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- 저자 : Xiaowu Cai (검색결과 3 건)
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SOI radiation‑hardened 300 V half‑bridge date driver IC design with high dv/dt noise immunity
Yuexin Gao,Xiaowu Cai,Zhengsheng Han,Yun Tang,Liqiang Ding,Ruirui Xia,Mali Gao,Fazhan Zhao 전력전자학회 2023 JOURNAL OF POWER ELECTRONICS Vol.23 No.5
Noise immunity is a critical index of high-voltage half-bridge gate driver integrated circuits (IC). Various noise cancelation technologies have been proposed to improve dv/dt noise immunity with sacrifices in terms of area and propagation delay time. Besides, when it is applied to an inductive load, the half-bridge driver is vulnerable to negative surges at the VS terminal, which is the offset ground of the high-side channel. A 300 V half-bridge gate driver IC with noise rejection module is designed in this paper. The noise immunity can be improved to 87.5 V/ns. The VS negative swing region can be extended to − 5.1 V. In addition, the proposed driver IC can work normally at a working frequency of 500 kHz and the delay matching time between the high-side and the low-side is less than 4 ns. The propagation delay time of the high-side channel is measured at 71.6 ns. Furthermore, gamma ray irradiation experimental results show that the proposed structure presents a good radiation tolerance of 100 krad (Si). The presented half-bridge gate driver IC is fabricated with the silicon-on-insulator (SOI) bipolar-CMOS-DMOS (BCD) process, which occupied an area of 1.86 mm2.
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Lianmin Ji,Liang Cai,Yuze zhang,Xiaowu Peng,Dong Shi,Lijuan Li 한국공업화학회 2023 Journal of Industrial and Engineering Chemistry Vol.123 No.-
Based on the exchangeability of anions between the layers of magnesium-based LDHs, LDHs intercalatedby tartaric acid anion (TA-LDH) was prepared by co-precipitation method to adsorb boron, and confirmedby XRD and FT-IR that TA had successfully entered the interlayer of LDH. The adsorption kinetics showedthat the adsorption efficiency of B was mainly controlled by the chemisorption mechanism. The thermodynamicsrevealed that the relationship between the equilibrium concentration of B in solution and theadsorption capacity of TA-LDH for B was consistent with the Freundlich model. Cl or Li+ in solution hadlittle effect on the adsorption of B by TA-LDH, while SO4 2 had a great effect on that compared with NO3-LDH. Boron adsorption was accomplished through the interaction between the hydroxyl of TA anion inthe interlayer and that of B(OH)3 and B(OH)4. The elution efficiency of TA-LDH was greater than 70% withammonium chloride used as the eluent. While TA-LDH still maintained a good adsorption capacity after 5cycles, and the solubility loss efficiencies of Mg2+ in a single adsorption and elution were 1.5% and 5.4%,respectively. Our study can provide a new idea and method for the development and utilization of magnesiumresources.
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Dihydroartemisinin inhibits HepG2.2.15 proliferation by inducing cellular senescence and autophagy
( Jiang Zou ),( Qiang Ma ),( Ru Sun ),( Jiajing Cai ),( Hebin Liao ),( Lei Xu ),( Jingruo Xia ),( Guangcheng Huang ),( Lihua Yao ),( Yan Cai ),( Xiaowu Zhong ),( Xiaolan Guo ) 생화학분자생물학회(구 한국생화학분자생물학회) 2019 BMB Reports Vol.52 No.8
Dihydroartemisinin (DHA) has been reported to possess anti-cancer activity against many cancers. However, the pharmacologic effect of DHA on HBV-positive hepatocellular carcinoma (HCC) remains unknown. Thus, the objective of the present study was to determine whether DHA could inhibit the proliferation of HepG2.2.15 cells and uncover the underlying mechanisms involved in the effect of DHA on HepG2.2.15 cells. We found that DHA effectively inhibited HepG2.2.15 HCC cell proliferation both in vivo and in vitro. DHA also reduced the migration and tumorigenicity capacity of HepG2.2.15 cells. Regarding the underlying mechanisms, results showed that DHA induced cellular senescence by up-regulating expression levels of proteins such as p-ATM, p-ATR, γ-H<sub>2</sub>AX, P53, and P21 involved in DNA damage response. DHA also induced autophagy (green LC3 puncta gathered together and LC3II/LC3I ratio increased through AKT-mTOR pathway suppression). Results also revealed that DHA-induced autophagy was not linked to senescence or cell death. TPP1 (telomere shelterin) overexpression could not rescue DHA-induced anticancer activity (cell proliferation). Moreover, DHA down-regulated TPP1 expression. Gene knockdown of TPP1 caused similar phenotypes and mechanisms as DHA induced phenotypes and mechanisms in HepG2.2.15 cells. These results demonstrate that DHA might inhibit HepG2.2.15 cells proliferation through inducing cellular senescence and autophagy. [BMB Reports 2019; 52(8): 520-525]
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