ライフサイエンスコーパス: BRB

1 BRB breakdown was quantified 24 hours later.

2 BRB decreased expression of survival/proliferation-assoc

3 BRB loss in vivo was studied in the mouse oxygen-induced

4 BRB permeability occurred as early as 4 hours and increa

5 BRB PS (cm(3)/min) was measured using DCE-MRI and Gd-DTP

6 BRB reduced mRNA and protein expression levels of COX-2,

7 BRB was intact (P > 0.05) after saline and distilled wat

8 BRB-ArrayTools is a widely used software system for the

9 At week 25, BRB inhibited tumor multiplicity, the standard end point

10 nts of VEGF in the vitreous cavity induces a BRB breakdown even earlier than 3 days after implantatio

11 Ellagic acid, its metabolite urolithin A, BRB extract, and the anthocyanin metabolite protocatechu

12 Acute BRB of BP was 47% smaller in the women (3.3+/-0.5 versus

13 F neutralization, and the protection against BRB dysfunction was additive when both targets were inhi

14 Our previous work revealed that HHcy altered BRB in retinal endothelial cells in vivo.

15 -induced BRB breakdown by 93% (P < 0.05) and BRB breakdown in early experimental diabetes by 40.6% (P

16 GF and Norrin, coordinating angiogenesis and BRB formation.

17 activity regulates retinal angiogenesis and BRB maturation by modulating endothelial Norrin/beta-cat

18 activity, regulates retinal angiogenesis and BRB maturation remains unclear.

19 in signaling, which is essential for BBB and BRB function.

20 nal vascularization and maintain the BBB and BRB.

21 ssion, vitreal glutamate concentrations, and BRB leakage compared with nondiabetic control rats.

22 decreased vitreoretinal VEGF expression and BRB breakdown to levels similar to those observed in con

23 tein levels in retina and vitreous fluid and BRB breakdown compared with control nondiabetic rats.

24 vels (2.2-fold), leukostasis (1.9-fold), and BRB breakdown (2.1-fold, P < 0.01 for all), despite negl

25 retinal VEGF protein, vitreal glutamate, and BRB breakdown were then measured.

26 ent reduces neurotoxicity, inflammation, and BRB breakdown in diabetic animals through activities tha

27 icant suppression of retinal leukostasis and BRB breakdown in both early (72.4% and 82.6%, respective

28 s VEGF(164) mediates retinal leukostasis and BRB breakdown in early and established diabetes.

29 cing ICAM-1-mediated retinal leukostasis and BRB breakdown in vivo.

30 s, and the effect on retinal leukostasis and BRB breakdown was quantified.

31 Retinal leukostasis and BRB breakdown were compared in nondiabetic rats receivin

32 Retinal leukostasis and BRB breakdown were simultaneously quantified by combinin

33 hibition of diabetic retinal leukostasis and BRB breakdown with EYE001 in early and established diabe

34 ores tight junction complex organization and BRB properties in a beta-catenin-dependent manner.

35 Because both PEITC and BRB maintain near-normal levels of expression of these 5

36 t are positively modulated by both PEITC and BRB.

37 to streptozotocin-induced diabetic rats, and BRB breakdown was quantified.

38 ls down-regulated beta-catenin signaling and BRB gene expression that is rescued by Ctnnb1 overactiva

39 response that may alter retina structure and BRB integrity following long-term spaceflight.

40 quired for developmental vascularization and BRB formation.

41 rupted retinal vascular perfusion as well as BRB integrity.

42 ed by terminal dUTP nick-end labeling assay; BRB function by quantifying extravasation of bovine seru

43 We assessed BRB protection in diabetic rats through use of species-s

44 e of TNFalpha had no effect on DR-associated BRB breakdown, even though it prevented retinal leukosta

45 s of premenopausal women, whereas attenuated BRB of BP may help explain less effective BP regulation

46 g Ang2 or activating Tie2 greatly attenuates BRB breakdown, suggesting potential therapeutic approach

47 lood-retina barrier and blood-brain barrier (BRB/BBB) are selective and semipermeable and are critica

48 ther disruption of the blood-retina barrier (BRB) increases spread of murine cytomegalovirus (MCMV) t

49 The breakdown of the blood-retina barrier (BRB) is a common feature of diabetic retinopathy.

50 The integrity of the blood-retina barrier (BRB) is crucial for phototransduction and vision, by tig

51 ar development, normal blood-retina barrier (BRB) permeability, and retinal function.

