ライフサイエンスコーパス: retinopathy

1 y severe to severe nonproliferative diabetic retinopathy).

2 ose was greater in individuals with diabetic retinopathy.

3 2, regulates antioxidant defense in diabetic retinopathy.

4 shown to have an association with autoimmune retinopathy.

5 itive effect of increased FLCN expression on retinopathy.

6 pathological vascular remodeling in diabetic retinopathy.

7 (FLCN) as a susceptibility gene for diabetic retinopathy.

8 ge-related macular degeneration and diabetic retinopathy.

9 l dynamics and genomic stability in diabetic retinopathy.

10 ameliorated retinal dysfunction and diabetic retinopathy.

11 ording to the presence and stage of diabetic retinopathy.

12 reating patients with proliferative diabetic retinopathy.

13 celerating mitochondrial damage and diabetic retinopathy.

14 ut increased in PRPH2-related Stargardt-like retinopathy.

15 onal RD associated with proliferative vitreo-retinopathy.

16 plicated FLCN as a disease gene for diabetic retinopathy.

17 cipants versus diabetic participants without retinopathy.

18 who had not previously screened for diabetic retinopathy.

19 d an association of FLCN eQTLs with diabetic retinopathy.

20 al blinding eye diseases, including diabetic retinopathy.

21 f Keap1-Nrf2-antioxidant defense in diabetic retinopathy.

22 ral and retinal diseases, including diabetic retinopathy.

23 idemia is also closely related with diabetic retinopathy.

24 ns is the hallmark of proliferative diabetic retinopathy.

25 nstrated signs of significant hyperviscosity retinopathy.

26 rowth of blood vessels in mice with ischemic retinopathy.

27 lasting for 10 years or more, with diabetic retinopathy.

28 history of diabetes, and history of diabetic retinopathy.

29 history of diabetes, and history of diabetic retinopathy.

30 al vascular occlusive disorders and ischemic retinopathy.

31 phenotypic manifestation of CERKL-associated retinopathy.

32 objective detection of preclinical diabetic retinopathy.

33 de for therapeutic benefit in early diabetic retinopathy.

34 VKH presented with unilateral proliferative retinopathy.

35 prevent or slow the development of diabetic retinopathy.

36 damage and to prevent or slow down diabetic retinopathy.

37 iduals with type 1 diabetes with and without retinopathy.

38 concerning for hereditary versus autoimmune retinopathy.

39 before the clinical development of diabetic retinopathy.

40 maneuver is a risk factor for venous stasis retinopathy.

41 values in patients with and without diabetic retinopathy.

42 angiogenesis in experimental oxygen-induced retinopathy.

43 pediatric neuro-ophthalmology, and diabetic retinopathy.

44 CI, 0.721-1.290) compared with eyes with no retinopathy.

45 es were tested for association with diabetic retinopathy.

46 ir cancer within 6 months after the onset of retinopathy.

47 transformed therapy for these proliferative retinopathies.

48 t or treat aberrant angiogenesis of ischemic retinopathies.

49 etinoid therapeutics for managing RP-related retinopathies.

50 people are affected by eye diseases, such as retinopathies.

51 tion and glia proliferation in proliferative retinopathies.

52 cataract surgery in eyes with proliferative retinopathy (0.903; 95% CI, 0.725-1.124), and nonprolife

53 ; 95% CI, 0.725-1.124), and nonproliferative retinopathy (0.965; 95% CI, 0.721-1.290) compared with e

54 9%), screening for diabetic and hypertensive retinopathy (13.1%), referral (9.7%), sudden vision loss

55 Hypertensive retinopathy (18.9%) was the commonest VR disease, follow

56 except in patients with diabetes and without retinopathy (4.086; 95% CI, 3.511-4.754).

57 ucose and hemoglobin concentrations, malaria retinopathy, acute kidney injury, and prolonged coma dur

58 e and imaging findings of a similar AMN-like retinopathy after treatment with atezolizumab.

59 following dependent factors to differentiate retinopathy; age, T1D duration, gingivitis, periodontiti

60 diabetic mice and human donors with diabetic retinopathy also presented similar increases in LncRNA M

61 With an increase in the stage of diabetic retinopathy, alterations in corneal findings also increa

62 practice and associated factors of diabetic retinopathy among adult diabetic patients at Debark hosp

63 proportion of good knowledge about diabetic retinopathy among diabetic patients at Debark hospital w

64 n leaflet can increase knowledge of diabetic retinopathy, an important screening predictor.

