ライフサイエンスコーパス: arterial thrombosis

1 (15%) and thrombosis (6%, including 4% with arterial thrombosis).

2 botic or pro-inflammatory conditions such as arterial thrombosis.

3 fect that impacts on platelet reactivity and arterial thrombosis.

4 al event, referred to here as an unexplained arterial thrombosis.

5 cid (ALA) reduces atherogenesis and inhibits arterial thrombosis.

6 illebrand factor (VWF) plays a major role in arterial thrombosis.

7 aling and establish it as a key regulator of arterial thrombosis.

8 lator in platelets, a critical mechanism for arterial thrombosis.

9 ole for supervillin in platelet adhesion and arterial thrombosis.

10 a newly recognized contributor to venous and arterial thrombosis.

11 ed with an increased risk of both venous and arterial thrombosis.

12 dysfunction that promotes platelet-dependent arterial thrombosis.

13 ) mice had increased ferric chloride-induced arterial thrombosis.

14 cal development as a potential treatment for arterial thrombosis.

15 he acute and chronic treatment of venous and arterial thrombosis.

16 exhibited a bleeding tendency and defective arterial thrombosis.

17 as a potential target for the prevention of arterial thrombosis.

18 ulted in 100% mortality within 4 days due to arterial thrombosis.

19 c protection against ferric chloride-induced arterial thrombosis.

20 bbeta3 signaling and confers protection from arterial thrombosis.

21 asis, and plays a critical role in mediating arterial thrombosis.

22 arget in the prevention and the treatment of arterial thrombosis.

23 months) with a cardiac condition at risk for arterial thrombosis.

24 d TF is critical in a macrovascular model of arterial thrombosis.

25 r thrombin formation and the acceleration of arterial thrombosis.

26 vascular thrombin formation, and accelerated arterial thrombosis.

27 ndent negative-feedback mechanism regulating arterial thrombosis.

28 plays a critical role in the development of arterial thrombosis.

29 t a novel therapeutic opportunity to prevent arterial thrombosis.

30 s and may open new avenues for prevention of arterial thrombosis.

31 In vivo, Rap1b-null mice are protected from arterial thrombosis.

32 al efficacy in two different models of acute arterial thrombosis.

33 esion and aggregation during hemo stasis and arterial thrombosis.

34 n of more specific therapeutic inhibitors of arterial thrombosis.

35 nhuman primate model of electrolytic-induced arterial thrombosis.

36 s of vascular injury is the primary event in arterial thrombosis.

37 b-IIIa antagonists are effective in blocking arterial thrombosis.

38 vide effective treatment for both venous and arterial thrombosis.

39 is a promising tool to noninvasively detect arterial thrombosis.

40 s contributes to the development of coronary arterial thrombosis.

41 agulant, widely used to treat and to prevent arterial thrombosis.

42 to blood is sufficient for the occurrence of arterial thrombosis.

43 ssociated with increased risks of venous and arterial thrombosis.

44 k vascular occlusion in an in vivo model for arterial thrombosis.

45 ulation and is thought to play a key role in arterial thrombosis.

46 c stroke results most commonly from cerebral arterial thrombosis.

47 quently examined in a stasis/injury model of arterial thrombosis.

48 ned subsequently in a stasis/injury model of arterial thrombosis.

49 mutation does not seem to increase risks for arterial thrombosis.

50 may play a major role in the development of arterial thrombosis.

51 otein C deficiency is a weak risk factor for arterial thrombosis.

52 hrombomodulin gene may constitute a risk for arterial thrombosis.

53 testing of this mutant in a rabbit model of arterial thrombosis.

54 efficacious in a rat FeCl3-induced model of arterial thrombosis.

55 heparins uniquely suitable for prevention of arterial thrombosis.

56 tion at different doses in various models of arterial thrombosis.

57 ion and preventing platelet CXCL12-dependent arterial thrombosis.

58 between potential risk factors and venous or arterial thrombosis.

59 ove the standard of care in the treatment of arterial thrombosis.

60 the basis of having an outcome of venous or arterial thrombosis.

61 tential therapeutic target for prevention of arterial thrombosis.

62 that contributes to hypertension-associated arterial thrombosis.

63 potentially contributing to postvaccination arterial thrombosis.

64 d cells, play a major role in hemostasis and arterial thrombosis.

