简介：Symptomatichepato-diaphragmaticinterpositionofabowellooporChilaiditi'ssyndromeisapeculiaranatomicalconditionmostoftenfoundbychance.Itsdescribedsymptomsrangefromintermittent,mildabdominalpainanddyspepsiatoacuteintestinalobstruction.Wereportacaseofhepato-diaphragmaticmigrationofthehepaticflexureofthecolonassociatedtoanunusual,heretoforeunreported,angina-likepainexclusivelyevokedbytheleftlateraldecubitus.Tomaximizethechanceofobservinganatomicalchangesindifferentpostures,computedtomographyofthechestandabdomenwasperformedafterairinsufflationintothecolon.Whilefrankherniationintothechestwasexcluded,thescanshowedthatthehepaticflexure-withtheinterpositionofthediaphragm-cameincontactwiththerightsideoftheheartintheleftlateral,butnotinthesupine,decubitus.Thisfindingwasreproducedbyechocardiographywhichalsoshowedvirtuallyunalteredhemodynamicsafterthechangeofposture.ECG,leftandrightventricularglobalandregionalfunctionaswellascardiacinjurymarkersalsoremainedunchangedduringthemaneuver,indicatingthatthepainevokedbythelatterwasunlikelyduetomyocardialischemia.ThiscasesuggeststhatChilaiditi'ssyndromeshouldbeincludedamongthepossible,althoughrare,causesofunexplainedangina-likesymptoms.

简介：煽动性的肠疾病(IBD)经常与象眼的神经炎那样的extraintestinal表明(EIM)被联系(在上)尽管这到目前为止在仅仅一些成年病人被描述了，所有谁与Crohns疾病(CD)被影响。而且，在上并且demyelinating疾病比的被表明了在IBD病人更经常在控制人口。在我们的当前的案例报告，我们与活跃CD描述一个孩子开发了突然的盲目由于在那上双边不与任何已知的原因有关，并且那即时对类固醇的高剂量作出回应。调查和临床的后续到目前为止在这个病人排除了demyelinating疾病的发展。到我们的知识，这是第一份报告在上在有CD的一个小儿科的病人。对这个案例的可能的解释包括活跃的肠疾病的阵发性的EIM，联系自体免疫的混乱例如一周期性孤立在上，多重硬化的第一表明，或能出现在以后的后续的另一demyelinating疾病。

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简介：AIM:Toinvestigatethelifetimeriskofdevelopmentofesophagealadenocarcinomaand/orhigh-gradedysplasiainpatientsdiagnosedwithBarrett’sesophagus.METHODS:DatawereextractedfromtheUnitedKingdomNationalBarrett’sOesophagusRegistryondateofdiagnosis,patientageandgenderof7877patientsfromwhohadbeenregisteredfrom35UnitedKingdomcenters.LifeexpectancywasevaluatedfromUnitedKingdomNationalStatisticsdatabasedupongenderandageatyearatdiagnosis.Thesedatawerethenusedwithpublishedestimatesofannualadenocarcinomaandhigh-gradedysplasiaincidencesfrommetaanalysesandlargepopulation-basedstudiestoestimateoveralllifetimeriskofdevelopmentofthesestudyendpoints.RESULTS:ThemeanageatdiagnosisofBarrett’sesophaguswas61.6yearsinmalesand67.3yearsinfemales.Themeanlifeexpectancyatdiagnosiswas23.1yearsinmales,20.7yearsinfemalesand22.2yearsoverall.Usingdatafrompublishedmeta-analyses,thelifetimeriskofdevelopmentofadenocarcinomawasbetween1in8and1in14andthelifetimeriskofhigh-gradedysplasiaoradenocarcinomawas1in5to1in6.Usingdatafrom3largerecentpopulation-basedcohortstudiesthelifetimeriskofadenocarcinomawasbetween1in10and1in37andofthecombinedendpointofhigh-gradedysplasiaandadenocarcinomawasbetween1in8and1in20.AgeatBarrett’sesophagusdiagnosisisreducingandlifeexpectancyisincreasing,whichwillpartiallycounter-balancelowerannualcancerincidence.CONCLUSION:Thereisasignificantlifetimeriskofdevelopmentofhigh-gradedysplasiaandadenocarcinomainBarrett’sesophagus.

