4,928 research outputs found

    Pragma-Oriented Parallelization of the Direct Sparse Odometry SLAM Algorithm

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    Monocular 3D reconstruction is a challenging computer vision task that becomes even more stimulating when we aim at real-time performance. One way to obtain 3D reconstruction maps is through the use of Simultaneous Localization and Mapping (SLAM), a recurrent engineering problem, mainly in the area of robotics. It consists of building and updating a consistent map of the unknown environment and, simultaneously, saving the pose of the robot, or the camera, at every given time instant. A variety of algorithms has been proposed to address this problem, namely the Large Scale Direct Monocular SLAM (LSD-SLAM), ORB-SLAM, Direct Sparse Odometry (DSO) or Parallel Tracking and Mapping (PTAM), among others. However, despite the fact that these algorithms provide good results, they are computationally intensive. Hence, in this paper, we propose a modified version of DSO SLAM, which implements code parallelization techniques using OpenMP, an API for introducing parallelism in C, C++ and Fortran programs, that supports multi-platform shared memory multi-processing programming. With this approach we propose multiple directive-based code modifications, in order to make the SLAM algorithm execute considerably faster. The performance of the proposed solution was evaluated on standard datasets and provides speedups above 40% without significant extra parallel programming effort.info:eu-repo/semantics/publishedVersio

    Meta-analysis of Penetrance and Systematic Review on Transition to Disease in Genetic Hypertrophic Cardiomyopathy

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    BACKGROUND: Hypertrophic cardiomyopathy (HCM) is characterized by unexplained left ventricular hypertrophy (LVH) and is classically caused by pathogenic or likely pathogenic variants (P/LP) in genes encoding sarcomere proteins. Not all subclinical variant carriers will manifest clinically overt disease, as penetrance (proportion of G+ who develop disease) is variable, age-dependent, and not reliably predicted. METHODS: A systematic search of the literature was performed. We employed random effects generalized linear mixed model meta-analyses to contrast the cross-sectional prevalence and penetrance of sarcomere genes in two different contexts: clinically-based studies on patients and families with HCM versus population/community-based studies. Longitudinal family/clinical studies were additionally analyzed to investigate the rate of phenotypic conversion from subclinical to overt HCM during follow-up. FINDINGS: 455 full text manuscripts were assessed. In family/clinical studies, the prevalence of sarcomere variants in patients diagnosed with HCM was 34%. The penetrance across all genes in non-proband relatives carrying P/LP variants identified during cascade screening was 57% (95% confidence interval [CI] [52,63]) and the mean age of HCM diagnosis was 38 years (95% CI [36, 40]). Penetrance varied from ~32% for myosin light chain (MYL3) to ~55% for myosin binding protein C (MYBPC3), ~60% troponin T (TNNT2) and troponin I (TNNI3), and ~65% for myosin heavy chain (MYH7). Population-based genetic studies demonstrate that P/LP sarcomere variants are present in the background population, but at a low prevalence of <1%. The penetrance of HCM in incidentally identified P/LP variant carriers was also substantially lower; approximatively 11%, ranging from 0% in Atherosclerosis Risk in Communities to 18% in UK Biobank. In longitudinal family studies, the pooled phenotypic conversion across all genes was 15% over an average of ~8 years of follow up, starting from a mean age of ~16 years. However, short-term gene-specific phenotypic conversion varied between ~12% for MYBPC3 to ~23% for MYH7. CONCLUSIONS: The penetrance of P/LP variants is highly variable and influenced by currently undefined and context-dependent genetic and environmental factors. Additional longitudinal studies are needed to improve understanding of true lifetime penetrance in families and in the community, and to identify drivers of the transition from subclinical to overt HCM

    An empirical evaluation of imputation accuracy for association statistics reveals increased type-I error rates in genome-wide associations

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    <p>Abstract</p> <p>Background</p> <p>Genome wide association studies (GWAS) are becoming the approach of choice to identify genetic determinants of complex phenotypes and common diseases. The astonishing amount of generated data and the use of distinct genotyping platforms with variable genomic coverage are still analytical challenges. Imputation algorithms combine directly genotyped markers information with haplotypic structure for the population of interest for the inference of a badly genotyped or missing marker and are considered a near zero cost approach to allow the comparison and combination of data generated in different studies. Several reports stated that imputed markers have an overall acceptable accuracy but no published report has performed a pair wise comparison of imputed and empiric association statistics of a complete set of GWAS markers.</p> <p>Results</p> <p>In this report we identified a total of 73 imputed markers that yielded a nominally statistically significant association at <it>P </it>< 10 <sup>-5 </sup>for type 2 Diabetes Mellitus and compared them with results obtained based on empirical allelic frequencies. Interestingly, despite their overall high correlation, association statistics based on imputed frequencies were discordant in 35 of the 73 (47%) associated markers, considerably inflating the type I error rate of imputed markers. We comprehensively tested several quality thresholds, the haplotypic structure underlying imputed markers and the use of flanking markers as predictors of inaccurate association statistics derived from imputed markers.</p> <p>Conclusions</p> <p>Our results suggest that association statistics from imputed markers showing specific MAF (Minor Allele Frequencies) range, located in weak linkage disequilibrium blocks or strongly deviating from local patterns of association are prone to have inflated false positive association signals. The present study highlights the potential of imputation procedures and proposes simple procedures for selecting the best imputed markers for follow-up genotyping studies.</p

