ライフサイエンスコーパス: ocular hypertension

1 f the ciliary body had the largest impact on ocular hypertension.

2 icroglia/macrophages soon after induction of ocular hypertension.

3 Adult patients with open-angle glaucoma or ocular hypertension.

4 nocturnal, period in open-angle glaucoma and ocular hypertension.

5 tissues and prevented dexamethasone-induced ocular hypertension.

6 on syndrome (PDS) at risk for progressing to ocular hypertension.

7 patients with primary open-angle glaucoma or ocular hypertension.

8 ints in patients with open-angle glaucoma or ocular hypertension.

9 t there is a dose effect for steroid-induced ocular hypertension.

10 o in individuals with open-angle glaucoma or ocular hypertension.

11 stigate RGC degeneration in a mouse model of ocular hypertension.

12 s in a mouse model of induced, chronic, mild ocular hypertension.

13 el in patients with a history of glaucoma or ocular hypertension.

14 patients with primary open-angle glaucoma or ocular hypertension.

15 with the correlations seen in patients with ocular hypertension.

16 s to create a mouse model of steroid-induced ocular hypertension.

17 y contribute to disc hemorrhage formation in ocular hypertension.

18 atients with primary open-angle glaucoma and ocular hypertension.

19 t eyes do not remodel in response to chronic ocular hypertension.

20 sure appears to be elevated in patients with ocular hypertension.

21 rrent knowledge of global risk assessment in ocular hypertension.

22 GCs and that their expression is affected by ocular hypertension.

23 n enhanced glucocorticoid responsiveness and ocular hypertension.

24 ts effect on optic nerve injury in rats with ocular hypertension.

25 and management of patients with glaucoma and ocular hypertension.

26 tic nerve damage in mice after laser-induced ocular hypertension.

27 owed caspase-3 activation in RGCs damaged by ocular hypertension.

28 k between MYOC mutations and steroid-induced ocular hypertension.

29 nd EDA null mice blocked Ad5.TGFbeta-induced ocular hypertension.

30 in MYOC might be involved in steroid-induced ocular hypertension.

31 sterior subcapsular opacities, glaucoma, and ocular hypertension.

32 proposed to be involved in the generation of ocular hypertension.

33 cell loss as a consequence of long-standing ocular hypertension.

34 cell loss as a consequence of long-standing ocular hypertension.

35 All affected eyes featured ocular hypertension.

36 n treatment option for managing glaucoma and ocular hypertension.

37 ated a mouse model of corticosteroid-induced ocular hypertension.

38 d both eyes of 100 patients with glaucoma or ocular hypertension.

39 or, in patients with open-angle glaucoma and ocular hypertension.

40 adults diagnosed with open-angle glaucoma or ocular hypertension.

41 retinal tau that was markedly exacerbated by ocular hypertension.

42 flow pathway and a novel target for treating ocular hypertension.

43 R4 and FN-EDA contribute to TGFbeta2 induced ocular hypertension.

44 -year (EY); cornea decompensation, 0.001 EY; ocular hypertension, 0.008 EY; pupil ovalization, 0.020

45 28.5%) had a suspicious nerve, 62 (6.8%) had ocular hypertension, 102 (11.3%) had diabetic retinopath

46 trol participants, 126 eyes of patients with ocular hypertension, 128 eyes of patients with preperime

47 eral ulcerative keratitis (7.4% vs. 0%), and ocular hypertension (14.2% vs. 3.5%; P<0.0001 for each).

48 in difference was greatest for patients with ocular hypertension (2.00 mmHg) and for patients with pr

49 Most frequent complications were de novo ocular hypertension (29 eyes, 10%) and transient cystoid

50 all, 47 persons (2.4%) were categorized with ocular hypertension, 32 persons (1.6%) were categorized

51 He experienced episodes of marked ocular hypertension (53 mmHg OD and 60 mmHg) likely due

52 g term complications in both groups included ocular hypertension (67.4% vs 66.7%), keratopathy due to

53 We report that ocular hypertension, a major risk factor in glaucoma, up

54 ries, such as penetrating corneal trauma and ocular hypertension also cause similar changes.

55 ing increased risk of corticosteroid-induced ocular hypertension among first-degree relatives of affe

56 ar pressure (IOP) in patients with glaucoma, ocular hypertension, anatomic narrow angles, and in glau

57 individuals (11 male and 19 female), 16 had ocular hypertension and 14 had primary open-angle glauco

58 IMK2 may be an effective target for treating ocular hypertension and associated glaucoma.

59 mic fibrillopathy, which often presents with ocular hypertension and exfoliation glaucoma (XFG).

