THREE AMERICAN INTERNATIONAL PIANO COMPETITIONS: THE PIANO WORKS THEY COMMISSIONED BETWEEN 1962 AND 2012

Over a period of 50 years—between 1962 and 2012—three preeminent American piano competitions, the Van Cliburn International Piano Competition, the University of Maryland International Piano Competition/William Kapell International Piano Competition and the San Antonio International Piano Competition, commissioned for inclusion on their required performance lists 26 piano works, almost all by American composers. These compositions, works of sufficient artistic depth and technical sophistication to serve as rigorous benchmarks for competition finalists, constitute a unique segment of the contemporary American piano repertoire. Although a limited number of these pieces have found their way into the performance repertoire of concert artists, too many have not been performed since their premières in the final rounds of the competitions for which they were designed. Such should not be the case. Some of the composers in question are innovative titans of 20th-century American music—Samuel Barber, Aaron Copland, Leonard Bernstein, John Cage, John Corigliano, William Schuman, Joan Tower and Ned Rorem, to name just a few—and many of the pieces themselves, as historical touchstones, deserve careful examination. This study includes, in addition to an introductory overview of the three competitions, a survey of all 26 compositions and an analysis of their expressive characteristics, from the point of view of the performing pianist. Numerous musical examples support the analysis. Biographical information about the composers, along with descriptions of their overall musical styles, place these pieces in historical context. Analytical and technical comprehension of this distinctive and rarely performed corner of the modern classical piano world could be of inestimable value to professional pianists, piano pedagogues and music educators alike.

MECHANISM OF UPREGULATION OF PHOSPHATIDYLCHOLINE SYNTHESIS DURING PICORNAVIRUS INFECTION AND ITS ROLE IN THE DEVELOPMENT OF VIRAL REPLICATION ORGANELLES

Picornaviruses are a group of human and animal pathogens capable of inflicting serious public health diseases and economic burdens. Treatments options through vaccines for prevention or antivirals to cure infection are not available for the vast majority of these viruses. These shortcomings, in the development of vaccines or antivirals therapeutic, are linked to the genetic diversity and to an incomplete understanding of the biology of these viruses. Despite the diverse host range, this group of positive-strand RNA viruses shares the same replication mechanisms, including the development of membranous structures (replication organelles) in the cytoplasm of infected cells. The development of these membranous structures, which serve as sites for the replication of the viral RNA genome, has been linked to the hijacking of elements of the cellular membrane metabolism pathways. Here we show that upon picornavirus infection, there is a specific activation of acyl-CoA synthetase enzymes resulting in strong import and accumulation of long chain fatty acids in the cytoplasm of infected cells. We show that the newly imported fatty acids serve as a substrate for the upregulation of phosphatidylcholine synthesis required for the structural development of replication organelles. In this work, we identified that acyl-CoA synthetase long chain 3 (ACSL3) is required for the upregulation of lipids syntheses and the replication of poliovirus. We have shown that the poliovirus protein 2A was required but not sufficient for the activation of import of long chain fatty acids in infected cells. We demonstrated that the fatty acid import is upregulated upon infection by diverse picornaviruses and that such upregulation is not dependent on activation of ER stress response or the autophagy pathways. In this work, we have demonstrated that phosphatidylcholine was required for the structural development of replication organelles. Phosphatidylcholine synthesis was dispensable for the production of infectious particles at high MOI but required at a low MOI for the protection of the replication complexes from the cellular innate immunity mechanisms.