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THIS ONE IS FOR KATHY AND RKAISER.......LOL TSS ;-)

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flounder

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Environmental Factors that Affect the Development of Prion Diseases.

Project funded by the European Commission under the Quality of Life Programme.



Contract No: QLK4-CT-2002-02723

Project No: QLRT-2001-02723

Start Date

1st January 2003

Duration

36 months plus 6 month extension

Partners

1. The University of Bristol, UK (Co-ordinator)
2. National Environment Research Council-The British Geological Society, UK
3. University of Bath, UK
4. Free University of Berlin, Germany
5. University of Iceland, Iceland
6. Universita degli studi di Perugia, Italy
7. Universite Joseph Fourier Grenoble, France
8. Alpine Institute of Environmental Dynamics, France

Introduction

The work proposed here brings together top EU geo and biochemists focusing on determining the environmental factors that affect the development of prion diseases such as scrapie, bovine spongiform enchpalitis (BSE), chronic wasting disease (CWD) and Creutzfeld-Jacobs disease (CJD). First the geographical distribution of manganese and copper in soils will be investigated as risk factors. This will be undertaken due to the fact that prion diseases often are found in clusters. It now has been established that the normal metal for prion protein is copper but if that metal is replaced with manganese, the structure of the prion protein is altered. The role of organophosphate pesticides will also be investigated because it has been suggested that copper is complexed with organophosphate, preventing copper absorption.

Objectives

There is clear evidence that the occurrence of prion diseases often has a non-random distribution, suggesting a link to some environmental factors. The work proposed here will investigate risk factors, including the role of trace elements and organophosphates. Analysis of regional variation in local manganese/copper levels will be determined and compared to the incidence of the diseases. The ability of manganese and/or organophosphates in influencing conversion of the prion protein to an abnormal and/or infectious protein will be determined. In combination with geographical occurrence and geo-chemical considerations this program will identify whether these environmental considerations should be acted upon to bring about effective prevention or at least risk minimalisation of prion diseases in the EU and further afield.

Description of the Work

Recently it has been suggested that disbalance in dietary trace-elements and/or exposure to organophosphates might either cause or be a risk factor for prion disease development. In particular, high incidence of scrapie (e.g. in Iceland), chronic wasting disease, and in Slovakia and Italy CJD are associated with regions where soil and foliage are reported to be low in copper and high in manganese. This proposal will address whether exposure to a diet that has a high manganese/copper ratio can influence prion disease will also be addressed. In particular, we shall investigate this theory at the level of protein, cells, animals as well as geographical and geo-chemical associations with prion diseases. Animal models of prion disease and sheep from farms in regions of high scrapie will be investigated for a possible influence of level of manganese and copper on incidence or onset of these diseases. Bio-chemical and biophysical techniques will be used to investigate interaction of the prion protein with copper and manganese to determine the mechanism by which Mn substitution for Cu influences conversion to the abnormal isoform of the protein and whether such conversion results in protein that is infectious in mouse bioassay for infectivity. Additionally, a cell culture model will be used to generate abnormal prion protein by exposure to manganese. Cell culture model of infection will be used to assay whether prion disease alters manganese metabolism and transport of manganese into cells. The level of expression of the prion protein is in itself a risk factor for prion disease as it shortens the incubation time for the disease. This research will result in understanding of the role of disbalance in the trace elements Cu and Mn on the onset and mechanisms behind the occurrence of prion diseases and will for the first time define whether there are environmental risk factors for prion diseases.

Milestones and Expected Results

The study proposed here will produce a geo-chemical map of Europe for manganese and copper. These maps will be used to target field areas where prion diseases have occurred as clusters. The bio-chemical studies will establish whether the replacement of manganese for copper in prion protein is a risk factor for the disease _development_. Organophosphate will also be investigated as a risk factor. The study aims at minimising the risk of prion diseases for humans and animals in the EU.





http://www.arp-manchester.org.uk/FatePride.htm






a) As regards the involvement of organophosphates in the origin of BSE, no new scientific
information providing evidence or supporting the hypothesis by valid data became
available after the adoption of the last opinion of the SSC on this issue. Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for registration of
plant protection products and veterinary medicines – addressed in the enquiries – provide
the basis for safe use of registered compounds and their formulations. Regarding the
alleged intoxication cases reported and OP exposure it must be concluded that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R., Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar, H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and transmission of BSE. Adopted
on 29-30 November 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf


transmission studies do not lie, amplification and transmission!


