TRUESSEC.EU is a CSA on certification and labelling of trustworthiness properties from a multidisciplinary SSH-ICT perspective and with emphasis on human rights. The current complexity of ICT products and services makes it difficult to appraise their trustworthiness. Thus, certification becomes a must to restore transparency and trust. TRUESSEC.EU aims at exploring the situation, the barriers, and the benefits of security and privacy labels; engaging stakeholders in the discussions, and issuing recommendations that may foster the adoption and acceptance of labels. With that aim, TRUESSEC.EU works and results are sustained by three pillars: 1) A StakeHolders' Online Platform (SHOP), where associated cluster projects and stakeholders from industry, academia, governments and civil society will gather, participate in debates, get informed, and provide their opinions and feedback on the topics of the project. 2) A series of Support Analysis and Studies (SUPPA) from multidisciplinary perspectives on issues of trustworthiness certification and assurance, to study the situation of trust-enhancing labels, barriers/incentives to industry adoption and consumer acceptance. Information will be gathered from both public sources and the interactions with stakeholders through SHOP. Four different approaches will be applied: -Socio-cultural -Legal & ethical -Technological -Business 3) A set of Recommendations on European Trust-Enhancing Labels (ETEL) dealing with: methodological aspects of certification and assurance, a catalogue of criteria for labels and certifications, and regulatory aspects to foster their adoption, plus a strategic agenda. These recommendations reflect the conclusions obtained from the support analysis and from the stakeholders. The community of stakeholders will nourish, among others, from: (a) members of the consortium partners that are stakeholder networks themselves (DIGICAT, APWG, KTN, AUI), and (b) H2020 RIAs & IAs from the associated cluster.

Parkinson’s disease (PD) is the most common neurodegenerative movement disorder, currently incurable. Studies in the PD field show that leucine-rich repeat kinase 2 (LRRK2) is both a major player in PD pathogenesis and a promising PD therapeutic target. LRRK2 functions in health and disease are not defined; however the applicant and others have shown that LRRK2 phosphorylation is the key to understanding LRRK2 biology. This project’s goal is therefore to understand the role of LRRK2 phosphorylation in PD by pursuing 3 specific aims: 1) elucidate the regulation of LRRK2 phosphorylation by phosphatases, 2) determine LRRK2 phosphorylation downstream phenotypes in cellular models through transcriptome profiling, protein translation profiling and protein tau related phenotypes, and 3) verify these findings from experimental models in PD biosamples. The project builds on the applicant’s extensive expertise in the field of LRRK2 biology (24 papers in 8 years) required for aim 1 and will leverage expertise on PD biosample analysis of the host institution (training for aims 2 and 3). The research program will be performed at the JPA research center (a mixed Inserm-Lille 2 University-Lille University Hospital center for excellence research, Lille, France), with a network of strategically chosen collaborating research groups locally and internationally, coordinated by the applicant. The study of LRRK2 phosphorylation in experimental models and translation of experimental results to clinical samples will reveal the most relevant molecular mechanisms of LRRK2 in PD which can be exploited in follow up work as diagnostic biomarkers and targeted for disease-modifying therapy. Given the importance of PD and neurodegeneration in Europe, this project is fertile ground for a high visibility fellowship and will reposition the applicant in the international neurodegenerative diseases research community by adding a clinical translation dimension to his signalling neurobiologist profile.

