ライフサイエンスコーパス: night blindness

1 inical vitamin A deficiency (Bitot spots and night blindness).

2 otinib was limited by toxicities, especially night blindness.

3 ith the Nougaret form of dominant stationary night blindness.

4 l molecular mechanism in dominant stationary night blindness.

5 were diarrhea, skin rash, hyperglycemia, and night blindness.

6 deficiency that causes congenital stationary night blindness.

7 se have Oguchi disease, a form of stationary night blindness.

8 85 with recessive RP, and 10 with stationary night blindness.

9 li women with (cases) and without (controls) night blindness.

10 e identified in the patients with stationary night blindness.

11 netic heterogeneity in congenital stationary night blindness.

12 efect is implicated as a cause of stationary night blindness.

13 is pigmentosa (RP) and congenital stationary night blindness.

14 eceptor molecule rhodopsin causes congenital night blindness.

15 of CORD except that patients did not report night blindness.

16 only 54% of the patients with CSNB2 reported night blindness.

17 ion and are a model of congenital stationary night blindness.

18 mission, resulting in a novel mouse model of night blindness.

19 teins lead to complete congenital stationary night blindness.

20 activity and leads to congenital stationary night blindness.

21 an autosomal recessive congenital stationary night blindness.

22 and is referred to as congenital stationary night blindness.

23 een linked to autosomal-recessive stationary night blindness.

24 factors resulting in retinal dysfunction and night blindness.

25 rods, provide an animal model for congenital night blindness.

26 rget through which the retinoic acids induce night blindness.

27 ected in autosomal dominant human congenital night blindness.

28 Congenital stationary night blindness 1, despite different causative mutations

29 Congenital stationary night blindness 2 caused by mutations in CABP4 merely sh

30 Congenital stationary night blindness 2 was primarily caused by mutations in C

31 reduced, but did not eliminate, gestational night blindness (7.1% for vitamin A vs 9.2% for placebo

32 We have isolated a dominant mutation, night blindness a (nba), that causes a slow retinal dege

33 r the complete form of congenital stationary night blindness, a human disorder in which patients have

34 cy may result in abnormal dark adaptation or night blindness, a symptom primarily of vitamin A defici

35 nown rhodopsin mutants that cause congenital night blindness, A292E and G90D, have been shown in vitr

36 inal diseases, such as congenital stationary night blindness, albinism, blue cone monochromatism, and

37 rnal death during and after a pregnancy with night blindness among women participating in a cluster-r

38 Subjects were 877 women with night blindness and 9,545 women without night blindness

39 vessels, ultimately resulting in progressive night blindness and constriction of the visual field.

40 vessels, ultimately resulting in progressive night blindness and constriction of the visual field.

41 Although night blindness and delayed dark adaptation are hallmark

42 le, children with ESCS had an early onset of night blindness and hyperopia but no nystagmus.

43 fer from vitamin A deficiency are plagued by night blindness and longer vision-restoration times.

44 neration of the peripheral retina leading to night blindness and loss of peripheral visual field.

45 neration of the peripheral retina leading to night blindness and loss of visual fields.

46 ssociated with a congenital variant of human night blindness and other closely related nonstationary

47 ally heterogeneous disorder characterized by night blindness and peripheral vision loss, and in many

48 RP is characterized by night blindness and progressive degeneration of the midp

49 osa (adRP), a rare disorder characterized by night blindness and progressive vision loss.

50 nal diseases including congenital stationary night blindness and retinitis pigmentosa.

51 ned for mutations with congenital stationary night blindness and RP genotyping arrays.

52 Although the predominant clinical symptom of night blindness and the electroretinography results sugg

53 sociated with greater awareness of cataract, night blindness and trachoma (p<0.05).

54 with lower awareness of cataract, glaucoma, night blindness and trachoma (p<0.05).

55 of cataract, glaucoma, diabetic retinopathy, night blindness and trachoma (p<0.05).

56 of cataract, glaucoma, diabetic retinopathy, night blindness and trachoma compared to those from a se

57 tic condition that causes visual symptoms of night-blindness and photopsias.

