简介：尽管有在动物模型获得的出色的结果，船边交货ligand(FasL)的临床的使用被严重毒性作为anticancer药限制。死亡ligands的全身的毒性可以被使用编码膜界限死亡ligands的基因阻止，由指向的transgene，通过也的表示指向了transduction或指向了抄写。肿瘤房间死亡的选择正式就职是有希望的anticancer策略。熔化蛋白质被熔化船边交货ligand(FasL)的细胞外的领域到有选择地在肿瘤endothelial房间上指向av3-integrins的肽arginine-glycine-aspartic酸(RGD)创造。这研究的目的是在鼠科的hepatocellular癌(HCC)在肿瘤生长和幸存上评估RGD-FasL的效果肿瘤模型。有与FasL作为与那相比在HCC肿瘤模型上显示明显的镇压效果的RGD-FasL的处理(p<0.05)并且在这个模型在肿瘤生长延期上导致了更多的添加剂效果。RGD-FasL处理显著地提高了老鼠幸存并且没引起有毒的效果，例如重量损失，机关失败，或另外的处理相关的毒性。Apoptosis被流动cytometric分析和TUNEL试金检测；那些结果也证明RGD-FasL比FasL是为H22和H9101房间线的房间apoptosis的更多的有势力inducer(p<0.05)。在结论，RGD-FasL看起来是肿瘤房间死亡的低毒性的选择inducer，它在现出症状之前的潜、临床的研究应得进一步的调查。而且，这条途径与治疗学的recombinant蛋白质为complexing目标ligands提供一种万用的技术。为了在vivo，肿瘤和肝区分FasL的反肿瘤效果，纸巾被收获由染色的Hematoxylin和曙红(H&E)为坏死的房间，肿瘤房间，或apoptotic房间的证据检验。

简介：PreviousstudieshaveshownthatoligodeoxynucleotidescontainingunmethylatedCpGmotifswereusedasadjuvantsforimmunoregulationandimmuneresponse.ThisstudywastoexploretheactivationeffectsofBifidobacteriaDNAcontainingunmethylatedCpGmotifs(CpGDNA)onmurinemacrophageJ774A.1cells.ThegenomicDNAofBifidobacteriawasextractedandpurified,andthemethylationdegreeofCpGmotifswastested.Thephagocyticabilityofthemacrophageswasdetectedbyflowcytometry.Thecytokines(IL-1β,IL-6,IL-12p40andTNF-α)levelsintheculturesupernatantsofBifidobacteriaDNAtreatedJ774A.1cellswereassayedbyELISA.Thecontentofnitricoxide(NO)wasdetectedbyGriessreagent.AftertreatedwithBifidobacteriaDNAfor24h,NileRedstainincreasedinJ774A.1macrophage,whichsuggestedthatthelipidmetabolismincreasedinthemacrophages.ThephagocyticabilityandlevelsofNOandcytokinesofIL-1β,IL-6,IL-12p40andTNF-αweresignificantlyhigherthanPBSgroupandCTDNAgroup.TheresultsindicatedthatBifidobacteriaDNAcouldactivatemurinemacrophagesJ774A.1,whichcouldprovidescientificbasisfortheresearchandapplicationofmicroorganismDNApreparation.

简介：Col1a1(骨胶原的子单元之一打字我)是骨胶原，它属于细胞外的矩阵(ECM)的一个家庭在细胞的增长和区别起一个重要作用的蛋白质。然而，特别在增长的控制和spermatogonial干细胞(SSC)的区别，在精子发生的Col1a1的角色仍然保持未知。在这研究，我们在老鼠spermatogonia的区别和增长上探索了Col1a1的downregulation的效果。Loss-of-function学习揭示了那Oct4和Plzf，SSC自强的标记，，显著地被减少c工具包和haprin的表示，SSC区别的特点，在Col1a1以后被提高击倒。房间周期分析显示三分之二spermatogonia在Col1a1以后在S阶段被逮捕击倒。在vivo实验，睾丸的DNA注射和electroporation证明那个spermatogonia自强能力与Col1a1的loss-of-function显著地被损害。我们的数据建议Col1a1的silencing能压制spermatogonia自强并且支持spermatogonia区别。

