Seguimiento y evaluación de graduados en Sociología y Ciencias Políticas. Comparación de competencias obtenidas en estudios de grado y competencias necesarias

El proyecto pretendía la búsqueda de mejoras y nuevas líneas de desarrollo de contenidos y competencias en las asignaturas de los grados de Ciencias Políticas y Sociología, en la UCM y, eventualmente, en otras universidades. El aporte de esta investigación es recabar datos de la realidad a la que se enfrentan los graduados una vez egresados de la universidad. A partir de la obtención de datos empíricos obtenidos de los procesos de empleabilidad y adaptación al mercado que han vivido jóvenes egresados, en sus experiencias de prácticas y primeros empleos, y de la información acumulada que poseen los tutores de prácticas en empresas u organizaciones privadas. Esta información se obtiene a partir de dos encuestas on-line que se desarrollaron tomando en cuenta las experiencias en la mediación y observación de las competencias y desempeños profesionales. Estas encuestas se enviaron a sendas bases de datos de jóvenes egresado y de empleadores/tutores proporcionadas por el Colegio de Politólogos y Sociólogos de Madrid

Mapping mobility - pathways, institutions and structural effects of youth mobility: Descriptive Analysis Report

This document presents the Deliverable Descriptive Analysis Report (D.4.5 internal)1 of the MOVE Project Survey (Work Package 4) that has received funding from the Horizon 2020 research and innovation programme of the European Union under Grant Agreement No.649263. All the descriptive analysis committed in the Grant Agreement have been performed and shared with all partners in the internal intranet Project Angel due to its size and format. This document presents simpli ed more manageable and visual version that was shared amongst partners who were asked to contribute with speci c country analysis or explanations. The central aim of MOVE is to provide evidence-based knowledge on mobility of young people in Europe as a prerequisite to improve mobility conditions, and to identify fostering and hindering factors of "beneficial" mobility. This aim is pursued using a multilevel interdisciplinary research approach, aiming at a comprehensive and systematic analysis of the mobility of young people in Europe

Master Plan para UNIMAK

El Master Plan de UNIMAK se presenta como una apuesta a futuro, no solo para la Universidad de Makeni, sino también para la propia ciudad de Makeni. Se pretende potencias la Universidad como una referencia a nivel regional y como desencadenante de la estructura de trazado de la ciudad. El proyecto plantea potencial la dualidad que existe entre la infraestructura viaria y la red verde , existente en la ciudad, introduciéndola en el nuevo desarrollo del campus universitario y dotándola de la importancia suficiente para que se convierta en un elemento vinculante de la ciudad. El nuevo sistema de infraestructura rodada que se plantea está ligado entre sí por medio de unos "nodos equipados" que actúan como nuevos espacios públicos de relación en la ciudad y que albergan servicios urbanos. Este sistema de nodos se distribuye por toda la ciudad de manera que cada uno de ellos dé servicio a las viviendas de un radio de 500m

Cambios en las características de los inmigrantes durante la crisis económica

Exponemos a continuación uno de los pocos trabajos de investigación del fenómeno inmigratorio en España, que se focaliza en un aspecto cualitativo importante como es el de la formación o educación previamente adquirida en los países de origen, y en la formación o educación de aquellos inmigrantes con nivel de estudios superiores o medios. Es precisamente, la confusión de los trabajos reales y la dimensión simbólica de los trabajos atribuidos a la mayor formación o preparación, una de las claves de estudio que hemos realizado: ¿Qué trabajo hacían y qué expectativas tanto laborales como vitales expresaban los inmigrantes que vinieron a España con un nivel de educación que, supuestamente, les destinaba a empleos más calificados

Balance y futuro de la migración de los jóvenes españoles: Movilidad, emigración y retorno

Depto. de Antropología Social y Psicología SocialFac. de Ciencias Políticas y SociologíaTRUEpu

A microRNA Cluster Controls Fat Cell Differentiation and Adipose Tissue Expansion By Regulating SNCG

