简介:Objective:ToinvestigatethemembranelocalizationfunctionoftheCX26proteinwhenits86thaminoacidisThr,SerorArg,anditsrelationstodeafness.Methods:CX26-GFPproteinwitheitherThr,SerorArgasthe86thaminoacidwasexpressedinmouseSGNcellsviatheGFPfusiontypelentivirusexpressionsystem.Themembranelocalizationofthefusionproteinwasobservedunderafluorescencemicroscope.Results:ThemutatedproteinofCX26T86Swaslocalizedtocellmembraneandformgapconjunctionstructures,showingnodifferencetothewildtypeCX26protein(withThrasthe86thaminoacid).However,thegapconjunctionstructuredisappearedwhenthemutationwasCX26T86A.Conclusion:TheseresultsindicatethattheCX26T86Rmutationmaybeacauseofhearingloss,butCX26T86Sasanon-pathogenicpolymorphismmutationdoesnotaffectfunctionsoftheCX26protein.Theresultsareinaccordancewiththeresultsofclinicalscreening.
简介:Thisyearmarksthe50thanniversaryofthebeginningofdiplomaticrelationsbetweenChinaandAfricancountries.Overthepasthalfacentury,withthejointeffortsbytheleadersandpeoplesofChinaandAfrica,thefriendshipbetweenChinaandAfricahasbeenincreasinglyconsolidatedandtherelationsbetweenthetwosideshavegrowntoanewhigh.InNovemberthisyear,theBeijingSummitandtheThirdMinisterialMeetingoftheChina-AfricaCooperationForumwillbeheldinBeijingtodiscussthefurtherstrengtheningoftherelationsandcooperationbetweenChinaandAfrica.Tocommemoratethesehistoricevents,thecurrentissueofthisJournalisbringingoutfourarticleswithregardtoSino-AfricanrelationsandthesituationinAfricatosharewithourreaders.
简介:Brucella流产胎是zoonotic在ruminants和人引起brucelosis的克否定的病原体。像使用费的受体(TLR)认出Brucella流产胎并且开始影响天生、适应的免疫的介绍抗原的房间活动。在这研究,我们集中了于recombinantBrucella房间表面蛋白质31(rBCSP31)在老鼠巨噬细胞上决定它的效果。我们表明的结果rBCSP31导致了TNF-α;,IL-6和IL-12p40生产,由刺激p38和JNK和抄写因素NF-κ的激活的快速的phosphorylation取决于激活mitogen的蛋白质kinases(MAPK)的激活,在巨噬细胞的B。另外,连续暴露(>;24h)RAW264.7,到rBCSP31的房间显著地提高了IFN-γ;MHC-II的导致的表示和介绍rBCSP31肽给CD4+T房间的能力。而且,我们发现rBCSP31能与TLR2和TLR4交往。由从TLR2−/−和TLR4−/−老鼠的巨噬细胞的导致rBCSP31的cytokine生产从NF-κ的C57BL/6巨噬细胞,和激活是比那低的;B和MAPK从TLR2−/−和TLR4−/−老鼠在巨噬细胞被稀释。另外,从与rBCSP31使免疫的C57BL/6老鼠的CD4+T房间生产了IFN-γ的高水平;并且IL-2与从TLR2−/−和TLR4−/−老鼠的CD4+T房间相比。从使免疫的C57BL/6老鼠的巨噬细胞从TLR2−/−和TLR4−/−老鼠比那些生产了IL-12p40的高水平。而且,有rBCSP31的免疫在B以后比在TLR2−/−和TLR4−/−老鼠在C57BL/6老鼠提供了更好的保护。流产胎2308挑战。这些结果显示rBCSP31是导致cytokine生产的TLR2和TLR4收缩筋,upregulates巨噬细胞功能并且导致Th1有免疫力的反应。
简介:二次根式(a~2)~(1|2)和((a~2)~(1|2))有什么区别吗?主要表现在下面三个方面:1.读法不同.(a~2)~(1|2)读作根号a的平方,而((a~2)~(1|2))读作括号根号a括号的平方.2.表示的意义不同.(a~2)~(1|2)是求a~2。的算术平方根.((a~2)~(1|2))求的是a的算术平方根的平方.一个表示求一