65 A total of 77 patients with ABCA4-related retinopathy and 110 control subjects underwent quantitat

66 eyes of 20 diabetic subjects type 2 without retinopathy and 20 eyes of 20 healthy controls of the sa

67 inopathy or severe nonproliferative diabetic retinopathy and a high suspicion of NV based on clinical

68 tomography (OCT) mainly focused on diabetic retinopathy and age-related macular degeneration.

69 lpha is a promising drug target for diabetic retinopathy and age-related macular degeneration.

70 glutide and canagliflozin increased diabetic retinopathy and amputation, respectively.

71 nce of diabetic retinopathy, as Group I with retinopathy and Group II without.

72 tinal angiogenesis in proliferative diabetic retinopathy and its modulation has proven to be effectiv

73 associated complications, including diabetic retinopathy and loss of vision, are major health concern

74 ssociated with increased risk of T2D-related retinopathy and modestly associated with chronic kidney

75 s (such as diabetic kidney disease, diabetic retinopathy and neuropathy) lead to increased mortality,

76 icient diabetes (SIDD) had increased risk of retinopathy and neuropathy, whereas the severe insulin-r

77 derlies diseases like proliferative diabetic retinopathy and retinopathy of prematurity.

78 the nature and the consequences of diabetic retinopathy and routine eye checkup helps for timely ide

79 rs are beneficial for patients with diabetic retinopathy and suggest that antagonizing the RAAS impro

80 patients with diabetes mellitus on diabetic retinopathy and their eye check-up practices in Ethiopia

81 /or cone fluorescent reporters, manifested a retinopathy and thin optic nerves (ON).

82 taract, glaucoma, near-sightedness, diabetic retinopathy, and macular degeneration, respectively, wit

83 ct, macular degeneration, glaucoma, diabetic retinopathy, and near-sightedness using the Google searc

84 an 1500 g who met criteria for treatment for retinopathy, and randomised patients equally (1:1:1) to

85 urpose was to assess periodontal conditions, retinopathy, and serum glutamic acid decarboxylase antib

86 nificant role in the development of diabetic retinopathy, and unraveling the mechanism responsible fo

87 , MI, CHF, and death, with higher degrees of retinopathy appearing to carry a heightened risk for eac

88 ge-related macular degeneration and diabetic retinopathy are prevalent causes of vision loss requirin

89 The majority of patients with retinopathy are unaware of this diagnosis, including the

90 Retinopathy as a complication to T1D is linked to the du

91 uperficial and deep capillary bed with worse retinopathy as measured on the Diabetic Retinopathy Seve

92 groups according to the presence of diabetic retinopathy, as Group I with retinopathy and Group II wi

93 ity, gestational age, birth weight, stage of retinopathy at prematurity, and presence of pre-plus or

94 f retinal perfusion associated with diabetic retinopathy but also may be able to improve retinal perf

95 DNA methylation can prevent/reverse diabetic retinopathy by maintaining mitochondrial dynamics and DN

96 reous hemorrhage from proliferative diabetic retinopathy can cause loss of vision.

97 Proliferative retinopathy can present variably in VKH patients and ind

98 , age-related macular degeneration, diabetic retinopathy, cataract, glaucoma surgery, cataract surger

99 P1-implicit time indiabetic patients without retinopathy compared to normal controls.

100 delays in individuals with diabetes without retinopathy compared with age-matched control subjects (

101 etinal function (electroretinogram), and the retinopathy continued to progress.

102 Retinopathy continues to progress even when diabetic pat

103 as did patients with proliferative diabetic retinopathy (CVA: HR, 2.53; 95% CI, 1.84-3.48; MI: HR, 1

104 duration of DM nor the presence of diabetic retinopathy did have a significant effect on the CCT.

