ライフサイエンスコーパス: retinal neovascularization

1 oxygen (variable oxygen exposure) to induce retinal neovascularization.

2 n a dose-dependent manner, resulting in less retinal neovascularization.

3 ity, to examine the roles of MMP-2 and -9 in retinal neovascularization.

4 e an important factor in the pathogenesis of retinal neovascularization.

5 VEGF expression, in vivo in ischemia-induced retinal neovascularization.

6 ge role in diabetic maculapathy and diabetic retinal neovascularization.

7 ty and diabetic retinopathy are often due to retinal neovascularization.

8 signaling, suggesting a possible therapy for retinal neovascularization.

9 documented protein kinase CK2 involvement in retinal neovascularization.

10 hypothesis in a well-characterized model of retinal neovascularization.

11 for feedback inhibition of angiogenesis and retinal neovascularization.

12 H oxidase in causing VEGF overexpression and retinal neovascularization.

13 field loss, vitrectomy, DME development, and retinal neovascularization.

14 s, normalized VEGF expression, and prevented retinal neovascularization.

15 -stimulated increases in VEGF expression and retinal neovascularization.

16 and pStat3 was observed in association with retinal neovascularization.

17 paramount importance in the pathogenesis of retinal neovascularization.

18 tion and VEGF production in a mouse model of retinal neovascularization.

19 w prospects for their therapeutic utility in retinal neovascularization.

20 tors in endothelial cells are protected from retinal neovascularization.

21 d to room air for 5 days (P12-P17) to induce retinal neovascularization.

22 ptor uPAR is essential to the development of retinal neovascularization.

23 ences between physiological and pathological retinal neovascularization.

24 ignal intermediates can significantly retard retinal neovascularization.

25 etinal vascular development and pathological retinal neovascularization.

26 in a significant reduction in the extent of retinal neovascularization.

27 ceptor (IGF-1R) are associated with abnormal retinal neovascularization.

28 ctions regulate the extent of oxygen-induced retinal neovascularization.

29 n-induced retinal ischemia without provoking retinal neovascularization.

30 RORalpha substantially suppressed pathologic retinal neovascularization.

31 ble NOS (iNOS) suppresses choroidal, but not retinal neovascularization.

32 f extracellular proteinase expression during retinal neovascularization.

33 Brown Norway (BN) rats with ischemia-induced retinal neovascularization.

34 a rat strain difference in susceptibility to retinal neovascularization.

35 itors of eNOS may be needed for treatment of retinal neovascularization.

36 s on P13 and P15, during the early stages of retinal neovascularization.

37 al endothelial cell growth and migration and retinal neovascularization.

38 d in the retina of experimental animals with retinal neovascularization.

39 lled and eyes enucleated for quantitation of retinal neovascularization.

40 ed in maintaining homeostasis and preventing retinal neovascularization.

41 e, or IPDX showed a significant reduction in retinal neovascularization.

42 tnatal days 7 through 12) was used to create retinal neovascularization.

43 s plays a permissive role in ischemia-driven retinal neovascularization.

44 xpression in tumors and during developmental retinal neovascularization.

45 tinopathy, they developed the same amount of retinal neovascularization.

46 nt and for ischemia-related tumor, iris, and retinal neovascularization.

47 GF2 in the retina affects the development of retinal neovascularization.

48 hyperoxia-induced retinopathy that exhibits retinal neovascularization.

49 pression are not likely to be complicated by retinal neovascularization.

50 essary nor sufficient for the development of retinal neovascularization.

51 duced Src-PLD1-PKCgamma-cPLA2 activation and retinal neovascularization.

52 duced Src-PLD1-PKCgamma-cPLA2 activation and retinal neovascularization.

53 al outcomes in rodent models of diabetes and retinal neovascularization.

54 S-antigen-induced uveitis and laser-induced retinal neovascularization.

55 d modulation of MEF2C may prevent pathologic retinal neovascularization.

56 n effective strategy for treating pathologic retinal neovascularization.

57 g its inhibitory effects on ischemia-induced retinal neovascularization.

58 e results in enhanced tumor angiogenesis and retinal neovascularization.

59 netic deletion suppressed both choroidal and retinal neovascularization.

60 LD1-PKCgamma signaling in retina, leading to retinal neovascularization.

61 ion of PDGF-DD suppressed both choroidal and retinal neovascularization.

