

14 s expressing cell surface tissue factor (TF, thromboplastin) in persons with HIV infection.

15 oved event-free survival in a mouse model of thromboplastin-induced generalized and invariably fatal

16 ministration of the diabody (0.8 mg/kg) in a thromboplastin-induced model of thromboembolism led to d

17 usceptible to thrombosis than females in the thromboplastin-induced pulmonary embolism model and show

18 ombosis of mesenteric arterioles and against thromboplastin-induced pulmonary embolism.

19 low serum albumin concentration, and partial thromboplastin time < or =25 seconds predict a high risk

20 low serum albumin concentration, and partial thromboplastin time < or =25 seconds.

21 ms had a three-fold longer activated partial thromboplastin time (124 s; p<0.001) than both nondrowni

22 a (13% and 23%); prolonged activated partial thromboplastin time (8% and 18%); elevated aspartate ami

23 ct as assessed by anti-Xa, activated partial thromboplastin time (aPTT) and activated clotting time (

24 The activated partial thromboplastin time (aPTT) and anti-factor X (anti-Xa) l

25 The activated partial thromboplastin time (APTT) and prothrombin time (PT) are

26 Activated partial thromboplastin time (aPTT) and prothrombin time (PT) are

27 had reduced activity in an activated partial thromboplastin time (aPTT) assay and was activated by fa

28 atively normal activity in activated partial thromboplastin time (aPTT) assays.

29 up without prolongation of activated partial thromboplastin time (aPTT) before and after the treatmen

30 as measured by a one-stage activated partial thromboplastin time (aPTT) clotting assay (36% +/- 9.6%

31 s were characterized using activated partial thromboplastin time (APTT) clotting assays and FVa inact

32 Finally, the activated partial thromboplastin time (aPTT) coagulation assay was perform

33 We examined the activated partial thromboplastin time (aPTT) in 29,656 patients in the Glo

34 infusion of thrombin, the activated partial thromboplastin time (APTT) increased by 11+/-3 seconds b

35 Reduced activated partial thromboplastin time (aPTT) is a risk marker for incident

36 Activated partial thromboplastin time (aPTT) is associated with risk of th

37 prothrombin time (PT) and activated partial thromboplastin time (aPTT) obtained before elective surg

38 prothrombin time (PT) and activated partial thromboplastin time (APTT) of 14.2 and 35.5s respectivel

39 were titrated to a target activated partial thromboplastin time (aPTT) of 55 to 85 seconds and were

40 n thawed washed platelets, activated partial thromboplastin time (aPTT) reagent and prothrombin time

41 he clotting time using the activated partial thromboplastin time (APTT) test.

42 specific validation of the activated partial thromboplastin time (aPTT) therapeutic range is required

43 normalized ratio (INR) and activated partial thromboplastin time (aPTT) values were 1.5 and 48, respe

44 dditional association with activated partial thromboplastin time (aPTT) was tested for the top SNPs.

45 the thrombin time and the activated partial thromboplastin time (aPTT) when added to normal plasma,

46 complete correction of the activated partial thromboplastin time (aPTT), and that injection of 10(11)

47 carin clotting time (ECT), activated partial thromboplastin time (aPTT), and thrombin time (TT) were

48 Increases in activated partial thromboplastin time (aPTT), anti-factors IIa and Xa, and

49 vated clotting time (ACT), activated partial thromboplastin time (APTT), heparin concentration, and p

50 CTs [prothrombin time (PT)/activated partial thromboplastin time (aPTT), international normalized rat

51 We tested the activated partial thromboplastin time (APTT), international normalized rat

52 nt 43% prolongation of the activated partial thromboplastin time (aPTT), over controls (P < 0.05).

53 measured ACT (Hemochron), activated partial thromboplastin time (aPTT), plasma anti-Xa and anti-IIa

54 ses that significantly prolonged the partial thromboplastin time (APTT), prothrombin time (PT), and b

55 ATS-112 in prolonging the activated partial thromboplastin time (APTT), whereas ATS-119 inhibited fa

56 ly combined with tests for activated partial thromboplastin time (aPTT).