105 ded into groups: the groups without diabetic retinopathy (DR) (n = 68); the nonproliferative DR (NPDR

106 wo major blinding retinal diseases, diabetic retinopathy (DR) and age-related macular degeneration (A

107 ost common indications for RLT were diabetic retinopathy (DR) and diabetic macular oedema (DMO) (542

108 the accuracy of coding for stage of diabetic retinopathy (DR) and DR-related complications (including

109 Diabetic retinopathy (DR) is a common complication of diabetes an

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

111 Diabetic retinopathy (DR) is a microvascular complication of diab

112 Diabetic retinopathy (DR) is a severe retinal disorder that can l

113 Diabetic retinopathy (DR) is diagnosed clinically by directly vie

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

115 The main therapeutic goal for diabetic retinopathy (DR) is to prevent vision loss in patients w

116 e vascular features associated with diabetic retinopathy (DR) may improve assessment and treatment of

117 anosine (8-OHdG) as a biomarker for diabetic retinopathy (DR) screening.

118 The diabetic retinopathy (DR) severity score improved by at least 1 s

119 Patients with diabetic retinopathy (DR) show reduced ipRGC function, as inferre

120 untries set screening intervals for diabetic retinopathy (DR) that are insufficiently informed by con

121 Diabetic retinopathy (DR), the most common cause of vision loss,

122 prevent irreversible blindness from diabetic retinopathy (DR), which is the leading cause of visual i

123 y provide new markers associated to diabetic retinopathy (DR).

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

125 creening patients with diabetes for diabetic retinopathy (DR).

126 n pathological conditions including diabetic retinopathy (DR).

127 from retinal vein occlusion (RVO), diabetic retinopathy (DR; diabetic macular edema, DME), or noninf

128 The retinopathy (EMERALD) study tested diagnostic accuracy,

129 In patients with diabetic retinopathy, especially PDR, who are managed with anti-V

130 the first autonomous point-of-care diabetic retinopathy examination de novo authorized by the FDA, a

131 sed the robust mouse model of oxygen-induced retinopathy exposing C57BL/6 mice to 75% oxygen from pos

132 study was to assess knowledge about diabetic retinopathy, eye check-up practice and associated factor

133 ts or age-related diseases, such as diabetic retinopathies, glaucoma, and macular degeneration, cause

134 related macular degeneration (AMD), diabetic retinopathy, glaucoma, or cornea guttata (aOR, 1.35; P =

135 fied Airlie House classification of diabetic retinopathy has been extended for use in the Early Treat

136 d to reassess the risk of hydroxychloroquine retinopathy (HR) in obese women using the American Acade

137 s and outcome of management of proliferative retinopathy in 2 patients with VKH.

138 found in 68.2%, periodontitis in 21.2%, and retinopathy in 64.7%, GADA (>=35 U/mL) in 54.1%, and ser

139 present an impressive case of venous stasis retinopathy in a 10-year-old boy with ocular hypertensio

140 were assessed for association with diabetic retinopathy in a genome-wide association study meta-anal

141 The aim was to investigate retinopathy in a model closely mimicking the normal prog

142 The total caseload of diabetic retinopathy in adults age 40 and older is expected to in

143 By now, venous stasis retinopathy in children due to Valsalva maneuver has not

144 xylase antibody (GADA) titers in relation to retinopathy in individuals with type 1 diabetes (T1D).

145 ion plays a vital role in detecting diabetic retinopathy in its earliest stage before the onset of bl

146 netic modifications and preventing/retarding retinopathy in patients with diabetes.

147 idered as a potential etiology of autoimmune retinopathy in patients without other autoimmune or mali

148 A as a nutritional supplement for preventing retinopathy in preterm infants.

149 n of retinal vascular diseases like diabetic retinopathy in small animal models is often complicated

150 nt increased risk for proliferative diabetic retinopathy in the multivariate model included hemorrhag

151 this process using a mouse model of ischemic retinopathy, in which vessel closure and EC apoptosis ca

152 VEGFR2 pY949 limits vascular permeability in retinopathy induced by high oxygen or by laser-wounding.

153 Diabetic retinopathy is a potentially blinding eye disease that t

154 Proliferative retinopathy is an uncommon feature of Vogt Koyanagi Hara

155 Diabetic retinopathy is significantly associated with future risk

156 Currently, myopic retinopathy is the most common irreversible blinding dis

157 s, which is an essential element of diabetic retinopathy, is driven by chronic elevation of vascular

158 nt for cataract (kappa >= 0.71) and diabetic retinopathy (kappa >= 0.61) and moderate to substantial

159 re involved in the progression of almost all retinopathies leading to blindness.

