Prototipo de sistema de gestion para la fuente de soda y schoperia "Los Reales del Valle"

87 p.La presente memoria consiste en un análisis estratégico del negocio de la Fuente de Soda y Schoperia "Los Reales del Valle", uno de los principales negocios de la ciudad de Rengo. Posteriormente, se brinda, dada las necesidades de la empresa, en un requerimiento de tecnologías de información, lo que se traduce en un análisis informativo, el cual, se implementa en un prototipo de sistema de gestión de negocios, adaptado a los requerimientos de la empresa. En si, el objetivo que promueve la presente memoria, es la elaboración de un prototipo de software, que genere información relevante y oportuna, que sirva como apoyo de las decisiones gerenciales, lo cual se menciona en el capitulo de Introducción. En el capitulo 2, se hace referencia al Análisis Del Ambiente Interno de La Empresa; ya sea su identificación y descripción, visión, misión, objetivos general y específicos, definición de negocio, la cadena de valor de la empresa y el análisis las Fortalezas y Debilidades, lo cual es un estudio completo a la empresa y sus características internas que posee. En el Capitulo 3, se hace referencia al Ambiente Externo De La Empresa, el cual se traduce en el análisis de las Oportunidades y Amenazas, Las variables que tienen influencia en la empresa, el Análisis Porter, lo que brinda, junto al capitulo anterior, varias estrategias a seguir en la empresa, las cuales se hacen mención en el capitulo 4. En el Capitulo 4, se hace referencia a la estrategia genérica de la empresa y las estrategias a implementar dado el resultado de los análisis anteriores. En el capitulo 5, se efectúa el Análisis De Requerimientos del prototipo de software que se desarrollara para la fuente de Soda y Schoperia, lo que desencadena al Diseño Lógico ( capitulo 6 ), sus requerimientos iniciales, el Modelo Entidad - Relación, Diagramas de Flujos de Datos; y al Diseño Físico ( Capitulo 7 ), el que consiste en la organización del sistema y el diccionario de datos. En el Capitulo 8, se hace referencia al diseño del prototipo del sistema, en el cual se muestran los diseños de las pantallas que consiste este sistema como su primera versión. Posteriormente, en el capitulo 9 se hace mención a los anexos de la Memoria y en el Capitulo 10 a su Bibliografía

Fructose consumption reduces hippocampal synaptic plasticity underlying cognitive performance

AbstractMetabolic syndrome (MetS) is a global epidemic, which involves a spectrum of metabolic disorders comprising diabetes and obesity. The impact of MetS on the brain is becoming to be a concern, however, the poor understanding of mechanisms involved has limited the development of therapeutic strategies. We induced a MetS-like condition by exposing mice to fructose feeding for 7weeks. There was a dramatic deterioration in the capacity of the hippocampus to sustain synaptic plasticity in the forms of long-term potentiation (LTP) and long-term depression (LTD). Mice exposed to fructose showed a reduction in the number of contact zones and the size of postsynaptic densities (PSDs) in the hippocampus, as well as a decrease in hippocampal neurogenesis. There was an increase in lipid peroxidation likely associated with a deficiency in plasma membrane excitability. Consistent with an overall hippocampal dysfunction, there was a subsequent decrease in hippocampal dependent learning and memory performance, i.e., spatial learning and episodic memory. Most of the pathological sequel of MetS in the brain was reversed three month after discontinue fructose feeding. These results are novel to show that MetS triggers a cascade of molecular events, which disrupt hippocampal functional plasticity, and specific aspects of learning and memory function. The overall information raises concerns about the risk imposed by excessive fructose consumption on the pathology of neurological disorders

Adiponectin and resistin modulate the progression of Alzheimer´s disease in a metabolic syndrome model

Metabolic syndrome (MetS), a cluster of metabolic conditions that include obesity, hyperlipidemia, and insulin resistance, increases the risk of several aging-related brain diseases, including Alzheimer’s disease (AD). However, the underlying mechanism explaining the link between MetS and brain function is poorly understood. Among the possible mediators are several adipose-derived secreted molecules called adipokines, including adiponectin (ApN) and resistin, which have been shown to regulate brain function by modulating several metabolic processes. To investigate the impact of adipokines on MetS, we employed a diet-induced model to induce the various complications associated with MetS. For this purpose, we administered a high-fat diet (HFD) to both WT and APP/PSN1 mice at a pre-symptomatic disease stage. Our data showed that MetS causes a fast decline in cognitive performance and stimulates Aβ42 production in the brain. Interestingly, ApN treatment restored glucose metabolism and improved cognitive functions by 50% while decreasing the Aβ42/40 ratio by approximately 65%. In contrast, resistin exacerbated Aβ pathology, increased oxidative stress, and strongly reduced glucose metabolism. Together, our data demonstrate that ApN and resistin alterations could further contribute to AD pathology

Insulin-like growth factor 2 (IGF2) protects against Huntington's disease through the extracellular disposal of protein aggregates

