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Very Interesting Prion Study from Iowa State Univ.

Kathy

Well-known member
Sadly, this research gets published after Mark Purdey has passed away.

Toxicol Sci. 2007 May 4; [Epub ahead of print]

Normal Cellular Prion Protein Protects against Manganese-induced Oxidative Stress and Apoptotic Cell Death.

Choi CJ, Anantharam V, Saetveit NJ, Houk R, Kanthasamy A, Kanthasamy AG.
Neuroscience and Toxicology graduate Programs, Iowa Center for Advanced Neurotoxicology, Department of Biomedical Sciences, Iowa State University.

The normal prion protein is abundantly expressed in the CNS, but its biological function remains unclear. The prion protein has octapeptide repeat regions that bind to several divalent metals, suggesting that the prion proteins may alter the toxic effect of environmental neurotoxic metals. In the present study, we systematically examined whether prion protein modifies the neurotoxicity of manganese (Mn) by comparing the effect of Mn on mouse neural cells expressing prion protein (PrP(C)-cells) and prion-knockout (PrP(KO)-cells). Exposure to Mn (10 muM-1 mM) for 24 hr produced a dose-dependent cytotoxic response in both PrP(C)-cells and PrP(KO)-cells. Interestingly, PrP(C)-cells (EC(50) 117.6muM) were more resistant to Mn-induced cytotoxicity, as compared to PrP(KO)-cells (EC(50) 59.9muM), suggesting a protective role for PrP(C) against Mn neurotoxicity. Analysis of intracellular Mn levels showed less Mn accumulation in PrP(C)-cells as compared to PrP(KO)-cells, but no significant changes in the expression of the metal transporter proteins transferrin and DMT-1. Furthermore, Mn-induced mitochondrial depolarization and ROS generation were significantly attenuated in PrP(C)-cells as compared to PrP(KO)-cells. Measurement of antioxidant status revealed similar basal levels of glutathione (GSH) in PrP(C)-cells and PrP(KO)-cells; however, Mn treatment caused greater depletion of GSH in PrP(KO)-cells. Mn-induced mitochondrial depolarization and ROS production were followed by time- and dose-dependent activation of the apoptotic cell death cascade involving caspase-9 and -3. Notably, DNA fragmentation induced by both Mn treatment and the oxidative stress inducer hydrogen peroxide (100muM) was significantly suppressed in PrP(C) -cells as compared to PrP(KO)-cells. Together, these results demonstrate that prion protein interferes with divalent metal Mn uptake and protects against Mn-induced oxidative stress and apoptotic cell death.

PMID: 17483122

Manganese caused "mitochondrial depolarization and ROS (reactive oxygen species) production" followed by "apoptotic cell death cascade"...

So the question is, why does manganese flood to the brain with TSEs? Answer: ROS - production of reactive oxygen species caused by ?

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

Do you really believe FATEPRiDE, and others, when they claim that OPs did not influence the BSE catastrophe in the UK, and elsewhere? The UK government mandated the treatment of warbles in 1982 and most farms used PHOSMET, an organophosphate, because the withdrawal time was only a matter of hours, and their dairy cattle could be treated after the morning milking and they could still sell the evening milk - ie; no waste of milk or loss of income.

Exposure to OPs, whether as a warblecide or as a spray on crops, will cause increased reactve oxygen (or nitrogen) species [ROS], thus upregulating the production of various antioxidant mechanisms, including the manganese based superoxide dismutase.

Also, radiation [ie: external or internalized] exposure also upregulates manganese SOD activity. If the internalized radiation [for example inhalation of Depleted Uranium, strontion 90, lead 210, cesium 137, etc] into the nasal cavity can cause co-localization to various parts of the brain and body, which would trigger the upregulation of manganese based SOD.

Acta Physiol Hung. 2006 Dec;93(4):341-6.

Regional differences in antioxidative response of rat brain after cranial irradiation.

Todorovic A, Pejic S, Kasapovic J, Stojiljkovic V, Pajovic SB, Kanazir DT.
Laboratory of Molecular Biology and Endocrinology, Vinda Institute of Nuclear Sciences, P.O. Box 522, 11000 Belgrade, Serbia.

In order to examine if differences in activity and inducibility of antioxidative enzymes in rat cerebral cortex and hippocampus are underlying their different sensitivity to radiation, we exposed four-day-old female Wistar rats to cranial radiation of 3 Gy of gamma-rays. After isolation of hippocampus and cortex 1 h or 24 h following exposure, activities of copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD) and catalase (CAT) were measured and compared to unirradiated controls. MnSOD protein levels were determined by SDS-PAGE electrophoresis and Western blot analysis. Our results showed that CuZnSOD activity in hippocampus and cortex was significantly decreased 1 h and 24 h after irradiation with 3 Gy of gamma-rays. MnSOD activity in both brain regions was also decreased 1 h after irradiation. 24 h following exposure, manganese SOD activity in hippocampus almost achieved control values, while in cortex it significantly exceeded the activity of the relevant controls. CAT activity in hippocampus and cortex remained stable 1 h, as well as 24 h after irradiation with 3 Gy of gamma-rays. MnSOD protein level in hippocampus and cortex decreased 1 h after irradiation with 3 Gy of gamma-rays. 24 h after exposure, MnSOD protein level in cortex was similar to control values, while in hippocampus it was still significantly decreased. We have concluded that regional differences in MnSOD radioinducibility are regulated at the level of protein synthesis, and that they represent one of the main reasons for region-specific radiosensitivity of the brain.

PMID: 17191666
 

Kathy

Well-known member
At the Wikipedia site [on-line dictionary], the depleted uranium page has been regularly updated with some information which was not there earlier.

