基于DVB-T的OFDM系统的信道估计研究

DVB-T标准中采用了OFDM编码调制技术来提高系统的频谱利用率和抗多径干扰的能力,为了能够准确地解调OFDM信号,需要对接收到的信号进行信道估计.而基于导频的信道估计是通过导频子信道的响应计算出整个信道的响应,它能够很好地跟踪信道的变化,在计算复杂度不是很高的情况下能够达到较好的性能,是一种比较实用的信道估计方法.本文讨论了DVB-T系统中基于导频的信道估计方法,并提出了一种时频二维插值信道估计方法.仿真结果表明,二维插值信道估计较一维插值具有更好的误码率性能.     

基于导频的OFDM系统信道估计

本文介绍了基于导频的OFDM系统信道估计的基本方法,并给出在不同估计准则、不同导频图案下,信道估计性能的对比分析。采用广义平非相关散射下的多径时变瑞利信道模型,对各个算法进行仿真,得出不同算下信道估计的均方误差曲线。仿真结果表明：在快变信道中,梳状导频较块导频有更好的性能;基于MMSE准则的信道估计比基于LS准则的估计有更的性能,但前者复杂度较高。     

基于导频的OFDM水下通信信道估计

信道估计是OFDM水下通信相干解调的必要步骤。通过插入位置已知的导频信息,OFDM接收机可以知道水声信道在导频位置的频率响应。根据插入导频位置的不同,信道估计的性能也有很大的差异。块状、梳状和分散型3种导频分布方式被证明分别适用于不同的水声信道环境。水声信道可以看做是一个梳状滤波器,通过信道估计可以得到试验信道的通带和阻带。阻带的信道估计错误往往要大于通带,尤其是当信道的相干带宽较小时,这种现象则更为明显。子载波间干扰会对信道估计性能造成很大影响,利用改进的变换域滤波器导频降噪方法可以有效地降低这种影响。     

一种新的基于判决反馈的OFDM系统信道估计方法

提出了一种基于判决反馈机制的信道估计方法,采用少量导频估计出初始信道信息,再从接收端检测出的符号中选取一组包含了少量错误的符号作为准导频,反馈到信道估计器,与初始的导频一起构成数量更多的导频序列,经过几次迭代,达到提高信道估计精度的目的.为提高初始估计的精度,信道估计采用了一种频域分集的方法.计算机仿真表明,在多径瑞利衰落信道下,本文的方法可以在较低的复杂度下有效地提高信道估计的精度,在MMSE接收条件下,系统具有良好的误比特率(BER)性能.     

OFDM系统中最优导频序列的设计方案

在正交频分复用(OFDM)系统中,接收信号易受频率选择性衰落信道的影响产生失真,准确的信道估计变得必不可少。考虑到无线信道的内在稀疏性、压缩感知技术挖掘信道稀疏特征的有效性,研究了基于压缩感知技术的OFDM稀疏信道估计。针对导频位置影响信道估计性能的问题,提出了一种反馈型的导频优化算法,该算法基于离散傅里叶变换(DFT)子矩阵中各个列之间互相干性最小的原则,同时结合信道状态信息的反馈机制,实现了对导频序列的联合优化。仿真结果表明,与当前的随机优化算法、传统最小二乘信道估计相比,该优化方法有效降低干扰和噪声对信道估计的影响,从而改善了信道估计的性能。     

基于压缩感知的DRM信道估计

针对数字调幅广播(Digital Radio Mondiale,DRM) 系统频谱有限的特点,为了以较少的导频开销获得精确的信道状态信息,本文将压缩感知理论与信道估计问题相联系,建立基于压缩感知的DRM 信道估计模型,并分析和验证导频插入方式和数量对信道估计性能的影响.与LS(Least Square) 方法相比,基于压缩感知的DRM 信道估计不但能够以更少的导频获得精确可靠的估计结果,而且在提升信道估计性能的同时提高频谱利用率.     

正交频分复用系统中基于子空间跟踪的信道估计

基于导频的正交频分复用（OFDM）系统信道估计方法是通过在确定的时频位置发送已知的导频符号来获取信道参数的,通常包括导频位置的最小二乘估计和内插滤波两步。如果能够提高导频位置信道频域特性的估计精度,那么后续内插滤波的精度也就能相应地得到提高,为此,在建立通用参数化信道模型的基础上,提出一种子空间跟踪的改进算法,该算法通过基于Givens旋转的时延子空间跟踪和基于RLS滤波的幅度跟踪,提高了导频符号信道估计的精度,降低了跟踪算法的复杂度。仿真结果表明,基于子空间跟踪的信道估计方法具有较低的复杂度和较高的估计精度。     

一种新的基于伪导频搜索的MB-LSF信道估计算法

针对伪导频搜索算法复杂度高的情况,对基于伪导频的MB-LSF信道估计算法进行了研究。提出先估计导频位置的信道响应,然后通过线性插值得到所有位置的信道响应,进而检测得到伪导频的估计值,将其作为第1次搜索的符号。理论分析和仿真结果都证明了这种新算法在不影响信道估计性能的前提下,能够很大程度地降低伪导频的搜索次数。     

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。     

基于改进的离散随机近似方案的导频研究

为解决传统信道估计方法在稀疏信道估计的性能不够理想,许多算法没有考虑到导频放置等问题,将压缩感知理论(Compressed Sensing,CS)应用到稀疏信道估计中.基于CS理论测量矩阵互相关最小化的导频图案设计的分析,提出信道估计均方误差最小准则来选择CS算法的方法,建立OFDM系统模型和导频设计方案.仿真结果表明:改进的离散随机近似方案的导频设计,比遍历性搜索收敛更快更有效,对基于OMP算法的信道估计性能有较大幅度提升.     

