ライフサイエンスコーパス: artery wall

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

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

3 reducing nitric oxide bioavailability in the artery wall.

4 allow noninvasive assessment of the coronary artery wall.

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

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

7 ctive nitrogen species in the circulation or artery wall.

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

9 supporting leukocyte entry into the coronary artery wall.

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

11 ncreased trafficking of macrophages into the artery wall.

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

13 intermolecular protein cross-linking in the artery wall.

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

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

16 levels and enhanced APN localization in the artery wall.

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

18 that MPO oxidatively modifies targets in the artery wall.

19 inhibitor that has been detected within the artery wall.

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

21 eoglycans in the extracellular matrix of the artery wall.

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

23 , 16, 20, or 24 Gy to a depth of 1 mm in the artery wall.

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

25 erosclerosis by trapping lipoproteins in the artery wall.

26 and effective gene delivery to the coronary artery wall.

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

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

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

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

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

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

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

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

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

36 loperoxidase in lipoprotein oxidation in the artery wall.

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

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

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

40 thophysiological process within the diseased artery wall.

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

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

43 ount the nonlinear elastic properties of the artery wall.

44 stribution of apoA1 recovered from the human artery wall.

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

46 on and apoptosis resistance in the pulmonary artery wall.

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

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

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

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

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

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

53 erosclerosis by retaining macrophages in the artery wall.

54 onic inflammatory processes in the pulmonary artery wall.

55 ecules limiting monocyte infiltration of the artery wall.

56 he tumor lesion without also irradiating the artery wall.

57 iven leukocyte migration into and within the artery wall.

58 producers were readily detectable within the artery wall.

59 phage accumulation in adipose tissue and the artery wall.

60 holesterol from macrophage foam cells in the artery wall.

61 esident vascular SMC progenitor cells in the artery wall.

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

63 tionately increase lipid accumulation in the artery wall.

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

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

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

67 is by impairing cholesterol removal from the artery wall.

68 anize into trabecular bone tissue within the artery wall.

69 by lipoprotein aggregation and deposition in artery walls.

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

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

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

73 used contrast agent distribution in coronary artery walls.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 Carotid artery wall imaging was performed in 10 healthy voluntee

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

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

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

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

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

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

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

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

136 The artery wall is equipped with a water permeation barrier

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

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

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

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

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

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

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

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

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

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

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

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

149 Radial artery wall might be damaged after cannulation for cardi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 levels promote localized oxidative damage to artery wall proteins.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 Carotid artery wall thickening is more prevalent in patients wit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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