I am quite shocked to learn that DU is being used as "counterweights and sinker bars in oil drills"... This might help explain how deer with CWD were exposed to a radioactive substance... "drilling mud" spread on the land which they [and our cattle, sheep, goats, horses, etc] graze. Not to mention the land which grows crops for human consumption.

Another area of interest, also new to the Wikipedia site, is its use in dental porcelain for false teeth. ... my god, where else will we find out DU is being used?

Civilian applications for depleted uranium are fairly limited and are typically unrelated to its radioactive properties. It primarily finds application as ballast because of its high density. Such applications include sailboat keels, as counterweights and sinker bars in oil drills, gyroscope rotors, and in other places where there is a need to place a weight that occupies as little space as possible. However other high density materials are sometimes preferred because uranium is prone to corrosion.

Other relatively minor consumer product uses have included: incorporation into dental porcelain used for false teeth to simulate the fluorescence of natural teeth; and in uranium-bearing reagents used in chemistry laboratories (eg. uranyl acetate, used in analytical chemistry and as a stain in electron microscopy).

http://en.wikipedia.org/wiki/Depleted_uranium
 

flounder

Well-known member
Kathy said:
Sadly, this research gets published after Mark Purdey has passed away.

Do you really believe FATEPRiDE, and others, when they claim that OPs did not influence the BSE catastrophe in the UK, and elsewhere?
[/quote]


simple fact is, purdey was wrong. what part of that do you not understand ???


Subject: FATEPriDE KEY FINDINGS ORGANOPHOSPHATE NO RELATIONSHIP TO CAUSE TSE
Date: May 3, 2007 at 8:41 am PST

KEY FINDINGS

Organophosphate Studies

6. Studies using phosmet (an organophosphate pesticide) were
carried out throughout the project. No relationship between this
compound and the potential to cause a TSE were identified. In
studies with oral dosing of rats, it was shown that PrP expression
levels increased in the brain but there was no association between
this and formation of proteinase K (PK) resistant PrP.


snip...


12. A model of seed protein aggregation and fibril formation was
established using PrP charged with Mn2+. PrP-Mn2+ was found to
form small circular aggregates able to catalyse further protein
aggregation and fibrilisation of PrP. This model unlike other
published models (for example those of Baskakov et al.1) does not
require the presence of denaturants and is not an autocatalytic
process (i.e. the substrate of the reaction did not aggregate). The
results suggest that Mn2+ may play a role in the formation of prion
seeds

__although further studies showed that this material was not
infectious in mouse bioassay.__

snip...

24. The project also generated information concerning the relation of
TSEs to environmental factors:
• __Potentially no role for organophosphates in TSEs.__
• Increased Mn in the diet results in higher PrP levels in the
brain.
• No conclusion is yet possible in terms of the relationship
between environmental trace element concentrations and the
geographical occurrence of TSEs (classical scrapie or BSE).
• Some confirmation was provided that in some specific farms
occurrence of classical scrapie correlates with high Mn levels.


http://www.seac.gov.uk/papers/97-4.pdf

OP'S MEETING WITH PURDEY

http://www.bseinquiry.gov.uk/files/yb/1994/02/09001001.pdf



simply put, as i have said time and time again, op's and or metals, do NOT
cause any TSE. ...TSS
 

Kathy

Well-known member
I see Terry (via google searches) that you were very quick to post the SEAC 97 FATEPRiDE preliminary report infor onto many, many, many sites including the veggie source site and CJD sites......

Your enthusiasm for getting this type of preliminary data out is ..... well it is what it is....

And no! Purdey was not entirely wrong, anymore than he was entirely correct....

The OP connection may not directly causal of prion malformation.... but it is directly responsible for chelating and tying-up copper in the animals AND caused a major un-natural (artificially induced) up-regulation of production of the prion protein at a time when copper deficiency was a known problem in the UK and when Chernobyl showered down its radio-active fallout over Europe and other nations!

Fatepride can claim that OPs did not cause the malformation of prions; but, they are (as I said earlier) criminally neglegent if they state that the organophosphates had nothing to do with the BSE crisis in the UK.

You can huff and puff all you want Terry, on every website there is; but it will not change the FACT the OPs causing harm to humans and animals.

The mandated warble eradication program of the early 1980's in the UK put cattle in a very "un-natural state" of hyper-prion-production and it bound up copper binding sites somehow making copper unavailable for attachment to copper-loading proteins. This had more than an effect on prions, it would have also damaged the abilities of various antioxidants (like Cu/Zn SOD) which would be required to deal with the oxidative stress resulting from the use of OPs and daily insults.

The USA patent which identifies the use of Organophosphates as a tool to chelate radiological metals out of acidic aqueous solutions, also shows that OPs could have made these nuclides MORE BIO-AVAILABLE to the animals biological systems - thus exacerbating the situation when meat and bone meal was fed back to these animals. Bones being a major absorber of these metals.

One example:
United States Patent 5,770,085
Wai , et al. June 23, 1998

Extraction of metals and/or metalloids from acidic media using supercritical fluids and salts

Abstract
A method of extracting metalloid and metal species from a solid or liquid material by exposing the material to a fluid solvent, particularly supercritical carbon dioxide, containing a chelating agent is described. The chelating agent forms chelates that are soluble in the fluid to allow removal of the species from the material. In preferred embodiments, the extraction solvent is supercritical carbon dioxide and the chelating agent comprises a trialkyl phosphate, a triaryl phosphate, a trialkylphosphine oxide, a triarylphosphine oxide, or mixtures thereof. The method provides an environmentally benign process for removing contaminants from industrial waste. The method is particularly useful for extracting actinides from acidic solutions, and the process can be aided by the addition of nitrate salts. The chelate and supercritical fluid can be regenerated, and the contaminant species recovered, to provide an economic, efficient process.


quote:
The results from these extraction procedures also are provided in Table XVI. These results show that actinides were efficiently extracted from acidic solutions using both organophosphate and organophosphine oxides in supercritical carbon dioxide.

