柴油机燃用二甲醚排放实验研究

在ZS195直喷式柴油机实验台上进行了二甲醚的燃烧与排放试验,着重研究了甲醛及甲酸甲酯等非常规污染物的排放,并同时进行了常规排放物的研究．实验表明,DME燃烧物中HC的排放与甲醛的排放具有基本相同的规律：随平均有效压力的增加排放浓度下降．甲醛排放浓度与HC的排放浓度密切相关,实验数据表明,除少量数据外,HC的排放浓度与甲醛排放浓度呈线性关系．甲酸甲酯的排放与甲醛及HC无直接关系．同时,在DME的燃烧排放物中发现有微量甲酸甲酯的排放,但尚未发现DME燃烧排放物中有蚁酸存在．     

铜离子对铜锌超氧化物歧化酶二聚作用的影响

观测了Cu^2＋在脱辅基SOD（apoSOD）二聚过程中的作用．探讨了过氧化氢和pH值对SOD二聚体形成的影响,以及缺锌多铜SOD（Cu^2＋SOD）诱导其他蛋白质聚集的作用．结果显示Cu^2＋SOD自聚集成二聚体,在SDS作用下不解聚;pH值为5．6～6．8最有利于Cu^2＋SOD二聚体的形成．而过氧化氢的存在导致Cu^2＋SOD二聚体解聚成单体．另一方面,发现Cu^2＋SOD能够诱导结构类似的apoSOD,Zn4SOD和Cu2Zn2SOD形成不被SDS解聚的二聚体,而对其他蛋白质没有影响,表明Cu^2＋SOD诱导蛋白质聚集时有一定的空间结构选择性．     

燃料电池汽车开发及产业化的关键技术研究

燃料电池电动汽车技术是当今世界上正在进行研究的一项高新技术,文章介绍了燃料电池电动汽车的动力系统和燃料电池系统的基本结构和工作原理。从燃料电池电动汽车的车身和底盘设计、燃料电池系统、驱动电机系统、电控系统以及系统优化等方面,分析了燃料电池电动汽车开发及产业化需要解决的关键技术,同时提出了相应的技术路线和对策。     

一类具有不同Virasoro-向量的顶点算子子代数

根据X_I型Cartan矩阵的一类主子矩阵_J,构造出无扭仿射李代数■的同构于g(A_J)的子代数■_J的导代数■_J,以及■_J-模V_■(l,0).证明了V_■(l,0)不仅是顶点算子代数.而且是V_■(l,0)的具有不同Virasoro-向量的顶点算子子代数.     

基于烟花算法的基站群协作计算卸载模型研究

车联网、AR、AI等计算密集、时延敏感型应用迅速发展,而移动设备因自身计算能力相对不足,执行此类应用任务时会因高时延而严重影响用户体验甚至无法满足用户需求。针对此问题,提出综合考虑时延与成本的多用户、多MEC (mobile edge computing)服务器的基站群协作计算卸载模型。并提出基于凸优化的改进烟花算法（improved fireworks algorithm based on convex optimization, CVX-FWA）来对模型进行求解,对用户任务进行合理的卸载与资源分配。仿真结果表明,提出的计算卸载方案有效降低了任务总时延成本值,实现计算卸载资源的整体优化配置。     

PPAR γ partial agonist, KR-62776, inhibits adipocyte differentiation via activation of ERK

Indenone KR-62776 acts as an agonist of PPARγ without inducing obesity in animal models and cells. X-ray crystallography reveals that the indenone occupies the binding pocket in a different manner than rosiglitazone. 2-Dimensional gel-electrophoresis showed that the expression of 42 proteins was altered more than 2.0-fold between KR-62776- or rosiglitazone-treated adipocyte cells and control cells. Rosiglitazone down-regulated the expression of ERK1/2 and suppressed the phosphorylation of ERK1/2 in these cells. However, the expression of ERK1/2 was up-regulated in KR-62776-treated cells. Phosphorylated ERK1/2, activated by indenone, affects the localization of PPARγ, suggesting a mechanism for indenone-inhibition of adipogenesis in 3T3-L1 preadipocyte cells. The preadipocyte cells are treated with ERK1/2 inhibitor PD98059, a large amount of the cells are converted to adipocyte cells. These results support the conclusion that the localization of PPARγ is one of the key factors explaining the biological responses of the ligands. Received 04 March 2009; received after revision 13 March 2009; accepted 17 March 2009     

