The mitochondrial lineage U8a reveals a Paleolithic settlement in the Basque country

BACKGROUND: It is customary, in population genetics studies, to consider Basques as the direct descendants of the Paleolithic Europeans. However, until now there has been no irrefutable genetic proof to support this supposition. Even studies based on mitochondrial DNA (mtDNA), an ideal molecule for constructing datable maternal genealogies, have failed to achieve this. It could be that incoming gene flow has replaced the Basque ancient lineages but it could also be that these lineages have not been detected due to a lack of resolution of the Basque mtDNA genealogies. To assess this possibility we analyzed here the mtDNA of a large sample of autochthonous Basques using mtDNA genomic sequencing for those lineages that could not be unequivocally classified by diagnostic RFLP analysis and control region (HVSI and HVSII) sequencing. RESULTS: We show that Basques have the most ancestral phylogeny in Europe for the rare mitochondrial subhaplogroup U8a. Divergence times situate the Basque origin of this lineage in the Upper Palaeolithic. Most probably, their primitive founders came from West Asia. The lack of U8a lineages in Africa points to an European and not a North African route of entrance. Phylogeographic analysis suggest that U8a had two expansion periods in Europe, the first, from a south-western area including the Iberian peninsula and Mediterranean France before 30,000 years ago, and the second, from Central Europe around 15,000–10,000 years ago. CONCLUSION: It has been demonstrated, for the first time, that Basques show the oldest lineages in Europe for subhaplogroup U8a. Coalescence times for these lineages suggest their presence in the Basque country since the Upper Paleolithic. The European U8 phylogeography is congruent with the supposition that Basques could have participated in demographic re-expansions to repopulate central Europe in the last interglacial periods

Autologous and Allogeneic Stem Cell Transplantation for Treatment of Crohn’s Fistulae

Up to 20% of patients with Crohn’s disease (CD) may have perianal fistula disease. Classically, surgery has played an important role; in recent years, medical treatment has taken a leading role. Immunosuppressants and biological trea tments have proven beneficial in many patients, but still, the percentage of patients who do not respond remains significant. In this scenario, cell therapy is envisaged as an effective alternative to surgery. The promising preclinical and clinical data that we review below suggest that cell therapy could represent a major advance in the clinical management of this difficult problem

El papel del voluntariado universitario en la creación de una comunidad de aprendizaje.

La comunicación que presentamos describe el proceso de participación del voluntariado universitario en la comunidad de aprendizaje CEIP Albolafia de Córdoba. Dado que el papel del voluntariado en este tipo de experiencias es clave para la puesta en práctica de las actuaciones transformadoras, nuestra tarea ha estado centrada en articular la presencia de un grupo de alumnos y alumnas en el centro educativo. Por ello consideramos de interés valorar sus conocimientos previos sobre el tema, sus deseos de transformación social y sus motivaciones para participar en este proyecto. La información obtenida ha permitido reformular las actuaciones en relación a la formación, el compromiso y la participación en la comunidad de aprendizaje

Invoking Chiral Vector Leptoquark to explain LFU violation in B Decays

LHCb has recently reported more than $2\sigma$ deviation from the Standard Model prediction in the observable $R_{J/\psi}$. We study this anomaly in the framework of a vector leptoquark along with other lepton flavor universality violating measurements which include $R_{K^{(*)}}$, and $R_{D^{(*)}}$. We show that a chiral vector leptoquark can explain all the aforementioned anomalies consistently while also respecting other experimental constraints

Lyman break and ultraviolet-selected galaxies at z ~ 1 - II. PACS 100μm/160μm FIR detections

