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1 schemia, neovascularization, and incompetent blood-retinal barrier).
2 ke by glucose in the cells that comprise the blood-retinal barrier.
3 pate in the induction and maintenance of the blood-retinal barrier.
4 rotein activity in cells that form the outer blood-retinal barrier.
5  disorder associated with dysfunction of the blood-retinal barrier.
6 cyte function at sites of a breakdown in the blood-retinal barrier.
7      It can pass the blood-brain barrier and blood-retinal barrier.
8 h OIR, suggesting a protective effect on the blood-retinal barrier.
9 optosis, thereby preserving the integrity of blood-retinal barriers.
10 lly significant increase in breakdown of the blood-retinal barrier (AGE Alb versus Alb, 8.2 vs. 1.6 n
11 n identified as an important mediator of the blood-retinal barrier alteration in diabetic retinopathy
12  localized breakdown in the integrity of the blood-retinal barrier and aberrations in the organizatio
13                             Breakdown of the blood-retinal barrier and leakage from the retinal vascu
14  role for Mvarphi-derived CD in altering the blood-retinal barrier and reveal a potential therapeutic
15 , which are a crucial component of the outer blood-retinal barrier and the damage is related to retin
16  suggests that there may be breakdown of the blood-retinal barrier and tight junction integrity in a
17 patial buffering of ions, maintenance of the blood-retinal barrier, and response to injury.
18 by ischemia, neovascularization, incompetent blood-retinal barrier, and vascular occlusion.
19 )], pericytes (anti-neural/glial antigen 2), blood-retinal barrier [anti-zonula occludens protein 1 (
20 ve acquired the ability to break through the blood-retinal barrier are thought to be causally involve
21 ecome more important during breakdown of the blood-retinal barrier, as seen after TNF-alpha treatment
22  not bind IGF-1 (IGFBP-3NB), to regulate the blood retinal barrier (BRB) using two distinct experimen
23        We hypothesized that Edn2 damages the blood-retinal barrier (BRB) and that this is mediated by
24     Diabetic retinopathy is characterized by blood-retinal barrier (BRB) breakdown and neurotoxicity.
25                                              Blood-retinal barrier (BRB) breakdown and related vascul
26 kostasis) within the retinal vasculature and blood-retinal barrier (BRB) breakdown and to determine w
27  previously showed that lovastatin mitigates blood-retinal barrier (BRB) breakdown in db/db mice.
28                                              Blood-retinal barrier (BRB) breakdown is a hallmark of d
29 ial growth factor (VEGF) protein levels, and blood-retinal barrier (BRB) breakdown of the animals wer
30 role of reactive oxygen species (ROS) in the blood-retinal barrier (BRB) breakdown that characterizes
31                                              Blood-retinal barrier (BRB) breakdown was quantified usi
32                                          The blood-retinal barrier (BRB) consists of tightly intercon
33 sophosphatidylcholine (LPC), are involved in blood-retinal barrier (BRB) damage during diabetic retin
34                 Here, by studying functional blood-retinal barrier (BRB) formation in mice, we found
35 lop and characterize a quantitative assay of blood-retinal barrier (BRB) function in mice and to dete
36                                              Blood-retinal barrier (BRB) function was assayed by dete
37 p54/PSF heterodimer may contribute to normal blood-retinal barrier (BRB) induction in vivo.
38  studies, functional MRI was used to measure blood-retinal barrier (BRB) integrity after Gd-DTPA inje
39               In a subgroup of male SD rats, blood-retinal barrier (BRB) integrity was also assessed
40                            In vertebrates, a blood-retinal barrier (BRB) is established by tight junc
41                             Breakdown of the blood-retinal barrier (BRB) is linked to vision loss in
42 cular endothelial cells comprising the inner blood-retinal barrier (BRB) is mediated by the GLUT1 glu
43 scular permeability due to alteration of the blood-retinal barrier (BRB) is one of the major complica
44                                     In vivo, blood-retinal barrier (BRB) leakage was studied using th
45  block vascular permeability and restore the blood-retinal barrier (BRB) may lead to new therapies.
