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Biomedical subjects

S L Smith

Publications and source records attributed to S L Smith.

At least 199 records · Page 11Linked to original sources
PubMed1985

Sensitization and histamine release by cells of the sand dollar, Mellita quinquiesperforata.

The coelomic fluid of the sand dollar, Mellita quinquiesperforata, contains cells (coelomocytes) that release red granules when the animal is stressed. Preliminary evidence suggests that the red pigment is protective, but its release from the coelomocytes is similar to that of allergy-inducing mediators from mammalian basophils and mast cells. The present study revealed further links with allergy, e.g., the coelomocytes can be sensitized to foreign proteins and release histamine on challenge. These and other findings suggest that the coelomocyte stress response may be an evolutionary precursor to the mammalian allergic response.

Animals↗
PubMed1984

Effect of the stable endoperoxide analog U-46619 on prostacyclin production and cyclic AMP levels in bovine endothelial cells.

The effects of the stable endoperoxide analog U46619 (U) on the regulation of prostacyclin (PGI2) formation and cyclic adenosine monophosphate (cAMP) were investigated in cultured bovine aortic endothelial (BAE) cells. Incubation of U (0.3, 3.0 and 30 microM) with BAE cells for 5 min results in a dose-dependent increase in PGI2. Cyclic AMP levels were not changed at 0.3 and 3.0 microM but were stimulated at 30 microM U. When cells were exposed to U for a second and third 5 min period, PGI2 formation at 0.3 and 3.0 microM U remained stimulated while at 30 microM, PGI2 was not increased. Five min incubation of BAE cells with the cyclooxygenase inhibitor indomethacin blocked the stimulation of PGI2 at all concentrations of U and also prevented the increase of cAMP levels at 30 microM. In cells prelabeled with 3H-arachidonate, U stimulated release of labeled products at 0.3 and 3.0 microM but not at 30 microM U. In cells treated with bradykinin in the presence of U, PGI2 production was stimulated at 0.3 and 3.0 microM but not 30 microM U. When cells were exposed to U and stimulated with PGI2 (with and without phosphodiesterase inhibition), U caused significant increases in cAMP. We conclude that incubation of BAE cells with U results in an initial dose-dependent increase in PGI2 formation. Cyclic AMP levels are increased at high concentrations of U. This increase in cAMP is mediated by the initial stimulated PGI2 and results in decreased PGI2 on further exposure to U. Data suggest that U stimulates phospholipase activity and, at high concentrations, inhibits phosphodiesterase.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1984

Effects of thyroid status on presynaptic alpha 2-adrenoceptor function and beta-adrenoceptor binding in the rat brain.

The effect of thyroid status on noradrenergic synaptic function in the mature rat brain was examined by measuring presynaptic alpha 2- and post-synaptic beta-adrenoceptors. Repeated triiodothyronine (T3) administration to rats (100 micrograms/kg X 14 days: hyperthyroid) caused an 18% increase in striatal beta-adrenoceptors as shown by [3H]-dihydroalprenolol binding with no change in membranes from cerebral cortex or hypothalamus. In contrast, hypothyroidism (propylthiouracil, PTU X 14 days) produced significant 12% and 30% reductions in striatal and hypothalamic beta-adrenoceptors respectively with no change in the cerebral cortex. Presynaptic alpha 2-adrenoceptor function was measured in the two dysthyroid states using the clonidine-induced hypoactivity model. Experimental hyperthyroidism increased the degree of clonidine-induced hypoactivity, and suggests increased presynaptic alpha 2-adrenoceptor function compared with control rats, whereas hypothyroidism suppressed presynaptic alpha 2-adrenoceptor function. These results show firstly that changes in thyroid status in the mature rat may produce homeostatic alterations at central noradrenergic synapses as reflected by changes in pre- and post-synaptic adrenoceptor function. Secondly, there appear to be T3-induced changes in beta-adrenoceptors in the striatum where changes in dopaminergic neuronal activity have previously been demonstrated.

Animals↗
PubMed1984

Medical education provided by a clinical pharmacist: impact on the use and cost of corticosteroid therapy in chronic obstructive pulmonary disease.

