Análisis del funcionamiento de un método basado en wavelets borrosos para la detección de bordes en imágenes sintéticas del tipo SAR

La detección automática de líneas costeras y riberas, a partir de imágenes de radar de apertura sintética (conocidas como SAR, por las siglas en inglés de Synthetic Aperture Radar) es una tarea difícil dentro del campo del procesamiento de imágenes, debido a la presencia de retrodispersiones similares al ruido moteado multiplicativo. Recientemente, se presentó un Marco Wavelet Borroso (Fuzzy Wavelet Framework, FWF) para la detección de líneas costeras en imágenes SAR basado en una combinación de Wavelets unidimensionales, como filtro para la eliminación de parte del ruido moteado, y Lógica Difusa, para la detección de las líneas costeras, ya que tiene su potencialidad en la toma de decisiones en ambientes ruidosos y mal definidas (K. Nemer Pelliza, tesis doctoral, Universidad Tecnológica Nacional, Facultad Regional Córdoba, Argentina, 2016). Para realizar la detección de líneas costeras, se construye un mapa borroso de la imagen Wavelet intermedia, extrayéndose sus bordes. Dicho algoritmo codifica las filas y columnas de píxeles de la imagen, por lo que posee buena exactitud y preferencia en identificar bordes verticales y horizontales; la ventaja de este algoritmo es su rapidez y eficiencia. En el presente trabajo se presenta un estudio para analizar la detección de bordes en situaciones desfavorables para el algoritmo con el objetivo de mejorarlo y resolver el problema con mayor exactitud. Para esto se generan imágenes dicotómicas, con figuras de bordes lisos con presencia de líneas no alineadas con filas o columnas (por ej. círculo, rombo, estrella, etc.), se les aplican las 120 combinaciones distribuciones de retrodispersiones, para obtener imágenes similares a las del tipo SAR. Se calcula el error de detección de borde y se muestran las características de las imágenes que generan un mayor nivel de error en el método. Finalmente, se indican las posibles vías de acción para mejorar el FWF.Publicado en: Mecánica Computacional vol. XXXV, no. 43Facultad de Ingenierí

Signal-to-noise measurements utilizing a novel dual-energy multimedia detector

Dual-energy measurements are presented utilizing a novel slot-scan digital radiographic imaging detector, operating on gaseous solid state ionization principles. The novel multimedia detector has two basic functional components: a noble gas-filled detector volume operating on gas microstrip principles, and a solid state detector volume. The purpose of this study is to investigate the potential use of this multimedia detector for enhanced dual-energy imaging. The experimental results indicate that the multimedia detector exhibits a large subtracted signal-to-noise ratio. Although the intrinsic merit of this device is being explored for medical imaging, potential applications of the multimedia detector technology in other industrial areas, such as aerospace imaging, aviation security, and surveillance, are also very promising

ABCG2 Is Overexpressed on Red Blood Cells in Ph-Negative Myeloproliferative Neoplasms and Potentiates Ruxolitinib-Induced Apoptosis

Acknowledgments: The authors would like to thank Dominique Gien, Sirandou Tounkara, and Eliane Véra at Centre National de Référence pour les Groupes Sanguins for the management of blood samples. Funding: The work was supported by Institut National de la Santé et de la Recherche Médicale (Inserm), Institut National de la Transfusion Sanguine (INTS), the University of Paris, and grants from Laboratory of Excellence (Labex) GR-Ex, reference No. ANR-11-LABX-0051. The Labex GR-Ex is funded by the IdEx program “Investissements d’avenir” of the French National Research Agency, reference No. ANR-18-IDEX-0001. R.B. was funded by the European Union’s Horizon 2020 Research and Innovation Program under grant agreement No. 675115-RELEVANCE-H2020-MSCA-ITN-2015. M.B. was funded by Ministère de l’Enseignement Supérieur et de la Recherche at the BioSPC Doctoral School. R.B. and M.B. also received financial support from Société Française d’Hématologie (SFH) and Club du Globule Rouge et du Fer (CGRF).Peer reviewedPublisher PD

Clinical and genetic characterisation of dystrophin-deficient muscular dystrophy in a family of Miniature Poodle dogs

