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Biomedical subjects

T D Tyler

Publications and source records attributed to T D Tyler.

10 recordsLinked to original sources
PubMed1987

Efficacy of a morantel sustained-release bolus for control of gastrointestinal parasites in winter-grazed steers in Mississippi.

From Nov 22, 1983 through May 15, 1984, 36 crossbred steers were allotted into 3 treatment groups (12/group) and were grazed on separate 3.4-hectare pastures. On Nov 22, 1983, the steers were administered a single morantel sustained-release bolus (MSRB), orally (group 1), or a single dose of thiabendazole (TBZ; 66 mg/kg of body weight, orally; group 2), or were left untreated (group 3; controls). Animal weights, nematode egg counts in fecal specimens, and plasma pepsinogen concentrations were monitored monthly. At the termination of the study, 4 steers from each treatment group were slaughtered and necropsied and worm counts were determined. A set of parasite-free tracer calves (3/treatment group) were grazed with each treatment group for 1 month, beginning on Nov 22, 1983; a second set of tracer calves (3/group) were grazed with each treatment group for 1 month, beginning Apr 3, 1984. At the end of their respective grazing periods, tracer calves were held for 3 weeks and then were slaughtered and necropsied and their worm counts were determined. Mean nematode egg counts in fecal specimens of group 1 (MSRB treated) were significantly lower (P less than 0.05) than that of the TBZ-treated or nontreated steers. Differences in worm counts were not found between treatment groups. Differences in worm counts of tracer calves were not found among the 3 groups for November 1983 nor for April 1984. Steers treated with the MSRB had a higher mean weight gain (P less than 0.06) than did the control or TBZ-treated steers.

Animals↗
PubMed1985

Field efficacy of a morantel sustained release bolus for control of gastrointestinal nematodes in yearling steers.

The efficacy of a morantel sustained release bolus (MSRB) for control of gastrointestinal nematodes in yearling steers was evaluated over a 6-month grazing period commencing on 26 March 1982. Three groups of 15 steers were allotted to the following treatments: Group 1 -- one MSRB at start of trial; Group 2 -- one therapeutic dose of thiabendazole at start of trial; Group 3 -- untreated control. The treatment groups were grazed separately. Parasite egg counts (EPG), herbage larval counts, pepsinogen levels and weight gains were monitored. Every other month, sets of 2 parasite-free tracer calves were placed in the pasture grazed by each treatment group and allowed to graze for 3 weeks before being subsequently necropsied for worm counts. At the end of the trial, 6 animals from each group were also necropsied for worm counts. The MSRB treatment resulted in significantly lower egg counts, fewer infective larvae on pasture, lower pepsinogen levels and lower worm burdens in tracer calves than was the case for the untreated group, but generally the levels were not significantly different from those associated with the thiabendazole treatment. The mean weight gain for the MSRB treated steers showed a significant advantage (70.9 lb) over the untreated animals, but was not significantly different from those which received thiabendazole. Total worm counts at the end of the trial were not different from any treatment group.

Abomasum↗
PubMed1980

Norepinephrine uptake inhibitors as biochemically and behaviorally selective antagonists of the locomotor stimulation induced by indirectly acting sympathomimetic aminetic amines in mice.

Pretreatment with the selective noradrenergic uptake inhibitors nisoxetine and desipramine antagonized the locomotor stimulant effect of d-amphetamine without reducing the drug's stereotypy-inducing action. A similar antagonism was observed with imipramine but not with fluoxetine, a selective serotonin uptake inhibitor and structural analog of nisoxetine. The order of potency of antagonism was desipramine greater than nisoxetine greater than imipramine. Nisoxetine also selectively reduced the locomotor activity induced by maximally effective doses of cocaine, d-N-ethyl-amphetamine, and methylphenidate, but not that induced by morphine. Biochemically, nisoxetine blocked the selective reduction in cerebral cortical endogenous and 3H-norepinephrine produced by amphetamine with itself significantly altering either measure. These data support the involvement of norepinephrine in the locomotor stimulant action of indirectly acting sympathomimetic amines.

Animals↗
PubMed1980

Calcium enhancement of alcohol and drug-induced sleeping time in mice and rats.

Calcium injected intracerebroventricularly (IVT) at various times before a hypnotic dose of ethanol significantly enhanced the duration of sleeping time (loss of righting reflex, LRR) in mice and rats. This cation also enhanced the duration of LRR induced by t-butanol and chloral hydrate, but not that induced by sodium pentobarbital. Other cations injected IVT (manganese, cadmium, and zinc) also enhanced ethanol-induced LRR. The synergistic effects of the ionophores X537A and A23187 on calcium-enhanced LRR, and the antagonism of ethanol-induced LRR by EDTA and EGTA suggest the involvement of a membrane-associated calcium pool in the hypnotic effect of ethanol. These studies show the generality of cation enhancement of alcohol-induced sleeping time in mice and rats, and confirm earlier reports which suggested that calcium is involved with the central nervous system depressant effects of alcohols.

Animals↗
PubMed1978

Ethanol: modifications of acute intoxication by divalent cations.

Calcium, other divalent cations, and calcium antagonists were tested for their ability to alter ethanol-induced sleeping time, hypothermia, and behavioral intoxication in mice and rats. Calcium given intraventricularly significantly enhanced sleeping time and behavioral intoxication in a dose-related manner. The ionophores X537A and A23187 accentuated the effect of a low dose of calcium, whereas the calcium chelators EDTA and EGTA decreased sleeping time. Calcium also enhanced tertiary butanol- and chloral hydrate-induced sleeping time. The effects of cations on ethanol-induced hypothermia were less significant. The results suggest the existence of a central calcium pool that is involved in ethanol intoxication in rodents.

Alcoholic Intoxication↗