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Thermal switches that switch the thermal conductivity (κ) of the active layers are attracting increasing attention as thermal management devices. For electrochemical thermal switches, several transition metal oxides (TMOs) are proposed as active layers. After electrochemical redox treatment, the crystal structure of the TMO is modulated, which results in the κ switching. However, the κ switching width is still small (<4 W m−1 K−1). In this study, it demonstrates that LaNiOx‐based solid‐state electrochemical thermal switches have a κ switching width of 4.3 W m−1 K−1. Fully oxidized LaNiO3 (on state) has a κ of 6.0 W m−1 K−1 due to the large contribution of electron thermal conductivity (κele, 3.1 W m−1 K−1). In contrast, reduced LaNiO2.72 (off state) has a κ of 1.7 W m−1 K−1 because the phonons are scattered by the oxygen vacancies. The LaNiOx‐based electrochemical thermal switch is cyclable of κ and the crystalline lattice of LaNiOx. This electrochemical thermal switch may be a promising platform for next‐generation devices such as thermal displays. [ABSTRACT FROM AUTHOR]

Abstract Recently, magnetic nanoparticles of iron oxide (Fe3O4, γ-Fe2O3) have shown an increasing number of applications in the field of biomedicine, but some questions have been raised about the potential impact of these nanoparticles on the environment and human health. In this work, the three types of magnetic nanoparticles (DMSA-Fe2O3, APTS-Fe2O3, and GLU-Fe2O3) with the same crystal structure, magnetic properties, and size distribution was designed, prepared, and characterized by transmission electronic microscopy, powder X-ray diffraction, zeta potential analyzer, vibrating sample magnetometer, and Fourier transform Infrared spectroscopy. Then, we have investigated the effect of the three types of magnetic nanoparticles (DMSA-Fe2O3, APTS-Fe2O3, and GLU-Fe2O3) on smooth muscle cells (SMCs). Cellular uptake of nanoparticles by SMC displays the dose, the incubation time and surface property dependent patterns. Through the thin section TEM images, we observe that DMSA-Fe2O3is incorporated into the lysosome of SMCs. The magnetic nanoparticles have no inflammation impact, but decrease the viability of SMCs. The other questions about metabolism and other impacts will be the next subject of further studies.

Mitochondria are key regulators of cell fate, maintaining self‐stability by a fine‐tuned quality‐control network including mitophagy, biogenesis, fission and fusion processes. Myocardial mitochondria can be impaired by hypercholesterolemia. Statins, such as atorvastatin, are considered the cornerstone in the management of hypercholesterolaemia primarily due to their marked cholesterol‐lowering ability. The direct effect of atorvastatin on myocardial mitochondria remains unclear. We aimed to explore whether atorvastatin could attenuate myocardial mitochondrial defects induced by high cholesterol, and whether cycloastragenol, a potent telomerase activator, could be used as a potential complementary bioactive compound for obesity and hypercholesterolaemia treatment. We found that atorvastatin at a low dose (3 mg/kg) did not reduce elevated serum cholesterol, but reversed cardiac remodelling and dysfunction in C57BL/6J mice fed with high‐fat diet (HFD). Atorvastatin reversed the upregulated mitophagy, mitochondrial fission and fusion, accompanied by mitochondrial biogenesis activation in HFD‐fed mice hearts. Mitochondrial structural impairments were attenuated by atorvastatin in HFD‐fed mice and oxidized low‐density lipoprotein (ox‐LDL) exposed HL‐1 cardiomyocytes. The depolarized mitochondrial membrane potential and increased mitochondrial oxygen consumption rates in ox‐LDL exposed HL‐1 cells were recovered by atorvastatin. Furthermore, atorvastatin co‐treated with cycloastragenol had better effects on reducing body weight, improving cardiac remodelling and dysfunction, and protecting mitochondria in high cholesterol. Conclusively, low‐dose atorvastatin exhibited a cholesterol‐independent cardioprotective effect through improving the mitochondrial quality‐control network and repairing mitochondrial ultrastructure in high cholesterol. Atorvastatin plus cycloastragenol supplement therapy has a better effect on treating obesity and hypercholesterolaemia. [ABSTRACT FROM AUTHOR]

Hydrogenation, an effective way to tune the properties of transition metal oxide (TMO) thin films, has been long awaited to be performed safely and without an external energy input. Recently, metal-acid-TMO has been reported to be an effective approach for hydrogenation, but the requirement of acid limits its application. In this work, the reversible and rapid hydrogen doping of WO 3 in NaOH(aq) | Al(s) | WO 3 (s) is revealed by structural and electrical measurements. Accompanied by the structural phase transition identified by in situ X-ray diffraction, the electric resistance of the WO 3 film is found to be able to change by 5 orders of magnitude. A significant electrical response of touching, 8-fold in amplitude and 3 s in a cycle, can be achieved in the low-resistance state. These reactions are reversible at room temperature. This study unambiguously proves that the hydrogenation-driven dynamic phase transition of WO 3 in metal-solution-WO 3 systems could occur not only in acid solutions but also in some non-acid environments. Unlike the monotonic increase of resistance revealed during H δ WO 3 to WO 3 transition, an intriguing non-monotonic evolution was found for crystal lattice parameter c , indicating that the mechanism of WO 3 hydrogenation involves a series of metastable states, more comprehensive and reasonable. This work sheds light on the potential applications of metal-solution-TMO hydrogenation in touching sensors, circuits survey, and information storage.