简介：ObjectivesIschemiainducedarrhythmia(ventriculartachycardia/ventricularfibrillation)isoneofthemajorcausesofdeath.Potassiumchannelschangearelikelytoberesponsiblefortheischemia-relatedarrhythmias.Cardiacpotassiumcurrentisthemajoroutwardcurrentinvolvedincardiacrepolarization.Thepropertiesofpotassiumchannelshavebeenintensivelystudied.Here,weinvestigatedtheassociationbetweenischemiainducedarrhythmiaandpotassiumchannelsgeneticvariations.Methods23patientswithventriculartachycardia/ventricularfibrillationinducedbyischemiawereselectedasobjects.5MLperipheralbloodweretakenfromeachperson,fromwhichDNAwasextractedus-ingastandardenzymaticphenol-chloroformmethod.Candidategenes(HERG、KCNJ2、KCNQ1、Mink、Mirp1、Kir2.1、KV4.3、Kir3.1、KV1.5、Kir6.1、Kir6.2、Kir2.1)Werescreenedforpotassiumchannelsgenemutationswithdirectsequencingmethods.ResultsHere4potassiumchannelsgenemutationshavebeendiscovered.InthegenecodingfortheATP-sensitiveK~+channelssubunitKir6.2,thereisachangefromvalinetoisoleucineatthepositionof326(V326I).Attheposition448,argininesubstitutesproline(P448R)intheKC-NQ1gene.InthegeneKCNJ2twomutationshavebeenfound(P156L,Q193H).ConclusionsThisstudyimplicatedthatthereisahighrelationshipbetweenischemiainducedarrhythmiaandthemutationofpotassiumchannels.Inordertoidentifythepreciselyrelationshipthereisneedfunctionalanalysis.

简介：无

简介：

简介：

简介：

简介：背景：为疼痛地势的Opioid药方正在增加。Codeine是在几个欧洲国家的统治opioid，与在最高的codeine用户之中的挪威。瞄准：决定codeine是否首先为剧烈疼痛被使用或是否有一个药方模式，显示有问题的opioid使用。方法：在挪威的所有药店被强迫在所有分配药方上在公共健康的挪威的研究所电子地提交数据到挪威的药方数据库。因为所有药方与一个独特的人标识符被识别，识别所有药方到一个题目是可能的。codeine的有的药方在2004，2005或2006分配了到他们的所有题目在学习被包括。结果：385190个挪威的人有在2005由于非癌症疼痛分配到他们的codeine的至少一张药方，相应于8.3%的1年的周期的流行。223(58%)778在2005收到了仅仅一张药方，121(31%)025收到了超过一张药方，但是<120定义每日的剂量(DDD)，30(8%)939在120和365DDD之间收到了，7661(2%)在365和730DDD之间，当(0.5%)仅仅1787超过了730DDD的最大的推荐剂量时。在后者组，有benzodiazepines(65%)和carisoprodol(45%)的合作药是流行的。结论：大约一在在挪威的10个成年的人是在2005的分配codeine。一个多数(58%)收到了codeine仅仅一次，为剧烈疼痛最可能，而一个小少数(0.5%)有一个药方模式显示有问题的opioid，使用。

