ライフサイエンスコーパス: neointimal hyperplasia

1 d both BRSs to be patent with nonobstructive neointimal hyperplasia.

2 cell loss, heterophils/eosinophils, and late neointimal hyperplasia.

3 ituted endothelium, leading to inhibition of neointimal hyperplasia.

4 all at the time of angioplasty might prevent neointimal hyperplasia.

5 1) in EPCs enhances their ability to inhibit neointimal hyperplasia.

6 utics; NP delivering rapamycin inhibit patch neointimal hyperplasia.

7 ffect of flow disturbances on the pattern of neointimal hyperplasia.

8 grity in injured vessels, thereby inhibiting neointimal hyperplasia.

9 smooth muscle cell apoptosis and subsequent neointimal hyperplasia.

10 tatus and suggest a novel target to minimize neointimal hyperplasia.

11 nificantly to late vein graft failure due to neointimal hyperplasia.

12 with dexamethasone (DEX) to reduce in-stent neointimal hyperplasia.

13 0 activity increased NFkappaB activation and neointimal hyperplasia.

14 in foreign body contamination and increased neointimal hyperplasia.

15 migration and proliferation contributing to neointimal hyperplasia.

16 hanced vascular NO production, and decreased neointimal hyperplasia.

17 promotes inflammation in atherosclerosis and neointimal hyperplasia.

18 ulnerable to restenosis, caused primarily by neointimal hyperplasia.

19 sma cholesterol levels and drug treatment on neointimal hyperplasia.

20 may therefore be therapeutically useful for neointimal hyperplasia.

21 y agonists implicated in the pathogenesis of neointimal hyperplasia.

22 ing atherogenesis, plaque stabilization, and neointimal hyperplasia.

23 an arrest cell cycle progression and inhibit neointimal hyperplasia.

24 xtracellular matrix deposition, and vascular neointimal hyperplasia.

25 ed differences existed in the development of neointimal hyperplasia.

26 d vice versa, that were also associated with neointimal hyperplasia.

27 tic obstruction occurring on a foundation of neointimal hyperplasia.

28 However, dexamethasone did not decrease neointimal hyperplasia.

29 ession, accompanied by a reduction in venous neointimal hyperplasia.

30 In-stent restenosis results primarily from neointimal hyperplasia.

31 ly reduces in-stent restenosis by inhibiting neointimal hyperplasia.

32 nd late arterial remodeling while triggering neointimal hyperplasia.

33 al contributor to experimental stent-induced neointimal hyperplasia.

34 e involved in the preventive action of E2 on neointimal hyperplasia.

35 case 2 (70.9%) without evidence of excessive neointimal hyperplasia.

36 t Orai3 knockdown inhibited LRC currents and neointimal hyperplasia.

37 e injured using balloon angioplasty to cause neointimal hyperplasia.

38 apeutic agents targeted to inhibit localized neointimal hyperplasia.

39 hus contributing to vascular remodelling and neointimal hyperplasia.

40 xide production in medial VSMCs and enhanced neointimal hyperplasia.

41 be centrally involved in the development of neointimal hyperplasia.

42 ormal vascular homeostasis and regulation of neointimal hyperplasia.

43 novel regulators for VSMC proliferation and neointimal hyperplasia.

44 rolimus effectively inhibits leptin-enhanced neointimal hyperplasia.

45 ed Akt activity in a stretch injury model of neointimal hyperplasia.

46 ures at six months, possibly attributable to neointimal hyperplasia.

47 n of p27(kip1) in the VSMC and inhibition of neointimal hyperplasia.

48 heparin (90 mg/kg BID) effectively inhibited neointimal hyperplasia (0.11+/-0.02 and 0.09+/-0.07 mm(2

49 The LFA-1 blockade profoundly attenuated neointimal hyperplasia (61.6 vs 23.8%; P < 0.05), CAV-af

50 lockade of the IIb/IIIa receptor, may reduce neointimal hyperplasia after arterial balloon injury.

51 A central role for leukocytes in neointimal hyperplasia after arterial injury is suspecte

52 rapy with mTOR and PI3K inhibitors, inhibits neointimal hyperplasia after arterial injury.

53 vascular inflammation, atherosclerosis, and neointimal hyperplasia after arterial injury.

54 ble ceramide as a novel therapy for reducing neointimal hyperplasia after balloon angioplasty.

55 frequent (BID) subcutaneous dosing inhibits neointimal hyperplasia after balloon injury or stent imp

56 rin beta-subunit CD18 was required to reduce neointimal hyperplasia after balloon injury.

57 t studies have demonstrated reduction in the neointimal hyperplasia after intracoronary radiation (IR

58 Neointimal hyperplasia after percutaneous coronary inter

59 de that nonablative infrared laser inhibited neointimal hyperplasia after PTCA in cholesterol-fed rab

60 Neointimal hyperplasia after PTCA is an important compon

61 ed antisense oligonucleotides (Resten-NG) on neointimal hyperplasia after stenting in a pig model.

