基带传输系统码间干扰及其消除问题讨论

以基带传输系统为例,给出码间干扰的概念,并推导出系统无码间干扰的条件——奈奎斯特第一准则,并通过算例探讨了奈奎斯特准则的应用。     

平方根升余弦滤波器的FPGA实现

通信系统中使用根升余弦滤波器作为成型滤波器,使系统满足奈奎斯特准则。随着滤波器工作频率的不断提高,使用DSP实现已经不太现实,而FPGA的成本不断降低,采用FPGA设计工作在高频率的滤波器更加适合。本文介绍了一种根升余弦滤波器的FPGA实现方法。     

一种可调横向滤波器的设计分析

针对在数字信号传输系统中存在码间串扰时,在基带传输系统中,必须采用在系统中插入滤波器(如频域均衡器或时域均衡器)来补偿的问题。采用奈奎斯特准则和抽样值函数的方法,对可调横向滤波器进行设计分析。并在此基础上,进一步对该滤波器的实现方法进行了较详细而全面的分析。     

等效于奈奎斯特第二准则的传输函数及构造

讨论了满足奈奎斯特第二准则传输函数的等效形式及其构造。首先将依降的概念引入到等效传输函数中，继而论证了依降函数应满足的条件。最后构造了满足奈奎斯特第二准则的等效传输函数。实践表明，该传输函数易于实现且具有良好的时频域特性。     

基于逐符号检测的部分响应系统分析

利用部分响应信号(双二进制脉冲)可控地引入符号间干扰(ISI),设计可近似物理实现的发送滤波器和接收滤波器收发信号,牺牲功率利用率来换取较高的频谱利用率,使得符号传输速率达到奈奎斯特速率.在调制信号前采用数据预编码,对接收信号进行相应译码,以消除信道中噪声引起的差错传播.     

基于系统开环频率特性曲线的奈奎斯特判据用法研究

为了解决系统中奈氏曲线、积分环节处理和正负穿越次数等开环频率曲线的特性,基于奈奎斯特判据法,通过画奈奎斯特曲线、正确完善奈氏曲线和应用奈氏判据研究确定系统的相对稳定性,研究得到奈奎斯特稳定判据能够有效判断系统的稳定性,研究结论对于系统相对稳定性的理解提供参考．     

OFDM系统的信道估计算法的研究

目前基于导频的OFDM信道估计算法都是针对满足二维奈奎斯特准则的规则导频点阵而设计的。如果奈奎斯特准则被违反．或者导频分布构成不规则的点阵,这些基于规则导频的信道估计算法不再适用。针对此情形本文介绍了一种利用不规则采样技术的基于不规则导频分布的算法进行信道估计。该算法先利用最小二乘算法估计出导频位置的信道信息,再利用合适的权及块状托普利兹矩阵,通过共轭梯度迭代算法获得整个信道信息的估计值。     

预失真系统的采样率和滤波器带宽的设计

给出了预失真系统中信号源采样率和滤波器带宽的合理设计方法.考虑到腔体滤波器能较好地滤除射频信号的高阶互调分量,预失真信号通常只需补偿功放的3阶互调失真,因此3阶互调分量应尽可能少地有混叠、有损失送至功放.根据奈奎斯特定理,应对信号源进行3～4倍过采样,带通滤波器的带宽应取3～4倍过采样对应的带宽.仿真结果表明,设计方法合理,能以较低的计算复杂度和硬件成本获得良好的线性化性能.     

基于调制宽带转换器的倒谱恢复算法

亚奈奎斯特采样主要应用于宽带通信和射频(RF)技术中。目前理论成熟且硬件实现的亚奈奎斯特采样技术有随机解调器和调制宽带转换器。随机解调器主要用于谱线的检测,而调制宽带转换器是用于稀疏多频带信号。调制宽带转换器(MWC)是一种用于获取频域稀疏、时域连续信号的一种亚奈奎斯特采样方法。其平均采样速率要低于奈奎斯特速率。亚奈奎斯特采样是一种全盲采样方法,即在信号采样和信号重构时都是不知道频谱信息和频谱位置。本文提出一种基于调制宽带转换器的时域对偶信号的倒谱恢复算法,能在极小误差(0.0098)范围内完美的恢复出原始信号。     

