919 resultados para Joaquín Sorolla


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Studia Palaeohispanica: actas del IV Coloquio sobre lenguas y Culturas Paleohispánicas (Vitoria-Gasteiz, 6-10 mayo 1985 / editadas por Joaquín Gorrochategui, José L. Melena y Juan Santos

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Studia Palaeohispanica: actas del IV Coloquio sobre lenguas y Culturas Paleohispánicas (Vitoria-Gasteiz, 6-10 mayo 1985 / editadas por Joaquín Gorrochategui, José L. Melena y Juan Santos

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Introduction. Obesity and obstructive sleep apnea syndrome (OSA) are common coexisting conditions associated with a chronic low-grade inflammatory state underlying some of the cognitive, metabolic, and cardiovascular morbidities. Aim. To examine the levels of inflammatory markers in obese community-dwelling children with OSA, as compared to no-OSA, and their association with clinical and polysomnographic (PSG) variables. Methods. In this cross-sectional, prospective multicenter study, healthy obese Spanish children (ages 4-15 years) were randomly selected and underwent nocturnal PSG followed by a morning fasting blood draw. Plasma samples were assayed for multiple inflammatory markers. Results. 204 children were enrolled in the study; 75 had OSA, defined by an obstructive respiratory disturbance index (RDI) of 3 events/hour total sleep time (TST). BMI, gender, and age were similar in OSA and no-OSA children. Monocyte chemoattractant protein-1 (MCP-1) and plasminogen activator inhibitor-1 (PAI-1) levels were significantly higher in OSA children, with interleukin-6 concentrations being higher in moderate-severe OSA (i.e., AHI > 5/hrTST; P < 0.01), while MCP-1 levels were associated with more prolonged nocturnal hypercapnia (P < 0.001). Conclusion. IL-6, MCP-1, and PAI-1 are altered in the context of OSA among community-based obese children further reinforcing the proinflammatory effects of sleep disorders such as OSA. This trial is registered with ClinicalTrials.gov NCT01322763.

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[ES] Análisis computacional de un modelo (además de su fenomenología emergente) de red asociativa tipo Hopfield que se ha modificado para de cabida a evidencias biológicas como es la del balanceado entre las neuronas excitadoras e inhibidoras en la corteza cerebral.

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Background: In contrast with the recommendations of clinical practice guidelines, the most common treatment for anxiety and depressive disorders in primary care is pharmacological. The aim of this study is to assess the efficacy of a cognitive-behavioural psychological intervention, delivered by primary care psychologists in patients with mixed anxiety-depressive disorder compared to usual care. Methods/Design: This is an open-label, multicentre, randomized, and controlled study with two parallel groups. A random sample of 246 patients will be recruited with mild-to-moderate mixed anxiety-depressive disorder, from the target population on the lists of 41 primary care doctors. Patients will be randomly assigned to the intervention group, who will receive standardised cognitive-behavioural therapy delivered by psychologists together with usual care, or to a control group, who will receive usual care alone. The cognitive-behavioural therapy intervention is composed of eight individual 60-minute face-to face sessions conducted in eight consecutive weeks. A follow-up session will be conducted over the telephone, for reinforcement or referral as appropriate, 6 months after the intervention, as required. The primary outcome variable will be the change in scores on the Short Form-36 General Health Survey. We will also measure the change in the frequency and intensity of anxiety symptoms (State-Trait Anxiety Inventory) and depression (Beck Depression Inventory) at baseline, and 3, 6 and 12 months later. Additionally, we will collect information on the use of drugs and health care services. Discussion: The aim of this study is to assess the efficacy of a primary care-based cognitive-behavioural psychological intervention in patients with mixed anxiety-depressive disorder. The international scientific evidence has demonstrated the need for psychologists in primary care. However, given the differences between health policies and health services, it is important to test the effect of these psychological interventions in our geographical setting.

