简介：INTRODUCTIONThedisease,damageorlossoftissueandorgancanseriouslyaffectthehumanlife,evenleadstomaimedordeath,thatitshouldnotbeignored.Todate,autograftsandallograftstransplantationarethemostusuallyusedmethodstorepairdefectsoftissuesandorgans.

简介：Thisstudyaimedtoexploretheroleofmechanicaltensioninhypertrophicscarsandthechangeinnervedensityusinghematoxylin-eosinstainingandS100immunohistochemistry,andtoobservetheexpressionofnervegrowthfactorbywesternblotanalysis.Theresultsdemonstratedthatmechanicaltensioncontributedtotheformationofahyperplasticscarinthebackskinofrats,inconjunctionwithincreasesinbothnervedensityandnervegrowthfactorexpressioninthescartissue.Theseexperimentalfindingsindicatethatthecutaneousnervoussystemplaysaroleinhypertrophicscarformationcausedbymechanicaltension.

简介：BACKGROUND:Pattern-visualevokedpotential(PVEP)canreflectthefunctionalstatusofretinalganglialcells(RGC)andvisualcortex,andisanobjectiveexaminationforvisualpathwayfunction.Itisauniquemethodforobjectivelyexaminingtheopticnervefunctionofopticganglioncells.OBJECTIVE:Toobservetheeffectsofnervegrowthfactor(NGF)onPVEFinthetreatmentofopticnervecontusion,evaluatetheclinicalefficacyofNGF,andmakeanefficacycomparisonwithvitaminB12.DESIGN:Arandomlygrouping,controlledobservation.SETTING:DepartmentofOphthalmology,TangshanGongrenHospitalAffiliatedtoHebeiMedicalUniversity.PARTICIPANTS:Fortypatientswithopticnervecontusioncausedbyeyetrauma,whoreceivedthetreatmentintheTangshanWorkerHospitalAffiliatedtoHebeiMedicalUniversitybetweenJanuary2006andJune2007,wererecruitedinthisstudy.Theinvolved40patients,including34malesand6females,wereaged14-59years.TheywereconfirmedtohaveopticnervecontusionbyophthalmologicconsultationcombinedwithhistoryofdiseaseandorbitalCTexamination.Informedconsentsoftreatmentsanddetecteditemswereobtainedfromallthepatients.Thepatientswererandomlydividedinto2groupswith20ineach:NGFgroupandvitaminB12group.METHODS:Conservativetreatmentwasusedinthetwogroups.Inaddition,patientsintheNGFgroupwereintramuscularlyinjectedwithNGFsolution18μg/time,onceaday.ThoseinthevitaminB12groupwereinjectedbythesamemethodwithcommonvitaminB12of500μgcombinedwithvitaminB1of100mg,onceaday.MAINOUTCOMEMEASURES:PVEPexaminationwasconductedinallthepatientsbefore,oneandtwoweeksaftertreatment,andlatencyandamplitudeatP100weredetected.RESULTS:Fortypatientswithopticnervecontusionparticipatedinthefinalanalysis.Beforetreatment,significantdifferencesinthelatencyandamplitudeatP100werenotfoundinpatientsbetweentwogroups(P>0.05).ForeachpatientintheNGF

简介：Guidedtissueregenerationisanewapproachinthereconstructivesurgeryofperipheralnerves.Biomimeticconductswereconstructfromtheexpandedveinonwhoseinnersurfacecompositedwithamnionfilaments(cf.Fig1).

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简介：Objective:Tostudytheeffectofnervegrowthfactor(NGF)andSchwanncellsonaxonregenerationoftheinferioralveolarnervefollowingmandibularlengtheningwithdistractionosteogenesis.Methods:Unilateralmandibularosteodistractionwasperformedin9healthyadultmalegoatswithadistractionrateof1mm/d.Every3goatswerekilledondays7,14and28aftermandibularlengthening,respectively.TheinferioralveolarnervesinthedistractioncalluswereharvestedandprocessedforultrastructuralandNGFimmunohistochemicalstudy.Theinferioralveolarnervesfromthecontralateralsidewereusedascontrols.Results:Onday7afterdistraction,axondegenerationandSchwanncellproliferationwereobserved,andverystrongstainingofNGFinthedistractednervewasdetected.Onday14afterdistraction,axonregenerationandremyelinationwereeasilyobserved,andNGFexpressionstartedtodecline.Onday28afterdistraction,thegrayscaleofNGFimmunoreactivityrecoveredtothenormalvalueandtheSchwanncellsalmostrecoveredtotheirnormalstate.Conclusions:Gradualmandibularosteodistractioncanresultinmildormoderateaxondegenerationoftheinferioralveolarnerve.NervetraumamaystimulatetheproliferationofSchwanncellsandpromotethesynthesisandsecretionofNGFintheSchwanncells.SchwanncellsandNGFmightplayimportantrolesinaxonregenerationoftheinjuredinferioralveolarnervefollowingmandibularlengthening.

