ライフサイエンスコーパス: arteriopathy

1 matization of inflammation (e.g., multifocal arteriopathy).

2 ss the presence and severity of small-vessel arteriopathy.

3 to elastin haploinsufficiency, underlie the arteriopathy.

4 with a single wire to investigate transplant arteriopathy.

5 hort and 14% validation cohort have a remote arteriopathy.

6 ot affect cardiac survival or development of arteriopathy.

7 vation and is required to suppress allograft arteriopathy.

8 opment of graft vasculitis, as well as graft arteriopathy.

9 th HIV suggest the presence of an underlying arteriopathy.

10 may be more appropriately termed an elastin arteriopathy.

11 ng the complications of segmental mediolytic arteriopathy.

12 ogation of the development of posttransplant arteriopathy.

13 ammation and the development of obliterative arteriopathy.

14 l injury and the development of obliterative arteriopathy.

15 SEM, n = 9), and by 8-12 wk evolved coronary arteriopathy.

16 model of chronic rejection and obliterative arteriopathy.

17 ontribution of myeloid subpopulations to NF1 arteriopathy.

18 ed pathobiology predisposing to small vessel arteriopathy.

19 SCAD in an individual with family history of arteriopathy.

20 the NF1 tumor suppressor gene are linked to arteriopathy.

21 these populations in the pathogenesis of NF1 arteriopathy.

22 ation class-specific benefit in hypertensive arteriopathy.

23 ata from the Genetic Epidemiology Network of Arteriopathy.

24 ulmonary arteries combined with small-vessel arteriopathy.

25 delay the onset of diabetic retinopathy and arteriopathy.

26 y is associated with markers of hypertensive arteriopathy.

27 significant network associated with cardiac arteriopathy.

28 anastomoses in the development of plexogenic arteriopathy.

29 t they result from an occlusive small-vessel arteriopathy.

30 herapeutic strategy for preventing allograft arteriopathy.

31 ikely involves minor trauma with preexisting arteriopathy.

32 ing results, and 53% of those (n=277) had an arteriopathy.

33 rdiac disease and sepsis reduced the risk of arteriopathy.

34 ardioembolic (21 [30.9%]) and focal cerebral arteriopathy (17 [25.0%]).

35 89; cardioembolic, 6 of 40; steno-occlusive arteriopathies, 24 of 79; p = 0.08).

36 Segmental mediolytic arteriopathy, a rare, noninflammatory arterial disease,

37 t indicate different underlying small vessel arteriopathies according to PVS anatomical distribution,

38 The common nonatherosclerotic, large-vessel arteriopathies affecting the cerebrovasculature include

39 luminal coronary angioplasty and accelerated arteriopathy after cardiac transplantation.

40 ared the relative importance of hypertensive arteriopathy and CAA scores as predictors of [(11)C]PK11

41 Small vessel disease (mainly hypertensive arteriopathy and cerebral amyloid angiopathy (CAA)) is a

42 SVD burden, and SVD subtypes of hypertensive arteriopathy and cerebral amyloid angiopathy (CAA).

43 of SVD burden, and subtypes of hypertensive arteriopathy and cerebral amyloid angiopathy.

44 and dissection, which result from a diffuse arteriopathy and continued hypertension that may be caus

45 ession techniques to determine predictors of arteriopathy and FCA among those subjects who received v

46 per respiratory infection predicted cerebral arteriopathy and FCA in particular, suggesting a possibl

47 gic features by light microscopy (transplant arteriopathy and glomerulopathy); (3) widespread C4d dep

48 opolyamine nanoparticles to repair pulmonary arteriopathy and improve cardiac function in rats with s

49 sociated with discernible allograft coronary arteriopathy and is predictive of outcome in patients af

50 We present a case of focal cerebral arteriopathy and ischemic stroke in a pediatric patient

51 Cerebral arteriopathy and its subtypes were defined using publish

52 , with development of more severe transplant arteriopathy and markedly augmented effector autoantibod

53 ial for inhibiting progression of transplant arteriopathy and prolonging transplant survival.

54 ed primitive ECs promote occlusive pulmonary arteriopathy and severe PH.

55 manifested in this BM group by obliterative arteriopathy and the epicardium and endocardium contains

56 ed with atrial tachyarrhythmia, extracardiac arteriopathy, and a high body mass index.