62 P-1 receptor CCR2, was effective at reducing neointimal hyperplasia after stenting.

63 n tip of an embolectomy catheter would limit neointimal hyperplasia after stretch injury.

64 e the effects of orally delivered heparin on neointimal hyperplasia after varying forms of arterial i

65 ever, the role of RAGE/ligand interaction in neointimal hyperplasia after vascular injury remains unc

66 l tetrahydrobiopterin availability modulates neointimal hyperplasia after vascular injury via acceler

67 Deletion of mPGES-1 in mice attenuates neointimal hyperplasia after vascular injury, in part by

68 the genes that influence the development of neointimal hyperplasia after vascular injury.

69 nt of arterial thrombosis, inflammation, and neointimal hyperplasia after vascular injury.

70 ys) of nitro-oleic acid (OA-NO(2)) inhibited neointimal hyperplasia after wire injury of the femoral

71 Colchicine is associated with less neointimal hyperplasia and a decreased ISR rate when adm

72 s, in fact, been developed that inhibits the neointimal hyperplasia and accelerated atherosclerosis t

73 he response to vascular injury that leads to neointimal hyperplasia and accelerated atherosclerosis.

74 central to the initiation and progression of neointimal hyperplasia and arterial stenosis.

75 e intima during vascular remodelling such as neointimal hyperplasia and arteriosclerosis.

76 Increased endothelial BH4 reduces vein graft neointimal hyperplasia and atherosclerosis through a red

77 otes vascular inflammatory disorders such as neointimal hyperplasia and atherosclerosis.

78 ion of CaMKII delta prevented injury-induced neointimal hyperplasia and cell proliferation in the int

79 ion is a major contributor to injury-induced neointimal hyperplasia and depends on alteration of the

80 tency, the cell-seeded TEV demonstrated less neointimal hyperplasia and fewer proliferating cells tha

81 ESS with the localization and progression of neointimal hyperplasia and in-stent clotting.

82 Neointimal hyperplasia and inflammation around stent str

83 ery, NAD(P)H oxidase activity contributes to neointimal hyperplasia and is involved in vascular cell

84 affords mice with a protected status against neointimal hyperplasia and lumen narrowing in vivo.

85 d a significant dose-dependent inhibition of neointimal hyperplasia and luminal encroachment in the p

86 he time of angioplasty significantly reduced neointimal hyperplasia and prevented restenosis.

87 inhibitor of NOS activity, increased venous neointimal hyperplasia and pro-inflammatory gene express

88 tent-based therapies that can both attenuate neointimal hyperplasia and promote re-endothelialization

89 ent with that of a bare metal stent (BMS) on neointimal hyperplasia and re-endothelialization in a ra

90 s relevant to vascular remodeling along with neointimal hyperplasia and relevant histological changes

91 n and devising strategies that may interrupt neointimal hyperplasia and relevant pathogenetic pathway

92 or later obstruction by vein graft disease (neointimal hyperplasia and remodelling).

93 C) migration and proliferation contribute to neointimal hyperplasia and restenosis after vascular inj

94 vascular injury may reduce the incidence of neointimal hyperplasia and restenosis.

95 ion of drugs to a vascular segment to reduce neointimal hyperplasia and restenosis.

96 ial cell layer lining the lumen and prevents neointimal hyperplasia and restenosis.

97 from diabetic mice developed more extensive neointimal hyperplasia and showed greater proliferation

98 Systemic treatment produced the least neointimal hyperplasia and significantly reduced in-sten

99 apy of experimental vein grafts inhibits the neointimal hyperplasia and subsequent accelerated athero

100 dependent risk factor for the development of neointimal hyperplasia and subsequent vein graft failure

101 Both neointimal hyperplasia and the intima/media ratio of the

102 ll migration and proliferation contribute to neointimal hyperplasia and vascular stenosis after endot

103 Acute thrombosis, neointimal hyperplasia, and accelerated atherosclerosis

104 constitutes a key event in atherosclerosis, neointimal hyperplasia, and the response to vascular inj

105 ivation of membrane ERalpha does not prevent neointimal hyperplasia; and (3) ERalphaAF1 is necessary

106 Furthermore, SMC migration and neointimal hyperplasia are promoted by degradation of th

107 Histologic assessment demonstrated neointimal hyperplasia around the IVC filter within 2 we

108 nti-CD4 mAb-treated mice exhibited prominent neointimal hyperplasia associated with endothelial morph

109 The neointimal hyperplasia associated with this injury was l

110 l roles in vascular restenosis by preventing neointimal hyperplasia at the early stage via suppressio

111 Neointimal hyperplasia at the site of surgical intervent

112 Neointimal hyperplasia (at 14 d) was notably attenuated

113 regulatory gene expression inhibits not only neointimal hyperplasia, but also diet-induced, accelerat

114 Intracoronary ultrasound showed severe neointimal hyperplasia, but only at the proximal interfa

115 elium-dependent vasoconstriction and promote neointimal hyperplasia, but the intracellular signaling

116 d thrombocytopenia and suppressed postinjury neointimal hyperplasia by 88%.

