195 research outputs found

    Topcrosses in the selection of testers and inbred lines S3 for the yield and bromatological quality of silage maize.

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    The study aiming to evaluate the combining ability of maize partially inbred lines (S3) in crosses with testers ofnarrow genetic base aiming at the selection of the inbred lines, testers and topcross hybrids. Three simple latticetrials with 81 treatments were carried out in the 2014/2015 and 2015/2016 growing seasons. For each growingseason, trials were used to evaluate the topcross hybrids obtained in combination with the testers AG8088,DKB330 (single-cross hybrids) and 9.H33.3 (line). The hybrid AG8088 and line 9.H3.33 were the best testers forgrain yield. The line 9.H3.33 was the best tester for the traits related to yield and quality of silage maize. Theinbred lines that stood out for their combining abilities and capacity of generating great topcross hybrids with thetesters (i.e., 201-23.2, 201-59.1, 201-80.2, 201-81.5, 203-195.3, 201-100.4, 201-145.4, 201-169.3, 202-155, 202-159, 203-23, 203- 31, 203-32, 203-38, 203-75, 203-98, 203-111, 203-135, 203-139, 203-150, 203-188, 203-235,and 203-237) should be maintained in the UEM silage maize breeding program. Progenies 201-59.01, 201-100.4,203-135, 203-150, 203-235 and 203-254 were selected as tester lines of progenies derived from selfing of thetesters AG8088 and DKB330 to improve the silage maize quality. The topcross hybrids 201-95.3 x 9.H3.33, 203-71x 9.H3.33, 203-72 x 9.H3.33, 203-88 x 9.H3.33, 203-139 x 9.H3.33, and 203-150 x 9.H3.33 were selected for goodperformance for agronomic and bromatological silage maize traits. These hybrids are indicated for evaluationsin more environments, with a view to recommending commercial cultivars for grain and silage production in thefuture

    Stress ocupacional e alteração do Estatuto da Carreira Docente português

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    Este estudo foi realizado com 1162 professores, tendo como objetivo analisar a experiência de stress e a síndrome de “burnout”, antes a após a alteração do Estatuto da Carreira Docente em Portugal. Assim, foram efetuadas duas avaliações em momentos temporais distintos, assumindo-se um plano transversal de recolha de dados (2004/2005, n=689 e 2008/2009, n=473). O protocolo de avaliação incluiu medidas de fontes de stress (Questionário de Stress nos Professores, Gomes, Silva, Mourisco, Mota, & Montenegro, 2006) e de “burnout” (Inventário de “Burnout” de Maslach – Versão para Professores, Maslach, Jackson, & Leiter, 1996; Maslach, Jackson, & Schwab, 1996, Adaptação de Gomes et al., 2006). Os resultados indicaram que a experiência de stress e de “burnout” aumentou entre as duas avaliações, verificando-se em 2008/2009 aumentos em áreas relacionadas com as pressões de tempo/excesso de trabalho e com o trabalho burocrático/administrativo e, inversamente, diminuições em áreas relacionadas com as diferentes capacidades e motivações dos alunos. Quanto à predição da síndrome de “burnout”, não se verificaram alterações substanciais nas variáveis preditoras nos dois momentos. Em síntese, os resultados indicaram aumentos nas exigências profissionais dos professores, mas não se pode afirmar que tal se deva às alterações do Estatuto da Carreira Docente uma vez que não observámos alterações no stress associado à carreira docente.(undefined

    Overexpression of CD97 in Intestinal Epithelial Cells of Transgenic Mice Attenuates Colitis by Strengthening Adherens Junctions

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    The adhesion G-protein-coupled receptor CD97 is present in normal colonic enterocytes but overexpressed in colorectal carcinoma. To investigate the function of CD97 in colorectal carcinogenesis, transgenic Tg(villin-CD97) mice overexpressing CD97 in enterocytes were generated and subjected to azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced colitis-associated tumorigenesis. Unexpectedly, we found a CD97 cDNA copy number-dependent reduction of DSS-induced colitis in Tg compared to wild-type (WT) mice that was confirmed by applying a simple DSS protocol. Ultrastructural analysis revealed that overexpression of CD97 strengthened lateral cell-cell contacts between enterocytes, which, in contrast, were weakened in CD97 knockout (Ko) mice. Transepithelial resistance was not altered in Tg and Ko mice, indicating that tight junctions were not affected. In Tg murine and normal human colonic enterocytes as well as in colorectal cell lines CD97 was localized preferentially in E-cadherin-based adherens junctions. CD97 overexpression upregulated membrane-bound but not cytoplasmic or nuclear β-catenin and reduced phospho-β-catenin, labeled for degradation. This was associated with inactivation of glycogen synthase kinase-3β (GSK-3β) and activation of Akt. In summary, CD97 increases the structural integrity of enterocytic adherens junctions by increasing and stabilizing junctional β-catenin, thereby regulating intestinal epithelial strength and attenuating experimental colitis

    Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

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    Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

    Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

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    Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

    Networks of Neuronal Genes Affected by Common and Rare Variants in Autism Spectrum Disorders

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    Autism spectrum disorders (ASD) are neurodevelopmental disorders with phenotypic and genetic heterogeneity. Recent studies have reported rare and de novo mutations in ASD, but the allelic architecture of ASD remains unclear. To assess the role of common and rare variations in ASD, we constructed a gene co-expression network based on a widespread survey of gene expression in the human brain. We identified modules associated with specific cell types and processes. By integrating known rare mutations and the results of an ASD genome-wide association study (GWAS), we identified two neuronal modules that are perturbed by both rare and common variations. These modules contain highly connected genes that are involved in synaptic and neuronal plasticity and that are expressed in areas associated with learning and memory and sensory perception. The enrichment of common risk variants was replicated in two additional samples which include both simplex and multiplex families. An analysis of the combined contribution of common variants in the neuronal modules revealed a polygenic component to the risk of ASD. The results of this study point toward contribution of minor and major perturbations in the two sub-networks of neuronal genes to ASD risk

    Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

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    This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

    Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images

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    Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and correlation with overall survival. TIL map structural patterns were grouped using standard histopathological parameters. These patterns are enriched in particular T cell subpopulations derived from molecular measures. TIL densities and spatial structure were differentially enriched among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for the TCGA image archives with insights into the tumor-immune microenvironment

    Measurement of the cosmic ray spectrum above 4×10184{\times}10^{18} eV using inclined events detected with the Pierre Auger Observatory

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    A measurement of the cosmic-ray spectrum for energies exceeding 4×10184{\times}10^{18} eV is presented, which is based on the analysis of showers with zenith angles greater than 6060^{\circ} detected with the Pierre Auger Observatory between 1 January 2004 and 31 December 2013. The measured spectrum confirms a flux suppression at the highest energies. Above 5.3×10185.3{\times}10^{18} eV, the "ankle", the flux can be described by a power law EγE^{-\gamma} with index γ=2.70±0.02(stat)±0.1(sys)\gamma=2.70 \pm 0.02 \,\text{(stat)} \pm 0.1\,\text{(sys)} followed by a smooth suppression region. For the energy (EsE_\text{s}) at which the spectral flux has fallen to one-half of its extrapolated value in the absence of suppression, we find Es=(5.12±0.25(stat)1.2+1.0(sys))×1019E_\text{s}=(5.12\pm0.25\,\text{(stat)}^{+1.0}_{-1.2}\,\text{(sys)}){\times}10^{19} eV.Comment: Replaced with published version. Added journal reference and DO
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