Suchergebnisse

Colombian musician and activist César López has comforted victims of the Colombian civil war throughout his career. His songs, albums, and artistic-social projects memorialize painful recent-history events and human rights violations. In 2003, López created the escopetarra, a musical instrument that combines a rifle and a guitar. Thereafter, López has been a UN messenger of non-violence. I consider that his compositions are not only sonic memorials but are also musical gifts and, thus, technologies of care. Moreover, as Lopez's works challenges the logics of heteronormative masculinity, I analyze this case through the feminist and gender studies lenses. I support these claims with data gathered through netnography of several online-concerts and talks, interviews with López, reading journalistic sources, and observing Lopez's interventions' online records. I propose that López's musical gifts operate homologously to memorializations as both share the categorization of technologies of care. Finally, I conclude that Lopez's activism promotes the democratization of care as he destabilizes the exclusive association of care to the feminine and proposes new masculinities. ; La carrera artística del músico bogotano César López ha estado dedicada al acompañamiento y memorialización de las víctimas del conflicto armado colombiano. Sus composiciones y canciones conmemoran eventos de violación de derechos humanos en el país y reconocen a las víctimas. En 2003, López creó la escopetarra, un instrumento musical que combina un fusil y una guitarra. Todo esto lo llevó a convertirse en "mensajero de la no violencia" de las Naciones Unidas. Este ensayo propone conceptualizar la música de López y su escopetarra como regalos musicales y, en consecuencia, como tecnologías del cuidado. Además, ya que la obra de López refuta la lógica de la masculinidad heteronormativa, es necesario apoyarse también en la crítica feminista y la perspectiva de género para analizar la materialización del cuidado. A través de una etnografía virtual, la ...

La implantación de prácticas de Responsabilidad Social Corporativa (RSC) en las empresas es un tema relevante en los últimos años. Entre las cuestiones analizadas destaca la importancia de correlacionar la RSC con el comportamiento de los clientes por la influencia que puede tener en los beneficios de las empresas. Si bien diferentes investigaciones han estudiado esta relación previamente, son pocos los trabajos que han tratado la influencia de la RSC percibida en la actitud del consumidor en el sector de la distribución comercial minorista de España y menos aún en un contexto de crisis económica. En esta investigación se analiza la relación entre la RSC percibida y la actitud del consumidor de los tres grupos empresariales del sector minorista con mayor facturación en España: la empresa familiar Mercadona y las enseñas Carrefour y Eroski. Los resultados corroboran que las acciones de RSC influyen de manera directa y positiva en la actitud del consumidor, por lo que la investigación contribuye a consolidar el conocimiento de la relación entre estas dos variables y orienta a los gestores hacia la implantación de políticas de RSC para mejorar sus resultados.

Objetivo: inferir los activos financieros del mercado colombiano que pueden ser cubiertos mediante posiciones con bitcoin, determinando el vínculo frente a dicha criptomoneda, así como contribuir al entendimiento de las criptodivisas (en este caso en particular, al bitcoin), en pro de su uso y aplicabilidad como vehículo de inversión.
Diseño/metodología: este estudio usó un modelo de correlación condicional dinámico (DCC), el cual tiene capacidad para recoger las relaciones dinámicas y la variabilidad de las series en el tiempo cuando son volátiles y brinda la flexibilidad propia univariante del modelo autorregresivo generalizado condicional heterocedástico (GARCH), que permite encontrar momentos donde la volatilidad tienda a un equilibro que proporcione coeficientes, el cual, al evaluar pares de variables, favorece la diferenciación e interpretación entre diversificación, refugio seguro y cobertura financiera.
Resultados: los hallazgos evidenciaron que los coeficientes proporcionados por el modelo permiten concretar las propiedades del bitcoin como mecanismo de cobertura de riesgo frente a algunos instrumentos de renta fija y variable del mercado nacional, así como la inhabilidad de su uso como refugio seguro para todos los activos estudiados, por lo que contribuye para que los inversionistas cuenten con más bases para la toma de decisiones.
Conclusiones: esta investigación soporta que el bitcoin es apto para ser utilizado como un innovador producto de inversión en la economía nacional, dado que posee características que lo convierten en activo financiero, con enfoque hacia la construcción de portafolios y generación de coberturas frente a riesgos financieros.
Originalidad: a través de la aplicación del modelo econométrico y el análisis de sus salidas, surge la necesidad de comenzar a difundir educación en activos digitales, debido a que en el largo plazo desarrollan solidez y rentabilidad, lo que genera la oportunidad de lograr beneficios bajo un adecuado nivel de riesgo, siendo materia de interés para inversionistas.

