汽车甩挂运输最佳运距的研究

汽车甩挂运输是先进的公路运输形式之一。从汽车甩挂运输生产工艺的全过程和昼提高车时利用率出发，提出了适合我国目前推行汽车甩挂运输的最佳单程运距为５３－１００ｋｍ、１３３－２２０ｋｍ和２９３－４６０ｋｍ。     

^4He^＋离子在C和Cu上能量沉积系数的理论计算

利用部分地考虑能量损失的角关联的改进离子输运双群模型，计算了＾４Ｈｅ＾＋离子垂直入射到Ｃ和Ｃｕ上的能量沉积参数，改进了早期的离子输运双群模型。     

维修“天窗”对电气化重载专线输送能力的影响

采用运行图模拟和理论分析相结合的方法,论证了电气化重载专线维修“天窗”的预留方式,并分析了各种“天窗”的预留方案对输送能力的影响.     

一类具有非齐次边界条件的迁移方程的适应性及谱特征

本文讨论了一类具有一般边界条件的中子迁移方程的适定性.利用Banach空间的锥理论和积分半群理论证明了该方程的具有物理意义的正解的存在唯一性,并且,我们还讨论了相应的迁移算子的本征值的一系列性质.     

探测深度对心脏光学标测中荧光信号的影响

为了估计心脏光学标测过程中不同探测深度对光标测结果的影响，利用电兴奋跨壁传导模型和荧光传输模型，模拟了心室电兴奋跨壁传播时跨膜电位的分布和不同光探测深度的荧光信号，并将深度权重的荧光信号与组织表层细胞的荧光信号做了比较，并分析了产生差异的原因．研究表明：如果大多数荧光来自组织的近表层（小于0．5mm），光探测深度的影响几乎可以忽略；当探测深度增加时（大于等于0．5mm），尤其在螺旋波条件下，两种动作电位在上升时间、幅度和时程上的差异随探测深度的增加而加大，所以需要对以往由心肌表面电标测得到的电生理指标做相应修正．     

双向运输带式输送机的动力学设计

矿山掘进工作面,需要同时向工作面运送支护材料和向外运输采掘下来的岩石（或煤炭）,两者运行方向相反,同时使用输送带的上、下分支恰好解决这一问题。以这一上、下分支同时运输物料的双向运输带式输送机为例,对其建立了动力学计算模型。依据作用于滚筒上力的平衡方程式,给出了双向运输带式输送机启动加速度和制动减速度的计算公式;按照匀加减速转动,给出了加速和减速时间的计算公式;依据输送带作用于滚筒上的静张力和动张力,给出了输送带在滚筒上不打滑的条件;按照不打滑条件和垂度条件分别给出了输送带最小张力的计算公式;依据托辊不圆造成对输送带的扰动,给出了激励频率的计算公式;依据弹性体动力学,给出了输送机的固有振动频率和输送带最大弹性变形量的计算公式,并附有设计计算实例。     

Axonal transport of neurofilaments in normal and disease states

Neurofilaments are among the most abundant organelles in neurones. They are synthesised in cell bodies and then transported into and through axons by a process termed 'slow axonal transport' at a rate that is distinct from that driven by conventional fast motors. Several recent studies have now demonstrated that this slow rate of transport is actually the consequence of conventional fast rates of movement that are interrupted by extended pausing. At any one time, most neurofilaments are thus stationary. Accumulations of neurofilaments are a pathological feature of several human neurodegenerative diseases suggesting that neurofilament transport is disrupted in disease states. Here, we review recent advances in our understanding of neurofilament transport in both normal and disease states. Increasing evidence suggests that phosphorylation of neurofilaments is a mechanism for regulating their transport properties, possibly by promoting their detachment from the motor(s). In some neurodegenerative diseases, signal transduction mechanisms involving neurofilament kinases and phosphatases may be perturbed leading to disruption of transport. Received 11 July 2001; received after revision 30 August 2001; accepted 31 August 2001     

