106 research outputs found

    Plan de mercadeo lanzamiento y comercialización del nuevo producto panela instantánea Tierranela

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    TIERRANELA LTDA es una empresa dedicada al diseño, desarrollo, producción y comercialización de endulzantes y bebidas refrescantes e hidratantes naturales instantáneas, elaboradas a base de jugo de caña panelera. Orgullosamente Boyacense ubicada en la región panelera de la hoya del río Suárez en el municipio de Chitaraque Boyacá, Zona que representa el 39% de la producción nacional de panela. Es así como surge la oportunidad para proponer la comercialización directa del producto “Panela instantánea TIERRANELA” enfocado a amas de casa de Bogotá, tomando como referencia inicial los supermercados ROMI debido a su alta concentración de habitantes en los estratos 4 y 5 catalogados entre los consumidores potenciales de productos naturales que puedan hacer la vida más práctica, según datos de Fedepanela. De esta manera, en los primeros siete capítulos del trabajo se plantea el problema de investigación, los objetivos, hipótesis, marco de referencia, y el diseño metodológico necesarios para orientar el desarrollo del proyecto

    Plan de mercadeo lanzamiento y comercialización del nuevo producto panela instantánea Tierranela

    Get PDF
    TIERRANELA LTDA es una empresa dedicada al diseño, desarrollo, producción y comercialización de endulzantes y bebidas refrescantes e hidratantes naturales instantáneas, elaboradas a base de jugo de caña panelera. Orgullosamente Boyacense ubicada en la región panelera de la hoya del río Suárez en el municipio de Chitaraque Boyacá, Zona que representa el 39% de la producción nacional de panela. Es así como surge la oportunidad para proponer la comercialización directa del producto “Panela instantánea TIERRANELA” enfocado a amas de casa de Bogotá, tomando como referencia inicial los supermercados ROMI debido a su alta concentración de habitantes en los estratos 4 y 5 catalogados entre los consumidores potenciales de productos naturales que puedan hacer la vida más práctica, según datos de Fedepanela. De esta manera, en los primeros siete capítulos del trabajo se plantea el problema de investigación, los objetivos, hipótesis, marco de referencia, y el diseño metodológico necesarios para orientar el desarrollo del proyecto

    Impact of glucocorticoid on a cellular model of parkinson’s disease: Oxidative stress and mitochondrial function

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    Stress seems to contribute to the neuropathology of Parkinson’s disease (PD), possibly by dysregulation of the hypothalamic–pituitary–adrenal axis. Oxidative distress and mitochondrial dysfunction are key factors involved in the pathophysiology of PD and neuronal glucocorticoid-induced toxicity. Animal PD models have been generated to study the effects of hormonal stress, but no in vitro model has yet been developed. Our aim was to examine the impact of corticosterone (CORT) administration on a dopaminergic neuronal cell model of PD induced by the neurotoxin MPP+, as a new combined PD model based on the marker of endocrine response to stress, CORT, and oxidative-mitochondrial damage. We determined the impact of CORT, MPP+ and their co-incubation on reactive oxygen species production (O2−• ), oxidative stress cellular markers (advanced-oxidation protein products and total antioxidant status), mitochondrial function (mitochondrial membrane potential and mitochondrial oxygen consumption rate) and neurodegeneration (Fluoro-Jade staining). Accordingly, the administration of MPP+ or CORT individually led to cell damage compared to controls (p < 0.05), as determined by several methods, whereas their co-incubation produced strong cell damage (p < 0.05). The combined model described here could be appropriate for investigating neuropathological hallmarks and for evaluating potential new therapeutic tools for PD patients suffering mild to moderate emotional stress

    Neuronal Metabolism and Neuroprotection: Neuroprotective Effect of Fingolimod on Menadione-Induced Mitochondrial Damage