65 inositol 3- kinase (PI3K) and contributes to arterial thrombosis.

66 as a potential target for the prevention of arterial thrombosis.

67 seeks to investigate the role of miR-223 in arterial thrombosis.

68 ggering atherosclerotic plaque formation and arterial thrombosis.

69 important role for 14-3-3zeta in regulating arterial thrombosis.

70 lators of thrombin-induced EC activation and arterial thrombosis.

71 unction, which contribute to pathogenesis of arterial thrombosis.

72 antithrombotic activity in a rabbit model of arterial thrombosis.

73 s that play a central role in hemostasis and arterial thrombosis.

74 platelet aggregates is a critical process in arterial thrombosis.

75 te cardiovascular events are attributable to arterial thrombosis.

76 nhibition of DUSP3 may prove therapeutic for arterial thrombosis.

77 art Gd analogue, EP-2104R, in a rat model of arterial thrombosis.

78 its implications in platelet maturation and arterial thrombosis.

79 was assessed in detail in 2 animal models of arterial thrombosis.

80 thereby inhibiting platelet aggregation and arterial thrombosis.

81 rmation and stability in different models of arterial thrombosis.

82 otic state that was sufficient to accelerate arterial thrombosis.

83 ic stability were assessed in a rat model of arterial thrombosis.

84 3 of 1008]; aHR, 0.92; 95% CI, 0.72-1.18) or arterial thrombosis (1.2% [n = 12 of 1014] vs 1.5% [n =

85 as characterized by the highest incidence of arterial thrombosis (17.4%), venous thrombosis (25.7%),

86 einuria (2%; 0), venous thrombosis (4%; 2%), arterial thrombosis (2%; 0), fatigue (8%; 0), infection

87 vels of ET-1 were found in APS patients with arterial thrombosis (2.00 +/- 0.87 versus 0.96 +/- 0.37

88 three probands were asymptomatic, 11 had had arterial thrombosis, 7 obstetrical complications, and 15

89 Relevant to both venous and arterial thrombosis, a Blood Systems Biology approach sh

90 No arterial thrombosis, acute cardiovascular events, or sud

91 s in HIT were associated with higher odds of arterial thrombosis (adjOR = 3.4, 95%CI = 1.2-9.5) and m

92 s in TTP were associated with higher odds of arterial thrombosis (adjOR = 5.8, 95%CI = 1.3-26.6), AMI

93 cuments the key role of TF activity in acute arterial thrombosis after atherosclerotic plaque disrupt

94 Adjusted hazard ratios for first arterial thrombosis after COVID-19 diagnosis compared wi

95 xidation of cellular lipids, contributing to arterial thrombosis after plaque rupture.

96 telet-delivered rADAMTS13 is able to inhibit arterial thrombosis after vascular injury and prevent th

97 aling pathway that plays a prominent role in arterial thrombosis and abdominal aortic aneurysm (AAA)

98 nts with aspirin for secondary prevention in arterial thrombosis and aspirin with anticoagulants for

99 hrombosis is well established, its effect on arterial thrombosis and atherosclerosis is controversial

100 opoietic Lnk deficiency leads to accelerated arterial thrombosis and atherosclerosis, but only in the

101 r the FVL mutation in mice leads to enhanced arterial thrombosis and atherosclerosis.

102 pathological conditions,including occlusive arterial thrombosis and bleeding disorders.

103 antithrombotic in mouse models of venous and arterial thrombosis and blocked the inflammatory effect

104 tant role of platelets in the development of arterial thrombosis and cardiovascular disease is well e

105 ulation factor XII (fXII) are protected from arterial thrombosis and cerebral ischemia-reperfusion in

106 of the role of hypercoagulable disorders in arterial thrombosis and discuss our approach to thrombop

107 for platelet adhesion and aggregation during arterial thrombosis and hemostasis.

108 sociated with heightened risks of venous and arterial thrombosis and hospitalization due to respirato

109 ignificant protection in different models of arterial thrombosis and in a model of ischemic stroke.

110 patients with (n = 16) and without (n = 11) arterial thrombosis and in non-APS patients with arteria

111 atelet (hem)ITAM signaling in the setting of arterial thrombosis and ischemic stroke.

