RESUMO
Near-field radiative heat transfer (NFRHT) can exceed the blackbody limit by several orders of magnitude owing to the tunneling evanescent waves. Exploiting this near-field enhancement holds significant potential for emerging technologies. It has been suggested that coupled polaritons can give rise to orders of magnitude enhancement of NFRHT. However, a thorough experimental verification of this phenomenon is still missing. Here this work experimentally shows that NFRHT mediated by coupled polaritons in millimeter-size graphene/SiC/SiO2 composite devices in planar plate configuration can realize about 302.8 ± â 35.2-fold enhancement with respect to the blackbody limit at a gap distance of 87â ± â 0.8 nm. The radiative thermal conductance and effective gap heat transfer coefficient can reach unprecedented values of 0.136 WK-1 and 5440 Wm-2K-1. Additionally, a scattering-type scanning near-field optical measurement, in conjunction with full-wave numerical simulations, provides further evidence for the coupled polaritonic characteristics of the devices. Notably, this work experimentally demonstrates dynamic regulation of NFRHT can be achieved by modulating the bias voltage, leading to an ultrahigh dynamic range of ≈4.115. This work ambiguously elucidates the important role of coupled polaritons in NFRHT, paving the way for the manipulation of nanoscale heat transport, energy conversion, and thermal computing via the strong coupling effect.
RESUMO
Age-related dysfunction of salivary glands (SGs) leading to xerostomia or dry mouth is typically associated with increased dental caries and difficulties in mastication, deglutition or speech. Inflammaging-induced hyposalivation plays a significant role in aged SGs; however, the mechanisms by which ageing shapes the inflammatory microenvironment of SGs remain unclear. Here, we show that reduced salivary secretion flow rate in aged human and mice SGs is associated with impaired autophagy and increased M1 polarization of macrophages. Our study reveals the crucial roles of SIRT6 in regulating macrophage autophagy and polarization through the PI3K/AKT/mTOR pathway, as demonstrated by generating two conditional knock out mice. Furthermore, triptolide (TP) effectively rejuvenates macrophage autophagy and polarization via targeting this pathway. We also design a local delivery of TP-loaded apoptotic extracellular vesicles (ApoEVs) to improve age-related SGs dysfunction therapeutically. Collectively, our findings uncover a previously unknown link between SIRT6-regulated autophagy and macrophage polarization in age-mediated hyposalivation, while our locally therapeutic strategy exhibits potential preventive effects for age-related hyposalivation.