Microglial activation has been considered a crucial player in the pathological process of multiple human neurodegenerative diseases. In some of these pathologies, such as Amyotrophic Lateral Sclerosis or Multiple Sclerosis, the immune system and microglial cells (as part of the cerebral immunity) play a central role. In other degenerative processes, such as Alzheimer's disease (AD), the role of microglia is far to be elucidated. In this "mini-review" article, we briefly highlight our recent data comparing the microglial response between amyloidogenic transgenic models, such as APP/PS1 and AD patients. Since the AD pathology could display regional heterogeneity, we focus our work at the hippocampal formation. In APP based models a prominent microglial response is triggered around amyloid-beta (Aβ) plaques. These strongly activated microglial cells could drive the AD pathology and, in consequence, could be implicated in the neurodegenerative process observed in models. On the contrary, the microglial response in human samples is, at least, partial or attenuated. This patent difference could simply reflect the lower and probably slower Aβ production observed in human hippocampal samples, in comparison with models, or could reflect the consequence of a chronic long-standing microglial activation. Beside this differential response, we also observed microglial degeneration in Braak V–VI individuals that, indeed, could compromise their normal role of surveying the brain environment and respond to the damage. This microglial degeneration, particularly relevant at the dentate gyrus, might be mediated by the accumulation of toxic soluble phospho-tau species. The consequences of this probably deficient immunological protection, observed in AD patients, are unknown. ; This work was supported by Fondo de Investigación Sanitaria (FIS) from the Instituto de Salud Carlos III (ISCiii) of Spain, co-financed by FEDER funds from European Union, through grants PI15/00957 (to JV) and PI15/00796 (to AG), CIBERNED (to AG and JV), and by Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucia Proyecto de Excelencia (CTS-2035) (to JV and AG). ; Peer reviewed

Background: Executive functions and attention play a key role to achieve academic goals in scholars. However, research have shown multiple social factors that might impact educational outcomes in typically developed children. Colombia faces one major issue in its border with Venezuela due to historical, social, cultural and economic conditions that have contributed to low quality of education - among others problems. This situation is far worse in rural areas where government assistance programs are limited, and teaching methodologies vary considerably. The aim of this study was to explore children's performances in attention and executive functions tasks according to teaching methodology used in urban (regular) and rural (multigrade) areas in the northeast of Colombia and close to the border with Venezuela. Methods: data were collected in two types of settings: 26 children from one local school (in Cucuta- Norte de Santander) and 29 children from three rural schools. All of them were 6 years old and enrolled in the first grade of primary school. Participants were tested using attentional (visual and auditory) and executive function tasks (planning, inhibitory control, and working memory). Results: lower performance was found in visual attention tasks for both groups in comparison with the reference group (children from other regions in Colombia). Moreover, there was a significant difference between the two conditions according to the teaching methodology: children from multigrade methodologies showed better performance in inhibitory control tasks, meanwhile children from regular methodologies showed better results in planning and attentional tasks. Conclusions: this study has identified differences in executive functions and attention of children depending on social contexts (urban-rural) and teaching methodologies. Findings are discussed in order to highlight social variables such as physical environment, limited cognitive stimulation, parenting, and some habits that impact Latin American contexts and have a strong relationship with children's scholar outcomes. ; Introducción: La frontera colombo-venezolana enfrenta dinámicas sociales particulares que han contribuido en los bajos indicadores de calidad educativa, presente también en contextos rurales donde problemas como la migración y la violencia, dificultan la calidad y cobertura. Este estudio tuvo como objetivo analizar las diferencias en el desarrollo de habilidades de atención y funciones ejecutivas según el contexto (urbano -rural) y la metodología escolar recibida (urbana regular y rural multigrado). Métodos: Se empleó un diseño no experimental, de alcance comparativo y corte transversal, evaluando una muestra intencional de 55 niños emparejados por edad, sin dificultades académicas y matriculados en diferentes instituciones de Norte de Santander- Colombia, en zona de frontera con Venezuela. Los estudiantes fueron evaluados con tareas neuropsicológicas de atención visual, planificación, inhibición y memoria de trabajo de la Evaluación neuropsicológica Infantil (ENI y Neuro psi). Los resultados fueron analizados mediante estadística no-paramétrica dadas las características de los datos recolectados. Resultados: Se encontraron desempeños inferiores en tareas de atencional visual en los participantes de ambas metodologías en comparación con el grupo de referencia. Así mismo, se encontraron diferencias según el tipo de metodología escolar recibida, siendo destacados en control inhibitorio los participantes de metodología multigrado, mientras que los niños escolarizados en metodología regular mostraron mejores resultados en capacidad de atención visual, atención auditiva y planeación. Conclusiones: Se encontraron diferencias en funciones ejecutivas de control inhibitorio, atención y planeación de acuerdo con el contexto escolar urbano-rural. Los hallazgos se discuten con el fin de argumentar la importancia de variables intervinientes asociadas a contextos rurales latinoamericanos, donde se destaca el entorno físico, la limitada estimulación cognitiva, prácticas particulares de crianza y cuidado y algunos hábitos que han mostrado una relación con el desempeño cognitivo.