60 Corticosteroid-induced ocular hypertension and glaucoma has been recognized for

61 Recent randomized prospective trials of ocular hypertension and glaucoma have provided evidence

62 on seem to play a role in the development of ocular hypertension and glaucoma in these families.

63 patients affected by corticosteroid-induced ocular hypertension and glaucoma provides new opportunit

64 apitulates several critical aspects of human ocular hypertension and glaucoma, and results in early c

65 genetic component to corticosteroid-related ocular hypertension and glaucoma, but specific genetic r

66 iew the literature of corticosteroid-induced ocular hypertension and glaucoma, its risk factors, the

67 r anterior segment in some cases can lead to ocular hypertension and glaucoma.

68 ion of early retinal ganglion cell damage in ocular hypertension and glaucoma.

69 ture in the detection of early ONH damage in ocular hypertension and glaucoma.

70 ganglion cell function, is altered early in ocular hypertension and glaucoma.

71 t, monitor, and treat corticosteroid-induced ocular hypertension and glaucoma.

72 ial new class of agents for the treatment of ocular hypertension and glaucoma.

73 ht on the pathophysiology of steroid-induced ocular hypertension and glaucoma.

74 gulated and its persistent increase leads to ocular hypertension and glaucoma.

75 ritical role in increasing RGC resistance to ocular hypertension and glaucomatous damage.

76 initial therapy for open-angle glaucoma and ocular hypertension and have demonstrated efficacy in ot

77 Dysfunction of these tissues leads to ocular hypertension and increases the risk for developin

78 ration atropine for one year does not induce ocular hypertension and is effective for retarding myopi

79 stasis retinopathy in a 10-year-old boy with ocular hypertension and megalocornea due to increased in

80 t-naive patients with open angle glaucoma or ocular hypertension and no ocular comorbidities were rec

81 types of ERG had reduced mean amplitudes in ocular hypertension and open-angle glaucoma groups compa

82 nfortunately in some, dysfunction results in ocular hypertension and open-angle glaucoma.

83 tolerated for the treatment of patients with ocular hypertension and open-angle glaucoma.

84 ants with non-endstage glaucoma or high-risk ocular hypertension and performed standard automated per

85 of TAO may be associated with more sustained ocular hypertension and require topical therapy.

86 ch allows normal SC development and prevents ocular hypertension and RGC loss.

87 f one or more resident cell types results in ocular hypertension and risk for glaucoma, a leading cau

88 stress contributes to glucocorticoid-induced ocular hypertension and suggest that reducing ER stress

89 n for patients with a history of glaucoma or ocular hypertension and switching to a 'PRN' injection p

90 of 233 patients with open-angle glaucoma or ocular hypertension and with mean intraocular pressure (

91 Normal subjects, patients with ocular hypertension and with pigment dispersion syndrome

92 s a much lower penetrance for rs74315329 for ocular hypertension (and thus glaucoma), in comparison w

93 nt for open-angle glaucoma, 23 subjects with ocular hypertension, and 28 healthy subjects in a contro

94 es had glaucomatous optic neuropathy, 37 had ocular hypertension, and 28 served as age-matched normal

95 progressive optic neuropathy (PGON) 53 with ocular hypertension, and 51 with no disease were include

96 d with PDS (1 with PDS alone, 2 with PDS and ocular hypertension, and 7 with PG).

97 ular hypertension or glaucoma, 6 had PDS and ocular hypertension, and 91 had PG.

98 lammation of more than 2+, anterior uveitis, ocular hypertension, and associated infectious disease.

99 having glaucomatous optic disc appearance or ocular hypertension, and patients with primary open angl

100 sectoral iris atrophy, keratic precipitates, ocular hypertension, and poor response to steroids.

101 tected high rate of suspicious optic nerves, ocular hypertension, and retinal pathology.

102 Validated risk calculators for ocular hypertension are currently available mostly deriv

103 Primary open angle glaucoma and ocular hypertension are habitually treated with eye drop

104 Ocular hypertension arising from increased resistance to

105 d efficacy in this nonhuman primate model of ocular hypertension as well as a desirable physicochemic

106 However, the rates of cataract formation and ocular hypertension at 10 years have important clinical

107 treated patients with open-angle glaucoma or ocular hypertension at a hospital-based glaucoma service

108 Anatomic results, ocular hypertension, best-corrected distance visual acui

109 ony, 5 had a previous history of glaucoma or ocular hypertension, but only 3 had a glaucoma drainage

110 ion in Tlr4, in our inducible mouse model of ocular hypertension by injection of Ad5.TGFbeta2.

