ライフサイエンスコーパス: retinal disease

1 MacTel) is a rare neurovascular degenerative retinal disease.

2 therapeutically modulating immune aspects in retinal disease.

3 ts into the pathophysiology underlying USH2A-retinal disease.

4 linical diagnosis and assessing treatment of retinal disease.

5 apies aimed at photoreceptor regeneration in retinal disease.

6 ional potential of these drugs for inherited retinal disease.

7 genic mutation in MAPKAPK3 associated with a retinal disease.

8 nificant therapies for currently untreatable retinal disease.

9 e of autologous cells for transplantation in retinal disease.

10 zed iPSC-based transplantation therapies for retinal disease.

11 get for optogenetic restoration of vision in retinal disease.

12 rease the risk of glaucoma for patients with retinal disease.

13 redox status in a well-established model of retinal disease.

14 individuals aged 63 years and older without retinal disease.

15 on of genes, including genes associated with retinal disease.

16 review the role of UWFA in the management of retinal disease.

17 ng cis-regulatory variants in the context of retinal disease.

18 the retina may have therapeutic effects for retinal disease.

19 to an innate immune response in neovascular retinal disease.

20 e genes in this network are risk factors for retinal disease.

21 Most irreversible blindness results from retinal disease.

22 n-related changes in vivo in mouse models of retinal disease.

23 amounts prior to development of most severe retinal disease.

24 zation for stroke among Ontario seniors with retinal disease.

25 the multifocal ERG is superior in localized retinal disease.

26 r oedema, such as uveitis, diabetes or other retinal disease.

27 em cell therapy to be a viable treatment for retinal disease.

28 tants lead to loss of Cav1.4 function and to retinal disease.

29 c indicator for patients with this inherited retinal disease.

30 and the generation of mouse models of human retinal disease.

31 estoring sight to individuals suffering from retinal disease.

32 a therapeutic option for transplantation in retinal disease.

33 Mutation of BEST1 causes retinal disease.

34 stem/progenitor cell-based interventions for retinal disease.

35 investigate the genetic causes of inherited retinal disease.

36 a new approach for the treatment of blinding retinal diseases.

37 ded novel insights in clinical evaluation of retinal diseases.

38 r range of findings to those of other severe retinal diseases.

39 to FLIM and spectral data in mouse models of retinal diseases.

40 cted by central or peripheral scotoma due to retinal diseases.

41 ction can reduce irreversible blindness from retinal diseases.

42 a (RP) is a heterogeneous group of inherited retinal diseases.

43 m photoreceptor cell degeneration or related retinal diseases.

44 PUFAs among patients with different types of retinal diseases.

45 ecedented details of vascular involvement in retinal diseases.

46 aving the way for the treatment of disparate retinal diseases.

47 ar telangiectasia, neovascular AMD and other retinal diseases.

48 ducted at a tertiary referral eye center for retinal diseases.

49 ortant for the management of a wide range of retinal diseases.

50 ntanglement of the exact role MMPs in ocular/retinal diseases.

51 to retina scar formation in many devastating retinal diseases.

52 ular diseases, including recently in certain retinal diseases.

53 re favorably with costs of therapy for other retinal diseases.

54 sts, and the implementation of therapies for retinal diseases.

55 of vision loss in ischemic and inflammatory retinal diseases.

56 ic target in the treatment of human vascular retinal diseases.

57 costs for cataract surgery and treatment of retinal diseases.

58 rtance in the pathophysiology of a number of retinal diseases.

59 ponse to light and is involved in congenital retinal diseases.

60 retinal neuronal and vascular pathologies in retinal diseases.

61 tment under active investigation in multiple retinal diseases.

62 w insights into the roles of PNR mutation in retinal diseases.

63 agents are now used for treatment of common retinal diseases.

64 ness and other closely related nonstationary retinal diseases.

65 DME) compared with diabetic patients without retinal diseases.

66 apy holds great promise for the treatment of retinal diseases.

