Glaucoma is defined as an optic disc neuropathy meaning the nerve fibers are being atrophied similar to the fate occurring in non-glaucomatous optic atrophies. Furthermore, the nerve fibers are always being destroyed ...Glaucoma is defined as an optic disc neuropathy meaning the nerve fibers are being atrophied similar to the fate occurring in non-glaucomatous optic atrophies. Furthermore, the nerve fibers are always being destroyed randomly in all the non-glaucomatous optic atrophies. In contrast, the nerve fibers in glaucoma are invariably destroyed in an orderly tandem fashion, from peripheral to central, never randomly. Is glaucoma really an optic disc neuropathy in light of orderly destruction of nerve fibers in glaucoma? The current prevailing theories in glaucoma such as posterior bowing of the lamina cribrosa or cupping can’t explain the orderly destruction of nerve fibers occurring in glaucoma. In fact, there is no biological mechanism acting directly on the nerve fibers or their RGCs which could lead to their orderly destruction. Therefore, there should be some mechanical way, which could result in the orderly destruction of nerve fibers even though this mechanical scenario may have resulted from the direct biological effect of raised IOP on some important component of the optic disc. It is proposed that the border tissue of Elschnig (BT) atrophies due to chronic ischemia caused by raised IOP, and as a result, the lamina cribrosa (LC) begins sinking in the scleral canal—a mechanical problem. Due to sinking of the LC, the nerve fibers get stretched and broken starting with the most peripheral nerve fibers being closest to the edge of the scleral opening and ending with the most central nerve fibers in an orderly tandem fashion. Therefore, in view of the orderly destruction of nerve fibers, glaucoma may not be an optic disc neuropathy but an optic disc axotomy.展开更多
Aim: To present a case of hamartoma of the optic disc and Retinal Pigment Epithelium (RPE) and follow up of the visual function over three-years period. Methods: A seventeen-year-old boy has observed reduced visual ac...Aim: To present a case of hamartoma of the optic disc and Retinal Pigment Epithelium (RPE) and follow up of the visual function over three-years period. Methods: A seventeen-year-old boy has observed reduced visual acuity in his left eye. The visual acuity was 0.2 and there was RAPD in the left eye. Fundoscopy revealed an elevation of the optic disc obscuring disc vessels with epiretinal gliosis. Fluorescein angiography demonstrated hyperfluorescent saccular dilatations with leakage in the late phase. Ocular Coherence Tomography (OCT) showed hyperreflective elevation of the optic disc and epiretinal membrane. There was a juxtapapillary scotoma in Semi-automated Kinetic Perimetry (SKP). There was no systemic diseases. Results of blood tests, CT and MRI of CNV were normal. Results: After 3 years period of the follow-up the visual acuity was 0.1 and there was a progression of the visual field defect to the altitudinal scotoma in the upper hemisphere. Fluorescein anhiography and OCT revealed the same. Conclusion: Hamartoma of RPE and optic disc is a rare condition consisting of glial, vascular and RPE cells. It should be differentiated from optic disc oedema and vascular tumors of the retina. Assessment of the visual function is very important in the longitudinal follow-up.展开更多
Background： The mechanisms of pathological retinal neovascularization （RNV） remain unknown. Several microRNAs were reported to be involved in the process of RNV. Oxygen-induced retinopathy （O1R） is a useful model...Background： The mechanisms of pathological retinal neovascularization （RNV） remain unknown. Several microRNAs were reported to be involved in the process of RNV. Oxygen-induced retinopathy （O1R） is a useful model to investigate RNV. Our present work explored the expression and the role of microRNA-128 （miR-218） in oxygen-induced RNV. Methods： OIR was used to establish RNV model. The expression level ofmiR-218 in the retina from OIR mice was assessed by quantitative real-time reverse transcriptase polymerase chain reaction. Fluorescein angiography was performed in retinae of OIR mice, and RNV was quantified by hematoxylin and eosin staining to evaluate the effect of pCDH-CMV-miR-218 intravitreal injection on RNV in OIR mice. Roundabout 1 （Robol） expression was detected by Western blotting in mouse retinal vascular endothelial cells expressing a high or low level of miR-218 and retinal tissues from OIR mice. Cell migration was evaluated by scratch wound assay. Results： In OIR mice, the expression level of miR-218 was significantly down-regulated （P = 0.006）. Retinal Robol expression was significantly increased at both mRNA and protein levels （P = 0.001, 0.008： respectively）, miR-218 intravitreal injection inhibited retinal angiogenesis in OIR mice, and the restoration of miR-218 in retina led to down-regulation of Robol. Conelusions： Our experiments showed that restoration ofmiR-218 inhibited retinal angiogenesis via targeting Robo 1. MiR-218 contributed to the inhibition of retinal angiogenesis and miR-218 might be a new therapeutic target for preventing RNV.展开更多
