离散型二维竞争系统中某群体消亡的条件

研究了离散型二维竞争系统的渐近稳定性,得到了这类竞争系统中各类平衡点的坐标及其性质,获得了系统在边界上的平衡点处渐近稳定的一系列充分条件.这些条件等价于该系统中的某个群体在竞争过程中消亡或被淘汰的相应条件.     

矿井下CAN总线节点地址的设计

针对矿井监控系统网络存在的传输速率较低问题，提出了无主式CAN总线网络结构。为了扩大CAN的网络覆盖面，采用了节点分支的方法，并对节点分支的系统地址和节点分支内地址作了详细的说明。实践证明，该种方法既增大了网络覆盖面积，又能够满足矿井监控系统实时传输的要求。     

基于LabVIEW的温差测量化学虚拟仪器

介绍了基于LabVIEW的温差测量化学虚拟仪器，并通过物质燃烧热测定的实例说明了基于LabVIEW的虚拟仪器用于化学测试不仅可以降低人为误差，提高测量准确度，而且具有操作简便，界面友好、易开发等优点．     

一类非线性演化方程新的多级准确解

利用摄动法对NLS方程和Zakharov方程作展开.应用Jacobi椭圆函数展开法求得了零级近似方程的准确解,并在Lamé方程和Lamé函数的基础上分别求得一级近似方程和二级近似方程的准确解.这样,就求得此类非线性演化方程的多级准确解.     

Structure of a nanobody-stabilized active state of the β(2) adrenoceptor

G protein coupled receptors (GPCRs) exhibit a spectrum of functional behaviours in response to natural and synthetic ligands. Recent crystal structures provide insights into inactive states of several GPCRs. Efforts to obtain an agonist-bound active-state GPCR structure have proven difficult due to the inherent instability of this state in the absence of a G protein. We generated a camelid antibody fragment (nanobody) to the human β(2) adrenergic receptor (β(2)AR) that exhibits G protein-like behaviour, and obtained an agonist-bound, active-state crystal structure of the receptor-nanobody complex. Comparison with the inactive β(2)AR structure reveals subtle changes in the binding pocket; however, these small changes are associated with an 11?? outward movement of the cytoplasmic end of transmembrane segment 6, and rearrangements of transmembrane segments 5 and 7 that are remarkably similar to those observed in opsin, an active form of rhodopsin. This structure provides insights into the process of agonist binding and activation.     

Crystal structure of the β2 adrenergic receptor-Gs protein complex

G protein-coupled receptors (GPCRs) are responsible for the majority of cellular responses to hormones and neurotransmitters as well as the senses of sight, olfaction and taste. The paradigm of GPCR signalling is the activation of a heterotrimeric GTP binding protein (G protein) by an agonist-occupied receptor. The β(2) adrenergic receptor (β(2)AR) activation of Gs, the stimulatory G protein for adenylyl cyclase, has long been a model system for GPCR signalling. Here we present the crystal structure of the active state ternary complex composed of agonist-occupied monomeric β(2)AR and nucleotide-free Gs heterotrimer. The principal interactions between the β(2)AR and Gs involve the amino- and carboxy-terminal α-helices of Gs, with conformational changes propagating to the nucleotide-binding pocket. The largest conformational changes in the β(2)AR include a 14 ? outward movement at the cytoplasmic end of transmembrane segment 6 (TM6) and an α-helical extension of the cytoplasmic end of TM5. The most surprising observation is a major displacement of the α-helical domain of Gαs relative to the Ras-like GTPase domain. This crystal structure represents the first high-resolution view of transmembrane signalling by a GPCR.     

进化论的故乡

加拉帕戈斯群岛位于东太平洋,距离南美大陆约1000千米。群岛由大大小小19座岛屿和无数的岸礁组成,这些岛屿都是远古时代由海底火山喷发出的岩浆堆积而成的火山岛。几百万年以来,许多动植物被洋流和季风由美洲、加勒比海和南极送往这座群岛,与世隔绝地在不同的岛屿上各自进化。19世纪30年代,达尔文曾上岛研究这些独特的动植物,这对他后来提出进化论起到了重大影响。因此,加拉帕戈斯群岛被誉为“进化论的故乡”。进化论的故乡~~     

Trak1 mutation disrupts GABA(A) receptor homeostasis in hypertonic mice

Hypertonia, which results from motor pathway defects in the central nervous system (CNS), is observed in numerous neurological conditions, including cerebral palsy, stroke, spinal cord injury, stiff-person syndrome, spastic paraplegia, dystonia and Parkinson disease. Mice with mutation in the hypertonic (hyrt) gene exhibit severe hypertonia as their primary symptom. Here we show that hyrt mutant mice have much lower levels of gamma-aminobutyric acid type A (GABA(A)) receptors in their CNS, particularly the lower motor neurons, than do wild-type mice, indicating that the hypertonicity of the mutants is likely to be caused by deficits in GABA-mediated motor neuron inhibition. We cloned the responsible gene, trafficking protein, kinesin binding 1 (Trak1), and showed that its protein product interacts with GABA(A) receptors. Our data implicate Trak1 as a crucial regulator of GABA(A) receptor homeostasis and underscore the importance of hyrt mice as a model for studying the molecular etiology of hypertonia associated with human neurological diseases.