简介：Hydraulicspinalcordandcaudaequinanerveinjuriesareveryuncommon.Since1996,wehavereceivedandtreated4patientswithhydraulicspinalcordandcaudaequinainjuries.Thisreportgivesadetaildescription.Fourpatientswithhydraulicspinalcordandcaudaequinanerveinjuries,male:3,female:1,aging13-56yearshavebeentreatedinourhospitalsince1996.Extraduralblockinginjurywasin1patient,extraduralanaesthesiainjuryin1patientandintraspinalcanalmyelographyinjuryin2patients;thesegmentsofintraspinalcanalwereL2-3andL3-4.Onepatientwasaccompaniedbyfemoralfracture,2patientsbyintraspinaltumorand1patienthadoperationbecauseofprolapseoflumbarintervertebraldisc.

简介：客观：在老鼠在试验性的针的绳索损害(SCI)上观察橡黄素的效果。方法：六十只Sprague-Dawley老鼠随机被划分成四个组；仅仅为laminectomy的组A，为有SCI的laminectomy的组B，为有为SCI和intraperitoneal注射的200mg/kg橡黄素和组D的一丸大丸药的SCI和intraperitonealinjection的组C盐。SCI模型被使用修改侨民做“T_(12)上的s方法。每个组的六只老鼠在损害和免费的铁的层次以后在4h被打死，深奥针的绳索片断的malondialdehyde(MDA)被bleomycin和thiobarbituric酸(TBA)测量试金独立。后部的手足功能的Therecovery被修改Tarlov估计“在在SCI以后的7d，14d和21d的s规模和斜面方法。损坏针的绳索的组织学的变化也在SCI以后在7d被检验。结果：在SCI以后，免费的铁和MDA的层次显著地在组B和D被增加，当时不在组C。修改Tarlov“s分数和斜面角度显著地在组B，C和D被减少。组织学的调查结果没被改进。结论：在SCI以后，橡黄素能每氧化减少类脂化合物的水平，然而并非改进功能的恢复。

简介：Tostudythechangesofexcitatoryaminoacids(EAAs)andintracellularcalcium([Ca2+]i),andtheprotectiveeffectofEAAsreceptorantagonistsinthetissuesofrabbitlumbarspinalcordafter40-minuesischemiaand4-hoursreperfusion.Methods:Thirtyhealthyrabbitsweredividedintosixgroups:sham-operation,40-minuesischemia,4-hourreperfusion,ketamineandMgSO4treatment,ketaminetreatment,andsalinetreatmentgroups.ThecontentsofEAAs(glutamateandaspartate)and[Ca2+]iweremeasured.Results:Thecontentsofglutamateandaspartateweredecreasedto15.18μmol/g±2.33μmol/gand9.99μmol/g±0.69μmol/g,respectively;13.75μmol/g±2.58μmol/gand6.49μmol/g±1.39umol/gafterreperfusion.Intheischemiagroup,the[Ca2+]iwaselevatedto221.2μg/g±4.27μg/g,andelevatedfurtherto298.3μg/g±9.26μg/gafterreperfusion,beingsignificantlyhigherthanthatofischemiaandcontrolgroups.Ketaminecouldobviouslyincreasethelevelofglutamateandaspartateanddecreasethelevelof[Ca2+]iduringtheischemiaandreperfusioninjury.Conclusions:TheexcitotoxicityofEAAsandtheoverloadofcalciuminducedbyEAAsplayaharmfulroleinischemiaandreperfusioninjury.Ketaminehasaneffectiveinhibitoryeffect.

