简介：Traumaticbraininjury(TBI)istheleadingcauseofdeathanddisabilityofpersonsunder45yearsoldintheUnitedStates,affectingover1.5millionindividualseachyear.Ithadbeenthoughtthatrecoveryfromsuchinjuriesisseverelylimitedduetotheinabilityoftheadultbraintoreplacedamagedneurons.However,recentstudiesindicatethatthematuremammaliancentralnervoussystem(CNS)hasthepotentialtoreplenishdamagedneuronsbyproliferationandneuronaldifferentiationofadultneuralstem/progenitorcellsresidingintheneurogenicregionsinthebrain.Furthermore,increasingevidenceindicatesthattheseendogenousstem/progenitorcellsmayplayregenerativeandreparativerolesinresponsetoCNSinjuriesordiseases.Insupportofthisnotion,heightenedlevelsofcellproliferationandneurogenesishavebeenobservedinresponsetobraintraumaorinsultssuggestingthatthebrainhastheinherentpotentialtorestorepopulationsofdamagedordestroyedneurons.Thisreviewwilldiscussthepotentialfunctionsofadultneurogenesisandrecentdevelopmentofstrategiesaimingatharnessingthisneurogeniccapacityinordertorepopulateandrepairtheinjuredbrain.

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简介：OnbehalfoftheEditors-in-ChiefandEditorialBoard,wewishtoexpressourgratitudetothefollowing'anonymous'reviewerswhogavetheirtimeandenergyforreviewingthearticles(eitherpublishedorrejected)fromJanuary1,2014,throughDecember31,2014,ensuringthequalityofNeuralRegenerationResearch.

简介：Neurodegenerativedisordersaffectmorethan30millionindividualsthroughouttheworldandleadtosignificantdisabilityaswellasdeath.Thesestatisticswillincreasealmostexponentiallyasthelifespanandageofindividualsincreasegloballyandindividualsbecomemoresusceptibletoacutedisorderssuchasstrokeaswellaschronicdiseasesthatinvolvecognitiveloss,Alzheimer’sdisease,andParkinson’sdisease.Currenttherapiesforsuchdisordersareeffectiveonlyforasmallsubsetofindividualsorprovidesymptomaticreliefbutdonotalterdiseaseprogression.Oneexcitingtherapeuticapproachthatmayturnthetideforaddressingneurodegenerativedisordersinvolvesthemammaliantargetofrapamycin(mTOR).mTORisacomponentoftheproteincomplexesmTORComplex1(mTORC1)andmTORComplex2(mTORC2)thatareubiquitousthroughoutthebodyandcontrolmultiplefunctionssuchasgenetranscription,metabolism,cellsurvival,andcellsenescence.mTORthroughitsrelationshipwithphosphoinositide3-kinase(PI3-K)andproteinkinaseB(Akt)andmultipledownstreamsignalingpathwayssuchasp70ribosomalS6kinase(p70S6K)andprolinerichAktsubstrate40kDa(PRAS40)promotesneuronalcellregenerationthroughstemcellrenewalandoverseescriticalpathwayssuchasapoptosis,autophagy,andnecroptosistofosterprotectionagainstneurodegenerativedisorders.TargetingbymTORofspecificpathwaysthatdrivelong-termpotentiation,synapticplasticity,andβ-amyloidtoxicitymayoffernewstrategiesfordisorderssuchasstrokeandAlzheimer’sdisease.Overall,mTORisanessentialneuroprotectivepathwaybutmustbecarefullytargetedtomaximizeclinicalefficacyandeliminateanyclinicaltoxicsideeffects.

简介：MolecularmechanismsoftheKru?ppel-likefamilyoftranscriptionfactors(KLFs)havebeenstudiedmoreinproliferatingcellsthaninpost-mitoticcellssuchasneurons.WerecentlyfoundthatKLFsregulateintrinsicaxongrowthabilityincentralnervoussystem(CNS)neuronsincludingretinalganglioncells,andhippocampalandcorticalneurons.Withatleast15of17KLFfamilymembersexpressedinneuronsandatleast5structurallyuniquesubfamilies,itisimportanttodeterminehowthiscomplexfamilyfunctionsinneuronstoregulatetheintricategeneticprogramsofaxongrowthandregeneration.BycharacterizingthemolecularmechanismsoftheKLFfamilyinthenervoussystem,includingbindingpartnersandgenetargets,andcomparingthemtodefinedmechanismsdefinedoutsidethenervoussystem,wemaybetterunderstandhowKLFsregulateneuritegrowthandaxonregeneration.

