北京谱仪Ⅱ（BESⅡ）顶点探测器数据获取系统

北京谱仪（ＢＥＳⅡ）顶点探测器数据获取系统是北京谱仪数据获取系统的一部分，该子系统电子学采用快总线标准，本文描述了该系统的硬件结构和软件系统，软件包括快总线系统的微码软件和上层控制软件，该系统的死时间为１．５ｎｓ，对ＢＥＳⅡ系统总死时间的贡献小于０．５ｍｓ。     

3^n阶矩阵乘法的分块算法

针对３＾ｎ阶矩阵的乘法运行，给出了一种分块算法，其乘法运行量比常规的矩阵乘法计算方法和补零的基－２算法都有所减少。     

含油废水处理

在水量水质调查的基础上，本文提出了以出水回用为目的的含油废水隔油调节沉淀－混凝沉淀－砂滤处理工艺，动态模型试验表明，废水中油和ＣＯＤ的去除率分别达到９５％和９０％，出水浊度低于２，此水质完全可回用于有关生产车间。     

InGaAs（P）分别限制应变单量子阱激光器的优化设计

针对较常用的ＩｎＧａＡｓ（Ｐ）分别限制应变单量子阱激光器，给出了为得到最大净增益的优化设计参数。对于激射波长为１．５５μｍ的无应变激光器，最佳的光限制层波长为１．２４μｍ，厚度为１００ｎｍ。当阱材料引入压缩应变后．由于价带的有效状态密度减小，量子阱激光器的微分增益变大，阱深的增大对增大线性增益的效果更加明显．所以最佳光限制层的波长将变短，为１．２０μｍ     

Effects of EGb 761 on nitric oxide and oxygen free radicals, myocardial damage and arrhythmia in ischemia-reperfusion injury in vivo

The cardioprotective effects of EGb 761 on the release of nitric oxide (NO), the concentration of serum thiobarbituric acid reaction substance (TBARS), the activity of creatine kinase (CK) and the incidence of ventricular arrhythmias were investigated in myocardial ischemia-reperfusion injury in vivo. Using sodium nitrite (NaNO2) as standard source of nitric oxide (NO), we compared the correlation coefficients of the three measuring methods used currently in the determination of NOFe2+(DETC)2 complex with that of the measuring method suggested in this study. The result showed that measuring the whole height of three splitting signals is the best linear correlation to the concentration of NO comparing with other methods in this system. Using this method, we observed the effects of EGb 761 on NOFe2+(DETC)2 complex in myocardial ischemia-reperfusion injury in vivo. The hearts of the Wistar rats were subjected to 30 min of ischemia and 10 min of reperfusion in vivo. Different doses of EGb 761 (25, 50, 100, 200 mg/kg i.p.), superoxide dismutase (SOD, 10(4) U/kg), l-arginine (50 mg/kg i.p.) and nitric oxide synthase (NOS) inhibitor NG-nitro-l-arginine (NNA, 50 mg/kg i.p.) were administered to the ischemia-reperfusion rats. EGb 761 under the dose of 100 mg/kg increased the signal intensity of NOFe2+(DETC)2 complex, while EGb 761 at 200 mg/kg showed an effect of decreasing the signal intensity of NOFe2+(DETC)2 complex. EGb 761 inhibited the formation of TBARS, the release of CK, and mitigated the incidence of ventricular arrhythmias in a dose dependent way. Both l-arginine and SOD increased the signal intensity of NOFe2+(DETC)2 complex and inhibited the formation of TBARS, the leakage of CK and the incidence of ventricular arrhythmia. NNA not only had no protective effects on myocardial injury, but also increased the incidence of reperfusion-induced arrhythmia. In conclusion, EGb 761 has cardiovascular protective effects by means of adjusting the level of NO and inhibiting oxygen free radicals induced lipid peroxidation in myocardial ischemia-reperfusion injury in vivo.