基于在线神经网络的自适应控制器的设计与应用

针对线性控制系统自适应性较弱的缺点,在其基础上设计了一种基于在线神经网络的自适应控制器．该控制器根据被控对象和参考模型之间的误差调整网络权值,在线抵消被控对象的未建模动态特性和不确定因素．文中以某小卫星姿态控制系统为例,对所提出的自适应控制器进行设计和仿真．结果表明,神经网络以很高的精度跟踪和在线补偿不确定项,改善了线性控制系统的动态性能．     

白腐菌对焦化废水中吲哚的降解及其机理

选用白腐菌BP降解吲哚,研究了白腐菌在不同培养基中对两种浓度吲哚的降解过程和机理,以及吲哚的降解与白腐菌漆酶酶活、生物量、培养基pH值的关系.结果显示不同培养基中白腐菌可去除99%以上的吲哚;吲哚去除率与白腐菌漆酶活率具有较好的相关性,白腐菌漆酶活率达到最高时,可去除97%以上的吲哚;高浓度吲哚会抑制白腐菌的生长,同时也激发了白腐菌漆酶的产生,秸秆滤出液能促进白腐菌的生长和漆酶活力的增长;白腐菌BP最适pH值为6~7,pH值在5~8之间对吲哚都具有较强的降解能力;在HPLC谱图3~6 min之间出现的新物质可能有氧化吲哚和靛红.     

An Agent-based Adaptive Mechanism for Efficient Job Scheduling in Open and Large-scale Environments

Agent-based scheduling refers to applying intelligent agents to autonomously allocate resources to jobs.Decentralized agent-based scheduling approaches have ach...     

过站航班地面保障流程效能评估

为了感知过站航班地面保障流程运行状况和优化机场协同决策信息系统,研究了单航班条件下的保障流程效能评估问题。通过系统分析地面保障流程,得到各场景的效能评估指标。结合评估指标的大小、重要性及聚散状态3个维度,构建了流程效能评估指标体系。设计了一种基于雷达图周长-面积的过站航班地面保障流程动态效能评估方法,并结合实际运行数据开展仿真验证。研究表明,流程效能评估结果整体上直观描述了保障流程效能的动态变化。通过客观性对比和敏感性分析可知,结果一定程度反映了过站航班离港属性,为航班推出控制提供依据。     

基于Unity3D的水下机器人半实物仿真系统

基于Unity3D研制了一种由地面控制终端、机器人本体和三维仿真系统3部分组成的水下机器人半实物仿真系统,为水下机器人开发过程中的性能测试、控制算法分析和人员操作培训提供了仿真和测试平台。该系统采用同一地面控制终端作为三维仿真系统和机器人控制系统的统一指令输入源,以实现虚拟对象和机器人本体的同步工作,可对系统进行实时监测、调参。采用多目视觉技术对机器人位置采集,对传感器数据进行卡尔曼滤波处理。机器人运动仿真试验结果表明,机器人实际运动路径和仿真规划路径基本相同,该系统动态响应性和控制系统同步性较好。     

The start-up of biohydrogen-producing process by bioaugmentation in the EGSB reactor

Expanded granular sludge bed (EGSB) reactor and bioaugmentation were employed to investigate biohydrogen production with molasses wastewater. The start-up experiments consisted of two stages. In the first stage (0～24d) seeded with activated sludge, the butyric acid type-fermentation formed when the initial expanding rate, organic loading rate (OLR), the initial redox potential (ORP) and hydraulic retention time (HRT) were 10%, 10.0 kg COD/(m3·d), - 215 mV and 6.7 h, respectively. At the beginning of the second stage on day 25, the novel hydrogen-producing fermentative bacterial strain B49 (AF481148 in EMBL) were inoculated into the reactor under the condition of OLR 16. 0 kg COD/(m3·d), ORP and HRT about - 139 mV and 6.7 h, respectively, and then the reaction system transformed to ethanol-type fermentation gradually with the increase in OLR. When OLR, ORP and HRT were about 94.3 kg COD/(m3·d), -250 mV and 1.7 h, respectively, the system achieved the maximum hydrogen-producing rate of 282.6 mL H2/L reactor· h and hydrogen percentage of 51%～53% in the biogas.     

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.     

Common variants at 12q14 and 12q24 are associated with hippocampal volume

Aging is associated with reductions in hippocampal volume that are accelerated by Alzheimer's disease and vascular risk factors. Our genome-wide association study (GWAS) of dementia-free persons (n = 9,232) identified 46 SNPs at four loci with P values of <4.0 × 10(-7). In two additional samples (n = 2,318), associations were replicated at 12q14 within MSRB3-WIF1 (discovery and replication; rs17178006; P = 5.3 × 10(-11)) and at 12q24 near HRK-FBXW8 (rs7294919; P = 2.9 × 10(-11)). Remaining associations included one SNP at 2q24 within DPP4 (rs6741949; P = 2.9 × 10(-7)) and nine SNPs at 9p33 within ASTN2 (rs7852872; P = 1.0 × 10(-7)); along with the chromosome 12 associations, these loci were also associated with hippocampal volume (P < 0.05) in a third younger, more heterogeneous sample (n = 7,794). The SNP in ASTN2 also showed suggestive association with decline in cognition in a largely independent sample (n = 1,563). These associations implicate genes related to apoptosis (HRK), development (WIF1), oxidative stress (MSR3B), ubiquitination (FBXW8) and neuronal migration (ASTN2), as well as enzymes targeted by new diabetes medications (DPP4), indicating new genetic influences on hippocampal size and possibly the risk of cognitive decline and dementia.     

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.