ライフサイエンスコーパス: PDR

1 PDR is a metric similar to chromatographic resolution th

2 PDR is responsible for transferring electrons from NADH

3 PDR patients had significantly lower blood flow ( approx

4 PDR prevalence in ARV-naive women 18-24 years old was 21

5 PDR prevalence was calculated by demographics and codon,

6 PDR prevalences (95% confidence interval [CI]) in 815 AR

7 PDR was defined as >/=2% mutant frequency in a participa

8 genes, while P. sojae contains 20 MRP and 49 PDR genes.

9 n real time using a Micro-Aethalometer and a PDR-1500 DataRAM, respectively.

10 one ABCG type transporter is derived from a PDR transporter, while transporters in the ABCB-half fam

11 as 3.6 +/- 0.2 mm, while the EMD alone had a PDR of 4.0 +/- 0.3 mm.

12 ar age decrease was associated with adjusted PDR prevalence ratio 1.20 (95% CI, 1.06-1.36; P = .004).

13 found in PDR; overexpression did not affect PDR, nor was its presence required for Ssz1's or Zuo1's

14 diabetes, the prevalence of DME was 4.6% and PDR, 7.4%.

15 ects of therapy in patients with wet AMD and PDR.

16 widely used in the treatment of wet-AMD and PDR.

17 association of severe stages of DR (DME and PDR) with incident CVD in patients with type 2 diabetes.

18 were detected, particularly from the MDR and PDR subfamilies, which often showed expression in either

19 to 26.4% among anti-VEGF groups for NPDR and PDR eyes, respectively.

20 V was lower in NDR than NPDR and PDR subjects (P </= 0.02).

21 r ratio of VEGF to its receptors in NPDR and PDR vitreous.

22 luding 28% macular edema, 2% severe NPDR and PDR.

23 emical and biological predictors for PNR and PDR were assigned through path analysis.

24 ification and denitrification rates (PNR and PDR) and gross mineralization rates.

25 II were increased in eyes with PVR, RRD, and PDR when compared with control eyes (P < 0.002).

26 The presence of both the substrate and PDR was synergistic, making PDO fully catalytically acti

27 The Vt and PDR necessary to decrease end-tidal CO2 20% (from 75 to

28 esulted in a significant increase in average PDR values and prediction accuracies.

29 With both PDR(ox) and phthalate present, most of the PDO(red) (app

30 variation in the lung model driving chamber (PDR).

31 Time from randomization to a composite PDR-worsening outcome defined as the first occurrence of

32 < 0.001 PD and -0.0 mm test; +0.4 mm control PDR).

33 Ten patients with poorly controlled PDR (mean hemoglobin A1C = 9.2 +/- 2.0%) and 10 control

34 nal vascular parameters in poorly controlled PDR patients.

35 this parameter may be the signal controlling PDR gene expression.

36 We determined PDR prevalence and correlates in a Kenyan cohort.

37 4.80, and 28.19 times more likely to develop PDR, respectively.

38 % of eyes in the sham/0.5 mg group developed PDR, as measured by composite outcome, compared with 18.

39 ly increased hazard ratio (HR) of developing PDR (HR 1.77, 95% confidence interval [CI] 1.25-2.49, P

40 (IRRs) were estimated for patients with DME, PDR, and vision-threatening DR, compared with persons wi

41 32.4%; severe NPDR, 17.6%; proliferative DR (PDR), 19.1%; and high-risk PDR, 4.4%; with PPL present i

42 ) levels with incidence of proliferative DR (PDR), and soluble intercellular adhesion molecule-1 (sIC

43 DR (NPDR), severe NPDR, or proliferative DR (PDR), with or without maculopathy or mild NPDR with macu

44 r edema (DME), and 18 with proliferative DR (PDR)-and 64 age-matched nondiabetic control eyes.

45 ession, and development of proliferative DR (PDR).

46 ive DR (NPDR, N = 45), and proliferative DR (PDR, N = 35).

47 oliferative DR [NPDR], 155 proliferative DR [PDR]) were analyzed; 302 (46.5%) were women and mean (SD

48 rtion of participants with proliferative DR [PDR], clinically significant macular edema [CSME], or bo

49 onproliferative DR [NPDR], proliferative DR [PDR], or diabetic macular edema [DME]) or "any DR" (furt

50 es), proliferative DR without macular edema (PDR) (10 eyes), and diabetic macular edema (DME) (14 eye

51 sham control-treated subjects, time to first PDR event was significantly delayed in subjects treated

52 Adjustment for PDR did not alter HRs by race/ethnicity, but differences

53 retreatment protocol or PRP at baseline for PDR.

