ライフサイエンスコーパス: neuroretinal

1 h the technique in its current form leads to neuroretinal and RPE tissue loss, and graft shrinkage.

2 n 91 (65%) eyes in the periphery beneath the neuroretinal and scleral rims or vascular structures.

3 serves choroid and prevents protracted outer neuroretinal anomalies in OIR, suggesting IL-1beta as a

4 ions in thickness, such as macular edema and neuroretinal atrophy.

5 l dysfunction is associated with significant neuroretinal cell death.

6 We have transplanted quail neuroretinal cell lines QNR/D, a putative amacrine or ga

7 ntial differentiation from RPCs to the seven neuroretinal cell types in maturated NR-like structures

8 These NRPCs differentiated into multiple neuroretinal cell types, similar to OV cultures from hum

9 Neuroretinal cells (RGC-5) were incubated with serum eit

10 the ability to influence protein profiles of neuroretinal cells and possibly hold neuroprotective pot

11 t effects of serum antibodies on proteins of neuroretinal cells especially of the mitochondrial apopt

12 n together with SOCS1-mediated protection of neuroretinal cells from apoptosis, suggest that SOCS1 ha

13 and antibody effect of glaucoma patients on neuroretinal cells in more detail and also determine the

14 retinal glia either regenerate lost RPE and neuroretinal cells or form nonfunctional scars.

15 OCS3 may be a common physiologic response of neuroretinal cells to cellular stress.

16 Furthermore the neuroretinal cells were preincubated with different and

17 GF was found predominantly in the nucleus of neuroretinal cells, including photoreceptor cells.

18 in the transplants was tightly surrounded by neuroretinal cells, suggesting their active role in neur

19 of fusion between donor cells and endogenous neuroretinal cells.

20 n and disease pathogenesis in a well-defined neuroretinal circuitry.

21 ulation are therefore likely attributable to neuroretinal compromise.

22 ischemia, preretinal neovascularization, or neuroretinal degeneration in OIR.

23 diabetic macular edema (DME) with subfoveal neuroretinal detachment (SND+) vs DME without SND (SND-)

24 the therapy was started again and the serous neuroretinal detachment appeared once more, however with

25 To report a case of uveitis and neuroretinal detachment in a patient treated with Tramet

26 Fundoscopy showed serous neuroretinal detachment of the fovea accompanied with wh

27 therapeutic implications in the treatment of neuroretinal diseases, which are characterized by apopto

28 HIV-associated neuroretinal disorder (HIV-NRD), a visual impairment of

29 This condition, termed HIV-related neuroretinal disorder (HIV-NRD), is a risk factor for vi

30 r understanding of the structural changes in neuroretinal disorder as an indicator of other end-organ

31 Regarding the neuroretinal disorder associated with HIV, new ophthalmi

32 Sixteen percent of participants had HIV neuroretinal disorder at enrollment.

33 Patients with HIV neuroretinal disorder had a 70% excess mortality versus

34 Patients with HIV neuroretinal disorder had increased risks of bilateral v

35 Risk factors for HIV neuroretinal disorder included hepatitis C infection, lo

36 Human immunodeficiency virus neuroretinal disorder is a common finding among patients

37 Human immunodeficiency virus neuroretinal disorder was more common in women and Afric

38 Patients with HIV neuroretinal disorder were identified by a contrast sens

39 eases but does not eliminate the risk of HIV neuroretinal disorder.

40 incidence, risk factors, and outcomes of HIV neuroretinal disorder.

41 2.8-13.7; P = 0.01) versus those without HIV neuroretinal disorder.

42 ential disease mechanism for HIV-associated "neuroretinal disorder."

43 rmed the "human immunodeficiency virus (HIV) neuroretinal disorder." The objectives of this study wer

44 rine OIR offers a valuable model of ischemic neuroretinal dysfunction and degeneration in which to in

45 in wild-type animals with OIR did not rescue neuroretinal dysfunction or degeneration.