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：BACKGROUND:Astrocytesreactsensitivelytocerebralischemia,causingreactiveproliferationandactivation,whichmaycontributetotheireffectinprotectingorinjuringneuronalregeneration.Whetheracupuncture,asatreatmentforcerebralischemia,regulatestheactivatedstateofastrocyteshasbecomeafocusofrecentinvestigations.OBJECTIVE:Toobservetheeffectsofelectroacupuncture(EA)onultrastructurechangesandreactiveproliferationofastrocytesinthemarginalzoneoffocalcerebralischemiainrats.DESIGN,TIMEANDSETTING:Randomized,controlledanimalstudy.ThisstudywasperformedattheExperimentalAnimalCenterofGuangzhouUniversityofTraditionalChineseMedicinebetweenDecember2007andJuly2008.MATERIALS:Atotalof90maleWistarratswererandomlydividedintoshamoperated,modelandEAgroups.Eachgroupwassubdividedinto1hour,1,3,7,and21dayspost-cerebralischemiagroups,withsixanimalsforeachtimepoint.Rabbitanti-ratglialfibrillaryacidicprotein(GFAP)andgoatanti-rabbitIgG/tetramethylrhodamineisothiocyanatewereprovidedbyBeijingBiosynthesisBiotechnology.TheG-6805electricacupunctureapparatuswasprovidedbyShanghaiHuayi.METHODS:Heat-coagulation-inducedocclusionofthemiddlecerebralarterywasperformedtoestablishamodeloffocalcerebralischemia,inthemodelandEAgroups.Middlecerebralarterieswereexposedwithoutocclusioninshamoperatedgroup.EAwasappliedimmediatelyaftersurgeryintheEAgroup,4/20Hz,2.0-3.0V,1-3mA,toBaihui(GV20)andDazhui(GV14),for30minutes.Thetreatmentwasperformedonceaday.Theshamoperatedandmodelgroupsdidnotreceiveacupuncture.MAINOUTCOMEMEASURES:Inthemarginalzoneoffocalcerebralischemiainratsatdifferenttimepointsafterintervention,theultrastructurechangesofastrocyteswereobservedbyusingtransmissionelectronicmicroscopy.GFAPexpressioninastrocyteswasalsomeasuredbylaserconfocalscanningmicroscopy.RESULTS:Cellswellingandrapidproliferationofastrocytes

简介：

简介：Proteasomeactivityreductionisanimportantpathologicalphenomenon,resultinginproteinsaggregationandneuronaldeathintheinjuredneuronsinducedbytransientischemia.Ourpreviousreportshowedthatthetrapofproteasomeintheproteinaggregateswasareasontoleadtothereductionofproteasomeactivity.However,thepatternsofproteasomeenteredintoproteinaggregatesarenotclear.Inthisstudy,weusedaglobalischemiamodel,Hematoxylin-Eosinstaining,differentialcentrifuge,proteasomeactivityassay,sucrosegradientdensitycentrifuge,andWesternblotanalysistoinvestigatethisproblem.Ourresultsshowthattherearetwoaggregationpatternsofproteasomeaftertransientischemiaandreperfusion.Oneisthat26Sproteasomeistrappedbyproteinaggregatesasawholeunit,andtheotheristhat19Sor20Sistrappedintheproteinaggregates,respectively,after26Sdisassociates.

简介：Objective:Toobservetheeffectofelectroacupuncture(EA)onsynapticstructureofhippocampalnervefeltsandsynaptophysin(SYN)expressioninratswithcerebralischernicinjury.Methods:SixtyWistarratswererandomizedintoshah-operationgroup,cerebralischemia(CI)groupandEAgroup,eachofwhichwasfurtherdividedinto1week(W)and5Wsubgroups.Clinjurymodelwasestablishedbyocclusionofthebilateralcomrnoncarotidarter-ies.“Baihui”(百会GV20),“Dazhui”(大椎GV14),“Renzhong”(人中GV26)and“Guenyuan”(关元CV4)werepuncturedandstimulatedelectrically.Thebraintissuesectionscontaininghippocampusregionwerestainedwithirnrrunohistochernicaltechniqueandobservedunderlightmicroscopeandtransmissionelectronicmicroscope.Results:AfterCI,theischemicinjuryasdegenerationofthepresynapsecompositions,decreaseofthesynapticnumeraldensity,andlowexpressionofSYNwereobservedinhippocampalCA1area.Bythe5^thweekafterCI,theneonatalsynapsesofCIandEAgroupsappeared,andSYNexpressionwasupregulated.InEAgroup,therecoveryofthenumeraldensityofsynapseswasespeciallynoticeable,being93.8%ofthatofsham-operationgroupandsignificantlyhigherthanthatinCIgroup(P<0.01).Comparedwithsham-operationgroup,thecalibratedopticaldensity(COD)valuesofSYNincreasedto70%inCIgroup,and93.3%inEAgroup,andCODvalueinEAgroupwassignificantlyhigherthanthatinCIgroup(P<0.01).Conclusion,EAcanfunctioninpromotingsynapticregenerationandenhancingandperfectingtheactionsofthereconstructedsynapsesinhippocampalCA1areainCIrats.

