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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
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
40 coherence tomography and dynamic and static retinal vessel analysis, using the Dynamic Vessel Analyz
43 n evidence of both bioavailability of RBX to retinal vessels and amelioration of diabetes-induced ret
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
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
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
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
70 t this difference or to find a difference in retinal vessel arteriovenous ratio between smokers and n
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
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
80 he gliotoxin fluorocitrate (150 mum) dilated retinal vessels by 52.3 +/- 1.1% (P < 0.001) and inhibit
84 suggest that computer-based measurements of retinal vessel caliber may be useful to identify people
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
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
113 presence of factors that are associated with retinal vessel diameters should be considered when using
117 significant associations of albuminuria and retinal vessel diameters with depression were reported.
119 tively across genes with summary measures of retinal vessel diameters, referred to as the central ret
121 ngles relative to the long axes of the major retinal vessels during anaphase were calculated from pho
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,
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
132 peroxia (75% oxygen) for 5 d, which inhibits retinal vessel growth and causes significant vessel loss
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)
138 sure was the first detectable abnormality of retinal vessels in subjects with well-controlled type 1
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
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
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
158 lls, anterior chamber protein concentration, retinal vessel leukocyte adhesion, and protein leakage w
164 sured from stereoscopic photographs, whereas retinal vessel measurements were taken from a single dig
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
171 sults indicate that leukocyte recruitment in retinal vessels near the ON head is an early event in TO
177 uct of complement activation, in the wall of retinal vessels of human eye donors with 9 +/- 3 years o
179 ase in the rate of apoptosis was observed in retinal vessels of PECAM-1-/- mice, which was compensate
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
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
190 od, SDRA demonstrated a marked difference in retinal vessel responses to flickering light (P < 0.05).
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
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
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
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
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
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
215 ght line between two points; the diameter of retinal vessels was determined using ImageJ software, an
218 ous adhesions beyond major arcades and along retinal vessels was noted during surgery in all eyes.
220 ocalization of fibronectin and its amount in retinal vessels were examined with the immunoperoxidase
223 n of FGF2 in the retina by Western blot, but retinal vessels were not different in appearance or tota
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
228 ed angiogenic sprouting and regrowth of lost retinal vessels while suppressing ectopic pathological n
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
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