ライフサイエンスコーパス: artery wall

1 f myeloperoxidase-dependent oxidation in the artery wall.

2 is by impairing cholesterol removal from the artery wall.

3 anize into trabecular bone tissue within the artery wall.

4 HDL, suggesting that the two interact in the artery wall.

5 reducing nitric oxide bioavailability in the artery wall.

6 allow noninvasive assessment of the coronary artery wall.

7 that MPO promotes HDL oxidation in the human artery wall.

8 ctive nitrogen species in the circulation or artery wall.

9 d on persistent, chronic inflammation in the artery wall.

10 nd lipid-specific chemical information of an artery wall.

11 supporting leukocyte entry into the coronary artery wall.

12 production of HL by donor macrophages in the artery wall.

13 ncreased trafficking of macrophages into the artery wall.

14 n may be another target of HDL action in the artery wall.

15 intermolecular protein cross-linking in the artery wall.

16 s, suggesting that HDL may be trapped by the artery wall.

17 iven leukocyte migration into and within the artery wall.

18 ion, and therefore to plaque rupture, in the artery wall.

19 ting that this oxidant activates MMPs in the artery wall.

20 that MPO oxidatively modifies targets in the artery wall.

21 inhibitor that has been detected within the artery wall.

22 omplete, and precise cell eradication in the artery wall.

23 eoglycans in the extracellular matrix of the artery wall.

24 ons of VLDL surface and core lipids with the artery wall.

25 , 16, 20, or 24 Gy to a depth of 1 mm in the artery wall.

26 ochlorous acid in LDL oxidation in the human artery wall.

27 particularly low-density lipoprotein, in the artery wall.

28 erosclerosis by trapping lipoproteins in the artery wall.

29 and effective gene delivery to the coronary artery wall.

30 the intima and media of the normal coronary artery wall.

31 s that may increase the amount of LDL in the artery wall.

32 st LDL oxidation in a coculture model of the artery wall.

33 al ions as catalysts of LDL oxidation in the artery wall.

34 e mechanism of oxidative damage in the human artery wall.

35 in [LpL]) by increasing LDL retention in the artery wall.

36 ng this entry of adherent monocytes into the artery wall.

37 hway for oxidation of LDL cholesterol in the artery wall.

38 levels and enhanced APN localization in the artery wall.

39 loperoxidase in lipoprotein oxidation in the artery wall.

40 than the interaction of ETS-plasma with the artery wall.

41 st LDL oxidation in a coculture model of the artery wall.

42 ere detected in the endothelial layer of the artery wall.

43 modulating the maladaptive responses in the artery wall.

44 ascular adipose tissue and adventitia to the artery wall.

45 hts into the chemical environment within the artery wall.

46 annot target lesion-determinant cells in the artery wall.

47 ed apoA-I form in atherosclerotic and normal artery wall.

48 thophysiological process within the diseased artery wall.

49 y to monitor a proatherogenic process in the artery wall.

50 edia (I/M) ratio are signs of a less healthy artery wall.

51 ount the nonlinear elastic properties of the artery wall.

52 stribution of apoA1 recovered from the human artery wall.

53 and expression of receptors for RvD1 in the artery wall.

54 on and apoptosis resistance in the pulmonary artery wall.

55 is of the lumen caused by amyloidosis of the artery wall.

56 from a passive buildup of cholesterol in the artery wall.

57 ssion, within the underlying location in the artery wall.

58 rotein expression in the balloon-injured rat artery wall.

59 ersistence of lipid-laden macrophages in the artery wall.

60 erosclerosis by retaining macrophages in the artery wall.

61 ation of leukocyte-derived foam cells in the artery wall.

62 onic inflammatory processes in the pulmonary artery wall.

63 ecules limiting monocyte infiltration of the artery wall.

64 he tumor lesion without also irradiating the artery wall.

65 producers were readily detectable within the artery wall.

66 phage accumulation in adipose tissue and the artery wall.

67 holesterol from macrophage foam cells in the artery wall.

68 esident vascular SMC progenitor cells in the artery wall.

69 ion of cholesterol outflow from cells of the artery wall.

70 tionately increase lipid accumulation in the artery wall.

71 mbospondin) in TGF-beta(1) activation in the artery wall.

72 vely regulates TGF-beta(1) expression in the artery wall.

73 ession of uncoupling protein-1 (UCP1) in the artery wall.

74 by lipoprotein aggregation and deposition in artery walls.

75 kening of both the popliteal and the carotid artery walls.

76 promising new tool for MR imaging of carotid artery walls.

77 solution fast T1-weighted imaging of carotid artery walls.

78 used contrast agent distribution in coronary artery walls.