160 mpt diagnosis is crucial for the patient, as retinopathy may be a herald sign that precedes systemic

161 ch are subsumed under the term venous stasis retinopathy, may occur as transient blurred vision and w

162 jury and repair caused by the oxygen-induced retinopathy model reduced visual acuity thresholds, redu

163 tering YK-4-279 to mice in an oxygen-induced retinopathy model that generates disorganized and poorly

164 iated trials studying proliferative diabetic retinopathy, neovascular age-related macular degeneratio

165 amatic declines in the development of severe retinopathy, nephropathy, and neuropathy in those treate

166 e effect of prevalent microvascular disease (retinopathy, neuropathy, and nephropathy) and peripheral

167 primary outcome was survival with no active retinopathy, no unfavourable structural outcomes, or nee

168 trols, 36 diabetic subjects without clinical retinopathy (NoDR), 38 with nonproliferative retinopathy

169 nd specificity for nonproliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopath

170 those with minimal nonproliferative diabetic retinopathy (NPDR) had a higher risk of CVA (hazard rati

171 s, 30 of them had non-proliferative diabetic retinopathy (NPDR), and 30 had proliferative diabetic re

172 retinopathy (NoDR), 38 with nonproliferative retinopathy (NPDR), and 38 with proliferative retinopath

173 Bronchopulmonary dysplasia (BPD) and retinopathy of prematurity (ROP) are two debilitating di

174 al weight gain are known predictors of worse retinopathy of prematurity (ROP) but the role of prenata

175 685 patients, including 8 cases of bilateral retinopathy of prematurity (ROP) received RLT.

176 isease between clinicians using an automated retinopathy of prematurity (ROP) vascular severity score

177 In the Multicenter Trial of Cryotherapy for Retinopathy of Prematurity (ROP), 4099 infants weighing

178 Patients with PDR, retinopathy of prematurity (ROP), and wet age-related ma

179 iratory disorders, perinatal infections, and retinopathy of prematurity (ROP).

180 acid (DHA) positively affect the outcome of retinopathy of prematurity (ROP).

181 g the progression of ocular diseases such as retinopathy of prematurity and diabetic retinopathy, ove

182 Goals for retinopathy of prematurity are to optimize prenatal and

183 The overall goal is to clarify retinopathy of prematurity currently and formulate quest

184 Worldwide, retinopathy of prematurity differs and, in emerging coun

185 o that experienced in the United States when retinopathy of prematurity first manifested.

186 Retinopathy of prematurity has evolved from affecting in

187 Retinopathy of prematurity is a leading cause of childho

188 Retinopathy of prematurity is located asymmetrically aro

189 from the retrospective Postnatal Growth and Retinopathy of Prematurity Study (G-ROP) 1 study (2006-2

190 patients born after the Early Treatment for Retinopathy of Prematurity Study.

191 28.4%) vs 126/485 (26.0%); and treatment for retinopathy of prematurity was required in 41/472 (8.7%)

192 ose regarding pathophysiologic risk factors, retinopathy of prematurity worldwide, basic and clinical

193 strabismus, optic neuropathy, nystagmus, or retinopathy of prematurity) by ICD-9 codes in typically

194 fferences between the groups in the rates of retinopathy of prematurity, intracranial hemorrhage, sep

195 like proliferative diabetic retinopathy and retinopathy of prematurity.

196 ase mouse models, such as the oxygen-induced retinopathy (OIR) model, including a previously unapprec

197 nd chemical approaches in the oxygen-induced retinopathy (OIR) mouse model.

198 ) pathway in a mouse model of oxygen-induced retinopathy (OIR).

199 is associated with diseases such as diabetic retinopathy or cancer.

200 gh LDL-C did not associate with high risk of retinopathy or neuropathy.

201 Eyes with proliferative diabetic retinopathy or severe nonproliferative diabetic retinopa

202 I 1.00-1.19; p = 0.048), but less likely for retinopathy (OR 0.88, 95% CI 0.79-0.97; p = 0.01) and ne

203 1.73 m(2) of body-surface area, and diabetic retinopathy, or they had a urinary albumin-to-creatinine

204 e infants did not demonstrate differences in retinopathy outcomes, age at worst ROP stage, or postnat

205 h as retinopathy of prematurity and diabetic retinopathy, overgrowth of retinal blood vessels results

206 dary outcome variable: knowledge of diabetic retinopathy (p = .03) with moderate effect (partial eta

207 tients diagnosed with proliferative diabetic retinopathy (PDR) be considered for pan-retinal photocoa

208 to be associated with proliferative diabetic retinopathy (PDR) in Caucasian patients with diabetes.

