ライフサイエンスコーパス: diabetic retinopathy

1 moderately severe to severe nonproliferative diabetic retinopathy).

2 r mild, moderate, or severe nonproliferative diabetic retinopathy).

3 icipants who had not previously screened for diabetic retinopathy.

4 s revealed an association of FLCN eQTLs with diabetic retinopathy.

5 in several blinding eye diseases, including diabetic retinopathy.

6 ulation of Keap1-Nrf2-antioxidant defense in diabetic retinopathy.

7 larizations is the hallmark of proliferative diabetic retinopathy.

8 mellitus lasting for 10 years or more, with diabetic retinopathy.

9 acuity, history of diabetes, and history of diabetic retinopathy.

10 es in neural and retinal diseases, including diabetic retinopathy.

11 ent age, history of diabetes, and history of diabetic retinopathy.

12 hyperlipidemia is also closely related with diabetic retinopathy.

13 r earlier objective detection of preclinical diabetic retinopathy.

14 ene cascade for therapeutic benefit in early diabetic retinopathy.

15 herapy to prevent or slow the development of diabetic retinopathy.

16 strategies such as screening programmes for diabetic retinopathy.

17 meability, features commonly associated with diabetic retinopathy.

18 ns such as age-related macular degeneration, diabetic retinopathy.

19 urine retinal microvasculature in a model of diabetic retinopathy.

20 eration, and edema) in the initial stages of diabetic retinopathy.

21 e, smoking, HT randomization, education, and diabetic retinopathy.

22 that are characteristic of non-proliferative diabetic retinopathy.

23 reflect the medical record for patients with diabetic retinopathy.

24 deficiency impairs this process and prevents diabetic retinopathy.

25 ths among those with severe nonproliferative diabetic retinopathy.

26 such as age-related macular degeneration and diabetic retinopathy.

27 on to determine the presence and severity of diabetic retinopathy.

28 development of PDR and slows progression of diabetic retinopathy.

29 sfunction before the clinical development of diabetic retinopathy.

30 e of Jurkat cells and disease progression in diabetic retinopathy.

31 oxidative damage and to prevent or slow down diabetic retinopathy.

32 the CCT values in patients with and without diabetic retinopathy.

33 glaucoma, pediatric neuro-ophthalmology, and diabetic retinopathy.

34 ponse genes were tested for association with diabetic retinopathy.

35 Keap1-Nrf2, regulates antioxidant defense in diabetic retinopathy.

36 pment of pathological vascular remodeling in diabetic retinopathy.

37 lliculin (FLCN) as a susceptibility gene for diabetic retinopathy.

38 such as age-related macular degeneration and diabetic retinopathy.

39 ochondrial dynamics and genomic stability in diabetic retinopathy.

40 ion, and ameliorated retinal dysfunction and diabetic retinopathy.

41 roups according to the presence and stage of diabetic retinopathy.

42 e to glucose was greater in individuals with diabetic retinopathy.

43 rmed in treating patients with proliferative diabetic retinopathy.

44 tions, accelerating mitochondrial damage and diabetic retinopathy.

45 ession implicated FLCN as a disease gene for diabetic retinopathy.

46 euritis (18), retinitis pigmentosa (17), and diabetic retinopathy (16).

47 million [0.6 million to 13.3 million]), and diabetic retinopathy (2.6 million [0.2 million to 9.9 mi

48 ractive error (60.8%), cataract (20.1%), and diabetic retinopathy (5.2%).

49 teractions and mechanisms that contribute to diabetic retinopathy, a visually debilitating complicati

50 Ocular conditions, including diabetic retinopathy, age-related macular degeneration,

51 -induced diabetic mice and human donors with diabetic retinopathy also presented similar increases in

52 With an increase in the stage of diabetic retinopathy, alterations in corneal findings al

53 check-up practice and associated factors of diabetic retinopathy among adult diabetic patients at De

54 The proportion of good knowledge about diabetic retinopathy among diabetic patients at Debark h

55 promotion leaflet can increase knowledge of diabetic retinopathy, an important screening predictor.

56 patients were recruited (90 patients with no diabetic retinopathy and 90 patients with NPDR) into the

57 betic retinopathy or severe nonproliferative diabetic retinopathy and a high suspicion of NV based on

58 coherence tomography (OCT) mainly focused on diabetic retinopathy and age-related macular degeneratio

59 ch, PPARalpha is a promising drug target for diabetic retinopathy and age-related macular degeneratio

60 eous semaglutide and canagliflozin increased diabetic retinopathy and amputation, respectively.

