54 research outputs found

    Estimation of productivity change of NBA teams from 2006-07 to 2012-13 seasons

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    "... acknowledgements at FiT Publishing"The aim of this work is to evaluate the productivity change of the NBA teams during the last seven seasons (from 2006-07 to 2012-13). Within that period of time, a new collective bargaining agreement (CBA) of the National Basketball Association (NBA) was ratified before season 2011-12, ending a 161-day lockout. The Malmquist Productivity Index (MPI) has been used to measure the total factor productivity, while an input-oriented Network DEA approach is used to compute the distance of each observation to the corresponding frontier. The results reveal that there has been technological progress for the last few seasons, excluding that of the 2011 lockout, and an increasing efficiency change. This means that best practices are improving and that most teams have been reducing their payrolls to catch up with these practices, thus backing up the owners’ proposal to reduce players’ income. Also regression results show that changes in the number of wins are more dependent upon scale efficiency change than upon budget or efficiency changes

    A linear relational DEA model to evaluate two-stage processes with shared inputs

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    Two-stage data envelopment analysis (DEA) efficiency models identify the efficient frontier of a two-stage production process. In some two-stage processes, the inputs to the first stage are shared by the second stage, known as shared inputs. This paper proposes a new relational linear DEA model for dealing with measuring the efficiency score of two-stage processes with shared inputs under constant returns-to-scale assumption. Two case studies of banking industry and university operations are taken as two examples to illustrate the potential applications of the proposed approach

    Convergencia y gestión del cambio como factores clave de supervivencia para las empresas editoras de periódicos: ABC (2006)

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    Partiendo del marco teórico sobre diversos tipos de convergencia, el autor incide en la Convergencia Estructural. La CE está unida a los cambios que se producen con el uso de TIC para análisis de la información, edición, producción, distribución y comercialización del periódico. Dado que la CE introduce cambios en la organización redaccional y en prácticas de trabajo se propone un estudio sistémico desde la teoría de Análisis de procesos. Entendido todo proceso como cambio, el autor muestra que el paso a estructuras de CE supone la evolución, “desaprendizaje” o abandono de determinadas estructuras, procedimientos y comportamientos en el periódico

    Posverdad y sistema de medios desde los postulados de la Teoría General de Sistemas (TGS)

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    This work offers a review of the comparative analysis of media systems proposed by Hallin and Mancini (2004-2017). In line with one of the hypotheses proposed by these authors, the structuring idea of the work is established: Old and new media, digital content platforms and social networks, the disinformation industry and the big Internet players are constituted as the new order for the media system, that would discontinue the previous dominant liberal/commercial traditional model. An "open supra system" whose scope is the “meta medium” of the social network; hosted and influenced by global technology companies capable of interfering in the contemporary social system and facilitating the diffusion of a toxic atmosphere of post-truth as a result of postmodernism. To articulate the idea, we proceed to a free interpretation from the postulates of the General Systems Theory of Bertalanffy (1968). This work reveals systemic imbalances due to polarization, the phenomenon of disinformation, and glimpses a sophisticated manifestation of social control in which the social network merges with, subdues, and presumably, devours the social system with unpredictable consequences. This work proposes a graphic interpretation of the post-truth phenomenon as a "toxic atmosphere" from the perspective of the classical systemic studies, together with suggestions for improvement actions.Este trabajo ofrece una revisión del análisis comparado de sistemas de medios propuesto por Hallin y Mancini (2004-2017). En línea con una de las hipótesis propuestas por estos autores, se establece la idea vertebradora del trabajo: Los viejos y nuevos medios, las plataformas de contenido digital y redes sociales, la industria de la desinformación y las grandes tecnológicas se constituyen como el nuevo orden del sistema de medios que discontinuaría el modelo tradicional liberal/comercial dominante anterior. Un “suprasistema abierto” cuyo ámbito es el metamedio de la red social; hospedado e influenciado, por empresas tecnológicas globales capaces de interferir en el sistema social contemporáneo y que facilita la difusión de una atmósfera tóxica de posverdad como resultado del posmodernismo. Para articular la idea, se procede a una interpretación libre desde los postulados de la Teoría General de Sistemas de Bertalanffy (1968). Este trabajo desvela desequilibrios sistémicos por la polarización, el fenómeno de la desinformación y atisba una sofisticada manifestación de control social en el que la red social se funde con, somete y presumiblemente, devora al sistema social con consecuencias imprevisibles. Este trabajo propone una interpretación gráfica del fenómeno de la posverdad como “atmósfera tóxica” desde la perspectiva de la sistémica clásica junto a sugerencias de acciones de mejora

