ライフサイエンスコーパス: vessel wall

1 s into the PCSK6 role in normal and diseased vessel wall.

2 ant source of the measured anisotropy in the vessel wall.

3 ppressed innate and adaptive immunity in the vessel wall.

4 geted for collagen exposed on diseased blood vessel wall.

5 differ considerably in retention time in the vessel wall.

6 borne lipids to initially traverse the blood vessel wall.

7 facilitate transport across the endothelial vessel wall.

8 ues can allow direct characterisation of the vessel wall.

9 ters as well as through direct impact on the vessel wall.

10 ulation, VWF recruited S. lugdunensis to the vessel wall.

11 mechanical and inflammatory stresses to the vessel wall.

12 ifferentially affect the compartments of the vessel wall.

13 blood cell hematocrit as platelets move to a vessel wall.

14 ng from angiogenesis to calcification of the vessel wall.

15 of the metallic stent frame in the coronary-vessel wall.

16 o the vasculature following breaching of the vessel wall.

17 at there is an excess concentration near the vessel wall.

18 oting an inflammatory environment within the vessel wall.

19 ated astrocyte end-feet from the endothelial vessel wall.

20 or biological signalling that operate in the vessel wall.

21 othelial barrier and transmigrate across the vessel wall.

22 d CRP-induced elevation of superoxide in the vessel wall.

23 lation of apo(a) in the intimal layer of the vessel wall.

24 ration and increased oxidative stress in the vessel wall.

25 cells to activated endothelial cells in the vessel wall.

26 leukocytes and oxidized lipoproteins in the vessel wall.

27 poptosis and increasing efferocytosis in the vessel wall.

28 ocal microscopy of the full thickness of the vessel wall.

29 by endothelial cells to form the surrounding vessel wall.

30 equired for platelet adhesion to the injured vessel wall.

31 othelial-associated cells that contribute to vessel wall.

32 e, at least in part, to calcification of the vessel wall.

33 l narrowing rather than abnormalities in the vessel wall.

34 ation and prevents leukocyte adhesion to the vessel wall.

35 ammatory and progenitor cell delivery to the vessel wall.

36 abolic and chronic inflammatory state in the vessel wall.

37 can induce the structural remodeling of the vessel wall.

38 , reducing the likelihood of adhesion to the vessel wall.

39 ing the adhesion of VWF to platelets and the vessel wall.

40 effects on the endothelial cells lining the vessel wall.

41 umulation and subsequent inflammation in the vessel wall.

42 by binding platelets to plug ruptures in the vessel wall.

43 ed by the accumulation of macrophages in the vessel wall.

44 ssed vasculitis-associated remodeling of the vessel wall.

45 microcrystalline form of sirolimus into the vessel wall.

46 tion, whereas VSMC proliferation repairs the vessel wall.

47 d blood vessels and penetrates deep into the vessel wall.

48 oping largely as sterile inflammation in the vessel wall.

49 tribution of stresses and strains across the vessel wall.

50 h are known to damage the integrity of blood vessel walls.

51 lood cells are known to marginate toward the vessel walls.

52 enesis but are not believed to directly form vessel walls.

53 he sprouting tip cells or tethered along the vessel walls.

54 avoid excessive heating and damaging of the vessel walls.

55 es newly implicating biological processes in vessel walls.

56 re independently associated with thicker RCA vessel walls.

57 development of lipid-laden plaques in blood vessel walls.

58 (IgG) deposited on beta cells and along the vessel walls.

59 ale formulation for the NP adhesion to blood vessel walls.

60 entially negligible toxic effect on arterial vessel walls.

61 wever, OCT imaging revealed that significant vessel wall abnormalities were present in all children i

62 ls, cell debris and modified proteins in the vessel wall, accumulate in response to hypercholesterole

63 high and persistent sirolimus levels in the vessel wall after administration by a coated balloon.

64 s for evaluating the healing response of the vessel wall after injury.