Microglial cells are crucial players in the pathological process of neurodegenerative diseases, such as Alzheimer's disease (AD). Microglial response in AD has been principally studied in relation to amyloid-beta pathology but, comparatively, little is known about inflammatory processes associated to tau pathology. In the hippocampus of AD patients, where tau pathology is more prominent than amyloid-beta pathology, a microglial degenerative process has been reported. In this work, we have directly compared the microglial response in two different transgenic tau mouse models: ThyTau22 and P301S. Surprisingly, these two models showed important differences in the microglial profile and tau pathology. Where ThyTau22 hippocampus manifested mild microglial activation, P301S mice exhibited a strong microglial response in parallel with high phospho-tau accumulation. This differential phospho-tau expression could account for the different microglial response in these two tau strains. However, soluble (S1) fractions from ThyTau22 hippocampus presented relatively high content of soluble phospho-tau (AT8-positive) and were highly toxic for microglial cells in vitro, whereas the correspondent S1 fractions from P301S mice displayed low soluble phospho-tau levels and were not toxic for microglial cells. Therefore, not only the expression levels but the aggregation of phospho-tau should differ between both models. In fact, most of tau forms in the P301S mice were aggregated and, in consequence, forming insoluble tau species. We conclude that different factors as tau mutations, accumulation, phosphorylation, and/or aggregation could account for the distinct microglial responses observed in these two tau models. For this reason, deciphering the molecular nature of toxic tau species for microglial cells might be a promising therapeutic approach in order to restore the deficient immunological protection observed in AD hippocampus. ; This work was supported by Fondo de Investigacion Sanitaria (FIS) from the Instituto de Salud Carlos III (ISCiii) of Spain, co-financed by FEDER funds from European Union, through grants PI15/00957 (to JV) and PI15/00796 (to AG), CIBERNED (to AG and JV), and by Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucia Proyecto de Excelencia (CTS-2035) (to JV and AG). CR-M was supported by Fundación Tatiana Pérez de Guzmán el Bueno and a FPU fellowship from the Spanish Ministry of Science, Innovation and Universities. JF-V, MS-M, and CM-C were supported by FPU fellowships from the Spanish Ministry of Science, Innovation and Universities. ; Peer reviewed

Alzheimer's disease is a major neurodegenerative disorder that leads to severe cognitive deficits in the elderly population. Over the past two decades, multiple studies have focused on elucidating the causative factors underlying memory defects in Alzheimer's patients. In this regard, new evidence linking Alzheimer's disease-related pathology and neuronal stem cells suggests that hippocampal neurogenesis impairment is an important factor underlying these cognitive deficits. However, because of conflicting results, the impact of Aβ pathology on neurogenesis/gliogenesis remains unclear. Here, we investigated the effect of Aβ on neuronal and glial proliferation by using an APP/PS1 transgenic model and in vitro assays. Specifically, we showed that neurogenesis is affected early in the APP/PS1 hippocampus, as evidenced by a significant decrease in the proliferative activity due to a reduced number of both radial glia-like neural stem cells (type-1 cells) and intermediate progenitor cells (type-2 cells). Moreover, we demonstrated that soluble Aβ from APP/PS1 mice impairs neuronal cell proliferation using neurosphere cultures. On the other hand, we showed that oligomeric Aβ stimulates microglial proliferation, whereas no effect was observed on astrocytes. These findings indicate that Aβ has a differential effect on hippocampal proliferative cells by inhibiting neuronal proliferation and triggering the formation of microglial cells. ; This study was supported by Institute of Health Carlos III (ISCiii, Spain) through grants PI12/01431, PI15/00796 (to AG) and PI12/01439, PI15/00957 (to JV) that were co-financed by FEDER funds from European Union, by Junta de Andalucia Proyecto de Excelencia CTS-2035 (to JV and AG), Alzheimer's Association NIRG-15-363477 (to DBV) and The Larry Hillblom Foundation #2013-A-016-FEL (to DBV). ; Peer reviewed

