简介：目的:评价大剂量甲基强的松龙对原田病急性期浆液性视网膜脱离的治疗作用.方法:对2001-12/2003-07就诊本院患者11例(22眼)在临床诊断当天即给予甲基强的松龙静脉滴注,剂量为500mg,1次/d,连续用3d后迅速减量,于7d内减为强的松口服.OCT和间接眼底镜观察炎症渗出吸收情况,检查视功能恢复情况.结果:大剂量甲基强的松龙静脉滴注次日即可观察到22眼视网膜下液均明显减少,静滴3d后浆液性视网膜脱离基本消失,视网膜复位,出院时21眼视网膜下液完全吸收,14眼(64%)视力恢复至0.5以上.结论:甲基强的松龙冲击疗法可促进原田病急性期视网膜下液迅速吸收,恢复视功能,疗效可靠,值得临床推广.

简介：为探讨迷路的老化过程,应用透射电镜观察了新生、青年、老年豚鼠的耳蜗和迷路血管系统的变化。发现老年豚鼠血浆成分有改变、听力呈下降倾向;毛细胞、迷路血管及螺旋神经和螺旋神经节细胞均可见一系列损害。作者推测在耳蜗老化过程中血管系统的变化非常重要,至少是耳蜗其他部位老年性改变的原因之一。

简介：目的研究C-MYC蛋白表达在雏鸡耳蜗毛细胞庆大霉素损伤后再生过程中的意义。方法采用C-MYC蛋白单克隆抗体免疫组织化学技术,检测雏鸡内耳基底乳头庆大霉素损伤后修复1、3、7、14、21和28天时C-MYC蛋白表达情况。结果损伤后修复的早期,C-MYC蛋白首先在基底乳头的部分支持细胞中高水平表达,随后腔面细胞亦有明显表达,修复第七天时,C-MYC蛋白在基底乳头中表达水平达高峰。结论C-MYC蛋白高水平表达可能与毛细胞再生的前体细胞增殖密切相关。

简介：AIM:ExcessivedissolveofcornealtissueinducedbyMMPswhichwereactivatedbycytokinsandchemokineswillleadtocornealulcer.ThemolecularmechanismofLipoxinA4(LXA4)oncornealcollagendegradationinthreedimensionswasinvestigated.·METHODS:Rabbitcornealfibroblastswereharvestedandsuspendedinserum-freeMEM.TypeIcollagen,DMEM,collagenreconstitutionbufferandcornealfibroblastsuspensionweremixedonice.Theresultantmixturesolidifiedinanincubator,afterwhichtestreagentsandplasminogenwasoverlaidandthecultureswerereturnedtotheincubator.Thesupernatantsfromcollagengelincubationswerecollectedandtheamountofhydroxyprolineinthehydrolysatewasmeasured.ImmunoblotanalysisofMMP-1,-3andTMMP-1,-2wasperformed.MMP-2,-9wasdetectedbythemethodofGelatinzymography.Cytotoxicityassaywasmeasured.RESULTS:LXA4inhibitedcornealcollagendegradationinadoseandtimemanner.LXA4inhibitedtheIL-1βinducedincreasesinthepro-MMP-1,-2,-3,-9andactiveMMP-1,-2,-3,-9inaconcentrationdependentmanner.LXA4alsoinhibitedtheIL-1βinducedincreasesinTIMP-1,-2.CONCLUSION:Asapotentanti-inflammationreagent,LXA4caninhibitcornealcollagendegradationinducedbyIL-1βincornealfibroblaststhusinhibitingcornealdissolvingpathologyprocess.

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：AIM:TodiscusstheimpactofLyciumBarbarumPolysaccharide(LBP)andDanshensupurifiedfromTraditionalChineseMedicine(TCM)onvascularendothelialgrowthfactor(VEGF)ofrabbitswithretinalneovascularization.METHODS:Fortyrabbitsweredividedintonormalcontrolgroup,modelcontrolgroup,LBPgroupandDanshensugroup.Animalsinthenormalcontrolgroupwerefedinthenormaloxygenenvironment.Animalsintheotherthreegroupswereputintotheenvironmentwith70%oxygenfor5daysinordertobuildthemodelofoxygen-inducedvascularproliferationretinopathy.AndthendifferentTCMextractwasinjectedintotheabdominalcavitiesoftheseannimals.After7days,theVEGFcontentofintheserumofrabbitwasmeasuredbydoubleantibodysandwichmethod.RESULTS:DataanalysisindicatedthatVEGFcontentwasasfollows:Danshensugroupwaslowerthanmodelcontrolgroup(12.92±3.84ng/Lvs19.32±4.15ng/L,P<0.05);LBPgroupandnormalcontrolgroupwerelowerthanmodelcontrolgroup(12.92±3.84ng/L,9.26±1.61ng/Lvs19.32±4.15ng/L,P<0.01);totalbloodviscosity,plasmaviscosity,cholesterolcontent,fibrinogencontentandtriacylglycerolcontentafterperitonealinjectionofLBPandDanshensuwereobviouslylowerthanbeforeinjection.CONCLUSION:TCMextract-LBPandDanshensucanprominentlyreducethecontentofVEGFintheprocessofvascularproliferativeretinopathyofrabbit;canpreventtheoccurrenceofretinalmicrovasculardiseasebyimprovingpartialoxygen-deficientenvironmentoraffectingallkindsofnewgrowthfactor.