采用系统理论思想实现新一代防病毒技术

本文从防病毒角度把病毒分为三类：可检测型病毒、半可检测型病毒和非检测型病毒；提出系统状态转移网络这一中心概念，根据系统状态的可测性、状态间的相容性和循环性来判别ＤＯＳ系统的安全性，并提出了仿真检测判别技术。新一代防病毒技术从传统地剖析病毒转移到ＤＯＳ系统状态的研究，为全面预防各种计算机病毒奠定了系统理论基础。     

软件补偿方法在测温智能仪表中的应用

软件补偿方法具有效果好、精确度高、成本低的优点。介绍了在研制多点巡回检测仪中采用的几种软件补偿方法：前向通道特性补偿使放大器等元件不因外界条件的变化而受到任何影响；引线电阻的补偿可实现引线电阻对系统无任何影响；热电阻、热电偶的非线性度补偿效果明显，节省开销。     

大尺寸YBa2Cu3O7—δ超导体的研制

利用固相反应法成功地制备了直径为100mm,厚为5mm的大尺寸YBa_2Cu_3O_(7-δ)超导体。在通氧,930℃热处理45min后,超导体的上限转变温度为94K,零电阻温度为92K。x射线衍射进行物相定性,扫描电镜进行形貌和超导电性关系的对比观察。选区电子衍射给出YBa_2Cu_3O_(7-δ)超导体的晶格参数为a=0.348nm,b=0.377nm,c=0.716nm,属于正交晶系。     

偏头痛的遗传:从性性状的遗传假说

偏头痛被公认为一种家族高聚集性神经系统疾病 ,尽管欧美白种人群的患病率远高于亚洲人种 ,但全球范围内的患病率女性是男性的 2～ 4倍却是恒定的 .临床及遗传医学仅仅沿用常染色体显性或染色体隐性遗传、多基因遗传及线粒体遗传理论均不能满意地解释所有家系的特征 ,笔者率先在国际上提出的从性性状遗传模式sex conditionedgeneticmodel(即男性为常隐、女性为常显遗传 )似可较好地解释偏头痛复杂的“不一致”的遗传方式 .自然界中的生物体内一条染色体的基因会对另一条染色体致病基因的表达实施功能调控 ,此种遗传疾病范例在遗传性秃顶、肝豆状核变性等症中已得到验证 .当然对于环境的因素也有待考虑 ,时下对于复杂遗传病的研究正是最富有挑战性的 .     

一种新型粘土稳定剂的合成与应用研究

本文简要报导了有机阳离子聚和物(氯化N,N—二甲基二烯丙基铵—二氧化硫)的合成方法,并对其作为粘土稳定剂的性能进行了评价。结果表明,该共聚物稳定粘土的能力高于目前国内外广泛使用的同类聚合物TDC。     

Ca2+ release induced by inositol 1,4,5-trisphosphate is a steady-state phenomenon controlled by luminal Ca2+ in permeabilized cells.

Low concentrations of inositol 1,4,5-trisphosphate (InsP3) evoke a very rapid mobilization of intracellular Ca2+ stores in many cell types, which can be followed by a further, much slower efflux. Two explanations have been suggested for this biphasic release. The first proposes that the Ca2+ stores vary in their sensitivity to InsP3, and each store releases either its entire contents or nothing (all-or-none release); the second proposes instead that the stores are uniformly sensitive to the effects of InsP3, but that they can release only a fraction of their Ca2+ before their sensitivity is somehow attenuated (steady-state release). Experiments using purified InsP3 receptor molecules reconstituted into lipid vesicles have shown heterogeneity of the receptors in their response to InsP3 under conditions in which the total Ca2+ level at both sides of the receptor is held constant. We now report that in permeabilized A7r5 smooth-muscle cells incubated in Ca(2+)-free medium, the amount of 45Ca2+ remaining in the stores after the rapid transient phase of release is independent of their initial Ca2+ levels, indicating that partially depleted stores are less sensitive to InsP3. Moreover, if the stores are reloaded with 40Ca2+ after the first stimulus, reapplication of the same low concentration of InsP3 will release further 45Ca2+. This recovery of InsP3 sensitivity is almost complete. Under these conditions, Ca2+ release must thus occur by a steady-state mechanism, in which the decreasing Ca2+ content of the stores slows down further release.     

柔性变截面滑移式机械手的控制

研究了柔性变截面滑移式机械手臂的控制。首先，基于有限元法导出系统的动力学方程，然后分别建立了两种控制方式的状态方程：１）以加速度和角加速度作为控制变量：２）以力和力矩作为控制变量。控制过程分为“粗控”和“精控”两步进行。“精控”过程采用线性二次型高斯控制。最后给出了数值模拟的结果。     

Exocytotic fusion is activated by Rab3a peptides.

Studies of intracellular traffic in yeast and mammalian systems have implicated members of the Rab family of small GTP-binding proteins as regulators of membrane fusion. We have used the patch clamp technique to measure exocytotic fusion events directly and investigate the role of GTP-binding proteins in regulating exocytosis in mast cells. Intracellular perfusion of mast cells with GTP-gamma S is sufficient to trigger complete exocytotic degranulation in the absence of other intracellular messengers. Here we show that GTP is a potent inhibitor of GTP-gamma S-induced degranulation, indicating that sustained activation of a GTP-binding protein is sufficient for membrane fusion. We have found that synthetic oligopeptides, corresponding to part of the effector domain of Rab3a, stimulate complete exocytotic degranulation, similar to that induced by GTP-gamma S. The response is selective for Rab3a sequence and is strictly dependent on Mg2+ and ATP. This suggests that sustained activation of a Rab3 protein causes exocytotic fusion. The peptide response can be accelerated by GDP-beta S, suggesting that Rab3a peptides compete with endogenous Rab3 proteins for a binding site on a target effector protein, which causes fusion on activation.