An open environment for cooperative equational solving

We describe a system called CFLP which aims at the integration of the best features of functional logic programming (FLP), cooperative constraint solving (CCS), and distributed computing. FLP provides support for defining one’s own abstractions over a constraint domain in an easy and comfortable way, whereas CCS is employed to solve systems of mixed constraints by iterating specialized constraint solving methods in accordance with a well defined strategy. The system is a distributed implementation of a cooperative constraint functional logic programming scheme that combines higher-order lazy narrowing with cooperative constraint solving. The model takes advantage of the existence of several constraint solving resources located in a distributed environment (e. g., a network of computers), which communicate asynchronously via message passing. To increase the openness of the system, we are redesigning CFLP based on CORBA. We discuss some design and implementation issues of the system.     

土壤渗滤系统中土壤酶活性与系统脱氮效果的关系研究

研究了土壤渗滤系统污水脱氮效果及其与内部酶活性空间分布的关系.7个工况的研究结果表明:①在水力负荷0.01 m3·m-2·d-1条件下,系统对COD,NH3-N,TN,TP的去除率达到了90%以上,具有良好的脱氮除磷效果;②系统内部中层和底层的脲酶活性均与系统的TN去除率显著正相关,底层的亚硝酸盐还原酶(NIR)活性与出水的NO3--N,TN浓度显著负相关,硝酸盐还原酶(NAR)活性与系统脱氮效果的关系不明显.现将前两种酶活性(脲酶,NIR)作为指示系统脱氮效果的重要指标.     

三维初应变问题中区域变量的边界型积分公式

给出了用边界单元法求解三维初应变问题时区域型变量的边界型积分公式的显式．首先将区域型变量用完全多项式展开,然后利用积分核之间的内在联系以及高阶基本解,将相应的区域型积分转化成边界型积分,并简述了边界型积分公式的应用．     

Haploinsufficiency of NSD1 causes Sotos syndrome

We isolated NSD1 from the 5q35 breakpoint in an individual with Sotos syndrome harboring a chromosomal translocation. We identified 1 nonsense, 3 frameshift and 20 submicroscopic deletion mutations of NSD1 among 42 individuals with sporadic cases of Sotos syndrome. The results indicate that haploinsufficiency of NSD1 is the major cause of Sotos syndrome.     

基于概率局域搜索的动车组平日运用计划编制算法

介绍动车组运用计划的含义、计划方案的评价准则;平日运用计划自动编制的启发式算法;算法将问题分为两个部分,即定期检修计划生成和动车组接续运用部分.将接续运用部分转化为某种旅行商问题,定义了动车组运用网络;在构造新的回路时能够考虑日常检修条件和动车组的利用效率.利用实际线路数据进行实验,证明算法有效.     

Mutations affecting components of the SWI/SNF complex cause Coffin-Siris syndrome

By exome sequencing, we found de novo SMARCB1 mutations in two of five individuals with typical Coffin-Siris syndrome (CSS), a rare autosomal dominant anomaly syndrome. As SMARCB1 encodes a subunit of the SWItch/Sucrose NonFermenting (SWI/SNF) complex, we screened 15 other genes encoding subunits of this complex in 23 individuals with CSS. Twenty affected individuals (87%) each had a germline mutation in one of six SWI/SNF subunit genes, including SMARCB1, SMARCA4, SMARCA2, SMARCE1, ARID1A and ARID1B.     

Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice

A fundamental question about the pathogenesis of spontaneous autoimmune diabetes is whether there are primary autoantigens. For type 1 diabetes it is clear that multiple islet molecules are the target of autoimmunity in man and animal models. It is not clear whether any of the target molecules are essential for the destruction of islet beta cells. Here we show that the proinsulin/insulin molecules have a sequence that is a primary target of the autoimmunity that causes diabetes of the non-obese diabetic (NOD) mouse. We created insulin 1 and insulin 2 gene knockouts combined with a mutated proinsulin transgene (in which residue 16 on the B chain was changed to alanine) in NOD mice. This mutation abrogated the T-cell stimulation of a series of the major insulin autoreactive NOD T-cell clones. Female mice with only the altered insulin did not develop insulin autoantibodies, insulitis or autoimmune diabetes, in contrast with mice containing at least one copy of the native insulin gene. We suggest that proinsulin is a primary autoantigen of the NOD mouse, and speculate that organ-restricted autoimmune disorders with marked major histocompatibility complex (MHC) restriction of disease are likely to have specific primary autoantigens.     

Roberts syndrome is caused by mutations in ESCO2, a human homolog of yeast ECO1 that is essential for the establishment of sister chromatid cohesion

Roberts syndrome is an autosomal recessive disorder characterized by craniofacial anomalies, tetraphocomelia and loss of cohesion at heterochromatic regions of centromeres and the Y chromosome. We identified mutations in a new human gene, ESCO2, associated with Roberts syndrome in 15 kindreds. The ESCO2 protein product is a member of a conserved protein family that is required for the establishment of sister chromatid cohesion during S phase and has putative acetyltransferase activity.