ライフサイエンスコーパス: bleeding time

1 re antithrombotic and prolonged the template bleeding time.

2 ice, accompanied by a slight prolongation of bleeding time.

3 inhibitors administered to mice prolong the bleeding time.

4 est influence on bleeding severity score and bleeding time.

5 These results were reflected in a prolonged bleeding time.

6 o vWF or low doses of thrombin and prolonged bleeding time.

7 hemophilia A mice and normalized their tail-bleeding time.

8 racterized by pigment dilution and prolonged bleeding time.

9 dependent of vWf and was able to reduce skin bleeding time.

10 with any changes in platelet aggregation or bleeding time.

11 n (100%) resulted in an approximately 10-min bleeding time.

12 y useful and safe separation of efficacy and bleeding time.

13 these findings, GP V -/- mice had a shorter bleeding time.

14 nd modest twofold to threefold elevations in bleeding time.

15 ing as judged by measurements of the cuticle bleeding time.

16 e muscle tissue and by the standard template bleeding time.

17 d by normal platelet numbers and a prolonged bleeding time.

18 partial thromboplastin time, and the cuticle bleeding time.

19 ation induced by ADP and prolonging template bleeding time.

20 n sites and shortened DENV-induced prolonged bleeding time.

21 vimentin knockout mice had a prolonged tail bleeding time.

22 s high-dose non-targ-CD39, without prolonged bleeding time.

23 t differ from wild-type mice with respect to bleeding time.

24 lusive arterial thrombosis without affecting bleeding time.

25 Anti-ADAMTS-18 Ab shortens the tail vein bleeding time.

26 m diameter grafts without affecting template bleeding times.

27 gregation, P-selectin secretion, and shorter bleeding times.

28 on circulating platelets exhibited improved bleeding times.

29 a lower species such as mouse and to extend bleeding times.

30 lbumin or Pf4 BAC exhibit nearly normal tail bleeding times.

31 hese models and similar prolongation of tail bleeding times.

32 surprisingly the mutant mice display normal bleeding times.

33 e with these platelets exhibited normal tail bleeding times.

34 rabbit thrombosis models and did not prolong bleeding times.

35 ultimers and a corresponding prolongation of bleeding times.

36 tting times to baseline levels and corrected bleeding times.

37 e a macrothrombocytopenia and increased tail bleeding times.

38 uently, Unc13d(Jinx) mice had prolonged tail-bleeding times.

39 tivated partial thromboplastin and tail vein bleeding times.

40 botic doses, there is little prolongation of bleeding time (1.4-fold), which is in marked contrast to

41 s (58 +/- 4 minutes to 38 +/- 4 minutes) and bleeding times (170 +/- 13 seconds to 88 +/- 8 seconds)

42 (3) normal coagulation assays; (4) prolonged bleeding time; (5) absent clot retraction; (6) decreased

43 ce show macrothrombocytopenia with prolonged bleeding times, a defect in clot retraction, and increas

44 fivefold to sixfold or greater elevations in bleeding time; a single oral 30-microg/kg dose of L-738,

45 DMHD/NO had no effects on bleeding time, ACT, or blood pressure.

46 The average bleeding time also increased significantly (P <0.01) whe

47 ed in a significant increase in the template bleeding time, an increase in platelet PAR-1 thrombin re

48 Mice lacking apelin displayed a shorter bleeding time and a prothrombotic profile.

49 E2 treatment led to increased bleeding time and a resistance to thromboembolism.

50 Based on a prolonged bleeding time and absence of platelet aggregation in res

51 The GPx-3((-/-)) mice showed an attenuated bleeding time and an enhanced aggregation response to th

52 The tail bleeding time and blood loss remained unaltered, indicat

53 Bleeding time and carotid artery occlusion time were sig

54 saccharide from Fucus vesiculosus, decreases bleeding time and clotting time in hemophilia, possibly

55 Mice showed less prolonged bleeding time and fewer embolized vessels in the liver,

56 rmal clotting activity, enough to reduce the bleeding time and have a therapeutic benefit.

57 r to severe bleeding still reduced prolonged bleeding time and hemorrhage.

