ライフサイエンスコーパス: macular

1 All 22 RCNs (21 eyes of 14 patients) were macular.

2 Study participants underwent macular 3- x 3-mm OCTA scans with spectral domain OCTA.

3 Peripapillary (4.5 x 4.5-mm) and macular (3 x 3-mm) OCTA scans were acquired with AngioVu

4 For the diagnosis of early glaucoma, both macular and optic disc scans should be used.

5 40 and 80 years from LVPEI-GLEAMS underwent macular and optic nerve head imaging with spectral-domai

6 rence tomography and confocal microscopy for macular and peripapillary neuroretinal layer thicknesses

7 isual dysfunction that correspond with early macular architectural changes characteristic of multiple

8 ep large choroidal vessels over the superior macular area even after tumor removal.

9 One or more drusen were present in the macular area of at least 1 eye in 95.5% of the populatio

10 ith established open-angle glaucoma from the Macular Assessment and Progression Study (MAPS; developm

11 ow eye was associated with increased risk of macular atrophy (hazard ratio [HR], 1.70; 95% confidence

12 re was not associated with increased risk of macular atrophy (HR, 1.03; 95% CI, 0.90-1.17; P = 0.67).

13 Previous studies of macular atrophy (MA) in HARBOR analyzed color fundus pho

14 20/40]; P < 0.0001), higher proportion with macular atrophy 2 years earlier (26.8% vs. 12.3%; P = 0.

15 Incident macular atrophy after nAMD was examined by Kaplan-Meier

16 The rate of incident macular atrophy after untreated nAMD is relatively high,

17 The cumulative risks of incident macular atrophy after untreated nAMD were 9.6% (standard

18 Central macular atrophy does not develop universally in eyes rec

19 ing, the cause of poor vision appeared to be macular atrophy in 60% and subretinal fibrosis in 40%.

20 entrations in the junctional zone and future macular atrophy may represent progressive migration and

21 Macular atrophy was considered Definite if all 3 criteri

22 een the extent of angioid streaks and CNV or macular atrophy were investigated using regression analy

23 associated with an increased risk of CNV and macular atrophy, even after adjustment for age.

24 to identify factors predictive of presenting macular attachment status.

25 strated early emergence of peripapillary and macular capillary vasculature changes after I(125) plaqu

26 Efficient delivery of macular carotenoid lutein to target retinal tissue is po

27 cal aspect of sialidosis is the finding of a macular cherry-red spot on ocular fundus examination.

28 Fundoscopic examination showed a typical macular cherry-red spot with retinal pigment epithelium

29 The main outcome measure was the central macular ChT (0.5-mm radius around the fovea).

30 on between better BCVA and increased central macular ChT (P < .001), after adjusting for age, sex, et

31 The median central macular ChT was 370 mum (interquartile range 312-406 mum

32 ctors were identified for the development of macular complications in eyes with chronic CSC.

33 e last four point to shared aetiologies with macular condition, myopia and glaucoma.

34 ndard, the confounding effects of concurrent macular conditions including myopia, and the measurement

35 ts were observed in association with various macular conditions: presumed posterior vitreous detachme

36 RP and may improve suboptimally functioning macular cones.

37 The macular cube was analyzed for 10 time-points from baseli

38 ermediary step in the causal pathway between macular damage and impairment of facial recognition.

39 al visual acuity, patients with glaucomatous macular damage exhibit diminished facial recognition, wh

40 The presence or absence of macular damage was determined by comparing corresponding

41 In NAION and POAG with similar RNFL and macular damage, macular OCT-A shows less involvement of

42 r indirect costs associated with age-related macular degeneration ($17 379.41-$657 406.55).

43 abnormalities (26.6% versus 7.3%), exudative macular degeneration (5.2% versus 0.1%), and geographic

44 ing hypothesis of the Alabama Study on Early Macular Degeneration (ALSTAR2) is that early AMD is a di

45 to 90 years with GA secondary to age-related macular degeneration (AMD) and best-corrected visual acu

46 ssociated with increased risk of age-related macular degeneration (AMD) and disease progression, but

47 and anxiety among subjects with age-related macular degeneration (AMD) and its association with AMD

48 sociated with the development of age-related macular degeneration (AMD) and other complementopathies.

