ライフサイエンスコーパス: POAG

1 POAG (506.69 +/- 35.08 mum) and NTG (510.79 +/- 44.37 mu

2 POAG, PXS and PXG samples demonstrated higher MMP2, TIMP

3 lymorphisms (SNPs) and their proxies from 10 POAG-associated loci (CAV1-CAV2, CDKN2B-AS1, SIX1-SIX6,

4 067 (82.0%), including 807 controls and 1260 POAG cases, met all inclusion criteria and completed the

5 itus in a group of black South Africans (215 POAG cases and 214 controls).

6 Aqueous humour from 16 PACG, 28 POAG and 27 control eyes were sampled during intraocular

7 rmed Exome Array (Illumina) analysis on 3504 POAG cases and 9746 controls with replication of the mos

8 ls from Singapore and a further set of 1,374 POAG cases and 4,053 controls from China.

9 yes of 53 control subjects and 64 eyes of 39 POAG patients underwent OCTA imaging.

10 ion of the most significant findings in 9173 POAG cases and 26 780 controls across 18 collections of

11 Nitric oxide donation has emerged as a POAG therapeutic target.

12 idents' compliance with PPP guidelines for a POAG follow-up visit was very high for most elements, bu

13 e than 2000 African Americans eligible for a POAG genetics study.

14 hed healthy controls: (a) 15 patients with a POAG and a FS (POAG/FS+); (b) 15 patients with a POAG bu

15 Patients with a POAG and FS (POAG/FS+) had a significantly higher RVP co

16 and a FS (POAG/FS+); (b) 15 patients with a POAG but without a FS (POAG/FS-); (c) 14 healthy subject

17 was searched in August 2014 to identify AAO POAG guidelines.

18 lin mutations were identified in 45 advanced POAG patients (4.2%), which is significantly higher (P =

19 exons 1 and 2 in early-age-at-onset advanced POAG cases.

20 ns rose from 16% to 40% in selected advanced POAG subgroups based on different thresholds of maximum

21 cohort comprising 1,155 cases with advanced POAG and 1,992 controls.

22 t that the caveolins particularly may affect POAG pathogenesis in women and in patients with early pa

23 Independent of age, POAG and NTG patients demonstrated significantly lower G

24 In addition, almost all POAG patients are steroid responders.

25 45 or more servings per day was 0.82 for all POAG (95% CI, 0.69-0.97; P for trend = .02) and 0.52 for

26 also modulate optic nerve degeneration among POAG patients, underscoring the role of CDKN2B-AS1 in PO

27 significantly higher in PACG (p = 0.032) and POAG (p < 0.001) compared to controls.

28 PACG (0.426 +/- 0.126 mg/ml, p = 0.043) and POAG (0.578 +/- 0.360 mg/ml, p = 0.007) compared to cont

29 significantly higher in PACG (p = 0.049) and POAG (p = 0.010) compared to controls.

30 ratio was higher in PACG (0.83 +/- 0.80) and POAG (0.82 +/- 0.53) compared to controls (0.70 +/- 0.63

31 ified a novel association between CDKN1A and POAG.

32 The associations of myopia with AMD, DR, and POAG are mostly explained by longer AL.

33 OP- and VCDR-specific GRSs with glaucoma and POAG were determined using logistic regression analyses.

34 P = 2.0x10(-5)) likely to have glaucoma and POAG, respectively, compared with participants with both

35 P = 2.0x10(-4)) likely to have glaucoma and POAG, respectively, compared with those in the bottom.

36 P = 1.4x10(-4)) likely to have glaucoma and POAG, respectively.

37 The relationship between oral health and POAG has received limited attention.

38 Genes found to date associated with IOP and POAG are ABCA1, CAV1/CAV2, GAS7 and TMCO1.

39 a small part of the heritability of IOP and POAG.

