简介：Inflammatorydemyelinatingpseudotumorusuallyoccursinthebrainandrarelyoccursinthespinalcord.Onimaging,inflammatorydemyelinatingpseudotumorappearsverysimilartointramedullarytumorssuchasgliomas.Itisoftenmisdiagnosedasintramedullarytumorandsurgicallyresected.Inviewofthis,theclinicalandmagneticresonanceimagingmanifestationsandthepathologicalfeaturesof36casesofinflammatorydemyelinatingpseudotumorinthespinalcordwereretrospectivelyanalyzedandsummarized.Mostofthesecasessufferedfromacuteorsubacuteonsetandexhibitedasensorimotordisorder.Amongthem,sixcasesweremisdiagnosedashavingintramedullarygliomas,andinflammatorydemyelinatingpseudotumorwasonlyidentifiedandpathologicallyconfirmedaftersurgicalresection.Lesionsinthecervicalandthoracicspinalcordwerecommon.Magneticresonanceimagingrevealededemaandspace-occupyinglesionstovaryingdegreesatthecervical-thoracicjunction,withapredominantfeatureofnon-closedrosette-likereinforcement(open-loopsign).Pathologicalexaminationshowedperivascularcuffingofpredominantlydenselymphocytes,anddemyelinationwasobservedinsixofthemisdiagnosedcases.Theseresultssuggestthattumor-likeinflammatorydemyelinatingdiseaseinthespinalcordisakindofspecialdemyelinatingdiseasethatcanbecategorizedasinflammatorypseudotumor.Thesesolitarylesionsareeasilyconfusedwithintramedullaryneoplasms.Patchyornon-closedreinforcement(open-ringsign)onmagneticresonanceimagingisthepredominantpropertyofinflammatorydemyelinatingpseudotumor,andinflammatorycellinfiltrationanddemyelinationareadditionalpathologicalproperties.

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

简介：Hypertonicsaline(HS)hasbeenappliedinseveralmedicalareassuchaspneumology(asthma,cysticfibrosisandbronchiolytis),endocrinology(hyponatremia)andespeciallyinemergencymedicine,intraumaticandinflammatory/infectiousdisorders.Itmaybecomposedof

简介：Therearefewstudiesontheneuroprotectiveeffectsofsyringaldehydeinaratmodelofcerebralischemia.Thestudyaimedtoelucidatethemechanismsunderlyingtheneuroprotectiveeffectsofsyringaldehydeonischemicbraincells.Ratmodelsofcerebralischemiawereintraperitoneallyadministeredsyringaldehyde.At6and24hoursaftersyringaldehydeadministration,celldamageinthebrainofcerebralischemiaratswasobviouslyreduced,superoxidedismutaseactivityandnuclearrespiratoryfactor1expressioninthebraintissueweremarkedlyincreased,malondiadehydelevelwasobviouslydecreased,apoptosis-relatedcysteinepeptidasecaspase-3and-9immunoreactivitywasobviouslydecreased,andneurologicalfunctionwasmarkedlyimproved.Thesefindingssuggestthatsyringaldehydeexertsneuroprotectiveeffectsoncerebralischemiainjurythroughanti-oxidationandanti-apoptosis.