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Notes: Electrically active defects were generated in metal-oxide-silicon (MOS) structures by implantation of 16 keV Si ions into the oxide (350 A(ring) thick) of oxidized silicon wafers. Subsequently, hydrogenation was carried out at room temperature by 400 eV H ions from a Kaufman source. To examine the nature of interaction between the H ions and the electronic traps and the efficacy of ion beam hydrogenation, current-voltage, and comprehensive admittance-voltage-frequency measurements were made. The measured data were analyzed to yield information on the trap and other important parameters of the MOS structure. The experimental data indicated impressive passivation of the ion beam induced damage by room-temperature hydrogenation. Many and most of the insiduous effects of radiation damage were removed, some completely. However, the results also indicated generation of some H-defect complexes during hydrogenation, leading to residual traps in the hydrogenated samples.

Notes: As the ever-decreasing gate oxide thickness approaches the threshold for direct tunneling of electrons across the gate oxide, i.e., about 3 nm, a defect-generation mechanism, which is not present in thicker gate oxides, becomes inevitable. The source of this mechanism is the recombination of channel electrons into the interface traps and their subsequent tunneling through the gate oxide to the gate metal. This carrier transport process generates additional interface traps, and the resultant regenerative feedback cycle culminates in a soft breakdown of the gate oxide, fatally compromising its reliability, and setting the ultimate gate oxide thinness to a value in the neighborhood of 3 nm. © 2000 American Institute of Physics.

Notes: Abstract: The characteristic pathological features of the postmortem brain of Alzheimer's disease (AD) patients include, among other features, the presence of neuritic plaques composed of amyloid β-peptide (Aβ) and the loss of basal forebrain cholinergic neurons, which innervate the hippocampus and the cortex. Studies of the pathological changes that characterize AD and several other lines of evidence indicate that Aβ accumulation in vivo may initiate and/or contribute to the process of neurodegeneration and thereby the development of AD. However, the mechanisms by which Aβ peptide influences/causes degeneration of the basal forebrain cholinergic neurons and/or the cognitive impairment characteristic of AD remain obscure. Using in vitro slice preparations, we have recently reported that Aβ-related peptides, under acute conditions, potently inhibit K+-evoked endogenous acetylcholine (ACh) release from hippocampus and cortex but not from striatum. In the present study, we have further characterized Aβ-mediated inhibition of ACh release and also measured the effects of these peptides on choline acetyltransferase (ChAT) activity and high-affinity choline uptake (HACU) in hippocampal, cortical, and striatal regions of the rat brain. Aβ1–40 (10−8M) potently inhibited veratridine-evoked endogenous ACh release from rat hippocampal slices and also decreased the K+-evoked release potentiated by the nitric oxide-generating agent, sodium nitroprusside (SNP). It is interesting that the endogenous cyclic GMP level induced by SNP was found to be unaltered in the presence of Aβ1–40. The activity of the enzyme ChAT was not altered by Aβ peptides in hippocampus, cortex, or striatum. HACU was reduced significantly by various Aβ peptides (10−14 to 10−6M) in hippocampal and cortical synaptosomes. However, the uptake of choline by striatal synaptosomes was altered only at high concentration of Aβ (10−6M). Taken together, these results indicate that Aβ peptides, under acute conditions, can decrease endogenous ACh release and the uptake of choline but exhibit no effect on ChAT activity. In addition, the evidence that Aβ peptides target primarily the hippocampus and cortex provides a potential mechanistic framework suggesting that the preferential vulnerability of basal forebrain cholinergic neurons and their projections in AD could relate, at least in part, to their sensitivity to Aβ peptides.

Notes: Abstract. Field experiments were carried out to evaluate the relative efficacy of organic manures in improving the productivity and pest tolerance of rice growing in a lateritic soil. The effects of three commercial manures: processed city waste (PCW), vermicompost (VC) and oil cake pellets (OCP), were assessed in comparison to farmyard manure (FYM) and inorganic fertilizer all at the same total N applied. Of the organic manures tested, FYM produced the maximum straw and grain yields. Differences in yield among the organic manure treatments were mainly attributed to variation in the amounts of available N, P, K and micronutrients. Effect of manures on soil physical condition was not studied. The uptake of N, P and K by rice plants with FYM was significantly greater than all other commercial manures and inorganic fertilizer. The tolerance of rice plants to attack by pathogens and pests, measured in terms of grain yield was highest in the treatment with FYM. Among the commercial manures PCW showed the greatest promise and emerged as a potential alternative to FYM.

