@misc{HetenyiMolinariClintonetal.2018, author = {Hetenyi, Gyorgy and Molinari, Irene and Clinton, John and Bokelmann, Gotz and Bondar, Istvan and Crawford, Wayne C. and Dessa, Jean-Xavier and Doubre, Cecile and Friederich, Wolfgang and Fuchs, Florian and Giardini, Domenico and Graczer, Zoltan and Handy, Mark R. and Herak, Marijan and Jia, Yan and Kissling, Edi and Kopp, Heidrun and Korn, Michael and Margheriti, Lucia and Meier, Thomas and Mucciarelli, Marco and Paul, Anne and Pesaresi, Damiano and Piromallo, Claudia and Plenefisch, Thomas and Plomerova, Jaroslava and Ritter, Joachim and Rumpker, Georg and Sipka, Vesna and Spallarossa, Daniele and Thomas, Christine and Tilmann, Frederik and Wassermann, Joachim and Weber, Michael and Weber, Zoltan and Wesztergom, Viktor and Zivcic, Mladen and Abreu, Rafael and Allegretti, Ivo and Apoloner, Maria-Theresia and Aubert, Coralie and Besancon, Simon and de Berc, Maxime Bes and Brunel, Didier and Capello, Marco and Carman, Martina and Cavaliere, Adriano and Cheze, Jerome and Chiarabba, Claudio and Cougoulat, Glenn and Cristiano, Luigia and Czifra, Tibor and Danesi, Stefania and Daniel, Romuald and Dannowski, Anke and Dasovic, Iva and Deschamps, Anne and Egdorf, Sven and Fiket, Tomislav and Fischer, Kasper and Funke, Sigward and Govoni, Aladino and Groschl, Gidera and Heimers, Stefan and Heit, Ben and Herak, Davorka and Huber, Johann and Jaric, Dejan and Jedlicka, Petr and Jund, Helene and Klingen, Stefan and Klotz, Bernhard and Kolinsky, Petr and Kotek, Josef and Kuhne, Lothar and Kuk, Kreso and Lange, Dietrich and Loos, Jurgen and Lovati, Sara and Malengros, Deny and Maron, Christophe and Martin, Xavier and Massa, Marco and Mazzarini, Francesco and Metral, Laurent and Moretti, Milena and Munzarova, Helena and Nardi, Anna and Pahor, Jurij and Pequegnat, Catherine and Petersen, Florian and Piccinini, Davide and Pondrelli, Silvia and Prevolnik, Snjezan and Racine, Roman and Regnier, Marc and Reiss, Miriam and Salimbeni, Simone and Santulin, Marco and Scherer, Werner and Schippkus, Sven and Schulte-Kortnack, Detlef and Solarino, Stefano and Spieker, Kathrin and Stipcevic, Josip and Strollo, Angelo and Sule, Balint and Szanyi, Gyongyver and Szucs, Eszter and Thorwart, Martin and Ueding, Stefan and Vallocchia, Massimiliano and Vecsey, Ludek and Voigt, Rene and Weidle, Christian and Weyland, Gauthier and Wiemer, Stefan and Wolf, Felix and Wolyniec, David and Zieke, Thomas}, title = {The AlpArray seismic network}, series = {Surveys in Geophysics}, volume = {39}, journal = {Surveys in Geophysics}, number = {5}, publisher = {Springer}, address = {Dordrecht}, organization = {ETHZ SED Elect Lab AlpArray Seismic Network Team AlpArray OBS Cruise Crew AlpArray Working Grp}, issn = {0169-3298}, doi = {10.1007/s10712-018-9472-4}, pages = {1009 -- 1033}, year = {2018}, abstract = {The AlpArray programme is a multinational, European consortium to advance our understanding of orogenesis and its relationship to mantle dynamics, plate reorganizations, surface processes and seismic hazard in the Alps-Apennines-Carpathians-Dinarides orogenic system. The AlpArray Seismic Network has been deployed with contributions from 36 institutions from 11 countries to map physical properties of the lithosphere and asthenosphere in 3D and thus to obtain new, high-resolution geophysical images of structures from the surface down to the base of the mantle transition zone. With over 600 broadband stations operated for 2 years, this seismic experiment is one of the largest simultaneously operated seismological networks in the academic domain, employing hexagonal coverage with station spacing at less than 52 km. This dense and regularly spaced experiment is made possible by the coordinated coeval deployment of temporary stations from numerous national pools, including ocean-bottom seismometers, which were funded by different national agencies. They combine with permanent networks, which also required the cooperation of many different operators. Together these stations ultimately fill coverage gaps. Following a short overview of previous large-scale seismological experiments in the Alpine region, we here present the goals, construction, deployment, characteristics and data management of the AlpArray Seismic Network, which will provide data that is expected to be unprecedented in quality to image the complex Alpine mountains at depth.