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341.
A key aspect of human behaviour is cooperation. We tend to help others even if costs are involved. We are more likely to help when the costs are small and the benefits for the other person significant. Cooperation leads to a tension between what is best for the individual and what is best for the group. A group does better if everyone cooperates, but each individual is tempted to defect. Recently there has been much interest in exploring the effect of costly punishment on human cooperation. Costly punishment means paying a cost for another individual to incur a cost. It has been suggested that costly punishment promotes cooperation even in non-repeated games and without any possibility of reputation effects. But most of our interactions are repeated and reputation is always at stake. Thus, if costly punishment is important in promoting cooperation, it must do so in a repeated setting. We have performed experiments in which, in each round of a repeated game, people choose between cooperation, defection and costly punishment. In control experiments, people could only cooperate or defect. Here we show that the option of costly punishment increases the amount of cooperation but not the average payoff of the group. Furthermore, there is a strong negative correlation between total payoff and use of costly punishment. Those people who gain the highest total payoff tend not to use costly punishment: winners don't punish. This suggests that costly punishment behaviour is maladaptive in cooperation games and might have evolved for other reasons. 相似文献
342.
基于压缩感知过程的语音增强 总被引:2,自引:0,他引:2
压缩感知(compressive sensing,CS)是一种基于信号稀疏性的采样方法,可以有效提取信号中所包含的信息。该文提出了一种基于CS过程的语音增强新算法。算法利用语音在离散余弦变换(discrete cosine transform,DCT)域下的稀疏性,采用Hadamard矩阵对带噪语音进行压缩测量,通过改进的正交匹配跟踪(orthogonal matching pursuit,OMP)算法恢复语音信号,实现语音增强。与经典谱减法和子空间算法进行实验对比分析,结果表明:该算法在降噪性能上优于经典谱减法和子空间算法。 相似文献
343.
Gerlach B Cordier SM Schmukle AC Emmerich CH Rieser E Haas TL Webb AI Rickard JA Anderton H Wong WW Nachbur U Gangoda L Warnken U Purcell AW Silke J Walczak H 《Nature》2011,471(7340):591-596
Members of the tumour necrosis factor (TNF) receptor superfamily have important functions in immunity and inflammation. Recently linear ubiquitin chains assembled by a complex containing HOIL-1 and HOIP (also known as RBCK1 and RNF31, respectively) were implicated in TNF signalling, yet their relevance in vivo remained uncertain. Here we identify SHARPIN as a third component of the linear ubiquitin chain assembly complex, recruited to the CD40 and TNF receptor signalling complexes together with its other constituents, HOIL-1 and HOIP. Mass spectrometry of TNF signalling complexes revealed RIP1 (also known as RIPK1) and NEMO (also known as IKKγ or IKBKG) to be linearly ubiquitinated. Mutation of the Sharpin gene (Sharpin(cpdm/cpdm)) causes chronic proliferative dermatitis (cpdm) characterized by inflammatory skin lesions and defective lymphoid organogenesis. Gene induction by TNF, CD40 ligand and interleukin-1β was attenuated in cpdm-derived cells which were rendered sensitive to TNF-induced death. Importantly, Tnf gene deficiency prevented skin lesions in cpdm mice. We conclude that by enabling linear ubiquitination in the TNF receptor signalling complex, SHARPIN interferes with TNF-induced cell death and, thereby, prevents inflammation. Our results provide evidence for the relevance of linear ubiquitination in vivo in preventing inflammation and regulating immune signalling. 相似文献