The anode materials that have been developed for solid oxide fuel cells (SOFCs) are vulnerable to deactivation by carbon buildup (coking) from hydrocarbon fuels or by sulfur contamination (poisoning). We report on a mixed ion conductor, BaZr(0.1)Ce(0.7)Y(0.2-)(x)Yb(x)O(3-delta), that allows rapid transport of both protons and oxide ion vacancies. It exhibits high ionic conductivity at relatively low temperatures (500 degrees to 700 degrees C). Its ability to resist deactivation by sulfur and coking appears linked to the mixed conductor's enhanced catalytic activity for sulfur oxidation and hydrocarbon cracking and reforming, as well as enhanced water adsorption capability.

The existing Ni-yttria-stabilized zirconia anodes in solid oxide fuel cells (SOFCs) perform poorly in carbon-containing fuels because of coking and deactivation at desired operating temperatures. Here we report a new anode with nanostructured barium oxide/nickel (BaO/Ni) interfaces for low-cost SOFCs, demonstrating high power density and stability in C3H8, CO and gasified carbon fuels at 750°C. Synchrotron-based X-ray analyses and microscopy reveal that nanosized BaO islands grow on the Ni surface, creating numerous nanostructured BaO/Ni interfaces that readily adsorb water and facilitate water-mediated carbon removal reactions. Density functional theory calculations predict that the dissociated OH from H2O on BaO reacts with C on Ni near the BaO/Ni interface to produce CO and H species, which are then electrochemically oxidized at the triple-phase boundaries of the anode. This anode offers potential for ushering in a new generation of SOFCs for efficient, low-emission conversion of readily available fuels to electricity.

A carefully designed test cell platform with a new electrode structure is utilized to determine the intrinsic surface catalytic properties of an electrode. With this design, the electrocatalytic activity and stability of an La 0.6 Sr 0.4 Co 0.2 Fe 0.8 O 3Àd (LSCF) cathode is enhanced by a dense thin La 0.85 Sr 0.15 MnO 3AEd (LSM) coating, suggesting that an efficient electrode architecture has been demonstrated that can make effective use of desirable properties of two different materials: fast ionic and electronic transport in the backbone (LSCF) and facile surface kinetics on the thin-film coating (LSM). Theoretical analyses suggest that the enhanced electrocatalytic activity of LSM-coated LSCF is attributed possibly to surface activation under cathodic polarization due to the promotion of oxygen adsorption and/or dissociation by the surface layer and the dramatically increased oxygen vacancy population in the surface film. Further, the observed time-dependent activation over a few hundreds of hours and durability are likely associated with the formation of a favorable hybrid surface phase intermediate between LSM and LSCF. This efficient electrode architecture was successfully applied to the state-of-the-art LSCF-based cathodes by a simple solution infiltration process, achieving reduced interfacial resistance and improved stability under fuel cell operating conditions.

Mitochondrial homeostasis is critical for keeping functional heart in response to metabolic or environmental stresses. Mitochondrial fission and fusion (mitochondrial dynamics) play essential roles in maintaining mitochondrial homeostasis, defects in mitochondrial dynamics lead to cardiac diseases such as ischemia-reperfusion injury (IRI), heart failure and diabetic cardiomyopathy. Mitochondrial dynamics is determined by mitochondrial fission and fusion proteins, including OPA1, mitofusins and Drp1. These proteins are tightly regulated by a series of signaling pathways through different aspects such as transcription, post translation modifications (PTMs) and proteasome-dependent protein degradation. By modulating these mitochondrial fission and fusion proteins, mitochondria fine-tune their metabolic status to meet the energy demands of the heart. Moreover, these mitochondrial fission and fusion proteins are essential for mediating mitochondrial autophagy (mitophagy), leading to clearance of damaged mitochondria to maintain a healthy population of mitochondria in heart under stressed conditions. Mitochondrial dynamics dependent improvement in mitochondrial metabolism and quality could partially reverse the pathological conditions of heart. This review describes an overview of mechanisms on mitochondrial dynamics regulation and provides potential therapeutic targets for treating cardiovascular diseases.

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