@article{MontiglioDammhahnMessieretal.2018,
  author    = {Montiglio, Pierre-Olivier and Dammhahn, Melanie and Messier, Gabrielle Dubuc and Reale, Denis},
  title     = {The pace-of-life syndrome revisited},
  series = {Behavioral ecology and sociobiology},
  volume    = {72},
  journal   = {Behavioral ecology and sociobiology},
  number    = {7},
  publisher = {Springer},
  address   = {New York},
  issn      = {0340-5443},
  doi       = {10.1007/s00265-018-2526-2},
  pages     = {9},
  year      = {2018},
  abstract  = {The pace-of-life syndrome (i.e., POLS) hypothesis posits that behavioral and physiological traits mediate the trade-off between current and future reproduction. This hypothesis predicts that life history, behavioral, and physiological traits will covary under clearly defined conditions. Empirical tests are equivocal and suggest that the conditions necessary for the POLS to emerge are not always met. We nuance and expand the POLS hypothesis to consider alternative relationships among behavior, physiology, and life history. These relationships will vary with the nature of predation risk, the challenges posed by resource acquisition, and the energy management strategies of organisms. We also discuss how the plastic response of behavior, physiology, and life history to changes in ecological conditions and variation in resource acquisition among individuals determine our ability to detect a fast-slow pace of life in the first place or associations among these traits. Future empirical studies will provide most insights on the coevolution among behavior, physiology, and life history by investigating these traits both at the genetic and phenotypic levels in varying types of predation regimes and levels of resource abundance.},
  language  = {en}
}
@article{MuellerFinkeEbertetal.2018,
  author    = {M{\"u}ller, S. M. and Finke, Hannah and Ebert, Franziska and Kopp, Johannes Florian and Schumacher, Fabian and Kleuser, Burkhard and Francesconi, Kevin A. and Raber, G. and Schwerdtle, Tanja},
  title     = {Arsenic-containing hydrocarbons},
  series = {Archives of toxicology : official journal of EUROTOX},
  volume    = {92},
  journal   = {Archives of toxicology : official journal of EUROTOX},
  number    = {5},
  publisher = {Springer},
  address   = {Heidelberg},
  issn      = {0340-5761},
  doi       = {10.1007/s00204-018-2194-z},
  pages     = {1751 -- 1765},
  year      = {2018},
  abstract  = {Arsenic-containing hydrocarbons (AsHCs), a subgroup of arsenolipids found in fish and algae, elicit substantial toxic effects in various human cell lines and have a considerable impact on cellular energy levels. The underlying mode of action, however, is still unknown. The present study analyzes the effects of two AsHCs (AsHC 332 and AsHC 360) on the expression of 44 genes covering DNA repair, stress response, cell death, autophagy, and epigenetics via RT-qPCR in human liver (HepG2) cells. Both AsHCs affected the gene expression, but to different extents. After treatment with AsHC 360, flap structure-specific endonuclease 1 (FEN1) as well as xeroderma pigmentosum group A complementing protein (XPA) and (cytosine-5)-methyltransferase 3A (DNMT3A) showed time- and concentration-dependent alterations in gene expression, thereby indicating an impact on genomic stability. In the subsequent analysis of epigenetic markers, within 72 h, neither AsHC 332 nor AsHC 360 showed an impact on the global DNA methylation level, whereas incubation with AsHC 360 increased the global DNA hydroxymethylation level. Analysis of cell extracts and cell media by HPLC-mass spectrometry revealed that both AsHCs were considerably biotransformed. The identified metabolites include not only the respective thioxo-analogs of the two AsHCs, but also several arsenic-containing fatty acids and fatty alcohols, contributing to our knowledge of biotransformation mechanisms of arsenolipids.},
  language  = {en}
}