ライフサイエンスコーパス: vascular injury

1 is one of the first lines of defence against vascular injury.

2 siRNA delivery to ameliorate the response to vascular injury.

3 ge accumulation in hyperlipidemic mice after vascular injury.

4 mediating the rapid response of platelets to vascular injury.

5 giotensin system (RAS) exacerbates renal and vascular injury.

6 rmed in 11 of the 22 patients with contained vascular injury.

7 hesion to damaged subendothelium at sites of vascular injury.

8 togenic therapy for epilepsy associated with vascular injury.

9 ering/translocation of platelets to sites of vascular injury.

10 rin formation, and thrombus growth following vascular injury.

11 ll growth, angiogenesis, and the response to vascular injury.

12 ether FLAP deletion modifies the response to vascular injury.

13 well located to interact with platelets upon vascular injury.

14 ted delivery of ectopic proteins to sites of vascular injury.

15 pathogenic, fibroproliferative responses to vascular injury.

16 black individuals appear more susceptible to vascular injury.

17 nd acute (ischemia-reperfusion [I/R]) ocular vascular injury.

18 little is known about resolution pathways in vascular injury.

19 nt vasculature and is frequently lost during vascular injury.

20 ng endothelial progenitor cell numbers after vascular injury.

21 y increased after angiogenic stimuli such as vascular injury.

22 cells rescued the proliferative response to vascular injury.

23 ular smooth muscle cell (VSMC) phenotype and vascular injury.

24 mbus body that guides leukocytes to sites of vascular injury.

25 n and fibrin deposition in in vivo models of vascular injury.

26 e gap between in-vitro and in-vivo models of vascular injury.

27 rterial thrombosis model in combination with vascular injury.

28 molecules that facilitate homing at sites of vascular injury.

29 t critically mediates hemostasis at sites of vascular injury.

30 erentiation in response to flow cessation or vascular injury.

31 ed proliferation in vitro and in response to vascular injury.

32 tin-T-cadherin association protected against vascular injury.

33 eration and a hyperproliferative response to vascular injury.

34 a therapeutic target in neutrophil-mediated vascular injury.

35 that atherosclerosis occurs as a response to vascular injury.

36 ential for hemostasis initiation at sites of vascular injury.

37 ts protection from neutrophil-mediated acute vascular injury.

38 mediated platelet aggregation at the site of vascular injury.

39 the formation of an occlusive thrombus after vascular injury.

40 einase-9 (MMP-9) gene, a crucial mediator of vascular injury.

41 eficient in nitrate/nitrite each exacerbated vascular injury.

42 ns as critical mediators of VSMC response to vascular injury.

43 ontributing to a pro-thrombotic status after vascular injury.

44 rtality in the developed world, results from vascular injury.

45 ited the development of IH in a rat model of vascular injury.

46 te dependence of FVIII activity on extent of vascular injury.

47 stores hemostasis in hemophilic animals upon vascular injury.

48 ls acute and long-term responses to arterial vascular injury.

49 ated in the pathogenesis of inflammation and vascular injury.

50 that mediates platelet adhesion to sites of vascular injury.

51 od platelets mediate the primary response to vascular injury.

52 vent overly robust platelet activation after vascular injury.

53 ntly recognized as a critical participant in vascular injury.

54 imes in both prdx2-/- and nrf2-/- mice after vascular injury.

55 or endothelial regeneration and repair after vascular injury.

56 that has been implicated in diverse forms of vascular injury.

57 may contribute to neointimal formation after vascular injury.

58 MR that mediates aldosterone augmentation of vascular injury.

59 ling modulates platelet function at sites of vascular injury.

60 rin polymers to form blood clots at sites of vascular injury.

61 ical task of stemming blood flow at sites of vascular injury.

62 atelet adhesion and thrombus formation after vascular injury.

63 ssential for endothelial proliferation after vascular injury.

