We demonstrate simultaneous lasing at two well-separated wavelengths in self-assembled InAs quantum-dot lasers, via ground-state (GS) and excited-state (ES) transitions. This effect is reproducible and strongly depends on the cavity length. By a master-equation model, we attribute it to incomplete clamping of the ES population at the GS threshold.

Background and purpose: The clinical use of arsenic trioxide (As 2 O 3 ), a potent antineoplastic agent, is limited by its severe cardiotoxic effects. QT interval prolongation and apoptosis have been implicated in the cardiotoxicity of As 2 O 3 . The present study was designed to evaluate the effects of resveratrol on As 2 O 3 -induced apoptosis and cardiac injury. Experimental approach: In a mouse model of As 2 O 3 -induced cardiomyopathy in vivo, QT intervals and plasma enzyme activities were measured; cardiac tissues were examined histologically and apoptosis assessed. In H9c2 cardiomyocyte cells, viability, apoptosis, generation of reactive oxygen species (ROS) and cellular calcium levels were measured. Key results: In the mouse model, resveratrol reduced As 2 O 3 -induced QT interval prolongation and cardiomyocyte injury (apoptosis, myofibrillar loss and vacuolization). In addition, increased lactate dehydrogenase activity and decreased activities of glutathione peroxidase, catalase and superoxide dismutase were observed in the plasma of As 2 O 3 -treated mice; these changes were prevented by pretreatment with resveratrol. In As 2 O 3 -treated H9c2 cardiomyocytes, resveratrol significantly increased cardiomyocyte viability and attenuated cell apoptosis as measured by acridine orange/ethidium bromide staining, TdT-mediated dUTP nick end labelling assay and caspase-3 activity. As 2 O 3 -induced generation of ROS and intracellular calcium mobilization in H9c2 cells was also suppressed by pretreatment with resveratrol. Conclusions and implications: Our results showed that resveratrol significantly attenuated As 2 O 3 -induced QT prolongation, structural abnormalities and oxidative damage in the heart. In H9c2 cardiomyocytes, resveratrol also decreased apoptosis, production of ROS and intracellular calcium mobilization induced by treatment with As 2 O 3 . These observations suggested that resveratrol has the potential to protect against cardiotoxicity in As 2 O 3 -exposed patients.

International audienceWe present a comparative study of carrier diffusion in semiconductor heterostructures with different dimensionality [InGaAs quantum wells (QWs), InAs quantum dots (QDs), and disordered InGaNAs QWs (DQWs)]. In order to evaluate the diffusion length in the active region of device structures, we introduce a method based on the measurement of the current-voltage and light-current characteristics in light-emitting diodes where current is injected in an area <1 μm2. By analyzing the scaling behavior of devices with different sizes, we deduce the effective active area, and thus the diffusion length. A strong reduction in the diffusion length is observed going from QWs (Ld≈2.7 μm) to QDs (Ld<100 nm), DQWs being an intermediate case (Ldiff≈0–200 nm depending on the carrier density). These results show that lateral composition fluctuations, either intended or unintended, produce strong carrier localization and significantly affect the carrier profile in a device even at room temperatur

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Electrically injected InGaAs/GaAs quantum-dot microcavity light-emitting diode operating at 1.3 μm and grown by metalorganic chemical vapor deposition Appl. Phys. Lett. 84, 4155 (2004); 10.1063/1.1755411 Dependence of the emission wavelength on the internal electric field in quantum-dot laser structures grown by metal-organic chemical-vapor deposition Appl. Phys. Lett. 79, 1435 (2001); 10.1063/1.1400088 Room-temperature 1.3 μm emission from InAs quantum dots grown by metal organic chemical vapor deposition Structural and optical properties of 1.3 μ m wavelength tensile-strained InGaAsP multiquantum wells grown by metalorganic molecular beam epitaxy

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Oesterle, U.; Fiore, A.; Stanley, R.P.; Ilegems, M.; Todaro, T.

Tri- ortho–cresyl phosphate (TOCP) has been widely used as plasticizers, plastic softeners, and flame retardants in industry and reported to have delayed neurotoxicity and reproductive toxicology in animals. However, it remains to be elusive whether TOCP induces liver injury. In this study, male mice were orally administered different concentrations of TOCP (100, 200, or 400 mg/kg/day) for 28 days. Histological examination showed that TOCP led to serious hepatocellular injury. In addition, administration of TOCP induced a marked elevation in the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in mice. The content of malondialdehyde (MDA) was increased significantly in the liver after the mice were treated with TOCP; while there was a dramatic decrease in the content of glutathione (GSH) and the activities of antioxidative enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX). TOCP inhibited viability of mouse liver cancer Hepa 1-6 cells in a dose-dependent manner. Meanwhile, TOCP significantly increased MDA content and inhibited GSH content and the activities of SOD and GSH-PX in the cells, respectively. Oxidative stress dramatically inhibited viability of Hepa 1-6 cells; while inhibition of oxidative stress by N-acetyl-l-cysteine could rescue the cell viability inhibited by TOCP to a certain extent. In summary, oxidative stress might be involved in TOCP-induced hepatocellular injury in male mice.