ライフサイエンスコーパス: balloon injury

1 gnificantly increased in the neointima after balloon injury.

2 f rat decorin expression up to 8 weeks after balloon injury.

3 ima formation and adventitial reaction after balloon injury.

4 t carotid arteries of rats immediately after balloon injury.

5 imal formation in rat carotid arteries after balloon injury.

6 in the development of stenotic lesions after balloon injury.

7 worsens atherosclerosis and restenosis after balloon injury.

8 are downregulated in rat carotid arteries on balloon injury.

9 RNA was found to be expressed markedly after balloon injury.

10 proliferation and neointima formation after balloon injury.

11 ns play a role in SMC growth responses after balloon injury.

12 Adventitial neovascularization occurs after balloon injury.

13 le cells of the arterial wall in response to balloon injury.

14 could reduce intimal hyperplasia induced by balloon injury.

15 fed New Zealand White rabbits 6 months after balloon injury.

16 , was examined in rat carotid arteries after balloon injury.

17 -selectin and L-selectin are expressed after balloon injury.

18 nous arteries and from arteries subjected to balloon injury.

19 for both gelatinases were upregulated after balloon injury.

20 arteries but declined again by 21 days after balloon injury.

21 tinases from pig carotid artery tissue after balloon injury.

22 and promote recovery of EC dysfunction after balloon injury.

23 iac artery of each animal was subjected to a balloon injury.

24 reduce neointimal hyperplasia after arterial balloon injury.

25 aque in rats feeding with high fat diet plus balloon injury.

26 rantly expressed in the vascular walls after balloon injury.

27 ects on preventing intimal hyperplasia after balloon injury.

28 the neointima of rat carotid arteries after balloon injury.

29 uired to reduce neointimal hyperplasia after balloon injury.

30 n vascular smooth muscle cells (VSMCs) after balloon injury.

31 d vascular smooth muscles in the media after balloon injury.

32 ccelerate reendothelialization after carotid balloon injury.

33 Tenascin-C is expressed in response to balloon injury.

34 is expressed locally in arteries at sites of balloon injury.

35 artery wall promotes neointima growth after balloon injury.

36 by treatment with M1/70 (intimal area after balloon injury, 0.12 +/- 0.09 mm2, compared with 0.32 +/

37 inflammation (-0.82 versus -0.24, P = 0.03), ballooning injury (-1.27 versus -0.53, P = 0.03) and NAS

38 An oversized balloon injury, 1.15 to 1.30 times the reference vessel

39 Sequential balloon injury, 3 weeks after the first balloon denudati

40 of adventitial microvessels was enhanced by balloon injury 4 days before gene transfer.

41 Zealand White rabbits (n = 7) by a repeated balloon injury (4 wk apart) and 4 mo of hyperlipemic die

42 eration increases significantly 4 days after balloon injury (45%) in this animal model.

43 , and in neointimal cells 3 and 7 days after balloon injury; 72-kD gelatinase mRNA persisted after 21

44 Local CMMC administration at the time of balloon injury accelerated reendothelialization at 4 wee

45 show that Ad-E2F1 overexpression at sites of balloon injury accelerates functional endothelial recove

46 We hypothesized that balloon injury activated a redox-sensitive signaling pat

47 Balloon injury also caused increased STAT-3 phosphorylat

48 abbits (n = 37) by the combination of double-balloon injury and a nine-month high-cholesterol (HC) di

49 duced experimental atheroma in 33 rabbits by balloon injury and an atherogenic diet (0.3% cholesterol

50 n of intimal SMCs in 33 rabbits subjected to balloon injury and cholesterol feeding (0.3%) for 4 mont

51 ty, we produced atheroma in rabbit aortas by balloon injury and cholesterol feeding for 4 months (Bas

52 ion of a fibrocellular plaque by overstretch balloon injury and cholesterol feeding.

53 g(-1) x d(-1) beginning 2 days before aortic balloon injury and continued for the total 8 weeks of th

54 his trend was also observed at 28 days after balloon injury and gene transfer during which AV-W9-trea

55 Zealand White rabbits underwent simultaneous balloon injury and gene transfer of one femoral artery w

56 n 37 coronary artery segments by overstretch balloon injury and high cholesterol diet.

57 s was induced in rabbits (n=31) using aortic balloon injury and high-cholesterol diet.

58 Animals underwent balloon injury and immediate delivery of autologous CMMC

59 retrieved 3, 7, 14, 28, 42, or 56 days after balloon injury and immunostained as well for proliferati

60 17 beta prevents neointimal thickening after balloon injury and in rabbit cardiac transplant allograf

61 in rat neointima at 7 days and 14 days after balloon injury and is also present in early human athero

62 gelatinase production occurs in response to balloon injury and may play a role in permitting migrati

63 carotid artery model at 1 and 4 weeks after balloon injury and PDT.

