用Zubarev非平衡统计算子法讨论非平衡定态中的不可逆过程

本文是用Zubarev非平衡统计算子讨论处于非平衡定态的系统在受到力学拢动时的线性响应问题。仅限于讨论一级近似下的非平衡定态。主要结论是:证明了定态统计算子与定态哈密顿对易,从而证明了定态时间相关函数的稳恒性。导出了以定态为参考态的起伏耗散定理。证明了定态时间相关函数不存在时间反演对称性。根据定态时间相关函数时间反演对称性破缺,证明了对广义极化率的Onsager倒易关系不成立。根据因果律在定态得到满足,证明了对广义极化率的色散关系仍然成立。     

电压型母线差动保护

本文拟制的电压型母线差动保护和普通电流型差动保护主要的区别是:在差动回路中采用了电压继电器来代替电流继电器。保护的原理是,当正常运行和外部故障时,利用选择继电器的整定值大于最大的不平衡电压来防止误动作;而当内部故障时,利用差动回路上能产生较高电压而达到灵敏动作的目的。在双母线对,故障母线是利用联络开关流过的电流和差动回路上电压之间的相位关系来确定。这种保护方式在正常运行时电流回路的工作情况和普通差动保护类似,但是在母线上故障时能保证有较高的动作灵敏度和较快的速废。特别当电流差动回路由于电流互感器特性不一致而不平衡电流较大时,这种保护方式的优点就更为突出。此外当双母线时不要求出线固定地联接在一定的母线上也是显著的优点。文中给出了保护的原理和接线图,整定计算公式和实验室内的试验结果。     

配电电缆绝缘劣化的极化去极化电流特性仿真

为实现对6 kV交联聚乙烯(XLPE)电缆绝缘状态的可靠检测,基于德拜扩展模型建立了整体受潮、局部受潮、绝缘老化、含水树枝电缆的仿真模型,采用极化-去极化电流法(polarization-depolarization current,PDC)对电缆绝缘状态进行诊断,研究电缆在不同绝缘状态下PDC特性变化规律。结果表明:电缆受潮较严重时,电压电流呈现明显的非线性关系,绝缘电阻下降速率更快;水树枝程度越深,极化去极化电流初始值越大,电缆绝缘性能越差。     

无须考虑电源接法和性质的三相电压型整流器平均模型

为克服三相电压型整流器现有平均模型的局限性,提出并推导一种无须考虑电源接法和性质的统一形式的平均模型.在建立开关模型过程中,处理纯电感割集时对独立状态变量个数以及独立方程数进行了严格界定;推导平均模型时,引入了冗余变量和冗余方程,使得所得模型更加直观易用.模型直接采用电感电流作状态变量,除基尔霍夫电流定律(KCL)和基尔霍夫电压定律(KVL)外,没有依赖任何额外假设.与现有模型相比,该模型去除了对输入三相交流电压波形性质的要求,因此完全适用于非正弦、非平衡、非对称的场合.仿真结果证明了模型的有效性.进一步的讨论说明,在三相正弦输入时,该模型与现有模型兼容.     

反应控制时固定床电化学反应器特性研究

本文建立了反应控制操作条件下的固定床电化学反应器模型，从理论上对Ｔａｆｅｌ极化区和线性极化区操作下的反应速率、电流分布进行了讨论，并将实验测定的床层内电势分布与模型计算值进行了比较，为固定床电化学反应器非定态操作特性研究奠定了基础。     

基于p-q变换的改进i_p-i_q基波正序有功和无功电流检测算法

针对非理想电压下不能获取基波正序有功和无功电流的问题,通过对三相电压和电流并行地进行p-q坐标变换和低通滤波以降低系统延时,并获取三相基波正序电压和电流的综合相位信息,通过坐标反变换求出基波正序电流中的有功和无功分量,从而提出1种改进的ip-iq算法。研究结果表明:该算法在电网电压对称无畸变、电网电压不对称、电网电压同时存在畸变和不对称条件下,均能获取正确的基波正序有功和无功电流,为在有源电力滤波系统中实现对谐波电流、无功电流和不对称分量的综合补偿提供了合理的参考指令电流。     

