简介：ObjectivesToob-servetheeffectofdifferentestrogenlevelsonthesecretoryfunctionofvascularendothelialcellsoffemalerats,andstudytheeffectofmodulationofestrogenlevelontheexpressionofvascularcelladhesionmolecule-1andtheconcentrationofestrogenreceptorinvascularendothelialcells.MethodsRadioim-munologywasusedtomeasuretheserumconcentrationofendothelinandPGI2,andcopper-cadmiumreductionwasemployedtomeasuretheserumcontentofnitrogenmonoxide.Radioligandbindingandflowcy-tometrywereusedtomeasuretheexpressionofestrogenreceptorandvascularcelladhesionmolecule(VCAM-1)ofvascularendothelialcellsrespectively.Results1.TheserumconcentrationofnitricoxideandPGI2decreasedwhentheovariesoffemaleratswereremoved.Inovariectomizedrats,givenestrogen,theconcentrationrose(P<0.05),buttheplasmaconcentrationofendothelinwasadversetoit.2.Theconcentrationofestrogenreceptorofvascularendothelialcel

简介：锁骨下的脉管的损害说明所有脉管的损害的1%-5%。如果没及时发现或迅速设法，锁骨下的脉管的损害是可能的引起出血性的吃惊甚至死亡。从通过2003的8月的1998的三月，有锁骨下的脉管的损害的15个盒子的一个总数在我们的部门被对待。细节在这份报告的redescribed。

简介：Apoptosisisaformofgeneticallyprogrammedcelldeath,whichplaysakeyroleinregulationofcellularityinavarietyoftissueandcelltypesincludingthecardiovasculartissues.Underbothphysiologicalandpathophysiologicalconditions,variousbiophysiologicalandbiochemicalfactors,includingmechanicalforces,reactiveoxygenandnitrogenspecies,cytokines,growthfactors,oxidizedlipoproteins,etc.,mayinfluenceapoptosisofvascularcells.TheFas/Fasligand/caspasedeath-signalingpathway,Bcl-2proteinfamily/mitochondria,thetumorsuppressivegenep53,andtheproto-oncogenec-mycmaybeactivatedinatheroscleroticlesions,andmediatesvascularapoptosisduringthedevelopmentofatherosclerosis.Abnormalexpressionanddysfunctionoftheseapoptosis-regulatinggenesmayattenuateoracceleratevascularcellapoptosisandaffecttheintegrityandstabilityofatheroscleroticplaques.Clarificationofthemolecularmechanismthatregulatesapoptosismayhelpdesignanewstrategyfortreatmentofatherosclerosisanditsmajorcomplication,theacutevascularsyndromes.

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简介：Objective:Toinvestigatetheneointimaformationandtheexpressionofmonocytechemoattractantprotein-1(MCP-1)andtumornecrosisfactor-α(TNF-α)incuff-inducedvascularinjuryinmousemodel,andtoexaminetheeffectofangiotensinIItype1receptor(AT1)blocker,olmesartan,onMCP-1andTNF-αexpressionandconsequentlyvascularremodeling.Methods:Vascularinjurywasinducedbypolyethylenecuff-placementaroundthemousefemoralartery.SomemiceweretreatedwithAT1receptorblocker,olmesartan,atthedoseof3mg*kg-1*day-1withanosmoticminipump.Neointimaformationandtheproliferationofvascularsmoothmusclecells(VSMCs)weremeasuredbymorphometricanalysisandbromodeoxyuridine(BrdU)incorporation.MCP-1andTNF-αexpressionwasdetectedbyWesternblotandimmunohistochemicalstaining.Results:Weobservedneointimaformation14daysaftercuffplacementaswellasVSMCsproliferationinthemediaandneointima.CuffplacementalsoinducedMCP-1andTNF-αexpressioninthemediaandneointimathattheVSMCsspecificallyexisted.Treatmentofmicewitholmesartanatadoseof3mg*kg-1*day-1,whichdidnotinfluencesystolicbloodpressure,significantlydecreasedneointimaformationandtheproliferationofVSMCs.OlmesartanalsoinhibitedMCP-1andTNF-αexpressionintheinjuredarteries.Conclusions:OurresultsdemonstratethatblockadeofAT1receptorinhibitsMCP-1andTNF-αexpressionandtherebyimprovesvascularremodeling.

