ライフサイエンスコーパス: retinopathy

1 oderate, or severe nonproliferative diabetic retinopathy).

2 creased visual acuity secondary to radiation retinopathy.

3 ities were present in the absence of visible retinopathy.

4 lomerular filtration rate, or progression of retinopathy.

5 at cells and disease progression in diabetic retinopathy.

6 y vascular effects of RORalpha deficiency in retinopathy.

7 diabetic eyes that do not manifest clinical retinopathy.

8 o develop a rational screening frequency for retinopathy.

9 al complications and vision loss in diabetic retinopathy.

10 aches may enhance early screening for sickle retinopathy.

11 measured by reactive hyperaemia index, or on retinopathy.

12 rs, suppress pathological vascular growth in retinopathy.

13 pathy, 97.9% (94.9%-99.1%) for proliferative retinopathy.

14 severe NPDR or PDR than among those with no retinopathy.

15 ckness compared to patients with no diabetic retinopathy.

16 promised vascular integrity such as diabetic retinopathy.

17 retinal barrier and the damage is related to retinopathy.

18 malities to those seen in diabetic mice with retinopathy.

19 ts with no history of proliferative diabetic retinopathy.

20 ly effective and cost-effective detection of retinopathy.

21 ling codes used in the treatment of diabetic retinopathy.

22 characteristic of non-proliferative diabetic retinopathy.

23 nship was not seen among those with diabetic retinopathy.

24 portant role in the pathogenesis of diabetic retinopathy.

25 reduced in more advanced stages of diabetic retinopathy.

26 es or targets to investigate and inhibit the retinopathy.

27 ion of the blood-retinal barrier in diabetic retinopathy.

28 d recognized risk factors for progression of retinopathy.

29 he medical record for patients with diabetic retinopathy.

30 deep plexus with sickle SC or proliferative retinopathy.

31 y impairs this process and prevents diabetic retinopathy.

32 th adequate UWFA studies demonstrated sickle retinopathy.

33 those with severe nonproliferative diabetic retinopathy.

34 with macroaneurysm, and 1 eye with radiation retinopathy.

35 ge-related macular degeneration and diabetic retinopathy.

36 ermine the presence and severity of diabetic retinopathy.

37 ent of PDR and slows progression of diabetic retinopathy.

38 se model of Matrigel plug and oxygen-induced retinopathy.

39 eferentially protects against oxygen-induced retinopathy.

40 arious ischemic diseases, including ischemic retinopathies.

41 r pathological angiogenesis in proliferative retinopathies.

42 hology of metastatic cancers and age-related retinopathies.

43 alue for the treatment of human RP and other retinopathies.

44 [0.6 million to 13.3 million]), and diabetic retinopathy (2.6 million [0.2 million to 9.9 million]).

45 0.2% (95% CI, 16.3%-24.1%) for those with no retinopathy, 20.4% (95% CI, 15.3%-27.8%) for those with

46 44.8-52.9]), the prevalence was 72.3% for no retinopathy, 25.4% for mild and moderate nonproliferativ

47 nations at 4 years among patients who had no retinopathy, 3 years among those with mild retinopathy,

48 drainage-vitrectomy developed less radiation retinopathy (30.5% and 37.4% after 5 years, P = .001 and

49 rror (60.8%), cataract (20.1%), and diabetic retinopathy (5.2%).

50 o retinopathy, 3 years among those with mild retinopathy, 6 months among those with moderate retinopa

51 ections that were for proliferative diabetic retinopathy), 8.3% to treat retinal vein occlusions, and

52 athy; Retmarker 73.0% (72.0 %-74.0%) for any retinopathy, 85.0% (83.6%-86.2%) for referable retinopat

53 follows: EyeArt 94.7% (94.2%-95.2%) for any retinopathy, 93.8% (92.9%-94.6%) for referable retinopat

54 tinopathy, 85.0% (83.6%-86.2%) for referable retinopathy, 97.9% (94.9%-99.1%) for proliferative retin

55 severe NPDR or PDR relative to those with no retinopathy (adjusted odds ratio [aOR], 3.59; 95% CI, 1.

