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 ole for supervillin in platelet adhesion and arterial thrombosis.

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

4 dysfunction that promotes platelet-dependent arterial thrombosis.

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

6 cal development as a potential treatment for arterial thrombosis.

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

8 exhibited a bleeding tendency and defective arterial thrombosis.

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

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

11 c protection against ferric chloride-induced arterial thrombosis.

12 bbeta3 signaling and confers protection from arterial thrombosis.

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

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

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

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

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

18 r thrombin formation and the acceleration of arterial thrombosis.

19 vascular thrombin formation, and accelerated arterial thrombosis.

20 ndent negative-feedback mechanism regulating arterial thrombosis.

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

22 t a novel therapeutic opportunity to prevent arterial thrombosis.

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

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

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

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

27 esion and aggregation during hemo stasis and arterial thrombosis.

28 n of more specific therapeutic inhibitors of arterial thrombosis.

29 nhuman primate model of electrolytic-induced arterial thrombosis.

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

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

32 vide effective treatment for both venous and arterial thrombosis.

33 is a promising tool to noninvasively detect arterial thrombosis.

34 s contributes to the development of coronary arterial thrombosis.

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

36 ggering atherosclerotic plaque formation and arterial thrombosis.

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

38 ssociated with increased risks of venous and arterial thrombosis.

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

40 c stroke results most commonly from cerebral arterial thrombosis.

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

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

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

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

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

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

47 hrombomodulin gene may constitute a risk for arterial thrombosis.

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

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

50 heparins uniquely suitable for prevention of arterial thrombosis.

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

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

53 unction, which contribute to pathogenesis of arterial thrombosis.

54 tential therapeutic target for prevention of arterial thrombosis.

55 antithrombotic activity in a rabbit model of arterial thrombosis.

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

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

58 te cardiovascular events are attributable to arterial thrombosis.

59 nhibition of DUSP3 may prove therapeutic for arterial thrombosis.

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

61 its implications in platelet maturation and arterial thrombosis.

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

63 thereby inhibiting platelet aggregation and arterial thrombosis.

64 rmation and stability in different models of arterial thrombosis.

65 otic state that was sufficient to accelerate arterial thrombosis.

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

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

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

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

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

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

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

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

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

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

76 No arterial thrombosis, acute cardiovascular events, or sud

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 2 infusions in wild-type mice interfere with arterial thrombosis and protect animals from activated p

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

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

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

105 Recurrent arterial thrombosis and venous thrombosis are frequent c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 1 are associated with age-dependent coronary arterial thrombosis in mice transgenic for human PAI-1.

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

154 thesis that hyperhomocysteinemia accelerates arterial thrombosis in mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 Arterial thrombosis is considered to arise from the inte

176 Arterial thrombosis is initiated by platelet activation,

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

178 Acute arterial thrombosis is the proximal cause of most cases

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

199 0.6 was associated with higher incidence of arterial thrombosis (nine of 123 vs zero of 217, respect

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

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

202 Arterial thrombosis occurring early after liver transpla

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

223 in lowers plasma prostacyclin and normalizes arterial thrombosis times.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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