简介：Similarlytootheradulttissues,ahierarchicalstructurehasbeenestablishedforthebrain,wherethedifferentiatedcelltypes(neurons,oligodendrocytesandastrocytes)aregeneratedfromprimaryprogenitorcells,knownastypeB

简介：Objective:Humaninducedpluripotentstem(iPS)cellsexhibitgreatpotentialforgeneratingfunctionalhumancellsformedicaltherapies.Inthispaper,wereportforuseofhumaniPScellslabeledwithfluorescentmagneticnanoparticles(FMNPs)fortargetedimagingandsynergistictherapyofgastriccancercellsinvivo.Methods:HumaniPScellswerepreparedandculturedfor72h.Theculturemediumwascollected,andthenwascoincubatedwithMGC803cells.CellviabilitywasanalyzedbytheMTTmethod.FMNP-labeledhumaniPScellswerepreparedandinjectedintogastriccancer-bearingnudemice.Themousemodelwasobservedusingasmall-animalimagingsystem.Thenudemicewereirradiatedunderanexternalalternatingmagneticfieldandevaluatedusinganinfraredthermalmappinginstrument.Tumorsizesweremeasuredweekly.Results:iPScellsandthecollectedculturemediuminhibitedthegrowthofMGC803cells.FMNP-labeledhumaniPScellstargetedandimagedgastriccancercellsinvivo,aswellasinhibitedcancergrowthinvivothroughtheexternalmagneticfield.Conclusion:FMNP-labeledhumaniPScellsexhibitconsiderablepotentialinapplicationssuchastargeteddual-modeimagingandsynergistictherapyforearlygastriccancer.

简介：Recentadvancesinstemcelltechnologieshaveopenednewavenuesforthetreatmentofanumberofdiseasesstilllackingeffectivetherapeuticoptions.Celltransplantationhasemergedasamongthemostpromisingclinicalinterventionfordisorderssuchasinjuries,diabetes,liver

简介：规章的T(Treg)房间被认为由于他们在维持有免疫力的动态平衡和自我忍耐的必要角色对autoimmunity是保护的CD4+T房间的一个亚系的Foxp3+。然而，Treg房间以系专门化和镇压功能在vivo是不稳定的。这些不稳定的Treg房间在疾病的致病起作用，它关于人的Treg房间治疗引起安全担心。在这评论，我们加亮最近的调查结果在不同疾病模型表明Treg房间的病原的变换。

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简介：Cancercellsdifferfromnormalcellsinvariousparameters,andthesedifferencesarecausedbygenomicmutationsandconsequentialalteredgeneexpression.Thegeneticandfunctionalheterogeneityoftumorcellsisamajorchallengeincancerresearch,detection,andeffectivetreatment.Assuch,theuseofdiagnosticmethodsisimportanttorevealthisheterogeneityatthesingle-celllevel.Dropletmicrofluidicdevicesareeffectivetoolsthatprovideexceptionalsensitivityforanalyzingsinglecellsandmolecules.Inthisreview,wehighlighttwonovelmethodsthatemploydropletmicrofluidicsforultrasensitivedetectionofnucleicacidsandproteinmarkersincancercells.Wealsodiscussthefuturepracticalapplicationsofthesemethods.

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简介：Circulatingtumorcells(CTCs)areapopulationoftumorcellsmediatingmetastasis,whichresultsinmostofthecancerrelateddeaths.ThenumberofCTCsintheperipheralbloodofpatientsisrare,andmanyplatformshavebeenlaunchedfordetectionandenrichmentofCTCs.EnumerationofCTCshasalreadybeenusedasaprognosismarkerpredictingthesurvivalrateofcancerpatients.YetCTCsshouldbemorepotential.StudiesonCTCsatsinglecelllevelmayhelprevealingtheunderlyingmechanismoftumorigenesisandmetastasis.Thoughfarfromdeveloped,thisareaofstudyholdsmuchpromiseinprovidingnewclinicalapplicationanddeepunderstandingtowardsmetastasisandcancerdevelopment.