65 Immunohistochemistry revealed increased vessel wall albumin and microvessel density in diseased

66 sition and ongoing biologic processes in the vessel wall, allowing the early diagnosis and risk strat

67 associated with concentric splitting of the vessel wall (an advanced form of cerebral amyloid angiop

68 Endothelial cells line the lumen of the vessel wall and are exposed to flow.

69 echanisms mediating homing of B cells to the vessel wall and B-cell effects on atherosclerosis are po

70 ing shear forces and for its adhesion to the vessel wall and cardiac valves.

71 We show that mtDNA damage in vessel wall and circulating cells is widespread and caus

72 o investigate the motion of platelets near a vessel wall and close to an intravascular thrombus.

73 cells interacted with B. burgdorferi at the vessel wall and disrupted dissemination attempts by thes

74 le the passage of the drug through the tumor vessel wall and enhance its interaction with liver macro

75 latelets are promoted to marginate to near a vessel wall and form blood clots.

76 onary imaging to detect early changes in the vessel wall and high-risk plaques.

77 uggesting that circadian fluctuations in the vessel wall and in the circulation contribute to atherog

78 s a local dilatation of the abdominal aortic vessel wall and is among the most challenging cardiovasc

79 It is the most complex compartment of the vessel wall and is composed of a variety of cells, inclu

80 aused by immune-mediated inflammation of the vessel wall and is diagnosed in some cases by the presen

81 he tunica media accounts for the bulk of the vessel wall and is the chief determinant of mechanical c

82 Given the small size of the vessel wall and its proximity with blood, molecular imag

83 including its ability to be retained in the vessel wall and mediate pro-inflammatory and proapoptoti

84 to remove the majority of histones from the vessel wall and only partly reduces injury.

85 mework for automated 3D segmentation of CCTA vessel wall and quantification of atherosclerotic plaque

86 termed lncRNA-MAP3K4 that is enriched in the vessel wall and regulates vascular inflammation.

87 pturing, adhesion, and crawling on the blood vessel wall and require Galphai signaling in neutrophils

88 d spectroscopy that detects lipid within the vessel wall and that has recently been combined with gra

89 ctor (VWF) mediate bacterial adhesion to the vessel wall and the cardiac valves under flow.

90 Remodeling of the vessel wall and the formation of vascular networks are d

91 he exposed extracellular matrix (ECM) of the vessel wall and the surrounding tissues.

92 brogates mesoangioblast ability to cross the vessel wall and to engraft into damaged myofibres throug

93 les, and higher abilities to attach onto the vessel wall and transmigrate across endothelia.

94 nous tissue, which may represent elements of vessel wall and valvelike structures, was identified.

95 lymphangion segment has mechanically-active vessel walls and is flanked by deformable valves.

96 l for tumor cell extravasation through blood vessel walls and is mediated by a combination of tumor s

97 to estimate air-seeding pressures for inter-vessel walls and pits.

98 bundant stem/progenitor cells present in the vessel wall are largely responsible for SMC accumulation

99 eractions between cancer cells and the blood vessel wall as facilitating this process, in a manner si

100 elastin can directly exhibit changes in the vessel wall associated with disease.

101 cells (4%) were almost never present in the vessel wall at the site of bleeding, but Abeta was frequ

102 tion and the re-entry of mature cells in the vessel wall back into cell cycle.

103 acterization of the relatively thin arterial vessel wall, because it allows imaging with high spatial

104 ole of autophagic flux in maintaining normal vessel wall biology and a growing suspicion that autopha

105 ing provides important information regarding vessel wall biology in the course of aneurysm developmen

106 utic targets to modulate inflammation in the vessel wall, brain, and heart.

107 f active and passive stress distributions of vessel wall, but also enables reliable estimations of ma

108 distinguished from endothelial cells of the vessel wall by production of high amounts of CYTL1.

109 represent a means of traversal of the blood vessel wall by yeast during disseminated candidiasis, an

110 facilitate an association of RAS with blood vessel walls by an as-yet-unknown mechanism, ultimately

111 y to collagen IV) to measure the coverage of vessel walls by astrocyte processes.

112 in SEAs from old vs. young mice; the rise in vessel wall [Ca(2+) ](i) induced by H(2) O(2) was attenu

113 gadolinium enhancement (LGE) of the coronary vessel wall can detect and grade coronary allograft vasc

114 osis by generating mice with blood cells and vessel wall cells lacking PDI (Mx1-Cre Pdifl/fl mice) an

115 ect and quantify morphological and molecular vessel-wall changes in atherosclerosis.