79 ation of MGd and trypan blue within coronary artery walls.

80 d skin; plus aortic, carotid, and mesenteric artery walls.

81 chronic inflammation and remodelling of the artery wall(2).

82 For myeloablative therapy, artery wall ADs were in general less than those typical

83 rients and oxygen to the outer layers of the artery wall, adventitia, and perivascular adipose tissue

84 HA is also produced in the artery wall after angioplasty, where it may inhibit cons

85 nvestigated structural changes of the radial artery wall after catheterization to understand whether

86 Within the scenario of uncontrolled artery wall aging processes, CKD (chronic kidney disease

87 al to noninvasively image the human coronary artery wall and define the degree and nature of coronary

88 nsity lipoprotein (LDL) cholesterol into the artery wall and its engulfment by macrophages, which lea

89 gh-resolution in vivo images of the coronary artery wall and lesions were obtained with a double-inve

90 chymal stem cells are also present in normal artery wall and microvessels and that they also may ente

91 ogen species such as ONOO- form in the human artery wall and provide direct evidence for a specific r

92 presence of sterol-laden macrophages in the artery wall and reduced plasma HDL levels.

93 flect a balance between local effects in the artery wall and systemic effects on lipid metabolism.

94 cally reduced macrophage accumulation in the artery wall and the subsequent development of atheroscle

95 mvastatin attenuates hypoxia in the coronary artery wall and VV neovascularization in experimental hy

96 nvolved, including specialized properties of artery walls and a negative impact of lipid mediators on

97 osclerosis is an inflammatory disease of the artery walls and involves immune cells such as macrophag

98 oxidation in a co-cultured cell model of the artery wall, and both HDLs and LDLs isolated from PON1-k

99 luded thrombus, calcification, valve tissue, artery wall, and foreign material.

100 O) colocalizes with macrophages in the human artery wall, and its characteristic oxidation products h

101 cluded measurement of the area of the lumen, artery wall, and main plaque components; fibrous cap sta

102 ) Collagen IV (COL4A1/A2) is abundant in the artery wall, and several lines of evidence indicate a pr

103 ocational group, nerves were absent from the artery wall, and starting 0.5-1.0 mm from the lumen exhi

104 the accumulation of free cholesterol in the artery wall, and that this promotes, rather than inhibit

105 asured based on displacements of the carotid artery wall, and Young's modulus was 2-fold greater in s

106 Moreover, both lesion and normal artery wall apoA1 are highly cross-linked (50% to 70% of

107 The change in mean carotid artery wall area was -3.37 mm(2) after 12 months with ca

108 xtracellular space of the grey matter and in artery walls as cerebral amyloid angiopathy and tau prot

109 tributes to restenosis when cells shrink the artery wall at sites of injury.

110 AdCMV.hTIMP-2 (2.5x10(9) pfu) to the carotid artery wall at the time of balloon withdrawal injury inh

111 A-I (apoA-I) is oxidatively modified in the artery wall at tyrosine 166 (Tyr(166)), serving as a pre

112 erosclerosis begins as local inflammation of artery walls at sites of disturbed flow.

113 ion and engraft other tissues, including the artery wall, at sites of injury.

114 senchymal stem cells from the bone marrow or artery wall bring about vascular regeneration and repair

115 approximately 8% of total apoA-I within the artery wall but was nearly undetectable (>100-fold less)

116 High-density lipoprotein (HDL) protects the artery wall by removing cholesterol from lipid-laden mac

117 to maintain physiological homeostasis of the artery wall by supplying nutrients and oxygen to the out

118 LDL enters the artery wall by transcytosis and, in vulnerable regions,

119 protein B-containing lipoproteins within the artery wall causes atherosclerosis.

120 , the formation of fibrofatty lesions in the artery wall, causes much morbidity and mortality worldwi

121 duced monocyte chemotactic activity in human artery wall cell cocultures decreased with time after in

122 The impact of lutein on monocyte response to artery wall cell modification of LDL was assessed in vit

123 itial cells, and the expression of leptin by artery wall cells and atherosclerotic lesions in mice.

124 stimulated lipid hydroperoxide formation in artery wall cells and induced monocyte transmigration, i

125 t the induction of inflammatory responses in artery wall cells through the production of the antioxid

126 tein (HDL), which mobilizes cholesterol from artery wall cells.

127 gainst LDL oxidation in co-cultures of human artery wall cells.

128 ay help determine the prooxidant activity of artery wall cells.

129 nocyte chemotactic activity (MCA) in a human artery wall coculture.

130 was also higher in the injured left carotid artery wall compared with the intact right carotid arter

131 These results suggest that the artery wall contains cells that have the potential for m

132 kely to have a significant role in signaling artery wall damage.