56 ion loss in eye pathologies such as diabetic retinopathy, age-related macular degeneration, and centr

57 ions to retinopathy of prematurity, diabetic retinopathy, age-related macular degeneration, and glauc

58 ding adaptive optics, outcomes in autoimmune retinopathy (AIR) patients treated with rituximab.

59 tic target in the treatment of proliferative retinopathies and other diseases dependent on pathologic

60 tients without clinical evidence of diabetic retinopathy and 40 eyes of 40 healthy nondiabetic subjec

61 d with the comparator group (52.3% radiation retinopathy and 57.8% neovascular glaucoma after 5 years

62 were recruited (90 patients with no diabetic retinopathy and 90 patients with NPDR) into the study.

63 Paraneoplastic retinopathy and autosomal recessive bestrophinopathy clo

64 lar to human macula-in the study of diabetic retinopathy and diabetic macular edema (DME).

65 (age-related macular degeneration, diabetic retinopathy and glaucoma) segments of the eye.

66 enesis in the mouse models of oxygen-induced retinopathy and laser-induced choroid neovascularization

67 enesis in the mouse models of oxygen-induced retinopathy and laser-induced choroid neovascularization

68 Five- and 10-year freedom from radiation retinopathy and optic neuropathy rates were higher in th

69 and appears to promote experimental diabetic retinopathy and that Muller cells orchestrate inflammato

70 an diseases including proliferative diabetic retinopathy and wet age-related macular degeneration.

71 diabetes mellitus patients with no diabetic retinopathy and with non-proliferative diabetic retinopa

72 tive retinopathy, or progression of diabetic retinopathy), and nerve events (a composite of new loss

73 inopathy, 6 months among those with moderate retinopathy, and 3 months among those with severe nonpro

74 7.7) microL/min in the diabetic eyes without retinopathy, and 44.4 (8.3) microL/min in age-matched he

75 ce displayed symptoms of stroke and ischemic retinopathy, and 48% died prematurely.

76 cluding retinopathy of prematurity, diabetic retinopathy, and age-related macular degeneration, as we

77 cluding retinopathy of prematurity, diabetic retinopathy, and age-related macular degeneration, threa

78 a set of images from patients with malarial retinopathy, and found it compares favourably with the r

79 determinant in the pathogenesis of diabetic retinopathy, and inhibition of sEH can prevent progressi

80 Microvascular outcomes were nephropathy, retinopathy, and neuropathy.

81 Retinopathies are a group of monogenetic or complex reti

82 macular degeneration, glaucoma, and diabetic retinopathy, are ideal candidates for home monitoring pr

83 012 Preferred Practice Patterns for Diabetic Retinopathy as 91 answerable clinical research questions

84 ntial treatment strategy for STGD1 and other retinopathies associated with complement dysregulation.

85 dies in 25 cases of acute zonal occult outer retinopathy (AZOOR) identified using the classification

86 Acute zonal occult outer retinopathy (AZOOR) remains a challenging diagnosis.

87 nt microalbuminuria (not reported), incident retinopathy, bodyweight, insulin dose, and endothelial f

88 55%, 40%, 44%, and 30% reported, blindness, retinopathy, cataracts, glaucoma, and double vision resp

89 Retinopathy changes over time were determined by DRSS st

90 elopment of microalbuminuria, progression of retinopathy, changes in the glomerular filtration rate,

91 Diabetic Retinopathy Clinical Research Network (DRCR.net) investi

92 on Treatments Trials (CATT) and the Diabetic Retinopathy Clinical Research Network (DRCR.net).

93 The Diabetic Retinopathy Clinical Research Network Protocol S randomi

94 asily incorporated in the automated diabetic retinopathy detection algorithms.