    Genetic mapping of a new heart rate QTL on chromosome 8 of spontaneously hypertensive rats

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    BACKGROUND: Tachycardia is commonly observed in hypertensive patients, predominantly mediated by regulatory mechanisms integrated within the autonomic nervous system. The genetic loci and genes associated with increased heart rate in hypertension, however, have not yet been identified. METHODS: An F2 intercross of Spontaneously Hypertensive Rats (SHR) × Brown Norway (BN) linkage analysis of quantitative trait loci mapping was utilized to identify candidate genes associated with an increased heart rate in arterial hypertension. RESULTS: Basal heart rate in SHR was higher compared to that of normotensive BN rats (365 ± 3 vs. 314 ± 6 bpm, p < 0.05 for SHR and BN, respectively). A total genome scan identified one quantitative trait locus in a 6.78 cM interval on rat chromosome 8 (8q22–q24) that was responsible for elevated heart rate. This interval contained 241 genes, of which 65 are known genes. CONCLUSION: Our data suggest that an influential genetic region located on the rat chromosome 8 contributes to the regulation of heart rate. Candidate genes that have previously been associated with tachycardia and/or hypertension were found within this QTL, strengthening our hypothesis that these genes are, potentially, associated with the increase in heart rate in a hypertension rat model

    Wind-CSP short-term coordination by MILP approach

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    This paper is on the maximization of total profit in a day-ahead market for a price-taker producer needing a short-term scheduling for wind power plants coordination with concentrated solar power plants, having thermal energy storage systems. The optimization approach proposed for the maximization of profit is a mixed-integer linear programming problem. The approach considers not only transmission grid constraints, but also technical operating constraints on both wind and concentrated solar power plants. Then, an improved short-term scheduling coordination is provided due to the more accurate modelling presented in this paper. Computer simulation results based on data for the Iberian wind and concentrated solar power plants illustrate the coordination benefits and show the effectiveness of the approach

    A high-fat meal impairs muscle vasodilatation response to mental stress in humans with Glu27 β2-adrenoceptor polymorphism

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    <p>Abstract</p> <p>Background</p> <p>Forearm blood flow responses during mental stress are greater in individuals homozygous for the Glu27 allele. A high-fat meal is associated with impaired endothelium-dependent dilatation. We investigated the impact of high-fat ingestion on the muscle vasodilatory responses during mental stress in individuals with the Glu27 allele and those with the Gln27 allele of the β<sub>2</sub>-adrenoceptor gene.</p> <p>Methods</p> <p>A total of 162 preselected individuals were genotyped for the Glu27Gln β<sub>2</sub>-adrenoceptor polymorphism. Twenty-four individuals participated in the study. Fourteen were homozygous for the Gln27 allele (Gln27Gln, 40 ± 2 years; 64 ± 2 kg), and 10 were homozygous for the Glu27 allele (Glu27Glu, 40 ± 3 years; 65 ± 3 kg). Forearm blood flow was evaluated by venous occlusion plethysmography before and after ingestion of 62 g of fat.</p> <p>Results</p> <p>The high-fat meal caused no changes in baseline forearm vascular conductance (FVC, 2.2 ± 0.1 vs. 2.4 ± 0.2; <it>P </it>= 0.27, respectively), but reduced FVC responses to mental stress (1.5 ± 0.2 vs. 0.8 ± 0.2 units; <it>P </it>= 0.04). When volunteers were divided according to their genotypes, baseline FVC was not different between groups (Glu27Glu = 2.4 ± 0.1 vs. Gln27Gln = 2.1 ± 0.1 units; <it>P </it>= 0.08), but it was significantly greater in Glu27Glu individuals during mental stress (1.9 ± 0.4 vs. 1.0 ± 0.3 units; <it>P </it>= 0.04). High-fat intake eliminated the difference in FVC responses between Glu27Glu and Gln27Gln individuals (FVC, 1.3 ± 0.4 vs. 1.2 ± 0.4; <it>P </it>= 0.66, respectively).</p> <p>Conclusion</p> <p>These findings demonstrate that a high-fat meal impairs muscle vasodilatation responses to mental stress in humans. However, this reduction can be attributed to the presence of the homozygous Glu27 allele of the β<sub>2</sub>-adrenoceptor gene.</p

    CD47 expression is decreased in hematopoietic progenitor cells in patients with myelofibrosis

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    Myelofibrosis (MF) is characterized by increased circulating hematopoietic progenitor cells (HPCs), abnormal cytokine levels, and the survival advantage of neoplastic progenitors over their normal counterparts, which leads to progressive disappearance of polyclonal hematopoiesis. CD47 is a surface glycoprotein with many functions, such as acting as a phagocytosis inhibitor of the expressing cell, that is increased in normal hematopoietic stem and progenitor cells mobilized into the blood and several human cancer-initiating cells, such as in acute myeloid leukemia. We compared CD47 expression in hematopoietic stem and progenitor cells of patients with MF and controls and found it to be decreased in progenitors of MF. Exposure of control HPCs to the cytokines transforming growth factor β and stromal-derived factor 1, which are important regulators of hematopoietic stem cell cycling and are overexpressed in patients with MF, did not modulate CD47 expression
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