58 A standard bleeding time and papillary bleeding index score were re

59 In mice, the effects of CpG DNA on bleeding time and plasma levels of thrombin-antithrombin

60 e, as was hemostatic potential determined by bleeding time and platelet plug formation after venous i

61 of the anti-PAR4 pepducin into mice extended bleeding time and protected against systemic platelet ac

62 vivo, the lack of P2Y1 expression increased bleeding time and protected from collagen- and ADP-induc

63 e RIIIS/J mouse strain, exhibits a prolonged bleeding time and reduced plasma VWF levels.

64 ith mAb 2E8 shortened DENV-induced prolonged bleeding time and reduced viral Ag expression in the ski

65 In vivo assays revealed longer tail bleeding time and resistance to thromboembolism in Ip6k1

66 efects in hemostasis with a highly prolonged bleeding time and spontaneous bleeding events in approxi

67 ts in hemostasis, including highly prolonged bleeding time and spontaneous bleeding events, closely m

68 pinephrine-stimulated VWF release, prolonged bleeding time and thrombosis, largely due to defective e

69 In addition, shorter bleeding times and a prothrombotic phenotype were observ

70 have platelet defects resulting in increased bleeding times and a reduction in the number of platelet

71 Five of these patients had prolonged bleeding times and all had diminished responsiveness to

72 lt, G alpha(q)-deficient mice have increased bleeding times and are protected from collagen and adren

73 Paradoxically, the BKB2R(-/-) mice have long bleeding times and delayed carotid artery thrombosis, 78

74 Twf2a deficiency resulted in shortened tail bleeding times and faster occlusive arterial thrombus fo

75 fic sGC deficient mice showed prolonged tail-bleeding times and impaired FeCl(3)-induced carotid arte

76 hemostasis defects, including prolonged tail bleeding times and impaired mesenteric arteriole and car

77 HS1-null mice displayed increased bleeding times and increased time to occlusion in the Fe

78 unction in DKO mice is revealed by prolonged bleeding times and ineffective platelet activation in vi

79 iving mice displayed severely prolonged tail-bleeding times and macrothrombocytopenia.

80 ce lacking Galpha(i2) exhibit prolonged tail-bleeding times and markedly impaired thrombus formation

81 In contrast, tail bleeding times and thrombus formation in small arteriole

82 otic phenotype exemplified by prolonged tail-bleeding times and times-to-occlusion after FeCl(3) vess

83 , PAR4-deficient mice had markedly prolonged bleeding times and were protected in a model of arteriol

84 0.5 secs and increased to 63+/-21 secs after bleeding time, and 217+/-32 secs after 60-min shock.

85 n platelet aggregation (PA), blood pressure, bleeding time, and activated clotting time (ACT) were al

86 aggregation, platelet P-selectin expression, bleeding time, and activated clotting time (ACT) were qu

87 ystem results in thrombocytopenia, prolonged bleeding time, and giant platelets that are clinically i

88 Mutant mice also manifested an abnormal bleeding time, and histologic surveys of mouse tissues,

89 ightened platelet reactivity, shortened tail-bleeding time, and reduced survival following collagen/e

90 ithout a significant increase in the primary bleeding time, and secondary bleeding did not occur.

91 eta1-tubulin(-/-) mice also have a prolonged bleeding time, and their platelets show an attenuated re

92 g-chain n-3 fatty acids prolong the template bleeding time, and they may exert some beneficial effect

93 ion for its dramatic increase, the shortened bleeding time, and, possibly, the adverse cardiovascular

94 t aggregation and clot retraction, prolonged bleeding times, and cutaneous and gastrointestinal bleed

95 reoperative risk factor assessment, template bleeding times, and flow cytometry may allow the identif

96 ender, race, body weight, diabetes mellitus, bleeding times, and lipid profiles, indicated that this

97 e, presents with hypopigmentation, prolonged bleeding times, and platelet storage pool deficiency due

98 espans, but abnormal hepatic detoxification, bleeding times, and postnatal growth, the latter being a

99 ar normal, but they exhibit highly prolonged bleeding times, and their platelets aggregate poorly in

100 rac) causes macrothrombocytopenia, prolonged bleeding times, anemia, leukopenia, infertility, cardiom

101 In some mice, tail bleeding times are extremely prolonged, and thrombus for

102 ets maintain their normal discoid shape, and bleeding times are normal.

