ライフサイエンスコーパス: primary open-angle glaucoma

1 of the TM may be possible in human eyes with primary open angle glaucoma.

2 ed 50 mmHg and he was found to have advanced primary open angle glaucoma.

3 th juvenile glaucoma and some cases of adult primary open angle glaucoma.

4 (s) of TIGR/MYOC in both steroid-induced and primary open angle glaucoma.

5 ssociated with both juvenile-and adult-onset primary open angle glaucoma.

6 rove early diagnosis of visual field loss in primary open angle glaucoma.

7 oss is measurable by conventional methods in primary open angle glaucoma.

8 has been associated with the development of primary open angle glaucoma.

9 nce for genetic heterogeneity of adult-onset primary open angle glaucoma.

10 e damage, is involved in the pathogenesis of primary open angle glaucoma.

11 omy in patients with coexisting cataract and primary open angle glaucoma.

12 coagulation (ECP) surgeries in patients with primary open angle glaucoma.

13 ous ocular diseases, such as keratoconus and primary open angle glaucoma.

14 sub-types were mostly pseudo-exfoliative and primary open angle glaucoma.

15 ffective in lowering intraocular pressure in primary open-angle glaucoma.

16 gene are the most common genetic factors of primary open-angle glaucoma.

17 g the onset of the prevalent ocular disorder primary open-angle glaucoma.

18 ) which have previously been associated with primary open-angle glaucoma.

19 ing diabetic retinopathy, uveoretinitis, and primary open-angle glaucoma.

20 related to mutations in the MYOCILIN gene is primary open-angle glaucoma.

21 N gene may lead to juvenile- and adult-onset primary open-angle glaucoma.

22 ay be on a multiple topical drug regimen for primary open-angle glaucoma.

23 similar at baseline; 68% were diagnosed with primary open-angle glaucoma.

24 F-beta2 because TGF-beta2 is associated with primary open-angle glaucoma.

25 are associated with juvenile and adult-onset primary open-angle glaucoma.

26 N gene may lead to juvenile- and adult-onset primary open-angle glaucoma.

27 ween antioxidant consumption and the risk of primary open-angle glaucoma.

28 s in the initial management of patients with primary open-angle glaucoma.

29 documented to occur in eyes of patients with primary open-angle glaucoma.

30 surgical therapy are similar to treatment of primary open-angle glaucoma.

31 eature of the outflow system in aging and in primary open-angle glaucoma.

32 laucoma and 2121 control individuals without primary open-angle glaucoma.

33 hwork and possibly some of the extra loss in primary open-angle glaucoma.

34 rat model appears to mimic some features of primary open-angle glaucoma.

35 also may be involved in the pathogenesis of primary open-angle glaucoma.

36 from juvenile glaucoma to typical late-onset primary open-angle glaucoma.

37 may contribute to changes seen with age and primary open-angle glaucoma.

38 lantation following previous GDD surgery had primary open-angle glaucoma.

39 Genetic variants associated with primary open-angle glaucoma.

40 Presence of primary open-angle glaucoma.

41 es in a transgenic mouse model of hereditary primary open-angle glaucoma.

42 forms of myocilin, a protein associated with primary open-angle glaucoma.

43 male), 16 had ocular hypertension and 14 had primary open-angle glaucoma.

44 risk and be a new risk factor to consider in primary open-angle glaucoma.

