Asignación de recursos en una micro-red social con sistemas fotovoltaicos basado en el control de carga

Este articulo analiza la implementación de un sistema fotovoltaico con respaldo de bancos de baterías, para la asignación de recursos empleando una optimización LP (Linear Programming). El estudio realizado se basa en una micro-red (MR) social con control de carga en lugares aislados, que permitirá abastecer la demanda de energía eléctrica de acuerdo a las necesidades de la comunidad. Para ello se plantea un despacho económico para cada estación del año. En verano se busca minimizar los costos con una mayor participación de los paneles, debido al alto índice de irradiancia que puede ser captado. En invierno la situación es totalmente adversa, por lo que el modelo asigna mayor cantidad de recursos de almacenamiento de energía, por la baja irradiancia. Para lograr tener continuidad de servicio eléctrico la MR despacha de manera prioritaria. Los usuarios de mayor prioridad como pistas de aterrizaje y escuelas, tendrán asegurado el servicio, mientras que hogares y otros servicios comunitarios no serán abastecidos en las horas de mayor consumo.This article analyzes the implementation of a photovoltaic system with the support of battery banks, for the allocation of resources using LP (Linear Programming) optimization. The study being carried out is based on a social micro-grid (MG) with load control in isolated places, which will allow it to supply the demand for electrical energy according to the needs of the community. For this, an economic dispatch is proposed for each season of the year. In summer, the aim is to minimize costs with a greater participation of the panels, due to the high index of irradiance that can be captured. In winter the situation is completely adverse, so the model allocates more energy storage resources due to low irradiance. To achieve continuity of electrical service, the MG dispatches as a priority. Higher priority users, such as airstrips and schools, will have guaranteed service, while homes and other community services will not be supplied during the hours of greatest consumption

Increasing Jaundice Secondary to an Acute Toxic Hepatitis Induced by Levofloxacin in a 20-year-old Man with a Fibrolamellar Hepatocarcinoma

Introduction: Levofloxacin-induced liver injury is rare and usually mild and transient. Presentations in the form of acute fulminant hepatitis are extremely uncommon.Presentation of the case: We report the case of a 20-year old man with a fibrolamellar hepatocellular carcinoma (fHCC), with affected retroperitoneal lymph nodes but no hepatic disease involvement. After receiving levofloxacin for the treatment of a community-acquired pneumonia, he developed hyperbilirrubinemia and abnormal liver function tests in the context of an acute cholestasic toxic hepatitis. In spite of optimal supportive treatment, that included admission in the Intensive Unit Care and extracorporeal albumin dialysis detoxification, the patient developed a rapidly progressive liver failure and died a month after the beginning of the process. The necropsy findings confirmed extensive drug-induced hepatic necrosis. No liver involvement by the fHCC was found in the autopsy.Conclusion: Rarer intercurrent conditions, such as drug-induced hepatotoxicity, should be taken into account in cancer patients with deranged liver function tests, even in those patients with advanced disease.

Microglial response differences between amyloidogenic transgenic models and Alzheimer’s disease patients

Aims: The continuing failure to develop an effective treatment for Alzheimer’s disease (AD) reveals the complexity for AD pathology. Increasing evidence indicates that neuroinflammation involving particularly microglial cells contributes to disease pathogenesis. Here we analyze the differences in the microglial response between APP/PS1 model and human brains. Methods: RT-PCR, western blots, and immunostaining were performed in the hippocampus of human post mortem samples (from Braak II to Braak V-VI) and APP751SL/PS1M146L mice. In vitro studies to check the effect of S1 fractions on microglial cells were assayed. Results: In APP based models the high Abeta accumulation triggers a prominent microglial response. On the contrary, the microglial response detected in human samples is, at least, partial or really mild. This patent difference could simple reflect the lower and probably slower Abeta production observed in human hippocampal samples, in comparison with models or could reflect the consequence of a chronic long-standing microglial activation. However, beside this differential response, we also observed a prominent microglial degenerative process in Braak V-VI samples 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 of the hippocampal formation, might be mediated by the accumulation of toxic soluble phospho-tau species. Conclusions: These differences need to be considered when delineating animal models that better integrate the complexity of AD pathology and, therefore, guarantee clinical translation. Correcting dysregulated brain inflammatory responses might be a promising avenue to restore cognitive function. Supported by grants FIS PI15/00796 and FIS PI15/00957 co-financed by FEDER funds from European Union, and by Junta de Andalucia Proyecto de Excelencia CTS385 2035.Financiado por FIS PI15/00796 y FIS PI15/0095, cofinanciado por los fondos FEDER de la Unión Europea, y por Junta de Andalucia Proyecto de Excelencia CTS385 2035. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

