Nickel concentration in the environment of Caenorhabditis elegans may affect its longevity. Furthermore, it would be expected that the genetic variants of C. elegans known to promote advanced longevity (clk-1, daf-2, and daf-2/clk-1) would be affected in an inverse proportion if the ability to detoxify nickel in the substrate were disrupted. Ten nematodes per variant were subjected to varying concentrations of nickel treated K Agar gel plates and monitored daily for 12 days for developmental disruptions and LC50. Four repetitions of this experiment were run simultaneously. Data from these tests were analyzed using TOXSTAT. The null hypothesis is that there is no significant difference between the sensitivity to nickel of the mutated C. elegans and the wild type. From the statistical analysis, the null hypothesis was rejected. Related research conducted by Barsyte showed an increase in heavy metal tolerance, specifically cadmium and copper, in 24-hour test trials with the wild type C. elegans. This research is in contrast to the results achieved using nickel in 12-day test trials, which could be due to the difference in length of the experiments and/or the heavy metals tested. Other nematode aging studies have shown that there is no tradeoff in fertility or reproductivity. There is an increase in life span that is related to starvation of the nematodes for the daf-2 mutation. Additional research in these areas may show a relationship between the mutations in these nematodes, nickel exposure, and the human disease genes that are known to be of similar genetic constitution.

Deer mice (Peromyscus maniculatus) are the principal reservoir hosts of Sin Nombre hantavirus (SNV). Once infected, deer mice remain persistently infected for the remainder of their lives. It is unknown what immune evasion strategies SNV uses to elude the host immune response, but evidence suggests that macrophages may be one target of viral infection. If so, SNV may interfere with normal macrophage functions that impair the immune response and contribute to evasion. Previous attempts to isolate and culture deer mouse macrophages have not been successful. We report here the first successful isolation and activation of deer mouse peritoneal macrophages. Isolated cells exhibited macrophage morphology and expressed several macrophage cytokine and chemokine genes when stimulated with lipopolysaccharide, including tumor necrosis factor, macrophage inflammatory protein-1α and interleukin-12. The ability to culture deer mouse macrophages will permit examination of SNV infectivity and consequences in macrophage functions.

In this study, we sought to determine if resistance to the antibacterial agent, triclosan, correlates with ciprofloxacin resistance in Staphylococcus aureus. To these ends, we isolated 8 mutant strains of S. aureus that were cross-resistant to both triclosan and ciprofloxacin when the drugs are present in bacterial media simultaneously. Surprisingly, the 8 mutant strains were as sensitive to triclosan as the wild type strain when grown in triclosan containing bacterial media lacking ciprofloxacin. This data suggests that triclosan resistance in these mutants is dependant on the presence of ciprofloxacin. These strains also displayed resistance to various concentrations of ethidium bromide. In other bacterial systems, resistance to ciprofloxacin and ethidium bromide is mediated by multi-drug efflux pumps. In order to evaluate the mechanism behind the triclosan/ciprofloxacin/ethidium bromide cross-resistance in our 8 mutant strains, we performed sequencing analyses on the promoter region of the S. aureus multi-drug efflux pump, NorA. NorA is the most well characterized drug efflux pump in S. aureus and is responsible for the efflux of both ciprofloxacin and ethidium bromide. The results from the sequencing analyses demonstrated that 3 of the 8 mutant strains displayed alterations in the NorA promoter region. Taken together, our results demonstrated that triclosan resistance can be correlated with ciprofloxacin resistance in S. aureus and that alterations in the NorA promoter may be responsible for the cross-resistant phenotypes of 3 of these mutant strains.