ライフサイエンスコーパス: intimal

1 search on atherosclerosis has focused on the intimal accumulation of lipids and inflammatory cells, t

2 IL-6 on endothelial cell integrity or on the intimal accumulation of smooth muscle cells, macrophages

3 Phenotypic transformation of intimal and adventitial lymphatics in atherosclerosis: a

4 r BMP activity, atherosclerotic lesion size, intimal and medial calcification, and inflammation.

5 Intimal and medial hyperplasia correlated significantly

6 Intimal and medial hyperplasia was significantly inhibit

7 p67phox, immunoreactive NoxA1 is present in intimal and medial SMCs of human early carotid atheroscl

8 The importance of CyPA for intimal and medial thickening was shown by strong correl

9 Both intimal and valvular calcifications are closely associat

10 ients who received ATG by changes in maximal intimal area (1.0 +/- 1.2 versus 2.3 +/- 2.6 mm(2); P =

11 odel (OA-NO(2) treatment resulted in reduced intimal area and intima to media ratio versus vehicle- o

12 acity to deliver drug more evenly within the intimal area rather than concentrating drug around the s

13 At 1 year, the SVG mean intimal area was 4.3 +/- 2.1 mm(2), and the occlusion ra

14 ne concentration to an evolution law for the intimal area, we reduce the problem to a single nonlinea

15 with intimal gathering without alteration of intimal area.

16 lear if the category of acute rejection with intimal arteritis (ARV) is relevant to short- and long-t

17 Intimal arteritis (Banff v-lesion) was an independent hi

18 Intimal arteritis (the presence of v-lesions) in kidney

19 teria of AMR: T cell-mediated rejection with intimal arteritis (v) lesion (TCMRV; n = 78), total anti

20 The Banff scores of intimal arteritis (v1, v2 and v3) represented low, moder

21 l activation, a response resembling clinical intimal arteritis.

22 aft outcomes are affected by the severity of intimal arteritis.

23 pathomechanisms of arterial calcifications: intimal associated with atherosclerosis and medial knows

24 nd other inflammatory cells are found in the intimal atherosclerotic lesions.

25 The spasm lesion more frequently showed an intimal bump at baseline and intimal gathering during sp

26 ic state and facilitates the formation of an intimal bump in patients with vasospastic angina.

27 An intimal bump was defined as 1 or more intimal projection

28 of chondrocyte-like cells in atherosclerotic intimal calcification of C57BL/6 LDLr(-/-) mice using bo

29 that this effect could be due to a defect in intimal cell differentiation from endothelial to mesench

30 cpep1-null mice show decreases in medial and intimal cell proliferation as well as vessel remodeling

31 rtant source from which TGF-beta(1) recruits intimal cells and suggest instead that TGF-beta(1) induc

32 l-derived factor (SDF)-1alpha and medial and intimal cells coexpressing SM-alpha-actin and CXCR4, the

33 ed how well vascular elastography can detect intimal changes in a mouse model of carotid remodeling.

34 d elastography method for early detection of intimal changes in small animals.

35 mic stresses have normalized without obvious intimal changes.

36 Increased accumulation of less organized intimal collagen, laminin, alpha-smooth muscle actin, an

37 ll pathology contributes to AAD with typical intimal damage at sites of mechanical trauma.

38 solving inflammatory response that can cause intimal destruction, arterial thrombosis, and end-organ

39 Focal intimal disruption (FID) has been described in >20% of t

40 FID was defined as an intimal disruption with contrast material-filled outpouc

41 Nearly all the intimal dissection tears were located at sites of previo

42 Thrombi because of superficial intimal erosion characteristically complicate matrix-ric

43 y until day 42, at which point the degree of intimal expansion (IE) of vessels was assessed by histol

44 y until day 42, at which point the degree of intimal expansion (IE) of vessels was assessed by histol

45 peratively results in T cell infiltrates and intimal expansion 4 wk later.

46 eic arterial interposition grafts, producing intimal expansion and calcification in the absence of T

47 ation of human IL-6 reduces the magnitude of intimal expansion and total T cell infiltration but incr

48 Intimal expansion can give rise to dangerous events such

49 enhances allogeneic T cell infiltration and intimal expansion in a model of human allograft rejectio

50 odels characterized by VSMC accumulation and intimal expansion to determine the function of AIP1.

