ライフサイエンスコーパス: aphakia

1 the differential in a patient with presumed aphakia.

2 lantation in posttraumatic and postoperative aphakia.

3 atients with posttraumatic and postoperative aphakia.

4 n before age 7 months has no advantages over aphakia.

5 nt secondary IOL implantation for unilateral aphakia.

6 result in significant periods of uncorrected aphakia.

7 opmental defect that finally progresses into aphakia.

8 pecification and organogenesis, resulting in aphakia.

9 opacities with this treatment compared with aphakia.

10 a (141 eyes, group 1), post-cataract surgery aphakia (122 eyes, group 2), and in cases in which penet

11 ormed RPICIOL implantation in post-traumatic aphakia (141 eyes, group 1), post-cataract surgery aphak

12 % CI, 8%-17%) in participants with bilateral aphakia, 33% (95% CI, 26%-39%) in those with bilateral p

13 optic atrophy (6.4%), phthisis bulbi (6.4%), aphakia (5.6%) and glaucoma (5.2%).

14 17 with retinal tear or detachment, 683 with aphakia, 534 with pseudophakia, and 2465 with myopia.

15 CI, 28%-59%) in participants with bilateral aphakia, 7% (95% CI, 1%-12%) in those with bilateral pse

16 corneal opacity (90%; sclerocornea in 47%), aphakia (83%) and microphthalmia (80%), but some had mil

17 who underwent secondary IOL implantation for aphakia after congenital cataract surgery at L. V. Prasa

18 Diabetes (OR, 0.90) and aphakia after surgery (OR, 0.60) seemed to be protective

19 Eyes with aphakia after surgery for traumatic cataracts and other

20 Despite prior documentation of aphakia after treatment for congenital cataracts, detail

21 Mouse aphakia (ak) is a recessive phenotype that spontaneously

22 Here, we demonstrate that Pitx3-deficient aphakia (ak) mice, which have been shown previously to e

23 The recessive aphakia (ak) mouse mutant is characterized by bilateral

24 em (LCS) makes use of a mutant mouse strain, aphakia (ak), homozygotes of which fail to develop an oc

25 provides the first direct evidence that the aphakia allele of Pitx3 is a hypomorph and that Pitx3 is

26 , 20/20 to worse than 20/800) in 6 eyes with aphakia and 20/63 (range, 20/20 to 20/200) in 26 eyes wi

27 s was 29% (95% CI, 25%-34%) in 443 eyes with aphakia and 7% (95% CI, 5%-9%) in 606 eyes with pseudoph

28 tion is approximately 7% more expensive than aphakia and CL correction.

29 ater understanding of the natural history of aphakia and pseudophakia have changed the approach to th

30 The Toddler Aphakia and Pseudophakia Study (TAPS) is a registry of c

31 The Toddler Aphakia and Pseudophakia Study is a registry of children

32 ated separately for unilateral and bilateral aphakia and pseudophakia.

33 eyes previous pars plana vitrectomy, 2 eyes aphakia, and 1 eye each with aniridia, anterior chamber

34 % (95% CI, 15%-34%) in those with unilateral aphakia, and 17% (95% CI, 5%-28%) in those with unilater

35 1% (95% CI, 6%-15%) in those with unilateral aphakia, and 34% (95% CI, 28%-39%) in those with unilate

36 iridocorneal endothelial syndrome, aniridia, aphakia, and anterior chamber intraocular lenses, among

37 fferences between eyes having primary IOL vs aphakia, and optimal timing of unilateral congenital cat

38 ry of ocular surgery, PVR at time of repair, aphakia, and redetachment were risk factors for a poor o

39 lana vitrectomy; secondary implantations for aphakia; and iris suture fixation at primary cataract ex

40 rating keratoplasty, ICE syndrome, aniridia, aphakia, complex anterior chambers with anterior chamber

41 that a cell autonomous defect underlies the aphakia condition assures that lenses generated through

42 to either primary intraocular lens (IOL), or aphakia (contact lens [CL]).

43 To assess the constants and formula for aphakia correction with iris-claw IOLs to achieve the be

44 n of accommodation, reduction of the risk of aphakia, glaucoma, and development of secondary lens rep

45 ris-fixated claw IOL, ACIOL implantation for aphakia has regained popularity.

46 Recent studies of mouse mutant aphakia have implicated the homeobox gene Pitx3 in the s

47 Risk factors for GFCS included aphakia (hazard ratio [HR], 2.63; 95% CI, 1.96-3.57), un

48 The aphakia homozygous mouse is characterized by small eyes

49 io [HR], 2.22; 95% CI 1.39-3.57; P < 0.001), aphakia (HR, 2.10; 95% CI, 1.43-3.10; P < 0.001), premat

50 tients with glaucoma, cataract, and surgical aphakia in better coping with the impact of these condit

51 ular lenses are a well-accepted treatment of aphakia in children 2 years of age and older, with many

52 Options available to treat aphakia in children with inadequate support for posterio

53 tion in Foxe3 that causes congenital primary aphakia in humans marks an important milestone.

54 WCLs) for the optical treatment of infantile aphakia in humans.

55 trial comparing the treatment of unilateral aphakia in patients under 7 months of age with a primary

56 Contact lenses were used to correct aphakia in patients who did not receive IOLs.

57 erally sutured intraocular lenses to correct aphakia in pediatric patients.

58 , presence of epiretinal membrane (ERM), and aphakia in the study eye.

