ライフサイエンスコーパス: RPE

1 RPE adenoma/adenocarcinoma can simulate choroidal melano

2 RPE has several well-delineated phenotypes and functions

3 psoid zone disruption (83% vs 3%, P < .001), RPE disruption (77% vs 3%, P < .001), and choroidal neov

4 ubretinal drusenoid deposits and drusen, (2) RPE cell bodies, and (3) the choriocapillaris' vascular

5 hy with treatment-naive quiescent CNV (n=7), RPE atrophy with a history of exudative CNV (n=10), and

6 ction of YAP1 is essential to maintain adult RPE differentiation.

7 and prevention of dedifferentiation of adult RPE.

8 he cellular and molecular landscape of adult RPE/choroid and uncover a Hedgehog-regulated choroidal i

9 annel affecting Ca(2+) signaling and altered RPE function.

10 Alternatively, RPEs might promote learning about the sensory features (

11 epithelium (RPE) of the AMD donor eyes (AMD RPE).

12 ics revealed dysregulated metabolites in AMD RPE as compared to normal RPE, including glycerophosphol

13 activity, and overactive mTOR pathway in AMD RPE as compared to normal RPE.

14 nd annular LAMP-1-positive organelles in AMD RPE.

15 Here, we generated an RPE event in the milliseconds before movement onset and

16 rm iRORA should not be used when there is an RPE tear.

17 with a history of exudative CNV (n=10), and RPE atrophy without evidence of coexisting CNV (n=81).

18 therapeutic preservation of the choroid and RPE in age-related retinal disorders.

19 enous interaction in HCT116, 293T, HeLa, and RPE-hTERT cells; demonstrated that the interaction occur

20 d retinal function, retinal inflammation and RPE/photoreceptor degeneration.

21 PE degeneration or intact IS/OS junction and RPE.

22 isolated RPE atrophy, and matched IS/OS and RPE degeneration or intact IS/OS junction and RPE.

23 Photoreceptor and RPE degeneration exhibited a strong relationship wherein

24 ficant correlation was found between qAF and RPE/BM complex thickness (r = 0.27, P = 0.004).

25 er adjusting for age and iris color, qAF and RPE/BM complex thickness were still correlated in subjec

26 ked electrical responses from the retina and RPE.

27 zone, hyperreflective dots above the RPE and RPE thickening.

28 ole in maintaining choroidal vasculature and RPE cells, implicating insufficiency in choroidal macrop

29 These precede other anatomic heralds such as RPE changes and drusen substructure emergence detectable

30 ingle retinal layer identification to assess RPE/BM complex thickness in vivo.

31 n important step toward accurately assessing RPE lipofuscin concentrations by FAF.

32 t study, we quantified outcome history-based RPE signals in the ventral pallidum (VP), a basal gangli

33 2))/year and was independent of the baseline RPE area (r = -0.18; P = 0.15) and age (r = 0.06; P = 0.

34 al RPE strongly correlated with the baseline RPE area (r = 0.90 and 0.61, respectively; P < 0.001).

35 ted whether there was a relationship between RPE and vigor.

36 We demonstrated that light attenuation by RPE melanin can be assessed and corrected using the dept

37 -associated phenotype secretome, followed by RPE and PRC demise, and that ELVs 32 and 34 blunt these

38 l CNV: 1) progression to type A, followed by RPE erosion and subretinal hyperreflective material, the

39 vidence for retinal pigment epithelial cell (RPE) involvement.

40 loss of visual acuity lagged behind central RPE atrophy in AF images.

41 Mean choroid, RPE, PR, and ONL thicknesses were compared across quarti

42 ing of the interaction partners in confluent RPE monolayers.

43 with genetically proven MIDD and demarcated RPE atrophy on serial fundus autofluorescence (AF) image

44 ne approaches that utilise stem cell-derived RPE cells to treat conditions such as age-related macula

45 nduced pluripotent stem cell (hiPSC)-derived RPE (iRPE) was extensively characterized, and then used

46 -dependent Cl(-) currents in patient-derived RPE cells by WT BEST1 gene supplementation.

47 igms using virtual reality that disambiguate RPEs from values.

48 l cystoid spaces, ellipsoid zone disruption, RPE disruption, and choroidal neovascularization in peri

49 In the dorsal RPE of the optic cup, Nf2 inactivation leads to a robust

50 Neural activation during RPE and other phases of reward processing were determine

51 better detection and understanding of early RPE changes in the course of AMD, potentially before cli

52 We found that a subset of VP neurons encoded RPEs and did so more robustly than the nucleus accumbens

53 en implicated in retinal pigment epithelial (RPE) cell differentiation.

