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In the present dissertation, the interband optical transition and carrier lifetime of InAs/GaAsSb QDs with different silicon delta-doping densities have been first studied by time-integrated and time-resolved photoluminescence (PL). It is found that an optimized silicon delta-doping density in the QDs enables to fill the QD electronic states with electrons for sub-bandgap photon absorption and to improve carrier lifetime of the QDs.
After that, the crystal quality and QD morphology of single- and multi-stack InAs/GaAsSb QDs with different Sb compositions have been investigated by transmission electron microscopy (TEM) and x-ray diffraction (XRD). The TEM studies reveal that QD morphology of single-stack QDs is affected by Sb composition due to strain reducing effect of Sb incorporation. The XRD studies confirm that the increase of Sb composition increases the lattice mismatch between GaAs matrix and GaAsSb spacers, resulting in increase of the strain relaxation in GaAsSb of the multi-stack QDs. Furthermore, the increase of Sb composition causes a PL redshift and increases carrier lifetime of QDs.
Finally, the spacer layer thickness of multi-stack InAs/GaAsSb QDs is optimized for the growth of InAs/GaAsSb QD solar cells (QDSCs). The InAs/GaAsSb QDSCs with GaP strain compensating layer are grown and their device performances are characterized. The increase of GaP coverage is beneficial to improve the conversion efficiency of the QDSCs. However, the conversion efficiency is reduced when using a relatively large GaP coverage.
Our previous studies show reduced abundance of the β-subunit of mitochondrial H+-ATP synthase (β-F1-ATPase) in skeletal muscle of obese individuals. The β-F1-ATPase forms the catalytic core of the ATP synthase, and it is critical for ATP production in muscle. The mechanism(s) impairing β-F1-ATPase metabolism in obesity, however, are not completely understood. First, we studied total muscle protein synthesis and the translation efficiency of β-F1-ATPase in obese (BMI, 36±1 kg/m2) and lean (BMI, 22±1 kg/m2) subjects. Both total protein synthesis (0.044±0.006 vs 0.066±0.006%·h-1) and translation efficiency of β-F1-ATPase (0.0031±0.0007 vs 0.0073±0.0004) were lower in muscle from the obese subjects when compared to the lean controls (P<0.05). We then evaluated these same responses in a primary cell culture model, and tested the specific hypothesis that circulating non-esterified fatty acids (NEFA) in obesity play a role in the responses observed in humans. The findings on total protein synthesis and translation efficiency of β-F1-ATPase in primary myotubes cultured from a lean subject, and after exposure to NEFA extracted from serum of an obese subject, were similar to those obtained in humans. Among candidate microRNAs (i.e., non-coding RNAs regulating gene expression), we identified miR-127-5p in preventing the production of β-F1-ATPase. Muscle expression of miR-127-5p negatively correlated with β-F1-ATPase protein translation efficiency in humans (r = – 0.6744; P<0.01), and could be modeled in vitro by prolonged exposure of primary myotubes derived from the lean subject to NEFA extracted from the obese subject. On the other hand, locked nucleic acid inhibitor synthesized to target miR-127-5p significantly increased β-F1-ATPase translation efficiency in myotubes (0.6±0.1 vs 1.3±0.3, in control vs exposure to 50 nM inhibitor; P<0.05). Our experiments implicate circulating NEFA in obesity in suppressing muscle protein metabolism, and establish impaired β-F1-ATPase translation as an important consequence of obesity.