TCVI工艺制备C／C复合材料的多物理场耦合模拟

采用2D轴对称瞬态模型对热梯度化学气相渗积（TCVI）22艺制备高性能C／C复合材料过程进行模拟．模型包括对流、热传导、扩散、沉积反应和孔隙演变等物理化学过程．采用有限元方法实现了多物理场迭代耦合计算，得到了各时刻流场、温度场和密度分布规律，研究表明对流对温度场分布具有重要影响．对于采用TCVI工艺致密化100h的C／C复合材料，对比实验测得的预制体平均密度径向分布，计算结果与实验结果符合一致规律，验证了模型的可靠性和模拟计算的预测能力．     

基于交易成本理论的网络购物满意度影响因素分析

本文将交易成奉理论应用于网络购物满意度研究,在分析网络购物的优势并界定网络购物满意度的基础上,从交易成本的视角,探讨网络购物满意度的影响因素,指出这些影响因素与顾客满意度的关系,进而提出研究命题,以及相关的营销建议.     

应力水平对3D C/C复合材料的弯弯疲劳损伤模式的影响

测定了3D C/C复合材料的弯弯疲劳寿命曲线以及疲劳加载过程中的载荷-挠度回滞曲线, 通过试件实物照片和SEM疲劳断口分析, 研究了在不同应力水平下材料的损伤模式. 研究结果表明, 3D C/C复合材料的弯弯疲劳极限为203 MPa, 应力水平为静弯曲强度的92%, 远高于2D C/C复合材料. 随应力水平的提高, 材料的疲劳载荷-挠度回滞曲线由弹性滞后环向非弹性滞后环转化, 挠度显著增加. 揭示了纤维与基体界面的滑动磨损在疲劳失效中起重要的作用, 应力水平的高低控制着这种滑动磨损的程度和速度.     

乙醇热解制备C/C复合材料工艺及组织结构研究

以整体碳毡为预制体,无水乙醇为前躯体,N2做为载气和稀释气,在负压条件下,沉积温度为1050~1200°C,采用压力梯度ICVI工艺制备出C/C复合材料制品,采用偏光显微镜、扫描电镜、透射电镜分析材料的组织结构和断口形貌,利用三点弯曲测定了材料的弯曲强度.结果表明：制备的C/C复合材料基体组织结构在1050°C条件下为中织构与高织构并存的组织,当沉积温度上升为1100~1200°C时,热解碳为均一的高织构组织.制备试样的弯曲破坏应力应变曲线及断口形貌分析表明：断裂特征受热解碳与基体界面结合强弱的影响,弯曲断口以纤维断裂、纤维拔出为主,材料具有假塑性断裂特征,并且随着沉积温度的提高,热解碳基体与纤维的界面结合逐渐增强,断裂方式由假塑性断裂向脆性断裂逐渐转变.     

疲劳载荷下C/C复合材料的基体皱褶现象研究

采用专门设计的非常规交替式疲劳试验, 对碳纤维三维整体编织C/C复合材料在拉-拉循环载荷作用下的力学行为进行了探索性研究. 试验中发现, 在C/C复合材料内部热解碳沉积层的某些微区域形成了丝绸状“皱褶”. 进一步对试验过程进行了热力学理论分析, 阐明了产生皱褶现象的原因主要是疲劳振动过程导致热解碳沉积微层之间发生微摩擦, 并进而形成高温微区所致.     

C和Mo双注入H13钢纳米结构和抗腐蚀特性

用多次扫描电位法研究了C+Mo双注入和两种元素注入的顺序对抗腐蚀特性的影响,研究了抗腐蚀相生成的条件,观察到细丝状纳米碳化物镶嵌相的形成,以及这些相对抗腐蚀特性的作用,并对其改性机理进行了讨论. 实验结果表明,在C+Mo双注入H13钢中,生成了含Fe₂Mo,FeMo合金相和MoC,Mo₂C,MoCx,FeMo₂C,Fe₂C,Mo和MoO等的表面钝化膜.双注入则具有C和Mo单注入双重优点; 可有效地提高H13钢的耐腐蚀性和抗点蚀特性;效果比Mo单注入更好,与C+Mo双注入注入次序相反的Mo+C双注入生成的钝化膜抗腐蚀性更强. 特别可贵的是这种注入能有效地提高抗点蚀特性.     