46 OIR was associated with significant neuroretinal dysfunction, with reduced photopic and scot

47 Neuroretinal dystrophies occupy a prominent place among

48 In 3 patients OCT revealed subfoveal neuroretinal elevation, often asymptomatic, also after d

49 These data demonstrate that neuroretinal expression of Lhx2 and neuroretina-derived

50 e the adjacent neuroepithelium to assume the neuroretinal fate.

51 ught to determine the effects of ischemia on neuroretinal function and survival in murine oxygen-indu

52 se concentration is associated with degraded neuroretinal function in adolescents with type 1 diabete

53 Endogenous EPO can protect neuroretinal function in ischemic retinopathy.

54 Neuroretinal function in Type 2 diabetes is worse than i

55 Neuroretinal function is more abnormal in males than in

56 Local neuroretinal function is not associated with full retina

57 purpose of our study is to determine whether neuroretinal function, measured by the multifocal electr

58 Over 20% of these patients have abnormal neuroretinal function.

59 unterparts in two separate analyses of local neuroretinal function.

60 anges are detected with similar frequency as neuroretinal parameter changes.

61 depth occurs more frequently than change in neuroretinal parameters in glaucoma, and (2) Bruch's mem

62 Age-related loss of neuroretinal parameters may explain a large proportion o

63 of controls who had significant reduction of neuroretinal parameters was 35% for BMO-MRW, 31% for RNF

64 meters, but not on laminar depth, changes in neuroretinal parameters were adjusted for age-related re

65 s of significant change in laminar depth and neuroretinal parameters were compared with survival mode

66 Because normal aging has a clear effect on neuroretinal parameters, but not on laminar depth, chang

67 Two neuroretinal parameters, minimum rim width and retinal n

68 Longitudinal changes in laminar depth and neuroretinal parameters.

69 red with the same frequencies as thinning in neuroretinal parameters.

70 near homogeneous population of proliferating neuroretinal progenitor cells (NRPCs).

71 Mean BMO disc and neuroretinal rim (NRR) areas ranged from 0.94 to 4.06 mm

72 red by optical coherence tomography, and the neuroretinal rim (rim area, rim/disc area, and rim volum

73 a, independently undertook planimetry of the neuroretinal rim and of the disc margin from 1 eye of ea

74 Global disc margin-based neuroretinal rim area (DMRA) was measured with confocal

75 ckness (HRT II, StratusOCT, and GDx VCC) and neuroretinal rim area (HRT II) and SAP sensitivity expre

76 rrelation between 1/Lambert DLS and temporal neuroretinal rim area (R(2) = 0.30, P = 0.0000).

77 adratic fit between decibel DLS and temporal neuroretinal rim area (R(2) = 0.38, P = 0.0000) was sign

78 To evaluate and compare rates of change in neuroretinal rim area (RA) and retinal nerve fiber layer

79 re was a linear correlation between temporal neuroretinal rim area and PERG amplitude (transient PERG

80 Software automatically calculated the neuroretinal rim area in 10 degrees , 30 degrees , 40 de

81 The first consisted of measurements of neuroretinal rim area in the superior-temporal sector pa

82 tral 18 degrees of the visual field and with neuroretinal rim area in the temporal part of the optic

83 The neuroretinal rim area of the patients was measured with

84 in terms of the 3 Boolean comparisons of the neuroretinal rim area was specified in terms of the sens

85 SITA PSD for 10%, 30%, 50%, and 70% loss of neuroretinal rim area were 0.638, 0.756, 0.852, and 0.92

86 ld mean deviation (MD) and global optic disc neuroretinal rim area with follow-up time.

87 ween decibel DLS and both PERG amplitude and neuroretinal rim area, and a linear relationship between

88 (including optic disc area, optic cup area, neuroretinal rim area, cup volume, rim volume, cup-disc

89 be obeyed, the 3 Boolean comparisons of the neuroretinal rim area, I>S, S>N, and N>T, had to be true

90 e relations between contrast sensitivity and neuroretinal rim area.

