ライフサイエンスコーパス: retinal disease

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

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

3 individuals aged 63 years and older without retinal disease.

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

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

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

7 the retina may have therapeutic effects for retinal disease.

8 to an innate immune response in neovascular retinal disease.

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

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

11 amounts prior to development of most severe retinal disease.

12 zation for stroke among Ontario seniors with retinal disease.

13 the multifocal ERG is superior in localized retinal disease.

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

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

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

17 c indicator for patients with this inherited retinal disease.

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

19 estoring sight to individuals suffering from retinal disease.

20 a therapeutic option for transplantation in retinal disease.

21 o(-/-) were reminiscent of findings in human retinal disease.

22 rphic mutations in human LAMA1 could lead to retinal disease.

23 he use of SD-OCT in detecting and diagnosing retinal disease.

24 ndergoing surgery for cataract, glaucoma, or retinal disease.

25 s of relevance to both Mendelian and complex retinal disease.

26 at might account for phenotypic diversity in retinal disease.

27 investigate the genetic causes of inherited retinal disease.

28 m-cell therapy a viable treatment for select retinal disease.

29 herapies that aim to alleviate ABCA4-related retinal disease.

30 pectralis OCT, in subjects without any known retinal disease.

31 o-associated virus-mediated gene therapy for retinal disease.

32 eurologic disorders, including glaucoma, and retinal disease.

33 ns in rodent models of the visual system and retinal disease.

34 e variants of angle closure in patients with retinal disease.

35 nt efficacy in patients and animal models of retinal disease.

36 nization of the visual system in people with retinal disease.

37 for the application of hNPC(ctx) in treating retinal disease.

38 enetic analysis, and treatment of hereditary retinal disease.

39 MacTel) is a rare neurovascular degenerative retinal disease.

40 therapeutically modulating immune aspects in retinal disease.

41 linical diagnosis and assessing treatment of retinal disease.

42 apies aimed at photoreceptor regeneration in retinal disease.

43 ional potential of these drugs for inherited retinal disease.

44 genic mutation in MAPKAPK3 associated with a retinal disease.

45 nificant therapies for currently untreatable retinal disease.

46 e of autologous cells for transplantation in retinal disease.

47 zed iPSC-based transplantation therapies for retinal disease.

48 get for optogenetic restoration of vision in retinal disease.

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

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

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

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

53 to retina scar formation in many devastating retinal diseases.

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

55 ular diseases, including recently in certain retinal diseases.

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

57 of vision loss in ischemic and inflammatory retinal diseases.

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

59 costs for cataract surgery and treatment of retinal diseases.

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

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

62 retinal neuronal and vascular pathologies in retinal diseases.

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

64 tment under active investigation in multiple retinal diseases.

65 tion in patients suffering from degenerative retinal diseases.

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

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

68 ness and other closely related nonstationary retinal diseases.

69 DME) compared with diabetic patients without retinal diseases.

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

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

72 ceptors is a common endpoint in degenerative retinal diseases.

73 he features of AMD as well as those of other retinal diseases.

74 as grown since its first use in glaucoma and retinal diseases.

75 play several key roles in normal and various retinal diseases.

76 ion may provide therapeutic benefit for such retinal diseases.

77 ough which to study genetic heterogeneity in retinal diseases.

78 dpoint may be warranted in treating ischemic retinal diseases.

79 ents for the therapy of angiogenesis-related retinal diseases.

80 e photoreceptor organization and its role in retinal diseases.

81 lls for cell-based therapies of degenerative retinal diseases.

82 s and may play a role in the pathogenesis of retinal diseases.

83 apeutic effects against certain degenerative retinal diseases.

84 e RPE/phagocyte interaction in AMD and other retinal diseases.

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

86 ded novel insights in clinical evaluation of retinal diseases.

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

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

89 ction can reduce irreversible blindness from retinal diseases.

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

91 m photoreceptor cell degeneration or related retinal diseases.

92 PUFAs among patients with different types of retinal diseases.

93 ecedented details of vascular involvement in retinal diseases.

94 ar telangiectasia, neovascular AMD and other retinal diseases.

