Infectious Prions in the Saliva and Blood of Deer with CWD

[flounder]

For someone who doesn't care what Randy or I (or anyone that disagrees with whatever you are stating at the time), you sure like to pay alot of attention to us. Always trying to discredit the things we say.

Transmissibility of the disease is not argued, we disagree on what the actual transmissible agent is which initiates the disease process. We also have a problem, because of your insistance that metals are not involved with these diseases, and that inhalation of fine and ultrafine metal particles can contaminate the brain initiating oxidative stress and other disease processes.

When I argued for iatrogenic transmission, ie: via injection of naturally derived beef growth hormones, you and flounder ignores or denied this possible route of transmission in cattle (especially in the UK). The UK banned naturally derived growth hormones in cattle for a reason, their use was transmitting the "agent" which initiated disease. The pituatary gland is a target organ for metals.

It is really sad that you and flounder make the bold statements that metals have nothing to do with this, or that OPs had nothing to do with these neurological disease processes. Do you care/know how many researchers you a presently insulting by these statements?

When I argue against the "infectious" prion, I am not saying that the research on prions should stop. I am asking for deeper investigation and complete characterization of the prions. It appears Manuelidis and others are finally moving deeper into this process.

Neurotoxicology. 2006 May;27(3):437-44. Epub 2006

Free radical generation of protease-resistant prion after substitution of manganese for copper in bovine brain homogenate.

Deloncle R, Guillard O, Bind JL, Delaval J, Fleury N, Mauco G, Lesage G.
Universite Francois Rabelais de Tours, Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, 31 Avenue Monge, 37200 Tours, France. [email protected]

The exchange between copper and seven transition metals is studied in a bovine brain obex homogenate according to the redox status of the medium. In reductive conditions, almost all the studied metals can substitute for copper when it is in the reduced form Cu+. This substitution is reversible, since copper uptake as Cu++ is restored in an oxidizing medium but only Co++, Ni++ and Mn++, in this decreasing order, can substitute perfectly for copper in bovine brain homogenate. To study free radical effects on bovine brain proteins, at first a copper substitution was processed in order to inhibit superoxide dismutase-like protective properties against free radicals in copper metalloproteins. Manganese was selected since a brain copper decrease correlated with a manganese increase is well-known in transmissible spongiform encephalopathies. Results for bovine brain homogenate, initially negative in the Western blot Prionics test, indicate that the substitution of manganese for copper in a reducing medium and exposure to UVA-induced free radicals produce proteinase K resistant prion. These findings suggest that an impairment in brain metal homeostasis leading to oxidative abnormalities may be involved in transmissible spongiform encephalopathies.

PMID: 16481041

Angew Chem Int Ed Engl. 2006 Sep 28;

Charge-Induced Molecular Alignment of Intrinsically Disordered Proteins.

Skora L, Cho MK, Kim HY, Becker S, Fernandez CO, Blackledge M, Zweckstetter M.
Department of NMR-based Structural Biology, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077 Gottingen, Germany, Fax: (+49) 551-201-2202 http://www.mpibpc.gwdg.de/abteilungen/030/zweckstetter.

PMID: 17009286

ScientificWorldJournal. 2006 Feb 28;6:295-310.

Anticholinesterase toxicity and oxidative stress.

Milatovic D, Gupta RC, Aschner M.
Department of Pediatrics, Medical School, Vanderbilt University, Nashville, TN, USA. [email protected].

Anticholinesterase compounds, organophosphates (OPs) and carbamates (CMs) are commonly used for a variety of purposes in agriculture and in human and veterinary medicine. They exert their toxicity in mammalian system primarily by virtue of acetylcholinesterase (AChE) inhibition at the synapses and neuromuscular junctions, leading into the signs of hypercholinergic preponderance. However, the mechanism(s) involved in brain/muscle damage appear to be linked with alteration in antioxidant and the scavenging system leading to free radical-mediated injury. OPs and CMs cause excessive formation of F2-isoprostanes and F4-neuroprostanes, in vivo biomarkers of lipid peroxidation and generation of reactive oxygen species (ROS), and of citrulline, a marker of NO/NOS and reactive nitrogen species (RNS) generation. In addition, during the course of these excitatory processes and inhibition of AChE, a high rate of ATP consumption, coupled with the inhibition of oxidative phosphorylation, compromise the cell's ability to maintain its energy levels and excessive amounts of ROS and RNS may be generated. Pretreatment with N-methyl D-aspartate (NMDA) receptor antagonist memantine, in combination with atropine sulfate, provides significant protection against inhibition of AChE, increases of ROS/RNS, and depletion of high-energy phosphates induced by DFP/carbofuran. Similar antioxidative effects are observed with a spin trapping agent, phenyl-N-tert-butylnitrone (PBN) or chain breaking antioxidant vitamin E. This review describes the mechanisms involved in anticholinesterase-induced oxidative/nitrosative injury in target organs of OPs/CMs, and protection by various agents.

PMID: 16518518

there you go again kathy, when you cannot prove your statements, you then lie :liar:


nothing you referenced above has anything to do with the CAUSE of TSE.



kathy wrote ;


When I argued for iatrogenic transmission, ie: via injection of naturally derived beef growth hormones, you and flounder ignores or denied this possible route of transmission in cattle (especially in the UK). ...........end


kathy, please reference where i said this ???

IN fact i have argued of the contrary from inoculations of cattle of the drugs to super ovulate ;


Super-ovulate cattle. (Not to forget about the potential for some BSE cases to come from vaccinations containing pituitary-derived SRMs.)

TWA LITTLE minute

http://www.bseinquiry.gov.uk/files/yb/1988/06/10001001.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/06/13010001.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/06/14006001.pdf

COMMERCIAL IN CONFIDENCE

http://www.bseinquiry.gov.uk/files/yb/1988/09/06005001.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/10/06005001.pdf

NOT FOR PUBLICATION

http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf

http://www.bseinquiry.gov.uk/yb/1988/11/04003001.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/04/00007001.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/07/00007001.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/09/00004001.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/10/00003001.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/01/26007001.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/01/30001001.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf

NON-LICENSED HUMAN TISSUE DEVICES WERE NOT COMMERCIALLY AVAILABLE

snip...

