ライフサイエンスコーパス: microvessel

1 T-shaped bifurcation on the scale of a large microvessel.

2 smooth muscle cells to stabilize functional microvessels.

3 vo and lower gelatinase activity in cerebral microvessels.

4 VWF fibers and platelet aggregation in tumor microvessels.

5 tained positively for insulin, glucagon, and microvessels.

6 CD34(+) stem and early progenitor cells with microvessels.

7 s and prevent their accumulation in cerebral microvessels.

8 to the emission of NO by the endothelium of microvessels.

9 aracterized by progressive loss of pulmonary microvessels.

10 proinflammatory, procoagulant state in brain microvessels.

11 nds required for leukocyte rolling in dermal microvessels.

12 bosis, macrophages, smooth muscle cells, and microvessels.

13 cell culture with explicit, endothelialized microvessels.

14 d increase in the permeability of mouse lung microvessels.

15 tes that obstruct/occlude up to 88% of tumor microvessels.

16 ith wild-type (WT) inflamed cremaster muscle microvessels.

17 limiting the delivery effect at or near the microvessels.

18 HepG2 cells were entwined with a network of microvessels.

19 , because they actually display a paucity of microvessels.

20 pression and 20-HETE levels in preglomerular microvessels.

21 ibrin deposition and platelet aggregation in microvessels.

22 GF signalling increases pericyte coverage in microvessels.

23 , affected plasticity, and promoted death of microvessels.

24 oth as effector and target cells in inflamed microvessels.

25 with controls, and lesions had fewer CD31(+) microvessels.

26 eric microvessels and fenestrated glomerular microvessels.

27 GF) on activity, plasticity, and survival of microvessels.

28 Ps also compromised vasodilation in perfused microvessels.

29 g SUV(mean) had significantly fewer perfused microvessels.

30 ns, accompanied by massive losses of retinal microvessels.

31 a velocity of 36 mum/min, 3x faster than in microvessels.

32 also contribute to FIV in human subcutaneous microvessels.

33 intermediary step in MV reversion to normal microvessels.

34 perivascular cells to stabilize newly formed microvessels.

35 articles to reversibly occlude blood flow in microvessels.

36 with a VEGF trap reverted MV back to normal microvessels.

37 vasodilatation in human subcutaneous adipose microvessels.

38 (LSECs) constitute discontinuous, permeable microvessels.

39 lially to the spatially remote thrombin-free microvessels.

40 rowth of new blood vessels from pre-existing microvessels.

41 ls had impaired rolling on TNF-alpha-treated microvessels.

42 n nutrient delivery through living, perfused microvessels.

43 s embedded in the basement membrane of blood microvessels.

44 ow of deformable red blood cells in stenosed microvessels.

45 platelet aggregate formation within cerebral microvessels.

46 microhemorrhage related to branched dilated microvessels.

47 ocytes with disrupted end-feet juxtaposed to microvessels.

48 flow changes in SMC but not pericyte-covered microvessels.

49 jority of participants with branched dilated microvessels (11 of 13) (McNemar Test for equal distribu

50 Based on detection of flow in low-flow microvessels, a new sharp contrast image was derived.

51 L-PAM analysis also pinpointed microvessels ablated or resistant to VEGFR2 immuno-block

52 The shedding was also blocked in microvessels after knockdown of a complex III component

53 P, and subsequent reversion of GMP to normal microvessels, all without extensive vascular killing.

54 contrast to old mdx mice, displaying marked microvessel alterations, and the functional repercussion

55 the loss of occludin from ischemic cerebral microvessels and a massive BBB leakage at 4.5-hour post-

56 he development of pericyte coverage of tumor microvessels and aPL-induced tumor cell expression of ch

57 uated a decrease in occludin levels in brain microvessels and BBB permeability of METH-injected mice.

58 Testicular microvessels and blood flow are known to contribute to t

59 s a critical factor in persistent leaky lung microvessels and edema formation in the disease.

60 increased c-kit(+) CSC-derived myocytes and microvessels and enhanced functional recovery in myocard

61 sm of self-regulation of thrombosis in blood microvessels and explains experimentally observed distin

62 r and albumin, in both continuous mesenteric microvessels and fenestrated glomerular microvessels.