57 esis, peribiliary fibroinflammation, hepatic arteriopathy, and ciliopathy.

58 ration, a contributor to graft proliferative arteriopathy, and does not increase blood pressure, chol

59 atherosclerosis, restenosis, posttransplant arteriopathy, and pulmonary hypertension.

60 etardation or learning difficulties, elastin arteriopathy, and striking neurocognitive and social-beh

61 postangioplasty restenosis, transplantation arteriopathy, and stroke.

62 terial hypertension (PAH) is a proliferative arteriopathy associated with glucose transporter-1 (Glut

63 Fibromuscular dysplasia (FMD) is an arteriopathy associated with hypertension, stroke and my

64 chronic" transplant rejection, including the arteriopathy (atherosclerosis) commonly present.

65 a concomitant diagnosis of CADASIL (cerebral arteriopathy, autosomal dominant, with subcortical infar

66 In multivariate analysis, arteriopathy, bilateral ischaemia, and decreased conscio

67 ries dissected from cardiac transplants with arteriopathy, but the prevelance and patterns of B cell

68 Animals in group 4 developed arteriopathy by postoperative day (POD) 28.

69 Transplant arteriopathy can be excluded by an MPR of >2.3 with sens

70 hoectasia of intracranial arteries is a rare arteriopathy characterized by elongation and widening of

71 EBV infection also demonstrated large-vessel arteriopathy characterized by thickening of the intimae

72 h a variety of conditions including cerebral arteriopathies, congenital heart disease, infection, hea

73 SRL plus CsA prevented allograft arteriopathy, correlating with suppression of intragraft

74 ticularly in regions typical of hypertensive arteriopathy: deep microbleeds (beta=0.63, F(1,35)=35.24

75 alloantibody responses and progressive graft arteriopathy developed in FcgammaRIIb(-/-) recipients.

76 Based on the underlying arteriopathy distributions, we hypothesised that severe

77 esent in one patient who had severe coronary arteriopathy documented by intravascular ultrasound.

78 chemic stroke (AIS) caused by focal cerebral arteriopathy (FCA) versus cardioembolism (CE).

79 ismatched murine aortic graft model of graft arteriopathy (GA) in wild-type and inducible smooth musc

80 Graft arteriopathy (GA), characterized by diffuse concentric n

81 Graft coronary arteriopathy (GCA) after heart transplantation is a majo

82 I), Maywood, Genetic Epidemiology Network of Arteriopathy (GENOA) and Howard University Family Study

83 ) and in the Genetic Epidemiology Network of Arteriopathy (GENOA) sibships (1381 African-Americans in

84 ans from the Genetic Epidemiology Network of Arteriopathy (GENOA) study to identify a substantially l

85 ans from the Genetic Epidemiology Network of Arteriopathy (GENOA) study.

86 sure Project Genetic Epidemiology Network of Arteriopathy (GENOA) study.

87 part of the Genetic Epidemiology Network of Arteriopathy (GENOA) study.

88 w reserve (FFR) to assess cardiac transplant arteriopathy has not been evaluated.

89 ted immunity in generating chronic allograft arteriopathy have been considered for several years.

90 infection and rejection, as well as coronary arteriopathy, have led to development of new immunosuppr

91 We also place these cerebrocervical arteriopathies in the context of other systemic nonather

92 the BNP/GC-A/cGMP pathway may play a role in arteriopathies in women, while GC-A agonists may provide

93 maRIIB-deficient mice develop severe chronic arteriopathy in a murine cardiac allograft model.

94 A concomitant small-vessel arteriopathy in addition to major pulmonary artery obstr

95 e investigated the distribution of pulmonary arteriopathy in chronic pulmonary hypertension (PH) in a

96 erefore, this review will focus on plexiform arteriopathy in experimental animal models of PAH.

97 cules may contribute to the lack of coronary arteriopathy in hearts allografted into GKO mice.

98 himeric humanized mouse system to model this arteriopathy in human vessels, and found that the morpho

99 oculated with allogeneic human PBMC to study arteriopathy in human vessels.

100 is analysis, we aimed to examine the role of arteriopathy in PHACES syndrome as a potential contribut

101 followed by development of a postobstructive arteriopathy in the resistance arteries of the occluded

102 ponsiveness to these Ags on the formation of arteriopathy in transplanted mouse hearts.