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

62 errant retinal angiogenesis in proliferative diabetic retinopathy and its modulation has proven to be

63 Diabetes associated complications, including diabetic retinopathy and loss of vision, are major healt

64 plications (such as diabetic kidney disease, diabetic retinopathy and neuropathy) lead to increased m

65 ll have a major impact on inhibiting/halting diabetic retinopathy and preventing the loss of vision.

66 which underlies diseases like proliferative diabetic retinopathy and retinopathy of prematurity.

67 dge about the nature and the consequences of diabetic retinopathy and routine eye checkup helps for t

68 inhibitors are beneficial for patients with diabetic retinopathy and suggest that antagonizing the R

69 wledge of patients with diabetes mellitus on diabetic retinopathy and their eye check-up practices in

70 ty of human diseases including proliferative diabetic retinopathy and wet age-related macular degener

71 proliferative retinopathy, or progression of diabetic retinopathy), and nerve events (a composite of

72 eases, including retinopathy of prematurity, diabetic retinopathy, and age-related macular degenerati

73 mmation in age-related macular degeneration, diabetic retinopathy, and glaucoma.

74 .4 for cataract, glaucoma, near-sightedness, diabetic retinopathy, and macular degeneration, respecti

75 of cataract, macular degeneration, glaucoma, diabetic retinopathy, and near-sightedness using the Goo

76 ave a significant role in the development of diabetic retinopathy, and unraveling the mechanism respo

77 ascular age-related macular degeneration and diabetic retinopathy are prevalent causes of vision loss

78 -related macular degeneration, glaucoma, and diabetic retinopathy, are ideal candidates for home moni

79 , using wide-field non-perfusion analysis in diabetic retinopathy as a model widefield OCTA usage-cas

80 into two groups according to the presence of diabetic retinopathy, as Group I with retinopathy and Gr

81 Main outcome measurements were any signs of diabetic retinopathy, as measured by diagnosis codes for

82 rsening of retinal perfusion associated with diabetic retinopathy but also may be able to improve ret

83 ation of DNA methylation can prevent/reverse diabetic retinopathy by maintaining mitochondrial dynami

84 ty, and described variations in incidence of diabetic retinopathy by region with a focus on populatio

85 Vitreous hemorrhage from proliferative diabetic retinopathy can cause loss of vision.

86 glaucoma, age-related macular degeneration, diabetic retinopathy, cataract, glaucoma surgery, catara

87 omponents in the pathogenic cascade of early diabetic retinopathy, characterized by neuronal and vasc

88 Diabetic Retinopathy Clinical Research Network (DRCR.net

89 The Diabetic Retinopathy Clinical Research Network Protocol

90 32-1.82), as did patients with proliferative diabetic retinopathy (CVA: HR, 2.53; 95% CI, 1.84-3.48;

91 Diabetic retinopathy, diabetic macular edema (DME), visi

92 ither the duration of DM nor the presence of diabetic retinopathy did have a significant effect on th

93 severity based on the International Clinical Diabetic Retinopathy disease severity scale in each of 3

94 es), divided into groups: the groups without diabetic retinopathy (DR) (n = 68); the nonproliferative

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

96 tients with DM without clinically detectable diabetic retinopathy (DR) and 57 age-matched control sub

97 logy of two major blinding retinal diseases, diabetic retinopathy (DR) and age-related macular degene

98 The in vivo function of microRNAs (miRs) in diabetic retinopathy (DR) and age-related macular degene

99 Previous studies on the relationship between diabetic retinopathy (DR) and cardiovascular disease (CV

100 The most common indications for RLT were diabetic retinopathy (DR) and diabetic macular oedema (D

101 acterize the accuracy of coding for stage of diabetic retinopathy (DR) and DR-related complications (

102 of four ocular diseases; cataract, glaucoma, diabetic retinopathy (DR) and dry eye disease (DED) was

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

104 : 210 normal (NL), 183 glaucoma (GL), and 18 diabetic retinopathy (DR) at Tilganga Institute of Ophth

105 prevalence of diabetes, annual screening for diabetic retinopathy (DR) by expert human grading of ret

106 Ltd., Bengaluru, India) in detecting diabetic retinopathy (DR) compared with a conventional t

107 hy (DPN), diabetic kidney disease (DKD), and diabetic retinopathy (DR) contribute to significant morb

108 Diabetic retinopathy (DR) is a common complication of di

109 Diabetic retinopathy (DR) is a major cause of blindness

110 Diabetic retinopathy (DR) is a major cause of blindness,

111 Diabetic retinopathy (DR) is a microvascular complicatio

112 Diabetic retinopathy (DR) is a severe retinal disorder t

113 Diabetic retinopathy (DR) is characterized by apoptotic

114 Diabetic retinopathy (DR) is diagnosed clinically by dir

115 Ophthalmic screening to check for diabetic retinopathy (DR) is important to prevent vision

116 , and its role in ocular angiogenesis and in diabetic retinopathy (DR) is not yet fully understood.

