原油沥青质吸附与沉积对储层岩石润湿性和渗透率的影响

原油沥青质吸附引起的油藏岩石润湿性改变和沥青质沉积对储层孔喉的堵塞是造成储层损害、导致油井产能下降的重要机理之一。首先 ,采用改进的自吸速率法和分光光度法 ,研究了原油沥青质吸附所引起的砂岩岩样润湿指数的变化 ;然后 ,利用岩心流动实验方法 ,定量评价了稠油沥青质沉积对储层岩石渗透率的影响。实验结果表明 ,岩心润湿指数随沥青质吸附量的增加而减小 ,从而导致油相的相对渗透率降低。地层水的离子组成是影响水湿性的主要因素之一。地层水所含无机阳离子的化合价价数越高 ,它与沥青质的协同作用所引起的润湿指数下降的程度越大。储层岩心油相渗透率下降的程度与沥青质沉积量和储层岩心的原始渗透率有关 ,沉积量越大或原始渗透率越低 ,则油相渗透率下降幅度越大。因此 ,对于原油中富含沥青质的油藏 ,特别是稠油油藏 ,尽可能抑制沥青质的吸附和沉积是保护储层的一项重要措施。     

界面处理和冷却条件对玻璃纤维与聚丙烯界面结合的影响 Ⅱ.不同冷却速度对界面剪切强度的影响

通过对玻璃纤维与聚丙烯界面剪切强度的测量,以及对其界面结晶形态的观测,发现界面产生横晶的充分条件是界面存在较强的相互作用和样品的缓慢冷却。提出了横晶形成机理,并推断横晶的形成会导致玻璃纤维与聚丙烯树脂界面结合强度的明显下降。用观测到的横晶与基体球晶的冲击线进一步证实了横晶形成机理     

界面处理和冷却条件对玻璃纤维与聚丙烯界面结合的影响 I.不同界面处理对界面剪切强度的影响

通过测定,得出马来酸酐改性聚丙烯（ＭＰＰ）是提高玻璃纤维与聚丙烯树脂界面剪切强度的关键因素,而偶联剂的变化对体系界面剪切强度的影响较少,用仪器分析证实了酸酐基团与玻璃纤维表面发生化学反应的实质,以及当界面存在改性聚丙烯时,应选择Ａ－１７４ＴＭ硅烷偶联剂处理增强聚丙烯的玻璃纤维,而不是传统的Ａ－１１００ＴＭ硅烷偶联剂。     

油藏数值模拟在剩余油预测中的不确定性分析

油藏数值模拟作为一种定量的剩余油饱和度预测方法 ,在油田开发后期剩余油分布研究中起着越来越重要的作用 ,但其预测精度也不可避免地受到多种因素的影响。对剩余油预测中油藏数值模拟精度的影响因素进行了分析 ,结果表明 ,地层对比的多解性、储层物性参数求取的不确定性以及储层非均质描述的局限性是影响数值模拟精度的主要地质因素。此外 ,相对渗透率曲线的选取、动态数据的获取及数值模拟软件本身都存在较大的不确定性 ,这些都会影响到油藏数值模拟的精度。因此 ,在剩余油研究过程中 ,不能过分依赖油藏数值模拟。应该综合运用地质、地震、测井、油藏工程、油藏数值模拟等多学科知识进行研究 ,以提高剩余油饱和度的预测精度。     

原子吸收光谱法测定污水中镉的最佳操作条件研究

主要研究了测定波长、工作电流、燃烧器高度、光谱通带、燃气与助燃气流量等操作条件对测定工业污水中镉含量的影响，确定了最佳的测试条件。     

幂律流体管内充分发展的对流换热分析

将非牛顿流体的动量方程、能量方程和幂律流体的本构方程相结合 ,建立了幂律流体管内流动和换热充分发展时的对流换热控制方程组 ,并在恒热流和恒壁温边界条件下分别对方程组进行了求解 ,得到了两种不同边界条件下的温度分布和无量纲对流换热系数 (Nu数 )的表达式。结果表明 ,幂律流体的流变指数对流体流动的影响要大于对换热的影响 ;在恒热流边界条件下 ,幂律流体的温度在管内沿轴向呈线性分布 ;而在恒壁温条件下 ,其截面平均温度沿轴向呈指数规律变化。幂律流体的无量纲对流换热系数与幂律流体的流变指数有关 ,并且在两种边界条件下 ,均随着流变指数的增加而减小     

