17 research outputs found

    Sills and gabions as countermeasures at bridge pier in presence of debris accumulations

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    Transverse structures, such as sills, can reduce local scour at bridge piers. However, in the presence of a sill, the scour hole evolves more rapidly with a debris accumulation, yielding a different behaviour of the countermeasure. This research aims to analyse the efficiency of sills and gabions as countermeasures against local scour in the presence of simplified debris geometry. Experiments were conducted under clear-water conditions with the approach flow velocity set at the threshold of the sediment motion. The temporal evolution and the scour morphology in the presence of smooth sills and gabions were investigated. The efficiency of the countermeasures was assessed by referring to a pilot test with an unprotected pier. Although a delay occurs in the scour development, the main findings reveal an insufficient countermeasure efficiency for large scour development in the presence of large debris accumulation, while gabions were able to further delay the scour process mainly due to larger surface roughness when compared with smooth sills

    Studi di Filologia romanza offerti a Valeria Bertolucci Pizzorusso

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    Raccolta di studi di Filologia romanza in onore di Valeria Bertolucci Pizzoruss

    Blood to skin recirculation of CD4(+) memory T cells associates with cutaneous and systemic manifestations of psoriatic disease

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    Blood to skin recirculation could play a role in the pathogenesis of psoriasis. To investigate this possibility we dissected the phenotype of circulating T cells in psoriasis patients, calculated the correlation the clinical parameters of the disease and performed a parallel bioinformatics analysis of gene expression data in psoriatic skin. We found that circulating CCR6(+) CD4(+) TEM and TEFF cells significantly correlated with systemic inflammation. Conversely, the percentage of CXCR3(+) CD4(+) TEM cells negatively correlated with the severity of the cutaneous disease. Importantly CLA(+) CD4(+) TCM cells expressing CCR6(+) or CCR4(+)CXCR3(+) negatively correlated with psoriasis severity suggesting recruitment to the skin compartment. This assumption was reinforced by gene expression data showing marked increase of CCR7 and CLA-encoding gene SELPLG expression in psoriatic skin and strong association of their expression. The data enlightens a role for CD4(+) T cells trafficking between blood and skin in cutaneous and systemic manifestations of psoriasis

    Inositol-triphosphate 3-kinase B promotes calcium mobilization and the inflammatory activity of dendritic cells.

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    peer reviewedInnate immune responses to Gram-negative bacteria depend on the recognition of lipopolysaccharide (LPS) by a receptor complex that includes CD14 and TLR4. In dendritic cells (DCs), CD14 enhances the activation not only of TLR4 but also that of the NFAT family of transcription factors, which suppresses cell survival and promotes the production of inflammatory mediators. NFAT activation requires Ca2+ mobilization. In DCs, Ca2+ mobilization in response to LPS depends on phospholipase C γ2 (PLCγ2), which produces inositol 1,4,5-trisphosphate (IP3). Here, we showed that the IP3 receptor 3 (IP3R3) and ITPKB, a kinase that converts IP3 to inositol 1,3,4,5-tetrakisphosphate (IP4), were both necessary for Ca2+ mobilization and NFAT activation in mouse and human DCs. A pool of IP3R3 was located on the plasma membrane of DCs, where it colocalized with CD14 and ITPKB. Upon LPS binding to CD14, ITPKB was required for Ca2+ mobilization through plasma membrane-localized IP3R3 and for NFAT nuclear translocation. Pharmacological inhibition of ITPKB in mice reduced both LPS-induced tissue swelling and the severity of inflammatory arthritis to a similar extent as that induced by the inhibition of NFAT using nanoparticles that delivered an NFAT-inhibiting peptide specifically to phagocytic cells. Our results suggest that ITPKB may represent a promising target for anti-inflammatory therapies that aim to inhibit specific DC functions
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