In this work, we report the Photodetector Array Camera and Spectrometer (PACS) 100 μm/160 μm detections of a sample of 42 GALEX-selected and far-infrared (FIR)-detected Lyman break galaxies (LBGs) at z ~ 1 located in the Cosmic Evolution Survey (COSMOS) field and analyse their ultraviolet (UV) to FIR properties. The detection of these LBGs in the FIR indicates that they have a dust content high enough so that its emission can be directly detected. According to a spectral energy distribution (SED) fitting with stellar population templates to their UV-to-near-IR observed photometry, PACS-detected LBGs tend to be bigger (Reff ~ 4.1 kpc), more massive [log (M*/M⊙) ~ 10.7], dustier [Es(B - V) ~ 0.40], redder in the UV continuum (β ~ -0.60) and UV-brighter [log (LUV/L⊙) ~ 10.1] than PACSundetected LBGs. PACS-detected LBGs at z ~ 1 are mostly disc-like galaxies and are located over the green valley and red sequence of the colour-magnitude diagram of galaxies at their redshift. By using their UV and IR emission, we find that PACS-detected LBGs tend to be less dusty and have slightly higher total star formation rates (SFRs) than other PACS-detected UV-selected galaxies within the same redshift range. As a consequence of the selection effect due to the depth of the FIR observations employed, all our PACS-detected LBGs have total IR luminosities, LIR, higher than 1011 L⊙ and thus are luminous IR galaxies. However, none of the PACS-detected LBGs are in the ultra-luminous IR galaxy (ULIRG) regime, LIR =1012 L⊙, where the FIR observations are complete. The finding of ULIRGs-LBGs at higher redshifts (z ~ 3) suggests an evolution of the FIR emission of LBGs with cosmic time. In an IRX-β diagram, PACS-detected LBGs at z~1 tend to be located around the relation for local starburst similarly to other UV-selected PACS-detected galaxies at the same redshift. Consequently, the dust-correction factors obtained with theirUVcontinuum slope allowus to determine their total SFR, unlike at higher redshifts. However, the dust attenuation derived from UV to NIR SED fitting overestimates the total SFR for most of our PACS-detected LBGs in an age-dependent way: the overestimation factor is higher in younger galaxies. This is likely due to the typical degeneracy between dust attenuation and age in the SED fitting with synthetic templates and highlights the importance of the FIR measurements in the analysis of star-forming galaxies at intermediate redshifts.Generalitat Valenciana PROMETEO-2008/132NASA Office of Space Science NNX09AF08GEuropean Southern Observatory LP175.A-0839Junta de Andalucía TIC-114, P08-TIC-03531Ministerio de Economía y Competitividad AYA2011- 29517-C03-01, AYA2010-22111-C03-02, AYA2010-1516

Resistance to Bleomycin-Induced Lung Fibrosis in MMP-8 Deficient Mice Is Mediated by Interleukin-10

BACKGROUND: Matrix metalloproteinases (MMPs) may have pro and antifibrotic roles within the lungs, due to its ability to modulate collagen turnover and immune mediators. MMP-8 is a collagenase that also cleaves a number of cytokines and chemokines. METHODOLOGY AND PRINCIPAL FINDINGS: To evaluate its relevance in lung fibrosis, wildtype and Mmp8(-/-) mice were treated with either intratracheal bleomycin or saline, and lungs were harvested at different time points. Fibrosis, collagen, collagenases, gelatinases, TGFβ and IL-10 were measured in lung tissue. Mmp8(-/-) mice developed less fibrosis than their wildtype counterparts. This was related to an increase in lung inflammatory cells, MMP-9 and IL-10 levels in these mutant animals. In vitro experiments showed that MMP-8 cleaves murine and human IL-10, and tissue from knockout animals showed decreased IL-10 processing. Additionally, lung fibroblasts from these mice were cultured in the presence of bleomycin and collagen, IL-10 and STAT3 activation (downstream signal in response to IL-10) measured by western blotting. In cell cultures, bleomycin increased collagen synthesis only in wildtype mice. Fibroblasts from knockout mice did not show increased collagen synthesis, but increased levels of unprocessed IL-10 and STAT3 phosphorylation. Blockade of IL-10 reverted this phenotype, increasing collagen in cultures. CONCLUSIONS: According to these results, we conclude that the absence of MMP-8 has an antifibrotic effect by increasing IL-10 and propose that this metalloprotease could be a relevant modulator of IL-10 metabolism in vivo

