简介:目的研究c—erbB—2和c—myc癌基因在胃癌组织中扩增的意义。方法应用非放射性原位杂交技术检测81例胃癌标本中c—erbB—2和c—myc的扩增情况。结果C—erbB—2和c—myc在胃癌中的扩增率分别为50.6%和67.9%。c—erbB—2基因与胃癌组织分化程度、浸润深度及淋巴结转移有关(P〈0.05),分化程度越差、浸润深度越深、淋巴结有转移,c—erbB—2基因表达率越高,而C—myc癌基因与胃癌组织分化程度、浸润深度及淋巴结转移无关。两基因的扩增具有显著的相关性(x^2=7.26,P〈0.01)。结论c—erbB—2和c—myc扩增是胃癌发生过程中的一个重要的生物学因素,且两者具有较好的协同作用。
简介:目的掌握影响肝性脑病(HE)预后的危险因素。方法对国内发表资料完整、统计设计合理的11个HE研究(共1131例)进行荟萃分析。结果HE诱因分别为:消化道出血43.8%,感染33.9%,电解质紊乱29.1%,大量利尿和/或放腹水14.5%,饮食不节14.2%,肾功能衰竭13.0%,手术/创伤6.0%,药物4.5%,输血/输复合氨基酸3.2%,腹泻2.4%,便秘1.8%,原因未明/无2.7%.与HE死亡率相关因素包括:①诱因数:单一诱因死亡率33%,二种诱因为71.4%;三种或以上诱因为92.3%;三组间差异显著(P〈0.01)。②诱因纠正情况:可纠正组死亡率为18.2%,未纠正组为100%,二组间差异显著(P〈0.01)。③HE分期:Ⅰ期死亡率为O%,Ⅱ期为4.9%.Ⅲ期为34.4%,Ⅳ期为85.1%,四组间差异显著(P〈0.01)。④肝功(Child—pugh分级):A级死亡率为19.8%,B级为49.8%,C级为80.8%,三组间差异显著(P〈0.01)。结论重视HE预后的危险因素,警惕多种诱因并存,消除其不利影响。保护肝功能是改善HE预后的重要途径。
简介:AIMToinvestigatetheroleofthecomplement5a(C5a)/C5areceptor(C5aR)pathwayinthepathogenesisofacuteliverfailure(ALF)inamousemodel.METHODSBALB/cmicewererandomlyassignedtodifferentgroups,andintraperitonealinjectionsoflipopolysaccharide(LPS)/D-galactosamine(D-GalN)(600mg/kgand10μg/kg)wereusedtoinduceALF.TheKaplanMeiermethodwasusedforsurvivalanalysis.Serumalanineaminotransferase(ALT)levels,atdifferenttimepointswithina1-wkperiod,weredetectedwithabiochemistryanalyzer.Pathologicalexaminationoflivertissuewasperformed36hafterALFinduction.Serumcomplement5(C5),C5a,tumornecrosisfactor-α(TNF-α),interleukin(IL)-1β,IL-6,high-mobilitygroupproteinB1(HMGB1)andsphingosine-1-phosphatelevelsweredetectedbyenzyme-linkedimmunosorbantassay.Hepaticmorphologicalchangesat36hafterALFinductionwereassessedbyhematoxylinandeosinstaining.ExpressionofC5aR,sphingosinekinase1(SphK1),p38-MAPKandp-p38-MAPKinlivertissue,peripheralbloodmononuclearcells(PBMCs)andperitonealexudativemacrophages(PEMs)ofmiceorRAW264.7cellswasanalyzedbywesternblotting.C5aRmRNAlevelsweredetectedbyquantitativereal-timePCR.RESULTSActivationofC5andup-regulationofC5aRwereobservedinlivertissueandPBMCsofmicewithALF.BlockadeofC5aRwithaC5aRantagonist(C5aRaC5aRa)significantlyreducedthelevelsofserumALT,inflammatorycytokines(TNF-α,IL-1βandIL-6)andHMGB1,aswellasthelivertissuedamage,butincreasedthesurvivalrates(P<0.01forall).BlockadeofC5aRdecreasedSphK1expressioninbothlivertissueandPBMCssignificantlyat0.5hafterALFinduction.C5aRapretreatmentsignificantlydownregulatedthephosphorylationofp38-MAPKinlivertissuesofALFmiceandC5astimulatedPEMsorRAW264.7cells.Moreover,inhibitionofp38-MAPKactivitywithSB203580reducedSphK1proteinproductionsignificantlyinPEMsafterC5astimulation.CONCLUSIONTheC5a/C5aRpath
