Biomedical subjects
Publications and source records attributed to P Thurman.
Mycobacterium microti readily incorporates radioactive propionate into phenolic glycolipids and phthiocerol dimycocerosates. This process is inhibited by 2- and 3-fluoropropionic acids at concentrations which do not affect overall growth. Incorporation is also inhibited by N-(phosphonomethyl) glycine, an inhibitor of the synthesis of aromatic units, but only at high concentrations which also inhibit bacterial growth.
While taking orally administered anticoagulants, three patients had hemorrhages into their retropharyngeal and submandibular spaces, suffering eventual acute airway obstruction. One of the patients died. Despite the life-threatening nature of this complication of anticoagulant therapy, the diagnosis was obscure and initially veiled in complaints of sore throat or hoarseness, suggesting infection. Thorough investigation of such complaints is necessary in patients receiving anticoagulation therapy. If a hematoma is discovered, the patient should be admitted to the hospital for close observation and prompt reversal of anticoagulation with plasma. Intubation or tracheostomy also may be required.
Sodium ion was shown to stimulate strongly the transport of l-glutamic acid into cells of Bacillus licheniformis 6346 His(-). Lithium ion had a slight capacity to replace Na(+) in this capacity, but K(+) was without effect. Three of five amino acids tested. l-glutamic acid, l-aspartic acid, and l-alanine, were concentrated against a gradient in the cells. Intracellular pools of these amino acids were extractable with 5% trichloroacetic acid. Pools of l-histidine and l-lysine could not be detected. No evidence of active transport of lysine into cells could be detected, and histidine was taken up in the absence of chloramphenicol but not in its presence. The uptake of glutamic acid by membrane vesicle preparations was strongly stimulated by reduced nicotinamide adenine dinucleotide (NADH) and to a lesser extent by succinate. The presence of phenazine methosulfate increased uptake in the presence of succinate. Either l- or d-lactate and adenosine triphosphate were without effect. None of these compounds stimulated the uptake of glutamic acid by mesosomes, although some mesosome preparations contained separable membrane which was very active. NADH strongly stimulated the uptake of aspartic acid and alanine by membrane vesicles but had only a slight effect on the uptake of histidine and lysine. No evidence of active transport of any of the amino acids into mesosomes could be detected either in the presence or absence of NADH. NADH stimulation of the uptake of glutamic acid by membrane vesicles was destroyed by exposure to light of 360 nm; this inactivation was reversible by vitamin K(2(5)) or K(2(10)). Sodium ion stimulated transport of glutamic acid by membrane vesicles.