Understanding if and how species are able to rapidly adapt to climate change is a major and challenging problem of modern biology. Can evolution operate quickly enough? Theory suggests that the genetic basis of most phenotypic traits is polygenic, and evolution can be rapid if it harnesses this reservoir of standing variation spread across the genome - ‘Poly2Adapt’. Recent theoretical advances suggest that the signature of real-time polygenic selection can be identified using time-series genomic data. Moreover, a recent paradigm-shift, framed in the ‘omnigenic model’ suggests that all genes which are broadly expressed, or in general all genomic regions broadly available in euchromatin, contribute to the heritability of complex traits. How can we use these theoretical advances in concert? Benefiting from a unique genomic time-series dataset comprising 1,000 samples from 2000 to 2021, the aim of Poly2Adapt is to quantify the polygenic variation relevant to real-time adaptation to climate change in the King penguin, a keystone species occupying one of the most climate change-impacted ecosystems. Coupling genomic time-series analysis with gene expression and chromatin accessibility data, I will rigorously test the theories of the polygenic (O1) and omnigenic (O2) models, using this information to develop metrics of adaptation potential (O3) for the conservation of other at-risk species. This will be the first study to detect the footprints of real-time adaptation proposed by the polygenic and omnigenic models in a wild species. The objectives are directly relevant to the priorities of Horizon Europe, ‘to tackle climate change’, in particular Mission 1: Adaptation to Climate Change. I will harness interdisciplinary expertise from the host, secondment and collaborators to deepen my skills in evolutionary theory, bioinformatics, and population and conservation genetics. Together, we are well-positioned to employ powerful new approaches to pursue this timely research.

The project "Structural Health Assessment of Bridges during and after FLOOD events" (FLOOD-SHAB) aims to investigate the structural behaviour of critical infrastructures such as bridges, focusing on the studying and assessing the structural response of bridges during and after flood events. The main objective is to improve the understanding of bridge structural behaviour under various health conditions and enhance the capacity to detect structural damage caused by component failure or foundation scouring. Climate changes increasingly impact our life. It has become less predictable. Droughts, floods, and new temperature records are becoming more common worldwide, including in Europe. The rising global temperature intensifies the water cycle, which increases wet and dry extremes and affects the critical infrastructure essential for the functioning of a society and economy. Due to their significance, bridges need protection from potential hazards, including natural disasters and ageing. The increased water levels result in the additional force from fast-moving water, which can lead to structural damage, and scouring of bridge foundations. Regular inspections, continuous structural health monitoring (especially during flood events), and maintenance programs are vital to ensure bridges' structural integrity and safety. The bridge monitoring research focuses around addressing the challenges of data capture and data interpretation. In the aspect of floodings, there is a lack of knowledge about correct measuring techniques and data interpretation for these instantaneous phenomena. By comprehensive data collection of bridges’ structural behaviour on-site for the selected local case studies (at least 2 bridges) and further rigorous analysis, interpretation, and wide numerical simulations, the patterns and trends in the bridges’ structural behaviour, especially during and after flood events, and feature thresholds will be defined and established.

Autism Spectrum Disorder (ASD) is a severe permanent neurodevelopmental disorder, affecting 1 in 59 children, worldwide. Researchers have reported a markedly increased prevalence of ASD in preterm populations. Performing early screening of ASD in Neonatal Intensive Care Units (NICUs) would be a unique opportunity to provide a prompt and proper intervention. However, no quantitative solutions are present in the literature. The project “Crib with ARtificial InteLLigence fOr ASD diagnosis in Neonatal intensive care units” (ASD-carillon) aims to design, implement and validate a smart crib for analyzing visual preference and motor patterns in preterm infants in NICUs for early ASD screening. The smart crib integrates a Monitoring Framework, consisting of RGB-D and thermal cameras, and sensors already available in NICUs (e.g., those in the cardiomonitor) for collecting infants data. The smart crib is equipped with an Artificial Intelligence (AI) engine, for processing these data and providing healthcare professionals with quantitative parameters for early ASD screening in NICUs. During the outgoing phase of the fellowship, the ER will benefit from the experience of Prof Zuomin Dong, from University of Victoria (UVic), in the field of sensors and intelligent system, to develop the Monitoring Framework and build the prototype of the smart crib. During the incoming phase, she will collaborate with her main mentor, Prof Emanuele Frontoni from Università Politecnica delle Marche (UNIVPM), to refine the AI Engine. Expert neonatologists as well as neuropsychiatrists from UNIVPM and UVic will be involved as clinical collaborators of ASD-carillon. In the last decades, there has been an increasingly growing number of manuscripts dealing with AI in medicine, but the AI potential in the field of ASD screening in NICUs has not being unlocked, yet. With ASD-carillon, the ER aims to fill this gap, while building the basis for a solid career in the field of AI in neonatology and ASD.

Myelin, the fatty substance surrounding nerve fibers, is essential for proper brain functioning. Loss of myelin integrity characterizes several debilitating diseases, such as multiple sclerosis. Thus, understanding the factors that can modulate myelin formation and maintenance is crucial for these diseases. My recent work has shown that: - Sleep favors the expression of genes implicated in myelin formation and myelin lipid turnover. - Oligodendrocyte precursors that form the major source of newly formed myelinating-oligodendrocytes in the brain proliferate preferentially during sleep. - By contrast, sleep restriction leads to myelin thinning, suggesting sleep is an essential requirement for maintaining myelin integrity. These results raise the intriguing question: can we promote myelination by enhancing sleep? Here, I will use closed-loop acoustic stimulation in sleeping mice to enhance NREM and REM sleep. Increasing evidence has shown that this method can reliably boost cardinal neurophysiological features of NREM and REM sleep in both rodents and humans. This approach will allow me to verify whether sleep enhancement promotes myelination in the mouse forebrain. This research will advance our knowledge about the factors that regulate myelination. Furthermore, it will provide insight into new possible ways of intervention in Multiple Sclerosis and related disorders based on sleep enhancement. In order to function properly the brain needs myelin, an electrically insulating substance that surrounds nerve fibers. Myelin is continuously remodeled in the brain and sleep is one of key factors contributing to the formation and maintenance of myelin in the brain. The objective of my research is to understand whether we can promote myelin formation and maintenance by enhancing sleep. Recent research demonstrated that playing tones while one is asleep can boost sleep. Here I will apply this approach to mice, in which I will then evaluate the extent of myelin formation. This research will help clarify why sleep is beneficial to our health and whether sleep can be manipulated to enhance the capability of our brain to produce more myelin, particularly in the pathological context of debilitating neurological diseases, where myelin formation is crucial for the recovery process.