简介:目的观察端粒酶催化亚基(hTERT)、c-myc在胆囊癌中的表达,探讨hTERT及c-myc与胆囊癌的相关性。方法采用免疫组织化学方法检测15例胆囊癌组织、癌旁组织、正常胆囊黏膜及20例胆囊腺瘤性息肉组织hTERT、c-myc的表达。结果①正常胆囊黏膜、胆囊腺瘤性息肉组织、癌旁组织及胆囊癌组织hTERT的阳性表达率分别为6,67%(1/15)、10.00%(2/20)、33.33%(5/15)及80%(12/15);c-myc阳性表达率分别为20.00%(3/15)、45.00%(9/20)、40%(6/15)及86.67%(13/15);胆囊癌组织中hTERT与c-myc阳性表达率明显高于其它组织(P〈0.05);②胆囊癌组织hTERT和c-myc表达与淋巴结转移有关,伴淋巴结转移的胆囊癌hTERT及c-myc阳性表达率明显高于无淋巴结转移者(P〈0.05);③c-myc在hTERT阳性的胆囊癌组织的表达率明显高于hTERT阴性组(P〈0.05)。结论hTERT过度表达在胆囊癌的发生发展过程中具有重要作用,c-myc在转录水平上调控hTERT的表达,进而激活端粒酶促进胆囊癌的形成。
简介:背景:临床上评估炎症性肠病活动性的方法有临床活动度、C反应蛋白(CRP)和血沉等,三者常不一致。目的:探讨CRP评估炎症性肠病活动性的价值。方法:以Logistic回归法分析80例克罗恩病(CD)、70例溃疡性结肠炎(UC)患者血清CRP与血沉、临床活动度、内镜表现活动性、组织学活动性、低白蛋白血症、贫血、白细胞升高的关系;比较临床严重度、病变部位和药物治疗对CRP的影响。结果:CD中CRP与血沉相关;UC中CRP与血沉、外周血白细胞升高相关。CRP在活动性CD中显著升高(P〈0.01),重度CD和结肠CD中CRP升高较其他各组明显(P〈0.05);活动性UC中CRP亦显著升高(P〈0.01),重度组中CRP升高较其他组明显(P〈0.05)。药物有效控制临床表现时.CRP显著下降(P〈0.01),复发时重新升高(P〉0.05)。结论:CRP升高更适于反映中至重度结肠CD和UC的活动性:具有快速反映药物治疗有效性的特点。
简介:AIM:Toevaluatetheimpactofsociodemographic/clinicalfactorsonearlyvirologicalresponse(EVR)topegin-terferon/ribavirinforchronichepatitisC(CHC)inclinicalpractice.METHODS:Weconductedamulticenter,cross-sectional,observationalstudyinHepatologyUnitsof91Spanishhospitals.CHCpatientstreatedwithpeginterferonα-2aplusribavirinwereincluded.EVRwasdefinedasundetectablehepatitisCvirus(HCV)-ribonucleicacid(RNA)or≥2logHCV-RNAdecreaseafter12wkoftreatment.AbivariateanalysisofsociodemographicandclinicalvariablesassociatedwithEVRwascarriedout.IndependentfactorsassociatedwithanEVRwereanalyzedusingamultipleregressionanalysisthatincludedthefollowingbaselinedemographicandclinicalvariables:age(≤40yearsvs>40years),gender,race,educationallevel,maritalstatusandfamilystatus,weight,alcoholandtobaccoconsumption,sourceofHCVinfection,alanineaminotransferase(ALT)andaspartateaminotransferase(AST)levels,andgammaglutamyltranspeptidase(GGT)(≤85IU/mLvs>85IU/mL),serumferritin,serumHCV-RNAconcentration(<400000vs≥400000),genotype(1/4vs3/4),cirrhoticstatusandribavirindose(800/1000/1200mg/d).RESULTS:Atotalof1014patientswereincludedinthestudy.Meanageofthepatientswas44.3±9.8years,70%weremale,and97%wereCaucasian.ThemainsourcesofHCVinfectionwereintravenousdrugabuse(25%)andbloodtransfusion(23%).SeventyeightpercentwereinfectedwithHCVgenotype1/4(68%hadgenotype1)and22%withgenotypes2/3.TheHCV-RNAlevelwas>400000IU/mLin74%ofpatients.ThemeanALTandASTlevelswere88.4±69.7IU/mLand73.9±64.4IU/mL,respectively,andmeanGGTlevelwas82±91.6IU/mL.Themeanferritinlevelwas266±284.8μg/L.Only6.2%ofpatientspresentedwithcirrhosis.Allpatientsreceived180mgofpeginterferonα-2a.Themostfrequentlyusedribavirindoseswere1000mg/d(41%)and1200mg/d(41%).Theplannedtreatm
