ライフサイエンスコーパス: macular

1 roidal vascular and stromal areas within the macular (6 mm) and foveal (1.5 mm) regions, and choroida

2 Macular abnormalities included mild to severe pigment mo

3 shunts and tangles were noted in 3 eyes, and macular abnormalities were noted in 3 eyes.

4 oretinal atrophy with a predilection for the macular area, congenital glaucoma and optical nerve hypo

5 To compare the enlargement rate of macular atrophy (ERMA) in eyes treated with ranibizumab

6 ol eyes, as well as analyze risk factors for macular atrophy (MA) development and progression.

7 ase with no visual symptoms despite temporal macular atrophy.

8 udy reports a high frequency of microcystoid macular changes in the inner nuclear layer in eyes with

9 Microcystoid macular changes in the inner nuclear layer were diagnose

10 The likelihood to develop microcystoid macular changes increased at advanced glaucoma and epire

11 vailable OCT devices also permit analysis of macular changes over time, for example, changes in the g

12 yzed in a subgroup of eyes with microcystoid macular changes treated with pars plana vitrectomy and e

13 The morphology of microcystoid macular changes was similar between glaucomatous and non

14 Cystoid macular changes were found in 53% of patients and 22% of

15 ineffective in the treatment of microcystoid macular changes.

16 SS OCT was used to obtain automatic macular choroidal thickness (CT) maps, according to the

17 Specific macular clinic user interfaces within the institutional

18 e to quantify a biological characteristic of macular CNP in malaria that had previously only been des

19 ted macular degeneration may be more than a "macular" condition but one that involves the entire reti

20 The central macular CVV was significantly decreased by 19% in eyes w

21 Recent evidence supports the presence of macular damage (within 8 degrees of the central field) t

22 own about the association between structural macular damage and self-reported visual function of peop

23 irment) and a high prevalence of age-related macular degeneration (>14% of blindness) as causes in th

24 ith no sex difference related to age-related macular degeneration (0.91 [0.70-1.14]).

25 r (61.3%), cataract (13.2%), and age-related macular degeneration (10.3%).

26 ilable for cataract surgery (10 metrics) and macular degeneration (7 metrics).

27 18.2 million to 109.6 million]), age-related macular degeneration (8.4 million [0.9 million to 29.5 m

28 Age-related macular degeneration (AMD) affects millions of people th

29 Age-related macular degeneration (AMD) affects the retinal pigment e

30 for the treatment of neovascular age-related macular degeneration (AMD) among Medicare beneficiaries.

31 geographic atrophy secondary to age-related macular degeneration (AMD) and 2 eyes (5%) had geographi

32 s were diagnosed with coincident age-related macular degeneration (AMD) and 2 with myopic macular deg

33 Age-related macular degeneration (AMD) and related macular dystrophi

34 ges of patients with neovascular age-related macular degeneration (AMD) and to demonstrate its use to

35 non-neovascular and neovascular age-related macular degeneration (AMD) and to provide recommendation

36 icity on the association between age-related macular degeneration (AMD) and vision-specific functioni

37 ecline in the risk of developing age-related macular degeneration (AMD) continued for people born dur

38 gene and their association with age-related macular degeneration (AMD) have been described.

39 year incidence of early and late age-related macular degeneration (AMD) in a Singaporean Malay popula

40 ve eyes diagnosed with exudative age-related macular degeneration (AMD) in comparison with eyes with

41 terranean diet and prevalence of age-related macular degeneration (AMD) in countries ranging from Sou

42 incidence of intermediate-stage age-related macular degeneration (AMD) in patients with acquired imm

43 Age-related macular degeneration (AMD) is a leading cause of irrever

44 Age-related macular degeneration (AMD) is a major cause of visual im

45 Age-related macular degeneration (AMD) is a progressive retinal neur

46 Age-related macular degeneration (AMD) is the leading cause of irrev

47 Age-related macular degeneration (AMD) is the most common cause of b

48 To evaluate the impact of age-related macular degeneration (AMD) on short out-loud and sustain

49 d (TREX) regimen for neovascular age-related macular degeneration (AMD) or fellow control eyes, as we

50 , 1 from a 78-year-old exudative age-related macular degeneration (AMD) patient, 1 from a 58-year-old

51 ascularization (NV) in eyes with age-related macular degeneration (AMD) receiving anti-vascular endot

52 in diabetic retinopathy (DR) and age-related macular degeneration (AMD) remains unclear.

