A 12 μm ISOCAM survey of the ESO-Sculptor field

We present a detailed reduction of a mid-infrared 12 μm (LW10 filter) ISOCAM open time observation performed on the ESOSculptor Survey field (Arnouts et al. 1997, A&AS, 124, 163). A complete catalogue of 142 sources (120 galaxies and 22 stars), detected with high significance (equivalent to 5σ), is presented above an integrated flux density of 0.24 mJy. Star/galaxy separation is performed by a detailed study of colour-colour diagrams. The catalogue is complete to 1 mJy and, below this flux density, the incompleteness is corrected using two independent methods. The first method uses stars and the second uses optical counterparts of the ISOCAM galaxies; these methods yield consistent results. We also apply an empirical flux density calibration using stars in the field. For each star, the 12 μm flux density is derived by fitting optical colours from a multi-band χ^2 to stellar templates (BaSel-2.0) and using empirical optical-IR colour-colour relations. This article is a companion analysis to our 2007 paper (Rocca-Volmerange et al. 2007, A&A, 475, 801) where the 12 μm faint galaxy counts are presented and analysed per galaxy type with the evolutionary code PÉGASE.3

The 12 μm ISO-ESO-Sculptor and 24 μm Spitzer faint counts reveal a population of ULIRGs as dusty massive ellipticals: Evolution by types and cosmic star formation

Context. Multi-wavelength galaxy number counts provide clues to the nature of galaxy evolution. The interpretation per galaxy type of the mid-IR faint counts obtained with ISO and Spitzer, consistent with the analysis of deep UV-optical-near IR galaxy counts, provide new constraints on the dust and stellar emission. Discovering the nature of new populations, such as high redshift ultra-luminous (≥10^(12) L_⊙) infrared galaxies (ULIRGs), is also crucial for understanding galaxy evolution at high redshifts. Aims. We first present the faint galaxy counts at 12 μm from the catalogue of the ISO-ESO-Sculptor Survey (ISO-ESS) published in a companion article (Seymour et al. 2007a, A&A, 475, 791). They go down to 0.31 mJy after corrections for incompleteness. We verify the consistency with the existing ISO number counts at 15 μm. Then we analyse the 12 μm (ISO-ESS) and the 24 μm (Spitzer) faint counts, to constrain the nature of ULIRGs, the cosmic star formation history and time scales for mass buildup. Methods. We show that the “normal” scenarios in our evolutionary code PÉGASE, which had previously fitted the deep UV-opticalnear IR counts, are unsuccessful at 12 μm and 24 μm. We thus propose a new ULIRG scenario adjusted to the observed cumulative and differential 12 μm and 24 μm counts and based on observed 12 μm and 25 μm IRAS luminosity functions and evolutionary optical/mid-IR colours from PÉGASE. Results. We succeed in simultaneously modelling the typical excess observed at 12 μm, 15 μm (ISO), and 24 μm (Spitzer) in the cumulative and differential counts by only changing 9% of normal galaxies (1/3 of the ellipticals) into ultra-bright dusty galaxies evolving as ellipticals, and interpreted as distant ULIRGs. These objects present similarities with the population of radio-galaxy hosts at high redshift. No number density evolution is included in our models even if minor starbursts due to galaxy interactions remain compatible with our results. Conclusions. Higher spectral and spatial resolution in the mid-IR, together with submillimeter observations using the future Herschel observatory, will be useful to confirm these results

The 12 μm ISO-ESO-Sculptor and 24 μm Spitzer faint counts reveal a population of ULIRGs as dusty massive ellipticals: Evolution by types and cosmic star formation

Context. Multi-wavelength galaxy number counts provide clues to the nature of galaxy evolution. The interpretation per galaxy type of the mid-IR faint counts obtained with ISO and Spitzer, consistent with the analysis of deep UV-optical-near IR galaxy counts, provide new constraints on the dust and stellar emission. Discovering the nature of new populations, such as high redshift ultra-luminous (≥10^(12) L_⊙) infrared galaxies (ULIRGs), is also crucial for understanding galaxy evolution at high redshifts. Aims. We first present the faint galaxy counts at 12 μm from the catalogue of the ISO-ESO-Sculptor Survey (ISO-ESS) published in a companion article (Seymour et al. 2007a, A&A, 475, 791). They go down to 0.31 mJy after corrections for incompleteness. We verify the consistency with the existing ISO number counts at 15 μm. Then we analyse the 12 μm (ISO-ESS) and the 24 μm (Spitzer) faint counts, to constrain the nature of ULIRGs, the cosmic star formation history and time scales for mass buildup. Methods. We show that the “normal” scenarios in our evolutionary code PÉGASE, which had previously fitted the deep UV-opticalnear IR counts, are unsuccessful at 12 μm and 24 μm. We thus propose a new ULIRG scenario adjusted to the observed cumulative and differential 12 μm and 24 μm counts and based on observed 12 μm and 25 μm IRAS luminosity functions and evolutionary optical/mid-IR colours from PÉGASE. Results. We succeed in simultaneously modelling the typical excess observed at 12 μm, 15 μm (ISO), and 24 μm (Spitzer) in the cumulative and differential counts by only changing 9% of normal galaxies (1/3 of the ellipticals) into ultra-bright dusty galaxies evolving as ellipticals, and interpreted as distant ULIRGs. These objects present similarities with the population of radio-galaxy hosts at high redshift. No number density evolution is included in our models even if minor starbursts due to galaxy interactions remain compatible with our results. Conclusions. Higher spectral and spatial resolution in the mid-IR, together with submillimeter observations using the future Herschel observatory, will be useful to confirm these results

Can Systems Biology Advance Clinical Precision Oncology?

