ライフサイエンスコーパス: arterial injury

1 od, isolated platelets, and animal models of arterial injury.

2 n the areas of regenerated endothelium after arterial injury.

3 osclerosis, and neointimal hyperplasia after arterial injury.

4 and increased neointima formation following arterial injury.

5 egulation target of mitogenic signals during arterial injury.

6 colocalized in neointimal macrophages after arterial injury.

7 ion is critical in neointima formation after arterial injury.

8 f intimal hyperplasia in response to femoral arterial injury.

9 esion formation in nonmouse animal models of arterial injury.

10 s, TF and active caspase-3 were absent after arterial injury.

11 ected from neointimal lesion formation after arterial injury.

12 e oxidase (Nox2)-deficient (Nox2-/-) mice to arterial injury.

13 n the formation of intimal hyperplasia after arterial injury.

14 pair and inhibited neointima formation after arterial injury.

15 VEGF with high affinity, in a mouse model of arterial injury.

16 and neointima formation in a mouse model of arterial injury.

17 in our understanding of the pathogenesis of arterial injury.

18 proliferation and neointimal formation after arterial injury.

19 n CRP-transgenic (CRPtg) mice to 2 models of arterial injury.

20 untoward neointimal expansion consequent to arterial injury.

21 tid thrombi were induced in swine (n = 7) by arterial injury.

22 eparin administration in the rabbit model of arterial injury.

23 smooth muscle cell (SMC) proliferation after arterial injury.

24 of T lymphocytes on intimal thickening after arterial injury.

25 by a variety of agents and in vivo following arterial injury.

26 ntribute to the formation of neointima after arterial injury.

27 itment to sites of neointima formation after arterial injury.

28 inflammatory responses of atherogenesis and arterial injury.

29 let accumulation in FeCl3-induced mesenteric arterial injury.

30 uates neointima formation after perivascular arterial injury.

31 ia of VSMC, we used a mouse model of femoral arterial injury.

32 tant determinant of thrombolysis at sites of arterial injury.

33 luation of a patient with suspected thoracic arterial injury.

34 inhibitor, prevents thrombus formation after arterial injury.

35 hat there are different response patterns to arterial injury.

36 and impaired vascular regeneration following arterial injury.

37 te and cover the denuded area at the site of arterial injury.

38 are-stented coronary segments with regard to arterial injury.

39 n and luminal stenosis after balloon-induced arterial injury.

40 ing type and severity of angioplasty-induced arterial injury.

41 otoxicity and neointimal formation following arterial injury.

42 ng atherosclerotic plaque rupture or balloon arterial injury.

43 egulation of endothelial integrity following arterial injury.

44 s, have a role in neointimal formation after arterial injury.

45 t role in smooth muscle cell migration after arterial injury.

46 n neointimal formation after balloon-induced arterial injury.

47 thought to mediate neointima formation after arterial injury.

48 s the response of the adventitia to coronary arterial injury.

49 ased thrombin deposition at the site of deep arterial injury.

50 are important for neointimal formation after arterial injury.

51 lial adhesion molecule in an animal model of arterial injury.

52 icantly enhances intimal proliferation after arterial injury.

53 mits neointimal formation and stenosis after arterial injury.

54 nce thrombosis potential in recipients after arterial injury.

55 nce thrombosis potential in recipients after arterial injury.

56 was mildly increased in an ex vivo model of arterial injury.

57 very of TSP-2 siRNA to mitigate IH following arterial injury.

58 rrant vascular repair processes in models of arterial injury.

59 lified the degree of arterial stenosis after arterial injury.

60 y, such as CD34(+)CXCR4(+)cells, at sites of arterial injury.

61 of contemporary access techniques that limit arterial injury.

62 cells enhances neointima formation following arterial injury.

63 PCs) participate in endothelial repair after arterial injury.

64 thrombosis in a chemically induced model of arterial injury.

65 on and delays endothelial regeneration after arterial injury.

66 ase activity in atheromata and stent-induced arterial injury.

67 their preferential localization to sites of arterial injury.

68 ion, atherosclerosis, and EPC function after arterial injury.

69 ation as well as vessel remodeling following arterial injury.

70 ons, fractures, intracranial hemorrhage, and arterial injury.

71 ibition of neointimal hyperplasia induced by arterial injury.

72 52.2%, respectively) were at highest risk of arterial injury.

73 dependent predictors of an increased risk of arterial injury.

74 c deletion reduced intimal hyperplasia after arterial injury.

75 viewed all the CT angiograms for evidence of arterial injury.

76 itors, inhibits neointimal hyperplasia after arterial injury.

77 muscle cells (VSMCs) in atherosclerosis and arterial injury.

78 and increases neointima formation following arterial injury.

