Coupled-barrier diffusion: the case of oxygen in silicon

Oxygen migration in silicon corresponds to an apparently simple jump between neighboring bridge sites. Yet, extensive theoretical calculations have so far produced conflicting results and have failed to provide a satisfactory account of the observed $2.5$ eV activation energy. We report a comprehensive set of first-principles calculations that demonstrate that the seemingly simple oxygen jump is actually a complex process involving coupled barriers and can be properly described quantitatively in terms of an energy hypersurface with a ``saddle ridge'' and an activation energy of $\sim 2.5$ eV. Earlier calculations correspond to different points or lines on this hypersurface.Comment: 4 Figures available upon request. Accepted for publication in Phys. Rev. Let

Geometry and quantum delocalization of interstitial oxygen in silicon

The problem of the geometry of interstitial oxygen in silicon is settled by proper consideration of the quantum delocalization of the oxygen atom around the bond-center position. The calculated infrared absorption spectrum accounts for the 517 and 1136 cm$^{-1}$ bands in their position, character, and isotope shifts. The asymmetric lineshape of the 517 cm$^{-1}$ peak is also well reproduced. A new, non-infrared-active, symmetric-stretching mode is found at 596 cm$^{-1}$. First-principles calculations are presented supporting the nontrivial quantum delocalization of the oxygen atom.Comment: uuencoded, compressed postscript file for the whole. 4 pages (figures included), accepted in PR

Semiconductor Surface Studies

Contains research summary and reports on two research projects.Joint Services Electronics Program (Contract DAAL03-86-K-0002)Joint Services Electronics Program (Contract DAAL03-89-C-0001

Semiconductor Surface Studies

Contains an introduction and reports on two research projects.Joint Services Electronics Program Contract DAAL03-89-C-000

Optically modulated magnetic resonance of erbium implanted silicon

Er implanted Si is an important candidate for quantum and photonic applications, but the Er centres involved are poorly understood, which has hindered development of these applications. Here we present the first measurement of the crystal field splitting of the 4I13/2 manifold of Er implanted Si, using a technique we call optically modulated magnetic resonance (OMMR). Crystal field analysis allows us to determine that this splitting originates from a photoluminescence (PL) active O coordinated Er centre with orthorhombic symmetry, which is highly localised with, and magically coupled to, an electron paramagnetic resonance (ERP) active O coordinated Er centre with monoclinic symmetry. The orthorhombic centre has a g-factor in agreement with previous Zeeman measurements, and is associated with a previously unreported acceptor state at ~ Ev+425 cm-1, showing that Er in Si is amphoteric, and not a pure donor, as previously thought. The OMMR mechanism involves transitions from this acceptor state to the 4I13/2 manifold, followed by relaxation to the Zeeman ground state

Neuron-glia cross talk in rat striatum after transient forebrain ischemia

Striatum is highly vulnerable to transient forebrain ischemia induced by the 4 vessel occlusion (4V0) method (Brierley 1976. Pulsinelli et al. 1982, Zini et al. 1990a). Massive degeneration and loss of Nissl-stained neurons occur within 24 hr from an ischemia of long duration (30 min) (Pulsinelli et al. 1982). Neuronal loss is mainly restricted to the lateral part of caudate-putamen (Pulsinelli et al. 1982, Zini et al. 1990a). Cellular alterations include loss of medium-size spiny projection neurons (Pulsinelli et al. 1982, Francis and Pulsinelli 1982), largely corresponding to dopaminoceptive neurons (Benfenati et al. 1989, Zoli et al. 1989), and increase in reactive astrocytes (Pulsinelli et al. 1982, Grimaldi et al. 1990) and microglia (Gehrmann et al. 1982). On the other hand, large cholinergie (Francis and Pulsinelli 1982) and medium-size aspiny somatostatin (SS)/neuropeptide Y (NPY)-containing interneurons are resistant to the ischemic insult (Pulsinelli et al. 1982, Grimaldi et al. 1990). In a few instances, such as in the case of SS and NPY immunoreactivity (IR), the initial loss is followed by full recovery within 7 (SS) or 40 (NPY) days post-ischemia (Grimaldi et al. 1990). However, it is not known whether some kind of recovery is present for the bulk of medium-size spiny projections neurons after the first days post-ischemia