简介：Wehavereviewedthegenetherapyingastrointestinaldiseases^[1].GastriccanceriscommoninChina^(2-20),anditsearlydiagnosisandtreatmentarestilldifficultuptonow^(13-36).Theex-pressionofanexogenousgeneintroducedbygenetherapyintopa-tientswithgliomascanbemonitorednon-invasivelybypositron-emissiontornography^[4].

简介：AIM:Toconductasystematicreviewofthepublishedepidemiologicalstudiesinvestigatingtheassociationoftheinteractionsbetweengenevariantsanddietaryintakewithgastriccancerrisk.METHODS:AliteraturesearchwasconductedinPubMed,EMBASE,andMEDLINEforarticlespublishedbetweenJanuary2000andJuly2013,and38studieswereidentified.Previousstudiesincludedvariousdietaryfactors(e.g.,fruitsandvegetables,soybeanproducts,salt,meat,andalcohol)andgeneticvariantsthatareinvolvedinvariousmetabolicpathways.RESULTS:Studiessuggestthatindividualswhocarryhigh-riskgeneticvariantsanddemonstrateparticulardietaryhabitsmayhaveanincreasedriskofgastriccancercomparedwiththosewhodonotcarryhigh-riskgeneticvariants.Distinctivedietarypatternsandvariationsinthefrequencyofgeneticvariantsmayexplainthehigherincidenceofgastriccancerinaparticularregion.However,mostpreviousstudieshavelimitations,suchasasmallsamplesizeandaretrospectivecasecontroldesign.Inaddition,paststudieshavebeenunabletoelucidatethespecificmechanismingene-dietinteractionassociatedwithgastriccarcinogenesis.CONCLUSION:Additionallargeprospectiveepidemiologicalandexperimentalstudiesarerequiredtoidentifythegene-dietmetabolicpathwaysrelatedtogastriccancersusceptibility.

简介：瞄准：为了由学习在IFN-gamma基因多型性，包括的IFN-gamma+874A/T单个核苷酸多型性(SNP)和CA之间的关系探索孩子的危险性到子宫内的HBV感染，重复微卫星多型性和子宫内的HBV感染。方法：在IFN-gamma+874A/T单个核苷酸多型性的TaqMan荧光聚合酶链反应在子宫内的HBV感染组被测试(组我)并且孩子们组织的正常免疫者(组II)。毛状的电气泳动在上述二个组被执行到试金IFN-gammaCA重复微卫星多型性。结果：AA的频率，在并且TT遗传型在感染组织的子宫内的HBV是67.4%，19.6%和13.0%，并且45.2%，30.1%和24.7%分别地在正常有免疫力的孩子组织。有效差量在在二个组之间的IFN-gamma+874遗传型的频率分发被发现(chi2=5.102，P=0.02389)。在子宫内的HBV感染组，AA遗传型比在正常免疫者组织是更普通的。IFN-gamma+874A等位基因的频率在子宫内的HBV感染组是77.17%，并且60.27%在正常有免疫力的孩子组织。在子宫内的HBV感染组，IFN-gamma+874A等位基因比在正常免疫者组织是更普通的。有效差量在在二个组之间的频率分发被发现(chi2=7.238，P=0.02389，或=2.228，95%CI=1.244-3.992)。(CA12)IFN-gammaCA微卫星多型性的+/(CA12)+在子宫内的HBV感染组是11.90%，26.47%在正常有免疫力的孩子组织。有效差量在在二个组之间的频率分发被发现(chi2=5.64，P=0.0176)。IFN-gammaCA重复的频率在子宫内的HBV感染组是25%，43.38%在正常有免疫力的孩子组织。IFN-gammaCA重复的频率比在正常免疫者组织是在子宫内的HBV感染组的更少。有效差量在在二个组之间的频率分发被发现(chi2=7.548，P=0.0060)。结论：在IFN-gamma+874A/TSNP和子宫内的HBV感染之间以及在IFN-gammaCA微卫星多型性和子宫内的HBV感染之间有一种关系。IFN-gamma基因多型性可能在决定个人的危险�

简介：AIM:ToinvestigatetheeffectofhepatitisBvirus(HBV)XgeneonapoptosisandexpressionsofapoptosisfactorsinXgene-transfectedHepG2cells.METHODS:TheHBVXgeneeukaryonexpressionvectorpcDNVA3-XwastransientlytransfectedintoHepG2cellsbylipid-mediatransfection.UntransfectedHepG2andHepG2transfectedwithpcDNA3wereusedascontrols.ExpressionofHBxinHepG2wasidentifiedbyPT-PCR.MTTandTUNELwereemployedtomeasureproliferationandapoptosisofcellsin.threegroups.Semi-quantifiedRT-PCRwasusedtoevaluatetheexpressionlevelsofFas/FasL,Bax/Bcl-xL,andc-mycineachgroup.RESULTS:HBVXgenewastransfectedintoHepG2cellssuccessfully.RT-PCRshowedthatHBxwasonlyexpressedinHepG2/pcDNA3-Xcells,butnotexpressedinHepG2andHepG2/pcDNA3cells.AnalyzedbyMTT,cellproliferationcapacitywasobviouslylowerinHepG2/pcDNA3-Xcells(0.08910±0.003164)thaninHepG2(0.14410±0.004927)andHepG2/pcDNA3cells(0.12150±0.007159)(P＜0.05andP＜0.01).AnalyzedbyTUNEL,cellapoptosiswasmuchmoreinHepG2/pcDNA3-Xcells(980/2000)thanHepG2(420/2000),HepG2/pcDNA3cells(520/2000)(P＜0.05andP＜0.01).Evaluatedbysemi-quantifiedRT-PCR,theexpressionlevelofFas/FasLwassignificantlyhigherinHepG2cellstransfectedwithHBxthaninHepG2andHepG2/pcDNA3cells(P＜0.05andP＜0.01).Bax/Bcl-xLexpressionlevelwasalsoelevatedinHepG2/pcDNA3-Xcells(P＜0.05andP＜0.01).Expressionofc-mycwasmarkedlyhigherinHepG2/pcDNA3-XcellsthaninHepG2andHepG2/pcDNA3cells(P＜0.05andP＜0.01).CONCLUSION:HBVXgenecanimpaircellproliferationcapacity,improvecellapoptosis,andupregulateexpressionofapoptosisfactors.TheinterventionofHBVXgeneontheexpressionofapoptosisfactorsmaybeapossiblemechanismresponsibleforthechangeincellapoptosisandproliferation.

简介：AIMTocompareKAI1incancerofpapillaofVaterandpancreastoevaluatewhethertherearedifferencesinbiologicbehaviorwhichmightaccountforprognosis.METHODSWecomparedtheexpressionin24papillayand29pancreaticcancersusingNorthernblotanalysis,immunochemicalassayandinsituhybridization,andinvestigatedwhetherearlydiagnosisormoleculardifferencespredicttheoutcomeinthesetumorentities.RESULTSByNorthernblotanalysisthereisnostatisticaldifferenceofKAI1levelsinnormalandcancerouspapilla.NoassociationbetweenKAI1mRNAexpressionandtumorstageortumordifferentiationwasfoundinthetumors.Byimmunohistochemicalassay,KAI1stainingincytoplasmofpapillarycancercellswassimilartothatofnormalpapillarycells.Byinsituhybridization,theresultsofKAI1mRNAexpressioninnormalandcancerouspapillaweresimilartothosewithimmunohistochemicalassay.Thenormalandcancerouspancreastissueswerealsoanalyzedbythemethodsusedinpapillarysamples.CONCLUSIONAlthoughthebiologicrolesofKAI1havenotbeenclarified,ourresultssuggestthatKAI1mayrestricttheprogressionofmalignantpapillarycancer,butitsexpressionmightnothaveanyeffectonthecharacteristicsofpapillarytumor,whereasbytheanalysisofKAl1gene,itsreducedexpressioniscloselyrelatedtotheprogressionandmetastasesofpancreaticcancer.

简介：AIM:Toinvestigatethemutationsofthe5'noncodingregionofBCL-6geneinChinesepatientswithprimarygastriclymphomas.METHODS:PCRanddirectDNAsequencingwereusedtoidentifyBCL-6genemutationsinthe5'noncodingregionin29casesofgastricdiffuselargeB-celllymphoma(DLBCL)and18casesofgastricmucosa-associatedlymphoidtissue(MALT)lymphomaaswellas10casesofreactivehyperplasiaoflymphnode(LRH).RESULTS:Sixof29gastricDLBCLs(20.7%),4of18gastricMALTlymphomas(22.2%)and1of10LRHs(10%)werefoundtohavemutations.Allmutationsweresingle-basesubstitutionsandthefrequencyofsingle-basechangeswas0.20x10-2-1.02x10-2perbp.CONCLUSION:Pointmutationsinthe5'noncodingregionofBCL-6genearefoundinChinesepatientswithprimarygastricDLBCLsandMALTlymphomas,suggestingthattheymay,insomeextent,participateinthepathogenesisofprimarygastricDLBCLsandMALTlymphomas.