45 8591 (3.9%) with glaucoma, 3412 (1.6%) with primary open-angle glaucoma, 1515 (0.7%) with exfoliatio

46 glaucoma 2.66 mm Hg, 95% CI: 2.36-2.97; and primary open-angle glaucoma 2.92 mm Hg, 95% CI: 2.75-3.0

47 spective study included 122 eyes treated for primary open angle glaucoma, 50 eyes (study group) in wh

48 Main diagnoses in descending prevalence were primary open-angle glaucoma (55.9%), chronic angle-closu

49 identified 354 eyes in 180 subjects (97 with primary open-angle glaucoma, 83 with glaucoma suspicion)

50 he potential role of superoxide dismutase in primary open angle glaucoma, a disorder of the aging tra

51 The etiology of primary open angle glaucoma, a leading cause of age-rela

52 laucoma have identified novel loci for POAG (primary-open-angle glaucoma) (ABCA1, AFAP1, GMDS, PMM2,

53 educed cell survival is also associated with primary open angle glaucoma, ageing, cellular senescence

54 Family and personal history of primary open-angle glaucoma also increases the risk of c

55 aucoma, one locus (GLC1A) for juvenile-onset primary open angle glaucoma and a further two loci (GLC1

56 essure is a highly heritable risk factor for primary open angle glaucoma and currently the only targe

57 mans with Weill-Marchesani-like syndrome and primary open angle glaucoma and ectopia lentis in dogs.

58 ng female patient with choroidal infarction, primary open angle glaucoma and Flammer syndrome.

59 actor for the development and progression of primary open angle glaucoma and is due to trabecular mes

60 Primary open angle glaucoma and ocular hypertension are

61 discovery data set of 2320 individuals with primary open-angle glaucoma and 2121 control individuals

62 Twenty-one patients with newly diagnosed primary open-angle glaucoma and 34 age- and gender-match

63 We screened 716 patients with primary open-angle glaucoma and 596 control subjects for

64 amples were collected from 111 patients with primary open-angle glaucoma and an age-matched control g

65 A total of 609 patients (609 eyes) with primary open-angle glaucoma and cataract were included.

66 of dementia, including Alzheimer's disease, primary open-angle glaucoma and Helicobacter pylori (H.p

67 in which CCT has been implicated, including primary open-angle glaucoma and keratoconus.

68 ts with NTG when compared with patients with primary open-angle glaucoma and nonglaucomatous control

69 traocular lens implantation in patients with primary open-angle glaucoma and ocular hypertension.

70 The two most common types of glaucoma--primary open-angle glaucoma and primary angle-closure gl

71 ntly identified as causative for adult-onset primary open-angle glaucoma and provides additional evid

72 One eye per patient with primary open-angle glaucoma and stable intraocular press

73 d from patients undergoing trabeculotomy for primary open-angle glaucoma and the normal aqueous from

74 asured by 24-2 and 10-2 VFs in patients with primary open-angle glaucoma and to test the hypothesis t

75 A total of 234 patients (104 with primary open angle glaucoma, and 130 control subjects wi

76 wed up until death; 203 patients (65.7%) had primary open-angle glaucoma, and 106 patients (34.2%) ha

77 n "high-pressure" forms of glaucoma, such as primary open-angle glaucoma, and in cases in which the i

78 tis pigmentosa, while Bardet-Biedl syndrome, primary open-angle glaucoma, and tumor cell invasiveness

79 these mice may be useful as a mouse model of primary open angle glaucoma as well as for assessing the

80 t quintile have a 2.5-fold increased risk of primary open-angle glaucoma as compared with those in th

81 To determine the stage of primary open angle glaucoma at presentation at a tertiar

82 utoimmune uveitis, diabetic retinopathy, and primary open angle glaucoma, but its role in normal visi

83 autosomal dominant juvenile- and adult-onset primary open angle glaucoma, but the mechanism by which

84 ive oxygen species play a pathogenic role in primary open angle glaucoma by fostering changes that re

85 s demonstrated differential association with primary open-angle glaucoma by ancestry.

86 the gene have been found in 2-4% of sporadic primary open angle glaucoma cases.

87 ed, and they lead to approximately 5% of all primary open-angle glaucoma cases.

