Pr3+/Tm3+共掺LaF3纳米体系中能量转移效应的光谱学研究

在较低的温度下用水热法制备了分散性良好的Pr³⁺/Tm³⁺共掺的LaF₃纳米颗粒. X射线衍射、原子力显微镜和透射电子显微镜等技术对纳米颗粒进行表征的结果显示, 纳米颗粒呈六方相, 平均粒径为30 nm. 通过激光激发LaF3:Pr³⁺/Tm³⁺共掺纳米体系中的Tm3+离子, 实现了Tm³⁺离子到Pr³⁺离子的能量转移, 观测到了因此而产生的荧光辐射. 运用光谱学方法对共掺纳米体系的荧光辐射性质进行了研究分析, 并对相应的能量转移机理进行了探讨.     

直波导耦合输出AlGaInAs多量子阱环形激光器研究

采用InP基InAlGaAs多量子阱激光器外延材料结构, 利用感应耦合等离子体(ICP)干法刻蚀技术和聚酰亚胺介质平坦化工艺, 研制了多量子阱半导体环形激光器样品. 该器件通过加正偏压的环形结构谐振腔实现光激射, 然后借助紧邻的直线波导耦合将光信号输出. 环形谐振腔直径为700 μm, 波导宽度为3 μm. 用光纤对准直线波导端口耦合测试了环形激光器的光功率-电流特性曲线和激射光谱, 其阈值电流为120 mA, 在注入电流160 mA时从直波导耦合输出得到激射光谱的中心波长为1602 nm, 并结合光功率-电流特性曲线对环形激光器中的工作模式进行了初步分析.     

中华绒螯蟹首次排卵后卵巢发育的组织学研究

利用组织切片技术,结合外观特征,在光学水平对江苏南通地区第一次排卵后18天内（即卵巢的二次发育）的中华绒螯蟹的卵巢发育进行组织学和细胞学的观察研究．本实验可以观察到卵细胞发育的四个不同时期：初级卵母细胞小生长期、初级卵母细胞大生长期、成熟期以及退化时期的卵细胞．排卵后的卵巢在营养贫乏的情况下,出现直接退化现象;而在营养丰富的情况下,处于大生长前期的卵细胞则会迅速生长,为二次排卵做好准备．     

网络教育资源Web挖掘研究

针对网络教育资源建设中存在的问题，着重对网络教育资源的获取、分类和标准化描述模型进行了研究．在分析Web挖掘技术和任务分类的基础上，提出了网络教育资源的Web文本挖掘、模型及其相关算法，将数据挖掘技术应用到网络教育领域，有助于在网络上获取高品质的网络教育资源，一定程度上解决了网络教育资源获取缺乏智能的问题．     

The hyh mutation uncovers roles for alpha Snap in apical protein localization and control of neural cell fate

The hyh (hydrocephalus with hop gait) mouse shows a markedly small cerebral cortex at birth and dies postnatally from progressive enlargement of the ventricular system. Here we show that the small hyh cortex reflects altered cell fate. Neural progenitor cells withdraw prematurely from the cell cycle, producing more early-born, deep-layer cerebral cortical neurons but depleting the cortical progenitor pool, such that late-born, upper-layer cortical neurons are underproduced, creating a small cortex. hyh mice carry a hypomorphic missense mutation in the gene Napa encoding soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein alpha (alpha Snap), involved in SNAP receptor (SNARE)-mediated vesicle fusion in many cellular contexts. A targeted null Napa mutation is embryonically lethal. Altered neural cell fate is accompanied by abnormal localization of many apical proteins implicated in regulation of neural cell fate, including E-cadherin, beta-catenin, atypical protein kinase C (aPKC) and INADL (inactivation-no-afterpotential D-like, also known as protein associated with Lin7, or Pals1). Apical localization of the SNARE Vamp7 is also disrupted. Thus, alpha Snap is essential for apical protein localization and cell fate determination in neuroepithelial cells.     

模糊滑动控制的一般方法(英文)

陈述了一种新的模糊逻辑控制方法,它可消除滑动控制所固有的抖动问题。方法的推导是将多开关滑动控制问题简化成等效的单开关问题。控制规律显示它是一种模糊滑动控制的一般方法。文献中的其他方法可由此法导出。模糊推理规则由两个输入变量组成。第一个输入变量是系统状态到所预定的状态空间中的超平面之间的方向距离;第二个输入变量的选择可根据应用而定,例如方向距离的导数、控制设计者所感兴趣的特定变量,或者某些状态变量的加权之和。这个新方法易于在高阶系统中实现,并且可以直接而明确地控制系统的动态过程。它消除了滑动控制和经典模糊滑动控制中的抖动问题。此外。新方法比其他类似方法的控制要简单。稳定性和性能分析显示了此法的有效性。此法已用于一带有典型驱动和反馈传感器的工业直流电机的位置控制之中。     

The VASE exon downregulates the neurite growth-promoting activity of NCAM 140.

Axonal growth, guidance and synapse formation are controlled by receptors on neuronal growth cones that can recognize positive and inhibitory cues in the local microenvironment. Four well characterized receptor systems are known that recognize the growth-promoting activities associated with the extracellular matrix and the membranes of cells such as astrocytes, muscle cells and Schwann cells; these are the integrins and the homophilically binding cell adhesion molecules neural-cell adhesion molecule (NCAM), N-cadherin and L1 (refs 5-12). Alternative splicing generates 20-30 isoforms of NCAM and these can also be differentially glycosylated. There are two sites where alternative splicing changes the extracellular structure of membrane-bound NCAM and one of these (the MSD1 region) does not obviously affect function. Here we report that the variable alternatively spliced exon (VASE) in immunoglobulin domain 4 downregulates the neurite outgrowth-promoting activity of NCAM. The high level of VASE expression in the adult central as compared with peripheral nervous system could contribute to the poor regenerative capacity of the former.     

Calcium-dependent enhancement of calcium current in smooth muscle by calmodulin-dependent protein kinase II.

Calcium entry through voltage-activated Ca2+ channels is important in regulating many cellular functions. Activation of these channels in many cell types results in feedback regulation of channel activity. Mechanisms linking Ca2+ channel activity with its downregulation have been described, but little is known of the events responsible for the enhancement of Ca2+ current that in many cells follows Ca2+ channel activation and an increase in cytoplasmic Ca2+ concentration. Here we investigate how this positive feedback is achieved in single smooth muscle cells. We find that in these cells voltage-activated calcium current is persistently but reversibly enhanced after periods of activation. This persistent enhancement of the Ca2+ current is mediated by activation of calmodulin-dependent protein kinase II because it is blocked when either the rise in cytoplasmic Ca2+ is inhibited or activation of calmodulin-dependent protein kinase II is prevented by specific peptide inhibitors of calcium-calmodulin or calmodulin-dependent protein kinase II itself. This mechanism may be important in different forms of Ca2+ current potentiation, such as those that depend on prior Ca2+ channel activation or are a result of agonist-induced release of Ca2+ from internal stores.