Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
The production of work. Welfare, labour-market and the disputed boundaries of labour (1880-1938). (PRODUCTION OF WORK)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Cultures and cultural production
Countries involved: Austria
Call:  (ERC-2007-StG, 2007)
Start date: 2008-10-01
End date: 2013-09-30
Duration (months): 60.0
Total project cost (EUR): 1372759.7
EU funding (EUR): 1372759.7
Participants: 1
Project status: CLOSED

Since the late 19th century modern social welfare policy has established social insurances in certain formalized cases of non-work: in case of old age, illness, invalidity, and unemployment. Doing so, it gained importance to control the entitlement to social welfare, national affiliation, willingness or (in-)ability to work. These new regulations of work and non-work also manifested new concepts of work and vocation. Simultaneously and with reference to the new social status of labour and to the new social rights debates on vagrancy, begging and the work-shy relived a new boom. Who should receive help? Who is a threat to the greater public good by refusing labour? Not every way to find income was equally acknowledged as work. There was a variety of activities changeable between work, hunting for a job, non-work, begging and vagrancy. These activities were suspected of being a cover of work-shyness and negative work. Through that they belonged to a disputed sphere at the margins of welfare, labour market and criminality. Within this context unskilled, occasional, seasonal labour were further marginalized and subject of re-definition. The project analyses these disputed boundaries of work. It will focus on Austria 1918-1938, but it aims at an international comparison and will consider relevant developments since the late 19th century, too. The project will study precarious forms of waged labour and non-work within the context of the organisations of labour market, search for employment and job placement. Therefore it is of fundamental importance to include marginal perspectives and practices into the analysis. How did concepts of vocational work and their binding character vary according to age, gender and ethnicity? In which ways were work and non-work defined? How were the distinctions and hierarchies practically implemented? Of particular interest is the tramping of the unemployed and forms of integration, support and control of ramblers being related to it.

Keywords: work,unemployment,social welfare,labour market,mobility,poverty
Natural course, pathophysiology, models for early diagnosis, prevention and innovative treatment of TNF Receptor Associated Periodic Syndrome TRAPS with application for all hereditary recurrent fevers (EUROTRAPS)

Framework: FP7 — Cooperation
Programme: Health
Destination: Translating research for human health
Action type: Collaborative project
Countries involved: France,France,United Kingdom,United Kingdom,Italy,Italy,Germany,Israel,Austria
Call:  (FP7-HEALTH-2007-A, 2007)
Start date: 2008-04-01
End date: 2011-09-30
Duration (months): 42.0
Total project cost (EUR): 3840772.0
EU funding (EUR): 2963225.0
Participants: 9
Project status: CLOSED

The TNF Receptor Associated Syndrome (TRAPS) is a rare disease of innate immunity, caused by mutations in TNFR1. It is characterised by recurrent bouts of fever and pain and mainly affects patients of European ancestry. The development of renal amyloidosis in up to 20% of cases makes it a potentially fatal disease. Corticosteroids and anti-TNF therapeutics have not been consistently effective in controlling attacks and preventing amyloidosis. EUROTRAPS is a multidisciplinary consortium, which by combining ideas, resources, and data from 7 academic participants and 2 SMEs from 6 countries, aims to gain insights into the natural course and pathophysiology of TRAPS, particularly in children. The creation of a European registry for TRAPS patients will facilitate the delineation of scores and outcome measures for diagnosis and treatment. We will examine additional pathways and genes involved in the phenotype. Kit assays will be developed to facilitate identification of disease mutations and susceptibility factors for amyloidosis and resistance to treatment. TNFR1 signalling, apoptosis and IL1 secretion abnormalities associated with TRAPS will be studied. We will also develop in vitro and humanised animal models to investigate innovative therapies. We expect that future developments in TRAPS will impact on all aspects of hereditary paediatric fevers, and thereby improve the wellbeing of patients and their families. A dedicated bipartite committee will undertake the complex task of managing this ambitious project, create a secure intranet, organise regular meetings, issue progress reports, oversee ethical, legal, financial, and gender issues (over 50% of the participants are female), adjust the workplan at each milestone, and guarantee dissemination, exploitation and protection of scientific information. The requested funding will cover salaries (over 200 person/months newly generated employments), equipment acquisition, consumables, and dissemination of knowledge.