C/C复合材料CVI工艺人工神经网络建模

C/C复合材料CVI制备工艺过程的本质繁杂性限制了该材料的广泛应用. 尝试利用人工神经网络技术对该工艺过程进行辨识与仿真, 采用Levenberg-Marquardt算法建立了通用的CVI工艺神经网络模型. 根据CVI工艺复杂、参数众多等特点, 结合有限元技术及工艺实验从教师样本处理、网络拓扑结构设计和学习参数调整等方面对网络学习算法作了进一步的改进. 通过对等温CVI样本集的学习, 初步建立了管类零件等温CVI工艺知识库. 结果表明: 该模型可以挖掘样本蕴含的领域知识, 不仅可以对单个工艺参数的时间效应进行预测和分析, 而且可以分析任意两个工艺参数对致密化过程的偶合作用.     

μC/OS-Ⅱ在LPC2114上的移植与应用

介绍了当前流行的μC／OS-Ⅱ实时多任务操作系统，分析了ARM嵌入式微处理器LPC2114与移植相关的一些概念，并在此基础上介绍了将μC／OS-Ⅱ移植到LPC2114上的过程以及其应用。     

热压烧结ZrB2／B4C陶瓷材料的组织与性能

以B4C、C、ZrO2为主要原料,采用反应热压法制备ZrB2／B4C陶瓷材料。通过对ZrB2／B4C陶瓷材料的显微组织及力学性能的综合分析,发现第二相ZrB2含量为20wt％时,材料具有较好的综合力学性能,相对密度为99．3％,维氏硬度为36．1GPa,抗弯强度为533．3MPa,断裂韧性为6．95MPa·m^1/2,比纯B4C陶瓷材料的性能均有所提高。材料为穿晶和沿晶断裂的混合断裂模式。     

基于S3C2416的公交电子站牌系统设计

为了提高城市公交的运营效率和服务质量,让乘客及时了解公交车实时车况,设计了一种基于S3C2416微处理器的新型公交电子站牌系统,并对该系统的组成、工作原理、关键技术及主要模块的软硬件设计进行了详细的阐述.系统以ARM为嵌入式硬件平台,采用当前先进的嵌入式技术和GPRS无线网络通信技术,实现了车辆到站预报、车辆到站提示、公交站点查询、公交车次查询等功能.测试结果表明,该系统性能良好、实时性强、稳定性高,具有巨大的市场价值.     

Subtypes of protein kinase C in rat cerebral microvessels

Summary Protein kinase C in rat cerebral microvessels was characterized. By hydroxyapatite column chromatography, protein kinase C in the soluble fraction was resolved into two major peaks corresponding to type II and III enzymes, in the proportions of 57% and 38%, respectively. Since each subtype is considered to have a distinct role, the high proportion of type II enzyme found in this study suggests that this type may be involved in specific functions of the cerebral microvessels.     

香烟烟雾提取物对人内皮细胞细胞色素C氧化酶活性及细胞凋亡的影响

目的探讨香烟烟雾提取物（cigarette smoking extract,CSE）对内皮细胞细胞色素C氧化酶（cytochmme Coxidase,COX）活性及凋亡的影响。方法体外培养ECV304,分别给予0％、0．5％、1％、5％CSE刺激12h,及5％CSE刺激0h、6h、12h、24h后,生化法检测COX活性;投射电镜和流式细胞仪观察细胞凋亡情况。结果CSE引起COX活性下降,且随着刺激浓度和时间的增加而下降（P〈0．05）;电镜示CSE干预组细胞出现明显的凋亡形态学改变;流式细胞仪结果示不同浓度CSE分别作用12h后凋亡率依次增高,除O％CSE组和0．5％CSE组间比较无统计学意义（P〉0．05）,余各组间比较均有统计学意义（P〈0．05）;5％CSE作用不同时间后,随着干预时间的延长细胞凋亡率逐渐升高（P〈0．05）。结论CSE抑制内皮细胞COX活性,呈浓度和时间依赖性;CSE诱导内皮细胞凋亡,呈浓度和时间依赖性;COX活性的下降可能在CSE所致的内皮细胞凋亡中具有重要作用。     

Spermine protects protein kinase C from phospholipid-induced inactivation

Phosphatidylserine (PS), an activator of protein kinase C (PKC) in the assay of protein phosphorylation, inhibited this enzyme in a time-dependent manner following preincubation in the absence of Ca²⁺. The phospholipid-induced inactivation of kinase activity was dependent on the PS content and on the charge density of liposomes. This inactivation of PKC could be reduced, but not completely eliminated, by addition of Ca²⁺. In the present work the effect of a naturally occurring polyamine (spermine) on the PS-induced inactivation of PKC was investigated. The presence of spermine during preincubation without Ca²⁺ was effective in suppressing the PS-induced inactivation of PKC over the period (20 min) required for PS to inhibit the enzyme by 95%. PKC exists in two membrane-bound states: a reversible one which can be dissociated by Ca²⁺ chelators (membrane-associated form) and an irreversible one which is chelator-stable (membrane-inserted form). Gel filtration experiments on the PKC-PS complex formed in the presence of Ca²⁺ indicated that less insertion of enzyme into liposomes occurred in the presence of spermine and that the kinase activity of the reversibly membrane-associated PKC was protected from PS inactivation.     