117 The main therapeutic goal for diabetic retinopathy (DR) is to prevent vision loss in p

118 The presence and severity of diabetic retinopathy (DR) may contribute to the risk of

119 ics of the vascular features associated with diabetic retinopathy (DR) may improve assessment and tre

120 vidence on diagnostic test accuracy (DTA) of diabetic retinopathy (DR) screening utilising photograph

121 '-deoxyguanosine (8-OHdG) as a biomarker for diabetic retinopathy (DR) screening.

122 The diabetic retinopathy (DR) severity score improved by at

123 Patients with diabetic retinopathy (DR) show reduced ipRGC function, a

124 n most countries set screening intervals for diabetic retinopathy (DR) that are insufficiently inform

125 , their results regarding the progression of diabetic retinopathy (DR) were neutral with liraglutide

126 ctions are used commonly in the treatment of diabetic retinopathy (DR), but the need for treatment an

127 ous forms of exudative maculopathy including diabetic retinopathy (DR), retinal vein occlusion (RVO),

128 Diabetic retinopathy (DR), the most common cause of visi

129 ment can prevent irreversible blindness from diabetic retinopathy (DR), which is the leading cause of

130 thms in screening patients with diabetes for diabetic retinopathy (DR).

131 nctions in pathological conditions including diabetic retinopathy (DR).

132 l processes associated with the induction of diabetic retinopathy (DR).

133 ature) with the incidence and progression of diabetic retinopathy (DR).

134 -retinal barrier due to hyperpermeability in diabetic retinopathy (DR).

135 eir mechanism of action were investigated in diabetic retinopathy (DR).

136 have not identified any robust risk loci for diabetic retinopathy (DR).

137 creasing diabetic microvasculopathy based on diabetic retinopathy (DR).

138 he decision-making processes before treating diabetic retinopathy (DR).

139 ethods may provide new markers associated to diabetic retinopathy (DR).

140 Retinal vascular caliber has been linked to diabetic retinopathy (DR).

141 d with ME from retinal vein occlusion (RVO), diabetic retinopathy (DR; diabetic macular edema, DME),

142 role in retinal ischemia and angiogenesis in diabetic retinopathy, especially in the proliferative st

143 In patients with diabetic retinopathy, especially PDR, who are managed wi

144 example, the first autonomous point-of-care diabetic retinopathy examination de novo authorized by t

145 of this study was to assess knowledge about diabetic retinopathy, eye check-up practice and associat

146 Fundus photographs from 7 Early Treatment Diabetic Retinopathy fields were graded in a masked mann

147 tic defects or age-related diseases, such as diabetic retinopathies, glaucoma, and macular degenerati

148 age-related macular degeneration, cataracts, diabetic retinopathy, glaucoma, and intraocular cancers.

149 than age-related macular degeneration (AMD), diabetic retinopathy, glaucoma, or cornea guttata (aOR,

150 changes associated with various disease i.e. Diabetic Retinopathy, Glaucoma.

151 The modified Airlie House classification of diabetic retinopathy has been extended for use in the Ea

152 response were assessed for association with diabetic retinopathy in a genome-wide association study

153 The total caseload of diabetic retinopathy in adults age 40 and older is expec

154 examination plays a vital role in detecting diabetic retinopathy in its earliest stage before the on

155 ions of erythropoietin on the development of diabetic retinopathy in patients with diabetes mellitus

156 rogression of retinal vascular diseases like diabetic retinopathy in small animal models is often com

157 significant increased risk for proliferative diabetic retinopathy in the multivariate model included

158 Diabetic retinopathy is a common complication of diabete

159 Diabetic retinopathy is a leading cause of vision impair

160 billing claim codes used during the care of diabetic retinopathy is a necessary precursor to fully u

161 Diabetic retinopathy is a potentially blinding eye disea

162 Diabetic retinopathy is significantly associated with fu

163 od vessels, which is an essential element of diabetic retinopathy, is driven by chronic elevation of

164 l agreement for cataract (kappa >= 0.71) and diabetic retinopathy (kappa >= 0.61) and moderate to sub

165 ator-initiated trials studying proliferative diabetic retinopathy, neovascular age-related macular de

166 ), moderate (27.2%), severe nonproliferative diabetic retinopathy (NPDR) (45.5%).