64 mediating the early immune response and lung vascular injury.

65 s immune factors involved in the response to vascular injury.

66 by increased hydrodynamic forces at sites of vascular injury.

67 e reparative, proliferative state induced by vascular injury.

68 be implicated in transplantation and related vascular injury.

69 ulation is a hallmark of atherosclerosis and vascular injury.

70 on and neointimal VSM hyperplasia induced by vascular injury.

71 factor (TF) initiates blood coagulation upon vascular injury.

72 plete or delayed re-endothelialization after vascular injury.

73 f the endothelial barrier after inflammatory vascular injury.

74 vessels to establish hemostasis by repairing vascular injury.

75 tion in neointima obstruction in response to vascular injury.

76 4 promotes leukocyte recruitment to sites of vascular injury.

77 is may require an initiating insult, such as vascular injury.

78 surface, in circulation, and at the sites of vascular injury.

79 -stress, it adheres to platelets at sites of vascular injury.

80 ctivation and thrombus formation at sites of vascular injury.

81 ss for the endothelium, linking hemolysis to vascular injury.

82 tiation and resolution of inflammation after vascular injury.

83 ignificantly reduced in HPS6(-/-) mice after vascular injury.

84 formation and clot stability at the site of vascular injury.

85 deposition is a consequence or a trigger of vascular injury.

86 that 1,25-VitD3 promotes regeneration after vascular injury.

87 eta, which enhanced cell-based therapy after vascular injury.

88 ioplasty and stent implantation, often cause vascular injury.

89 emorrhage and 22 (15%) had several contained vascular injuries.

90 wn as Reticulon 4B, plays important roles in vascular injuries.

91 vs 3.9%; P = .03), repair and/or ligation of vascular injury (15.1% vs 5.4%; P = .001), complex leg f

92 vs 5.5%; P = .02), repair and/or ligation of vascular injury (54.8% vs 25.3%; P < .001), 4 or more tr

93 failure (1.9%; 95% CI, 1.6%-2.2%), and major vascular injury (6.4%; 95% CI, 5.8%-6.9%).

94 yte recruitment and inflammation at sites of vascular injury, a function thought to involve primarily

95 that CD39-null mice are protected from acute vascular injury after single-lobe warm IRI, and, relativ

96 Vascular injury also was associated with increased level

97 platelets per day into the blood that repair vascular injuries and prevent excessive bleeding.

98 uction are now applied to nearly half of the vascular injuries and should be a focus of training for

99 ves detection of traumatic contained splenic vascular injuries and should be considered to optimize d

100 Many markers of vascular injury and angiogenesis are elevated in severe

101 Markers of vascular injury and angiogenesis were measured before an

102 lls that aggregate to seal leaks at sites of vascular injury and are important in the pathology of at

103 e and lipid accumulation in animal models of vascular injury and atherosclerosis.

104 Vascular injury and atherothrombosis involve vessel infi

105 rmation and ameliorated hyperlipidemia after vascular injury and during atherosclerosis.

106 Endovascularly implanted leads risk vascular injury and endocarditis, and can be difficult t

107 Moreover, these MPs bind to sites of vascular injury and enhance thrombosis.

108 o correspond to the balloon dilation-induced vascular injury and healing processes.

109 ith the degree of injury in murine models of vascular injury and human atherosclerotic disease.

110 oviding a unique opportunity for quantifying vascular injury and immune response in vivo.

111 to induce apoptosis, a pathogenic feature of vascular injury and inflammation from multiple pathogene

112 apoptosis and its consequences in mediating vascular injury and inflammation.

113 nimal models, estrogen protects females from vascular injury and inhibits atherosclerosis.

114 Orai1 is upregulated in VSMC during vascular injury and is required for NFAT activity, VSMC

115 traits, including tau, amyloid beta plaques, vascular injury and Lewy bodies.

