简介：Deareditor,Itiswithgreatinterestthatwereadthearticle“Relationshipofcalcitoningene-relatedpeptidewithdiseaseprogressionandprognosisofpatientswithseveretraumaticbraininjury”(Chenetal.,2018).Inthisstudy,theauthorsevaluated121patientswhoweredividedintomild/moderatetraumaticbraininjury(TBI)(n=61),severeTBI(n=35)andcontrol(n=25)groups,andmeasuredserumlevelsofcalcitoningene-relatedpeptide(CGRP)andserumendothelin-1(ET-1).TheyfoundthatlowlevelsofCGRPandhighlevelsofET-1wereassociatedwithhighmortalityat6months.IdentificationofmorphologicalabnormalitiesonCTscansisveryimportantforevaluatingpatientswithTBIbecausedifferentdiagnosesaremadebasedondifferentimagingfindings(Maasetal.,2005).

简介：Itisaverydifficulttasktodevelopamethodofreducingturbulentboundarylayerdrag.However,inrecentyears,plasmaflowcontroltechnologyhasdemonstratedhugepotentialinfrictiondragreduction.Tofurtherinvestigatethisissue,asmoothplatemodelwasdesignedasatestingobjectarrangedwithabidirectionaldielectric-barrier-discharge(DBD)plasmaactuator.Inaddition,measurementofskinfrictiondragwasachievedbyapplyinghotwireanemometrytoobtainthevelocitydistributionoftheturbulentboundarylayer.AmethodofquantifyingthefrictiondrageffectwasadoptedbasedontheSpaldingformulafittedwiththeexperimentdata.Whenplasmaactuationwasconducted,avelocitydefectoccurredatthetwomeasuringpositions,comparedwiththenoplasmacontrolcondition;thismeansthattheDBDplasmaactuationcouldreducethedragsuccessfullyinthedownstreamoftheactuator.Moreover,dragreductioncausedbybackwardactuationwasslightlymoreefficientthanthatcausedbyforwardactuation.Withanincreasingdistancefromplasmaactuation,thedrag-reductioneffectcouldbecomeweaker.Experimentalresultsalsoshowthattheimprovementofdrag-reductionefficiencyusingaDBDplasmaactuatorcanachieveabout8.78%inthelocalregionoftheexperimentalflatmodel.

简介：Objective:MemorystemTcells(Tscm)haveattractedattentionbecauseoftheirenhancedself-renewal,multipotentcapacity,andanti-tumorcapacities.However,littleisknownaboutTscminpatientswithrenalclearcellcarcinoma(RCC)andtheroleofWntsignalinginthesecells.WeevaluatedTscmfromRCCpatientsconcerningtheiractivationofWntsignalinginvitroandexploredthemechanismofpreferentialsurvival.Methods:FlowcytometryidentifiedsurfacemarkersandcytokinesproducedfromaccumulatedTscminthepresenceoftheglycogensynthasekinasebetainhibitorTWS119.Apoptosiswasevaluatedafterinductionusingtumornecrosisfactor-alpha.ImmunofluorescenceandWesternblotanalyseswereusedtoinvestigatetheactivationofthenuclearfactor-kappaB(NF-КB)pathway.Results:RCCpatientshadasimilarpercentageofCD4~+andCD8~+Tscmashealthydonors.ActivationofWntsignalingbyTWS119resultedintheaccumulationofTscminactivatedTcells,butreversalofdifferentiatedTcellstoTscmwasnotachieved.PreferentialsurvivalofTscmwasassociatedwithincreasedanti-apoptoticabilitymediateddownstreamoftheNF-КBactivationpathway.Conclusions:ThefindingthatTscmcanaccumulatebyWntsignalinginvitroinbloodfromRCCpatientswillhelpindevisingnewcancertherapystrategiesofTscm-basedadoptiveimmunotherapy,suchasdendriticcell-stimulatedTscm,andTcellreceptororchimericantigenreceptor-engineeredTscm.