57 research outputs found

    Érase una vez…la ciencia. Los relatos como nexo de unión entre enseñar ciencia y aprender soñando

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    Este proyecto se basa en la confección de relatos breves que involucren contenidos científicos de aprendizaje. Los autores de los relatos fueron los alumnos de la Facultad de Educación

    Activation-induced cytidine deaminase targets SUV4-20-mediated histone H4K20 trimethylation to class-switch recombination sites

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    Activation-induced cytidine deaminase (AID) triggers antibody diversification in B cells by catalysing deamination and subsequently mutating immunoglobulin (Ig) genes. Association of AID with RNA Pol II and occurrence of epigenetic changes during Ig gene diversification suggest participation of AID in epigenetic regulation. AID is mutated in hyper-IgM type 2 (HIGM2) syndrome. Here, we investigated the potential role of AID in the acquisition of epigenetic changes. We discovered that AID binding to the IgH locus promotes an increase in H4K20me3. In 293F cells, we demonstrate interaction between co-transfected AID and the three SUV4-20 histone H4K20 methyltransferases, and that SUV4-20H1.2, bound to the IgH switch (S) mu site, is replaced by SUV4-20H2 upon AID binding. Analysis of HIGM2 mutants shows that the AID truncated form W68X is impaired to interact with SUV4-20H1.2 and SUV4-20H2 and is unable to bind and target H4K20me3 to the Smu site. We finally show in mouse primary B cells undergoing class-switch recombination (CSR) that AID deficiency associates with decreased H4K20me3 levels at the Smu site. Our results provide a novel link between SUV4-20 enzymes and CSR and offer a new aspect of the interplay between AID and histone modifications in setting the epigenetic status of CSR sites

    The tumor suppressor SirT2 regulates cell cycle progression and genome stability by modulating the mitotic deposition of H4K20 methylation

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    The establishment of the epigenetic mark H4K20me1 (monomethylation of H4K20) by PR-Set7 during G2/M directly impacts S-phase progression and genome stability. However, the mechanisms involved in the regulation of this event are not well understood. Here we show that SirT2 regulates H4K20me1 deposition through the deacetylation of H4K16Ac (acetylation of H4K16) and determines the levels of H4K20me2/3 throughout the cell cycle. SirT2 binds and deacetylates PR-Set7 at K90, modulating its chromatin localization. Consistently, SirT2 depletion significantly reduces PR-Set7 chromatin levels, alters the size and number of PR-Set7 foci, and decreases the overall mitotic deposition of H4K20me1. Upon stress, the interaction between SirT2 and PR-Set7 increases along with the H4K20me1 levels, suggesting a novel mitotic checkpoint mechanism. SirT2 loss in mice induces significant defects associated with defective H4K20me1-3 levels. Accordingly, SirT2-deficient animals exhibit genomic instability and chromosomal aberrations and are prone to tumorigenesis. Our studies suggest that the dynamic cross-talk between the environment and the genome during mitosis determines the fate of the subsequent cell cycle

    Lecciones y practicum de Derecho Constitucional

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    El presente proyecto de innovación docente persigue un doble objetivo: la actualización de los contenidos de Lecciones de Derecho Constitucional II y la reorganización y difusión de las prácticas de Derecho Constitucional II. Mientras que la primera finalidad ya ha sido satisfecha, la segunda se está desarrollando al tiempo en el que se imparten las lecciones por parte de los distintos profesores.Departamento de Derecho Constitucional, Procesal y Eclesiástico del Estad

    Post-Hospital Syndrome and Hyponatremia

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    Introduction: Post-hospital syndrome (PHS) is defined as a period of vulnerability during the first 30 days after a patient is discharged from hospital, in which multiple factors come into play. Hyponatremia is the most frequent hydroelectrolytic disorder in hospitalized patients and may be related to the appearance of PHS. Objective: The objective is to estimate the prevalence of PHS that is assessed as the rate of readmissions in the first 30 days after discharge, in patients with hyponatremia. Material and Methods: It is a descriptive observational study of patients with hyponatremia who were discharged from 1 September 2010 to 2 February 2020 at the Internal Medicine Service of the Hospital University of San Juan (Alicante, Spain). Results: Of the 25 included patients, 5 (20%) were readmitted within a month of discharge, after a mean of 11.4 days (standard deviation [SD] 5.1). The overall mortality of the study was 20% (n = 5), with one case of death in the first 30 days post-hospitalization (4%). In 12 patients (48%) the origin of the hyponatremia was undetermined. The most frequently recorded etiology for the condition was pharmacological (n = 7, 28%), and there was pronounced variability in its clinical and laboratory study. The most widely used corrective measure was drug withdrawal, in 16 patients (64%). Water intake restriction was the most common treatment after discharge (5 patients, 20%), followed by urea (2 patients, 8%), while tolvaptan was not used. Conclusion: Hyponatremia may be the cause of PHS, which could increase the rate of early readmission. Hyponatremia is an underdiagnosed and undertreated entity, so it is necessary to apply an appropriate system to optimize its management and, in future studies, to assess its impact on PHS

    In vivo partial cellular reprogramming enhances liver plasticity and regeneration.

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    Mammals have limited regenerative capacity, whereas some vertebrates, like fish and salamanders, are able to regenerate their organs efficiently. The regeneration in these species depends on cell dedifferentiation followed by proliferation. We generate a mouse model that enables the inducible expression of the four Yamanaka factors (Oct-3/4, Sox2, Klf4, and c-Myc, or 4F) specifically in hepatocytes. Transient in vivo 4F expression induces partial reprogramming of adult hepatocytes to a progenitor state and concomitantly increases cell proliferation. This is indicated by reduced expression of differentiated hepatic-lineage markers, an increase in markers of proliferation and chromatin modifiers, global changes in DNA accessibility, and an acquisition of liver stem and progenitor cell markers. Functionally, short-term expression of 4F enhances liver regenerative capacity through topoisomerase2-mediated partial reprogramming. Our results reveal that liver-specific 4F expression in vivo induces cellular plasticity and counteracts liver failure, suggesting that partial reprogramming may represent an avenue for enhancing tissue regeneration

    Lo tangible e intangible del diseño

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    1 archivo PDF (366 páginas)"El Departamento de Evaluación del Diseño, en el Tiempo de la División de Ciencias y Artes para el Diseño de la Universidad Autónoma Metropolitana, Azcapotzalco, publica este libro colectivo, donde se aborda la discusión y el análisis sobre "Lo tangible e intangible del diseño". Este libro tiene como finalidad el profundizar en distintas posiciones teóricas, metodológicas y empíricas, donde un grupo interdisciplinario de profesores investigadores del Departamento de Evaluación, desde la arquitectura, los estudios urbanos, la educación, la historia, la semiótica, el diseño de la comunicación gráfica y el industrial; buscan convergencias y discuten divergencias que puedan generar servir como referentes intelectuales y teóricos, en el diseño. Este libro es resultado del Cuarto Coloquio Departamental: Lo tangible e Intangible del Diseño. Evaluación de Objetos, Espacios, Mensajes, realizado durante el mes de septiembre del año 2004, el cual se constituyó como un espacio para el intercambio de experiencias académicas y profesionales, desde una perspectiva interdisciplinaria, centrada en la reflexión y la discusión sobre la manera de cómo se puede analizar, definir y evaluar, lo tangible y lo intangible en el diseño"
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