ライフサイエンスコーパス: retinal vessel

1 d to identify and remove pixels belonging to retinal vessels.

2 increased surface area and remodeling of the retinal vessels.

3 that preempt the effects of hyperglycemia on retinal vessels.

4 and protein and in leukocyte adhesion to the retinal vessels.

5 signature that the polyol pathway leaves on retinal vessels.

6 t epithelium and endothelial membrane of the retinal vessels.

7 tinal neovascularization (SNV) evolving from retinal vessels.

8 ns of retinal vasculature confirm attenuated retinal vessels.

9 sprout development; for instance, in growing retinal vessels.

10 PH oxidase catalytic subunit NOX2 within the retinal vessels.

11 lar endothelial (VE) -cadherin expression in retinal vessels.

12 f microglia that was closely associated with retinal vessels.

13 orientation in vivo, in flow-exposed forming retinal vessels.

14 was preferentially localized to neovascular retinal vessels.

15 with the epiretinal vessels than with inner retinal vessels.

16 r birth and lack of or abnormal outgrowth of retinal vessels.

17 can be dissected without damage to the major retinal vessels.

18 as phenotype of the hyperpermeable diabetic retinal vessels.

19 analysis revealed PSF mainly associated with retinal vessels.

20 unoreactivity was associated with developing retinal vessels.

21 omata that were closely apposed to the large retinal vessels.

22 as no identifiable adverse effects on mature retinal vessels.

23 ble metabolite of PGI2) from isolated bovine retinal vessels.

24 ing overlying retinal pigment epithelium and retinal vessels.

25 ctive spots mainly located near second-order retinal vessels.

26 A) allows direct, non-invasive estimation of retinal vessels.

27 active recruitment of pericytes onto growing retinal vessels.

28 strocyte pattern and defective remodeling of retinal vessels.

29 ss, high levels of VEGF can cause closure of retinal vessels.

30 -VEGF treatment on development of peripheral retinal vessels (1 article), refractive outcomes (1 arti

31 Cross-sectional study of 387 retinal vessels (193 arterioles, 194 veins) from 28 eyes

32 alpha were detected in the GCL, INL, and the retinal vessels 24 hours after reperfusion.

33 MCP-1, MIP-1alpha, and MIP-1beta mRNA in the retinal vessels 3 hours after reperfusion.

34 /26, 8%), glaucoma (5/26, 19%), and tortuous retinal vessels (4/26, 15%).

35 rst- or second-order branches of the central retinal vessels (95%).

36 Similarly, the number of retinal vessel-adherent leukocytes and protein leakage w

37 aphy revealed normal vascular patency of the retinal vessels after vitrectomy.

38 layer (INL), outer nuclear layer (ONL), and retinal vessels, after laser capture microdissection of

39 e to our knowledge, the associations between retinal vessel alterations and subclinical WM pathology

40 ular function was assessed using the Dynamic Retinal Vessel Analyser (DVA), and systemic macrovascula

41 (TCD) during cognitive stimulation, dynamic retinal vessel analysis (DVA) during flicker light stimu

42 -Stage Renal Disease) study, data on dynamic retinal vessel analysis (DVA) was available in a sub-coh

43 to flicker light was assessed using dynamic retinal vessel analysis (Imedos, GmbH).

44 Furthermore, on dynamic retinal vessel analysis, both glaucoma groups exhibited

45 coherence tomography and dynamic and static retinal vessel analysis, using the Dynamic Vessel Analyz

46 ssed in 201 participants by means of dynamic retinal vessel analysis.

47 red with established methods as delivered by retinal vessel analyzer (RVA) software.

48 cular reactivity was assessed by the dynamic retinal vessel analyzer.

49 d fluorescence angiography revealed narrower retinal vessels and a reduced perfusion area in the peri

50 n evidence of both bioavailability of RBX to retinal vessels and amelioration of diabetes-induced ret

51 tizer effectively produced FVT closure, both retinal vessels and anastomoses remained patent.

52 Retinal vessels and angiogenic gene expression in retina

53 s of nonproliferative DR, including tortuous retinal vessels and defective pericyte coverage.

