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“While the neuropsychological effects of high manganese

(Mn) exposure in occupational settings are well known, the effects of lower levels of exposure are less understood. In this study, we investigated the neuropsychological effects of lower level occupational Mn exposure in 46 male welders (mean age = 37.4, S.D. = 11.7 years). Each welders’ cumulative Mn exposure indices (Mn-CEI) for the past 12 months and total work history Mn exposure were constructed based on air Mn measurements and work histories. selleck products The association between these exposure indices and performance on cognitive, motor control, and psychological tests was examined. In addition, among a subset of welders (n = 24) who completed the tests both before and after a work shift, we examined the association between cross-shift Mn exposure assessed Tucidinostat from personal monitoring and acute changes in test scores.

Mn exposures in this study (median = 12.9 mu g/m(3)) were much lower, as compared to those observed in other similar studies. Increasing total Mn-CEI was significantly associated with slower reaction time on the continuous performance test (CPT;

p < 0.01), as well as worse mood for several scales on the Profile of Mood States (POMS; confused, tired, and a composite of tired and energetic, all p <= 0.03). Increasing Mn-CEI over the previous 12 months was significantly associated with worse mood on the sad, tense, and confused POMS scales (all p <= 0.03) and the association with worse CPT performance approached significance (p = 0.10). Higher Mn exposure over the course of a workday was associated with worse performance on the CPT test across the day (p = 0.06) as well as declines in fine motor control over the

work-shift (p = 0.04), adjusting for age and time between the 2 tests. Our study suggests that even at relatively low Mn exposure levels neuropsychological effects may manifest particularly with respect to attention, mood, and fine motor control. (C) 2011 Elsevier Inc. All rights reserved.”
“Recently it has been shown that the check details proinflammatory NF-kappa B pathway promotes efficient influenza virus propagation. Based on these findings, it was suggested that NF-kappa B blockade may be a promising approach for antiviral intervention. The classical virus-induced activation of the NF-kappa B pathway requires proteasomal degradation of the inhibitor of NF-kappa B, I kappa B. Therefore, we hypothesized that inhibition of proteasomal I kappa B degradation should impair influenza A virus (IAV) replication. We chose the specific proteasome inhibitor PS-341, which is a clinically approved anticancer drug also known as Bortezomib or Velcade. As expected, PS-341 treatment of infected A549 cells in a concentration range that was not toxic resulted in a significant reduction of progeny virus titers.