ライフサイエンスコーパス: lens opacity

1 a common and clinically significant form of lens opacity.

2 ll aberrations as well as the development of lens opacity.

3 ropic lens fibers and homozygotes show total lens opacity.

4 ng of the gamma-crystallin(s) and results in lens opacity.

5 reared under standard conditions produced no lens opacity.

6 correlates positively with the preoperative lens opacity.

7 nt risk factors associated with each type of lens opacity.

8 egation, insolubilization, and mild cortical lens opacity.

9 notype comprised of microphthalmic eyes with lens opacity.

10 series, 5.9% required lensectomy because of lens opacity.

11 nd MAP kinases in signaling the induction of lens opacities.

12 ent intakes and age-related cortical and PSC lens opacities.

13 of SFK activity suppresses the formation of lens opacities.

14 sociated inversely with nuclear and cortical lens opacities.

15 tially reduce the development of age-related lens opacities.

16 ins may affect the occurrence of age-related lens opacities.

17 only lens opacities, and 88 (2.5%) had mixed lens opacities.

18 usen were independent risk factors for mixed lens opacities.

19 independent risk factors for incident mixed lens opacities.

20 ndependent risk factor for incident PSC-only lens opacities.

21 27 had PSC only opacities, and 364 had mixed lens opacities.

22 acuity after DSEK in cases with significant lens opacities.

23 (when >1 opacity type developed in a person) lens opacities.

24 rmalities, as well as a higher rate of minor lens opacities.

25 abetes were independent risk factors for PSC lens opacities.

26 re independent risk factors for nuclear only lens opacities.

27 cident nuclear-only, cortical-only and mixed lens opacities.

28 prevention may reduce the risk of developing lens opacities.

29 e independent risk factors for cortical only lens opacities.

30 ns and protocols were used to define OAG and lens opacities.

31 nuclear, cortical, and posterior subcapsular lens opacities.

32 mapped an autosomal semi-dominant cataract [lens opacity 10 (Lop10)] mutation to mouse chromosome 3

33 Lens opacity 11 (lop11) is an autosomal recessive mouse

34 Lens opacity 12 (Lop12) is a semidominant mutation that

35 etrant gene, which we have designated lop18 (lens opacity 18).

36 py injection (2 eyes) and nonaxial posterior lens opacity (2 eyes).

37 with gradable lenses, 468 had cortical only lens opacities, 217 had nuclear only lens opacities, 27

38 al only lens opacities, 217 had nuclear only lens opacities, 27 had PSC only opacities, and 364 had m

39 Incident cataract was defined as a lens opacity, age related in origin, and responsible for

40 nces in the prevalence of different types of lens opacities and cataract surgery.

41 ystallin at near-physiological levels causes lens opacities and fiber cell defects, confirming the pa

42 enter for cortical and posterior subcapsular lens opacities and for AMD severity.

43 The results show that lens opacities and posterior sutural defects occur when

44 d 6/18 OS, bilateral corneal decompensation, lens opacities and raised intraocular pressures 4 years

45 crystallin subunits are sufficient to induce lens opacities and sutural defects.

46 ontrol may help to reduce the risk of having lens opacities and their associated vision loss.

47 cross-sectional relation between age-related lens opacities and vitamin C supplement use over a 10-12

48 n 28 patients with (DM-1) and without (DM-0) lens opacity and 18 controls.

49 in those without any clinically significant lens opacity and in persons with visual acuity better th

50 eight was associated with the development of lens opacity and phacoemulsification (P = .005 and .008,

51 y opacities, 16 (0.5%) had incident PSC-only lens opacities, and 88 (2.5%) had mixed lens opacities.

52 Instead, the lens opacities appeared to result from gross abnormaliti

53 Lens opacities are present in 9.3-44 % (five studies).

54 and may be useful for centralized objective lens opacity assessment in clinical trials using widely

55 Association of the change in lens opacities at 2 years with these outcomes at 5 years

56 Significant QTL with effects on lens opacity at 24 months were detected on mouse chromos

57 ls in persons without clinically significant lens opacity at each preceding examination (interval 1,

58 nces in the prevalence of different types of lens opacities by racial group.

59 For cataract, a high grade of lens opacity by biomicroscopy to which best-corrected vi

60 f intraocular inflammation and assessment of lens opacity by the Lens Opacities Classification System

61 or eyes with only a single, or pure, type of lens opacity by using the generalized estimating approac

62 lly in those with ocular inflammation, ARMD, lens opacities/cataract, and thyroid-associated orbitopa

63 s, cytoskeletal proteins, and crystallins in lens opacities caused by the absence of the major chaper

64 To understand the molecular mechanism of lens opacity caused by this mutation, we expressed human

65 ity in these volunteers was graded using the Lens Opacities Classification System (LOCS) III.

66 mation and assessment of lens opacity by the Lens Opacities Classification System (LOCS) III.

67 -lamp assessment of lens opacities using the Lens Opacities Classification System II (LOCS II) at bas

68 fraction, applanation tonometry, gonioscopy, Lens Opacities Classification System II cataract grading

69 -lamp assessment of lens opacities using the Lens Opacities Classification System II.

70 t each follow-up visit were graded using the Lens Opacities Classification System III protocol.

71 capsular opacities as grade > or =0.3 of the Lens Opacities Classification System III.

72 Lens opacification was assessed by the Lens opacities classification system III.

73 lar opacity as grade >/=0.5 according to the Lens Opacities Classification System III.

74 cataract was diagnosed clinically using the Lens Opacity Classification System (LOCS) III system.

