在砂土液化的危险性评价中确定性与不确定性方法的应用研究

地震导致的砂土液化具有很大的随机性。据此，提出了评价砂土液化危险性的确定性与不确定性两种方法。确定性方法是以液化指数为变量的多因子判别分析方法，不确定性方法是分析法，即用概率密度函数判断砂土液化灾害的期望损失值。     

风险决策中不同决策准则决策一致性条件

首先给出了理想条件收益值的概念,证明了一个风险决策问题的理想条件收益值是一个定数,并给出了条件收益值与条件损失值的关系.其次给出了理想期望收益值的概念,证明了一个风险决策问题的理想期望收益值是一个定数,并在以上概念和结论的基础上给出了期望收益值与期望损失值的关系.最后给出了风险决策中按不同决策准则决策的一致性条件.     

不均衡数据情形的基于聚焦损失的CGAN的集成分类方法

针对非均衡数据的情形,基于条件生成对抗网络(conditional generative adversarial networks, CGAN),利用梯度提升树研究了聚焦损失的CGAN的集成分类方法.该方法首先通过CGAN降低不均衡率,通过聚焦损失的权值均衡结合GBDT算法,适当增加对少数类样本的关注度进而进一步提升分类器的分类性能.对方法的性质进行了研究,获得了若干理论成果.证明了:在一定条件下,由CGAN产生的经验条件分布收敛于相应总体的条件分布;聚集损失的CGAN方法其经验风险收敛到期望风险;该方法的估计量会收敛到使得期望风险最小化的函数.实验结果显示了聚焦损失的CGAN方法具有良好的表现.     

EMV、EOL和EUV理论在风险决策中的应用分析

文章简要介绍了最大期望收益决策准则、最小机会损失决策准则和最大效用值决策准则,将它们应用于风险决策案例并进行分析,最大期望收益决策准则和最小机会损失决策准则结论基本相同,二者与最大效用值决策准则结合使用,可使决策更为合理.     

基于高阶期望损失的投资组合优化模型

金融风险管理的第一步是风险的识别和度量,选择一种满足实践需要的风险测度指标是风险管理的关键.首先提出了高阶期望损失风险测度的定义,其次建立了高阶期望损失风险测度的投资组合优化模型,并对其进行求解,该模型的解在获得指定回报率的全部投资组合中具有最小的高阶期望损失风险.模型和求解方法将在金融理论和实践两方面有多种应用.     

基于多伴随直觉模糊粗糙集的三支决策

决策粗糙集提供了处理不确定数据和风险数据决策问题的一个新方法,基于决策粗糙集的三支决策理论是典型的风险决策理论的推广.传统的直觉模糊粗糙集采用一对三角模与蕴涵算子来构造逻辑算子,未考虑属性之间的差别,而多伴随直觉模糊粗糙集采用多个伴随对构造逻辑算子,更好地体现了用户偏好.构造了多伴随直觉模糊粗糙集模型,研究了基于多伴随直觉模糊粗糙集的三支决策.首先,定义了乐观多伴随直觉模糊粗糙集,并用于处理直觉模糊数的复杂计算问题;然后利用隶属函数和非隶属函数计算损失函数,通过期望损失函数对事件对象进行评估,进一步构造了相应的三支决策模型;基于期望损失函数值最小的原则诱导出三支决策,并得到相应决策的风险值.此模型中期望损失函数的构造是基于支持度与非支持度两种度量的综合讨论,考虑更全面,更能有效地反映实际生活情况,满足用户偏好.最后用医学诊断的例子来验证该模型的有效性.     

用Gauss-Laguerre积分算法确定风速数学期望

在分析了风速离散性与连续性特点基础上,通过引入连续型风速的Weibull概率分布和数学期望表达式,分别给出离散型和连续型风速数学期望的计算方法.为求解风速的Weibull数学期望,首先提出用梯度法求出Weibull函数的两个参数,然后以Gauss-Laguerre积分公式作为标准模型,将Weibull数学期望表达式转化为此标准模型,进而求出数学期望的值.最后以内蒙古新巴尔虎旗为例,通过上述方法求出该地区风速的数学期望.实验结果和分析显示,这种方法求得的数学期望和经验平均风速与气象上平均风速基本吻合.     

