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 12,000 U/24 hr aiming for activated partial thromboplastin time < 45 s).

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

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

22 oagulation variables (mean activated partial thromboplastin time <= 50 s, international normalized ra

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

24 004), daily geometric mean activated partial thromboplastin time (48.1 s [95% CI, 43.5-53.2 s] vs 55.

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

26 inear correlation with the activated partial thromboplastin time (aPTT) (r = 0.99).

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

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

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

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

31 aring the PA signal to the activated partial thromboplastin time (aPTT) as well as the activated clot

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

33 ion and is captured by the activated partial thromboplastin time (aPTT) assay.

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

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

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

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

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

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

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

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

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

43 (INR) greater than 1.4, or activated partial thromboplastin time (APTT) longer than 39 seconds.

44 s were tested for modified activated partial thromboplastin time (aPTT) measured on an optical-mechan

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

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

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

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

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

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

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

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

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

54 DeltaSBP), platelet count, activated partial thromboplastin time (APTT), and injury severity score (I

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

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

57 ing prothrombin time (PT), activated partial thromboplastin time (APTT), and thrombin time (TT).

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

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

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

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

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

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

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

65 re studied for their blood activated partial thromboplastin time (APTT), prothrombin time (PT), inter

66 ing prothrombin time (PT), activated partial thromboplastin time (aPTT), thrombin time (TT), as well

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

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

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

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

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

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

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

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

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

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

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

78 alized ratio (p = 0.99) or activated partial thromboplastin time (p = 0.29).

79 ion (P=0.04), higher final activated partial thromboplastin time (P=0.05), lower final von Willebrand

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

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

82 es, including prothrombin time (PT), partial thromboplastin time (PTT), and D-dimer concentrations, r

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

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

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

86 ivity correlated well with activated partial thromboplastin time (r = -0.789; p = 0.007).

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

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

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

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

91 Xa activity but comparable activated partial thromboplastin time activity.

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

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

94 t difference in mean daily activated partial thromboplastin time and anti-Xa levels between groups.

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

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

97 sustained prolongation of activated partial thromboplastin time and FXI suppression for up to 4 week

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

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

100 Plasma activated partial thromboplastin time and prothrombin time increased over

101 Activated partial thromboplastin time and prothrombin time were shortened

102 The activated partial thromboplastin time and prothrombin time, as well as act

103 -dependent prolongation of activated partial thromboplastin time and reduction of FXI clotting activi

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

105 ctivity in assays (diluted activated partial thromboplastin time and thrombin generation), similar to

106 uction treatment increased activated partial thromboplastin time and thrombin time, while reducing fi

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

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

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

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

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

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

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

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

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

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

117 ation with heparin (target activated partial thromboplastin time between 50 and 70 s) or lower dose h

118 ce in daily geometric mean activated partial thromboplastin time between groups when considering only

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

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

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

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

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

124 with both the anti-Xa assay and the partial thromboplastin time due to cirrhosis-related antithrombi

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

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

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

128 on factor XII activity and activated partial thromboplastin time in heparinase-treated samples in vit

129 2 caused a doubling of the activated partial thromboplastin time in human plasma at 2.4 microM and wa

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

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

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

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

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

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

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

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

138 -2-macroglobulin (A2M) and activated partial thromboplastin time measurement for coagulation factor X

139 nation, which may confound activated partial thromboplastin time measurements and limit its clinical

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

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

142 first dose of emicizumab, activated partial thromboplastin time normalized in 1 to 3 days, FVIII (hu

143 S or heparin, targeting an activated partial thromboplastin time of 150 +/- 10 seconds and 50 +/- 5 s

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

145 hich consisted of a target activated partial thromboplastin time of 45 to 60 seconds, for continuous

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

147 15H8 prolonged the activated partial thromboplastin time of baboon and human plasmas.

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

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

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

151 05, respectively), and the activated partial thromboplastin time prolonged significantly at 2 and 4 h

152 parin required to maintain activated partial thromboplastin time ratio 1.5-2.

153 entage of patients with an activated partial thromboplastin time ratio greater than 1.8 (47.8% vs 20%

154 ) despite it having a mean activated partial thromboplastin time ratio of 1.60 +/- 0.31.

155 The mean activated partial thromboplastin time ratio was higher in the severe acute

156 eference value, 0.80-1.25; activated partial thromboplastin time ratio, 0.88 second; reference range,

157 othrombin time, as well as activated partial thromboplastin time reagent and tissue factor-induced th

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

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

160 international normalized ratio, and partial thromboplastin time testing after a best practices advis

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

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

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

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

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

166 were associated with subtherapeutic partial thromboplastin time values.

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

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

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

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

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

172 Partial thromboplastin time was increased six- to sevenfold over

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

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

175 The activated partial thromboplastin time was unchanged.

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

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

178 gus monkeys as assessed by activated partial thromboplastin time without any evidence of bleeding.

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

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

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

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

183 mer, fibrinogen level, and activated partial thromboplastin time) or inflammation (WBC count, C-react

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

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

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

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

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

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

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

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

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

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

194 s abnormalities in prothrombin time, partial thromboplastin time, and platelet counts are relatively

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

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

197 ed liver enzymes, fatigue, prolonged partial thromboplastin time, arthralgia/myalgia, COVID-19, and h

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

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

200 national normalized ratio, activated partial thromboplastin time, d-dimers, factor VIII coagulant act

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

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

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

204 vity, magnesium, globulin, activated partial thromboplastin time, lymphocyte count (L%), and platelet

205 national normalized ratio, activated partial thromboplastin time, prothrombin activity, thrombin time

206 e of respiratory supports, activated partial thromboplastin time, prothrombin time, and deep vein thr

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

208 included prothrombin time, activated partial thromboplastin time, thrombin time, fibrinogen, D-dimer,

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

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

211 a parallel anti-Factor Xa/activated partial thromboplastin time-guided anticoagulation algorithm and

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

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

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

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

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

217 marked prolongation of the activated partial thromboplastin time.

218 n-linear relationship with activated partial thromboplastin time; curves were similar to those for ad

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

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

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

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

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

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

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

226 ) more rapidly and exhibited shorter partial thromboplastin times compared with HP controls.

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

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

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

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

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

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

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

234 Systemic partial thromboplastin times were not affected by local hirudin

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

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

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

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

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

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