Auranofin is a gold compound that is widely used for the treatment of rheumatoid arthritis. It is a monomeric linear complex with triethylphosphine and thiolate moieties bounded to an Au(I) center. Gold compounds are well known for their neurological and nephrotoxic implications. However, haematological toxicity is one of the most serious toxic and less studied effects. The lack of information on these aspects of auranofin prompted us to study the structural effects induced on cell membranes, particularly that of human erythrocytes. Auranofin was incubated with intact erythrocytes and molecular models of the erythrocyte membrane. The latter consisted of multibilayers of dimyristoylphosphatidylcholine (DMPC) and dimyristoylphosphatidylethanolamine (DMPE), phospholipids classes located in the outer and inner monolayers of the human erythrocyte membrane, respectively. This report presents evidence in order that auranofin interacts with red cell membranes as follows: a) in scanning electron microscopy studies on human erythrocytes it was observed that auranofin induced shape changes; b) X-ray diffraction studies showed that auranofin induced increasing structural perturbation to DMPC and to a lower extent to DMPE bilayers. Additional experiments were performed in human neuroblastoma cells SH-SY5Y. A statistically significant decrease of cell viability was observed.
In 2015, Legionnaires’ disease was diagnosed in a street cleaning worker. We found Legionella pneumophila serogroup 1 in the water and internal foam from the tanks of 2 trucks used by the worker during the incubation period. The internal foam was removed, and a Legionella prevention program was implemented.
Cluster EK2 Akoni, Ashton, and Truong are lytic
Podoviridae
actinobacteriophages that were isolated from soil in Florida using
Microbacterium foliorum
NRRL B-24224 as the host. The genomes are 54,307 bp, 54,560 bp, and 54,309 bp, respectively, and are 60% GC rich. Each genome contains a novel 13,464-bp gene that encompasses 25% of the genome.
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