简介：Objective:Todetecttheexistenceofimmunetoleranceinducedbygamma-rayirradiation.Methods:Peritonealcellswereharvestedfrommicesubjectedto5Gy60Cogamma-raytotalbodyirradiationat3d,7d,15dand30d,thentheircounts,morphologicalchangesandIL-12geneexpressionwereinvestigated.Results:Afterirradiation,theperitonealcellsweresharplyreduced,thecellmorphologyshiftedfromround-liketopolymorphicandfusiformwithsomeprocesses,expressionofIL-12p35wasseriouslysuppressed,whilethatofIL-12p40greatlyenhanced.Conclusion:Ourdatahighlysuggestthatthegamma-rayirradiationcouldpotentiallyinducedendriticcell(DC)commitmentandimmunetolerance.

简介：OBJECTIVE:Radiation-inducedmeningiomasareknowntooccurafterhighandlow-dosecranialradiationtherapy.Thegoalofthisstudywastodiscernthedistinguishingfindingsandcharacteristicsofradiation-inducedmeningiomas.METHODS:Therecordsof16patients(sevenmenandninewomen)whofulfilledthecriteriaforradiation-inducedmeningiomaswereretrospectivelyreviewed.Clinical,histopathological,cytokinetic,andcytogeneticfindingsaswellasthepatients'outcomewereanalyzed.Themeanageofthepatientswas38.8yearsandthemeantumorlatencywas26.5years.Fivepatientshadmultiplemeningiomasintheirradiatedfield.Therecurrenceratewas100%aftertheinitialresection;62%ofpatientshadasecondrecurrenceand17%hadathirdrecurrence.Thirtyeightpercentofpatientshadatypicalormalignanthistopathologicalfindings.Thepresenceofprogesteronereceptorsandlowproliferation

简介：ＧＲＡＮＩＳＥＴＲＯＮＣＯＭＰＡＲＥＤＷＩＴＨＯＮＤＡＮＳＥＴＲＯＮＰＬＵＳＤＥＸＡＭＥＴＨＡＳＯＮＥＩＮＴＨＥＰＲＥＶＥＮＴＩＯＮＯＦＮＡＵＳＥＡＡＮＤＶＯＭＩＴＩＮＧＩＮＤＵＣＥＤＢＹＡＩＮＴＥＮＳＥＬＹＥＭＥＴＯＧＥＮＩＣＣＨＥＭＯＴＨＥＲＡＰ...

简介：Objective:Laser-inducedCoulombexplosionofgoldnanoparticlesforbreastcancerhasbeenstudiedbynanophotolysistechnique.Thisstudyaimedtoinvestigatewhetherlaser-inducedbubbleformationduetoCoulombexplosioncanprovideaneffectiveapproachforselectivedamageofbreastcancerwithgoldnanoparticles.Method:Numericalmethodinvolveslaser-inducedCoulombexplosionofgoldnanoparticles.Differentparametersrelatedtonanophotolysissuchaslaserfluence,tumordepth,clusterradius,laserpulseduration,andbubbleformationisstudiednumerically.NumericalsimulationwasperformedusingMatlab.Results:Thegoldnanoparticlesof10,20,30,40,and50nminradiuscouldpenetrateintotumor1.14,1.155,1.189,1.20and1.22cmindepthrespectively.Themaximumpenetrationdepthintumorcouldbeobtainedwithnanoparticlesof50nmradius.Shortlaserpulseof40nswithnanoparticlesof10nmradiuscouldpenetrateintotumor1.14cmindepth.Bubbleswitharadiusof9μmcouldeffectivelykillbreastcancercellswithoutdamaginghealthyones.Thebubbleradiusincreasedfrom4to9μmwithanincreaseinpulsedurationintherangeof10to30ns.Conclusions:Goldnanoparticleswithincreasingradiusandbubbleformationforselectivedamageofbreastcancercellsaresuccessfullyprobed.Thepresentcalculatedresultsarecomparedwithotherexperimentalfindings,andgoodcorrelationisfoundbetweenthepresentworkandpreviousexperimentalvalues.Itwasdemonstratedthatbubbleformationintumormayfurtherincreasetheefficacyofbreastcancertreatment.

