@unpublished{AcharyaActisAghajanietal.2013,
  author    = {Acharya, B. S. and Actis, M. and Aghajani, T. and Agnetta, G. and Aguilar, J. and Aharonian, Felix A. and Ajello, M. and Akhperjanian, A. G. and Alcubierre, M. and Aleksic, J. and Alfaro, R. and Aliu, E. and Allafort, A. J. and Allan, D. and Allekotte, I. and Amato, E. and Anderson, J. and Ang{\"u}ner, Ekrem Oǧuzhan and Antonelli, L. A. and Antoranz, P. and Aravantinos, A. and Arlen, T. and Armstrong, T. and Arnaldi, H. and Arrabito, L. and Asano, K. and Ashton, T. and Asorey, H. G. and Awane, Y. and Baba, H. and Babic, A. and Baby, N. and Baehr, J. and Bais, A. and Baixeras, C. and Bajtlik, S. and Balbo, M. and Balis, D. and Balkowski, C. and Bamba, A. and Bandiera, R. and Barber, A. and Barbier, C. and Barcelo, M. and Barnacka, Anna and Barnstedt, J{\"u}rgen and Barres de Almeida, U. and Barrio, J. A. and Basili, A. and Basso, S. and Bastieri, D. and Bauer, C. and Baushev, Anton N. and Becerra Gonzalez, J. and Becherini, Yvonne and Bechtol, K. C. and Tjus, J. Becker and Beckmann, Volker and Bednarek, W. and Behera, B. and Belluso, M. and Benbow, W. and Berdugo, J. and Berger, K. and Bernard, F. and Bernardino, T. and Bernl{\"o}hr, K. and Bhat, N. and Bhattacharyya, S. and Bigongiari, C. and Biland, A. and Billotta, S. and Bird, T. and Birsin, E. and Bissaldi, E. and Biteau, Jonathan and Bitossi, M. and Blake, S. and Blanch Bigas, O. and Blasi, P. and Bobkov, A. A. and Boccone, V. and Boettcher, Markus and Bogacz, L. and Bogart, J. and Bogdan, M. and Boisson, Catherine and Boix Gargallo, J. and Bolmont, J. and Bonanno, G. and Bonardi, A. and Bonev, T. and Bonifacio, P. and Bonnoli, G. and Bordas, Pol and Borgland, A. W. and Borkowski, Janett and Bose, R. and Botner, O. and Bottani, A. and Bouchet, L. and Bourgeat, M. and Boutonnet, C. and Bouvier, A. and Brau-Nogue, S. and Braun, I. and Bretz, T. and Briggs, M. S. and Bringmann, T. and Brook, P. and Brun, Pierre and Brunetti, L. and Buanes, T. and Buckley, J. H. and Buehler, R. and Bugaev, V. and Bulgarelli, A. and Bulik, Tomasz and Busetto, G. and Buson, S. and Byrum, K. and Cailles, M. and Cameron, R. A. and Camprecios, J. and Canestrari, R. and Cantu, S. and Capalbi, M. and Caraveo, P. A. and Carmona, E. and Carosi, A. and Carr, John and Carton, P. H. and Casanova, Sabrina and Casiraghi, M. and Catalano, O. and Cavazzani, S. and Cazaux, S. and Cerruti, M. and Chabanne, E. and Chadwick, Paula M. and Champion, C. and Chen, Andrew and Chiang, J. and Chiappetti, L. and Chikawa, M. and Chitnis, V. R. and Chollet, F. and Chudoba, J. and Cieslar, M. and Cillis, A. N. and Cohen-Tanugi, J. and Colafrancesco, Sergio and Colin, P. and Calome, J. and Colonges, S. and Compin, M. and Conconi, P. and Conforti, V. and Connaughton, V. and Conrad, Jan and Contreras, J. L. and Coppi, P. and Corona, P. and Corti, D. and Cortina, J. and Cossio, L. and Costantini, H. and Cotter, G. and Courty, B. and Couturier, S. and Covino, S. and Crimi, G. and Criswell, S. J. and Croston, J. and Cusumano, G. and Dafonseca, M. and Dale, O. and Daniel, M. and Darling, J. and Davids, I. and Dazzi, F. and De Angelis, A. and De Caprio, V. and De Frondat, F. and de Gouveia Dal Pino, E. M. and de la Calle, I. and De La Vega, G. A. and Lopez, R. de los Reyes and De Lotto, B. and De Luca, A. and de Mello Neto, J. R. T. and de Naurois, M. and de Oliveira, Y. and de Ona Wilhelmi, E. and de Souza, V. and Decerprit, G. and Decock, G. and Deil, C. and Delagnes, E. and Deleglise, G. and Delgado, C. and Della Volpe, D. and Demange, P. and Depaola, G. and Dettlaff, A. and Di Paola, A. and Di Pierro, F. and Diaz, C. and Dick, J. and Dickherber, R. and Dickinson, H. and Diez-Blanco, V. and Digel, S. and Dimitrov, D. and Disset, G. and Djannati-Ata{\"i}, A. and Doert, M. and Dohmke, M. and Domainko, W. and Prester, Dijana Dominis and Donat, A. and Dorner, D. and Doro, M. and Dournaux, J-L. and Drake, G. and Dravins, D. and Drury, L. and Dubois, F. and Dubois, R. and Dubus, G. and