40 ed a stronger association between myopia and POAG among non-Hispanic whites (OR, 1.12; 95% CI, 1.11-1

41 The difference between PACG and POAG was also not significant (p = 0.133).

42 The difference between PACG and POAG was also not significant (p = 0.961).

43 The difference between PACG and POAG was not significant (p = 0.158).

44 een oral health history and risk of POAG and POAG subtypes.

45 e main outcome was the incidence of POAG and POAG subtypes; 1483 cases were confirmed with medical re

46 low diastolic ocular perfusion pressure and POAG (OR = 0.84 per 10 mm Hg, 95% CI = 0.70-1.01, P = .0

47 re likely to have nuclear cataract, PSC, and POAG.

48 t associations between 10 CAV1/CAV2 SNPs and POAG (top SNP, rs4236601; pooled P = 2.61 x 10(-7)).

49 nd an association between CAV1/CAV2 SNPs and POAG with paracentral VF defects.

50 2 single nucleotide polymorphisms (SNPs) and POAG in a large case-control dataset and to explore asso

51 Subjects were classified as POAG (open drainage angle, glaucomatous optic neuropathy

52 orphisms (SNPs) in other genes in the beagle POAG locus that segregate with disease.

53 tures in other cohorts were compared between POAG cases and controls in the OHTS cohort using analyse

54 lary choroidal volume did not differ between POAG, OH, and control eyes when beta-zone parapapillary

55 wed an overbalance of TIMPsover MMPs in both POAG & PXG groups,especially of TIMP4.

56 In both POAG and PACG, there were no significant differences in

57 demonstrates, for the first time, that both POAG and NTG patients exhibit lower GSH and t-GSH levels

58 id not differ (P for heterogeneity = .75) by POAG subtypes defined by IOP (997 case patients with IOP

59 ation and separated by gender, as well as by POAG subtypes defined by type of VF defect (peripheral o

60 highest in PACG (2.83 +/- 7.40), followed by POAG (1.38 +/- 1.55) and controls (1.34 +/- 3.05).

61 highest in PACG (1.50 +/- 1.69), followed by POAG (1.40 +/- 0.77) and controls (1.15 +/- 0.92).

62 All consecutive POAG new patient visits were reviewed from each study si

63 ths of follow-up in patients with controlled POAG, PXG, or PACG was 0% and was 7% in patients with un

64 glaucoma suspect/POAG combined and definite POAG increased substantially when best-performing criter

65 diabetic pseudophakic patients with definite POAG were recruited; 29 eyes of 16 individuals participa

66 Of these, 209 developed POAG (cases) and 848 did not develop glaucoma (controls)

67 63 eligible enrollees, 2925 (1.9%) developed POAG.

68 e of an ODH increased the risk of developing POAG 2.6-fold in the multivariate analysis (95% confiden

69 AS1 SNPs, which influence risk of developing POAG, also modulate optic nerve degeneration among POAG

70 on of care for patients with newly diagnosed POAG.

71 of rim area loss in eyes with an optic disc POAG endpoint was significantly faster than in those wit

72 rcumpapillary scan) in both eyes of 50 early POAG and 50 control subjects.

73 re to achieve the goal of facilitating early POAG detection and ultimately preventing irreversible bl

74 parameters performed well, identifying early POAG as well as RNFL thickness.

75 hickness were related independently to early POAG.

76 s in St. Lucia and Dominica with established POAG were randomized to prompt washout of IOP-lowering m

77 tly faster than in those with a visual field POAG endpoint.

78 This first POAG genetic association study in black South Africans h

79 For POAG, 9 studies (total, 461 patients; follow-up, 17 mont

80 was stronger (P for heterogeneity = .01) for POAG with early paracentral VF loss (433 cases; quintile

81 , 0.69-0.97; P for trend = .02) and 0.52 for POAG with paracentral VF loss (95% CI, 0.29-0.96; P for

82 ndividual tests gave acceptable accuracy for POAG detection.