}, language = {en} } @article{SchulzThierbachVoigtetal.2006, author = {Schulz, Tim Julius and Thierbach, Ren{\`e} and Voigt, Anja and Drewes, Gunnar and Mietzner, Brun and Steinberg, Pablo and Pfeiffer, Andreas F. H. and Ristow, Michael}, title = {Induction of oxidative metabolism by mitochondrial frataxin inhibits cancer growth : Otto Warburg revisited}, doi = {10.1074/jbc.M511064200}, year = {2006}, abstract = {More than 80 years ago Otto Warburg suggested that cancer might be caused by a decrease in mitochondrial energy metabolism paralleled by an increase in glycolytic flux. In later years, it was shown that cancer cells exhibit multiple alterations in mitochondrial content, structure, function, and activity. We have stably overexpressed the Friedreich ataxia-associated protein frataxin in several colon cancer cell lines. These cells have increased oxidative metabolism, as shown by concurrent increases in aconitase activity, mitochondrial membrane potential, cellular respiration, and ATP content. Consistent with Warburg's hypothesis, we found that frataxin-overexpressing cells also have decreased growth rates and increased population doubling times, show inhibited colony formation capacity in soft agar assays, and exhibit a reduced capacity for tumor formation when injected into nude mice. Furthermore, overexpression of frataxin leads to an increased phosphorylation of the tumor suppressor p38 mitogen-activated protein kinase, as well as decreased phosphorylation of extracellular signal-regulated kinase. Taken together, these results support the view that an increase in oxidative metabolism induced by mitochondrial frataxin may inhibit cancer growth in mammals}, language = {en} } @article{ThierbachDrewesFusseretal.2010, author = {Thierbach, Ren{\´e} and Drewes, Gunnar and Fusser, Markus and Voigt, Anja and Kuhlow, Doreen and Blume, Urte and Schulz, Tim Julius and Reiche, Carina and Glatt, Hansruedi and Epe, Bernd and Steinberg, Pablo and Ristow, Michael}, title = {The Friedreich's ataxia protein frataxin modulates DNA base excision repair in prokaryotes and mammals}, issn = {0264-6021}, doi = {10.1042/Bj20101116}, year = {2010}, abstract = {DNA-repair mechanisms enable cells to maintain their genetic information by protecting it from mutations that may cause malignant growth. Recent evidence suggests that specific DNA-repair enzymes contain ISCs (iron-sulfur clusters). The nuclear-encoded protein frataxin is essential for the mitochondrial biosynthesis of ISCs. Frataxin deficiency causes a neurodegenerative disorder named Friedreich's ataxia in humans. Various types of cancer occurring at young age are associated with this disease, and hence with frataxin deficiency. Mice carrying a hepatocyte- specific disruption of the frataxin gene develop multiple liver tumours for unresolved reasons. In the present study, we show that frataxin deficiency in murine liver is associated with increased basal levels of oxidative DNA base damage. Accordingly, eukaryotic V79 fibroblasts overexpressing human frataxin show decreased basal levels of these modifications, while prokaryotic Salmonella enterica serotype Typhimurium TA 104 strains transformed with human frataxin show decreased mutation rates. The repair rates of oxidative DNA base modifications in V79 cells overexpressing frataxin were significantly higher than in control cells. Lastly, cleavage activity related to the ISC-independent repair enzyme 8-oxoguanine glycosylase was found to be unaltered by frataxin overexpression. These findings indicate that frataxin modulates DNA-repair mechanisms probably due to its impact on ISC-dependent repair proteins, linking mitochondrial dysfunction to DNA repair and tumour initiation.