Diss.--Hamburg, 2001. / Bibliogr. p. 371-397.

Diss.--Geschichtswissenschaft--Mainz--Johannes Gutenberg-Universität, 1999. / Bibliogr. p. 250-272. Index.

Texte remanié de: Thesis Ph. D.--University of Leeds, GB. / Bibliogr. p. 270-284.

Texte remanié de: Thèse de doctorat--Études littéraires--Paris 7, 1996. / Bibliogr. p. 264-269.

Texte remanié de: Th. doct.--Litt. française--Caen, 2002. Titre de soutenance : L'écriture autobiographique de l'oeuvre de J.-M. G. Le Clézio. / Bibliogr. p. 311-312. Bibliogr. des oeuvres de J.-M. G. Le Clézio p. 309-311.

Texte remanié de: Th. 3e cycle--Litt. française--Paris 4, 1986. Titre de soutenance : La Grande Mademoiselle mémorialiste : une autobiographie dans le temps. / Bibliogr. p. 403-420. Index.

Texte remanié de: Thèse de doctorat--Art et archéologie--Paris 1, 1996. Titre de soutenance : La scène initiale de l'incarnation à Byzance et dans l'art occidental à la fin du Moyen âge. / Résumé en grec. Bibliogr. p. 405-427.

Thesis (Ph. L.)--Catholic University of America, 2008. / Includes bibliographical references (leaves 81-83).

The present study is focused on understanding the aetiology of the human clubfoot deformity. Although this pathology has been studied since Classical Antiquity, the mechanisms that lead to this abnormality in new-born patients remain elusive. Clubfoot is a deformity of one or both feet present at birth, in which the foot is abnormally positioned in a hand-like position, that is, the foot is turned and rotated inwards while pointing down; and is resistant to any further movements. Very little is known about the aetiology and genetics of clubfoot in the human population. Only recently, mutations in the PITX1 gene have been associated with a small number of patients. Because the genetic basis is not understood and the phenotypic observations are complex and variable in human patients, many mechanisms have been proposed to explain clubfoot. In this study, these pressing questions were addressed using the peroneal muscular atrophy (pma) mouse, a spontaneous mutant that has been shown to be a surprisingly good model for clubfoot, recapitulating the key features of the human phenotype. In order to confirm that the pma mouse is in fact an idiopathic model of clubfoot, it was important to understand if the pma clubfoot-like phenotype occurs in isolation or within a syndromic pathology. In addition to clubfoot, it was found that these animals show a retinal degeneration phenotype. However, this phenotype was associated with the Pde6brd1 mutation, suggesting that clubfoot occurs independently of the retinal phenotype and thus the pma is a good model for human idiopathic clubfoot. Clubfoot in the pma mouse has been associated with the observed failure of the foot rotation during embryonic development. This defect is thought to result from the extensive regional muscular atrophy that occurs at earlier stages. The peroneal nerve is also absent in the adult pma mouse, a defect that has remained unexplored. As such, this neuronal defect was studied to understand the reason for the peroneal nerve absence in the adult animals. The results indicate that the nerve fails to branch from the developing sciatic nerve during embryogenesis and is unable to innervate its target muscles. This abnormal branching process is associated with a neural growth delay. In respect to the genetics of the pma, it was not possible to identify the exact mutation that is responsible for the inheritance of the clubfoot phenotype. However, strong evidence was found in favour of a regulatory mutation resulting in over-expression of the gene Limk1, which encodes for a kinase involved in neuronal guidance and growth. Further work was performed on chicken embryos to understand the foot rotation process. By removing defined regions of muscle tissue from the developing limb zeugopod, it was possible to conclude that lack of function of the anterior and lateral hindlimb tissue is associated with abnormal foot rotation, resulting in a similar phenotype to clubfoot. By examining the affected muscles, it was possible to identify the tibialis cranialis and the peroneus longus muscles as relevant candidates involved in clubfoot aetiology. In summary, the evidence presented here suggests that the pma clubfoot results from a regulatory mutation that induces Limk1 over-expression and nerve growth delay. This in turn prevents the proper development of the peroneal nerve, resulting in the degeneration of its target muscle tibialis anterior and peroneus longus muscles. This degeneration will interfere with foot rotation and result in clubfoot. Thus, the results described by this work are of utmost importance for the understanding of the clubfoot pathology, as it supports a neuro-muscular aetiology dependent on a physical dynamic equilibrium of muscular forces. This is of scientific interest as it expands the current understanding of the foot rotation and the integrative interactions during the limb organogenesis; poorly described developmental processes, and of clinical relevance as it establishes important ideas and concepts for study in human patients.

Within the body of "migrant" literature, the work of Marie-Celie Agnant is distinguished by its strong testimonial nature. The author herself ascribes a certain instrumental role to literature; through her fictional narratives, Agnant bears witness to the collective experiences of women in Haiti and also of female Haitian immigrants in Montreal. What, then, of the function or literary value of her work? This thesis responds to this question through the study of three works by Marie-Celie Agnant: La Dot de Sara (1995), Le Livre d'Emma (2001), and Le Silence comme le sang (1997). The analysis of the complex relationship between testimony and fiction in Agnant's writing leads to a reflection on the specific character of socially impelled female literature: women writers are driven by the imperative of memory and the desire to convey their occulted history.