111 igoxin derivatives efficiently normalize the ocular hypertension, by comparison with digoxin, digoxig

112 Thyroid orbitopathy combined with ocular hypertension can produce true glaucoma.

113 ing adverse event of glucocorticoid usage is ocular hypertension, caused by dysfunction of the conven

114 e elevated outflow resistance and consequent ocular hypertension characteristic of glaucoma is unknow

115 We found that chronic ocular hypertension (COH) in rat down-regulated Muller c

116 ior chamber angle was used to induce chronic ocular hypertension (COHT) in the right eye of 18 macaqu

117 ior chamber angle was used to induce chronic ocular hypertension (COHT) in the right eyes of 18 macaq

118 200 patients with glaucoma or ocular hypertension, controlled on the unfixed combinati

119 The TGFbeta2-induced ocular hypertension correlated with anterior segment TGF

120 Rat RGCs subjected to chronic ocular hypertension demonstrate caspase activation and a

121 ound in eyes in which glucocorticoid-induced ocular hypertension developed.

122 that reducing IOP in eyes without glaucoma (ocular hypertension) does not increase perimetric contra

123 large cup-to-disc ratio without glaucoma or ocular hypertension exhibited lower global cognitive fun

124 at Cav-1-deficient (Cav-1(-/-)) mice display ocular hypertension explained by reduced pressure-depend

125 clinical diagnosis of open-angle glaucoma or ocular hypertension from a referred sample were enrolled

126 None of the participants had any evidence of ocular hypertension, glaucoma, or other ocular disease.

127 To alleviate oxidative stress-induced ocular hypertension, grafting of antioxidant molecules t

128 In the ocular hypertension group, the N95 and the L&M-pathway p

129 Eyes with ocular hypertension had thicker CCs than did normal and

130 Dexamethasone, which can induce ocular hypertension, has been found to increase resistan

131 tionally and morphologically resembles human ocular hypertension, having titratable, robust, and sust

132 Ocular hypertension (hazard ratio [HR], 4.6; 95% confide

133 loss after the injection was associated with ocular hypertension, hemorrhagic retinopathy, vitreous h

134 IOP) in patients with open-angle glaucoma or ocular hypertension; however, these medications may affe

135 ly, their administration frequently leads to ocular hypertension, i.e., elevated intraocular pressure

136 e suspicion in 10 subjects (11.5%), and with ocular hypertension in 2 subjects (2.2%).

137 The most common complication was glaucoma/ocular hypertension in 29 eyes (34.1%) without prior gla

138 stoperative complications included transient ocular hypertension in 44 eyes (11.3%), vitreous hemorrh

139 stoperative complications included transient ocular hypertension in 8 eyes (8.4%), transient hypotony

140 lin may play an important pathogenic role in ocular hypertension in addition to its role in certain f

141 imbal and episcleral veins induces transient ocular hypertension in albino CD-1 mice.

142 n the aqueous outflow pathway contributes to ocular hypertension in Col1a1(r/r) mice.

143 al procedure for the management of postgraft ocular hypertension in DSAEK patients, and DSAEK may hav

144 underlying extracellular matrix as cause for ocular hypertension in glaucoma.

145 tanding mechanisms affecting steroid-induced ocular hypertension in humans.

146 These results demonstrate ocular hypertension in mice with a targeted type I colla

147 ibronectin-EDA (FN-EDA), in TGFbeta2-induced ocular hypertension in mice.

148 Laser-induced ocular hypertension in mouse eyes can induce optic nerve

149 expression decreased glucocorticoid-induced ocular hypertension in mouse eyes.

150 the pattern of RGC loss after laser-induced ocular hypertension in rats is similar to that previousl

151 Administration of glucocorticoids induces ocular hypertension in some patients.

152 therapy drugs for the potential treatment of ocular hypertension in steroid-responsive patients.

153 Ocular hypertension in the mouse eye sufficient to cause

154 To establish an experimental model of ocular hypertension in the mouse.

155 This report presents a case of severe ocular hypertension in which emotional stress was the on

156 Ad5.TGFbeta2 induced ocular hypertension in wildtype C57BL/6J mice and furthe

157 enylbutyrate prevented dexamethasone-induced ocular hypertension in WT mice.