简介：Objective:Toanalyzethechangesofgeneexpressioninphenylbutyrateinduceddifferentiationofgliomacells.Methods:Theexpressionlevelsof14000genesingliomacellsbeforeandafterinducementwithsodiumphenyl-butyratefor2hor6dayswereevaluatedbycDNAarraytechniqueandprovedbymulti-dotblotting.Results:expressionof98genesingliomacellsshowedchangesaftertheinducement.Somegenesinvolvedintranscriptionandtranslationandsomeoncogenesaredown-regulated,whilesomegeneinvolvedindifferentiationorapoptosisareup-regulated.18unknownexpressionsequencingtag(EST)changedtoo.Conclusion:Ageneexpressionprofileassociatedwithdifferentiationofgliomacellswasestablished.

简介：Objective:Chemotherapyisthestandardtreatmentforsmall-celllungcancer(SCLC),andleukopeniaisacommonsideeffect.Thisstudyassesseswhetherchemotherapy-inducedleukopeniaisapredictorofefficacyandwhetheritisassociatedwiththesurvivalofSCLCpatients.Methods:Aretrospectiveanalysiswasconductedondatafrom445patientswithSCLCwhoreceivedstandardchemotherapyfor4to10cycles.TheWorldHealthOrganizationgradingsystemclassifiesleukopeniaduringchemotherapyasfollows:absent(grade0),mild(grades1and2),orsevere(grades3and4).Theprimaryendpointisoverallsurvival(OS).Results:Theassociationbetweenchemotherapy-inducedleukopeniaandOSwasassessed.AccordingtoamultivariateCoxmodelwithtime-varyingcovariates,thehazardratioofdeathwassignificantlyloweramongpatientswithmildleukopeniathanamongpatientswithsevereleukopeniaat0.687(0.506to0.943)and1.414(1.147to1.744),respectively.Themediansurvivalwas13months(95%CI:11to15months)forpatientswhodidnotexperienceleukopenia,17months(95%CI:14to18months)forthosewithmildleukopenia,and14months(95%CI:13to16months)forthosewithsevereleukopenia(absentvs.mildvs.severeleukopenia,P=0.047).Conclusion:LeukopeniaduringchemotherapyisassociatedwiththesurvivalofSCLCpatients.Mildleukopeniaisstronglyassociatedwithlongersurvivaltime.

简介：Severaldrug-resistantvariantshavebeendevelopedbygrowingtheparentalMELcellsinpresenceofcolchicine,adriamycinandvincristinerespectivelywithstepwiseincreasingconcentration.Boththecolchicine-resistantSc9(ColO)andvincristine-resis-tantSc9(VCR5)cellsdisplayedanacceleratedHMBA-inducedcommitmenttoterminalcelldifferentiation,whereastheadriamycin-resistantSC9(A120)showednoaccelerationbutratherasubstantialdelayinHMBA-induceddifferentiation.ThestudiesprovidemorecluesaswellasexperimentalmodelsforfurtherstudyonthemechanismofinduceddifferentiationofMELcells.

简介：Objective:ToinvestigatewhethertheBc1-2antisenseoligonucleotide(ASODN)mayenhanceradiation-inducedapoptosisinRajicellline.Methods:Cellsurvivingfractionwasdeterminedusingthetrypanbluedyeexclusionassay.Theexpressionlevelofbc1-2proteinwasassayedbyimmunofluorescenceusingfluoresceisothiocyanatelabel.ApoptosiswasdetectedbyGiemsastainingandflowcytomertriccellcycleanalysis.Results:ItwasfoundthatBc1-2ASODNcombinedwithradiationhadsignificantlyreducedthenumberofviablecells(P<0.05).TherewasnodifferenceoncellsurvivalbetweenmismatchBc1-2oligodeoxynucleotide/radiationcombinationandradiation-treatedcellsalone.Bc1-2ASODNcombinedwithradiationcouldsignificantlyinhibitexpressionofBc1-2proteininRajicells(P<0.05).CellstreatedwithBc1-2ASODNcombinedwithradiationat72hdisplayedclassicapoptoticchanges.ApoptosisratesofRajicellstreatedwithBc1-2oligodeoxynucleotide/radiationcombinationandradiation-treatedcellsalone,respectively.Conclusion:Bc1-2antisenseoligonucleotidecanenhanceradiation-inducedapoptosisinRajicellline.

