ライフサイエンスコーパス: arteriosclerosis

1 HSP70 effects are undesirable (arthritis and arteriosclerosis).

2 ells would reduce the severity of transplant arteriosclerosis.

3 sistent with an infectious disease origin of arteriosclerosis.

4 nulomatosis, Behcet syndrome, and transplant arteriosclerosis.

5 is a key mechanism by which Ang II mediates arteriosclerosis.

6 atment of edema, endotoxemia, and transplant arteriosclerosis.

7 grafts correlates with absence of transplant arteriosclerosis.

8 h cerebral amyloid angiopathy, but not HS or arteriosclerosis.

9 elopment of chronic rejection and transplant arteriosclerosis.

10 y donors, knowing that aging per se promotes arteriosclerosis.

11 ications for the pathophysiology of AAAs and arteriosclerosis.

12 096 may be able to prevent chronic allograft arteriosclerosis.

13 I-1096 decreases the incidence of transplant arteriosclerosis.

14 ons, most notably coronary heart disease and arteriosclerosis.

15 c target for preservation of vessel lumen in arteriosclerosis.

16 s important roles in coronary thrombosis and arteriosclerosis.

17 xpression, links early dysfunction with late arteriosclerosis.

18 vents in the pathogenesis of transplantation arteriosclerosis.

19 s with heart failure, diabetes mellitus, and arteriosclerosis.

20 the formation of microvessels in transplant arteriosclerosis.

21 by attenuating the development of transplant arteriosclerosis.

22 from immune injury and attenuates transplant arteriosclerosis.

23 important role in the process of transplant arteriosclerosis.

24 rogression of transplant-associated coronary arteriosclerosis.

25 he kinetics of the development of transplant arteriosclerosis.

26 y were associated with increased severity of arteriosclerosis.

27 he kinetics of the development of transplant arteriosclerosis.

28 of the presence of risk factors for coronary arteriosclerosis.

29 ortant role in the development of transplant arteriosclerosis.

30 umber of disease states such as diabetes and arteriosclerosis.

31 e to the development of accelerated coronary arteriosclerosis.

32 ard the progression of transplant-associated arteriosclerosis.

33 y disorders such as atherosclerosis or graft arteriosclerosis.

34 ble to diet (high-fat diet)-induced diabetic arteriosclerosis.

35 plays a central role in the pathogenesis of arteriosclerosis.

36 have utility in the treatment of transplant arteriosclerosis.

37 hin the lesions of atherosclerosis and graft arteriosclerosis.

38 immune inflammation characteristic of graft arteriosclerosis.

39 her glomerulosclerosis, tubular atrophy, and arteriosclerosis.

40 e of preventing the development of allograft arteriosclerosis.

41 tion and migration into the neointima during arteriosclerosis.

42 essel wall may promote transplant-associated arteriosclerosis.

43 eopontin (OPN), a matricellular regulator of arteriosclerosis.

44 F-I may be a major factor in mediating graft arteriosclerosis.

45 e of chronic rejection, including transplant arteriosclerosis.

46 IGF-I) is crucial in accelerating transplant arteriosclerosis.

47 ent protects against experimental transplant arteriosclerosis.

48 ays an important role in the pathogenesis of arteriosclerosis.

49 phenotypic modulation in the pathogenesis of arteriosclerosis.

50 ntral role in the pathogenesis of transplant arteriosclerosis.

51 ne sources of TGF-beta1 attenuate transplant arteriosclerosis.

52 ultimately promote the development of graft arteriosclerosis.

53 ect grafts against development of transplant arteriosclerosis.

54 OS) is upregulated in grafts with transplant arteriosclerosis.

55 etic approach to the treatment of transplant arteriosclerosis.

56 hereby IGF-I exposure accelerates transplant arteriosclerosis.

57 t NO suppresses the development of allograft arteriosclerosis.

58 NO) may play in the development of allograft arteriosclerosis.

59 than 90% of graft vessels due to accelerated arteriosclerosis.

60 lipoprotein, playing a role in inhibition of arteriosclerosis.

