Search PubMed⌕ Search

Biomedical subjects

A E Roberts

Publications and source records attributed to A E Roberts.

23 records · Page 2Linked to original sources
PubMed1971

Conditioned suppression of an avoidance response.

A signal followed by shock was presented at irregular intervals during a free-operant avoidance schedule. The effects of this procedure were studied in terms of the rate of unavoided shock in the presence and absence of the signal and the rate of response before and during the signal. Three shock intensities were employed. Response enhancement as well as response suppression were observed; irrespective of changes in responding, shock rates substantially increased during signalled periods compared to non-signalled periods. Shock rates in non-signalled periods were generally higher than during training.

Journal Article↗
PubMed1970

The effect of a pre-shock signal on a free-operant avoidance response.

After 25 free-operant avoidance training sessions, a 1-min signal followed by a brief shock was presented on the average of once every 4 min. During the signal, the avoidance schedule was suspended (20 sessions). Response rates during the signal were markedly reduced. Shock rates during non-signalled periods increased. Fifteen additional sessions were given during which the signal was presented without shock. Response rates during signalled periods were greater than previously observed during signalled periods, indicating that signalled shock had suppressive control over a previously acquired avoidance response rate.

Journal Article↗
PubMedDate not supplied

Metabolism of acrylonitrile to 2-cyanoethylene oxide in F-344 rat liver microsomes, lung microsomes, and lung cells.

The metabolism of acrylonitrile to the epoxide, 2-cyanoethylene oxide (ANO) was examined in rat liver microsomes, lung microsomes, and isolated enriched lung cell preparations. GC/high resolution MS was used to quantitate ANO in microsomal and cellular extracts by monitoring the fragment ion C2H3N (m/z 41.0265). The limit of detection was 0.05 pmol of ANO/0.5 microliter of standard solution, microsomal extract, or cellular extract injected onto the column, and the linear range of analysis was 0.05 to 12.5 pmol of ANO. Kinetic parameters of Vmax, V/K, and Km were calculated for microsomal ANO formation. Liver microsomes were quantitatively more active than lung microsomes on a mg of protein basis. The Vmax (pmol of ANO formed/min/mg of protein) was 666.61 for liver and 45.07 for lung microsomes. The V/K (pmol of ANO/min/mg of protein/microM) was 12.83 for liver and 0.02 for lung microsomes. The apparent Km was 51.93 microM and 1853.83 microM for liver and lung microsomes, respectively. When calculated as nmol of ANO formed/min/nmol of microsomal P-450, the Vmax for lung was equivalent to the Vmax for liver. ANO formation in the rat lung was cell specific. The rates of metabolism in the Clara cell-enriched fraction, the alveolar type II cell-enriched fraction, and the cell suspension were 2.55, 0.38, and 0.67 pmol of ANO formed/min/mg of protein, respectively. No metabolism was observed in the endothelial (small) cell-enriched fraction or in the alveolar macrophages. The results suggest that the lung contributes to the metabolism and disposition of inhaled acrylonitrile.

Acrylonitrile↗