Nanocarbons in a unique spring-like helical structure were prepared by a simple and low-cost flame combustion method to act as active and conductive nano-springs in constructing a mattress-like graphene-based paper as a flexible freestanding electrode. As the electrode is applied in a supercapacitor, it simultaneously exhibits high activity, cycling and mechanical stability owing to its unique structure. At a working current density of 0.2 mA cm−2, the areal capacitance of this electrode is as high as 1.07 F cm−2, which is 228% higher than that of the electrode without the helical interlayer. In addition, the capacitive retention of the electrode reaches 93.02% after 1000 charge-discharge cycles at a current density of 2 mA cm−2, and it can remain at 81.22% even if the electrodes are bent 120° in a symmetrical supercapacitor. Such a preparation route is simple and effective, which makes it a promising method for fabricating general spring-like nanomaterials for high-performance wearable electronic devices.
Autism spectrum disorder (ASD) is a complex mental illness with a high incidence and considerable impact. More than half of the affected individuals have self-harm behaviors, resulting in high mortality and morbidity. The impact of ASD on education and employment opportunities, the need for family care and support, as well as the burden on families and society is enormous. The underlying pathogenesis of ASD is still unclear, and effective interventions are lacking. Microglia are key immune cells in the central nervous system (CNS), and they function far beyond classical innate immunity, as they can affect normal neuronal activity by secreting cytokines and pruning synapses through phagocytosis. On the one hand, the abnormal activity of microglia may contribute to the development of ASD; on the other hand, it provides a potential target for intervention and treatment. In this review, we comprehensively analyze the mechanism of action of microglia in ASD development and summarize the current methods for targeting microglia in treating ASD.
Aging is a natural and complex biological process that is associated with widespread functional declines in numerous physiological processes, terminally affecting multiple organs and tissues. Fibrosis and neurodegenerative diseases (NDs) often occur with aging, imposing large burdens on public health worldwide, and there are currently no effective treatment strategies for these diseases. Mitochondrial sirtuins (SIRT3-5), which are members of the sirtuin family of NAD + -dependent deacylases and ADP-ribosyltransferases, are capable of regulating mitochondrial function by modifying mitochondrial proteins that participate in the regulation of cell survival under various physiological and pathological conditions. A growing body of evidence has revealed that SIRT3-5 exert protective effects against fibrosis in multiple organs and tissues, including the heart, liver, and kidney. SIRT3-5 are also involved in multiple age-related NDs, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. Furthermore, SIRT3-5 have been noted as promising targets for antifibrotic therapies and the treatment of NDs. This review systematically highlights recent advances in knowledge regarding the role of SIRT3-5 in fibrosis and NDs and discusses SIRT3-5 as therapeutic targets for NDs and fibrosis.
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