简介:以质子泵抑制剂(PPI)为基础的三联疗法的幽门螺杆菌(H.pylori)根除率不尽相同,可能与细胞色素P450(CYP)2C19基因多态性有部分关联。目的:研究CYP2C19基因多态性对亚洲人群中以PPI为基础的三联疗法H.pylori根除率的影响。方法:在PubMed、EMBASE、CNKI和万方数据中进行系统文献检索,以RevMan4.2.8软件行荟萃分析。结果:共17篇文献纳入荟萃分析。不考虑PPI类型,CYP2C19弱代谢型(PM)与杂合子强代谢型(HetEM)之间、PM与纯合子强代谢型(HomEM)之间、HetEM与HomEM之间H.pylori根除率均有显著差异(PM对HetEM:OR=1.75,95%CI1.24—2.47.舟0.002;PM对HomEM:OR=2.82,95%CI1.73~4.60,P〈0.0001;HetEM对HomEM:OR=1.84,95%CI1.33-2.57,P=-0.0003)。在以奥美拉唑或兰索拉唑为基础的三联疗法中,PM与HomEM之间、HetEM与HomEM之间且pylori根除率均有显著差异(含奥美拉唑方案PM对HomEM:OR=4.37,95%CI1.86—10.26.P=0.0007,HetEM对HomEM:OR=3.15,95%CI1.75—5.66,P=0.0001;含兰索拉唑方案PM对HomEM:OR=3.06.95%CI1.56-6.00。P=0.001。HetEM对HomEM:OR=1.95,95%CI1.03~3.70,P=0.04)。在以雷贝拉唑为基础的三联疗法中,PM、HetEM、HomEM三组间H.pylori根除率均无明显差异。结论:在亚洲人群中,以奥美拉唑和兰索拉唑为基础的三联疗法.其H.pylori根除率受CYP2C19基因多态性影响,以雷贝拉唑为基础的三联疗法则否。
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: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:AIM:Tocomparetwotypesofclassificationofintestinalmetaplasia(IM)ofthestomachandtoexploretheirrelationshiptogastriccarcinoma.METHODS:Forty-sevencasesofgastricIMwereclassifiedintotypeortypeaccordingtomucinhistochemicalstainingandcomparedwithanovelclassificationinwhichthespecimenswereclassifiedintosimpleIM(SIM)oratypicalIMaccordingtopolymorphismintermsofatypicalchangesofthemetaplasticepithelium.Forty-sevenIMandthirty-sevengastriccarcinomasa...
简介:AIM:Toelucidatethemechanism(s)bywhichS-adenosyl-L-methionine(SAM)decreaseshepatitisCvirus(HCV)expression.METHODS:WeexaminedtheeffectsofSAMonviralexpressionusinganHCVsubgenomicrepliconcellculturesystem.Huh7HCV-repliconcellsweretreatedwith1mmol/LSAMfordifferenttimes(24-72h),thentotalRNAandproteinswereisolated.cDNAwassynthesizedandrealtime-PCRwasachievedtoquantifyHCV-RNA,superoxidedismutase1and2(SOD-1,SOD-2)catalase,thioredoxin1,methionineadenosyltransferase1Aand2A(MAT1A,MAT2A)expression,andGAPDHandRPS18asendogenousgenes.Expressionofcellularandviralproteinwasevaluatedbywestern-blotanalysisusingantibodiesvsHCV-NS5A,SOD-1,SOD-2,catalase,thioredoxin-1,MAT1A,MAT2A,GAPDHandactin.TotalglutathionelevelsweremeasuredatdifferenttimesbyEllman’srecyclingmethod(0-24h).Reactiveoxidativespecies(