235 research outputs found

    Q+\mathcal{Q}^{+}: Characterising the structure of young star clusters

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    Many young star clusters appear to be fractal, i.e. they appear to be concentrated in a nested hierarchy of clusters within clusters. We present a new algorithm for statistically analysing the distribution of stars to quantify the level of sub-structure. We suggest that, even at the simplest level, the internal structure of a fractal cluster requires the specification of three parameters. (i) The 3D fractal dimension, D\mathcal{D}, measures the extent to which the clusters on one level of the nested hierarchy fill the volume of their parent cluster. (ii) The number of levels, L\mathcal{L}, reflects the finite ratio between the linear size of the large root-cluster at the top of the hierarchy, and the smallest leaf-clusters at the bottom of the hierarchy. (iii) The volume-density scaling exponent, C=dln[δn]/dln[L]\mathcal{C}=-\textrm{d}\ln[\delta n]/\textrm{d}\ln[L] measures the factor by which the excess density, δn\delta n, in a structure of scale LL, exceeds that of the background formed by larger structures; it is similar, but not exactly equivalent, to the exponent in Larson's scaling relation between density and size for molecular clouds. We describe an algorithm which can be used to constrain the values of (D,L,C)({\cal D},{\cal L},{\cal C}) and apply this method to artificial and observed clusters. We show that this algorithm is able to reliably describe the three dimensional structure of an artificial star cluster from the two dimensional projection, and quantify the varied structures observed in real and simulated clusters.Comment: Accepted by MNRA

    Star Formation triggered by cloud-cloud collisions

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    We present the results of SPH simulations in which two clouds, each having mass Mo ⁣= ⁣500MM_{_{\rm{o}}}\!=\!500\,{\rm M}_{_\odot} and radius Ro ⁣= ⁣2pcR_{_{\rm{o}}}\!=\!2\,{\rm pc}, collide head-on at relative velocities of Δvo=2.4,  2.8,  3.2,  3.6  and  4.0kms1\Delta v_{_{\rm{o}}} =2.4,\;2.8,\;3.2,\;3.6\;{\rm and}\;4.0\,{\rm km}\,{\rm s}^{-1}. There is a clear trend with increasing Δvo\Delta v_{_{\rm{o}}}. At low Δvo\Delta v_{_{\rm{o}}}, star formation starts later, and the shock-compressed layer breaks up into an array of predominantly radial filaments; stars condense out of these filaments and fall, together with residual gas, towards the centre of the layer, to form a single large-NN cluster, which then evolves by competitive accretion, producing one or two very massive protostars and a diaspora of ejected (mainly low-mass) protostars; the pattern of filaments is reminiscent of the hub and spokes systems identified recently by observers. At high Δvo\Delta v_{_{\rm{o}}}, star formation occurs sooner and the shock-compressed layer breaks up into a network of filaments; the pattern of filaments here is more like a spider's web, with several small-NN clusters forming independently of one another, in cores at the intersections of filaments, and since each core only spawns a small number of protostars, there are fewer ejections of protostars. As the relative velocity is increased, the {\it mean} protostellar mass increases, but the {\it maximum} protostellar mass and the width of the mass function both decrease. We use a Minimal Spanning Tree to analyse the spatial distributions of protostars formed at different relative velocities.Comment: 10 pages, 11 figure

    Correspondence

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    Evidence for low-density lipoprotein–induced expression of connective tissue growth factor in mesangial cells

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    Evidence for low-density lipoprotein–induced expression of connective tissue growth factor in mesangial cells.BackgroundAlthough hyperlipidemia is a risk factor for the progression of renal damage, the relationship between increased plasma lipoproteins and glomerular injury is poorly defined. Connective tissue growth factor (CTGF) is emerging as a key determinant of progressive fibrotic diseases and its expression is up-regulated by diabetes. To define the mechanisms through which low-density lipoproteins (LDLs) promote glomerular injury, we evaluated whether LDL can modulate the expression of CTGF and collagen I.MethodsThe effects of LDL on CTGF and collagen I expression were carried out in rat mesangial cells.ResultsTreatment of mesangial cells with LDL for 24 hours produced a significant increase in the protein levels of CTGF and collagen I compared to unstimulated controls. To explore if CTGF and collagen I are downstream targets for regulation by transforming growth factor-β (TGF-β), mesangial cells were treated with various concentration of TGF-β for 24 hours. TGF-β produced a concentration-dependent increase in the protein levels of CTGF and collagen I. The increase in CTGF and collagen I induced by LDL was significantly inhibited by neutralizing anti-TGF-β antibodies. Inhibition of p38mapk or p42/44mapk activities did not affect LDL-induced TGF-β1, CTGF, and collagen I expression, whereas inhibition of c-Jun NH2-terminal kinase (JNK) suppressed LDL-induced TGF-β, CTGF, and collagen I expression.ConclusionThese findings implicate JNK pathway and TGF-β1 as key players in LDL signaling leading to CTGF and collagen I expression in mesangial cells. The data also point to a potential mechanistic pathway through which lipoproteins may promote glomerular injury

