一类具反应扩散项的时滞耦合神经网络的同步

主要讨论一类具有反应扩散项混合时滞耦合神经网络的同步问题.同时,考虑系统参数的范数有界不确定性及其切换依赖某个马尔可夫链等方面对其的影响.文中通过构造新颖的Lyapunov-Krasovskii泛函,运用线性矩阵不等式(LMI)技术并结合Kronecker积来获得耦合神经网络的鲁棒均方全局指数同步的充分性条件,并且所获得的判据依赖于时滞.该条件可由MATLAB的LMI工具箱进行有效的验证.此外,细胞激活函数更为一般的假设,可进一步减少结论的保守性.     

具有leakage时滞与随机干扰的离散神经网络渐近稳定性分析

研究了一类具有leakage时滞与随机干扰的离散型神经网络的全局渐近稳定性问题．利用一种新的时滞分割方法将时滞区间分割为多个区间．通过构造新的Lyapunov泛函得到了基于线性矩阵不等式（LMI）的渐近稳定性判据．该判据在获得更小的保守性同时也降低了计算的复杂度．     

一类带有阈的神经网络模型的全局稳定性

利用分析技巧,获得了一类带有阈的神经网络模型全局稳定性的判据,去掉了文「１」相应结果的一个较强条件∫＾∞０ｓｋ（ｓ）ｄｓ〈＋∞。     

动态神经网络中的同步振荡

目前有一种假设认为同一视觉对象是由一群神经元的同步振荡活动来表征的。这一神经元发放活动的时间特性,是解决视觉信息处理中“结合问题（Ｂｉｎｄｉｎｇｐｒｏｂｌｅｍ）”的可能机制。本文用我们所提出的一种简化现实性神经网络模型［１］所构造的时滞非线性振子网络［２］,模拟生物神经网络的同步振荡活动。并考虑了振子各参数的设置与振荡活动的关系,以及网络振子间耦联对同步活动的影响．     

Hindmarsh-Rose 神经网络的混沌同步

研究了通过特殊构造的非线性函数耦合连接的神经网络的混沌同步问题。在发展基于稳定性准则的混沌同步方法的基础上,给出了计算同步稳定性的误差发展方程,当耦合强度取参考值时,可实现稳定的混沌同步而不需要计算最大条件Lyapunov指数去判定是否稳定。通过对按照完全连接形式构成的Hindmarsh-Rose神经网络的数值模拟,显示可仅从两个耦合神经的耦合强度的稳定性范围预期到许多耦合神经实现同步的稳定性范围。该方法在噪声影响下,对实现神经元的混沌同步仍具有较强的鲁棒性。此外发现随着耦合神经数的增加,满足同步稳定性的耦合强度减小,与耦合神经的数量成反比。     

功能柱结构神经网络模型中的同步振荡现象

功能柱作为大脑皮层一个普遍存在的基本结构, 有着重要的功能意义. 基于皮层功能柱的生理特点, 构建一个模块式的神经网络模型. 当施以恒定密度的脉冲刺激时, 单个功能柱能产生同步振荡. 根据外界输入和网络结构参数的不同, 振荡频率在3~43 Hz之间变化. 由多个功能柱构成的网络之间能在各振荡子之间出现复杂的同步现象, 网络中可以出现部分同步的亚集群.     

带时间延迟的Cohen-Grossberg神经网络全局鲁棒稳定性的一个结果（英文）

在本文中,我们讨论了一类带时间延迟的Cohen-Grossberg神经网络,并研究了这个系统平衡点的全局鲁棒稳定性。利用Lyapunov函数,我们得出了全局鲁棒收敛性的几个充分条件。这些条件以线性矩阵不等式（LMI）的形式表达。因此,从计算的角度出发他们是高效的。另外,这些条件不依赖于时间延迟和神经网络的激发函数。     

捕食者有病的食饵-捕食者模型

建立了捕食者有病的食饵-捕食者模型;由Hurwitz判据、LaSalle不变性原理获得了平衡点稳定的条件;并给出了模型的撮动解．     

局域种群的Allee效应和集合种群的同步性

从包含Allee效应的局域种群出发,建立了耦合映像格子模型,即集合种群模型.通过分析和计算机模拟表明:(1)当局域种群受到Allee效应强度较大时,集合种群同步灭绝;(2)而当Allee效应强度相对较弱时,通过稳定局域种群动态(减少混沌)使得集合种群发生同步波动,而这种同步波动能够增加集合种群的灭绝风险;(3)斑块间的连接程度对集合种群同步波动的发生有很大的影响,适当的破碎化有利于集合种群的续存.全局迁移和Allee效应结合起来增加了集合种群同步波动的可能,从而增加集合种群的灭绝风险.这些结果对理解同步性的机理、利用同步机理来制定物种保护策略和害虫防治都有重要的意义.     

一类具有漏泄时滞的混沌神经网络的反同步

利用矩阵测度方法和微分不等式技巧,研究了一类具有漏泄时滞的混沌神经网络的反同步问题.数值模拟验证了理论分析的正确性.     