51 ascular smooth muscle cell proliferation and intimal expansion were associated with phosphorylation o

52 -J(2), ciglitazone, and pioglitazone reduced intimal expansion, intimal infiltration of CD45RO(+) mem

53 Rejecting grafts demonstrated robust intimal expansion, outward vascular remodeling, and vari

54 effector T cells into the artery intima and intimal expansion.

55 of the mesenchymal cells responsible for the intimal fibrosis in systemic sclerosis (SSc) has not bee

56 However, dissections with intimal flap extension into the aortic arch between the

57 ocedure time, number of fenestrations of the intimal flap per patient, necessity of additional aortic

58 In four patients, fenestration of the intimal flap was performed twice.

59 However, only 3 patients presented an intimal "flap" on angiography.

60 cular targets through which PAI-1 stimulates intimal formation and suppresses TGF-beta(1) expression

61 as a negative regulator in IFN-gamma-induced intimal formation, in part by downregulating IFN-gamma-J

62 all may reveal new approaches for inhibiting intimal formation.

63 ently showed an intimal bump at baseline and intimal gathering during spasm compared with the nonspas

64 Intimal gathering was defined as a folding/gathering of

65 al narrowing during spasm is associated with intimal gathering without alteration of intimal area.

66 . 22.3%; p = 0.006) and tendency for greater intimal growth (percent intimal volume: 9.2 +/- 9.3% vs.

67 Therefore, PAI-1 stimulates intimal growth and suppresses TGF-beta(1) expression thr

68 howed previously that TGF-beta(1) stimulates intimal growth through early upregulation of plasminogen

69 ctor (TGF)-beta(1) is a potent stimulator of intimal growth.

70 aths produced pronounced (85%) inhibition of intimal hyperplasia (0.15+/-0.05 vs 1.01+/-0.16), withou

71 cold ischemia time developed severe TV with intimal hyperplasia (alpha-smooth muscle actin positive

72 sue factor (TF) and thrombin are involved in intimal hyperplasia (IH) and remodelling following vascu

73 Intimal hyperplasia (IH) and restenosis limit the long-t

74 This leads to intimal hyperplasia (IH) formation that induces inflamma

75 Intimal hyperplasia (IH) limits the patency of all cardi

76 Intimal hyperplasia (IH) remains a major cause of poor p

77 r processes, constrictive vessel remodeling, intimal hyperplasia (IH), and retarded re-endothelializa

78 e major pro-restenotic pathologies including intimal hyperplasia (IH), endothelium impairment, and ve

79 emodeling and the formation of flow-limiting intimal hyperplasia (IH).

80 vs. 0.77+/-0.10 micromol/L; P<0.01) and less intimal hyperplasia (risk ratio [95% confidence interval

81 re associated with subsequent development of intimal hyperplasia (risk ratio [95% confidence interval

82 cent VSMCs; however, CD98hc deletion reduced intimal hyperplasia after arterial injury.

83 n shown to be involved in the development of intimal hyperplasia after vascular injury.

84 igating mechanisms of hemodynamically driven intimal hyperplasia and arterial wall remodeling.

85 Moreover, HB-EGF is augmented at sites of intimal hyperplasia and atherosclerosis, conditions favo

86 ID(-/-) recipients with further reduction of intimal hyperplasia and fibrosis scores.

87 lly challenging and can lead to failure from intimal hyperplasia and foreign body reaction.

88 and protects against injury-induced arterial intimal hyperplasia and inflammation, providing protecti

89 Intimal hyperplasia and lesion size were measured histol

90 Frequently, this leads to intimal hyperplasia and lumen narrowing, with significan

91 d induce ischemic organ damage through rapid intimal hyperplasia and luminal occlusion.

92 perone function is an important regulator of intimal hyperplasia and may have implications for molecu

93 ors, and medications are associated with SVG intimal hyperplasia and occlusion after CABG.

94 We assessed the following correlates for intimal hyperplasia and occlusion: patient characteristi

95 /-) mice, which displayed significantly more intimal hyperplasia and perivascular fibrosis compared t

96 rotid arteries attenuated the development of intimal hyperplasia and reduced arterial wall thickening

97 namic manipulations can reproducibly augment intimal hyperplasia and remodeling end points in mouse v

98 clinically relevant mouse model of arterial intimal hyperplasia and remodeling.

