Probing the Timescale of the 1.4 GHz Radio emissions as a Star formation tracer

Radio used as a star formation rate (SFR) tracer presents enormous advantages by being unaffected by dust and radio sources being pinpointed at the sub-arc-second level. The interpretation of the low frequency 1.4 GHz luminosity is hampered by the difficulty in modeling the cosmic ray paths in the interstellar medium, and their interactions with the magnetic field. In this work, we compare the SFR derived from radio observations, and the ones derived from spectral energy distribution (SED) modeling. We aim at better understand the behavior of the SFR radio tracer, with a specific emphasis on the link with star-formation histories. We used the SED modeling code Code Investigating GALaxy Emission, CIGALE, with a non-parametric star formation history model (SFH) and fit the data over the wavelength range from the ultraviolet (UV) up to the mid-infrared (mid-IR). We interpret the difference between radio and SED-based SFR tracers in the light of recent gradients in the derived SFH. To validate the robustness of the results, we checked for any remaining active galaxy nuclei (AGN) contribution and tested the impact of our SFH modeling approach. Approximately 27% our galaxies present a radio SFR (SFR$_{\rm radio}$) at least ten times larger than the instantaneous SFR from SED-fitting (SFR$_{\rm SED}$). This trend affects primarily the galaxies that show a declining SFH activity over the last 300 Myr. Both SFR indicators converge toward a consistent value, when the SFHs are averaged over a period larger than 150 Myr to derive SFR$_{\rm SED}$. Although the radio at low frequency 1.4 GHz is a good tracer of the star formation activity of galaxies with constant or increasing SFH, our results indicate that this is not the case for galaxies that are quenching. Our analysis suggests that the star formation time sensitivity of the radio low frequency could be longer than 150 Myr.Comment: 10 pages, 10 figure

Involvement of focal adhesion kinase in cellular invasion of head and neck squamous cell carcinomas via regulation of MMP-2 expression

Focal adhesion kinase (FAK) is considered intimately involved in cancer progression. Our previous research has demonstrated that overexpression of FAK is an early and frequent event in squamous cell carcinomas of the supraglottic larynx, and it is associated with the presence of metastases in cervical lymph nodes. The purpose of this study was to examine the functional role of FAK in the progression of head and neck squamous cell carcinomas (HNSCC). To this end, expression of FAK-related nonkinase (FRNK) or small interfering RNA (siRNA) against FAK was used to disrupt the FAK-induced signal transduction pathways in the HNSCC-derived SCC40 and SCC38 cell lines. Similar phenotypic effects were observed with the two methodological approaches in both cell lines. Decreased cell attachment, motility and invasion were induced by FRNK and FAK siRNA, whereas cell proliferation was not impaired. In addition, increased cell invasion was observed upon FAK overexpression in SCC cells. FRNK expression resulted in a downregulation of MMP-2 and MMP-9 expression. Interestingly, MMP-2 overexpression in FRNK-expressing cells rescued FRNK inhibition of cell invasion. This is the first demonstration of a direct rescue of impaired cell invasion by the re-expression of MMP-2 in a tumour cell type with decreased expression of functional FAK. Collectively, these data reported here support the conclusion that FAK enhances invasion of HNSCC by promoting both increased cell motility and MMP-2 production, thus providing new insights into possible therapeutic intervention strategies

Identification of a transition from stochastic to secular star formation around z=9 with JWST

tar formation histories (SFH) of early (6 9, 87% of massive galaxies, (log(M∗/M⊙) ≳9), have SFR gradients consistent with a stochastic star-formation activity during the last 100 Myr, while this fraction drops to 15% atz < 7. On the other hand, we see an increasing fraction of galaxies with a star-formation activity following a common stream on the SFR-M∗ plane with cosmic time, indicating that a secular mode of star-formation is emerging. We place our results in the context of the observed excess of UV emission as probed by the UV luminosity function at z ≳ 10, by estimating σUV , the dispersion of the UVabsolute magnitude distribution, to be of the order of 1.2 mag and compare it with predictions from the literature. In conclusion, we find a transition of star-formation mode happening around z ∼9: Galaxies with stochastic SFHs dominates at z ≳ 9, although this level of stochasticity is too low to reach those invoked by recent models to reproduce the observed UV luminosity function

"Organización, fragmentación y posibilidades de cambio: la brecha como vacío fértil"

En este trabajo buscamos comprender los complejos procesos de aprendizaje colectivo, y explorar y diseñar herramientas que posibiliten desarrollarlo. De este modo, observamos brechas y fragmentaciones en la red organizativa, que se enquistan en un vacío estéril que impide el flujo y tensión creativa que requieren los procesos de transformación y cambio. Primeramente se explicitan conceptos, seguido de ejemplos de brechas en torno a las cuales venimos trabajando. Finalmente concluimos con una síntesis integradora para abrir nuevos horizontes que nos conduzcan a una articulación compleja de dichas brechas

Defective glycosylation and multisystem abnormalities characterize the primary immunodeficiency XMEN disease.

