简介:Objective:TheresultsofapreviousstudyshowedthatacleardysregulationwasevidentintheglobalgeneexpressionoftheBCL11A-suppressedB-lymphomacells.Inthisstudy,thebonemorphogeneticproteinreceptor,typeII(BMPR2),E1Abindingproteinp300(EP300),transforminggrowthfactor-β2(TGFβ2),andtumornecrosisfactor,andalpha-inducedprotein3(TNFAIP3)geneexpressionpatternsinB-cellmalignancieswerestudied.Methods:TherelativeexpressionlevelsofBMPR2,EP300,TGFβ2,andTNFAIP3mRNAinB-lymphomacelllines,myeloidcelllines,aswellasincellsfromhealthyvolunteers,weredeterminedbyreal-timequantitativereversetranscriptpolymerasechainreaction(qRT-PCR)withSYBRGreenDye.Glyceraldehyde-3-phosphatedehydrogenase(GAPDH)wasusedasreference.Results:TheexpressionlevelofTGFβ2mRNAinB-lymphomacelllineswassignificantlyhigherthanthoseinthecellsfromthehealthycontrol(P<0.05).However,theexpressionlevelofTNFAIP3mRNAinB-malignantcellswassignificantlylowerthanthatofthehealthycontrol(P<0.05).TheexpressionlevelsofBMPR2andEP300mRNAshowednosignificantdifferencebetweenB-malignantcelllinesandthehealthygroup(P>0.05).InB-lymphomacelllines,correlationanalysesrevealedthattheexpressionofBMPR2andTNFAIP3(r=0.882,P=0.04)hadsignificantpositiverelation.TheexpressionlevelsofBMPR2,EP300,andTNFAIP3mRNAincelllinesfrommyeloidleukemiaweresignificantlylowerthanthoseinthecellsfromthehealthycontrol(P<0.05).TheexpressionlevelsofTGFβ2mRNAshowednosignificantdifferencebetweenmyeloidleukemiacelllinesandthehealthycontrolorB-malignantcelllines(P>0.05).TheexpressionlevelsofBMPR2,EP300,andTNFAIP3mRNAinB-lymphomacellsweresignificantlyhigherthanthoseofthemyeloidleukemiacells(P<0.05).Conclusion:DifferentexpressionpatternsofBMPR2,EP300,TGFβ2,andTNFAIP3genesinB-lymphomacellsexist.更多还原
简介:Inthiswork,boththethermalexpansionandelectricalconductivityofnanocrystallineLa2Mo2O9werestudied.ThenanocrystallinepowderofLa2Mo2O9wasobtainedbysol-gelmethod,andwiththehelpofSHP(superhighpressure)upto4.5×104atmat700℃forashorttime,andthenanocrystallinepowderwasdensifiedwithoutobviousparticlesizegrowth.TheelectricalconductivityofnanocrystallineLa2Mo2O9wasoneorderofmagnitudelowerthanthatofthemicrocrystallinesampleatthesametemperature.Owingtothephasetransition,themicrocrystallineLa2Mo2O9hasanabruptincreaseofthermalexpansionwithapeakvalueof48×10-6K-1at556℃.Forthenanocrystallinematerial,thepeakvalueincreasesto112×10-6K-1at520℃.Ontheotherhand,above600℃thesignificantgrowthofparticlesizeofthenanocrystallineLa2Mo2O9wasobserved,accompanyingbyatremendousincreaseofthermalexpansionwithapeakvalueofthirdhigherthanthatofLa2Mo2O9.
