Background: Retinal ischemia-refusion (I/R) is a leading cause of irreversible blindness worldwide. This study aims to explore the regulatory role of SOX9 in retinal I/R injury, and attempts to elucidate its potential regulatory mechanism. Methods: Retinal I/R injury model was established in vivo, and the histological changes was examined by hematoxylin and eosin (H&E) staining and immunofluorescent assay was performed to examine SOX9 expression. Oxygenation-glucose deprivation/reoxygenation (OGD/R)-induced retinal ischemia/reperfusion (I/R) injury in 661 W cells was constructed as an in vitro cellular model of glaucoma. The production of cytokines, lactate dehydrogenase (LDH) and the antioxidant enzymes were assessed by their commercial kits. Cellular reactive oxygen species (ROS) and lipid ROS was detected using DCFH-DA and C11-BODIPY 581/591 staining, respectively. Lipid peroxidation and Fe2+ level were detected to assess the ferroptosis level. Protein expression was examined by western blot. LM22B-10, the agonist of ERK signaling, was used to pretreat 661 W cells for mechanism investigation. Results: SOX9 was aberrantly upregulated following retinal I/R injury both in vivo and in vitro. SOX9 knockdown exerted a protective role against OGD/R-triggered oxidative stress, inflammatory response and ferroptosis in 661 W cells. Further, ERK/p38 signaling was activated in 661 W cells following OGD/R induction, which was repressed by SOX9 knockdown, and the ERK signaling agonist partially counteracted the protective role of SOX9 knockdown against oxidative stress, inflammatory response and ferroptosis in OGD/R-induced 661 W cells. Conclusion: Collectively, inhibiting SOX9 to block oxidative stress, inflammation and ferroptosis by inactivating ERK/p38 signaling might be effective to prevent retinal I/R injury, thereby alleviating glaucoma.

目的 本研究旨在揭示黄芩苷对氧化应激状态下视网膜色素上皮细胞的保护作用.方法 AMD模型构建及氧化应激损伤评估;实验组、对照组及黄芩苷干预组分别作用于细胞,检测细胞衰老状态,ROS(reactive oxidative species)累积,细胞增殖、凋亡(apoptosis)状态以及Real-Time定量荧光聚合酶链反应分析SIRT1 mRNA水平.结果 1.氧化应激能造成ARPE损伤,并导致SIRT1 mRNA表达水平下降,差异有统计学意义(P<0.05).2.黄芩苷高、低剂量组能显著改善细胞衰老状态,促进增殖,降低凋亡,并显著改善SIRT1 mRNA水平,差异有统计学意义(P<0.05).结论 ARPE细胞氧化应激损伤中黄芩苷能起到负向调节作用,意味着黄芩苷具有抗氧化应激损伤的作用,为临床AMD治疗提供了思路.

目的 探讨白内障超声乳化并人工晶体植入术对睑板腺功能的影响.方法 随机选取我院2018年1月至2019年1月接受白内障超声乳化联合人工晶体植入手术的患者60例.采取临床OSDI问卷评分、非接触泪膜破裂时间[NITBUT]测量、睑板腺(MGs)评分、泪膜脂质层厚度检查、睑板腺分泌物评分进行研究.在白内障术前和术后1个月、2个月分3次检测.结果 术后1个月和2个月,OSDI量表评分较术前增加[(20.3±13.6)分,P＜0.05;(23.2±10.4)分,P＜0.05];非接触泪膜破裂时间缩短[(6.5±2.6)s,P＜0.05;(6.2±3.6)s,P＜0.05];泪膜脂质层厚度下降[(62.1±21.4)nm,P＜0.05;(65.7±15.7)nm,P＜0.05];术后1个月睑板腺结构评分与术前差异无统计学意义[(2.2±1.6)分,P＞0.05],术后2个月评分显著降低[(2.1±1.5)分,P＜0.05];术后1个月和2个月睑板腺分泌物性状评分与术前差异无统计学意义(P＞0.05).结论 白内障超声乳化并人工晶体植入术对睑板腺存在明确影响,术后患者干眼症状出现或加重,睑板腺腺体丢失,泪膜脂质层厚度下降.远期影响需继续研究.