103 Bleeding times are prolonged in Tp-/- mice and their pla

104 Bleeding times are significantly prolonged in mutant ani

105 In other littermates, tail bleeding times are within the range of wild-type mice, a

106 cking HMGB1 in platelets exhibited increased bleeding times as well as reduced thrombus formation, pl

107 e of platelet inhibition and prolongation of bleeding times, as was sudden death due to acute thrombo

108 Additionally, a tail cutting bleeding time assay revealed that ACH-11 did not prolong

109 tanding in vivo efficacy; in fact, the mouse bleeding time at 1 mg/kg was 0.85 min compared to 29.28

110 Cutaneous bleeding time (BT) and platelet aggregation tests were o

111 Bleeding time (BT) was assessed in a separate study.

112 aggregation (PA), platelet CD62 expression, bleeding time (BT), heart rate, and mean arterial blood

113 stin time (APTT), prothrombin time (PT), and bleeding time (BT).

114 In this study of hemodialysis patients, bleeding times (BT) and the response of their platelets

115 eptor agonist peptide (TRAP) and to template bleeding times (BTs).

116 7E3 significantly prolonged bleeding time but had no effect on ACT and platelet P-se

117 motif signaling defect resulted in prolonged bleeding times but affected arterial thrombus formation

118 ficiency resulted in markedly prolonged tail bleeding times but also significant protection in differ

119 etreatment with aspirin (32 mg/kg) prolonged bleeding times but failed to prevent graft occlusion, su

120 aused a dose-dependent increase in tail vein bleeding time, but intracerebral hemorrhage (ICH) was no

121 n vivo where EHNA dramatically prolonged the bleeding time, but only in Abcc4 KO mice.

122 vivo, Vps34 deficiency had no impact on tail bleeding time, but significantly reduced platelet prothr

123 mice twice weekly for 6 weeks shortened tail bleeding time by 43% (n = 3; P < .01 vs L1-injected mice

124 ial thrombosis with no significant prolonged bleeding time by inhibiting platelet activation and extr

125 while only prolonging cuticle and mesenteric bleeding times by 3.3- and 3.1-fold, respectively, in pr

126 Prolonged bleeding time can result from defects in platelet adhesi

127 ted in thromboelastography (TEG) and cuticle bleeding time (CBT) tests.

128 platelet morphology under light microscopy, bleeding time, clot retraction, and platelet aggregation

129 and Bambi(+/-) mice exhibit mildly prolonged bleeding times compared with Bambi(+/+) littermates.

130 Correction of bleeding time correlated clinically with a dramatic redu

131 philia raises the possibility that decreased bleeding times could be achieved through activation of p

132 fold reduced blood loss, and improved buccal bleeding times decreased to 4 min for up to 5 y after tr

133 10 microM in diameter exhibited a shortened bleeding time, decreased prothrombin and partial thrombo

134 of beta1 integrins on platelets show normal bleeding times despite reduced platelet adhesion.

135 from skin incisions made using standardized bleeding time devices.

136 1 hour, neither systemic blood pressure nor bleeding time differed.

137 s.c. infusion of 20-HETE shortened the tail bleeding time dramatically.

138 mice that lacked eNOS had markedly decreased bleeding times even after endothelial NO production was

139 Bleeding times, ex vivo platelet aggregation, receptor o

140 on and aggregation were reduced in vitro and bleeding times extended.

141 ion of its metabolism and that the shortened bleeding time following rofecoxib administration is attr

142 Here, we report a prolonged bleeding time (>30 minutes in 10 of 11 rats tested) with

143 as well as blood urea nitrogen, creatinine, bleeding time, hematuria or proteinuria, and aspartate a

144 d cell differential counts, platelet number, bleeding time, hemoglobin, hematocrit, thyroid hormones,

145 (Delta760-762) mice exhibited prolonged tail bleeding times; however, none demonstrated spontaneous b

146 ling of Candida albicans by neutrophils, and bleeding time in 88 healthy subjects aged >65 y particip

147 correlates with a significantly shorter tail bleeding time in a murine model.