简介:瞄准:为了在病人调查胰岛素抵抗和糖尿病的临床的参数的流行,由长期的丙肝(CHC)或长期的肝炎B(CHB)影响了。方法:我们回顾地评估了经历了肝活体检视的852个连续病人(726CHC和126CHB)。我们记录了年龄,性别,中高音,类型2糖尿病或新陈代谢的症候群(MS),身体团索引(BMI),和明显的疾病持续时间(增加)。结果:年龄,增加,BMI,在有温和/中等的肝纤维变性的病人的MS和糖尿病的流行在CHC是显著地更高的。然而,脂肪变性的度和在肝活体检视评估的肝纤维变性没在CHC和CHB病人之间不同。在多变量分析,年龄,性别,BMI,中高音和糖尿病是为在CHC的肝纤维变性的独立风险因素,而仅仅年龄与在CHB的肝纤维变性有关。我们也评估了在重要脂肪变性之间的协会(>30%)并且年龄,性别,BMI,糖尿病,MS和肝纤维变性。糖尿病,BMI和肝纤维变性与脂肪变性>被联系30%在CHC,而仅仅年龄和BMI与在CHB的脂肪变性有关。结论:这些数据可以显示丙肝病毒感染是为胰岛素抵抗的一个风险因素。
简介:瞄准:估计临床,生物化学并且virological在长期的丙肝(CHC)的长期的结果有在加ribavirin的peginterferon(PEG-IFN)以后的持续virological回答(SVR)的病人联合治疗。方法:有在有PEG-IFN正ribavirin的治疗以后的SVR的一百和53个病人在一个单个西班牙的中心在5年的后续研究被包括,基于标准临床的实践。临床的回忆,生物化学的分析,丙肝病毒RNA和alpha-fetoprotein测量,ultrasonography和短暂elastography每年被执行。结果:153个病人的吝啬的后续经期是76??敦瑥吗?
简介:AIM:ToinvestigatehowweightgainafterOLTaffectsthespeedoffibrosisprogression(SFP)duringrecurrenthepatitisCvirus(HCV)infectionofthegraft.METHODS:Ninetyconsecutivepatients(63males,medianage53years;55withHCV-relatedliverdisease),transplantedatasingleinstitution,werestudied.Allwerefollowedforatleast2yearsafterOLTandhadatleastonefollow-upgraftbiopsy,performednotearlierthan1yearafterthetransplantoperation.Foreachbiopsy,asingle,experiencedpathologistgaveanestimateofboththestagingaccordingtoIshakandthedegreeofhepaticsteatosis.TheSFPwasquantifiedinfibrosisunits/month(FU/mo).Thelipidmetabolismstatusofpatientswassummarizedbytheplasmatriglycerides/cholesterol(T/C)ratio.Bodymassindex(BMI)wasmeasuredbeforeOLT,and1and2yearsafterit.RESULTS:IntheHCVpositivegroup,thehighestSFPwasobservedinthefirstpost-OLTyear.Atthattimepoint,aSFP≤0.100FU/mowasobservedmorefrequentlyamongrecipientswhohadreceivedtheirgraftfromayoungdonorandhadapre-transplantBMIvalue>26.0kg/m2.Atcompletionofthefirstpost-transplantyear,aBMIvalue>26.5kg/m2wasassociatedwithaT/Cratio≤1.TheproportionofpatientswithSFP>0.100FU/modescendedinthefollowingorder:femalerecipientswithahighT/Cratio,malerecipientswithhighT/Cratio,andrecipientsofeithergenderwithlowT/Cratio.Hepaticsteatosiswasobservedmorefrequentlyinrecipientswho,inthefirstpost-transplantyear,hadincreasedtheirBMI≥1.5kg/m2incomparisontothepre-transplantvalue.Hepaticsteatosiswasinverselyassociatedwiththestagingscore.CONCLUSION:AmongHCVpositiverecipients,excessweightgainpost-OLTdoesnotrepresentafactorfavoringearlyliverfibrosisdevelopmentandmightevenbeprotectiveagainstit.
简介:AIM:Tocomparetwotypesofclassificationofintestinalmetaplasia(IM)ofthestomachandtoexploretheirrelationshiptogastriccarcinoma.METHODS:Forty-sevencasesofgastricIMwereclassifiedintotypeortypeaccordingtomucinhistochemicalstainingandcomparedwithanovelclassificationinwhichthespecimenswereclassifiedintosimpleIM(SIM)oratypicalIMaccordingtopolymorphismintermsofatypicalchangesofthemetaplasticepithelium.Forty-sevenIMandthirty-sevengastriccarcinomasa...