简介：对骨胳的肌肉新生的成长兴趣在损伤，以及几个肌肉发达的退化病理以后为肌肉损害与新治疗学的策略的开始被联系，包括营养障碍，肌肉发达的萎缩，和极度瘦弱。集中于细胞外的因素的能力支持myogenesis的研究因此是高度有希望的。我们现在报导那一个导出adipocyte的因素，球状的adiponectin(荡者)，能导致肌肉基因表示和房间区别。除它在肌肉调整几新陈代谢的功能的著名能力以外，包括葡萄糖举起和消费和丰满的酸分解代谢，荡者能堵住myoblasts的房间周期入口，到导致象肌浆球蛋白那样的特定的骨胳的肌肉标记的表示重链或caveolin-3，象一样挑起房间熔化进multinucleatedsyncytia并且，最后肌肉纤维形成。荡者通过p38，Akt和5鈥?的氧化还原作用依赖者激活施加它的pro-differentiative活动激活安培的蛋白质kinase小径。有趣地，区分myoblasts是为adiponectin的autocrine，并且到氧化应力的支持inflammatory背景或暴露的mimicking强烈从区分房间增加荷尔蒙的生产。这些数据建议adiponectin的一个新奇函数，直接协调myogenic区别程序并且在骨胳的myogenesis期间服务一个autocrine函数。

简介：这研究是在RGD-FasL和内在的机制导致的垂体腺瘤房间线GH3/MMQ/AtT20上调查细胞毒素的效果。Fas/DcR3mRNAs被RT-PCR检测，他们的表面表情被流动cytometry测量。RGD-FasL在肿瘤房间上施加的Cytotoxicity与MTT试金被测量，导致的apoptosis被agarose胶化电气泳动决定。房间周期和apoptosis被流动cytometry估计，PI染色。caspase8/9/3，Bcl-2，RANKL和JNK2的表情被西方的弄污检测。约13.7%GH3房间，25.5%MMQ房间，，22.2%AtT20房间表示船边交货23.9%GH3房间，24.1%MMQ房间，4.6%AtT20房间表示DcR3。肿瘤房间上的FasL/RGD-FasL的细胞毒素的效果都以一种剂量依赖者方式被拿。房间线MMQ/AtT20至于FasL显示出一样的敏感到RGD-FasL，当房间线GH3对RGD-FasL不太敏感时。房间周期分析显示RGD-FasL能在G0/G1阶段和G2/M阶段禁止房间。在与RGD-FasL对待的MMQ和AtT20房间，AI不与，在与RGD-FasL对待的GH3房间与FasL对待那显著地不同，AI比与FasL对待的低。当Bcl-2的与RGD-FasL在处理以后被减少时，caspase-8/9/3，RANKL和JNK2的表情被增加，建议RGD-FasL导致通过caspase激活的apoptosis。我们断定RGD-FasL能可能被看作垂体腺瘤的处理的一个新奇therapeutical候选人。

简介：Gradingprocedureinroutineseacucumberhatcheryproductionisthoughttoaffectjuvenileseacucumberimmunologicalresponse.Thepresentstudyinvestigatedtheimpactofa3-minmechanicalperturbationmimickingthegradingprocedureonneuroendocrineandimmuneparametersoftheseacucumberApostichopusjaponicus.Duringtheapplicationofstress,concentrationsofnoradrenalineanddopamineincoelomicfluidincreasedsignificantly,indicatingthatthemechanicalperturbationresultedinatransientstateofstressinseacucumbers.Coelomocytesconcentrationincoelomicfluidincreasedtransientlyafterthebeginningofstressing,andreachedthemaximumin1h.Whereas,coelomocytesphagocytosisat3min,superoxideanionproductionfrom3minto0.5h,acidphosphataseactivityat0.5h,andphenoloxidaseactivityfrom3minto0.5hwereallsignificantlydown-regulated.Alloftheimmuneparametersrecoveredtobaselinelevelsaftertheexperimentwasconductedfor8h,andanimmunostimulationoccurredafterthestressconsideringthephagocytosisandacidphosphataseactivity.Theresultssuggestedthat,asinothermarineinvertebrates,neuroendocrine/immuneconnectionsexistinseacucumberA.japonicus.Mechanicalstresscanelicitaprofoundinfluenceonseacucumberneuroendocrinesystem.Neuroendocrinemessengersactinturntomodulatetheimmunityfunctions.Therefore,theseeffectsshouldbeconsideredfordevelopingbetterhusbandryprocedures.

