No abstract

Recently, flexible stretchable sensors have been gaining attention for their excellent adaptability for electronic skin applications. However, the preparation of stretchable strain sensors that achieve dual‐mode sensing while still retaining ultra‐low detection limit of strain, high sensitivity, and low cost is a pressing task. Herein, a high‐performance dual‐mode stretchable strain sensor (DMSSS) based on biomimetic scorpion foot slit microstructures and multi‐walled carbon nanotubes (MWCNTs)/graphene (GR)/silicone rubber (SR)/Fe3O4 nanocomposites is proposed, which can accurately sense strain and magnetic stimuli. The DMSSS exhibits a large strain detection range (≈160%), sensitivity up to 100.56 (130–160%), an ultra‐low detection limit of strain (0.16% strain), and superior durability (9000 cycles of stretch/release). The sensor can accurately recognize sign language movement, as well as realize object proximity information perception and whole process information monitoring. Furthermore, human joint movements and micro‐expressions can be monitored in real‐time. Therefore, the DMSSS of this work opens up promising prospects for applications in sign language pose recognition, non‐contact sensing, human‐computer interaction, and electronic skin.

Stretchable strain sensors with high stability, high responsiveness, and low detection limit provide the broad potential for intelligent robots and electronic skin. However, developing low‐cost strain sensors with contact and non‐contact sensing modes remains a significant challenge. In this study, a flexible magnetic strain sensor based on a sandwich structure is proposed to address this challenge. The proposed structure utilizes the coordination between carbon black and Fe3O4 microparticles in the silicone rubber matrix to enhance the sensor's sensitivity to external strain and magnetic stimuli. The sensor exhibits excellent tensile properties with a strain range of up to 180%, fast response/recovery time (78 ms/65 ms), high stability, and durability after 9000 cycles. Moreover, the flexible magnetic strain sensors can detect micro‐vibration and micro‐strain signals. It can also be performed as electronic skin to precisely sense human movements. Furthermore, the newly developed sensor can accurately sense oncoming objects and bicycle riding speed/distance, and a flexible magnetic keyboard is conceived. Consequently, the dual‐modal magnetic strain sensor exhibits an excellent ability to identify contact and non‐contact states and has broad application prospects in next‐generation intelligent products.

Aims Sustained activation of β-adrenergic signalling induces cardiac fibrosis, which marks progression to heart failure. GHSR (growth hormone secretagogue receptor) is the receptor for ghrelin, which is an orexigenic gastric hormone with newly defined cardiovascular effects. The present study determined the effects of GHSR deficiency in a mouse model of isoproterenol (ISO)-induced cardiac fibrosis and examined the underlying mechanism. Methods and results Histochemical studies showed that GHSR deficiency exacerbated cardiac fibrosis. Quantitative RT–PCR, western blotting, and immunofluorescence staining demonstrated that cardiac fibroblasts isolated from GHSR−/− mice exhibited increased expression of marker genes for myofibroblast trans-differentiation (α-SMA, SM22, and calponin) upon transforming growth factor-β treatment compared to wild-type mice. RNA-sequencing of heart transcriptomes revealed that differentially expressed genes in GHSR−/− hearts were enriched in such biological processes as extracellular matrix organization, inflammatory response, lipid metabolism, cell cycle, migration, and adhesion. Particularly, GHSR deficiency increased Wnt/β-catenin pathway activation in ISO-induced myocardial fibrosis. In addition, loss of GHSR in macrophages instigated inflammasome activation with increased cleavage and release of interleukin-18. Conclusion These results for the first time demonstrated that GHSR deficiency aggravated ISO-induced cardiac fibrosis, suggesting that GHSR was a potential target for the intervention of cardiac fibrosis.