116 erformed to test within-group differences in vessel wall CNReff effective contrast-to-noise ratio .

117 ladaptive paracrine interactions between the vessel wall compartments.

118 ascular adventitia is a complex layer of the vessel wall consisting of vasa vasorum microvessels, ner

119 ascular adventitia is a complex layer of the vessel wall consisting of vasa vasorum microvessels, ner

120 Brain linear tracks such as blood vessel walls constitute their main invasive routes.

121 eas variable stretch maintains-physiological vessel-wall contractility through mitochondrial ATP prod

122 Endothelial cells lining the vessel wall control important aspects of vascular homeos

123 ctionally, the intrinsic vasodilation of the vessel wall decreased at 12 weeks compared with 3 weeks

124 The formation of N-cadherin AJs in the vessel wall depends on the intraluminal pressure and was

125 on in brain blood vessels is associated with vessel wall disruption and abnormal surrounding neuropil

126 through diverting coagulation away from the vessel wall due to eoxPL deficiency, instead activating

127 cclusion, and hyperintense signal within the vessel wall due to intramural haematoma on T1 fat-satura

128 minished accumulation of [Ca(2+) ](i) in the vessel wall during H(2) O(2) exposure.

129 s to the migration of particles toward blood vessel walls during blood flow.

130 ating T cells in the maladaptive behavior of vessel wall endogenous cells.

131 resulted in higher vascular permeability and vessel wall enhancement 7 days after injury in both stra

132 in the spatial distribution of intracranial vessel wall enhancement between CNS vasculitis and risk

133 Intracranial arteries were evaluated for vessel wall enhancement by branching pattern (e.g., prim

134 results suggest the spatial distribution of vessel wall enhancement is an important consideration wh

135 Similarly, vessel wall enhancement was higher in NOS3(-/-) but reco

136 f vascular permeability (R1) and remodeling (vessel wall enhancement, mm(2)) after gadofosveset injec

137 uing massive bleeding was due to superficial vessel wall erosion induced by the ulceration.

138 reased bioavailability of NO in the arterial vessel wall facilitates atherosclerosis.

139 flowing leukocytes from the blood to luminal vessel walls, facilitating the initial stages of their e

140 imal proliferation, transplant vasculopathy, vessel wall fibrosis, progressive luminal occlusion, and

141 h experimental autoimmune encephalomyelitis, vessel-wall fibrosis was detected early in the demyelina

142 source of endothelial cells repopulating the vessel wall following injury.

143 rmeabilized retinal artery and normalize the vessel wall formation by localized inhibition of VEGF.

144 he monolayer of endothelial cells lining the vessel wall forms a semipermeable barrier (in all tissue

145 he direction of flow, thereby protecting the vessel wall from inflammation and permeability.

146 ly from the inner to outer boundaries of the vessel wall (from 11 kPa to zero).

147 n, storage, and release of key regulators of vessel wall function.

148 s or paclitaxel from durable polymers to the vessel wall, have been consistently shown to reduce the

149 atherogenesis in key target tissues (liver, vessel wall, hematopoietic cells) can assist in the desi

150 ation, thereby modulating the maintenance of vessel wall homeostasis.

151 plays a critical role in the maintenance of vessel wall homeostasis.

152 ll cells, which are critical for maintaining vessel wall homeostasis.

153 New advanced MR intracranial vessel wall imaging (IVW) techniques can allow direct ch

154 inally, the clinical feasibility of arterial vessel wall imaging at unenhanced and contrast material-

155 ly, recent advances in preclinical molecular vessel wall imaging will be reviewed.

156 oronary magnetic resonance angiogram and LGE vessel wall imaging with 1.5 T (n=12) and 3.0 T (n=12).

157 expression and macrophage recruitment to the vessel wall in a carotid ligation model in ApoE-/- mice.

158 ctional and morphological alterations of the vessel wall in a murine atherosclerosis model.