117 rtery SMC after balloon angioplasty prevents neointimal hyperplasia by blocking SMC proliferation and

118 Although inhibition of neointimal hyperplasia by cell cycle gene blockade thera

119 is feasible and effectively reduces in-stent neointimal hyperplasia by inhibiting cellular proliferat

120 esulting in decreased O2*-, would lessen the neointimal hyperplasia caused by balloon injury to the c

121 tenosis, although early stent thrombosis and neointimal hyperplasia causing vessel renarrowing were k

122 Neointimal hyperplasia characterized by abnormal accumul

123 ed femoral arteries showed a 20% increase in neointimal hyperplasia compared with similarly injured w

124 l activation, less inflammation, and reduced neointimal hyperplasia compared with the E1-AV vector-tr

125 2, p = 0.044) owing to significantly reduced neointimal hyperplasia (cross-sectional area, 0.46 +/- 0

126 lack of endothelium and compliance mismatch, neointimal hyperplasia develops aggressively, resulting

127 sion revascularization (consistent with less neointimal hyperplasia), especially after PES implantati

128 selectin antagonism using rPSGL-Ig decreases neointimal hyperplasia following balloon injury, by inhi

129 nd both agents attenuated the development of neointimal hyperplasia following endothelial injury.

130 s of OA-NO(2) in vivo, because inhibition of neointimal hyperplasia following femoral artery injury w

131 dels of angioplasty have suggested a role in neointimal hyperplasia for endothelins (ETs), potent vas

132 elivery in a manner that virtually abolishes neointimal hyperplasia for months after stent implantati

133 lymer could produce a sustained reduction in neointimal hyperplasia for up to six months after stenti

134 A) receptor antagonism significantly reduced neointimal hyperplasia forming over porcine coronary ste

135 Three weeks after injury, neointimal hyperplasia (from alpha-smooth muscle actin-p

136 helialization, but also effectively improved neointimal hyperplasia, hypercoagulability, and vasoreac

137 ar ultrasound (IVUS) measurement of in-stent neointimal hyperplasia (IH) volumes.

138 ent and selective ET(A) antagonist to reduce neointimal hyperplasia in a porcine coronary artery sten

139 al nonablative infrared laser irradiation on neointimal hyperplasia in a rabbit balloon injury model.

140 fibrin turnover/deposition, (3) exacerbates neointimal hyperplasia in an experimental model of stasi

141 erial injury correlates with the severity of neointimal hyperplasia in animal models and postangiopla

142 pterin, in an EC-specific manner and reduced neointimal hyperplasia in experimental vein grafts in GC

143 The examination of neointimal hyperplasia in injured animal artery models h

144 gamma-irradiation reduces recurrent in-stent neointimal hyperplasia in long, diffuse ISR lesions; how

145 overexpression of the apoE gene also reduces neointimal hyperplasia in mice after endothelial denudat

146 PES compared with BMS significantly reduce neointimal hyperplasia in patients with ST-segment eleva

147 , named W9, inhibited balloon injury-induced neointimal hyperplasia in rabbit carotid arteries.

148 angiogenesis in tumor implants and sustained neointimal hyperplasia in response to arterial injury, i

149 direct effect of apoE in protection against neointimal hyperplasia in response to mechanically induc

150 in (apo) E in vivo was explored by measuring neointimal hyperplasia in response to vascular injury in

151 ion and degradation of p27(Kip1) accentuates neointimal hyperplasia in response to wire injury.

152 , the rat subtotal nephrectomy model, venous neointimal hyperplasia in the arteriovenous fistula was

153 s been shown to attenuate the development of neointimal hyperplasia in the balloon injury model, this

154 Ad2/betaARKct significantly reduced neointimal hyperplasia in the graft/vein anastomosis.

155 AV-W9 treatment significantly inhibited neointimal hyperplasia in this porcine arterial balloon

156 enhance endothelial regeneration and reduce neointimal hyperplasia in vascular injury states.

157 defects, improve EPC survival, and decrease neointimal hyperplasia in Zucker fatty rats postangiopla

158 gulator of SMC proliferation, migration, and neointimal hyperplasia, in part through modulating endos

159 linically significant outcome, inhibition of neointimal hyperplasia induced by arterial injury.

