退火条件对LDPE空间电荷特性的影响研究

使用冷却速率不同的3种退火方法制备了不同微观形态的LDPE薄膜,对薄膜试品进行了显微观测,并运用傅立叶红外分析对3种试品的结晶度进行了比较,同时使用PEA空间电荷测量技术对不同电场下这3种试品的空间电荷分布进行了观测,并基于结晶度和微观形态对LDPE空间电荷特性做了讨论.研究结果表明施加电场撤压后,高速冷却试品比低速冷却试品和正常冷却试品积聚更多的空间电荷,而随着撤压时间的增加,低速冷却试品中积聚的空间电荷衰减得最快.     

面向5G新空口技术的LDPC码标准化研究进展

第5代移动通信系统(5th generation mobile communication system,5G)业务需求的多样性以及各业务场景的典型特性给新空口(new radio,NR)的信道编码技术带来困难及挑战,信道编码方案成为通信业界及学术界的重要研究课题之一。因具备优越性能,低密度奇偶校验(low-density parity-check, LDPC)码被确定为5G增强移动宽带(enhanced mobile broadband, eMBB)场景数据信道编码方案。在对5G及LDPC码进行概述的基础上,阐述了包括码设计、译码算法、速率匹配和性能评估在内的面向NR的LDPC码标准化工作研究内容。此外,对近年来第3代合作伙伴计划(3rd generation partnership project, 3GPP)各成员机构在无线接入网层一(radio access network layer 1, RAN1)标准化工作组历次会议中提出的LDPC码编码方案进行分析和对比,并在此基础上对LDPC码标准化相关工作进行总结。     

Weighted symbol-flipping decoding algorithm for nonbinary LDPC codes with flipping patterns

A novel low-complexity weighted symbol-flipping algorithm with flipping patterns to decode nonbinary low-density parity-check codes is proposed.The proposed decoding procedure updates the hard-decision received symbol vector iteratively in search of a valid codeword in the symbol vector space.Only one symbol is flipped in each iteration,and symbol flipping function,which is employed as the symbol flipping metric,combines the number of failed checks and the reliabilities of the received bits and calculated symbols.A scheme to avoid infinite loops and select one symbol to flip in high order Galois field search is also proposed.The design of flipping pattern’s order and depth,which is dependent of the computational requirement and error performance,is also proposed and exemplified.Simulation results show that the algorithm achieves an appealing tradeoff between performance and computational requirement over relatively low Galois field for short to medium code length.     

Tight lower bound of consecutive lengths for QC-LDPC codes with girth at least ten

For an arbitrary (3,L) quasi-cyclic(QC) low-density parity-check (LDPC) code with girth at least ten, a tight lower bound of the consecutive lengths is presented. For an arbitrary length above the bound the corresponding LDPC code necessarily has a girth at least ten, and for the length equal to the bound, the resultant code inevitably has a girth smaller than ten. This new conclusion can be well applied to some important issues, such as the proofs of the existence of large girth QC-LDPC codes, the construction of large girth QC-LDPC codes based on the Chinese remainder theorem, as well as the construction of LDPC codes with the guaranteed error correction capability.     

丝氨酰-天冬氨酰-谷氨酸三肽吸附低密度脂蛋白的机理的探讨

以聚丙烯酰胺(PAM)微球为载体,丝氨酰-天冬氨酰-谷氨酸(SDE)三肽为配体,通过两种方法将配体偶联到载体上制成吸附剂。采用体外静态吸附法检测吸附剂的吸附效果,考察SDE三肽仿生吸附剂对低密度脂蛋白(LDL)的吸附并探讨其机理。结果表明:两种方法制备的吸附剂对LDL都有一定的亲和吸附能力,Ca2 可通过桥接LDL所含磷脂极性头部的磷酸基团和吸附微珠配体上的羧基及交联相邻LDL磷脂间的磷酸基团,增大LDL吸附到吸附微珠上的机率,进而提高其吸附率。用戊二醛固定化配体制成的吸附剂因表面含有更多能与LDL相互作用的基团(COOH),更有利于LDL的吸附。     

跳频抗干扰通信系统中LDPC码的编码优化设计

为进一步提升低密度奇偶校验(low-density parity-check, LDPC)编码跳频通信系统抗干扰能力,提出一种对抗部分频带干扰样式的LDPC编码构造方法。首先针对不同干扰因子参数优化了LDPC码字在干扰环境下的度分布序列,然后通过基于渐进边增长和近似环外信息算法构造基矩阵,最后采用改进部分分割移位系数矩阵扩展得到校验矩阵,并结合不等差错保护特性应用到信息位的干扰保护上。该构造方法兼顾优化的度分布和准循环结构。仿真结果表明,所构造的码字性能良好,相同条件下,抗干扰性能优于现行主流类型码字的抗干扰性能。     

基于粒子群算法的非规则LDPC码度序列设计

研究了非规则低密度奇偶校验（low-density parity-check, LDPC）码度序列阈值计算方法，详细讨论了构造具有较高阈值度序列的步骤与约束条件的处理，提出了一种基于粒子群优化（particle swarm optimization, PSO）算法的度序列优化方法。仿真了此方法的寻优效果，给出了一些接近Shannon限的优秀度序列和分析比较。     

基于LDPC的不均等错误保护H.264抗误码算法

从最新的H.264视频压缩标准出发,提出一种基于数据分类和LDPC的不均等错误保护的策略。根据H.264数据分类中信息比特重要性的不同,对其进行不均等错误保护,即对信道中优先级较高的数据,采用码率低,抗误码性能更好的LDPC编码传输,以提高传输效率。仿真结果表明,这种联合的信源信道编码算法在AWGN信道下具有比以前的一般算法(如Turbo码)更好的适应性和更强的健壮性。     

中华猕猴桃营养生物学效应研究——Ⅱ.浓缩果汁对家兔血清脂蛋白和高密度脂蛋白胆固醇及其亚组分的效应

采用琼脂糖凝胶电泳分析法和PEG化学沉降分析法,对口服中华猕猴桃浓缩果汁家兔血清脂蛋白组分和高密度脂蛋白胆固醇及其亚组分的动态变化进行实验观察。结果表明,持续30d口服浓缩果汁血清总胆固醇呈明显下降,高密度脂蛋白亚组分胆固醇HDL2-C/HDL3-C比率明显升高。凝胶电泳分析结果,α-脂蛋白与β-脂蛋白的比值明显升高。     

Molecular pathogenesis of apolipoprotein E-mediated amyloidosis in late-onset Alzheimer’s disease

Apolipoprotein E (apoE) ɛ4 allele is a genetic risk factor for late-onset familial and sporadic Alzheimer’s disease (AD). In the central nervous system, apoE is secreted mainly by astrocytes as a constituent of high-density lipoproteins. A recent study using apoE knockout mice provided strong evidence that apoE promotes cerebral deposition of amyloid β protein (Aβ). However, no clear explanation of the pathogenesis of apoE-induced AD has been provided. Here we discuss two possible mechanisms by which apoE might enhance Aβ deposition. One is the intracellular pathway in which apoE is internalized by neurons and induces lysosomal accumulation of Aβ and amyloidogenic APP (amyloid precursor protein) fragments, leading to neuronal death. The other is the extracellular pathway in which apoE-containing lipoproteins are trapped by Aβ1–42 deposits mobilizing soluble Aβ peptides and consequently enlarge amyloid plaques. These two mechanisms may operate at different stages of AD pathogenesis and suggest a chaperone-like function for the apoE molecule. Received 4 February 1999; received after revision 9 April 1999; accepted 23 April 1999