67 vision-threatening complication in ischemic retinal diseases.

68 ne therapy by scAAV2/8 delivery for dominant retinal diseases.

69 re or regulation can result in several human retinal diseases.

70 nding of the molecular etiology of inherited retinal diseases.

71 ession of >190 genes associated with 7 human retinal diseases.

72 ew insights into the underlying pathology of retinal diseases.

73 nerve head morphology is affected by several retinal diseases.

74 c interventions for managing PDE6-associated retinal diseases.

75 w mutations in rod PDE6 subunits can lead to retinal diseases.

76 might be helpful for C5-mediated thrombotic retinal diseases.

77 nvestigating new treatments for degenerative retinal diseases.

78 l be safe and effective for individuals with retinal diseases.

79 ues of research into the treatment of common retinal diseases.

80 ) in eyes receiving ranibizumab for 3 common retinal diseases.

81 tion in patients suffering from degenerative retinal diseases.

82 ceptors is a common endpoint in degenerative retinal diseases.

83 apeutic effects against certain degenerative retinal diseases.

84 cizumab use increased each year for diabetic retinal disease (2.4 injections/1000 patients with diabe

85 Perioperative control of retinal disease activity is desired, but level 1 evidenc

86 hic findings suggestive of (choroidal and/or retinal) disease activity were not observed on FA.

87 in achromatopsia patients and in other human retinal diseases affecting foveal function.

88 thickness and for comparisons with specific retinal diseases affecting the macula.

89 s new insights into the underlying causes of retinal disease and age-related vision loss.

90 quencing in 28 individuals with "cone-first" retinal disease and clinical features atypical for ABCA4

91 Exclusion criteria were non-DR retinal disease and inability to image the macula.

92 Retinal disease and loss of vision can result from any d

93 nts who presented with isolated nonsyndromic retinal disease and mutations in CLN3.

94 ountries that share broadly similar rates of retinal disease and risk factor distributions to Scotlan

95 tform genetic testing strategy for inherited retinal disease and to describe its performance in 1000

96 This was based on visualized retinal disease and/or optic nerve pathology.

97 offering a new platform with which to study retinal diseases and degeneration, test prospective drug

98 ious stem cell-based approaches for treating retinal diseases and discuss future directions and chall

99 sting of ABEs for the treatment of inherited retinal diseases and for the correction of pathological

100 exosomes in the molecular pathophysiology of retinal diseases and help identify potential therapeutic

101 required to treat Muller cell deficiency in retinal diseases and in other parts of the CNS associate

102 ncreased each year in patients with diabetic retinal diseases and retinal vein occlusions (both <0.1

103 Mutations in RDS cause rod and cone-dominant retinal disease, and it is well established that both ce

104 netic nonhuman primate model of an inherited retinal disease, and provide an ideal testing ground for

105 onia, pathological gastro-esophageal reflux, retinal disease, and sinus-node dysfunction, whereas rel

106 s of liver disease and neurologic disorders, retinal diseases, and possibly heart disease.

107 blood vessel growth is a key feature of many retinal diseases, and recently, anti-VEGF therapy has be

108 inal changes in animal models of neovascular retinal disease approximately 3-4-fold longer than unmod

109 enes traditionally associated with syndromic retinal disease are increasingly found to cause nonsyndr

110 As many retinal diseases are accompanied by low carotenoid level

111 Vitreo-retinal diseases are among the leading causes of visual

112 Many retinal diseases are associated with pathological cell s

113 Retinal diseases are frequently characterized by the acc

114 Retinal diseases are the leading causes of irreversible

115 -related macular degeneration, a devastating retinal disease, are limited.

116 on of common variants in the ABCA4 gene with retinal disease, assessed by a score-based variance-comp

117 in developing anti-complement therapies for retinal diseases associated with complement activation.

118 ld identify new molecular therapies to treat retinal diseases associated with ER protein misfolding.

