ライフサイエンスコーパス: vessel

1 micrographs of the same portion of the same vessel.

2 ocal recurrences occurred at the site of the vessel.

3 providing the energy required to reopen the vessel.

4 y over an order of magnitude within the same vessel.

5 sly repopulated the lining of decellularized vessels.

6 ity of cases with acceptable sizes of access vessels.

7 + cells supported the assembly of perfusable vessels.

8 beaking" and "criss-cross" of the mesenteric vessels.

9 ns of microbubbles are confined to the blood vessels.

10 ic resonance angiography of the cerebropetal vessels.

11 t was (largely) the consequence of collapsed vessels.

12 for instance, by recruiting blood and lymph vessels.

13 passing through abnormally leaky tumor blood vessels.

14 distant sites, tumor cells migrate to blood vessels.

15 s lymphangiogenesis and obstructed lymphatic vessels.

16 of transplanted converted cells into injured vessels.

17 to electronics and astronauts onboard space vessels.

18 combination fermentation, aging, and serving vessels.

19 action, fibrosis, and formation of new blood vessels.

20 matory, and antiatherogenic actions in blood vessels.

21 -cadherin at the cell surface in these blood vessels.

22 blood conductance through sites of narrowed vessels.

23 ctivity, to produce relaxation of some blood vessels.

24 ular signature from blood and true lymphatic vessels.

25 ol to differentiate between normal and tumor vessels.

26 h matrix molecules, fibroblasts, nerves, and vessels.

27 as enlarged jugular lymph sacs and lymphatic vessels.

28 electively upregulated in regenerating blood vessels.

29 ransport across bioengineered human cerebral vessels.

30 eatment on development of peripheral retinal vessels (1 article), refractive outcomes (1 article), or

31 lmonary artery side branches <300 mum per cm vessel (3.8 +/- 1.1 vs. 1.8 +/- 1.1; p = 0.010) and not

32 Structural and functional alterations of vessels accumulate throughout life, culminating in incre

33 bility of catheter-only, closed-chest, large-vessel anastomosis (superior vena cava and pulmonary art

34 MicroCT imaging of the models defined vessel anatomy to our analyses threshold of 100 microm d

35 F) as a result of residual shunts, anomalous vessel anatomy, progressive valvulopathy, hypertension,

36 cellulose biosynthesis, regulators of xylem vessel and fiber differentiation and lignification.

37 infarcts can be manifestations of both small vessel and large vessel disease, that cerebral microinfa

38 e-related reduction of type CD31(hi)Emcn(hi) vessels and bone loss.

39 WF), which binds exposed collagen at damaged vessels and captures platelets.

40 ion of sub-nanometre AuNCs from normal blood vessels and enhances their passive targeting to cancerou

41 tment with tPA led to decompression of blood vessels and improved tumor perfusion.

42 suggest that downstream mesenteric lymphatic vessels and lymph drainage into mesenteric lymph nodes m

43 which leads to vasodilatation of the uterine vessels and might improve fetal growth in utero.

44 The brain lacks lymph vessels and must rely on other mechanisms for clearance

45 electroactive sites in the interior tubular vessels and outer surfaces for ultrasensitive detection

46 Tie2 signaling-dependent specialized hybrid vessels and provide genetic evidence of the critical rol

47 are in tight contact with neurons and blood vessels and shape excitatory synaptic transmission due t

48 sulted in an increase in the number of blood vessels and sub-epithelial connective tissue matrix comp

49 e recently characterized meningeal lymphatic vessels and their role in drainage of the brain ISF, CSF

50 cancer, their role in tumor-associated blood vessels and tumor immunity, and provide an update on mTO

51 ructure of tissues, including muscles, blood vessels, and connective tissues, adapts to mechanical st

52 ere less abundant, concentrated around blood vessels, and round in shape.