58 presented with photopsias, 56% (14/25) with night blindness, and 56% (14/25) with loss of peripheral

59 carrying LCA5 mutations presented nystagmus, night blindness, and progressive loss of visual acuity a

60 ummary statistics on iron deficiency anemia, night blindness, and risk of zinc deficiency are summari

61 of cataract, glaucoma, diabetic retinopathy, night blindness, and trachoma.

62 hanisms by which human NCKX1 mutations cause night blindness are not understood.

63 , such as retinitis pigmentosa or congenital night blindness, are linked to rhodopsin malfunctions.

64 racterized in the early stages of disease by night blindness as a result of rod photoreceptor loss, p

65 T94I may play a causative role in congenital night blindness as has been suggested by the Oprian and

66 ized, autosomal recessive form of congenital night blindness associated with a negative ERG waveform.

67 We previously isolated a dominant mutation, night blindness b (nbb), which causes a late onset of re

68 We describe here a dominant mutation, night blindness b (nbb), which causes an age-related vis

69 omolog of the Stil gene in zebrafish mutant (night blindness b, nbb), which showed neural defects in

70 All patients had night blindness (before age 6 years in 10).

71 sed in the treatment of acne but that causes night blindness, binds to RPE65 with a K(D) of 195 nM.

72 Night blindness can result from impaired photoreceptor f

73 patients with complete congenital stationary night blindness caused by mutations in GRM6, 2 brothers

74 anding the molecular mechanism of congenital night blindness caused by the G90D mutation in human rho

75 Complete congenital stationary night blindness (cCSNB) is a clinically and genetically

76 Complete congenital stationary night blindness (cCSNB) is associated with loss of funct

77 dus albipunctatus, a rare form of stationary night blindness characterized by a delay in the regenera

78 atus (FA) is a form of congenital stationary night blindness characterized by yellow-white spots, whi

79 e been associated with congenital stationary night blindness, considered to be a relatively nonprogre

80 ized by progressive photoreceptor cell loss, night blindness, constriction of the visual field, and p

81 eta has been linked to congenital stationary night blindness (CSNB) in a large Danish family (Rambusc

82 rectly associated with congenital stationary night blindness (CSNB) in Appaloosa horses.

83 Congenital stationary night blindness (CSNB) is a heterogeneous group of non-p

84 ocular albinism (OA), congenital stationary night blindness (CSNB), and blue-cone monochromatism (BC

85 ction resembling human congenital stationary night blindness (CSNB), characterized by the loss of the

86 without cells included congenital stationary night blindness (CSNB), LCA, Stargardt disease, and blue

87 tinitis pigmentosa and congenital stationary night blindness (CSNB).

88 complete form of human congenital stationary night blindness (CSNB).

89 patients with complete congenital stationary night blindness (CSNB1), where signaling through the ON

90 form of human X-linked congenital stationary night blindness (CSNB1).

91 n humans with complete congenital stationary night blindness (CSNB1).

92 ith that of incomplete congenital stationary night blindness (CSNB2) patients.

93 wn to cause incomplete congenital stationary night blindness (CSNB2).

94 s a recessively inherited form of stationary night blindness due to malfunction of the rod photorecep

95 Night blindness due to vitamin A deficiency is common du

96 We describe a case of night blindness due to vitamin A deficiency resulting fr

97 ated hyporetinolemia may predispose women to night blindness during pregnancy in Nepal.

98 These findings show that night blindness during pregnancy is a risk factor of bot

99 ced but failed to eliminate the incidence of night blindness during pregnancy, suggesting a role for

100 with night blindness and 9,545 women without night blindness during pregnancy.

101 retinitis pigmentosa (RP) typically develop night blindness early in life due to loss of rod photore

102 Patients with congenital stationary night blindness enjoy normal daytime vision, which is me

103 man Hermansky-Pudlak syndrome and congenital night blindness, for which the pearl mouse is an appropr

104 Vitamin A deficiency and resulting night blindness have previously been reported in patient

105 world's population with consequences such as night blindness, higher child mortality, anemia, poor pr

106 forms part of the differential diagnosis of night blindness in childhood.