Reactive astrocytes and dystrophic neurites, most aberrant presynaptic elements, are found surrounding amyloid‐β plaques in Alzheimer's disease (AD). We have previously shown that reactive astrocytes enwrap, phagocytose, and degrade dystrophic synapses in the hippocampus of APP mice and AD patients, but affecting less than 7% of dystrophic neurites, suggesting reduced phagocytic capacity of astrocytes in AD. Here, we aimed to gain insight into the underlying mechanisms by analyzing the capacity of primary astrocyte cultures to phagocytose and degrade isolated synapses (synaptoneurosomes, SNs) from APP (containing dystrophic synapses and amyloid‐β peptides), Tau (containing AT8‐ and AT100‐positive phosphorylated Tau) and WT (controls) mice. We found highly reduced phagocytic and degradative capacity of SNs‐APP, but not AT8/AT100‐positive SNs‐Tau, as compared with SNs‐WT. The reduced astrocyte phagocytic capacity was verified in hippocampus from 12‐month‐old APP mice, since only 1.60 ± 3.81% of peri‐plaque astrocytes presented phagocytic structures. This low phagocytic capacity did not depend on microglia‐mediated astrocyte reactivity, because removal of microglia from the primary astrocyte cultures abrogated the expression of microglia‐dependent genes in astrocytes, but did not affect the phagocytic impairment induced by oligomeric amyloid‐β alone. Taken together, our data suggest that amyloid‐β, but not hyperphosphorylated Tau, directly impairs the capacity of astrocytes to clear the pathological accumulation of oligomeric amyloid‐β, as well as of peri‐plaque dystrophic synapses containing amyloid‐β, perhaps by reducing the expression of phagocytosis receptors such as Mertk and Megf10, thus increasing neuronal damage in AD. Therefore, the potentiation or recovery of astrocytic phagocytosis may be a novel therapeutic avenue in AD. ; Research funding: Centro de Invesitgacion Biomedica en Red Enfermedades Neurodegenetativas (CIBERNED). Grant Numbers: CB06/05/0094, CB06/05/1116; Instituto de Salud Carlos III co‐financed by FEDER funds from European Union. Grant Numbers: PI18/01556, PI18/01557; Junta de Andalucia Consejería de Economía y Conocimiento co‐financed by Programa Operativo FEDER 2014‐2020. Grant Numbers: PY18‐RT‐2233, UMA18‐FEDERJA‐211, US‐1262734; La Marató‐TV3 Foundation. Grant Numbers: 20141430, 20141431, 20141432.

In Alzheimer's disease (AD), and other tauopathies, microtubule destabilization compromises axonal and synaptic integrity contributing to neurodegeneration. These diseases are characterized by the intracellular accumulation of hyperphosphorylated tau leading to neurofibrillary pathology. AD brains also accumulate amyloid-beta (Aβ) deposits. However, the effect of microtubule stabilizing agents on Aβ pathology has not been assessed so far. Here we have evaluated the impact of the brain-penetrant microtubule-stabilizing agent Epothilone D (EpoD) in an amyloidogenic model of AD. Three-month-old APP/PS1 mice, before the pathology onset, were weekly injected with EpoD for 3 months. Treated mice showed significant decrease in the phospho-tau levels and, more interesting, in the intracellular and extracellular hippocampal Aβ accumulation, including the soluble oligomeric forms. Moreover, a significant cognitive improvement and amelioration of the synaptic and neuritic pathology was found. Remarkably, EpoD exerted a neuroprotective effect on SOM-interneurons, a highly AD-vulnerable GABAergic subpopulation. Therefore, our results suggested that EpoD improved microtubule dynamics and axonal transport in an AD-like context, reducing tau and Aβ levels and promoting neuronal and cognitive protection. These results underline the existence of a crosstalk between cytoskeleton pathology and the two major AD protein lesions. Therefore, microtubule stabilizers could be considered therapeutic agents to slow the progression of both tau and Aβ pathology. ; This study was supported by Instituto de Salud Carlos III (ISCiii) of Spain, co-financed by FEDER funds from European Union, through grants PI15/00796 and PI18/01557 (both to AG), PI15/00957 and PI18/01556 (both to JV), and CIBERNED (CB06/05/1116 to AG and CB06/05/0094 to JV); by Malaga University grant PPIT.UMA.B1.2017/26 (to RSV). JJFV and CMC were supported by FPU PhD fellowships (Spanish Ministry of Science, Innovation and Universities). RSV held a postdoctoral contract from Malaga University. IMG is recipient of a senior postdoctoral contract from Ramon y Cajal Program (Spain Government).