52 The outer blood-retina barrier (BRB) separates the neural retina from the choroidal vasc

53 1) is expressed at the blood-retina barrier (BRB), where it may control distribution of drugs from bl

54 The blood-retina barrier (BRB), which is disrupted in diabetic retinopathy (DR) an

55 rain barrier (BBB) and blood-retina barrier (BRB).

56 that Edn2 damages the blood-retinal barrier (BRB) and that this is mediated by interactions with the

57 y is characterized by blood-retinal barrier (BRB) breakdown and neurotoxicity.

58 Blood-retinal barrier (BRB) breakdown and related vascular changes are implicat

59 tinal vasculature and blood-retinal barrier (BRB) breakdown and to determine whether endogenous VEGF(

60 ate the mechanisms of blood-retinal barrier (BRB) breakdown at a global level, we studied the gene re

61 lovastatin mitigates blood-retinal barrier (BRB) breakdown in db/db mice.

62 Blood-retinal barrier (BRB) breakdown is a hallmark of diabetic retinopathy, bu

63 Blood-retinal barrier (BRB) breakdown is responsible for multiple ocular diseas

64 ) protein levels, and blood-retinal barrier (BRB) breakdown of the animals were measured.

65 species (ROS) in the blood-retinal barrier (BRB) breakdown that characterizes the early stages of va

66 Blood-retinal barrier (BRB) breakdown was quantified using the Evans blue (EB)

67 The blood-retinal barrier (BRB) consists of tightly interconnected capillary endoth

68 LPC), are involved in blood-retinal barrier (BRB) damage during diabetic retinopathy.

69 ransport at the inner blood-retinal barrier (BRB) do not completely retain several in vivo functions,

70 (VEGF) contributes to blood-retinal barrier (BRB) dysfunction in several blinding eye diseases, inclu

71 y studying functional blood-retinal barrier (BRB) formation in mice, we found that immature vessel le

72 quantitative assay of blood-retinal barrier (BRB) function in mice and to determine the effect of sev

73 Blood-retinal barrier (BRB) function was assayed by determining extravasation o

74 ity of the retina and blood-retinal barrier (BRB) in the eye.

75 contribute to normal blood-retinal barrier (BRB) induction in vivo.

76 I was used to measure blood-retinal barrier (BRB) integrity after Gd-DTPA injection intravenously and

77 roup of male SD rats, blood-retinal barrier (BRB) integrity was also assessed with dynamic contrast-e

78 In vertebrates, a blood-retinal barrier (BRB) is established by tight junctions (TJs) present in

79 Breakdown of the blood-retinal barrier (BRB) is linked to vision loss in DR and AMD.

80 comprising the inner blood-retinal barrier (BRB) is mediated by the GLUT1 glucose transporter, chang

81 to alteration of the blood-retinal barrier (BRB) is one of the major complications in early diabetes

82 In vivo, blood-retinal barrier (BRB) leakage was studied using the Evans Blue dye techni

83 inal angiogenesis and blood-retinal barrier (BRB) maturation.

84 ility and restore the blood-retinal barrier (BRB) may lead to new therapies.

85 rain barrier (BBB) or blood-retinal barrier (BRB) occur in disorders ranging from stroke, cancer, dia

86 st differences in the blood-retinal barrier (BRB) of mice and rabbits and indicate that penetration t

87 Blood-retinal barrier (BRB) permeability in uninfected diabetic mice also was d

88 ermine to what extent blood-retinal barrier (BRB) permeability occurred during experimental Bacillus

89 Blood-retinal barrier (BRB) permeability surface area product (PS) was measured

90 e has been related to blood-retinal barrier (BRB) permeability through delocalization and down-regula

91 Loss of blood-retinal barrier (BRB) properties induced by vascular endothelial growth f

92 The blood-retinal barrier (BRB) serves as a physiological boundary regulating the p

93 3NB), to regulate the blood retinal barrier (BRB) using two distinct experimental mouse models, laser

94 the alteration of the blood-retinal barrier (BRB) was further assessed in wild-type C57BL/6J mice int

95 Breakdown of the blood-retinal barrier (BRB), as occurs in diabetic retinopathy and other chroni

96 and breakdown of the blood-retinal barrier (BRB).