Dufour, C. and Dumas, D. and Dumm, J. and Durand, D. and Dyks, J. and Dyrda, M. and Ebr, J. and Edy, E. and Egberts, Kathrin and Eger, P. and Einecke, S. and Eleftheriadis, C. and Elles, S. and Emmanoulopoulos, D. and Engelhaupt, D. and Enomoto, R. and Ernenwein, J-P and Errando, M. and Etchegoyen, A. and Evans, P. and Falcone, A. and Fantinel, D. and Farakos, K. and Farnier, C. and Fasola, G. and Favill, B. and Fede, E. and Federici, S. and Fegan, S. and Feinstein, F. and Ferenc, D. and Ferrando, P. and Fesquet, M. and Fiasson, A. and Fillin-Martino, E. and Fink, D. and Finley, C. and Finley, J. P. and Fiorini, M. and Firpo Curcoll, R. and Flores, H. and Florin, D. and Focke, W. and Foehr, C. and Fokitis, E. and Font, L. and Fontaine, G. and Fornasa, M. and Foerster, A. and Fortson, L. and Fouque, N. and Franckowiak, A. and Fransson, C. and Fraser, G. and Frei, R. and Albuquerque, I. F. M. and Fresnillo, L. and Fruck, C. and Fujita, Y. and Fukazawa, Y. and Fukui, Y. and Funk, S. and Gaebele, W. and Gabici, S. and Gabriele, R. and Gadola, A. and Galante, N. and Gall, D. and Gallant, Y. and Gamez-Garcia, J. and Garcia, B. and Garcia Lopez, R. and Gardiol, D. and Garrido, D. and Garrido, L. and Gascon, D. and Gaug, M. and Gaweda, J. and Gebremedhin, L. and Geffroy, N. and Gerard, L. and Ghedina, A. and Ghigo, M. and Giannakaki, E. and Gianotti, F. and Giarrusso, S. and Giavitto, G. and Giebels, B. and Gika, V. and Giommi, P. and Girard, N. and Giro, E. and Giuliani, A. and Glanzman, T. and Glicenstein, J. -F. and Godinovic, N. and Golev, V. and Gomez Berisso, M. and Gomez-Ortega, J. and Gonzalez, M. M. and Gonzalez, A. and Gonzalez, F. and Gonzalez Munoz, A. and Gothe, K. 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  title     = {Introducing the CTA concept},
  series = {Astroparticle physics},
  volume    = {43},
  journal   = {Astroparticle physics},
  number    = {2},
  publisher = {Elsevier},
  address   = {Amsterdam},
  organization    = {CTA Consortium},
  issn      = {0927-6505},
  doi       = {10.1016/j.astropartphys.2013.01.007},
  pages     = {3 -- 18},
  year      = {2013},
  abstract  = {The Cherenkov Telescope Array (CTA) is a new observatory for very high-energy (VHE) gamma rays. CTA has ambitions science goals, for which it is necessary to achieve full-sky coverage, to improve the sensitivity by about an order of magnitude, to span about four decades of energy, from a few tens of GeV to above 100 TeV with enhanced angular and energy resolutions over existing VHE gamma-ray observatories. An international collaboration has formed with more than 1000 members from 27 countries in Europe, Asia, Africa and North and South America. In 2010 the CTA Consortium completed a Design Study and started a three-year Preparatory Phase which leads to production readiness of CTA in 2014. In this paper we introduce the science goals and the concept of CTA, and provide an overview of the project.},
  language  = {en}
}
@article{BriestGrassSeddingetal.2017,
  author    = {Briest, Franziska and Grass, Irina and Sedding, Dagmar and Moebs, Markus and Christen, Friederike and Benecke, Joana and Fuchs, Karolin and Mende, Stefanie and Kaemmerer, Daniel and S{\"a}nger, J{\"o}rg and Kunze, Almut and Geisler, Christina and Freitag, Helma and Lewens, Florentine and Worpenberg, Lina and Iwaszkiewicz, Sara and Siegmund, Britta and Walther, Wolfgang and Hummel, Michael and Grabowski, Patricia},
  title     = {Mechanisms of Targeting the MDM2-p53-FOXM1 Axis in Well-Differentiated Intestinal Neuroendocrine Tumors},
  series = {Neuroendocrinology : international journal for basic and clinical studies on neuroendocrine relationships},
  volume    = {107},
  journal   = {Neuroendocrinology : international journal for basic and clinical studies on neuroendocrine relationships},
  number    = {1},
  publisher = {Karger},
  address   = {Basel},
  issn      = {0028-3835},
  doi       = {10.1159/000481506},
  pages     = {1 -- 23},
  year      = {2017},
