Search PubMed⌕ Search

Biomedical subjects

P B Hamilton

Publications and source records attributed to P B Hamilton.

At least 127 records · Page 7Linked to original sources
PubMed1975

Effects of dietary aflatoxin on certain egg yolk parameters.

Aflatoxicosis was induced in laying hens by incorporating graded amounts of aflatoxin into a commercial layer ration (0, 1.25, 2.5, 5.0, and 10.0 mug./g. of feed). After four weeks liver size and liver lipid were increased by aflatoxin while egg production and egg size were decreased (P less than 0.05). Total yolk weight and the yolk as percent of total egg weight were lowered (P less than 0.05). The dry weight and lipid content of the yolk were not affected. Yolk and plasma carotenoid concentrations were elevated (P less than 0.05). The data suggest that plasma and yolk lipids respond to the inhibition of lipid synthesis and transport from the liver by aflatoxin, but plasma and yolk carotenoids which are dietary in origin necessarily increase when egg production decreases during aflatoxicosis.

Aflatoxins↗
PubMed1975

Proof of mycotoxicoses being a field problem and a simple method for their control.

A field trial in which moldy caked feed was removed from the feed delivery truck, storage bins, conveyors, and feeding troughs by scrubbing and disinfecting resulted in improved body weight, pigmentation, and carcass grade of broiler chickens. This improvement which occurred despite the presence of only small and infrequent quantities of aflatoxin and ochratoxin suggest that mycotoxicoses, as yet undefined, can have a deleterious economic effect and further suggests that the mycotoxicoses can be partially controlled by simple preventive measures.

Animal Feed↗
PubMed1974

Activation of carbamoyl phosphate synthase by N-acetyl-L-aspartate.

Carbamoyl phosphate synthase from liver of both rat and frog, normally dependent on N-acetyl-l-glutamate (on the basis of K(m) and physiological concentrations) as an activator, was shown to be activated by high concentrations of N-acetyl-l-aspartate. However, the high concentrations of N-acetyl-l-aspartate required for activation produce non-competitive inhibition. Similarly, high concentrations of N-acetyl-l-glutamate, in very large excess of the amount required to activate the enzyme, inhibit. The limit for N-acetyl-l-glutamate as an impurity in N-acetyl-l-aspartate was found to be less than 1 in 5000 parts, far below the 1 in 250 parts needed to produce the activation observed with N-acetyl-l-aspartate.

Animals↗
PubMed1973

Improved yield of aflatoxin by incremental increases of temperature.

Increasing the initial temperature of the rice fermentation of Aspergillus parasiticus NRRL 2999 from 15 to 21 C after 24 h of incubation and then to 28 C after 48 h resulted in about a fourfold increase in total aflatoxin over the usual fermentation which is held constant at 28 C for 6 days. The percentage of aflatoxin B(1), the most toxic component, in the total aflatoxin was also increased.

Aflatoxins↗
PubMed1973

Neural disturbances in chickens caused by dietary T-2 toxin.

Graded concentrations of dietary T-2 toxin (0, 1, 2, 4, 8, and 16 mug/g) were fed to groups of 40 chickens. T-2 toxin was found to cause an abnormal positioning of the wings, hysteroid seizures, and impaired righting reflex in young chickens. The abnormal wing positioning occurred spontaneously or as the result of dropping from a height of 1 meter. The seizures could be elicited by rough handling or loud noises. The seizures and the abnormal wing posture would not occur again when the stimulus was repeated unless a rest period of 3 to 6 h was allowed. The loss of righting reflex could be demonstrated at any time. The total incidence of neural symptoms was dependent on the length of exposure to T-2 toxin and to its concentration. Neural toxicity occurred at dosages of 4, 8, and 16 mug per g of diet, which are the same doses that retard growth. This neural toxicity of T-2 toxin in chickens is similar to the neural disturbances associated with alimentary toxic aleukia, a nutritional toxicosis of humans produced by eating moldy grain. T-2 toxin has been implicated also in moldy corn toxicosis which has neural manifestations in horses and swine.

Animal Feed↗