简介：AIMToinvestigatetherolesandinteractionsofmutThomolog（MTH）-1andhypoxia-induciblefactor（HIF）-1αinhumancolorectalcancer（CRC）.METHODS：TheexpressionanddistributionofHIF-1αandMTH-1proteinsweredetectedinhumanCRCtissuesbyimmunohistochemistryandquantitativerealtimepolymerasechainreaction（qRT-PCR）.SW480andHT-29cellswereexposedtonormoxiaorhypoxia.ProteinandmRNAlevelsofHIF-1αandMTH-1wereanalyzedbywesternblottingandqRT-PCR,respectively.InordertodeterminetheeffectofHIF-1αontheexpressionofMTH-1andtheamountof8-oxodeoxyguanosinetriphosphate（dGTP）inSW480andHT-29cells,HIF-1αwassilencedwithsmallinterferingRNA（siRNA）.GrowthstudieswereconductedoncellswithHIF-1αinhibitionusingaxenografttumormodel.Finally,MTH-1proteinwasdetectedbywesternblottinginvivo.RESULTS：HighMTH-1mRNAexpressionwasdetectedin64.2%ofcases（54/84）,andthiswassignificantlycorrelatedwithtumorstage（P=0.023）andsize（P=0.043）.HIF-1αproteinexpressionwascorrelatedsignificantlywithMTH-1expression（R=0.640;P〈0.01）inhumanCRCtissues.HypoxicstressinducedmRNAandproteinexpressionofMTH-1inSW480andHT-29cells.InhibitionofHIF-1αbysiRNAdecreasedtheexpressionofMTH-1andledtotheaccumulationof8-oxo-dGTPinSW480andHT-29cells.Intheinvivoxenografttumormodel,expressionofMTH-1wasdecreasedintheHIF-1αsiRNAgroup,andthetumorvolumewasmuchsmallerthanthatinthemocksiRNAgroup.CONCLUSION：MTH-1expressioninCRCcellswasupregulatedviaHIF-1αinresponsetohypoxicstress,emphasizingthecrucialroleofHIF-1α-inducedMTH-1intumorgrowth.

简介：这研究的目的是在老鼠模型在肝移植以后在早时期(24h)观察在接枝的损害和氧化还原作用factor-1(Ref-1)的表示之间的关系。150只成年男威斯特老鼠随机包括肝被划分成三个组移植组，假冒的外科组和未经治疗的控制组。在肝移植以后，动物在不同时间点被牺牲，并且Ref-1的表示的变化和意义然后被immunohistochemistry，血清学和组织病理学说探索。作为与假冒的外科组和未经治疗的控制组相比，Ref-1蛋白质在的表示移植组在在肝移植以后的早时期是更强壮的。与病理分析，大量渗透的发炎房间在门静脉附近被发现。肝的纸巾是损害。然而，在假冒的外科的损害和未经治疗的控制组是比较地细微的。浆液中高音和著名计算机生产厂商层次在6-12h到达了山峰，并且在12h以后显著地减少了。这些数据建议在在移植以后的更早的时期的肝损害的度在6h达到顶点然后减少。并且Ref-1蛋白质由肝的ischemic灌注损害导致了可能在修理损害起一个关键作用。

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

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：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.