53 -function (pLoF) variants within age-related macular degeneration (AMD) risk loci and AMD sub-phenoty

54 redictors of lipid fractions and age-related macular degeneration (AMD) risk.

55 LLQ) in patients with a range of age-related macular degeneration (AMD) severity are associated with

56 ophy (GA) is an advanced form of age-related macular degeneration (AMD) that leads to progressive and

57 ome in patients with neovascular age-related macular degeneration (AMD) treated initially with bevaci

58 bolomic profile of patients with age-related macular degeneration (AMD) using mass spectrometry (MS).

59 igment epithelium (RPE) cells in age-related macular degeneration (AMD) using polarimetry.

60 standard care for patients with age-related macular degeneration (AMD) who are being considered for

61 y SD OCT study participants with age-related macular degeneration (AMD) with bilateral large drusen o

62 iking phenotypic similarities to age-related macular degeneration (AMD), a common and genetically com

63 Age-related macular degeneration (AMD), a leading contributor of vis

64 Age-related macular degeneration (AMD), a multifactorial disease wit

65 zation (CNV) among patients with age-related macular degeneration (AMD), but no economic evaluation h

66 Other diseases, such as age-related macular degeneration (AMD), develop late in life and are

67 ls for management of neovascular age-related macular degeneration (AMD), diabetic macular edema (DME)

68 rse range of diseases, including age-related macular degeneration (AMD), glaucoma and refractive erro

69 In age-related macular degeneration (AMD), rare variants in the complem

70 uited patients with intermediate age-related macular degeneration (AMD), without other vitreoretinal

71 ations in eyes with intermediate age-related macular degeneration (AMD).

72 intakes with a high incidence of age-related macular degeneration (AMD).

73 d lesions which are hallmarks of age-related macular degeneration (AMD).

74 o contribute the pathogenesis of age-related macular degeneration (AMD).

75 tory marker associated with late age-related macular degeneration (AMD).

76 s from images from patients with Age-related Macular Degeneration (AMD).

77 ermediate and advanced stages of age-related macular degeneration (AMD).

78 aflibercept to treat neovascular age-related macular degeneration (AMD).

79 ibute to the oxidative stress in Age-related macular degeneration (AMD).

80 n OCT findings in the setting of age-related macular degeneration (AMD).

81 tered in patients with exudative age-related macular degeneration (AMD).

82 matory retinal disorders such as age-related macular degeneration (AMD).

83 flammation increases the risk of age-related macular degeneration (AMD).

84 inal pigment epithelium (RPE) of age-related macular degeneration (ARMD) patients and therefore could

85 d with neovascularization in wet age-related macular degeneration (ARMD), choriocapillaris degenerati

86 (nGA) in eyes with intermediate age-related macular degeneration (iAMD).

87 mes in patients with neovascular age-related macular degeneration (nAMD) during anti-vascular endothe

88 ens in patients with neovascular age-related macular degeneration (nAMD) from the TReat and extEND (T

89 he natural course of neovascular age-related macular degeneration (nAMD) is essential in discussing p

90 ment-naive eyes with neovascular age-related macular degeneration (nAMD) tracked by the Fight Retinal

91 hy (GA) in eyes with neovascular age-related macular degeneration (nAMD) treated with ranibizumab.

92 with ranibizumab for neovascular age-related macular degeneration (nAMD), diabetic macular oedema (DM

93 apy in patients with neovascular age-related macular degeneration (nAMD).

94 guiding therapy for neovascular age-related macular degeneration (nvAMD) to the research investments

95 occlusion (RVO), and neovascular-age related macular degeneration (nvAMD).

96 nd (TAE) regimen for neovascular age-related macular degeneration (NVAMD).

97 is for patients with neovascular age-related macular degeneration (nvAMD).

