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The neutralizing ability of commercially available antivenom prepared against 'milked' box-jellyfish (Chironex fleckeri) venom was tested intravenously in mice against crude nematocyst venom obtained by crushing isolated nematocysts and against each of two lethal toxins (T1 and T2) present in this venom. The in vitro neutralizing ability of the antivenom against crude venom was reduced markedly compared with its reported neutralizing ability against 'milked' venom whilst the in vivo neutralizing ability of the antivenom tested in both prophylactic and rescue experiments involving crude nematocyst venom was reduced approximately threefold. When tested in vitro and prophylactically in vivo the neutralizing ability of the antivenom was much more pronounced against T2 than against T1. This finding was in accord with the view that T1 was absent from the 'milked' venom against which the antivenom was prepared. Doses of crude venom in excess of twice the lethal dose killed mice within 2-3 min emphasizing the need for speed in the administration of antivenom.

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Transferrin-iron uptake by peripheral blood monocytes was studied in vitro to test the hypothesis that the relative paucity of mononuclear phagocyte iron loading in hereditary hemochromatosis results from a defect in uptake of iron from transferrin. Monocytes from nine control subjects and 17 patients with hemochromatosis were cultured in the presence of 59Fe-labelled human transferrin. There was no difference in 59Fe uptake between monocytes from control subjects and monocytes from patients with hemochromatosis who had been treated by phlebotomy and who had normal body iron stores. However, 59Fe uptake by monocytes from iron-loaded patients with hemochromatosis was significantly reduced compared with either control subjects or treated hemochromatosis patients. It is likely that this was a secondary effect of iron loading since iron uptake by monocytes from treated hemochromatosis patients was normal. Assuming that monocytes in culture reflect mononuclear phagocyte iron metabolism in vivo, this study suggests that the relative paucity of mononuclear phagocyte iron loading in hemochromatosis is not related to an abnormality in transferrin-iron uptake by these cells.

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Tissue ferritin metabolism was compared in control and ascorbic acid (AA) deficient guinea-pigs. Concentrations of ferritin protein in the liver (0.98 +/- 0.61 mg/g wet weight) and spleen (0.48 +/- 0.23 mg/g) of control animals did not change after tissue depletion of AA. Iron dextran (75 mg/kg weight, i.m.) caused a 4-5-fold increase in tissue ferritin concentrations in controls whereas no increase in tissue ferritin occurred in scorbutic animals. The rise in tissue total iron concentration was similar in the two groups. Liver ferritin synthesis was similar in control and scorbutic animals. After stimulation with iron (8 mg/kg iron dextran i.v.), ferritin synthesis rose in both groups of animals. However, the pattern of response differed. At 24 h after iron dextran, ferritin synthesis in controls was still significantly elevated (P less than 0.001) and liver ferritin protein continued to rise, whereas in scorbutic animals, ferritin synthesis had declined to pre-iron injection levels, and no rise in ferritin protein values occurred. It is concluded that the ferritin synthetic apparatus in AA deficient tissues remained intact and capable of responding to added iron. The absence of a sustained elevation in tissue ferritin protein after an iron load appeared to be due to inadequate stimulation of ferritin synthesis by intracellular iron. It is suggested that AA has a physiological role in the reduction of intracellular iron and that it is the reduced form of iron which stimulates ferritin synthesis. Abnormalities of iron metabolism occur in AA depleted tissues when the quantity of Fe3+ entering cells exceeds the residual reducing capacity of those cells.

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A pellicle-forming yeast, identified as Candida ingens, was found to grow on substrates derived from the anerobic fermentation of monogastric animal wastes. The organism used volatile fatty acids C2 to C6 and ammonia nitrogen. It had a preferential uptake of the acids in increasing order of molecular weight, removing 90% of the total titratable volatile acid. The nonwrinkled pellicle had a doubling time of 3.2 h, and the doubling time of the wrinkled pellicle was 4.2 h. Proximate amino acid and nucleic acid analyses suggested that the organism might be acceptable as a source of single cell protein. Its vitamin B group content compared favorably with that of other yeasts. It contained 6% calcium and 7% phosphorus. It could be useful in removing these minerals from effluents as well as in providing them as nutrients in livestock rations.

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