ライフサイエンスコーパス: DME

1 DME demonstrated a convincing relationship between BCVA

2 DME with SND correlates with greater CT, more HRS, disru

3 ive risk, 1.00; 95% CI, 0.47-2.11; P = 1.00; DME: relative risk, 1.18; 95% CI, 0.75-1.86; P = 0.48).

4 with NMFP (DR, 2.8% vs. 26.9% [P < 0.0001]; DME, 3.8% vs. 26.2% [P < 0.0001]).

5 anium(IV) alkoxide complex U(OCPh3)4(DME) (3.DME).

6 omplex [TolC identical withMo(OCCH3(CF3)2)3].DME with 2 equiv of functional ynamines or ynamides yiel

7 o the uranium(IV) alkoxide complex U(OCPh3)4(DME) (3.DME).

8 VISTA and VIVID randomized 872 DME patients to receive intravitreal aflibercept injecti

9 fference, 9%; 95% CI, 4%-15%; P < .001), and DME development was more frequent (28% vs 9%; difference

10 ites, with visual acuity 20/32 to 20/320 and DME involving the central macula were randomly assigned

11 Patients with type 2 diabetes and DME or PDR have an increased risk of incident CVD, which

12 gaporeans have a higher prevalence of DR and DME compared with Chinese and Malays.

13 The ungradable rate per patient for DR and DME was significantly lower with UWF imaging compared wi

14 associations between the severity of DR and DME with symptoms of anxiety and depression and commonal

15 aded for the presence and severity of DR and DME.

16 e of an association between dyslipidemia and DME.

17 c, the relationship between lipid levels and DME deserves further investigation.

18 strong relationship between lipid levels and DME, this was not confirmed by the meta-analysis that in

19 relationship between blood lipid levels and DME.

20 al aspects of the production of methanol and DME and outline future research and development directio

21 and 11 of 27 (41%) eyes with NPDR, PDR, and DME, respectively, demonstrated this feature (P = .0001)

22 y control, diabetes without retinopathy, and DME groups.

23 izumab disposition was determined in RVO and DME patients and compared with that previously seen in A

24 ate studies for the decomposition of THF and DME are consistent with monomer-based mechanisms.

25 6 weeks]); MEfBRVO (VIBRANT [52 weeks]); and DME (DA VINCI [52 weeks], VIVID [100 weeks], VISTA [100

26 = 0.012); a similar trend was noted for any DME (P = 0.001) and CSME (P = 0.032).

27 presence and area of HE did not increase as DME resolved (either in the ranibizumab or sham groups).

28 ercent of incident individuals had bilateral DME and 39% had unilateral DME, but DME could develop in

29 ilateral DME and 39% had unilateral DME, but DME could develop in the fellow eye.

30 in subgroups with more severe DR and chronic DME at baseline.

31 or more was significantly greater in chronic DME patients (FAc 0.2 mug/day, 34.0% vs. sham, 13.4%; P<

32 contributions of these 3 factors to chronic DME.

33 ps could receive ranibizumab for concomitant DME.

34 Using NHANES definitions, DME and CSME prevalences from monocular fundus photograp

35 ologic surveys using photographs to diagnose DME.

36 Dimethoxyethane (DME) and N,N,N',N'-tetramethylethylenediamine quantitati

37 fluoroslufonyl)imide (KFSI)-dimethoxyethane (DME) electrolyte forms a uniform SEI on the surface of p

38 endo,exo-norbornenyl dialkylesters (dimethyl DME, diethyl DEE, di-n-butyl DBE) were strategically des

39 enge for the commercialization of the direct DME fuel cell.

40 mine the association of severe stages of DR (DME and PDR) with incident CVD in patients with type 2 d

41 9) and patients with diabetic macular edema (DME) (n = 31) were compared with healthy control partici

42 ved for treatment of diabetic macular edema (DME) after demonstration of its efficacy and safety in t

43 alence of persistent diabetic macular edema (DME) after months of anti-vascular endothelial growth fa

44 Patients with diabetic macular edema (DME) are at high risk of vascular complications, includi

45 ion of patients with diabetic macular edema (DME) are important for individualizing treatment and opt

46 rse) center-involved diabetic macular edema (DME) at baseline were required to receive ranibizumab fo

47 tion of diabetes and diabetic macular edema (DME) at baseline, were less likely to have proliferative

48 njections (IAIs) for diabetic macular edema (DME) during the phase III VISTA DME trial were maintaine

49 ti-VEGF) therapy for diabetic macular edema (DME) favorably affects diabetic retinopathy (DR) improve

50 Diagnosing diabetic macular edema (DME) from monocular fundus photography vs optical cohere

51 mg) for treatment of diabetic macular edema (DME) involving the center of the retina and associated w

52 e implant therapy in diabetic macular edema (DME) is associated with long-term outcome.

