Correction: Long cyclic stability of acidic aqueous zinc-ion batteries achieved by atomic layer deposition: the effect of the induced orientation growth of the Zn anode.

Correction for 'Long cyclic stability of acidic aqueous zinc-ion batteries achieved by atomic layer deposition: the effect of the induced orientation growth of the Zn anode' by Zhisen Zeng et al., Nanoscale, 2021, 13, 12223-12232, https://doi.org/10.1039/d1nr02620h.

Iron oxide nanoparticles size-dependently activate mouse primary macrophages via oxidative stress and endoplasmic reticulum stress.

Iron oxide nanoparticles (IONPs) are widely used in cosmetics, food additives, and biomedical fields. There are a few adverse effects of IONPs according to clinical reports and animal studies. However, the immunotoxicity and, in particular, the size effects and mechanisms of IONPs on macrophages have not been fully clarified. This study aimed to explore the impacts of 10 nm and 30 nm IONPs on immune responses both in mice and bone marrow-derived macrophages (BMMs). We found that 10 mg/kg IONPs elevated the number of neutrophils and the level of interleukin-6 (IL-6) in peritoneal lavage fluids in mice. IONPs also provoked BMMs and induced the production of IL-6 and tumor necrosis factor-α (TNF-α). The impacts of IONPs on inflammatory responses were size-dependent, and 30 nm IONPs were stronger. Consistently, RNA-sequencing and bioinformatic analysis showed that 30 nm IONPs activated numerous biological processes, including many immune responses, endoplasmic reticulum (ER) stress, and oxidative stress. Furthermore, the inflammatory response caused by IONPs could be attenuated by blocking actin polymerization, ER stress, or oxidative stress. This study is helpful to understand the biosafety of IONPs and protect humans from their potential adverse immune effects.

Long cyclic stability of acidic aqueous zinc-ion batteries achieved by atomic layer deposition: the effect of the induced orientation growth of the Zn anode.

Aqueous Zn-ion batteries with economical ZnSO4 solution as the electrolyte suffer from a tremendous tendency of dendrite formation under mildly acidic conditions; moreover, utilization of Zn(CF3SO3)2 delivers superior performance, but is expensive. Herein, we optimize the ZnSO4 electrolyte by inducing 50 µL of 10 M sulfuric acid in 10 mL electrolyte, which can achieve long cycle life (1000 h at 0.1 mA cm-2, 300 h at 1 mA cm-2 and 250 h at 10 mA cm-2) when the Zn foil is protected by three metallic oxides deposited by atomic layer deposition (ALD). The nucleation behaviour of the (002) facet has proved to play a critical role in the reversible lifespan. The Al2O3 layer would restrict the stripping procedure, leading to the highest overpotential, while the TiO2 layer and Fe2O3 layer tended to strip all orientations but the (002) facet. Al2O3@Zn demonstrated a preference for a compact hillock-like (101) orientation texture in the deposition procedure, while TiO2@Zn and Fe2O3@Zn were favourable to obtain a smooth terrace texture. Additionally, symmetric cells with Fe2O3@Zn expressed the lowest overpotential (31.64 mV) and minimal voltage hysteresis (23.6 mV) at 1 mA cm-2. A Zn-MnO2 battery with Fe2O3@Zn also displayed superior capacity, which could reach 280 mA h g-1 at a current density of 1 A g-1. The diffusion coefficient of Zn2+ discloses that among the three ALD layers, full cells with Fe2O3@Zn are the most favourable for diffusion of Zn2+ in acidic electrolyte.

Ultrathin interfacial modification of Li-rich layered oxide electrode/sulfide solid electrolyte via atomic layer deposition for high electrochemical performance batteries.

Herein, Li-rich layered oxides (LLOs) are modified by sulfide solid electrolyte Li10GeP2S12 (LGPS) with high ionic conductivity to enhance the diffusion of Li+ and an ultrathin Al2O3 layer is interposed between LLOs and LGPS through the atomic layer deposition (ALD) technique to inhibit the development of the highly resistive space-charge layer, the side reactions and structure transition of the composites, thus excellently promoting the electrochemical properties of the composites in liquid electrolyte. Among the different ALD cycles of Al2O3, 10 cycles of ultrathin Al2O3 layer achieves the greatest electrochemical performance. The beginning discharge capacity of LLOs@Al2O3/LGPS composites comes up to 233.4 mA h g-1 with a capacity retention of 90.6% and a voltage retention of 97.3% after 100 cycles at 0.2 C. The composites also exhibit the optimal rate capability and a high energy density of 581 Wh kg-1 at 1 C. The galvanostatic intermittent titration technique test indicates that the composites (LLOs@Al2O3/LGPS) possess the greatest Li+ diffusion coefficient (1.58 × 10-10 cm2 s-1) compared to LLOs (0.85 × 10-10 cm2 s-1) and LLOs/LGPS (1.10 × 10-10 cm2 s-1). More importantly, charge curves at the beginning of the initial charge and electrochemical impedance spectroscopy curves clearly reveal the inhibition of the development of the highly resistive space-charge layer.

Superparamagnetic iron oxide nanoparticles attenuate lipopolysaccharide-induced inflammatory responses through modulation of toll-like receptor 4 expression.

Superparamagnetic iron oxide nanoparticles (SPIONs) are extensively applied in biomedical fields, such as magnetic resonance imaging and as nanocarriers. However, the biosafety of SPIONs is not completely established, especially their effect on the immune system and inflammatory responses. Toll-like receptor (TLR) signaling is essential for many acute and chronic human inflammatory diseases. Regulation of TLR responses with drugs is helpful for these inflammatory conditions. In this study, we investigated the effects of 10 and 30 nm SPIONs on macrophages in the presence or absence of the TLR4 agonist lipopolysaccharide (LPS). We found that SPIONs inhibited the release of inflammatory cytokines induced by LPS both in murine and human macrophages in a concentration-dependent manner. Meanwhile, SPIONs suppressed inducible nitric oxide synthase expression activated by SPIONs in RAW264.7 macrophages. Additionally, TLR4 mRNA transcription and expression were attenuated with SPIONs treatment, which positively correlated with the release of inflammatory cytokines. In summary, our study demonstrates that SPIONs can suppress inflammatory responses, and the underlying mechanism may be regulated by TLR4 expression. Our present work contributes to clarifying the biosafety of SPIONs and provides a potential approach to alleviate human inflammatory diseases.