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A correlation exists between obstructive sleep apnoea (OSA) and the severity of metabolic dysfunction-associated steatotic liver disease (MASLD), OSA can induce more severe MASLD. However, the underlying regulatory mechanism between the two is unclear. To this end, this study explored the role and possible molecular mechanisms of adipocyte-derived exosomes under OSA in aggravating MASLD. Through sequencing technology, miR-455-3p was identified as a co-differentially expressed miRNA between the MASLD + OSA and Control groups and between the MASLD + OSA and MASLD groups. Upregulation of TCONS-00039830 and Smad2 and downregulation of miR-455-3p in the MASLD and MASLD + OSA groups were validated in vivo and in vitro. TCONS-00039830, as a differentially expressed LncRNA in exosomes found in the sequencing results, transfection notably downregulated miR-455-3p and upregulated Smad2 in hepatocytes. TCONS_00039830 overexpression increased fat, triglyceride and cholesterol levels, while miR-455-3p overexpression decreased these levels. Furthermore, exosome administration promoted the accumulation of fat, triglyceride and cholesterol, upregulated TCONS_00039830 and Smad2, and downregulated miR-455-3p. Overexpression of miR-455-3p reversed the increased fat accumulation and upregulated TCONS_00039830 and Smad2. In conclusion, OSA-derived exosomes promoted hepatocyte steatosis by regulating TCONS_00039830/miR-455-3p/Smad2 axis, thereby aggravating liver damage in MASLD. Exosomes from rats with obstructive sleep apnoea aggravate metabolic dysfunction-associated steatotic liver disease by delivering the lncRNA TCONS_00039830 to hepatocytes and regulating Smad2 expression through targeting miR-455-3p. [ABSTRACT FROM AUTHOR]

This paper is concerned with a periodic nonlinear competition model governed by impulsive differential equation with infinitely distributed delays and feedback controls. By means of coincidence degree theory and Lyapunov functional, a set of sufficient criteria are obtained to guarantee the existence and globally asymptotic stability of a unique positive periodic solution of the model. Furthermore, applying our main results to some important competition models which have been well studied in the literature, we establish some new criteria to supplement and generalize some well-known results. [ABSTRACT FROM AUTHOR]

In this paper, a Gilpin-Ayala predator-prey model with time-dependent delay with m preys and $(n-m)$ predators is studied, which can be seen as a modification of the traditional Lotka-Volterra competition predator-prey system model. Two sets of sufficient conditions on the permanence of the system are obtained. One set is delay dependent, while the other set is delay independent. [ABSTRACT FROM AUTHOR]

The structural, electronic, elastic, and thermodynamic properties and the superconducting transition temperature of MNiBN (M = La, Ca) compounds are investigated by using the first principles within the generalized gradient approximation (GGA). The calculated lattice constants are found in an agreement with the available experimental data, and the deviations are underestimated by less than 2 %. The calculated elastic constants indicate that both of the MNiBN (M = La, Ca) compounds are mechanically stable. The shear modulus, Young's modulus, Poisson's ratio σ, and the ratio B/ G are also calculated. Finally, the Debye temperature ( 휃) and the superconducting transition temperature are obtained. [ABSTRACT FROM AUTHOR]

A discrete semi-ratio-dependent predator-prey system with Holling type IV functional response and time delay is investigated. It is proved the general nonautonomous system is permanent and globally attractive under some appropriate conditions. Furthermore, if the system is periodic one, some sufficient conditions are established, which guarantee the existence and global attractivity of positive periodic solutions. We show that the conditions for the permanence of the system and the global attractivity of positive periodic solutions depend on the delay, so, we call it profitless. [ABSTRACT FROM AUTHOR]