148 ark, Delaware), a test that has replaced the bleeding time in many clinical settings, was used.

149 platelet aggregation in vitro and elongates bleeding time in mice (iv administration of 30 mg of 3A/

150 emostatic plug as evidenced by the increased bleeding time in mice and humans with dense granule defi

151 e assay revealed that ACH-11 did not prolong bleeding time in mice at a dose of 3 mg/kg.

152 ro under arterial flow conditions, increased bleeding time in mice, and a decrease in experimentally

153 Tail bleeding time in platelet-specific PDI-deficient mice we

154 s, may help explain the relationship between bleeding time in vessel trauma and red blood cell hemato

155 t compound 35 did not significantly increase bleeding times in a rabbit model except at the highest d

156 The long bleeding times in BKB2R(-/-) mice also correct with L-NA

157 thrombin/antithrombin complex, and decreased bleeding times in Cdkn2a-deficient mice compared with co

158 IIA amounts and activity, as well as reduced bleeding times in homeostatic conditions and during seps

159 under flow is associated with prolonged tail-bleeding times in mice lacking one or both collagen rece

160 The bleeding times in mice transfused with eNOS-deficient pl

161 In in vivo studies, Slit2 prolonged bleeding times in murine tail bleeding assays.

162 this report we demonstrate prolonged in vivo bleeding times in PECAM-1-deficient mice.

163 e to spread normally may relate to prolonged bleeding times in vivo and defective clot formation in W

164 ve wound-triggered haemostasis and decreased bleeding times in vivo in a traumatic injury model.

165 complex and GPVI, but not of GPIIbIIIa, and bleeding time increased in WT mice.

166 lasma and activity levels as well as reduced bleeding times, indicating that mast cells are more effi

167 The prolonged bleeding times induced by ASA were unaffected by the inf

168 T the platelet morphology is normal, and the bleeding time is disproportionately prolonged.

169 dothelium- versus platelet-derived NO to the bleeding time, isolated platelets from either eNOS-defic

170 clopidogrel treatment strongly prolonged the bleeding time, it did not impact on bacterial loads duri

171 Nevertheless, tail bleeding time measurements revealed no severe bleeding t

172 Template bleeding time measurements were shorter (3.5 +/- 0.12 mi

173 Moreover, despite normal tail vein bleeding times, mKng1(-/-) mice displayed a significantl

174 and 3.1-fold, respectively, in provoked rat bleeding time models.

175 either a significant increase in the primary bleeding time nor secondary bleeding (total blood loss).

176 There were no gross differences in bleeding times nor in agonist-induced aggregation measur

177 of exogenous LPA recapitulated the prolonged bleeding time observed in Enpp2-Tg mice.

178 Further, the tail bleeding time of hemizygous mice was markedly prolonged

179 WHI-P131 prolonged the bleeding time of mice in a dose-dependent manner and imp

180 potently than factor VIIa and shortened the bleeding time of mice treated with enoxaparin.

181 eficient mice show a 40% prolongation of the bleeding time on amputation of the tip of the tail.

182 s after thrombolysis, without prolonging the bleeding time or causing systemic hypotension.

183 In wild-type mice, CpG DNA shortened the bleeding time parallel with dramatic increases in plasma

184 pa animals suffer from prolonged bleeding time, pigment dilution, kidney lysosomal enzyme

185 In functional assays including tail bleeding time, plasma clotting times, and tissue factor-

186 DMP 728 effects on bleeding time prolongation could be reversed more rapidl

187 tion attenuated platelet function, prolonged bleeding times, reduced or prevented cyclic flows and ab

188 d after 16 weeks of ALA feeding, whereas the bleeding time remained similar.

