环状磷酰基硫脲的合成研究

采用2-异硫氰基-5，5-二甲基-2-氧代-1，3，2-二氧磷杂环己烷与不同的胺反应合成了13个新型的环状磷酰基硫脲衍生物，它们的结构经^1H NMR、IR和元素分析证实．     

基于J2ME与WebService架构的无线Internet应用研究

对比了J2ME与WAP,阐述了基于J2ME与WebService架构的无线Internet应用开发模式,并应用此架构设计了面向手机、PDA等无线手持设备的实时航班查询系统.     

基于谱分析的实时波浪模拟

海洋表面有各种各样的波浪，作为一种自然现象，其模拟已成为计算机图形学中最具挑战性的问题之一。风浪是最主要的一种波浪，其模拟在工程及影视中的应用已日益引起人们的关注。本文从海洋学已有的统计观测结果出发，利用海浪频谱与方向谱的相关公式，对开阔海面深水域的风成波浪进行了模拟。实践证明，该方法对波浪的模拟在实时性与真实感方面均取得了不错的效果。     

CeO_2纳米线阵列的制备

以阳极氧化铝膜(AAO)为模板通过溶胶-凝胶法合成了CeO2 纳米线阵列,并通过扫描电子显微镜(SEM)、透射电子显微镜(TEM)以及X射线光电子能谱(XPS)等对CeO2 纳米线进行了表征.     

同步时序逻辑电路设计方法改进

用卡诺图化简法求电路激励方程的方法进行改进。     

利用矩阵和分块矩阵的乘法计算行列式的值

利用矩阵乘积的行列式公武计算行列式的值;将矩阵巧妙合理地分块后,利用分块矩阵的乘法计算行列式的值.     

藏东南高寒区尼洋河河谷地带不同土地利用方式土壤抗蚀性研究

土壤抗蚀性是评价土壤侵蚀潜在发生可能性的重要综合性指标,研究高寒河谷地带不同土地利用方式土壤抗蚀性为土地利用模式优化和资源整合提供理论依据.本文应用主成分分析法对藏东南高寒区尼洋河流域5种不同土地利用方式下的3大类、13个土壤抗蚀性指标进行分析研究.研究结果表明:土壤团粒类指标和有机质能很好地反映土壤抗蚀性,0.25 mm水稳性团聚体质量分数、0.5mm水稳性团聚体质量分数、0.25 mm非水稳性团聚体质量分数、水稳性指数、平均重量直径、团聚体结构破坏率、有机质7个指标对土壤抗蚀性的影响最为明显,是表现不同土地利用方式土壤抗蚀性的最佳指标.各抗蚀性指标值基本表现出(0～15)cm(16～30)cm规律.通过建立权重求和模型发现0～15 cm表层土壤抗蚀性能远远大于16～30 cm;最终,通过叠加法得出不同土地利用类型土壤抗蚀性评价从强到弱顺序为:灌木林地(SL)、天然林地(NF)、农耕地(CL)、河滩林地(BL)、人工林地(AF).     

Epigenetics: a link between addiction and social environment

The detrimental effects of drug abuse are apparently not limited to individuals but may also impact the vulnerability of their progenies to develop addictive behaviours. Epigenetic signatures, early life experience and environmental factors, converge to influence gene expression patterns in addiction phenotypes and consequently may serve as mediators of behavioural trait transmission between generations. The majority of studies investigating the role of epigenetics in addiction do not consider the influence of social interactions. This shortcoming in current experimental approaches necessitates developing social models that reflect the addictive behaviour in a free-living social environment. Furthermore, this review also reports on the advancement of interventions for drug addiction and takes into account the emerging roles of histone deacetylase (HDAC) inhibitors in the etiology of drug addiction and that HDAC may be a potential therapeutic target at nucleosomal level to improve treatment outcomes.     

0.18μm CMOS高集成度可编程分频器的设计

采用标准0.18 μm CMOS工艺,提出了一种高集成度可编程分频器.该电路所采用技术的新颖之处在于：基于基本分频单元的特殊结构,对除2/除3单元级联式可编程分频器的关键模块进行改进,将普通的CML型锁存器集成为包含与门的锁存器,从而大大提高了电路的集成度,有效地降低了电路功耗,提升了整体电路速度,并使版图更紧凑.仿真结果表明,在1.8V电压、输入频率Fin=1 GHz的情况下,可实现任意整数且步长为1的分频比,相位噪声为-173.1 dBc/Hz@1 MHz,电路功耗仅为9 mW.     

Tyrosine 842 in the activation loop is required for full transformation by the oncogenic mutant FLT3-ITD

The type III receptor tyrosine kinase FLT3 is frequently mutated in acute myeloid leukemia. Oncogenic FLT3 mutants display constitutive activity leading to aberrant cell proliferation and survival. Phosphorylation on several critical tyrosine residues is known to be essential for FLT3 signaling. Among these tyrosine residues, Y842 is located in the so-called activation loop. The position of this tyrosine residue is well conserved in all receptor tyrosine kinases. It has been reported that phosphorylation of the activation loop tyrosine is critical for catalytic activity for some but not all receptor tyrosine kinases. The role of Y842 residue in FLT3 signaling has not yet been studied. In this report, we show that Y842 is not important for FLT3 activation or ubiquitination but plays a critical role in regulating signaling downstream of the receptor as well as controlling receptor stability. We found that mutation of Y842 in the FLT3-ITD oncogenic mutant background reduced cell viability and increased apoptosis. Furthermore, the introduction of the Y842 mutation in the FLT3-ITD background led to a dramatic reduction in in vitro colony forming capacity. Additionally, mice injected with cells expressing FLT3-ITD/Y842F displayed a significant delay in tumor formation, compared to FLT3-ITD expressing cells. Microarray analysis comparing gene expression regulated by FLT3-ITD versus FLT3-ITD/Y842F demonstrated that mutation of Y842 causes suppression of anti-apoptotic genes. Furthermore, we showed that cells expressing FLT3-ITD/Y842F display impaired activity of the RAS/ERK pathway due to reduced interaction between FLT3 and SHP2 leading to reduced SHP2 activation. Thus, we suggest that Y842 is critical for FLT3-mediated RAS/ERK signaling and cellular transformation.