ライフサイエンスコーパス: dark adaptation

1 ery of rhodopsin to the ground state and rod dark adaptation.

2 by PKA is likely to be involved in light and dark adaptation.

3 li of various durations were presented after dark adaptation.

4 contrast sensitivity, color perception, and dark adaptation.

5 ole in mediating gene repression to maintain dark adaptation.

6 ice during a 90 min illumination followed by dark adaptation.

7 ity, contrast sensitivity, visual field, and dark adaptation.

8 uppresses bleached rhodopsin activity during dark adaptation.

9 ion and is inhibited by a shift to pH 7 upon dark adaptation.

10 alpha-GCs when compared to levels seen under dark adaptation.

11 upled receptor, each can influence light and dark adaptation.

12 ration ratio, and improved ERG responses and dark adaptation.

13 isin content in association with acute light/dark adaptation.

14 s-R-Ac for 6 or 10 months exhibited improved dark adaptation.

15 onse to 24 hours of light exposure following dark adaptation.

16 nd Rdh8 knockout mice displayed only delayed dark adaptation.

17 ics of all-trans-retinal reduction, delaying dark adaptation.

18 exhibited a similar time course of neuronal dark adaptation.

19 a critical contributing factor to light and dark adaptation.

20 overed progressively in darkness, indicating dark adaptation.

21 recycling capacity of ABCA4 and may improve dark adaptation.

22 rious intensities of illumination and during dark adaptation.

23 e full recovery of visual sensitivity during dark adaptation.

24 cally, HPR treatment caused modest delays in dark adaptation.

25 nogram traces were recovered after prolonged dark adaptation.

26 igh Ca2+ concentrations as should occur with dark adaptation.

27 ng both light adaptation and early stages of dark adaptation.

28 robe flash presented at varying times during dark adaptation.

29 able difference in the rates of rod and cone dark adaptation.

30 11-cis-retinal and opsin affects the rate of dark adaptation.

31 failed to restore night vision or to improve dark adaptation.

32 ogram amplitudes were normal after prolonged dark adaptation.

33 LBP gene cause retinal pathology and delayed dark adaptation.

34 precedes sensitivity recovery, thus slowing dark adaptation.

35 the size of the absorption changes seen upon dark adaptation.

36 hom had punctate fundus lesions and abnormal dark adaptation.

37 flow of retinoids in the eye in vivo during dark adaptation.

38 low-luminance visual acuity and rod-mediated dark adaptation.

39 onstriction was recorded after bleaching and dark adaptation.

40 or completely dephosphorylated after a long dark adaptation.

41 d when cytoplasmic [Ca2+]free increase after dark adaptation.

42 ather than a secondary response to long-term dark adaptation.

43 low-white lesions in one fundus and abnormal dark adaptation.

44 cted cats have a marked delay in recovery of dark adaptation.

45 al trade-off between rod photoprotection and dark adaptation.

46 with LO-SD primarily complained of difficult dark adaptation.

47 hore recycling, and ultimately photoreceptor dark adaptation.

48 eated fundus photography following prolonged dark adaptation.

49 ysis of rod-intercept time data in measuring dark adaptation.

50 l monitoring of photoreceptor changes during dark adaptation.

51 -6.5) minutes, and 1 individual had impaired dark adaptation.

52 contrast sensitivity and slower rod-mediated dark adaptation.

53 e systemic and ocular safety and recovery of dark adaptation.

54 e after photobleaching, suggesting a delayed dark adaptation.

55 sicles at presynaptic ribbons after light or dark adaptation.

56 eria and plant plastids, contributes to this dark adaptation.

57 sensitivity in the macula, and rod-mediated dark adaptation.

58 choroidal thickness might affect the rate of dark adaptation.

59 mal cone-driven vision and accelerating cone dark adaptation.

60 se of the PFDA as a reliable tool to measure dark adaptation.

61 at rods suppress, whereas RPE promotes, cone dark adaptation.

62 ed so at month 36 with no clinical impact on dark adaptation.

63 ion of cone function, it did not rescue cone dark adaptation.