考虑可再生能源配额制的售电公司组合购电优化研究

以风电购电量和绿色证书购买量作为实行配额的方法,协调售电公司在远期合约、现货、期权等多个市场的购电量,考虑负荷需求、风电购电量及电价的不确定性,采用条件风险价值度量损失的大小,以期望费用最小和遭受损失的风险最小为目标,建立期望购电费用-损失风险模型,并通过多目标粒子群优化法和模糊集理论进行求解. 最后,通过算例分析可再生能源配额制、期权合约对售电公司的购电费用、损失的风险值和在各市场的购电量的影响,从而为售电公司在多市场环境下的购电策略提供参考.     

基于非对称GARCH与极值理论的商业银行信用风险度量模型

提出一种基于ARMA-TGARCH-EVT模型并适用于商业银行内部信用风险评估的新方法.首先通过广义矩法估计ARMA-TGARCH模型,获得近似独立同分布的残差序列zt;然后选用极值理论的越槛高峰模型(POT)对残差序列进行拟合分析,得到风险价值和期望损失的估计值,并采用Bootstrap方法给出95%置信水平下的置信区间;最后利用某商业银行2000-02-19～2010-12-15的日信贷资产对数收益率进行仿真,得到控制信用风险价值V和期望损失E值及置信区间,并与未经调整的预测值进行比较.研究结果表明,该方法在一定程度上克服了单纯进行极值分析时,由于序列的非独立同分布不能满足极值理论假设所造成的估计误差,改进了采用似然比率法估计置信区间时,由于极值事件的小样本所造成的偏差.     

粉体与聚合物相容性的一种表征法

在曾提出的表征粉体表面化学特征的参数ATRHL值(即亲水-亲油比)的基础上,测定了几种粉体的ATRHL值,并用DSC及相差显微镜法研究了这几种粉体与PS及PVA的相容性。结果表明,粉体的ATRHL值越小,与PS相容性越好。因此,ATRHL值可做为判定粉体与聚合物相容性的一种表征方法。     

基于C++表达的AI/ES语言和工具的实现

介绍了C＋＋表达的人工智能（AD）／专家系统（ES）的设计和实现。针对以前在人工智能研究中的函数式程序语言－LISP，建立了一个C＋＋和LISP语言之间的转换工具。基于C＋＋的专家系统开发模式构造了ES系统中的部分底层模块（如：表操作）。通过使用该模块能够直接把各种LISP开发的系统映射到新的C＋＋开发平台，实现高效的、实用的人工智能专家系统。     

Nanog promotes transfer of pluripotency after cell fusion

Through cell fusion, embryonic stem (ES) cells can erase the developmental programming of differentiated cell nuclei and impose pluripotency. Molecules that mediate this conversion should be identifiable in ES cells. One candidate is the variant homeodomain protein Nanog, which has the capacity to entrain undifferentiated ES cell propagation. Here we report that in fusions between ES cells and neural stem (NS) cells, increased levels of Nanog stimulate pluripotent gene activation from the somatic cell genome and enable an up to 200-fold increase in the recovery of hybrid colonies, all of which show ES cell characteristics. Nanog also improves hybrid yield when thymocytes or fibroblasts are fused to ES cells; however, fewer colonies are obtained than from ES x NS cell fusions, consistent with a hierarchical susceptibility to reprogramming among somatic cell types. Notably, for NS x ES cell fusions elevated Nanog enables primary hybrids to develop into ES cell colonies with identical frequency to homotypic ES x ES fusion products. This means that in hybrids, increased Nanog is sufficient for the NS cell epigenome to be reset completely to a state of pluripotency. We conclude that Nanog can orchestrate ES cell machinery to instate pluripotency with an efficiency of up to 100% depending on the differentiation status of the somatic cell.     

