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 ng a mechanistic explanation for the lack of thrombus formation.

3 eta3 to support stable platelet adhesion and thrombus formation.

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

5 d following vessel injury and participate in thrombus formation.

6 functions thus plays a role in pathological thrombus formation.

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

8 ibute significantly to platelet function and thrombus formation.

9 nfluences blood coagulation and pathological thrombus formation.

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

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

12 yphosphate make significant contributions to thrombus formation.

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

14 RAP1 is critical for platelet activation and thrombus formation.

15 crovascular dysfunction, plaque erosion, and thrombus formation.

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

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

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

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

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

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

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

23 n is imperative in preventing arrhythmia and thrombus formation.

24 put parameters reflecting distinct stages of thrombus formation.

25 ving platelet cross-linking during occlusive thrombus formation.

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

27 mechanism of regulation of the initiation of thrombus formation.

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

29 ent mice increases fibrin generation but not thrombus formation.

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

31 onstrated poor vascularization and increased thrombus formation.

32 e effective hemostasis and prevent occlusive thrombus formation.

33 and platelet activation heterogeneity during thrombus formation.

34 ved from intravascular cells is required for thrombus formation.

35 integrin alphaIIbbeta3 is a prerequisite for thrombus formation.

36 ets, coagulation abnormalities, and enhanced thrombus formation.

37 a significant incidence of left ventricular thrombus formation.

38 e electrical isolation (LAAEI) could lead to thrombus formation.

39 ptors in supporting platelet aggregation and thrombus formation.

40 ntribution by Gas6 from both compartments to thrombus formation.

41 intravital imaging of laser-induced arterial thrombus formation.

42 nfarction risk, possibly through accelerated thrombus formation.

43 therosclerotic plaque rupture and subsequent thrombus formation.

44 in so doing blunts platelet aggregation and thrombus formation.

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

46 alysis of leukocytic tissue infiltration and thrombus formation.

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

48 a source other than platelets contributes to thrombus formation.

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

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

51 namic microenvironment plays a major role in thrombus formation.

52 negative regulator of platelet function and thrombus formation.

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

54 od vessel injury while preventing pathologic thrombus formation.

55 out activation of integrin alphaIIbbeta3 and thrombus formation.

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

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

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

59 itrullinates plasma proteins, thus affecting thrombus formation.

60 ects of PXR ligands on platelet function and thrombus formation.

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

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

63 that precedes development of carotid artery thrombus formation.

64 in subsequent platelet activation and stable thrombus formation.

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

66 planin expression in the venous wall trigger thrombus formation.

67 activity and plays an important role during thrombus formation.

68 hese observations suggest RBCs contribute to thrombus formation.

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

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

71 bleeding times and faster occlusive arterial thrombus formation.

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

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

74 Pathogenic thrombus formation accounts for the etiology of many ser

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

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

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

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

79 Although thrombus formation allows for Eph-ephrin engagement and

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

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

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

83 2 signaling is involved in the regulation of thrombus formation and clot retraction.

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

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

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

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

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

89 esterol increased platelet responsiveness in thrombus formation and ensuing fibrin formation, resulti

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

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

92 The kinetics of thrombus formation and fibrin generation were drasticall

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

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

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

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

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

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

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

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

101 PK drives thrombus formation and inflammation via activation of th

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

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

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

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

106 Defective thrombus formation and platelet activation were confirme

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

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

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

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

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

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

113 een published on the role of lamellipodia in thrombus formation and stability.

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

115 Accordingly, thrombus formation and stabilization under high arterial

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

117 The identification of a ruptured plaque with thrombus formation and subsequent occlusion or downstrea

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

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

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

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

122 elet aggregation, oxygen radical output, and thrombus formation, and carotid occlusion, while tail he

123 exhibited prolonged bleeding times, impaired thrombus formation, and reduced survival following major

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

125 ipodium formation is not required for stable thrombus formation, and that morphological changes of pl

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

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

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

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

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

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

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

137 gen all attenuated along with a reduction in thrombus formation (both in vitro and in vivo).

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

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

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

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

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

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

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

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

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

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

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

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

150 egulator of platelet activation and arterial thrombus formation dynamics.

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

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

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

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

155 tive phenotyping approach of platelet-fibrin thrombus formation has revealed interaction mechanisms o

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

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

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

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

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

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

162 event or block VWF oligomerization attenuate thrombus formation in a murine model of HIT.

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

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

165 we studied platelet activation and arterial thrombus formation in Apoe(-/-) and Ldlr(-/-) mice fed a

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

167 tion in the lungs, but the cancer-associated thrombus formation in CLEC-2-depleted mice was significa

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

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

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

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

172 Defective thrombus formation in Hermansky-Pudlak syndrome, associa

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

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

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

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

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

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

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

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

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

182 Thrombus formation in the cerebral microcirculation has

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

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

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

186 y inoculated in the back skin showed massive thrombus formation in the lungs, but the cancer-associat

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

188 croscopy demonstrated reduced post-traumatic thrombus formation in the pericontusional cortical micro

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

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

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

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

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

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

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

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

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

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

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

200 3 mug/g body weight inhibited laser-induced thrombus formation in vivo by causing a 70% decrease in

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

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

203 c ligand, SR12813, was observed to attenuate thrombus formation in vivo in humanised PXR transgenic m

204 om vascular cells, is essential for complete thrombus formation in vivo, but other extracellular ERp5

205 Consequently, targeting of EETs diminished thrombus formation in vivo, which identifies this approa

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

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

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

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

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

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

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

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

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

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

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

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

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

219 isorders indicated characteristic defects in thrombus formation, in cases of factor V, XI or XII defi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 mounts of serotonin that they release during thrombus formation or acute inflammation.

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

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

243 While thrombin is the key protease in thrombus formation, other coagulation proteases, such as

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

245 Thrombus formation over a ruptured atherosclerotic plaqu

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

247 Thrombus formation plays a major role in cardiovascular

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

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

250 oles of factor XIIIa-specific cross-links in thrombus formation, regression, or probability for embol

251 which platelet polyphosphate contributes to thrombus formation remains unclear.

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

253 Given that coagulation is involved in the thrombus formation stage on atherosclerotic plaque ruptu

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

255 en-dependent platelet aggregation, adhesion, thrombus formation, superoxide anion generation, and sur

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

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

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

259 on on biomaterials and related mechanisms of thrombus formation (thrombosis).

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

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

262 Thrombus formation time was markedly prolonged after ind

263 MIF reduced thrombus formation under arterial flow conditions in vit

264 Platelet aggregation responses, as well as thrombus formation under arterial flow conditions on col

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

266 tive Ca2+ signaling translated into impaired thrombus formation under flow and a protection of Bin2fl

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

268 differ between a static spreading assay and thrombus formation under flow.

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

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

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

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

273 gation at low doses of collagen and impaired thrombus formation under shear stress.

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 addition to its effects on acute thrombosis, thrombus formation was also markedly suppressed in alpha

277 Arterial thrombus formation was analyzed in a murine carotid arte

278 The poststenotic thrombus formation was critically dependent on bloodborn

279 Markedly, thrombus formation was enhanced in blood from chimeric m

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 Thrombus formation was quantified by intravital microsco

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

286 No significant thrombus formation was seen in alpha2AP(-/-) mice (P < .

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

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

289 Similarly, arterial thrombus formation was significantly reduced in response

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

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

292 The inhibition of thrombus formation was subsequently accomplished by inco

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

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 eptor 1), leading to platelet activation and thrombus formation, which can be inhibited by rivaroxaba

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

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

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