Alzheimer's disease (AD) is a progressive neurodegenerative disease in which the formation of extracellular aggregates of amyloid beta (Aβ) peptide, fibrillary tangles of intraneuronal tau and microglial activation are major pathological hallmarks. One of the key molecules involved in microglial activation is galectin-3 (gal3), and we demonstrate here for the first time a key role of gal3 in AD pathology. Gal3 was highly upregulated in the brains of AD patients and 5xFAD (familial Alzheimer's disease) mice and found specifically expressed in microglia associated with Aβ plaques. Single-nucleotide polymorphisms in the LGALS3 gene, which encodes gal3, were associated with an increased risk of AD. Gal3 deletion in 5xFAD mice attenuated microglia-associated immune responses, particularly those associated with TLR and TREM2/DAP12 signaling. In vitro data revealed that gal3 was required to fully activate microglia in response to fibrillar Aβ. Gal3 deletion decreased the Aβ burden in 5xFAD mice and improved cognitive behavior. Interestingly, a single intrahippocampal injection of gal3 along with Aβ monomers in WT mice was sufficient to induce the formation of long-lasting (2 months) insoluble Aβ aggregates, which were absent when gal3 was lacking. High-resolution microscopy (stochastic optical reconstruction microscopy) demonstrated close colocalization of gal3 and TREM2 in microglial processes, and a direct interaction was shown by a fluorescence anisotropy assay involving the gal3 carbohydrate recognition domain. Furthermore, gal3 was shown to stimulate TREM2–DAP12 signaling in a reporter cell line. Overall, our data support the view that gal3 inhibition may be a potential pharmacological approach to counteract AD. ; This work was supported by Grants from the Swedish Research Council, and the Strong Research Environment MultiPark (Multidisciplinary Research in Parkinson's and Alzheimer's Disease at Lund University), Bagadilico (Linné consortium sponsored by the Swedish Research Council), the Swedish Alzheimer's Foundation, Swedish Brain Foundation, A.E. Berger Foundation, Gyllenstiernska Krapperup Foundation, the Royal Physiographic Society, Crafoord Foundation, Olle Engkvist Byggmästare Foundation, Wiberg Foundation, G&J Kock Foundation, Stohnes Foundation, Swedish Dementia Association and the Medical Faculty at Lund University. This work was supported by Grant SAF2015-64171R (Spanish MINECO/FEDER, UE), by Instituto de Salud Carlos III (ISCiii) of Spain, co-financed by FEDER funds from European Union through grants PI15/00796 and PI18/01557 (to AG), PI15/00957 and PI18/01556 (to JV), and CIBERNED (to AG and JV), by Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucia Proyecto de Excelencia (CTS-2035) (to JV and AG), and by Malaga University grant PPIT.UMA.B1.2017/26 (to RSV). AV and GCB received funding from the Innovative Medicines Initiative 2 Joint Undertaking under Grant agreement no. 115976 (PHAGO). CIBERNED "Centro de Investigacion Biomedica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid (Spain)". HL and AF were supported by the Swedish Research Council, the Swedish Brain Foundation, the Alzheimer Foundation and the Åhlén Foundation. UJN was supported by Grants from the Knut and Alice Wallenberg Foundation (KAW 2013.0022) and the Swedish Research Council (Grant no. 621-2012-2978). ; Peer reviewed