Brain-derived neurotrophic factor prevents neuronal death in vivo

Developing vertebrate neurons are thought to depend for their survival on specific neurotrophic proteins present in their target fields. The limited availability of these proteins does not allow the survival of all neurons initially innervating a target, resulting in the widely observed phenomenon of naturally occurring neuronal death. Although a variety of proteins have been reported to promote the survival of neurons in tissue culture, the demonstration that these proteins increase neuronal numbers and/or decrease neuronal death in vivo has only been possible with nerve growth factor (NGF). The generalization of the concept that neurotrophic proteins regulate neuronal survival during normal development critically depends on the demonstration that the survival of neurons in vivo can be increased by the administration of a neurotrophic protein different from NGF. We report here that this is the case with brain-derived neurotrophic factor, a protein of extremely low abundance purified from the central nervous system.     

Identity of the 19S 'prosome' particle with the large multifunctional protease complex of mammalian cells (the proteasome)

There have been many reports that eukaryotic cells contain ring-shaped 19S or 20S particles which are composed of numerous polypeptide subunits ranging in size between 25 and 35 kilodaltons. Because these particles seemed to copurify with inactive mRNA, they were assumed to function in regulating mRNA translation and hence were named 'prosomes' (for 'programmed-o-some'). A number of properties have been reported for these structures, including an association with specific RNA species or with certain heat-shock proteins and involvement in tRNA processing or aminoacyl tRNA synthesis. However, these proposed activities have not been supported by definitive evidence. During studies of the proteolytic systems in mammalian tissues, we noted many similarities between these 19S particles and the high molecular weight protease complexes that are present in most or all eukaryotic cells. This (700 kilodalton) enzyme complex, designated here as LAMP for 'large alkaline multi-functional protease', contains three distinct endoproteolytic sites which function at neutral or alkaline pH and are specific for hydrolysis of proteins, hydrophobic peptides, or basic peptides. This protease also exists in a latent form which can be activated by polylysine, fatty acids, or ATP. In this report, we show that the prosomes and these protease complexes are very similar or identical with respect to their size, polypeptide composition, immunological cross-reactivity, appearance in the electron microscope, radial symmetry of subunits, subcellular localization, and proteolytic activities. Therefore, the 'prosome' probably plays a critical role in intracellular protein breakdown, and we propose that it be renamed 'proteasome'.     

Chronic ethanol causes heterologous desensitization of receptors by reducing alpha s messenger RNA

One of the biochemical results of ethanol exposure is a change in the amount of the intracellular second messenger cyclic AMP (cAMP) produced in response to receptor stimulation. In general, acute ethanol exposure increases the amount of cAMP produced on stimulation of receptors coupled to the enzyme adenylyl cyclase via the GTP-binding protein Gs, whereas chronic ethanol exposure has the opposite effect (results for receptors coupled via Gi have been more variable). We previously reported that adaptation to continuous ethanol exposure reduces receptor-stimulated cAMP production by 25-35% in a neuroblastoma cell line (NG108-15), and an even greater reduction of 75% was observed in lymphocytes taken from actively-drinking alcoholics. This reduction in receptor-stimulated cAMP levels was recently confirmed in platelets from alcoholics. None of these studies, however, determined whether more than one receptor coupled to adenylyl cyclase activity was affected in the same cell. Here we report that chronic ethanol exposure causes desensitization of heterologous receptors coupled to Gs as cAMP production mediated by prostaglandin E1 as well as by adenosine is reduced by approximately 30% in NG108-15 cells. We show that, after chronic ethanol exposure, the activity of the alpha subunit of Gs is decreased by 29%, the amount of alpha s protein is decreased by 38.5%, and alpha s messenger RNA is decreased by 30%. Thus, cellular adaptation to ethanol involves a reduction in alpha s mRNA and, as a consequence, reduced cAMP production by heterologous receptors coupled to Gs. Such changes in cAMP production may account for the tolerance and physical dependence on ethanol in alcoholism.     

一种新的有限元与边界元的对称耦合方法

本文从弹性力学分区变分原理出发,提出一种新的有限元与边界元的对称耦合方法.与目前通用的超单元形式的对称耦合法相比,本文的方法理论上比较直接,计算上更为经济,易于利用现有的有限元与边界元程序予以实现,也易于推广应用于局部的材料非线性或接触非线性问题,文中通过有限域、无限域及半无限域等问题的算例,对该方法的有效性作了比较全面的验证.     

聚甲醛的分子链柔性研究

Stockmayer以六氟丙酮水合物为溶剂,在25℃时测定了聚甲醛的分子量和特性粘数[η],由此计算出Flory特征比C_∞为10.5,与中等柔性聚苯乙烯的C_∞值接近。作者认为该值偏高,是由于聚甲醛与溶剂形成强的氢键所致。本文以间甲酚(100℃)和对氯苯酚(60℃)为溶剂,采用Salchard-Stockmayer-Fixman外推法求得C_∞为6.19,比聚乙烯的C_∞值还小些,并指出聚甲醛的无扰尺寸与温度的关系不大。还订定了聚甲醛在两种不同溶剂体系中的MHS方程为[η]=3.87×10~(-2)M_η~(0.705) (间甲酚,100℃) [η]=2.00×10~(-2)M_η~(0.79) (对氯苯酚,60℃)     

4DPSK调制中的差分编码与解码

本文以简明、直观的论述方式讨论了4DPSK调制中的差分编码与解码原理,给出一种与差分算法直接对应的简单而实用的电路。     

大熊猫毛发微量元素研究

用原子吸收分光光度法测定了四川野外203只大熊猫(其中包括岷山山系48只、邛崃山系67只)和三个人工饲养场的21只大熊猫毛发及三个饲养场大熊猫精饲料中的Cu、Zn、Mn、Fe、Ca、Mg、K等七种元素的含量,看出:野外健康大熊猫毛发中的这七种元素的含量呈现较好的正态分布;雌性和雄性大熊猫毛发中Mn、Ca、Mg三元素存在着显著性差异;野外大熊猫毛发中的七种元素的含量均高于人工饲养的大猫猫;三个饲养场的大熊猫毛发中的这七种元素含量与他们所食的精饲料有正相关的关系。因此,人工饲养条件下补充适当的微量元素是非常必要的。     

稀土对铬合金铸铁热塑性的影响

本文介绍了加入微量稀土元素可显著提高铬合金铸铁热塑性的试验結果。通过金相显微镜、电子探针、离子探针等手段,研究了稀土元素在铬合金铸铁中对硫、硅、碳化物及夹杂物的影响。初步探讨了稀土元素提高铬合金铸铁热塑性的机理。     

回火方式和时间对高速钢的组织与性能的影响

采用透射电镜、X—射线等手段研究了不同回火方式和时间下 W6Mo5Cr4V2高速纲力学性能与组织的变化。发现淬火该钢经560和630℃多次回火后马氏体内孪晶清晰完整,板条马氏体中仍然存在着以魏氏组织形态分布的 M_3C 型碳化物。证实380℃×(0.5～5)h+560℃×1h×2次的低高温配合回火工艺与560℃×1h×3次的普通回火相比,可使高速钢的硬度、红硬性及冲击韧性提高.采用560℃×(1～3)h×3次的回火工艺时,随每次回火时间延长,高速钢的强度、冲击韧性和断裂韧性提高,红硬性变化不大,但硬度则稍稍下降(约1HRC).