95 Diabetic retinopathy, diabetic macular edema (DME), vision-threat

96 layers of diabetic patients without diabetic retinopathy (DR) after 1 year of follow-up.

97 y factors associated with prevalent diabetic retinopathy (DR) among Chinese American adults with type

98 generation in the initial stages of diabetic retinopathy (DR) and 2) the presence of neurodegeneratio

99 ivo function of microRNAs (miRs) in diabetic retinopathy (DR) and age-related macular degeneration (A

100 ral human visual disorders, such as diabetic retinopathy (DR) and age-related macular degeneration (A

101 studies on the relationship between diabetic retinopathy (DR) and cardiovascular disease (CVD) focuse

102 cular diseases; cataract, glaucoma, diabetic retinopathy (DR) and dry eye disease (DED) was assessed.

103 al stages leading to vision loss in diabetic retinopathy (DR) are highlighted.

104 the United States, severe forms of diabetic retinopathy (DR) are significantly associated with a gre

105 mal (NL), 183 glaucoma (GL), and 18 diabetic retinopathy (DR) at Tilganga Institute of Ophthalmology,

106 A diabetic retinopathy (DR) biomarker, tumor necrosis factor-alpha

107 e of diabetes, annual screening for diabetic retinopathy (DR) by expert human grading of retinal imag

108 hows multiple vascular hallmarks of diabetic retinopathy (DR) due to BRB disruption.

109 cular edema (DME) favorably affects diabetic retinopathy (DR) improvement and worsening.

110 the prevalence and risk factors for diabetic retinopathy (DR) in the Singapore Epidemiology of Eye Di

111 Ophthalmic screening to check for diabetic retinopathy (DR) is important to prevent vision loss in

112 Diabetic retinopathy (DR) is one of the leading causes of prevent

113 Early diagnosis of diabetic retinopathy (DR) is vital but challenging.

114 The presence and severity of diabetic retinopathy (DR) may contribute to the risk of falling i

115 nty-six eyes of 69 patients with no diabetic retinopathy (DR) or mild or moderate nonproliferative DR

116 ssion after stratifying by baseline diabetic retinopathy (DR) severity and adjusting for age, sex, ra

117 Diabetic Retinopathy Study (ETDRS) diabetic retinopathy (DR) severity scale (DRSS) grade during the

118 esults regarding the progression of diabetic retinopathy (DR) were neutral with liraglutide (LEADER)

119 tes (HEs) are the classical sign of diabetic retinopathy (DR) which is one of the leading causes of b

120 tal of 143 diabetic eyes-27 with no diabetic retinopathy (DR), 47 with nonproliferative DR (NPDR), 51

121 Diabetic retinopathy (DR), a major microvascular complication of

122 y (OCTA) may have value in managing diabetic retinopathy (DR), but there is limited information on th

123 ized controlled trials for managing diabetic retinopathy (DR), including diabetic macular edema (DME)

124 s, under chronic diseases including diabetic retinopathy (DR), mitophagy dysregulation and NLRP3 infl

125 of exudative maculopathy including diabetic retinopathy (DR), retinal vein occlusion (RVO), and neov

126 diabetic microvasculopathy based on diabetic retinopathy (DR).

127 on-making processes before treating diabetic retinopathy (DR).

128 nown about their risk of developing diabetic retinopathy (DR).

129 the pathogenesis and progression of diabetic retinopathy (DR).

130 l rat streptozotocin (STZ) model of diabetic retinopathy (DR).

131 nism of action were investigated in diabetic retinopathy (DR).

132 identified any robust risk loci for diabetic retinopathy (DR).

133 (DSM) may affect his or her risk of diabetic retinopathy (DR); however, few studies have examined thi

134 cular degeneration [AMD], cataract, diabetic retinopathy [DR], and glaucoma) and the overlap between

135 nd >/=2 lines of Early Treatment of Diabetic Retinopathy (ETDRS)-letters, respectively.

