Room-temperature quantum emitters in gallium nitride (GaN) are reported. The emitters originate from cubic inclusions in hexagonal lattice and exhibit narrowband luminescence in the red spectral range. The sources are found in different GaN substrates, and therefore are promising for scalable quantum technologies.

Microcrystalline Cs2AgxNa1−xBiyIn1−yCl6 perovskites with tailored composition emitting broadband yellow-white photoluminescence with a quantum yield of up to 92% were produced by a new “green” approach under ambient conditions.

BackgroundFetal growth impacts cardiovascular health throughout postnatal life in humans. Various animal models of intrauterine growth restriction exhibit reduced heart size at birth, which negatively influences cardiac function in adulthood. The mechanistic target of rapamycin complex 1 (mTORC1) integrates nutrient and growth factor availability with cell growth, thereby regulating organ size. This study aimed at elucidating a possible involvement of mTORC1 in intrauterine growth restriction and prenatal heart growth.Methods and ResultsWe inhibited mTORC1 in fetal mice by rapamycin treatment of pregnant dams in late gestation. Prenatal rapamycin treatment reduces mTORC1 activity in various organs at birth, which is fully restored by postnatal day 3. Rapamycin‐treated neonates exhibit a 16% reduction in body weight compared with vehicle‐treated controls. Heart weight decreases by 35%, resulting in a significantly reduced heart weight/body weight ratio, smaller left ventricular dimensions, and reduced cardiac output in rapamycin‐ versus vehicle‐treated mice at birth. Although proliferation rates in neonatal rapamycin‐treated hearts are unaffected, cardiomyocyte size is reduced, and apoptosis increased compared with vehicle‐treated neonates. Rapamycin‐treated mice exhibit postnatal catch‐up growth, but body weight and left ventricular mass remain reduced in adulthood. Prenatal mTORC1 inhibition causes a reduction in cardiomyocyte number in adult hearts compared with controls, which is partially compensated for by an increased cardiomyocyte volume, resulting in normal cardiac function without maladaptive left ventricular remodeling.ConclusionsPrenatal rapamycin treatment of pregnant dams represents a new mouse model of intrauterine growth restriction and identifies an important role of mTORC1 in perinatal cardiac growth.

Lithium niobate Mach−Zehnder modulators (MZMs) are present in a wide range of technologies and though fulfilling the performance and reliability requirements of present applications, they are becoming progressively too bulky, power inefficient, and slow in switching to keep pace with future technological demands. Here, we utilize plasmonics to demonstrate the most efficient (V π L = 0.23 Vcm) lithium niobate MZM to date, consisting of gold nanostripes on lithium niobate that guide both plasmonic modes and electrical signals that control their relative optical phase delay, thereby enabling efficient electro-optic modulation. For high linearity (modulation depth of >2 dB), the proposed MZM inherently operates near its quadrature point by shifting the relative phase of the signal in the interferometric arms. The demonstrated lithium niobate MZM manifests the benefits of employing plasmonics for applications that demand compact (<1 mm 2 ) and fast (>10 GHz) photonic components operating reliably at ambient temperatures.

Large reflection losses at interfaces in light emitting semiconductor devices cause a significant reduction in their light emission and energy efficiencies. Metal nanoparticle (NP) surface coatings have been demonstrated to increase the light extraction efficiency from planar high refractive index semiconductor surfaces. This emission enhancement in Au NP-coated ZnO is widely attributed to involvement of a green (~ 2.5 eV) deep level ZnO defect exciting localized surface plasmons in the NPs that non-radiatively decay into hot electrons, which return to ZnO and radiatively recombine. In this work, we achieve a 6 times enhancement of the ultra-violet excitonic emission in ZnO nanorods that are coated with 5 nm Au NPs without the aid of ZnO defects. Cathodoluminescence (CL), photoluminescence (PL) and a novel concurrent CL-PL technique as well as time resolved PL spectroscopy revealed that the increase in UV emission is due to the formation of an additional fast excitonic relaxation pathway that increases the exciton spontaneous emission rate. Concurrent CL-PL measurements ruled out the presence of charge transfer mechanism in the emission enhancement process. While time resolved PL results confirmed the existence of a new excitonic recombination channel that is attributed to exciton relaxation via the plasmon-assisted excitation of rapid non-radiative Au interband transitions. Our results establish that ZnO defect levels ~ 2.5 eV are not required to facilitate Au NP induced enhancement of the ZnO UV emission.