The Dragonfly Galaxy: II. ALMA unveils a triple merger and gas exchange in a hyper-luminous radio galaxy at z = 2

The Dragonfly Galaxy (MRC 0152-209), at redshift z ~  2, is one of the most vigorously star-forming radio galaxies in the Universe. What triggered its activity? We present ALMA Cycle 2 observations of cold molecular CO(6−5) gas and dust, which reveal that this is likely a gas-rich triple merger. It consists of a close double nucleus (separation ~4 kpc) and a weak CO-emitter at ~10  kpc distance, all of which have counterparts in HST/NICMOS imagery. The hyper-luminous starburst and powerful radio-AGN were triggered at this precoalescent stage of the merger. The CO(6−5) traces dense molecular gas in the central region, and complements existing CO(1−0) data, which reveal more widespread tidal debris of cold gas. We also find ~1010 M☉ of molecular gas with enhanced excitation at the highest velocities. At least 20−50% of this high-excitation, high-velocity gas shows kinematics that suggests it is being displaced and redistributed within the merger, although with line-of-sight velocities of |v| < 500 km s-1, this gas will probably not escape the system. The processes that drive the redistribution of cold gas are likely related to either the gravitational interaction between two kpc-scale discs, or starburst/AGN-driven outflows. We estimate that the rate at which the molecular gas is redistributed is at least [Ṁentity!#x2009!]~ 1200 ± 500 M☉ yr-1, and could perhaps even approach the star formation rate of ~3000 ± 800 M☉ yr-1. The fact that the gas depletion and gas redistribution timescales are similar implies that dynamical processes can be important in the evolution of massive high-z galaxies

Attention to Speech-Accompanying Gestures: Eye Movements and Information Uptake

There is growing evidence that addressees in interaction integrate the semantic information conveyed by speakers’ gestures. Little is known, however, about whether and how addressees’ attention to gestures and the integration of gestural information can be modulated. This study examines the influence of a social factor (speakers’ gaze to their own gestures), and two physical factors (the gesture’s location in gesture space and gestural holds) on addressees’ overt visual attention to gestures (direct fixations of gestures) and their uptake of gestural information. It also examines the relationship between gaze and uptake. The results indicate that addressees’ overt visual attention to gestures is affected both by speakers’ gaze and holds but for different reasons, whereas location in space plays no role. Addressees’ uptake of gesture information is only influenced by speakers’ gaze. There is little evidence of a direct relationship between addressees’ direct fixations of gestures and their uptake

SPT 0538-50: Physical conditions in the ISM of a strongly lensed dusty star-forming galaxy at z=2.8

We present observations of SPT-S J053816-5030.8, a gravitationally-lensed dusty star forming galaxy (DSFG) at z = 2.7817, first discovered at millimeter wavelengths by the South Pole Telescope. SPT 0538-50 is typical of the brightest sources found by wide-field millimeter-wavelength surveys, being lensed by an intervening galaxy at moderate redshift (in this instance, at z = 0.441). We present a wide array of multi-wavelength spectroscopic and photometric data on SPT 0538-50, including data from ALMA, Herschel PACS and SPIRE, Hubble, Spitzer, VLT, ATCA, APEX, and the SMA. We use high resolution imaging from HST to de-blend SPT 0538-50, separating DSFG emission from that of the foreground lens. Combined with a source model derived from ALMA imaging (which suggests a magnification factor of 21 +/- 4), we derive the intrinsic properties of SPT 0538-50, including the stellar mass, far-IR luminosity, star formation rate, molecular gas mass, and - using molecular line fluxes - the excitation conditions within the ISM. The derived physical properties argue that we are witnessing compact, merger-driven star formation in SPT 0538-50, similar to local starburst galaxies, and unlike that seen in some other DSFGs at this epoch.Comment: 16 pages, 11 figures. Accepted for publication in Ap

The diacylglycerol kinase α/Atypical PKC/β1 integrin pathway in SDF-1α mammary carcinoma invasiveness

