• Publicationsclose
• Research dataclose
• Other research productsclose
• Open Access close
• Article close
• EU close
• IRIS - Università degli Studi di Verona close

In the context of finite elasticity, we propose plate models describing the spontaneous bending of nematic elastomer thin films due to variations along the thickness of the nematic order parameters. Reduced energy functionals are deduced from a three-dimensional description of the system using rigorous dimension reduction techniques, based on the theory of Γ-convergence. The two-dimensional models are non-linear plate theories, in which deviations from a characteristic target curvature tensor cost elastic energy. Moreover, the stored energy functional cannot be minimised to zero, thus revealing the presence of residual stresses, as observed in numerical simulations. Three nematic textures are considered: splay-bend and twisted orientations of the nematic director, and a uniform director perpendicular to the mid-plane of the film, with variable degree of nematic order along the thickness. These three textures realise three very different structural models: one with only one stable spontaneously bent configuration, a bistable model with two oppositely curved configurations of minimal energy, and a shell with zero stiffness to twisting.

Elevated serum urate concentrations can cause gout, a prevalent and painful inflammatory arthritis. By combining data from >140,000 individuals of European ancestry within the Global Urate Genetics Consortium (GUGC), we identified and replicated 28 genome-wide significant loci in association with serum urate concentrations (18 new regions in or near TRIM46, INHBB, SFMBT1, TMEM171, VEGFA, BAZ1B, PRKAG2, STC1, HNF4G, A1CF, ATXN2, UBE2Q2, IGF1R, NFAT5, MAF, HLF, ACVR1B-ACVRL1 and B3GNT4). Associations for many of the loci were of similar magnitude in individuals of non-European ancestry. We further characterized these loci for associations with gout, transcript expression and the fractional excretion of urate. Network analyses implicate the inhibins-activins signaling pathways and glucose metabolism in systemic urate control. New candidate genes for serum urate concentration highlight the importance of metabolic control of urate production and excretion, which may have implications for the treatment and prevention of gout. © 2013 Nature America, Inc. All rights reserved.

Background. Epidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent. Methods. In 12 cohorts from 6 European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: Particulate matter (PM) ≥2.5,≥10, and 2.5-10 FÊm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant, and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses. Results. Of 282 194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts also had data on nonmalignant brain tumor, where among 106 786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically nonsignificant association between malignant brain tumor and PM2.5 absorbance (hazard ratio and 95% CI: 1.67; 0.89.3.14 per 10.5/m3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38.2.71 per 10-5/m3) and all other pollutants were lower for nonmalignant than for malignant brain tumors. Conclusion. We found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors. © 2018 The Author(s). Chemicals/CAS: nitric oxide, 10102-43-9; nitrogen dioxide, 10102-44-0

Both Michel Foucault and Barbara Cassin address Aristotle’s thought and the 5th century BCE sources attributed to the rhetorician Gorgias in order to reconstruct the history of the strategic exclusion of the Sophistics from the Western philosophical tradition. They retrace the scene of the rhetoric agon that Aristotle engaged with Gorgias. Both theorists’ arguments illuminate that the sophist has formulated an original account of political theatricality by talking about the scenes of the logos.

Heart failure (HF) is a leading cause of mortality. Inflammation is implicated in HF, yet clinical trials targeting pro-inflammatory cytokines in HF were unsuccessful, possibly due to redundant functions of individual cytokines. Searching for better cardiac inflammation targets, here we link T cells with HF development in a mouse model of pathological cardiac hypertrophy and in human HF patients. T cell costimulation blockade, through FDA-approved rheumatoid arthritis drug abatacept, leads to highly significant delay in progression and decreased severity of cardiac dysfunction in the mouse HF model. The therapeutic effect occurs via inhibition of activation and cardiac infiltration of T cells and macrophages, leading to reduced cardiomyocyte death. Abatacept treatment also induces production of anti-inflammatory cytokine interleukin-10 (IL-10). IL-10-deficient mice are refractive to treatment, while protection could be rescued by transfer of IL-10-sufficient B cells. These results suggest that T cell costimulation blockade might be therapeutically exploited to treat HF. Abatacept is an FDA-approved drug used for treatment of rheumatoid arthritis. Here the authors show that abatacept reduces cardiomyocyte death in a mouse model of heart failure by inhibiting activation and heart infiltration of T cells and macrophages, an effect mediated by IL-10, suggesting a potential therapy for heart failure.