The effect of sporidesmin toxicity on ovine serum vitamin B12 levels.

A field outbreak of facial eczema occurred during a vitamin B12 response trial in young growing sheep. Pasture cobalt levels were in the low range for sheep (<0.08 mg/kg, 1.358 micromol/kg) and mean (of 3) liver vitamin B12 levels in the sheep were low (<400 nmol/kg) during the period in which facial eczema occurred. Mean serum vitamin B12 levels of the untreated group were low (<485 pmol/l) for the two months (January and February) preceding the period of facial eczema. However, levels showed an approximate 3.5 fold increase in both cobalt supplemented and unsupplemented groups with the onset of facial eczema in March. From February to March the mean serum vitamin B12 and glutamyl transferase (GGT) activity showed parallel increases with a positive correlation (r = 0.73) between log serum vitamin B12 and log serum GGT activity during the period January to July for both groups. This finding suggested that the increase in serum vitamin B12 was due to sporidesmin induced liver damage. The diagnostic implication is that, in areas where facial eczema is a problem, liver is the sample of choice for determining vitamin B12 status. because sporidesmin toxicity can elevate low serum vitamin B12 levels to diagnostically normal levels.

Neonatal data base and automated discharge summary using a personal computer and proprietary software.

A computerized neonatal data base and a program to develop automated neonatal discharge summaries were developed using a personal computer and proprietary software. The system has been relatively inexpensive, simple to operate, and easy to expand. The current program can produce a discharge summary in less than five minutes, as well as provide detailed summary statistics regarding patients admitted to the intensive care facility. The personal computer and proprietary software are a cost-effective mechanism of improving efficiency in obtaining neonatal statistics and discharge summaries.

Fatty acid composition of phospholipids and neutral lipids during embryonic and early larval development in Atlantic herring (Clupea harengus, L.).

The fatty acid compositions of total polar and total neutral lipids of Atlantic herring eggs and larvae were determined immediately before fertilization, after fertilization and at various times during subsequent embryonic and early larval development. Within 3 hr after fertilization the percentage of total PUFA in neutral lipid decreased from 33% to 20%, with a reciprocal increase in monoenes. Thereafter the percentage of PUFA in the neutral lipids increased progressively, attaining the original level in ripe eggs by the time of yolk sac absorption. During the larval stages the percentage of PUFA continued to increase in the neutral lipid, reaching almost 44% of the total by day 32 after fertilization, although it was reduced to 32% by day 36. The percentage of monoenes in the neutral lipid displayed a progressive decrease during the whole period of development from 3 hr after fertilization. Throughout all the developmental periods the fatty acid composition of total polar lipids remained essentially constant. The polar lipids of the yolk sac displayed virtually the same fatty acid composition as the larval bodies, but the neutral lipids of the yolk sac were low in PUFA compared to the larval bodies. The results are discussed with reference to changes in lipid class composition during development. The conservation of high levels of PUFA in lipids during embryogenesis and early larval development reflects the importance of these fatty acids during development.

Lipid class composition during embryonic and early larval development in Atlantic herring (Clupea harengus, L.).

The lipid class compositions of Atlantic herring eggs and larvae were determined immediately before fertilization, after fertilization and at various times during subsequent embryonic and early larval development. Total lipid constituted 15% of the dry wt of ripe eggs, 70% of the total lipid being polar lipid with phosphatidylcholine (PC) accounting for almost 90% of the polar lipid. In general, the total lipid content decreased gradually during embryogenesis and in particular during larval development. Within 3 hr after fertilization the relative percentage of neutral lipid decreased slightly. This was followed by a general decrease in polar lipid which, by the stage of yolk sac absorption, was reduced to 52% of the total lipid. The decreased percentage of polar lipid was due entirely to a decrease in PC, which was reduced to 66% of the polar lipids at the stage of yolk sac absorption. The accompanying increase in the percentage of neutral lipids was mainly due to increased percentages of triacylglycerols (TAG) up to yolk sac absorption and cholesterol esters in the larval stages. During the first 4 days after hatching, phospholipids and to a lesser extent cholesterol were preferentially depleted in the yolk sacs, which also had higher levels of free fatty acids. The results are discussed in relation to possible roles of different lipids during embryonic and early larval development.

Some observations on the liver copper status of pigs in the northern part of New Zealand.