简介：Carbonnanotubescancarryproteinintocellstoinducebiologicaleffects.Amino-functionalizedcarbonnanotubesaresolubleandbiocompatible,havehighreactivityandlowtoxicity,andcanhelppromotenervecellgrowth.Inthisstudy,amino-functionalizedethylenediamine-treatedmulti-walledcarbonnanotubeswereusedtopreparecarbonnanotubes-nervegrowthfactorcomplexesbynon-covalentgrafting.Thephysicochemicalproperties,cytotoxicitytoPC12andchickembryodorsalrootganglion,andbiologicalactivityofthecarbonnanotubes-nervegrowthfactorcomplexeswereinvestigated.Theresultsshowedthataminofunctionalizationimprovedcarbonnanotubes-nervegrowthfactorcomplexdispersibility,reducedtheirtoxicitytoPC12cells,andpromotedPC12celldifferentiationandchickembryodorsalrootganglion.

简介：Toexplorethemolecularmechanismoftheprotectiveeffectofnervegrowthfactor(NGF)oninjuredspinalcord.Methods:TheposteriorT8(the8ththoracicsegment)spinalcordsof60Wistarratswereinjuredbyimpactscausedbyobjects(weighing10g)fallingfromaheightof2.5cmwithAllensway.Solutionwithnervegrowthfactors(NGF)wasgivento30rats(theNGFgroup)throughamicrotubuleinsertedintothesubarachnoidcavityimmediately,andat2,4,8,12and24hoursafterspinalcordinjury(SCI)respectively.Normalsaline(NS)withsamevolumewasgiventotheother30rats(theNSgroup)withthesamemethod.And5normalratsweretakenasthenormalcontrols.Theexpressionofbcl-2andbaxproteinsinspinalcordwasdetectedwithimmunohistochemistry.Theapoptoticneuronsinspinalcordweremeasuredwithterminaldeoxynucleotidyltransferase-mediateddUTP-biotinnickend-labelingofDNAfragments(TUNEL)staining.Results:Thepositiveexpressionofbcl-2proteinwasstronginthenormalcontrols,butdecreasedintheNSgroup,andincreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).Thepositiveexpressionofbaxproteinwasalsostronginthenormalcontrols,butincreasedintheNSgroup,anddecreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).ApoptoticneuronswerefoundintheNSgroup,andtheydecreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).Conclusions:NGFcanprotecttheinjurednervetissuesthroughstimulatingtheexpressionofbcl-2protein,inhibitingtheexpressionofbaxproteinandinhibitingtheneuronalapoptosisafterSCI.

简介：很多研究调查了外部煽动性的索引，包括根据痴呆的子类型的血浆cytokines和相关分子，然而并非在温和认知缺陷(媒体控制接口)。在这研究，我们使用了复合cytokine试金作为amnestic和non-amnestic与媒体控制接口subtyped在病人估计22cytokines的血浆层次，根据认知特征。当比较血浆生长因素，chemokines和cytokines的层次时，血浆单核白血球铺平趋化性的蛋白质3(MCP-3)，并且贝它神经生长因素(在这二的-NGF)组织，他们被发现比在non-amnestic媒体控制接口病人在amnestic媒体控制接口病人显著地更高级，在好久调整和性以后。这建议血浆MCP-3和-NGF可能在区分媒体控制接口的子类型是有用的。

简介：Objective:Toexaminetheeffectsofratmarrowstromalcells(rMSCs)ongeneexpressionoflocalbrain-derivedneurotrophicfactor(BDNF)andnervegrowthfactor(NGF)afterinjectionofrMSCsintoCisternMagnumofadultratssubjectedtotraumaticbraininjury(TBI).Results:GroupcelltransplantationhadhigherBDNFandNGFgeneexpressionsthanGroupsalinecontrolduringaperiodoflessthan3weeks(P<0.05).Conclusions:rMSCstransplantationviaCisternMagnuminratssubjectedtotraumaticbraininjurycanenhanceexpressionsoflocalbrainNGFandBDNFtoacertainextent.

