Compartments revealed in food-web structure

Compartments in food webs are subgroups of taxa in which many strong interactions occur within the subgroups and few weak interactions occur between the subgroups. Theoretically, compartments increase the stability in networks, such as food webs. Compartments have been difficult to detect in empirical food webs because of incompatible approaches or insufficient methodological rigour. Here we show that a method for detecting compartments from the social networking science identified significant compartments in three of five complex, empirical food webs. Detection of compartments was influenced by food web resolution, such as interactions with weights. Because the method identifies compartmental boundaries in which interactions are concentrated, it is compatible with the definition of compartments. The method is rigorous because it maximizes an explicit function, identifies the number of non-overlapping compartments, assigns membership to compartments, and tests the statistical significance of the results. A graphical presentation reveals systemic relationships and taxa-specific positions as structured by compartments. From this graphic, we explore two scenarios of disturbance to develop a hypothesis for testing how compartmentalized interactions increase stability in food webs.     

BAD and glucokinase reside in a mitochondrial complex that integrates glycolysis and apoptosis

Glycolysis and apoptosis are considered major but independent pathways that are critical for cell survival. The activity of BAD, a pro-apoptotic BCL-2 family member, is regulated by phosphorylation in response to growth/survival factors. Here we undertook a proteomic analysis to assess whether BAD might also participate in mitochondrial physiology. In liver mitochondria, BAD resides in a functional holoenzyme complex together with protein kinase A and protein phosphatase 1 (PP1) catalytic units, Wiskott-Aldrich family member WAVE-1 as an A kinase anchoring protein, and glucokinase (hexokinase IV). BAD is required to assemble the complex in that Bad-deficient hepatocytes lack this complex, resulting in diminished mitochondria-based glucokinase activity and blunted mitochondrial respiration in response to glucose. Glucose deprivation results in dephosphorylation of BAD, and BAD-dependent cell death. Moreover, the phosphorylation status of BAD helps regulate glucokinase activity. Mice deficient for BAD or bearing a non-phosphorylatable BAD(3SA) mutant display abnormal glucose homeostasis including profound defects in glucose tolerance. This combination of proteomics, genetics and physiology indicates an unanticipated role for BAD in integrating pathways of glucose metabolism and apoptosis.     

Chromosome cohesion is regulated by a clock gene paralogue TIM-1

Faithful transmission of the genome requires that a protein complex called cohesin establishes and maintains the regulated linkage between replicated chromosomes before their segregation. Here we report the unforeseen participation of Caenorhabditis elegans TIM-1, a paralogue of the Drosophila clock protein TIMELESS, in the regulation of chromosome cohesion. Our biochemical experiments defined the C. elegans cohesin complex and revealed its physical association with TIM-1. Functional relevance of the interaction was demonstrated by aberrant mitotic chromosome behaviour, embryonic lethality and defective meiotic chromosome cohesion caused by the disruption of either TIM-1 or cohesin. TIM-1 depletion prevented the assembly of non-SMC (structural maintenance of chromosome) cohesin subunits onto meiotic chromosomes; however, unexpectedly, a partial cohesin complex composed of SMC components still loaded. Further disruption of cohesin activity in meiosis by the simultaneous depletion of TIM-1 and an SMC subunit decreased homologous chromosome pairing before synapsis, revealing a new role for cohesin in metazoans. On the basis of comparisons between TIMELESS homologues in worms, flies and mice, we propose that chromosome cohesion, rather than circadian clock regulation, is the ancient and conserved function for TIMELESS-like proteins.     

多孔泡沫材料的声吸收特性

为了结合泡沫金属兼有的高吸声和高热传导两种特性以进一步提高其吸声性能,回顾了泡沫金属材料的应用和声学建模;通过对泡沫金属和用于制造泡沫金属的高分子基体材料的实验,比较了作者提出的声波通过泡沫金属传播的3种黏滞模型的预测结果,表明所有模型在泡沫金属典型胞元尺寸所对应的低雷诺数范围内是有效的(假定声波为线性,幅值低于160 dB).第一种模型考虑了声波沿平行于刚性圆柱束轴线方向传播时所受到的空气曳力,第二种模型考虑了声波沿垂直于刚性圆柱束轴线方向的传播,第三种模型考虑了声波通过球形节点的传播.结合这3种模型,提出了一种泡沫金属声学性能的综合模型,可以用来预测泡沫金属的声吸收特性.此外,还介绍了一种用于泡沫金属材料基本声传播特性实验的后处理技术.     

基于光流场模型的医学图像配准

基于最大化互信息的配准方法因其复杂性高而不能满足临床的实时性要求；基于光流场模型的图像配准方法计算简单快速，但已有的采用光流场进行配准的方法都直接采用原始的Horn模型，该模型简单地采用速度场的模作为光滑性约束，而导致配准过程不能保持图像的不连续性，使得图像严重模糊以致无法应用，该模型还存在不能处理大位移的问题．为了能在配准过程中尽可能地保持图像特征，采用了Lucas等人提出的窗口化光流场模型，通过选用小的窗口减轻对图像造成的模糊；对于大位移问题，可以采用金字塔结构来有效处理．实验结果证明，Lucas光流场模型应用于医学图像配准能够得到较准确的配准结果，具有很高的运行效率．