83 Several genetic risk factors for POAG and optic nerve features have been identified.

84 associated with an increased likelihood for POAG (CDR asymmetry >/=0.3; LR, 7.3; 95% CI, 3.3-16).

85 nset glaucoma have identified novel loci for POAG (primary-open-angle glaucoma) (ABCA1, AFAP1, GMDS,

86 the development of POAG, the risk of ODH for POAG, and risk factors for ODH were determined using a m

87 rol before surgery are few, particularly for POAG and PXG.

88 was associated with a 0.4% reduced risk for POAG (HR, 0.996 [95% CI, 0.993-0.999]; P = .02).

89 FR C677T polymorphism increases the risk for POAG development in Saudi population and can be a geneti

90 The risk for POAG did not differ with each additional month of use of

91 aining estrogen may help reduce the risk for POAG.

92 re may be associated with increased risk for POAG.

93 ic regression models were run separately for POAG and PEXG.

94 trated that MYOC cascade genetic testing for POAG allows identification of at-risk individuals at an

95 CI, 0.40-0.79; P for trend < .001) than for POAG with peripheral VF loss only (835 cases; quintile 5

96 eter (inferior quadrant RNFL thickness); for POAG, sensitivity was 62% (39-84) for FDT, 58% (37-78) f

97 actors for ODH are very similar to those for POAG in OHT patients.

98 Treatment for POAG currently relies completely on lowering the intraoc

99 Thirty-four POAG patients, 30 NTG patients, and 53 controls were sub

100 humour of PACG eyes that were different from POAG and non-glaucoma control eyes.

101 trols: (a) 15 patients with a POAG and a FS (POAG/FS+); (b) 15 patients with a POAG but without a FS

102 igher RVP compared to patients without a FS (POAG/FS-) (p = 0.0301).

103 b) 15 patients with a POAG but without a FS (POAG/FS-); (c) 14 healthy subjects with a FS (healthy/FS

104 Patients with a POAG and FS (POAG/FS+) had a significantly higher RVP compared to pat

105 Furthermore, POAG eyes with beta-zone parapapillary atrophy had subst

106 d patients with primary open angle glaucoma (POAG group, n = 30) and controls (non POAG group, n = 25

107 7 patients with primary open angle glaucoma (POAG) and 9 patients with normal tension glaucoma (NTG)

108 he pathology of primary open angle glaucoma (POAG) and amyotrophic lateral sclerosis.

109 oci for IOP and primary open-angle glaucoma (POAG) and identify four new IOP-associated loci located

110 imary glaucoma [primary open angle glaucoma (POAG) and primary angle closure glaucoma (PACG)] patient

111 differs between primary open-angle glaucoma (POAG) and primary angle-closure glaucoma (PACG) eyes.

112 l prevalence of primary open-angle glaucoma (POAG) and primary angle-closure glaucoma (PACG), and pro

113 d risk of a new primary open-angle glaucoma (POAG) diagnosis within 365 days after cataract surgery.

114 ueous humour of primary open-angle glaucoma (POAG) eyes have been described.

115 ation study for primary open-angle glaucoma (POAG) in 1,007 cases with high-pressure glaucoma (HPG) a

116 ole therapy for primary open-angle glaucoma (POAG) in an Afro-Caribbean population.

117 ild-to-moderate primary open-angle glaucoma (POAG) in patients undergoing cataract surgery.

