ライフサイエンスコーパス: ocular hypertension

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

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

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

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

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

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

7 with the correlations seen in patients with ocular hypertension.

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

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

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

11 rrent knowledge of global risk assessment in ocular hypertension.

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

13 n enhanced glucocorticoid responsiveness and ocular hypertension.

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

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

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

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

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

19 sterior subcapsular opacities, glaucoma, and ocular hypertension.

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

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

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

23 retinal tau that was markedly exacerbated by ocular hypertension.

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

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

26 icroglia/macrophages soon after induction of ocular hypertension.

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

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

29 tissues and prevented dexamethasone-induced ocular hypertension.

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

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

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

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

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

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

36 28.5%) had a suspicious nerve, 62 (6.8%) had ocular hypertension, 102 (11.3%) had diabetic retinopath

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 Ocular hypertension arising from increased resistance to

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

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

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

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

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

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

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

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

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

85 200 patients with glaucoma or ocular hypertension, controlled on the unfixed combinati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 Administration of glucocorticoids induces ocular hypertension in some patients.

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

114 Ocular hypertension in the mouse eye sufficient to cause

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

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

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

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

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

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

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

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

123 Ocular hypertension is sufficiently common in eyes treat

124 Ocular hypertension is the most significant known risk f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 Steroid-induced ocular hypertension resembles several characteristics ob

172 Ocular hypertension responsible for GC-induced glaucoma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 The Ocular Hypertension Treatment Study (OHTS) provided impo

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

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

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

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

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

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

198 The Ocular Hypertension Treatment Study has confirmed that d

199 The Ocular Hypertension Treatment Study has effectively demo

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

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

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

203 In the Ocular Hypertension Treatment Study, patients were rando

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

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

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

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

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

209 Chronic ocular hypertension was associated with a reduction in t

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

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

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

213 Ocular hypertension was induced unilaterally in 13 NIH B

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

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

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

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

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

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

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

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

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

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

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

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