Role of ERas in promoting tumour-like properties in mouse embryonic stem cells

Embryonic stem (ES) cells are pluripotent cells derived from early mammalian embryos. Their immortality and rapid growth make them attractive sources for stem cell therapies; however, they produce tumours (teratomas) when transplanted, which could preclude their therapeutic usage. Why ES cells, which lack chromosomal abnormalities, possess tumour-like properties is largely unknown. Here we show that mouse ES cells specifically express a Ras-like gene, which we have named ERas. We show that human HRasp, which is a recognized pseudogene, does not contain reported base substitutions and instead encodes the human orthologue of ERas. This protein contains amino-acid residues identical to those present in active mutants of Ras and causes oncogenic transformation in NIH 3T3 cells. ERas interacts with phosphatidylinositol-3-OH kinase but not with Raf. ERas-null ES cells maintain pluripotency but show significantly reduced growth and tumorigenicity, which are rescued by expression of ERas complementary DNA or by activated phosphatidylinositol-3-OH kinase. We conclude that the transforming oncogene ERas is important in the tumour-like growth properties of ES cells.     

Mismatch repair genes identified using genetic screens in Blm-deficient embryonic stem cells

Phenotype-driven recessive genetic screens in diploid organisms require a strategy to render the mutation homozygous. Although homozygous mutant mice can be generated by breeding, a reliable method to make homozygous mutations in cultured cells has not been available, limiting recessive screens in culture. Cultured embryonic stem (ES) cells provide access to all of the genes required to elaborate the fundamental components and physiological systems of a mammalian cell. Here we have exploited the high rate of mitotic recombination in Bloom's syndrome protein (Blm)-deficient ES cells to generate a genome-wide library of homozygous mutant cells from heterozygous mutations induced with a revertible gene trap retrovirus. We have screened this library for cells with defects in DNA mismatch repair (MMR), a system that detects and repairs base-base mismatches. We demonstrate the recovery of cells with homozygous mutations in known and novel MMR genes. We identified Dnmt1(ref. 5) as a novel MMR gene and confirmed that Dnmt1-deficient ES cells exhibit micro-satellite instability, providing a mechanistic explanation for the role of Dnmt1 in cancer. The combination of insertional mutagenesis in Blm-deficient ES cells establishes a new approach for phenotype-based recessive genetic screens in ES cells.     

单层和多层Ehrlich-Schwoebel势垒对薄膜粗糙度随温度变化的影响

以Cu为原型,利用动力学蒙特卡洛(KMC)方法模拟了在一定的沉积速率下,单层、多层台阶Ehrlich-Schwoebel(ES)势及温度对成膜质量的影响.结果表明,在一定沉积速率和ES势垒下,薄膜的粗糙度在一定范围内随着温度的升高而降低,当多层ES势垒大于单层ES势垒时,此温度范围受单层ES势垒的影响,而与多层ES势垒关系不大;当单层ES势垒大于多层ES势垒时,多层ES势垒与粗糙度下降的起始温度密切相关,单层ES势垒与粗糙度趋于平稳的温度相关.     

The molecular mechanism of embryonic stem cell pluripotency maintenance

In vitro cultured embryonic stem （ES） cells are derived from the inner cell mass （ICM） of pre-implantation embryos, and are capable of giving rise to all cell and tissue types of the three germ layers upon being injected back into blastocysts. These ceils are therefore said to possess pluripotency that can be maintained infinitely in culture under optimal conditions. Such pluripotency maintenance is believed to be due to the symmetrical cleavage of the cells in an undifferentiated state. The pluripotency of ES cells is the basis for their various practical and potential applications. ES cells can be used as donor cells to generate knockout or transgenic animals, as in vitro models of mammalian development, and as cell resources for cell therapy in regenerative medicine. The further success in these applications, particularly in the last two, is dependent on the establishment of a culture system with components in the medium clearly defined and the subsequent procedures for controlled differentiation of the cells into specific lineages. In turn, elucidating the molecular mechanism for pluripotency maintenance of ES cells is the prerequisite. This paper summarizes the recent progresses in this area, focusing mainly on the LIF/STAT3, BMPs/Smads, canonical Wnt, TGFβ/activin/nodal, PI3K and FGF signaling pathways and the genes such as oct4, nanog that are crucial in ES cell pluripotency maintenance. The regulatory systems of pluripotency maintenance in both mouse and human ES cells are also discussed. We believe that the cross-talkings between these signaling pathways, as well as the regulatory system underlying pluripotency maintenance will be the main focus in the area of ES cell researches in the future.