Detection and correction of inclination shallowing in deep sea sediments using the anisotropy of anhysteretic remanence

Paleomagnetic data from recent Pleistocene to recent deep sea sediments from the continental rise of eastern North America exhibit a cyclical inclination shallowing, up to 30° with respect to the geocentric axial dipole value. This shallowing is strongly correlated with a ratio of anhysteretic remanent magnetization (ARM) anisotropy determined from a four position ARM anisotropy method. It is therefore proving that inclination variations in these cores are not due to paleosecular variation but in part to a bias in the remanence recording processes linked to depositional anisotropy. This study suggests that ARM anisotropy could provide a method to identify and correct for inclination shallowing in natural sediments

Skopos Theory as an Extension of Rhetoric

This essay, which pertains to translation studies, presents a reflection aiming at defining intersections between the areas covered respectively by rhetoric and by skopos theory, which, in the field of translation studies, is one of the most frequently used theoretical frameworks that structures practice, and therefore teaching. It aims to lay the foundations of a translatorial theoretical framework based on an extension of the skopos model including the stylistic elements of classical rhetoric, and perhaps also on an extension of the rhetorical model to embrace a wide range of text types

Reprogramming into pancreatic endocrine cells based on developmental cues.

Due to the increasing prevalence of type 1 diabetes and the complications arising from actual therapies, alternative treatments need to be established. In order to compensate the beta-cell deficiency associated with type 1 diabetes, current research focuses on new strategies to generate insulin-producing beta-cells for transplantation purpose, including the differentiation of stem or progenitor cells, as well as the transdifferentiation of dispensable mature cell types. However, to successfully force specific cells to adopt a functional beta-cell fate or phenotype, a better understanding of the molecular mechanisms underlying beta-cell genesis is required. The present short review summarizes the hitherto known functions and interplays of several key factors involved in the development of the different endocrine cell lineages during pancreas morphogenesis, as well as their potential to direct the generation of beta-cells. Furthermore, an emphasis is made on beta-cell regeneration and the determinants implicated

Pax4 and Arx Represent Crucial Regulators of the Development of the Endocrine Pancreas

The development of the endocrine pancreas is under the control of highly orchestrated, cross-interacting transcription factors. Pancreas genesis is initiated by the emergence of a Pdx1/Ptf1a marked territory at the foregut/midgut junction. A small fraction of pancreatic fated cells activates the expression of the bHLH transcription factor Ngn3 triggering the endocrine cell program, thus giving rise to beta-, alpha-, delta-, PP-, and epsilon-cells, producing insulin, glucagon, somatostatin, pancreatic polypeptide, and ghrelin, respectively. Two transcription factors, Pax4 and Arx, play a crucial role in differential endocrine cell subtype specification. They were shown to be necessary and sufficient to endow endocrine progenitors with either a beta- or alpha-cell destiny. Interestingly, whereas the forced expression of Arx in beta-cells converts these into cells exhibiting alpha- and PP-cell characteristics, the sole expression of Pax4 in alpha-cells promotes alpha-cell-neogenesis and the acquisition of beta-cell features, the resulting beta-like cells being capable of counteracting chemically induced diabetes. Gaining new insights into the molecular mechanisms controlling Pax4 and Arx expression in the endocrine pancreas may therefore pave new avenues for the therapy of diabetes.</jats:p

« Vague rose » et syndicalisme : enseignements des expériences argentine et brésilienne

Cet article propose une analyse comparative de l’action des syndicats argentins et brésiliens pendant la période appelée « vague rose », soit celle durant laquelle un grand nombre de gouvernements progressistes furent au pouvoir en Amérique du Sud, ainsi qu’à la fin de celle-ci, quand des partis politiques de droite reviennent au pouvoir. À partir d’un cadre d’analyse ancré dans l’économie politique critique et le néo-institutionnalisme historique, l’approche comparée permet de faire ressortir la résilience des dynamiques corporatistes, mais aussi leurs spécificités nationales, induites par des héritages politiques et juridiques distincts. L’implantation différenciée des syndicats argentins et brésiliens dans les milieux de travail, ainsi que leurs rapports distincts à la scène partisane et à l’unité syndicale expliquent en grande partie les différences observées au moment de la chute des gouvernements progressistes.This article offers a comparative analysis of Argentina and Brazil’s labour movement during and immediately after the “Pink Tide”, a period during which most South American countries elected progressive governments. We adopt an analytical framework combining critical political economy and historical neo-institutionalism that points to the resilience of corporatist dynamics but also to their domestic specificities, due to divergent political and legal legacies. The contrasting implementations of Argentinean and Brazilian unions in workplaces, as well as their relations to political parties and to organizational unity explain most of the differences observed after the fall of the progressive governments in their respective countries

