ライフサイエンスコーパス: neovascular

1 nonindigenous participants (atrophic, 0.72%; neovascular, 0.24%).

2 There were 1727 cases of late AMD (1151 neovascular, 384 geographic atrophy, and 192 mixed [neov

3 th primary PED presenting as the hallmark of neovascular activity and was induced by secondary format

4 long-term outcome of bevacizumab therapy for neovascular age related macular degeneration (NVAMD) in

5 variant of choroidal neovascularization and neovascular age related macular degeneration presenting

6 In contrast to neovascular age related macular degeneration, polypoidal

7 bizumab and bevacizumab for the treatment of neovascular age-related macular degeneration (AMD) among

8 trophy due to late-stage non-neovascular and neovascular age-related macular degeneration (AMD) and t

9 nce tomography (OCT) images of patients with neovascular age-related macular degeneration (AMD) and t

10 39.7% of eyes; retinal tear in 8.9% of eyes; neovascular age-related macular degeneration (AMD) in 7.

11 Neovascular age-related macular degeneration (AMD) is ch

12 using a treat-and-extend (TREX) regimen for neovascular age-related macular degeneration (AMD) or fe

13 There is a subset of eyes with neovascular age-related macular degeneration (AMD) that

14 ss (CMT) and visual outcome in patients with neovascular age-related macular degeneration (AMD) treat

15 lop predictive models of anatomic outcome in neovascular age-related macular degeneration (AMD) treat

16 rospective clinical trials for management of neovascular age-related macular degeneration (AMD), diab

17 inal degenerative diseases including dry and neovascular age-related macular degeneration (AMD), reti

18 In eyes with neovascular age-related macular degeneration (AMD), SHRM

19 tinal angiomatous proliferation, a subset of neovascular age-related macular degeneration (AMD), whic

20 growth factor (VEGF) drug, in patients with neovascular age-related macular degeneration (AMD).

21 dothelial growth factor (VEGF) treatment for neovascular age-related macular degeneration (AMD).

22 apy is the major therapeutic breakthrough in neovascular age-related macular degeneration (AMD).

23 emulsification surgery on the progression of neovascular age-related macular degeneration (AMD).

24 ty of brolucizumab with aflibercept to treat neovascular age-related macular degeneration (AMD).

25 nsisted of 1200 OCT volumes of patients with neovascular age-related macular degeneration (AMD, n = 4

26 Novartis Pharma AG, Basel, Switzerland) for neovascular age-related macular degeneration (nAMD) afte

27 (OCT) with alternative tests for monitoring neovascular age-related macular degeneration (nAMD) and

28 ocks all isoforms of VEGF-A in patients with neovascular age-related macular degeneration (nAMD) demo

29 d long-term visual outcomes in patients with neovascular age-related macular degeneration (nAMD) duri

30 to investigate preferences of patients with neovascular age-related macular degeneration (nAMD) for

31 &E) versus monthly regimens in patients with neovascular age-related macular degeneration (nAMD) from

32 t outcomes with intravitreal aflibercept for neovascular age-related macular degeneration (nAMD) in r

33 Describing the natural course of neovascular age-related macular degeneration (nAMD) is e

34 Neovascular age-related macular degeneration (nAMD) is t

35 Treatment-naive eyes with neovascular age-related macular degeneration (nAMD) trac

36 sion of geographic atrophy (GA) in eyes with neovascular age-related macular degeneration (nAMD) trea

37 al-world visual acuity (VA) in patients with neovascular age-related macular degeneration (nAMD) trea

38 us adverse events (SAEs) among patients with neovascular age-related macular degeneration (nAMD) who

39 the outcomes over 12 months in patients with neovascular age-related macular degeneration (nAMD) with

40 anti-VEGF injections in patients treated for neovascular age-related macular degeneration (nAMD), dia

41 rolled patients treated with ranibizumab for neovascular age-related macular degeneration (nAMD), dia

42 using anti-VEGF therapy for the treatment of neovascular age-related macular degeneration (nAMD), oph

43 ith ranibizumab monotherapy in patients with neovascular age-related macular degeneration (nAMD).

44 Aflibercept in treatment-naive patients with neovascular age-related macular degeneration (nvAMD) in

45 Neovascular age-related macular degeneration (NVAMD) is

46 ence tomography (OCT) in guiding therapy for neovascular age-related macular degeneration (nvAMD) to

47 (HE) and all other eyes among patients with neovascular age-related macular degeneration (NVAMD) tre

48 used in a treat-and-extend (TAE) regimen for neovascular age-related macular degeneration (NVAMD).

