深层培养技术在食用菌产业中的应用

本文介绍我国食用菌产业现状和深层培养技术在食用菌产业中四个方面的应用;获得高白蛋菌丝;制备药物;开发利用野生菌途径之一;液体菌种制备。运用深层培养技术原理提出这一技术应用广泛的理论依据。针对深层培养技术存在的问题提出相应对策。     

DNA fingerprinting transforms the art of cell authentication.

The increasing diversity of new cell cultures is seriously stretching the capabilities of traditional methods of identification. DNA fingerprinting is set to play an important role in increasing confidence in the authenticity of cultures in research and industry.     

用钼蓝反应动力学方法作微量磷的分光光度测定

提出用ｄ－葡萄糖试剂做钼蓝反应的还原剂测定磷的动力学方法。用吸光度监测反应速度，用假一级反应的关系式测定了反应速度与磷浓度的线性范围为０．６～２．５μｇ／ｍＬ。用内标法计算五种土壤样品中的含磷量，分析结果与常规方法比较，符合程度令人满意。     

KNA算法计算单零点多项式全部零点的复杂性

证明用KNA算法计算n次单零点多项式全部零点所需的多项式计值次数不超过O(n~3 log_2(n/ε)),其中ε是计算精度。     

Prediction of the structure of a receptor-protein complex using a binary docking method.

To validate procedures of rational drug design, it is important to develop computational methods that predict binding sites between a protein and a ligand molecule. Many small molecules have been tested using such programs, but examination of protein-protein and peptide-protein interactions has been sparse. We were able to test such applications once the structures of both the maltose-binding protein (MBP) and the ligand-binding domain of the aspartate receptor, which binds MBP, became available. Here we predict the binding site of MBP to its receptor using a 'binary docking' technique in which two MBP octapeptide sequences containing mutations that eliminate maltose chemotaxis are independently docked to the receptor. The peptides in the docked solutions superimpose on their original positions in the structure of MBP and allow the formation of an MBP-receptor complex. The consistency of the computational and biological results supports this approach for predicting protein-protein and peptide-protein interactions.     

Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.     

苯乙烯基取代的缩杂环卓酮化合物的合成

探讨了３－肉桂酰基酚酮及其亲电取代产物与盐酸羟氨和盐酸苯肼的反应，合成了１０个苯乙烯基取代的缩杂环酮新化合物，并用元素分析及光谱分析证实了它们的结构。     

Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1.

Neurofibromatosis type I (NF1) is one of the most common single-gene disorders that causes learning deficits in humans. Mice carrying a heterozygous null mutation of the Nfl gene (Nfl(+/-) show important features of the learning deficits associated with NF1 (ref. 2). Although neurofibromin has several known properties and functions, including Ras GTPase-activating protein activity, adenylyl cyclase modulation and microtubule binding, it is unclear which of these are essential for learning in mice and humans. Here we show that the learning deficits of Nf1(+/-) mice can be rescued by genetic and pharmacological manipulations that decrease Ras function. We also show that the Nf1(+/-) mice have increased GABA (gamma-amino butyric acid)-mediated inhibition and specific deficits in long-term potentiation, both of which can be reversed by decreasing Ras function. Our results indicate that the learning deficits associated with NF1 may be caused by excessive Ras activity, which leads to impairments in long-term potentiation caused by increased GABA-mediated inhibition. Our findings have implications for the development of treatments for learning deficits associated with NF1.