Precision oncology is perceived as a way forward to treat individual cancer patients. However, knowing particular cancer mutations is not enough for optimal therapeutic treatment, because cancer genotype-phenotype relationships are nonlinear and dynamic. Systems biology studies the biological processes at the systems’ level, using an array of techniques, ranging from statistical methods to network reconstruction and analysis, to mathematical modeling. Its goal is to reconstruct the complex and often counterintuitive dynamic behavior of biological systems and quantitatively predict their responses to environmental perturbations. In this paper, we review the impact of systems biology on precision oncology. We show examples of how the analysis of signal transduction networks allows to dissect resistance to targeted therapies and inform the choice of combinations of targeted drugs based on tumor molecular alterations. Patient-specific biomarkers based on dynamical models of signaling networks can have a greater prognostic value than conventional biomarkers. These examples support systems biology models as valuable tools to advance clinical and translational oncological research

Information content of the weak-charge form factor

Parity-violating electron scattering provides a model-independent determination of the nuclear weak-charge form factor that has widespread implications across such diverse areas as fundamental symmetries, nuclear structure, heavy-ion collisions, and neutron-star structure. We assess the impact of precise measurements of the weak-charge form factor of ${}^{48}$Ca and ${}^{208}$Pb on a variety of nuclear observables, such as the neutron skin and the electric-dipole polarizability. We use the nuclear Density Functional Theory with several accurately calibrated non-relativistic and relativistic energy density functionals. To assess the degree of correlation between nuclear observables and to explore systematic and statistical uncertainties on theoretical predictions, we employ the chi-square statistical covariance technique. We find a strong correlation between the weak-charge form factor and the neutron radius, that allows for an accurate determination of the neutron skin of neutron-rich nuclei. We determine the optimal range of the momentum transfer $q$ that maximizes the information content of the measured weak-charge form factor and quantify the uncertainties associated with the strange quark contribution. Moreover, we confirm the role of the electric-dipole polarizability as a strong isovector indicator. Accurate measurements of the weak-charge form factor of ${}^{48}$Ca and ${}^{208}$Pb will have a profound impact on many aspects of nuclear theory and hadronic measurements of neutron skins of exotic nuclei at radioactive-beam facilities.Comment: 10 pages, 4 figure

Evolution equation for a model of surface relaxation in complex networks

In this paper we derive analytically the evolution equation of the interface for a model of surface growth with relaxation to the minimum (SRM) in complex networks. We were inspired by the disagreement between the scaling results of the steady state of the fluctuations between the discrete SRM model and the Edward-Wilkinson process found in scale-free networks with degree distribution $P(k) \sim k^{-\lambda}$ for $\lambda <3$ [Pastore y Piontti {\it et al.}, Phys. Rev. E {\bf 76}, 046117 (2007)]. Even though for Euclidean lattices the evolution equation is linear, we find that in complex heterogeneous networks non-linear terms appear due to the heterogeneity and the lack of symmetry of the network; they produce a logarithmic divergency of the saturation roughness with the system size as found by Pastore y Piontti {\it et al.} for $\lambda <3$.Comment: 9 pages, 2 figure

CRISPR-Cas9 Gene Editing of Hematopoietic Stem Cells from Patients with Friedreich's Ataxia.

Friedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disorder caused by expansion of GAA repeats in intron 1 of the frataxin (FXN) gene, leading to significant decreased expression of frataxin, a mitochondrial iron-binding protein. We previously reported that syngeneic hematopoietic stem and progenitor cell (HSPC) transplantation prevented neurodegeneration in the FRDA mouse model YG8R. We showed that the mechanism of rescue was mediated by the transfer of the functional frataxin from HSPC-derived microglia/macrophage cells to neurons/myocytes. In this study, we report the first step toward an autologous HSPC transplantation using the CRISPR-Cas9 system for FRDA. We first identified a pair of CRISPR RNAs (crRNAs) that efficiently removes the GAA expansions in human FRDA lymphoblasts, restoring the non-pathologic level of frataxin expression and normalizing mitochondrial activity. We also optimized the gene-editing approach in HSPCs isolated from healthy and FRDA patients' peripheral blood and demonstrated normal hematopoiesis of gene-edited cells in vitro and in vivo. The procedure did not induce cellular toxic effect or major off-target events, but a p53-mediated cell proliferation delay was observed in the gene-edited cells. This study provides the foundation for the clinical translation of autologous transplantation of gene-corrected HSPCs for FRDA