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简介：这张手稿用设计策略的织物集中于骨头修理/新生，并且加亮导致新奇nanocomposite系统的nanobiotechnology开发。大约650万破裂在美国每年发生，并且大约550,000个这些单个盒子要求了骨头接枝的申请。自然发生并且allogenous骨头最广泛地为骨头接枝被使用了基于的治疗；然而，象施主缺乏和感染的风险那样有重要问题。用合成、自然的biomaterials的选择被开发了，并且一些为要求骨头接枝的临床的应用程序是商业地可得到的。然而，设计很仔细模仿骨头织物在结构上，和罐头的理想的合成接枝仍然是大挑战在造骨细胞和祖先房间人口调制需要的功能。Nanobiomaterials，明确地，nanocompositeshydroxyapatite创作了(哈)或骨胶原极其正在答应接枝代用品。biocomposites能被制作模仿本国的骨头织物的材料作文，并且另外，当使用nano时--哈(减少的谷物尺寸)，一个人模仿本国的骨头的结构的安排。骨头生物学和结构的好理解对骨头mimicking接枝代用品的开发批评。哈并且能进一步调制regenerative/healing的优秀osteoconductive性质处理跟随破裂损害的骨胶原展览。与另外的聚合biomaterials结合将增强因此做新奇nano的机械性质--哈比得上人的骨头的基于的composites。我们用nanocomposites在最近的研究上报导为部分骨头缺点的新生作为粒子和nanofibers被制作了。在nanocomposites的研究，在理想的未来发展加亮一个枢轴的角色整形外科植入设备，然而进一步的重要前进是必要的完成临床的使用。

简介：ProfessorKowk-faiSo,theeditor-in-chiefofNeuralRegenerationResearch,hasbeennamedaFellowoftheNationalAcademyofInventors(NAI)ProfessorKwok-faiSo,DepartmentofOphthalmology,LiKaShing,FacultyofMedicine,TheUniversityofHongKong(HKU),hasbeennamedaFellowoftheNationalAcademyofInventors(NAI).

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简介：NeuralRegenerationResearch(NRR)isafirst-classinternationalacademicjournalpublishedinEnglish.ItissupervisedbytheMinistryofHealth,P.R.China.NRR(CN11-5422/R,ISSN1675-5374)isamonthlyjournal,distributedallovertheworld.

简介：Immunobiologicalstudyisakeytorevealingtheimportantbasisoffacialnerverepairandregenerationforbothresearchanddevelopmentofclinictreatments.Themicroenvironmentalchangesaroundaninjuriedfacialmotoneuron,i.e.,theaggregationandexpressionofvarioustypesofimmunecellsandmoleculesinadynamicequilibrium,impenetratefromthestarttotheendoftherepairofaninjuredfacialnerve.Theconceptof'immunemicroenvironmentforfacialnerverepairandregeneration',mainlyconcernswiththedynamicexchangebetweenexpressionandregulationnetworksandavariatyofimmunecellsandimmunemoleculesintheprocessoffacialnerverepairandregenerationforthemaintenanceofaimmunemicroenvironmentfavorablefornerverepair.Investigationonmicroglialactivationandrecruitment,Tcellbehavior,cytokinenetworks,andimmunologicalcellularandmolecularsignalingpathwaysinfacialnerverepairandregenerationarethecurrenthotspotsintheresearchonimmunobiologyoffacialnerveinjury.Thecurrentpaperprovidesacomprehensivereviewoftheabovementionedissues.Researchoftheseissueswilleventuallymakeimmunologicalinterventionspracticabletreatmentsforfacialnerveinjuryintheclinic.

