简介：INTRODUCTIONInterventiontherapyhasbecomeoneofthemaintherapiesofhepaticcancer.Theintroductionofhepaticarterialperfusionandembolizationhasprovidedopportunitiesforasecondaryoperationonpatientswithintermediateandadvancedcancer,thusprolonging

简介：Objective:Toprobeintoeffectivesurgicalproceduresandimprovetheoutcomeoftreatmentforpatientswithseverehepaticinjury.Methods:Aretrospectivestudyinvolving113patientswithseverehepatictrauma(AASTgradeIVandV)duringthepast12yearswascarriedout.Ninety-eightpatientsunderwentsurgicaltreatment.SurgicalinterventionsincludinghepatectomyordirectcontrolofbleedingvesselsbyfingerfracturetechniquewithPringlemaneuver,selectiveligationofhepaticartery,retrohepaticcavalrepairwithtotalhepaticvascularocclusion,andperihepaticpackingweremainlyused.Results:Inthe98patientstreatedoperatively,thesurvivalratewas69.4%(68/98).Among40patientswithjuxtahepaticvenousinjury(JHVI),15werecuredwiththemaximumbloodtransfusionof12000ml.EightcasesofGradeIVinjurytreatednonoperativelywerecured.Thepercentageoffailureofnonoperativemanagementwas42.9%(6/14).Theoverallmortalityratewas32.7%(37/113),and57%ofthedeathswereduetoexsanguination.Conclusions:Reasonablesurgicalproceduresbasedonclassificationofhepaticinjuriescanincreasethesurvivalrateofseverelivertrauma.AccurateperihepaticpackingiseffectiveindealingwithJHVI.

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简介：Objective:toobserveeffectofendothelin-1(ET-1)onhepaticdamageinducedbyendotoxin.Methods:atotalof90ratswererandomlydividedintocontrolgroup(groupc),endotoxintreatedgroup(groupLPS)andendotoxinplusET-1antibodytreatedgroup(groupLEA).AnobservationwasdoneonthechangesofET-1concentration,andtranscriptionandexpressionofET-1mRNA.Plasmaglutamicpyruvictransaminaseenzyme(GPT),hepaticlactatedehydrogenase(LDH),adenosinetriphosphate(ATP)andmalondialdehyde(MDA)werealsoobservedat3,6,9,12,24hoursaftersaline,endotoxin(10mg·kg^-1)andET-1antibody(dalubine1:2000,2ml·kg^-1)administration.Results:TheresultsindicatedthattheconcentrationofplasmaandhepaticET-1andexpressionofET-1mRNAinliversignificantlyincreasedfollowingendotoxemia.ThehepaticET-1levelswereinverselycorrelatedwiththeATPconcentration,andpositivelyrelatedtotheMDAconcentration.ET-1antibodycouldpartiallyprotecttheliveragainstdamageinducedbyendotoxin.Conclusions:Theseresultssuggestthatendotoxinmay,ontranscriptionandtranslationlevel,leadtoanincreaseofET-1insynthesis.ET-1maycontributetohepaticdamageduringendotoxemia.

简介：肝的动脉pseudoaneurysm(幸运)是很稀罕的疾病但是在复杂并发症的情况下，有很高的死亡。幸运的最普通的原因是象肝活体检视那样的因医生之治疗而引的损伤，transhepatic胆汁的排水，胆囊炎和hepatectomy。幸运可以也与象与联系的感染或发炎那样的复杂并发症发生腐败emboli。幸运与尖锐胰腺炎在病人很少被报导了。根据我们知道，没有尖锐自发的胰腺炎特别地引起的一个案例的报告。我们报导在一个61岁的女人发展了的尖锐自发的胰腺炎引起的幸运的一个案例。开始由于未知原因与尖锐胰腺炎介绍的女人。在保守管理以后，她的症状似乎改善了。但是在承认以后的八天，腹的疼痛突然地再变得更坏。腹的计算断层摄影术(CT)被再核对，它检测了没在以前的腹的CT被看见的新幸运。内视镜后退因为hemobilia的怀疑，cholangiopancreatography(ERCP)作为加重的腹的疼痛的一个原因被执行。ERCP由在cholangiogram上在远侧的普通胆汁管在两耳细颈瓶和几充满缺点的开始观察新鲜的血块证实了hemobilia。没有象embolization或外科的结扎那样的任何特别治疗，幸运thrombosed自发地。在分泌物以后的三个月，腹的CT证明在左侧面的片断的那幸运消失了。