Binding of estradiol to synaptosomal mitochondria: physiological significance

The subsynaptosomal distribution and specific binding of 17beta-estradiol in vitro to mitochondria isolated from presynaptic nerve endings of female rat brain were examined. 17Beta-estradiol is (i) distributed unequally in synaptosomes and mitochondria posses the highest capacity to bind estradiol with respect to the available amount of the hormone. (ii) Estradiol binds specifically to isolated synaptosomal mitochondria. A Michaelis-Menten plot of specific binding was sigmoidal within a concentration range of 0.1-5 nM of added estradiol, with a saturation plateau at 3 nM. Binding of higher estradiol concentrations demonstrated an exponential Michaelis-Menten plot, indicating non-specific binding to mitochondria. Vmax and Km for the sigmoidal-shape range were estimated as 46 +/- 6 fmol of estradiol/mg of mitochondrial proteins and 0.46 +/- 0.07 nM free estradiol respectively. (iii) Estradiol binding is not affected by the removal of ovaries. The results show that inhibition of Na-dependent Ca2+ efflux from mitochondria by estradiol occurs according to an affinity change of the translocator for Na+, at the same estradiol concentrations that show specific binding to mitochondrial membranes. These data imply that physiological concentrations of estradiol, acting on mitochondrial membrane properties, extragenomically modulate the mitochondrial, and consequently the synaptosomal content of Ca2+, and in that way exert a significant change in nerve cell homeostasis.     

Cardiac protective role of a novel erythrocyte-derived depressing factor on rats and its Ca^2＋ mechanism

The cardiac protective role of a novel erythro-cyte-derived depressing factor (EDDF) on spontaneous hy-pertensive rats (SHR), calcium overload (CaO) rats and Wistar rats and its mechanism was evaluated. Mean artery pressure (MAP), heart rate (HR) and LVdp/dtmax were measured by physiological recorder. The effect of EDDF on the Ca2+-ATPase activity in myocardial sarcoplasmic reticu-lum (SR) of CaO rats was determined by inorganic phos-phate assay. Calcium transport in myocytes was measured by 45Ca2+ radioactive isotope measurement. The phosphoryla-tion levels of extracellular signal-regulated protein kinases (ERK1/2) in myocardial tissue of SHR and CaO rats were measured by Western blot method. And the ultrastructures of cardiac muscle cells were observed with the transmission electron microscope. The results indicated that EDDF could significantly decrease MAP, HR and LVdp/dtmax in a dose dependent manner (P < 0.05). It seems that the mechanism might relate with activating the Ca2+-APTase, enhancing the uptake and release of Ca2+ from SR (P < 0.05), decreasing the phosphorylation levels of ERK1/2 of myocytes (P < 0.01) and lightening the ultrastructural lesion of cardiac muscle cells. In CaO rats, the Ca2+-ATPase activity decreased clearly com-pared to control (64.99 7.16 vs 94.48 7.68 nmol·min-1 ·mg-1 protein, P < 0.01), while EDDF (100 mg/mL) could significantly increase the activity (87.93 ?9.54 vs 64.99 ?7.16, P < 0.05, n = 7). Both uptake and release rate of Ca2+ (祄ol 45Ca2+/g protein/min) from myocardial SR of CaO rats re-markably decreased compared to control (32.40 ?2.70 and 15.46 ?1.49 vs 61.09 ?10.89 and 25.47 ?4.29, P < 0.05); EDDF (100 mg/mL) could significantly stimulate their activi-ties (50.48 6.76 and 21.76 2.75 vs 32.40 2.70 and 15.46 1.49, P < 0.05). EDDF could evidently down-regulate the phosphorylation of ERK1/2 in myocardial tissue from SHR and CaO rats (P < 0.01), lighten the ultrastructural lesion of cardiac muscle cells of SHR as well. It is concluded that EDDF seems to play protective roles on both structure and function of heart, which closely related with amelioration of Ca2+ transport and inhibition of Ca2+-MAP kinase pathway.