@article{MayrKleinRutzingeretal.2021,
  author    = {Mayr, Stefan and Klein, Igor and Rutzinger, Martin and Kuenzer, Claudia},
  title     = {Determining temporal uncertainty of a global inland surface water time series},
  series = {Remote Sensing},
  volume    = {13},
  journal   = {Remote Sensing},
  number    = {17},
  issn      = {2072-4292},
  doi       = {10.3390/rs13173454},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-245234},
  year      = {2021},
  abstract  = {Earth observation time series are well suited to monitor global surface dynamics. However, data products that are aimed at assessing large-area dynamics with a high temporal resolution often face various error sources (e.g., retrieval errors, sampling errors) in their acquisition chain. Addressing uncertainties in a spatiotemporal consistent manner is challenging, as extensive high-quality validation data is typically scarce. Here we propose a new method that utilizes time series inherent information to assess the temporal interpolation uncertainty of time series datasets. For this, we utilized data from the DLR-DFD Global WaterPack (GWP), which provides daily information on global inland surface water. As the time series is primarily based on optical MODIS (Moderate Resolution Imaging Spectroradiometer) images, the requirement of data gap interpolation due to clouds constitutes the main uncertainty source of the product. With a focus on different temporal and spatial characteristics of surface water dynamics, seven auxiliary layers were derived. Each layer provides probability and reliability estimates regarding water observations at pixel-level. This enables the quantification of uncertainty corresponding to the full spatiotemporal range of the product. Furthermore, the ability of temporal layers to approximate unknown pixel states was evaluated for stratified artificial gaps, which were introduced into the original time series of four climatologic diverse test regions. Results show that uncertainty is quantified accurately (>90\%), consequently enhancing the product's quality with respect to its use for modeling and the geoscientific community.},
  language  = {en}
}
@article{JostKleinBrandetal.2023,
  author    = {Jost, Priska and Klein, Franziska and Brand, Benjamin and Wahl, Vanessa and Wyatt, Amanda and Yildiz, Daniela and Boehm, Ulrich and Niemeyer, Barbara A. and Vaeth, Martin and Alansary, Dalia},
  title     = {Acute downregulation but not genetic ablation of murine MCU impairs suppressive capacity of regulatory CD4 T cells},
  series = {International Journal of Molecular Sciences},
  volume    = {24},
  journal   = {International Journal of Molecular Sciences},
  number    = {9},
  issn      = {1422-0067},
  doi       = {10.3390/ijms24097772},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-313621},
  year      = {2023},
  abstract  = {By virtue of mitochondrial control of energy production, reactive oxygen species (ROS) generation, and maintenance of Ca\(^{2+}\) homeostasis, mitochondria play an essential role in modulating T cell function. The mitochondrial Ca\(^{2+}\) uniporter (MCU) is the pore-forming unit in the main protein complex mediating mitochondrial Ca\(^{2+}\) uptake. Recently, MCU has been shown to modulate Ca\(^{2+}\) signals at subcellular organellar interfaces, thus fine-tuning NFAT translocation and T cell activation. The mechanisms underlying this modulation and whether MCU has additional T cell subpopulation-specific effects remain elusive. However, mice with germline or tissue-specific ablation of Mcu did not show impaired T cell responses in vitro or in vivo, indicating that 'chronic' loss of MCU can be functionally compensated in lymphocytes. The current work aimed to specifically investigate whether and how MCU influences the suppressive potential of regulatory CD4 T cells (Treg). We show that, in contrast to genetic ablation, acute siRNA-mediated downregulation of Mcu in murine Tregs results in a significant reduction both in mitochondrial Ca\(^{2+}\) uptake and in the suppressive capacity of Tregs, while the ratios of Treg subpopulations and the expression of hallmark transcription factors were not affected. These findings suggest that permanent genetic inactivation of MCU may result in compensatory adaptive mechanisms, masking the effects on the suppressive capacity of Tregs.},
  language  = {en}
}
@incollection{Klein2023,
  author    = {Klein, Martin},
  title     = {Metaphors, Dead and Alive},
  series = {Metaphysics Through Semantics: The Philosophical Recovery of the Medieval Mind},
  booktitle = {Metaphysics Through Semantics: The Philosophical Recovery of the Medieval Mind},
  editor    = {Hochschild, Joshua P. and Nevitt, Turner C. and Wood, Adam and Borb{\´e}ly, G{\´a}bor},
  publisher = {Springer},
  doi       = {10.1007/978-3-031-15026-5_8},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-359678},
  publisher      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2023},
  abstract  = {This paper examins how the medieval distinction between proper and improper signification can give a plausible explanation of both metaphorical use and the usual transformations a language can undergo. I will show how Thomas Aquinas distinguishes between ordinary ambiguous terms and metaphors, whereas William of Ockham and Walter Burley do not leave room for this distinction. I will argue that Ockham's conception of transfer of sense through subsequent institution of words is best thought of as an explanation of how ordinary usage can contain ambiguities, whereas Burley's conception of transfer of sense without new imposition is more plausible when it comes to explaining metaphors. If metaphorical use is lumped together with equivocation, the account of how they work cannot do full justice to either, an insight that we already find in Peter Abelard, if not in Boethius.},
  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}
}