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简介：AbstractObjective:Rubicon is an inhibitory interacting protein of the autophagy-related protein Uvrag. We previously showed that Rubicon deficiency promotes autophagic flux in vivo and that autophagy can degrade lipid droplets. This study aimed to investigate the effects of Rubicon deficiency on fasting-induced hepatic steatosis.Methods:Two-month-old wild-type (WT) and Rubicon-deficient mice were subjected to feeding or fasting for 24 hours to induce hepatic steatosis. The distribution of liver lipid droplets was revealed by oil red O staining. Hepatic and plasma triglyceride, non-esterified fatty acid (NEFA), and cholesterol levels were detected using commercially available kits. Real-time reverse transcriptasepolymerase chain reaction was performed to analyze the mRNA expression of genes related to lipid metabolism in the liver. Western blot was conducted to assess autophagy-related protein levels in the liver. The animal experiments were approved by the Institutional Animal Care and Use Committee at Shanghai Jiao Tong University, China.Results:We showed that under fasting conditions, Rubicon-deficient mice had more lipid droplets in the liver than WT controls. Consistent with these results, the hepatic triglyceride, NEFA, and cholesterol levels in fasted Rubicon-deficient mice were significantly higher than those of fasted WT controls. The levels of SREBP-1, a key regulator of lipid synthesis, were significantly lower in livers from fasted WT mice than those of fed WT mice. However, the decrease in SREBP-1 in fasted mice was attenuated by Rubicon deficiency. Western blot analysis demonstrated that the fasting-induced increase in autophagic flux was amplified by Rubicon deficiency. Finally, we showed that Rubicon deficiency in mice led to elevated plasma triglyceride and NEFA acid levels under fasting conditions.Conclusion:Rubicon deficiency exacerbates fasting-induced hepatic steatosis in mice.

简介：Hepaticinvolvementinaggressivesystemicmastocytosis(ASM)isrelativelycommon,andthemainclinicalfeaturesofthisdiseaseincludehepatomegaly,portalhypertension,ascites,andfibrosis.CirrhosisisarareASMsymptom.WereportanASMcasethatinitiallymimickedcirrhosisbasedonclinicalandradiographicanalyses.Theportaltractwasexpandedbymononuclearinflammatorycells,andanincreaseincollagenamountwasobservedinroutinehistologicalsectionsofthebiopsiedliver.Adiagnosisofsystemicmastocytosis(SM)wasmadeafterancillarytestsformastcellsusingbonemarrowaspirates.Extensiveinvolvementoftheliverandgastrointestinaltractwasobserved.CliniciansandpathologistsneedtoconsiderASMasadiagnosisordifferentialdiagnosisinaclinicalcaseofcirrhosiswithunknownetiology.Thediagnosiscanbeconfirmedordisregardedbyimmunohistochemicalstainingandmolecularanalysis.

简介：AbstractFibroblast growth factor 21 (FGF21) is a fasting or stress inducible metabolic hormone produced mainly in the liver. It plays important roles in regulating both glucose and lipid homeostasis via interacting with a heterodimeric receptor complex comprising FGF receptor 1 (FGFR1) and β-klotho (KLB). For the past decade, great effort has been made on developing FGF21 derivatives or specific FGF21 receptor agonists into therapeutic agents for various metabolic disorders including type 2 diabetes (T2D), obesity, and more importantly, nonalcoholic fatty liver disease (NAFLD). Here we have reviewed FGF21 gene and protein structures, its expression pattern, cellular signaling cascades that mediate FGF21 production and function. We have then summarized the six clinical trials utilizing four FGF21 analogues. Finally, two recent literatures on the development of GLP-1 and FGF21 dual agonists were presented briefly.

简介：Neuroendocrinetumors(NET)areaheterogeneousgroupofcancers,withindolentbehavior.Themostcommonprimaryoriginisthegastro-intestinaltractbutcanalsoappearinthelungs,kidneys,adrenals,ovariesandotherorgans.Ingeneral,NETisusuallydiscoveredinthemetastaticphase(40%-80%).Theliveristhemostcommonorganinvolvedwhenmetastasesoccur(40%-93%),followedbybone(12%-20%)andlung(8%-10%).Anumberofdifferenttherapeuticoptionsareavailableforthetreatmentofhepaticmetastasesincludingsurgicalresection,transplantation,ablation,trans-arterialchemoembolization,chemotherapyandsomatostatinanalogues.Recently,moleculartargetedtherapieshavebeenused,usuallyincombinationwithothertreatmentoptions,toimproveoutcomesinpatientswithmetastases.ThisarticleemphasizesontheroleofsurgeryinthetreatmentoflivermetastasesfromNET.