Keywords: traps natural course pathophysiology auto-inflammatory innate immunity hereditary recurrent fevers
Mucosal protease and their inhibitors in inflammatory bowel disease: From etiopathogenetic insight to innovative therapy (IBDASE)

Framework: FP7 — Cooperation
Programme: Health
Destination: Translating research for human health
Action type: Collaborative project
Countries involved: Switzerland,Belgium,France,Germany,Spain,Italy,Sweden,United Kingdom
Call:  (FP7-HEALTH-2007-A, 2007)
Start date: 2008-03-01
End date: 2011-05-31
Duration (months): 39.0
Total project cost (EUR): 4120034.35
EU funding (EUR): 2973550.0
Participants: 10
Project status: CLOSED

IBDase addresses the etiology and pathogenesis of inflammatory bowel disease (IBD) with a multidisciplinary plan for innovative diagnosis and therapy focused on mucosal proteases and their inhibitors (P/PIs). The incidence of IBD, a multifactorial disease influenced by environmental factors in a background of complex genetic susceptibility, is rising, particularly among European children. Current therapies lack efficacy and specificity. The gut microflora plays a crucial role in IBD but the cause for this is still poorly understood. Research implicating P/PIs in gut mucosal inflammation requires further mechanistic insight and the P/PIs relevant in human IBD need to be identified. To this end we will identify human mucosal P/PI polymorphisms affecting expression levels and/or activity of P/PIs and analyse their genotype/phenotype associations in IBD patient cohorts across Europe. IBD-associated P/PIs will be characterised by biochemical properties, expression in human clinical samples and manipulation of experimental models. Their interaction with microflora will be examined in animal models with controlled colonisation of the gut and in vitro co-culture models of intestinal mucosa and bacteria. In vivo studies will use targeted, well-established and new mouse models and evaluate zebrafish as an IBD model. Molecular mechanisms for involvement of IBD specific P/PI gene variants in the inflammatory response will be proposed. Therapeutics development will focus on specific inhibition or promotion of proteolysis in the intestinal mucosa, and select at least three validated P/PI of the intestinal mucosa for follow-up in clinical trials. Embracing the concept of tailoring treatment to individual patient characteristics to increase efficacy and reduce side-effects, IBDase strengthens international visibility of IBD related research, policies and industry and fosters IBD related research to the benefit of European society in both patient care and economic interest.

Keywords: animal model gene polymorphism ibd microflora pathogenesis personalised medicine proteolysis therapy intestine
Identification and characterization of novel human telomere-related biomarkers that aid cancer management by improving patient diagnosis, treatment selection, response monitoring, and drug development (TELOMARKER)

Framework: FP7 — Cooperation
Programme: Health
Destination: Translating research for human health
Action type: Collaborative project
Countries involved: United Kingdom,United Kingdom,Switzerland,Germany,Sweden,Spain,France,Germany
Call:  (FP7-HEALTH-2007-A, 2007)
Start date: 2008-02-01
End date: 2011-01-31
Duration (months): 36.0
Total project cost (EUR): 3683902.4
EU funding (EUR): 2848490.0
Participants: 8
Project status: CLOSED