116 egulatory T cells normally function to limit vascular injury and may protect against the development

117 ll-known coagulation factor generated during vascular injury and plays an important role in lung infl

118 is able to inhibit arterial thrombosis after vascular injury and prevent the onset and progression of

119 and sufficient for neointima formation after vascular injury and provide evidence of vascular inflamm

120 is to investigate the effect of salsalate on vascular injury and repair in a rat model of carotid art

121 As such, fibrin(ogen) lies at the nexus of vascular injury and repair.

122 est that salsalate may be useful in reducing vascular injury and restenosis following interventional

123 paranase in controlling thrombosis following vascular injury and stent-induced flow disturbance.

124 ful mediator of thrombosis in the context of vascular injury and stent-induced flow disturbance.

125 , consolidates the platelet plug at sites of vascular injury and supports the recruitment of circulat

126 gulated in medial and neointimal VSMCs after vascular injury and that Orai3 knockdown inhibited LRC c

127 FVIIa that circulates in the blood prior to vascular injury and the molecular details of its activit

128 to localization of inflammation at sites of vascular injury and thrombosis.

129 ed NET formation contributes to inflammatory vascular injury and tissue damage.

130 2alpha promoter was markedly increased after vascular injury and was G/C Repressor dependent.

131 gulators of CaMKIIdelta expression following vascular injury and whether ectopic expression of miR-30

132 s feasible, helps detect clinically relevant vascular injuries, and results in diagnostic image quali

133 intravascular hemolysis, acute hypertension, vascular injury, and kidney dysfunction associated with

134 remity CT angiograms, noting the presence of vascular injury, and measured the attenuation in the low

135 odies exacerbates anticoagulant suppression, vascular injury, and plasma leakage.

136 cells mediate Ang II-induced SBP elevation, vascular injury, and T-cell activation in mice.

137 T cells blunted Ang II-induced hypertension, vascular injury, and T-cell activation; and gammadelta T

138 damage associated with ischemia-reperfusion, vascular injury, and/or rejection creates permissive con

139 Vascular injury appeared in 2 patients, in 1 case associ

140 s that regulate the activity of NR4A1 during vascular injury are not clear.

141 Neoangiogenesis and vascular injury are observed in IBD along with increased

142 eract directly with platelets in response to vascular injury, are among the main sources of properdin

143 the extent of platelet activation following vascular injury arise from the integration of different

144 ze but also these manifestations of coronary vascular injury, as do drugs which recruit signal transd

145 Access-site and access-related vascular injury (ASARVI) is still a major limiting facto

146 esonance imaging are part of the spectrum of vascular injury associated with aging of the brain and a

147 ndothelial progenitor cells after iatrogenic vascular injury associated with balloon angioplasty and

148 ia A, the complex normalized hemostasis upon vascular injury at a dose of 0.3 nmol/kg compared with 3

149 hi) or CD4(+)CD25(-) T cell subsets prior to vascular injury attenuated the development of PAH.

150 and is involved in the cellular response to vascular injury, but the regulation of TGFB1I1 expressio

151 ALK1 is upregulated in ECs during vascular injury by a synergistic cooperative mechanism b

152 nst diabetes mellitus-induced aggravation of vascular injury by promoting EPC function and reendothel

153 KII stimulates neointima proliferation after vascular injury by regulating cell proliferation through

154 Vascular injuries can be observed and their management i

155 loss of precapillary arterioles results from vascular injury causing endothelial dysfunction.

156 epileptogenesis in 2 different rat models of vascular injury, combining in vitro and in vivo biochemi

157 Following vascular injury, damaged or dysfunctional endothelial ce

158 contrast to exaggeration of the response to vascular injury, deletion of mPGES-1 in VSMCs, ECs, or b

159 standing of how platelets attach to sites of vascular injury, describing a new, to the best of our kn

160 ation and aggregation must occur at sites of vascular injury despite the constant presence of NO.