64 cycle dramatically accelerated the mouse rod dark adaptation.

65 he retina visual cycle is key for rapid cone dark adaptation.

66 ange their distribution in rods during light/dark adaptation.

67 dosing did not induce changes in kinetics of dark adaptation.

68 he retinas in awake animals during light and dark adaptation.

69 on of TRPL in the rhabdomeres upon prolonged dark-adaptation.

70 enhanced degradation of TRPL after prolonged dark-adaptation.

71 oncentrations >1.4 micromol/L predict normal dark adaptation 95% of the time.

72 s carrying a A249T mutation, such that after dark-adaptation a significant percentage of the QA sites

73 with alitretinoin: an asymptomatic delay in dark adaptation, a marked decrease in high-density lipop

74 r a full bleach, the patients showed typical dark adaptation abnormalities reported for these disease

75 er rod-b wave recovery consistent with early dark adaptation abnormalities, accumulation of hyperauto

76 Early phenotypic features of L-ORD include: dark adaptation abnormalities, nyctalopia, and drusen de

77 Dark-adaptation abnormalities can precede symptoms and f

78 24 hours of exposure or at 6 or 24 hours of dark adaptation after 24 hours of light exposure.

79 regeneration, 11-cis-retinal production, and dark adaptation after illumination are delayed by >10-fo

80 targardt disease exhibit abnormally slow rod dark adaptation after illumination that bleaches a subst

81 This phenotype is exacerbated with dark adaptation, age and in white mutants.

82 n ERG responses, such as a decreased rate of dark adaptation and a lowered rhodopsin/opsin ratio.

83 terval of 80 ms was ~fourfold after 5 min of dark adaptation and approximately twofold after 20 min.

84 ween any of the two measures of rod-mediated dark adaptation and choroidal thickness (time to rod int

85 nuclei in the ONL is required for the timely dark adaptation and efficient synaptic transmission in c

86 n of the donor had normal fundi but abnormal dark adaptation and electroretinography.

87 o its well-established role during long-term dark adaptation and etiolation.

88 lly this is manifest as delayed rod-mediated dark adaptation and eventually as rod-mediated visual dy

89 e imaged 5 of the patients after a period of dark adaptation and examined layer reflectivity on optic

90 ation of 9-cis-retinal increased the rate of dark adaptation and improved cone function in Rdh5-/-Rdh

91 ght blindness because of markedly slowed rod dark adaptation and in some patients, macular atrophy.

92 of the retinylidene chromophore during light-dark adaptation and photochemical reactions of Anabaena

93 vitamin A from food or synthetic sources on dark adaptation and plasma retinol concentrations in nig

94 hown in physiological experiments to promote dark adaptation and recovery of photoresponsiveness of b

95 rdt phenotypes, such as improved recovery of dark adaptation and reduced lipofuscin granules.

96 evels of rhodopsin protein, and the rates of dark adaptation and rhodopsin regeneration.

97 osphorylation/dephosphorylation during light/dark adaptation and the subsequent effects on G(t)beta g

98 roperimeter grid pattern after 20 minutes of dark adaptation and without dilation.

99 econdary behavioral screens measuring visual dark-adaptation and learning suggest that the defects we

100 al equilibration of retinal isomeric states (dark adaptation) and the deprotonation kinetics of the S

101 ction deficits in reading, night vision, and dark adaptation, and produce dense, irreversible scotoma

102 ity, cone-mediated sensitivity, rod-mediated dark adaptation, and SDOCT were obtained in 1 eye per su

103 Although night blindness and delayed dark adaptation are hallmarks of this condition, recent

104 to the IS/ST and its return to the OS during dark adaptation are not well understood.

