@article{HommersRichterYangetal.2018,
  author    = {Hommers, L. G. and Richter, J. and Yang, Y. and Raab, A. and Baumann, C. and Lang, K. and Schiele, M. A. and Weber, H. and Wittmann, A. and Wolf, C. and Alpers, G. W. and Arolt, V. and Domschke, K. and Fehm, L. and Fydrich, T. and Gerlach, A. and Gloster, A. T. and Hamm, A. O. and Helbig-Lang, S. and Kircher, T. and Lang, T. and Pan{\´e}-Farr{\´e}, C. A. and Pauli, P. and Pfleiderer, B. and Reif, A. and Romanos, M. and Straube, B. and Str{\"o}hle, A. and Wittchen, H.-U. and Frantz, S. and Ertl, G. and Lohse, M. J. and Lueken, U. and Deckert, J.},
  title     = {A functional genetic variation of SLC6A2 repressor hsa-miR-579-3p upregulates sympathetic noradrenergic processes of fear and anxiety},
  series = {Translational Psychiatry},
  volume    = {8},
  journal   = {Translational Psychiatry},
  doi       = {10.1038/s41398-018-0278-4},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-322497},
  year      = {2018},
  abstract  = {Increased sympathetic noradrenergic signaling is crucially involved in fear and anxiety as defensive states. MicroRNAs regulate dynamic gene expression during synaptic plasticity and genetic variation of microRNAs modulating noradrenaline transporter gene (SLC6A2) expression may thus lead to altered central and peripheral processing of fear and anxiety. In silico prediction of microRNA regulation of SLC6A2 was confirmed by luciferase reporter assays and identified hsa-miR-579-3p as a regulating microRNA. The minor (T)-allele of rs2910931 (MAFcases = 0.431, MAFcontrols = 0.368) upstream of MIR579 was associated with panic disorder in patients (pallelic = 0.004, ncases = 506, ncontrols = 506) and with higher trait anxiety in healthy individuals (pASI = 0.029, pACQ = 0.047, n = 3112). Compared to the major (A)-allele, increased promoter activity was observed in luciferase reporter assays in vitro suggesting more effective MIR579 expression and SLC6A2 repression in vivo (p = 0.041). Healthy individuals carrying at least one (T)-allele showed a brain activation pattern suggesting increased defensive responding and sympathetic noradrenergic activation in midbrain and limbic areas during the extinction of conditioned fear. Panic disorder patients carrying two (T)-alleles showed elevated heart rates in an anxiety-provoking behavioral avoidance test (F(2, 270) = 5.47, p = 0.005). Fine-tuning of noradrenaline homeostasis by a MIR579 genetic variation modulated central and peripheral sympathetic noradrenergic activation during fear processing and anxiety. This study opens new perspectives on the role of microRNAs in the etiopathogenesis of anxiety disorders, particularly their cardiovascular symptoms and comorbidities.},
  language  = {en}
}
@article{BaumannBurschkaSchenk1986,
  author    = {Baumann, Franz Erich and Burschka, Christian and Schenk, Wolfdieter A.},
  title     = {Ligandensubstitution an cis-Mo(CO)\(_2\)(PPh\(_3\)h(MeCN)(\(\eta^2\)-S0\(_2\)), Kristall- und Molek{\"u}lstruktur von cis-Mo(CO)\(_2\)(PMe\(_3\))\(_3\)(\(\eta^2\)-S0\(_2\)) [1]},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47143},
  year      = {1986},
  abstract  = {No abstract available},
  subject      = {Chemie},
  language  = {de}
}
@article{HornBaumannPereiraetal.2012,
  author    = {Horn, Michael and Baumann, Reto and Pereira, Jorge A. and Sidiropoulos, P{\´a}ris N. M. and Somandin, Christian and Welzl, Hans and Stendel, Claudia and L{\"u}hmann, Tessa and Wessig, Carsten and Toyka, Klaus V. and Relvas, Jo{\~a}o B. and Senderek, Jan and Suter, Ueli},
  title     = {Myelin is dependent on the Charcot-Marie-Tooth Type 4H disease culprit protein FRABIN/FGD4 in Schwann cells},
  series = {Brain},
  volume    = {135},
  journal   = {Brain},
  doi       = {10.1093/brain/aws275},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-125390},
  pages     = {3567-3583},
  year      = {2012},