54 mutant-TIMP3 in retinal pigment epithelial (RPE) cells showed increased secretion of bFGF and condit

55 ular atrophy and retinal pigment epithelial (RPE) changes including structural disruption, downregula

56 s to accelerated retinal pigment epithelial (RPE) senescence in vitro and in vivo.

57 chment (RD) with retinal pigment epithelial (RPE) tear is a rare and severe variant of chronic centra

58 Retinal pigmented epithelial (RPE) cells are essential for maintaining normal visual f

59 photoreceptor, retinal pigmented epithelial (RPE), and-more recently-choroidal endothelial cells has

60 ity of amphibian retinal pigment epithelium (RPE) allows them to regenerate the entire retina, a trai

61 The human retinal pigment epithelium (RPE) and choroid are complex tissues that provide crucia

62 performed by the retinal pigment epithelium (RPE) and on oxygen and nutrients delivered by blood vess

63 ents of complete retinal pigment epithelium (RPE) and outer retinal atrophy (e.g., RPE perturbation w

64 model presented retinal pigment epithelium (RPE) and photoreceptor degeneration which was similar to

65 e disease of the retinal pigment epithelium (RPE) and the retina leading to loss of central vision.

66 may require the retinal pigment epithelium (RPE) and/or retinal Muller glia.

67 ocular history: retinal pigment epithelium (RPE) atrophy with treatment-naive quiescent CNV (n=7), R

68 Retinal pigment epithelium (RPE) cells are cultured on top of custom-made electrodes

69 In human retinal pigment epithelium (RPE) cells, the primary site for the fusion of optic fis

70 ncorporated into retinal pigment epithelium (RPE) cells.

71 fluid drainage, retinal pigment epithelium (RPE) changes, and choroidal thickness in both eyes.

72 revealed that in retinal pigment epithelium (RPE) elevations with a greatest transverse linear dimens

73 SRF), 36% had subretinal pigment epithelium (RPE) fluid, and 66% had subretinal hyper-reflective mate

74 with respect to retinal pigment epithelium (RPE) in 836 spectral-domain OCT slices from 44 eyes of 3

75 rk in DR and the retinal pigment epithelium (RPE) in AMD.

76 on phases of the Retinal Pigment Epithelium (RPE) in-vitro at the cell layer level using impedance sp

77 The retinal pigment epithelium (RPE) is a highly polarized epithelial cell type maintain

78 The retinal pigment epithelium (RPE) is a monolayer of cobblestone-like epithelial cells

79 The retinal pigment epithelium (RPE) is a particularly vulnerable tissue to age-dependen

80 ipofuscin in the retinal pigment epithelium (RPE) is the major source of fundus autofluorescence (FAF

81 of the residual retinal pigment epithelium (RPE) is unclear, with reported RPE area decline rates va

82 al damage in the retinal pigment epithelium (RPE) layer in serous retinal pigment epithelium detachme

83 unctional in the retinal pigment epithelium (RPE) of the AMD donor eyes (AMD RPE).

84 vation mainly in retinal pigment epithelium (RPE) or rather in non-RPE cells promotes CNV, (2) whethe

85 s on retinal and retinal pigment epithelium (RPE) structure and function.

86 cular mean EZ to retinal pigment epithelium (RPE) thickness (2q4: 26.6 mum to 31.6 mum, P < 0.001; 2q

87 n vivo in murine retinal pigment epithelium (RPE) tissue and skeletal muscle after local administrati

88 n vivo in murine retinal pigment epithelium (RPE) tissue via subretinal injection, providing a highly

89 perturbation of retinal pigment epithelium (RPE) transcriptional programs in any model, although off

90 the obelix(td15) retinal pigment epithelium (RPE) uncovered reduced phagosome clearance and increased

91 Proteins in the retinal pigment epithelium (RPE), a cell layer adjacent to the photoreceptor outer s

92 em involving the retinal pigment epithelium (RPE), Bruch's membrane, and the choriocapillaris in the

93 terial below the retinal pigment epithelium (RPE), have long been established as a hallmark early fea

94 material (SHRM), retinal pigment epithelium (RPE), hyperreflective foci (HRF), fibrovascular pigment

95 eptors, while in retinal pigment epithelium (RPE), TH regulates expression of a cytochrome P450 enzym

96 , despite intact retinal pigment epithelium (RPE), to approximately 70% of baseline thicknesses, as w

97 and cells of the retinal pigment epithelium (RPE), which provide essential metabolites, phagocytose w

98 l opsin known as retinal pigment epithelium (RPE)-retinal G-protein-coupled receptor (RGR) was previo

99 l retina than in retinal pigment epithelium (RPE).

