109 research outputs found

    Dance as a means of educational inclusion

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    Uno de los objetivos de la educación, es de reducir o eliminar las barreras que pudieran obstaculizar la participación de las personas en el proceso de enseñanza-aprendizaje. En este sentido, la UNESCO destaca la educación como un vehículo transcendental para conseguir la inclusión social de quienes pudieran estar en riesgo o en situación de exclusión, siendo la danza un medio muy valioso para paliar estas desigualdades. Siguiendo el protocolo PRISMA, se realizó una revisión sistemática a partir de una búsqueda en Web of Sciencie y Scopus, utilizando como criterios de búsqueda “danza” “educación” e “inclusión” tanto en español como en inglés, que arrojó un total de 419 resultados de los cuales se seleccionaron 23. Las investigaciones muestran que el concepto de danza puede entenderse como el arte de mover el cuerpo al ritmo de una música, expresando emociones, ideas, pensamientos o historias. Este arte incide en el proceso de formación del ser humano, estimulando el desarrollo intelectual, motor, afectivo y social de los individuos. El baile es utilizado para alcanzar el bienestar físico y psicológico, y permite al individuo reforzar su identidad grupal y sentido comunitario, independientemente de sus capacidades, habilidades o competencias. Los pocos estudios existentes que emplean la danza como vía de inserción social, evidencian un fomento de oportunidades de participación y desarrollo de las personas, pero para ello se requiere un proceso de transformación que permita la eliminación de barreras socialmente impuestas y una reforma educativa.Este trabajo ha sido financiado por la Universidad de Málaga (Campus de Excelencia Internacional Andalucía Tech) y por el Ministerio de Educación, Cultura y Deporte a través de las ayudas para la Formación de Profesorado Universitario (FPU17/01554) y a través de las Becas de Colaboración con departamentos universitarios para el curso 2020/2021

    Modelo matemático mediante líneas de espera para el desarrollo de un simulador

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    El presente proyecto se desarrolló en el marco de la convocatoria a proyectos cofinanciados UBA-UNDAV del año 2012. El objetivo fue proveer una herramienta para la mejora de la gestión del mantenimiento del casco céntrico de una ciudad mediana para lo que se decidió desarrollar un simulador. Con los datos del relevamiento inicial se confeccionó un modelo matemático que consistió en un conjunto de variables aleatorias de acuerdo a la Teoría de Colas para alimentar a un simulador de tránsito. Los datos relevados permitieron elaborar los estimadores (media y varianza muestral) para los parámetros de las variables aleatorias definidas. Este modelo matemático proveyó de lógica al simulador. Éste fue desarrollado para SUMO (Simulation of Urban Mobility) versión 0.25, mediante un script Python que interactúa con la plataforma, más un conjunto de utilitarios entre los que se cuentan editores y graficadores.Sociedad Argentina de Informática e Investigación Operativ

    Modelo matemático mediante líneas de espera para el desarrollo de un simulador

    Get PDF
    El presente proyecto se desarrolló en el marco de la convocatoria a proyectos cofinanciados UBA-UNDAV del año 2012. El objetivo fue proveer una herramienta para la mejora de la gestión del mantenimiento del casco céntrico de una ciudad mediana para lo que se decidió desarrollar un simulador. Con los datos del relevamiento inicial se confeccionó un modelo matemático que consistió en un conjunto de variables aleatorias de acuerdo a la Teoría de Colas para alimentar a un simulador de tránsito. Los datos relevados permitieron elaborar los estimadores (media y varianza muestral) para los parámetros de las variables aleatorias definidas. Este modelo matemático proveyó de lógica al simulador. Éste fue desarrollado para SUMO (Simulation of Urban Mobility) versión 0.25, mediante un script Python que interactúa con la plataforma, más un conjunto de utilitarios entre los que se cuentan editores y graficadores.Sociedad Argentina de Informática e Investigación Operativ

    Modelo matemático mediante líneas de espera para el desarrollo de un simulador

    Get PDF
    El presente proyecto se desarrolló en el marco de la convocatoria a proyectos cofinanciados UBA-UNDAV del año 2012. El objetivo fue proveer una herramienta para la mejora de la gestión del mantenimiento del casco céntrico de una ciudad mediana para lo que se decidió desarrollar un simulador. Con los datos del relevamiento inicial se confeccionó un modelo matemático que consistió en un conjunto de variables aleatorias de acuerdo a la Teoría de Colas para alimentar a un simulador de tránsito. Los datos relevados permitieron elaborar los estimadores (media y varianza muestral) para los parámetros de las variables aleatorias definidas. Este modelo matemático proveyó de lógica al simulador. Éste fue desarrollado para SUMO (Simulation of Urban Mobility) versión 0.25, mediante un script Python que interactúa con la plataforma, más un conjunto de utilitarios entre los que se cuentan editores y graficadores.Sociedad Argentina de Informática e Investigación Operativ