Objective To investigate the interactions between histone deacetylas-1 (silent information regulator of transcription 1,SirT1) and signal transducer and activator of transcription 3 (STAT3) following exposure to oxidative stress of retinal pigmented epithelium (RPE) cells through gene knockout and overexpression techniques.Methods RPE cell line was cultured in vitro,followed by addition of H2O2 for inducing oxidative stress.The targeting knockout strategy (siRNA/shRNA) was used for silencing SirT1/STAT3 gene and lentiviral vectors (pRC/CMV STAT3 and PCRC/CMV) were transfected to RPE cells.RT-qPCR and Western blot were used to detect the expression of SirT1/STAT3 due to gene knockout and overexpression and deeply analyze the effects of SirT1/STAT3 on RPE cells exposed to oxidative stress.Results SirT1 activator (resveratrol) significantly reduced the expression of STAT3 mRNA to (3.0 ± 0.2) (P =0.048);and after SifT1 knockout,the expression of STAT3 mRNA in RPE cells was significantly increased to (6.9 ± 1.1) (P =0.025).During the oxidative stress of RPE cells after SifT1 knockout,the expression of STAT3 and phosphorylated STAT3 protein were significantly increased to 0.990 ±0.031 and 0.544 ±0.019,respectively (P =0.000,0.003).With the condition of oxidative stress,the over-expression of STAT3 reduced the SirT1 mRNA expression to 0.42 ± 0.16 (P =0.022),but SifT1 mRNA expression was significantly increased to 2.8 ±0.85 (P =0.015) during STAT3 knockdown.Conclusion SifT1 has a negative effect on the regulation of STAT3 expression during oxidative stress,which suggests that there is an equilibrium mechanism between SirT1 and STAT3 against oxidative stress.

目的 本研究旨在观察信号转导/转录激活因子3(signal transduction/activation of transcription factor3,STAT3)对视网膜色素上皮细胞(retinal pigment epithelium cells,RPE)氧化应激损伤的保护作用,并探讨STAT3在年龄相关性黄斑变性(age-related macular degeneration,AMD)发病机制中的意义.方法 体外培养ARPE-19细胞系,氧化低密度脂蛋白及H2O2干预培养细胞诱导氧化应激损伤,通过对细胞增殖、凋亡、活性氧族(reactive oxygen species,ROS)水平及细胞衰老分析研究,评估氧化应激损伤对RPE的影响;实时荧光定量技术分析氧化应激过程中STAT3-mRNA表达状况;STAT3过表达载体转染ARPE-19细胞,烟酰胺预处理细胞再经H2O2及氧化低密度脂蛋白干预后通过对增殖、凋亡、ROS及细胞衰老状态的分析,了解STAT3抗RPE氧化应激效果.结果 与对照组相比,H2O2和氧化低密度脂蛋白能显著增加ROS水平,促使细胞衰老增加,细胞的增殖显著下降而细胞凋亡显著上升(均为P＜0.05).氧化应激状况下STAT3上游产物表达上升,氧化低密度脂蛋白及H2O2组荧光表达强度分别是3.3±1.2及3.5±1.1,与对照组相比差异均有统计学意义(均为P＜0.05);STAT3能保护ARPE-19细胞抗氧化应激损伤,使细胞增殖增加、凋亡减少及ROS累积,但不造成细胞衰老状况加剧,说明ARPE-19细胞衰老不受STAT3调节.结论 STAT3在细胞氧化损伤中能独立地发挥抗氧化应激作用,提示了STAT3在AMD治疗过程中的应用前景.