79 Rose Bengal administration and laser-induced arterial injury.

80 Cs) contribute to endothelial recovery after arterial injury.

81 m of findings that one would expect in renal arterial injuries.

82 new questions in the management of thoracic arterial injuries.

83 iliac arteries in patients without any iliac arterial injury (20 +/- 9, P =.009).

84 eointimal hyperplasia after varying forms of arterial injury, 57 New Zealand White rabbits underwent

85 In a model of transluminal arterial injury, absence of early leukocyte recruitment

86 Coronary arterial injury after ablation procedures is rare.

87 on the presentation and outcome of coronary arterial injury after ablation procedures.

88 sis factor-alpha (TNF-alpha) at the sites of arterial injury after balloon angioplasty, suppresses en

89 Arterial injury after percutaneous transluminal coronary

90 F and PR39 to the level seen with mechanical arterial injury alone.

91 od reconstructs 3D neointima formation after arterial injury and allows for volumetric analysis of re

92 ficient mouse in combination with a model of arterial injury and aortic explant SMC culture.

93 icantly decreased neointimal expansion after arterial injury and decreased smooth muscle cell prolife

94 Arterial injury and disruption of the endothelial layer

95 te to the vascular remodeling observed after arterial injury and during disease.

96 expressed in the adventitia and neointima on arterial injury and found that it functionally increases

97 Neointima formation in response to arterial injury and IGF-1R phosphorylation in neointima

98 t1, mammalian Atr expression increased after arterial injury and in VSMCs stimulated with growth and

99 carotid thrombosis was low at low levels of arterial injury and increased along with the contributio

100 ZPI deficiency enhances thrombosis following arterial injury and increases mortality from pulmonary t

101 enger ribonucleic acid mediators involved in arterial injury and inflammation have been found.

102 Experimental studies suggest that arterial injury and inflammation lead to increased neoin

103 : protection from occlusive thrombosis after arterial injury and markedly diminished metastatic poten

104 rmines neointimal thickness independently of arterial injury and may be useful for predicting pattern

105 a pivotal role in neointima formation after arterial injury and might represent an attractive target

106 neointima formation by 94% (P<0.0001) after arterial injury and reduced the intima-to-media ratio co

107 ooth muscle cells (VSMCs) in vitro and after arterial injury and regulates both cell proliferation an

108 ntral feature, namely an accelerated form of arterial injury and remodeling.

109 luminal size, whereas animal data show that arterial injury and stent design determine late neointim

110 les for PKCbeta in the SMC response to acute arterial injury and suggest that blockade of PKCbeta may

111 ity contributes to neointima formation after arterial injury and suggest that local delivery of a hig

112 tion; a relationship between acute allograft arterial injury and TA has been suggested.

113 it plays a role in neointima formation after arterial injury and that 17beta-estradiol (E(2)) modulat

114 PAI-1 might decrease lesion formation after arterial injury and that PAI-1 gene transfer might preve

115 rtant as platelets to thrombosis at sites of arterial injury and that platelets contribute to venous

116 nappreciated antithrombotic role at sites of arterial injury and that this activity may be mediated,

117 MCs express functional flt-1 receptors after arterial injury and that VEGF has synergistic effects wi

118 We studied the response to arterial injury and the development of atherosclerosis i

119 orrelations were found between the degree of arterial injury and the extent of the inflammatory react

120 telet P2Y(12) in the vessel wall response to arterial injury and thrombosis.

121 le of P2Y(12) in the vessel wall response to arterial injury and thrombosis.

122 expressed in the adult organism at sites of arterial injury and to inhibit monocyte migration.

123 After 1 week, mice underwent arterial injury and treatments were maintained for 4 wee

124 um cromoglycate (DSCG) immediately following arterial injury and were able to show a reduction in neo

125 dependent predictors of an increased risk of arterial injury and were used to construct a scoring sys

126 decreases lesions in a variety of models of arterial injury, and inhibition of NO synthase exacerbat

127 ly regulate cellular proliferation following arterial injury, and strategies to increase its expressi

128 ulation during the first 24 hours after deep arterial injury appears to be particularly effective for

129 Blunt vertebral arterial injuries are more common than previously report

130 he physiologic role of endogenous VEGF after arterial injury are not well described.

131 actors underlying VSMC growth in response to arterial injury are not well understood.

132 Nineteen (32%) patients had the following arterial injuries at CT angiography: arterial occlusion

133 Compared with carotid arterial injuries, BVIs have been considered innocuous.

134 ivo in the porcine carotid artery after deep arterial injury by balloon angioplasty.

135 vo, decorin was overexpressed at the site of arterial injury by cell-mediated gene transfer.

