Stellar populations of galaxies in the ALHAMBRA survey up to z∼1z \sim 1. I. MUFFIT: A Multi-Filter Fitting code for stellar population diagnostics

We present MUFFIT, a new generic code optimized to retrieve the main stellar population parameters of galaxies in photometric multi-filter surveys, and we check its reliability and feasibility with real galaxy data from the ALHAMBRA survey. Making use of an error-weighted $\chi^2$-test, we compare the multi-filter fluxes of galaxies with the synthetic photometry of mixtures of two single stellar populations at different redshifts and extinctions, to provide through a Monte Carlo method the most likely range of stellar population parameters (mainly ages and metallicities), extinctions, redshifts, and stellar masses. To improve the diagnostic reliability, MUFFIT identifies and removes from the analysis those bands that are significantly affected by emission lines. We highlight that the retrieved age-metallicity locus for a sample of $z \le 0.22$ early-type galaxies in ALHAMBRA at different stellar mass bins are in very good agreement with the ones from SDSS spectroscopic diagnostics. Moreover, a one-to-one comparison between the redshifts, ages, metallicities, and stellar masses derived spectroscopically for SDSS and by MUFFIT for ALHAMBRA reveals good qualitative agreements in all the parameters. In addition, and using as input the results from photometric-redshift codes, MUFFIT improves the photometric-redshift accuracy by $\sim 10$-$20\%$, and it also detects nebular emissions in galaxies, providing physical information about their strengths. Our results show the potential of multi-filter galaxy data to conduct reliable stellar population studies with the appropiate analysis techniques, as MUFFIT.Comment: 31 pages, 18 figures, accepted for publication in A&

The ALHAMBRA Survey: Bayesian Photometric Redshifts with 23 bands for 3 squared degrees

The ALHAMBRA (Advance Large Homogeneous Area Medium Band Redshift Astronomical) survey has observed 8 different regions of the sky, including sections of the COSMOS, DEEP2, ELAIS, GOODS-N, SDSS and Groth fields using a new photometric system with 20 contiguous ~ $300\AA$ filters covering the optical range, combining them with deep $JHKs$ imaging. The observations, carried out with the Calar Alto 3.5m telescope using the wide field (0.25 sq. deg FOV) optical camera LAICA and the NIR instrument Omega-2000, correspond to ~700hrs on-target science images. The photometric system was designed to maximize the effective depth of the survey in terms of accurate spectral-type and photo-zs estimation along with the capability of identification of relatively faint emission lines. Here we present multicolor photometry and photo-zs for ~438k galaxies, detected in synthetic F814W images, complete down to I~24.5 AB, taking into account realistic noise estimates, and correcting by PSF and aperture effects with the ColorPro software. The photometric ZP have been calibrated using stellar transformation equations and refined internally, using a new technique based on the highly robust photometric redshifts measured for emission line galaxies. We calculate photometric redshifts with the BPZ2 code, which includes new empirically calibrated templates and priors. Our photo-zs have a precision of $dz/(1+z_s)=1$ for I<22.5 and 1.4% for 22.5<I<24.5. Precisions of less than 0.5% are reached for the brighter spectroscopic sample, showing the potential of medium-band photometric surveys. The global $P(z)$ shows a mean redshift =0.56 for I=0.86 for I<24.5 AB. The data presented here covers an effective area of 2.79 sq. deg, split into 14 strips of 58.5'x15.5' and represents ~32 hrs of on-target.Comment: The catalog data and a full resolution version of this paper is available at https://cloud.iaa.csic.es/alhambra

Quantum Quench in the Transverse Field Ising chain I: Time evolution of order parameter correlators

We consider the time evolution of order parameter correlation functions after a sudden quantum quench of the magnetic field in the transverse field Ising chain. Using two novel methods based on determinants and form factor sums respectively, we derive analytic expressions for the asymptotic behaviour of one and two point correlators. We discuss quenches within the ordered and disordered phases as well as quenches between the phases and to the quantum critical point. We give detailed account of both methods.Comment: 65 pages, 21 figures, some typos correcte

Characterization of Patients with Chronic Diseases and Complex Care Needs: A New High-Risk Emergent Population

