Attribution de la dénomination "unité biologique" au constituant 10S de l'Antigène Somatique de Shigella flexneri

info:eu-repo/semantics/publishe

Etude physico-chimique de la structure de l'antigène somatique de Shigella flexneri

Doctorat en Sciencesinfo:eu-repo/semantics/nonPublishe

Nomenclature of genes encoding aminoglycoside-modifying enzymes36680

NA</p

Chimiotypes de mutants R de Shigella Flexneri et récepteurs de phages: I. Étude chimique des lipopolyosides

The F6R rough mutants isolated from Shigella flexneri F6S, serotype 5b, and the FH rough mutants, derived from other serotypes of S. flexneri, were chemotyped according to the chemical analysis of their lipopolysaccharides. Further, the following stages of lipopolysaccharide core biosynthesis in S. flexneri have been established: --(KDO)3--heptose--heptose--glucose--galactose; the last three stages are: either --glucose--glucosamine--glucose, or --glucosamine--glucose--glucose. The results of the chemical study of the R lipopolysaccharides are compatible with the assumption of the existence of a similar core in all considered S. flexneri serotypes.info:eu-repo/semantics/publishe

Nomenclature of Genes Encoding Aminoglycoside-Modifying Enzymes

NA</p

Chimiotypes de mutants R de Shigella Flexneri et récepteurs de phages: II. Localisation des récepteurs de phages

Receptor sites for phages FP3, V, P1kcvir, H+, C21, T4, T3, T7 and 6SR have been investigated, by comparing the lytic activity of these phages on R mutants of strain F6 (F6R) and of various serotypes (FH) of Shigella flexneri with their inhibition by the lipopolysaccharides isolated from these mutants. The results suggest the following localizations for the receptor sites: phage FP3: lipid A-KDO; phage V: heptose or glucose; phage C21: heptose-glucose; phages H+, P1kcvir, T4 and T3: glucose; phage T7: glucose-galactose; phage 6SR: complete core structure.info:eu-repo/semantics/publishe

The role of lipopolysaccharide anionic binding sites in aminoglycoside uptake in Stenotrophomonas (Xanthomonas) maltophilia36660

Aminoglycoside resistance was investigated in six clinical isolates of Stenotrophomonas (Xanthomonas) maltophilia by studying the uptake kinetics and by using a radiochemical method to detect aminoglycoside modifying enzymes. Furthermore, the lipopolysaccharides (LPS) were extracted and characterized by SDS-PAGE and chemical analysis. Dansyl-polymyxin displacement experiments confirmed the availability of anionic binding sites. Growing cells of the isolates bound dansyl-polymyxin but were not lysed</p

Rapid purification of Bordetella pertussis toxin by alternating affinity and hydrophobic chromatography

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Study of the structure of Shigella Flexneri o antigen: I. Chemical degradation

info:eu-repo/semantics/publishe

Aminoglycoside resistance in Gram-negative blood isolates from various hospitals in Belgium and the Grand Duchy of Luxembourg. Aminoglycoside Resistance Study Group36690

A total of 1102 consecutive clinical blood isolates, including 897 Enterobacteriaceae and 205 non-fermenting bacilli, were obtained from 13 university and university-affiliated hospitals, which were divided into a Northern and a Southern group. Resistance to gentamicin, tobramycin, netilmicin, amikacin and isepamicin was determined using a microdilution technique according to NCCLS procedures. The overall mean resistance level was 5.9% for gentamicin, 7.7% for tobramycin, 7.5% for netilmicin, 2.8% for amikacin and 1.2% for isepamicin. Resistance to amikacin and isepamicin was significantly higher in the Northern hospitals than in the Southern hospitals. In total, 157 isolates were found not to be susceptible to aminoglycosides. By PCR, 179 aminoglycoside resistance mechanisms, i.e. 150 genes encoding modifying enzymes and 29 permeability mechanisms, were detected in 148 isolates. A resistance mechanism could not be detected in nine isolates. Moreover, in a further 14 isolates the resistance profile was not fully explained by the detected genes. The aac(6&#039;)-I genes were found to be the most predominant resistance mechanism in both the Northern and Southern isolates, followed by aac(3) genes and permeability resistance. A total of 29 non-susceptible isolates harboured a combination of genes, 72.4% of which were a combination with the aac(6&#039;)-lb gene. The majority of these combinations were broad-spectrum combinations which represented 9.0% of the resistance mechanisms in non-susceptible Enterobacteriaceae and 19.3% in the non-fermenting bacilli</p