140 research outputs found
Grammaticae hebraicae et chaldaicae, ex optimis quae hactenus prodierunt nova facilique methodo concinnata, tomus II : complectens syntaxim figuratam sive rhetoricam sacram, grammaticae chaldaicae compendium, nec non varia ad literaturam hebraicam spectantia, cum indicibus locupletissimis
Sign. : a-o\p4\s, p\p2\s, A-Z\p4\s, 2A-2Z\p4\s, 3A-3Z\p4\s, 4A-4Z\p4\s, 5A-5D\p4\sPort. con grab. xilLas ilustraciones xil. y cal
Grammaticae hebraicae et chaldaicae, ex optimis, quae hactenus prodierunt, nova facilique methodo concinnatae, tomus II : complectens syntaxim figuratam, sive rhetoricam sacram, grammaticae chaldaicae compendium, necnon varia ad literaturam hebraicam spectantia, cum indicibus locupletissimis
Copia digital : Google BooksLa segunda fecha consta en colofón, en verso de 5D\b4\sSign. : a-o\p4\s, p\p2\s, A-Z\p4\s, 2A-2Z\p4\s, 3A-3Z\p4\s, 4A-4Z\p4\s, 5A-5D\p4\sPortada con grabado xilográficoParte del texto a dos columnasLas ilustraciones xilográficas y calcográfica
Thomas Borrel, Amzat Boukari Yabara, Benoît Collombat, Thomas Deltombe (2021) - L\u27Empire qui ne veut pas mourir. Une histoire de la Françafrique
Critical review: Thomas Borrel, Amzat Boukari Yabara, Benoît Collombat, Thomas Deltombe, L’Empire qui ne veut pas mourir. Une histoire de la Françafrique, Paris, Seuil, 2021, 1008 p.Recensé : Thomas Borrel, Amzat Boukari Yabara, Benoît Collombat, Thomas Deltombe, L’Empire qui ne veut pas mourir. Une histoire de la Françafrique, Paris, Seuil, 2021, 1008 p.
Traduction : Louise Barré et Camille Evrard
A genetic mouse model for progressive ablation and regeneration of insulin producing beta-cells
<div><p>The putative induction of adult β-cell regeneration represents a promising approach for the treatment of type 1 diabetes. Toward this ultimate goal, it is essential to develop an inducible model mimicking the long-lasting disease progression. In the current study, we have established a novel β-cell ablation mouse model, in which the β-cell mass progressively declines, as seen in type 1 diabetes. The model is based on the β-cell specific genetic ablation of the transcription initiation factor 1A, TIF-IA, essential for RNA Polymerase I activity (TIF-IA<sup>Δ/Δ</sup>). Using this approach, we induced a slow apoptotic response that eventually leads to a protracted β-cell death. In this model, we observed β-cell regeneration that resulted in a complete recovery of the β-cell mass and normoglycemia. In addition, we showed that adaptive proliferation of remaining β-cells is the prominent mechanism acting to compensate for the massive β-cell loss in young but also aged mice. Interestingly, at any age, we also detected β-like cells expressing the glucagon hormone, suggesting a transition between α- and β-cell identities or <i>vice versa</i>. Taken together, the TIF-IA<sup>Δ/Δ</sup> mouse model can be used to investigate the potential therapeutic approaches for type 1 diabetes targeting β-cell regeneration.</p></div
Pancreatic beta-cells: From generation to regeneration.
The pancreas is composed of two main compartments consisting of endocrine and exocrine tissues. The majority of the organ is exocrine and responsible for the synthesis of digestive enzymes and for their transport via an intricate ductal system into the duodenum. The endocrine tissue represents less than 2% of the organ and is organized into functional units called islets of Langerhans, comprising alpha-, beta-, delta-, epsilon- and PP-cells, producing the hormones glucagon, insulin, somatostatin, ghrelin and pancreatic polypeptide (PP), respectively. Insulin-producing beta-cells play a central role in the control of the glucose homeostasis. Accordingly, absolute or relative deficiency in beta-cells may ultimately lead to type 1 and/or type 2 diabetes, respectively. One major goal of diabetes research is therefore to understand the molecular mechanisms controlling the development of beta-cells during pancreas morphogenesis, but also those underlying the regeneration of adult injured pancreas, and assess their significance for future cell-based therapy. In this review, we will therefore present new insights into beta-cell development with focus on beta-cell regeneration
The mouse orthologue of ARX, a gene mutated in several X-linked forms of mental retardation and epilepsy, is an early marker of most forebrain GABAergic neurons
L’empathie rationnelle : vers un nouveau paradigme traductionnel
This article sets out to show that translation, far from being a mere impersonation, is an activity involving a complex form of rational empathy. In order to do their work to the best of their abilities, translators must adopt an empathetic attitude not only toward the author of the source text, but also toward the text and the future reader whose knowledge skills he needs to consider in the same way the original author did.