救荒野豌豆对根竞争的响应及其识别机制

以救荒野豌豆为材料,研究其对邻体根的响应机制以及根之间的识别方式.结果表明:邻体根存在时,叶、茎、冠、根生物量,根冠比和花数量均没有变化,而繁殖生物量明显增加,表明根的生长与繁殖不存在权衡,也表明救荒野豌豆能够检测到邻体根的存在并做出响应;根之间的识别方式既有直接接触,也有间接的化感作用.     

Estimating the proportion of variation in susceptibility to schizophrenia captured by common SNPs

Schizophrenia is a complex disorder caused by both genetic and environmental factors. Using 9,087 affected individuals, 12,171 controls and 915,354 imputed SNPs from the Schizophrenia Psychiatric Genome-Wide Association Study (GWAS) Consortium (PGC-SCZ), we estimate that 23% (s.e. = 1%) of variation in liability to schizophrenia is captured by SNPs. We show that a substantial proportion of this variation must be the result of common causal variants, that the variance explained by each chromosome is linearly related to its length (r = 0.89, P = 2.6 × 10(-8)), that the genetic basis of schizophrenia is the same in males and females, and that a disproportionate proportion of variation is attributable to a set of 2,725 genes expressed in the central nervous system (CNS; P = 7.6 × 10(-8)). These results are consistent with a polygenic genetic architecture and imply more individual SNP associations will be detected for this disease as sample size increases.     

Conditional and joint multiple-SNP analysis of GWAS summary statistics identifies additional variants influencing complex traits

We present an approximate conditional and joint association analysis that can use summary-level statistics from a meta-analysis of genome-wide association studies (GWAS) and estimated linkage disequilibrium (LD) from a reference sample with individual-level genotype data. Using this method, we analyzed meta-analysis summary data from the GIANT Consortium for height and body mass index (BMI), with the LD structure estimated from genotype data in two independent cohorts. We identified 36 loci with multiple associated variants for height (38 leading and 49 additional SNPs, 87 in total) via a genome-wide SNP selection procedure. The 49 new SNPs explain approximately 1.3% of variance, nearly doubling the heritability explained at the 36 loci. We did not find any locus showing multiple associated SNPs for BMI. The method we present is computationally fast and is also applicable to case-control data, which we demonstrate in an example from meta-analysis of type 2 diabetes by the DIAGRAM Consortium.     

Disruption of mouse Slx4, a regulator of structure-specific nucleases, phenocopies Fanconi anemia

The evolutionarily conserved SLX4 protein, a key regulator of nucleases, is critical for DNA damage response. SLX4 nuclease complexes mediate repair during replication and can also resolve Holliday junctions formed during homologous recombination. Here we describe the phenotype of the Btbd12 knockout mouse, the mouse ortholog of SLX4, which recapitulates many key features of the human genetic illness Fanconi anemia. Btbd12-deficient animals are born at sub-Mendelian ratios, have greatly reduced fertility, are developmentally compromised and are prone to blood cytopenias. Btbd12(-/-) cells prematurely senesce, spontaneously accumulate damaged chromosomes and are particularly sensitive to DNA crosslinking agents. Genetic complementation reveals a crucial requirement for Btbd12 (also known as Slx4) to interact with the structure-specific endonuclease Xpf-Ercc1 to promote crosslink repair. The Btbd12 knockout mouse therefore establishes a disease model for Fanconi anemia and genetically links a regulator of nuclease incision complexes to the Fanconi anemia DNA crosslink repair pathway.