49 has changed the prognosis for patients with neovascular age-related macular degeneration (nvAMD).

50 afety of rAAV.sFlt-1 subretinal injection in neovascular age-related macular degeneration (wet AMD) o

51 Patients aged 50 years or older with neovascular age-related macular degeneration and a basel

52 Neovascular age-related macular degeneration is among th

53 helial growth factor agents for treatment of neovascular age-related macular degeneration or diabetic

54 Importance: When a patient with neovascular age-related macular degeneration or diabetic

55 helial growth factor agents for treatment of neovascular age-related macular degeneration or diabetic

56 When a patient with neovascular age-related macular degeneration or diabetic

57 Patients with neovascular age-related macular degeneration received in

58 19 patients with advanced neovascular age-related macular degeneration were enroll

59 A total of 1097 patients with neovascular age-related macular degeneration were random

60 An oral treatment for neovascular age-related macular degeneration would be le

61 eeded basis (PRN) in patients with subfoveal neovascular age-related macular degeneration).

62 Thirty-five participants with neovascular age-related macular degeneration, 7 of whom

63 ) had diabetic macular edema, 32 (25.8%) had neovascular age-related macular degeneration, and 32 (25

64 Subretinal fibrosis is an end stage of neovascular age-related macular degeneration, characteri

65 ch as proliferative diabetic retinopathy and neovascular age-related macular degeneration, uncontroll

66 reventing subretinal fibrosis development in neovascular age-related macular degeneration.

67 ent of individualized treatment regimens for neovascular age-related macular degeneration.

68 e an unmet medical need in the management of neovascular age-related macular degeneration.

69 and present a novel therapeutic approach for neovascular age-related macular degeneration.

70 ion Fab (DAF) as a potential therapeutic for neovascular age-related macular degeneration.

71 issue to regulate disease conditions such as neovascular age-related macular degeneration.

72 Thirty-one eyes had CNV associated with neovascular age-related macular degeneration.

73 ing protein sFLT01 in patients with advanced neovascular age-related macular degeneration.

74 reserve central vision in many patients with neovascular age-related macular degeneration.

75 athy (DR), retinal vein occlusion (RVO), and neovascular-age related macular degeneration (nvAMD).

76 variants more frequently than patients with neovascular AMD (11 of 93 [11.8%] vs 40 of 835 [4.8%]; P

77 For neovascular AMD (133 scans), 7 25-line raster scans conf

78 ion, patients with MPNs had a higher risk of neovascular AMD (adjusted HR, 1.4; 95% CI, 1.2-1.6).

79 Age-related macular degeneration 4 included neovascular AMD (nvAMD) and geographic atrophy (GA).

80 e age-related macular degeneration (AMD) and neovascular AMD (nvAMD) with serum 25-hydroxy vitamin D

81 nce of late AMD, geographic atrophy (GA) and neovascular AMD (NVAMD), year of recruitment, AMD gradin

82 gment epithelial (RPE) hemorrhage related to neovascular AMD (odds ratio 1.55 [95% confidence interva

83 cant after conditioning on participants with neovascular AMD (P = 2.42 x 10(-4)).

84 3CR1 promoter region and was associated with neovascular AMD (RR, 0.75; P = .03).

85 In studies of non-neovascular AMD (without evident signs of active or regr

86 ng 4 risk alleles in CFH and ARMS2 developed neovascular AMD 12.2 (95% CI, 6.2-18.3) years earlier th

87 the complement factor H (CFH) gene developed neovascular AMD 2.8 (95% CI, 0.5-5.0) years earlier (P =

88 In addition, HRs of neovascular AMD after 2006 were calculated since antivas

89 izumab vs ranibizumab as initial therapy for neovascular AMD among US Medicare beneficiaries varied s

90 Twelve eyes (32%) had neovascular AMD and 1 eye (3%) had neovascularization se

91 MD, 85.7% (95% CI, 57.2%-98.2%; n = 12) were neovascular AMD and 14.3% (95% CI, 2.0%-42.8%; n = 2) we

92 hat included 106 referral eyes for suspected neovascular AMD and 63 eyes with stable neovascular AMD.