I was quite prepared to believe in unofficial pituitary hormones, also in the 1970's, whether as described by Dr. Little, or in other circumstances, for animal use.

snip...

The fact that there were jars of pituitaries (or extract) around on shelves is attested by the still potent 1943 pituitaries, described in Stockell Hartree et al. (J/RF/17/291) which had come from the lab. at Mill Hill. Having taken the trouble to collect them, they were not lightly thrown out...

http://www.bseinquiry.gov.uk/files/ws/s467bx.pdf

more on the 1968 medicine act, they forgot to follow

http://www.bseinquiry.gov.uk/files/yb/1989/01/30008001.pdf

Draft cover letter to product licence holders (considered by Human and Vet Medicines including deer)

http://www.bseinquiry.gov.uk/files/yb/1989/02/22008001.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/02/22011001.pdf

(It was noted with concern that hormone extracts could be manufactured by a veterinary surgeon for administration to animals under his care without any Medicines Act Control.)

http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/06/07010001.pdf

TWA LITTLE STATEMENT 331

http://www.bseinquiry.gov.uk/files/ws/s331.pdf

snip...end



http://www.prwatch.org/node/4624


http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm

OF course, these had nothing to do with metals or ops. it's the transmission of the infectious agent TSE. i know you and rkaiser cannot understand these things :roll:


kathy, you only disgredit yourself when you start lying.


TSS

 

[bse-tester]

Kathy worte:

Isn't it interesting how Kuru showed up after the USA nuked the sh@% out of the Marshall Islands.

First of all Kathy, by way of introducing Kuru to you Kathy, it was first recognized in Papua New Guinea in 1900. You might also note that this was long before the first nuke was ever designed, let alone detonated!!!!

Secondly, the Marshall Islands are so far removed from Papua (on the other side of the Solomons, Micronesia and the Gilbert Islands. If I recall, there is about 2000 miles of ocean between Papua and the Marshall Islands.

Too suggest that Kuru resulted from a nuke is totally out to lunch in my opinion.

First you suggest that Kuru "showed up after the USA nuked the sh@& out of the Marshall Islands," but fail to add that Kuru was already there 45 or 50 years prior to the first nuke being built and then detonated. You need to do some more research Kathy.

Further:

Kathy, if you would read some of my replies you would have noticed this one wherein I asked you to give me a definition of the term "Infectious."

Ron.

Posted: Sun Oct 15, 2006 3:51 pm Post subject: Rogue Metals

--------------------------------------------------------------------------------

Kathy worte:

Quote:
The "unconventional transmissible AGENT" (UTA) involved with TSEs has been identified as the rogue metals attached to the normally copper loaded octapeptide repeats.

You wish to ignore this fact, and continue to call these diseases "infectious" rather than a toxin found in the environment.



So when an "infected" deer, licks another deers vulva during the rutting season and happens to transfer some PrPsc into the vaginal fluid of the female deer from its own infected saliva, is that not by its very act referred to as an infection caused by directed implantation of PrPsc via saliva thus being able to be described as an infective sharing of contaminated fluids which will bring about the growth of PrPsc within the now infected animal to a point where the numbers of the PrPsc will, by replication, bring about the death of that individual. To this end, can we therefore not classify this transferral of PrPsc as being caused by an animal that was infected and subsequently discretely sharing the infectious paticulate with a non-infected animal which, after the act occurred could be considered to be now "infected" and therefore having received an infection from an animal that was originally infected by whatever means - rogue metals, or by continuous exposure to amorous and affectionate rutting practices commonly found in wild deer?

It would be foolish to consider that rogue metals are to be the sole means by which PrPsc can develop from their normal counterparts into the isoform we call PrPsc so early in this relatively new science, even if it has some important merit. But to constantly throw out the word "infectious" is akin to closing one's eyes on potential that may well prove to be factual rather than whimsical.

The cause or at least one of the causes of the disease may well be found to rogue metals (associatively or directly) - but once the disease is manifested within the animal, do we consider the animal to be simply suffering from a lack of or abundance of a metal contaminant or, in fact, to be classified as a now infectious animal??? I consider it to be not only infected, but also infectious!! And most certainly suffering from what is now an infectious disease!

Define for me, if you will, the true meaning of the word "Infectious?"

[/quote]

 

[rkaiser]

Around and around we go.

But what is the purpose of each of the debaters. I for one am a cattle person here in Canada who's industry has been devastated by this BS. The main thing that has hurt our industry is the fear of human death related to eating cattle that have BSE. Not so much how they got the problem, but how they are going to cause human suffering because of it. I don't argue against the removal of SRM's, or a feed ban of MBM, and support testing to identify BSE animals. What I do have a problem with is the continual drive of those to tell the terrible human when even R2 herself has questions about the human cases of vCJD in Europe.

It seems that the only goal of Terry and R2 is to continue the fear. Post about the infectious prion theory and support unproven stories of humans dying by eating beef.

You would think that if the goal of R2 and Terry were to save human lives, they would explore every alternative rather than simply discredit and continue the fear.

I wonder what their purpose is? No effect from BSEconomics but obvious connections to personal TSE problems. Why are the two of you even here on this Beef Cattle site? What are you trying to tell us? That we need more SRM removal and more testing. I don't think anyone on this site would argue those points, unless they are part of the packer commucapitalist agenda that has seen nothing but opportunity in this debacle.

What else do you want us to believe R2 and Terry? Do you want me and the rest of the ranchers on this site to admit that cows are the problem. To say - yes R2 cows have it --- we don't know how they got it but they certainly spread it and despite no solid proof - these cows caused a bunch of humans to die and will cause more? Forget it R2 - Forget it Terry. Fight your battle with others who have not seen the economic and political games played at their expense. Go prove your theory somewhere else. Any with any sense on this site already agree with most of what you propose, so go play somewhere else.

