Gamma-Ray Emission From Be/X-Ray Binaries

Be/X-ray binaries are systems formed by a massive Be star and a magnetized neutron star, usually in an eccentric orbit. The Be star has strong equatorial winds occasionally forming a circumstellar disk. When the neutron star intersects the disk the accretion rate dramatically increases and a transient accretion disk can be formed around the compact object. This disk can last longer than a single orbit in the case of major outbursts. If the disk rotates faster than the neutron star, the Cheng-Ruderman mechanism can produce a current of relativistic protons that would impact onto the disk surface, producing gamma-rays from neutral pion decays and initiating electromagnetic cascades inside the disk. In this paper we present calculations of the evolution of the disk parameters during both major and minor X-ray events, and we discuss the generation of gamma-ray emission at different energies within a variety of models that include both screened and unscreened disks.Comment: 14 pages, to appear in: "The multiwavelength approach to unidentified gamma-ray sources", Eds. K. S. Cheng & G.E. Romero, Kluwer Academic Publisher (Astrophysics and Space Sciences Journal). The present version has two additional figures respect to the version to be published in the journa

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

Negative regulation of TLX by IL-1β correlates with an inhibition of adult hippocampal neural precursor cell proliferation

Adult hippocampal neurogenesis is modulated by a number of intrinsic and extrinsic factors including local signalling molecules, exercise, aging and inflammation. Inflammation is also a major contributor to several hippocampal-associated disorders. Interleukin-1beta (IL-1β) is the most predominant pro-inflammatory cytokine in the brain, and an increase in its concentration is known to decrease the proliferation of both embryonic and adult hippocampal neural precursor cells (NPCs). Recent research has focused on the role of nuclear receptors as intrinsic regulators of neurogenesis, and it is now established that the orphan nuclear receptor TLX is crucial in maintaining the NPC pool in neurogenic brain regions. To better understand the involvement of TLX in IL-1β-mediated effects on hippocampal NPC proliferation, we examined hippocampal NPC proliferation and TLX expression in response to IL-1β treatment in an adult rat hippocampal neurosphere culture system. We demonstrate that IL-1β reduced the proliferation of hippocampal NPCs and TLX expression in a dose and time-dependent manner and that co-treatment with IL-1β receptor antagonist or IL-1 receptor siRNA prevented these effects. We also report a dose-dependent effect of IL-1β on the composition of cell phenotypes in the culture and on expression of TLX in these cells. This study thus provides evidence of an involvement of TLX in IL-1β-induced changes in adult hippocampal neurogenesis, and offers mechanistic insight into disorders in which neuroinflammation and alterations in neurogenesis are characteristic features

The gut microbiome and adult hippocampal neurogenesis:A new focal point for epilepsy?

Temporal lobe epilepsy (TLE) is a neurological disorder affecting millions of people worldwide and currently represents the most common form of focal epilepsy. Thus, the search for aetiological and pathophysiological parameters of TLE is ongoing. Preclinical work and post-mortem human studies suggest adult hippocampal neurogenesis as a potentially relevant factor in TLE pathogenesis. Although progress has been made in elucidating the molecular links between TLE and hippocampal neurogenesis, recent evidence suggests that additional peripheral mediators may be involved. The microbiota-gut-brain axis mediates bidirectional communication between the gut and the brain and could comprise a link between neurogenesis and TLE. In this review, we discuss emerging evidence highlighting a potential role for the gut microbiome in connecting TLE pathogenesis and hippocampal neurogenesis. We focus in particular on mechanisms associated with neuronal excitability, neuroinflammation and gut microbial metabolites. As the evidence does not yet support a direct link between gut microbiota-regulated hippocampal neurogenesis and TLE aetiology or pathophysiology, future studies are needed to establish whether current findings comprise circumstantial links or a potentially novel avenue for clinically relevant research

A New TeV Source Confirmed in Whipple Archival Data: TeV J2032+41

A re-analysis of data near Cygnus X-3 in 1989-1990 using the Whipple Observatory atmospheric Cherenkov imaging telescope confirms the existence of the TeV J2032 + 4130 source first reported at a conference by the Crimean Astrophysical Observatory and confirmed independently by the HEGRA Collaboration in a referred publication. The significance of the Whipple observations at the a priori HEGRA position is 3.3$\sigma. The peak signal was found at RA = 20 h 32 m, Dec = +41$\degres$33'. This is 0.6$\degres$ north of Cygnus X-3. The flux level (12\% of the level of the Crab Nebula) is intermediate between that reported by the Crimean (100\%) and HEGRA (3\%) groups