Hydriding and Dehydriding Characteristics of Mechanically Alloyed LaMg_(17) Ni Composite Material

Magnesiumandmagnesiumalloyshavebeenin vestigatedashydrogenstoragematerialsforseveralde cadesbecausefarmorehydrogenbyweightcanbestoredinthemthaninmostoftheothercurrentlyknownhydrogenstoragealloys .Moreover ,thehighnaturalabundanceofMg ,itslightmassandenviron mentalcompatibilitypotentiallymakemagnesiumoneofthemostprospectivecandidatesforfuturehydrogenstoragematerials .Unfortunately ,thepracticalappli cationofMganditsalloyshasbeenlimitedonlytocertainstoragedevicebecauseoftheirpoorhydriding dehydr…     

有色金属行业信息化述评

通过大量调查资料 ,分析有色金属行业信息化建设的现状、存在的差距和问题 ,探讨了有色信息化建设面临的形势和要求、方向和任务。     

酚醛树脂复合板在热连轧机中的应用

重点分析了现有F7机架出口导卫装置的情况。原导卫材料是由铸钢制造 ,由于摩擦和高温常常引起热连轧带钢表面划伤 ,根据现场实际情况用酚醛树脂复合板替代铸钢导卫装置。实践表明 ,这种改造即可行又可靠 ,并取得了好的效果     

NMR structure and mutagenesis of the FADD (Mort1) death-effector domain

When activated, membrane-bound receptors for Fas and tumour-necrosis factor initiate programmed cell death by recruiting the death domain of the adaptor protein FADD to the membrane. FADD then activates caspase 8 (also known as FLICE or MACH) through an interaction between the death-effector domains of FADD and caspase 8. This ultimately leads to the apoptotic response. Death-effector domains and homologous protein modules known as caspase-recruitment domains have been found in several proteins and are important regulators of caspase (FLICE) activity and of apoptosis. Here we describe the solution structure of a soluble, biologically active mutant of the FADD death-effector domain. The structure consists of six antiparallel, amphipathic alpha-helices and resembles the overall fold of the death domains of Fas and p75. Despite this structural similarity, mutations that inhibit protein-protein interactions involving the Fas death domain have no effect when introduced into the FADD death-effector domain. Instead, a hydrophobic region of the FADD death-effector domain that is not present in the death domains is vital for binding to FLICE and for apoptotic activity.     

建立数据库用微机进行钻井液设计

为了更好地指导现场钻井液施工,利用微机建立有关数据库和相应的设计软件,根据地质、工程的要求和井下情况进行钻井液设计,其特点是资料全面、程序运行可靠且操作简便,设计符合现场情况,施工顺利。在千12区块,用微机设计的109口井与人工设计的75口井相比,钻井速度提高,井下复杂情况减少,提高了经济效益。     

用于生产甲基丙烯酸的杂多酸催化剂的研究

以异丁烯为原料的两段直接氧化生产甲基丙烯酸最新工艺有许多优点。其技术关键在于研制出高效的甲基丙烯醛选择性氧化催化剂。本文报道P-Mo-As-Cu杂多化合物催化剂的组成、制备条件对催化剂活性的影响。经优化后获得高选择性、高活性的二段氧化催化剂，其甲基丙烯酸收率达60％以上。     

���þ��ܰ�ȫ�Բ�������������

本文通过对在用钻机井架的现场实际测试,建立数据库、测评模型,对实测的数据用计算机技术进行分析,提出了初始弯曲应力;数据正态分布检验——x～2检验;建立回归方程;在给定置信度下测评当前承载能力的技术概念。解决了在用钻机A型井架的安全性评估问题,是一种较为合理、可靠、科学的测评技术和方法。     

含淀粉聚乙烯膜的时控光降解研究

使用复合光降解剂，得到了可光降解的生物降解膜。对膜的光降解进行了考察，并对影响光降解的因素进行了讨论，结果表明，我们所制得的膜是一种较好的时控光降解膜。     

Protein C Osaka 10 with aberrant propeptide processing: loss of anticoagulant activity due to an amino acid substitution in the protein C precursor

We studied the molecular basis of protein C deficiency in a family with a history of thromboembolic disease. An approximately 50% reduction in anticoagulant activity despite normal levels of protein C amidolytic activity and antigen was detected in plasma from the proband. All the exons and intron/exon junctions of the protein C gene were studied using a strategy that combined polymerase chain reaction amplification with DNA sequencing of the amplified fragments. We identified a C-to-A change at nucleotide number 1387 of the protein C gene in the proband and his mother, and this mutant was designated protein C Osaka 10. The C-to-A change resulted in the substitution of Ser for Arg at position -1, which is the processing protease cleavage site. The mutant protein C was partially purified from plasma of the patient's mother using barium adsorption followed by ion-exchange column chromatography. It eluted at the same sodium chloride concentration as normal protein C, and thus gamma-carboxylation of the mutant protein appeared to be normal. The apparent molecular weight of this mutant protein C was the same as that of the normal protein on immunoblotting. Amino-terminal sequence analysis showed that the light chain of the mutant protein C had an additional Ser at position-1. Thus, the loss of anticoagulant activity of protein C Osaka 10 can be explained by alteration of the conformation of the Gla domain by the additional Ser in the mutant molecule.