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Volume 25, Number 1—January 2019
Research

Variable Protease-Sensitive Prionopathy Transmission to Bank Voles

Romolo Nonno1, Silvio Notari1, Michele Angelo Di Bari, Ignazio Cali, Laura Pirisinu, Claudia d’Agostino, Laura Cracco, Diane Kofskey, Ilaria Vanni, Jody Lavrich, Piero Parchi, Umberto Agrimi, and Pierluigi GambettiComments to Author 
Author affiliations: Istituto Superiore di Sanità, Rome, Italy (R. Nonno, M.A. Di Bari, L. Pirisinu, C. d’Agostino, I. Vanni, U. Agrimi); Case Western Reserve University, Cleveland, Ohio, USA (S. Notari, I. Cali, L. Cracco, D. Kofskey, J. Lavrich, P. Gambetti); University of Bologna, Bologna, Italy (P. Parchi); Istituto delle Scienze Neurologiche di Bologna, Bologna (P. Parchi)

Main Article

Figure 5

Glycoform ratio of protease-resistant, disease-related prion protein (resPrPD) in phenotypes T1 and T2. The ratio of resPrPD associated with T1 (T1 109I) was 48% for diglycosylated, 44% for monoglycosylated, and 8% for unglycosylated conformers and significantly differed in each glycoform from the 17%, 63%, and 20% corresponding ratio of T2 (T2 109I). *p<0.0001; †p<0.005; ‡p<0.05). Glycoform ratios of T1 109I and T1 109M as well as that of type 1 control (from bank voles 109I inoculated

Figure 5. Glycoform ratio of protease-resistant, disease-related prion protein (resPrPD) in phenotypes T1 and T2. The ratio of resPrPD associated with T1 (T1 109I) was 48% for diglycosylated, 44% for monoglycosylated, and 8% for unglycosylated conformers and significantly differed in each glycoform from the 17%, 63%, and 20% corresponding ratio of T2 (T2 109I). *p<0.0001; †p<0.005; ‡p<0.05). Glycoform ratios of T1 109I and T1 109M as well as that of type 1 control (from bank voles 109I inoculated with sporadic Creutzfeldt-Jakob disease MV1 and used as human type 1 controls) did not significantly differ from each other. Each bar represents mean ± SD of n = 4 for T1 109M, n = 6 for T1 109I, n = 6 for T2, and n = 2 for type 1 control.

Main Article

1These authors contributed equally to this article.

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