简介：

简介：BackgroundRecentresearcheshavefoundthatstainscanimproveacutemyocardialischemiareperfusioninjurywhichisachievedbyinhibitinginflammatoryreaction.Xuezhikangisextractedfromredrice,atailor-madeChinesecrudedrug.MaincomponentofXuezhikangthatcaninhibitblood-fatisstatins.MethodsFortyhealthySDrats(halfmaleandhalffemale,200gorso)wererandomlydividedintofourgroups:A:normalcontrol;B:shamoperation;C:MIRgroup;D:Xuezhikanggroup.Theacutemyocardialischemiareperfusioninjurymodelwasproduced.Infarctsizes,MYO,CK-MB,cTnI,IL-10andIL-18weredetectedafterreperfusion.ResultsComparedwithCandDgroup,inAandBgroup,infarctsizewereincreasedsignificantly(P<0.01),thelevelofserumMYO,CK-MB,cTnIwereincreasedsignificantly(P<0.01),thelevelofIL-10weredecreasedsignificantly(P<0.01)andIL-18,CRPwereincreasedsignificantly(P<0.01).ComparedwithCgroup,infarctsizeweredecreasedsignificantly(P<0.05),thelevelofserumMYO,CK-MBandcTnIwereincreasedsignificantly(P<0.05),thelevelofIL-10wereincreasedsignificantly(P<0.05)andIL-18weredecreasedsignificantly(P<0.05).ThelevelofIL-10andIL-18werenodifferencebetweenAandBgroup.ConclusionTheapplicationofXuezhikangcapsulesonratsbeforetheoperationofmyocardialischemiareperfusioncanlesseninflammatoryreactionandreduceinfarctsizesandprotectacutemyocardialischemiareperfusion.

简介：BACKGROUND:Synapsesundergohighlevelsofplasticitywithinthenervoussystem,andcerebralischemiainducessynapticplasticitychanges.OBJECTIVE:Todemonstratetheeffectsofelectroacupunctureonultrastructuralsynapticchangesinthefocalcerebralischemiamarginalzoneinratsusingquantitativeanalysisofstereologicalmeasurement.DESIGN,TIMEANDSETTING:Arandomized,controlled,animalexperimentwasperformedattheExperimentalAnimalCenterandLaboratoryofElectronMicroscopy,GuangzhouUniversityofTraditionalChineseMedicinefromJanuary2008toJanuary2009.MATERIALS:TheG-6805electricacupunctureapparatuswasprovidedbyShanghaiHuayiInstrumentFactory,China.METHODS:Atotalof90male,Wistarratswererandomlyassignedtosham-surgery,model,andelectroacupuncturegroups,with30animalsineachgroup.Eachgroupwassubdividedinto1hour,aswellas1,3,7,and21dayspost-surgerygroups,withsixanimalsassignedtoeachtimepoint.Heatcoagulation-inducedocclusionofthemiddlecerebralarterywasperformedtoestablishamodeloffocalcerebralischemia.Electroacupuncturewasappliedimmediatelyfollowingsurgerytotheelectroacupuncturegroup[4/20Hz,2.0-3.0V,1-3mA,toBaihui(GV20)andDazhui(GV14)]for30minutes.Treatmentwasperformedonceaday,andexperimentalanimalsweresacrificed,at1hour,aswellas1,3,7and21dayspost-surgery.MAINOUTCOMEMEASURES:Atdifferenttimepointsafterintervention,changesinsynapticultrastructure,suchaspostsynapticdensitythickness,synapticcleftwidth,andsynapticinterfacecurvature,wereobservedinthefocalcerebralischemiamarginalzoneinratsthroughtheuseoftransmissionelectronicmicroscopy.RESULTS:Brokensynapseswereobservedfollowingcerebralischemia,andthenumberofsynapseswassignificantlydecreased.Comparedtothemodelgroup,synapticultrastructurewassignificantlyimprovedintheelectroacupuncturegroup.Comparedtothesham-surgerygroup,postsynapticdensitythicknesswassignificantlydecreased,asweresynaptic

简介：Brainischemicstrokeistheleadingcauseoflong-lastinginjury,disability,anddeathinadults.Althoughthebrainrepresentsonlyabout2%ofthetotalbodymass,itconsumesalmost20%ofthebody’soxygen.Asaresult,braincellsareextremelysensitivetohypoxia.Oncecerebralischemiaoccurs,thecoreofthe