119 athies are a group of monogenetic or complex retinal diseases associated with high unmet medical need

120 opathologic mechanisms of MacTel 2 and other retinal diseases associated with telangiectasia.

121 To identify retinal-disease-associated genes, we performed exome seq

122 ut age-related macular degeneration (AMD) or retinal disease at fundus examination were matched for e

123 visualization of structural abnormalities in retinal disease at the cellular level.

124 ents who participated in clinical trials for retinal diseases at the Sydney Eye Hospital.

125 cules, which had been linked to neuronal and retinal diseases, atherosclerosis, and aging.

126 This study showed that ERM is not a static retinal disease but a dynamic condition in which retinal

127 ngiography to differentiate optic nerve from retinal disease can be very helpful in formulating a dif

128 Structural changes in retinal diseases can also lead to functional rewiring.

129 uction and is likely to affect the course of retinal diseases caused by cGMP toxicity.

130 encing (NGS), we screened mutations in known retinal disease-causing genes in an RP cohort of 35 unre

131 RPGRIP1 interacts with other retinal disease-causing proteins and has been proposed t

132 nstrumentation and imaging methods to detect retinal diseases changing indications for surgery, impro

133 rmine the prevalence of CPR-type diplopia in retinal disease clinic patients with ERM and to determin

134 sectional study of 31 patients with ERM from retinal disease clinics to determine the prevalence of C

135 Of the 31 patients with ERM seen in retinal disease clinics, 16 were women and 15 were men;

136 R-type diplopia in patients with ERM seen in retinal disease clinics, and whether or not clinical fin

137 for prioritizing genes associated with human retinal diseases compared to both mouse single-cell RNA-

138 understanding of the pathobiologic basis of retinal diseases, coupled with growth of gene transfer a

139 ceptor-interacting protein-like 1), leads to retinal diseases culminating in blindness.

140 ese clinical efforts for several significant retinal diseases, describe the challenges involved and d

141 seem to improve the accuracy of glaucoma or retinal disease detection when added to the standard TEC

142 olved in the pathology of two major blinding retinal diseases, diabetic retinopathy (DR) and age-rela

143 could help to form a better understanding of retinal disease diagnosis and prognosis.

144 The age at onset and natural progression of retinal disease differs greatly between syndromic and no

145 elated macular degeneration (nAMD), diabetic retinal disease (DRD), and retinal venous occlusive dise

146 We investigated the retinal disease due to mutations in the retinitis pigmen

147 systemic neurologic disease, optic nerve or retinal disease (even if unilateral) or any bilateral oc

148 inistration-approved stem cell therapies for retinal disease exist.

149 fected by retinitis pigmentosa, an inherited retinal disease, experience a decline in vision due to p

150 clinical/genetic spectrum of EYS-associated retinal disease (EYS-RD), and to discover disease-associ

151 cataract surgery in patients with coexisting retinal disease, focusing on factors that are important

152 ighted the potential for curing degenerative retinal diseases from intrinsic cellular sources.

153 Our study firmly establishes ATOH7 as a retinal disease gene and provides a functional basis to

154 The retinal disease gene peripherin 2 (PRPH2) is essential f

155 ty of AAVs combined with the large number of retinal disease genes exceeding that capacity make the d

156 GS), we screened mutations in over 200 known retinal disease genes in a cohort of 12 unrelated Uyghur

157 Direct sequencing of all retinal disease genes on chromosome 6 revealed a novel p

158 whereas no mutations were detected in other retinal disease genes on chromosome 6.

159 For example, retinal disease genes were discovered to be among the mo

160 pression of cell differentiation markers and retinal disease genes, as well as in mRNA alternative sp

161 l was designed, which incorporated 195 known retinal disease genes, including 61 known RP genes.

162 e performance of these programs in eyes with retinal diseases has not been independently evaluated.