99 id focal stenosis yields reproducible murine intimal hyperplasia and substantial differentials in art

100 ew mechanism for the development of vascular intimal hyperplasia and suggest a novel therapeutic stra

101 istic insight into the formation of vascular intimal hyperplasia and suggest a novel therapeutic stra

102 werful tool for unraveling the mechanisms of intimal hyperplasia and vascular remodeling, although th

103 Two of our recipients developed severe intimal hyperplasia and vasculopathy early post-transpla

104 ft failure includes thrombotic occlusion and intimal hyperplasia at the site of vascular anastomosis.

105 afts are prone to thrombosis, infection, and intimal hyperplasia at the venous anastomosis.

106 Stenosis due to intimal hyperplasia development often occurs after place

107 pression in A20 heterozygote mice aggravated intimal hyperplasia following partial carotid artery lig

108 Although intimal hyperplasia has been reported in human hand tran

109 Drugs that inhibit intimal hyperplasia have been developed, however there i

110 The effect of NO-ELIP delivery to attenuate intimal hyperplasia in a balloon-injured artery was dete

111 Average intimal hyperplasia in all arteries was 2+/-4%.

112 ing EC repair and the ensuing development of intimal hyperplasia in eNOS(-/-) mice.

113 We noted significantly greater intimal hyperplasia in HET versus WT allografts, indicat

114 ide a novel clinical approach for decreasing intimal hyperplasia in vein grafts.

115 external stent to reduce the development of intimal hyperplasia in vein grafts.

116 ctile gene expression and greatly attenuates intimal hyperplasia in vivo.

117 esis, we used an established mouse model for intimal hyperplasia in wild-type mice that had been tran

118 e for some of the smooth muscle cells within intimal hyperplasia lesions of vein grafts.

119 Within intimal hyperplasia lesions, smooth muscle cells are a m

120 respectively, of smooth muscle cells within intimal hyperplasia lesions.

121 Intimal hyperplasia of autologous vein grafts is a criti

122 Intimal hyperplasia of saphenous vein grafts (SVGs) can

123 No intimal hyperplasia of the coronary arteries was observe

124 rvival, myocardial lesion size and degree of intimal hyperplasia of the coronary arteries were analyz

125 Intimal hyperplasia produces restenosis (re-narrowing) o

126 echnically flexible method for enhancing the intimal hyperplasia response.

127 atelet Treatment After Grading Stent-Induced Intimal Hyperplasia Study (PRODIGY) trial assessed unsel

128 erplasia, hampering efforts to identify anti-intimal hyperplasia therapies.

129 heath that is highly effective in preventing intimal hyperplasia through perivascular delivery of rap

130 Intimal hyperplasia with luminal obliteration developed

131 atelet Treatment After Grading Stent-Induced Intimal Hyperplasia) trial and randomized to short (6 mo

132 re small, whereas wild-type mice had diffuse intimal hyperplasia, a high intima/media ratio, and infl

133 om the development of vascular inflammation, intimal hyperplasia, and accelerated atherosclerosis.

134 xpression and function in the development of intimal hyperplasia, and discern a potential mechanism o

135 , fracturing of the internal elastic lamina, intimal hyperplasia, and eyelid vessel damage.

136 as cerebral and coronary arterial vasospasm, intimal hyperplasia, and hypertension.

137 preventing smooth muscle cell proliferation, intimal hyperplasia, and proteoglycan deposition.

138 GF-beta) has profound stimulatory effects on intimal hyperplasia, but it is unknown whether these eff

139 However, in wild-type mice, there is limited intimal hyperplasia, hampering efforts to identify anti-

140 ype recipient mice which had severe vascular intimal hyperplasia, interstitial fibrosis, and inflamma

141 However, despite their involvement in intimal hyperplasia, neither LPA1 nor LPA2 was required

142 ated plasma ADMA is associated with coronary intimal hyperplasia, supporting the importance of nitric

143 he response to vascular injury that leads to intimal hyperplasia, this study investigated the in vivo

144 The former is pathophysiologic resulting in intimal hyperplasia, whereas the latter is physiological

145 ial role in the formation and development of intimal hyperplasia, which is the main cause of graft fa

146 orphologic adaptations included proximal LCA intimal hyperplasia, which was exacerbated by diet-induc

147 oangiogenesis and results in lumen-occlusive intimal hyperplasia.

148 ascular graft that resists both clotting and intimal hyperplasia.

