Numerical investigation on heat transfer characterization of liquid lithium metal in pipe

Liquid Li metal is a promising nuclear reactor coolant; however, relevant research regarding its heat transfer characteristics remains insufficient. In this study, a steady-state two-dimensional mathematical model is established to describe the heat transfer process of liquid Li in a straight pipe. A numerical analysis is conducted to investigate the effects of inlet velocity, inlet temperature, and wall heat flux on heat transfer in liquid Li. The results indicate the advantage of using liquid Li for improving heat transfer at high inlet temperatures (> 1000 K) compared with using liquid sodium and lead–bismuth eutectic. Considering the mechanism of the outlet radial heat flow model, the ratio of turbulent to molecular diffusion coefficients presents a parabolic distribution along the radius of the pipe. Increasing the inlet velocity, decreasing the inlet temperature, and decreasing the wall heat flux can effectively weaken the dominant role of molecular heat transfer owing to the low Prandtl number of liquid Li. The heat transfer of liquid Li is investigated comprehensively in this study, and the results provide a basis for the practical application of liquid Li as a promising coolant.     

基于作战环的不同节点攻击策略下的作战网络效能评估

基于作战环思想, 以作战网络抽象模型为基础, 围绕作战环的分类、定义、形式化描述、数学模型等基本问题开展了理论研究, 进一步丰富了作战环理论体系。同时, 以能否快速有效打击对方目标实体为根本依据, 建立了基于目标节点打击率和基于目标节点打击效率的作战网络效能评估指标。通过仿真实验, 将作战环相关理论运用于不同节点攻击策略下的作战网络效能评估, 为实际作战体系对抗中双方的攻击与防护提供应用指导, 也为进一步开展基于作战环的作战网络应用研究提供参考借鉴。     

基于改进Lagrange乘子法的交通信号配时优化研究

为提高交叉口的机动车通行效率及环境效益,采用改进罚参数来构造一种新的Lagrange乘子法对交叉路口的交通信号进行优化配时。通过权重系数建立车辆延误与尾气排放的数学模型,利用改进Lagrange乘子法进行优化,将其结果与两种典型智能算法的优化结果进行对比,并利用VISSIM(Verkehr in Stadten Simulation)微观交通可视化仿真软件进行验证。实验结果表明,该方法优化的信号配时使车辆延误降低19.89%,尾气排放量降低2.379%,可见大比例优化了交叉口的车辆延误,同时可以降低尾气排放量。     

基于回波预处理和相参积累的C&I干扰抑制算法

C&I(chopping and interleaving)干扰是一种针对线性调频(linear frequency modulation, LFM)雷达的典型干扰样式, 干扰子信号调频斜率与雷达发射信号相同, 利用信号处理工具分离真实回波与干扰信号难度较大。针对该问题, 以LFM相参雷达抗自卫式C&I干扰为背景, 提出基于回波预处理和相参积累的干扰抑制算法。根据估计的回波时延, 设置距离窗截取受干扰回波段, 在此基础上, 通过对回波预处理, 改变不同重复周期内假目标的快时间位置分布, 通过相参积累实现干扰抑制。仿真试验表明, 所提算法能够有效抑制强干扰背景下的C&I干扰, 干扰抑制后真实目标检测概率大幅提高, 虚假目标数量明显减少。     

Improving the photocatalytic activity of graphitic carbon nitride by thermal treatment in a high-pressure hydrogen atmosphere

Extending visible light absorption range and suppressing the recombination of photogenerated charge carriers are always important topics in developing efficient solar-driven photocatalysts. In this study, the thermal treatment process at 400 °C in a high-pressure hydrogen atmosphere was applied to modify graphitic carbon nitride. Compared to the normal atmospheric hydrogen treatment process, this process has the merit of producing nitrogen deficient graphitic carbon nitride in high-yield. The optimal photocatalytic activity of modified graphitic carbon nitride was demonstrated by controlling the treatment duration in the hydrogen atmosphere.The changes in the crystal structure, microstructure and optical properties of carbon nitrides were investigated by several characterizations. The relationship between the photocatalytic activity and structures of graphitic carbon nitride was preliminarily established. The results obtained in this study could provide some new ways of improving the activity of graphitic carbon nitride based photocatalyst.     

A Method to Visualize the Skeleton Industrial Structure with Input-Output Analysis and Its Application in China,Japan and USA

The paper established a double filtering method (DFM) to visualize the skeleton industrial structure (SIS) of one economy and find its evolution rule. Different with the previous researches, this method is from a new view of industrial conjunctions combined by leading sectors to depict the industrial structure. It was proved that the leading sector selected by DFM must be key sector selected by Hirschman-Rasmussen method. Applied DFM to input-output tables of China, Japan and USA and MFA to Japan and USA, the results analysis showed that DFM could overtake the two main shortcomings of minimum flow analysis (MFA), scratch SIS of each economy with its own characteristics, visualize the general evolution rules of the industrial structure with crisscrossed conjunctions among leading sectors.     

Defining G protein-coupled receptor peptide ligand expressomes and signalomes in human and mouse islets

Introduction

Islets synthesise and secrete numerous peptides, some of which are known to be important regulators of islet function and glucose homeostasis. In this study, we quantified mRNAs encoding all peptide ligands of islet G protein-coupled receptors (GPCRs) in isolated human and mouse islets and carried out in vitro islet hormone secretion studies to provide functional confirmation for the species-specific role of peptide YY (PYY) in mouse islets.

Materials and methods

GPCR peptide ligand mRNAs in human and mouse islets were quantified by quantitative real-time PCR relative to the reference genes ACTB, GAPDH, PPIA, TBP and TFRC. The pathways connecting GPCR peptide ligands with their receptors were identified by manual searches in the PubMed, IUPHAR and Ingenuity databases. Distribution of PYY protein in mouse and human islets was determined by immunohistochemistry. Insulin, glucagon and somatostatin secretion from islets was measured by radioimmunoassay.

Results

We have quantified GPCR peptide ligand mRNA expression in human and mouse islets and created specific signalomes mapping the pathways by which islet peptide ligands regulate human and mouse GPCR signalling. We also identified species-specific islet expression of several GPCR ligands. In particular, PYY mRNA levels were ~ 40,000-fold higher in mouse than human islets, suggesting a more important role of locally secreted Pyy in mouse islets. This was confirmed by IHC and functional experiments measuring insulin, glucagon and somatostatin secretion.

Discussion

The detailed human and mouse islet GPCR peptide ligand atlases will allow accurate translation of mouse islet functional studies for the identification of GPCR/peptide signalling pathways relevant for human physiology, which may lead to novel treatment modalities of diabetes and metabolic disease.

     

基于LabVIEW与SQL server设计的浮标电源远程管理系统

针对现有海洋浮标缺乏对电源有效监控管理的问题，提出了一种基于LabVIEW与SQL server编程，结合C8051F021单片机硬件的方法，设计了岸站服务器的终端监控软件和安装于浮标上的硬件电路。通过网络或北斗通讯等实时通讯方式，实现对浮标上电源的实时监控和管理，提高了浮标电源的利用和管理的能力。     

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.