Synergistically engineered in-situ self-assembled heterostructure composite nanofiber cathode with superior oxygen reduction reaction catalysis for solid oxide fuel cells.

The engineering and exploration of cathode materials to achieve superior oxygen reduction catalytic activity and resistance to CO2 are crucial for enhancing the performance of solid oxide fuel cells (SOFCs). Herein, a novel heterostructure composite nanofiber cathode comprised of PrBa0.5Sr0.5Co2O5+δ and Ce0.8Pr0.2O1.9 (PBSC-CPO-ES) was prepared for the first time through a synergistic approach involving in-situ self-assembly and electrostatic spinning techniques. PBSC-CPO-ES exhibits exceptionally high oxygen reduction catalytic activity and CO2 resistance, which is attributed to its unique nanofiber microstructure and abundant presence of heterointerfaces, significantly accelerating the charge transfer process, surface exchange and bulk diffusion of oxygen. The introduction of CPO not only effectively reduces the thermal expansion of PBSC but also changes the characteristics of oxygen ion transport anisotropy in layered perovskite materials, forming three-dimensional oxygen ion transport pathways. At 750 °C, the single cell employing the PBSC-CPO-ES heterostructure nanofiber attains an impressive peak power density of 1363 mW cm-2. This represents a notable 60.7 % improvement in comparison to the single-phase PBSC powder. Moreover, PBSC-CPO-ES exhibits excellent CO2 tolerance and performance recovery after CO2 exposure. This work provides new perspectives to the design and advancement of future high-performance and high-stability SOFC cathode materials.

Lead exposure disrupted ileal barrier of developmental Japanese quails(Coturnix japonica): Histopathological damages, microbiota dysbiosis and immune disorder.

The gut barrier plays an essential role in maintaining homeostasis and is usually composed of a mechanical barrier, a chemical barrier, an immune barrier, and a biological barrier. However, the impacts of lead (Pb) exposure on avian gut barrier are still unclear. Therefore, the present study tried to determine the toxic effects of Pb on ileal barrier of a biological model-Japanese quail (Coturnix japonica). One-week old quails were exposed to 0, 50, 500 and 1000 ppm Pb in drinking water for 5 weeks. The results showed mechanic barrier in the ileum was disrupted with microstructural deformation featured by epithelial cell abscission, villi contractions and goblet cells reduction as well as ultrastructural changes characterized by swollen mitochondria, blurry tight junctions and microvilli subtraction. Meanwhile, the expression of genes associated with intestinal tight junctions was downregulated in Pb-treated groups indicating tight junction malfunction. Moreover, less mucus and downregulation of expression of mucin2 (Muc2) and Krüppel-like factor 4 (Klf4) indicated chemical barrier disturbance by Pb. In addition, the alteration of microbial diversity and emergence of pathogen bacteria suggested ileal biological barrier disruption by Pb. Furthermore, Pb caused immune dysfunction in the ileum through promoting the expression of pro-inflammatory factors including interleukin 1 beta (IL-1ß), interleukin 6 (IL-6), Interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α) and nuclear factor kappa B (NF-κB) and inhibiting the expression of anti-inflammatory factor interleukin 10 (IL-10). The present study demonstrated that Pb may pose health risks to birds through gut barrier damages.