简介：Enterovesicalfistulasarenotuncommoninpatientswithinflammatoryormalignantcolonicdisease,however,fistulassecondarytoprimarybladdercarcinomasareextremelyrare.Wehereinreportedapatientpresentingwithintractableurinarytractinfectionduetoenterovesicalfistulaformationcausedbyasquamouscellcarcinomaoftheurinarybladder.Thispatientunderwentenblocresectionofthebladderdomeandinvolvedileum,andrecovereduneventfullywithouturinarycomplaint.Tothebestofourknowledge,thisisthefirstcasereportedintheliterature.

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：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：AIM:Todeterminetheclinicalvalueofdiffusion-weight-edimaging(DWI)forthediagnosisofextrahepaticcholangiocarcinoma(EHCC)bycomparingthediagnosticsensitivityofDWIandmagneticresonancecholan-giopancreatography(MRCP).METHODS:Magneticresonanceimagingexaminationwasperformedin56patientswithsuspectedEHCC.T1-weightedimaging,T2-weightedimaging,MRCPandDWIsequence,DWIusingsingle-shotspin-echoechoplanarimagingsequencewithdifferentbvalues(100,300,500,800and1000s/mm2),wereperformed.Allcaseswerefurtherconfirmedbysurgeryorhistopathologicaldiagnosis.TworadiologistsjointlyperformedtheanalysisoftheDWIandMRCPimages.Apparentdiffusioncoefficient(ADC)valueandsignal-noiseratiowerecalculatedforEHCC.Sensitivity,specificity,accuracy,positivepredictivevalueandnegativepredictivevalueweretestedusingDWIwithabvalueof500s/mm2andMRCPimages,respectively.RESULTS:Histopathologicaldiagnosisconfirmedthatamongthe56cases,35wereEHCC(20hilarand15distalextrahepatic),16werecholangitis,and5werecal-culusofbileduct.Thirty-threeoutofthe35EHCCcasesweredetectedbyDWI.EHCCexhibiteddifferentiallevelsofhighsignalintensityinDWIandlowsignalintensityintheADCmap.ThemeanvalueforADCwas(1.31±0.29)×10-3mm2/s.ThedetectionrateofEHCCwassignificantlyhigherbyDWI(94.3%)thanbyMRCP(74.3%)(P<0.05).Therewasasignificantdifferenceinsensitivity(94.3%vs74.3%),specificity(100%vs71.4%),accu-racy(96.4%vs73.2%),positivepredictivevalue(100%vs81.3%),andnegativepredictivevalue(91.3%vs62.5%)betweenDWIandMRCPindiagnosingEHCC.CONCLUSION:DWIhasahighsensitivityforthedetectionofEHCCasitshowstheEHCClesionmoreunambiguouslythanMRCPdoes.DWIcanalsoprovideadditionalclinicallyimportantinformationinEHCCpatientswhenaddedtoroutinebileductMRimagingprotocols.

简介：关于为心脏性的吃惊的处理的levosimendan的使用的编辑的一封信被介绍。

简介：瞄准：在食道的有鳞的房间癌(ESCC)调查midkine的表示并且与clinicopathological特征分析它的关系。方法：RT-PCR和免疫细胞化学的染色被用来分别地在EC109房间检测midkinemRNA和蛋白质的表示。然后，在ESCC样品的66种情况中的midkine的表示被免疫组织化学对人的midkine用单音的同种细胞的抗体检测。结果：Midkine被RT-PCR和免疫细胞化学在EC109房间表示。免疫反应在56.1%被检测(37/66)ESCC样品。midkine的表示在肿瘤房间的细胞质被发现。尤其是，midkine的紧张在充满容器和肿瘤的入侵的边阶的区域是更强壮的。Midkine更强烈地比在中等并且糟糕区分的肿瘤在很好区分的肿瘤(76.9%)被表示(43.1%和41.2%，分别地)(P<0.05)。在midkine之间没有统计上重要的关联在ESCC的表示和性，年龄，临床的阶段，淋巴节点转移或幸存。结论：Midkine完了在ESCC表示了。它可以在肿瘤血管生成和侵略起一个作用。midkine的表示在ESCC与肿瘤细胞分化被相关。肿瘤房间区分越多糟糕，midkine表示越多weaker。

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.