59 Angle recession, uveitis, and aphakia increased the odds of a nonresponse (ORs 2.46, 1

60 Congenital primary aphakia is a rare developmental disease in which the len

61 Appropriate correction of aphakia is key to good outcomes.

62 ay also be appropriate when the patient with aphakia is young and has a relatively long life expectan

63 Aphakia (lack of lens) is a rare human congenital disord

64 Although aphakia management did not affect VA outcome or AE incid

65 , we took advantage of PITx3-deficient mice (aphakia mice), in which DA in the dorsal striatum is red

66 When transplanted into PD model animals, aphakia mice, and 6-OHDA-lesioned rats, mDA NPs differen

67 that the abnormal ocular development in the aphakia mouse is due to the deletion upstream of the Pit

68 Our results from the Pitx3-deficient aphakia mouse suggest that pre-existing DA neurons modul

69 However, when we examined the aphakia mouse, which is deficient in nigrostriatal neuro

70 The inclusion criteria were aphakia, no capsular support, and a minimal 1 year of fo

71 Pitx3 was mapped close to aphakia on mouse chromosome 19.

72 Patients presenting with aphakia or dislocated IOL without capsular support were

73 All eyes presented with aphakia or luxated or subluxated posterior chamber intra

74 amples include the glaucomas associated with aphakia or pseudophakia, neovascular glaucoma, and glauc

75 Patients with aphakia or pseudophakia, orbital injuries, secondary cat

76 st, but some individuals had microphthalmia, aphakia or sclerocornea, more typical of recessive disea

77 hy (PVR; OR, 0.39 [0.16 - 0.92]; P = 0.032), aphakia (OR, 0.25 [0.08 - 0.77]; P = 0.016), and redetac

78 Age >=60 years (OR<0.82), pseudophakia/aphakia (OR=0.58), or residence outside of the Northeast

79 ination with the presence of pseudophakia or aphakia, or reported during telephone calls at 6-month i

80 a make Pitx3 a strong candidate gene for the aphakia phenotype in the mouse and suggest a role for th

81 associated with a history of ocular trauma, aphakia, premature retina, persistent fetal vasculature,

82 Exclusion criteria included aphakia, pseudophakia, late age-related macular degenera

83 ry causes than in patients being treated for aphakia resulting from other causes (71% vs 29%).

84 The indications were postsurgical aphakia, subluxated cataract, ectopia lentis, traumatic

85 Data from the Infant Aphakia Treatment Study (IATS) are used in a cohort desi

86 tral corneal thickness (CCT) from the Infant Aphakia Treatment Study (IATS) patients at the 5-year ex

87 Fifty-seven infants in the Infant Aphakia Treatment Study (IATS) with a unilateral catarac

88 lantation for infants enrolled in the Infant Aphakia Treatment Study (IATS).

89 ly studied and were excluded from the Infant Aphakia Treatment Study (IATS).

90 Infants enrolled in the Infant Aphakia Treatment Study (IATS).

91 The just completed Infant Aphakia Treatment Study aims to answer questions regardi

92 glaucoma suspect were created for the Infant Aphakia Treatment Study and applied for surveillance and

93 The Infant Aphakia Treatment Study enrolled 114 children; 57 were r

94 Results of the Infantile Aphakia Treatment Study have concluded that primary IOL

95 ars of age by a traveling examiner using the Aphakia Treatment Study HOTV protocol.

96 The Infant Aphakia Treatment Study is a randomized clinical trial w

97 The Infant Aphakia Treatment Study is a randomized, multicenter (n

98 The Infant Aphakia Treatment Study randomized 114 patients with uni

99 lysis of a randomized clinical trial (Infant Aphakia Treatment Study) of infants born from August 1,

100 Data came from the Infant Aphakia Treatment Study, a randomized clinical trial of

101 l of 114 infants were enrolled in the Infant Aphakia Treatment Study, a randomized, multi-center (12)

102 ollowed for 10.5 years as part of the Infant Aphakia Treatment Study.

103 at 10.6 (+/-0.3) years of age in the Infant Aphakia Treatment Study.

104 dverse events than reported in the Infantile Aphakia Treatment Study.

105 eived primary IOL implantation in the Infant Aphakia Treatment Study.

106 ge, axial length, maturity, pseudophakia v/s aphakia, type of IOL and type of cataract surgery, there

107 IRIS Registry was associated with young age, aphakia, unilateral cataract, and Black race.

108 emoval in infancy, yet their relationship to aphakia vs primary intraocular lens (IOL) implantation r

109 was 38.8 years, and the most common cause of aphakia was congenital cataract surgery (55%).

110 Aphakia was due to eye trauma (19) or complicated catara

111 before the first visit when pseudophakia or aphakia was observed.

112 baseline IOP, angle recession, uveitis, and aphakia were associated with increased odds of nonrespon

113 Those with pseudoexfoliation or aphakia were more likely to progress to blindness.

114 otal posterior capsulectomy, vitrectomy, and aphakia were once the standard of care, many physicians

115 OP spike, whereas diabetes and postoperative aphakia were protective against a spike after stand-alon

116 ntation is the standard of care for treating aphakia when spectacle or contact lens correction is not

117 (n=12) clinical trial comparing treatment of aphakia with a primary IOL or contact lens in 114 infant

118 = 12), clinical trial comparing treatment of aphakia with a primary IOL or contact lens in 114 infant

119 cal trial comparing the optical treatment of aphakia with either primary IOL implantation (n = 57) or

120 rative complications, neonatal correction of aphakia with IOLs combined with EWCLs can lead to normal

121 The ideal intraocular lens in cases of aphakia without capsular support is debated.