160 ated balloon catheters significantly reduced neointimal hyperplasia induced by balloon angioplasty in

161 Atherosclerosis and arterial injury-induced neointimal hyperplasia involve medial smooth muscle cell

162 Neointimal hyperplasia involves activation of smooth mus

163 Neointimal hyperplasia is a critical component of resten

164 Exaggerated neointimal hyperplasia is considered as the primary mech

165 ysis arteriovenous fistulas, and that venous neointimal hyperplasia is exacerbated when this model is

166 ggest that apoE inhibition of injury-induced neointimal hyperplasia is not due to the inhibition of i

167 Recalcitrant neointimal hyperplasia is postulated to be involved in t

168 ver, and if the media is not made quiescent, neointimal hyperplasia is simply delayed rather than pre

169 Patches delivering rapamycin developed less neointimal hyperplasia, less smooth muscle cell prolifer

170 articles, causing a significant reduction in neointimal hyperplasia, lipid burden, cholesterol clefts

171 1 to negatively regulate cell proliferation (neointimal hyperplasia) may have an antiatherogenic effe

172 is characterized by increased vascular tone, neointimal hyperplasia, medial hypertrophy, and adventit

173 , a retinal ischemia/reperfusion model and a neointimal hyperplasia model of the femoral artery.

174 remodeling, morphometry, graft patency, and neointimal hyperplasia (NH) development.

175 In view of the inflammatory nature of neointimal hyperplasia (NIH), we tested the hypothesis t

176 ss was 0.04, 0.05, and 0.06 mm, whereas mean neointimal hyperplasia obstruction was 4.5+/-2.4%, 5.2+/

177 Neointimal hyperplasia occurred in variable degrees by 5

178 Neointimal hyperplasia of restenosis after coronary arte

179 vulnerability in atherosclerosis and in the neointimal hyperplasia of restenosis.

180 To trigger neointimal hyperplasia of VSMC, we used a mouse model of

181 asty model, control patches developed robust neointimal hyperplasia on the patch luminal surface char

182 sis within Palmaz-Schatz stents results from neointimal hyperplasia or chronic stent recoil and occur

183 ese EPCs given to Zucker fatty rats decrease neointimal hyperplasia post-carotid angioplasty.

184 nactivation of ERalpha in VSMC abrogates the neointimal hyperplasia protection induced by E2, whereas

185 implantation may lower the intensity of late neointimal hyperplasia, reducing the incidence of in-ste

186 only used in cardiovascular surgery, however neointimal hyperplasia remains a significant concern, es

187 Because ISR is due to neointimal hyperplasia, rotational ablation may be a mor

188 Moreover, the reduction in neointimal hyperplasia seen in beta-arrestin2(-/-) mice

189 and at 4 weeks, the venous segment displayed neointimal hyperplasia, smooth muscle proliferation, and

190 , especially negative remodeling, influences neointimal hyperplasia suppression after implantation of

191 e sirolimus drug-eluting stent in inhibiting neointimal hyperplasia, the process underlying restenosi

192 Although much attention has focused on neointimal hyperplasia, the repetitive trauma to vessel

193 The median neointimal hyperplasia thickness was 0.04, 0.05, and 0.0

194 A20 prevents neointimal hyperplasia through combined anti-inflammator

195 Venous neointimal hyperplasia (VNH) at the outflow vein of hemo

196 tively, and intravascular ultrasound percent neointimal hyperplasia was 8.10+/-5.81 and 8.85+/-7.77,

197 Neointimal hyperplasia was assayed 8 weeks after the vas

198 Neointimal hyperplasia was assessed after carotid balloo

199 e recruitment (41%) were reduced at 3 d, and neointimal hyperplasia was attenuated (29%) at 28 d by R

200 Neointimal hyperplasia was enhanced in beta-arrestin1(-/

201 of EPCs was done at various time points, and neointimal hyperplasia was measured 3 weeks later.

202 ablishing the fistula, and by 16 weeks, such neointimal hyperplasia was progressive and pronounced; a

203 Accordingly, the origin of neointimal hyperplasia-was examined in porcine arteriali

204 smooth muscle cell (VSMC) proliferation and neointimal hyperplasia were evaluated in cultured VSMCs

205 d of intima (percentage intima) secondary to neointimal hyperplasia were noted among the different ra

206 ected from the development of injury-induced neointimal hyperplasia, whereas LPA1(-/-) mice developed

207 odeling, including interstitial fibrosis and neointimal hyperplasia, which are characteristic of chro

208 Control allografts showed severe neointimal hyperplasia, which consists mainly of alpha-a

209 s in venous endothelial cells (ECs) to cause neointimal hyperplasia, which correlated with the high e

210 Cav-1 in mice stimulates SMC proliferation (neointimal hyperplasia), with concomitant activation of

211 The frequency of neointimal hyperplasia within the stent was also decreas