简介：Glyceraldehyde-3-phosphatedehydrogenase(GAPDH),initiallyidentifiedasaglycolyticenzymeandconsideredasahousekeepinggene,iswidelyusedasaninternalcontrolinexperimentsonproteins,mRNA,andDNA.However,emergingevidenceindicatesthatGAPDHisimplicatedindiversefunctionsindependentofitsroleinenergymetabolism;theexpressionstatusofGAPDHisalsoderegulatedinvariouscancercells.OneofthemostcommoneffectsofGAPDHisitsinconsistentroleinthedeterminationofcancercellfate.Furthermore,studieshavedescribedGAPDHasaregulatorofcelldeath;otherstudieshavesuggestedthatGAPDHparticipatesintumorprogressionandservesasanewtherapeutictarget.However,relatedregulatorymechanismsofitsnumerouscellularfunctionsandderegulatedexpressionlevelsremainunclear.GAPDHistightlyregulatedattranscriptionalandposttranscriptionallevels,whichareinvolvedintheregulationofdiverseGAPDHfunctions.Severalcancer-relatedfactors,suchasinsulin,hypoxiainduciblefactor-1(HIF-1),p53,nitricoxide(NO),andacetylatedhistone,notonlymodulateGAPDHgeneexpressionbutalsoaffectproteinfunctionsviacommonpathways.Moreover,posttranslationalmodifications(PTMs)occurringinGAPDHincancercellsresultinnewactivitiesunrelatedtotheoriginalglycolyticfunctionofGAPDH.Inthisreview,recentfindingsrelatedtoGAPDHtranscriptionalregulationandPTMsaresummarized.MechanismsandpathwaysinvolvedinGAPDHregulationanditsdifferentrolesincancercellsarealsodescribed.

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

简介：Brainmicrovascularendothelialcellsformtheinterfacebetweennervoustissueandcirculatingblood,andregulatecentralnervoussystemhomeostasis.Brainmicrovascularendothelialcellsdifferfromperipheralendothelialcellswithregardsexpressionofspecificiontransportersandreceptors,andcontainfewerfenestrationsandpinocytoticvesicles.Brainmicrovascularendothelialcellsalsosynthesizeseveralfactorsthatinfluencebloodvesselfunction.Thisreviewdescribesthemorphologicalcharacteristicsandfunctionsofbrainmicrovascularendothelialcells,andsummarizescurrentknowledgeregardingchangesinbrainmicrovascularendothelialcellsduringstrokeprogressionandtherapies.Futurestudiesshouldfocusonidentifyingmechanismsunderlyingsuchchangesanddevelopingpossibleneuroprotectivetherapeuticinterventions.

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：IL-37是仅仅最近被识别的反煽动性的cytokine，并且它高度与煽动性、自体免疫的疾病从病人在纸巾被表示。煽动性的cytokines和煽动性的刺激能导致IL-37的upregulation。然而，反煽动性的药是否导致IL-37的表示，没被报导。在这个工作，第一次，我们揭开了那主要bioactive二个部件，triptolide和triptonide，从植物Tripterygiumwilfordii钩f。(TwHF)，它拥有反煽动性的活动，upregulateIL-37的表示，和这表情被ERK1/2和p38MAPK禁止者压制。总的来说，第一次，我们的研究表明了那反煽动性的活跃部件(triptolide和triptonide)upregulated经由ERK1/2和p38MAPK小径的激活最可能的IL-37的表示。