1: J Infect Dis 1980 Aug;142(2):205-8


Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri
sciureus) that were exposed to the infectious agents only by their
nonforced consumption of known infectious tissues. The asymptomatic
incubation period in the one monkey exposed to the virus of kuru was
36 months; that in the two monkeys exposed to the virus of
Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and
that in the two monkeys exposed to the virus of scrapie was 25 and
32 months, respectively. Careful physical examination of the buccal
cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has
remained asymptomatic during the 39 months that it has been under
observation.

PMID: 6997404

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


and for Gods sake, if someone is smearing this [email protected] all over there kids
heads for lice and did not come up with a TSE, i would say this is good case study;


1) None of our animals that contracted BSE were treated with OP's, even
in utero.
2) My kids were treated with OP's as infants to control head lice. This
seems to be endemic as infection waves in UK primary schools (and
possibly elsewhere).
3) One might argue if the continued use of british beef in the UK was
ethical, none the less it happened. We have a duty to learn from it, not
least a duty to learn on behalf of those people who died so horribly....



However, i have never dusputed the remote possibility that ;



Phosmet induces up-regulation of surface levels of the cellular prion protein.
Neuroreport. 9(7):1391-1395, May 11, 1998.
Gordon, Irit 1; Abdulla, Elizabeth M. 1; Campbell, Iain C. 1; Whatley, Stephen A. 1,2
Abstract:
CHRONIC (2 day) exposure of human neuroblastoma cells to the organophosphate pesticide phosmet induced a marked concentration-dependent increase in the levels of PrP present on the cell surface as assessed by biotin labelling and immunoprecipitation. Levels of both phospholipase C (PIPLC)-releasable and non-releasable forms of PrP were increased on the plasma membrane. These increases appear to be due to post-transcriptional mechanisms, since PrP mRNA levels as assessed by Northern blotting were unaffected by phosmet treatment. These data raise the possibility that phosmet exposure could increase the _susceptibility to the prion agent by altering the levels of accessible PrP_.

(C) Lippincott-Raven Publishers.



http://www.neuroreport.com/pt/re/neuroreport/abstract.00001756-199805110-00026.htm;jsessionid=D3XI1RSXL8uyd5FtR23dvWP1753t5Cv0lY8VXIid8eyvzvuM7qJ5!-477899252!-949856144!9001!-1?index=1&database=ppvovft&results=1&count=10&searchid=1&nav=search





WHAT some of the OPiest/Metalist dont understand (refuse to understand to further there plight to squash the truth of the ruminant feeding spreads and amplifies the TSE agent) is that no where in science literature does it show that Phosmet or metals _CAUSE_ TSE, there is a big difference. TO distort, confuse, lie about the true aspect of this theory into trying to make people believe that Phosmet and or Metals _CAUSE_ TSE, only weakens the whole aspect of the study. but there will always be those that cannot admit the truth about the amplification and transmission of TSE, want to blame others, and will continue this deceit. ...TSS
 

Kathy

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Terry, it is a good thing that you don't listen. I get to repeat myself over and over and over and over and over......

The people who believe that Phosmet contributed to the incidence of these spongiform diseases are not saying it solely (all by itself) caused the disease.

Now repeat that one hundred times.

The people who believe that Phosmet contributed to the incidence of these spongiform diseases know that this Organophosphate (OP) chelated copper from the animals biological systems.

Now repeat that two hundred times.

The people who believe that Phosmet contributed to the incidence of these spongiform diseases know that the chemical was recirculated in the rendered feed, as the chemical was lipophilic (stored in the fats) and had an tiny, tiny 8 hour withdrawal period.

