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RISS 인기검색어
- 검색키워드
- 저자 : Fangping Yuan (검색결과 2 건)
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Hiren V. Trada,Venkat Vendra,Joseph P. Tinney,Fangping Yuan,Douglas J. Jackson,Kevin M. Walsh,Bradley B. Keller 한국바이오칩학회 2015 BioChip Journal Vol.9 No.2
We have designed, fabricated, and validated a novel porous, multielectrode array (P-MEA) device capable of low-voltage electrical stimulation of engineered cardiac tissues (ECTs). The primary advantage of this device is the ability to successfully function at a very low voltage thus minimizing any undesirable oxidative by-products in the culture environment or cell injury. Major features of our P-MEA include dimensions of 10 mm width and 82 mm length, four arms to allow movement of the individual pads within ECTs, each embedded electrode arm incorporates eight 100 μm×200 μm rectangular pores surrounding a 950 μm×340 μm exposed electrode, large pads on either side of the porous embedded device to function as current return electrodes, suture holes to aid in vivo suturing and stabilization, and an eight electrode connector pads. Average thickness of the Ni/Au electrodes was 20 nm of nickel and 400 nm of old, an average electrode film thickness of 0.4 μm, and a double polyimide layer thickness of 16 μm. Electrode resistance ranged from 69.45 Ω to 78.52 Ω. Electrochemical impedance spectroscopy confirmed that the P-MEA operates in the 0.01 V to 1.0 V range with favorable charge transfer characteristics. Proof of principle experiments confirmed the ability of the P-MEA to effectively embed within ECT and electricallystimulate ECT during chronic, in vitro culture. Histology imaging shows that the embedding of the device has no adverse effects on the ECT and the cardiomyocytes are aligned within the tissue. Experiments are ongoing to evaluate the role of electrical stimulation on the maturation and function of ECTs. We have designed, fabricated, and validated a novel porous, multielectrode array (P-MEA) device capable of low-voltage electrical stimulation of engineered cardiac tissues (ECTs). The primary advantage of this device is the ability to successfully function at a very low voltage thus minimizing any undesirable oxidative by-products in the culture environment or cell injury. Major features of our P-MEA include dimensions of 10 mm width and 82 mm length, four arms to allow movement of the individual pads within ECTs, each embedded electrode arm incorporates eight 100 μm×200 μm rectangular pores surrounding a 950 μm×340 μm exposed electrode, large pads on either side of the porous embedded device to function as current return electrodes, suture holes to aid in vivo suturing and stabilization, and an eight electrode connector pads. Average thickness of the Ni/Au electrodes was 20 nm of nickel and 400 nm of gold, an average electrode film thickness of 0.4 μm, and a double polyimide layer thickness of 16 μm. Electrode resistance ranged from 69.45 Ω to 78.52 Ω. Electrochemical impedance spectroscopy confirmed that the P-MEA operates in the 0.01 V to 1.0 V range with favorable charge transfer characteristics. Proof of principle experiments confirmed the ability of the P-MEA to effectively embed within ECT and electrically stimulate ECT during chronic, in vitro culture. Histology imaging shows that the embedding of the device has no adverse effects on the ECT and the cardiomyocytes are aligned within the tissue. Experiments are ongoing to evaluate the role of electrical stimulation on the maturation and function of ECTs.
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Prevention of acetaminophen-induced hepatocyte injury: JNK inhibition and GSTA1 involvement
Chang Yicong,He Jingshan,Ma Bingke,Ishfaq Muhammad,Wang Jiaqi,Zhang Ruichen,Yuan Liang,Liu Jiarui,Li Changwen,Liu Fangping 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.2
Background Glutathione S-transferase A1 (GSTA1) is a detoxification enzyme and a sensitive marker for hepatotoxicity. We investigated the effects of JNK inhibition on different degrees of Acetaminophen (APAP)-induced hepatocyte injury and GSTA1 expression. Objective This study aimed to investigate the role of JNK signaling pathway in APAP-induced different degrees of hepatocyte injury and its correlation with GSTA1 by inhibiting the phosphorylation of JNK by SP600125. Results 6 and 8 mM APAP induced different degrees of hepatocyte injury and apoptosis, both activated JNK signaling pathway. In contrast, JNK inhibitor significantly reduced activation of JNK and c-JUN on exposure to APAP. Meanwhile, the levels of hepatocyte injury, oxidative stress, and apoptosis obviously decreased. Importantly, GSTA1 expression was significantly increased by JNK inhibition. Conclusions JNK inhibition attenuates APAP-induced hepatocyte injury and oxidative stress and increases GSTA1 expression. Furthermore, GSTA1 may be involved in this signaling pathway for detoxification. Background Glutathione S-transferase A1 (GSTA1) is a detoxification enzyme and a sensitive marker for hepatotoxicity. We investigated the effects of JNK inhibition on different degrees of Acetaminophen (APAP)-induced hepatocyte injury and GSTA1 expression. Objective This study aimed to investigate the role of JNK signaling pathway in APAP-induced different degrees of hepatocyte injury and its correlation with GSTA1 by inhibiting the phosphorylation of JNK by SP600125. Results 6 and 8 mM APAP induced different degrees of hepatocyte injury and apoptosis, both activated JNK signaling pathway. In contrast, JNK inhibitor significantly reduced activation of JNK and c-JUN on exposure to APAP. Meanwhile, the levels of hepatocyte injury, oxidative stress, and apoptosis obviously decreased. Importantly, GSTA1 expression was significantly increased by JNK inhibition. Conclusions JNK inhibition attenuates APAP-induced hepatocyte injury and oxidative stress and increases GSTA1 expression. Furthermore, GSTA1 may be involved in this signaling pathway for detoxification.
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