In fact the Commission Energy Atomic of France even KNEW back in 1980's that organophosphates could extract these actinide from an solution and patented a process that would prevent certain ones like uranium from being pulled out by organophosphates:

United States Patent 4,764,352
Bathellier , et al. August 16, 1988

Process for preventing the extraction of technetium and/or rhenium, particularly during the extraction of uranium and/or plutonium by an organic solvent


Abstract
Process for preventing the extraction of technetium and/or rhenium, particularly during the extraction of uranium and/or plutonium by an organic solvent. This process permitting the extraction of a chemical element, such as uranium or plutonium present in an aqueous solution containing both said element, technetium and/or rhenium and zirconium and/or hafnium consists of contacting the aqueous solution with an organic solvent able to extract said element, wherein for preventing the extraction of the technetium and/or rhenium with said element, to the aqueous solution is added a zirconium and/or hafnium complexing agent in a quantity adequate for complexing all the zirconium and/or hafnium, said agent being soluble in the aqueous solution.

Inventors: Bathellier; Andre (Sceaux, FR), Pasquiou; Jean-Yves (Gif sur Yvette, FR), Vialard; Etienne (Paris, FR)
Assignee: Commissariat a l'Energie Atomique (Paris, FR)

Appl. No.: 06/878,131
Filed: June 25, 1986

quote:
What is claimed is:

1. A process for the extraction of at least one first element selected from the group consisting of actinides and present in an aqueous solution containing both said first element, at least one second element selected from the group consisting of rhenium and technetium and at least one third element selected from the group consisting of hafnium and zirconium, said process comprising the steps of bringing the aqueous solution into contact with an organic solvent comprising a phosphorous compound having only one electron donor oxygen atom and able to extract said first element, in order to prevent the extraction of the second element with the said first element, adding to the aqueous solution a complexing agent of the third element in a quantity adequate for completely complexing said third element, said agent being soluble in the aqueous solution.

2. A process according to claim 1, wherein the second element is technetrium and the third element is zirconium.

3. A process according to claim 1, wherein the complexing agent is a carboxylic acid.

4. A process according to claim 3, wherein the complexing agent is oxalic acid.

5. A process according to claim 3, wherein the complexing agent is glycolic acid.

6. A process according to claim 1, wherein the first element is uranium.

7. A process according to claim 1, wherein the organic solvent is tributyl phosphate.

8. A process according to claim 1, wherein the aqueous solution is a nitric acid solution.

9. A process according to claim 1, wherein the first element is plutonium.

10. A process according to claim 1, wherein the organic solvent is selected from the group consisting of a neutral phosphine oxide and an organophosphate.

11. A process according to claim 1, wherein the first element is selected from the group consisting of neptunium, plutonium, uranium and thorium.

12. A process according to claim 1, wherein the complexing agent is oxalic acid and the third element is zirconium.

13. A process according to claim 12, wherein the ratio R of the oxalic acid concentration to the zirconium concentration is 1.ltoreq.R.ltoreq.2.

.....

It has also been found that the extraction of technetium by the organic solvent was more particularly increased in the presence of zirconium ions. It would appear that this extraction is due to the formation of a mixed nitric complex of technetium and zirconium in the organic solvent.

[----- the organic solvent being an organophosphate.....]

United States Patent 4,548,790
Horwitz , et al. October 22, 1985

Method for extracting lanthanides and actinides from acid solutions

Abstract
A process for the recovery of actinide and lanthanide values from aqueous acidic solutions with an organic extractant having the formula: ##STR1## where .phi. is phenyl, R.sup.1 is a straight or branched alkyl or alkoxyalkyl containing from 6 to 12 carbon atoms and R.sup.2 is an alkyl containing from 3 to 6 carbon atoms. The process is suitable for the separation of actinide and lanthanide values from fission product values found together in high level nuclear reprocessing waste solutions.

Inventors: Horwitz; E. Philip (Naperville, IL), Kalina; Dale G. (Naperville, IL), Kaplan; Louis (Lombard, IL), Mason; George W. (Clarendon Hills, IL)
Assignee: The United States of America as represented by the United States (Washington, DC)

Appl. No.: 06/517,475
Filed: July 26, 1983

quote:
....One group of extractants which have been considered for the extraction of lanthanide and actinide values from aqueous acid waste solutions are the bidentate organophosphorous compounds.

The extractant may be one of a series of several neutral bifunctional organophosphorous compounds containing a phenyl.

BSE inquiry supplementary testimony by Dr. Anthony Andrews:
http://www.bseinquiry.gov.uk/files/ws/s269a.pdf
45. It would appear that the data for usage of OPs in treatment and prevention of warble fly are now lost,

[and where did all this data disappear to?]

See Mark's information on OPs and copper chelation here:
http://www.markpurdey.com/science_ecosystems8.htm

I don't believe Mark ever did researched about the OPs chelating the heavy metals and actinides from the Meat and Bone Meal, thus providing a highly concentrated source of these metals for the animals consuming it.

Phosmet induces up-regulation of surface levels of the cellular prion protein.

