MgFeSiO_4 prepared via a molten salt method as a new cathode material for rechargeable magnesium batteries

Well-crystallized MgFeSiO4 microparticles were synthesized at different temperatures by a simple molten salt method using KCl flux. As a new cathode for rechargeable magnesium batteries,the material shows a reversible Mg2+ intercalation-deintercalation process. In 0.25 mol/L Mg(AlCl2EtBu) 2/THF electrolyte,MgFeSiO4 synthesized at 900°C can deliver a 125.1 mAh/g initial dis-charge capacity and a 91.4% capacity retention on the 20th cycle at a rate of 0.1C(about 15.6 mA/g) . The results show that MgFeSiO4 cou...     

论沈光文诗歌的用典艺术

沈光文诗歌中的典故来源丰富，经史子集无所不涉。作者善于以典抒怀，以史明志，体现了活用典故、以故为新、如水着盐、浑融无迹等用典技巧。沈光文诗歌通过对典故的娴熟运用，自然贴切而又含蓄蕴藉地表现了明清之际遗民诗人复杂深沉的思想感情，赋予了诗作古雅凝重、沉致深婉的审美风格，也折射了作者崇高峻洁的人格之美。     

《普洱茶文化赏析》通识课“三合一”教改实践与反思

在深化教育领域综合改革大背景下,近两年来,大理学院面向全校各专业学生开设的《普洱茶文化赏析》通识选修课,积极适应教育发展改革新形势;将课堂教学、实训、大学生创业指导"三合一",创新教改模式,不仅使学生学到通识教育知识,还培养其创新创业能力,提高学生的实践实训能力,在教改实践中取得了较好效果,受到学生普遍欢迎。     

论媒体与司法的关系——以药家鑫案为背景的分析

社会公众通过新闻媒体、网络媒体关注司法机关对一些社会影响力较大案件的审判活动,本身就是法制的进步和公民意识的觉醒.它保障了司法审判的公正性与透明性,有效地防止司法腐败及暗箱操作的发生.然而,过度与不合适宜的报道与宣传也有其负面效应发酵的一面,如不能在法治的轨道上加以引导,就很有可能损害司法的独立性与公正性,从而滑向众口铄金的泥淖,这是司法独立所必须面对的现实之一.     

楚调“唐音”歌吟源流及其基本特点

楚凋“唐音”歌吟是我国传统吟诵众多流派中的一个重要分支，文章阐述了楚调“唐音”歌吟（江西省级非物质文化遗产）的源流，并对其基本特点进行归纳与总结。楚调“唐音”歌吟可吟多种诗词体裁，且在同一首诗（词）中可分别采用如歌、如诉、如泣三种吟唱模式，为丰富吟诵音乐形态的地域研究提供参考。     

基于神经网络技术自动筛选Monastrol抑制剂的算法研究

带自动荧光显微镜的HCS（high content screening）系统是一种新兴的显微摄影、筛选和处理系统.HCS系统在摄影过程中会产生大量数据,人工筛选和识别费时费力.本文为了进行Monastrol抑制剂的筛选,基于前馈式神经网络技术研究了一种对HCS系统摄影的大量细胞同时进行特征提取和细胞显型识别的自动算法.在得到各个通道分离的图像后,对不同通道图像进行并行预处理,并采用神经网络和逻辑运算相结合的算法进行处理.我们将该方法运用于Monastrol抑制剂的筛选中,并将结果与人工识别结果进行分析比较.相比较前人提出的multi-phenotypic mitotic analysis（MMA）算法自动识别的正确率得以提高,可更好评估抗癌药剂效用.     

基于异构数据库银行业绩考核系统的构建

针对从异种操作系统平台事后下载、解压、提取当日银行业务报表数据,采用Visual FoxPro数据库语言进行银行业绩考核统计应用程序设计中涉及的异种数据库数据格式转换、数据筛选等几个难点问题进行分析,提出采用基于中间数据格式转换的方法,有效地解决了Informix 数据、FoxPro 数据格式转换问题,使该程序得以成功开发和应用.     

