ライフサイエンスコーパス: dark adaptation

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

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

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

4 nd Rdh8 knockout mice displayed only delayed dark adaptation.

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

6 sicles at presynaptic ribbons after light or dark adaptation.

7 exhibited a similar time course of neuronal dark adaptation.

8 a critical contributing factor to light and dark adaptation.

9 overed progressively in darkness, indicating dark adaptation.

10 recycling capacity of ABCA4 and may improve dark adaptation.

11 rious intensities of illumination and during dark adaptation.

12 e full recovery of visual sensitivity during dark adaptation.

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

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

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

16 robe flash presented at varying times during dark adaptation.

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

18 11-cis-retinal and opsin affects the rate of dark adaptation.

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

20 ogram amplitudes were normal after prolonged dark adaptation.

21 LBP gene cause retinal pathology and delayed dark adaptation.

22 precedes sensitivity recovery, thus slowing dark adaptation.

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

24 hom had punctate fundus lesions and abnormal dark adaptation.

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

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

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

28 onstriction was recorded after bleaching and dark adaptation.

29 or completely dephosphorylated after a long dark adaptation.

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

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

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

33 choroidal thickness might affect the rate of dark adaptation.

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

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

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

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

38 hore recycling, and ultimately photoreceptor dark adaptation.

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

40 cycle dramatically accelerated the mouse rod dark adaptation.

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

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

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

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

45 e after photobleaching, suggesting a delayed dark adaptation.

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

47 li of various durations were presented after dark adaptation.

48 contrast sensitivity, color perception, and dark adaptation.

49 ole in mediating gene repression to maintain dark adaptation.

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

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

52 uppresses bleached rhodopsin activity during dark adaptation.

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

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

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

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

57 enhanced degradation of TRPL after prolonged dark-adaptation.

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

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

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

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

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

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

64 Dark-adaptation abnormalities can precede symptoms and f

65 24 hours of exposure or at 6 or 24 hours of dark adaptation after 24 hours of light exposure.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 3, the pigment is purple and shows light and dark adaptation, but almost no light-induced Schiff base

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

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

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

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

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

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

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

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

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

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

104 During dark adaptation, dephosphorylation of rhodopsin occurs i

105 Improvement in dark adaptation did not differ significantly between wom

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

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

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

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

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

111 The biphasic dark adaptation functions resulting from fractional blea

112 Psychophysical dark adaptation functions were measured after bleaching

113 Dark adaptation has been used as a tool for identifying

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

115 05, repeated-measures analysis of variance); dark adaptation improved in 5 dyslexia patients after su

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

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

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

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

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

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

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

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

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

125 0 x 20 x 700 mum was used to study light and dark adaptation in the same animals (N = 10) in which on

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 Dark adaptation kinetics was normal.

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

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

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

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

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

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

149 Impaired dark adaptation occurs commonly in vitamin A deficiency.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 Dark adaptation requires timely deactivation of phototra

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

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

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

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

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

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

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

183 43 vs. 70.64+/-47.14 seconds; P = 0.001) and dark adaptation speed (12.80+/-5.15 vs. 9.74+/-2.56 minu

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

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

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

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

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

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

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

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

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

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

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

195 Dark-adaptation threshold was associated with serum reti

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

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

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

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

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

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

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

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

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

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

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

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

208 Initially during dark adaptation, transduction activity wanes as multiple

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

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

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

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

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

214 The rate of dark adaptation was analyzed using electroretinography (

215 Dark adaptation was assessed by PT score.

216 Dark adaptation was assessed weekly by using the pupilla

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

218 Dark adaptation was delayed by a factor of approximately

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

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

221 Dark adaptation was monitored by electroretinography.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

236 3%) of 22 patients had reversible changes in dark adaptation, which correlated with relative decrease

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

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

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