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This Week in PNAS: Jan 30, 2018

In the early, online edition of the Proceedings of the National Academy of Sciences, New York University researchers describe DNA damage associated with e-cigarette exposure in mice. The team used a combination of immuno-slot-blot, DNA repair, and other assays to look for mutagenic DNA changes in tissues from mice exposed to the combustion-free nicotine delivery system for a few hours per day, five days per week over three months. Based on these analyses and follow up studies on cultured human lung or bladder epithelial cells, the authors argue that minor metabolic products of nicotine, called nitrosamines, can damage DNA in mouse lung, bladder, and heart tissue and produce potentially tumorigenic changes in human cells in vitro.

Researchers at Brown University and the University of California, San Francisco, explore ties between lifespan and mitochondrial metabolic regulators called sirtuins in Drosophila melanogaster. By comparing sequences for five sirtuin ortholog genes in Drosophila, the team narrowed in on one authentic mitochondrial sirtuin protein in the fruit fly, called Sirt4. Following a series of protein staining, gene knockout, altered feeding, and metabolic analyses in the flies, the authors suggest that Sirt4 regulates long chain and very long chain fatty acids in a manner that affects everything from starvation sensitivity and fertility to overall lifespan in Drosophila.

An international team led by investigators at the University of Colorado at Denver present evidence of inflammasome inhibition by a compound called OLT1177. The researchers began by tracing cytokine activity in mouse and human immune cells with activated NLRP3 pathways — inflammasomes that prompt the release of IL-1-beta and IL-18 cytokines involved in acute and chronic inflammation. In the presence of OLT1177, a candidate compound proposed from prior research, they saw a notable dip in IL-1-beta and IL-18 cytokine secretion following immune stimulation. From these and other experiments in mice treated with OLT1177, the authors note that OLT1177 appears to selectively inhibit the NLRP3 inflammasome "with unique properties to reverse the metabolic costs of inflammation and to treat IL-1beta- and IL-18-mediated diseases."