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The discrete effect on the boundary condition has been a fundamental topic for the lattice Boltzmann method (LBM) in simulating heat and mass transfer problems. In previous works based on the anti-bounce-back (ABB) boundary condition for convection-diffusion equations (CDEs), it is indicated that the discrete effect cannot be commonly removed in the Bhatnagar–Gross–Krook (BGK) model except for a special value of relaxation time. Targeting this point in this paper, we still proceed within the framework of BGK model for two-dimensional CDEs, and analyze the discrete effect on a non-halfway single-node boundary condition which incorporates the effect of the distance ratio. By analyzing an unidirectional diffusion problem with a parabolic distribution, the theoretical derivations with three different discrete velocity models show that the numerical slip is a combined function of the relaxation time and the distance ratio. Different from previous works, we definitely find that the relaxation time can be freely adjusted by the distance ratio in a proper range to eliminate the numerical slip. Some numerical simulations are carried out to validate the theoretical derivations, and the numerical results for the cases of straight and curved boundaries confirm our theoretical analysis. Finally, it should be noted that the present analysis can be extended from the BGK model to other lattice Boltzmann (LB) collision models for CDEs, which can broaden the parameter range of the relaxation time to approach 0.5. [ABSTRACT FROM AUTHOR]

The article examines the pathological characters and pathogenesis of piglets naturally infected with high-pathogenic porcine reproductive and respiratory syndrome virus (PRRSV) and artificially infected by American strain. It is intended to find the pathogenic traits of the virus. The typical pathological changes are cyanosis of feet and flecked bleeding in skin. The tissue pathological change in natural cases include necrosis of lymphoid tissues and viral encephalitis.

Despite recent advances in cancer therapy, anthracycline-based combination therapy remains the standardized first-line strategy and has been found to have effective antitumor actions. Anthracyclines are extremely cardiotoxic, which limits the use of these powerful chemotherapeutic agents. Although numerous studies have been conducted on the cardiotoxicity of anthracyclines, the precise mechanisms by which doxorubicin causes cardiomyocyte death and myocardial dysfunction remain incompletely understood. This review highlights recent updates in mechanisms and therapies involved in doxorubicin-induced cardiomyocyte death, including autophagy, ferroptosis, necroptosis, pyroptosis, and apoptosis, as well as mechanisms of cardiovascular dysfunction resulting in myocardial atrophy, defects in calcium handling, thrombosis, and cell senescence. We sought to uncover potential therapeutic approaches to manage anthracycline cardiotoxicity via manipulation of crucial targets involved in doxorubicin-induced cardiomyocyte death and dysfunction., Competing Interests: The authors declare no conflict of interest., (Copyright: © 2023 The Author(s). Published by IMR Press.)