The copper content of the livers from 347 pigs was analysed. Two hundred and three of these samples were from animals varying in age from full term foetus to five years, which were submitted to the laboratory (laboratory cases) for a variety of diagnostic tests. The remaining 144 liver samples were obtained from pigs slaughtered at an abattoir (abattoir survey) at 75-85 kg liveweight (approximately 20-30 weeks old). Liver copper levels of 12 mg/kg D.M. (Dry Matter) or less, a level consistent with copper deficiency, were found in 6.9% of the laboratory cases and in 9.0% of the abattoir survey pigs. Liver levels less than 20 mg/kg suggesting insufficient dietary copper to produce a growth-promoting effect, were found in 21.6% of the former and 36.1% of the latter pigs. A significantly greater frequency of illthrift and anaemia was found in the laboratory cases in which liver copper levels were less than 20 mg/kg compared with animals with higher levels. Liver copper levels less than 20 mg/kg were also more common in pigs derived from dairy farms or fed garbage than in animals from pig farms or fed on meal. All of 26 samples of commercial pig meal analysed contained sufficient copper to satisfy the daily essential copper requirements of pigs (greater than 5-6 mg/kg) but 14 of these (53.8%) contained less than 125 mg/kg levels of copper and were unlikely to produce a growth-promoting effect.

Superphosphate poisoning of sheep: the role of fluoride.

Earlier work confirmed that the fundamental lesion of superphosphate poisoning is an acute toxic tubular nephritis in which both phosphate and fluoride may play a part but their respective roles could not be determined. In this study, sheep poisoned by sodium fluoride (NaF) were compared with sheep poisoned by superphosphate containing approximately 1.5% fluoride. The LD50 of NaF was in the range 100 to 300 mg/kg (45 to 135 mg F/kg). This range is of the same order as the amount of fluoride in a toxic dose of superphosphate (70 to 90 mg F/kg). A lethal dose of NaF caused severe depression, salivation, hyperpnoea, blindness, ataxia and incoordination. Death ensued three to 52 hours after dosing. Acute necrotizing rumino-reticulitis and abomasitis and necrosis of epithelial cells in the proximal convoluted tubules of the kidney were the characteristic lesions of NaF toxicity. Superphosphate poisoning took a more protracted course with depression and diarrhoea as the predominant clinical signs until the terminal coma. As with NaF, the notable lesions were in the gastrointestinal tract and kidneys, but were less severe. Although there were differences in the clinical and pathological manifestations of the two forms of poisoning, the comparable toxic dose of NaF and of the fluoride in a toxic dose of superphosphate, and the similar target organs involved, support the view that fluoride plays a dominant role in the pathogenesis of superphosphate poisoning. It is probable that phosphate plays a contributory role but the nature of the interaction of fluoride and phosphate remains to be established.

Glutathione peroxidase activity in bovine serum and erythrocytes in relation to selenium concentrations of blood, serum and liver.

The concentration of selenium (Se) in liver, serum and whole blood, and the activity of glutathione peroxidase (GSH-px) in serum and erythrocytes were monitored for seven months after the administration of Se to Se-deficient calves. There was a rapid increase in Se concentration in liver and serum, followed by an exponential decline with half-lives of 22.1 +/- 0.2 days and 28.3 +/- 2.0 days respectively. Whole blood Se concentration also increased rapidly but declined more slowly than liver or serum Se concentraations. The rise in Se concentration and GSH-px activity in erythrocytes was delayed and both levels remained elevated several months after liver and serum Se concentrations had become marginal or deficient. GSH-px activity in serum increased more rapidly after dosing and declined more rapidly than GSH-px activity in erythrocytes. The results suggest that liver and serum Se concentration and serum GSH-px activity respond to changes in dietary Se intake more rapidly than either whole blood Se or erythrocyte GSH-px activity. Two-monthly administrations of Se, at the current recommended therapeutic dose (0.1 mg Se/kg as sodium selenate) appears to be necessary to maintain adequate Se levels in calves on Se-deficient pasture.

Fate of surviving low-birth-weight infants with coagulation deficiencies on the first day of life.

Fifty-two surviving low-birth-weight infants who had low Thrombotest (Owren) results on the first day, together with the same number of matched controls with higher Thrombotest results, were examined for the integrity of their central nervous system. Gross abnormalities were found in 13.5% of the low Thrombotest group compared with 1.9% in the higher group. Minor brain damage syndromes were more common in the low Thrombotest group. The combined brain damage syndromes were 23.1% in the low Thrombotest group compared with 3.8% in the higher group.It is suggested that the causes of the brain damage in the low Thrombotest group are either non-fatal cerebral haemorrhage or intravascular fibrin deposition associated with disseminated intravascular coagulation.