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Esta serie tiene como propósito mostrar diferentes expresiones artísticas relacionadas con la Ictiología nacional y regional, generadas en diferentes épocas y que surgen por diversas motivaciones personales que, en algún caso, muestran casi con exactitud a los modelos que inspiraron la obra, en otras, por lo contrario, responden a la imaginación y creatividad del autor. En este caso tomamos una imagen de Tomás Gurvich artista uruguayo de origen lituano quién fuera uno de los discípulos preferidos del maestro oriental Joaquín Torres García. Sólo me resta invitar a quienes quieran sumarse a esta iniciativa, se acerquen con sus aportes para consolidar esta idea, ya que podría ser otro instrumento de difusión del conocimiento de nuestra disciplina a los diferentes estamentos de la sociedad.

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McArdle disease, caused by inherited deficiency of the enzyme muscle glycogen phosphorylase (GP-MM), is arguably the paradigm of exercise intolerance. The recent knock-in (p.R50X/p.R50X) mouse disease model allows an investigation of the phenotypic consequences of muscle glycogen unavailability and the physiopathology of exercise intolerance. We analysed, in 2-month-old mice [wild-type (wt/wt), heterozygous (p.R50X/wt) and p.R50X/p.R50X)], maximal endurance exercise capacity and the molecular consequences of an absence of GP-MM in the main glycogen metabolism regulatory enzymes: glycogen synthase, glycogen branching enzyme and glycogen debranching enzyme, as well as glycogen content in slow-twitch (soleus), intermediate (gastrocnemius) and glycolytic/fast-twitch (extensor digitorum longus; EDL) muscles.

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The intent of this review is to summarize current body of knowledge on the potential implication of the xanthine oxidase pathway (XO) on skeletal muscle damage. The possible involvement of the XO pathway in muscle damage is exemplified by the role of XO inhibitors (e.g., allopurinol) in attenuating muscle damage. Reliance on this pathway (as well as on the purine nucleotide cycle) could be exacerbated in conditions of low muscle glycogen availability. Thus, we also summarize current hypotheses on the etiology of both baseline and exertional muscle damage in McArdle disease, a condition caused by inherited deficiency of myophosphorylase. Because myophosphorylase catalyzes the first step of muscle glycogen breakdown, patients are unable to obtain energy from their muscle glycogen stores. Finally, we provide preliminary data from our laboratory on the potential implication of the XO pathway in the muscle damage that is commonly experienced by these patients.

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McArdle disease is a metabolic disorder caused by pathogenic mutations in the PYGM gene. Timely diagnosis can sometimes be difficult with direct genomic analysis, which requires additional studies of cDNA from muscle transcripts. Although the "nonsense-mediated mRNA decay" (NMD) eliminates tissue-specific aberrant transcripts, there is some residual transcription of tissue-specific genes in virtually all cells, such as peripheral blood mononuclear cells (PBMCs).We studied a subset of the main types of PYGM mutations (deletions, missense, nonsense, silent, or splicing mutations) in cDNA from easily accessible cells (PBMCs) in 12 McArdle patients.Analysis of cDNA from PBMCs allowed detection of all mutations. Importantly, the effects of mutations with unknown pathogenicity (silent and splicing mutations) were characterized in PBMCs. Because the NMD mechanism does not seem to operate in nonspecific cells, PBMCs were more suitable than muscle biopsies for detecting the pathogenicity of some PYGM mutations, notably the silent mutation c.645G>A (p.K215=), whose effect in the splicing of intron 6 was unnoticed in previous muscle transcriptomic studies.We propose considering the use of PBMCs for detecting mutations that are thought to cause McArdle disease, particularly for studying their actual pathogenicity.

