The performance of the heart depends on the concentrations of free calcium ions in the cytoplasm of the myocytes. However, direct evidence for changes in free Ca concentration in physiological events during response to drugs and in pathogenesis has been difficult to obtain because of technical problems in measuring free Ca at 10(-7) M in cells with a volume of only a few picolitres. Here we describe measurements made with the Ca-sensitive photoprotein aequorin in single ventricular myocytes isolated from rat heart. We have detected signals from resting and contracting cells, and from cells exposed to media of altered ionic composition (raised K, lowered Na), ouabain and metabolic inhibitors. We report that free Ca in metabolically-poisoned myocytes is remarkably stable and that severe injury to the cell occurs before the free Ca concentration rises above 1-3 X 10(-7) M, hence cell damage seems to be a cause, not a consequence, of a rise in free Ca. The technique used here should help to resolve many uncertainties regarding free Ca in heart function, and should be particularly valuable for investigating the role of free Ca in ischaemic pathogenesis.

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SUMMARY1. The principal pathways of Na+ and K+ transport in trout erythrocytes have been characterized.2. Approximately 50 % of K+ influx in steady-state erythrQaytes was inhibited by ouabain (1 mM) and 46 % by furosemide (1 mM). Furosemide-sensitive K+ influx was a saturable function of external K+ concentration with a Km of 25 mm. This flux component was also inhibited by SITS (4-acetamido-4'-isothiocyanatostilbene-2'2-disulphonate) (concentration required for 50 % inhibition, I50 = 7-6 x 10-6 M) and by the removal ofexternal Cl-. An increase in cell volume stimulated furosemide-sensitive K+ influx and cell shrinkage inhibited this flux.3. K+ efflux was mainly furosemide-sensitive (64 % of total). This pathway was unaffected by variations in extracellular K+ concentration and is therefore not exchange diffusion. However, it was affected by variations in cell volume in a similar way to the furosemide-sensitive K+ influx. 4. Na+ influx was only slightly sensitive to furosemide (13 % of total) but this component was very sensitive to changes in cell volume; decreased cell volume increased Na+ influx whilst increased cell volume inhibited Na+ influx.5. Furosemide-sensitive K+ influx was unaffected by variations in external Na+ concentration. Similarly, furosemide-sensitive Na+ influx was unaffected by variations in external K+ concentration. This indicates that the passive influxes of Na+ and K+ were not coupled, in contrast to the situation in avian erythrocytes.6. The opposite effects of cell volume upon passive Na+ and K+ fluxes are in good agreement with the net movements of these cations during volume regulation in erythrocytes of the flounder (Cala, 1977) and the toadfish (Lauf, 1982).

Neural transdifferentiation is increasingly recognized in neural crest and neural stem cell tumors. Neuronal differentiation has been anecdotally described primarily in somatotroph cell adenomas associated with acromegaly, but its prevalence in adenomas and relationship to adenoma type has not been completely established. In this study we performed a retrospective morphological and immunohistochemical analysis of neurofilament, phosphoneurofilament, Neu-N, class III tubulin, and Hu in WHO grade I pituitary adenomas. Limited numbers of cells with neuronal features and neuron-associated epitopes may be more common in pituitary adenomas than previously recognized. These may occur in many forms of adenomas including somatotroph, lactotroph, mixed somatotroph and lactotroph, null cell/gonadotroph cell and, rarely, corticotroph cell adenomas.

In this study, conducted in collaboration with the Western Australian rock lobster industry during the 1992–93 fishing season, daily records were made on morbidity and mortality of western rock lobsters, Panulirus cygnus, held in commercial shipping (export) cartons. The aims were to measure the rates of morbidity + mortality and to identify patterns of correlation of morbidity + mortality rates for a range of environmental variables recorded by the processors. In three processing units, the rate of morbidity + mortality in simulated live shipments averaged 5á2% (±0·6), with a highly significant difference (P<0·001) between processing units. Three factors, holding time in export cartons, ambient temperature within the export cartons and chilling period before packing lobsters, had the greatest influence on the rate of morbidity + mortality. Morbidity + mortality rate of animals held for 30–36 h (10·4 ± 2·3%) was twice that of animals held for 20–24 h (5·2 ± 0·6%). A positive significant correlation (r = 0·25, P = 0·001) was identified between morbidity + mortality rate and the internal carton temperature. Aprolongation of the chilling period was reflected by improved survival, possibly resulting from an anaesthesic effect of the chilling treatment.