53 otype 1 (rAAV1) transduces ECs of pathologic vessels, and that editing of genomic VEGFR2 locus using

54 ped erythrocytes disrupt blood flow in small vessels, and this vaso-occlusion leads to distal tissue

55 come in ischaemic stroke patients with large vessel anterior circulation occlusion undergoing endovas

56 Our results show that major trunk lymphatic vessels are conserved in the zebrafish, and provide a th

57 anistic details of how mural cells stabilize vessels are not fully understood.

58 .06 [0.01]; 95% CI, 0.04-0.09; P < .001) and vessel area density (0.04% [0.02%]; 95% CI, 0.02%-0.08%;

59 lt1 (from 881 +/- 98% increase in functional vessel area to 279 +/- 72%) and by inhibition of angiopo

60 diameter was 2.9+/-0.6 mm and mean reference vessel area was 6.8+/-2.6 mm(2).

61 rix, there was an increase in the mean lumen vessel area with a decrease in the ratio of neointima ar

62 roved owing to decompression of intratumoral vessels as a result of increased killing of cancer cells

63 n and resultant vascular image compared with vessels as seen in histologic section.

64 and complete description of trunk lymphatic vessel assembly.

65 to drive strong EGFP expression in lymphatic vessels at all stages of development and in adult zebraf

66 Vessel-based analysis revealed statistically significant

67 erficial and deep retinal vasculatures using vessel-based and FAZ-based metrics.

68 the ultrastructure of collagen fibers in the vessel basement membrane, and the kinetics of regression

69 Thus, in diabetes, retinal vessels become dependent on a small increase in TGF-beta

70 onse to growth factor activation to form new vessel branches.

71 accumulated in a higher number in angiogenic vessels, but extravasated less toward the implanted cyto

72 associated with stromal cells or near blood vessels, but was absent in the amnion.

73 maintaining the resting tone of the cerebral vessels by releasing ATP and COX-1 derivatives.

74 (VWF) mediates platelet adhesion to injured vessels by sequestering platelets from blood flow and de

75 ermit robust discrimination between coronary vessels causing ischemia versus not causing ischemia.

76 mass index (BMI)] and greater odds of large-vessel cerebral vascular disease or history of cardiovas

77 rdiovascular disease but lower odds of small-vessel cerebral vascular disease.

78 Pathological proliferation of retinal blood vessels commonly causes vision impairment in proliferati

79 For example, widespread vessel constriction (vessel tone) is induced by brainste

80 ous coronary intervention, or previous multi-vessel coronary artery bypass graft surgery.

81 rdial infarction in the past 20 years, multi-vessel coronary artery disease, history of stable or uns

82 The abundance of type CD31(hi)Emcn(hi) vessels decrease during ageing.

83 he AUC and sensitivity at 95% specificity of vessel densities within the ONH (0.76 and 42%) and macul

84 occur earlier than the reduction in retinal vessel densities.

85 f superficial and deep foveal and parafoveal vessel density (FVD, PFVD) and choricapillary density us

86 Ex vivo investigation revealed a higher mean vessel density and poorly differentiated extracellular m

87 ficient mice exhibit a transient increase in vessel density at ages P10-P12 due to delayed vessel pru

88 Lymphatic vessel density did not impact the time to development of

89 Lymphatic vessel density in CLAD patients did not differ from thos

90 Macular vessel density of the deep capillary plexus in the 6 x 6

91 iderably different between groups: mean (SD) vessel density of the deep retinal capillary plexus was

92 OCTA showed vessel density reduction in BRVO and CRVO with main invo

93 A novel algorithm was used to adjust the vessel density to compensate for local variations in OCT

94 Flow index and vessel density were calculated from the en face angiogra

95 also contributed to decreased growth, blood vessel density, and VEGF and hypoxia-inducible factor 1a

96 iris and tumor vasculature, and quantitative vessel density.

97 s then utilized in a series of patients with vessel-depleted neck anatomy.

98 an 10 DA remains the key risk factor for new vessel development compared to areas of nonperfusion con

99 gulates macrophage dynamics during lymphatic vessel development.

100 signaling pathway dedicated to regulating GM vessel development.

101 suggesting a role for thrombin signaling in vessel development.

