92 research outputs found

    Pulsed electron beam induced recrystallization and damage in GaAs

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    Single-pulse electron-beam irradiations of 300-keV 10^(15)Kr+/cm^2 or 300-keV 3×10^(12)Se+/cm^2 implanted layers in unencapsulated GaAs are studied as a function of the electron beam fluence. The electron beam pulse had a mean electron energy of ~-20 keV and a time duration of ~-10^(–7) s. Analyses by means of MeV He + channeling and TEM show the existence of narrow fluence window (0.4–0.7 J/cm^2) within which amorphous layers can be sucessfully recrystallized, presumably in the liquid phase regime. Too high a fluence produces extensive deep damage and loss of As

    Steady-state thermally annealed GaAs with room-temperature-implanted Si

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    Semi-insulating Cr-doped single-crystal GaAs samples were implanted at room temperature with 300-keV Si ions in the dose range of (0.17–2.0)×1015 cm–2 and were subsequently steady-state annealed at 900 and 950°C for 30 min in a H2 ambient with a Si3N4 coating. Differential Hall measurements showed that an upper threshold of about 2×1018/cm3 exists for the free-electron concentration. The as-implanted atomic-Si profile measured by SIMS follows the theoretical prediction, but is altered during annealing. The Cr distribution also changes, and a band of dislocation loops ~2–3 kÅ wide is revealed by cross-sectional TEM at a mean depth of Rp~3 kÅ. Incomplete electrical activation of the Si is shown to be the primary cause for the effect

    Cyanobacterial lipopolysaccharides and human health – a review

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    Cyanobacterial lipopolysaccharide/s (LPS) are frequently cited in the cyanobacteria literature as toxins responsible for a variety of heath effects in humans, from skin rashes to gastrointestinal, respiratory and allergic reactions. The attribution of toxic properties to cyanobacterial LPS dates from the 1970s, when it was thought that lipid A, the toxic moiety of LPS, was structurally and functionally conserved across all Gram-negative bacteria. However, more recent research has shown that this is not the case, and lipid A structures are now known to be very different, expressing properties ranging from LPS agonists, through weak endotoxicity to LPS antagonists. Although cyanobacterial LPS is widely cited as a putative toxin, most of the small number of formal research reports describe cyanobacterial LPS as weakly toxic compared to LPS from the Enterobacteriaceae. We systematically reviewed the literature on cyanobacterial LPS, and also examined the much lager body of literature relating to heterotrophic bacterial LPS and the atypical lipid A structures of some photosynthetic bacteria. While the literature on the biological activity of heterotrophic bacterial LPS is overwhelmingly large and therefore difficult to review for the purposes of exclusion, we were unable to find a convincing body of evidence to suggest that heterotrophic bacterial LPS, in the absence of other virulence factors, is responsible for acute gastrointestinal, dermatological or allergic reactions via natural exposure routes in humans. There is a danger that initial speculation about cyanobacterial LPS may evolve into orthodoxy without basis in research findings. No cyanobacterial lipid A structures have been described and published to date, so a recommendation is made that cyanobacteriologists should not continue to attribute such a diverse range of clinical symptoms to cyanobacterial LPS without research confirmation
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