ライフサイエンスコーパス: thrombus formation

1 an optimal ADME and safety profile (e.g., no thrombus formation).

2 diminished both in vitro and in vivo during thrombus formation.

3 RAP1 is critical for platelet activation and thrombus formation.

4 crovascular dysfunction, plaque erosion, and thrombus formation.

5 th, whereas a lower value is associated with thrombus formation.

6 p57) are emerging as important regulators of thrombus formation.

7 d vessel is believed to be the main cause of thrombus formation.

8 /g body weight, a dose that does not inhibit thrombus formation.

9 l, Abcc4 KO mice exhibited markedly impaired thrombus formation.

10 orifice may play a role in the reduction of thrombus formation.

11 othelial cells after injury, is required for thrombus formation.

12 n is imperative in preventing arrhythmia and thrombus formation.

13 put parameters reflecting distinct stages of thrombus formation.

14 ving platelet cross-linking during occlusive thrombus formation.

15 tance of ERp5 and ERp57 in the initiation of thrombus formation.

16 mechanism of regulation of the initiation of thrombus formation.

17 merases, are important for the initiation of thrombus formation.

18 ent mice increases fibrin generation but not thrombus formation.

19 of fibrin, and subsequent platelet-dependent thrombus formation.

20 e effective hemostasis and prevent occlusive thrombus formation.

21 and platelet activation heterogeneity during thrombus formation.

22 ved from intravascular cells is required for thrombus formation.

23 integrin alphaIIbbeta3 is a prerequisite for thrombus formation.

24 ets, coagulation abnormalities, and enhanced thrombus formation.

25 a significant incidence of left ventricular thrombus formation.

26 ss in platelet function and life-threatening thrombus formation.

27 ptors in supporting platelet aggregation and thrombus formation.

28 ntribution by Gas6 from both compartments to thrombus formation.

29 intravital imaging of laser-induced arterial thrombus formation.

30 nfarction risk, possibly through accelerated thrombus formation.

31 in so doing blunts platelet aggregation and thrombus formation.

32 stem, such as diabetes, atherosclerosis, and thrombus formation.

33 alysis of leukocytic tissue infiltration and thrombus formation.

34 ice elicited a dose-dependent enhancement of thrombus formation.

35 a source other than platelets contributes to thrombus formation.

36 ll death in multiple organs, which triggered thrombus formation.

37 rom the vascular wall plays a role in venous thrombus formation.

38 namic microenvironment plays a major role in thrombus formation.

39 negative regulator of platelet function and thrombus formation.

40 ization, granule secretion, aggregation, and thrombus formation.

41 ular traps (NETs) have been shown to promote thrombus formation.

42 od vessel injury while preventing pathologic thrombus formation.

43 out activation of integrin alphaIIbbeta3 and thrombus formation.

44 h a role for ADP in platelet recruitment and thrombus formation.

45 emostasis is to prevent blood loss by stable thrombus formation.

46 at has recently been shown to participate in thrombus formation.

47 hycardia/AF itself, enhanced post-RFA atrial thrombus formation.

48 collagen is one of the initiating events in thrombus formation.

49 fully activated state, which is critical for thrombus formation.

50 enhance platelet aggregation, and accelerate thrombus formation.

51 antiplatelet agents because of their role in thrombus formation.

52 serves to prevent inappropriate or premature thrombus formation.

53 loited to control platelet activation during thrombus formation.

54 sruption and results in luminal dilation and thrombus formation.

55 ation impairs vascular function and enhances thrombus formation.

56 planin expression in the venous wall trigger thrombus formation.

57 activity and plays an important role during thrombus formation.

58 hese observations suggest RBCs contribute to thrombus formation.

59 al cells on vascular injury, is required for thrombus formation.

60 I and FIX supports efficient FVIII-dependent thrombus formation.

61 oteins, among them vitronectin, critical for thrombus formation.

62 bleeding times and faster occlusive arterial thrombus formation.

63 that precedes development of carotid artery thrombus formation.

64 ng a mechanistic explanation for the lack of thrombus formation.