118 Primary open-angle glaucoma (POAG) is a blinding disease.

119 Primary open-angle glaucoma (POAG) is a highly prevalent condition worldwide and the

120 Primary open-angle glaucoma (POAG) is a leading cause of blindness worldwide.

121 Primary open-angle glaucoma (POAG) is a leading cause of irreversible vision loss wor

122 Primary open-angle glaucoma (POAG) is a major cause of blindness and visual disabilit

123 Primary open-angle glaucoma (POAG) is a major cause of irreversible blindness worldwi

124 ted with either primary open angle glaucoma (POAG) or heritable ocular quantitative traits associated

125 in the eyes of primary open-angle glaucoma (POAG) patients and healthy subjects with and without a F

126 y of disease in primary open-angle glaucoma (POAG) patients with a Myocilin (MYOC) disease-causing va

127 was examined in primary open-angle glaucoma (POAG) patients with cataract and nonglaucomatous catarac

128 of the TM as in primary open-angle glaucoma (POAG) patients, and is characterized by increased resist

129 ive (OH) and in primary open-angle glaucoma (POAG) patients.

130 Ophthalmology's Primary Open-angle Glaucoma (POAG) Preferred Practice Pattern (PPP) guidelines.

131 rol TM and most primary open angle glaucoma (POAG) TM were collected from cadaver donors.

132 somal recessive primary open angle glaucoma (POAG) to a 4-Mb interval on chromosome 20, and identifie

133 uding 28 (4.4%) primary open angle glaucoma (POAG), 27 (4.2%) primary angle closure glaucoma (PACG),

134 us: (67 PXG, 42 Primary Open Angle Glaucoma (POAG), 28 PACG, 14 Normal Tension Glaucoma (NTG), 5 Juve

135 ied 1 eye of 63 primary open-angle glaucoma (POAG), 30 ocular hypertension (OH), and 48 control subje

136 Primary open angle glaucoma (POAG), a major cause of blindness worldwide, is a comple

137 associated with primary open-angle glaucoma (POAG), although replication among independent studies ha

138 n patients with primary open angle glaucoma (POAG), in which there is specific RGC loss.

139 angle glaucoma: primary open-angle glaucoma (POAG), normal-tension glaucoma (NTG), pigmentary glaucom

140 y patients with primary open angle glaucoma (POAG), ocular hypertension (OHTN), or suspicion of glauc

141 f patients with primary open angle glaucoma (POAG), pseudoexfoliation syndrome (PXS) and pseudoexfoli

142 Primary open-angle glaucoma (POAG), the most common optic neuropathy, is a heritable

143 rocedures) with primary open angle glaucoma (POAG).

144 that resembles primary open-angle glaucoma (POAG).

145 se the risk for primary open-angle glaucoma (POAG).

146 associated with primary open-angle glaucoma (POAG).

147 n implicated in primary open-angle glaucoma (POAG).

148 e implicated in primary open-angle glaucoma (POAG).

149 development of primary open-angle glaucoma (POAG); determine the prognostic significance of ODH for

150 , consisting of primary open-angle glaucoma (POAG, 3.2%, including high-tension glaucoma [1.7%] and n

151 fects of T2D on primary open-angle glaucoma (POAG; 3,554 cases).

152 standard examination, 26 subjects (5.1%) had POAG and 32 subjects (6.4%) were glaucoma suspects.

153 Subjects had POAG with mean diurnal unmedicated intraocular pressure

154 myopia (SE <-6.0 D) were more likely to have POAG (OR, 5.90; 95% CI, 2.68-12.97); each millimeter inc

155 of African ancestry were more likely to have POAG than people of European ancestry (OR, 2.80; 95% CrI

156 ving in urban areas were more likely to have POAG than those in rural areas (OR, 1.58; 95% CrI, 1.19-

157 gression model, men were more likely to have POAG than women (odds ratio [OR], 1.36; 95% CrI, 1.23-1.

158 n a mouse model of elevated IOP and in human POAG eyes.

159 In POAG, a short chromatic pupillometry test that evaluates

160 significantly lower diagnostic abilities in POAG than the peripapillary density.

161 ents, underscoring the role of CDKN2B-AS1 in POAG.

162 role for caveolin 1, caveolin 2, or both in POAG and suggest that the caveolins particularly may aff

163 nally, a lower redox index was found, but in POAG patients only, in comparison to both NTG and contro

164 trophy and associated vascular compromise in POAG.