简介：为回顾1949-2004年针灸治疗血管性头痛的状况，以推动针灸临床的发展，根据《中国现代针灸信息数据库》数据，计量分析针灸治疗血管性头痛的临床文献。从1956年起针灸治疗血管性头痛的文献报道逐年增加，呈平稳增长趋势，临床治疗以针刺为主，临床选穴以邻近取穴与辨证取穴相结合。

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简介：Objective:Toinvestigatethebindingcharacteristicsofendothelialcell(EC)withLPSfreefromtheparticipationofserumfactors.Methods:LaserconfocalmicroscopewasemployedintheobservationofthebindingofECwithFITC-LPS.TheKDandthebindingsitesofeachECwerecalculatedbyradioligandbindingassayofreceptors(RBA)using[3H]-LPS.Results:ThebindingofECwithLPSwassaturable,timeandconcentrationdependentanditcouldbecompetedwithoverdosedLPSofthesametype.Thefluorescencemainlydistributedincytoplasm,especiallynearthenucleus,whichcouldalsobestained.Conclusions:TheremightbesomespecificLPSbindingsitesexistingonEcsandLPScouldfunctionintracellularily.

简介：AIM:Tumorangiogenesishasbeenshowntobepromotedbyvascularendothelialgrowthfactor(VEGF)viastimulatingendothelialcellproliferation,migration,andsurvival.BlockadeofVEGFsignalingbydifferentmeanshasbeendemonstratedtoresultinreducedtumorgrowthandsuppressionoftumorangiogenesisindistincttumorentities.Here,wetestedarecombinantadenovirus,AdsFIt1-3,thatencodesanantagonisticallyactingfragmentoftheVEGFreceptor1(Flt-1),forsystemicantitumoreffectsinpre-establishedsubcutaneousCRCtumorsinmice.METHODS:Murinecolorectalcarcinomacells(CT26)wereinoculatedsubcutaneouslyintoBalb/cmiceforinvivostudies.Tumorsizeandsurvivalweredetermined.293celllinewasusedforpropagationoftheadenoviralvectors.HumanlungcancerlineA549andhumanumbilicalveinendothelialcellsweretransfectedforinvitroexperiments.RESULTS:InfectionoftumorcellswithAdsFlt1-3resultedinproteinsecretionintocellsupernatant,demonstratingcorrectvectorfunction.Asexpected,thesecretedsFlt1-3proteinhadnodirecteffectonCT26tumorcellproliferationinvitro,butendothelialcellfunctionwasinhibitedbyabout46%ascomparedtotheAdLacZcontrolinatubeformationassay.WhenAdsFlt1-3(5×109PFU/animal)wasappliedtotumorbearingmice,wefoundatumorinhibitionby72%atd12aftertreatmentinitiation.Inspiteoftheseantitumoraleffects,thesurvivaltimewasnotimproved.AccordingtoreducedintratumoralmicrovesseldensityinAdsFIt1-3-treatedmice,theantitumormechanismcanbeattributedtoangiostaticvectoreffects.WedidnotdetectincreasedsystemicVEGFlevelsafterAdsFlt1-3treatmentandlivertoxicitywaslowasjudgedbyserumalanineaminotransferasedetermination.CONCLUSION:InthisstudyweconfirmedthevalueofasystemicadministrationofAdsFIt1-3toblockVEGFsignalingasantitumortherapyinanexperimentalmetastaticcolorectalcarcinomamodelinmice.

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简介：ObjectivesToevaluatetheimpactofstentimplantationonproliferationandapop-tosisininjuredmediavascularsmoothmusclecells(VSMC)andtoexplorethemechanismofrestenosisafterstentimplantation.MethodsFiftymaleNewZealandrabbitswererandomizedintotwogroups,includingballoongroupandstentgroup.Controlgroupwassetup.Thesampleswereharvestedon3,7,14,28,56daysafteroperationandthefollowinginvestigationwascarriedout:(1)Assessingtheexpressionofproliferatingcellnuclearantigen(PCNA)ofmediaVSMCbythemethodofimmunohistochemistry;(2)AnalyzingapoptosisofmediaVSMCbyDNAagarosegelelectrophoresisandTUNELtechnique.ResultsTheexpressionofPCNAandapoptosisinstentandballoongroupsweremarkedlyincreasedcomparedwithcontrolgroups.(1)StentgroupinducedsignificantincreasedexpressionofPCNAinthemediaVSMCcomparedwithballoongroupon3to28days.Onday7,thepositiveratesofPCNAwere24.36±0.55%vs18.74±1.09%

