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Vitamin A is an essential nutrient in animals, playing important roles in animal health. In the pig industry, proper supplementation of vitamin A in the feed can improve pork production performance, while deficiency or excessive intake can lead to growth retardation or disease. However, the specific molecular mechanisms through which vitamin A operates on pig skeletal muscle growth as well as muscle stem cell function remain unexplored. Therefore, in this study, we isolated the pig primary skeletal muscle stem cells (pMuSCs) and treated with retinoic acid (RA), the natural metabolite of vitamin A, and then examined the myogenic capacity of pMuSCs via immunostaining, real-time PCR, CCK8 and western-blot analysis. Unexpectedly, the RA caused a significant decrease in the proliferation and differentiation of pMuSCs. Mechanistically, the RA addition induced the activation of retinoic acid receptor gamma (RARγ), which inhibited the myogenesis through the blockage of protein translation of the master myogenic regulator myogenic differentiation 1 gene (MYOD). Specifically, RARγ inactivate AKT kinase (AKT) signalling and lead to dephosphorylation of eukaryotic translation initiation factor 4E binding protein 1 (eIF4EBP1), which in turn repress the eukaryotic translation initiation factor 4E (eIF4E) complex and block mRNA translation of MYOD. Inhibition of AKT could rescue the myogenic defects of RA-treated pMuSCs. Our findings revealed that retinoid acid signalling inhibits the skeletal muscle stem cell proliferation and differentiation in pigs. Therefore, the vitamin A supplement in the feedstuff should be cautiously optimized to avoid the potential adverse consequences on muscle development associated with the excessive levels of retinoic acid. [ABSTRACT FROM AUTHOR]

The sustainable development of urban communities has attracted widespread attention from all sectors. So, the question regarding how to promote sustainable development in communities has become an important issue that warrants consideration and research. Sustainable development thinking can help create more effective strategies, enhance the ability to organize information, and build a preferred future. During the COVID-19 pandemic, the nucleic acid testing booths in China played an important role in providing fast screening to determine community outbreaks and effectively prevent the spread of the virus. However, with the overall relaxation of the zero COVID-19 policy, many nucleic acid testing booths are currently largely idle. The question regarding how to leverage these testing booths scientifically and reasonably by redesigning them for local conditions is a ready-to-research topic. Based on theories such as future design and sustainable development construction of future urban communities, we focused on old urban communities in China and explored how to use idle testing booths by conducting field research and resident interviews. We thus aimed to explore how to redesign idle nucleic acid testing booths and transform them into products or smart mobile convenience service stations by applying the study's qualitative results. Through a case analysis, we constructed design models for intelligent mobile convenience service stations in old communities that met the needs of the future urban community residents and promoted the sustainable development of the community. We hope that our results will be further verified via the design of intelligent convenience service stations in other cities. [ABSTRACT FROM AUTHOR]

The development of high-performance nonprecious metal catalysts for oxygen reduction reactions is critical for the commercialization of fuel cells. In this paper, we report a non-precious catalyst with high-performance, in which Fe and Fe3C is embedded in nitrogen-doped carbon nanofibers (MIL-N-CNFs) by co-electrospinning Fe-MIL and polyacrylonitrile (PAN) and pyrolyzing. The mass ratio of Fe-MIL to PAN in the precursors and the pyrolysis temperature were optimized to be 1.5 and treated at 800 °C, respectively. The optimized catalyst exhibited an onset potential of 0.950 V and a half-wave potential of 0.830 V in alkaline electrolytes, thanks to the improved mass transfer kinetics in a meso-porous structure and enhanced reaction kinetics by confined Fe and Fe3C particles. Additionally, the optimized catalyst showed a better methanol tolerance than the commercial 20 wt.% Pt/C, indicating a potential application in direct methanol fuel cells. Serving as the cathode in CCM, the anion-exchange membrane fuel cell reaches a power density of 192 mW cm−2 at 428 mA cm−2 and 80 °C. [ABSTRACT FROM AUTHOR]

The H19 gene promotes skeletal muscle differentiation in mice, but the regulatory models and mechanisms of myogenesis regulated by H19 are largely unknown in pigs. Therefore, the regulatory modes of H19 in the differentiation of porcine skeletal muscle satellite cells (PSCs) need to be determined. We observed that H19 gene silencing could decrease the expressions of the myogenin ( MYOG ) gene, myogenic differentiation ( MYOD ), and myosin heavy chain ( MYHC ) in PSCs. Therefore, we constructed and sequenced 12 cDNA libraries of PSCs after knockdown of H19 at two differentiation time points to analyze the transcriptome differences. A total of 11,419 differentially expressed genes (DEGs) were identified. Among these DEGs, we found through bioinformatics analysis and protein interaction experiment that SRY-box transcription factor 4 ( SOX4 ) and Drebrin 1 ( DBN1 ) were the key genes in H19 -regulated PSC differentiation. Functional analysis shows that SOX4 and DBN1 promote PSC differentiation. Mechanistically, H19 regulates PSC differentiation through two different pathways. On the one hand, H19 functions as a molecular sponge of miR-140-5p , which inhibits the differentiation of PSCs, thereby modulating the derepression of SOX4 . On the other hand, H19 regulates PSC differentiation through directly binding with DBN1. Furthermore, MYOD binds to the promoters of H19 and DBN1 . The knockdown of MYOD inhibits the expression of H19 and DBN1 . We determined the function of H19 and provided a molecular model to elucidate H19 's role in regulating PSC differentiation., (Copyright © 2020 Li, Su, Zou, Luo, Shi, Chen, Fang and Li.)