}, language = {en} } @article{ThierbachBlumeWolfrumetal.2010, author = {Thierbach, Ren{\´e} and Blume, Urte and Wolfrum, K. and Drewes, Gunnar and Voigt, Anja and Ristow, Michael and Steinberg, Pablo}, title = {Altered carbohydrate metabolism in a tumour developing knock-out mice model}, issn = {0028-1298}, doi = {10.1007/s00210-010-0508-7}, year = {2010}, language = {en} } @article{ThierbachSchulzIskenetal.2005, author = {Thierbach, Ren{\`e} and Schulz, Tim Julius and Isken, Frank and Voigt, Aanja and Mietzner, Brun and Drewes, Gunnar and von Kleist-Retzow, J{\"u}rgen-Christoph and Wiesner, Rudolf J. and Magnuson, Mark A. and Puccio, Helene and Pfeiffer, Andreas F. H. and Steinberg, Pablo and Ristow, Michael}, title = {Targeted disruption of hepatic frataxin expression causes impaired mitochondrial function, decreased life span and tumor growth in mice}, year = {2005}, abstract = {We have disrupted expression of the mitochondrial Friedreich ataxia protein frataxin specifically in murine hepatocytes to generate mice with impaired mitochondrial function and decreased oxidative phosphorylation. These animals have a reduced life span and develop multiple hepatic tumors. Livers also show increased oxidative stress, impaired respiration and reduced ATP levels paralleled by reduced activity of iron-sulfur cluster (Fe/S) containing proteins (ISP), which all leads to increased hepatocyte turnover by promoting both apoptosis and proliferation. Accordingly, phosphorylation of the stress-inducible p38 MAP kinase was found to be specifically impaired following disruption of frataxin. Taken together, these findings indicate that frataxin may act as a mitochondrial tumor suppressor protein in mammals}, language = {en} } @article{ThierbachSchulzVoigtetal.2004, author = {Thierbach, Rene and Schulz, Tim Julius and Voigt, Aanja and Drewes, Gunnar and Isken, F. and Pfeiffer, Andreas F. H. and Ristow, Michael and Steinberg, Pablo}, title = {Targeted disruption of frataxin in hepatocytes causes spontaneous neoplasia accompanied by increased ROS formation}, issn = {0028-1298}, year = {2004}, language = {en} } @article{ThierbachFlorianWolfrumetal.2012, author = {Thierbach, Rene and Florian, Simone and Wolfrum, Katharina and Voigt, Anja and Drewes, Gunnar and Blume, Urte and Bannasch, Peter and Ristow, Michael and Steinberg, Pablo}, title = {Specific alterations of carbohydrate metabolism are associated with hepatocarcinogenesis in mitochondrially impaired mice}, series = {Human molecular genetics}, volume = {21}, journal = {Human molecular genetics}, number = {3}, publisher = {Oxford Univ. Press}, address = {Oxford}, issn = {0964-6906}, doi = {10.1093/hmg/ddr499}, pages = {656 -- 663}, year = {2012}, abstract = {Friedreich's ataxia is an inherited neurodegenerative disease caused by the reduced expression of the mitochondrially active protein frataxin. We have previously shown that mice with a hepatocyte-specific frataxin knockout (AlbFxn(-/-)) develop multiple hepatic tumors in later life. In the present study, hepatic carbohydrate metabolism in AlbFxn(-/-) mice at an early and late life stage was analyzed. In young (5-week-old) AlbFxn(-/-) mice hepatic ATP, glucose-6-phosphate and glycogen levels were found to be reduced by similar to 74, 80 and 88\%, respectively, when compared with control animals. This pronounced ATP, G6P and glycogen depletion in the livers of young mice reverted in older animals: while half of the mice die before 30 weeks of age, the other half reaches 17 months of age and exhibits glycogen, G6P and ATP levels similar to those in age-matched controls. A key event in this respect seems to be the up-regulation of GLUT1, the predominant glucose transporter in fetal liver parenchyma, which became evident in AlbFxn(-/-) mice being 5-12 weeks of age. The most significant histological findings in animals being 17 or 22 months of age were the appearance of multiple clear cell, mixed cell and basophilic foci throughout the liver parenchyma as well as the development of hepatocellular adenomas and carcinomas. The hepatocarcinogenic process in AlbFxn 2/2 mice shows remarkable differences regarding carbohydrate metabolism alterations when compared with all other chemically and virally driven liver cancer models described up to now.