简介:今天,我们在这里召开2005年全国防盲工作研讨会。这次会议的主要内容是:分析全国防盲工作面临的形势和挑战,研究开展防盲工作的重点和策略;研究制定2006-2010年全国防盲工作规划。同时,还要对“视觉第一中国行动”二期启动以来的工作进行总结,对中期评估事宜和下一步工作进行部署。两天的时间,任务还是比较重的,我希望大家借此机会,广泛交流各地防盲治盲工作情况,借鉴各地有益的工作经验,在充分研讨,制定出我国2006-2010年防盲工作规划的同时,研究探索适合我国国情、进一步推进我国防盲治盲工作的政策措施、有效途径。
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.