一种新的蠕虫检测和控制方法

在分析网络蠕虫连接请求和网络正常连接请求差异的基础上,提出一种新的蠕虫检测和控制方法.该方法针对网络蠕虫攻击特定端口以及攻击地址发散的特性,采用基于端口的多工作集区分网络蠕虫连接请求和网络正常连接请求,在蠕虫控制中使用多延迟队列处理可疑连接请求,避免了不同端口流量之间的相互影响;针对网络正常连接请求的暂时突发特征,利用令牌桶控制多延迟队列的输出,缩短了正常连接请求在延迟队列中的停留时间.测试表明,在主机感染了蠕虫后,新方法将误报率从85%降低到12%,对正常连接请求的平均延迟时间从95.4s降低到5.6s.     

二甲醚HCCI发动机微量排放物的研究

根据优化气相色谱仪工作条件,对二甲醚均质充量压燃(HCCI)发动机排气中的甲醛和甲酸甲酯进行了检测.通过二甲醚简化反应机理与Fluent的耦合联算,以及结合Woschni传热模型和DME详细反应机理的Chemkin反应动力学数值模拟,对二甲醚HCCI发动机的燃烧过程及其微量排放物(甲醛、甲酸和甲酸甲酯)进行了预测分析.结果表明:在一定条件下,甲醛、甲酸和甲酸甲酯存在于排气中,其排放量均随过量空气系数的减小而减小,发动机转速、进气温度和压力对其影响也很大.     

仿生六足机器人步态规划策略实验研究

采用日本弓背蚁进行常规步态实验学研究和仿生学探索,通过对高速数字摄像机采样结果的判断和分析,发现了蚂蚁后足的滑行过程并定义为“滑动相“.此外,还针对蚂蚁直线前进步态给出了合理的步态关系表达式,通过与周期规则步态的对比证明了该式的现实可行性,为仿生六足机器人进行周期不规则步态的规划奠定了理论基础.所采用的实验学研究和仿生学探索相结合的方法能有效提高仿生机器人的技术水平.     

BRD7 regulates the insulin-signaling pathway by increasing phosphorylation of GSK3β

Reduced hepatic expression levels of bromodomain-containing protein 7 (BRD7) have been suggested to play a role in the development of glucose intolerance in obesity. However, the molecular mechanism by which BRD7 regulates glucose metabolism has remained unclear. Here, we show that BRD7 increases phosphorylation of glycogen synthase kinase 3β (GSK3β) in response to activation of the insulin receptor-signaling pathway shortly after insulin stimulation and the nutrient-sensing pathway after feeding. BRD7 mediates phosphorylation of GSK3β at the Serine 9 residue and this effect on GSK3β occurs even in the absence of AKT activity. Using both in vitro and in vivo models, we further demonstrate that BRD7 mediates phosphorylation of ribosomal protein S6 kinase (S6K) and leads to increased phosphorylation of the eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) and, therefore, relieves its inhibition of the eukaryotic translation initiation factor 4E (eIF4E). However, the increase in phosphorylation of 4E-BP1 with BRD7 overexpression is blunted in the absence of AKT activity. In addition, using liver-specific BRD7 knockout (LBKO) mice, we show that BRD7 is required for mTORC1 activity on its downstream molecules. These findings show a novel basis for understanding the molecular dynamics of glucose metabolism and suggest the unique function of BRD7 in the regulation of glucose homeostasis.