Long-term stability of carbon dioxide electrolysis in a large-scale flat-tube solid oxide electrolysis cell based on double-sided air electrodes

Solid oxide electrolysis cell is a highly promising technology for CO2 electrolysis and has attracted wide attention. But the durability is insufficient by known designed structure of solid oxide electrolysis cell due to structure damage. In this work, a new flat-tube solid oxide electrolysis cell (SOEC) based on double-sided air electrodes with mechanically-strong redox properties and larger active area was proposed and applied to electrolysis of CO2, and its electrochemical performance and long-term durability were investigated. The results showed that the charging current density reaches -600 mA/cm(2) at 1.5 V and 750 degrees C under H-2/CO2 atmosphere. The CO2 conversion rate achieves 47.4% with energy conversation efficiency of 91.4% at the electrolysis voltage of 1.305 V under the charging current density of -400 mA/cm(2), corresponding to 210 mL/min of CO production rate. This new cell architecture for CO2 electrolysis was stable at the current density of -300 mA/cm(2) for 1910 h at 750 degrees C with a degradation rate of 4.89%/kh. The new flat-tube solid oxide electrolysis cell is capable to conduct CO2 electrolysis with high efficiency and long-term stability

Durability of direct-internally reformed simulated coke oven gas in an anode-supported planar solid oxide fuel cell based on double-sided cathodes

A simulated coke oven gas (COG) is used as internally-reformed (IR) fuel in an anode of solid oxide fuel cell based on double-sided cathodes (DSC-SOFC) and the durability of the cell is studied. The DSC-SOFC operates stably for over 240 h when the steam to methane (H2O/CH4) ratio is above 3 with performance degradation of about 0.01% per hour, but it has a larger degradation of about 0.08% per hour when the H2O/CH4 ratio is lower than 2.5. The mechanism of the cell degradation has been analyzed in detail. It is found that the H2O/CH4 ratio approximately equal to 1 is the key point affecting cell performance. The results of cell analysis by energy dispersive spectroscopy and Raman spectroscopy indicate that carbon deposition mainly takes place at the inlet and at the middle of DSC-SOFC. Due to thick anode substrate in this type of cell, carbon distribution on the cross-section reveals that there are two carbon producing areas, one close to the anode surface, and the other near the three-phase boundary. Some of the deposited carbon can be carried by the fuel gas to exhaust which lowers the actual carbon amount in the cell, thus prolonging the cell operation

SIRT1 Suppresses Doxorubicin-Induced Cardiotoxicity by Regulating the Oxidative Stress and p38MAPK Pathways

Background: SIRT1, which belongs to the Sirtuin family of NAD-dependent enzymes, plays diverse roles in aging, metabolism, and disease biology. It could regulate cell survival and has been shown to be a protective factor in heart function. Hence, we verified the mechanism by which SIRT1 regulates doxorubicin induced cardiomyocyte injury in vivo and in vitro. Methods: We analyzed SIRT1 expression in doxorubicin-induced neonatal rat cardiomyocyte injury model and adult mouse heart failure model. SIRT1 was over-expressed in cultured neonatal rat cardiomyocyte by adenovirus mediated gene transfer. SIRT1 agonist resveratrol was used to treat the doxorubicin-induced heart failure mouse model. Echocardiography, reactive oxygen species (ROS) production, TUNEL, qRT-PCR, and Western blotting were performed to analyze cell survival, oxidative stress, and inflammatory signal pathways in cardiomyocytes. Results: SIRT1 expression was down-regulated in doxorubicin induced cardiomocyte injury, accompanied by elevated oxidative stress and cell apoptosis. SIRT1 over-expression reduced doxorubicin induced cardiomyocyte apoptosis with the attenuated ROS production. SIRT1 also reduced cell apoptosis by inhibition of p38MAPK phosphorylation and caspase-3 activation. The SIRT1 agonist resveratrol was able to prevent doxorubicin-induced heart function loss. Moreover, the SIRT1 inhibitor niacinamide could reverse SIRT1's protective effect in cultured neonatal rat cardiomyocytes. Conclusions: These results support the role of SIRT1 as an important regulator of cardiomyocyte apoptosis during doxorubicin-induced heart injury, which may represent a potential therapeutic target for doxorubicin-induced cardiomyopathy