46        These data suggest differences in the blood-retinal barrier (BRB) of mice and rabbits and indi
47                                              Blood-retinal barrier (BRB) permeability in uninfected d
48 f this study was to determine to what extent blood-retinal barrier (BRB) permeability occurred during
49                                              Blood-retinal barrier (BRB) permeability surface area pr
50              Its absence has been related to blood-retinal barrier (BRB) permeability through delocal
51                                      Loss of blood-retinal barrier (BRB) properties induced by vascul
52                             Breakdown of the blood-retinal barrier (BRB), as occurs in diabetic retin
53 trophin Dp71 gene induces a highly permeable blood-retinal barrier (BRB).
54 is important to measure the integrity of the blood-retinal barrier (BRB).
55 esion molecule (ICAM)-1 and breakdown of the blood-retinal barrier (BRB).
56 ntry into the endothelial cells of the inner blood-retinal barrier (BRB).
57                                              Blood-retinal barrier [BRB] breakdown, characteristic of
58 ffected by hyperglycemia simultaneously with blood retinal barrier breakdown, suggesting that glial a
59 ular endothelial cell injury, apoptosis, and blood-retinal barrier breakdown (P<0.0001) but did not d
60  adhesion molecule-1 (ICAM-1) and results in blood-retinal barrier breakdown and capillary nonperfusi
61 receptor apoptosis, vascular telangiectasis, blood-retinal barrier breakdown and, later, intraretinal
62 IF-1alpha and VEGF increases and the related blood-retinal barrier breakdown are suppressed by inhibi
63 oteinases (MMPs) as a potential cause of the blood-retinal barrier breakdown at the onset of angiogen
64  drops significantly reduced leukostasis and blood-retinal barrier breakdown in a dose-dependent mann
65                                              Blood-retinal barrier breakdown in diabetic animals trea
66 dothelial cell apoptosis as a major cause of blood-retinal barrier breakdown in early diabetes.
67                                        Early blood-retinal barrier breakdown in experimental diabetes
68  role in the pathogenesis of blood-brain and blood-retinal barrier breakdown in vivo.
69                                              Blood-retinal barrier breakdown is markedly increased wi
70 ry cytokines that initiate neuronal loss and blood-retinal barrier breakdown seen in diabetic retinop
71 y produces a transient worsening of diabetic blood-retinal barrier breakdown via an HIF-1alpha-mediat
72                                              Blood-retinal barrier breakdown was assessed using (3)H-
73                             Diabetes-induced blood-retinal barrier breakdown was dose-dependently inh
74                                              Blood-retinal barrier breakdown was induced in rats with
75                             Spatially, early blood-retinal barrier breakdown was localized to the ret
76                                              Blood-retinal barrier breakdown was quantified using the
77  circulation with an anti-platelet antibody, blood-retinal barrier breakdown worsened in the diabetic
78 rrent study, diabetic vascular permeability (blood-retinal barrier breakdown) is demonstrated to resu
79 elial growth factor (VEGF) triggers diabetic blood-retinal barrier breakdown, and (2) identify the si
80 n apoptosis, oxidative stress, inflammation, blood-retinal barrier breakdown, and neuroprotection.
81 iabetic retinal vasculature results in early blood-retinal barrier breakdown, capillary nonperfusion,
82  the diabetic retinal vasculature results in blood-retinal barrier breakdown, capillary nonperfusion,
83 adhesion molecule-1 levels, leukostasis, and blood-retinal barrier breakdown, in a relevant animal mo
84 sening of diabetic retinopathy, specifically blood-retinal barrier breakdown, that follows the instit
85 ocyte adhesion, endothelial cell injury, and blood-retinal barrier breakdown.
86 yte adhesion and endothelial cell injury and blood-retinal barrier breakdown.
87 ch reduced leukocyte adhesion and suppressed blood-retinal barrier breakdown.
88 the isotope-dilution method for quantitating blood-retinal barrier breakdown.
89  approach in the treatment of early diabetic blood-retinal barrier breakdown.
90 as the isotope-dilution method for measuring blood-retinal barrier breakdown.
91 model by determining retinal leukostasis and blood-retinal barrier breakdown.
92 titating vascular leakage and especially the blood-retinal barrier breakdown.