49 t prediction models for advanced age-related macular degeneration (AMD) are based on a restrictive se

50 d in eyes with large drusen from age-related macular degeneration (AMD) before and after the drusen s

51 nning may be secondary to active age-related macular degeneration (AMD) disease progression in both e

52 Offspring of parent(s) with age-related macular degeneration (AMD) have a 45% lifetime risk of d

53 Age-related macular degeneration (AMD) is a chronic eye condition th

54 Age-related macular degeneration (AMD) is a common multifactorial di

55 (VEGF) treatment of neovascular age-related macular degeneration (AMD) is a highly effective advance

56 Age-related macular degeneration (AMD) is the leading cause of legal

57 t often in eyes with neovascular age-related macular degeneration (AMD) that had type 1 macular neova

58 re implicated in the etiology of age-related macular degeneration (AMD), a major cause of blindness i

59 as retinitis pigmentosa (RP) and age-related macular degeneration (AMD), are among the leading causes

60 ng ocular comorbidity other than age-related macular degeneration (AMD), diabetic retinopathy, glauco

61 ic loci that are associated with age-related macular degeneration (AMD), the most common cause of inc

62 ntributes to the pathogenesis of age-related macular degeneration (AMD), the role of retinal perfusio

63 80 years of age or later, showed age-related macular degeneration (AMD)-like fundus changes.

64 ts and graded centrally for late age-related macular degeneration (AMD).

65 e first cell classes affected by age-related macular degeneration (AMD).

66 atrophy (GA) onset secondary to age-related macular degeneration (AMD).

67 ger age than in individuals with age-related macular degeneration (AMD).

68 coherence tomography (SS-OCT) in age-related macular degeneration (AMD).

69 link Periodontal disease(PD) to age-related macular degeneration (AMD).

70 al and breast cancers as well as age-related macular degeneration (AMD).

71 or delay development to advanced age-related macular degeneration (AMD).

72 Progression to exudative 'wet' age-related macular degeneration (exAMD) is a major cause of visual

73 uro-ophthalmology.(1-5) Humans with juvenile macular degeneration (JMD) show significant blood-oxygen

74 change in real-world neovascular age-related macular degeneration (nAMD) patients.

75 ion in patients with neovascular age-related macular degeneration (nAMD) treated with intravitreal in

76 mes in patients with neovascular age-related macular degeneration (nAMD) who received anti-vascular e

77 igible patients with neovascular age-related macular degeneration (nAMD).

78 for the treatment of neovascular age-related macular degeneration (nAMD).

79 CA) in patients with neovascular age-related macular degeneration (nAMD).

80 ersus aflibercept in neovascular age-related macular degeneration (nAMD).

81 pt monotherapies for neovascular age-related macular degeneration (NVAMD).

82 hy of prematurity (ROP), and wet age-related macular degeneration (wet AMD) have been found to have e

83 r glaucoma, Brolucizumab for wet age-related macular degeneration (wet AMD), Luxturna for retinitis p

84 s common in eye diseases such as age-related macular degeneration and diabetic retinopathy.

85 atform for understanding the pathogenesis of macular degeneration and other related degenerative diso

86 body donor eyes with neovascular age-related macular degeneration are limited by the time span from d

87 tformin were less likely to have age-related macular degeneration compared with those not taking the

88 roidal neovascularization due to age-related macular degeneration in the study eye were randomized an

89 Age-related macular degeneration is a leading cause of vision loss w

90 Age-related macular degeneration is a major cause of vision impairme

91 raphic atrophy (GA) secondary to age-related macular degeneration is considered a single entity.

92 (GA), a progressive dry form of age-related macular degeneration is elusive and there is currently n

93 f age or older with a diagnosis of exudative macular degeneration or diabetic macular edema requiring

94 rcept injections for neovascular age-related macular degeneration presented 4 weeks after his most re

95 from the early drusen stage to the advanced macular degeneration stage that leads to blindness, rema

96 Age-related macular degeneration was diagnosed and graded based on f

97 ic multivitamin formulations for age-related macular degeneration were obtained.

98 ophy outcome(s) in patients with age-related macular degeneration who received anti-VEGF treatment we

99 g 1185 patients with neovascular age-related macular degeneration who were enrolled in the clinical t

100 ether individuals with retinal damage due to macular degeneration will have stereopsis.