189 d artery thrombosis times and prolonged tail bleeding time resulting from elevated angiotensin II (An

190 gation and activation were also impaired and bleeding times significantly prolonged in these mutant m

191 In a cuticular bleeding time study, these animals also had only a parti

192 thermore, iNOS knock-out mice have prolonged bleeding time, suggesting that this novel mode of regula

193 tivated-clotting time (ACT) and template cut bleeding times, suggesting that CTRP-1 has promising ant

194 K-beta activity significantly prolonged tail bleeding times, suggesting that currently available IKK

195 By two different bleeding-time techniques, the treated hemophilic mice ga

196 Akt-1 null mice showed significantly longer bleeding times than wild-type mice.

197 We found that Pyk2-knockout mice had a tail bleeding time that was slightly increased compared with

198 idence of spontaneous bleeding, and had tail bleeding times that were not prolonged compared with wil

199 dministration of 30 mg of 3A/kg), increasing bleeding time to 16 vs 9 min for Prasugrel.

200 resulted in reduced viability with increased bleeding time to 28.6 min (control 6.4 min, P < 0.05).

201 ditional doses were required to increase the bleeding time to the maximum time allowed in the protoco

202 We compared a bleeding severity score and bleeding times to candidate gene haplotypes within pedig

203 -type platelets to SERT(-/-) mice normalized bleeding times to wild-type levels, suggesting that loss

204 The bleeding time was >2SD above the normal mean in 4 of 5 t

205 hrombocytopenic eNOS-deficient mouse and the bleeding time was measured.

206 Tail bleeding time was normal, and in vivo, the absence of AP

207 Most important, bleeding time was normalized by 48 hours after the deliv

208 otected against arterial thrombosis, whereas bleeding time was not affected.

209 Skin bleeding time was not modified or was moderately prolong

210 mpaired in sgk1(-/-) platelets, whereas tail bleeding time was not significantly enhanced.

211 A prolonged bleeding time was observed; platelet count and platelet

212 Tail bleeding time was prolonged in DREAM KO control mice, bu

213 arterial occlusion was delayed and the tail bleeding time was prolonged.

214 Accordingly, the tail bleeding time was prolonged.

215 The tail bleeding time was significantly lower in laropiprant gro

216 Bleeding time was significantly prolonged in all groups

217 Tail bleeding time was significantly prolonged with this high

218 hat induced a larger than 3-fold increase in bleeding time were 33 and 100 mug/kg/min for 3 and 13, r

219 romboplastin time, complete blood count, and bleeding time were recorded.

220 Systemic arterial blood pressure and bleeding time were unchanged with any treatment.

221 ranule components, platelet aggregation, and bleeding times were highly dependent on genetic backgrou

222 Bleeding times were increased (P < .05) in both the 7E3+

223 thrombus formation were attenuated and tail bleeding times were increased in comparison with those o

224 mice was not significantly altered; however, bleeding times were markedly decreased in eNOS-deficient

225 bset of preoperative aspirin users (n = 40), bleeding times were measured before and after aspirin us

226 cromol/liter adenosine diphosphate (ADP) and bleeding times were measured.

227 Bleeding times were moderately prolonged in the aspirin-

228 Interestingly, tail bleeding times were normal in RhoG(-/-) mice, suggesting

229 eline phenotype, hematological profiles, and bleeding times were normal, cd39(-/-) mice exhibited inc

230 However, mouse tail-bleeding times were not affected by deletion of TRAF3.

231 Intriguingly, bleeding times were not altered in DUSP3-deficient mice.

232 Furthermore, normal bleeding times were observed when marrow-ablated wild-ty

233 factor IX in the murine coagulation system, bleeding times were performed in normal, hemophilic, and

234 e nadir of platelet counts and restored tail bleeding time when applied to two passive ITP models ind

235 rolonged diluted thrombin time and tail-vein bleeding time, which were reversed by idarucizumab.

236 mboelastography and prolonged saphenous-vein bleeding times, which are consistent with FVIII deficien

237 resulted in a moderate 2.5-fold increase in bleeding time, while complete inhibition (100%) resulted

238 xpectedly, cd39-deficient mice had prolonged bleeding times with minimally perturbed coagulation para

239 ation in platelet aggregates emerging from a bleeding time wound, (ii) binding to Dacron in an arteri