88 of the posterior sclera in a canine model of primary open-angle glaucoma caused by the G661R missense

89 -85 years with a minimum 2-year diagnosis of primary open-angle glaucoma, chronic primary angle-closu

90 The pooled multivariate rate ratios for primary open-angle glaucoma comparing the highest versus

91 s elevated in aqueous humor of patients with primary open-angle glaucoma, contributes to the increase

92 rmal eyes and of the increased resistance in primary open-angle glaucoma eyes (POAG).

93 lens and vitreous status and the presence of primary open-angle glaucoma for statistical analyses.

94 Primary open angle glaucoma (GLC1) is a common ocular di

95 Individuals with primary open-angle glaucoma had open iridocorneal angles

96 e of progression from ocular hypertension to primary open-angle glaucoma has been established in the

97 sty reduces elevated intraocular pressure in primary open-angle glaucoma has been established.

98 the progression from ocular hypertension to primary open-angle glaucoma has been the subject of two

99 ld sustained IOP reduction for patients with primary open-angle glaucoma (hazard ratio [HR], 1.19; 95

100 he authors investigated the genetic cause of primary open angle glaucoma in a large four-generation f

101 ld female was being followed and treated for primary open angle glaucoma in our tertiary referral cen

102 lance of benefits and harms of screening for primary open-angle glaucoma in adults.

103 variants of LOXL1 play a significant role in primary open-angle glaucoma in the Caucasian, African-Am

104 nces may contribute to the predisposition of primary open-angle glaucoma in various high-risk populat

105 o cause the most common form of the disease, primary open angle glaucoma, in selected families.

106 It may also be important in primary open angle glaucoma influencing aqueous outflow.

107 A 63-year-old male patient affected by primary open angle glaucoma (IOP = 25 mmHg) and a full t

108 Adult onset primary open angle glaucoma is a leading cause of blindn

109 ntraocular pressure-independent component of primary open angle glaucoma is associated with 26 differ

110 associated with progression of patients with primary open angle glaucoma is essential to our clinical

111 CACNA2D1 single-nucleotide polymorphism and primary open angle glaucoma is found.

112 Primary open angle glaucoma is the most prevalent type o

113 Primary open-angle glaucoma is a progressive optic neuro

114 Primary open-angle glaucoma is characterized by increase

115 number of persons in the United States with primary open-angle glaucoma is estimated to be 2.47 mill

116 The common form of adult-onset primary open-angle glaucoma is inherited as a complex tr

117 Primary open-angle glaucoma is the second leading cause

118 s not contain any of the previously reported primary open angle glaucoma loci.

119 This study identifies a new primary open angle glaucoma locus, GLC1Q, in a region on

120 A total of 2320 individuals with primary open-angle glaucoma (mean [interquartile range]

121 [45.5%] women) and 2121 individuals without primary open-angle glaucoma (mean [interquartile range]

122 size (P < 0.001) in both eyes with incident primary open-angle glaucoma (mean, 10.6%; standard devia

123 yndrome (MetS) with intraocular pressure and primary open angle glaucoma (OAG) have been reported.

124 Primary open-angle glaucoma (OAG) was diagnosed in 3.1%

125 2 (APBB2; chromosome 4, rs59892895T>C) with primary open-angle glaucoma (odds ratio [OR], 1.32 [95%

126 ce or ocular hypertension, and patients with primary open angle glaucoma or primary angle closure gla

127 A total of 560 patients with primary open-angle glaucoma or ocular hypertension who h

128 ) and dorz/brim/tim in Mexican patients with primary open-angle glaucoma or ocular hypertension.

129 ation of 0.005% (50 mug/mL) in patients with primary open-angle glaucoma or ocular hypertension.

130 Our results suggest that patients with primary open-angle glaucoma or with narrow angles or chr

131 gery were elevated in surgical patients with primary open-angle glaucoma (OR, 1.48; 95% CI, 1.08-2.01

132 5; 95% CI, 1.31-10.13; P = .01), presence of primary open-angle glaucoma (OR, 3.82; 95% CI, 1.60-9.14

133 e of trabeculectomy surgery in patients with primary open angle glaucoma over a 3-year period of foll

134 ely 1.8 fold; n=20) in AH derived from human primary open angle glaucoma patients as compared to AH d

135 tly was shown to harbor mutations in 2-4% of primary open angle glaucoma patients.