65 eta3 to support stable platelet adhesion and thrombus formation.

66 d PAI-1 in the treatment of lenti-miR-30c to thrombus formation.

67 in subsequent platelet activation and stable thrombus formation.

68 d following vessel injury and participate in thrombus formation.

69 functions thus plays a role in pathological thrombus formation.

70 apex with the typical 3-layer appearance and thrombus formation.

71 ibute significantly to platelet function and thrombus formation.

72 nfluences blood coagulation and pathological thrombus formation.

73 ase in platelets) in platelet activation and thrombus formation.

74 erase (PDI), all of which serve to stabilize thrombus formation.

75 yphosphate make significant contributions to thrombus formation.

76 sists well beyond red cell escape and mature thrombus formation, (3) the most critical events for lim

77 provide evidence for a novel role of ERp5 in thrombus formation, a function that may be mediated thro

78 without PN2KPI treatment, the propagation of thrombus formation after 10 minutes and the amount of th

79 of neutrophils, monocytes, and platelets in thrombus formation after a laser-induced injury in vivo.

80 Data on left ventricular (LV) thrombus formation after primary percutaneous coronary i

81 adhesion and bleeding defects due to delayed thrombus formation after vessel injury.

82 ance to elucidate the mechanisms of platelet thrombus formation after vessel wall injury.

83 Although thrombus formation allows for Eph-ephrin engagement and

84 ice displayed accelerated occlusive arterial thrombus formation and a dramatically worsened outcome a

85 phosphate has been associated with increased thrombus formation and activation of coagulation factor

86 fully restored injury-induced microvascular thrombus formation and brain damage.

87 2 signaling is involved in the regulation of thrombus formation and clot retraction.

88 elet TLR4 exhibited prolonged times to first thrombus formation and complete occlusion (P < .05 vs Fn

89 -/-) mice exhibited prolonged times to first thrombus formation and complete occlusion and a signific

90 ential requirements of platelet integrins in thrombus formation and demonstrate that correct integrin

91 On the one hand, this could enhance thrombus formation and embolization of thrombi around th

92 istic studies suggests that RBCs can promote thrombus formation and enhance thrombus stability.

93 functional CLP36 translated into accelerated thrombus formation and enhanced procoagulant activity, a

94 They also displayed increased thrombus formation and fibrin deposition in in vivo mode

95 ide isomerase (PDI) is required for platelet thrombus formation and fibrin generation after arteriola

96 The kinetics of thrombus formation and fibrin generation were drasticall

97 ets, that inhibition of PDI blocked platelet thrombus formation and fibrin generation, and that endot

98 with platelets and their localization during thrombus formation and fibrinolysis under flow are not d

99 hesion of platelets is crucial in predicting thrombus formation and growth following a thrombotic eve

100 ypothesis that targeting factor XII prevents thrombus formation and has a beneficial effect on outcom

101 anules, release proteins that participate in thrombus formation and hemostasis.

102 n mice minimize trauma-induced microvascular thrombus formation and improve outcome, as reflected by

103 Ablation of Tregs reduced microvascular thrombus formation and improved cerebral reperfusion on

104 KNG appears to be instrumental in pathologic thrombus formation and inflammation but dispensable for

105 PK drives thrombus formation and inflammation via activation of th

106 adhesion and aggregation, and downregulates thrombus formation and inflammation.

107 tes (ZPI, PZ), kinetics of light/dye-induced thrombus formation and microhemodynamics were assessed i

108 lled platelet activation leads to pathologic thrombus formation and organ failure.

109 Integrin ligation mediates thrombus formation and outside-in signalling, which requ

110 Defective thrombus formation and platelet activation were confirme

111 f a vulnerable atherosclerotic plaque causes thrombus formation and precipitates cardiovascular disea

112 vivo that translated into defective arterial thrombus formation and protection from thrombo-inflammat

113 scent albumin marker to simultaneously track thrombus formation and protein transport following injur

114 suggests that this action is independent of thrombus formation and requires the engagement of glycop

115 ed tail-bleeding times and markedly impaired thrombus formation and stability in different models of

116 atelet BAMBI as a positive regulator of both thrombus formation and stability.