X-linked immunodeficiency with magnesium defect, EBV infection, and neoplasia (XMEN) disease are caused by deficiency of the magnesium transporter 1 (MAGT1) gene. We studied 23 patients with XMEN, 8 of whom were EBV naive. We observed lymphadenopathy (LAD), cytopenias, liver disease, cavum septum pellucidum (CSP), and increased CD4-CD8-B220-TCR alpha beta(+) T cells (alpha beta DNTs), in addition to the previously described features of an inverted CD4/CD8 ratio, CD4(+) T lymphocytopenia, increased B cells, dysgammaglobulinemia, and decreased expression of the natural killer group 2, member D (NKG2D) receptor. EBV-associated B cell malignancies occurred frequently in EBV-infected patients. We studied patients with XMEN and patients with autoimmune lymphoproliferative syndrome (ALPS) by deep immunophenotyping (32 immune markers) using time-of-flight mass cytometry (CyTOF). Our analysis revealed that the abundance of 2 populations of naive B cells (CD20(+)CD27(-)CD22(+)IgM(+)HLA-DR(+)CXCR5(+)CXCR4(++)CD10(+)CD38(+) and CD20(+)CD27(-)CD22(+)IgM(+)HLA-DR(+)CXCR5(+)CXCR4(+)CD10(-)CD38(-)) could differentially classify XMEN, ALPS, and healthy individuals. We also performed glycoproteomics analysis on T lymphocytes and show that XMEN disease is a congenital disorder of glycosylation that affects a restricted subset of glycoproteins. Transfection of MAGT1 mRNA enabled us to rescue proteins with defective glycosylation. Together, these data provide new clinical and pathophysiological foundations with important ramifications for the diagnosis and treatment of XMEN disease

Defective glycosylation and multisystem abnormalities characterize the primary immunodeficiency XMEN disease

X-linked immunodeficiency with magnesium defect, EBV infection, and neoplasia (XMEN) disease are caused by deficiency of the magnesium transporter 1 (MAGT1) gene. We studied 23 patients with XMEN, 8 of whom were EBV naive. We observed lymphadenopathy (LAD), cytopenias, liver disease, cavum septum pellucidum (CSP), and increased CD4-CD8-B220-TCRαβ+ T cells (αβDNTs), in addition to the previously described features of an inverted CD4/CD8 ratio, CD4+ T lymphocytopenia, increased B cells, dysgammaglobulinemia, and decreased expression of the natural killer group 2, member D (NKG2D) receptor. EBV-associated B cell malignancies occurred frequently in EBV-infected patients. We studied patients with XMEN and patients with autoimmune lymphoproliferative syndrome (ALPS) by deep immunophenotyping (32 immune markers) using time-of-flight mass cytometry (CyTOF). Our analysis revealed that the abundance of 2 populations of naive B cells (CD20+CD27-CD22+IgM+HLA-DR+CXCR5+CXCR4++CD10+CD38+ and CD20+CD27-CD22+IgM+HLA-DR+CXCR5+CXCR4+CD10-CD38-) could differentially classify XMEN, ALPS, and healthy individuals. We also performed glycoproteomics analysis on T lymphocytes and show that XMEN disease is a congenital disorder of glycosylation that affects a restricted subset of glycoproteins. Transfection of MAGT1 mRNA enabled us to rescue proteins with defective glycosylation. Together, these data provide new clinical and pathophysiological foundations with important ramifications for the diagnosis and treatment of XMEN disease

COSMOS-Web: An Overview of the JWST Cosmic Origins Survey

We present the survey design, implementation, and outlook for COSMOS-Web, a 255 hour treasury program conducted by the James Webb Space Telescope in its first cycle of observations. COSMOS-Web is a contiguous 0.54 deg$^2$ NIRCam imaging survey in four filters (F115W, F150W, F277W, and F444W) that will reach 5$\sigma$ point source depths ranging $\sim$27.5-28.2 magnitudes. In parallel, we will obtain 0.19 deg$^2$ of MIRI imaging in one filter (F770W). COSMOS-Web will build on the rich heritage of multiwavelength observations and data products available in the COSMOS field. The design of COSMOS-Web is motivated by three primary science goals: (1) to discover thousands of galaxies in the Epoch of Reionization ($64$ and place constraints on the formation of the Universe's most massive galaxies ($M_\star>10^{10}$ M$_\odot$), and (3) directly measure the evolution of the stellar mass to halo mass relation using weak gravitational lensing out to $z\sim2.5$ and measure its variance with galaxies' star formation histories and morphologies. In addition, we anticipate COSMOS-Web's legacy value to reach far beyond these scientific goals, touching many other areas of astrophysics, such as the identification of the first direct collapse black hole candidates, ultracool sub-dwarf stars in the Galactic halo, and possibly the identification of $z>10$ pair-instability supernovae. In this paper we provide an overview of the survey's key measurements, specifications, goals, and prospects for new discovery