简介：Hirschsprungs疾病是现场发生在1:5000的先天的混乱出生。它被伤寒神经原的缺席沿着胃肠的道的一个可变区域描述。Hirschsprungs疾病作为multigenic混乱被分类，因为一样的显型在多重不同基因与变化被联系。而且，Hirschsprungs疾病的遗传高度复杂、不严格地孟德尔。在Hirschsprungs疾病观察的phenotypic可变性和不完全的外显率也建议修饰词基因的参与。这里，我们总结基于人和动物研究位于Hirschsprungs疾病下面的遗传的当前的知识，集中于修饰词基因的主要原因的基因，他们的相互作用，和角色。

简介：内镜对粘膜病变由于其镜下特殊表现并可病理活检而能作出正确诊断，但对胃腔狭窄尤其当内镜不能通过狭窄部位时会对病变定位或病变性质判断错误。

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

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简介：hepatocellular癌(HCC)的发展被归因于几个因素，包括长期的病毒的感染，白酒消费，到黄麴毒素B1的暴露和新陈代谢的混乱。几份最近的报告证明了HCC能当另外的内在的高风险的肝疾病不在时与长期的Crohns疾病(CD)发生在病人。然而，可以在CD和hepatocarcinogenesis之间有一个协会为这的精确机制要求进一步的调查。

简介：AIM:Toevaluatetherelationshipbetweenthiopu-rineS-methyltransferase(TPMT)polymorphismsandthiopurine-inducedadversedrugreactions(ADRs)ininflammatoryboweldisease(IBD).METHODS:EligiblearticlesthatcomparedthefrequencyofTPMTpolymorphismsamongthiopurine-tolerantand-intolerantadultIBDpatientswereincluded.StatisticalanalysiswasperformedwithReviewManager5.0.Sub-analysis/sensitivityanalysiswasalsoperformed.RESULTS:Ninestudiesthatinvestigatedatotalof1309participantsmetourinclusioncriteria.Theinci-denceofTPMTgenemutationwasincreased2.93-fold(95%CI:1.68-5.09,P=0.0001)and5.93-fold(95%CI:2.96-11.88,P<0.00001),respectively,inIBDpatientswiththiopurine-inducedoverallADRsandbonemarrowtoxicity(BMT),comparedwithcontrols.TheORforTPMTgenemutationinIBDpatientswiththiopurine-inducedhepatotoxicityandpancreatitiswas1.51(95%CI:0.54-4.19,P=0.43)and1.02(95%CI:0.26-3.99,P=0.98)vscontrols,respectively.CONCLUSION:Thismeta-analysissuggeststhattheTPMTpolymorphismsareassociatedwiththiopurine-inducedoverallADRsandBMT,butnotwithhepatotoxicityandpancreatitis.

简介：目的观察早期胃癌组织中GTP酶激活蛋白SH3功能区结合蛋白G3BP1和G3BP2的表达变化并探讨其意义。方法选择早期胃癌组织89例和正常对照组织35例，采用免疫组织化学方法检测两组G3BP1蛋白和G3BP2蛋白的表达情况。结果早期胃癌组和正常组G3BP1的阳性率分别为87.64%和60.00%，G3BP2阳性率分别为86.51%和54.28%，两组比较差异有统计学意义（P=0.000，0.000）；早期胃癌G3BP1和G3BP2的表达均与幽门螺杆菌感染相关（P=0.000）；早期胃癌组织中G3BP1与G3BP2表达呈正相关（rs=0.252，P=0.017）。结论早期胃癌组织中G3BP1和G3BP2呈高表达，可能与幽门螺杆菌感染紧密相关，两指标异常表达可能在早期胃癌的发生和发展中起重要作用。

简介：目的探讨PreS1抗原检测的临床价值。方法采用酶联免疫吸附试验法检测421例慢性乙型肝炎患者血清PreS1抗原和HBV标记物;采用荧光定量PCR法检测HBVDNA。结果在421例慢性乙型肝炎患者中,HBVDNA阳性者367例,其中PreS1Ag阳性者188例（51.2%）,HBeAg阳性者119例（32.4%）,后两者有显著性差异（P〈0.01）;在高HBVDNA载量（105～107copies/ml和〉107copies/ml）组患者中,PreS1Ag阳性率（60.2%,60.0%）显著高于HBVDNA阴性组（33.3%）和低载量（103～105copies/ml）组（41.9%,P〈0.01）;但在421例患者中,PreS1Ag阳性率（48.9%）低于HBVDNA（87.2%,P〈0.01）。结论PreS1Ag能够较HBeAg更好地反映HBV在体内的复制状态,但尚不能代替HBVDNA的检测。