98 antly with sets found by GWAS of age-related macular degeneration (P=1.4 x 10(-12)), ulcerative colit

99 Recessive Stargardt macular degeneration (STGD1) is caused by mutations in t

100 r inhibitors (anti-VEGF) for wet age-related macular degeneration (wAMD), and to acquire a snapshot o

101 Age-related macular degeneration 4 included neovascular AMD (nvAMD)

102 years or older with neovascular age-related macular degeneration and a baseline best-corrected visua

103 To report patients with age-related macular degeneration and atypical central retinal pigmen

104 al degenerative diseases such as age-related macular degeneration and diabetic retinopathy.

105 es for retinal diseases, such as age-related macular degeneration and inherited retinal dystrophies,

106 in both eyes of adult mammals is a model for macular degeneration and leads to retinotopic map reorga

107 ss in many eye diseases, such as age-related macular degeneration and macular telangiectasia.

108 Age-related macular degeneration automated detection was applied to

109 cizumab injections for exudative age-related macular degeneration between January 1, 2009, and Decemb

110 ic atrophy is a blinding form of age-related macular degeneration characterized by retinal pigmented

111 ancestry from the International Age-related Macular Degeneration Genomics Consortium.

112 Age related macular degeneration is the leading cause of blindness i

113 Age-related macular degeneration may be more than a "macular" condit

114 When a patient with neovascular age-related macular degeneration or diabetic macular edema does not

115 nts for treatment of neovascular age-related macular degeneration or diabetic macular edema.

116 that iPSC-derived RPE cells from age-related macular degeneration patients express increased levels o

117 .9 million to 124.1 million), by age-related macular degeneration to 8.8 million (0.8 million to 32.1

118 articipants in the Comparison of Age-Related Macular Degeneration Treatments Trials (CATT).

119 t study within the Comparison of Age-Related Macular Degeneration Treatments Trials (CATT).

120 Age-related macular degeneration was attributed as the main cause of

121 ur method to an in-depth GWAS of age-related macular degeneration with 33,976 individuals and 9,857,2

122 nant I62-CFH (protective against age-related macular degeneration) and V62-CFH functioned equivalentl

123 g the normal and diseased state (age related macular degeneration, AMD) in the retina.

124 dema, 32 (25.8%) had neovascular age-related macular degeneration, and 32 (25.8%) had other causes of

125 n various pathologies, including age-related macular degeneration, arthritis, and cancer.

126 urity, diabetic retinopathy, and age-related macular degeneration, as well as corneal diseases with a

127 f ophthalmic diseases, including age-related macular degeneration, cataracts, diabetic retinopathy, g

128 dry eye syndrome) and posterior (age-related macular degeneration, diabetic retinopathy and glaucoma)

129 ould be of clinical and research interest in macular degeneration, for example in estimating visual p

130 Ophthalmic diseases, such as age-related macular degeneration, glaucoma, and diabetic retinopathy

131 The other, age-related macular degeneration, is the most common form of blindne

132 ly contributes to vision loss in age-related macular degeneration, is unclear.

133 emplary search for patients with age-related macular degeneration, performed cataract surgery, and at

134 urity, diabetic retinopathy, and age-related macular degeneration, threaten the visual health of chil

135 diseases, including stroke, AD, age-related macular degeneration, traumatic brain injury, Parkinson'

136 isual outcomes for patients with age-related macular degeneration.

137 n eye diseases like glaucoma and age-related macular degeneration.

138 mes and drives the pathogenesis of Stargardt macular degeneration.

139 tients with advanced neovascular age-related macular degeneration.

140 ive diabetic retinopathy and wet age-related macular degeneration.

141 tis pigmentosa (RP) and atrophic age-related macular degeneration.

142 liferative vitreoretinopathy and age-related macular degeneration.

143 ve effect of FHR-1 deficiency in age-related macular degeneration.

144 macular degeneration (AMD) and 2 with myopic macular degeneration.

145 lassification of Age-related Maculopathy and Macular Degeneration.

146 olamine elimination in a cell-based model of macular degeneration.

147 ambiguity about cone survival in age-related macular degeneration.

148 her macular disease including AMD and myopic macular degeneration.

149 n mouse and human eyes, both normal and with macular degeneration/choroidal neovascularization.

150 tinoschisis (XLRS) is one of the most common macular degenerations in young males, with a worldwide p

151 during the first month following iatrogenic macular detachment surgery.

152 into the genetic pathways involved in human macular development.

153 (NCMD) is believed to represent a failure of macular development.