 

[Anonymous]

kaiser- I don't think you can even relate to the compassion both these folks have for finding the truth about the disease- since both have lost close relatives...And from what I've seen both are much more educated and studied on the disease than anyone else who has posted on this board- with BSE tester being a close third...I know Reader 2 has spent extensive time travelling and attending meetings and seminars on the disease- besides extensive reading and study....

How you can condemn them for this I do not know...

They appear to be much more open minded than either you, Kathy, or several others on here- but they also are not afraid to see what they see...

 

[PORKER]

Man tested for human mad cow disease
Clara Pirani, Medical reporter
October 12, 2006
NSW health authorities are conducting tests to confirm if a hospital patient died as the result of a brain disease that may have infected other patients.

Doctors at John Hunter Hospital in Newcastle began to suspect on Tuesday that a middle-aged man who died on Wednesday had Creutzfeldt-Jakob Disease - the human form of mad cow disease.

The man was admitted to hospital 10 weeks ago, suffering neurological symptoms including severe headaches and involuntary muscle movements, and underwent several operations.

Hunter New England Health director of clinical operations, Nigel Lyons, said the likelihood that the patient had CJD was "very remote".

Initial results of a brain biopsy were negative for CJD, however further tests to rule out the disease will take 10 days to complete.

"We sent the brain biopsy down to a specialist at the Royal Prince Alfred Hospital and he said it showed no signs of CJD so that's an encouraging sign," Dr Lyons said.

"It's 95 per cent likely that it's not CJD, but it will take 10 days to perform further tests that will completely rule it out.

"There is no evidence at this stage that the patient had CJD and he did not have any typical symptoms of the disease.

"However, as his condition could not be definitively diagnosed, CJD cannot be excluded as a remote cause for his condition.''

Dr Lyons said the CJD germ was very difficult to destroy, even through rigorous cleaning and sterilisation of medical equipment. However, he said there had been no transmissions of the disease through surgical instruments around the world since 1980.

Surgical instruments used at the hospital during the past 10 weeks have been quarantined to limit any potential risk of infection to other surgical patients.

If tests confirm the patient had CJD, health authorities will need to contact patients who had surgery at the hospital during the past 10 weeks.

"If there is a diagnosis of CJD, then we will need to go back and have a look at everyone who has had potential contact with instruments since the surgery was performed," Dr Lyons said.

 

[rkaiser]

Oldtimer -

kaiser- I don't think you can even relate to the compassion both these folks have for finding the truth about the disease- since both have lost close relatives...And from what I've seen both are much more educated and studied on the disease than anyone else who has posted on this board- with BSE tester being a close third...I know Reader 2 has spent extensive time travelling and attending meetings and seminars on the disease- besides extensive reading and study....

How you can condemn them for this I do not know...

They appear to be much more open minded than either you, Kathy, or several others on here- but they also are not afraid to see what they see...

And what would the Old Rcalf boys agenda be? Does he like the feed transmission theory at the moment. You bet your ass. It fits to a tee at the moment. Atypical BSE in the good old USA after all. :roll:

I just told you that I support most everything that these two (educated on one topic) folks support. I just wish that they were open minded enough to look for the cause of BSE more than their goal of keeping the cow story in the headlines day after day.

If "for instance" metal contamination could be proven to have caused a cluster like the one in Britain - things could be done to change the situation. Once again not arguing that the feed ban may have already done some of that be removing metal contaminated material from MBM.
But it could have been taken a step further, and clean up of environmentally problematic things could have followed.

Simple enough for your Oldtimer - or would you rather show some more support for these two just because their current theory has your cull cows worth more than mine?

 

[Anonymous]

rkaiser- Your and Kathy's arguments do more for R-CALF or border closure than anybody- shows that there are still way too many unknowns/unprovens and theories about BSE to go changing the long standing isolation and quarantine rules that have been in effect- and have proven to be somewhat effective in the UK, Europe and other countries for so many years.

Even IF its chemical/minerals that infect the cattle- can these cattle than still transmit to humans thru prions, SRM's, blood, or nerves in the muscle meat?...

Or does this throw the governments safe beef by SRM removal theory out the door? Maybe they should be testing for some mysterious metal or chemical that is actually triggering the disease instead of removing SRM's?

Does Canada have a chemical/mineral/radioactive area causing the Alberta cluster?...

Could these supposed radioactive Canadian cattle of Kathy's pass on that radioactivity to US cows if comingled? Many cancer treatments require isolation for several days so the radioactivity can wear off- Is there the same thing in Kathy's radioactive Canadian cows? Then should all the Canadian live cattle coming into the US be isolated and quarantined for 30 days first to wear off the radioactivity?

Yep- Opens up a whole other book of questions- and what I, and I think R-CALF, want first is some answers....

 

[Kathy]

Tell me why the PrPC prion changes its shape? What physical conditions cause this?

The "infectious prion" hypothesis does not deal with these questions at all.

Replacement of copper on the PrPC prion with other metals, like manganese, is 100% proven to mis-shapen the prion into a tertiary confirmation very similar, if not the same, as PrPSc.

Once these rogue metals attach to the PrPC, it is disfunctional and accumulates. Reactive oxygen species and free radicals continue to damage the cells in the absence of the antioxidant effects of PrPC, and downstream effects.

However, the expression of PrPC continues - at least it keeps trying to produce the healthy form. Without feedback that the tells the cell, PrPC is there and working, expression is enhanced, similar in exposures to chemicals like OPs.

The metals attached to the prion are directly related to the bio-availability of metals in the body. A brain challenged by the iatrogenic insertion of radioactive isotopes will eventually succumb to the oxidative stressors, because of a breakdown in the anti-oxidant defence mechanisms. Holding metallic surgical instruments against the brain tissue will also provide bio-available rogue metals.

There is a connection to radio-active materials - if they got there in a graft, injection, consumption or inhalation, it is all the same result. Of course, iatrogenic tranmission and inhalation are more likely to concentrate the metals in the brain faster than ingestion.

Are you agreeing that naturally derived growth hormones from diseased cattle spread BSE?


Oldtimer states:

Could these supposed radioactive Canadian cattle of Kathy's pass on that radioactivity to US cows if comingled? Many cancer treatments require isolation for several days so the radioactivity can wear off- Is there the same thing in Kathy's radioactive Canadian cows? Then should all the Canadian live cattle coming into the US be isolated and quarantined for 30 days first to wear off the radioactivity?

