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Oxidative stress is one of the important mechanisms of inner ear cell damage, which can lead to age-related hearing loss (ARHL). LncRNA H19 is significantly downregulated in the cochlea of old mouse, however, the role of H19 in the development of ARHL remains unclear. In this study, we aim to investigate the expression and function of H19 in oxidative stress injury of cochlear hair cells induced by H2O2. RT-qPCR and western blot analysis confirms that HEI-OC1 cells stimulated with H2O2 decreases the expressions of H19 and SIRT1, but increases the expression of miR-653-5p. Overexpression of H19 could increase cell viability, ATP level and mitochondrial membrane potential, but reduce mitochondrial ROS generation and cell apoptosis ratio in H2O2-stimulated HEI-OC1 cells. MiR-653-5p is a target of H19, which can bind to the 3′-UTR of SIRT1. H19 is found to regulate the expression of SIRT1 through miR-653-5p. Further experiments demonstrates that H19 regulates HEI-OC1 cell viability, ATP level, mitochondrial membrane potential, mitochondrial ROS generation, and cell apoptosis ratio via the miR-653-5p/SIRT1 axis. In conclusion, lncRNA H19 inhibits oxidative stress injury of cochlear hair cells via the miR-653-5p/SIRT1 axis.

Horses were domesticated 5500 years ago, thousands of years later than other domestic animals; however, in this relatively short period, domestic horses have had a great impact on human history by accelerating civilization, revolutionizing warfare and advancing agricultural production. Modern breeding using marker-assisted selection has greatly accelerated breeding progress. Therefore, identification of genetic markers underlying the traits of interest in domestic horses is the basis for the modern breeding system. In this review, we present an overview of genetic mapping studies and genome wide analyses to identify the genomic regions targeted by positive selection for four important aspects of horses, coat color, racing performance, gait and height at withers. The MC1R locus, for example, has been shown to be the main gene responsible for chestnut color, and the MSTN locus has been shown to control the muscle fiber growth in racing breeds. The missense mutation in DMRT3 is the causal mutation for the alternate gaits in horses. Height at withers, a quantitative trait, was mapped to four major loci (3:105547002, 6:81481064, 9:75550059 and 11:232597 32) that can explain 83% of the height variations in domestic horses.

The high energy density, low cost, and low toxicity of LiNi0.8Co0.1Mn0.1O2 (NCM811) cathodes has led to their large‐scale mass production. However, the poor interfacial stability between NCM811 and organic electrolytes impairs the long‐cycle performance of lithium ions batteries. In this study, carbonized polymer dots (CPDs) are successfully introduced onto the surface of NCM811 (NCM811@CPDs) via a simple physical mixing process. CPDs with rich surface oxygen functional groups form strong covalent bonds with transition metal (TM) ions at the NCM811 surface, distinctly restraining surface structure degradation, and transition metal ion dissolution. Furthermore, CPDs facilitate the formation of a compact and steady cathode electrolyte interface (CEI) layer during electrochemical cycling. As a result, the NCM811@1 wt% CPDs exhibit enhanced cycling performance with a capacity retention of 89.77% after 100 cycles at 0.5 C compared to 55.39% of the bare NCM811. This facile and effective surface decoration strategy provides valuable guidance for improving the stability and cycling performance of Ni‐rich cathodes. [ABSTRACT FROM AUTHOR]

Laryngocarcinoma is one of the most frequent malignancies occurring in the head and neck. The roles of spindle- and kinetochore-associated complex 1 (SKA1) in the malignant progression of several cancers have already been discussed. However, the precise significance and action's mechanism of SKA1 in laryngocarcinoma remain largely unknown. In this study, SKA1 was shown to be strongly expressed in laryngocarcinoma tissues and cells, and higher expression of SKA1 was associated with more severe tumor infiltration, larger tumor diameter, higher risk of lymphatic metastasis and later pathological stage. Additionally, loss-of-function assays in vitro suggested that SKA1 depletion caused a reduction in cell proliferation, migration, and colony formation as well as an increase in apoptosis. In animal experiments, tumors generated from AMC-HN-8 cells with SKA1 depletion exhibited declined tumor volume and weight. Similarly, the detection of Ki67 protein in xenograft tumor tissues reflected that knocking down SKA1 curbed tumor growth in vivo. Further exploration on downstream mechanism revealed that after treatment with Pifithrin-α, the suppression in proliferation level caused by SKA1 knockdown was reversed, while the increase of cell apoptosis was withdrawn; at the molecular level, Pifithrin-α treatment caused p-P53 and Bax diminished, while Bcl-2 ameliorated. In short, SKA1 promotes the development of laryngocarcinoma via activating the P53 signaling pathway. [ABSTRACT FROM AUTHOR]