A PRICE DUOPOLY GAME MODEL WITH UNCERTAIN PARAMETERS

1 IntroductionIn the Bayesian game modeIs[1t2], the uncertainty of objectives is described with probability. But sometbe the uncertainty in practice i8 gben by some fuzzy parnders, and theobjectives of players mny not be to mallmize the expected payOffs[3'4'5j. [6,7l discussed themodeIs for endogenous Stackelberg and price leadership under complete infOmation. In [8,9],we studied the Cournot and Stackelberg models with fuzzy parameters. In this paPer, we givea new subjective equllibrinm fo…     

基于Android 手机言行记录系统的设计与实现

针对手机用户的个性化需求较高及传统方法的进程监控问题, 设计并实现了基于Android 开发平台的手机言行记录系统。该系统通过控制手机通讯录信息、文件加密操作、应用程序监控以及日志监控等方式实时监控分析手机用户的言行记录, 方便用户的自我监控与管理。该方法主要运用Intent 和日志监控实现软件监控功能,通过类FileEncrpter 对文件系统加密, 对录音加密则使用流加密, 运用MediaRecord 类和ACC(Advanced AudioCoding)编码实现音频录制。实验结果表明, 该系统达到了较为理想的实验效果, 证明了该系统的可行性。     

基于ARM的列车运行控制算法仿真测试系统

介绍了列车运行控制系统的基本组成和原理,采用通用ARM芯片S3C2440设计了列车运行控制仿真硬件系统以及包含列车模型的PC端仿真软件.使用串口UART实现下位机控制系统硬件和上位机列车仿真模型软件之间的数据通信.最后,设计了基于滑动模态状态观测器的列车控制算法,并在仿真测试系统中进行了测试.     

一种混合退化系统剩余寿命预测方法

针对传统的预测方法不能同时考虑线性和非线性退化问题,提出了一种基于维纳过程的带随机参数和确定参数的混合退化模型.基于首达时间(FHT)的概念给出了剩余寿命(RUL)的解析渐进显式形式,模型中随机参数通过Kalman滤波技术实时更新,确定参数采用极大似然估计进行估计.最后,采用陀螺仪实验数据验证了该方法的有效性.     

考虑侧壁效应修正的循环水槽船模斜航试验水动力计算

采用计算流体动力学技术,以KVLCC2船模为对象研究速度修正方法对斜航水动力修正的影响及其适用工况,并与循环水槽试验结果对比以验证速度修正方法的有效性;采用Tamura速度修正公式对宽阔水域的试验流速进行修正,将速度修正前后的水动力及流场特征与循环水槽斜航试验的计算结果进行对比.结果表明:Tamura速度修正公式在阻塞比为3.5%~5.0%时有效,阻塞比过大将会加大船体两侧流场流速的变化;循环水槽中船体两侧的压力分布与其在宽阔水域中的差别较大;速度修正方法会同时增大船体两侧的压力,因此,在一定的阻塞比范围内可以减小两者的水动力差异,但当阻塞比继续增大时会增大两者的水动力差异.同时,基于低速风洞试验的阻塞效应修正方法提出了低速肥大型船循环水槽斜航试验的横向水动力修正公式.     

环形流道内周向流对摩擦因子的修正公式

针对屏蔽电动机定转子环形流道内转子转动对其摩擦因子的影响作定量分析.搭建缩尺实验台,实验分析了不同转子转速下定转子间的压力分布规律.实验结果表明:转速的升高会引起压降增大,间隙环流的摩擦因子需要在经验公式上进行修正,分析拟合数据得到了修正系数与切向、轴向雷诺数比值的映射关系,从而推导出了环形流道内考虑周向流动下摩擦因子的修正公式.为了验证该公式的准确性与普遍性,利用计算流体动力学(CFD)软件对缩尺实验台与主泵屏蔽电动机定转子间的流场分别进行仿真,对比数值仿真与该修正公式所求得的摩擦因子,结果表明偏差在合理范围内.     

H型梁与矩形钢管柱单板简支连接性能

对H型梁和矩形管柱的单板简支连接的受力性能进行分析,着重研究节点连接对矩形管柱壁的影响.通过建立理论计算模型,提出了该连接节点的设计原则,并通过试验和有限元分析来验证理论模型的正确性,探讨该种连接形式的优点和缺点,得到了适合工程设计人员使用的该连接节点的设计公式.
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Evaluation of Novel 3D Architectures Based on Knitting Technologies for Engineering Biological Tissues

Textile-based technologies are considered as potential routes for the production of 3D porous architectures for tissue engineering( TE) applications. We describe the use of two polymers,namely polybutylene succinate( PBS) and silk fibroin(SF) to produce fiber-based finely tuned porous architectures by weft and warp knittings. The obtained knitted constructs are described in terms of their morphology, mechanical properties,swelling ability,degradation behaviour,and cytotoxicity. Each type of polymer fibers allows for the processing of a very reproducible intra-architectural scaffold geometry,with distinct characteristics in terms of the surface physicochemistry,mechanical performance,and degradation capability,which has an impact on the resulting cell behaviour at the surface of the respective biotextiles. Preliminary cytotoxicity screening shows that both materials can support cell adhesion and proliferation. Furthermore, different surface modifications were performed( acid /alkaline treatment, UV radiation,and plasma) for modulating cell behavior. An increase of cell-material interactions were observed,indicating the important role of materials surface in the first hours of culturing. Human adipose-derived stem cells( hASCs) became an emerging possibility for regenerative medicine and tissue replacement therapies. The potential of the recently developed silk-based biotextile structures to promote hASCs adhesion,proliferation,and differentiation is also evaluated. The obtained results validate the developed constructs as viable matrices for TE applications. Given the processing efficacy and versatility of the knitting technology, and the interesting structural and surface properties of the proposed polymer fibers,it is foreseen that our developed systems can be attractive for the functional engineering of tissues such as bone,skin,ligaments or cartilage and also for develop more complex systems for further industrialization of TE products.     

Synaptotagmin I functions as a calcium regulator of release probability

In all synapses, Ca2+ triggers neurotransmitter release to initiate signal transmission. Ca2+ presumably acts by activating synaptic Ca2+ sensors, but the nature of these sensors--which are the gatekeepers to neurotransmission--remains unclear. One of the candidate Ca2+ sensors in release is the synaptic Ca2+-binding protein synaptotagmin I. Here we have studied a point mutation in synaptotagmin I that causes a twofold decrease in overall Ca2+ affinity without inducing structural or conformational changes. When introduced by homologous recombination into the endogenous synaptotagmin I gene in mice, this point mutation decreases the Ca2+ sensitivity of neurotransmitter release twofold, but does not alter spontaneous release or the size of the readily releasable pool of neurotransmitters. Therefore, Ca2+ binding to synaptotagmin I participates in triggering neurotransmitter release at the synapse.