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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：AbstractBackground:Angiogenesis and hypoxia-inducible factor 1α (HIF-1α) play major roles in solid tumors. This study aimed to establish a longitudinal and multimodal imaging model for in vivo evaluation of HIF1α and angiogenesis in breast cancer.Methods:By transfection of a 5 hypoxia-responsive element (HRE)/green fluorescent protein (GFP) plasmid, the cell line Ca761-hregfp was established, which emitted green fluorescence triggered by HIF-1α under hypoxia. The cells were subjected to CoCl2-simulated hypoxia to confirm the imaging strategy. We grew Ca761-hre-gfp cells in the left rear flanks of twelve 615 mice. Experiments were conducted on days 4, 9, 15, and 19. For in vivo analysis, Ca761-hre-gfp subcutaneous allografted tumors were imaged in vivo using contrast-enhanced ultrasound (CEUS) and fluorescence imaging (FLI) during tumor development. The tumor size, CEUS peak intensity, and FLI photons were measured to evaluate tumor growth, angiogenesis, and HIF-1α activity, respectively. After each experiment, three mice were randomly sacrificed and tumor specimens were collected to examine HIF-1α activity and the microvessel density (MVD).Results:In vitro, both green fluorescence and HIF-1α expression were detected in Ca761-hre-gfp cells treated with CoCl2, indicating the suitability of the cells to detect HIF-1α activity. In vivo, HIF-1α activity first increased and then decreased, which was significantly correlated with angiogenic changes (r = 0.803, P = 0.005). These changes were confirmed by immunohistochemical staining of HIF-1α and MVD.Conclusions:The findings validated the Ca761-hre-gfp murine allograft model for reliable evaluation of HIF-1α activity and angiogenesis longitudinally using both molecular and pre-clinical non-invasive imaging modalities. The cell line may be useful for studies of anti-HIF pathway therapies.

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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：Objective:TostudythesequentialchangesofHIF-1α(hypoxia-induciblefactor1alpha)inexperimentalspinalcordinjuryinratsandtoanalyzeitspotentialeffectsinSCI.Methods:AstaticcompressionmodelofSCIwasemployedinthisstudy.ExpressionsofHIF-1αweremeasuredwithimmunohistochemicalstaining,whileflowcytometrywasusedtodeterminetheapoptoticratioandbcl-2expressions.Results:HIF-1αbegantoincrease1dayafterinjury,andreachedthepeakat3-7days.Twoweekslater,itdeclinedsignificantly.ThesequentialchangesofHIF-1αcoincidedwellwiththealterationsofapoptoticratioandcontentsofbel-2.Conclusions:HIF-1αpossiblyparticipatesinthesecondaryischemicandhypoxicproceduresafterspinalcordinjury,andmaymediatethetraumaticapoptosis.FurtherunderstandingofHIF-1αmayprovidenewtherapeuticregimensforSCI.

简介：我们识别了米饭花的机关发展异种，称为的同样开的壳和男性无菌1(ohms1)，从indicarestorer线的子孙，Zhonghui8015与60Co光线照耀对待。ohms1异种展出了开的壳并且像词根并且象palea一样组织在花药和耻辱之间的变换，它导致了显示出‘tridentatelemma’的ohms1异种小穗状花小穗。ohms1异种是完全无菌却有的60%-70%肥沃的花粉。印射的基因分析和基因证明ohms1被单个后退的基因控制，并且变异的基因对在标记KY2和KY29之间的染色体3的短手臂上的42-kb间隔印射罚款。在这个区域的四个开的读物框架的顺序分析表明异种在第五intron的最后底带了单个核苷酸转变(到G的A)，它多半被通信到ohms1phynotype，在一种MIKC类型疯盒子的基因OsMADS1(LOC_Os03g11614)。进一步定序的酶消化和cDNA显示可变拼接在MADS领域或氨基酸框架为在ohms1，而是没有结构的变化的第六exon的删除负责移动出现了。另外，即时荧光灯量的PCR分析证明OsMADS1表示水平在ohms1异种显著地减少了。发展相关的基因也显著地改变了的米饭flowering因素和花的颖的表示层次。这些结果证明OsMADS1可以在米饭起一个重要作用花的机关开发，特别地在花的颖开发和小花原基区别。