    Технология сборки и дуговой сварки пластин из титанового сплава

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    Цель работы – является разработка технологии дуговой сварки пластин из сплава ВТ5-1. В процессе исследования проводился анализ повышения эффективности и сравнение способов сварки, ручной аргонодуговой сварки неплавящимся электродом и механизированной сварки плавящимся электродом в среде защитного газа. В результате работы были рассчитаны параметры и выбран наиболее производительный способ для сварки сплава ВТ5-1.The purpose of the work is to develop a technology for arc welding of plates made of VT5-1 alloy. In the course of the study, the analysis of efficiency improvement and comparison of welding methods, manual argon arc welding with a non-melting electrode and mechanized welding with a melting electrode in a protective gas environment were carried out. As a result of the work, the parameters were calculated and the most productive method for welding the VT5-1 alloy was selected

    Reduced Efficacy of d-Amphetamine and 3,4-Methylenedioxymethamphetamine in Inducing Hyperactivity in Mice Lacking the Postsynaptic Scaffolding Protein SHANK1

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    Genetic defects in the three SH3 and multiple ankyrin repeat domains (SHANK) genes (SHANK1, SHANK2, and SHANK3) are associated with multiple major neuropsychiatric disorders, including autism spectrum disorder (ASD), schizophrenia (SCZ), and bipolar disorder (BPD). Psychostimulant-induced hyperactivity is a commonly applied paradigm to assess behavioral phenotypes related to BPD and considered to be the gold standard for modeling mania-like elevated drive in mouse models. Therefore, the goal of our present study was to test whether Shank1 plays a role in the behavioral effects of psychostimulants and whether this is associated with genotype-dependent neurochemical alterations. To this aim, male and female null mutant Shank1-/- mice were treated with d-amphetamine (AMPH; 2.5 mg/kg) and 3,4-methylenedioxymethamphetamine (MDMA, commonly known as ecstasy; 20 mg/kg), and psychostimulant-induced hyperactivity was compared to heterozygous Shank1+/- and wildtype Shank1+/+ littermate controls. Results show that Shank1-/- mice display reduced psychostimulant-induced hyperactivity, although psychostimulants robustly stimulated locomotor activity in littermate controls. Shank1 deletion effects emerged throughout development, were particularly prominent in adulthood, and seen in response to both psychostimulants, i.e., AMPH and MDMA. Specifically, while AMPH-induced hyperactivity was reduced but still detectable in Shank1-/- mice, MDMA-induced hyperactivity was robustly blocked and completely absent in Shank1-/- mice. Reduced efficacy of psychostimulants to stimulate hyperactivity in Shank1-/- mice might be associated with alterations in the neurochemical architecture in prefrontal cortex, nucleus accumbens, and hypothalamus. Our observation that psychostimulant-induced hyperactivity is reduced rather than enhanced in Shank1-/- mice clearly speaks against a behavioral phenotype with relevance to BPD. Lack of BPD-like phenotype is consistent with currently available human data linking mutations in SHANK2 and SHANK3 but not SHANK1 to BPD

    A Multifaceted Analysis of Immune-Endocrine-Metabolic Alterations in Patients with Pulmonary Tuberculosis

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    Our study investigated the circulating levels of factors involved in immune-inflammatory-endocrine-metabolic responses in patients with tuberculosis with the aim of uncovering a relation between certain immune and hormonal patterns, their clinical status and in vitro immune response. The concentration of leptin, adiponectin, IL-6, IL-1β, ghrelin, C-reactive protein (CRP), cortisol and dehydroepiandrosterone (DHEA), and the in vitro immune response (lymphoproliferation and IFN-γ production) was evaluated in 53 patients with active untreated tuberculosis, 27 household contacts and 25 healthy controls, without significant age- or sex-related differences. Patients had a lower body mass index (BMI), reduced levels of leptin and DHEA, and increased concentrations of CRP, IL-6, cortisol, IL-1β and nearly significant adiponectin values than household contacts and controls. Within tuberculosis patients the BMI and leptin levels were positively correlated and decreased with increasing disease severity, whereas higher concentrations of IL-6, CRP, IL-1β, cortisol, and ghrelin were seen in cases with moderate to severe tuberculosis. Household contacts had lower DHEA and higher IL-6 levels than controls. Group classification by means of discriminant analysis and the k-nearest neighbor method showed that tuberculosis patients were clearly different from the other groups, having higher levels of CRP and lower DHEA concentration and BMI. Furthermore, plasma leptin levels were positively associated with the basal in vitro IFN-γ production and the ConA-driven proliferation of cells from tuberculosis patients. Present alterations in the communication between the neuro-endocrine and immune systems in tuberculosis may contribute to disease worsening

    Development and validation of a clinical score to estimate progression to severe or critical state in Covid-19 pneumonia hospitalized patients