63 formed by the endothelial cells of cerebral microvessels and forms the critical interface regulating

64 larger size, increasing proliferation, more microvessels and less apoptosis.

65 eceptor expression in isolated preglomerular microvessels and microvascular smooth muscle cells.

66 gulation of SUR1, the target of SU drugs, in microvessels and neurons.

67 mic the in vivo spatial relationship between microvessels and nonendothelial cells embedded in extrac

68 s of tumor cell interactions with functional microvessels and provide evidence for a mitosis-mediated

69 Astrocyte feet surround cerebral microvessels and release molecules that can trigger vasc

70 tein receptor-related protein (LRP) in brain microvessels and the Abeta-degrading protease neprilysin

71 environment and induces injury to both tumor microvessels and tumor cells using intrinsic SSRBC-deriv

72 islet grafts stained positively for insulin, microvessels, and a collagen scaffold.

73 r density, loss of the radial orientation of microvessels, and altered expression of VEGF receptors.

74 ly assessed by visualizing clot formation in microvessels, and correlations can be made to thromboela

75 genesis and quantification of the developing microvessels, and it can be used to identify new modulat

76 e-dimensional co-culture self-assembled into microvessels, and platelet-derived growth factor had che

77 gers photodynamic damage of tumour cells and microvessels, and simultaneously initiates release of XL

78 from pericytes, mural cells associated with microvessels, and that these cells are present in adults

79 ree; pericytes supporting the endothelium of microvessels; and smooth muscle cells forming the bulk o

80 Myocardial microvessels appear as strandlike structures on high-spa

81 Cerebral microvessels are formed by endothelial cells (ECs), whic

82 However, normal microvessels are hierarchical and vasoreactive with sing

83 Retinal and cerebral microvessels are structurally and functionally homologou

84 a transporters, which include UT-B in kidney microvessels, are potential targets for development of d

85 t least half of the TH cells were apposed to microvessels at these ages, and many of these cells cont

86 Loss of KRIT1 leads to decreased microvessel barrier function and to the development of t

87 Spinal microvessels became enlarged during the hypoxic period,

88 in vivo two-photon imaging was used to track microvessels before and after photothrombotic stroke in

89 In an in vitro model of 3D microvessels, both tumor-derived and matched normal Line

90 Analysis of microvessel branching patterns revealed that stroke led

91 pecimens contained C5b-9 reactive endomysial microvessels but none of these or other vessels reacted

92 s, but unlike cerebral microvessels, retinal microvessels can be noninvasively measured in vivo by re

93 or histocompatibility complex class II), and microvessels (CD31) in plaque and control regions.

94 of endothelial cells, a rarefaction of brain microvessels, cerebral hypoperfusion, a disrupted blood-

95 Microvessel Chaste can be used to build simulations of v

96 process, because EndMT mainly occurs in the microvessels close to these cells, and because megakaryo

97 pericyte alpha-SMA phenotype mediates acute microvessel constriction after SAH possibly by hemoglobi

98 e found between K(trans) and the endothelial microvessel content determined on histologic slices (Pea

99 of endothelial progenitor cells (EPCs) into microvessels contributes to the vascularization of endom

100 ession of matrix adhesion receptors in brain microvessels decreases in ischemic stroke; this contribu

101 espite the presence of heterogeneously leaky microvessels, dense extracellular matrix and high inters

102 ckage to anticancer effects, VEGF levels and microvessel densities (MVD) were quantified.

103 Microvessel density (MVD) and microvessel size (MVS) ran

104 usion CT parameters were correlated with the microvessel density (MVD) count at both corresponding si

105 CT and immunohistochemical markers Ki67 and microvessel density (MVD) in patients with non-small cel

106 the viable zones of tumors and compared with microvessel density (MVD), cellularity, and micronecrosi

107 onse was associated with significantly lower microvessel density (P < 0.01) and lower uptake of the p

108 vasive measures reflected a 30% reduction in microvessel density and increased vessel maturation in e

109 s had increased FGF18 expression levels with microvessel density and M2 macrophage infiltration, conf

110 roRNA-126 (miR-126) downregulation decreases microvessel density and promotes the transition from a c

111 in neoplastic mast cells resulted in reduced microvessel density and reduced tumor growth in vivo com

112 tly, miR-126 upregulation in the RV improves microvessel density and RV function in experimental PAH.