Background: To analyze the prevalence and main epidemiological, clinical and outcome features of in-Patients with Complex Chronic conditions (PCC) in internal medicine areas, using a pragmatic working definition. Methods: Prospective study in 17 centers from Spain, with 97 in-hospital, monthly prevalence cuts. A PCC was considered when criteria of polypathological patient (two or more major chronic diseases) were met, or when a patient suffered one major chronic disease plus one or more of nine predefined complexity criteria like socio-familial risk, alcoholism or malnutrition among others (PCC without polypathology). A complete set of baseline features as well as 12-months survival were collected. Then, we compared clinical, outcome variables, and PROFUND index accuracy between polypathological patients and PCC without polypathology. Results: The global prevalence of PCC was 61% (40% of them were polypathological patients, and 21% PCC withouth polypathology) out of the 2178 evaluated patients. Their median age was 82 (59.5% men), suffered 2.3 ± 1.1 major diseases (heart diseases (70.5%), neurologic (41.5%), renal (36%), and lung diseases (26%)), 5.5 ± 2.5 other chronic conditions, met 2.5 ± 1.5 complexity criteria, and presented functional decline (Barthel index 55 (25-90)). Compared to polypathological patients, the subgroup of PCC without polypathology were younger, with a different pattern of major diseases and comorbidities, a better functional status, and lower 12-months mortality rates ((36.2% vs 46.8%; p = .003; OR 0.7(0.48-0.86). The PROFUND index obtained adequate calibration and discrimination power (AUC-ROC 0.67 (0.63-0.69)) in predicting 12-month mortality of PCC. Conclusion: Patients with complex chronic conditions are highly prevalent in internal medicine areas; their clinical pattern has changed in parallel to socio-epidemiological modifications, but their death-risk is still adequately predicted by PROFUND index

Measurement of the Xe 136 two-neutrino double -decay half-life via direct background subtraction in NEXT

[EN] We report a measurement of the half-life of the 136Xe two-neutrino double-ß decay performed with a novel direct-background-subtraction technique. The analysis relies on the data collected with the NEXT-White detector operated with 136Xe-enriched and 136Xe-depleted xenon, as well as on the topology of double-electron tracks. With a fiducial mass of only 3.5 kg of Xe, a half-life of 2.34+0.80(stat)+0.30(sys)×1021 yr is derived from ¿0.46 ¿0.17 the background-subtracted energy spectrum. The presented technique demonstrates the feasibility of unique background-model-independent neutrinoless double-ß-decay searches.The NEXT Collaboration acknowledges support from the following agencies and institutions: the European Research Council (ERC) under Grant No. 951281-BOLD; the European Union's Framework Programme for Research and Innovation Horizon 2020 (2014-2020) under Grant No. 957202-HIDDEN; the MCIN/AEI/10.13039/501100011033 of Spain and ERDF "A way of making Europe" under Grant No. RTI2018-095979, the Severo Ochoa Program Grant No. CEX2018-000867-S, and the Maria de Maeztu Program Grant No. MDM-2016-0692; the Generalitat Valenciana of Spain under Grants No. PROMETEO/2021/087 and No. CIDEGENT/2019/049; the Portuguese FCT under Project No. UID/FIS/04559/2020 to fund the activities of LIBPhys-UC; the Pazy Foundation (Israel) under Grants No. 877040 and No. 877041; the U.S. Department of Energy under Contracts No. DE-AC02-06CH11357 (Argonne National Laboratory), No. DE-AC02-07CH11359 (Fermi National Accelerator Laboratory), No. DE-FG02-13ER42020 (Texas A&M), No. DE-SC0019054 (Texas Arlington), and No. DE-SC0019223 (Arlington, TX); the U.S. National Science Foundation under Grant No. CHE 2004111; and the Robert A. Welch Foundation under Grant No. Y-203120200401. D.G.D. acknowledges support from the Ramon y Cajal program (Spain) under Contract No. RYC-2015-18820. Finally, we are grateful to the Laboratorio Subterraneo de Canfranc for hosting and supporting the NEXT experiment.Novella, P.; Sorel, M.; Usón, A.; Adams, C.; Almazán, H.; Álvarez-Puerta, V.; Aparicio, B.... (2022). Measurement of the Xe 136 two-neutrino double -decay half-life via direct background subtraction in NEXT. Physical Review C (Online). 105(5):055501-1-055501-8. https://doi.org/10.1103/PhysRevC.105.055501055501-1055501-8105

Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead.

Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology

Vav3 oncogene activates estrogen receptor and its overexpression may be involved in human breast cancer

<p>Abstract</p> <p>Background</p> <p>Our previous study revealed that Vav3 oncogene is overexpressed in human prostate cancer, activates androgen receptor, and stimulates growth in prostate cancer cells. The current study is to determine a potential role of Vav3 oncogene in human breast cancer and impact on estrogen receptor a (ERα)-mediated signaling axis.</p> <p>Methods</p> <p>Immunohistochemistry analysis was performed in 43 breast cancer specimens and western blot analysis was used for human breast cancer cell lines to determine the expression level of Vav3 protein. The impact of Vav3 on breast cancer cell growth was determined by siRNA knockdown of Vav3 expression. The role of Vav3 in ERα activation was examined in luciferase reporter assays. Deletion mutation analysis of Vav3 protein was performed to localize the functional domain involved in ERα activation. Finally, the interaction of Vav3 and ERα was assessed by GST pull-down analysis.</p> <p>Results</p> <p>We found that Vav3 was overexpressed in 81% of human breast cancer specimens, particularly in poorly differentiated lesions. Vav3 activated ERα partially via PI3K-Akt signaling and stimulated growth of breast cancer cells. Vav3 also potentiated EGF activity for cell growth and ERα activation in breast cancer cells. More interestingly, we found that Vav3 complexed with ERα. Consistent with its function for AR, the DH domain of Vav3 was essential for ERα activation.</p> <p>Conclusion</p> <p>Vav3 oncogene is overexpressed in human breast cancer. Vav3 complexes with ERα and enhances ERα activity. These findings suggest that Vav3 overexpression may aberrantly enhance ERα-mediated signaling axis and play a role in breast cancer development and/or progression.</p

Promoter- and cell-specific epigenetic regulation of CD44, Cyclin D2, GLIPR1 and PTEN by Methyl-CpG binding proteins and histone modifications

<p>Abstract</p> <p><it>Background</it></p> <p>The aim of the current study was to analyze the involvement of methyl-CpG binding proteins (MBDs) and histone modifications on the regulation of CD44, Cyclin D2, GLIPR1 and PTEN in different cellular contexts such as the prostate cancer cells DU145 and LNCaP, and the breast cancer cells MCF-7. Since global chromatin changes have been shown to occur in tumours and regions of tumour-associated genes are affected by epigenetic modifications, these may constitute important regulatory mechanisms for the pathogenesis of malignant transformation.</p> <p><it>Methods</it></p> <p>In DU145, LNCaP and MCF-7 cells mRNA expression levels of CD44, Cyclin D2, GLIPR1 and PTEN were determined by quantitative RT-PCR at the basal status as well as after treatment with demethylating agent 5-aza-2'-deoxycytidine and/or histone deacetylase inhibitor Trichostatin A. Furthermore, genomic DNA was bisulfite-converted and sequenced. Chromatin immunoprecipitation was performed with the stimulated and unstimulated cells using antibodies for MBD1, MBD2 and MeCP2 as well as 17 different histone antibodies.</p> <p><it>Results</it></p> <p>Comparison of the different promoters showed that MeCP2 and MBD2a repressed promoter-specifically Cyclin D2 in all cell lines, whereas in MCF-7 cells MeCP2 repressed cell-specifically all methylated promoters. Chromatin immunoprecipitation showed that all methylated promoters associated with at least one MBD. Treatment of the cells by the demethylating agent 5-aza-2'-deoxycytidine (5-aza-CdR) caused dissociation of the MBDs from the promoters. Only MBD1v1 bound and repressed methylation-independently all promoters. Real-time amplification of DNA immunoprecipitated by 17 different antibodies showed a preferential enrichment for methylated lysine of histone H3 (H3K4me1, H3K4me2 and H3K4me3) at the particular promoters. Notably, the silent promoters were associated with unmodified histones which were acetylated following treatment by 5-aza-CdR.</p> <p><it>Conclusions</it></p> <p>This study is one of the first to reveal the histone code and MBD profile at the promoters of CD44, Cyclin D2, GLIPR1 and PTEN in different tumour cells and associated changes after stimulation with methylation inhibitor 5-aza-CdR.</p