54 kade both lead to AVM formation in postnatal retinal vessels and internal organs including the gastro

55 ed infiltration of CCR2(+) leukocytes across retinal vessels and into the parenchyma within 48 hours

56 proliferating endothelial cells in reforming retinal vessels and intravitreal neovascularization afte

57 mmunoreactivity was very strong in reforming retinal vessels and intravitreal neovascularization in o

58 others previously achieved oximetry on major retinal vessels and measured the total retinal oxygen me

59 qualitative and quantitative assessments of retinal vessels and neovascularization (NV).

60 RT-PCR in whole retina and on laser-captured retinal vessels and neuronal layers.

61 val NF-kappaB via Epo receptor activation on retinal vessels and neurons.

62 c photograph by matching the position of the retinal vessels and of Bruch's membrane opening.

63 eceptor mosaic cannot be visualized clearly, retinal vessels and other retinal changes can be seen),

64 nized mouse line (R3), displaying attenuated retinal vessels and pigmented patches, was identified by

65 blocked VEGF-induced leakage from dermal and retinal vessels and prevented exudative retinal detachme

66 include neovascular growth originating from retinal vessels and progressing to the subretinal space

67 re the cells preferentially recruited to the retinal vessels and protect vessels from diabetic damage

68 of the eye by using corresponding points on retinal vessels and RVPs using UWF-FAF.

69 Similar complement activation in retinal vessels and selective reduction in the levels of

70 arly activation of complement in the wall of retinal vessels and the decreased levels of complement i

71 ions were observed in the endothelium of the retinal vessels and the nearby retinal cells, the endoth

72 betes increases the amount of fibronectin in retinal vessels and upregulates its expression without c

73 y was only weakly associated with developing retinal vessels and was not observed in angioblasts thro

74 comprehensive endocrine, neuropsychological, retinal vessel, and diffusion tensor imaging-based cereb

75 aled severe retinal degeneration, attenuated retinal vessels, and depigmentation in mice lacking Sema

76 ar connective tissue surrounding the central retinal vessels, and in the dura mater, arachnoid, and p

77 across most areas of the retina, attenuated retinal vessels, and RPE thinning in both eyes.

78 Appearance of the optic nerve head, retinal vessels, and surrounding retina was documented w

79 queous fluid, firm leukocyte adhesion in the retinal vessels, and the number of extravasated leukocyt

80 (2) prevascular vitreous fissures overly the retinal vessels; and (3) cisterns are continuous with pr

81 sculopathy of the central nervous system and retinal vessels; and a fetal akinesia deformation sequen

82 GC) loss induced by glaucoma and in what way retinal vessels are involved in this process.

83 e retina, suggesting that only proliferating retinal vessels are sensitive to Nutlin-3.

84 t this difference or to find a difference in retinal vessel arteriovenous ratio between smokers and n

85 terations in the density and distribution of retinal vessels, astrocytes and microglia, (3) decreased

86 Retinal vessel attenuation, pigment spots, and optic atr

87 ase stages, despite the observed progressive retinal vessel attenuation.

88 ripheral nail-fold capillary (P = 0.009) and retinal vessel (average baseline corrected flicker respo

89 not be accurately quantitated in lysates of retinal vessels because of variable degrees of glial con

90 Thus, in diabetes, retinal vessels become dependent on a small increase in

91 nal injury and intraretinal hemorrhages from retinal vessel bleeding, with no rupture of choroidal bl

92 ly associated with normal developing primary retinal vessels but was strongly expressed by proliferat

93 uman diabetic retinas associated with normal retinal vessels but were absent from proliferative lesio

94 g Smad2 phosphorylation, was enhanced in the retinal vessels, but not in the neural retina.

95 he gliotoxin fluorocitrate (150 mum) dilated retinal vessels by 52.3 +/- 1.1% (P < 0.001) and inhibit

96 Retinal vessel caliber and fractal dimension were measur

97 The association between retinal vessel caliber and heart failure was nonsignific

98 Early retinal vessel caliber changes are seemingly early marke

99 suggest that computer-based measurements of retinal vessel caliber may be useful to identify people

100 Extended-zone retinal vessel caliber predicts moderate DR in adolescen

101 Retinal vessel caliber reclassified 21% of low-risk wome

102 ciations between a posteriori-derived DP and retinal vessel caliber.

