简介：Objective:Tostudytheexpressionofactivatedepi-dermalgrowthfactorreceptor(EGFR)andtranscrip-tionfactorE2F(E2F)inCondylomaAccuminata(CA)patients.Methods:ImmunofluorescenttechniqueswereusedtoinvestigatetheexpressionofactivatedEGFRandE2FinCApatients.Results:TheexpressionofactivatedEGFRonthemembraneofepithelialcellsinCAlesionswassig-nificantlygreatercomparedtoexpressionleversinthecontrolgroup(P<0.01).Moreover,theco-expres-sionofactivatedEGFRandE2Fwassignificantlyin-creasedcomparedtothecontrolgroup(P<0.01).Conclusion:Ourobservationssuggestthatthein-creaseinactivatedEGFRexpressionmaystimulatehyperplasiainCApatientsthroughtheactivationoftranscriptionfactorE2F.

简介：Objective:Tostudytheexpressionlevelsofplatelet-derivedgrowthfactor(PDGF)andgranulocytecolony-stimulatingfactor(G-CSF)inperipheralbloodandtheirroleinthepathogenesisofCondylomaacuminatum(CA).Methods:Seraweretakenfrom70patientswithCondylomaacuminatumandcomparedwith35healthycontrols.PDGFandG-CSFinserumwerequantitatedusingadualantibodysandwichenzyme-linkedimmunoabsorbentassay(ELISA).Results:SerumconcentrationsofPDGFandG-CSFweresignificantlyincreasedinpatientswithCondylomaacuminatum(CA)comparedtocontrols(P<0.001andP<0.005respectively).SerumlevelsofPDGFandG-CSFcorrelatedwithclinicalseverityofCA,butnosignificantdifferencewasobservedbetweendifferentdurationofdiseasegroups.AsignificantpositivecorrelationwasnoticedbetweenneutrophilcountandG-CSFlevels(γ=0.38,P<0.001),andtheneutrophilcountshowednosignificantcorrelationwithPDGF.Conclusion:TheresultsindicatedthatincreasedexpressionofPDGFandG-CSFinperipheralbloodmightbeinvolvedinpathogenesisofCA.

简介：客观：为了与M-CSFR验证MAF-J6-1受体的抗原协会并且进一步学习M-CSF和它的受体的角色，调停了在支持白血病的房间增长的juxtacrine。方法：MAF-J6-1RRE2的Monoclonal抗体(McAb)和rhM-CSFR的polyclonal抗体(PolyAb)被准备。到M-CSFR的McAbRE2的特性被ELISA被间接ELISA，有J6-1房间殖民地形成的跨neutralizing试金和中立化测试证实。结果：到M-CSFR的净化的RE2的反应活动是超过1：16000。M-CSFR和MAF-J6-1R的禁止的活动能被RE2和anti-M-CSFR抗体堵住。到M-CSFR的RE2的反应能被M-CSFR减少。结论：到M-CSFR的RE2的特性被证实，有M-CSFR的MAF-J6-1R的抗原协会被证明。它建议M-CSF和它的受体调停了auto-juxtacrine刺激能是在白血病或nonhematological恶意的起作用的机制。

简介：无

简介：Objective:ThisstudyaimstoexploretheassociationbetweenthedensityofHimalayanmarmot(Marmotahimalayana)andclimaticfactorssuchastemperature,precipitation,humidity,vapourpressure,sunshinepercentage,windvelocity,whicharecloselyassociatedwithglobalclimatechange,andtoprovideareferenceforplaguepreventionandcontrol.Methods:WeconductedaregressionanalysistofindthepossibleclimatefactorsassociatedwiththedensityofHimalayamarmot,andanalyzedtheresponsecharactersofHimalayanmarmottoclimatechange.Results:Dailyprecipitationdays(>=0.1mm)andsunshinepercentageweresignificantlyassociatedwiththedensityofHimalayanmarmot(p<0.01).Conclusion:Climatechangewasassociatedwiththeriskofplague.ThisphenomenonisvaluableforHimalayanmarmotandplagueprevention.MorestudiesareneededtounderstandtheimpactofclimatechangeonHimalayanmarmotandplague.

简介：客观：在在人的创伤的奔流和正常透镜的上皮的房间之间的原子factor-KB(NF-κB)的表示学习差别。方法：全部的RNAof前面的囊标本从受不了创伤的奔流做半量的RT-PCR并且在在他们之间的NF-κB的表示进行差别的分析的正常cadaveric眼睛施主和那些在显微镜下面被拿。结果：作为与在正常控制组的0.8337的平均数相比，NF-κB的表示等价物为在创伤的奔流患者的透镜的上皮的房间是0.9074，并且差别具有显著意义(t=2.447，P<0.05)因此。结论：NF-κB是可能的对必要的一种抄写因素维持正常透镜的上皮的房间的新陈代谢。在创伤的奔流患者可得到的更高的NF-κB“透镜的上皮的房间工具NF-κB具有到创伤的奔流的出现和开发的可能的关联的s。

简介：INTRODUCTIONThedisease,damageorlossoftissueandorgancanseriouslyaffectthehumanlife,evenleadstomaimedordeath,thatitshouldnotbeignored.Todate,autograftsandallograftstransplantationarethemostusuallyusedmethodstorepairdefectsoftissuesandorgans.