101 pigment epithelium), and H35.50 (unspecified macular degeneration).

102 bnormal deposits associated with age-related macular degeneration, Alzheimer's disease, and many othe

103 oid-associated diseases, including dementia, macular degeneration, and diabetes mellitus, in epidemio

104 ic features, including glaucoma, age-related macular degeneration, and epiretinal membrane, require s

105 Glaucoma, macular degeneration, and near-sightedness searches more

106 uch as diabetic retinopathies, glaucoma, and macular degeneration, cause the death of retinal neurons

107 sting for age, gender, glaucoma, age-related macular degeneration, diabetic retinopathy, cataract, gl

108 d for information on the topics of cataract, macular degeneration, glaucoma, diabetic retinopathy, an

109 without concomitant ocular pathology such as macular degeneration, glaucoma, Sicca syndrome, epiretin

110 telangiectasia type 2 (MacTel), a late-onset macular degeneration, has been linked to a loss in the r

111 near-sightedness, diabetic retinopathy, and macular degeneration, respectively, with all pairwise co

112 In age-related macular degeneration, the retinal pigment epithelium can

113 r age, gender, and a documented diagnosis of macular degeneration, the use of a BLF IOL was not predi

114 ncluding an epiretinal membrane, age-related macular degeneration, vitreomacular traction, and cystoi

115 lume scans of 1094 patients with age-related macular degeneration, we generated a vocabulary of 20 lo

116 used on diabetic retinopathy and age-related macular degeneration.

117 recommended for patients who are at risk for macular degeneration.

118 te unexpected cell types in diseases such as macular degeneration.

119 lytic uremic syndrome (aHUS) and age-related macular degeneration.

120 tics and diagnostics directed at age-related macular degeneration.

121 s less than that for other diseases, such as macular degeneration.

122 atrophy, and 2 eyes (2.8%) developed cystoid macular degeneration.

123 atients affected by dry atrophic age-related macular degeneration.

124 nd monitoring human eye disorders, including macular degeneration.

125 membrane probably also has implications for macular degeneration.

126 get in patients with neovascular age-related macular degeneration.

127 y (GA) secondary to nonexudative age-related macular degeneration.

128 ells to treat conditions such as age-related macular degeneration.

129 al ocular diseases including keratoconus and macular degeneration.

130 erited retinal degenerations and age-related macular degeneration.Literature discussed here focuses o

131 eyes of 4 patients demonstrated neurosensory macular detachment with treatment-resistant submacular f

132 and synthesis rates in eyes with and without macular disease.

133 ilateral rapidly progressive vision loss and macular disturbance, blood film microscopy to detect vac

134 d SLC16A8), and 3 genes that cause inherited macular dystrophies (ABCA4, CTNNA1, and PRPH2).

135 atrophy spectrum disorder, including retinal macular dystrophy and kidney insufficiency leading to tr

136 gmentation to treat Best disease, a dominant macular dystrophy caused by over 200 missense mutations

137 s to understand symptoms of Best vitelliform macular dystrophy such as reduced electro-oculogram, lip

138 Stargardt disease, the most common inherited macular dystrophy, is characterized by vision loss due t

139 There was one family with macular dystrophy, nine with cone-rod dystrophy (CORD),

140 50.9%), posterior synechiae (21.7%), cystoid macular edema (16%), epiretinal membrane (13.2%), glauco

141 face changes, or both (24 eyes); sequelae of macular edema (3 eyes); blunt trauma (2 eyes); retinal p

142 Center-involved diabetic macular edema (ci-DME) is a major cause of vision loss.

143 Patients with center-involved diabetic macular edema (CI-DME) with good visual acuity (VA) repr

144 kness (2.9 mm vs. 3.2 mm; P = 0.01), cystoid macular edema (CME) involving the foveola (30% vs. 70%;

145 tion, epiretinal membrane (ERM), and cystoid macular edema (CME), were analyzed.

146 n naive and previously treated (PT) diabetic macular edema (DME) eyes in a real-life setting.

147 ased macular thickness in eyes with diabetic macular edema (DME) in clinical trials.

148 Diabetic macular edema (DME) is a leading cause of vision loss in

149 Diabetic macular edema (DME) is the most common cause of vision l

150 e <75 years, absence of preexisting diabetic macular edema (DME) or postvitrectomy persistent cystoid

151 ercept monotherapy for treatment of diabetic macular edema (DME).