简介：MaleWistar7-day-oldratswereinjectedwith40mg/kgketamineintraperitoneally,followedbythreeadditionalinjectionsof20mg/kgketamineeachuponrestorationoftherightingreflex.Neonatalratsinjectedwithequivalentvolumesofsalineservedascontrols.Hippocampalsampleswerecollectedat1,7or14daysfollowingadministration.Electronmicroscopyshowedthatneuronalstructurechangednoticeablyfollowingketaminetreatment.Specifically,microtubularstructurebecameirregularanddisorganized.Quantitativerealtime-PCRrevealedthatphosphorylatedtaumRNAwasupregulatedafterketamine.Westernblotanalysisdemonstratedthatphosphorylatedtaulevelsatserine396initiallydecreasedat1dayafterketamineinjection,andthengraduallyreturnedtocontrolvalues.At14daysafterinjection,levelsofphosphorylatedtauwerehigherintheketaminegroupthaninthecontrolgroup.Tauproteinphosphorylatedatserine404significantlyincreasedafterketamineinjection,andthengraduallydecreasedwithtime.However,thelevelsoftauproteinatserine404weresignificantlygreaterintheketaminegroupthaninthecontrolgroupuntil14days.ThepresentresultsindicatethatketamineinducesanincreaseofphosphorylatedtaumRNAandexcessivephosphorylationoftauproteinatserine404,causingdisruptionofmicrotubulesintheneonatalrathippocampusandpotentiallyresultingindamagetohippocampalneurons.

简介：

简介：Inthisstudy,weaimedtoexploretheroleofursolicacidintheneuralregenerationoftheinjuredsciaticnerve.BALB/cmicewereusedtoestablishmodelsofsciaticnerveinjurythroughunilateralsciaticnervecompletetransectionandmicroscopicanastomosisat0.5cmbelowtheischialtuberosity.Thesuccessfullygeneratedmodelmiceweretreatedwith10,5,or2.5mg/kgursolicacidviaintraperitonealinjection.Enzyme-linkedimmunosorbentassayresultsshowedthatserumS100proteinexpressionlevelgraduallyincreasedat1-4weeksaftersciaticnerveinjury,andsignificantlydecreasedat8weeks.Assuch,ursolicacidhasthecapacitytosignificantlyincreaseS100proteinexpressionlevels.Real-timequantitativePCRshowedthatS100mRNAexpressionintheL4-6segmentsontheinjurysidewasincreasedafterursolicacidtreatment.Inaddition,themuscularmassindexinthesoleusmusclewasalsoincreasedinmicetreatedwithursolicacid.Toluidinebluestainingrevealedthatthequantityandaveragediameterofmyelinatednervefibersintheinjuredsciaticnerveweresignificantlyincreasedaftertreatmentwithursolicacid.10and5mg/kgofursolicacidproducedstrongereffectsthan2.5mg/kgofursolicacid.Ourfindingsindicatethatursolicacidcandose-dependentlyincreaseS100expressionandpromoteneuralregenerationinBALB/cmicefollowingsciaticnerveinjury.

简介：真菌经常被用来在Aquilaria树上导致agarwood。这研究被进行在年轻Aquilariamalaccensis随着时间的过去在agarwood形成上评估几真菌的效果(打)树。在长度和产生褪色的轻紧张的典型变化在三和六月时期追随者接种以后被观察。伍德样品是观察用显微镜并且分类进几个轻紧张组。褪色长度是测量的纵。在接种以后的持续时间影响了褪色长度的平均数：当时，6月的旧样品(1.70厘米)有一个更宽的褪色地区与3月的旧样品(1.17厘米)相比。当测量褪色紧张时，与时间的一种积极关系被察觉。数字图象，使用一台装备照相机的显微镜捕获，表明在六个月以后收集的木头样品显得是1.8-times比在三个月以后黑暗。我们结束了那时间，不是任何测试真菌的种类，褪色长度和紧张上的有的重要效果。6月的旧样品的煤气的层析/团spectrometry(GCMS)分析产出象benzylacetone，anisylacetone，guaiene和palustrol那样的一些重要agarwood混合物。这证明测试真菌有能力在托儿所A导致agarwood形成。malaccensis树。