"Bioadsorption of silver ions by calcareous chitin, chitin and chitosan"

"Context: Calcareous chitin, chitin, chitosan, and their modifications are used as bioadsorbents of metals and dyes that cause environmental pollution, endocrine disruption, and human diseases. Aims: To evaluate the selective bioadsorption of silver ions (Ag+ ) by calcareous chitin, chitin, and chitosan. Methods: Experimental and prospective study. The presence of functional groups of the bioadsorbents was identified by Fourier-transformed infrared spectroscopy (FT-IR), 1H-NMR spectroscopy and scanning electron microscopy (SEM). The Langmuir, Freundlich, and Elovich models were applied to describe the adsorption capacity of bioadsorbents according to granule size (20-40, 40-60, 60-80 meshes) and temperature (10, 20, and 30°C). Results: The FT-IR spectrum of calcareous chitin indicates the presence of carbonate (CO3 = 1420 cm-1 ), amide III (1313 cm-1 ), –OH groups (3441.90 cm-1 ), and pyranose structure (952.83 cm-1 ); chitin has –OH groups (3441.90 cm-1 ), NH (3268 cm-1 ), amide I (1654 cm-1 ) and II (1559 cm-1 ); chitosan has –OH groups (3419.90 cm-1 ), –NH (3200 cm-1 ), amide I (1712.18 cm-1 ), –NH2 (1654.46 cm-1 ), amide III (1317.11 cm-1 ) and pyranose structure (1070.12 cm-1 and 1031 cm-1 ). The Langmuir model indicates greater bioadsorption of Ag+ ions at smaller particle sizes (60-80 = 0.25-0.18 mm) and at a temperature of 20-30°C. Conclusions: The bioadsorption of silver ions (Ag+ ) by chitosan is greater with respect to calcareous chitin and chitin; the Langmuir model fits for the Ag+ isotherm and suggests that the process is controlled by physisorption.

Autologous Platelet-Rich Plasma in the Treatment of Perianal Fistula in Crohn’s Disease

[Aim] To assess clinical healing in patients with perianal Crohn’s disease with local intrafistular injection of autologous platelet-rich plasma.[Method] The pilot study was conducted at a single centre between January 2013 and December 2015. Autologous platelet-rich plasma was prepared in platelet-rich and platelet-poor fractions for local intrafistular injection in patients with proven, established perianal Crohn’s disease. Patients were permitted biological therapies, and the Perianal Crohn’s Disease Activity Index was recorded. Patients were followed for 48 weeks for clinical signs of healing (complete, partial or non-healing), monitoring fistula drainage, closure and epithelialization.[Results] The study included 29 patients (19 males; mean age 38 ± 12.8 years) with four exclusions in the operating room because surgery was not indicated and four lost to follow-up. Five adverse events were recorded, with two requiring the drainage of abscess collections. Of the 21 patients assessable at 24 weeks, there was complete healing, partial healing and non-healing in 7 (33.3%), 8 (38.1%) and 6 (28.6%) patients, respectively. By 48 weeks, there was complete healing, partial healing and non-healing in 6 (40%), 6 (40%) and 3 (20%) patients, respectively, with a reduction in the number of visible external fistula openings at both time points (P = 0.021). By the end of the study, there was a higher trend of healing if biological therapies were continued (85.7% with biologics vs. 75% without, P = 0.527), but there were no statistically significant differences and no differences in the Perianal Crohn’s Disease Activity Index.[Conclusion]Autologous platelet-rich plasma is safe in patients with perianal Crohn’s disease, with an acceptable healing rate over a medium-term follow-up, particularly if biological therapies are used concomitantly

Viruses Previously Identified in Brazil as Belonging to HIV-1 CRF72_BF1 Represent Two Closely Related Circulating Recombinant Forms, One of Which, Designated CRF122_BF1, Is Also Circulating in Spain

