@article{WuWinklerWieseretal.2015,
  author    = {Wu, Lingdan and Winkler, Markus H. and Wieser, Matthias J. and Andreatta, Marta and Li, Yonghui and Pauli, Paul},
  title     = {Emotion regulation in heavy smokers: experiential, expressive and physiological consequences of cognitive reappraisal},
  series = {Frontiers in Psychology},
  volume    = {6},
  journal   = {Frontiers in Psychology},
  number    = {1555},
  doi       = {10.3389/fpsyg.2015.01555},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-145225},
  year      = {2015},
  abstract  = {Emotion regulation dysfunctions are assumed to contribute to the development of tobacco addiction and relapses among smokers attempting to quit. To further examine this hypothesis, the present study compared heavy smokers with non-smokers (NS) in a reappraisal task. Specifically, we investigated whether non-deprived smokers (NDS) and deprived smokers (DS) differ from non-smokers in cognitive emotion regulation and whether there is an association between the outcome of emotion regulation and the cigarette craving. Sixty-five participants (23 non-smokers, 22 NDS, and 20 DS) were instructed to down-regulate emotions by reappraising negative or positive pictorial scenarios. Self-ratings of valence, arousal, and cigarette craving as well as facial electromyography and electroencephalograph activities were measured. Ratings, facial electromyography, and electroencephalograph data indicated that both NDS and DS performed comparably to nonsmokers in regulating emotional responses via reappraisal, irrespective of the valence of pictorial stimuli. Interestingly, changes in cigarette craving were positively associated with regulation of emotional arousal irrespective of emotional valence. These results suggest that heavy smokers are capable to regulate emotion via deliberate reappraisal and smokers' cigarette craving is associated with emotional arousal rather than emotional valence. This study provides preliminary support for the therapeutic use of reappraisal to replace maladaptive emotion-regulation strategies in nicotine addicts.},
  language  = {en}
}
@article{PreisingSchneiderBucheretal.2015,
  author    = {Preising, Christina and Schneider, Reinhard and Bucher, Michael and Gekle, Michael and Sauvant, Christoph},
  title     = {Regulation of expression of renal organic anion transporters OAT1 and OAT3 in a model of ischemia/reperfusion injury},
  series = {Cellular Physiology and Biochemistry},
  volume    = {37},
  journal   = {Cellular Physiology and Biochemistry},
  number    = {1},
  doi       = {10.1159/000430328},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-144504},
  year      = {2015},
  abstract  = {Background: Recently, we gained evidence that impairment of rOat1 and rOat3 expression induced by ischemic acute kidney injury (AKI) is mediated by COX metabolites and this suppression might be critically involved in renal damage. Methods: (i) Basolateral organic anion uptake into proximal tubular cells after model ischemia and reperfusion (I/R) was investigated by fluorescein uptake. The putative promoter sequences from hOAT1 (SLC22A6) and hOAT3 (SCL22A8) were cloned into a reporter plasmid, transfected into HEK cells and (ii) transcriptional activity was determined after model ischemia and reperfusion as a SEAP reporter gen assay. Inhibitors or antagonists were applied with the beginning of reperfusion. Results: By using inhibitors of PKA (H89) and PLC (U73122), antagonists of E prostanoid receptor type 2 (AH6809) and type 4 (L161,982), we gained evidence that I/R induced down regulation of organic anion transport is mediated by COX1 metabolites via E prostanoid receptor type 4. The latter signaling was confirmed by application of butaprost (EP2 agonist) or TCS2510 (EP4 agonist) to control cells. In brief, the latter signaling was verified for the transcriptional activity in the reporter gen assay established. Therein, selective inhibitors for COX1 (SC58125) and COX2 (SC560) were also applied. Conclusion: Our data show (a) that COX1 metabolites are involved in the regulation of renal organic anion transport(ers) after I/R via the EP4 receptor and (b) that this is due to transcriptional regulation of the respective transporters. As the promoter sequences cloned were of human origin and expressed in a human renal epithelial cell line we (c) hypothesize that the regulatory mechanisms described after I/R is meaningful for humans as well.},
  language  = {en}
}