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Biomedical subjects

M J Ryan

Publications and source records attributed to M J Ryan.

At least 145 records · Page 8Linked to original sources

Staphylococcus aureus mastitis in nursing mink affected with aleutian disease.

An outbreak of staphylococcal mastitis in nursing female ranch mink (Mustela vison) is described. Lesions were acute necrotizing mastitis, fatty infiltration of the liver and renal tubules, and adrenal cortical hyperplasia. The presence of Aleutian disease in the herd suggests a role of immunosuppression in the outbreak.

Aleutian Mink Disease↗

CCNU, vinblastine, and delalutin therapy in renal cell carcinoma.

Advanced renal cell carcinoma is relatively resistant to most adequately evaluated chemotherapeutic agents. The combination of CCNU and vinblastine, which has antitumor activity in a frog renal carcinoma model system, has demonstrated activity in initial studies in man. The current study investigated this combination of drugs together with a progestational agent, Delalutin. Seventeen patients with metastatic renal cell carcinoma were treated with CCNU, vinblastine and Delalutin. There were no objective responses. Four patients with stable disease had a mean survival of 18 months compared to 13 patients with progressive disease who had a mean survival of 5 months. The survival of the four patients with stable disease was in large part due to the slowly progressive natural history of their disease.

Adenocarcinoma↗

Influence of prostaglandin precursors and synthesis inhibitors in vascular bed perfused without a pump.

The present investigation was coducted to examine the role of endogenous prostaglandin (PG) on blood flow and arenergic responses in the paw vasculature perfused without a pump. The PG precursors, arachidonic acid and dihomo-gamma-linolenic acid, given i.a. caused only small increments in paw blood flow which were much less than that caused by PGE2 and PGE1. The i.a. administration of the PG synthesis inhibitors, indomethacin, meclofenamate and naproxen, caused a decrease in paw blood flow and increase in vascular resistance, whereas eicosa-5,8,11,14-tetraynoic acid had no significant effect. Vasoconstrictor responses evoked by norepinerphrine were unaffected after administration of indomethacin or eicosa-5,8,11,14-tetraynoic acid, whereas slight potentiation of the response to sympathetic nerve stimulation was obtained after indomethacin. These results suggest that in the cutaneous vascular bed of the paw, endogenous PG decreases the vascular resitance, but plays only a minor adrenergic modulating role, and then only on the response to adrenergic nerve stimulation.

5,8,11,14-Eicosatetraynoic Acid↗

Coumermycin A1: A preferential inhibitor of replicative DNA synthesis in Escherichia coli. I. In vivo characterization.

Coumermycin A1, an antibiotic related to novobiocin, inhibited nucleic acid synthesis in intact Escherichia coli with replication being slightly more sensitive to this drug than transcription. The ultraviolet-induced repair synthesis of DNA was only partially inhibited under conditions where replication was eliminated by coumermycin A1. Inhibition of protein synthesis was a secondary effect. Coumermycin A1-resistant E. coli were isolated and the mutation was mapped near dnaA. Chromatography of crude protein extracts of sensitive and resistant bacteria on drug affinity columns implicated a soluble protein of approximately 37,000 molecular weight as the target site for coumermycin A1. Depending on the medium used, this antibiotic had either a bacteriocidal or a bacteriostatic effect on E. coli. Results showed that the effect of coumermycin A1 cannot be explained by the degradation of DNA under bacteriocidal growth conditions.

Aminocoumarins↗

Coumerimycin A1: A preferential inhibitor of replicative DNA synthesis in Escherichia coli. II. In vivo characterization.

In vitro inhibitions by coumermycin A1 of DNA and RNA synthesis in toluenized cells were studied. In a sensitive strain, 50% inhibitions of replication and transcription were observed at 0.035 and 0.600 mug/ml, respectively. DNA synthesis in a toluenized-resistant mutant was 50% inhibited at 0.140 mug/ml of coumermycin A1, whereas RNA synthesis was unaffected at all concentrations tested. Studies with a mixture of toluenized-sensitive and -resistant bacteria ruled out the presence of a diffusable activator or inhibitor of coumermycin A1 action. Density label studies with toluenized pol A+ and pol A- strains indicated that replicative DNA synthesis was specifically inhibited, in agreement with the in vivo studies in the preceding paper of this issue (Ryan, M. J. (1976), Biochemistry 15). Highly purified Escherichia coli DNA polymerase III and RNA polymerase both were inhibited by this antibiotic. However, the high concentrations necessary for these inhibitions suggest that they are not biologically relevant. No interaction between DNA and coumermycin A1 was observed with the following analytical procedures: ultraviolet difference spectra, DNA absorbance-temperature transitions, equilibrium buoyant density centrifugation, and DNA cross-linking determinations.

Anti-Bacterial Agents↗

Effect of prostaglandins on vascular resistance and adrenergic vasoconstrictor responses in the canine uterus.

Prostaglandins appear to play an important role in a number of reproductive processes. The effect of prostaglandins on numerous vascular beds has been extensively studied, but the effects on uterine hemodynamics have not. The present study was designed to determine the effects of prostaglandins of the A and E series on uterine vascular resistance and responses to adrenergic nerve stimulation in the canine uterus. PGE1, PGE2 and PGA1 were found to be potent uterine vasodilators. In addition, these agents were able to modify adrenergic vasoconstrictor responses. These effects on uterine vascular resistance and adrenergic vasoconstrictor responses were separable. The results of these studies suggest that prostaglandins of the A and E series may play an important role in regulating uterine blood flow in the nonpregnant animal.

Animals↗