64 proliferation and neointima formation after balloon injury and suggest that LXR ligands may constitu

65 Rat carotid arteries that were subjected to balloon injury and transduced with Ad-15-LOX1 upon expos

66 rea of the AV-W9-treated group 10 days after balloon injury and treatment was 0.42+/-0.36 mm(2), wher

67 the neointima reached a maximum 7 days after balloon injury and was associated with the presence of p

68 imals were killed at days 4, 8, and 14 after balloon injury, and coronary artery segments were studie

69 Four pigs were killed 28 d after coronary balloon injury, and four pigs with uninjured coronary ar

70 efore injury, 4 days after, or 12 days after balloon injury, and maintained under circumferential ten

71 line was randomly administered 15 min before balloon injury as an intravenous bolus.

72 otid artery in a time-dependent manner after balloon injury as compared with its levels in uninjured

73 ed intravenously beginning 15 minutes before balloon injury as either a high dose (0.5 mg/kg bolus an

74 timal hyperplasia was assessed after carotid balloon injury at 21 days by computerized morphometry.

75 was 7.6-fold elevated 3 hours (P<.05) after balloon injury, back to baseline at 2 days, increased ag

76 d Results- Rabbits subjected to iliac artery balloon injury (balloon denudation with or without stent

77 Balloon injury (BI) induced EGFR, Src, Jak2, and STAT3 p

78 Consistent with these observations, balloon injury (BI) induced p115 RhoGEF tyrosine phospho

79 vided into 3 groups of 10 each: control (C), balloon injury (BI), and BI followed by ICBT (16 Gy at 0

80 After balloon injury, biliary stents (Johnson & Johnson) were

81 After balloon injury, both intravenous (0.3 mg/kg per hour) an

82 lateral femoral artery was also subjected to balloon injury but not to gene transfer.

83 24 hours, 3 days, 7 days, and 14 days after balloon injury by in situ hybridization, immunohistochem

84 g decreases neointimal hyperplasia following balloon injury, by inhibiting the inflammatory and throm

85 Immediately after balloon injury, cell proliferation increased as p27Kip1

86 increased at 72 h, 1 week, and 2 weeks after balloon injury compared with its levels in uninjured lef

87 uli present at the site of coronary arterial balloon injury contribute to the progression and develop

88 nant genes in atherosclerotic arteries after balloon injury could inhibit intimal cell proliferation.

89 Tissue sections from arteries 3 days after balloon injury demonstrated rFGF2-SAP binding to medial

90 For the long-term study, after balloon injury, drugs were delivered as above into the i

91 Simultaneous with balloon injury, each artery was treated locally with eit

92 t New Zealand White rabbits underwent aortic balloon injury followed by a 1% cholesterol diet for 8 w

93 Twenty-one pigs underwent balloon injury followed by implantation of oversized, tu

94 nary arteries) were subjected to overstretch balloon injury followed by IR with doses of 0 to 18 Gy o

95 Balloon injury followed by percutaneous delivery of a 15

96 In experimental models, balloon injury has been shown to induce NAD(P)H oxidase

97 ation promotes medial cell replication after balloon injury; however, signaling of intimal cell repli

98 Carotid artery CTO was created by balloon injury in 19 lipid-overfed swine.

99 iven locally in vivo at the site of coronary balloon injury in a porcine model, it can inhibit neoint

100 this hypothesis, we examined the response to balloon injury in atherosclerotic rabbit arteries after

101 of RAGE and S100/calgranulins in response to balloon injury in diabetic compared with nondiabetic rat

102 ons in vascular function and structure after balloon injury in hypercholesterolemic rabbits could be

103 red the myointimal proliferative response to balloon injury in male rats.

104 utes to rapid endothelial regeneration after balloon injury in nonatherosclerotic rabbits.

105 and dissection repair following overstretch balloon injury in porcine coronary arteries.

106 tion and dissection repair after overstretch balloon injury in porcine coronary arteries.

107 ling alters adventitial cell migration after balloon injury in rat carotid arteries.

108 CaMKIIgamma protein decreased 90% 14 d after balloon injury in rat carotid artery.

109 ore injury suppresses stenosis after carotid balloon injury in rats as well as in mice.

110 ein were significantly elevated 7 days after balloon injury in the rat carotid artery.

111 tered in a single, 180-second infusion after balloon injury in the rat carotid model.

112 alcification on neointimal hyperplasia after balloon injury in the rat carotid.

113 r events leading to intimal thickening after balloon injury in the rat.

114 s able to reduce neointimal thickening after balloon injury in the rat.

