重介质旋流器分选机理研究

物料分选过程 ,是整个体系能量降低的过程 ,从这一原理出发 ,不同性质的固体颗粒在重介质旋流器中将位于不同的位置 ,使不同性质的固体颗粒得以分离。固体颗粒在重介质旋流器中的运动轨迹大体呈圆锥螺旋线形状 ,实测出的密度线验证了该结论     

播种方式对紫花苜蓿＋无芒雀麦人工草地土壤剖面养分分布的影响

采用田间调查取样和室内分析相结合的方法,2007年在内蒙古民族大学农学院试验农场以2年生单播紫花苜蓿、单播无芒雀麦、隔行混播和同行混播人工草地为研究对象,采用分层取样法研究了不同播种方式对土壤理化性质的影响,结果表明：在牧草生长期间单播无芒雀麦草地土壤容重最小,紫花苜蓿草地土壤容重最大;单播无芒雀麦、隔行混播和同行混播草地0～20cm土层有机质含量大于单播紫花苜蓿草地,20～30cm不显著,30～40cm单播紫花苜蓿草地显著增加,分别是隔行混播草地、同行混播和单播无芒雀麦草地的1.11、1.72和1.94倍;速效N单播无芒雀麦草地最低,速效P、速效K单播紫花苜蓿草地最低.     

藏药波棱瓜花质量标准的初步研究

对藏药波棱瓜花药材的质量标准进行初步研究.根据2010年版《中国药典》附录IX相关方法,对波棱瓜花药材的水分、总灰分、酸不溶性灰分、醇溶性浸出物进行测定;并对该药材的性状、显微特征进行描述;采用薄层色谱(TLC)法进行定性鉴别.初步明确了波棱瓜花药材性状、显微和薄层鉴别方法,并确立了波棱瓜花药材水分、总灰分、酸不溶性灰分、浸出物的限量.本研究为波棱瓜花的质量标准的的制定提供参考依据.     

基于CVaR的能源互补联合系统优化配置模型研究

由于风电、光电出力具有不确定性,因此会引起电网频率的较大波动,严重影响电能质量.为了保证含有新能源电力系统的稳定运行,特提出风光水储联合调度优化模型.首先,建立含新能源的电力系统优化调度数学模型,该模型追求系统机组耗量最小.在进行含新能源发电的电力系统优化调度中,可被用来调度的出力实际为满足负荷功率后,扣除新能源输出功率的那部分火电机组出力.算例结果表明,本文采取CVaR具有良好的性能;风电与光伏清洁能源机组并入系统中增加了日前调度的不确定性风险,但通过CVaR评估计算系统风险,采取有效的措施会使系统发电成本减少与碳排放量减少.     

Nanomechanics: response of a strained semiconductor structure

The nanomechanical properties of thin silicon films will become increasingly critical in semiconductor devices, particularly in the context of substrates that consist of a silicon film on an insulating layer (known as silicon-on-insulator, or SOI, substrates). Here we use very small germanium crystals as a new type of nanomechanical stressor to demonstrate a surprising mechanical behaviour of the thin layer of silicon in SOI substrates, and to show that there is a large local reduction in the viscosity of the oxide on which the silicon layer rests. These findings have implications for the use of SOI substrates in nanoelectronic devices.     

A transforming mutation in the pleckstrin homology domain of AKT1 in cancer

Although AKT1 (v-akt murine thymoma viral oncogene homologue 1) kinase is a central member of possibly the most frequently activated proliferation and survival pathway in cancer, mutation of AKT1 has not been widely reported. Here we report the identification of a somatic mutation in human breast, colorectal and ovarian cancers that results in a glutamic acid to lysine substitution at amino acid 17 (E17K) in the lipid-binding pocket of AKT1. Lys 17 alters the electrostatic interactions of the pocket and forms new hydrogen bonds with a phosphoinositide ligand. This mutation activates AKT1 by means of pathological localization to the plasma membrane, stimulates downstream signalling, transforms cells and induces leukaemia in mice. This mechanism indicates a direct role of AKT1 in human cancer, and adds to the known genetic alterations that promote oncogenesis through the phosphatidylinositol-3-OH kinase/AKT pathway. Furthermore, the E17K substitution decreases the sensitivity to an allosteric kinase inhibitor, so this mutation may have important clinical utility for AKT drug development.