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

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

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

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

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

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

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

102 RPE function, modeling of RPE dysfunction in retinal disease and in vitro evaluation of new therapies

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

104 fected with two different forms of inherited retinal disease and should be useful as a means of asses

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

106 Thirty-six subjects with no history of retinal disease and with normal vision and normal intrao

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

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

109 signature genes are excellent candidates for retinal diseases and for physiological investigations (e

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

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

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

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

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

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

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

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

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

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

120 The question now is which retinal diseases are most appropriate targets for clinic

121 Retinal diseases are the leading causes of irreversible

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

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

124 imal model for studying the visual cycle and retinal diseases associated with chromophore regeneratio

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

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

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

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

129 These inhibitors may be beneficial against retinal diseases associated with the loss of RPE cells.

130 Third, we also predicted novel retinal disease-associated genes based on the network an

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

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

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

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

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

136 ons suggests that MPDZ plays a role in human retinal disease, but the precise nature of this role rem

137 l structure and function in rodent models of retinal disease, but translation to clinical practice wi

138 en implicated in the pathogenesis of various retinal diseases, but their basic function and cellular

139 s were analyzed for pigmentation defects and retinal disease by histology, immunohistochemistry, and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 We defined the retinal disease expression in vivo in human USH using op

158 ut also identify a form of pathology wherein retinal disease first manifests at the POS-RPE junction.

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

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

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

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

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

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

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

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

167 ession of photoreceptor genes including most retinal disease genes.

168 The study of inherited retinal diseases has advanced our knowledge of the cellu

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

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

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

172 Many degenerative retinal diseases illustrate retinal inflammatory changes

173 (2.4 injections/1000 patients with diabetic retinal disease in 2009 to 13.6 per 1000 in 2015) while

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

175 on interventions to minimize progression of retinal disease in diabetic patients undergoing cataract

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

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

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

179 making it the most common cause of heritable retinal disease in this population and MAK-associated RP

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

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

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

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

184 Retinal diseases included acute posterior multifocal pla

185 number of desirable qualities for a model of retinal disease including a large eye and an existing an

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

187 sels, is a key feature of many proliferative retinal diseases including diabetic retinopathy, retinal

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

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

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

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

192 helial dysfunction and death in degenerative retinal diseases, including age-related macular degenera

193 S may provide new insights and treatments of retinal diseases, including AMD.

194 s associated with a broad range of inherited retinal diseases, including Stargardt disease, autosomal

195 Further testing of DFP for retinal disease involving oxidative stress is warranted.

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

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

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

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

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 oretinal research, the spectrum of treatable retinal disease is likely to expand significantly in the

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 ore common as the genetic basis of inherited retinal diseases is further elucidated.

207 A common thread in many retinal diseases is reactive Muller cell gliosis, an unt

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

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

210 unction that is known to contribute to human retinal diseases like age-related macular degeneration.

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

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

213 l is regulated in the normal retina, and how retinal diseases may affect oxygen response.

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

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

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

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

218 Gene therapy for a number of retinal diseases necessitates efficient transduction of

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

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

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

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

223 fts, or double-transgenic mice, also gave no retinal disease or signs of Ag recognition.

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

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

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

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

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

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

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

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

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

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

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

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

236 neurons, the biological functions of NGB in retinal diseases remain largely unknown.

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

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

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

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

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

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

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

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

245 Retinal disease staging was done by indirect funduscopy

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

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

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

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

250 Retinal diseases such as macular degeneration and glauco

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

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

253 hese ZFNs may be useful for the treatment of retinal diseases such as retinitis pigmentosa, one of th

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

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

256 cumulating for a role of complement in other retinal diseases, such as diabetic retinopathy and proli

257 potential molecular mechanisms of inherited retinal diseases, such as Oguchi disease and Arr1-associ

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

275 In many retinal diseases, the malfunction that results in photor

276 s well as rods, an important requirement for retinal disease therapy.

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

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

279 llowed by reperfusion (IR) to model ischemic retinal disease, this study compares the effects of isch

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

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

282 reduce the dosing frequency associated with retinal disease treatments.

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

284 Retinal disease was determined by ophthalmoscopy, fundus

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

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

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

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

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

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

291 rly detection and longitudinal monitoring of retinal diseases where retinal and choroidal hemodynamic

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

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

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

295 iew the evidence for progression of diabetic retinal disease with cataract surgery and critically ana

296 angiectasia (MacTel) is a vision-threatening retinal disease with unknown pathogenesis and no approve

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

298 ated gene therapy for treatment of inherited retinal diseases, with early intervention resulting in t

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

300 Iron dysregulation can cause retinal disease, yet retinal iron regulatory mechanisms