高中学生的物理成绩的调查与分析

经过两年广泛的调查，对调查结果进行统计，按教育统计学相关分析的计算方法，逐条求出各单元的相应系数。并对量化的部分结果进行了初步分析，指出了高中学生学习物理困难的主要原因，以及进行矫治的初步措施。该调查采集面广，样本大，计算方法科学，量化结果数据可靠，所反映的信息具有一定的代表性，可供中学物理同仁在教学改革中参考。     

有关勾股定理、射影定理的研究性论题

本文对勾股定理、射影定理的研究性论题进行了研究。     

Science Letters： A synthetic Toll-like receptor 2 ligand decreases allergic immune responses in a mouse rhinitis model sensitized to mite allergen

It has been proposed that activation of Toll-like receptors （TLRs） plays crucial roles in the polarization of adaptive immune responses. A synthetic Toll-like receptor 2 （TLR2） ligand, Pam3CSK4, has been reported to modulate the balance of Th1/Th2 responses. We evaluated the modulation effect of Pam3CSK4 on allergic immune response in a mouse rhinitis model sensitized to house dust mite allergen （HDM）. Mice were sensitized and challenged with Dermatophagoidesfarinae allergen （Der f）, and then the allergic mice were treated by Pam3CSK4. Nasal allergic symptoms and eosinophils were scored. Der f-specific cytokine responses were examined in the splenocytes and bronchoalveolar lavage fluid （BALF）. Serum level of total IgE was also detected. After establishing a mouse allergic rhinitis model with HDM, we have showed that Pam3CSK4 treatment not only ameliorated the nasal allergic symptoms remarkably but also decreased the eosinophils and total inflammation cells in BALF significantly. Analysis of cytokine profile found that IFN-7 released from either BALF or stimulated splenocytes increased markedly in Pam3CSK4-treated mice, while IL-13 decreased significantly. Moreover, serum level of total IgE was significantly lower in Pam3CSK4-treated mice than in the untreated. Thus, in an allergic rhinitis mouse model developed with HDM, Pam3CSK4 was shown to exhibit an antiallergic effect, indicating its potential application in allergic diseases.     

序列模式挖掘的两种典型算法及比较

序列模式挖掘是数据挖掘的重要分支,GSP算法与PSP算法是序列模式挖掘中的两种典型算法。本文介绍了这两种算法并对其进行了分析与比较。     

怀地黄不同品种块根显微结构与糖分含量的比较研究

采用石蜡切片和分光光度计对不同品种怀地黄块根的显微结构和糖分含量进行了研究,并用SPSS 10.0软件分析了两者之间的相关性.结果表明,怀地黄不同品种块根的显微结构差异明显,且还原糖含量的差异达到了显著水平.块根中还原糖含量、总糖含量均与块根各解剖结构特征呈正相关关系.     

PbI_2－PbBr_2－KCl系统玻璃的形成及其析晶行为

ＰｂＩ_２可以单独形成玻璃。ＰｂＩ_２－ＰｂＢｒ_２－ＫＣｌ三元系统玻璃具有良好的玻璃形成能力。通过恰当的热处理，不仅可获得透红外性能与原始玻璃一致的微晶玻璃，同时还可克服自发析晶倾向和大幅度地提高玻璃的显微硬度。以此三元系统为基础，有望开发出一类具有实用前景的透红外玻璃材料。     

非线性系统两变量控制下的分枝特性

采用分枝理论推导非线性系统两变量P和PI控制下的分枝特性,所导得的几个定理阐明了简单分枝点和Hopf分枝点的位置和性质。一个简化精馏塔模型用于演示这一过程,展示出精馏塔系统在闭环时,可能出现多态和极限环。     

矿区铁路专用线下综采放顶煤开采的试验研究

介绍了国内第一个综采放顶煤开采矿区铁路线下压煤试验面的成功经验，总结了试采中对铁路所采取的各种分析和维护措施，分析了该采煤方法下的地在移动和变形特点，为我国“三下”采煤领域提供了具有特色的成功实例。     

Electrochemical studies of glutathione monolayer assembled on a polycrystalline gold electrode

The glutathione (GSH) monolayer and complex monolayer of GSH-metallic ion on polycrystalline gold electrode were studied by using K₃Fe(CN)₆ as the redox probe. As for the GSH monolayer, it was found that the metallic ions could open the ion-gate in the monolayer dramatically in the order La³⁺> Pb²⁺>>Ba²⁺>Ca²⁺ whereas Zn²⁺ ion closed the ion-gate. The complexes of GSH-metallic ions were capable of self-assembling the different kind of monolayer. All the differences were related to the structural configuration of the anchored GSH molecule, which changed with different metallic ions or pH. Biography:Fang Cheng (1971-) male, Ph. D, research direction: electroanlysis.     

The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease

The recycling of the amyloid precursor protein (APP) from the cell surface via the endocytic pathways plays a key role in the generation of amyloid beta peptide (Abeta) in Alzheimer disease. We report here that inherited variants in the SORL1 neuronal sorting receptor are associated with late-onset Alzheimer disease. These variants, which occur in at least two different clusters of intronic sequences within the SORL1 gene (also known as LR11 or SORLA) may regulate tissue-specific expression of SORL1. We also show that SORL1 directs trafficking of APP into recycling pathways and that when SORL1 is underexpressed, APP is sorted into Abeta-generating compartments. These data suggest that inherited or acquired changes in SORL1 expression or function are mechanistically involved in causing Alzheimer disease.