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Advanced oxysulfur radical-based advanced oxidation processes (OSR-AOPs) usually use heterogeneous catalysts to activate sulfite to degrade organic pollutants in water. In this study, we report the mechanism of sulfite activation by amorphous Fe1−xNixS to degrade rhodamine B (RhB) in different pH ranges. Compared with FeS, Fe1−xNixS had a wide pH application range and high activity. For Fe1−xNixS, Ni-doping sped up electron transfer inside the catalyst and the reduced S2− promoted the ≡Fe(III)/≡Fe(II) cycle, which together improved the sulfite activation by Fe1−xNixS. The results indicated a pH dependence of RhB degradation in the Fe1−xNixS/sulfite system. The free radical pathway of SO3˙−, SO5˙− and ˙OH generated in the process was dominant under acidic condition, whereas it was mainly a non-free radical pathway of electron transfer between the catalyst and the pollutant under alkaline conditions. Both free radical and non-free radical pathways existed in Fe1−xNixS/sulfite under neutral conditions. The results shed significant light on promoting sulfite-based AOPs to remove pollutants from water. [ABSTRACT FROM AUTHOR]

The liver exhibits remarkable regenerative capacity. However, the limited ability of primary human hepatocytes to proliferate in vitro, combined with a compromised regenerative capacity induced by pathological conditions in vivo, presents significant obstacles to effective liver regeneration following liver injuries and diseases. Developing strategies to compensate for the loss of endogenous hepatocytes is crucial for overcoming these challenges, and this remains an active area of investigation. Lineage reprogramming, the process of directly converting one cell type into another bypassing the intermediate pluripotent state, has emerged as a promising method for generating specific cell types for therapeutic purposes in regenerative medicine. Here, we discuss the recent progress and emergent technologies in lineage reprogramming into hepatic cells, and their potential applications in enhancing liver regeneration or treating liver disease models. We also address controversies and challenges that confront this field., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)