The cat study shows that radio-active isotopes can be found in the urine and saliva (attached to what proteins, if any?) and we know this is also true with depleted uranium contaminated people/soldiers.

Canada has naturally occurring radio-active material in various areas, mostly under the surface. But cattle ranching doesn't bring it to the surface. Drilling for water, oil & gas, mining etc. can translocate the NORMs from their deposited underground locations to the surface and/or atmosphere.

The USA also has naturally occurring radio-active materials (NORMs) as well as 104 nuclear power plants and hundreds of military testing ranges used for DU testing and nuclear bomb testing, nuclear and DU weapons manufacturing plants (eg. Hanford Super-fund sight, Rocky Flats Nuclear Weapons Facility near Denver, etc. etc.)

We can continue to ignore this problem until it gets beyond repair, or we can stop this now, and implement environmental regulations that will force stiffer emission restrictions for "ultrafine particulate" with the hope that we can prevent their translocation or contamination. We must concentrate on methods of energy production which are "clean" (like wind) which cannot possible contaminate the environment with metals and radioactive nuclides. This won't make Halliburton or Suncore as much money though.

This is a very big can of worms, and sooner or later, there will be no avoiding the situation.

 

[Kathy]

Most importantly, the use of nuclear weapons including depleted uranium weapons must be halted.

"Since 1991, the U.S.. has released the radioactive atomicity equivalent of at least 400,000 Nagasaki bombs into the global atmosphere. That is 10 times the amount released during atmospheric testing which was the equivalent of 40,000 Hiroshima bombs." (Leuren Moret, geophysicist/nuclear industry whistleblower.)

Since 1991 .....(man made contamination) ... disgusting!

We have enouth naturally occurring radiation to deal with, including releases from volcanos, and cosmic radiation which is made worse by thinning of the ozone layer.

 

[flounder]

Tell me why the PrPC prion changes its shape? What physical conditions cause this?

The "infectious prion" hypothesis does not deal with these questions at all.

Replacement of copper on the PrPC prion with other metals, like manganese, is 100% proven to mis-shapen the prion into a tertiary confirmation very similar, if not the same, as PrPSc.

Once these rogue metals attach to the PrPC, it is disfunctional and accumulates. Reactive oxygen species and free radicals continue to damage the cells in the absence of the antioxidant effects of PrPC, and downstream effects.

However, the expression of PrPC continues - at least it keeps trying to produce the healthy form. Without feedback that the tells the cell, PrPC is there and working, expression is enhanced, similar in exposures to chemicals like OPs.

The metals attached to the prion are directly related to the bio-availability of metals in the body. A brain challenged by the iatrogenic insertion of radioactive isotopes will eventually succumb to the oxidative stressors, because of a breakdown in the anti-oxidant defence mechanisms. Holding metallic surgical instruments against the brain tissue will also provide bio-available rogue metals.

There is a connection to radio-active materials - if they got there in a graft, injection, consumption or inhalation, it is all the same result. Of course, iatrogenic tranmission and inhalation are more likely to concentrate the metals in the brain faster than ingestion.

Are you agreeing that naturally derived growth hormones from diseased cattle spread BSE?


Oldtimer states:

Could these supposed radioactive Canadian cattle of Kathy's pass on that radioactivity to US cows if comingled? Many cancer treatments require isolation for several days so the radioactivity can wear off- Is there the same thing in Kathy's radioactive Canadian cows? Then should all the Canadian live cattle coming into the US be isolated and quarantined for 30 days first to wear off the radioactivity?

The cat study shows that radio-active isotopes can be found in the urine and saliva (attached to what proteins, if any?) and we know this is also true with depleted uranium contaminated people/soldiers.

Canada has naturally occurring radio-active material in various areas, mostly under the surface. But cattle ranching doesn't bring it to the surface. Drilling for water, oil & gas, mining etc. can translocate the NORMs from their deposited underground locations to the surface and/or atmosphere.

The USA also has naturally occurring radio-active materials (NORMs) as well as 104 nuclear power plants and hundreds of military testing ranges used for DU testing and nuclear bomb testing, nuclear and DU weapons manufacturing plants (eg. Hanford Super-fund sight, Rocky Flats Nuclear Weapons Facility near Denver, etc. etc.)

We can continue to ignore this problem until it gets beyond repair, or we can stop this now, and implement environmental regulations that will force stiffer emission restrictions for "ultrafine particulate" with the hope that we can prevent their translocation or contamination. We must concentrate on methods of energy production which are "clean" (like wind) which cannot possible contaminate the environment with metals and radioactive nuclides. This won't make Halliburton or Suncore as much money though.

This is a very big can of worms, and sooner or later, there will be no avoiding the situation.

yep, but it has nothing to do with the cause of TSEs kathy. science has proven this via transmission studies. the usda and industry are the ones responsible for this via feed. you know, i know it, and everyone else on this board knows it. and there still feeding likely TSE cows to cows in 2006. feed ban has failed, and the surveillance of TSE in the USA bovine has come to a hault. they just could not keep covering them up, so they stopped all together. ...TSS

 

[Big Muddy rancher]

Man tested for human mad cow disease
Clara Pirani, Medical reporter



Ever wonder why it couldn't be written Cow tested for Bovine form of Creutzfeldt-Jakob .

 

[bse-tester]

Kathy wrote:

Once these rogue metals attach to the PrPC, it is disfunctional and accumulates. Reactive oxygen species and free radicals continue to damage the cells in the absence of the antioxidant effects of PrPC, and downstream effects.

At what point does a metal fragment become a "Rogue?"

What species are you describing to be a "Reactive oxygen species?"

What "Free Radicals" are you describing that damage cells in lieu of PrPsc?

Describe the antioxident effects that occur on PrPsc?

Also, please outline what you think PrPsc does to cells and what cells in particular when not absent but present???

I am simply asking Kathy and not trying to be petty - I hope you understand?