54 ed ratio (1 point) and less than 10%/min for PDR (2 points).

55 ation for additional therapeutic options for PDR patients.

56 PRP), or (3) pars plana vitrectomy (PPV) for PDR; and study eye changes on the DRSS.

57 nd features of initial DR are prognostic for PDR development.

58 xygen-induced retinopathy (OIR), a proxy for PDR.

59 bizumab as an alternative therapy to PRP for PDR, at least through 2 years.

60 ios of 0.5-mg ranibizumab therapy vs PRP for PDR.

61 o differences between treatment regimens for PDR were identified for most of the other patient-center

62 N-terminal ATPase domain, is sufficient for PDR induction as well, indicating that Ssz1 does not fun

63 bosome, is both necessary and sufficient for PDR induction by Zuo1.

64 ening of PDR might lead to new therapies for PDR.

65 P compared with IVR as primary treatment for PDR is less expensive over 2 years, but both fall well b

66 Treatment for PDR, panretinal photocoagulation, is inherently destruct

67 factor agents are proposed as treatments for PDR that spare peripheral vision.

68 Study eyes had vitreous hemorrhage from PDR precluding panretinal photocoagulation completion.

69 red with saline for vitreous hemorrhage from PDR that precludes placement or confirmation of complete

70 weeks in eyes with vitreous hemorrhage from PDR.

71 as detected in ECs in retinal NV tissue from PDR patients, whereas MMP-2 protein levels were elevated

72 The high PDR prevalence may warrant resistance testing and/or alt

73 scular endothelial cells obtained from human PDR fibrovascular membranes (FVMs) via transcriptomic an

74 ICG-PDR significantly deteriorated after TIPS (P = .006).

75 of the plasma disappearance rate of ICG (ICG-PDR) and various factors derived from MR imaging, includ

76 cyanine green plasma disappearance rate [ICG-PDR]) was performed.

77 he factors significantly correlated with ICG-PDR (R = 0.87).

78 The liver function correlating with ICG-PDR can be estimated quantitatively from the signal inte

79 ns as a surrogate marker of CCN1 activity in PDR distinguishing pathological from physiological angio

80 ter reduction of active NV than PRP alone in PDR, although no differences were seen between the two o

81 ing concentrations in more severe PVR and in PDR when measured by ELISA, and, conversely, there was e

82 hat Ssz1 does not function as a chaperone in PDR.

83 No role for Ssb was found in PDR; overexpression did not affect PDR, nor was its pres

84 e propose that Ssz1's and Zuo1's function in PDR is distinct from their role as ribosome-associated c

85 t Muller cell tractional force generation in PDR is driven by vitreous IGF activity and proliferation

86 e findings that serum sTNF-Rs were higher in PDR than in PVR (P < 0.016) and that vitreous levels of

87 rstand the regulation of MMPs by ischemia in PDR.

88 PDF is known to increase cAMP levels in PDR receptor (PDFR)-containing neurons.

89 and NPDR (P </= 0.03), while V was lower in PDR (P = 0.04).

90 in-binding angiogenic factors upregulated in PDR vitreous humor besides VEGF, thus inhibiting their b

91 perations, and grade of severity, whereas in PDR these levels were not related to the type or duratio

92 n overexpressed, a possible role for Zuo1 in PDR was investigated.

93 and Zuo1 must be free of ribosomes to induce PDR, we propose that Ssz1's and Zuo1's function in PDR i

94 Cambodia, Indonesia (Jakarta and Bali), Lao PDR, Taiwan, Thailand and Vietnam.

95 duce malaria was carried out in southern Lao PDR to determine whether the use of repellent and long-l

96 gst agricultural populations in southern Lao PDR.

97 eyes with PDR, ranibizumab resulted in less PDR worsening compared with PRP, especially in eyes not

98 amily was the presence of a large yeast-like PDR subfamily, and the absence of genes encoding bona fi

99 The very low PDR suggests poor access to diagnosis and care.

100 demonstrated less rebreathed CO2 and a lower PDR than either the Facial-WS or Total Face masks.

101 ved colonoscopy from physicians with a lower PDR.

