The interaction-driven starburst contribution to the cosmic star formation rate density

An increasing amount of observational evidence supports the notion that there are two modes of star formation: a quiescent mode in disk-like galaxies, and a starburst mode, which is generally interpreted as driven by merging. Using a semi-analytic model of galaxy formation, we derive the relative contribution to the cosmic star formation rate density of quiescently starforming and starburst galaxies, predicted under the assumption that starburst events are triggered by galaxy encounters (merging and fly-by kind) during their merging histories. We show that, within this framework, quiescently starforming galaxies dominate the cosmic star formation rate density at all redshifts. The contribution of the burst-dominated starforming galaxies increases with redshift, rising from <5% at low redshift (z5. We estimated that the fraction of the final (z=0) galaxy stellar mass which is formed through the burst component of star formation is ~10% for 10^10 M_\odot<M_*<10^11.5 M_\odot. Starburst galaxies, selected according to their distance from the galaxy main sequence, account for ~10% of the star formation rate density in the redshift interval 1.5<z<2.5, i.e. at the cosmic peak of the star formation activity.Comment: 11 pages, 8 figures. Accepted for publication in A&

The PEP Survey: evidence for intense star-forming activity in the majority of radio-selected AGN at z>~1

In order to investigate the FIR properties of radio-active AGN, we have considered three different fields where both radio and FIR observations are the deepest to-date: GOODS-South, GOODS-North and the Lockman Hole. Out of a total of 92 radio-selected AGN, ~64% are found to have a counterpart in Herschel maps. The percentage is maximum in the GOODS-North (72%) and minimum (~50%) in the Lockman Hole, where FIR observations are shallower. Our study shows that in all cases FIR emission is associated to star-forming activity within the host galaxy. Such an activity can even be extremely intense, with star-forming rates as high as ~10^3-10^4 Msun/yr. AGN activity does not inhibit star formation in the host galaxy, just as on-site star-formation does not seem to affect AGN properties, at least those detected at radio wavelengths and for z>~1. Furthermore, physical properties such as the mass and age distributions of the galaxies hosting a radio-active AGN do not seem to be affected by the presence of an ongoing star-forming event. Given the very high rate of FIR detections, we stress that this refers to the majority of the sample: most radio-active AGN are associated with intense episodes of star-formation. However, the two processes proceed independently within the same galaxy, at all redshifts but in the local universe, where powerful enough radio activity reaches the necessary strength to switch off the on-site star formation. Our data also show that for z>~1 the hosts of radio-selected star-forming galaxies and AGN are indistinguishable from each other both in terms of mass and IR luminosity distributions. The two populations only differentiate in the very local universe, whereby the few AGN which are still FIR-active are found in galaxies with much higher masses and luminosities.Comment: 20 pages, 22 figures, to appear in MNRA

Due "insolite" testimonianze arangiane

The essay republishes two testimonies relating to the complex figure of Vincenzo Arangio-Ruiz. The first reproduces a radio speech pronounced when the Professor held the office of Minister of Public Education. Then it was published in the fourth issue of 1945 of a post-war periodical, Oratoria, very difficult to find. The second testimony is a portrait of Arangio-Ruiz reported by the lawyer Ercole Graziadei, on the occasion of a meeting in Rome with the ambassador of France Gaston Palewsky. Two little-known and very different testimonies that can contribute to reconstruct the tone of the Professor’s humanity and political commitment

growth factor enhancement of cardiac regeneration

The potential for endogenous or supplementary stem cells to restore the form and function of damaged tissues is particularly promising for overcoming the restricted regenerative capacity of the mammalian heart. To maintain blood circulation, this essential organ needs to launch a rapid response to repair damage of the muscle wall and to prevent muscle loss. The capacity of growth factors to supplement the repair process has been successfully applied to restore the integrity of damaged skeletal muscle, reducing the fibrotic response to injury, and recruiting local populations of self-renewing precursor cells and circulating stem cells. We review the recent evidence that extension of growth factor supplementation to the heart may overcome its inherent regenerative impediments through improvement of the local tissue environment and stimulation of cell replacement, and we speculate on future research directions for treatment of myocardial damage

