| PubMed |
Abstract |
RScore(About this table) |
| 9572563 |
Purdey M: High-dose exposure to systemic phosmet insecticide modifies the phosphatidylinositol anchor on the prion protein: the origins of new variant transmissible spongiform encephalopathies?. Med Hypotheses. 1998 Feb;50(2):91-111.
|
162(2,2,2,2) |
Details |
| 8735882 |
Purdey M: The UK epidemic of BSE: slow virus or chronic pesticide-initiated modification of the prion protein? Part 2: An epidemiological perspective. Med Hypotheses. 1996 May;46(5):445-54.
An alternative hypothesis is proposed that cites exposure of the bovine embryo to various specific high-dose lipophilic formulations of organophosphates, such as the high-dose phthalimide containing organophosphate phosmet, (which were applied compulsorily and exclusively in the UK during the 1980s/early 1990s) as the primary trigger that initiated the deformation of prion protein and the onset of the bovine spongioform encephalopathy epidemic. |
85(1,1,1,5) |
Details |
| 12184497 |
Shaw I, Berry C, Lane E, Fitzmaurice P, Clarke D, Holden A: Studies on the putative interactions between the organophosphorus insecticide Phosmet and recombinant mouse PrP and its implication in the BSE epidemic. Vet Res Commun. 2002 Jun;26(4):263-71.
It has been suggested that exposure of cattle to the ectoparasiticide Phosmet in the 1980s caused a conformational change in the cellular prion protein (PrP (C)) to form the BSE prion (PrP (SC)), which initiated the epidemic of bovine spongiform encephalopathy (BSE). |
6(0,0,1,1) |
Details |
| 9631435 |
Gordon I, Abdulla EM, Campbell IC, Whatley SA: Phosmet induces up-regulation of surface levels of the cellular prion protein. Neuroreport. 1998 May 11;9(7):1391-5.
|
6(0,0,1,1) |
Details |