149 ay in the TEV's resistance to occlusion from intimal hyperplasia.

150 roliferate is essential for the formation of intimal hyperplasia.

151 et proteins (HSP27 and CREB) associated with intimal hyperplasia.

152 ay provide a novel approach to inhibition of intimal hyperplasia.

153 s (SMCs) is essential for the development of intimal hyperplasia.

154 identified patients who would have developed intimal hyperplasia.

155 of CD8+ T cell infiltration and reduced neo-intimal hyperplasia.

156 contributes to vascular pathologies such as intimal hyperplasia.

157 e characterized histologically by concentric intimal hyperplasia.

158 It is a concentric vascular intimal hyperplastic lesion composed of smooth muscle-li

159 s characteristically develop severe, diffuse intimal hyperplastic lesions that eventually compromise

160 coefficient was 0.80 (P<0.001) and with mean intimal index was 0.92 (P<0.001).

161 Maximal intimal thickness and mean intimal index were 0.73+/-0.50 mm and 20.9+/-10.6%, resp

162 Maximal intimal thickness and mean intimal index were recorded.

163 and pioglitazone reduced intimal expansion, intimal infiltration of CD45RO(+) memory T cells, and pl

164 specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and calcificat

165 Toll-like receptor 2 ligation in superficial intimal injury, a process implicated in superficial eros

166 n maintaining the health and function of the intimal layer in vasculature.

167 NTN1 protein was highly expressed in the intimal layer of the control vessels.

168 h an increased accumulation of apo(a) in the intimal layer of the vessel wall.

169 f medial vascular smooth muscle cells to the intimal layer, and ultimately acute thrombosis.

170 eoangiogenesis as well as hyperplasia of the intimal layer, implicating T cells in the maladaptive be

171 endothelial progenitors able to assemble the intimal layers.

172 entiated into smooth muscle cells within the intimal lesion and may provide a novel clinical approach

173 ring inflammatory cells do not contribute to intimal lesion formation.

174 blockade by TAK-779 reduced the severity of intimal lesions (53+/-10% vs. 16+/-2%; P<0.05) and decre

175 recipients with D-4F reduced the severity of intimal lesions (62.5+/-3.4% vs. 31.1+/-8.7%, P<0.009).

176 tantly, the donor hearts did not display any intimal lesions characteristic of chronic rejection.

177 After wire-injury, intimal lesions in AGER1-tg mice were small, whereas wil

178 els with medial hypertrophy or initial-stage intimal lesions in lung sections from VM macaques demons

179 iple lineages, and potentially contribute to intimal lesions in vivo.

180 expression of Id1 was observed in concentric intimal lesions of heritable PAH cases.

181 D In mouse carotid arteries with established intimal lesions tailored to resemble the substrate of hu

182 severe and irreversible PAH, associated with intimal lesions, colocalizing with proliferating ECs and

183 bone marrow transplantation did not develop intimal lesions, which indicates that CCR1-bearing infla

184 contribution of host cell precursors to the intimal lesions.

185 Axl-dependent survival is very important for intimal leukocytes; however, Axl expression in BM cells

186 last-like synoviocytes (FLS) in the synovial intimal lining of the joint are key mediators of inflamm

187 Expression in synovium was mainly in the intimal lining.

188 ia reflected the alterations observed in the intimal lipids, yet being more subtle.

189 Intimal lymphatics in the atherosclerotic lesions exhibi

190 aging of atherosclerotic lesions in terms of intimal macrophage accumulation and distribution and dis

191 of maladapted endothelial cells and triggers intimal macrophage accumulation.

192 Intimal macrophage infiltration promotes atherosclerotic

193 assess the distribution and accumulation of intimal macrophages using CD36-targeted nanovesicles.

194 argeted delivery of therapeutic compounds to intimal macrophages.

195 s were associated with common carotid artery intimal media thickness (CC IMT) in European-Americans [

196 unction was assessed by using carotid-artery intimal media thickness (cIMT) and flow-mediated dilatio

197 onary artery calcification (CAC) and carotid intimal media thickness at baseline in 2000-2002 among p

198 nic variation in sex differences for carotid intimal media thickness was less pronounced.

199 ions also included body composition, carotid intimal-media thickness (c-IMT), ambulatory blood pressu

200 subclinical atherosclerosis (common carotid intimal-media thickness) and 2) associated risk factors

201 , resting and treadmill exercise BP, carotid intimal-media thickness, retinal vascular photography, m

202 Intimal medial thickness (IMT) of both carotid arteries

203 osclerosis measured by common carotid artery intimal medial thickness (IMT).