113 They had higher bone marrow microvessel density and vascular endothelial growth fact

114 Immunohistochemistry confirmed the lower microvessel density and VEGFR2-positive area fraction in

115 chemotherapy consistently showed an enhanced microvessel density compared with the corresponding samp

116 gh-cholesterol mice had significantly higher microvessel density compared with tumors from the other

117 from Ptp4a3-null mice revealed reduced tumor microvessel density compared with wild type controls.

118 Increased microvessel density contributes to abnormal BM and splee

119 Tumor cell density and microvessel density correlated significantly and positiv

120 In contrast, angiogenesis, as assessed by microvessel density count, was similar between tumors wi

121 tumor partial pressure of oxygen (pO(2)) and microvessel density during treatments with a multi-tyros

122 on, TFF3 expression correlated strongly with microvessel density evaluated with CD31 and CD34.

123 Intratumoral proliferation, apoptosis and microvessel density findings correlated with tumor growt

124 y revealed increased vessel wall albumin and microvessel density in diseased aortas and especially in

125 th Gal-3 neutralizing antibody decreased the microvessel density in ischemic brain.

126 ntriguingly, glipizide significantly reduces microvessel density in PC tumor tissues, while not inhib

127 We also assessed microvessel density in the Bristol (UK) samples, by meas

128 ted with CD11b(+)Gr1(+) cell recruitment and microvessel density in the tumor tissue, with evidence f

129 rowth factor, and was accompanied by reduced microvessel density in vivo.

130 acellular IL1R2 levels with tumor growth and microvessel density in xenograft mouse models.

131 ural integrity of the endothelium and higher microvessel density increase vascular permeability.

132 ed from these tumors had significantly lower microvessel density than tissue from the other groups as

133 expression were significantly decreased; and microvessel density was increased without changes in ult

134 Microvessel density was inhibited by sorafenib treatment

135 At 72h after microsphere infusion, microvessel density was significantly reduced in tumors

136 uates in vivo expression of SPARC, increases microvessel density, and enhances drug delivery to the t

137 ascularization activity (microvessel radius, microvessel density, and microvessel type indicator [MTI

138 hological abnormalities (fibrosis, increased microvessel density, and osteosclerosis).

139 activated fibroblasts, collagen deposition, microvessel density, and vascular function.

140 sed tumor mitotic index, and decreased tumor microvessel density, compared with bolus therapy.

141 Furthermore, the induction of VEGF protein, microvessel density, decrease of infarct volumes and neu

142 es correlated with advanced stage, increased microvessel density, metastasis, and poor overall surviv

143 thologic correlation with tumor stage, CD105 microvessel density, vascular endothelial growth factor

144 a-inducible factor expression, and decreased microvessel density.

145 ew more slowly in xenografts, with decreased microvessel density.

146 e while concurrently demonstrating decreased microvessel density.

147 ed higher levels of phospho-Akt, -p44/42 and microvessel density.

148 stratify breast cancer patients with a high microvessel density.

149 MMP-9 release, tumor-infiltrating PMNs, and microvessel density.

150 mast cell numbers positively correlated with microvessel density.

151 ffect that was associated with a decrease in microvessel density.

152 treatments, accompanied by a 45% decrease in microvessel density.

153 genic form and was associated with increased microvessel density.

154 on in tumor growth, proliferating cells, and microvessel density.

155 normal flow of red blood cells in pulmonary microvessels depends in part on the release of antiadhes

156 (NOD-SCID) mice resulted in the formation of microvessels derived from human fibroblasts perfused wit

157 for the lumenization of new capillaries and microvessels developing in ischemic muscles to allow suf

158 ase in capillary tortuosity, and widening of microvessel diameter.