Molecular Neuroscience

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.

link to abstract: http://www.neuroreport.com/pt/re/neuroreport/abstract.00001756-199805110-00026.htm;jsessionid=GGsbmYJMmwFxZpLQLQq22G55Nlb0p4psCX2GHMG2jfjycR7m4Qgn!3145886!-949856145!8091!-1
 

flounder

Well-known member
Kathy said:
I see Terry (via google searches) that you were very quick to post the SEAC 97 FATEPRiDE preliminary report infor onto many, many, many sites including the veggie source site and CJD sites......

Your enthusiasm for getting this type of preliminary data out is ..... well it is what it is....

And no! Purdey was not entirely wrong, anymore than he was entirely correct....

The OP connection may not directly causal of prion malformation.... but it is directly responsible for chelating and tying-up copper in the animals AND caused a major un-natural (artificially induced) up-regulation of production of the prion protein at a time when copper deficiency was a known problem in the UK and when Chernobyl showered down its radio-active fallout over Europe and other nations!

Fatepride can claim that OPs did not cause the malformation of prions; but, they are (as I said earlier) criminally neglegent if they state that the organophosphates had nothing to do with the BSE crisis in the UK.

You can huff and puff all you want Terry, on every website there is; but it will not change the FACT the OPs causing harm to humans and animals.


kathy,

why don't you just admit when you are wrong and move on. you are only discrediting yourself. also, please show me where i said op's do not cause harm? never said that. i said OP's do not cause TSE. and i will continue to huff and puff when people continue to pass false data, and believe in junk science, only to detour, deceive, confuse, or distort the facts, just to save the industry. these are the facts;


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



2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)


http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml



look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused
7% (1 of 14) of the cows to come down with BSE;


Risk of oral infection with bovine spongiform encephalopathy agent in
primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys
Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to
non-human primates. We gave two macaques a 5 g oral dose of brain homogenate
from a BSE-infected cow. One macaque developed vCJD-like neurological
disease 60 months after exposure, whereas the other remained free of disease
at 76 months. On the basis of these findings and data from other studies, we
made a preliminary estimate of the food exposure risk for man, which
provides additional assurance that existing public health measures can
prevent transmission of BSE to man.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a
similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of
disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic
ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula


Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa




It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf




2

6. It also appears to me that Mr Bradley's answer (that it would take less
than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise
that it

could take as little of 1 gram of brain to cause BSE by the oral route
within the

same species. This information did not become available until the "attack
rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to
ensure

that the actual result was within both a lower and an upper limit within the
study

and the designing scientists would not have expected all the dose levels to
trigger

infection. The dose ranges chosen by the most informed scientists at that
time

ranged from 1 gram to three times one hundred grams. It is clear that the
designing

scientists must have also shared Mr Bradley's surprise at the results
because all the

dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s147f.pdf


Calves were challenged by mouth with homogenised brain from confirmed cases
of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They
were then left to develop BSE, but were not subjected to the normal stresses
that they might have encountered in a dairy herd. Animals in all four groups
developed BSE. There has been a considerable spread of incubation period in
some of the groups, but it appears as if those in the 1 and 10g challenge
groups most closely fit the picture of incubation periods seen in the
epidemic. Experiments in progress indicate that oral infection can occur in
some animals with doses as low as 0.01g and 0.001g. .........



http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose




10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA
2007



Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was
cross-contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI

___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL
Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal,
TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY
Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST
POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL
DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK
CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC
MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY,
A-BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not
bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007


http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html


USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN

18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.


snip...



64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD.


snip...



http://www.seac.gov.uk/minutes/95.pdf




3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve
University

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years.

***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.***


6:30 Close of Day One


http://www.healthtech.com/2007/tse/day1.asp




SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...


http://www.cjdsurveillance.com/resources-casereport.html



There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
collection.

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf


THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;


CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006


The U.S. Department of Agriculture was quick to assure the public earlier
this week that the third case of mad cow disease did not pose a risk to
them, but what federal officials have not acknowledged is that this latest
case indicates the deadly disease has been circulating in U.S. herds for at
least a decade.

The second case, which was detected last year in a Texas cow and which USDA
officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is
thought that cows usually contract the disease from contaminated feed they
consume as calves. The concern is that humans can contract a fatal,
incurable, brain-wasting illness from consuming beef products contaminated
with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the
National Institutes of Health's Laboratory for Central Nervous System
Studies and an expert on mad cow-like diseases, told United Press
International. "The question was, 'How many?' and we still can't answer
that."

Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before
one year ago" because of the agency's reluctance to retest the Texas cow
that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything USDA did before 2005
suspect," Brown said. ...snip...end


http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r


CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ...
Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central
Nervous System ... Address for correspondence: Paul Brown, Building 36, Room
4A-05, ...


http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm





PAUL BROWN COMMENT TO ME ON THIS ISSUE

Tuesday, September 12, 2006 11:10 AM


"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."


OR, what the Honorable Phyllis Fong of the OIG found ;


Audit Report

Animal and Plant Health Inspection Service

Bovine Spongiform Encephalopathy (BSE) Surveillance Program – Phase II

and

Food Safety and Inspection Service

Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III

Report No. 50601-10-KC January 2006

Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain


http://www.usda.gov/oig/webdocs/50601-10-KC.pdf




EXPORTATION AND IMPORTATION OF ANIMALS AND ANIMAL PRODUCTS:
BSE; MRR AND IMPORTATION OF COMMODITIES, 65758-65759 [E6-19042]



http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&T=0&P=3854




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0611&L=sanet-mg&T=0&P=3381




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=498




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0702&L=sanet-mg&T=0&P=10277




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&T=0&P=9972




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=4492




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=2583




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=2470


Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.


http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535





BRITISH MEDICAL JOURNAL


BMJ


http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2





BMJ


http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1




Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States


Email Terry S. Singeltary:


[email protected]


I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?


http://www.neurology.org/cgi/eletters/60/2/176#535




LANCET INFECTIOUS DISEASE JOURNAL


Volume 3, Number 8 01 August 2003


Newsdesk


Tracking spongiform encephalopathies in North America


Xavier Bosch

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost

my mom to hvCJD (Heidenhain variant CJD) and have been searching for

answers ever since. What I have found is that we have not been told the

truth. CWD in deer and elk is a small portion of a much bigger problem.


