Abstract
Nature and biologically inspired metaheuristics can be powerful tools to design PID controllers. The grey wolf optimization is one of these promising and interesting metaheuristics, recently introduced. In this study the grey wolf optimization algorithm is proposed to design PID controllers, and the results obtained compared with the ones obtained with gravitational search and particle swarm optimization algorithms. Simulation results obtained with these three bio-inspired metaheuristics applied to a set of benchmark linear plants are presented, considering the design objective of set-point tracking. The results are also compared with two non-iterative PID tuning techniques. © Springer International Publishing Switzerland 2017.

Abstract
Massive changes in electricity markets have occurred during the last years, as a consequence of the massive introduction of renewable energies. These changes have led to a restructuring process that had an impact throughout the electrical industry. The case of the electricity markets is a relevant example, where new forms of trading emerged and new market entities were created. With these changes, the complexity of electricity markets increased as well, which brought out the need from the involved players for adequate support to their decision making process. Artificial intelligence plays an important role in the development of these tools. Multi-agent systems, in particular, have been largely explored by stakeholders in the sector. Artificial intelligence also provides intelligent solutions for optimization, which enable troubleshooting in a short time and with very similar results to those achieved by deterministic techniques, which usually result from very high execution times. The work presented in this paper aims at solving a portfolio optimization problem for electricity markets participation, using an approach based on NPSO-LRS (New Particle Swarm Optimization with Local Random Search). The proposed method is used to assist decisions of electricity market players. © 2016 IEEE.

Abstract
A highly non-linear solid core photonic crystal fiber (SCPCF) is designed in the present work. Three hexagonal air hole rings in cladding region and four very small air holes are present in a symmetric manner in the core region. By using full vectorial finite element method (FVFEM) with the perfectly matched layer, we study numerically the effective area of modal pattern as well as the nonlinear coefficient of this proposed SCPCF. For this proposed fiber a small modal effective area 5.58 µm2 and a high nonlinear coefficient 21.38 W-1 km-1 are obtained at communication wavelength 1.55 µm for the small air holes in the core with diameter 0.15 µm. This type of SCPCF is useful for different nonlinear applications. © Springer Nature Singapore Pte Ltd. 2017.

Abstract
X chromosome inactivation (XCI) silences transcription from one of the two X chromosomes in female mammalian cells to balance expression dosage between XX females and XY males. XCI is, however, incomplete in humans: up to one-third of X-chromosomal genes are expressed from both the active and inactive X chromosomes (Xa and Xi, respectively) in female cells, with the degree of 'escape' from inactivation varying between genes and individuals1,2. The extent to which XCI is shared between cells and tissues remains poorly characterized3,4, as does the degree to which incomplete XCI manifests as detectable sex differences in gene expression5 and phenotypic traits6. Here we describe a systematic survey of XCI, integrating over 5,500 transcriptomes from 449 individuals spanning 29 tissues from GTEx (v6p release) and 940 single-cell transcriptomes, combined with genomic sequence data. We show that XCI at 683 X-chromosomal genes is generally uniform across human tissues, but identify examples of heterogeneity between tissues, individuals and cells. We show that incomplete XCI affects at least 23% of X-chromosomal genes, identify seven genes that escape XCI with support from multiple lines of evidence and demonstrate that escape from XCI results in sex biases in gene expression, establishing incomplete XCI as a mechanism that is likely to introduce phenotypic diversity6,7. Overall, this updated catalogue of XCI across human tissues helps to increase our understanding of the extent and impact of the incompleteness in the maintenance of XCI.

Abstract
Phonocardiogram signals contain very useful information about the condition of the heart. It is a method of registration of heart sounds, which can be visually represented on a chart. By analyzing these signals, early detections and diagnosis of heart diseases can be done. Intelligent and automated analysis of the phonocardiogram is therefore very important, to determine whether the patient's heart works properly or should be referred to an expert for further evaluation. In this work, we use electrocardiograms and phonocardiograms collected simultaneously, from the Physionet challenge database, and we aim to determine whether a phonocardiogram corresponds to a "normal" or "abnormal" physiological state. The main idea is to translate a 1D phonocardiogram signal into a 2D image that represents temporal and Mel-frequency cepstral coefficients features. To do that, we develop a novel approach that uses both features. First we segment the phonocardiogram signals with an algorithm based on a logistic regression hidden semi-Markov model, which uses the electrocardiogram signals as reference. After that, we extract a group of features from the time and frequency domain (Mel-frequency cepstral coefficients) of the phonocardiogram. Then, we combine these features into a two-dimensional time-frequency heat map representation. Lastly, we run a binary classifier to learn a model that discriminates between normal and abnormal phonocardiogram signals. In the experiments, we study the contribution of temporal and Mel-frequency cepstral coefficients features and evaluate three classification algorithms: Support Vector Machines, Convolutional Neural Network, and Random Forest. The best results are achieved when we map both temporal and Mel-frequency cepstral coefficients features into a 2D image and use the Support Vector Machines with a radial basis function kernel. Indeed, by including both temporal and Mel-frequency cepstral coefficients features, we obtain sligthly better results than the ones reported by the challenge participants, which use large amounts of data and high computational power.

Abstract
Adenosine-to-inosine (A-to-I) RNA editing is a conserved posttranscriptional mechanism mediated by ADAR enzymes that diversifies the transcriptome by altering selected nucleotides in RNA molecules1. Although many editing sites have recently been discovered2-7, the extent to which most sites are edited and how the editing is regulated in different biological contexts are not fully understood8-10. Here we report dynamic spatiotemporal patterns and new regulators of RNA editing, discovered through an extensive profiling of A-to-I RNA editing in 8,551 human samples (representing 53 body sites from 552 individuals) from the Genotype-Tissue Expression (GTEx) project and in hundreds of other primate and mouse samples. We show that editing levels in non-repetitive coding regions vary more between tissues than editing levels in repetitive regions. Globally, ADAR1 is the primary editor of repetitive sites and ADAR2 is the primary editor of nonrepetitive coding sites, whereas the catalytically inactive ADAR3 predominantly acts as an inhibitor of editing. Cross-species analysis of RNA editing in several tissues revealed that species, rather than tissue type, is the primary determinant of editing levels, suggesting stronger cis-directed regulation of RNA editing for most sites, although the small set of conserved coding sites is under stronger trans-regulation. In addition, we curated an extensive set of ADAR1 and ADAR2 targets and showed that many editing sites display distinct tissue-specific regulation by the ADAR enzymes in vivo. Further analysis of the GTEx data revealed several potential regulators of editing, such as AIMP2, which reduces editing in muscles by enhancing the degradation of the ADAR proteins. Collectively, our work provides insights into the complex cis-and trans-regulation of A-to-I editing.