简介：Ahallmarkofallformsofneurodegenerativediseasesisimpairmentofneuronalfunctions,andinmanycasesneuronalcelldeath.Althoughtheetiologyofneurodegenerativediseasesmaybedistinct,differentdiseasesdisplayasimilarpathogenesis,forexampleabnormalimmunitywithinthecentralnervoussystem(CNS),activationofmacrophage/microgliaandtheinvolvementofproinflammatorycytokines.Recentstudiesshowthatneuronsinaneurodegenerativestateundergoahighlyregulatedprogrammedcelldeath,alsocalledapoptosis.TNF-relatedapoptosis-inducingligand(TRAIL),amemberoftheTNFfamily,hasbeenshowntobeinvolvedinapoptosisduringmanydiseases.Asonememberofadeathligandfamily,TRAILwasoriginallythoughttotargetonlytumorcellsandwasnotpresentinCNS.However,recentdatashowedthatTRAILwasunregulatedinHIV-1-infectedandimmune-activatedmacrophages,amajordiseaseinducingcellduringHIV-1-associateddementia(HAD).TRAILisalsoinducedonneuronbyβ-amyloidprotein,animportantpathogenforAlzheimer'sdisease.Inthisreview,wesummarizethepossiblecommonaspectsthatTRAILinvolvedthoseneurodegenerativediseases,TRAILinducedapoptosissignalingintheCNScells,andspecificroleofTRAILinindividualdiseases.Cellular&MolecularImmunology.2005;2(2):113-122.

简介：Objective:Toinvestigatetheexpressionofmatrixmetalloproteinase-7(MMP-7)andFasligand(FasL)ingastriccancerandexploretheirroleinprogressionofgastriccancer.Methods:Formalin-fixedparaffinandembeddedtissuesofprimarygastriccancerandadjacentnon-tumormucosafrom113caseswereevaluatedforMMP-7,FasLandCapase-3expressionbystreptavidin-peroxidase(S-P)immunohistochemistry.Theexpressionofthefirsttwoproteinsincancercellsofprimaryfociwascomparedwithclinicopathologicalparametersoftumors.WealsoobservedthecorrelationofMMP-7andFasLexpressionwithCaspase-3expressionincancercellsofprimaryfoci.Results:MMP-7positiveimmunostainingwaslessfrequentlydetectedinadjacentepithelialcellsthanincancercellsofprimaryfociofgastriccancer(P<0.05,29.2%vs69.0%),andsowasFasL(P<0.05,34.5%vs54.0%).MMP-7expressionwasassociatedwithtumorsize,Borrmann'sclassification,invasivedepth,metastasisandTNMstaging(P<0.05),butnotwithgrowthpattern,Lauren'sclassification,orhistologicalclassification(P>0.05).FasLexpressionwascorrelatedwithtumorsize,invasivedepth,metastasis,Lauren'sclassification,histologicalclassification(P<0.05),whilenotwithBorrmann'sclassification,TNMstagingorgrowthpattern(P>0.05).CancercellsofprimaryfociexpressedlessCaspase-3thantheiradjacentepithelialcells(P<0.05,32.7%vs50.4%).TherewasanobviouscorrelationbetweenFasL,MMP-7andCaspase-3expressionincancercellsofprimaryfoci(P<0.05).Co-expressionofMMP-7andFasLparalleledwithCaspase-3expressionincancercellsofprimaryfoci(P<0.05).Conclusion:MMP-7andFasLexpressionwasup-regulatedingastriccarcinogenesisandwasprincipallyinvolvedinprogressionofgastriccancer.FasLexpressioncouldreflectthedifferentiationofgastriccancercellsandunderliethemolecularmechanismsofdifferentpathwaysofgastrictumorigenesis.Co-expressionofMMP-7andFasLcouldhaveapoptosis-inducingeffe

