ライフサイエンスコーパス: retinal vessel

1 active recruitment of pericytes onto growing 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 strocyte pattern and defective remodeling of retinal vessels.

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

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

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

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

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

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

32 /26, 8%), glaucoma (5/26, 19%), and tortuous retinal vessels (4/26, 15%).

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

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

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

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

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

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

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

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

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

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

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

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

45 Retinal vessels and angiogenic gene expression in retina

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

71 Retinal vessel attenuation, pigment spots, and optic atr

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

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

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

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

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

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

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

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

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

81 Retinal vessel caliber and fractal dimension were measur

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

83 Early retinal vessel caliber changes are seemingly early marke

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

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

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

87 We investigated whether retinal vessel calibers are associated with cardiovascul

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

89 Retinal vessel calibers have been associated with the pr

90 Retinal vessel calibers of baseline retinal photographs

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

92 Changes in retinal vessel calibre may reflect cumulative structural

93 Summarised retinal vessel calibre measurements obtained from oximet

94 Retinal vessel calibre was measured using computer-assis

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

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

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

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

99 Development of peripheral retinal vessels continued after treatment with intravitr

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

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

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

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

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

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

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

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

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

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

110 Retinal vessel diameters are being measured to examine t

111 Summarised retinal vessel diameters are linked to systemic vascular

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

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

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

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

116 Major retinal vessel diameters were analyzed from ADPase-stain

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

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

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

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

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

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

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

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

125 Retinal vessel equivalents were more highly correlated b

126 1(+), cells were preferentially entrapped in retinal vessels (fivefold increase compared with nondiab

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

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

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

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

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

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

133 Retinal vessel homeostasis ensures normal ocular functio

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

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

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

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

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

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

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

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

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

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

144 Histology showed overgrown retinal vessels in the subretinal space.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 The retinal vessel movements correlated to worsening of BCVA

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

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

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

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

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

175 The retinal vessels of diabetic rats showed differential exp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 Retinal vessel tortuosity was measured from digitized re

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

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

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

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

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

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

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

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

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

221 Individual retinal vessels were identified on infrared reflectance

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

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

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

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

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

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

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

229 The retinal vessel width relationship at vessel branch point

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

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

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