BACKGROUND:Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes. The present study aimed to identify a possible connection between gene polymorphisms and the risk of developing DR. MATERIALS AND METHODS:A total of 319 patients with type 2 diabetes mellitus (T2DM) were selected. All patients underwent a complete eye examination. Based on this, the patients with T2DM were divided into two subgroups: 175 patients with retinopathy (DR) and 144 patients without retinopathy (NDR). We calculated the genotype frequencies of case and control subjects using the chi-squares test. The odds ratio (OR) and 95% confidence intervals (CIs) were calculated by unconditional logistic regression adjusted for age and sex. RESULTS:The finding by analysis is that the mean of duration of diabetes, total cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL), glomerular filtration rate and C-peptide were significantly different between DR and NDR. We found significant differences in cystatin-C concentrations with LEKR1-CCNL1 rs13064954 and NOS3 rs3918227 of different genotypes. Significant differences in serum TG levels were seen among the three genotypes of MTHFR rs1537516. Subjects carried the T allele of IGSF21-KLHDC7A rs3007729 had higher serum LDL concentrations (p = 0.015). In the allele model, LEKR1-CCNL1 rs13064954 decreased the risk of DR (OR =0.57, 95% CI = 0.34-0.96, p = 0.032). Under the dominant model, the IGSF21-KLHDC7A rs3007729 CT-TT genotype increased the risk of DR (OR =1.84, 95% CI = 1.14-2.99, p = 0.013). CONCLUSIONS:Our results suggest that LEKR1-CCNL1 and IGSF21-KLHDC7A influence the development of DR.

Objective:To evaluate the changes in intraocular pressure ( IOP ) after intravitreal injection of triamcinolone acetonide for the management of diabetic macular edema( DME) . Methods:The study design is a prospective, interventional, dose-response study. 83 eyes with DME were included,Randomly divided into two groups,eyes of one group underwent intravitreal injection of 4 mg triamcinolone acetonide(42 eyes),and eyes of another group underwent intravitreal injection of 8 mg triamcinolone acetonide ( 41 eyes ); The patients were followed up for 6 months after injection;Intraocular pressure was measuremented and controled. Results:After injection. Significant IOP rise was observed in both groups with an incidence of 76. 2%and 73. 2%in groups A and B,respectively. IOP-lowering drugs were used to control IOP,satisfactory effect was achieved. however,six eyes needed glaucoma filtration surgery after intractable glaucoma with failure of medical treatme-nt. Conclusion:Although intravitreal injection of triamcinolone acetonide is very effective in managing DME and with lower cost than other modalities,the rise in IOP and the burden of glaucoma are major concerns. High corticosteroid responder is an individualized reaction irrespective of the intravitreal triamcinolone acetonide dose used.

Retinal pigmented epithelial cell (RPE) oxidative stress is known to have a vital role in the etiology of age‑related macular degeneration (AMD). The present study aimed to investigate whether allicin, a natural product with antioxidant activity, was able to protect RPEs (ARPE‑19) from hydrogen peroxide (H2O2)‑induced damage, and to determine the underlying mechanisms. The 3-(4,5-dimethylthiazol-2-yl)-2,5‑diphenyl tetrazolium bromide assay was used to determine cellular viability, and reactive oxygen species (ROS) were detected using a ROS Assay kit. The results demonstrated that allicin was able to protect ARPE‑19 cells from H2O2‑induced damage in a dose‑dependent manner. In addition, allicin attenuated oxidative stress by reducing the levels of intracellular ROS and malondialdehyde (MDA), and enhancing the glutathione/glutathione disulfide (GSSG) ratio. With regards to the underlying mechanism, allicin was able to markedly modulate the expression levels of ROS‑associated enzymes, including superoxide dismutase, NADPH oxidase 4 and NAD(P)H dehydrogenase quinone 1, and elevate the activity of nuclear factor erythroid 2‑related factor 2 in the H2O2‑stimulated ARPE‑19 cells. These results suggested that allicin may exert protective effects against H2O2‑induced cytotoxicity in RPEs via ROS regulation.