136 el), volume (ONVol), and flow (ONFlow) in 19 primary open-angle glaucoma patients and 15 age-matched

137 ce glaucoma and that disease pathogenesis in primary open-angle glaucoma patients is dependent upon t

138 be controlled and treated more strictly than primary open-angle glaucoma patients to avoid visual fie

139 us level of TGF-beta2 has been found in many primary open-angle glaucoma patients.

140 th early paracentral visual field defects in primary open-angle glaucoma patients.

141 ual field progression in exfoliation than in primary open-angle glaucoma patients.

142 The study included patients with primary open angle glaucoma (POAG group, n = 30) and con

143 12 normal controls, 7 patients with primary open angle glaucoma (POAG) and 9 patients with n

144 neurin (OPTN) are linked to the pathology of primary open angle glaucoma (POAG) and amyotrophic later

145 This study was designed to evaluate if primary open angle glaucoma (POAG) and its severity are

146 ssure (IOP) in patients with newly diagnosed primary open angle glaucoma (POAG) and ocular hypertensi

147 and alleles frequencies in primary glaucoma [primary open angle glaucoma (POAG) and primary angle clo

148 tly has testing for a disease risk factor in primary open angle glaucoma (POAG) become available.

149 nctional changes of optic nerve in eyes with primary open angle glaucoma (POAG) by the joint use of o

150 re recently associated with 6.0% of cases of primary open angle glaucoma (POAG) in patients from Oreg

151 ltiple loci have been associated with either primary open angle glaucoma (POAG) or heritable ocular q

152 e sought between groups of eyes differing in primary open angle glaucoma (POAG) outcome, how POAG was

153 optosis (codon 72 Pro/Arg) and the subset of primary open angle glaucoma (POAG) patients with early l

154 d in aqueous humor as well as circulation of primary open angle glaucoma (POAG) patients.

155 symptoms in a population of newly-diagnosed primary open angle glaucoma (POAG) patients.

156 Control TM and most primary open angle glaucoma (POAG) TM were collected fro

157 s in the beagle model of autosomal recessive primary open angle glaucoma (POAG) to a 4-Mb interval on

158 separate and combined screening for PACG and primary open angle glaucoma (POAG) to evaluate costs and

159 mutations in the myocilin (MYOC) gene cause primary open angle glaucoma (POAG) with varying age-of-o

160 A total of 226 primary open angle glaucoma (POAG), 132 primary angle cl

161 ollow-up of 30.8 months, including 28 (4.4%) primary open angle glaucoma (POAG), 27 (4.2%) primary an

162 five subjects were glaucomatous: (67 PXG, 42 Primary Open Angle Glaucoma (POAG), 28 PACG, 14 Normal T

163 Primary open angle glaucoma (POAG), a major cause of bli

164 (MYOC) are the most common genetic cause of primary open angle glaucoma (POAG), but the mechanisms u

165 omplex 1 defects also occur in patients with primary open angle glaucoma (POAG), in which there is sp

166 Genetically complex disorders, such as primary open angle glaucoma (POAG), may include highly h

167 ity clinic or glaucoma faculty patients with primary open angle glaucoma (POAG), ocular hypertension

168 The mean IOP for primary open angle glaucoma (POAG), ocular hypertension

169 (MMP) in the aqueous humor of patients with primary open angle glaucoma (POAG), pseudoexfoliation sy

170 cular pressure (IOP) sensor in patients with primary open angle glaucoma (POAG).

171 esembles several characteristics observed in primary open angle glaucoma (POAG).

172 very closely mimics the pathologic course of primary open angle glaucoma (POAG).

173 retinogram (ERG) is reduced in patients with primary open angle glaucoma (POAG).