165 retinal ganglion cell (RGC) degeneration in POAG remains unknown.

166 omarkers of cerebral small vessel disease in POAG and NTG will show different characteristics.

167 4 %) and genotype CT (38.89 %) were found in POAG patients compared to controls (12.5 % and 25 % resp

168 TIMP-2 was significantly higher in POAG (p = 0.004) compared to controls.

169 MMP-3 was significantly higher in POAG compared to controls (p = 0.002) and PACG (p = 0.02

170 genetic variation in CDKN1A is important in POAG risk.

171 The main cause of elevated IOP in POAG is thought to be an increased outflow resistance vi

172 w extends this by directly implicating it in POAG disease pathogenesis.

173 -CDC7) was associated with VF progression in POAG patients.

174 the optic nerve was significantly reduced in POAG eyes when beta-zone parapapillary atrophy was prese

175 horoidal volume was significantly reduced in POAG vs control eyes when beta-zone parapapillary atroph

176 horoidal volume was significantly reduced in POAG vs OH and control eyes (1.057 vs 1.228 vs 1.255 muL

177 to establish if systemic oxidative status in POAG patients was elevated compared with the cataract on

178 acellular matrix homeostasis is suggested in POAG, PXS and PXG.

179 predict success of trabeculectomy surgery in POAG patients during the first 3 years of follow-up.

180 tential to alleviating the fibrosis of TM in POAG patients.

181 humor is the main cause of fibrosis of TM in POAG patients.

182 ion of this population demonstrated incident POAG.

183 Hazard ratios (HRs) for developing incident POAG.

184 risk factors that could predict the incident POAG.

185 In 6 years, incident POAG developed in 129 subjects (2.9%; 95% confidence int

186 ng that metabolic dysregulation may increase POAG risk prior to T2D diagnosis.

187 iable estimates indicated that T2D increased POAG risk (odds ratio = 2.53, 95% confidence interval: 1

188 er observational evidence that T2D increases POAG risk.

189 Separate meta-analyses of 4 independent POAG cohorts, totaling 4,284 cases and 95,560 controls,

190 as assumed that genetic variation influenced POAG either through IOP or via changes to the optic nerv

191 Upon stratification of our results into POAG and PACG, significantly higher frequencies of allel

192 o association was detected between the known POAG risk alleles when the OHTS cohort was examined as a

193 vegetable intake was associated with a lower POAG risk, particularly POAG with early paracentral VF l

194 345, His141Asn) is enhanced by another major POAG risk gene, p16INK4a (cyclin-dependent kinase inhibi

195 CA1, CAV1/CAV2 and GAS7 pathway to Mendelian POAG genes (MYOC, OPTN, WDR36).

196 onal surgical treatment for mild-to-moderate POAG.

197 A total of 274 new POAG patient visits from phase 1 and 280 visits from pha

198 ificant indicator of increased risk of a new POAG diagnosis.

199 ucoma (POAG group, n = 30) and controls (non POAG group, n = 25).

200 laucoma suspect, ocular hypertension, or non-POAG/nonocular hypertension.

201 in individuals with advanced and nonadvanced POAG.

202 higher (P = 0.02) compared with nonadvanced POAG patients (1.6%).

203 systolic ocular perfusion pressure and OAG, POAG, or PEXG, regardless of the use of antihypertensive

204 logistic regression models were run for OAG, POAG, and PEXG in subjects with and without antihyperten

205 ns have been reported in approximately 4% of POAG cases.

206 During follow-up, 485 incident cases of POAG were confirmed with medical records and classified

207 n-years of follow-up, 1483 incident cases of POAG were identified.

208 mutation of ADAMTS10 as the likely cause of POAG in beagles.

209 verage of 13 years before the development of POAG and 1.2% per year during an average of 6 years afte

210 ent predictive factor for the development of POAG in patients with ocular hypertension (OHT) and the

211 e of ODH before and after the development of POAG, the risk of ODH for POAG, and risk factors for ODH

212 ee loci newly associated with development of POAG.