133 cluded ophthalmic artery and central retinal artery wall dissection, fracturing of the internal elast

134 Median carotid artery wall echodensity and carotid-femoral pulse wave v

135 tein E (apoE) secreted by macrophages in the artery wall exerts an important protective effect agains

136 Carotid artery wall FDG uptake was quantified in 134 patients (a

137 ecific drug delivery to the porcine coronary artery wall for at least 28 days.

138 Macrophage production of apoE in the artery wall has been demonstrated to provide protection

139 tion of cholesterol-laden macrophages in the artery wall, has remained elusive.

140 to allow early dismantling synchronized with artery wall healing in comparison with a bare metal sten

141 Time-resolved coronary artery wall images at three to five cine phases were obt

142 ascular magnetic resonance (DE-CMR) coronary artery wall imaging correlated with atherosclerosis dete

143 We performed DE-CMR coronary artery wall imaging in 14 patients with cardiovascular r

144 Carotid artery wall imaging was performed in 10 healthy voluntee

145 ition, alpha tocopherol can partition in the artery wall in critical cells such as smooth muscle cell

146 igated whether the absorbed dose (AD) to the artery wall in radioimmunotherapy of NHL is of potential

147 y MPO levels similar to those present in the artery walls in atherosclerosis can promote apoA-I struc

148 emic plasma, dextran accumulation within the artery wall increased > 4-fold (0.024 +/- 0.01 mV/min [c

149 Rapid efflux of LDL from the artery wall indicated that increased endothelial layer p

150 are introduced, the incidence of acute renal artery wall injury with relation to the denervation meth

151 ity lipoprotein) that has accumulated in the artery wall is a key autoantigen in atherosclerosis, and

152 ecruitment of circulating monocytes into the artery wall is an important feature of early atherogenes

153 sis in mice, here we show that the pulmonary artery wall is constructed radially, from the inside out

154 The artery wall is equipped with a water permeation barrier

155 e presence of ectopic tissue in the diseased artery wall is evidence for the presence of multipotenti

156 Thus, the artery wall is not only a destination but also a source

157 mulated in peripheral tissues, including the artery wall, is transported to the liver for excretion.

158 w density lipoproteins (LDL) by cells in the artery wall leads to a proatherogenic particle that may

159 the presence of leptin receptor in the mouse artery wall, localized to subpopulations of medial and a

160 the hypothesis that overexpression of uPA by artery wall macrophages is atherogenic and suggest that

161 e protein expressed by select populations of artery wall macrophages, initiates one potentially mutag

162 of LDL into arteries and its accumulation by artery wall macrophages, thereby promoting atheroscleros

163 yeloperoxidase (MPO), a major constituent of artery wall macrophages.

164 calcification of vascular cells and that the artery wall may be an important peripheral tissue target

165 and suppresses TGF-beta(1) expression in the artery wall may reveal new approaches for inhibiting int

166 inhibit the endothelial delivery of LDL into artery walls may represent a new therapeutic category in

167 o, noninvasive technique to measure brachial artery wall mechanics under baseline conditions and foll

168 ure and function and therefore their role in artery wall metabolism.

169 Radial artery wall might be damaged after cannulation for cardi

170 Thus, LPL in the artery wall might increase the atherogenicity of oxidize

171 lar context for cell-based therapy to remove artery wall mineral deposits.

172 edded within the collagen-rich matrix of the artery wall mobilize uncharacterized proteolytic systems

173 novirus-mediated transgene expression in the artery wall must be redirected.

174 ned the direct effects of pravastatin on the artery wall of atherosclerotic monkeys after dietary lip

175 rypan blue was locally infused into coronary artery walls of six cadaveric pig hearts with MR monitor

176 elevated uPA activity in the atherosclerotic artery wall, of a magnitude similar to elevations report

177 and its role in cholesterol efflux from the artery wall, offer a means of assessing the efficiency o

178 As more LDL becomes trapped within the artery wall over time, the atherosclerotic plaque burden

179 sed supply of unsaturated fatty acids in the artery wall promotes atherogenesis by impairing the ABCA

180 dicate that macrophage LPL expression in the artery wall promotes atherogenesis during foam cell lesi

181 vo that LPL expression by macrophages in the artery wall promotes foam cell formation and atheroscler

182 Increased expression of PAI-1 in the artery wall promotes neointima growth after balloon inju

183 erglycemia in primates promotes oxidation of artery wall proteins by a species that resembles hydroxy

184 Myeloperoxidase, therefore, may oxidize artery wall proteins in vivo, cross-linking their L-tyro

185 levels promote localized oxidative damage to artery wall proteins.

