基于NVH性能的排气系统悬挂点位置设计

基于平均驱动自由度位移（ADDOFD）理论,同时考虑车身侧与排气系统侧的NVH性能,以及各阶模态频率的不同权值的影响,对某车型排气系统吊点位置进行优化布置,并对布置吊点后的排气系统做声学稳健性分析。实际应用表明该设计方法能对汽车排气系统悬挂点选择提供可行性参考建议,在整车开发的初期,有效预测和控制车身结构的NVH性能。     

大入射余角CFAR检测器

雷达在大入射余角高分辨率海杂波背景下检测时,等效后向散射面积增大,大部分海杂波能量投射到少数距离单元,能量分布不均,出现功率突然增大的杂波“异常单元”,导致检测器参考窗口所处的背景环境复杂多变,传统检测器检测概率降低,虚警率及误检率增加。为解决此问题,通过参考滑窗单元的协方差矩阵构造正定矩阵,求解其矩阵范数用以估计杂波功率水平,并采用支持向量机改进传统恒虚警率(constant false alarm rate,CFAR)检测器,得到基于正定矩阵杂波功率估计训练支持向量机的改进CFAR检测器。实验结果表明,新检测器在均匀杂波、多目标环境下检测性能稳定,在杂波边缘的虚警控制能力良好。     

Functions and pathologies of BiP and its interaction partners

The endoplasmic reticulum (ER) is involved in a variety of essential and interconnected processes in human cells, including protein biogenesis, signal transduction, and calcium homeostasis. The central player in all these processes is the ER-lumenal polypeptide chain binding protein BiP that acts as a molecular chaperone. BiP belongs to the heat shock protein 70 (Hsp70) family and crucially depends on a number of interaction partners, including co-chaperones, nucleotide exchange factors, and signaling molecules. In the course of the last five years, several diseases have been linked to BiP and its interaction partners, such as a group of infectious diseases that are caused by Shigella toxin producing E. coli. Furthermore, the inherited diseases Marinesco-Sj?gren syndrome, autosomal dominant polycystic liver disease, Wolcott-Rallison syndrome, and several cancer types can be considered BiP-related diseases. This review summarizes the physiological and pathophysiological characteristics of BiP and its interaction partners. Received 20 November 2008; received after revision 09 December 2008; accepted 12 December 2008     

The genomic basis of the Williams – Beuren syndrome

The Williams-Beuren syndrome is a genomic disorder (prevalence: 1/7,500 to 1/20,000), caused by a hemizygous contiguous gene deletion on chromosome 7q11.23. Typical symptoms comprise supravalvular aortic stenosis, mental retardation, overfriendliness and visuospatial impairment. The common deletion sizes range of 1.5–1.8 mega base pairs (Mb), encompassing app. 28 genes. For a few genes, a genotype-phenotype correlation has been established. The best-explored gene within this region is the elastin gene; its haploinsufficiency causes arterial stenosis. The region of the Williams-Beuren syndrome consists of a single copy gene region (~1.2 Mb) flanked by repetitive sequences – Low Copy Repeats (LCR). The deletions arise as a consequence of misalignment of these repetitive sequences during meiosis and a following unequal crossing over due to high similarity of LCRs. This review presents an overview of the Williams-Beuren syndrome region considering the genomic assembly, chromosomal rearrangements and their mechanisms (i.e. deletions, duplications, inversions) and evolutionary and historical aspects. Received 11 July 2008; received after revision 15 October 2008; accepted 16 October 2008     

POLSAR图像杂波L分布建模及其参数估计

基于乘积模型的杂波统计建模是进行高分辨极化合成孔径雷达(POLSAR)图像非均匀区域杂波统计特性分析的有效方法,其核心在于纹理分量随机分布的类型选择.广义伽马分布(GΓD)是一种普适性很强的分布类型,Weibull分布、伽马分布、逆伽马分布等都是GΓD分布的特例,因此基于GΓD分布的图像乘性杂波建模既满足杂波建模的高精度要求,同时成为各种雷达杂波辨识的有效工具.本文首先推导了服从GΓD分布的随机变量的高阶矩特征及其对数累积量(MLC),利用纹理分量服从GΓD分布情形构建了乘积相干斑模型,得到了适用于POLSAR图像处理的L分布杂波多视处理的协方差矩阵的概率分布函数,同时推导了其高阶矩特征及其对数累积量,提出了基于对数累积量的L分布参数估计新方法.针对样本数较少的情况下对数累积量参数估计失效问题提出了基于混合矩(MME)的参数估计方法来解决.然后给出了不同分布的高阶矩和对数累积量,通过二三阶对数累积量关系图辨析了常用分布与L分布的内在关系,得到了L分布是目前乘积模型中适用范围较为广泛的统计分布的结论.最后用仿真数据验证了理论推导的正确性,并将基于对数累积量的参数估计方法与已有方法进行了比较,结果证明新参数估计方法具有更高的估计精度和运算效率;另外,还用实测数据进行了统计模型检验,其结果验证了理论推导的正确性.极化SAR中多视图像L分布杂波的统计建模及其参数估计方法为极化SAR目标检测和识别等领域的新技术研究提供了新手段.     

