实验性免疫应激雏鸡胸腺T细胞研究

用ND（新城疫）I系疫苗大剂量肌肉注射2周龄雏鸡的方法建立实验性免疫应激模型，检测胸腺中CIM＋、CD8＋T细胞动态变化以及超微结构变化．结果显示：免疫应激前期（1—5d）表现为CIM＋T细胞数目减少，CD8＋T细胞数目增加的趋势；部分T细胞发生凋亡，并且是一个逐渐加剧的过程，呈现从凋亡到坏死的病理学变化过程．     

广义凸集值向量优化问题的弱有效解

在序线性拓扑空间中定义了广义凸集值映射．引进了相对内部．应用凸集分离定理建立了一个广义凸集值映射的择一性定理．运用此定理获得了弱有效解意义下的集值向量优化问题的最优性条件．     

急性力竭游泳后小鼠血液成分变化的动态观察

为了观察急性力竭游泳对小鼠血液成分的影响,分别于小鼠力竭游泳停止后0(即刻)、1、4、8和24 h时进行尾静脉取血,测定了其白细胞、红细胞、血小板和血红蛋白等指标.结果表明:白细胞的数量在小鼠力竭游泳后0 h为(8.46±3.20)×109/L,与对照组的(10.65±2.29)×109/L比较明显减少(P＜0.05);在4 h时为(17.67±3.41)×109/L,与对照组比较显著增多(P＜0.01);在8 h以后恢复正常.红细胞的数量在小鼠力竭游泳后4 h时为(9.99±0.95)×1012/L,与对照组的(10.87±0.79)×1012/L比较明显减少(P＜0.05);在8h以后恢复正常.血小板的数量在小鼠力竭游泳后1、4、8和24 h时分别为(856.5±129.0)×109、(859.5±67.9)×109、(874.1±96.5)×109和(875.7±124.8)×109/L,与对照组的(721.5±115.7)×109/L比较均明显增多(P＜0.05).说明急性力竭游泳对小鼠血液中不同成分的作用存在差异,在一定时间内导致红细胞数减少、血小板增多和白细胞数先降后升的现象.     

骨髓干细胞与急性心肌梗死的血管新生

骨髓干细胞可分化为心肌细胞、血管内皮细胞、平滑肌细胞等，能再生心肌和血管，可用于心肌梗死的治疗。本文就骨髓干细胞在血管新生方面的生物学特性及其对心梗后的血管新生作用作一综述。     

生物种群增长模型的研究

根据种群生物量增长模式,提出一种新的种群增长的数学模型.该模型改进了Logistic模型,可以用来描述种群数量随时间和环境条件变化的增长规律,具有更广泛的代表性和适用性.在新的模型中,Logistic模型仅为它的一个特例.     

精巢间质细胞雄激素合成及其调节的研究进展

本文综述了近年来精巢间质细胞雄激素的合成及其分泌调节的研究进展。间质细胞内的雄激素合成的限速步骤是胆固醇转化为孕烯醇酮时的胆固醇跨线粒体膜转运。在此转运过程中，PBR可能是作为依赖于配体的通道蛋白，对胆固醇分子进行跨膜转移；StAR则通过解离线粒体膜与胆固醇分子的吸附作用，加速了胆固醇分子的转运。雄激素的合成还受垂体、支持细胞、巨噬细胞和其自身分泌激素和细胞因子的调控。同时对今后研究的方向做了总结和展望。     

B-样条曲面的G1连续性

得到了关于两个双三次内部重结点B-样条曲面片G1连续的充分必要条件和在公共边界线上控制向量的本征条件,这些条件直接由两个B-样条曲面的控制向量表示.利用本文所给的条件,得到了具有局部性质且是真正G1光滑的曲面模型.     

Inhibitory effect of the adenovirus type 5 E1A protein expressed in the yeast system

The human adenovirus type 5 E1A, a tumor- suppressor gene[1], codes for two major related proteins of 243 amino acids (12S) and 289 amino acids (13S) by al-ternative splicing in two exons[2]. Studies have been shown that E1A can regulate expression of many genes and cell cycle[3]. Both in vitro and in vivo experiments indicated that E1A could induce tumor cells differentia-tion, convert tumor cells into an epithelial phenotype, in-hibit tumor cell growth and metastasis and strongly en-ha…     

Mechanical Studies on Treatment of Malignant Tumour by Ultralow Frequency Pulsed-Gradient Magnetic Fields

Ultralow frequency (ULF) pulsed-gradient magnetic field (with the maximum intensity of 0.6-2.0 T, gradient of 10-100 T·m-1, pulse width of 20-200 ms and frequency of 0. 16-1. 34 Hz) treatment of mice can inhibit murine malignant tumour growth and can induce apoptosis of cancer cell. The apoptotic cancer cell contracted, became rounder and divorced from adjacent cells; the heterochromatin condensed and coagulated together along the inner side of the nuclear membrane; the endoplasmic reticulums expanded and fused with the cellular membrane; many apoptotic bodies which were packed by the cellular membrane appeared and were devoured by some lymphocytes and plasma. By Lorentz force the magnetic field keeps the moving ions within bounds of Larmor radius. Thus, penetrating capability of the positive and negative ions through the cell membrane was affected, even the role on the cell membrane formed.     

Compact difference approximation with consistent boundary condition

For simulating multi-scale complex flow fields it should be noted that all the physical quantities we are interested in must be simulated well. With limitation of the computer resources it is preferred to use high order accurate difference schemes. Because of their high accuracy and small stencil of grid points computational fluid dynamics (CFD) workers pay more attention to compact schemes recently. For simulating the complex flow fields the treatment of boundary conditions at the far field boundary points and near far field boundary points is very important. According to authors' experience and published results some aspects of boundary condition treatment for far field boundary are presented, and the emphasis is on treatment of boundary conditions for the upwind compact schemes. The consistent treatment of boundary conditions at the near boundary points is also discussed. At the end of the paper are given some numerical examples. The computed results with presented method are satisfactory.