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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 e potential for payload transport across the blood-retinal barrier.
8 tinal cells that includes the formation of a blood-retinal barrier.
9  diseases such as DME with compromised outer blood-retinal barrier.
10      It can pass the blood-brain barrier and blood-retinal barrier.
11 h OIR, suggesting a protective effect on the blood-retinal barrier.
12 he extracellular matrix underlying the outer blood/retinal barrier.
13 tinitis, inflamed vasculature, and disrupted blood-retinal barriers.
14 optosis, thereby preserving the integrity of blood-retinal barriers.
15 lly significant increase in breakdown of the blood-retinal barrier (AGE Alb versus Alb, 8.2 vs. 1.6 n
16 n identified as an important mediator of the blood-retinal barrier alteration in diabetic retinopathy
17 l and biological factors possibly related to blood-retinal barrier alterations.
18           Consequent impairment of the outer blood retinal barrier and colonic intestinal epithelial
19  localized breakdown in the integrity of the blood-retinal barrier and aberrations in the organizatio
20 profound vascular abnormalities, loss of the blood-retinal barrier and impaired neuronal function.
21                             Breakdown of the blood-retinal barrier and leakage from the retinal vascu
22 arrier (BBB), blood-spinal cord barrier, and blood-retinal barrier and play key roles in maintaining
23  role for Mvarphi-derived CD in altering the blood-retinal barrier and reveal a potential therapeutic
24 , which are a crucial component of the outer blood-retinal barrier and the damage is related to retin
25  suggests that there may be breakdown of the blood-retinal barrier and tight junction integrity in a
26  to cross RPE cell membranes (i.e. the outer blood retinal barrier) and with potential roles in certa
27 patial buffering of ions, maintenance of the blood-retinal barrier, and response to injury.
28 by ischemia, neovascularization, incompetent blood-retinal barrier, and vascular occlusion.
29 )], pericytes (anti-neural/glial antigen 2), blood-retinal barrier [anti-zonula occludens protein 1 (
30 ve acquired the ability to break through the blood-retinal barrier are thought to be causally involve
31 ecome more important during breakdown of the blood-retinal barrier, as seen after TNF-alpha treatment
32  not bind IGF-1 (IGFBP-3NB), to regulate the blood retinal barrier (BRB) using two distinct experimen
33        We hypothesized that Edn2 damages the blood-retinal barrier (BRB) and that this is mediated by
34     Diabetic retinopathy is characterized by blood-retinal barrier (BRB) breakdown and neurotoxicity.
35                                              Blood-retinal barrier (BRB) breakdown and related vascul
36 kostasis) within the retinal vasculature and blood-retinal barrier (BRB) breakdown and to determine w
37  an attempt to investigate the mechanisms of blood-retinal barrier (BRB) breakdown at a global level,
38  previously showed that lovastatin mitigates blood-retinal barrier (BRB) breakdown in db/db mice.
39                                              Blood-retinal barrier (BRB) breakdown is a hallmark of d
40                                              Blood-retinal barrier (BRB) breakdown is responsible for
41 ial growth factor (VEGF) protein levels, and blood-retinal barrier (BRB) breakdown of the animals wer
42 role of reactive oxygen species (ROS) in the blood-retinal barrier (BRB) breakdown that characterizes
43                                              Blood-retinal barrier (BRB) breakdown was quantified usi
44                                          The blood-retinal barrier (BRB) consists of tightly intercon
45 sophosphatidylcholine (LPC), are involved in blood-retinal barrier (BRB) damage during diabetic retin
46 es for analyzing drug transport at the inner blood-retinal barrier (BRB) do not completely retain sev
47 othelial growth factor (VEGF) contributes to blood-retinal barrier (BRB) dysfunction in several blind
48                 Here, by studying functional blood-retinal barrier (BRB) formation in mice, we found
49 lop and characterize a quantitative assay of blood-retinal barrier (BRB) function in mice and to dete
50                                              Blood-retinal barrier (BRB) function was assayed by dete
51 he structure and integrity of the retina and blood-retinal barrier (BRB) in the eye.