167 tivity, and specificity for nonproliferative diabetic retinopathy (NPDR) and proliferative diabetic r

168 nopathy, those with minimal nonproliferative diabetic retinopathy (NPDR) had a higher risk of CVA (ha

169 h diabetes, 30 of them had non-proliferative diabetic retinopathy (NPDR), and 30 had proliferative di

170 ured by diagnosis codes for nonproliferative diabetic retinopathy (NPDR), proliferative diabetic reti

171 abetic retinopathy (PDR) or nonproliferative diabetic retinopathy (NPDR), with or without diabetic ma

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

173 eir loss is associated with diseases such as diabetic retinopathy or cancer.

174 probability of progression to proliferative diabetic retinopathy or clinically significant macular e

175 ression from no retinopathy to proliferative diabetic retinopathy or clinically significant macular e

176 e likelihood of progression to proliferative diabetic retinopathy or clinically significant macular e

177 Eyes with proliferative diabetic retinopathy or severe nonproliferative diabetic

178 nute per 1.73 m(2) of body-surface area, and diabetic retinopathy, or they had a urinary albumin-to-c

179 eases such as retinopathy of prematurity and diabetic retinopathy, overgrowth of retinal blood vessel

180 elitis (P < 0.001), prostatitis (P < 0.001), diabetic retinopathy (P < 0.001), and vascular catheter

181 one secondary outcome variable: knowledge of diabetic retinopathy (p = .03) with moderate effect (par

182 nd risk factors for developing proliferative diabetic retinopathy (PDR) and vitreous hemorrhage (VH).

183 s that patients diagnosed with proliferative diabetic retinopathy (PDR) be considered for pan-retinal

184 ovascular changes in eyes with proliferative diabetic retinopathy (PDR) following panretinal photocoa

185 reported to be associated with proliferative diabetic retinopathy (PDR) in Caucasian patients with di

186 ts that represent worsening of proliferative diabetic retinopathy (PDR) in eyes treated with panretin

187 -world outcomes of people with proliferative diabetic retinopathy (PDR) in India and highlight opport

188 The hallmark of proliferative diabetic retinopathy (PDR) is retinal neovascularization

189 of neovascularization (NV) in proliferative diabetic retinopathy (PDR) on ultra-widefield (UWF) fluo

190 ely with anti-VEGF therapy for proliferative diabetic retinopathy (PDR) or nonproliferative diabetic

191 iabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR) were excellent (>90%).

192 VR) (n = 30), PVR (n = 16) and proliferative diabetic retinopathy (PDR) with tractional RD (n = 8).

193 ed macular degeneration (AMD), proliferative diabetic retinopathy (PDR), and proliferative vitreoreti

194 e diabetic retinopathy (NPDR), proliferative diabetic retinopathy (PDR), or diabetic macular edema (D

195 oagulation (PRP) when managing proliferative diabetic retinopathy (PDR), with or without concomitant

196 PRP alone in the treatment of proliferative diabetic retinopathy (PDR).

197 retinopathy (NPDR), and 30 had proliferative diabetic retinopathy (PDR).

198 onperfusion (RNP) in eyes with proliferative diabetic retinopathy (PDR).

199 ) in eyes with treatment-naive proliferative diabetic retinopathy (PDR).

200 s hemorrhage (VH) secondary to proliferative diabetic retinopathy (PDR).

201 evere manifestations of active proliferative diabetic retinopathy (PDR).

202 ) in treatment-naive eyes with proliferative diabetic retinopathy (PDR).

203 plicated in the progression of proliferative diabetic retinopathy (PDR).

204 abetic macular edema [DME] and proliferative diabetic retinopathy [PDR]), which require frequent life

205 s and document within the natural history of diabetic retinopathy processes of protection and repair

206 inal nonperfusion, which are associated with diabetic retinopathy progression.

207 The annual incidence of diabetic retinopathy ranged from 2.2% to 12.7% and progr

208 Diabetic retinopathy remains the leading cause of acquir

209 sions were intended to simulate glaucoma and diabetic retinopathy, respectively.

