浅谈建筑工程招投标现状

文章主要对目前建筑工程招投标现状进行分析,即对当前招标投标工作中存在的问题进行分析,对改进和完善现行建设工程招投标工作进行剖析,深刻说明了建筑工程招标现状,同时也提出了解决这一问题的方法.     

Optimal design and experiment research of an orthogonal-parallel six-axis force/torque sensor

A novel orthogonal-parallel six-axis force/torque sensor is studied based on a modified Stewart platform architecture,and the optimal design and experiment rese...     

基于区间直觉模糊数ANP的体系贡献率计算方法

体系贡献率主要用于体系建设中度量装备对体系的贡献程度。为解决目前体系贡献率计算存在的一些问题,提出一种“任务–能力–指标–装备”的多层次装备指标体系结构。考虑了装备指标体系结构、网络分析法和区间直觉模糊数的特点,提出了一种基于区间直觉模糊数的网络分析法以得到更准确的体系贡献率。实验表明,该方法不仅能够解决体系贡献率计算公式现存的问题,而且与AHP(analytic hierarchy process)和ANP(analytic network process)相比,可以得到更准确的体系贡献率,为体系建设提供更有效的支持。     

基于仿真驱动的高速公路主动限速效用评价与推荐

传统的路侧被动限速方式对于特定的惩处区域以外缺少管控,间接导致车辆行为在时空上的不一致性甚至突变,影响了交通的通行效率与安全性。从车侧主动限速方式入手,提出主动限速效用评价与推荐方法,结合道路线形、交通流量、车型比例,开展多情景主动、被动限速交通仿真,利用安全间接分析模型及交通流运行状态,从安全与效率2个层面提取效用评价指标及其权重,采用集成学习方法进行预测分析。结果显示：主动限速方式相较于被动限速方式更有利于提高安全性和调节效率,而在主动限速方面,GBDT(gradient boosting decision tree)回归模型的预测稳定性和准确率更高(R²=0.984)。     

基于烟花算法的基站群协作计算卸载模型研究

车联网、AR、AI等计算密集、时延敏感型应用迅速发展,而移动设备因自身计算能力相对不足,执行此类应用任务时会因高时延而严重影响用户体验甚至无法满足用户需求。针对此问题,提出综合考虑时延与成本的多用户、多MEC (mobile edge computing)服务器的基站群协作计算卸载模型。并提出基于凸优化的改进烟花算法（improved fireworks algorithm based on convex optimization, CVX-FWA）来对模型进行求解,对用户任务进行合理的卸载与资源分配。仿真结果表明,提出的计算卸载方案有效降低了任务总时延成本值,实现计算卸载资源的整体优化配置。     

基于HMM的多维数据下扶贫对象状态预测

针对扶贫领域中贫困、脱贫和返贫状态预测不准确,影响状态变迁的关键因素难以识别的问题,从扶贫基础数据和多个行业数据中提取8个关键特征和22个观测状态,构建观察状态和隐含状态关联关系,建立扶贫对象状态预测隐马尔可夫模型(hidden markov model,HMM)。以某深度贫困县连续3年的数据为样本,进行参数训练、测试实验和结果验证,结果表明该方法对返贫、贫困和脱贫状态有较强的预测能力,误差率较低,且能准确识别出影响返贫的关键要素。该方法对指导精准扶贫工作具有非常重要的实际意义。     

MicroRNA Mirn140 modulates Pdgf signaling during palatogenesis

Disruption of signaling pathways such as those mediated by sonic hedgehog (Shh) or platelet-derived growth factor (Pdgf) causes craniofacial abnormalities, including cleft palate. The role that microRNAs play in modulating palatogenesis, however, is completely unknown. We show that, in zebrafish, the microRNA Mirn140 negatively regulates Pdgf signaling during palatal development, and we provide a mechanism for how disruption of Pdgf signaling causes palatal clefting. The pdgf receptor alpha (pdgfra) 3' UTR contained a Mirn140 binding site functioning in the negative regulation of Pdgfra protein levels in vivo. pdgfra mutants and Mirn140-injected embryos shared a range of facial defects, including clefting of the crest-derived cartilages that develop in the roof of the larval mouth. Concomitantly, the oral ectoderm beneath where these cartilages develop lost pitx2 and shha expression. Mirn140 modulated Pdgf-mediated attraction of cranial neural crest cells to the oral ectoderm, where crest-derived signals were necessary for oral ectodermal gene expression. Mirn140 loss of function elevated Pdgfra protein levels, altered palatal shape and caused neural crest cells to accumulate around the optic stalk, a source of the ligand Pdgfaa. These results suggest that the conserved regulatory interactions of mirn140 and pdgfra define an ancient mechanism of palatogenesis, and they provide candidate genes for cleft palate.     

The emerging link between O-GlcNAcylation and neurological disorders

O-linked β-N-acetylglucosaminylation (O-GlcNAcylation) is involved in the regulation of many cellular cascades and neurological diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and stroke. In the brain, the expression of O-GlcNAcylation is notably heightened, as is that of O-linked N-acetylglucosaminyltransferase (OGT) and β-N-acetylglucosaminidase (OGA), the presence of which is prominent in many regions of neurological importance. Most importantly, O-GlcNAcylation is believed to contribute to the normal functioning of neurons; conversely, its dysregulation participates in the pathogenesis of neurological disorders. In neurodegenerative diseases, O-GlcNAcylation of the brain’s key proteins, such as tau and amyloid-β, interacts with their phosphorylation, thereby triggering the formation of neurofibrillary tangles and amyloid plaques. An increase of O-GlcNAcylation by pharmacological intervention prevents neuronal loss. Additionally, O-GlcNAcylation is stress sensitive, and its elevation is cytoprotective. Increased O-GlcNAcylation ameliorated brain damage in victims of both trauma-hemorrhage and stroke. In this review, we summarize the current understanding of O-GlcNAcylation’s physiological and pathological roles in the nervous system and provide a foundation for development of a therapeutic strategy for neurological disorders.     

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.