Madurez ciudadana. Requisito para la consolidación de una democracia ética

La ciudadanía, decían los filósofos griegos, es la condición por la que el hombre puede, en lugar de limitarse a vivir, aspirar a una vida buena. La teoría política enseña que los ciudadanos son importantes sencillamente porque son la esencia y existencia de todo Estado. Sin ciudadanos no hay Estado. ¿Cuál es la situación del ciudadano en la actualidad? ¿Cuál es su nivel de participación y compromiso con los fines del Estado? Ser ciudadano supone desarrollar el sentido de identidad y pertenencia en el lugar en el que se interactúa socialmente; implica desenvolverse con responsabilidad, lo cual nos conduce al meollo de la ciudadanía: la participación política. La participación ciudadana en política se asocia estrechamente al concepto de democracia, la cual se caracteriza por la necesidad de conciliar las exigencias de la participación con la gobernabilidad. Pero para lograr una actitud de compromiso y participación se requiere de una ciudadanía madura. En la antigüedad se decía que el “ciudadano virtuoso” era aquel ciudadano libre y bien formado, con capacidad crítica, que actuaba con ética y responsabilidad, participando en la decisión sobre los derroteros de su comunidad. Para volver a ese ciudadano virtuoso, libre y activo, que se evocaba en la antigüedad, es necesario desenmarañar el entramado actual y salir del laberinto creado por la sociedad de consumo. Indudablemente, es fundamental que cada individuo encuentre o recupere su libertad. Quienes participamos en la obra Madurez ciudadana y gobernanza para la consolidación de una democracia ética invitamos a la ciudadanía a caminar en ese sentido

SSolution of series-parallel photovoltaic generator model using optimization algorithms Trust Region Dogleg and PSO

El modelo matemático de un generador fotovoltaico en conexión Serie-Paralelo representado mediante el modelo de diodo simple, tiene asociado a él un sistema de ecuaciones no lineales. En este trabajo se propone la solución de estos sistemas empleando los métodos de optimización Trust Region Dogleg y Optimización por Enjambre de Partículas, para resolver el modelo de un generador fotovoltaico operando en condiciones homogéneas y no homogéneas, variando el número de submódulos y el patrón de sombreado que incide sobre el generador. Se realizó la simulación de los modelos para generadores compuestos por 3 y 15 submódulos en serie, bajo diferentes condiciones de sombreado. De los métodos implementados, Trust Region Dogleg mostró un mejor desempeño con tiempos de cómputo 2 y 14 veces menores que el método de referencia y Optimización por Enjambre de Partículas, respectivamente. Y un error medio cuadrático igual o un 50 % inferior a los otros métodos.Mathematical Model of a Series-Parallel (SP) photovoltaic (PV) generator represents each module through an equivalent electrical circuit denominated single diode model, this model has associated a nonlinear equation system that describes the electrical behavior of SP generator. This paper presents a solution of this system using optimization methods widely using: Trust Region Dogleg and Particle swarm optimization (PSO) for solving the electrical model of PV generator operating under homogeneous or non-homogeneous conditions, changing the number of submodules and shading pattern. It has been made simulations about generators composed by 3 and 15 series submodules, operating under different partial shading conditions. Between the implemented methods, Trust Region Dogleg show a better performance than other methods, with 2 and 14 times less computation time than the reference method and PSO, respectively, and a RMSE equal or 50 % lower than PSO. &nbsp

High plasticity of axonal pathology in Alzheimer's disease mouse models

Axonal dystrophies (AxDs) are swollen and tortuous neuronal processes that are associated with extracellular depositions of amyloid beta (Abeta) and have been observed to contribute to synaptic alterations occurring in Alzheimer's disease. Understanding the temporal course of this axonal pathology is of high relevance to comprehend the progression of the disease over time. We performed a long-term in vivo study (up to 210 days of two-photon imaging) with two transgenic mouse models (dE9xGFP-M and APP-PS1xGFP-M). Interestingly, AxDs were formed only in a quarter of GFP-expressing axons near Abeta-plaques, which indicates a selective vulnerability. AxDs, especially those reaching larger sizes, had long lifetimes and appeared as highly plastic structures with large variations in size and shape and axonal sprouting over time. In the case of the APP-PS1 mouse only, the formation of new long axonal segments in dystrophic axons (re-growth phenomenon) was observed. Moreover, new AxDs could appear at the same point of the axon where a previous AxD had been located before disappearance (re-formation phenomenon). In addition, we observed that most AxDs were formed and developed during the imaging period, and numerous AxDs had already disappeared by the end of this time. This work is the first in vivo study analyzing quantitatively the high plasticity of the axonal pathology around Abeta plaques. We hypothesized that a therapeutically early prevention of Abeta plaque formation or their growth might halt disease progression and promote functional axon regeneration and the recovery of neural circuits