152 hy (OCTA) and treatment response in diabetic macular edema (DME).

153 nal vein occlusion disease (BRVO) cases with macular edema (ME).

154 a (DME) or postvitrectomy persistent cystoid macular edema (P < .05).

155 r until macular edema resolved or until both macular edema and HEs resolved.

156 patients with radiation retinopathy-related macular edema and prevent vision loss through 48 weeks o

157 sociated with presenting vision in eyes with macular edema and RVO, most eyes treated with ranibizuma

158 treal aflibercept (IVA) for the treatment of macular edema associated with CRVO based on data from th

159 FAi-treated eyes had investigator-determined macular edema at month 36 compared with sham-treated eye

160 In the treatment of macular edema in CRVO, IVB yields the best cost utility

161 iss Meditec, Dublin, CA) OCTA images with no macular edema or significant motion artifact were acquir

162 Cystoid macular edema refractory to carbonic anhydrase inhibitor

163 f exudative macular degeneration or diabetic macular edema requiring bilateral anti-vascular endothel

164 avitreal ranibizumab injections either until macular edema resolved or until both macular edema and H

165 The risk for the development of cystoid macular edema was found to be associated with recurrence

166 nicity aged 18 years and older with diabetic macular edema who received intravitreal injections of be

167 y (BCVA) change from baseline, resolution of macular edema, and number of adjunctive treatments.

168 on (RVO), diabetic retinopathy (DR; diabetic macular edema, DME), or noninfectious uveitis (NIU).

169 % vs. 14.7% and 13.0% vs. 27.3% for BCVA and macular edema, respectively).

170 provement of best-corrected visual acuity or macular edema.

171 eration, vitreomacular traction, and cystoid macular edema.

172 erity scale score or development of diabetic macular edema.

173 OCT analysis identified various patterns of macular fibrosis in eyes with nAMD.

174 s from HARBOR participants were analyzed for macular fluid secondary to macular neovascularization.

175 Interventions were 1) macular function as measured by 10-2 VF and 2) CS as mea

176 major contributions from Tmc2a and Tmc2b to macular function; however, Tmc1 had less overall impact.

177 illary retinal nerve fiber layer (pRNFL) and macular ganglion cell + inner plexiform layer (GCIPL) th

178 Macular ganglion cell complex (GCC) and peripapillary re

179 e tomography (OCT)-based measurements of the macular ganglion cell complex (GCC) in healthy children

180 Circumpapillary retinal nerve fiber layer, macular ganglion cell layer (mGCL), and macular inner pl

181 inal nerve fibre layer thickness (mRNFL) and macular ganglion cell layer-inner plexiform layer thickn

182 The purpose was to study the macular ganglion cell- inner plexiform layer (GC-IPL) th

183 A similar trend was noted in our analysis of macular GC-IPL thickness.

184 d that while averaged peripapillary RNFL and macular GCC were not different between NAION and POAG ey

185 cohort of 480 older adults either in normal macular health or with early AMD will be enrolled and fo

186 s. 12.3%; P = 0.003), higher proportion with macular hemorrhage (25.5% vs. 13.2%; P = 0.014), and few

187 Subretinal hyperreflective material, macular hemorrhage, or RPE tear occurred in 14 of 47, 13

188 Most study eyes (89% [973/1095]) showed macular hemorrhages at baseline, declining to 31% (319/1

189 LM removal in the treatment of large stage 4 macular hole (MH) > 400 mum and to evaluate reconstructi

190 termining which factors influence idiopathic macular hole (MH) size is important because it is a majo

191 OVD to stabilize inverted ILM flap onto the macular hole (MH) were reviewed.

192 ere graded for vitreomacular traction (VMT), macular hole (MH), and epiretinal membrane (ERM) accordi

193 clusively, and not to epiretinal membrane or macular hole codes.

194 o a disorder of the vitreomacular interface (macular hole or epimacular membrane).

