简介：AIM:ToinvestigateapathophysiologicalroleofcathepsinW(CatW),aputativethiol-dependentcysteineprotease,whichisspecificallyexpressedincytotoxiclymphocytes,indifferenttypesofchronicinflammationofthegastricmucosa.METHODS:GastricandduodenalbiopsiesofpatientswithHelicobacterpylori(Hpylori)-associatedactivegastritis(Hp,n=19),chemicallyinducedreactivegastritis(CG,n=17),autoimmuneatrophicgastritis(AIG,n=20),lymphocyticcorpusgastritis(LG,n=29),celiacdisease(CD,n=10),andcorrespondingcontrols(n=24)wereanalyzedbyimmunohistochemistryfortheexpressionofCatWandCD45.Furthermore,immunohistochemicaldoublestainingwithanti-CD3andanti-cathepsinwasperformedforthesamplesofAIG.RESULTS:MedianvaluesofCatW-expressingcellsamongCD45-positiveimmunecellswerebetween2%and6%fornormalgastricmucosa,CG,andLG,whereasthecorrespondingvaluewassignificantlyincreasedforAIG(24.7%,P＜0.001)andsignificantlydecreasedforHP(0.7%,P＜0.05).Doublestainingwithanti-CD3andantiCatWantibodiesrevealedthat＞90%ofCatW-expressingcellsingastricmucosaofAIGwereTcells.DuodenalmucosahadsignificantlymoreCatW/CD45-positivecellsthannormalgastricmucosa(median:17.8%vs2%,P＜0.01).ThecorrespondingproportionofCatW/CD45-positivecellswasdecreasedinCDcomparedtoduodenalmucosa(median:2.1%vs17.8%,P＜0.05).CONCLUSION:TheoppositefindingsregardingthepresenceofCatW-positivecellsinAIG(increase)andCD(decrease)reflectsthedifferentcellularcompositionofimmunecellsinvolvedinthepathogenesisofthesediseases.

简介：AIM:Toidentifythosewithamicropapillarypattern,ascertainrelativefrequencyanddocumentclinicopathologicalcharacteristicsbyreviewinggastriccarcinomas.METHODS:Onehundredandfifty-onepatientsdiagnosedwithgastriccancerwhounderwentgastrectomywereretrospectivelystudiedandthepresenceofaregionalinvasivemicropapillarycomponentwasevaluatedbylightmicroscopy.Allavailablehematoxylin-eosin(HE)-stainedslideswerehistologicallyreviewedand5tumorswereselectedasp...

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：Historically,mastcellswereknownasakeycelltypeinvolvedintypeIhypersensitivity.Untillasttwodecades,thiscelltypewasrecognizedtobewidelyinvolvedinanumberofnon-allergicdiseasesincludinginflammatoryboweldisease(IBD).MarkedlyincreasednumbersofmastcellswereobservedinthemucosaoftheileumandcolonofpatientswithIBD,whichwasaccompaniedbygreatchangesofthecontentinmastcellssuchasdramaticallyincreasedexpressionofTNFα,IL-16andsubstanceP.TheevidenceofmastcelldegranulationwasfoundinthewallofintestinefrompatientswithIBDwithimmunohistochemistrytechnique.ThehighlyelevatedhistamineandtryptaselevelsweredetectedinmucosaofpatientswithIBD,stronglysuggestingthatmastcelldegranulationisinvolvedinthepathogenesisofIBD.However,littleisknownoftheactionsofhistamine,tryptase,chymaseandcarboxypeptidaseinIBD.Overthelastdecade,heparinhasbeenusedtotreatIBDinclinicalpractice.Thelowmolecularweightheparin(LMWH)waseffectiveasadjuvanttherapy,andthepatientsshowedgoodclinicalandlaboratoryresponsewithnoseriousadverseeffects.TherolesofPGD2,LTC4,PAFandmastcellcytokinesinIBDwerealsodiscussed.Recently,aseriesofexperimentswithdispersedcolonmastcellssuggestedthereshouldbeatleasttwopathwaysinmanformastcellstoamplifytheirownactivation-degranulationsignalsinanautocrineorparacrinemanner.Thehypothesisisthatmastcellsecretogoguesinducemastcelldegranulation,releasehistamine,thenstimulatetheadjacentmastcellsorpositivelyfeedbacktofurtherstimulateitshostmastcellsthroughH1receptor.Whereasreleasedtryptaseactssimilarlytohistamine,butactivatesmastcellsthroughitsreceptorPAR-2.Theconnectionsbetweencurrentanti-IBDtherapiesorpotentialtherapiesforIBDwithmastcellswerediscussed,implicatingfurtherthatmastcellisakeycelltypethatisinvolvedinthepathogenesisofIBD.Inconclusion,whilepathoge