117 Thereby, CLEC-2 not only contributes to thrombus formation and stabilization but also plays a ce

118 Accordingly, thrombus formation and stabilization under high arterial

119 LAAI, an unexpectedly high incidence of LAA thrombus formation and stroke was observed despite OAC t

120 (AF) and underlies the potential for atrial thrombus formation and subsequent stroke.

121 -Infestin-4) on trauma-induced microvascular thrombus formation and the subsequent outcome in 2 mouse

122 This study evaluated the incidence of LAA thrombus formation and thromboembolic events after LAAI.

123 nological synapse formation, shear-dependent thrombus formation, and agonist-driven blood clotting.

124 able target for small molecule inhibition of thrombus formation, and its inhibition may prove to be a

125 P2Y12R regulates platelet activation and thrombus formation, and several antithrombotic drugs tar

126 quires integrin activation for adherence and thrombus formation, and thus regulation of talin present

127 siological mechanisms that may lead to valve thrombus formation; and 3) provide perspective on the im

128 es linking hypoxia, platelet reactivity, and thrombus formation are limited.

129 3) induces endothelial injury and subsequent thrombus formation are little understood, we used scanni

130 the atherosclerotic plaques responsible for thrombus formation are not necessarily those that imping

131 MNs and the subsequent fibrin generation and thrombus formation are strongly affected in mice deficie

132 Platelet activation and thrombus formation are under the control of signaling sy

133 vascular thiol isomerases that contribute to thrombus formation are yet to be defined at the molecula

134 A comprehensive understanding of thrombus formation as a physicochemical process that has

135 of postnatal vascular injury with subsequent thrombus formation as the leading cause of pediatric str

136 acking supervillin exhibit enhanced platelet thrombus formation at high shear stress.

137 ained RAP1-dependent platelet activation and thrombus formation at sites of vascular injury.

138 Assays measuring platelet aggregation (thrombus formation) at arterial shear rate mostly use co

139 ents a new mechanism in controlling arterial thrombus formation but also might be a useful target for

140 Because extracellular PDI is critical for thrombus formation but its extracellular substrates are

141 evidence that platelet PDI is essential for thrombus formation but not for hemostasis in mice.

142 bosis, systemic delivery of miR-181b reduced thrombus formation by 73% in carotid arteries and prolon

143 , suggesting that these factors may regulate thrombus formation by distinct mechanisms.

144 endothelial protein C receptor (EPCR) limits thrombus formation by enhancing activation of the protei

145 n of platelet function and the prevention of thrombus formation by GLP-1R agonists represent potentia

146 itions that promote platelet aggregation and thrombus formation by increased accumulation and activit

147 urred, integrin alpha(IIb)beta(3) stabilizes thrombus formation by providing agonist-independent "out

148 Three types of thrombus formation can be identified with a predicted hi

149 on a phenomenological mathematical model of thrombus formation, coagulation and platelet function ca

150 tration of cLDL in mice accelerated arterial thrombus formation compared to treatment with native LDL

151 led pulmonary fibrin deposition, and trebled thrombus formation compared with wildtype littermates in

152 ng anti-CLEC-2 antibody, INU1, resulted in a thrombus formation defect in vivo and ex vivo, revealing

153 e critically regulates platelet adhesion and thrombus formation during ischemic vascular events.

154 egulator of platelet activation and arterial thrombus formation dynamics.

155 n eptifibatide was infused to block platelet thrombus formation, enhanced fibrin generation and endot

156 radiation chimeras) attenuated shear-induced thrombus formation ex vivo, and PRT060318 strongly inhib

157 After each exposure, ex vivo thrombus formation, fibrinolysis, platelet activation, a

158 Anti-miR-148a also reduced thrombus formation following intravascular platelet acti

159 oietic cell DREAMs are required for platelet thrombus formation following laser-induced arteriolar in

160 he effects of Slit2 on platelet function and thrombus formation have never been explored.