简介：AIMTocharacterizepunctualmutationsin23SrRNAgeneofclarithromycin-resistantHelicobacterpylori(H.pylori)anddeterminetheirassociationwiththerapeuticfailure.METHODSPCRproductsof23SrRNAgeneVdomainof74H.pyloriisolates;34resistanttoclarithromycin(29fromalow-riskgastriccancer(GC)population:Tumaco-Colombia,and5fromahigh-riskpopulation:Tuquerres-Colombia)and40fromasusceptiblepopulation(28fromTumacoand12fromTúquerres)weresequencedusingcapillaryelectrophoresis.TheconcordancebetweenmutationsofVdomain23SrRNAgeneofH.pyloriandtherapeuticfailurewasdeterminedusingtheKappacoefficientandMcNemar’stestwasperformedtodeterminetherelationshipbetweenH.pylorimutationsandclarithromycinresistance.RESULTS23SrRNAgenefromH.pyloriwasamplifiedin56/74isolates,ofwhich25wereresistanttoclarithromycin(20fromTumacoand5fromTúquerres,respectively).In17resistantisolates(13fromTumacoand4fromTúquerres)thefollowingmutationswerefound:A1593T1,A1653G2,C1770T,C1954T1,andG1827CinisolatesfromTumaco,andA2144GfromTúquerres.ThemutationsT2183C,A2144GandC2196TinH.pyloriisolatesresistanttoclarithromycinfromColombiaarereportedforthefirsttime.NoassociationbetweentheH.pylorimutationsandinvitroclarithromycinresistancewasfound.However,therapeuticfailureoferadicationtreatmentwasassociatedwithmutationsof23SrRNAgeneinclarithromycin-resistantH.pylori(κ=0.71).CONCLUSIONThetherapeuticfailureoferadicationtreatmentinthetwopopulationsfromColombiawasassociatedwithmutationsofthe23SrRNAgeneinclarithromycinresistantH.pylori.

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：AIM:ToassesstheutilityofanautologousCD34+andCD133+stemcellsinfusionasapossibletherapeuticmodalityinpatientswithend-stageliverdiseases.METHODS:Onehundredandfortypatientswithendstageliverdiseaseswererandomizedintotwogroups.Group1,comprising90patients,receivedgranulocytecolonystimulatingfactorforfivedaysfollowedbyautologousCD34+andCD133+stemcellinfusionintheportalvein.Group2,comprising50patients,receivedregularlivertreatmentonlyandserveda...

简介：瞄准：在Crohn的疾病(CD)调查单核白血球的函数病人并且相关这与联系疾病的核苷酸绑定oligomerizationdomain-2(NOD2)基因变体。方法：从47个连续地提交的CD病人和9健康供血者的单核白血球与interleukin(IL)是有教养的-4和granulocyte巨噬细胞刺激殖民地的因素(GM-CSF)，并且与脂肪的多糖(LPS)或muramyldipeptide(MDP)刺激了，NOD2的通常认为的ligand。结果：我们发现从CD病人的单核白血球区分了在试管内到成熟树枝状的房间(DC)，由免疫显型和形态学决定了。NOD2遗传型在所有题目被估计，并且我们观察到在NOD2的不成熟、刺激LPS的DC上的高CD86表示变异CD病人，作为与wtNOD2CD病人和控制相比。由对比，导致到成熟，MDP源于变异NOD2的题目的DC的CD86表示层次比得上正常题目的那些。在耐心房间的文化的IL-12p70的数量与MDP比在在LPS治疗，然而并非术后疗法以后的控制大。结论：我们的结果建议在NOD2基因与变化从病人获得的DC显示高CD86表示描绘的激活的显型，但是当与终端相比区别分阶段执行时，有减少的回答到MDP。我们推测单核白血球的改变的区别可能导致在发炎和单核白血球的杀死的能力之间的不平衡，并且可能与CD的致病相关。