Arx and Nkx2.2 compound deficiency redirects pancreatic alpha- and beta-cell differentiation to a somatostatin/ghrelin co-expressing cell lineage

<p>Abstract</p> <p>Background</p> <p>Nkx2.2 and Arx represent key transcription factors implicated in the specification of islet cell subtypes during pancreas development. Mice deficient for <it>Arx </it>do not develop any alpha-cells whereas beta- and delta-cells are found in considerably higher numbers. In <it>Nkx2.2 </it>mutant animals, alpha- and beta-cell development is severely impaired whereas a ghrelin-expressing cell population is found augmented.</p> <p>Notably, <it>Arx </it>transcription is clearly enhanced in <it>Nkx2.2</it>-deficient pancreata. Hence in order to precise the functional link between both factors we performed a comparative analysis of <it>Nkx2.2/Arx </it>single- and double-mutants but also of <it>Pax6</it>-deficient animals.</p> <p>Results</p> <p>We show that most of the ghrelin⁺cells emerging in pancreata of <it>Nkx2.2</it>- and <it>Pax6</it>-deficient mice, express the alpha-cell specifier Arx, but also additional beta-cell related genes. In <it>Nkx2.2</it>-deficient mice, Arx directly co-localizes with iAPP, PC1/3 and Pdx1 suggesting an Nkx2.2-dependent control of <it>Arx </it>in committed beta-cells. The combined loss of <it>Nkx2.2 </it>and <it>Arx </it>likewise results in the formation of a hyperplastic ghrelin⁺cell population at the expense of mature alpha- and beta-cells. Surprisingly, such <it>Nkx2.2^-/-Arx^-</it>ghrelin⁺cells also express the somatostatin hormone.</p> <p>Conclusions</p> <p>Our data indicate that Nkx2.2 acts by reinforcing the transcriptional networks initiated by Pax4 and Arx in early committed beta- and alpha-cell, respectively. Our analysis also suggests that one of the coupled functions of Nkx2.2 and Pax4 is to counteract <it>Arx </it>gene activity in early committed beta-cells.</p

The Homeodomain-Containing Transcription Factors Arx and Pax4 Control Enteroendocrine Subtype Specification in Mice

Intestinal hormones are key regulators of digestion and energy homeostasis secreted by rare enteroendocrine cells. These cells produce over ten different hormones including GLP-1 and GIP peptides known to promote insulin secretion. To date, the molecular mechanisms controlling the specification of the various enteroendocrine subtypes from multipotent Neurog3+ endocrine progenitor cells, as well as their number, remain largely unknown. In contrast, in the embryonic pancreas, the opposite activities of Arx and Pax4 homeodomain transcription factors promote islet progenitor cells towards the different endocrine cell fates. In this study, we thus investigated the role of Arx and Pax4 in enteroendocrine subtype specification. The small intestine and colon of Arx- and Pax4-deficient mice were analyzed using histological, molecular, and lineage tracing approaches. We show that Arx is expressed in endocrine progenitors (Neurog3+) and in early differentiating (ChromograninA−) GLP-1-, GIP-, CCK-, Sct- Gastrin- and Ghrelin-producing cells. We noted a dramatic reduction or a complete loss of all these enteroendocrine cell types in Arx mutants. Serotonin- and Somatostatin-secreting cells do not express Arx and, accordingly, the differentiation of Serotonin cells was not affected in Arx mutants. However, the number of Somatostatin-expressing D-cells is increased as Arx-deficient progenitor cells are redirected to the D-cell lineage. In Pax4-deficient mice, the differentiation of Serotonin and Somatostatin cells is impaired, as well as of GIP and Gastrin cells. In contrast, the number of GLP-1 producing L-cells is increased concomitantly with an upregulation of Arx. Thus, while Arx and Pax4 are necessary for the development of L- and D-cells respectively, they conversely restrict D- and L-cells fates suggesting antagonistic functions in D/L cell allocation. In conclusion, these finding demonstrate that, downstream of Neurog3, the specification of a subset of enteroendocrine subtypes relies on both Arx and Pax4, while others depend only on Arx or Pax4