ERC FUNDED PROJECTS

Today, Europe’s linguistic landscape is shaped almost entirely by a single language family: Indo-European. Even by the dawn of history, a patchwork of Indo-European subgroups, Germanic, Celtic, Italic, Baltic, Slavic and Greek, was covering the continent, and over the centuries, these subgroups evolved into the modern European languages, among which Russian, Italian, German, Lithuanian and Swedish, as well as the global lingua francas French, Spanish, and English. The Indo-Europeanization of Europe was probably one of the most profound linguistic shifts ever to have taken place in the prehistory of Europe. The origin of the European languages, unsurprisingly, is therefore a matter of intense academic debate. There are currently only two prehistoric events that in the present academic debate are considered as likely driving factors behind the spread of Indo-European speech. One the one hand, there are those historical linguists who by meticulous comparison of the different Indo-European languages have reconstructed a language and culture that is typical of the early Bronze Age. Terminology for horse-riding and wagon technology provides a possible link to the expansion of the Yamnaya culture on the Pontic-Caspian steppes, which was fueled by the invention of the wheel and the domestication of the horse. Others have suggested that the Indo-European languages diffused from Anatolia together with another major prehistoric event, the spread of agriculture to Europe between the 8th and 5th millennium. The debate has remained unresolved for over two decades, but a new approach produces potentially decisive results. By studying prehistoric loanwords absorbed by the speakers of Indo-European when they entered Europe, and test the resulting cultural implications against the available archaeological record, new light can be shed on the language of Europe’s first farmers, and whether or not they spoke a form of Indo-European.

1 499 578 €

Start date: 2017-07-01, End date: 2022-06-30

The Great Hunger (1845-49) radically transformed Ireland: it led to the wide-scale eviction of farmers, killed one million of the rural population, and caused massive emigration to other parts of the British Empire and the United States. Moreover, the Great Famine encouraged anti-English, nationalist sentiments and its trauma is pivotal to the development of an Irish postcolonial consciousness between 1847-1921. There is a vast unexplored transatlantic corpus of prose fiction, written between the aftermath of the Famine and the Anglo-Irish Treaty of 1921, which remembers the years of starvation and diaspora. My project is the first to inventorise and bring together this under-researched body of literature, written in Ireland and by Irish immigrants in England, Canada and the United States. This fiction requires intensive examination for significant reasons, offering alternative perspectives on how the Famine was culturally experienced than previous studies have displayed, and representing subaltern voices and recollections. Moreover, the texts are written in the homeland as well as in diaspora, by migrated Irish or their descendants. An examination of the corpus will therefore move beyond the largely nation-oriented frontiers of cultural memory studies towards innovative, transnational approaches. The project specifically investigates how remembrance is mediated through time, from one generation to another, and space, in diaspora. It aims to evolve a novel theoretical model about the interaction between temporal and spatial relocation in literary remembrance. This pioneering model will generate groundbreaking insights into the interaction between memory and ethnic identity in comparative contexts of cultural dislocation, a colonised homeland and migrant communities; and in processes of cultural relocation: de-colonisation and ethnic integration. At the same time, the project will analyse genre aspects which play a dynamic role in processes of cultural remembrance, contributing a new perspective to the interdisciplinary debate on media of recollection in cultural memory studies.

741 000 €

Start date: 2010-10-01, End date: 2015-09-30

Obesity has reached epidemic proportions globally. At least 2.8 million people die each year as a result of being overweight or obese, the biggest burden being obesity-related diseases. It is now clear that inflammation is an underlying cause or contributor to many of these diseases, including type 2 diabetes, atherosclerosis, and cancer. Recognition that the immune system can regulate metabolic pathways has prompted a new way of thinking about diabetes and weight management. Despite much recent progress, most immunometabolic pathways, and how to target them, are currently unknown. One such pathway is the cross-talk between invariant natural killer (iNKT) cells and neighboring adipocytes. iNKT cells are the innate lipid-sensing arm of the immune system. Since our discovery that mammalian adipose tissue is enriched for iNKT cells, we have identified a critical role for iNKT cells in regulating adipose inflammation and body weight. The goal of this project is to use a multi-disciplinary approach to identify key signals and molecules used by iNKT cells to induce metabolic control and weight loss in obesity. Using immunological assays and multi-photon intravital microscopy, cells and pathways that control the unique regulatory functions of adipose iNKT cells will be identified and characterised. Novel lipid antigens in adipose tissue will be identified using a biochemical approach, perhaps explaining iNKT cell conservation in adipose depots, and providing safe tools for iNKT cell manipulation in vivo. Finally, using proteomics and whole body metabolic analysis in vivo, novel ‘weight-loss inducing’ factors produced by adipose iNKT cells will be identified. This ambitious and high impact project has the potential to yield major insights into immunometabolic interactions at steady state and in obesity. The ability to activate or induce adipose iNKT cells holds remarkable potential as an entirely new therapeutic direction for treating obesity and type 2 diabetes.

1 804 052 €

Start date: 2016-09-01, End date: 2021-08-31

"Inflammasomes are intracellular danger-sensing protein complexes that are important for host protection. They initiate inflammation by controlling the activity of the proinflammatory cytokine interleukin-1β (IL-1β). Unlike most other cytokines, IL-1β is produced and retained in the cytoplasm in an inactive pro-form. Inflammasome-dependent maturation of proIL-1β is mediated by the common component of all inflammasomes, the protease caspase-1. Caspase-1 also controls the secretion of IL-1β, but the mechanism and route of secretion are unknown. We have recently demonstrated that the ability of caspase-1 to control IL-1β secretion is not dependent on its protease activity, but rather on a scaffold or adapter function of caspase-1. Furthermore, we and others could show that caspase-1 can control the secretion of non-substrates like IL-1α. These insights provide us with new and potentially revealing means to investigate the downstream effector functions of caspase-1, including the route and mechanism of IL-1 secretion. We will develop new tools to study the process of IL-1 secretion by microscopy and the novel mode-of-action of caspase-1 through the generation of transgenic models. Despite the important role of IL-1 in host defence against infection, dysregulated inflammasome activation and IL-1 production has a causal role in a number of acquired and hereditary auto-inflammatory conditions. These include particle-induced sterile inflammation (as is seen in gout and asbestosis), hereditary periodic fever syndromes, and metabolic diseases like diabetes and atherosclerosis. Currently, recombinant proteins that block the IL-1 receptor or deplete secreted IL-1 are used to treat IL-1-dependent diseases. These are costly treatments, and are also therapeutically cumbersome since they are not orally available. We hope that a better understanding of caspase-1-mediated secretion of IL-1 will unveil mechanisms that may serve as targets for future therapies for these diseases."

1 495 533 €

Start date: 2014-03-01, End date: 2019-02-28