103 to determine if, in a community based-study, retinal vessel calibers and change in caliber over 8 yea

104 We investigated whether retinal vessel calibers are associated with cardiovascul

105 We examined retinal vessel calibers as 16-year predictors of diabeti

106 Retinal vessel calibers at baseline (upper 3 quartiles v

107 significant associations were found between retinal vessel calibers at Exam 2 and 5 with the subsequ

108 Retinal vessel calibers have been associated with the pr

109 Retinal vessel calibers of baseline retinal photographs

110 Retinal vessel calibers were measured at an optic disc c

111 Singapore I Vessel Assessment: standard zone retinal vessel calibers were summarized as central retin

112 d pressure was not associated with childhood retinal vessel calibers.

113 Changes in retinal vessel calibre may reflect cumulative structural

114 Summarised retinal vessel calibre measurements obtained from oximet

115 Retinal vessel calibre was measured using computer-assis

116 The relationship of retinal vessel calibre with clinical and demographic cha

117 ders in associations between measurements of retinal-vessel calibre and CVD risk factors, including b

118 ning models for the automated measurement of retinal-vessel calibre in retinal photographs, using div

119 Retinal-vessel calibre measured by the models and by exp

120 PTX inhibited radial extension of retinal vessels, causing increases in AVA of 65% (P < 0.

121 and the retinal microvasculature, including retinal vessels, choroidal vessels, and capillaries in t

122 the capacity to express AQP1, though intact retinal vessels chronically suppress AQP1 expression.

123 EGF inhibition improves retinal hemorrhages, retinal vessel closure, and progression of nonproliferat

124 Development of peripheral retinal vessels continued after treatment with intravitr

125 dus examination revealed marked narrowing of retinal vessels, cotton wool spots and few retinal hemor

126 Reflectance-compensated retinal vessel densities were calculated on projection-r

127 Peripapillary superficial retinal vessel densities were significantly reduced in p

128 in PACG occur earlier than the reduction in retinal vessel densities.

129 (54.2%) and exudative (45.8%) AMD to measure retinal vessel density (VD) from the superficial capilla

130 ysis using normalized deviation compared the retinal vessel density in GA regions, 500-mum GA rim reg

131 Eyes with GA have reduced retinal vessel density in SVC, ICP, and DCP compared to

132 Retinal vessel density in the GA rim region decreased in

133 The current study therefore evaluated the retinal vessel density in the peripapillary and macular

134 ships between the vertical asymmetrical deep retinal vessel density reduction (ADRVD) across the temp

135 roidal thickness, choroidal vascularity, and retinal vessel density were measured across the central

136 Retinal vessel density within the GA region decreased si

137 , and area), fovea (distance and angle), and retinal vessel density.

138 Ischemia was identified by metrics of retinal vessel density.

139 inner retina, forming a template upon which retinal vessels develop.

140 We prevented retinal vessel development by raising newborn mice in a

141 ation of intravitreal neovascularization and retinal vessel development in OIR.

142 ith increased endothelial cell death, and in retinal vessels development that is abnormally reduced.

143 e rat retina in vivo by measuring changes in retinal vessel diameter and red blood cell (RBC) flux ev

144 RA showed a strong relation between baseline retinal vessel diameter and subsequent dilatory response

145 el diameters should be considered when using retinal vessel diameter as an outcome or when using thes

146 latory function was measured with continuous retinal vessel diameter assessment and nail-fold capilla

147 1.55 uL min(-1)) across the full spectrum of retinal vessel diameters (3.2-45.8 um), without requirin

148 puter grading was used to determine the mean retinal vessel diameters (central retinal arteriole equi

149 Retinal vessel diameters are being measured to examine t

150 Summarised retinal vessel diameters are linked to systemic vascular

151 Recently it was shown that retinal vessel diameters could be measured using spectra

152 presence of factors that are associated with retinal vessel diameters should be considered when using

153 A reduction in retinal vessel diameters was less consistent and not sig

154 The significant reduction in retinal vessel diameters was only apparent for the small

155 Major retinal vessel diameters were analyzed from ADPase-stain

156 significant associations of albuminuria and retinal vessel diameters with depression were reported.

157 ntral macular thickness, macular volume, and retinal vessel diameters).

