Biomedical subjects

E F Remmers

Publications and source records attributed to E F Remmers.

76 records · Page 5Linked to original sources

PubMed1980

Isolation of drug-resistant Aeromonas hydrophila from aquatic environments.

Antibiotic-resistant strains of Aeromonas hydrophila have been isolated from the natural environment in the Chesapeake Bay and areas surrounding Dacca and the Matlab region of Bangladesh. The Bangladesh strains carried resistance to chloramphenicol, streptomycin, and tetracycline, and 57% of them had a multiple streptomycin-tetracycline resistance phenotype correlated with the presence of a large plasmid. The Chesapeake Bay strains were resistant to polymyxin B ane tetracycline, but showed neither multiple resistance nor R-factor carriage. Twenty-five percent of the environmental strains were toxigenic in a Y-1 adrenal cell assay. Toxigenicity showed no positive correlation with drug resistance or with plasmid carriage. Environmental areas of heavy human impact appear to be associated with a higher incidence of antibiotic-resistant strains of aeromonads.

Aeromonas↗

PubMed1980

R-factor carriage in a group F vibrio isolated from Bangladesh.

Two group F vibrio organisms have been identified among a collection of vibrio strains isolated from the aquatic environment in Bangladesh. Neither group F strain produced a cholera-like enterotoxin. One of the isolates, BV12, contained an R plasmid conferring resistance to streptomycin and chloramphenicol.

Aeromonas↗

PubMedDate not supplied

Analysis of CARD15/NOD2 haplotypes fails to identify common variants associated with rheumatoid arthritis susceptibility.

OBJECTIVES: The CARD15/NOD2 gene product plays an important role in host response to bacterial lipopolysaccharides and bacterial muramyl dipeptide via activation of NF-kappaB in monocytes. Mutations in CARD15 are associated with Crohn's disease (CD), a chronic inflammatory bowel disease. In this study we sought to determine whether CD-associated mutations or any common variants of this gene might contribute to susceptibility to another chronic inflammatory disease, rheumatoid arthritis (RA). METHODS: We genotyped 376 Caucasian RA cases and 376 ethnically matched healthy controls for three CD-associated CARD15 mutations. We also genotyped these 752 individuals for 12 common CARD15 single nucleotide polymorphisms (SNPs), determined the linkage disequilibrium structure of the gene, and compared the frequencies of the common CARD15 haplotypes in the RA cases and controls. RESULTS: None of the CD-associated mutations or the CARD15 SNPs was associated with susceptibility to RA. We also found no significant difference in the frequencies of any of the common haplotypes of the CARD15 gene in RA patients and controls. Our haplotype analysis was consistent with earlier observations that all three CD-associated variants independently arose on the same ancestral haplotype. CONCLUSIONS: These data suggest that CARD15 variants are not associated with RA susceptibility.

Adolescent↗

PubMedDate not supplied

Mechanisms of bone and cartilage destruction in rheumatoid arthritis: lessons from the streptococcal cell wall arthritis model in LEW/N rats.

Rheumatoid arthritis is a proliferative and erosive disease which has been described as tumor-like. Streptococcal cell wall-induced arthritis in the LEW/N rat is also tumor-like and closely simulates the features of joint destruction that develop in rheumatoid arthritis. This article discusses the mechanisms of bone and cartilage destruction in streptococcal cell wall arthritis with particular emphasis on the tumor-like behavior of synovial connective tissue cells and the role of cytokines, such as platelet-derived growth factor, transforming growth factor beta and interleukin 1, in regulating this abnormal behavior.

Animals↗