I understand the hypothesis of metal contamination and I am following it with great interest, but I am wondering why you would describe the metals within that contaminant as being "Rogue?"

I am also wondering why you would use a term such a "antioxidant to describe an effect that is caused by PrPc??

I am also wondering what you mean by "downstream effects" and what they might be in your estimation?

I am also wondering why you would mention an effect that an absense of "Reactive oxygen species and Free Radicals" would have on a cell or any specific cell when there is an absense of those things???

Can you also explain how PrPc becomes "dysfunctional and accumulates" when the "Rogue Metals" attach to them???

Can you lastly define what PrPc acually is please and how it affects the host???[/b]

Kathy, please do not get all bent out of shape - I am simply asking you to explain your comments in more detail. Ron.

One last observation:

Kathy wrote:

The USA also has naturally occurring radio-active materials (NORMs) as well as 104 nuclear power plants and hundreds of military testing ranges used for DU testing and nuclear bomb testing, nuclear and DU weapons manufacturing plants (eg. Hanford Super-fund sight, Rocky Flats Nuclear Weapons Facility near Denver, etc. etc.)

In light of this last comment, how many actually detonation sites for nukes are there in the USA and where?? Other than the well known underground facility in Nevada of course? I know that there are certainly not hundreds as you stated, but in order to find out if I am wrong, please let us know how many there are and where they are. I would be most interested. Ron.

 

[flounder]

Radioactivity report published
Monday 23 October 2006
The radioactivity people absorb through food remained below the EU legal limit during 2005, says a report published today by the Agency.


Radioactivity in Food and the Environment (RIFE) 2005 is the fourth annual report combining the Agency's monitoring results with those of the Environment Agency, the Scottish Environment Protection Agency and the Environment and Heritage Services of Northern Ireland.
It is the most comprehensive annual independent report of radioactivity in food over the whole of the UK. The survey measures radioactivity from different parts of the food chain, including local food eaten by people who live close to nuclear sites. Overall, it also works out how much radioactivity people would absorb from authorised radioactive discharges in our environment, such as in the air.

By combining these sources the report works out how much radioactivity people take in from all these sources, whether they live near a nuclear site or not. It found that the total dose is under the EU annual dose limit for members of the public of 1 millisievert for all authorised discharges of radiation.


The science behind the story
Radioactivity has been around since the Earth was created and it exists naturally in the atmosphere, soil, seas and rivers. It's also created by human activity during energy production and military operations. Inevitably some of this gets into the food and drink we consume.
The main purpose of the Agency's monitoring programme is to make sure that levels of radioactivity in food and drink from authorised discharges do not lead to us receiving unacceptable amounts of radioactivity through our food. Authorised discharges are those that nuclear sites or industrial manufacturers are allowed to make under their operating licences.




Radioactivity in Food and the Environment (RIFE) 2005
Read the full report



http://www.food.gov.uk/news/newsarchive/2006/oct/rife



Radioactivity in Food and the Environment (RIFE) 2005
Monday 23 October 2006

RIFE 11 is the fourth joint annual report combining the results of the radiological monitoring programmes of the Food Standards Agency, the Environment Agency, the Scottish Environment Protection Agency and the Environment and Heritage Services of Northern Ireland. The RIFE 11 report includes data for samples collected in 2005.

The main purposes of the Food Standards Agency's monitoring programme are to ensure that authorised discharges of radioactivity do not result in unacceptable doses to people through their diet and to show that levels of radioactivity in food are low.
The RIFE report is the only independent report of radioactivity in food over the whole UK. The data are mainly used to calculate the potential dose to consumers eating locally grown food around the UK's nuclear sites. Other dose assessments are included for consumers in areas well away from nuclear sites where sources of naturally occurring radiation are known to contribute to the radioactivity in the general diet.

The report contains sections on radiological dose assessment methods, recently published surveys and research, current legislation and updates on UK, EU and international commitments pertinent to the radiological protection area.

As in previous years, data from surveys of consumers' diets have been used to calculate doses from 'terrestrial' and 'aquatic' food pathways separately. The report uses methodology recommended by the National Dose Assessment Working Group to calculate 'total' doses to consumers from all exposure pathways. The doses calculated by this new methodology lead to a more reliable assessment of total dose to members of the public from discharges to the environment. RIFE 11 includes the dose estimates using this methodology for consumers around 16 sites, and it is hoped that by 2008 (when necessary surveys of dietary habits have been completed) this methodology will be used to calculate total doses for consumers around all nuclear sites.

The report shows that in 2005, consumers' exposure to artificially produced radioactivity via the food chain (for aquatic, terrestrial and 'total' dose pathways) remained below the EU annual dose limit to members of the public of 1 millisievert for all artificial sources of radiation.