163 nsights into the pathophysiology of advanced retinal disease highlighting a role for Muller cells and

164 presence of these cells in mouse models for retinal disease; however, only limited aspects of their

165 MPG2 has previously been implicated in human retinal disease; however, until now no canine PRAs have

166 Many degenerative retinal diseases illustrate retinal inflammatory changes

167 (2.4 injections/1000 patients with diabetic retinal disease in 2009 to 13.6 per 1000 in 2015) while

168 tic neuropathy in 3, corneal opacities in 3, retinal disease in 3, and undetermined in 5) that preven

169 lth literacy levels of patients with chronic retinal disease in Denmark.

170 nes related to phagocytosis, metabolism, and retinal disease in humans.

171 sted that apoptosis contributed minimally to retinal disease in MCMV-infected eyes of MAIDS-10 mice.

172 These results suggest that retinal disease in the diabetic milieu may progress thro

173 We propose that the retinal disease in this model is primarily a failure of

174 tion, and neovascularization associated with retinal diseases in animal models.

175 visual photoresponse and trigger congenital retinal diseases in humans, but GCAP interaction with it

176 study aims to explore the awareness of these retinal diseases in Nepal.

177 n actual practice for treating patients with retinal diseases in Thailand.

178 reports the prevalence and pattern of vitreo-retinal diseases in the Bhaktapur Glaucoma Study (BGS),

179 kle cell retinopathy, uveitis, and pediatric retinal disease, in turn guiding both diagnosis and mana

180 sia type 2 (MacTel) is an uncommon bilateral retinal disease, in which glial cell and photoreceptor d

181 Retinal diseases included acute posterior multifocal pla

182 Several point mutations in rhodopsin cause retinal diseases including congenital stationary night b

183 underlie the majority of vision threatening retinal diseases including retinal detachment (RD).

184 reversible vision loss in incurable blinding retinal diseases including retinitis pigmentosa (RP) and

185 degeneration (AMD), 16.1% to treat diabetic retinal diseases (including 0.9% of all injections that

186 following cataract surgery in patients with retinal disease, including uveitis, diabetic macular ede

187 tential nonhematopoietic roles in neural and retinal diseases, including diabetic retinopathy.

188 ifferent types of damage that underpin major retinal diseases, including macular degeneration and gla

189 or age-related macular degeneration (AMD), a retinal disease involving neurodegeneration and microgli

190 genital amaurosis (LCA) is a known inherited retinal disease (IRD) associated with severe visual loss

191 ness (iCSNB), is a non-progressive inherited retinal disease (IRD) characterized by night blindness,

192 ohort of molecularly characterized inherited retinal disease (IRD) families, we investigated proporti

193 Inherited retinal disease (IRD) is a category of genetic disorders

194 major cause of autosomal recessive inherited retinal disease (IRD), with a high prevalence in the Asi

195 ing in a pediatric population with inherited retinal disease (IRD).

196 Inherited retinal diseases (IRDs) are a diverse group of genetical

197 ase composed of 1385 patients with inherited retinal diseases (IRDs) from 1192 families.

198 e genetic defects in patients with inherited retinal diseases (IRDs) using WES.

199 ated with autosomal recessive (AR) inherited retinal diseases (IRDs).

200 Inherited retinal disease is a common cause of visual impairment a

201 Neovascular retinal disease is a leading cause of blindness orchestr

202 of genes that can, when mutated, cause human retinal disease is a powerful means to understand the mo

203 A common inherited retinal disease is caused by mutations in RHO expressed

204 Genetic testing for inherited retinal disease is now more than 75% sensitive.

205 Stem cell therapy for retinal disease is under way, and several clinical trial

206 generation, a neurodegenerative and vascular retinal disease, is the most common cause of blindness i

207 Many retinal diseases lead to the loss of retinal neurons and

208 al and genetic heterogeneity associated with retinal diseases makes stem-cell-based therapies an attr

209 been tested in preclinical animal models of retinal disease, many postnatal stem/progenitor cell pop

210 cations in the study of optic nerve head and retinal disease mechanisms.