100 (POS) within the retinal pigment epithelium (RPE).

101 channels in the retinal pigment epithelium (RPE).

102 ina to reach the retinal pigment epithelium (RPE)/choroid with minimal subsequent systemic exposure.

103 he ER-associated retinal pigment epithelium (RPE)65 isomerase necessary for recycling 11-cis-retinal,

104 ipsoid zone, and retinal pigment epithelium (RPE, P < 0.001 and P = 0.005-0.045, respectively).

105 ression in the retinal pigmented epithelium (RPE) and limited expression in the Muller glia.

106 ofuscin in the retinal-pigmented epithelium (RPE) and of lipoproteins at the Bruch's membrane (BrM),

107 ally increased retinal pigmented epithelium (RPE) proliferation in the fissure region with concomitan

108 oss, increased retinal pigmented epithelium (RPE) stress, and increased basal laminar deposits was de

109 unction of the retinal pigmented epithelium (RPE) underlies the pathogenesis of age-related macular d

110 s (ROS) in the retinal pigmented epithelium (RPE).

111 hyperreflective retinal pigment epithelium [RPE] from Bruch's membrane, with the gap between them sh

112 cally activation to reward prediction error (RPE), are impacted by trauma and predict the future cour

113 urons are to encode reward prediction error (RPE), in addition to other signals, such as salience.

114 vidence implicates reward prediction errors (RPEs) as a key factor in the acquisition of episodic mem

115 hesized to compute reward prediction errors (RPEs) to promote adaptive behavior.

116 rch has shown that reward prediction errors (RPEs), a key concept of reinforcement learning theory, a

117 ed on the basis of reward prediction errors (RPEs), defined as the discrepancy between expectations a

118 thought to signal reward prediction errors (RPEs), resembling temporal difference errors used in mac

119 of signed (i.e., better/worse-than-expected) RPEs (SRPEs).

120 erall flat or variable morphologic features, RPE layer irregularity, and nonhomogeneous reflectivity

121 h iRPE displayed features close to bona fide RPE, no or a modest increase of the RPE65 protein level

122 Focal RPE damage was indicated by hyper-transmission beneath t

123 , 11 mum (33) for SHRM, and 103 mum (95) for RPE + RPE elevation.

124 er age was associated with lower volumes for RPE, SRF, NSR, and sPED; in second-treated eyes, older a

125 The odds for future RPE atrophy involvement were reduced by a factor of 0.21

126 elium (RPE) and outer retinal atrophy (e.g., RPE perturbation with associated hypotransmission or hyp

127 We found that the LCA16 hiPSC-RPE cells had normal morphology but did not express a fu

128 d Pluripotent Stem Cells (iPSCs) and a human RPE cell line.

129 m another hiPSC source and from foetal human RPE.

130 -204 expression in primary cultures of human RPE using anti-miR-204.

131 first study to demonstrate invasion of human-RPEs, begin to characterize intracellular localization a

132 These changes in RPE further prompted the loss of adjacent photoreceptor

133 tivation of ADAMTS9 impaired ciliogenesis in RPE-1 cells, which was restored by catalytically active

134 eramide desaturase-1 (DES1), is expressed in RPE and Muller cells.

135 in normal subjects, adding great interest in RPE cell biology.

136 asome activation in non-RPE cells but not in RPE cells promotes CNV.

137 AnxA8 suppression in RPE cells via siRNA or administration of FR induced neur

138 rmissive chromatin state and unmethylated in RPE.

139 mice are resistant to sodium iodate-induced RPE cell death.

140 Blue light-induced RPE cellular damage preceded the photoreceptors loss.

141 ate regression models, the total average INL-RPE was observed to be thinner in older aged, females, B

142 f some photoreceptor reflectivity and intact RPE after SDD regression should be seen in the larger co

143 to differentiate pluripotent stem cells into RPE cells suitable for disease modelling and therapy dev

144 ssociated with progressive disease involving RPE atrophy and photoreceptor cell degeneration.

145 nd improved rhodopsin degradation in an iPSC-RPE model of recessive bestrophinopathy as well as in tw

146 rived retinal pigment epithelial cells (iPSC-RPE).

