简介：CellsregulatephospholipaseD(PLD)activityinresponsetonumerousextracellularsignals.Here,weinvestigatedtheinvolvementofPLDactivityintransforminggrowthfactor-β(TGF-β1)-mediatedgrowthinhibitionofepithelialcells.TGF-β1)-mediatedgrowthinhibitionofepithelialcells.TGF-β1inhibitsthegrowthofMDCK,Mv1Lu,andA-549cells.Inthepresenceof0.4%butanol,TGF-β1inducesanincreaseintheformationofphosphatidylbutanol,auniqueproductcatalyzedbyPLD.TGF-β1alsoinducesanincreaseinphosphatidicacid(PA)levelinA-549andMDCKcells.TGF-β1inducesanincreaseinthelevelsofDAGlabeledwith[^3H]-myristicacidinA-549andMDCKcellsbutnotinMv1Lucells.NoincreaseofDAGwasobservedincellsprelabeledwith[^3H]-arachidonicacid.ThedatapresentedsuggestthatPLDactivationisinvolvedintheTGF-β1-inducedcellgrowthinhibition.

简介：Formationofapoptoticbodiesisatypicalcharacterofapoptoticcelldeath,buthowtheprocessesarecontrolledisnotknown.Inthisstudy,wecomparedtwoapoptosisinducingsystemsinvascularendothelialcells(VEC).Wefoundthattheformationofapoptoticbodiesduringapoptosisinducedbyrattlesnakevenom,whichisanuniqueandspecificapoptosisinducertovascularendothelialcells,wasmuchfasterthanthatinducedbydeprivationofsurvivalfactors(aFGFandserum).WhenweblockedthesynthesisofmRNAsincellstreatedwithrattlesnakevenombyDRB(5,6-dichloro-1-β-D-ribofuranosylbenzimidazole),aninhibitoroftranscription,theformationofapoptoticbodieswasdramaticallyinhibited.WeexaminedtheexpressionofP^53geneandfoundthatitsexpressionwasmuchhigherinapoptosisinducedbyrattlesnakevenomthatthatinapoptosisinducedbydeprivationofaFGFandserum.OurresultssuggestthatgeneexpressionisimportantandP^53genemayplayamajorroleininducingtheformationofapoptoticbodiesinVEC.

简介：WereportedinthismanuscriptthatTGF-β1inducesapoptosisinAML12murinehepatocytes,whichisassociatedwiththeactivationofp38MAPKsignalingpathway.SB202190,aspecificinhibitorofp38MAPK,stronglyinhibitedtheTGF-β1-inducedapoptosisandPAI-1promoteractivity.TreatmentofcellswithTGF-β1activatesp38.Furthermore,over-expressionofdominantnegativemutantp38alsoreducedtheTGF-β1-inducedapoptosis.Thedataindicatethattheactivationofp38isinvolvedinTGF-β1-mediatedgeneexpressionandapoptosis.

简介：MYB蛋白质在真核细胞的有机体起重要作用。在植物，R1R2R3类型MYB蛋白质在房间周期控制工作。然而，R2R3类型MYB蛋白质是否也涉及房间部门过程，仍然保持未知。这里，我们报导那R2R3类型抄写因素基因，AtMYB59，涉及房间周期前进和根生长的规定。AtMYB59蛋白质在洋葱的原子核是局部性的表皮的房间并且transactivation活动。在酵母房间的AtMYB59的表示压制房间增长，和transformants与更长的房间有更多的原子核和更高的aneuploidDNA内容。在AtMYB59的保存领域的变化在酵母细胞生长上废除它的效果。在同步Arabidopsis房间暂停，AtMYB59基因明确地在房间周期前进期间在S阶段被表示。表示和promoter-GUS分析表明AtMYB59基因富有地在根被表示。转基因的植物overexpressingAtMYB59更短的根与野类型的植物(Arabidopsis就职Col-0)相比，并且在在根尖端的有丝分裂的房间的一半附近在中期。相反地，空变异的myb59-1比关口在中期让更长的根和更少有丝分裂的房间，建议那AtMYB59可以由扩大有丝分裂的房间的中期禁止根生长。AtMYB59调整许多下游的基因，包括CYCB1；1基因，可能通过到MYB应答的元素的绑定。这些结果在细胞周期规定和植物根生长为AtMYB59支持一个角色。

