The Physical Conditions in Starbursts Derived from Bayesian Fitting of Mid-IR SEDS: 30 Doradus as a Template

To understand and interpret the observed Spectral Energy Distributions (SEDs) of starbursts, theoretical or semi-empirical SED models are necessary. Yet, while they are well-founded in theory, independent verification and calibration of these models, including the exploration of possible degeneracies between their parameters, are rarely made. As a consequence, a robust fitting method that leads to unique and reproducible results has been lacking. Here we introduce a novel approach based on Bayesian analysis to fit the Spitzer-IRS spectra of starbursts using the SED models proposed by Groves et al. (2008). We demonstrate its capabilities and verify the agreement between the derived best fit parameters and actual physical conditions by modelling the nearby, well-studied, giant HII region 30 Dor in the LMC. The derived physical parameters, such as cluster mass, cluster age, ISM pressure and covering fraction of photodissociation regions, are representative of the 30 Dor region. The inclusion of the emission lines in the modelling is crucial to break degeneracies. We investigate the limitations and uncertainties by modelling sub-regions, which are dominated by single components, within 30 Dor. A remarkable result for 30 Doradus in particular is a considerable contribution to its mid-infrared spectrum from hot ({\simeq} 300K) dust. The demonstrated success of our approach will allow us to derive the physical conditions in more distant, spatially unresolved starbursts.Comment: 17 pages, 10 figures. Accepted por publication in the Astrophysical Journa

D25V apolipoprotein C-III variant causes dominant hereditary systemic amyloidosis and confers cardiovascular protective lipoprotein profile

Apolipoprotein C-III deficiency provides cardiovascular protection, but apolipoprotein C-III is not known to be associated with human amyloidosis. Here we report a form of amyloidosis characterized by renal insufficiency caused by a new apolipoprotein C-III variant, D25V. Despite their uremic state, the D25V-carriers exhibit low triglyceride (TG) and apolipoprotein C-III levels, and low very-low-density lipoprotein (VLDL)/high high-density lipoprotein (HDL) profile. Amyloid fibrils comprise the D25V-variant only, showing that wild-type apolipoprotein C-III does not contribute to amyloid deposition in vivo. The mutation profoundly impacts helical structure stability of D25V-variant, which is remarkably fibrillogenic under physiological conditions in vitro producing typical amyloid fibrils in its lipid-free form. D25V apolipoprotein C-III is a new human amyloidogenic protein and the first conferring cardioprotection even in the unfavourable context of renal failure, extending the evidence for an important cardiovascular protective role of apolipoprotein C-III deficiency. Thus, fibrate therapy, which reduces hepatic APOC3 transcription, may delay amyloid deposition in affected patients