Overcompensation and population cycles in an ungulate.

Although theoretical studies show that overcompensatory density-dependent mechanisms can potentially generate regular or chaotic fluctuations in animal numbers, the majority of realistic single-species models of invertebrate populations are not overcompensatory enough to cause sustained population cycles. The possibility that overcompensation may generate cycles or chaos in vertebrate populations has seldom been considered. Here we show that highly overcompensatng density-dependent mortality can generate recurrent population crashes consistent with those observed in a naturally limited population of Soay sheep. The observed interval of three or more years between crashes points to sharp 'focusing' of mortality over a narrow range of population density.     

熔炼数据库的建立和应用

熔炼数据库是合金熔炼多功能软件中的一个模块，本文结合作者在研究和开发软件中的体会，对建立熔炼数据库的必要性、建库过程和应用情况进行了论述．     

特征结构提取的高阶Hopfield神经网络实现

本文首先建立了特征结构提取问题的罚函数表示，通过对罚函数求极小可以求得原始协方差矩阵的主特征向量及其对应的特征值。为了求得其他特征结构，特构造了一个协方差矩阵序列。如果将罚函数展开并进行整理，高阶Ｈｏｐｆｉｅｌｄ神经网络可被引入到特征结构提取中。这种方法比较直观，它将网络稳定时的输出与所求协方差矩阵的主特征向量的各个分量相对应，而网络稳定时的能量则对应于协方差矩阵的迹与所求特征值之差，计算机仿真结果验证了这种方法的正确性。     

炭黑／结晶性含氟树脂合金在自控温加热电缆中应用

选择了结晶性含氟树脂添加改性剂为树脂基体，与炭黑制居复合导电体系。通过这个对体系不同条件下ＰＴＣ特性的研究，对其配方与加工工艺进行优化。并利用扫描电镜，Ｘ射线衍射，ＤＳＣ等分析测试手段，对体系的各种开矿结构进行了研究，阐明了该导电复合体系的形态结构与性能的关系。     

从猪血中制备原卟啉甲酯的新方法

本文报导由猪血制备原卟啉甲酯的一种新方法,木法成本低廉,设备简单,产率较高,得到的产物容易纯化,并对产物进行了IR_.~iHNMR.UV等波谱解析。     

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.     

Retrograde transport of endocytosed Shiga toxin to the endoplasmic reticulum.

Shiga toxin and some other protein toxins that act on targets in the cytosol have previously been shown to enter the trans-Golgi network. Transport by this route may be necessary for translocation of the toxin to the cytosol and for intoxication, but it is not known whether the enzymatically active part of the toxins actually enters the cytosol from the trans-Golgi network. It has been suggested that such toxins are transported in a retrograde manner to the endoplasmic reticulum and that translocation occurs in this organelle, but retrograde transport of endocytosed material beyond the trans-Golgi network has never been demonstrated. Here we show that in butyric acid-treated A431 cells endocytosed Shiga toxin is not only transported to the trans-Golgi network, but also to all Golgi stacks, to the endoplasmic reticulum and to the nuclear envelope. Furthermore, butyric acid sensitizes the cells to Shiga toxin, which is consistent with the possibility that retrograde transport is required for translocation of the toxin to the cytosol.