62 or mechanism by which omega3-PUFAs attenuate retinal neovascularization.

63 RNA approach also suppressed hypoxia-induced retinal neovascularization.

64 identify the genes and pathways involved in retinal neovascularization.

65 RAIL(-/-) mice had a significant increase in retinal neovascularization.

66 EGF-B targeting inhibited both choroidal and retinal neovascularization.

67 enesis and discover novel drugs that inhibit retinal neovascularization.

68 ascular endothelial growth factor (VEGF) and retinal neovascularization.

69 in the retinas of mice with hypoxia-induced retinal neovascularization.

70 nd dose-dependent deficiency of the expected retinal neovascularization.

71 pproach for ocular diseases characterized by retinal neovascularization.

72 r obstruction (23%), retinal traction (20%), retinal neovascularization (6%), and retinal hole with d

73 ther species of PEDF significantly inhibited retinal neovascularization (83% for PEDF A and 55% for P

74 ischemic insult typically leads to aberrant retinal neovascularization, a major cause of blindness.

75 -FasL interaction plays an important role in retinal neovascularization after hyperoxia-induced injur

76 l tube formation in vitro and in vivo during retinal neovascularization after induction of VEGF expre

77 p.)-injected rBPI21 reduced ischemia-induced retinal neovascularization and diabetes-induced retinal

78 onditional knockout strain, but pathological retinal neovascularization and growth of heterotopically

79 cts developmental angiogenesis, pathological retinal neovascularization and heterotopic tumor growth.

80 c-abl is required for the hyperoxia-induced retinal neovascularization and hyperoxia-induced decreas

81 as a comprehensive resource for the study of retinal neovascularization and identification of potenti

82 Ischemia-induced hypoxia elicits retinal neovascularization and is a major component of s

83 ory effects of adiponectin overexpression on retinal neovascularization and leukocyte adhesion were a

84 suggest calcitriol is a potent inhibitor of retinal neovascularization and may be of benefit in the

85 exhibit critical features of MacTel such as retinal neovascularization and photoreceptor degeneratio

86 studies have shown that angiostatin inhibits retinal neovascularization and reduces retinal vascular

87 ly to be useful adjuncts in the treatment of retinal neovascularization and therapies designed to inc

88 d c-Met in the initiation and development of retinal neovascularization and to determine whether inhi

89 rference as a potential strategy to suppress retinal neovascularization and to prevent proliferative

90 lls and in a mouse model of ischemia-induced retinal neovascularization and to study the regulation o

91 TM significantly inhibits retinal neovascularization and VEGF production in a mous

92 xynucleotides against murine VEGF to inhibit retinal neovascularization and VEGF synthesis in a murin

93 iogenesis is increased in some tissues (e.g. retinal neovascularization) and decreased in others (e.g

94 ecreased level of Matrigel plug and neonatal retinal neovascularization, and aortas isolated from Rap

95 cause of new blindness in young patients is retinal neovascularization, and in the elderly is choroi

96 RORalpha is a novel regulator of pathologic retinal neovascularization, and RORalpha inhibition may

97 A6 peptide showed significant inhibition of retinal neovascularization, and the response was dose de

98 creased in a mouse model of ischemia-induced retinal neovascularization, and VEGF induced time- and d

99 ion is highly enhanced at the early stage of retinal neovascularization, and we found simultaneous re

100 Diseases characterized by retinal neovascularization are among the principal cause

101 rgeting pathological, but not physiological, retinal neovascularization are outlined.

102 hypoxia, VENIRKO mice show a 57% decrease in retinal neovascularization as compared with controls.

103 ression patterns in adult homeostasis and in retinal neovascularization associated with diabetes.

104 le human paradigm: spontaneous regression of retinal neovascularization associated with long-standing

105 d increased superoxide formation in areas of retinal neovascularization associated with relative reti

106 njection of 100 ng of digoxin at P12 reduced retinal neovascularization by >70% at P17.

107 ctin attenuated hypoxia-induced pathological retinal neovascularization by 35% in wild-type mice and

108 al administration of alpha-defensins reduced retinal neovascularization by 45% and 60%, respectively,

109 mRNA expression and significantly suppressed retinal neovascularization by approximately 40%.