147 f polarized RPE (porcine primary cells, iPSC-RPE) that endogenously express Ca(V) 1.3 and wild-type b

148 A third dominant Best disease iPSC-RPE model did not respond to gene augmentation, but show

149 bjected all three dominant Best disease iPSC-RPE models to gene editing, which produced premature sto

150 ell-derived retinal pigment epithelium (iPSC-RPE) to test the potential of gene augmentation to treat

151 Gene augmentation in iPSC-RPE fully restored BEST1 calcium-activated chloride chan

152 th factor (VEGF) secretion, and matched iPSC-RPE monolayers to the stem cell donors.

153 QBAM images of iPSC-RPE were used to train DNNs that predicted iPSC-RPE mono

154 nd off-target events using personalized iPSC-RPE model systems is warranted.

155 In summary, personalized iPSC-RPE models can be used to select among a growing list of

156 were used to train DNNs that predicted iPSC-RPE monolayer transepithelial resistance, predicted pola

157 dimension of 1000 mum or more, an irregular RPE layer with a height of predominantly less than 100 m

158 collective features as a shallow, irregular RPE elevation (SIRE).

159 as regions of isolated IS/OS loss, isolated RPE atrophy, and matched IS/OS and RPE degeneration or i

160 g status, SBP and refractive error; and ISOS-RPE was additionally associated with smoking status, IOP

161 no evidence of retinal breaks, while a large RPE tear was detected in the temporal quadrant.

162 n, the retinal pigment epithelial cell line, RPE-Neo was used as a healthy cell line for comparison.

163 Cells lining the OF margin can maintain RPE fate ectopically and fail to transition from neuroep

164 ice task where we experimentally manipulated RPEs and found support for key neural predictions with f

165 The mean RPE/BM complex thickness significantly increased with ag

166 own-regulated upon fenretinide (FR)-mediated RPE transdifferentiation.

167 Knockout of Yap1 in the adult mouse RPE caused cell depolarization and tight junction breakd

168 nd bulk RNA sequencing, we categorized mouse RPE/choroid cell types and characterized the tissue-spec

169 ivity were significantly increased in mutant RPE.

170 ures reflecting distress of the neuroretina, RPE, or choroid were assessed and included ellipsoid zon

171 In contrast, wild-type mice showed no RPE degeneration after blue light illumination.

172 el that NLRP3 inflammasome activation in non-RPE cells but not in RPE cells promotes CNV.

173 al pigment epithelium (RPE) or rather in non-RPE cells promotes CNV, (2) whether inflammasome activat

174 metabolites in AMD RPE as compared to normal RPE, including glycerophospholipid metabolism, involved

175 TOR pathway in AMD RPE as compared to normal RPE.

176 ge was associated with lower volumes of NSR, RPE, sPED, fvPED, and SRF.

177 coefficient) between predicted and observed RPE atrophy progression was evaluated to estimate the mo

178 high overlap between predicted and observed RPE atrophy progression with a cross-validated Dice coef

179 ssure region with concomitant acquisition of RPE cell fate.

180 he area, radius, and log-transformed area of RPE change linearly with time, respectively.

181 f macular complications (CNV, large areas of RPE atrophy [at least 250 mum in diameter], and CMD).

182 layed CNV, 9 eyes (12.7%) had large areas of RPE atrophy, and 2 eyes (2.8%) developed cystoid macular

183 membrane band when there are small areas of RPE damage.

184 n, is to compensate the light attenuation of RPE melanin.

185 nges occurred prior to structural changes of RPE and retinal degeneration.

186 lator of Wnt signalling and a determinant of RPE phenotype, with implications for regenerative medici

187 Factors associated with the development of RPE atrophy were also identified: ONL thinning had an HR

188 ibition of RPE65 expression, diminishment of RPE pigments, and retraction of microvilli and basal inf

189 Distribution of RPE melanin was calculated using the dataset from multi-

190 ventral striatum increased as a function of RPE value (during learning), suggesting a central role o

191 Collectively, invasion of RPE by Pg and its prolonged survival by autophagy evasio

192 antly hypoautofluorescent on FAF and loss of RPE, ellipsoid zone, and external limiting membrane on S

193 eposited in both the extracellular matrix of RPE cells and aged donor BrM tissue.

