简介：Thechiralclusters(μ3-S)MCoW(CO)8[η^5-C5H4C(O)OCH3][M=Ru(2),Fe(3)]weresynthesizedbyasymmetricinductionofN-benzylcinchoniumchlorideasphase-transfercatalyst(PTC).ThemostsuitableamountofPTCis70mol%.Cluster3wasdeterminedbysinglecrystalX-raydiffractionanalysis.Thebesteeofthechiralclusterisover20%.

简介：Ring-closingmetathesisreactionsinvolvingdiallyldiphenylsilaneanddiallyloxydiphenylsilaneweresuccessfullyperformedbyusingonly0.01molorevenlessofGrubbscatalyst1.Theeffectsofreactionparameters,suchassolvents,temperatureandconcentrationofthecatalystarediscussed.

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简介：Thevisualsystemisvitaltohumanhealth,andtheeffectsofionizingradiationonvisionhavereceivedincreasingattention.Usingazebrafishmodel,thisstudywasdesignedtoinvestigatetheapoptosisineyesinducedbycarbonionirradiation.Zebrafishembryosat12hpost-fertilization(hpf)wereirradiatedusing12C6+ionbeamsatdosesof2,4and8Gy.

简介：Intrinsicapoptosis,apossibleresponsetomitochondrialdamage,inMDA-MB-231cellsexposedtodifferentdosesofcarbonionswasinvestigatedinthisstudy.WeassessedBaxandBcl-2expressionandcytochromecreleaseinthemitochondriaandcytosolofcellsexposedtolow(0.5Gy)andhigh(3Gy)dosesofcarbonionsusingwesternblotanalysis.

简介：Caspasesfunctionasacomponentincellsignalingpathwayswhichareinvolvedineventssuchasapoptosis,cellgrowthanddifferentiation.Caspase-9(CASP9)isamemberoftheintrinsicapoptosispathway,whichisactivatedasaresultofmitochondrialdamageandcytochromecrelease.Onceactivated,CASP9cleavesandactivatestherelevantcaspases,suchascaspase-3,thattargetavarietyofcellularcomponentstodismantleacellandpresentthefragmentsforphagocytosis[1].

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简介：cJUNNH2-terminalkinase(JNK)hasbeenreportedtoplayimportantrolesinregulatingthecellularapoptosisandautophagy.However,accuratemechanismandhowthebalanceoftheseactivitiesdeterminesthecellularradiosensitivityremainunclear.

简介：TodepictthedetailsthatCHOP(C/EBPhomologousprotein)regulatesautophagyandapoptosisinbreastcancercells,theexpressionofCHOPwasinhibitedbytransfectionwithsiRNAsequence.AsshowninFig.1,radiati-Fig.1CHOPinhibitionbysiRNAatmRNAandproteinlevelsafterradiation.onelicitedahigherexpressionofCHOPintheNCgroupcomparedwithcontrol.However,thishigherexpressionwassignificantlyinhibitedinthesiRNAgroup.

简介：Theeffectandmechanismofcarmustine(BCNU)combinedwithall-transretinoicacid(ATRA)ontheapoptosisofhumanglioblastomaU251cellswereinvestigatedbymeansof3-(4,5-dimethylthiazol-2-yl)-2,5-diphe-nyltetrazoliumbromide(MTT)assay,flowcytometry,reversetranscription-polymerasechainreaction(RT-PCR)andWesternblotanalysis.TheresultsshowthatBCNUorATRAshowstime-anddose-dependentinhibitioneffectsonhumanglioblastomaU251cellsandthecombinationofBCNUwithATRAshowsansynergisticinhibitioneffectonhumanglioblastomaU251cells,andthecombinedBCNUandATRAcansignificantlyinhibittheproliferationofhumanglioblastomaU251cells,andinducetheapoptosisofthem,makingthecellsarrestinthestageofG1phase,thestageofSandG2phasesdecline,therateoftheapoptosisofhumanglioblastomaU251cellsincrease,thecorrespondingmRNAexpressionofcyclinEandcyclin-dependentkinase2(CDK2)downregulatedandthecorrespon-dingmRNAexpressionofp27kip1unregulated.Inaddition,thecombinedBCNUandATRAreducedtheproteinexpressionofnuclearfactorkappaB(NF-κB).Takentogether,theseresultssuggestthatthetreatmentofhumanglioblastomaU251cellswithacombinationapplicationofATRAandBCNUcanexertsynergisticeffect,thecourseofthiskindofcombinationchemotherapymaylikelybeassociatedwithmultiplemolecularmechanismsforapoptosis,furthermore,thecyclinEandp27kip1shouldbeconsideredasnoveltargetsforcontrollingthegrowthofglioblastomacells.