简介：增加的证据证明磁场和磁性的应答的脚手架能在支持骨头修理和新生起唯一的作用。这篇文章在situ在骨头新生上响应外部磁场探讨磁性的脚手架的synergistic效果。另外，使用在骨头的工具植入固定，本地药交货和干细胞区别的mimicking微型环境的磁性的脚手架的探索被介绍。我们也在骨头修理和新生讨论了磁性的应答的脚手架的可能的内在的机制和观点。

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简介：Theirretrievablefateofneuronsdominatedtheneurosciencerhetoricforthefirsthalfofthiscentury,apositionthatwasfiercelycontestedandrecentlydebunkedbyextensivestudiescarriedoutinthefieldofneuroregenerationresearch.Theturningpointcameintheyear1928,whenRamonY.Cajal’s(Lobato,2008)worksuggestedthattheregenerativecapacityof

简介：Thisstudyproposesapost-processortoimprovetheharmonicstructureofavowelinanenhancedspeech,enablingthespeechqualitytobeimproved.Initially,aspeechenhancementalgorithmisemployedtoreducethebackgroundnoiseforanoisyspeech.Hencetheenhancedspeechispost-processedbyahybrid-medianfiltertoreducethemusicaleffectofresidualnoise.Sincetheharmonicspectraareimpactedbybackgroundnoiseandaspeechenhancementprocess,thequalityofavowelisdeteriorated.Aharmonicregeneratedmethodisdevelopedtoimprovethequalityofpost-processedspeech.Experimentalresultsshowthattheproposedmethodcanimprovethequalityofpost-processedspeechbyadequatelyregeneratingharmonicspectra.

简介：Braindevelopmentisoneofthemostfascinatingsubjectsinthefieldofbiologicalsciences.Nonetheless,ourscientificcommunitystillfaceschallengesintryingtounderstandtheconceptsthatdefinetheunderlyingmechanismsofneuraltissuedevelopment.Afterall,itisaverycomplexsubjecttograspandmany

简介：Recentstudieshaveshownthattheglycation-associateddamageisnotlimitedtopatientswithdiabetes.Becauseoftheirassociationwithoxidativestress,advancedglycationend-products(AGEs)havealsobeenimplicatedinmanyneurodegenerativediseases,suchasHuntingtondisease,amyotrophiclateralsclerosis,andAlzheimerdisease(Yanetal.,

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简介：采用5水平Box-Behnken设计的反应表面方法论(RSM)被用来优化铈(III)的biosorption到动物和植物起源viz的biowaste材料上。对虾甲壳(PC)和玉米风格(CS)。各种各样的过程参数viz。pH(一：3.0–9.0)，生物资源剂量(B：0.05–0.35g/L)，起始的金属集中(C：50–350mg/L)，接触时间(D：2–6h)并且温度(E：20–60°C)为优化被选择。木头转变被盒子艇长阴谋在现在的盒子中建议。低p值<0.0001验证了模型的意义。为PC的218.3mg/g和为CS的180.2mg/g的最大的Ce(III)举起在最佳条件下面被注意。在平衡等温线之中，Freundlich模型被发现是而兰米尔模型证明最好适合在CS上建议铈biosorption的同类的模式，在PC上建议biosorption的一个异构的模式的最好适合的那个。这被扫描电子显微镜学(SEM)进一步证实。运动研究显示出作为位于这个过程下面的现象建议physisorption的伪first顺序模型的更好的适用性。电影散开被博伊德阴谋的非线性建议。热力学的研究证明这个过程吸热、自发。FTIR分析在Ce(III)biosorption期间证实了酰胺，胺，酉同类和主要白酒组的参予的主要参与。EDAX分析在Ce(III)biosorption期间证实了碳组的主要参予。这是Ce(III)biosorption的参数优化上的第一份报告到用可能从水的环境对Ce(III)的恢复有用的5水平Box-Behnken试验性的设计的biowaste材料上。