Drug-dependent, alcohol-dependent, and mental patients: clinical study of oral surgery procedures.
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Biomedical subjects
Publications and source records attributed to C L Davis.
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The time course of hydrogenation of linoleic acid to trans-11-octadecenoic acid was observed in a growing culture of Treponema (Borrelia) strain B(2)5. A conjugated fatty acid, cis-9, trans-11-octadecadienoic acid, was identified as an intermediate in the process. The isomerase responsible for the conversion of linoleic acid to the conjugated fatty acid was found to be associated with a particulate fraction characterized by a high protein and lipid content in a 2:1 ratio. Optimum pH for isomerase activity was found to be 7.0 in 0.05 m potassium phosphate buffer. No cofactor requirements could be demonstrated for the isomerase. The sulfhydryl inhibiting agents, iodoacetamide, N-ethylmaleimide, and p-chloromercuribenzoate, inhibited isomerase activity. Isomerase activity was also inhibited by the metal chelators, o-phenanthroline, alpha, alpha'-bipyridyl, ethylenediaminetetraacetic acid, and 8-hydroxyquinoline. Linoleic (Delta9, 12), linolenic (Delta9, 12, 15), and gamma-linolenic (Delta6, 9, 12) acids served as effective substrates for the isomerase; however, the derivatives of linoleic and linolenic acid did not.
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Borrelia sp. B(2)5, when grown in a medium containing [1-(14)C] linoleic acid in an atmosphere of CO(2), was found to hydrogenate linoleic acid to trans-11-octadecenoic acid.
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Of six antibiotics investigated, streptovaricin C had the most marked chemotherapeutic effect on Mycobacterium kansasii infections in mice. By the intraperitoneal route this antibiotic caused elimination of the pathogens from all organs. Kanamycin eliminated the pathogens from the lungs of all animals and from the spleens and livers of most of them. Bluensomycin also removed the pathogens from the lungs of all animals, and spectinomycin and lincomycin, from the lungs of the majority of the animals. The three latter antibiotics lowered the bacterial counts in liver and spleen. Streptovaricin C also decreased the bacterial counts in brain, spleen, and liver of mice inoculated intracerebrally with M. kansasii. In one experiment it completely eliminated this pathogen from the spleen and almost completely from the liver. The effect of streptovaricin C on the cerebral infection was more marked than that of streptovaricin complex. Respiratory and cerebral infections of mice with M. avium, serotypes I and II, were limited by streptovaricin C, and marked decreases of the bacterial counts in brain, lungs, spleen, and liver were observed.
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