102 The overall per-vessel diagnostic accuracy of FFR-CT was 81.9% (95% CI,

103 f stent oversizing to angiographic reference vessel diameter (RVD) was calculated as (nominal stent d

104 induced 51% (p = 0.001) and 37% (p = 0.018) vessel diameter reductions respectively.

105 Mean reference vessel diameter was 2.9+/-0.6 mm and mean reference vess

106 Mutant tissues show no difference in blood vessel diameter, density/growth, and branching from embr

107 angles in several scenarios using different vessel diameters, orientations, diffusion rates, and sus

108 mines serotonin and noradrenaline, and local vessel dilation is induced by glutamatergic neuron activ

109 abnormalities associated with impaired blood vessel dilation.

110 65%/94% for retinal whitening, 62%/100% for vessel discoloration, and 73%/96% for hemorrhages.

111 tive impairment, but also for cerebral small vessel disease (CSVD) and Abeta-positivity.

112 neurological syndrome characterized by small vessel disease (SVD), stroke, and vascular cognitive imp

113 in and may reflect underlying cerebral small vessel disease (SVD).

114 The resulting cerebral small vessel disease and heart failure may contribute to early

115 emyelinating disorders such as chronic small vessel disease and other inflammatory, granulomatous, in

116 Large and small cerebral vessel disease can trigger stroke and contribute to the

117 genesis of cardiovascular and cerebral large-vessel disease compared with that of small-vessel diseas

118 , dyslipidemia, smoking, infarcts from small-vessel disease, and "other definite" causes and worse on

119 anifestations of both small vessel and large vessel disease, that cerebral microinfarcts are independ

120 e-vessel disease compared with that of small-vessel disease.

121 are a neuroimaging marker of cerebral small vessel disease.

122 es may reflect the underlying cerebral small vessel disease.

123 ivation of Wnt/beta-catenin signaling in CNS vessels during EAE/MS partially restores functional BBB

124 Hdac3 in mice led to blood-filled lymphatic vessels, edema, defective lymphovenous valve morphogenes

125 fiber and pith refilling was associated with vessel emptying, indicating a link between tissue connec

126 on promotes strong activation of brain blood vessel endothelial cells.

127 Normalization of tumor blood vessels enhances the infiltration and functions of T cel

128 ng GCV at 14 d postinjury, scar elements and vessels entered the lesions over the next 7 d, as did la

129 d tight junctions are functional as early as vessel entry into the CNS.

130 The primary end point was target-vessel failure (a composite of cardiac death, target-ves

131 Target vessel failure (TVF), a composite of cardiac death, targ

132 significant difference in the rate of target-vessel failure between the patients who received a biore

133 In commercial fisheries, communities and vessels fishing a greater diversity of species have less

134 ts was associated with increased risk of new vessel formation (HR 2.7, 95% CI 1.3-5.5, P = .003).

135 d, identifying the genes essential for blood vessel formation and elucidating their function are cruc

136 to study the mechanisms underlying lymphatic vessel formation, remodeling and function in a human cel

137 nib-treated patients and increased lymphatic vessels found in 70% of neoadjuvant treated patients.

138 Mesenteric lymphatic vessels from MetSyn or LPS-injected rats exhibited impai

139 oit angiogenesis, the formation of new blood vessels from pre-existing vasculature, in order to obtai

140 In ex vivo rings, aortic and mesenteric vessels from SHR treated with DHI exhibited significantl

141 Vessel function was further improved owing to decompress

142 In the lymphatic vasculature, collecting vessels generate rapid contractions coordinated along ly

143 in vivo, and reveal the crucial role of the vessel geometry in the margination by calculations when

144 l Chaste can be used to build simulations of vessel growth and adaptation in response to mechanical a

145 ndothelial cells, granulocytes promote blood vessel growth and hematopoietic regeneration.

146 Excess blood vessel growth contributes to the pathology of metastatic

147 ified, but the mechanisms controlling venous vessel growth have been obscure.

148 involved in elevated FSS-induced collateral vessel growth in rat hind limbs.