53 Diabetic macular edema (DME) is the major cause of vision loss in diabetic perso

54 and ranibizumab for diabetic macular edema (DME) might influence interpretation of study results.

55 ct of treatments for diabetic macular edema (DME) on driving should be of value to patients and clini

56 ty factors (PPFs) in diabetic macular edema (DME) patients before and after injection of dexamethason

57 graphs, we evaluated diabetic macular edema (DME) progression and DR progression.

58 iod) (2q8) and other diabetic macular edema (DME) therapies at doses licensed outside the USA.

59 st-line treatment of diabetic macular edema (DME) to inform technology assessments such as those cond

60 SS) in patients with diabetic macular edema (DME) treated with intravitreal ranibizumab.

61 have revolutionized diabetic macular edema (DME) treatment.

62 Patients with diabetic macular edema (DME) who received sham control or FAc 0.2 or 0.5 mug/day

63 ema, and 27 eyes had diabetic macular edema (DME) with either NPDR or PDR.

64 ristics in eyes with diabetic macular edema (DME) with subfoveal neuroretinal detachment (SND+) vs DM

65 therapy in eyes with diabetic macular edema (DME) with vision loss after macular laser photocoagulati

66 therapy in eyes with diabetic macular edema (DME) with vision loss after macular laser photocoagulati

67 R), 51 with NPDR and diabetic macular edema (DME), and 18 with proliferative DR (PDR)-and 64 age-matc

68 also contributes to diabetic macular edema (DME), and because of the absence of good animal models,

69 degeneration (AMD), diabetic macular edema (DME), and retinal vein occlusion (RVO) were evaluated by

70 et for patients with diabetic macular edema (DME), perhaps in combination with currently administered

71 degeneration (nAMD), diabetic macular edema (DME), retinal vein occlusion, choroidal neovascularizati

72 ity, with or without diabetic macular edema (DME), using en face Doppler OCT.

73 iabetic retinopathy, diabetic macular edema (DME), vision-threatening diabetic retinopathy (VTDR), de

74 for center-involving diabetic macular edema (DME).

75 with center-involved diabetic macular edema (DME).

76 on loss or worsening diabetic macular edema (DME).

77 778 in patients with diabetic macular edema (DME).

78 of dyslipidemia and diabetic macular edema (DME).

79 lved center-involved diabetic macular edema (DME).

80 eatment paradigm for diabetic macular edema (DME).

81 concomitant baseline diabetic macular edema (DME).

82 etic retinopathy and diabetic macular edema (DME).

83 athy (DR), including diabetic macular edema (DME).

84 generation (AMD) and diabetic macular edema (DME).All patients were operated at a small procedure roo

85 tion (AMD, n = 400), diabetic macular edema (DME, n = 400), or retinal vein occlusion (RVO, n = 400)

86 severe stages of DR (diabetic macular edema [DME] and proliferative diabetic retinopathy [PDR]) have

87 erative DR [PDR], or diabetic macular edema [DME]) or "any DR" (further subclassified as NPDR or PDR,

88 ect-feed fuel cells but lack of an efficient DME oxidation electrocatalyst has remained the challenge

89 %-47.1%) were not diagnosed as having either DME or CSME on monocular fundus photographs using MESA a

90 tery with a MgTFSI2 /MgCl2 /DME electrolyte (DME=1,2-dimethoxyethane, TFSI=bis(trifluoromethanesulfon

91 Dimethyl ether (DME) has been considered as a promising alternative fuel

92 nversion of synthesis gas to dimethyl ether (DME) was imaged simultaneously and in situ using synchro

93 % (25.9-30.6) for any DR, 7.6% (6.5-9.0) for DME, and 7.7% (6.6-9.0) for VTDR.

94 -step DRSS score improvement at week 100 for DME patients in VISTA and VIVID.

95 patients treated for nAMD, 167 (12.5 %) for DME, and 144 (10.8 %) for other reasons.

