T-S模糊延迟系统延迟脉冲控制的指数稳定性分析

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"这篇论文探讨了Takagi-Sugeno(T-S)模糊延迟系统中带延迟脉冲的指数稳定性问题。通过结合时间依赖的Lyapunov函数方法和Razumikhin技术,得到了一个关于延迟脉冲的T-S模糊延迟系统指数稳定性的线性矩阵不等式(LMIs)的充分条件。这个稳定性条件同时依赖于脉冲间隔的下界和上界,具有对小脉冲输入延迟的鲁棒性。通过求解一组LMIs,可以轻松构建脉冲状态反馈控制器。文中通过两个数值示例来验证理论发现的有效性。关键词包括延迟脉冲、模糊脉冲控制、Takagi-Sugeno(T-S)模糊系统。" 这篇论文关注的是T-S模糊系统的延迟脉冲控制,这是一个在复杂系统控制领域的重要研究主题。T-S模糊系统是一种广泛应用的模型,因为它能以一种结构化的方式近似非线性动态系统。延迟脉冲在实际系统中很常见,例如在生物系统、电力网络和自动化过程控制中,它们可能会引起系统的不稳定。 论文的核心贡献是提出了一种新的稳定性分析方法。通过时间依赖的Lyapunov函数,研究人员能够分析系统随时间演变的行为,并结合Razumikhin技术,这是一种处理延迟系统稳定性问题的有力工具。这种方法允许他们建立一个关于延迟脉冲的稳定性条件,该条件不仅考虑了脉冲间隔的边界,还具有对小幅度脉冲延迟的适应性。这意味着即使存在一定的输入延迟,系统仍可能保持稳定。 此外,论文还提供了基于线性矩阵不等式的充分条件,这是控制系统设计中的一个标准工具。利用这些不等式,设计者可以构造一个脉冲状态反馈控制器,以确保系统的指数稳定性。这样的控制器设计方法简化了实现过程,使得控制策略能够直接从理论分析中得出。 最后,论文通过两个具体的数值示例来验证所提方法的实际效果。这些示例有助于读者理解理论结果如何应用于解决实际问题,同时也展示了该方法的有效性和实用性。 这篇论文为T-S模糊延迟系统中延迟脉冲的控制问题提供了一个新的视角,其成果对于理解和设计这类系统的控制器具有重要意义。

Rab GTPases serve as master regulators of membrane trafficking. They can be activated by guanine nucleotide exchange factors (GEF) and be inactivated by GTPase-activating proteins (GAPs). The roles of some GAPs have been explored in Saccharomyces cerevisiae, but are largely unknown in filamentous fungi. Here, we investigated the role of GAP Gyp3 gene, an ortholog of S. cerevisiae Gyp3, in an entomopathogenic fungus, Metarhizium acridum. We found that MaGyp3 is mainly localized to the endoplasmic reticulum (ER) of vegetative hyphae, nuclei of mature conidia, and both ER and nuclei in invasive hyphae. Lack of MaGyp3 caused a decreased tolerance to hyperosmotic stress, heat-shock and UV-B radiation. Moreover, the ΔMaGyp3 mutant showed a significantly decreased pathogenicity owing to delayed germination, reduced appressorium-mediated penetration and impaired invasive growth. Loss of MaGyp3 also caused impaired fungal growth, advanced conidiation and defects in utilization of carbon and nitrogen sources, while overexpression of MaGyp3 exhibited delayed conidiation on nutrient-rich medium and conidiation pattern shift from microcycle conidiation to normal conidiation on nutrient-limited medium. Mavib-1, a tanscription factor invloved in conidiation by affecting nutrient utilizaiton, can directly bind to the promoter of MaGyp3. ΔMaGyp3 and ΔMavib-1 mutants shared similar phenotypes, and overexpression mutants of MaGyp3 and Mavib-1 (Mavib-1-OE) exhibited similar phenotypes in growth, conidiation and pathogenicity. Reintroduction of the Magyp3 driven by strong promoter gpd in ΔMavib-1 mutant recovered the defects in growth and conidiation for dysfunction of Mavib1. Taken together, our findings uncovered the role of GAP3 in a filamentous pathogenic fungus and and illustrated the upstream regulatory mechanism by direct interaction with Mavib-1.请用nature杂志的风格润色成学术论文的形式。

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