    Study of the genotype-phenotype correlation in fibroblasts of patients with mutations in COQ4

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    Motivation: Coenzyme Q10 (CoQ10), or ubiquinone, has a crucial role in the energetic metabolism due to its redox capacity in the electron transport chain (ETC), where it shuttles electrons from complex I or II to complex III. Lack of this essential component leads to mitochondrial disorders characterized by a rare condition with a huge spectrum of different phenotypes and different genetic mutations. To date, specific genotype-phenotype correlations do not exist because the link between specific genetic defects and phenotypes is unclear. In this way, the diagnosis and treatment of this patients is so complicated. The diagnosis on time is extremely important to start the treatment in order to avoid the fulminant course of the disease with an irreversible damage and a fatal outcome. In a previous study reported in our lab it was described that CoQ10-deficient fibroblasts (independently from the etiology) showed a common transcriptomic profile. The expression of certain genes was modified in the same way, that it to say, they were always increased or decreased. COQ4 is one of the genes involved in CoQ10 biosynthesis. It has been also demonstrated that COQ4 mutations are responsible for early-onset mitochondrial diseases with heterogeneous clinical presentations and associated with CoQ10 deficiency. The aim of this work is to find a possible correlation between different COQ4 mutations, the pathological phenotype, the clinical severity of the disease and the level of markers genes expression.Methods: To achieve this goal, we have used two fibroblast cell lines as control, and four mutant fibroblast cell lines from patients with different COQ4 mutations. We have performed different genetic and biochemical assays such as analysis of the expression profile by microarray, Seahorse or flow cytometry.Results: Fibroblasts from subjects with COQ4 mutations show similar profiles between them, and at the same time, they show a different profile when we compared them to control fibroblasts. In adittion, a more differentiated profile is observed according as the severity of the symptoms increases. Taken together, these results suggest a correlation between the phenotype and the clinical severity.Conclusions: Cells with COQ4 mutations look for an adaptative biological response to face the mithocondrial damage due to the CoQ10 deficiency. And interestingly, our results suggest an association between genothype and phenotype in these patients

    Evaluation of post-graduate programs using a network data envelopment analysis model

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    Despite standard Data Envelopment Analysis (DEA) models having been widely used in assessing efficiency in education, a few studies use Network DEA (NDEA) models in educational evaluation. In this paper, we proposed an alternative to the official evaluation performed every three years by CAPES (Brazilian agency for post-graduation programs regulation) using an NDEA model. The use of NDEA is justified because depending on the point of view, some variables can be considered either inputs or outputs. The use of NDEA avoids the need to decide whether a variable is an input or output of the entire process. This happens because a variable can be both an output for one stage and an input for another. Our relational NDEA model computes both productivity and quality assessments together with global efficiency using bibliometric data.A pesar de que los modelos estándar del Análisis Envolvente de Datos (DEA) han sido ampliamente utilizados en la evaluación de la eficiencia en educación, existen pocos estudios que utilizan modelos DEA en red (Network DEA – NDEA) en la evaluación educativa. En el presente trabajo, se ha propuesto una alternativa a la evaluación oficial realizada a cada tres años por la CAPES (agencia brasileña para la regulación de los programas de post-graduación) mediante un modelo DEA en red. El uso de NDEA se justifica ya que dependiendo del punto de vista algunas variables pueden ser consideradas como entradas o como salidas. El uso de NDEA evita la necesidad de decidir si una variable es una entrada o una salida de todo el proceso. Esto ocurre porque una variable puede ser tanto una salida para una etapa y una entrada para otro. Nuestro modelo relacional NDEA evalúa tanto la productividad como la calidad junto con la eficiencia global, a partir de datos bibliométricos

    Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients: implications in the pathogenesis of the disease

