Socioeconomic inequalities in children’s neurodevelopment and mental health are observed from early onwards and widen over time. Moreover, children whose parents are immigrant, particularly if they belong to ethnic minority groups, may be especially vulnerable. Yet there are important inter-individual differences in development, implying the possibility of resilience. My project will examine the consequences of multiple forms of socioeconomic adversity in children’s family and broader social environment with regard to their neurodevelopment and mental health, testing the role of social supports as sources of resilience. Specifically, I will rely upon longitudinal data collected from the ELFE child cohort study, a nationally representative sample of 18 321 children born in France in 2011 and followed-up to age 10.5 years, which will be linked with longitudinal administrative and geographical information characterizing neighbourhoods of children’s school and residence, as well as healthcare use data. Potential resilience factors will include familial (e.g. relations between the child and his/her mother and father, grandparents’ involvement) and contextual social supports (e.g. childcare prior to school entry, neighborhood social capital). Lifecourse patterns of adversity and resilience at each level of analysis will be identified using statistical methods developed for high-dimensional data and their influence on children’s development will be ascertained applying methods that strengthen causal inference (e.g. propensity scores). The results will help clarify 1) the ways in which lifecourse patterns of exposure to adversity in the family and children’s broader social environment can influence neurodevelopment and mental health, particularly among children of immigrants; 2) familial and collective factors that can help children overcome the odds and should be promoted.

Heart failure (HF) affects 14 million people in Europe, and this number is expected to increase to 30 million by 2020. Early diagnosis of HF is essential for successfully addressing underlying causes. However, initial diagnosis is difficult in many situations so that HF is correctly diagnosed in only half of patients. Diastolic HF, that accounts for more than 50% of all HF patients, is due to abnormal ventricular stiffness which remains very difficult to diagnose. The characterization of myocardial properties remains today a challenge and there is no technique that can assess myocardial stiffness in clinical practice. Shear Wave Imaging (SWI), a novel ultrasound technique, has been shown capable of quantifying myocardial stiffness. The development of SWI for transthoracic evaluation of myocardial stiffness in patients is one of the major goal of ULTRAECHOCARDIO, the related ERC-funded project. To achieve this goal, ultrafast ultrasound imaging is developed in order to provide thousands of images per second of the heart requiring the development of complex equipment and imaging methodology. In ElastoCardioScope, a novel portable ultrasound device will be developed for non-invasive quantification of myocardial stiffness. The idea of ElastoCardioScope is to develop a simple and innovative approach for SWI that 1) quantifies myocardial stiffness transthoracically, 2) evaluates myocardial function through time-varying stiffness and 3) is cost effective. In contrast with SWI that requires costly and complex multichannel electronics and transducers, this project aims to develop a low cost and portable approach which does not rely on ultrafast imaging of the heart. The clinical proof of concept of this technology will be performed on patients with diastolic HF. This simple and low cost innovative technology will provide a clear solution to unmet medical needs and thus has great potential for take-up and use by clinicians at hospital but also in other points of cares.

mRNA translation consists on translating the genetic code to proteins by the ribosome that is universally conserved in all cells. However, its structure presents significant differences between bacteria and eukaryotes. Partly because of these differences, the bacterial ribosome can be targeted specifically by a number of antibiotics without affecting the eukaryotic host cells. However, the conservation of the ribosome among eukaryotes complicates the search for specific drugs against eukaryotic pathogens such as certain protozoa like plasmodium and kinetoplastids. Our work along with other studies demonstrates the existence of significant structural differences between ribosomes of protozoa and mammals. Using Cryogenic electron microscopy, we endeavor to investigate such structural differences that are anticipated to affect some of the vital steps of mRNA translation, especially the initiation process, because of their position on the ribosome. 1. Thus we will focus on the structural differences in translation initiation between kinetoplastids and their mammalian hosts (i) by characterizing initiation complexes from several plasmodium and kinetoplastids species and compare them to their mammalian counterparts. (ii) We will also follow up on our previous works in solving the structures of various conventional, but also unconventional mammalian initiation complexes, in interaction with special mRNAs. 2. We will focus on the structure of protozoa-specific features characterized from elongating ribosomal complexes and (i) attempt to fish for regulators that they interact with from cell extracts. In addition, (ii) we will investigate the ribosomal structures from plasmodium at different stages of the parasite life cycle, as they vary according to the latter. Our results will significantly advance our understanding of protein synthesis regulation in protozoa and will represent a promising step in the search for more efficient treatments against these eukaryotic pathogens