简介：Adultstem/progenitorcellsplayimportantrolesintissuehomeostasisandhaveimportantimplicationsforregenerativemedicine.Itwasoncethoughtthatformationofnewbloodvesselsinadultonlyoccursthroughangiogenesis,aprocesswherebynewvesselsareformedfromexistingmatureendothelialcells;whilevasculogenesis,wherenewvesselsarederivedfromdifferentiationofendothelialprogenitorcells(EPCs),wasthoughttooccurexclusivelyinembryos.ThediscoveryofadultEPCsafewyearsagohaschangedthisoldparadigm;andsubsequentstudiesshowedthatEPCsmaybeapromisingtoolforthetreatmentofvasculardisorders.However,therehavebeenconflictingreportsonsubtypes,surfacemarkers,andfunctionsofEPCs;andthustheexactoriginandidentityofEPCsremaintobedefined.AcommonapproachtoobtainEPCsistoisolateandculturemononuclearcellsfromperipheralbloodandtoselectadherentcellsfor

简介：<正>WeandothershavefirmlyestablishedthatsurfaceIgMreceptor(sIgM-R)crosslinkingwithantibodiestotheiheavychain(anti-i)leadstogrowtharrestandapoptosisinaseriesofwellcharacterizedB-celllymphomas.Thisrequiresablationofc-Mycproteinexpressionandtheconcomitantinductionofthecyclin-dependent-kinaseinhibitor,p27Kip1.Thesignalingmechanismsregulatingc-Mycandp27Kip1proteinexpressionarepoorlyunderstood.However,werecentlyestablishedthatsIgM-Rmediateddown-modulationofthePI-3Kpathwaydirectlyaffectedc-Mycandp27Kip1expressionandaccuratelypredictedgrowtharrest

简介：转变生长因素(TGF)-尾家庭成员是多功能的cytokines在细胞上得到他们的效果包括endothelial和墙壁的细胞，经由特定的类型我和类型IIserine/threoninekinase受体和细胞内部的Smad抄写因素。为表明小径部件的TGF-尾家庭的猛烈老鼠模型在合适的蛋黄囊angiogenesis揭示了他们的批评重要性。在人的基因研究在这些发信号的部件连接了变化到象世袭出血性的毛细管扩张，主要肺的高血压和Marfan症候群那样的特定的心血管的症候群。在这评论，我们在我们TGF-尾受体在脉管的生物学和疾病发信号的角色的理解的现在的最近的进展，并且讨论这怎么可以被申请治疗。

简介：Apoptosisisaformofgeneticallyprogrammedcelldeath,whichplaysakeyroleinregulationofcellularityinavarietyoftissueandcelltypesincludingthecardiovasculartissues.Underbothphysiologicalandpathophysiologicalconditions,variousbiophysiologicalandbiochemicalfactors,includingmechanicalforces,reactiveoxygenandnitrogenspecies,cytokines,growthfactors,oxidizedlipoproteins,etc.,mayinfluenceapoptosisofvascularcells.TheFas/Fasligand/caspasedeath-signalingpathway,Bcl-2proteinfamily/mitochondria,thetumorsuppressivegenep53,andtheproto-oncogenec-mycmaybeactivatedinatheroscleroticlesions,andmediatesvascularapoptosisduringthedevelopmentofatherosclerosis.Abnormalexpressionanddysfunctionoftheseapoptosis-regulatinggenesmayattenuateoracceleratevascularcellapoptosisandaffecttheintegrityandstabilityofatheroscleroticplaques.Clarificationofthemolecularmechanismthatregulatesapoptosismayhelpdesignanewstrategyfortreatmentofatherosclerosisanditsmajorcomplication,theacutevascularsyndromes.