213 average of 6 years after the development of POAG.

214 c significance of ODH for the development of POAG; and identify predictive factors for ODH.

215 e is strongly associated with a diagnosis of POAG and with the severity of abnormalities in CDR and v

216 rticipants were aged 40+ years, were free of POAG, and reported eye examinations.

217 cipants were 40 years or older, were free of POAG, and reported eye examinations.

218 The main outcome was the incidence of POAG and POAG subtypes; 1483 cases were confirmed with m

219 The cumulative incidence of POAG in eyes with ODH was 25.6% compared with 12.9% in e

220 IOP at baseline had the highest incidence of POAG.

221 human TM cells and in a MYOC mouse model of POAG to knock down expression of mutant MYOC, resulting

222 We used logistic regression models of POAG in the overall population and separated by gender,

223 encing the major clinical risk predictors of POAG and showed that genetic variation in CDKN1A is impo

224 L was associated with a higher prevalence of POAG (OR, 1.43; 95% CI, 1.13-1.80).

225 ss the association between the prevalence of POAG and the relevant factors.

226 The prevalence of POAG is highest in Africa (4.20%; 95% CrI, 2.08-7.35), a

227 ssociated with a 1.45-fold increased risk of POAG (95% CI, 1.06-1.97); in particular, a report within

228 ssociated with a 1.85-fold increased risk of POAG (95% CI, 1.07-3.18).

229 n the association of myopia with the risk of POAG and NTG.

230 tion between oral health history and risk of POAG and POAG subtypes.

231 receptor 1B gene (MTNR1B) predicted risk of POAG independently of T2D status, indicating possible pl

232 atural teeth was not associated with risk of POAG, recent tooth loss was associated with an increased

233 oss was associated with an increased risk of POAG.

234 d validated our findings in multiple sets of POAG cases and controls.

235 Siblings of POAG cases have a ten-fold increased risk of developing

236 A select subset of POAG surgical TM samples also were collected for analyse

237 yes were measured and compared with those of POAG as well as non-glaucoma control eyes.

238 Follow-up visits of POAG patients were evaluated for documentation of 19 ele

239 The effect of antihypertensive treatment on POAG was not statistically significant (OR = 1.20, 95% C

240 fference between PACG and either controls or POAG was not significant (p > 0.05).

241 ed with POAG with peripheral VF loss only or POAG among men.

242 ociated with a lower POAG risk, particularly POAG with early paracentral VF loss at diagnosis.

243 TIMP4 was elevated in glaucoma patients(POAG: 0.95 +/- 0.49 PXG: 1.28 +/- 1.38 pg/ml. p < 0.001)

244 aracteristics are used clinically to predict POAG risk.

245 l dysregulation also significantly predicted POAG (odds ratiobeta-cell = 5.26, 95% confidence interva

246 data indicate that SIX6 and/or IOP promotes POAG by directly increasing p16INK4a expression, leading

247 le A associated with increased disease risk, POAG patients with A alleles had larger cup-to-disc rati

248 isease risk (eg, the G allele at rs2157719), POAG patients carrying these minor alleles had smaller c

249 Post-test probability of glaucoma suspect/POAG combined and definite POAG increased substantially

250 pecificity for detection of glaucoma suspect/POAG combined was 41% (28-55) for FDT, 35% (21-48) for M

251 oss were not significantly different for the POAG subtypes (P for heterogeneity >/=0.36), although as

252 Mean TM heights in the POAG and PACG groups were 812 +/- 13 mum and 732 +/- 27

253 be a factor in the toxicity of sCD44 in the POAG disease process.