空间矢量控制的三相四桥臂逆变器建模与硬件实现

在三相负载不平衡时,传统逆变器无法控制三相输出电压达到平衡状态,因此运用三相四桥臂结构控制零序电压和电流来应对不平衡负载。通过对三相输出电压进行解耦,并增加了电压和电流的双环控制,使得空间矢量调制(SVM)对逆变器控制的稳定性增强,提高了动态响应特性,运用Matlab/Simulink进行建模仿真,分模块搭建了仿真模型,仿真达到了预期应对不对称负载和负载突变的效果,并结合仿真模型算法部分编写了DSP程序,实验观察SVPWM波形,验证了算法的合理性和有效性。     

非平衡系统的规格化模型及其临界广义势

非平衡临界的参考态是非平衡定态,在该参考态下存在一个描述系统状态稳定的广义势。本文从一般非平衡系统出发,注意到非平衡临界与平衡临界的差别和联系,建立了非平衡系统的规格化模型,考察了非平衡系统广义势的存在形式,得到了该广义势在非平衡临界点无限小邻域内的具体结构。还讨议了该模型及其广义势在位形空间和动量空间中的粗粒化过程,为对非平衡相变系统临界性质更深一步的考察和研究创造了条件。     

TRAAK离子通道第4次跨膜结构对其机械敏感性的作用

TRAAK通道(KCNK4)是双孔钾通道的成员,在哺乳动物神经系统中表达,其产生的钾电流是能改变神经元兴奋性的背景电流的重要组成部分.TRAAK通道是机械力和温度门控的通道,并且受到电压、胞内pH以及脂质的调节,然而它们的机制在很大程度上仍然是未知的.为了研究TRAAK通道的机械力门控机制,本研究将TRAAK通道的第4次跨膜结构域(the fourth transmembrane domain,M4)和非机械敏感性离子通道TWIK-1之间的同源区域进行替换,构建了3个嵌合突变体,通过全细胞和细胞贴附式记录,发现当TRAAK通道M4的上半部分被TWIK-1的同源序列替换之后,显著降低了通道半激活压力值(P_(50)),极大增强了TRAAK通道的机械敏感性,表明M4的上半部分对TRAAK通道机械敏感性具有重要的调控作用,为研究TRAAK通道的机械力门控机制提供了基础.     

双馈风电机组在电网对称故障下低压穿越仿真

以双馈式风力发电机（DFIG）为主体的大型风力发电机组在电网中所占的比例快速提高,为了确保风电接入电力系统运行的可靠性、安全性与稳定性,电力系统对并网风力发电机在电网故障,特别是电网电压骤降故障下的低压运行能力提出了更高的要求。文中介绍了电网对称故障时DFIG的暂态特性,通过对转子电流与定子磁链的关系分析得出优化转子侧变换器控制策略的方案,通过配合改进网侧变流器控制方法为DFIG在电网电压跌落期间提供了一个稳定的直流母线电压,从而使电网对称故障时的定转子过电流和直流母线侧过电压的情况得到解决。在研究模型的基础上,通过改变转子侧和网侧变换器控制策略的Matlab模型进行仿真实验,结果表明该方案对于对称电压跌落故障时的LVRT有一定的可行性。     

驱动电流密度对低压容性射频鞘电势及离子动能的影响

研究了离子轰击被加工材料表面的能量与射频驱动电流密度之间的关系，在Lieberman的低压容性射频等离子鞘模型基础上，考虑Bohm速度对应的鞘前电势差，将鞘前电势差与Lieberman的鞘内电势合并，发展了Lieberman的模型，并推出了总电势差与驱动电流密度的关系式，利用总鞘电势差计算了经时间平均的鞘电场加速后离子获得的动能，由于鞘电势差和平均离子动能及其增幅随电流密度的增加而增加，因此射频驱动电流密度对鞘电势差及平均离子动能起激励作用，通过实验，测量了时间平均鞘电势差及驱动电流密度值，实验结果与理论结果吻合较好，因此验证了理论分析的正确性。     