112 mbotic target because of its central role in arterial thrombosis and its minor relevance for normal h

113 tions of platelet lysosomes to inflammation, arterial thrombosis and macrophage biology.

114 d allow real-time molecular imaging of acute arterial thrombosis and monitoring of the success or fai

115 nsfusions are associated with higher odds of arterial thrombosis and mortality among TTP and HIT pati

116 Smoking is a known risk factor for arterial thrombosis and myocardial infarction, and it ca

117 t aggregation, which plays a central role in arterial thrombosis and plaque formation.

118 in platelets and its efficacy in inhibiting arterial thrombosis and preventing hereditary and acquir

119 2 infusions in wild-type mice interfere with arterial thrombosis and protect animals from activated p

120 abeled fibrin deposition in baboon models of arterial thrombosis and related to platelet aggregation

121 uate evidence for endogenous fibrinolysis in arterial thrombosis and review techniques to assess it,

122 ction of Bin2fl/fl,Pf4-Cre mice in models of arterial thrombosis and stroke.

123 f the contribution of thrombin generation to arterial thrombosis and the role of platelets in venous

124 l for studying the molecular determinants of arterial thrombosis and thrombolysis.

125 Recurrent arterial thrombosis and venous thrombosis are frequent c

126 e studies with angiographic documentation of arterial thrombosis and, in the case of thrombolysis, re

127 that of large vessels (atherosclerosis with arterial thrombosis) and might suggest novel approaches

128 2 were due to early venous thrombosis, 2 to arterial thrombosis, and 2 to failure of desensitization

129 f intravascular thrombin, an acceleration of arterial thrombosis, and an increase in bronchoalveolar

130 d in polyphosphate accumulation, accelerated arterial thrombosis, and augmented activated platelet-dr

131 response that can cause intimal destruction, arterial thrombosis, and end-organ ischemia.

132 nionic phospholipid exposure in platelets in arterial thrombosis, and inhibition of this activity cou

133 ase characterized by venous thromboembolism, arterial thrombosis, and obstetric morbidities in the se

134 n vitro, but its in vivo role in hemostasis, arterial thrombosis, and postischemic infarct progressio

135 ice are resistant to ferric chloride-induced arterial thrombosis, and this resistance can be reversed

136 three etiologic subsets: arterial embolism, arterial thrombosis, and venous thrombosis.

137 tion of PIKfyve in mice leads to accelerated arterial thrombosis, and, unexpectedly, also to inapprop

138 tive in atherosclerotic vascular disease and arterial thrombosis, are thought to be centrally involve

139 pendent platelet activation and pathological arterial thrombosis, as tested in vivo by carotid occlus

140 VTE and arterial thrombosis (associated with anti-phospholipid s

141 to being fully efficacious in a rat model of arterial thrombosis at an infusion rate of 10 micrograms

142 VLeiden mutation may not as readily predict arterial thrombosis, because the normal and variant plat

143 e, poor graft function, primary nonfunction, arterial thrombosis, biliary complication, or serious in

144 g-related (eltrombopag: acute kidney injury, arterial thrombosis, bone pain, diarrhoea, myocardial in

145 a pivotal role not only in the formation of arterial thrombosis but also in the progression of ather

146 a) plays a central role in the initiation of arterial thrombosis, but its contribution to disseminate

147 These data suggest RBCs promote arterial thrombosis by enhancing platelet accumulation a

148 Thus, GPIbalpha contributes to arterial thrombosis by important adhesion mechanisms ind

149 thrombin-mediated endothelial activation and arterial thrombosis by targeting caspase recruitment dom

150 in might be due to its favourable effects on arterial thrombosis caused by vascular disease.

151 These results reveal that arterial thrombosis, cerebral infarction, and hemostasis

152 ease 2019 is associated with lower-extremity arterial thrombosis characterized by a greater clot burd

153 ubsequent vascular injury, we observed rapid arterial thrombosis compared with Hmox1+/+ mice receivin

154 ) did not demonstrate significantly enhanced arterial thrombosis compared with wild-type mice (n = 6)

155 In a mouse model of arterial thrombosis, CyPA-deficient mice were protected

156 eptor-delta antagonist, which predisposes to arterial thrombosis, decreased SIRT1 expression and incr

157 may explain the association between aPLs and arterial thrombosis, despite the lack of evidence of sur

158 sociations with the occurrence of venous and arterial thrombosis during follow-up.

