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.

The crack density within a fault's damage zone is thought to vary as seismic rupture is approached, as well as in the postseismic period. Moreover, external stress loads, seasonal or tidal, may also change the crack density in rocks, and all such processes can leave detectable signatures on seismic attenuation. Here we show that attenuation time histories from the San Andreas Fault at Parkfield are affected by seasonal loading cycles, as well as by 1.5-3-year periodic variations of creep rates, consistent with Turner et al.

Background: Neutrophils are one of the key players in the human innate immune system (HIIS). In the event of an insult where the body is exposed to inflammation triggering moieties (ITMs), neutrophils are mobilized towards the site of insult and antagonize the inflammation. If the inflammation is cleared, neutrophils go into a programmed death called apoptosis.

Phosphoinositides (PtdIns) control fundamental cell processes, and inherited defects of PtdIns kinases or phosphatases cause severe human diseases, including Lowe syndrome due to mutations in OCRL, which encodes a PtdIns(4,5)P2 5-phosphatase. Here we unveil a lysosomal response to the arrival of autophagosomal cargo in which OCRL plays a key part. We identify mitochondrial DNA and TLR9 as the cargo and the receptor that triggers and mediates, respectively, this response.

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.

Many studies have shown that Physarum polycephalum slime mold is able to find the shortest path in a maze. Here we study this behavior in a network, using a hyperbolic model of chemotaxis [1]. Suitable transmission and boundary conditions at each node are considered to mimic the behavior of such an organism in the feeding process. Several numerical tests are presented for special network geometries to show the qualitative agreement between our model and the observed behavior of the mold.

The effects of a nonminimally coupled curvature-matter model of gravity on planetary orbits are computed. The parameters of the model are then constrained by the observation of Mercury orbit.

Background: The high contagiousness and rapid spreading of the coronavirus disease 2019 (COVID-19) has caused a high number of critical to severe life-threatening cases, which required urgent hospital admission and treatment in intensive care units (ICUs). The pandemic has been a tough test for all European national health systems and their capability to provide an adequate reaction. Methods: The present work aims to reveal correlations between parameters such as COVID-19 incidence, ICU bed occupancy, ICU excess area, and mortality in Italian regions.

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.