154 These findings, which support the macular diattenuator model of polarization sensitivity,

155 wise healthy patients who may manifest other macular disease including AMD and myopic macular degener

156 2010, to July 31, 2014, of 323 veterans with macular diseases and best-corrected distance visual acui

157 r Stargardt disease type 1 (STGD1) and other macular diseases are needed.

158 l use of the visual streak in modeling human macular diseases.

159 able for the detection and quantification of macular dysfunction.

160 lated macular degeneration (AMD) and related macular dystrophies (MDs) are a major cause of vision lo

161 laris (CC) in patients with Best vitelliform macular dystrophy (BVMD) by means of optical coherence t

162 y of vitelliform lesions in Best vitelliform macular dystrophy (BVMD) using spectral-domain optical c

163 ily excluded linkage with the North Carolina macular dystrophy (MCDR1) locus.

164 Autosomal dominant North Carolina macular dystrophy (NCMD) is believed to represent a fail

165 milies found no pathogenic variants in known macular dystrophy genes.

166 epiretinal membrane (0.16/EY), and recurrent macular edema (0.09/EY).

167 a vitreous haze score of >/=1.5+ or cystoid macular edema (CME) of >300 mum were enrolled.

168 ar pressure (IOP) increase (n = 12), cystoid macular edema (CME; n = 3), and nonarteritic anterior is

169 proliferative DR, or clinically significant macular edema (CSME).

170 Patients with diabetic macular edema (DME) are at high risk of vascular complic

171 (VA 20/32 or worse) center-involved diabetic macular edema (DME) at baseline were required to receive

172 l aflibercept injections (IAIs) for diabetic macular edema (DME) during the phase III VISTA DME trial

173 owth factor (anti-VEGF) therapy for diabetic macular edema (DME) favorably affects diabetic retinopat

174 erity score (DRSS) in patients with diabetic macular edema (DME) treated with intravitreal ranibizuma

175 growth factor therapy in eyes with diabetic macular edema (DME) with vision loss after macular laser

176 related macular degeneration (AMD), diabetic macular edema (DME), and retinal vein occlusion (RVO) we

177 Diabetic retinopathy, diabetic macular edema (DME), vision-threatening diabetic retinop

178 ith or without concomitant baseline diabetic macular edema (DME).

179 f 456 patients with center-involved diabetic macular edema (DME).

180 nterval {CI}, 2.15-4.35], P < .001), cystoid macular edema (HR = 2.87 [95% CI, 1.41-5.82], P = .004),

181 fficacy variables were: patients (%) in whom macular edema (ME) developed (>/=30% increase from preop

182 Macular edema (ME) is the leading cause of decreased vis

183 erapeutic alternatives for the management of macular edema (ME) secondary to branch retinal vein occl

184 retinal vein occlusion (BRVO) complicated by macular edema (ME).

185 n for the prevention of pseudophakic cystoid macular edema (PCME) using a prospective, randomized, do

186 oliferative DR [PDR], clinically significant macular edema [CSME], or both who had evidence of retina

187 age-related macular degeneration or diabetic macular edema does not respond to an initial anti-vascul

188 nited States, and included 362 patients with macular edema due to central retinal or hemiretinal vein

189 th Intravitreal Aflibercept in Subjects with Macular Edema Due to Retinal Vein Occlusion (TANZANITE)

190 38 eyes of 38 treatment-naive patients with macular edema due to RVO, enrolled in the prospective Su

191 abetic retinopathy or clinically significant macular edema in patients with various initial retinopat

192 Pseudophakic cystoid macular edema is common after phacoemulsification catara

193 Diabetic macular edema is one of the leading causes of vision los

194 Macular edema is the leading cause of vision loss in bil

195 reatment of decreased vision attributable to macular edema owing to CRVO or HRVO.

196 ia in patients with visual impairment due to macular edema secondary to branch retinal vein occlusion

197 inferior to aflibercept for the treatment of macular edema secondary to central retinal or hemiretina

198 Questionnaire (NEI VFQ-25), in patients with macular edema secondary to central retinal vein occlusio

199 Sixteen patients with NPDR without macular edema underwent SDOCT and OCTA.

200 abetic retinopathy or clinically significant macular edema was 1.0% over 5 years among patients with

201 Macular edema was less likely to resolve in eyes that re

202 abetic retinopathy or clinically significant macular edema was limited to approximately 5% between re

203 raphs of 30 eyes (20 patients) with diabetic macular edema were obtained.

