NUMERICAL ANALYSIS AND EXPERI- MENT OF UNSTEADY THERMAL FIELD OF ROTOR PLATE FOR EDDY CURRENT RETARDER

The physical model based on heat transfer theory and virtual boundary method for analyzing unsteady thermal field of rotor plate for eddy current retarder used in automobile is established and boundary conditions are also defined. The finite element governing equation is derived by Galerkin method. The time differential item is discrete based on Galerkin format that is stable at any condition. And a new style of varying time step method is used in iteration process. The thermal field on the rotor plate at the radial and axle directions is analyzed and varying temperature at appointed points on two side-surfaces is measured. The testing and analytical data are uniform approximately. Finite element method can be used for estimating thermal field of the rotor plate at initial design stage of eddy current retarder.     

以外供液氮替代膨胀机的深度冷冻循环

介绍空分制氮装置采用膨胀机循环与液氮循环的两种工艺流程及能量平衡 ,示出了两种循环的实例比较。指出外供液氮可以作为冷源替代膨胀机 ,且单耗低、操作更方便 ,设备维护量更小、氮气提取率更高     

TEMIC射频卡的速率自适应读卡算法

提出种基于TEMIC射频卡Manchester编码的速率自适应读卡算法,并对该算法进行了说明和示例。     

BYJ型防喷脱接器的设计与应用

本文介绍了BYJ型防喷脱接器的结构和工作原理。它既有抽油杆与大泵活塞脱接功能,又能实现不压井作业施工,是大型抽油泵理想的配套工具。现场应用表明,该防喷脱接器对接成功率较高,并实现了大泵井不压井施工。     

粘土作为高放废物处置回填材料的可行性研究

本文以西北粘土为对象,对其压实行为、热传导、膨胀特性,以及吸附和渗透性能进行了初步研究,借以探讨西北粘土在高放废物处置中用作回填材料的可行性。试验表明,以西北粘土为基材,经过适当的热改性和吸附改性,在初始含水量约为9%,于70MPa 下成型,用作高放废物处置中的回填材料是可行的。     

分析再热器超温爆漏与水冷壁结焦控制量的关系

文章介绍了宝钢自备电厂在改善锅炉燃烧工况，控制锅炉水冷壁结焦所采取的技术措施，分析了锅炉水冷壁结焦量与锅炉二次再热器烟气出口平均温度的关系，为解决锅炉水冷壁结焦所引发的二次再热器超温爆漏问题提供了依据。     

Electrical passivation in hydrogen plasma exposed GaN

Lightly p-doped (3×10¹⁷ cm^-3) GaN grown on GaAs substrates by metal organic molecular beam epitaxy (MOMBE) shows deactivation of the residual acceptors on exposure to a microwave (2.45 GHz) hydrogen plasma at 250°C. Subsequent annealing to 350°C produces further dopant passivation, while higher temperatures (450°C) restore the initial conductivity. These results suggest that hydrogen carrier gases should be avoided during vapour phase growth of III-V nitrides     

Comparison of production of choriogonadotropin inhibitory protein, prolactin and insulin-like growth factor binding protein-1 by human decidua in vitro

BACKGROUND: Tissue plasminogen activator (tPA) is elevated in cancer patients and is thought to promote tumor angiogenesis by facilitating endothelial cell migration through plasmin-mediated degradation of extracellular matrix. Due to the presence of an epidermal growth factor (EGF)-finger domain in the tPA A-chain and the existence of an endothelial cell (EC) receptor that binds this domain, it was hypothesized that tPA has a direct receptor-mediated effect on EC proliferation, independent of plasmin. METHODS AND RESULTS: Using cultured canine ECs, tPA (7.25 microg/ml, approximately 107 nM) increased proliferation as much as 50 and 170% in the absence and presence of growth factors, respectively. tPA-induced increases in EC proliferation occurred independent of plasmin generation, as the plasmin inhibitor, aprotinin (10 microg/ml) did not inhibit tPA-induced proliferation. However, tPA-induced proliferation was inhibited dose-dependently to a maximum of 78% using a monoclonal antibody against the tPA EGF-finger domain. This antibody, known to inhibit tPA binding to its receptor, did not inhibit tPA-induced plasmin generation. To investigate the role of potential signal transduction pathways, ECs were exposed to lavendustin A, a tyrosine kinase inhibitor, at 33.5 microM (IC50 for basic fibroblast growth factor). Lavendustin A did not inhibit tPA-induced EC proliferation. However, Rp-cAMP, an inhibitor of cAMP-dependent kinases, specifically inhibited tPA-induced EC proliferation in a dose-dependent manner (IC50 = 50.5 microM). Pertussis toxin at maximal concentrations for this system (0.5 ng/ml) did not inhibit tPA-induced EC proliferation. CONCLUSION: These results lend support to the hypothesis that tPA may have a direct receptor-mediated effect on EC proliferation and that this effect occurs independent of plasmin and may be dependent upon protein kinase A activity.