93 l, 275 patients with a known age at onset of neovascular AMD and a genetic risk analysis were include

94 VEGF treatment for subfoveal and juxtafoveal neovascular AMD and a minimum follow-up of 24 months wer

95 ular, 384 geographic atrophy, and 192 mixed [neovascular AMD and geographic atrophy]) and 1153 contro

96 se, 47 met inclusion criteria; most targeted neovascular AMD and investigated anti-vascular endotheli

97 All patients with non-neovascular AMD and no retinal pigment epithelial (RPE)

98 e a driving force in macular telangiectasia, neovascular AMD and other retinal diseases.

99 New referrals for patients with suspected neovascular AMD and patients with stable neovascular AMD

100 patients (n = 115 eyes) with treatment-naive neovascular AMD and PED (>150 mum), who were treated wit

101 Eyes with neovascular AMD and PED showed significant functional an

102 Patients with neovascular AMD and persistent macular edema despite fix

103 recall of 0.81, with superior performance in neovascular AMD and RVO compared with DME, which was rep

104 ation included 101 eyes of 101 patients with neovascular AMD and thick submacular hemorrhage who unde

105 The photopsias from neovascular AMD are more centrally located (83%), quick

106 396 eyes of 295 patients were diagnosed with neovascular AMD between 2009 and 2014.

107 196 patients diagnosed with treatment-naive neovascular AMD between January 2009 and March 2013; the

108 iaries (N = 195 812) with an index claim for neovascular AMD between July 1, 2006, and June 30, 2009,

109 riants (SNVs) across the whole genome of 216 neovascular AMD cases and 1,553 controls.

110 As a follow-up validation, we evaluate 3,772 neovascular AMD cases and 6,942 controls from five indep

111 ficant decrease of the RGCL in patients with neovascular AMD compared to the fellow (untreated) eye.

112 oint increase in sFlt-1, the odds for having neovascular AMD compared with non-AMD and neovascular AM

113 ng neovascular AMD compared with non-AMD and neovascular AMD decrease by 27.8%, odds ratio (OR) = 0.7

114 This study demonstrates that eyes with neovascular AMD display reduced RNFL and GCC thickness.

115 terns in anti-VEGF therapy for patients with neovascular AMD do not reflect optimal treatment strateg

116 intravitreal bevacizumab for treatment-naive neovascular AMD does not increase initial fluid-free int

117 l and anatomic improvements in patients with neovascular AMD for up to 3 years of treatment.

118 um sFlt-1 differentiates those patients with neovascular AMD from both early AMD and non-AMD particip

119 Rim area was significantly thinner in the neovascular AMD group compared with controls (P = .047);

120 = .047); cup-to-disc ratio was higher in the neovascular AMD group compared with the control group (P

121 e log-rank test indicated that subjects with neovascular AMD had a significantly lower 3-year Parkins

122 ular endothelial growth factor therapies for neovascular AMD had decreased mortality compared with th

123 ts (7.0%) and 2 of 40 donor eyes (5.0%) with neovascular AMD had layered, hyperreflective sub-RPE lin

124 of these SNPs with angiographic features of neovascular AMD has been inconsistent in previous studie

125 Participants with neovascular AMD in 1 eye at baseline had a statistically

126 Sixty patients with treatment-naive neovascular AMD in 1 eye randomized 1:2 to monthly or TR

127 The frequency of the onion sign in neovascular AMD in a referral practice and a pathology a

128 fellow eye have focused on the incidence of neovascular AMD in the fellow eye of participants with n

129 chment, and geographic atrophy/fibrotic scar/neovascular AMD in the fellow eye.

130 g first-generation offspring of parents with neovascular AMD in the LIMPIA trial, MPOD as measured wi

131 r AMD in the fellow eye of participants with neovascular AMD in the other eye.

132 onsecutive patients with iAMD in one eye and neovascular AMD in their fellow eye were imaged with FA,

133 The efficacy of antiangiogenic therapy in neovascular AMD is strongly determined by morphologic fe

134 Eyes like those enrolled in CATT with neovascular AMD lesions composed of >50% blood can be ma

135 Longer-term follow-up of neovascular AMD managed with anti-VEGF therapy suggests

136 Neovascular AMD management imposes a substantial time bu

137 The TREX neovascular AMD management strategy used in this prospec

138 For neovascular AMD monitoring, the average recurrence to tr

139 Past smokers and current smokers developed neovascular AMD on average 4.9 (95% CI, 3.0-6.8) and 7.7

140 ders for the development of late AMD, either neovascular AMD or geographic atrophy (GA).