49-year-old Singeltary is one of a number of people who have remained

largely unsatisfied after being told that a close relative died from a

rapidly progressive dementia compatible with spontaneous

Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of

documents on transmissible spongiform encephalopathies (TSE) and

realised that if Britons could get variant CJD from bovine spongiform

encephalopathy (BSE), Americans might get a similar disorder from

chronic wasting disease (CWD) the relative of mad cow disease seen among

deer and elk in the USA. Although his feverish search did not lead him

to the smoking gun linking CWD to a similar disease in North American

people, it did uncover a largely disappointing situation.


Singeltary was greatly demoralised at the few attempts to monitor the

occurrence of CJD and CWD in the USA. Only a few states have made CJD

reportable. Human and animal TSEs should be reportable nationwide and

internationally, he complained in a letter to the Journal of the

American Medical Association (JAMA 2003; 285: 733). I hope that the CDC

does not continue to expect us to still believe that the 85% plus of all

CJD cases which are sporadic are all spontaneous, without route or source.


Until recently, CWD was thought to be confined to the wild in a small

region in Colorado. But since early 2002, it has been reported in other

areas, including Wisconsin, South Dakota, and the Canadian province of

Saskatchewan. Indeed, the occurrence of CWD in states that were not

endemic previously increased concern about a widespread outbreak and

possible transmission to people and cattle.


To date, experimental studies have proven that the CWD agent can be

transmitted to cattle by intracerebral inoculation and that it can cross

the mucous membranes of the digestive tract to initiate infection in

lymphoid tissue before invasion of the central nervous system. Yet the

plausibility of CWD spreading to people has remained elusive.


Part of the problem seems to stem from the US surveillance system. CJD

is only reported in those areas known to be endemic foci of CWD.

Moreover, US authorities have been criticised for not having performed

enough prionic tests in farm deer and elk.


Although in November last year the US Food and Drug Administration

issued a directive to state public-health and agriculture officials

prohibiting material from CWD-positive animals from being used as an

ingredient in feed for any animal species, epidemiological control and

research in the USA has been quite different from the situation in the

UK and Europe regarding BSE.


Getting data on TSEs in the USA from the government is like pulling

teeth, Singeltary argues. You get it when they want you to have it,

and only what they want you to have.


Norman Foster, director of the Cognitive Disorders Clinic at the

University of Michigan (Ann Arbor, MI, USA), says that current

surveillance of prion disease in people in the USA is inadequate to

detect whether CWD is occurring in human beings; adding that, the

cases that we know about are reassuring, because they do not suggest the

appearance of a new variant of CJD in the USA or atypical features in

patients that might be exposed to CWD. However, until we establish a

system that identifies and analyses a high proportion of suspected prion

disease cases we will not know for sure. The USA should develop a

system modelled on that established in the UK, he points out.


Ali Samii, a neurologist at Seattle VA Medical Center who recently

reported the cases of three hunters two of whom were friends who died

from pathologically confirmed CJD, says that at present there are

insufficient data to claim transmission of CWD into humans; adding that

[only] by asking [the questions of venison consumption and deer/elk

hunting] in every case can we collect suspect cases and look into the

plausibility of transmission further. Samii argues that by making both

doctors and hunters more aware of the possibility of prions spreading

through eating venison, doctors treating hunters with dementia can

consider a possible prion disease, and doctors treating CJD patients

will know to ask whether they ate venison.


CDC spokesman Ermias Belay says that the CDC will not be investigating

the [Samii] cases because there is no evidence that the men ate

CWD-infected meat. He notes that although the likelihood of CWD

jumping the species barrier to infect humans cannot be ruled out 100%

and that [we] cannot be 100% sure that CWD does not exist in humans&

the data seeking evidence of CWD transmission to humans have been very

limited.



http://infection.thelancet.com/journal/journal.isa




UPDATE, ATYPICAL SCRAPIE NOR98 DOCUMENTED IN USA ;

SCRAPIE UPDATE USA AS OF MARCH 2007 NOR98 INCLUDED

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps


NOR98-LIKE STRAIN OF SCRAPIE FOUND IN WYOMING (1791 lines)
From: Terry S. Singeltary Sr.
Date: Wed, 11 Apr 2007 15:08:15 -0500



http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=8315


THE SEVEN SCIENTIST REPORT ***


http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf


Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)


http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf


[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk
Materials for Human Food and Requirement for the Disposition of
Non-Ambulatory Disabled Cattle

03-025IFA
03-025IFA-2
Terry S. Singeltary


9/13/2005

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf




Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

http://www.chron.com/disp/story.mpl/ap/fn/4796252.html
 

Kathy

Well-known member
Flounder,

why don't you leave us alone at rancher's.... my information upsets you so much, I am passing on scientific papers and patent info which shows data I feel is pertinent to BSE and other TSEs... you don't agree... move on.... I have yet to see a prion experimental transmission or consumptions study where they analyzed the tissue for actinides

So you know, Terry. I don't do this to save the industry... it is doing a fine job on its own (with the help of several cattle organizations) to destroy itself... for example... the continued use of growth hormones when harm has been shown and when the educated consumer does not want them used..

