@article{VogtMottaghyRathetal.2014,
  author    = {Vogt, C. and Mottaghy, Darius and Rath, V. and Marquart, G. and Dijkshoorn, L. and Wolf, A. and Clauser, C.},
  title     = {Vertical variation in heat flow on the Kola Peninsula: palaeoclimate or fluid flow?},
  series = {Geophysical Journal International},
  volume    = {199},
  journal   = {Geophysical Journal International},
  number    = {2},
  publisher = {Oxford University Press},
  address   = {Oxford},
  issn      = {1365-246X},
  doi       = {10.1093/gji/ggu282},
  pages     = {829 -- 843},
  year      = {2014},
  abstract  = {Following earlier studies, we present forward and inverse simulations of heat and fluid transport of the upper crust using a local 3-D model of the Kola area. We provide best estimates for palaeotemperatures and permeabilities, their errors and their dependencies. Our results allow discriminating between the two mentioned processes to a certain extent, partly resolving the non-uniqueness of the problem. We find clear indications for a significant contribution of advective heat transport, which, in turn, imply only slightly lower ground surface temperatures during the last glacial maximum relative to the present value. These findings are consistent with the general background knowledge of (i) the fracture zones and the corresponding fluid movements in the bedrock and (ii) the glacial history of the Kola area.},
  language  = {en}
}
@article{ScheerMclaughlinRodeetal.2014,
  author    = {Scheer, Nico and Mclaughlin, Lesley A. and Rode, Anja and MacLeod, Alastair Kenneth and Henderson, Colin J. and Wolf, Roland C.},
  title     = {Deletion of thirty murine cytochrome P450 genes results in viable mice with compromised drug metabolism},
  series = {Drug Metabolism and Disposition},
  volume    = {42},
  journal   = {Drug Metabolism and Disposition},
  number    = {6},
  publisher = {ASPET},
  address   = {Bethesda, Md.},
  issn      = {1521-009X},
  doi       = {10.1124/dmd.114.057885},
  pages     = {1022 -- 1030},
  year      = {2014},
  abstract  = {In humans, 75\% of all drugs are metabolized by the cytochrome P450-dependent monooxygenase system. Enzymes encoded by the CYP2C, CYP2D, and CYP3A gene clusters account for ∼80\% of this activity. There are profound species differences in the multiplicity of cytochrome P450 enzymes, and the use of mouse models to predict pathways of drug metabolism is further complicated by overlapping substrate specificity between enzymes from different gene families. To establish the role of the hepatic and extrahepatic P450 system in drug and foreign chemical disposition, drug efficacy, and toxicity, we created a unique mouse model in which 30 cytochrome P450 genes from the Cyp2c, Cyp2d, and Cyp3a gene clusters have been deleted. Remarkably, despite a wide range of putative important endogenous functions, Cyp2c/2d/3a KO mice were viable and fertile, demonstrating that these genes have evolved primarily as detoxification enzymes. Although there was no overt phenotype, detailed examination showed Cyp2c/2d/3a KO mice had a smaller body size (15\%) and larger livers (20\%). Changes in hepatic morphology and a decreased blood glucose (30\%) were also noted. A five-drug cocktail of cytochrome P450 isozyme probe substrates were used to evaluate changes in drug pharmacokinetics; marked changes were observed in either the pharmacokinetics or metabolites formed from Cyp2c, Cyp2d, and Cyp3a substrates, whereas the metabolism of the Cyp1a substrate caffeine was unchanged. Thus, Cyp2c/2d/3a KO mice provide a powerful model to study the in vivo role of the P450 system in drug metabolism and efficacy, as well as in chemical toxicity.},
  language  = {en}
}