158 Patients with uncontrolled early OAG or ocular hypertension (inadequate IOP control requiring ad

159 mRNA and protein levels in rat retinas with ocular hypertension-induced ganglion cell death.

160 rting a critical role for tau alterations in ocular hypertension-induced neuronal damage.

161 Moreover, overexpression of NGB attenuated ocular hypertension-induced superoxide production and th

162 E scores at the time of the eye examination, ocular hypertension (intraocular pressure >23 mm Hg, Gol

163 clearly established that medically treating ocular hypertension is efficacious in delaying or preven

164 The ophthalmologist treating patients with ocular hypertension is frequently faced with the clinica

165 Ocular hypertension is sufficiently common in eyes treat

166 Ocular hypertension is the most significant known risk f

167 f irreversible and preventable blindness and ocular hypertension is the strongest known risk factor.

168 that glaucomatous damage, more than uveitic ocular hypertension, is in fact occurring.

169 Using a laser-induced ocular hypertension (LIOH) mouse model of glaucoma, we f

170 (lacZ/lacZ)) were subjected to laser-induced ocular hypertension (LIOH), an experimental mouse model

171 nmental mechanisms impacting steroid-induced ocular hypertension may provide important insight into p

172 Children with ocular hypertension might be at higher risk for impendin

173 A laser-induced mouse model of chronic ocular hypertension mimicked human high-tension glaucoma

174 sion was assessed in vivo, in the Morrison's ocular hypertension model of glaucoma in rats.

175 atures of glaucomatous degeneration in a rat ocular hypertension model.

176 GCs and preserved visual function in a mouse ocular hypertension model.

177 For eyes with ocular hypertension (n = 45) at baseline, the incidence

178 eitis patients also had the highest rates of ocular hypertension (n = 465; 17.9%, 95% CI 16.4-19.3%)

179 However, cataract and ocular hypertension occurred in a substantial minority.

180 rabeculoplasty were reduced in patients with ocular hypertension (odds ratio [OR], 0.27; 95% CI, 0.10

181 iological mechanisms in glaucoma, we induced ocular hypertension (OH) in mice by angle closure via la

182 of 63 primary open-angle glaucoma (POAG), 30 ocular hypertension (OH), and 48 control subjects.

183 c for detecting early glaucomatous damage in ocular hypertension (OH).

184 Improving adherence to ocular hypertension (OH)/glaucoma therapy is highly like

185 is of glaucomatous optic neuropathy (GON) or ocular hypertension (OHT) and at least 2 disc stereophot

186 measurements between patients with glaucoma, ocular hypertension (OHT) and glaucoma-like optic discs

187 for the development of POAG in patients with ocular hypertension (OHT) and the predictive factors for

188 the outer retina is affected in experimental ocular hypertension (OHT) and, second, whether whole ret

189 To describe the risk and risk factors for ocular hypertension (OHT) in adults with noninfectious u

190 k patients with newly diagnosed glaucoma and ocular hypertension (OHT) in South West Ethiopia.

191 Glucocorticoid (GC)-induced ocular hypertension (OHT) is a serious adverse effect of

192 intraocular pressure (IOP) in patients with ocular hypertension (OHT) or glaucoma.

193 n patients with open-angle glaucoma (OAG) or ocular hypertension (OHT) treated for 6 months.

194 dependent group of 191 patient eyes (66 with ocular hypertension (OHT), 12 with suspected glaucoma by

195 olled trials of open-angle glaucoma (OAG) or ocular hypertension (OHT), bimatoprost 0.01 % improved t

196 g a well-established rodent model of chronic ocular hypertension (OHT), comparing single intravitreal

197 IOP for primary open angle glaucoma (POAG), ocular hypertension (OHT), normal tension glaucoma (NTG)

198 s and defined 2.82 mm Hg as the threshold of ocular hypertension (OHT), which equals mean pressure ch

199 n patients with open-angle glaucoma (OAG) or ocular hypertension (OHT).

200 n patients with open-angle glaucoma (OAG) or ocular hypertension (OHT).

201 nosed primary open angle glaucoma (POAG) and ocular hypertension (OHT).