158 tively across genes with summary measures of retinal vessel diameters, referred to as the central ret

159 Important factors that directly affect retinal vessel diameters, such as medication use, should

160 ngles relative to the long axes of the major retinal vessels during anaphase were calculated from pho

161 oxidase in turn blocks leukocyte adhesion to retinal vessels during diabetes and uveitis.

162 t of AMG 386 on established and newly formed retinal vessels, either as a single agent or when combin

163 Two masked graders evaluated scans for (1) retinal vessel elevation, (2) scalloped retinal layers,

164 Retinal vessel equivalents were more highly correlated b

165 Correspondingly, retinal vessels experienced tensile stress of up to 2.3

166 ant difference between Color and IR based on retinal vessel features (all p values > 0.05).

167 statistically significant difference in the retinal vessel features between Color and IR.

168 reement between Color and IR images based on retinal vessel features.

169 1(+), cells were preferentially entrapped in retinal vessels (fivefold increase compared with nondiab

170 al membranes, distortion of myelin wings and retinal vessels, fixed retinal folds, and traction retin

171 vestigated the causal role of adiponectin in retinal vessel formation and inflammation under conditio

172 s tested on more than 5000 cross-sections of retinal vessels from the REVIEW dataset through comparat

173 Gene expression profiling of isolated retinal vessels from these mutant rodent models and wild

174 Only during normal retinal vessel growth (P1-P10) and before the appearance

175 otein thioredoxin 2 (TRX2), exhibit retarded retinal vessel growth and arteriovenous malformations (A

176 peroxia (75% oxygen) for 5 d, which inhibits retinal vessel growth and causes significant vessel loss

177 ing or genetic deficiency of SMAD2 prevented retinal vessel growth retardation and AVM in all three m

178 Retinal vessel homeostasis ensures normal ocular functio

179 layer/inner nuclear layer plus the embedded retinal vessels, (ii) the avascular outer nuclear (photo

180 y vascular injury models: laser occlusion of retinal vessels in adult green fluorescent protein (GFP)

181 Notably, the retinal vessels in Apoa1bp(-/-) mice manifested normal p

182 r patient showed mild straightening of nasal retinal vessels in both eyes.

183 owed less adhesion of leukocytes on inflamed retinal vessels in endotoxin-induced uveitis mice.

184 cally affects the vascular response in small retinal vessels in order to maintain hemodynamic regulat

185 riolar (aMax) and venular dilation (vMax) of retinal vessels in response to flicker light stimulation

186 Rapid dilation of retinal vessels in response to flickering light (functio

187 ction of CVD on the basis of the features of retinal vessels in retinal photographs.

188 sure was the first detectable abnormality of retinal vessels in subjects with well-controlled type 1

189 ted the formation and maturation of new host retinal vessels in the area of the transplant.

190 imilar sequence of events, with sprouts from retinal vessels in the deep capillary bed seen on P14 an

191 of beta1-integrin and FN was observed in the retinal vessels in the mouse model of hypoxia-induced re

192 n a statistically significant reperfusion of retinal vessels in the rabbit experimental model of RVO.

193 allowed visualization of small pathological retinal vessels in the retinal periphery that were obscu

194 Histology showed overgrown retinal vessels in the subretinal space.

195 neovascularization or other abnormalities of retinal vessels; in the ischemic retinopathy model, they

196 release of NO and PGI2 from isolated bovine retinal vessels, indicating that the increase in EDRF ma

197 nct experimental mouse models, laser-induced retinal vessel injury and vascular endothelial growth fa

198 e evidence that adiponectin protects against retinal vessel injury following pathological stimuli thr

199 Fractal analysis of the retinal vessels is a method to quantify the global geome

200 h factor (VEGF) immunoreactivity in diabetic retinal vessels is related to increased vascular permeab

201 D We examined the gene expression profile of retinal vessels isolated from rats with 6 months of stre

202 the foveal avascular zone in the superficial retinal vessel layer increased significantly after surge

203 the foveal avascular zone in the superficial retinal vessel layer, more pronounced in group 2, may be

204 vascular development, absence of deep layer retinal vessels, leading to increased levels of vascular

205 By contrast, deletion of Cdc42 in postnatal retinal vessels leads to aberrant vascular remodeling an

206 vitreous injection of CA-I in rats increased retinal vessel leakage and caused intraretinal edema.