简介：Itisstandardpractice,wheneveraresearcherfindsanewgene,tosearchdatabasesforgenesthathaveasimilarsequence.Itisnotstandardpractice,wheneveraresearcherfindsanewgene,tosearchforgenesthathavesimilarexpression(coexpression).Failuretoperformco-expressionsearcheshasleadtoincorrectconclusionsaboutthelikelyfunctionofnewgenes,andhasleadtowastedlaboratoryattemptstoconfirmfunctionsincorrectlypredicted.WepresentheretheexampleofGliaMaturationFactorgamma(GMF-gamma).Despiteitsname,ithasnotbeenshowntoparticipateingliamaturation.ItisageneofunknownfunctionthatissimilarinsequencetoGMF-beta.ThesequencehomologyandchromosomallocationledtoanunsuccessfulsearchforGMF-gammamutationsinglioma.WeexaminedGMF-gammaexpressionin1432humancDNAlibraries.Highestexpressionoccursinphagocytic,antigen-presentingandotherhematopoieticcells.WefoundGMF-gammamRNAinalmosteverytissueexamined,withexpressioninnervoustissuenohigherthaninanyothertissue.OurevidenceindicatesthatGMF-gammaparticipatesinphagocytosisinantigenpresentingcells.Searchesforgeneswithsimilarsequencesshouldbesupplementedwithsearchesforgeneswithsimilarexpressiontoavoidincorrectpredictions.

简介：Thepaperpresentsadetailedanalysisofexperimentaldatainordertocharacterizetheelasticpropertiesofarteries.Suchanalysiswouldprovideagoodbasisforevaluationofbiomimeticvasculargrafts.Sincethelatterneedstoexhibitsimilarpropertiesofnativetissue,itisimportanttoaccuratelycharacterizethebiomimeticsampleinalargerangeofappliedstresses.Thestress-strainpropertiesvaryaccordingtothespecificpathology(e.g.arteriosclerosis,aneurism)andthetissuegraftmustbechosencorrectly.Twomodelsareproposedinthispaperonthestress-straincharacteristics.Anextensionforfrequency-domainanalysisisprovidedforoneofthemodels.Thecomparisonbetweenvasculargraftsandnativetissueforcarotidandthoracicarteriesinpigsareingoodagreementwithresultsfromliterature.Theproposedexperimentalmethodofferssuitableparametersforidentifyingmodelswhichcharacterizebothelasticityandstiffnesspropertiesoftheanalyzedtissues(stress-strain).Theproposedmodelsshowgoodperformanceincharacterizingtheintrinsicmaterialproperties.

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简介：Insufficientgrowthandrarefactionofcapillaries,followedbyendothelialdysfunctionmayrepresentoneofthemostcriticalmechanismsinvolvedinheartdamage.Inthisstudyweexaminedhistochemicalandultrastructuralchangesinmyocardialcapillaryendotheliumintwomodelsofheartfailurestreptozotocin-induceddiabetesmellitus(STZ)andNOdeficienthypertensioninmaleWistarrats.Diabeteswasinducedbyasinglei.v.doseofSTZ(45mg/kg)andchronic9-weekstagewasanalysed.ToinduceNO-deficienthypertension,animalsweretreatedwithinhibitorofNOsynthaseLnitroargininemethylester(L-NAME)(40mg/kg)for4weeks.Leftventriculartissuewasprocessedforenzymecatalytichistochemistryofcapillaryalkalinephosphatase(AlPh),dipeptidylpeptidaseⅣ(DPPⅣ),andendothelialNOsynthase/NADPH-diaphorase(NOS)andforultrastructuralanalysis.Indiabeticandhypertensiverats,lower/absentAlPhandDPPⅣactivitieswerefoundinfocalmicro-areas.NOSactivitywassignificantlyreducedandpersistedonlylocally.QuantitativeevaluationdemonstratedreductionofreactionproductintensityofAlPh,DPPandNOSby49.50%,74.36%,20.05%indiabeticand62.93%,82.71%,37.65%inhypertensiverats.Subcellularalterationsofendothelialcellswerefoundinheartofbothgroupssuggestinginjuryofcapillaryfunctionaswellascompensatoryprocesses.Endothelialinjurywasmoresignificantindiabeticanimals,incontrasttheadaptationwasmoreevidentinhypertensiveones.Concluding:bothSTZ-induceddiabetes-andNO-deficienthypertension-relatedcardiomyopathywereaccompaniedbysimilarfeaturesofstructuralremodellingofcardiaccapillarynetworkmanifestedasangiogenesisandangiopathy.Thelatterwashowever,predominantandmayacceleratedisappearanceofcapillaryendotheliumcontributingtomyocardialdysfunction.