Caracterización Avanzada de Tanques de Fermentación de Café mediante una Red Multidistribuida de Sensores RFID

La fermentación de las bayas de café se considera una et apa crítica en el procesado del café debido a su impacto en la calidad final del producto. La temperatura es una de las principales variables de control que puede ser utilizada para predecir el final del proceso, teniendo en cuenta que varios autores indican que el control de esta etapa es fundamental para evitar la mala calidad de la be bida final. En la práctica, la fermentación es el paso \ud menos controlado del proceso, haciendo que los beneficiaderos operen lejos de sus condiciones óptimas en términos de costes de operación (es decir, elevados consumos de energía y agua) y de calidad del producto final. El objetivo de este trabajo es caracterizar los gradientes de temperatura que se dan en los tanques de fermentación mediante una red multi-distribuida de sensores autónomos, inalámbricos y de bajo coste (registradores de temperatura del tipo RFID, identificadores de radiofrecuencia semipasivos modelo TurboTag®).Para ello se utilizan dos metodologías: la interpolación espacial en coordenadas polares y los diagramas de espacio de fase. Se supervisaron dos fermentaciones reales de café, en El Cauca (Colombia), mediante sensores sumergidos directamente en la masa en fermentación. Los fermentadores eran tanques de plástico cubiertos, uno de ellos colocado en el interior de un almacén, permaneciendo el otro a la intemperie. El rango de variación máximo de temperatura en los tanques fue de 4,5ºC. La interpolación espacial mostró, incluso en el fermentador bajo las condiciones menos desfavorables en el interior del almacén, un gradiente radial de temperatura instantáneo de 0,1 °C/cm desde el centro hasta el perímetro del tanque y un gradiente vertical de temperatura de 0,25 °C/cm para sensores con coordenadas polares iguales. La combinación de ambas metodologías permitió la identificación consistente de los puntos calientes y fríos de ambas fermentaciones

Understanding microglial responses in the frontal cortex of alzheimer´s disease patients

Microglial cells, the immune cells of the brain, and the neuroinflammatory process associated, have been postulated as a critical factor in AD pathogenesis, since the identification of genetic risk factors related to microglial function. However, the microglial role in the development/progression of AD has not been determined yet. In this sense, we have previously reported a limited activation and microglial degeneration in the hippocampus of AD patients in contrast to the proinflammatory view based on findings in amyloidogenic models. Here, we have further analyzed the functional/phenotypic profile displayed by microglial cells in other vulnerable brain region of AD patients, the frontal cortex. Immunohistochemistry and image analysis approaches were performed in the frontal cortex of post mortem samples from controls (Braak 0-II) and AD patients (Braak V-VI) including familial cases. Microglia of Braak V-VI individuals were observed forming clusters and showed, both plaque (Iba1+/TMEM119+/P2ry12-/CD45high/Trem2+) and inter-plaque (Iba1+/ TMEM119+/P2ry12-/CD45high/Trem2-) microglial activation, similar that observed in amyloidogenic mice. By contrast, homeostatic and ramified microglial cells of non-demented Braak II cases presented Iba1+/P2ry12+/TMEM119+/CD45low/Trem2- profile. Furthermore, different microglial responses were observed between sporadic and familial AD cases. These different microglial phenotypes associated with AD pathology show the heterogeneity and complexity of the microglial phenotypes and suggest different functional states of these glial cells in a region-specific manner. These data need to be considered for better understand the immunological mechanisms underlying AD progression. Modulating brain inflammatory responses might be a promising avenue to prevent cognitive dysfunction in AD patients. ISCiii:PI18/01557(AG)-PI18/01556(JV);Junta Andalucia:UMA18-FEDERJA211(AG). All cofinanced by FEDER funds (European-Union).Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

