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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
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.
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
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
34 Diabetic retinopathy is characterized by blood-retinal barrier (BRB) breakdown and neurotoxicity.
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,
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
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
49 lop and characterize a quantitative assay of blood-retinal barrier (BRB) function in mice and to dete
53 studies, functional MRI was used to measure blood-retinal barrier (BRB) integrity after Gd-DTPA inje
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
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
65 f this study was to determine to what extent blood-retinal barrier (BRB) permeability occurred during
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
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
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
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
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
121 racteristics of tight junctions in the outer blood-retinal barrier change during embryonic developmen
123 GF) plays a crucial role in breakdown of the blood-retinal barrier due to hyperpermeability in diabet
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
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
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,
141 l pigmented epithelium (RPE) forms the outer blood-retinal barrier in the eye and its polarity is res
147 tion-dependent manner and that loss of inner blood-retinal barrier integrity induced by diabetes cont
149 fic systemic antibodies through the impaired blood-retinal barrier is higher in patients with neovasc
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
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
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
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
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