简介：Theactivationandselectiveconversionofenergy-relatedmoleculesisanimportantresearchareaofenergychemistry.Thedepletionofpetroleumhasstimulatedresearchactivitiesintotheutilizationofnon-petroleumcarbonresourcessuchasnaturalgas(includingconventionaland

简介：AIMTo探索α的效果；在在眼的神经压碎(ONC)和α的机制以后的星形细胞gliosis的A-crystallin；在neuroprotection和轴突regeneration.METHODSONC的-crystallin在Sprague-Dawley老鼠模型和α上被建立；A-crystallin(10−4g/L，4µ；L)intravitreously被注入老鼠模型。闪光视觉的唤起的潜力(F-VEP)是在ONC，和酸的蛋白质(GFAP)在视网膜铺平的glialfibrillary以后的检验14d，压碎地点被分析1，3，5，7并且在由immunohistochemistry(IHC)和西方的污点的ONC以后的14d分别地。在在视网膜和眼的神经的ONC.RESULTSGFAP水平显著地在ONC以后增加了1d以后，贝它导管素(TUJ1)的层次，联系生长的膜phosphoprotein-43(GAP-43)，chondroitin硫酸盐proteoglycans(CSPG)和neurocan被IHC14d也决定，并且到达了山峰水平7dpost-ONC。α的注射；A-crystallin显著地减少了在在ONC以后的视网膜和压碎地点3d的GFAP水平，并且导致的星形细胞建筑学在压碎地点改变。网膜的中心房间(RGC)的Quantification轴突显示了α；A-crystallin显著地在ONC老鼠支持了轴突新生并且提高了渗透进glial疤的改革轴突。CSPG和neurocan表示也减少了在α以后的14d；A-crystallin注射。振幅(N1-P1)和F-VEP的潜伏(P1)也是restored.CONCLUSIONOur结果建议α；-crystallin支持RGC的轴突新生并且压制星形细胞的激活。

简介：AIM:Toinvestigatetheanti-apoptoticcapabilityofthehepatitisBvirus(HBV)intheHepG2hepatomacelllineandtheunderlyingmechanisms.METHODS:CellviabilityandapoptosisweremeasuredbyMTTassayandflowcytometry,respectively.Targetedknockdownofmanganesesuperoxidedismutase(MnSOD),AMP-activatedproteinkinase(AMPK)andhepatitisBvirusXprotein(HBx)genesaswellasAMPKagonistAICARandantagonistcompoundCwereemployedtodeterminethecorrelationsofexpressionofthesegenes.RESULTS:HBVmarkedlyprotectedthehepatomacellsfromgrowthsuppressionandcelldeathintheconditionofserumdeprivation.AdecreaseofsuperoxideanionproductionaccompaniedwithanincreaseofMnSODexpressionandactivitywasfoundinHepG2.215cells.Moreover,AMPKactivationcontributedtotheup-regulationofMnSOD.HBxproteinwasidentifiedtoinducetheexpressionofAMPKandMnSOD.CONCLUSION:OurresultssuggestthatHBVsuppressesmitochondrialsuperoxidelevelandexertsanantiapoptoticeffectbyactivatingAMPK/MnSODsignalingpathway,whichmayprovideanovelpharmacologicalstrategytopreventHCC.

简介：全身的豺狼座erythematosus(SLE)是B房间hyperreactivity描绘的自体免疫的疾病。像使用费的受体7(TLR7)表明小径反常地在SLEB房间被激活。CyclinD3(CCND3)在B房间增长，开发，和区别起一个重要作用。尽管以前的研究为自发的幼芽的中心的发展集中了于TLR7的B房间内在的角色，在SLEB房间的CCND3上的TLR7的影响仍然不是清楚的。这里，我们使用了介绍薄片的B房间并且发现CCND3与SLE有关并且显著地在SLEB房间提高了。而且，我们决定CCND3的表示水平更高，当miR-15b与正常题目相比在从SLE病人和B6.MRL-Faslpr/J豺狼座老鼠的B房间是显著地更低的时。而且，我们证明TLR7的激活戏剧性地增加了CCND3表示，但是显著地减少了在在vitro的B房间的miR-15b并且我们鉴别CCND3是miR-15b的一个直接目标。为了推进，证实我们的结果，我们由谈论地对待C57BL/6(B6)建立了另一个豺狼座模型有为8个星期的TLR-7收缩筋imiquimod(IMQ)的老鼠根据以前描述的协议。Expectedly，有IMQ的热门治疗显著地也增加了CCND3并且减少在B6老鼠的B房间的miR-15b。一起拿，我们的结果鉴别TLR7的激活在Bcells;经由miR-15b的downregulation增加了CCND3表示；因此，这些调查结果建议那外来的导致因素的CCND3表情可以在SLE贡献B房间的反常。