基于S3C2410构建PDA数据采集节点系统

描述了以现代的无损检测技术为基础,以S3C2410为核心构建的PDA数据采集系统。该系统实现了无线网络节点的数据采集功能。在此基础上设计了一套PDA数据采集,其硬件结构由S3C2410、无线网络节点和通信模块等组成;系统软件分为驱动程序模块、通信协议模块等,可应用于高校的教室温度采集系统。     

Chemical evidence for interactions between vitamins E and C

Summary Experimental proof is provided for interactions between radicals of vitamin E/vitamin C as generated by air-oxidized lipids (liquid fraction of subcutaneous chicken fat). Using ESR spectroscopy, hydrogen atom exchange is shown to take place between vitamin C and the radical of vitamin E. Sequential consumption of these two vitamins in oxidized lipid, first vitamin C then vitamin E, is demonstrated by means of differential pulse polarography. These results elucidate the in vitro radical scavenging functions attributed to vitamin E and vitamin C as well as their synergism in lipid antioxidation.The authors very much thank Dr A. Dieffenbacher and P. Ducret for the preparation of the chicken fat fraction.     

T-cell signal transduction and the role of protein kinase C

The T lymphocyte has a vital part to play in maintaining the host response to bacterial and viral infection and also appears to play a key pathological role in autoimmune diseases such as rheumatoid arthritis. In this review, we summarize the signalling pathways which trigger antigen-driven T-cell proliferation and examine the evidence which suggests that protein kinase C (PKC) is fundamental to this process. Finally, we discuss the therapeutic potential that PKC inhibitors may have in the treatment of autoimmune disease. Received 31 March 1998; received after revision 19 May 1998; accepted 19 May 1998     

Effect of protein kinase C activation and depletion on insulin stimulation of glycogen synthesis in cultured hepatoma cells

Summary Insulin stimulation of glycogen synthesis was nearly abolished in hepatoma cells shortly treated with 4 ß-phorbol 12 \-myristate, 13 -acetate (protein kinase C activation) but remained unmodified in cells chronically treated with the phorbol ester (protein kinase C depletion). Thus, although exogenous activation of protein kinase C results in an inhibition of insulin action, protein kinase C depletion has no influence on this process. The results suggest that, in hepatoma cells, no endogenous activation of protein kinase C may occur in response to the signal triggered by insulin.     

Protein kinase C regulation of GABAA receptors

Pharmacological studies with drugs that activate or inhibit several protein kinase C (PKC) isozymes have identified the PKC family of serine-threonine kinases as important in the regulation of -aminobutyric acid type A (GABA_A) receptor function. PKC modulates GABA_A receptor surface density, chloride conductance and receptor sensitivity to positive allosteric modulators such as neurosteroids, ethanol, benzodiazepines and barbiturates. Recent studies using PKC isozyme-selective reagents and gene-targeted mice have begun to identify critical roles for three isozymes, PKCII, PKC and PKC, in various aspects of GABA_A receptor regulation. Progress in this field touches upon therapeutic areas that are of great clinical importance such as anxiety and addiction. Increased understanding of how PKC regulates GABA_A receptors and which PKC isozymes are involved holds promise for development of new treatments for diverse neuropsychiatric disorders.Received 2 August 2004; received after revision 17 August 2004; accepted 21 August 2004     

Phospholipase C activation via a GTP-binding protein in tumoral islet cells stimulated by carbamylcholine

Summary Carbamylcholine and GTP act synergistically in stimulating the production of [³H]inositol-1-phosphate by digitonized tumoral islet cells (RINm5F line) prelabeled with myo-[2-³H(N)]inositol. The response to these two agents is similar to that evoked by GTPS. These findings suggest that a GTP-binding regulatory protein couples the occupancy of muscarinic receptors to activation of phospholipase C in pancreatic islet cells.This work was supported by grants from the Belgian Foundation for Scientific Medical Research.