174 rk (TM) cells is known to be associated with primary open angle glaucoma (POAG).

175 identified 61 patients (80 procedures) with primary open angle glaucoma (POAG).

176 of 771 previously undiagnosed patients with primary open angle glaucoma (POAG, 622 patients) or ocul

177 IOP is a principal risk factor for primary open-angle glaucoma (POAG) a leading cause of bl

178 Primary open-angle glaucoma (POAG) affects 33 million in

179 A total of 47 patients with primary open-angle glaucoma (POAG) and 36 normal partici

180 A total of 60 patients with primary open-angle glaucoma (POAG) and 37 healthy partic

181 nd trabecular meshwork (TM) of patients with primary open-angle glaucoma (POAG) and appears to contri

182 cutive eyes of 75 patients with uncontrolled primary open-angle glaucoma (POAG) and cataract who unde

183 s performed on 27 consecutive eyes with both primary open-angle glaucoma (POAG) and cataract; each ey

184 descent (AD) and European descent (ED) with primary open-angle glaucoma (POAG) and control participa

185 enetic association of known loci for IOP and primary open-angle glaucoma (POAG) and identify four new

186 ed to assess the NOS-2 level in the ONH from primary open-angle glaucoma (POAG) and nonglaucomatous h

187 haracterize the role of osteopontin (OPN) in primary open-angle glaucoma (POAG) and normal eyes.

188 ematically examined the global prevalence of primary open-angle glaucoma (POAG) and primary angle-clo

189 becular meshwork (TM) height differs between primary open-angle glaucoma (POAG) and primary angle-clo

190 atched subjects, one of each pair with early primary open-angle glaucoma (POAG) and the other with no

191 thelin (ET)-1 are increased in patients with primary open-angle glaucoma (POAG) as well as in animal

192 ) has been implicated in the pathogenesis of primary open-angle glaucoma (POAG) based on elevated lev

193 and damage to the optic disc in humans with primary open-angle glaucoma (POAG) can be measured using

194 (40+ days) endophthalmitis and risk of a new primary open-angle glaucoma (POAG) diagnosis within 365

195 proteinases (TIMPs) in the aqueous humour of primary open-angle glaucoma (POAG) eyes have been descri

196 erformed a genome-wide association study for primary open-angle glaucoma (POAG) in 1,007 cases with h

197 er trabeculoplasty (SLT) as sole therapy for primary open-angle glaucoma (POAG) in an Afro-Caribbean

198 enlo Park, CA) for treating mild-to-moderate primary open-angle glaucoma (POAG) in patients undergoin

199 A, and CDKN2B genes has been associated with primary open-angle glaucoma (POAG) in several independen

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

201 Primary open-angle glaucoma (POAG) is a complex disease

202 Primary open-angle glaucoma (POAG) is a complex disease

203 Primary open-angle glaucoma (POAG) is a complex inherite

204 Primary open-angle glaucoma (POAG) is a genetically comp

205 Primary open-angle glaucoma (POAG) is a genetically comp

206 Primary open-angle glaucoma (POAG) is a highly prevalent

207 Primary open-angle glaucoma (POAG) is a leading cause of

208 Primary open-angle glaucoma (POAG) is a leading cause of

209 Primary open-angle glaucoma (POAG) is a leading cause of

210 Primary open-angle glaucoma (POAG) is a major cause of b

211 Primary open-angle glaucoma (POAG) is a major cause of i

212 Primary open-angle glaucoma (POAG) is a progressive neur

213 of cataract surgery on IOP in patients with primary open-angle glaucoma (POAG) is a subject of debat

214 sk factor for optic nerve damage in cases of primary open-angle glaucoma (POAG) is an increased intra

