简介:摘要:目的: 本次实验将采用全科诊疗 针对 高血压患者的效果 进行探究。 方法: 本次实验选取了 2018 年 12 月 -2019 年 12 月前来本院进行疾病检查及治疗的高血压患者为对象,在自愿参与实验调查的患者中,采用 计算机随机数字表 法,对 62 例患者进行病情结果讨论。对照组患者采用专科联合就诊措施的患者,观察组则为全科门诊就诊的患者。 结果: 对于患者生活质量上来看 ,观察组的 31 名患者中,健康知识掌握程度平均为 ( 8.8±0.4 )分,对照 组的 31 名患者中,生活质量评分 ( 6.2±0.6 )分,组间对比差异较为显著,具有统计学意义( P < 0.05 )。 与此同时,对患者 治疗有效率 进行比较, 观察组患者 临床效果有效率 为93.5% ,明显优于对照组的 77.4% 。因此,我们认为观察组治疗效果更佳。 结论: 采用 全科诊疗的高血压患者效果显著,治疗有效率更高,改善了患者生活质量,值得进一步推广应用。
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:CytoehromeP450norgenewasclonedintotheexpressionvectorpET-28toyieldtherecombinantexpressionplasmidpET-P450nor,whichcoulddirectthesynthesisofaeukaryoticderivedproteininEscherichiacoliBL21.Thevectorallowsoverproductionandsingle-steppurificationof(His)6-taggedcytoehromeP450norbythefacifitationofmetal(Ni^2+)chelateafl]nitychromatography.TheexpressionlevelofcytoehromeP450norwashighat30℃afterIPTGinduction.SDSPAGEandWesternblotanalysisshowedaspecificband(about43kDa).TheoverproducedcytochromeP450norwaspurifiedtoeleetrophoretichomogeneitywithin2.5handabout20.8mgpurifiedproteinwasobtainedfrom2Lcellculture.TheproliferationofSSMC-7721celllinecouldbeinhibitedbycytoehromeP450nor.Rabbitpolyclonalantibodies(titerover64000)wereproducedagainstrecombinantcytoehromeP450norandprovedtobeveryusefulforimmunoblottingstudy.AvailabilityofthisexpressionsystemandspecificantibodiesshouldfacilitatecharacterizationoftheroleofcytochromeP450norinthemetabolismofNO.
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简介:ThisstudywasaimedtoobservetheexpressionofP70S6kinase(P70S6K)inoralaciniccellcarcinoma.PT0S6kinaseexpressionwasexaminedbymeansofWestern-blottestandActivityas-say.Specimenswerefrom30casesoforalaciniccellcarcinomaand15casesofnormaloraltissuewereusedascontrols.StatisticalanalysissoftwareSPSS10.0wasusedforttesttodeterminetherelationshipbetweengeneexpressionandclinicalfeatures.TheexpressionlevelofP70S6Kincreasedobviouslyinoralaciniccellcarcinomatissue(P<0.01).ActivityassaywasthesameastheWestemblottest(P<0.01).P70S6Kexpressionlevelandactivityplayedanimportantroleinthedevelopmentoforalaciniccellcarcinoma.Inconclusion,P70S6Kisamplifiedandoverexpressedinoralaciniccellcarci-nomatissue,whichsuggestsapotentialoncogenicfunction.P70S6KandotherpossibletargetsofmTORcontributesignificantlytotumordevelopmentandthatinhibitionoftheseproteinsmaybethera-peuticforcancerpatients.OverexpressionofP70S6Kmaybeinvolvedinthepathogenesisoforalacin-iccellcarcinoma.
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简介:ToobservetheeffectofGardeniaextractZGontheadsorptionquantityofherpessimplexvirustype1(HSV-1)soastoexplorethemechanismofitsantiviralactivity,fluoresceinisothiocyanate(FITC)wasusedasthefluorescentprobetolabelvirusesandheparinsodiumwasusedascontrol.Meanwhile,theeffectofGardeniaextractZGontheadsorptionquantityonthesurfaceofHep-2cellswasdeterminedbyflowcytometry.ItwasdemonstratedthatadsorptionofHSV-1onthesurfaceofHep-2cellsexhibitedthecharacterofsaturationandspecificityandheparinsodiumcouldpreventattachmentofvirusesonthesecells.Theseresultsareinaccordwiththosereportedpreviously.Itwasalsoprovedthatthemannerofdrug-usepriortoadsorptionorsimultaneoususeofdrugandadsorptionwasbetterthanadsorptionpriortodrug-use,andtheinhibitionratesoftheformerandlattermannerwere84.76%and82.92%respectively.Threemannersofdrug-usewithGardeniaextractZGwerealleffectivetoreducetheadsorptionquantityofviruses,especiallythemannerofsimultaneoususeofdrugandadsorptionwithanadsorptioninhibitionrateof68.46%.Fromtheaboveobservation,itisapparentthatthemechanismofanti-viralactivityofGardeniaextractZGmaybeviaseveralstepsinvolvedintheHSV-1adsorption.