The clustering properties of high-redshift passive galaxies

We investigate the clustering properties of 3<z<5 candidate passive galaxies from the Merlin et al. (2019) sample residing in the GOODS-North (35 sources) and GOODS-South (33 sources) fields. Within the large uncertainties due to the paucity of sources we do not detect clustering signal in GOODS-North, while this is present in GOODS-South, highlighting the importance of the effects of cosmic variance. The estimated correlation length in GOODS-South is r_0=12^+4_-5 Mpc, while the estimated minimum mass for a halo capable to host one of such high-redshift quenched galaxies is log10(M_min/M_sun) =13.0\pm 0.3, once also the constraints from their space density are taken into account. Both values are compatible with the results from GOODS-North. Putting the above findings in a cosmological context, these suggest no evolution of the dark matter content of the hosts of passive galaxies during the past 12.5 Gyr, i.e. during more than 90% of the age of the Universe. We discuss possible scenarios for the observed trend.Comment: 6 pages, 3 figures, letter to appear in MNRA

mIGF-1 regulates heart physiology and induces complete regeneration of infarcted myocardial tissue

ABSTRACT The mammalian heart is particularly susceptible to traumatic injury or sustained disease, suffering tissue deterioration, scarring and loss of contractile function. Clinical interventions to prevent or reverse the devastating effects of cardiac damage have met with limited success, presumably due to restricted cardiac regenerative potential. We tested the ability of a locally acting mIGF-1 isoform to regenerate the injured heart, restricting expression of a mIGF-1 transgene to the mouse myocardium to exclude endocrine effects on other tissues. Transgenic mIGF-1 hearts displayed accelerated postnatal cardiac growth that never exceeded the wild-type adult cardiac size. Early remodelling of the transgenic hearts was accompanied by transient activation of MAPKs and increased function of the translational machinery, without perturbing cardiac performance, and by modest upregulation of hypertrophic markers at one and two months. Notably, AKT the downstream effector of IGF-1 signalling was not activated in the hearts of transgenic mIGF-1 animals, indicating that a different kinase regulates mIGF-1 downstream signalling in the heart. The regenerative capacity of mIGF-1 was analyzed either by LAD ligation or by direct cardiotoxin (CTX) injection into the ventricles of adult mice. Injury to both wild-type and transgenic mIGF-1 hearts produced reproducible and localized infarctions coupled with early cell death and marked inflammation. In contrast to the characteristic progression of scar formation in wild-type hearts, transgenic mIGF-1 hearts induced complete repair of the injured tissue after 1 month, without scar formation. mIGF-1-induced regeneration was associated with a marked decrease in pro-inflammatory cytokines and an increase in anti-inflammatory cytokines, indicating that mIGF-1 drives regeneration in part by modulating the inflammatory response in pathological conditions. At later stages, mIGF-1 transgenic hearts displayed increased proliferative activity proximal to the infarct, and restored cardiac functionality. By enabling myocardial reconstruction following injury, the mIGF-1 isoform appears to bypass the evolutionary restrictions on mammalian regeneration. The enhancement of cardiac regeneration by localized expression of this growth factor suggests novel and clinically feasible therapeutic strategies to decrease inflammation and increase cell replacement after tissue damage

Toxicity of aflatoxin B1 towards the vitamin D receptor (VDR)