简介：AIM:Toinvestigatewhethergenemethylationintheperitonealfluid(PF)predictsperitonealrecurrenceingastriccancerpatients.METHODS:ThegenemethylationofCHFR(checkpointwithforkheadandringfingerdomains),p16,RUNX3(runt-relatedtranscriptionfactor3),E-cadherin,hMLH1(mutLhomolog1),ABCG2(ATP-bindingcassette,sub-familyG,member2)andBNIP3(BCL2/adenovirusE1B19kDainteractingprotein3)wereanalyzedin80specimensofPFbyquantitativemethylation-specificpolymerasechainr...

简介：瞄准：评估在人的肝细胞癌的房间增长和apoptosis上的基因衬里的人的易碎的组氨酸三个一组(FHIT)的禁止的效果Hep3B在试管内。方法：包括FHIT基因的功能的区域的recombinantpcDNA3.1(+)/FHIT被构造并且转了进人的肝细胞癌房间在试管内。mRNA和在transfected房间的FHIT基因的蛋白质表示被RT-PCR和西方的污点分别地检测。增长上的FHIT的效果被MTT试金检测。在房间周期和apoptosis的变化是由流动血细胞计数的assayed。五只老鼠收到了Hep3B-FHIT的下的移植；5只老鼠作为控制收到了正常Hep3B和Hep3B-C的下的移植。裸体老鼠和肿瘤生长的体重被测量。结果：RT-PCR和西方的污点分析证明FHIT-mRNA和FHIT蛋白质的表示水平在在有pcDNA3.1(+)/FHIT的感染以后的Hep3B房间是更高的。与pcDNA3.1(+)/FHIT对待的Hep3B细胞的生长显著地被禁止。pcDNA3.1(+)/FHIT-transfectedHep3B房间在G0-G1阶段显示出显著地更高的房间率并且与控制比较增加了apoptosis(P<0.05)。移植肿瘤的生长被FHIT显著地禁止。从Hep3B-FHIT房间产生的肿瘤比那些从Hep3B和Hep3B-C房间产生晚很发生了。Hep3B-FHIT房间的生长是慢的，肿瘤体积是低的。结论：FHIT基因的转导变异禁止人的肝细胞癌细胞的生长并且导致细胞apoptosis在活体内和在试管内。

简介：瞄准：调查影响他我有教养的老鼠小岛的生存能力和功能上的oxygenase-1(HO-1)基因转移在试管内。方法：小岛被管内胶原酶消化从Sprague-Dawley老鼠的胰孤立，并且由不连续的Ficoll密度坡度远心沉淀净化了。净化的老鼠小岛是有包含人的HO-1基因(Ad-HO-1)的adenoviral向量的transfected或提高了绿荧光灯的蛋白质基因(Ad-EGFP)，然后为七天有教养。Transfection被萤光显微镜检查和西方的污点证实。小岛生存能力被氮蒽orange/propidium碘化物评估荧光灯的染色。刺激葡萄糖的胰岛素版本用胰岛素放射性免疫测定工具包被检测并且被用来估计小岛的功能。刺激索引(SI)被在低葡萄糖刺激之上由胰岛素版本在高葡萄糖刺激之上划分胰岛素版本计算。结果：在七种天文化以后，有教养的老鼠小岛的生存能力显著地减少了(92%+/-6%对52%+/-13%，P<0.05)，并且刺激葡萄糖的胰岛素版本也显著地减少了(6.47+/-0.55mIU/L/30IEQ对4.57+/-0.40mIU/L/30IEQ，14.93+/-1.17mIU/L/30IEQ对9.63+/-0.71mIU/L/30IEQ，P<0.05)。有在20的MOI的adenoviral向量的老鼠小岛的Transfection是有效的，并且没损害小岛功能。在7dpost-transfection，Ad-HO-1transfected小岛的生存能力比控制小岛的高(71%+/-15%对52%+/-13%，P<0.05)。在Ad-HO-1transfected组之中在在低葡萄糖刺激(2.8mmol/L)之上的胰岛素版本没有有效差量，Ad-EGFPtransfected组织，并且控制组织P>0.05)，当时当由高葡萄糖(16.7mmol/L)刺激了时答案，在Ad-HO-1transfected组的胰岛素版本比在Ad-EGFP，transfected组织并且控制组显著地高，分别地(12.50+/-2.17mIU/L/30IEQ对8.87+/-0.65mIU/L/30IEQ；12.50+/-2.17mIU/L/30IEQ对9.63+/-0.71mIU/L/30IEQ，P<0.05)。Ad-HO-1transfected组的SI比Ad-EGFP，transfected组织并且控制组也显著地高，分

