Bioaccumulation of perfluoroalkyl compounds in midge (Chironomus riparius) larvae exposed to sediment

Midge larvae (Chironomus riparius) were exposed to sediments from a deposition sampled at a site along the Rhône River (France) downstream of an industrial site releasing various perfluorinated chemicals. This sediment is characterized by high concentrations of perfluoroundecanoic acid (PFUnA) and perfluorotridecanoic acid (PFTrDA) and a low perfluorooctane sulfonate (PFOS) concentration. Concentrations of 23 perfluoroalkyl compounds, including C4eC14 carboxylate acids, C4eC10 sulfonates, and seven precursors, were analyzed in overlying and pore water, sediment, and larvae. Midge larvae accumulated carboxylate acids (C11eC14), PFOS, and two precursors (perfluorooctane sulfonamide: FOSA and 6:2 fluorotelomer sulfonic acid, 6:2 FTSA). These substances accumulated mainly during the fourth instar larvae exponential growth phase. Accumulation of 6:2 FTSA, PFUnA, and PFOS occured via trophic and tegumentary routes. Other compounds mainly accumulated from food. Kinetics followed a partition model, from which uptake and elimination constants were derived

Geometry unites synchrony, chimeras, and waves in nonlinear oscillator networks

One of the simplest mathematical models in the study of nonlinear systems is the Kuramoto model, which describes synchronization in systems from swarms of insects to superconductors. We have recently found a connection between the original, real-valued nonlinear Kuramoto model and a corresponding complex-valued system that permits describing the system in terms of a linear operator and iterative update rule. We now use this description to investigate three major synchronization phenomena in Kuramoto networks (phase synchronization, chimera states, and traveling waves), not only in terms of steady state solutions but also in terms of transient dynamics and individual simulations. These results provide new mathematical insight into how sophisticated behaviors arise from connection patterns in nonlinear networked systems

Geometry unites synchrony, chimeras, and waves in nonlinear oscillator networks

One of the simplest mathematical models in the study of nonlinear systems is the Kuramoto model, which describes synchronization in systems from swarms of insects to superconductors. We have recently found a connection between the original, real-valued nonlinear Kuramoto model and a corresponding complex-valued system that permits describing the system in terms of a linear operator and iterative update rule. We now use this description to investigate three major synchronization phenomena in Kuramoto networks (phase synchronization, chimera states, and traveling waves), not only in terms of steady state solutions but also in terms of transient dynamics and individual simulations. These results provide new mathematical insight into how sophisticated behaviors arise from connection patterns in nonlinear networked systems

Reduction in oxidatively generated DNA damage following smoking cessation

<p>Abstract</p> <p>Background</p> <p>Cigarette smoking is a known cause of cancer, and cancer may be in part due to effects of oxidative stress. However, whether smoking cessation reverses oxidatively induced DNA damage unclear. The current study sought to examine the extent to which three DNA lesions showed significant reductions after participants quit smoking.</p> <p>Methods</p> <p>Participants (n = 19) in this study were recruited from an ongoing 16-week smoking cessation clinical trial and provided blood samples from which leukocyte DNA was extracted and assessed for 3 DNA lesions (thymine glycol modification [d(T^gpA)]; formamide breakdown of pyrimidine bases [d(T^gpA)]; 8-oxo-7,8-dihydroguanine [d(G^h)]) via liquid chromatography tandem mass spectrometry (LC-MS/MS). Change in lesions over time was assessed using generalized estimating equations, controlling for gender, age, and treatment condition.</p> <p>Results</p> <p>Overall time effects for the d(T^gpA) (χ²(3) = 8.068, p < 0.045), d(P^fpA) (χ²(3) = 8.477, p < 0.037), and d(G^h) (χ²(3) = 37.599, p < 0.001) lesions were seen, indicating levels of each decreased significantly after CO-confirmed smoking cessation. The d(T^gpA) and d(P^fpA) lesions show relatively greater rebound at Week 16 compared to the d(G^h) lesion (88% of baseline for d(T^gpA), 64% of baseline for d(P^fpA), vs 46% of baseline for d(G^h)).</p> <p>Conclusions</p> <p>Overall, results from this analysis suggest that cigarette smoking contributes to oxidatively induced DNA damage, and that smoking cessation appears to reduce levels of specific damage markers between 30-50 percent in the short term. Future research may shed light on the broader array of oxidative damage influenced by smoking and over longer durations of abstinence, to provide further insights into mechanisms underlying carcinogenesis.</p