简介:【摘要】目的:分析对 老年 2型糖尿病 (T2DM)患者采用利拉鲁肽治疗的 临床效果。方法:选取我院 2018年 2月 -2019年 4月收治的 110例 老年 2型糖尿病 (T2DM)患者为分析对象,给予所有患者利拉鲁肽进行治疗,经治疗 8 周后,对患者治疗前与治疗后的空腹血糖、餐后 2h 血糖、体重指数以及胰岛 β 细胞 功能指数进行对比。 结果:经所有患者 8 周治疗后所有相关临床指标均优于治疗前,治疗前后指标对比差异存在显著临床可比性 ( P<0.05)。 结论:临床上对 老年 2型糖尿病 (T2DM)患者采用利拉鲁肽治疗效果显著,在改善患者胰岛功能以及血糖时具有较高的安全性,值得在临床推广应用 。
简介:Wehaveconfirmedefficientanti-tumoractivitiesoftheperipherallymphocytestransducedwithap185HER2-specificchimericT-cellreceptorgenebothinmurineandinhumaninourpreviousstudies.TofurthertestthefeasibilityofchimericT-cellreceptorinabonemarrowtransplantationmodel,wefirst,madetwomurinetumorcelllines:MT901andMCA-205,toexpresshumanp185HER2byretroviralgenetransduction.MurinebonemarrowcellswereretrovirallytransducedtoexpressthechimericT-cellreceptorandgene-modifiedbonemarrowcellsweretransplantedintolethallyirradiatedmouse.Sixmonthsposttransplantation,p185HER2-positivetumorcells:MT-901/HER2orMCA-205/HER2wassubcutaneouslyorintravenouslyinjectedtomakemousemodelssimulatingprimarybreastcancerorpulmonarymetastasis.Theinvivoanti-tumoreffectsweremonitoredbythesizeofthesubcutaneoustumororcountingthetumornodulesinthelungsafterIndiainkstaining.ThesizeofthesubcutaneoustumorwassignificantlyinhibitedandthenumberofpulmonarynodulesweresignificantlydecreasedinmouserecipientstransplantedwithchimericT-cellreceptormodifiedbonemarrowcellscomparedwiththecontrolgroup.Ourresultssuggesttheefficientinvivoanti-tumoractivitiesofchimericT-cellreceptorgenemodifiedbonemarrowcells.
简介:【摘要】目的:对布地奈德联合孟鲁司特钠对儿童支气管哮喘患儿肺功能、T细胞免疫功能所造成的影响进行研究分析。方法:将我院2017年7月-2018年7月所收治的88例支气管哮喘患儿设为本次实验研究对象,随机均分为对照组以及试验组各44例。其中对照组患儿采用布地奈德雾化剂进行治疗,试验组患儿在对照组的基础之上联合孟鲁司特钠进行治疗,并对两组研究对象的肺功能指标以及T 淋巴细胞及亚群水平进行对比分析。结果:试验组患儿在肺功能指标以及T 淋巴细胞及亚群水平上均显著优于对照组,且各项数据比较差异均具有统计学意义(P<0.05)结论:采用布地奈德联合孟鲁司特钠治疗儿童支气管哮喘具有十分突出的治疗效果,能够有效改善患儿肺功能,提升T淋巴细胞及亚群水平,临床价值较高,可予以推广应用。
简介:ExposureofnaivemurineCD4^+TlymphocytestosuperantigensuchasstaphylococcalenterotoxinB(SEB)inducesastrongproliferativeresponse.ProlongedexposureorsubsequentrestimulationoftherespondingTcellpopulationwithSEBleadstotheapoptoticeventsofactivation-inducedcelldeath(AICD).ThesignalingmechanismresponsiblefortheAICDisatargetofintensiveinvestigation.However,theprecisedownstreamsignahngpathwaysofSEB-inducedAICDremainsunclear.Ourresultshereshowthatthesequentialactivationofcaspase-1/ICE-hkeandcaspase-3/CPP32-hkecysteineproteasesprobablyplaysaroleinthesignalingtransductionofSEB-inducedAICD,butcaspase-3/CPP32-hkeproteasesactivationdoesnotdependoncaspase-1-likeproteasesactivation.HerbimycinA,aspecificinhibitorofproteintyresinekinases,inhibitcaspase-3/CPP32-1ikecysteineproteasesactivation.However,itdoesnotpreventDNAfragmentationofCD4^+TcellsapoptosisinducedbySEB.TheseresultsindicatethatproteintyrosinekinasespathwayisprobablyinvolvedinthesignalingtransductionofCD4^+TcellsapoptosisinducedbySEBand“crosstalks”withthepathwayofcaspase-3/CPP32-1ikeproteasesactivation.