Integration of Open Slag Bath Furnace with Direct Reduction Reactors for New‐Generation Steelmaking

The present paper illustrates an innovative steel processing route developed by employing hydrogen direct reduced pellets and an open slag bath furnace. The paper illustrates the direct reduction reactor employing hydrogen as reductant on an industrial scale. The solution allows for the production of steel from blast furnace pellets transformed in the direct reduction reactor. The reduced pellets are then melted in open slag bath furnaces, allowing carburization for further refining. The proposed solution is clean for the decarbonization of the steel industry. The kinetic, chemical and thermodynamic issues are detailed with particular attention paid to the slag conditions. The proposed solution is also supported by the economic evaluation compared to traditional route

Recuperando prestaciones en clusters tras ocurrencia de fallos utilizando RADIC

Tras la recuperación de un fallo, las aplicaciones pierden prestaciones debido, en gran parte, a que el número planificado de nodos ha disminuido y de la pérdida que provoca la existencia no planificada de procesos compartiendo el mismo nodo. Este trabajo presenta una propuesta para mitigar las pérdidas de prestaciones en sistemas paralelos con tolerancia a fallos basados en rollback-recovery, después de un fallo, donde la máquina paralela queda reconfigurada con un nodo menos, con la consiguiente repercusión en el tiempo de ejecución de la aplicación. Proponemos para recuperar las prestaciones, una solución que extiende la arquitectura RADIC: la posibilidad de permitir, durante la ejecución de la aplicación, el reemplazo de nodos que han fallado o disponer de nodos extras que pueden ser iniciados con la aplicación, pero sin procesos de la aplicación activos, de forma que cuando falle un nodo pase a ejecutar los procesos en dicho nodoAfter a fault recovering, the reduction of the planned nodes number and the existence of unplanned process node sharing, leads to application performance lost. This work presents a proposal to minimize the performance lost in rollback-recovery based fault tolerant parallel systems, after a fault occurrence, when the parallel machine reconfigure itself with one node less, affecting the application total execution time. In order to restore the performance, we propose a solution that extends the RADIC architecture: the possibility of, during the application execution, allow the faulty nodes replacement or to have process free spare nodes that may or not be started with the application, in order to under a node failure assumes the process that was in execution on the faulty node.VII Workshop de Procesamiento Distribuido y Paralelo (WPDP)Red de Universidades con Carreras en Informática (RedUNCI

A hybrid of deep and textural features to differentiate glomerulosclerosis and minimal change disease from glomerulus biopsy images

The minimal change disease (MCD) and glomerulosclerosis (GS) are two common kidney diseases. Unless adequately treated, these diseases leads to chronic kidney diseases. Accurate differentiation of these two diseases is of paramount importance as their methods of treatment and prognoses are different. Thus, this article propose a method capable of differentiating MCD from GS in glomerulus biopsies images based on a new hybrid deep and texture feature space. We conducted an extensive study to determine the best set of features for image representation. Our feature extraction methodology, which includes Haraliks and geostatistics texture descriptors and pre-trained CNNs, resulted in 13,476 characteristics. We then used mutual information to order the elements by importance and select the best set for differentiating MCD from GS using the random forest classifier. The proposed method achieved an accuracy of 90.3% and a Kappa index of 80.5%. Representation of glomerulus biopsy images with a hybrid of deep and textural features facilitates the accurate differentiation of GS and MCD

Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

Comparative modeling of DNA and RNA polymerases from Moniliophthora perniciosa mitochondrial plasmid

<p>Abstract</p> <p>Background</p> <p>The filamentous fungus <it>Moniliophthora perniciosa </it>(Stahel) Aime & Phillips-Mora is a hemibiotrophic Basidiomycota that causes witches' broom disease of cocoa (<it>Theobroma cacao </it>L.). This disease has resulted in a severe decrease in Brazilian cocoa production, which changed the position of Brazil in the market from the second largest cocoa exporter to a cocoa importer. Fungal mitochondrial plasmids are usually invertrons encoding DNA and RNA polymerases. Plasmid insertions into host mitochondrial genomes are probably associated with modifications in host generation time, which can be involved in fungal aging. This association suggests activity of polymerases, and these can be used as new targets for drugs against mitochondrial activity of fungi, more specifically against witches' broom disease. Sequencing and modeling: DNA and RNA polymerases of <it>M. perniciosa </it>mitochondrial plasmid were completely sequenced and their models were carried out by Comparative Homology approach. The sequences of DNA and RNA polymerase showed 25% of identity to 1XHX and 1ARO (pdb code) using BLASTp, which were used as templates. The models were constructed using Swiss PDB-Viewer and refined with a set of Molecular Mechanics (MM) and Molecular Dynamics (MD) in water carried out with AMBER 8.0, both working under the ff99 force fields, respectively. Ramachandran plots were generated by Procheck 3.0 and exhibited models with 97% and 98% for DNA and RNA polymerases, respectively. MD simulations in water showed models with thermodynamic stability after 2000 ps and 300 K of simulation.</p> <p>Conclusion</p> <p>This work contributes to the development of new alternatives for controlling the fungal agent of witches' broom disease.</p

EFSA Panel on Food Contact Materials, Enzymes, Flavourings and Processing Aids (CEF); Scientific Opinion on Flavouring Group Evaluation 96 (FGE.96): Consideration of 88 flavouring substances considered by EFSA for which EU production volumes / anticipated production volumes have been submitted on request by DG SANCO. Addendum to FGE. 51, 52, 53, 54, 56, 58, 61, 62, 63, 64, 68, 69, 70, 71, 73, 76, 77, 79, 80, 83, 84, 85 and 87

Overgrowth disorders are a heterogeneous group of conditions characterized by increased growth parameters and other variable clinical features such as intellectual disability and facial dysmorphism1. To identify new causes of human overgrowth, we performed exome sequencing in ten proband-parent trios and detected two de novo DNMT3A mutations. We identified 11 additional de novo mutations by sequencing DNMT3A in a further 142 individuals with overgrowth. The mutations alter residues in functional DNMT3A domains, and protein modeling suggests that they interfere with domain-domain interactions and histone binding. Similar mutations were not present in 1,000 UK population controls (13/152 cases versus 0/1,000 controls; P &lt; 0.0001). Mutation carriers had a distinctive facial appearance, intellectual disability and greater height. DNMT3A encodes a DNA methyltransferase essential for establishing methylation during embryogenesis and is commonly somatically mutated in acute myeloid leukemia2, 3, 4. Thus, DNMT3A joins an emerging group of epigenetic DNA- and histone-modifying genes associated with both developmental growth disorders and hematological malignancie