@article{IsaiasSpiegelBrumbergetal.2014,
  author    = {Isaias, Ioannis Ugo and Spiegel, J{\"o}rg and Brumberg, Joachim and Cosgrove, Kelly P. and Marotta, Giorgio and Oishi, Naoya and Higuchi, Takahiro and K{\"u}sters, Sebastian and Schiller, Markus and Dillmann, Ulrich and van Dyck, Christopher H. and Buck, Andreas and Herrmann, Ken and Schloegl, Susanne and Volkmann, Jens and Lassmann, Michael and Fassbender, Klaus and Lorenz, Reinhard and Samnick, Samuel},
  title     = {Nicotinic acetylcholine receptor density in cognitively intact subjects at an early stage of Parkinson's disease},
  series = {Frontiers in Aging Neuroscience},
  volume    = {6},
  journal   = {Frontiers in Aging Neuroscience},
  doi       = {10.3389/fnagi.2014.00213},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-119351},
  pages     = {213},
  year      = {2014},
  abstract  = {We investigated in vivo brain nicotinic acetylcholine receptor (nAChR) distribution in cognitively intact subjects with Parkinson's disease (PD) at an early stage of the disease. Fourteen patients and 13 healthy subjects were imaged with single photon emission computed tomography and the radiotracer 5-[(123)I]iodo-3-[2(S)-2-azetidinylmethoxy]pyridine ([(123)I]5IA). Patients were selected according to several criteria, including short duration of motor signs (<7 years) and normal scores at an extensive neuropsychological evaluation. In PD patients, nAChR density was significantly higher in the putamen, the insular cortex and the supplementary motor area and lower in the caudate nucleus, the orbitofrontal cortex, and the middle temporal gyrus. Disease duration positively correlated with nAChR density in the putamen ipsilateral (ρ = 0.56, p < 0.05) but not contralateral (ρ = 0.49, p = 0.07) to the clinically most affected hemibody. We observed, for the first time in vivo, higher nAChR density in brain regions of the motor and limbic basal ganglia circuits of subjects with PD. Our findings support the notion of an up-regulated cholinergic activity at the striatal and possibly cortical level in cognitively intact PD patients at an early stage of disease.},
  language  = {en}
}
@article{WeberLorenzHemmings2019,
  author    = {Weber, Silvana and Lorenz, Christopher and Hemmings, Nicola},
  title     = {Improving stress and positive mental health at work via an app-based intervention: a large-scale multi-center randomized control trial},
  series = {Frontiers in Psychology},
  volume    = {10},
  journal   = {Frontiers in Psychology},
  number    = {2745},
  issn      = {1664-1078},
  doi       = {10.3389/fpsyg.2019.02745},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-194337},
  year      = {2019},
  abstract  = {Mobile health interventions (i.e., "apps") are used to address mental health and are an increasingly popular method available to both individuals and organizations to manage workplace stress. However, at present, there is a lack of research on the effectiveness of mobile health interventions in counteracting or improving stress-related health problems, particularly in naturalistic, non-clinical settings. This project aimed at validating a mobile health intervention (which is theoretically grounded in the Job Demands-Resources Model) in preventing and managing stress at work. Within the mobile health intervention, employees make an evidence-based, personalized, psycho-educational journey to build further resources, and thus, reduce stress. A large-scale longitudinal randomized control trial, conducted with six European companies over 6 weeks using four measurement points, examined indicators of mental health via measures of stress, wellbeing, resilience, and sleep. The data were analyzed by means of hierarchical multilevel models for repeated measures, including both self-report measures and user behavior metrics from the app. The results (n = 532) suggest that using the mobile health intervention (vs. waitlist control group) significantly improved stress and wellbeing over time. Higher engagement in the intervention increased the beneficial effects. Additionally, use of the sleep tracking function led to an improvement in sleeping troubles. The intervention had no effects on measures of physical health or social community at work. Theoretical and practical implications of these findings are discussed, focusing on benefits and challenges of using technological solutions for organizations to support individuals' mental health in the workplace.},
  language  = {en}
}
@article{DammertBraegelmannOlsenetal.2019,
  author    = {Dammert, Marcel A. and Br{\"a}gelmann, Johannes and Olsen, Rachelle R. and B{\"o}hm, Stefanie and Monhasery, Niloufar and Whitney, Christopher P. and Chalishazar, Milind D. and Tumbrink, Hannah L. and Guthrie, Matthew R. and Klein, Sebastian and Ireland, Abbie S. and Ryan, Jeremy and Schmitt, Anna and Marx, Annika and Ozretić, Luka and Castiglione, Roberta and Lorenz, Carina and Jachimowicz, Ron D. and Wolf, Elmar and Thomas, Roman K. and Poirier, John T. and B{\"u}ttner, Reinhard and Sen, Triparna and Byers, Lauren A. and Reinhardt, H. Christian and Letai, Anthony and Oliver, Trudy G. and Sos, Martin L.},
  title     = {MYC paralog-dependent apoptotic priming orchestrates a spectrum of vulnerabilities in small cell lung cancer},
  series = {Nature Communications},
  volume    = {10},
  journal   = {Nature Communications},
  doi       = {10.1038/s41467-019-11371-x},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-223569},
  year      = {2019},
  abstract  = {MYC paralogs are frequently activated in small cell lung cancer (SCLC) but represent poor drug targets. Thus, a detailed mapping of MYC-paralog-specific vulnerabilities may help to develop effective therapies for SCLC patients. Using a unique cellular CRISPR activation model, we uncover that, in contrast to MYCN and MYCL, MYC represses BCL2 transcription via interaction with MIZ1 and DNMT3a. The resulting lack of BCL2 expression promotes sensitivity to cell cycle control inhibition and dependency on MCL1. Furthermore, MYC activation leads to heightened apoptotic priming, intrinsic genotoxic stress and susceptibility to DNA damage checkpoint inhibitors. Finally, combined AURK and CHK1 inhibition substantially prolongs the survival of mice bearing MYC-driven SCLC beyond that of combination chemotherapy. These analyses uncover MYC-paralog-specific regulation of the apoptotic machinery with implications for genotype-based selection of targeted therapeutics in SCLC patients.},
  language  = {en}
}