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简介：PlatycodinD(PD)，从Platycodonis根值孤立的triterpenoidsaponin，是被显示了在几根癌症房间线有anti-proliferative效果的一副著名中草药。这研究的目的是用proteomics途径与PD在hepatocellular癌HepG2房间的治疗以后在细胞的蛋白质决定变化。房间生存能力用MTT试金被决定。proteome被二维的差别胶化电气泳动和帮助矩阵的激光解吸附作用/电离time-of-flight团spectrometry分析。西方的污点分析被用来证实改变的蛋白质的表示。我们的结果证明PD在集中依赖者和时间依赖者礼貌禁止了HepG2房间的增长。十六蛋白质被识别在对待PD的HepG2房间起来调整包括ATP5HOXCT1，KRT9，CCDC40，ERP29，RCN1，ZNF175，HNRNPH1，HSP27，PA2G4，哲学学士，BANF1，TPM3，ECH1，LGALS1，和MYL6三蛋白质(即，RPS12，EMG1，和KRT1)与PD在治疗以后在HepG2房间减少了。在HSP27和哲学学士的变化被西方的弄污进一步证实。在结论，我们的结果为PD的反癌症活动在行动的机制上打开新灯。

简介：Polyreactive天生类型的B房间说明在圆周表示自我反应的许多B房间。这些B房间的不适当的规定可以是位于自体免疫的疾病下面的一个重要因素。这里，我们在导致骨胶原的关节炎(中央情报局)的开发探索了自我反应的天生的B房间的影响，风湿性关节炎的一个鼠标模型。我们显示出那个脾的边缘的地区(MZ)，然而并非B-1B房间在naı展出自发的IgM反应到自体同源的骨胶原II；¨；ve老鼠。在有在完全的Freund’的heterologous骨胶原II的免疫之上；骨胶原反应的MZB房间很快扩展了的s助手，当B-1B房间显示出谦虚反骨胶原回答时。MZB房间被像使用费的受体(TLR)容易激活4并且在vitro，导致的增长和cytokine分泌物的9-ligands，暗示B房间受体和TLR的那个双约会可以把有免疫力的反应提升到自我抗原。而且，告知骨胶原的MZB房间显示出在vivo在IgG反骨胶原抗体的vitro和正式就职由血缘的T房间增长思考了的重要介绍抗原的能力。在1和2表明了的补充受体是缺乏的MZB房间增加了增长和cytokine生产，当时Fcγ；房间的受体IIb缺乏导致增加的cytokine生产和抗原表示。在结论，我们的数据在中央情报局作为自体免疫的反应的开始者加亮自我反应的MZB房间，在补充和Fc受体在在房间控制自我反应是相关的的地方。

简介：BackgroundStudyhasshownthatratbonemesenchymalstemcells(MSCs)canbedifferentiatedintoendothelialcellsbyVEGFandb-FGFinvitro.OurpreviousresearchfoundthatafterratboneMSCstreatedbyVEGFandb-FGFgainedthephenotypicandfunctionalfeaturesofendothelialcelllines,withsomedifferencesfromendothelialcelllinesregardtothestabilityandself-replicating.ThisstudywastoexploretheeffectofNotchsignalingonthefunctionsofMSCsdifferentiatedendothelialcells.MethodsRatboneMSCswerecultivatedandtreatedbyVEGF165andb-FGFfor2weekstoinduceendothelialcelldifferentiation.ThegeneofVEGF165wasimportedintodifferentiatedendothelialcells.ThereceptorofNotch1andtheligandofNotchsignalingJagged1weredetectedbyRT-PCRbeforeandafterthetransfection.γ-secretaseinhibitorwasusedtoblockNotchpathway,Cellmigrationabilitywasdetectedbyscarificationtest.Cellswereinoculatedonsemisolidgeltostudytheirabilityofcapillary-likestructureformation.ResultsAftertransfection,VEGF165mRNAwasdetectedonthedifferentiatedendothelialcells.TheexpressionofJagged1’smRNAwasupregulated(1.08±0.01comparedto1.01±0.02,P<0.01)andtherewasnochangeabouttheNotch1.Cellsmigrationabilitywasenhanced[numberofcellsonthescratchedarea:44.95±3.14comparedto41.61±1.42,P<0.05]andtheabilityofformingcapillary-likestructureonsemisolidgelwasnotchanged.Theγ-secretaseinhibitorL-685,458furtherenhancedtheabilitiesofcellmigration[numberofcellsonthescratchedarea:50.28±2.76comparedto44.95±3.14,P<0.05])andcapillary-likestructureformationonsemisolidgel(cellsclassification:4.00±0.63comparedto3.00±0.63,P<0.05).ConclusionsInhibitionofNotchsignalingcanenhancethefunctionsoftheendothelialcellsdifferentiatedfromratMSCs.