BFSK信号在高斯和瑞利信道中传输性能仿真分析

本文首先建立了高斯白噪声信道和瑞利衰落信道数学模型,并用MATLAB软件进行了仿真.以BFSK信号为例,对该信号在此两种信道中的性能进行了仿真分析,得出了对于相同的信噪比,信号在高斯白噪声信道中的误比特率低于瑞利衰落信道的结论.     

Voltage and Ca2+-activated K+ channel in baso-lateral acinar cell membranes of mammalian salivary glands

Nervous or hormonal stimulation of many exocrine glands evokes release of cellular K+ (ref. 1), as originally demonstrated in mammalian salivary glands2,3, and is associated with a marked increase in membrane conductance1,4,5. We now demonstrate directly, by using the patch-clamp technique6, the existence of a K+ channel with a large conductance localized in the baso-lateral plasma membranes of mouse and rat salivary gland acinar cells. The K+ channel has a conductance of approximately 250 pS in the presence of high K+ solutions on both sides of the membrane. Although mammalian exocrine glands are believed not to possess voltage-activated channels1,7, the probability of opening the salivary gland K+ channel was increased by membrane depolarization. The frequency of channel opening, particularly at higher membrane potentials, was increased markedly by elevating the internal ionized Ca2+ concentration, as previously shown for high-conductance K+ channels from cells of neural origin8-10. The Ca2+ and voltage-activated K+ channel explains the marked cellular K+ release that is characteristically observed when salivary glands are stimulated to secrete.     

FPGA多通道视皮层刺激器

设计了一款用于视皮层视觉修复的基于FPGA的多通道视皮层刺激器。该刺激器由FPGA和外围电压/电流转换电路两部分组成。FPGA内部包括刺激脉冲发生器和多个多路选择器:刺激脉冲发生器产生各种形式的脉冲序列信号;多路选择器作为控制端实现对信号的选择,每一通道对应一个多路选择器,增加多路选择器即可实现通道的增加。FPGA输出的电压信号通过外围电压/电流转换电路,转换为电流信号后传入电极阵列。采用Altera公司Cyclone系列EP1C6型FPGA制作了四通道实验样机进行动物实验。采用猫作为实验对象,在猫的视皮层硬脑膜外左右两侧植入微电极,左侧接入刺激信号,右侧记录脑电,实验结果显示,视皮层能够响应来自对硬脑膜的电刺激,验证了所设计的刺激器是可行的。     

Glycine binding primes NMDA receptor internalization

NMDA (N-methyl-d-aspartate) receptors (NMDARs) are a principal subtype of excitatory ligand-gated ion channel with prominent roles in physiological and disease processes in the central nervous system. Recognition that glycine potentiates NMDAR-mediated currents as well as being a requisite co-agonist of the NMDAR subtype of 'glutamate' receptor profoundly changed our understanding of chemical synaptic communication in the central nervous system. The binding of both glycine and glutamate is necessary to cause opening of the NMDAR conductance pore. Although binding of either agonist alone is insufficient to cause current flow through the channel, we report here that stimulation of the glycine site initiates signalling through the NMDAR complex, priming the receptors for clathrin-dependent endocytosis. Glycine binding alone does not cause the receptor to be endocytosed; this requires both glycine and glutamate site activation of NMDARs. The priming effect of glycine is mimicked by the NMDAR glycine site agonist d-serine, and is blocked by competitive glycine site antagonists. Synaptic as well as extrasynaptic NMDARs are primed for internalization by glycine site stimulation. Our results demonstrate transmembrane signal transduction through activating the glycine site of NMDARs, and elucidate a model for modulating cell-cell communication in the central nervous system.     

改进的子波过零电子耳蜗语音编码策略

提出改进的倍频程小波过零刺激方案(WZCS),以改善电子耳蜗语音编码策略的性能.在语音信号倍频程小波变换域的过零点通过幅度调制合成刺激脉冲,并基于Matlab对该算法和连续间隔采样(CIS)、通道专用采样序列(CSSS)、频率幅度联合调制编码(FAME)等编码策略进行仿真,将合成信号与原始语音、合成信号频谱与原始语音频谱进行了相关性分析.仿真结果表明,WZCS算法合成信号的频谱与原始语音信号的频谱相关系数最大,WZCS算法合成信号频谱与原始语音最为相关,且相关显著,即与其他算法相比其保留了原始语音信号的更多频率和相位成分.     

