带有测量噪声的Ⅱ型T-S模糊建模

实际工业生产过程中,系统的数据带有测量噪声.Ⅱ型模糊集的二阶隶属度用来表征一阶隶属度的模糊度,这种模糊度的增加意味着处理不确定信息能力增加.因此,提出了一种基于Ⅱ型模糊集的T-S模糊建模方法来减少由噪声带来不确定信息的影响.首先采用改进的最小邻域算法对带有测量噪声的数据进行聚类,继而确定Ⅱ型模糊集的一阶隶属度,接着根据数据的聚类信息采用高斯混和模型得到二阶隶属度值,然后用正交最小二乘算法确定模糊模型的后件参数,最后通过仿真实验来验证该方法的有效性.     

一种基于自适应网格IMM的自适应采样周期算法

提出一种自适应网格交互多模型下采样周期自适应的算法。在自适应网格交互多模型算法中,中心模型参数变化率反映了系统模型与目标机动水平间的匹配程度,而两者的匹配程度直接影响目标的跟踪精度。利用中心模型参数变化率对采样周期进行控制,并引入可控参数对平均采样周期进行灵活调整。仿真结果表明在自适应网格交互多模型下,提出的自适应采样周期算法比固定采样周期算法及基于预测协方差的自适应采样周期算法具有更好的性能。     

一种节能的无线传感网异构配置模型

依据对实际传感信息分布与无线传感网络工程需求的分析,提出一种新的无线传感网异构配置模型(WSNHEDPM).对传感节点中的传感模块按需要进行组合,使其与感知物理特征量空间分布特征相适应,以减少信息冗余,降低无线传感节点的能量负担.对两种配置方法进行了配置成本、能量消耗与生存周期方面的理论和实验分析比较.理论和仿真实验表明,该模型使无线传感网在面向实际普通应用环境时更为能量有效和合理.     

Multiple targets vector miss distance measurement accuracy based on 2-D assignment algorithms

An extension of 2-D assignment approach is proposed for measurement-to-target association for improving multiple targets vector miss distance measurement accuracy. When the multiple targets move so closely, the measurements can not be fully resolved due to finite resolution. The proposed method adopts an auction algorithm to compute the feasible measurement-to-target assignment with unresolved measurements for solving this 2-D assignment problem. Computer simulation results demonstrate the effectiveness and feasibility of this method.     

基于二维几何特征的微地形快速识别算法

为满足水下超声波准确、实时探测海底微地形的需要,研制出一种摆动式单波束探测系统.该系统在探测实验过程中,因出现高程奇异值而造成数字"伪"地形产生,由此提出一种基于二维几何特征的水平、斜坡和凹凸不平三种微地形模式的快速识别算法.该算法建立在现代统计分析与模糊聚类的理论基础上,具有准确性高、实时性好以及抗干扰能力强等优点;并由物理模拟实验证明,利用该算法能有效消除高程奇异值的影响,识别出来的微地形模式准确可靠,为下一步快速重构逼真的数字微地形提供了保障,能够应用于真实的海底微地形探测.     

单车型确定性动态车辆调配问题

给出了单车型确定性动态车辆调配问题的定义,引入网络图描述该问题.建立了问题的线性规划模型,鉴于线性模型的缺点,利用函数逼近技术构造一个特殊的线性函数来近似目标函数中未来时段部分,从而建立起问题的时空分解模型,把问题从时间和空间上分解为多个单时段单节点问题,并根据单时段单节点问题特点设计简单的排序求解方法.最后,给出了模型的完整求解过程,从而使问题得到有效地解决.     

The roles of poly(ADP-ribose)-metabolizing enzymes in alkylation-induced cell death

Poly(ADP-ribose) (PAR) has been identified as a DNA damage-inducible cell death signal upstream of apoptosis-inducing factor (AIF). PAR causes the translocation of AIF from mitochondria to the nucleus and triggers cell death. In living cells, PAR molecules are subject to dynamic changes pending on internal and external stress factors. Using RNA interference (RNAi), we determined the roles of poly(ADP-ribose) polymerases-1 and -2 (PARP-1, PARP-2) and poly(ADP-ribose) glycohydrolase (PARG), the key enzymes configuring PAR molecules, in cell death induced by an alkylating agent. We found that PARP-1, but not PARP-2 and PARG, contributed to alkylation-induced cell death. Likewise, AIF translocation was only affected by PARP-1. PARP-1 seems to play a major role configuring PAR as a death signal involving AIF translocation regardless of the death pathway involved. Received 7 November 2007; received after revision 19 December 2007; accepted 21 December 2007 O. Cohausz, C. Blenn: These two authors contributed equally to this work.     

Zinc binding to peptide analogs of the structural zinc site in alcohol dehydrogenase: Implications for an entatic state

Zinc binding to the peptide replica and analogs to residues 93–115 of horse liver alcohol dehydrogenase (ADH) was examined by competition of the peptides and the chromophoric chelator 4-(2- pyridylazo)resorcinol for zinc and X-ray absorption fine structure analysis of the zinc ligands. In the enzyme, zinc is coordinated by four Cys residues. In the peptide replica, zinc is bound to three Cys and one His residue. A four-Cys zinc coordination is observed only when His is removed, leading to increased zinc stability. ADH crystal structures reveal that the ε-amino group of the conserved residue Lys323 is within H-bond distance of the backbone amide oxygens of residues 103, 105 and 108, likely stabilizing the zinc coordination in the enzyme. The peptide data thus indicate structural strain and increased energy in the zinc-binding site in the protein, characteristic of an entatic state, implying a functional nature for this zinc site. Received 3 July 2008; received after revision 11 August 2008; accepted 1 September 2008     

On the mechanism of inhibition of p27 degradation by 15-deoxy-Δ12,14-prostaglandin J 2 in lymphoblasts of Alzheimer’s disease patients

It has been proposed that neuroinflammation, among other factors, may trigger an aberrant neuronal cell cycle re-entry leading to neuronal death. Cell cycle disturbances are also detectable in peripheral cells from Alzheimer’s disease (AD) patients. We previously reported that the anti-inflammatory 15- deoxy-Δ^12,14-prostaglandin J ₂ (15d-PGJ ₂) increased the cellular content of the cyclin-dependent kinase inhibitor p27, in lymphoblasts from AD patients. This work aimed at elucidating the mechanisms of 15d-PGJ ₂-induced p27 accumulation. Phosphorylation, half-life, and the nucleo-cytoplasmic traffic of p27 protein were altered by 15d-PGJ2 by mechanisms dependent on PI3K/Akt activity. 15d-PGJ ₂ prevents the calmodulin-dependent Akt overactivation in AD lymphoblasts by blocking its binding to the 85-kDa regulatory subunit of PI3K. These effects of 15d-PGJ ₂ were not mimicked by 9,10-dihydro-15-deoxy-Δ^12,14- prostaglandin J ₂, suggesting that 15d-PGJ ₂ acts independently of peroxisome proliferator-activated receptor γ activation and that the α,β-unsaturated carbonyl group in the cyclopentenone ring of 15d-PGJ ₂ is a requisite for the observed effects. Received 14 July 2008; received after revision 2 September 2008; accepted 12 September 2008