ライフサイエンスコーパス: vascular injury

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

2 plete or delayed re-endothelialization after vascular injury.

3 f the endothelial barrier after inflammatory vascular injury.

4 vessels to establish hemostasis by repairing vascular injury.

5 ER stress and apoptosis, are associated with vascular injury.

6 tion in neointima obstruction in response to vascular injury.

7 4 promotes leukocyte recruitment to sites of vascular injury.

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

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

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

11 ctivation and thrombus formation at sites of vascular injury.

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

13 tiation and resolution of inflammation after vascular injury.

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

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

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

17 two harvesting approaches on the donor site vascular injury.

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

19 ioplasty and stent implantation, often cause vascular injury.

20 ge accumulation in hyperlipidemic mice after vascular injury.

21 mediating the rapid response of platelets to vascular injury.

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

23 hesion to damaged subendothelium at sites of vascular injury.

24 togenic therapy for epilepsy associated with vascular injury.

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

26 rin formation, and thrombus growth following vascular injury.

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

28 ether FLAP deletion modifies the response to vascular injury.

29 well located to interact with platelets upon vascular injury.

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

31 pathogenic, fibroproliferative responses to vascular injury.

32 black individuals appear more susceptible to vascular injury.

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

34 little is known about resolution pathways in vascular injury.

35 e their presence was aligned with regions of vascular injury.

36 nt vasculature and is frequently lost during vascular injury.

37 ng endothelial progenitor cell numbers after vascular injury.

38 y increased after angiogenic stimuli such as vascular injury.

39 cells rescued the proliferative response to vascular injury.

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

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

42 rmation are hallmarks of atherosclerosis and vascular injury.

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

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

45 rterial thrombosis model in combination with vascular injury.

46 molecules that facilitate homing at sites of vascular injury.

47 t critically mediates hemostasis at sites of vascular injury.

48 erentiation in response to flow cessation or vascular injury.

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

50 a therapeutic target in neutrophil-mediated vascular injury.

51 that atherosclerosis occurs as a response to vascular injury.

52 ts protection from neutrophil-mediated acute vascular injury.

53 mediated platelet aggregation at the site of vascular injury.

54 the formation of an occlusive thrombus after vascular injury.

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

56 ting levels of tPA and to fibrinolysis after vascular injury.

57 eficient in nitrate/nitrite each exacerbated vascular injury.

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

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

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

61 omoting recruitment of platelets to sites of vascular injury.

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

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

64 stores hemostasis in hemophilic animals upon vascular injury.

65 RNA-223 as a potential therapeutic target in vascular injury.

66 y and as a contributor to fibrinolysis after vascular injury.

67 been implicated in intimal remodeling during vascular injury.

68 scores or alter markers of inflammation and vascular injury.

69 ated in dog, which was attributed to diffuse vascular injury.

70 romotes endothelial activation and pulmonary vascular injury.

71 rated, with no histopathological evidence of vascular injury.

72 signaling regulates intima hyperplasia after vascular injury.

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

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

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

76 siRNA delivery to ameliorate the response to vascular injury.

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

78 decreases neutrophil recruitment to sites of vascular injury.

79 eration and a hyperproliferative response to vascular injury.

80 ential for hemostasis initiation at sites of vascular injury.

81 ed with smooth muscle cells (SMCs) following vascular injury.

82 or endothelial regeneration and repair after vascular injury.

83 by increased hydrodynamic forces at sites of vascular injury.

84 ng platelets in the blood stream to sites of vascular injury.

85 e reparative, proliferative state induced by vascular injury.

86 be implicated in transplantation and related vascular injury.

87 ulation is a hallmark of atherosclerosis and vascular injury.

88 on and neointimal VSM hyperplasia induced by vascular injury.