115 cells as well as in the arterial wall after balloon injury in vivo.

116 Balloon injury induced cyclin A expression and CDK2 acti

117 Furthermore, balloon injury induced IL-6 expression both at mRNA and

118 Balloon injury induced PAK1 activity and interference wi

119 Balloon injury induced PKN1 activation in NFAT-dependent

120 Balloon injury-induced cyclin D1-CDK4 activity requires

121 This resistance to balloon injury-induced death was associated with an upre

122 ignaling by recombinant hirudin also blocked balloon injury-induced EGFR tyrosine phosphorylation and

123 d 15-HETE as a major eicosanoid and enhanced balloon injury-induced expression of MCP-1 in smooth mus

124 s administered to rat carotid arteries after balloon injury-induced intimal hyperplasia.

125 cineurin-NFAT activation pathway, suppressed balloon injury-induced neointima formation by 40%.

126 We found less balloon injury-induced neointima formation in hyperbilir

127 nduced VSMC growth and motility in vitro and balloon injury-induced neointima formation in vivo.

128 -BB)-stimulated VSMC growth and motility and balloon injury-induced neointima formation.

129 p27-p16 fusion protein, named W9, inhibited balloon injury-induced neointimal hyperplasia in rabbit

130 Furthermore, CsA and GFPVIVIT attenuated balloon injury-induced neointimal smooth muscle cell pro

131 In addition, VIVIT attenuated balloon injury-induced SMC proliferation, resulting in r

132 ation of its levels substantially suppressed balloon injury-induced smooth muscle cell migration and

133 duction of Ad-15-LOX1 into arteries enhanced balloon injury-induced smooth muscle cell migration from

134 -mediated expression of dnSTAT-5B attenuated balloon injury-induced smooth muscle cell migration from

135 expression of dngp130 or dnSTAT-3 attenuated balloon injury-induced STAT-3 phosphorylation and cyclin

136 ome the blockade effect of NFATs by VIVIT on balloon injury-induced vascular wall remodeling events,

137 The local delivery of ZVAD-fmk during balloon injury inhibits smooth muscle cell apoptosis.

138 The response to arterial balloon injury involves MMP-dependent SMC migration and

139 trated that endothelial recovery at sites of balloon injury is a critical determinant of consequent i

140 Rat aortae were isolated 4 days after balloon injury, maintained in organ culture under circum

141 Using the rat carotid balloon injury model and a PAI-1-expressing adenoviral v

142 e similarly regulated in vivo in a rat aorta balloon injury model and found that p47(phox) protein wa

143 intimal hyperplasia in this porcine arterial balloon injury model compared with untreated or control

144 was evaluated in vitro and in a rat arterial balloon injury model following transduction with Ad-p27-

145 ed in an arterialized vein graft model and a balloon injury model in rats.

146 In the arterial balloon injury model in the rat, platelet-derived growth

147 neointima formation in a rat carotid artery balloon injury model of restenosis.

148 nsic pathway of coagulation, in a sequential balloon injury model of the rabbit abdominal aorta.

149 We previously found in a pig coronary balloon injury model that vitamins C and E as well as pr

150 In a rat carotid artery balloon injury model, CD44 and CD44-V6 mRNAs were unregu

151 development of neointimal hyperplasia in the balloon injury model, this strategy has not been tested

152 and upregulated after 5 days in rat carotid balloon injury model, with positive correlation to PDGFB

153 antiproliferative effects in the rat carotid balloon injury model.

154 neointima formation in a rat carotid artery balloon injury model.

155 iation on neointimal hyperplasia in a rabbit balloon injury model.

156 e in vitro findings, the in vivo rat carotid balloon-injury model of restenosis evidenced that AC8 de

157 As early as 30 minutes after balloon injury, myocytes appear to undergo apoptotic cel

158 r smooth muscle cells in vivo was induced by balloon injury of carotid arteries in the rat.

159 e role of Orai1 in neointima formation after balloon injury of rat carotid arteries and its potential

160 Balloon injury of rat carotid arteries upregulated prote

161 on and role during neointima formation after balloon injury of rat carotid arteries.

162 was increased in the neointimal layer after balloon injury of rat carotid artery.

163 iferation, and neointima formation following balloon injury of rat carotids.

164 ) less neointima/media area ratio 14 d after balloon injury of the aorta compared with injured rats t

165 male, and the responsiveness of this gene to balloon injury of the artery is more rapid and more robu

166 the expression of RAGE and its ligands after balloon injury of the carotid artery in both Zucker diab

167 nts the neointimal proliferative response to balloon injury of the carotid artery in intact female ra

168 administered to rats for various times after balloon injury of the carotid artery.