110 nepafenac inhibits CNV and ischemia-induced retinal neovascularization by decreasing production of V

111 h CD13/APN inhibitors significantly impaired retinal neovascularization, chorioallantoic membrane ang

112 imals demonstrated a significant decrease in retinal neovascularization compared with control animals

113 hy (OIR) developed significantly less severe retinal neovascularization compared with wild-type (Wt)

114 but showed no difference in ischemia-induced retinal neovascularization compared with wild-type mice.

115 d no significant difference in the amount of retinal neovascularization compared with wild-type mice.

116 Retinal neovascularization decreased with increasing PAI

117 F therapy to prevent further vision loss and retinal neovascularization due to extensive retinal isch

118 optic disk demonstrate a higher incidence of retinal neovascularization due to heat-induced obstructi

119 o ischemia-induced retinopathy, pathological retinal neovascularization during ischemia was exacerbat

120 -2 in development of retinal vasculature and retinal neovascularization during oxygen-induced ischemi

121 ostnatal retinal vascularization, as well as retinal neovascularization during oxygen-induced ischemi

122 natal development of retinal vasculature and retinal neovascularization during oxygen-induced ischemi

123 mouse and human data indicate that reactive retinal neovascularization either fails to develop or re

124 hough chemical- and injury-induced models of retinal neovascularization exist, the need for a genetic

125 of CCN1 significantly decreases pathological retinal neovascularization following OIR.

126 tuation is more complex for ischemia-induced retinal neovascularization for which NO produced in endo

127 PPARgamma-mediated effect of omega3-PUFAs on retinal neovascularization formation and retinal angioge

128 by later vascular signs of DR, specifically retinal neovascularization, formation of new capillary b

129 vascular cells from tissues of patients with retinal neovascularization from PDR, we examined the eff

130 e presumed ocular histoplasmosis syndrome or retinal neovascularization from proliferative diabetic r

131 The association of retinal hypoxia with retinal neovascularization has been recognized for decad

132 Do agents that inhibit retinal neovascularization have any effect on choroidal

133 n of the NISAs RFE-007 and RFE-011 inhibited retinal neovascularization in a dose-dependent manner, c

134 fic inhibitors were tested for inhibition of retinal neovascularization in a mouse model of oxygen-in

135 16K hPRL inhibited retinal neovascularization in a mouse model of oxygen-in

136 to determine the effect of the ribozymes on retinal neovascularization in a mouse model of oxygen-in

137 (Pdeb(rd1)/Pdeb(rd1)) fail to mount reactive retinal neovascularization in a mouse model of oxygen-in

138 Captopril reduces retinal neovascularization in a mouse model of oxygen-in

139 eptor (EGFR) signaling, reduces pathological retinal neovascularization in a mouse model of oxygen-in

140 , was reported to protect against pathologic retinal neovascularization in a mouse model of oxygen-in

141 ic molecule, carboxyamido-triazole (CAI), on retinal neovascularization in a mouse model.

142 The extent of retinal neovascularization in a mouse OIR model was redu

143 iogenic inhibitor, inhibits ischemia-induced retinal neovascularization in a rat model.

144 We developed a novel model of retinal neovascularization in adult mice to examine the

145 AR interactions could suppress the extent of retinal neovascularization in an animal model of ischemi

146 re during normal development but had reduced retinal neovascularization in an OIR protocol.

147 Since VEGF is required for iris and retinal neovascularization in animal models of retinal i

148 dies have demonstrated partial inhibition of retinal neovascularization in animal models using antago

149 xia followed by normoxia induced significant retinal neovascularization in BN rats but not in SD rats

150 iogenesis may define new targets to suppress retinal neovascularization in diabetes and other ocular

151 ar, vessel loss resulting in hypoxia induces retinal neovascularization in diabetic retinopathy and i

152 CAI almost completely abolished retinal neovascularization in group A, and neovascular f

153 or investigation and treatment of peripheral retinal neovascularization in her right eye(RE).

154 ypoxia and is a major stimulatory factor for retinal neovascularization in ischemic retinopathies suc

155 VEGF-specific antagonists markedly suppress retinal neovascularization in mice and primates with isc

156 ibin expression cassette strongly suppressed retinal neovascularization in mice with ischemic retinop

157 eceptors (rho/VEGF mice) but did not inhibit retinal neovascularization in mice with ischemic retinop

158 study, we demonstrate complete inhibition of retinal neovascularization in mice with oxygen-induced i

159 mals, XMP.Z also suppressed ischemia-induced retinal neovascularization in mice.

