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Volume 14, Number 9—September 2008

Research

Excretion of Transmissible Spongiform Encephalopathy Infectivity in Urine

Luisa Gregori, Gabor G. Kovacs, Irina Alexeeva, Herbert Budka, and Robert G. RohwerComments to Author 
Author affiliations: Veterans Affairs Medical Center, Baltimore, Maryland, USA (L. Gregori, I. Alexeeva, R.G. Rohwer); University of Maryland, Baltimore (L. Gregori, R.G. Rohwer); Medical University of Vienna, Vienna, Austria (G.G. Kovacs, H. Budka);

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Figure 2

Immunostaining for prion protein (PrP) in control and scrapie-infected hamsters. Deposition of disease-associated PrP is lacking in the brain (A), spleen (B), and kidneys (C,D) of control hamsters. Fine synaptic and plaque-like PrP immunoreactivity in the frontal cortex (E), granular immunoreactivity in the germinal center of spleen (F) and in the collecting tubules of kidneys (G,H) in a representative scrapie-infected animal. Original magnification ×200 for panels A, B, D, E, F, and H and ×40 for panels C and G.

Figure 2. Immunostaining for prion protein (PrP) in control and scrapie-infected hamsters. Deposition of disease-associated PrP is lacking in the brain (A), spleen (B), and kidneys (C,D) of control hamsters. Fine synaptic and plaque-like PrP immunoreactivity in the frontal cortex (E), granular immunoreactivity in the germinal center of spleen (F) and in the collecting tubules of kidneys (G,H) in a representative scrapie-infected animal. Original magnification ×200 for panels A, B, D, E, F, and H and ×40 for panels C and G.

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