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Biomedical subjects

H C Neu

Publications and source records attributed to H C Neu.

At least 451 records · Page 25Linked to original sources
PubMed1972

In vitro studies of tobramycin, an aminoglycoside antibiotic.

Tobramycin is an aminoglycoside antibiotic which has excellent antibacterial activity against Pseudomonas, Staphylococcus aureus, and many members of the Enterobacteriaceae. Most strains of Serratia, Providence, Streptococcus, and Diplococcus pneumoniae were resistant to concentrations of tobramycin which could be achieved in man. Tobramycin was effective against certain Pseudomonas strains resistant to gentamicin. The growth medium used to determine the inhibitory level of tobramycin had a significant effect upon the minimal inhibitory concentration. Calcium and magnesium ions inhibited the bactericidal effect of tobramycin. Tobramycin and carbenicillin acted in a synergistic manner. Ethylenediaminetetraacetic acid did not act in a synergistic manner with tobramycin. Broth-dilution susceptibility tests and disc-diffusion tests in agar (10-mug discs) showed excellent correlation except with Proteus strains.

Aminoglycosides↗
PubMed1972

Relation of beta-lactamase activity and cellular location to resistance of Enterobacter to penicillins and cephalosporins.

The Enterobacter species E. aerogenes, E. cloacae, and E. hafnia were examined for resistance to penicillin and cephalosporin derivatives. All were resistant to benzyl penicillin, ampicillin, 6 [d(-)alpha-amino-p-hydroxyphenylacetamido] penicillanic acid, cephaloridine, cephalothin, and cephalexin. A significant number were sensitive to carbenicillin and 6 [d(-)alpha-carboxy-3-thienylacetamido] penicillanic acid. No differences among the three species were noted. The beta-lactamase activity was cell-bound, and was not released by osmotic shock, toluene treatment, or diphenylamine treatment. It was rarely released into the growth medium. The beta-lactamase activity was primarily directed against cephalosporin derivatives. Synthesis of beta-lactamase was chromosomally mediated. Resistance to ampicillin seemed to be partly related to entry of the molecule into the bacteria since exposure to ethylenediaminetetraacetate lowered the minimal inhibitory concentration.

Amidohydrolases↗
PubMed1971

Semisynthetic penicillin 6-(D(--)-alpha-carboxy-3-thienylacetamido) penicillanic acid active against Pseudomonas in vitro.

The activity of 6-[d(-)-alpha-carboxy-3-thienylacetamido] penicillanic acid, BRL2288, was determined against Pseudomonas aeruginosa and various gram-negative bacilli. The majority of Pseudomonas strains (89%) were inhibited by 100 mug of the antibiotic per ml. BRL2288 is twofold more active than carbenicillin against Pseudomonas at 100 mug/ml or less. Among Enterobacteriaceae tested, 87% Enterobacter and 87% of Proteus mirabilis strains were inhibited by 25 mug/ml or less. Indole-positive Proteus were inhibited by 10 mug/ml or less. Fifty-five per cent of ampicillin-resistant Escherichia coli were inhibited by 100 mug/ml. Klebsiella were uniformly resistant. BRL2288 is not hydrolyzed by most resistant Pseudomonas, but it is destroyed by the beta-lactamases of E. coli and P. mirabilis. The antibiotic shows synergy with gentamicin but not with penicillinase-resistant penicillins such as cloxacillin. Activity of BRL2288 against gram-positive organisms is two- to eightfold less than that of ampicillin or benzylpenicillin G.

Drug Synergism↗
PubMed1970

Relation of lipopolysaccharide and fatty acid ester release to the ethylenediaminetetraacetic acid alteration of permeability in enterobacteriaceae.

Escherichia coli subjected to cold osmotic shock released 30 to 40% of their fatty acid esters and 42% of their cellular hexosamine. In contrast, Enterobacter, although they released 40% of fatty acid esters, release only 25% of hexosamine. Proteus released less than 15% of either fatty acid esters or hexosamine. These differences are taken to explain the differences among the Enterobacteriaceae in releasing surface enzymes after osmotic shock. It is felt that the release of additional lipopolysaccharide after osmotic shock is necessary for the release of surface enzymes that are not freed by ethylenediaminetetraacetic acid-tris(hydroxymethyl)aminomethane exposure.

Buffers↗