简介:AIM:ToidentifythegeneticdefectinaChinesefamilywithbilateralprogressivechildhoodposteriorcataract.METHODS:Atwo-generationfamilywasrecruitedinthisstudy.Familyhistoryandclinicaldatawererecorded.AllreportedcandidategenesassociatedwithcongenitalposteriorcataractwerescreenedbydirectDNAsequencing.·RESULTS:Allaffectedindividualspresentedposterioropacitiesinthelens.Directsequencingofthecandidategenesshowedaheterozygousc.2668C>TvariationinEPHA2gene,whichresultedinthereplacementofargininebycysteineatcodon890(p.R890C).Thismutationwasfoundintwoaffectedindividuals,butwasnotobservedin200normalcontrols.·CONCLUSION:Wereportanovelmutation(p.R890C)intheEPHA2receptortyrosinekinasegene.ThefindingexpandsthemutationspectrumofEPHA2inassociationwithposteriorcataract.
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简介:目的:探讨线粒体膜电位(△ψm)、Caspase3在As2O3诱导ACC-2细胞凋亡中的作用。方法:进行ACC-2细胞培养,将As2O3建立不同药物浓度梯度(0,1.0,2.0,4.0,8.0μmol/L)分别作用于ACC-2细胞,用Rh123染色,流式细胞仪检测8.0μmol/LAs2O3作用前、后(24h),ACC-2细胞的线粒体膜电位(△ψm)变化;用多功能酶标仪进行Caspase3活性检测。结果:空白对照组ACC-2细胞内Rh123荧光强度最强,8.0μmol/LAs2O3处理组ACC-2细胞内Rh123荧光强度减弱,其差异有显著性(P〈0.05);随着As2O3药物浓度的增高(0,1,2,4,8μmol/L),ACC-2细胞的Caspase3酶活力单位逐渐增加。结论:As2O3作用于ACC-2细胞,可通过降低线粒体膜电位从而引起细胞凋亡。随着As2O3药物浓度的增高,ACC-2细胞的Caspase3酶活力单位逐渐增加,Caspase3被激活,细胞可发生不可逆转的凋亡过程。
简介:AIMTo在划分的类型2糖尿病的patients.METHODSWe估计在choroidal厚度(CT)和糖尿病的retinopathy(医生)的早阶段之间的关联83个糖尿病的病人(51-80岁;50女性)进非糖尿病的retinopathy,组(NDR)和温和/中等的nonproliferative糖尿病患者retinopathy(NPDR)组织,并且把他们与26个非糖尿病的控制题目作比较(51-78岁;16女性)。Subfovealchoroidal厚度(SFCT)和parafovealchoroidal厚度(PFCT)用提高的深度成像被测量光谱域的光连贯断层摄影术(EDI10月)。眼睛的健康地位,疾病持续时间,身体团索引,和血红素A1c(HbA1c)是NDR,NPDR,和控制组的recorded.RESULTSThe平均数年龄68.0是戠牥晥?景吗?
简介:AIM:Toinvestigatetheprevalenceandriskfactorsofdiabeticretinopathy(DR)innorthernChinesepatientswithtype2diabetesmellitus(T2DM).METHODS:Thisretrospectivecross-sectionalstudywasperformedbetweenMay2011andApril2012.Atotalof1100patients(male/female,483/617)wereincludedinthisstudy.DRwasdefinedfollowingtheEarlyTreatmentDiabeticRetinopathyStudy(ETDRS)severityscale.Allincludedpatientsacceptedacomprehensiveophthalmicexaminationincludingretinalphotographs.Logisticregressionmodelswereusedtoestimateoddsratios(ORs)and95%confidenceinterval(CI)afteradjustingforageandgender.RESULTS:Retinopathywaspresentin307patientswithaprevalenceof27.9%.Inunivariatelogisticanalysis,presenceofDRwasassociatedwithlongerdurationofdiabetes(OR,5.70;95%CI,2.91-12.56),higherconcentrationoffastingbloodglucose(OR,12.94;95%CI,2.40-67.71),higherlevelofglycosylatedhemoglobinHbA1c(OR,5.50;95%CI,3.78-11.97)andinsulintreatment(OR,6.99;95%CI,1.39-35.12).ThelifestyleofpatientswithT2DMincludingsmoking,alcoholconsumptionandregularexerciseseemednotassociatedwiththedevelopmentofDR.CONCLUSION:Ourstudysuggeststhatfastingserumglucoseconcentration,HbA1clevel,durationofdiabetesandinsulintreatmentarepotentialriskfactorsforDRinnorthernChinesepatientswithT2DM,whilethelifestyleofincludedpatientsseemsnotassociatedwithDR.