215 Primary open-angle glaucoma (POAG) is associated with a

216 The primary causative factor of primary open-angle glaucoma (POAG) is elevated intraocul

217 Adult-onset primary open-angle glaucoma (POAG) is the most common fo

218 Primary open-angle glaucoma (POAG) is the most common fo

219 Primary open-angle glaucoma (POAG) is the second leading

220 rein, we report mapping of a new adult-onset primary open-angle glaucoma (POAG) locus on 5q22.1 (GLC1

221 , prospective cross-sectional study: 68 mild primary open-angle glaucoma (POAG) patients according to

222 retinal venous pressure (RVP) in the eyes of primary open-angle glaucoma (POAG) patients and healthy

223 ess the difference in severity of disease in primary open-angle glaucoma (POAG) patients with a Myoci

224 tus (solitary determination) was examined in primary open-angle glaucoma (POAG) patients with catarac

225 emodeling can cause fibrosis of the TM as in primary open-angle glaucoma (POAG) patients, and is char

226 eyedrops in ocular hypertensive (OH) and in primary open-angle glaucoma (POAG) patients.

227 e to the American Academy of Ophthalmology's Primary Open-angle Glaucoma (POAG) Preferred Practice Pa

228 , was identified by sequencing an EST in the primary open-angle glaucoma (POAG) region on 3q21.

229 rent literature continues to be that NTG and primary open-angle glaucoma (POAG) represent a continuum

230 Analysis of aqueous humor from patients with primary open-angle glaucoma (POAG) revealed marked incre

231 Economic viability of treatments for primary open-angle glaucoma (POAG) should be assessed ob

232 the type and amount of GAGs in normal and in primary open-angle glaucoma (POAG) TM and adjacent anter

233 The beagle model of primary open-angle glaucoma (POAG) was used to correlate

234 prevalence was 1.24% (95% CI, 1.14-1.34) for primary open-angle glaucoma (POAG), 0.39% (95% CI, 0.34-

235 We studied 1 eye of 63 primary open-angle glaucoma (POAG), 30 ocular hypertensi

236 enomic region previously was associated with primary open-angle glaucoma (POAG), although replication

237 ressure in greater than 90% of patients with primary open-angle glaucoma (POAG), compared with 30% to

238 EN microstent was implanted in patients with primary open-angle glaucoma (POAG), normal-tension glauc

239 G); 1 of the 4 forms of open-angle glaucoma: primary open-angle glaucoma (POAG), normal-tension glauc

240 Primary open-angle glaucoma (POAG), the most common opti

241 In cadaver eyes with primary open-angle glaucoma (POAG), TSP1 is increased in

242 A prior clinic-based study of primary open-angle glaucoma (POAG)-related DH showed tha

243 develop a secondary glaucoma that resembles primary open-angle glaucoma (POAG).

244 sting that PMH use may decrease the risk for primary open-angle glaucoma (POAG).

245 in the TM, similar to those associated with primary open-angle glaucoma (POAG).

246 ) are the most common known genetic cause of primary open-angle glaucoma (POAG).

247 ated disorders of blindness, with a focus on primary open-angle glaucoma (POAG).

248 enes for population-specific genetic risk of primary open-angle glaucoma (POAG).

249 for insights into the molecular pathology of primary open-angle glaucoma (POAG).

250 are involved in the etiology of adult-onset primary open-angle glaucoma (POAG).

251 ylation of aqueous humor sCD44 in normal and primary open-angle glaucoma (POAG).

252 erapies for retinal ganglion cells (RGCs) in primary open-angle glaucoma (POAG).

253 mined dietary fat consumption in relation to primary open-angle glaucoma (POAG).

254 ce of aqueous outflow and the development of primary open-angle glaucoma (POAG).

255 ctroretinogram (PERG) in the early stages of primary open-angle glaucoma (POAG).

256 nal layer thickness in eyes with and without primary open-angle glaucoma (POAG).

257 of the current knowledge on risk factors for primary open-angle glaucoma (POAG).

258 d with various ocular pathologies, including primary open-angle glaucoma (POAG).