97 al cells of the inner blood-retinal barrier (BRB).

98 es a highly permeable blood-retinal barrier (BRB).

99 the integrity of the blood-retinal barrier (BRB).

100 the retina and causes blood-retinal-barrier (BRB) dysfunction in mice.

101 Blood-retinal barrier [BRB] breakdown, characteristic of diabetic retinopathy (

102 ern of changes in the group without baseline BRB permeability alterations, as probed by psychophysica

103 ts of the well-tolerated alkaloid Berberine (BRB), used for treating metabolic disorders, were studie

104 ctive strategy for the development of better BRB/BBB models and novel EC barrier-inducing therapeutic

105 an) and less effective baroreflex buffering (BRB) of BP (potentiation of the systolic BP [SBP] respon

106 cid inhibited drug efflux in CRPC cells, but BRB extract and PCA did not.

107 Ellagic acid increased, but BRB extract inhibited, microtubule assembly.

108 and indicate need for further research, but BRB consumption appears safe.

109 total nitrite levels were also decreased by BRB in papillomas.

110 tored to near-normal levels of expression by BRB.

111 muM might be mediated, at least in part, by BRB-induced impairment of oxidative phosphorylation and

112 unction converges in protection of capillary BRB integrity.

113 retinal vessels surprisingly does not cause BRB disintegration, it sensitizes retinal vascular endot

114 uorum-sensing mutant B. cereus strain caused BRB permeability comparable to that of wild-type B. cere

115 thesized that excess formation of ROS causes BRB breakdown in diabetes.

116 nt retinal leakage into the vitreous cavity (BRB breakdown) of the VEGF-implanted eyes.

117 In this context, BRB triggered mitochondrial dysfunction and aberrant cel

118 nificantly different (P > 0.05) from control BRB PS values.

119 l cell gene expression program that controls BRB integrity.

120 the VEGF in vitro release study, this 3-day BRB breakdown corresponded to a total sustained release

121 an important mediator of leukocyte-dependent BRB breakdown secondary to VEGF.

122 At 3 months of diabetes, BRB breakdown was significantly suppressed and at 6 mont

123 nhibition of VEGF-induced and early diabetic BRB breakdown with aprotinin indicates that azurocidin m

124 se were compared with a group with disrupted BRB (with normal fundus or initial DR) and normal contro

125 lpha nor inflammation is essential for early BRB breakdown in DR in either model of diabetes.

126 lpha nor inflammation is necessary for early BRB breakdown in DR, TNFalpha is critical for later comp

127 related ANS support of BP and less effective BRB of BP than men of similar age.

128 can be proposed to mitigate diabetes-evoked BRB breakdown.

129 We examined BRB integrity and vasculature in Cav-1 knockout mice and

130 naling through beta-catenin was required for BRB restoration, but glycogen synthase kinase 3 alpha/be

131 osis governs the development of a functional BRB, and suppression of transcytosis is a principal cont

132 endothelial cells to form a fully functional BRB.

133 in order to re-establish a proper functional BRB and retina homeostasis thus preventing retina from o

134 onth diabetic mice had significantly greater BRB permeability than control mice.

135 ce for ABCB1 transport activity at the human BRB.

136 ce for ABCB1 transport activity at the human BRB.

137 xhibited an eightfold increase (P < 0.05) in BRB PS compared to that in control animals.

138 NMF analysis plug-in is freely available in BRB-ArrayTools for non-commercial users.

139 There was no significant difference in BRB permeability between control and 1-month uninfected

140 We have developed a NMF analysis plug-in in BRB-ArrayTools for unsupervised sample clustering of mic

141 strated a correlation between an increase in BRB permeability and an increase in EBE incidence, suppo

142 out mice and found a significant increase in BRB permeability, compared with wild-type controls, with

143 eated rats exhibited a threefold increase in BRB PS (P < 0.05) compared to eyes injected with HSA.

144 s and glia, but the role of the pericytes in BRB regulation is not fully understood.

145 ical resistance reduction induced by VEGF in BRB models in vitro and significantly increased transend

146 c denervation did not significantly increase BRB PS.

147 eoretinal VEGF protein levels, and increased BRB breakdown.

148 al occludin protein expression and increases BRB permeability.

149 < 0.05) and did not increase with increasing BRB PS'.