Impaired neuronal proteostasis is a salient feature of many neurodegenerative diseases, highlighting alterations in the function of the endoplasmic reticulum (ER). We previously reported that targeting the transcription factor XBP1, a key mediator of the ER stress response, delays disease progression and reduces protein aggregation in various models of neurodegeneration. To identify disease modifier genes that may explain the neuroprotective effects of XBP1 deficiency, we performed gene expression profiling of brain cortex and striatum of these animals and uncovered insulin-like growth factor 2 (Igf2) as the major upregulated gene. Here, we studied the impact of IGF2 signaling on protein aggregation in models of Huntington's disease (HD) as proof of concept. Cell culture studies revealed that IGF2 treatment decreases the load of intracellular aggregates of mutant huntingtin and a polyglutamine peptide. These results were validated using induced pluripotent stem cells (iPSC)-derived medium spiny neurons from HD patients and spinocerebellar ataxia cases. The reduction in the levels of mutant huntingtin was associated with a decrease in the half-life of the intracellular protein. The decrease in the levels of abnormal protein aggregation triggered by IGF2 was independent of the activity of autophagy and the proteasome pathways, the two main routes for mutant huntingtin clearance. Conversely, IGF2 signaling enhanced the secretion of soluble mutant huntingtin species through exosomes and microvesicles involving changes in actin dynamics. Administration of IGF2 into the brain of HD mice using gene therapy led to a significant decrease in the levels of mutant huntingtin in three different animal models. Moreover, analysis of human postmortem brain tissue and blood samples from HD patients showed a reduction in IGF2 level. This study identifies IGF2 as a relevant factor deregulated in HD, operating as a disease modifier that buffers the accumulation of abnormal protein species

Lithium Enhances Hippocampal Glucose Metabolism in an In Vitro Mice Model of Alzheimer’s Disease

Impaired cerebral glucose metabolism is an early event that contributes to the pathogenesis of Alzheimer’s disease (AD). Importantly, restoring glucose availability by pharmacological agents or genetic manipulation has been shown to protect against Aβ toxicity, ameliorate AD pathology, and increase lifespan. Lithium, a therapeutic agent widely used as a treatment for mood disorders, has been shown to attenuate AD pathology and promote glucose metabolism in skeletal muscle. However, despite its widespread use in neuropsychiatric disorders, lithium’s effects on the brain have been poorly characterized. Here we evaluated the effect of lithium on glucose metabolism in hippocampal neurons from wild-type (WT) and APPSwe/PS1ΔE9 (APP/PS1) mice. Our results showed that lithium significantly stimulates glucose uptake and replenishes ATP levels by preferential oxidation of glucose through glycolysis in neurons from WT mice. This increase was also accompanied by a strong increase in glucose transporter 3 (Glut3), the major carrier responsible for glucose uptake in neurons. Similarly, using hippocampal slices from APP-PS1 mice, we demonstrate that lithium increases glucose uptake, glycolytic rate, and the ATP:ADP ratio in a process that also involves the activation of AMPK. Together, our findings indicate that lithium stimulates glucose metabolism and can act as a potential therapeutic agent in AD

Some ideological considerations in the Bauhaus for the development of didactic activities: the influence of the Montessori method, the modernism and the gothic

The way in which Industrial Design confronts materiality and transforms it into products of use, obeys influences that are not always scientific. From its origin, artistic movements, ideologies, culture, technology and market demands, among many others, have continually modeled its epistemology and phenomenology. The Bauhaus, established a conception of Design almost a century ago but that is still valid in Latin America, even though its extreme dogmatism was the cause of its decline. In this opportunity, we review the influence of the Gothic, the Montessori pedagogy, the ideologies of the late nineteenth century, intuition and modernism, as central aspects in the original didactic and with it we have developed a simple classroom exercise, where they apply to identify the original elements that still prevail in the teaching practice of Design. These influences tend to be forgotten, but they have evolved since 1919, until decanting in the "Design Thinking" method, which, with the filters of contemporaneity, has put the own way of "thinking and doing" of the design at the disposal of other disciplines

Study on Li ion diffusion in LixV2O5 using first principle calculations and kinetic Monte Carlo simulations

We study the Li diffusion in Li x V2O5 (0 < x ≤ 1) - a potential cathode material for Lithium ion batteries. Different diffusion pathways in this material with dependence on the Li ion concentration are investigated by applying first-principles calculations. The results are used to obtain the corresponding diffusion coefficients by employing two complementary methodologies: Kinetic Monte Carlo (KMC) simulations and a statistical thermodynamics approach. The KMC simulations for two different crystal planes give new evidence that the diffusion occurs mainly along the [010] direction, while the corresponding diffusion coefficients show a temperature dependence obeying Arrhenius' Law. The necessity of the consideration of concentration-dependent barrier heights in the KMC simulations are demonstrated by looking at the significant changes of the concentration-dependence of the diffusion coefficients. The simulated diffusion coefficients of the combined approach show a good quantitative agreement with experimental data reported previously.Fil: Dietrich, Fabian. Universidad de La Frontera; ChileFil: Cisternas, Eduardo. Universidad de La Frontera; ChileFil: Pasinetti, Pedro Marcelo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich". Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich"; ArgentinaFil: Dos Santos Mendez, Gonzalo Joaquín. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich". Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich"; Argentina. Universidad de Mendoza. Facultad de Ingenieria; Argentin