简介：RapamycintreatmenthasbeenshowntoincreaseautophagyactivityandactivateAktphosphorylation,suppressingapoptosisinseveralmodelsofischemiareperfusioninjury.However,littlehasbeenstudiedontheneuroprotectiveeffectsonspinalcordinjurybyactivatingAktphosphorylation.Wehypothesizedthatbotheffectsofrapamycin,theincreasedautophagyactivityandAktsignaling,wouldcontributetoitsneuroprotectiveproperties.Inthisstudy,acompressivespinalcordinjurymodelofratwascreatedbyananeurysmclipwitha30gclosingforce.Ratmodelswereintraperitoneallyinjectedwithrapamycin1mg/kg,followedbyautophagyinhibitor3-methyladenine2.5mg/kgandAktinhibitorIV1μg/kg.Westernblotassay,immunofluorescencestainingandterminaldeoxynucleotidyltransferase-mediateddUTPnickendlabelingassaywereusedtoobservetheexpressionofneuronalautophagymoleculeBeclin1,apoptosis-relatedmoleculesBcl-2,Bax,cytochromec,caspase-3andAktsignaling.OurresultsdemonstratedthatrapamycininhibitedtheexpressionofmTORininjuredspinalcordtissueandup-regulatedtheexpressionofBeclin1andphosphorylated-Akt.Rapamycinpreventedthedecreaseofbcl-2expressionininjuredspinalcordtissue,reducedBax,cytochromecandcaspase-3expressionlevelsandreducedthenumberofapoptoticneuronsininjuredspinalcordtissue24hoursafterspinalcordinjury.3-MethyladenineandAktinhibitorIVinterventionsuppressedtheexpressionofBeclin-1andphosphorylated-Aktininjuredspinalcordtissueandreducedtheprotectiveeffectofrapamycinonapoptoticneurons.TheaboveresultsindicatethattheneuroprotectiveeffectofrapamycinonspinalcordinjuryratscanbeachievedbyactivatingautophagyandtheAktsignalingpathway.

简介：Somestudieshavesuggestedthatearlysurgicaltreatmentcaneffectivelyimprovetheprognosisofcervicalspinalcordinjurywithoutradiologicalabnormality,butnoresearchhasfocusedonthedevelopmentofaprognosticmodelofcervicalspinalcordinjurywithoutradiologicalabnormality.Thisretrospectiveanalysisincluded43patientswithcervicalspinalcordinjurywithoutradiologicalabnormality.Sevenpotentialfactorswereassessed:age,sex,externalforcestrengthcausingdamage,durationofdisease,degreeofcervicalspinalstenosis,JapaneseOrthopaedicAssociationscore,andphysiologicalcervicalcurvature.Amodelwasestablishedusingmultiplebinarylogisticregressionanalysis.Themodelwasevaluatedbyconcordantprofilingandtheareaunderthereceiveroperatingcharacteristiccurve.Bootstrappingwasusedforinternalvalidation.Theprognosticmodelwasasfollows:logit(P)=-25.4545+21.2576VALUE+1.2160SCORE-3.4224TIME,whereVALUEreferstothePavlovratioindicatingtheextentofcervicalspinalstenosis,SCOREreferstotheJapaneseOrthopaedicAssociationscore(0–17)aftertheoperation,andTIMEreferstothediseaseduration(frominjurytooperation).Theareaunderthereceiveroperatingcharacteristiccurveforallpatientswas0.8941(95%confidenceinterval,0.7930–0.9952).Threefactorsassessedinthepredictivemodelwereassociatedwithpatientoutcomes:agreatextentofcervicalstenosis,apoorpreoperativeneurologicalstatus,andalongdiseaseduration.Thesethreefactorscouldworsenpatientoutcomes.Moreover,thediseaseprognosiswasconsideredgoodwhenlogit(P)≥-2.5105.Overall,themodeldisplayedacertainclinicalvalue.ThisstudywasapprovedbytheBiomedicalEthicsCommitteeoftheSecondAffiliatedHospitalofXi’anJiaotongUniversity,China(approvalnumber:2018063)onMay8,2018.

简介：Ourpreviousstudieshaveconfirmedthatduringnervetranspositionrepairtoinjuredperipheralnerves,theregeneratednervefibersofmotorneuronsintheanteriorhornofthespinalcordcaneffectivelyrepairdistalnerveandtargetmuscletissueandrestoremusclemotorfunction.Toobservetheeffectofnerveregenerationandmotorfunctionrecoveryafterseveraltypesofnervetranspositionformediannervedefect(2mm),30Sprague-Dawleyratswererandomlydividedintoshamoperationgroup,epineurialneurorrhaphygroup,musculocutaneousnervetranspositiongroup,medialpectoralnervetranspositiongroup,andradialnervemuscularbranchtranspositiongroup.Threemonthsafternerverepair,thewristflexiontestwasusedtoevaluatetherecoveryofwristflexionafterregenerationofmediannerveintheaffectedlimbsofrats.Thenumberofmyelinatednervefibers,thethicknessofmyelinsheath,thediameterofaxonsandthecross-sectionalareaofaxonsintheproximalanddistalsegmentsoftherepairednervesweremeasuredbyosmicacidstaining.Theratioofnewlyproduceddistalmyelinatednervefiberstothenumberofproximalmyelinatednervefiberswascalculated.Wetweightsoftheflexordigitorumsuperficialismusclesweremeasured.Musclefibermorphologywasdetectedusinghematoxylin-eosinstaining.Thecross-sectionalareaofmusclefiberswascalculatedtoassesstherecoveryofmuscles.Resultsshowedthatwristflexionfunctionwasrestored,andthenervegrewintothedistaleffectorinallthreenervetranspositiongroupsandtheepineurialneurorrhaphygroup.Thereweredifferencesinthenumberofmyelinatednervefibersineachgroup.Themagnificationofproximaltodistalnerveswas1.80,3.00,2.50,and3.12inepineurialneurorrhaphygroup,musculocutaneousnervetranspositiongroup,medialpectoralnervetranspositiongroup,andradialnervemuscularbranchtranspositiongroup,respectively.Nevertheless,axondiametersofnewnervefibers,cross-sectionalareasofaxons,thicknessesofmyelinsheath,wet