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：AbstractObjective:Structural abnormalities and dysfunction of the placenta contribute to pregnancy-related complications, such as preeclampsia. Syncytin-A (synA) has been reported to be expressed in the placenta. The contribution of synA to developmental abnormalities and dysfunction of the placenta remains elusive. In this study, we aimed to explore the role of synA in placental development and functions.Methods:SynA-knockout mice were generated using the CRISPR-Cas9 method, and the phenotypes of the placenta and fetus of synA-knockout mice were observed. Real-time quantitative polymerase chain reaction (PCR) and routine PCR were employed to detect the genotypes of the offspring. CD31 immunohistochemistry was used to evaluate the vessel density of the placenta, and the protein levels of key molecules were measured by western blotting.Results:SynA knockout caused fetal death. Furthermore, synA-knockout mice showed placental developmental abnormalities, indicated by a thinner labyrinth layer, thicker spongiotrophoblast layer, lower blood vessel density, and significantly higher numbers of apoptotic trophoblasts, when compared with wild-type littermates. Mechanistically, synA ablation induced apoptosis-inducing factor (AIF) cleavage and nuclear localization and promoted placental trophoblast apoptosis. In addition, synA knockout increased the calpain1 protein levels. The calpain1 inhibitor calpeptin blocked synA knockout-induced AIF cleavage, partially restoring the placental structural abnormalities of synA-knockout mice.Conclusions:SynA knockout leads to placental developmental abnormalities by inducing trophoblastic apoptosis via the calpain1-AIF pathway.

简介：AIMTo在透镜调查Aquaporin-1(AQP-1)的角色上皮的房间(LEC)和它的潜在的目标基因。AQP-1明确地在眼睛的LEC被表示并且为透镜动态平衡和透明性维护是重要的。此处，在LEC的AQP-1表示被调查在奔流formation.METHODSLECs与它的潜在的角色联合在房间幸存上评估它的影响是有带AQP-1的lentivirus的transfected小介入RNA(siRNA)。实时聚合酶链反应(PCR)并且西方的弄污被进行从不同的组在LEC检测AQP-1表示。同时，房间数kit-8(CCK-8)试金和流动cytometry被执行测量LEC增长和apoptosis，respectively.RESULTSAQP-1表示显著地在LEC被减少，两个都在mRNA和蛋白质铺平(P<；0.05)，在siRNA处理以后。减少的房间生存能力被CCK-8试金与siRNA干扰在LEC检测，与控制房间相比(P<；0.05)。apoptosis率显著地在siRNA干扰以后在房间增加了(P<；0.05).CONCLUSIONThe减少了在规定下面的房间生存能力追随者AQP-1大部分由于它LEC的apoptosis的正式就职。AQP-1减小可能在LEC导致生理的功能的变化，它可能与奔流的出现和发展被联系。

简介：Toexplorethemolecularmechanismoftheprotectiveeffectofnervegrowthfactor(NGF)oninjuredspinalcord.Methods:TheposteriorT8(the8ththoracicsegment)spinalcordsof60Wistarratswereinjuredbyimpactscausedbyobjects(weighing10g)fallingfromaheightof2.5cmwithAllensway.Solutionwithnervegrowthfactors(NGF)wasgivento30rats(theNGFgroup)throughamicrotubuleinsertedintothesubarachnoidcavityimmediately,andat2,4,8,12and24hoursafterspinalcordinjury(SCI)respectively.Normalsaline(NS)withsamevolumewasgiventotheother30rats(theNSgroup)withthesamemethod.And5normalratsweretakenasthenormalcontrols.Theexpressionofbcl-2andbaxproteinsinspinalcordwasdetectedwithimmunohistochemistry.Theapoptoticneuronsinspinalcordweremeasuredwithterminaldeoxynucleotidyltransferase-mediateddUTP-biotinnickend-labelingofDNAfragments(TUNEL)staining.Results:Thepositiveexpressionofbcl-2proteinwasstronginthenormalcontrols,butdecreasedintheNSgroup,andincreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).Thepositiveexpressionofbaxproteinwasalsostronginthenormalcontrols,butincreasedintheNSgroup,anddecreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).ApoptoticneuronswerefoundintheNSgroup,andtheydecreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).Conclusions:NGFcanprotecttheinjurednervetissuesthroughstimulatingtheexpressionofbcl-2protein,inhibitingtheexpressionofbaxproteinandinhibitingtheneuronalapoptosisafterSCI.