194 The expected hexagonal mosaic of RPE cells was only sometimes seen in normal eyes, while

195 The localized progression of RPE atrophy in topographic relation to the CNV lesion wa

196 F group demonstrated a greater proportion of RPE changes in fellow eyes (30.8% vs. 1.7%; P = 0.03) an

197 The mean progression rate of RPE atrophy was 2.33 mm(2)/year, revealing a dependence

198 rformed on macular and peripheral regions of RPE-choroid from 7 human donor eyes in 2 independent exp

199 IS/OS loss was 1.6-fold greater than that of RPE atrophy, supporting the theory that photoreceptor de

200 Correlates of RPEs have been observed in the midbrain dopamine system,

201 the pathological effects, as dysfunction of RPEs leads to AMD.

202 nt neural predictions related to the role of RPEs in episodic memory acquisition remain to be tested.

203 ssion analyses to determine their effects on RPE and NR production.

204 rreflective material, macular hemorrhage, or RPE tear occurred in 14 of 47, 13 of 47, and 10 of 47 ey

205 create masks to measure total IS/OS loss or RPE atrophy as well as regions of isolated IS/OS loss, i

206 ar degeneration and ameliorated pathological RPE alterations.

207 Transfection of polarized RPE (porcine primary cells, iPSC-RPE) that endogenously

208 polipoproteins secreted from primary porcine RPE cells.

209 ory that photoreceptor degeneration precedes RPE in STGD.

210 Progressive RPE atrophy could be traced in all eyes using AF imaging

211 ults indicate that there is markedly reduced RPE atrophy progression in areas co-localizing with quie

212 show lipid accumulation in the RPE, reduced RPE and retinal function, retinal inflammation and RPE/p

213 : medial VTA activity more closely reflected RPE, while lateral VTA activity more closely reflected a

214 bove the RPE, and as type C if the remaining RPE was undistinguishable.

215 t epithelium (RPE) is unclear, with reported RPE area decline rates varying widely among patients.

216 The loss of residual RPE area in untreated eyes with CHM follows the AEM over

217 of the area and effective radius of residual RPE strongly correlated with the baseline RPE area (r =

218 The residual RPE area followed a trend of exponential decay as a func

219 identify studies that assessed the residual RPE area in untreated eyes with CHM using fundus autoflu

220 Log-transformed residual RPE area measured by FAF can serve as an anatomic endpoi

221 um (33) for SHRM, and 103 mum (95) for RPE + RPE elevation.

222 Using fMRI, we show that signed RPEs (SRPEs) are encoded in the ventral striatum (VS), a

223 gmentation, were averaged to obtain a single RPE/BM complex thickness value in each eye.

224 Eyes from Black individuals had higher SRF, RPE, and serous PED volumes compared with other ethnic g

225 e reinforcement learning theory and striatal RPEs as key factors subtending the formation of episodic

226 We propose that RPE hyperproliferation is the primary cause for the obse

227 Our data show that RPE cells with constitutively high mTORC1 activity were

228 The data suggest that RPE events, which are thought to transiently alter the r

229 experimental techniques has established that RPEs are signaled by midbrain dopamine neurons.

230 The RPE decline rate was estimated using a 2-stage random-ef

231 The RPE+drusen complex layer becomes thinner over time in fe

232 The RPE/BM complex thickness could reflect the lipofuscin/me

233 ipsoide zone, hyperreflective dots above the RPE and RPE thickening.

234 eath the RPE, as type B if located above the RPE, and as type C if the remaining RPE was undistinguis

235 deposits, SDD), which are located above the RPE.

236 The correlation among the RPE/BM complex thickness, the qAF value, and the age of

237 n standard OCT for displaying changes at the RPE-Bruch's membrane band when there are small areas of

238 indicated by hyper-transmission beneath the RPE-Bruch's membrane band in standard OCT images.

239 r with light-dependent processes in both the RPE and neural retina to ensure adequate 11-cis-retinal

240 from movement error was not modulated by the RPE event.

241 infrared autofluorescence (AO-IRAF) from the RPE layer in healthy retinas and patients with AMD.

242 The loss of lactate transporters from the RPE most closely resembled the phenotype of the Bsg(-/-)

243 ial homeostatic role for lipid efflux in the RPE and suggest a pathogenic contribution of reduced ABC

244 that the regulation of lactate levels in the RPE and the subretinal space is essential for the viabil

245 al consequences of hyperactive mTORC1 in the RPE are unclear.

246 e beginning of light-dark transitions in the RPE by targeting Ezrin, a cytoskeleton-associated protei

247 that contribute to lipid accumulation in the RPE cells during aging and age-related degeneration.

248 l biogenesis and function is impaired in the RPE from miR-211(-/-) mice that show severely compromise

249 t limiting proliferation particularly in the RPE layer is a critical mechanism during OF closure.

