简介：瞄准：在与clinicopathological特征和成纤维细胞生长因素受体1的表示(FGFR1)和ephrinligands的关系在胃的癌症澄清Ephrin受体A4(EphA4)的表示和角色。方法：十一根胃的癌房间线，胃的腺癌的24个配对的外科的新鲜标本并且邻近非，肿瘤组织，74个常规修理福尔马林的、嵌入石蜡的肿瘤标本，和55个标本在组织上看到微数组(TMA)被分析。反向的transcription-PCR(RT-PCR)，即时RT-PCR，免疫组织化学，和房间生长试金被执行。结果：EphA4mRNA表示的Overexpression在8被观察(73%)11胃的癌症，房间排队并且10(42%)24胃的癌症纸巾。EphA4的Overexpression，由免疫组织化学分析了，在62被观察(48%)129胃的癌症纸巾。在蛋白质水平，在表示上的EphA4显著地与侵略和复发的深度被联系。在表示上的EphA4也在表示上与FGFR1被相关。有EphA4积极的癌症的病人比有显著地更短的全面幸存时期与EphA4否定的癌症做了那些(P=0.0008)。为ephrinligands的mRNAs是在在胃的癌症房间线和癌症纸巾的各种各样的联合的coexpressed。由在EphA4-overexpressing胃的癌症房间线的siRNA的EphA4表示的Downregulation在房间生长导致了重要减少。结论：我们的结果建议那在胃的癌症在EphA4的表示上起一个作用。

简介：AIM:Tumorangiogenesishasbeenshowntobepromotedbyvascularendothelialgrowthfactor(VEGF)viastimulatingendothelialcellproliferation,migration,andsurvival.BlockadeofVEGFsignalingbydifferentmeanshasbeendemonstratedtoresultinreducedtumorgrowthandsuppressionoftumorangiogenesisindistincttumorentities.Here,wetestedarecombinantadenovirus,AdsFIt1-3,thatencodesanantagonisticallyactingfragmentoftheVEGFreceptor1(Flt-1),forsystemicantitumoreffectsinpre-establishedsubcutaneousCRCtumorsinmice.METHODS:Murinecolorectalcarcinomacells(CT26)wereinoculatedsubcutaneouslyintoBalb/cmiceforinvivostudies.Tumorsizeandsurvivalweredetermined.293celllinewasusedforpropagationoftheadenoviralvectors.HumanlungcancerlineA549andhumanumbilicalveinendothelialcellsweretransfectedforinvitroexperiments.RESULTS:InfectionoftumorcellswithAdsFlt1-3resultedinproteinsecretionintocellsupernatant,demonstratingcorrectvectorfunction.Asexpected,thesecretedsFlt1-3proteinhadnodirecteffectonCT26tumorcellproliferationinvitro,butendothelialcellfunctionwasinhibitedbyabout46%ascomparedtotheAdLacZcontrolinatubeformationassay.WhenAdsFlt1-3(5×109PFU/animal)wasappliedtotumorbearingmice,wefoundatumorinhibitionby72%atd12aftertreatmentinitiation.Inspiteoftheseantitumoraleffects,thesurvivaltimewasnotimproved.AccordingtoreducedintratumoralmicrovesseldensityinAdsFIt1-3-treatedmice,theantitumormechanismcanbeattributedtoangiostaticvectoreffects.WedidnotdetectincreasedsystemicVEGFlevelsafterAdsFlt1-3treatmentandlivertoxicitywaslowasjudgedbyserumalanineaminotransferasedetermination.CONCLUSION:InthisstudyweconfirmedthevalueofasystemicadministrationofAdsFIt1-3toblockVEGFsignalingasantitumortherapyinanexperimentalmetastaticcolorectalcarcinomamodelinmice.

