简介：Guidedtissueregenerationisanewapproachinthereconstructivesurgeryofperipheralnerves.Biomimeticconductswereconstructfromtheexpandedveinonwhoseinnersurfacecompositedwithamnionfilaments(cf.Fig1).

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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：ThestudywasconductedinManglingVillageunderDehongPerfecture,YunnanProvince,forthoroughinvestigationofforesttenurestructure,managementmodeandforestlandtransferofcollectiveforestsaswellasoffarmers'preferenceformanagementandtransferintention.TheimpactfactorsofmanagementorientationoffarmerhouseholdswereanalyzedwithLogisticModel.Theresultsshowedthattenurestructureandmanagementmodesofcollectiveforesthavebeendiversifiedafterthecollectiveforestte...

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：Objective:Chroniclymphocyticleukemia(CLL)andmantlecelllymphoma(MCL)cellsover-expressaguanineexchangefactor(GEF),Rasgrf-1.ThisGEFincreasesactiveRasasitcatalyzestheremovalofGDPfromRassothatGTPcanbindandactivateRas.ThisstudyaimstostudythemechanismofactionofRasgrf-1inB-cellmalignancies.Methods:N-terminustruncatedRasgrf-1variantshaveahigherGEFactivityascomparedtothefull-lengthtranscriptthereforeaMCLcelllinewithstableover-expressionoftruncatedRasgrf-1wasestablished.TheB-cellreceptor(BCR)andchemokinesignalingpathwayswerecomparedintheRasgrf-1over-expressingandacontroltransfectedcellline.Results:Cellsover-expressingtruncatedformofRasgrf-1haveahigherproliferativerateascomparedtocontroltransfectedcells.BCRwasactivatedbylowerconcentrationsofanti-IgMantibodyinRasgrf-1over-expressingcellsascomparedtocontrolcellsindicatingthatthesecellsaremoresensitivetoBCRsignaling.BCRsignalingalsophosphorylatesRasgrf-1thatfurtherincreasesitsGEFfunctionandamplifiesBCRsignaling.ThisactivationofRasgrf-1inover-expressingcellsresultedinahigherexpressionofphospho-ERK,AKT,BTKandPKC-alphaascomparedtocontrolcells.BesidesBCR,Rasgrf-1over-expressingcellswerealsomoresensitivetomicroenvironmentstimuliasdeterminedbyresistancetoapoptosis,chemotaxisandERKpathwayactivation.Conclusions:ThisGEFproteinsensitizesB-cellstoBCRandchemokinemediatedsignalingandalsoupregulatesanumberofothersignalingpathwayswhichpromotesgrowthandsurvivalofthesecells.

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

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简介：BACKGROUND:Brainischemiainvolvessecondaryinflammation,whichsignificantlycontributestotheoutcomeofischemicinsults.Vascularendothelialgrowthfactor(VEGF)mayplayanimportantroleinthevascularresponsetocerebralischemia,becauseischemiastimulatesVEGFexpressioninthebrain,andVEGFpromotesformationofnewcerebralbloodvessels.Minocycline,atetracyclinederivative,protectsagainstcerebralischemiaandreducesinflammation,oxidativestress,andapoptosis.OBJECTIVE:ToobservetheinfluenceofminocyclineonVEGF,interleukin-1beta(IL-1β),andtumornecrosisfactoralpha(TNF-α)expressioninWistarratswithfocalcerebralischemia/reperfusioninjury,andtostudytheneuroprotectionmechanismofminocyclineagainstfocalcerebralischemia/reperfusioninjury.DESIGN,TIMEANDSETTING:Randomized,controlledexperiment,whichwasperformedintheChongqingKeyLaboratoryofNeurologybetweenMarch2007andMarch2008.MATERIALS:Atotalof36female,Wistarratsunderwentsurgerytoinsertathreadintotheleftmiddlecerebralartery.Animalswererandomlydividedintosham-operation,minocyclinetreatment,andischemia/reperfusiongroups,with12ratsineachgroup.Minocycline(HuishiPharmaceuticalLimitedCompany,China)wasdissolvedto0.5g/Linnormalsaline.METHODS:A0.5-1.0cmthreadwasinsertedintoratsfromthesham-operationgroup.Ratsintheischemia/reperfusiongroupunderwentischemiaandreperfusion.Theminocyclinegroupreceivedminocycline(50mg/kg)12and24hoursfollowingischemiaandreperfusion,whereastheothergroupsreceivedsalineatthecorrespondingtimepoints.MAINOUTCOMEMEASURES:mRNAandproteinexpressionofIL-1βandTNF-αwasmeasuredbyreversetranscriptase-polymerasechainreaction(RT-PCR)andenzymelinkedimmunosorbentassay(ELISA),respectively.VEGFmRNAandproteinexpressionwasexaminedbyRT-PCR,Westernblot,andELISA.RESULTS:Minocyclinedecreasedthefocalinfarctvolume.VEGF,IL-1β,andTNF-αexpressionw