202 open angle glaucoma (POAG, 622 patients) or ocular hypertension (OHT, 149 patients) at Zhongshan Oph

203 nts with primary open angle glaucoma (POAG), ocular hypertension (OHTN), or suspicion of glaucoma wer

204 e identified 34 040 members with glaucoma or ocular hypertension (OHTN; cases) and 403 398 members wi

205 ce, we examined the effects of laser-induced ocular hypertension on the structure and function of a s

206 Both eyes of 185 individuals with high-risk ocular hypertension or early glaucoma were evaluated.

207 xamination of 168 individuals with high-risk ocular hypertension or early glaucoma, were used as pred

208 ated perimetry (SAP), in eyes with high-risk ocular hypertension or early glaucoma.

209 Twenty-five patients (aged 43-82 years) with ocular hypertension or early primary open-angle glaucoma

210 glaucoma (both open-angle and closed-angle), ocular hypertension or glaucoma suspects (mean age, 71 y

211 ded were poor-quality scans and diagnoses of ocular hypertension or glaucoma suspects.

212 Four of the patients had PDS without ocular hypertension or glaucoma, 6 had PDS and ocular hy

213 Compared with glaucoma suspects, ocular hypertension (OR, 1.55), pigmentary glaucoma (OR,

214 01), anterior uveitis (OR, 1.78; P = 0.033), ocular hypertension (OR, 3.19; P<0.001), and associated

215 risk allele of the variant who had high IOP (ocular hypertension) or glaucoma.

216 suspected glaucoma and those with glaucoma, ocular hypertension, or anatomically narrow angles were

217 g both ICD-10 codes of uveitis and glaucoma, ocular hypertension, or corticosteroid response diagnose

218 laucomatous field defect), glaucoma suspect, ocular hypertension, or non-POAG/nonocular hypertension.

219 In this group of patients with early OAG or ocular hypertension, our short-term results confirmed SL

220 aract surgery decreases IOP in patients with ocular hypertension over a long period of time.

221 eye pain (p = 0.013), hypopyon (p = 0.003), ocular hypertension (p = 0.003), positive intraocular fl

222 ed trial (RCT) with glaucoma (open angle) or ocular hypertension patients attending a glaucoma clinic

223 H outflow through the trabecular meshwork in ocular hypertension patients.

224 In patients with open-angle glaucoma or ocular hypertension, polyquaternium-1-preserved travopro

225 Cataract surgery in patients with ocular hypertension produced sustained reductions in the

226 res: Rate of cataract surgery, lens opacity, ocular hypertension, refractive safety, predictability,

227 mplication have a greater risk of developing ocular hypertension requiring treatment and phthisis.

228 Steroid-induced ocular hypertension resembles several characteristics ob

229 Ocular hypertension responsible for GC-induced glaucoma

230 ), glaucoma (RR = 6.0, 95% CI: 3.9-9.3), and ocular hypertension (RR = 2.0, 95% CI: 1.3-3.0), while c

231 iagnosis of glaucoma, suspected glaucoma, or ocular hypertension seen in the Massachusetts Eye and Ea

232 g useful guidelines for determining who with ocular hypertension should be offered medical treatment.

233 effectively demonstrated that patients with ocular hypertension should be risk stratified prior to i

234 Although ocular hypertension showed the highest OPA values (3.53

235 IOP in patients with open-angle glaucoma or ocular hypertension, showing significantly superior IOP-

236 he classification of open-angle glaucoma and ocular hypertension, significant electrophysiological lo

237 t-line treatment for open angle glaucoma and ocular hypertension, supporting a change in clinical pra

238 Among this cohort, 40.8% had ocular hypertension/suspected glaucoma, 70% had 0-to-mil

239 es (12.9%; 95% CI, 5.6%-19.6%) had developed ocular hypertension that required topical medication.

240 Glucocorticoid-induced ocular hypertension (the steroid response) may result in

241 the eye in a steroid induced mouse model of ocular hypertension, the compounds reduce intraocular pr

242 r meshwork cells and leads to early onset of ocular hypertension, the major risk factor for glaucoma.

243 aqueous humor in the eye is responsible for ocular hypertension, the only treatable risk factor in p

244 medical treatments in patients with POAG or ocular hypertension through a systematic review and netw

245 c medications may lead to the development of ocular hypertension through the induction of morphologic

246 of assessing global risk for conversion from ocular hypertension to glaucoma is to identify patients

247 ssure to reduce the rate of progression from ocular hypertension to primary open-angle glaucoma has b

248 apy to delay or prevent the progression from ocular hypertension to primary open-angle glaucoma has b

249 tients diagnosed with open-angle glaucoma or ocular hypertension; to suggest approaches ophthalmologi

250 central corneal thickness of subjects in the Ocular Hypertension Treatment Study (OHTS) and determine

251 progression to glaucoma as determined by the Ocular Hypertension Treatment Study (OHTS) Optic Disc Re

252 ODHs were evaluated in 3236 eyes of 1618 Ocular Hypertension Treatment Study (OHTS) participants

253 The Ocular Hypertension Treatment Study (OHTS) provided impo

254 yes of 1636 subjects who participated in the Ocular Hypertension Treatment Study (OHTS) were included

255 profile of DH from fundus photographs in the Ocular Hypertension Treatment Study (OHTS).