简介：AIM:Toevaluatetheroleofsurvivinandcaspase-3inapoptosisofgastriccarcinoma,aswellasinprognosisofpatientswithgastriccarcinoma.METHODS:Expressionsofsurvivinandcaspase-3wereinvestigatedimmunohistochemicallyin80gastriccarcinomapatientswithoutahistoryofchemo-radiationtherapy.TumorcellapoptosiswasexaminedbyTUNELmethod.RESULTS:Immunohistochemicalanalysisshowedthatsurvivinexpressionwaspositivein61of80patients(76%)withgastriccarcinoma.Incontrast,noexpressionofsurvivininadjacentnormaltissueswasdetected.Expressionlevelofcaspase-3washigherinnormaltissuesthanincarcinoma.Patientswithhigherexpressionofsurvivinhadworsehistologicalgradesandpathologicalstages.Expressionofcaspase-3wassignificantlyassociatedwithhistologicalstages,butnotwiththepathologicalstages.Althoughsurvivinexpressionincarcinomawasnotinverselyrelatedtocaspase-3,patientswithsurvivin(-)andcaspase-3(+)hadthemaximumapoptosisindex.CONCLUSION:Expressionlevelofsurvivinwasassociatedwithhistologicalgradesandpathologicalstagesofthetumor,indicatingthatsurvivinmaybeapoorprognosisfactorforgastriccarcinoma.Unlikecaspase-3,survivin(anapoptosisinhibitor)canmarkedlyinhibittheapoptosisoftumorcells.

简介：Perivascularepithelioidcelltumor(PEComa)ofthepancreasisanunusualtumorderivingfrommesenchyma.ThispaperdescribedacaseofpancreaticPEComa,whichwasinitiallysuspectedasneuroendocrinecarcinomabybiopsy,andthereforesurgicaltreatmentwasrecommendedduetoundetermineddiagnosis.Examinationofthesurgicalspecimenunderamicroscopeshowedthatthetumorcell’smorphologywasepithelioidorspindle-shaped,andrangedinanestedpattern.Additionally,thesecellshadalargeextentofacidophiliccytoplasm,nomitoticfigures,andexpressedHMB-45,melan-p,andsmoothmuscleactinimmunohistochemically.PathologicalexaminationindicatedthatPEComaoriginatedfromthepancreas,butsymptomsrelatedtotuberoussclerosiswereabsent.SincePEComaisextremelyrareinthepancreas,itislikelytobeignoredindifferentialdiagnosis.Inconclusion,ourarticlehighlightedtheclinicopathologicalfeaturesofPEComa,andweconductedaliteraturereviewfocusingonPEComasoastodeepentheunderstandingofthistumortype.

简介：

简介：AIMToevaluatetheclinicaloutcomesofpatientswhounderwentendoscopicsubmucosaltunneldissection(ESTD)foresophagealsquamouscellcarcinoma(ESCC)andprecancerouslesions.METHODSESTDwasperformedin289patients.Theclinicaloutcomesofthepatientsandpathologicalfeaturesofthelesionswereretrospectivelyreviewed.RESULTSAtotalof311lesionswereincludedintheanalysis.Theenblocrate,completeresectionrate,andcurativeresectionratewere99.04%,81.28%,and78.46%,respectively.TheESTDproceduretimewas102.4±35.1min,themeanhospitalizationtimewas10.3±2.8d,andtheaverageexpenditurewas3766.5±846.5dollars.Theintraoperativebleedingratewas6.43%,thepostoperativebleedingratewas1.61%,theperforationratewas1.93%,andthepostoperativeinfectionratewas9.65%.Esophagealstrictureandpositivemarginweresevereadverseevents,withanincidencerateof14.79%and15.76%,respectively.Notumorrecurrenceoccurredduringthefollow-upperiod.CONCLUSIONESTDforESCCandprecancerouslesionsisfeasibleandrelativelysafe,butforlargemucosallesions,therateofesophagealstrictureandpositivemarginishigh.