Now repeat that three hundred times.

The use of this chemical to eradicate a warble problem, which was not a serious problem at all (only 1% of the hides showed evidence of warbles), made these animals susceptible to replacement of copper on the PrPC protein, by other metals which screwed it up. These malformed proteins did not function as the copper loaded PrPC protein did and a cascade of biological malfunctions (loss of antioxidant defenses) lead to extreme oxidation of the brain lipids, etc. which resulted in spongioform of the brain.

Repeat that four hundred times. Then come back and tell the board that people like Randy and myself, are saying that Phosmet caused BSE. Your look pretty ridiculous when you keep harping on the 'Phosmet caused BSE' propaganda.

Organophosphate will also be investigated as a risk factor.
 

flounder

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kathy, please make your mind up, it is either op's/metals or nuclear power plants, now which one is it girlfriend :roll:


kathy writes;


> The people who believe that Phosmet contributed to the incidence of

> these spongiform diseases are not saying it solely (all by itself) caused

> the disease.


but you have. thanks for finally admitting this.



TSS wrote;


>>>WHAT some of the OPiest/Metalist dont understand (refuse to understand to further there plight to squash the truth of the ruminant feeding spreads and amplifies the TSE agent) is that no where in science literature does it show that Phosmet or metals _CAUSE_ TSE, there is a big difference. TO distort, confuse, lie about the true aspect of this theory into trying to make people believe that Phosmet and or Metals _CAUSE_ TSE, only weakens the whole aspect of the study. but there will always be those that cannot admit the truth about the amplification and transmission of TSE, want to blame others, and will continue this deceit. <<<


i knew i could count on you to prove my point kathy :lol: tss :lol:
 

flounder

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kathy posted Fri Feb 03, 2006 1:43 am



>>> If BSE has nothing to do with radiation, then why did the CEA (commission energy atomic) develop the first rapid BSE test?

Why was Dr. Elizabeth Williams, (American top CWD expert who died Xmas 2004), working on reports about "ionizing-radiation" before she died?<<<






kathy posted Sun Feb 05, 2006 4:41 pm ;


>>> I do not believe that BSE causes vCJD. They are similar diseases caused by each individual mammals bio-accumulation of metals, improperly balanced -(accumulation) in the brain. Two species can have similar effects resulting from simultaneous exposure to the causative metal(s). Just because they happened at the same time, does not mean that one caused the other.

I believe that BSE can happen without feeding MBM to cattle.

I believe that metals were transmitted via their bio-accumulation in the organs and bones of cattle (and other animals) fed back to cows. Similar to the warnings about eating fish with mercury. Don't forget the feeding of chicken manure (very high in manganese) back to cattle. <<<<




kathy posted Wed Feb 01, 2006 12:20 am


>>> He stated that on the consent form for the MRI (done in USA somewhere), the document stated that "a MRI could potentially cause CJD" <<<


unbelievable kathy, i am still trying to figure out that one?


you just dont get it kathy, these poisonings from metals are NOT transmissible. TSEs are.
show me a study that these diseases from metals are transmissible, then we will have something to talk about. or maybe you can explain away scrapie, a transmissible TSE around for 100s of years, where were your ops and nuclear power plants back then?


tss
 

Kathy

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Just for R2, again, NORMs - naturally occurring radioactive material.

So much for flounder's, Terry's, comments of no nuclear contamination in the hot, hot spot for CWD in North America.

I wonder why these doctors don't "characterize" the prions they use for their inoculation tests?

Rocky Flats judgment more than half a billion
Wednesday, February 15, 2006
The Denver Business Journal
Homeowners who lived downwind of the now-closed Rocky Flats Nuclear Weapons Plant won a $553.9 million judgment from a federal jury Tuesday after a four-month trial that accused the plant's former operators of contaminating their land with plutonium released from the plant.

The defendants were The Dow Chemical Company and Rockwell International Corp., who operated the plant for the U.S. Department of Energy from 1952 to 1989. But those companies have been indemnified in the case by the federal government -- which will pay any judgment and has been paying the companies' legal fees.

