Analysis of the coding genome of diffuse large B-cell lymphoma

Diffuse large B-cell lymphoma (DLBCL) is the most common form of human lymphoma. Although a number of structural alterations have been associated with the pathogenesis of this malignancy, the full spectrum of genetic lesions that are present in the DLBCL genome, and therefore the identity of dysregulated cellular pathways, remains unknown. By combining next-generation sequencing and copy number analysis, we show that the DLBCL coding genome contains, on average, more than 30 clonally represented gene alterations per case. This analysis also revealed mutations in genes not previously implicated in DLBCL pathogenesis, including those regulating chromatin methylation (MLL2; 24% of samples) and immune recognition by T cells. These results provide initial data on the complexity of the DLBCL coding genome and identify novel dysregulated pathways underlying its pathogenesis.     

科学普及,一个重要的政治问题

公众科学素养是城市文明的重要内涵,也是城市综合竞争力的重要基础。大力开展城市科普工作是提高公众科学素养水平的重要途径。去年在上海举行的首届“城市科普发展国际论坛”中,中外专家从不同角度阐述了“城市科普发展”的模式、经验及思考,给城市科普工作发展带来崭新的理念。本期摘录了几位专家在此次论坛上的精彩观点,以飨读者。     

性能分析和网格计算

随着信息技术的迅速发展，计算机领域需要持续地在性能理论、方法和工具上取得进步。性能科学和技术的发展包括性能建模、评价、测量、分析、检测、解释、优化和预测。传统的计算机性能分析局限在特定的并行处理机上，但随着网格的流行，高性能计算必须从单个并行机向大规模网络计算发展。本书正是填补了网格计算方面性能分析的空白，提供了对于网格共享资源的理论分析方法。本书综合了近年来在Dagstuhl Workshop上关于网格性能分析和分布式计算方面的论文，给读者展示了网格性能分析的模型、工具和应用。     

自然生物动力学

人体运动是一个非常复杂的过程，涉及人体肌肉、骨骼模型、人脑控制机制以及人体和环境的复杂交互。本书从数学角度，论述了一个非线性动力学系统。这个系统当它包含几百个非线性关联变量时是无序的，但是在同样复杂的人体运动时却是有序的。书中使用微分几何、代数拓扑、非线性控制、混沌和协同学等工具，为具有神经一肌肉一骨骼的类人复杂系统建立数学、物理模型，并提供了一种方法来理解、预测、控制类人复杂系统的行为。     

Laser hardening processing on tool steel SKD61

This paper is aimed at overcoming different degree defects of crystalline structure in SKD61 carbide tool steel under quenching in solid phase and liquid phase. The paper studies the micro-structure an...     

Treatment of diabetes and atherosclerosis by inhibiting fatty-acid-binding protein aP2

Adipocyte fatty-acid-binding protein, aP2 (FABP4) is expressed in adipocytes and macrophages, and integrates inflammatory and metabolic responses. Studies in aP2-deficient mice have shown that this lipid chaperone has a significant role in several aspects of metabolic syndrome, including type 2 diabetes and atherosclerosis. Here we demonstrate that an orally active small-molecule inhibitor of aP2 is an effective therapeutic agent against severe atherosclerosis and type 2 diabetes in mouse models. In macrophage and adipocyte cell lines with or without aP2, we also show the target specificity of this chemical intervention and its mechanisms of action on metabolic and inflammatory pathways. Our findings demonstrate that targeting aP2 with small-molecule inhibitors is possible and can lead to a new class of powerful therapeutic agents to prevent and treat metabolic diseases such as type 2 diabetes and atherosclerosis.