141 Telephone interviews were conducted with 13 neovascular AMD patient caregivers.

142 A survey was administered to 75 neovascular AMD patients aged >/=50 years who received >

143 participants, 53 early AMD patients, and 97 neovascular AMD patients from Belfast in Northern Irelan

144 sFlt-1 from neovascular AMD patients was significantly decreased com

145 Teleophthalmologic monitoring for neovascular AMD recurrence resulted in longer wait times

146 For neovascular AMD screening, the average referral-to-diagn

147 Daily pazopanib eye drops in neovascular AMD subjects did not result in therapeutic b

148 All patients with neovascular AMD treated by the same physician during a 1

149 er patients received ranibizumab for initial neovascular AMD treatment in 2009 vs 2006.

150 he 3-year follow-up period for subjects with neovascular AMD was 2.57 (95% CI: 1.42-4.64) that of com

151 iciaries that first received ranibizumab for neovascular AMD was 35%, and varied significantly (0.9%-

152 An average patient visit for neovascular AMD was 90 minutes (range: 13 minutes to >4

153 ity in future studies in non-neovascular and neovascular AMD was held.

154 t-1 concentration of non-AMD, early AMD, and neovascular AMD were 90.8 +/- 2.9 pg/mL (+/- standard er

155 dvanced AMD, drusen, geographic atrophy, and neovascular AMD were determined by using a modified Wisc

156 od long-term outcomes of VEGF inhibition for neovascular AMD were found in this study.

157 In 39 patients, 52 eyes with neovascular AMD were identified.

158 Patients with treatment-naive neovascular AMD were randomized 1:1:1 into 1 of 3 groups

159 ted neovascular AMD and patients with stable neovascular AMD were randomized into either routine or t

160 This study included patients with neovascular AMD who presented vitreomacular adhesion (VM

161 Treatment of neovascular AMD with a VEGF-neutralizing protein can res

162 g teleophthalmologic screening for suspected neovascular AMD with retinal specialist-based screening.

163 t of late AMD (central geographic atrophy or neovascular AMD) or pseudophakia.

164 diate and 1356 advanced AMD cases (primarily neovascular AMD) were confirmed by medical record review

165 diate and 1118 advanced AMD cases (primarily neovascular AMD) with a visual acuity of 20/30 or worse

166 diate and 1356 advanced AMD cases (primarily neovascular AMD) with a visual acuity of 20/30 or worse,

167 category 2, 26 for AREDS category 3, 26 for neovascular AMD, 26 with atrophic AMD, and 26 controls.

168 isease Study (AREDS) category 2 and 3, naive neovascular AMD, and atrophic AMD.

169 may better guide evaluation and treatment of neovascular AMD, and may contribute to the development o

170 yes with treatment-naive CNV due to AMD, non-neovascular AMD, and normal controls.

171 RN effectively treated PEDs in patients with neovascular AMD, and significant vision gains resulted r

172 ome use of a monitoring device for detecting neovascular AMD, and the proportion who established a ba

173 line and the various components of late AMD (neovascular AMD, central GA, or any GA) also showed no s

174 ry RNFL thickness was significantly lower in neovascular AMD, compared to controls (P = .004); peripa

175 and specifically for geographic atrophy and neovascular AMD, compared with those without AMD.

176 T specifically images RPE-related changes in neovascular AMD, contrary to conventional imaging method

177 Compared with PEDs associated with neovascular AMD, DPEDs had different crystallization pat

178 role in response to anti-VEGF treatment for neovascular AMD, especially for Caucasians.

179 For studies in patients with neovascular AMD, increased need for visualization of the

180 In neovascular AMD, only IRC at baseline and persistent thr

181 In eyes with neovascular AMD, SHRM is an important morphologic biomar

182 influence on new MA development in eyes with neovascular AMD, whether dosed monthly or per TREX regim

183 has a strong anatomical effect in eyes with neovascular AMD.

184 n first-generation offspring of parents with neovascular AMD.

185 B vitamin was significantly associated with neovascular AMD.

186 terval intravitreous anti-VEGF treatment for neovascular AMD.

187 as a major long-term therapeutic advance for neovascular AMD.

188 d development of RTH258 for the treatment of neovascular AMD.

189 support the use of EMB for chronic, active, neovascular AMD.

190 , FMT can be considered for second eyes with neovascular AMD.

191 sponse to anti-VEGF therapy in patients with neovascular AMD.

192 eems to indicate a particularly high risk of neovascular AMD.

