10 resultados para repeat synchronization
em Archivo Digital para la Docencia y la Investigación - Repositorio Institucional de la Universidad del País Vasco
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[EN]This work analyzes the problem of community structure in real-world networks based on the synchronization of nonidentical coupled chaotic Rössler oscillators each one characterized by a defined natural frequency, and coupled according to a predefined network topology. The interaction scheme contemplates an uniformly increasing coupling force to simulate a society in which the association between the agents grows in time. To enhance the stability of the correlated states that could emerge from the synchronization process, we propose a parameterless mechanism that adapts the characteristic frequencies of coupled oscillators according to a dynamic connectivity matrix deduced from correlated data. We show that the characteristic frequency vector that results from the adaptation mechanism reveals the underlying community structure present in the network.
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9 p. : il.
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Gene-culture co-evolution emphasizes the joint role of culture and genes for the emergence of altruistic and cooperative behaviors and behavioral genetics provides estimates of their relative importance. However, these approaches cannot assess which biological traits determine altruism or how. We analyze the association between altruism in adults and the exposure to prenatal sex hormones, using the second-to-fourth digit ratio. We find an inverted U-shaped relation for left and right hands, which is very consistent for men and less systematic for women. Subjects with both high and low digit ratios give less than individuals with intermediate digit ratios. We repeat the exercise with the same subjects seven months later and find a similar association, even though subjects' behavior differs the second time they play the game. We then construct proxies of the median digit ratio in the population (using more than 1000 different subjects), show that subjects' altruism decreases with the distance of their ratio to these proxies. These results provide direct evidence that prenatal events contribute to the variation of altruistic behavior and that the exposure to fetal hormones is one of the relevant biological factors. In addition, the findings suggest that there might be an optimal level of exposure to these hormones from social perspective.
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179 p.
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Smart and mobile environments require seamless connections. However, due to the frequent process of ''discovery'' and disconnection of mobile devices while data interchange is happening, wireless connections are often interrupted. To minimize this drawback, a protocol that enables an easy and fast synchronization is crucial. Bearing this in mind, Bluetooth technology appears to be a suitable solution to carry on such connections due to the discovery and pairing capabilities it provides. Nonetheless, the time and energy spent when several devices are being discovered and used at the same time still needs to be managed properly. It is essential that this process of discovery takes as little time and energy as possible. In addition to this, it is believed that the performance of the communications is not constant when the transmission speeds and throughput increase, but this has not been proved formally. Therefore, the purpose of this project is twofold: Firstly, to design and build a framework-system capable of performing controlled Bluetooth device discovery, pairing and communications. Secondly, to analyze and test the scalability and performance of the \emph{classic} Bluetooth standard under different scenarios and with various sensors and devices using the framework developed. To achieve the first goal, a generic Bluetooth platform will be used to control the test conditions and to form a ubiquitous wireless system connected to an Android Smartphone. For the latter goal, various stress-tests will be carried on to measure the consumption rate of battery life as well as the quality of the communications between the devices involved.
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[ES]El trabajo fin grado desarrollado en este documento consiste en la realización de una interfaz gráfica que permita analizar la precisión, en la medida de armónicos e interarmónicos de señales eléctricas de tensión y corriente, de diferentes técnicas que buscan la sincronización de la frecuencia de muestreo con la frecuencia fundamental. Se estudian diferentes técnicas de estimación de la frecuencia fundamental y diferentes técnicas de remuestreo aplicadas a señales analíticas de las que se conocen su frecuencia fundamental y su contenido armónico. Estas técnicas de procesado tienen como objetivo mejorar en la medida del contenido armónico haciendo disminuir, mediante la sincronización de la frecuencia de muestreo, el error que se comete debido a la dispersión espectral provocada por el enventanado de las señales.