简介:目的建立c-Met慢病毒载体转染人脐带间充质干细胞(hUMSC),为治疗肝衰竭作为种子细胞.方法培养hUMSC,经流式细胞技术检测细胞表面表型,转染c-Met慢病毒载体,在荧光显微镜下观察转染效率,确定最佳多重感染复数(MOI).采用嘌呤霉素抗性筛选稳定表达c-Met的hUMSC细胞系,采用Western-blot法检测细胞c-met蛋白表达量.结果P5代细胞高表达CD44、CD90和CD105抗原,不表达CD31、CD45和CD34相关造血细胞抗原,符合人脐带间充质干细胞的特性;构建成功的c-Met慢病毒载体转染人脐带间充质干细胞最佳MOI=80,经嘌呤霉素筛药,在荧光显微镜下观察发现荧光阳性率为100%,且经Western-blot法检测证实该细胞过表达c-Met蛋白.结论成功构建过表达c-Met基因的脐带间充质干细胞,为进-步实验打下了基础.
简介:胃内幽门螺杆菌(简称Hp)感染与消化疾病密切相关[1],故诊断Hp感染显得尤为重要.目前诊断Hp的方法很,多为侵人性(包括快速尿素酶、病理染色、细菌培养等),对患者具有一定创伤和痛苦;血清Hp-IgG抗体测定为非侵人性,但根除Hp后血清Hp抗体需长时间才能转阴,不宜疗效考核.无创伤性呼气试验可作为根除Hp前后诊断的金标准[2].我院于1998年5月至1999年5月,采用微量14C-尿素呼气法(简称14C-UBT)诊断Hp感染,同时予快速尿素酶法(RUT)、病理染色(W-S染色)对照,及追踪根除Hp后疗效检测.旨在观察14C-UBT法在诊断胃内Hp感染的临床价值.
简介:AIM:TotestthehypothesisthatE-cadheringene(CDH1)C-160Apromotervariantgenotypeisassociatedwithanincreasedriskfordevelopinggastriccancer.METHODS:Inthispopulation-basedcase-controlstudyofgastriccancerinJiangsuProvince,China,weperformedpolymerasechainreaction-restrictionfragmentlengthpolymorphism(PCR-RFLP)togenotypetheC-160ApolymorphismofCDH1promoterin206non-cardiagastriccancerpatientsand261age-andsex-matchedbutunrelatedcancer-freecontrols.RESULTS:ThefrequenciesofgenotypesCC,CAandAAwere57.8%,36.4%and5.8%ingasfriccancercases,respectively,and58.2%,34.9%and6.9%incontrolsrespectively.ThedistributionsofCDH1genotypeswerenotsignificantlydifferentbetweengastriccancercasesandcontrols(P=0.87forgenotypefrequencyandP=0.92forallelefrequency).ComparedwiththeCCgenotype,theCAandAAgenotypeswerenotassociatedwithanincreasedriskfornon-cardiagastriccancer(adjustedoddsratios(OR)=1.15,and95%confidenceinterval(95%CI)=0.78-1.72forCAgenotype,andOR=0.90and95%CI=0.42-2.01forAAgenotype).CONCLUSION:E-cadheringeneC-160Apromoterpolymorphismmaynotplayamajorroleintheetiologyofnon-cardiagastriccancerinChinesepopulation.
简介:AIM:Toinvestigatetheeffectsofc-mybantisenseRNAoncellproliferationandtheexpressionofc-myb,TGF-β1andα1-Ⅰcollageninculturedhepaticstellatecells(HSC)fromrats.METHODS:Recombinantretroviralvectorofc-mybantisensegene(pDOR-myb)wasconstructed,andthentransfectedintoretroviralpackagecelllinePA317bymeansofDOTAP.ThepseudovirusesproducedfromtheresistantPA317cellswereselectedwithG418toinfectHSCsisolatedfromratlivers.Thecellproliferationwasmeasuredby3-[4,5-Dimethylthiazolzyl]-2,5-diphenyltetrazo-diumbromide(MTT)method.Theexpressionofc-myb,α1-ⅠcollagenandTGF-β1rnRNA,andc-mybproteininHSCswasdetectedwithsemi-quantitivereversetranseription-polymerasechainreaction(RT-PCR)andWestern-blotrespectively.RESULTS:HSCsfromratswereisolatedsuccessfullywiththeviability>98%.InthepDOR-mybinfectedHSCs,thecmybproteinexpression,cellproliferation,andα1-ⅠcollagenandTGF-β1mRNAexpressionwererepressedsignificantlycomparedwiththeircorrespondingcontrolgroups(P<0.01).CONCLUSION:c-mybplaysakeyroleinactivationandproliferationofHSC.c-mybantisenseRNAcaninhibitcellproliferation,α1-ⅠcollagenandTGF-β1mRNAexpression,suggestingthatinhibitionofc-mybgeneexpressionmightbeapotentialwayforthetreatmentofliverfibrosis.