Aperture-free star formation rate of SDSS star-forming galaxies

Large area surveys with a high number of galaxies observed have undoubtedly marked a milestone in the understanding of several properties of galaxies, such as star-formation history, morphology, and metallicity. However, in many cases, these surveys provide fluxes from fixed small apertures (e.g. fibre), which cover a scant fraction of the galaxy, compelling us to use aperture corrections to study the global properties of galaxies. In this work, we derive the current total star formation rate (SFR) of Sloan Digital Sky Survey (SDSS) star-forming galaxies, using an empirically based aperture correction of the measured $\rm H\alpha$ flux for the first time, thus minimising the uncertainties associated with reduced apertures. All the $\rm H\alpha$ fluxes have been extinction-corrected using the $\rm H\alpha/H\beta$ ratio free from aperture effects. The total SFR for $\sim$210,000 SDSS star-forming galaxies has been derived applying pure empirical $\rm H\alpha$ and $\rm H\alpha/H\beta$ aperture corrections based on the Calar Alto Legacy Integral Field Area (CALIFA) survey. We find that, on average, the aperture-corrected SFR is $\sim$0.65dex higher than the SDSS fibre-based SFR. The relation between the SFR and stellar mass for SDSS star-forming galaxies (SFR--$\rm M_\star$) has been obtained, together with its dependence on extinction and $\rm H\alpha$ equivalent width. We compare our results with those obtained in previous works and examine the behaviour of the derived SFR in six redshift bins, over the redshift range $\rm 0.005 \leq z\leq 0.22$. The SFR--$\rm M_\star$ sequence derived here is in agreement with selected observational studies based on integral field spectroscopy of individual galaxies as well as with the predictions of recent theoretical models of disc galaxies

The extended HeII4686-emitting region in IZw18 unveiled: clues for peculiar ionizing sources

New integral field spectroscopy has been obtained for IZw18, the nearby lowest-metallicity galaxy considered our best local analog of systems forming at high-z. Here we report the spatially resolved spectral map of the nebular HeII4686 emission in IZw18, from which we derived for the first time its total HeII-ionizing flux. Nebular HeII emission implies the existence of a hard radiation field. HeII-emitters are observed to be more frequent among high-z galaxies than for local objects. So investigating the HeII-ionizing source(s) in IZw18 may reveal the ionization processes at high-z. HeII emission in star-forming galaxies, has been suggested to be mainly associated with Wolf-Rayet stars (WRs), but WRs cannot satisfactorily explain the HeII-ionization at all times, in particular at lowest metallicities. Shocks from supernova remnants, or X-ray binaries, have been proposed as additional potential sources of HeII-ionizing photons. Our data indicate that conventional HeII-ionizing sources (WRs, shocks, X-ray binaries) are not sufficient to explain the observed nebular HeII4686 emission in IZw18. We find that the HeII-ionizing radiation expected from models for either low-metallicity super-massive O stars or rotating metal-free stars could account for the HeII-ionization budget measured, while only the latter models could explain the highest values of HeII4686/Hbeta observed. The presence of such peculiar stars in IZw18 is suggestive and further investigation in this regard is needed. This letter highlights that some of the clues of the early Universe can be found here in our cosmic backyard.Comment: 6 pages, 3 figures. Accepted for publication in ApJ Letter

Spatially resolved integral field spectroscopy of the ionized gas in IZw18

We present a detailed 2D study of the ionized ISM of IZw18 using new PMAS-IFU optical observations. IZw18 is a high-ionization galaxy which is among the most metal-poor starbursts in the local Universe. This makes IZw18 a local benchmark for understanding the properties most closely resembling those prevailing at distant starbursts. Our IFU-aperture (~ 1.4 kpc x 1.4 kpc) samples the entire IZw18 main body and an extended region of its ionized gas. Maps of relevant emission lines and emission line ratios show that higher-excitation gas is preferentially located close to the NW knot and thereabouts. We detect a Wolf-Rayet feature near the NW knot. We derive spatially resolved and integrated physical-chemical properties for the ionized gas in IZw18. We find no dependence between the metallicity-indicator R23 and the ionization parameter (as traced by [OIII]/[OII]) across IZw18. Over ~ 0.30 kpc^2, using the [OIII]4363 line, we compute Te[OIII] values (~ 15000 - 25000 K), and oxygen abundances are derived from the direct determinations of Te[OIII]. More than 70% of the higher-Te[OIII] (> 22000 K) spaxels are HeII4686-emitting spaxels too. From a statistical analysis, we study the presence of variations in the ISM physical-chemical properties. A galaxy-wide homogeneity, across hundreds of parsecs, is seen in O/H. Based on spaxel-by-spaxel measurements, the error-weighted mean of 12 + log(O/H) = 7.11 +/- 0.01 is taken as the representative O/H for IZw18. Aperture effects on the derivation of O/H are discussed. Using our IFU data we obtain, for the first time, the IZw18 integrated spectrum.Comment: Accepted for publication in MNRAS, 13 pages, 10 figures, 4 table