简介：Hepaticencephalopathy(HE)isasevereneuropsychiatricsyndromethatmostcommonlyoccursindecompensatedlivercirrhosisandincorporatesaspectrumofmanifestationsthatrangesfrommildcognitiveimpairmenttocoma.AlthoughtheetiologyofHEisnotcompletelyunderstood,itisbelievedthatmultipleunderlyingmechanismsareinvolvedinthepathogenesisofHE,andoneofthemainfactorsisthoughttobeammonia;however,theammoniahypothesisinthepathogenesisofHEisincomplete.Recently,ithasbeenincreasinglydemonstratedthatinflammation,includingsystemicinflammation,neuroinflammationandendotoxemia,actsinconcertwithammoniainthepathogenesisofHEincirrhoticpatients.Meanwhile,agoodnumberofstudieshavefoundthatcurrenttherapiesforHE,suchaslactulose,rifaximin,probioticsandthemolecularadsorbentrecirculatingsystem,couldinhibitdifferenttypesofinflammation,therebyimprovingtheneuropsychiatricmanifestationsandpreventingtheprogressionofHEincirrhoticpatients.TheantiinflammatoryeffectsofthesecurrenttherapiesprovideanoveltherapeuticapproachforcirrhoticpatientswithHE.ThepurposeofthisreviewistodescribetheinflammatorymechanismsbehindtheetiologyofHEincirrhosisanddiscussthecurrenttherapiesthattargettheinflammatorypathogenesisofHE.

简介：Anewcaseofepithelioidhemangioendotheliomaisreportedtohaveoccurredtoa67-year-oldpatientwhoconsultedforrightsidedchestpain.Thework-upshowedmultiplerightpulmonarylesionsassociatedwithbilateralmoderatepleuraleffusionandleft-sidedpleuralthickeningandthreehypodensenodulesintherightlobeoftheliver,peritonealthickening,ascites,andmultiplevertebrallyticlesions.Thediagnosisofanepithelioidhemangioendotheliomawasconcludedthroughahistologicalexaminationofacomputedtomographyscanguidedbiopsyoftheliver.Thepatientreceivedaprimarymono-chemotherapywithAdriamycin(75mg/m~2everythreeweeks)andintravenousbisphosphonateswithoutresponseandgeneralstatusimpairment.Thepatientdiedafter16monthsoffollow-up.

简介：AIM:Todeterminethecorrelationbetweenthehepaticvenouspressuregradientandtheendoscopicgradeofesophagealvarices.METHODS:FromSeptember2009toMarch2013,atotalof176measurementsofhepaticvenouspressuregradient(HVPG)weredonein146patients.EachtransjugularHVPGwasmeasuredtwice,firstusinganendwholecatheter(EH-HVPG),andthenusingaballooncatheter(B-HVPG).TheHVPGwascomparedwiththeendoscopicgradeofesophagealvarices(accordingtothegeneralrulesforrecordingendoscopicfindingsofesophagogastricvarices),whichwasrecordedwithinamonthofthemeasurementofHVPG.RESULTS:Thestudyincluded110menand36women,withameanageof56.1years(range,43-76years).Thetechnicalsuccessrateofthepressuremeasurementswas100%andtherewerenocomplicationrelatedtotheprocedures.MeanHVPGwas15.3mmHgasmeasuredusingtheendholecathetermethodand16.5mmHgasmeasuredusingtheballooncathetermethod.MeanHVPG(bothEHHVPGandB-HVPG)wasnotsignificantlydifferentamongpatientswithdifferentcharacteristics,includingsexandcomorbidfactors,exceptforcaseswithhepatocellularcarcinoma(B-HVPG,P=0.01;EH-HVPG,P=0.02).Portalhypertension(>12mmHgHVPG)occurredin66%ofpatientsaccordingtoEH-HVPGand83%ofpatientsaccordingtoB-HVGP,andsignificantlycorrelatedwithChild’sstatus(B-HVPG,P<0.000;EHHVGP,P<0.000)andesophagealvariesobserveduponendoscopy(EH-HVGP,P=0.003;B-HVGP,P=0.006).Onehundredandthirty-fiveendoscopieswereperformed,ofwhich15showednormalfindings,27showedgrade1endoscopicesophagealvarices,49showedgrade2varices,and44showedgrade3varices.WhencomparingendoscopicesophagealvaricealgradesandHVPGusingunivariateanalysis,thePvaluewas0.004forEH-HVPGand0.002forB-HVPG.CONCLUSION:BothEH-HVPGandB-HVPGshowedapositivecorrelationwiththeendoscopicgradeofesophagealvarices,withB-HVPGshowingastrongercorrelationthanEH-HVPG.