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：Objective:Tobetterunderstandthecharacteristicsoftheneurogenicmotorevokedpotential(NMEP)beforeandafteracutespinalcordinjury.Methods:WerecordedandcharacterizedthespinalcordNMEPfrom48normalratsandfrom38ratswithspinalcordhemisectionlesion.SpinalcordNMEPswereelicitedbyapplyingarangeofcurrentintensitieswithbipolarmicroelectrodestimulitotheC4cordsegmentandrecordingtheresponsesfromsciaticnerveswithbipolarmicroelectrodesplacedintheneurilemma.Results:Theevokedpotentialsconsistedofthreestableandreproduciblenegativeandthreepositivepeaks.Themean±SDlatenciesofN1were2.89±0.22msontherightsideand2.89±0.24msontheleftside.Themeanconductionvelocitywas47.9m/s.Themean±SDamplitudesofN1were3.61±2.10μVontherightsideand3.83±2.32μVontheleftside.TheamplitudesofN1weresignificantlydifferentamongtheeightstimulusintensitygroups(rightside:F=2.22,df=7201,P=0.03;leftside:f=2.11,df=7206,P=0.04).Theamplitudewaslargestwhenthestimulusintensitywas1.1-2.5mA.ThelatenciesofN1werenotsignificantlydifferentamongtheeightstimulusintensitygroups(rightside:F=0.40,df=7201,P=0.9;leftside:F=1.20,df=7206,P=0.3).TheamplitudesandlatenciesofN2,N3werenotsignificantlydifferentamongtheeightstimulusintensitygroups.Therewerenosignificantchangesinlatencyandamplitudebetweentheleftandtherightsidenerveresponses.Thirty-eightratsundewentT9cordrightsidehemisection.Amongthem,20(53%),30(79%),and32(84%)ratscouldnotberecordedincorrespondingtoN1,N2,andN3,respectively,intheright-sidesciaticnerves;and13(79%),18(47%),and21(55%),incorrespondingtoN1,N2,andN3intheleft-sidesciaticnerves.Thelatencywassignificantlydelayedonthebothrightandleftsides.TheamplitudeN1wassignificantlydepressedonthebothsides,withN3significantlydepressedontherightsideandN2notsignificantlydepressed.Conclusions:TheamplitudeofNissignificantlydiffere

简介：Objective:Toobservetheeffectsofcryopreservedolfactoryensheathingcells(OECs)transplantationonaxonalregenerationandfunctionalrecoveryfollowingspinalcordinjuryinadultrats.Methods:Twenty-fourratsweredividedintoexperimentalandcontrolgroups,eachgrouphaving12rats.ThespinalcordinjurywasestablishedbytransectingthespinalcordatT10levelwithmicrosurgeryscissors.OECswerepurifiedfromSDratolfactorybulbandculturedinDMEM(Dulbecco'sminimumessentialmedium)andcryopreserved(-120℃)fortwoweeks.OECssuspension[(1-1.4)×105/ul]wastransplantedintotransectedspinalcord,whiletheDMEMsolutionwasinjectedinsteadinthecontrolgroup.At6and12weeksaftertransplantation,theratswereevaluatedwithclimbingtestandMEP(moterevokedpotentials)monitoring.Thesamplesofspinalcordwereprocuredandstudiedwithhistologicalandimmunohistochemicalstainings.Results:At6weeksaftertransplantation,alloftheratsinbothtransplantedandcontrolgroupswereparaplegic,andMEPscouldnotberecorded.MorphologyoftransplantedOECswasnormal,andOECswereinterfusedwithhostwell.Axonscouldregrowintogaptissuebetweenthespinalcords.BothOECsandregrownaxonswereimmunoreactiveforMBP.Noregrownaxonswerefoundinthecontrolgroup.At12weeksaftertransplantation,2rats(2/7)hadlowerextremitiesmusclecontraction,2rats(2/7)hadhipand/orkneeactivemovement,andMEPof5rats(5/7)couldberecordedinthecalfinthetransplantationgroup.Noneoftherats(7/7)inthecontrolgrouphadfunctionalimprovement,andnonehadMEPsrecorded.Inthetransplantedgroup,histologicalandimmunohistochemicalmethodsshowedthenumberoftransplantedOECsreducedandsomeregrownaxonshadreachedtheendoftransectedspinalcord.However,noregrownaxonscouldbeseenexceptscarformationinthecontrolgroup.Conclusions:CryopreservedOECscouldintegratedwiththehostandpromoteregrowingaxonsacrossthetransectedsp