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    This is an open access article distributed under the terms of the Creative Commons Attribution License.[Introduction]: Fibromyalgia is a chronic pain syndrome with unknown etiology. Recent studies have shown some evidence demonstrating that oxidative stress may have a role in the pathophysiology of fibromyalgia. However, it is still not clear whether oxidative stress is the cause or the effect of the abnormalities documented in fibromyalgia. Furthermore, the role of mitochondria in the redox imbalance reported in fibromyalgia also is controversial. We undertook this study to investigate the role of mitochondrial dysfunction, oxidative stress, and mitophagy in fibromyalgia. [Methods]: We studied 20 patients (2 male, 18 female patients) from the database of the Sevillian Fibromyalgia Association and 10 healthy controls. We evaluated mitochondrial function in blood mononuclear cells from fibromyalgia patients measuring, coenzyme Q10 levels with high-performance liquid chromatography (HPLC), and mitochondrial membrane potential with flow cytometry. Oxidative stress was determined by measuring mitochondrial superoxide production with MitoSOX™ and lipid peroxidation in blood mononuclear cells and plasma from fibromyalgia patients. Autophagy activation was evaluated by quantifying the fluorescence intensity of LysoTracker™ Red staining of blood mononuclear cells. Mitophagy was confirmed by measuring citrate synthase activity and electron microscopy examination of blood mononuclear cells. [Results]: We found reduced levels of coenzyme Q10, decreased mitochondrial membrane potential, increased levels of mitochondrial superoxide in blood mononuclear cells, and increased levels of lipid peroxidation in both blood mononuclear cells and plasma from fibromyalgia patients. Mitochondrial dysfunction was also associated with increased expression of autophagic genes and the elimination of dysfunctional mitochondria with mitophagy. [Conclusions]: These findings may support the role of oxidative stress and mitophagy in the pathophysiology of fibromyalgia.This work was supported by grants FIS PI080500 and FIS EC08/00076, Ministerio de Sanidad, Spain. The authors dedicate this manuscript to FM patients and AFIBROSE (Asociación de Fibromialgia de Sevilla) for their unconditional help.Peer Reviewe

    An educational robotic approach for improvements of learning in technology courses / Uma abordagem de robótica educacional para melhoria da aprendizagem em cursos de tecnologia

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    The Rubik’s cube is one of the most popular puzzles in the world. It is estimated that one in seven people have already played with the cube. There are several ways to solve the cube problem and some people solve without a technique help, however, this is a laborious and tiring practice. The existing methods range from the simplest to the most complex, and it influences the time that will be spent in the solution. A robotic solution can implement one or more of these methods to solve the Rubik’s cube in an automatic way. Considering this, this work proposes a low-cost micro controlled system to solve Rubik’s cube. This prototype is intended to be used in classrooms for the teaching-learning process improvement, and consequently also improve the students’ performance in disciplines of logic and algorithms

    Mitochondrial Na+ controls oxidative phosphorylation and hypoxic redox signalling

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    All metazoans depend on O2 delivery and consumption by the mitochondrial oxidative phosphorylation (OXPHOS) system to produce energy. A decrease in O2 availability (hypoxia) leads to profound metabolic rewiring. In addition, OXPHOS uses O2 to produce reactive oxygen species (ROS) that can drive cell adaptations through redox signalling, but also trigger cell damage1–4, and both phenomena occur in hypoxia4–8. However, the precise mechanism by which acute hypoxia triggers mitochondrial ROS production is still unknown. Ca2+ is one of the best known examples of an ion acting as a second messenger9, yet the role ascribed to Na+ is to serve as a mere mediator of membrane potential and collaborating in ion transport10. Here we show that Na+ acts as a second messenger regulating OXPHOS function and ROS production by modulating fluidity of the inner mitochondrial membrane (IMM). We found that a conformational shift in mitochondrial complex I during acute hypoxia11 drives the acidification of the matrix and solubilization of calcium phosphate precipitates. The concomitant increase in matrix free-Ca2+ activates the mitochondrial Na+/Ca2+ exchanger (NCLX), which imports Na+ into the matrix. Na+ interacts with phospholipids reducing IMM fluidity and mobility of free ubiquinone between complex II and complex III, but not inside supercomplexes. As a consequence, superoxide is produced at complex III, generating a redox signal. Inhibition of mitochondrial Na+ import through NCLX is sufficient to block this pathway, preventing adaptation to hypoxia. These results reveal that Na+ import into the mitochondrial matrix controls OXPHOS function and redox signalling through an unexpected interaction with phospholipids, with profound consequences in cellular metabolism
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