简介：ＱＵＡＬＩＴＡＴＩＶＥＳＴＵＤＹＯＦＳＩＡＬＯＭＵＣＩＮＳＣＨＡＮＧＥＳＤＵＲＩＮＧＮ－ＭＥＴＨＹＬ－Ｎ－ＮＩＴＲＯＳＯＵＲＥＡ－ＩＮＤＵＣＥＤＣＯＬＯＮＩＣＣＡＲＣＩＮＯＧＥＮＥＳＩＳＩＮＭＩＣＥＷａｎｇＱｉａｎｇ王强；ＷａｎｇＹｕａｎｈｅ王元和；...

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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：Objective:TostudythesynergiceffectsofIL-12andB7-1transfectantonantitumorimmunityinvivo.Methods:TheretrovirusvectorencodingmIL-12andmB7-1genewastranfectedintoEL-4thymiclymphomacellsrespectively.Thecellswereusedastumorvaccineandthetherapeuticeffectwasobserved.Results:IncontrasttothemiceimmunizedwithEL-4/WtorEL-4/Neogroups,thetumorigenicityofEL-4/IL-12transfectantwasdecreased(P<0.001).TheEL-4/IL-12andEL-4/B7-1cellsirradiatedwith60CoshowedsignificantsystematicprotectiveeffectsagainsttherechallengeofEL-4/Wt.60CoirradiatedEL-4/IL-12cellsdelayedtheoccurrenceoftumorandprolongedthesurvivalperiodoftumorbearingmice.CombinationofthevaccinesofEL-4/IL-12andEL-4/B7-1resultedintheenhancedtherapeuticeffectcomparedwitheachsingletransfectantgroup(P<0.001).Conclusion:TheresultsshowedthatIL-12transducedcellscouldenhancetheantitumorimmunityofhostascancervaccine.CombinationoftheEL-4/IL-12andEL-4/B7-1transfectantcouldimproveimmunityofhostandisaprospectcancervaccine.

简介：Objective:Todeterminewhetherpyrrolidinedithio-carbamate(PDTC)enhancesTNFα-inducedapoptosisinculturedbreastcancercellsandexploretheroleofNF-κBinTNFα-inducedapoptosis.Methods:HumanbreastcancercelllinesMCF-7andMDA-MB-435sweretreatedwithTNFα,PDTCandcombinationtherapy.CellsurvivalsweredeterminedbyMTTassay.ApoptosiswasdetectedbyTUNELandflowcytometry.NF-κBDNAbindingactivitywasdetectedusingelectrophoresismobilityshiftassay(EMSA).WesternblotswereperformedtodemonstrateIκBα(InhibitorproteinofnuclearfactorκB)phosphorylationanddegradation.Results:CellgrowthwasnotsuppressedbyeitherTNFα(2000U/mlorless)orPDTCalone.BothcelllinestreatedwithTNFα(2000U/ml)combinedwithPDTC(50μmol/L)showedsignificantgrowthinhibition.PDTCinhibitedTNFα-inducedIκBαphosphorylationanddegradationinbothcelllines.EMSAshowedthatPDTCcontinuouslyinhibitedTNFαinducedNF-κBDNAbindingactivity.TNFαinducedapoptosis(TUNEL)wasincreasedsignificantlywhenbothcellswerepretreatedwithPDTC,andthiswasconfirmedbyFlowcytometry.Conclusion:PDTCenhancesTNFα-inducedapoptosisviainhibitingIκBαphosphorylationanddegradationinhumanbreastcancercells.NF-κBprotectsagainstTNFα-inducedapoptosis.

简介：Effectsoftwodosesoftheanti-diabeticdrug,metformin(MF),onhormonalandmetaboliclevelsofserumofnon-diabeticmaleWistarratswith1,2-dimethylhydrazine(DMH)-inducedcolontumoradenocarcinomaswerestudied.Carcinogenesisintheanimalswasalsoobserved.RatswithDMH-inducedcolonadenocarcinomashadelevatedlevelsofserumglucose,insulin,insulinlikegrowthfactor-1,totalcholesterol,triglycerides,catalase,malonicdialdehyde,glycatedhemoglobin,aspartateaminotransferase,andalanineaminotransferaseanddecreasedhemoglobin.TreatmentwithtwodosesofMFnormalizedmajorityofthesechangesinDMH-treatedrats,whereasthedrugwasineffectiveinratswithoutDMHtreatment.TheonlyexceptionwasthedecreasedtriglyceridelevelsinMF-treatedrats.A100mg/kgdoseofMFincreasedDMH-inducedexophyticcoloncarcinomasanddecreasedendophytictumorscomparedwithuntreatedrats.Moreover,bothMFdosesincreasedDMH-inducedandhighlydifferentiatedtumorsanddecreasedtheinvasivenessofcoloncarcinomascomparedwithratsprovidedwithDMHandwater.Therefore,effectsofMFonmetabolichomeostasisarecriticalforpreventingcoloncancer.