159 , we hypothesized that HO-1 protects against arterial thrombosis during oxidant stress.

160 During arterial thrombosis, eosinophils are quickly recruited i

161 venous thromboembolism (VTE), mortality, and arterial thrombosis following a diagnosis of superficial

162 nclusion, platelet miR-223 is a regulator of arterial thrombosis following endothelial injury through

163 Leptin contributes to arterial thrombosis following vascular injury in vivo an

164 lism accounted for 38% (22/58) of the cases, arterial thrombosis for 36% (21/58), and venous thrombos

165 The construct prevented arterial thrombosis formation in all animals, while vira

166 n the endothelial integrity might also favor arterial thrombosis formation.

167 Five grafts were lost because of arterial thrombosis (four en bloc and one solitary).

168 ombosis group was further subdivided into an arterial thrombosis group (n = 17).

169 ls at presentation predicted higher rates of arterial thrombosis (hazard ratio [HR], 1.8; 95% CI, 1.1

170 ociated with an increased risk of venous and arterial thrombosis, hemorrhage, myelofibrosis, and acut

171 eficient mice presented a marked decrease in arterial thrombosis in 3 models of injury of the carotid

172 They were also protected against arterial thrombosis in a chemically induced model of art

173 eficiency of bioactive NO is associated with arterial thrombosis in animal models, individuals with e

174 telet aggregation plays an important role in arterial thrombosis in coronary heart disease, stroke, a

175 y an important role in the increased risk of arterial thrombosis in diabetic patients.

176 as rapid and suppressed PAR1 aggregation and arterial thrombosis in guinea pigs and baboons and stron

177 ed role for monocytes in the pathogenesis of arterial thrombosis in HIT and suggest that therapies ta

178 eceding platelet accumulation for initiating arterial thrombosis in injured vessels.

179 1 are associated with age-dependent coronary arterial thrombosis in mice transgenic for human PAI-1.

180 n, and that plasma HK contributes to induced arterial thrombosis in mice.

181 thesis that hyperhomocysteinemia accelerates arterial thrombosis in mice.

182 nds UHRA-9 and UHRA-10 significantly reduced arterial thrombosis in mice.

183 emic HO-1/CO for protection against vascular arterial thrombosis in murine aortic allotransplantation

184 mation can reduce atherosclerosis burden and arterial thrombosis in murine systems.

185 incidence of and risk factors for venous and arterial thrombosis in patients hospitalized with COVID-

186 s correlated significantly with a history of arterial thrombosis in patients with APS.

187 r gangrene or significant tissue loss and/or arterial thrombosis in peripheral arteries).

188 determine the effect of the FVL mutation on arterial thrombosis in the mouse, wild-type (Fv+/+), het

189 ggesting that TFPI gene transfer can prevent arterial thrombosis in the presence of severe shear stre

190 nicians should include the potential risk of arterial thrombosis in their assessment of the benefits

191 The construct effectively prevented arterial thrombosis in treated animals, whereas viral an

192 we show that LIMK1(-/-) mice have defective arterial thrombosis in vivo but do not differ from wild-

193 We studied how A1-A1 affects arterial thrombosis in vivo in lupus-prone (NZW x BXSB)F

194 on ex vivo, and PRT060318 strongly inhibited arterial thrombosis in vivo in multiple animal species w

195 fibers ex vivo and in 2 models of occlusive arterial thrombosis in vivo.

196 s, Ca(2+)-dependent platelet activation, and arterial thrombosis in vivo.

197 n VI (GPVI) is critical for the formation of arterial thrombosis in vivo.

198 nstrate that platelet-derived TSP1 modulates arterial thrombosis in vivo.

199 ing to bleeding complications, but unaltered arterial thrombosis, in these mice.

200 Current treatments for arterial thrombosis include anti-platelet agents such as

201 ed TF in vivo and in vitro and prevented the arterial thrombosis induced by CSE/IL-1beta.

202 vasorelaxation, and markedly delayed time to arterial thrombosis induced by photochemical injury.

