Conservação e restauro de uma urna em vidro do século I d.C., encontrada em Mértola (Portugal)

International audienceThe evolution of capillary forces during evap-oration and the corresponding changes in the geometrical characteristics of liquid (water) bridges between two glass spheres with constant separation are examined experimen-tally. For comparison, the liquid bridges were also tested for mechanical extension (at constant volume). The obtained results reveal substantial differences between the evolution of capillary force due to evaporation and the evolution due to extension of the liquid bridges. During both evaporation and extension, the change of interparticle capillary forces consists in a force decrease to zero either gradually or via rupture of the bridge. At small separations between the grains (short & wide bridges) during evaporation and at large volumes during extension, there is a slight initial increase of force. During evaporation, the capillary force decreases slowly at the begin-ning of the process and quickly at the end of the process; during extension, the capillary force decreases quickly at the beginning and slowly at the end of the process. Rup-ture during evaporation of the bridges occurs most abruptly for bridges with wider separations (tall and thin), sometimes occurring after only 25 % of the water volume was evapo-rated. The evolution (pinning/depinning) of two geometri-cal characteristics of the bridge, the diameter of the three-phase contact line and the "apparent" contact angle at the solid/liquid/gas interface, seem to control the capillary force evolution. The findings are of relevance to the mechanics of unsaturated granular media in the final phase of drying

Circulating free testosterone and risk of aggressive prostate cancer: Prospective and Mendelian randomisation analyses in international consortia

Previous studies had limited power to assess the associations of testosterone with aggressive disease as a primary endpoint. Further, the association of genetically predicted testosterone with aggressive disease is not known. We investigated the associations of calculated free and measured total testosterone and sex hormone-binding globulin (SHBG) with aggressive, overall and early-onset prostate cancer. In blood-based analyses, odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression from prospective analysis of biomarker concentrations in the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group (up to 25 studies, 14 944 cases and 36 752 controls, including 1870 aggressive prostate cancers). In Mendelian randomisation (MR) analyses, using instruments identified using UK Biobank (up to 194 453 men) and outcome data from PRACTICAL (up to 79 148 cases and 61 106 controls, including 15 167 aggressive cancers), ORs were estimated using the inverse-variance weighted method. Free testosterone was associated with aggressive disease in MR analyses (OR per 1 SD = 1.23, 95% CI = 1.08-1.40). In blood-based analyses there was no association with aggressive disease overall, but there was heterogeneity by age at blood collection (OR for men aged <60 years 1.14, CI = 1.02-1.28; Phet = .0003: inverse association for older ages). Associations for free testosterone were positive for overall prostate cancer (MR: 1.20, 1.08-1.34; blood-based: 1.03, 1.01-1.05) and early-onset prostate cancer (MR: 1.37, 1.09-1.73; blood-based: 1.08, 0.98-1.19). SHBG and total testosterone were inversely associated with overall prostate cancer in blood-based analyses, with null associations in MR analysis. Our results support free testosterone, rather than total testosterone, in the development of prostate cancer, including aggressive subgroups

Differential activation of jnk1 isoforms by trail receptors modulate apoptosis of colon cancer cell lines

Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis on binding to its receptors, death receptor 4 and 5 (DR4, DR5). TRAIL can also activate c-Jun N-terminal kinase (JNK) through the adaptor molecules, TNF receptor-associated factor 2 (TRAF2) and receptor-interacting protein (RIP). The role of JNK in TRAIL-induced tumour cell apoptosis is unclear. In this study, we demonstrate that JNK is activated by TRAIL in colon cancer cells. Inhibition of JNK with L-JNKI reduced rhTRAIL-induced cell death but enhanced cell death induced by selective activation of DR4 or DR5. This difference was unrelated to receptor internalisation or differential activation of c-Jun, but activation of different JNK isoforms. Our data demonstrate that JNK1, but not JNK2 is activated by rhTRAIL in the examined colon cancer cell lines. Although rhTRAIL activated both the long and short isoforms of JNK1, selective activation of DR4 or DR5 led to predominant activation of the short JNK1 isoforms (JNK1 alpha 1 and/or JNK1 beta 1). Knockdown of JNK1 alpha 1 by shRNA enhanced apoptosis induced by TRAIL, agonistic DR4 or DR5 antibodies. On the other hand, knockdown of the long JNK1 isoforms (JNK1 alpha 2 and JNK1 beta 2) had the opposite effect; it reduced TRAIL-induced cell death. These data indicate that the short JNK1 isoforms transmit an antiapoptotic signal, whereas the long isoforms (JNK1 alpha 2 or JNK1 beta 2) act in a proapoptotic manner