简介：AIM:Tostudythepossibleactionsandmechanismsofperoxisomeproliferator-activatedreceptorγ(PPARγ),aligand-activatedtranscriptionfactor,inpancreaticcarcinogenesis,especiallyinangiogenesis.METHODS:ExpressionsofPPARγandretinoidacidreceptor(RXRα)wereexaminedbyreverse-transcriptionpolymerasechainreaction(RT-PCR)withimmunocytochemicalstaining.Pancreaticcarcinomacells,PANC-1,weretreatedeitherwith9-cis-RA,aligandofRXRα,orwith15-deoxy-Δ12,14prostaglandinJ2(15d-PGJ2),aligandofPPARγ,orboth.Antiproliferativeeffectwasevaluatedbycellviabilityusingmethyltetrazolium(MTT)assay.ApancreaticcarcinomaxenografttumormodelofnudemicewasestablishedbyinoculatingPANC-1cellssubcutaneously.Rosiglitazone,aspecificligandofPPARγ,wasadministeredviawaterdrinkinginexperimentalgroupofnudemice.After75d,allmiceweresacrificed.Expressionofproliferatingcellnuclearantigen(PCNA)intumortissuewasexaminedwithimmunohistochemicalstaining.Expressionofvascularendothelialgrowthfactor(VEGF)mRNAinPANC-1cells,whichweretreatedwith15d-PGJ2or9-cis-RAatvariousconcentrationsordifferentduration,wasdetectedbysemi-quantitativeRT-PCR.EffectsofRosiglitazoneonchangesofmicrovasculardensity(MVD)andVEGFexpressionwereinvestigatedinxenografttumortissue.Neovasculaturewasdetectedwithimmunohistochemistrystaininglabeledwithanti-Ⅳcollagenantibody,andindicatedbyMVD.RESULTS:RT-PCRandimmunocytochemicalstainingshowedthatPPARγandRXRαwereexpressedinPANC-1cellsatbothtranscriptionlevelandtranslationlevel.MTTassaydemonstratedthat15d-PGJ2,9-cis-RAandtheircombinationinhibitedthegrowthofPANC-1cellsinadose-dependentmanner.9-cis-RAhadacombinedinhibitingactionwith15d-PGJ2onthegrowthofpancreaticcarcinoma.InvivostudiesrevealedthatRosiglitazonesignificantlysuppressedthegrowthofpancreaticcarcinomaascomparedtocontrolgroup(0.48±0.23cm3vs2.488±0.59cm3,P<0.05),andthegro

简介：瞄准：为了为在肝炎B估计肝的纤维变性决定结缔组织生长因素(CCN2/CTGF)的用途，病毒(HBV)导致了长期的肝疾病(CLD-B)。方法：连接酶的immunosorbent试金被用来与导致HBV的活跃的肝肝硬化和30个健康个人与长期的肝炎B(CHB)和39个病人从107个病人在sera测量CCN2。从有CHB，有导致HBV的肝肝硬化的8个病人和有正常的肝组织学的8个HBV搬运人的31个病人的肝样品为转变生长因素-1(TGF-1)或CCN2mRNA层次由被检验在situ杂交，并且计算机图象分析被执行在肝纸巾测量CCN2mRNA积极的房间的综合最佳的密度(IOD)。组织学的发炎分级和纤维变性阶段被H并且E染色和凡·吉森斯方法评估。结果：分别地，浆液CCN2集中作为与健康个人相比在有CHB或活跃的肝肝硬化的病人更高是4.0褶层或4.9褶层(P<0.01)。在肝纸巾在在sera和CCN2mRNA表示的CCN2的层次之间有好一致性(r=0.87，P<0.01)。在sera的CCN2的层次与CLD-B在病人与组织学的纤维变性阶段的改进被增加(r=0.85，P<0.01)。浆液CCN2是为对肝纤维变性的评价的一个可靠标记，与在操作为从有F1阶段肝纤维变性的病人的分别地，区分的正常的肝控制的0.94或0.85的特征(巨鸟)曲线(AUC)或在温和、重要的纤维变性之间区别的接收装置下面的区域。结论：在有CLD-B的病人的浆液CCN2的察觉可以为对肝的纤维变性的严厉的评价有临床的意义。

简介：瞄准：在老鼠碳在Kupffer房间决定激活血小板的因素(PAF)合成和它的受体表示导致四氯化物的肝硬化。方法：Kupffer房间，从控制和导致CCl4的肝脏硬化症的老鼠的肝孤立，一夜间被放在没有浆液的媒介。PAF浸透绑定，ET-1浸透和比赛绑定是assayed。导致的PAF合成，PAF的mRNA表示，preproendothelin-1，endothelinA(希腊语字母的第七字)和endothelinB(ETB)受体也是的ET-1决定了。结果：PAF合成的双重的增加(1.42+/-0.14对0.66+/-0.04pg/mugDNA)并且膜界限PAF的1.48褶层增加(1.02+/-0.06对0.69+/-0.07pg/mugDNA)在肝脏硬化症的老鼠的激活的Kupffer房间被观察。到Kupffer房间的ET-1的申请在激活的Kupffer房间经由ETB受体，而是PAF合成在肝脏硬化症、正常的老鼠以一种集中依赖者方式导致了PAF合成在正常Kupffer房间是比那更有效的。在激活的Kupffer房间，PAF受体表示和PAF绑定能力显著地被提高。激活的Kupffer房间涨了[125I]-ET-1绑定能力，而是改变的两个都不受体的亲密关系，也不希腊语字母的第七字的表达式受体。结论：在导致CCl4的肝硬化期间的Kupffer房间是增加的PAF的主要来源。ET-1内长地涉及由paracrine经由ETB受体在激活的Kupffer房间刺激PAF合成。希腊语字母的第七字受体没出现在激活的Kupffer房间，它可以加重肝硬化的肝、额外的肝的复杂并发症。