Four full-sibling intact male Miniature Poodles were evaluated at 4–19 months of age. One was clinically normal and three were affected. All affected dogs were reluctant to exercise and had generalised muscle atrophy, a stiff gait and a markedly elevated serum creatine kinase activity. Two affected dogs also showed poor development, learning difficulties and episodes of abnormal behaviour. In these two dogs, investigations into forebrain structural and metabolic diseases were unremarkable; electromyography demonstrated fibrillation potentials and complex repetitive discharges in the infraspinatus, supraspinatus and epaxial muscles. Histopathological, immunohistochemical and immunoblotting analyses of muscle biopsies were consistent with dystrophin-deficient muscular dystrophy. DNA samples were obtained from all four full-sibling male Poodles, a healthy female littermate and the dam, which was clinically normal. Whole genome sequencing of one affected dog revealed a >5 Mb deletion on the X chromosome, encompassing the entire DMD gene. The exact deletion breakpoints could not be experimentally ascertained, but we confirmed that this region was deleted in all affected males, but not in the unaffected dogs. Quantitative polymerase chain reaction confirmed all three affected males were hemizygous for the mutant X chromosome, while the wildtype chromosome was observed in the unaffected male littermate. The female littermate and the dam were both heterozygous for the mutant chromosome. Forty-four Miniature Poodles from the general population were screened for the mutation and were homozygous for the wildtype chromosome. The finding represents a naturally-occurring mutation causing dystrophin-deficient muscular dystrophy in the dog

Base-editing-mediated dissection of a γ-globin cis-regulatory element for the therapeutic reactivation of fetal hemoglobin expression

: Sickle cell disease and β-thalassemia affect the production of the adult β-hemoglobin chain. The clinical severity is lessened by mutations that cause fetal γ-globin expression in adult life (i.e., the hereditary persistence of fetal hemoglobin). Mutations clustering ~200 nucleotides upstream of the HBG transcriptional start sites either reduce binding of the LRF repressor or recruit the KLF1 activator. Here, we use base editing to generate a variety of mutations in the -200 region of the HBG promoters, including potent combinations of four to eight γ-globin-inducing mutations. Editing of patient hematopoietic stem/progenitor cells is safe, leads to fetal hemoglobin reactivation and rescues the pathological phenotype. Creation of a KLF1 activator binding site is the most potent strategy - even in long-term repopulating hematopoietic stem/progenitor cells. Compared with a Cas9-nuclease approach, base editing avoids the generation of insertions, deletions and large genomic rearrangements and results in higher γ-globin levels. Our results demonstrate that base editing of HBG promoters is a safe, universal strategy for treating β-hemoglobinopathies

Avaliação de linhagens/cultivares de arroz de sequeiro em condição de cerrado do Amazonas.

Informacoes preliminares sobre avaliacao e selecao de genotipos de arroz de sequeiro com grande potencial produtivo, com graos do tipo agulhinha, resistentes a pragas, doencas e acamamento, para servir de suporte a acao governamental de incrementar a producao de graos para o Estado do Amazonas. Tanto no ensaio comparativo quanto no avancado, muitas linhagens avaliadas apresentaram alto potencial produtivo, com destaque para: CNA8826, CNA8824, CNA8832, CNA8170, CNA8540, CNA8817, CNA8812, CNA8548, CNA8555, CNA8796, CNA8775, CNA8545 e CNA8793. As cultivares Maravilha, Progresso e Xingu ja constam da lista de recomendacao para o estado do Amazonas, sendo que as duas primeiras, para areas com uso intensivo de tecnologia de producao, e a ultima, para areas com baixo nivel tecnologicao e de plantio em toco.bitstream/item/82575/1/Pesquisa-04-1999.pd

A gain-of-function TBX20 mutation causes congenital atrial septal defects, patent foramen ovale and cardiac valve defects

BACKGROUND: Ostium secundum atrial septal defects (ASDII) account for approximately 10% of all congenital heart defects (CHD) and mutations in cardiac transcription factors, including TBX20, were identified as an underlying cause for ASDII. However, very little is known about disease penetrance in families and functional consequences of inherited TBX20 mutations. METHODS: The coding region of TBX20 was directly sequenced in 170 ASDII patients. Functional consequences of one novel mutation were investigated by surface plasmon resonance, CD spectropolarymetry, fluorescence spectrophotometry, luciferase assay and chromatin immunoprecipitation. RESULTS: We found a novel mutation in a highly conserved residue in the T-box DNA-binding domain (I121M) segregating with CHD in a three generation kindred. Four mutation carriers revealed cardiac phenotypes in terms of cribriform ASDII, large patent foramen ovale or cardiac valve defects. Interestingly, tertiary hydrophobic interactions within the mutant TBX20 T-box were significantly altered leading to a more dynamic structure of the protein. Moreover, Tbx20-I121M resulted in a significantly enhanced transcriptional activity, which was further increased in the presence of co-transcription factors GATA4/5 and NKX2-5. Occupancy of DNA binding sites on target genes was also increased. CONCLUSIONS: We suggest that TBX20-I121M adopts a more fluid tertiary structure leading to enhanced interactions with cofactors and more stable transcriptional complexes on target DNA sequences. Our data, combined with that of others, suggest that human ASDII may be related to loss- as well as gain-of-function TBX20 mutations