52 p54/PSF heterodimer may contribute to normal blood-retinal barrier (BRB) induction in vivo.
53  studies, functional MRI was used to measure blood-retinal barrier (BRB) integrity after Gd-DTPA inje
54               In a subgroup of male SD rats, blood-retinal barrier (BRB) integrity was also assessed
55                            In vertebrates, a blood-retinal barrier (BRB) is established by tight junc
56                             Breakdown of the blood-retinal barrier (BRB) is linked to vision loss in
57 cular endothelial cells comprising the inner blood-retinal barrier (BRB) is mediated by the GLUT1 glu
58 scular permeability due to alteration of the blood-retinal barrier (BRB) is one of the major complica
59                                     In vivo, blood-retinal barrier (BRB) leakage was studied using th
60 nts are crucial for retinal angiogenesis and blood-retinal barrier (BRB) maturation.
61  block vascular permeability and restore the blood-retinal barrier (BRB) may lead to new therapies.
62 ngements of the blood-brain barrier (BBB) or blood-retinal barrier (BRB) occur in disorders ranging f
63        These data suggest differences in the blood-retinal barrier (BRB) of mice and rabbits and indi
64                                              Blood-retinal barrier (BRB) permeability in uninfected d
65 f this study was to determine to what extent blood-retinal barrier (BRB) permeability occurred during
66                                              Blood-retinal barrier (BRB) permeability surface area pr
67              Its absence has been related to blood-retinal barrier (BRB) permeability through delocal
68                                      Loss of blood-retinal barrier (BRB) properties induced by vascul
69                                          The blood-retinal barrier (BRB) serves as a physiological bo
70 fect of neutrophils in the alteration of the blood-retinal barrier (BRB) was further assessed in wild
71 Uveitis is characterised by breakdown of the blood-retinal barrier (BRB), allowing infiltration of im
72                             Breakdown of the blood-retinal barrier (BRB), as occurs in diabetic retin
73 ntry into the endothelial cells of the inner blood-retinal barrier (BRB).
74 trophin Dp71 gene induces a highly permeable blood-retinal barrier (BRB).
75 is important to measure the integrity of the blood-retinal barrier (BRB).
76 esion molecule (ICAM)-1 and breakdown of the blood-retinal barrier (BRB).
77 nto the deep layers of the retina and causes blood-retinal-barrier (BRB) dysfunction in mice.
78                                              Blood-retinal barrier [BRB] breakdown, characteristic of
79 ffected by hyperglycemia simultaneously with blood retinal barrier breakdown, suggesting that glial a
80 ular endothelial cell injury, apoptosis, and blood-retinal barrier breakdown (P<0.0001) but did not d
81  adhesion molecule-1 (ICAM-1) and results in blood-retinal barrier breakdown and capillary nonperfusi
82 receptor apoptosis, vascular telangiectasis, blood-retinal barrier breakdown and, later, intraretinal
83 IF-1alpha and VEGF increases and the related blood-retinal barrier breakdown are suppressed by inhibi
84 oteinases (MMPs) as a potential cause of the blood-retinal barrier breakdown at the onset of angiogen
85  drops significantly reduced leukostasis and blood-retinal barrier breakdown in a dose-dependent mann
86                                              Blood-retinal barrier breakdown in diabetic animals trea
87 dothelial cell apoptosis as a major cause of blood-retinal barrier breakdown in early diabetes.
88                                        Early blood-retinal barrier breakdown in experimental diabetes
89  role in the pathogenesis of blood-brain and blood-retinal barrier breakdown in vivo.