57 coagulation time (ACT) and activated partial thromboplastin time (aPTT).

58 a concomitant increase in activated partial thromboplastin time (APTT).

59 The activated partial thromboplastin time (APTT; baseline, 28 seconds) increas

60 fibrinogen, platelets, and activated partial thromboplastin time (but not prothrombin index) differed

61 nt (five [12%]), prolonged activated partial thromboplastin time (four [10%]), and decreased platelet

62 Longer activated partial thromboplastin time (hazards ratio, 0.98; p = 0.002) and

63 E. coli further increased activated partial thromboplastin time (p < .0001 vs. placebo) within or ab

64 rombin time (p < .02), and activated partial thromboplastin time (p < .05).

65 ith placebo) increased the activated partial thromboplastin time (p = .002) close to the therapeutic

66 in the prothrombin time (PT) and the partial thromboplastin time (PTT) in response to the first FFP t

67 r examinations, virus isolation, and partial thromboplastin time (PTT) were evaluated during the stud

68 jury, prolonged prothrombin time and partial thromboplastin time (PTT), and lower levels of both pro-

69 Prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen/fibrin degradation

70 linear prolongation of the activated partial thromboplastin time (PTT).

71 (r=0.72) but less so with activated partial thromboplastin time (r=0.56; all P<0.001).

72 , adjusted to maintain the activated partial thromboplastin time 1.5 to 3.0 times baseline value.

73 nce ratio values (ratio of activated partial thromboplastin time [APTT] clotting times with and witho

74 d clotting time [ACT], and activated partial thromboplastin time [aPTT]) have remained at the upper l

75 Xa activity but comparable activated partial thromboplastin time activity.

76 ese functional studies and activated partial thromboplastin time analysis validate predictions made f

77 ating more than 90% of its activated partial thromboplastin time and anti-factor Xa activity.

78 y components prolonged the activated partial thromboplastin time and decreased target protein activit

79 associated with prolonged activated partial thromboplastin time and extravascular hemorrhage.

80 een the peak posttreatment activated partial thromboplastin time and post hoc weight-adjusted dose of

81 missive range and returned activated partial thromboplastin time and prothrombin time clotting times

82 Plasma activated partial thromboplastin time and prothrombin time increased over

83 Activated partial thromboplastin time and prothrombin time were shortened

84 of heparin to prolong the activated partial thromboplastin time and the factor Xa- one-stage clottin

85 XI deficient plasma in an activated partial thromboplastin time assay, with a specific activity 50%

86 n specific activity in the activated partial thromboplastin time assay.

87 ed the clotting time in an activated partial thromboplastin time assay.

88 ots, prothrombin time, and activated partial thromboplastin time assays and fibrinopeptide A generati

89 (APC) cofactor activity in activated partial thromboplastin time assays in PS-depleted plasma.

90 ity in modified prothrombin time and partial thromboplastin time assays, respectively.

91 and <5%, respectively, in activated partial thromboplastin time assays.

92 both prothrombin time and activated partial thromboplastin time assays; however, it exhibited a simi

93 se dependently; the median activated partial thromboplastin time at 10 minutes after a single intrave

94 ctivated clotting time and activated partial thromboplastin time at the higher dose.

95 red in a factor VIII-based activated partial thromboplastin time clot assay.

96 anticoagulant activity in activated partial thromboplastin time clotting assays but retained high af

97 In activated partial thromboplastin time clotting assays, the specific activi

98 paired liver function, and activated partial thromboplastin time confounding may interfere with monit

99 RB006 increased the activated partial thromboplastin time dose dependently; the median activat

100 In contrast, activated partial thromboplastin time for 7.5% NaCl adenocaine/Mg(2)(+) wa

101 in the prolongation of the activated partial thromboplastin time identified in patients with streptoc

102 f the prothrombin time and activated partial thromboplastin time in affected individuals.

