Rachmaninoff, one of the greatest Romantic composer of the turn of 19-20 centuries, characterized by his lyrical melody, rich changing chords, and others unique personal style, is considered an important late Romantic composer. After the October Revolution of 1917, Rachmaninoff left Russia to begin a new life in the United States, was a significant turning point in Rachmaninoff's career of music composition. After that, he lived in the United States as a pianist, and devoted himself to transcriptions. Kreisler, creator of ¡§Liebesfreud,¡¨ was a violinist. Besides performance, he also created some of the sketches as the concert repertoire. He composed ¡§Liebesfreud¡¨ in the style of the Austrian Landler. Rachmaninoff and Kreisler met and became friendly in the United States, and later Rachmaninoff transcribed the piece to memorize their friendship. He not only reedited of original pieces and arrangements for piano with great skill in piano but also remarked the transcriptions his personal style to enrich it with artiness and skills. The study aims to explore Rachmaninoff¡¦s piano transcription ¡§Liebesfreud¡¨ to understand its adaptation practices. We finally discuss the innovation and meaning of the transcriptions by Rachmaninoff.

Thèse de doctorat : Aspects moléculaires et cellulaires de la biologie : Strasbourg 1 : 2007. / Titre provenant de l'écran-titre. Bibliogr. p. 188-205.

Thesis (M. Phil.)--University of Hong Kong, 2010. / Includes bibliographical references (leaves 103-114). Also available in print.

Source: Dissertation Abstracts International, Volume: 69-07, Section: B, page: 4115. Advisers: Mary Ann Smith; Benoit de Crombrugghe. Includes bibliographical references.

Previously a t(2;14)(p13;q32) translocation was characterized in four unusually aggressive cases of B cell chronic lymphocytic leukemia (B-CLL). A gene located near the 2p13 breakpoint, B cell lymphoma/leukemia 11A (BCL11A), was shown to overexpress 3 isoforms (BCL11A-XL, L and S). Bcl11a knockout mice are severely impaired in B cell development at the early (pro-B) stage. I have further characterized BCL11A, focusing on the most abundant and evolutionarily conserved isoform, BCL11A-XL (XL). I demonstrated that XL resides in the nuclear matrix, is modified by ubiquitination, and is destabilized by B cell antigen receptor ligation. I identified domains within XL required for its localization within nuclear paraspeckles and for its transcriptional repression. While BCL11A-XL represses model promoters in non-B cells, its biologically relevant targets in B lymphocytes were unknown. I have identified and confirmed a number of XL targets which are both up- and down-regulated by XL over-expression in B cell lines. A number of these genes have been implicated in B cell function, including the V(D)J recombination activating (RAG) genes. Both RAG1 and RAG2 transcripts were up-regulated by XL. XL binds to the RAG1 promoter and RAG enhancer (Erag) in vivo as well as in vitro. Unexpectedly, XL repressed RAG1 transcription in non-B cells, indicating that additional B cell-specific factors are required for activation. Overexpression of XL in a V(D)J recombination-competent pre-B cell line markedly induced RAG expression and VDJ recombination. IRF4 and IRF8, transcription factors previously shown to be required for early B cell development, were also induced by BCL11A-XL. I propose that the early B cell progenitor block in Bcl11a knockout mice is, at least in part, a direct result of BCL11A-XL regulation of V(D)J recombination. Further experiments are required to establish how other XL targets promote B cell lineage development and how malignant transformation such as in B-CLL may corrupt BCL11A function.

published_or_final_version / abstract / toc / Zoology / Master / Master of Philosophy

I present a method that regroups cis-regulatory modules by shared sequences motifs. The goal of this approach is to search for clusters of modules that may share some function, using only sequence similarity. The proposed similarity measure is based on a variable-order Markov model likelihood scoring of sequences. I also introduce an extension of the variable-order Markov model which could better perform the required task. Results. I show that my method may recover subsets of sequences sharing a pattern in a set of generated sequences. I found that the proposed approach is successful in finding groups of modules that shared a type of transcription factor binding site.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karol Inst., 2003. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 4 uppsatser.