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We recently generated a knock-in mouse model (PYGM p.R50X/p.R50X) of McArdle disease (myophosphorylase deficiency). One mechanistic approach to unveil the molecular alterations caused by myophosphorylase deficiency, which is arguably the paradigm of 'exercise intolerance', is to compare the skeletal-muscle tissue of McArdle, heterozygous, and healthy (wild type (wt)) mice. We analyzed in quadriceps muscle of p.R50X/p.R50X (n=4), p.R50X/wt (n=6) and wt/wt mice (n=5) (all male, 8 wk-old) molecular markers of energy-sensing pathways, oxidative phosphorylation (OXPHOS) and autophagy/proteasome systems, oxidative damage and sarcoplamic reticulum (SR) Ca handling. We found a significant group effect for total AMPK (tAMPK) and ratio of phosphorylated (pAMPK)/tAMPK (P=0.012 and 0.033), with higher mean values in p.R50X/p.R50X mice vs. the other two groups. The absence of massive accumulation of ubiquitinated proteins, autophagosomes or lysosomes in p.R50X/p.R50X mice suggested no major alterations in autophagy/proteasome systems. Citrate synthase activity was lower in p.R50X/p.R50X mice vs. the other two groups (P=0.036) but no statistical effect existed for respiratory chain complexes. We found higher levels of 4-hydroxy-2-nonenal-modified proteins in p.R50X/p.R50X and p.R50X/wt mice compared with the wt/wt group (P=0.011). Sarco(endo)plasmic reticulum ATPase 1 (SERCA1) levels detected at 110kDa tended to be higher in p.R50X/p.R50X and p.R50X/wt mice compared with wt/wt animals (P=0.076), but their enzyme activity was normal. We also found an accumulation of phosphorylated SERCA1 in p.R50X/p.R50X animals. Myophosphorylase deficiency causes alterations in sensory energetic pathways together with some evidence of oxidative damage and alterations in Ca handling but with no major alterations in OXPHOS capacity or autophagy/ubiquitination pathways, which suggests that the muscle tissue of patients is likely to adapt overall favorably to exercise training interventions.

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Periodistas, científicos, sociólogos, ingenieros, economistas... En multitud de profesiones nos encontramos con la necesidad de interpretar o de realizar gráficas. Las gráficas son elementos habituales en multitud de textos: periódicos, revistas, informes, publicaciones científicas, etc. Y no es de extrañar dado que constituyen un excelente método de comunicación de información cuantitativa. No es improbable, sin embargo, encontrar gráficas que no resultan adecuadas, que no se entienden o que transmitan impresiones equívocas. Del mismo modo que los textos están sujetos a una gramática que aprendemos desde pequeños en la escuela, las gráficas también disponen de una estructura, sólo que mucho menos formalizada y, que desde luego, no se enseña en la escuela. El objetivo de este texto es ofrecer unas guías muy simples, basadas en la analogía con la gramática del lenguaje, que ayuden a comprender y especialmente a realizar representaciones gráficas correctas. Está dirigido a todos los públicos, buscándose la máxima sencillez en las ideas, sin ninguna apoyatura matemática o lingüística. Del mismo modo, los ejemplos están tomados casi exclusivamente de periódicos, de forma que el contenido de las gráficas tampoco despiste de su forma, que es lo que se pretende analizar aquí.

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This paper reviews the fingerprint classification literature looking at the problem from a double perspective. We first deal with feature extraction methods, including the different models considered for singular point detection and for orientation map extraction. Then, we focus on the different learning models considered to build the classifiers used to label new fingerprints. Taxonomies and classifications for the feature extraction, singular point detection, orientation extraction and learning methods are presented. A critical view of the existing literature have led us to present a discussion on the existing methods and their drawbacks such as difficulty in their reimplementation, lack of details or major differences in their evaluations procedures. On this account, an experimental analysis of the most relevant methods is carried out in the second part of this paper, and a new method based on their combination is presented.

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In the first part of this paper we reviewed the fingerprint classification literature from two different perspectives: the feature extraction and the classifier learning. Aiming at answering the question of which among the reviewed methods would perform better in a real implementation we end up in a discussion which showed the difficulty in answering this question. No previous comparison exists in the literature and comparisons among papers are done with different experimental frameworks. Moreover, the difficulty in implementing published methods was stated due to the lack of details in their description, parameters and the fact that no source code is shared. For this reason, in this paper we will go through a deep experimental study following the proposed double perspective. In order to do so, we have carefully implemented some of the most relevant feature extraction methods according to the explanations found in the corresponding papers and we have tested their performance with different classifiers, including those specific proposals made by the authors. Our aim is to develop an objective experimental study in a common framework, which has not been done before and which can serve as a baseline for future works on the topic. This way, we will not only test their quality, but their reusability by other researchers and will be able to indicate which proposals could be considered for future developments. Furthermore, we will show that combining different feature extraction models in an ensemble can lead to a superior performance, significantly increasing the results obtained by individual models.