简介：Mammaliancelltotipotencyisasubjectthathasfascinatedscientistsforgenerations.AlonglastingquestionwhethersomeofthesomaticcellsretainstotipotencywasansweredbythecloningofDollyattheendofthe20thcentury.Thedawnofthe218thasbroughtforwardgreatexpectationsinharnessingthepoweroftotipotentcyinmedicine.Throughstemcellbiology,itispossibletogenerateanypartsofthehumanbodybystemcellengineering.Considerableresourceswillbedevotedtoharnesstheuntappedpotentialsofstemcellsintheforeseeablefuturewhichmaytransformmedicineasweknowtoday.Atthemolecularlevel,totipotencyhasbeenlinkedtoasingulartranscriptionfactoranditsexpressionappearstodefinewhetheracellshouldbetotipotent.NamedOct4,itcanactivateorrepresstheexpressionofvariousgenes.Curiously,verylittleisknownaboutOct4beyonditsabilitytoregulategeneexpression.ThemechanismbywhichOct4specifiestotipotencyremainsentirelyunresolved.Inthisreview,wesummarizerethestructureandfunctionofOct4andaddresstoOct4functioninmaintainingtotipotencyorpluripotencyofembryonicstemcels.

简介：Tumor-targetingantibodieswereinitiallydefinedasagroupoftherapeuticmonoclonalantibodies(mAb)thatrecognizetumor-specificmembraneproteins,blockcellsignaling,andinducetumor-killingthroughFc-driveninnateimmuneresponses.However,inthepastdecade,ampleevidencehasshownthattumor-targetingmAb(TTmAb)eradicatestumorcellsviaactivationofcytotoxicTcells(CTLs).Inthisreview,wespecificallyfocusonhowTTmAbsinduceadaptiveanti-tumorimmunityanditspotentialincombinationtherapywithimmunecytokines,checkpointblockade,radiation,andenzymetargetedsmallmoleculedrugs.ExploringthemechanismsofthesepreclinicalstudiesandretrospectiveclinicaldatawillsignificantlybenefitthedevelopmentofhighlyefficientandspecificTTmAb-orientedanti-tumorremedies.

简介：导致的模仿的微严肃(SMG)的知识在微生物的致病力变化为长期的空间飞行的成功是重要的。在用高方面比率容器生物反应器的以前的研究，当在建模的微严肃成长时，我们证明酵母种类Saccharomycescerevisiae经历了重要phenotypic回答，它在基因表达侧面的分析被反映。在这研究，我们证实Candidaalbicans以一种类似的方式对SMG作出回应，证明在到这个环境压力的酵母之中有保存回答。我们也报导C的生长。在SMG的albicans导致与提高的致病力一致的一个morphogenic开关。明确地，我们在有机体的细丝状的形式观察了增加，在二基因的表示伴随变化与酵母菌丝的转变联系了。词法反应可以为宇航员的安全有重要含意，当真菌的病原体可以在空间飞行期间变得更剧毒。

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简介：ThisworkprovidessomeevidencesforthesaponinproductionofPanaxnotoginsengcallusbyusingbiologi-callyactive,wall-relatedoligosaccharins.Inanappropriateconcentration,threekindsofoligosaccharinsstimulatedsaponinformationorcallusgrowth.TheconcentrationofDO,GOandCOforsaponinproductionofPanaxnotoginsengcallusculturewere15ppm,15ppmaud20ppmrespectivelybycomparingsaponinyield.ItwasveryobviousforDOtoincreasesaponincontentwhentheconcentrationwas10ppm,andforGOtostimulatecallusgrowthwhentheconcentrationwas20ppm.Itwouldbeagoodwaytoproducesaponinbyusingoligosaccharinsinlargescalecultureinthefuture.