超支化不饱和聚(酰胺-酯)的改性及热分解动力学

采用不同链长的十四酰氯和十八酰氯对超支化不饱和聚(酰胺-酯)(MHBP)的端羟基进行原位端基改性,制备出2种改性超支化聚合物,用傅立叶红外光谱(FTIR)、热重分析(TGA)、黏度法等对其结构及性能进行表征,并研究了它们的热分解行为及其热分解动力学.结果表明,其热分解反应不是一级反应,改性超支化聚合物的热稳定性与末端烷烃链的长度有关,用Ozawa法求出了热分解表观活化能.     

Taming theory with thought experiments: Understanding and scientific progress

I claim that one way thought experiments contribute to scientific progress is by increasing scientific understanding. Understanding does not have a currently accepted characterization in the philosophical literature, but I argue that we already have ways to test for it. For instance, current pedagogical practice often requires that students demonstrate being in either or both of the following two states: 1) Having grasped the meaning of some relevant theory, concept, law or model, 2) Being able to apply that theory, concept, law or model fruitfully to new instances. Three thought experiments are presented which have been important historically in helping us pass these tests, and two others that cause us to fail. Then I use this operationalization of understanding to clarify the relationships between scientific thought experiments, the understanding they produce, and the progress they enable. I conclude that while no specific instance of understanding (thus conceived) is necessary for scientific progress, understanding in general is.     

Glycogen synthase kinase 3β and Alzheimer’s disease: pathophysiological and therapeutic significance

Alzheimer’s disease (AD) is a neurodegenerative disorder associated with cognitive and behavioral dysfunction and is the leading cause of dementia in the elderly. Several studies have implicated molecular and cellular signaling cascades involving the serine-threonine kinase, glycogen synthase kinase β(GSK-3β) in the pathogenesis of AD. GSK-3β may play an important role in the formation of neurofibrillary tangles and senile plaques, the two classical pathological hallmarks of AD. In this review, we discuss the interaction between GSK-3β and several key molecules involved in AD, including the presenilins, amyloid precursor protein, tau, and β-amyloid. We identify the signal transduction pathways involved in the pathogenesis of AD, including Wnt, Notch, and the PI3 kinase/Akt pathway. These may be potential therapeutic targets in AD. Received 19 December 2005; received after revision 24 January 2006; accepted 6 February 2006     

On the mechanism of inhibition of p27 degradation by 15-deoxy-Δ12,14-prostaglandin J 2 in lymphoblasts of Alzheimer’s disease patients

It has been proposed that neuroinflammation, among other factors, may trigger an aberrant neuronal cell cycle re-entry leading to neuronal death. Cell cycle disturbances are also detectable in peripheral cells from Alzheimer’s disease (AD) patients. We previously reported that the anti-inflammatory 15- deoxy-Δ^12,14-prostaglandin J ₂ (15d-PGJ ₂) increased the cellular content of the cyclin-dependent kinase inhibitor p27, in lymphoblasts from AD patients. This work aimed at elucidating the mechanisms of 15d-PGJ ₂-induced p27 accumulation. Phosphorylation, half-life, and the nucleo-cytoplasmic traffic of p27 protein were altered by 15d-PGJ2 by mechanisms dependent on PI3K/Akt activity. 15d-PGJ ₂ prevents the calmodulin-dependent Akt overactivation in AD lymphoblasts by blocking its binding to the 85-kDa regulatory subunit of PI3K. These effects of 15d-PGJ ₂ were not mimicked by 9,10-dihydro-15-deoxy-Δ^12,14- prostaglandin J ₂, suggesting that 15d-PGJ ₂ acts independently of peroxisome proliferator-activated receptor γ activation and that the α,β-unsaturated carbonyl group in the cyclopentenone ring of 15d-PGJ ₂ is a requisite for the observed effects. Received 14 July 2008; received after revision 2 September 2008; accepted 12 September 2008     

阿罗不可能性定理和社会选择的无矛盾性问题

2017年2月21日,国际著名数理经济学家、1972年度诺贝尔(Nobel)经济学奖获得者阿罗(K.J.Arrow)于美国辞世。谨作此文,以纪念他在社会选择理论,特别是其中将有关数学应用于研究经济学领域发现的"阿罗不可能性定理"作出的重大贡献。     