102 .1 cm H2O/sec; Total Face, Vt 790 +/- 12 mL, PDR 11.4 +/- 0.2 cm H2O/sec, p <.001).

103 0.1 cm H2O/sec; Facial-WS, Vt 745 +/- 9 mL, PDR 10.2 +/- 0.1 cm H2O/sec; Total Face, Vt 790 +/- 12 m

104 e tested masks (Facial-MEP, Vt 701 +/- 9 mL, PDR 8.1 +/- 0.1 cm H2O/sec; Facial-WS, Vt 745 +/- 9 mL,

105 % [high-risk PDR or worse] vs. 23% [moderate PDR or better]; HR, 3.97; 99% CI, 2.48 to 6.36; P < 0.00

106 more of the following: (1) worsening from no PDR to PDR, (2) worsening of 2 or more severity levels o

107 When no PDR or phthalate is present, the oxidation of the Rieske

108 ch scores, severe nonproliferative DR (NPDR)/PDR was independently associated with greater depressive

109 20 (55%), and 11 of 27 (41%) eyes with NPDR, PDR, and DME, respectively, demonstrated this feature (P

110 d year, 66 (59.5%) of NPDR and 28 (70.0%) of PDR eyes that manifested improvement at 1 year maintaine

111 We evaluated the ability of PDR to predict early mortality or retransplantation afte

112 Addition of PDR(ox) to native PDO(red) resulted in a large fraction

113 otein levels were elevated in the aqueous of PDR patients compared with controls.

114 g pars plana vitrectomy for complications of PDR.

115 The treatment coverage of PDR and CSME was 75% (56/75) in Indigenous Australians a

116 aocular delivery of FAc slows development of PDR and slows progression of diabetic retinopathy.

117 Although uncommon, the development of PDR still occurs in a small percentage of eyes undergoin

118 Time to first development of PDR was analyzed by Kaplan-Meier methods to calculate cu

119 ds with progression of DR and development of PDR were weaker and not significant after adjustment for

120 e potential associations with development of PDR.

121 in patients with a new clinical diagnosis of PDR.

122 Distinguishing the effects of PDR and PRP may guide the development of restorative vis

123 gression of DR severity and establishment of PDR.

124 PRP in this group of PDR patients did not have a statistically significant ef

125 this study, noteworthy was the percentage of PDR.

126 Time to progression of PDR and VH were calculated with Cox regression after str

127 For these eyes, the rate of PDR-worsening was greater with PRP than ranibizumab (45%

128 IRMA increases risk of PDR whereas 4Q DBH increases risk of VH.

129 ears to be associated with a reduced risk of PDR worsening.

130 PV compared to 1-3 days for the treatment of PDR-related complications.

131 ) undergoing vitrectomy for the treatment of PDR.

132 ntify MMP-2 as a target for the treatment of PDR.

133 macular edema on development or worsening of PDR might lead to new therapies for PDR.

134 ence required for Ssz1's or Zuo1's effect on PDR.

135 with PVR than in eyes with RRD (P < 0.01) or PDR (P < 0.03).

136 Binding of phthalate and/or PDR(ox) to reduced PDO-APO increases the reactivity of t

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

138 Persons with DME or PDR were more likely to have incident CVD (IRR, 1.39; 95

139 .49-3.67) compared with those without DME or PDR.

140 , 25.6%-71.5%) for those with severe NPDR or PDR (P = .02).

141 e in depressive symptoms, and severe NPDR or PDR contributed to 19.1% (95% CI, 1.7%-44.4%) of the tot

142 Those with severe NPDR or PDR did not have a statistically significant greater odd

143 roximately half of those with severe NPDR or PDR had difficulty with at least one visual function tas

144 ces) with 1 or more eyes with severe NPDR or PDR less than Early Treatment Diabetic Retinopathy Study

145 ntly greater among those with severe NPDR or PDR relative to those with no retinopathy (adjusted odds

146 ntly greater among those with severe NPDR or PDR than among those with no retinopathy.

147 Severe NPDR or PDR, but not DME, was independently associated with depr

148 r "any DR" (further subclassified as NPDR or PDR, without or with DME).

149 etic macular edema (DME) with either NPDR or PDR.

150 Thus, the binding of phthalate or PDR(ox) to PDO(red) each results in greater reactivity o

151 cally unaffected by the presence of oxidized PDR.

152 conserved domain present in all known plant PDR transporters.

153 proach for elucidating the function of plant PDR proteins.

