一种减小TOA测量距离中NLOS影响的DMS模型和估计算法

有效的滤波方法和多尺度估计是无线定位技术的重要研究方向。为了减小在蜂窝网无线定位中非视距传 播(NLOS)对波达时间(TOA)测量距离的误差影响,先结合NLOS误差特性对标准Kalman滤波进行修正,然后提 出将不同采样率的修正Kalman滤波方程与多个尺度联系起来,建立了一种动态多尺度系统(DMS)模型,并给出基 于Haar小波的实现方法。仿真结果表明,基于上述方法优于直接进行Kalman滤波的效果,能较大幅度地提高 TOA测量距离的精度。     

虚拟现实技术支持下的三维地形仿真系统设计研究

将虚拟现实技术应用到地形仿真中的相关理论与关键技术,确定了系统实现的技术路线,并以黑龙江省8511农场数据作为本系统的实验数据,以武汉吉奥公司的CCGIS4.0作为二次开发平台,使用Visual Basic6.0重新定制与开发了三维地形仿真系统,在普通PC机上成功建立了桌面型虚拟现实系统.系统实现了三维场景的漫游、查询定位、空间分析和视频输出等功能,达到了虚拟三维场景实时动态显示与交互的目的.     

基于支持向量机的信用评估模型及风险评价

运用基于支持向量机理来建立一个新的个人信用评估预测模型,以期取得更好的预测分类能力.并对SVM分类结果与三层全连接BPN分类结果进行了比较.结果表明,在判别潜在的贷款申请者中支持向量的判别结果比神经网络的要好.为了减小训练集偏差及为了验证两种方法的鲁棒性,基于两种策略(平衡样本与非平衡样本)交叉验证来进一步评价SVM分类准确性,并对两种方法基于两种策略的误分类作了风险代价分析.     

质量功能展开中自相关关系确定的粗糙集方法

针对质量功能展开中各项工程特性之间的自相关关系具有模糊、不确定和不分明等特质,提出了自相关关系确定的粗糙集方法.对于每一项顾客需求,由每一项工程特性组成相应的决策属性集,并由其它工程特性组成相应的条件属性集,分别构造了相应于该决策属性集的决策系统.基于粗糙集中相对约简和相对核等方法,分别建立了其相应的修正决策系统.利用信息熵和等价类的集成方法,获取了修正决策系统中各条件属性的重要度.引入了自相关关系的比例因子概念,确定了各项工程特性之间的自相关关系.以洗衣机的产品研发为例,说明了方法的应用.     

基于结构层贡献率的沥青路面抗车辙措施

采用环道试验及德国汉堡车辙试验方法,研究在中面层使用改性沥青对路面结构和组合结构抗车辙性能的影响,包括对结构层贡献率和对沥青层剪切流动变形的影响;探讨在中面层添加纤维对路面结构抗车辙能力的影响.研究结果表明:中面层使用改性沥青,能提高路面结构的整体抗车辙性能;使剪切流动变形由95.2%下降至84.4%;中面层变形贡献率达到60%以上,应该重视提高中面层的抗车辙能力;对于中面层采用普通沥青的结构,在中面层添加纤维可明显减少整个结构车辙深度,但对于中面层已采用改性沥青的结构,添加纤维减少车辙的效果不明显.     

基于管道配置的电液位置控制系统同步特性研究

针对径锻机一级先导缸电液位置控制系统同步精度低的问题,运用AMESim软件研究了第一类管道配置对径锻机一级先导缸电液位置控制系统同步特性的影响。研究发现:系统同步误差随着管道长度的增加而增大,且伴有波动现象,管道长度为3m时最大同步误差是管道长度为1m时的1.4倍;管道长度为1m时的最大同步误差为无管道时的1.1倍;管道材料的杨氏弹性模量越小,对应系统的同步误差越大。     

Interleukin-33 stimulates formation of functional osteoclasts from human CD14+ monocytes

Interleukin (IL)-33 is a recently described pro-inflammatory cytokine. Here we demonstrate IL-33 as a regulator of functional osteoclasts (OCs) from human CD14⁺ monocytes. IL-33 stimulates formation of tartrate-resistant acid phosphatase (TRAP)⁺ multinuclear OCs from monocytes. This action was suppressed by anti-ST2 antibody, suggesting that IL-33 acts through its receptor ST2, but not by the receptor activator of NF-κB ligand (RANKL) decoy, osteoprotegerin, or anti-RANKL antibody. IL-33 stimulated activating phosphorylations of signaling molecules in monocytes that are critical for OC development. These included Syk, phospholipase Cγ2, Gab2, MAP kinases, TAK-1, and NF-κB. IL-33 also enhanced expression of OC differentiation factors including TNF-α receptor-associated factor 6 (TRAF6), nuclear factor of activated T cells cytoplasmic 1, c-Fos, c-Src, cathepsin K, and calcitonin receptor. IL-33 eventually induced bone resorption. This study suggests that the osteoclastogenic property of IL-33 is mediated through TRAF6 as well as the immunoreceptor tyrosine-based activation motif-dependent Syk/PLCγ pathway in human CD14⁺ monocytes.     

Mutations in the RNA exosome component gene EXOSC3 cause pontocerebellar hypoplasia and spinal motor neuron degeneration

RNA exosomes are multi-subunit complexes conserved throughout evolution and are emerging as the major cellular machinery for processing, surveillance and turnover of a diverse spectrum of coding and noncoding RNA substrates essential for viability. By exome sequencing, we discovered recessive mutations in EXOSC3 (encoding exosome component 3) in four siblings with infantile spinal motor neuron disease, cerebellar atrophy, progressive microcephaly and profound global developmental delay, consistent with pontocerebellar hypoplasia type 1 (PCH1; MIM 607596). We identified mutations in EXOSC3 in an additional 8 of 12 families with PCH1. Morpholino knockdown of exosc3 in zebrafish embryos caused embryonic maldevelopment, resulting in small brain size and poor motility, reminiscent of human clinical features, and these defects were largely rescued by co-injection with wild-type but not mutant exosc3 mRNA. These findings represent the first example of an RNA exosome core component gene that is responsible for a human disease and further implicate dysregulation of RNA processing in cerebellar and spinal motor neuron maldevelopment and degeneration.     

Frequent mutations of chromatin remodeling genes in transitional cell carcinoma of the bladder

Transitional cell carcinoma (TCC) is the most common type of bladder cancer. Here we sequenced the exomes of nine individuals with TCC and screened all the somatically mutated genes in a prevalence set of 88 additional individuals with TCC with different tumor stages and grades. In our study, we discovered a variety of genes previously unknown to be mutated in TCC. Notably, we identified genetic aberrations of the chromatin remodeling genes (UTX, MLL-MLL3, CREBBP-EP300, NCOR1, ARID1A and CHD6) in 59% of our 97 subjects with TCC. Of these genes, we showed UTX to be altered substantially more frequently in tumors of low stages and grades, highlighting its potential role in the classification and diagnosis of bladder cancer. Our results provide an overview of the genetic basis of TCC and suggest that aberration of chromatin regulation might be a hallmark of bladder cancer.