在动作间的状态未知条件下,利用遗传算法,从不完整的领域描述和规划实例中学习动作模型,并且设计了AMLS-GA(Action Model Learning System Based on Genetic Algorithm)系统来具体实现这一思想.作者为每一个动作构建一个可能谓词集,这...在动作间的状态未知条件下,利用遗传算法,从不完整的领域描述和规划实例中学习动作模型,并且设计了AMLS-GA(Action Model Learning System Based on Genetic Algorithm)系统来具体实现这一思想.作者为每一个动作构建一个可能谓词集,这个谓词集覆盖了动作前提表、增加表和删除表中的所有谓词.采用二进制编码的方式,把动作模型编码成GA搜索空间中的一个假设,学习过程是在标准的遗传算法框架下进行的.把学习结果的正确性定义为尽可能多的解释规划实例,并且通过实验的方法对比学习到的模型与专家预定义模型之间的差别.实验结果表明,算法能在较短的时间内,学习到一个逼近专家描述的动作模型.展开更多
TRIM5α restricts retroviruses in a species-specific manner. Cyclophilin A was independently retrotransposed into the TRIM5 loci in different species, leading to the generation of antiviral TR1M5-cyclophilin A （TRIM...TRIM5α restricts retroviruses in a species-specific manner. Cyclophilin A was independently retrotransposed into the TRIM5 loci in different species, leading to the generation of antiviral TR1M5-cyclophilin A （TRIMCyp） proteins. Previously, we found that assam macaques express a TRIMCyp chimera （amTRIMCyp）, along with a TRIM5α allelic protein （amTRIM5α）. Herein, we investigated the antiviral activity of amTRIMCyp and amTRIM5α individually, as well as their interaction and joint effects. amTRIMCyp showed a divergent restriction pattern from amTRIM5αc Although both proteins potently restricted the replication of HIV-1, only amTRIM5αt inhibited N-MLV. Remarkably, cellular anti-HIV-1 activity increased when amTRIMCyp and amTRIM5αt were coexpressed, indicating a synergistic block of HIV-1 replication. Consistently, PMBCs from heterozygous amTRIM50t/TRIMCyp showed stronger resistance to HIV-1 infection than those from amTRIM5a/TRIM5α homozygotes. The anti-HIV-1 synergistic effect was dependent on the amTRIMCyp-amTRIM5α interaction. In contrast, amTRIMCyp completely abrogated the anti-N-MLV activity mediated by amTRIM5α, showing a dominant-negative effect, indicating that the generation of amTRIMCyp was involved in the trade-off between divergent restriction activities. Our results provide a new paradigm to study functional trade-offs mediated by allelic proteins, a theoretical basis for utilizing animal models with various TRIM5 alleles, as well as novel HIV-1 gene therapy strategies.展开更多
文摘在动作间的状态未知条件下,利用遗传算法,从不完整的领域描述和规划实例中学习动作模型,并且设计了AMLS-GA(Action Model Learning System Based on Genetic Algorithm)系统来具体实现这一思想.作者为每一个动作构建一个可能谓词集,这个谓词集覆盖了动作前提表、增加表和删除表中的所有谓词.采用二进制编码的方式,把动作模型编码成GA搜索空间中的一个假设,学习过程是在标准的遗传算法框架下进行的.把学习结果的正确性定义为尽可能多的解释规划实例,并且通过实验的方法对比学习到的模型与专家预定义模型之间的差别.实验结果表明,算法能在较短的时间内,学习到一个逼近专家描述的动作模型.
文摘动作模型学习可以使Agent主动适应动态环境中的变化,从而提高Agent的自治性,同时也可为动态域建模提供一个初步模型,为后期的模型完善和修改提供了基础。通过结合归纳逻辑程序设计(Inductive Logic Programming,ILP)和回答集程序设计(Answer Set Programming,ASP),设计了一个学习B语言描述的动作模型算法,该算法可以在混合规模的动态域中进行学习,并采用经典规划实例验证了该学习算法的有效性。
基金supported by grants from the National Natural Science Foundation of China (81471620, 81671627, 81571606, 81172876, U0832601)the 13th Five-Year Key Scientific and Technological Program of China (2017ZX10304402-002-004, 2017ZX10202102-001-005)+2 种基金the Knowledge Innovation Program of the Chinese Academy of Sciences (KJZD-EW-L1002, KSCX2-EW-R-13)the National Key Research & Development Plan (2016YFC1201000)the National Basic Research Program of China (2012CBA01305)
文摘TRIM5α restricts retroviruses in a species-specific manner. Cyclophilin A was independently retrotransposed into the TRIM5 loci in different species, leading to the generation of antiviral TR1M5-cyclophilin A （TRIMCyp） proteins. Previously, we found that assam macaques express a TRIMCyp chimera （amTRIMCyp）, along with a TRIM5α allelic protein （amTRIM5α）. Herein, we investigated the antiviral activity of amTRIMCyp and amTRIM5α individually, as well as their interaction and joint effects. amTRIMCyp showed a divergent restriction pattern from amTRIM5αc Although both proteins potently restricted the replication of HIV-1, only amTRIM5αt inhibited N-MLV. Remarkably, cellular anti-HIV-1 activity increased when amTRIMCyp and amTRIM5αt were coexpressed, indicating a synergistic block of HIV-1 replication. Consistently, PMBCs from heterozygous amTRIM50t/TRIMCyp showed stronger resistance to HIV-1 infection than those from amTRIM5a/TRIM5α homozygotes. The anti-HIV-1 synergistic effect was dependent on the amTRIMCyp-amTRIM5α interaction. In contrast, amTRIMCyp completely abrogated the anti-N-MLV activity mediated by amTRIM5α, showing a dominant-negative effect, indicating that the generation of amTRIMCyp was involved in the trade-off between divergent restriction activities. Our results provide a new paradigm to study functional trade-offs mediated by allelic proteins, a theoretical basis for utilizing animal models with various TRIM5 alleles, as well as novel HIV-1 gene therapy strategies.