Telomeres are DNA-nucleoprotein structures that protect the ends of human chromosomes through the formation of a ‘cap’ that prevents exonucleolytic degradation, inter- & intra-chromosomal fusion and subsequent chromosomal instability. Telomerase, the ribonucleoprotein enzyme that maintains linear chromosomal DNA ends by the addition of TTAGGG repeats, is completely repressed or present only at low, tightly regulated levels in normal human cells as a safeguard against cancer. Normally, telomere shortening in the absence of sufficient telomerase leads to telomere uncapping, activation of a DNA damage response, and either replicative senescence or apoptosis. Paradoxically, however, under certain conditions (when damage response pathways are defective, eg through p53 gene mutation) unchecked telomere shortening can generate a chronic genomic instability that drives and accelerates clonal evolution and cancer progression. As a result, telomeres are dysfunctional in human cancers. Individual protein components of the core telomere higher-order structure (known as the telosome, or the ‘shelterin’ complex) represent highly promising candidates for novel biomarkers of telomere dysfunction and human cancer progression. In this project (‘TeloMarker’) we have assembled the most experienced and talented scientists in telomere biology in the EU into a collaborative research consortium that will identify, characterize and validate novel telomere-related biomarkers. Biomarker discovery will be based both on known telosomal components and newly discovered affiliated proteins, as well as on telomerase and its recruitment factors. Novel telomere-related cancer biomarkers promise radically to improve early diagnosis, patient treatment selection, prognostic evaluation, and outcome monitoring, as well as furnishing new molecular targets for the development of novel small molecule anti-cancer drugs.

Keywords: cancer,biomarkers,diagnosis,telomere,telomerase,drug targets
The Design of International Institutions: Legitimacy, Effectiveness and Distribution in Global Governance (DII)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Institutions, values, beliefs and behaviour
Countries involved: Sweden
Call:  (ERC-2007-StG, 2007)
Start date: 2009-01-01
End date: 2014-12-31
Duration (months): 72.0
Total project cost (EUR): 1651200.0
EU funding (EUR): 1651200.0
Participants: 1
Project status: CLOSED

One of the most profound trends in global governance over the past two decades is the growing extent to which international institutions offer mechanisms for the participation of transnational actors. This project will explore two central research questions, pertaining to the causes and effects of this shift in the design of international institutions: (1) Why have international institutions increasingly opened up to transnational actor involvement? (2) What are the consequences of involving transnational actors for the democratic legitimacy, problem-solving effectiveness, and distributional effects of international institutions? These are research questions that previously have not been explored systematically in existing literatures on international institutional design, transnational actors in global governance, and democracy beyond the nation-state. This project opens up a new research agenda on the design of international institutions through an ambitious combination of novel theory development and comparative empirical research. Theoretically, the project develops and tests alternative hypotheses about the causes and effects of transnational participation in international policy-making. Empirically, the project explores the dynamics of transnational participation through comparative case studies of five major international institutions, supplemented with a large-n mapping of formal mechanisms of transnational access in a broader sample of institutions. The project will help to establish an internationally competitive research group of post-doc researchers and Ph.D. students devoted to international institutional design, and consolidate the position of the principal investigator as a leading researcher in this field.

Keywords: international institutions,global governance,transnational actors,legitimacy,effectiveness,distribution
Vesicular protein sorting in the Golgi apparatus (PROTEIN SORTING)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: United Kingdom
Call:  (FP7-PEOPLE-2007-4-3-IRG, 2007)
Start date: 2007-09-03
End date: 2011-09-02
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