150 Aprotinin inhibited azurocidin-induced BRB breakdown by more than 95% (P < 0.05).

151 ediated VEGF expression and diabetes-induced BRB breakdown.

152 lar endothelial growth factor (VEGF)-induced BRB breakdown, rats were treated intravenously with apro

153 otinin significantly suppressed VEGF-induced BRB breakdown by 93% (P < 0.05) and BRB breakdown in ear

154 PCA allowed stratification of VEGF-induced BRB dysfunction and inhibitory effects of bevacizumab th

155 vivo, ANP significantly reduced VEGF-induced BRB leakage and the size of laser-induced choroidal neov

156 VAP is an essential cofactor in VEGF-induced BRB permeability and may become an interesting novel tar

157 xpression resulted in decreased VEGF-induced BRB permeability of fluorescent tracers, both in vivo an

158 in with VEGF completely ablated VEGF-induced BRB permeability to Evans Blue-albumin.

159 ANP significantly reversed VEGF-induced BRB TEER reduction in both HuREC and ARPE-19 cells, mode

160 nesis, and Norrin, a Wnt ligand that induces BRB properties, are decreased after activity blockade.

161 Six hours after VEGF injection, BRB breakdown was quantified in the injected eye and was

162 es and pathways possibly implicated in inner BRB breakdown during non-infectious posterior uveitis.

163 d lamc3) was validated at the level of inner BRB cells.

164 ers the expression and distribution of inner BRB GLUT1, changes in immunoreactive retinal endothelial

165 diabetic retinopathy, breakdown of the inner BRB (iBRB) results in damage to the neurovascular unit a

166 to evaluate drug transport across the inner BRB help us understand the role of this barrier in maint

167 nsatory downregulation of GLUT1 on the inner BRB in an animal model of long-standing diabetes.

168 er, changes in GLUT1 expression on the inner BRB in long-standing diabetes mellitus may have a direct

169 pregulation of GLUT1 expression at the inner BRB occurs in long-standing diabetes mellitus with minim

170 ful tool to study transport across the inner BRB.

171 Interestingly, BRB lowered the apoptotic threshold of ABT-199/Venetocla

172 This method is incorporated into BRB-ArrayTools version 3.0.

173 The effects of processing on other key BRB compound groups, including ellagitannins, are also d

174 ii) vasoinhibins can block TRPV4 to maintain BRB and endothelial permeability.

175 endothelial CYP2J2 overexpression maintained BRB integrity after ischemia-reperfusion injury and cons

176 eta signalling is expendable for maintaining BRB integrity in adult mice.

177 hese findings implicate Cav-1 in maintaining BRB integrity in retinal vasculature and suggest a previ

178 o investigate whether azurocidin may mediate BRB breakdown in early diabetes, aprotinin or vehicle wa

179 on can effectively prevent diabetes-mediated BRB dysfunction and that LPC impacts on the retinal vasc

180 In the animal models, BRB permeability was quantified by intravenous injection

181 After 3 months, BRB permeability was quantified by intravenous injection

182 ice deficient for Ntn1 or Unc5b display more BRB leakage at the arterial end of the vasculature, whil

183 DCE-MRI BRB PS measurements are expected to provide a useful sur

184 xogenous VEGF restores vessel growth but not BRB function, whereas stabilizing beta-catenin in endoth

185 ated that the cytotoxic/cytostatic action of BRB at 10-30 muM might be mediated, at least in part, by

186 nique was then used to compare the amount of BRB breakdown that occurs after intravitreous injection

187 n mice provides a quantitative assessment of BRB function that is normalized and can therefore be com

188 The quantifiable change of BRB breakdown by the contrast-enhanced MRI method is ide

189 ols gave strong indication of disturbance of BRB integrity.

190 Comparison of the extent and duration of BRB breakdown after intravitreous injection of vasoactiv

191 derstanding the mechanism of GC induction of BRB properties may provide novel therapies for macular e

192 ases in vitreoretinal VEGF and inhibition of BRB breakdown in diabetic rats.

193 ickness increased (P < 0.05) without loss of BRB integrity.

194 retinal capillaries associates with loss of BRB properties and correlates with increased vascular pe

195 g is critical in formation and maturation of BRB through active recruitment of pericytes onto growing

196 ouping has its basis in shared mechanisms of BRB disruption.