136 visual acuity (VA; Early Treatment Diabetic Retinopathy [ETDRS] letters) from baseline to 24 weeks.

137 photographs from 7 Early Treatment Diabetic Retinopathy fields were graded in a masked manner using

138 ed macular degeneration, cataracts, diabetic retinopathy, glaucoma, and intraocular cancers.

139 level of mean serum uric acid in no diabetic retinopathy group (p = 0.004 respectively).

140 Proliferative diabetic retinopathy has been managed by panretinal laser photoco

141 ly important for the development of diabetic retinopathy; however, the interplay between these cells

142 tinopathy, 93.8% (92.9%-94.6%) for referable retinopathy (human graded as either ungradable, maculopa

143 Percentages with retinopathy improvement at 1 and 2 years and cumulative

144 genes associated with the different forms of retinopathies in general do not overlap despite their ov

145 s observed in 45%, carotidodynia in 10%, and retinopathy in 4%.

146 CASE PRESENTATION: A retinopathy in a 16 year-old child with no history of co

147 This case report describes a proliferative retinopathy in a 16 year-old patient with co-inheritance

148 phy angiography (OCT-A) detect more-frequent retinopathy in adolescents with SCD.

149 sis (LCA), the most severe form of inherited retinopathy in early childhood.

150 ein paxillin, growth factor-induced ischemic retinopathy in the murine oxygen-induced retinopathy mod

151 mmendations regarding screening for diabetic retinopathy include annual dilated retinal examinations

152 ly causes vision impairment in proliferative retinopathies, including retinopathy of prematurity.

153 Diabetic retinopathy is a common complication of diabetes mellitu

154 claim codes used during the care of diabetic retinopathy is a necessary precursor to fully understand

155 oidal angiogenesis, including oxygen-induced retinopathy, laser-induced choroidal neovascularization,

156 cular edema in patients with various initial retinopathy levels (no retinopathy or mild, moderate, or

157 clinical evidence (0%) of radiation-induced retinopathy, maculopathy, or optic neuropathy.

158 s already in development for targeting these retinopathies may also prove useful for the treatment of

159 These findings suggest that pediatric sickle retinopathy may be more prevalent than previously suspec

160 mic retinopathy in the murine oxygen-induced retinopathy model could be inhibited.

161 hological angiogenesis in the oxygen-induced retinopathy mouse model by promoting glycolysis in endot

162 malaria parasites are innocent bystanders in retinopathy-negative CM and the etiology of the coma is

163 tinopathy-positive CM, their contribution to retinopathy-negative CM is largely unknown.

164 A lower bound for the fraction of retinopathy-negative CM that would be prevented if malar

165 ate the contribution of malaria infection to retinopathy-negative CM.

166 temia does contribute to the pathogenesis of retinopathy-negative CM.

167 can be classified as retinopathy-positive or retinopathy-negative, based on the presence or absence o

168 and cerebrovascular morbidity and mortality; retinopathy, nephropathy, and neuropathy; and harms.

169 The proportions of retinopathy, nephropathy, peripheral neuropathy, diabeti

170 te (27.2%), severe nonproliferative diabetic retinopathy (NPDR) (45.5%).

171 ) progression from nonproliferative diabetic retinopathy (NPDR) to PDR based on graded fundus photogr

172 mild and moderate nonproliferative diabetic retinopathy (NPDR), and 2.3% for severe NPDR or prolifer

173 ) in patients with nonproliferative diabetic retinopathy (NPDR).

174 inopathy and with non-proliferative diabetic retinopathy (NPDR).

175 patients who have non-proliferative diabetic retinopathy (NPDR).