149 ng season (BS), angiogenic VEGF-A stimulates vessel growth in the infundibulum, aiding vascular commu

150 We conclude that enhanced collateral vessel growth is controlled by miRNAs, among which miR-3

151 e VEGF165-induced edema without compromising vessel growth.

152 he specific growth of arteries and lymphatic vessels have been identified, but the mechanisms control

153 To assess the vessel-healing pattern of Ultimaster drug-eluting stent

154 ield and purity: conventional reflux, sealed vessel heated in an oil bath, and microwave assisted rea

155 hree-dimensional analyses of human placental vessels; (ii) demonstrate the utility of the technique i

156 ots in nonvascular areas and more continuous vessel images than those of images without averaging.

157 intravascular ultrasound was performed in 57 vessels in 20 asymptomatic individuals (90% on statins)

158 Eight hundred thirty-eight vessels in 639 patients were analyzed.

159 etaining in-situ flow signal from real blood vessels in deeper layers.

160 Although histological analysis of lymphatic vessels in donor grafts can yield information on the str

161 er and by the aberrant nature of tumor blood vessels in general.

162 report the existence of meningeal lymphatic vessels in human and nonhuman primates (common marmoset

163 elta T cells promoted the formation of blood vessels in the dermis underlying the HPV-induced lesions

164 logical and biochemical features of coronary vessels in vivo.

165 increased the permeability of retinal blood vessels in wild type but not in TRPV4 knockout mice.

166 ependent associates of perforation in native vessels included age, chronic occlusive disease interven

167 a convenient visualization of all lymphatic vessels, including those in the central nervous system,

168 revealed the presence of paraportal shunting vessels, increased numbers of portal vascular structures

169 therapy dedicated to destroying tumor blood vessels induced the development of lymphatic vessels, wh

170 h poor prognosis and increased risk of blood vessel infiltration.

171 ral artery injury with or without additional vessel injuries (risk ratio, 0.90; 95% CI, 0.21-3.83).

172 hancing platelet accumulation at the site of vessel injury.

173 to improve the imaging quality of deep-lying vessels inside the abdominal cavity.

174 n mice, improving hemodynamic parameters and vessel integrity.

175 Here, we have analysed neutrophil-lymphatic vessel interactions in real time and in vivo using intra

176 toreceptors in a model of pathological blood vessels invading photoreceptors: the very low-density li

177 nterstitial fluid and solutes into lymphatic vessels is important for maintaining interstitial homeos

178 rstitial space combined with advection along vessels is likely to substitute for the lymphatic draina

179 moderate=early positive treadmill or single-vessel ischemia, and severe=large ischemic region abnorm

180 ence proteases often circulate in host blood vessels leading to life-threatening diseases.

181 B) formation in mice, we found that immature vessel leakage occurs entirely through transcytosis, as

182 to evaluate the impact of number of diseased vessel, lesion location, and severity of the noninfarct-

183 hypertension collapsing blood and lymphatic vessels, limiting drug delivery.

184 lformation (CM-AVM) is a blood and lymphatic vessel (LV) disorder that is caused by inherited inactiv

185 th cancer cells and tumor-infiltrating blood vessels, making it a potentially ideal dual-compartment

186 The sealed vessel method is a new approach for fast cleavage of PCB

187 on with concentrations obtained using closed vessel microwave digestion was also realized.

188 T for ex-vivo examination of human placental vessel morphology.

189 gers endothelial communication to mesenteric vessel muscle cells, leading to vasoconstriction.

190 ided by intravascular ultrasound on the main vessel (MV) stent expansion and SB fractional flow reser

191 target lesion failure (cardiac death, target vessel myocardial infarction [TVMI], or ischemia-driven

192 ailure (a composite of cardiac death, target-vessel myocardial infarction, or target-vessel revascula

193 of mFlt1, suggesting new ways to manipulate vessel network formation.

194 Vessel networks expand when sprouts form new connections

195 In vivo, expanding vessel networks favor interactions with Flt1 mutant mous

196 the technique in the comparison of placental vessel networks in normal and fetal growth restriction (

197 erarchy that induces vascular sprouting, APC vessel niche affinity and APC vessel occupancy.