简介：AIMToinvestigatetheeffectoffenugreeklactone（FL）onpalmitate（PA）-inducedapoptosisanddysfunctionininsulinsecretioninpancreaticNIT-1β-cells.METHODS：CellswereculturedinthepresenceorabsenceofFLandPA（0.25mmol/L）for48h.Then,lipiddropletsinNIT-1cellswereobservedbyoilredOstaining,andtheintracellulartriglyceridecontentwasmeasuredbycolorimetricassay.Theinsulincontentinthesupernatantwasdeterminedusinganinsulinradioimmunoassay.Oxidativestress-associatedparameters,includingtotalsuperoxidedismutase,glutathioneperoxidaseandcatalaseactivityandmalondialdehydelevelsinthesuspensionswerealsoexamined.Theexpressionofupstreamregulatorsofoxidativestress,suchasproteinkinaseC-α（PKC-α）,phospho-PKC-αandP47phox,weredeterminedbyWesternblotanalysisandreal-timePCR.Inaddition,apoptosiswasevaluatedinNIT-1cellsbyflowcytometryassaysandcaspase-3viabilityassays.RESULTS：Ourresultsindicatedthatcomparedtothecontrolgroup,PAinducedanincreaseinlipidaccumulationandapoptosisandadecreaseininsulinsecretioninNIT-1cells.OxidativestressinNIT-1cellswasactivatedafter48hofexposuretoPA.However,FLreversedtheabovechanges.TheseeffectswereaccompaniedbytheinhibitionofPKC-α,phospho-PKC-αandP47phoxexpressionandtheactivationofcaspase-3.CONCLUSION：FLattenuatesPA-inducedapoptosisandinsulinsecretiondysfunctioninNIT-1pancreaticβ-cells.Themechanismforthisactionmaybeassociatedwithimprovementsinlevelsofoxidativestress.

简介：AIM:Toinvestigatetheabilityofproteaseinhibitorstomodulatehistaminereleasefromhumancolonmastcells.METHODS:Enzymaticallydispersedcellsfromhumancolonwerechallengedwithanti-IgEorcalciumionophoreA23187intheabsenceorpresenceoftryptaseandchymaseinhibitors,andhistaminereleasewasdetermined.RESULTS:IgEdependenthistaminereleasefromcolonmastceilswasinhibitedbyuptoapproximately37%,26%and36.8%bychymaseinhibitorsZ-Ile-Glu-Pro-Phe-CO2Me(ZIGPFM),N-TosyI-L-phenylalanyl-chloromethylketone(TPCK),andC~l-antitrypsin,respectively.Similarly,inhibitorsoftryptaseleupeptin,N-tosyI-L-lysinechloromethylketone(TLCK),lactoferrinandprotaminewerealsoabletoinhibitanti-IgEinducedhistaminereleasebyamaximumofsome48%,37%,40%and34%,respectively.Preincubationoftheseinhibitorswithcellsfor20rainbeforechallengedwithanti-IgEhadsmalleffectontheinhibitoryactionsoftheseinhibitorsoncolonmastcells.Aspecificinhibitorofaminopeptidaseamastatinhadnoeffectonanti-IgEinducedhistaminerelease.Thesignificantinhibitionofcalciumionophoreinducedhistaminereleasewasalsoobservedwiththeinhibitorsoftryptaseandchymaseexamined.Apartfromleupeptinandprotamine,theinhibitorstestedbythemselvesdidnotstimulatecolonmastcells.CONCLUSION:ItwasdemonstratedthatbothtryptaseandchymaseinhibitorscouldinhibitIgEdependentandcalciumionophoreinducedhistaminereleasefromdispersedcolonmastcellsinaconcentrationdependentofmanner,whichsuggestthattheyarelikelytobedevelopedasanovelclassofanti-inflammatorydrugstotreatchronicofcolitisinman.