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简介：POU抄写因素OCT4不仅在维持pluripotent和房间而且幕作为通过基因剂量的一个房间命运决定因素完成的胚胎的茎(ES)的自我更新的状态起一个必要作用。然而，控制细胞内部的OCT4蛋白质水平的分子的机制留下逃犯。这里，我们报导那人的WWP2，E3ubiquitin(Ub)蛋白质ligase，通过它的WW领域明确地与OCT4交往并且在vitro并且在vivo提高OCT4的Ub修正。我们首先证明在人的ES房间的内长的OCT4能被Ubpost-translationally修改。而且，我们发现WWP2以一种剂量依赖者方式，和WWP2的活跃地点半胱氨酸残余通过26Sproteasome支持了OCT4的降级在OCT4上为它的酶的活动和解朊的效果被要求。显著地，我们当WWP2表示是由特定的RNA干扰(RNAi)的downregulated时，内长的OCT4蛋白质水平显著地被提高的数据表演，建议那WWP2是为在人的ES房间维持合适的OCT4蛋白质水平的一个重要管理者。而且，北污点分析证明WWP2抄本在多样的人的织物/器官是广泛地在场的并且高度在无差别的人的ES房间表示了。然而，它的表示水平快速在区分的人的ES房间以后被减少，显示WWP2表示力量发展地被调整。我们的调查结果证明WWP2是在人的ES房间的OCT4蛋白质水平的一个重要管理者。

简介：运动评价髌(VISA-P)规模的BackgroundThe维多利亚式的研究所是过去常与膝盖骨的tendinopathy在运动员估计症状严厉的最条件特定的报导病人的结果措施。以前的探索因素分析被进行了评估规模维数，与不一致的结果，并且规模的因素结构仍然保持不清楚。现在的学习的目的是越过包括的sexes.MethodsThe学习用确定的因素分析(CFA)和测试测量不变性决定VISA-P规模的因素的结构有膝盖骨的tendinopathy的249个西班牙的运动员的一件便利样品。CFA被执行估计因素的有效性。假设1因素和2因素模型被测试。越过性的测量不变性用EQS6.1software.ResultsThe与几个合适的索引经由多组CFA被评估内部一致性系数0.74。几个CFA模特儿被检查，在为项目的错误，7和8被相关的1因素模型出现了可接受装入比较合适的索引(CFI)和goodness-of-fit索引(GFI)的术语统计(CFI=0.93；GFI=0.94；标准化根平均数平方residual=0.06；approximation=0.10的根均方差；90%信心间隔：0.08-0.13)。这个模型越过在为项目的错误，7和8被相关的VISA-P规模(VISA-P-Sp)的西班牙的版本的1因素模型表明了的sexes.ConclusionThe是不变的亲戚装入CFA。没有性偏爱，经由VISA-P-Sp获得的分数能在男人和女人之间被比较。进一步的研究应该并发地检验VISA-P规模和另外的单个分数的报导病人的结果措施。

简介：AbstractThe chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family (CMTM) is widely expressed in the immune system. Abnormal expression of CMTM is associated with the development of various diseases. This article summarizes the relevant research on the role of the CMTM family in immune disorders. This information will increase our understanding of pathogenesis and identify promising targets for the diagnosis and treatment of autoimmune diseases. The CMTM family is highly expressed in peripheral blood mononuclear cells. CKLF1 may be involved in the development of arthritis through its interaction with C-C chemokine receptor 4. CKLF1 is associated with the pathogenesis of lupus nephritis and psoriasis. Both CMTM4 and CMTM5 are associated with the pathogenesis of systemic lupus erythematosus. CMTM1, CMTM2, CMTM3, and CMTM6 play a role in rheumatoid arthritis, systemic sclerosis, Sjögren syndrome, and anti-phospholipid syndrome, respectively. The CMTM family has been implicated in various autoimmune diseases. Further research on the mechanism of the action of CMTM family members may lead to the development of new treatment strategies for autoimmune diseases.