210 allmark of CADASIL and other SVDs, including diabetic retinopathy, resulting in vascular instability.

211 in the incidence of PME among patients with diabetic retinopathy (RR 1.06, 95% 0.81-1.38).

212 lor photographs using the Early Treatment of Diabetic Retinopathy scale.

213 Diabetic retinopathy screening can be accomplished in an

214 To evaluate self-reported adherence to diabetic retinopathy screening examinations among diabet

215 Scottish Diabetic Retinopathy Screening Programme data from 1 Jan

216 Implementation of an automated diabetic retinopathy screening system in a primary care

217 icantly associated with adherence to initial diabetic retinopathy screening.

218 Diabetic retinopathy searches related to other diseases

219 Diabetic retinopathy severity improvements with ranibizu

220 more precise and complete staging system for diabetic retinopathy severity in the future.

221 d exploratory outcome measures included CST, Diabetic Retinopathy Severity Scale (DRSS) score, and du

222 dary outcomes included ischemic index (ISI), diabetic retinopathy severity scale (DRSS) scores, visua

223 ed with worse retinopathy as measured on the Diabetic Retinopathy Severity Scale.

224 EGF) therapy show significant improvement in diabetic retinopathy severity score (DRSS), in particula

225 Diabetic Retinopathy Severity Score level was determined

226 cross-sectional study, eyes were grouped by diabetic retinopathy severity using the 7-field Early Tr

227 Diabetic retinopathy severity was evaluated photographic

228 or axis length were strongly associated with diabetic retinopathy severity.

229 scular catheter, internal organ abscess, and diabetic retinopathy showed a significant risk (P < 0.00

230 f referral and best-corrected visual acuity, diabetic retinopathy status in both eyes.

231 quivalent (VAE), approximate Early Treatment Diabetic Retinopathy Study (appETDRS) letter score, was

232 ng as compared with standard Early Treatment Diabetic Retinopathy Study (ETDRS) 7-field photographs (

233 For each patient, the BCVA [Early Treatment Diabetic Retinopathy Study (ETDRS) charts] and macular t

234 areas in 9 subfields on the Early Treatment Diabetic Retinopathy Study (ETDRS) grid and correlated t

235 inner and outer rings of the Early Treatment Diabetic Retinopathy Study (ETDRS) grid, generated by th

236 ved on conventional reported early treatment diabetic retinopathy study (ETDRS) grid-based optical co

237 e of patients to achieve >=5 Early Treatment Diabetic Retinopathy Study (ETDRS) letter gain postopera

238 of patients with 15 or more Early Treatment Diabetic Retinopathy Study (ETDRS) letter score change,

239 t DR gained a median of 11.0 Early Treatment Diabetic Retinopathy Study (ETDRS) letters (interquartil

240 rom 60.3 to 61.0 approximate Early Treatment Diabetic Retinopathy Study (ETDRS) letters (mean change,

241 l acuity (BCVA) of 5 or more Early Treatment Diabetic Retinopathy Study (ETDRS) letters (Snellen equi

242 tients gaining 15 or more Early Treatment of Diabetic Retinopathy Study (ETDRS) letters from baseline

243 e patient's greatest gain in Early Treatment Diabetic Retinopathy Study (ETDRS) letters from baseline

244 hange from baseline was -3.2 Early Treatment Diabetic Retinopathy Study (ETDRS) letters, -0.5 ETDRS l

245 hange from baseline was -4.6 Early Treatment Diabetic Retinopathy Study (ETDRS) letters, -2.3 ETDRS l

246 nts and lost a median of 7.0 Early Treatment Diabetic Retinopathy Study (ETDRS) letters, HD-1 patient

247 as lower in patients with Early Treatment of Diabetic Retinopathy Study (ETDRS) level 20-35 than in p

248 duration >=5 years and an Early Treatment of Diabetic Retinopathy Study (ETDRS) level of <=35 were ra

249 g mydriatic 7-standard field Early Treatment Diabetic Retinopathy Study (ETDRS) photographs.

250 y severity using the 7-field Early Treatment Diabetic Retinopathy Study (ETDRS) protocol (levels 10-2

251 cuity was measured using the Early Treatment Diabetic Retinopathy Study (ETDRS) protocol.

252 ured with EDI-OCT in nine Early Treatment of Diabetic Retinopathy Study (ETDRS) subfields before and

253 e primary outcome was 1-year Early Treatment Diabetic Retinopathy Study (ETDRS) visual acuity (VA).

254 been extended for use in the Early Treatment Diabetic Retinopathy Study (ETDRS).