简介：AIM:ToinvestigatetheeffectofhepatitisBvirus(HBV)XgeneonapoptosisandexpressionsofapoptosisfactorsinXgene-transfectedHepG2cells.METHODS:TheHBVXgeneeukaryonexpressionvectorpcDNVA3-XwastransientlytransfectedintoHepG2cellsbylipid-mediatransfection.UntransfectedHepG2andHepG2transfectedwithpcDNA3wereusedascontrols.ExpressionofHBxinHepG2wasidentifiedbyPT-PCR.MTTandTUNELwereemployedtomeasureproliferationandapoptosisofcellsin.threegroups.Semi-quantifiedRT-PCRwasusedtoevaluatetheexpressionlevelsofFas/FasL,Bax/Bcl-xL,andc-mycineachgroup.RESULTS:HBVXgenewastransfectedintoHepG2cellssuccessfully.RT-PCRshowedthatHBxwasonlyexpressedinHepG2/pcDNA3-Xcells,butnotexpressedinHepG2andHepG2/pcDNA3cells.AnalyzedbyMTT,cellproliferationcapacitywasobviouslylowerinHepG2/pcDNA3-Xcells(0.08910±0.003164)thaninHepG2(0.14410±0.004927)andHepG2/pcDNA3cells(0.12150±0.007159)(P＜0.05andP＜0.01).AnalyzedbyTUNEL,cellapoptosiswasmuchmoreinHepG2/pcDNA3-Xcells(980/2000)thanHepG2(420/2000),HepG2/pcDNA3cells(520/2000)(P＜0.05andP＜0.01).Evaluatedbysemi-quantifiedRT-PCR,theexpressionlevelofFas/FasLwassignificantlyhigherinHepG2cellstransfectedwithHBxthaninHepG2andHepG2/pcDNA3cells(P＜0.05andP＜0.01).Bax/Bcl-xLexpressionlevelwasalsoelevatedinHepG2/pcDNA3-Xcells(P＜0.05andP＜0.01).Expressionofc-mycwasmarkedlyhigherinHepG2/pcDNA3-XcellsthaninHepG2andHepG2/pcDNA3cells(P＜0.05andP＜0.01).CONCLUSION:HBVXgenecanimpaircellproliferationcapacity,improvecellapoptosis,andupregulateexpressionofapoptosisfactors.TheinterventionofHBVXgeneontheexpressionofapoptosisfactorsmaybeapossiblemechanismresponsibleforthechangeincellapoptosisandproliferation.

简介：瞄准：评估在人的肝细胞癌的房间增长和apoptosis上的基因衬里的人的易碎的组氨酸三个一组(FHIT)的禁止的效果Hep3B在试管内。方法：包括FHIT基因的功能的区域的recombinantpcDNA3.1(+)/FHIT被构造并且转了进人的肝细胞癌房间在试管内。mRNA和在transfected房间的FHIT基因的蛋白质表示被RT-PCR和西方的污点分别地检测。增长上的FHIT的效果被MTT试金检测。在房间周期和apoptosis的变化是由流动血细胞计数的assayed。五只老鼠收到了Hep3B-FHIT的下的移植；5只老鼠作为控制收到了正常Hep3B和Hep3B-C的下的移植。裸体老鼠和肿瘤生长的体重被测量。结果：RT-PCR和西方的污点分析证明FHIT-mRNA和FHIT蛋白质的表示水平在在有pcDNA3.1(+)/FHIT的感染以后的Hep3B房间是更高的。与pcDNA3.1(+)/FHIT对待的Hep3B细胞的生长显著地被禁止。pcDNA3.1(+)/FHIT-transfectedHep3B房间在G0-G1阶段显示出显著地更高的房间率并且与控制比较增加了apoptosis(P<0.05)。移植肿瘤的生长被FHIT显著地禁止。从Hep3B-FHIT房间产生的肿瘤比那些从Hep3B和Hep3B-C房间产生晚很发生了。Hep3B-FHIT房间的生长是慢的，肿瘤体积是低的。结论：FHIT基因的转导变异禁止人的肝细胞癌细胞的生长并且导致细胞apoptosis在活体内和在试管内。

