Robust fault detection and diagnosis for uncertain nonlinear systems

This paper considers robust fault detection and diagnosis for input uncertain nonlinear systems. It proposes a multi-objective fault detection criterion so that the fault residual is sensitive to the fault but insensitive to the uncertainty as much as possible. Then the paper solves the proposed criterion by maximizing the smallest singular value of the transformation from faults to fault detection residuals while minimizing the largest singular value of the transformation from input uncertainty to the fault detection residuals. This method is applied to an aircraft which has a fault in the left elevator or rudder. The simulation results show the proposed method can detect the control surface failures rapidly and efficiently.     

Structure and function of human perforin

Perforin (P1) is a cytolytic protein with similarity to complement component C9. P1 has been described as a unique component of murine cytolytic T-cell and rat natural killer cell granules Previous studies indicated that human granules and P1 differed from murine granules and P1 in that they appeared to be cytolytically less active and lacked the haemolytic activity characteristic of P1. It has been suggested that P1, like C9, is under the control of the homologous restriction factor. Here we determine the primary structure of human P1, re-examine its functional properties, and address the question of homologous restriction.     

最优同伦渐近法在带滑移的6常数Oldroyd流体模型中的应用

应用最优同伦渐近法（OHAM）研究了6常数Oldroydl流体的平面Couette流、平面Poiseuille流和平面Couette Poiseuille流这三个非线性问题.介绍了6常数Oldroyd流体的平面Couette流、平面Poiseuille流和平面Couette Poiseuille流的控制方程和边界条件,应用最优同伦渐近法对上述问题进行求解,并给出模拟仿真,根据仿真结果讨论了滑移参数对速度分布的影响.      

Unusual selection on the KIR3DL1/S1 natural killer cell receptor in Africans

Interactions of killer cell immunoglobulin-like receptors (KIRs) with major histocompatibility complex (MHC) class I ligands diversify natural killer cell responses to infection. By analyzing sequence variation in diverse human populations, we show that the KIR3DL1/S1 locus encodes two lineages of polymorphic inhibitory KIR3DL1 allotypes that recognize Bw4 epitopes of protein">HLA-A and HLA-B and one lineage of conserved activating KIR3DS1 allotypes, also implicated in Bw4 recognition. Balancing selection has maintained these three lineages for over 3 million years. Variation was selected at D1 and D2 domain residues that contact HLA class I and at two sites on D0, the domain that enhances the binding of KIR3D to HLA class I. HLA-B variants that gained Bw4 through interallelic microconversion are also products of selection. A worldwide comparison uncovers unusual KIR3DL1/S1 evolution in modern sub-Saharan Africans. Balancing selection is weak and confined to D0, KIR3DS1 is rare and KIR3DL1 allotypes with similar binding sites predominate. Natural killer cells express the dominant KIR3DL1 at a high frequency and with high surface density, providing strong responses to cells perturbed in Bw4 expression.