90                                              Blood-retinal barrier breakdown is markedly increased wi
91 ry cytokines that initiate neuronal loss and blood-retinal barrier breakdown seen in diabetic retinop
92 y produces a transient worsening of diabetic blood-retinal barrier breakdown via an HIF-1alpha-mediat
93                                              Blood-retinal barrier breakdown was assessed using (3)H-
94                             Diabetes-induced blood-retinal barrier breakdown was dose-dependently inh
95                                              Blood-retinal barrier breakdown was induced in rats with
96                             Spatially, early blood-retinal barrier breakdown was localized to the ret
97                                              Blood-retinal barrier breakdown was quantified using the
98  circulation with an anti-platelet antibody, blood-retinal barrier breakdown worsened in the diabetic
99 rrent study, diabetic vascular permeability (blood-retinal barrier breakdown) is demonstrated to resu
100 elial growth factor (VEGF) triggers diabetic blood-retinal barrier breakdown, and (2) identify the si
101 n apoptosis, oxidative stress, inflammation, blood-retinal barrier breakdown, and neuroprotection.
102  the diabetic retinal vasculature results in blood-retinal barrier breakdown, capillary nonperfusion,
103 iabetic retinal vasculature results in early blood-retinal barrier breakdown, capillary nonperfusion,
104 adhesion molecule-1 levels, leukostasis, and blood-retinal barrier breakdown, in a relevant animal mo
105 sening of diabetic retinopathy, specifically blood-retinal barrier breakdown, that follows the instit
106  cell death and serves, in part, to suppress blood-retinal barrier breakdown.
107 appaB DNA-binding activity, leukostasis, and blood-retinal barrier breakdown.
108 urs, endothelial cell injury ensues, as does blood-retinal barrier breakdown.
109 ocyte adhesion, endothelial cell injury, and blood-retinal barrier breakdown.
110 yte adhesion and endothelial cell injury and blood-retinal barrier breakdown.
111 ch reduced leukocyte adhesion and suppressed blood-retinal barrier breakdown.
112 the isotope-dilution method for quantitating blood-retinal barrier breakdown.
113  approach in the treatment of early diabetic blood-retinal barrier breakdown.
114 as the isotope-dilution method for measuring blood-retinal barrier breakdown.
115 model by determining retinal leukostasis and blood-retinal barrier breakdown.
116 titating vascular leakage and especially the blood-retinal barrier breakdown.
117 xtracted and assayed for leukocyte adhesion; blood-retinal barrier breakdown; VEGF, TNF-alpha, IL-1be
118 etinopathy increases the permeability of the blood-retinal barrier, but the specific vessels that bec
119  TGF-beta may contribute to breakdown of the blood-retinal barrier by stimulating endothelial cell MM
120                                              Blood-retinal barrier cells are known to exhibit a massi
121 racteristics of tight junctions in the outer blood-retinal barrier change during embryonic developmen
122        Macular oedema typically results from blood-retinal barrier disruption.
123 GF) plays a crucial role in breakdown of the blood-retinal barrier due to hyperpermeability in diabet
124 ivo was demonstrated that was accompanied by blood-retinal barrier dysfunction.
125 ontributing to the pathologic progression of blood-retinal barrier dysfunction.
126 agenase-like activity that may contribute to blood-retinal barrier dysfunction.
127 ssion of pathologic retinal angiogenesis and blood-retinal barrier dysfunction.
128  diabetic retinopathy and macular edema, the blood-retinal barrier fails to function properly, and th
129 ibitor (HDACi), ITF2357, in regulating outer blood-retinal barrier function and investigates the unde
130                                     Impaired blood-retinal barrier function leads to macular edema th
131 ivo Fluorescein angiography indicated normal blood-retinal barrier function.
132  enhanced apoptotic cell death, and impaired blood-retinal barrier function.
133 erentially contribute to the inner vs. outer blood-retinal barrier function.