96 evacizumab, ranibizumab, and aflibercept for DME.

97 endothelial growth factor (VEGF) agents for DME.

98 e, no comparable estimates are available for DME specifically.

99 ty improvement compared with bevacizumab for DME, with superior anatomic outcomes and fewer injection

100 We investigated OCT biomarkers for DME treated by intravitreal dexamethasone (DEX) implant.

101 and then under model reaction conditions for DME synthesis (H2:CO:CO2 ratio of 16:8:1, up to 250 degr

102 vascular endothelial growth factor drugs for DME.

103 ne whether reduced TRBF is a risk factor for DME.

104 om 284 patients treated with DEX implant for DME (naive, n = 209; refractory, n = 90).

105 t evaluated monthly anti-VEGF injections for DME for 2 years and reported the outcome measures of cer

106 focal/grid laser treatment was performed for DME, the only participants to have a substantial reducti

107 nd 25 to the PRP group (plus ranibizumab for DME).

108 eatment groups could receive ranibizumab for DME.

109 ST) can yield different prevalence rates for DME.

110 Pd catalyst was designed and synthesized for DME electrooxidation.

111 ckness decreases after anti-VEGF therapy for DME after 6 months, but may not be associated with funct

112 lowed by maintenance ranibizumab therapy for DME.

113 a suggest less than half of eyes treated for DME with intravitreous ranibizumab have persistent centr

114 d dose) or sham based on prior treatment for DME at study entry.

115 whether an eye received laser treatment for DME during the study.

116 gulation has been the standard treatment for DME for nearly 3 decades, there is increasing evidence t

117 with NPDR receiving anti-VEGF treatment for DME may experience improvement in DR severity.

118 macular laser photocoagulation treatment for DME.

119 th and without prior anti-VEGF treatment for DME.

120 macular laser photocoagulation treatment for DME.

121 t, bevacizumab, or ranibizumab treatment for DME.

122 trial among eyes with vision impairment from DME, long-term improvement in visual acuity from baselin

123 A total of 483 adults with vision loss from DME treated with ranibizumab were included in this analy

124 ents for patients with decreased vision from DME found that at 1 year aflibercept (2.0 mg) achieved b

125 In eyes with decreased vision from DME, treatment costs of aflibercept and ranibizumab woul

126 atients with specific characteristics (e.g., DME).

127 or CSME on monocular fundus photographs have DME on OCT.

128 5% CI, 12.9%-24.2%) were diagnosed as having DME on monocular fundus photographs using MESA and NHANE

129 a suggest that many eyes diagnosed as having DME or CSME on monocular fundus photographs have no DME

130 CST, while many eyes diagnosed as not having DME or CSME on monocular fundus photographs have DME on

131 dividualize treatment options, especially if DME patients respond differently to various therapies.

132 photocoagulation was added after 6 months if DME persisted.

133 6 participants with PDR and vision-impairing DME at baseline, 21 were assigned to the ranibizumab gro

134 rticipants without baseline vision-impairing DME, 80 and 87 were in the ranibizumab and PRP groups, r

135 yes presenting with PDR and vision-impairing DME, but not for those with PDR without vision-impairing

136 s with and without baseline vision-impairing DME, the incremental cost-effectiveness ratios of ranibi

137 for those with PDR without vision-impairing DME.

138 e) DME and without baseline vision-impairing DME.

139 y PtRu catalyst shows much lower activity in DME than methanol oxidation.

140 otable differences were found in nAMD and in DME, with VA significantly higher in some RCTs and lower

141 However, the response to anti-VEGF drugs in DME is not as robust as in proliferative diabetic retino

142 l in identifying various imaging findings in DME.

143 to the 25-line raster at detecting fluid in DME, BRVO/CRVO, and central serous chorioretinopathy, bu

144 ular endothelial growth factor inhibitors in DME could be associated with an increase in cardiovascul

145 compared with sham with and without laser in DME.

146 0.27) and RVO (r = -0.72) trials, but not in DME trial data.

147 GF-induced worsening of retinal perfusion in DME is superimposed on another cause of more gradually w

148 C6 H3 ) with H2 SiI2 in a 3:1 molar ratio in DME afforded a mixture of the separated ion pair [(cAACM

149 causes a significantly greater reduction in DME than that seen with suppression of VEGF alone.

150 sponsored (Genentech or Novartis) studies in DME completed as of December 31, 2013.

