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ULB

Université Libre de Bruxelles
Country: Belgium
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309 Projects, page 1 of 62
  • Open Access mandate for Publications and Research data
    Funder: EC Project Code: 950289
    Overall Budget: 1,499,970 EURFunder Contribution: 1,499,970 EUR
    Partners: ULB

    Popular and scientific accounts describe how the phenomenon of overprotective parenting (also labeled “helicopter parenting” or “overparenting”) is on the rise. This evolution is highly problematic, as it puts future generations of adolescents and parents at risk for mental health problems, including anxiety and depression. Although past research offered some insights into the causes of overprotection, thereby identifying a number of parent-related and child-related determinants, there is no systematic research on the societal, economic, and cultural causes of overprotective parenting. By bringing together theories from multiple disciplines (including developmental psychology, social psychology, sociology, economics, and gender studies), the aim of this project is to test whether overprotection is rooted in parents’ context-related representations, such as their perceptions of societal expectations about how parents ought to raise children. Second, I will examine whether specific characteristic of their cultural context shape these representations and intensify their tendency to engage in overprotective parenting. Third, I aim to identify parental risk and resilience factors, which explain why some parents are either vulnerable or immune to these socio-cultural pressures. To address these research goals, I will adopt a multi-method approach, relying on longitudinal, experimental, observational and cross-cultural research. The present project has the potential to generate a paradigm shift in the study of overprotective parenting, and in the field of developmental psychology more generally, by highlighting the fundamental importance of considering the complexities related to the socio-economic and cultural context in which parent-child interactions take place. Further, findings may be highly informative for policy-makers and practitioners, and, accordingly, may help to better equip parents for facing the challenges of parenthood in a complex and changing social world.

  • Open Access mandate for Publications
    Funder: EC Project Code: 660449
    Overall Budget: 160,800 EURFunder Contribution: 160,800 EUR
    Partners: ULB

    Type 1 diabetes (T1D) is a chronic autoimmune disease in which pancreatic beta cells are killed by infiltrating immune cells and by cytokines released by these cells. The mechanisms by which autoimmunity is triggered and aggravated in T1D and the nature of the intracellular signals that decide beta cell fate between survival or death remain to be clarified. Alternative splicing (AS) is a complex mechanism of gene expression regulation and a potent generator of proteome diversity. It provides cells with an exquisite capacity to rapidly modify their transcriptome and proteome in response to intra and extracellular cues. AS affects more than 90% of human genes and has a major impact in many cellular processes, including cell survival and generation of new antigenic epitopes. There is a growing interest in the role of AS in autoimmune diseases but nearly nothing is known on its role in beta cells and diabetes. Recent findings by the host group indicate that pro-inflammatory cytokines change the expression of >30 RNA-binding proteins (RBPs) and modify AS of >3000 genes in human beta cells. Importantly, the host group has discovered that the diabetes candidate gene GLIS3 affects beta cell apoptosis by regulating the splicing of the pro-apoptotic BH3-only protein Bim. These findings suggest that AS plays an important role in the regulation of beta cell dysfunction and death by mechanisms that remain to be clarified. We hypothesise that pro-inflammatory signals activate splicing networks contributing to beta cell functional lost and death. We propose in the present project a systems biology approach that will combine RNA-seq, network inference and analysis of individual RBPs to characterize and validate inflammation-activated splicing networks in beta cells. The ultimate goal is to identify key splicing networks and mRNA splice variants that will be targeted by splicing-modulation molecules as a novel therapeutic strategy to prevent progressive beta cell loss in T1D.