160 previously described model of oxygen-induced retinal neovascularization in newborn mouse pups was use

161 on of blocking antibodies to SDF-1 prevented retinal neovascularization in our murine model, even in

162 oncentrations, retinal vascular leakage, and retinal neovascularization in P17 mice subjected to oxyg

163 beta 2 isoform and a significant decrease in retinal neovascularization in PKC beta isoform null mice

164 ntly decreases the formation of pathological retinal neovascularization in retinopathy.

165 rences in susceptibility to ischemia-induced retinal neovascularization in SD and BN rats.

166 retinal inflammation, vascular leakage, and retinal neovascularization in the DR models.

167 o be a useful tool for assessing the risk of retinal neovascularization in the newborn rat ROP model.

168 Arg-Gln dramatically inhibited retinal neovascularization in the OIR model.

169 ndothelial growth factor expression precedes retinal neovascularization in the retinas and the optic

170 gon laser in effecting lasting regression of retinal neovascularization in the setting of previously

171 s investigated by quantitating the extent of retinal neovascularization in the uPAR(-/-) mouse.

172 oroidal neovascularization and regression of retinal neovascularization in two models, transgenic mic

173 ve AdoR antagonists inhibited oxygen-induced retinal neovascularization in vivo and may provide a bas

174 show that alpha-defensins inhibit pathologic retinal neovascularization in vivo and may provide a cli

175 that an IGF-1 receptor antagonist suppresses retinal neovascularization in vivo, and infer that inter

176 , migration, and tube formation in vitro and retinal neovascularization in vivo.

177 endothelial capillary outgrowth in vitro and retinal neovascularization in vivo.

178 F-1 signaling are now shown to contribute to retinal neovascularization, in part, by modulating the e

179 f proteinases in the final common pathway of retinal neovascularization indicates that inhibition of

180 Proliferative retinopathy because of retinal neovascularization is a leading cause of blindne

181 Retinal neovascularization is a major cause of blindness

182 Retinal neovascularization is one of the leading causes

183 Retinal neovascularization is the major cause of untreat

184 e retinopathy, characterized by pathological retinal neovascularization, is a major cause of blindnes

185 In addition to retinal neovascularization, it involves retinal degenera

186 is a reproducible model of ischemia-induced retinal neovascularization; it is used commonly to devel

187 Cre mice display reduced angiogenesis in the retinal neovascularization model and in response to VEGF

188 cts of intravitreous bevacizumab in a rabbit retinal neovascularization model.

189 ,5,6,7-tetrabromobenzotriazole blocked mouse retinal neovascularization more efficiently than either

190 rrhage (n = 2), vitreous hemorrhage (n = 1), retinal neovascularization (n = 1), and cystoid macular

191 icated by the ICD-9-CM diagnosis of "362.16: Retinal Neovascularization NOS." RESULTS: The estimated

192 Clinical Modification diagnosis of "362.16: Retinal Neovascularization NOS." Type of initial treatme

193 The present study investigates whether retinal neovascularization (NV) and apoptosis are altere

194 perimental retinopathy of prematurity (ROP), retinal neovascularization (NV) and vessel tortuosity ha

195 echanisms are implicated in the induction of retinal neovascularization (NV) during ischemic retinopa

196 ll types, the role of TRAIL in regulation of retinal neovascularization (NV) has not been described.

197 fect of administration of exogenous PAI-1 on retinal neovascularization (NV) in an animal model of re

198 tions of DXR or DNR suppressed choroidal and retinal neovascularization (NV), but also perturbed reti

199 growth factor (VEGF) has been implicated in retinal neovascularization (NV), but it has been difficu

200 ina triggers both normal vessel regrowth and retinal neovascularization (NV), which is maximal at P17

201 pout in early OIR and mitigated pathological retinal neovascularization (NV).

202 o investigate whether 12-LOX plays a role in retinal neovascularization (NV).

203 Changes in retinal neovascularization occur in the Nrl(-/-)Grk1(-/-

204 Retinal neovascularization occurring as a complication o

205 as a model for one of the variants of type 3 retinal neovascularization occurring in some patients wi

206 tinal detachment were increased if there was retinal neovascularization (odds ratio, 11.61; 95% CI, 1

207 2 in retinal photoreceptors but developed no retinal neovascularization or other abnormalities of ret

208 des did not cause a significant reduction in retinal neovascularization or VEGF protein levels.