197 n Comparison kit is developed as a module of BRB-ArrayTools for discovering biologically meaningful p

198 rison kit is freely available as a module of BRB-ArrayTools for non-commercial users.

199 Using this module of BRB-ArrayTools, researchers can efficiently analyze pre-

200 l and cycling armamentarium, the presence of BRB affects this process.

201 anges that result from thermal processing of BRB powder into a nectar beverage.

202 not seem to contribute to the regulation of BRB and RPE permeability by vasoinhibins under diabetic

203 ts suggest a novel tumor suppressive role of BRB through inhibition of COX-2, iNOS, and c-Jun.

204 edominately in retinal venules, the sites of BRB breakdown, cell adhesion, and extravasation, from da

205 ture research on the impact of processing on BRB product bioactivity.

206 antigen presentation at the inner and outer BRB, respectively.

207 imaging assay was developed to examine outer BRB breakdown.

208 thors demonstrated the significance of outer BRB breakdown in diabetes and ischemia, which will have

209 To determine the significance of outer BRB breakdown in diabetic retinopathy, the outer BRB-spe

210 The number of severe outer BRB leakage sites is inversely proportional to the size

211 leakages of macromolecules through the outer BRB in diabetic and ischemic rodents were detected with

212 zing macromolecules leaked through the outer BRB in rodents was developed.

213 indicate that penetration through the outer BRB may be needed for topically administered drugs to ex

214 E-19 cells, modeling the inner and the outer BRB, respectively.

215 The outer BRB-specific leakage in diabetic and ischemic rodents wa

216 The outer BRB-specific leakage of fluorescent macromolecules was v

217 breakdown in diabetic retinopathy, the outer BRB-specific leakage of macromolecules in diabetic and i

218 r edema and other ocular diseases with outer BRB defects.

219 t, deep plexus angiogenesis and paracellular BRB maturation are accelerated in Gnat1(-/-) retinas, wh

220 in deep plexus angiogenesis and paracellular BRB maturation.

221 sociated with death and enucleation, passive BRB PS in experimental diabetes.

222 rs per rat in animals treated with NMBA plus BRB (P < 0.005).

223 terminal fragments of prolactin that prevent BRB breakdown during diabetes.

224 l barrier permeability surface area product (BRB PS') was determined using MRI after Gd-DTPA injectio

225 g that TNFalpha is essential for progressive BRB breakdown.

226 target for the prevention of the progressive BRB breakdown, retinal leukostasis, and apoptosis associ

227 vere, relatively delayed, and more prolonged BRB breakdown.

228 VEGF caused prominent BRB breakdown at 6 hours that returned to near normal by

229 thetic diet containing 5% black raspberries (BRB) for the duration of the bioassay (25 weeks).

230 Black raspberries (BRB) have anti-cancer effects, but have not been evaluat

231 ontaining 5% freeze-dried black raspberries (BRB) instead of PEITC.

232 In 2-, 4-, and 6-month diabetic rats, BRB PS was not significantly different (P > 0.05) from c

233 BRI also significantly reduced BRB breakdown in aged diabetic rats at 10 weeks after ST

234 presence of VEGF or laser injury by reducing BRB permeability in part by modulating sphingomyelinase

235 The molecules and mechanisms regulating BRB integrity and pathophysiology are not fully elucidat

236 a potential therapeutic target for relieving BRB impairments.

237 ng beta-catenin in endothelial cells rescues BRB dysfunction but not vessel formation.

238 antagonists (RN-1734 and GSK2193874) resolve BRB breakdown in diabetic rats.

239 (GSK-3alpha/beta) inhibition did not restore BRB properties.

240 umin, and a single norrin injection restored BRB properties.

241 CYP2J2 metabolites restored BRB integrity in the presence of ANXA1.

242 nal angiogenesis deficits, but also restores BRB and BBB function.

243 e tested the hypothesis that norrin restores BRB properties after VEGF-induced vascular permeability

244 itreoretinal VEGF protein levels and retinal BRB leakage in the diabetic rats.

245 affected in normal B lymphocytes at the same BRB concentrations.