254 There were 199 eyes (123 patients) in the POAG group and 61 eyes (38 patients) in the PACG group.

255 In the POAG group, optic cup-to-disc ratio (CDR) was positively

256 S10 was an affected beagle, unrelated to the POAG colony.

257 sociations were strongest in relation to the POAG subtypes with IOP <22 mmHg (MVRR, 1.93; 95% CI, 1.0

258 d one SNP showing significant association to POAG (CDC7-TGFBR3 rs1192415, ORG-allele = 1.13, Pmeta =

259 juxtapapillary choroidal volume compared to POAG eyes without beta-zone parapapillary atrophy (0.957

260 ight is shorter in PACG patients compared to POAG patients.

261 4-hour intraocular pressure (IOP) in treated POAG patients.

262 ese results identify new pathways underlying POAG susceptibility and suggest new targets for preventa

263 pproximately 5 times faster in eyes in which POAG developed compared with eyes in which it did not.

264 ally significant change in the eyes in which POAG did not develop represents normal aging or glaucoma

265 th multiple-ethnic populations affected with POAG to strengthen these findings.

266 other population-based studies in Asia, with POAG accounting for the majority of cases.

267 en genomic regions have been associated with POAG (including the normal tension glaucoma (NTG) subgro

268 sh model we show that six6b (associated with POAG and optic nerve head variation) alters the expressi

269 n pressure was significantly associated with POAG in subjects using antihypertensive treatment (OR =

270 e SNP was also significantly associated with POAG in two independent case-control studies [n = 1225 c

271 f 13 risk alleles previously associated with POAG or with optic disc features in other cohorts were c

272 lymorphism are significantly associated with POAG while allele C and CC genotype may be protective fo

273 f the 10 CAV1/CAV2 SNPs were associated with POAG with early paracentral VF (top SNP, rs17588172; poo

274 4)), and none of the 10 were associated with POAG with peripheral VF loss only or POAG among men.

275 ore diagnosis were inversely associated with POAG, but more strongly for NTG.

276 d low BMI were significantly associated with POAG.

277 these loci for IOP were also associated with POAG.

278 oot canal treatment were not associated with POAG.

279 No association with POAG was identified with tagging SNPs in TMCO1, CAV1/CAV

280 ne regions showed marginal associations with POAG.

281 ysis, 87 (70.7%) of whom were diagnosed with POAG.

282 nt IOP reduction in Afro-Caribbean eyes with POAG.

283 l visual parameters in some individuals with POAG, suggesting that neuronal energy substrate delivery

284 examined the association of these loci with POAG, with central corneal thickness (CCT), vertical cup

285 Compared with controls, patients with POAG and those with NTG exhibited similarly increased no

286 Patients with POAG do not manifest a reproducible diurnal IOP pattern

287 Patients with POAG had significantly greater white matter lesion load

288 ry light reflex was reduced in patients with POAG only at higher irradiance levels, corresponding to

289 articipants with a FS (whether patients with POAG or healthy subjects), had a significantly higher RV

290 Patients with POAG or NTG exhibit similar alterations in ocular and sy

291 rst-line medical treatments in patients with POAG or ocular hypertension through a systematic review

292 A single diurnal IOP curve in patients with POAG poorly characterizes IOP fluctuations and has limit

293 We reviewed the records of patients with POAG who underwent 4 diurnal IOP curve measurements 6 mo

294 stemic vascular function of 19 patients with POAG, 19 patients with NTG, and 20 healthy individuals s

295 In patients with POAG, pupillary responses were evaluated relative to sta

296 ons of IOP and medications for patients with POAG, PXG, and PACG, respectively, and using 1 to 2 medi

297 CAV2 SNPs were associated significantly with POAG overall, particularly among women.

298 The ONHs of 9 subjects with POAG (pre-TE IOP: 25.3+/-13.9 mmHg; post-TE IOP: 11.8+/-

299 ared between control subjects and those with POAG by constructing dose-response curves across a wide

300 A total of 4316 subjects without POAG at baseline who were 40 years of age and older from