Resistant orthogonal procrustes analysis

In this paper two alternative loss criteria for the least squares Procrustes problem are studied. These alternative criteria are based on the Huber function and on the more radical biweight function, which are designed to be resistant to outliers. Using iterative majorization it is shown how a convergent reweighted least squares algorithm can be developed. In asimulation study it turns out that the proposed methods perform well over a specific range of contamination. When a uniform dilation factor is included, mixed results are obtained. The methods also yield a set of weights that can be used for diagnostic purposes.     

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.     

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.     

矿区铁路专用线下综采放顶煤开采的试验研究

介绍了国内第一个综采放顶煤开采矿区铁路线下压煤试验面的成功经验，总结了试采中对铁路所采取的各种分析和维护措施，分析了该采煤方法下的地在移动和变形特点，为我国“三下”采煤领域提供了具有特色的成功实例。     

Electrochemical studies of glutathione monolayer assembled on a polycrystalline gold electrode

The glutathione (GSH) monolayer and complex monolayer of GSH-metallic ion on polycrystalline gold electrode were studied by using K₃Fe(CN)₆ as the redox probe. As for the GSH monolayer, it was found that the metallic ions could open the ion-gate in the monolayer dramatically in the order La³⁺> Pb²⁺>>Ba²⁺>Ca²⁺ whereas Zn²⁺ ion closed the ion-gate. The complexes of GSH-metallic ions were capable of self-assembling the different kind of monolayer. All the differences were related to the structural configuration of the anchored GSH molecule, which changed with different metallic ions or pH. Biography:Fang Cheng (1971-) male, Ph. D, research direction: electroanlysis.     

Der Einfluß der Nebenniere auf die Kreislaufwirkung des Adrenalins

Summary Traces of nor-adrenaline restore the vascular action of adrenaline altered in epinephrectomized dogs to the reaction of the normal animal. Therefore it is claimed that the adrenals discharge one or several substances into the blood stream, which are necessary for the usual peripheral vascular action of adrenaline. Further investigations are in progress.