198 This influence of vessel noise on communication space exceeded natural var

199 these impacts, we investigated the effect of vessel noise on the communication space of the Bryde's w

200 led that gene expression features related to vessel normalization correlate with immunostimulatory pa

201 Although disruption of vessel normalization reduced T lymphocyte infiltration a

202 activation of CD4(+) T lymphocytes decreased vessel normalization, indicating a mutually regulatory l

203 ytes by immune checkpoint blockade increased vessel normalization.

204 vascular density and branching suggestive of vessel normalization.

205 immunohistochemistry showed that high-CE and vessel number were neither associated with an elevated t

206 In this study, we coated decellularized vessels obtained from porcine carotid arteries with poly

207 For small vessel occlusion (17.8%), outcomes tended to vary by whi

208 e for patients with suspected emergent large-vessel occlusion (ELVO), efficient systems of care must

209 acilitate more rapid identification of large-vessel occlusion and direct routing to endovascular-capa

210 Although the dynamics of vessel occlusion have been studied extensively, it remai

211 patients with acute stroke suffering a large-vessel occlusion, although treatment efficacy is highly

212 sprouting, APC vessel niche affinity and APC vessel occupancy.

213 erior pole), only 1 (7.7%) eye developed new vessels, odds ratio (OR) 0.12 [95% confidence interval (

214 Previous optical studies of microbubbles in vessels of approximately 20 microns have shown that expa

215 and showed lymphadenopathy around the major vessels of the abdomen.

216 e fibroids were embolized, leaving the large vessels of the fibroids patent.

217 Diabetes mellitus destabilized microvascular vessels of the heart, affecting the amplitude of therape

218 3CR1(high), Ly-6C(low)) patrolling along the vessels of the microcirculation is critical for endothel

219 s line to describe the assembly of the major vessels of the trunk lymphatic vascular network, includi

220 Ocean going vessels (OGVs) operating within emission control areas (

221 sible in the right lobe while avoiding large vessels, on imager-generated parametric maps to measure

222 oronary intervention (MV-PCI) versus culprit vessel-only PCI (CO-PCI) in patients with multivessel di

223 s of DES-PCI versus CABG for patients with 3-vessel or left main CAD.

224 and Cardiac Surgery) trial, patients with 3-vessel or left main coronary artery disease (CAD) had im

225 njection (P = 0.003), conjunctival corkscrew vessels (P < 0.001), corneal scarring (P = 0.01) and pin

226 Animals underwent vessel painting perfusion to label the entire cortex at

227 Doppler ultrasound showed normal testicular vessels passing through the mass which were undisturbed,

228 d points were fractional flow reserve during vessel patency, the quantitative intracoronary ECG ST-se

229 that coordination of HSC specification with vessel patterning might involve modulatory regulatory fa

230 of stable or unstable angina, previous multi-vessel percutaneous coronary intervention, or previous m

231 ensity and facilitated the recovery of blood vessel perfusion function in a murine hindlimb ischemia

232 Cerebral vessels play a major role in AD, as Abeta is cleared fro

233 dense autonomic innervation of the choroidal vessels predisposes them particularly to vasospasms.

234 Vessel preparation with directional atherectomy (DA) pot

235 shows that polymer coating of decellularized vessels provides a new strategy to improve re-endothelia

236 essel density at ages P10-P12 due to delayed vessel pruning.

237 Imaging outcomes included rates of vessel recanalization and infarct growth at 24 hours and

238 new therapeutic approaches to improve blood vessel regeneration and increase survival and hematopoie

239 regression of the entire network, with some vessels regressing >10 mm within 16 h.

240 yes (62.0%), out of which 29 (38.1%) had new vessel relapse and required additional laser treatment.

241 (TVF), a composite of cardiac death, target vessel-related myocardial infarction, or target vessel r

242 rtant for flow-dependent vasodilation, blood vessel remodeling, and atherosclerosis.

