西湖凹陷西部斜坡带花港组、平湖组储层裂缝发育特征及有效裂缝测井识别

以西湖凹陷西斜坡花港组、平湖组致密砂岩储层为研究对象,通过录井资料分析及岩心和显微薄片观察,研究裂缝的宏观与微观发育特征及其影响因素.结果显示其主要发育层理缝和构造缝.层理缝主要为水平缝和低角度缝,且已被充填;构造缝主要为垂直缝和高角度缝,充填缝和未充填缝各占一半.裂缝的发育受岩性、单层厚度、断裂及地应力场的综合影响.在交会图法(定性)和概率判别法(半定量)研究的基础上,将岩心观察统计结果与常规测井曲线和成像测井成果相对比,综合预测与评价裂缝发育段,认为有利的裂缝发育层段为花港组下段和平湖组中下段.     

螺栓连接大变形梁非线性振动特性的实验研究

柔性机械臂、大型可展开天线等机械结构的动作精度受运动过程中大变形几何非线性和连接处接触非线性的影响十分显著。以含螺栓连接结构的大变形梁作为研究对象，针对动力学建模和振动特性开展了实验研究，通过数值计算验证了实验发现的非线性振动特性。搭建了含螺栓连接柔性大变形梁的实验台架，开展了敲击和正弦激振的实验测试。实验结果表明，螺栓连接的柔性梁较连续梁的（无螺栓连接）模态频率降低，阻尼增加，反映出随着激励能量增大，模态频率降低的非线性模态特征。改变螺栓连接位置会显著影响结构的模态频率，其变化规律可由求解线性矩阵特征值定性反映。     

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.     

财政性科技经费监管体系探析

我国初步建立了财政性科技经费监管体系,但是在监督主体、监督制度等方面还存在缺陷,科技经费监督出现诸多问题。建立要加强宏观层面的统筹规划,建立由政府、承担单位和外部主体上下联动、横向联合的立体监督体系。     

仿生非光滑花纹沟对轮胎抗滑水性能的影响

以205/55R16乘用车轮胎为研究对象,采用计算流体动力学建立了考虑胎面花纹变形的轮胎滑水分析模型;以气-液二相流数值模型分析了轮胎的滑水性能,并将临界滑水速度仿真值与NASA滑水速度预测值及轮胎发生滑水时力平衡下的速度进行对比.在此基础上,引入仿生减阻理念,研究了夹角为60°、高度为0.6mm的仿生对称V形结构对花纹沟排水量和水流阻力的影响,并将其结构特征信息等效移植到接地区轮胎花纹沟底,进行了仿生花纹轮胎的滑水性能分析.结果表明:所建滑水分析模型可用来分析轮胎滑水时的流体运动特性;相对原花纹轮胎,仿生非光滑花纹沟轮胎通过提高接地区花纹沟内水流速度,降低了胎面动水压力,提高了临界滑水速度.     

青藏铁路含保温夹层路基厚度与地温关系的研究

通过对青藏铁路风火山段含有保温夹层的路基建立均匀介质分层纯导热模型并运用分层近似解法求出冻土表层的温度函数,结合Lachenbruch给出的冻土层的理论温度表达式,得到了路基填料层、保温层、地表年平均温度与正弦变化温度的振幅比三者之间的隐式方程,并应用该方程对三者之间的关系进行了分析.     

含砂雾封层在桥面铺装工程中的应用

结合含砂雾封层在国道205桥面铺装上的应用,深入分析了含砂雾封层的防水、防老化作用机理,本文系统总结了国道205桥面雾封层施工质量的控制要点,并对施工前后封层各项性能指标进行跟踪检测,分析结果表明采取含砂雾封层措施确实能对桥面早期微裂缝进行有效封水,延缓桥面病害的发生,延长沥青路面的使用寿命。     

利用SRTM数据修测高山区地貌的探讨

在高海拔区域测制地形图,如青藏高原地区,所获取的遥感影像局部存在着大范围的高山阴影或云雪覆盖,造成立体观测地貌困难的现象,探讨应用SRTM数据对这类特殊区域地貌进行修测补绘。介绍了数据处理的作业过程,并对实验区SRTM与SPOT5影像立体测图成果进行实验对比分析,成果符合要求。     

兰州黄河岸边卵石层大吨位桩基自平衡法试验研究

对兰州深安黄河大桥进行桩基自平衡法试验。在对黄河岸边的岩土层进行桩基试验时,对桩基的极限侧阻力和端阻力标准值的取值提出建议,并在兰州地区进行自平衡法桩基试验时,对桩基侧摩阻力的取值提出建议。     

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.