  abstract  = {Background/Aims: The tumor suppressor p53 is rarely mutated in gastroenteropancreatic neuroendocrine neoplasms (GEP-NEN) but they frequently show a strong expression of negative regulators of p53, rendering these tumors excellent targets for a p53 recovery therapy. Therefore, we analyzed the mechanisms of a p53 recovery therapy on intestinal neuroendocrine tumors in vitro and in vivo. Methods: By Western blot and immunohistochemistry, we found that in GEP-NEN biopsy material overexpression of MDM2 was present in intestinal NEN. Therefore, we analyzed the effect of a small-molecule inhibitor, nutlin-3a, in p53 wild-type and mutant GEP-NEN cell lines by proliferation assay, flow cytometry, immunofluorescence, Western blot, and by multiplex gene expression analysis. Finally, we analyzed the antitumor effect of nutlin-3a in a xenograft mouse model in vivo. During the study, the tumor volume was determined. Results: The midgut wild-type cell line KRJ-I responded to the treatment with cell cycle arrest and apoptosis. By gene expression analysis, we could demonstrate that nutlins reactivated an antiproliferative p53 response. KRJ-I-derived xenograft tumors showed a significantly decreased tumor growth upon treatment with nutlin-3a in vivo. Furthermore, our data suggest that MDM2 also influences the expression of the oncogene FOXM1 in a p53-independent manner. Subsequently, a combined treatment of nutlin-3a and cisplatin (as chemoresistance model) resulted in synergistically enhanced antiproliferative effects. Conclusion: In summary, MDM2 overexpression is a frequent event in p53 wild-type intestinal neuroendocrine neoplasms and therefore recovery of a p53 response might be a novel personalized treatment approach in these tumors. (c) 2017 S. Karger AG, Basel},
  language  = {en}
}
@article{StoesselStellmannWillingetal.2018,
  author    = {Stoessel, Daniel and Stellmann, Jan-Patrick and Willing, Anne and Behrens, Birte and Rosenkranz, Sina C. and Hodecker, Sibylle C. and Stuerner, Klarissa H. and Reinhardt, Stefanie and Fleischer, Sabine and Deuschle, Christian and Maetzler, Walter and Berg, Daniela and Heesen, Christoph and Walther, Dirk and Schauer, Nicolas and Friese, Manuel A. and Pless, Ole},
  title     = {Metabolomic Profiles for Primary Progressive Multiple Sclerosis Stratification and Disease Course Monitoring},
  series = {Frontiers in human neuroscienc},
  volume    = {12},
  journal   = {Frontiers in human neuroscienc},
  publisher = {Frontiers Research Foundation},
  address   = {Lausanne},
  issn      = {1662-5161},
  doi       = {10.3389/fnhum.2018.00226},
  pages     = {13},
  year      = {2018},
  abstract  = {Primary progressive multiple sclerosis (PPMS) shows a highly variable disease progression with poor prognosis and a characteristic accumulation of disabilities in patients. These hallmarks of PPMS make it difficult to diagnose and currently impossible to efficiently treat. This study aimed to identify plasma metabolite profiles that allow diagnosis of PPMS and its differentiation from the relapsing remitting subtype (RRMS), primary neurodegenerative disease (Parkinson's disease, PD), and healthy controls (HCs) and that significantly change during the disease course and could serve as surrogate markers of multiple sclerosis (MS)-associated neurodegeneration over time. We applied untargeted high-resolution metabolomics to plasma samples to identify PPMS-specific signatures, validated our findings in independent sex- and age-matched PPMS and HC cohorts and built discriminatory models by partial least square discriminant analysis (PLS-DA). This signature was compared to sex- and age-matched RRMS patients, to patients with PD and HC. Finally, we investigated these metabolites in a longitudinal cohort of PPMS patients over a 24-month period. PLS-DA yielded predictive models for classification along with a set of 20 PPMS-specific informative metabolite markers. These metabolites suggest disease-specific alterations in glycerophospholipid and linoleic acid pathways. Notably, the glycerophospholipid LysoPC(20:0) significantly decreased during the observation period. These findings show potential for diagnosis and disease course monitoring, and might serve as biomarkers to assess treatment efficacy in future clinical trials for neuroprotective MS therapies.},