103 2 caused a doubling of the activated partial thromboplastin time in human plasma at 2.4 microM and wa

104 ides (PS ODNs) prolong the activated partial thromboplastin time in human plasma by inhibition of int

105 performance characteristics for the partial thromboplastin time in predicting postoperative hemorrha

106 Prolongation of activated partial thromboplastin time in streptococcal toxic shock syndrom

107 ocyte count, and prolonged activated partial thromboplastin time in the soft-tissue sarcoma group (th

108 both prothrombin time and activated partial thromboplastin time in vitro or ex vivo.

109 he baseline (pretreatment) activated partial thromboplastin time is prolonged.

110 valirudin anticoagulation (activated partial thromboplastin time less than twice the control time).

111 or 2500 units/kg produced activated partial thromboplastin time levels less than, within, or greater

112 -2-macroglobulin (A2M) and activated partial thromboplastin time measurement for coagulation factor X

113 mic response, reflected in activated partial thromboplastin time measurements, was seen after adminis

114 that compared therapeutic (activated partial thromboplastin time more than twice the control time) wi

115 ional normalized ratio of 1.2, and a partial thromboplastin time of 29.3 seconds.

116 udies revealed a prolonged activated partial thromboplastin time of 49.2 seconds, a normal prothrombi

117 15H8 prolonged the activated partial thromboplastin time of baboon and human plasmas.

118 The activated partial thromboplastin time of the treated mice was fully correc

119 Severe activated partial thromboplastin time prolongation may be a marker of comb

120 Grade I post-partial thromboplastin time prolongations were noted.

121 05, respectively), and the activated partial thromboplastin time prolonged significantly at 2 and 4 h

122 ose of heparin was decreased and the partial thromboplastin time returned towards the normal referenc

123 activator inhibitor 1, and activated partial thromboplastin time showed variability but no significan

124 ged prothrombin time to 113% +/- 2%, partial thromboplastin time to 122% +/- 4%, activated clotting t

125 RB007 reversed the activated partial thromboplastin time to baseline levels within a median o

126 s) and sustained return of activated partial thromboplastin time to within the normal range.

127 nogen level <60 mg/dL, and activated partial thromboplastin time values >100 seconds were the stronge

128 At 60-min resuscitation, activated partial thromboplastin time values for untreated, 7.5% NaCl, 7.5

129 were associated with subtherapeutic partial thromboplastin time values.

130 Baseline plasma activated partial thromboplastin time was 17+/-0.5 secs and increased to 6

131 dose was 588 units/hr, and the mean partial thromboplastin time was 37 secs.

132 , dose-related increase in activated partial thromboplastin time was accompanied by a trend toward a

133 Prolongation of activated partial thromboplastin time was associated with reduced factor X

134 thrombin was inhibited and activated partial thromboplastin time was increased after treatment with C

135 Partial thromboplastin time was increased six- to sevenfold over

136 The activated partial thromboplastin time was prolonged in only the rTPA plus

137 The activated partial thromboplastin time was prolonged to a similar extent by

138 The activated partial thromboplastin time was unchanged.

139 both prothrombin time and activated partial thromboplastin time were normal.

140 ere normal, but prothrombin time and partial thromboplastin time were prolonged and bone alkaline pho

141 e acoustic assays namely ''activated Partial Thromboplastin Time'' (aPTT) and ''Prothrombinase comple

142 s (index normalized ratio, activated partial thromboplastin time) after reperfusion were similar betw

143 thrombosis in vitro (e.g. activated partial thromboplastin time) and in vivo (e.g. rat FeCl(2)-induc

144 coagulation times (prothrombin time, partial thromboplastin time) indicated that iNO improved the rat

145 V was analyzed in an aPTT (activated partial thromboplastin time)-based APC sensitivity assay, the AP

146 f heparin (n = 50) (target activated partial thromboplastin time, 65 to 90 seconds or 90 to 110 secon

