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1 th juvenile glaucoma and some cases of adult primary open angle glaucoma.
2 (s) of TIGR/MYOC in both steroid-induced and primary open angle glaucoma.
3 ssociated with both juvenile-and adult-onset primary open angle glaucoma.
4 rove early diagnosis of visual field loss in primary open angle glaucoma.
5 oss is measurable by conventional methods in primary open angle glaucoma.
6 has been associated with the development of primary open angle glaucoma.
7 nce for genetic heterogeneity of adult-onset primary open angle glaucoma.
8 e damage, is involved in the pathogenesis of primary open angle glaucoma.
9 ous ocular diseases, such as keratoconus and primary open angle glaucoma.
10 ed 50 mmHg and he was found to have advanced primary open angle glaucoma.
11 es in a transgenic mouse model of hereditary primary open-angle glaucoma.
12 similar at baseline; 68% were diagnosed with primary open-angle glaucoma.
13 F-beta2 because TGF-beta2 is associated with primary open-angle glaucoma.
14 are associated with juvenile and adult-onset primary open-angle glaucoma.
15 N gene may lead to juvenile- and adult-onset primary open-angle glaucoma.
16 ween antioxidant consumption and the risk of primary open-angle glaucoma.
17 s in the initial management of patients with primary open-angle glaucoma.
18 documented to occur in eyes of patients with primary open-angle glaucoma.
19 surgical therapy are similar to treatment of primary open-angle glaucoma.
20 eature of the outflow system in aging and in primary open-angle glaucoma.
21 hwork and possibly some of the extra loss in primary open-angle glaucoma.
22 rat model appears to mimic some features of primary open-angle glaucoma.
23 also may be involved in the pathogenesis of primary open-angle glaucoma.
24 from juvenile glaucoma to typical late-onset primary open-angle glaucoma.
25 may contribute to changes seen with age and primary open-angle glaucoma.
26 male), 16 had ocular hypertension and 14 had primary open-angle glaucoma.
27 risk and be a new risk factor to consider in primary open-angle glaucoma.
28 ffective in lowering intraocular pressure in primary open-angle glaucoma.
29 gene are the most common genetic factors of primary open-angle glaucoma.
30 g the onset of the prevalent ocular disorder primary open-angle glaucoma.
31 ) which have previously been associated with primary open-angle glaucoma.
32 ing diabetic retinopathy, uveoretinitis, and primary open-angle glaucoma.
33 related to mutations in the MYOCILIN gene is primary open-angle glaucoma.
34 forms of myocilin, a protein associated with primary open-angle glaucoma.
35 N gene may lead to juvenile- and adult-onset primary open-angle glaucoma.
36 ay be on a multiple topical drug regimen for primary open-angle glaucoma.
37 spective study included 122 eyes treated for primary open angle glaucoma, 50 eyes (study group) in wh
38 identified 354 eyes in 180 subjects (97 with primary open-angle glaucoma, 83 with glaucoma suspicion)
39 he potential role of superoxide dismutase in primary open angle glaucoma, a disorder of the aging tra
41 laucoma have identified novel loci for POAG (primary-open-angle glaucoma) (ABCA1, AFAP1, GMDS, PMM2,
42 educed cell survival is also associated with primary open angle glaucoma, ageing, cellular senescence
43 aucoma, one locus (GLC1A) for juvenile-onset primary open angle glaucoma and a further two loci (GLC1
44 essure is a highly heritable risk factor for primary open angle glaucoma and currently the only targe
45 mans with Weill-Marchesani-like syndrome and primary open angle glaucoma and ectopia lentis in dogs.
47 Twenty-one patients with newly diagnosed primary open-angle glaucoma and 34 age- and gender-match
49 amples were collected from 111 patients with primary open-angle glaucoma and an age-matched control g
51 of dementia, including Alzheimer's disease, primary open-angle glaucoma and Helicobacter pylori (H.p
53 ts with NTG when compared with patients with primary open-angle glaucoma and nonglaucomatous control
54 traocular lens implantation in patients with primary open-angle glaucoma and ocular hypertension.
