简介：Withtheadventofmoderntechniques,drugs,andmonitoring,generalanesthesiahascometobeconsideredanunlikelycauseofharm,particularlyforhealthypatients.Whilethisislargelytrue,newlyemergingclinicalandlaboratorystudieshavesuggestedthatexposuretoanestheticagentsduringearlychildhoodmayhavelong-lastingadverseeffectsoncognitivefunction.Thisconcernhasbeenthefocusofintensestudyinthefieldof

简介：Objective:Toidentifypresenceofinflammasomeactivatedinmousecochleawithsensorineuralhearingloss(SNHL)causedbycytomegalovirus(CMV)infection.Method:MCMVwasinjectedintotherightcerebralhemisphereinneonatalBALB/cmiceat2000pfuvirustiters.Auditorybrainstemresponses(ABRs)weretestedtoevaluatehearingat21days.HistopathologicalstudieswereconductedtoconfirmlocalizationsofMCMVinfectedcellsintheinnerear.Expressionofinflammasomerelatedfactorswasassessedbyimmunofluorescence,Quantitativereal-timePCRandWesternblotting.Results:InthemousemodelofCMVinducedSNHL,inflammasomerelatedkinaseCaspase-1anddownstreaminflammatoryfactorIL-1bandIL-18werefoundincreasedandactivatedafterCMVinfectioninthecochlea.Thesefactorscouldfurtherup-regulateexpressionofIL-6andTNFa.Theseinflammatoryfactorsareneurotoxicityandmaycontributetohearingimpairment.Furthermore,wealsodetectedsignificantlyincreasedAIM2proteinthataccumulatedintheSGNofcochleaewithCMVinfection.Significance:Wehaveshownthatinflammasomeasanovelinherentimmunitymechanismmaycontributetohearingimpairment.Conclusion:OurdataindicatethatimflammasomeassembleinmouseinnerearinresponsetoCMVinfection.WehaverevealedanovelpathologyeventinCMVinducedSNHLinvolvingactivationofinflammasomeinmousecochlea.Additionally,wehaveshownthatinflammasomemaybeanoveltargetforpreventionandtreatmentofCMVrelatedSNHL.

简介：AIMToinvestigatetheeffectoffenugreeklactone（FL）onpalmitate（PA）-inducedapoptosisanddysfunctionininsulinsecretioninpancreaticNIT-1β-cells.METHODS：CellswereculturedinthepresenceorabsenceofFLandPA（0.25mmol/L）for48h.Then,lipiddropletsinNIT-1cellswereobservedbyoilredOstaining,andtheintracellulartriglyceridecontentwasmeasuredbycolorimetricassay.Theinsulincontentinthesupernatantwasdeterminedusinganinsulinradioimmunoassay.Oxidativestress-associatedparameters,includingtotalsuperoxidedismutase,glutathioneperoxidaseandcatalaseactivityandmalondialdehydelevelsinthesuspensionswerealsoexamined.Theexpressionofupstreamregulatorsofoxidativestress,suchasproteinkinaseC-α（PKC-α）,phospho-PKC-αandP47phox,weredeterminedbyWesternblotanalysisandreal-timePCR.Inaddition,apoptosiswasevaluatedinNIT-1cellsbyflowcytometryassaysandcaspase-3viabilityassays.RESULTS：Ourresultsindicatedthatcomparedtothecontrolgroup,PAinducedanincreaseinlipidaccumulationandapoptosisandadecreaseininsulinsecretioninNIT-1cells.OxidativestressinNIT-1cellswasactivatedafter48hofexposuretoPA.However,FLreversedtheabovechanges.TheseeffectswereaccompaniedbytheinhibitionofPKC-α,phospho-PKC-αandP47phoxexpressionandtheactivationofcaspase-3.CONCLUSION：FLattenuatesPA-inducedapoptosisandinsulinsecretiondysfunctioninNIT-1pancreaticβ-cells.Themechanismforthisactionmaybeassociatedwithimprovementsinlevelsofoxidativestress.