256 lly randomized to the observation arm of the Ocular Hypertension Treatment Study (OHTS).

257 To summarize the major findings of the Ocular Hypertension Treatment Study (OHTS).

258 se factors contribute to participants in the Ocular Hypertension Treatment Study (OHTS).

259 To understand the results of the Ocular Hypertension Treatment Study and the European Gla

260 ecently completed large clinical trials, the Ocular Hypertension Treatment Study and the European Gla

261 rom the Genetic Analysis Workshop 17 and the Ocular Hypertension Treatment Study demonstrated that SK

262 The Ocular Hypertension Treatment Study has confirmed that d

263 The Ocular Hypertension Treatment Study has effectively demo

264 Three experts used the Ocular Hypertension Treatment Study reading center crite

265 This study uses data from the Ocular Hypertension Treatment Study to assess whether th

266 Laser Ophthalmoscopy Ancillary Study to the Ocular Hypertension Treatment Study were included.

267 In the Ocular Hypertension Treatment Study, patients were rando

268 g its performance in an independent dataset (Ocular Hypertension Treatment Study-Confocal Scanning La

269 currently available mostly derived from the Ocular Hypertension Treatment Study.

270 n-angle glaucoma has been established in the Ocular Hypertension Treatment Study.

271 ata and an analysis of genetic data from the Ocular Hypertension Treatment Study.

272 of open-angle glaucoma and 26 patients with ocular hypertension underwent perimetry (Octopus G1; Haa

273 Patients with open-angle glaucoma or ocular hypertension (unmedicated baseline IOP >20 to <30

274 Adults with open-angle glaucoma or ocular hypertension (unmedicated intraocular pressure [I

275 xonal loss in the optic nerve after inducing ocular hypertension using a laser glaucoma model in adul

276 phenotypes in human TM (hTM) cells to cause ocular hypertension, via a yet unknown mechanism.

277 Chronic ocular hypertension was associated with a reduction in t

278 Furthermore, dexamethasone-induced ocular hypertension was associated with chronic ER stres

279 Fisher exact test); however, development of ocular hypertension was associated with worse final BCVA

280 Reproducible and reversible ocular hypertension was induced in approximately 40% of

281 Ocular hypertension was induced in the right eye of 7 cy

282 Ocular hypertension was induced unilaterally in 13 NIH B

283 The ocular hypertension was responsive to topical medicines.

284 within the trabecular meshwork may result in ocular hypertension, we investigated the effects of expr

285 Forty subjects with open-angle glaucoma or ocular hypertension were admitted to our sleep laborator

286 n = 27 subjects) with open-angle glaucoma or ocular hypertension were enrolled during standard-of-car

287 with newly diagnosed open-angle glaucoma and ocular hypertension were included and followed up until

288 with latanoprost for open-angle glaucoma or ocular hypertension were randomly assigned to refill the

289 nduced trabecular meshwork scarification and ocular hypertension, were observed with optical coherenc

290 is obscuration occurred in 9.4% of eyes, and ocular hypertension which required eye drop medication o

291 ic contrast sensitivity and IOP reduction in ocular hypertension, which suggests that previous sensit

292 patients with primary open-angle glaucoma or ocular hypertension who had insufficient IOP reduction w

293 Patients with open-angle glacuoma or ocular hypertension who received phaco-ELT between 01/20

294 with a diagnosis of any kind of glaucoma or ocular hypertension who were aged >=40 years, were takin

295 Patients with open-angle glaucoma or ocular hypertension who were intolerant of latanoprost 0

296 IOP in patients with open-angle glaucoma or ocular hypertension who were intolerant of latanoprost.

297 support a novel and flexible model of modest ocular hypertension with axon loss.

298 blindness (glaucoma suspects and those with ocular hypertension with mild visual field loss) and may

299 P) lowering in an in vivo transient model of ocular hypertension, with the maximal effect at 120 min

300 a typical POAG, normal tension glaucoma, or ocular hypertension without glaucoma.