简介：Hypoxia-induciblefactor1(HIF-1)attenuatesamyloid-betaproteinneurotoxicityanddecreasesapoptosisinducedbyoxidativestressorhypoxiaincorticalneurons.Inthisstudy,weconstructedarecombinantadeno-associatedvirus(rAAV)vectorexpressingthehumanHIF-1αgene(rAAV-HIF-1α),andtestedtheassumptionthatrAAV-HIF-1αrepresseshippocampalneuronalapoptosisinducedbyamyloid-betaprotein.OurresultsconfirmedthatrAAV-HIF-1αsignificantlyreducesapoptosisinducedbyamyloid-betaproteininprimaryculturedhippocampalneurons.DirectintracerebralrAAV-HIF-1αadministrationalsoinducedrobustandprolongedHIF-1αproductioninrathippocampus.SinglerAAV-HIF-1αadministrationresultedindecreasedapoptosisofhippocampalneuronsinanAlzheimer’sdiseaseratmodelestablishedbyintracerebroventricularinjectionofaggregatedamyloid-betaprotein(25–35).OurinvitroandinvivofindingsdemonstratethatHIF-1haspotentialforattenuatinghippocampalneuronalapoptosisinducedbyamyloid-betaprotein,andprovidesexperimentalsupportfortreatmentofneurodegenerativediseasesusinggenetherapy.

简介：AbstractBackground:Pulmonary microvascular endothelial cells (PMVECs) were not complex, and the endothelial barrier was destroyed in the pathogenesis progress of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Previous studies have demonstrated that hepatocyte growth factor (HGF), which was secreted by bone marrow mesenchymal stem cells, could decrease endothelial apoptosis. We investigated whether mTOR/STAT3 signaling acted in HGF protective effects against oxidative stress and mitochondria-dependent apoptosis in lipopolysaccharide (LPS)-induced endothelial barrier dysfunction and ALI mice.Methods:In our current study, we introduced LPS-induced PMEVCs with HGF treatment. To investigate the effects of mammalian target of rapamycin (mTOR)/signal transducer and activator of transcription 3 (STAT3) pathway in endothelial oxidative stress and mitochondria-dependent apoptosis, mTOR inhibitor rapamycin and STAT3 inhibitor S3I-201 were, respectively, used to inhibit mTOR/STAT3 signaling. Moreover, lentivirus vector-mediated mTORC1 (Raptor) and mTORC2 (Rictor) gene knockdown modifications were introduced to evaluate mTORC1 and mTORC1 pathways. Calcium measurement, reactive oxygen species (ROS) production, mitochondrial membrane potential and protein, cell proliferation, apoptosis, and endothelial junction protein were detected to evaluate HGF effects. Moreover, we used the ALI mouse model to observe the mitochondria pathological changes with an electron microscope in vivo.Results:Our study demonstrated that HGF protected the endothelium via the suppression of ROS production and intracellular calcium uptake, which lead to increased mitochondrial membrane potential (JC-1 and mitochondria tracker green detection) and specific proteins (complex I), raised anti-apoptosis Messenger Ribonucleic Acid level (B-cell lymphoma 2 and Bcl-xL), and increased endothelial junction proteins (VE-cadherin and occludin). Reversely, mTOR inhibitor rapamycin and STAT3 inhibitor S3I-201 could raise oxidative stress and mitochondria-dependent apoptosis even with HGF treatment in LPS-induced endothelial cells. Similarly, mTORC1 as well as mTORC2 have the same protective effects in mitochondria damage and apoptosis. In in vivo experiments of ALI mouse, HGF also increased mitochondria structural integrity via the mTOR/STAT3 pathway.Conclusion:In all, these reveal that mTOR/STAT3 signaling mediates the HGF suppression effects to oxidative level, mitochondria-dependent apoptosis, and endothelial junction protein in ARDS, contributing to the pulmonary endothelial survival and barrier integrity.