61 VEC damage is a hallmark of arteriosclerosis.

62 d, in particular, with transplant-associated arteriosclerosis.

63 ying events that culminate in posttransplant arteriosclerosis.

64 f xenografts and the avoidance of transplant arteriosclerosis.

65 orine (CsA) on iNOS expression and allograft arteriosclerosis.

66 inhibitory effect of estradiol on transplant arteriosclerosis.

67 ral-mediated iNOS gene transfer on allograft arteriosclerosis.

68 an important and independent risk factor for arteriosclerosis.

69 edict the development of transplant coronary arteriosclerosis.

70 minal narrowing characteristic of transplant arteriosclerosis.

71 oth muscle cell proliferation, a hallmark of arteriosclerosis.

72 ion, which resulted in attenuated transplant arteriosclerosis.

73 of cockerels to ETS significantly accelerate arteriosclerosis.

74 togenic peptide in the pathogenesis of graft arteriosclerosis.

75 cytomegalovirus (HCMV) in the development of arteriosclerosis.

76 proliferation and migration is important in arteriosclerosis.

77 aft rejection and transplantation-associated arteriosclerosis.

78 response to injury, one of the hallmarks of arteriosclerosis.

79 mall arteries indicative of early transplant arteriosclerosis.

80 ors that favor the progression of transplant arteriosclerosis.

81 modelling such as neointimal hyperplasia and arteriosclerosis.

82 rogramming of aortic progenitors in diabetic arteriosclerosis.

83 rosclerosis and medial knows as Monckeberg's arteriosclerosis.

84 aortic root disease seems to protect against arteriosclerosis.

85 induction strategies that prevent transplant arteriosclerosis.

86 tes, and has been linked to some cancers and arteriosclerosis.

87 lls) expanded ex vivo can prevent transplant arteriosclerosis.

88 tubular atrophy, interstitial fibrosis, and arteriosclerosis.

89 may contribute to the inflammatory milieu of arteriosclerosis.

90 oxidative injury, and attenuates transplant arteriosclerosis.

91 leading to increased formation of transplant arteriosclerosis.

92 ceptor CCR7 in the development of transplant arteriosclerosis.

93 s is implicated in the pathogenesis of graft arteriosclerosis.

94 determinant of luminal loss in cardiac graft arteriosclerosis.

95 cellular immunotherapy to control transplant arteriosclerosis.

96 ta-chains identified previously in allograft arteriosclerosis.

97 prevent CD25-CD4+ T-cell-mediated transplant arteriosclerosis.

98 were AD, subcortical vascular pathology, and arteriosclerosis.

99 amycin therapy for atherosclerosis and graft arteriosclerosis.

100 present in the intimal lesions of transplant arteriosclerosis?

101 d CD8+ T-cell depletion abrogated transplant arteriosclerosis (9%+/-4% luminal occlusion 60 days afte

102 titer correlates with severity of allograft arteriosclerosis after cardiac transplantation.

103 C to chronic rejection and accelerated graft arteriosclerosis (AGA) in long-term cardiac allografts,

104 2) reduces the severity of accelerated graft arteriosclerosis (AGA) in transplanted organs, although

105 . pneumoniae infection and accelerated graft arteriosclerosis (AGA), also known as cardiac allograft

106 splanted human hearts with accelerated graft arteriosclerosis (AGA).

107 e involved in the pathogenesis of transplant arteriosclerosis, an alloimmune initiated vascular steno

108 Patients with severe arteriosclerosis and anti-HLA antibodies (n=91, 12.2%) d

109 e ageing disease, characterized by premature arteriosclerosis and degeneration of vascular smooth mus

110 ural remodelling of arteries, which leads to arteriosclerosis and end-organ damage.

111 16-24 weeks, including widespread transplant arteriosclerosis and focal and segmental glomerulosclero

112 llograft vascular dysfunction predisposes to arteriosclerosis and graft loss.