136 VN participate in the thrombotic response to arterial injury by preventing premature thrombus dissolu

137 gnaling may promote endothelial repair after arterial injury by selective recruitment and functional

138 e exhibited severe intimal hyperplasia after arterial injury compared with controls, whereas CBP(iKO)

139 t the inflammatory response after mechanical arterial injury correlates with the severity of neointim

140 immune system may differentially respond to arterial injury depending on the severity of injury, whi

141 rix degradation and cellular migration after arterial injury, does not appear to be so important in v

142 The severity of arterial injury during stent placement correlates with i

143 On arterial injury, Egfl7 expression was up-regulated in th

144 In response to arterial injuries, existing smooth muscle cells give ris

145 Because it is induced after arterial injury, Fat1 may control VSMC functions central

146 ical evidence on the role of microRNAs after arterial injury, focusing on practical aspects of their

147 role of the immune system in the response to arterial injury has been impressive.

148 an atypical cadherin induced robustly after arterial injury, has significant effects on mammalian va

149 Blunt carotid arterial injuries have the potential for devastating com

150 its role in vascular repair after mechanical arterial injury (i.e., percutaneous transluminal coronar

151 Finally, in a rat carotid model of arterial injury, Id2 was expressed in a temporal pattern

152 rt greater risk for the development of iliac arterial injuries in patients undergoing transfemoral de

153 migration in vitro and delayed EC healing of arterial injuries in vivo.

154 n to prevent thrombosis and restenosis after arterial injury in a variety of animal models.

155 herosclerotic lesions on alloimmune-mediated arterial injury in an experimental setting is not known.

156 mation and inflammation after collar-induced arterial injury in ApoE(-/-) mice, and reduced cytokine

157 nd other vascular changes that develop after arterial injury in apolipoprotein E-deficient (apoE(-/-)

158 a model of accelerated atherosclerosis after arterial injury in apolipoprotein E-deficient (ApoE(-/-)

159 Arterial injury in CRPtg mice results in an expedited an

160 tic and nondiabetic EPCs intravenously after arterial injury in diabetic and nondiabetic mice.

161 of estrogen administration on mouse carotid arterial injury in ERbeta-deficient mice.

162 ling was characterized 4 weeks after femoral arterial injury in FLAP knockout mice and wild-type cont

163 of cell proliferation and inflammation after arterial injury in local vascular cells and that the SDF

164 CI, Kovacic et al. show that, in response to arterial injury in mice, the cytokine TNF-alpha triggers

165 expression alters the thrombotic response to arterial injury in mice.

166 reaction plays an equally important role as arterial injury in neointimal formation after coronary s

167 treatment suppresses the intimal response to arterial injury in nonatherosclerotic rodents and rabbit

168 oral and cellular immune responses can cause arterial injury in organ transplants, but the manifestat

169 Here, we show that balloon-mediated arterial injury in rabbits resulted in expression of sur

170 rombus formation were measured in mice after arterial injury in the cremaster muscle.

171 and risk of new plaque formation, suggesting arterial injury in this cohort.

172 ded thrombotic occlusion after FeCl3-induced arterial injury in vivo, an effect mediated through CXCR

173 cts of the terminal complement components on arterial injury in vivo.

174 interactions post-myocardial infarction and arterial injury in vivo.

175 arrow accelerated endothelial recovery after arterial injury in WT mice.

176 the potential to support several pathways of arterial injury, including the release of reactive oxyge

177 arkedly accelerates thrombus formation after arterial injury, increases vascular oxidative stress, an

178 tained neointimal hyperplasia in response to arterial injury, indicating the in vivo role of R-ras as

179 Arterial injury indices were no different among the grou

180 Atherosclerosis and arterial injury-induced neointimal hyperplasia involve m

181 Arterial injury induces a series of proliferative, vasoa

182 ylcholine (lysoPC) accumulate at the site of arterial injury, inhibiting endothelial cell (EC) migrat

183 neointimal formation after balloon and stent arterial injury is accompanied by subacute and late thro

184 Neointimal proliferation in response to arterial injury is an important contributor to restenosi

185 r leukocytes in neointimal hyperplasia after arterial injury is suspected.

186 VSM), is markedly upregulated in response to arterial injury, is essential for normal VSM proliferati

187 hronic forms of limb ischemia and iatrogenic arterial injury, limiting the true assessment of ALI inc

188 hronic allograft dysfunction may result from arterial injury, manifest as transplant arteriosclerosis

189 ctin observed in the adventitial cells after arterial injury may constrict the injured vessel and con

190 nced endothelium regeneration after denuding arterial injury (mean [SEM] percent recovered area, wild

191 In response to arterial injury, medial vascular smooth muscle cells (VS

192 in mice and found that immediately following arterial injury, medial VSMCs upregulated Rantes in an a

193 Using a different arterial injury model (balloon catheter injury), we show

194 We developed a murine arterial injury model and applied it to wild-type (PAI-1

195 f mutant mice by the ferric chloride-induced arterial injury model suggests that the Capn1-/- mice ar

196 In a rat balloon carotid arterial injury model, adenovirus-mediated gene transfer

197 , on neointimal formation in a mouse femoral arterial injury model.