  • Open Access mandate for Publications and Research data
    Funder: EC Project Code: 842676
    Overall Budget: 166,320 EURFunder Contribution: 166,320 EUR
    Partners: ULB

    The project aims for the implementation of a novel technological platform based on compact all-fibre resonators (CAFRs). I will exploit silica optical fibres treated via thermal poling to induce a second order nonlinear polarization. Periodically poled silica fibres (PPSFs), equipped with Bragg mirrors on both their facets, will be converted into quadratic nonlinear optical resonators with the target of exploiting the significant enlargement of the nonlinear interaction lengths. A complete study of the experimental conditions necessary to observe up and down conversion of light in the telecom wavelengths range inside those resonators will be realised. The main goal of the project consists in the implementation of an optical parametric oscillator (OPO) by exploiting the CAFR in doubly resonant configuration. This outcome would allow to open the way to a totally revolutionary type of all-fibre, integrated and compact laser/light sources based on nonlinear parametric processes. Another significant goal of the project is the first experimental observation of dissipative structures in these compact all-fibre resonators, with the main target of testing the theoretical predictions present in literature and shed new light onto some still unveiled aspects of dynamics of purely quadratic resonators.

  • Open Access mandate for Publications
    Funder: EC Project Code: 950220
    Overall Budget: 1,447,460 EURFunder Contribution: 1,447,460 EUR
    Partners: ULB

    AgricultureAgriculture condenses the most pressing challenges we are facing today: ecological degradation, financial deregulation and demographic explosion. Value discrepancies are key obstacles toward integrated agriculture which are not rewarding in the capitalist economy overwhelmed by a profit-driven agroindustry. However, we still lack fundamental knowledge to identify the manifold values of agricultural assets. While the value of crop varieties is usually assessed in economic terms, we need to also consider the ethical values that incentivies farmers to perpetuate biodiverse agriculture. Beside empirical timeliness, this study contributes to the elaboration of a general anthropology of value still lacking to date. The SeedsValues contends that agriculture offers a unique object to overcome the current split between the economic and the ethical studies on value. This will be achieved by producing interspecies ethnographies into seed-human relatedness - both affective and instrumental - in three agrobiodiversity hotspots: potato cultivation in Peru, maize in Mexico and rice in Laos. Prominent on global markets, also distinguished by international institutions as highly promising to reach global food security, these crops bear outstanding value to the Indigenous people who cultivate and eat them daily. Sometimes, they are treated as organisms imbued with a subjectivity, challenging Western dichotomies between object and subject, nature and culture. In this light, this project aims at unravelling (a) the ethics of seed growing, (b) the appreciation of seeds in exchange and consumption, and (c) the entanglements between growers' and seeds’ qualities. Beside addressing critical ecological questions regarding the sustainable feeding of an increasing human population, this research at the interface of anthropology and biology promises significant theoretical advances in the anthropology of value by investigating a vital object: the cultivation of flourishing seeds.

  • Open Access mandate for Publications
    Funder: EC Project Code: 708408
    Overall Budget: 172,800 EURFunder Contribution: 172,800 EUR
    Partners: ULB

    Attention-deficit/hyperactivity disorder (ADHD) like many other mental illnesses probably results from a combination of genetic and developmental factors pointing at abnormalities in brain monoamines (MA). Imaging studies in ADHD patients also indicate deficits in activity of various brain regions including the prefrontal cortex (PFC) and basal ganglia (BG). The mechanisms by which PFC and BG dysfunctions are triggered, and can be corrected with MA-based treatment are unknown. Although there is a consistent frontal hypoactivity detected in ADHD, some variations are seen amongst executive processes including attention or impulse control, in which MA have specific functions. Besides, the limited spatial resolution of brain imaging does not allow to detect certain subregions or discriminate neuronal subpopulations. In order to identify brain network impairments in ADHD, we need models to further dissect frontal dysfunctions looking at MA signaling, cell excitability and behavioral correlates of activity in identified neurons. The goal of this project is to untangle brain circuits involved in a novel mouse model of ADHD, which fulfills the major criteria reflecting human condition, showing specific BG dysfunctions and differential MA involvement. Innovative approaches have been chosen to accomplish this challenge that include transgenesis, opto- and pharmaco-genetics, and in vivo measurement of neuronal activity in translational behavioral tasks assessing attention and impulsivity. Importantly, while the most common medication using psychotimulants has proven the best efficiency, it has also been shown to affect children growth and their adult mental health highlighting the urge for alternatives. We believe that our model and multidisciplinary methodology provide new insights in ADHD ætiology and allow to develop new concepts and/or targets for therapeutic alternatives further based on the manipulation of neurons activity to reverse or attenuate ADHD symptoms.