151 at visual response to ranibizumab therapy in DME was not influenced by nonocular factors related to s

152 priority for the management of DR, including DME, but few were associated with Cochrane reviews.

153 id not have vision-impairing center-involved DME at baseline.

154 VEGF treatments in eyes with center-involved DME causing vision impairment.

155 tive effectiveness trial for center-involved DME was conducted in 650 participants receiving afliberc

156 b for vision impairment from center-involved DME, patients not driving at initiation of treatment are

157 d to receive ranibizumab for center-involved DME.

158 d to receive ranibizumab for center-involved DME.

159 10, an estimated 37 274 had central-involved DME and VI eligible for ranibizumab treatment.

160 through 3 years, even when central-involved DME chronically persists.

161 ence of 1 or both eyes with central-involved DME in 2010 were estimated based on the 2010 United Stat

162 abetes mellitus, and 1-year central-involved DME incidence rate.

163 s in the United States with central-involved DME that has caused vision loss.

164 ranibizumab have persistent central-involved DME through 24 weeks after initiating treatment.

165 hen have chronic persistent central-involved DME through 3 years, longer-term visual acuity outcomes

166 4 consecutive patients with center-involving DME and VA </=79 ETDRS letters, central subfield macular

167 ial ranibizumab therapy for center-involving DME likely have better long-term vision improvements tha

168 SND-) with treatment-naive, center-involving DME were evaluated.

169 ine laser control eyes with center-involving DME were included.

170 growth factor treatment of center-involving DME with visual acuity loss may decrease long-term treat

171 zontal lineN bonded moiety in the complex [K(DME)2][Ce horizontal lineN(3,5-(CF3)2C6H3)(TriNOx)], who

172 The [K(DME)2][Ce horizontal lineN(3,5-(CF3)2C6H3)(TriNOx)] comp

173 Furthermore, the superconcentrated KFSI-DME electrolyte shows excellent electrochemical stabilit

174 ecco's modification of Eagle's basal medium (DME) produce no transformed foci when grown to confluenc

175 argeable Mg/S battery with a MgTFSI2 /MgCl2 /DME electrolyte (DME=1,2-dimethoxyethane, TFSI=bis(trifl

176 action pathway of sulfur cathode in MgTFSI2 -DME electrolyte, as well as the associated kinetics are

177 m 42 patients diagnosed with treatment-naive DME were treated with 3 monthly intravitreal injections

178 Although eyes with naive DME gained more vision than refractory eyes (P < 0.001),

179 also obtainable from LiN(SiMe3 )2 and NiCl2 (DME).

180 No DME-like condition was noticed even after 7 months.

181 CSME on monocular fundus photographs have no DME based on OCT CST, while many eyes diagnosed as not h

182 001), compared with patients with nonchronic DME (FAc 0.2 mug/day, 22.3% vs. sham, 27.8%; P = 0.275).

183 Severe NPDR or PDR, but not DME, was independently associated with depressive sympto

184 egeneration (nAMD), diabetic macular oedema (DME) or branch/central retinal vein occlusion (B/CRVO).

185 These data may improve characterization of DME in eyes with SND.

186 ean age was 63.7 years, the mean duration of DME was 40 months, and 77.1% of the participants had rec

187 and severe thickening are important goals of DME treatment, and in patients with renal disease, treat

188 emokines are involved in the pathogenesis of DME, with multiple cellular involvement affecting the ne

189 Presence of DME on OCT used Diabetic Retinopathy Clinical Research N

190 Presence of DME, including clinically significant macular edema (CSM

191 Prevalence of DME based on monocular fundus photographs or OCT.

192 ents with type 2 diabetes, the prevalence of DME was 4.6% and PDR, 7.4%.

193 Among the 246 eyes, the prevalences of DME (61.4%) and CSME (48.5%) based on MESA definitions f

194 me measures were incidence or progression of DME or DR and change in visual acuity.

195 or FAc 0.2 mug/day was similar regardless of DME duration.

196 n worsening of hard exudates and severity of DME in the lipid-lowering group compared with placebo (h

197 Retrospective cross-sectional study of DME grading based on monocular fundus photographs and OC

198 n compared with laser alone for treatment of DME concluded that there was no significant between-grou

199 eal ranibizumab therapy for the treatment of DME confers considerable patient (human) value gain.

