量子元胞自动机可编程逻辑阵列单元的缺陷研究

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"该文研究了基于量子元胞自动机(QCA)的可编程逻辑阵列(PLA)结构,探讨了元胞缺失、移位缺陷和未对准缺陷对PLA单元逻辑功能的影响,通过QCADesigner软件进行仿真,并得出在特定结构下缺陷的参数标准,为提高PLA阵列单元利用率提供了依据。" 量子元胞自动机(QCA)是一种新兴的纳米电子技术,其基本工作原理是利用量子力学现象来实现信息的存储和处理。与传统的CMOS技术不同,QCA的计算单元是量子点,这些量子点通过量子相互作用进行信息传递和逻辑运算。这种技术有望解决传统半导体技术面临的尺寸缩小和功耗增加等问题,为构建大规模集成的可编程逻辑电路提供新的可能。 可编程逻辑阵列(PLA)是一种常用的数字逻辑电路,它允许用户根据需要配置其内部连接,以实现各种不同的逻辑函数。在QCA框架下设计PLA结构,可以充分利用QCA的并行性和高密度特性,实现更高效、低功耗的逻辑运算。 在本文中,作者李政操、蔡理和黄宏图对基于QCA的PLA结构进行了深入研究。他们关注的是QCA PLA单元在实际应用中可能出现的缺陷,如元胞缺失、移位缺陷和未对准缺陷。这些缺陷会直接影响PLA的逻辑功能和整体性能。通过使用QCADesigner仿真软件,研究人员能够模拟这些缺陷对PLA单元的影响,并找出在特定结构下每个元胞移位和未对准的最大允许错位距离。 元胞缺失是指在阵列中某些量子点未能正确形成或消失,这可能导致逻辑路径中断。移位缺陷则是指量子点的位置发生偏移,使得相邻元胞之间的相互作用不准确。未对准缺陷通常指的是布线图案中的问题,导致信号在传输过程中出现错误。在实验中,作者发现导线模式中存在特定位置的8个可缺失元胞,这可能与QCA阵列的结构布局和设计规则有关。 这些研究成果为理解和优化QCA PLA结构提供了关键的参数标准,有助于在设计时考虑和规避这些缺陷,从而提高PLA阵列的单元利用率和整体系统的可靠性。通过设定合理的容错机制和补偿策略,可以进一步增强QCA PLA的鲁棒性,推动QCA技术在逻辑电路设计领域的实际应用。

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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