简介：ThepresentstudywasdesignedtodeterminetheeffectsofatraditionalChinesemedicine,calledQishenYiqiDroppingPillonchronichypoxia-inducedmyocardialinjury.ToestablisharatchronichypoxiamodeltobeusedintheevaluationofthetherapeuticeffectsoftheQishenYiqiDroppingPill,Sprague-Dawley(SD)ratswererandomlydividedintothreegroups:thecontrol,model,andtreatmentgroups(n=10pergroup).Theanimalswerehousedinaplexiglasscontainer.Thecontrolanimalswereundernormaloxygenconcentrationandthemodelandtreatmentgroupswereexposedtoairandnitrogenfor5weeks.TheratsinthetreatmentgroupwereorallyadministeredtheQishenYiqiDroppingpill(35mg·kg-1·d-1)for5weeks.Afterthetreatment,thecardiacfunctionandmorphologywereanalyzed,andtheexpressionlevelsofhypoxia-induciblefactor1α(HIF-1α)weredeterminedusingWesternblotting.Ourresultsindicatedthatthecardiacfunctionwasimpaired,cellapoptosiswasenhanced,andHIF-1αexpressionwasup-regulatedinthemodelgroup,comparedtothecontrolgroup.ThesechangeswereamelioratedbythetreatmentwiththeQishenYiqiDroppingPill.Inconclusion,QishenYiqiDroppingpillcanamelioratemyocardialinjuryinducedbychronichypoxia,improvecardiacfunction,anddecreasemyocardialcellapoptosis,whichmayprovideabasisforitsclinicaluseforthetreatmentofchroniccardiovasculardiseases

简介：自发的术语劳动在包括cytokine生产和白血球渗入的myometrium与放大煽动性的事件被联系；然而，调整如此的事件的潜在的机制充分没被理解。我们由成长胎儿假设了子宫的墙的那机械段由子宫的myocytes通过各种各样的cytokines的版本便于外部白血球溢出进术语myometrium。人的myometrial房间(hTERT-HM)受到静态的机械段；调节段的媒介被收集并且分析了使用48-plexLuminex试金和ELISA。人的子宫的microvascularendothelial房间(UtMVEC-Myo)的房间粘附分子表示上的调节段的媒介的效果被量的聚合酶链反应(qPCR)和流动cytometry检测；测试leukocyte-endothelial相互作用的功能的试金：到endothelial房间和象THP-1monocytic房间的移植一样的标记calcein的主要人的neutrophils的transendothelial移植的白血球的粘附被萤光计估计。在vitro学习的水流证明机械段(i)直接由hTERT-HM细胞导致多重cytokines和chemokines的分泌物(IL-6，CXCL8，CXCL1，移植禁止的因素(MIF)，VEGF，G-CSF，IL-12p70，bFGF和导出血小板的生长因素子单元B(PDGF-bb)，P<；0.05)；导致段的cytokines(ii)提高白血球粘附到包围的内皮细胞层子宫的微脉管系统由(iii)导致endothelial房间粘附分子的表示并且(iv)指导外部白血球的transendothelial迁居。(vi)抵销Chemokine抗体和用途广泛的chemokine禁止者堵住白血球移植。我们的数据从子宫的血容器为白血球招募提供机械规定的一个证明给myometrium，为白血球建议通常认为的机制在劳动和产后的复杂物期间渗透到子宫。

简介：Inthisstudy,ratswereputintotraumaticbraininjury-inducedcomaandtreatedwithmediannerveelectricalstimulation.Weexploredthewake-promotingeffect,andpossiblemechanisms,ofmediannerveelectricalstimulation.Electricalstimulationupregulatedtheexpressionlevelsoforexin-AanditsreceptorOX1Rintheratprefrontalcortex.Orexin-Aexpressiongraduallyincreasedwithincreasingstimulation,whileOX1Rexpressionreachedapeakat12hoursandthendecreased.Inaddition,aftertheOX1Rantagonist,SB334867,wasinjectedintothebrainofratsaftertraumaticbraininjury,fewerratswererestoredtoconsciousness,andorexin-AandOXIRexpressionintheprefrontalcortexwasdownregulated.Ourfindingsindicatethatmediannerveelectricalstimulationinducedanup-regulationoforexin-AandOX1Rexpressionintheprefrontalcortexoftraumaticbraininjury-inducedcomarats,whichmaybeapotentialmechanisminvolvedinthewake-promotingeffectsofmediannerveelectricalstimulation.