  language  = {en}
}
@article{DeFrenneRodriguezSanchezCoomesetal.2013,
  author    = {De Frenne, Pieter and Rodriguez-Sanchez, Francisco and Coomes, David Anthony and B{\"a}ten, Lander and Verstr{\"a}ten, Gorik and Vellend, Mark and Bernhardt-R{\"o}mermann, Markus and Brown, Carissa D. and Brunet, J{\"o}rg and Cornelis, Johnny and Decocq, Guillaume M. and Dierschke, Hartmut and Eriksson, Ove and Gilliam, Frank S. and Hedl, Radim and Heinken, Thilo and Hermy, Martin and Hommel, Patrick and Jenkins, Michael A. and Kelly, Daniel L. and Kirby, Keith J. and Mitchell, Fraser J. G. and Naaf, Tobias and Newman, Miles and Peterken, George and Petrik, Petr and Schultz, Jan and Sonnier, Gregory and Van Calster, Hans and Waller, Donald M. and Walther, Gian-Reto and White, Peter S. and Woods, Kerry D. and Wulf, Monika and Graae, Bente Jessen and Verheyen, Kris},
  title     = {Microclimate moderates plant responses to macroclimate warming},
  series = {Proceedings of the National Academy of Sciences of the United States of America},
  volume    = {110},
  journal   = {Proceedings of the National Academy of Sciences of the United States of America},
  number    = {46},
  publisher = {National Acad. of Sciences},
  address   = {Washington},
  issn      = {0027-8424},
  doi       = {10.1073/pnas.1311190110},
  pages     = {18561 -- 18565},
  year      = {2013},
  abstract  = {Recent global warming is acting across marine, freshwater, and terrestrial ecosystems to favor species adapted to warmer conditions and/or reduce the abundance of cold-adapted organisms (i.e., "thermophilization" of communities). Lack of community responses to increased temperature, however, has also been reported for several taxa and regions, suggesting that "climatic lags" may be frequent. Here we show that microclimatic effects brought about by forest canopy closure can buffer biotic responses to macroclimate warming, thus explaining an apparent climatic lag. Using data from 1,409 vegetation plots in European and North American temperate forests, each surveyed at least twice over an interval of 12-67 y, we document significant thermophilization of ground-layer plant communities. These changes reflect concurrent declines in species adapted to cooler conditions and increases in species adapted to warmer conditions. However, thermophilization, particularly the increase of warm-adapted species, is attenuated in forests whose canopies have become denser, probably reflecting cooler growing-season ground temperatures via increased shading. As standing stocks of trees have increased in many temperate forests in recent decades, local microclimatic effects may commonly be moderating the impacts of macroclimate warming on forest understories. Conversely, increases in harvesting woody biomass-e.g., for bioenergy-may open forest canopies and accelerate thermophilization of temperate forest biodiversity.},
  language  = {en}
}
@article{RaafatMrochenAl’Sholuietal.2020,
  author    = {Raafat, Dina and Mrochen, Daniel M. and Al'Sholui, Fawaz and Heuser, Elisa and Ryll, Ren{\´e} and Pritchett-Corning, Kathleen R. and Jacob, Jens and Walther, Bernd and Matuschka, Franz-Rainer and Richter, Dania},
  title     = {Molecular epidemiology of methicillin-susceptible and methicillin-resistant Staphylococcus aureus in wild, captive and laboratory rats},
  series = {Toxins},
  volume    = {12},
  journal   = {Toxins},
  number    = {2},
  publisher = {MDPI},
  address   = {Basel},
  issn      = {2072-6651},
  doi       = {10.3390/toxins12020080},
  pages     = {1 -- 22},
  year      = {2020},
