低成本纳米复合材料70％ CeO2·30％ NiO的合成及其催化性能的研究

分别选用水热,浸渍,柠檬酸络合燃烧,共沉淀方法合成了多种前驱体,再经过600 ℃煅烧处理4h,成功合成出纳米复合材料70％ CeO2·30％ NiO,对这些复合材料进行系统的XRD、BET、H2-TPR、O2-TPD表征和CO催化氧化性能测试.     

316L不锈钢表面纳米化残余应力对材料性能的影响

高速旋转丝表面纳米化是一种新型的表面纳米化方法,本文对316L不锈钢表面进行纳米化处理,测定残余应力在材料内部的分布.通过分析、对比实验数据,表面纳米化处理方法,能够在材料内部引入大量残余压应力,提升材料的力学性能.     

我国化学化工领域毕业生及学位授予情况的调研与分析

本文基于对我国化学化工领域2006-2010年间本科生、硕士研究生和博士研究生培养情况的调研数据,分析了不同学位层次毕业生数量变化趋势、毕业生在各学科门类及培养单位的分布情况,进而讨论了我国化学化工领域学生培养的结构特点及人才队伍趋势.     

Vapor-deposited CsPbI3 solar cells demonstrate an efficiency of 16％

Hybrid organic-inorganic perovskite solar cells (PSCs) have made rapid progress in efficiency from 3.8％ to 25.5％ in the past decade [1-3].The hybrid perovskite ...     

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。     

基于CPN的智能合约交易顺序依赖漏洞的验证

智能合约的形式化验证工作主要集中在编程语言层面的漏洞研究,而交易顺序依赖作为区块链层面的漏洞更不易被检测。基于着色Petri网对智能合约中潜在的交易顺序依赖漏洞进行形式化验证。以Decode悬赏合约为对象,分析合约中潜在的漏洞,自顶向下地对合约本身及其执行环境建立着色Petri网模型,并引入攻击者模型来考虑合约遭受攻击的情况。通过运行模型以验证合约存在交易顺序依赖漏洞,最后基于Remix平台在以太坊网络中证实结论的正确性。     

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.

     

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.