简介：Sheng-Mai-San(SMS),awell-knownChinesemedicinalplantformula,iswidelyusedforthetreatmentofcardiacdiseasescharacterizedbydeficiencyofQiandYinsyndrome.Amousechronicintermittenthypoxia(CIH)modelwasestablishedtomimictheprimaryclinicalfeaturesofdeficiencyofQiandYinsyndrome.MiceexperiencedCIHfor28days(nadir7%topeak8%oxygen,20minperday),resultinginleftventricle(LV)dysfunctionandstructureabnormalities.AfteradministrationofSMS(0.55,1.1,and5.5g·kg-1·d-1)forfourweeks,improvedcardiacfunctionwasobserved,asindicatedbytheincreaseintheejectionfractionfromtheLVonechocardiography.SMSalsopreservedthestructuralintegrityoftheLVagainsteccentrichypotrophy,tissuevacuolization,andmitochondrialinjuryasmeasuredbyhistology,electronmicroscopy,andultrasoundassessments.Mechanistically,theantioxidanteffectsofSMSweredemonstrated;SMSwasabletosuppressmitochondrialapoptosisasindicatedbythereductionofseveralpro-apoptoticfactors(Bax,cytochromec,andcleavedcaspase-3)andup-regulationoftheanti-apoptosisfactorBcl-2.Inconclusion,theseresultsdemonstratethatSMStreatmentcanprotectthestructureandfunctionoftheLVandthattheprotectiveeffectsofthisformulaareassociatedwiththeregulationofthemitochondrialapoptosispathway.

简介：ThepresentstudywasdesignedtoevaluatetheprotectiveeffectsofethanolextractsofRabdosiajaponicavar.glaucocalyx(Maxim.)Hara(RJ)onlipopolysaccharide(LPS)-inducedacutelunginjury(ALI)inmiceandthepossibleunderlyingmechanismsofaction.ThemicewereorallyadministratedwithRJextract(16,32or64mg?kg–1)dailyforconsecutive7daysbeforeLPSchallenge.Theungspecimensandthebronchoalveolarlavagefluid(BALF)werecollectedforhistopathologicalexaminationsandbiochemicalanalyses.PretreatmentwithRJsignificantlyenhancedsuperoxidedismutase(SOD)activityandreducedthewet-to-dryweight(W/D)ratio,thelevelsofnitricoxide(NO)andproteinleakage,andmyeloperoxidase(MPO)activityinmicewithALI,inadose-dependentmanner.RJreducedcomplementdepositionandsignificantlyattenuatedLPS-inducedALIbyreducingproductionsofinflammatorymediators,suchastumornecrosisfactor-α(TNF-α),interleukin-6(IL-6),andinterleukin-1β(IL-1β).TheresultsdemonstratedthatRJmayattenuateLPS-inducedALIviareducingtheproductionofpro-inflammatorymediators,andreducingcomplementdepositionandradicals.

简介：Objective:Humaninducedpluripotentstem(iPS)cellsexhibitgreatpotentialforgeneratingfunctionalhumancellsformedicaltherapies.Inthispaper,wereportforuseofhumaniPScellslabeledwithfluorescentmagneticnanoparticles(FMNPs)fortargetedimagingandsynergistictherapyofgastriccancercellsinvivo.Methods:HumaniPScellswerepreparedandculturedfor72h.Theculturemediumwascollected,andthenwascoincubatedwithMGC803cells.CellviabilitywasanalyzedbytheMTTmethod.FMNP-labeledhumaniPScellswerepreparedandinjectedintogastriccancer-bearingnudemice.Themousemodelwasobservedusingasmall-animalimagingsystem.Thenudemicewereirradiatedunderanexternalalternatingmagneticfieldandevaluatedusinganinfraredthermalmappinginstrument.Tumorsizesweremeasuredweekly.Results:iPScellsandthecollectedculturemediuminhibitedthegrowthofMGC803cells.FMNP-labeledhumaniPScellstargetedandimagedgastriccancercellsinvivo,aswellasinhibitedcancergrowthinvivothroughtheexternalmagneticfield.Conclusion:FMNP-labeledhumaniPScellsexhibitconsiderablepotentialinapplicationssuchastargeteddual-modeimagingandsynergistictherapyforearlygastriccancer.