through the copyediting, typesetting, pagination and proofreading process which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1002/jgm.2926 This article is protected by copyright. All rights reserved. Association between LEKR1-CCNL1, IGSF21-KLHDC7A gene polymorphism and Diabetic Retinopathy of Type 2 Diabetes mellitus in Chinese Han Population Xiaohui Lin 1, # , Jihong Wang 2 , Lixia Yun 1 , Shuhong Jiang 1 , Langen Li 1 , Xiaohai Chen 1 , Zhen Li 1 , Qiang Lu 1 , Yihui Zhang 1 , Xiaocheng Ma 1

Objective To evaluate the relationship between the rate of development of juvenile myopia, the position of the eye, accommodation, the myopia, the corneal curvature and the outdoor activities , and provide evidence of myopia prevention and treatment .Methods Collected from May 2012 to March 2016&nbsp;in Inner Mongolia Region People′s Hospital optometry clinic teen-agers with complete data reviewed 386 cases (772 eyes).In age from 6 to 13 years old.Cycloplegic refraction measured by spherical equivalent -0.75 D of myopia or more was defined as the onset of myopia .Be wearing best corrected visual acuity maximum positive lens of the principle of prescription glasses .A year later review of the refractive state of the patient , for statistical analysis .Results The comparison results between the eye position display , exophoria person increase in myopia degree is the average (0.82±0.16) D, (0.62±0.14) D and (0.71±0.19) D, as those who, through the single factor variance analysis between the three groups there were statistically significant differences ( F=42.87, P<0.05); further pairwise comparisons exophoria , implicit strabismus and implicit strabismus difference were statistically significant ( t=3.75, 3.16;P<0.05) , and intraocular heterophoria is a myopic development speed between groups comparison , difference of no statistical significance ( t=1.94, P>0.05) .Regulation mode comparison results shows , accommodative lag myopia increased the average speed for (0.91±0.36) D, (0.52±0.22) D and (0.67±0.15) D, through the single factor variance analysis , differences between the three groups have statistical significance ( F=36.76, P<0.05); further pairwise comparisons of accommodative lag , regulation of normal and regulating the lead difference and the statistical significance ( t=6.81, 7.21;P<0.05) .Regulation of lead and regulate normal were compared statistically significant ( t=-1.78, P>0.05) .Whether parents with myopia comparison results shows , both parents myopia myopia increased speed are the average of (0.98±0.15) D, (0.73±0.14) D and (0.53±0.09) D; after the single factor variance analysis , differences between the three groups have statistical significance ( F=347.76, P<0.05);further pairwise comparisons two myopic parents , unilateral myopia , parents both myopia and myopia differences have statistical significance ( t=14.36, 29.56;P<0.05);parents unilateral myopia and parents not myopic group comparison , the differences have statistical significance ( t=14.37, P<0.05) .Corneal curvature test comparison results shows , corneal curvature according to <43 D, 43 to 44 D, and>44 D points into three groups, diopter increased degree respectively (0.72±0.23) D, (0.74±0.25) Dand (0.81±0.34) D, through the single factor variance analysis , differences between the three groups of no statistical significance ( F=2.17, P>0.05); size and diopter corneal curvature increases little correlation .Outdoor activity time comparison results shows, the time for outdoor activities according to the <1 h/d,1 h/d-2 h/d, and>2 h/d divided into three groups, diopter increased degree respectively (1.02±0.24) D, (0.70±0.18) D and (0.41±0.14) D, through the single factor variance analysis , among the three groups there were statistically significant differences ( F=122.71, P<0.05); Further pairwise comparisons of outdoor activities time more than 2 h/d myopia increased speed is lower than 1-2 h/d and <1 h/d, the difference is statistically significant ( t=-10.78,-15.46;P<0.05);outdoor activities time 1 h/d-2 h/d myopia development speed is lower than the time <1 h/d( t=-9.85, P<0.05) .Conclusion Juvenile exophoria , accommodative lag , and parents myopia are the development of myopia factors , outdoor activities are the impediment of myopia , the size of corneal curvature was correlated little with the increase of the refractive degree .