259 ct surgery in subjects with mild to moderate primary open-angle glaucoma (POAG).

260 al dysfunction, which has been implicated in primary open-angle glaucoma (POAG).

261 blood flow autoregulation are implicated in primary open-angle glaucoma (POAG).

262 raocular pressure (IOP) in the evaluation of primary open-angle glaucoma (POAG); and to determine the

263 rrhage (ODH) before and after development of primary open-angle glaucoma (POAG); determine the progno

264 confidence interval, 3.3-5.4), consisting of primary open-angle glaucoma (POAG, 3.2%, including high-

265 Among glaucoma subtypes, primary open-angle glaucoma (POAG, N = 5756) and normal-

266 85; 1995-2013) to estimate effects of T2D on primary open-angle glaucoma (POAG; 3,554 cases).

267 e factor [CRF], cup-to-disc ratio [CDR], and primary open-angle glaucoma [POAG]).

268 sera from 65 patients with glaucoma (25 with primary open-angle glaucoma [POAG]; 40 with normal-press

269 PRIMARY OPEN-ANGLE GLAUCOMA PREFERRED PRACTICE PATTERN(R

270 (R) GUIDELINES: Evidence-based update of the Primary Open-Angle Glaucoma Preferred Practice Pattern(R

271 Primary open-angle glaucoma presents with increased prev

272 to identify possible risk factors leading to primary open angle glaucoma progression and blindness.

273 f prostaglandin analog eye drops in treating primary open-angle glaucoma, published between December

274 expressed sequence tag, which maps near the primary open angle glaucoma region on chromosome 3q21, s

275 ation between dietary antioxidant intake and primary open-angle glaucoma risk was examined in partici

276 ons with suspected glaucoma or patients with primary open-angle glaucoma, selected to have clinically

277 Primary open-angle glaucoma, status as a glaucoma suspec

278 PRIMARY OPEN-ANGLE GLAUCOMA SUSPECT PREFERRED PRACTICE P

279 he diagnosis and management of patients with primary open-angle glaucoma suspect with detailed recomm

280 With age, and particularly in eyes with primary open angle glaucoma, the number of cells residin

281 In 57 patients with primary open-angle glaucoma, the IOP decreased by 7.7 mm

282 ry cause of elevated intraocular pressure in primary open-angle glaucoma, the present study was condu

283 Risk factors for primary open-angle glaucoma-the most common form of glau

284 that Cochlin contributes to elevated IOP in primary open angle glaucoma through altered interactions

285 Lucia with medically treated primary open-angle glaucoma underwent a 30-day washout,

286 azard ratio [HR] 2.51; 95% CI 1.12-5.65) and primary open-angle glaucoma vs secondary open-angle glau

287 The prevalence of primary open-angle glaucoma was 6.8% overall, increasing

288 Primary open-angle glaucoma was the underlying diagnosis

289 , 45 clinical questions on the management of primary open-angle glaucoma were derived from practice g

290 -82 years) with ocular hypertension or early primary open-angle glaucoma were enrolled.

291 allele was associated with increased risk of primary open-angle glaucoma when all data were included

292 One of the major causes of blindness is primary open-angle glaucoma, which affects millions of e

293 to January 1, 2013, including patients with primary open-angle glaucoma who had a best-corrected vis

294 OMPASS study of the Cypass micro-stent) with primary open-angle glaucoma who were using 0-4 classes o

295 A total of 603 patients (603 eyes) with primary open-angle glaucoma who were using up to 3 glauc

296 The analysis included 186 patients with primary open-angle glaucoma with a mean age of 59.1 year

297 enotyping was performed in 117 patients with primary open-angle glaucoma with a minimum treatment dur

298 he diagnosis and management of patients with primary open-angle glaucoma with an algorithm for patien

299 -related quality of life among patients with primary open-angle glaucoma with structural macular reti

300 es confirmed by medical chart review to have primary open-angle glaucoma with visual field loss.