My part in the beef industry, is converting grass to muscle. I have many acres of land that is best suited for raising cattle and grass fed beef is the future.

You don't agree with me, that does not give you grounds to say that I am distorting or deceiving, etc...

You should not worry yourself about the comments of someone that you have so little respect for. The grown adults that use this "ranchers" message board can read and think for themselves. Their opinions are valuable to me. Even your comments have aided me in finding new data.

You are the first, most of the time, to post new cases of BSE. You should use your talent to find out where the he$$ these animals are being raised, so all can review the environmental factors that may, or may not, be giving rise to BSE, CWD, scrapie et al.

....exposed to the infectious agents only by their nonforced consumption of known infectious tissues

ya, that's real science. Even Gadjusek was changing his opinion and requested all of Mark Purdey's papers (right before he was thrown in jail)...

One man's junk science, is another man's treasure.

Here is a older comment from Neil Cashman which I found at the link below:
http://www.newmediaexplorer.org/chris/2004/01/07/re_mad_cow_disease_pesticides_organophosphate.htm
Date: Mon, 26 May 2003 07:12:09 -0400
From: [email protected]
To: [email protected]
Subject: Re: Mad Cow disease & pesticides (Organophosphate)
I'm sorry to say that I believe the organophosphate theory to be nonsense.
Likewise with manganese. There are plenty of other reasons to minimize or avoid the use of these agents, but "causing" BSE is not one of them.

Best,

Neil Cashman

Considering the mountains of information coming to light about manganese and the prion protein, Neil Cashman had better change his tune or get left behind in the dust. As for OPs, note his very careful choice of words. "...but "causing" BSE is not one of them."

Causing the malformed protein - alone, by itself....

contributing to the susceptibility of the animal is a whole other matter.

Chow man, I have real work to do!
 
A

Anonymous

Guest
Hey Kathy-- Heres another conspiracy you better check on...Since you don't believe in terrorists it must be that now we got madcows committing suicide by drowning themselves....!!!

Looks like a hot lead to me......
:roll: :wink: :lol:

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

Mystery sparks speculation




May 11 2007


On May 4 there was an article headline which read, Bloated structure inappropriate.

Then the following week we have the story of the beached bovine and directly underneath another of mad cow disease. Could this be some plot or terrorist attack?

Is it possible the said bovine was so overtaken with madness that it thought it was a whale, and is it possible, that just like information regarding air flight bombings, that its plight was planned?

My suspicion is if this is the case, the terrorists missed their target with the mad bovine by miles.

Their real target was likely right smack in front of the new condos being erected in downtown Parksville beachfront and not on some obscure beach in Bowser.

I know that’s where my target would have been.

So, why did the cow cross the straits? To get to the other side, of course.

Tami Jones

Coombs

http://www.pqbnews.com/portals-code/list.cgi?paper=50&cat=45&id=982046&more=
 

Mrs.Greg

Well-known member
Oldtimer said:
Hey Kathy-- Heres another conspiracy you better check on...Since you don't believe in terrorists it must be that now we got madcows committing suicide by drowning themselves....!!!

Looks like a hot lead to me......
:roll: :wink: :lol:

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

Mystery sparks speculation




May 11 2007


On May 4 there was an article headline which read, Bloated structure inappropriate.

Then the following week we have the story of the beached bovine and directly underneath another of mad cow disease. Could this be some plot or terrorist attack?

Is it possible the said bovine was so overtaken with madness that it thought it was a whale, and is it possible, that just like information regarding air flight bombings, that its plight was planned?

My suspicion is if this is the case, the terrorists missed their target with the mad bovine by miles.

Their real target was likely right smack in front of the new condos being erected in downtown Parksville beachfront and not on some obscure beach in Bowser.

I know that’s where my target would have been.

So, why did the cow cross the straits? To get to the other side, of course.

Tami Jones

Coombs

http://www.pqbnews.com/portals-code/list.cgi?paper=50&cat=45&id=982046&more=
:lol: :lol:
 

flounder

Well-known member
ITEM 6 FATEPRIDE (SEAC 97/4)
35. The Chair explained that FATEPriDE is a multi-centre European
Union funded project that examined the possible influence of
environmental trace elements on the occurrence of TSEs.
36. Professor David Brown (University of Bath) explained that the
project had principally studied potential interactions between prion
disease and copper and manganese, although interactions with
other environmental factors such as organophosphates had also
been assessed. No link, other than with manganese, between
many environmental factors studied, including organophosphates,
and TSEs was found. The key experiments and findings had been
summarised in SEAC paper 97/4. The main conclusions were that
manganese binds to PrP with similar affinity to known manganese
binding proteins, induces conformational change in PrP, catalyses
PrP aggregation, induces protease resistance in PrP, increases
PrP expression levels and increases cellular susceptibility to prion
infection. Manganese had also been found at high levels on farms
with a high classical scrapie incidence and manganese was found
to increase the stability of PrP in soil. Although it had been the
intention to create maps of bioavailable manganese and compare
those to similar maps of TSE hotspots, this had not been possible
as no data of sufficient precision relating the location of BSE or
scrapie cases was made available. Further studies were required
to investigate the interactions of manganese and prions.


37. Members noted that the study suggested an association between
high levels of bioavailable manganese, low levels of bioavailable
copper and classical scrapie in field studies. However, it was likely
that other factors such as soil pH and organic matter may also be
involved. It was acknowledged that it was very difficult in
environmental studies to exclude potential confounding factors.
The experimental and field data suggested that manganese may
influence the susceptibility to TSEs.