Our text situates the translation process in a functionalist perspective and subordinates it to the preliminary establishment of a translation postulate (“postulat traductif”) in accordance with which the translator lays down a translation strategy based on the type of text, the origin of the text, for whom the text is intended as well the function of the text. At this stage, the translator seeks to achieve maximum objectivity based on rational empathy. 
As a rule, empathy in translation is associated with literary translation, in keeping with a lyrical view of the latter and with an inordinate focusing on the author. We will try to show that the empathy factor is a constant, whether the text be literary or pragmatic, and that rational empathy is an indispensable tool for all translators since few of them are in a position to both choose their texts and hope to feel a spontaneous emotional empathy with their author or text.
Lastly, we will see that a broad general culture, including both a knowledge of the source language and culture, combined with an acute awareness of one’s own culture, is an essential basis for rational empathy, and conditions the intercultural and communication skills of the translator. Seen from this angle, the translator must master the various linguistic codes, namely language levels and diatopic variations, which he must use in order to best fulfil his role as a translator according to the most efficient translation postulate.</jats:p
Sp8 controls the anteroposterior patterning at the midbrain-hindbrain border.
The specification of neuronal cell types in the developing neural tube is orchestrated by signaling centers. However, how patterned territories of the central nervous system (CNS) are organized into structures with appropriate size and shape is still unclear. We report that in the absence of the mouse transcription factor mBtd/Sp8, a posterior shift of the isthmic organizer (IsO) occurs, suggesting a crucial role for Sp8 in this process. In addition, large patches of cells ectopically expressing Fgf8, Otx2 and/or Wnt1 in the rostral hindbrain are detected in Sp8 mutant embryos. In this context, midbrain dopaminergic neurons are found posterior to the IsO. Furthermore, we provide evidence that cell proliferation in the mid- and hindbrain is tightly controlled by Sp8 activity. Our observations are consistent with a role for Sp8 in restricting Fgf8 expression at the Is
In vivo and in vitro tissue-specific expression of green fluorescent protein using the cre-lox system in mouse embryonic stem cells
Embryonic stem cells (ES) are pluripotent and may therefore serve as a source for the generation of specific cell types required for future therapies based on cell replacement. The isolation of defined cell populations from a certain lineage or tissue is a prerequisite for the analysis of the potential of such ES-derived cells in animal transplantation studies. Here, using the Cre/loxP system, we report the generation of murine ES cells conditionally expressing the hrGFP gene at the cell surface. Such ES cells can be differentiated in vitro into neurons displaying GFP activity in neurites. Transgenic mice derived from these ES cells permit the targeting of GFP-expression to specific tissues and provide material from the three germ layers suitable for molecular and biochemical analysis
A regulatory path associated with X-linked intellectual disability and epilepsy links KDM5C to the polyalanine expansions in ARX
Intellectual disability (ID) and epilepsy often occur together and have a dramatic impact on the development and quality of life of the affected children. Polyalanine (polyA)-expansion-encoding mutations of aristaless-related homeobox (ARX) cause a spectrum of X-linked ID (XLID) diseases and chronic epilepsy, including infantile spasms. We show that lysine-specific demethylase 5C (KDM5C), a gene known to be mutated in XLID-affected children and involved in chromatin remodeling, is directly regulated by ARX through the binding in a conserved noncoding element. We have studied altered ARX carrying various polyA elongations in individuals with XLID and/or epilepsy. The changes in polyA repeats cause hypomorphic ARX alterations, which exhibit a decreased trans-activity and reduced, but not abolished, binding to the KDM5C regulatory region. The altered functioning of the mutants tested is likely to correlate with the severity of XLID and/or epilepsy. By quantitative RT-PCR, we observed a dramatic Kdm5c mRNA downregulation in murine Arx-knockout embryonic and neural stem cells. Such Kdm5c mRNA diminution led to a severe decrease in the KDM5C content during in vitro neuronal differentiation, which inversely correlated with an increase in H3K4me3 signal. We established that ARX polyA alterations damage the regulation of KDM5C expression, and we propose a potential ARX-dependent path acting via chromatin remodeling.Loredana Poeta, Francesca Fusco, Denise Drongitis, Cheryl Shoubridge, Genesia Manganelli, Stefania Filosa, Mariateresa Paciolla, Monica Courtney, Patrick Collombat, Maria Brigida Lioi, Jozef Gecz, Matilde Valeria Ursini, and Maria Giuseppina Mian
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