204 he main outcome measure was the diagnosis of macular edema within 90 days of cataract surgery.

205 ibercept Injection in Patients With Diabetic Macular Edema) and VIVID (Intravitreal Aflibercept Injec

206 f 124 eyes analyzed, 60 (48.4%) had diabetic macular edema, 32 (25.8%) had neovascular age-related ma

207 ties, such as angle closure glaucoma, cystic macular edema, and exudative retinal detachment.

208 change, proportion of patients with resolved macular edema, and leakage on fluorescein angiography.

209 rative retinopathy or clinically significant macular edema, both of which require timely intervention

210 e best-corrected visual acuity, incidence of macular edema, posterior capsular opacification, epireti

211 control, worsening of visual acuity, cystoid macular edema, retroprosthetic membrane formation, persi

212 age-related macular degeneration or diabetic macular edema.

213 VO and HRVO patients receiving treatment for macular edema.

214 r leakage observed in patients with diabetic macular edema.

215 53 and/or presence of clinically significant macular edema; n = 95) using the modified Airlie House c

216 Only 1 of 11 patients (9%) had recurrence of macular fluid (14 months postoperatively).

217 SDOCT data, including presence or absence of macular fluid and automated central subfield macular thi

218 reduction in CSMT was 79 mum with absence of macular fluid in 72.7% of the 88 eyes with SDOCT data av

219 equired additional procedures to resolve the macular fluid.

220 to detect true clinical change in eyes with macular fluid.

221 Electrophysiologic studies identified normal macular function in 17 of 19 subjects and normal full-fi

222 HRS, disruption of the ELM, and significant macular functional impairment (RS decrease) vs SND-.

223 Atrophy of the macular ganglion cell layer and inner plexiform layer (G

224 s; in severe glaucoma eyes, rates of average macular GCIPL loss were significant, but rates of global

225 in early and moderate glaucoma, and average macular GCIPL thickness loss was detectable in early, mo

226 both global circumpapillary RNFL and average macular GCIPL thickness were detectable in early and mod

227 yes were found in the peripapillary RNFL and macular GCIPL.

228 a, 644 persons 60 years or older with normal macular health per medical record based on their most re

229 vitreous hemorrhage (n = 40), full-thickness macular hole (n = 33), recurrent proliferative vitreoret

230 (RR 13.1), retinal vein occlusion (RR 12.9), macular hole (RR 7.7), and epiretinal membrane (RR 5.7).

231 d unless patients developed a full-thickness macular hole or required surgical intervention for sympt

232 Idiopathic macular holes (MHs) are a cause of decreased vision amon

233 , 8%), or iris (36/1059, 3%), with 19% being macular in location.

234 Retinal sensitivity was assessed by Macular Integrity Assessment microperimetry, and a neuro

235 However, macular intraretinal measurements still have not overcom

236 ntitative OCTA parameters reveal subclinical macular ischemia at both the superficial and deep retina

237 Presence of macular ischemia did not affect BCVA outcome or treatmen

238 Thirty-seven (62%) patients met macular laser criteria at a mean of 19.5 weeks with no s

239 patients receiving no IAIs, and the role of macular laser in decreasing treatment burden among patie

240 c macular edema (DME) with vision loss after macular laser photocoagulation is clinically valuable.

241 b 0.3 mg with and without angiography-guided macular laser photocoagulation significantly decreased t

242 s experiencing substantial vision loss after macular laser photocoagulation treatment for DME.

243 very 8 weeks after 5 monthly doses (2q8), or macular laser photocoagulation.

244 nce in the frequency of IAIs before or after macular laser.

245 es have compared rates of change in RNFL and macular measurements, with some suggesting that the rela

246 and quantify the size and vessel density of macular neovascularization (MNV) using optical coherence

247 of each participant was imaged using 6x6-mm macular OCT angiography (OCTA) scan pattern by 70-kHz 84

248 nical datapoints from the EMR, 52,690 normal macular OCT images and 48,312 AMD macular OCT images wer

249 690 normal macular OCT images and 48,312 AMD macular OCT images were selected.