Diacylglycerol kinase α (DGKα), by phosphorylating diacylglycerol into phosphatidic acid, provides a key signal driving cell migration and matrix invasion. We previously demonstrated that in epithelial cells activation of DGKα activity promotes cytoskeletal remodeling and matrix invasion by recruiting atypical PKC at ruffling sites and by promoting RCP-mediated recycling of α5β1 integrin to the tip of pseudopods. In here we investigate the signaling pathway by which DGKα mediates SDF-1α-induced matrix invasion of MDA-MB-231 invasive breast carcinoma cells. Indeed we showed that, following SDF-1α stimulation, DGKα is activated and localized at cell protrusion, thus promoting their elongation and mediating SDF-1α induced MMP-9 metalloproteinase secretion and matrix invasion. Phosphatidic acid generated by DGKα promotes localization at cell protrusions of atypical PKCs which play an essential role downstream of DGKα by promoting Rac-mediated protrusion elongation and localized recruitment of β1 integrin and MMP-9. We finally demonstrate that activation of DGKα, atypical PKCs signaling and β1 integrin are all essential for MDA-MB-231 invasiveness. These data indicates the existence of a SDF-1α induced DGKα - atypical PKC - β1 integrin signaling pathway, which is essential for matrix invasion of carcinoma cells

Detecting small low emission radiating sources

The article addresses the possibility of robust detection of geometrically small, low emission sources on a significantly stronger background. This problem is important for homeland security. A technique of detecting such sources using Compton type cameras is developed, which is shown on numerical examples to have high sensitivity and specificity and also allows to assign confidence probabilities of the detection. 2D case is considered in detail

Perlecan Maintains microvessel integrity in vivo and modulates their formation in vitro

Perlecan is a heparan sulfate proteoglycan assembled into the vascular basement membranes (BMs) during vasculogenesis. In the present study we have investigated vessel formation in mice, teratomas and embryoid bodies (EBs) in the absence of perlecan. We found that perlecan was dispensable for blood vessel formation and maturation until embryonic day (E) 12.5. At later stages of development 40% of mutant embryos showed dilated microvessels in brain and skin, which ruptured and led to severe bleedings. Surprisingly, teratomas derived from perlecan-null ES cells showed efficient contribution of perlecan-deficient endothelial cells to an apparently normal tumor vasculature. However, in perlecan-deficient EBs the area occupied by an endothelial network and the number of vessel branches were significantly diminished. Addition of FGF-2 but not VEGF165 rescued the in vitro deficiency of the mutant ES cells. Furthermore, in the absence of perlecan in the EB matrix lower levels of FGFs are bound, stored and available for cell surface presentation. Altogether these findings suggest that perlecan supports the maintenance of brain and skin subendothelial BMs and promotes vasculo- and angiogenesis by modulating FGF-2 function

Inhibition of miR-29 by TGF-beta-Smad3 Signaling through Dual Mechanisms Promotes Transdifferentiation of Mouse Myoblasts into Myofibroblasts

MicroRNAs (miRNAs) are non-coding RNAs that regulate gene expression in post-transcriptional fashion, and emerging studies support their importance in regulating many biological processes, including myogenic differentiation and muscle development. miR-29 is a promoting factor during myogenesis but its full spectrum of impact on muscle cells has yet to be explored. Here we describe an analysis of miR-29 affected transcriptome in C2C12 muscle cells using a high throughput RNA-sequencing platform. The results reveal that miR-29 not only functions to promote myogenic differentiation but also suppresses the transdifferentiation of myoblasts into myofibroblasts. miR-29 inhibits the fibrogenic differentiation through down-regulating both extracellular matrix genes and cell adhesion genes. We further demonstrate that miR-29 is under negative regulation by TGF-beta (TGF-β)–Smad3 signaling via dual mechanisms of both inhibiting MyoD binding and enhancing Yin Yang 1 (YY1)-recruited Polycomb association. Together, these results identify miR-29 as a pleiotropic molecule in both myogenic and fibrogenic differentiation of muscle cells