Retinopathy of prematurity (ROP) is the leading cause of blindness for children, early detection and treatment can prevent ROP progression and improve the visual prognosis. ROP prevention system, including advocacy, screening, diagnosis/treatment and follow-up, is the key to reducing the rate of blindness in children. The proposed tertiary ROP prevention network includes primary health centers in county-level, secondary health centers in municipal-level and tertiary health centers in provincial-level or national-level. The idea is to explore the greatest benefits in the ROP prevention process from the existing allocation of medical resources, but also to avoid wasting at the current stage of social development. We tested this idea in Shaanxi Province recently. The preliminary practice results indicated that ROP tertiary prevention network can increase the ROP screening coverage, promote the prevention and treatment of ROP. However this work is still in its infancy. We need to expand its scope and strength the advocacy efforts to find a way to prevent and treat ROP in China.
PURPOSE:In search of the mechanism for photic retinal injury. METHODS:A visible light damage model was established in the primary cultured healthy,adult human RPE cells by using intense fluorescence light (2 400 Lx). RESULTS:Electron microscopy revealed swelling of the mitochondria and obscurity of nuclear membranous structure in the light damaged cells. The decrease or dissolution of organelle,vacuolization of cytoplasm and myelinic degeneration were found in some severely damaged cells. The level of intracellular SOD was decreased to 41% of that of the controls (P＜0.05). CONCLUSION:The structure of the RPE was damaged by the light radiation and the level of intracellular SOD was decreased. These suggested the light damage might be associated with the production of free radicals and the lipid perioxide reaction in membranous structure of cell. （Chin J Ocul Fundus Dis,1996,12: 174-175 ）
Objective To clarify the relationship between inhibition of proliferation and cxpression of Ki-67 in cultured human retinal pigment epithelial(RPE) cells. Methods The cultured human RPE cells were treated with daunoblastina at a dose of 180 mu;g/L for 12h.Twenty-four hours later,DNA inhibiting rate was studied by using tritium-labelled thymidine deoxyribose(3H-TdR)incorporation assay.The expression of Ki-67 was evaluated by immunocytochemical staining technique and image analysis system.Flow cytometry was used to analyse cell cycle. Results DNA inhibiting rate was directly proportional to the dosage of daunoblastina.The proportion of the cells positive staining to Ki-67 in the control and the daunoblastina-treated group were 89.3% and 45.6%(Plt;0. 01),and the integral optical density values for expression of Ki-67 in the two groups were 68.1plusmn;6.2 and 27.3plusmn;5.5(Plt;0.01),respectively.The percen tage of cells in G2 phase of cell cycle increased from 8.9% to 29.5%. Conclusion G2 block was induced and poliferation was inhibited by daunoblastina in cultured human RPE cells.There is a relatively good correlation between Ki-67 immunostaining and inhibition of RPE cell proliferation. (Chin J Ocul Fundus Dis，2000，16：1-70)
The introduction of anti-vascular endothelial growth factor (VEGF) therapy represents a landmark in the management of wet age-related macular degeneration (AMD). However, as a new therapy, several problems such as durability of the therapeutic effects, medication side effects, and medication selection have emerged. We should make appoint of improving the therapeutic effect and safety by realizing the limitation of the therapy, monitoring the clinical potential adverse reactions of anti-VEGF agents, and recommending individualized treatment.
Objective To investigate the molecular mechanism of apoptosis in cultured human retinal pigment epithelial (RPE) cells. Methods The growth media of confluency human RPE cells were replaced with a daunoblastinacontaining one at a dose of 180mu;g/L,and the cells were incubated for 12 hr at 37℃.After incubation with the drug,the medium was withdrawn,fresh medium was added and incubation was carried out for an additional 24 hr.Apoptosis was monitored by light microscopy,enzyme linked immunosorbent assay(ELISA)and terminal deoxynucleotidyl transferase mediated biotin-dUTP nick-end labelling(TUNEL)staining.The expression of bax and bcl-2 were evaluated by immuncoytochemical staining with anti-human bcl-2 and bax antibodies. Results After the RPE cells treated with daunoblastina,shrinkage of cytoplasm and nucleus was identified.The ratio of nucleus to cytoplasm was increased.TUNEL staining showed that many cells were positive staining.The amount of apoptotic cells was directly proportional to the drug dose.The integral optical desity values for expression of bax inereased by 22.0%(Plt;0.05), and that of bcl-2 did not change significantly(Pgt;0.05). Conclusions During human RPE cell apoptosis induced by daunoblastina,overexpression of bax or low bcl-2/bax ratio were demonstrated.The results suggest that bax and bcl-2 gene expression could play a role in regulation of RPE cell apoptosis. (Chin J Ocul Fundus Dis, 1999, 15: 153-156)