134  in the cells comprising the inner and outer blood-retinal barriers: human retinal pigment epithelial
135 icrovascular disorder characterized by inner blood-retinal barrier (iBRB) breakdown and irreversible
136 port for fluids and solutes across the inner blood-retinal barrier (iBRB).
137 nce leukocytes cannot gain entry through the blood-retinal barrier, illustrating that microglia play
138 , through neutrophil recruitment, alters the blood-retinal barrier in diabetic retinopathy and, thus,
139 ricyte interactions during alteration of the blood-retinal barrier in diabetic retinopathy.
140 lity with implications for alteration of the blood-retinal barrier in diabetic retinopathy.
141 l pigmented epithelium (RPE) forms the outer blood-retinal barrier in the eye and its polarity is res
142 th diabetes and induces the breakdown of the blood-retinal barrier in vitro.
143 th diabetes and induces the breakdown of the blood-retinal barrier in vitro.
144  derangements observed in the diabetic inner blood-retinal barrier in vivo.
145 retinal thickness, intraocular pressure, and blood retinal barrier integrity.
146 l layer thickness, intraocular pressure, and blood retinal barrier integrity.
147 tion-dependent manner and that loss of inner blood-retinal barrier integrity induced by diabetes cont
148         We used retinal angiography to study blood-retinal barrier integrity.
149 fic systemic antibodies through the impaired blood-retinal barrier is higher in patients with neovasc
150                            Alteration of the blood-retinal barrier is the hallmark of this disease, c
151 helium (RPE), which helps maintain the outer blood-retinal barrier, is a local source for ET-1 and wh
152 olic parameters, key inflammatory mediators, blood-retinal barrier junction molecules, retinal struct
153 cations of diabetes is the alteration of the blood-retinal barrier, leading to retinal edema and cons
154 A may have a protective effect against outer blood-retinal barrier leakage associated with diabetic r
155 tein, the vitreous-plasma protein ratio, and blood-retinal barrier leakage by 3-, 1.7-, 3.1-, and 2.7
156 nd retinal PGE2 secretion, VEGF protein, and blood-retinal barrier leakage were estimated.
157 abetes-induced elevations in PGE2, VEGF, and blood-retinal barrier leakage.
158                      Disruption of the outer blood-retinal barrier (oBRB) is a central feature of ret
159 , but transporters for DHA uptake across the blood-retinal barrier or retinal pigment epithelium have
160 ansport, phagocytosis and formation of outer blood-retinal barrier, or possible involvement of JN exp
161                    Choroidal contribution or blood-retinal barrier permeability surface area product
162 hese results suggest that astrocytes enhance blood-retinal barrier properties, at least in part by in
163 rowth factor (VEGF)-induced breakdown of the blood-retinal barrier requires protein kinase C (PKC)bet
164 in ICAM-1, leukostasis, and breakdown of the blood-retinal barrier, suggesting that NOX2 is primarily
165 igmented epithelial (RPE) cells maintain the blood-retinal barrier, sustain retinal photoreceptor cel
166 d Fpn is expressed in cells constituting the blood-retinal barrier, the authors tested whether the re
167 litis" based on fundamental knowledge of the blood-retinal barrier, the neurovascular unit, and patho
168 lay important roles in the alteration of the blood-retinal barrier through proteolytic degradation of
169 ining retinal homeostasis and regulating the blood-retinal barrier through secreted factors.
170    There is no evidence of a blood-ocular or blood-retinal barrier to activated T cell blasts.
171  protein [anti-GFAP]) and to investigate the blood-retinal barrier using the tight junction markers z
172 onditions in the subretinal space, the outer blood-retinal barrier was disrupted by compromising reti
173 udy, the potential side effects on the outer blood-retinal barrier were examined.
174 at is highly enriched at the blood-brain and blood-retinal barriers, where it mediates Na(+)-dependen
175 esis during development and formation of the blood-retinal barrier, which is linked to significant do
176 lature itself that results in opening of the blood-retinal barrier with or without retinal vascular o

 
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