含过期火药粉状工业炸药的研究

文章概要论述了一种新型民用炸药－含过期火药粉状工业炸药在配方、制造工艺等方面所进行的实验研究。结果表明，该炸药性能良好、制造技术安全可靠，值得推广。     

抽油机球铁齿轮的化学成分及生产工艺

为提高抽油机减速器齿轮铸件的机械性能，提出以Sn代替Mo作为合金元素，并通过试验确定了合理的Si、Cu、Sn的加入量。指出Si加入量应控制在1．9％－2．1％范围内，同时加入0．36％～0．9％的Cu和0．025％～0．07％的Sn，可保证球铁的强度和延伸率都满足QT700－2的要求。鉴于试件与实际铸件的表面硬度有一定的差值，为提高铸件表面硬度，进行了余热正火试验，并给出了铸件在铸型内的时间－冷却温度曲线。最后根据球铁化学成分的选择结果，进行了齿轮生产试验。     

用αβ谱仪测量人工αβ放射性气溶胶体积活度的试验研究

本文介绍了用αβ谱仪系统同时测量αβ谱、实现Ｒｎ／Ｔｈ子体补偿、确定超铀α核素气溶胶体积活度及人工放射性气溶胶总β体积活度的技术途径。利用ＲａＡ、ＲａＣ′ａ峰的二段时间计数可确定空气中ＲａＡ、ＲａＢ、ＲａＣ的气溶胶体积活度，相应的，也能给出ＲａＢ、ＲａＣ对总β计数的贡献。根据一般环境条件下的平衡比，用ＴｈＣ′的。计数修正Ｔｈ子体对αβ测量的影响。￣［２３９］ｐｕ或／和￣［２４１］Ａｍ人工核素的α计数，可通过两段时间分别扣除ＲａＡ、ＲａＣ′拖尾的方法确定；β计数分别扣除Ｒｎ／Ｔｈ子体β贡献即可确定。在本文规定的测量条件下，对室内天然Ｒｎ子体水平在１５Ｂｑ／ｍ￣３以下，超铀α核素气溶胶体积活度的测量下限可达到０．１Ｂｑ／ｍ￣３；即使在７５Ｂｑ／ｍ￣３环境下，人工核素总β的测量下限也可达ｌＢｑ／ｍ￣３以下。     

Chrestenson函数序列的生成方法及其数学分析

本文提出了适于三种序号的Ｃｈｒｅｓｔｅｎｓｏｎ函数序列的复制方法，对其复制过程进行了数学分析，并指出当Ｃｈｒｅｓｔｅｎｓｏｎ函数退化为Ｗａｌｓｈ函数时，此方法即为复制理论中的平移复制方法。     

Java语言及其虚拟机技术探讨

随着Internet的迅猛发展，Internet编程语言Java愈来愈成为计算机行业的焦点。本文在简述了Java的主要特点后，重点对Java最关键的技术──虚拟机进行了深入的探讨。     

桥丝电阻分布的均匀性对发火电流的影响

文中分析了桥丝电阻分布的均匀性对电雷管发火电流的影响，并对试验结果作了分析和讨论。     

利用计算机进行油气资源评价和勘探决策

本文着重介绍了构成《现代勘探决策理论系统》的5个主要计算机模块,即:生油岩热演化处理、求任意曲边形面积、数学模拟预测资源量、勘探经济评价分析及决策、辅助处理等模块。该系统曾在塔里木盆地和准噶尔盆地的油气资源评价和勘探决策中发挥了作用,受到了专家和用户的好评。     

Substance P modulates NMDA responses and causes long-term protein synthesis-dependent modulation of the lamprey locomotor network

