简介：目的：研究在高糖诱导人晶状体上皮细胞向间充质转化的过程中JAK-STAT通路的作用及AG490对此过程的影响。方法：低糖（5.5mmol/L）DMEM培养液体外培养人晶状体上皮细胞系SRA01/04。高糖（30.5mmol/L）处理细胞,按照是否加入AG490及其浓度的不同分为实验组和对照组。CCK-8试剂盒检测晶状体上皮细胞的活性,选择实验组AG490浓度为10μmol/L和50μmol/L,处理时间分别为6,12,24和48h；细胞划痕实验检测细胞迁移能力的变化；RT-PCR方法半定量检测TGF-β1,FN和α-SMA的mRNA表达量变化。结果：在不同的处理时间（6,12,24,48h）,高糖组（HG组）与低糖组相比,细胞的迁移能力增加（P〈0.05）,TGF-β1,FN和α-SMA表达量增高（P〈0.05）；AG490组与HG组相比,细胞的迁移能力降低（P〈0.05）,TGF-β1,FN和α-SMA的mRNA表达量下降。结论：JAK-STAT通路通过影响TGF-β1和细胞外基质转录表达参与了高糖诱导的人晶状体上皮细胞向间充质转化的过程。JAK抑制剂AG490对此过程有抑制作用,且随着AG490浓度的增加其抑制作用增强。

简介：突发性耳聋一般认为是由内耳微循环障碍所致,我科自1997年1月至2000年12月,用利多卡因作星状神经节封闭加丹参治疗突聋32例和同期临床随机分组的用等量利多卡因静脉滴注加丹参治疗者33例进行比较,现报告如下.

简介：目的探讨康柏西普联合激光光凝治疗视网膜分支静脉阻塞继发黄斑水肿的效果。方法选择本院2016年1月至2017年6月收治的90例（98眼）视网膜分支静脉阻塞继发黄斑水肿患者,根据随机数字表法将其分为两组,各45例（49眼）。对照组采用激光光凝治疗,观察组采用康柏西普联合激光光凝治疗,比较两组最佳矫正视力、黄斑中心视网膜厚度。结果观察组治疗1周后、治疗3个月后BCVA水平较对照组高,CMI水平均较对照组低,差异具有统计学意义（P〈0.05）。结论康柏西普联合激光光凝治疗视网膜分支静脉阻塞继发黄斑水肿效果确切,可明显改善黄斑中心视网膜厚度,促进患者视力恢复。

简介：目的：研究家兔静脉注射头孢哌酮钠／舒巴坦钠在眼内的透过性及蓄积作用。方法：用高效液相色谱法（highperformanceliquidchromatography，HPLC）测定给药后不同疗程时间点各组兔眼房水和玻璃体中的药物浓度。结果：房水中舒巴坦钠的药物浓度分别为23．4±4．8和23．6±3．7mg／L；头孢哌酮钠浓度分别为8．9±1．2和8．9±1．7mg／L；玻璃体中舒巴坦钠浓度分别为71．2±4．6和69．3±6．8mg／L，头孢哌酮钠未检出。结论：头孢哌酮Ca／舒巴坦钠静脉注射后在正常的眼内透过性不良。

简介：AIM:Toinvestigatethelevelsofserumsolubleintercellularadhesionmolecules-1(sICAM-1)andneutrophilicexpressionofCD18inpatientswithvariousstagesofdiabeticretinopathyandtodeterminetheirdifferentexpressionpatterninthedevelopmentofdiabeticretinopathy(DR).·METHODS:LevelsofserumsICAM-1andCD18onthesurfaceofneutrophileweremeasuredin41DRpatients,theywereclassifiedinthreesubgroupsaccordingtothestageofretinopathyasdeterminedbyfund’sophthalmoscopy;10controlsubjectswerealsostudied.sICAM-1weremeasuredbyenzyme-linkedimmunosorbentassayandCD18byflowcytometry.·RESULTS:TheneutrophilicCD18expressionandserumsICAM-1levelwereallsignificantlyelevatedinalldiabeticsubgroupscomparedtocontrolsubjects(P<0.01).ThedifferencesofCD18andsICAM-1amongthediabeticsubgroupsweresignificantinCD18butnotinsICAM-1.TheprogressionofretinopathywasassociatedwithanincreasebothinCD18andinsICAM-1levelsbysimplecorrelationanalysis(β=0.74,P<0.001;β=0.38,P<0.01,respectively).ButstepwisemultipleregressionanalysisrevealedthatonlyCD18wasindependentdeterminantofretinopathy(β=1.04,P<0.01).·CONCLUSION:OurresultsconfirmthecontributionofendothelialandneutrophilicactivationinthedevelopmentofDRasindicatedbyincreasedlevelsofCD18andsICAM-1.However,adirectimplicationofCD18andICAM-1intheprogressionofDRcanbesupportedonlyintheCD18butnotICAM-1.CD18andICAM-1mayplaydifferentroleinthedevelopmentofdiabeticretinopathy.

简介：AIM:ToInvestigatetheeffectsoftransforminggrowthfactorβ2(TGF-β2)andconnectivetissuegrowthfactor(CTGF)ontransdifferentiationofhumanlensepithelialcells(HLECs)culturedinvitroandsynthesisofextracellularmatrix(ECM).METHODS:HLECsweretreatedwithTGF-β2(0,0.5,1.0,5,10μg/L)andCTGF(0,15,30,60,100μg/L)fordifferenttimes(0,24,48,72h)invitroandtheexpressionofα-smoothmuscleactin(α-SMA),themaincomponentoftheextracellularmatrixtypeⅠcollagen(Col-1)andfibronectin(Fn)weremeasuredbyusingreal-timepolymerasechainreaction(PCR)andwestern-blot.RESULTS:TGF-β2andCTGFsignificantlyincreasedexpressionofα-SMAmRNAandprotein(P<0.05,P<0.001),FnmRNAandprotein(P<0.001),Col-1mRNAandprotein(P<0.001).TGF-β2couldinduceHLECsexpressionofCTGFmRNAandproteinindosedependentmanner(P<0.05,P<0.001).TGF-β2andCTGFcouldinduceHLECstoexpressα-SMA,FnandCol-1intime-dependentmanner.EachtimeofTGF-β2andCTGFinducedHELCsexpressionofα-SMA,Fn,Col-1mRNAandproteinwassignificantincreasecomparedwithcontrol(P<0.05,P<0.001).CONCLUSION:TGF-β2andCTGFcouldinduceHLECsepithelialmesenchymaltransitionandECMsynthesis.