电子电路设计有关问题的探讨

分析了电子电路设计在低频电子电路,高频电子电路,数字电路,印制版制作过程中应注意的实际问题,以提高设计者设计成功的一次性。     

场助纳米二氧化钛薄膜光催化降解甲紫的研究

纳米二氧化钛是一种重要的无机功能材料。本文采用溶胶-凝胶法制备了TiO_2薄膜,利用"场助"影响其光催化特性。光催化实验以可能具有致癌性并且难以生化降解的三苯甲烷类染料——甲紫作为降解物质,用2100型分光光度计来测量降解率,以确定电场、磁场强度对光催化特性的影响。光催化实验结果表明,外加电场(未参与水的电解)、磁场对于协助光催化降解甲紫有着明显的效果。随着外加电场、磁场强度的增加,甲紫溶液的降解率有大幅提高。反应符合一级动力学方程。     

有色金属物性数据库面向服务的体系结构研究与设计

本文在分析目前流行的两层、三层网络数据库体系结构存在的问题的基础上,根据有色金属物性数据库的特点,提出一种基于SOA、多层、分布式体系结构应用开发模型.该模型着重解决以下几个方面的问题：利用软件开发新技术,提出了基于RIA的有色金属物性数据库客户端实现方式,吸取了＂胖客户端＂和＂度客户端＂的优点,解决了传统客户端部署或动态图形绘制等方面的问题 在模型中,增加了服务层,实现了系统服务的对外发布.解决了异构平台、跨系统的业务集成和重组 采用了服务器集群技术,动态的实现了负载均衡,优化了系统性能 改进了数据访问层,增加了O/R映射,屏蔽了下层数据库的细节信息,使系统能够架构在多种类型的数据库上,提高了系统的灵活性.     

高中频CPM数字接收机设计

本文给出了一种适用于软件无线电的突发模式非相干二进制CPM接收机。该接收机采用前馈结构,利用FFT算法对前导进行捕获和分析,可以快速实现载波频偏和符号定时误差的联合估计,采用多符号检测算法来对CPM信号实现解调。通过仿真和对硬件的需求分析验证了本接收机可以有效检测信号的到来,快速实现载波和符号的联合同步,且比传统接收机具有更低的误码率。相对较低的硬件复杂度也使得接收机容易在FPGA上实现。     

锶铁氧体的结构特征及制备方法研究现状

对锶铁氧体的结构、性能特征以及主要制备方法进行了综合评述.锶铁氧体为六角晶系,属于M型铁氧体,其矫顽力主要取决于磁晶各向异性;制备方法主要有陶瓷法、化学共沉淀法、水热法、溶胶-凝胶法、熔盐合成法和自蔓延高温合成法等.水热法和溶胶-凝胶法因具有工艺简单、产品磁性能高等优点,是今后高性能锶铁氧体制备技术的主要研究方向.     

基于UDEC巷道掘进矿压显现的数值模拟

通过采用UDEC软件,依据钻孔柱状图和采掘应力影响范围建立了相应的几何模型,根据煤岩体物理力学性质建立相应的材料模型,在此基础上结合地应力数据,从而完成数值模型.通过模拟实际巷道开挖尺寸及方位,得出巷道前方的应力分布和巷道两帮位移分布,为巷道冲击地压显现防治提供了理论支持.     

基于复扩散模型憎水性图像多尺度亮点检测算法研究

在多尺度框架下,提出基于非线性复扩散模型憎水性图像水珠亮点检测算法,最后采用模糊均类算法对多尺度虚部图像水珠亮点进行提取。实验结果表明：对于不同憎水性等级憎水性图像,水珠亮点检测都达到95％以上,这为对绝缘子憎水性等级估判及水珠（水迹）的进一步分割提供了重要的信息。     

Ranbp2 haploinsufficiency mediates distinct cellular and biochemical phenotypes in brain and retinal dopaminergic and glia cells elicited by the Parkinsonian neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)

Many components and pathways transducing multifaceted and deleterious effects of stress stimuli remain ill-defined. The Ran-binding protein 2 (RanBP2) interactome modulates the expression of a range of clinical and cell-context-dependent manifestations upon a variety of stressors. We examined the role of Ranbp2 haploinsufficiency on cellular and metabolic manifestations linked to tyrosine-hydroxylase (TH(+)) dopaminergic neurons and glial cells of the brain and retina upon acute challenge to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a parkinsonian neurotoxin, which models facets of Parkinson disease. MPTP led to stronger akinetic parkinsonism and slower recovery in Ranbp2 (+/-) than wild-type mice without viability changes of brain TH(+)-neurons of either genotype, with the exception of transient nuclear atypia via changes in chromatin condensation of Ranbp2 (+/-) TH(+)-neurons. Conversely, the number of wild-type retinal TH(+)-amacrine neurons compared to Ranbp2 (+/-) underwent milder declines without apoptosis followed by stronger recoveries without neurogenesis. These phenotypes were accompanied by a stronger rise of EdU(+)-proliferative cells and non-proliferative gliosis of GFAP(+)-Müller cells in wild-type than Ranbp2 (+/-) that outlasted the MPTP-insult. Finally, MPTP-treated wild-type and Ranbp2 (+/-) mice present distinct metabolic footprints in the brain or selective regions thereof, such as striatum, that are supportive of RanBP2-mediated regulation of interdependent metabolic pathways of lysine, cholesterol, free-fatty acids, or their β-oxidation. These studies demonstrate contrasting gene-environment phenodeviances and roles of Ranbp2 between dopaminergic and glial cells of the brain and retina upon oxidative stress-elicited signaling and factors triggering a continuum of metabolic and cellular manifestations and proxies linked to oxidative stress, and chorioretinal and neurological disorders such as Parkinson.     

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.     

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.