ライフサイエンスコーパス: arteriopathy

1 delay the onset of diabetic retinopathy and arteriopathy.

2 with a single wire to investigate transplant arteriopathy.

3 ot affect cardiac survival or development of arteriopathy.

4 vation and is required to suppress allograft arteriopathy.

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

6 th HIV suggest the presence of an underlying arteriopathy.

7 may be more appropriately termed an elastin arteriopathy.

8 ng the complications of segmental mediolytic arteriopathy.

9 ogation of the development of posttransplant arteriopathy.

10 ammation and the development of obliterative arteriopathy.

11 l injury and the development of obliterative arteriopathy.

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

13 model of chronic rejection and obliterative arteriopathy.

14 y is associated with markers of hypertensive arteriopathy.

15 significant network associated with cardiac arteriopathy.

16 ata from the Genetic Epidemiology Network of Arteriopathy.

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

18 herapeutic strategy for preventing allograft arteriopathy.

19 ikely involves minor trauma with preexisting arteriopathy.

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

21 ulmonary arteries combined with small-vessel arteriopathy.

22 rdiac disease and sepsis reduced the risk of arteriopathy.

23 to elastin haploinsufficiency, underlie the arteriopathy.

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

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

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

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

28 luminal coronary angioplasty and accelerated arteriopathy after cardiac transplantation.

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

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

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

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

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

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

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

36 Cerebral arteriopathy and its subtypes were defined using publish

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

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

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

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

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

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

43 postangioplasty restenosis, transplantation arteriopathy, and stroke.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 Cerebral arteriopathies, including an idiopathic focal cerebral a

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

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

81 Arteriopathy-including arterial dissection and other pro

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

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

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

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

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

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

88 ELN arteriopathy is genetically heterogeneous and occurs as

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

90 Plexiform arteriopathy is not merely an end stage or postthromboti

91 Carotid arteriopathy is present in children with successful rena

92 Arteriopathy is prevalent among children with arterial i

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

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

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

96 ELN arteriopathy may be present in a nonsyndromic condition

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

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

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

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

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

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

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

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

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

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

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

108 Transplant arteriopathy often lacks clinical symptoms and is the re

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

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

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

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

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

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

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

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

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

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

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

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

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

122 Arteriopathy, sometimes termed accelerated atheroscleros

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

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

125 concentrations and more extensive transplant arteriopathy (TA).

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

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

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

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

130 0-CD40L blockade will also prevent allograft arteriopathy, the major long-term limitation to transpla

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

132 mutations causing known genetically mediated arteriopathies was unrevealing.

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

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

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

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

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

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

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

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

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

142 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephal

143 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephal

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

145 Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephal

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

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

148 Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephal

149 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

150 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

151 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

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

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

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

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

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

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

158 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephal

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

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

161 oencephalopathy, cerebral autosomal dominant arteriopathy with subcortical ischaemic leucoencephalopa

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