ライフサイエンスコーパス: vessel wall

1 microcrystalline form of sirolimus into the vessel wall.

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

3 ng from angiogenesis to calcification of the vessel wall.

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

5 o the vasculature following breaching of the vessel wall.

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

7 oting an inflammatory environment within the vessel wall.

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

9 or biological signalling that operate in the vessel wall.

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

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

12 ration and increased oxidative stress in the vessel wall.

13 cells to activated endothelial cells in the vessel wall.

14 leukocytes and oxidized lipoproteins in the vessel wall.

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

16 by endothelial cells to form the surrounding vessel wall.

17 equired for platelet adhesion to the injured vessel wall.

18 othelial-associated cells that contribute to vessel wall.

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

20 ation and prevents leukocyte adhesion to the vessel wall.

21 ammatory and progenitor cell delivery to the vessel wall.

22 abolic and chronic inflammatory state in the vessel wall.

23 can induce the structural remodeling of the vessel wall.

24 aracterized by leukocyte accumulation in the vessel wall.

25 segments were completely integrated into the vessel wall.

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

27 cally, suggesting long-term residence in the vessel wall.

28 pes that have long-term consequences for the vessel wall.

29 ry lesion in Foxo1(KR/KR) mice occurs in the vessel wall.

30 f the HEV and their chemotaxis away from the vessel wall.

31 enotypic switch in VSMCs) and in the injured vessel wall.

32 of inflammation and destruction of the blood vessel wall.

33 oping largely as sterile inflammation in the vessel wall.

34 mote an immunoregulatory response within the vessel wall.

35 where angioplasty balloon interacts with the vessel wall.

36 cholesterol on inflammasome activity in the vessel wall.

37 e shape, representing a segment of the blood vessel wall.

38 he thrombus proximal, but not distal, to the vessel wall.

39 programming for applications directed to the vessel wall.

40 tribution of stresses and strains across the vessel wall.

41 tion, whereas VSMC proliferation repairs the vessel wall.

42 ppressed innate and adaptive immunity in the vessel wall.

43 geted for collagen exposed on diseased blood vessel wall.

44 differ considerably in retention time in the vessel wall.

45 borne lipids to initially traverse the blood vessel wall.

46 facilitate transport across the endothelial vessel wall.

47 ues can allow direct characterisation of the vessel wall.

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

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

50 mechanical and inflammatory stresses to the vessel wall.

51 ifferentially affect the compartments of the vessel wall.

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

53 es newly implicating biological processes in vessel walls.

54 re independently associated with thicker RCA vessel walls.

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

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

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

58 mooth muscle cells forming the bulk of large vessel walls.

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

60 entially negligible toxic effect on arterial vessel walls.

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

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

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

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

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

66 n glomeruli, tubular basement membranes, and vessel walls, albeit at lower intensity than in C3 glome

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 d to the mechanical environment of the blood vessel wall, and point to cell-cell interactions as crit

93 cephalic artery lesion size, cellularity, or vessel wall apoptosis.

94 t dimensions and positioning relative to the vessel wall are critical factors in modulating stent thr

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

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

97 mphatic vessels, yet regulation of lymphatic vessel wall assembly and lymphatic pumping are poorly un

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

99 [AF660]FPR-ProT bound rapidly to the vessel wall at the site of injury, preceding platelet ac

100 f the redistribution of platelets toward the vessel walls at high shear rates, then thrombin activati

101 Inter-vessel walls averaged 1.02 MPa air-seeding pressure, sim

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

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

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

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

112 nclude that peristaltic motions of the blood vessel walls can facilitate fluid and solute transport i

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

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

115 ladaptive paracrine interactions between the vessel wall compartments.

116 nction was present in both hematopoietic and vessel wall compartments.

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

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

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

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

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

122 se to reduce immune-mediated endothelial and vessel wall damage.

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

124 are key pathogenic regulators, instructed by vessel wall dendritic cells to differentiate into vascul

125 Acute injury of the vessel wall denudes the endothelial lining, removing hom

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

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

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

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

130 ese in vitro findings, histopathology showed vessel wall endothelial cell changes, leukostasis, and v

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

132 injection of gadofosveset, showed increased vessel wall enhancement and relaxation rate (R(1)) with

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

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

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

136 o the physiological phenomenon whereby blood vessel walls exhibit rhythmic oscillations in diameter,

137 The vessel wall experiences progressive stiffening with age

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

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

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

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

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

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

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

145 using whole body gene deletion that affects vessel wall function.