This research describes an unexpected toxicity of the aflatoxin B1 towards the vitamin D receptors. Rickets is a childhood disease, and calcium deficiency is the aetiological cause in Africa, being primarily associated with nutritional problems; in this research the contribution of aflatoxin B1 exposure during the early months of life is an interesting factor to deepen in order to prevent liver damages or the development of rickets. The results show that the expression of vitamin D receptor in osteosarcoma cell line SAOS-2 is significantly down-modulated by exposure to aflatoxin B1. This seems to suggest that Aflatoxin B1, toxic towards the vitamin D receptor, interferes with the actions of the vitamin D on calcium binding gene expression in the kidney and intestine. Experimental data indicate a 58% and 86% decrease if the cells are exposed to 5 ng/mL and 50 ng/mL of aflatoxin B1, respectively. These results seem to indicate that natural occurrence of the aflatoxin B1 and allelic variant of vitamin D receptor on (F allele) increase the risk of developing rickets of African children

Increased cardiogenesis in P19-GFP teratocarcinoma cells expressing the propeptide IGF-1Ea

AbstractThe mechanism implicated in differentiation of endogenous cardiac stem cells into cardiomyocytes to regenerate the heart tissue upon an insult remains elusive, limiting the therapeutical goals to exogenous cell injection and/or gene therapy. We have shown previously that cardiac specific overexpression of the insulin-like growth factor 1 propeptide IGF-1Ea induces beneficial myocardial repair after infarct. Although the mechanism is still under investigation, the possibility that this propeptide may be involved in promoting stem cell differentiation into the cardiac lineage has yet to be explored. To investigate whether IGF-1Ea promote cardiogenesis, we initially modified P19 embryonal carcinoma cells to express IGF-1Ea. Taking advantage of their cardiomyogenic nature, we analyzed whether overexpression of this propeptide affected cardiac differentiation program. The data herein presented showed for the first time that constitutively overexpressed IGF-1Ea increased cardiogenic differentiation program in both undifferentiated and DMSO-differentiated cells. In details, IGF-1Ea overexpression promoted localization of alpha-actinin in finely organized sarcomeric structure compared to control cells and upregulated the cardiac mesodermal marker NKX-2.5 and the ventricular structural protein MLC2v. Furthermore, activated IGF-1 signaling promoted cardiac mesodermal induction in undifferentiated cells independently of cell proliferation. This analysis suggests that IGF-1Ea may be a good candidate to improve both in vitro production of cardiomyocytes from pluripotent stem cells and in vivo activation of the differentiation program of cardiac progenitor cells

Local IGF-1 isoform protects cardiomyocytes from hypertrophic and oxidative stresses via SirT1 activity

Oxidative and hypertrophic stresses contribute to the pathogenesis of heart failure. Insulin-like growth factor-1 (IGF-1) is a peptide hormone with a complex post-transcriptional regulation, generating distinct isoforms. Locally acting IGF-1 isoform (mIGF-1) helps the heart to recover from toxic injury and from infarct. In the murine heart, moderate overexpression of the NAD+-dependent deacetylase SirT1 was reported to mitigate oxidative stress. SirT1 is known to promote lifespan extension and to protect from metabolic challenges. Circulating IGF-1 and SirT1 play antagonizing biological roles and share molecular targets in the heart, in turn affecting cardiomyocyte physiology. However, how different IGF-1 isoforms may impact SirT1 and affect cardiomyocyte function is unknown. Here we show that locally acting mIGF-1 increases SirT1 expression/activity, whereas circulating IGF-1 isoform does not affect it, in cultured HL-1 and neonatal cardiomyocytes. mIGF-1-induced SirT1 activity exerts protection against angiotensin II (Ang II)-triggered hypertrophy and against paraquat (PQ) and Ang II-induced oxidative stress. Conversely, circulating IGF-1 triggered itself oxidative stress and cardiomyocyte hypertrophy. Interestingly, potent cardio-protective genes (adiponectin, UCP-1 and MT-2) were increased specifically in mIGF-1-overexpressing cardiomyocytes, in a SirT1-dependent fashion. Thus, mIGF-1 protects cardiomyocytes from oxidative and hypertrophic stresses via SirT1 activity, and may represent a promising cardiac therapeutic