176 pairment at all ages in 2015 due to diabetic retinopathy (odds ratio 2.52 [1.48-3.73]) and cataract (

177 The Children's Hospital of Philadelphia Retinopathy of Prematurity (CHOP ROP) model uses birth w

178 and The Children's Hospital of Philadelphia Retinopathy of Prematurity (CHOP-ROP) postnatal weight g

179 edicine Approaches to Evaluating Acute-Phase Retinopathy of Prematurity (e-ROP) Study telemedicine sy

180 edicine Approaches to Evaluating Acute-Phase Retinopathy of Prematurity (e-ROP) study was conducted f

181 medicine study) and the Postnatal Growth and Retinopathy of Prematurity (G-ROP) Study (a multicenter

182 alysis of data from the Postnatal Growth and Retinopathy of Prematurity (G-ROP) Study.

183 eveloped to improve diagnostic competency in retinopathy of prematurity (ROP) by ophthalmologists-in-

184 on retinal image grading of fellow eyes for retinopathy of prematurity (ROP) features (stage, zone a

185 Telemedicine in retinopathy of prematurity (ROP) has the potential for d

186 Retinopathy of prematurity (ROP) is one of the targets f

187 Retinopathy of prematurity (ROP) is the leading cause of

188 undred thirty-one preterm infants undergoing retinopathy of prematurity (ROP) screenings.

189 625 mg) is increasingly used to treat type 1 retinopathy of prematurity (ROP), but there remain conce

190 ight gain rate to predict the risk of severe retinopathy of prematurity (ROP).

191 optic components in children with or without retinopathy of prematurity (ROP).

192 sparing vitrectomy (LSV) surgery in advanced retinopathy of prematurity (ROP).

193 f treatment strategies for the management of retinopathy of prematurity (ROP).

194 h conventional laser photoablation in type 1 retinopathy of prematurity (ROP).

195 e the rate from the best quartile for severe retinopathy of prematurity and severe intraventricular h

196 ment concepts for diagnosis and treatment of retinopathy of prematurity and to provide interpretation

197 tamin A deficiency, perinatal infections and retinopathy of prematurity as well as specialist pediatr

198 There was no association with retinopathy of prematurity in the preterm group, which s

199 the ffERG recordings and gestational age or retinopathy of prematurity in the preterm group.

200 m, birth weight percentile, gestational age, retinopathy of prematurity occurrence, maternal age at c

201 Sensitivity for Early Treatment of Retinopathy of Prematurity type 1 ROP and potential redu

202 their associations with gestational age and retinopathy of prematurity were examined.

203 We also review the applications to retinopathy of prematurity, diabetic retinopathy, age-re

204 many vision-threatening diseases, including retinopathy of prematurity, diabetic retinopathy, and ag

205 Neovascular eye diseases, including retinopathy of prematurity, diabetic retinopathy, and ag

206 injury on postnatal ultrasonography, severe retinopathy of prematurity, necrotizing enterocolitis, o

207 were no differences in chronic lung disease, retinopathy of prematurity, or NDI among survivors.

208 fection more than 3 days after birth, severe retinopathy of prematurity, severe intraventricular hemo

209 al insufficiency (UPI) increases severity of retinopathy of prematurity, we developed a composite rat

210 nt in proliferative retinopathies, including retinopathy of prematurity.

211 rate-severe chronic lung disease, and severe retinopathy of prematurity.

212 selectively protected against oxygen-induced retinopathy (OIR) in mice.

213 eloped in room air (RA) or an oxygen-induced retinopathy (OIR) model.

214 In the mouse model of oxygen-induced retinopathy (OIR), pericytes become the predominant CCN1

215 ed in the retina of mice with oxygen-induced retinopathy (OIR).

