Robert C. Eisenberg

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Independently controlled, inducible, catabolic genes in Pseudomonas aeruginosa are subject to strong catabolite repression control by intermediates of the tricarboxylic acid cycle. Mutants which exhibited a pleiotropic loss of catabolite repression control of multiple pathways were isolated. The mutations mapped in the 11-min region of the P. aeruginosa(More)
To examine further the role of immune-complex deposition in infective endocarditis, we studied 29 patients with infective endocarditis for presence of complement-containing circulating immune complexes. Ninety-seven per cent (28 of 29) had serum levels of immune complexes greater than 12 mug per milliliter. Mean levels in these patients were significantly(More)
Induction of Entner-Doudoroff pathway enzymes in Pseudomonas fluorescens was investigated to study the role of gluconate as a possible inducer. Glucose oxidase-deficient mutants were isolated and characterized. One of these mutants, gox-7, was deficient in particulate glucose oxidase; another mutant, gox-17, was deficient in particulate glucose and(More)
Pseudomonas fluorescens ATCC 13525 and a particulate glucose oxidase (d-glucose:oxygen oxidoreductase, EC 1.1.3.4) mutant of this organism, gox-7, were examined to determine if glucose oxidation via particulate glucose oxidase is a required first step for glucose uptake. Initial [(14)C]glucose-uptake rates in parent and gox-7 cells were qualitatively(More)
On the basis of information available in the literature, gluconate dissimilation in Escherichia coli is thought to occur via the hexose monophosphate pathway. Evidence is presented in this study that gluconate is catabolized in this organism via an inducible Entner-Doudoroff pathway. This evidence is based on chromatographic examination of end products(More)
A thrombotic thrombocytopenic purpura (TTP)-like syndrome was the chief presenting feature in two patients with infective endocarditis. Clinical and laboratory aberrations of the syndrome were rapidly reversed by specific antimicrobial therapy. Hypocomplementemia and high levels of circulating immune complexes were detected initially in both patients.(More)
Deoxycholate disruption of Micrococcus lysodeikticus protoplast membranes resulted in solubilization of both l-malate and reduced nicotinamide adenine dinucleotide (NADH) dehydrogenase enzymes (substrate: 2,6-dichlorophenolindophenol oxidoreductases). Insoluble residues contained cytochromes of the b, c, and a type. Solubilized dehydrogenases were(More)
Membrane-associated l-malate and reduced nicotinamide adenine dinucleotide (NADH) oxidase complexes of Micrococcus lysodeikticus were inactivated with deoxycholate. Reactivation of NADH oxidase by addition of Mg(2+) occurred in these detergent-membrane mixtures, but reactivation of l-malate oxidase did not occur in the presence of deoxycholate. Removal of(More)
Solubilization of a reduced nicotinamide adenine dinucleotide (NADH)-2,6 dichlorophenol indophenol (DCIP) oxidoreductase associated with the membrane NADH oxidase system of Bacillus megaterium KM was effected by treatment with 0.2% sodium deoxycholate, 8 m urea, or buffer (pH 9.0) in the presence of ethyl-enediaminetetraacetate. These treatments inactivated(More)