Resultados de investigación

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This dataset contains the BOCATS2 2023 (A25-Ovide line) pre-qualified measurements of CTD data and qualified microstructure data, BOCATS2, a continuation of the previous BOCATS project (2014-2017), will be a main contribution to the observation of the NA subpolar gyre by continuing the occupation of the biennial section A25-Ovide (2021 and 2023) within the framework of the international GO-SHIP programme. A particular focus will be given to the new challenge of assessing the variability of the deep circulation in the NA, improving the spatial-temporal resolution of deep currents and water mass characteristics by deploying a regional deep-ARGO array and, at a submillenary scale, using paleoceanographic data obtained in sedimentary records from key sites, such as the Bight and Charlie-Gibbs fracture zones. The high-quality observations foreseen in the SPNA will contribute to the early detection of the alteration of the carbon cycle allowing the precise estimation of the heat, CO2 and N2O storage rates and, ultimately, to find the connection between these changes and the variability of the AMOC at different time scales. The natural and anthropogenic fluxes of heat, CO2 and N2O will be evaluated, as well as the present and submillenary scale transport of sediments and biogenic elements, and the impact of acidification on these timescales by means of the analysis of CaCO3 and organic carbon fluxes to the sediment. Besides, the current ocean acidification rates will also be quantified by evaluating the present situation and establishing future projections. These new observation-based estimates will be a valuable result that will be used to validate the predictions from the models (GCMs and ESMs from CMIP5-6) for the 2°C warming scenario. Finally, special attention will be paid to the rates of elevation of aragonite saturation horizons in deep layers, where the impact on the ecosystems sustained by calcareous organisms is potentially imminent, The Spanish project BOCATS2 with the number PID2019-104279GB-C21 was funded by MCIN/AEI/10.13039/501100011033. The French contribution was funded by Ifremer, and is a contribution to the European project Euro GO-SHIP (Grant agreement n°101094690), Peer reviewed

[Introduction]: In monoclonal B cell lymphocytosis (MBL) and chronic lymphocytic leukemia (CLL), the expansion of malignant B cells disrupts the normal homeostasis and interactions between B cells and T cells, leading to immune dysregulation. CD20+ T cells are a subpopulation of T cells that appear to be involved in autoimmune diseases and cancer., [Methods]: Here, we quantified and phenotypically characterized CD20+ T cells from MBL subjects and CLL patients using flow cytometry and correlated our findings with the B-cell receptor mutational status and other features of the disease., [Results and discussion]: CD20+ T cells were more represented within the CD8+ T cell compartment and they showed a predominant memory Tc1 phenotype. CD20+ T cells were less represented in MBL and CLL patients vs healthy controls, particularly among those with unmutated IGVH gene. The expansion of malignant B cells was accompanied by phenotypic and functional changes in CD20+ T cells, including an increase in follicular helper CD4+ CD20+ T cells and CD20+ Tc1 cells, in addition to the expansion of the TCR Vβ 5.1 in CD4+ CD20+ T cells in CLL., Peer reviewed

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29 ficheros pdf, The target of rapamycin (TOR) signalling pathway plays a key role in the coordination between cellular growth and the cell cycle machinery in eukaryotes. The underlying molecular mechanisms by which TOR might regulate events after anaphase remain unknown. We show for the first time that one of the 2 TOR complexes in budding yeast, TORC1, blocks the separation of cells following cytokinesis by phosphorylation of a member of the NDR (nuclear Dbf2-related) protein-kinase family, the protein Cbk1. We observe that TORC1 alters the phosphorylation pattern of Cbk1 and we identify a residue within Cbk1 activation loop, T574, for which a phosphomimetic substitution makes Cbk1 catalytically inactive and, indeed, reproduces TORC1 control over cell separation. In addition, we identify the exocyst component Sec3 as a key substrate of Cbk1, since Sec3 activates the SNARE complex to promote membrane fusion. TORC1 activity ultimately compromises the interaction between Sec3 and a t-SNARE component. Our data indicate that TORC1 negatively regulates cell separation in budding yeast by participating in Cbk1 phosphorylation, which in turn controls the fusion of secretory vesicles transporting hydrolase at the site of division., Peer reviewed

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