154 to test VEGF antagonists to treat or prevent PDR in humans.

155 easured by physicians' polyp detection rate (PDR).

156 w the calculation of patient diagnosis rate (PDR).

157 en clearance, the plasma disappearance rate (PDR), has been associated with initial graft function.

158 Reduction of PDO by reduced PDR was also slower in the D178A and D178N variants.

159 Fe(II) center per monomer, and a reductase (PDR) that contains flavin mononucleotide (FMN) and a pla

160 onomer, and phthalate dioxygenase reductase (PDR), which contains flavin mononucleotide (FMN) and a p

161 thalate dioxygenase (PDO) and its reductase (PDR) are parts of a two-component Rieske oxygenase syste

162 The probing depth reduction (PDR) for the EMD + DFDBA was 3.6 +/- 0.2 mm, while the E

163 -buccal probing depth (PD) and PD reduction (PDR) reduction favored the test group (1.4 +/- 0.4 mm, t

164 of the productivity-diversity relationship (PDR) for marine phytoplankton has been suggested to be u

165 ers involved in pleiotropic drug resistance (PDR) and in the cellular efflux of a wide variety of dru

166 members of the pleiotropic drug resistance (PDR) family of ATP-binding cassette transporters.

167 P) genes and 49 pleiotropic drug resistance (PDR) genes, while P. sojae contains 20 MRP and 49 PDR ge

168 re-antiretroviral-treatment drug resistance (PDR) is a predictor of human immunodeficiency virus (HIV

169 sporter family, pleiotropic drug resistance (PDR) transporters play essential functions, such as in h

170 subfamily, the Pleiotropic Drug Resistance (PDR) transporters, or full-size ABCG transporters, are f

171 at Ssz1 induces pleiotropic drug resistance (PDR) when overexpressed, a possible role for Zuo1 in PDR

172 s (PCA) and projected difference resolution (PDR) metrics were used to evaluate the data quality and

173 so that the projected difference resolution (PDR) or signal-to-noise ratio (SNR) was maximized.

174 the average projected difference resolution (PDR).

175 strategy and projected distance resolution (PDR) method.

176 Health DNA Polymorphism Discovery Resource (PDR).

177 tes with proliferative diabetic retinopathy (PDR) and 61 individuals with type 1 or 2 diabetes withou

178 eatening proliferative diabetic retinopathy (PDR) and diabetic macular edema (DME).

179 ssion to proliferative diabetic retinopathy (PDR) and the impact of FAc on changes in Early Treatment

180 veloping proliferative diabetic retinopathy (PDR) and vitreous hemorrhage (VH).

181 AMD) and proliferative diabetic retinopathy (PDR) are one of the major causes of blindness caused by

182 te-stage proliferative diabetic retinopathy (PDR) had elevated vitreous semaphorin 3A (SEMA3A).

183 in 69%, proliferative diabetic retinopathy (PDR) in 31% and advanced diabetic eye disease (ADED) in

184 ening of proliferative diabetic retinopathy (PDR) in eyes treated with panretinal photocoagulation (P

185 yes with proliferative diabetic retinopathy (PDR) in need of PRP were randomly assigned to 1 of 4 gro

186 Proliferative diabetic retinopathy (PDR) is a common cause of blindness in the developed wor

187 PRP) for proliferative diabetic retinopathy (PDR) may lead to peripheral field loss that prevents dri

188 to treat proliferative diabetic retinopathy (PDR) that is unresponsive to laser therapy and to retard

189 nts with proliferative diabetic retinopathy (PDR) undergoing pars plana vitrectomy (PPV) for vitreous

190 care for proliferative diabetic retinopathy (PDR) usually is panretinal photocoagulation, an inherent

191 nts with proliferative diabetic retinopathy (PDR) were enriched with a two-module form of CCN1 compri

192 eyes had proliferative diabetic retinopathy (PDR) without macular edema, and 27 eyes had diabetic mac

193 treated proliferative diabetic retinopathy (PDR), and branch retinal vein occlusion (BRVO).

194 28 with proliferative diabetic retinopathy (PDR), previously treated with panretinal photocoagulatio

195 In proliferative diabetic retinopathy (PDR), retinal ischemia promotes neovascularization (NV),

196 tment of proliferative diabetic retinopathy (PDR), the leading cause of visual impairments in the wor

197 ase with proliferative diabetic retinopathy (PDR), vitrectomy was resorted for non clearing vitreous

198 managing proliferative diabetic retinopathy (PDR), with or without concomitant baseline diabetic macu

199 pment of proliferative diabetic retinopathy (PDR).

