CMS环境下基于智能优化算法的单元间布局问题研究*

研究了单元制造系统(CMS)设计中单元间布局设计问题,从单元制造系统的实际出发,提出了一种基于割树(Slicing-tree)的单元间布局设计模型.该模型考虑了单元形状约束、单元I/O点位置优化等诸因素对布局结果的影响.针对基于割树的描述形式,采用遗传算法求解,提出了一种新的割树编码方案,克服了以往编码方案易产生非法子串、不能覆盖整个解空间以及实现困难等缺点.计算结果表明,该算法是有效的、可行的.     

一种基于全IP蜂窝网络的实时业务传输机制*

针对无线蜂窝网络和Internet的业务特点,分析了在信道带宽有限、传输误码率高的无线网络中传输基于IP的实时业务所面临的问题.针对下一代蜂窝网络中基于IP技术实现多媒体业务要求,从无线网络上实际传送的码流角度,结合ROHC机制提出一种在信道传输速率不变的条件下,提高码流传输效率的方法,并且探究了空中链路的全IP机制.从采样编码后输出的净码流和经过封装后的码流两个角度来分析,提出了高效的针对全IP的蜂窝网络的实时交互式语音业务的新方案.     

Therapeutic Potential for Regulation of the Nuclear Factor Kappa-B Transcription Factor p65 to Prevent Cellular Senescence and Activation of Pro-Inflammatory in Mesenchymal Stem Cells

Mesenchymal stem cells have an important potential in the treatment of age-related diseases. In the last years, small extracellular vesicles derived from these stem cells have been proposed as cell-free therapies. Cellular senescence and proinflammatory activation are involved in the loss of therapeutic capacity and in the phenomenon called inflamm-aging. The regulators of these two biological processes in mesenchymal stem cells are not well-known. In this study, we found that p65 is activated during cellular senescence and inflammatory activation in human umbilical cord-derived mesenchymal stem cell. To demonstrate the central role of p65 in these two processes, we used small-molecular inhibitors of p65, such as JSH-23, MG-132 and curcumin. We found that the inhibition of p65 prevents the cellular senescence phenotype in human umbilical cord-derived mesenchymal stem cells. Besides, p65 inhibition produced the inactivation of proinflammatory molecules as components of a senescence-associated secretory phenotype (SASP) (interleukin-6 and interleukin-8 (IL-6 and IL-8)). Additionally, we found that the inhibition of p65 prevents the transmission of paracrine senescence between mesenchymal stem cells and the proinflammatory message through small extracellular vesicles. Our work highlights the important role of p65 and its inhibition to restore the loss of functionality of small extracellular vesicles from senescent mesenchymal stem cells and their inflamm-aging signature.     

Tau Exon 10 Inclusion by PrPC through Downregulating GSK3β Activity

Tau protein is largely responsible for tauopathies, including Alzheimer’s disease (AD), where it accumulates in the brain as insoluble aggregates. Tau mRNA is regulated by alternative splicing, and inclusion or exclusion of exon 10 gives rise to the 3R and 4R isoforms respectively, whose balance is physiologically regulated. In this sense, one of the several factors that regulate alternative splicing of tau is GSK3β, whose activity is inhibited by the cellular prion protein (PrP^C), which has different physiological functions in neuroprotection and neuronal differentiation. Moreover, a relationship between PrP^C and tau expression levels has been reported during AD evolution. For this reason, in this study we aimed to analyze the role of PrP^C and the implication of GSK3β in the regulation of tau exon 10 alternative splicing. We used AD human samples and mouse models of PrP^C ablation and tau overexpression. In addition, we used primary neuronal cultures to develop functional studies. Our results revealed a paralleled association between PrP^C expression and tau 4R isoforms in all models analyzed. In this sense, reduction or ablation of PrP^C levels induces an increase in tau 3R/4R balance. More relevantly, our data points to GSK3β activity downstream from PrP^C in this phenomenon. Our results indicate that PrP^C plays a role in tau exon 10 inclusion through the inhibitory capacity of GSK3β.     