209 tcomes of people with proliferative diabetic retinopathy (PDR) in India and highlight opportunities f

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

211 scularization (NV) in proliferative diabetic retinopathy (PDR) on ultra-widefield (UWF) fluorescein a

212 etinopathy (NPDR) and proliferative diabetic retinopathy (PDR) were excellent (>90%).

213 etinopathy (NPDR), and 38 with proliferative retinopathy (PDR) were imaged using spectral-domain opti

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

215 e in the treatment of proliferative diabetic retinopathy (PDR).

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

217 on (RNP) in eyes with proliferative diabetic retinopathy (PDR).

218 tment-naive eyes with proliferative diabetic retinopathy (PDR).

219 in the progression of proliferative diabetic retinopathy (PDR).

220 cular edema [DME] and proliferative diabetic retinopathy [PDR]), which require frequent life-long fol

221 ument within the natural history of diabetic retinopathy processes of protection and repair that can

222 erfusion, which are associated with diabetic retinopathy progression.

223 es had developed clinical signs of radiation retinopathy, radiation optic neuropathy, or both.

224 gression, with rituximab showing efficacy in retinopathy refractory to other agents.

225 ision and anatomy in patients with radiation retinopathy-related macular edema and prevent vision los

226 Retinopathies remain major causes of visual impairment i

227 e intended to simulate glaucoma and diabetic retinopathy, respectively.

228 osis within a murine model of oxygen-induced retinopathy resulting from the intravitreal injection of

229 graphs using the Early Treatment of Diabetic Retinopathy scale.

230 Diabetic retinopathy screening can be accomplished in an urban se

231 Implementation of an automated diabetic retinopathy screening system in a primary care clinic se

232 ssociated with adherence to initial diabetic retinopathy screening.

233 Diabetic retinopathy searches related to other diseases (41.5%),

234 Lactate accumulation during ischemic retinopathy selectively activates GPR81-extracellular si

235 d DCP were all significantly correlated with retinopathy severity (P < .0001).

236 ise and complete staging system for diabetic retinopathy severity in the future.

237 omes included ischemic index (ISI), diabetic retinopathy severity scale (DRSS) scores, visual acuity,

238 orse retinopathy as measured on the Diabetic Retinopathy Severity Scale.

239 apy show significant improvement in diabetic retinopathy severity score (DRSS), in particular at DRSS

240 Diabetic Retinopathy Severity Score level was determined at basel

241 thological neoangiogenesis in oxygen-induced retinopathy, similarly sized lesions leak less in mutant

242 The relationship between retinopathy status and the 5-year risk of first-time CVA

243 l and best-corrected visual acuity, diabetic retinopathy status in both eyes.

244 (VAE), approximate Early Treatment Diabetic Retinopathy Study (appETDRS) letter score, was calculate

245 patient, the BCVA [Early Treatment Diabetic Retinopathy Study (ETDRS) charts] and macular thickness

246 9 subfields on the Early Treatment Diabetic Retinopathy Study (ETDRS) grid and correlated them with

247 outer rings of the Early Treatment Diabetic Retinopathy Study (ETDRS) grid, generated by the softwar

248 ents to achieve >=5 Early Treatment Diabetic Retinopathy Study (ETDRS) letter gain postoperatively.

249 ed a median of 11.0 Early Treatment Diabetic Retinopathy Study (ETDRS) letters (interquartile range [

250 to 61.0 approximate Early Treatment Diabetic Retinopathy Study (ETDRS) letters (mean change, +0.6 let

251 (BCVA) of 5 or more Early Treatment Diabetic Retinopathy Study (ETDRS) letters (Snellen equivalent, 2

252 ining 15 or more Early Treatment of Diabetic Retinopathy Study (ETDRS) letters from baseline at 6, 12

253 's greatest gain in Early Treatment Diabetic Retinopathy Study (ETDRS) letters from baseline was achi

254 m baseline was -3.2 Early Treatment Diabetic Retinopathy Study (ETDRS) letters, -0.5 ETDRS letters, +

255 m baseline was -4.6 Early Treatment Diabetic Retinopathy Study (ETDRS) letters, -2.3 ETDRS letters, +

256 ic 7-standard field Early Treatment Diabetic Retinopathy Study (ETDRS) photographs.