简介：AIMTocharacterizepunctualmutationsin23SrRNAgeneofclarithromycin-resistantHelicobacterpylori(H.pylori)anddeterminetheirassociationwiththerapeuticfailure.METHODSPCRproductsof23SrRNAgeneVdomainof74H.pyloriisolates;34resistanttoclarithromycin(29fromalow-riskgastriccancer(GC)population:Tumaco-Colombia,and5fromahigh-riskpopulation:Tuquerres-Colombia)and40fromasusceptiblepopulation(28fromTumacoand12fromTúquerres)weresequencedusingcapillaryelectrophoresis.TheconcordancebetweenmutationsofVdomain23SrRNAgeneofH.pyloriandtherapeuticfailurewasdeterminedusingtheKappacoefficientandMcNemar’stestwasperformedtodeterminetherelationshipbetweenH.pylorimutationsandclarithromycinresistance.RESULTS23SrRNAgenefromH.pyloriwasamplifiedin56/74isolates,ofwhich25wereresistanttoclarithromycin(20fromTumacoand5fromTúquerres,respectively).In17resistantisolates(13fromTumacoand4fromTúquerres)thefollowingmutationswerefound:A1593T1,A1653G2,C1770T,C1954T1,andG1827CinisolatesfromTumaco,andA2144GfromTúquerres.ThemutationsT2183C,A2144GandC2196TinH.pyloriisolatesresistanttoclarithromycinfromColombiaarereportedforthefirsttime.NoassociationbetweentheH.pylorimutationsandinvitroclarithromycinresistancewasfound.However,therapeuticfailureoferadicationtreatmentwasassociatedwithmutationsof23SrRNAgeneinclarithromycin-resistantH.pylori(κ=0.71).CONCLUSIONThetherapeuticfailureoferadicationtreatmentinthetwopopulationsfromColombiawasassociatedwithmutationsofthe23SrRNAgeneinclarithromycinresistantH.pylori.

简介：AIM:TOexplorethefeasibilityofenhancingapoptosis-inducingeffectsofchemotherapeuticdrugsonhumangastriccancercellsbystabletransfectionofextrinsicSmacgene.METHODS:AfterSmacgenewastransferredintogastriccancercelllineMKN-45,subclonecellswereobtainedbypersistentG418selection.CellularSmacgeneexpressionwasdeterminedbyRT-PCRandWesternblotting.Aftertreatmentwithmitomycin(MMC)asanapoptoticinducer,invitrocellgrowthactivitieswereinvestigatedbytrypanblue-stainingmethodandMI-Icolorimetry.Cellapoptosisanditsratesweredeterminedbyelectronicmicroscopy,annexinV-FITCandpropidiumiodidestainingflowcytometry.Cellularcaspase-3proteinexpressionanditsactivitieswereassayedbyWesternblottingandcolorimetry.RESULTS:WhencomparedwithMKN-45cells,theselectedsubclonecelllineMKN-45/SmachadsignificantlyhigherSmacmRNA(3.12±0.21vs0.82:1:0.14,t=7.52,P<0.01)andproteinlevels(4.02±0.24vs0.98:1:0.11,t=8.32,P<0.01).Aftertreatmentwith10μg/mLMMCfor6-24h,growthinhibitionrateofMKN-45/Smac(15.8±1.2-54.8±2.9%)wassignificantlyhigherthanthatofMKN-45(5.8±0.4-24.0±1.5%,t=6.42,P<0.01).PartialMKN-45/Smaccancercellspresentedcharacteristicmorphologicalchangesofapoptosisundertheelectronicmicroscopewithanapoptosisrateof36.4=1=2.1%,whichwassignificantlyhigherthanthatofMKN-45(15.2±0.8%,t=9.25,P<0,01).ComparedwithMKN-45,caspase-3expressionlevelsinMKN-45/Smacwereimprovedsignificantly(3.39±0.42vs0.96:1:0.14,t=8.63,P<0.01),whileitsactivitieswere3.25timesasmanyasthoseofMKN-45(0.364±0.010vs0.112:1:0.007,t=6.34,P<0.01).CONCLUSION:StabletransfectionofextrinsicSmacgeneanditsover-expressioningasbiccancercelllinecansignificantlyenhancecellularcaspase-3expressionandactivities,ameliorateapoptosis-inducingeffectsofmitomycinConcancercells,whichisanovelstrategytoimprovechemotherapeuticeffectsongastriccancer.

