Highly Efficient Electrochemical Reforming of CH\u3csub\u3e4\u3c/sub\u3e/CO\u3csub\u3e2\u3c/sub\u3e in a Solid Oxide Electrolyser

Reforming CH4 into syngas using CO2 remains a fundamental challenge due to carbon deposition and nanocatalyst instability. We, for the first time, demonstrate highly efficient electrochemical reforming of CH4/CO2 to produce syngas in a solid oxide electrolyser with CO2 electrolysis in the cathode and CH4 oxidation in the anode. In situ exsolution of an anchored metal/oxide interface on perovskite electrode delivers remarkably enhanced coking resistance and catalyst stability. In situ Fourier transform infrared characterizations combined with first principle calculations disclose the interface activation of CO2 at a transition state between a CO2 molecule and a carbonate ion. Carbon removal at the interfaces is highly favorable with electrochemically provided oxygen species, even in the presence of H2 or H2O. This novel strategy provides optimal performance with no obvious degradation after 300 hours of high-temperature operation and 10 redox cycles, suggesting a reliable process for conversion of CH4 into syngas using CO2

Herbal formula Xinshuitong capsule exerts its cardioprotective effects via mitochondria in the hypoxia-reoxygenated human cardiomyocytes

Abstract Background The collapse of mitochondrial membrane potential (ΔΨm) resulted in the cell apoptosis and heart failure. Xinshuitong Capsule (XST) could ameliorate left ventricular ejection fraction (LVEF), New York Heart Association (NYHA) classes and the quality of life in patients with chronic heart failure in our clinical study, however, its cardioprotective mechanisms remain unclear. Methods Primary human cardiomyocytes were subjected to hypoxia-reoxygenation and treated with XST200, 400 and 600 μg/ml. The model group was free of XST and the control group was cultured in normal conditions. Cell viability, ΔΨm, the activity of mitochondrial respiratory chain complexes, ATPase activity, reactive oxygen species (ROS) and apoptosis cells were determined in all the groups. Results The cell viability in the XST-treated groups was significantly higher than that in the model group (P < 0.05). Coupled with the restoration of the ΔΨm, the number of polarized cells increased dose dependently in the XST-treated groups. XST also restored the lost activities of mitochondrial respiratory chain complexes I-IV induced by the oxidative stress. The total of mitochondrial ATPase activity was significantly elevated at XST400 and 600 μg/ml compared to the model group (P < 0.05). The levels of mitochondrial ROS and the number of apoptosis cells declined in the XST-treated groups compared to those in the model group (P < 0.05). Conclusions XST, via restoration of ΔΨm and the mitochondrial respiratory chain complexes I-IV activities, and suppression of mitochondrial ROS generation and the apoptosis cells, maintained the integrity of the mitochondrial membrane to exert its cardioprotective effects in the hypoxia-reoxygenated human cardiomyocytes

Inflammatory cytokines via up-regulation of aquaporins deteriorated the pathogenesis of early osteoarthritis.

BackgroundInflammatory cytokines enhanced the progress of the pathogenesis of osteoarthritis, however the mechanisms remain unclear. The objective is to determine aquaporins (AQPs) in the pathogenesis of osteoarthritis.Methods and findingsPrimary rat articular chondrocytes were treated with IL-1β to mimic the early stage of osteoarthritis in vitro. Early osteoarthritis animal model was established by intra-articular injection of 4% papain. Micro- or ultra-structure histopathologic changes, cell viability, apoptosis cells and cell membrane permeability, locations and expressions of AQP1 and AQP3 and matrix were detected in the cartilage or in the chondrocytes of knee. IL-1β could reduce the chondrocytes viability, increase the apoptosis cells, and also impair the cell membrane and organelles. IL-1β significantly induced the up-regulation of AQP1 and AQP3 in the chondrocytes. In the chondrocytes, AQPs were mainly clustered in both membrane and perinuclear region of cytoplasm, while higher AQPs were detected in the superficial and middle layers of the cartilage. With the up-regulation of AQPs, the cartilage matrix was considerably decreased in both the chondrocytes and in the osteoarthritis cartilage. In the early osteoarthritis rat model, serum and synovial fluid confirmed that higher IL-1β could increase the expressions of AQPs, and decrease the cartilage matrix in both the chondrocytes and the cartilage.ConclusionsInflammatory cytokine IL-1β via up-regulation of AQPs caused the abnormal metabolism of water transport and loss of the cartilage matrix in the chondrocytes, and ultimately exacerbated the pathogenesis of early osteoarthritis. Therefore, AQPs may be a candidate therapeutic target for prevention and treatment of osteoarthritis