200 role in proliferative diabetic retinopathy (PDR).

201 ndary to proliferative diabetic retinopathy (PDR).

202 without proliferative diabetic retinopathy (PDR).

203 evant to proliferative diabetic retinopathy (PDR).

204 tic with proliferative diabetic retinopathy (PDR).

205 f active proliferative diabetic retinopathy (PDR).

206 nts with proliferative diabetic retinopathy (PDR).

207 milar to proliferative diabetic retinopathy (PDR).

208 NPDR or proliferative diabetic retinopathy (PDR).

209 nts with proliferative diabetic retinopathy (PDR; respectively, 2.0 +/- 0.9 vs. 2.9 +/- 0.9, P = 0.00

210 DME] and proliferative diabetic retinopathy [PDR]) have a higher risk of CVD will allow physicians to

211 egardless of treatment group (64% [high-risk PDR or worse] vs. 23% [moderate PDR or better]; HR, 3.97

212 r of patients with newly diagnosed high-risk PDR treated with panretinal photocoagulation (PRP) using

213 proliferative DR (PDR), 19.1%; and high-risk PDR, 4.4%; with PPL present in 61.8%.

214 Diabetic Retinopathy Study-defined high-risk PDR.

215 g PASCAL pattern laser therapy for high-risk PDR.

216 he setting of previously untreated high-risk PDR.

217 as examined to determine risk for subsequent PDR development.

218 Venular V and Q were higher in NPDR than PDR subjects (P </= 0.04).

219 The PDR group treated with ALP had significantly lower subba

220 The PDR in 2011 was 0.34 (95% CI 0.25-0.44).

221 The PDR transporters Pdr5p of Saccharomyces cerevisiae and C

222 Recent duplication events in the PDR and ABCG families in both the P. ramorum and the P.

223 Tortuosity was significantly higher in the PDR group (2.2 +/- 0.8 vs. 2.8 +/- 0.9, P = 0.008).

224 in the PDR sample, and two SNPs found in the PDR sample were not found in the Old World sample.

225 ected in the Old World sample but not in the PDR sample, and two SNPs found in the PDR sample were no

226 the Old World sample were also found in the PDR sample.

227 s suggest that the physiological role of the PDR genes might be to regulate membrane homeostasis and

228 ound to be significantly associated with the PDR group (OR = 18.45 [2.35, 144.67], P = 0.00622).

229 ndida albicans are important members of this PDR subfamily, which comprises up to 10 phylogenetic clu

230 proliferative diabetic retinopathy (NPDR) to PDR based on graded fundus photographs, (2) panretinal p

231 the following: (1) worsening from no PDR to PDR, (2) worsening of 2 or more severity levels on readi

232 a 4.7-fold increased risk for progression to PDR (3 [6%] vs. 14 [25%]; P = 0.005).

233 R progression (P = 0.004) and progression to PDR (P = 0.009).

234 Study eye progression to PDR based on a composite clinical outcome of (1) progres

235 Progression to PDR in 5 years differed by baseline DR: no DR (2.2%), mi

236 e seems to be associated with progression to PDR in ranibizumab-treated eyes but did not meaningfully

237 e showed greater reduction in progression to PDR with FAc treatment.

238 he risk of DR progression and progression to PDR, especially with less severe DR at baseline.

239 2)), was predictive of future progression to PDR.

240 on of severe nonproliferative retinopathy to PDR.

241 and January 2015 with a new VH secondary to PDR and treated with IVB were included.

242 management of patients with VH secondary to PDR.

243 POBF is decreased in eyes with laser-treated PDR.

244 Eyes with glaucoma, NAION, treated PDR, and BRVO had significantly decreased retinal blood

245 to examine POBF in subjects with PRP-treated PDR.

246 n explains the negative side of the unimodal PDR curve.

247 theory to explain the shape of the unimodal PDR we obtain at the global scale.

248 Patients with untreated PDR exhibited inner retinal dysfunction, as evidenced by

249 independent predictors of the endpoint were PDR (odds ratio [OR], 0.85; 95% confidence interval, 0.7

250 ndance followed by ammonium content, whereas PDR was best explained directly by nosZ gene abundance a

251 eated patients (1.56+/-0.20; P = 0.001) with PDR.

