6. REFERENCES
Bruce, M.E., Will, R.G., Ironside, J.W., McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H., & Bostock, C.J. (1997) Transmissions to mice indicate that new variant CJD is caused by the BSE agent. Nature 389 498-501.
Collinge, J., Hill, A.F., Desbruslais, M., Joiner, S., Sidle, K.C.L. and Gowland, I. (1997) The same prion strain causes vCJD and BSE. Nature 389 448-450.
Crystal Ball Version 4.0; Decisioneering Inc, Denver, Colorado (www.decisioneering.com ).
Diringer, H., (1999) Bovine spongiform Encephalopathy (BSE) and Public Health. In Aggett, P.J., Kuiper,H.A., (Eds) 1999. Risk Assessment in the food chain of children. Nestlé Nutrition Worksop Series, 44, 225-233. Nestlé Ltd,, Vevey/Lippncott Williams & Wilkins Publishers, Philadelphia.
DNV (1997a): “Assessment of risk from Possible BSE Infectivity in Dorsal Root Ganglia”, Report to the Ministry of Agriculture Fisheries and Food and the Spongiform Encephalopathy Advisory Committee, Det Norske Veritas C7831, December 1997.
DNV (1997b): “Overview of Risks from BSE via Environmental Pathways”, Report to Environment Agency, Det Norske Veritas C7243, June 1997.
Scientific Steering Committee, EC (2000) Opinion: Oral Exposure to Humans of the BSE Agent: Infective Dose and Species Barrier Adopted by the SSC at its meeting on the 13th - 14th April 2000.
Wells, G.A.H. et al (1998): “Preliminary Observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update”, The Veterinary Record 142, 103-106.