243 gional vasoconstriction and subsequent blood vessel remodeling.

244 uggest a potential target for the control of vessel restenosis.

245 1.69-3.23; P<0.0001), ischemia-driven target vessel revascularization (adjusted hazard ratio, 1.82; 9

246 trong trend was preserved in terms of target vessel revascularization (harzard ratio, 1.55; 95% confi

247 vents, myocardial infarction (MI), or target vessel revascularization in SVG intervention with and wi

248 rget-vessel myocardial infarction, or target-vessel revascularization).

249 , stent thrombosis, heart failure, or target vessel revascularization.

250 sel-related myocardial infarction, or target vessel revascularization.

251 iac death, myocardial infarction, and target vessel revascularization.

252 The topography of these vessels, running alongside dural venous sinuses, recapit

253 g the HEC-1A cell line and the rotating wall vessel (RWV) bioreactor technology.

254 sex, hypertension, diabetes mellitus, target vessel, serial stenosis, and baseline percentage diamete

255 H without causing endothelium impairment and vessel shrinkage.

256 lts showed that mpJX-594 targets tumor blood vessels, spreads secondarily to tumor cells, and produce

257 decreased its stability, and elevated blood vessel sprouting and in vivo angiogenesis.

258 elial glutamine and asparagine metabolism in vessel sprouting.

259 and tight junction pathways and normalizing vessel structure and function.

260 esponse to tumor stiffening may help restore vessel structure, minimize metastasis, and aid in drug d

261 node voltages of the circuit reflecting the vessel structures were used for node registration.

262 ective pericyte loss in stable adult retinal vessels surprisingly does not cause BRB disintegration,

263 tion of picogram amounts of NGR-TNF, a tumor vessel-targeted TNFalpha derivative currently in phase I

264 neuronal-astrocytic signaling to local blood vessels to a multidimensional one in which mediators rel

265 In partial UFE, only the small arterial vessels to the fibroids were embolized, leaving the larg

266 nd resistance analogous to the role of blood vessel tone in regulating blood flow.

267 For example, widespread vessel constriction (vessel tone) is induced by brainstem neurons that releas

268 th intermediate AMD, choroidal thickness and vessel volume are reduced in the presence of subretinal

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

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

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

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

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

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

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

276 Expansive vessel wall remodeling was more frequent and intense wit

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

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

279 microcrystalline form of sirolimus into the vessel wall.

280 tion, whereas VSMC proliferation repairs the vessel wall.

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

282 entially negligible toxic effect on arterial vessel walls.

283 The data suggests that the El Faro vessel was drifting at an average speed of approximately

284 The number of vessels was also significantly higher in carotid plaque

285 To investigate the effect of NAC on larger vessels, we also performed ferric chloride-induced carot

286 >/=70% stenosis in at least 1 major coronary vessel were identified from >200 candidate variables, in

287 and alpha-smooth muscle actin-positive blood vessels were assayed at postoperative day 7 by colony fo

288 Tibial artery vessels were classified as completely occluded, signific

289 Pathological tumor vessels were closed using particles filling the entire v

290 in a pulmonary thromboembolism model, larger vessels were occluded.

291 The medium- and large-scale vessels were run for 52 consecutive weeks as semibatch r

292 loss of side branches and the enlargement of vessels when pericyte function is impaired or lost.

293 ble liquid can provide miniaturised reaction vessels which can be manipulated in microfluidic network

294 rods are confined and separated by the wood vessels, which deliver directional electron transport pa

295 vessels induced the development of lymphatic vessels, which may have contributed to the treatment fai

296 y undergo senescence in vascular sprouts and vessels, which suggests that pathologic outcomes of cent

297 orrelated well with percentage area of blood vessels, while other US perfusion parameters did not.

298 ration-dependent relaxation of precontracted vessels with a maximal effect observed at 90 minutes.

299 to induce arteriolargenesis (8.6 +/- 1.3% of vessels with recruitment of vascular smooth muscle cells

300 east two reaction steps in a single reaction vessel without isolation of the intermediates, whereby a