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简介：InordertorevealvariationandrevolutionofNPgenesofhumanavianH_5N_1influenzavirusstrains,theNPgeneofahumanavianH_5N_1influenzavirusstraininGuangdongwassequencedandtheglobalNPgenesofstrainswereretrieved.ThesequenceswereanalyzedbyDNAStar5.0,andtheevolu-tionaryspeedwasstudiedwithreferencetotheepidemiologicaldata.ItwasfoundthatNPgenesof45strainsduring1997-2006werehomologicallyclassifiedintothreegroups:strainsin1997-1998,strainsin2004-2005andstrainsfrom2003to2006.Therewere35substitutionsinNPsinallstrainsaccountingforaratioof7.03%(35/498).Anadditionalglycoproteindomain(NGT_(430-432))wasfoundinNPgenesinthestrainsof2003-2006,themutationofN_(370)SinGD-01-06resultedinoccurrenceofonemoreglyco-proteindomain(NES_(368-370)).Inthesynonymousvariation,K_svaluesinNPwere2.03×10~(-5)-2.55×10~(-5)Nt/dandK_avaluesinNPwere1.58×10(-6)-3.10×10~(-6)Nt/d.Theredidn′texistobviouslyselectivepres-sure.Anadditionalglycoproteindomainineverystrainof2003-2006andonemoreinstrainGD-01-06mightchangetheantigenicityofhumanavianH_6N_1influenzavirus.ThevariationonhumanavianH_5N_1influenzastrainsoccurredfrequentlyinthenaturalworld,whichwouldresultinhighprobabilityofhu-man-humantransmissionalongwiththenaturalevolutionofthevirus.

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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

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