Normal-state properties of the antiperovskite oxide Sr3−x_{3-x}SnO revealed by 119^{119}Sn-NMR

We have performed $^{119}$Sn-NMR measurements on the antiperovskite oxide superconductor Sr$_{3-x}$SnO to investigate how its normal state changes with the Sr deficiency. A two-peak structure was observed in the NMR spectra of all the measured samples. This suggests that the phase separation tends to occur between the nearly stoichiometric and heavily Sr-deficient Sr$_{3-x}$SnO phases. The measurement of the nuclear spin-lattice relaxation rate $1/T_1$ indicates that the Sr-deficient phase shows a conventional metallic behavior due to the heavy hole doping. In contrast, the nearly stoichiometric phase exhibits unusual temperature dependence of $1/T_1$, attributable to the presence of a Dirac-electron band.Comment: 5 pages, 4 figure

Growth of quantum three-dimensional structure of InGaAs emitting at ~1 µm applicable for a broadband near-infrared light source

We obtained a high-intensity and broadband emission centered at ~1 µm from InGaAs quantum three-dimensional (3D) structures grown on a GaAs substrate using molecular beam epitaxy. An InGaAs thin layer grown on GaAs with a thickness close to the critical layer thickness is normally affected by strain as a result of the lattice mismatch and introduced misfit dislocations. However, under certain growth conditions for the In concentration and growth temperature, the growth mode of the InGaAs layer can be transformed from two-dimensional to 3D growth. We found the optimal conditions to obtain a broadband emission from 3D structures with a high intensity and controlled center wavelength at ~1 µm. This method offers an alternative approach for fabricating a broadband near-infrared light source for telecommunication and medical imaging systems such as for optical coherence tomography

Penetration depth and gap structure in the antiperovskite oxide superconductor Sr3−x_{3-x}SnO revealed by μ\muSR

We report a $\mu$SR study on the antiperovskite oxide superconductor Sr$_{3-x}$SnO. With transverse-field $\mu$SR, we observed the increase of the muon relaxation rate upon cooling below the superconducting transition temperature $T_{\mathrm{c}}=5.4$ K, evidencing bulk superconductivity. The exponential temperature dependence of the relaxation rate $\sigma$ at low temperatures suggests a fully gapped superconducting state. We evaluated the zero-temperature penetration depth $\lambda(0)\propto1/\sqrt{\sigma(0)}$ to be around 320-1020 nm. Such a large value is consistent with the picture of a doped Dirac semimetal. Moreover, we revealed that the ratio $T_{\mathrm{c}}/\lambda(0)^{-2}$ is larger than those of ordinary superconductors and is comparable to those of unconventional superconductors. The relatively high $T_{\mathrm{c}}$ for small carrier density may hint at an unconventional pairing mechanism beyond the ordinary phonon-mediated pairing. In addition, zero-field $\mu$SR did not provide evidence of broken time-reversal symmetry in the superconducting state. These features are consistent with the theoretically proposed topological superconducting state in Sr$_{3-x}$SnO, as well as with $s$-wave superconductivity.Comment: 9 pages, 9 figures, to be published in Physical Review

Wireless optogenetics protects against obesity via stimulation of non-canonical fat thermogenesis.

Cold stimuli and the subsequent activation of β-adrenergic receptor (β-AR) potently stimulate adipose tissue thermogenesis and increase whole-body energy expenditure. However, systemic activation of the β3-AR pathway inevitably increases blood pressure, a significant risk factor for cardiovascular disease, and, thus, limits its application for the treatment of obesity. To activate fat thermogenesis under tight spatiotemporal control without external stimuli, here, we report an implantable wireless optogenetic device that bypasses the β-AR pathway and triggers Ca2+ cycling selectively in adipocytes. The wireless optogenetics stimulation in the subcutaneous adipose tissue potently activates Ca2+ cycling fat thermogenesis and increases whole-body energy expenditure without cold stimuli. Significantly, the light-induced fat thermogenesis was sufficient to protect mice from diet-induced body-weight gain. The present study provides the first proof-of-concept that fat-specific cold mimetics via activating non-canonical thermogenesis protect against obesity

Mitochondrial lipoylation integrates age-associated decline in brown fat thermogenesis.

Thermogenesis in brown adipose tissue (BAT) declines with age; however, what regulates this process remains poorly understood. Here, we identify mitochondria lipoylation as a previously unappreciated molecular hallmark of aged BAT in mice. Using mitochondrial proteomics, we show that mitochondrial lipoylation is disproportionally reduced in aged BAT through a post-transcriptional decrease in the iron-sulfur (Fe-S) cluster formation pathway. A defect in the Fe-S cluster formation by the fat-specific deletion of Bola3 significantly reduces mitochondrial lipoylation and fuel oxidation in BAT, leading to glucose intolerance and obesity. In turn, enhanced mitochondrial lipoylation by α-lipoic acid supplementation effectively restores BAT function in old mice, thereby preventing age-associated obesity and glucose intolerance. The effect of α-lipoic acids requires mitochondrial lipoylation via the Bola3 pathway and does not depend on the anti-oxidant activity of α-lipoic acid. These results open up the possibility to alleviate the age-associated decline in energy expenditure by enhancing the mitochondrial lipoylation pathway