The H19X-encoded miR-424(322)/503 cluster regulates multiple cellular functions. Here, it is reported for the first time that it is also a critical linchpin of fat mass expansion. Deletion of this miRNA cluster in mice results in obesity, while increasing the pool of early adipocyte progenitors and hypertrophied adipocytes. Complementary loss and gain of function experiments and RNA sequencing demonstrate that miR-424(322)/503 regulates a conserved genetic program involved in the differentiation and commitment of white adipocytes. Mechanistically, it is demonstrated that miR-424(322)/503 targets gamma-Synuclein (SNCG), a factor that mediates this program rearrangement by controlling metabolic functions in fat cells, allowing adipocyte differentiation and adipose tissue enlargement. Accordingly, diminished miR-424(322) in mice and obese humans co-segregate with increased SNCG in fat and peripheral blood as mutually exclusive features of obesity, being normalized upon weight loss. The data unveil a previously unknown regulatory mechanism offat mass expansion tightly controlled by the miR-424(322)/503 through SNCG.Peer reviewe

HuertAula Comunitaria de Agroecología “Cantarranas” UCM 2010-2017: Hacia una educación transformadora y emancipadora

Depto. de Química AnalíticaFac. de Ciencias QuímicasFALSEsubmitte

Insulin regulates neurovascular coupling through astrocytes

Mice with insulin receptor (IR)-deficient astrocytes (GFAP-IR knockout [KO] mice) show blunted responses to insulin and reduced brain glucose uptake, whereas IRdeficient astrocytes show disturbed mitochondrial responses to glucose. While exploring the functional impact of disturbed mitochondrial function in astrocytes, we observed that GFAP-IR KO mice show uncoupling of brain blood flow with glucose uptake. Since IR-deficient astrocytes show higher levels of reactive oxidant species (ROS), this leads to stimulation of hypoxia-inducible factor-1¿ and, consequently, of the vascular endothelial growth factor angiogenic pathway. Indeed, GFAP-IR KO mice show disturbed brain vascularity and blood flow that is normalized by treatment with the antioxidant N-acetylcysteine (NAC). NAC ameliorated high ROS levels, normalized angiogenic signaling and mitochondrial function in IR-deficient astrocytes, and normalized neurovascular coupling in GFAP-IR KO mice. Our results indicate that by modulating glucose uptake and angiogenesis, insulin receptors in astrocytes participate in neurovascular coupling.We are thankful to M.Garcia and R. Cañadas for technical support. This work was funded by Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED) (Instituto de Salud CarlosIII, Spain) to I.T.A., A.G., and T.I.; an Inter-CIBER project (PIE14/00061) to I.T.A.that forms part of the projects PID2019-104376RB-I00 (I.T.A.) and RTI2018-094887-B-I00 (M.N.) funded by MCIN/AEI/10.13039/501100011033; a grant from Junta de Andalucia Consejería de Economía y Conocimiento (P18-RT-2233 to A.G.) cofinanced by Programa Operativo FEDER 2014–2020; a grant from Instituto de Salud Carlos III Spain (cofinanced by FEDER funds from the European Union; PI21/00915 to A.G.); Grant PID2020-115218RB-I00 to T.I. funded by Ministerio de Ciencia e Innovación/Agencia Española de Investigación (MCIN/AEI/10.13039/501100011033); and a grant from Comunidad de Madrid through the European Social Fund (ESF)–financed programme Neurometabolismo-Comunidad de Madrid (NEUROMETAB-CM) (B2017/BMD-3700 to I.T.A.and T.I.). M.N. was also supported by the Spanish Ministry of Science and Innovation (Ramón y Cajal RYC-2016-20414). J.P.-U. was contracted by CIBERNED

Modulation of SHBG binding to testosterone and estradiol by sex and morbid obesity.