107 psin mutation is known to produce congenital night blindness in humans.

108 dominant retinitis pigmentosa and congenital night blindness in humans.

109 known to cause autosomal dominant congenital night blindness in humans.

110 e, an autosomal recessive form of stationary night blindness in man characterized in part by delayed

111 ity of rhodopsin, potentially accounting for night blindness in the early stages of RP.

112 he relative risk among women with or without night blindness in the vitamin A/beta-carotene group was

113 One form of dominantly inherited congenital night blindness is eponymously named "Nougaret' because

114 The Nougaret form of dominant stationary night blindness is linked to a G38D mutation in the rod

115 argardt's disease, and congenital stationary night blindness is presented, along with a guide for cli

116 s involved in rod phototransduction cascade; night blindness is the only symptom and eye examination

117 hic diseases, is characterized by late-onset night blindness, loss of peripheral vision, and diminish

118 naptic disruption differed from other murine night-blindness models with an electronegative electrore

119 , the one phenotype shared by all congenital night blindness mutants that is different from the wild-

120 chromophore), like the other known rhodopsin night blindness mutants, is not active in the dark and h

121 However, in contrast to the other night blindness mutants, the T94I MII intermediate decay

122 nd compared to the two other known rhodopsin night blindness mutants.

123 This effect does not appear to be general to night blindness mutations as the two other mutants (A292

124 examination of the effect of three rhodopsin night blindness mutations on the rate of association of

125 ople with ESCS also suffer visual loss, with night blindness occurring from early in life, varying de

126 ypes are associated with variable degrees of night blindness or photophobia, reduced visual acuity, h

127 in arrestin are a cause of RP or stationary night blindness other than Oguchi disease.

128 reported to be associated with a congenital night blindness phenotype in a large Irish pedigree.

129 ciated retinopathy (MAR) is characterized by night blindness, photopsias, and a selective reduction o

130 The loss of GPR179 in a mouse model of night blindness prevented targeting of RGS to the postsy

131 al degenerations characterized clinically by night blindness, progressive constriction of the visual

132 splantation into a mouse model of stationary night-blindness, raising the critical question of whethe

133 ed with Fundus albipunctatus, a mild form of night blindness (RDH5) and an autosomal recessive, child

134 stered isotretinoin to rats to learn whether night blindness resulted from rod cell death or from rod

135 The affected patients had night blindness since early childhood, consistent with a

136 showed symptoms early in life, ranging from night blindness to decreased visual acuity, and were dia

137 with poorer awareness of cataract, glaucoma, night blindness, trachoma and diabetic retinopathy (p<0.

138 ocular diseases, namely cataract, glaucoma, night blindness, trachoma and diabetic retinopathy in Ne

139 nder (p<0.05) whereas awareness of cataract, night blindness, trachoma and diabetic retinopathy was a

140 in the development of congenital stationary night blindness type 1 (CSNB1).

141 gene cause incomplete congenital stationary night blindness type 2 (CSNB2), a non-progressive, clini

142 associated with human congenital stationary night blindness type-2.

143 , we have examined the mechanism of Nougaret night blindness using transgenic mice expressing TalphaG

144 Age at diagnosis; age at onset of night blindness, visual field loss, visual acuity loss,

145 nished generally many years before symptomic night blindness, visual-field scotomas, or decreased vis

146 cataract across the entire sample was 49.6%, night blindness was 48.3%, diabetic retinopathy was 29%,

147 wareness of cataract, glaucoma, trachoma and night blindness was associated with female gender (p<0.0

148 To elucidate the mechanism of Nougaret night blindness, we have examined the key functional pro

149 Supplement use and daily history of night blindness were obtained at home twice every week.

150 o the retinal disorder congenital stationary night blindness which is characterized by defective nigh

151 night vision of pregnant women who developed night blindness while routinely receiving either vitamin

152 The mother developed night blindness with undetectable serum vitamin A concen