207 rom retinal astroglial cells (RACs) suppress retinal vessel leakage and inhibit choroidal neovascular

208 Improved retinal circulation and decreased retinal vessel leakage were found in the follow-up fluor

209 n using FN-439 reverses RAC exosome-mediated retinal vessel leakage.

210 lls, anterior chamber protein concentration, retinal vessel leukocyte adhesion, and protein leakage w

211 rfold the absolute number of PMo adherent to retinal vessels (leukostasis).

212 Subsequent to oxygen-induced retinal vessel loss, Igfbp3(-/-) mice had a 31% decrease

213 a dose-dependent increase in oxygen-induced retinal vessel loss.

214 and flow in interconnected small parafoveal retinal vessels (< 50 um) of nine healthy participants.

215 It has also been suggested that retinal vessels manifest different features on spectral

216 Although retinal vessels may be viewed through the pupil using st

217 hanges (e.g. decreased flow or occlusion) in retinal vessels may serve as a useful diagnostic indicat

218 e of a relationship between extracted DP and retinal vessel measurements in this population.

219 sured from stereoscopic photographs, whereas retinal vessel measurements were taken from a single dig

220 flatmounts from one cohort were prepared and retinal vessel morphology examined.

221 e 9 vectors was summed to describe the total retinal vessel movement (retinal tangential movement [RT

222 nal disease but a dynamic condition in which retinal vessel movement associated with ERM was measurea

223 secondary outcome was to correlate measured retinal vessel movement with changes in BCVA, CMT, and p

224 The retinal vessel movements correlated to worsening of BCVA

225 cular area was divided into 9 subfields, and retinal vessel movements were calculated.

226 eral vascular leakage (n = 3 eyes), aberrant retinal vessels (n = 1 eyes), vascular tortuosity (n = 1

227 sults indicate that leukocyte recruitment in retinal vessels near the ON head is an early event in TO

228 Furthermore, in the absence of bim retinal vessel obliteration and neovascularization did n

229 ult chimeric mice subjected to laser-induced retinal vessel occlusion injury.

230 The central retinal vessels occupied approximately 20% of the centra

231 The retinal vessels of diabetic rats showed differential exp

232 ed, but not the basal, Tgf-beta signaling in retinal vessels of diabetic rats.

233 uct of complement activation, in the wall of retinal vessels of human eye donors with 9 +/- 3 years o

234 er the mesenteric vessels of EAU mice or the retinal vessels of OVA-immunized mice.

235 ase in the rate of apoptosis was observed in retinal vessels of PECAM-1-/- mice, which was compensate

236 ast reduction of the intraluminal pattern of retinal vessels on OCT.

237 Ps) and VE-cadherin was examined in isolated retinal vessels or cultured endothelial cells in respons

238 Flash intensity has a significant impact on retinal vessel oxygen saturation measurements using dual

239 , and seven Caucasian individuals) underwent retinal vessel oxygen saturation measurements using dual

240 Although alterations in retinal vessel oxygenation and morphology have been repo

241 ned from 16 volunteer participants and seven retinal vessel parameters, i.e. Fractal Dimension (FD),

242 oups, pigmentation, retinal fibrosis, shape, retinal vessel pattern, and choroidal vessel visibility

243 ase preparations showed dilated and tortuous retinal vessels, pigmentary changes, incomplete vascular

244 responding points on retinal vasculature and retinal vessel printings (RVPs) within Zone 1, a circula

245 study was to investigate the role of AQP1 in retinal vessel proliferation.

246 that leads to attenuated and hyperpermeable retinal vessels, recapitulating some pathological featur

247 al monkey eyes were overlaid onto 3D central retinal vessel reconstructions generated as part of post

248 loss, Igfbp3(-/-) mice had a 31% decrease in retinal vessel regrowth versus controls after returning

249 al cells, the endothelial cell lining of the retinal vessels remained intact.

250 od, SDRA demonstrated a marked difference in retinal vessel responses to flickering light (P < 0.05).

