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involved in the action of peptide hormones, startling in its breadth of coverage. Professor Catt came armed with no less than 6 other seminars -a remarkable achievement. The greatest demand was for those on angiotensin and aldosterone, as well as those on the gonadotrophin-releasing hormones. He had detailed laboratory discussions with between 5 and 12 endocrine investigators each day, and all remarked on his perspicacity and helpfulness in discussing their research. Professor Catt proved to be indefatigable, despite what a distinguished British professor described as 'an itinerary for his destruction', and the educational value of his visits to young British researchers proved immense. Perhaps his only moments of peace and quiet were on a train, or when staying at the Domus Medica. He was, of course, entertained by the Clinical Endocrinology Trustees and also by the officers of the Section of Endocrinology.The value of such visits, however, is not just oneway, and is well exemplified by Professor Catt's remark to me that he had not previously realized how well focused is British endocrine research, nor how diverse. British endocrinology and the Section of Endocrinology in particular express their gratitude to Professor Catt and the Trustees for making such a marvellous visit possible.

This pilot programme shows the benefits of a high-fidelity, in situ, multidisciplinary simulation training course for core medical trainees in developing the key crisis resource management skills necessary at medical registrar level. As a historical apprenticeship model of training becomes increasingly variable and absent, we present a novel complimentary training strategy for tomorrow's medical registrars.

We have studied in 12 patients the effect of desflurane in nitrous oxide on the electroencephalogram (EEG) and the early cortical auditory evoked response (AER). After induction with desflurane, patients' lungs were ventilated to maintain three different end-expiratory concentrations of desflurane (1.5, 3 and 6%) during four consecutive 10-min periods before surgery. As the end-expiratory concentration of desflurane was increased, Pa and Nb (AER) amplitudes decreased and their latencies increased, and spontaneous EEG showed an increase in amplitude and a slowing of frequency. A linear relationship was demonstrated between log10 concentration of desflurane and all variables (P = 0.001). Pa amplitude showed the greatest linearity followed by the derived variable F95 of the EEG. From regression slopes, mean percentage changes of each variable were calculated for a 1 MAC change in desflurane concentration, Pa amplitude showed the largest change (mean 49% (95% confidence interval 40-56%) decrease for a 1 MAC increase). This was greater than that of F95 for a similar confidence interval, indicating better resolution. This study confirms that the early cortical AER is affected by desflurane in a similar manner to that of other anaesthetic agents and as such remains the most promising EEG derived measure of depth of anaesthesia.

We have studied the effect of a bolus dose of midazolam on the auditory evoked response (AER) of the electroencephalogram (EEG) in nine patients. We measured the AER in the awake patient, at the point of loss of the eyelash reflex and when airway support was required. The eyelash reflex was lost at mean 1.78 (SD 0.5) min after administration of the midazolam bolus dose. Time to airway support in the seven patients who required it was 2.74 (1.26) min. Mean Nb latency in awake patients was 44.3 ms (95% CI 41.9-46.9) which was significantly shorter than Nb latency at the clinical end-points (P < 0.001). When the eyelash reflex was lost, Nb latency was 55.7 ms (95% CI 51.4-60.3) and when airway support was needed, it was 50.9 ms (95% CI 48.6-53.2). We conclude that loss of consciousness after midazolam was associated with an increase in mean Nb latency.