Cox比例风险模型的桥估计

在经济领域和生物科学领域的研究中,经常会遇到包括有变量指标多、样本量大的数据集.一般来说,在一个复杂模型中如果包括有很多微不足道的变量,统计结果往往很难解释.因此,为了减少这种误差,在没有先验的专业知识情况下,研究变量的选择方法非常重要.Cox比例风险模型是生存分析中重要的模型之一.本文将桥估计的变量选择方法应用于Cox比例风险模型中,该方法使用的惩罚函数是p∑j=1｜βj｜γ.用桥估计方法估计未知参数和变量选择,在一定条件下,讨论了基于惩罚部分似然的桥估计方法在Cox比例风险模型中的Oracle性质,即：相合性和渐近正态性.     

表达FLP重组酶pCEP4-FLP载体的构建及其在FLP/FRT重组系统中的应用

构建重组载体pCEP4-FLP和pEF1a-FRT-stop-FRT-GFP,重组载体pEF1a-FRT-stop-FRT-GFP瞬时转染PK-15细胞24h后,再将重组载体pCEP4-FLP瞬时转染该细胞,利用荧光显微镜观察PK-15细胞GFP蛋白的表达情况,利用细胞流式技术统计绿色荧光蛋白表达效率.结果表明:重组载体pCEP4-FLP在细胞内能够表达FLP重组酶,并且表达的FLP重组酶能够识别FRT位点,删除两同向FRT位点间的DNA片段,为FLP/FRT位点特异性重组系统在转基因猪的应用奠定了基础.     

尼古丁对人脐带间充质干细胞氧化应激的影响

目的:研究尼古丁对人脐带间充质干细胞(HUCMSCs)超微结构及氧化应激的影响,探讨尼古丁诱导HUCMSCs凋亡的作用机制.方法:不同浓度尼古丁作用HUCMSCs后,透射电镜(TEM)观察HUCMSCs超微结构变化.分光光度计法检测HUCMSCs胞内过氧化氢酶(CAT)活性,黄嘌呤氧化酶法检测超氧化物歧化酶(SOD)活性,化学比色法检测还原型谷胱甘肽(GSH)活性,硫代巴比妥酸法检测丙二醛(MDA)含量.分光光度计法检测一氧化氮合酶(NOS)、诱生型一氧化氮合酶(iNOS)活性.结果:尼古丁作用HUCMSCs后,细胞内出现大量空泡状结构,粗面内质网扩张成池,线粒体嵴扩张.细胞内CAT、SOD、GSH活性均显著降低,脂质过氧化产物MDA含量显著增加,呈浓度依赖性.NOS、iNOS活性随尼古丁浓度上升而逐渐增加.结论:尼古丁可增加HUCMSCs的NOS、iNOS活性,使细胞发生凋亡结构改变,呈氧化应激状态,发生氧化-抗氧化系统失衡.     

聚氨酯复合乳液制备研究进展

聚氨酯乳液具有环境友好和节能减排的特点,但是其耐水、耐溶剂以及机械性能等不足,限制了它的应用价值。为了充分发挥其优点,与其它材料复合是提高其性能的重要手段。总结了近年来国内外关于环氧树脂、丙烯酸酯、聚硅氧烷、含氟聚合物、SiO2、聚倍半硅氧烷、粘土、碳纳米管、石墨和生物纳米材料改性聚氨酯复合乳液的制备方法并比较了性能之间的差异。     

近20年来黄河三角洲土地利用与覆被动态变化——以东营市为例

以黄河三角洲东营市为例,对东营市1989年、1999年、2009年三期遥感影像用ERDAS和ARCGIS软件进行融合、镶嵌、裁剪和解译,分析1989—2009的东营市土地利用／覆被变化．结果表明黄河三角洲东营市近二十年来建筑用地、水域、盐田、养殖水面、耕地面积呈总体增加趋势,而草地、未利用地、滩涂和林地呈现总体减少的趋势,其中盐田的增加速度最快,建设用地面积增加最大．1999—2009与1989—1999相比综合土地利用动态度和土地利用综合程度都提高了,土地利用更加集约化．     

空地机器人协作导航方法与实验研究

飞行机器人和地面移动机器人所具有的功能互补性使得通过二者间的协作执行使命具有明显的优越性,这对于提高移动机器人使命完成度具有重要的作用.因此,空地机器人协作近年越来越受到研究人员的重视.空地机器人协作的一个重要工作模式是通过飞行机器人的大范围环境感知能力为地面机器人提供导航信息.针对该问题,首先讨论了利用机载视觉传感信息实现地面环境建模(主要是地面障碍物)及地面机器人识别方法;然后,利用波门跟踪算法实现了对地面移动机器人的运动跟踪;最后,提出了空地机器人协作策略;最后,搭建了室内试验平台,进行了实验验证.     