多径衰落信道下准正交时分复用的研究

基于时频对偶原理，提出了一种准正交时分复用（QOTDM）系统．该系统利用频域具有升余弦性质的脉冲波形的平移准正交特性，采用自适应信道均衡方法，使发送滤波器、信道和接收滤波器的频域总特性具有升余弦性质，信道等效脉冲响应满足奈奎斯特采样点无失真准则．发送端利用上述信道进行时域波形准正交的离散信息符号序列传输；接收端根据信息符号波形的准正交特性，实现准正交分离．与正交频分复用（OFDM）系统相比，QOTDM系统在略微降低频带利用率的条件下，可以降低峰值平均功率比，并且当信噪比较高时具有更强的抗多径衰落能力．仿真结果表明，在准静态多径衰落信道下，采用正交幅度调制，在误比特率为10^-3时，QOTDM比OFDM的平均比特信噪比值约低3dB．     

A neurofibromatosis-1-regulated pathway is required for learning in Drosophila

The tumour-suppressor gene Neurofibromatosis 1 (Nf1) encodes a Ras-specific GTPase activating protein (Ras-GAP). In addition to being involved in tumour formation, NF1 has been reported to cause learning defects in humans and Nf1 knockout mice. However, it remains to be determined whether the observed learning defect is secondary to abnormal development. The Drosophila NF1 protein is highly conserved, showing 60% identity of its 2,803 amino acids with human NF1 (ref. 12). Previous studies have suggested that Drosophila NF1 acts not only as a Ras-GAP but also as a possible regulator of the cAMP pathway that involves the rutabaga (rut)-encoded adenylyl cyclase. Because rut was isolated as a learning and short-term memory mutant, we have pursued the hypothesis that NF1 may affect learning through its control of the Rut-adenylyl cyclase/cAMP pathway. Here we show that NF1 affects learning and short-term memory independently of its developmental effects. We show that G-protein-activated adenylyl cyclase activity consists of NF1-independent and NF1-dependent components, and that the mechanism of the NF1-dependent activation of the Rut-adenylyl cyclase pathway is essential for mediating Drosophila learning and memory.     

Aberrant regulation of ras proteins in malignant tumour cells from type 1 neurofibromatosis patients.

Defects in the NF1 gene have been implicated in the inherited disorder neurofibromatosis type 1, which is characterized by several developmental abnormalities including an increased frequency of benign and malignant tumours of neural crest origin (neurofibromas and neurofibrosarcomas respectively). The NF1 gene encodes a ubiquitous protein homologous to p120GAP, the GTPase-activating protein (GAP) for the products of the ras protooncogenes. When expressed in non-mammalian systems, the region of the NF1 gene homologous to p120GAP produces a protein with GAP-like activity. Here we present evidence that the ras proteins in malignant tumour cell lines from patients with type 1 neurofibromatosis are in a constitutively activated state, as judged by the guanine nucleotide bound to them, and are necessary for cellular proliferation. These cells contain p21ras and p120GAP that are both functionally wild type, but barely any functional NF1 protein. Our results show that the NF1 protein is normally essential for correct negative regulation of ras proteins in the cell, even in the presence of normal p120GAP, and they support the hypothesis that NF1 is a tumour-suppressor gene whose product acts upstream of ras.     

覆盖矩阵P的(0,1)-矩阵类u_p(R,S)的结构

本文研究了覆盖矩阵P的(0,1)-矩阵类U_p(R,S)的结构,给出了U_p(R,S)中恒元的存在性定理.取P=0,即得Ryser关于U(R,S)中恒1的结果.     

Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1.