216 While 22 of 32 SCD eyes (68.8%) had retinopathy on biomicroscopy, by UWFA 4 of 24 (16.7%) SC

217 The role of diabetic retinopathy on the relationship between NSAID use and PM

218 local failure, death, enucleation, radiation retinopathy, optic neuropathy, and best-corrected visual

219 ood of progression to proliferative diabetic retinopathy or clinically significant macular edema in p

220 ity of progression to proliferative diabetic retinopathy or clinically significant macular edema was

221 rom no retinopathy to proliferative diabetic retinopathy or clinically significant macular edema was

222 retinal examinations to detect proliferative retinopathy or clinically significant macular edema, bot

223 er 31, 2014, using the search terms diabetic retinopathy OR macular edema AND stroke OR cerebrovascul

224 with various initial retinopathy levels (no retinopathy or mild, moderate, or severe nonproliferativ

225 atio [OR], 2.58; 95% CI, 1.39-4.81; P=.003), retinopathy (OR, 2.24; 95% CI, 1.11-4.50; P = .02), and

226 us images and classified them as healthy (no retinopathy) or having DR, identifying relevant cases fo

227 The risk of heart failure, stroke, or retinopathy, or prevalent fasting versus postprandial hy

228 or vitrectomy, development of proliferative retinopathy, or progression of diabetic retinopathy), an

229 on the progression to proliferative diabetic retinopathy (PDR) and the impact of FAc on changes in Ea

230 actors for developing proliferative diabetic retinopathy (PDR) and vitreous hemorrhage (VH).

231 epresent worsening of proliferative diabetic retinopathy (PDR) in eyes treated with panretinal photoc

232 Proliferative diabetic retinopathy (PDR) is a common cause of blindness in the

233 n (PRP) when managing proliferative diabetic retinopathy (PDR), with or without concomitant baseline

234 ifestations of active proliferative diabetic retinopathy (PDR).

235 3% for severe NPDR or proliferative diabetic retinopathy (PDR).

236 age (VH) secondary to proliferative diabetic retinopathy (PDR).

237 cular edema [DME] and proliferative diabetic retinopathy [PDR]) have a higher risk of CVD will allow

238 Diabetic kidney disease, retinopathy, peripheral neuropathy, cardiovascular auton

239 re considered central to the pathogenesis of retinopathy-positive CM, their contribution to retinopat

240 Cerebral malaria (CM) can be classified as retinopathy-positive or retinopathy-negative, based on t

241 TGF-beta signaling may protect against rapid retinopathy progression and should not be a target of in

242 te recent advances in therapeutics, diabetic retinopathy remains a leading cause of vision impairment

243 sed on standard screening techniques, sickle retinopathy reportedly occurs in 10% of adolescents with

244 f CADASIL and other SVDs, including diabetic retinopathy, resulting in vascular instability.

245 tive), 99.6% (97.0%-99.9%) for proliferative retinopathy; Retmarker 73.0% (72.0 %-74.0%) for any reti

246 terval (CI) 0.58-0.72] and diabetics without retinopathy (RR 0.51, 95% CI 0.32-0.82).

247 ncidence of PME among patients with diabetic retinopathy (RR 1.06, 95% 0.81-1.38).

248 nt in contralateral PCME (RR 19.5), diabetic retinopathy (RR 13.1), retinal vein occlusion (RR 12.9),

249 evaluate self-reported adherence to diabetic retinopathy screening examinations among diabetic subjec

250 Worse baseline levels of diabetic retinopathy severity (Early Treatment Diabetic Retinopat

251 -field fundus photography using the Diabetic Retinopathy Severity Scale.

252 e clinical importance of changes in diabetic retinopathy severity score (DRSS) in patients with diabe

253 Acute zonal occult outer retinopathy should be considered in patients with acute

254 pared with standard Early Treatment Diabetic Retinopathy Study (ETDRS) 7-field photographs (ETDRS pho

255 f FAc on changes in Early Treatment Diabetic Retinopathy Study (ETDRS) diabetic retinopathy (DR) seve

256 nts with 15 or more Early Treatment Diabetic Retinopathy Study (ETDRS) letter score change, mean cont

257 olution (logMAR) or Early Treatment Diabetic Retinopathy Study (ETDRS) letter scores.

258 in patients with Early Treatment of Diabetic Retinopathy Study (ETDRS) level 20-35 than in patients w

259 measured using the Early Treatment Diabetic Retinopathy Study (ETDRS) protocol.