200 rowth factor (VEGF) agents, the treatment of DME has been revolutionized, and the indication for lase

201 The most effective treatment of DME is VEGF inhibitor injections with or without laser t

202 ive relative to bevacizumab for treatment of DME unless their prices decrease substantially.

203 cular fundus photography, while treatment of DME uses OCT CST.

204 gest patient-level data sets on treatment of DME with ranibizumab.

205 b compared with bevacizumab for treatment of DME, using a markedly reduced sample size relative to a

206 A2 inhibitory mechanism for the treatment of DME.

207 RISE studies of ranibizumab for treatment of DME.

208 in haplotypes) and the presence of any DR or DME in white participants with T1DM and T2DM.

209 eferable DR (moderate nonproliferative DR or DME or worse) was increased using UWF imaging from 11.7%

210 = Li, K, Rb, Cs; solv = TMEDA, THF, Et2O, or DME), was isolated and fully characterized.

211 etween TZD use and visual acuity outcomes or DME progression, and no consistent evidence of increased

212 ere similar among patients with AMD, RVO, or DME.

213 cluded them from the RCT, such as persistent DME despite recent anti-VEGF treatment.

214 e 3-year probabilities of chronic persistent DME (failure to achieve a central subfield thickness <25

215 The probability of chronic persistent DME among eyes with persistent DME at the 24-week visit

216 in eyes with and without chronic persistent DME through the follow-up period, respectively, by a mea

217 Conversion to aflibercept for persistent DME resulted in significant anatomic improvements.

218 ly as 74 weeks from baseline, for persistent DME with vision impairment.

219 ter 6 months for the treatment of persistent DME.

220 igned to receive ranibizumab with persistent DME (central subfield thickness >/=250 mum on time domai

221 ic persistent DME among eyes with persistent DME at the 24-week visit decreased from 100% at the 32-w

222 correlations were identified in both pooled DME (r = -0.45) and pooled RVO (r = -0.35) trial data at

223 medium correlation was identified in pooled DME trial data (r = -0.42).

224 n at cataract surgery prevents postoperative DME concluded that intravitreal ranibizumab injection at

225 ictor of VA in eyes with present or previous DME and more highly correlated with VA than other widely

226 n array of monodisperse polymers (PLA(x)-ran-DME(1-x))n bearing variable grafting densities (x = 1.0,

227 elected by literature search: nAMD: 13 RCTs, DME: 9, RVO: 5), the OCEAN patients' mean age was signif

228 IAIs in the presence of clinically relevant DME.

229 of 142 patients with clinically significant DME and from 20 controls.

230 and clinical studies strongly indicate that DME is an inflammatory disease.

231 5% and 21.0%, respectively) approximated the DME prevalence from OCT (21.1%).

232 lar fundus photographs were greater than the DME prevalence based on OCT (21.1%) by 40.2% (95% CI, 32

233 ) to identify potential PPFs contributing to DME.

234 ly implicated VEGF as a major contributor to DME and have been confirmed by several large multicenter

235 ercept Injection in Vision Impairment Due to DME)-in a multicenter setting.

236 ercept Injection in Vision Impairment Due to DME)-in a multicenter setting.

237 ed when choosing an anti-VEGF agent to treat DME.

238 reatment in patients with previously treated DME.

239 Twenty DME patients randomized to dexamethasone implant or VEGF

240 Under DME reaction conditions at 1 bar, the coexistence of Cu(

241 als had bilateral DME and 39% had unilateral DME, but DME could develop in the fellow eye.

242 Sixty patients completing VISTA DME elected to enter the ENDURANCE extension study.

243 ed visual acuity gains achieved during VISTA DME were maintained and stable with individualized dosin

244 cular edema (DME) during the phase III VISTA DME trial were maintained with individualized, as-needed

245 ision gains achieved during the 3-year VISTA DME trial were maintained through M12 of the ENDURANCE e

246 e, peripheral visual field loss, vitrectomy, DME development, and retinal neovascularization.

247 subfoveal neuroretinal detachment (SND+) vs DME without SND (SND-).

248 nt criteria: Treatment was administered when DME was identified by the investigator on optical cohere

249 o be slightly worse than in the 60% in which DME does not persist.

250 ted for 3,614 patients with nAMD, 1,211 with DME, 204 with BRVO and 121 with CRVO.

251 ne whether the VHRF score is associated with DME and may serve as a noninvasive measure of inflammati

252 697515 Was also specifically associated with DME in those with T2DM (P = 0.004; OR, 0.53; CI, 0.35-0.

