简介：·Thetherapeuticeffectofselenium(Se)hasalreadybeenproveninthyroiddiseaseandthyroidassociatedophthalmopathy(TAO).InspiteofclearscientificproofofitsbenefitsinTAO,thereappearstobenoclearagreementamongthecliniciansregardingitsoptimumdose,durationofthetreatment,efficacyandsafetytodate.Inthisreview,theauthorsummarisesthefindingsof135Englishlanguagearticlespublishedonthissubjectoverthepastfourdecadesfrom1973to2013.TheregulationandmetabolismofthyroidhormonesrequireasteadysupplyofSeandrecentstudieshaverevealedseveralpossiblemechanismsbywhichSeimprovestheseverityofthyroiddiseaseandTAO.Thesemechanismsinclude1)inhibitoryeffectofHLA-DRmoleculeexpressiononthyrocytes;2)profoundreductionsofthyroidstimulatinghormone(TSH)receptorantibodies(TSHR-Ab)andTPOantibodies(TPO-Ab);3)preventionofdysregulationofcell-mediatedimmunityandBcellfunction;4)neutralisingreactiveoxygenspecies(ROS)andinhibitionofredoxcontrolprocessesrequiredfortheactivation,differentiationandactionoflymphocytes,macrophages,neutrophils,naturalkillercellsinvolvedinbothacuteandchronicorbitalinflammationinTAO;5)inhibitionofexpressionofproinflammatorycytokinesand6)inhibitionofprostaglandinandleukotrienesynthesis.AnincreasedoxidativestresshasbeenobservedinbothacuteandchronicphasesofthyroiddiseasewithraisedtissueconcentrationsofROS.ThebenefitsofSesupplementationinindividualswithTAOappeartobeproportionatetothedegreeofsystemicactivityofthethyroiddisease.ThemaximalbenefitofSesupplementationisthereforeseeninthesubjectswhoarehyperthyroid.RestorationofeuthyroidismisoneofthemaingoalsinthemanagementofTAOandwhenanti-thyroiddrugsarecombinedwithSe,thepatientswithGraves’disease(GD)andautoimmunethyroiditis(AIT)achievedeuthyroidismfasterthanthosetreatedwithanti-thyroiddrugsalone.SestatusofnormaladulthumanscanvarywidelyandSe

简介：AIM:Todeterminewhethersinglenucleotidepolymorphism(SNP)rs641153isassociatedwiththeriskofage-relatedmaculardegeneration(AMD),weperformedasystematicmeta-analysisof15eligiblestudies.SNPinthecomplementfactorB(CFB)geneisconsideredtohavesignificantassociationwithAMDsusceptibility,butthereisgreatdiscrepancyintheseresults.METHODS:TheeligiblestudieswereidentifiedbysearchingthedatabasesofPubMed,EMBASE,andWebofScience.Oddsratios(ORs)with95%confidenceintervals(CIs)wereusedtoassesstheassociation.AlldatawereanalyzedusingStatasoftware.RESULTS:Theassociationbetweenrs641153andAMDriskwasstatisticallysignificantunderthehomozygousmodel(AAvsGG:OR=0.26,95%CI=0.15-0.45,P_h=0.973,/~2=0.0%,fixedeffects),dominantmodel(AA+GAvsGG:OR=0.49,95%CI=0.40-0.59,P_h=0.004,/~2=56.4%,randomeffects)andrecessivemodel(AAvsGA+GG:OR=0.30,95%CI=0.17-0.51,R_n=0.983,I~2=0.0%,fixedeffects).Thesameresultswerealsoobservedinthestratifiedanalysesbyethnicity,sourceofcontrolandsamplesize.CONCLUSION:Ourmeta-analysissuggeststhatrs641153intheCFBgenemayplayaprotectiveroleinAMDsusceptibility,thelateAMDinparticular,bothinCaucasiansandinAsians.