113 ted and disease-related processes, including arteriosclerosis and inflammatory, endocrine, and immune

114 class I/II-mismatched mouse allografts with arteriosclerosis and intragraft T-cell activation.

115 antibodies are major determinants of severe arteriosclerosis and major adverse cardiovascular events

116 ng for risk factors associated with coronary arteriosclerosis and MI, a stress-induced increase in WM

117 bstantial insight into future treatments for arteriosclerosis and osteoporosis, which are strongly as

118 ole of circulating antibodies in accelerated arteriosclerosis and the role of immune-associated arter

119 Risk factors for arteriosclerosis and type of bypass conduit influence th

120 t activation, in stabilizing thrombi, and in arteriosclerosis and vascular remodeling.

121 s of interstitial fibrosis, tubular atrophy, arteriosclerosis, and arteriolar hyalinosis were graded

122 ocardial fiber disarray, intramural coronary arteriosclerosis, and interstitial fibrosis.

123 diseases, including coronary artery disease, arteriosclerosis, and leukemias.

124 factors for diabetes mellitus, dyslipidemia, arteriosclerosis, and mortality.

125 ogenesis of conditions such as vasculititis, arteriosclerosis, and rheumatoid arthritis.

126 allografts from the development of allograft arteriosclerosis, and that iNOS gene transfer strategies

127 Atherosclerosis and post-transplant graft arteriosclerosis are both characterized by expansion of

128 Atherosclerosis and graft arteriosclerosis are characterized by leukocytic infiltr

129 stem cells to the pathogenesis of transplant arteriosclerosis are controversial, eg, whether bone mar

130 el, the histologic signs of nephrosclerosis (arteriosclerosis/arteriolosclerosis, global glomeruloscl

131 sfer completely prevented the development of arteriosclerosis associated with eNOS deficiency.

132 murine model to demonstrate distal coronary arteriosclerosis associated with evidence of myocardial

133 nimals studied developed peripheral coronary arteriosclerosis, associated with perivascular and myoca

134 omponent has been demonstrated to accelerate arteriosclerosis, at a dose that is environmentally rele

135 N and end-organ damage from DM contribute to arteriosclerosis, atherosclerosis, and endothelial dysfu

136 The homocysteine theory of arteriosclerosis attributes one of the underlying causes

137 role of interferon (IFN)-gamma in transplant arteriosclerosis, BALB/c hearts were transplanted in imm

138 s also been referred to as accelerated graft arteriosclerosis because it has features of arterioscler

139 ngestive heart failure, Alzheimer's disease, arteriosclerosis, breast neoplasms, hypertension, myocar

140 ted plasma homocysteine is a risk factor for arteriosclerosis, but a cause-and-effect relationship re

141 arteriosclerosis because it has features of arteriosclerosis, but it is limited to the graft and dev

142 n CD40L-/- hosts developed significant graft arteriosclerosis by 8-12 wk posttransplant.

143 Our hypothesis that vasculitis results in arteriosclerosis by causing vascular endothelial dysfunc

144 assess immune contributions of TGF-beta1 to arteriosclerosis by comparing the effect of TGF-beta1-de

145 Acceleration of transplant arteriosclerosis by exposure to IGF-I is associated with

146 at human T(reg) cells can inhibit transplant arteriosclerosis by impairing effector function and graf

147 terial injuries, vein grafts, and transplant arteriosclerosis, by which the major progress in underst

148 ociated with increased incidence of coronary arteriosclerosis (CAD), the pathogen burden correlated w

149 In a mouse model of transplant-associated arteriosclerosis, CD44 protein was induced in the neoint

150 Patients develop severe premature arteriosclerosis characterized by vascular smooth muscle

151 pravastatin group (cerebrovascular accident, arteriosclerosis coronary artery, myocardial infraction,

152 iseases such as ischemia-reperfusion injury, arteriosclerosis, cystic fibrosis, inflammatory bowel di

153 ed and diffuse form of obliterative coronary arteriosclerosis, determines long-term function of the t

154 iltrate, but completely prevented transplant arteriosclerosis, diminished myocardial injury, and abro

155 Graft arteriosclerosis directly induced by human IFN-gamma in

156 arch on the role of stem cells in transplant arteriosclerosis, discusses the mechanisms of stem cell

157 nction predicts the development of allograft arteriosclerosis during the initial year posttransplant.

