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The excess pore-water pressures (u) induced by piezocone penetration and their dissipation around the cone have been investigated by laboratory model tests and theoretical-numerical analyses. Based on the test results, a method for predicting cone penetration-induced distribution of u has been proposed. By numerical analysis using the predicted initial distribution of u it has been demonstrated that dissipation of the pore-water pressure measured at the shoulder of the cone ([u.sub.2]- type cone) is a two-dimensional (horizontal radial and vertical) process. Aback-fitted coefficient of consolidation in the horizontal direction ([c.sub.h]) can be obtained by comparing the simulated and laboratory-measured two-dimensional dissipation curves. It has also been shown that a published method for estimating [c.sub.h] from measured nonstandard dissipation curves (in which [u.sub.2] increases initially and then decreases) results in values of [c.sub.h] that agree well with values of [c.sub.h] deduced from the two- dimensional analysis. Key words: piezocone test, excess pore pressure, coefficient of consolidation, numerical analysis. L'exces de pression interstitielle (u) induit par la penetration d'un piezocone dans le sol et sa dissipation autour du cone ont ete analyses a l'aide d'essais sur modeles effectues en laboratoire et d'analyses theoriques et numeriques. A partir des resultats de ces essais, on a propose une methode de prediction de la distribution de l'exces de pression interstitielle, u, induit par la penetration du cone dans le sol. Grace a une analyse numerique basee sur la distribution initiale predite de u, on a pu montrer que la dissipation de la pression interstitielle mesuree autour du cone (cone de type [u.sub.2]) est un mecanisme bidimensionnel (radial-horizontal et vertical). En comparant les courbes de dissipation bidimensionnelles simulees a celles mesurees en laboratoire, on peut obtenir un coefficient de consolidation retroajuste dans la direction horizontale ([c.sub.h]). En outre, on a montre qu'une methode deja publiee et permettant d'estimer [c.sub.h] a partir de courbes de dissipation non standard mesurees (sur lesquelles [u.sub.2] augmente d'abord, puis diminue) produisait des valeurs de [c.sub.h] qui concordaient bien avec celles obtenues grace a l'analyse bidimensionnelle. [Traduit par la Redaction] Mots-cles: essai au piezocone, exces de pression interstitielle, coefficient de consolidation, analyse numerique., Introduction The piezocone is widely used as an in situ site investigation tool. Piezocone tests consist of a penetration phase followed by a dissipation test conducted by holding the cone [...]

Introduction: Pattern recognition receptor-mediated signaling pathways have recently been elucidated to bridge the innate immune system and atherosclerosis. NLRP3 is a member of the NLR family. Upon activation, it initiates IL-1β and IL-18 processing, a key step in the inflammatory process of atherosclerosis. Material and methods: We used three different types of lipoproteins, ox- LDL, ox-HDL, and HDL, in Thp-1 at the concentration of 50 mg/l, 100 mg/l, and 150 mg/l respectively. Using real-time polymerase chain reaction and western blot, ELISA detected the expression of NLRP3 and downstream cytokines. NLRP3 siRNA was constructed to down-regulate expression of the NLRP3 gene via the RNA interference technique. 150 mg/l of ox-LDL, ox-HDL and HDL was added to the Thp-1 cell line respectively. We observed the changes in the expression of caspase-1, IL-1β and IL-18 when the NLRP3 gene was down-regulated. Results: Ox-LDL and ox-HDL addition not only increases the expression of NLRP3, but also activates the NLRP3 downstream cytokines and caspase-1 and induces IL-1β and IL-18 secretion. Moreover, the effects of activation and induction are shown to have a dose-dependent manner. Expression of NLRP3 and its downstream inflammatory cytokines is reduced in the presence of HDL (p < 0.05). Furthermore, our data demonstrated that NLRP3 siRNA downregulates NLRP3 expression in mononuclear cells, thus leading to a dramatic reduction in the expression of caspase-1, IL-1β and IL-18 (p < 0.05). Conclusions: The data suggest that activation of the NLRP3 inflammasome is a critical step in caspase-1 activation and IL-1β and IL-18 secretion. Interference with the NLRP3 inflammasome can significantly inhibit the generation of cytokines, thus impeding the pathogenesis of inflammation. [ABSTRACT FROM AUTHOR]