}, language = {en} } @article{TuckerBoehningGaeseFaganetal.2018, author = {Tucker, Marlee A. and Boehning-Gaese, Katrin and Fagan, William F. and Fryxell, John M. and Van Moorter, Bram and Alberts, Susan C. and Ali, Abdullahi H. and Allen, Andrew M. and Attias, Nina and Avgar, Tal and Bartlam-Brooks, Hattie and Bayarbaatar, Buuveibaatar and Belant, Jerrold L. and Bertassoni, Alessandra and Beyer, Dean and Bidner, Laura and van Beest, Floris M. and Blake, Stephen and Blaum, Niels and Bracis, Chloe and Brown, Danielle and de Bruyn, P. J. Nico and Cagnacci, Francesca and Calabrese, Justin M. and Camilo-Alves, Constanca and Chamaille-Jammes, Simon and Chiaradia, Andre and Davidson, Sarah C. and Dennis, Todd and DeStefano, Stephen and Diefenbach, Duane and Douglas-Hamilton, Iain and Fennessy, Julian and Fichtel, Claudia and Fiedler, Wolfgang and Fischer, Christina and Fischhoff, Ilya and Fleming, Christen H. and Ford, Adam T. and Fritz, Susanne A. and Gehr, Benedikt and Goheen, Jacob R. and Gurarie, Eliezer and Hebblewhite, Mark and Heurich, Marco and Hewison, A. J. Mark and Hof, Christian and Hurme, Edward and Isbell, Lynne A. and Janssen, Rene and Jeltsch, Florian and Kaczensky, Petra and Kane, Adam and Kappeler, Peter M. and Kauffman, Matthew and Kays, Roland and Kimuyu, Duncan and Koch, Flavia and Kranstauber, Bart and LaPoint, Scott and Leimgruber, Peter and Linnell, John D. C. and Lopez-Lopez, Pascual and Markham, A. Catherine and Mattisson, Jenny and Medici, Emilia Patricia and Mellone, Ugo and Merrill, Evelyn and Mourao, Guilherme de Miranda and Morato, Ronaldo G. and Morellet, Nicolas and Morrison, Thomas A. and Diaz-Munoz, Samuel L. and Mysterud, Atle and Nandintsetseg, Dejid and Nathan, Ran and Niamir, Aidin and Odden, John and Oliveira-Santos, Luiz Gustavo R. and Olson, Kirk A. and Patterson, Bruce D. and de Paula, Rogerio Cunha and Pedrotti, Luca and Reineking, Bjorn and Rimmler, Martin and Rogers, Tracey L. and Rolandsen, Christer Moe and Rosenberry, Christopher S. and Rubenstein, Daniel I. and Safi, Kamran and Said, Sonia and Sapir, Nir and Sawyer, Hall and Schmidt, Niels Martin and Selva, Nuria and Sergiel, Agnieszka and Shiilegdamba, Enkhtuvshin and Silva, Joao Paulo and Singh, Navinder and Solberg, Erling J. and Spiegel, Orr and Strand, Olav and Sundaresan, Siva and Ullmann, Wiebke and Voigt, Ulrich and Wall, Jake and Wattles, David and Wikelski, Martin and Wilmers, Christopher C. and Wilson, John W. and Wittemyer, George and Zieba, Filip and Zwijacz-Kozica, Tomasz and Mueller, Thomas}, title = {Moving in the Anthropocene}, series = {Science}, volume = {359}, journal = {Science}, number = {6374}, publisher = {American Assoc. for the Advancement of Science}, address = {Washington}, issn = {0036-8075}, doi = {10.1126/science.aam9712}, pages = {466 -- 469}, year = {2018}, abstract = {Animal movement is fundamental for ecosystem functioning and species survival, yet the effects of the anthropogenic footprint on animal movements have not been estimated across species. Using a unique GPS-tracking database of 803 individuals across 57 species, we found that movements of mammals in areas with a comparatively high human footprint were on average one-half to one-third the extent of their movements in areas with a low human footprint. We attribute this reduction to behavioral changes of individual animals and to the exclusion of species with long-range movements from areas with higher human impact. Global loss of vagility alters a key ecological trait of animals that affects not only population persistence but also ecosystem processes such as predator-prey interactions, nutrient cycling, and disease transmission.