简介:Thetitlecompoundchlorpropham(CASnumber:101-21-3,C10H12ClNO2,Mr=213.66)waspreparedbytheadditionreactionof3-chlorophenylisocyanatewithisopropanol.Spectraldata,IR,NMRandMS,werereported.ThispaperprovidessomerelatedinformationaboutRegulatoryStatus,ToxicologicalEffects,EcologicalEffectsandEnvironmentalFatealso.
简介:Ameloblastomaisabenignbutlocallyaggressiveodontogenieneoplasmthataccountsfor10%ofalltumorsarisinginthemandibleandmaxilla(1).Eightypercentofameloblastomasariseinthemandible,andtheyareusuallyfoundinyoungadults.Itfrequentlyrecursifnotadequatelyresected.Therefore,thestandardtherapyforthistumoriscompleteboneresectionwithanadequatemarginofsafety:marginalorsegmentalosteotomy.However,aestheticdeformities,functionalimpairmentsandpsychologicalimpairmentsafterradicalsurgeryforlargeameloblastoma,havebeenseriousissues(1).
简介:Apotentialdualinhibitor(4)forexogenousabsorptionandendogenicsynthesisofcholesterolwasdesignedbasedontheconjugationoftheβ-lactampharmacophoreofezetimibeandtheδ-lactonepharmacophoreofstatins.Themergerofezetimibeandstatin4wassynthesizedfromp-hydroxybenzaldehydethroughaten-steproute.1HNMRanalysisshowedexistenceoffourpairsofenantiomers(5.7:5.7:1:1,molarratio).Andcompound4wasfoundtolowertotalglucose(TG)levelinratserumviaahigh-cholesterolandhigh-fatfeedingexperiment.
简介:Objective:ToinvestigatetheeffectsofE7080andN5-(1-iminoethyl)-L-ornithinedihydrochloride(L-NIO)oncolorectalcanceraloneandincombination.Methods:HT29colorectalcancercelllinefromSapInstitutewasused.Real-timecellanalysis(xCELLigencesystem)wasperformedtodeterminetheeffectsofE7080andL-NIOoncolorectalcellproliferation.WhileapoptosiswasdeterminedwithAnnexinVstaining,andtheeffectofagentsonangiogenesiswasdeterminedwithchorioallantoicmembrane(CAM)model.Results:WefoundthatE7080hasastrongantiproliferativeeffectwithanhalfmaximuminhibitionofconcentration(IC50)valueof5.60×10–8mol/L.AlsoithasbeenobservedthatE7080showedantiangiogenicandapoptoticeffectsonHT29colorectalcancercells.AntiangiogenicscoresofE7080were1.2,1.0and0.6for100,10and1nmol/LE7080concentrations,respectively.Furthermore,apoptosishasbeendetectedin71%ofHT29colorectalcancercellsafteradministrationof100nmol/LE7080whichmayindicatestrongapoptoticeffect.MeanwhileadministrationofL-NIOalonedidnotshowanyeffect,butthecombinationofE7080withL-NIOincreasedtheantiproliferative,antiangiogenicandapoptoticeffectsofE7080.Conclusions:ResultsofthisstudyindicatethatE7080maybeagoodchoiceintreatmentofcolorectaltumors.FurthermoretheincreasedeffectsofE7080whencombinedwithL-NIOraisethepossibilitytousealowerdoseofE7080andthereforeavoid/minimizethesideeffectsobservedwithE7080.
简介:[摘要 ]: JAK/STAT信号通路参与体内多种细胞的增殖、分化及免疫调节等过程,这一通路更参与与造血干细胞的存活、增殖、分化等有关的细胞因子的表达。当信号通路过度激活时,将与多种血液系统疾病密切相关。芦可替尼是一种非选择性 JAK1/2抑制剂,可有效阻断 JAK/STAT信号通路过度激活,在治疗相关疾病中发挥不容忽视的作用。本文就此进行综述。
简介:BOUNDEDNESSANDBLOWUPFORTHEGENERALACTIVATOR-INHIBITORMODELLiMINGDE(李名德);CHENSHAOHUA(陈绍华);QINYUCHUN(秦禹春)(DepartmentofMathematic...
简介:TheethanecrackeratasteamcrackerofYangziPetrochemicalCompany(YPC)hasbeensafelyoperatingformorethan100dayssinceapplicationofdomesticN360cokeinhibitorstartingAugust28,2004tosetanewrecordontheoperatingcycleofethanecracker,whichhasrevealedgreatsuccessincommercialapplicationofthisinhibitor.