简介：TherearetwopossibleoutcomeswhenDNAdamageoccursinnormalmammaliancells:eitherinductionofcell-cyclecheckpointwhichinhibitstheprogressofthecellcyclesaswellasactivatesDNArepairpathways,oractivationofapoptosistoeliminatedamagedcells.Thep53tumour-suppressorgeneplaysakeyroleinselectingthesepathways.Inourpresentworks,thehumangastriccancercelllineAGSwastreatedwithtripchlorolide,apotentantitumorcompoundpurifiedfromaChineseherbTripterygiumWilfordiiHook.Singlecellgelelectrophoresis(Cometassay)showedthatthetreatmentoftripchlorolideresultedinDNAdamageinAGScells.ThedamagedAGScellswentthroughapoptosis,whichwastime-anddose-dependent.

简介：Intheprocessofoxidativephosphorylation,protonsarepumpedintotheintermembranespacetoestablishthemitochondrialmembranepotential(MMP).Relyingontheelectrochemicalgradient,protonscanreturntothematrixthroughtheATPsynthasecomplexwithATPgeneration.MitoQ,alipophiliccationdrug,canbebsorbedtotheinnermitochondrialmembranewiththecationicmoietystayingattheintermembranespace[1].

简介：biflavonoidisochamaejasmin主要在StellerachamaejasmeL的根被散布。(Thymelaeaceae)那在繁体中文药(TCM)被使用治疗肿瘤，肺结核，和干癣。此处，isochamaejasmin被发现对Bcl-2家庭蛋白质显示出类似的bioactivity到参考Bcl-2ligand(−)通过3D类似搜索的-gossypol。它有选择地跳了到Bclx有K和Mcl-1>是的i价值1.93±0.13mol·L−1和9.98±0.21mol·L−1,分别地。另外，isochamaejasmin显示出细微生长对有是的IC50价值的HL-60的禁止的活动50.40±1.21mol·L−1和中等生长对有IC50价值的K562细胞的禁止的活动是24.51±1.62mol·L−1。而且，isochamaejasmin由增加在Bcl-2-inducedapoptosis小径包含了的caspase-9，caspase-3，和PARP的劈开的蛋白质的细胞内部的表示层次导致了K562房间的apoptosis。这些结果显示isochamaejasmin由禁止Bcl-2家庭蛋白质的活动在白血病房间导致apoptosis，提供为进一步学习S的内在的反癌症机制的证据。chamaejasmeL。

简介：AbstractObjective:Despite the fact that adenomyosis is a fairly common gynecological disorder, its pathogenesis remains elusive. Several theories on the pathogenesis of adenomyosis have been proposed, but none of them has been proven experimentally. So far, the most used one is the neonatal feeding of tamoxifen (TAM) in Institute of Cancer Research/cryopreserved (ICR/CD-1) mouse. However, its underlying mechanism of action is unknown. To further delineate the mechanism of TAM-induced adenomyosis in ICR/CD-1 mouse with regard to specific estrogen receptor (ER), we conducted an experiment that neonatal mice were fed with either TAM, or 4,4′,4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (PPT; an ERα agonist), or 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN; an ERβ agonist), or G-1 (a G-protein coupled receptor 30 agonist), or just vehicle, in an attempt to tease out which specific receptor plays a dominant role in the genesis of adenomyosis induced by neonatal feeding of TAM.Methods:Forty female neonatal mice were randomly divided into 5 equal-sized groups: CTL (control), TAM, PPT, DPN, and G-1. Three months later, all mice were sacrificed and their uterine horns were harvested, weighed, and processed for histological evaluation.Results:All mice in the TAM group developed adenomyosis, so did 4 mice (50%) in the DPN group, a result that should be considered significant given that mice in the CTL group would not develop adenomyosis. No mouse in the PPT or G-1 group developed adenomyosis. Remarkably, all lesions in the DPN group were seen exclusively near the uterine serosa, which are dramatically different from that of TAM mice and reminiscent of extrinsic or external adenomyosis in humans.Conclusions:Neonatal feeding of DPN induces adenomyosis, but the adenomyotic lesions appear to be different from those induced by TAM. Thus, the cause of TAM-induced adenomyosis in ICR/CD-1 mouse cannot be attributable to one specific ER alone. This suggests that the extrinsic/external adenomyosis may have a pathogenesis that is different from other sub-types of adenomyosis.