56 ntly identified as causative for adult-onset primary open-angle glaucoma and provides additional evid
58 d from patients undergoing trabeculotomy for primary open-angle glaucoma and the normal aqueous from
59 asured by 24-2 and 10-2 VFs in patients with primary open-angle glaucoma and to test the hypothesis t
61 wed up until death; 203 patients (65.7%) had primary open-angle glaucoma, and 106 patients (34.2%) ha
62 n "high-pressure" forms of glaucoma, such as primary open-angle glaucoma, and in cases in which the i
63 tis pigmentosa, while Bardet-Biedl syndrome, primary open-angle glaucoma, and tumor cell invasiveness
64 these mice may be useful as a mouse model of primary open angle glaucoma as well as for assessing the
65 t quintile have a 2.5-fold increased risk of primary open-angle glaucoma as compared with those in th
67 utoimmune uveitis, diabetic retinopathy, and primary open angle glaucoma, but its role in normal visi
68 autosomal dominant juvenile- and adult-onset primary open angle glaucoma, but the mechanism by which
69 ive oxygen species play a pathogenic role in primary open angle glaucoma by fostering changes that re
72 of the posterior sclera in a canine model of primary open-angle glaucoma caused by the G661R missense
73 -85 years with a minimum 2-year diagnosis of primary open-angle glaucoma, chronic primary angle-closu
75 s elevated in aqueous humor of patients with primary open-angle glaucoma, contributes to the increase
78 e of progression from ocular hypertension to primary open-angle glaucoma has been established in the
80 the progression from ocular hypertension to primary open-angle glaucoma has been the subject of two
81 he authors investigated the genetic cause of primary open angle glaucoma in a large four-generation f
82 ld female was being followed and treated for primary open angle glaucoma in our tertiary referral cen
84 variants of LOXL1 play a significant role in primary open-angle glaucoma in the Caucasian, African-Am
85 nces may contribute to the predisposition of primary open-angle glaucoma in various high-risk populat
89 associated with progression of patients with primary open angle glaucoma is essential to our clinical
94 number of persons in the United States with primary open-angle glaucoma is estimated to be 2.47 mill
99 size (P < 0.001) in both eyes with incident primary open-angle glaucoma (mean, 10.6%; standard devia
100 yndrome (MetS) with intraocular pressure and primary open angle glaucoma (OAG) have been reported.
102 ce or ocular hypertension, and patients with primary open angle glaucoma or primary angle closure gla
104 ation of 0.005% (50 mug/mL) in patients with primary open-angle glaucoma or ocular hypertension.
105 ) and dorz/brim/tim in Mexican patients with primary open-angle glaucoma or ocular hypertension.
106 5; 95% CI, 1.31-10.13; P = .01), presence of primary open-angle glaucoma (OR, 3.82; 95% CI, 1.60-9.14
107 e of trabeculectomy surgery in patients with primary open angle glaucoma over a 3-year period of foll
108 ely 1.8 fold; n=20) in AH derived from human primary open angle glaucoma patients as compared to AH d
110 el), volume (ONVol), and flow (ONFlow) in 19 primary open-angle glaucoma patients and 15 age-matched
111 ce glaucoma and that disease pathogenesis in primary open-angle glaucoma patients is dependent upon t
116 neurin (OPTN) are linked to the pathology of primary open angle glaucoma (POAG) and amyotrophic later
117 and alleles frequencies in primary glaucoma [primary open angle glaucoma (POAG) and primary angle clo
118 tly has testing for a disease risk factor in primary open angle glaucoma (POAG) become available.
119 nctional changes of optic nerve in eyes with primary open angle glaucoma (POAG) by the joint use of o
120 re recently associated with 6.0% of cases of primary open angle glaucoma (POAG) in patients from Oreg
121 ltiple loci have been associated with either primary open angle glaucoma (POAG) or heritable ocular q
122 e sought between groups of eyes differing in primary open angle glaucoma (POAG) outcome, how POAG was
123 optosis (codon 72 Pro/Arg) and the subset of primary open angle glaucoma (POAG) patients with early l
125 s in the beagle model of autosomal recessive primary open angle glaucoma (POAG) to a 4-Mb interval on
126 mutations in the myocilin (MYOC) gene cause primary open angle glaucoma (POAG) with varying age-of-o
127 ollow-up of 30.8 months, including 28 (4.4%) primary open angle glaucoma (POAG), 27 (4.2%) primary an
128 five subjects were glaucomatous: (67 PXG, 42 Primary Open Angle Glaucoma (POAG), 28 PACG, 14 Normal T
130 (MYOC) are the most common genetic cause of primary open angle glaucoma (POAG), but the mechanisms u
131 omplex 1 defects also occur in patients with primary open angle glaucoma (POAG), in which there is sp
134 ity clinic or glaucoma faculty patients with primary open angle glaucoma (POAG), ocular hypertension
135 (MMP) in the aqueous humor of patients with primary open angle glaucoma (POAG), pseudoexfoliation sy
142 nd trabecular meshwork (TM) of patients with primary open-angle glaucoma (POAG) and appears to contri
143 enetic association of known loci for IOP and primary open-angle glaucoma (POAG) and identify four new
144 ed to assess the NOS-2 level in the ONH from primary open-angle glaucoma (POAG) and nonglaucomatous h
145 haracterize the role of osteopontin (OPN) in primary open-angle glaucoma (POAG) and normal eyes.