Hyperglycemia or high-glucose (HG)-induced apoptosis in human retinal pigment epithelial (RPE) cells is a characteristic process in diabetic retinopathy. In our study, we examined whether microRNA-29 (miR-29) may regulate HG-induced RPE cell apoptosis. Human RPE cell line, ARPE-19 cells, was treated with various high concentration of glucose in vitro. HG-induced RPE cell apoptosis was examined by terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) assay and miR-29 gene expression by quantitative RT-PCR (qRT-PCR). miR-29 was then downregulated in RPE cells, and its effect on HG-induced apoptosis was examined by TUNEL assay and western blot assay on caspase-7 protein. Association of miR-29 on its downstream target, PTEN, in HG-induced RPE cell apoptosis was evaluated by dual-luciferase assay and qRT-PCR. PTEN was silenced in RPE cells. The effects of PTEN downregulation on miR-29-mediated HG-induced RPE cell apoptosis were also examined by TUNEL and western blot assays. HG induced significant apoptosis in RPE cells in a dose-dependent manner. miR-29 was upregulated by HG in RPE cells. miR-29 downregulation protected HG-induced apoptosis and reduced the production of caspase-7 protein in RPE cells. PTEN was shown to be directly downregulated by HG and then upregulated by miR-29 downregulation in RPE cells. Small interfering RNA (siRNA)-mediated PTEN downregulation reversed the protective effect of miR-29 downregulation on HG-induced RPE cell apoptosis. This study demonstrates that miR-29, through inverse association of PTEN, plays an important role in the process of HG-induced apoptosis in RPE cells.

Objective To observe the protection role of the sirtuin 1 (SIRT1)towards the retinal pigmented epithelium (RPE)cells following exposure to oxidative stress.Methods The rates of proliferation and apoptosis,levels of intra-cellular reactive oxygen species(ROS)and cell senescence of RPEs,induced by oxidants (H2 O2 ),were evaluated. Results The results revealed a down-regulation of SIRT1 expression during oxidative stress.Furthermore,SIRT1 acti-vator resveratrol (RSV)and inhibitors nicotinamide (NA)were respectively treated on RPE cells following exposure by H2 O2 intervention;the expression of SIRT1 gene were detected by RT-PCR technology after RNA interfering on SIRT1.The experiments indicated that cell proliferation,apoptosis and ROS levels were significantly different compared with the control group after intervention by H2 O2 ,and cell senescence were significantly increased;NA was significant-ly increased the toxicity of H2 O2 ,however RSV had the opposite anti-cytotoxicity of H2 O2;RT-PCR analysis showed that SIRT1 levels were significantly reduced.Conclusion These results therefore suggested that down-regulation of SirT1 expression during oxidative stress,further investigation indicated that SIRT1 protected RPEs from oxidative stress-induced damage.Appropriate increase of the activity of SIRT1 may be a therapeutic strategy to delay AMD.

It has been previously demonstrated that there are interactions between sirtuin 1 (SirT1) and signal transducer and activator of transcription 3 (STAT3), which have versatile roles in various microenvironments. However, whether or not there is crosstalk between these two molecules during oxidative stress, and what mechanism of crosstalk occurs in retinal pigmented epithelium cells (RPEs), the protection of which may delay the process of age-related macular degeneration (AMD), has required further elucidation. The present study aimed to investigate the interactions between SirT1 and STAT3 in RPEs, following exposure to oxidative stress. The rates of proliferation and apoptosis, levels of intracellular reactive oxygen species and cell senescence of RPEs, induced by oxidants [H2O2 and oxidized low density lipoprotein (oxLDL)], were evaluated. The results revealed a downregulation of SirT1 expression, and an upregulation of STAT3 expression during oxidative stress. Further investigation indicated that SirT1 protected RPEs from oxidative stress-induced damage. Furthermore, gain- and loss-of-function experiments indicated that SirT1 had negative effects on the regulation of STAT3 expression in RPEs during oxidative stress. Notably, STAT3 directly protected the cells from oxidative stress, rather than depending on SirT1. Additionally, the protective effects of STAT3 had no association with the modulation of cell senescence during oxidative stress. In conclusion, SirT1 had negative effects on the regulation of STAT3 expression during oxidative stress. However, SirT1 and STAT3 demonstrated protective roles against oxidative stress in RPEs. These results therefore suggested that there was an equilibrium mechanism between SirT1 and STAT3 against oxidative stress, meaning that an equilibrium mechanism is required to be considered when combined application of STAT3 and SirT1 were performed to treat AMD.