105 s, together with the increase in the rate of dark adaptation as the temperature increases, leads to a

106 ikely to have greater change in the speed of dark adaptation, as indicated by the rod slope parameter

107 Rod-mediated dark adaptation at 5 degrees reached the test ceiling in

108 Dark adaptation at dusk triggered extensive widening of

109 Notably, their cone-driven dark adaptation both in vivo and in isolated retina was

110 Following a 5-minute period of dark adaptation, both static and dynamic pupillographic

111 rans <=> 13-cis thermal isomerization during dark adaptation but also of the reisomerization of the c

112 ure and had no effect on cone sensitivity or dark adaptation but did slightly accelerate the rate of

113 PTA-AM blocked Ser-54 phosphorylation during dark adaptation but had no effect on Ser-73 phosphorylat

114 3, the pigment is purple and shows light and dark adaptation, but almost no light-induced Schiff base

115 ur results do not support that variations in dark adaptation can be attributed to variations in choro

116 Objective measurement of dark adaptation can facilitate early diagnosis to enable

117 Moreover, complete dark adaptation can only occur when all rhodopsin has be

118 In more severe cases of AMD, dark adaptation cannot always be recorded within a maxim

119 six-month treatment with vitamin A shortened dark adaptation considerably in one affected member.

120 c patients experience functional deficits in dark adaptation, contrast sensitivity, and color percept

121 ents often experience functional deficits in dark adaptation, contrast sensitivity, and color percept

122 his daily melatonin-driven modulation of rod dark adaptation could potentially protect the retina fro

123 The outcome measures were the area under dark adaptation curve (AUDAC) and the time for visual se

124 The early, linear part of the rod-mediated dark adaptation curve was analyzed to extract the time r

125 e associated with their performance on focal dark adaptation (DA) testing and with choroidal thicknes

126 One study eye per participant underwent dark adaptation (DA) testing to measure rod intercept ti

127 Impaired dark adaptation (DA), a defect in the ability to adjust

128 n-based characteristics were associated with dark adaptation (DA).

129 s by knocking out rhodopsin accelerated cone dark adaptation, demonstrating the interplay between rod

130 These results indicate that the effects of dark adaptation depend on the time of day and are regula

131 During dark adaptation, dephosphorylation of rhodopsin occurs i

132 Improvement in dark adaptation did not differ significantly between wom

133 xustat-treated larvae raised under extensive dark-adaptation displayed significantly attenuated immed

134 Delayed dark adaptation due to impaired rod photoreceptor homeos

135 markably, the mouse retina promoted M/L-cone dark adaptation eightfold faster than the RPE.

136 ld fundus imaging, retinal autofluorescence, dark adaptation, electroretinography (ERG), Goldmann kin

137 l of the subjects were given pupil light and dark adaptation examination and optical coherence tomogr

138 r has previously been seen in psychophysical dark adaptation experiments, for the dependence of the '

139 Part two involves 20 min of dark adaptation followed by two-colour scotopic microper

140 In contrast, rod dark adaptation following exposure to bright bleaching l

141 ht-adapted conditions, but exhibited delayed dark adaptation following high bleaching levels.

142 However, dark adaptation for as little as 8 h triggers a switch t

143 persisted in cyclic light-reared rats after dark adaptation for up to 3 additional days.

144 The biphasic dark adaptation functions resulting from fractional blea

145 Psychophysical dark adaptation functions were measured after bleaching

146 related macular degeneration (AMD) research, dark adaptation has been found to be a promising functio

147 Dark adaptation has been used as a tool for identifying

148 Over the last two decades, ERG studies of dark adaptation have generated insights into underlying

149 After 2 hr of dark adaptation, however, visual thresholds of nbb(+/-)

150 05, repeated-measures analysis of variance); dark adaptation improved in 5 dyslexia patients after su

151 ophore structural changes to those caused by dark adaptation in bacteriorhodopsin.

152 gth had no detectable effect on rod-mediated dark adaptation in healthy young subjects.

153 f retinol increased the rate of rod-mediated dark adaptation in older adults who were in the early ph

154 limit the efficacy of vitamin A to normalize dark adaptation in pregnant Nepali women.

155 litude of these oscillatory potentials after dark adaptation in seven patients with type 2 diabetes a

156 decreased oscillatory potentials induced by dark adaptation in the diabetic patients increased durin

157 w cost, and easily operated device to assess dark adaptation in the field.

158 Finally, we also observed cone dark adaptation in the isolated mouse retina.

159 ure, and/or changes in polarity occur during dark adaptation in the S(1) state.