147 rolonged prothrombin time, partial activated thromboplastin time, activated clotting time were consis

148 rolonged prothrombin time, partial activated thromboplastin time, activated clotting time, and thromb

149 eration, prothrombin time, activated partial thromboplastin time, activated clotting time, and thromb

150 rombin generation, prothrombin time, partial thromboplastin time, activated clotting time, R+K, alpha

151 relationship was seen with activated partial thromboplastin time, activated protein C resistance, hem

152 inogen, prothrombin index, activated partial thromboplastin time, and d-dimer as well as the DIC scor

153 imer, prolonged prothrombin time and partial thromboplastin time, and falling fibrinogen) resulting i

154 s and increases of prothrombin time, partial thromboplastin time, and fibrin split products.

155 leeding, fibrinogen level, activated partial thromboplastin time, and somnolence.

156 tivated clotting time, the activated partial thromboplastin time, and the cuticle bleeding time.

157 d TF, and has no effect on activated partial thromboplastin time, but is 70-fold less potent as an in

158 f laboratory-based prothrombin time, partial thromboplastin time, complete blood count, and bleeding

159 The activated partial thromboplastin time, factor VIII activity, von-Willebran

160 ounts, with plasma prothrombin time, partial thromboplastin time, fibrinogen levels, fibrin split pro

161 anges in prothrombin time, activated partial thromboplastin time, fibrinogen, fibrinogen-fibrin degra

162 Mean activated partial thromboplastin time, prothrombin time, and international

163 ation time, T(GP), and the activated partial thromboplastin time, whereas the association of D(f) wit

164 , P = 0.035), but not with activated partial thromboplastin time-based APC resistance ratios.

165 vel, prothrombin time, and activated partial thromboplastin time.

166 fect on the TF-independent activated partial thromboplastin time.

167 ets, prothrombin time, and activated partial thromboplastin time.

168 d, at higher doses, of the activated partial thromboplastin time.

169 in III, platelet count, or activated partial thromboplastin time.

170 marked prolongation of the activated partial thromboplastin time.

171 han 35% of patients having activated partial thromboplastin times (aPTTs) within a range of 55 to 85

172 m with centrally monitored activated partial thromboplastin times (aPTTs).

173 ding time, decreased prothrombin and partial thromboplastin times (decreased plasma clotting times),

174 x min, adjusted to achieve activated partial thromboplastin times 1.5-3 times baseline

175 kb1(-/-) plasmas have long-activated partial thromboplastin times and defective contact activation-in

176 ulation was assessed using activated partial thromboplastin times and prothrombin times.

177 increased prothrombin and activated partial thromboplastin times and tissue factor, tissue factor pa

178 Patients with prolonged partial thromboplastin times did not have a statistically signif

179 ients achieved therapeutic activated partial thromboplastin times generally within 4 to 5 hours of st

180 is, heparin titrated using activated partial thromboplastin times may be efficacious.

181 The treated mice exhibited activated partial thromboplastin times that were comparable to those of wi

182 -dependent prolongation of activated partial thromboplastin times that were two- to three-fold greate

183 Prolongation of prothrombin and partial thromboplastin times was accompanied by evidence for tis

184 r values for Quick's test and higher partial thromboplastin times were associated with a higher rate

185 Systemic partial thromboplastin times were not affected by local hirudin

186 ions and increase in prothrombin and partial thromboplastin times were significantly attenuated by TN

187 necrotizing fasciitis, the activated partial thromboplastin times were significantly prolonged in inf

188 ing times were normalized, activated partial thromboplastin times were substantially reduced, and ant

189 prolonged prothrombin, and activated partial thromboplastin times, in whom no classifying diagnosis w

190 secreted protein (50 kDa) that reconstituted thromboplastin-triggered thrombin generation in immunode

191 from zebrafish plasma selectively inhibited thromboplastin-triggered thrombin generation.