Gating pore current in an inherited ion channelopathy

Ion channelopathies are inherited diseases in which alterations in control of ion conductance through the central pore of ion channels impair cell function, leading to periodic paralysis, cardiac arrhythmia, renal failure, epilepsy, migraine and ataxia. Here we show that, in contrast with this well-established paradigm, three mutations in gating-charge-carrying arginine residues in an S4 segment that cause hypokalaemic periodic paralysis induce a hyperpolarization-activated cationic leak through the voltage sensor of the skeletal muscle Na(V)1.4 channel. This 'gating pore current' is active at the resting membrane potential and closed by depolarizations that activate the voltage sensor. It has similar permeability to Na+, K+ and Cs+, but the organic monovalent cations tetraethylammonium and N-methyl-D-glucamine are much less permeant. The inorganic divalent cations Ba2+, Ca2+ and Zn2+ are not detectably permeant and block the gating pore at millimolar concentrations. Our results reveal gating pore current in naturally occurring disease mutations of an ion channel and show a clear correlation between mutations that cause gating pore current and hypokalaemic periodic paralysis. This gain-of-function gating pore current would contribute in an important way to the dominantly inherited membrane depolarization, action potential failure, flaccid paralysis and cytopathology that are characteristic of hypokalaemic periodic paralysis. A survey of other ion channelopathies reveals numerous examples of mutations that would be expected to cause gating pore current, raising the possibility of a broader impact of gating pore current in ion channelopathies.     

Cyclic AMP-dependent protein kinase closes the serotonin-sensitive K+ channels of Aplysia sensory neurones in cell-free membrane patches

Selected actions of neurotransmitters and hormones on ion channels in nerve and muscle cells are now thought to be mediated by cyclic AMP-dependent protein phosphorylation. Although the cyclic AMP-dependent protein kinase (cAMP-PK) affects the cellular properties of several neurones, its mode of action at the single-channel level has not been characterized. In addition, little is known about the identity or subcellular localization of the phosphoproteins that control channel activity and, in particular, whether the critical substrate proteins are cytoplasmic or membrane-associated. In Aplysia sensory neurones, serotonin produces a slow modulatory synaptic potential mediated by cAMP-PK that contributes to presynaptic facilitation and behavioural sensitization. Previously, we have found that serotonin acts on cell-attached membrane patches to produce prolonged all-or-none closures of a specific class of K+ channels (S channels) whose gating is weakly dependent on voltage and independent of intracellular calcium. We demonstrate here that in cell-free membrane patches from Aplysia sensory neurones, the purified catalytic subunit of cAMP-PK produces all-or-none closures of the S channel, simulating most (but not all) aspects of the action of serotonin on cell-attached patches. This result suggests that protein kinase acts on the internal surface of the membrane to phosphorylate either the channel itself or a membrane-associated protein that regulates channel activity.     

单电子量子同心环的基态特性

给出了单电子量子同心环基态能量随其半径和势垒的变化规律, 并根据动力学和不确定关系对变化规律进行分析,  通过密度函数显示基态的电子几率分布. 结果表明, 即使基态能量小于势垒, 电子在势垒中的几率也不为零.     

Energetics of ion conduction through the K+ channel.

K+ channels are transmembrane proteins that are essential for the transmission of nerve impulses. The ability of these proteins to conduct K+ ions at levels near the limit of diffusion is traditionally described in terms of concerted mechanisms in which ion-channel attraction and ion-ion repulsion have compensating effects, as several ions are moving simultaneously in single file through the narrow pore. The efficiency of such a mechanism, however, relies on a delicate energy balance-the strong ion-channel attraction must be perfectly counterbalanced by the electrostatic ion-ion repulsion. To elucidate the mechanism of ion conduction at the atomic level, we performed molecular dynamics free energy simulations on the basis of the X-ray structure of the KcsA K+ channel. Here we find that ion conduction involves transitions between two main states, with two and three K+ ions occupying the selectivity filter, respectively; this process is reminiscent of the 'knock-on' mechanism proposed by Hodgkin and Keynes in 1955. The largest free energy barrier is on the order of 2-3 kcal mol-1, implying that the process of ion conduction is limited by diffusion. Ion-ion repulsion, although essential for rapid conduction, is shown to act only at very short distances. The calculations show also that the rapidly conducting pore is selective.     