158 Coronary arteriosclerosis, essential hypertension, angina, and pr

159 y T cells suffices to evoke subsequent graft arteriosclerosis, even in the absence of additional T-ce

160 Only when glomerulosclerosis and arteriosclerosis exceed that expected for age is there a

161 This may result from arteriosclerosis following inflammatory damage to the ve

162 t rejection presents pathologically as graft arteriosclerosis (GA) characterized by recipient T cell

163 Graft arteriosclerosis (GA) is an important factor limiting lo

164 role of SENP1-mediated SUMOylation in graft arteriosclerosis (GA), the major cause of allograft fail

165 cellular infiltrates and moderate transplant arteriosclerosis (>75% of arteries showed 10-20% occlusi

166 Patients with antibody-associated severe arteriosclerosis had decreased allograft survival and in

167 ed arteriosclerosis in 1910, suggesting that arteriosclerosis has an infectious cause.

168 dysfunction and the development of allograft arteriosclerosis has not been analyzed serially with int

169 roke, the mechanisms by which it accelerates arteriosclerosis have not been elucidated, mostly becaus

170 veral mouse models for studying all types of arteriosclerosis have recently been established.

171 gnificantly associated with severe allograft arteriosclerosis (hazard ratio, 2.9; P<0.0001), independ

172 ever and syphilis at younger ages, predicted arteriosclerosis in 1910, suggesting that arterioscleros

173 o separate strategies, to prevent transplant arteriosclerosis in a clinically relevant chimeric human

174 prevent the development of accelerated graft arteriosclerosis in a rat model of chronic cardiac allog

175 r-I (IGF-I) on the development of transplant arteriosclerosis in a rat orthotopic aorta allotransplan

176 fts, and prevented development of transplant arteriosclerosis in an MHC class II-mismatched allograft

177 also inhibited the development of transplant arteriosclerosis in aortic allografts partially, but was

178 o the media and neointima during athero- and arteriosclerosis in ApoE(-/-) mice with chronic kidney d

179 lopment of therapeutics targeting transplant arteriosclerosis in both allograft transplantation and o

180 ssed completely the development of allograft arteriosclerosis in both untreated recipients and recipi

181 NV, supporting the hypothesis that premature arteriosclerosis in chronic inflammatory rheumatic disor

182 reductions in the frequency and severity of arteriosclerosis in comparison with cyclosporine A-treat

183 Estrogen prevents transplant arteriosclerosis in experimental cardiac and aortic allo

184 osclerosis and the role of immune-associated arteriosclerosis in graft and patient survival and the o

185 The severity of arteriosclerosis in hGSTA4-4 transduced allografts was c

186 d that the in vivo development of transplant arteriosclerosis in human arteries was prevented by trea

187 ent in diagnosis, prevention, and therapy of arteriosclerosis in humans.

188 dentified in areas of glomerulosclerosis and arteriosclerosis in idiopathic and secondary focal segme

189 hanisms of CD40-CD154-independent transplant arteriosclerosis in major histocompatibility complex (MH

190 ble to prevent the development of transplant arteriosclerosis in MHC class I-mismatched aortic allogr

191 We examined the development of arteriosclerosis in mouse carotid artery loops allograft

192 ecomes a novel therapeutic target to prevent arteriosclerosis in patients with hypertension.

193 ist that protects against the development of arteriosclerosis in rat cardiac allograft.

194 es not prevent the development of transplant arteriosclerosis in several models.

195 cipient's age matters the most in transplant arteriosclerosis in the absence of such variables.

196 mined predicted the development of allograft arteriosclerosis in the initial year posttransplant.

197 or to transplantation accelerates transplant arteriosclerosis in the rat aorta allograft model.

