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The AlpArray seismic network
(2018)
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.
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
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.
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
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.
Moving in the Anthropocene
(2018)
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.
Geschlechter in Un-Ordnung
(2023)
Wie blicken verschiedene Wissenschaftsdisziplinen (auch intersektional) auf trans, inter und nicht-binäre (TIN) Subjektpositionen jenseits der zweigeschlechtlichen Norm und Devianzen heterosexueller Lebensweisen? Wie werden Geschlechtervielfalt und Geschlechterrollen(-bilder) in zivilgesellschaftlichen Einrichtungen thematisiert? Die Autor*innen erörtern hochaktuelle gesellschaftliche, rechtliche und alltagspraktische Diskurse und Forderungen: Unter anderem werden die Änderung des Personenstandsgesetzes, das geplante Selbstbestimmungsrecht, geschlechtergerechte Sprache und die Idee der „TINklusiven“ Universität behandelt.
Der erste Teil der Anthologie bietet theoretische Auseinandersetzungen über Wechselwirkungen zwischen Gesellschaft und Geschlechterkonstruktionen. Der zweite Teil wendet sich den praktischen Handlungsfeldern und institutionellen Bewältigungsstrategien zu, mit in denen binär strukturierte Organisationen und Instanzen realer Geschlechtervielfalt begegnen und intentional oder unbeabsichtigt Zweigeschlechtlichkeit und Heteronormativität (re-)produzieren bzw. dekonstruieren. Auch mögliche Verstärkungen anderer Diskriminierungsformen durch Othering-Prozesse im Genderdiskurs werden thematisiert. Im dritten und letzten Teil werden hochschulpolitische Spielräume anhand verfassungsrechtlicher Prüfung und digitaler Handlungsoptionen ausgelotet.
Geschlechter in Un-Ordnung
(2023)
Wie blicken verschiedene Wissenschaftsdisziplinen (auch intersektional) auf trans, inter und nicht-binäre (TIN) Subjektpositionen jenseits der zweigeschlechtlichen Norm und Devianzen heterosexueller Lebensweisen? Wie werden Geschlechtervielfalt und Geschlechterrollen(-bilder) in zivilgesellschaftlichen Einrichtungen thematisiert? Die Autor*innen erörtern hochaktuelle gesellschaftliche, rechtliche und alltagspraktische Diskurse und Forderungen: Unter anderem werden die Änderung des Personenstandsgesetzes, das geplante Selbstbestimmungsrecht, geschlechtergerechte Sprache und die Idee der „TINklusiven“ Universität behandelt.
Der erste Teil der Anthologie bietet theoretische Auseinandersetzungen über Wechselwirkungen zwischen Gesellschaft und Geschlechterkonstruktionen. Der zweite Teil wendet sich den praktischen Handlungsfeldern und institutionellen Bewältigungsstrategien zu, mit in denen binär strukturierte Organisationen und Instanzen realer Geschlechtervielfalt begegnen und intentional oder unbeabsichtigt Zweigeschlechtlichkeit und Heteronormativität (re-)produzieren bzw. dekonstruieren. Auch mögliche Verstärkungen anderer Diskriminierungsformen durch Othering-Prozesse im Genderdiskurs werden thematisiert. Im dritten und letzten Teil werden hochschulpolitische Spielräume anhand verfassungsrechtlicher Prüfung und digitaler Handlungsoptionen ausgelotet.