简介：因为它启用自由并且从而的光子旋转度的敏感控制，光的纺纱轨道相互作用(SOI)强烈地在nanophotonics被学习了光子的轨道，它为象信号编码和路由那样的应用程序是有用的。最近的研究[Phys。加快。Lett。117，166803(2016)]证明光子的SOI在光子通过宣传的媒介的介电常数面对一个坡度表明；这提高在沿着扭曲的轨道宣传的光子散布循环地极化的光和结果。这里，我们理论上预言那，因为在不同类的绝缘的媒介和在转变光学表明的一个重力的领域之间的等价，重要SOI被导致到一个黑洞的重力的透镜过去的循环地极化的光上。这导致：我)如果黑洞的尺寸比事件光子的波长小，沿着chiral轨道宣传的光子；ii)重力的透镜到的产生图象因为这些chiral轨道，表明方位角的旋转。为探查为并且用循环地极化的光发现subwavelength尺寸黑人洞的一个方法开的调查结果。

简介：Objective:TodeterminewhetherInterferon-alpha-2b(IFN-α2b)canmodulatetheautophagicresponseinhepatocellularcarcinomacells.Methods:HepatocellularcarcinomacellsweretreatedwithIFN-α2b.Autophagywasassessedbyacridineorangestaining,GFP-LC3dottedassay,transmissionelectronmicroscopyandimmunoblotting.Results:AcridineorangestainingshowedthatIFN-α2btriggeredtheaccumulationofacidicvesicularandautolysosomesinHepG2cells.TheacridineorangeHepG2cellratioswere(4.3±1.0)%,(6.9±1.4)%,and(13.1±2.3)%,respectively,aftertreatmentwith100,1,000,and10,000IU/mLIFN-α2bfor48h.AmarkedlypunctatepatternwasobservedinHepG2cellstreatedwith10,000IU/mLIFN-α2bfor48h,butonlydiffuseandweaklyfluorescentGFP-LC3punctawasobservedincontrolcells.HepG2cellstreatedwith10,000IU/mLIFN-α2bfor48hdevelopedautophagosome-likecharacteristics,includingsingle-ordouble-membranevacuolescontainingintactanddegradedcellulardebris.TheBeclin1andLC3-IIproteinexpressionwasup-regulatedbyIFN-α2btreatment.Conclusion:Autophagycanbeinducedinadose-dependentmannerbytreatmentwithIFN-α2binHepG2cells,andtheBeclin1signalingpathwaywasstimulatedbyIFN-α2b.

简介：雄激素受体(AR)和它的coregulators在前列腺癌症的carcinogenesis有重要角色。p53是重要的瘤suppressor基因，并且基本p53回答的缺席可以预先安排到癌症。Transgelin，作为一个联系ARA54的AR禁止者知道，能在LNCaP房间压制AR功能。除了这些效果，我们试图阐明LNCaP和它的内在的机制上的蛋白质的proapoptotic效果，特别在transgelin和p53之间的相互作用。数的房间，流动cytometric分析和把试金标记的终端deoxynucleotidyltransferase-dUTP刻痕结束被使用测量transgelin的proapoptotic效果。用与transgelinp53染色的p53和两倍immunofluorescence的西方的弄污，我们在增加p53的细胞质的translocation和p53表示的upregulation显示出transgelin结果的那transfection。我们也在vivo发现了在transgelin和p53之间的一个相互作用由哺乳动物二混血儿并且coimmunoprecipitation试金。联系线粒体的apoptosis小径的激活与transgelin在transfection以后在LNCaP房间被观察。这些结果除了它AR小径上的已知的镇压效果的LNCaP房间上的transgelin的调停p53的联系线粒体的apoptotic效果是指示的。