159 evated collagen fiber density, and increased microvessel diameter.

160 And hemoglobins significantly reduced the microvessel diameters at pericyte sites, due to the effe

161 Increased F-actin was evident in microvessels directly treated with thrombin and in those

162 ctive oxygen species (ROS) in cultured brain microvessel endothelial cells and central neurons.

163 esses can quickly lead to dysfunction of the microvessel endothelial cells, including disruption of b

164 alterations in the permeability of pulmonary microvessel endothelial monolayers (PMEM) that result fr

165 It was better tolerated by brain microvessel endothelial/neuronal cells, and accumulated

166 of pericytes, supporting cells that surround microvessel endothelium.

167 gh the use of a detailed simulation model of microvessel flow in two principal configurations: a diam

168 m cells contribute to both encapsulation and microvessel formation.

169 epresent important support cells surrounding microvessels found in solid organs.

170 Conversely, treatment of microvessels from CAD patients with the telomerase activ

171 However, tumor microvessels from EC JAM-C-deficient mice exhibited redu

172 and laser-capture microdissected endoneurial microvessels from four cryopreserved normal adult human

173 UDM patients were decreased as compared with microvessels from the ND or CDM patients (P<0.05).

174 sociations between ambient air pollution and microvessel function measured by peripheral arterial ton

175 lore the distribution of the intramyocardial microvessels (group 2, n = 4; three-dimensional fast ima

176 We conclude that MRTF-A promotes microvessel growth (via CCN1) and maturation (via CCN2),

177 H(2)S-induced wound healing and microvessel growth in matrigel plugs is suppressed by ph

178 ndocapillary layer on the luminal surface of microvessels has a major role in the exclusion of macrom

179 Increased permeability of brain microvessels has the most profound effects as it may lea

180 Radiation-induced microvessel hyalinosis mimicked tumor microvascularity a

181 nctional permeability properties of the same microvessel in vivo.

182 as observed in rectal mucosal and submucosal microvessels in a preclinical model of radiation proctit

183 diated agonist, thrombin, was instilled into microvessels in a restricted region of isolated blood-pe

184 ormed correlated UM of fluorescently labeled microvessels in cleared brains.

185 Cs after OGD as well as in isolated cerebral microvessels in mice after MCAO.

186 d alterations of ZO-1 was confirmed in brain microvessels in mice with CREB shRNA lentiviral particle

187 changes occurring in central nervous system microvessels in patients harbouring mitochondrial DNA de

188 rns revealed that stroke led to a pruning of microvessels in peri-infarct cortex, with very few insta

189 thelial enzymatic changes in skeletal muscle microvessels in response to ET and SIT.

190 e islet endocrine cells, juxtaposed to islet microvessels in T1D.

191 ractional system of neurons, astrocytes, and microvessels in the brain.

192 ilatation, by comparing the phenotype of new microvessels in the mesentery during induction of vascul

193 recursor cells that accumulate with cerebral microvessels in the perilesional tissue further stimulat

194 SI within groups revealed significantly more microvessels in the subepicardium with MR (group 1: P =

195 cent restricted regions increased F-actin in microvessels in the thrombin-treated and adjacent region

196 ascular microhemorrhage and branched dilated microvessels in the tissues lining the clinically health

197 ap could be detected in the branched dilated microvessels in tissues lining the GC.

198 s and endothelium under flow in vitro and to microvessels in vivo and we characterized their migrator

199 ty to roll at tenfold higher shear stress in microvessels in vivo.

200 played an enhanced ability of recruiting new microvessels in vivo.

201 retinal endothelial injury, primarily in the microvessels, including vascular tortuosity, obliterated

202 er when they extravasate across the walls of microvessels into inflamed tissues or when they enter in

203 Thrombin colocalization with microvessels is closely associated with remarkably eleva

204 l cells, the membrane potential along intact microvessels is remarkably uniform.

205 he thrombogenic transcriptome changes in the microvessels is rudimentary.

206 tional assessment of gated individual dermal microvessels is therefore of outstanding interest.

