基于用户QoE的室内可见光通信系统接入策略

在可见光通信网络室内场景中,针对用户难以选择合适的发光二极管进行接入从而实现高质量流量服务的问题,以用户为中心,引入系统性能指标:用户体验质量(QoE).以QoE概率覆盖模型为基础,提出基于用户QoE优化的贪婪接入算法.通过MATLAB进行仿真,将贪婪接入算法与就近接入方法在用户数量、覆盖概率、接入阈值、接收视角等方面...     

基于VR运动模拟器的体感模拟算法的研究

针对VR(Virtual Reality)运动模拟器使用的经典体感模拟控制算法存在相位延迟、虚假暗示的缺点导致虚实运动一致性不够,引发VR晕动症的问题,提出了一种改进体感模拟算法。改进体感模拟算法在经典模拟算法的基础上加入了前庭感知系统,对算法的输出误差进行反馈,采用模糊控制算法对输入加速度和角速度进行修正和预测,并且对虚拟现实中地形的起伏变化进行模拟。在MATLAB/Simulink中对改进体感模拟算法进行建模仿真,仿真结果表明改进体感模拟算法降低了相位延迟和虚假暗示,提高了虚实运动的一致性。     

分布式呼叫中心系统的设计

呼叫中心目前在各行各业中有着广泛的应用,但由于传统的集中式呼叫中心系统中存在语音服务平台和具体业务平台没有分离的缺点,对业务扩展产生了较大的阻碍。本文提出的分布式呼叫中心系统结构通过使用互联网络并采用分布式处理的思想对原有系统进行改造,将业务与呼叫中心通讯和设备控制分离,实现分布式的信息处理并简化业务流程控制,使系统整体的可扩展性和可维护性得到提升。     

Turbo／MAP编译码器中的交织器优化设计

讨论采用软输出迭代译交织级联卷积码（Ｔｕｒｂｏ码）编译码器中的交织器优化设计问题．从基于最大后验概率（ＭＡＰ）算法与迭代译码的Ｔｕｒｂｏ码编译码原理出发,给出交织器设计的一些基本方法并分析其特点;提出“保奇偶”的随机交织器设计方案,它能有效地改善某些以提高编码效率为目的的“删余截短”Ｔｕｒｂｏ码的纠错性能．通过计算机仿真得出一些Ｔｕｒｂｏ码在加性高斯白噪声信道中采用不同交织器时的误码率数据,分析了交织类型和交织深度的变化对Ｔｕｒｂｏ码纠错性能的影响．针对Ｔｕｒｂｏ码的特点提出了在卫星通信等应用中交织器设计的实用性结论．     

浅谈网络语言在词汇层面上的变异

随着网络在中国的迅猛发展,一种新的社会方言———网络语言兴起并蓬勃发展。互联网的出现对我们的生活产生了巨大影响。网络语言是广泛应用于虚拟世界的信息符号。网络语言与现实语言相比,它受现实语言的制约,同时又反作用于现实语言。本文试图从词汇层面对网络语言进行浅析。     

Granzyme B is recovered by natural killer cells via clathrin-dependent endocytosis

When they recognize a target cell, natural killer (NK) cells mount an attack to kill the target by exerting their cytotoxicity via the exocytosis of cytotoxic granules. Although the details of this process (which includes the movement of cytotoxic granules in the immune synapse and their fusion with the plasma membrane, releasing granzymes and perforin into the synaptic cleft) are relatively better understood, the post-exocytosis regulation of the process is still largely unknown. Here we show that a clathrin-dependent endocytosis stimulated by target cell occurs in NK92 cell line, which is closely correlated with granzyme B recovery. Inhibition of the endocytosis significantly attenuates the cytotoxicity of NK92 cells. The NK cell recovery of its released effector molecules, in turn, suggests that endocytosis may well play a key role in the post exocytosis regulation of immune cells.     

A genome-wide association study in Han Chinese identifies new susceptibility loci for ankylosing spondylitis

To identify susceptibility loci for ankylosing spondylitis, we performed a two-stage genome-wide association study in Han Chinese. In the discovery stage, we analyzed 1,356,350 autosomal SNPs in 1,837 individuals with ankylosing spondylitis and 4,231 controls; in the validation stage, we analyzed 30 suggestive SNPs in an additional 2,100 affected individuals and 3,496 controls. We identified two new susceptibility loci between EDIL3 and HAPLN1 at 5q14.3 (rs4552569; P = 8.77 × 10(-10)) and within ANO6 at 12q12 (rs17095830; P = 1.63 × 10(-8)). We also confirmed previously reported associations in Europeans within the major histocompatibility complex (MHC) region (top SNP, rs13202464; P < 5 × 10(-324)) and at 2p15 (rs10865331; P = 1.98 × 10(-8)). We show that rs13202464 within the MHC region mainly represents the risk effect of HLA-B*27 variants (including HLA-B*2704, HLA-B*2705 and HLA-B*2715) in Chinese. The two newly discovered loci implicate genes related to bone formation and cartilage development, suggesting their potential involvement in the etiology of ankylosing spondylitis.     

Mutations in NMNAT1 cause Leber congenital amaurosis and identify a new disease pathway for retinal degeneration

Leber congenital amaurosis (LCA) is a blinding retinal disease that presents within the first year after birth. Using exome sequencing, we identified mutations in the nicotinamide adenine dinucleotide (NAD) synthase gene NMNAT1 encoding nicotinamide mononucleotide adenylyltransferase 1 in eight families with LCA, including the family in which LCA was originally linked to the LCA9 locus. Notably, all individuals with NMNAT1 mutations also have macular colobomas, which are severe degenerative entities of the central retina (fovea) devoid of tissue and photoreceptors. Functional assays of the proteins encoded by the mutant alleles identified in our study showed that the mutations reduce the enzymatic activity of NMNAT1 in NAD biosynthesis and affect protein folding. Of note, recent characterization of the slow Wallerian degeneration (Wld(s)) mouse model, in which prolonged axonal survival after injury is observed, identified NMNAT1 as a neuroprotective protein when ectopically expressed. Our findings identify a new disease mechanism underlying LCA and provide the first link between endogenous NMNAT1 dysfunction and a human nervous system disorder.     

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.