246 95 at 10 mg/kg (i.p.) effectively suppressed BRB breakdown in streptozotocin-diabetic Brown Norway ra

247 Given that BRB breakdown is involved in retinal inflammation and th

248 These results indicate that BRB permeability occurs during the early stages of exper

249 ed and maintained in the BRB and reveal that BRB gene expression is regulated at the level of endothe

250 The BRB is composed of endothelial cell tight junctions, per

251 The BRB of the left eye of normal and immunosuppressed mice

252 The BRB was assessed at 1, 1.5, 3, and 6 months.

253 onstants for radiotracer transfer across the BRB (K1, k2) and total retinal distribution volume VTDur

254 onstants for radiotracer transfer across the BRB (K1, k2) and total retinal distribution volume VTRes

255 orchestrate immune cell migration across the BRB, with implications for inflammatory ocular diseases

256 , through neutrophil recruitment, alters the BRB in DR and, thus, serves as a potential novel therape

257 ctions that may regulate permeability at the BRB.

258 Ly6C+ monocytes crossed the BRB proximal to perivascular macrophages.

259 160 mg/kg/day) blocked the breakdown in the BRB and prevented the increases in formation of lipid pe

260 onation is established and maintained in the BRB and reveal that BRB gene expression is regulated at

261 al ocular fundus and absent breakdown of the BRB (confirmed with vitreous fluorometry).

262 as delayed, but substantial breakdown of the BRB after injection of TNF-alpha.

263 ssion in the maintenance and function of the BRB and may provide a model for studying pathologic cond

264 y regulate the tight junction complex of the BRB and may restore barrier properties after cytokine-in

265 betes, independently of the breakdown of the BRB and onset of vasculopathy.

266 cells, which influence the integrity of the BRB and prevent retinal edema, became gliotic and expres

267 that early diabetes causes breakdown of the BRB by a mechanism involving the action of reactive nitr

268 es in susceptibility to the breakdown of the BRB in diabetic retinopathy using two rat models.

269 Breakdown of the BRB leads to the development of retinal diseases.

270 tracellular proteinases in alteration of the BRB seen in diabetic retinopathy.

271 administered Edn2 exhibited breakdown of the BRB with increased vascular leakage, vascular endothelia

272 l pigment epithelium (RPE) components of the BRB, and that TRPV4-selective antagonists (RN-1734 and G

273 lso caused relatively rapid breakdown of the BRB, but its effect was more prolonged than that caused

274 atially and temporally with breakdown of the BRB, cell adhesion, and extravasation.

275 ICAM-1 and P-selectin, and breakdown of the BRB, leading to transendothelial migration of leukocytes

276 is have delayed or precocious sealing of the BRB, respectively.

277 Despite the importance of the BRB, retinal perivascular macrophage function remains un

278 M-1) and a decrease in the expression of the BRB-related tight junction protein, Zonula occludens-1 (

279 akage confirmed a prominent breakdown of the BRB.

280 clusion, Edn2 has detrimental effects on the BRB and Muller cells that involve interactions with the

281 al purported vasopermeability factors on the BRB.

282 creases in VEGF and ICAM-1 and preserves the BRB by a process involving blockade of diabetes/high-glu

283 igated whether absence of PLVAP protects the BRB from VEGF-induced permeability.

284 otential therapeutic strategy to restore the BRB.

285 DCE-MRI demonstrated that the BRB becomes leaky immediately before death, possibly cau

286 Using the BRB array program, we identified genes differentially ex

287 Data were analyzed using the BRB ArrayTools system.

288 significantly higher in the eye in which the BRB had been disrupted.

289 re significantly higher in eyes in which the BRB had been disrupted.

290 Endothelial cells (ECs) within the BRB/BBB are tightly coupled, express high levels of Clau

291 factors may not significantly contribute to BRB permeability.

292 e mechanism by which diabetes contributes to BRB breakdown through proteolytic degradation of VE-cadh

293 allmarks of diabetic retinopathy (DR) due to BRB disruption.

294 was compared by microarrays, analyzed using BRB ArrayTools (National Cancer Institute, Bethesda, MD)

295 oss of function causes predominantly venular BRB leakage.

296 The barrier properties of in vitro BRB models were assessed by measuring transendothelial e

297 Here we studied whether BRB and some of their constituents interact with docetax

298 rescued by Ctnnb1 overactivation, along with BRB integrity.

299 treatment of ocular diseases associated with BRB leakage, such as diabetic macular edema and retinopa

300 tic strategies in dealing with diseases with BRB breakdown and macular oedema such as diabetic retino

301 e analyzed by using univariate t test within BRB tools.