146 becular meshwork (TM) height differs between primary open-angle glaucoma (POAG) and primary angle-clo
147 ematically examined the global prevalence of primary open-angle glaucoma (POAG) and primary angle-clo
148 atched subjects, one of each pair with early primary open-angle glaucoma (POAG) and the other with no
149 thelin (ET)-1 are increased in patients with primary open-angle glaucoma (POAG) as well as in animal
150 ) has been implicated in the pathogenesis of primary open-angle glaucoma (POAG) based on elevated lev
151 and damage to the optic disc in humans with primary open-angle glaucoma (POAG) can be measured using
152 (40+ days) endophthalmitis and risk of a new primary open-angle glaucoma (POAG) diagnosis within 365
153 proteinases (TIMPs) in the aqueous humour of primary open-angle glaucoma (POAG) eyes have been descri
154 erformed a genome-wide association study for primary open-angle glaucoma (POAG) in 1,007 cases with h
155 er trabeculoplasty (SLT) as sole therapy for primary open-angle glaucoma (POAG) in an Afro-Caribbean
156 enlo Park, CA) for treating mild-to-moderate primary open-angle glaucoma (POAG) in patients undergoin
157 A, and CDKN2B genes has been associated with primary open-angle glaucoma (POAG) in several independen
170 sk factor for optic nerve damage in cases of primary open-angle glaucoma (POAG) is an increased intra
175 rein, we report mapping of a new adult-onset primary open-angle glaucoma (POAG) locus on 5q22.1 (GLC1
176 retinal venous pressure (RVP) in the eyes of primary open-angle glaucoma (POAG) patients and healthy
177 ess the difference in severity of disease in primary open-angle glaucoma (POAG) patients with a Myoci
178 tus (solitary determination) was examined in primary open-angle glaucoma (POAG) patients with catarac
179 emodeling can cause fibrosis of the TM as in primary open-angle glaucoma (POAG) patients, and is char
181 e to the American Academy of Ophthalmology's Primary Open-angle Glaucoma (POAG) Preferred Practice Pa
183 rent literature continues to be that NTG and primary open-angle glaucoma (POAG) represent a continuum
184 Analysis of aqueous humor from patients with primary open-angle glaucoma (POAG) revealed marked incre
186 the type and amount of GAGs in normal and in primary open-angle glaucoma (POAG) TM and adjacent anter
188 prevalence was 1.24% (95% CI, 1.14-1.34) for primary open-angle glaucoma (POAG), 0.39% (95% CI, 0.34-
190 enomic region previously was associated with primary open-angle glaucoma (POAG), although replication
191 ressure in greater than 90% of patients with primary open-angle glaucoma (POAG), compared with 30% to
192 G); 1 of the 4 forms of open-angle glaucoma: primary open-angle glaucoma (POAG), normal-tension glauc
210 raocular pressure (IOP) in the evaluation of primary open-angle glaucoma (POAG); and to determine the
211 rrhage (ODH) before and after development of primary open-angle glaucoma (POAG); determine the progno
212 confidence interval, 3.3-5.4), consisting of primary open-angle glaucoma (POAG, 3.2%, including high-
214 sera from 65 patients with glaucoma (25 with primary open-angle glaucoma [POAG]; 40 with normal-press
216 (R) GUIDELINES: Evidence-based update of the Primary Open-Angle Glaucoma Preferred Practice Pattern(R
217 to identify possible risk factors leading to primary open angle glaucoma progression and blindness.
218 f prostaglandin analog eye drops in treating primary open-angle glaucoma, published between December
219 expressed sequence tag, which maps near the primary open angle glaucoma region on chromosome 3q21, s
220 ation between dietary antioxidant intake and primary open-angle glaucoma risk was examined in partici
221 ons with suspected glaucoma or patients with primary open-angle glaucoma, selected to have clinically
224 he diagnosis and management of patients with primary open-angle glaucoma suspect with detailed recomm
226 ry cause of elevated intraocular pressure in primary open-angle glaucoma, the present study was condu
228 that Cochlin contributes to elevated IOP in primary open angle glaucoma through altered interactions
232 , 45 clinical questions on the management of primary open-angle glaucoma were derived from practice g
234 One of the major causes of blindness is primary open-angle glaucoma, which affects millions of e
235 to January 1, 2013, including patients with primary open-angle glaucoma who had a best-corrected vis
236 A total of 603 patients (603 eyes) with primary open-angle glaucoma who were using up to 3 glauc
237 The analysis included 186 patients with primary open-angle glaucoma with a mean age of 59.1 year
238 enotyping was performed in 117 patients with primary open-angle glaucoma with a minimum treatment dur
239 he diagnosis and management of patients with primary open-angle glaucoma with an algorithm for patien
240 -related quality of life among patients with primary open-angle glaucoma with structural macular reti
241 es confirmed by medical chart review to have primary open-angle glaucoma with visual field loss.
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