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- Aad, G, et al.
(författare)
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- 2015
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swepub:Mat__t
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- Heuzé, Céline, 1988, et al.
(författare)
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Increasing vertical mixing to reduce Southern Ocean deep convection in NEMO3.4
- 2015
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Ingår i: Geoscientific Model Development. - : Copernicus GmbH. - 1991-959X .- 1991-9603. ; 8:10, s. 3119-3130
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Tidskriftsartikel (refereegranskat)abstract
- Most CMIP5 (Coupled Model Intercomparison Project Phase 5) models unrealistically form Antarctic Bottom Water by open ocean deep convection in the Weddell and Ross seas. To identify the mechanisms triggering Southern Ocean deep convection in models, we perform sensitivity experiments on the ocean model NEMO3.4 forced by prescribed atmospheric fluxes. We vary the vertical velocity scale of the Langmuir turbulence, the fraction of turbulent kinetic energy transferred below the mixed layer, and the background diffusivity and run short simulations from 1980. All experiments exhibit deep convection in the Riiser-Larsen Sea in 1987; the origin is a positive sea ice anomaly in 1985, causing a shallow anomaly in mixed layer depth, hence anomalously warm surface waters and subsequent polynya opening. Modifying the vertical mixing impacts both the climatological state and the associated surface anomalies. The experiments with enhanced mixing exhibit colder surface waters and reduced deep convection. The experiments with decreased mixing give warmer surface waters, open larger polynyas causing more saline surface waters and have deep convection across the Weddell Sea until the simulations end. Extended experiments reveal an increase in the Drake Passage transport of 4 Sv each year deep convection occurs, leading to an unrealistically large transport at the end of the simulation. North Atlantic deep convection is not significantly affected by the changes in mixing parameters. As new climate model overflow parameterisations are developed to form Antarctic Bottom Water more realistically, we argue that models would benefit from stopping Southern Ocean deep convection, for example by increasing their vertical mixing.
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- Tejada, Thor, et al.
(författare)
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IGF-1 degradation by mouse mast cell protease 4 promotes cell death and adverse cardiac remodeling days after a myocardial infarction
- 2016
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 113:25, s. 6949-6954
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Tidskriftsartikel (refereegranskat)abstract
- Heart disease is a leading cause of death in adults. Here, we show that a few days after coronary artery ligation and reperfusion, the ischemia-injured heart elaborates the cardioprotective polypeptide, insulin-like growth factor-1 (IGF-1), which activates IGF-1 receptor prosurvival signaling and improves cardiac left ventricular systolic function. However, this signaling is antagonized by the chymase, mouse mast cell protease 4 (MMCP-4), which degrades IGF-1. We found that deletion of the gene encoding MMCP-4 (Mcpt4), markedly reduced late, but not early, infarct size by suppressing IGF-1 degradation and, consequently, diminished cardiac dysfunction and adverse structural remodeling. Our findings represent the first demonstration to our knowledge of tissue IGF-1 regulation through proteolytic degradation and suggest that chymase inhibition may be a viable therapeutic approach to enhance late cardioprotection in post-ischemic heart disease.
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