91 between 1/Lambert DLS and PERG amplitude and neuroretinal rim area.

92 (P < 0.0001) and negatively correlated with neuroretinal rim area.

93 We determined whether neuroretinal rim assessment based on Bruch's membrane op

94 Neuroretinal rim assessment based on the clinical optic

95 At FU1, neuroretinal rim decreased and ALCS depth increased sign

96 f localized retinal nerve fiber layer and/or neuroretinal rim defects, and disc haemorrhages).

97 To investigate possible differences in neuroretinal rim distribution, vascular pattern, and per

98 lar signs and characteristics related to the neuroretinal rim distribution, vascular pattern, peripap

99 Presently, the clinician evaluates neuroretinal rim health according to the appearance of t

100 from normal, by 28% in the inferior temporal neuroretinal rim location (P = 0.001) and by 24% in the

101 appa = 0.7), disc hemorrhages (kappa = 0.7), neuroretinal rim loss (kappa = 0.5), and retinal nerve f

102 ificantly associated with RBV shift included neuroretinal rim loss (OR, 21.9; 95% CI, 5.7-83.6; P< 0.

103 chronic experimental high-pressure glaucoma, neuroretinal rim loss and an increase of beta zone may b

104 holes or disinsertions) are associated with neuroretinal rim loss and APON.

105 ease severity was evaluated by the amount of neuroretinal rim loss assessed by confocal scanning lase

106 eyes with functionally progressive glaucoma, neuroretinal rim loss, and DH.

107 tructural progression (2 graders), including neuroretinal rim loss, parapapillary atrophy progression

108 laminar disinsertions corresponded to focal neuroretinal rim loss, with no evidence of APON in disc

109 Conventional optic disc margin-based neuroretinal rim measurements lack a solid anatomic and

110 een the retinal nerve fiber layer (RNFL) and neuroretinal rim measurements.

111 he AUC for the RNFL also was higher than the neuroretinal rim measures.

112 y (SD OCT) for quantification of a BMO-based neuroretinal rim parameter, minimum rim width (BMO-MRW),

113 the 2D RNFL thickness parameter, the 3D MDB neuroretinal rim thickness parameter had uniformly equal

114 optic neuropathy defined by the presence of neuroretinal rim thinning, notching or excavation of the

115 a central ODP had glaucoma with glaucomatous neuroretinal rim thinning, RNFL loss, and corresponding

116 and glaucomatous optic disc changes such as neuroretinal rim thinning/notching and acquired pits of

117 ptic disc and optic cup and the width of the neuroretinal rim were drawn and measured.

118 Increase of beta zone and loss of neuroretinal rim were independent of presence and size o

119 cups possess greater variability of relative neuroretinal rim width around the disc, greater relative

120 azard ratio [HR], 5.737; P = .012), narrower neuroretinal rim width at baseline (HR, 2.91; P = .048),

121 In discs with small cups, neuroretinal rim width conforms to the overall oval shap

122 Study patients, migraine, baseline narrower neuroretinal rim width, low systolic blood pressure and

123 DP were otherwise normal with intact macula, neuroretinal rim, RNFL, and visual field.

124 sitivity for glaucoma detection than did the neuroretinal rim.

125 seen in measurements of both the cup and the neuroretinal rim.

126 tion of the disc margin and estimates of the neuroretinal rim.

127 es were defined as clinically having healthy neuroretinal rims and an MRA analysis of within normal l

128 optic epithelium, lack of expression of the neuroretinal-specific CHX10 transcription factor, and co

129 milieu may progress through inflammatory and neuroretinal stages long before the development of vascu

130 e capacity to self-assemble into rudimentary neuroretinal structures and express markers indicative o

131 nations were obtained from four sites on the neuroretinal tissue and from the center of the cup.

132 a causes severe retinal injury with death of neuroretinal tissue, scarring, and permanent visual loss

133 um transcription factors, gain expression of neuroretinal transcription factors, and eventually trans