211 tic approaches to blocking VEGF signaling in retinal diseases might have unexpected detrimental side

212 We propose that in retinal disease, mislocalized rod opsin gains access to

213 Spatial and temporal heterogeneities in retinal disease models have hampered validation of this

214 cts (n = 3519) and diabetes controls without retinal disease (n = 10557) were matched by age and gend

215 Among patients with retinal disease, neither the trend nor the level of the

216 or sophisticated monitoring and diagnosis of retinal diseases, OCTA capable of providing wide-field a

217 for pediatric and adult cataract, glaucoma, retinal disease, oculoplastic disorders, and other visio

218 telangiectasia type 2 (MacTel 2), which is a retinal disease of unknown cause.

219 lants are now available for the treatment of retinal disease, offering control of macular edema and i

220 , observational study, 20 volunteers with no retinal diseases or risk factors, ranging in age between

221 s of screening for glaucoma, the presence of retinal disease, or decreased acuity in a population-bas

222 lyopia, high myopia or hyperopia, coexisting retinal disease, or prior surgery were excluded.

223 acking of visual development, progression of retinal disease, or therapeutic interventions, such as i

224 has been associated with the development of retinal diseases, particularly age-related macular degen

225 uently, well-defined NHP models of heritable retinal diseases, particularly cone disorders that are p

226 Here we characterize the development of the retinal disease phenotype in a genetic model of type 1 d

227 nd provide insights into the pathogenesis of retinal disease phenotypes caused by NR2E3 mutations.

228 (sgRho) vs. intronless cDNA in ameliorating retinal disease phenotypes in a rhodopsin knockout (RKO)

229 nducted on a patient with distinct inherited retinal disease presenting in childhood, with a phenotyp

230 effect of pharmacological PERK inhibition on retinal disease process in the P23H-1 transgenic rat mod

231 ch has the potential to aid in understanding retinal disease processes and will facilitate preclinica

232 ssociated with a broad spectrum of inherited retinal diseases ranging from severe autosomal recessive

233 when compared with other treatment of other retinal diseases regardless of treatment modality.

234 s included previously known risk factors for retinal diseases related to oxidative stress, inflammati

235 ive gliosis, but its biological functions in retinal diseases remain elusive.

236 contribution of Muller glial dysfunction to retinal diseases remains largely unknown.

237 ion, which were resistant and susceptible to retinal disease, respectively, but which harbored equiva

238 or cause of retinitis pigmentosa, a blinding retinal disease resulting from photoreceptor degeneratio

239 ted eyes, 9 were enucleated, 6 for recurrent retinal disease, resulting in an overall globe salvage r

240 rs in diabetic retinopathy and other chronic retinal diseases, results in vasogenic edema and neural

241 ve error, no visual impairment, and no known retinal disease served as age-similar controls.

242 The involvement of mast cells in retinal diseases should be further investigated.

243 Consecutive cases with retinal diseases showing outer retinal disruption and at

244 Low health literacy of patients with retinal disease signify a need for more health literacy

245 Retinal disease staging was done by indirect funduscopy

246 Additionally, specific retinal disease states and anatomic variables such as ex

247 The complexity of treating a retinal disease such as choroideremia that affects multi

248 ve to the intravitreal injection for chronic retinal diseases such as age-related macular degeneratio

249 strategies for the treatment of degenerative retinal diseases such as age-related macular degeneratio

250 ential to study oxygen metabolism in hypoxic retinal diseases such as diabetic retinopathy.