250 e constructed at an independent image level, macular OCT level, and patient level.

251 All patients underwent macular OCT-A (Avanti RTVue XR).

252 Normal and AMD patients who had a macular OCT.

253 Macular OCTA images were acquired from all participants

254 elated macular degeneration (nAMD), diabetic macular oedema (DME) or branch/central retinal vein occl

255 Macular oedema responded to intravitreal treatment with

256 Furthermore, the macular origin and sensitivity of human polarization pat

257 etection and quantification of IRC for all 3 macular pathologies with a mean accuracy (AUC) of 0.94 (

258 To detect macular perfusion defects in glaucoma using projection-r

259 Ocular findings were focal macular pigment mottling, chorioretinal atrophy with a p

260 fore might represent a more potent source of macular pigments than green leafy vegetables like spinac

261 ng whom 3 patients had bilateral early-onset macular pseudocoloboma.

262 cal arRP in some individuals associated with macular pseudocoloboma.

263 densities within the ONH (0.76 and 42%) and macular region (0.69 and 18%) in PACG were significantly

264 01) than control eyes with emmetropia at the macular region.

265 The qAF8 within nondiseased macular regions were within the normal range.

266 preserved visual acuity but showing temporal macular retinal atrophy were included.

267 pillary retinal nerve fiber layer (RNFL) and macular retinal ganglion cell-inner plexiform layer (GCI

268 Macular retinal VD, ganglion cell complex (GCC) thicknes

269 Characteristic patterns of glaucoma-related macular RGC+IPL loss appeared to be more important predi

270 univariable analyses, patients with diffuse macular RGC+IPL loss had mean composite Rasch-calibrated

271 Macular RGC+IPL loss was determined by diffuse or focal

272 Macular RNFL, mGCL-IPL, and mGCC measurements showed a h

273 BCVA unchanged in 3 eyes due to preexisting macular scar and advanced glaucoma.

274 ortices with subcortical calcifications; (3) macular scarring and focal pigmentary retinal mottling;

275 thickness at inferotemporal and inferonasal macular sectors (rho = 0.222, P = .023 and rho = 0.209,

276 who developed bilateral anterior uveitis and macular serous retinal detachment during nivolumab treat

277 f bilateral anterior uveitis associated with macular serous retinal detachment related to anti-PD-1 t

278 ndred five eyes of 65 patients who underwent macular spectral-domain optical coherence tomography ima

279 We identified predictors of final macular status, and developed two predictive models.

280 ion into a luminance signal by diattenuating macular structures.

281 Macular Telangiectasia Type 2 (MacTel) is an uncommon, l

282 c juxtafoveal retinal telangiectasis type 2 (macular telangiectasia type 2; MacTel) is a rare neurova

283 such as age-related macular degeneration and macular telangiectasia.

284 To evaluate changes in central macular thickness (CMT) and visual outcome in patients w

285 macular fluid and automated central subfield macular thickness (CSMT) at year 1 and 2, were recorded.

286 acid showed a poor correlation with RNFL and macular thickness among type 2 diabetic patients.

287 the strongest of which was with the central macular thickness in the superior 6 x 3-degree region (r

288 d demonstrated higher correlations with full macular thickness measurements, the strongest of which w

289 L thickness of the temporal quadrant and the macular thickness of the superior outer, inferior outer

290 The BCVA and central macular thickness were recorded at baseline and at 1, 2,

291 tion of retinal nerve fibre layer (RNFL) and macular thickness with serum uric acid in type 2 diabeti

292 from preoperative baseline central subfield macular thickness) within 90 days after cataract surgery

293 pigment epithelium (RPE) thickness, central macular thickness, and integrity of the ellipsoid zone.

294 the adolescent population, detected abnormal macular thinning and flow abnormalities undetected by bi

295 For the macular variables, retinal thickness was significantly r

296 lgorithms were used to quantify FAZ area and macular vascular density.

297 Among the overall macular VD parameters, the SVC VD had the best diagnosti

298 Macular vessel density of the deep capillary plexus in t

299 The macular vessel density of the superficial capillary plex

300 Tracking the area of EZ loss on SD-OCT macular volume scans longitudinally is a reliable way of