The impact of medical education provided by a clinical pharmacist on the use and cost of corticosteroid therapy in acute exacerbations of chronic obstructive pulmonary disease was evaluated. Three separate two-month audits of corticosteroid use were conducted on the pulmonary medicine service (PMS) of a teaching hospital. For the first audit period, no education was given and no clinical pharmacist was on the PMS. During the second audit period, no education was given, but a clinical pharmacist was on-service. For the third audit period, education (brief discussion and a handout) was given to new house staff members by the clinical pharmacist on the PMS. A significant reduction in the mean number of intravenous steroid doses, steroid cost per day, and patient steroid charges per day occurred in the third vs. the first period. Steroid cost per day and patient steroid charges per day were lower in the third period than the second, but the difference was not statistically significant.

Adrenal Cortex Hormones↗
PubMed1983

Hypophysectomy alters both 5-hydroxytryptamine- and alpha 2-adrenoceptor-mediated behavioural changes in the rat.

Hypophysectomy, but not sham-hypophysectomy, reduced tranylcypromine/L-tryptophan hyperactivity when compared with unoperated controls although brain 5-hydroxytryptamine concentrations were not different. Hypophysectomy also reduced quipazine locomotor activity but did not alter spontaneous locomotion. Hypophysectomy potentiated clonidine hypoactivity but did not itself produce sedation. Furthermore, noradrenaline concentrations were not altered in either hypothalamus or nucleus accumbens. This suggests that pituitary function is necessary for the normal manifestation of behaviours mediated by postsynaptic 5-hydroxytryptamine receptors and presynaptic alpha 2-adrenoceptors.

Animals↗
PubMed1983

Biocidal braided sutures.

Once sutures become contaminated it is difficult for local tissue defenses or antibiotics to eliminate the bacteria and prevent infection. Impregnation of sutures with antibiotics before implantation is one way to prevent bacterial seeding of the suture surface. In this study, braided silk and Dacron sutures were impregnated with the antibiotic complex, neomycin palmitate. Using our standard wound model in the mouse, the efficacy of these biocidal sutures was determined in the presence of Staphylococcus aureus, Escherichia coli, Proteus mirabilis, and Pseudomonas aeruginosa. Implantation of these biocidal sutures into tissue contaminated with 10(7) organisms resulted in substantially decreased numbers of bacteria as compared with that of tissue receiving control sutures. In most cases, the tissue bacterial counts in the presence of biocidal sutures were also considerably lower than that for similarly contaminated tissue without a suture. Consequently, the presence of the neomycin palmitate eliminated the infection-potentiating effect of the suture. The therapeutic benefit of the biocidal sutures was related to the dose of antibiotic complex and was not adversely affected by delaying suture implantation.

Animals↗
PubMed1983

The effects of acute and repeated administration of various antidepressant drugs on clonidine-induced hypoactivity in mice and rats.

Small doses of clonidine produce hypoactivity in mice and rats, probably by stimulating pre-synaptic alpha 2-adrenoceptors in the brain. When mice were injected with desmethylimipramine (DMI, 5 mg/kg) before clonidine it attenuated the hypoactivity, while pretreatment with amitriptyline (5 mg/kg) or mianserin (5 mg/kg) potentiated this behaviour. In rats, desmethylimipramine (20 mg/kg) inhibited and mianserin (5 mg/kg) potentiated the clonidine-induced hypoactivity. Amitriptyline (20 mg/kg), however, had no effect on this behaviour in rats. Mice were also given repeated injections of these 3 antidepressant drugs (5 mg/kg twice daily for 14 days) and were tested with clonidine 12 and 60 hr after the final treatment. At 12 hr desmethylimipramine and amitriptyline both attenuated the hypoactivity responses while the reduction by mianserin was marginal (potency DMI greater than amitriptyline greater than mianserin). At 60 hr, however, amitriptyline and mianserin both decreased the clonidine-induced responses while the attenuation by desmethylimipramine was slight (potency amitriptyline congruent to mianserin greater than DMI). In rats, repeated injections of desmethylimipramine (20 mg/kg), administered twice daily for 14 days, attenuated the clonidine-induced hypoactivity 12 hr after the final treatment and this effect persisted for at least 72 hr. Furthermore, the degree of inhibition of the behavioural responses did not correlate with plasma concentrations of desmethylimipramine and persisted after disappearance of the drug from plasma. In conclusion, these data suggest that after repeated injection, desmethylimipramine, amitriptyline and mianserin all produce an adaptive decrease in the function of central alpha 2-adrenoceptors but the time course of this change differs with the individual antidepressant drug administered.