简介：Astodeterminetheeffectofpost-remissiontherapyinprolongingsurvivalanddurationofremissionaftercompleteremission,50patientswithAPLIncompleteremissionInducedbyretinolcacid(RA)weredividedintothreegroupsrandomly:(A)30cases,treatedbyalternatechemotherapywithRA;(B)10cases,withRAalone;(C)10cases,onlywithchemotherapy.ThesurvivalcurvesshowedmatGroupAhadthesurvivaltimemorethan1yearIn87.4%,morethan2yearin80.7%.26/30casesweresurvivalandstillinremission,thesurvivalcurvetendtobeaplateauat16months.InGroupBmorethan1yearin45.7%.InGroupC,morethan1yearIn50%.(Keplan-Melerx2=8.93P<0.01).ThisresultshowedthatthealternatechemotherapywithRAforpost-InductionremissiontherapycouldbeusefultoImprovelong-termsurvivorsandtoprolongthedurationofremission.

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简介：FivehundredsandfiftyLACAmicewereusedin3batchesforstudyingtheanticarcinogeniceffectofKonjakupowderonMNNG-inducedlungcancers.Thesemice(withineachbatch)wererandomlyallocatedtofourgroups,namely,positivecontrol(MNNG),Amorphophalluskonjac(A.K.),complex(MNNG+A.K.),andblankcontrol(C)group.InMNNGgroup,MNNG(250μg)wasinjectedintravenouslyoncefivedaysforseventimesineachmouse,thetotaldosageofMNNGbeing1.75mk.InA.K.group,accordingtow/w,8%A.K.waswellmixedinto92%commondietforlong-termbreeding.Incomplexgroup,MNNGwasgivenasthatinMNNGgroupandthemicewererearedasthoseinA.K.group.ThemiceinMNNGgroupandinCgroupwereallrearedbycommondiet.TheresultsshoweddifferentdegreesofanticarcinogenicandpreventiveeffectofrefinedA.K.onMNNG-inducedlungcancersinLACAmice.A.K.notonlyexertedeffectonthenumberofinducedcancerandprecancer,causingadropofthecancerousratefrom70.87%to19.3

简介：Objective:B-celllymphoma2(Bcl-2)isanimportantmemberoftheBcl-2familyofproteinsthatregulatetheinductionofapoptosis.ThisstudyaimstoinvestigatewhetherBcl-2smallinterferingRNA(siRNA)combinedwithmiR-15aoligonucleotides(ODN)couldenhancemethotrexate(MTX)-inducedapoptosisinRajicells.Methods:ChemicallysynthesizedmiR-15aODNandBcl-2siRNAweretransfectedinRajicellsbyusingaHiPerFectTransfectionReagentandthencombinedwithMTX.ExpressionlevelsofBcl-2proteinweredetectedbyWesternblot.CellproliferationwasdeterminedbyCCK8assay.TherateofcellapoptosiswasdeterminedbyAnnexinV/PIdoublestaining.ThemorphologyofapoptoticcellswasobservedbyHoechst-33258staining.Results:AfterthecellsweretransfectedwithmiR-15aODNcombinedwithBcl-2siRNA,Bcl-2proteinlevelswereevidentlydecreased.CCK8assayshowedthatcellproliferationwassignificantlydecreasedandwassignificantlylowerinmiR-15aODNcombinedwithBcl-2siRNAplusMTXgroupthaninmiR-15aODNwithmethotrexategroup,Bcl-2siRNAwithMTXgroup,andsingleMTXgroup(P<0.05).Hoechst33258stainingrevealednumerousapoptoticcells.AnnexinV/PIdoublestainingshowedthattheapoptoticrateswere(13.13±1.60)%,(34.47±2.96)%,(32.87±3.48)%,and(45.47±2.16)%inMTX,Bcl-2siRNAplusMTX,miR-15aODNplusMTX,andmiR-15aODNcombinedwithBcl-2siRNAplusMTXgroups,respectively.Amongthesegroups,theapoptoticrateofmiR-15aODNcombinedwithBcl-2siRNAplusMTXgroupwasthehighest;thisapoptoticratewasalsosignificantlydifferentfromthatofmiR-15aODNorBcl-2siRNAplusMTX(P<0.05).Conclusions:Bcl-2siRNAcombinedwithmiR-15aODNcouldenhanceMTX-inducedapoptosisinRajicells.Bcl-2siRNAandmiR-15acombinedwithMTXmaybeausefulapproachtoimprovethetreatmenteffectsonlymphoma.更多还原