195 If a neovascularization or macular hole were present, bilateral occurrence was freq

196 All cases had at least 4 sets of RNFL and macular images at 6-month intervals.

197 Macular imaging with optical coherence tomography (OCT)

198 yer, macular ganglion cell layer (mGCL), and macular inner plexiform layer (mIPL) were significantly

199 umphrey visual fields (Carl Zeiss Meditech), macular integrity assessment perimetry, OCT, motion disc

200 ikely to be treated earlier and to have less macular involvement, but the final VA outcomes were simi

201 hyperautofluorescence and mottling indicated macular involvement.

202 i.e., CST) was associated significantly with macular leakage index and posterior pole microaneurysm c

203 al assessments of macular microaneurysms and macular leakage index values revealed that eyes with DME

204 Higher doses of NAC reduced risk of macular loci sensitivity loss in RP.

205 Zonal assessments of macular microaneurysms and macular leakage index values

206 ondition outer foveal microdefect instead of macular microhole, which is usually associated with a vi

207 diffusion, provides a quantitative metric of macular microvascular remodeling with a strong physiolog

208 d macular degeneration (AMD) that had type 1 macular neovascularization (MNV) (91.1%).

209 dothelial growth factor (VEGF) treatment for macular neovascularization (MNV).

210 were analyzed for macular fluid secondary to macular neovascularization.

211 Atezolizumab-associated acute macular neuroretinopathy (AMN) with retinal venulitis is

212 Vessel leak and macular non-perfusion were associated with neurological

213 Macular OCT features and layer thicknesses for untreated

214 We captured macular OCT from 169 eyes (1 eye excluded because of pri

215 and issues related to detection of change on macular OCT images in glaucoma eyes.

216 factors affecting the detection of change on macular OCT images.

217 es to detection of glaucoma progression with macular OCT imaging and propose ways to enhance its perf

218 posterior vitreous cortex are visualized on macular OCT, an accurate determination of attached vitre

219 d POAG with similar RNFL and macular damage, macular OCT-A shows less involvement of superficial and

220 mic retina practice and obtained 3-mm x 3-mm macular OCTA scans with the AngioVue system and standard

221 d-extend protocol of aflibercept for cystoid macular oedema (CMO) secondary to central retinal vein o

222 were diabetic retinopathy (DR) and diabetic macular oedema (DMO) (542 cases, 66.0%), followed by ret

223 tatistical significance between AUCs for the macular parameter and cpRNFL thickness measurement at an

224 t patients with DR without severe concurrent macular pathologic features.

225 It was assumed that patients with macular pathologies detected before surgery would receiv

226 atients undergoing cataract surgery may have macular pathologies, of which 11% may not be detected on

227 For example, we observed a macular pattern that was sparse centrally and peaked per

228 ssociated with retinitis pigmentosa (RP) and macular/pattern dystrophies, but the origin of this phen

229 e-control review of 38 consecutive PDT-naive macular PCV patients who underwent verteporfin PDT using

230 a high dose lutein/zeaxanthin supplement on macular pigment optical density (MPOD) and skin caroteno

231 coincides with the loss of Muller cells and macular pigment.

232 tenuator, compatible with the arrangement of macular pigments in Henle fibres; (ii) the morphology of

233 ization, differential absorption of light by macular pigments is perceived as the entoptic phenomena

234 0-373 mum) and thinnest nasally at the outer macular region (median 256 mum).

235 inal vessel density in the peripapillary and macular region of POAG patients with normal IOP treated

236 rior sector of the superficial plexus in the macular region was also significantly higher in the Tafl

237 superior-inner, inferior-inner, and central macular regions (370-373 mum) and thinnest nasally at th

238 y plexus in the foveal, parafoveal, and full macular regions and foveal avascular zone (FAZ) area, pe

239 ection as needed, and thicknesses in various macular regions were compared using mixed effects models

240 of GA varies significantly across different macular regions.

241 eficits (FDa) were compared within the given macular regions.

242 ctural changes in both the peripapillary and macular retina and changes in vascular parameters have b

243 he superior and inferior quadrants and total macular retinal nerve fibre layer thickness (mRNFL) and

244 concurrent 4-AP therapy, degeneration of the macular retinal nerve fibre layer was reduced over 2 yea

245 ted with these two loci drive differences in macular retinal thickness prior and subsequent to the on

246 xamined the incidence and natural history of macular retinochoroidal neovascularization (RCN) in enha

247 RFI volatility with an aggregate increase in macular RFI by >=10 points from those timepoints with in

248 Early RFI volatility with a central macular RFI increase by >=5 points from week 4 to 8 (P =

249 gnificantly associated with artifacts on the macular scan (P < .001).