简介：瞄准：为了阐明，在在各种各样的铁地位下面的含铁锡，转铁蛋白和转铁蛋白受体之中的铁的顺序的转移调节。方法：进粘膜、钠的蛋白质的59Fe的加入在控制WKY老鼠被执行。在含铁锡，转铁蛋白和转铁蛋白受体之中的铁的顺序的转移在铁被执行缺乏，控制和铁过载了老鼠。十二指肠的蛋白质被microautoradiography和免疫组织化学被特定的ELISA和原位本地化在双人脚踏车受到免疫降水和quantitation十二指肠的节。人的十二指肠的活体检视(n=36)从有不同的铁的题目镇定地位也为这些蛋白质被染色。结果：铁蛋白作为主要蛋白质被识别在十二指肠的粘膜以一种时间依赖者方式合并了铁。粘膜含铁锡的集中在与控制相比的铁过量组是显著地更高的，熨缺乏的组(731.5+/-191.96对308.3+/-123.36，731.5+/-191.96对256.0+/-1.19，P<0.005)，当比粘膜显著地高的钠转铁蛋白的没在这些组之中不同时(10.9+/-7.6对0.87+/-0.79，11.1+/-10.3对0.80+/-1.20，6.8+/-4.7对0.61+/-0.63，P<0.001)。蛋白质和熨斗分级的原位，和他们的重迭，建议了铁的顺序的转移的出现。这被表明然后通过铁的起始的绑定发生到钠转铁蛋白到吸收性的房间表面转铁蛋白受体。这些蛋白质的染色的紧张在人根据铁营养变化了，与在铁观察的转铁蛋白受体的强烈染色缺乏的题目。结论：肠通过包含钠转铁蛋白，transferrin-transferrin受体和含铁锡的相互作用的顺序的转移收起铁，这被结束。

简介：AIM:Toinvestigatetheassociationbetweenendogenousgeneexpressionandgrowthregulationincludingproliferationandapoptosisinducedbytransforminggrowthfactor-β1(TGF-β1)inhumangastriccancer(GC)cells.METHODS:Reversetranscriptionpolymerasechainreaction(RT-PCR)wasperformedtodetectthemaincomponentsoftheTGF-β1/SmadssignalpathwayinhumanpoorlydifferentiatedGCcelllineBGC-823.LocalizationofSmadproteinswasalsodeterminedusingimmunofluorescence.Then,theBGC-823cellswereculturedinthepresenceorabsenceofTGF-β1(10ng/mL)for24and48h,andtheeffectsofTGF-β1onproliferationandapoptosisweremeasuredbycellgrowthcurveandflowcytometry(FCM)analysis.TheultrastructuralfeaturesofBGC-823cellswithorwithoutTGF-β1treatmentwereobservedundertransmissionelectronmicroscope.Theapoptoticcellswerevisualizedbymeansoftheterminaldeoxynucleotidyltransferase(TdT)-mediateddTUPinsitunickend-labeling(TUNEL)method.Meanwhile,theexpressionlevelsofendogenousp15,p21andSmad7mRNAandthecorrespondingproteinsinthecellsweredetectedat1,2and3haftercultureinthepresenceorabsenceofTGF-β1(10ng/mL)bysemi-quantitativeRT-PCRandWesternblot,respectively.RESULTS:TheTGF-β1/SmadsignalingwasfoundtobeintactandfunctionalinBGC-823cells.ThegrowthcurverevealedthemostevidentinhibitionofcellproliferationbyTGF-β1at48h,andFCMassayshowedG1arrestaccompaniedwithapoptosisinducedbyTGF-β1.ThetypicalmorphologicalchangesofapoptosiswereobservedincellsexposedtoTGF-β1.Theapoptosisindex(AI)inTGF-β1-treatedcellswassignificantlyhigherthanthatintheuntreatedcontrols(10.7±1.3%vs0.32±0.06%,P＜0.01).Thelevelsofp15,p21andSmad7mRNAandcorrespondingproteinsincellsweresignificantlyup-regulatedat1h,butgraduallyreturnedtobasallevelsat3hfollowingTGF-β1(10ng/mL)treatment.CONCLUSION:TGF-β1affectsbothproliferationandapoptosisofGCcellsth