简介：Objective:　Tocomparethedynamicchangesofinterleukin-1(IL-1),interleukin-6(IL-6),andtumornecrosisfactor(TNF)inintermingledskingraftwiththoseinothertypesofskingraftsinrats.　　Methods:　A10%-15%third-degreeburnwascreatedin180Spregue-Dawley(SD)rats.Afterremovingthescar,skingraftswereperformedontheopenwoundsimmediatelywithautoskin(aus,n=54),alloskin(als,n=54)andintermingledskin(n=36).Thatistosay,intheintermingledskingraft,abigpieceofalloskin(mals)wasgraftedfirst,and3dayslater,smallpiecesofautoskin(maus)wereembeddedinthealloskin.Therest36ratsweretakenasthecontrols.AndthebiologicalactivitiesofIL-1,IL-6andTNFingraftsheetsineachgroupweredetectedafterskingraft.　　Results:　ThelevelsofIL-1,IL-6andTNFintheausgroupdecreasedsteadilyaftertheirinitialelevations,whereasinthealsgrouptheyincreasedsignificantlyandkeptonthepeaklevelinthelaterphases.Intheintermingledgroup,thereappearedalowestIL-1levelinthemalsandahighestoneinthemaussimultaneouslyat7(4)days(Thenumberoutofparenthesisisthedaysaftertransplantingwithalloskinsheets,andthenumberinparenthesisisthedaysafterembeddingautoskinsheetsintheintermingledskingraft.Similarlyhereinafter.)afterskingraft(P<0.01),andthehighlevelinthemausabruptlydecreasedat14(11)daysafterskingraft.Atexactlythesamephaseonday7(4),aprominentpeakedIL-6inthemalsoccurred.Inthelaterphases,thelevelsofTNFremainedrelativelylowbothinthemalsandinthemaus.Fromday7(4)on,eachcytokinefluctuationinthemalssynchronizedwiththatinthemaus.Thelongertheposttransplantationperiodlasted,themorethepositivecytokinecorrelatedbetweenthemalsandthemaus.　　Conclusions:　ThelowlevelsofIL-1andTNFmaybeimportantfactorstolightentheintensityoflocalrejectionintheintermingledskingraft.Thetempo

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

简介：TheinvivoeffectsofPhytolaccaacinosapoly-saccharidesI(PEP-I)onimmunologiccytotoxicityofmouseperitonealmacrophagesanditsproductionoftumornecrosisfactor(TNF)andinterleukin1(IL-1)werestudied.PEP-I80or160mgkgwasgiveniptwiceevery4day.BothdoseswerefoundtohavesignificantenhancingactivityonmacrophagescytotoxicityagainstS180sarcomacellsandmalignanttransformedfibroblastL929cells.PeritonealactivatedmacrophageswereincubatedwithLPSfor2and24hrstoinduceTNFandIL-1,respectively.TheTNFandIL-1activitiesweretestedfromcytotoxicityagainstL929cellsinanabsorbenceassayofenzymaticreactionandproliferationofthymocytesco-stimulatedassayseparately.TheoptimaltimeforTNFproductionwasfoundonday8.SignificantincreasesinTNFandIL-1wereobserved.IncomparisonoftheeffectofPEP-IonTNFwiththatofknownprimingagentBCG,therewasnodifferencebetweenthem,butPEP-IhadahigheffectonIL-1.Theseresultssug