252 genous and Indigenous Australian adults with PDR or CSME have received laser treatment.

253 The study included 305 adults with PDR, the mean age was 52 years, 44% were women, and 52%

254 ninety-four study eyes from 305 adults with PDR, visual acuity (VA) 20/320 or better, and no history

255 follow-up at 55 US sites for 213 adults with PDR.

256 52A, -141A, -116A, +405C was associated with PDR (OR [95% CI] = 29.92 [3.91, 228.78], P = 1.62 x 10(-

257 simulates neovascular growth associated with PDR and assesses treatment outcomes.

258 Only age in females associated with PDR: A 5-year age decrease was associated with adjusted

259 ed significant independent associations with PDR, as well as the minihaplotype CAA (P = 0.00017).

260 significantly decreased by 19% in eyes with PDR (0.020 +/- 0.005 mm(3), ss = -0.01, P = .01) compare

261 nonproliferative DR (89%), 9 of 10 eyes with PDR (90%), and 13 of 14 eyes with DME (93%) compared wit

262 ness were significantly reduced in eyes with PDR (P < .05) and DME (P < .05) compared with controls.

263 For 93 eyes with PDR at baseline, 1-year improvement rates were 75.9% for

264 For eyes with PDR at baseline, the 3-year cumulative probabilities for

265 levels of TNFalpha were higher in eyes with PDR than in eyes with PVR (P < 0.0005).

266 9%) eyes with NPDR, 11 of 20 (55%) eyes with PDR, and 11 of 27 (41%) eyes with DME (P = .0001).

267 8%) eyes with NPDR, 13 of 20 (65%) eyes with PDR, and 17 of 27 (63%) eyes with DME (P = .007).

268 In eyes with PDR, ranibizumab resulted in less PDR worsening compared

269 yes with uncomplicated RRD, and 29 eyes with PDR.

270 Of the 46 participants with PDR and vision-impairing DME at baseline, 21 were assign

271 in the smaller subgroup of participants with PDR at baseline.

272 ) was exhibited in PRP-treated patients with PDR (MD +/- standard deviation, -8.20+/-5.76 dB; P < 0.0

273 Untreated patients with PDR also had diffusely thinned RPE layers (P = 0.031) co

274 of sTNF-Rs were measured in 17 patients with PDR and 21 patients with PVR.

275 s are significantly reduced in patients with PDR and DME.

276 n measures were compared among patients with PDR and PRP, untreated patients with PDR, and controls.

277 center included 43 laser-naive patients with PDR that required bilateral PRP.

278 elial growth factor therapy in patients with PDR who might otherwise receive laser treatment.

279 ts with PDR and PRP, untreated patients with PDR, and controls.

280 In 60 eyes of 45 patients with PDR, PRP (PRP group), PRP with IVT (IVT group), or PRP w

281 One hundred and fifty-six patients with PDR-related complications requiring PPV were prospective

282 sel formation in the retina of patients with PDR.

283 s fluid samples collected from patients with PDR.

284 er in the vitreous of diabetic patients with PDR.

285 only in sections from diabetic patients with PDR.

286 reretinal membranes in eyes of patients with PDR.

287 n the United States for eyes presenting with PDR and vision-impairing DME, but not for those with PDR

288 Among PRP-treated subjects with PDR, ocular blood flow was 22% below the control (mean O

289 vision-impairing DME, but not for those with PDR without vision-impairing DME.

290 ach eye received a different treatment) with PDR, visual acuity 20/320 or better, no history of PRP.

291 In eyes without PDR (n = 109) at baseline, 56 (51%) had at least 1 field

292 In eyes without PDR (n = 52), increasing NPA and NPI was associated with

293 ssment of fundus photographs in eyes without PDR at baseline, (3) having panretinal photocoagulation,

294 For eyes without PDR at baseline, the 3-year cumulative probabilities for

295 of worsening of retinopathy, with or without PDR, does not seem warranted at this time.

296 etinopathy worsening in eyes with or without PDR.

297 t PRP also were at higher risk for worsening PDR (60% vs. 39%; HR, 2.04; 99% CI, 1.02 to 4.08; P = 0.

298 ars, the cumulative probability of worsening PDR was 42% (PRP) versus 34% (ranibizumab; hazard ratio

299 associated with increased risk of worsening PDR, regardless of treatment group (64% [high-risk PDR o

300 Resource Center Public Data Repository (YRC PDR) serves as a single point of access for the experime