简介:摘要目的比对两种不同的免疫检测系统测定胃泌素释放肽前体(ProGRP)结果的可比性,以评估磁微粒化学发光法检测ProGRP是否能够满足临床需求。方法以罗氏Cobase601电化学发光法(ECLIA)为参考方法,安图AutoLumoA2000磁微粒化学发光法(CMIA)为待评价方法,根据美国临床和实验室标准协会(CLSI)新指南EP9-A3文件的要求,对两种方法学检测ProGRP的结果进行方法学比对和偏移评估。结果在6.73-4536.65pg/mL范围内,两种方法学的ProGRP检测结果具有较好的相关性,相关系数r=0.9975,截距4.185。结论安图AutoLumoA2000磁微粒化学发光法和罗氏Cobase601电化学发光法检测ProGRP结果具有可比性。
简介:ThefourthilnternationalExhibi-tiononEnergy(power)(EPChina’92heldfromMay19to24,1992wassuccessfullyconcluded.ExhibitsattheEx-hibitioncomefrom280factoriesandcom-panies,researchinstitutesanduniversitiesofthe10EECmembercountries,Australia,Canada,Norway,theUnitedStates,Japan
简介:摘要目的评价两种方法学检测糖类抗原242(CA242)结果的可比性,以评估磁微粒化学发光法检测CA242是否能够满足临床的需求。方法根据美国临床和实验室标准协会(CLSI)新指南EP9-A3文件要求,收集2018年1-7月首都医科大学附属北京康复医院和北京大学首钢医院肿瘤患者检测剩余的新鲜血清标本100例,以Fujirebio Diagnostics AB的酶联免疫法为参比方法,安图生物的磁微粒化学发光法为评估方法,对2种方法检测CA242的结果进行方法学比对和偏移评估。选择Passing-Baklok回归方法进行线性拟合,采用Wilcoxon符号秩检验及Spearman相关分析。结果在4.31~295.63 U/ml范围内,2种方法学的CA242检测结果具有较好的相关性(r=0.991,截距0.652)。参比方法和评估方法比较,差异无统计学意义[(53.75±6.69)U/ml比(56.11±6.86)U/ml,t=0.246,P=0.806]。将CA242的医学决定水平25.00 U/ml代入选取的最佳回归模型拟合方程,计算得到的相对偏移3.52%,<1/2TEa±12.5%(TEa为国家卫生健康委临床检验中心室间质量评审允许总误差),满足要求。结论安图生物的磁微粒化学发光法和Fujirebio Diagnostics AB酶联免疫法检测CA242结果具有可比性,满足临床需要。
简介:Chip:Idon’thaveashirttowear!Where’sMom?Joe:She’smakingourlunches.Chip:WhataboutDad?Joe:He’sfixingbreakfast.Chip:Well,whataboutTrevor?Heknowshowtoinron!Joe:He’stakingashower.Chip:Where’sPatrick?
简介:WejoinedtheSEASTAR(ShellEvolutionAndSearchfor2+energiesAtRIBF)collaborationatRIKENandareanalyzingthedataofn-richVandMnisotopeswithN40.Three-raysineachof63;65;67Mnareidentified.The??coincidencerelationshipsarebeinganalyzedforestablishingtheirlevelschemes.TheprogressinthedataanalysisispresentedinRef.[1].
简介:BackgroundTaxifolin(Tax)isanessentialnaturalantioxidant.MultiplestudieshaveshownthatTaxcanprotectcardiomyocytesfromischemia-reperfusioninjury.However,theunderlyingmechanismisstillunclear.MethodsH9C2cellswererandomlydividedintocontrol,H_2O_2group,Taxpretreatmentgroup(Tax+H_2O_2);Taxeffectgroup.CellactivitywasdetectedbyCCK-8andtheintracellularstructurewasobservedbytransmissionelectronmicroscopy.AutophagywasdeterminebyWesternblottinganalysisofBeclin-1,Bcl-2andPKC.ResultsTaxpretreatmentsignificantlyincreasedanti-apoptoticproteinBcl-2andautophagyproteinBeclin-1.ExpressionofPKCwasinhibitedbyTax.ConclusionsTaxpretreatmentcouldprotectH9C2cellsagainstH_2O_2-induceddamagethroughtheBcl-2andautophagypathways.