    Risk Factors Related to Inflammation and Endothelial Dysfunction in the DCCT/EDIC Cohort and Their Relationship With Nephropathy and Macrovascular Complications

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    OBJECTIVE—Because endothelial cell dysfunction and inflammation are key contributors to the development of complications in type 1 diabetes, we studied risk factors related to endothelial dysfunction and inflammation (C-reactive protein and fibrinogen, soluble vascular cell adhesion molecule-1, intracellular adhesion molecule-1, and E-selectin, and fibrinolytic markers) in a subgroup of patients from the Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Intervention and Complications (EDIC) study cohort

    The Hi-GAL compact source catalogue – I. The physical properties of the clumps in the inner Galaxy (−71. ◦ 0 < ℓ < 67.◦ 0)

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    Hi-GAL (Herschel InfraRed Galactic Plane Survey) is a large-scale survey of the Galactic plane, performed with Herschel in five infrared continuum bands between 70 and 500 µm. We present a band-merged catalogue of spatially matched sources and their properties derived from fits to the spectral energy distributions (SEDs) and heliocentric distances, based on the photometric catalogues presented in Molinari et al., covering the portion of Galactic plane −71.◦ 0 < ℓ < 67.◦ 0. The band-merged catalogue contains 100 922 sources with a regular SED, 24 584 of which show a 70-µm counterpart and are thus considered protostellar, while the remainder are considered starless. Thanks to this huge number of sources, we are able to carry out a preliminary analysis of early stages of star formation, identifying the conditions that characterize different evolutionary phases on a statistically significant basis. We calculate surface densities to investigate the gravitational stability of clumps and their potential to form massive stars. We also explore evolutionary status metrics such as the dust temperature, luminosity and bolometric temperature, finding that these are higher in protostellar sources compared to pre-stellar ones. The surface density of sources follows an increasing trend as they evolve from pre-stellar to protostellar, but then it is found to decrease again in the majority of the most evolved clumps. Finally, we study the physical parameters of sources with respect to Galactic longitude and the association with spiral arms, finding only minor or no differences between the average evolutionary status of sources in the fourth and first Galactic quadrants, or between 'on-arm' and 'interarm' positions

    CTGF is a central mediator of tissue remodeling and fibrosis and its inhibition can reverse the process of fibrosis

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    CTGF is a secreted matricellular protein with very complex biology. It has been shown to modulate many signaling pathways leading to cell adhesion and migration, angiogenesis, myofibroblast activation, and extracellular matrix deposition and remodeling, which together lead to tissue remodeling and fibrosis. It has been reported in the literature that inhibition of CTGF expression by siRNA prevents CCl4-induced liver fibrosis and can reverse fibrosis when administered after significant collagen deposition is observed. A monoclonal antibody to CTGF that is currently in clinical development (FG-3019) has demonstrated the ability to reverse vascular stiffening and improve cardiac function in a rat model of diabetic complications. FG-3019 has also exhibited activity in a murine radiation-induced pulmonary fibrosis model. When FG-3019 was administered to mice after a significant radiation-induced increase in lung density could be observed by CT imaging, the density of the lungs was observed to decrease over the period during which the antibody was administered and to remain stable after therapy had ceased. When considered together, these data indicate that inhibition of CTGF can prevent and reverse the process of fibrosis

    Violent masculinities: Gendered dynamics of policing in Rio de Janeiro

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    Historically, policing in Rio de Janeiro has been shaped by the equation of racialized violence and masculinity. Attempts to reform the police have paradoxically drawn on forms of male violence that are centered on the rational and professional use of force and on “softer” practices, such as dialogue and collaboration, symbolically coded as feminine. The failure of police reform reflects the cultural salience of understandings of masculinity centered around violence within the police, historical patterns of policing in Rio, and political actors’ strategic cultivation of male violence. Through Rio de Janeiro's failed attempt at police reform, we theorize the relation between racialized state violence, authoritarian political projects, and transgressive forms of male violence, arguing that an important appeal of authoritarianism lies in its promise to carve out a space for performing what we call wild masculinity. [masculinity, race, police, violence, gender, politics, favela, Rio de Janeiro, Brazil]publishedVersio
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