Notes: Important characteristics of the Si-SiO2 interface states, such as the interface state density distributions and the electron and the hole capture cross section versus energy profiles, were investigated in unannealed metal/silicon dioxide/silicon (MOS) structures with the gate oxide thickness in the range of 70–230 A(ring), using the optical MOS admittance technique. The experimentally obtained interface state density distribution, in case of p-Si/SiO2/Al structures, exhibited two peaked profiles, one near the valence-band edge Ev and the other near the conduction-band edge Ec, overlying a concave background. The state density at the peak was observed to undergo a maximum, preceded by a minimum, as the gate oxide thickness tox was increased. The peak energy versus tox and the capture cross section versus tox profiles also indicated strong features.

Notes: For the present investigation n-Si/SiO2/In2O3 transparent gate structures were fabricated by electron-beam evaporation of a tin-doped indium oxide layer on thermally oxidized silicon. Admittance measurements were carried out in dark and under three different levels of illumination. A comprehensive technique has been presented for obtaining interface state density distribution from illuminated capacitance data as well as from illuminated conductance data, and hole and electron capture cross sections from the latter. This technique includes a procedure for identification of the dominant quasi-Fermi level (imref) under illumination for determination of the state energy level, three independent methods for evaluating the imref separation from measured data, and a procedure for ascertaining whether electron or hole exchange is the source of a set of Gp/ω vs V or ω characteristics. The interface state density distribution of unannealed structures exhibited two peaked profiles. One peak was located about 0.36–0.41 eV above the valence-band edge, while the other was located about 0.30–0.17 eV below the conduction-band edge. The peak magnitude was found to increase with the illumination intensity and the peak position moved towards the respective band edge. Electron capture cross sections of states in the upper band gap half were found to be in the range of 10−18–10−20 cm2, and hole capture cross sections of states in the lower band gap half in the range of 10−15–10−16 cm2. Both σe and σh were found to vary with band-gap energy and illumination level.

Notes: Glycogen synthase kinase-3β (GSK-3β) is a multifunctional enzyme involved in a variety of biological events including development, glucose metabolism and cell death. Its activity is inhibited by phosphorylation of the Ser9 residue and up-regulated by Tyr216 phosphorylation. Activated GSK-3β increases phosphorylation of tau protein and induces cell death in a variety of cultured neurons, whereas phosphorylation of phosphatidylinositol-3 (PI-3) kinase-dependent protein kinase B (Akt), which inhibits GSK-3β activity, is one of the best characterized cell survival signaling pathways. In the present study, the cholinergic immunotoxin 192 IgG-saporin was used to address the potential role of GSK-3β in the degeneration of basal forebrain cholinergic neurons, which are preferentially vulnerable in Alzheimer's disease (AD) brain. GSK-3β co-localized with a subset of forebrain cholinergic neurons and loss of these neurons was accompanied by a transient decrease in PI-3 kinase, phospho-Ser473Akt and phospho-Ser9GSK-3β levels, as well as an increase in phospho-tau levels, in the basal forebrain and hippocampus. Total Akt, GSK-3β, tau and phospho-Tyr216GSK-3β levels were not significantly altered in these brain regions in animals treated with 192 IgG-saporin. Systemic administration of the GSK-3β inhibitor LiCl did not significantly affect cholinergic marker or phospho-Ser9GSK-3β levels in control rats but did preclude 192-IgG saporin-induced alterations in PI-3 kinase/phospho-Akt, phospho-Ser9GSK-3β and phospho-tau levels, and also partly protected cholinergic neurons against the immunotoxin. These results provide the first evidence that increased GSK-3β activity, via decreased Ser9 phosphorylation, can mediate, at least in part, 192-IgG saporin-induced in vivo degeneration of forebrain cholinergic neurons by enhancing tau phosphorylation. The partial protection of these neurons following inhibition of GSK-3β kinase activity suggests a possible therapeutic role for GSK-3β inhibitors in attenuating the loss of basal forebrain cholinergic neurons observed in AD.

Notes: In this investigation, the efficacy of remote plasma hydrogenation, in the passivation of bonding and other electronic defects in amorphous silicon, has been compared with those of ion beam and radio-frequency plasma hydrogenations. The amorphous silicon film was obtained by amorphization of the subsurface of ultrapure crystalline silicon by a Si ion beam. Electrical measurements indicated remote plasma hydrogenation to be a promising low- temperature defect removal technique, without the damaging effect of a plasma or the etching effects of low-energy hydrogen ions.