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R O'Kelly

Publications and source records attributed to R O'Kelly.

5 recordsLinked to original sources
PubMed1984

Efficacy of nosiheptide as a growth promotant for growing-finishing swine--a cooperative study.

A cooperative study involving 296 pigs was conducted at two experiment stations and at a commercial research farm to evaluate the efficacy of nosiheptide as a growth promotant for growing-finishing swine. At each station, five or six replicate pens of four or five pigs/pen were fed a fortified, corn-soybean meal basal diet with 0, 5.5, 11 or 22 ppm nosiheptide. Initial and final weights averaged 11 and 92 kg, respectively. Daily gain increased quadratically (623, 664, 669, 678 g/d; P less than .03) and feed/gain decreased quadratically (3.35, 3.24, 3.24, 3.28; P less than .02) with increasing level of nosiheptide. Breakpoint analysis indicated that gain plateaued at 6.8 ppm and feed/gain at 5.5 ppm of nosiheptide. Averaged across all levels of nosiheptide, gain and feed/gain during the growing phase (11 to 52 kg body weight) were improved by 13.1 and 7.6%, respectively, by feeding the antibiotic. For the entire growing-finishing period, gain was improved by 5.3% and feed/gain by 2.9% in pigs fed nosiheptide. Although there were large differences in gain and feed/gain, the responses to dietary treatments were similar among the three stations. The results indicate that nosiheptide is an effective growth-promoting agent for growing-finishing swine.

Analysis of Variance↗
PubMed1983

Routine heparin therapy inhibits adrenal aldosterone production.

While heparin-induced aldosterone deficiency has been sporadically reported, it is not known whether heparin always inhibits aldosterone production to a variable extent or if this is an idiosyncratic effect, nor is the mechanism underlying the phenomenon known. We have examined plasma aldosterone, PRA, and aldosterone to renin activity ratios in 20 patients before, during and after treatment with heparin. Aldosterone cell during heparin treatment from 73.5 +/- 20.5 to 36.8 +/- 11.2 pg/ml (P less than 0.05) and rose after its withdrawal to 94.8 +/- 37.1 p/ml (P less than 0.05). PRA rose with heparin treatment from 2.8 +/- 1.0 to 6.1 +/- 1.6 ng/ml . h (P less than 0.05) and fell to 2.4 +/- 0.5 ng/ml . h (P less than 0.05) when the drug was withdrawn. Aldosterone to renin activity ratios, which are indices of aldosterone responsiveness to angiotensin, fell from 59.5 +/- 1.7 to 25 +/- 14.9 (P less than 0.01) with heparin treatment and rose after withdrawal of the drug to 58.5 +/- 24.9 (P less than 0.01). There was a significant small fall in serum sodium levels with the introduction of heparin, but none of the patients developed clinical mineralocorticoid deficiency. Although heparin consistently perturbs aldosterone production in the glomerulosa cell, this effect is not clinically significant when normal adjustments can be made in the generation of angiotensin. However, where limitations in the renin-angiotensin-aldosterone axis exist, e.g. in diabetes mellitus, mineralocorticoid insufficiency may be precipitated by heparin.

Adrenal Cortex↗