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Interesting website....

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ranchwife

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Very interesting, indeed!!!! Something for me to print off and take to work to see how many of my "professional" co-workers know about the facts this article listed!!!
 

Kathy

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This Anthony (Gerry) Parish fellow was a real character. He had alot on his table, yet spent is last years fighting for our health, while his failed.

Taken from his bio:
His American doctor had taken a medical history and attributed his condition to the two years spent working in a drycleaners when he was 16 and exposed to the solvent trichloroethylene. He set out to prove the association. He discovered that this solvent could cause a latent poisoning and began compiling a case against the manufacturers, ICI, who he claimed knew of the dangers as early as the 1930s.

Interesting that the manufacturer of the solvent "trichloroethylene" was ICI: they were also the same manufacturer of "Phosmet", the warblecide used by UK farmers which Purdey and others, claim a relationship to BSE (trigger mechanism due to its Cu chelation affects, oxidative stressor).

Right up until his death he worked tirelessly with his son Ben on his research; writing to successive Prime Ministers, politicians, the Department for Environment Food and Rural Affairs and scientists. Unfortunately, a combination of having no academic background and controversial views meant that his work was often dismissed. However, he published his much-referenced findings on the Internet from 1996 onwards and in several publications including the Journal ‘Medical Hypotheses’. He was invited to become a fellow of the New York Academy of Sciences in 1988. ....

Anthony Royal Gerry died from cancer on 16th December 2002 leaving wife Rema, and from previous marriages, two daughters and three sons
 

Tam

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two days and still no comment from R2 or Mike . This has got to be a record of some kind. :wink:
 

fedup2

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I will admit that I know very little about this so don't read to much into this question. The information on that site was over 5 yrs old. Has there been any new research since then to dispute any of this? No hidden agenda here, just wondering.
 

Tam

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fedup2 said:
I will admit that I know very little about this so don't read to much into this question. The information on that site was over 5 yrs old. Has there been any new research since then to dispute any of this? No hidden agenda here, just wondering.

Well if there was I think Reader would have found it by now and posted it. But I have read some of the stuff she has posted only to find out later it was older than this article.
 

Mike

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Authors

Benjamin Parish M.Sc.

Anthony Parish PhD.

Two Scientists, (Only ONE with a Doctor's Degree), refutes hundreds, if not thousands, of scientists worldwide?


Skeptical? You bet! Calling it hogwash? I wouldn't go that far. Lets see if any more scientists are convinced and get on board before we say this is the gospel.
 

Kathy

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You want something recent and by a reputable group of doctors, check this out, just published in Nature:

"The most infectious prion protein particles"

Jay R. Silveira, Gregory J. Raymond, Andrew G. Hughson, Richard E. Race, Valerie L. Sim, Stanley F. Hayes, and Byron Caughey

Quote:
Abstract
Neurodegenerative diseases such as Alzheimer's, Parkinson's and the transmissible spongiform encephalopathies (TSEs) are characterized by abnormal protein deposits, often with large amyloid fibrils. However, questions have arisen as to whether such fibrils or smaller subfibrillar oligomers are the prime causes of disease1, 2. Abnormal deposits in TSEs are rich in PrPres, a protease-resistant form of the PrP protein with the ability to convert the normal, protease-sensitive form of the protein (PrPsen) into PrPres (ref. 3). TSEs can be transmitted between organisms by an enigmatic agent (prion) that contains PrPres (refs 4 and 5). To evaluate systematically the relationship between infectivity, converting activity and the size of various PrPres-containing aggregates, PrPres was partially disaggregated, fractionated by size and analysed by light scattering and non-denaturing gel electrophoresis. Our analyses revealed that with respect to PrP content, infectivity and converting activity peaked markedly in 17−27-nm (300−600 kDa) particles, whereas these activities were substantially lower in large fibrils and virtually absent in oligomers of 5 PrP molecules. These results suggest that non-fibrillar particles, with masses equivalent to 14−28 PrP molecules, are the most efficient initiators of TSE disease.

This throws a big wrench in the "infectious" theory. How come only prion aggregates of a "specific size variant" are capable of initiating further PrPC mutation?

Another quote from the summary discussion which is suggesting that other factors make up the content of the aggregates, which have not been identified yet (at least not by mainstream infectioun promotors):

Quote:
PrP content of PrP-res aggregates

Based on protein assays and ultra-microbalance measurements, 47±9% of the vacuum-dried weight of the washed, unfractionated SUS-treated PrP-res particles was protein (data not shown), and, according to semi-quantitative western blots (data not shown), >87% of the protein was PrP. Adjusting for the glycan and glycophosphatidylinositol content (~25%) of PK-treated PrP molecules, we estimate that at least 54% of the mass was attributable to PrP molecules

Will this lead to a break-through? I certainly hope so.
 

Maple Leaf Angus

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reader (the Second) Thanks MLA and Tam. :roll: :roll: [/quote said:
I think I just discovered what it means to be collateral damage! :?

Thanks for what, reader2?

Oh well, you're welcome!

If you liked it, I'll try to do more of it.

Enough.
 

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