Sub-ångstrom experimental validation of molecular dynamics for predictive modeling of extended defect structures in Si.

In this Letter we present the detailed, quantitative comparison between experimentally and theoretically derived structures of the extended {311} defect in silicon. Agreement between experimental and theoretical column positions of better than ±0.05 nm has been achieved for all 100 atomic columns in the defect structure. This represents a calculated density of 5.5×10(14) silicon interstitials per cm(2) on {311} planes, in agreement with previous work [S. Takeda, Jpn. J. Appl. Phys., Part 2, 30, L639 (1991)]. We show that although the {311} defect is made up of five-, six-, seven-, and eight-member rings, the shape of these rings varies as a function of position along the defect, and these variations can be determined experimentally with high precision and accuracy. The excellent agreement between the calculated and experimentally derived structure, including the position of atomic columns and the shape of the distinct structural units of the defect, provides strong evidence for the quality and robustness of the molecular dynamics simulation approach for structural studies of defects. The experimental approach is straightforward, without the need for complicated image processing methods, and is therefore widely applicable.

Quantitative statistical analysis, optimization and noise reduction of atomic resolved electron energy loss spectrum images.

In this work we investigate methods of statistical processing and background fitting of atomic resolution electron energy loss spectrum image (SI) data. Application of principal component analysis to SI data has been analyzed in terms of the spectral signal-to-noise ratio (SNR) and was found to improve both the spectral SNR and its standard deviation over the SI, though only the latter was found to improve significantly and consistently across all data sets analyzed. The influence of the number of principal components used in the reconstructed data set on the SNR and resultant elemental maps has been analyzed and the experimental results are compared to theoretical calculations.

The presence of a magnocellular defect depends on the type of dyslexia.

Previous studies have identified a magnocellular pathway defect in approximately 75% of dyslexics. Since these experiments have not classified dyslexia into subtypes, the purpose of this experiment was to determine if adult dyseidetic dyslexics or dysphoneidetic dyslexics suffer from a defect in the magnocellular pathway. Nine dyseidetic dyslexics, eight dysphoneidetic dyslexics, and nine normal readers participated in the experiment. Contrast sensitivity functions (CSF) were determined with vertically oriented sine wave gratings (0.5, 1.0, 2.0, 4.0, 8.0, 12.0 c/deg drifting at 1 and 10 Hz) by employing a two-alternative, forced-choice technique. The results of the experiment indicated that dysphoneidetic dyslexics had reduced sensitivity to low spatial frequencies at 10 Hz, whereas dyseidetic dyslexics did not have reduced sensitivity at either 1 or 10 Hz. These results suggest that the type of dyslexia influences whether losses in perception are found which are consistent with a magnocellular deficit.

Evidence for inherent differences in the system A carrier from normal and transformed liver tissue. Differential inactivation and substrate protection in membrane vesicles and reconstituted proteoliposomes.

Plasma membrane vesicles isolated from intact rat liver (normal hepatocyte) or cultured rat H4 hepatoma cells retain Na+-dependent uptake of 2-aminoisobutyric acid mediated by System A. The carrier was inactivated in normal liver membrane vesicles by either N-ethylmaleimide (NEM) or p-chloromercuribenzene sulfonate (PCMBS). The concentrations required to produce half-maximal inhibition were approximately 370 and 110 microM for NEM and PCMBS, respectively. In contrast, transport of System A in H4 hepatoma membrane vesicles was sensitive to PCMBS (K 1/2 = 180 microM), yet totally unaffected by NEM at concentrations up to 5 mM. Substrate-dependent protection from PCMBS activation was observed for the System A activity in H4 hepatoma membranes, but not in vesicles from normal hepatocytes. Subsequent inactivation of the substrate-protected carrier by sulfhydryl-specific reagents, added following the removal of the protective amino acid, suggests that one or more cysteine residues become less reactive in the presence of System A substrates. Treatment of solubilized membrane proteins with NEM prior to reconstitution into artificial proteoliposomes showed that the selective inactivation by NEM of the carrier in normal liver membranes is not dependent on the lipid environment or on the integrity of the plasma membrane. The results support the hypothesis that there are inherent differences in the System A carriers that are present in normal and transformed liver tissue.