159 f contact of at least 1 stent strut with the vessel wall in a segment not overlying a side branch; it

160 mtDNA damage occurred early in the vessel wall in apolipoprotein E-null (ApoE(-/-)) mice, b

161 age occurs in both circulating cells and the vessel wall in human atherosclerosis.

162 llations in leukocytes and components of the vessel wall in this process.

163 based imaging techniques to characterize the vessel wall in vivo.

164 (HSPCs) emerge and develop adjacent to blood vessel walls in the yolk sac, aorta-gonad-mesonephros re

165 end to preferentially accumulate next to the vessel walls, in a size-dependent manner (~70% for 1,000

166 s stretch is statically condensed to enforce vessel wall incompressibility via a plane stress conditi

167 In giant cell arteritis, vessel-wall infiltrating CD4 T cells and macrophages for

168 MMP-targeted imaging reflects vessel wall inflammation and can predict future aortic e

169 We have examined whether persistent vessel wall inflammation is maintained by lesional T cel

170 However, the chronic vessel wall inflammation related to permanent polymer pe

171 a activation in cDCs is necessary to control vessel wall inflammation.

172 ) may contribute to the inconsistency of FDG vessel wall inflammation.

173 HHcy causes vessel wall inflammatory MC differentiation and macropha

174 or an equal volume of saline before venular vessel wall injuries was made by directed laser irradiat

175 hanisms of platelet thrombus formation after vessel wall injury.

176 facilitated gene delivery strategies to heal vessel wall injury.

177 abdominal aortic aneurysm (AAA) resulting in vessel wall instability thereby predisposing the vessel

178 al cells (ECs), with each EC residing in the vessel wall integrating local signals to determine wheth

179 endothelial growth factors (angiogenesis and vessel wall integrity), FOXC2 (vascular development), he

180 uired arms of the immune system and platelet-vessel wall interactions that drive inflammatory disease

181 elial stiffness, permeability, and leukocyte-vessel wall interactions.

182 rane potential is depolarized by ~20 mV, and vessel wall intracellular [Ca(2+)] is elevated relative

183 s. vein) or the presence of histology-proven vessel wall invasion.

184 s blockade of leukocyte interaction with the vessel wall is being studied to reduce the inflammation

185 Activation of cells intrinsic to the vessel wall is central to the initiation and progression

186 on-dependent intracerebral remodeling of the vessel wall is directly associated with the prominence o

187 Leukocyte transmigration across vessel walls is a critical step in the innate immune res

188 Abnormal HA accumulation within blood vessel walls is associated with tissue inflammation and

189 rmation of calcium phosphate crystals in the vessel wall, is mediated by vascular smooth muscle cells

190 for a blood-borne NP to firmly adhere to the vessel walls, is a fundamental parameter in this analysi

191 of competent platelets causes changes in the vessel wall itself, accounting for the time required for

192 Following shear-resistant adhesion to the vessel wall, L-selectin has frequently been reported to

193 igher number and enhancement of intracranial vessel wall lesions at 7-T MRI in individuals evaluated

194 oneal application improves the uptake within vessel wall lesions compared with intravenous injection.

195 .02) were associated with a higher number of vessel wall lesions in the anterior circulation.

196 Contrast material-enhancing vessel wall lesions were associated only with increasing

197 ar risk factors and number or enhancement of vessel wall lesions.

198 was found between smoking and the number of vessel wall lesions.

199 sed for number, location, and enhancement of vessel wall lesions.

200 The TFA data obtained in umbilical blood vessel wall lipids were related to the neurologic condit

201 ensitive dual inversion recovery black-blood vessel wall magnetic resonance imaging (TRAPD) was used

202 udy who underwent 3-dimensional intracranial vessel wall magnetic resonance imaging from October 18,

203 ized wall index) and number were assessed by vessel wall magnetic resonance imaging.

204 The adventitia, the outer layer of the blood vessel wall, may be the most complex layer of the wall a

205 ion coefficient, 0.69-0.99) for quantitative vessel wall measurements.

