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 fusion model, runcaciguat treatment improved neuroretinal and visual function as measured by electror

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

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

6 l dysfunction is associated with significant neuroretinal cell death.

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

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

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

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

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

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

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

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

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

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

17 Furthermore the neuroretinal cells were preincubated with different and

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

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

20 of fusion between donor cells and endogenous neuroretinal cells.

21 diseases and partly explains the progressive neuroretinal changes observed in optic coherence tomogra

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

23 ulation are therefore likely attributable to neuroretinal compromise.

24 ork can be trained to quantify the amount of neuroretinal damage on optic disc photographs using SDOC

25 to prevent severe visual loss as a result of neuroretinal damage.

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

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

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

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

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

31 , through the complement C3/C3aR axis during neuroretinal development.

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

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

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

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

36 Regarding the neuroretinal disorder associated with HIV, new ophthalmi

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

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

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

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

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

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

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

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

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

46 2.8-13.7; P = 0.01) versus those without HIV neuroretinal disorder.

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

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

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

50 ble role of mfERG in evaluating the expected neuroretinal dysfunction before the clinical development

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

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

53 Neuroretinal dystrophies occupy a prominent place among

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

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

56 e the adjacent neuroepithelium to assume the neuroretinal fate.

57 at model, runcaciguat significantly improved neuroretinal function and improved inner plexiform layer

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

59 es suggest that sGC signaling is involved in neuroretinal function and vision and that diabetes negat

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

61 Endogenous EPO can protect neuroretinal function in ischemic retinopathy.

62 Neuroretinal function in Type 2 diabetes is worse than i

63 Neuroretinal function is more abnormal in males than in

64 Local neuroretinal function is not associated with full retina

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

66 unterparts in two separate analyses of local neuroretinal function.

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

68 cal microscopy for macular and peripapillary neuroretinal layer thicknesses and corneal nerve length/

69 g and thinning at times, mostly in the inner neuroretinal layers and the ganglion cell-inner plexifor

70 Thinner neuroretinal layers are associated with delayed P100 lat

71 Among neuroretinal layers, solely the peripapillary retinal ne

72 istent immaturity of retinal vasculature and neuroretinal layers.

73 unclear, though inflammatory, vascular, and neuroretinal mechanisms are implicated.

74 al edema, reduced inflammation and preserved neuroretinal morphology and function following RVO.

75 rent ocular media and the pattern of macular neuroretinal opacification that evolves as upstream tiss

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

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

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

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

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

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

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

83 Two neuroretinal parameters, minimum rim width and retinal n

84 Longitudinal changes in laminar depth and neuroretinal parameters.

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

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

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

88 structural damage is often characterized by neuroretinal rim (NRR) thinning of the optic nerve head,

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

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

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

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

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

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

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

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

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

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

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

100 The neuroretinal rim area of the patients was measured with

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

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

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

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

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

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

107 e relations between contrast sensitivity and neuroretinal rim area.

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

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

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

111 Neuroretinal rim assessment based on the clinical optic

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

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

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

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

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

117 ents were associated with faster loss of the neuroretinal rim in glaucoma, as measured by MRW.

118 attern, with most of them located within the neuroretinal rim in the inferior and superior quadrant o

119 ma, as thinning of the superior and inferior neuroretinal rim is a hallmark of the disease.

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

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

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

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

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

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

126 Neuroretinal rim loss was classified as diffuse or local

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

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

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

130 er (RNFL) thickness measurements, and 3D OCT neuroretinal rim measurements (i.e., minimum distance ba

131 High-density 3D SD OCT neuroretinal rim measurements detected glaucoma progress

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

133 ogression detected by high-density 3D SD-OCT neuroretinal rim measurements preceded DH occurrence in

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

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

136 f vertical cup-to-disc ratio of 0.7 or more, neuroretinal rim notching, retinal nerve fiber layer def

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

138 e band (MDB) thickness, a 3-dimensional (3D) neuroretinal rim parameter, was calculated from optic ne

139 minimum distance band (MDB) thickness, a 3D neuroretinal rim parameter.

140 w studies have examined the stability of OCT neuroretinal rim parameters after glaucoma surgery for o

141 Likewise, the following neuroretinal rim parameters showed significant changes w

142 although shadowing from blood vessels at the neuroretinal rim remains an issue.

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

144 nce of a DH was associated with localized 3D neuroretinal rim thickness progression (superior MDB pro

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

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

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

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

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

150 ers of the macula in contrast to the minimum neuroretinal rim width (MRW) and peripapillary retinal n

151 to <6/60; vertical cup-to-disc ratio 0.85 or neuroretinal rim width 0.1); moderate VI (BCDVA 6/60 to

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

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

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

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

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

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

158 sitivity for glaucoma detection than did the neuroretinal rim.

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

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

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

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

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

164 nderscoring the detrimental effect of IRF on neuroretinal structures.

165 herence tomography demonstrating progressive neuroretinal thinning in the absence of optic neuritis.

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

167 al coherence tomography (OCT) imaging of the neuroretinal tissue could improve the feasibility of suc

168 normal neuroglia remodeling that exacerbates neuroretinal tissue damage.

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

170 telencephalic, optic-stalk, optic-disc, and neuroretinal tissues along the center-periphery axis.

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