Robust stability of genetic regulatory networks with distributed delay

This paper investigates robust stability of genetic regulatory networks with distributed delay. Different from other papers, distributed delay is induced. It says that the concentration of macromolecule depends on an integral of the regulatory function of over a specified range of previous time, which is more realistic. Based on Lyapunov stability theory and linear matrix inequality (LMI), sufficient conditions for genetic regulatory networks to be global asymptotic stability and robust stability are derived in terms of LMI. Two numerical examples are given to illustrate the effectiveness of our theoretical results.     

一类具有广义Logistic增长的比率型捕食模型的定性分析

对具有广义Logistic增长的比率型捕食模型进行了分析,得到了系统永久持续生存的充分条件．通过对系统进行无量纲代换和应用Liapunov函数的方法,进一步得到了正平衡点全局渐近稳定的充分条件．     

Global robust power-rate stability of delayed genetic regulatory networks with noise perturbations

In this paper, by using the Lyapunov method, Itô’s differential formula and linear matrix inequality (LMI) approach, the global robust power-rate stability in mean square is discussed for genetic regulatory networks with unbounded time-varying delay, noise perturbations and parameter uncertainties. Sufficient conditions are given to ensure the robust power-rate stability (in mean square) of the genetic regulatory networks. Meanwhile, the criteria ensuring global power-rate stability in mean square are a byproduct of the criteria guaranteeing global robust power-rate stability in mean square. The obtained conditions are derived in terms of linear matrix inequalities (LMIs) which are easy to be verified via the LMI toolbox. An illustrative example is given to show the effectiveness of the obtained result.     

Leukocyte migration inhibition by a specific antigen in human typhoid fever.

Cellular reactivity to heat-killed Salmonella typhi antigen was investigated by the leukocyte migration inhibition (LMI) method in 33 S. typhi infected patients and in 32 control persons. In the typhoid group a statistically significant LMI was observed as compared to the members of the control group. A correlation was found between the level of the cellular sensitivity and the time elapsed between onset of the disease and performance of the test. Previous typhoid vaccination had no influence on the LMI. No correlation was found between the agglutinin titres and the sensitivity demonstrated by the LMI test. The value of the method in studies of cellular immunity in typhoid fever is discussed.     

LATE MERISTEM IDENTITY2 acts together with LEAFY to activate APETALA1

The switch from producing vegetative structures (branches and leaves) to producing reproductive structures (flowers) is a crucial developmental transition that significantly affects the reproductive success of flowering plants. In Arabidopsis, this transition is in large part controlled by the meristem identity regulator LEAFY (LFY). The molecular mechanisms by which LFY orchestrates a precise and robust switch to flower formation is not well understood. Here, we show that the direct LFY target LATE MERISTEM IDENTITY2 (LMI2) has a role in the meristem identity transition. Like LFY, LMI2 activates AP1 directly; moreover, LMI2 and LFY interact physically. LFY, LMI2 and AP1 are connected in a feed-forward and positive feedback loop network. We propose that these intricate regulatory interactions not only direct the precision of this crucial developmental transition in rapidly changing environmental conditions, but also contribute to its robustness and irreversibility.     

Robust synchronization analysis in nonlinear stochastic cellular networks with time-varying delays, intracellular perturbations and intercellular noise

Naturally, a cellular network consisted of a large amount of interacting cells is complex. These cells have to be synchronized in order to emerge their phenomena for some biological purposes. However, the inherently stochastic intra and intercellular interactions are noisy and delayed from biochemical processes. In this study, a robust synchronization scheme is proposed for a nonlinear stochastic time-delay coupled cellular network (TdCCN) in spite of the time-varying process delay and intracellular parameter perturbations. Furthermore, a nonlinear stochastic noise filtering ability is also investigated for this synchronized TdCCN against stochastic intercellular and environmental disturbances. Since it is very difficult to solve a robust synchronization problem with the Hamilton-Jacobi inequality (HJI) matrix, a linear matrix inequality (LMI) is employed to solve this problem via the help of a global linearization method. Through this robust synchronization analysis, we can gain a more systemic insight into not only the robust synchronizability but also the noise filtering ability of TdCCN under time-varying process delays, intracellular perturbations and intercellular disturbances. The measures of robustness and noise filtering ability of a synchronized TdCCN have potential application to the designs of neuron transmitters, on-time mass production of biochemical molecules, and synthetic biology. Finally, a benchmark of robust synchronization design in Escherichia coli repressilators is given to confirm the effectiveness of the proposed methods.     

Membranes of EBV-carrying virus nonproducer cells inhibit leukocyte migration of EBV-seropositive but not seronegative donors

We have previously shown that the leukocytes of healthy EBV-seropositive (but not seronegative) donors respond with migration inhibition (LMI) when confronted with extracts of EBV-carrying (but not EBV negative) cells. In the present study, we have examined whether this EBV-specific LMI response is capable of detecting a membrane antigen on the surface of EBV-carrying virus nonproducer cells. Crude membranes from EBV-genome carrying and EBV-negative cell lines were used as antigen. Contamination with the EBV-determined nuclear antigen (EBNA) was ruled out. Membranes from EBV-genome carrying nonproducer cells inhibited the migration of leukocytes from healthy seropositive donors, whereas membranes from EBV-negative lines had no such effect. Seronegative donors did not show any LMI. The clear difference between the EBV-negative Ramos line and its EBV-converted sublines was particularly conclusive in showing that the membrane component is determined or induced by the viral genome.