Local-Density Driven Clustered Star Formation

A positive power-law trend between the local surface densities of molecular gas, $\Sigma_{gas}$, and young stellar objects, $\Sigma_{\star}$, in molecular clouds of the Solar Neighbourhood has been identified by Gutermuth et al. How it relates to the properties of embedded clusters, in particular to the recently established radius-density relation, has so far not been investigated. In this paper, we model the development of the stellar component of molecular clumps as a function of time and initial local volume density so as to provide a coherent framework able to explain both the molecular-cloud and embedded-cluster relations quoted above. To do so, we associate the observed volume density gradient of molecular clumps to a density-dependent free-fall time. The molecular clump star formation history is obtained by applying a constant SFE per free-fall time, \eff. For volume density profiles typical of observed molecular clumps (i.e. power-law slope $\simeq -1.7$), our model gives a star-gas surface-density relation $\Sigma_{\star} \propto \Sigma_{gas}^2$, in very good agreement with the Gutermuth et al relation. Taking the case of a molecular clump of mass $M_0 \simeq 10^4 Msun$ and radius $R \simeq 6 pc$ experiencing star formation during 2 Myr, we derive what SFE per free-fall time matches best the normalizations of the observed and predicted ($\Sigma_{\star}$, $\Sigma_{gas}$) relations. We find \eff \simeq 0.1. We show that the observed growth of embedded clusters, embodied by their radius-density relation, corresponds to a surface density threshold being applied to developing star-forming regions. The consequences of our model in terms of cluster survivability after residual star-forming gas expulsion are that due to the locally high SFE in the inner part of star-forming regions, global SFE as low as 10% can lead to the formation of bound gas-free star clusters.Comment: 16 pages, 15 figures, Astronomy & Astrophysics, in pres

On the origin of the radial mass density profile of the Galactic halo Globular Cluster System

We investigate what may be the origin of the presently observed spatial distribution of the mass of the Galactic Old Halo globular cluster system. We propose its radial mass density profile to be a relic of the distribution of the cold baryonic material in the protoGalaxy. Assuming that this one arises from the profile of the whole protoGalaxy minus the contribution of the dark matter (and a small contribution of the hot gas by which the protoglobular clouds were bound), we show that the mass distributions around the Galactic centre of this cold gas and of the Old Halo agree satisfactorily. In order to demonstrate our hypothesis even more conclusively, we simulate the evolution with time, up to an age of 15 Gyr, of a putative globular cluster system whose initial mass distribution in the Galactic halo follows the profile of the cold protogalactic gas. We show that beyond a galactocentric distance of order 2 to 3 kpc, the initial shape of such a mass density profile is preserved in spite of the complete destruction of some globular clusters and the partial evaporation of some others. This result is almost independent of the choice of the initial mass function for the globular clusters, which is still ill-determined. The shape of these evolved cluster system mass density profiles also agree with the presently observed profile of the Old Halo globular cluster system, thus strengthening our hypothesis. Our result might suggest that the flattening shown by the Old Halo mass density profile at short distance from the Galactic centre is, at least partly, of primordial origin.Comment: 10 pages, accepted in MNRA

Impact of a star formation efficiency profile on the evolution of open clusters

We study the effect of the instantaneous gas expulsion on star clusters wherein the residual gas has a density profile shallower than that of the embedded cluster. This is expected if star formation proceeds with a given SFE per free-fall time in a centrally-concentrated molecular clump. We perform direct N-body simulations whose initial conditions are generated by the program "mkhalo" "falcON" adapted for our models. Our model clusters initially have a Plummer profile and are in virial equilibrium with the gravitational potential of the cluster-forming clump. The residual gas contribution is computed based on the model of Parmentier&Pfalzner(2013). Our simulations include mass loss by stellar evolution and the tidal field of the Galaxy. We find that a star cluster with a minimum global SFE of 15% is able to survive instantaneous gas expulsion and to produce a bound cluster. Its violent relaxation lasts no longer than 20 Myr, independently of its global SFE and initial stellar mass. At the end of violent relaxation the bound fractions of surviving clusters with the same global SFEs are similar regardless of their initial stellar mass. Their subsequent lifetime in the gravitational field of the Galaxy depends on their bound stellar masses. We therefore conclude that the critical SFE needed to produce a bound cluster is 15%, which is twice smaller than earlier estimates of 33%. Thus we have improved the survival likelihood of young clusters after instantaneous gas expulsion. Those can now survive instantaneous gas expulsion with global SFEs as low as those observed for embedded clusters of Solar Neighbourhood (15-30%). This is the consequence of the star cluster having a density profile steeper than that of the residual gas. However, in terms of the effective SFE, measured by the virial ratio of the cluster at gas expulsion, our results are in agreement with previous studies.Comment: Accepted for publication in Astronomy&Astrophysics, 13 pages, 10 figure