161 ha2beta1-collagen interaction and subsequent thrombus formation, however its practical application su

162 e suppression activates platelets, increases thrombus formation, impairs vascular function, and promo

163 tion and limits platelet accumulation during thrombus formation, implicating TFPI in modulating plate

164 ntly, while injection of Cangrelor inhibited thrombus formation in a FeCl(3)-induced thrombosis model

165 Combined, both lead to increased thrombus formation in a mouse blood stasis model.

166 an in vivo model of thrombosis and defect in thrombus formation in an ex vivo blood flow system.

167 Here, we visualized thrombus formation in an in vivo murine model and an end

168 This study provides evidence for accelerated thrombus formation in arterioles and venules in the cere

169 l microvasculature is rendered vulnerable to thrombus formation in beta(s) mice via a neutrophil-depe

170 ner, reduces fibrin accumulation and impedes thrombus formation in blood under flow.

171 PKK or fXII deficiency reduced thrombus formation in both arterial and venous thrombosi

172 mbin, are responsible for increased arterial thrombus formation in COX-2 knockout mice.

173 aggregation response, and light/dye-induced thrombus formation in cremaster muscle arterioles were m

174 on of miR-30c increases PAI-1 expression and thrombus formation in DM2.

175 e of Blood, Ciciliano et al demonstrate that thrombus formation in ferric chloride (FeCl3) thrombosis

176 However, thrombus formation in FXII(-/-) mice is largely defectiv

177 Defective thrombus formation in Hermansky-Pudlak syndrome, associa

178 ular injury showed that defective hemostatic thrombus formation in HPS mice largely reflected reduced

179 Infusion of wild-type platelets rescued thrombus formation in HPS6(-/-) mice.

180 Targeting KNG reduced thrombus formation in ischemic vessels and improved cere

181 ignificantly reduced human platelet-mediated thrombus formation in laser-injured arterioles by > 75%

182 intravenous injection of exenatide inhibited thrombus formation in normoglycemic and hyperglycemic mi

183 model in wild-type mice, it failed to affect thrombus formation in P2Y(12) deficient mice.

184 ient blood reveals distinct abnormalities in thrombus formation in patients with severe combined immu

185 These findings support a role for fXII in thrombus formation in primates.

186 In contrast, tail bleeding times and thrombus formation in small arterioles were largely unaf

187 ntibody complexes and does not affect normal thrombus formation in the absence of anti-beta2GPI antib

188 ly decreased the progress of FeCl(3)-induced thrombus formation in the carotid artery.

189 Thrombus formation in the cerebral microcirculation has

190 nd in vivo, the absence of APP did not alter thrombus formation in the femoral artery.

191 t(-/-) mice) had a shorter time to occlusive thrombus formation in the injured carotid artery and a h

192 Medical therapy to eliminate thrombus formation in the LAA has been the standard of c

193 in alpha1-sGC protein displayed accelerated thrombus formation in the microcirculation after local t

194 platelets contain supervillin; (2) platelet thrombus formation in the PFA-100 is associated with hum

195 s enhance platelet activation and accelerate thrombus formation in the placenta and that this leads t

196 m for in vitro evaluation of shear-dependent thrombus formation in the setting of atherosclerosis.

197 th corresponds to an increased prevalence of thrombus formation in vessels injured by focused laser i

198 iated with accelerated, yet highly unstable, thrombus formation in vitro and in vivo.

199 a range of platelet functional responses and thrombus formation in vitro and in vivo.

200 and specifically MASP-1, play a key role in thrombus formation in vitro and in vivo.

201 ation, adhesion, spreading, aggregation, and thrombus formation in vitro and in vivo.

202 greater inhibition of platelet function and thrombus formation in vitro than chrysin under physiolog

203 agonists and S. aureus and reduced platelet thrombus formation in vitro.

204 emonstrate that vascular Gas6 contributes to thrombus formation in vivo and can be explained by the a

205 Results showed effective inhibition of thrombus formation in vivo and enhancement of vascular t

206 pected important contribution of laminins to thrombus formation in vivo and suggests that targeting t

207 3 mug/g body weight inhibited laser-induced thrombus formation in vivo by causing a 70% decrease in

208 onstrated that quercetin-3-rutinoside blocks thrombus formation in vivo by inhibiting PDI.