206 of ~10 mum, enabling visualization of blood vessel wall microstructure in vivo at an unprecedented l

207 Vessel wall motion is passively affected by fluid pressu

208 Fifty-five vessel wall MR imaging (VWI) exams were included in this

209 Conclusion Vessel wall MR imaging is a reliable tool for identifyin

210 tiated and characterized by using unenhanced vessel wall MR imaging.

211 urden of intracranial arteries assessed with vessel wall MRI at 7 T in participants with ischemic str

212 dentify a new type of stem cell in the blood vessel wall, named multipotent vascular stem cells.

213 (SMCs), a major structural component of the vessel wall, not only play a key role in maintaining vas

214 erosis before macroscopic alterations of the vessel wall occur.

215 s dramatically reduced within the plaque and vessel wall of Il1r1(-)/(-)Apoe(-)/(-) mice, and Mmp3(-)

216 Tracer accumulation in the vessel wall of major arteries was analyzed qualitatively

217 fragmentation, and effacement of HA from the vessel wall of small pulmonary arteries.

218 (125)I-pentixafor uptake in the vessel wall on autoradiographies was located in macropha

219 ck the initiation of LDL accumulation in the vessel wall or augment hepatic LDLR-dependent clearance

220 en bleeding and thrombosis within either the vessel wall or circulation was revealed that can either

221 des a source of FA for adjacent cells in the vessel wall or tissues.

222 ty across natural barriers of tumors such as vessel walls or cellular membranes, allowing for enhance

223 Initial fibrin deposition at the vessel wall over 6 hours in this model was dependent on

224 ghly lipophilic sirolimus analogue, into the vessel wall over a period of 1 month.

225 ndent manner, with changes in all three true vessel wall permeability coefficients (hydraulic conduct

226 activation, plaque microvascularization, and vessel wall permeability in subjects with carotid plaque

227 ontribution of the endothelial glycocalyx to vessel wall permeability.

228 defect in platelet activation in vitro, and vessel wall platelet deposition and initial hemostasis i

229 Following binding to the injured vessel wall, PMNs are activated and release elastase.

230 deposition in the brain parenchyma and blood vessel walls, potentially resulting in cerebral amyloid

231 ed transmural necrosis and thickening of the vessel wall progressing to the point of luminal obstruct

232 A 27% reduction in the vessel wall pulsatility of intracortical arterioles and

233 The plaque-to-healthy vessel wall ratio of (68)Ga-FOL was significantly higher

234 l muscle differentiation and cross the blood vessel wall regardless of the developmental stage at whi

235 structures and facilitates stiffening of the vessel wall, regulating blood flow return to the heart.

236 remodeling and calculate the plaque area and vessel wall relaxation rate (R1 = 1/T1).

237 Rupture-prone plaques had higher vessel wall relaxation rate (R1; 2.30+/-0.5 versus 1.86+

238 lular sources for these autacoids within the vessel wall remain unclear.

239 The ECM-based hydrogel promotes arterial vessel wall remodeling and a fibroinflammatory response

240 ized that RGS5 may play an important role in vessel wall remodeling and blood pressure regulation.

241 Expansive vessel wall remodeling was more frequent and intense wit

242 ntrast agent that measures plaque burden and vessel wall remodeling.

243 endothelial cell (EC) targets that modulate vessel wall remodelling and arterial-venous specificatio

244 l knockout mice die in utero with defects in vessel wall remodelling in association with losses in mu

245 including Hb extravasation across the blood vessel wall, scavenging of endothelial nitric oxide (NO)

246 Reductions in vessel wall shear stress and, consequently, nitric oxide

247 ct borders, vascular and optic disc leakage, vessel wall staining, or capillary nonperfusion.

248 In fact, vessel wall stiffening, and microcirculatory endothelial

249 Here, we review the cross talk among vessel wall stiffening, endothelial contractility, and v

250 bited the attachment of fluid-phase VWF onto vessel wall strands.

251 ystem allows homogenous drug delivery to the vessel wall, such that the drug release per unit surface

252 We hypothesized that damaged vessel walls, such as those involved in atherosclerosis,

253 ymphoid cells that had invaded the lymphatic vessel wall, suggesting these cells may be mediators of

254 ion of cholesterol in macrophages within the vessel wall, supporting the role of Nef in pathogenesis

255 t achieves high drug concentration along the vessel wall surface, intended to correspond to the ballo

256 de body (WPB) P-selectin and VWF onto EC and vessel wall surfaces and activated EC nuclear factor kap

257 f intervessel pit membranes and deposited on vessel wall surfaces.