简介：ToexploretherelationshipbetweensubstanceP(SP)releasedfromperipheralnerveendingsandtheexpressionofepidermalgrowthfactor(EGF)andepidermalgrowthfactorreceptor(EGFR)duringwoundhealing.Methods:FiftyWistarratswererandomlydividedinto2groups,injurygroupandcapsaicingroup.Intheinjurygroup,afull-thicknessskinwoundonthebackoftheratwastaken.Thewoundedgeandgranulationtissuesweretakenonthe1st,3rd,6th,9th,12thdaysafterinjury,respectively.Inthecapsaicingroup,capsaicinwasinjectedsubcutaneouslyonthebackoftheratstodestroythesensorynervetopreventthesecretionofSP,thenawoundandsamplewasmadeinthesameway.ImmunohistochemistryandinsituhybridizationwereemployedtodetecttheexpressionofSP,EGF/EGFR,andEGFmRNA/EGFRmRNAinthegranulationtissues.Results:Intheinjurygroup,immunohistochemicalstainofSPandEGF/EGFRwaslocatedonthehairfolliclesandsebaceousglandsatthe1stday.AndthestainofSPwasobviousatthe3rddayinthegranulationtissues,thendecreasedgradually.EGF/EGFRwasatlowlevelatthe3rdday,thenincreasedgraduallyandreachedthepeakatthe9thday,thendeclined.Inthecapsaicingroup,theimmunohistochemicalstainofSPandEGF/EGFRwasfaintandwithoutobviouschangeduringthewoundhealingprocess.ThetendencyoftheEGFmRNA/EGFRmRNAexpressionwassimilartothatofEGF/EGFR.Conclusions:Duringwoundhealing,SPmaypromotethehealingprocessbyaffectingtheexpressionofEGF/EGFRinthegranuationtissues.

简介：Thegrowthofdevelopingcountriesisanimportanteventofhistoricsignificanceinthecurrentworld.Withthechangesoftheconditionsofthetimes,theirpoliticalandeconomicpursuits

简介：Osteoblastsofratculturedinvitrowerestimulatedwithpulsed50Hzelectromagneticfieldandbasicfibroblastgrowthfactor(bFGF).TheMTTmethod,flowcytometryandhistochemistrystainingwereusedtodetectcellproliferation,cellcycleandalkalinephosphatase.Theresultsindicated:afterstimulatedby1mTelectromagneticfield,thecellsaremoreabundant,havemoreSphasepercentages,2mTelectromagneticfieldhavenoevidenteffectoncells'growth;comparedwithelectromagneticfield,thecellsstimulatedbybFGFaremoreabundantandhavelargerSphaseratios.ElectromagneticfieldandbFGFhavenoeffectoncells,alkalinephosphatase.Therefore,weconcludedthatelectromagneticfieldcanenhanceosteoblastsgrowthlikesomegrowthfactorsuchasbasicfibroblastgrowthfactor,andtheosteoblasts',characteristicswasnotchanged.

简介：CellsregulatephospholipaseD(PLD)activityinresponsetonumerousextracellularsignals.Here,weinvestigatedtheinvolvementofPLDactivityintransforminggrowthfactor-β(TGF-β1)-mediatedgrowthinhibitionofepithelialcells.TGF-β1)-mediatedgrowthinhibitionofepithelialcells.TGF-β1inhibitsthegrowthofMDCK,Mv1Lu,andA-549cells.Inthepresenceof0.4%butanol,TGF-β1inducesanincreaseintheformationofphosphatidylbutanol,auniqueproductcatalyzedbyPLD.TGF-β1alsoinducesanincreaseinphosphatidicacid(PA)levelinA-549andMDCKcells.TGF-β1inducesanincreaseinthelevelsofDAGlabeledwith[^3H]-myristicacidinA-549andMDCKcellsbutnotinMv1Lucells.NoincreaseofDAGwasobservedincellsprelabeledwith[^3H]-arachidonicacid.ThedatapresentedsuggestthatPLDactivationisinvolvedintheTGF-β1-inducedcellgrowthinhibition.