简介：biflavonoidisochamaejasmin主要在StellerachamaejasmeL的根被散布。(Thymelaeaceae)那在繁体中文药(TCM)被使用治疗肿瘤，肺结核，和干癣。此处，isochamaejasmin被发现对Bcl-2家庭蛋白质显示出类似的bioactivity到参考Bcl-2ligand(−)通过3D类似搜索的-gossypol。它有选择地跳了到Bclx有K和Mcl-1>是的i价值1.93±0.13mol·L−1和9.98±0.21mol·L−1,分别地。另外，isochamaejasmin显示出细微生长对有是的IC50价值的HL-60的禁止的活动50.40±1.21mol·L−1和中等生长对有IC50价值的K562细胞的禁止的活动是24.51±1.62mol·L−1。而且，isochamaejasmin由增加在Bcl-2-inducedapoptosis小径包含了的caspase-9，caspase-3，和PARP的劈开的蛋白质的细胞内部的表示层次导致了K562房间的apoptosis。这些结果显示isochamaejasmin由禁止Bcl-2家庭蛋白质的活动在白血病房间导致apoptosis，提供为进一步学习S的内在的反癌症机制的证据。chamaejasmeL。

简介：cAMPsignalingandthecontrolofSchwanncellfate:Theubiquitoussecondmessengercyclicadenosinemonophosphate(cAMP)controlsavarietyofcellularresponsesinacelltype-specificandstimulus-dependentmannerthroughanelaboratenetworkofsignalingintermediariesthatconnectstimulationofcellmembranereceptors(typicallyG

简介：·AIM:ToexploretheimmunomodulatoryeffectsofcurdlanoninnateimmuneresponsesagainstAspergillusfumigatus(A.fumigatus)inculturedhumancornealepithelialcells(HCECs),andwhetherC-typelectinreceptorDectin-1mediatestheimmunomodulatoryeffectsofcurdlan.·METHODS:TheHCECswerestimulatedbycurdlanindifferentconcentrations(50,100,200,400μg/mL)forvarioustime.ThenHCECspretreatedwithorwithoutlaminarin(Dectin-1blocker,0.3mg/mL)andcurdlanwerestimulatedbyA.fumigatushyphae.ThemRNAandproteinproductionoftumornecrosisfactor-α(TNF-α)andinterleukin-6(IL-6)weredeterminedbyreal-timequantitativepolymerasechainreactionandenzyme-linkedimmunosorbentassay,respectively.TheproteinlevelofDectin-1wasmeasuredbyWesternblot.·RESULTS:CurdlanstimulatedmRNAexpressionofTNF-αandIL-6inadoseandtimedependentmannerinHCECs.CurdlanpretreatmentbeforeA.fumigatushyphaestimulationsignificantlyenhancedtheexpressionofTNF-αandIL-6atmRNAandproteinlevelscomparedwithA.fumigatushyphaestimulationgroup(P<0.05).BothcurdlanandA.fumigatushyphaeup-regulatedDectin-1proteinexpressioninHCECs,andDectin-1expressionwaselevatedto1.5-to2-foldbycurdlanpretreatmentfollowedhyphaestimulation.TheDectin-1blockerlaminarinsuppressedthemRNAexpressionandproteinproductionofTNF-αandIL-6inducedbycurdlanandhyphae(P<0.05).·CONCLUSION:ThesefindingsdemonstratedthatcurdlanpretreatmentenhancedtheinflammatoryresponseinducedbyA.fumigatushyphaeinHCECs.Dectin-1isessentialfortheimmunomodulatoryeffectsofcurdlan.Curdlanmayhavehighclinicalapplicationvaluesinfungalkeratitistreatment.