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Goethe University Frankfurt

Goethe University Frankfurt

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278 Projects, page 1 of 56
  • Funder: European Commission Project Code: 707932
    Overall Budget: 171,461 EURFunder Contribution: 171,461 EUR

    The left ventral occipito-temporal cortex (lvOT) is an integral part of the ventral visual processing stream and is consistently activated in response to visual words. Recently, I developed a computational implementation of the lvOT functioning during visual word recognition, the sparse familiarity model (SFM). The single assumption of the SFM is that the statistical patterns of letter string familiarity are the fundament of lvOT functioning. The SFM is able to simulate prominent lvOT benchmark contrasts and its simulations predict brain activation of the lvOT in multiple fMRI studies. The main aim of the present proposal is to use the model to systematically investigate hotly debated topics in word recognition research concerning current theoretical approaches for the lvOT: (1) The influence of learning and (2) domain specificity (i.e. for words) vs. generalization (i.e., to face and object recognition) of lvOT function and neuronal populations. In the course of these investigations, the SFM will be developed into a learning model and a generalized model for word, face, and object recognition. Central to this will be high-density electrophysiological measurements (MEG) that sample brain activation with high temporal resolution and reasonable spatial resolution, to allow connectivity analysis at different time points. The MEG measurement, in addition to fMRI measures, will be essential to test theoretical assumptions concerning the proposed two stages of the SFM that differ fundamentally in terms of neuronal and cognitive mechanisms. Critical will be the association of these stages to different time windows and assumptions about the brain networks involved. The host, Prof. Fiebach at Frankfurt University, has a strong focus on the neurocognitive basis of language and access to an MEG, which is essential for realizing this project. To summarize, the goal of the project is to establish the sparse familiarity model and extend its functioning to resolve current debates.

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  • Funder: European Commission Project Code: 101040070
    Overall Budget: 1,498,860 EURFunder Contribution: 1,498,860 EUR

    The rise of the far right poses a profound challenge to global politics. Diverse far-right actors, such as political parties, civil society groups, and social movements, have been gaining support in domestic contexts, while intensifying their transnational contacts. As these groups focus on national sovereignty and share a stance against globalization, they often contest international organizations (IOs) and their policies. Yet their impact on international organizations differs: On the one hand, far-right groups have profoundly changed negotiations on the Global Compact for Migration in the UN. On the other hand, radical-right parties in the European Parliament have hardly brought about any deeper policy changes. Why does transnational far-right contestation have varying effects on international organizations? While scholars have analyzed far-right actors in domestic politics, knowledge about their transnational activities and effects is limited. FARRIO fills this gap empirically, theoretically, and methodologically. Empirically, it compares effects of far-right contestation on the EU, the UN, and its specialized agencies/treaties in four central policy fields (migration, women's rights, climate change, and public health). Theoretically, it proposes that IO changes depend on the directness of far-right strategies and the liberal character of international organizations. It thereby breaks new ground in identifying scope conditions for far-right impact highly relevant for research on transnational protest as well as IO resilience and change. Methodologically, FARRIO draws on and further develops quantitative and qualitative methods. It adapts protest event and networks analysis to map transnational far-right contestation, also including social media data. Bridging Comparative Politics, Social Movement Studies, and the study of International Relations, FARRIO assesses the challenge far-right actors pose to IOs as well as what measures are suited to respond to it.

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  • Funder: European Commission Project Code: 101104566
    Funder Contribution: 189,687 EUR

    Many heterothermic mammals exploit multi-day torpor (i.e. hibernation) to face harsh climates. The timings and the regulations of this process are controlled and influenced by several intrinsic and extrinsic factors such as e.g. the circannual biological clock of the animal, the day-length, the spring temperature, the snow-melt date. Yet, how these animals answer(ed) global climate changes is still a matter of debate. With the AROUSE project I will examine the hibernation timing and the bone elemental metabolism of small mammals from a new unexplored perspective, by analyzing well-dated fossil and modern hibernating rodent teeth straddling the last glacial-interglacial cycle. Specifically, I will exploit the enamel incisor micro-chemistry (high-spatially resolved elements and isotopes), histomorphometry and proteomics of geographically-constrained Alpine marmots to: 1) precisely measure sex-specific hibernation length; 2) investigate metabolic changes in relation to (paleo)climate seasonal fluctuations; 3) unravel dental enamel secretion and mineralization behavior during winter torpor; 4) search for specific dental chemical biomarkers of hibernation, transferable to other disciplines. For the first time, this project will provide a robust tool for the retrospective study of hibernation events in dental specimens, allowing to deepen our knowledge about hibernation plasticity but also to possibly investigate the evolutionary trajectories of torpor in deep-time. AROUSE will also help to understand how marmots adapted to secular climate variations, possibly forecasting the effects of global warming on modern hibernating mammals.

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  • Funder: European Commission Project Code: 617891
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  • Funder: European Commission Project Code: 101055213
    Overall Budget: 2,496,690 EURFunder Contribution: 2,496,690 EUR

    The endoplasmic reticulum (ER) is the most extensive endomembrane system of the cell that undergoes continuous remodelling and adaptation to fulfil required functions in synthesis and transport of cellular components. A major driver of ER remodelling is ER-phagy, a selective autophagy pathway that targets excess or damaged portions of ER for degradation. By linking the ER membrane to the autophagic machinery, ER-phagy receptors play central roles in this process. However, beyond the identities of ER-phage receptors, we have little understanding of the mechanisms underlying ER-phagy and the dynamics of ER remodelling. This proposal aims to decipher the mechanisms by which ER-phagy receptors, especially those containing reticulon-homology domains (RHD), drive the dynamic process of ER remodelling in a cell-type specific fashion. We will determine how ER-phagy is regulated by site-specific receptor ubiquitination and by the formation of ER-phagy receptor clusters, particularly how ubiquitination regulates cluster size, dynamics, localization, identity and composition. We will combine structural, computational and functional approaches to determine, at the highest possible resolution, how ubiquitination and clustering of ER-phagy receptors controls the multistep process of ER-phagy and membrane remodelling. We aim for a comprehensive understanding of the distinct mechanisms involved in ER remodelling in different cell types and in response to various stress conditions. This mechanistic knowledge is essential to explain how changes in ER-phagy and ER remodelling impact on the pathophysiology of human diseases from bacterial infections to neurological disorders. These novel and ground-breaking discoveries will elucidate an ER-phagy receptor code controlling ER remodelling in health and disease. Moreover, ER-REMODEL will provide a conceptual framework for future studies into the dynamic regulation of other cellular organelles via ubiquitin-driven selective autophagy.

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