简介：瞄准：调查角色和骨头髓的潜在的机制在严重尖锐腹膜炎(树液)的间充质的干细胞(MSC)。方法：从SpragueDawley老鼠的胰腺的acinar房间随机被划分成三个组：非钠deoxycholate(SDOC)组(non-SODC组)，SDOC组，和MSC干预组织(即，MSC的一个合作文化系统和胰腺的acinar房间+SDOC)。房间幸存率，malonaldehyde(MDA)的集中，superoxidedismutase(草皮)的密度，浆液淀粉酶(AMS)分泌物评价并且喂奶脱氢酶(LDH)漏率在各种各样的时间点被检测。在分开的研究，SpragueDawley老鼠随机被划分成一个树液组或MSC组织的树液+。浆液AMS，MDA和草皮，interleukin(IL)-6,IL-10，和肿瘤坏死因素(TNF)-层次，肠的mucosa损害分数和小肠的mucosa的增殖的房间在注射任何一个MSC以后在各种各样的时间点被测量或进老鼠盐。在两学习，MSC的保护的效果被评估。结果：在vitro，胰腺的acinar房间和草皮的密度的房间幸存率显著地被减少，并且MDA，AMS分泌物率和LDH漏率的集中显著地与MSC干预组和Non-SDOC组相比在SDOC组被增加在每次指。在vivo，在SAP+MSC组的浆液AMS，IL-6，TNF-和疯水平比SAP组低；然而，浆液IL-10水平比SAP组高。浆液草皮水平比SAP组在高每次指，而在草皮水平的重要在组之间差别仅仅在24h以后被注意。肠的mucosa损害分数显著地被减少，小肠的mucosa的增殖的房间在注射MSC以后变得明显。结论：MSC能有效地减轻损害到胰腺的acinar房间和小肠的上皮，支持伤寒上皮的增长并且mucosa修理，与树液一起在老鼠稀释全身的发炎。

简介：AIM:ToinvestigatethetryptaseandhistaminereleaseabilityofhumancolonmastcellsuponIgEdependentorindependentactivationandthepotentialmechanisms.METHODS:Enzymaticallydispersedcellsfromhumancolonswerechallengedwithanti-IgEorcalciumionophoreA23187,andthecellsupernatantsafterchallengewerecollected.Bothconcentrationdependentandtimecoursestudieswithanti-IgEorcalciumionophoreA23187wereperformed.TryptasereleasewasdeterminedwithasandwichELISAprocedureandhistaminereleasewasmeasuredusingaglassfibre-basedfiuorometricassay.RESULTS:Bothanti-IgEandcalciumionophorewereabletoinducedosedependentreleaseofhistaminefromcolonmastcellswithuptoapproximately60%and25%nethistaminereleasebeingachievedwith1μg/mLcalciumionophoreand10μg/mLanti-IgE,respectively.Dosedependentreleaseoftryptasewasalsoobservedwithuptoapproximately19ng/mLand21ng/mLreleaseoftryptasebeingachievedwith10μg/mLanti-IgEand1μg/mLcalciumionophore,respectively.Timecoursestudyrevealedthatbothtryptaseandhistaminereleasefromcolonmastcellsstimulatedbyanti-IgEinitiatedwithin10secandreachedtheirmaximumreleaseat6minfollowingchallenge.Pretreatmentofcellswithmetabolicinhibitorsabolishedtheactionsofanti-IgEaswellascalciumionophore.Tryptaseandhistaminerelease,particularlythatinducedbycalciumionophorewasinhibitedbypretreatmentofcellswithpertussistoxin.CONCLUSION:Bothanti-IgEandcalciumionophoreareabletoinducesignificantreleaseoftryptaseandhistaminefromcolonmastcells,indicatingthatthiscelltypeislikelytocontributetothepathogenesisofcolitisandothermastcellassociatedintestinaldiseases.