简介：AIM:ToexploreexpressionsofPIK3CAintheprogressionofgastriccancerfromprimarytometastasisanditseffectsonactivationofphosphatidylinositol3-kinase(PI3K)/Aktpathway.METHODS:mRNAandproteinlevelsofPIK3CAwereassessed,respectively,byreal-timequantitativepolymerasechainreactionandimmunohistochemistryinspecimensofnormalgastricmucosa,primaryfociandlymphnodeanddistantmetastasisofgastriccancer.AktandphosphorylatedAktproteinwerealsoexaminedbyWesternblottinginthesetissues,inordertoanalyzetheeffectofPIK3CAexpressionlevelchangesontheactivationofPI3K/Aktsignalingpathway.RESULTS:PIK3CAmRNAinlymphnodemetastasiswereapproximately5and2foldshigher,respectively,thanthatinthecorrespondingnormalgastricmucosaandprimarygastriccancertissues(P<0.05),whilenostatisticalsignificancewasfoundcomparedwithdistantmetastasis.Immunohistochemically,PIK3CAproteinexpressionwasdiscoveredin7(35%)specimensof20primaryfocivs10(67%)of15oflymphnodemetastasisor11(61%)of18ofdistantmetastasis(35%vs67%,P=0.015;35%vs61%,P=0.044).WiththeincreasedlevelofPIK3CAexpression,thetotalAktproteinexpressionremainedalmostunchanged,butp-Aktproteinwasupregulatedmarkedly.CONCLUSION:IncreasedexpressionofPIK3CAisexpectedtobeapromisingindicatorofmetastasisingastriccancer.Up-regulationofPIK3CAmaypromotethemetastasisofgastriccancerthroughaberrantactivationofPI3K/Aktsignaling.

简介：目的观察小鼠对HBVS基因和基因疫苗的应答。方法用已构建的HBVS基因疫苗(pCR3.1-S)和C基因疫苗(pCR3.1-C)分别给Balb/c小鼠多点肌肉注射,2wk后追加免疫一次,用ELISA法及MTT法检测小鼠血清抗体及脾细胞对HBsAg或HBcAg的特异性增殖反应。结果免疫接种2wk后小鼠血清抗体滴度明显高于对照组,pCR3.1-C组的刺激指数明显高于pCR3.1-S注射组。结论HBVS和C基因疫苗诱导较强的体液和细胞免疫应答强度;C基因尤以细胞免疫增高明显。

简介：目的研究MPP3表达减少与大肠癌发病的关系。方法RT-PCR法检测正常大肠黏膜、大肠腺瘤和大肠癌的MPP3mRNA表达;WesternBlotting法检测正常大肠黏膜、大肠腺瘤和大肠癌的MPP3蛋白表达。结果大肠腺瘤中MPP3表达无明显减少（P〉0.05）,部分大肠癌组织中MPP3表达减少,且有淋巴结转移患者比无淋巴结转移患者更常见（P〈0.05）,DukesC期和D期患者比DukesA期和B期患者更常见（P〈0.05）。结论MPP3表达减少在大肠癌中为常见现象,而且在晚期肿瘤更明显,因此,MPP3在大肠癌发病中可能发挥重要作用。

简介：目的调查分析我院近3年来住院的药物性肝损伤(DILI)患者临床特点及转归,为提高医师对该病的认识以及保证患者合理用药提供参考。方法2014年3月~2017年5月我院收治115例DILI患者,回顾性分析了其临床资料。结果引起DILI的主要药物为中药、抗生素药物、免疫抑制剂、循环系统用药和抗肿瘤药物,所占比例分别为20.9%、18.3%、13.0%、10.4%、8.7%;本组胆汁淤积型66例(57.4%),肝细胞型16例(13.9%),混合型33例(28.7%);发病时血清ALT水平为(151.2±56.8)U/L,AST为(136.5±25.4)U/L,ALP为(251.6±79.4)U/L,TBIL为(39.8±11.3)μmol/L,GGT为(101.5±28.8)U/L,经2~3w治疗,分别降至(21.7±10.2)U/L、(39.3±8.3)U/L、(120.8±70.5)U/L、(15.2±9.4)μmol/L、(37.6±7.2)U/L;76例(66.1%)DILI患者完全恢复,25例(21.7%)患者病情基本恢复,10例(8.7%)患者肝功能指标反复,4例(3.5%)因肝衰竭而死亡。结论引起DILI的药物种类繁多,中药、抗生素和免疫抑制剂等为主要的诱发药物,临床表现无特异性,治疗后预后良好,但临床医生应注意用药安全,尽量避免或降低DILI的发生。