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

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

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

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

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

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

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

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

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

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

99 Vascular injury and atherothrombosis involve vessel infi

100 s insight into the synergy between pulmonary vascular injury and diminished BMP9 signaling in the pat

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

102 Vascular injury and dysfunction of the perivascular adip

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

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

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

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

107 Vascular injury and inflammation during percutaneous cor

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

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

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

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

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

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

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

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

116 signaling under normal conditions and after vascular injury and regrowth into the retina.

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

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

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

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

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

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

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

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

125 2alpha promoter was markedly increased after vascular injury and was G/C Repressor dependent.

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

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

128 is a complex process that includes atrophy, vascular injury, and a variety of age-associated neurode

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

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

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

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

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

134 ic differentiation, ADAM17-induced renal and vascular injury, and TNFalpha-induction of neutral-sphin

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

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

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

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

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

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

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

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

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

144 ous vitamin C may attenuate inflammation and vascular injury associated with sepsis and acute respira

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

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

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

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

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

150 Vascular injuries can be observed and their management i

151 y highlights an important mechanism by which vascular injury can impair brain function.

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

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

154 Following vascular injury, damaged or dysfunctional endothelial ce

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

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

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

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

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

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

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

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

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

164 stemic inflammation in health, and renal and vascular injury favoring VC in hyperphosphatemic CKD.

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

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

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

168 es the first discussion of the management of vascular injuries in the island-hopping battles of the P

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

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

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

172 indings are validated in other VCA patients, vascular injury in mild rejection might warrant a differ

173 nvestigated whether these purines can impact vascular injury in more clinically-relevant E.coli (non-

174 d disabling visible manifestation of digital vascular injury in patients with SSc.

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

176 Here we show that vascular injury in rodent carotid arteries induces YY1 e

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

178 results highlight the possible relevance of vascular injury in the context of VCA, as its presence m

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

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

181 Because vascular injury in the superior vena cava-right atrium d

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

183 Vascular injury in vivo results in rapid changes in CaMK

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

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

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

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

191 Vascular injury induces a potent inflammatory response t

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

193 ild closed-head impact injury, and rats with vascular injury inflicted by photothrombosis.

194 Vascular injury initiates rapid platelet activation that

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 Vascular injury leads to membrane disruption, ATP releas

212 traumatic microbleeds as a form of traumatic vascular injury may aid in identifying patients who coul

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

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

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

216 normalities in markers indicating axonal and vascular injury, metabolic and mitochondrial dysfunction

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

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

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

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

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

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

223 naling, ECM deposition, and proliferation in vascular injury models.

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

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

226 For the management of vascular injuries occurring after different orthopaedic

227 eries of patients presenting with iatrogenic vascular injuries of the lower limbs following orthopaed

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

229 y safety outcomes were accessed site-related vascular injury or bleeding complications.

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 fluences platelet plug formation at sites of vascular injury (primary hemostasis).

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

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

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

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

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

248 se C-delta) regulates multiple components of vascular injury response including apoptosis of SMCs and

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

250 red endothelium is an important component of vascular injury response.

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

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

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

254 ains its role in developmental angiogenesis, vascular injury responses, and cell migration.

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

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

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

258 receptor DARC on endothelial cells leads to vascular injury, shedding light on pathogen-driven contr

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

260 Blood clotting at the vascular injury site is a complex process that involves

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

262 nsmural infiltration of myeloid cells at the vascular injury site.

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

264 eration and reduce neointimal hyperplasia in vascular injury states.

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

266 utcome in diseases that are characterized by vascular injury, such as atherosclerosis, restenosis, pe

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

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

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

270 Vascular injury that results in proliferation and dediff

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

272 Even without lymphatic vascular injury, the loss of LEC-specific Hif2alpha caus

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

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

275 inflammation (C-reactive protein levels) and vascular injury (thrombomodulin levels) measured at 0, 4

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

277 Platelets engage cues of pending vascular injury through coordinated adhesion, secretion,

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

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

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

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

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

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

284 Vascular injury was introduced by carotid air-dry endoth

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

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

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

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

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

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

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

292 Vascular injuries were seen in eight cases, of which sev

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

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

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

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

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

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

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

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