By Committee on Transmissible Spongiform Encephalopathies: Assessment of Relevant Science
Period in-between record of the Institute of Medicine's Committee on Transmissible Spongiform Encephalopathies: evaluation of proper technological know-how, convened to supply suggestion to the U.S. division of security concerning prion illness. specializes in the learn had to enhance diagnostics for prion ailments and discusses prion learn infrastructure matters. Softcover.
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1983. Pathogenesis of mouse scrapie. Evidence for direct neural spread of infection to the CNS after injection of sciatic nerve. Journal of the Neurological Sciences 61(3):315-325. Klatzo I, Gajdusek DC, Zigas V. 1959. Pathology of kuru. Laboratory Investigation 8:799-847. Klitzman RL, Alpers MP, Gadjusek DC. 1984. The natural incubation period of kuru and the episodes of transmission in three clusters of patients. Neuroepidemiology 3:320. 38 ADVANCING PRION SCIENCE Kretzschmar HA, Honold G, Seitelberger F, Feucht M, Wessely P, Mehraein P, Budka H.
1967; Griffith 1967; Lewin, 1972; Pattison and Jones, 1967). Until Prusiner’s entry into the field, however, no other investigator had provided compelling data to support his hypothesis. Applying advanced biochemical techniques, Prusiner generated a purified infectious scrapie preparation that yielded a peptide fragment. By determining the nucleic acid sequence that encoded the peptide, he located the gene where the sequence for the peptide was embedded, allowing him to decipher the full-length protein PrP (the prion protein) (Brown and Bradley, 1998).
1. Rohwer RG. 1991. ” Current Topics in Microbiology and Immunology 172:195-232. Scott MR, Will R, Ironside J, Nguyen HO, Tremblay P, DeArmond SJ, Prusiner SB. 1999. Compelling transgenetic evidence for transmission of bovine spongiform encephalopathy prions to humans. Proceedings of the National Academy of Sciences of the United States of America 96(26):15137-15142. Telling GC, Scott M, Mastrianni J, Gabizon R, Torchia M, Cohen FE, DeArmond SJ, Prusiner SB. 1995. Prion propagation in mice expressing human and chimeric PrP transgenes implicates the interaction of cellular PrP with another protein.