RESUMO
The emerging intelligent piezoresistive yarn/textile-based sensors are of paramount importance for skin-interface electronics, owing to their unparalleled features including softness, breathability, and easy integration with functional devices. However, employing a facile way to fabricate 1D sensing yarns with mechanical robustness, multi-functional integration, and comfortability is still demanded for satisfying the practical applications. Herein, a facile one-step synchronous conjugated electrospinning and electrospraying technique is innovatively employed to continuously construct an Ag NW-embedded polyurethane (PU) nanofiber sensing yarn (AENSY) with hierarchical architecture. This 1D AENSY with weavability and stretchability can be woven into AENSY textile-based sensors integrated with functions of strain and pressure sensing. In this embedded multi-scale architecture, Ag NWs are evenly embedded and locked in the oriented and twisted PU nanofiber (PUNF) scaffold, forming the hierarchical mechanical sensing layer on the surface of the AENSY with favorable stability. Meanwhile, the presence of the elastic PUNFs enhances porosity, elasticity, and considerable deformation space, which in turn endow the AENSY textile-based sensor with a gauge factor (GF) up to 1010, a pressure sensitivity up to 16.7 N-1, high stretchability up to 160%, and high stability under long-term cycles. In addition, the AENSY textile-based sensor exhibits light weight and the unique advantage of skin-friendliness with the human body, which can be directly and conformally attached to the curved human skin to monitor the various human movements. Furthermore, the weavable AENSYs can be integrated into smart textiles with sensing arrays, which are capable for spatial pressure and strain mapping. Thus, the continuous one-step developing process and the stable embedded-twisted fiber structure provide a promising strategy to develop innovative smart yarns and textiles for personalized healthcare and human-machine interfaces.
RESUMO
Neurokinin-1 receptor (NK1R) occurs naturally on human glioblastomas. Its activation mediates glioma cell proliferation. However, it is unknown whether NK1R is directly involved in tumor cell migration. In this study, we found human hemokinin-1 (hHK-1), via NK1R, dose-dependently promoted the migration of U-251 and U-87 cells. In addition, we showed that hHK-1 enhanced the activity of MMP-2 and the expression of MMP-2 and MT1-matrix metalloproteinase (MMP), which were responsible for cell migration, because neutralizing the MMPs with antibodies decreased cell migration. The involved mechanisms were then investigated. In U-251, hHK-1 induced significant calcium efflux; phospholipase C inhibitor U-73122 reduced the calcium mobilization, the up-regulation of MMP-2 and MT1-MMP, and the cell migration induced by hHK-1, which meant the migration effect of NK1R was mainly mediated through the G(q)-PLC pathway. We further demonstrated that hHK-1 boosted rapid phosphorylation of ERK, JNK, and Akt; inhibition of ERK and Akt effectively reduced MMP-2 induction by hHK-1. Meanwhile, inhibition of ERK, JNK, and Akt reduced the MT1-MMP induction. hHK-1 stimulated significant phosphorylation of p65 and c-JUN in U-251. Reporter gene assays indicated hHK-1 enhanced both AP-1 and NF-κB activity; inhibition of ERK, JNK, and Akt dose-dependently suppressed the NF-κB activity; only the inhibition of ERK significantly suppressed the AP-1 activity. Treatment with specific inhibitors for AP-1 or NF-κB strongly blocked the MMP up-regulation by hHK-1. Taken together, our data suggested NK1R was a potential regulator of human glioma cell migration by the up-regulation of MMP-2 and MT1-MMP.