250 lated with expression levels of FATP4 in the RPE of the KI, KI;Fatp4 (+/-) , and KI;Fatp4 (-/-) mice.

251 tion with the FATP4 expression levels in the RPE of the three mutant lines.

252 Here we show that FATP4-deficiency in the RPE results in 2.8-fold and 1.7-fold increase of 11-cis-

253 rements of lipofuscin fluorophore A2E in the RPE using liquid chromatography/mass spectrometry (LC/MS

254 In the RPE, isomerization of all-trans-retinyl esters to 11-cis

255 Mutant mice show lipid accumulation in the RPE, reduced RPE and retinal function, retinal inflammat

256 images clearly showed melanin defects in the RPE-Bruch's membrane band at all points.

257 RPE to increase active Rap1a protein in the RPE.

258 nstitutively active Rap1a (CARap1a) into the RPE of wild type mice, self-complementary AAV2 (scAAV2)

259 ght individual-eye data and investigated the RPE decline pattern using 3 models: the area linear mode

260 tems routinely evaluate the structure of the RPE at the tissue level, but cellular level information

261 than 1000 mum in length were: height of the RPE elevation, overall flat or variable morphologic feat

262 es as biological signals at the level of the RPE is in the order of minutes to hours, depending on th

263 cular degeneration with frank atrophy of the RPE or neovascularization.

264 ing zone of attenuation or disruption of the RPE, and (3) evidence of overlying photoreceptor degener

265 OCT images failed to show disruption of the RPE-Bruch's membrane band at 5 of the 24 hyper-transmiss

266 ective, irregular, knobbly elevations of the RPE.

267 ogenic retinal degenerative disorders of the RPE.

268 ntial protective effect of type 1 CNV on the RPE and overlying neurosensory retina.

269 Over the life span, the RPE develops an expanded endo-lysosomal compartment to m

270 In our study, the RPE identity of human induced pluripotent stem cell (hiP

271 inally, microglia transiently adhered to the RPE before which RPE cells appeared dysmorphic.

272 d that choroidal endothelium adjacent to the RPE expresses high levels of Indian Hedgehog and identif

273 ture strategy to deliver active Rap1a to the RPE in order to protect against both atrophic and neovas

274 While applied to the RPE, this work is also suitable for the study of any kin

275 rix (Bruch's membrane (BrM)) adjacent to the RPE.

276 specifically and efficiently transduced the RPE to increase active Rap1a protein in the RPE.

277 slices, as type A if located underneath the RPE, as type B if located above the RPE, and as type C i

278 By the final visit, the RPE+drusen complex was significantly thinner when compar

279 ssociated significantly with NE-MNV when the RPE elevation was more than 1000 mum in length were: hei

280 O-IRAF could be seen even in areas where the RPE appeared relatively normal in clinical imaging modal

281 ) grid, generated by the software using the "RPE" segmentation, were averaged to obtain a single RPE/

282 mygdala (beta = 0.58, p = .04) activation to RPE and future hypo/mania severity trajectory: the inter

283 greater left ventral striatum activation to RPE was associated with a shallower increase in hypo/man

284 uma and greater right amygdala activation to RPE was associated with increasing hypo/mania severity.

285 can have similar downstream consequences to RPE-like signals, although with different temporal depen

286 iating downstream effects that contribute to RPE dysfunction/death.

287 ation and dimension were spatially mapped to RPE atrophy.

288 valuated and expression profiles specific to RPE and major choroidal cell populations were identified

289 In the first experiment, total RPE/choroid preparations were evaluated and expression p

290 The decline rate of log-transformed RPE area was 0.050 (95% confidence interval, 0.046-0.055

291 lular level information may provide valuable RPE biomarkers of health, aging and disease.

292 her trials, this content was less valuable (-RPE event).

293 VP RPEs predicted changes in task engagement, and optogenet

294 transiently adhered to the RPE before which RPE cells appeared dysmorphic.

295 ain dopamine system, but the extent to which RPE signals exist in other reward-processing regions is

296 While RPE is known to support learning, the role of salience i

297 nosis of bullous variant of chronic CSC with RPE tear is critical to avoid inappropriate procedures a

298 and genomic approaches to examine mice with RPE-specific deletion of the tuberous sclerosis 1 (Tsc1)

299 fold) as well as in an experimental set with RPE derived from another hiPSC source and from foetal hu

300 ramping dopamine signals are consistent with RPEs rather than value, and this ramping is observed at