204 sed ultrasonography to demonstrate increased intimal medial thickness and alterations in the structur

205 n coronary atherosclerosis or carotid artery intimal medial thickness as compared with subjects on at

206 onographic investigations of fatty liver and intimal medial thickness of the common carotid arteries,

207 y calcium score, common and internal carotid intimal medial thickness, and major electrocardiographic

208 linical cardiovascular disease (CAC, carotid intimal medial thickness, stenosis, and ankle brachial i

209 ncluding multiple areas of patchy or diffuse intimal, medial or adventitial abnormalities with thicke

210 accumulation of fatty cells in the arterial intimal-medial layers.

211 The estimated mean differences in carotid intimal-medial thickness between groups of men with vari

212 Intimal-medial thickness was weakly, positively associat

213 the relation of baldness pattern to carotid intimal-medial thickness, a measure of atherosclerosis,

214 al disease (coronary calcium, common carotid intimal-medial thickness, and ankle-brachial index) in 5

215 res, including ankle-brachial index, carotid intimal-medial thickness, and echocardiographic left ven

216 Type IV collagen was strictly intimal/medial.

217 e B(4)-dependent VSMC phenotypic modulation, intimal migration, and proliferation.

218 their expression of ABCA1 in comparison with intimal monocyte-derived macrophages, however, are unkno

219 ectively, 5 and 2 cases), 5 scaffolds showed intimal neovessels or marked peristrut low-intensity are

220 ncy of this innate immune receptor decreased intimal neutrophil adherence in regions of local flow di

221 xperiments with vessel walls stripped of the intimal or adventitial layer identified dendritic cells

222 An intimal bump was defined as 1 or more intimal projections into the lumen that disappeared afte

223 monocytes/macrophages significantly enhances intimal proliferation after arterial injury.

224 s from atherogenic damage by reducing vessel intimal proliferation and inhibiting adhesion molecule e

225 with standard-dose cyclosporine and reduces intimal proliferation at 12 months in de novo heart tran

226 ation with anti-CD8 antibody did not prevent intimal proliferation compared with untreated controls (

227 injury, Nf1(+/-) mice demonstrated increased intimal proliferation compared with wild-type mice.

228 hypothesis that Ras-Erk signaling regulates intimal proliferation in a murine model of NF1 arterial

229 Intimal proliferation in low-flow carotid arteries was d

230 ion molecule expression, and enhanced aortic intimal proliferation.

231 phospholipids, increasing their affinity for intimal proteoglycans; contribute to cholesterol loading

232 e that graft-derived IL-1 can promote T cell intimal recruitment and IL-17 production during human ar

233 o luminal region, their proliferation in the intimal region, and neointima formation.

234 artery characterized by an expansion of the intimal region.

235 muscle cell migration from the media to the intimal region.

236 on stabilization of PECAM-1, which reverses intimal remodeling in vivo.

237 f cytokines and chemokines in human synovial intimal resident fibroblast-like synoviocytes (FLS).

238 OCT readily identified the intimal rupture site (n = 7), the thickness (348 +/- 84

239 rsus WT allografts correlated with increased intimal SMC proliferation, and a higher number of infilt

240 decreased expression of PTEN was observed in intimal SMCs of human atherosclerotic lesions underlying

241 ABCA1 expression by intimal SMCs was significantly reduced between early and

242 The intimal SMLCs in mouse GAD lesions differ from medial sm

243 Although intimal SMLCs may originate by migration and modulation

244 Intimal SMLCs, but not medial smooth muscle cells, expre

245 Intimal smooth muscle cells (SMCs) contribute to the foa

246 These data suggest that targeting intimal stiffening and/or the EC response to intima stif

247 Intimal surface areas of ascending aortas were measured

248 h there might be a catastrophic transection, intimal tear or flap, or subadventitial tear.

