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 is associated with pre-existing HTN, suggesting tha

3 POAG was significantly associated with prior HTN (OR 1.3

4 3.9 +/- 7.4 to 15.4 +/- 5.1 mmHg (p < 0.01); POAG: 22.8 +/- 6.5 to 15.1 +/- 4.6 mmHg (p < 0.01); NTG:

5 067 (82.0%), including 807 controls and 1260 POAG cases, met all inclusion criteria and completed the

6 CMvD was detected in 21 POAG (58.3%) and 10 PACG (35.7%) eyes (P = .07).

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

8 DF (teaching set: 34 healthy subjects and 34 POAG patients) using a combination of MRW and pRNFL para

9 (validating set: 34 healthy subjects and 34 POAG patients).

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

11 Structured EHR data of 385 POAG patients from a single academic institution were in

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

13 Seventy eyes of 40 POAG patients undergoing cataract surgery by phacoemulsi

14 eyes, 36 preperimetric glaucoma eyes, and 80 POAG eyes) of 94 patients who had at least 3 visits were

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

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

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

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

19 participants in this report include 2146 AD POAG patients, 695 ED POAG patients, 198 AD control part

20 After adjusting for age, AD POAG patients had different phenotypic characteristics c

21 The AD POAG patients and control participants were significantl

22 Advanced POAG was defined by age-based mean deviation of visual f

23 etween controls, mild-moderate, and advanced POAG groups.

24 polymorphisms (SNPs) with POAG and advanced POAG was tested by linear mixed model correcting for rel

25 Thirty-seven eyes with moderate and advanced POAG, 19 eyes with atrophic NAION, and 40 eyes of normal

26 novel locus, EN04, was observed for advanced POAG (rs185815146 beta, 0.36; standard error, 0.065; P <

27 the LC-GSI was most negative in the advanced POAG group (mean [standard error] = -0.34 [0.05]), follo

28 Patients with uncontrolled mild to advanced POAG (according to Glaucoma Grading Scale HODAPP) 2) cat

29 A novel association with advanced POAG in the EN04 locus was identified putatively in pers

30 Among all POAG eyes, peripapillary VD and IOS of the affected hemi

31 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

32 ified a novel association between CDKN1A and POAG.

33 0.45; P <= 3.0 x 10(-4)) and between CDR and POAG were high (r(g) = 0.57; P = 2.8 x 10(-10)).

34 en corneal properties (CCT, CRF, and CH) and POAG were low (r(g) range -0.18 to 0.11) and nonsignific

35 tistical power using all-cause endpoints and POAG endpoints.

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

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

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

39 ntrast, genetic correlations between IOP and POAG (r(g) >= 0.45; P <= 3.0 x 10(-4)) and between CDR a

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

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

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

43 lar GCC were not different between NAION and POAG eyes, both were significantly thinner than control

44 In NAION and POAG with similar RNFL and macular damage, macular OCT-A

45 to obtain prevalence estimates for PACG and POAG.

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

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

48 ificant negative correlation between T2D and POAG (r(g) = -0.14; P = .16).

49 The uveitis and POAG groups had 23 of 205 (11%) and 331 of 4600 (7%) "ra

50 artile range) baseline MD in the uveitis and POAG groups was -3.8 (-8.7, -1.5) dB and -3.1 (-6.6, -1.

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

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

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

54 -causing gene, accounting for ~2% of British POAG cases.

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

56 113 eyes were affected by POAG (74%), 5 eyes by NTG (3%), 22 eyes by PEX (14%) and

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

58 sification in eyes with medically controlled POAG resulted at 1 year in a very small IOP decrease wit

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

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

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

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

63 low-up in this population of newly diagnosed POAG patients.

64 (median age 77.3 years) with newly diagnosed POAG, those with XFG had more office visits (mean, 9.1 v

65 on of care for patients with newly diagnosed POAG.

66 Consecutive newly-diagnosed POAG patients were enrolled and followed-up for one year

67 examined an independent cohort of 624 early POAG patients.

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

69 (number of medications) results in the early POAG cohort (P <= 0.01).

70 report include 2146 AD POAG patients, 695 ED POAG patients, 198 AD control participants, and 227 ED c

71 of glaucoma did not differ between AD and ED POAG patients.

72 ificantly younger (both, 67.4 years) than ED POAG patients and control participants (73.4 and 70.2 ye

73 phenotypic characteristics compared with ED POAG patients, including higher intraocular pressure, wo

74 s observed at the 9p21 European descent (ED) POAG signal (rs79721419; P < 6.5x10(-5)) independent of

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

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

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

78 For POAG, an AD signal was observed at the 9p21 European des

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

80 , 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

81 as 0.94 for all-cause endpoints and 0.99 for POAG endpoints.

