We present a statistical analysis of the mid-infrared (MIR) spectra of 248 luminous infrared (IR) galaxies (LIRGs) which comprise the Great Observatories All-sky LIRG Survey (GOALS) observed with the ...Infrared Spectrograph (IRS) on board the Spitzer Space Telescope. The GOALS sample enables a direct measurement of the relative contributions of star formation and active galactic nuclei (AGNs) to the total IR emission from a large sample of local LIRGs. The AGN contribution to the MIR emission (f AGN) is estimated by employing several diagnostics based on the properties of the Ne V, O IV, and Ne II fine-structure gas emission lines, the 6.2 Delta *mm polycyclic aromatic hydrocarbon (PAH), and the shape of the MIR continuum. We find that 18% of all LIRGs contain an AGN and that in 10% of all sources the AGN contributes more than 50% of the total IR luminosity. Summing up the total IR luminosity contributed by AGNs in all our sources suggests that AGNs supply ~12% of the total energy emitted by LIRGs. The average spectrum of sources with an AGN looks similar to the average spectrum of sources without an AGN, but it has lower PAH emission and a flatter MIR continuum. AGN-dominated LIRGs have higher IR luminosities, warmer MIR colors, and are found in interacting systems more often than pure starburst LIRGs. However, we find no linear correlations between these properties and f AGN. We used the IRAC colors of LIRGs to confirm that finding AGNs on the basis of their MIR colors may miss ~40% of AGN-dominated (U)LIRGs.
The Chandra component of the Great Observatories All-Sky Luminous Infrared Galaxy Survey (GOALS) presently contains 44 luminous and ultraluminous infrared galaxies (ULIRGs) with log (L IR/L ) = ...11.73-12.57. Omitting 15 obvious active galactic nuclei (AGNs), the other galaxies are, on average, underluminous in the 2-10 keV band by 0.7 dex at a given far-infrared luminosity, compared with nearby star-forming galaxies with lower star formation rates. The integrated spectrum of these hard X-ray quiet galaxies shows strong high-ionization Fe K emission (Fe XXV at 6.7 keV), which is incompatible with X-ray binaries as its origin. The X-ray quietness and the Fe K feature could be explained by hot gas produced in a starburst, provided that the accompanying copious emission from high-mass X-ray binaries is somehow suppressed. Alternatively, these galaxies may contain deeply embedded supermassive black holes that power the bulk of their infrared luminosity and only faint photoionized gas is visible, as seen in some ULIRGs with a Compton-thick AGN.
Given substantial advances in venovenous extracorporeal membrane oxygenation (ECMO) technology, long-term support is increasingly feasible. Although the benefits of short-term ECMO as a bridge to ...recovery in acute respiratory distress syndrome (ARDS) are well described, the utility and outcomes of long-term support remain unclear.
Patients requiring ECMO for ARDS between January 2009 and November 2012 were retrospectively reviewed and analyzed separately for those requiring ECMO support for less than 3 weeks or for 3 weeks or longer. Demographic factors, ECMO variables, and outcomes were assessed.
Fifty-five patients with ARDS received ECMO during the study period, with 11 patients requiring long-term ECMO support and a median duration of 36 (interquartile range: 24 to 68) days. Recovery was the initial goal in all patients. Pre-ECMO mechanical ventilatory support, indices of disease severity, and the ECMO cannulation strategy were similar between the two groups. Eight (73%) patients receiving long-term support were bridged to recovery, and 1 patient was bridged to transplantation after a refractory course. Eight (73%) patients receiving long-term support and 25 (57%) patients receiving short-term support survived to 30 days and hospital discharge.
Previously, long-term ECMO support was thought to be associated with unfavorable outcomes. This study, however, may provide support for the efficacy of ECMO support even for 3 weeks or more as a bridge to recovery or transplantation.
The RNA modification N6-methyladenosine (m6A) post-transcriptionally regulates RNA function. The cellular machinery that controls m6A includes methyltransferases and demethylases that add or remove ...this modification, as well as m6A-binding YTHDF proteins that promote the translation or degradation of m6A-modified mRNA. We demonstrate that m6A modulates infection by hepatitis C virus (HCV). Depletion of m6A methyltransferases or an m6A demethylase, respectively, increases or decreases infectious HCV particle production. During HCV infection, YTHDF proteins relocalize to lipid droplets, sites of viral assembly, and their depletion increases infectious viral particles. We further mapped m6A sites across the HCV genome and determined that inactivating m6A in one viral genomic region increases viral titer without affecting RNA replication. Additional mapping of m6A on the RNA genomes of other Flaviviridae, including dengue, Zika, yellow fever, and West Nile virus, identifies conserved regions modified by m6A. Altogether, this work identifies m6A as a conserved regulatory mark across Flaviviridae genomes.
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•The RNA genomes of HCV, ZIKV, DENV, YFV, and WNV contain m6A modification•The cellular m6A machinery regulates HCV infectious particle production•YTHDF proteins reduce HCV particle production and localize at viral assembly sites•m6A-abrogating mutations in HCV E1 increase infectious particle production
N6-methyladenosine (m6A) post-transcriptionally regulates RNA function. Gokhale et al. demonstrate that the RNA genomes of HCV, ZIKV, DENV, YFV, and WNV are modified by m6A. Depletion of cellular machinery that regulates m6A or introduction of m6A-abrogating mutations within HCV RNA increase viral particle production, suggesting that m6A negatively regulates HCV.
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