Analysis of the effect of repair materials for orbital blowout fracture on complications

AIM: To investigate the effect of repair materials for orbital blowout fractures on the occurrence of postoperative complications. METHODS: The clinical data and follow-up data of 54 subjects with orbital blowout fractures were retrospectively analyzed. The study was divided into three groups according to the used repair materials: titanium mesh(16 cases), Medpor(12 cases), and Medpor titanium mesh(26 cases). All test data were analyzed using the SPSS version 23.0 statistical software. The mean age and duration of disease between the groups were compared through oneway analysis of variance. The Chi-square(χ~2) test was used to compare the number of males and females, different fracture types, and different surgical approaches among groups. The χ~2 test was used to compare the frequencies for complications in each group.RESULTS: The baseline characteristics of age and gender in each group were matched(F=1.763, P=0.172;χ~2=0.026, P=0.987). In addition, there was no difference in the type of fracture and surgical approach(χ~2=0.460, P=0.977;χ~2=0.691, P=0.952), or the incidence of complications(χ~2=0.081, P=0.960) between the three groups. CONCLUSION: Although there is no difference in effect of various repair materials on the incidence of complications, the effect of repair materials on postoperative complications of orbital blowout fractures should not be ignored.

Effect of luteolin on apoptosis and vascular endothelial growth factor in human choroidal melanoma cells

AIM:To investigate the effects of luteolin on apoptosis,the cell cycle,and the expression and secretion of vascular endothelial growth factor(VEGF)in human choroidal melanoma cells(C918 and OCM-1).METHODS:C918 and OCM-1 cells cultured in vitro were treated with various concentrations of luteolin(0,5,10,15μmol/L).Cell growth was observed with an inverted microscope,and cell cycle arrest was detected by propidium iodide(PI)staining using flow cytometry.Apoptosis was detected by Hoechst33342 staining,and apoptosis rate was determined by Annexin V-FITC/PI experiments using flow cytometry.The expression of apoptosis-related proteins Bcl-2,Bax and VEGF was analyzed using Western blots.The levels of VEGF secreted by the cells into the supernatant was analyzed using ELISA.RESULTS:After treating with 5 to 15μmol/L luteolin for 48 h,the fusion degree of C918 and OCM-1 cells decreased,and more floating apoptotic cells appeared.Luteolin treatment increased the G0-G1 phase ratio of the C918 and OCM-1 cells,blocked cell cycle progression,and increased the apoptosis rate of the C918 and OCM-1 cells.Western blot showed that luteolin decreased the expression of Bcl-2 and VEGF in the C918 and OCM-1 cells and increased the expression of Bax protein.The ELISA results showed that 10 to 15μmol/L luteolin decreased the cell secretion of VEGF.CONCLUSION:Luteolin may induce apoptosis by regulating the levels of apoptosis-related proteins in C918 and OCM-1 cells.Luteolin can induce cell cycle arrest,decrease the expression of VEGF.

Mitochondrial dysfunction in glaucomatous degeneration

Glaucoma is a kind of optic neuropathy mainly manifested in the permanent death of retinal ganglion cells(RGCs),atrophy of the optic nerve,and loss of visual ability.The main risk factors for glaucoma consist of the pathological elevation of intraocular pressure(IOP)and aging.Although the mechanism of glaucoma remains an open question,a theory related to mitochondrial dysfunction has been emerging in the last decade.Reactive oxygen species(ROS)from the mitochondrial respiratory chain are abnormally produced as a result of mitochondrial dysfunction.Oxidative stress takes place when the cellular antioxidant system fails to remove excessive ROS promptly.Meanwhile,more and more studies show that there are other common features of mitochondrial dysfunction in glaucoma,including damage of mitochondrial DNA(mt DNA),defective mitochondrial quality control,ATP reduction,and other cellular changes,which are worth summarizing and further exploring.The purpose of this review is to explore mitochondrial dysfunction in the mechanism of glaucomatous optic neuropathy.Based on the mechanism,the existing therapeutic options are summarized,including medications,gene therapy,and red-light therapy,which are promising to provide feasible neuroprotective ideas for the treatment of glaucoma.

A pedigree with retinitis pigmentosa and its concomitant ophthalmic diseases

AIM:To characterize the ophthalmic clinical phenotype of a family with retinitis pigmentosa(RP)and closed-angle glaucoma and to detect pathogenic genes and mutation sites causing RP in this family.METHODS:Ophthalmic clinic performance was examined in detail in 8 enrolled family members.Genomic DNA was extracted from the peripheral blood of 4 family members for whole-exome sequencing(WES)to select potential genetic mutations whose structures were identified by bioinformatics analysis.Then,Sanger sequencing was used in 12 family members and control group members to validate and confirm the disease-causing mutation loci,and we analyzed the genotype-phenotype relationships.RESULTS:The known c.512C>T(p.P171L)mutation in the rhodopsin(RHO)gene was only found in afflicted family members and was confirmed by WES and Sanger sequencing as the pathogenic mutation in this family.In addition to being diagnosed with RP,family member III:4 was found to have bilateral closed-angle glaucoma,high myopia,and concurrent cataracts,and family members II:2 and II:4 had pathological changes of anterior chamber angle narrowing.Family members IV:3 and IV:4 were found to have retinoschisis.CONCLUSION:Glaucoma and related pathological changes,such as retinoschisis,in family members are preliminarily considered RP complications caused by RHO mutation.