简介：AIM:Heatshockprotein(HSP)70isover-expressedinhumangastriccancerandplaysanimportantroleintheprogressionofthiscancer.WeinvestigatedtheeffectsofantisenseHSP70oligomeronhumangastriccancercelllineSGC-7901,anditspotentialroleingenetherapyforthiscancer.METHODS:HumangastriccancercelllineSGC-7901wastreatedinvitrowithvariousconcentrationsofantisenseHSP70oligonucleotidesatdifferentintervals.Growthinhibitionwasdeterminedaspercentagebytrypanbluedyeexclusiontest.ExtractedDNAwaselectrophoresedonagarosegel,anddistributionofcellcycleandkineticsofapoptosisinductionwereanalyzedbypropidiumiodideDNAincorporationusingflowcytometry,whichwasalsousedtodetecttheeffectsofantisenseoligomerpretreatmentonthesubsequentapoptosisinducedbyheatshockinSGC-7901cells.ProteinswereextractedforsimultaneousmeasurementofHSP70expressionlevelbySDS-PAGEWesternblotting.RESULTS:Thenumberofviablecellsdecreasedinadoseandtime-dependentmanner,andladder-likepatternsofDNAfragmentswereobservedinSGC-7901cellstreatedwithantisenseHSP70oligomersataconcentrationof10μmol/Lfor48hor8μmol/Lfor72h,whichwereconsistentwithinter-nucleosomalDNAfragmentation.Flowcytometricanalysisshowedadose-andtime-dependentincreaseinapoptoticratebyHSP70antisenseoligomers.ThisresponsewasaccompaniedwithadecreaseinthepercentageofcellsintheG1andSphasesofthecellcycle,suggestinginhibitionofcellproliferation.Inaddition,flowcytometryalsoshowedthatpretreatmentofSGC-7901cellswithHSP70antisenseoligomersenhancedthesubsequentapoptosisinducedbyheatshocktreatment.WesternblottingdemonstratedthatHSP70antisenseoligomersinhibitedHSP70expression,whichprecededapoptosis,andHSP70wasundetectableattheconcentrationof10μmol/Lfor48hor8μmol/Lfor72h.CONCLUSION:AntisenseHSP70oligomerscanabrogateHSP70expressioninSGC-7901cells,wh

简介：瞄准：学习SSTR1，2，3，4，有在颜色的clinico病理学的因素，房间增长，Bcl-2和p53表示的5表示和他们的关系表面的癌症房间。方法：五种SSTR子类型，Ki-67，Bcl-2和p53染色的Immunohistochemical被标准streptavidin-peroxidase(SP)执行为127颜色的石蜡节的技术表面的癌症。并且在正常的40个标本的五种SSTR子类型的表示渲染表面的mucosae与一样的方法被检测。结果：为五种SSTR子类型的积极染色在颜色被观察表面的癌症房间和正常颜色表面的mucosae。SSTR1是最占优势的子类型在渲染表面的癌症，正常渲染表面的粘膜，并且第二是SSTR5或SSTR2。作为与正常相比渲染表面的粘膜，SSTR4更经常在颜色被表示表面的癌症房间(2.5%对18.9%，P<0.05)；SSTR2的表示，4，5在里面中等到很好区分的颜色，表面的腺癌在糟糕区分的(P<0.05)比那显著地高，在有积极淋巴节点转移的表面的癌症是的颜色的SSTR1表示比那显著地高与否定淋巴节点转移(72.2%和54.5%，P<0.05)。另外，颜色在溃疡的打表面的癌症，SSTR2表示显然被减少(P<0.05)；关联没到达在五SSTR子类型表情和Dukes'stages(P>0.05)之间的统计意义，但是SSTR1表示的频率与Dukes'stage增加，当SSTR3和SSTR5表示与公爵的阶段减少了时。而且，在象年龄那样的五种SSTR子类型和另外的clinicopathological因素的表示之间没有关联，性别，肿瘤地点，肿瘤深度，远转移。在肤色的增生的索引有SSTR2和SSTR3的否定表示的表面的癌症房间与积极表示(P<0.05)比那显著地高。在肤色的Bcl-2表示有SSTR1的积极表示的表面的癌症房间，2，3，5与否定表示(P<0.05)是比那显著地低的。在五种SSTR子类型和p53表示之间没有关联。结论：最占优势的SSTR子类型是SSTR1，并且第二是SSTR2或SSTR5。五�

简介：AIMToexploretheprotectiveeffectsandunderlyingmechanismsoftotalpolysaccharidesoftheSijunzidecoction(TPSJ)ontheepithelialbarriersinvitro.METHODSCaco-2cellmonolayersweretreatedwithorwithoutTPSJinthepresenceorabsenceofTNF-α,andparacellularpermeabilityandtransepithelialelectricalresistance(TEER)weremeasuredtoevaluatetheepithelialbarrierfunction.Immunofluorescenceandwesternblottingwererespectivelyusedtoevaluatethedistributionandexpressionofthetightjunctionproteinsclaudin1,claudin2,zo3,andoccludininCaco-2cells.Westernblottingwasalsousedtoevaluatethecellularexpressionofmyosinlightchain(MLC),phosphorylatedMLC(pMLC),MLCkinase(MLCK),andnuclearfactor(NF)-κBp65.RESULTSTPSJpromotedtheproliferationofCaco-2cellsandinhibitedTNF-α-inducedsecretionofpro-inflammatorycytokines.Furthermore,TPSJsignificantlyamelioratedboththereductionofTEERandtheincreasedparacellularpermeabilityobservedintumornecrosisfactor(TNF)-α-damagedCaco-2monolayers.Furthermore,TPSJremarkablyattenuatedTNF-α-inducedmorphologicalchanges,downregulatedtheexpressionofclaudin1,claudin2,zo3,andoccludin,andmarkedlysuppressedTNF-α-mediatedupregulationofp-MLCandMLCKexpression.Finally,TPSJinhibitedtheactivationandexpressionofNF-κBp65.CONCLUSIONOurresultsdemonstratethatTPSJalleviatestheTNF-α-inducedimpairmentoftheintestinalepithelialcellbarrierfunctionbysuppressingNF-κBp65-mediatedphosphorylationofMLCKandMLC.

简介：AIM:ToinvestigatethepreciserolesofCARinCCl4-inducedacutehepatotoxicity.METHODS:Toprepareanacuteliverinjurymodel,CCl4wasintraperitoneallyinjectedinCAR+/+andCAR-/-mice.RESULTS:ElevationofserumalanineaminotransferaseandextensionofcentrilobularnecrosiswereslightlyinhibitedinCAR-/-micecomparedtoCAR+/+micewithoutPB.AdministrationofaCARinducer,PB,revealedthatCCl4-inducedlivertoxicitywaspartiallyinhibitedinCAR-/-micecomparedwithCAR+/+mice.Ontheotherhand,androstanol,aninverseagonistligand,inhibitedhepatotoxicityinCAR+/+butnotinCAR-/-mice.Thus,CARactivationcausedCCl4hepatotoxicitywhileCARinhibitionresultedinpartialprotectionagainstCCl4-inducedhepatotoxicity.TherewerenodifferencesintheexpressionofCYP2E1,themainmetabolizingenzymeforCCl4,betweenCAR+/+andCAR-/-mice.However,theexpressionofotherCCl4-metabolizingenzymes,suchasCYP2B10and3A11,wasinducedbyPBinCAR+/+butnotinCAR-/-mice.AlthoughthemainpathwayofCCl4-inducedacuteliverinjuryismediatedbyCYP2E1,CARmodulatesitspathwayviainductionofCYP2B10and3A11inthepresenceofactivatororinhibitor.CONCLUSION:ThenuclearreceptorCARmodulatesCCl4-inducedliverinjuryviainductionofCCl4-metabolizingenzymesinthepresenceofanactivator.OurresultssuggestthatdrugsinteractingwithnuclearreceptorssuchasPBmightplaycriticalrolesindrug-inducedliverinjuryordrugdruginteractioneventhoughsuchdrugsthemselvesarenothepatotoxic.

