Comparison of proteomic and metabolomic profiles of mutants of the mitochondrial respiratory chain in Caenorhabditis elegans.

Single-gene mutations that disrupt mitochondrial respiratory chain function in Caenorhabditis elegans change patterns of protein expression and metabolites. Our goal was to develop useful molecular fingerprints employing adaptable techniques to recognize mitochondrial defects in the electron transport chain. We analyzed mutations affecting complex I, complex II, or ubiquinone synthesis and discovered overarching patterns in the response of C. elegans to mitochondrial dysfunction across all of the mutations studied. These patterns are in KEGG pathways conserved from C. elegans to mammals, verifying that the nematode can serve as a model for mammalian disease. In addition, specific differences exist between mutants that may be useful in diagnosing specific mitochondrial diseases in patients.

Molecular epidemiology of an SHV-5 extended-spectrum beta-lactamase in enterobacteriaceae isolated from infants in a neonatal intensive care unit.

Klebsiella oxytoca that produced extended-spectrum beta-lactamase (ESBL) and were resistant to ceftazidime were isolated from infants in a neonatal intensive care unit (NICU). During a 30-week period, 3 infants developed infections and an additional 60 infants were colonized with these bacteria. The molecular typing data suggested transmission of a single strain of ceftazidime-resistant K. oxytoca among 48 of the 63 infants. The ESBL of 46 of the 48 similar isolates, 14 of the remaining 15 isolates, and 6 other Enterobacteriaceae appeared to be associated with a conjugative plasmid of approximately 85 kb. The ESBL gene was cloned, and DNA sequencing confirmed that the ESBL was an SHV-5. Hybridization data suggested that the SHV-5 gene was transmitted to other Enterobacteriaceae in vivo. The spread of the ESBL was reduced through adherence to infection control practices.