Wearing masks has been a recommended protective measure due to the risks of coronavirus disease 2019 (COVID-19) even in its coming endemic phase. Therefore, deploying a "smart mask" to monitor human physiological signals is highly beneficial for personal and public health. This work presents a smart mask integrating an ultrathin nanocomposite sponge structure-based soundwave sensor (≈400 µm), which allows the high sensitivity in a wide-bandwidth dynamic pressure range, i.e., capable of detecting various respiratory sounds of breathing, speaking, and coughing. Thirty-one subjects test the smart mask in recording their respiratory activities. Machine/deep learning methods, i.e., support vector machine and convolutional neural networks, are used to recognize these activities, which show average macro-recalls of ≈95% in both individual and generalized models. With rich high-frequency (≈4000 Hz) information recorded, the two-/tri-phase coughs can be mapped while speaking words can be identified, demonstrating that the smart mask can be applicable as a daily wearable Internet of Things (IoT) device for respiratory disease identification, voice interaction tool, etc. in the future. This work bridges the technological gap between ultra-lightweight but high-frequency response sensor material fabrication, signal transduction and processing, and machining/deep learning to demonstrate a wearable device for potential applications in continual health monitoring in daily life.

The brain-derived neurotrophic factor/tropomyosin receptor kinase B/cAMP response element-binding protein (BDNF/TrkB/CREB) signaling pathway is a critical therapeutic target for inducing adult hippocampal neurogenesis and antidepressant therapy. In this study, we tested the hypothesis that naringin, a natural medicinal compound, could promote adult hippocampal neurogenesis and improve depression-like behaviors via regulating the BDNF/TrkB/CREB signaling pathway. We first investigated the effects of naringin on promoting adult hippocampal neurogenesis in both normal and chronic corticosterone (CORT)-induced depressive mice. Under physiological condition, naringin treatment enhanced the proliferation of neural stem/progenitor cells (NSPCs) and accelerated neuronal differentiation. In CORT-induced depression mouse model, naringin treatment promoted neuronal differentiation and maturation of NSPCs for hippocampal neurogenesis. Forced swim test, tail suspension test, and open field test confirmed the antidepressant and anxiolytic effects of naringin. Co-treatment of temozolomide (TMZ), a neurogenic inhibitor, abolished these antidepressant and anxiolytic effects. Meanwhile, naringin treatment increased phosphorylation of cAMP response element binding protein (CREB) but had no effect on the expression of brain-derived neurotrophic factor and phosphorylation of TrkB in the hippocampus of CORT-induced depressive mice. Co-treatment of CREB inhibitor 666-15, rather than TrkB inhibitor Cyc-B, abolished the neurogenesis-promoting and antidepressant effects of naringin. Taken together, naringin has antidepressant and anxiolytic effects, and the underlying mechanisms could be attributed to enhance hippocampal neurogenesis via activating CREB signaling.