193 irty patients (31 eyes) with treatment-naive neovascular AMD.

194 eal drugs rarely induce PVD in patients with neovascular AMD.

195 was associated with a >6-fold higher risk of neovascular AMD.

196 lt-1 could be a biomarker for development of neovascular AMD.

197 cted neovascular AMD and 63 eyes with stable neovascular AMD.

198 ysicians provided data for 221 patients with neovascular AMD.

199 l, and ocular factors on the age at onset of neovascular AMD.

200 We assessed 1400 OCT scans of patients with neovascular AMD.

201 ystem may play a role in the pathogenesis of neovascular AMD.

202 l risk factors influence the age at onset of neovascular AMD.

203 oral X-82 administered for the treatment of neovascular AMD.

204 T software algorithm, and the development of neovascular AMD.

205 L11 receptor/ligand complex in patients with neovascular AMD.

206 e first-generation offspring of parents with neovascular AMD.

207 group, becoming progressively thinner up to neovascular and atrophic AMD groups (P < .0001).

208 t and quantify atrophy due to late-stage non-neovascular and neovascular age-related macular degenera

209 le of each modality in future studies in non-neovascular and neovascular AMD was held.

210 yes revealed a significant reduction in both neovascular and non-neovascular areas from baseline to m

211 mab injections, overall in the macula and in neovascular and non-neovascular areas, from baseline to

212 sification system that distinguishes between neovascular and nonneovascular iAMD.

213 ficant reduction in both neovascular and non-neovascular areas from baseline to month 3 and month 6 (

214 all in the macula and in neovascular and non-neovascular areas, from baseline to month 3 (loading pha

215 We speculate that neovascular buds may be a precursor to neovascular disea

216 Hypercellular, apparent neovascular buds were adjacent to areas of CC loss in 22

217 We identified a large mature neovascular complex in approximately 75% of eyes, typica

218 erapy, indicating a more mature longstanding neovascular complex resistant to anti-VEGF therapy.

219 e SD OCT features and FA leakage of IRMA and neovascular complex.

220 t voltage from aberrantly located preretinal neovascular complexes is transmitted into the intraretin

221 in occlusion (CRVO) and stratify the risk of neovascular complication based on wider areas of visible

222 ficantly improve visual outcomes and prevent neovascular complications.

223 Development of neovascular complications.

224 y of evidence supports a strong link between neovascular disease and inflammation.

225 ded good visual gains without progression of neovascular disease or increased need for intravitreal a

226 tors may be a useful therapeutic strategy in neovascular disease to reduce VEGF165-induced edema with

227 I, 32.1%-45.4%; P < .001), and 38.2% loss in neovascular disease where RPE remained intact (95% CI, 2

228 ed stages of AMD (geographic atrophy, n = 5; neovascular disease, n = 13) were evaluated.

229 al growth factor, providing the stimulus for neovascular disease.

230 that neovascular buds may be a precursor to neovascular disease.

231 se postnatal retina and in a model of ocular neovascular disease.

232 scular protection and reduced progression to neovascular disease.

233 ibit angiogenesis in individuals with ocular neovascular disease.

234 ole of these lipid metabolites in regulating neovascular disease.

235 Ocular neovascular diseases are a leading cause of blindness.

236 Robo1 expression is altered in ocular neovascular diseases, and previous in vitro studies have

237 ulators are potential therapeutic targets in neovascular diseases.

238 or (VEGF) is a common treatment strategy for neovascular eye disease, a major cause of vision loss in

239 Neovascular eye diseases, including retinopathy of prema

240 LC-PUFAs and their enzymatic metabolites in neovascular eye diseases.

241 s open-angle (2/26), exfoliative (2/26), and neovascular following central retinal vein occlusion fro

242 cts can be used for studying the dynamics of neovascular formation in-vitro by a combination of live

243 .048 [Kaplan-Meier], respectively) and less neovascular glaucoma (11.6% and 21.3% after 5 years, P =

244 Rates of neovascular glaucoma (NVG) and enucleation (mainly for l

245 group (52.3% radiation retinopathy and 57.8% neovascular glaucoma after 5 years).

246 es treated with EBRT, and one that developed neovascular glaucoma after completion of therapy.