简介：WereportedinthismanuscriptthatTGF-β1inducesapoptosisinAML12murinehepatocytes,whichisassociatedwiththeactivationofp38MAPKsignalingpathway.SB202190,aspecificinhibitorofp38MAPK,stronglyinhibitedtheTGF-β1-inducedapoptosisandPAI-1promoteractivity.TreatmentofcellswithTGF-β1activatesp38.Furthermore,over-expressionofdominantnegativemutantp38alsoreducedtheTGF-β1-inducedapoptosis.Thedataindicatethattheactivationofp38isinvolvedinTGF-β1-mediatedgeneexpressionandapoptosis.

简介：AbstractBackground:Pulmonary arterial hypertension (PH) is a progressive disease with limited therapeutic options, ultimately leading to right heart failure and death. Recent findings indicate the role of the Warburg effect (aerobic glycolysis) in the development of PH. However, the effect of the glycolysis inhibitor 3-bromopyruvate (3-BrPA) on the pathogenesis of PH has not been well investigated. This study aimed to determine whether 3-BrPA inhibits PH and its possible mechanism.Methods:PH was induced in adult Sprague-Dawley rats by a single intraperitoneal injection of monocrotaline (MCT). 3-BrPA, or phosphate-buffered saline (PBS) was administered via intraperitoneal injection every other day from the first day of MCT-injection to 4 weeks of follow-up, and indices such as right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI), pulmonary arteriolar remodeling indicated by percent media thickness (% MT), lactate levels and glucose consumption, were evaluated. Pulmonary arteriolar remodeling and right ventricular hypertrophy were observed in hematoxylin-eosin-stained lung sections. Western blotting, immunohistochemistry, and/or immunofluorescence analyses were used to measure the expression of relevant proteins. A cytochrome C release apoptosis assay and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining were used to measure cell apoptosis.Results:MCT-induced PH showed a significant increase in glucose consumption (0 vs. 4 weeks: 0.87 ± 0.23 vs. 2.94 ± 0.47, P = 0.0042) and lactate production (0 vs. 4 weeks: 4.19 ± 0.34 vs. 8.06 ± 0.67, P = 0.0004). Treatment with 3-BrPA resulted in a concomitant reduction in glucose consumption (1.10 ± 0.35 vs. 3.25 ± 0.47, P = 0.0063), lactate production (5.09 ± 0.55 vs. 8.06 ± 0.67, P= 0.0065), MCT-induced increase in RVSP (39.70 ± 2.94 vs. 58.85 ± 2.32, P= 0.0004), pulmonary vascular remodeling (% MT, 43.45% ± 1.41% vs. 63.66% ± 1.78%, P < 0.0001), and right ventricular hypertrophy (RVHI, 38.57% ± 2.69% vs. 62.61% ± 1.57%, P < 0.0001) when compared with those of the PBS-treated group. 3-BrPA, a hexokinase 2 inhibitor, exerted its beneficial effect on PH by decreasing aerobic glycolysis and was also associated with inhibiting the expression of glucose transporter protein-1, inducing apoptosis, and suppressing inflammation.Conclusions:3-BrPA might have a potential beneficial effect on the PH treatment.