198 erosis of native coronary arteries and graft arteriosclerosis in transplanted hearts are characterize

199 attenuates key histologic features of graft arteriosclerosis, in association with inhibition of mult

200 timulation prevents the development of graft arteriosclerosis, in the LEW into F344 rat cardiac trans

201 Transplant arteriosclerosis initiated by CD4+ T cells was associate

202 s resulted in a similar degree of transplant arteriosclerosis (intimal proliferation, 20+/-9%) in MHC

203 Because arteriosclerosis is a complicated disease, which include

204 Accelerated coronary arteriosclerosis is a major complication in long-term su

205 affects the entire graft vasculature, graft arteriosclerosis is a suitable term to describe the prob

206 hibition of SMC proliferation and transplant arteriosclerosis is down-regulation of IGF-IR.

207 Although the pathogenesis of transplant arteriosclerosis is not yet fully understood, recent dev

208 munosuppression, E2 inhibition of transplant arteriosclerosis is still associated with inhibition of

209 Transplant arteriosclerosis is still the major complication for lon

210 Transplant arteriosclerosis is the hallmark of chronic allograft dy

211 Accelerated coronary arteriosclerosis is the major obstacle to long-term surv

212 The etiology of transplant arteriosclerosis is unknown, but current data point to t

213 scular cell injury and consequent transplant arteriosclerosis is unknown.

214 The precise pathogenesis of graft arteriosclerosis is unknown.

215 lografts and is protective against allograft arteriosclerosis; it suppresses neointimal smooth muscle

216 Graft arteriosclerosis-like arteriopathy induced by PBMCs was

217 Accelerated arteriosclerosis limits the survival of transplanted hea

218 scle cells (ASMC) during the pathogenesis of arteriosclerosis, little is known about genes that defin

219 ipal cohort, 250 (33.6%) patients had severe arteriosclerosis (luminal narrowing >25% via fibrointima

220 s associated with acceleration of transplant arteriosclerosis may occur at an earlier time.

221 protocol significantly reduced the amount of arteriosclerosis; mean vascular luminal occlusion was 11

222 This transplant arteriosclerosis model uses a 0.5% cholesterol diet and

223 We used mouse graft arteriosclerosis models characterized by VSMC accumulati

224 86, attenuated the development of transplant arteriosclerosis, mononuclear cell infiltration, and par

225 event in the cascade that culminates in the arteriosclerosis of chronic rejection.

226 To determine the contribution to transplant arteriosclerosis of MHC and adhesion molecules from cell

227 ue to acute rejection, transplant-associated arteriosclerosis of the coronary arteries remains a sign

228 Cardiac transplant arteriosclerosis or cardiac allograft vasculopathy remai

229 minal geometry in mouse models of transplant arteriosclerosis or flow-induced vascular remodeling.

230 e often regarded as secondary to concomitant arteriosclerosis or related to aging.

231 During the development of transplant arteriosclerosis, PECAM-1 donor endothelial cells were r

232 lls attenuates the development of transplant arteriosclerosis, possibly by affecting macrophage infil

233 use also prevented development of transplant arteriosclerosis post-CD154 mAb therapy.

234 cytokine linked to atherosclerosis and graft arteriosclerosis, potentiated the inflammatory responses

235 The 1910 black arteriosclerosis rate was six times higher than the whit

236 ter lifelong burden of infection led to high arteriosclerosis rates in 1910.

237 Transplant-associated arteriosclerosis remains an obstacle to long-term graft

238 le of NOS2 in the pathogenesis of transplant arteriosclerosis remains unclear.

239 in the development of transplant-associated arteriosclerosis remains unclear.

240 of vascular elastin occurs in patients with arteriosclerosis, renal failure, diabetes, and vascular

241 tecting a vascularized graft from transplant arteriosclerosis requires inhibition of host immune effe

242 use the mouse as an experimental system for arteriosclerosis research.

243 without antibodies and patients with minimal arteriosclerosis, respectively (P<0.0005).

244 cy instead of the a-smooth muscle actin-rich arteriosclerosis seen in wild-type recipients.