247 Neovascular glaucoma developed in 20 of 36 eyes (56%).

248 Neovascular glaucoma developed in 7 eyes, and all eyes r

249 ucleation were tumor recurrence in 60 (61%), neovascular glaucoma in 21 (21%), and tumor nonresponse

250 There were no reports of neovascular glaucoma or iris neovascularization.

251 Here we report a neovascular glaucoma patient who experienced a substanti

252 ts that in larger tumors the enucleation and neovascular glaucoma rates might be reduced by adjuvant

253 set cataract was noted in 22 patients (44%), neovascular glaucoma was noted in 1 patient (2%), and th

254 Unresponsive neovascular glaucoma was the leading cause of secondary

255 al photocoagulation are important to prevent neovascular glaucoma, a common complication.

256 ns for uveal melanoma were tumor recurrence, neovascular glaucoma, and tumor nonresponse.

257 ent, anterior segment neovascularization, or neovascular glaucoma.

258 ully managed IOP increase during dialysis in neovascular glaucoma.

259 revent additional vision loss resulting from neovascular glaucoma.

260 glaucoma and diabetic retinopathy developed neovascular glaucoma.

261 CN1 and significantly decreases pathological neovascular growth in OIR.

262 erited blinding disorder, autosomal dominant neovascular inflammatory vitreoretinopathy (ADNIV, OMIM

263 vides noninvasive measurement of the area of neovascular lesions in AMD.

264 epth-resolved identification of nonexudative neovascular lesions in eyes with iAMD suggests the need

265 , retinal pigment epithelial depigmentation, neovascular lesions, and geographic atrophy using the mo

266 proved visualization and measurements of the neovascular lesions.

267 allowing 2 monthly visits for patients with neovascular macular degeneration (nAMD) compared with mo

268 treatment for patients with newly diagnosed neovascular macular degeneration: monthly or as-needed b

269 tched at baseline for VA, age, and choroidal neovascular membrane (CNV) size.

270 at risk factors for development of choroidal neovascular membrane (CNVM) and visual loss.

271 nitis (n = 5), hemangioma (n = 1), choroidal neovascular membrane (n = 1), or nerve fiber layer infar

272 For analyses by visit: choroidal neovascular membrane activity graded by the treating phy

273 is cohort of patients had advanced choroidal neovascular membrane upon enrollment (recurrent or resis

274 e the characteristics of pediatric choroidal neovascular membranes (CNVs) associated with retinochoro

275 ts affected by C3 glomerulopathy can develop neovascular membranes as retinal complications of pigmen

276 ity to study the morphology of occult type 1 neovascular membranes in AMD and allows precise structur

277 ic patterns and quantifiable features of the neovascular membranes were studied on en face projection

278 namic therapy for the treatment of choroidal neovascular membranes, has also been shown to be an effe

279 The choroidal neovascular morphology of the 17 eyes of 14 consecutive

280 AMD - geographic atrophy (GA) and Late AMD - neovascular (NV).

281 The neovascular or "wet" form of AMD can be treated to varyi

282 months, any other surgeries or diagnosis of neovascular or active uveitic glaucoma.

283 Neovascular, or wet, age-related macular degeneration ca

284 of hypoxia in experimental and human retinal neovascular pathogenesis.

285 as a novel therapeutic agent to treat ocular neovascular pathologies and may complement current anti-

286 Neovascular pathologies in the eye like age-related macu

287 progress requires a better understanding of neovascular pathophysiology.

288 d comparisons of histologic features between neovascular PED and DPED resulting from AMD.

289 f AMD (2 with nonneovascular DPED and 2 with neovascular pigment epithelium detachment [PED]) and 49

290 in OCT and may be confused with fluid from a neovascular process.

291 hage dysfunction plays a pivotal role during neovascular proliferation in diseases of ageing includin

292 -induced retinal changes in animal models of neovascular retinal disease approximately 3-4-fold longe

293 o measure vascular voltages in human retinal neovascular specimens and rodent models of retinal neova

294 tor for the early detection of the choroidal neovascular stage before substantial vision loss has occ

295 With OCT angiography, type 1 neovascular tissue was visualized in 21 out of 22 study

296 cular/total retina (AVA) and of intravitreal neovascular/total retina (IVNV).

297 of pathologic retinal angiogenesis, reducing neovascular tuft formation and increased avascular area,

298 ecule resulted in a significant reduction of neovascular tufts in oxygen-induced retinopathy, support

299 ed a high level of Cavin-2 expression in the neovascular tufts in the mouse model of oxygen-induced r

300 ovascularization (CNV), is a hallmark of the neovascular (wet) form of advanced AMD and leads to sign