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RISS 인기검색어
- 검색키워드
- 저자 : Xiangliang Yang (검색결과 4 건)
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Cathode Side Engineering to Raise Holding Voltage of SCR in a 0.5-μm 24 V CDMOS Process
Yang Wang,Xiangliang Jin,Acheng Zhou,Liu Yang 대한전자공학회 2015 Journal of semiconductor technology and science Vol.15 No.6
A set of novel silicon controlled rectifier (SCR) devices’ characteristics have been analyzed and verified under the electrostatic discharge (ESD) stress. A ring-shaped diffusion was added to their anode or cathode in order to improve the holding voltage (Vh) of SCR structure by creating new current discharging path and decreasing the emitter injection efficiency (γ) of parasitic Bipolar Junction Transistor (BJT). ESD current density distribution imitated by 2- dimensional (2D) TCAD simulation demonstrated that an additional current path exists in the proposed SCR. All the related devices were investigated and characterized based on transmission line pulse (TLP) test system in a standard 0.5-μm 24 V CDMOS process. The proposed SCR devices with ring-shaped anode (RASCR) and ring-shaped cathode (RCSCR) own higher Vh than that of Simple SCR (S_SCR). Especially, the Vh of RCSCR has been raised above 33 V. What’s more, their holding current is kept over 800 mA, which makes it possible to design power clamp with SCR structure for on chip ESD protection and keep the protected chip away from latch-up risk.
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Cathode Side Engineering to Raise Holding Voltage of SCR in a 0.5-㎛ 24 V CDMOS Process
Wang, Yang,Jin, Xiangliang,Zhou, Acheng,Yang, Liu The Institute of Electronics and Information Engin 2015 Journal of semiconductor technology and science Vol.15 No.6
A set of novel silicon controlled rectifier (SCR) devices' characteristics have been analyzed and verified under the electrostatic discharge (ESD) stress. A ring-shaped diffusion was added to their anode or cathode in order to improve the holding voltage (Vh) of SCR structure by creating new current discharging path and decreasing the emitter injection efficiency (${\gamma}$) of parasitic Bipolar Junction Transistor (BJT). ESD current density distribution imitated by 2-dimensional (2D) TCAD simulation demonstrated that an additional current path exists in the proposed SCR. All the related devices were investigated and characterized based on transmission line pulse (TLP) test system in a standard $0.5-{\mu}m$ 24 V CDMOS process. The proposed SCR devices with ring-shaped anode (RASCR) and ring-shaped cathode (RCSCR) own higher Vh than that of Simple SCR (S_SCR). Especially, the Vh of RCSCR has been raised above 33 V. What's more, their holding current is kept over 800 mA, which makes it possible to design power clamp with SCR structure for on chip ESD protection and keep the protected chip away from latch-up risk.
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The Combination of Gefitinib and Acetaminophen Exacerbates Hepatotoxicity via ROS-Mediated Apoptosis
Xu Jiangxin,Huang Xiangliang,Zhou Yourong,Xu Zhifei,Cai Xinjun,Yang Bo,He Qiaojun,Luo Peihua,Yan Hao,Jin Jie 한국응용약물학회 2024 Biomolecules & Therapeutics(구 응용약물학회지) Vol.32 No.5
Gefitinib is the well-tolerated first-line treatment of non-small cell lung cancer. As it needs analgesics during oncology treatment, particularly in the context of the coronavirus disease, where patients are more susceptible to contract high fever and sore throat. This has increased the likelihood of taking both gefitinib and antipyretic analgesic acetaminophen (APAP). Given that gefitinib and APAP overdose can predispose patients to liver injury or even acute liver failure, there is a risk of severe hepatotoxicity when these two drugs are used concomitantly. However, little is known regarding their safety at therapeutic doses. This study simulated the administration of gefitinib and APAP at clinically relevant doses in an animal model and confirmed that gefitinib in combination with APAP exhibited additional hepatotoxicity. We found that gefitinib plus APAP significantly exacerbated cell death, whereas each drug by itself had little or minor effect on hepatocyte survival. Mechanistically, combination of gefitinib and APAP induces hepatocyte death via the apoptotic pathway obviously. Reactive oxygen species (ROS) generation and DNA damage accumulation are involved in hepatocyte apoptosis. Gefitinib plus APAP also promotes the expression of Kelch-like ECH-associated protein 1 (Keap1) and downregulated the antioxidant factor, Nuclear factor erythroid 2-related factor 2 (Nrf2), by inhibiting p62 expression. Taken together, this study revealed the potential ROS-mediated apoptosis-dependent hepatotoxicity effect of the combination of gefitinib and APAP, in which the p62/Keap1/Nrf2 signaling pathway participates and plays an important regulatory role.
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Nobiletin promotes adipogenesis in 3T3-L1 cells through the activation of Akt
Huimin Peng,Xiayu Tian,Lu Gan,Xiangliang Yang 경희대학교 융합한의과학연구소 2023 Oriental Pharmacy and Experimental Medicine Vol.23 No.1
The objective of the study was to investigate the effect of nobiletin on adipogenesis in 3T3-L1 cells. Here, we found that nobiletin could promote adipogenesis in 3T3-L1 cells in the absence of adipogenic inducers such as insulin, 3-Isobutyl-1-methylxanthine and dexamethasone. In addition, Real time quantitative PCR showed that the expression of adipogenic genes such as CCAAT/enhancer binding proteins, peroxisome proliferator-activated receptors-γ and fatty acid-binding protein aP2 were up-regulated in 3T3-L1 cells in the presence of nobiletin. Next, we investigated the role of Akt in the effect of nobiletin on the adipogenesis in 3T3-L1 cells by LY294002 blocking PI3K/Akt pathway. The experimental results showed that the promotive effect of nobiletin on adipogenesis was attenuated, accompanied by the down-regulation of adipogenic genes expression, after the activity of Akt was inhibited, suggesting that Akt plays an important role in the effect of nobiletin on promoting adipogenesis in 3T3-L1 cells. Still, the inhibition of Akt pathway by LY294002 was attenuated in the presence of nobiletin. These findings provide a possibility that nobiletin may be a potential candidate agent for stimulating Akt pathway in 3T3-L1 cells.
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