Tachykinin immunoreactivity is found in a ventromedial spinal plexus in the lamprey. Neurons in this plexus project bilaterally and are thus in a position to modulate locomotor networks on both sides of the spinal cord. We have examined the effects of the tachykinin substance P on NMDA-evoked locomotor activity. Brief (10 min) application of tachykinin neuropeptides results in a prolonged concentration-dependent (>24 hr) modulation of locomotor activity, shown by the increased burst frequency and more regular burst activity. These effects are blocked by the tachykinin antagonist spantide II. There are at least two phases to the burst frequency modulation. An initial phase (approximately 2 hr) is associated with the protein kinase C-dependent potentiation of cellular responses to NMDA. The long-lasting phase (>2 hr) appears to be protein synthesis-dependent, with protein synthesis inhibitors causing the increased burst frequency to recover after washing for 2-3 hr. The modulation of the burst regularity is caused by a separate effect of tachykinins, because unlike the burst frequency modulation it does not require the modulation of NMDA receptors for its induction and is blocked by H8, an inhibitor of cAMP- and cGMP-dependent protein kinases. The effects of substance P were mimicked by the dopamine D2 receptor antagonist eticlopride. The effects of eticlopride were blocked by the tachykinin antagonist spantide II, suggesting that eticlopride may endogenously release tachykinins. Because locomotor activity in vitro corresponds to that during swimming in intact animals, we suggest that endogenously released tachykinins will result in prolonged modulation of locomotor behavior.     

Endothelium-dependent effect of perindopril and enalaprilat in rat thoracic aorta

AIM: To study the effect of the angiotensin-converting enzyme (ACE) inhibitors perindopril (Per) and enalaprilat (Ena) on the reactivity of the endothelium in normal rats. METHODS: Male rats were treated intragastrically with Per (2 mg.kg-1.d-1) or placebo (n = 18) for 6 wk. Aorta was isolated for experiment. Another set of isolated aortic rings with and without endothelium were incubated with Ena (0.1 mumol.L-1) for 30 min. Responses to acetylcholine, serotonin, phenylephrine, sodium nitroprusside (SN), and nitroglycerin (Nit) were observed. RESULTS: Endothelium-dependent relaxation to acetylcholine was augmented in aortic rings from rats treated with Per in comparison with control. The IC50 value (95% confidence limits) decreased from 3.8 (0.56-26.1) mumol.L-1 (control group) to 0.98 (0.28-3.41) mumol.L-1 (Per-treated group). The maximal relaxation was augmented from 62 +/- 9% to 78 +/- 10% (P < 0.01). However, the responses to the endothelium-independent vasodilators, SN and Nit, were similar. Serotonin- and phenylephrine-induced contractions were decreased, which were influenced by basal release of endothelium-derived relaxing factor (EDRF). EC50 values was 6.1 (2.6-14.4) nmol.L-1 vs 8.3 (3.6-18.8) nmol.L-1 in comparison with control group and Per-treated group. The maximal contraction was decreased from 2.42 +/- 0.29 g (control group) to 1.96 +/- 0.25 g (treated group) (P < 0.01). Similar results were found in incubation with Ena. CONCLUSION: Ena and Per enhanced the basic release of EDRF from vascular endothelium.     

Neuronal migration disorders increase susceptibility to hyperthermia-induced seizures in developing rats

PURPOSE: Retrospective studies suggest that adult patients with intractable epilepsy may have a history of febrile seizures in childhood. Risk factors for a febrile seizure may include the rate of increase in the core temperature (T-core), its peak (Tmax), the duration of the temperature increase, or an underlying brain pathology. Recently, neuronal migration disorders (NMD) have been diagnosed with increasing frequency in patients with epilepsy, but the link between NMD, febrile seizures, and epilepsy is unclear. We studied rat pups rendered hyperthermic to ascertain the incidence of seizures, mortality, and extent of hippocampal cell loss in each group. METHODS: We exposed 14-day-old rat pups with experimentally induced NMD (n = 39) and age-matched controls (n = 30) to hyperthermia (core body temperature > 42 degrees C). RESULTS: The incidence of hyperthermia-induced behavioral seizures and mortality rate were significantly higher in rats with NMD than in controls (p < 0.05). The longer duration of hyperthermia resulted in a higher incidence of behavioral seizures and higher mortality rate (p < 0.05). In rats with NMD, hyperthermia resulted in hippocampal pyramidal cell loss independent of seizure activity; the extent of neuronal damage correlated positively with the duration of hyperthermia. In control rats, occasional neuronal loss and astrocytosis occurred only after prolonged hyperthermia. CONCLUSIONS: In immature rats, NMD lower the threshold to hyperthermia-induced behavioral seizures and hyperthermia in the presence of NMD may cause irreversible hippocampal neuronal damage.