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 ion of inflammatory signs and a reduction of neovascular activity.

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

5 In contrast to neovascular age related macular degeneration, polypoidal

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

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

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

9 ndothelial growth factor (VEGF) treatment of neovascular age-related macular degeneration (AMD) is a

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

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

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

13 SLG were encountered most often in 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 tinal angiomatous proliferation, a subset of neovascular age-related macular degeneration (AMD), whic

19 the risk of subsequent ION in patients with neovascular age-related macular degeneration (AMD).

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

21 ation (CNV), a hallmark of the human wet, or neovascular age-related macular degeneration (AMD).

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

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

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

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

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

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

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

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

30 with visual acuity (VA) change in real-world neovascular age-related macular degeneration (nAMD) pati

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

32 mber 2012 were identified from a registry of neovascular age-related macular degeneration (nAMD) trea

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

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

35 retinal vascular occlusion in patients with neovascular age-related macular degeneration (nAMD) trea

36 tcomes from real-world data of patients with neovascular age-related macular degeneration (nAMD) trea

37 -associated visual outcomes in patients with neovascular age-related macular degeneration (nAMD) who

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

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

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

41 py plays a central role in the management of 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 anibizumab 0.5 mg for eligible patients with neovascular age-related macular degeneration (nAMD).

45 acuity is the main goal for the treatment of neovascular age-related macular degeneration (nAMD).

46 rcept are both approved for the treatment of neovascular age-related macular degeneration (nAMD).

47 sistent disease activity among patients with neovascular age-related macular degeneration (nAMD).

48 l growth factor (VEGF) injection therapy for neovascular age-related macular degeneration (nAMD).

49 h, South San Francisco, CA) in patients with neovascular age-related macular degeneration (nAMD).

50 trials of brolucizumab versus aflibercept in neovascular age-related macular degeneration (nAMD).

51 used patient data regarding the treatment of neovascular age-related macular degeneration (nAMD).

52 othelial growth factor (VEGF) inhibitors for neovascular age-related macular degeneration (nAMD).

53 dapted (DA) retinal sensitivity in eyes with neovascular age-related macular degeneration (nAMD).

54 Neovascular age-related macular degeneration (NVAMD) is

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

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

57 nibizumab, and aflibercept monotherapies for neovascular age-related macular degeneration (NVAMD).

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

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

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

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

62 increase in prevalence during treatment for neovascular age-related macular degeneration and are ass

63 Neovascular age-related macular degeneration and diabeti

64 ascularization (CNV) in body donor eyes with neovascular age-related macular degeneration are limited

65 Neovascular age-related macular degeneration is among th

66 Neovascular age-related macular degeneration is one of t

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

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

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

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

71 l growth factor (VEGF) treatment patterns in neovascular age-related macular degeneration patients in

72 ving intravitreal aflibercept injections for neovascular age-related macular degeneration presented 4

73 from a multisite, international registry of neovascular age-related macular degeneration was analyze

74 19 patients with advanced neovascular age-related macular degeneration were enroll

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

76 Patients with neovascular age-related macular degeneration who demonst

77 ed up during year 2 among 1185 patients with neovascular age-related macular degeneration who were en

78 choroidal vasculopathy (PCV) is a variant of neovascular age-related macular degeneration with distin

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

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

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

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

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

84 studying proliferative diabetic retinopathy, neovascular age-related macular degeneration, diabetic m

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

86 Neovascular age-related macular degeneration-free surviv

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

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

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

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

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

92 a novel therapeutic target in patients with neovascular age-related macular degeneration.

93 idualized ranibizumab retreatment schemes in neovascular age-related macular degeneration.

94 urther clinical validation for patients with neovascular age-related macular degeneration.

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

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

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

98 other conditions could affect progression to neovascular AMD (nAMD).

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

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

101 e AMD, defined as geographic atrophy (GA) or neovascular AMD (NVAMD), was identified.

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

103 gnificantly with progression to late AMD and neovascular AMD (P = 2.40 x 10(-5) and P = 0.002, respec

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

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

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

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

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

109 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

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

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

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

113 Patients with neovascular AMD and persistent macular edema despite fix

114 apy for exudative AMD including both typical neovascular AMD and polypoidal choroidal vasculopathy (P

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

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

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

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

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

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

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

122 a analysis of eyes previously diagnosed with neovascular AMD in a tertiary eye care center (Medical R

123 Large SMH in neovascular AMD in a treat-and-extend regimen does not s

124 naive lesions in 1 eye and without signs of neovascular AMD in the fellow eye were included in the a

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

126 The prevalence of subclinical nonexudative neovascular AMD in the fellow eyes of patients with unil

127 Exclusion criteria included neovascular AMD in the intervention eye, glaucoma with i

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

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

130 Here we show in a neovascular AMD mouse model that NLRP3 inflammasome acti

131 (>=125 mum) macular druse in the absence of neovascular AMD or central geographic atrophy.