  abstract  = {Studying the function and malfunction of genes and proteins associated with inherited forms of peripheral neuropathies has provided multiple clues to our understanding of myelinated nerves in health and disease. Here, we have generated a mouse model for the peripheral neuropathy Charcot-Marie-Tooth disease type 4H by constitutively disrupting the mouse orthologue of the suspected culprit gene FGD4 that encodes the small RhoGTPase Cdc42-guanine nucleotide exchange factor Frabin. Lack of Frabin/Fgd4 causes dysmyelination in mice in early peripheral nerve development, followed by profound myelin abnormalities and demyelination at later stages. At the age of 60 weeks, this was accompanied by electrophysiological deficits. By crossing mice carrying alleles of Frabin/Fgd4 flanked by loxP sequences with animals expressing Cre recombinase in a cell type-specific manner, we show that Schwann cell-autonomous Frabin/Fgd4 function is essential for proper myelination without detectable primary contributions from neurons. Deletion of Frabin/Fgd4 in Schwann cells of fully myelinated nerve fibres revealed that this protein is not only required for correct nerve development but also for accurate myelin maintenance. Moreover, we established that correct activation of Cdc42 is dependent on Frabin/Fgd4 function in healthy peripheral nerves. Genetic disruption of Cdc42 in Schwann cells of adult myelinated nerves resulted in myelin alterations similar to those observed in Frabin/Fgd4-deficient mice, indicating that Cdc42 and the Frabin/Fgd4-Cdc42 axis are critical for myelin homeostasis. In line with known regulatory roles of Cdc42, we found that Frabin/Fgd4 regulates Schwann cell endocytosis, a process that is increasingly recognized as a relevant mechanism in peripheral nerve pathophysiology. Taken together, our results indicate that regulation of Cdc42 by Frabin/Fgd4 in Schwann cells is critical for the structure and function of the peripheral nervous system. In particular, this regulatory link is continuously required in adult fully myelinated nerve fibres. Thus, mechanisms regulated by Frabin/Fgd4-Cdc42 are promising targets that can help to identify additional regulators of myelin development and homeostasis, which may crucially contribute also to malfunctions in different types of peripheral neuropathies.},
  language  = {en}
}
@article{BaumannTvingstedtHeiberetal.2014,
  author    = {Baumann, A. and Tvingstedt, K. and Heiber, M. C. and V{\"a}th, S. and Momblona, C. and Bolink, H. J. and Dyakonov, V.},
  title     = {Persistent photovoltage in methylammonium lead iodide perovskite solar cells},
  series = {APL Materials},
  volume    = {2},
  journal   = {APL Materials},
  number    = {8},
  doi       = {10.1063/1.4885255},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-119397},
  pages     = {081501},
  year      = {2014},
  abstract  = {We herein perform open circuit voltage decay (OCVD) measurements on methylammonium lead iodide (CH3NH3PbI3) perovskite solar cells to increase the understanding of the charge carrier recombination dynamics in this emerging technology. Optically pulsed OCVD measurements are conducted on CH3NH3PbI3 solar cells and compared to results from another type of thin-film photovoltaics, namely, the two reference polymer-fullerene bulk heterojunction solar cell devices based on P3HT:PC60BM and PTB7:PC70BM blends. We observe two very different time domains of the voltage transient in the perovskite solar cell with a first drop on a short time scale that is similar to the decay in the studied organic solar cells. However, 65\%-70\% of the maximum photovoltage persists on much longer timescales in the perovskite solar cell than in the organic devices. In addition, we find that the recombination dynamics in all time regimes are dependent on the starting illumination intensity, which is also not observed in the organic devices. We then discuss the potential origins of these unique behaviors.},
  language  = {en}
}
@article{BurschkaBaumannSchenk1983,
  author    = {Burschka, Christian and Baumann, F.-E. and Schenk, W. A.},
  title     = {Schwefel(IV)-Verbindungen als Liganden. II. Die Kristall- und Molek{\"u}lstruktur von Pentacarbonyl-(schwefeldioxid)chrom},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31388},
  year      = {1983},
  abstract  = {Die Struktur von Pentacarbonyl(schwefeldioxid)chrom (1) wurde r{\"o}ntgenographisch aus Einkristalldaten bestimmt. Die Verbindung kristallisiert mit acht Formeleinheiten in der rhombischen Elementarzelle (Raumgruppe Pbn2\(_1\)) folgender Dimensionen: a = 657,8(2) pm, b = 1245,2(4) pm, c = 2177,4(5) pm (bei 180 K). Das Schwefeldioxid ist \(\eta^1\)-koplanar koordiniert, der Cr-S-Abstand ist mit 219 pm der k{\"u}rzeste bisher gefundene Abstand zwischen Chrom(O) und Schwefel. Die Cr-C(ax)-Bindung ist mit 189 pm fast genau so lang wie die Cr-C(eq).Bindungen (190 pm), ein Beleg f{\"u}r das hohe \(\pi\)-Akzeptorverm{\"o}gen des S0\(_2\).},
  subject      = {Chemie},
  language  = {de}
}