Environmental Stressors on Skin Aging. Mechanistic Insights

An accurate fine-resolution surface of the chemical composition of fine particulate matter (PM2.5) would offer valuable information for epidemiological studies and health impact assessments. We develop geoscience-derived estimates of PM2.5 composition from a chemical transport model (GEOS-Chem) and satellite observations of aerosol optical depth, and statistically fuse these estimates with ground-based observations using a geographically weighted regression over North America to produce a spatially complete representation of sulfate, nitrate, ammonium, black carbon, organic matter, mineral dust, and sea-salt over 2000-2016. Significant long-term agreement is found with cross-validation sites over North America (R2 = 0.57-0.96), with the strongest agreement for sulfate (R2 = 0.96), nitrate (R2 = 0.90), and ammonium (R2 = 0.86). We find that North American decreases in population-weighted fine particulate matter (PM2.5) concentrations since 2000 have been most heavily influenced by regional changes in sulfate and organic matter. Regionally, the relative importance of several chemical components are found to change with PM2.5 concentration, such as higher PM2.5 concentrations having a larger proportion of nitrate and a smaller proportion of sulfate. This data set offers information for research into the health effects of PM2.5 chemical components.

Inflammasomes are innate immune signaling pathways that sense pathogens and injury to direct the proteolytic maturation of inflammatory cytokines such as IL-1beta and IL-18. Among inflammasomes, the NLRP3/NALP3 inflammasome is the most studied. However, little is known on the molecular mechanisms that mediate its assembly and activation. Recent findings suggest that ROS are produced by NLRP3/NALP3 activators and are essential secondary messengers signaling NLRP3/NALP3 inflammasome activation.

There is evidence that L-tyrosine and L-dihydroxyphenylalanine (L-DOPA), besides serving as substrates and intermediates of melanogenesis, are also bioregulatory agents acting not only as inducers and positive regulators of melanogenesis but also as regulators of other cellular functions. These can be mediated through action on specific receptors or through non-receptor-mediated mechanisms. The substrate induced (L-tyrosine and/or L-DOPA) melanogenic pathway would autoregulate itself as well as regulate the melanocyte functions through the activity of its structural or regulatory proteins and through intermediates of melanogenesis and melanin itself. Dissection of regulatory and autoregulatory elements of this process may elucidate how substrate-induced autoregulatory pathways have evolved from prokaryotic or simple eukaryotic organisms to complex systems in vertebrates. This could substantiate an older theory proposing that receptors for amino acid-derived hormones arose from the receptors for those amino acids, and that nuclear receptors evolved from primitive intracellular receptors binding nutritional factors or metabolic intermediates. © 2011 John Wiley & Sons A/S.