Publications by authors named "Q Lung"

Integration of graphene and quantum dots (QD) is a promising route to improved material and device functionalities. Underlying the improved properties are alterations in carrier dynamics within the graphene/QD heterostructure. In this study, it is shown that graphene functions as a carrier redistribution and supply channel when integrated with InAs QDs.

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Monolithic integration of III-V quantum dot (QD) lasers onto a Si substrate is a scalable and reliable approach for obtaining highly efficient light sources for Si photonics. Recently, a combination of optimized GaAs buffers and QD gain materials resulted in monolithically integrated butt-coupled lasers on Si. However, the use of thick GaAs buffers up to 3 μm not only hinders accurate vertical alignment to the Si optical waveguide but also imposes considerable growth costs and time constraints.

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Fabrication of high quantum efficiency nanoscale device is challenging due to increased carrier loss at surface. Low dimensional materials such 0D quantum dots and 2D materials have been widely studied to mitigate the loss. Here, we demonstrate a strong photoluminescence enhancement from graphene/III-V quantum dot mixed-dimensional heterostructures.

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We report on the photoluminescence enhancement of 1.3 μm InAs quantum dots (QDs) epitaxially grown on an ultrathin 250 nm GaAs buffer on a Si substrate. Decreasing the GaAs buffer thickness from 1000 to 250 nm was found to not only increase the coalesced QD density from 6.

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Detailed data are presented concerning the relative amounts of Hb A and two alpha chain variants (Hb Duan with alpha 75 Asp----Ala, and Hb Westmead with alpha 122 His----Gln), and the occurrence of an alpha-thalassemia-2 heterozygosity in five members of a small Chinese family. The three children who have the three abnormalities inherited the alpha-Duan and alpha-thalassemia-2 heterozygosities from their father, and the alpha-Westmead heterozygosity from their mother. The base substitution which leads to the synthesis of the alpha-Duan chain occurred at codon 75 of the alpha 1 globin gene of the chromosome which also carried the alpha-thalassemia-2 deletion; the concentration of alpha-Duan (37% of total alpha) is similar to that observed for other alpha chain variants, linked to an alpha-thalassemia-2 condition.

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