简介：AIM:Toinvestigatetheanti-apoptoticcapabilityofthehepatitisBvirus(HBV)intheHepG2hepatomacelllineandtheunderlyingmechanisms.METHODS:CellviabilityandapoptosisweremeasuredbyMTTassayandflowcytometry,respectively.Targetedknockdownofmanganesesuperoxidedismutase(MnSOD),AMP-activatedproteinkinase(AMPK)andhepatitisBvirusXprotein(HBx)genesaswellasAMPKagonistAICARandantagonistcompoundCwereemployedtodeterminethecorrelationsofexpressionofthesegenes.RESULTS:HBVmarkedlyprotectedthehepatomacellsfromgrowthsuppressionandcelldeathintheconditionofserumdeprivation.AdecreaseofsuperoxideanionproductionaccompaniedwithanincreaseofMnSODexpressionandactivitywasfoundinHepG2.215cells.Moreover,AMPKactivationcontributedtotheup-regulationofMnSOD.HBxproteinwasidentifiedtoinducetheexpressionofAMPKandMnSOD.CONCLUSION:OurresultssuggestthatHBVsuppressesmitochondrialsuperoxidelevelandexertsanantiapoptoticeffectbyactivatingAMPK/MnSODsignalingpathway,whichmayprovideanovelpharmacologicalstrategytopreventHCC.

简介：肠道T细胞淋巴瘤（intestinalT-celllymphoma，ITCL）病情凶险，临床表现复杂，以非特异性症状为主。发病年龄轻，无明显的乳糜泻，EB病毒检出率高，回盲部、升结肠和降结肠受累多见是我国患者的特点，与西方国家报道不同。ITCL由于临床少见，极易误诊，且易复发，对治疗的反应和预后极差，死亡率高，应引起临床医师的广泛重视。

简介：AIM:TOexplorethefeasibilityofenhancingapoptosis-inducingeffectsofchemotherapeuticdrugsonhumangastriccancercellsbystabletransfectionofextrinsicSmacgene.METHODS:AfterSmacgenewastransferredintogastriccancercelllineMKN-45,subclonecellswereobtainedbypersistentG418selection.CellularSmacgeneexpressionwasdeterminedbyRT-PCRandWesternblotting.Aftertreatmentwithmitomycin(MMC)asanapoptoticinducer,invitrocellgrowthactivitieswereinvestigatedbytrypanblue-stainingmethodandMI-Icolorimetry.Cellapoptosisanditsratesweredeterminedbyelectronicmicroscopy,annexinV-FITCandpropidiumiodidestainingflowcytometry.Cellularcaspase-3proteinexpressionanditsactivitieswereassayedbyWesternblottingandcolorimetry.RESULTS:WhencomparedwithMKN-45cells,theselectedsubclonecelllineMKN-45/SmachadsignificantlyhigherSmacmRNA(3.12±0.21vs0.82:1:0.14,t=7.52,P<0.01)andproteinlevels(4.02±0.24vs0.98:1:0.11,t=8.32,P<0.01).Aftertreatmentwith10μg/mLMMCfor6-24h,growthinhibitionrateofMKN-45/Smac(15.8±1.2-54.8±2.9%)wassignificantlyhigherthanthatofMKN-45(5.8±0.4-24.0±1.5%,t=6.42,P<0.01).PartialMKN-45/Smaccancercellspresentedcharacteristicmorphologicalchangesofapoptosisundertheelectronicmicroscopewithanapoptosisrateof36.4=1=2.1%,whichwassignificantlyhigherthanthatofMKN-45(15.2±0.8%,t=9.25,P<0,01).ComparedwithMKN-45,caspase-3expressionlevelsinMKN-45/Smacwereimprovedsignificantly(3.39±0.42vs0.96:1:0.14,t=8.63,P<0.01),whileitsactivitieswere3.25timesasmanyasthoseofMKN-45(0.364±0.010vs0.112:1:0.007,t=6.34,P<0.01).CONCLUSION:StabletransfectionofextrinsicSmacgeneanditsover-expressioningasbiccancercelllinecansignificantlyenhancecellularcaspase-3expressionandactivities,ameliorateapoptosis-inducingeffectsofmitomycinConcancercells,whichisanovelstrategytoimprovechemotherapeuticeffectsongastriccancer.

