16nm FinFET工艺在28Gb/s SerDes模拟前端设计中的挑战与解决方案

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"这篇论文由Avago Technologies的工程师Freeman Zhong和Ashutosh Sinha在2014年撰写,探讨了在16nm FinFET半导体工艺中设计高速SerDes(串行器/解串器)模拟前端的问题。论文主要关注28Gb/s SerDes,比较了28nm平面CMOS工艺与16nm FinFET工艺对电路性能的影响,并提出了一些应对技术来减轻不良设备特性的影响。" 在高速通信系统中,SerDes扮演着至关重要的角色。随着数据流量的指数级增长和半导体工艺的进步,SerDes的数据速率已从1.25Gb/s提升至28+Gb/s。一个典型的串行链路包括发射机、信道和接收机,它不仅负责数据的串行化(N到1位)和反串行化(1到N位),还包含了通道均衡等功能,以确保在高速传输下的信号完整性。 传统的28nm平面CMOS工艺在制造高速SerDes时面临一些挑战,如信号衰减、噪声和功耗问题。而16nm FinFET工艺引入了三维鳍式场效应晶体管,其更小的尺寸和更好的栅极控制理论上能提供更高的速度、更低的功耗以及更好的性能。然而,FinFET工艺也带来了新的设计难题,如寄生效应、工艺变异性以及热效应等。 论文中详细讨论了几种架构选择,以及在16nm FinFET工艺下如何设计模拟电路来应对这些挑战。这可能包括优化的电路拓扑结构,如差分放大器、均衡器和时钟恢复电路的改进设计。为了减轻FinFET工艺特有的不良设备特性,论文提出了各种技术和策略,例如使用补偿电路来减少噪声,采用新型的电源管理方案来降低功耗,以及采用先进的信号处理算法来改善信道性能。 通过应用这些先进技术及缓解措施,作者开发出了一款原型28Gb/s SerDes,并展示了理想的性能、功耗和芯片面积。实验结果证明,16nm FinFET工艺在实现高速SerDes方面具有显著优势,但同时也强调了在设计过程中对模拟电路和设备特性的深入理解是至关重要的。 "Analog Circuit and Device Interaction in High-Speed SerDes"论文提供了对高速SerDes设计的深入洞察,尤其是在16nm FinFET工艺中的挑战和解决方案,对于理解和优化这类高速通信组件具有重要价值。

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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