249 CAV was defined as an intimal thickening >/= 0.5 mm in the follow-up with rega

250 nd specificity of 81% and 75% to detect CAV (intimal thickening >0.5 mm), whereas the PPV and NPV wer

251 ophy, arteriolar hyaline thickening, fibrous intimal thickening (CV), and fraction of sclerotized glo

252 ities were present in all children including intimal thickening (intima/lumen cross-sectional area ra

253 recipients, angiography was normal; however, intimal thickening (intima/media cross-sectional area ra

254 LITA showed a significant intimal thickening (P=0.05) and a nonsignificant medial

255 Lesions were classified into pathological intimal thickening (PIT), VH-IVUS-derived thin-capped fi

256 ly, restenosis after angioplasty, vein graft intimal thickening and atherogenesis.

257 day 24 posttransplantation and analyzed for intimal thickening and cellular infiltration.

258 rol allografts, which also developed greater intimal thickening and stenosis than hGSTA4-4 transduced

259 nges in coronary artery structure, including intimal thickening and vessel remodeling, occur early af

260 evealed patent ductus arteriosus with normal intimal thickening but dilated cardiac chambers.

261 , whereas arteriolar hyalinosis and vascular intimal thickening did not.

262 Intimal thickening is driven by damage to the endotheliu

263 Vascular remodeling rather than intimal thickening is the most important determinant of

264 Intimal thickening is usually attributed to the migratio

265 e, changes in right ventricular pressure and intimal thickening of pulmonary small artery are a littl

266 Cs together with fibrosis provoke concentric intimal thickening of the coronary arteries, which is th

267 (plaque erosion), most often on pathological intimal thickening or fibroatheromas.

268 typically characterized by diffuse coronary intimal thickening with pathological vessel remodeling,

269 CCR1-deficient recipients, it increased GAD intimal thickening with SMLC proliferation in only the w

270 cimens comprised an undiseased portion (thin intimal thickening with the underlying media) and a dise

271 olar hyalinosis, and 32.9% abnormal vascular intimal thickening).

272 patterns are observed: (1) shear stabilized intimal thickening, (2) tension induced wall thinning an

273 o the coronary circulation, LITA grafts show intimal thickening, increased intima/media ratio, and ma

274 ially drive the various vascular phenotypes (intimal thickening, media hypertrophy, adventitial thick

275 we propose and study a mathematical model of intimal thickening, posed as a free boundary problem.

276 lates most strongly with venous and small IV intimal thickening, similar to the pattern observed in P

277 tion ensues within 4 weeks, characterized by intimal thickening, T-cell infiltrates, and vascular cel

278 ity, as indicated by the loss of Eph-B4, and intimal thickening.

279 SMC) proliferation and migration and thereby intimal thickening.

280 cent medial thickness (arteries) and percent intimal thickness (%IT) (arteries, veins, and IV) relati

281 7.9 versus 12.8 +/- 12.3%; = 0.003), maximal intimal thickness (0.2 +/- 0.2 versus 0.3 +/- 0.3 mm; P

282 e demonstrated no difference in mean maximal intimal thickness (0.35+/-0.36 versus 0.36+/-0.26 mm; P=

283 On the basis of maximum intimal thickness (MIT) at BL, recipients were divided i

284 Maximal intimal thickness and mean intimal index were 0.73+/-0.5

285 Maximal intimal thickness and mean intimal index were recorded.

286 revealed significant differences of arterial intimal thickness between rejecting and AD-MSC-treated a

287 ng's modulus was most associated with higher intimal thickness but not medial or adventitial thicknes

288 point included change in first-year maximal intimal thickness by intravascular ultrasound, a recogni

289 In contrast, maximum intimal thickness did not predict long-term mortality.

290 Morphometry showed that intimal thickness increased by 26% via carotid branch li

291 Correlation of LGE with maximal intimal thickness using the Pearson coefficient was 0.80

292 The mean (SD) 12-month increase in maximal intimal thickness was 0.03 (0.05) mm with everolimus 1.5

293 protein-coupled receptor 180, also known as intimal thickness-related receptor (ITR).

294 ES coating is distributed in the surrounding intimal tissue over the course of several weeks.

295 Exposure of intimal tissue to drug revealed differential distributio

296 aortic segments revealed the distribution of intimal TLR2 expression and the atheroprotective outcome

297 l-known inflammatory reactions consequent to intimal trapping and oxidation of LDL.

298 Change in intimal volume greater than the median and vascular remo

299 tendency for greater intimal growth (percent intimal volume: 9.2 +/- 9.3% vs. 4.4 +/- 5.3%; p = 0.07)

300 EBP50 is up-regulated in intimal VSMC following endoluminal injury and promotes n