浅议运动后骨骼肌疲劳的原因

疲劳是人或动物对体力训练失去反应能力．内环境发生紊乱的具体表现，本文阐述了引起疲劳的几个主要原因．     

Induction of autotomy in the American bird grasshopperSchistocerca americana (Drury) by the ecdysone agonist RH-5849 and investigation of its mode of action

The non-steroidal ecdysone agonist RH-5849 (1,2-dibenzoyl-l-tert-butylhydrazine) was found to be an effective neurotoxicant on injection into the American bird grasshopper,Schistocerca americana (Drury). Treated grasshoppers became immediately hyperactive, followed by loss of coordination, paralysis and eventually death. We also discovered that this compound induced bilateral autotomy of the metathoracic legs during the early stages of intoxication. However, no evidence of ecdysonergic or morphogenetic activities was observed. Synergism studies with neurotoxins of known mode of action suggested that RH-5849 has a mechanism of action similar to that of 4-amino pyridine, which blocks potassium channels.     

42CrMo钢回火方程的建立

通过回归分析给出了４２ＣｒＭｏ钢的回火硬度、回火温度及回火时间的函数关系式。该关系式具有精度高，使用方便。同时分析了回火参量Ｐ＝ｆ［Ｔ（Ｃ＋ｌｇτ）］的算法，指出了其存在较大误差的原因     

高等化学教育与市场经济研究

试从高等化学教育与市场经济发展的历史必然生活动同步等方面分析论述，从而揭示高等化学教育与市场经济两者相互依存和相互促进的关系。     

仿射Weyl群族afs（W）s∈R的结构

本文给出有限维单李代数g( )的s-仿射Weyl群afs(W) (s∈R)的定义 ,讨论了这类变换群的结构性质 .并且证明了以下结论 : 对每个s∈R ,s-仿射Weyl群afs(W)同构于仿射型Kac -Moody代数g(A)的Weyl群W ; 对s∈Z ,afs(W)可由af1 (W)生成 . 对于每个λ∈η s 设Wλ 是λ在W中的稳定子群 ,则afs(Wλ)=(Wafs) λ, λ是λ在 η 上的投影     

微机控高精度高压脉冲电源的研制

介绍利用大功率绝缘栅极晶体管(IGBT)配合脉冲升压变压器组成的高精度高压脉冲电源。该电源利用复杂可编程逻辑器件(CPLD)产生触发信号，通过微机、单片机、CPLD实现脉冲频率、脉冲宽度和脉冲个数的微机控制。且脉冲宽度能够以1μs步长增减，满足了脉冲电场非热效应处理技术应用的研究。     

射序对多管火箭武器性能影响

研究多管火箭射击顺序对其振动特性和密集度等系统性能的影响，为优化射击顺序提高射击密集度提供直接的方法。应用多体系统传递矩阵法和发射动力学理论，建立了多管火箭武器射击顺序与多管火箭武器系统性能之间的定量关系。对某多管火箭武器不同射击顺序下对应的振动特性和密集度进行数值仿真。仿真结果表明多管火箭武器不同射击顺序下的振动特性和密集度不同。该文方法为优化射击顺序提高射击密集度提供了直接的方法。     

高效液相色谱法检测蜂蜜中残留的抗生素

采用高效液相色谱、紫外检测器、C18,10μm,300mm×4.6mm色谱柱,波长348nm,CH3CN:0.05mol/LH3PO4(V:V)=60:40流动相,对蜂蜜中的残留四环素、土霉素和金霉素进行了检测。方法检出限分别为: 四环素、土霉素为0.03mg/L,金霉素为0,06mg/L。结果令人满意。     

Minimum information about a microarray experiment (MIAME)-toward standards for microarray data.

Microarray analysis has become a widely used tool for the generation of gene expression data on a genomic scale. Although many significant results have been derived from microarray studies, one limitation has been the lack of standards for presenting and exchanging such data. Here we present a proposal, the Minimum Information About a Microarray Experiment (MIAME), that describes the minimum information required to ensure that microarray data can be easily interpreted and that results derived from its analysis can be independently verified. The ultimate goal of this work is to establish a standard for recording and reporting microarray-based gene expression data, which will in turn facilitate the establishment of databases and public repositories and enable the development of data analysis tools. With respect to MIAME, we concentrate on defining the content and structure of the necessary information rather than the technical format for capturing it.     

Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency

Collagen VI is an extracellular matrix protein that forms a microfilamentous network in skeletal muscles and other organs. Inherited mutations in genes encoding collagen VI in humans cause two muscle diseases, Bethlem myopathy and Ullrich congenital muscular dystrophy. We previously generated collagen VI-deficient (Col6a1-/-) mice and showed that they have a muscle phenotype that strongly resembles Bethlem myopathy. The pathophysiological defects and mechanisms leading to the myopathic disorder were not known. Here we show that Col6a1-/- muscles have a loss of contractile strength associated with ultrastructural alterations of sarcoplasmic reticulum (SR) and mitochondria and spontaneous apoptosis. We found a latent mitochondrial dysfunction in myofibers of Col6a1-/- mice on incubation with the selective F1F(O)-ATPase inhibitor oligomycin, which caused mitochondrial depolarization, Ca2+ deregulation and increased apoptosis. These defects were reversible, as they could be normalized by plating Col6a1-/- myofibers on collagen VI or by addition of cyclosporin A (CsA), the inhibitor of mitochondrial permeability transition pore (PTP). Treatment of Col6a1-/- mice with CsA rescued the muscle ultrastructural defects and markedly decreased the number of apoptotic nuclei in vivo. These findings indicate that collagen VI myopathies have an unexpected mitochondrial pathogenesis that could be exploited for therapeutic intervention.