103 Predictors of arteriopathy include early school age (5 to 9 years), re

104 ngiographic findings of segmental mediolytic arteriopathy include the "string of beads" and microaneu

105 Cerebral arteriopathies, including an idiopathic focal cerebral a

106 lating vascular repair and other accelerated arteriopathies, including transplant vasculopathy and ve

107 pproximately 100 mm Hg) and severe pulmonary arteriopathy, including concentric neointimal and comple

108 Arteriopathy-including arterial dissection and other pro

109 However, BMT at 4 months did not reverse arteriopathy, indicating the importance of early interve

110 Two resected specimens showed obliterative arteriopathy indicative of chronic rejection.

111 Graft arteriosclerosis-like arteriopathy induced by PBMCs was reduced by atorvastati

112 ine model of PAH-like plexiform/obliterative arteriopathy induced via a two-hit pathophysiological me

113 ild-type B6 recipients showed severe chronic arteriopathy (intimal thickening, alpha-smooth muscle ac

114 erstanding of the nature and course of these arteriopathies is crucial to the development of secondar

115 ta suggest that the human cardiac transplant arteriopathy is associated with reduction in circulating

116 ELN arteriopathy is genetically heterogeneous and occurs as

117 Transplant-associated coronary arteriopathy is manifested in its early stages by parado

118 Plexiform arteriopathy is not merely an end stage or postthromboti

119 Carotid arteriopathy is present in children with successful rena

120 Arteriopathy is prevalent among children with arterial i

121 We propose that a primary arteriopathy is the initiating event in the genesis of s

122 tion characteristic of transplant-associated arteriopathy, is important in regulating MCP-1 expressio

123 hy (CADASIL), an autosomal dominant cerebral arteriopathy, is variable, but the reasons for this rema

124 e peritubular capillary basement membrane or arteriopathy manifesting as intimal fibrosis.

125 ELN arteriopathy may be present in a nonsyndromic condition

126 dney suggests that a previously unrecognized arteriopathy may contribute to disease pathogenesis in p

127 on and other progressive and non-progressive arteriopathies-might account for up to 80% of childhood

128 liams syndrome (n=23), non-Williams familial arteriopathy (n=12), and Alagille syndrome (n=3).

129 g lymphocytic myocarditis (n=9) and coronary arteriopathy (n=6), with complete vessel occlusion (n=4)

130 ectious organisms, transplant (obliterative) arteriopathy, neoplasia, relative proportions of alpha a

131 undetermined, cardioembolic, steno-occlusive arteriopathies), no statistically significant difference

132 . none, odds ratio 1.75, 7.98), extracardiac arteriopathy (odds ratio 2.63), preoperative intra-aorti

133 raphic studies; and (3) it suggests that the arteriopathy of ADPKD may be more generalized than previ

134 hies, including an idiopathic focal cerebral arteriopathy of childhood (FCA), are common in children

135 hat are indistinguishable from the pulmonary arteriopathy of human pulmonary arterial hypertension.

136 rozygotes, are predominantly due to dilative arteriopathy of the vertebrobasilar circulation, frequen

137 Transplant arteriopathy often lacks clinical symptoms and is the re

138 d type of small-vessel disease (hypertensive arteriopathy or cerebral amyloid angiopathy) in a multic

139 stenosis was more frequent in focal cerebral arteriopathy (P < .01).

140 litis (P=0.0021), and more chronic allograft arteriopathy (P=0.0527).

141 nd is associated with pregnancy and systemic arteriopathies, particularly fibromuscular dysplasia.

142 ans from the Genetic Epidemiology Network of Arteriopathy, phase 2, study population, we examined the

143 tential links between elastin expression and arteriopathy, possible explanations for disease variabil

144 cephelopathy (CADASIL) syndrome, a heritable arteriopathy predisposing to early onset stroke.

145 FMD have demonstrated that FMD is a systemic arteriopathy presenting as arterial stenosis, aneurysm,

146 ings, with a hallmark feature of generalized arteriopathy presenting as stenoses of elastic arteries

147 e used as a noninvasive method for assessing arteriopathy progression and demonstrates that the timin

148 dhood arterial ischaemic stroke and cerebral arteriopathy, provided by current knowledge of Mendelian

149 AntimiR-145 reduced the degree of pulmonary arteriopathy, reduced the severity of pulmonary hyperten

150 or SCD, in halting or reversing SCD-mediated arteriopathy remains unclear.