简介：Objective:Toexploretheeffectsofdexamethasone(DXM)andvincristine(VCR)oncytosinearabinoside(Ara-C)inducedapoptosisandactivationofnuclearfactor-κ-genebinding(NF-κB)inleukemiccelllineHL60-n.Methods:ApoptosisofHL60-ncellswasanalysedbyTdT-mediatedX-dUTPnickandendlabeling(TUNEL)andDNAelectrophoresis.NF-κBactivityofHL60-ncellswasdetectedbyelectrophoreticmobilityshiftassay(EMSA).Results:TherewasslightactivationofNF-κBinHL60-ncellswithoutdruginduction.Ara-Cat1μmol/LsignificantlyenhancedtheactivationofNF-κBinHL60-ncells.ThelevelofNF-κBactivationinducedbyDXMat1μmol/LorVCRat0.1μmol/Lhadnosignificantdifferencecomparedwiththatofthecontrolgroup.However,inHL60-ncellspre-treatedwith1μmol/LofDXMor0.1μmol/LofVCR,theactivationofNF-κBinducedby1μmol/LofAra-Cwassignificantlysuppressedwithinhibitionratesof31.0%and47.0%,respectively.TheapoptosisratesofHL60-ncellsinducedby1.0μmol/L,10μmol/Land100μmot/LAra-Cwere45.00±3.16%,61.88±3.40%and77.62±4.75%,respectively.TheapoptoticratesofHL60-ncellsinducedbyDXMat1μmol/LorVCRat0.1μmol/Lweresimilartothatofthecontrolgroup.However,eitherDXMat1μmol/LorVCRat0.lμmol/LcouldenhancetheapoptosisofHL60-ncellsinducedbyAra-Cat1μmol/Lwithratesof39.1%and59.2%,respectively.Conclusion:Ara-CcaninduceapoptosisandactivationofNF-κBinHL60-ncells.ThemechanismofincreasedapoptosisofHL60-ncellsbyDXMorVCRmayberelatedtosuppressionofNF-κBactivation.

简介：Objectives:Toinvestigatetheeffectsofadenovirus-mediatedinduciblenitricoxidesynthasegenetransfectiononbladdertransitionalcellcarcinomaT24cells,andtoprovidenovelinsightsandapproachestoclinicaltherapiesagainstbladdertransitionalcellcarcinoma.Methods:Firstly,constructrecombinantadenovirusvectorpAd-iNOSofiNOS,followedbytransfectionofpAd-iNOSintoHECK293packagingcells.Thirdly,harvestrecombinantadenovirusrAd-iNOSafteramplificationandpurificationprocedures.Finally,transfecttherecombinantadenovirusrAd-iNOSintohumanbladdercarcinomaT24cellsandexaminetheeffectofrAd-iNOStransfectiononapoptosisofT24andpossiblemechanism.Results:Asshownbythisstudy,therecombinantadenovirusrAd-iNOSwasconstructedsuccessfully.Thevirustiterwas5.8×108PFU/mLandrecombinantwasverifiedbyPCRanalysis.TransfectionofadenovirusrAd-iNOSintoT24cellscouldinducesecretionofhighNOconcentration,P53proteinexpressionupregulation,aswellaspromotionofT24cellapoptosis.Conclusions:ThetransfectionofhumanbladdercarcinomaT24cellsfromrecombinantadenovirusrAdiNOSwasconfirmedtoinduceintracellulariNOSover-expression,highproductionofNO,up-regulationofintracellularP53expressionandpromotionofcellapoptosis.