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    Imbalance in the oxidative status in neurons, along with mitochondrial damage, are common characteristics in some neurodegenerative diseases. The maintenance in energy production is crucial to face and recover from oxidative damage, and the preservation of different sources of energy production is essential to preserve neuronal function. Fingolimod phosphate is a drug with neuroprotective and antioxidant actions, used in the treatment of multiple sclerosis. This work was performed in a model of oxidative damage on neuronal cell cultures exposed to menadione in the presence or absence of fingolimod phosphate. We studied the mitochondrial function, antioxidant enzymes, protein nitrosylation, and several pathways related with glucose metabolism and glycolytic and pentose phosphate in neuronal cells cultures. Our results showed that menadione produces a decrease in mitochondrial function, an imbalance in antioxidant enzymes, and an increase in nitrosylated proteins with a decrease in glycolysis and glucose-6-phosphate dehydrogenase. All these effects were counteracted when fingolimod phosphate was present in the incubation media. These effects were mediated, at least in part, by the interaction of this drug with its specific S1P receptors. These actions would make this drug a potential tool in the treatment of neurodegenerative processes, either to slow progression or alleviate symptoms

    Insulin-like growth factor II prevents oxidative and neuronal damage in cellular and mice models of Parkinson's disease

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    Oxidative distress and mitochondrial dysfunction, are key factors involved in the pathophysiology of Parkinson's disease (PD). The pleiotropic hormone insulin-like growth factor II (IGF-II) has shown neuroprotective and antioxidant effects in some neurodegenerative diseases. In this work, we demonstrate the protective effect of IGF-II against the damage induced by 1-methyl-4-phenylpyridinium (MPP+) in neuronal dopaminergic cell cultures and a mouse model of progressive PD. In the neuronal model, IGF-II counteracts the oxidative distress produced by MPP + protecting dopaminergic neurons. Improved mitochondrial function, increased nuclear factor (erythroid-derived 2)-like2 (NRF2) nuclear translocation along with NRF2-dependent upregulation of antioxidative enzymes, and modulation of mammalian target of rapamycin (mTOR) signalling pathway were identified as mechanisms leading to neuroprotection and the survival of dopaminergic cells. The neuroprotective effect of IGF-II against MPP + -neurotoxicity on dopaminergic neurons depends on the specific IGF-II receptor (IGF-IIr). In the mouse model, IGF-II prevents behavioural dysfunction and dopaminergic nigrostriatal pathway degeneration and mitigates neuroinflammation induced by MPP+. Our work demonstrates that hampering oxidative stress and normalising mitochondrial function through the interaction of IGF-II with its specific IGF-IIr are neuroprotective in both neuronal and mouse models. Thus, the modulation of the IGF-II/IGF-IIr signalling pathway may be a useful therapeutic approach for the prevention and treatment of PD

    La velocidad de ejecución como marcador de la salud metabólica en estudiantes universitarios

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    The aim of this research was to evaluate execution velocity (EV) as a marker of metabolic health in university students. During the year 2020 and the first semester of 2021, a descriptive and cross-sectional study was carried out on 57 students (45 men and 12 women) belonging to a higher education institution located in the city of Bogotá, Colombia. To measure VE, the T-Force System, Ergotech, was used during the development of a direct protocol to determine the value of one repetition maximum (1RM) in the squat and bench press exercise. To assess the metabolic profile, a blood sample was taken, which was deposited in the Cardiocheck equipment with which total cholesterol, triglycerides, high-density lipoproteins (HDL), low-density lipoproteins (LDL), and glucose levels. Participants who developed a lower average mean propulsive speed in all the series developed, both in the squat test and in the flat press exercise, presented a higher Metabolic Risk Score compared to those who had a better performance (p < .001).El objetivo de esta investigación fue evaluar la velocidad de ejecución como marcador de la salud metabólica en estudiantes universitarios. Durante el año 2020 y el primer semestre del 2021, se desarrolló un estudio descriptivo y transversal, en 57 estudiantes (45 hombres y 12 mujeres) pertenecientes a una institución de educación superior ubicada en la ciudad de Bogotá, Colombia. Para la medición de la velocidad de ejecución (VE) se utilizó el sistema T-Force System, Ergotech durante el desarrollo de un protocolo directo para determinar el valor de una repetición máxima(1RM) en los ejercicios de sentadilla completa libre y press banca. Para la valoración del perfil metabólico se realizó la toma de una muestra sanguínea la cual se depositó en el equipo Cardiocheck con el que se determinó el colesterol total, triglicéridos, lipopreteinas de alta densidad (HDL), lipoproteínas de baja densidad (LDL), y los niveles de glucosa. Los participantes que desarrollaron una velocidad media propulsiva promedio menor en la totalidad de las series desarrolladas, tanto en la prueba de sentadilla como en el ejercicio de press plano, presentaron un Score de riesgo metabólico más alto en comparación con los que tuvieron un mejor desempeño (p < .001).Actividad Física y Deport

    Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015

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    SummaryBackground The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. Methods We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors—the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). Findings Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6–58·8) of global deaths and 41·2% (39·8–42·8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa. Interpretation Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden. Funding Bill & Melinda Gates Foundation

    Getting it right when budgets are tight: Using optimal expansion pathways to prioritize responses to concentrated and mixed HIV epidemics

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    Published: October 3, 2017Background: Prioritizing investments across health interventions is complicated by the nonlinear relationship between intervention coverage and epidemiological outcomes. It can be difficult for countries to know which interventions to prioritize for greatest epidemiological impact, particularly when budgets are uncertain. Methods: We examined four case studies of HIV epidemics in diverse settings, each with different characteristics. These case studies were based on public data available for Belarus, Peru, Togo, and Myanmar. The Optima HIV model and software package was used to estimate the optimal distribution of resources across interventions associated with a range of budget envelopes. We constructed “investment staircases”, a useful tool for understanding investment priorities. These were used to estimate the best attainable cost-effectiveness of the response at each investment level. Findings: We find that when budgets are very limited, the optimal HIV response consists of a smaller number of ‘core’ interventions. As budgets increase, those core interventions should first be scaled up, and then new interventions introduced. We estimate that the cost-effectiveness of HIV programming decreases as investment levels increase, but that the overall cost-effectiveness remains below GDP per capita. Significance: It is important for HIV programming to respond effectively to the overall level of funding availability. The analytic tools presented here can help to guide program planners understand the most cost-effective HIV responses and plan for an uncertain future.Robyn M. Stuart, Cliff C. Kerr, Hassan Haghparast-Bidgoli, Janne Estill, Laura Grobicki, Zofia Baranczuk, Lorena Prieto, Vilma Montañez, Iyanoosh Reporter, Richard T. Gray, Jolene Skordis-Worrall, Olivia Keiser, Nejma Cheikh, Krittayawan Boonto, Sutayut Osornprasop, Fernando Lavadenz, Clemens J. Benedikt, Rowan Martin-Hughes, S. Azfar Hussain, Sherrie L. Kelly, David J. Kedziora, David P. Wilso

    Global monitoring of antimicrobial resistance based on metagenomics analyses of urban sewage

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    Antimicrobial resistance (AMR) is a serious threat to global public health, but obtaining representative data on AMR for healthy human populations is difficult. Here, we use meta-genomic analysis of untreated sewage to characterize the bacterial resistome from 79 sites in 60 countries. We find systematic differences in abundance and diversity of AMR genes between Europe/North-America/Oceania and Africa/Asia/South-America. Antimicrobial use data and bacterial taxonomy only explains a minor part of the AMR variation that we observe. We find no evidence for cross-selection between antimicrobial classes, or for effect of air travel between sites. However, AMR gene abundance strongly correlates with socio-economic, health and environmental factors, which we use to predict AMR gene abundances in all countries in the world. Our findings suggest that global AMR gene diversity and abundance vary by region, and that improving sanitation and health could potentially limit the global burden of AMR. We propose metagenomic analysis of sewage as an ethically acceptable and economically feasible approach for continuous global surveillance and prediction of AMR.Peer reviewe
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