Neurofibromatosis type I (NF1) is one of the most common single-gene disorders that causes learning deficits in humans. Mice carrying a heterozygous null mutation of the Nfl gene (Nfl(+/-) show important features of the learning deficits associated with NF1 (ref. 2). Although neurofibromin has several known properties and functions, including Ras GTPase-activating protein activity, adenylyl cyclase modulation and microtubule binding, it is unclear which of these are essential for learning in mice and humans. Here we show that the learning deficits of Nf1(+/-) mice can be rescued by genetic and pharmacological manipulations that decrease Ras function. We also show that the Nf1(+/-) mice have increased GABA (gamma-amino butyric acid)-mediated inhibition and specific deficits in long-term potentiation, both of which can be reversed by decreasing Ras function. Our results indicate that the learning deficits associated with NF1 may be caused by excessive Ras activity, which leads to impairments in long-term potentiation caused by increased GABA-mediated inhibition. Our findings have implications for the development of treatments for learning deficits associated with NF1.     

基于自相关理论的GM(1,1)和GM(1,N)联合预测

通过引入自相关分析，将GM（1，1）与GM（1，N）两者的优点有机结合，运用GM（1，1）预测模型所需的数据量，达到GM（1，N）预测模型所具有的预测精度，减少灰色模型的预测误差。     

天然航道船行波波高计算方法

介绍了７０年代－８－年代国外较典型的有关船行波波高计算公式及其适用条件，根据我国近期对双体客船的船行波试验资料，给出了相应的计算船行波波高的方法。并了单体船和双体船船行波形态以及影响船行波波高的诸因素。     

Differential regulation of rasGAP and neurofibromatosis gene product activities

The ras-encoded p21ras proteins bind GTP very tightly, but catalyse hydrolysis to GDP very slowly. In humans, two genes encode proteins that stimulate this GTPase activity (GAP, or GTPase-activating proteins), one of relative molecular mass 120,000, referred to as p120-GAP, and another NF1-GAP, which is encoded by the neurofibromatosis type-1 gene. Both GAPs are widely expressed in mammalian tissues. Here we show that although they will both bind oncogenic mutants of p21ras, neither will stimulate their GTPase activity. NF1-GAP binds to the p21ras proteins up to 300 times more efficiently than p120-GAP. The two GAPs are inhibited to different extents by certain lipids: micromolar concentrations of arachidonate, phosphatidate and phosphatidylinositol-4,5-bisphosphate affect only NF1-GAP. This inhibition does not compete with p21ras, and lipid-inactivated NF1-GAP can still bind p21ras. We used the detergent dodecyl maltoside, which inhibits only NF1-GAP, to distinguish between the two activities in cell extracts and found both types present together in several mammalian cell lines. In contrast, GAP activity in extracts of Xenopus oocytes was not affected by dodecyl maltoside. By these criteria, the mammalian cells contain both GAP activities and the oocytes have only p120-like GAP activity. These results indicate that more than one GAP regulates p21ras in the same cell.     

界面缩聚法制备聚芳酯复合纳滤膜 III.NF-1复合纳滤膜的结构和性能

通过 Ｉ Ｒ, Ｘ射线衍射分别研究了复合纳滤膜致密层的化学结构及其与性能的关系。采用扫描电镜（ Ｓ Ｅ Ｍ ）和原子力显微镜（ Ａ Ｆ Ｍ ）分别对膜的断面、表面形态作了研究。     

新疆库车县沙尘暴变化特征及突变分析

根据新疆气象局地面观测资料,整理出库车县1951～2009年沙尘暴年日数资料,运用小波分析、累积距平、滑动t检验等方法对沙尘暴年日数序列的变化趋势、周期特征、突变特征进行了分析,结果表明:(1)近60年间,库车县沙尘暴年日数呈显著减少的趋势,趋势系数为-0.34,通过α=0.05的显著性检验。20世纪50年代、60年代和70年代是近60年库车县沙尘暴的三个频发期。(2)沙尘暴年日数序列存在7年、15年、22年的周期;在不同的时间尺度上,沙尘暴经历了多个频发期和少沙尘暴期,在未来几年可能会再次迎来一个沙尘暴的频发期。(3)研究区内沙尘暴年日数变化趋势确实存在1985年的突变年份,而且这次突变并不是简单的均值突变或转折突变,是这两种突变的组合。