93  cell death and serves, in part, to suppress blood-retinal barrier breakdown.
94 appaB DNA-binding activity, leukostasis, and blood-retinal barrier breakdown.
95 urs, endothelial cell injury ensues, as does blood-retinal barrier breakdown.
96 xtracted and assayed for leukocyte adhesion; blood-retinal barrier breakdown; VEGF, TNF-alpha, IL-1be
97 etinopathy increases the permeability of the blood-retinal barrier, but the specific vessels that bec
98  TGF-beta may contribute to breakdown of the blood-retinal barrier by stimulating endothelial cell MM
99 racteristics of tight junctions in the outer blood-retinal barrier change during embryonic developmen
100        Macular oedema typically results from blood-retinal barrier disruption.
101 ontributing to the pathologic progression of blood-retinal barrier dysfunction.
102 agenase-like activity that may contribute to blood-retinal barrier dysfunction.
103 ssion of pathologic retinal angiogenesis and blood-retinal barrier dysfunction.
104 ivo was demonstrated that was accompanied by blood-retinal barrier dysfunction.
105  diabetic retinopathy and macular edema, the blood-retinal barrier fails to function properly, and th
106                                     Impaired blood-retinal barrier function leads to macular edema th
107 erentially contribute to the inner vs. outer blood-retinal barrier function.
108 ivo Fluorescein angiography indicated normal blood-retinal barrier function.
109  enhanced apoptotic cell death, and impaired blood-retinal barrier function.
110  in the cells comprising the inner and outer blood-retinal barriers: human retinal pigment epithelial
111 port for fluids and solutes across the inner blood-retinal barrier (iBRB).
112 lity with implications for alteration of the blood-retinal barrier in diabetic retinopathy.
113 ricyte interactions during alteration of the blood-retinal barrier in diabetic retinopathy.
114 l pigmented epithelium (RPE) forms the outer blood-retinal barrier in the eye and its polarity is res
115  derangements observed in the diabetic inner blood-retinal barrier in vivo.
116 retinal thickness, intraocular pressure, and blood retinal barrier integrity.
117 l layer thickness, intraocular pressure, and blood retinal barrier integrity.
118                            Alteration of the blood-retinal barrier is the hallmark of this disease, c
119 helium (RPE), which helps maintain the outer blood-retinal barrier, is a local source for ET-1 and wh
120 cations of diabetes is the alteration of the blood-retinal barrier, leading to retinal edema and cons
121 A may have a protective effect against outer blood-retinal barrier leakage associated with diabetic r
122 tein, the vitreous-plasma protein ratio, and blood-retinal barrier leakage by 3-, 1.7-, 3.1-, and 2.7
123 nd retinal PGE2 secretion, VEGF protein, and blood-retinal barrier leakage were estimated.
124 abetes-induced elevations in PGE2, VEGF, and blood-retinal barrier leakage.
125 , but transporters for DHA uptake across the blood-retinal barrier or retinal pigment epithelium have
126 ansport, phagocytosis and formation of outer blood-retinal barrier, or possible involvement of JN exp
127                    Choroidal contribution or blood-retinal barrier permeability surface area product
128 hese results suggest that astrocytes enhance blood-retinal barrier properties, at least in part by in
129 rowth factor (VEGF)-induced breakdown of the blood-retinal barrier requires protein kinase C (PKC)bet
130 in ICAM-1, leukostasis, and breakdown of the blood-retinal barrier, suggesting that NOX2 is primarily
131 igmented epithelial (RPE) cells maintain the blood-retinal barrier, sustain retinal photoreceptor cel
132 d Fpn is expressed in cells constituting the blood-retinal barrier, the authors tested whether the re
133 lay important roles in the alteration of the blood-retinal barrier through proteolytic degradation of
134    There is no evidence of a blood-ocular or blood-retinal barrier to activated T cell blasts.
135  protein [anti-GFAP]) and to investigate the blood-retinal barrier using the tight junction markers z
136 onditions in the subretinal space, the outer blood-retinal barrier was disrupted by compromising reti
137 udy, the potential side effects on the outer blood-retinal barrier were examined.
138 esis during development and formation of the blood-retinal barrier, which is linked to significant do

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