L形钛板黄斑外垫压治疗近视牵拉性黄斑病变

目的评价L形硅海绵钛板黄斑外垫压联合玻璃体切割术治疗近视牵拉性黄斑病变的临床疗效。方法前瞻性研究收集2015年8~11月在中南大学湘雅医院行L形硅海绵钛板黄斑外垫压联合玻璃体切割术的7例7眼近视牵拉性黄斑病变患者的临床资料,术后随访观察黄斑形态变化(如劈裂腔有无缩小或消失),最佳矫正视力、眼轴长度及眼压变化情况。计量资料采用t检验进行统计学分析。结果随访时间为4~6个月,黄斑部劈裂腔完全消失者2例,明显缩小者5例。患者术前平均LogMAR视力为(1.50±0.50),末次随访平均LogMAR视力为(0.87±0.32),差异有统计学意义(P<0.05)。至末次随访时,患者的平均眼轴为(27.72±1.75)mm,术前平均眼轴为(28.72±1.97)mm,差异有统计学意义(P<0.05)。其中1例患者术后1周出现高眼压,加用2种局部降压滴眼液,眼压恢复正常,至术后1.5个月停药。结论 L形硅海绵钛板黄斑外垫压联合玻璃体切割术治疗近视牵拉性黄斑病变是一种有效的手术方法。

Treatment of myopic foveoschisis via macular buckling and vitrectomy

The aim of the present study was to evaluate the efficacy and safety of the treatment of myopic foveoschisis patients using the macular buckling with L-shaped titanium plate and silicon sponge combined with vitrectomy. The data of the patients who underwent macular buckling combined with vitrectomy was collected. The study recorded the following parameters：best corrected visual acuity（BCVA）, axial length, intraocular pressure, central macular thickness, and the position of the titanium plate. Following the surgery, the BCVA of the included patients were improved, whereas the axial lengths were reduced followed by resolution of the foveoschisis compared with that noted prior to the operations. All patients had orbital CT examination and the results indicated that the titanium plates were appropriately placed and were not in contact with the optic nerve. Therefore, it is effective to treat myopic foveaschisis by macular buckling using the L-shaped titanium plate and silicon sponge in the presence of vitrectomy.

Effect of pyridone agent on blood-retinal barrier in diabetic mice

AIM： To evaluate the therapeutic effect of fluorofenidone on disrupted blood-retinal barrier in the diabetic mice and uncover its underlying mechanism. METHODS： db/db mice were randomly chosen for treatment with daily doses of fluorofenidone or placebo at 5-week-old, treatment continued until mice reach 24-week- old. Then, expression of transcriptiona factor insulin gene enhancer binding protein-1 （Islet-I） and vascular endothelial growth factor （VEGF） in murine retinas were evaluated. Retinal vascular permeability was assessed by examining the level of albumin in db/db murine retinas. Furthermore, the retinal vessel tight junction was estimated by checking the level of occludin in the murine retinal tissues. RESULTS： After occurrence of diabetic retinopthy in db/ db mice, expressions of transcritpional factor Islet-1 was found to be upregulated in db/db murine retinas compared with non-diabetic controls. Similar to expression pattern of Islet-l, VEGF were also demonstrated to be increased in retinas of db/db mice, which was accompanied by increased retinal vascular leakage and decreased tight junction protein level. Systemetic administration of fluorofenidone repaired broken retinal vascular tight junction by restoring occludin expression in db/db retinal tissue. Consequently, retinal vascular premeability were indicated to be reduced by examining the transudative albumin level in diabetic retinal tissues. Both Islet-1 and VEGF expression were inhibited in the retinas of db/db mice after treatment with fluorofenidone. CONCLUSION： Fluorofenidone significantly protectes retinal tight junction and reduces retinal vascular leakage. The phenomenon can be partially attributed to reducing overexpression of Islet-1 and VEGF in diabetic retinal tissues.

Activation of the ERK 1/2 and STAT3 signaling pathways is required for 661W cell survival following oxidant injury

AIM: To evaluate the influence of hydrogen peroxide (H2O2) on mouse photoreceptor-derived 661W cell survival and to determine the effect of PD98059, an inhibitor for MEK1 (the direct upstream activator of ERK1/2), and S3I201, a STAT3-specific inhibitor on 661W cell survival after H2O2 exposure. METHODS: The mouse photoreceptor-derived 661W cells were cultured. 661W cells were treated for 12 hours with different concentrations (0, 0.25, 0.50, 0.75, 1mmol/L) of H2O2 and cell viability was determined by 3- (4, 5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide) (MTT) assay. 661W cells were treated with different concentrations H2O2 (0, 5, 10, 50, 500, 1000 mu mol/L) for 15 minutes or 1mmol/L H2O2 for different time points (0,5,10,15,30 minutes), and p-Tyr705-STAT3, STAT3, Phospho-p44/42 MAPK (Thr202/Tyr204), ERK1/2 were surveyed by immunoblot analysis. After treatment with 50 mu mol/L PD98059, or S3I201 for 1 hour, the inhibition efficiency of cell signal pathways was analyzed by immunoblot analysis and the effects of inhibitors on cell viability were determined by MTT. RESULTS: After treating with different concentrations of H2O2 for 12 hours, the cell viability of 661W cells decreased in concentration-dependent manner (P<0.05). Moreover, H2O2 induced phosphorylation of ERK1/2 and STAT3 in 661W cells (P <0.05). After pretreatment with 50 mu mol/L PD98059 or S3I201 for 1 hour, H2O2-induced phosphorylation of ERK1/2 or STAT3 was suppressed separately (P<0.05). Using PD98059 or S3I201 to inhibit ERK1/2 or STAT3 signal pathway, the cell viability of 661W cells decreased significantly (P<0.05). CONCLUSION: We demonstrated that the exposure of 661W cells to H2O2 increased the activation of ERK1/2 and STAT3 signal pathways. Activation of these pathways is required for 661W cell survival following oxidant injury.