No description available.

No description available.

No description available.

No description available.

We present the results of GaInNAs/GaAs quantum dot structures with GaAsN barrier layers grown by solid source molecular beam epitaxy. Extension of the emission wavelength of GaInNAs quantum dots by ~170nm was observed in samples with GaAsN barriers in place of GaAs. However, optimization of the GaAsN barrier layer thickness is necessary to avoid degradation in luminescence intensity and structural property of the GaInNAs dots. Lasers with GaInNAs quantum dots as active layer were fabricated and room-temperature continuous-wave lasing was observed for the first time. Lasing occurs via the ground state at ~1.2μm, with threshold current density of 2.1kA/cm[superscript 2] and maximum output power of 16mW. These results are significantly better than previously reported values for this quantum-dot system. / Singapore-MIT Alliance (SMA)

Inhalation of gallium arsenide (GaAs) particulates represent a potential health hazard in the semiconductor industry. Our results showed that GaAs was soluble under a variety of in vitro conditions. Arsenic levels in phosphate buffer filtrates indicated 78% dissolution by 36 hours. The in vivo dissolution of GaAs was dependent upon particle size, time, and route of administration. Intratracheal (i.t.) instillation of GaAs particulates (10-100 mg/kg) to rats resulted in blood arsenic levels of 5-187 ppm at 14-28 days, depending upon particle size. Dissolution doubled as the mean volume particle diameter was halved. Oral administration of GaAs particulates (10-1000 mg/kg) resulted in blood arsenic levels of 3-18 ppm at 14 days. Gallium was not detected in blood at any dose level by any route of exposure. Indices of toxicity that correlated to GaAs exposure were decreased weight gain and porphyria. These effects were maximal at 100 mg/kg GaAs i.t. Uroporphyrin replaced coproporphyrin as the major urinary metabolite. GaAs (10-100 mg/kg i.t.) resulted in an increase in the lung:body weight ratio (136-228%) at 14-28 days, depending upon particle size. Lungs retained 14-42% of the dose as gallium or arsenic. The increase in lung wet weight was not primarily due to edema although pulmonary edema increased in magnitude as particle size decreased. Lung dry weight, DNA, protein, and lipid content were also elevated 14 days after 100 mg/kg GaAs i.t. (large fraction). At this time and dose, major pathological lesions were a thickening in the alveolar wall, pneumonocyte hyperplasia, and interstitial pneumonia. Gallium, as Ga₂O₃ (65 mg/kg), accounted for the increase in lung lipids. Arsenic, as As₂O₃ (17 mg/kg), was responsible for the remaining changes in lung composition observed with GaAs administration. As₂O₃, but not GaAs, resulted in acute fibrosis at 14 days. With 100 mg/kg GaAs i.t. (smaller fraction), proteinosis, edema, mild fibrosis, and increased reticulin formation were observed over 1-28 days in addition to lesions previously described for the larger fraction. These results showed that oral and i.t. GaAs resulted in systematic arsenic intoxication. Intoxication was proportional to in vivo dissolution which was dependent upon particle size. GaAs i.t. was relatively more toxic to rats than an equivalent oral dose. The finding that urinary uroporphyrin levels were greater than coproporphyrin levels may serve as a sensitive, pretoxic indicator of GaAs exposure.

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published_or_final_version / Physics / Doctoral / Doctor of Philosophy

published_or_final_version / abstract / Physics / Master / Master of Philosophy

published_or_final_version / Physics / Master / Master of Philosophy