Et quand nous sommes entrés dans Rome. L'énigme de la fin du livre des Actes (28,16-31)

Pour composer la fin des Actes (28,16-31), Luc s'est inspiré d'un procédé littéraire que l'on retrouve à la fois dans l'oeuvre d'Homère, dans la poétique gréco-romaine et dans l'historiographie grecque (Hérodote): la suspension narrative. Il s'agit d'une rhétorique du silence, qui conduit le lecteur à porter lui-même le récit à son achèvement. Le souvenir de la mort de Paul est réinterprété par l'inversion du schéma du procès (Ac 27,28); dans le sommaire conclusif (28,30-31) se déploie le portrait du pasteur exemplaire, anticipation du programme missionnaire des Actes.

The Enigma of the Silent Closing of Acts (28,16-31)

(Résumé de l'ouvrage) In the first volume of this long-anticipated collection by Moessner and Tiede, seventeen leading scholars of antiquity present an amazing "sea change" of opinion that Luke is indeed the interpreter of Israel. The book represents an unprecedented international consensus that the Hellenistic author Luke composed a carefully crafted narrative in two parts to claim Jesus of Nazareth as Israel's true heritage and enduring legacy to the world. Part One explores the nature of Luke's prologues and his intention to write a narrative of "events brought to fruition," using the narrative conventions and audience expectations of the Greco-Roman milieu. Part Two illuminates the relation of Luke's second "volume" to the first by inquiring about the consistency and coherence of his narrative-thematic strategies in retelling the story of Israel's legacy of "the Christ." Whether Luke completed Acts, the larger role of Paul and, most significantly, the meaning of Israel by the end of Acts are approached from new perspectives and charged with provocative insights. In addition to the volume editors, the contributors include L. Alexander, D. Schmidt, V. Robbins, C. Thornton, R. Pervo, W. Kurz, C. Holladay, G. Sterling, D. Balch, E. Plmacher, Charles H. Talbert, J.H. Hayes, D. Marguerat, M. Wolter, R. Tannehill, and I. H. Marshall.

40Ar/39Ar dating of Penninic Front tectonic displacement (W Alps) during the Lower Oligocene (31-34 Ma)

Direct absolute dating of the Penninic Frontal Thrust tectonic motion is achieved using the Ar-40/Ar-39 technique in the Pelvoux Crystalline Massif (Western Alps). The dated phengites were formed syn-kinematically in shear zones. They underline the brittle-ductile stretching lineation, pressure-shadow fibres and slickensides consistent with underthrusting of the European continental slab below the propagating Penninic Thrust. Chlorite-phengite thermobarometry yields 10-15 km and T similar to 280 degrees C, while Ar-40/Ar-39 phengite ages mainly range between 34 and 30 Ma, with one younger age at 27 Ma. This Early Oligocene age range matches a major tectonic rearrangement of the Alpine chain. Preservation of prograde Ar-40/Ar-39 ages is ascribed to passive exhumation of the Pelvoux shear zone network, sandwiched between more external thrusts and the Penninic Front reactivated as an E-dipping detachment fault. Partial resetting in the Low Temperature part of argon spectra below 24 Ma is ascribed to brittle deformation and alteration of phengites.

Human natural Treg microRNA signature: role of microRNA-31 and microRNA-21 in FOXP3 expression.

Treg are the main mediators of dominant tolerance. Their mechanisms of action and applications are subjects of considerable debate currently. However, a human microRNA (miR) Treg signature has not been described yet. We investigated human natural Treg and identified a signature composed of five miR (21, 31, 125a, 181c and 374). Among those, two were considerably under-expressed (miR-31 and miR-125a). We identified a functional target sequence for miR-31 in the 3' untranslated region (3' UTR) of FOXP3 mRNA. Using lentiviral transduction of fresh cord blood T cells, we demonstrated that miR-31 and miR-21 had an effect on FOXP3 expression levels. We showed that miR-31 negatively regulates FOXP3 expression by binding directly to its potential target site in the 3' UTR of FOXP3 mRNA. We next demonstrated that miR-21 acted as a positive, though indirect, regulator of FOXP3 expression. Transduction of the remaining three miR had no direct effect on FOXP3 expression or on the phenotype and will remain the subject of future investigations. In conclusion, not only have we identified and validated a miR signature for human natural Treg, but also unveiled some of the mechanisms by which this signature was related to the control of FOXP3 expression in these cells.

Estimating and explaining the effect of education and income on head and neck cancer risk : INHANCE consortium pooled analysis of 31 case-control studies from 27 countries

Low socioeconomic status has been reported to be associated with head and neck cancer risk. However, previous studies have been too small to examine the associations by cancer subsite, age, sex, global region, and calendar time, and to explain the association in terms of behavioural risk factors. Individual participant data of 23,964 cases with head and neck cancer and 31,954 controls from 31 studies in 27 countries pooled with random effects models. Overall, low education was associated with an increased risk of head and neck cancer (OR = 2·50; 95%CI 2·02- 3·09). Overall one-third of the increased risk was not explained by differences in the distribution of cigarette smoking and alcohol behaviours; and it remained elevated among never users of tobacco and non-drinkers (OR = 1·61; 95%CI 1·13 - 2·31). More of the estimated education effect was not explained by cigarette smoking and alcohol behaviours: in women than in men, in older than younger groups, in the oropharynx than in other sites, in South/Central America than in Europe/North America, and was strongest in countries with greater income inequality. Similar findings were observed for the estimated effect of low vs high household income. The lowest levels of income and educational attainment were associated with more than 2-fold increased risk of head and neck cancer, which is not entirely explained by differences in the distributions of behavioural risk factors for these cancers, and which varies across cancer sites, sexes, countries, and country income inequality levels. © 2014 Wiley Periodicals, Inc.