Controlled synthesis of HBsAg in a differentiated human liver carcinoma-derived cell line.

A significant aspect of primary hepatic carcinoma in man is the high positive correlation of hepatocellular carcinoma with infection with hepatitis B virus (HBV)1. Analysis of the relationship between HBV infection and oncogenesis is difficult because natural infection with HBV is limited to man and experimental infection has been achieved only in chimpanzees and gibbons. Furthermore, because HBV has not been successfully propagated in cell culture, basic study of virus-cell interaction of the aetiological agent of one of the most widespread infections of man has been impossible. Recently, however, a cell line (PLC/PRF/5) derived from a human hepatoma biopsy was described which produces the HRV surface antigen (HBsAg) and so provides a tool for the experimental investigation of HBV in viro. We now report the derivation and characterisation of two additional cell lines primary liver carcinomas. In contrast to the PLC/PRF/5 cell line, these cell lines retain the capacity to synthesise many human plasma proteins, including both albumin and alpha-fetoprotein (AFP). One of these lines also produces BHsAg. We also present evidence that HBsAg synthesis and secretion in this cell line are correlated with the growth state of the culture. This finding is in contrast to the continuous HBsAg production found in the PLC/PRF/5 cell line.     

Crystallographic studies on the activity of glycogen phosphorylase b

High resolution studies on the crystal structure of glycogen phosphorylase b have identified the catalytic site to which the substrate glucose-1-phosphate binds strongly with some local conformational changes. The site is situated 8 A (phosphate-to-phosphate distance) from pyridoxal phosphate, an essential cofactor of all glycogen phosphorylases. The catalytic site is 33 A from the site in the N-terminal portion of the molecule to which adenine nucleotides bind. In contrast to phosphorylase a (the active form of the enzyme which is phosphorylated at Ser 14), the positions of the first 19 residues of phosphorylase b are not well defined.     

昆虫精子获能与顶体反应的研究

综述了近年来国内外在昆虫精子获能与顶体反应方面的研究概况,并系统地简述了昆虫精子顶体复合体基本结构,以及目前用于动物精子获能与顶体反应方面先进的方法和技术,同时对昆虫受精机理的研究进行了展望     

中祁连地块东段元古宙基底湟源群沉积构造环境

通过对中祁连地块东段元古宙基底湟源群原岩建造及其地球化学特征的研究,认为：湟源群主要由各种千枚岩、片岩、变粒岩、大理岩、石英岩和斜长角闪岩等组成的中浅变质的表壳岩组合;其原岩为一套由陆源碎屑岩、不纯碳酸盐岩、中基性大山岩等组成的火山岩沉积岩组合;湟源群中变质沉积岩系中沉积韵律、沉积条带构造的广泛发育以及浊积层的存在等,指示了其原岩建造具有复理石或类复理石建造的特征;其中变质杂砂岩的地球化学特征类似于大陆岛弧或安底斯岛弧型杂砂岩的特征;湟源群变质中基性火山岩的地球化学特征类似于岛弧或活动大陆边缘的钙碱性火山岩的特征。经综合分析得出,湟源群沉积构造环境可能为陆缘弧后盆地且靠近大陆一侧。     

极性小分子助剂对六甲基二硅氮烷改性纳米SiO2的作用机理

选择水、乙醇作为助剂,利用六甲基二硅氮烷(HMDS)在气固流化床中对纳米SiO2进行表面改性处理,采用FT—IR、TEM等多种手段表征了HMDS对纳米SiO2的改性效果。水和乙醇的引入能有效提高HMDS对纳米SiO2的改性效果及纳米SiO2的疏水程度,改善其在有机相中的分散性。极性小分子助剂在HMDS改性纳米SiO2中的作用机理分析表明：水可以促进HMDS水解。又可以补充纳米SiO2的表面羟基;乙醇一方面与纳米SiO2发生酯化反应,另一部分作为分散HMDS的溶剂。     

Abnormal mast cells in mice deficient in a heparin-synthesizing enzyme.

Heparin is a sulphated polysaccharide, synthesized exclusively by connective-tissue-type mast cells and stored in the secretory granules in complex with histamine and various mast-cell proteases. Although heparin has long been used as an antithrombotic drug, endogenous heparin is not present in the blood, so it cannot have a physiological role in regulating blood coagulation. The biosynthesis of heparin involves a series of enzymatic reactions, including sulphation at various positions. The initial modification step, catalysed by the enzyme glucosaminyl N-deacetylase/N-sulphotransferase-2, NDST-2, is essential for the subsequent reactions. Here we report that mice carrying a targeted disruption of the gene encoding NDST-2 are unable to synthesize sulphated heparin. These NDST-2-deficient mice are viable and fertile but have fewer connective-tissue-type mast cells; these cells have an altered morphology and contain severely reduced amounts of histamine and mast-cell proteases. Our results indicate that one site of physiological action for heparin could be inside connective-tissue-type mast cells, where its absence results in severe defects in the secretory granules.     

Leptin reverses insulin resistance and diabetes mellitus in mice with congenital lipodystrophy.

Congenital generalized lipodystrophy (CGL) is a rare autosomal recessive disorder characterized by a paucity of adipose (fat) tissue which is evident at birth and is accompanied by a severe resistance to insulin, leading to hyperinsulinaemia, hyperglycaemia and enlarged fatty liver. We have developed a mouse model that mimics these features of CGL: the syndrome occurs in transgenic mice expressing a truncated version of a nuclear protein known as nSREBP-1c (for sterol-regulatory-element-binding protein-1c) under the control of the adipose-specific aP2 enhancer. Adipose tissue from these mice was markedly deficient in messenger RNAs encoding several fat-specific proteins, including leptin, a fat-derived hormone that regulates food intake and energy metabolism. Here we show that insulin resistance in our lipodystrophic mice can be overcome by a continuous systemic infusion of low doses of recombinant leptin, an effect that is not mimicked by chronic food restriction. Our results support the idea that leptin modulates insulin sensitivity and glucose disposal independently of its effect on food intake, and that leptin deficiency accounts for the insulin resistance found in CGL.