Coal-tar pavement sealant use and polycyclic aromatic hydrocarbon contamination in urban stream sediments

Polycyclic aromatic hydrocarbons (PAHs) can occur at levels of environmental concern in stream sediments from urban and industrial watersheds. Recent studies indicate that coal-tar sealant use on parking lots may have been the major source of PAHs to urban streams in the eastern US over the past 40 years. This study evaluates the spatial distribution of PAHs in urban stream and pond sediments in Galloway Creek in Springfield, Missouri by focusing specifically on parking lots with and without coal-tar sealants as contamination source areas. Multiple-linear regression analysis is used to evaluate the spatial connectivity of contaminated sediment to potential source areas and compare the relative influence of watershed source factors and reach sediment variability on sediment PAH levels. Sediments from coal-tar sealed parking lots and the streams that drain them are enriched in PAHs at concentrations considered toxic to aquatic life, with concentrations that are, on average, 35 and 480 times greater than those of unsealed asphalt and concrete lots, respectively. Moreover, sediment PAH concentrations are strongly correlated with the percentage of sealed parking lot area within the upstream drainage area of the sampling site, in contrast to total parking lot area or sediment composition. Metal and nutrient contaminants are poorly correlated with sealed lot area indicating a wider range of urban source inputs. Finally, parking lots with coal-tar coatings contribute \u3e80% of the total PAH concentration in urban stream and pond sediments in Galloway Creek. If coal-tar sealant use ended, sediment PAH concentrations would probably decrease over time to levels not harmful to sediment-dwelling organisms

Glia fuel neurons with locally synthesized ketone bodies to sustain memory under starvation.

During starvation, mammalian brains can adapt their metabolism, switching from glucose to alternative peripheral fuel sources. In the Drosophila starved brain, memory formation is subject to adaptative plasticity, but whether this adaptive plasticity relies on metabolic adaptation remains unclear. Here we show that during starvation, neurons of the fly olfactory memory centre import and use ketone bodies (KBs) as an energy substrate to sustain aversive memory formation. We identify local providers within the brain, the cortex glia, that use their own lipid store to synthesize KBs before exporting them to neurons via monocarboxylate transporters. Finally, we show that the master energy sensor AMP-activated protein kinase regulates both lipid mobilization and KB export in cortex glia. Our data provide a general schema of the metabolic interactions within the brain to support memory when glucose is scarce

Sotrovimab therapy elicits antiviral activities against Omicron BQ.1.1 and XBB.1.5 in sera of immunocompromised patients [letter]

International audienc