The challenges for EU foreign policy increase in complexity and urgency. Scientific knowledge and networks contribute to the solution of a number of these challenges. The prospects for these contributions are promising, not least in light of Europe’s scientific capacities and the efforts towards open science, which the European Union is leading. However, the opportunities science and science cooperation offer for European Union foreign policy are underexploited. While the EU’s foreign policy landscape is now better set up to develop and exploit science diplomacy, the scientific and diplomatic communities often do not communicate with each other. Organising science diplomacy in a multi-level governance system is a challenge, as is dealing with interdependency. There is also no clear model for recruiting and employing science diplomats. The goal of the S4D4C project is to support current and future EU science diplomacy for the benefit of the Union’s strategic capacities, foreign policy goals and the development of solutions for societal challenges. In order to achieve this, S4D4C brings together scholars of foreign and science policy, advisors, science diplomacy professionals and diplomatic training institutions. We analyse cases of EU science diplomacy that relate to foreign policy goals, relevant EU-level instruments and important scientific developments. Employing a co-creation approach with stakeholders, we craft a governance framework for science diplomacy. It contains recommendations and models for science diplomacy interfaces, processes and knowledge resources. Furthermore, we develop training modules for current and future science diplomats. At the end of S4D4C, the EU will have strengthened science diplomacy capacities, which will contribute to its foreign policy goals and commitments. The EU will also be more visibly positioned as a global thought leader in exploiting science and science diplomacy for the benefit of foreign policy and society.

The escalating epidemic of obesity, type-2 diabetes and metabolic syndrome represents one of the most pressing and costly biomedical challenges confronting modern society. The impaired action of peripheral hormones on brain circuits controlling feeding and energy homeostasis, also known as "central hormone resistance", is increasingly recognized as playing a role in the pathophysiology of these disorders. The host laboratory has raised the groundbreaking notion that tanycytes, a specific type of hypothalamic glial cells, act as "gatekeepers" that regulate the access of blood-borne signals to the hypothalamus, and in particular, their vesicular transport into the cerebrospinal fluid, from where they enters other metabolic-hormone-sensitive regions. The overall objective of this proposal is to further develop this highly original angle by using state-of-the-art approaches to i) gain new insights into the molecular mechanisms underlying structural changes in the tanycytic barrier in response to fluctuating concentrations of circulating glucose, and determine how these processes are altered in animal models with acquired type-2 diabetes, and ii) explore the possibility that tanycytes are involved in the shuttling of circulating glucose into the cerebrospinal fluid (CSF) and that the tanycytic expression of the NMDA receptor plays a role in this process. This research promises to shed new light on the molecular mechanisms used by the hypothalamus to integrate key peripheral signals and coordinate energy homeostasis. The results will pave the way for the development of new treatment strategies to overcome hormone resistance in human obesity and associated metabolic syndromes.

The role of chronic inflammation in obesity, metabolic and cardiovascular diseases is increasingly recognized. Bile acids (BA), synthesized in the liver and modified by the gut flora, facilitate lipid absorption in the intestine. BA modulate lipid and glucose homeostasis by activating the nuclear receptor FXR and the GPCR TGR5. Intriguingly, peripheral BA concentrations are elevated in type 2 diabetes (T2D) and FXR mediates the beneficial metabolic response to gastric bypass in mice. The immune system plays an important role in the cross-talk with metabolic tissues, such as liver, intestine and adipose tissues. However, whether BA modulate immune cell function is unknown. Our unpublished results identifying FXR and TGR5 expression in lymphoid cells, prompt us to study their role in the regulation of glucose and lipid metabolism through immune cell modulation. Using reporter mice and specific ligands, we will characterize the immune cells expressing active FXR and TGR5. We will determine their role in metabolism and inflammation by immune cell-specific gene inactivation in models of obesity, T2D and elevated peripheral blood BA concentrations. Mass cytometry, cell sorting and single cell transcriptomic analysis will allow the identification of gene networks regulated by BA and their receptors. As microbiota generate biologically active secondary BA, we will assess the impact of microbiota depletion and subsequent BA acid pool modifications on immune cell populations. Translational studies in humans with altered BA metabolism and pharmacological treatment with anti-diabetic BA sequestrants will allow assessment of alterations in immune functions. This project aims to identify an hitherto unexplored role of BA through modulation of the immune system on T2D, NAFLD and dyslipidemia. Success of the project critically depends on an integrative approach uniquely undertaken in my laboratory through its unique multidisciplinary expertise in basic and translational biology.