14-3-3sigma controls mitotic translation to facilitate cytokinesis

14-3-3 proteins are crucial in a wide variety of cellular responses including cell cycle progression, DNA damage checkpoints and apoptosis. One particular 14-3-3 isoform, sigma, is a p53-responsive gene, the function of which is frequently lost in human tumours, including breast and prostate cancers as a result of either hypermethylation of the 14-3-3sigma promoter or induction of an oestrogen-responsive ubiquitin ligase that specifically targets 14-3-3sigma for proteasomal degradation. Loss of 14-3-3sigma protein occurs not only within the tumours themselves but also in the surrounding pre-dysplastic tissue (so-called field cancerization), indicating that 14-3-3sigma might have an important tumour suppressor function that becomes lost early in the process of tumour evolution. The molecular basis for the tumour suppressor function of 14-3-3sigma is unknown. Here we report a previously unknown function for 14-3-3sigma as a regulator of mitotic translation through its direct mitosis-specific binding to a variety of translation/initiation factors, including eukaryotic initiation factor 4B in a stoichiometric manner. Cells lacking 14-3-3sigma, in marked contrast to normal cells, cannot suppress cap-dependent translation and do not stimulate cap-independent translation during and immediately after mitosis. This defective switch in the mechanism of translation results in reduced mitotic-specific expression of the endogenous internal ribosomal entry site (IRES)-dependent form of the cyclin-dependent kinase Cdk11 (p58 PITSLRE), leading to impaired cytokinesis, loss of Polo-like kinase-1 at the midbody, and the accumulation of binucleate cells. The aberrant mitotic phenotype of 14-3-3sigma-depleted cells can be rescued by forced expression of p58 PITSLRE or by extinguishing cap-dependent translation and increasing cap-independent translation during mitosis by using rapamycin. Our findings show how aberrant mitotic translation in the absence of 14-3-3sigma impairs mitotic exit to generate binucleate cells and provides a potential explanation of how 14-3-3sigma-deficient cells may progress on the path to aneuploidy and tumorigenesis.     

Escape from HER-family tyrosine kinase inhibitor therapy by the kinase-inactive HER3

Oncogenic tyrosine kinases have proved to be promising targets for the development of highly effective anticancer drugs. However, tyrosine kinase inhibitors (TKIs) against the human epidermal growth factor receptor (HER) family show only limited activity against HER2-driven breast cancers, despite effective inhibition of epidermal growth factor receptor (EGFR) and HER2 in vivo. The reasons for this are unclear. Signalling in trans is a key feature of this multimember family and the critically important phosphatidylinositol-3-OH kinase (PI(3)K)/Akt pathway is driven predominantly through transphosphorylation of the kinase-inactive HER3 (refs 9, 10). Here we show that HER3 and consequently PI(3)K/Akt signalling evade inhibition by current HER-family TKIs in vitro and in tumours in vivo. This is due to a compensatory shift in the HER3 phosphorylation-dephosphorylation equilibrium, driven by increased membrane HER3 expression driving the phosphorylation reaction and by reduced HER3 phosphatase activity impeding the dephosphorylation reaction. These compensatory changes are driven by Akt-mediated negative-feedback signalling. Although HER3 is not a direct target of TKIs, HER3 substrate resistance undermines their efficacy and has thus far gone undetected. The experimental abrogation of HER3 resistance by small interfering RNA knockdown restores potent pro-apoptotic activity to otherwise cytostatic HER TKIs, re-affirming the oncogene-addicted nature of HER2-driven tumours and the therapeutic promise of this oncoprotein target. However, because HER3 signalling is buffered against an incomplete inhibition of HER2 kinase, much more potent TKIs or combination strategies are required to silence oncogenic HER2 signalling effectively. The biologic marker with which to assess the efficacy of HER TKIs should be the transphosphorylation of HER3 rather than autophosphorylation.     

基于GIS图谱法的中药资源生境恢复研究——以云南楚雄州彝药资源研究为例

为了对我国中药资源数字化的深入研究提供基础,提出利用现代GIS技术与地学图谱叠加相结合的方法进行生境恢复研究,建立了生境恢复的评价指标体系,并以云南楚雄州为研究区域,进行了彝药资源的生境恢复研究案例.结果表明: 1)生境恢复研究是实现我国中药资源可持续发展和利用的重要途径;2)GIS图谱法是进行生境恢复研究的科学有效技术方法.