Circulating recombinant forms (CRFs) are important components of the HIV-1 pandemic. Those derived from recombination between subtype B and subsubtype F1, with 18 reported, most of them of South American origin, are among the most diverse. In this study, we identified a HIV-1 BF1 recombinant cluster that is expanding in Spain, transmitted mainly via heterosexual contact, which, analyzed in near full-length genomes in four viruses, exhibited a coincident BF1 mosaic structure, with 12 breakpoints, that fully coincided with that of two viruses (10BR_MG003 and 10BR_MG005) from Brazil, previously classified as CRF72_BF1. The three remaining Brazilian viruses (10BR_MG002, 10BR_MG004, and 10BR_MG008) previously identified as CRF72_BF1 exhibited mosaic structures highly similar, but not identical, to that of the Spanish viruses and to 10BR_MG003 and 10BR_MG005, with discrepant subtypes in two short genome segments, located in pol and gp120env. Based on these results, we propose that the five viruses from Brazil previously identified as CRF72_BF1 actually belong to two closely related CRFs, one comprising 10BR_MG002, 10BR_MG004, and 10BR_MG008, which keep their CRF72_BF1 designation, and the other, designated CRF122_BF1, comprising 10BR_MG003, 10BR_MG005, and the viruses of the identified Spanish cluster. Three other BF1 recombinant genomes, two from Brazil and one from Italy, previously identified as unique recombinant forms, were classified as CRF72_BF1. CRF122_BF1, but not CRF72_BF1, was associated with protease L89M substitution, which was reported to contribute to antiretroviral drug resistance. Phylodynamic analyses estimate the emergence of CRF122_BF1 in Brazil around 1987. Given their close phylogenetic relationship and similar structures, the grouping of CRF72_BF1 and CRF122_BF1 in a CRF family is proposed.This work was funded through Acción Estratégica en Salud Intramural (AESI), Instituto de Salud Carlos III, projects “Estudios Sobre Vigilancia Epidemiológica Molecular del VIH-1 en España”, PI16CIII/00033, and “Epidemiología Molecular del VIH-1 en España y su Utilidad Para Investigaciones Biológicas y en Vacunas“, PI19CIII/00042, and through scientific agreement with Consellería de Sanidade, Government of Galicia (MVI 1004/16).S

Low-dose statin treatment increases prostate cancer aggressiveness

Altres ajuts: NM-M was supported by the Spanish Association Against Cancer (AECC), AECC JP Vizcaya. VT is supported by Fundación Vasca de Innovación e Investigación Sanitarias, BIOEF (BIO15/CA/052), the department of health of the Basque Government (2016111109) and the 2016 grant of the AECC (Junta provincial de Bizkaia). LA, AA-A and LV-J were supported by the Basque Government of education. The work of A.C. is supported by the Ramón y Cajal award, the Basque Department of Industry, Tourism and Trade (Etortek) and the department of education (IKERTALDE IT1106-16), FERO VIII Fellowship, the BBVA foundation, Severo Ochoa. Excellence Accreditation SEV-2016-0644) and the European Research Council (Starting Grant 336343; Proof of Concept 754627). The participation of AC, VT, NM-M, SF and AZ as part of CIBERONC was co-funded with FEDER funds.Prostate cancer is diagnosed late in life, when co-morbidities are frequent. Among them, hypertension, hypercholesterolemia, diabetes or metabolic syndrome exhibit an elevated incidence. In turn, prostate cancer patients frequently undergo chronic pharmacological treatments that could alter disease initiation, progression and therapy response. Here we show that treatment with anti-cholesterolemic drugs, statins, at doses achieved in patients, enhance the pro-tumorigenic activity of obesogenic diets. In addition, the use of a mouse model of prostate cancer and human prostate cancer xenografts revealed that in vivo simvastatin administration alone increases prostate cancer aggressiveness. In vitro cell line systems supported the notion that this phenomenon occurs, at least in part, through the direct action on cancer cells of low doses of statins, in range of what is observed in human plasma. In sum, our results reveal a prostate cancer experimental system where statins exhibit an undesirable effect, and warrant further research to address the relevance and implications of this observation in human prostate cancer