Rife 11: Part 1 - Introduction and summary

Rife 11: Part 2 - Chapters 1 and 2

Rife 11: Part 3 - Chapter 3

Rife 11: Part 4 - Chapter 4

Rife 11: Part 5 - Chapter 5

Rife 11: Part 6 - Chapter 6

Rife 11: Part 7 - Chapters 7 and 8

Rife 11: Part 8 - Chapter 9

Rife 11: Part 9 - Chapter 10 and 11

Rife 11: The Appendices


http://www.food.gov.uk/science/surveillance/radiosurv/rife11


http://www.food.gov.uk/multimedia/pdfs/rife11part1.pdf

http://www.food.gov.uk/multimedia/pdfs/rife11ch1and2.pdf


http://www.food.gov.uk/multimedia/pdfs/rife11ch3.pdf

http://www.food.gov.uk/multimedia/pdfs/rife11ch4.pdf

http://www.food.gov.uk/multimedia/pdfs/rife11ch5.pdf

http://www.food.gov.uk/multimedia/pdfs/rife11ch6.pdf

http://www.food.gov.uk/multimedia/pdfs/rife11ch7and8.pdf


9.1 Chernobyl
Following the Chernobyl accident of 1986, radiocaesium is detected in sheep grazing certain upland
areas in the UK, which were subjected to heavy rainfall after the accident. Restrictions are in place on
the movement, sale and slaughter of sheep from these areas, in order to prevent animals from entering
the food chain above the action level of 1,000 Bq kg- of caesium; a level based on the recommendations
of an EU expert committee in 1986. A programme of live monitoring, known as the Mark and Release
Scheme, allows food safety to be protected, whilst allowing established sheep farming practices to
continue. Results of the monitoring programme for 2005 are given in Table 9. .
In the summer of 2005, whole flock monitoring surveys of sheep on selected farms in the post-Chernobyl
restricted areas of Cumbria, Wales and Scotland were carried out (Food Standards Agency, 2006b,c,d). The
results of the survey in Scotland identified one farm where controls could be lifted and this decision was
implemented in January 2006, leaving 10 farms subject to restrictions. It is planned that further whole flock
monitoring surveys will be conducted on restricted farms in all areas during the summer of 006.
There remain a total of 374 farms, or part farms, and approximately 200,000 sheep within the restricted
areas of England, Scotland and Wales. This represents a reduction of over 95 per cent since 1986, when
approximately 9,700 farms and 4,225,000 sheep were under restriction. All remaining restrictions in
Northern Ireland were lifted in 2000. ..........

snip...

http://www.food.gov.uk/multimedia/pdfs/rife11ch9.pdf


http://www.food.gov.uk/multimedia/pdfs/rife11ch10and11.pdf


http://www.food.gov.uk/multimedia/pdfs/rife11appendices.pdf


kathy, please note, NO MENTION OF RADIOACTIVITY CAUSING ANY TSE.

so what's your excuse now kathy, are we back to the OPs??? :lol: :lol2: :arrow: :roll:


TSS

 

[rkaiser]

9.1 Chernobyl
Following the Chernobyl accident of 1986, radiocaesium is detected in sheep grazing certain upland
areas in the UK, which were subjected to heavy rainfall after the accident. Restrictions are in place on
the movement, sale and slaughter of sheep from these areas, in order to prevent animals from entering
the food chain above the action level of 1,000 Bq kg- of caesium; a level based on the recommendations
of an EU expert committee in 1986. A programme of live monitoring, known as the Mark and Release
Scheme, allows food safety to be protected, whilst allowing established sheep farming practices to
continue. Results of the monitoring programme for 2005 are given in Table 9. .
In the summer of 2005, whole flock monitoring surveys of sheep on selected farms in the post-Chernobyl
restricted areas of Cumbria, Wales and Scotland were carried out (Food Standards Agency, 2006b,c,d). The
results of the survey in Scotland identified one farm where controls could be lifted and this decision was
implemented in January 2006, leaving 10 farms subject to restrictions. It is planned that further whole flock
monitoring surveys will be conducted on restricted farms in all areas during the summer of 006.
There remain a total of 374 farms, or part farms, and approximately 200,000 sheep within the restricted
areas of England, Scotland and Wales. This represents a reduction of over 95 per cent since 1986, when
approximately 9,700 farms and 4,225,000 sheep were under restriction. All remaining restrictions in
Northern Ireland were lifted in 2000. ..........

Was it you bsetester who said most winds blow in a south easterly direction in Europe?

 

[bse-tester]

Having lived in England for over 20 years or so - at the height of the nuke power stations construction and startups - I think I know which way the predominant winds blew. They came mostly from the north west across Ireland and Scotland. Some winds came from the North Sea while others blew in from the Atlantic from a gain, a northerly direction. These winds did change through the seasons and have been known to completely reverse direction. On one occassion in the 1960's, all of southern England awoke to find a dusting of sand from the northern Sahara Desert practically covering everything across the southern part of the the UK. Freaky but true. So Randy - yes, the potential for Chenobyl is there but at that time, I think there may have been other home-grown fallout.

Like all things Randy, weather patterns do change and the climate today or even 20 years ago has changed dramatically since Chenobyl. I was questioning the potential for nuke fallout having come from Chenobyl when it was entirely possible that some of it may have originated in the UK itself due to the amount of incidences (accidents) that were occurring there with the UK Atomic Commission and the problems they had with some of the Power Stations.

 

[Kathy]

bse-tester, you are correct that there are certainly enough sources of man-made radioactive fallout, right in the UK (as well as other countries with nuclear power). Germany has legislation which states it must get rid of all its nuclear power stations in the future, not sure right now what the exact date is ? 2020. They are trying to convert to clean burning coal power stations where they will capture emissions, including C02.

Flounder was kind enough to acknowledge and post information which identifies that fallout from Chernobyl did indeed make its way to areas of the UK; and create a problem, worthy of government supervision and control.

The problem with statements like:

"The report shows that in 2005, consumers' exposure to artificially produced radioactivity via the food chain (for aquatic, terrestrial and 'total' dose pathways) remained below the EU annual dose limit to members of the public of 1 millisievert for all artificial sources of radiation. "

is that internalized radiation from nonsoluable ceramic nanoparticles, like depleted uranium (gas) for example, is handled differently in the body than soluable forms of isotopes. Also chronic long term exposure is now being identified as being more dangerous, in many scenarios, than acute one-time exposure.

Others have identified Strontium as a bigger problem than Caesium, even though less Strontium fell. It had a lingering effect on perinatal mortality.

Scientists are in the process of re-examining their "estimations" of internal dosage of radiation from various exposures.

Radiat Prot Dosimetry. 2001;97(3):241-50.
Human absorption and retention of polonium-210 from caribou meat.
Thomas PA, Fisenne I, Chorney D, Baweja AS, Tracy BL.
Toxicology Centre, University of Saskatchewan, Saskatoon, Canada.