High plasticity of axonal pathology in Alzheimer's disease mouse models

Axonal dystrophies (AxDs) are swollen and tortuous neuronal processes that are associated with extracellular depositions of amyloid beta (Abeta) and have been observed to contribute to synaptic alterations occurring in Alzheimer's disease. Understanding the temporal course of this axonal pathology is of high relevance to comprehend the progression of the disease over time. We performed a long-term in vivo study (up to 210 days of two-photon imaging) with two transgenic mouse models (dE9xGFP-M and APP-PS1xGFP-M). Interestingly, AxDs were formed only in a quarter of GFP-expressing axons near Abeta-plaques, which indicates a selective vulnerability. AxDs, especially those reaching larger sizes, had long lifetimes and appeared as highly plastic structures with large variations in size and shape and axonal sprouting over time. In the case of the APP-PS1 mouse only, the formation of new long axonal segments in dystrophic axons (re-growth phenomenon) was observed. Moreover, new AxDs could appear at the same point of the axon where a previous AxD had been located before disappearance (re-formation phenomenon). In addition, we observed that most AxDs were formed and developed during the imaging period, and numerous AxDs had already disappeared by the end of this time. This work is the first in vivo study analyzing quantitatively the high plasticity of the axonal pathology around Abeta plaques. We hypothesized that a therapeutically early prevention of Abeta plaque formation or their growth might halt disease progression and promote functional axon regeneration and the recovery of neural circuits

The Drinking Water, Sewerage, and Treatment Manual (MAPAS) As a New Support Tool for the Design of Urban Hydraulic Structures

Water industry companies need infrastructure capable of satisfying the hydraulic requirements for which they were designed. Moreover, in order to fulfill that objective, they should meet the structural requirements that assure an adequate lifespan and the capacity to withstand daily mechanical actions as well as the occurrence of earthquakes and/or gusts of wind. In Mexico there are local construction regulations that dictate the considerations that should be taken into account for a structural design, as well as diverse manuals that aid in this purpose, nonetheless, they commonly focus on the construction of conventional urban infrastructure. In the case of urban hydraulic works such as elevated tanks and treatment plants, which must be considered as priority structures of public interest, there isn't enough public information for their design and construction. For that reason, as part of the recent update of the Drinking Water, Sewerage, and Treatment Manual (MAPAS) the "Structural Design" book aids with the structural design of urban hydraulic works so as to standardize criteria for the design of buried, elevated and surface deposits, as well as support structures. Design and construction recommendations for these structures were also included based on the experience of the operators in charge of the distribution networks for drinking water, sewerage and water treatment. In the present article, the content and objectives of the book are broken down in a simplified form as well as their potential applications and usage. Interdisciplinary work in the design and construction of urban hydraulic infrastructure is also encouraged here

Transfusion related acute lung injury-TRALI: a review

Acute pulmonary damage caused by transfusion is characterized by the sudden onset of respiratory distress in newly transfused patients within 6 hours after the transfusion, bilateral infiltrative changes in chest X-ray, PaO2/FIO2 <300 mmHg, absence of other risk factors for acute lung injury and absence of signs suggesting cardiogenic origin of pulmonary edema. Being one of the most serious complications of blood transfusion, plasma is the most involved factor, although all blood components can cause it, and is caused by antigen reactions/leukocyte antibody and lipid activity with ability to modify the biological response on primitive leukocytes. The diagnosis is based on the integration of clinical, radiological and gasometric elements, ruling out the rest of the possible causes of acute lung injury. Its differential diagnosis should include hemodynamic overload, anaphylactic reaction, bacterial contamination of transfused blood products and transfusion hemolytic reaction. The treatment is supportive measures based on the needs and does not differ from the treatment of acute lung injury secondary to other etiologies, severe cases require endotracheal intubation and mechanical ventilation while the non-severe can be managed with oxygen therapy

High p16 expression and heterozygous RB1 loss are biomarkers for CDK4/6 inhibitor resistance in ER+ breast cancer