207 Here we explore the transcriptome of retinal microvessels isolated from mouse models of retinal disea

208 achment of astrocytic end-feet from cerebral microvessels, leakage of plasma proteins, reduction in e

209 y to cancer cells by decreasing intratumoral microvessel leakiness.

210 a-knockdown ECs are deficient in assembly of microvessel-like structures.

211 sociated vasculitis (AAV) are the restricted microvessel localization and the mechanism of inflammato

212 The microvessel localization of the disease is due to the AN

213 Hence, metabolically perturbed microvessels may contribute to central nervous system (C

214 Hence HTPCs via control of testicular microvessels may contribute to the regulation of spermat

215 ized that expression of E-selectin on marrow microvessels mediates osteotropism of hematopoietic stem

216 east cancer cells within a tissue-engineered microvessel model of the tumor microenvironment.

217 extensively, it remains an open question why microvessels need to be so narrow.

218 f the vessel wall consisting of vasa vasorum microvessels, nerves, fibroblasts, immune cells, and res

219 f the vessel wall consisting of vasa vasorum microvessels, nerves, fibroblasts, immune cells, and res

220 oma and is thought to result from mechanical microvessel obstruction and an excessive activation of i

221 synthase (eNOS) were determined in cerebral microvessels of BH(4)-deficient hph-1 mice.

222 Here, we employ engineered microvessels of complex geometry to examine the patholog

223 nitrotyrosine levels were higher in cerebral microvessels of diabetic animals.

224 vels of CYP4A12 and 20-HETE in preglomerular microvessels of doxycycline-treated transgenic mice appr

225 These results were confirmed in microvessels of HIV transgenic mice chronically administ

226 EndoMT was detected in microvessels of inflammatory bowel disease (IBD) mucosa

227 o induce the spatially extensive response in microvessels of mice lacking endothelial connexin43, sug

228 amma and GLUT-1 by the bacteria in the brain microvessels of newborn mice causes extensive pathophysi

229 Brain microvessels of S1pr1(iECKO) mice showed altered subcell

230 Microvessels of Syrian Golden hamsters fitted with a dor

231 d glucose transporter expression in cerebral microvessels of the BBB, but it also decreased 2-deoxy-g

232 The microvessels of the brain are very sensitive to mechanic

233 elevated in the tumor vasculature and dermal microvessels of VEGF-injected skin in R-Ras knockout mic

234 opositivity is detected only in the ischemic microvessels of wild-type mice and in the cerebrovascula

235 , while reducing endothelial NOX2 content in microvessels of young obese men.

236 nd nitrate (NO(2)+NO(3)) content in cerebral microvessels (P<0.05, n=6).

237 MR severity correlated with percentage of microvessels parasitized in the retina, brain, and nonre

238 erial movement between the vascular space of microvessels penetrating functioning organs and the cell

239 sulted in a 2-fold increase in the number of microvessels per square millimeter compared to lipid aft

240 in the immunohistochemical index termed the microvessel pericyte index (MPI), a measure of permeabil

241 chemic stroke; this contributes to increased microvessel permeability and detachment of astrocytes fr

242 ion in mice vasculature increased basal lung microvessel permeability and exaggerated permeability in

243 cellular fluid due to leakage of the brain's microvessel permeability barrier, and swelling of astroc

244 helial function in KRIT1-deficient cells and microvessel permeability in Krit1(+/-) mice; however, VE

245 rther, ANP and BNP elicit increases in blood microvessel permeability sufficient to cause protein and

246 glycocalyx regulate glycocalyx structure and microvessel permeability to both water and albumin.

247 mediator of angiogenesis and its associated microvessel permeability.

248 othelial glycocalyx structure and associated microvessel permeability.

249 -dependent vasoconstriction in preglomerular microvessels, predominantly afferent arterioles.

250 n producing thin-walled hyperdilated fragile microvessels prone to bleeding.

251 on in the number of functional intracortical microvessels (radii of 20-80 mum) has been observed in 2

252 omarker maps of neovascularization activity (microvessel radius, microvessel density, and microvessel

253 SCA was associated with microvessel rarefaction, decrease in capillary tortuosit

254 morphogenesis, arteriovenous remodeling, and microvessel regression.

