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The purpose of this study was to compare EEG current source densities in high IQ subjects vs. low IQ subjects. Resting eyes closed EEG was recorded from 19 scalp locations with a linked ears reference from 442 subjects ages 5 to 52 years. The Wechsler Intelligence Test was administered and subjects were divided into low IQ (< or =90), middle IQ (>90 to <120) and high IQ (> or =120) groups. Low-resolution electromagnetic tomographic current densities (LORETA) from 2,394 cortical gray matter voxels were computed from 1-30 Hz based on each subject's EEG. Differences in current densities using t tests, multivariate analyses of covariance, and regression analyses were used to evaluate the relationships between IQ and current density in Brodmann area groupings of cortical gray matter voxels. Frontal, temporal, parietal, and occipital regions of interest (ROIs) consistently exhibited a direct relationship between LORETA current density and IQ. Maximal t test differences were present at 4 Hz, 9 Hz, 13 Hz, 18 Hz, and 30 Hz with different anatomical regions showing different maxima. Linear regression fits from low to high IQ groups were statistically significant (P < 0.0001). Intelligence is directly related to a general level of arousal and to the synchrony of neural populations driven by thalamo-cortical resonances. A traveling frame model of sequential microstates is hypothesized to explain the results.

A reverse-phase liquid chromatography/mass spectrometry (LC/MS) method, incorporating gradient elution, is described for the characterization of residual erythromycin A and its metabolites in salmon tissue. The method uses ion-spray, a mild atmospheric pressure ionization technique which provides an abundant protonated molecule well suited for selected ion monitoring experiments. Tandem mass spectrometry (MS/MS) using collision-induced dissociation was used to provide structural information. The LC/MS method was tested for the analysis of salmon tissue spiked with erythromycin A at levels between 0.01 and 1 p.p.m. A simple extraction and clean-up procedure, slightly modified from that described by Takatsuki et al. (J. Assoc. Off. Anal. Chem. 70, 708 (1987)), was used in this work. Using selected ion and selected reaction monitoring techniques, the LC/MS and LC/MS/MS methods provided detection limits of < 10 and 50 ng g-1, respectively. Confirmatory full-scan LC/MS and LC/MS/MS spectra were obtained at the 0.5 and 1 microgram g-1 levels, respectively. Using a combination of these techniques, the presence of residual erythromycin A was confirmed in the tissue of fish administered medicated feed containing the antibiotic. In addition, several metabolites and degradation products of erythromycin A, including anhydro-erythromycin and N-demethyl-erythromycin, were detected and where possible confirmed by comparison with authentic compounds. Although this analytical method has been shown to afford the necessary sensitivity and precision, application of these techniques to high-throughput quantitative analyses will require development of an improved clean-up procedure and preferably also of a suitable surrogate internal standard.

The effects of cimetidine and ranitidine on tocainide pharmacokinetics were assessed in seven healthy subjects, using a randomized, double-blind, placebo-controlled, cross-over study design. After a 400-mg oral dose of tocainide, the area under the concentration-time curve decreased from (mean +/- SD) 31.64 +/- 14.16 micrograms.hr/mL during placebo, to 23.10 +/- 7.33 micrograms.hr/mL during cimetidine (P less than .05). Similarly, the peak tocainide concentrations were 2.81 +/- 0.89 micrograms/mL and 1.70 +/- 0.44 micrograms/mL with placebo and cimetidine, respectively (P less than .05). There was no change in the above parameters between ranitidine and placebo. The terminal half-life and renal clearance of tocainide were not altered by either H2-receptor antagonists, compared with placebo. However, the total amount of tocainide excreted unchanged in the urine, decreased from 159.8 +/- 14.7 mg with placebo to 136.8 +/- 26.8 mg with cimetidine (P less than .05), whereas there was no change with ranitidine. These data indicate that cimetidine, but not ranitidine, causes a decrease in the bioavailability of tocainide and that neither agent alters the apparent elimination rate of tocainide.