体域网中基于特征组合的步态行为识别

物联网(internet of things,IOT)拥有无处不在的识别、传感和通信能力,体域网(body area network,BAN)属于物联网中和人体相关的领域,其应用广泛,可以在日常生活中对人们进行监测及提供帮助.行走是许多日常活动的基本环节,因而步态分析能为体域网应用提供重要的生理行为信息.现有的步态分析已取得一定的研究成果,但仍存在一些问题,例如大多数步态特征提取是对加速度信号进行6重以上的变换,使得特征达到了45维以上,最后需要通过降维或优化来简化特征,较为复杂.本文设计一种灵活便捷的数据采集系统,并利用小波变换、傅里叶变换和四分位差提取出加速度信号中比较简单、低维度但能反应运动特征的步态参数,之后通过模式识别算法进行步态行为识别验证.实验结果表明该系统使用方便,特征提取方法简单实用,识别精确度为97%,EER(equal error rate)最小可到0.9%.     

基于磁性微泡对比剂的超声和磁共振影像融合算法

文中提出了一种新的基于磁性微泡对比剂的超声影像和磁共振影像之间的融合算法．首先利用磁性微泡对比剂对体模进行超声和磁共振显影,并对显影进行边缘分割．运用非采样contourlet变换（nonsubsampled contourlet transform．NSCT）对源图像进行分解,然后对低频子带系数采用自适应动态加权非负矩阵分解（dynamic weighted non-negative matrix factorization．DWNMF）结合分割图像进行融合．然后对各带通方向子带系数采用空间频率激励的脉冲耦合神经网络进行融合,最后利用NSCT逆变换得到融合图像．研究结果表明,利用磁性微泡对比剂并结合上述算法对超声影像和磁共振影像进行融合,可以获得预期的融合效果．     

基于EXCEL和MATLAB的矩形薄片热传导计算与仿真研究

对二维导热问题进行了离散化研究,推导出了节点差分方程,以矩形薄片为例,用MS.Excel对节点温度进行了计算,用MATLAB对计算结果进行了仿真,得到了薄片的温度分布仿真图.     

Activation and inactivation of thyroid hormone by deiodinases: Local action with general consequences

The thyroid hormone plays a fundamental role in the development, growth, and metabolic homeostasis in all vertebrates by affecting the expression of different sets of genes. A group of thioredoxin fold-containing selenoproteins known as deiodinases control thyroid hormone action by activating or inactivating the precursor molecule thyroxine that is secreted by the thyroid gland. These pathways ensure regulation of the availability of the biologically active molecule T3, which occurs in a time-and tissue-specific fashion. In addition, because cells and plasma are in equilibrium and deiodination affects central thyroid hormone regulation, these local deiodinase-mediated events can also affect systemic thyroid hormone economy, such as in the case of non-thyroidal illness. Heightened interest in the field has been generated following the discovery that the deiodinases can be a component in both the Sonic hedgehog signaling pathway and the TGR-5 signaling cascade, a G-protein-coupled receptor for bile acids. These new mechanisms involved in deiodinase regulation indicate that local thyroid hormone activation and inactivation play a much broader role than previously thought. Received 29 August 2007; received after revision 11 October 2007; accepted 16 October 2007     

ERK activation by Ca2+ ionophores depends on Ca2+ entry in lymphocytes but not in platelets, and does not conduct membrane scrambling

Rapid Ca²⁺-dependent phospholipid (PL) reorganization (scrambling) at the plasma membrane is a mechanism common to hematopoietic cells exposing procoagulant phosphatidylserine (PS). The aim of this research was to determine whether activation of the extracellular signal-regulated kinase (ERK) pathway was required for PL scrambling, based on a single report analyzing both responses induced by Ca²⁺ ionophores in megakaryoblastic HEL cells. Ca²⁺ ionophore-stimulated ERK phosphorylation was induced in platelets without external Ca²⁺, whereas exogenous Ca²⁺ entry was crucial for ERK activation in Jurkat T cells. In both cells, membrane scrambling only occurred following Ca²⁺ entry and was not blocked by inhibiting ERK phosphorylation. Furthermore, ERK proteins are strongly phosphorylated in transformed B lymphoblastic cell lines, which do not expose PS in their resting state. Overall, the data demonstrated that ERK activation and membrane scrambling are independent mechanisms. A. Arachiche, I. Badirou: These authors contributed equally to this work. Received 18 June 2008; received after revision 24 September 2008; accepted 1 October 2008