文摘Glaucoma is defined as an optic disc neuropathy meaning the nerve fibers are being atrophied similar to the fate occurring in non-glaucomatous optic atrophies. Furthermore, the nerve fibers are always being destroyed randomly in all the non-glaucomatous optic atrophies. In contrast, the nerve fibers in glaucoma are invariably destroyed in an orderly tandem fashion, from peripheral to central, never randomly. Is glaucoma really an optic disc neuropathy in light of orderly destruction of nerve fibers in glaucoma? The current prevailing theories in glaucoma such as posterior bowing of the lamina cribrosa or cupping can’t explain the orderly destruction of nerve fibers occurring in glaucoma. In fact, there is no biological mechanism acting directly on the nerve fibers or their RGCs which could lead to their orderly destruction. Therefore, there should be some mechanical way, which could result in the orderly destruction of nerve fibers even though this mechanical scenario may have resulted from the direct biological effect of raised IOP on some important component of the optic disc. It is proposed that the border tissue of Elschnig (BT) atrophies due to chronic ischemia caused by raised IOP, and as a result, the lamina cribrosa (LC) begins sinking in the scleral canal—a mechanical problem. Due to sinking of the LC, the nerve fibers get stretched and broken starting with the most peripheral nerve fibers being closest to the edge of the scleral opening and ending with the most central nerve fibers in an orderly tandem fashion. Therefore, in view of the orderly destruction of nerve fibers, glaucoma may not be an optic disc neuropathy but an optic disc axotomy.
文摘Aim: To present a case of hamartoma of the optic disc and Retinal Pigment Epithelium (RPE) and follow up of the visual function over three-years period. Methods: A seventeen-year-old boy has observed reduced visual acuity in his left eye. The visual acuity was 0.2 and there was RAPD in the left eye. Fundoscopy revealed an elevation of the optic disc obscuring disc vessels with epiretinal gliosis. Fluorescein angiography demonstrated hyperfluorescent saccular dilatations with leakage in the late phase. Ocular Coherence Tomography (OCT) showed hyperreflective elevation of the optic disc and epiretinal membrane. There was a juxtapapillary scotoma in Semi-automated Kinetic Perimetry (SKP). There was no systemic diseases. Results of blood tests, CT and MRI of CNV were normal. Results: After 3 years period of the follow-up the visual acuity was 0.1 and there was a progression of the visual field defect to the altitudinal scotoma in the upper hemisphere. Fluorescein anhiography and OCT revealed the same. Conclusion: Hamartoma of RPE and optic disc is a rare condition consisting of glial, vascular and RPE cells. It should be differentiated from optic disc oedema and vascular tumors of the retina. Assessment of the visual function is very important in the longitudinal follow-up.
基金This study was supported by the Natural Science Foundation of Tianjin
文摘Background： The mechanisms of pathological retinal neovascularization （RNV） remain unknown. Several microRNAs were reported to be involved in the process of RNV. Oxygen-induced retinopathy （O1R） is a useful model to investigate RNV. Our present work explored the expression and the role of microRNA-128 （miR-218） in oxygen-induced RNV. Methods： OIR was used to establish RNV model. The expression level ofmiR-218 in the retina from OIR mice was assessed by quantitative real-time reverse transcriptase polymerase chain reaction. Fluorescein angiography was performed in retinae of OIR mice, and RNV was quantified by hematoxylin and eosin staining to evaluate the effect of pCDH-CMV-miR-218 intravitreal injection on RNV in OIR mice. Roundabout 1 （Robol） expression was detected by Western blotting in mouse retinal vascular endothelial cells expressing a high or low level of miR-218 and retinal tissues from OIR mice. Cell migration was evaluated by scratch wound assay. Results： In OIR mice, the expression level of miR-218 was significantly down-regulated （P = 0.006）. Retinal Robol expression was significantly increased at both mRNA and protein levels （P = 0.001, 0.008： respectively）, miR-218 intravitreal injection inhibited retinal angiogenesis in OIR mice, and the restoration of miR-218 in retina led to down-regulation of Robol. Conelusions： Our experiments showed that restoration ofmiR-218 inhibited retinal angiogenesis via targeting Robo 1. MiR-218 contributed to the inhibition of retinal angiogenesis and miR-218 might be a new therapeutic target for preventing RNV.