203 marked protection against the development of arterial thrombosis, inflammation, and neointimal hyperp

204 rogress of VT is so much slower than that of arterial thrombosis initiated by subendothelial exposure

205 Platelet cross-linking during arterial thrombosis involves von Willebrand Factor (VWF)

206 Arterial thrombosis is a leading cause of death and disa

207 Arterial thrombosis is considered to arise from the inte

208 Arterial thrombosis is initiated by platelet activation,

209 Arterial thrombosis is less commonly documented, with 3%

210 of ADP in hemostasis and the development of arterial thrombosis is poorly understood.

211 Acute arterial thrombosis is the proximal cause of most cases

212 es not play a crucial role in hemostasis and arterial thrombosis, it aggravates thrombo-inflammatory

213 alphaIIbbeta3 antagonist, effectively blocks arterial thrombosis, it prolongs bleeding times at thera

214 been shown to regulate platelet function and arterial thrombosis, its effectors in platelets remain u

215 role of platelets, coagulation, and flow in arterial thrombosis, little attention has been paid to f

216 n rivaroxaban-treated patients with previous arterial thrombosis, livedo racemosa, or APS-related car

217 ow-dose aspirin in PV, and an excess rate of arterial thrombosis, major bleeding, and myelofibrotic t

218 It is concluded that venous and arterial thrombosis may develop in approximately 10% of

219 lly considered distinct disease states, with arterial thrombosis mediated predominantly by platelets

220 ombus weight reduction in an established rat arterial thrombosis model (10 mg/kg plus 10 mg/kg/h) whi

221 xhibit bleeding defects and protection in an arterial thrombosis model associated with platelet defic

222 the time to thrombosis using a laser-induced arterial thrombosis model in combination with vascular i

223 However, using a ferric chloride-induced arterial thrombosis model, the formation of stable throm

224 milar times to thrombosis in a laser-induced arterial thrombosis model.

225 o 10-fold higher than that of ANV in a mouse arterial thrombosis model.

226 sma level and perhaps even more potent in an arterial thrombosis model.

227 on and prolonged the time to occlusion in an arterial thrombosis model.

228 ithrombotic efficacies of DMP 728 in various arterial thrombosis models in dogs.

229 ntithrombotic activity in various venous and arterial thrombosis models, comparable with warfarin or

230 emostasis models; the converse was noted for arterial thrombosis models.

231 antibodies and challenged them in different arterial thrombosis models: the transient middle cerebra

232 bined abciximab/ticlopidine therapy inhibits arterial thrombosis more effectively than either treatme

233 Two eltrombopag recipients (arterial thrombosis n=1; myocardial infarction n=1) and

234 rial thrombosis and in non-APS patients with arterial thrombosis (n = 9).

235 0.6 was associated with higher incidence of arterial thrombosis (nine of 123 vs zero of 217, respect

236 ficant advances in regard to novel models of arterial thrombosis, novel mechanisms underlying thrombu

237 that mice lacking FXII are protected against arterial thrombosis (obstructive clot formation) and str

238 Arterial thrombosis occurring early after liver transpla

239 We tested the hypothesis that arterial thrombosis occurs in areas with high fluorodeox

240 ase), thrombosis of donor aorta (two cases), arterial thrombosis of one renal moiety (two cases), and

241 and symptoms of arterial compromise without arterial thrombosis or aneurysm were extracted from a pr

242 t at an increased risk of developing hepatic arterial thrombosis or other hepatic arterial complicati

243 nticoagulant therapy for suspected pulmonary arterial thrombosis or thromboembolism.

244 dded to the list of genetic risk factors for arterial thrombosis, particularly in younger patients an

245 d by the proposed model encompass venous and arterial thrombosis, ranging from low-shear-rate conditi

246 tory of severe obstetrical complications and arterial thrombosis received a diagnosis of hereditary t

247 ssociated with increased risks of venous and arterial thrombosis, recurrent fetal loss, and autoimmun

248 djustment for confounders, the occurrence of arterial thrombosis remained independently associated wi

249 tion to atherosclerotic plaque formation and arterial thrombosis remains unclear.

250 ) plays an important part in both venous and arterial thrombosis, rendering FXIa a potential target f

251 tainty regarding the magnitude of venous and arterial thrombosis risk associated with low protein S.

