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Doe
Fri, Aug-22-03, 06:10
http://www.redflagsweekly.com/conferences/mad_cow/aug18_P-
urdey.html

Does the rogue ferrimagnetic metal co partner of the misfolded
prion protein serve as the infectious / transmissible
component in TSEs ?

This theory explains why the so called ‘hyperinfectious’
property of the prion is a misnomer. It is the toxic
ferrimagnetic metal component of the prion that serves as the
so called ‘infectious’ pathogenic agent in TSEs. So
whenever scientists inoculate misfortunate lab animals with
TSE brain tissues ( eg tissues contaminated with this rogue
type of manganese or strontium atom ) and effectively transmit
TSE, they are actually transmitting ‘a magnetic field
inducing/radioactive capacity’ that is carried along with
the ferrimagnetically ordered metal contaminant into the
recipient animals, who, in turn, develop TSE.

Furthermore, the concept of the rogue ferrimagnetic manganese
atom as the ‘TSE agent’ also explains why the so called
‘infectious’ pathogenic capacity of the prion can survive
heating to temperatures in excess of 500 degrees — since
ferrimagnetic metals will hold onto their magnetic charge
until they are heated to temperatures beyond their respective
‘curie point’ temperature. ( eg, 550 degrees for manganese
3+)- whence its magnetic energy ( eg its pathogenic capacity )
is instantly drained.

The various strains of TSE disease could be explained by the
different prion protein phenotypes and their different metallo
binding affinities for the various combinations of rogue
replacement metals that could be involved in the aetiology of
TSEs. In this respect, a raft of specific metal valencies,
magnetic states and radioactive counts on the candidate
replacement metals could determine the particular strain of
TSE that emerges at the end of the day. Such factors as the
length of incubation, aggressiveness of the disease process is
determined by such factors as the radioactive, magnetic field
inducing capacity of the rogue replacement atoms.

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