75 orer vision-specific functioning occurred at Lens Opacity Classification System grades 4 (nuclear opa

76 he slit lamp by an ophthalmologist using the Lens Opacity Classification System II.

77 Opacities were assessed by using the Lens Opacity Classification System III (LOCS III).

78 examination and were graded according to the Lens Opacity Classification System III.

79 e alphaA-R49C mutant exhibit nearly complete lens opacity concurrent with small lenses and small eyes

80 oviding a comprehensive understanding of how lens opacity could result from this mutation.

81 (RR = 2.0, 95% CI: 1.3-3.0), while cortical lens opacities decreased risk (RR = 0.6, 95% CI: 0.4-0.9

82 The cataractous lens opacity decreases as the mice age.

83 ed with a decreased risk of moderate nuclear lens opacity developing compared with the lowest quintil

84 The rate of lens opacity development was 40.9% (95% CI, 32.7%-48.8%)

85 increased risk of mild posterior subcapsular lens opacity development.

86 portant to understand the molecular basis of lens opacity due to this mutation.

87 Nuclear lens opacities, glaucoma, and diabetes increase the risk

88 A prevalence survey for lens opacity, glaucoma, and visual impairment was carrie

89 Age, blood pressure, refractive error, and lens opacity had significant influence on retinal vascul

90 2/131 (24.4%) boys, and posterior spoke-like lens opacities in 3/97 (3.1%) girls and 2/130 (1.5%) boy

91 This study highlights the morphology of lens opacities in a family with genetically confirmed di

92 ected in the United States, and the basis of lens opacities in HHCS was determined.

93 Complications included worsening lens opacity in 242 of 443 phakic eyes (55%), loss of >/

94 g a slit-lamp examination and defined as any lens opacity in either eye or evidence of its removal (c

95 proliferation in tissue culture and induces lens opacity in organ culture.

96 efects in the AQP0 protein may contribute to lens opacity in patients with common, less fulminant for

97 cortical cataract increase of 5% or more in lens opacity in the central 5 mm of the lens compared wi

98 lens at birth and the gradual development of lens opacity in the second and third decades of life.

99 copy, and (f) development of a mild anterior lens opacity in the superior cortical region during the

100 Lens opacity in these volunteers was graded using the Le

101 Here we provide a molecular basis for lens opacity in two genetic cataracts and suggest that t

102 dent risk factors for incident cortical-only lens opacities included older age and having diabetes at

103 eline risk factors for incident nuclear-only lens opacities included older age, current smoking, and

104 trient intake that results when knowledge of lens opacities influences nutrition-related behavior or

105 f specific MAP kinases in the development of lens opacities, lenses were grown for 10 days in the pre

106 The lens opacity mutation is an amino-acid substitution that

107 Cataract was defined as high-grade lens opacity observed by biomicroscopy judged to be the

108 Lens opacity occurred when APH protein levels were >2.6%

109 omes and Measures: Rate of cataract surgery, lens opacity, ocular hypertension, refractive safety, pr

110 site and a 83% lower prevalence of moderate lens opacities (odds ratio: 0.17; 95% CI: 0.03, 0.85) at

111 ociated with a 77% lower prevalence of early lens opacities (odds ratio: 0.23; 95% CI: 0.09, 0.60) at

112 Progression of lens opacities on stereoscopic lens photographs at 2 yea

113 Two-year changes in severity of lens opacities on the AREDS lens grading scale are predi

114 nd 24 months of age and scored for degree of lens opacity on a 0 to 4+ scale, and the presence or abs

115 may report visual discomfort, despite minor lens opacity on slit-lamp examination, minor loss of bes

116 used to assess the effect of pupil size and lens opacity on the reliability of SD OCT in the acquisi

117 When affected children demonstrate lens opacities, ophthalmologists have the unique potenti

118 seline or development of nuclear or cortical lens opacity outcomes.

119 effect may influence development of nuclear lens opacity, possibly in conjunction with environmental

120 Moreover, increases in lens opacity (r = -0.728) and ERG implicit times (r = -0

121 ract was defined as an incident, age-related lens opacity responsible for a reduction in best-correct

122 ia risk increased with age, baseline nuclear lens opacities (risk ratio [RR] = 1.7; 95% confidence in

123 utation that results in an irregular nuclear lens opacity similar to the human Coppock cataract.

124 ing to progression of ROP and/or presence of lens opacity, then the hazard of having glaucoma signifi

125 retinal dysfunction versus diabetes-induced lens opacity, to the visual deficits found in early-stag

126 We investigated the incidence of lens opacities typical of cataracts in more than 1100 fr

127 We described the system for grading lens opacities using stereoscopic digital fundus reflex

128 ed visual acuity and slit-lamp assessment of lens opacities using the Lens Opacities Classification S

129 ed visual acuity and slit-lamp assessment of lens opacities using the Lens Opacities Classification S

130 y was to determine the relationships between lens opacity, vascular and lipid factors and retrobulbar

131 etrics pupillometer (iVIS Technologies), and lens opacity was measured by Pentacam densitometry (Ocul

132 Although mild lens opacity was noted, her postoperative VA remained 20

133 rable with that observed in mild to moderate lens opacity, was associated with a three- to fivefold o

134 Lens opacities were graded with the Lens Opacification C

135 Lens opacities were present in 26.6% of eyes at the time

136 Minor lens opacities were significantly more common in the JHS

137 t, p38 inhibitors blocked the development of lens opacities with an efficacy similar to that of the S

138 of cortical and posterior subcapsular (PSC) lens opacities within the central 5 mm diameter zone of