209 The compound inhibited thrombus formation in vivo following vascular injury wit

210 ballooning in vitro and markedly suppressed thrombus formation in vivo in a mouse model of thrombosi

211 (2)Cl ([AF660]FPR-ProT) during laser-induced thrombus formation in vivo in murine arterioles was exam

212 this interaction prevent platelet-dependent thrombus formation in vivo, without major bleeding compl

213 negative role in platelet activation and in thrombus formation in vivo.

214 hrough Galphaq but not Galpha13 in vitro and thrombus formation in vivo.

215 g blood in vitro and translated into reduced thrombus formation in vivo.

216 esion kinase Pyk2 in platelet activation and thrombus formation in vivo.

217 ted platelet activation, and is critical for thrombus formation in vivo.

218 platelets and whether cLDL enhances arterial thrombus formation in vivo.

219 ts of cLDL on vascular cells, platelets, and thrombus formation in vivo.

220 tg) mice, indicating a higher propensity for thrombus formation in vivo.

221 ctivation of the LOX-1 receptor and enhances thrombus formation in vivo.

222 binding and inhibit platelet aggregation and thrombus formation in vivo.

223 receptor 2-mediated platelet activation and thrombus formation in vivo.

224 ed stent was the most important correlate of thrombus formation in VLST.

225 d multi-parameter flow assay to characterize thrombus formation in whole blood from healthy subjects

226 These mediators can influence all aspects of thrombus formation, including platelet activation and ad

227 mal vWF multimers and impaired laser-induced thrombus formation, indicating that Galpha12 plays a pro

228 D) equations to represent three processes in thrombus formation: initiation, propagation and stabiliz

229 shown to potentiate platelet activation and thrombus formation, involving both CD40-dependent and -i

230 terial thrombus formation, it was shown that thrombus formation is associated with PDI secretion by p

231 Thus, after a short time, thrombus formation is governed by alphaIIbbeta3 binding

232 he use of fibrinolytic agents to prevent new thrombus formation is limited by an increased risk of bl

233 ynamics around a plaque promote pathological thrombus formation is not well understood.

234 c conditions in the absence of secreted PDI, thrombus formation is suppressed and maintains a quiesce

235 jury model, occlusion, but not initiation of thrombus formation, is delayed in GPVI-deficient and GPV

236 sis model in mice to induce in vivo arterial thrombus formation, it was shown that thrombus formation

237 s been identified as a predominant source of thrombus formation leading to significant thromboembolic

238 The time to occlusive thrombus formation lengthened in these mice and correlat

239 hatic valves revealed that platelet-mediated thrombus formation limits LV backflow under conditions o

240 croscopy to visualize endothelial damage and thrombus formation occurring in situ.

241 induced aggregation and approximately 80% of thrombus formation of human platelets on a collagen matr

242 ent static platelet adhesion to collagen and thrombus formation on collagen under low and high shear,

243 We found that platelet PDI is important for thrombus formation on collagen-coated surfaces under she

244 wild-type mice and showed severely impaired thrombus formation on ferric chloride-induced carotid ar

245 The NO releasing sensors induce less thrombus formation on the catheter surface in both veins

246 olonged bleeding times but affected arterial thrombus formation only after concomitant treatment with

247 associated complications either by enhancing thrombus formation or by initiating various signaling ev

248 hocardiographic examination without signs of thrombus formation or flow obstruction.

249 ret rate-limiting steps seen in experimental thrombus formation over a collagen-coated stenosis.

250 Thrombus formation over a ruptured atherosclerotic plaqu

251 increased bleeding times as well as reduced thrombus formation, platelet aggregation, inflammation,

252 Thrombus formation plays a major role in cardiovascular

253 uter simulations to predict patient-specific thrombus formation potential.(1) Their studies reveal a

254 dhesiveness, aggregation, degranulation, and thrombus formation, processes that contribute to the acc

255 which platelet polyphosphate contributes to thrombus formation remains unclear.