32位并行数据的CRC-16编码器的FPGA实现

在数据通信中,提高数据在通信中的可靠性,以及快速的数据处理能力一直是人们所追求的,循环冗余校验CRC就是一种广泛采用的差错控制方法,也是一种最常用的信道编码方法。在介绍CRC码原理之后,以经典的LFSR电路为基础,推导出产生32位并行数据的CRC-16编码表达式,用EDA工具设计出CRC-16编码模块,并对其进行综合仿真,验证其可行性。     

Activation by adrenaline of a low-conductance G protein-dependent K+ channel in mouse pancreatic B cells

Insulin is produced and secreted by the B cells in the endocrine pancreas. In vivo, insulin secretion is under the control of a number of metabolic, neural and hormonal substances. It is now clear that stimulation of insulin release by fuel secretagogues, such as glucose, involves the closure of K+ channels that are sensitive to the intracellular ATP concentration (KATP channels). This leads to membrane depolarization and the generation of Ca2(+)-dependent action potentials. The mechanisms whereby hormones and neurotransmitters such as adrenaline, galanin and somatostatin, which are released by intraislet nerve endings and the pancreatic D cells, produce inhibition of insulin secretion are not clear. Here we show that adrenaline suppresses B-cell electrical activity (and thus insulin secretion) by a G protein-dependent mechanism, which culminates in the activation of a sulphonylurea-insensitive low-conductance K+ channel distinct from the KATP channel.     

A constitutively open potassium channel formed by KCNQ1 and KCNE3

Mutations in all four known KCNQ potassium channel alpha-subunit genes lead to human diseases. KCNQ1 (KvLQT1) interacts with the beta-subunit KCNE1 (IsK, minK) to form the slow, depolarization-activated potassium current I(Ks) that is affected in some forms of cardiac arrhythmia. Here we show that the novel beta-subunit KCNE3 markedly changes KCNQ1 properties to yield currents that are nearly instantaneous and depend linearly on voltage. It also suppresses the currents of KCNQ4 and HERG potassium channels. In the intestine, KCNQ1 and KCNE3 messenger RNAs colocalized in crypt cells. This localization and the pharmacology, voltage-dependence and stimulation by cyclic AMP of KCNQ1/KCNE3 currents indicate that these proteins may assemble to form the potassium channel that is important for cyclic AMP-stimulated intestinal chloride secretion and that is involved in secretory diarrhoea and cystic fibrosis.     

Sympathetic regulation of cardiac calcium current is due exclusively to cAMP-dependent phosphorylation.

The positive inotropic effect of the sympathetic nervous system on the heart is partly mediated by an increase in the voltage-gated Ca2+ current (ICa). This increase is generally attributed to beta-adrenergic receptor-stimulated cyclic AMP-dependent phosphorylation of the Ca2+ channel. It has been suggested that cAMP-dependent phosphorylation cannot explain all the effects of beta-adrenergic agonists on ICa and that a parallel membrane-delimited pathway involving the 'direct' action of the G protein Gs also stimulates ICa. A precedent exists for such a membrane-delimited pathway in the activation of a K+ channel by acetylcholine in heart. A membrane-delimited pathway for stimulation of ICa might be important in rapid beat-to-beat regulation of contraction by the sympathetic nervous system, because isoproterenol may produce a biphasic increase in ICa with the rapid phase (tau = 150 ms) putatively mediated by the direct pathway and the slow phase (tau = 35 s) by cAMP-dependent phosphorylation. Here we report that in frog, rat, and guinea pig ventricular myocytes ICa increases slowly and monophasically in response to isoproterenol. The increase is completely blocked by inhibitors of cAMP-dependent phosphorylation. Furthermore, the time course of the increase in ICa closely parallels the increase in contractile force produced by sympathetic nerve stimulation. These data refute earlier suggestions that regulation of Ca2+ channels by the sympathetic nervous system involves or requires a direct G-protein pathway.     

Single-channel and whole-cell recordings of mitogen-regulated inward currents in human cloned helper T lymphocytes

Cytoplasmic free Ca2+ [( Ca2+]i) appears to be an important signal for DNA synthesis in early stages of lymphocyte activation. In spite of many experimental studies which employ fluorescent Ca2+ indicator dye to demonstrate an early increase of [Ca2+]i in T-lymphocytes after stimulation with lectins, specific antigens, and monoclonal antibodies to T-lymphocyte receptors, the mechanism responsible for the rise of [Ca2+]i is unknown. We have used the extracellular patch clamp technique to investigate this mechanism. Unitary inward currents, mediated by Ca2+ or Ba2+, were recorded in the membrane of T-lymphocytes. The inward current channel was characterized by a conductance of 7 pS and extrapolated reversal potential (Erev) 110 mV positive to resting potential (Vr). While gating kinetic parameters were not affected by membrane potential changes, the probability of channel opening markedly increased upon activation of the T-lymphocyte by the mitogenic lectin, phytohaemagglutinin (PHA). PHA also evoked a cadmium-sensitive, inward Ba2+ current on whole-cell clamp. We suggest that this mitogen-regulated channel introduces Ca2+ into the cytoplasm upon activation and represents a new class of voltage-independent Ca2+ channels.