简介：Thecorneahasuniquefeaturesthatmakeitausefulmodelforregenerativemedicinestudies.Itisanavascular,transparent,denselyinnervatedtissueandanypathologicalchangescanbeeasilydetectedbyslitlampexamination.Cornealsensitivityisprovidedbytheophthalmicbranchofthetrigeminalnervethatelicitsprotectivereflexessuchasblinkingandtearingandexertstrophicsupportbyreleasingneuromediatorsandgrowthfactors.Cornealnervesareeasilyevaluatedforbothfunctionandmorphologyusingstandardinstrumentssuchascornealesthesiometerandinvivoconfocalmicroscope.Alllocalandsystemicconditionsthatareassociatedwithdamageofthetrigeminalnervecausethedevelopmentofneurotrophickeratitis,araredegenerativedisease.Neurotrophickeratitisischaracterizedbyimpairmentofcornealsensitivityassociatedwithdevelopmentofpersistentepithelialdefectsthatmayprogresstocornealulcer,meltingandperforation.Currentneurotrophickeratitistreatmentsaimatsupportingcornealhealingandpreventingprogressionofcornealdamage.Novelcompoundsabletostimulatecornealnerverecoveryareinadvanceddevelopmentstage.Amongthem,nervegrowthfactoreyedropsshowedtobesafeandeffectiveinstimulatingcornealhealingandimprovingcornealsensitivityinpatientswithneurotrophickeratitis.Neurotrophickeratitisrepresentsanusefulmodeltoevaluateinclinicalpracticenovelneuro-regenerativedrugs.

简介：Theintrinsicgrowthabilityofalltheneuronsdeclinesduringdevelopmentalthoughsomemaygrowbetterthanothers.Numerousintracellularsignalingproteinsandtranscriptionfactorshavebeenshowntoregulatetheintrinsicgrowthcapacityinmatureneurons.Amongthem,PI3kinase/Aktpathwayisimportantforcontrollingaxonelongation.Asanegativeregulatorofthispathway,thetumorsuppressorphosphataseandtensinhomolog(PTEN)appearscriticaltocontroltheregenerativeabilityofyoungandadultneurons.ThisreviewwillfocusonrecentresearchprogressinaxonregenerationandneuralrepairbyPTENinhibitionandtherapeuticpotentialofblockingthisphosphataseforneurologicaldisorders.InhibitionofPTENbydeletioninconditionalknockoutmice,knockdownbyshort-hairpinRNA,orblockadebypharmacologicalapproaches,includingadministrationofselectivePTENantagonistpeptides,stimulatesvariousdegreesofaxonregrowthinjuvenileoradultrodentswithcentralnervoussysteminjuries.Importantly,post-injuryPTENsuppressioncouldenhanceaxonalgrowthandfunctionalrecoveryinadultcentralnervoussystemafterinjury.

简介：NeuralRegenerationResearch(NRR,CN11-5422/R,ISSN1673-5374)isaninternationaljournalpublishingpeer-reviewedoriginalEnglisharticleschargedbytheMinistryofHealth,

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

简介：AbstractThe regeneration capacity of cardiomyocytes (CMs) is retained in neonatal mouse hearts but is limited in adult mouse hearts. Myocardial infarction (MI) in adult hearts usually leads to the loss of large amounts of cardiac tissue, and then accelerates the process of cardiac remodeling and heart failure. Therefore, it is necessary to explore the potential mechanisms of CM regeneration in the neonates and develop potential therapies aimed at promoting CM regeneration and cardiac repair in adults. Currently, studies indicate that a number of mechanisms are involved in neonatal endogenous myocardial regeneration, including cell cycle regulators, transcription factors, non-coding RNA, signaling pathways, acute inflammation, hypoxia, protein kinases, and others. Understanding the mechanisms of regeneration in neonatal CMs after MI provides theoretical support for the studies related to the promotion of heart repair after MI in adult mammals. However, several difficulties in the study of CM regeneration still need to be overcome. This article reviews the potential mechanisms of endogenous CM regeneration in neonatal mouse hearts and discusses possible therapeutic targets and future research directions.

简介：Afterreviewingalargequantityofliteraturesathomeandabroad,thenaturalregenerationbarriermechanismsofforestweredescribed,includinglackofseed,animaleatingandtrespass,plantsallelopathy,microbialpathogenesis,unusualstateofecologicalfactorslikelight,temperature,humidityandrainfall,physicalobstructofunderstorygroundcoverandlitters,naturalandhumandisturbanceanddifferenceforestcommunitycharacteristics.Thepaperfinallycameupwiththeproblemsexistinginthecurrentresearchandthedevelopmentideaoftheresearch.

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.

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