一种改进的PSO-MBCV算法的车底阴影分割

针对当前车底阴影分割算法在复杂环境下鲁棒性较差以及最大类间方差（maximum between class variance,　MBCV）多阈值分割算法不能自动确定阈值个数的问题,提出利用峰值自适应方法自动确定MBCV多阈值分割算法中阈值个数;然后,以阈值的个数为粒子群优化算法（particle swarm optimization,　PSO）中粒子的维数,提出了一种改进的PSO MBCV算法的车底阴影分割。实验结果表明,该算法能有较低的误分类误差,能有效地分割出车底阴影。     

浅谈项目管理中施工组织设计重要性

施工组织是项目建设和指导工程施工的重要技术经济文件.能调节施工中人员、机器、原料、环境、工艺、设备、土建、安装、管理、生产等矛盾,要对施工组织设计进行监督和控制,才能科学合理的保证工程项目高质量、低成本、少耗能的完成.     

企业集成创新系统自组织演化机理浅析

面对技术与市场均不确定条件下的竞争环境,集成创新模式被提出.企业集成创新已成为企业重要的创新方式,通过运用自组织理论分析了企业集成创新系统的演化动因和过程.     

Methods, Models and Information Technologies for Decision Support Systems

Special Issue

Methods, Models and Information Technologies for Decision Support Systems     

5种外汇储备资产币种的投资组合

选取对我国外汇储备资产影响较大的美元、欧元、日元、港元、英镑等5个币种为研究对象,对2006-08-01--2010-04-08的汇率数据进行分析,从投资组合理论的角度出发,用预测值取代算术平均值来衡量各币种的汇率收益率,得出各币种的投资组合.     

基于群偏好与用户偏好协同演化的群推荐方法

群推荐系统已经成为社交网络平台的重要工具,为群体用户提供兼顾个性化和整体满意度的产品和服务.现有群推荐方法大多是对个性化推荐方法的集成和聚合,忽略了群体和用户的交互影响以及群偏好和成员偏好的动态变化,从而无法保障群推荐系统的效果.为此,本文提出一种基于群偏好和用户偏好协同演化的群推荐方法,能够建模群体和用户的动态交互.具体而言,本文将用户偏好建模成其历史偏好和群影响的加权聚合结果,将群偏好建模成群历史偏好和新加入成员偏好的加权聚合结果,最终预测群体可能消费的产品列表和成员可能加入的群体列表.实验结果表明,本文所提模型在群体消费行为和用户加群行为的预测表现都优于基准算法,并兼具很好的鲁棒性.     

考虑竞争企业定向能力的定向优惠券投放策略

针对竞争环境下企业优惠券投放问题,本文引入大众优惠券和定向优惠券,综合考虑消费者忠诚度和定向能力策略,构建优惠券影响下的企业利润模型,进而分析企业优惠券投放策略.结果表明:(1)当企业实施定向优惠券策略时,企业在优势市场投放强度要高于竞争市场;(2)当企业综合考虑价格歧视和定向优惠券策略时,通过在不同细分市场给予消费者...     

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...     

Forecasting stock volatility in the presence of extreme shocks: Short-term and long-term effects

This paper introduces a novel generalized autoregressive conditional heteroskedasticity–mixed data sampling–extreme shocks (GARCH-MIDAS-ES) model for stock volatility to examine whether the importance of extreme shocks changes in different time ranges. Based on different combinations of the short- and long-term effects caused by extreme events, we extend the standard GARCH-MIDAS model to characterize the different responses of the stock market for short- and long-term horizons, separately or in combination. The unique timespan of nearly 100 years of the Dow Jones Industrial Average (DJIA) daily returns allows us to understand the stock market volatility under extreme shocks from a historical perspective. The in-sample empirical results clearly show that the DJIA stock volatility is best fitted to the GARCH-MIDAS-SLES model by including the short- and long-term impacts of extreme shocks for all forecasting horizons. The out-of-sample results and robustness tests emphasize the significance of decomposing the effect of extreme shocks into short- and long-term effects to improve the accuracy of the DJIA volatility forecasts.     

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.