简介：Objective:Todetecttheconcentrationofmonocytechemoattractantprotein-1(MCP-1)intheserumofpatientswithincompletespinalcordinjuryandevaluateitsrelationwiththepathologicclassificationofthespinalcordinjury.Methods:MCP-1concentrationintheserumofpatientswithincompletespinalcordinjury(iSCI),singlespinecompressionandhealthysubjectsweredetectedbyELISA,respectivelyinthepresentstudyandthemagneticresonanceimagingdataofthesepatientswerestudiedatthesametimeonablindbase.Results:SerumlevelofMCP-1iniSCIpatientswas428pg/ml±11pg/mlbyELISA,whichwashigherthanboththatofthepatientswithsinglespinecompressionandofcontrols,withtheconcentrationof184pg/ml±21pg/mland124pg/ml±15pg/ml,respectively.Therewassignificantdifferencebetweenanytwogroups(P<0.01).iSCIpatientswithnormalMRIshowedalowerserumlevelofMCP-1as312pg/ml±30pg/ml.Pathologicalclassificationofspinalcordedemaandhematomacorrespondedto390pg/ml±16pg/mland508pg/ml±24pg/mlintheconcentrationofMCP-1.Conclusions:MCP-1mayinducesecondaryinflammatoryresponsebyrecruitinginflammatorycellstotheinjurysiteandthusaffecttheprognosisofspinalcordinjury.

简介：Objective:ToinvestigateCaspase-3expressionanditsroleinneuronalapoptosis.Methods:TheT13-L2spinalcordofratswasinjuredbytractionaftertheamplitudeofP1-N1wave,monitoredbyacorticalsomatosensoryevokedpotential(CSEP)monitor,decreasedtoseventypercentofthatbeforeoperation.Thenratswerekilledin6h,1d,4d,7d,14dand21drespectivelyafteroperation.Flowcytometerterminaldeoxynucleotldyltransferease-mediatedbiotinylateddeoxynuridinetriphosphatenickendlabeling(TUNEL),Caspase-3activityassayandimmunohistochemicalmethodwereappliedtoinvestigateCaspase-3expressioninthespinalcordtissueandtostudyneuronalapoptosisinrats.Results:Afterspinalcordinjury,apoptoticcellsdetectedbyflowcytometryandTUNEL-positivecellsweresignificantlymore,andpositiveimmunohistochemicalstainingofCaspase-3andCaspase-3activityweresignificantlyhigherinGroupinjurythaninGroupscontrolandlaminectomy,respectively(P>0.05,P>0.01).Similartrendofchangeswasnoticedinapoptoticcells,TUNEL-positivecellsandpositiveimmunohistochemicalstainingofCaspase-3,allofwhichreachedtheirrespectivepeak7daysafteroperation.Caspase-3activityreacheditspeak,however,4dayspostoperatively.Conclusions:IncreasedexpressionandactivityofCaspase-3proteininneuronsaftertractivespinalcordinjuryisthebiochemicalsignalofearlyspinalcellapoptosis.Itisofgreatsignificanceforunderstandingthemechanismofspinalcordinjury.

简介：Objective:TostudythechangesofthegeneexpressionpatternofspinalcordtissuesintheearlystageafterinjurybyDNAmicroarray(genechip).Methods:ThecontusionmodelofratspinalcordwasestablishedaccordingtoAllen'sfallingstrikemethodandthegeneexpressionpatternsofnormalandinjuredspinalcordtissueswerestudiedbygenechip.Results:Theexpressionof45geneswassignificantlychangedintheearlystageafterspinalcordinjury,inwhich22genesup-regulatedand23genesdown-regulated.Conclusions:Theexpressionofsomegeneschangessignificantlyintheearlystageafterspinalcordinjury,whichindicatesthecomplexityofsecondaryspinalcordinjury.