简介：Becauseconditionsforthegrainproductionarenotfavorableandtheinputintheproductionfactorsofmodernagricultureisnotsufficient,thegrainsupplyhasbeenlessthanthedemandforalongtime.Bymeansofgreycorrelationanalysis,thispaperdealswiththecorrelationsituationamongsuchinputfactorsasthegrainsownarea,thetotalpowerofagriculturalmachinery,thefertilizerutilizationvolume,theactualirrigationarea,thedamagearea,thenumberoffarminglaborforce,inordertounderstandthemajorrestrictinganddrivingforcesthathaveaffectedthegrainoutputintherecent23years.TheanalysisshowsthatthegrainsownareaandfertilizerutilizationvolumearethetwomostimportantleadingfactorsthataffectgrainproductioninGuizhouProvince,whilethedamageareaandthetotalpowerofthefarming-usedmachinesarethefollowingfactors.Fertilizerutilizationvolumeandtheactualagriculturalmachineryandirrigationareaarethetwoincreasinglyinfluentialfactorsthataffectgrainproduction.Theinfluenceofthefarminglaborforceupongrainproductionbecamelessstrong.ThemainmeasurestoincreasegrainproductionoutputinGuizhouProvincearetostabilizethearableland,increasetheactualirrigationarea,expeditethetransferofthefarminglaborforceandincreasetheinputofmodernagriculture.

简介：Endothelialprogenitorcellsareresidentinthebonemarrowbloodsinusoidsandcirculateintheperipheralcirculation.Theymobilizefromthebonemarrowaftervascularinjuryandhometothesiteofinjurywheretheydifferentiateintoendothelialcells.Activationandmobilizationofendothelialprogenitorcellsfromthebonemarrowisinducedviatheproductionandreleaseofendothelialprogenitorcell-activatingfactorsandincludesspecificgrowthfactorsandcytokinesinresponsetoperipheraltissuehypoxiasuchasafteracuteischemicstrokeortrauma.Endothelialprogenitorcellsmigrateandhometospecificsitesfollowingischemicstrokeviagrowthfactor/cytokinegradients.Somegrowthfactorsarelessstableunderacidicconditionsoftissueischemia,andsyntheticanaloguesthatarestableatlowpHmayprovideamoreeffectivetherapeuticapproachforinducingendothelialprogenitorcellmobilizationandpromotingcerebralneovascularizationfollowingischemicstroke.

简介：Basedonenergyequilibrium,anewprocedurecalledtheMembraneFactorMethodisdevel-opedtoanalyzethedynamicplasticresponseofplateswithdeflectionsintherangewherebothbendingmo-mentsandmembraneforcesareimportant.Thefinaldeflectionofasimply-supportedcircularrigid-plasticplateloadedbyauniformlydistributedimpulseisobtained.Incomparisonwithotherapproximatesolutions,thepresentresultsarefoundtobesimplerandinbetteragreementwiththecorrespondingexperimentalvaluesreoordedbyFlorence.

简介：AIMTo报告角膜的营养障碍(液晶显示器)与二个变化，R124C和A546D联系了的格子的一个phenotypic变体家谱，在导致贝它的基因(TGFBI).METHODSA详细说明了的转变生长因素，眼睛的检查为一个液晶显示器家庭的所有参加者被参加。从每个参加者的外部血白血球被提取获得DNA。TGFBI基因的所有十七exons的聚合酶链反应(PCR)被执行。产品被定序并且分析。在从proband.RESULTSGenetic分析的右眼睛的渗透的keratoplasty证明proband和所有6个影响个人两个都在codon怀有异质接合的CGC到TGC变化以后，组织学的检查被执行124并且异质接合的GCC到在codon的GAC变化546TGFBI。任何一个100个控制题目和未受影响的家庭成员都不为这二个变化是积极的。眼睛的检查显示了多重refractile在在外部角膜的中央角膜和小小粒的存款的前面的基质的像格子的暗。存款与红显示是的刚果断然被染色在自然淀粉、位于主要观察的前面、中间的stroma.CONCLUSIONWe在TGFBI基因带了二个病原的变化(R124C和A546D)的一个新奇液晶显示器家庭。phenotypic特征与与相应单个变化联系的那些显然不同。结果表明尽管明确的变化是疾病的最重要的基因原因，一些不同修饰词等位基因可以影响显型。

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