简介:Cisplatindamagescochlearhaircellsandspiralganglionneuronsthroughcelldeathsignalingpathwaysthatarenotfullyunderstood.Weusedfocusedapoptosisgenemicroarraystostudyearlychangesingeneexpres-sionincochlearculturesfromP3neonatalratstreatedwithcisplatin(0.2mM).After12hoursofcisplatintreat-ment,morethan50%ofthe96genesonthearrayshowedasignificantdecreaseinexpression,consistentwithwidespreadcelldeath.However,after3hoursofcisplatintreatment,10genesshowedsignificantincreaseinex-pressionintotalcochleartissue.Inexperimentswithsubsetsofcochleartissues,at3h,cisplatininducedincreasedexpressionof12genesinthecochlearsensoryepithelium(basilarmembrane)and11genesinthespiralganglion(tissueofRosenthal'scanal,containingthespiralganglion).Theseincludedpro-andanti-apoptoticgenesin-volvedinthep53signalingpathway,TNFreceptorfamily,NF-kappaBpathway,deathdomainfamily,deatheffec-tordomainfamily,Bcl-2family,CARDfamily,TRAFfamily,andGTPsignaltransduction.Althoughthechangesingeneexpressionshowedanoverlapbetweenbasilarmembraneandspiralganglion,otherchanges,whichmayreflecttheuniqueresponseofeachtissue,werealsoobserved.Pifithrin-αblockedcisplatin-inducedup-regulationofgenesinthep53signalingpathwaywhenassayedbybothsuperarrayandrealtimePCR.Thedataaddtoourunderstandingoftheinvolvementofp53incisplatin-inducedototoxicityandotoprotection,conferredbythep53inhibitorPifithrin-α.
简介:Here,theissueofrobustnessanalysisofcellJAK-STATsignaltransductionnetworksisaddressed.ThisisinvestigateduponamathematicalmodelofIFN-γinducedJAK-STATsignalingpathwaybyapplyingrobustnessanalysiswhichisbasedonabroadrangeofsimultaneousandsystematicalparametersvariation.Theeffectsofthevariationsoftheinitialsignalproteins'concentrationsontheoutputofthissystemarealsostudied.ThestudydemonstratesthattheJAK-STATsignalingpathwayisrobustwithrespecttoits"signaltime"and"signalduration",butsensitivewithrespecttoits"signalamplitude".Theseanalysisresultscanpointtoexperimentaldesignsthatcanfurthertesthowthepathwayactivitycanbeperturbed.
简介:ObjectiveThisstudywasinitiallydesignedtoevaluatetheeffectofcelecoxibontheregimenof5-fluorouracil,epirubicin,andcyclophosphamide(FEC)combination,followedbydocetaxel(T)inneoadjuvantsetting.AnunplannedpreliminaryreviewonsafetywasconductedafterahaltofthestudyduetotheconcernedpotentialcardiovascularriskofusingCOX-2inhibitors.MethodsWestudied23consecutivecasesofoperablebreastcancerhavingreceivedfourcyclesofFEC(500mg/m2,100mg/m2,500mg/m2)followedbyfourcyclesofT(100mg/m2)withconcurrentcelecoxib(400mgtwicedaily)(groupA)orsamechemotherapyregimenbutwithoutconcurrentcelecoxib(groupB).Thesecombinedchemotherapieswereadministeredevery3weeks.TheChi-squaretestorFisher'sexacttestwereusedtoassessthedifferenceinincidenceoflimitinghematologicaltoxicitesbetweengroups.Results23patients(groupA:n=12;groupB,n=11)receivedatotalof183outof184plannedtreatmentcycles;one(4%,1/23)ofthemomittedthefourthcycleofFECowingtorepeatedincidencesoffebrileneutropenia.Receiveddoseintensity(RDI)forFECingroupA(90%±11%)washigherthanthatingroupB(80%±8%)whileRDIforTwassimilarbetweengroupA(93%±8%)andgroupB(96%±9%).Ofthefirst91treatmentcyclesofFEC,limitinghematologicaltoxicity,severeneutropeniaincludingfebrileneutropenia,wassignificantlydifferentbetweengroupAandB[(10.4%,5/48)vs.(32.6%,14/43),P=0.009].Othertoxicitiescommonlyobservedinchemotherapyreceivingpatientsweremanageable.ConclusionsNeoadjuvantuseofFECfollowedbyTwithconcurrentcelecoxibappearedtobesafefortreatmentofoperableinvasivebreastcancer.Theobservedlowerincidenceofchemotherapy-inducedneutropeniaispossiblycontributedbytheadministrationofCOX-inhibitor.WebelievethatfurtherinvestigationmightprovidemoreevidenceontheuseofCOX-2inhibitorsinbreastcancer.
简介:XADisanapoptosisspecificDNaseinXenopusandcancutthelinker-DNAbetweennucleosomesduringapoptosisinXenopuslaeviseggextractinducedbycytochromec.XADismostlikelytobethehomologuetoDFF40inhumans.TheactivityofDFF40canbeinhibitedbyDFF45.WereportmolecularcloningandidentificationofanXADinhibitor,IXAD(inhibitorofXAD),inXenopuseggs.WeclonedthecompletecDNAoftheDFF45homologue,IXAD.ThereisaspecificDEVDsequenceinitsN-terminal,whichserves
简介:摘要:Janus激酶/信号转导与转录激活子(The Janus kinase/signal transducer and activator of transitions, JAK/STAT)信号通路调控多种重要的生物学进程,包括炎症与免疫、细胞分裂、细胞死亡以及肿瘤形成。近年来越来越多的证据表明JAK-STAT信号通路可能影响脂代谢。在肝脏中,JAK-STAT信号通路可以被许多不同的细胞因子或是生长因子激活,活化的STATs能够通过直接调控代谢相关分子的表达从而影响肝脏代谢。在本篇综述中,我们将主要讨论近年来关于JAK-STAT信号通路中的蛋白包括STAT1, 2, 3, 4, 5, 6在肝脏代谢中的调控作用。