  abstract  = {Rats are a reservoir of human- and livestock-associated methicillin-resistant Staphylococcus aureus (MRSA). However, the composition of the natural S. aureus population in wild and laboratory rats is largely unknown. Here, 144 nasal S. aureus isolates from free-living wild rats, captive wild rats and laboratory rats were genotyped and profiled for antibiotic resistances and human-specific virulence genes. The nasal S. aureus carriage rate was higher among wild rats (23.4\%) than laboratory rats (12.3\%). Free-living wild rats were primarily colonized with isolates of clonal complex (CC) 49 and CC130 and maintained these strains even in husbandry. Moreover, upon livestock contact, CC398 isolates were acquired. In contrast, laboratory rats were colonized with many different S. aureus lineages—many of which are commonly found in humans. Five captive wild rats were colonized with CC398-MRSA. Moreover, a single CC30-MRSA and two CC130-MRSA were detected in free-living or captive wild rats. Rat-derived S. aureus isolates rarely harbored the phage-carried immune evasion gene cluster or superantigen genes, suggesting long-term adaptation to their host. Taken together, our study revealed a natural S. aureus population in wild rats, as well as a colonization pressure on wild and laboratory rats by exposure to livestock- and human-associated S. aureus, respectively.},
  language  = {en}
}
@article{StoesselSchultedosSantosetal.2018,
  author    = {Stoessel, Daniel and Schulte, Claudia and dos Santos, Marcia C. Teixeira and Scheller, Dieter and Rebollo-Mesa, Irene and Deuschle, Christian and Walther, Dirk and Schauer, Nicolas and Berg, Daniela and da Costa, Andre Nogueira and Maetzler, Walter},
  title     = {Promising Metabolite Profiles in the Plasma and CSF of Early Clinical},
  series = {Frontiers in Aging Neuroscience},
  volume    = {10},
  journal   = {Frontiers in Aging Neuroscience},
  publisher = {Frontiers Research Foundation},
  address   = {Lausanne},
  issn      = {1663-4365},
  doi       = {10.3389/fnagi.2018.00051},
  pages     = {14},
  year      = {2018},
  abstract  = {Parkinson's disease (PD) shows high heterogeneity with regard to the underlying molecular pathogenesis involving multiple pathways and mechanisms. Diagnosis is still challenging and rests entirely on clinical features. Thus, there is an urgent need for robust diagnostic biofluid markers. Untargeted metabolomics allows establishing low-molecular compound biomarkers in a wide range of complex diseases by the measurement of various molecular classes in biofluids such as blood plasma, serum, and cerebrospinal fluid (CSF). Here, we applied untargeted high-resolution mass spectrometry to determine plasma and CSF metabolite profiles. We semiquantitatively determined small-molecule levels (<= 1.5 kDa) in the plasma and CSF from early PD patients (disease duration 0-4 years; n = 80 and 40, respectively), and sex-and age-matched controls (n = 76 and 38, respectively). We performed statistical analyses utilizing partial least square and random forest analysis with a 70/30 training and testing split approach, leading to the identification of 20 promising plasma and 14 CSF metabolites. The semetabolites differentiated the test set with an AUC of 0.8 (plasma) and 0.9 (CSF). Characteristics of the metabolites indicate perturbations in the glycerophospholipid, sphingolipid, and amino acid metabolism in PD, which underscores the high power of metabolomic approaches. Further studies will enable to develop a potential metabolite-based biomarker panel specific for PD},
  language  = {en}
}
@article{KleinOlonscheckWaltheretal.2013,
  author    = {Klein, Daniel R. and Olonscheck, Mady and Walther, Carsten and Kropp, J{\"u}rgen},
  title     = {Susceptibility of the European electricity sector to climate change},
  series = {Energy},
  volume    = {59},
  journal   = {Energy},
  number    = {6},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0360-5442},
  doi       = {10.1016/j.energy.2013.06.048},
  pages     = {183 -- 193},