132 anti-VEGF therapy is safe and effective for neovascular AMD over 2 years, the period for which data

133 Neovascular AMD patients receiving intravitreal injectio

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

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

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

137 ediate AMD, late AMD, geographic atrophy and neovascular AMD were 14.1% (95% CI, 13.1-15.1), 9.4% (95

138 te AMD, or late AMD, geographic atrophy, and neovascular AMD were 18.2% (95% confidence interval [CI]

139 e numbers who progressed to late AMD, GA, or neovascular AMD were 454 (23.3%), 345 (17.7%), and 278 (

140 Eyes that developed neovascular AMD were censored at the day of its detectio

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

142 ver, the existence of a nonexudative form of neovascular AMD would suggest that the term "neovascular

143 neovascular AMD would suggest that the term "neovascular AMD" should be preceded by either "exudative

144 without late AMD (geographic atrophy [GA] or neovascular AMD) in either eye at study baseline, aspiri

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

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

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

148 spect to the progression to late AMD (GA and neovascular AMD).

149 Regarding neovascular AMD, 9 nutrients were associated nominally w

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

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

152 sponse may improve therapeutic management of neovascular AMD, avoid discrepancies between clinicians/

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

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

155 e supporting the use of anti-VEGF agents for neovascular AMD, including intravitreal ranibizumab, afl

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

157 e a precursor for the formation of exudative neovascular AMD, there is evidence suggesting a protecti

158 Among patients with neovascular AMD, those who receive a higher number of an

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

160 e in fellow eyes of subjects with unilateral neovascular AMD.

161 ting CNV activity while monitoring eyes with neovascular AMD.

162 rely on OCT to guide treatment decisions in neovascular AMD.

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

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

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

166 ion of a novel range of baseline features in neovascular AMD.

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

168 marker of disease activity in patients with neovascular AMD.

169 se associations are stronger for GA than for neovascular AMD.

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

171 B vitamin was significantly associated with neovascular AMD.

172 terval intravitreous anti-VEGF treatment for neovascular AMD.

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

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

175 The signal was greater for GA than neovascular AMD.

176 agocytes in the laser-induced mouse model of neovascular AMD.

177 subclinical (treatment-naive), nonexudative, neovascular AMD.

178 for GA, and 0.84 (0.75-0.95, P = 0.005) for neovascular AMD.

179 VA) monitoring strategy in the detection of neovascular AMD.

180 n order to protect against both atrophic and neovascular AMD.

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

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

183 sification system that distinguishes between neovascular and nonneovascular iAMD.

184 tive analysis showed a significantly greater neovascular area and fractal dimension on the stress OCT

185 sensitive than en-face imaging in detecting neovascular blood flow signals under both rest (P = 0.12

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

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

188 f the retinal pigment epithelium (RPE) and a neovascular complex were seen in 3 older patients and 1

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

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

191 Development of neovascular complications.

192 ficantly improve visual outcomes and prevent neovascular complications.

193 to the pathophysiology in SFD and likely the neovascular component of the more commonly seen AMD.

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

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

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

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

198 et need, with only destructive therapies for neovascular disease.

199 ole of these lipid metabolites in regulating neovascular disease.

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

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

202 py development for sight-threatening corneal neovascular diseases.

203 ce of their interplay in the pathogenesis of neovascular diseases.

204 ulators are potential therapeutic targets in neovascular diseases.

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

206 apy for cancer and multitarget approaches in neovascular eye disease.

207 Neovascular eye diseases, including retinopathy of prema

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

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

210 .048 [Kaplan-Meier], respectively) and less neovascular glaucoma (11.6% and 21.3% after 5 years, P =

211 ow-up included vitreous hemorrhage (9 eyes), neovascular glaucoma (5 eyes), and traction retinal deta

212 9%), chronic angle-closure glaucoma (10.8%), neovascular glaucoma (9.0%), NTG (6.5%), and OHT (5.5%).