255 Microvessel relaxation response to adenosine 5'-diphosph

256 the major player in regulating acute dermal microvessel remodeling.

257 Pericytes represent a unique subtype of microvessel-residing perivascular cells with diverse ang

258 functionally homologous, but unlike cerebral microvessels, retinal microvessels can be noninvasively

259 othelial cells, as well as occluded rat pial microvessels, showed that luminal but not abluminal LPC

260 Microvessel density (MVD) and microvessel size (MVS) ranked with a semiquantitative th

261 CI, Rowlands et al. demonstrate that in lung microvessels, soluble TNF-alpha (sTNF-alpha) promotes th

262 horylation of ERK and AKT/eNOS, and promoted microvessel sprouting from an angiogenesis animal model.

263 Similarly, SAD suppressed VEGF-induced microvessel sprouting from rat aortic ring and blood ves

264 AVH and dilatation of dermal microvessels stimulated by vascular endothelial growth f

265 gmentation algorithm was utilized to extract microvessel structure from image data, and the distance

266 feration and the number, length, and area of microvessel structures in a concentration-dependent mann

267 mCRP co-localised with CD105 in microvessels suggesting angiogenesis.

268 evated GFAP immunoreactivity associated with microvessels suggests that the astrogliosis may be occur

269 cantly higher burden of immature intraplaque microvessels than carriers of the ancestral allele, irre

270 rolling interactions with TNF-alpha-treated microvessels than Th1 cells in wild-type mice but not in

271 tic cancer cells and a functional artificial microvessel that was lined with endothelial cells.

272 The grafts contain human microvessels that are perfused by the host coronary circ

273 tion of iron uptake and storage within brain microvessels that challenge the existing paradigm that t

274 very of FGF9 to renal tumors in mice yielded microvessels that were covered by pericytes, smooth musc

275 In the current study, we demonstrated that microvessel thrombin deposition is significantly increas

276 dies in endothelial cells derived from brain microvessels to determine the dose-response and time-cou

277 an engineered organotypic model of perfused microvessels to show that activation of the transmembran

278 pillary cell death was markedly decreased in microvessels treated with the polyamine synthesis inhibi

279 microvessel radius, microvessel density, and microvessel type indicator [MTI]) and oxygen metabolism

280 ing angiogenesis assays, in which developing microvessels undergo many key features of angiogenesis o

281 flow kinetics was performed on single gated microvessels using a free hand tool.

282 Cs, are the major target of IL-17 within the microvessel wall and that IL-17-activated PCs can modula

283 to WG22, the radial organization of cortical microvessels was clearly altered in pFAS/FAS patients fr

284 esolution, 39 mum) represent intramyocardial microvessels was tested.

285 thelial phenotype ex vivo using subcutaneous microvessels, we demonstrated that loss of EPCR and TM a

286 nB protein expression patterns along retinal microvessels were also assessed.

287 The diameters selected microvessels were determined by measuring the full width

288 Sharp images of low-flowing microvessels were enabled by introducing inverse varianc

289 g/day) for 14 days, and thereafter, cerebral microvessels were isolated and studied.

290 Microvessels were isolated from the motor cortex of 11 r

291 Single perfused rat mesenteric microvessels were perfused with fluorescent endothelial

292 ation of an extensive network of flowing neo-microvessels, which after 14 days structurally resembled

293 targets is the pericytes, the mural cells of microvessels, which regulate microvascular permeability,

294 AVMs arose from enlargement of preexisting microvessels with capillary diameter and blood flow and

295 lar remodeling effect, leading to normalized microvessels with infrequent vascular branches and incre

296 pore architectures and dedicated perfusable microvessels with rapidly degrading porous interfaces in

297 rier (BNB), formed by tight junction-forming microvessels within peripheral nerve endoneurium, exists

298 trast among biological tissues and can treat microvessels without causing collateral damage to the su

299 tentially allowing for long-term dilation of microvessels without substantial changes in cytosolic Ca

300 ion suggest that cocaine constricts coronary microvessels, yet direct evidence is lacking.