| 1. |
- Kanai, M, et al.
(författare)
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- 2023
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swepub:Mat__t
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| 2. |
- Giménez-Arteaga, C., et al.
(författare)
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Outshining in the spatially resolved analysis of a strongly lensed galaxy at z = 6.072 with JWST NIRCam
- 2024
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Ingår i: Astronomy and Astrophysics. - 0004-6361 .- 1432-0746. ; 686
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Tidskriftsartikel (refereegranskat)abstract
- We present JWST/NIRCam observations of a strongly lensed, sub-L∗, multiply imaged galaxy at z=6.072, with magnification factors μ³20 across the galaxy. The galaxy has rich HST, MUSE, and ALMA ancillary observations across a broad wavelength range. Aiming to quantify the reliability of stellar mass estimates of high redshift galaxies, we performed a spatially resolved analysis of the physical properties at scales of ~200 pc, inferred from spectral energy distribution (SED) modelling of five JWST/NIRCam imaging bands covering 0.16 μm < λrest < 0.63 μm on a pixel-by-pixel basis. We find young stars surrounded by extended older stellar populations. By comparing Hα+[Nâ¯II] and [Oâ¯III]+Hβ maps inferred from the image analysis with our additional NIRSpec integral field unit (IFU) data, we find that the spatial distribution and strength of the line maps are in agreement with the IFU measurements. We explore different parametric star formation history (SFH) forms with BAGPIPES on the spatially integrated photometry, finding that a double power-law (DPL) star formation history retrieves the closest value to the spatially resolved stellar mass estimate, and other SFH forms suffer from the dominant outshining emission from the youngest stars, thus underestimating the stellar mass - up to ~0.5 dex. On the other hand, the DPL cannot match the IFU-measured emission lines. Additionally, the ionising photon production efficiency may be overestimated in a spatially integrated approach by ~0.15 dex, when compared to a spatially resolved analysis. The agreement with the IFU measurements implies that our pixel-by-pixel results derived from the broadband images are robust, and that the mass discrepancies we find with spatially integrated estimates are not just an effect of SED-fitting degeneracies or the lack of NIRCam coverage. Additionally, this agreement points towards the pixel-by-pixel approach as a way to mitigate the general degeneracy between the flux excess from emission lines and underlying continuum, especially when lacking photometric medium-band coverage and/or IFU observations. This study stresses the importance of studying galaxies as the complex systems that they are, resolving their stellar populations when possible, or using more flexible SFH parameterisations. This can aid our understanding of the early stages of galaxy evolution by addressing the challenge of inferring robust stellar masses and ionising photon production efficiencies of high redshift galaxies.
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| 3. |
- Liang, Y., et al.
(författare)
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Desmosomal COP9 regulates proteome degradation in arrhythmogenic right ventricular dysplasia/cardiomyopathy
- 2021
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Ingår i: Journal of Clinical Investigation. - : American Society for Clinical Investigation. - 0021-9738 .- 1558-8238. ; 131:11
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Tidskriftsartikel (refereegranskat)abstract
- Dysregulated protein degradative pathways are increasingly recognized as mediators of human disease. This mechanism may have particular relevance to desmosomal proteins that play critical structural roles in both tissue architecture and cell-cell communication, as destabilization/breakdown of the desmosomal proteome is a hallmark of genetic-based desmosomal-targeted diseases, such as the cardiac disease arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). However, no information exists on whether there are resident proteins that regulate desmosomal proteome homeostasis. Here, we uncovered a cardiac constitutive photomorphogenesis 9 (COP9) desmosomal resident protein complex, composed of subunit 6 of the COP9 signalosome (CSN6), that enzymatically restricted neddylation and targeted desmosomal proteome degradation. CSN6 binding, localization, levels, and function were affected in hearts of classic mouse and human models of ARVD/C affected by desmosomal loss and mutations, respectively. Loss of desmosomal proteome degradation control due to junctional reduction/loss of CSN6 and human desmosomal mutations destabilizing junctional CSN6 were also sufficient to trigger ARVD/C in mice. We identified a desmosomal resident regulatory complex that restricted desmosomal proteome degradation and disease.
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| 4. |
- Omerovic, Elmir, 1968, et al.
(författare)
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Pathophysiology of Takotsubo syndrome - a joint scientific statement from the Heart Failure Association Takotsubo Syndrome Study Group and Myocardial Function Working Group of the European Society of Cardiology - Part 1: overview and the central role for catecholamines and sympathetic nervous system
- 2022
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Ingår i: European Journal of Heart Failure. - : Wiley. - 1388-9842 .- 1879-0844. ; 24:2, s. 257-273
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Tidskriftsartikel (refereegranskat)abstract
- This is the first part of a scientific statement from the Heart Failure Association (HFA) of the European Society of Cardiology focused upon the pathophysiology of Takotsubo syndrome and is complimentary to the previous HFA position statement on Takotsubo syndrome which focused upon clinical management. In part 1 we provide an overview of the pathophysiology of Takotsubo syndrome and fundamental questions to consider. We then review and discuss the central role of catecholamines and the sympathetic nervous system in the pathophysiology, and the direct effects of high surges in catecholamines upon myocardial biology including beta-adrenergic receptor signalling, G-protein coupled receptor kinases, cardiomyocyte calcium physiology, myofilament physiology, cardiomyocyte gene expression, myocardial electrophysiology and arrhythmogenicity, myocardial inflammation, metabolism and energetics. The integrated effects upon ventricular haemodynamics are discussed and integrated into the pathophysiological model.
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| 5. |
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