简介：Psychologicaldepressionisdrawingaccumulatingattentionnowadays,duetotheskyrocketingincidenceworldwideandtheenormousburdensitincurs.Physicalexercisehasbeenlongrecognizedforitstherapeuticeffectsondepressivedisorders,althoughknowledgeoftheunderlyingmechanismsremainslimited.Suppressedhippocampalneurogenesisinadultbrainshasbeenregarded,atleastpartly,contributivetodepression,whereasphysicalexercisethatrestoresneurogenesisaccordinglyexertstheanti-depressiveaction.Severalrecentpublicationshavesuggestedthepotentialroleofadiponectin,aproteinhormonesecretedbyperipheralmatureadipocytes,inmediatingphysicalexercise-triggeredenhancementofhippocampalneurogenesisandalleviationofdepression.Here,webrieflyreviewthesenovelfindingsanddiscussthepossibilityofcounteractingdepressionbymodulatingadiponectinsignalinginthehippocampuswithinterventionsincludingphysicalexerciseandadministrationofpharmacologicalagents.更多还原

简介：Curcumin,adietaryphytochemical,exhibitsmultifunctionalnaturalproductwithregulatoryeffectsoninflammation.However,thepoorbioavailabilitylimitsitsclinicalapplications.Thus,wedesignedandsynthesizedanovelmonocarbonylanalogueofcurcuminB7andtheirinhibitionagainstmonocytechemotacticprotein-1（MCP-1）andinterleukin-8（IL-8）releasewasevaluatedinH2O2-stimulatedhumanvascularendothelialcells（ECs）inadose-responsivemanner,whileexhibitingnocytotoxicityinECs.Takentogether,theseinsightsonthenovelcompoundB7mayserveaspotentialagentsforthetreatmentofatherosclerosis.

简介：Thispaperaimstotheresearchoftheimpactoffluidshearstressontheadhesionbetweenvascularendothelialcellsandleukocyteinducedbytumornecrosisfactor-α(TNF-α)bymicrofliudicchiptechnology.Microfluidicchipwasfabricatedbysoftlithograph;Endothelialmicrofluidicchipwasconstructedbyoptimizingtypesoftheextracellularmatrixproteinsmodifiedinthemicrochannelandcellincubationtime;humanumbilicalveinendothelialcellsEA.Hy926linedinthemicrochannelwereexposedtofluidshearstressof1.68dynes/cm~2and8.4dynes/cm~2respectively.Meanwhile,adhesionbetweenEA.Hy926cellsandleukocytewasinducedbyTNF-αunderaflowcondition.EA.Hy926cellculturedinthestaticconditionwasusedascontrolgroup.Thenumbersoffluorescently-labeledleukocyteinmicrochannelwerecountedtoquantizetheadhesionlevelbetweenEA.Hy926cellsandleukocyte;cellimmunofluorescencetechniquewasusedtodetecttheintercellularadhesionmolecule(ICAM-1)expression.TheconstructedendothelialmicrofluidicchipcanaffordtothefluidshearstressandrespondtoexogenousstimulusofTNF-α;comparedwiththeadhesionnumbersofleukocyteincontrolgroup,adhesionbetweenEA.Hy926cellsexposedtolowfluidshearstressandleukocytewasreducedunderthestimulusofTNF-αataconcentrationof10ng/ml(P<0.05);leukocyteadhesionwithEA.Hy926cellsexposedtohighfluidshearstresswasreducedsignificantlythanEA.Hy926cellsincontrolgroupandEA.1Hy926cellsexposedtolowfluidshearstress(P<0.01);theregulationmechanismoffluidshearstresstotheadhesionbetweenEA.Hy926cellsandleukocyteinducedbyTNF-αwasthroughthewayofICAM-1.Theendothelialmicrofluidicchipfabricatedinthispapercouldbeusedtostudythefunctionsofendothelialcellinvitroandprovideanewtechnicalplatformforexploringthepathophysiologyoftherelatedcardiovascularsystemdiseasesunderaflowenvironment.

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