Metallicity dependence of turbulent pressure and macroturbulence in stellar envelopes

Macroturbulence, introduced as a fudge to reproduce the width and shape of stellar absorption lines, reflects gas motions in stellar atmospheres. While in cool stars, it is thought to be caused by convection zones immediately beneath the stellar surface, the origin of macroturbulence in hot stars is still under discussion. Recent works established a correlation between the turbulent-to-total pressure ratio inside the envelope of stellar models and the macroturbulent velocities observed in corresponding Galactic stars. To probe this connection further, we evaluated the turbulent pressure that arises in the envelope convective zones of stellar models in the mass range 1-125 Msun based on the mixing-length theory and computed for metallicities of the Large and Small Magellanic Cloud. We find that the turbulent pressure contributions in models with these metallicities located in the hot high-luminosity part of the Hertzsprung-Russel (HR) diagram is lower than in similar models with solar metallicity, whereas the turbulent pressure in low-metallicity models populating the cool part of the HR-diagram is not reduced. Based on our models, we find that the currently available observations of hot massive stars in the Magellanic Clouds appear to support a connection between macroturbulence and the turbulent pressure in stellar envelopes. Multidimensional simulations of sub-surface convection zones and a larger number of high-quality observations are necessary to test this idea more rigorously.Comment: Accepted A&A, 8 p

Multiwavelength study of the fast rotating supergiant high-mass X-ray binary IGR J16465-4507

Since its launch, the X-ray and gamma-ray observatory INTEGRAL satellite has revealed a new class of high-mass X-ray binaries (HMXB) displaying fast flares and hosting supergiant companion stars. Optical and infrared (OIR) observations in a multi-wavelength context are essential to understand the nature and evolution of these newly discovered celestial objects. The goal of this multiwavelength study (from ultraviolet to infrared) is to characterise the properties of IGR J16465-4507, to confirm its HMXB nature and that it hosts a supergiant star. We analysed all OIR, photometric and spectroscopic observations taken on this source, carried out at ESO facilities. Using spectroscopic data, we constrained the spectral type of the companion star between B0.5 and B1 Ib, settling the debate on the true nature of this source. We measured a high rotation velocity of v = 320 +/- 8 km/s from fitting absorption and emission lines in a stellar spectral model. We then built a spectral energy distribution from photometric observations to evaluate the origin of the different components radiating at each energy range. We finally show that, having accurately determined the spectral type of the early-B supergiant in IGR J16465-4507, we firmly support its classification as an intermediate supergiant fast X-ray transient (SFXT).Comment: A&A in press, 14 pages, 15 tables, 13 figure

Spectral classification and properties of the O Vz stars in the Galactic O-Star Spectroscopic Survey (GOSSS)

On the basis of the Galactic O-Star Spectroscopic Survey (GOSSS), a detailed systematic investigation of the O Vz stars is presented. The currently used spectral classification criteria are rediscussed, and the Vz phenomenon is recalibrated through the addition of a quantitative criterion based on the equivalent widths of the He I 4471, He II 4542, and He II 4686 spectral lines. The GOSSS O Vz and O V populations resulting from the newly adopted spectral classification criteria are comparatively analyzed. The locations of the O Vz stars are probed, showing a concentration of the most extreme cases toward the youngest star forming regions. The occurrence of the Vz spectral peculiarity in a solar-metallicity environment, as predicted by the fastwind code, is also investigated, confirming the importance of taking into account several processes for the correct interpretation of the phenomenon.Comment: Accepted for publication in The Astronomical Journa

Glioblastoma cell fate is differentially regulated by the microenvironments of the tumour bulk and infiltrative margin