160 0 x 20 x 700 mum was used to study light and dark adaptation in the same animals (N = 10) in which on

161 There is no detectable dark-adaptation in PR, and the chromophore contains near

162 Other causes of abnormal dark adaptation include zinc and protein deficiencies.

163 Mice lacking RmP show delayed dark adaptation, increased all-trans-retinaldehyde (all-

164 s for retina-derived chromophore slowed cone dark adaptation, indicating that the cone specificity of

165 icroM rifampicin to illuminated cells before dark adaptation inhibited the transcription of lrtA in t

166 systemic injection of MnCl2 during light or dark adaptation; inner and outer retinal signal intensit

167 Dark adaptation is an energy-requiring process in the ou

168 Aberrant dark adaptation is common to many ocular diseases and pa

169 on the observation that the rate constant of dark adaptation is directly proportional to the fraction

170 ngs demonstrate that mammalian photoreceptor dark adaptation is dominated by the supply of chromophor

171 The dominant factor that limits dark adaptation is isomerization of retinal.

172 Delayed dark adaptation is likely due to accumulation in discs o

173 the return of GtalphaQ200L to the OS during dark adaptation is markedly slower than normal.

174 the recycling of chromophore that drives rod dark adaptation is regulated by the circadian clock and

175 Here, we demonstrate that mouse rod dark adaptation is slower during the day or after light

176 Rod-mediated dark adaptation is the only visual function of those tes

177 in the pH dependence of the rate constant of dark adaptation, k(da).

178 o intrinsic signal optoretinography (ORG) of dark adaptation kinetics in the C57BL/6J mouse retina.

179 Functional OCT of dark adaptation kinetics promises an objective method fo

180 Dark adaptation kinetics was normal.

181 Dark adaptation kinetics, the primary efficacy endpoint,

182 Dark-adaptation kinetics were abnormal in 6 of 12.

183 adaptation (SA) and those recorded after 3 h dark adaptation (LA).

184 Cone myoid elongation occurs during dark adaptation, leading to the positioning of the cone

185 y unappreciated mechanism by which prolonged dark adaptation leads to increased light sensitivity in

186 ERG tracking of dark adaptation may prove useful in future clinical cont

187 y eye per participant underwent rod-mediated dark adaptation, measuring rod intercept time (RIT) at 5

188 l processes and SDD in eyes with AMD, slower dark adaptation might be related to structural abnormali

189 tinal manganese uptake compared with that in dark adaptation; no effect on inner retinal uptake was f

190 Impaired dark adaptation occurs commonly in vitamin A deficiency.

191 2) Thermal isomerization of the chromophore (dark adaptation) occurs on transient protonation of Asp-

192 st and psbD transcription were studied after dark adaptation of 21-day-old light-grown Arabidopsis pl

193 n maximum and strongly decreases the rate of dark adaptation of ASR, confirming interaction between t

194 lbipunctatus, a disease expressed by delayed dark adaptation of both cones and rods.

195 Without this pathway, dark adaptation of cones was slow and incomplete.

196 In contrast, dark adaptation of cones was unaffected by the S21A muta

197 cassette transporter (ABCA4) accelerate the dark adaptation of cones, first, directly, by facilitati

198 on of cone arrestin suggests a role in light-dark adaptation of cones.

199 he deletion of RDH8 and ABCA4 suppressed the dark adaptation of M-cones driven by both the intraretin

200 the roles of rod photoreceptors and RPE for dark adaptation of M-cones.

201 This pathway supports rapid dark adaptation of mammalian cones and extends their dyn

202 P-binding cassette transporter 4 (ABCA4), in dark adaptation of mammalian cones.

203 Light sensitizes the animals; thus early dark adaptation of nbb(+/-) fish is normal.

204 sual pigment dephosphorylation regulates the dark adaptation of photoreceptors and provide insights i

205 grams, and show only modest anomalies in the dark adaptation of photoreceptors.

206 nt phosphorylation of GRK1 in regulating the dark adaptation of rod but not cone photoreceptors.