Star Clusters in the Galactic tidal field, from birth to dissolution

We study the evolution of star clusters in the Galactic tidal field starting from their birth in molecular clumps. Our model clusters form according to the local-density-driven cluster formation model in which the stellar density profile is steeper than that of gas. As a result, clusters resist the gas expulsion better than predicted by earlier models. We vary the impact of the Galactic tidal field {\lambda}, considering different Galactocentric distances (3-18 kpc), as well as different cluster sizes. Our model clusters survive the gas expulsion independent of {\lambda}. We investigated the relation between the cluster mass at the onset of secular evolution and their dissolution time. The model clusters formed with a high star-formation efficiency (SFE) follow a tight mass-dependent dissolution relation, in agreement with previous theoretical studies. However, the low-SFE models present a shallower mass-dependent relation than high-SFE clusters, and most dissolve before reaching 1 Gyr (cluster teenage mortality).Comment: 4 pages, 2 figures. Submitted for publication in the Proceedings of IAU Symposium 35

Star Clusters in the Galactic tidal field, from birth to dissolution

We study the evolution of star clusters in the Galactic tidal field starting from their birth in molecular clumps. Our model clusters form according to the local-density-driven cluster formation model in which the stellar density profile is steeper than that of gas. As a result, clusters resist the gas expulsion better than predicted by earlier models

G Protein-Dependent CCR5 Signaling Is Not Required for Efficient Infection of Primary T Lymphocytes and Macrophages by R5 Human Immunodeficiency Virus Type 1 Isolates

The requirement of human immunodeficiency virus (HIV)-induced CCR5 activation for infection by R5 HIV type 1 (HIV-1) strains remains controversial. Ectopic CCR5 expression in CD4(+)-transformed cells or pharmacological inhibition of G(α)i proteins coupled to CCR5 left unsolved whether CCR5-dependent cell activation is necessary for the HIV life cycle. In this study, we investigated the role played by HIV-induced CCR5-dependent cell signaling during infection of primary CD4-expressing leukocytes. Using lentiviral vectors, we restored CCR5 expression in T lymphocytes and macrophages from individuals carrying the homozygous 32-bp deletion of the CCR5 gene (ccr5 Δ32/Δ32). Expression of wild-type (wt) CCR5 in ccr5 Δ32/Δ32 cells permitted infection by R5 HIV isolates. We assessed the capacity of a CCR5 derivative carrying a mutated DRY motif (CCR5-R126N) in the second intracellular loop to work as an HIV-1 coreceptor. The R126N mutation is known to disable G protein coupling and agonist-induced signal transduction through CCR5 and other G protein-coupled receptors. Despite its inability to promote either intracellular calcium mobilization or cell chemotaxis, the inactive CCR5-R126N mutant provided full coreceptor function to several R5 HIV-1 isolates in primary cells as efficiently as wt CCR5. We conclude that in a primary, CCR5-reconstituted CD4(+) cell environment, G protein signaling is dispensable for R5 HIV-1 isolates to actively infect primary CD4(+) T lymphocytes or macrophages

High Risk of Anal and Rectal Cancer in Patients With Anal and/or Perianal Crohn’s Disease

International audienceBackground & AimsLittle is known about the magnitude of the risk of anal and rectal cancer in patients with anal and/or perineal Crohn’s disease. We aimed to assess the risk of anal and rectal cancer in patients with Crohn’s perianal disease followed up in the Cancers Et Surrisque Associé aux Maladies Inflammatoires Intestinales En France (CESAME) cohort.MethodsWe collected data from 19,486 patients with inflammatory bowel disease (IBD) enrolled in the observational CESAME study in France, from May 2004 through June 2005; 14.9% of participants had past or current anal and/or perianal Crohn’s disease. Subjects were followed up for a median time of 35 months (interquartile range, 29–40 mo). To identify risk factors for anal cancer in the total CESAME population, we performed a case-control study in which participants were matched for age and sex.ResultsAmong the total IBD population, 8 patients developed anal cancer and 14 patients developed rectal cancer. In the subgroup of 2911 patients with past or current anal and/or perianal Crohn’s lesions at cohort entry, 2 developed anal squamous-cell carcinoma, 3 developed perianal fistula–related adenocarcinoma, and 6 developed rectal cancer. The corresponding incidence rates were 0.26 per 1000 patient-years for anal squamous-cell carcinoma, 0.38 per 1000 patient-years for perianal fistula–related adenocarcinoma, and 0.77 per 1000 patient-years for rectal cancer. Among the 16,575 patients with ulcerative colitis or Crohn’s disease without anal or perianal lesions, the incidence rate of anal cancer was 0.08 per 1000 patient-years and of rectal cancer was 0.21 per 1000 patient-years. Among factors tested by univariate conditional regression (IBD subtype, disease duration, exposure to immune-suppressive therapy, presence of past or current anal and/or perianal lesions), the presence of past or current anal and/or perianal lesions at cohort entry was the only factor significantly associated with development of anal cancer (odds ratio, 11.2; 95% CI, 1.18-551.51; P = .03).ConclusionsIn an analysis of data from the CESAME cohort in France, patients with anal and/or perianal Crohn’s disease have a high risk of anal cancer, including perianal fistula–related cancer, and a high risk of rectal cancer