255 y (PD) in the SCP within the Early Treatment Diabetic Retinopathy Study 6-mm circle, 3-mm circle, and

256 ain OCT for DME, and 7-field Early Treatment Diabetic Retinopathy Study [ETDRS] and ultra-widefield [

257 0/40 or better vision (>= 69 Early Treatment Diabetic Retinopathy Study [ETDRS] letters) or an increa

258 an+/-standard deviation [SD] Early Treatment Diabetic Retinopathy Study [ETDRS] letters) were similar

259 rrected visual acuity (BCVA; Early Treatment Diabetic Retinopathy Study [ETDRS] letters), and central

260 sual acuity (VA) measured on Early Treatment Diabetic Retinopathy Study charts, injection episodes, a

261 d photographically using the Early Treatment Diabetic Retinopathy Study DR severity scale.

262 ease in VD and PD within all Early Treatment Diabetic Retinopathy Study inner ring quadrants; however

263 versus absence: 9.4 and 8.7 Early Treatment Diabetic Retinopathy Study letter scores, respectively (

264 , vision loss of more than 5 Early Treatment Diabetic Retinopathy Study letters from baseline, as wel

265 BCVA improved by 18.3+/-12.6 Early Treatment Diabetic Retinopathy Study letters in treated eyes.

266 ed vision gain of 15 or more Early Treatment Diabetic Retinopathy Study letters, vision loss of more

267 es into categories of no DR (Early Treatment Diabetic Retinopathy Study levels 10-15; n = 154), mild

268 defined as improvement in 3 Early Treatment Diabetic Retinopathy Study lines (doubling of the visual

269 with the drusen area in the Early Treatment Diabetic Retinopathy Study Report (ETDRS) grid (P = 2.29

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

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

272 oundary Segmentation at 9 Early Treatment of Diabetic Retinopathy Study subfields.

273 he best-corrected electronic Early Treatment Diabetic Retinopathy Study VALS (scores range from 0-100

274 surgical safety parameters, Early Treatment Diabetic Retinopathy Study visual acuity (VA), minimum r

275 eir distribution around the 5 North Carolina Diabetic Retinopathy Telemedicine Network sites by zip c

276 patients participating in the North Carolina Diabetic Retinopathy Telemedicine Network, (2) the locat

277 ophthalmology referral in the North Carolina Diabetic Retinopathy Telemedicine Network.

278 c pdx1 (-/-) zebrafish mutant as a model for diabetic retinopathy that lacks the transcription factor

279 important insights into the pathogenesis of diabetic retinopathy that will further guide us toward r

280 With the presence and advancement of diabetic retinopathy, the ECD and hexagonal cell ratio d

281 risk of early onset and rapid progression of diabetic retinopathy, the leading cause of blindness and

282 s had vitreous hemorrhage from proliferative diabetic retinopathy, there was no statistically signifi

283 illion (0.5 million to 15.4 million), and by diabetic retinopathy to 3.2 million (0.2 million to 12.9

284 rization (NV) in patients with proliferative diabetic retinopathy using swept-source optical coherenc

285 etic macular edema (DME), vision-threatening diabetic retinopathy (VTDR), defined as the presence of

286 Diabetic retinopathy was based on fundus photograph grad

287 Diabetic retinopathy was graded from 2-field retinal ima

288 Progression to proliferative diabetic retinopathy was higher in individuals with mild

289 he full picture of diabetic nephropathy, but diabetic retinopathy was prevented.

290 Diabetic retinopathy was significantly associated with a

291 In 542 (82%) of all patients, diabetic retinopathy was the most common diagnosis.

292 eyes of 45 patients with varying degrees of diabetic retinopathy were enrolled and analyzed.

293 tes from the Australian Registry of Advanced Diabetic Retinopathy were enrolled in this study.

294 wn to be associated with the pathogenesis of diabetic retinopathy were significantly elevated followi

295 rimary vitrectomy for TRD from proliferative diabetic retinopathy were studied.

296 g and best-corrected blindness; cataract and diabetic retinopathy were the top causes for best-correc

297 ue to vitreous hemorrhage from proliferative diabetic retinopathy who were enrolled from November 201

298 ors referred for retinal evaluation (16.7%), diabetic retinopathy with macular oedema (15.8%), and AM

299 ing data on the incidence and progression of diabetic retinopathy with stratification by age and sex

300 BCVA after cataract surgery in patients with diabetic retinopathy, with no unanticipated safety event