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

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

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

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

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

87 f 0.54-0.84) and a 56% reduction in risk for POAG endpoints (relative risk = 0.44, 95% CI of 0.31-0.6

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

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

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

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

92 Treatment for POAG currently relies completely on lowering the intraoc

93 eperimetric glaucoma eyes, and 2.6 years for POAG eyes.

94 As in eyes suffering from POAG, IOP and number of IOP-lowering drugs applied can b

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

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

97 7 patients with primary open-angle glaucoma (POAG) and 36 normal participants were analyzed.

98 7 patients with primary open angle glaucoma (POAG) and 9 patients with normal tension glaucoma (NTG)

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

100 th uncontrolled primary open-angle glaucoma (POAG) and cataract who underwent PKE combined with eithe

101 eyes with both primary open-angle glaucoma (POAG) and cataract; each eye was treated with combined p

102 scent (ED) with primary open-angle glaucoma (POAG) and control participants completed a detailed demo

103 to evaluate if primary open angle glaucoma (POAG) and its severity are associated with the shape of

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

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

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

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

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

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

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

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

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

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

114 Primary open-angle glaucoma (POAG) is a progressive neurodegenerative disease which l

115 n patients with primary open-angle glaucoma (POAG) is a subject of debate.

116 Primary open-angle glaucoma (POAG) is the most common form of glaucoma, prevalent in

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

118 study: 68 mild primary open-angle glaucoma (POAG) patients according to the Hodapp-Parrish-Anderson

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

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

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

122 newly-diagnosed primary open angle glaucoma (POAG) patients.

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

124 circulation of primary open angle glaucoma (POAG) patients.

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

126 ng for PACG and primary open angle glaucoma (POAG) to evaluate costs and benefits of community-level

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

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

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

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

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

132 n patients with primary open-angle glaucoma (POAG), normal-tension glaucoma (NTG), pseudoexfoliation

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

134 -based study of primary open-angle glaucoma (POAG)-related DH showed that they had grayscale pixel in

135 associated with primary open angle glaucoma (POAG).

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

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

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

139 n patients with primary open angle glaucoma (POAG).

140 ild to moderate primary open-angle glaucoma (POAG).

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

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

143 Population screening for glaucoma (POAG and PACG combined) is likely to be cost-effective i

144 ic (PPG), and 54 primary openangle glaucoma (POAG) eyes.

145 atio [CDR], and primary open-angle glaucoma [POAG]).

146 standardized incidences of primary glaucoma, POAG, and PACG were 1.68% (95% confidence interval [CI],

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

148 Subjects had POAG with mean diurnal unmedicated intraocular pressure

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

150 EHR has some predictive value in identifying POAG patients at risk of progression to surgical interve

151 Committee adjudication of endpoints improved POAG incidence estimates, increased statistical power, a

152 In POAG eyes, macular vessel density decrease was faster th

153 In POAG, a short chromatic pupillometry test that evaluates

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

155 fter performing phacoemulsification alone in POAG patients.

156 known that retinal blood flow is altered in POAG eyes.

157 As in POAG, CMvD in PACG was associated with advanced VF damag

158 CMvD in POAG eyes was associated with pretreatment intraocular p

159 trophy and associated vascular compromise in POAG.

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

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

162 , but may also enhance retinal blood flow in POAG patients with a normal IOP.

163 ovasculature showed decreased VD and flow in POAG with paracentral loss, supporting its importance in

164 4 %) and genotype CT (38.89 %) were found in POAG patients compared to controls (12.5 % and 25 % resp

165 genetic variation in CDKN1A is important in POAG risk.

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

167 Lamina cribrosa depth was larger in POAG eyes as compared with PXG, PACG, and healthy eyes.

168 enting intraocular pressure was 22.9 mmHg in POAG and 25.5 mmHg in PACG patients.

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

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

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

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

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

174 nding, this genome-wide association study in POAG patients of AD contributes to POAG genetics by iden

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

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

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

178 ssure, history of smoking and alcohol use in POAG patients and control participants were described.

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

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

181 er observational evidence that T2D increases POAG risk.

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

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

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

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

186 345, His141Asn) is enhanced by another major POAG risk gene, p16INK4a (cyclin-dependent kinase inhibi

187 ar pressure (IOP) in patients with medically POAG .

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

189 -0.34 [0.05]), followed by the mild-moderate POAG group (-0.31 [0.02]) and then controls (-0.23 [0.02

190 nd microstent placement for mild to moderate POAG is safe, more effective in lowering IOP with fewer

191 ion use among subjects with mild-to-moderate POAG who received a Schlemm canal microstent combined wi

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

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

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

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

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

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

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

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

200 uenced and variants reported for a cohort of POAG patients.