BACKGROUND:Advanced glycation end products (AGEs) accumulate in the retinal vascular cells, neurons, and glias of patients with diabetes mellitus and lead to the pathogenesis of diabetic retinopathy (DR).METHODS:In the present study, to elucidate the orchestrated interactions of high mobility group box 1 (HMGB1) and silent mating type information regulation 2 homolog 1 (Sirt 1) in the AGE-induced pro-inflammatory toxicity in retinal epithelial cells, we investigated the role of HMGB1 and Sirt 1 in the AGE-induced pro-inflammatory cytokines and chemokines.RESULTS:It was demonstrated that the expression of TNF-α, IL-1β, IL-6, MCP-1, RANTES and IP-10 was promoted by the AGE-BSA treatment dose-dependently. The treatment with AGE-BSA also significantly promoted the HMGB1 at both mRNA and protein levels, dose-dependently. And in addition, we confirmed that HMGB1 mediated the AGE-induced pro-inflammatory cytokines and chemokines in the AGE-treated ARPE-19 cells. Moreover, we found that the Sirt 1 was downregulated by the AGE-BSA treatment at both mRNA and protein levels in the ARPE-19 cells, dose-dependently. Our further investigation recognized the regulatory role of Sirt 1 in the AGE-promoted pro-inflammatory cytokines and chemokines. The Sirt 1 inhibitor aggravated, whereas the Sirt 1 activator inhibited, the translocation of HMGB1 and the promotion of AGE-induced IL-1β and IL-6.CONCLUSIONS:Taken together, we confirmed that AGE-BSA promoted HMGB1 but down regulated Sirt 1 in human retinal cells. Sirt 1 was confirmed to regulate AGE-induced pro-inflammatory cytokines and chemokines via inhibiting the nuclear-to-cytoplasmic translocation and release of HMGB1 in retinal ARPE-19 cells.

Objective:To reveal the oxidative damage effect on retinal pigment epithelial cells of two oxides hydrogen peroxide (H 2 O 2 )and oxidized low density lipoprotein (ox-LDL),and provide theoretical basis and foundation for antioxidant stress protection treatment.Methods:In vitro cultured ARPE-1 9 cell line,ox-LDL and H 2 O 2 respectively intervented cultured cells induced oxidative stress injury,cell proliferation and apoptosis rate were detected with flow cy-tometry combined AVFI/PI and MTS;the reactive oxygen species (ROS)of RPE and RPE cell senescence were determined by semi quantitative analysis with fluorescent labeling.Results:1 )The ROS level increased significantly compared with the normal control group after the intervention by ox-LDL and H 2 O 2 ,average size of fluorescence intensity were 537.495 and 958.533 and 644.994,respectively P =0.040 and P =0.01 6;and the ROS levels between two kinds of oxides(H 2 O 2 and ox-LDL)had significant difference;2)cell proliferation of RPE after the intervention by ox-LDL and H 2 O 2 was reduced significantly,respectively P = 0.020 and P =0.026;apoptosis rate of RPE after the intervention by ox-LDL and H 2 O 2 was increased sig-nificantly,respectively P =0.013及 P =0.003;3)the cell senescent state of two kinds of oxides (H 2 O 2 and ox-LDL)were both increased significantly compared with the normal cells,average size of fluorescence intensity were 218.571,320.240 and 293.868,and P = 0.045,but had no significant difference between H 2 O 2 and ox-LDL groups.Conclusion:Ox-LDL and H 2 O 2 can both cause oxidative stress injury of RPE,and a dramatic increase in ROS levels,and lead to ap-optosis and cell senescence obviously,and lay the foundation for the further study of age-related macular degeneration (AMD).

