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...     

Engineering of multiferroic BiFeO3 grain boundaries with head-to-head polarization configurations

Confined low dimensional charges with high density such as two-dimensional electron gas (2DEG) at interfaces and charged domain walls in ferroelectrics show gre...     

扰动累积下基于数字孪生的车间重调度

针对隐性扰动累积下车间重调度问题,搭建车间重调度决策服务,实现数字孪生驱动的扰动累积下的车间重调度。提出一种调度参数更新的方式,采用随机概率分布来描述调度参数的分布,提升调度参数的准确性;利用孪生网络搭建隐性扰动检测模型,以实时数据为输入,实现重调度的启动时刻的判定;从历史调度数据中提取用于调度知识挖掘的样本数据,利用伪孪生网络获取工序和机器的状态数据的映射关系作为调度规则,用于车间的重调度。仿真实验证明了所提数字孪生驱动的重调度模式的可行性。     

云仿真系统可信度评估问题探讨

云仿真平台支持“云仿真”模式,能够自动查找仿真资源、动态构建云仿真系统。由于云仿真平台具有按需构建仿真服务、多粒度资源共享等特点,云仿真系统的可信度评估工作在仿真资源的可信度、仿真子系统的可信度、仿真运行环境的可靠性等方面面临新的问题。从云仿真系统全生命周期角度,建立了云仿真系统的可信度评估过程模型和云仿真系统可信度评估指标体系,并给出了一种仿真资源排序评估方法,为云仿真系统可信度评估工作提供参考。     

基于X语言的起飞场景民机协同设计与仿真一体化方法

针对大型复杂产品,传统基于模型的系统工程(model-based system engineering, MBSE)方法存在系统设计和仿真验证的多语言、多平台集成实现,难以保证高效、准确地反馈系统设计的缺陷,无法达到快速优化设计目的等问题,提出采用基于面向复杂系统支持MBSE的新一代一体化建模仿真语言—X语言实现面向起飞场景的民机跨域子系统的一体化建模仿真。从民机起飞过程需求分析出发,建立了起飞场景的系统级模型和物理级模型,并在X语言的建模仿真软件—XLab进行统一的建模仿真验证,给出了基于X语言面向复杂产品协同设计与仿真一体化方法,为不同领域的设计人员实现复杂产品设计的协同与优化提供了全新的理论与方法参考。     

基于协作式深度强化学习的火灾应急疏散仿真研究

火灾是威胁公共安全的主要灾害之一,火灾产生的高温和有毒有害烟气严重影响了疏散路径的选择。将深度强化学习引入到应急疏散仿真研究,针对多智能体环境提出了协作式双深度Q网络算法。建立随时间动态变化的火灾场景模型,为人员疏散提供实时的危险区域分布信息;对各自独立的智能体神经网络进行整合,建立多智能体统一的深度神经网络,实现所有智能体之间的神经网络和经验共享,提高整体协作疏散效率。结果表明：所提方法具有良好的稳定性和适应性,训练和学习效率得到提升,具有良好的应用价值。     

信号交叉口人机混驾交通流速度控制策略建模

为分析人机混驾交通流下网联自动驾驶车辆（connected and autonomous vehicles,CAV）速度控制策略对交通流运行特征的影响,构建了考虑驾驶员对行车信息获取不确定性的人工驾驶车辆交叉口通行决策模型。提出考虑前车速度影响的自动驾驶速度控制策略,构建信号交叉口连续型元胞自动机更新规则,通过引入不同CAV渗透率、道路饱和度、控制区长度参数,研究CAV速度控制策略对信号交叉口交通流运行特征的影响。结果表明：CAV能显著提高交叉口通行能力,且车流通过交叉口区域的延误显著降低;同时速度控制策略的实施效果还受控制区长度的影响,呈现出随着控制区长度的增加,车均延误逐渐降低并趋于稳定。     

Act in contravention: a non-planar coupled electrode design utilizing "tip effect" for ultra-high areal capacity,long cycle life zinc-based batteries

Aqueous zinc-based batteries (ZBBs) have great potential as commercial energy storage devices.However,the poor cycling stability of zinc anode under high areal ...     

Blockage of the NLRP3 inflammasome by MCC950 improves anti-tumor immune responses in head and neck squamous cell carcinoma

The NLRP3 inflammasome is a critical innate immune pathway responsible for producing active interleukin (IL)-1β, which is associated with tumor development and immunity. However, the mechanisms regulating the inflammatory microenvironment, tumorigenesis and tumor immunity are unclear. Herein, we show that the NLRP3 inflammasome was over-expressed in human HNSCC tissues and that the IL-1β concentration was increased in the peripheral blood of HNSCC patients. Additionally, elevated NLRP3 inflammasome levels were detected in tumor tissues of Tgfbr1/Pten 2cKO HNSCC mice, and elevated IL-1β levels were detected in the peripheral blood serum, spleen, draining lymph nodes and tumor tissues. Blocking NLRP3 inflammasome activation using MCC950 remarkably reduced IL-1β production in an HNSCC mouse model and reduced the numbers of myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs) and tumor-associated macrophages (TAMs). Moreover, inhibiting NLRP3 inflammasome activation increased the numbers of CD4⁺ and CD8⁺ T cells in HNSCC mice. Notably, the numbers of exhausted PD-1⁺ and Tim3⁺ T cells were significantly reduced. A human HNSCC tissue microarray showed that NLRP3 inflammasome expression was correlated with the expression of CD8 and CD4, the Treg marker Foxp3, the MDSC markers CD11b and CD33, and the TAM markers CD68 and CD163, PD-1 and Tim3. Overall, our results demonstrate that the NLRP3 inflammasome/IL-1β pathway promotes tumorigenesis in HNSCC and inactivation of this pathway delays tumor growth, accompanied by decreased immunosuppressive cell accumulation and an increased number of effector T cells. Thus, inhibition of the tumor microenvironment through the NLRP3 inflammasome/IL-1β pathway may provide a novel approach for HNSCC therapy.     

Cystic fibrosis transmembrane conductance regulator—emerging regulator of cancer

Mutations of cystic fibrosis transmembrane conductance regulator (CFTR) cause cystic fibrosis, the most common life-limiting recessive genetic disease among Caucasians. CFTR mutations have also been linked to increased risk of various cancers but remained controversial for a long time. Recent studies have begun to reveal that CFTR is not merely an ion channel but also an important regulator of cancer development and progression with multiple signaling pathways identified. In this review, we will first present clinical findings showing the correlation of genetic mutations or aberrant expression of CFTR with cancer incidence in multiple cancers. We will then focus on the roles of CFTR in fundamental cellular processes including transformation, survival, proliferation, migration, invasion and epithelial–mesenchymal transition in cancer cells, highlighting the signaling pathways involved. Finally, the association of CFTR expression levels with patient prognosis, and the potential of CFTR as a cancer prognosis indicator in human malignancies will be discussed.