简介：Objective:Toinvestigatetheexpressionandpatternofvascularendothelialgrowthfactor(VEGF)anditsfetalliverkinase-1(Flk-1)receptorinspinalcordanddorsalrootgangliaafterneurotomyofsciaticnerveinrats.Methods:Forty-fiveadultmaleWistarratsweredividedrandomlyintoacontrolgroup(n=5)andanexperimentalgroup(n=40).ThebilateralsciaticnervesoftheratsintheexperimentalgroupunderwentneurotomyandtheL4-L6spinalcordandthecorrespondingdorsalrootgangliawereharvestedrespectivelyat8hours,and1,3,5,7,10,14and21days(8subgroupswith5ratseach)afteroperation.Theratsinthecontrolgrouponlyunderwentanexposureofsciaticnervewithoutneurotomy.ImmunohistochemistryandimageanalysiswereusedtostudytheexpressionofVEGFanditsFlk-1receptor.Results:BothVEGFandFlk-1receptorexpressedinthenormalratspinalcordanddorsalrootganglia.Inresponsetoneurotomy,theirexpressionreachedahigherlevelandpersistedforashorttimethendeclinedtothenormallevelrapidly.Besides,positivestainingofFlk-1wasobservedinbothglialcellsandnervefibers,whichlocatedinthewhitematterofthespinalcord.Conclusions:VEGFcanpromotetheregenerationofperipheralnervesfromtheangleofcentralneurons,whichestablishestheexperimentalandtheoreticalfoundationforVEGFtreatingperipheralnerveinjuries.

简介：组织缺氧和转变生长factor-β；1(TGF-β；1)在很多恶意增加脉管的endothelial生长因素A(VEGFA)表示。组织缺氧和TGF-β的这效果；1可能为肿瘤前进和先进前列腺癌症的转移负责。在现在的学习，TGF-β；1被显示从两根正常房间线(HPV7和RWPE1)和前列腺癌症房间线(DU145和PC3)导致VEGFA165分泌物。相反地，刺激组织缺氧的VEGFA165分泌物仅仅在前列腺癌症房间线被观察。组织缺氧导致了TGF-β；在PC3前列腺癌症房间的1表情，和TGF-β；打字我部分堵住的受体(ALK5)kinase禁止者调停组织缺氧的VEGFA165分泌物。组织缺氧的这效果提供新奇机制在前列腺癌症房间增加VEGFA表示。尽管VEGFA发信号的autocrine在前列腺癌症前进和转移被含有，联系机制糟糕被描绘。VEGFA活动经由VEGF受体(VEGFR)被调停1(Flt-1)并且2(Flk-1/KDR)。而VEGFR-1mRNA在正常前列腺被检测，上皮的房间，VEGFR-2mRNA和VEGFR蛋白质仅仅在PC3房间被表示。VEGFA165治疗在PC3房间然而并非在HPV7房间导致了细胞外的调整信号的kinase1/2(ERK1/2)的phosphorylation，建议VEGFA的autocrine功能可以特别地与前列腺癌症被联系。由VEGFA165的VEGFR-2的激活被显示提高PC3房间的移植。类似的效果也被观察，内长的VEGFA由TGF-β导致了；1并且组织缺氧。这些调查结果说明那经由VEGFR-2的VEGFA的一个autocrine环为TGF-β的tumorigenic效果是批评的；1并且变形前列腺癌症上的组织缺氧。

简介：Objective:Tostudytheexpressionofactivatedepi-dermalgrowthfactorreceptor(EGFR)andtranscrip-tionfactorE2F(E2F)inCondylomaAccuminata(CA)patients.Methods:ImmunofluorescenttechniqueswereusedtoinvestigatetheexpressionofactivatedEGFRandE2FinCApatients.Results:TheexpressionofactivatedEGFRonthemembraneofepithelialcellsinCAlesionswassig-nificantlygreatercomparedtoexpressionleversinthecontrolgroup(P<0.01).Moreover,theco-expres-sionofactivatedEGFRandE2Fwassignificantlyin-creasedcomparedtothecontrolgroup(P<0.01).Conclusion:Ourobservationssuggestthatthein-creaseinactivatedEGFRexpressionmaystimulatehyperplasiainCApatientsthroughtheactivationoftranscriptionfactorE2F.

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