分布式智能电网中电源失效时的电能优化分配

构建一种分布式智能电网的总体框架模型,给出分布式发电规划与优化控制总体模式;针对分布式智能电网中的电源故障问题采用一种改进微粒群算法进行优化潮流计算,获取系统正常工作发电设备的优化功率分配方案,并基于IEEE 14-bus系统进行了仿真,验证了所提方法的有效性.     

单桩式海上风力机支撑结构强度振动分析

以某型2MW海上风力机支撑结构为母型,运用有限元软件ANSYS建立了三维实体模型,并进行了模态、涡激振动及瞬态动力学等强度与振动特性分析.结果表明,非线性弹簧单元适用于模拟土壤对基础的约束,三维实体单元有限元模型在固有频率和应力分布计算上均比梁单元模型更为准确.在所提供的风况和海洋条件之下,海流涡激振动不会与支撑结构产生共振,支撑结构的应力水平主要受风载的影响,该结果可为海上风力机支撑结构强度与振动分析提供参考.针对不同环境,仅需调整载荷,所建模型宜可适用.     

Structural basis of ultraviolet-B perception by UVR8

The Arabidopsis thaliana protein UVR8 is a photoreceptor for ultraviolet-B. Upon ultraviolet-B irradiation, UVR8 undergoes an immediate switch from homodimer to monomer, which triggers a signalling pathway for ultraviolet protection. The mechanism by which UVR8 senses ultraviolet-B remains largely unknown. Here we report the crystal structure of UVR8 at 1.8?? resolution, revealing a symmetric homodimer of seven-bladed β-propeller that is devoid of any external cofactor as the chromophore. Arginine residues that stabilize the homodimeric interface, principally Arg?286 and Arg?338, make elaborate intramolecular cation-π interactions with surrounding tryptophan amino acids. Two of these tryptophans, Trp?285 and Trp?233, collectively serve as the ultraviolet-B chromophore. Our structural and biochemical analyses identify the molecular mechanism for UVR8-mediated ultraviolet-B perception, in which ultraviolet-B radiation results in destabilization of the intramolecular cation-π interactions, causing disruption of the critical intermolecular hydrogen bonds mediated by Arg?286 and Arg?338 and subsequent dissociation of the UVR8 homodimer.     

Deciphering a neuronal circuit that mediates appetite

Hypothalamic neurons that co-express agouti-related protein (AgRP), neuropeptide?Y and γ-aminobutyric acid (GABA) are known to promote feeding and weight gain by integration of various nutritional, hormonal, and neuronal signals. Ablation of these neurons in mice leads to cessation of feeding that is accompanied by activation of Fos in most regions where they project. Previous experiments have indicated that the ensuing starvation is due to aberrant activation of the parabrachial nucleus (PBN) and it could be prevented by facilitating GABA(A) receptor signalling in the PBN within a critical adaptation period. We speculated that loss of GABA signalling from AgRP-expressing neurons (AgRP neurons) within the PBN results in unopposed excitation of the PBN, which in turn inhibits feeding. However, the source of the excitatory inputs to the PBN was unknown. Here we show that glutamatergic neurons in the nucleus tractus solitarius (NTS) and caudal serotonergic neurons control the excitability of PBN neurons and inhibit feeding. Blockade of serotonin (5-HT(3)) receptor signalling in the NTS by either the chronic administration of ondansetron or the genetic inactivation of Tph2 in caudal serotonergic neurons that project to the NTS protects against starvation when AgRP neurons are ablated. Likewise, genetic inactivation of glutamatergic signalling by the NTS onto N-methyl D-aspartate-type glutamate receptors in the PBN prevents starvation. We also show that suppressing glutamatergic output of the PBN reinstates normal appetite after AgRP neuron ablation, whereas it promotes weight gain without AgRP neuron ablation. Thus we identify the PBN as a hub that integrates signals from several brain regions to bidirectionally modulate feeding and body weight.