Increased pulmonary susceptibility to streptococcal infection following inhalation of manganese oxide.
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Biomedical subjects
Publications and source records attributed to B Adkins.
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Inhalation of manganese oxide (Mn dose, 879.0 micrograms/m3) for 2 h reduced the total number of alveolar macrophages obtained by endotracheal lavage in pulmonary cell populations, slightly reduced cellular viability, and reduced both phagocytic capability and total protein in sonicated pulmonary cells. Increases in intracellular adenosine triphosphate and acid phosphatase specific activity were also exhibited by the pulmonary cells, but sonicated cells obtained from the exposed mice showed no change in lactic acid dehydrogenase specific activity. A slight increase in extracellular protein in the fluid phase of the lavage suspension was observed after manganese oxide exposure.
An acute inhalation exposure of laboratory mice to respirable Mn3O4 aerosols is described. The generation system consisted of a Wright dust generator which produced 1.40 micrometer aerosols. A non-linear loss of deposited manganese from mouse lungs over the inital 24-hour post-exposure period was observed. Systemic distribution of the manganese was observed in various tissues following exposure.
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The effects of intravenous infusions of prostaglandin E2 (PGE2) and arachidonic acid (AA) on histamine-stimulated gastric secretion have been studied in conscious dogs with either a simple gastric fistula or a denervated Heidenhain pouch. Both compounds produced a dose-related inhibition of acid secretion, though AA was 86-5 to 203-2 times less potent than PGE2. The maximal effect of AA was not achieved until 20 to 40 minutes after the infusion had ceased, suggesting that AA has to undergo some kinetic or metabolic process before it can act. Eicosatetraynoic acid (ETYN) 1-0 microgram.kg-1min-1, an inhibitor of PG biosynthesis, almost totally abolished the anti-secretory effect of AA up to 200 microgram.kg-1min-1. At 400 microgram AA.kg-1min-1, the antisecretory effect was reduced by about one half. The effect of PGE2 was not altered by ETYN. Furthermore, ETYN did not increase the response to histamine stimulation in control studies, which suggests that, in this model at least, prostaglandins are not involved in regulating gastric secretion.
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Two cases are presented of malignant hyperthermia in black patients. One patient developed signs of malignant hyperthermia during general anesthesia that was successfully treated with dantrolene sodium and cooling. A second patient was retrospectively diagnosed as having an atypical variant of malignant hyperthermia secondary to heat stroke and general anesthesia; this patient subsequently died. These cases illustrate that malignant hyperthermia can occur in blacks despite the very low incidence of this syndrome in nonwhite patients.