简介:AIM:Tocharacterizetemporalpatternofresolutionandrecurrenceofnaivechoroidalneovascularization(CNV)secondarytowetage-relatedmaculardegeneration(AMD)treatedwithintravitrealbevacizumabonasneededregimen,andtoanalyzebaselineriskfactorsforCNVresolutionorrecurrence.METHODS:Ninety-oneeyesof80patientswithnewlydiagnosedwetAMDwereretrospectivelystudied.Alleyesweretreatedwitharoundofthreemonthlyintravitrealbevacizumabinjections,followedbyoneadditional’bonus’injectionafterresolutionofCNVactivity.Duringfollow-up,eyesweremonitoredwithfluoresceinangiography,opticalcoherencetomography,andbest-correctedvisualacuity(BCVA).IncaseofrecurrencesofCNVactivity,eyeswereretreatedwithotherroundsofbevacizumabinjectionsfollowingthesametreatmentprotocol.RESULTS:Overamedianfollow-upof532d,themedianresolutiontimeofCNVactivityinthefirst,second,andthirdtreatmentroundwas98d,126d,and111d,respectively.Themedianrecurrencetimeforthethreeroundswas154d,126d,and151d,respectively.Nosignificantdifferenceinresolutiontime(P=0.09)orinrecurrencetime(P=0.11)wasdetectedamongtreatmentrounds.Age(P=0.0082)andlensstatus(P=0.035)werefoundtobeassociatedwithCNVresolution;forevery1-yearincreaseinagetherewas4%greaterchanceofCNVresolution;Phakiceyesdemonstrateda33%betterchancetoexperienceCNVresolutionthanpseudophakiceyes.ForCNVrecurrence,lensstatus(P=0.0009)andgender(P=0.0446)werefoundtobepredictive;pseudophakiceyeshada3.69-foldgreaterrisktoexperiencerecurrenceofCNVactivitycomparedtophakiceyes;maleshada2.19-foldgreaterrisktoexperiencerecurrenceofCNVactivitythanfemales.NosignificantBCVAchangesamongthreetreatmentroundswerenoted(P=0.56).CONCLUSION:ResolutiontimeandrecurrencetimeofCNVactivitywerenotsignificantlydifferentamongtreatmentrounds,suggestingabsenceoftachyphylaxistobevacizumab.Acautiousdecisionshouldbemadeupondisco
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.
简介:目的:研究在高糖诱导人晶状体上皮细胞向间充质转化的过程中JAK-STAT通路的作用及AG490对此过程的影响。方法:低糖(5.5mmol/L)DMEM培养液体外培养人晶状体上皮细胞系SRA01/04。高糖(30.5mmol/L)处理细胞,按照是否加入AG490及其浓度的不同分为实验组和对照组。CCK-8试剂盒检测晶状体上皮细胞的活性,选择实验组AG490浓度为10μmol/L和50μmol/L,处理时间分别为6,12,24和48h;细胞划痕实验检测细胞迁移能力的变化;RT-PCR方法半定量检测TGF-β1,FN和α-SMA的mRNA表达量变化。结果:在不同的处理时间(6,12,24,48h),高糖组(HG组)与低糖组相比,细胞的迁移能力增加(P〈0.05),TGF-β1,FN和α-SMA表达量增高(P〈0.05);AG490组与HG组相比,细胞的迁移能力降低(P〈0.05),TGF-β1,FN和α-SMA的mRNA表达量下降。结论:JAK-STAT通路通过影响TGF-β1和细胞外基质转录表达参与了高糖诱导的人晶状体上皮细胞向间充质转化的过程。JAK抑制剂AG490对此过程有抑制作用,且随着AG490浓度的增加其抑制作用增强。