Despite the international guidelines on the containment of the coronavirus disease 2019 (COVID-19) pandemic, the European scientific community was not sufficiently prepared to coordinate scientific efforts. To improve preparedness for future pandemics, we have initiated a network of nine European-funded Cooperation in Science and Technology (COST) Actions that can help facilitate inter-, multi-, and trans-disciplinary communication and collaboration.

Background: DNA methylation is the main epigenetic mechanism driving changes in phenotype without altering genotype. Since the end of the seventies the role of methylation in cancer has become increasingly clear. Objective: The aim of this work is to shed light on the impact of methylation events on cancer cells, providing evidence that differential methylation in small regions, mostly characterized by hypermethylation, affects gene regulation while differential methylation in large genomic regions, mostly characterized by hypomethylation, affects chromosomal organization.

The recent COVID-19 pandemic came alongside with an "infodemic", with online social media flooded by often unreliable information associating the medical emergency with popular subjects of disinformation. In Italy, one of the first European countries suffering a rise in new cases and dealing with a total lockdown, controversial topics such as migrant flows and the 5G technology were often associated online with the origin and diffusion of the virus.

A (2+2)-dimensional kinetic equation, directly inspired by the run-and-tumble modeling of chemotaxis dynamics is studied so as to derive a both ''2D well-balanced'' and ''asymptotic-preserving'' numerical approximation. To this end, exact stationary regimes are expressed by means of Laplace transforms of Fourier-Bessel solutions of associated elliptic equations. This yields a scattering S-matrix which permits to formulate a timemarching scheme in the form of a convex combination in kinetic scaling.

The present work is inspired by the recent developments in laboratory experiments made on chips, where the culturing of multiple cell species was possible. The model is based on coupled reaction-diffusion-transport equations with chemotaxis and takes into account the interactions among cell populations and the possibility of drug administration for drug testing effects.

Investigation about the mechanisms involved in the onset of type 2 diabetes in absence of familiarity is the focus of a research project which has led to the development of a computational model that recapitulates the aetiology of the disease. The model simulates the metabolic and immunological alterations related to type-2 diabetes associated to several clinical, physiological and behavioural characteristics of representative virtual patients.

A novel approach for extracting gauge-invariant information about spin-orbit coupling in gravitationally interacting binary systems is introduced. This approach is based on the "scattering holonomy", i.e. the integration (from the infinite past to the infinite future) of the differential spin evolution along the two worldlines of a binary system in hyperboliclike motion. We apply this approach to the computation, at the first post-Minkowskian approximation (i.e.

The Fokker--Planck approximation for an elementary linear, two-dimensional kinetic model endowed with a mass-preserving integral collision process is numerically studied, along with its diffusive limit. In order to set up a well-balanced discretization relying on an $S$-matrix, exact steady states of the continuous equation are derived. The ability of the scheme to keep these stationary solutions invariant produces the discretization of the local differential operator which mimics the collision process.

Background and limitations Impaired wound healing (WH) and chronic inflammation are hallmarks of non-communicable diseases (NCDs). However, despite WH being a recognized player in NCDs, mainstream therapies focus on (un)targeted damping of the inflammatory response, leaving WH largely unaddressed, owing to three main factors. The first is the complexity of the pathway that links inflammation and wound healing; the second is the dual nature, local and systemic, of WH; and the third is the limited acknowledgement of genetic and contingent causes that disrupt physiologic progression of WH.