A modified approach to actively remove high viscosity silicone oil through 23-gauge cannula

AIM：To report a simple approach to actively remove high viscosity silicone oil through a 23-gauge cannula via pars plana.METHODS：Forty-eight eyes of 48 patients underwent silicone oil（5700 centistokes） removal（SOR） were enrolled.A section of blood transfusion set was prepared to connect a standard 23-gauge cannula and vitrectomy machine.Silicone oil was removed with suction of500-mm Hg vacuum through the cannula.Main outcome measures were SOR duration,number of sutured sites,intraocular pressure（IOP）,best-corrected visual acuity（BCVA）,and complications.RESULTS：Silicone oil was successfully removed in all cases.The mean SOR time was 5.70±0.85 min.Nine eyes（18.75%） needed suture partial sclerotomies.No intraoperative complications were noted.Transient hypotony（≤8 mm Hg） was seen in 3 eyes（6.25%） on postoperative day 1,but all resolved within 1wk.Retinal reattachment was achieved in all cases and no other postoperative complications were noted during 3-month following-up.BCVA at the final visit improved or stabilized in all patients comparing to the preoperative level.CONCLUSION：Active removal of high viscosity silicone oil through a 23-gauge instrument cannula jointed with blood transfusion set is a practical and reliable technique when considering two sides of efficacy and safety.

The novel chalcone analog L2H17 protects retinal ganglion cells from oxidative stress-induced apoptosis

Chalcone is a plant metabolite widely found in fruits,vegetables,spices and tea,and has anti-tumor,anti-inflammation,immunomodulation,antibacterial and anti-oxidation activities,as well as many other pharmacological and biological effects.Our team has shown that its analogs have antioxidant activity,and oxidative stress is a pathological hallmark of retinal ischemia/reperfusion injury that can lead to retinal damage and visual loss.This investigation aims to identify a chalcone that protects retinal ganglion cells in vitro from the effects of oxidative stress and examine its mechanism.Rat retinal ganglion cell-5 cells were pretreated with chalcones and then exposed to tert-butyl hydroperoxide that causes oxidative damage.Controls received dimethyl sulfoxide only or tert-butyl hydroperoxide in dimethyl sulfoxide.Only（E）-3,4-dihydroxy-2′-methylether ketone（L2 H17）,of the five chalcone analogs,markedly increased the survival rate of oxidatively injured RGC-5 cells.Thus,subsequent experiments only analyzed the results of the L2 H17 intervention.Cell viability and apoptosis were measured.Intracellular superoxide dismutase and reactive oxygen species levels were used to assess induced oxidative stress.The mechanism of action by L2 H17 was explored by measuring the ER stress/UPR pathway and the expression and localization of Nrf2.All results demonstrated that L2 H17 could reduce the apoptosis of oxidatively injured cells,inhibit caspase-3 activity,increase Bcl-2 expression,decrease Bad expression,increase the activity of superoxide dismutase,inhibit the production of reactive oxygen species,increase Nrf2 immunoreactivity,and reduce the activating transcription factor 4,phospho-eukaryotic initiation factor 2 and CHOP expression.L2 H17 protects retinal ganglion cells induced by oxidative stress by regulating Nrf2,which indicates that it has the potential to become a drug for retinal ischemia/reperfusion.

PI3K-mediated glioprotective effect of epidermal growth factor under oxidative stress conditions

AIM:To determine the effects of epidermal growth factor(EGF)on the proliferation and migration of Müller cell line Moorfields/Institute of Ophthalmology-Müller 1(MIO-M1),and its related molecular mechanisms under normal and oxidative stress conditions.METHODS:Müller cells were cultured with different concentrations of EGF in the presence or absence of varied amounts of H2O2and glucose oxidase(GO)which induced oxidative stress.The proliferation and migration of Müller cells were examined by 5-Bromo-2-deoxy Uridine(BrdU),MTT assay,Transwell assay and scratch wound healing assays.The cell viability was determined with the MTT assay.The secretion of EGF by Müller cells was evaluated by ELISA.Western blot was performed to detect the activation of extracellular regulated protein kinases(ERK)1/2 and Akt signal pathways.RESULTS:EGF stimulated the proliferation and migration of Müller cells in a concentration-dependent manner in vitro.Under oxidative damage condition,2h of pretreatment with 10-100 ng/mL EGF can mostly inhibit 50% lethal dose of 0.08 mmol/L H2O2-induced cell damage.The Western blot results showed that after Müller cells were exposed to varying EGF for 24h,Akt and ERK1/2 were phosphorylated in a dose-dependent manner.In the presence of the LY294002,the potent PI3K inhibitor,the p-Akt was significantly attenuated.CONCLUSION:EGF may induce the proliferation and migration of human Müller cells through the Akt and the ERK1/2 signal pathways,and induce PI3K-mediated glioprotective effect under oxidative stress.