250 with the presence of true progression on the macular scan (P < .001).

251 alifornia, USA) using both 3x3-mm and 6x6-mm macular scan patterns.

252 SS-OCTA macular scanning was performed within a 3 x 3 mm (300 x

253 y prevalent on both circumpapillary RNFL and macular scans on SDOCT images acquired in a glaucoma cli

254 al of 190 eyes with 760 sets of OCT RNFL and macular scans were included.

255 Macular sensitivity and average macular thickness were m

256 Macular sensitivity as measured by microperimetry was de

257 Furthermore, macular sensitivity demonstrated a positive correlation

258 is study, we sought to determine the role of macular sensitivity measured by microperimetry in the de

259 Best-corrected visual acuity (BCVA), macular sensitivity, ellipsoid zone (EZ) width, and aque

260 targeting dendritic spines and displaying a macular shape, regardless of the layer examined.

261 that we have termed monoclonal gammopathy of macular significance.

262 Macular striae were seen in eyes with epiretinal membran

263 cluding myopia, and the measurement floor of macular structural outcomes.

264 with nAMD were retrospectively included when macular subretinal fibrosis was present.

265 FL) thicknesses were measured in addition to macular superficial and deep vasculature after projectio

266 er layer plexus capillary density (NFLP_CD), macular superficial vascular complex vessel density (mSV

267 rom laser or solar maculopathy (5 eyes); and macular telangiectasia type 2 (2 eyes).

268 e sign is an important OCT characteristic of Macular telangiectasia type 2 (MacTel 2).

269 Macular telangiectasia type 2 (MacTel), a late-onset mac

270 Severity of macular thickening (i.e., CST) was associated significan

271 jections for persistent HE in the absence of macular thickening.

272 OCT images were graded for central macular thickness (CMT) and the presence of fluid over t

273 0 letters or more in BCVA, change in central macular thickness (CMT), and time to maximum improvement

274 .001) with corresponding decrease in central macular thickness (IVOM: - 105 mum, p < 0.01; IVOM+Laser

275 d either the spherical equivalent or central macular thickness after 6 months, with p-values of 0.135

276 in the full GBC identified a combination of macular thickness and ONH VD measurements as the greates

277 Patients with higher baseline central macular thickness and with no previous central macular t

278 cular thickness and with no previous central macular thickness are more likely to require additional

279 ity demonstrated a positive correlation with macular thickness as measured by optical coherence tomog

280 Mean HE area and mean macular thickness at baseline and month 12 were compared

281 These eyes had significantly thicker central macular thickness at baseline and over the entire follow

282 The quadratic value of the retinal macular thickness decreased from the superior value of 2

283 Larger macular thickness fluctuations are associated with poore

284 nd aflibercept improved vision and decreased macular thickness in eyes with diabetic macular edema (D

285 may be used to interrupt measurement of the macular thickness in Middle Eastern population.

286 40 Snellen equivalent (P = .035) and central macular thickness increased from 268 +/- 27 mum to 339 +

287 ions did not coincide with the commonly used macular thickness scan.

288 Relapse of ME was defined as increase in macular thickness to >=240 mum in an eye that previously

289 al striae at the macula with the increase in macular thickness was observed in both eyes.

290 Best-corrected visual acuity and central macular thickness were measured every 2 months.

291 Macular sensitivity and average macular thickness were measured in all subjects using mi

292 l density decrease than GCC thinning; faster macular vessel density decrease rate was associated sign

293 re than two thirds of the eyes showed faster macular vessel density decrease than GCC thinning; faste

294 In POAG eyes, macular vessel density decrease was faster than GCC thin

295 es, the normalized rates of GCC thinning and macular vessel density decrease were comparable (all P >

296 Both GCC thinning and macular vessel density decrease were detectable over tim

297 Macular vessel density is useful for evaluating glaucoma

298 Whole image and parafoveal deep macular vessels in glaucoma eyes (21.0%+/-8.7%, 24.4%+/-

299 shortcomings in acquisition and analysis of macular volume scans can enhance its utility for measuri

300 Cirrus and Spectralis OCT macular volume scans were exported, data from the centra