Analyzing hippocampal synaptic damage and glial response in a mouse model of tauopathy

Tau pathology is highly related to synaptic and neuronal loss, leading to cognitive decline and dementia in Alzheimer’s disease (AD) and other tauopathies. Tau transgenic mice are widely used to investigate the specific contribution of this protein to AD since they reproduce the synaptic and cognitive dysfunction in parallel to an age-dependent accumulation of hyperphosphorylated forms of tau (phospho-tau). The aim of this study was to investigate the progression of tau aggregation and analyze its relationship with microglial activation and synaptic damage within the hippocampus of a transgenic tau model. 2, 6, 9, 12 and 18 month-old THY-Tau22 transgenic and WT mice were analyzed. Tau pathology was assessed by western blotting and immunohistochemistry (AT8, AT100). Confocal microscopy was used to study microglial/phospho-tau relationship, and Thioflavin-S staining to evidence fibrillar aggregates. Levels of general (Synaptophysin) and subtype-specific (ChAT, VGAT, VGLUT-1) synaptic proteins were determined by WB and immunohistochemistry. Inflammatory markers were assessed by quantitative PCR (CD45, CD68, TREM2), immunohistochemistry (Iba-1) and image analysis. Tau pathology was detectable in the hippocampus from 2 months of age and increased progressively during aging. Presynaptic protein levels were significantly decreased from 9-12 months compared to age-matched WT mice. Even though some inflammatory markers were slightly increased in the hippocampus, microglial reactivity was found to be generally attenuated and some cells even exhibited reduction in their prolongations and a clear degenerative phenotype at advanced ages similar to that seen in the hippocampus of AD patients. Finally, this model could be a relevant tool to further understand the specific role of tau in both microglial response and synaptic pathology in AD.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

Disentangling the contribution of tau and abeta pathologies in transgenic models of Alzheimer's disease

AIMS: Amyloid-beta (Abeta) deposits and intraneuronal hyperphosphorylated tau are major pathological hallmarks of Alzheimer’s disease (AD). The coexistence of these aggregates in AD brains leads to synaptic dysfunction, neuronal loss and cognitive decline. Failures in protein homeostasis, along with defective glial responses, have been identified as pathological mechanisms linked to this disorder. Thus, our main objective is to better understand the differential impact of Abeta- and tau-aggregates to these processes in the hippocampus of AD models. METHODS: We analyzed APP- (APPSL/PS1M146L) and Tau- (ThyTau22 and hP301S) based models from 2 to 18 months of age. Tau and Abeta pathologies were assessed by western blotting and immunohistochemistry. Confocal microscopy was used to study microglia/aggregates relationship. Levels of synaptic proteins, autophagy and inflammatory markers were determined by quantitative PCR, WB and immunohistochemistry. RESULTS: Tau and Abeta pathologies initiated as early as 2 months of age and increased progressively with aging. Even though only APP/PS1 hippocampus showed dystrophic neurites positive to proteostatic and presynaptic markers, their protein levels were altered in both types of models from 6-9 months compared to age-matched WT mice. Inflammatory markers and microglial reactivity were barely increased in the hippocampus of ThyTau mice in contrast to P301S and APP/PS1 mice which displayed a prominent microglial response. CONCLUSIONS: Clarifying the effects of Abeta and tau separately would indeed enable the development of novel therapeutic strategies and drugs targeting pathways related to these proteinopathies. Supported by grants FIS PI15/00796 and PI15/00957 co-financed by FEDER funds from European Union, by Junta de Andalucia Proyecto de Excelencia CTS385 2035 and by grant PPIT.UMA.B1/2017.26Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tec