简介：Arecentreportintroducedthephosphodiesterase-5inhibitionbyvardenafilasanoveltreatmentofportalhypertensioninpatientswithcirrhosis.Inthehereinpresented'lettertotheeditor',theadministrationoftadalafildidnotinfluenceportalhaemodynamicsbutimpairedsystemichaemodynamicsinpatientswithcirrhosis.OurobservationsconcurwiththeresultsofareportinapreviousissueofWorldJournalofGastroenterology(October2008).Moreover,tadalafiladverselyaffectedrenalfunctioninpatientswithdecompensatedliverdisease.

简介：Thecurrentstudydemonstratedthatinjuryofthespinalcordlateralfuniculusoccursinlivercirrhosis.Thisstudysoughttocomparethemorphologyofthethoracicandlumbarcord,theexpressionoffunctionalproteins,andchangesinvesselsbetweenlivercirrhosisandnon-cirrhosiscorpses.Resultsshowedthatinthelivercirrhosisgroup,thehepaticveinexpanded,thegastrointestinaltractwasfullofcoagulatedblood,blood-stasiswaseasilyseenintheveniplexofthevertebralcanalandthelumbarspinalcord,andthecellbodiesoftheanteriorhorninthethoracicandlumbarcordweresmallerthanthoseinnon-cirrhosiscorpses.Inaddition,nervecellsshrank,Nisslbodieswereconcentratedwithobscurednuclei,andneurofilamentandsynapsincontainingcellbodiesoftheanteriorhornandwhitematterdecreasedinthelivercirrhosisgroup.Theseexperimentalfindingsindicatethatabnormalcirculationofthespinalcord,resultingfromhemodynamicchangeofcirrhoticportalhypertension,maybethemostsignificantcauseofhepaticmyelopathy.

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

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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：Objective:TostudytheeffectofmoxibustiononhyperbilirubinemiainhepatitisBcirrhosispatients.Methods:56casesofinpatientswithhepatitisBcirrhosisweredividedintotreatmentgroup(n=27)andcontrolgroup(n=29)randomly.Allthepatientsofthesetwogroupsweregivenwithroutineexpectanttreatmentincludingadministrationofmedicines(Bifendate,Eessentiale,Potenline,etc)forprotectingliverfunctions,reducingthelevelofalanineaminotransferase(ALT),etc.,andinthemeantime,patientsofthetreatmentgroupwereAfter4weeksoftreatment,ofthe27and29casesoftreatmentandcontrolgroup,23and10patientshadimprovementinclinicalsymptoms,4and19failed,withthetotaleffectiveratesbeing85.18%and34.48%respectively.Serumtotalbilirubin(Tbil)contentsoftreatmentandcontrolgroupsdecreasedsignificantly,andthelevelofTbilinthetreatmentgroupwassignificantlylowerthanthatinthecontrolgroup(P<0.01).Conclusion:MoxibustionisaneffectiveremedyinrelievinghyperbilirubinemiaandimprovingclinicalsymptomsinthetreatmentofhepatitisBcirrhosispatients.

简介：Exosomes是endocytic起源的nanoparticles，由由他们调制cell-to-cell通讯的能力的优点正在吸引增加的注意的无数房间人口藏匿了。他们也在许多免疫学的问题正在吸引注意，包括autoimmunity和，特别地调整cytokine和chemokine激活的他们的能力。主要胆汁的肝硬化(PBC)被认为一个模型自体免疫疾病，它对胆汁的上皮的房间有高度集中的细胞毒素的回答。我们与PBC和30健康控制(HC)从29个病人从血浆孤立exosomes，并且用一个前vivo系统在mononuclear房间人口在co-stimulatory分子表示和cytokine生产上学习了这些exosomes的效果。我们也与HCexosomes相比在PBC识别了microRNA(miRNA)人口。我们此处报导尽管exosomes不改变cytokine生产，他们显著地确实在介绍抗原的人口上改变co-stimulatory分子表示。进一步，我们在CD14+单核白血球上表明了那CD86起来调整的表情，而在CD11c+上起来调整的CD40由从有PBC的病人的exosomes的树枝状的房间。另外，有在有PBC的病人的传播exosomes的miRNA表示的差别。这些数据基于co-stimulatory分子玩的观察有重要重要性在T房间激活的规定的一个微分角色。我们的观察显示从PBC的异常exosomes有选择地在介绍抗原的房间的不同子集导致co-stimulatory分子的表示。这些改变可以在自体免疫的肝疾病的致病包含。

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简介：AbstractBackground:Liver fibrosis (LF) continues to develop and eventually progresses to cirrhosis. However, LF and early-stage cirrhosis (ESC) can be reversed in some cases, while advanced cirrhosis is almost impossible to cure. Advances in quantitative imaging techniques have made it possible to replace the gold standard biopsy method with non-invasive imaging, such as radiomics. Therefore, the purpose of this study is to develop a radiomics model to identify LF and ESC.Methods:Patients with LF (n = 108) and ESC (n = 116) were enrolled in this study. As a control, patients with healthy livers were involved in the study (n = 145). Diffusion-weighted imaging (DWI) data sets with three b-values (0, 400, and 800 s/mm2) of enrolled cases were collected in this study. Then, radiomics features were extracted from manually delineated volumes of interest. Two modeling strategies were performed after univariate analysis and feature selection. Finally, an optimal model was determined by the receiver operating characteristic area under the curve (AUC).Results:The optimal models were built in plan 1. For model 1 in plan 1, the AUCs of the training and validation cohorts were 0.973 (95% confidence interval [CI] 0.946-1.000) and 0.948 (95% CI 0.903-0.993), respectively. For model 2 in plan 1, the AUCs of the training and validation cohorts were 0.944, 95% CI 0.905 to 0.983, and 0.968, 95% CI 0.940 to 0.996, respectively.Conclusions:Radiomics analysis of DWI images allows for accurate identification of LF and ESC, and the non-invasive biomarkers extracted from the functional DWI images can serve as a better alternative to biopsy.

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：测试假设这项活动的那改进他我有与周期性的肝损伤联系的纤维发生的过程的氧合酶罐头interfere，我们调查了在表示上的治疗学的潜力他我在CCl(4)的oxygense-1劝诱了微榴状的肝硬化模型。方法：带老鼠HO-1或GFP基因的Recombinant联系adeno的病毒被产生。1x10(12)联系adeno的病毒的vg在肝的正式就职的时候通过门注射被管理纤维变性。结果：有由rAAV/HO-1的HO-1的在表示上的老鼠肝显著地增加了的调节以一种稳定的方式的HO酶的活动。微榴状的肝硬化的开发显著地作为与控制相比在rAAV/HO-1-transduced动物被禁止。门静脉高血压显著地作为与控制相比在rAAV/HO-1-transduced动物被减少，而在收缩血压没有重要变化。这发现伴有激活的改进的肝生物化学，更少的渗透的巨噬细胞和更少在rAAV/HO-1-transduced肝的肝的星形细胞(HSC)。结论：改进惊讶在肝的活动压制肝硬化的发展。