简介：IntroductionAsIreflectbackonmytimeasaneditor,Irecallafewissuesthatbotheredmerelatingtopublicationsinmedicaljournals,e.g.Impactfactorandtherelationshipofeditorialsandself-citationontheimpactfactorandacceptanceratesfororiginalpublications.Whatfollowsaresomethoughtsonthesubject.

简介：Cytokineslikeinterferons(IFNs)playacentralroleinregulatinginnateandspecificimmunitiesagainstthepathogensandneoplasticcells.AnumberofsignalingpathwaysareinducedinresponsetoIFNinvariouscells.OneclassicmechanismemployedbyIFNsistheJAK-STATsignalingpathwayforinducingcellularresponses.Herewedescribethenon-STATpathwaysthatparticipateinIFN-inducedresponses.Inparticular,wewillfocusontheroleplayedbytranscriptionfactorC/EBP-βinmediatingtheseresponses.

简介：RecentinsituhybridizationstudiesshowedthatmRNAlevelsofOLIGlandOLIG2transcriptionfactorsareelevatedinoligodendrogliomas.Weraisedpolyclonalantibodiesagainstasyntheticpeptidehomologoustothehumantran-scriptionfactorOliglandstudiedbyimmunohistochemistrytheexpressionofOliglin84braintumorsandinnon-neoplasticbraintissues.Alloligodendrogliomas,oligoastrocytomas,anddysembryoplasticneuroepithelialtumorsshowedmoderatetostrongintranuclearimmunoreactivityincellsmorphologicallyidentifiedasoligodendrocytes.In

简介：组织缺氧和转变生长factor-β；1(TGF-β；1)在很多恶意增加脉管的endothelial生长因素A(VEGFA)表示。组织缺氧和TGF-β的这效果；1可能为肿瘤前进和先进前列腺癌症的转移负责。在现在的学习，TGF-β；1被显示从两根正常房间线(HPV7和RWPE1)和前列腺癌症房间线(DU145和PC3)导致VEGFA165分泌物。相反地，刺激组织缺氧的VEGFA165分泌物仅仅在前列腺癌症房间线被观察。组织缺氧导致了TGF-β；在PC3前列腺癌症房间的1表情，和TGF-β；打字我部分堵住的受体(ALK5)kinase禁止者调停组织缺氧的VEGFA165分泌物。组织缺氧的这效果提供新奇机制在前列腺癌症房间增加VEGFA表示。尽管VEGFA发信号的autocrine在前列腺癌症前进和转移被含有，联系机制糟糕被描绘。VEGFA活动经由VEGF受体(VEGFR)被调停1(Flt-1)并且2(Flk-1/KDR)。而VEGFR-1mRNA在正常前列腺被检测，上皮的房间，VEGFR-2mRNA和VEGFR蛋白质仅仅在PC3房间被表示。VEGFA165治疗在PC3房间然而并非在HPV7房间导致了细胞外的调整信号的kinase1/2(ERK1/2)的phosphorylation，建议VEGFA的autocrine功能可以特别地与前列腺癌症被联系。由VEGFA165的VEGFR-2的激活被显示提高PC3房间的移植。类似的效果也被观察，内长的VEGFA由TGF-β导致了；1并且组织缺氧。这些调查结果说明那经由VEGFR-2的VEGFA的一个autocrine环为TGF-β的tumorigenic效果是批评的；1并且变形前列腺癌症上的组织缺氧。

简介：BACKGROUND:Ithasbeendemonstratedthattransforminggrowthfactor-β(TGF-β)andbrain-derivedneurotrophicfactor(BDNF)caninducestemcelldifferentiationintoneuron-likecells.OBJECTIVE:ToinvestigatetheefficacyofTGF-βandBDNFatinducingthedifferentiationofadultratbonemarrowstromalcells(BMSCs)intoneuron-likecells,bothincombinationoralone.DESIGN,TIMEANDSETTING:AcomparativeobservationexperimentwasperformedattheDepartmentofOrthopedics,FirstAffiliatedHospitalofLiaoningMedicalUniversitybetweenOctober2007andJanuary2008.MATERIALS:TGF-βandBDNFwerepurchasedfromSigma,USA;mouseanti-ratneuronspecificenolase,neurofilamentandglialfibrillaryacidicproteinwerepurchasedfromBeijingHMHLBiochemLtd.,China.METHODS:BMSCswereisolatedfromratsaged4weeksandincubatedwithTGF-β(1μg/L)and/orBDNF(50μg/mL).MAINOUTCOMEMEASURES:Expressionofneuron-specificenolase,neurofilamentandglialfibrillaryacidicproteinweredeterminedbyimmunocytochemistry.RESULTS:BMSCsdifferentiatedintoneuron-likecellsfollowinginductionofTGF-βandBDNF,andexpressedbothneuron-specificenolaseandneurofilament.ThepercentofpositivecellswassignificantlygreaterinthecombinationgroupthanthoseinducedwithTGF-βorBDNFalone(P<0.01).CONCLUSION:TreatmentofBMSCswithacombinationofTGF-βandBDNFinduceddifferentiationintoneuron-likecells,withtheinductionbeingsignificantlygreaterthanwithTGF-βorBDNFalone.

