Ca2+ release induced by inositol 1,4,5-trisphosphate is a steady-state phenomenon controlled by luminal Ca2+ in permeabilized cells.

Low concentrations of inositol 1,4,5-trisphosphate (InsP3) evoke a very rapid mobilization of intracellular Ca2+ stores in many cell types, which can be followed by a further, much slower efflux. Two explanations have been suggested for this biphasic release. The first proposes that the Ca2+ stores vary in their sensitivity to InsP3, and each store releases either its entire contents or nothing (all-or-none release); the second proposes instead that the stores are uniformly sensitive to the effects of InsP3, but that they can release only a fraction of their Ca2+ before their sensitivity is somehow attenuated (steady-state release). Experiments using purified InsP3 receptor molecules reconstituted into lipid vesicles have shown heterogeneity of the receptors in their response to InsP3 under conditions in which the total Ca2+ level at both sides of the receptor is held constant. We now report that in permeabilized A7r5 smooth-muscle cells incubated in Ca(2+)-free medium, the amount of 45Ca2+ remaining in the stores after the rapid transient phase of release is independent of their initial Ca2+ levels, indicating that partially depleted stores are less sensitive to InsP3. Moreover, if the stores are reloaded with 40Ca2+ after the first stimulus, reapplication of the same low concentration of InsP3 will release further 45Ca2+. This recovery of InsP3 sensitivity is almost complete. Under these conditions, Ca2+ release must thus occur by a steady-state mechanism, in which the decreasing Ca2+ content of the stores slows down further release.     

多变量自校正控制计算机辅助设计软件系统

本文介绍了一个可帮助用户进行多变量自校正控制系统设计,而使用户不必了解算法细节的计算机辅助设计(CAD)软件系统;它既包括一些经典的自校正控制算法,又引入了一些近年来新研究的成果。使用情况表明,该系统算法先进,使用方便,控制效果较好,是一个实用的软件工具。     

Exocytotic fusion is activated by Rab3a peptides.

Studies of intracellular traffic in yeast and mammalian systems have implicated members of the Rab family of small GTP-binding proteins as regulators of membrane fusion. We have used the patch clamp technique to measure exocytotic fusion events directly and investigate the role of GTP-binding proteins in regulating exocytosis in mast cells. Intracellular perfusion of mast cells with GTP-gamma S is sufficient to trigger complete exocytotic degranulation in the absence of other intracellular messengers. Here we show that GTP is a potent inhibitor of GTP-gamma S-induced degranulation, indicating that sustained activation of a GTP-binding protein is sufficient for membrane fusion. We have found that synthetic oligopeptides, corresponding to part of the effector domain of Rab3a, stimulate complete exocytotic degranulation, similar to that induced by GTP-gamma S. The response is selective for Rab3a sequence and is strictly dependent on Mg2+ and ATP. This suggests that sustained activation of a Rab3 protein causes exocytotic fusion. The peptide response can be accelerated by GDP-beta S, suggesting that Rab3a peptides compete with endogenous Rab3 proteins for a binding site on a target effector protein, which causes fusion on activation.     

汽车拖拉机转向机构的优化设计

本文提出用一种新的时间离散化方法对汽车拖拉机的转向机构进行优化设计．该离散化方法是按被实现函数变化率的大小划分时间单元，在被实现函数变化率较大的区域，分点较密；在率化率较小的区域，分点较稀．笔者还分别用等间距的时间离散化及切比雪夫时间离散化方法，对同一机构使用同一种优化方法进行了优化设计，并将三种计算结果进行了比较．结果表明，笔者提出的方法，没有增加计算工作量，而能提高计算精度．     

接触载荷作用下的表面裂纹分析

用边界积分方法分析了表面裂纹在接触载荷作用下的张开位移和应力强度因子，该方法将埋在无穷大弹性介质中裂纹模拟为连续分布的位错环，根据两个位错环之间的相互作用能可以得到弹性体的应变能，对弹性体的势能取极值，可以得到关于裂纹张开位移的边界积分方程，通过把半空间的边界模拟成一个包含在无穷大弹性介质中大裂纹，该方法能用已有的边界积分方法很好的处理具有任意表面形状的表面裂纹，文中算例分析了不同倾角的表面裂纹在法向和切向接触载荷作用下，裂纹尖端的应力强度因子，其结果对于分析路面表面裂纹的扩展具有重要意义。     

Influence of hydrochlorothiazide on the pain threshold and on the antinociceptive activity of morphine,in rats

Summary Hydrochlorothiazide, acutely injected in rats, has a weak analgesic activity per se and potentiates and prolongs the antinociceptive effect of morphine.This work was supported in part by grants from Consiglio Nazionale delle Ricerche, and by Ministero della Pubblica Istruzione, Roma.