简介:摘要目的探究高压氧治疗(hyperbaric oxygen therapy,HBOT)对病毒性脑炎患儿神经功能、血清辅助性T细胞17(Th17)/调节性T细胞(regulatory T cells,Treg)水平以及Toll样受体2(Toll-like receptor 2,TLR2)/核因子κB(nuclear factor-kappa-B,NF-κB)通路的影响。方法选择重庆市大渡口区人民医院儿科2017年4月至2019年4月收治的病毒性脑炎患儿76例作为研究对象,按随机数字表法分为对照组和HBOT组(每组38例)。对照组患儿接受常规治疗,HBOT组在对照组基础上联合HBOT。对比2组的临床治疗效果、脑电图(EEG)检查结果、简易智力状态检查量表(mini-mental state examination, MMSE)、血清炎性因子、中枢神经特异性蛋白(central nerve specific protein,S100β)、神经元特异性烯醇化酶(neuron specific enolase,NSE)、外周血Th17/Treg以及TLR2/NF-κB通路水平。治疗前2组各项指标比较差异均无统计学意义(P>0.05)。结果HBOT组临床症状持续时间均显著短于对照组(P<0.05),HBOT组癫痫发作次数显著少于对照组(P<0.05)。治疗后HBOT组中度和重度EEG异常的比例显著少于对照组(P<0.05),EEG恢复正常的比例显著高于对照组(P<0.05),HBOT组EEG恢复时间显著短于对照组(P<0.05)。治疗后HBOT组的MMSE评分(28.16±8.29)高于对照组(20.21±4.40)(P<0.05)。HBOT组的白细胞介素1(IL-1)、C反应蛋白(CRP)、S100β和NSE水平显著低于对照组(P<0.05)。HBOT组的Th17[(0.024±0.004)%]显著低于对照组[(0.028±0.001)%](P<0.05),Treg[(0.016±0.003)%]显著高于对照组[(0.014±0.004)%](P<0.05)。HBOT组的TLR2、Myd88和NF-κB蛋白水平均显著低于对照组(P<0.05)。HBOT组未发现HBOT相关不良反应。结论HBOT可提高对病毒性脑炎患儿的疗效,减少癫痫的发生,并发挥脑保护作用,这可能与HBOT具有抑制TLR2/NF-κB通路、调节Th17/ Treg平衡的作用有关。
简介:IncessantpromotionofpowerefficiencySincelong,powerindustrialenergy-savingspecifications,standardsandmanagementsystemshasbeensystematicallyestablishedpursuanttostatelaws,regulationsandpolicies,andbeensteadilyimprovedthroughoptimization,structureupgrading,andtechnicalretrofitting.Theratioofprimaryenergytransformedintoelectricenergy,theratioofelectricenergyconsumedbyendusersandtheimportantpowertechnicalandeconomicindexeswhichweighnationaleconomicdevelopmentlevel,economicefficiency,energyutilizationef-
简介:<正>Iamverypleasedtoattendthe11thExecutiveCouncilMeetingofCAFIU,andwouldliketoexpressmyheartycongratulationstoPresidentYanJunqi,thenewleadershipandthenewly-electedExecutiveCouncil.IalsowanttoexpressmysincerethanksforchoosingmetobetheHonoraryPresidentofCAFIU!
简介:<正>Themeetingofthe11thExecutiveCouncilofCAFIUisconvenedsuccessfullytoday.Wehavereviewedtheachievementsofthe10thExecutiveCouncil,approvedtheamendedConstitutionandelectedthenewleadership.ItisagreathonorformetoserveasthePresidentofCAFIU.Therefore,IwouldliketoexpressmythanksforthetrustgivenbyallCouncilmembersandthecolleaguespresent
简介:摘要目的观察电针百会、太冲、三阴交对鱼藤酮致帕金森(PD)大鼠的行为学变化和中脑黑质中脑黑质酪氨酸羟化酶(TH)的影响,研究针刺治疗PD的作用机制。方法78只Wistar大鼠随机分为正常组、模型组、西药组和电针组,采用颈、背部皮下注射鱼藤酮溶液0.8mg/kg·d制备PD大鼠模型,造模成功后,西药组给予美多巴混悬液灌胃,1.67mg/kg·d,电针组选百会、三阴交、太冲穴,用φ0.30mm×13mm毫针刺入,接韩氏电针仪,采用疏密波,频率疏波2Hz、密波80Hz,强度2.0mA,每次10mg/kg·d,电针正极接一侧三阴交,负极接同侧太冲,双侧相同;西药和电针组均7d/疗程,共治疗2个疗程,疗程间休息1d;除西药组外,其余各组均灌服等体积的生理盐水;除电针组外,其余各组也均采用同一体位固定10min。各组大鼠行为学测试后脱臼处死,取脑,行中脑黑质TH免疫组化(S-P法)染色检查。结果悬挂实验模型组评分值低于正常组,P<0.05,电针组评分值均高于模型组,P<0.05,西药组评分值与模型组相比,P>0.05,电针组评分值与西药组相比,P>0.05;网格实验模型组大鼠移动潜伏期大于正常组P<0.05,电针组低于模型组,P<0.05,西药组与模型组相比,P>0.05,电针组与西药组相比,P>0.05。结论电针百会、太冲、三阴交具有改善PD大鼠行为学,可使模型大鼠中脑黑质区TH免疫反应阳性神经元数目明显增多,为临床应用电针治疗PD提供了理论支持。
简介:<正>OntheafternoonofMarch31st,the13thCPC-SPDDialogueofForeignAffairsandSecurityPoliciescosponsoredbytheInternationalDepartmentofCPCCentralCommittee(IDCPC),FriedrichEbertFoundationofGermany(FES)andCAFIUwasheldinBeijing.ThethemeoftheDialogueis"thechangesandadjustmentinChineseandGerman