简介：Toexploretheroleofnuclearfactor-κB(NF-κB)inthesignalpathwayofproteinkinaseC(PKC)regulatingtheproliferationandapoptosisofTlymphocytesinasthma.Tlymphocyteswereisolatedfromtheasthmaticmodelofguineapigsandtheasthmaticpatients.EithertheTcellsstimulatedwithPMAaloneorthosestimulatedwithPMAtogetherwithpyrrolidinedithiocarbamate(PDTC)wereincubatedfor1and24h.TheproliferationofandthepresenceofNF-κBinthecellsincubatedfor1hwereobservedbyMTTandimmunohistochemicalstaining,respectivelyAndthecellsincubatedfor24hwereobservedfortheapoptosisbyTUNEL.Alltheassayswereparalleledwithcontrols,andallthedatawereanalyzedstatisticallywiththesoftwareSAS.ThepercentageofcellsofnuclearpositivestainingofNF-scBandtheproliferationofTlymphocytesfromasthmaticguineapigsandasthmaticpatientsstimulatedwithPMAweresignificantlyhigherthanthoseofTlymphocytesfromasthmaticguineapigsandasthmaticpatientsstimulatedwithoutPMArespectively(P<0.01)andthoseofTlymphocytesfromnormalcontrolguineapigsandnormalcontrolpersonsstimulatedwithPMArespectively(P<0.01),andweresignificantlyreducedbyPDTC(P<0.01).TheapoptosisindexofTlymphocytesfromasthmaticguineapigsandasthmaticpatientsstimulatedwithPMAweresignificantlylowerthanthoseofTlymphocytesfromasthmaticguineapigsandasthmaticpatientsstimulatedwithoutPMArespectively(P<0.01)andthoseofTlymphocytesfromnormalcontrolguineapigsandnormalcontrolpersonsstimulatedwithPMArespectively(P<0.01),andweresignificantlyinducedbyPDTC(P<0.01).ThereweregoodpositivecorrelationbetweenthepercentageofcellsofnuclearstainingofNF-κBofTlymphocytesandtheproliferationofTlymphocytes(r=0.51-0.72,P<0.001),andalsogoodnegativecorrelationbetweenthepercentageofcellsofnuclearstainingofNF-scBandtheapoptosisindexofTlymphocytes(r=-0.55-0.71,P

简介：无

简介：CleavageofchromosomalDNAintooligonucleosomalsizefragmentsisanintegralpartofapoptosis.ElegantbiochemicalworkidentifiedtheDNAfragmentationfactor(DFF)asamajorapoptoticendonucleaseforDNAfragmentationinvitroGeneticstudiesinmicesupporttheimportenceofDFFinDNAfragmentationandpossiblyinapoptosisinvivo.RecentworkalsosuggeststheexistenceofadditionalendonucleasesforDNAdegradation.Understandingtherolesofindividualendonucleasesinapoptosis,andhowtheymightcoordinatetodegradeDNAindifferenttissuesduringnormaldevelopmentandhomeostasis,aswellasinvariousdiseasedstates,willbeamajorresearchfocusinthenearfuture.

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简介：<正>Apoptosisisahighlyregulatedphysiologicalprocesscriticalindevelopmentandtissuehomeostasis.Abnormalapoptosiscanleadtodiseaseconditionsincludingneurodegeneration,autoimmunityandcancer.DNAfragmentationisanintegralpartofapoptosisandhaslongbeensuspectedtobeofcriticalimportanceincleaninguppotentiallyantigenicDNAandgeneticmaterialcapableofinducingneoplasmictransformationinneighboringcells.DirectevidenceforthisfunctionofDNAfragmentationhowever,isstilllacking.TheidentificationofaheterodimericDNAfragmentationfactor45and40(DFF45andDFF40,alsocalledICADforInhibitorofCaspaseActivatedDNaseandCADforCaspaseActivatedDNaserespectively)aswellas

