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Xu, Ni,Shen, Yiyu,Lv, Sitao,Liu, Han,Rhee, Woogeun,Wang, Zhihua The Institute of Electronics and Information Engin 2016 Journal of semiconductor technology and science Vol.16 No.4
This paper describes a spread-spectrum clock generation method by utilizing a ${\Delta}{\Sigma}$ digital PLL (DPLL) which is solely based on binary phase detection and does not require a linear time-to-digital converter (TDC) or other linear digital-to-time converter (DTC) circuitry. A 1-bit high-order ${\Delta}{\Sigma}$ modulator and a hybrid finite-impulse response (FIR) filter are employed to mitigate the phase-folding problem caused by the nonlinearity of the bang-bang phase detector (BBPD). The ${\Delta}{\Sigma}$ DPLL employs a two-point modulation technique to further enhance linearity at the turning point of a triangular modulation profile. We also show that the two-point modulation is useful for the BBPLL to improve the spread-spectrum performance by suppressing the frequency deviation at the input of the BBPD, thus reducing the peak phase deviation. Based on the proposed architecture, a 3.2 GHz spread-spectrum clock generator (SSCG) is implemented in 65 nm CMOS. Experimental results show that the proposed SSCG achieves peak power reductions of 18.5 dB and 11 dB with 10 kHz and 100 kHz resolution bandwidths respectively, consuming 6.34 mW from a 1 V supply.
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Ni Xu,Yiyu Shen,Sitao Lv,Han Liu,Woogeun Rhee,Zhihua Wang 대한전자공학회 2016 Journal of semiconductor technology and science Vol.16 No.4
This paper describes a spread-spectrum clock generation method by utilizing a Δ∑ digital PLL (DPLL) which is solely based on binary phase detection and does not require a linear time-to-digital converter (TDC) or other linear digital-to-time converter (DTC) circuitry. A 1-bit high-order Δ∑ modulator and a hybrid finite-impulse response (FIR) filter are employed to mitigate the phase-folding problem caused by the nonlinearity of the bang-bang phase detector (BBPD). The Δ∑ DPLL employs a two-point modulation technique to further enhance linearity at the turning point of a triangular modulation profile. We also show that the two-point modulation is useful for the BBPLL to improve the spread-spectrum performance by suppressing the frequency deviation at the input of the BBPD, thus reducing the peak phase deviation. Based on the proposed architecture, a 3.2 ㎓ spread-spectrum clock generator (SSCG) is implemented in 65 ㎚ CMOS. Experimental results show that the proposed SSCG achieves peak power reductions of 18.5 ㏈ and 11 ㏈ with 10 ㎑ and 100 ㎑ resolution bandwidths respectively, consuming 6.34 ㎽ from a 1 V supply.
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Zhou Zhongcheng,Wu Bin,Chen Jing,Shen Yiyu,Wang Jing,Chen Xujian,Fei Faming,Li Liang 한국유전학회 2023 Genes & Genomics Vol.45 No.11
Background Metastasis of liver cancer (LC) is the main cause of its high mortality. ETV4 is a critical regulatory factor in promoting LC progression, but the mechanism that ETV4 impacts LC proliferation, migration, and invasion is poorly understood. Objective Investigation of the molecular mechanism of LC metastasis is conducive to developing effective drugs that prevent LC metastasis. Methods Expression of ETV4 and its target gene B3GNT3 in LC tissue was analyzed by bioinformatics, and the result was further verified in LC cells by qRT-PCR. In vitro cellular assays evaluated the impact of ETV4 on the proliferation, migration, and invasion of LC cells. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter gene assay were conducted to analyze the interaction between B3GNT3 and ETV4. SB525334 suppressor was used to treat and access the activation of ETV4 on the TGF-β pathway. Results We discovered that ETV4 and B3GNT3 were evidently up-regulated in LC, and high expression of ETV4 was coupled to the increase of proliferation, migration, and invasion of LC cells and epithelial-mesenchymal transition ability. Besides, ETV4 could bind to the B3GNT3 promoter and activate its transcription. Knockdown of B3GNT3 could prominently suppress the effect of up-regulated ETV4 on LC cells. Meanwhile, ETV4 could activate the TGF-β signaling pathway via B3GNT3, while SB525334 treatment notably repressed the functions of ETV4. Conclusion ETV4 emerges as a driven oncogene in LC, and the ETV4/B3GNT3-TGF-β pathway promotes proliferation, migration, invasion, and epithelial-mesenchymal transition progress of LC. Inhibition of the pathway may provide an underlying method for the prevention and treatment of LC metastasis.
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