The correct sorting of proteins is an important challenge for all eukaryotic cells. Problems in protein sorting are known to lead to various developmental defects or acquired diseases in humans. In the secretory pathway, whose main sorting hub is the Golgi apparatus, vesicular transport is used to sort proteins. To maintain the unique composition of different Golgi cisternae for example, resident Golgi-enzymes are continuously sorted away from their substrates, the secreted proteins. This is mostly mediated by COPI dependent retrograde vesicle transport, during which vesicles of different compositions are targeted to the various cisternae. The COG complex, several Rab GTPases and golgins, all function during the process referred to as vesicle tethering, to mediate the targeting of COPI vesicles. The molecular details of vesicle tethering, which is an essential process during every vesicle transport step, are unknown. It is believed to be the first encounter between vesicle and target membrane, and to encompass a series of protein-protein interactions leading to membrane fusion. This proposal aims to determine the interaction-topology of the involved proteins, and the identities of hitherto unknown factors, to establish a molecular mechanism of vesicle tethering at the Golgi. For this purpose we will use a combination of biochemical and genetic methods. Using in vivo immunoprecipitations and in vitro interaction assays we will reveal the interaction map of tethering. To uncover novel factors involved in the process we will take advantage of the known glycan processing defects associated with COG deficiencies. We will devise an RNAi based screen selecting for phenocopies of the glycosylation defects by using a specific combination of toxic lectins that selectively bind to the surface glycans of wild type cells. This work should expand our knowledge about both vesicle tethering and the organization of glycan chain synthesis in the Golgi.

Keywords: cell biology,molecular biology
Systems Biology of T-cell Activation in Health and Disease (SYBILLA)

Framework: FP7 — Cooperation
Programme: Health
Destination: Translating research for human health
Action type: Collaborative project
Countries involved: Germany,United Kingdom,Spain,Austria,Switzerland,Germany,Finland,France,Germany,France,Italy,United States,Finland,Spain,Germany,Italy,Czechia
Call:  (FP7-HEALTH-2007-A, 2007)
Start date: 2008-04-01
End date: 2013-09-30
Duration (months): 66.0
Total project cost (EUR): 14636311.41
EU funding (EUR): 11100000.0
Participants: 22
Project status: CLOSED

T-cell activation, whether induced by pathogens or auto-antigens, is a complex process relying on multiple layers of tightly controlled intracellular signalling modules that form an intricate network. Defects in this network can cause severe and chronic disorders such as autoimmune diseases. Although 5% of the population suffer from these diseases, only a few therapeutic treatments are available. To a large extent this is attributed to the lack of systems-level insights, which would provide concepts of how to modulate T-cell activation. The SYBILLA project groups 14 partners from 9 different EU countries, including 3 SMEs. Through a multidisciplinary effort it aims to understand at the systems’ level, how T-cells discriminate foreign from auto-antigens. Towards this goal, a transgenic mouse system will be used as a tractable physiological model. Data will be validated in human T-cells and a humanised mouse model for multiple sclerosis. SYBILLA will develop technological and mathematical tools to generate and integrate high-density quantitative data describing T-cell activation. Proteomics, transcriptomics, metabolomics, imaging and multiplexed biochemical techniques will be applied to obtain holistic maps of T-cell signalling networks and to achieve a quantitative understanding of the network and its regulation in response to different inputs. Building upon our existing network model, constant iterations will be used to develop more robust dynamic models to describe the network’s response to perturbations. This will culminate in the generation of a Virtual T-Cell, allowing computer simulation to refine the predictability of physiological and pathophysiological reactions. SYBILLA’s impact on EU biopharmaceutical competitiveness will be enormous through identification of new pharmacologic targets, optimised prediction of immunomodulatory drug efficacy, discovery of new concerted biomarkers and improvement of personalised medication for treating autoimmune diseases.

Keywords: dynamic models,multiple sclerosis,tcr/cd3,signalling network,auto-immune disease
Eukaryotic unicellular organism biology – systems biology of the control of cell growth and proliferation (UNICELLSYS)

Framework: FP7 — Cooperation
Programme: Health
Destination: Translating research for human health
Action type: Collaborative project
Countries involved: Sweden,Denmark,Switzerland,Spain,United Kingdom,United Kingdom,Italy,Germany,United Kingdom,Austria,United Kingdom,United Kingdom,Germany,Netherlands
Call:  (FP7-HEALTH-2007-A, 2007)
Start date: 2008-04-01
End date: 2013-03-31
Duration (months): 60.0
Total project cost (EUR): 15436639.65
EU funding (EUR): 11700000.0
Participants: 18
Project status: CLOSED

