简介：【摘要】目的： 分析 Q 热立克次体脑炎患者疾病诊断与治疗措施。 方法： 分析 1 例 Q 热立克次体脑炎患者临床疾病诊断与治疗方法。该患者因主诉“ 发热伴头痛 1周”，经临床误诊为上呼吸道感染治疗无效后，转入我科接受进一步治疗，确诊为 Q 热立克次体脑炎，并接受相应治疗措施。 结果： 该患者确诊后采取相应治疗措施后症状改善， 发病 1月后复查腰穿正常。 3月后化验呼吸道病原体 IgM筛查： Q热立克次体 IgM阴性，患者疾病痊愈出院。 结论： 临床针对 Q 热立克次体脑炎患者诊断存在一定误诊率，需采用多种方式准确诊断患者疾病类型，相应采取有效治疗措施，对提高患者治疗效果具有显著意义。

简介：

简介：Toclonethegenecodingtheimmunodominantregioninthechlamydialprotease-likeactivityfactor(CPAF)fromChlamydophilapneumoniae,toanalyzeimmunocompetenceoftheexpressedprotein,andtoevaluateitsvalueinserodiagnosis,theCPAFimmunodominantregiongenewasamplified,ligatedintoapGEX6p-2vector,andthentheexpressedrecombinantproteinwaspurifiedwithglutathioneS-transferase(GST)agarosegelFFafterrenaturation,thenidentifiedbySDS-PAGEandWesternblot.AnewindirectELISAwasdevelopedwiththepurifiedproteinascoatingantigen.TheimmunogenicityoftherecombinantproteinwasevaluatedbyimmunizationtoNewZealandrabbits,anditsimmunoreactivitywasanalyzedbyreactingwithanti-C,pneumoniaeantibody.300clinicalserasampleswererespectivelyde-tectedbymicroimmunofluorescence(MIF)asreferencemethodandtheindirectELISA,andthediffer-encebetweenthetwomethodswasanalyzed.Cross-reactivityagainstChlamydiatrachomatiswasinvesti-gatedwiththeindirectELISAtodetectanti-C,trachomatispositiveantisera.Theresultsindicatedthata51.3kDarecombinantproteinwasobtained.Westernblotassayprovedthattherecombinantproteincouldmerelyspecificallyreactwithhumananti-C.pneumoniaeantisera.ThetitersofthespecificIgGan-tibodiesintheimmunizedNewZealandrabbitswereabove1:16000.Anti-C.pneumoniaeIgGpositiveandnegativereferencesereweredetectedwiththeindirectELISA,andtheconcordancerateofnegativeandpositiveresultswereboth100%(40/40).ThesensitivityandspecificityoftheindirectELISAincomparisonwithMIFwere93.8%(45/48)and100%(252/252)separatelybydetecting300clinicalserasamples,andtheconcordanceratebetweenthetwomethodswas99.0%.NocrossreactionagainstC.trachomatiswasfoundwiththeindirectELISAtodetectanti-C,trachomatispositiveantisera.Incon-clusion,thepreparedrecombinantproteinoftheCPAFimmunodominantregionshowsexcellentimmuno-competenceandcanbeusedtodevelopanewindirect

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

简介：