257 nded for use in the Early Treatment Diabetic Retinopathy Study (ETDRS).

258 the SCP within the Early Treatment Diabetic Retinopathy Study 6-mm circle, 3-mm circle, and 3-mm rin

259 or DME, and 7-field Early Treatment Diabetic Retinopathy Study [ETDRS] and ultra-widefield [UWF] fund

260 dard deviation [SD] Early Treatment Diabetic Retinopathy Study [ETDRS] letters) were similar for 2012

261 isual acuity (BCVA; Early Treatment Diabetic Retinopathy Study [ETDRS] letters), and central retinal

262 D and PD within all Early Treatment Diabetic Retinopathy Study inner ring quadrants; however, especia

263 bsence: 9.4 and 8.7 Early Treatment Diabetic Retinopathy Study letter scores, respectively (P = 0.74)

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

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

266 gain of 15 or more Early Treatment Diabetic Retinopathy Study letters, vision loss of more than 5 Ea

267 as improvement in 3 Early Treatment Diabetic Retinopathy Study lines (doubling of the visual angle) o

268 nths of diabetes, T1D rats had no detectable retinopathy, T2D rats had significant retinopathy, their

269 or loss is the final common endpoint in most retinopathies that lead to irreversible blindness, and t

270 /-) zebrafish mutant as a model for diabetic retinopathy that lacks the transcription factor pdx1 thr

271 1 (PD-L1) inhibition with this rare form of retinopathy that was termed "anti-PD-L1-associated retin

272 ith the presence and advancement of diabetic retinopathy, the ECD and hexagonal cell ratio decreased,

273 arly onset and rapid progression of diabetic retinopathy, the leading cause of blindness and vision l

274 ctable retinopathy, T2D rats had significant retinopathy, their mitochondrial copy numbers were lower

275 reous hemorrhage from proliferative diabetic retinopathy, there was no statistically significant diff

276 pathy that was termed "anti-PD-L1-associated retinopathy." This irAE seems to be a consistent occurre

277 Compared with patients with no retinopathy, those with minimal nonproliferative diabeti

278 with diabetes, without clinically detectable retinopathy, to treatment with either low- or high-dose

279 ere born prematurely and who did not receive retinopathy treatment.

280 hanges in diabetic subjects without clinical retinopathy using multifocal electroretinogram (mfERG).

281 tosa GTPase regulator gene (RPGR)-associated retinopathy using spectral-domain optical coherence tomo

282 (NV) in patients with proliferative diabetic retinopathy using swept-source optical coherence tomogra

283 scular membrane (CNVM; 10,15), venous stasis retinopathy (VSR; 10,2), choroidal infarction (0,1), and

284 eriodontitis to differentiate a diagnosis of retinopathy was 7.3 (95%CI 1.6, 4.4, P <0.01).

285 At 6 months, retinopathy was comparable in T2D and T1D rats, suggesti

286 Retinopathy was detected in trypsin-digested microvascul

287 Retinopathy was evaluated in rats fed a 45% kcal as fat

288 icture of diabetic nephropathy, but diabetic retinopathy was prevented.

289 Diabetic retinopathy was significantly associated with all outcom

290 Using AO imaging in PXE-related retinopathy, we were able to observe the presence of the

291 e association of potential risk factors with retinopathy were assessed using univariate and multivari

292 trectomy for TRD from proliferative diabetic retinopathy were studied.

293 t-corrected blindness; cataract and diabetic retinopathy were the top causes for best-corrected VI, c

294 type-2 diabetics, free of pre-proliferative retinopathy, were included.

295 to study mechanisms of hyperglycemia-induced retinopathy wherein extensive proangiogenic alterations

296 reous hemorrhage from proliferative diabetic retinopathy who were enrolled from November 2016 to Dece

297 red for retinal evaluation (16.7%), diabetic retinopathy with macular oedema (15.8%), and AMD (11.0%)

298 iterion was a clinical diagnosis of AMN-like retinopathy with or without retinal vasculitis after ate

299 on the incidence and progression of diabetic retinopathy with stratification by age and sex are neede

300 development of clinically apparent radiation retinopathy within 1 year.