186 cts of sulfated glycoconjugates, heparin and artery wall proteoglycans, with human inflammatory and p

187 ins with heparin, subendothelial matrix, and artery wall purified proteoglycans was studied.

188 erest in techniques that assess the coronary artery wall, rather than the lumen.

189 the agent(s) that incite inflammation in the artery wall remain largely unknown.

190 tors associated with normal and pathological artery wall remodeling are induced by shear stress in en

191 K) is a large vessel vasculitis resulting in artery wall remodeling with segmental stenosis and/or an

192 e number of LDL particles trapped within the artery wall, slows the progression of atherosclerosis an

193 y material accumulation in the intima of the artery wall, smooth muscle cell proliferation, and Th1 i

194 ima-media-adventitia thickness], and carotid artery wall stress [CAWS]).

195 trasound technique to measure total brachial artery wall stress and incremental elastic modulus (Einc

196 molecular basis for shear-induced changes in artery wall structure is poorly defined.

197 eous inflammation in constitutively stressed artery walls, suggesting that expression of IL-1 is like

198 Hyaluronan (HA) accumulation into artery walls supports vessel thickening and is involved

199 olves the accumulation of plaques within the artery wall that can occlude blood flow to the heart and

200 (166) is an abundant modification within the artery wall that results in selective functional impairm

201 omain restricted to the adventitial layer of artery wall that supports resident Sca1-positive vascula

202 proinflammatory signals generated within the artery wall that suppress homeostatic and anti-inflammat

203 oblast-like calcifying vascular cells in the artery wall that undergo osteoblastic differentiation an

204 a decrease in macrophage recruitment to the artery wall that was associated with reduced chemokine l

205 egulation of IFN-gamma production within the artery wall, the effects of IFN-gamma on vessel wall cel

206 The normal coronary artery wall, the major components of the atherosclerotic

207 s reduced (left anterior descending coronary artery % wall thickening [mean+/-SD], 38+/-11% versus 83

208 treatment, left anterior descending coronary artery % wall thickening increased similarly after icCDC

209 Carotid artery wall thickening is more prevalent in patients wit

210 G ST-T segment abnormality, internal carotid artery wall thickness and decreased LV systolic function

211 Left anterior descending coronary artery wall thickness and external diameter are signific

212 rrelate pericardial fat volume with coronary artery wall thickness and plaque eccentricity.

213 es revealed significant increases in carotid artery wall thickness in burned rats at 6 h versus 3 day

214 on, peripheral arterial disease, and carotid artery wall thickness modestly and statistically signifi

215 t nondiabetic patients with MI had a carotid artery wall thickness similar to diabetic patients witho

216 Left anterior descending coronary artery wall thickness was larger in patients (1.9 +/- 0.

217 ricity (ratio of maximal to minimal coronary artery wall thickness) was determined by using magnetic

218 noid intake was unrelated to average carotid artery wall thickness, suggest that carotenoids may exer

219 laque, mononuclear leukocytes infiltrate the artery wall through vascular endothelial cells (ECs).

220 is-regulatory role of these USF1 variants in artery wall tissues in Caucasians.

221 eading from formation of oxidized LDL in the artery wall to cellular dysfunction and formation of les

222 It is unclear how circulating LDL enters the artery wall to instigate atherosclerosis.

223 poproteins provoke lipid accumulation in the artery wall, triggering early inflammatory responses cen

224 uPA gene transfer increased artery-wall uPA activity for at least 1 week, with a ret

225 factors and cells gain direct access to the artery wall via the vasa vasorum and may initiate, promo

226 ts with CGD had a 22% lower internal carotid artery wall volume compared with control subjects (361.3

227 Total coronary artery wall volume in all three vessels was measured by

228 MR protocol including measurement of carotid artery wall volume, assessment of left ventricular (LV)

229 Carotid artery wall volume, total vessel volume, and the wall:ou

230 kground ratio (TBR) of FDG uptake within the artery wall was assessed while blinded to time points an

231 sion of IE1-72 or IE2-86 protein in coronary artery walls was demonstrated after IE1-72 or IE2-86 gen

232 ure to ETS increases LDL accumulation in the artery wall, we developed a model to measure the rate of

233 est segment (SHS(gluc)) of FDG uptake in the artery wall were calculated.

234 nd contrast-to-noise ratio (CNR) of coronary artery walls were recorded by using different coils betw

235 on of osteoblast-like cells derived from the artery wall, were cocultured with human peripheral blood

236 accumulation of (125)I-MCP-1 in the damaged artery wall, with an average ratio of lesion to normal v

237 accompany Mvarphi foam cell formation in the artery wall, yet the relationship between Mvarphi lipid