简介：AIM:Toinvestigatetheassociationbetweenendogenousgeneexpressionandgrowthregulationincludingproliferationandapoptosisinducedbytransforminggrowthfactor-β1(TGF-β1)inhumangastriccancer(GC)cells.METHODS:Reversetranscriptionpolymerasechainreaction(RT-PCR)wasperformedtodetectthemaincomponentsoftheTGF-β1/SmadssignalpathwayinhumanpoorlydifferentiatedGCcelllineBGC-823.LocalizationofSmadproteinswasalsodeterminedusingimmunofluorescence.Then,theBGC-823cellswereculturedinthepresenceorabsenceofTGF-β1(10ng/mL)for24and48h,andtheeffectsofTGF-β1onproliferationandapoptosisweremeasuredbycellgrowthcurveandflowcytometry(FCM)analysis.TheultrastructuralfeaturesofBGC-823cellswithorwithoutTGF-β1treatmentwereobservedundertransmissionelectronmicroscope.Theapoptoticcellswerevisualizedbymeansoftheterminaldeoxynucleotidyltransferase(TdT)-mediateddTUPinsitunickend-labeling(TUNEL)method.Meanwhile,theexpressionlevelsofendogenousp15,p21andSmad7mRNAandthecorrespondingproteinsinthecellsweredetectedat1,2and3haftercultureinthepresenceorabsenceofTGF-β1(10ng/mL)bysemi-quantitativeRT-PCRandWesternblot,respectively.RESULTS:TheTGF-β1/SmadsignalingwasfoundtobeintactandfunctionalinBGC-823cells.ThegrowthcurverevealedthemostevidentinhibitionofcellproliferationbyTGF-β1at48h,andFCMassayshowedG1arrestaccompaniedwithapoptosisinducedbyTGF-β1.ThetypicalmorphologicalchangesofapoptosiswereobservedincellsexposedtoTGF-β1.Theapoptosisindex(AI)inTGF-β1-treatedcellswassignificantlyhigherthanthatintheuntreatedcontrols(10.7±1.3%vs0.32±0.06%,P＜0.01).Thelevelsofp15,p21andSmad7mRNAandcorrespondingproteinsincellsweresignificantlyup-regulatedat1h,butgraduallyreturnedtobasallevelsat3hfollowingTGF-β1(10ng/mL)treatment.CONCLUSION:TGF-β1affectsbothproliferationandapoptosisofGCcellsth

简介：AIM:TotestthehypothesisthatE-cadheringene(CDH1)C-160Apromotervariantgenotypeisassociatedwithanincreasedriskfordevelopinggastriccancer.METHODS:Inthispopulation-basedcase-controlstudyofgastriccancerinJiangsuProvince,China,weperformedpolymerasechainreaction-restrictionfragmentlengthpolymorphism(PCR-RFLP)togenotypetheC-160ApolymorphismofCDH1promoterin206non-cardiagastriccancerpatientsand261age-andsex-matchedbutunrelatedcancer-freecontrols.RESULTS:ThefrequenciesofgenotypesCC,CAandAAwere57.8%,36.4%and5.8%ingasfriccancercases,respectively,and58.2%,34.9%and6.9%incontrolsrespectively.ThedistributionsofCDH1genotypeswerenotsignificantlydifferentbetweengastriccancercasesandcontrols(P=0.87forgenotypefrequencyandP=0.92forallelefrequency).ComparedwiththeCCgenotype,theCAandAAgenotypeswerenotassociatedwithanincreasedriskfornon-cardiagastriccancer(adjustedoddsratios(OR)=1.15,and95%confidenceinterval(95%CI)=0.78-1.72forCAgenotype,andOR=0.90and95%CI=0.42-2.01forAAgenotype).CONCLUSION:E-cadheringeneC-160Apromoterpolymorphismmaynotplayamajorroleintheetiologyofnon-cardiagastriccancerinChinesepopulation.