Vitamins C and E prevent endothelial VEGF and VEGFR-2 overexpression induced by porcine hypercholesterolemic LDL

OBJECTIVE: Vascular endothelial growth factor (VEGF) is believed to play a role in the development of atherosclerosis and has been found to be increased in hypercholesterolemia. We examined the hypothesis that endothelial VEGF and VEGF receptor-2 (VEGFR-2) expression is upregulated by hypercholesterolemic low-density lipoprotein (LDL) and, because it could be driven by oxidative stress, we tested whether vitamin C and E supplementation could modulate it. METHODS: Native LDL were characterized after isolation from adult normal (C-LDL), hypercholesterolemic (HC-LDL) and hypercholesterolemic mini-pigs receiving vitamins C and E (HCV-LDL). VEGF, VEGFR-2, HIF-1 alpha and superoxide anion (O(2)(-)) productions were measured in porcine coronary endothelial cells (ECs) incubated for 48 h with native LDL. The effect of exogenous ascorbic acid and alpha- or beta-tocopherol was also studied. RESULTS: HC-LDL, with high cholesterol (P<0.05) and reduced tocopherol/cholesterol ratio (P<0.05), increased significantly VEGF and VEGFR-2 (p<0.001) in EC, associated with higher O(2)(-) and HIF-1 alpha expression, in comparison with C-LDL and HCV-LDL. The addition of vitamin C and alpha- or beta-tocopherol to the culture medium prevented the induction of VEGF and VEGFR-2 expression by HC-LDL, both at mRNA and protein levels. CONCLUSIONS: Our data suggest HC-LDL induce endothelial VEGF and VEGFR-2 overexpression at least by increasing oxidative stress, and HIF-1 alpha is one of the signaling mechanisms involved. Prevention of VEGF and VEGFR-2 upregulation could help explain the beneficial effects of vitamins C and E in hypercholesterolemia-induced experimental atherosclerosis

Antioxidant vitamins increase the collagen content and reduce MMP-1 in a porcine model of atherosclerosis: implications for plaque stabilization

Degradation of extracellular matrix, particularly interstitial collagen, promotes plaque instability and contributes to restenosis after vascular injury. We have explored the effects of vitamins C and E on the collagen content and metalloproteinase-1 (MMP-1) expression after angioplasty in hypercholesterolemic pigs. Iliac angioplasty was performed on 18 minipigs divided into three diet groups: a normal-cholesterol (NC), a high-cholesterol (HC) and a high-cholesterol plus vitamins C+E (HCV). Four weeks later, after sacrifice, the vascular collagen content and MMP-1 protein expression, along with the plasma caseinolytic activity and lipid peroxidation, were measured. MMP-1 was also determined in arterial rings stimulated with native low-density lipoproteins (LDL) isolated from experimental groups. Cholesterol-rich diet augmented plasma lipid peroxidation (P<0.05), reduced the collagen content and increased vascular MMP-1 expression after injury (P<0.05). Enhanced caseinolytic activity (identified as MMP-1) was also observed in HC plasma samples and in supernatants from arterial rings incubated with HC-LDL. Vitamins C and E markedly increased neointimal collagen content (P<0.01), reduced the hypercholesterolemia-induced changes in vascular MMP-1 (P<0.05) and diminished plasma and ex vivo caseinolytic activity. Vitamins C and E may help stabilize atherosclerotic plaque after angioplasty and favor vascular remodeling by increasing collagen content and reducing vascular MMP-1 expression in porcine hypercholesterolemia

Vitamins C and E downregulate vascular VEGF and VEGFR-2 expression in apolipoprotein-E-deficient mice

Anti-angiogenic therapy reduces both plaque growth and intimal neovascularization in apolipoprotein-E-deficient mice (apoE-/-). Vascular endothelial growth factor (VEGF) has been suggested as playing a role in the development of atherosclerosis. We examined the hypothesis that VEGF and VEGF receptor-2 (VEGFR-2) expression is upregulated in apoE-/- and, since it could be driven by oxidative stress, tested whether dietary supplementation with vitamins C and E could downregulate it.Two-month-old apoE-/- received vitamin C combined with alpha- or beta-tocopherol for 4 weeks. Aortic VEGF and VEGFR-2 expression were measured by RT-qPCR and western blot.ApoE-/- showed significantly higher expression of aortic VEGF and VEGFR-2 mRNA (P<0.001) and protein (P<0.001) than wild-type mice, as well as increased plasma VEGF (P<0.001). Vitamin C and alpha-tocopherol significantly reduced aortic VEGF and VEGFR-2 expression in apoE-/- (P<0.001), circulating VEGF (P<0.01) and plasma lipid peroxidation (P<0.01). apoE-/- receiving vitamin C and beta-tocopherol showed diminished lipid peroxidation and VEGFR-2, but only partial reduction of VEGF expression. These data demonstrate that augmented VEGF and VEGFR-2 expression in apoE-/- vasculature can be downregulated by vitamins C and E, at least partially through oxidative stress reduction. This novel mechanism could contribute to explaining the beneficial effects of antioxidant vitamins in experimental atherosclerosis