251 Retinal diseases such as macular degeneration and glauco

252 use of irreversible blindness in a number of retinal diseases such as retinitis pigmentosa (RP) and a

253 entials via retinal circuitry, degenerate in retinal diseases such as retinitis pigmentosa and age re

254 Degenerative retinal diseases such as retinitis pigmentosa and macula

255 incurable nature of hereditary and sporadic retinal diseases such as Stargardt disease, age-related

256 a critical role in normal physiology and in retinal diseases, such as age-related macular degenerati

257 idative properties protect the eye from many retinal diseases, such as age-related macular degenerati

258 ent a novel class of potential therapies for retinal diseases, such as age-related macular degenerati

259 cysts and ERMs were more common in eyes with retinal diseases, such as proliferative diabetic retinop

260 e deficiencies in Astyanax cavefish resemble retinal diseases, such as retinitis pigmentosa.

261 cycle is considered a treatment strategy for retinal diseases, such as Stargardt disease and dry age-

262 sfunction associated with incurable blinding retinal diseases, such as Stargardt disease, retinitis p

263 characterize cellular structure in inherited retinal disease; such information will be critical for s

264 ell as pathologies observed in age-dependent retinal diseases, suggesting that the responsible gene r

265 risk populations and revealed fewer cases of retinal disease than previously estimated, suggesting un

266 l microvessels isolated from mouse models of retinal disease that exhibit vascular pathology, and unc

267 igmentosa (RP) is an inherited, degenerative retinal disease that leads to blindness for which no the

268 (MacTel) is an uncommon, late-onset complex retinal disease that leads to central vision loss.

269 (ACHM) is a congenital, autosomal recessive retinal disease that manifests cone dysfunction, reduced

270 Differentiate between optic nerve and retinal disease that share common characteristics utiliz

271 OCT has revealed many details of retinal disease that were not available with older imagi

272 eceptors is sought and for investigations of retinal diseases that affect cone function.

273 tions have the potential to address blinding retinal diseases that affect hundreds of millions worldw

274 native approaches in patients with inherited retinal diseases that aim to improve surgical success an

275 an increased prevalence of both glaucoma and retinal diseases that can affect the visual outcomes aft

276 egeneration, retinitis pigmentosa, and other retinal diseases that can cause pathological changes in

277 ist to differentiate between optic nerve and retinal diseases that can share some common characterist

278 atment of neovascularization associated with retinal diseases that involve pathologic angiogenesis.

279 from the West Indies islands with a peculiar retinal disease, the Martinique crinkled retinal pigment

280 For the management of retinal disease, the use of intravitreous injections of

281 In many forms of degenerative retinal disease, there may be a window of opportunity to

282 a common pathological factor in degenerative retinal diseases; therefore, identifying novel strategie

283 OVs promise a more complete visualization of retinal disease, they also introduce new challenges to t

284 ructural level, and from characterization of retinal diseases to successful treatments.

285 ore health literacy research in the field of retinal diseases, to secure that patients have the timel

286 sh Columbia, such as those of the Provincial Retinal Diseases Treatment Program, who had received int

287 reduce the dosing frequency associated with retinal disease treatments.

288 cluding visual loss from the optic nerve and retinal disease, visual field loss from retrochiasmal vi

289 Retinal disease was determined by ophthalmoscopy, fundus

290 -fat diet-induced diabetes in mice can model retinal disease, we weaned mice to chow or a high-fat di

291 inical criteria for a diagnosis of inherited retinal disease were included in the study.

292 cts and patients diagnosed with AMD or other retinal diseases were collected during routine visits vi

293 mplicated in the promotion of ME in ischemic retinal disease, were not elevated by quantitative enzym

294 st of genes that will likely result in human retinal disease when mutated was identified and validate

295 bretinal space are thought to be involved in retinal diseases where low-grade chronic inflammation an

296 iously known to be associated with inherited retinal disease, which harbor biallelic predicted protei

297 hese channels result in severe, degenerative retinal diseases, which remain untreatable.

298 m a cohort of 722 individuals with inherited retinal disease, who have had whole-genome sequencing (n

299 of stem/progenitor cell-based approaches for retinal disease, with interpretation and perspective.

300 ) systems in the diagnosis and management of retinal diseases, with particular emphasis on choroidal