A functional polybenzimidazole nanofiber framework modified copper substrate was designed for dendrite-free Zn metal anodes.

Zinc metal holds a great potential as an anode material for next-generation aqueous batteries due to its suitable redox potential, high specific capacity, and low cost. However, the uncontrollable dendrite growth and detrimental side reactions with electrolytes hinder the practical application of this type of electrodes. To tackle the issues, an ultrathin (∼1 μm) sulfonated poly­(ether ether ketone) (SPEEK) solid–electrolyte interphase (SEI) is constructed onto the Zn anode surface by a facile spin-coating method. We demonstrate that the polymeric SEI simultaneously blocks the water molecules and anions, uniformizes the ion flux, and facilitates the desolvation process of Zn2+ ions, thus effectively suppressing the side reactions and Zn dendrite formation. As a result, the newly developed Zn@SPEEK anode enables a symmetric cell to stably operate over 1000 cycles at 5 mA cm–2 without degradation. Moreover, with the Zn anode paired with a MnO2 cathode, the full cell exhibits an improved Coulombic efficiency (over 99% at 0.1 A g–1), a superior rate capability (127 mA h g–1 at 2 A g–1), and excellent cycling stability (capacity retention of 70% over 1000 cycles at 1 A g–1). This work provides a facile yet effective strategy to address the critical challenges in Zn anodes, paving the way for the development of high-performance rechargeable aqueous batteries.

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Nafion membranes are extensively used in aqueous redox flow batteries due to high proton conductivity and excellent chemical stability, but their low ion selectivity and high cost restrict the further...

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Acute kidney injury (AKI) is often secondary to sepsis. Increasing evidence suggests that mitochondrial dysfunction contributes to the pathological process of AKI. In this study, we aimed to examine the regulatory roles of Sirt3 in Lipopolysaccharide (LPS)-induced mitochondrial damage in renal tubular epithelial cells (TECs). Sirt3 knockout mice were intraperitoneally injected with LPS, and cultured TECs were stimulated with LPS to evaluate the effects of Sirt3 on mitochondrial structure and function in TECs. Electron microscopy was used to assess mitochondrial morphology. Immunofluorescence staining was performed to detect protein expression and examine mitochondrial morphology.Western blotting was used to quantify protein expression. We observed that LPS increased apoptosis, induced disturbances in mitochondrial function and dynamics, and downregulated Sirt3 expression in a sepsis-induced AKI mouse model and human proximal tubular (HK-2) cells in vitro. Sirt3 deficiency further exacerbated LPS-induced renal pathological damage, apoptosis and disturbances in mitochondrial function and dynamics.On the contrary, Sirt3 overexpression in HK-2 cells alleviated these lesions. Functional studies revealed that Sirt3 overexpression alleviated LPS-induced mitochondrial damage and apoptosis in TECs by promoting OPA1-mediated mitochondrial fusion through the deacetylation of i-AAA protease (YME1L1), an upstream regulatory molecule of OPA1.Our study has identified Sirt3 as a vital factor that protects against LPS-induced mitochondrial damage and apoptosis in TECs via the YME1L1-OPA1 signaling pathway.