简介：Three-dimensional(3D)printing(3DP)isarapidprototypingtechnologythathasgainedincreasingrecognitioninmanydifferentfields.Inherentaccuracyandlow-costpropertyenableapplicabilityof3DPinmanyareas,suchasmanufacturing,aerospace,medical,andindustrialdesign.Recently,3DPhasgainedconsiderableattentioninthemedicalfield.Theimagedatacanbequicklyturnedintophysicalobjectsbyusing3DPtechnology.Theseobjectsarebeingusedacrossavarietyofsurgicalspecialties.Theshortageofcadaverspecimensisamajorprobleminmedicaleducation.However,thisconcernhasbeensolvedwiththeemergenceof3DPmodel.Custom-madeitemscanbeproducedbyusing3DPtechnology.Thisinnovationallows3DPuseinpreoperativeplanningandsurgicaltraining.Learningisdifficultamongmedicalstudentsbecauseofthecomplexanatomicalstructuresoftheliver.Thus,3Dvisualizationisausefultoolinanatomyteachingandhepaticsurgicaltraining.However,conventionalmodelsdonotcapturehapticqualities.3DPcanproducehighlyaccurateandcomplexphysicalmodels.Manytypesofhumanoranimaldifferentiatedcellscanbeprintedsuccessfullywiththedevelopmentof3Dbio-printingtechnology.Thisprogressrepresentsavaluablebreakthroughthatexhibitsmanypotentialuses,suchasresearchondrugmetabolismorliverdiseasemechanism.Thistechnologycanalsobeusedtosolveshortageoforgansfortransplantinthefuture.

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简介：Objective:Tostudytheprotectiveeffectofischemicpreconditioning(Ⅰ-pre)andischemicpostconditioning(Ⅰ-post)againstischemia/reperfusion(I/R)injuryinrat'sliver.Methods:UsingratmodelofhepaticsegmentalI/Rinjury,ratsweredividedinto5groups:GroupA(shamgroup),GroupB(I/Rinjury),GroupC(Ⅰ-pregroup),GroupD(Ⅰ-postgroup)andGroupE(combinedtreatmentofⅠ-preandⅠ-post).Serumalanineaminotransferase(ALT),aspartateaminotransferase(AST),malondiaidehyde(MDA),glutathione(GSH),superoxidedismutase(SOD),glutathioneperoxidase(GSH-Px)andmyeloperoxidase(MPO)inhepatictissuesweredetermined,respectively.Inaddition,7days'survivalofGroupsB,C,DandEwereevaluated.Results:ComparedwithGroupB,GroupsC,DandEexhibitedsignificantlydecreasedALTandASTrelease,minimizedtissueinjury,suppressedvaluesofMDAandMPO,increasedactivitiesofSOD,GSH-PxandGSH(P<0.05),aswellasimprovedanimalsurvival.ThedifferencesamongGroupsC,DandEwerenotstatisticallysignificant.Conclusions:Ⅰ-pre,Ⅰ-postandcombinedtherapyofⅠ-preandⅠ-posthaveprotectiveeffectagainsthepaticI/Rinjury,whichiscorrelatedwithitsfunctionofreducingtheproductionofreactiveoxygenspecies,maintainingtheactivitiesofantioxidantsystemsandsuppressingneutrophilsrecruitment.NoadditiveeffectcanbeobtainedinGroupE.

简介：TostudytheactionofKeGancapsuletoresistinjuryofhepaticcellsandfibrosisofliver.MethodsRephcatemodelofchronichepaticinjurywithCC14,atthebeginningofwhichKeGancapsulewasapplied;finishingexperiment,respectivelytestedthelevelofliverfimction,TP,ALB,A/G,L-hydroxyprolineandliverindexanddopathologicexaminationtofiver.ResultsKeGancapsulecanobviouslyreducethedegreeoffibrosisofliverandthelevelofL-hydroxyproline,improvethefiverfunction.Thehistologicalexaminationshowedthatcapsulehastheactionofprotectinghepaticcellsfrominjuryandresistingfibrosisoffivereither.ConclusionForKeGancapsulehastheactionofresistinginjuryoflivercellsandfibrosisofliver,it'shopedtobeappliedinprecautionandtreatmentoffibrosisoffiver.

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.