NH_4HCO_3作沉淀剂制备超细Ce-Zr-O粉末的研究

为寻求简便、合理的合成超细粉体的方法,利用NH4HCO3 作沉淀剂,通过考察料液配比、加料速度、升温速度等实验因素,得到了简单的合成超细 Ce Zr O粉末的工艺,并利用比表面积测定仪、激光粒度仪、XRD、Raman等仪器对相关产物进行了表征.结果表明:利用简单工艺合成的超细 Ce Zr O粉末具有中位粒径为0.30μm、比表面积为21.2 m2/g、悬浮性大于30 min、松装密度小于 1 g/cm3等性能,产物具有 CaF2 型的空间结构.     

Changes in glycosaminoglycan sulfation and protein kinase C subcellular distribution during differentiation of the human colon tumor cell line Caco-2

Summary During the spontaneous differentiation (day 5 to day 15 of the culture) of Caco-2 cells, the sulfation of cell layer glycosaminoglycans increased, whereas protein kinase C activity was concomitantly redistributed from the membrane to the cytosol. The protein kinase C activators, 4-phorbol 12-myristate, 13-acetate and 1,2-dioctanoyl-glycerol inhibited glycosaminoglycan sulfation. By contrast, 4-phorbol 12, 13 didecanoate was ineffective.These results suggest that membrane-bound PKC may exert a modulatory effect on glycosaminoglycan sulfation, and this effect is gradually attenuated as Caco-2 cell differentiation progresses.     

Effect of protein kinase C activation and depletion on insulin stimulation of glycogen synthesis in cultured hepatoma cells

Summary Insulin stimulation of glycogen synthesis was nearly abolished in hepatoma cells shortly treated with 4 ß-phorbol 12 \-myristate, 13 -acetate (protein kinase C activation) but remained unmodified in cells chronically treated with the phorbol ester (protein kinase C depletion). Thus, although exogenous activation of protein kinase C results in an inhibition of insulin action, protein kinase C depletion has no influence on this process. The results suggest that, in hepatoma cells, no endogenous activation of protein kinase C may occur in response to the signal triggered by insulin.     

Pharmacodynamic profile of CQP 201-403, a novel 8α-amino-ergoline

Summary The profile of action in animals of CQP 201-403, a novel 8-amino-ergoline, is in most aspects that of a very potent dopaminomimetic, both as a prolactin secretion inhibitor, and at the levels of the CNS and the cardiovascular system. Qualitatively CQP 201-403 differs slightly from bromocriptine and apomorphine in its effects on the CNS (no influence on serotonin metabolism in the rat cortex; induction of masculine mounting behavior in rats) and the cardiovascular system of the dog (reflex tachycardia in response to a blood-pressure fall). In man the new compound proved to be highly active in lowering prolactin serum levels and to be more potent than bromocriptine (Parlodel^®).In memory of Dr Annemarie Closse, who died 14 June 1987.     

一种防空C~3I系统的效能分析方法

本文讨论了一种评定C~3I系统效能的方法。这种方法是根据系统完成使命的能力和系统的内部结构两方面的分析来完成的。通过对IFFN系统的评定,对本方法进行了举例说明。     

Feller—Trotter算子的局部饱和定理

利用Bajsanski-Bajanic抛物线引理建立Feller-Trotter算子的局部小“ο”饱和定理,进一步地应用所得到结论建立了(C_)类算子半群概率表示的局部饱和定理。     

Proopiomelanocortin expression in the skin during induced hair growth in mice

We demonstrate for the first time a hair cycle-dependent gene and protein expression of proopiomelanocortin in mouse skin in vivo. Northern blot detected POMC mRNA with an apparent size of 0.9 kb in anagen but not telogen skin. Western blot emphasized a specific protein of 30–33 kDa recognized by anti -endorphin in late but not early anagen or telogen skin. By immunocytochemistry, -endorphin antigen was localized in the sebaceous gland in a hair cycle dependent manner.     

Preferential excretion of glycated albumin in C57BL-Ks-J mice: Effects of diabetes

Urinary excretion of glycated albumin was quantitated in genetically hyperglycemic mice (C57BL-Ks-J, db/db mice), a model for non-insulin-dependent diabetes mellitus, and compared with their non-diabetic littermates. The data indicated a preferential excretion of glycated albumin in non-diabetic mice. This phenomenon of editing of glycated albumin is decreased significantly in diabetic mice. Quantitative measurements of overall excretion of glycated albumin suggested that the loss of editing in diabetic mice is due to the dilution of glycated albumin by the unmodified albumin which is excreted in large amounts in diabetic mice. Therefore, the loss of editing observed in this model resembled the one we characterized in insulin-dependent diabetic humans and a streptozotocin-diabetic rat model³.