Chemical Compatibility and Electrochemical Performance of Ba7Ta3.7Mo1.3O20.15 Electrolytes for Solid Oxide Fuel Cells.

Hexagonal perovskite-related oxides Ba7Ta3.7Mo1.3O20.15 (BTM) have recently been reported as promising electrolyte materials for intermediate-temperature solid oxide fuel cells (IT-SOFCs). In this work, sintering properties, thermal expansion coefficient, and chemical stability of BTM were studied. In particular, the chemical compatibilities of (La0.75Sr0.25)0.95MnO3±Î´ (LSM), La0.6Sr0.4CoO3 (LSC), La0.6Sr0.4Co0.2Fe0.8O3+δ (LSCF), PrBaMn2O5+δ (PBM), Sr2Fe1.5Mo0.5O6-δ (SFM), BaCo0.4Fe0.4Zr0.1Y0.1O3-δ (BCFZY), and NiO electrode materials with the BTM electrolyte were evaluated. The results show that BTM is highly reactive with these electrodes, in particular, BTM tends to react with Ni, Co, Fe, Mn, Pr, Sr, and La elements in the electrodes to form resistive phases, thus deteriorating the electrochemical properties, which has not been reported before.

NLRP6 Induces Lung Injury and Inflammation Early in Brucella and Influenza Coinfection.

(1) Background: With the resurgence of brucellosis epidemics in China in recent years, the chances of a brucella coinfection with other common respiratory pathogens, such as the influenza virus, have increased dramatically. However, little is known about the pathogenicity or the mechanisms of brucella and influenza coinfections. (2) Methods: To clarify the interventions in the early stages of lung damage due to brucella and influenza coinfections, we evaluated the effect of the coinfection on disease progression and mortality using a coinfection model in WT mice and NLRP6-/- mice, and we verified the function of NLRP6 in infection and proinflammation. (3) Results: The coinfection induced significant respiratory symptoms, weight loss, and a high mortality rate in WT mice. Influenza in the coinfection group significantly increased brucella proliferation in a synergistic manner. Meanwhile, a histological examination showed severe lung tissue destruction and excessive inflammatory responses in coinfected WT animals, and the expression of NLRP6 and IL-18 was dramatically increased in the lung tissues. Furthermore, NLRP6 deletion attenuated lung injuries and inflammation, a reduced bacterial load, and decreased IL-18 protein expression. (4) Conclusions: Our findings indicated that NLRP6 plays a critical role and might be a promising potential therapeutic target for brucella-influenza coinfections.