Three-dimensional random Voronoi tessellations: From cubic crystal lattices to Poisson point processes

We perturb the SC, BCC, and FCC crystal structures with a spatial Gaussian noise whose adimensional strength is controlled by the parameter a, and analyze the topological and metrical properties of the resulting Voronoi Tessellations (VT). The topological properties of the VT of the SC and FCC crystals are unstable with respect to the introduction of noise, because the corresponding polyhedra are geometrically degenerate, whereas the tessellation of the BCC crystal is topologically stable even against noise of small but finite intensity. For weak noise, the mean area of the perturbed BCC and FCC crystals VT increases quadratically with a. In the case of perturbed SCC crystals, there is an optimal amount of noise that minimizes the mean area of the cells. Already for a moderate noise (a>0.5), the properties of the three perturbed VT are indistinguishable, and for intense noise (a>2), results converge to the Poisson-VT limit. Notably, 2-parameter gamma distributions are an excellent model for the empirical of of all considered properties. The VT of the perturbed BCC and FCC structures are local maxima for the isoperimetric quotient, which measures the degre of sphericity of the cells, among space filling VT. In the BCC case, this suggests a weaker form of the recentluy disproved Kelvin conjecture. Due to the fluctuations of the shape of the cells, anomalous scalings with exponents >3/2 is observed between the area and the volumes of the cells, and, except for the FCC case, also for a->0. In the Poisson-VT limit, the exponent is about 1.67. As the number of faces is positively correlated with the sphericity of the cells, the anomalous scaling is heavily reduced when we perform powerlaw fits separately on cells with a specific number of faces

Pulsar Wind Nebulae with Bow Shocks: Non-thermal Radiation and Cosmic Ray Leptons

Pulsars with high spin-down power produce relativistic winds radiating a non-negligible fraction of this power over the whole electromagnetic range from radio to gamma-rays in the pulsar wind nebulae (PWNe). The rest of the power is dissipated in the interactions of the PWNe with the ambient interstellar medium (ISM). Some of the PWNe are moving relative to the ambient ISM with supersonic speeds producing bow shocks. In this case, the ultrarelativistic particles accelerated at the termination surface of the pulsar wind may undergo reacceleration in the converging flow system formed by the plasma outflowing from the wind termination shock and the plasma inflowing from the bow shock. The presence of magnetic perturbations in the flow, produced by instabilities induced by the accelerated particles themselves, is essential for the process to work. A generic outcome of this type of reacceleration is the creation of particle distributions with very hard spectra, such as are indeed required to explain the observed spectra of synchrotron radiation with photon indices Γ≲ 1.5. The presence of this hard spectral component is specific to PWNe with bow shocks (BSPWNe). The accelerated particles, mainly electrons and positrons, may end up containing a substantial fraction of the shock ram pressure. In addition, for typical ISM and pulsar parameters, the e+ released by these systems in the Galaxy are numerous enough to contribute a substantial fraction of the positrons detected as cosmic ray (CR) particles above few tens of GeV and up to several hundred GeV. The escape of ultrarelativistic particles from a BSPWN—and hence, its appearance in the far-UV and X-ray bands—is determined by the relative directions of the interstellar magnetic field, the velocity of the astrosphere and the pulsar rotation axis. In this respect we review the observed appearance and multiwavelength spectra of three different types of BSPWNe: PSR J0437-4715, the Guitar and Lighthouse nebulae, and Vela-like objects. We argue that high resolution imaging of such objects provides unique information both on pulsar winds and on the ISM. We discuss the interpretation of imaging observations in the context of the model outlined above and estimate the BSPWN contribution to the positron flux observed at the Earth

Universal DNA methylation age across mammalian tissues

DATA AVAILABILITY STATEMENT : The individual-level data from the Mammalian Methylation Consortium can be accessed from several online locations. All data from the Mammalian Methylation Consortium are posted on Gene Expression Omnibus (complete dataset, GSE223748). Subsets of the datasets can also be downloaded from accession numbers GSE174758, GSE184211, GSE184213, GSE184215, GSE184216, GSE184218, GSE184220, GSE184221, GSE184224, GSE190660, GSE190661, GSE190662, GSE190663, GSE190664, GSE174544, GSE190665, GSE174767, GSE184222, GSE184223, GSE174777, GSE174778, GSE173330, GSE164127, GSE147002, GSE147003, GSE147004, GSE223943 and GSE223944. Additional details can be found in Supplementary Note 2. The mammalian data can also be downloaded from the Clock Foundation webpage: https://clockfoundation.org/MammalianMethylationConsortium. The mammalian methylation array is available through the non-profit Epigenetic Clock Development Foundation (https://clockfoundation.org/). The manifest file of the mammalian array and genome annotations of CpG sites can be found on Zenodo (10.5281/zenodo.7574747). All other data supporting the findings of this study are available from the corresponding author upon reasonable request. The chip manifest files, genome annotations of CpG sites and the software code for universal pan-mammalian clocks can be found on GitHub95 at https://github.com/shorvath/MammalianMethylationConsortium/tree/v2.0.0. The individual R code for the universal pan-mammalian clocks, EWAS analysis and functional enrichment studies can be also found in the Supplementary Code.SUPPLEMENTARY MATERIAL 1 : Supplementary Tables 1–3 and Notes 1–6.SUPPLEMENTARY MATERIAL 2 : Reporting SummarySUPPLEMENTARY MATERIAL 3 : Supplementary Data 1–14.SUPPLEMENTARY MATERIAL 4 : Supplementary Code.Aging, often considered a result of random cellular damage, can be accurately estimated using DNA methylation profiles, the foundation of pan-tissue epigenetic clocks. Here, we demonstrate the development of universal pan-mammalian clocks, using 11,754 methylation arrays from our Mammalian Methylation Consortium, which encompass 59 tissue types across 185 mammalian species. These predictive models estimate mammalian tissue age with high accuracy (r > 0.96). Age deviations correlate with human mortality risk, mouse somatotropic axis mutations and caloric restriction. We identified specific cytosines with methylation levels that change with age across numerous species. These sites, highly enriched in polycomb repressive complex 2-binding locations, are near genes implicated in mammalian development, cancer, obesity and longevity. Our findings offer new evidence suggesting that aging is evolutionarily conserved and intertwined with developmental processes across all mammals.https://www.nature.com/nataginghj2024Zoology and EntomologySDG-15:Life on lan

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Protect, correct, and eject: Ostracism as a social influence tool

Ostracism—ignoring and excluding—is an evolutionarily adaptive response that protects groups from burdensome members either by correcting the misbehavior while promoting sameness and civility, or, if correction is not achieved, then ejecting the member, resulting again in a homogeneous, albeit smaller, group. Over 20 years of research demonstrates that ostracism is a powerful tool of social influence. Being the target of ostracism activates brain regions associated with pain, threatens fundamental needs, worsens mood, and causes behavior changes aimed at fortifying threatened needs. We review research showing three functions of ostracism: (1) to protect—shielding groups from threatening members; (2) to correct—signaling to individuals that their behavior needs modification to remain in the group; and (3) to eject—permanently removing deviant individuals who resist correction. Although ostracism is a powerful and effective social influence tool, it can cause unintended and potentially dangerous consequences for those who employ it. Keywords: ostracism, social exclusion, rejection, Cyberball, social susceptibility, aggression, solitude, social pai