A key to the utilization of nitride-arsenides for long wavelength optoelectronic devices is obtaining low defect materials with long nonradiative lifetimes. Currently, these materials must be annealed to obtain device quality material. The likely defect responsible for the low luminescence efficiency is associated with excess nitrogen. Photoluminescence and capacitance–voltage measurements indicate the presence of a trap associated with excess nitrogen which decreases in concentration upon anneal. Our films are grown by elemental source molecular beam epitaxy and the background impurity concentration is low, thus we have investigated the role of crystalline defects. High resolution x-ray diffraction showed improved crystal quality after anneal. We observed that the lattice parameter does not decrease linearly with nitrogen concentration for levels of nitrogen above 2.9 mol % GaN. The fact that Vegard’s law is not observed, despite theoretical calculations that it should, indicates that nitrogen incorporates in locations other than the group V lattice sites. X-ray photoelectron spectroscopy revealed that nitrogen exists in two bonding configurations in not-annealed material: a Ga–N bond and another nitrogen complex in which N is less strongly bonded to gallium atoms. Annealing removes this second nitrogen complex. A combined nuclear reaction analysis and channeling technique showed that not annealed GaNAs contains a significant concentration of interstitial nitrogen that disappears upon anneal. We believe that this interstitial nitrogen is responsible for the deviation from Vegard’s law and the low luminescence efficiency of not annealed GaNAs and GaInNAs quantum wells.
Microparticles (MPs) are membrane-bound vesicles shed normally or as a result of various (pathological) stimuli. MPs contain a wealth of bio-active macromolecules. The aminophospholipid phosphatidylserine (PS) is present on the surface of many MPs. As PS and phosphatidylethanolamine (PE) are related, yet distinct aminophospholipids, the purpose of this study was to systematically and directly assess PE exposure on MPs. We examined MPs from various human cellular sources (human breast cancer, endothelial, red and white blood cells) by flow cytometry using a PE-specific probe, Duramycin, and two PS-specific probes, annexin V and lactadherin. PS and PE exposure percentage was comparable on vascular and blood cell-derived MPs (80-90% of MP-gated events). However, the percentage of malignant breast cancer MPs exposing PE (~90%) was significantly higher than PS (~50%). Thus, while PS and PE exposure can result from a general loss of membrane asymmetry, there may also be distinct mechanisms of PE and PS exposure on MPs that vary by cellular source.
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