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

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

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

204 average of 6 years after the development of POAG.

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

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

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

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

209 ess gaps in our knowledge of the genetics of POAG in this high-risk population.

210 y that are increased in the aqueous humor of POAG arising from a variety of conditions, it is likely

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

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

213 nsion (n = 45) at baseline, the incidence of POAG was 4.83% (95% CI, 1.24%-17.21%) and for eyes with

214 In our population, the incidence of POAG was only half and the incidence of PACG was similar

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

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

217 y in the peripapillary and macular region of POAG patients with normal IOP treated with topical Taflu

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

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

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

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

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

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

224 oss was associated with an increased risk of POAG.

225 red with no screening, combined screening of POAG and PACG in rural China is predicted to result in a

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

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

228 dentified Medicare beneficiaries with XFG or POAG and >=5 years of continuous enrollment from January

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

230 aracteristics are used clinically to predict POAG risk.

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

232 6 persons (median age 79.5) with preexisting POAG, persons with XFG had more office visits (mean 9.3

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

234 Thirty-six POAG eyes (36 patients) and 28 PACG eyes (28 patients) u

235 Sixty POAG patients with IOP >=21 mm Hg taking maximal topical

236 from IOP-associated variants and stratified POAG patients into 3 risk tiers.

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

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

239 The POAG eyes demonstrated the largest LC depths (P < 0.05),

240 The POAG groups had matched VF MD (-3.1 +/- 2.5 dB paracentr

241 The POAG groups were matched by VF mean deviation (MD).

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

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

244 l) of macular vessel density decrease in the POAG eyes (-7.12 [-8.36, -5.88]%/year) was significantly

245 7 eyes with IPFS and 1 of 13 with IND in the POAG group (P < .05) and 1 of 2 eyes with IPFS and 0 of

246 hicknesses were significantly thinner in the POAG group (p < 0.001).

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

248 In the POAG group, more than two thirds of the eyes showed fast

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

250 ne year after cataract surgery, 75.7% of the POAG eyes maintained the same number of glaucoma medicat

251 owed higher rates of VF progression than the POAG group (-0.37 dB/year; P < .01).

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

253 All patients had their POAG medically controlled without prior glaucoma surgery

254 1 patients, which accounts for 3.07% of this POAG cohort.

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

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

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

258 was significantly lower in PACG compared to POAG.

259 r for managing patients with XFG compared to POAG.

260 deep vascular plexus in NAION in contrast to POAG, which might show a primary vascular insult in addi

261 study in POAG patients of AD contributes to POAG genetics by identification of novel signals in prio

262 ributed 58% (155 of 267) of the endpoints to POAG.

263 4-hour intraocular pressure (IOP) in treated POAG patients.

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

265 The incidence of all-cause endpoints vs POAG endpoints was 19.5% and 13.2%, respectively, in the

266 ted RR for "rapid progression" in uveitic vs POAG eyes was 1.9 (95% confidence interval: 1.8-2.0).

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

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

269 yes), CMvD was significantly associated with POAG (OR > 3.5, P < .05) after accounting for glaucoma s

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

271 l previously identified loci associated with POAG in persons of AD were: 8q22, AFAP1, and TMC01.

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

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

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

275 oot canal treatment were not associated with POAG.

276 d low BMI were significantly associated with POAG.

277 An association with POAG in FNDC3B (rs111698934; P < 3.9x10(-5)) was observe

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

279 Compared with POAG eyes with peripheral VF loss, the paracentral group

280 e reduced LC and PLT thickness compared with POAG, PACG, and healthy eyes.

281 s glaucoma were compared with 4600 eyes with POAG only.

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

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

284 or all 112,929 newly diagnosed patients with POAG from January 2010 through December 2015 (cases), an

285 Patients with POAG had significantly greater white matter lesion load

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

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

288 Among patients with POAG, 3 had preperimetric glaucoma and 44 had perimetric

289 In patients with POAG, combined treatment with phacoemulsification, ab-in

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

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

292 In this study, patients with POAG, regularly scheduled for cataract surgery, were imp

293 single nucleotide polymorphisms (SNPs) with POAG and advanced POAG was tested by linear mixed model

294 head (OHN) were obtained from subjects with POAG (n = 99) and non-glaucomatous controls (n = 76).

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

296 The LPA was 3.40+/-2.29 mm(2) in those with POAG and 0.11+/-0.18 mm(2) in normal subjects (P < 0.001

297 The FPL was 21.8%+/-17.0% in those with POAG and 0.3%+/-0.7% in normal subjects (P < 0.001).

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

299 diagnosed and preexisting XFG vs those with POAG.

300 = .92) or between DH events with and without POAG (P >= .26).