209 s injected intraocularly in a mouse model of retinal neovascularization (oxygen-induced retinopathy [

210 ROP model showed a significant reduction in retinal neovascularization (P < 0.0001) and in the numbe

211 15 in rat) and to the later phase of maximum retinal neovascularization (P18 in mouse, P20 in rat) an

212 nhibition of the activity of uPAR suppresses retinal neovascularization, possibly through a reduction

213 or (TNF)-alpha as a regulator of MMPs in the retinal neovascularization process.

214 posure resulted in 78% and 82% inhibition of retinal neovascularization, respectively.

215 tic target in the prevention or treatment of retinal neovascularization seen in many ocular diseases.

216 ssion with siRNA is effective in suppressing retinal neovascularization, suggesting EPO siRNA is a po

217 ffective for neuronal survival did not cause retinal neovascularization, suggesting that VEGF-B is th

218 etinal nonperfusion and little likelihood of retinal neovascularization suggests the possibility that

219 GF-1 signaling in endothelium play a role in retinal neovascularization through the expression of vas

220 tulated to be involved in the development of retinal neovascularization through the regulation of ext

221 CTGF/CCN2 stimulates retinal neovascularization through transactivation of p5

222 Our results demonstrate human retinal neovascularization, thus revealing the functiona

223 d a novel mouse xenotransplantation model of retinal neovascularization to test human hematopoietic c

224 atic steroid, anecortave acetate, to inhibit retinal neovascularization using a rat model of ROP and

225 Is it possible to completely inhibit retinal neovascularization using drug treatment with a m

226 into ischemic retina and strongly suppressed retinal neovascularization, VEGF-induced subretinal neov

227 duced Src-PLD1-PKCgamma-cPLA2 activation and retinal neovascularization via activation of Kdr and Flt

228 icant reduction in vascular obliteration and retinal neovascularization vs. saline injection in the O

229 Cs), and the mouse model of ischemia-induced retinal neovascularization was assayed by real-time PCR

230 In addition, retinal neovascularization was assessed by quantificatio

231 In addition, retinal neovascularization was attenuated in PECAM-1-/-

232 the oxygen-induced ROP neonatal mouse model, retinal neovascularization was decreased by 40% +/- 16%

233 Oxygen-induced retinal neovascularization was established in neonatal m

234 Retinal neovascularization was evaluated using flatmount

235 Retinal neovascularization was evaluated using fluoresce

236 Retinal neovascularization was examined by fluorescein d

237 f AdoR antagonist administration in reducing retinal neovascularization was examined in a mouse pup m

238 Additional retinal neovascularization was found in 1 patient.

239 Retinal neovascularization was induced by exposing newbo

240 Retinal neovascularization was induced in mice pups by e

241 Abnormal retinal neovascularization was induced in rat pups by su

242 Retinal neovascularization was inhibited in these mice i

243 Stat3 in the mouse model of ischemia-induced retinal neovascularization was investigated to evaluate

244 ficant reduction in the severity of abnormal retinal neovascularization was observed in the steroid-t

245 Hyperoxia-induced retinal neovascularization was observed in wild-type and

246 Retinal neovascularization was scored, and avascular are

247 This effect was dose dependent, and retinal neovascularization was significantly inhibited i

248 However, the degree of ischemia-induced retinal neovascularization was significantly reduced in

249 f growth hormone (GH) in ischemia-associated retinal neovascularization was studied in transgenic mic

250 l neovascular specimens and rodent models of retinal neovascularization, we discovered that pathologi

251 n understanding the mechanisms of pathologic retinal neovascularization, we found that VEGF activates

252 In view of understanding the mechanisms of retinal neovascularization, we had reported previously t

253 Retinal vascular area and retinal neovascularization were assessed by adenosine di

254 Children with intraocular surgery or active retinal neovascularization were excluded from the study.

255 e uPA/uPAR interaction on the development of retinal neovascularization were studied in this animal m

256 n from injured eyes caused a 60% decrease in retinal neovascularization when injected into the vitreo

257 uced retinal vascular leakage and attenuated retinal neovascularization, when compared with the contr

258 Parstatin suppressed retinal neovascularization with maximum inhibition of 60

259 jection of VEGF in rabbits results in florid retinal neovascularization within the first week, follow

260 nal VEGF expression and reduces pathological retinal neovascularization without obvious side effects.

261 oss and consequent hypoxia-driven pathologic retinal neovascularization, yet relatively little is kno