简介：AIM:Toinvestigatetheanti-tumoreffectsofnuclearfactor-κB(NF-κB)inhibitorSN50andrelatedmechanismsofSGC7901humangastriccarcinomacells.METHODS:MTTassaywasusedtodeterminethecytotoxiceffectsofSN50ingastriccancercelllineSGC7901.Hoechst33258stainingwasusedtodetectapoptosismorphologicalchangesafterSN50treatment.Activationofautophagywasmonitoredwithmonodansylcadaverine(MDC)stainingafterSN50treatment.Immunofluorescencestainingwasusedtodetecttheexpressionoflightchain3(LC3).MitochondrialmembranepotentialwasmeasuredusingthefluorescentprobeJC-1.Westernblottinganalysiswereusedtodeterminetheexpressionofproteinsinvolvedinapoptosisandautophagyincludingp53,p53upregulatedmodulatorofapoptosis(PUMA),damage-regulatedautophagymodulator(DRAM),LC3andBeclin1.Wedetectedtheeffectsofp53-mediatedautophagyactivationontheapoptosisofSGC7901cellswiththep53inhibitorpifithrin-α.RESULTS:TheviabilityofSGC7901cellswasinhibitedafterSN50treatment.Inductionsintheexpressionofapoptoticproteinp53andPUMAaswellasautophagicproteinDRAM,LC3andBeclin1weredetectedwithWesternblottinganalysis.SN50-treatedcellsexhibitedpunctuatemicrotubule-associatedprotein1LC3inimmunoreactivityandMDC-labeledvesiclesincreasedaftertreatmentofSN50byMDCstaining.CollapseofmitochondrialmembranepotentialΔψweredetectedfor6to24hafterSN50treatment.SN50-inducedincreasesinPUMA,DRAM,LC3andBeclin1andcelldeathwereblockedbythep53specificinhibitorpifithrin-α.CONCLUSION:Theanti-tumoractivityofNF-κBinhibitorsisassociatedwithp53-mediatedactivationofautophagy.

简介：瞄准：在胃的很好区分的内分泌的肿瘤(GWDET)(ECL房间良性肿瘤)调查cyclin依赖的激酶禁止者p21和p27的表示。方法：p21和p27的表情从匹配GWDET的诊断标准的16个病人在内视镜的活体检视标本immunhistochemically被检验。弱或强壮的积极原子染色任何一个的百分比被注意。有年龄，性，肿瘤本地化，multifocality和伴随的长期的萎缩性胃炎，神经内分泌房间增生(NEH)，神经内分泌发育异常(NED)，肠的组织变形(IM)，Ki-67增长索引和临床的结果的免疫表情的协会也被评估。结果：所有情况与43.6%的一个吝啬的表示分数表示了p27，当31.3%案例显示出任何p21表示时。p21和p27免疫表情显著地与对方一起被相关(P<0.01)，并且表示p21组有更高的p27表示分数(68%对22%)。p21和p27表情在女人是更低的，在在某处除没有粘膜下层扩展的宫底以外，其肿瘤被定位的非衰退的粘膜和盒子。在上矛盾，p21和p27表情与粘膜下层扩展和萎缩性胃炎在男性和病人是更高的。介绍更低的p27分数的盒子有独居的肿瘤显示出既不NEH-NED也不IM。尽管有，有更低的p21表示的盒子介绍了NEH-NED伴随的多焦点的肿瘤。然而，p21的关联和p27表情都没与年龄和Ki-67表示被发现。结论：p27广泛地在GWDET被表示，当p21表示在三分之二个盒子中稀少、观察时。p21和p27表情的损失可以与不同良性肿瘤肿瘤子类型被相关；然而，更多的研究被需要在胃肠的内分泌的肿瘤估计这些未来的标记的角色。