256 presents one of the major sources of cardiac thrombus formation responsible for TIA/stroke in patient

257 scular mortality may be explained by reduced thrombus formation resulting from hypocoagulability.

258 the control group in 7 of 8 patients without thrombus formation (specificity, 88%).

259 ity, immunogenicity risks and the hazards of thrombus formation, still need to be addressed.

260 f secreted PDI blocks the earliest stages of thrombus formation, suppressing both pathways.

261 elets is directly involved in hemostasis and thrombus formation, the sequence of events by which G pr

262 spite the indispensable role of platelets in thrombus formation, the studies linking hypoxia, platele

263 dent FVIII activation sets the threshold for thrombus formation through contact phase-generated FIXa.

264 ocytes are actively recruited to the site of thrombus formation through interactions with platelets a

265 Thrombus formation time was markedly prolonged after ind

266 MIF reduced thrombus formation under arterial flow conditions in vit

267 o1, which may contribute to Ca(2+) entry and thrombus formation under arterial shear.

268 Incubation with exenatide also inhibited thrombus formation under flow conditions in ex vivo perf

269 3Kbeta and Pyk2 significantly contributed to thrombus formation under flow.

270 tify genetic factors that influence platelet thrombus formation under high shear stress, we performed

271 l microscopy and exhibited enhanced platelet thrombus formation under high-shear but not low-shear co

272 ntrol, exposure to fire simulation increased thrombus formation under low-shear (73+/-14%) and high-s

273 regation under static conditions and reduced thrombus formation under physiological flow conditions.

274 previously demonstrated its positive role in thrombus formation using a zebrafish thrombosis model.

275 We show here the involvement of ERp5 in thrombus formation using the mouse laser-injury model of

276 factor (vWF) mediates platelet adhesion and thrombus formation via its interaction with the platelet

277 Arterial thrombus formation was analyzed in a murine carotid arte

278 The poststenotic thrombus formation was critically dependent on bloodborn

279 Ex vivo thrombus formation was determined with the use of the Ba

280 Unexpected evidence of pulmonary artery thrombus formation was found in 19% of SSc-PAH patients.

281 High inhibition efficiency of L-PGMA NPs in thrombus formation was further confirmed in vivo with a

282 Thrombus formation was greater in mice transplanted with

283 l PVs were successfully isolated; no char or thrombus formation was observed.

284 secreted by platelets from WT mice and that thrombus formation was reduced in whole blood from Mrp14

285 ie2 and control mice; mean time to occlusive thrombus formation was shortened by 64% (P=0.002) in KC-

286 found that ferric chloride-induced arterial thrombus formation was significantly greater in COX-2 kn

287 helial cell granule contents on PDI-mediated thrombus formation was studied by intravital microscopy

288 x-4) or by chelation of extracellular Ca(2+) Thrombus formation was studied on collagen-coated surfac

289 The inhibition of thrombus formation was subsequently accomplished by inco

290 Similarly, hemostasis and arterial thrombus formation were indistinguishable between wild-t

291 PDI accumulation and platelet thrombus formation were markedly decreased after vessel

292 ed IgG, and of IgG from normal human sera on thrombus formation were measured in mice after arterial

293 ylserine exposure, aggregation, and in vitro thrombus formation were significantly impaired in sgk1(-

294 in clot faster, and showed markedly enhanced thrombus formation when perfused over a collagen-coated

295 l cell injury in the kidney that may lead to thrombus formation when severe or manifest by multilayer

296 Unlike the first steps of thrombus formation, which are GpIIb/IIIa-dependent, our

297 o the atherosclerotic material then triggers thrombus formation, which occludes the artery.

298 rect inhibition of FXIa can block pathologic thrombus formation while preserving normal hemostasis.

299 herogenic lipoproteins and platelet-mediated thrombus formation with a specific focus on stroke.

300 After a similar initial rate of thrombus formation with and without PN2KPI treatment, th