简介:抽象昆虫由被不变的微生物引起的表面分子的识别激活的一个有效天生的免疫系统保护自己免于微生物引起的感染。在水果苍蝇果蝇melanogaster,细菌的存在在主人与抗菌剂肽的表示被联系免疫者能干的纸巾。主人受体检测感染并且中继信号装适当有免疫力的反应。在果蝇像血球的l(2)有Pefabloc的mbn房间感染前处理,一个通常使用的丝氨酸朊酶禁止者,导致了二主要效果:它响应现场克否定的细菌和细菌的表面分子(peptidoglycans污染的粗略的lipopolysaccharide)堵住了抗菌剂肽Diptericin的表示,它导致了词法变化。
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:AIM:Toinvestigatetheabilityofproteaseinhibitorstomodulatehistaminereleasefromhumancolonmastcells.METHODS:Enzymaticallydispersedcellsfromhumancolonwerechallengedwithanti-IgEorcalciumionophoreA23187intheabsenceorpresenceoftryptaseandchymaseinhibitors,andhistaminereleasewasdetermined.RESULTS:IgEdependenthistaminereleasefromcolonmastceilswasinhibitedbyuptoapproximately37%,26%and36.8%bychymaseinhibitorsZ-Ile-Glu-Pro-Phe-CO2Me(ZIGPFM),N-TosyI-L-phenylalanyl-chloromethylketone(TPCK),andC~l-antitrypsin,respectively.Similarly,inhibitorsoftryptaseleupeptin,N-tosyI-L-lysinechloromethylketone(TLCK),lactoferrinandprotaminewerealsoabletoinhibitanti-IgEinducedhistaminereleasebyamaximumofsome48%,37%,40%and34%,respectively.Preincubationoftheseinhibitorswithcellsfor20rainbeforechallengedwithanti-IgEhadsmalleffectontheinhibitoryactionsoftheseinhibitorsoncolonmastcells.Aspecificinhibitorofaminopeptidaseamastatinhadnoeffectonanti-IgEinducedhistaminerelease.Thesignificantinhibitionofcalciumionophoreinducedhistaminereleasewasalsoobservedwiththeinhibitorsoftryptaseandchymaseexamined.Apartfromleupeptinandprotamine,theinhibitorstestedbythemselvesdidnotstimulatecolonmastcells.CONCLUSION:ItwasdemonstratedthatbothtryptaseandchymaseinhibitorscouldinhibitIgEdependentandcalciumionophoreinducedhistaminereleasefromdispersedcolonmastcellsinaconcentrationdependentofmanner,whichsuggestthattheyarelikelytobedevelopedasanovelclassofanti-inflammatorydrugstotreatchronicofcolitisinman.
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: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:Inthispaper,theeffectofaddingdifferentconcentrationsofkineticinhibitorsontheinductiontimeofhydrogensulfidehydrateformationinareactorequippedwithautomaticadjustabletemperaturecontrollerisstudied.Anovelmethodnamely"suddencooling"isusedforperformingtherelevantmeasurements,inwhichtheinductiontimeofH2Shydrateinthepresence/absenceofPVPandL-tyrosinewithdifferentconcentrations(100,500,and1000ppm)isdetermined.Asaresult,PVPwiththeconcentrationof1000ppminaqueoussolutionisdetectedasamoresuitablematerialforincreasingtheinductiontimeofH2Shydrateformationamongtheinvestigatedkinetichydrateinhibitors.
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简介:ObjectiveToinvestigatetheeffectsofselectivenitricoxidesynthase(NOS)inhibitorsondentategyrusneurogenesisafterdiffusebraininjury(DBI)intheadultratbrain.MethodsAdultmaleSDratsweresubjectedtodiffusebraininjury(DBI)model.Byusingsystemicbromodeoxyuridine(BrdU)tolabeldividingcells,wecomparedtheproliferationrateof