简介：

简介：AIM:ToinvestigatethemechanismsbywhichCskbindingprotein(CBP)inhibitstumorprogressioninesophagealcarcinoma.METHODS:ACBPoverexpressingesophagealcarcinomacellline(TE-1)wasestablished.Thegrowth,invasion,andmigrationofCBP-TE-1cells,aswellastheexpressionofSrcwerethendeterminedandcomparedwiththoseinnormalTE-1cells.RESULTS:TheexpressionofSrcwasdecreasedbytheoverexpressionofCBPinTE-1cells.Thegrowth,invasion,andmigrationofTE-1cellsweredecreasedbytheoverexpressionofCBP.CONCLUSION:ThisstudyindicatesthatCBPmaydecreasethemetastasisofesophagealcarcinomabyinhibitingtheactivationofSrc.CBPmaybeapotentialtumorsuppressorandtargetingtheCBPgenemaybeanalternativestrategyforthedevelopmentoftherapiesforesophagealcarcinoma.

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：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：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.

简介：Thisarticlediscussestheadequatetreatmentofearlygallbladdercancer(T1a,T1b)andisbasedonpublishedstudiesextendingovernearly3decades.Randomizedstudiesandmetaanalysescomparingdifferentsurgicaltreatmentsdonotexist.Theliteratureshowsthatinupto20%ofpatientslymphnodemetastasisarefoundinT1bgallbladdercancer.Duetohighmalignancywithearlyangiolymphaticspreadandresistancetochemotherapyandradiationontheonehand,andtherelativelowoperativeriskofextendedcholecystectomy(cholecystectomyandregionallymphadenectomy)ontheotherhand,webelievethatthisprocedureismandatoryinearlygallbladdercancer.

简介：AIM:ToinvestigatetheroleoftheoverexpressionofB7-H3inapoptosisincolorectalcancercelllinesandtheunderlyingmolecularmechanisms.METHODS:SW620cellsthathighlyoverexpressedB7-H3(SW620-B7-H3-EGFP)andHCT8cellsstablytransfectedwithB7-H3shRNA(HCT8-shB7-H3)werepreviouslyconstructedinourlaboratory.CellstransfectedwithpIRES2-EGFPwereusedasnegativecontrols(SW620-NCandHCT8-NC).Real-timePCRandwesternblottinganalysiswereusedtodetectthemRNAandproteinexpressionsoftheapoptosisregulatorproteinsBcl-2,Bcl-xlandBax.Acellproliferationassaywasusedtoevaluatethesurvivalrateanddrugsensitivityofthecells.Theeffectofdrugresistancewasdetectedbyacellcycleassay.Activecaspase-3westernblottingwasusedtoreflecttheanti-apoptoticabilityofcells.WesternblottingwasalsoperformedtodeterminetheexpressionofproteinsassociatedwiththeJak2-STAT3signalingpathwayandtheapoptosisregulatorproteinsafterthetreatmentwithAG490,aJak2specificinhibitor,inB7-H3overexpressingcells.ThedatawereanalyzedbyGraphPadPrism6usinganon-pairedt-test.RESULTS:WhetherbyoverexpressioninSW620cellsordownregulationinHCT8,B7-H3significantlyaffectedtheexpressionofanti-andpro-apoptoticproteins,atboththetranscriptionalandtranslationallevels,comparedwiththenegativecontrol(P<0.05).AcellproliferationassayrevealedthatB7-H3overexpressionincreasedthedrugresistanceofcellsandresultedinahighersurvivalrate(P<0.05).Inaddition,theresultsofcellcycleandactivecaspase-3westernblottingprovedthatB7-H3overexpressioninhibitedapoptosisincolorectalcancercelllines(P<0.05).B7-H3overexpressionimprovedJak2andSTAT3phosphorylationand,inturn,increasedtheexpressionofthedownstreamanti-apoptoticproteinsB-cellCLL/lymphoma2(Bcl-2)andBcl-xl,basedonwesternblotting(P<0.05).AftertreatingB7-H3overexpressingcellswiththeJak2-specificinhibitorAG490,thephosphorylationofJak2andSTAT3,andtheexp