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1.
International Eye Science ; (12): 2063-2066, 2016.
Article in Chinese | WPRIM | ID: wpr-638123

ABSTRACT

AIM:To compare the clinical efficacy of three combined surgical treatments for cataract induced by silicone oil -filled eye. METHODS: The data of 75 eyes of 75 patients with cataract induced by silicone oil-filled eye were reviewed. Those patients were divided into group A, B, C. The patients in group A were treated by phacoemulsification combined with silicone oil removal through pupil and IOL implantation, the patients in group B were treated by phacoemulsification combined with silicone oil removal through 23G vitrectomy system and IOL implantation, the patients in group C were treated by phacoemulsification combined with silicone oil removal through 20G vitrectomy system and IOL implantation. The operation time, intraocular pressure, best corrected visual acuity ( BCVA ) , discomfort days and complications before and after the surgery were compared. RESULTS: The differences of the intraocular pressure were not statistically significant between the three groups after the surgery. The BCVA of the three groups were all improved, but the differences were not statistically significant between three groups. The differences in postoperative complications showed no statistically significant. Otherwise, group A and B cost less operation time. The discomfort days of group A were less than other groups. CONCLUSION: Three different surgical methods were safe and effective, appropriate surgical approach could be chosen according to the patients' clinical manifestations. For patients with cataract induced by silicone oil-filled eye whose retina recovered well, phacoemulsification combined with silicone oil removal through pupil and IOL implantation is a time-saving, safe and effective method.

2.
Chinese Journal of Experimental Ophthalmology ; (12): 602-607, 2013.
Article in Chinese | WPRIM | ID: wpr-636144

ABSTRACT

Background Rhodopsin (RHO) gene is the most common disease gene for autosomal dominant retinitis pigmentosa (adRP),one of the main pathogenesis is that misfolded mutant RHO proteins accumulate in the endoplasmic reticulum and cause endoplasmic reticulum stress (ERS).Objective This study aimed to determine the genetic basis for a consanguineous Chinese Han adRP family.Methods This study procedure complied with Helsinki Declaration.All participants in the family were investigated under the informed consent.Regular ocular examination was performed on the patients in this family.Next-generation sequencing (NGS) was carried out to screen the mutations in 189 genes associated with hereditary retinal diseases (HRDs).After being analyzed and filtered,variations detected by NGS were validated by Sanger sequencing and evaluating of pathogenicity.The wild-type RHOWT and mutant RHOP53Rwere cloned into the vector pEGFP-N1.Then the two plasmids were transfected into adult retinal pigmentosa epithelium cell line(ARPE19) and human embryo kidney 293 line (HEK293) to observe the location of rhodopsin-GFP fusion protein in cells,and the expression of ERS related protein XBP1 in the cells was detected by quantitative-PCR and Western blot.Results This family included 5 generations with the typical adRP characteristics.Genetic analysis identified a heterozygous variation,p.P53R in RHO gene,which was fully cosegregated in the family.Wild-type RHOWT-GFP fusion proteins showed the green fluorescence on the endoplasmic reticulum and cytomembrane,but the misfolded mutant RHO-GFP fusion protein gathered only in endoplasmic reticulum.Compared to wild-type RHOWT,the XBP1 was activated and increased by (1.28 ±0.09) fold.The introns of 26 bases in XBP1 mRNA were removed in the HEK293 cells with mutant RHO-GFP fusion protein,and the expression of XBP1 was stronger in the HEK293 cells with mutant RHO-GFP than that in HEK293 cells with wild type RHO-GFP and cells with blank pEGFP-N1 plasmid.Conclusions Heterozygous variant RHO p.P53R is very likely the pathogenical mutation in the adRP family.The RHOP53R mutant rhodopsin protein can not be delivery effectively from the endoplasmic reticulum to the cell membrane,and these proteins accumulate in the endoplasmic reticulum,which causes ERS.

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