在Gramicidin膜通道中碱金属离子与多肽基团之间的相互作用

以Grimicidin A做为生物膜金属离子通道模型,在给定的通道结构参数条件下,用量子化学ASED-MO法研究了K~+,Na~+离子在通道内沿中心轴移动时,能量剖面,金属离子与肽骨架上各原子的相互作用规律。发现(1)Na~+离子在通道中总能量的下降较K~+离子情况的低,但受到周围的排斥作用较前者大;(2)金属离子与通道上原子的排斥能在中间区域表现为小波动变化,与前人结论是一致的。着重分析骨架原子的净电荷分布及其受金属离子的影响,讨论了金属离子与骨架原子排斥能周期性变化的原因。     

IS4 peptide forms ion channel in rat skeletal muscle cell membrane

A 22-mer peptide, identical to the primary sequence of domain I segment 4 (IS4) of rat brain sodium channel I, has been synthesized. IS4 peptide can incorporate into cultured rat skeletal myotube membranes and form ion channels. With patch clamp cell-attached technique single channel currents through IS4 channels can be recorded. The single channel conductances of IS4 channels are distributed heterogeneously. With different holding potentials, the mean open time, the mean closed time and the mean open probability are different respectively. IS4 channels are selective for Na⁺, Li⁺ and K⁺, but not for Cl⁻.     

交变电场作用下细胞膜离子通道电流的趋肤效应

自然状态下细胞跨膜通道开放后，离子在化学梯度力和膜电场力作用下运动，形成离子电流，维持细胞正常的电生理特性．在外电场作用下，离子通道暴露于感应电磁环境中．作为电生理活动基础的各种离子．在电磁力作用下，其运动状态受到影响，直接导致离子电流值的改变．为量化分析这一作用机理，可根据离子通道的物理性质将其等效为圆柱导体，建立通道的电学模型并推导离子电流密度的分布函数．分析可知，在外加交变电场作用下，细胞膜离子通道电流的径向密度分布发生了变化，越靠近通道壁，离子电流密度越大，即产生趋肤效应。进而影响跨膜通道对离子的通透性。     

Ion conduction pore is conserved among potassium channels.

Potassium channels, a group of specialized membrane proteins, enable K+ ions to flow selectively across cell membranes. Transmembrane K+ currents underlie electrical signalling in neurons and other excitable cells. The atomic structure of a bacterial K+ channel pore has been solved by means of X-ray crystallography. To the extent that the prokaryotic pore is representative of other K+ channels, this landmark achievement has profound implications for our general understanding of K+ channels. But serious doubts have been raised concerning whether the prokaryotic K+ channel pore does actually represent those of eukaryotes. Here we have addressed this fundamental issue by substituting the prokaryotic pore into eukaryotic voltage-gated and inward-rectifier K+ channels. The resulting chimaeras retain the respective functional hallmarks of the eukaryotic channels, which indicates that the ion conduction pore is indeed conserved among K+ channels.     

Single stretch-activated ion channels in vascular endothelial cells as mechanotransducers?

Endothelial cells line the inner surface of blood vessels and act as the main barrier to the passage of cells and large molecules from the blood stream to the tissues. Recent interest in the part played by the endothelium in regulating vascular tone has focused on the synthesis and secretion of prostacyclin and an endothelium-derived relaxing factor. Endothelial cells respond to blood-borne agonist, but how the endothelium senses and responds to mechanical forces generated by the flow of blood under pressure is not known. Here we report patch-clamp recordings of ion channel activity from cell-attached membrane patches on aortic endothelial cells. In most of the patches examined, we observed unitary inward currents associated with the opening of a cation-selective channel (approximately 40 pS in standard saline). The channel is permeable to Ca2+ and its opening frequency increases when the membrane is stretched by applying suction through the patch electrode. The presence of mechanotransducing ion channels in endothelial cells may help explain how the endothelium mediates vascular responses to haemodynamic stresses.