Objective: Sex hormone-binding globulin (SHBG) binds and transports testosterone and estradiol in plasma. The possibility that SHBG is a mixture of transporting proteins has been postulated. We analyzed in parallel the effects of obesity status on the levels and binding capacity of circulating SHBG and their relationship with testosterone and estradiol.Design: Anthropometric measures and plasma were obtained from apparently healthy young (i.e. 35 +/- 7 years) premenopausal women (n = 32) and men (n = 30), with normal weight and obesity (BMI > 30 kg/m(2)).Methods: SHBG protein (Western blot), as well as the plasma levels of testosterone, estradiol, cortisol and insulin (ELISA) were measured. Specific binding of estradiol and testosterone to plasma SHBG was analyzed using tritiumlabeled hormones.Results: Significant differences in SHBG were observed within the obesity status and gender, with discordant patterns of change in testosterone and estradiol. In men, testosterone occupied most of the binding sites. Estrogen binding was much lower in all subjects. Lower SHBG of morbidly obese (BMI > 40 kg/m(2)) subjects affected testosterone but not estradiol. The ratio of binding sites to SHBG protein levels was constant for testosterone, but not for estradiol. The influence of gender was maximal in morbid obesity, with men showing the highest binding/SHBG ratios.Conclusions: The results reported here are compatible with SHBG being a mixture of at least two functionally different hormone-binding globulins, being affected by obesity and gender and showing different structure, affinities for testosterone and estradiol and also different immunoreactivity

Mendelian Randomisation Confirms the Role of Y-Chromosome Loss in Alzheimer’s Disease Aetiopathogenesis in Men

Mosaic loss of chromosome Y (mLOY) is a common ageing-related somatic event and has been previously associated with Alzheimer’s disease (AD). However, mLOY estimation from genotype microarray data only reflects the mLOY degree of subjects at the moment of DNA sampling. Therefore, mLOY phenotype associations with AD can be severely age-confounded in the context of genome-wide association studies. Here, we applied Mendelian randomisation to construct an age-independent mLOY polygenic risk score (mloy-PRS) using 114 autosomal variants. The mloy-PRS instrument was associated with an 80% increase in mLOY risk per standard deviation unit (p = 4.22 × 10−20) and was orthogonal with age. We found that a higher genetic risk for mLOY was associated with faster progression to AD in men with mild cognitive impairment (hazard ratio (HR) = 1.23, p = 0.01). Importantly, mloy-PRS had no effect on AD conversion or risk in the female group, suggesting that these associations are caused by the inherent loss of the Y chromosome. Additionally, the blood mLOY phenotype in men was associated with increased cerebrospinal fluid levels of total tau and phosphorylated tau181 in subjects with mild cognitive impairment and dementia. Our results strongly suggest that mLOY is involved in AD pathogenesis.P.G.-G. (Pablo García-González) is supported by CIBERNED employment plan CNV-304-PRF-866. CIBERNED is integrated into ISCIII (Instituto de Salud Carlos III). I.d.R is supported by a national grant from the Instituto de Salud Carlos III FI20/00215. A.C. (Amanda Cano) acknowledges the support of the Spanish Ministry of Science, Innovation, and Universities under the grant Juan de la Cierva (FJC2018-036012-I). M.B. (Mercé Boada) and A.R. (Agustín Ruiz) are also supported by national grants PI13/02434, PI16/01861, PI17/01474, PI19/01240, and PI19/01301. The Genome Research @ Fundació ACE project (GR@ACE) is supported by Grifols SA, Fundación bancaria “La Caixa”, Fundació ACE, and CIBERNED. Acción Estratégica en Salud is integrated into the Spanish National R + D + I Plan and funded by ISCIII (Instituto de Salud Carlos III)—Subdirección General de Evaluación—and the Fondo Europeo de Desarrollo Regional (FEDER—“Una manera de hacer Europa”). Genotyping of the ACE MCI-EADB samples was performed in the context of EADB (European Alzheimer DNA biobank) funded by the JPco-fuND FP-829-029 (ZonMW project number 733051061). This work was supported by a grant (European Alzheimer DNA BioBank, EADB) from the EU Joint Program—Neurodegenerative Disease Research (JPND). Partial funding for open access charge: Universidad de Málag