ライフサイエンスコーパス: BRB

1 BRB breakdown was quantified 24 hours later.

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

3 BRB permeability occurred as early as 4 hours and increa

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

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

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

7 BRB-ArrayTools can be downloaded at http://linus.nci.nih

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

9 BRB-ArrayTools is available at http://linus.nci.nih.gov/

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

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

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 nal vascularization and maintain the BBB and BRB.

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

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

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

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

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

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

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

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

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

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

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

28 Retinal leukostasis and BRB breakdown were simultaneously quantified by combinin

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

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

31 t are positively modulated by both PEITC and BRB.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 3NB), to regulate the blood retinal barrier (BRB) using two distinct experimental mouse models, laser

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 endothelial cells to form a fully functional BRB.

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

102 an be downloaded at http://linus.nci.nih.gov/BRB-ArrayTools.html.

103 ols is available at http://linus.nci.nih.gov/BRB-ArrayTools.html.

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

105 ce for ABCB1 transport activity at the human BRB.

106 ce for ABCB1 transport activity at the human BRB.

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

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

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

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

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

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

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

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

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

116 c denervation did not significantly increase BRB PS.

117 eoretinal VEGF protein levels, and increased BRB breakdown.

118 al occludin protein expression and increases BRB permeability.

119 < 0.05) and did not increase with increasing BRB PS'.

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

121 ediated VEGF expression and diabetes-induced BRB breakdown.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 imaging assay was developed to examine outer BRB breakdown.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 g that TNFalpha is essential for progressive BRB breakdown.

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

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

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

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

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

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

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

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

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

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

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

187 95 at 10 mg/kg (i.p.) effectively suppressed BRB breakdown in streptozotocin-diabetic Brown Norway ra

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

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

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

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

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

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

194 ctions that may regulate permeability at the BRB.

195 160 mg/kg/day) blocked the breakdown in the BRB and prevented the increases in formation of lipid pe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 akage confirmed a prominent breakdown of the BRB.

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

213 al purported vasopermeability factors on the BRB.

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

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

216 otential therapeutic strategy to restore the BRB.

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

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

219 Data were analyzed using the BRB ArrayTools system.

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

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

222 factors may not significantly contribute to BRB permeability.

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

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

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

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

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

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

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