258 o differences in the change from baseline in vessel wall target-to-background ratio (TBR) from the as

259 Following vascular damage, vessel wall TF initiates the extrinsic coagulation casca

260 ar stiffness is a mechanical property of the vessel wall that affects blood pressure, permeability, a

261 daptation of fibroblasts in the hypertensive vessel wall that drives proliferative and proinflammator

262 g-eluting stents, which permanently cage the vessel wall, thereby preventing normal coronary vasomoti

263 femoral artery, Col8(-/-) mice had decreased vessel wall thickening and outward remodeling when compa

264 mina comparable to the control group suggest vessel wall thickening occurring in the early stage of d

265 We evaluated coronary vessel wall thickening, coronary plaque, and epicardial

266 right ventricular hypertrophy, and pulmonary vessel wall thickening.

267 Significantly increased vessel wall thickness was not found in ApoE(-/-) mice un

268 RCA vessel wall thickness was significantly increased in HIV

269 e IgE by extending cell processes across the vessel wall to capture luminal IgE.

270 posit that uremia modulates TF in the local vessel wall to induce postinterventional thrombosis in p

271 ent to be effective, it must cross the blood vessel wall to reach cancer cells in adequate quantities

272 ic nanoparticles to deliver rapamycin to the vessel wall to reduce inflammation in an in vivo model o

273 d to influence the tone and structure of the vessel wall; to initiate and perpetuate chronic vascular

274 sed to vascular diseases because of weakened vessel walls under stress conditions.

275 the pathophysiologic changes of the arterial vessel wall underlying the development of atherosclerosi

276 Persistence of sirolimus in the vessel wall until 1 month was 40% to 50% of the transfer

277 As the dominant cellular constituent of the vessel wall, vascular smooth muscle cells (VSMCs) and th

278 s preceded by cell rolling and arrest on the vessel wall via the formation of specific receptor-ligan

279 Automated vessel wall volume index remained unchanged from baselin

280 ues, severity of narrowing, composition, and vessel wall volume were measured.

281 Acute drug transfer to the vessel wall was 14.4+/-4.6% with the crystalline coating

282 On MRI, mean diameter of enhancement of vessel wall was 6.57+/-4.91 mm, and mean enhancement ind

283 n Alzheimer's disease and Abeta in the blood vessel walls was characteristic of cerebral amyloid angi

284 in the red-blood-cell depleted zone near the vessel walls was strongly influenced by nearby red blood

285 S/MS) and expression of RvD receptors in the vessel wall were assessed.

286 Acute injuries of the vessel wall were ubiquitous, but contrary to repeated pu

287 Before refilling, vessel walls were covered with a surface film, but vesse

288 entrated and stayed as clusters near a blood vessel wall when tumors were exposed to a magnetic field

289 es the drifting of the particles towards the vessel walls where they become trapped in the cell-free

290 e, individual platelets are mobilized to the vessel wall, where they interact with leukocytes and app

291 ive stress as well as eNOS uncoupling in the vessel wall, which can be prevented by ablation of LysM(

292 ent and activation of NK cells in the target vessel wall, which may participate in the necrotizing va

293 aging showed no thickening of the arteriolar vessel wall whilst OCT angiography showed extreme corksc

294 loss of the normal layered structure of the vessel wall, white thrombus, calcification, and neovascu

295 imaging of the aortic, carotid, and coronary vessel wall will be discussed.

296 nvasive detection of CXCR4 expression in the vessel wall with PET and emerges as a potential alternat

297 ombi formed after severe laser injury of the vessel wall with thrombin generation.

298 he outer to the inner surface of the damaged vessel wall, with a greater extent of platelet activatio

299 Re-endothelialization of the vessel wall, with functionally and structurally intact c

300 Kindlin-3-deficient T effectors arrested on vessel walls within inflamed skin-draining lymph nodes w