However, there was no
evidence that environmental factors, including manganese, cause
disease.


38. Members noted that data on BSE should allow spatial mapping of
cases, however sheep movements were so complex that it is not
possible to create similar maps for classical or atypical scrapie.
39. Members suggested that further research could investigate the
differential stability of a range of TSE agents bound with
manganese in soil, although other modifying factors in soil such as
12
© SEAC 2006
soil content and pH are likely. In addition, further animal studies
could examine the effect of manganese on a range of TSE agents.


http://www.seac.gov.uk/papers/draft98-1.pdf


flounder said:
Kathy said:
I see Terry (via google searches) that you were very quick to post the SEAC 97 FATEPRiDE preliminary report infor onto many, many, many sites including the veggie source site and CJD sites......

Your enthusiasm for getting this type of preliminary data out is ..... well it is what it is....

And no! Purdey was not entirely wrong, anymore than he was entirely correct....

The OP connection may not directly causal of prion malformation.... but it is directly responsible for chelating and tying-up copper in the animals AND caused a major un-natural (artificially induced) up-regulation of production of the prion protein at a time when copper deficiency was a known problem in the UK and when Chernobyl showered down its radio-active fallout over Europe and other nations!

Fatepride can claim that OPs did not cause the malformation of prions; but, they are (as I said earlier) criminally neglegent if they state that the organophosphates had nothing to do with the BSE crisis in the UK.

You can huff and puff all you want Terry, on every website there is; but it will not change the FACT the OPs causing harm to humans and animals.


kathy,

why don't you just admit when you are wrong and move on. you are only discrediting yourself. also, please show me where i said op's do not cause harm? never said that. i said OP's do not cause TSE. and i will continue to huff and puff when people continue to pass false data, and believe in junk science, only to detour, deceive, confuse, or distort the facts, just to save the industry. these are the facts;


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



2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)


http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml



look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused
7% (1 of 14) of the cows to come down with BSE;


Risk of oral infection with bovine spongiform encephalopathy agent in
primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys
Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to
non-human primates. We gave two macaques a 5 g oral dose of brain homogenate
from a BSE-infected cow. One macaque developed vCJD-like neurological
disease 60 months after exposure, whereas the other remained free of disease
at 76 months. On the basis of these findings and data from other studies, we
made a preliminary estimate of the food exposure risk for man, which
provides additional assurance that existing public health measures can
prevent transmission of BSE to man.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a
similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of
disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic
ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula


Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa




It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf




2

6. It also appears to me that Mr Bradley's answer (that it would take less
than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise
that it

could take as little of 1 gram of brain to cause BSE by the oral route
within the

same species. This information did not become available until the "attack
rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to
ensure

that the actual result was within both a lower and an upper limit within the
study

and the designing scientists would not have expected all the dose levels to
trigger

infection. The dose ranges chosen by the most informed scientists at that
time

ranged from 1 gram to three times one hundred grams. It is clear that the
designing

scientists must have also shared Mr Bradley's surprise at the results
because all the

dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s147f.pdf


Calves were challenged by mouth with homogenised brain from confirmed cases
of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They
were then left to develop BSE, but were not subjected to the normal stresses
that they might have encountered in a dairy herd. Animals in all four groups
developed BSE. There has been a considerable spread of incubation period in
some of the groups, but it appears as if those in the 1 and 10g challenge
groups most closely fit the picture of incubation periods seen in the
epidemic. Experiments in progress indicate that oral infection can occur in
some animals with doses as low as 0.01g and 0.001g. .........



http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose




10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA
2007



Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was
cross-contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI

___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL
Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal,
TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY
Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST
POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL
DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK
CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC
MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY,
A-BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not
bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007


http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html


USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN

18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.


snip...



64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD.


snip...



http://www.seac.gov.uk/minutes/95.pdf




3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve
University

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years.

***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.***


6:30 Close of Day One


http://www.healthtech.com/2007/tse/day1.asp




SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...


http://www.cjdsurveillance.com/resources-casereport.html



There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
collection.

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf


THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;


CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006


The U.S. Department of Agriculture was quick to assure the public earlier
this week that the third case of mad cow disease did not pose a risk to
them, but what federal officials have not acknowledged is that this latest
case indicates the deadly disease has been circulating in U.S. herds for at
least a decade.

The second case, which was detected last year in a Texas cow and which USDA
officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is
thought that cows usually contract the disease from contaminated feed they
consume as calves. The concern is that humans can contract a fatal,
incurable, brain-wasting illness from consuming beef products contaminated
with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the
National Institutes of Health's Laboratory for Central Nervous System
Studies and an expert on mad cow-like diseases, told United Press
International. "The question was, 'How many?' and we still can't answer
that."

Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before
one year ago" because of the agency's reluctance to retest the Texas cow
that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything USDA did before 2005
suspect," Brown said. ...snip...end


http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r


CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ...
Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central
Nervous System ... Address for correspondence: Paul Brown, Building 36, Room
4A-05, ...


http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm





PAUL BROWN COMMENT TO ME ON THIS ISSUE

Tuesday, September 12, 2006 11:10 AM


"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."