Glioblastoma recurrence originates from invasive cells at the tumour margin that escape surgical debulking, but their biology remains poorly understood. Here we generated three somatic mouse models recapitulating the main glioblastoma driver mutations to characterise margin cells. We find that, regardless of genetics, tumours converge on a common set of neural- like cellular states. However, bulk and margin display distinct neurogenic patterns and immune microenvironments. The margin is immune-cold and preferentially follows developmental-like trajectories to produce astrocyte-like cells. In contrast, injury-like programmes dominate in the bulk, are associated with immune infiltration and generate lowly-proliferative injured neural progenitor-like (iNPCs) cells. In vivo label-retention approaches further demonstrate that iNPCs account for a significant proportion of dormant glioblastoma cells and are induced by interferon signalling within T-cell niches. These findings indicate that tumour region is a major determinant of glioblastoma cell fate and therapeutic vulnerabilities identified in bulk may not extend to the margin residuum

Glioblastoma cell fate is differentially regulated by the microenvironments of the tumor bulk and infiltrative margin

Glioblastoma (GBM) recurrence originates from invasive margin cells that escape surgical debulking, but to what extent these cells resemble their bulk counterparts remains unclear. Here, we generated three immunocompetent somatic GBM mouse models, driven by subtype-associated mutations, to compare matched bulk and margin cells. We find that, regardless of mutations, tumors converge on common sets of neural-like cellular states. However, bulk and margin have distinct biology. Injury-like programs associated with immune infiltration dominate in the bulk, leading to the generation of lowly proliferative injured neural progenitor-like cells (iNPCs). iNPCs account for a significant proportion of dormant GBM cells and are induced by interferon signaling within T cell niches. In contrast, developmental-like trajectories are favored within the immune-cold margin microenvironment resulting in differentiation toward invasive astrocyte-like cells. These findings suggest that the regional tumor microenvironment dominantly controls GBM cell fate and biological vulnerabilities identified in the bulk may not extend to the margin residuum

Fibroblast Primary Cilia are Required for Cardiac Fibrosis

Background: The primary cilium is a singular cellular structure that extends from the surface of many cell types and plays crucial roles in vertebrate development, including that of the heart. Whereas ciliated cells have been described in developing heart, a role for primary cilia in adult heart has not been reported. This, coupled with the fact that mutations in genes coding for multiple ciliary proteins underlie polycystic kidney disease, a disorder with numerous cardiovascular manifestations, prompted us to identify cells in adult heart harboring a primary cilium and to determine whether primary cilia play a role in disease-related remodeling. Methods: Histological analysis of cardiac tissues from C57BL/6 mouse embryos, neonatal mice, and adult mice was performed to evaluate for primary cilia. Three injury models (apical resection, ischemia/reperfusion, and myocardial infarction) were used to identify the location and cell type of ciliated cells with the use of antibodies specific for cilia (acetylated tubulin, γ-tubulin, polycystin [PC] 1, PC2, and KIF3A), fibroblasts (vimentin, α-smooth muscle actin, and fibroblast-specific protein-1), and cardiomyocytes (α-actinin and troponin I). A similar approach was used to assess for primary cilia in infarcted human myocardial tissue. We studied mice silenced exclusively in myofibroblasts for PC1 and evaluated the role of PC1 in fibrogenesis in adult rat fibroblasts and myofibroblasts. Results: We identified primary cilia in mouse, rat, and human heart, specifically and exclusively in cardiac fibroblasts. Ciliated fibroblasts are enriched in areas of myocardial injury. Transforming growth factor β-1 signaling and SMAD3 activation were impaired in fibroblasts depleted of the primary cilium. Extracellular matrix protein levels and contractile function were also impaired. In vivo, depletion of PC1 in activated fibroblasts after myocardial infarction impaired the remodeling response. Conclusions: Fibroblasts in the neonatal and adult heart harbor a primary cilium. This organelle and its requisite signaling protein, PC1, are required for critical elements of fibrogenesis, including transforming growth factor β-1-SMAD3 activation, production of extracellular matrix proteins, and cell contractility. Together, these findings point to a pivotal role of this organelle, and PC1, in disease-related pathological cardiac remodeling and suggest that some of the cardiovascular manifestations of autosomal dominant polycystic kidney disease derive directly from myocardium-autonomous abnormalities