AIM: To observe theclinical effect of using triamcinolone acetonide ( TA ) to recognize posterior vitreous cortex (PVC) and help effective residual vitreous posterior cortex on pars plana vitrectomy (PPV). <br> METHODS: Thirty -five patients (35 eyes) underwent PPV with TA.An amount of 0.1mL TA solution was injected on the retinal surface to visualize and peel posterior vitreous cortex, epiretinal membranes (ERM) or internal limiting membrane (ILM) in these eyes.Among them, 16 cases were filled with silcon silicon oil and 9 cases were filled with C2 F6 .The follow-up time was for 6-12mo. <br> RESULTS: In 35 cases,intraoperative staining with TA consistently improved direct visualization and delineation of the posterior hyaloids, ERM or ILM and facilitated their removal.Among them, vitreous posterior cortex left in 13 cases and PVD was found in 19 cases.Postoperatively, macular hole closure rate reached at 100%, and retina reposition rate was 84.6%. <br> CONCLUSION: The good visibilityof TA formed during surgery is effective in recognizing residual vitreous posterior cortex, reducing the mechanical trauma to the retina, and improving operation success rate.And no serious complication related to TA was found in the study.

AIM: To evaluate the clinical effects of residual triamcinolone acetonide ( TA ) on the treatment of idiopathic macular hole ( IMH ) and lessening of tissue edema. <br> METHODS:A total of 32 patients (32 eyes) underwent closed vitrectomy.During the operation, TA was applied to 16 eyes of experimental group to assist internal limiting membrane peeling.A small amount of TA was left at the bottom of the macular hole.The others eyes of control group didn't use TA to assist internal limiting membrane peeling.Anatomical reduction, postoperative BCVA and macular hole index ( MHI ) were recorded and the statistical analysis was made. <br> RESULTS:All the macular holes reached the anatomical reduction after operation, the closing rate was 100%. Postoperative BCVA of the two groups were improved ( P=0.000).The visual improvement between the two groups had no statistical significance ( P>0.05 ). There is a positive correlation between postoperative BCVA and MHI, and there is no correlation between postoperative BCVA and the hole degree. The operation time in experimental group was shorter than in control group.No serious complications occurred in both groups. <br> CONCLUSION: Intraoperative application of TA was helpful for peeling off internal limiting membrane. Residual TA has no influence on the treatment of idiopathic macular hole or lessening of tissue edema.The MHI can be easily calculated to be used as a clinical index for visual acuity. It is an effective technique with no serious side effects.

The purpose was to investigate the protective effects of Vitamin C (Vit C) and the regulatory mechanism between Vit C and sirtuin 1 (SIRT1) in PREs during oxidative stress as Vit C and SIRT1 exerted famous effects as antioxidants. We found that moderate Vit C (100 µ M) prevented ARPE-19 cells from damages induced by H 2 O 2 , including increasing viability, reducing apoptosis, and attenuating intracellular ROS levels. But lower and higher concentration of Vit C had no effects. Further results indicated that Vit C caused the dysregulation of some stress responses factors (SIRT1, p53 and FOXO3) in ARPE-19 cells response to H 2 O 2 . Moreover we found that SIRT1 activator resveratrol (SRV) stimulated significantly the protective effects of moderate Vit C, provided the property of antioxidative stress for the lower and higher concentration of Vit C in ARPE-19 cells as well. Consistently, nicotinamide (NA) relieved the protective functions of moderate Vit C. Interestingly, data also revealed the dysregulation of p53 and FOXO3 was dependent on the regulation of SIRT1 rather than Vit C. Summarily, the protective effect of Vit C against oxidative stress was involved in regulation of SIRT1. It suggested that combined application of Vit C and RSV might be a promising therapeutic method for AMD.

根据临床神经病学教学特点和实践,从课堂教学方法、多媒体运用、考核方式等方面探索神经病教改的新方法.