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    The prognosis of a patient with Covid-19 pneumonia is uncertain. Our objective was to establish a predictive model of disease progression to facilitate early decision-making. A retrospective study was performed of patients admitted with Covid-19 pneumonia, classified as severe (admission to the intensive care unit, mechanic invasive ventilation, or death) or non-severe. A predictive model based on clinical, analytical, and radiological parameters was built. The probability of progression to severe disease was estimated by logistic regression analysis. Calibration and discrimination (receiver operating characteristics curves and AUC) were assessed to determine model performance. During the study period 1,152 patients presented with Covid-19 infection, of whom 229 (19.9%) were admitted for pneumonia. During hospitalization, 51 (22.3%) progressed to severe disease, of whom 26 required ICU care (11.4); 17 (7.4%) underwent invasive mechanical ventilation, and 32 (14%) died of any cause. Five predictors determined within 24 hours of admission were identified: Diabetes, Age, Lymphocyte count, SaO2, and pH (DALSH score). The prediction model showed a good clinical performance, including discrimination (AUC 0.87 CI 0.81, 0.92) and calibration (Brier score = 0.11). In total, 0%, 12%, and 50% of patients with severity risk scores ≤5%, 6-25%, and >25% exhibited disease progression, respectively. A simple risk score based on five factors predicts disease progression and facilitates early decision-making according to prognosis.Carlos III Health Institute, Spain, Ministry of Economy and Competitiveness (SPAIN) and the European Regional Development Fund (FEDER)Instituto de Salud Carlos II

    Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function

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    Non-alcoholic fatty liver disease (NAFLD) is a major health threat in both developed and developing countries and is a precursor of the more advanced liver diseases, including non-alcoholic steatohepatitis (NASH), cirrhosis, and liver cancer. Currently, understanding the multiple and complex molecular pathways implicated in NAFLD onset and progression is a major priority. The transcription factor p63, which belongs to a family comprising p53, p63, and p73,1 is one of many factors that contributes to the development of liver steatosis. The role of p63 as a tumor suppressor and in cell maintenance and renewal is well studied, but we have recently reported that it is also relevant in the control of lipid metabolism.2 p63 encodes multiple isoforms that can be grouped into 2 categories; isoforms with an acidic transactivation domain (TA) and those without this domain (domain negative). The TAp63α isoform is elevated in the liver of animal models of NAFLD as well as in liver biopsies from obese patients with NAFLD. Furthermore, downregulation of p63α in the liver attenuates liver steatosis in diet-induced obese (DIO) mice, while the activation of TAp63α increases hepatic fat content, mediated by the activation of IKKβ and endoplasmic reticulum stress.2 A specialized form of autophagy that degrades lipid droplets, termed “lipophagy”, is a major pathway of lipid mobilization in hepatocytes. Lipophagy is elevated in hepatoma cells upon exposure to free fatty acids,3 and reduces the fatty acid load in mouse hepatocytes.4 Its impairment has been associated with the development of fatty liver and insulin resistance3,5; in contrast, the autophagic flux is increased during the activation of hepatic stellate cells.6 In the present study, we used an unbiased proteomics approach to gain insight into novel proteins modulating lipid metabolism in the liver of mice with genetic knockdown or overexpression of TAp63α. We found that autophagy-related gene 3 (ATG3) was upregulated by TAp63α activation and downregulated after p63α inhibition. ATG3 is elevated in several animal models of NAFLD and in the liver of patients with NAFLD. Genetic overexpression of ATG3 increased the lipid load in hepatocytes, while its repression alleviated TAp63α- and diet-induced steatosis. ATG3 exerted its role in lipid metabolism by regulating SIRT1 and mitochondrial function. Collectively, these findings identify ATG3 as a novel factor implicated in the development of steatosisThis work has been supported by grants from FEDER/Ministerio de Ciencia, Innovación y Universidades-Agencia Estatal de Investigación (PA: RTI2018-095134-B-100; DS and LH: SAF2017-83813-C3-1-R; MLMC: RTC2019-007125-1; CD: BFU2017-87721; ML: RTI2018–101840-B-I00; GS; PID2019-104399RB-I00; RN: RTI2018-099413-B-I00 and RED2018-102379-T; MLMC: SAF2017-87301-R; TCD: RTI2018-096759-A-100), FEDER/Instituto de Salud Carlos III (AGR: PI19/00123), Xunta de Galicia (ML: 2016-PG068; RN: 2015-CP080 and 2016-PG057), Fundación BBVA (RN, GS and MLM), Proyectos Investigación en Salud (MLMC: DTS20/00138), Sistema Universitario Vasco (PA: IT971-16); Fundación Atresmedia (ML and RN), Fundación La Caixa (M.L., R.N. and M.C.), Gilead Sciences International Research Scholars Program in Liver Disease (MVR), Marató TV3 Foundation (DS: 201627), Government of Catalonia (DS: 2017SGR278) and European Foundation for the Study of Diabetes (RN and GS). This research also received funding from the European Community’s H2020 Framework Programme (ERC Synergy Grant-2019-WATCH- 810331, to RN, VP and MS). Centro de Investigación Biomédica en Red (CIBER) de Fisiopatología de la Obesidad y Nutrición (CIBERobn), Centro de Investigación Biomédica en Red (CIBER) de Enfermedades Hepáticas y Digestivas (CIBERehd) and CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERdem). CIBERobn, CIBERehd and CIBERdem are initiatives of the Instituto de Salud Carlos III (ISCIII) of Spain which is supported by FEDER funds. We thank MINECO for the Severo Ochoa Excellence Accreditation to CIC bioGUNE (SEV-2016-0644)S

    Precautionary Effect and Variations of the Value of Information

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