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

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

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

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

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

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

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

153 The TRAPD coronary vessel wall imaging sequence was developed and validated

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

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

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

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

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

159 oncentrations that are likely present in the vessel wall in atherosclerotic lesions, the effects prom

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

161 e cells and endothelial cells comprising the vessel wall in patients.

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

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

164 lls present in the medial layer of the blood vessels wall in the fully differentiated state (dVSMCs).

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

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

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

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

169 urysm (AAA) pathogenesis is distinguished by vessel wall inflammation.

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

171 HHcy causes vessel wall inflammatory MC differentiation and macropha

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

173 e protected from thrombosis after artificial vessel wall injury and lack the proinflammatory mediator

174 ly amplify thrombus size after laser-induced vessel wall injury in live mice.

175 facilitated gene delivery strategies to heal vessel wall injury.

176 hanisms of platelet thrombus formation after 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 Activation of cells intrinsic to the vessel wall is central to the initiation and progression

185 ctively recruited, and their egress from the vessel wall is dampened.

186 The blood vessel wall is largely composed of three cell types: end

187 endogenous retinoid mediators, exert in the vessel wall is less well understood.

188 l segments, we demonstrate that the adjacent vessel wall is the principal source of these endothelial

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

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

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

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

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

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

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

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

197 n of smooth muscle progenitor cell pools for vessel wall maintenance and repair, and aberrant activat

198 pnea, where their prolonged contact with the vessel wall may contribute to its overall deterioration.

199 els of TNF-alpha, IL-6, and MCP-1; increased vessel wall MC accumulation; and increased macrophage ma

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

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

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

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

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

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

206 erosis before macroscopic alterations of the vessel wall occur.

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

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

209 ith coated balloons, paclitaxel stays in the vessel wall of pigs long enough to explain persistent in

210 al arch arteries and for the assembly of the vessel wall of their derivatives.

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

212 agulation cofactor/receptor expressed in the vessel wall, on myeloid cells, and on microparticles (MP

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

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

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

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

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

218 elasticity and quantification of luminal and vessel wall parameters allows for a comprehensive and de

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

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

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

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

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

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

225 the inhibition of neutrophil binding to the vessel wall reduced the presence of TF and diminished th

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

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

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

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

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

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

232 Expansive vessel wall remodeling was more frequent and intense wit

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

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

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

236 struts often integrated completely into the vessel wall, resulting in characteristic morphological p

237 roles played by lipids and integrity of the vessel wall's constituent cells and matrix.

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

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

240 In fact, vessel wall stiffening, and microcirculatory endothelial

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

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

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

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

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

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

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

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

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

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

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

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

253 leagues provide evidence that in the injured vessel wall, the disruption of the NOS pathway is counte

254 After estimating the vessel wall, the vessel cross-section profile is divided

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

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

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

258 right ventricular hypertrophy, and pulmonary vessel wall thickening.

259 The difference in vessel wall thickness between healthy subjects and subje

260 This also resulted in vessel wall thickness measurements that show a more dist

261 er) densities were markedly reduced, whereas vessel wall thickness was increased in hypoxic MKP-1(-/-

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

263 RCA vessel wall thickness was significantly increased in HIV

264 trasound biomicroscopy (UBM) to evaluate the vessel wall thickness.

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

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

267 n tissue injury adhere to each other and the vessel wall to prevent blood loss and to facilitate woun

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

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

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

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

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

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

274 3) vs. 301.4 +/- 110.3 mm(3), p < 0.001) and vessel wall volume (467.7 +/- 166.8 mm(3) vs. 492.9 +/-

275 Automated vessel wall volume index remained unchanged from baselin

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

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

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

279 Without a stent, drug transfer to the vessel wall was somewhat reduced and elimination faster.

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

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

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

283 Platelets adherent to the blood vessel wall were observed in few areas in the heart samp

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

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

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

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

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

289 well known to bind nearly statically to the vessel walls, where they must resist the force exerted b

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

291 m a barrier between blood and the underlying vessel wall, which characteristically demonstrates infla

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

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

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

295 e cells and regulates the interaction of the vessel wall with circulating blood elements.

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

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

300 ung in nine of 10 specimens, and up to blood vessel walls without evidence of vessel (>4 mm) thrombos