简介:AIM:Toinvestigatewhethertheresponseofacentralhexagonalelementcorrespondingtothemacularareainconventionalmultifocalelectroretinography(mfERG)testswasthesameasthatofexperimentalmfERGusingsinglecentralhexagonalelementstimulation.METHODS:Prospective,observationalstudy.Thirtyhealthysubjectswereincludedinthisstudy.mfERGrecordingswereperformedaccordingtotwoprotocols:stimuluswith37hexagonalelements(protocol1),andstimuluswithasinglecentralelementcreatedbydeactivatingtheother36hexagonalelements(protocol2).Wecompareddifferencesbetweenring1parametersineachprotocol.RESULTS:Inprotocol1,thefirstpositivecomponent(P1)implicittimeandP1amplitudewere37.8±1.8msand6.3±2.7μV.Aftersingleelementstimulation(protocol2),doublepositivewavesappeared.TheimplicittimeandamplitudeofP1were40.7±2.4ms(P<0.001)and9.1±3.3μV(P=0.001),respectively.Theimplicittimeandamplitudeofthesecondpositivecomponent(P2)were68.0±4.5ms(P<0.001,comparedwithP1inprotocol1)and12.3±4.7μV(P<0.001,comparedwithP1inprotocol1),respectively.TheamplitudeofP2inprotocol2wasabouttwotimeshigherthanthatofP1inprotocol1.CONCLUSION:mfERGresponsesofacentralhexagonalelementinasingleelementstimulationprotocolaredifferentfromthoseofmultipleelementstimulation.Thepositivewaveismoreenhancedcomparedtothatoftheconventionalprotocolanditelongatedintotwowavelets.
简介:目的:构建表达小鼠CD4+T细胞钙支架蛋白AHNAK1的短发夹RNA(shorthairpinRNA,shRNA)慢病毒载体,并研究其对小鼠甲状腺相关性眼病(thyroid-associatedophthalmopathy,TAO)的抑制效应。方法:设计并筛选对AHNAK1具有良好干扰效力的shRNA序列,慢病毒载体包装干扰序列,感染小鼠CD4+T细胞,检测AHNAK1静默对T细胞功能的抑制作用,采用实验动物模型观察AHNAK1体内抑制甲状腺相关性眼病的效果。结果:成功筛选出具有良好干扰效力的shRNA,并包装入慢病毒。病毒滴度为1.0伊106TU/mL,转染慢病毒的CD4+T细胞展现出失能倾向,抑制炎症免疫反应;在动物模型中抑制T细胞中AHNAK1表达可以有效控制甲状腺眼病的发生发展,显著降低治疗组T细胞中IL-2、IL-1茁和IFN-酌的表达。结论:成功构建了表达小鼠AHNAK1shRNA的慢病毒,具有抑制T细胞分泌IL-2、IL-1茁和IFN-酌的表达效应,能够有效抑制甲状腺眼病的发生发展。
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:目的探讨OSA-18量表评价儿童睡眠呼吸紊乱严重程度的价值。方法我科收治的疑似阻塞性睡眠呼吸暂停低通气综合征(obstructivesleepapneahypopneasyndrome,OSAHS)儿童患者160例,均行多道睡眠描记术(polysomnography,PSG)监测。采用OSA-18评估患儿的生活质量。分析确诊为OSAHS患儿的呼吸暂停低通气指数(apneahypopneaindex,AHI)和最低血氧饱和度(10westoxygensaturation,LSaO2)与OSA-18评分的相关性。结果确诊OSAHS患者123例,单纯鼾症37例。OSAHS患者的OSA-18评分与AHI及LSaO2的相关系数分别为0.615和-0.496,P〈0.05。单纯鼾症及轻中度OSAHS患者各组间OSA-18中位数差异有统计学意义(P〈0.05);重度OSAHS患者OSA-18中位数为91.0,高于单纯鼾症及轻、中度OSAHS患者(OSA-18评分依次为64.0、76.0和87.0,P〈0.05)。以LSaO2为依据对OSAHS患者进行分组,发现无低氧血症组及轻、中度低氧血症患者各组间OSA-18中位数差异有统计学意义(P〈0.05),重度低氧血症患者OSA-18中位数为93.0,高于无低氧血症组及轻、中度低氧血症患者(OSA-18评分依次为69.0、81.0和89.0,P〈0.05)。结论OSA-18评分与PSG存在相关关系,在不同程度睡眠呼吸紊乱中有差异,可作为临床诊断儿童OSAHS的评价指标。(中国眼耳鼻喉科杂志,2011,11:19-21)
简介:目的:评价羊膜移植几种手术方法治疗大泡性角膜病变的临床效果。方法:对18例大泡性角膜病变患者,分别采取角膜层间烧烙术、新鲜羊膜移植术、角膜灼烙联合羊膜嵌入移植手术。结果:18例大泡性角膜病变患者,术后1~5d疼痛消失,7~12d角膜上皮修复,7~21d后羊膜植片常规溶解。角膜层间烧烙术1眼、新鲜羊膜移植术3眼术后1~2mo再次出现角膜大泡及角膜刺激症状而再次手术。角膜灼烙联合羊膜嵌入移植术,术后当天疼痛消失,14d角膜上皮光滑,角膜大泡消失。随访6~18mo无1例复发,部分患者视力有不同程度的提高。结论:角膜灼烙联合羊膜嵌入移植对大泡性角膜病变具有明显的治疗效果.
简介:AIM:ToexplorethemolecularmechanismsinlensdevelopmentandthepathogenesisofPetersanomalyinSmad4defectivemice.METHODS:Le-CretransgenicmouselinewasemployedtoinactivateSmad4inthesurfaceectodermselectively.PathologicaltechniqueswereusedtorevealthemorphologicalchangesoftheanteriorsegmentinSmad4defectiveeye.ImmunohistochemicalstainingwasemployedtoobservetheexpressionofE-cadherin,Ncadherinanda-SMAinanteriorsegmentofSmad4defectivemiceandcontrolmiceatembryonic(E)day16.5.Real-timequantitativepolymerasechainreaction(qPCR)wasperformedtodetecttheexpressionofSnail,Zeb1,Zeb2andTwist2inlensofSmad4defectivemiceandcontrolmiceatE16.5.RESULTS:ConditionaldeletionofSmad4oneyesurfaceectodermresultedincorneaidysplasia,iridocornealangleclosure,corneolenticularadhesionsandcataractresemblingPetersanomaly.LossofSmad4functioninhibitedE-cadherinexpressioninthelensepitheliumcellsandcorneaiepitheliumcellsinSmad4defectiveeye.ExpressionofN-cadherinwasupregulatedincorneaiepitheliumandcorneaistroma.BothE-cadherinandN-cadherinweredown-regulatedatthefuturetrabecularmeshworkregioninmutanteye.TheqPCRresultsshowedthattheexpressionofTwist2wasincreasedsignificantlyinthemutantlens(P<0.01).CONCLUSION:Smad4isessentialtoeyedevelopmentandlikelyacandidatepathogenicgenetoPetersanomalybyregulatingepithelial-mesenchymaltransition.Twist2canberegulatedbySmad4andplaysanessentialroleinlensdevelopment.