The gastrointestinal (GI) absorption factors and the biological retention times for polonium were determined for a group of 14 volunteers--seven men and seven women--from Saskatoon, Saskatchewan, Canada. Each volunteer consumed 2.0 kg of caribou meat containing known amounts of naturally occurring 210Po. Urine and faecal samples were collected for up to 65 days after meat consumption and analysed for 210Po. The average GI absorption factor for the 14 volunteers was 56 +/- 4% (range = 31-71%), not significantly different from the ICRP value of 50%. About 3% of absorbed polonium underwent prompt excretion by the urinary pathway. The remainder was retained by the body with a half-time >100 days, compared to the ICRP value of 50 days. The effect of these findings increases the dose estimate for ingestion of 210Po in food by a factor of 1.5 to 3.5. Thus, background doses to people consuming caribou and reindeer may be higher than previously thought.
PMID: 11843339

Radiats Biol Radioecol. 2003 Mar-Apr;43(2):197-202.
Strontium fallout from Chernobyl and perinatal mortality in Ukraine and Belarus. Korblein A.
Munich Evironmental Institute, Schwere-Reiter Str. 35/1B, 80797, Munich, Germany. [email protected]

Perinatal mortality rates in the regions of Ukraine and Belarus surrounding the Chernobyl site increased in 1987, the year following the Chernobyl accident. The same year, increases of perinatal mortality were also observed in Germany and Poland, and the effect can be associated with the caesium burden in pregnant women. After 1989, there is an unexpected second rise of perinatal mortality in Belarus and Ukraine. This increase is shown to correlate with the strontium content in pregnant women. The findings parallel an increase of perinatal mortality in Germany following the atmospheric bomb tests in the 1950's and 1960's. While the effect from caesium is essentially limited to 1987, the effect from strontium persists until the end of the study period in 1998. The cumulative effect from strontium around Chernobyl outweighs the effect from caesium by at least a factor of 10. This is contrary to the assertion that the caesium content in the Chernobyl fallout was more than 10-times greater than the strontium content. Thus, the dose factor presently used seems to severely underestimate the effect of strontium on perinatal mortality. PMID: 12754809

Inhal Toxicol. 2006 Oct;18(11):885-94.
Distribution and genotoxic effects after successive exposure to different uranium oxide particles inhaled by rats.Monleau M, De Meo M, Frelon S, Paquet F, Donnadieu-Claraz M, Dumenil G, Chazel V.
IRSN/DRPH/SRBE, Laboratoire de Radiotoxicologie Experimentale, Pierrelatte Cedex, France.

In nuclear fuel cycle facilities, workers may inhale airborne uranium compounds that lead to internal contamination, with various exposure scenarios depending on the workplace. These exposures can be chronic, repeated, or acute, and can involve many different compounds. The effect of uranium after multiple scenarios of exposure is unknown. The aim of this study, therefore, was to investigate the genotoxic and biokinetics consequences of exposure to depleted insoluble uranium dioxide (UO2) by repeated or acute inhalation on subsequent acute inhalation of moderately soluble uranium peroxide (UO4) in rats. The results show that UO2 repeated preexposure by inhalation increases the genotoxic effects of UO4 inhalation, assessed by comet assay, in different cell types, when UO4 exposure alone has no effect. At the same time, the study of UO4 bioaccumulation showed that the UO4 biokinetics in the kidneys, gastrointestinal tract, and excreta, but not in the lungs, were slightly modified by previous UO2 exposures. All these results show that both genotoxic and biokinetics effects of uranium may depend on preexposure and that repeated exposure induces a potentiation effect compared with acute exposure.

PMID: 16864406

Expression of the free radical scavenger manganese superoxide dismutase (Mn-SOD) is know to be increased with exposure to ionizing radiation (internally and externally). This correlates to the excessive amounts of manganese found in the brains of CJD victims (10 fold increase), and a 50% decrease in copper levels in the correlating brain tissue.

While the copper/zinc superoxide dismutase enzyme is continually expressed withing cells at a steady state the lack of bioavailable copper makes the Cu/Zn SOD susceptible to attachment with other metals more bioavailable, ie manganese. Yes, the manganese is responding to increased expression required to handle ionizing radiation in the tissue and free radicals.

Since copper is needed by other enzymes, and these enzymes are more prolific in the heart, kidneys and liver (than the brain), the copper is transferred from the brain to these other organs for their free-radical scavenging needs - robbing the brain of copper.

 

[Kathy]

Ron,

If I ever get a chance to sit down and put all the information together which you have asked me for in one statement/posting... you will read it in a published peer-reviewed paper first (before here).

The best thing you can do is go back and copy out all of the abstracts I have posted here on ranchers, and get the papers and read them. Then, if you like, come to see me at my home and we can review the hundreds of others that I have gathered.

I would like very much, to put all this information together into a paper and have it reviewed and published. It will take alot of work and considerable time away from my everyday life/ranching activities and family. It is a future goal of mine.

However, I am concerned that you do not know (or claim not to know) some of these answers for yourself already. The antioxidant activities of PrPC are well documented, and use of medical search engines can help you find the same information I have.

One source of info. on nuclear testing I have found is at:
http://nuclearweaponarchive.org
I have also made some personal acquaintances which have opened doors here.

I suggest you look up some of Dr. D.R. Brown's papers and others like Dr. G. Perry's, on oxidative damage and neurodegeneration.

J Neurochem. 2006 Aug;98(3):677-89. Epub 2006 Jun 19.
Prion protein reduces both oxidative and non-oxidative copper toxicity.Haigh CL, Brown DR.
Department of Biology and Biochemistry, University of Bath, Bath, UK.

The prion protein is a membrane tethered glycoprotein that binds copper. Conversion to an abnormal isoform is associated with neurodegenerative diseases known as prion diseases. Expression of the prion protein has been suggested to prevent cell death caused by oxidative stress. Using cell based models we investigated the potential of the prion protein to protect against copper toxicity. Although prion protein expression effectively protected neurones from copper toxicity, this protection was not necessarily associated with reduction in oxidative damage. We also showed that glycine and the prion protein could both protect neuronal cells from oxidative stress. Only the prion protein could protect these cells from the toxicity of copper. In contrast glycine increased copper toxicity without any apparent oxidative stress or lipid peroxidation. Mutational analysis showed that protection by the prion protein was dependent upon the copper binding octameric repeat region. Our findings demonstrate that copper toxicity can be independent of measured oxidative stress and that prion protein expression primarily protects against copper toxicity independently of the mechanism of cell death.

