Publications by authors named "McCall C"

The incorporation of uniformly labeled (14)C-amino acids into total protein of human polymorphonuclear leukocytes is inhibited when the cells are challenged with heat-killed Escherichia coli or latex particles. Parallel studies of amino acid incorporation and glucose oxidation indicate that the inhibition is dependent upon ingestion of the particles. It is suggested that the process of phagocytosis might inhibit the transport of amino acids into the cell either by competing for available energy or by internalizing specific transport sites.

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Promethazine hydrochloride at a concentration of 0.033 mg/ml has pronounced effects on leukocyte metabolism and function. The drug inhibits the phagocytosis-induced increases in O(2) consumption and hexose monophosphate shunt activity.

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An enzyme is present in extracts of rabbit alveolar macrophage which can catalyze the reaction of creatine phosphate with adenosine diphosphate to form adenosine triphosphate and creatine. The enzyme is moderately activated by reduced glutathione, has a pH optimum between pH 6.5 and 7.

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The effect of methylprednisolone sodium succinate treatment on Bacillus Calmette-Guérin (BCG) immunization was examined in alveolar macrophages of New Zealand White rabbits. Intravenous BCG injection caused a marked increase in cell number and in the hexosemonophosphate shunt activity. There was also a selective augmentation in the activity of acid phosphatase and beta-glucuronidase and an increase in lysosomal density.

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Epinephrine, norepinephrine, and dihydroxyphenylalanine at 8 mm concentrations prevented iodination of zymosan by intact neutrophils and decarboxylation of l-alanine by leukocyte sonic extracts. The same concentration of epinephrine also reduced bactericidal activity of the leukocyte against Staphylococcus aureus, Enterobacter cloacae, and Proteus rettgeri without decreasing phagocytosis of bacteria. Spectral studies indicated that epinephrine interferes with the myeloperoxidase-mediated reactions by competing for available H(2)O(2) via its enzymatic oxidation to adrenochrome.

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An enzyme is present in extracts of guinea pig polymorphonuclear leukocytes which can catalyze the hydrolysis of pyridine nucleotides. The enzyme is equally active toward nicotinamide adenine dinucleotide (NAD) or NAD phosphate, has an acid pH optimum, and is inhibited by either nicotinamide or isonicotinic acid hydrazide. This enzyme might be involved in the regulation of the pyridine nucleotide concentration within the leukocyte.

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The addition of either d- or l-amino acids fails to increase hexose monophosphate shunt activity of resting or phagocytizing neutrophils. This is presumptive evidence against a major role for amino acid oxidase in the bactericidal activity of the cell.

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A 52 yr old Caucasian female (F. E.) had hemolytic anemia, a leukemoid reaction, and fatal sepsis due to Escherichia coli.

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The addition of either ascorbic acid or dehydroascorbic acid to a suspension of polymorphonuclear leukocytes caused a dramatic increase in the resting hexose monophosphate shunt activity. A sequence of reactions involving dehydroascorbate, reduced glutathione, and reduced nicotinamide adenine dinucleotide phosphate is described to explain this stimulation. This sequence could provide an alternate method of producing H(2)O(2) and a bactericidal mechanism which is independent of myeloperoxidase.

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The increases in oxidation of glucose-1-(14)C and glucose-6-(14)C in BCG-sensitized alveolar macrophages are inhibited by administration of methylprednisolone sodium succinate. Both resting and phagocytizing cells are affected.

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An outbreak of nosocomial urinary-tract infection was caused by a strain of Proteus rettgeri that fermented lactose overnight and was resistant to all antimicrobial drugs tested. The nonmotile isolates shared an O (somatic) antigen that differed from those of wild-type P. rettgeri.

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Methylprednisolone sodium succinate was administered to New Zealand white rabbits sensitized with BCG in an attempt to define the effect of corticosteroid upon the interactions of lymphocytes and macrophages in the afferent and efferent limbs of delayed hypersensitivity. Daily intramuscular administration of the corticosteroid, beginning simultaneous with BCG sensitization of rabbits, prevented the inhibition of macrophage migration following tuberculin challenge 14 days after sensitization. If corticosteroid administration was delayed until 10 days following sensitization with BCG, the expected inhibition of macrophage migrations followed tuberculin challenge.

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