251 Fundus photography and retinal vessel responses were assessed by RVA, intraocul

252 ients also show areas of complete closure of retinal vessels (retinal nonperfusion [RNP]) that increa

253 A total of 170 retinal vessel-RVP pairs were identified from 54 UWF-FAF

254 ons in a wide range of applications, such as retinal vessel segmentation and cell membrane profiling

255 Our analysis demonstrates that the retinal vessel segmentation is far from solved when cons

256 Connective tissue was present in the central retinal vessel sheaths and was identified as longitudina

257 h muscle cells, and endothelial cells of the retinal vessels showed dense intracellular AGE IR.

258 standing of the genetic factors that mediate retinal vessel size.

259 New vessels originated from superficial retinal vessels, something that is widely recognized, bu

260 poptosis, retinal detachment, alterations in retinal vessel structure, and activation and translocati

261 ssion of PDGF-BB and its cognate receptor in retinal vessels suggests a vasoactive function.

262 of 67LR between proliferating and quiescent retinal vessels suggests that this laminin receptor is a

263 ough selective pericyte loss in stable adult retinal vessels surprisingly does not cause BRB disinteg

264 rs sought to identify early abnormalities of retinal vessels that are not prevented by the current th

265 ET, has been shown to cause constriction of retinal vessels, the expression and functional significa

266 To visualize mobility and transverse flow in retinal vessels, the statistical variance of phase for e

267 uced neovascular tufts while sparing healthy retinal vessels, thereby demonstrating the therapeutic p

268 ex, distorting it as necessary to match each retinal vessel to its cortical representation.

269 ramatically decreased angiogenic response of retinal vessels to an oxygen toxicity challenge.

270 s simulated with particular attention to the retinal vessels to analyze stress and strain on these st

271 cute constrictive response of the developing retinal vessels to hyperoxia (30 minutes to 96 hours of

272 n and severity of the reaction of developing retinal vessels to hyperoxia in the newborn dog is simil

273 ly affecting the physiological adaptation of retinal vessels to hyperoxia.

274 f Muller cells and exposure of the remaining retinal vessels to the more hypoxic environment near the

275 the potential of quantitative measurement of retinal vessel tortuosity for diabetic complication risk

276 Retinal vessel tortuosity was measured from digitized re

277 nd flickering light and inversely related to retinal vessel tortuosity--a characteristic that has bot

278 y was to compare the location of the central retinal vessel trunk (CRVT) in the LC and prelaminar tis

279 Oxygen tension was measured in retinal vessels using phosphorescence lifetime imaging a

280 ght line between two points; the diameter of retinal vessels was determined using ImageJ software, an

281 Binding of phage to retinal vessels was evaluated by confocal microscopy of

282 Increased tortuosity of the retinal vessels was found in 8 (27%) subjects in childho

283 The outer diameter of retinal vessels was monitored at 2 second intervals in r

284 ous adhesions beyond major arcades and along retinal vessels was noted during surgery in all eyes.

285 The vitreal surfaces of the large retinal vessels were covered by a meshwork of immunoreac

286 ocalization of fibronectin and its amount in retinal vessels were examined with the immunoperoxidase

287 Individual retinal vessels were identified on infrared reflectance

288 Retinal vessels were labelled by i.v. injection of a flu

289 n of FGF2 in the retina by Western blot, but retinal vessels were not different in appearance or tota

290 Venous congestion of the epiescleral and retinal vessels were observed.

291 grin preferentially colocalize in the mature retinal vessels, whereas NLGN1 deletion causes an aberra

292 m (P5), VEGFR-1 protein was colocalized with retinal vessels, whereas VEGFR-2 was detected only in th

293 he upregulation of proapoptotic caspase-3 in retinal vessels, which concomitantly reduced retinal cap

294 from deep retinal capillaries and from large retinal vessels, which is not generally known.

295 ed angiogenic sprouting and regrowth of lost retinal vessels while suppressing ectopic pathological n

296 Retinal vessel width associations with glaucoma and nove

297 The retinal vessel width relationship at vessel branch point

298 The connection of two remote retinal vessels with a fine tube was also achieved with

299 lectron microscopy revealed occlusion of the retinal vessels with ultrastructural changes in the endo

300 lized to its disc photograph by matching the retinal vessels within each photograph to vessel outline