镉污染土壤的植物修复研究进展与展望

近年来,重金属镉(Cd)及其复合污染问题越来越受到人们的关注.Cd污染土壤的植物修复技术因其具有治理成本的低廉性、环境美学的兼容性和治理过程的原位性等优势,随之成为具有广泛应用前景的技术.本文概述了Cd超积累植物的筛选及耐性机理与修复潜力的评价等方面的国内外进展,总结了Cd-重金属复合污染土壤、Cd-有机物复合污染土壤的植物修复相关的重要工作,着重评述了Cd复合污染土壤的化学强化、农业生态强化及其它方法的研发现状,展望了这一领域今后的重点研究内容和重要发展方向.     

体域网中基于特征组合的步态行为识别

物联网(internet of things,IOT)拥有无处不在的识别、传感和通信能力,体域网(body area network,BAN)属于物联网中和人体相关的领域,其应用广泛,可以在日常生活中对人们进行监测及提供帮助.行走是许多日常活动的基本环节,因而步态分析能为体域网应用提供重要的生理行为信息.现有的步态分析已取得一定的研究成果,但仍存在一些问题,例如大多数步态特征提取是对加速度信号进行6重以上的变换,使得特征达到了45维以上,最后需要通过降维或优化来简化特征,较为复杂.本文设计一种灵活便捷的数据采集系统,并利用小波变换、傅里叶变换和四分位差提取出加速度信号中比较简单、低维度但能反应运动特征的步态参数,之后通过模式识别算法进行步态行为识别验证.实验结果表明该系统使用方便,特征提取方法简单实用,识别精确度为97%,EER(equal error rate)最小可到0.9%.     

磁盘表面形貌对润滑剂分布及磁头／磁盘之间润滑剂转移的影响

磁盘表层润滑剂在磁头与磁盘之间转移会影响磁头飞行的稳定性．本文采用改进后的粗粒珠簧模型,运用分子动力学方法,研究了磁盘上类金刚石薄膜（diamondlikecarbon,DLC）层粗糙度和磁盘表面凸起对润滑剂在磁盘表面分布及磁头／磁盘之间润滑剂转移的影响．研究结果表明,DLC层粗糙度对润滑膜平均厚度及磁盘表层粗糙度的影响很小;磁盘表面凸起对磁盘表层润滑剂分布的影响明显．类金刚石薄膜层的粗糙度和磁盘表层凸起均可增加转移到磁头上的润滑剂的体积．但磁盘表层粗糙度对磁头／磁盘之间润滑剂转移量的影响明显低于由磁盘表层凸起导致的磁头／磁盘之间润滑剂的转移量．     

基于栅极信号的功率器件老化特征分析

本文研究栅极动态信号在功率器件故障预测上的应用.首先介绍了功率器件栅极动态信号反映的相关失效机制,并分析了栅极动态信号的老化特征及影响因素.提出了老化特征提取方法,选定动态过程时间,动态过程面积比率作为老化特征.使用降频错位采样的方法还原高频采样下计算的老化特征,降低利用动态信号进行故障预测的采样频率,以提高方法可行性.通过NASA公布的数据集进行实验验证,提取的老化特征明显,降频采样达到了预期效果.     

Metabolic engineering of Saccharomyces cerevisiae: a key cell factory platform for future biorefineries

Metabolic engineering is the enabling science of development of efficient cell factories for the production of fuels, chemicals, pharmaceuticals, and food ingredients through microbial fermentations. The yeast Saccharomyces cerevisiae is a key cell factory already used for the production of a wide range of industrial products, and here we review ongoing work, particularly in industry, on using this organism for the production of butanol, which can be used as biofuel, and isoprenoids, which can find a wide range of applications including as pharmaceuticals and as biodiesel. We also look into how engineering of yeast can lead to improved uptake of sugars that are present in biomass hydrolyzates, and hereby allow for utilization of biomass as feedstock in the production of fuels and chemicals employing S. cerevisiae. Finally, we discuss the perspectives of how technologies from systems biology and synthetic biology can be used to advance metabolic engineering of yeast.     

Exome sequencing of liver fluke-associated cholangiocarcinoma

Opisthorchis viverrini-related cholangiocarcinoma (CCA), a fatal bile duct cancer, is a major public health concern in areas endemic for this parasite. We report here whole-exome sequencing of eight O. viverrini-related tumors and matched normal tissue. We identified and validated 206 somatic mutations in 187 genes using Sanger sequencing and selected 15 genes for mutation prevalence screening in an additional 46 individuals with CCA (cases). In addition to the known cancer-related genes TP53 (mutated in 44.4% of cases), KRAS (16.7%) and SMAD4 (16.7%), we identified somatic mutations in 10 newly implicated genes in 14.8-3.7% of cases. These included inactivating mutations in MLL3 (in 14.8% of cases), ROBO2 (9.3%), RNF43 (9.3%) and PEG3 (5.6%), and activating mutations in the GNAS oncogene (9.3%). These genes have functions that can be broadly grouped into three biological classes: (i) deactivation of histone modifiers, (ii) activation of G protein signaling and (iii) loss of genome stability. This study provides insight into the mutational landscape contributing to O. viverrini-related CCA.     

Mutations in the RNA exosome component gene EXOSC3 cause pontocerebellar hypoplasia and spinal motor neuron degeneration

RNA exosomes are multi-subunit complexes conserved throughout evolution and are emerging as the major cellular machinery for processing, surveillance and turnover of a diverse spectrum of coding and noncoding RNA substrates essential for viability. By exome sequencing, we discovered recessive mutations in EXOSC3 (encoding exosome component 3) in four siblings with infantile spinal motor neuron disease, cerebellar atrophy, progressive microcephaly and profound global developmental delay, consistent with pontocerebellar hypoplasia type 1 (PCH1; MIM 607596). We identified mutations in EXOSC3 in an additional 8 of 12 families with PCH1. Morpholino knockdown of exosc3 in zebrafish embryos caused embryonic maldevelopment, resulting in small brain size and poor motility, reminiscent of human clinical features, and these defects were largely rescued by co-injection with wild-type but not mutant exosc3 mRNA. These findings represent the first example of an RNA exosome core component gene that is responsible for a human disease and further implicate dysregulation of RNA processing in cerebellar and spinal motor neuron maldevelopment and degeneration.     

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.     

Estimating the proportion of variation in susceptibility to schizophrenia captured by common SNPs

Schizophrenia is a complex disorder caused by both genetic and environmental factors. Using 9,087 affected individuals, 12,171 controls and 915,354 imputed SNPs from the Schizophrenia Psychiatric Genome-Wide Association Study (GWAS) Consortium (PGC-SCZ), we estimate that 23% (s.e. = 1%) of variation in liability to schizophrenia is captured by SNPs. We show that a substantial proportion of this variation must be the result of common causal variants, that the variance explained by each chromosome is linearly related to its length (r = 0.89, P = 2.6 × 10(-8)), that the genetic basis of schizophrenia is the same in males and females, and that a disproportionate proportion of variation is attributable to a set of 2,725 genes expressed in the central nervous system (CNS; P = 7.6 × 10(-8)). These results are consistent with a polygenic genetic architecture and imply more individual SNP associations will be detected for this disease as sample size increases.     

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.