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Country: Germany
623 Projects, page 1 of 125
  • Funder: EC Project Code: 659773
    Overall Budget: 171,461 EURFunder Contribution: 171,461 EUR

    As part of the Apollo lunar missions, four seismometers were deployed on the near-side of the Moon between 1969 and 1972, and operated continuously until 1977. There are many difficulties associated with determining lunar structure from these records. As a result, many properties of the moon, such as the thickness, density and porosity of the crust are poorly constrained. This hampers our ability to determine the structure, geochemical composition of the moon, its evolution, and ultimately the evolution of the solar system. This proposal uses modern seismic processing techniques to overcome these limitations. Using ambient noise tomography, it will provide a new, more accurate, model of the lunar crust and mantle. I will apply recent advances in the full waveform modelling of scattering at planetary scale by the host institution to the strongly scattering lunar crust. We will explore entirely new routes for planetary seismology by investigating single-station inverse problems building on recent work in rotational seismology pioneered at the host institution. The project is designed to develop a profile for myself as a planetary seismologist, and to position myself and the host institution to work on the Mars InSight mission in the future. InSight is a NASA Discovery mission, scheduled to land in September 2016, which will deploy a single seismometer on the surface of Mars. We combine the expertise of the researcher in surface wave analysis and tomographic modelling; the facilities and expertise of Ludwig Maximilian University (LMU) in ambient noise studies, full waveform modelling, modelling of seismic scatter and rotational seismology; and an interdisciplinary team of researchers with experience of the techniques and with diverse interests in geochemistry, geodynamics and planetary evolution.

  • Funder: EC Project Code: 752276
    Overall Budget: 159,461 EURFunder Contribution: 159,461 EUR

    Human fluid intelligence is characterized by a structured sequence of cognition, resulting in efficient application of rules to novel problems. In the brain, metabolic neuroimaging and lesion studies have linked fluid intelligence to a specific frontoparietal network, here called the multiple-demand (MD) network, comprising regions of lateral frontal, insular, dorsomedial frontal and parietal cortex. But how do MD functions determine fluid intelligence across stages of cognition? My extensive expertise in electroencephalography (EEG) source analyses and neural pattern classification techniques will allow me to assess time-resolved neural representations of novel rules in MD and perceptual cortex as a function of fluid intelligence, as well as the causal impact of MD cortex on earliest stages of perceptual encoding. Higher- and lower-intelligent subjects’ electrophysiological (EEG) and behavioural measures of novel rule implementation will be systematically analysed. Non-invasive neural stimulation (transcranial magnetic stimulation (TMS)) will be used in combination with EEG to draw causal conclusions on the specific role of MD and perceptual cortices in human fluid intelligence. My novel analysis approach may provide a new account on fluid intelligence: one aspect of low fluid intelligence may be the dysfunctional early filtering of task-relevant information in perceptual cortex, due to lack of top-down control from MD cortices, leading to sensory overload on later processing stages. The proposal’s outcomes will be both of high academic and commercial interest. Understanding the brain signatures underlying fluid intelligence is essential for more specific and cost-effective medical interventions. For example, decline of fluid intelligence due to healthy ageing is strongly correlated with high-cost medical conditions such as depression, which affect an increasing number of people in the ageing European population.

  • Funder: EC Project Code: 803302
    Overall Budget: 1,499,380 EURFunder Contribution: 1,499,380 EUR