简介：AIM:Toinvestigatetheassociationofcyclooxygenase-2(COX-2)expressionwithangiogenesisandthenumberandtypeofinflammatorycells(macrophages/Kupffercells;mastcells)withinprimaryhepatocellularcarcinoma(HCC)tissuesandadjacentnon-tumorous(MT)tissues.METHODS:ImmunohistochemistryforCOX-2,CD34,CD68andmastcelltryptase(MCT)wasperformedon14well-characterizedseriesofliver-cirrhosis-associatedHCCpatients.COX-2expressionandthenumberofinflammatorycellsintumorlesionsandsurroundinglivertissuesofeachspecimenwerecompared.Moreover,COX-2,CD34stainingandthenumberofinflammatorycellsinareaswithdifferenthistologicaldegreeswithineachtumorsamplewerecomparativelyanalyzed.RESULTS:ThepercentageofCOX-2positivecellswassignificantlyhigherinNTtissuesthanintumors.COX-2expressionwashigherinwell-differentiatedHCCthaninpoorly-differentiatedtissues.Fewmastcellswereobservedwithinthetumormass,whereasahighernumberwasobservedinthesurroundingtissue,especiallyinperi-portalspacesofNTtissues.Abundantmacrophages/KupffercellswereobservedinNTtissues,whereasthenumberofcellswassignificantlylowerinthetumormass.However,ahighercellnumberwasobservedinthewell-differentiatedtumorandprogressivelydecreasedinrelationtothedifferentiationgrade.Withinthetumor,apositivecorrelationwasfoundbetweenCOX-2expressionandthenumberofmacrophages/Kupffercellsandmastcells.Moreover,therewasapositivecorrelationbetweenCD34andCOX-2expressionintumortissues.Comparisonbetweenwell-andpoorly-differentiatedHCCshowedthatthenumberofCD34-positivecellsdecreasedwithdedifferentiation.However,COX-2wastheonlyindependentvariableshowingapositivecorrelationwithCD34inamultivariateanalysis.CONCLUSION:ThepresenceofinflammatorycellsandCOX-2expressioninlivertumorsuggestsapossiblerelationshipwithtumorangiogenesis.COX-2expressingcellsandthenumberofmacro

简介：Liverinjuryisacharacteristicfeatureofhumanimmunodeficiencyvirus(HIV)infection,whichisthesecondmostcommoncauseofmortalityinHIV-infectedpatients.NowitisrecognizedthatliverplaysakeyroleinHIVinfectionpathogenesis.Antiretroviraltherapy(ART),whichsuppressesHIVinfectioninpermissiveimmunecells,islesseffectiveinhepatocytes,therebymakingthesecellsasilentreservoirofHIVinfection.InadditiontodirecthepatotoxiceffectsofHIV,certainARTtreatmentmodalitiesprovidehepatotoxiceffects.TheexactmechanismsofHIV-triggeredchronichepatitisprogressionarenotelucidated,buttheliverisadverselyaffectedbyHIV-infectionandlivercellsareprominentlyinvolvedinHIV-elicitedinjury.Theseeffectsarepotentiatedbysecondhitslikealcohol.Here,wewillfocusontheincidenceofHIV,clinicalevidenceofHIVrelatedliverdamage,interactionsbetweenHIVandlivercellsandtheroleofalcoholandco-infectionwithhepatotropicvirusesinliverinflammationandfibrosisprogression.

简介：瞄准：为了孤立并且识别差别，由二维的电气泳动(2-DE)和帮助矩阵的激光解吸附作用/电离time-of-flight团分光术(MALDI-TOF-MS)表示了在癌症和胃的癌症的正常纸巾之间的蛋白质。方法：胃的癌症纸巾和配对的正常纸巾的可溶的部分蛋白质被2-DE分开。差别表示了蛋白质被MALDI-TOF-MS和数据库搜索选择并且识别。结果：有高分辨率和重制度的2-DE侧面被获得。23个蛋白质点从染色胶化的裂片被切除并且由胰岛素，十五个蛋白质点成功地在被识别在胶化消化了。在识别蛋白质之中，有十过去表示并且在胃癌症纸巾的五下面表示的蛋白质与正常纸巾相比。结论：在这研究，人的胃的癌症织物和配对的正常织物的解决得好的、可再现的2-DE模式被建立并且优化并且某些表示差别的蛋白质被识别。2-DE和MS的联合使用提供一条有效途径为潜在的肿瘤标记屏蔽。