MPTP慢性帕金森病小鼠海马内氧化应激与细胞凋亡蛋白的表达

目的 观察 MPTP慢性帕金森病小鼠海马氧化应激指标及细胞凋亡相关蛋白的表达.方法 应用MPTP制备慢性帕金森病模型,观察行为学改变,Morris水迷宫实验,检测模型组和对照组小鼠海马内超氧化物歧化酶（SOD）、还原型谷胱甘肽（GSH）及丙二醛（MDA）舍量变化,以及免疫组织化学方法、RT-PCR方法、Western blot方法检测海马Bax和Bel-2蛋白表达.结果 慢性帕金森病模型小鼠行为学特点为震颤、活动减少;水迷宫实验结果提示认知功能降低;与对照组海马比较：模型组海马SOD、GSH含量均下降,而MDA含量升高（P〈0.05）;模型组海马Bax蛋白表达增高,而Bel-2蛋白表达下降（P〈0.05）.结论 氧化应激在慢性帕全森病认知功能障碍发病机制中起重要作用,而Bax和Bcl-2蛋白参与了氧化应激诱导海马神经元凋亡的调控过程.     

基于磁性微泡对比剂的超声和磁共振影像融合算法

文中提出了一种新的基于磁性微泡对比剂的超声影像和磁共振影像之间的融合算法．首先利用磁性微泡对比剂对体模进行超声和磁共振显影,并对显影进行边缘分割．运用非采样contourlet变换（nonsubsampled contourlet transform．NSCT）对源图像进行分解,然后对低频子带系数采用自适应动态加权非负矩阵分解（dynamic weighted non-negative matrix factorization．DWNMF）结合分割图像进行融合．然后对各带通方向子带系数采用空间频率激励的脉冲耦合神经网络进行融合,最后利用NSCT逆变换得到融合图像．研究结果表明,利用磁性微泡对比剂并结合上述算法对超声影像和磁共振影像进行融合,可以获得预期的融合效果．     

基于SHPB试验的高速铁路CRTSⅡ型CA砂浆动态性能

采用分离式霍普金森压杆(Split Hopkinson Pressure Bar,SHPB)试验研究了高速铁路CRTS II型水泥乳化沥青砂浆(CA砂浆)的动态力学性能,并建立了CRTS II型CA砂浆的动态本构关系模型.结果表明:随着应变率的增大,CRTS II型CA砂浆峰值强度逐渐增加,但增加速率随应变率的增大而减小,当应变率从44.17增加至54.79 s-1和从54.79增加至108.47 s-1时,峰值强度分别增加了初始峰值强度的52.28%和7.5%,弹性模量随应变率的变化规律性较差;应变率越大,破坏时的贯通裂纹越多,碎裂程度越大;CRTS II型CA砂浆的比能量吸收随着应变率的增大而增大.所建立的动态本构模型拟合曲线与试验曲线具有较好的一致性.     

嫦娥三号“玉兔号”巡视器遥操作中的关键技术

2013年12月14日,"嫦娥三号"成功地将月面着陆器和"玉兔号"巡视器送抵月球,这标志着我国已完成了探月工程中"落"月的重要阶段.嫦娥三号任务的一个关键组成部分是由地面遥操作中心控制"玉兔号"巡视器在月面非结构化环境中进行巡视和科学探测,而遥操作技术正是该组成部分成功实施的关键."玉兔号"巡视器遥操作技术主要包括巡视器的导航定位、月面地形重构、行驶路径规划和机械臂探测等关键步骤,这些步骤相互支撑与融合,保证了嫦娥三号任务的顺利实施.本文在对上述4个方面关键技术的发展和应用现状进行总结的基础上,阐述了相关的主要技术途径及其应用特点,分析了各种技术在"玉兔号"月面巡视与科学探测任务实施中的发挥的重要作用,并评述了它们的发展潜力和应用前景,对中国探月工程以及后续火星探测工程中的遥操作具有一定的指导意义.     

高k栅MOSFET栅–源/漏寄生电容的半解析模型

文章针对高k栅MOSFET的栅介质层及其侧壁掩蔽层提出了一个二维定解问题,求出了二维电势和电荷分布.文章根据栅极电荷与栅源及栅漏电压关系,提出了MOSFET的栅极和源极/漏极之间的寄生电容的模型,用半解析法计算了这些寄生电容,得到了寄生电容与几何尺寸之间的关系.文章的计算结果表明改变栅极电介质常数可以得到一个寄生电容的最小值,计算结果与CST仿真结果能够很好地符合.