简介：AIM:Toinvestigatethemorphologicalalteringeffectoftransforminggrowthfactor-β2(TGF-β2)onuntransfectedhumancornealendothelialcells(HCECs)invitro.METHODS:AfteruntransfectedHCECsweretreatedwithTGF-β2atdifferentconcentrations,themorphology,cytoskeletondistribution,andtypeIVcollagenexpressionofthecellswereexaminedwithinvertedcontrastlightmicroscopy,fluorescencemicroscopy,immunofluorescenceorWesternBlot.RESULTS:TGF-β2attheconcentrationof3-15μg/LhadobviouslyalterativeeffectsonHCECsmorphologyindoseandtime-dependentmanner,and9μg/Lwasthepeakconcentration.TGF-β2(9μg/L)alteredHCEcellmorphologyaftertreatmentfor36h,increasedthemeanopticaldensity(P<0.01)andthelengthofF-actin,reducedthemeanopticaldensity(P<0.01)ofthecollagentypeIVinextracellularmatrix(ECM)andinducedtherearrangementofF-actin,microtubuleincytoplasmandcollagentypeIVinECMaftertreatmentfor72h.·CONCLUTION:TGF-β2hasobviouslyalterativeeffectonthemorphologyofHCECsfrompolygonalphenotypetoenlargedspindle-shapedphenotype,indoseandtime-dependencemannerbyinducingmore,elongationandalignmentofF-actin,rearrangementofmicrotubuleandlargerspreadareaofcollagentypeIV.

简介：hemolysinoligomer支持B-1a房间和CD25的表示的增长，它房间激活是指示的，在B-1a房间上。当单体没能导致这些效果时，oligomer导致的CD86的upregulation为B7家庭的B7-2成员显示出它的选择偏爱。oligomer导致了CXCR3的表示，当单体导致了CXCL4的表示时，与B房间激活联系了，强大的angiostaticchemokine。在结论，我们发现了房间由表示CXCL4回答了到apoptogenic单体的那B-1a，而immunogen的oligomerization导致了CXCR3向激活转移反应。

简介：目的将在对待matrine的K562房间上调查CGI-100-击倒的K562房间的特征和CGI-100RNA干扰(RNAi)的效果。指向CGI-100基因和与一个不同序列包含一样的核苷酸作文的一双否定控制的三oligonucleotides被设计并且化学上综合了的方法。由在K562房间的shRNA-CGI-100的CGI-100表示的抑制效率用semiquantitativeRT-PCR和点污点杂交被决定。K562房间的生长上的CGI-100RNAi的效果用MTT试金被检验，房间区别被不同途径包括流动cytometry，benzidine染色和电子显微镜测量。在CGI-100-konckdownK562细胞为48h与matrine的0.2mg/ml或hemin的30mol/L被孵化以后，GlycophorinA(GPA)(CD235a)和生长因素independence-1BmRNA(Gfi-1BmRNA)的表示层次被RT-PCR和GPA的蛋白质层次测量，CD14和CD15被流动cytometry检测。结果CGI-100RNAi的真核细胞的表示向量成功地被构造。K562/shRNA-CGI-100房间线在由shRNA-CGI-100的CGI-100基因表示的抑制效率在哪个是54%被建立。CGI-100-knockdown禁止了增长并且在K562房间导致了erythroid区别。与控制K562房间相比，K562/shRNA-CGI-100房间证明减少的吸收度价值由MTT试金，减少的enchromation，增加的heterochromation，G0/G1阶段房间的增加的百分比，S阶段房间的减少的人口，减少的PI(房间的增长索引)，和benzidine积极的房间的提高的百分比检测了。而且，到matrine或hemin的K562/shRNA-CGI-100房间的敏感被提高，到matrine的这些房间的敏感对hemin比那高。与控制K562房间相比，在K562/shRNA-CGI-100房间的matrine处理导致了增长，benzidine积极的房间的提高的百分比，GPA和Gfi-1B的显然起来调整的mRNA表达式，和GPA的增加的吝啬的荧光紧张(MFI)的增加的禁止的率。没有CD14表示被检测，没有统计意义被作出对有利的裁决检测CD15。最后，在与hemin对待并