简介：

简介：AbstractBackground:Glioma is a common malignant brain tumor. The purpose of this study was to investigate the role of the transcription factor SPI1 in glioma.Methods:SPI1 expression in glioma was identified using qRT-PCR and Western blotting. Cell proliferation was assessed using the CCK8 assay. Transwell and wound healing assays were utilized to evaluate cell migration. Additionally, cell cycle and apoptosis were detected using flow cytometry.Results:We observed that the expression level of SPI1 was up-regulated in glioma tissues, compared to normal tissues. Furthermore, we found that SPI1 is able to promote proliferation and migration of glioma cells in vitro. Flow cytometry results demonstrate that, compared to si-NC cells, si-SPI1 cells stagnated in the G1 phase, and downregulation of SPI1 expression is able to increase rates of apoptosis. Double luciferase activity and chromatin immunoprecipitation assay results indicated that SPI1 can bind to the promoter sites and promote the proliferation and migration of glioma cells by regulating the expression of oncogenic PAICS.Conclusions:Our results suggest that SPI1 can promote proliferation and migration of glioma. Furthermore, SPI1 can be utilized as a potential diagnostic marker and therapeutic target for glioma.

简介：无

简介：

简介：

简介：Toinvestigatetheeffectsofantisenseoligonucleotidesontheexpressionofmacrophagemigrationinhibitoryfactor(MIF)onmacrophages,themousephosphorothioateoligonucleotidesweredesignedandsynthesizedwiththesequencesofantisense,5'-TACGGATACAAGTAGCAC-3'；Sense,5'-ATGC-CTATGTTCATCGTG-3'；Missense,5'-CTCTCAGACTCGATCTGT-3'.Thesephosphorothioateoligonucleotideswerethentransfectedintoculturedmacrophages(RAW264.7)byluciferasevector,andthetransfectedmacrophageswereincubatedwithLipopolysaccharide(LPS)(1ng/ml)forvariousperiodsoftimesandcollectedafterwards.ThecontentofMIFproteinintheculturalsupernatantswasdeterminedbyELISA,cellularRNAextractedandtheexpressionofMIFmRNAwasexaminedbyRT-PCRanalysis.TheexperimentalresultsshowedthatLPScouldinduceatime-dependentspecificexpressionofMIFonmacrophages,inwhichtheMIFmRNAincellsandtheMIFproteininculturalsupernatantsappearedafter3handreachedtheirhighestconcentrationat9-12hafterLPSstimulation.ThelevelsofmRNAandproteinsinthemacrophagestreatedwithantisenseolignucleotidesweredecreasedsignificantlyafterstimulationwithLPSincomparisonwiththatofstimulationwithLPSaloneorwiththatwithLPSplussenseormissenseoligonucleotides.TherewerenodifferencesamongthosewithoutLPSstimulation.ItisconcludedthatmacrophagesstimulatedwithLPSexpressMIF,andtheantisenseolignucleotidesofMIFinhibittheexpressionofMIFmRNAaswellasthesecretionofMIFproteinsinmacrophages.

简介：无

简介：Objective:Toinvestigatetheproliferativeeffectofkeratinocytegrowthfactor(KGF-2)onhumanadultkeratinocytes.Methods:Thestandardmediumwaskeratinocytegrowthmediumwithoutbovinepituitaryextract(BPE),hydrocortisoneorepidermalgrowthfactor(EGF).Keratinocytesfroma48-year-oldsubjectwereculturedandseededondisheswithstandardmediumofEGFincelldensityof2×104/32mm2.After24hours,themediumwasreplacedbythestandardmediumwith0,4,16,125and500ng/mlKGF-2,respectively.ThestandardmediumwithEGFwasusedasthepositivecontrolandthestandardmediumwithoutEGForKGF-2wasusedasthenegativecontrols.Thegrowthofkeratinocyteswasmonitoredby3-(4,5-dimethythiazol-2-yl)-2,5dipheyltetrazoliumbromide(MTT)assayandbyphotographsondays3,5and7,respectively.Results:KGF-2inconcentrationsof4-500ng/mlshowedasignificantproliferativeeffectondays5and7ascomparedwiththatofthenegativecontrols(P<0.01).Onday3thecellswereproliferatedto1.5-2.5-fold,onday5to3-5-foldandonday7to3-12-foldinKGF-2mediumasthatofthenegativecontrols.TheoptimalresponseoccurredwhentheconcentrationofKGF-2was125ng/mlonday7.CellproliferationwasalsoconsistentlyhigherinallKGF-2concentrationsascomparedwiththatofthepositivecontrols.Conclusions:KGF-2hassignificanteffectsontheproliferationofadultkeratinocytes,whicharemoreeffectivethanthatofEGF.ThisstudysupportsKGF-2canimprovethehealingofchronicwoundsinadultsinclinic.