简介：瞄准：到表示人的gastric-cancer-related基因介绍的分析，GCRG123在人的胃的图章戒指房间癌纸巾，并且在GCRG123上执行生物信息学分析。方法：原位杂交被用来在嵌入石蜡的胃的纸巾探索GCRG123表示模式，包括图章戒指房间癌的15个盒子，15肠类型的腺癌，和15正常胃粘膜。北弄污被用来在在胃图章戒指房间癌和肠类型的腺癌纸巾之间的GCRG123表示分析差别。包括强风，Multalin和叫，联机软件被申请生物信息学分析。生物工学信息(NCBI)和加利福尼亚大学圣克鲁斯(UCSC)的国家中心数据库被用于分析。结果：当蓝色猛抛，原位杂交信号出现了限制了为细胞质。十从胃的环状体房间癌，正常胃的粘膜上皮和幽门腺的15个盒子显示出高GCRG123表示。低GCRG123表示在胃的肠类型的腺癌和正常胃腺被观察。北弄污表明GCRG123在图章戒指房间癌组织是起来调整的但是在肠类型的腺癌组织下面调整。强风和Multalin分析表明GCRG123顺序与人的长散布的原子元素retrotransposons的ORF2顺序有92%类似(LINE-1，L1)。叫分析显示了印射到所有染色体的那GCRG123。GCRG123被发现在Rb，IL-2的5'flanking区域和凝固第九因子基因的intron-17和-23集成。结论：GCRG123，L1家庭的一个积极成员，在人的胃的图章戒指是起来调整的房间癌。

简介：AIM:RecombinedplasmidpETNF-P16wasconstructedtoinvestigateitsexpressionpropertiesinesophagealsquamouscarcinomacelllineEC9706inducedbyX-rayirradiationandthefeasibilityofgene-radiotherapyforesophagealcarcinoma.METHODS:RecombinedplasmidpETNF-P16wasconstructedandtransfectedintoEC9706cellswithlipofectamine.ELISA,Westernblot,andimmunocytochemistrywereperformedtodeterminetheexpressionpropertiesofpETNF-P16inEC9706aftertransfectioninducedbyX-rayirradiation.RESULTS:EukaryoticexpressionvectorpETNF-P16wassuccessfullyconstructedandtransfectedintoEC9706cells.TNFαexpressionsweresignificantlyincreasedinthetransfectedcellsafterdifferentdosesofX-rayirradiationthaninthoseafter0Gyirradiation(1192.330-2026.518pg/mL,P<0.05-0.01),andtheTNFαexpressionsandP16weresignificantlyhigher6-48hafter2GyX-rayirradiation(358.963-585.571pg/mL,P<0.05-0.001).NoP16expressionwasdetectedinnormalEC9706cells.However,therewasstrongexpressioninthetransfectedandirradiationgroups.CONCLUSION:X-rayirradiationinductioncouldsignificantlyenhanceTNFαandP16expressioninEC9706cellstransfectedwithpETNF-P16plasmid.Theseresultsmayprovideimportantexperimentaldataandtherapeuticpotentialforgene-radiotherapyofesophagealcarcinoma.

简介：瞄准：调查在肝的卵形的房间在试管内的增长和区别上表明小径的正规Wnt的激活的效果。方法：WB-F344房间与recombinantWnt3a被对待(20，40，80，160，200ng/mL)在24h的没有浆液的媒介。房间增长被Brdu加入分析测量；未经治疗的WB-F344房间作为控制被拿。有为24h的Wnt3a(160ng/mL)的术后疗法，在对待的WB-F344房间代替细胞的本地化和beta-catenin的蛋白质表示并且与Wnt3a未经治疗被免疫荧光染色和西方的污点分析检验。CyclinD1mRNA表示被半量的反向抄本的聚合酶链反应(RT-PCR)决定。一些表型的标记的mRNA层次(法新社，CK-19，白长袍的)并且二个肝的原子因素(HNF-4，HNF-6)被RT-PCR测量。CK-19和法新社蛋白质的表情被西方的污点分析检测。结果：Wnt3a支持了WB-F344房间的增长。有recombinantWnt3a的WB-F344房间的刺激导致了transcriptional使活跃之物beta-catenin的累积，和它进原子核，和起来调整的典型Wnt目标基因CyclinD1的易位。在当浆液不在时的Wnt3a处理的3d以后，WB-F344房间保留了他们的双性人潜力表示hepatocytes和cholangiocytes的几个特定的表型的标记，例如法新社和CK-19，跟随表明小径的正规Wnt的激活。结论：表明小径的正规Wnt支持老鼠的增长和自强肝的卵形的房间。

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.