169 adherence was also evaluated after selective balloon injury of the CAs.

170 , with or without endothelial denudation via balloon injury of the infrarenal abdominal aorta.

171 ns were administered 7 days before oversized balloon injury of the left anterior descending coronary

172 evelopment of myointimal proliferation after balloon injury of the rat carotid artery in vivo, (2) wh

173 he rapid SMC proliferation that occurs after balloon injury of the rat carotid artery using en face c

174 approach to test the hypothesis that, after balloon injury of the rat carotid artery, adventitial fi

175 or their effect on neointima formation after balloon injury of the rat carotid artery, both full-leng

176 After balloon injury of the rat carotid artery, expression of

177 Our data indicate that in response to balloon injury of the rat carotid artery, NAD(P)H oxidas

178 lesions and late lesions that develop after balloon injury of the rat thoracic aorta.

179 Young adult male rats received balloon injury of the right carotid artery and were tran

180 ment with E2 or vehicle (V) and subjected to balloon injury of the right carotid artery.

181 E2, MPA, E2+MPA, or vehicle and subjected to balloon injury of the right carotid artery.

182 neously [S.C.]) or vehicle, beginning before balloon injury of the right common carotid artery and co

183 17 beta-estradiol + MPA, or (4) vehicle, and balloon injury of the right common carotid artery was ca

184 + MPA, or (4) vehicle and were subjected to balloon injury of the right common carotid artery.

185 However, the immediate effect of balloon injury on medial SMC viability has not been exam

186 Immediately after the balloon injury, one of the arteries was randomized to lo

187 raft survival, intimal hyperplasia following balloon injury or as seen in chronic graft rejection and

188 dosing inhibits neointimal hyperplasia after balloon injury or stent implantation.

189 ant improvements in steatosis (P = .006) and ballooning injury (P = .005), with a reduction of mean N

190 ATA-6 gene transfer to the vessel wall after balloon injury partially restored the levels of GATA-6 p

191 to the perivascular surface of arteries and balloon injury performed 4 days later.

192 body impaired reendothelialization following balloon injury performed in vivo.

193 Single balloon injury produced limited intimal thickening at 3

194 This report demonstrates that balloon injury results in both a rapid ACE inhibitor-ind

195 with a peak expression 24 to 48 hours after balloon injury, returning to baseline by 1 week.

196 ductions in steatosis and the hepatocellular ballooning injury seen in NASH.

197 -activated receptor gamma (PPAR gamma) after balloon injury significantly inhibits VSMC proliferation

198 mbus at the intervention site (3 stent and 2 balloon injury sites).

199 rotid arteries were harvested at the time of balloon injury (T = 0) and at 0.5, 1, 2, and 4 hours aft

200 reater increase in neointima formation after balloon injury than that observed in intact females (P <

201 tallic stents had been placed at the site of balloon injury; the contralateral iliac artery of each r

202 In animal models of restenosis after balloon injury, there is marked reduction of neointimal

203 at carotid arteries in the early hours after balloon injury, thus attenuating the stimulus for leukoc

204 Three to six months after balloon injury to the aorta, the rabbits were injected w

205 regulated in adventitial blood vessels after balloon injury to the carotid artery.

206 lessen the neointimal hyperplasia caused by balloon injury to the common carotid artery (CCA).

207 creen of 11 rat strains by use of a standard balloon injury to the left iliac artery to observe wheth

208 ure and for intimal migration of cells after balloon injury to the rat carotid artery.

209 gue-Dawley rats with intact gonads underwent balloon injury to the right common carotid artery.

210 creased again at 4 days, and by 7 days after balloon injury was 3.2-fold elevated (P<.05) when compar

211 Balloon injury was associated with oxidative stress as r

212 e production of O2- by vessels 14 days after balloon injury was determined and correlated with circul

213 Single iliac artery balloon injury was followed by placement of 2 overlappin

214 Balloon injury was induced in the left anterior descendi

215 Deendothelializing balloon injury was performed 1 week after pellet implant

216 Overstretch balloon injury was performed in the coronary arteries of

217 Balloon injury was performed on porcine coronary arterie

218 a formation in a model of rat carotid artery balloon injury was significantly attenuated after treatm

219 d rats, the induction of PAI-1 expression by balloon injury was significantly suppressed by 44% (P<.0

220 De-endothelializing balloon injury was then performed, and animals were kill

221 antibody to alphavbeta3, on the responses to balloon injury were tested in hyperlipidemic rabbits.

222 d wall, measured at both 4 and 29 days after balloon injury, were similar in the control and antibody

223 tory and thrombotic responses at the site of balloon injury, which appears to play a pivotal role in

224 Rat models of aortic balloon injury with or without subsequent stenting were