简介：客观：在兔子在针的绳索ischemia/reperfusion(I/R)以后在lipidperoxidation和apoptosis上学习白果树biloba摘录(GBE)的效果。方法：SpinalcordI/R损害模型根据对Erten等的描述被建立。27只NewZealand白兔子的一个总数随机被划分成三个组：一个假冒的组(9只兔子对待withs火腿操作但是没有大动脉的吸藏)，一个模型组(与大动脉的吸藏对待的9只兔子并且匹配卷盐)，并且一个GBE组(与大动脉的吸藏andGinaton(100mg/kg)对待的9只兔子在大动脉的夹钳前并且在灌注的发作注射了30分钟)。Theneurological结果分别地在灌注以后在24和48个小时被评估。针的绳索malondialdehyde(MDA)水平，超级氧化物dismutase(草皮)然后被检测。神经cellapoptosis被终端deoxynucleotidyltransferase(TdT)决定标记的-mediateddUTP-fluorescence刻痕结束(TUNEL)方法和bcl-2和bax的表示是examinedhistologically在有免疫组织化学的针的绳索。结果：I/Rproduced在神经病学的得分的重要减少。GBE组的马达分数比在在灌注以后的24和48个小时的模型组的那些显著地高(P<0.05)。与模型组相比，GBE改善了草皮的下面规定并且生产了MDA水平的重要减小(P<0.01)。为在模型组的TUNEL的积极房间是多于GBE组的那些的大部分(P<0.01)。bcl-2在I/R以后是起来调整的，特别在theGBE组(P<0.01)。bax的起来规定被GBE极大地减少(P<0.01).Conclusions：GBE对针的绳索I/R损害，和机制有保护的效果可以是它能清除氧释放激进分子并且禁止神经房间的apoptosis。

简介：Objective:TostudythesequentialchangesofHIF-1α(hypoxia-induciblefactor1alpha)inexperimentalspinalcordinjuryinratsandtoanalyzeitspotentialeffectsinSCI.Methods:AstaticcompressionmodelofSCIwasemployedinthisstudy.ExpressionsofHIF-1αweremeasuredwithimmunohistochemicalstaining,whileflowcytometrywasusedtodeterminetheapoptoticratioandbcl-2expressions.Results:HIF-1αbegantoincrease1dayafterinjury,andreachedthepeakat3-7days.Twoweekslater,itdeclinedsignificantly.ThesequentialchangesofHIF-1αcoincidedwellwiththealterationsofapoptoticratioandcontentsofbel-2.Conclusions:HIF-1αpossiblyparticipatesinthesecondaryischemicandhypoxicproceduresafterspinalcordinjury,andmaymediatethetraumaticapoptosis.FurtherunderstandingofHIF-1αmayprovidenewtherapeuticregimensforSCI.

简介：Objective:Peripheralnerveregenerationdependsongeneregulationbycentralneurons.Tosearchformoreeffectivetreatmentmethodstoimprovetheregenerationofwoundedperipheralnerves,geneexpressionprofileofspinalcordafterfirearminjurytorabbitsciaticnervesarestudiedwithDNAmicro-arraytechnique.Methods:Atotalof54rabbitswererandomlydividedinto4groups:Groupsdl,d3,d7andnormalcontrolgroup.Lumbarspinalcordsweresampled.RNAandmRNAwereextracted,labeledbyCy3andCy5,andanalyzedbymouse_8192Sgenechips.Results:Atotalof1367,923,and61geneswithdifferentialexpressionwerefoundonday1,day3,andday7aftertraumarespectively.Fiveexpressedsequencetag(EST)sequencesdemonstrateddifferentialexpressionduring7daysaftertrauma.Conclusions:Thereiscomplexgeneprofilewithdifferentialexpressionafterfirearmnerveinjury,amongwhichAW701496,U84291,W13926,X04017andAW822394ESTsequencesmaybeimportantregulationfactorsthatinvolvedinregenerationofperipheralnerveinjury.

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.