The overall objective of UNICELLSYS is a quantitative understanding of fundamental characteristics of eukaryotic unicellular organism biology: how cell growth and proliferation are controlled and coordinated by extracellular and intrinsic stimuli. Achieving an understanding of the principles with which bio-molecular systems function requires integrating quantitative experimentation with simulations of dynamic mathematical models. UNICELLSYS bring together a consortium of leading European experimental and computational systems biologists that will study cell growth and proliferation at the levels of cell population, single cell, cellular network, large-scale dynamic systems and functional module. Building computational reconstructions and dynamic models will involve different precise quantitative measurements as well as complementary approaches of mathematical modelling. A major challenge will be the generation of comprehensive dynamic models of the entire control system of cell growth and proliferation, which will require integration of smaller sub-models and reduction of complexity. Implementation of the models will allow observing responses to altered growth conditions zooming in seamlessly from populations consisting of cells of different replicative age and cell cycle stage via genome-wide molecular networks, large dynamic systems to detailed functional modules. Employing computational simulations combined with experimentation will allow discovering new and emerging principles of bio-molecular organisation and analysing the control mechanisms of cell growth and proliferation. The project will deliver new knowledge on fundamental eukaryotic biology as well as tools for quantitative experimentation and modelling. Detailed plans for dissemination and exploitation will ensure that UNICELLSYS will have major impact on the development of Systems Biology in Europe ensuring a competitive advantage of Europe in dynamic quantitative modelling of bio-molecular processes.

Keywords: cell cycle,signal transduction,metabolism,quantitative measurements,mathematical modelling,simulation
Neurobiological Mechanisms of Memory Loss in Alzheimer's Disease (MEMOLOAD)

Framework: FP7 — Cooperation
Programme: Health
Destination: Translating research for human health
Action type: Collaborative project
Countries involved: Finland,Hungary,Sweden,Germany,France,United Kingdom,Ireland
Call:  (FP7-HEALTH-2007-A, 2007)
Start date: 2008-02-01
End date: 2013-07-31
Duration (months): 66.0
Total project cost (EUR): 3928486.2
EU funding (EUR): 2998712.0
Participants: 7
Project status: CLOSED

The MEMOLOAD project will focus on the molecular and biological mechanisms underlying memory loss that occurs in Alzheimer’s disease, the leading cause of dementia and an enormous medical, social and economic challenge to Europe. Several lines of evidence point to accumulation of beta-amyloid peptide (Aß) in the brain as the key pathologic event in the disease. There is growing evidence that Aß causes memory loss by directly or directly interacting with the known key signalling pathways involved in memory consolidation. However, at present the data is fragmentary and consists mainly of single observations in particular models (cell culture, brain slice, in vivo). In most cases, we still lack the evidence that a clear molecular level interaction translates into memory impairment in vivo. The objective of this proposal is to elucidate the molecular level mechanisms by which accumulation of Aß in the brain results in impaired synaptic plasticity and memory loss. The MEMOLOAD consortium consists of a well-balanced mixture of the seven best available European research groups in terms of research experience on both the mechanisms of memory consolidation and the pathophysiology of Alzheimer’s disease. The current research topic is thus the primary research interest of all partners. MEMOLOAD will significantly contribute to a better understanding of brain memory mechanisms at the behavioural, network, synaptic and molecular levels and of dysfunction at all these levels in Alzheimer’s disease (AD). The knowledge acquired during the course of MEMOLOAD will translate into new validated in vitro and in vivo models for the memory impairing effect of Aß and will feed into industrial development leading to new therapies. The output of MEMOLOAD will include both identification of new drug targets and development of novel peptidomimetic compounds that neutralize the deleterious effects of most harmful Aß species.

Keywords: amyloid beta-peptide,oligomer,cortex,hippocampus,spatial memory,recognition memory,long-term potentiation,receptor trafficking,memory consolidation