245 d us to suggest that new therapies for graft arteriosclerosis should be optimized which focus on redu

246 rafts with 177/DST did not reduce transplant arteriosclerosis significantly (43.0+/-15.7%, n=5 vs. 56

247 ized organ grafts will be lost to transplant arteriosclerosis sometime posttransplantation.

248 a, heart failure, hypertension, arrhythmias, arteriosclerosis, stroke, and venous thrombosis.

249 Quantitative arteriosclerosis studies showed identical results in bot

250 ective role in the development of transplant arteriosclerosis, suppressing neointimal smooth muscle c

251 vascular rejection that leads to transplant arteriosclerosis (TA) are poorly understood.

252 -derived MSCs effectively control transplant arteriosclerosis (TA) by enhancing IL-10(+) and IFN-gamm

253 eg) numbers on the development of transplant arteriosclerosis (TA) in human arterial grafts transplan

254 Transplant arteriosclerosis (TA) is the pathognomonic feature of ch

255 from arterial injury, manifest as transplant arteriosclerosis (TA).

256 is central to the pathogenesis of transplant arteriosclerosis (TA).

257 ifested as a diffuse and accelerated form of arteriosclerosis, termed cardiac allograft vasculopathy.

258 ns on biopsy and more glomerulosclerosis and arteriosclerosis than would be expected for age.

259 lorecognition in the evolution of transplant arteriosclerosis, the main feature of chronic allograft

260 ic injury of allografts predisposes to graft arteriosclerosis, the major cause of late graft failure.

261 Long-term surviving grafts were assessed for arteriosclerosis, the sine qua non of chronic rejection

262 ake is believed to play an important role in arteriosclerosis, these results provide a link between H

263 c allograft recipients attenuates transplant arteriosclerosis; this was associated with inhibition of

264 in treatment successfully reduces vein graft arteriosclerosis through endothelial protection, resulti

265 atment may have a beneficial effect on graft arteriosclerosis through immune mechanisms.

266 tes the development of hepatic steatosis and arteriosclerosis, two common diet-induced metabolic dise

267 isease (CKD) represents an extreme model for arteriosclerosis, vascular calcification, and bone disor

268 taneous (native) atherosclerosis, transplant arteriosclerosis, vein graft atherosclerosis, and angiop

269 In hypertensive patients, we found that arteriosclerosis was associated with the activation of S

270 Transplant arteriosclerosis was evaluated in cardiac grafts placed

271 Moreover, arteriosclerosis was induced in allografts in immunoglob

272 scular cell injury and consequent transplant arteriosclerosis was investigated.

273 This CD40-CD154 pathway resistant transplant arteriosclerosis was mediated by IL-4, because neutraliz

274 ndardized scoring system, significantly less arteriosclerosis was seen in grafts from LMW-HA + CsA-tr

275 s into CCR7-deficient recipients, transplant arteriosclerosis was significantly elevated.

276 The development of arteriosclerosis was studied by use of intravascular ult

277 better understand the mechanisms of diabetic arteriosclerosis, we generated SM22-Cre;Msx1(fl/fl);Msx2

278 thways protect against or promote transplant arteriosclerosis, we used NOS2-deficient mice as recipie

279 Additional risk factors for arteriosclerosis were being born in the second relative

280 eta-gal+ cells of microvessels in transplant arteriosclerosis were derived from bone marrow progenito

281 Klotho-deficient mice display extensive arteriosclerosis when fed a normal diet, suggesting a po

282 ls of rejected hearts show florid transplant arteriosclerosis whereas those of accommodated hearts do

283 he blood supply can be tested in obstructive arteriosclerosis, which is essential for planning interv

284 eron (IFN)-gamma, is a key effector in graft arteriosclerosis, which, together with the IFN-gamma-ind

285 nd intimal thickening, two manifestations of arteriosclerosis with opposing effects on luminal size,

286 events compared with patients who had severe arteriosclerosis without antibodies and patients with mi

287 lay an important role in the pathogenesis of arteriosclerosis, yet the contribution of different IFN-