简介:WeareracingwithHIV-1,theetiologicagentforAIDSinhumanbeings[1,2],withtwopossibleendconsequences:ifwewin,HIV-1willbeunderourcontrolbyimmunologicortherapeuticmeasures;ifHIV-1wins,theSIVAfricanmonkeys'storywouldrepeatinhumans,i.e.,onlythefewindividualsthatarenotkilledbythevirus
简介:Wehavepreviouslydemonstratedtheabilityofmalariaparasitestointerferewithspecificimmuneresponses.CD4Tcellsspecifictoparasiteantigens,butnotCD4Tcellsspecifictoanirrelevantantigen,ovalbumin(OVA),aredeletedviaapoptosisduringmalariainfection.Itisofinterest,therefore,toinvestigatetheimmuneresponsesthatdevelopedfollowingvaccinationwiththe19kDacarboxylterminusofthemerozoitesurfaceprotein1(MSP119)inmicethathadpreviouslyexperiencedmalariainfection.Inthisstudy,pre-exposureofmicetoPlasmodiumyoeliielicitednativeanti-MSP119antibodyresponses,whichcouldbeboostedbyvaccinationwithrecombinantMSP119,Likewise,infectionofMSP119-primedmicewithPlasmodiumyoelii(P.yoelii)ledtoanincreaseofanti-MSP119antibodies.MSP119vaccinationofmalariapreexposedmiceorimmunizationbyinfection/cureofMSP119-primedmiceenabledthemicetosurvivechallengeinfection,withtheformergrouphavingslightlylowerparasitaemia.Thedatasuggestthatexposuretomalariainfectionprimesanaturalimmuneresponsewhichcanbeboostedbyvaccination.Thisinformationisrelevanttothedevelopmentofavaccineforuseinindividualslivinginmalaria-endemicareas.
简介:ToexplorethemechanismoftheinhibitionofHIV-1byMycoplasmafermerttans,culturesupernatantsandthallodicproteinsfromM.fermerttansPG18werepreparedandtheproteincomponentsofthesupernatantswerepurifiedwithhighperformanceliquidchromatography(HPLC).Theinhibitoryactivitiestoreversetranscriptase(RT)andthenucleaseactivitiesweredetected;theinfluenceofM.fermerttansonIL-10secretionbybothnormalandH1V-1infectedhumanPBMCweredetermined,andtheinhibitoryeffectofrhIL-10onH1V-1replicationwasdetectedwithEI,ISAmethod.Theresultsshowedthatthepurifiedproteinswithamolecularweightof67-100kDaor10-25kDashoweda36%or34%inhibitoryac-tivitytoRTandpartialnucleaseactivity.ThethallodicproteincouldinducebothnormalandH1V-1infectedPBMCtosecretIL-10remarkably,andtothelatter,thiseffectwasmoreapparent.WhilerhIL-10couldinhibitreplicationofH1V-1inPB-MCinvitroinadose-dependantmanner.ItconcludesthattheinhibitoryeffectoftheM.fermentansPG18culturesupernatantsonRTandthepromotingeffectofPG18thallodicproteinonIL-10secretioninPBMCexplainthemechanismsofinhibitiontoHIV-1byM.fermentansPG18.
简介:摘要:目的 通过建立骨关节炎模型探讨整合素pI和GIT 1对软骨细胞的影响,及二者之间的调控关系。对临床上骨性关节炎的治疗起指导作用。 方法 采用约一周龄的年乳大鼠20只,用定量PCR和Western Blotting检测对照组、pcDNA3.1空载体转染组、pcDNA3.1-GIT 1过表达组、pcDNA3 . I -integrin-p1过表达组、integrin-p 1 siRNA组和NC siRNA组中,integrin-p1和GIT1的mRNA和蛋白质的表达水平,来判断integrin-p1和GIT1之间的调控关系。结论 integrin-p1可以调控GIT1的表达,GTI1可能是位于integrin-pI下游的一个关键分子。
简介:ToinvestigatethephenotypicknockoutofHIV-1chemokinecoreceptorCXCR4andCCR5byintrakinesanditsinhibitoryeffectonHIV-1infection.PrimaryhumanPBLsweretransducedwiththerecombinantvectorpLNCX-R-K-S-K(△NGFR),followedbyanti-NGFR/anti-IgG-magneticbeadmethodselectionandFCMdetection.ThetransducedPBLswereinfectedwithDP1HIV-1virusthereafterenvelope-mediatedsyncytiumformationandp24detectionwerecarriedouttostudytheblockageofHIV-1infectionbyco-inactivationofCCR5andCXCR4.pLNCX-R-K-S-K(△NGFR)-transducedPBILswereisolatedwithananti-NGFR/anti-IgG-magneticbeadmethod.Afterisolation,about70%ofthePBLswerepositivefortheNGFRmarker.WhenthetransducedPBLswereinfectedwithDP1HIV-1virus,envelop-mediatedsyncytiumformationwasalmostcompletelyinhibitedbypLNCX-R-K-S-K(△NGFR)transfection.Also,p24antigenwasverylowintheculturesofpLNCX-R-K-S-K(△NGFR)transducedPBLs.pLNCX-R-K-S-K(△NGFR)transductioninhibitedtheproductionofDP1p24antigenby15%,43%and19%ondays4,7and10respectively.ThelymphocyteswiththephenotypicknockoutofCCR5andCXCR4couldprotectprimaryhumanPBLsfromDP1HIV-1virusinfection.