    10 years after the adoption of the United Nations Declaration on the Rights of Indigenous Peoples in 2007, indigenous stakeholders act as global players in arenas such as the UN Convention on Climate Change, the Dakota Access pipeline in the USA, and the Humboldt-Forum in Berlin. Yet, until the 1960s, anthropological inquiries considered the same people as ‘vanishing’ and doomed to disappear. The so-called Indigenous Renaissance presents a remarkable phenomenon of late (post)modernity. How can this surprising process be understood and explained? The objective of this project is to study how indigenous actors evolved from ‘vanishing people’ to global players. The project is located at the disciplinary intersections between anthropology, art, history, philosophy, and politics; and aims at making a future-oriented contribution to (re)emerging indigeneities and the (re)negotiation of their (post)colonial legacies in and with Europe. While the label ‘indigeneity’ circulates globally, it is also defined as a place-based marker of identity. This project breaks new ground by incorporating both dimensions – global circulation and local experience – in a common framework. It does so by studying entangled indigeneities as transregional and transcultural formations along the transpacific intersections between North and South America, Australia and the South Pacific. By untangling these intersections through museums as research sites and laboratories, the project’s sub-objectives are: 1. to historically identify the moments and processes through which indigenous people became re-ascribed through anthropological discourses and their involvement therein, 2. to ethnographically study the ways and forms in which indigenous people appropriate these external ascriptions for self-insertion into global affairs, 3. to experimentally research, in exhibitionary environments, the layers of indigenous continuity beneath the discursive transformation from ‘vanishing people’ to global players.

  • Funder: EC Project Code: 694559
    Overall Budget: 2,150,080 EURFunder Contribution: 2,150,080 EUR

    This research project proposes a fundamental re-examination of the historiography of theatre in emerging countries after 1945 . It investigates the institutional factors that led to the emergence of professional theatre in the post-war period throughout the decolonizing world. The particular focus will be on the massive involvement of internationally coordinated ‘development’ and ‘modernization’ programs both East and West. The project will introduce the concepts of epistemic community, expert networks and techno-politics to theatre historical research as a means to historicize theatre within transnational and transcultural paradigms and examine its imbrication in globalization processes. This institutional and transnational approach will enable theatre studies to overcome its still strong national and local focus on plays and productions and connect it to current discourses on transnational history. The main objectives of this project are to: • examine how a global ‘epistemic community’ centred around theatre emerged in the post-war period; • investigate how ‘expert networks’ composed of government bodies, private foundations, transnational corporate philanthropy, local elites and individual artists sought to institutionalize particular forms and practices of professional theatre as an interconnected, transnational phenomenon; • develop a new interdisciplinary approach to theatre historiography by focusing on institutional structures, path dependencies and transnational imbrications rather than on works and authors. The principal investigator will bring to this project two decades of internationally recognized research into intercultural and global theatre. With its combination of institutional historiography and innovative research methods the project will provide a new foundation for current discussions of cultural policy and sustainability in emerging societies.

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  • Funder: EC Project Code: 694913
    Overall Budget: 2,496,880 EURFunder Contribution: 2,496,880 EUR

    Arterial hypertension is a major cardiovascular risk factor that affects between 10-40% of the population. Primary aldosteronism (PA) due to adrenal excess production of aldosterone is the most common secondary form of hypertension affecting 4-12% of hypertensives. Given the severe cardiovascular adverse effects of aldosterone excess early detection and individualized treatment of PA has important impact on clinical outcome and survival. However, the pathophysiology of PA is not well understood: While we recently identified specific genes underlying aldosterone producing adenoma, the most prevalent form of PA, bilateral adrenal hyperplasia, has remained enigmatic. It is the first hypothesis of this proposal that the pathophysiology of PA is a process based on two ‘hits’: agonistic angiotensin II type 1 receptor (AT1R) autoantibodies (proliferation, nodular hyperplasia) and somatic mutations (adenoma formation). It is the second hypothesis, that together, both factors induce not only aldosterone but also marked glucocorticoid excess. 1.) I will analyze prevalence and binding characteristics of AT1R autoantibodies as a pathophysiologic basis of PA. 2.) I will determine the effect of AT1R antibodies and genetic factors on cellular adrenal cortex models in vitro. 3.) I will extend these studies to specific in vivo genetic rodent models of PA. 4.) I will quantify aldosterone and glucocorticoid excess as disease effectors of AT1R autoantibodies and somatic mutations using liquid chromatography–mass spectrometry in PA. 5.) Using the generated data I will develop a pathophysiology-based concept of PA. This groundbreaking approach using innovative in vitro and in vivo models, state-of-the art genetic, immunologic and steroidobolomic techniques will uniquely open new avenues to the pathophysiologic understanding of PA. It will change our current understanding of PA, has high health impact and, thus, will pave the way to novel concepts of aldosterone excess and hypertension.

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