207 The dark adaptation of the pigment and the last step of the

208 Continuous visual perception and the dark adaptation of vertebrate photoreceptors after brigh

209 Zinc deficiency may result in abnormal dark adaptation or night blindness, a symptom primarily

210 ot statistically different between light and dark adaptation (P > 0.05).

211 At 30-days, the dark-adaptation parameters of cone time-constant, cone t

212 The overall dark-adaptation period required for half-completion of 1

213 After closing the channels by dark adaptation, phosducin or inactive Galphao (both seq

214 ion between the time-to-rod-intercept or the dark adaptation rate and axial length, refraction, gende

215 Their fast dark adaptation rate and resistance to saturation are be

216 and 9-cis-retinals, respectively, improving dark-adaptation rates as well as survival and function o

217 sually responsive SCN neurones studied under dark adaptation received rod input (48 of 52, 92 %).

218 toreceptor function and delayed rod-mediated dark adaptation recovery, and pathological age-related m

219 n sensitivity was normal for both lines, and dark-adaptation recovery after bleaching rhodopsin was n

220 ologic visual cycle inhibition and prolonged dark adaptation-reduce photoreceptor anabolic lipid meta

221 apted conditions, but had a further delay in dark adaptation relative to either rdh11-/- or rdh5-/- m

222 Dark adaptation requires timely deactivation of phototra

223 Compared to the better-studied long-term dark adaptation response, the early response to darkness

224 Upon prolonged dark adaptation, RGS9-1 and Gbeta5L are primarily locate

225 Furthermore, after prolonged dark adaptation, RGS9-1 and transducin Galpha are locate

226 in early AMD, including delayed rod-mediated dark adaptation (RMDA) and impaired rod-mediated light a

227 dus-controlled perimetry [FCP], rod-mediated dark adaptation [RMDA]), and multimodal imaging.

228 ds (scotopic light sensitivity, rod-mediated dark adaptation [RMDA]).

229 CS, and rod intercept time (for rod mediated dark adaptation, RMDA) were worse in eyes with LHyperTD

230 e were compared, those recorded after 10 min dark adaptation (SA) and those recorded after 3 h dark a

231 In each subject the time course of dark adaptation, scotopic visual field sensitivity, and

232 idized and used for pigment regeneration and dark adaptation selectively in cones and not in rods.

233 ral retinas promote pigment regeneration and dark adaptation selectively in cones, but not in rods.

234 43 vs. 70.64+/-47.14 seconds; P = 0.001) and dark adaptation speed (12.80+/-5.15 vs. 9.74+/-2.56 minu

235 ing the molecular defects that cause delayed dark adaptation suggest that the desensitizing substance

236 rods, but not cones, change intensity after dark adaptation suggests that fundus changes in Oguchi d

237 phosphorylation increased much faster during dark adaptation (t((1/2)) approximately 3 min) to approx

238 Dark adaptation testing was performed using the AdaptDx

239 ence tomography (OCT), color vision testing, dark adaptation testing, full-field electroretinography

240 The improvement in pupillary dark-adaptation testing was not significant for children

241 omote cone-specific pigment regeneration and dark adaptation that are independent of the pigment epit

242 uces a strong effect on the pH dependence of dark adaptation that is interpreted as a drastic reducti

243 In the visual dark adaptation, the fundamental molecular event after p

244 On removal from dark adaptation, the intensity of the rods (but not cone

245 After 30 minutes of dark adaptation, the same eye underwent scotopic micrope

246 veral minutes without undergoing significant dark-adaptation, their vision remaining effectively adap

247 sholds were elevated so that by 14-18 min of dark adaptation, they were 2-3 log units above those of

248 We sought to examine the responsiveness of dark-adaptation threshold to vitamin A and beta-carotene

249 Dark-adaptation threshold was associated with serum reti

250 measured with the Goldmann perimeter, final dark-adaptation threshold, full-field electroretinogram

251 sing trial with pre- and postdose testing of dark-adaptation threshold.