Amitriptyline↗
PubMed1983

Ecdysone 20-monooxygenase activity during larval-pupal development of Manduca sexta.

Profiles of ecdysone 20-monooxygenase (E-20-M) activity in the fat body and midgut of Manduca sexta were determined during larval-pupal development. The E-20-M activities for both tissues were found to exhibit a single major fluctuation during this 10-day period of development: fat body, a 10-fold fluctuation with peak activity on day 4; midgut, a 60-fold fluctuation with peak activity on day 5. Substrate kinetics revealed that the apparent Km values of fat body and midgut monooxygenases for ecdysone were fairly constant during the instar, 2.42 X 10(-7) M and 4.67 X 10(-7) M, respectively. By contrast, the monooxygenase Vmax values in each tissue fluctuated in a manner both quantitatively and temporally coincident with the fluctuations in enzyme activity. These findings suggest that changes in E-20-M activity are a function of changes in the titer of the enzyme. The possible developmental significance of the fluctuations in E-20-M activity are discussed.

Animals↗
PubMed1983

Alpha-pyridine nucleotides as substrates for a plasmid-specified dihydrofolate reductase.

The alpha epimers of pyridine nucleotides are almost totally inactive as reductants in dehydrogenase reactions. In contrast, the R plasmid R67-specified dihydrofolate reductase (5,6,7,8-tetrahydrofolate: NADP+ oxidoreductase, EC 1.5.1.3) isolated from trimethoprim-resistant Escherichia coli utilized alpha-NADPH and alpha-NADH in addition to the "normal" beta-epimers. The enzymes from bacterial and mammalian sources used only beta-NADPH and beta-NADH. THe Km value for alpha-NADPH (16 microM) was 4-fold greater than that for beta-NADPH (4 microM), while the maximal velocity of the alpha-NADPH-catalyzed reaction was 70% of that seen with the beta-NADPH. beta-NADP+ and alpha-NADP+ were competitive inhibitors of the R67 enzyme. Pyridine nucleotide analogues such as deamino- and acetyl-NADPH were used readily by bacterial, plasmid, and mammalian enzymes, whereas thio-NADPH was used only by the plasmid enzyme. These data suggest that the enzyme from R plasmid R67 possesses a pyridine nucleotide binding site different from that of other dihydrofolate reductases and dehydrogenases.

Animals↗
PubMed1982

Hypophysectomy does not prevent the enhanced monoamine-mediated behavioural responses following repeated electroconvulsive shocks.

Groups of hypophysectomised rats were given either an electroconvulsive shock (ECS; 125V, 1 sec) once daily for 10 days or a sham-shock. Twenty-four hours after the final treatment both groups were tested for their responses to the dopamine agonist, apomorphine, the 5-hydroxytryptamine agonist, quipazine, and the alpha 2-adrenoceptor agonist, clonidine. Repeated electroconvulsive shock enhanced the locomotor activity produced by either quipazine (25 mg/kg i.p.) or apomorphine (0.2 mg/kg s.c.) compared to sham-shocked controls. This treatment also attenuated the hypoactivity produced by clonidine (0.5 mg/kg i.p.). These changes are identical to those produced in normal rats by repeated electroconvulsive shock. Hypophysectomy, therefore, did not abolish the increased 5-hydroxytryptaminergic and dopaminergic behavioural responses neither did it prevent the decreased functional activity of central alpha 2-adrenoceptors, which may be presynaptic. These data suggest that although electroconvulsive shock has been reported to stimulate the secretion of various pituitary hormones, this process is not essential for the development of the enhanced monoamine-mediated behavioural responses studied.

Animals↗