161 KLF4 mediates inflammatory responses after vascular injury/disease; however, the role of KLF4 in ab

162 Thus, platelets adherent to the site of vascular injury do not play the presumed preeminent role

163 he pulmonary microvasculature may exacerbate vascular injury during RBC transfusion.

164 m endothelial cells and leukocytes reflect a vascular injury during sepsis-induced disseminated intra

165 ofound changes in phenotype during repair of vascular injury, during remodeling in response to altere

166 odies, mTOR inhibition significantly reduced vascular injury, ERM phosphorylation, and macrophage inf

167 derived cells generating the neointima after vascular injury generally retained the expression of VSM

168 une modulation of neointimal formation after vascular injury has been investigated for several decade

169 However, the effect of salsalate on vascular injury has not been determined.

170 nisms regulating clot retraction at sites of vascular injury have been hampered by a paucity of in vi

171 as an important component of the response to vascular injury, having the potential to accelerate vasc

172 lls differentially modulates the response to vascular injury, implicating macrophage mPGES-1 as a car

173 n subsequent neointima formation elicited by vascular injury in a humanized mouse model.

174 matory, procoagulant states that induce lung vascular injury in an animal model of sepsis.

175 The absence of fibrin after vascular injury in beta3(-/-) mice is because of the abs

176 ted in more efficacious hemostasis following vascular injury in both the macro- and microcirculation.

177 The rate of vascular injury in modern combat is 5 times that reporte

178 lebrand factor (VWF), the first responder to vascular injury in primary hemostasis, is designed to ca

179 mostasis differs from hemostasis at sites of vascular injury in that it does not depend on major plat

180 loss of estrogen-mediated protection against vascular injury in the disrupting peptide mouse after ca

181 NRH is unclear, but has been associated with vascular injury in the liver sinusoids in clinical studi

182 study is to characterize the epidemiology of vascular injury in the wars of Iraq and Afghanistan, inc

183 ma Registry was interrogated (2002-2009) for vascular injury in US troops to identify specific injury

184 Vascular injury in vivo results in rapid changes in CaMK

185 wed increased neointimal formation following vascular injury in vivo, and SMCs explanted from these m

186 ation in vitro and neointimal formation with vascular injury in vivo.

187 control) was employed to examine effects on vascular injury in vivo.

188 sed in VSMCs, but it is down-regulated after vascular injury in vivo.

189 r EC migration in vitro and protects against vascular injury in vivo.

190 esence of various growth factors in vitro or vascular injury in vivo.

191 mice attenuates neointimal hyperplasia after vascular injury, in part by regulating tenascin-C expres

192 e, leukocyte-platelet-dependent responses to vascular injury, including inflammatory cell recruitment

193 tivated in vivo with increasing proteinuria, vascular injury induced a more robust thrombotic respons

194 e healing response of blood vessels from the vascular injury induced by therapeutic interventions is

195 Vascular injury induces a potent inflammatory response t

196 )tg and Lp(a)tg mice in both peritonitis and vascular injury inflammatory models, and was sufficient

197 Vascular injury initiates rapid platelet activation that

198 We have recently shown that vascular injury is associated with activation of albumin

199 In the systemic circulation, vascular injury is associated with downregulation of sar

200 helial progenitor cells (EPCs) into areas of vascular injury is critical to vascular repair.

201 Repair of the endothelium after vascular injury is crucial for preserving endothelial in

202 Platelet aggregation at sites of vascular injury is essential for hemostasis but also thr

203 Platelet activation at sites of vascular injury is essential for hemostasis, but it is a

204 Platelet aggregation at the site of vascular injury is essential in clotting.

205 inking AECAs of known specificity to in vivo vascular injury is lacking.