Breast cancer; Cancer models; Predictive markersCáncer de mama; Modelos de cáncer; Marcadores predictivosCàncer de pulmó; Models de càncer; Marcadors predictiusCDK4/6 inhibitors combined with endocrine therapy have demonstrated higher antitumor activity than endocrine therapy alone for the treatment of advanced estrogen receptor-positive breast cancer. Some of these tumors are de novo resistant to CDK4/6 inhibitors and others develop acquired resistance. Here, we show that p16 overexpression is associated with reduced antitumor activity of CDK4/6 inhibitors in patient-derived xenografts (n = 37) and estrogen receptor-positive breast cancer cell lines, as well as reduced response of early and advanced breast cancer patients to CDK4/6 inhibitors (n = 89). We also identified heterozygous RB1 loss as biomarker of acquired resistance and poor clinical outcome. Combination of the CDK4/6 inhibitor ribociclib with the PI3K inhibitor alpelisib showed antitumor activity in estrogen receptor-positive non-basal-like breast cancer patient-derived xenografts, independently of PIK3CA, ESR1 or RB1 mutation, also in drug de-escalation experiments or omitting endocrine therapy. Our results offer insights into predicting primary/acquired resistance to CDK4/6 inhibitors and post-progression therapeutic strategies

Role for Maternal Asthma in Severe Human Metapneumovirus Lung Disease Susceptibility in Children

Background: Severity of human metapneumovirus (hMPV) lower respiratory illness (LRTI) is considered similar to that observed for respiratory syncytial virus (RSV). However, differences in severity between these pathogens have been noted, suggesting the degree of illness may vary in different populations. Moreover, a potential association between hMPV and asthma also suggests that hMPV may preferentially affect asthmatic subjects. Methods: In a population-based surveillance study in children aged <2 years admitted for severe LRTI in Argentina, nasopharyngeal aspirates were tested by RT-PCR for hMPV, RSV, influenza A, and human rhinovirus. Results: Of 3947 children, 383 (10%) were infected with hMPV. The hospitalization rate for hMPV LRTI was 2.26 per 1000 children (95% confidence interval [CI], 2.04-2.49). Thirty-nine (10.2%) patients infected with hMPV experienced life-threatening disease (LTD; 0.23 per 1000 children; 95% CI,. 16-.31/1000), and 2 died (mortality rate 0.024 per 1000; 95% CI,. 003-.086). In hMPV-infected children birth to an asthmatic mother was an increased risk for LTD (odds ratio, 4.72; 95% CI, 1.39-16.01). We observed a specific interaction between maternal asthma and hMPV infection affecting risk for LTD. Conclusions: Maternal asthma increases the risk for LTD in children <2 years old hospitalized for severe hMPV LRTI.Fil: Libster, Romina Paula. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Esteban, Ignacio. Fundación para la Investigación en Infectología Infantil; Argentina. Gobierno de la Ciudad de Buenos Aires. Hospital de Pediatría "Juan P. Garrahan"; ArgentinaFil: Bianchi, Alejandra Silvina. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Alva Grimaldi, Luciano. Gobierno de la Provincia de Buenos Aires. Hospital Zonal General de Agudos Doctor Lucio Melendez.; ArgentinaFil: Dueñas, Karina. Gobierno de la Provincia de Buenos Aires. Hospital Interzonal de Agudos Evita.; ArgentinaFil: Sancillo, Andrea. Gobierno de la Provincia de Buenos Aires. Hospital Interzonal de Agudos Evita.; ArgentinaFil: Rodriguez, Andrea. Gobierno de la Provincia de Buenos Aires. Hospital Provincial Evita Pueblo.; ArgentinaFil: Ferrero, Fernando. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); ArgentinaFil: Stein, Katherine. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Acosta, Patricio Leandro. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Ferolla, Fausto Martín. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Bergel, Eduardo. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Caballero, Mauricio Tomás. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Polack, Fernando Pedro. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Pellegrino, Gustavo. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Fernandez Gago, Guadalupe. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Pozzolo, Cecilia. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Castro, Laura. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Almeida, Rodrigo Egues. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Rebec, Beatriz. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: González, Mariela. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Calvo, Mariel. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Henrichsen, Julieta. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Nocito, Celina. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Barbero, Guillermo. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Ves Losada, Juan. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Bonina, Angel. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Flamenco, Edgardo. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Rodriguez Perez, Alberto. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Kobylarz, Alicia. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Raggio, Mirta. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Schavlosky, Graciela. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Caria, Adriana. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Barboza, Edgar. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Sastre, Gustavo. Fundación para la Investigación en Infectología Infantil; Argentin