Cellular Senescence: Pathogenic Mechanisms in Lung Fibrosis

Pulmonary fibrosis is a chronic and fatal lung disease that significantly impacts the aging population globally. To date, anti-fibrotic, immunosuppressive, and other adjunct therapy demonstrate limited efficacies. Advancing our understanding of the pathogenic mechanisms of lung fibrosis will provide a future path for the cure. Cellular senescence has gained substantial interest in recent decades due to the increased incidence of fibroproliferative lung diseases in the older age group. Furthermore, the pathologic state of cellular senescence that includes maladaptive tissue repair, decreased regeneration, and chronic inflammation resembles key features of progressive lung fibrosis. This review describes regulatory pathways of cellular senescence and discusses the current knowledge on the senescence of critical cellular players of lung fibrosis, including epithelial cells (alveolar type 2 cells, basal cells, etc.), fibroblasts, and immune cells, their phenotypic changes, and the cellular and molecular mechanisms by which these cells contribute to the pathogenesis of pulmonary fibrosis. A few challenges in the field include establishing appropriate in vivo experimental models and identifying senescence-targeted signaling molecules and specific therapies to target senescent cells, known collectively as “senolytic” or “senotherapeutic” agents.     

Numerical simulation of microstructure formation ofAZ91 using mCA method

A stochastic model for simulating the microstructure formation of Mg alloy AZ91 during solidification was developed based on the finite element method（FEM） for macroscopic model of heat transfer calculation and a modified Cellular Automaton （mCA） for microscopic modeling of nucleation, growth of crystal. In this model, the effect of solute redistribution, interface curvature and preferred orientation was considered. A numerical simulation was developed with C＋＋ program language. The computation was carded out to understand the effect of varying processing parameters, such as nucleation parameters and heat transfer coefficient, on the microstructure formation of AZ91. The result of simulation was displayed on screen.     

共晶自生复合材料的晶形转变

自生复合材料的晶形转变受到成分过冷与曲面过冷两个因素的控制.非金属相具有较大的熔化熵且易形成小平面是改变领先相的因素,而领先相的改变则可能是晶形转变的根本原因.     

Solving a multi-floor layout design model of a dynamic cellular manufacturing system by an efficient genetic algorithm

This paper presents a mixed-integer programming model for a multi-floor layout design of cellular manufacturing systems (CMSs) in a dynamic environment. A novel aspect of this model is to concurrently determine the cell formation (CF) and group layout (GL) as the interrelated decisions involved in the design of a CMS in order to achieve an optimal (or near-optimal) design solution for a multi-floor factory in a multi-period planning horizon. Other design aspects are to design a multi-floor layout to form cells in different floors, a multi-rows layout of equal area facilities in each cell, flexible reconfigurations of cells during successive periods, distance-based material handling cost, and machine depot keeping idle machines. This model incorporates with an extensive coverage of important manufacturing features used in the design of CMSs. The objective is to minimize the total costs of intra-cell, inter-cell, and inter-floor material handling, purchasing machines, machine processing, machine overhead, and machine relocation. Two numerical examples are solved by the CPLEX software to verify the performance of the presented model and illustrate the model features. Since this model belongs to NP-hard class, an efficient genetic algorithm (GA) with a matrix-based chromosome structure is proposed to derive near-optimal solutions. To verify its computational efficiency in comparison to the CPLEX software, several test problems with different sizes and settings are implemented. The efficiency of the proposed GA in terms of the objective function value and computational time is proved by the obtained results.     

高铁车厢内部紧急情况下人员疏散仿真研究

在引入元胞自动机理论的基础上,模拟分析了紧急情况下人员生理及心理的不同对疏散过程的影响,通过人员动态调整自身行为,并引入人员竞争力,对人员疏散过程建立模型。在疏散过程中,根据存在着一定程度的外部干扰因素,提出疏散干扰度概念。计算机仿真的结果表明,考虑人员竞争力,以及出口疏散干扰的问题,可以更加真实地模拟人员紧急疏散过程和疏散状况。     

自动协议逆向工程研究综述

全面梳理了该领域国内外相关文献,归纳分析了自动协议逆向工程的研究现状和发展趋势。为了更清晰地刻画不同方法的特点和比较异同,提出一种基于协议逆向工程输出结果的分类方法,将协议逆向方法分为侧重于协议格式提取、侧重于协议状态机推断、侧重于完整协议规范描述、侧重于其他输出结果四类,并据此进行分析和比较。基于目前的进展情况和进一步的问题剖析发现,复杂交互场景分析、链路层协议逆向、加密协议分析以及协议状态机优化等应作为自动协议逆向工程领域下一步的重点研究方向。