252 ed with those in exons 1-14, had worse final dark adaptation thresholds and lower 0.5-Hz and 30-Hz ER

253 score, visual acuity, contrast sensitivity, dark adaptation thresholds, visual field parameters, and

254 measurement of Snellen visual acuity, final dark adaptation thresholds, visual fields, and ERGs.

255 regnant women receiving vitamin A had better dark-adaptation thresholds (-1.24 log cd/m(2)) than did

256 Among women receiving placebo, mean dark-adaptation thresholds were better during the first

257 tatistically significant difference in final dark-adaptation thresholds, visual field diameters, or c

258 or inner segments and delays the kinetics of dark adaptation through modulation of calcium homeostasi

259 s (SDD) vs 47 eyes without SDD, rod-mediated dark adaptation time was longer (mean +/- SD 13.5 +/- 7.

260 Longer rod-mediated dark adaptation time, the duration for rod-mediated sens

261 h-dose vitamin A accelerates the kinetics of dark adaptation to a limited degree.

262 lowly (t((1/2)) approximately 90 min) during dark adaptation to approximately 70% phosphorylated and

263 Initially during dark adaptation, transduction activity wanes as multiple

264 vesicle number at the ribbon after light and dark adaptation using electron microscopy.

265 gorithm 24-2 strategy, contrast sensitivity, dark adaptation, visual acuity, and quality of life) and

266 lgorithm 24-2 testing, contrast sensitivity, dark adaptation, visual acuity, and quality of life) and

267 During the first 6-8 min of dark adaptation, visual thresholds of DA-IPC-depleted an

268 The activity encoding of the light and dark adaptation was achieved in awake conditions and ima

269 The rate of dark adaptation was analyzed using electroretinography (

270 Dark adaptation was assessed by PT score.

271 Rod-mediated dark adaptation was assessed in 1 eye after photobleach

272 Dark adaptation was assessed weekly by using the pupilla

273 Rate of dark adaptation was defined by rod intercept time (RIT),

274 Dark adaptation was delayed by a factor of 2.5-3 compare

275 Dark adaptation was delayed by a factor of approximately

276 Improvement in dark adaptation was greater in the liver group than in t

277 cts in cones with mislocalized nuclei, their dark adaptation was impaired, consistent with a deficien

278 Additionally, M-cone dark adaptation was largely suppressed in CRALBP-deficie

279 Dark adaptation was monitored by electroretinography.

280 kinetics of 11-cis-retinal recycling during dark adaptation was not affected, suggesting that mRDH11

281 In the preliminary studies reported here, dark adaptation was shown to be impaired in 10 dyslexic

282 ertheless, translocation following prolonged dark adaptation was significantly slower in ninaC mutant

283 We found that dark adaptation was slower in Adfp(Delta2-3/Delta2-3) th

284 During pregnancy, pupillary dark adaptation was strongly associated with serum retin

285 At baseline and 30-day follow-up, dark adaptation was tested and the Low Luminance Questio

286 Notably, the rate of rod dark adaptation was unaffected by age.

287 However, rod dark adaptation was unaffected by the expression of RDH1

288 During daytime, only partial dark-adaptation was achieved and rhabdoms remained narro

289 The kinetics of dark adaptation were abnormal in all patients.

290 rey visual fields, photostress recovery, and dark adaptation were assessed.

291 right, steady light and the kinetics of cone dark adaptation were not affected in isolated retina or

292 Whereas rod-mediated parameters of dark adaptation were significantly associated with LLQ s

293 metabolic demand in the body particularly in dark adaptation when its sensitivity is enhanced.

294 One had fundus lesions and abnormal dark adaptation, whereas the others had normal fundi and

295 egeneration of mouse M/L-cone pigment during dark adaptation, whereas the slower RPE visual cycle is

296 3%) of 22 patients had reversible changes in dark adaptation, which correlated with relative decrease

297 escing leaves failed to recover after 6 h of dark adaptation, which suggests photo-oxidative damage.

298 study has directly compared the kinetics of dark adaptation with rates of the various chemical react

299 with VF, VA, contrast sensitivity (CS), and dark adaptation, with different predictive values depend

300 st were rod- and cone-mediated parameters of dark adaptation, with scores on the LLQ's six subscales