可自修复的高延性混凝土(ECC)在机场道面的适用性分析

在飞机荷载与环境荷载长期共同作用下,机场道面易出现裂缝、接缝和竖向位移类病害,使运营阶段维修成本高.提出将具有自修复功能的高延性水泥基材料(ECC)用于机场道面,以控制裂缝发展、实现无缝连接;并利用ECC因二次反应而使微裂缝愈合的特性,减少路面维护工作,延长使用寿命.通过试验手段研究了ECC材料应用于机场道面的力学行为、自修复行为和早期开裂潜能.试验结果表明:机场道面用ECC材料在拉伸荷载作用下,其拉伸应变可达3.67％(约为普遍混凝土的400倍);在弯曲荷载作用下,其竖向弯曲变形可达6.33 mm;抗压强度与弯曲强度分别为43.9 MPa和12.68 MPa,可满足机场道面的使用要求.在受约束条件下,ECC表现出较低的早期开裂潜能.由于自修复能力,裂损ECC的拉伸刚度、拉伸应变与拉伸强度几乎可恢复至未裂时的程度;其水渗透系数随自修复进程逐渐降低,最终达到未裂时的渗透水平.研究结果表明ECC材料用于无缝机场道面具有较高适用性.     

立德·铸魂·育人:新时代持续推进高校课程思政的三维审视

课程思政是当前高校人才培养的迫切任务,要将思想政治教育与其他课程有机结合起来.其基本着眼点是立德,即培养担当民族复兴大任的时代新人;其根本着力点在于铸魂,即用习近平新时代中国特色社会主义思想培育青年学生的价值观、世界观、人生观;其根本落脚点在于育人,即全面以学生为中心,打造高水平、高效率的黄金课堂.     

联程中转旅客的城市枢纽间换乘行为建模

针对旅客联程运输中旅客中转换乘行为,构建了多项Logit(Multinomial Logit,MNL)模型进行刻画分析.首先,设计了陈述偏好(Stated Preference,SP)调查问卷进行数据采集;其次,基于MNL模型对联程中转旅客的城市枢纽间换乘行为进行建模,并利用Biogeme软件对模型参数进行标定;最后,计算出各方式的分担率并与实际调查结果进行对比分析.结果表明:与出行目的、行李大小等因素相比,联程旅客个人特征(年龄、职业、收入等)的影响最为显著,考虑了旅客个人差异的MNL模型拟合误差在1.5％以内;此外,旅客对交通工具拥挤度、舒适度、班次数量以及准时性的关注程度也影响了其选择行为;联运旅客对时间效率尤为关注,超过50％的联运旅客选择地铁,当公交出行时间下调0％～20％时,可以一定程度上将换乘地铁的联运客流转移至公交上.研究结果对于枢纽间换乘需求预测、多方式协同调度以及提供旅客个性化出行服务具有一定的参考作用.     

企业生命周期下投资者关注对权益资本成本的影响

基于行为金融学的价格压力假说，结合企业生命周期理论，以2007—2014年的主板上市公司为样本，分析投资者关注对权益资本成本的影响以及这种影响在企业生命周期中存在的阶段性差异。研究发现，投资者关注与权益资本成本显著负相关，即权益资本成本随着投资者关注的提高而降低。对于不同生命周期的企业，投资者关注对权益资本成本的影响存在差异。新生期、衰退期企业的权益资本成本并不会随着投资者关注程度的提高而降低；成长期、成熟期企业的权益资本成本随着投资者关注程度的提高而降低。可以看出，投资者能够识别企业所处的生命周期，并愿意为成长期、成熟期的企业支付更高的溢价。     

目标边缘特征增强检测算法

针对分组角点检测网络在目标检测过程中,由于目标尺寸过小或同类目标空间距离较小而导致检测失效的问题,提出一种边缘特征增强的CornerNet目标检测算法OEC。该算法通过分离特征的高低频信息提取更多的高频信息,增强目标的边缘轮廓特征,解决关键点定位不准确的问题,提高目标的框定效果,进一步提升检测精度。仿真结果表明,该算法对行人、车辆等目标检测效果均有提高,在COCO数据集上的检测结果与CornerNet相比,mAP提高0.9%,可应用于无人驾驶与智能机器人等场景。     

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.