151 y reactive pupils with asymptomatic cerebral arteriopathy resembling her daughters.

152 This is a stage defined by plexogenic arteriopathy, resulting in obliteration and occlusion of

153 Based upon clinical evidence that CADASIL arteriopathy results in degeneration and loss of vascula

154 There is suspected correlation of cerebral arteriopathy risk with the presence of OPGs.

155 In dominance analysis, hypertensive arteriopathy score outperformed CAA in predicting [(11)C

156 recapitulate the plexiform and obliterative arteriopathy seen in PAH patients and help in defining t

157 oduced the muscularization and proliferative arteriopathy seen in the distal arteriolar vessels of PA

158 Earlier work demonstrated arteriopathy similar to that observed clinically, and id

159 Arteriopathy, sometimes termed accelerated atheroscleros

160 lerosis, and Genetic Epidemiology Network of Arteriopathy studies, we tested a 62 T2D-loci genetic ri

161 set from the Genetic Epidemiology Network of Arteriopathy study, which examined the genetics of hyper

162 with SVD, particularly with the hypertensive arteriopathy subtype of SVD.

163 concentrations and more extensive transplant arteriopathy (TA).

164 vere CN were subdivided into: (1) transplant arteriopathy (TA, n=233, 56%); (2) arteriolar hyalinosis

165 to-pelvis imaging allows detection of remote arteriopathies that may require follow-up, extracoronary

166 aortic stenosis is a systemic elastin (ELN) arteriopathy that disproportionately affects the suprava

167 rterial hypertension (PAH) is a degenerative arteriopathy that leads to right ventricular (RV) failur

168 tations of the Notch-3 receptor result in an arteriopathy that predisposes to early-onset stroke.

169 s from moyamoya disease were more widespread arteriopathy, the combination of arterial ectasia and st

170 0-CD40L blockade will also prevent allograft arteriopathy, the major long-term limitation to transpla

171 9 and Arg258 substitutions and ACTA2-related arteriopathy, this case illustrates the possibility that

172 goal of this study was to detect transplant arteriopathy (Tx-CHD) by a reduced myocardial perfusion

173 ntification of clinically significant remote arteriopathies was similar.

174 mutations causing known genetically mediated arteriopathies was unrevealing.

175 However, arteriopathy was more common among mice that did versus

176 ect biopsy diagnosis of segmental mediolytic arteriopathy was obtained through outside consultation.

177 Foam cell arteriopathy was rarely seen in needle biopsy specimens.

178 The most common arteriopathies were FCA (n=69, 25%), moyamoya (n=61, 22%

179 ents suggest that they may develop a similar arteriopathy which requires special management considera

180 eukoencephalopathy), a cerebral small-vessel arteriopathy, which thus complicates the genotype-phenot

181 e herein a patient with segmental mediolytic arteriopathy who presented with hemoperitoneum.

182 premature stroke and dementia is a heritable arteriopathy with alterations in vascular smooth muscle

183 the SVZ of patients with Cathepsin A-related arteriopathy with strokes and leukoencephalopathy correl

184 suggested to be cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephal

185 cal phenotype in cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephal

186 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephal

187 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephal

188 namely CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

189 ts with CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

190 dysostosis, and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

191 yndrome CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

192 Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephal

193 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

194 , monogenic SVD (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

195 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

196 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

197 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

198 by the study of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

199 stroke, CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

200 ith sporadic SVD/cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

201 NOTCH3 underlie cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

202 ll-characterized cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

203 essel disease or cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

204 in patients with Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephal

205 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

206 sed in detail include CSF1R, AARS2, cerebral arteriopathy with subcortical infarcts and leukoencephal

207 Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephal

208 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

209 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

210 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

211 -vessel disorder cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

212 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

213 activity causes cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephal

214 Arteries in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

215 manifestation of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

216 erative syndrome cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephal

217 cts and CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

218 or result in the cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephel

219 oencephalopathy, cerebral autosomal dominant arteriopathy with subcortical ischaemic leucoencephalopa

220 and these lesions, we measured predictors of arteriopathy within a large international series of chil