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Biomedical subjects

E D Lassen

Publications and source records attributed to E D Lassen.

22 records · Page 2Linked to original sources

Effects of dietary supplementation with ethoxyquin, magnesium oxide, methionine hydroxy analog, and B vitamins on tansy ragwort (Senecio jacobaea) toxicosis in beef cattle.

Dried tansy ragwort containing pyrrolizidine alkaloids was fed as 2.5% of a complete (control) diet to Hereford steers, with and without (basal) a mixture of additives. The additives provided a dietary supplement equivalent to 0.1% ethoxyquin, 1% methionine hydroxy analog, 2% MgO, 2.7 mg of vitamin B6/kg of diet, 50 micrograms of vitamin B12/kg of diet, 0.45 g of folic acid/kg of diet, and 0.2 g of cobalt/kg of diet. The additives did not alter tansy ragwort toxicity substantially, as assessed by liver histologic changes, sulfobromophthalein clearance rate, and serum gamma-glutamyl transpeptidase activity. After 281 days, 1 of 4 steers fed the basal diet was alive, whereas 3 of 4 steers in the basal plus additives group were alive, suggesting some protective activity. The chronic lethal dose of tansy ragwort in steers was 3.6% of initial body weight.

Animals↗

Increased susceptibility of lead-exposed swine to Salmonella choleraesuis var kunzendorf.

The effect of oral subclinical lead exposure on the susceptibility of swine to Salmonella choleraesuis var kunzendorf was studied in two experiments. In experiment 1, 18 pigs were exposed to lead acetate and 18 pigs were exposed to sodium acetate for 1, 2, or 3 weeks and then challenge exposed intraperitoneally. In experiment 2, 8 pigs were exposed to lead chloride for 2 weeks, 8 pigs were exposed to lead chloride for 1 week, and 8 pigs were exposed to sodium chloride for 2 weeks. These pigs were then challenge exposed orally. Only one pig (sodium acetate-exposed) died during experiment 1, but clinical signs were more severe in sodium acetate-exposed than in lead acetate-exposed animals. In experiment 2, 93.6% of the lead-exposed pigs died, whereas control pigs had 50.0% mortality. In experiment 2, clinical signs were more severe in lead-exposed pigs, and bacteria were more widespread in the tissues of these animals. Significant reductions of beta- or gamma-globulin concentrations or of agglutinating antibody titers were not observed in lead-exposed pigs in either of the trials. Possible mechanisms of the increased susceptibility in lead-exposed pigs of experiment 2 are discussed.

Animals↗

Activated coagulation times of normal cows.

The Activated Coagulation Time (ACT) was determined on 10 normal cows. Duplicate samples were taken from each cow. The mean ACT was 145 seconds with a range of 120-180 seconds. Standard deviations were 18 and 13 for the first and second sampling, respectively. Repeatability of the ACT was acceptable.

Journal Article↗

Experimental lead toxicosis in swine.

Thirty pigs, weighing 17 to 24 kg, were exposed to lead or sodium acetate orally or intraperitoneally (IP) 6 days each week for 13 weeks. These pigs were extremely tolerant of lead. Only mild clinical signs of lead toxicosis were observed in orally lead-exposed pigs despite blood lead concentrations of up to 290 micrograms/dl. Four IP lead-exposed pigs died, but eight other IP lead-exposed pigs survived the exposure period despite blood lead concentrations up to 14,300 micrograms/dl. Lead exposure caused marked decreases in blood delta-aminolevulinic acid dehydratase activities of all pigs and moderate decreases of blood hemoglobin concentrations, hematocrit percentages, mean corpuscular volumes, mean corpuscular hemoglobin concentrations, and mean corpuscular hemoglobins in IP lead-exposed, but not in orally lead-exposed pigs. Basophilic stippling was observed in erythrocytes of lead-exposed pigs, but not in those of control pigs.

Administration, Oral↗