  year      = {2013},
  abstract  = {The electricity system is particularly susceptible to climate change due to the close interconnectedness between electricity production, consumption and climate. This study provides a country based relative analysis of 21 European countries' electricity system susceptibility to climate change. Taking into account 14 quantitative influencing factors, the susceptibility of each country is examined both for the current and projected system with the result being a relative ranked index. Luxembourg and Greece are the most susceptible relatively due in part to their inability to meet their own electricity consumption demand with inland production, and the fact that the majority of their production is from more susceptible sources, primarily combustible fuels. Greece experiences relatively warm mean temperatures, which are expected to increase in the future leading to greater summer electricity consumption, increasing susceptibility. Norway was found to be the least susceptible, relatively, due to its consistent production surplus, which is primarily from hydro (a less susceptible source) and a likely decrease of winter electricity consumption as temperatures rise due to climate change. The findings of this study enable countries to identify the main factors that increase their electricity system susceptibility and proceed with adaptation measures that are the most effective in decreasing susceptibility.},
  language  = {en}
}
@article{MrochenSchulzFischeretal.2018,
  author    = {Mrochen, Daniel M. and Schulz, Daniel and Fischer, Stefan and Jeske, Kathrin and El Gohary, Heba and Reil, Daniela and Imholt, Christian and Truebe, Patricia and Suchomel, Josef and Tricaud, Emilie and Jacob, Jens and Heroldova, Marta and Br{\"o}ker, Barbara M. and Strommenger, Birgit and Walther, Birgit and Ulrich, Rainer G. and Holtfreter, Silva},
  title     = {Wild rodents and shrews are natural hosts of Staphylococcus aureus},
  series = {International Journal of Medical Microbiology},
  volume    = {308},
  journal   = {International Journal of Medical Microbiology},
  number    = {6},
  publisher = {Elsevier},
  address   = {Jena},
  issn      = {1438-4221},
  doi       = {10.1016/j.ijmm.2017.09.014},
  pages     = {590 -- 597},
  year      = {2018},
  abstract  = {Laboratory mice are the most commonly used animal model for Staphylococcus aureus infection studies. We have previously shown that laboratory mice from global vendors are frequently colonized with S. aureus. Laboratory mice originate from wild house mice. Hence, we investigated whether wild rodents, including house mice, as well as shrews are naturally colonized with S. aureus and whether S. aureus adapts to the wild animal host. 295 animals of ten different species were caught in different locations over four years (2012-2015) in Germany, France and the Czech Republic. 45 animals were positive for S. aureus (15.3\%). Three animals were co-colonized with two different isolates, resulting in 48 S. aureus isolates in total. Positive animals were found in Germany and the Czech Republic in each studied year. The S. aureus isolates belonged to ten different spa types, which grouped into six lineages (clonal complex (CC) 49, CC88, CC130, CC1956, sequence type (ST) 890, ST3033). CC49 isolates were most abundant (17/48, 35.4\%), followed by CC1956 (14/48, 29.2\%) and ST890 (9/48, 18.8\%). The wild animal isolates lacked certain properties that are common among human isolates, e.g., a phage-encoded immune evasion cluster, superantigen genes on mobile genetic elements and antibiotic resistance genes, which suggests long-term adaptation to the wild animal host. One CC130 isolate contained the mecC gene, implying wild rodents might be both reservoir and vector for methicillin-resistant. In conclusion, we demonstrated that wild rodents and shrews are naturally colonized with S. aureus, and that those S. aureus isolates show signs of host adaptation.},
  language  = {en}
}