Quantal transmitter secretion from myocytes loaded with acetylcholine.

It is well known that transmitter secretion requires specialized secretory organelles, the synaptic vesicles, for the packaging, storage and exocytotic release of the transmitter. Here we report that when acetylcholine (ACh) is loaded into an isolated Xenopus myocyte, there is spontaneous quantal release of ACh from the myocyte which results in activation of its own surface ACh channels and the appearance of membrane currents resembling miniature endplate currents. This myocyte secretion probably reflects Ca(2+)-regulated exocytosis of ACh-filled cytoplasmic compartments. Furthermore, step depolarization of the myocyte membrane triggers evoked ACh release from the myocyte with a weak excitation-secretion coupling. These findings suggest that quantal transmitter secretion does not require secretory pathways unique to neurons and that the essence of presynaptic differentiation may reside in the provision of transmitter supply and modification of the preexisting secretion pathway.     

新型全固态铁离子敏感电极研究

采用稀土电极材料六硼化镧制备了一种新的全固态铁离子敏感电极。研究了该敏感电极在常见介质中对Ｆｅ３＋的响应行为。结果表明，该铁离子敏感电极在１．５ｍｏｌ／ＬＨ３ＰＯ４介质中的线性响应范围、检测下限和响应斜率分别为１．０×１０－５～１．０×１０－１ｍｏｌ／ＬＦｅ３＋，６．０×１０－６ｍｏｌ／ＬＦｅ３＋和６０ｍＶ／ｐＣ，且具有较好的选择性。     

A calcium sensor in the sodium channel modulates cardiac excitability.

Sodium channels are principal molecular determinants responsible for myocardial conduction and maintenance of the cardiac rhythm. Calcium ions (Ca2+) have a fundamental role in the coupling of cardiac myocyte excitation and contraction, yet mechanisms whereby intracellular Ca2+ may directly modulate Na channel function have yet to be identified. Here we show that calmodulin (CaM), a ubiquitous Ca2+-sensing protein, binds to the carboxy-terminal 'IQ' domain of the human cardiac Na channel (hH1) in a Ca2+-dependent manner. This binding interaction significantly enhances slow inactivation-a channel-gating process linked to life-threatening idiopathic ventricular arrhythmias. Mutations targeted to the IQ domain disrupted CaM binding and eliminated Ca2+/CaM-dependent slow inactivation, whereas the gating effects of Ca2+/CaM were restored by intracellular application of a peptide modelled after the IQ domain. A naturally occurring mutation (A1924T) in the IQ domain altered hH1 function in a manner characteristic of the Brugada arrhythmia syndrome, but at the same time inhibited slow inactivation induced by Ca2+/CaM, yielding a clinically benign (arrhythmia free) phenotype.     

类DLVO理论与胆固醇单水结晶形成过程

就人体胆汁胆固醇单水结晶形成过程提出了类DLVO理论,应用该理论初步阐明了其结晶过程可能的化学物理机制,并分析了该理论在促、抗成核因子及溶石方面的意义.     

毕竟正则半群上的群同余

设S是一个半群,a∈S.如果存在x∈S,使得x=xax,则称x为a的一个弱逆.用W(a)表示a的所有弱逆的集合.本文利用元素的弱逆给出了毕竟正则半群S的群同余的若干等价刻画及一个表示.通过S的w-自共轭的、闭的,全子半群H定义了S上的一个二元关系(a,b)∈ρH( )(( )a'∈W(a),a'b∈H),证明了如果H是S的w-自共轭的、闭的全子半群,则ρH是S上的以H为核的群同余.反过来,如果ρ是S上的群同余,则kerρ是S的w-自共轭的,闭的全子半群,并且ρ=ρker ρ.     

吸附树脂对对甲苯胺的静态吸附行为及其热力学性质的研究

对比 Amberlite XAD-4与两种新型吸附树脂 NK和新 H对对甲苯胺的静态吸附行为 ,根据吸附等温线研究并讨论吸附热力学性质 .两种新型吸附树脂对对甲苯胺的吸附能力明显强于 Amberlite XAD-4 ,微孔作用机制及表面部分极性起决定作用 .吸附焓变 ΔH<0表明吸附为放热过程 ,降低温度有利于吸附 .对吸附焓变和自由能变的讨论同时表明树脂对对甲苯胺的吸附为多层物理吸附过程 .吸附熵变 ΔS表明吸附树脂表面的不均匀性和吸附质分子在树脂表面的分布及其局域运动与吸附有密切关系 .     

三峡钢丝绳卷扬全平衡式垂直升船机机电耦合系统动力学仿真

建立三峡钢丝绳卷扬全平衡式垂直式升船机的双闭环调速电力拖动控制系统的模型和升船机各子结构的动力学模型，并通过刚性子结构法形成了整体动力学模型，运用MATLAB中的SIMULINK模块，将电力拖动控制系统与整体动力学模型耦合，采用Wilson-θ法求解瞬态响,对误载水深为＋20cm，承船厢低点位置上向上启动运动的正常工况进行了仿真分析。     

(E)-3-(3,4-二甲氧基苯基)-2-氰基丙烯酸乙酯的合成和晶体结构

标题化合物C14 H15O4N(3)是由 3,4 二甲氧基苯甲醛 (1) 与氰乙酸乙酯 (2 ) 在KF/蒙脱土催化下以N ,N 二甲基甲酰胺 (DMF)作溶剂反应而得 .结构通过单晶X射线衍射分析确定 ,其晶体属于单斜晶系 ,空间群P2 1/n ,a =1.310 1(3) ,b =0 .80 32 (2 ) ,c =1.385 4 (2 )nm ,β =114 .2 1(1)° ,Mr=2 6 1.2 7,V =1.32 96 (5 )nm3 ,Dc=1.30 5 g/cm3 ,Z =4 ,μ(MoKα) =0 .0 96mm-1,F(0 0 0 ) =5 5 2 .晶体结构用直接法解出 ,使用全矩阵最小二乘法对原子参数进行修正 ,最后的偏离因子R =0 .0 398,RW =0 .0 816 .单晶X衍射分析表明标题化合物为 (E)式异构体产物 ,说明该反应具有立体选择性 .     

波动性比率与涨跌幅限制实证研究

从交易机制的角度解释了股市开盘收益率的波动大于收盘收益率的波动的原因。在考虑了涨跌幅限制的存在对股票价格行为的影响后，建立了一个简单的计量模型，提出涨跌停频率的大小与波动率的正相关关系及涨跌停日的日内收益率与次日隔夜收益率的正相关关系的假设，并就中国股市的情况进行了实证分析，得出了与假设一致的结论。这里的研究为“方差比率之谜”提供了新的解释思路。     

VPN 的构建方法

本文阐述了VPN的概念和采用隧道技术实现的原理,以及基于Internet的VPN构建方法和步骤.