简介：Objective:ToinvestigatetheeffectofsubstanceP(SP)ongeneexpressionoftransforminggrowthfactorβ-1(TGFβ-1),transforminggrowthfactorreceptor-1(TGFR-1)andtransforminggrowthfactorreceptor-2(TGFR-2)infibroblastsculturedinvitrofromrat'sgranulationtissues.Methods:Thefibroblastsfromthegranulationtissuesintheskeletalmuscleofrat'shindlimbsinjuredbyformaldehydewereculturedinvitro.Whendifferentconcentrations(10-9-10-5mol/L)ofSPwereaddedintotheculturemedium,thechangesofgeneexpressionofTGFβ-1,TGFR-1andTGFR-2intheculturedfibroblastswereobservedwithreversetranscriptionpolymerasechainreactionatdifferentintervals(0,3,6,12and24hoursafterincubation).Results:ThegeneexpressionofTGFβ-1,TGFR-1andTGFR-2inthefibroblastsculturedfromrat'sgranulationtissueswasup-regulatedbySP.ThepeaklevelofthemRNAexpressionwasfoundat10-8mol/LSPandtheup-regulationeffectwasnotfoundat10-5mol/Land10-6mol/L.ThepeaklevelsofgeneexpressionofTGFβ-1,TGFR-1andTGFR-2inthefibroblaststreatedwithSPwereachievedat6and12hours,respectively.Conclusions:SPhasup-regulationeffectonthegeneexpressionofTGFβ-1,TGFR-1andTGFR-2infibroblastsfromrat'sgranulationtissuesinvitro,andtheeffectisrelatedtodifferentstimulatingconcentrationsofSP.Itmaybeconcernedwithproliferationanddifferentiationoffibroblastsandformationofscartissuesduringwoundhealing.

简介：文章讨论了Factor定理的一些应用,特别对Auslander转置作了讨论.

简介：1毫无疑问，当2009年的德尔·波特罗在美网连续击败纳达尔和费德勒夺得冠军的时候，他就已经成为了打破巨头垄断的最好人选，可惜右手腕的伤病延缓了他的脚步，虽然在伤病恢复之后他的世界排名短暂来到过史上最高第四的位置，

简介：Asanresearchexampleofthewidelyexistingcooperation-competitionsystems,theauthorspresentanempiricalinvestigationonafruitnutritivefactornetwork.Itisdescribedbyanode-weightedbipartitegraph.Thefruitnutritivefactorsaredefinedasthenodes,andtwonodesareconnectedbyanedgeifatleastonefruitcontainsthesetwonutritivefactors.Thefruitsaredefinedasthecollaborationacts.Thenode-weightW_(nt),whichsignifiesthe'importancedegree'ofeachactornode,isdefinedasthecontentofanutritivefactorinafruit.Theempiricalinvestigationresultsshowsomeuniquefeatures.Thenode-weightdistributionstakeso-called'shiftedpowerlaw'functionforms,buttheact-weightdistributiontakesanormalform.Thedegreeandact-degreedistributionsshowimpulsive-spectrumlikeforms.Theseobservationsmaybehelpfulforthestudyoffruits.Thenetworkdescriptionmethodproposedinthisarticlemaybeuniversalforakindofcooperation-competitionsystems.

简介：Itisstandardpractice,wheneveraresearcherfindsanewgene,tosearchdatabasesforgenesthathaveasimilarsequence.Itisnotstandardpractice,wheneveraresearcherfindsanewgene,tosearchforgenesthathavesimilarexpression(coexpression).Failuretoperformco-expressionsearcheshasleadtoincorrectconclusionsaboutthelikelyfunctionofnewgenes,andhasleadtowastedlaboratoryattemptstoconfirmfunctionsincorrectlypredicted.WepresentheretheexampleofGliaMaturationFactorgamma(GMF-gamma).Despiteitsname,ithasnotbeenshowntoparticipateingliamaturation.ItisageneofunknownfunctionthatissimilarinsequencetoGMF-beta.ThesequencehomologyandchromosomallocationledtoanunsuccessfulsearchforGMF-gammamutationsinglioma.WeexaminedGMF-gammaexpressionin1432humancDNAlibraries.Highestexpressionoccursinphagocytic,antigen-presentingandotherhematopoieticcells.WefoundGMF-gammamRNAinalmosteverytissueexamined,withexpressioninnervoustissuenohigherthaninanyothertissue.OurevidenceindicatesthatGMF-gammaparticipatesinphagocytosisinantigenpresentingcells.Searchesforgeneswithsimilarsequencesshouldbesupplementedwithsearchesforgeneswithsimilarexpressiontoavoidincorrectpredictions.