The jury awarded the homeowners $354 million in compensatory damages and $200 million in punitive damages.

"It's been a long time coming, but it's a great victory for the plaintiffs," said Merrill Davidoff, the lead trial lawyer for the plaintiffs and a senior member of the law firm of Berger & Montague PC, based in Philadelphia, Pa., in a statement.

"This is what we have been waiting for, and working for, all these years. The jury found that fifty years of lies and cover up and pollution were enough," he said.

The case was filed in 1990 on behalf of 12,000 property owners near the plant, located in a highly populated area about 17 miles northeast of downtown Denver.


Rocky Flats History - The Rocky Flats Environmental Technology Site is a Department of Energy environmental cleanup site located 16 miles northwest of downtown Denver. Rocky Flats is designated by the U.S. Environmental Protection Agency (EPA) as a Superfund cleanup site. Historically, Rocky Flats made components for nuclear weapons using various radioactive and hazardous materials, including plutonium, uranium and beryllium. Nearly 40 years of nuclear weapons production left behind a legacy of contaminated facilities, soils and ground water.

Today, Rocky Flats is a DOE owned cleanup and closure site operated by Kaiser-Hill Company under an accelerated closure contract. The Rocky Flats mission includes the now completed special nuclear material management and shipment, nuclear deactivation and decommissioning, waste management and shipment, environmental cleanup and site closure. When cleanup is complete, the site will be transitioned to a National Wildlife Refuge managed by the US Fish & Wildlife Service.

Federal Bureau of Investigation Raid 1989 - On June 6, 1989 agents from the Federal Bureau of Investigation (FBI), the U. S. Department of Justice Department and the Environmental Protection Agency (EPA) raided and conducted an investigation at Rocky Flats to investigate into allegations of environmental violations of the Resource Conservation and Recovery Act (RCRA) and the Federal Water Pollution Control Act (known as the Clean Water Act) at Rocky Flats.

In March 1992, following a grand jury investigation, a plea agreement between the U.S. Department of Justice Department and Contractor Rockwell International was announced. Rockwell International paid a fine of $18.5 million.

In 2000, the U.S. House of Representatives Committee on Science permitted the FBI to appropriately dispose of any evidence being retained by the FBI from the 1989 Desert Glow investigation. The FBI agreed to return to the DOE Rocky Flats Field Office the Desert Glow evidence inventory it maintained of items taken from Rocky Flats (DOE and Contractor). The FBI transmitted to DOE the attached evidence control forms and printout of the FBI evidence inventory in 2001.
link: http://192.149.55.183/

The Rocky Flats Environmental Technology Site (RFETS) is situated on a 6,262 acre reserve (10.2 square miles) located 16 miles northwest of Denver, Colorado. The portion of the site where facilities are located and work is performed consists of 384 acres and has controlled access. The remaining 10 square miles serves as a buffer zone.

For nearly 40 years, the Rocky Flats Plant was a key part of the Federal government's nationwide complex for nuclear weapons research, development, and production. Rocky Flats provided unique processing capabilities for the fabrication of weapons components from plutonium, uranium, beryllium, and stainless steel. The Rocky Flats nuclear production mission was curtailed in 1989. As a legacy from past operations, RFETS has 12.9 metric tons of plutonium in the form of metals, oxides, solutions, and scrap/residue.
link: http://www.globalsecurity.org/wmd/facility/rocky_flats.htm

The best way to hide a great big elephant is to tell people he isn't there, even though it is right in front of them, constantly telling them there is "nothing here folks" is the standard operating procedure. Good work R2 and Flounder.

It reminds me of the 'emperor's new clothes' story.
 

Kathy

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Thank you Mike for this very informative link.

Who knew that Colorado was such a hot spot for uranium mining, processing, disposal and weapons testing.

If only more people knew about all this, and how it relates (I believe) to CWD.

Members of the board should definitely check out this site.

You have been a great help, thanks again.
 

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