ROS)levelswerequantifiedbythedichlorofluoresceinassay(0-48h);Pyrrolidindithiocarbamate(PDTC)wastestedasanantioxidantcontrolandH2O2asapositiveoxidantagent.RESULTS:SAMexpositiondecreasedHCV-RNAlevels50%-70%comparedtonon-treatedcontrols(24-72h).SAMinducedasynergicantiviraleffectwithstandardIFNtreatmentbutitwasindependentofIFNsignaling.Inaddition,1mmol/LSAMexpositiondidnotmodifyviralRNAstability,butitneedscellulartranslationmachineryinordertodecreaseHCVexpression.TotalglutathionelevelsincreaseduponSAMtreatmentinHCV-repliconcells.Transcriptionalantioxidantenzymeexpression(SOD-1,SOD-2andthioredoxin-1)wasincreasedatdifferenttimesbutinterestingly,therewasnosignificantchangeinROSlevelsuponSAMtreatment,contrarytowhatwasdetectedwithPDTCtreatment,whereanaverage40%reductionwasobservedinexposedcells.TherewasaturnoverfromMAT1A/MAT2A,sinceMAT1Aexpressionwasincreased(2.5fold-timesat48h)andMAT2Awasdiminished(from24h)uponSAMtreatmentatboththetranscriptionalandtranslationall
简介:瞄准:在根据操作特征(巨鸟)曲线分析的接收装置预言胰腺的癌的体面评估浆液CA19-9层次的临床的价值。方法:浆液CA19-9层次与可能根据成像是resected的胰腺的癌症在104个病人被测量。巨鸟曲线为CA19-9层次被阴谋。最近到图的上面的左边的角落的点被选择为截止的点。敏感,特性,在这个截止的点的CA19-9的积极、否定的预兆的价值被计算。结果:可切除的胰腺的癌症在58被检测(55.77%)病人和unresectable胰腺的癌症在46被检测(44.23%)病人。在ROC曲线下面的区域是0.918和95%CI是0.843-0.992。CA19-9水平是353.15U/mL,和敏感,在这个截止的点的CA19-9的特性分别地是93.1%和78.3%。积极、否定的预兆的价值分别地是84.38%和90%。结论:外科手术前的浆液CA19-9水平是为进一步评估胰腺的癌症的将切除能力的一个有用标记。CA19-9的显然增加的浆液层次(>353.15U/mL)能为unresectable被认为是一个辅助参数胰腺的癌症。
简介:目的:研究血清胃蛋白酶原及胃泌素17水平和胃癌的关系。方法:在2017年2月到2018年5月间选取210例患有胃病疾病患者作为此次实验研究的对象,对所有的患者首先进行胃镜下活检,研究人员根据活检的结果将患者的病种分为胃癌组,萎缩性胃炎组,非萎缩性胃炎组三组。然后对所有的患者采用酶联免疫吸附试验的方法来检测空腹血清PGⅠ、PGⅡ以及G-17水平,研究PGⅠ、PGⅡ以及G-17水平和胃癌关系。结果:经过实验研究可知,三组患者的PGⅡ、G-17水平及PGR(PGⅠ/PGⅡ)水平都有明显差异,胃癌组的PGR水平要显著低于萎缩性胃炎组和非萎缩性胃炎组,P<0.05;PGⅡ以及G-17水平都要明显高于萎缩性胃炎组和非萎缩性胃炎组,P<0.05,差异有统计学意义;PGⅠ水平在三组患者中并无明显差异,P>0.05,差异不具有统计学意义。另外,可以知道PGⅡ检测胃癌的灵敏度和特异度分别为78.57%(55/70)、82.14%(115/140);PGR检测胃癌的灵敏度和特异度分别为35.71%(25/70)、92.86%(130/140);G-17检测胃癌的灵敏度和特异度分别为64.29%(45/70)、89.29%(125/140)。结论:由此我们可以知道,用PGⅠ、PGⅡ以及G-17水平联合检测胃癌患者可以提早诊断出胃癌,提高胃癌诊断率,尤其是G-17联合PGR检测。对患者进行血清学检测可以让患者提早接受治疗,从而降低胃癌患者的死亡率,因此,在临床上可以大力的推广这种检测方法。
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