OR, what the Honorable Phyllis Fong of the OIG found ;


Audit Report

Animal and Plant Health Inspection Service

Bovine Spongiform Encephalopathy (BSE) Surveillance Program – Phase II

and

Food Safety and Inspection Service

Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III

Report No. 50601-10-KC January 2006

Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain


http://www.usda.gov/oig/webdocs/50601-10-KC.pdf




EXPORTATION AND IMPORTATION OF ANIMALS AND ANIMAL PRODUCTS:
BSE; MRR AND IMPORTATION OF COMMODITIES, 65758-65759 [E6-19042]



http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&T=0&P=3854




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0611&L=sanet-mg&T=0&P=3381




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=498




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0702&L=sanet-mg&T=0&P=10277




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&T=0&P=9972




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=4492




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=2583




http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=2470


Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.


http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535





BRITISH MEDICAL JOURNAL


BMJ


http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2





BMJ


http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1




Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States


Email Terry S. Singeltary:


[email protected]


I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?


http://www.neurology.org/cgi/eletters/60/2/176#535




LANCET INFECTIOUS DISEASE JOURNAL


Volume 3, Number 8 01 August 2003


Newsdesk


Tracking spongiform encephalopathies in North America


Xavier Bosch

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost

my mom to hvCJD (Heidenhain variant CJD) and have been searching for

answers ever since. What I have found is that we have not been told the

truth. CWD in deer and elk is a small portion of a much bigger problem.


49-year-old Singeltary is one of a number of people who have remained

largely unsatisfied after being told that a close relative died from a

rapidly progressive dementia compatible with spontaneous

Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of

documents on transmissible spongiform encephalopathies (TSE) and

realised that if Britons could get variant CJD from bovine spongiform

encephalopathy (BSE), Americans might get a similar disorder from

chronic wasting disease (CWD) the relative of mad cow disease seen among

deer and elk in the USA. Although his feverish search did not lead him

to the smoking gun linking CWD to a similar disease in North American

people, it did uncover a largely disappointing situation.


Singeltary was greatly demoralised at the few attempts to monitor the

occurrence of CJD and CWD in the USA. Only a few states have made CJD

reportable. Human and animal TSEs should be reportable nationwide and

internationally, he complained in a letter to the Journal of the

American Medical Association (JAMA 2003; 285: 733). I hope that the CDC

does not continue to expect us to still believe that the 85% plus of all

CJD cases which are sporadic are all spontaneous, without route or source.


Until recently, CWD was thought to be confined to the wild in a small

region in Colorado. But since early 2002, it has been reported in other

areas, including Wisconsin, South Dakota, and the Canadian province of

Saskatchewan. Indeed, the occurrence of CWD in states that were not

endemic previously increased concern about a widespread outbreak and

possible transmission to people and cattle.


To date, experimental studies have proven that the CWD agent can be

transmitted to cattle by intracerebral inoculation and that it can cross

the mucous membranes of the digestive tract to initiate infection in

lymphoid tissue before invasion of the central nervous system. Yet the

plausibility of CWD spreading to people has remained elusive.


Part of the problem seems to stem from the US surveillance system. CJD

is only reported in those areas known to be endemic foci of CWD.

Moreover, US authorities have been criticised for not having performed

enough prionic tests in farm deer and elk.


Although in November last year the US Food and Drug Administration

issued a directive to state public-health and agriculture officials

prohibiting material from CWD-positive animals from being used as an

ingredient in feed for any animal species, epidemiological control and

research in the USA has been quite different from the situation in the

UK and Europe regarding BSE.


Getting data on TSEs in the USA from the government is like pulling

teeth, Singeltary argues. You get it when they want you to have it,

and only what they want you to have.


Norman Foster, director of the Cognitive Disorders Clinic at the

University of Michigan (Ann Arbor, MI, USA), says that current

surveillance of prion disease in people in the USA is inadequate to

detect whether CWD is occurring in human beings; adding that, the

cases that we know about are reassuring, because they do not suggest the

appearance of a new variant of CJD in the USA or atypical features in

patients that might be exposed to CWD. However, until we establish a

system that identifies and analyses a high proportion of suspected prion

disease cases we will not know for sure. The USA should develop a

system modelled on that established in the UK, he points out.


Ali Samii, a neurologist at Seattle VA Medical Center who recently

reported the cases of three hunters two of whom were friends who died

from pathologically confirmed CJD, says that at present there are

insufficient data to claim transmission of CWD into humans; adding that

[only] by asking [the questions of venison consumption and deer/elk

hunting] in every case can we collect suspect cases and look into the

plausibility of transmission further. Samii argues that by making both

doctors and hunters more aware of the possibility of prions spreading

through eating venison, doctors treating hunters with dementia can

consider a possible prion disease, and doctors treating CJD patients

will know to ask whether they ate venison.


CDC spokesman Ermias Belay says that the CDC will not be investigating

the [Samii] cases because there is no evidence that the men ate

CWD-infected meat. He notes that although the likelihood of CWD

jumping the species barrier to infect humans cannot be ruled out 100%

and that [we] cannot be 100% sure that CWD does not exist in humans&

the data seeking evidence of CWD transmission to humans have been very

limited.



http://infection.thelancet.com/journal/journal.isa




UPDATE, ATYPICAL SCRAPIE NOR98 DOCUMENTED IN USA ;

SCRAPIE UPDATE USA AS OF MARCH 2007 NOR98 INCLUDED

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps


NOR98-LIKE STRAIN OF SCRAPIE FOUND IN WYOMING (1791 lines)
From: Terry S. Singeltary Sr.
Date: Wed, 11 Apr 2007 15:08:15 -0500



http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=8315


THE SEVEN SCIENTIST REPORT ***


http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf


Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)


http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf


[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk
Materials for Human Food and Requirement for the Disposition of
Non-Ambulatory Disabled Cattle

03-025IFA
03-025IFA-2
Terry S. Singeltary


9/13/2005

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf




Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

http://www.chron.com/disp/story.mpl/ap/fn/4796252.html
 
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