260 s, according to the Early Treatment Diabetic Retinopathy Study (ETDRS) sectors.

261 Early Treatment Diabetic Retinopathy Study BCVA and spectral-domain optical coher

262 dus photography and Early Treatment Diabetic Retinopathy Study best-corrected visual acuity.

263 ty (VA) measured on Early Treatment Diabetic Retinopathy Study charts, injection episodes, and compli

264 uity of at least 72 Early Treatment Diabetic Retinopathy Study letter score (20/40 Snellen equivalent

265 yes was 47.8 (16.9) Early Treatment Diabetic Retinopathy Study letter score (approximately 20/100 Sne

266 prespecified as -5 Early Treatment Diabetic Retinopathy Study letters.

267 [<5, 5-9, or >/=10; Early Treatment Diabetic Retinopathy Study letters] in BCVA) after treatment with

268 ategories of no DR (Early Treatment Diabetic Retinopathy Study levels 10-15; n = 154), mild to modera

269 drusen area in the Early Treatment Diabetic Retinopathy Study Report (ETDRS) grid (P = 2.29 x 10(-11

270 sified according to Early Treatment Diabetic Retinopathy Study Research Group - report no.

271 tinopathy severity (Early Treatment Diabetic Retinopathy Study scale) were associated with increased

272 grading, using the Early Treatment Diabetic Retinopathy Study severity scale.

273 egmentation at 9 Early Treatment of Diabetic Retinopathy Study subfields.

274 orrected electronic Early Treatment Diabetic Retinopathy Study VALS (scores range from 0-100; higher

275 r tufts in the mouse model of oxygen-induced retinopathy, suggesting a role for Cavin-2 in pathogenic

276 ts in the retina of mice with oxygen-induced retinopathy, suggesting that RUNX1 upregulation is a hal

277 ction of neovascular tufts in oxygen-induced retinopathy, supporting the feasibility of targeting RUN

278 ibution around the 5 North Carolina Diabetic Retinopathy Telemedicine Network sites by zip code and t

279 participating in the North Carolina Diabetic Retinopathy Telemedicine Network, (2) the locations of p

280 logy referral in the North Carolina Diabetic Retinopathy Telemedicine Network.

281 t insights into the pathogenesis of diabetic retinopathy that will further guide us toward rationally

282 .5 million to 15.4 million), and by diabetic retinopathy to 3.2 million (0.2 million to 12.9 million)

283 The risk of progression from no retinopathy to proliferative diabetic retinopathy or cli

284 echanisms of monogenic as opposed to complex retinopathies, using AMD as an example of the latter.

285 ciated with ocular hypertension, hemorrhagic retinopathy, vitreous hemorrhage, combined traction and

286 lar edema (DME), vision-threatening diabetic retinopathy (VTDR), defined as the presence of severe no

287 Diabetic retinopathy was attributed as the main cause of vision l

288 Diabetic retinopathy was based on fundus photograph grading, usin

289 Diabetic retinopathy was graded from 2-field retinal images into

290 Visible retinopathy was negatively associated with overall RT (c

291 This Edn2-mediated retinopathy was reduced by all treatments.

292 could be a therapeutic target for preventing retinopathy, we used a pharmacologic approach (SM16, a s

293 -laser treated active proliferative diabetic retinopathy were recruited from 22 UK ophthalmic centres

294 Insured patients with diabetic retinopathy were seen by the practices between 2011 and

295 chieved acceptable sensitivity for referable retinopathy when compared with that of human graders and

296 TATION: Patients with proliferative diabetic retinopathy who were treated with intravitreal afliberce

297 dy by assessing the association of worsening retinopathy with objectively measured functional outcome

298 r cataract surgery in patients with diabetic retinopathy, with no unanticipated safety events.

299 Two-year cumulative rates for retinopathy worsening ranged from 7.1% to 10.2% and 17.2

300 and 2 years and cumulative probabilities for retinopathy worsening through 2-year without adjustment