ERC FUNDED PROJECTS

The main goal of the proposed research is to investigate the possibility of allowing below-ground support systems to respond to strong seismic shaking by going beyond a number of thresholds that would conventionally imply failure and are today forbidden by codes. Such thresholds include : (a) sliding at the soil-foundation interface ; (b) separation and uplifting of a shallow foundation from the soils ; (c) mobilization of bearing capacity failure mechanism for shallow foundations ; (d) structural yielding of pile foundations ; (e) combination of some of the above. Whereas under static loading conditions a slight exceedance of such thresholds leads to failure, the oscillatory nature of seismic shaking will allow such exceedances for a short period of time, with perhaps no detrimental or irreparable consequences. The latter take the form of permanent foundation displacements, rotations, or injuries , which the designer will aspire to confine within rational limits. The motivation and the need for this research has come from : (i) observations of actual behaviour in a variety of earthquakes ; conspicuous examples : the permanent tilting , overturning, and often survival of numerous buildings on extremely soft soil in Adapazari during the Kocaeli 1999 earthquake ; (ii) the foundation design of a number of critical structures (e.g., major bridge pier, air control tower, tall monuments, elevated water tanks,) against large seismic actions ; the disproportionately large overturning moment and/or base shear force of such slender structures can hardly be faced with today s conventional foundation methods, (iii) the need to seismically retrofit and rehabilitate older structures and historical monuments; (iv) structural yielding of pile foundations is now detectable (thanks to technological advances), thus eliminating one of the reasons for avoiding it.

2 399 992 €

Start date: 2008-12-01, End date: 2013-10-31

Unconventional superconductivity is extensively sought for in contemporary research. Of particular interest are chiral superconductors which possess non-trivial topological properties resulting in superconducting (SC) order parameters (OPs) that may break time-reversal symmetry (TRS). The possibility of applications to topological quantum computation have placed such materials at the forefront of condensed matter research. Recent measurements of the polar Kerr effect (PKE), in which a rotation of polarization is detected for a beam of light reflected from the surface of a superconductor, have emerged as a key experimental probe of TRS breaking. Here we propose the development of a new generation of spectroscopic instrumentation for the PKE spectroscopy in the sub-THz frequency range, the energy scale that is comparable with the SC gap magnitude of unconventional superconductors. The THz range PKE spectroscopy will enable to study the broken symmetries, the origin of unconventional pairing, the in-gap collective modes, and the structures of the SC OPs. We plan to measure the PKE at sub-THz frequencies and with sub-milli-radian angular resolution from a variety of unconventional superconductors that are cooled to 100 mK, deep into SC state. The aim is to understand the basic mechanisms leading to unconventional superconductivity in these systems in order to find answers to the fundamental questions, such as: What is the structure of the SC gap in Sr2RuO4, URu2Si2, and UPt3? Is the TRS broken in (a) the Hidden Order state and in (b) SC state of URu2Si2? Which symmetries are broken at the transition from the HO state into the unconventional SC state? – and to elucidate the microscopic origin of superconductivity in the new families of unconventional superconductors. In a broader view, the project will keep Estonian physics on the forefront of science through new scientific contacts and will promote physics education by engaging students and postdocs in the research.

2 489 976 €

Start date: 2021-07-01, End date: 2026-06-30

Necrosis contributes critically in devastating human pathologies such as stroke, ischemia, and age-associated neurodegenerative disorders. Ageing increases susceptibility to neurodegeneration, in diverse species ranging from the lowly nematode Caenorhabditis elegans to humans. The mechanisms that govern necrotic neurodegeneration and its modulation by ageing are poorly understood. Autophagy has been implicated in necrosis and neurodegeneration, both with pro-survival and a pro-death roles. Autophagic flux declines with age, while induction of autophagy enhances longevity under conditions such as low insulin/IGF1 signalling and dietary restriction, which extend lifespan across diverse taxa. Our recent findings indicate that organelle-specific autophagy, including mitophagy, pexophagy and nucleophagy, is an important, evolutionarily conserved, determinant of longevity. We propose to dissect the molecular underpinnings of neuron vulnerability to necrosis during ageing, focusing on cargo-specific macroautophagy. To this end, we will implement a multifaceted approach that combines the power and versatility of C. elegans genetics with advanced, in vivo neuronal imaging and microfluidics technology. Our objectives are fourfold. First, we will monitor autophagic flux of organellar cargo, during neurodegeneration, under conditions that alter lifespan and identify mediators of organelle-specific autophagy in neurons. Second, we will conduct genome-wide screens for modifiers of age-inflicted neurodegeneration. Third, we will interrogate nematode models of human neurodegenerative disorders for organelle-specific autophagy and susceptibility to necrosis, upon manipulations that alter lifespan. Fourth, we will investigate the functional conservation of key mechanisms in mammalian models of neuronal necrosis. Together, these studies will deepen our understanding of age-related neurodegeneration and provide critical insights with broad relevance to human health and quality of life.

2 254 109 €

Start date: 2017-01-01, End date: 2021-12-31

Mesenchymal cells (MCs) of the intestinal lamina propria refer to a variety of cell types, most commonly intestinal myofibroblasts, fibroblasts, pericytes, and mesenchymal stromal cells, which show many similarities in terms of origin, function and molecular markers. Understanding the physiological significance of MCs in epithelial and immunological homeostasis and the pathophysiology of chronic intestinal inflammatory and neoplastic disease remains a great challenge. In this proposal, we put forward the challenging hypothesis that, especially during acute or chronic inflammatory and tumorigenic conditions, MCs play important physiological roles in intestinal homeostasis regulating key processes such as epithelial damage, regeneration and tumorigenesis, intestinal inflammation and lymphoid tissue formation. We further posit that a unifying principle underlying such functions would be the innate character of MCs, which we hypothesize are capable of directly sensing and metabolizing innate signals from microbiota or cytokines in order to exert homeostatic epithelial and immunological regulatory functions in the intestine. We will be using genetic approaches to target innate pathways in MCs and state of the art phenotyping to discover the physiologically important signals orchestrating intestinal homeostasis in various animal models of intestinal pathophysiology. We will also study MC lineage relations and plasticity during disease and develop ways to interfere therapeutically with MC physiology to achieve translational added value for intestinal diseases, as well as for a range of other pathologies sharing similar characteristics.

2 590 000 €

Start date: 2014-07-01, End date: 2019-06-30