ライフサイエンスコーパス: bleeding time

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

2 re antithrombotic and prolonged the template bleeding time.

3 inhibitors administered to mice prolong the bleeding time.

4 est influence on bleeding severity score and bleeding time.

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

6 These results were reflected in a prolonged bleeding time.

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

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

9 racterized by pigment dilution and prolonged bleeding time.

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

11 with any changes in platelet aggregation or bleeding time.

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

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

14 botic efficacy and no prolongation of kidney bleeding time.

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

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

17 nd modest twofold to threefold elevations in bleeding time.

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

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

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

21 partial thromboplastin time, and the cuticle bleeding time.

22 ation induced by ADP and prolonging template bleeding time.

23 ced mouse carotid artery thrombosis and tail bleeding time.

24 thrombosis with a mild effect in prolonging bleeding time.

25 aggregation and yet did not prolong in vitro bleeding time.

26 transmittance aggregometry without affecting bleeding time.

27 rved for enoxaparin with a similar effect on bleeding time.

28 odel of thrombocytopenia, and prolonged tail bleeding time.

29 growth and stability without increasing tail bleeding time.

30 sociated with a significant increase in tail bleeding time.

31 vimentin knockout mice had a prolonged tail bleeding time.

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

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

34 lusive arterial thrombosis without affecting bleeding time.

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

36 tivated partial thromboplastin and tail vein bleeding times.

37 m diameter grafts without affecting template bleeding times.

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

39 on circulating platelets exhibited improved bleeding times.

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

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

42 hese models and similar prolongation of tail bleeding times.

43 surprisingly the mutant mice display normal bleeding times.

44 e with these platelets exhibited normal tail bleeding times.

45 s compared with control mice but with normal bleeding times.

46 collagen but did not affect the murine tail bleeding times.

47 arotid arterial thrombosis without prolonged bleeding times.

48 ring ischemic stroke without prolonging tail bleeding times.

49 e to arterial thrombosis with unaltered tail bleeding times.

50 rabbit thrombosis models and did not prolong bleeding times.

51 ultimers and a corresponding prolongation of bleeding times.

52 tic defect and prolonged arterial and venous bleeding times.

53 tting times to baseline levels and corrected bleeding times.

54 e a macrothrombocytopenia and increased tail bleeding times.

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

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

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

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

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

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

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

62 s mutation on hemostasis as measured by tail-bleeding times, although the time to thrombus formation

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

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

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

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

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

68 uced platelet aggregation without increasing bleeding time and blocked TYRO3-dependent functions in t

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

70 Bleeding time and carotid artery occlusion time were sig

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 We also compared tail bleeding times and activation of platelets from WT and A

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

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

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

92 c44a2 null mice (Slc44a2(KO)) have increased bleeding times and delayed thrombosis compared to wild-t

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

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

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

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

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

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

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

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

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

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

103 0.5 secs and increased to 63+/-21 secs after bleeding time, and 217+/-32 secs after 60-min shock.

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

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

106 the increased arterial occlusion time, tail bleeding time, and blood coagulation parameters in rat m

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

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

109 post-MI), light transmittance aggregometry, bleeding time, and histological and molecular analyses w

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

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

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

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

114 lat, circulating tPA, fibrinolytic activity, bleeding time, and time to thrombosis, which are reverse

115 viral titers, soluble NS1 levels, mouse tail bleeding time, and vascular leakage at skin injection si

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

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

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

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

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

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

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

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

124 GT gene therapy showed significantly reduced bleeding time (approximately fivefold to eightfold) and

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

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

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

128 Bleeding times are significantly prolonged in mutant ani

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

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

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

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

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

134 vely blocks arterial thrombosis, it prolongs bleeding times at therapeutic doses.

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

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

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

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

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

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

141 7E3 significantly prolonged bleeding time but had no effect on ACT and platelet P-se

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

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

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

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

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

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

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

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

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

151 Prolonged bleeding time can result from defects in platelet adhesi

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

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

154 splayed significantly reduced blood loss and bleeding time compared with F8-/-mice.

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

156 dY311F mice have significantly enhanced tail-bleeding times compared with WT littermate controls, whi

157 hemostatic activity in vivo, as assessed by bleeding time correction in aspirin-treated mice.

158 Correction of bleeding time correlated clinically with a dramatic redu

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

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

161 10 microM in diameter exhibited a shortened bleeding time, decreased prothrombin and partial thrombo

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

163 from skin incisions made using standardized bleeding time devices.

164 osphorylation occurs through TXA(2) Although bleeding times did not significantly differ between PTPN

165 1 hour, neither systemic blood pressure nor bleeding time differed.

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

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

168 Bleeding times, ex vivo platelet aggregation, receptor o

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

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

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

172 d not significantly affect coagulation time, bleeding time, heart rate, and blood pressure.

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

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

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

176 F haploinsufficiency and exhibited prolonged bleeding times, impaired thrombus formation, and reduced

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

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

179 nt antithrombotic efficacy without increased bleeding time in animal models (Weitz, J.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 f aspirin and/or clopidogrel, did not affect bleeding time or platelet aggregation.

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

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

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

219 y of surface receptors, coagulation profile, bleeding time, plasma-dependent thrombin generation (thr

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

221 xcellent antithrombotic efficacy and minimal bleeding time prolongation in monkey models relative to

222 or decoupling of antithrombotic efficacy and bleeding time prolongation.

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

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

225 Col5a1+/- mice demonstrated increased tail bleeding time, reproduced the signaling defects observed

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

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

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

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

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

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

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

233 erapy alone but achieved a 5-to-7-fold lower bleeding time than UFH/bivalirudin.

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

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

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

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

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

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

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

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

242 end points included any clinically relevant bleeding, time to mobilization, duration of hospitalizat

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

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

245 telet abnormalities in CKD are inconsistent, bleeding time was mostly prolonged and platelet adhesion

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

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

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

249 Skin bleeding time was not modified or was moderately prolong

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

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

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

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

254 Accordingly, the tail bleeding time was prolonged.

255 The tail bleeding time was significantly lower in laropiprant gro

256 Bleeding time was significantly prolonged in all groups

257 Tail bleeding time was significantly prolonged with this high

258 Hemostasis, as measured by tail bleeding time, was not altered in Syk Y342F mice, but th

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

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

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

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

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

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

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

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

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

268 Bleeding times were moderately prolonged in the aspirin-

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

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

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

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

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

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

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

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

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

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

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

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