简介：Toexploretheprevalenceoftheplasmid-mediatedquinoloneresistancegeneqnrAinGram-negativebacteriaandtoinvestigateitsmoleculargeneticbackgroundandresistanceprofileinisolatesharboringthisgene,atotalof629nalidixicacid-resistantisolatesofnon-repetitiveGram-negativebac-teriawerecollectedfromclinicalspecimensbetweenApril2004andApril2006andtheseisolateswerescreenedforqnrAgenebyPCRusingspecificprimerscombinedwithDNAsequencing.Theextendedspectrumβ-lactamase(ESBL)orAmpC-producingisolatesweredistinguishedbythephenotypicconfir-matorytestcombinedwithDNAsequencing,andtheantibioticssusceptibilitytestforqnrA-positiveiso-lateswascarriedoutbyKirby-BauerandE-testmethod.TodetectthelocationoftheqnrAgene,plas-midconjugationandSouthernhybridizationwereperformedandtheintegronstructurecontainingtheqnrAgenewasclonedbyPCRstrategyandsequencedbyprimerwalking.ItwasdemonstratedthattheincidenceoftheqnrA-positivestrainsinnalidixicacid-resistantbacteriawas1.9%(12/629),inwhichthedetectionratesforKlebiesiellapneumoniae.Enterobactercloacae,Enterobacteraerogenes,CitrobacterfreundiiandSalmonellachoeraesuiswere2.2%(3/138),17.1%(6/35),9.1%(1/11),12.5%(1/8),and14.3%(1/7),respectively.TheqnrAgenewasfoundtobeembeddedinthecomplexsu/1-typeintegronlocatedonplasmidswithvariedsize(80-180kb).Amongthem,4qnrA-positiveisolatescarriedintegronIn37and8isolatescarriedanovelintegron,temporarilydesig-natedasInX.AlltheqnrA-positiveisolateswereESBL-producingandtransferableforthemuhi-drugresistance.Itisconcludedthattheplasmid-mediateddrug-resistancemechanismexistsinthequinoloneresistantstrainsofisolatesfromhospitalsinGuangdongarea,buttheincidencewasratherlow.Never-theless,itisstillpossiblethatthehorizontaltransferoftheresistantqnrAgenemightleadtothespreadingofdrug-resistance.

简介：Toinvestigatetheroleofnegative-regulatoryfactorsA20,IRF-4andTRAF4ofthetoll-likereceptor(TLR)signalpathwaysinimmunologicalpathogenesisofKawasakidisease(KD),48childrenwithKawasakidisease,16childrenwithinfectiousdisease(ID)and16age-matchedhealthychildrenwerestudied.Reverse-transcriptionPCR(RT-PCR)andreal-timePCRwereusedtoevaluatetheexpres-sionlevelsofnegative-regulatoryandeffectivefactorsintoll-likereceptor4(TLR4)signalpathwaysandproinflammatoryfactorsinperipheralbloodmonocyte/macrophage(MC).Inthisstudy,expressionlevelsofTLR4,MD-2,MyD88,IRAK-4,TRAF6,TAK1,andTAB2mRNAinKDgroupweredetectedtobeelevatedsignificantlyduringacutephaseofKD.Transcriptionlevelsofnegative-regulatoryfactorsA20,IRF-4andTRAF4mRNAinKDorIDpatientsincreasedremarkably.However,expressionsofIRF-4andTRAF4inKDpatientsweredetectedtobelowerthanthatinIDpatients,exceptthattran-scriptionlevelsofA20werefoundtobehigherthanthatinIDpatients.Simultaneously,expressionsofproinflammatorycytokinessuchasL-1β,IL-6andTNF-αinKDpatientsweresignificantlyelevatedcom-paredwiththoseinIDpatients.Furthermore,itwasfoundthatstimulationoflipopolysaccharide(LPS)remarkablyup-regulatedtheexpressionsofnegative-regulatoryfactorsA20,IRF-4andTRAF4inKDpa-tientsorhealthyvolunteers.ThemRNAlevelsofallthethreefactorsinKDpatientswerefoundtobelowerthanthatinthelatter.Inaddition,transcriptionlevelsofIRF-4andTRAF4inKDpatientswithcoronaryarterylesion(KD-CAL~+)weredetectedtobelowerthanthoseinKDpatientswithoutcoronaryarterylesion(KD-CAL~-)duringacutephase,whilethatofA20inKD-CAL~+groupwerelowerthanthatinthelatter.AndthelevelsofexpressionsofproinflammatorycytokinesinKD-CAL~+groupwerefoundtobehigherthanthoseinKD-CAL-group(P<0.01).Thesefindingssuggestthataberrantexpressionofnegative-regulatoryfactorsofTLRssignalpathwaysmaybeinvolved