Invoking Interfacial Engineering Boosts Structural Stability Empowering Exceptional Cyclability of Ni-Rich Cathode.

The cycling stability of LiNi0.8Co0.1Mn0.1O2 under high voltages is hindered by the occurrence of hybrid anion- and cation-redox processes, leading to oxygen escape and uncontrolled phase collapse. In this study, an interfacial engineering strategy involving a straightforward mechanical ball milling and low-temperature calcination, employing a Se-doped and FeSe2&Fe2O3-modified approach is proposed to design a stable Ni-rich cathode. Se2- are selectively adsorbed within oxygen vacancies to form O─TM─Se bond, effectively stabilizing lattice oxygen, and preventing structural distortion. Simultaneously, the Se-NCM811//FeSe2//Fe2O3 self-assembled electric field is activated, improving interfacial charge transfer and coupling. Furthermore, FeSe2 accelerates Li+ diffusion and reacts with oxygen to form Fe2O3 and SeO2. The Fe2O3 coating mitigates hydrofluoric acid erosion and acts as an electrostatic shield layer, limiting the outward migration of oxygen anions. Impressively, the modified materials exhibit significantly improved electrochemical performance, with a capacity retention of 79.7% after 500 cycles at 1C under 4.5 V. Furthermore, it provides an extraordinary capacity retention of 94.6% in 3-4.25 V after 550 cycles in pouch-type full battery. This dual-modification approach demonstrates its feasibility and opens new perspective for the development of stable lithium-ion batteries operating at high voltages.

The Role of M1 and M2 Myocardial Macrophages in Promoting Proliferation and Healing via Activating Epithelial-to-Mesenchymal Transition.

(1) Background: The activation of sequential processes for the formation of permanent fibrotic tissue following myocardial infarction (MI) is pivotal for optimal healing of heart tissue. M1 and M2 macrophages are known to play essential roles in wound healing by the activation of cardiac fibroblasts after an episode of MI. However, the molecular and cellular mechanisms mediated by these macrophages in cellular proliferation, fibrosis, and wound healing remain unclear. (2) Methods: In the present study, we aimed to explore the mechanisms by which M1 and M2 macrophages contribute to cellular proliferation, fibrosis, and wound healing. Using both in vivo and cellular models, we examined the remodeling effects of M1 and M2 macrophages on infarcted cardiac fibroblasts and their role in promoting cardiac healing post-MI. (3) Results: Our findings indicate that M1 macrophages induce a proliferative effect on infarcted cardiac fibroblasts by exerting an anti-apoptotic effect, thereby preventing cell death. Moreover, M1 macrophages were found to activate the mechanism of epithelial-to-mesenchymal transition (EMT), resulting in wound healing and inducing the fibrotic process. The present findings suggest that M1 macrophages play a crucial role in promoting cardiac remodeling post-MI, as they activate the EMT pathway and contribute to increased collagen production and fibrotic changes. (4) Conclusions: The present study provides insights into molecular and cellular mechanisms mediated by M1 and M2 macrophages in cellular proliferation, fibrosis, and wound healing post-MI. Our findings highlight the critical role of M1 macrophages in promoting cardiac remodeling by activating the EMT pathway. Understanding these mechanisms can potentially result in the development of targeted therapies aimed at enhancing the healing process and improving outcomes following MI.