简介：甲醇摘录ofStellerachamaejasmeL被antitumor为antitumor活动估计对鼠科的白血病P388invivo的活跃生物鉴定。摘录的bioassay-directcd分离供应了七diterpene混合物(stellerarin，stelleramacrin，gnidimacrin，pimelea因素P2，subtoxin，huratoxin，simplexin)并且二biflavanone混合物(neochemae茉莉属A和B)。在他们之中，gnidimacrin，stellerarin和stelleramacrin(新奇混合物)被发现对P388，L1210和K562invivoandinvitro有高antitumor和细胞毒素的活动。结果建议diterpene混合物是有势力antitumorprinciplesofStellerachamaejasmeL。

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简介：Havingbeenpassedfor160generations,acelllinedesignatedasH22-F25/LwasestablishedfromamurinetumorlymphaticmetastatlcmodelH22-F25whichhadbeensetupinourcollege.Thecelllinewasinsuspensionculturewitharapidproliferationandstablegrowth.Thepeaktuneofcelldivisionandproliferationwas48and96hoursafterculture.Inaweek,thecellnumberwasIncreasedby25tunes.H22-F25/Lstillkeepsthefeaturesofapoorlydifferentiatedcancer.Itstumorinducingrate(invivo)was100%in615mice.Lymphnodemetastasisratewas50%andpulmonarymetastasisrate10%.H22-F25/LIsapopulationofheterogenetlctumorcellsIncluding2stemcelllines(themodelnumberofchromosomesbeing43in40%tumorcellsand86in32%)andsomesidelines.ThecommonmarkerchromosomesM1,M2,M3andM4werepresentinallstemandsidelines.

简介：TheresponsetosingleheattreatmentandStep-downheat(SDH)treatmentinvitroofV79andLcellswasstudied.Colony-formingabilitywasassayedinmediumaftertreatmentinvitro.Time-responsecurveswereestablishedandsubjectedtoArrheniusanalysis.TheArrheniuscurvesshowedinflectionpointsat43℃forV79cellsandat42℃forLcells.Theactivationenergieswere145kcal/moleand400kcal/moleaboveandbelow43℃(P<0.05),respectively,forV79cells,while160kcal/moleand300kcal/moleaboveandbelow42℃(P<0.05),respectively,forLcells.ThermosensitivityofLcellsaremarkedlyhigherthanV79cells.BothV79andLcellsweresensitizedbySDH.TheSDHeffectwascharacterizedbyareductioninshoulder(anadditioneffecttosublethaldamage),anincreaseinslope(thermosensitization),andthedelayanddisappearanceofthermotolerant"tail"forV79andLcellsat45℃to40℃and44℃to42℃SDHtreatmentrespectively.Particularly,42℃to39℃or42℃to40℃SDHforLc

简介：Objective:TolookforthefurtherevidenceforHPVL1HPV16E6,HPV18E6andEBVascarcinogenicfactorsinlaryngealcarcinoma.Method:weexaminedrepresentativenumbersofspecimensfromlaryngealcancerwithhighlysensitivePCRtechniqueforthepresenceofHPVL1andhigh-risktypesHPV16E6,HPV18E6andEBVLMP1.Results:UsingPCRdetection,7.3%sampleswereHPVL1positive,52.03%wereHPV16E6positive,30.89%wereHPV18E6positiveand9.13%wereEBVLMP1positive.ThelowincidenceofHPVL1andhighincidenceofHPV-16E6andHPV18E6genessuggestthatHPVmightbeintegratedintotumorcells.OurresultssupportaroleofHPV-16andHPV-18infectioninthepathogenesisoflaryngealcarcinomainChina.Conclusion:IntegrationofE6intohostgenomeandstableexpressionofthesegenesmaybeassociatedwiththecarcinogenesisoflaryngealcarcinoma.HPV-16andHPV-18maysynergisticallyfunctiononthepathogenesisoflaryngealcarcinoma.Ourresultssuggestanassociationoflaryngealcarcinogenesisandinfectionwiththehigh-riskHPVtypes16,HPV18andEBV.

简介：客观：为了改进倔强的脸中部的外部T房间non-Hodgkin鈥檚的功效，有L天门冬氨酰胺酶(LASP)的淋巴瘤(MPTC-NHL)基于抢救化疗。方法：有倔强的MPTC-NHL的21个病人被分析，11patients(LASP组)收到了L天门冬氨酰胺酶基于的抢救化疗由L天门冬氨酰胺酶，长春新碱和dexame-thosone组成。没有L天门冬氨酰胺酶，10个病人(控制组)收到了抢救联合化疗。结果：完全的宽恕率为LASP组是45.6%，0.0%为控制组织(P<0.05)。全面反应率(CR+PR)为LASP组是63.6%，10.0%为控制组织，分别地(P<0.05)。2年的幸存率为LASP组是45.5%，0.0%为控制组织(P<0.05)。LASP的主要不利效果是白细胞减少，浆液bilirubin和多糖症的举起。结论：LASP基于的初步的临床的学习表演抢救化疗可以与倔强的MPTC-NHL改进反应率和病人的2年的幸存率。进一步继续学习是必要的。

简介：Objective:Tostudytheeffectofactivecompound6FandAfromPterissemipinnataL.(PsL)ontheactivitiesofDNAtopoisomerase(TOPO)IandII,activitiesofcytosolicandmembraneTPK,andexpressionofoncogenec-mycinlungadenocarcinomacells.Methods:Theeffectofcompound6FandAonactivitiesofcytosolicandmembraneTPKwasmeasuredbyscintillationcounting;theeffectofcompoundAonexpressionofoncogenec-mycwasdeterminedbyflowcytometryindirectfluorimetry.Results:compound6FandAcouldinhibittheactivitiesofTOPOI,andtheystronglyinhibitedtheTOPOIIin0.01mg/Land10.0mg/Lrespectively.CompoundAslightlyinhibitedtheactivitiesofmembraneTPK,butnotthecytosolicone.CompoundAcouldinhibittheexpressionofoncogenec-myc.Conclusion:Topoisomerasesaretargetofcompound6FandA.CompoundAcouldslightlyinhibittheactivitiesofTPK,andshowedaninhibitoryeffectontheexpressionofoncogenec-myc.