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JA-925
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During the last two decades, analysis of 1/f noise in cognitive science has led to a considerable progress in the way we understand the organization of our mental life. However, there is still a lack of specific models providing explanations of how 1/f noise is generated in coupled brain-body-environment systems, since existing models and experiments typically target either externally observable behaviour or isolated neuronal systems but do not address the interplay between neuronal mechanisms and sensorimotor dynamics. We present a conceptual model of a minimal neurorobotic agent solving a behavioural task that makes it possible to relate mechanistic (neurodynamic) and behavioural levels of description. The model consists of a simulated robot controlled by a network of Kuramoto oscillators with homeostatic plasticity and the ability to develop behavioural preferences mediated by sensorimotor patterns. With only three oscillators, this simple model displays self-organized criticality in the form of robust 1/f noise and a wide multifractal spectrum. We show that the emergence of self-organized criticality and 1/f noise in our model is the result of three simultaneous conditions: a) non-linear interaction dynamics capable of generating stable collective patterns, b) internal plastic mechanisms modulating the sensorimotor flows, and c) strong sensorimotor coupling with the environment that induces transient metastable neurodynamic regimes. We carry out a number of experiments to show that both synaptic plasticity and strong sensorimotor coupling play a necessary role, as constituents of self-organized criticality, in the generation of 1/f noise. The experiments also shown to be useful to test the robustness of 1/f scaling comparing the results of different techniques. We finally discuss the role of conceptual models as mediators between nomothetic and mechanistic models and how they can inform future experimental research where self-organized critically includes sensorimotor coupling among the essential interaction-dominant process giving rise to 1/f noise.
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Myotonic dystrophy type 1 (DM1 or Steinert's disease) and type 2 (DM2) are multisystem disorders of genetic origin. Progressive muscular weakness, atrophy and myotonia are the most prominent neuromuscular features of these diseases, while other clinical manifestations such as cardiomyopathy, insulin resistance and cataracts are also common. From a clinical perspective, most DM symptoms are interpreted as a result of an accelerated aging (cataracts, muscular weakness and atrophy, cognitive decline, metabolic dysfunction, etc.), including an increased risk of developing tumors. From this point of view, DM1 could be described as a progeroid syndrome since a notable age dependent dysfunction of all systems occurs. The underlying molecular disorder in DM1 consists of the existence of a pathological (CTG) triplet expansion in the 3' untranslated region (UTR) of the Dystrophia ll/Iyotonica Protein Kinase (DMPK) gene, whereas (CCTG)n repeats in the first intron of the Cellular Nucleic acid Binding Protein/Zinc Finger Protein 9 (CNBP/ZNF9) gene cause DM2. The expansions are transcribed into (CUG)n and (CCUG)n-containing RNA, respectively, which form secondary structures and sequester RNA binding proteins, such as the splicing factor muscleblind-like protein (MBNL), forming nuclear aggregates known as foci. Other splicing factors, such as CUGBP, are also disrupted, leading to a spliceopathy of a large number of downstream genes linked to the clinical features of these diseases. Skeletal muscle regeneration relies on muscle progenitor cells, known as satellite cells, which are activated after muscle damage, and which proliferate and differentiate to muscle cells, thus regenerating the damaged tissue. Satellite cell dysfunction seems to be a common feature of both age-dependent muscle degeneration (sarcopenia) and muscle wasting in DM and other muscle degenerative diseases. This review aims to describe the cellular, molecular and macrostructural processes involved in the muscular degeneration seen in DM patients, highlighting the similarities found with muscle aging.
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Age of onset (AO) of Huntington disease (HD) is mainly determined by the length of the CAG repeat expansion (CAGexp) in exon 1 of the HTT gene. Additional genetic variation has been suggested to contribute to AO, although the mechanism by which it could affect AO is presently unknown. The aim of this study is to explore the contribution of candidate genetic factors to HD AO in order to gain insight into the pathogenic mechanisms underlying this disorder. For that purpose, two AO definitions were used: the earliest age with unequivocal signs of HD (earliest AO or eAO), and the first motor symptoms age (motor AO or mAO). Multiple linear regression analyses were performed between genetic variation within 20 candidate genes and eAO or mAO, using DNA and clinical information of 253 HD patients from REGISTRY project. Gene expression analyses were carried out by RT-qPCR with an independent sample of 35 HD patients from Basque Country Hospitals. We found suggestive association signals between HD eAO and/or mAO and genetic variation within the E2F2, ATF7IP, GRIN2A, GRIN2B, LINC01559, HIP1 and GRIK2 genes. Among them, the most significant was the association between eAO and rs2742976, mapping to the promoter region of E2F2 transcription factor. Furthermore, rs2742976 T allele patient carriers exhibited significantly lower lymphocyte E2F2 gene expression, suggesting a possible implication of E2F2-dependent transcriptional activity in HD pathogenesis. Thus, E2F2 emerges as a new potential HD AO modifier factor.