混合式可重构数字多核并行处理器平台

一种高性能、RISC-VLIW融合的多核、可重构数字媒体处理器已经从专利发明顺利形成了一个先进的数据处理器设计平台(Digital Multi-processor Platform)。研发的结果体现若干先进处理器技术的融合。(1)应用:低功耗并行运算处理覆盖数字信号处理(DSP)、数字媒体处理(DMP)和超级并行处理器(SPP)的应用扩展领域;(2)体系结构:精简指令(RISC)和超常指令字(VLIW)处理器融合于同一个可配置的平台;(3)运算能力:处理器群调用异构的通用处理器核,使用两类处理器核实例:通用处理器核(包括ALU等的通用运算)和专用处理器核(包括DDCU的用户自定义运算核);(4)可配置和可重构:硅编译器、SoC集成工具、用户自定义运算单元、多核间的和槽内的流水线、包括运算单元的现场编程;(5)设计自动化平台:专用工具用于设计、分析与验证;与商业电子自动化设计(EDA)流程接口;(6)产品模式:硅知识产权(Silicon IP)、通用处理器芯片系列(IC Series)、定制单片系统(SoC)。命名为Fusion的融合式数字多核处理器平台把数个先进处理器技术集成到一个统一的体系结构和设计环境之中...     

Loss of ACTN3 gene function alters mouse muscle metabolism and shows evidence of positive selection in humans

More than a billion humans worldwide are predicted to be completely deficient in the fast skeletal muscle fiber protein alpha-actinin-3 owing to homozygosity for a premature stop codon polymorphism, R577X, in the ACTN3 gene. The R577X polymorphism is associated with elite athlete status and human muscle performance, suggesting that alpha-actinin-3 deficiency influences the function of fast muscle fibers. Here we show that loss of alpha-actinin-3 expression in a knockout mouse model results in a shift in muscle metabolism toward the more efficient aerobic pathway and an increase in intrinsic endurance performance. In addition, we demonstrate that the genomic region surrounding the 577X null allele shows low levels of genetic variation and recombination in individuals of European and East Asian descent, consistent with strong, recent positive selection. We propose that the 577X allele has been positively selected in some human populations owing to its effect on skeletal muscle metabolism.     

Tissue repair and stem cell renewal in carcinogenesis

Cancer is increasingly being viewed as a stem cell disease, both in its propagation by a minority of cells with stem-cell-like properties and in its possible derivation from normal tissue stem cells. But stem cell activity is tightly controlled, raising the question of how normal regulation might be subverted in carcinogenesis. The long-known association between cancer and chronic tissue injury, and the more recently appreciated roles of Hedgehog and Wnt signalling pathways in tissue regeneration, stem cell renewal and cancer growth together suggest that carcinogenesis proceeds by misappropriating homeostatic mechanisms that govern tissue repair and stem cell self-renewal.