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UM

Maastricht University
Country: Netherlands
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498 Projects, page 1 of 100
  • Funder: EC Project Code: 628276
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  • Funder: EC Project Code: 101024942
    Overall Budget: 187,572 EURFunder Contribution: 187,572 EUR

    Elderly poverty is a prominent problem, and financial well-being in elderly is often considered low. A common cause for elderly poverty is a lack of sufficient pension awareness and engagement, especially at a young age. Independent of the pension scheme in a particular country, pension funds and policymakers around the world struggle to increase the engagement of pension plan consumers that would affect a consumer's future financial well-being positively. An often-proposed intervention to overcome the present bias that leads to not engaging with pension communications is to stimulate the imagery of the future self in pension plan consumers. Yet, current pension communications fall behind expectations in stimulating imagery of the future self and thus fail to improve pension awareness and engagement. In light of recent evidence on a new technology coined Augmented Reality (AR), this project proposes an experimental approach to investigate the impact of AR on the imagery of the future self and the downstream effects on pension awareness and engagement. Building on a series of laboratory, online, and field experiments, I apply findings from recent AR research in consumer behavior to find evidence and theoretically explain the effects AR can have on pension awareness and engagement. Combining findings from laboratory studies with field-evidence from the world’s third largest pension provider (APG) will shine light on how to improve pension communication with AR to improve future financial well-being. The proposed results are societally relevant as they can help to promote pension engagement that results in future financial well-being. My strong background in experimental consumer behavior research with a focus on AR technology and consumer engagement, combined with my supervisor’s expertise in pension and financial well-being research, and the strong research and training environment at Maastricht University (UM) will guarantee a successful project completion.

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  • Funder: EC Project Code: 665647
    Overall Budget: 150,000 EURFunder Contribution: 150,000 EUR

    Cardiac hypertrophy is the principal risk factor for the development of heart failure and lethal arrhythmias. A complex web of interconnected signalling pathways has been implicated in hypertrophy and species of non-coding RNA molecules, microRNAs, have been shown to regulate these pathways. The recognition of microRNAs as potential therapeutic targets marks the principal step towards new therapeutic concepts. The SIRENE project represents the advancement of the therapeutic strength of miRNA silencing in clinically relevant heart failure models towards a valuable proposition for counteracting pathological hypertrophic signalling and heart failure development. In specific, during the related ERC CALMIRS project, it was found that sustained knockdown of endogenous miR-199b in the adult mouse heart in vivo leads to profound protective effects against symptoms of heart failure. Therefore, a new class of RNA antagonists, targeting miRNAs is powerful and holds great promise to become the next generation therapeutics. At this stage the newly developed antagonists are unique in their affinity and specificity for miR-199b and current data demonstrates a profound rescue by miR-199b antagonists on heart failure symptoms such as pressure overload induced cardiac morphological, histological, functional and molecular abnormalities in mice. The challenge of the SIRENE project is to identify immediate and longer term opportunities for commercialisation with high clinical and commercial feasibility. Therefore different business models will be studied in terms of market research, IP strategy and business development to eventually consolidate a commercial strategy and business case for presenting our business proposition to strategic partners or venture capitalists. Simultaneously, dose-range finding and efficacy studies will be conducted in rats, a clinically relevant and larger animal model of heart failure, for further preclinical development.

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  • Funder: EC Project Code: 748944
    Overall Budget: 165,599 EURFunder Contribution: 165,599 EUR

    Problem: Muscle atrophy is defined as a decrease in muscle mass, and is a major problem in many patients with type 2 diabetes (T2D). Previous studies have linked a fatty liver to the development of muscle atrophy in T2D patients, but the exact mechanisms are unknown. Background: Many T2D patients are characterised by hepatic steatosis. We have preliminary data to suggest that secretion products from the steatotic liver play an important role in the development of muscle atrophy. Aim: we will identify how hepatic steatosis affects the liver secretory profile, and we will determine the impact of these secretion products on muscle protein metabolism. We will also identify novel liver-secreted proteins that are causally related to muscle atrophy, and validate these proteins in patients with hepatic steatosis and T2D. Hypothesis: We hypothesize that hepatic steatosis changes the liver protein secretion profile which negatively impacts muscle mass. We also expect to identify proteins that are causally related to muscle atrophy, and to validate these proteins in patients with liver steatosis and T2D. Methods: We will use a translational approach in which leads from human studies will be investigated in cell- and animal experiments and subsequently tested again in human subjects. We will combine functional metabolic assays, high-throughput molecular biology approaches, cell biology and in vivo studies to investigate whether secretion products from the liver play a role in the development of muscle atrophy. Outcome: This project is the first to investigate whether secretion products from the liver directly contribute to the loss of muscle mass in T2D patients. Our research is innovative and will provide crucial proof-of-concept information to further develop therapeutic approaches to treat or prevent muscle atrophy in T2D patients.

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  • Funder: EC Project Code: 277033
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