253 TZD use was not associated with DME incidence in either the analysis of any use (adjuste

254 nce in neovascular AMD and RVO compared with DME, which was represented rarely in the population stud

255 eyes with PDR, and 11 of 27 (41%) eyes with DME (P = .0001).

256 eyes with PDR, and 17 of 27 (63%) eyes with DME (P = .007).

257 uence visual acuity improvement in eyes with DME after ranibizumab therapy.

258 Diabetic eyes with DME exhibited lower TRBF than healthy eyes (P </= .001).

259 s led to improved visual acuity in eyes with DME involving the center of the retina and visual acuity

260 s led to improved visual acuity in eyes with DME involving the center of the retina and with visual a

261 laser treatment for >/=24 weeks in eyes with DME involving the central macula with vision impairment.

262 Among eyes with DME on OCT, 26.9% (95% CI, 15.6%-41.0%) and 32.7% (95% C

263 e TRBF was consistently low in the eyes with DME regardless of DR severity.

264 with DME that were treated and the eyes with DME that were not treated was not identified.

265 A difference in TRBF between the eyes with DME that were treated and the eyes with DME that were no

266 ctive review of medical records of eyes with DME treated with 0.7 mg intravitreal dexamethasone impla

267 F was 28.0 (8.5) microL/min in the eyes with DME, 48.8 (13.4) microL/min in the eyes with DR but with

268 Among eyes with DME, those with submacular fluid, no HRF, and a continuo

269 functional or anatomic outcomes in eyes with DME.

270 ubclassified as NPDR or PDR, without or with DME).

271 Patients with DME and submacular fluid, intraretinal cysts, severe thi

272 Patients with DME are more likely to be treated bilaterally with anti-

273 s mean (SD), were increased in patients with DME by 2.95-fold (5.60 [8.65]) compared with healthy con

274 Higher VHRF scores in patients with DME compared with controls and diabetic patients without

275 ) were significantly higher in patients with DME compared with those without DME (TC: 30.08; 95% conf

276 diabetic retinopathy, and many patients with DME do not show complete resolution of fluid despite mul

277 anibizumab, as administered to patients with DME for 12 to 36 months in these studies, can both impro

278 nce of VMA should not preclude patients with DME from receiving treatment.

279 isual and anatomic outcomes in patients with DME previously treated with laser, intravitreal anti-vas

280 In the READ-3 study, patients with DME received monthly intravitreal injections of either 0

281 Between the 2 studies, 759 patients with DME were randomized to receive monthly 0.3 or 0.5 mg int

282 wever, uncertainty remains for patients with DME who are at high risk for vascular disease and were n

283 mprovement similar to those of patients with DME who had immediate anatomic response.

284 xposure group (those high-risk patients with DME who received 2 years of monthly treatment) revealed

285 ickness may help predict which patients with DME will respond more favorably in the short term to int

286 tinued treatment, at month 24, patients with DME with delayed anatomic response (</=10% CFT reduction

287 ion of AKB-9778 for 4 weeks in patients with DME, and doses of 15 mg or more twice daily reduced macu

288 alysis of anti-VEGF agents for patients with DME, assessment of the highest-level exposure group (tho

289 am-controlled phase 3 study in patients with DME, best-corrected visual acuity (BCVA) of 34-68 Early

290 tios (IRRs) were estimated for patients with DME, PDR, and vision-threatening DR, compared with perso

291 occlusion, the same is true in patients with DME, suggesting that regardless of the underlying diseas

292 In patients with DME, vision improvement with ranibizumab was not influen

293 Persons with DME or PDR were more likely to have incident CVD (IRR, 1

294 In subjects with DME, sustained intraocular delivery of FAc slows develop

295 ith moderate nonproliferative DR but without DME exhibited a wide range of TRBF from 31.1 to 75.0 mic

296 ) microL/min in the eyes with DR but without DME, 40.1 (7.7) microL/min in the diabetic eyes without

297 However, among eyes without DME on OCT, 58.2% (95% CI, 51.0%-65.3%) and 18.0% (95% C

298 atients with DME compared with those without DME (TC: 30.08; 95% confidence interval [CI], 21.14-39.0

299 % CI, 1.49-3.67) compared with those without DME or PDR.

300 mpairing (Snellen equivalent 20/32 or worse) DME and without baseline vision-impairing DME.