Foetal rat pancreatic rudiments explanted on day 14 of gestation were grown for 6 days in organ culture in medium containing glucose (5\m=.\5 or 16\m=.\5 mmol/1) and amino acids at the 'physiological' or seven times the 'physiological' concentration. At the end of the period of culture, the rudiments were compared with normal 20-day foetal pancreas for DNA content, insulin concentration and quantitative morphology. The secretion of insulin from the explants was tested during 2 h incubations in medium containing glucose (5\m=.\5 or 16\m=.\5 mmol/1). Amino acid, but not glucose enrichment of the culture medium stimulated cellular growth of the rudiment which remained, nevertheless, smaller than that occurring in vivo. All culture conditions produced a smaller proportion of exocrine cells and a greater proportion of \ g=b\ and duct cells than were found in normal 20-day foetal pancreas. Enrichment with amino acids favoured the development of exocrine cells at the expense of duct cells. Glucose had no effect on the development of any type of cell. Enrichment with amino acids resulted in a higher concentration of insulin per \ g=b\ cell but the highest value observed in vitro was only one sixth of that occurring in vivo. The absolute number of \ g=b\ cells cultured in amino-acid-enriched medium was twice that occurring in vivo. Culture in a gl ucose\x=req-\ enriched medium had no effect on the ability of the explant to respond to an acute glucose challenge during a short incubation, but the basal and glucose-stimulated release of insulin from cultures grown in amino-acid-enriched medium were significantly greater.
A patient is described who had an inhibitor to coagulation factor XIII associated with serum autoantibodies to certain tissues. The relationship of these abnormal findings to practolol therapy suggests that this was practolol-induced lupus erythematosus. Further investigations delineating the site of action of the inhibitor to factor XIII are reported.
The natural history and haematological features of 18 patients with a chronic form of myelomonocytic leukaemia are described. The majority were elderly and, in this series, females predominated. Haematological prodomata, such as unexplained monocytosis, leucopenia, or thrombocytopenia were common, and the clinical onset was insidious. Splenomegaly was variable but tended to increase as the disease progressed. Anaemia was usually less than in the acute disease, unless compounded by iron deficiency. The blood film typically showed a mixed monocytosis and granulocytosis, cells in both lines showing abnormalities. 'Paramyeloid' cells, appearing in Romanowsky stained films intermediate between myelocytes and monocytes, were characteristic, although cytochemical and electron microscopical analysis suggests that these cells may be allotted to one or other cell line. The marrow aspirate was characteristically hypercellular, showed granulocytic hyperplasia, and, in contrast to the well-differentiated blood picture, the proportion of poorly differentiated cells, including blasts, was high. Serum lysozyme levels were usually raised. Five of the 18 cases survived more than 5 years, while 10 lived 2 years or longer. The morphological and clinical features form part of a spectrum including acute myelomonocytic leukaemia, into which several of the patients transformed. Recognition of the syndrome is important because the patients are probably best managed without intensive chemotherapy.
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