简介：Ephedrinehasaprotectiveeffectagainstcerebralischemia,butitssideeffectslimititsclinicalapplication.Resultsfromapreviousstudyshowedthat1.5mg/kgperdayephedrinecanpromotemotionrecoveryinratsfollowingcerebralischemia/reperfusionwithoutsignificantsideeffects.Inthepresentstudy,ephedrineatdosesof3.0,2.5and2.0mg/kgwasusedtotreatratswithcerebralischemia/reperfusionandtheeffectsofephedrineontheheart,liver,kidneyandcerebrumwereobserved.Resultsshowedthatthebloodpressureofratswithcerebralischemia/reperfusioninjuryfollowingephedrinetreatmentwaslowerthaninratsthatrecoverednaturallyfromcerebralischemia/reperfusion,butthepressuredecreasedwithincreasingdosesofephedrine.Inaddition,serumaspartatetransaminase,alkalinephosphataseandcreatinineconcentrationinratswithcerebralischemia/reperfusioninjuryfollowingephedrinetreatmentweregreaterthaninratsthatrecoverednaturallyfromcerebralischemia/reperfusion.Theconcentrationsoftheseenzymesweredecreasedwithincreasingdosesofephedrine.Ephedrine-treatedratsdisplayedhyperemia,degenerationandedemainthecerebrum,liver,heartandkidney.Resultsdemonstratedthatephedrineexhibitedsideeffectsonthecerebrum,heart,liverandkidneyinratsfollowingcerebralischemia/reperfusioninadose-dependentmanner.

简介：Objective:Toobserveeffectsofarginineonarterialendotheliuminjuredbyischemia-reperfusion(IR),andexploreitspossiblemechanism.Methods:Fifty-fourratsweredividedinto3groupsandtreatedinrespectiveways:(1)drinkingtapwaterasthecontrol;(2)drinkingtapwatercontaining2.5%L-arginine;(3)drinkingtapwatercontaining2.5L-argininetogetherwithintraperitonealinjectionofN^G-nitro-L-argininemethylester5mg·kg^-1·d^-1.asegmentofthecommoncarotidarterywasoccludedfor1h,andthenreperfused.Samplestakenatdifferentpost-IRtimefromthesegmentwerepreparedfortheultrastructuralandCeH2O2cytochemicalobservation.Thenakedindex(NI)ofinternalelasticlamina(IEL)wasmeasuredforcomparingtheendothelialinjureextentanditsrepairprocess.Results:Lessdamageofendothelialcells(EC),moreplateletsadheringtonakedIELandmoreregeneratingECwereobservedinGroup2.TheNIvaluesofsamplestakenat1,2,3daftertheIRwererespectively0.92±0.08,0.88±0.03and0.41±0.02inGroup1,andreducedto0.52±0.05,0.19±0.08and0.06±0.01inGroup2(P<0.05-0.01).InGroup3,theendotheliumdamagewasnotalleviated,andsoweretheNI.TheCe-H2O2particlesdepositedonthelumensurfaceofendotheliumweremuchlessinGroup2thaninGroups1and3.Conclusions:L-argininepromotestherepairprocessofIR-injuredendotheliumprobablythroughtheremovalofoxygenfreeradicalsbyNO.

简介：AbstractPanax notoginseng is an ancient Chinese medicinal plant that has great clinical value in regulating cardiovascular disease in China. As a single component of panax notoginosides, notoginsenoside R1 (NGR1) belongs to the panaxatriol group. Many reports have demonstrated that NGR1 exerts multiple pharmacological effects in ischemic stroke, myocardial infarction, acute renal injury, and intestinal injury. Here, we outline the available reports on the pharmacological effects of NGR1 in ischemia-reperfusion (I/R) injury. We also discuss the chemistry, composition and molecular mechanism underlying the anti-I/R injury effects of NGR1. NGR1 had significant effects on reducing cerebral infarct size and neurological deficits in cerebral I/R injury, ameliorating the impaired mitochondrial morphology in myocardial I/R injury, decreasing kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin in renal I/R injury and attenuating jejunal mucosal epithelium injury in intestinal I/R injury. The various organ anti-I/R injury effects of NGR1 are mainly through the suppression of oxidative stress, apoptosis, inflammation, endoplasmic reticulum stress and promotion of angiogenesis and neurogenesis. These findings provide a reference basis for future research of NGR1 on I/R injury.

简介：

简介：