简介：Objective:Toobservehumanneuronalapoptosissecondarytotraumaticbraininjury,andtoelucidateitsregulativemechanismandthechangeofexpressionofapoptosis-relatedgenes.Methods:Specimensofbrainwerecollectedfromcasesoftraumaticbraininjuryinhumans.Thehistologicalandcellularmorphologywasexaminedbylightandelectronmicroscopy.TheextentofDNAinjurytocorticalneuronswasdetectedbyusingTUNEL.ByinsituhybridisationandimmunohistochemistrythemRNAchangesandproteinexpressionofBcl-2,Bax,p53,andcaspase3p20subunitwereobserved.Results:Apoptoticneuronsappearedfollowingtraumaticbraininjury,peakedat24hoursandlastedfor7days.Innormalbraintissueactivatedcaspase3wasrare,butashorttimeaftertraumaitbecameactivated.Theactivitypeakedat20-28hoursandremainedhigherthannormalfor5-7days.TherewasnoexpressionofBcl-2mRNAandBcl-2proteininnormalbraintissuebut8hoursafterinjurytheirexpressionbecameevidentandthenincreased,peakedat2-3daysandremainedhigherthannormalfor5-7days.TheprimaryexpressionofBax-mRNAandBaxproteinwashighinnormalbraintissue.At20-28hourstheyincreasedandremainedhighfor2-3days;onthe7thdaystheyreturnedtoanormallevel.Innormalbraintissue,p53mRNAandP53wereminimallyexpressed.Increasedexpressionwasdetectedatthe8thhour,anddecreasedat20-28hoursbutstillremainedhigherthannormalonthe5thday.Conclusions:Followingtraumaticinjurytothehumanbrain,apoptoticneuronsappeararoundthefocusoftrauma.ThemRNAandproteinexpressionofBcl-2,Baxandp53andtheactivityofcaspase3enzymeareincreased.

简介：Inordertodeterminetheroleofalginate-derivedoligosaccharides(ADO)indroughtstressresistanceoftomato(Ly-copersiconesculentumMiller)seedlings,theleaveswereexposedtodifferentconcentrationsofADO(0.05%,0.10%,0.20%,0.30%and0.50%)afterdroughtstresswassimulatedbyexposingtherootsto0.6molL-1PEG-6000solutionfor6h.Changesinbiomass,electrolyteleakageandmalondialdehyde(MDA),freeproline,totalsolublesugars(TSS)andabscisicacid(ABA),theenzymeactivitiesofcatalase(CAT),superoxidedismutase(SOD),peroxidase(POD)andphenylalanineammonia-lyase(PAL)weremeasuredtoinvestigatetheeffectsofADOtreatment.TheresultsshowedthatthetreatmentwithanADOconcentrationof0.20%exhibitedthehighestperformanceofdroughtstressresistanceinthetomatoseedlingsbydecreasingtheelectrolyteleakageandtheconcentrationofMDA,increasingthecontentsoffreeproline,TSSandABA,andincreasingtheactivitiesofCAT,SOD,PODandPALaftertreatmentwithADO.Itissuggestedthatchangesinelectrolyteleakage,MDA,osmoticsolutes,ABA,anti-oxidativeenzymeandPALactivitieswereresponsiblefortheincreaseddroughtstressresistanceintomatoseedlings.Toourbestknowledge,thisisthefirstreportoftheeffectofADOtreatmentonenhancingthedroughtstressresistanceoftomatoseedlings.

简介：Thechiralclusters(μ3-S)MCoW(CO)8[η^5-C5H4C(O)OCH3][M=Ru(2),Fe(3)]weresynthesizedbyasymmetricinductionofN-benzylcinchoniumchlorideasphase-transfercatalyst(PTC).ThemostsuitableamountofPTCis70mol%.Cluster3wasdeterminedbysinglecrystalX-raydiffractionanalysis.Thebesteeofthechiralclusterisover20%.

简介：Ring-closingmetathesisreactionsinvolvingdiallyldiphenylsilaneanddiallyloxydiphenylsilaneweresuccessfullyperformedbyusingonly0.01molorevenlessofGrubbscatalyst1.Theeffectsofreactionparameters,suchassolvents,temperatureandconcentrationofthecatalystarediscussed.

简介：Wehaveidentifiedseveralkeyeventsinthymocyteapoptosisoverthepastfewyears,includingarequiredroleforproteasomefunctionandtheproductionofROS.WhileweourdataestablishedthatproteasomefunctionandROSproductionarerequiredforapoptosisinthymocytes,wehadnotestablishedtheorderofeventsleadingfromtheprimaryapoptoticstimulustotheactivationofcaspases.Recently,wehavedemonstratedthatbothTcellreceptorinducedapoptosisandglucocorticoidinducedapoptosissignalthymocytestodiethroughactivationoftheproteasomeandthiseventisupstreamoftheproductionofROS.