PMID: 16787422

Folia Neuropathol. 2005;43(4):229-43.
Neurodegeneration and oxidative stress: prion disease results from loss of antioxidant defence. Brown DR.
Department of Biology and Biochemistry, University of Bath, Bath, BA2 7AY, UK. [email protected]

Prion diseases or transmissible spongiform encephalopathies (TSEs) are rare neurodegenerative disorders that can be acquired either by direct transmission, inherited through dominant mutations in the prion protein gene or via an unknown sporadic cause. This latter group constitutes the vast majority of cases. Like many neurodegenerative diseases the hallmarks of oxidative damage can be readily detected throughout the brain of the affected individual. However, unlike most other neurodegenerative diseases, prion diseases are connected with a dramatic loss of antioxidant defence. As abnormal protein accumulates in the diseased brain there is both an increase of oxidative substances and a loss of the defences that keep them in check. In particular the normal cellular prion protein has been shown to be an antioxidant. Conversion of this protein to the protease resistant isoform is accompanied by a loss of this antioxidant activity. This change creates a paradox as the loss of activity is not accompanied by a loss of protein expression. It is likely that this prevents other cellular defences from responding sufficiently to protect neurons from the heightened oxidative burden. Recent experiments with transgenic mice have shown that when prion protein expression is switched off during the course of prion disease, cell death is dramatically halted and the mouse recovers from the disease. This result clearly illustrates that the continued expression of non-function prion protein is essential for disease progression. This implies that the presence of this abnormal protein during prion disease causes a failure of cellular antioxidant defence. This failed defence is the fundamental cause of the massive neurodegeneration that results in the fatal nature of TSEs. The role of oxidative stress in TSEs and other neurodegenerative disorders are discussed in this review.

PMID: 16416388

This is an interesting new paper which discusses the need to use nanoparticles attached to metal chelators to breach the blood-brain barrier.

Neurosci Lett. 2006 Oct 9;406(3):189-93. Epub 2006 Aug 21.
Nanoparticle iron chelators: a new therapeutic approach in Alzheimer disease and other neurologic disorders associated with trace metal imbalance.
Liu G, Men P, Harris PL, Rolston RK, Perry G, Smith MA.
Department of Radiology, University of Utah, Salt Lake City, UT 84102, USA. [email protected].

Accumulating evidence suggests that oxidative stress may be a major etiologic factor in initiating and promoting neurodegeneration in Alzheimer disease. Contributing to this, there is a dyshomeostasis of metal ions in Alzheimer disease with abnormally high levels of redox-active metals, particularly iron, in affected areas of the brain. Although it is unclear whether metal excesses are the sole cause of oxidative stress and neurodegeneration or a by-product of neuronal loss, the finding that metal chelators can partially solubilize amyloid-beta deposits in Alzheimer disease suggests a promising therapeutic role for chelating agents. However, the blood-brain barrier and toxicity of known chelators limit their utility. In this study, we suggest that covalent conjugation of iron chelators with nanoparticles may help overcome the limitations in blood-brain barrier permeability of existing chelation therapy. Using in vitro studies, we have shown that a chelator-nanoparticle system and the chelator-nanoparticle system complexed with iron, when incubated with human plasma, preferentially adsorb apolipoprotein E and apolipoprotein A-I, that would facilitate transport into and out of the brain via mechanisms used for transporting low-density lipoprotein. Our studies suggest a unique approach, utilizing nanoparticles, to transport chelators and chelator-metal complexes in both directions across the blood-brain barrier, thus providing safer and more effective chelation treatment in Alzheimer disease and other neurodegenerative diseases.

PMID: 16919875

Ann N Y Acad Sci. 2005 Jun;1043:545-52. Links
Oxidative stress and neurodegeneration.
Moreira PI, Smith MA, Zhu X, Nunomura A, Castellani RJ, Perry G.
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA.

Oxidative stress is a well-studied early response in chronic neurodegenerative diseases, including Alzheimer's disease, where neuronal loss can exceed 90% in the vulnerable neuronal population. Oxidative stress affects all classes of macromolecules (sugar, lipids, proteins, and DNA), leading inevitably to neuronal dysfunction. We observed that Nepsilon-(carboxymethyl)lysine (CML), the predominant advanced glycation end product that accumulates in vivo, along with its glycation-specific precursor hexitol-lysine, are increased in neurons from cases of Alzheimer's disease, especially those containing intracellular neurofibrillary pathology. The increase in hexitol-lysine and CML can result from either lipid peroxidation or advanced glycation, whereas hexitol-lysine is solely a product of glycation, suggesting that two distinct oxidative processes act in concert in the neuropathology of the disease. Furthermore, using olfactory neurons as an experimental model, we observed an increase in glycation products in neurons derived from Alzheimer's disease patients. Our findings support the idea that aldehyde-mediated modifications, in concert with oxyradical-mediated modifications, are critical early pathogenic factors in Alzheimer's disease.

PMID: 16037277

I will keep your list of questions, as they make a good outline for a review.

 

[bse-tester]

Kathy wrote:

I would like very much, to put all this information together into a paper and have it reviewed and published. It will take alot of work and considerable time away from my everyday life/ranching activities and family. It is a future goal of mine.

However, I am concerned that you do not know (or claim not to know) some of these answers for yourself already. The antioxidant activities of PrPC are well documented, and use of medical search engines can help you find the same information I have.

Should make an extremely interesting read Kathy. Go for it.

As for being concerned about me not knowing the answers - please don't be. I do most certainly know the answers but just wanted to see how far you were into it. It is one thing to read papers and quote others but to have the knowledge and know what it is all about is another. I commend you for your efforts to dig deeper and I suspect that when you do read a paper or any other material that you gather, you absorb it to a point where you become very intimately aware of what it is all about.

I may not always agree with what is posted on this board but that doesn't mean that the info or the data has to be thrown out because of it not being proven as yet or in the so-called mainstream thinking. All information should be considered valuable until it is catagorically proven to be worthless. But then, even worthless information tends to stimulate the inquisitive nature in us humans.

Kathy, keep it up. Who can say where it may lead but also be aware that you may not be able to include a lot of the info you have in any future publication without first getting the permission of the original author(s) due to copyright law. Just a thought. Ron.