206 In conclusion, NMDA-induced retinal neuro/vascular injury is mediated by peroxynitrite-altered Trx

207 y-induced repression of SM22alpha gene after vascular injury is mediated through KLF4 binding to the

208 f circulating progenitors in the response to vascular injury is necessary if we are to develop effect

209 Platelet aggregation at sites of vascular injury is not only essential for hemostasis, bu

210 the pulmonary circulation, but the origin of vascular injury is unknown.

211 ters vascular neointima formation induced by vascular injury is unknown.

212 The role of mPGES-1 in the response to vascular injury is unknown.

213 elet adhesion on subendothelial matrix after vascular injury is well characterized, how the matrix bi

214 for vascular homeostasis and the response to vascular injury, is regulated by hydrolysis of proinflam

215 creted by platelets and endothelial cells on vascular injury, is required for thrombus formation.

216 s CD8+ effector T cells might directly cause vascular injury, iTregs may attenuate this response.

217 y to simultaneously block multiple events in vascular injury may allow Slit2 to effectively prevent a

218 The release of PDI during vascular injury may serve as a regulatory switch that al

219 ons from physiological pH (e.g., at sites of vascular injury) may represent a means to enhance VWF's

220 nd that, after IgG-APS or 4C5 injections and vascular injury, mean thrombus size was significantly sm

221 apolipoprotein E-deficient (ApoE(-/-)) mouse vascular injury model and a spontaneous ApoE(-/-) mouse

222 of these chemokine receptors in both a mouse vascular injury model and a spontaneously developed mous

223 tection from bleeding in acute and prolonged vascular injury model in hemophilia A mice.

224 Here we test that prediction in a mouse vascular injury model.

225 apolipoprotein E knock-out (ApoE(-/-)) mouse vascular injury model.

226 synthetic SMCs in vitro and in various mouse vascular injury models in vivo.

227 In response to vascular injuries, multipotent vascular stem cells, inst

228 In response to vascular injury, Myh11(R247C/R247C) mice showed signific

229 pendently recorded the presence of contained vascular injuries or active hemorrhage and the phase or

230 argets for control of VSMC remodeling during vascular injury or disease.

231 target for control of VSMC remodeling during vascular injury or disease.

232 paranase in controlling thrombosis following vascular injury or endovascular stenting.

233 in several pathological situations, such as vascular injury or organ fibrosis of various etiologies,

234 coreleased agonists, such as ADP at sites of vascular injury or synaptic transmitters acting at metab

235 ble analysis, only repair and/or ligation of vascular injury (OR, 3.32; 95% CI, 1.37-8.03), Abbreviat

236 cured by EVH have revealed retained clot and vascular injury, particularly during the 'learning curve

237 lar amyloid-beta accumulation, activation of vascular injury pathways and impaired vascular physiolog

238 r smooth muscle cells (VSMCs) in response to vascular injury plays a critical role in vascular lesion

239 s augmented as an adaptive response to limit vascular injury/proliferation and can be harnessed for i

240 sodic exposure to PM(2.5) induces reversible vascular injury, reflected in part by depletion of circu

241 lls differentially regulates the response to vascular injury, reflecting distinct effects of mPGES-1-

242 y which thrombi guide leukocytes to sites of vascular injury remain ill-defined.

243 Mechanisms of ischemic neuronal and vascular injury remain obscure.

244 Selective ligation of vascular injury remains an important management strategy

245 A normal hemostatic response to vascular injury requires both factor VIII (FVIII) and vo

246 Achieving hemostasis following vascular injury requires the rapid accumulation of plate

247 implicating aggrecan and aggrecanases in the vascular injury response after stenting.

248 may offer new opportunities to regulate the vascular injury response and promote vascular homeostasi

249 docosahexaenoic acid (DHA) can modulate the vascular injury response.

250 itochondrial Hsp90 as a key modulator of the vascular injury response.

251 ical for expression of genes involved in the vascular injury response.

252 induced platelet aggregation and an impaired vascular injury response.

253 highly associated with inhibition of chronic vascular injury responses and not due to the inhibition

254 herapeutic opportunity for the regulation of vascular injury responses.