简介：AIMToinvestigatetheroleofthecomplement5a(C5a)/C5areceptor(C5aR)pathwayinthepathogenesisofacuteliverfailure(ALF)inamousemodel.METHODSBALB/cmicewererandomlyassignedtodifferentgroups,andintraperitonealinjectionsoflipopolysaccharide(LPS)/D-galactosamine(D-GalN)(600mg/kgand10μg/kg)wereusedtoinduceALF.TheKaplanMeiermethodwasusedforsurvivalanalysis.Serumalanineaminotransferase(ALT)levels,atdifferenttimepointswithina1-wkperiod,weredetectedwithabiochemistryanalyzer.Pathologicalexaminationoflivertissuewasperformed36hafterALFinduction.Serumcomplement5(C5),C5a,tumornecrosisfactor-α(TNF-α),interleukin(IL)-1β,IL-6,high-mobilitygroupproteinB1(HMGB1)andsphingosine-1-phosphatelevelsweredetectedbyenzyme-linkedimmunosorbantassay.Hepaticmorphologicalchangesat36hafterALFinductionwereassessedbyhematoxylinandeosinstaining.ExpressionofC5aR,sphingosinekinase1(SphK1),p38-MAPKandp-p38-MAPKinlivertissue,peripheralbloodmononuclearcells(PBMCs)andperitonealexudativemacrophages(PEMs)ofmiceorRAW264.7cellswasanalyzedbywesternblotting.C5aRmRNAlevelsweredetectedbyquantitativereal-timePCR.RESULTSActivationofC5andup-regulationofC5aRwereobservedinlivertissueandPBMCsofmicewithALF.BlockadeofC5aRwithaC5aRantagonist(C5aRaC5aRa)significantlyreducedthelevelsofserumALT,inflammatorycytokines(TNF-α,IL-1βandIL-6)andHMGB1,aswellasthelivertissuedamage,butincreasedthesurvivalrates(P<0.01forall).BlockadeofC5aRdecreasedSphK1expressioninbothlivertissueandPBMCssignificantlyat0.5hafterALFinduction.C5aRapretreatmentsignificantlydownregulatedthephosphorylationofp38-MAPKinlivertissuesofALFmiceandC5astimulatedPEMsorRAW264.7cells.Moreover,inhibitionofp38-MAPKactivitywithSB203580reducedSphK1proteinproductionsignificantlyinPEMsafterC5astimulation.CONCLUSIONTheC5a/C5aRpath

简介：我们表明白氨酸应答的规章的蛋白质(rLrp)禁止的那Mycobacterium肺结核recombinantlipopolysaccharide(LPS)导致了肿瘤坏死因素alpha(TNF-α；)，interleukin-6，和interleukin-12生产和块原子受体的抄写因素NF-κ的子单元的原子translocation；B(原子factor-kappaB)。而且，rLrp稀释导致LPS的DNA绑定和NF-κ；Btranscriptional活动，被禁止的Iκ的降级伴随，Bα；并且在NF-κ的原子translocation的作为结果的减少；Bp65子单元。RLrp防碍TNF联系受体的因素的导致LPS的聚类6并且与interleukin-1联系受体的kinase1绑定到TAK1。而且，rLrp没稀释proinflammatorycytokines或CD86和interferon-gamma在像使用费的受体的巨噬细胞导致的主要histocompatibility建筑群class-II的表示2删除(TLR2−/−)老鼠并且在蛋白质kinase，b(Akt)弄空老鼠房间，显示rLrp的禁止的效果依赖于phosphatidylinositol3-OHkinase(PI3K)的调停TLR2的激活/Akt小径。RLrp能也由刺激PI3K，Akt，和肝糖synthasekinase的快速的phosphorylation激活PI3K/Akt小径在巨噬细胞的3贝它。另外，在rLrp的N终点的19氨基酸残余决心重要、要求因为禁止的效果由TLR2调停了。rLrp的这19氨基酸的禁止的功能提起模仿的禁止的肽能被用来处于发信号的延长TLR在有有害效果的状况限制天生的有免疫力的回答的可能性。我们的学习提供新卓见进调停TLR2的PI3K/Akt小径由保证有势力的短暂表示的禁止的机制煽动性的调停人。