简介:目的探讨榄香烯对人喉癌Hep-2细胞生长的影响和作用机制.方法用四甲基偶氮唑盐法(methylthiazolyltetrazoliumassay,MTT)测定榄香烯对喉癌细胞的抑制作用;以透射电镜来观察其形态学变化;采用DNA末端标记法(terminaldeoxynucleotidy1transferasemediateddeoxyuridinetriphosphatenickendlabelingmethod,TUNEL)研究细胞凋亡数;用免疫组化分析bcl-2蛋白在Hep-2细胞中的表达.结果榄香烯明显抑制Hep-2细胞的生长;透射电镜观察到染色质浓缩,沿着核膜排列,形成不同形状和大小的块状;DNA末端标记法说明,凋亡细胞数随药物浓度的提高逐渐增高;免疫组化结果提示榄香烯能使Hep-2细胞bcl-2蛋白表达降低.结论榄香烯能够抑制喉癌细胞的生长,其抑制作用与细胞凋亡有关,作用机制可能与bcl-2表达降低有关.
简介:AIMTo与类型2糖尿病mellitus(T2DM)在中国病人的一个队调查在C反应的蛋白质(CRP)和糖尿病的retinopathy(医生)之间的关系基于.METHODSCommunity的观察的队学习。有1131个参加者,在城市的北京在Desheng社区从2009年11月招募到2011年9月。病人们诊断了T2DM被招募并且经历由一张问询表,眼睛、人体测量的检查和实验室调查组成的标准化评估。医生的存在和严厉由七个领域被估计30°;渲染宫底相片。题目然后没有医生,任何医生,或威胁视觉的克尔普博士被分类进组与T2DM从1007个病人全部的学习subjects.RESULTSA的浆液被分析为分析被包括,包括408(40.5%)男人并且599(59.5%)女人。中部的CRP水平为男人是为女人和1.1mg/L的1.5mg/L(P=0.004,或0.37,95%CI0.18-0.74)。在为可能的covariates调整以后,CRP的高水平与任何医生的更低的流行被联系(P=0.02,或0.55,95%CI0.35-0.89),然而并非与威胁视觉的医生联系了(P=0.62,或0.78,95%CI0.28-2.14)。在由性的层化以后,在CRP和医生之间的反的协会被发现在男人统计上重要(P=0.006,或0.35,95%CI0.16-0.73),然而并非在女人(P=0.58,或0.88,95%CI0.29-1.16)与T2DM从一张中国人口拉的.CONCLUSIONThe数据建议那增加的CRP层次可以相反地与医生的开发被联系。
简介:AIM:Toinvestigatethemorphologicalalteringeffectoftransforminggrowthfactor-β2(TGF-β2)onuntransfectedhumancornealendothelialcells(HCECs)invitro.METHODS:AfteruntransfectedHCECsweretreatedwithTGF-β2atdifferentconcentrations,themorphology,cytoskeletondistribution,andtypeIVcollagenexpressionofthecellswereexaminedwithinvertedcontrastlightmicroscopy,fluorescencemicroscopy,immunofluorescenceorWesternBlot.RESULTS:TGF-β2attheconcentrationof3-15μg/LhadobviouslyalterativeeffectsonHCECsmorphologyindoseandtime-dependentmanner,and9μg/Lwasthepeakconcentration.TGF-β2(9μg/L)alteredHCEcellmorphologyaftertreatmentfor36h,increasedthemeanopticaldensity(P<0.01)andthelengthofF-actin,reducedthemeanopticaldensity(P<0.01)ofthecollagentypeIVinextracellularmatrix(ECM)andinducedtherearrangementofF-actin,microtubuleincytoplasmandcollagentypeIVinECMaftertreatmentfor72h.·CONCLUTION:TGF-β2hasobviouslyalterativeeffectonthemorphologyofHCECsfrompolygonalphenotypetoenlargedspindle-shapedphenotype,indoseandtime-dependencemannerbyinducingmore,elongationandalignmentofF-actin,rearrangementofmicrotubuleandlargerspreadareaofcollagentypeIV.