简介：Purpose:Tostudythecorrelationbetweenfunctionalandstructurallossinchronicglaucoma,asdetectedbyFrequencyDoublingTechnology(FDT)andHeilderbergRetinaTomograph(HRT).MaterialandMethods:60eyesof60patientswitheitherocularhypertensionorchronicopen-angleglaucomaunderwentvisualfieldtestingwithbothstandardautomated

简介：

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：Theratfunctionalmaldigestionmodelwasmadebyirregularfeedingforstudyingmechanismsofacupunctureinregulatingrastroidtestinalactivities.ThechangesofthenumberandtheopticaldensityofNo-neuronsingastrointestinalintermuscularnerveswereusedastheindexes.Wistarratswererandomlydividedintoacupuncture,Domperidone,modelandcontrolgroupswithfourratsineachgroup.ThoseratswerefedwithDomperidome1mL/100g/dayatthebeginningofthemodelmakingprocess.Bilateral“Zusanli”(ST36)andright“Weishu”(BL21)werestimulatedfor20minineverysession,onceeverytwodays,continuouslyforonemonth.Onemonthlater,theratswerekilledforsamplingthegastrointestinalwalls.Thesampleswerecutintosectionswhichwerestainedwithimmunohistochemicalmethodforexaminingthenitricoxidesynthase(NOS)reactionwiththereductivecoenzymeⅡ.Theresultsshowedthatacupunctureof“Zusanli”and“Weishu”pointsmightrestoretheNOSactivityofthestomachtothenormallevel.Comparedwiththemodelgroup,Noimmuno-reactionpositiveneurons'numberinacupuncturegroupdecreasedandtheopticaldensityincreased.Theinfluenceofacupunctureontheupperpartofthesmallintestinewasindistinct.ChangesofNOIr-positiveneuronsmaycontributetotheeffectofacupunctureinmodulatinggastrointestinalactivitiesoffunctionalindigestioninclinic.

简介：Highlevelsoflowmolecularweight(LMW)IgMincertaindiseasesareassociatedwithclinicalandlaboratoryindiceswhichreflecttheseverityofthedisease.TheseassociationssuggestthatLMWIgMmayplayanimportantroleintheimmunopathogenesisofthesediseases.TofurtherapproachthequestionconcerningthefunctionalactivityofLMWIgMindisease,apanelofLMWIgMandhighmolecularweight(HMW)IgMpreparationswithorwithoutrheumatoidfactor(RF)activitywereusedtoinvestigatetheirantibodybindingactivityandtheireffectorfunction.ItwasfoundthatLMWIgM-RFandHMWIgM-RFhadasimilarbindingcapacitytoFcfragmentastherewasnosignificantdifferenceintheaffinityindexbetweenthem.ItfurthershowedthattherateofactivationandtotalamountofutilizationofcomplementbyLMWIgMandHMWIgMwassimilar,althoughthemeanfluorescenceofC3depositionbyIgM-RFandHMWIgM-RFwasslightlyhigherthanthatofLMWIgM-RFandothercontrolRFantibodies.However,thecurrentstudydemonstratedthatLMWIgMhadstrongneutrophilactivatingpropertieswhencomparedwithHMWIgM.ThesefindingssuggestthatonemechanismofLMWIgMcontributingtotheimmunopathogenesisofRAmaybeduetotheformationofcirculatingimmunecomplex(CIC)byLMWIgMwithsubsequentactivationofneutrophils.WhetherLMWIgMhasotherfunctionalactivityindiseaseisunclearandneedsfurtherinvestigation.

简介：Functionalindigestionisalsotermednon-ulcerativeindigestion.Becauseofunknownpathogenesis,thereisnospecifictherapyclinically.Theauthorhadtreated72casesofthisdiseasebytheacupointcatgut-embeddingmethodfrom2000to2003.

简介：Mycoplasmagenitaliumisthemaincausativeagentfornon-gonococcalandnon-chlamydialurethritis.P32istheputativesurface-exposedmembraneproteinofM.genitaliumandithassubstaintialidentityinaminoacidsequencewithadhesinproteinP30fromM.pnewnoniae.SinceM.pneumoniaemutantslackingP30proteinisdefectiveincytadherence,P32proteinhasbeenproposedtobeanessentialadhesinimplicatedintheadherenceofM.genitaliumtohostcells.TheprokaryoticexpressionvectorpET-30(+)/p32wasconstructedinthepresentstudy,andtherecombinantproteinwasexpressedinE.coliandpurifiedunderdenaturingcondition.Asdemonstratedbytheimmunoblottinganalysis,therecombinantproteincouldreactwithrabbitantiseraagainstM.genitalium,andadherenceinhibitionassayswerepetformedwithantiseraagainstthisrecombinantprotein.ItwasdemonstratedthatP32proteinapperaredtobeanadhesionproteinofM.genitalium,thusprovidingtheexperimentalbasisforbetterunderstandingofthepathogenesisofM.genitaliuminfectionandforthedevelopmentoftherelatedvaccinesagainsttheinfection.

简介：

简介：

简介：

简介：