简介：AIM:Toinvestigatewhetherthesimultaneoustreatmentwithhumangrowthhormone(hGH)abolishesthenegativeeffectsofeverolimusonanastomotichealing.METHODS:Forty-eightmaleSprague-Dawley-ratswererandomizedtothreegroupsof16animalseach(Ⅰ:vehicle;Ⅱ:everolimus3mg/kgpo;Ⅲ:everolimus3mg/kgpo+hGH2.5mg/kgsc).AnimalswerepretreatedwithhGHand/oreverolimusdailyforsevendays.Thenastandardanastomosiswascreatedinthedescendingcolonandtreatmentwascontinuedforanothersevendays.Theanastomosiswasresectedintotoandtheburstingpressurewasassessedasamechanicalparameterofintestinalhealing.Moreover,biochemical(Hydroxyproline,PCNA,MPO,MMP-2andMMP-9)andhistological(celldensity,angiogenesis,amountofgranulationtissue)parametersofintestinalhealingwereassessed.RESULTS:AnastomoticburstingpressurewassignificantlyreducedbyeverolimusandasimultaneoustreatmentwithhGHresultedinconsiderablyhighervalues(Ⅰ:134±19mmHg,Ⅱ:85±25mmHg,Ⅲ:114±25mmHg;P<0.05,ⅠvsⅡ;P=0.09,ⅠvsⅢandⅡvsⅢ)HydroxyprolineconcentrationwassignificantlyincreasedbyhGHcomparedtoeverolimusalone(Ⅰ:14.9±2.5μg/mg,Ⅱ:8.9±3.6μg/mg,Ⅲ:11.9±2.8μg/mg;P<0.05,?ⅠvsⅡ/ⅢandⅡvsⅢ).ThenumberofMPO-positivecellswasreducedsignificantlybyhGHcomparedtoeverolimusalone(Ⅰ:10±1n/mm~2,Ⅱ:15±3n/mm~2,Ⅲ:9±2n/mm~2;P<0.05,ⅠvsⅡandⅡvsⅢ),whilethenumberofPCNA-positivecellswereincreasedbyhGH(Ⅰ:28±3/mm~2,Ⅱ:12±3/mm~2,Ⅲ:26±12/mm~2;P<0.05,?Ⅰ?vsⅡandⅡvsⅢ).Correspondingtothesebiochemicalfindings,HEhistologyrevealedsignificantlyincreasedamountofgranulationtissueinhGH-treatedanimals.CONCLUSION:InhibitionofintestinalwoundhealingbyeverolimusispartiallyneutralizedbysimultaeoustreatmentwithhGH.BothinflammationaswellascollagendepositionisinfluencedbyhGH.

简介：瞄准：为了学习不同Helicobacterpylori(Hpylori)的效果，文化在胃的上皮细胞的生长上过滤。方法：肉汤文化Hpylori过滤被准备。胃的上皮细胞与filtrates被对待，并且房间生长被生长曲线和流动血细胞计数决定。胃的上皮细胞的DNA损坏被单个房间的微胶化电气泳动测量。结果：当由CagA-gene-positive对待时，胃的上皮细胞活跃地增殖了肉汤文化过滤，并且到达的菌落形成40%。在S阶段的房间的数字与控制相比增加了。彗星试金在对待与的GES-1房间显示出41.2%彗星房间CagA积极过滤(P<0.05)。结论：CagA积极过滤在形态学和人的胃的上皮细胞瘤细胞的生长特征提高变化。也许，涉及生长的机制之一改变的DNA损坏。

简介：AIM:Toinvestigatewhethergenemethylationintheperitonealfluid(PF)predictsperitonealrecurrenceingastriccancerpatients.METHODS:ThegenemethylationofCHFR(checkpointwithforkheadandringfingerdomains),p16,RUNX3(runt-relatedtranscriptionfactor3),E-cadherin,hMLH1(mutLhomolog1),ABCG2(ATP-bindingcassette,sub-familyG,member2)andBNIP3(BCL2/adenovirusE1B19kDainteractingprotein3)wereanalyzedin80specimensofPFbyquantitativemethylation-specificpolymerasechainr...

简介：AIM:Toinvestigatethedamagingeffectofhigh-intensityfocusedultrasound(HIFU)oncancercellsandtheinhibitoryeffectontumorgrowth.METHODS:MurineH22hepaticcancercellsweretreatedwithHIFUatthesameintensityfordifferentlengthsoftimeandatdifferentintensitiesforthesamelengthoftimeinvitro,thedeadcancercellsweredeterminedbytrypanbluestaining.TwogroupsofcancercellstreatedwithHIFUatthelowestandhighestintensitywereinoculatedintomice.Tumormasseswereremovedandweighedafter2wk,tumorgrowthineachgroupwasconfirmedpathologically.RESULTS:ThedeathrateofcancercellstreatedwithHIFUat1000W/cm2for0.5,1,2,4,8,and12swas3.11±1.21%,13.37±2.56%,38.84±3.68%,47.22±5.76%,87.55±7.32%,and94.33±8.11%,respectively.ApositiverelationshipbetweenthedeathratesofcancerceilsandthelengthofHIFUtreatmenttimewasfound(r=0.96,P＜0.01).ThedeathrateofcancercellstreatedwithHIFUattheintensityof100,200,400,600,800,and1000W/cm2for8swas26.31±3.26%,31.00±3.87%,41.97±5.86%,72.23±8.12%,94.90±8.67%,and99.30±9.18%,respectively.ApositiverelationshipbetweenthedeathratesofcancercellsandtheintensitiesofHIFUtreatmentwasconfirmed(r=0.98,P＜0.01).ThecancercellstreatedwithHIFUat1000W/cm2for8swereinoculatedintomiceexvivo.Thetumorinhibitoryratewas90.35%comparedtothecontrol(P＜0.01).IntheexperimentalgroupinoculatedwiththecancercellstreatedwithHIFUat1000W/cm2for0.5s,thetumorinhibitoryratewas22.9%(P＜0.01).Bypathologicalexamination,tumorgrowthwasconfirmedin8outof14mice(57.14%,8/14)inoculatedwiththecancercellstreatedwithHIFUat1000W/cm2for8s,whichwassignificantlylowerthanthatinthecontrol(100%,15/15,P＜0.05).CONCLUSION:HIFUiseffectiveonkillingordamageofH22hepaticcancercellsinvitroandoninhibitingtumorgrowthinmiceexvivo.

