| 1. |
- Cicone, C., et al.
(författare)
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Massive molecular outflows and evidence for AGN feedback from CO observations
- 2014
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Ingår i: Astronomy and Astrophysics. - : EDP Sciences. - 0004-6361 .- 1432-0746. ; 562, s. 25-
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Tidskriftsartikel (refereegranskat)abstract
- We study the properties of massive, galactic-scale outflows of molecular gas and investigate their impact on galaxy evolution. We present new IRAMPdBI CO(1-0) observations of local ultra-luminous infrared galaxies (ULIRGs) and quasar-hosts: a clear signature of massive and energetic molecular outflows, extending on kpc scales, is found in the CO(1-0) kinematics of four out of seven sources, with measured outflow rates of several 100M(circle dot)yr(-1). We combine these new observations with data from the literature, and explore the nature and origin of massive molecular outflows within an extended sample of 19 local galaxies. We find that starburst-dominated galaxies have an outflow rate comparable to their star formation rate (SFR), or even higher by a factor of similar to 2-4, implying that starbursts can indeed be effective in removing cold gas from galaxies. Nevertheless, our results suggest that the presence of an active galactic nucleus (AGN) can boost the outflow rate by a large factor, which is found to increase with the L-AGN/L-bol ratio. The gas depletion time scales due to molecular outflows are anti-correlated with the presence and luminosity of an AGN in these galaxies, and range from a few hundred million years in starburst galaxies down to just a few million years in galaxies hosting powerful AGNs. In quasar hosts, the depletion time scales due to the outflow are much shorter than the depletion time scales due to star formation. We estimate the outflow kinetic power and find that, for galaxies hosting powerful AGNs, it corresponds to about 5% of the AGN luminosity, as expected by models of AGN feedback. Moreover, we find that momentum rates of about 20 L-AGN/c are common among the AGN-dominated sources in our sample. For "pure" starburst galaxies, our data tentatively support models in which outflows are mostly momentum-driven by the radiation pressure from young stars onto dusty clouds. Overall, our results indicate that, although starbursts are effective in powering massive molecular outflows, the presence of an AGN may strongly enhance such outflows, and therefore have a profound feedback effect on the evolution of galaxies by efficiently removing fuel for star formation, hence quenching star formation.
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| 2. |
- Beyder, Arthur, et al.
(författare)
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Loss-of-Function of the Voltage-Gated Sodium Channel Na(V)1.5 (Channelopathies) in Patients With Irritable Bowel Syndrome
- 2014
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Ingår i: Gastroenterology. - : Elsevier BV. - 0016-5085 .- 1528-0012. ; 146:7, s. 1659-1668
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND & AIMS: SCN5A encodes the a-subunit of the voltage-gated sodium channel Na(V)1.5. Many patients with cardiac arrhythmias caused by mutations in SCN5A also have symptoms of irritable bowel syndrome (IBS). We investigated whether patients with IBS have SCN5A variants that affect the function of Na(V)1.5. METHODS: We performed genotype analysis of SCN5A in 584 persons with IBS and 1380 without IBS (controls). Mutant forms of SCN5A were expressed in human embryonic kidney-293 cells, and functions were assessed by voltage clamp analysis. A genome-wide association study was analyzed for an association signal for the SCN5A gene, and replicated in 1745 patients in 4 independent cohorts of IBS patients and controls. RESULTS: Missense mutations were found in SCN5A in 13 of 584 patients (2.2%, probands). Diarrhea-predominant IBS was the most prevalent form of IBS in the overall study population (25%). However, a greater percentage of individuals with SCN5A mutations had constipation-predominant IBS (31%) than diarrhea-predominant IBS (10%; P < .05). Electrophysiologic analysis showed that 10 of 13 detected mutations disrupted Na(V)1.5 function (9 loss-of-function and 1 gain-of-function function). The p. A997T-Na(V)1.5 had the greatest effect in reducing Na(V)1.5 function. Incubation of cells that expressed this variant with mexiletine restored their sodium current and administration of mexiletine to 1 carrier of this mutation (who had constipation-predominant IBS) normalized their bowel habits. In the genome-wide association study and 4 replicated studies, the SCN5A locus was strongly associated with IBS. CONCLUSIONS: About 2% of patients with IBS carry mutations in SCN5A. Most of these are loss-of-function mutations that disrupt Na(V)1.5 channel function. These findings provide a new pathogenic mechanism for IBS and possible treatment options.
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| 3. |
- Beyder, Arthur, et al.
(författare)
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Loss-of-function of the voltage-gated sodium channel NaV1.5 (channelopathies) in patients with irritable bowel syndrome.
- 2014
-
Ingår i: Gastroenterology. - : Elsevier BV. - 0016-5085 .- 1528-0012. ; 146:7
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND & AIMS: SCN5A encodes the α-subunit of the voltage-gated sodium channel NaV1.5. Many patients with cardiac arrhythmias caused by mutations in SCN5A also have symptoms of irritable bowel syndrome (IBS). We investigated whether patients with IBS have SCN5A variants that affect the function of NaV1.5.METHODS: We performed genotype analysis of SCN5A in 584 persons with IBS and 1380 without IBS (controls). Mutant forms of SCN5A were expressed in human embryonic kidney-293 cells, and functions were assessed by voltage clamp analysis. A genome-wide association study was analyzed for an association signal for the SCN5A gene, and replicated in 1745 patients in 4 independent cohorts of IBS patients and controls.RESULTS: Missense mutations were found in SCN5A in 13 of 584 patients (2.2%, probands). Diarrhea-predominant IBS was the most prevalent form of IBS in the overall study population (25%). However, a greater percentage of individuals with SCN5A mutations had constipation-predominant IBS (31%) than diarrhea-predominant IBS (10%; P < .05). Electrophysiologic analysis showed that 10 of 13 detected mutations disrupted NaV1.5 function (9 loss-of-function and 1 gain-of-function function). The p. A997T-NaV1.5 had the greatest effect in reducing NaV1.5 function. Incubation of cells that expressed this variant with mexiletine restored their sodium current and administration of mexiletine to 1 carrier of this mutation (who had constipation-predominant IBS) normalized their bowel habits. In the genome-wide association study and 4 replicated studies, the SCN5A locus was strongly associated with IBS.CONCLUSIONS: About 2% of patients with IBS carry mutations in SCN5A. Most of these are loss-of-function mutations that disrupt NaV1.5 channel function. These findings provide a new pathogenic mechanism for IBS and possible treatment options.
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