255 a defect in thrombus consolidation following vascular injury, resulting in an increase in intrathromb

256 We hypothesized that vascular injury results in decreased bioavailability of

257 Thus platelet activation at sites of vascular injury results in the release of high local con

258 for hematopoietic stem cell abnormalities in vascular injury, right ventricular hypertrophy, and morb

259 ntravital microscopy following laser-induced vascular injury showed that defective hemostatic thrombu

260 ntribute to extracellular PDI binding at the vascular injury site.

261 et-platelet interactions may be localized to vascular injury sites because integrins must be activate

262 After vascular injury, SMC-derived AdvSca1 cells expand in num

263 eration and reduce neointimal hyperplasia in vascular injury states.

264 to improve, concerns remain with respect to vascular injury, stroke, paravalvular regurgitation, and

265 s broadly reduce VSMC responses and modulate vascular injury, suggesting that local activation of res

266 In an effort to inhibit the response to vascular injury that leads to intimal hyperplasia, this

267 re important determinants of the response to vascular injury that leads to neointimal hyperplasia and

268 ophil cytoplasmic autoantibody (ANCA) causes vascular injury that leads to small-vessel vasculitis.

269 Vascular injury that results in proliferation and dediff

270 Since aldosterone plays a key role in vascular injury, the aim of this study was to determine

271 However, in the presence of vascular injury, the time to thrombosis was dramatically

272 eration and phenotypic switch in response to vascular injury, therefore, representing a therapeutic t

273 eins in the systemic vasculature, leading to vascular injury, thrombosis, and occlusion.

274 m and the adaptive immune system at sites of vascular injury through increased T-cell motility and pr

275 oth hemostasis and thrombosis in response to vascular injury, thus identifying promising new targets

276 The contribution of (micro)vascular injury to CRMS is considered to be substantial.

277 telets aggregate and activate at the site of vascular injury to stem bleeding, they are subjected to

278 Inflammation and vascular injury triggered by ischemia/reperfusion (I/R)

279 ility modulates neointimal hyperplasia after vascular injury via accelerated EC repopulation and grow

280 The beneficial effect of salsalate on vascular injury was associated with upregulation of eNOS

281 Vascular injury was introduced by carotid air-dry endoth

282 A varying extent of vascular injury was observed after renal denervation in

283 Here, using multiple models of vascular injury, we found that time to arterial thrombot

284 od platelets mediate the primary response to vascular injury, we hypothesize that storage of coagulat

285 In a mouse model of vascular injury, we observed reduced neointima hyperplas

286 Using 2 models of vascular injury, we show that ISG12-deficient mice are p

287 Capsular, ureteric and vascular injuries were all significantly more frequent (

288 image acquisition; the other nine contained vascular injuries were seen at all phases.

289 ro and increases platelet accumulation after vascular injury when expressed either as a global knock-

290 Haemostasis occurs at sites of vascular injury, where flowing blood forms a clot, a dyn

291 ably, forces on VWF are elevated at sites of vascular injury, where VWF's hemostatic potential is imp

292 ficiency enhanced the thrombotic response to vascular injury, whereas protein Z deficiency increased

293 ) mice have prolonged thrombosis times after vascular injury, which can be protective in the state of

294 In the absence of vascular injury, wild type and heparanase overexpressing

295 hibited thrombus formation in vivo following vascular injury with an IC(50) of approximately 1 mg/kg.

296 k analysis suggest a major role of postnatal vascular injury with subsequent thrombus formation as th

297 By pairing localized vascular injury with thrombin microinjection in the mese

298 d show ultrastructural evidence of pulmonary vascular injury within 5 min of anti-MHC class I mAb inj

299 (mPGES-1) in mice attenuates the response to vascular injury without a predisposition to thrombogenes

300 ates both the acute and chronic responses to vascular injury without affecting hemostasis.