简介：AIMToinvestigatetherolesandinteractionsofmutThomolog（MTH）-1andhypoxia-induciblefactor（HIF）-1αinhumancolorectalcancer（CRC）.METHODS：TheexpressionanddistributionofHIF-1αandMTH-1proteinsweredetectedinhumanCRCtissuesbyimmunohistochemistryandquantitativerealtimepolymerasechainreaction（qRT-PCR）.SW480andHT-29cellswereexposedtonormoxiaorhypoxia.ProteinandmRNAlevelsofHIF-1αandMTH-1wereanalyzedbywesternblottingandqRT-PCR,respectively.InordertodeterminetheeffectofHIF-1αontheexpressionofMTH-1andtheamountof8-oxodeoxyguanosinetriphosphate（dGTP）inSW480andHT-29cells,HIF-1αwassilencedwithsmallinterferingRNA（siRNA）.GrowthstudieswereconductedoncellswithHIF-1αinhibitionusingaxenografttumormodel.Finally,MTH-1proteinwasdetectedbywesternblottinginvivo.RESULTS：HighMTH-1mRNAexpressionwasdetectedin64.2%ofcases（54/84）,andthiswassignificantlycorrelatedwithtumorstage（P=0.023）andsize（P=0.043）.HIF-1αproteinexpressionwascorrelatedsignificantlywithMTH-1expression（R=0.640;P〈0.01）inhumanCRCtissues.HypoxicstressinducedmRNAandproteinexpressionofMTH-1inSW480andHT-29cells.InhibitionofHIF-1αbysiRNAdecreasedtheexpressionofMTH-1andledtotheaccumulationof8-oxo-dGTPinSW480andHT-29cells.Intheinvivoxenografttumormodel,expressionofMTH-1wasdecreasedintheHIF-1αsiRNAgroup,andthetumorvolumewasmuchsmallerthanthatinthemocksiRNAgroup.CONCLUSION：MTH-1expressioninCRCcellswasupregulatedviaHIF-1αinresponsetohypoxicstress,emphasizingthecrucialroleofHIF-1α-inducedMTH-1intumorgrowth.

简介：AIM:Tostudytheblockingeffectsofgenisteinoncellproliferationcycleinhumangastriccarcinomacells(SGC-7901)andthepossiblemechanism.METHODS:MTTassaywasappliedinthedetectionoftheinhibitoryeffectsofgenisteinoncellproliferation.Flowcytometrywasusedtoanalyzethecellcycledistribution.ImmunocytochemicaltechniqueandWesternblottingwereperformedtodetecttheproteinexpressionofcyclinD1,cyclinB1andp21waf1/cip1.RESULTS:Genisteinsignificantlyinhibitedthegrowthandproliferationofhumangastriccarcinomacells(SGC-7901).Sevendaysaftertreatmentwithdifferentconcentrationsofgenistein(2.5,5.0,10.0,20.0μg/mL),thegrowthinhibitoryrateswere11.2%,28.8%,55.3%,84.7%respectivelyandcellcycleswerearrestedattheG(2)/Mphase.GenisteindecreasedcyclinD1proteinexpressionandenhancedcyclinB1andp21waf/cip1proteinexpressioninaconcentration-dependentmanner.CONCLUSION:ThegrowthandproliferationofSGC-7901cellscanbeinhibitedbygenisteinviablockingthecellcycle,withreducedexpressionofcyclinD1andenhancedexpressionofcyclinB1andp21waf/cip1proteinintheconcentrationrangeof0-20μg/mL.