装药结构对传爆药柱起爆能力的影响研究

为了适应钝感弹药对传爆序列提出的新要求,根据炸药冲击起爆理论,研究了凹球形和半球形两种新结构传爆药柱,并对两种新结构传爆药柱与普通圆柱形传爆药柱的起爆威力进行了实验对比.研究结果表明,改变传爆药柱的结构可提高其输出威力,新结构传爆药柱较普通圆柱形传爆药柱的起爆威力有明显提高.研究结果对解决钝感弹药的可靠起爆问题具有重要意义.     

杆式侵彻体冲击起爆反应装甲影响因素研究

该文对杆式侵彻体冲击起爆反应装甲进行了试验研究，分析侵彻体对夹层炸药的盖板、面板的分层侵彻机理，在Held准则基础上，提出了与杆式侵彻体的密度、长度、直径、速度因素有关的冲击起爆反应装甲的关系式。该关系式对于研究对付反应装甲的动能弹具有指导意义，并对反导冲击起爆机制研究具有一定的参考价值。     

OCCL编译器中符号表的研究及设计

OCCL是笔者做的一个新型ANSIC编译器，文中介绍在前人的工作基础上，笔者用哈希表———层次独立对应法以及最迟分配初始化法对OCCL的符号表进行设计。最终结果使编译器的时间开销得到缩减，提高了性能。     

中碳钢缺口疲劳裂纹的萌生及扩展规律的研究

经研究中碳合金结构钢３５ＣｒＭｏ，４２ＣｒＭｏ在不同应力比下（Ｒ＝０．１和Ｒ＝０．３）三点弯曲缺口试件的疲劳裂纹萌生及长，短裂纹的扩展规律，确定了该钢的缺口根部最大应力范围△σｍａｘ和疲劳裂纹萌生周次Ｎｉ的关系及疲劳裂纹萌生门截坎值（△σｍａｘ）ｔｈ，并得出了这两种钢在长，短期纹阶段的扩展规律。     

有机过氧化物与药物体系引发烯类聚合反应的热效应

研究了有机过氧化物（ＢＰＯ）分别与含叔胺基结构的药物（如利福中，奋乃静，水杨酸毒扁豆碱，硝酸毛果芸香碱）组成的引发体系，在４０℃的温度下引发甲基丙烯酸β羟乙酯（ＨＥＭＡ）聚合的放热过程，并与纯ＢＰＯ、ＢＰＯ－ＤＭＴ体系引发ＨＥＭＡ聚合的放热过程比较．实验表明：（１）有机过氧化物与药物引发体系的引发机理与氧化还原引发体系的引发机理相似，其引发活性比ＢＰＯ－ＤＭＴ体系的低．（２）有机过氧化物与药物引发体系，能在４０℃温度下引发ＨＥＭＡ聚合成型，聚合过程放热较为平稳     

学生情绪对体育教学的影响

非智力因素对课堂教学的影响日益受到重视.就非智力因素的一个组成———情绪的重要作用,从情绪的引发、维持、调节控制等几个方面讨论学生情绪对体育教学的重要影响.     

多破片命中时炸药的冲击起爆研究

研究破片撞击炸药的过程中多破片的作用，提出在两破片撞击炸药存在一定的时间间隔和空间间隔距离的情况下炸药的冲击起爆机理，建立工程模型。该研究对于研究反导的协和毁伤效应以及优化反导战斗部的结构具有实际意义。     

聚能射流水中侵爆盖板B炸药仿真研究

为获得聚能射流对水中盖板B炸药侵爆作用能力,开展水层厚度影响规律研究.基于准定常侵彻理论得到了紫铜聚能射流侵彻水介质时射流速度计算式;建立侵爆仿真模型,研究了聚能射流水中成型与运动、侵彻盖板及起爆装药的变化特性,计算给出了射流侵彻盖板前后的速度和直径的变化,结果表明,射流侵爆水中盖板B炸药的临界水层厚度为261 mm,并依据Held判据得出B炸药的起爆阈值为18.598 mm³·μs^-2.研究结果对聚能射流水下毁伤技术的应用提供技术参考.     

Characteristic investigation of trilayered Cu/Al8011/Al1060 composite: Interface morphology,microstructure, and in-situ tensile deformation

In this work, Cu/Al8011/Al1060 trilayered composite with an ultrathin copper layer was fabricated successfully by the hybrid process of cast-rolling and hot-roll-bonding. The effects of heat treatment were investigated on the microstructure and mechanical behavior of the composite. The results showed that annealing temperatures above 300 ​°C led to the formation of new intermetallic compounds that joined their initial counterparts. Also, the interface growth was fast above 340 ​°C. It was found that the annealing temperature of 320 ​°C led to the optimal tensile properties of the composite. Through rolling, hard-brittle IMCs imposed intense plastic strains on the surrounding regions, resulting in further grain refinement of both metals in the vicinity of the interface. Although the kernel average misorientation of the trilayered composite was almost identical with the Cu/Al8011 bimetal, its amount was considerably decreased after heat treatment, as the distorted structure changed into a nearly strain-free one using the restoration phenomenon. The SEM-based in-situ tensile test showed that crack initiation occurred within the IMCs and propagated into the Cu strip, leading to its early fracture. However, the strength-displacement curve during in-situ tensile deformation did not decrease significantly due to the ultrathin copper layer.     

Transient and constitutive repression of cytoplasmic translation signaling in cells with mtDNA mutation

Cytoplasmic translation is under sophisticated control but how cells adapt its rate to constitutive loss of mitochondrial oxidative phosphorylation is unknown. Here we show that translation is repressed in cells with the pathogenic A3243G mtDNA mutation or in mtDNA-less ρ⁰ cells by at least two distinct pathways, one transiently targeting elongation factor eEF-2 and the other initiation factor eIF-2α constitutively. Under conditions of exponential cell growth and mammalian target of rapamycin (mTOR) activation, eEF-2 becomes transiently phosphorylated by an AMP-activated protein kinase (AMPK)-dependent pathway, especially high in mutant cells. Independent of AMPK and mTOR, eIF-2α is constitutively phosphorylated in mutant cells, likely a signature of endoplasmic reticulum (ER)-stress response induced by the loss of oxidative phosphorylation. While the AMPK/eEF-2K/eEF-2 pathway appears to function in adaptation to physiological fluctuations in ATP levels in the mutant cells, the ER stress signified by constitutive protein synthesis inhibition through eIF-2α-mediated repression of translation initiation may have pathobiochemical consequences. Received 29 October 2008; received after revision 11 December 2008; accepted 16 December 2008