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  • Neil Peart

    Canadian and American drummer (1952–2020)

    For the footballer, see Neil Peart (footballer).

    Neil Ellwood Peart (PEERT; September 12, 1952 – January 7, 2020) was a Canadian and American musician, known as the drummer, percussionist, and primary lyricist of the rock band Rush. He was known to fans by the nickname "the Professor",[1] derived from the Gilligan's Islandcharacter of the same name.[2] His drumming was renowned for its technical proficiency and his live performances for their exacting nature and stamina. Peart earned numerous awards for his musical performances, including an induction into the Modern DrummerReaders Poll Hall of Fame in 1983 at the age of thirty, making him the youngest person ever so honoured.[3]

    Peart was born in Hamilton, Ontario,[4] and grew up in Port Dalhousie (now part of St. Catharines). During adolescence, he floated between regional bands in pursuit of a career as a full-time drummer. After a discouraging stint in England, Peart returned home to concentrate on music where he joined Rush, a Toronto band, in mid-1974, six years after its formation. Together they released 19 studio albums, with 10 exceeding a million copies sold in the United States. Billboard lists the band third

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  • A nucleotide resolution map of Top2-linked DNA breaks in the yeast and human genome

    Introduction

    DNA topoisomerases are a broad and ubiquitous family of enzymes that tackle topological constraints to replication, transcription, the maintenance of genome structure and chromosome segregation in mitosis and meiosis1. Although the specific mechanisms by which this is accomplished vary considerably across the family, key aspects are shared: including single or double-strand DNA cleavage to form a transient covalent complex (CC), which allows alteration of the topology of the nucleic acid substrate prior to religation2. These processes are essential but carry with them a significant risk to genome stability because the CC may be stabilised as a permanent protein-linked DNA break by several physiological factors; such as the proximity of other DNA lesions, the collision of transcription and replication complexes, denaturation of the topoisomerase, or by the binding of small molecules that inhibit religation1,3. Topoisomerase-induced DNA strand breaks have been proposed to constitute a significant fraction of the total damage to genomic DNA per day, and have been linked to the genesis and development of various cancers4,5, including a subset of therapy-related acute myeloi