198 ttenuation of neointimal lesions in a murine arterial injury model.

199 able hypoperfusion: Protocol 1) or a site of arterial injury (model of recurrent platelet-mediated th

200 ith the histology of thrombi in large-animal arterial injury models and human acute coronary syndrome

201 In an in vivo model of mechanical arterial injury NAB2 levels also increase transiently in

202 gnant uterus, and in two different models of arterial injury, namely ballooning and ferric chloride i

203 Upon arterial injury, neointimal expansion was strikingly sup

204 tial imaging suggestive of a cerebrovascular arterial injury not classifiable by the Denver criteria.

205 lication (SRC) was defined as an iliofemoral arterial injury not including a cannulation site.

206 ned in cholesterol-fed rabbits 4 weeks after arterial injury of the iliac artery (9 rabbits) and the

207 nine phosphokinase increase (four patients), arterial injury (one), neutropenia (one), and pneumoniti

208 ibrosis could be valuable in the presence of arterial injuries or anastomotic strictures.

209 ssion in VSMCs increases significantly after arterial injury or growth factor stimulation.

210 Challenging the R-Ras-null mice with arterial injury or tumor implantation showed exaggerated

211 endothelial cell proliferation 2 weeks after arterial injury (P<0.05), resulting in decreased neointi

212 uminal endothelial cells 2 and 4 weeks after arterial injury (P<0.05).

213 nd recruitment and neointima formation after arterial injury, potentially through enhancement of plat

214 For example, although arterial injury provokes thrombosis in both lean and obe

215 ct of platelets on neointima formation after arterial injury remains undetermined.

216 By studying vascular smooth muscle cells and arterial injury response, we find a specific requirement

217 Arterial injury results in the formation of neointimal l

218 P-selectin or PSGL-1 blockade at the time of arterial injury significantly limits plaque macrophage c

219 lized in the adventitia and neointima at the arterial injury site.

220 Targeted inactivation of JNK1 at arterial injury sites may represent a potential therapeu

221 d injury-induced vasoconstriction after deep arterial injury, suggesting that a major inhibition of p

222 ce compared with WT after chemically induced arterial injury, suggesting that CD36 may contribute to

223 proliferation and migration are responses to arterial injury that are highly important to the process

224 malities in rapidly proliferating SMCs after arterial injury that could contribute to the growth of a

225 e acute events transpiring immediately after arterial injury that establish the blueprint for this in

226 th muscle cell (SMC) proliferation following arterial injury that results in neointimal growth.

227 Thus, at sites of arterial injury, the factor VLeiden mutation may not as

228 are protected from neointima formation after arterial injury through inhibition of monocyte trafficki

229 by initiating platelet adhesion at sites of arterial injury through interactions with the platelet r

230 upted and have used a mouse model of carotid arterial injury to compare the effects of estrogen on wi

231 The mice were then observed in a model of arterial injury to evaluate their capacity to form throm

232 (FvQ/Q) mice underwent photochemical carotid arterial injury to induce occlusive thrombosis.

233 e relative contributions of inflammation and arterial injury to neointimal formation in a porcine cor

234 at lack MRP-8/14 complexes with experimental arterial injury, vasculitis, or atherosclerosis.

235 s of mouse models, rather focus on models of arterial injuries, vein grafts, and transplant arteriosc

236 Arterial injury was driven by macrophages that accumulat

237 A copper-induced arterial injury was found to generate a lesion with char

238 inally, neointima formation after mechanical arterial injury was increased in AMPKalpha2(-/-) but not

239 Lesion formation after mechanical arterial injury was markedly increased in mice with homo

240 THODS AND Using a model of guidewire-induced arterial injury, we demonstrate decreased neointima form

241 Sixty-three arterial injuries were identified in 44 (15.5%) of 284 p

242 .3%), femoral (56.6%), and popliteal (41.1%) arterial injuries were included.

243 In vivo murine models of arterial injury were employed alone and in combination w

244 g progenitor cells are recruited to sites of arterial injury where they may then differentiate into s

245 genase-2 knockout increased thrombosis after arterial injury, which was associated with the accumulat

246 Inflammation is a key component of arterial injury, with VSMC proliferation and neointimal

247 predictor of luminal loss in immune-mediated arterial injury, yet little is known about its mechanism