252 Maintaining a normal hematocrit may reduce arterial thrombosis risk in humans.

253 We observed that arterial thrombosis seemed to be related to the donor (o

254 As a symbolic feature of arterial thrombosis, severe stenosis in the blood vessel

255 us respiratory virus that can lead to venous/arterial thrombosis, stroke, renal failure, myocardial i

256 eral infarctions, upper- and lower-extremity arterial thrombosis, strokes, and repeated graft occlusi

257 n vitro flow chamber experiments and in vivo arterial thrombosis studies have been proved to be of vi

258 The consequences of arterial thrombosis such as myocardial infarction, strok

259 production and activation may predispose to arterial thrombosis, suggesting an explanation, at least

260 nto HO-1(+/+) (Balb/cJ) mice did not develop arterial thrombosis, surviving more than 56 days.

261 in response to photochemical injury-induced arterial thrombosis, systemic delivery of miR-181b reduc

262 than 40 years old had a higher incidence of arterial thrombosis than did younger recipients (eight o

263 , gangrene, or tissue loss and/or peripheral arterial thrombosis) that occurred after diagnosis were

264 (PAI-1) and its cofactor vitronectin (VN) to arterial thrombosis/thrombolysis in vivo is controversia

265 , 2021, excluding those with prior venous or arterial thrombosis, thrombophilia, cancer (except non-m

266 erhomocysteinemia enhances susceptibility to arterial thrombosis through a mechanism that is not caus

267 in lowers plasma prostacyclin and normalizes arterial thrombosis times.

268 come of a composite of adjudicated venous or arterial thrombosis, treatment with extracorporeal membr

269 Platelet-dependent arterial thrombosis triggers most heart attacks and stro

270 Arterial thrombosis triggers myocardial infarction and i

271 erial thrombus stability in a mouse model of arterial thrombosis using intravital microscopy.

272 Patients who present with arterial thrombosis usually develop their disease as a c

273 al link between inflammation and thrombosis, arterial thrombosis was assessed in KC-Tie2 and control

274 udy was to determine whether lower-extremity arterial thrombosis was associated with COVID-19 and whe

275 and TxA2 receptor function in GPIb-dependent arterial thrombosis was confirmed in vivo by characteriz

276 Arterial thrombosis was independently associated with ma

277 s thrombosis was observed more often in men; arterial thrombosis was more frequent in women.

278 transplantation; an 8% prevalence of hepatic arterial thrombosis was observed.

279 al complications; a 5% prevalence of hepatic arterial thrombosis was observed.

280 In addition to the aPL thrombophilic effect, arterial thrombosis was related to accelerated atheroscl

281 use of the potential role of TF in mediating arterial thrombosis, we have examined its expression in

282 , CyPA-deficient mice were protected against arterial thrombosis, whereas bleeding time was not affec

283 Hyperreactive RPs drive arterial thrombosis, whereas procoagulant platelets ampl

284 Platelets are critical in haemostasis and in arterial thrombosis, which causes heart attacks and othe

285 was proven efficacious in an animal model of arterial thrombosis, which demonstrates in vivo efficacy

286 ta) is considered a potential drug target in arterial thrombosis, which is a major cause of death wor

287 ntrolled activation of platelets may lead to arterial thrombosis, which is a major cause of myocardia

288 DIC score significantly predicted venous and arterial thrombosis with a hazard ratio (HR) for a high

289 /aggregation induced by collagen and in vivo arterial thrombosis with a mild effect in prolonging ble

290 utaneous coronary intervention and may cause arterial thrombosis with consequent myocardial necrosis.

291 K/STAT signaling in eosinophils, and carotid arterial thrombosis with increased eosinophil abundance

292 promising therapeutic role, as they inhibit arterial thrombosis with limited risk of bleeding.

293 we show, metformin prevents both venous and arterial thrombosis with no significant prolonged bleedi

294 n antithrombotic effect in a rabbit model of arterial thrombosis with rTFAA giving full efficacy at a

295 ibrinogen-platelet interactions that support arterial thrombosis with severe challenge.

296 in the rat wire coil model, more relevant to arterial thrombosis, with 15 (blood loss increase of 2-f

297 se its inhibition is protective in models of arterial thrombosis, with only minor effects on hemostas

298 integrin ligation, and suppresses occlusive arterial thrombosis without affecting bleeding time.

299 eta3 integrin activation and protection from arterial thrombosis without pathological bleeding.

300 group, 2 of 20 grafts (10%) were lost due to arterial thrombosis without patient mortality.