}, language = {en} } @misc{HarkHackmannWolffetal.2023, author = {Hark, Sabine_ and Hackmann, Nina and Wolff, Christina and Voigt, Anna and Krall, Lisa and Niehus-Kettler, Melinda and Barry, C{\´e}line and Malmedie, Lydia and Rain Hornstein, Ren{\´e}_ and Giesche-von R{\"u}den, Doro* and Beck, Florian and Busch-Geertsema, Max and von R{\"o}mer, Jasper and Sch{\"u}tze, Christin and Rothermel, Ann-Kathrin and Lembke, Ulrike and Tischbirek, Alexander and G{\"o}tschel, Helene and H{\"u}hne, RyLee}, title = {Geschlechter in Un-Ordnung}, editor = {Hackmann, Nina and Shirchinbal, Dulguun and Wolff, Christina}, doi = {10.25932/publishup-59994}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-599948}, pages = {234}, year = {2023}, abstract = {Wie blicken verschiedene Wissenschaftsdisziplinen (auch intersektional) auf trans, inter und nicht-bin{\"a}re (TIN) Subjektpositionen jenseits der zweigeschlechtlichen Norm und Devianzen heterosexueller Lebensweisen? Wie werden Geschlechtervielfalt und Geschlechterrollen(-bilder) in zivilgesellschaftlichen Einrichtungen thematisiert? Die Autor*innen er{\"o}rtern hochaktuelle gesellschaftliche, rechtliche und alltagspraktische Diskurse und Forderungen: Unter anderem werden die {\"A}nderung des Personenstandsgesetzes, das geplante Selbstbestimmungsrecht, geschlechtergerechte Sprache und die Idee der „TINklusiven" Universit{\"a}t behandelt. Der erste Teil der Anthologie bietet theoretische Auseinandersetzungen {\"u}ber Wechselwirkungen zwischen Gesellschaft und Geschlechterkonstruktionen. Der zweite Teil wendet sich den praktischen Handlungsfeldern und institutionellen Bew{\"a}ltigungsstrategien zu, mit in denen bin{\"a}r strukturierte Organisationen und Instanzen realer Geschlechtervielfalt begegnen und intentional oder unbeabsichtigt Zweigeschlechtlichkeit und Heteronormativit{\"a}t (re-)produzieren bzw. dekonstruieren. Auch m{\"o}gliche Verst{\"a}rkungen anderer Diskriminierungsformen durch Othering-Prozesse im Genderdiskurs werden thematisiert. Im dritten und letzten Teil werden hochschulpolitische Spielr{\"a}ume anhand verfassungsrechtlicher Pr{\"u}fung und digitaler Handlungsoptionen ausgelotet.}, language = {de} } @book{HarkHackmannWolffetal.2023, author = {Hark, Sabine_ and Hackmann, Nina and Wolff, Christina and Voigt, Anna and Krall, Lisa and Niehus-Kettler, Melinda and Barry, C{\´e}line and Malmedie, Lydia and Rain Hornstein, Ren{\´e}_ and Giesche-von R{\"u}den, Doro* and Beck, Florian and Busch-Geertsema, Max and von R{\"o}mer, Jasper and Sch{\"u}tze, Christin and Rothermel, Ann-Kathrin and Lembke, Ulrike and Tischbirek, Alexander and G{\"o}tschel, Helene and H{\"u}hne, RyLee}, title = {Geschlechter in Un-Ordnung}, editor = {Hackmann, Nina and Shirchinbal, Dulguun and Wolff, Christina}, publisher = {Verlag Barbara Budrich}, address = {Opladen, Berlin, Toronto}, isbn = {978-3-8474-2679-0}, doi = {10.3224/84742679}, pages = {234}, year = {2023}, abstract = {Wie blicken verschiedene Wissenschaftsdisziplinen (auch intersektional) auf trans, inter und nicht-bin{\"a}re (TIN) Subjektpositionen jenseits der zweigeschlechtlichen Norm und Devianzen heterosexueller Lebensweisen? Wie werden Geschlechtervielfalt und Geschlechterrollen(-bilder) in zivilgesellschaftlichen Einrichtungen thematisiert? Die Autor*innen er{\"o}rtern hochaktuelle gesellschaftliche, rechtliche und alltagspraktische Diskurse und Forderungen: Unter anderem werden die {\"A}nderung des Personenstandsgesetzes, das geplante Selbstbestimmungsrecht, geschlechtergerechte Sprache und die Idee der „TINklusiven" Universit{\"a}t behandelt. Der erste Teil der Anthologie bietet theoretische Auseinandersetzungen {\"u}ber Wechselwirkungen zwischen Gesellschaft und Geschlechterkonstruktionen. Der zweite Teil wendet sich den praktischen Handlungsfeldern und institutionellen Bew{\"a}ltigungsstrategien zu, mit in denen bin{\"a}r strukturierte Organisationen und Instanzen realer Geschlechtervielfalt begegnen und intentional oder unbeabsichtigt Zweigeschlechtlichkeit und Heteronormativit{\"a}t (re-)produzieren bzw. dekonstruieren. Auch m{\"o}gliche Verst{\"a}rkungen anderer Diskriminierungsformen durch Othering-Prozesse im Genderdiskurs werden thematisiert. Im dritten und letzten Teil werden hochschulpolitische Spielr{\"a}ume anhand verfassungsrechtlicher Pr{\"u}fung und digitaler Handlungsoptionen ausgelotet.}, language = {de} }