16 research outputs found

    Mergers, AGN, and 'Normal' Galaxies: Contributions to the Distribution of Star Formation Rates and Infrared Luminosity Functions

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    We use a novel method to predict the contribution of normal star-forming galaxies, merger-induced bursts, and obscured AGN, to IR luminosity functions (LFs) and global SFR densities. We use empirical halo occupation constraints to populate halos with galaxies and determine the distribution of normal and merging galaxies. Each system can then be associated with high-resolution hydrodynamic simulations. We predict the distribution of observed luminosities and SFRs, from different galaxy classes, as a function of redshift from z=0-6. We provide fitting functions for the predicted LFs, quantify the uncertainties, and compare with observations. At all redshifts, 'normal' galaxies dominate the LF at moderate luminosities ~L* (the 'knee'). Merger-induced bursts increasingly dominate at L>>L*; at the most extreme luminosities, AGN are important. However, all populations increase in luminosity at higher redshifts, owing to increasing gas fractions. Thus the 'transition' between normal and merger-dominated sources increases from the LIRG-ULIRG threshold at z~0 to bright Hyper-LIRG thresholds at z~2. The transition to dominance by obscured AGN evolves similarly, at factor of several higher L_IR. At all redshifts, non-merging systems dominate the total luminosity/SFR density, with merger-induced bursts constituting ~5-10% and AGN ~1-5%. Bursts contribute little to scatter in the SFR-stellar mass relation. In fact, many systems identified as 'ongoing' mergers will be forming stars in their 'normal' (non-burst) mode. Counting this as 'merger-induced' star formation leads to a stronger apparent redshift evolution in the contribution of mergers to the SFR density.Comment: 16 pages, 9 figures (+appendices), accepted to MNRAS. A routine to return the galaxy merger rates discussed here is available at http://www.cfa.harvard.edu/~phopkins/Site/mergercalc.htm

    Complex Evolutionary History of the Aeromonas veronii Group Revealed by Host Interaction and DNA Sequence Data

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    Aeromonas veronii biovar sobria, Aeromonas veronii biovar veronii, and Aeromonas allosaccharophila are a closely related group of organisms, the Aeromonas veronii Group, that inhabit a wide range of host animals as a symbiont or pathogen. In this study, the ability of various strains to colonize the medicinal leech as a model for beneficial symbiosis and to kill wax worm larvae as a model for virulence was determined. Isolates cultured from the leech out-competed other strains in the leech model, while most strains were virulent in the wax worms. Three housekeeping genes, recA, dnaJ and gyrB, the gene encoding chitinase, chiA, and four loci associated with the type three secretion system, ascV, ascFG, aexT, and aexU were sequenced. The phylogenetic reconstruction failed to produce one consensus tree that was compatible with most of the individual genes. The Approximately Unbiased test and the Genetic Algorithm for Recombination Detection both provided further support for differing evolutionary histories among this group of genes. Two contrasting tests detected recombination within aexU, ascFG, ascV, dnaJ, and gyrB but not in aexT or chiA. Quartet decomposition analysis indicated a complex recent evolutionary history for these strains with a high frequency of horizontal gene transfer between several but not among all strains. In this study we demonstrate that at least for some strains, horizontal gene transfer occurs at a sufficient frequency to blur the signal from vertically inherited genes, despite strains being adapted to distinct niches. Simply increasing the number of genes included in the analysis is unlikely to overcome this challenge in organisms that occupy multiple niches and can exchange DNA between strains specialized to different niches. Instead, the detection of genes critical in the adaptation to specific niches may help to reveal the physiological specialization of these strains

    Correction to: Cluster identification, selection, and description in Cluster randomized crossover trials: the PREP-IT trials

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    An amendment to this paper has been published and can be accessed via the original article

    Patient and stakeholder engagement learnings: PREP-IT as a case study

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    Injury stimulates an innate respiratory immunoglobulin a immune response in humans

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    BACKGROUND: Secretory immunoglobulin A (SIgA) is the specific immune antibacterial defense. Since pneumonia frequently complicates the course of trauma patients, we studied early airway immune responses after injury. METHODS: Twelve severely injured, intubated (expected for >/=5 d) patients had tracheal and bilateral lung lavage (BAL) within 30 hours of injury (n = 12). Epithelial lining fluid (ELF) volume and SIgA were measured by urea dilution and enzyme-linked immunosorbent assay (ELISA), respectively. Control BAL specimens were obtained from eight healthy elective surgical patients. Anatomically based comparisons were made between groups with Welch's unpaired t test. To verify human data, 30 male mice received no injury (time 0, n = 7) or injury with abdominal and neck incisions and were killed for airway IgA at 4 (n = 7), 8 (n = 8), and 24 (n = 8) hours. Analysis of variance (ANOVA) and Fisher's protected least significant difference testing was used to analyze animal data. RESULTS: Initial trauma patient SIgA concentration (SIgA/mL ELF) increased compared with control in the lungs bilaterally (p < 0.05 both right and left). ELF volume was significantly higher in the right lung (p = 0.02) and just missed statistical significance (p = 0.07) on the left. Mouse IgA increased 8 hours after stress (p < 0.05 versus 0, 4, and 24 hours) and returned to normal by 24 hours. CONCLUSION: A previously unrecognized innate human airway mucosal immune response with increased airway SIgA and ELF occurs after severe injury and is reproducible experimentally. This accessible, quantifiable human response allows study of clinical strategies to reduce infections via mucosal immune therapies
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