简介：瞄准：测试假设这项活动的那改进他我有与周期性的肝损伤联系的纤维发生的过程的氧合酶罐头interfere，我们调查了在表示上的治疗学的潜力他我在CCl(4)的oxygense-1劝诱了微榴状的肝硬化模型。方法：带老鼠HO-1或GFP基因的Recombinant联系adeno的病毒被产生。1x10(12)联系adeno的病毒的vg在肝的正式就职的时候通过门注射被管理纤维变性。结果：有由rAAV/HO-1的HO-1的在表示上的老鼠肝显著地增加了的调节以一种稳定的方式的HO酶的活动。微榴状的肝硬化的开发显著地作为与控制相比在rAAV/HO-1-transduced动物被禁止。门静脉高血压显著地作为与控制相比在rAAV/HO-1-transduced动物被减少，而在收缩血压没有重要变化。这发现伴有激活的改进的肝生物化学，更少的渗透的巨噬细胞和更少在rAAV/HO-1-transduced肝的肝的星形细胞(HSC)。结论：改进惊讶在肝的活动压制肝硬化的发展。

简介：瞄准：到表示人的gastric-cancer-related基因介绍的分析，GCRG123在人的胃的图章戒指房间癌纸巾，并且在GCRG123上执行生物信息学分析。方法：原位杂交被用来在嵌入石蜡的胃的纸巾探索GCRG123表示模式，包括图章戒指房间癌的15个盒子，15肠类型的腺癌，和15正常胃粘膜。北弄污被用来在在胃图章戒指房间癌和肠类型的腺癌纸巾之间的GCRG123表示分析差别。包括强风，Multalin和叫，联机软件被申请生物信息学分析。生物工学信息(NCBI)和加利福尼亚大学圣克鲁斯(UCSC)的国家中心数据库被用于分析。结果：当蓝色猛抛，原位杂交信号出现了限制了为细胞质。十从胃的环状体房间癌，正常胃的粘膜上皮和幽门腺的15个盒子显示出高GCRG123表示。低GCRG123表示在胃的肠类型的腺癌和正常胃腺被观察。北弄污表明GCRG123在图章戒指房间癌组织是起来调整的但是在肠类型的腺癌组织下面调整。强风和Multalin分析表明GCRG123顺序与人的长散布的原子元素retrotransposons的ORF2顺序有92%类似(LINE-1，L1)。叫分析显示了印射到所有染色体的那GCRG123。GCRG123被发现在Rb，IL-2的5'flanking区域和凝固第九因子基因的intron-17和-23集成。结论：GCRG123，L1家庭的一个积极成员，在人的胃的图章戒指是起来调整的房间癌。

简介：AIM:Toobservethereversaleffectsofwide-typep53geneonmulti-drugresistanceto5-FU(LOVO/5-FU).METHODS:AftertreatmentwithAd-p53,LOVO/5-FUsensitivityto5-Fuwasinvestigatedusingtetrazoliumdyeassay.Multidrugresistancegene-1(MDR1)geneexpressionwasassayedbysemi-quantitativereversetranscriptionpolymerasechainreactionandtheexpressionofp53proteinwasexaminedbyWesternblotting.RESULTS:Thereversalactivityaftertreatmentwithwidetypep53genewasincreasedupto4.982foldat48h.TheexpressionofMDR1genedecreasedsignificantlyaftertreatmentwithwide-typep53gene,andtheexpressionofp53proteinlastedforabout5d,withapeakat48h,andbegantodecreaseat72h.CONCLUSION:Wide-typep53genehasaremarkablereversalactivityforthehighexpressionofMDR1geneincolorectalcancers.Thereversaleffectsseemtobeinatimedependentmanner.Itmighthavegoodprospectsinclinicalapplication.