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

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

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

216 Concomitant secondary neovascular glaucoma and cataract needed appropriate man

217 One additional patient developed neovascular glaucoma and retinal detachment.

218 Neovascular glaucoma and retinal detachments may occur,

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

220 ulloepithelioma with concomitant seeding and neovascular glaucoma in the right eye was seen for a sec

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

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

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

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

225 Unresponsive neovascular glaucoma was the leading cause of secondary

226 vitreous hemorrhage, retinal detachment, and neovascular glaucoma) during this transition.

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

228 e to 20% of cornea had the largest impact on neovascular glaucoma, and dose to 20% of the ciliary bod

229 The diagnoses of neovascular glaucoma, CRVO and CRAO were established as

230 vitreous hemorrhage, retinal detachment, and neovascular glaucoma, respectively).

231 ent, anterior segment neovascularization, or neovascular glaucoma.

232 CN1 and significantly decreases pathological neovascular growth in OIR.

233 s or more predicted higher incidence of both neovascular (hazard ratio, 11.036; 95% confidence interv

234 CAPN5 Neovascular Inflammatory Vitreoretinopathy (CAPN5-NIV; O

235 -such as NOD2 (Blau syndrome) and CAPN5 NIV (neovascular inflammatory vitreoretinopathy)-as well as v

236 , (3) time to first grading of the choroidal neovascular lesion as inactive, and (4) maximum rate of

237 n, irradiated NP-[CPP] significantly reduces neovascular lesion size.

238 mented period of inactivity of the choroidal neovascular lesion with no further treatments unless the

239 T) lying within the maximum footprint of the neovascular lesion.

240 on rotational 3D OCTA images, a total of 35 neovascular lesions (vs 22 lesions detected on 2D OCTA i

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

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

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

244 ion of the eye allows NP accumulation in the neovascular lesions.

245 proved visualization and measurements of the neovascular lesions.

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

247 ward for 164,188 Medicare beneficiaries with neovascular macular degeneration receiving >=1 anti-vasc

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

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

250 0,68), macular exudate (ME; 20,5), choroidal neovascular membrane (CNVM; 10,15), venous stasis retino

251 was considered to be evidence of epiretinal neovascular membrane (ERNM).

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

253 to counting fingers in the left eye with the neovascular membrane as a consequence of sub-retinal fib

254 Choroidal neovascular membrane can also be a late complication of

255 l characteristics, for example, in choroidal neovascular membrane development and treatment received.

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

257 None of the eyes showed a choroidal neovascular membrane.

258 e, however one of them developed a choroidal neovascular membrane.

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

260 These neovascular membranes are visualized best using OCT and

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

262 e such as outer retinal atrophy or exudative neovascular membranes develop, which could produce irrev

263 ions were eyes with large active or inactive neovascular membranes); (3) reduced retinal thickness me

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

265 h lipid globules found in the choroid and in neovascular membranes.

266 tes to late AMD: geographic atrophy (GA) and neovascular (NV)-AMD.

267 y has prevented blindness from exudative and neovascular ocular diseases worldwide while saving healt

268 of AMD, no therapy is successful for the non-neovascular or "dry" form.

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

270 While treatment is effective for the neovascular or "wet" form of AMD, no therapy is successf

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

272 ive analysis to assess the rate of change in neovascular parameters during the stress condition.

273 of hypoxia in experimental and human retinal neovascular pathogenesis.

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

275 Neovascular pathologies in the eye like age-related macu

276 ogies, including geographic atrophy (GA) and neovascular pathologies, were also seen.

277 progress requires a better understanding of neovascular pathophysiology.

278 ultifactorial and may follow, in part, a non-neovascular pathway.

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

280 The increased neovascular perfusion following the induced increase of

281 hat Fzd7 controls both vaso-obliteration and neovascular phases (NV).

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

283 2 are key regulators of the inflammatory and neovascular responses to injury.

284 Aberrant, neovascular retinal blood vessel growth is a vision-thre

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

286 s, injection details, and the development of neovascular sequelae or need for adjunct therapies were

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

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

289 tive" or "nonexudative" when describing this neovascular stage of AMD.

290 Hence, perilesional nonexudative choroidal neovascular tissue (presumably present before the develo

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

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

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

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

295 els results in the formation of pathological neovascular tufts that impair vision.

296 t generates disorganized and poorly perfused neovascular tufts that mimic human ocular diseases.

297 YK-4-279 treatment significantly reduced neovascular tufts while sparing healthy retinal vessels,

298 fore, strategies that eliminate pathological neovascular tufts while sparing normal blood vessels are

299 ression is upregulated and co-localized with neovascular tufts.

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