简介：ObjectivesTounderstandtheeffectofcarvedilolonthecoronaryvascularendothelialfunctionofthepatientswithcoronaryheartdiseaseafterpercutaneoustransluminalcoronaryangioplasty(PTCA).Methods51cases,havingoneormorethantwobranchesnarrow(≥70%),werediagnosedbycoronaryangiography.Thesepatientsweredividedrandomlyintocarvedilolgroup(n=28)andcontrolgroup(n=23)whodidnottakecarvedilol.Endothelin(ET)andnitrodioxide(NO)levelsofperipheralbloodweremeasuredbeforeandafterPTCA,beforeandaftertwoweeksbytakingcarvedilol.ResuitsComparedwiththeETandNOlevelsbeforePTCA,ETweremarkedlyincreasedandNOweredecreasedafterPTCA(p<0.05);comparedwiththeETandNOlevelsbeforetakingcarvedilol,ETweredecreasedandNOwereincreasedaftertwoweek(p<0.05),buttheETandNOlevelsofthecontrolgroupdidnotchangeintheperiodoftwoweeksobservation(p>0.05).ConclusionsCarvedilolmayimprovethecoronaryvascularendothelialfunctionafterPTCA.

简介：Formationofapoptoticbodiesisatypicalcharacterofapoptoticcelldeath,buthowtheprocessesarecontrolledisnotknown.Inthisstudy,wecomparedtwoapoptosisinducingsystemsinvascularendothelialcells(VEC).Wefoundthattheformationofapoptoticbodiesduringapoptosisinducedbyrattlesnakevenom,whichisanuniqueandspecificapoptosisinducertovascularendothelialcells,wasmuchfasterthanthatinducedbydeprivationofsurvivalfactors(aFGFandserum).WhenweblockedthesynthesisofmRNAsincellstreatedwithrattlesnakevenombyDRB(5,6-dichloro-1-β-D-ribofuranosylbenzimidazole),aninhibitoroftranscription,theformationofapoptoticbodieswasdramaticallyinhibited.WeexaminedtheexpressionofP^53geneandfoundthatitsexpressionwasmuchhigherinapoptosisinducedbyrattlesnakevenomthatthatinapoptosisinducedbydeprivationofaFGFandserum.OurresultssuggestthatgeneexpressionisimportantandP^53genemayplayamajorroleininducingtheformationofapoptoticbodiesinVEC.

简介：Objective:Toexploretheprobabilityofvascularendothelialgrowthfactor(VEGF)antisenseoligodeoxynucleotidesasadevelopingnewtherapeuticstrategyforglioma.Methods:VEGFproteinexpressionwasdetectedbyS-Pimmunohistochemicaltechnique.TumorcellapoptosiswasobservedbyTUNELmethod.Results:Comparedwithcontrol,VEGFproteinexpressionwasinhibitedbyantisenseoligodeoxynucleotidesinvitro.Andtheinhibitoryeffectsincreasedwiththeincreasingconcentration.VEGFpositiveratewas82.10%incontrolgroup,whilein2.5,5,10(mol/LAODNgroups,theywere70.00%,57.85%,53.20%respectively.Noinhibitioneffectwasfoundinthecelllinestreatedwithmissenseandsenseoligodeoxynucleotides.Invivo,antisenseoligodeoxy-nucleotidestherapyalsoinhibitedVEGFproteinexpressionandinducedtheincreaseofapoptotictumorcells.However,ithasnoeffectontumorcellproliferation.Conclusion:ItishopefulthatVEGFantisenseoligodeoxynucleotidesmaybeanewgenetherapymethodtogliomathroughitsantiangiogenesiseffectbyinhibitionofVEGF.

简介：Objective:Toanalyzetheexpressionofinduciblenitricoxidesynthase(iNOS),endothelialnitricoxidesynthase(eNOS)andvascularendothelialgrowthfactor(VEGF)inhepatocellularcarcinoma(HCC)anditsrelationtoangiogenesis.Methods:Tissuesectionsfrom71HCCpatientswereexaminedimmunohistochemicallyforproteinexpressionofiNOS,eNOS,andVEGF.Microvessaldensity(MVD)wascountedbyendothelialcellsimmunostainedbyanti-CD34antibody.Results:PositiveimmunostainingforiNOS,eNOSwasdetectedin83.1%and85.9%ofHCCrespectively.INOSandeNOSwerenotdetectedinnormalhepatictissue.MVDwas34.3±1.5/HPand38.6±1.6/HPinHCCwithpositivestainingforiNOSandVEGFwhileitwas31.2±2.8/HP,and22.4±2.0/HPinHCCwithnegativestainingforiNOSandVEGF(P<0.01).AcorrelationbetweenNOSexpressionandVEGFinHCCwasnotobserved.Conclusion:iNOSandeNOSmayplayaroleinmalignanttransformationfpost-hepaticcirrhosis.TheexpressionofiNOSandVEGFfavorsangiogenesisofHCC.

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简介：综合应用耳针,针刺合或灌疗法治疗21例脑血管意外引起的呃逆患者,经3～10次治疗后,全部治愈.

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