单电极直流电弧炉电热特性理论研究

运用电磁理论与流体静压力原理,导出了电弧自身的电磁向心压缩力以及电弧对熔池冲力的解析式。又运用辐射传热原理,导出了单电极电弧对熔池与炉衬辐射传热的解析式。解析式揭示出电弧自身电磁向心压缩力、电弧对熔池冲力,单电极电弧对熔池以及对炉衬辐射传热的规律。     

混合氯化稀土催化合成DOP,DOM和DOA

本文报道:价廉的混合氯化稀土,对合成DOP等增塑剂有明显的催化效果。产品精制简单,转化率高,有应用前景。     

求Ramsey数最优下界值的递归算法

要确定每个具体的Ramsey数的数值是相当困难的,至今人们只求出了为数很少的几个Ramsey数的数值.人们在研究Ramsey数性质的同时,也在估计Ramsey数的数值,得出了某些Ramsey数的下界值,但工作进展缓慢.本文提出了一种计算Ramsey数最优下界值的递归算法,该算法利用当今关于Ramsey数的最新结果,能得出Ramsey数的目前最优下界值.1 算法描述不妨将本算法定名为G,参数个数为1个以上(可变化),算法允许递归调用,其输出值为Ramsey数的目前最优下界值.C(k_1,k_2…,k_n)表示以k_1,k_2…,k_n作为输入,通过算法G所得到的输出结果,即C(k_1,k_2…,k_n)表示的是G算出的Ramsey数N(k_1,k_2,…,k_n;2)的目前最优下界值,其中N(k_1,k_2…,k_n;2)的含意与文献[2]中有关含意相同.算法G:     

Clustering of voltage-dependent sodium channels on axons depends on Schwann cell contact.

In myelinated nerves, segregation of voltage-dependent sodium channels to nodes of Ranvier is crucial for saltatory conduction along axons. As sodium channels associate and colocalize with ankyrin at nodes of Ranvier, one possibility is that sodium channels are recruited and immobilized at axonal sites which are specified by the subaxolemmal cytoskeleton, independent of glial cell contact. Alternatively, segregation of channels at distinct sites along the axon may depend on glial cell contact. To resolve this question, we have examined the distribution of sodium channels, ankyrin and spectrin in myelination-competent cocultures of sensory neurons and Schwann cells by immunofluorescence, using sodium channel-, ankyrin- and spectrin-specific antibodies. In the absence of Schwann cells, sodium channels, ankyrin and spectrin are homogeneously distributed on sensory axons. When Schwann cells are introduced into these cultures, the distribution of sodium channels dramatically changes so that channel clusters on axons are abundant, but ankyrin and spectrin remain homogeneously distributed. Addition of latex beads or Schwann cell membranes does not induce channel clustering. Our results suggest that segregation of sodium channels on axons is highly dependent on interactions with active Schwann cells and that continuing axon-glial interactions are necessary to organize and maintain channel distribution during differentiation of myelinated axons.     

用栅板剪切干涉法确定应力强度因子

本文介绍了一种用栅板剪切干涉法确定应力强度因子的新方法,阐明了该方法的基本原理与实验技术,通过三点弯曲梁确定了Ⅰ型裂纹应力强度因子,实验结果与理论上近似计算结果相符合。     

锁具装箱方案

讨论了锁具装箱问题，首先用穷举法统计符合要求的一批锁具的数量，然后根据奇数和偶数的转换关系，给出装箱的销售方案。应用本方法比较完满地解决了锁具装箱问题，而且经过简单改动，可以进行推广。     

有限水深慢船理论及波阻计算

本文推广E.Baba的无限水深慢船理论,建立了有限水深慢船理论.基于低速与量级假定,将总速度势Φ分为合模势(?)_r和波动势(?),分别给出了各自的表达式,进而推导了有限水深兴波的波高、波阻公式.编制了波阻计算程序,并以半浸圆球为例进行验算,计算了Series 60船型在8种水深时的波阻.理论分析和数值计算表明:当水深趋于无穷时,本理论与Baba理论是一致的.     

A ground‐level ozone forecasting model for Santiago,Chile

A physically based model for ground‐level ozone forecasting is evaluated for Santiago, Chile. The model predicts the daily peak ozone concentration, with the daily rise of air temperature as input variable; weekends and rainy days appear as interventions. This model was used to analyse historical data, using the Linear Transfer Function/Finite Impulse Response (LTF/FIR) formalism; the Simultaneous Transfer Function (STF) method was used to analyse several monitoring stations together. Model evaluation showed a good forecasting performance across stations—for low and high ozone impacts—with power of detection (POD) values between 70 and 100%, Heidke's Skill Scores between 40% and 70% and low false alarm rates (FAR). The model consistently outperforms a pure persistence forecast. Model performance was not sensitive to different implementation options. The model performance degrades for two‐ and three‐days ahead forecast, but is still acceptable for the purpose of developing an environmental warning system at Santiago. Copyright © 2002 John Wiley & Sons, Ltd.     

Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1.

Neurofibromatosis type I (NF1) is one of the most common single-gene disorders that causes learning deficits in humans. Mice carrying a heterozygous null mutation of the Nfl gene (Nfl(+/-) show important features of the learning deficits associated with NF1 (ref. 2). Although neurofibromin has several known properties and functions, including Ras GTPase-activating protein activity, adenylyl cyclase modulation and microtubule binding, it is unclear which of these are essential for learning in mice and humans. Here we show that the learning deficits of Nf1(+/-) mice can be rescued by genetic and pharmacological manipulations that decrease Ras function. We also show that the Nf1(+/-) mice have increased GABA (gamma-amino butyric acid)-mediated inhibition and specific deficits in long-term potentiation, both of which can be reversed by decreasing Ras function. Our results indicate that the learning deficits associated with NF1 may be caused by excessive Ras activity, which leads to impairments in long-term potentiation caused by increased GABA-mediated inhibition. Our findings have implications for the development of treatments for learning deficits associated with NF1.