Mark Purdey had it right!

[Kathy]

Hello to the board.

Kaiser has been at me for quite awhile to get my butt over here from the www.ranchers.net message board, so finally, I'm here.

We just started calving this weekend, right on schedule with the annual April blizzard.

Not to many calves coming, thank goodness. And we are happy for the moisture.

I was a friend and fellow detective with the late Mark Purdey.... He has, in my opinion, really been the best to demonstrate what actually causes prion disorders. Dr. David Brown of Bath University is doing a good job also, revealing the damage caused by oxidative stress.

Dr. Vitaly Vodyanoy of Auburn University in Alabama, USA has some very interesting work, and USA patent applications which I recommend reviewing.

United States Patent Application 20070122799
Kind Code A1
Vodyanoy; Vitaly J. ; et al. May 31, 2007

------------------------------------------------------------------------------
Method of isolation and self-assembly of small protein particles from blood and other biological materials

Abstract

Compositions and methods for the isolation and manipulation of misfolded, or partially misfolded, proteins present in blood and other biological materials are provided. In one aspect of the invention, the compositions, hereinafter termed "proteons" are misfolded or partially misfolded proteins surrounding a metallic nanocluster, termed "proteon nucleation center" (PNC). Also provided are compositions and methods for the isolation and manipulation of proteon nucleation centers (PNCs) upon which the proteons of the present in blood and other biological materials form.


and definitely check out this one page review with its own links:

http://ott.auburn.edu/overview/PNC-Misfolded-Proteins.pdf

At a recent meeting in Nisku, about CWD, Dr. Neil Cashman stated that he believes we are looking at a "process of protein crystallization". Golly, isn't that exactly what Mark Purdey talked about!

I'm going to leave you with this to ponder for today.

When I get a chance I'll give some more evidence demonstrating Mark Purdey was on the right path.

Chow!

[per]

Hi Kathy,

I am curious, do you make a living with all the research you do in this subject area or is it a hobby? I have followed this argument on Ranchers and it is obvious you have thoroughly researched this subject. As with any real science the truth eventually comes out. Even then it is usually refuted and denied. The science truly is important but I am interested in selling a product. A safe product yes, but also a product my customer believes is safe.

Phil

[rkaiser]

Hay Kathy, we were due to start April 20th as well and as of today we have almost 1/4 of the 100 head here at home calved out. Dropping like radioactive fallout in Iraq in this lovely weather. So far we are up one as we had three sets of twins but only managed to save one complete set.

Good on you for keeping us up on the work begun by Mark. I have Mark's book but have not had time to get in to it much yet.

[Kathy]

Phil,

I make my living selling cattle. Since May 2003, we have been in the business of selling yearlings off grass in the fall, and occasionally giving away our old or dry cows at auction.

The research is just an area of huge interest to me. It's hard to explain why I care soo much, I just do.

The only thing that will free us from our shackles, is the truth. The consumer will demand their food be protected from pollutants, chemicals and fallout - but only if they know that these products are causing harm.

If everyone sits back on the couch and believes all that the slick commercials tell us about their drugs, and chemicals - we will never get rid of the toxic crap that is creating disease.

The pharmaceutical industry has a few good soldiers, but for the most part... they are a solution looking for a problem. What better way to sell drugs/treatments than to create the diseases to start with. It is perfect corporate capitalism, with no morals.

I am living two lives in one body, or so it feels. The researcher and activist, and the rancher/mother.

Since 1998 when my own government came after all the "welfare cowboys" {so named by former Alberta premier Ralph Klein} re: the grazing lease issue, living on the ranch has taken a different tone, and it ISN'T a good feeling! Cancer in 2002, and BSE in 2003 made me look at my farm life with less foundness and an acute awareness that every day sees some new control measure dumped on us.

Take for example the Agristability program. Have you seen the "Applicant Declaration" document? It is a blood-oath! You will be signing away your freedom forever. The government will have complete access to your farm and farm records - FOREVER, no matter what material or non-material changes they make to AgriStability. Clause 12 states your obligations will survive your termination from the program/or termination of the program itself.

[AFSC's ?] Lawyers have drafted this document, and are fully aware that they are asking you to sign a "floating document". You sign it, and your farm will float in the direction the government tells it to.

One lady from AFSC, basically said to me, "If you take government handouts, you surrender your privacy and rights."

Sorry lady, not me! We won't sign.

[per]

Thanks Kathy. Kinda interesting how the status quo establishment creates strong activists. Good to have you aboard.

[cpallett]

Hi Kathy,

I read the AgriStability Participant Declaration you are taliking about. It sure does appear to be a bit over the top. It also is limited to Alberta. This declaration is not required anywhere else in Canada, as far as I can determine. Seems that Fast Eddie's troops don't trust y'all to tell the whole truth and nothing but the truth when it comes to subsidy money.

As for Mark Purdey, I read Animal Pharm closely and with great interest and recommend it to all and sundry. Excellent read. Interesting man. I have some personal experience with having people not read the material, and even if they do to wilfully misconstrue it. Frustrating indeed.

I wonder what Mr. Purdey would have made of the recent attack rate studies as well as the recent dissection studies that demonstrate the movement of the misfolded prion protein from the Peyer's patches through the central nervous system and finally to the brain over time as the disease progresses? I very much wish he and I had the opportunity to chat. We all have to go, but he had to leave a bit too soon for my liking.

All the best.

[Kathy]

There is an interesting study by a French team that demonstrates how the Peyer's Patches of the distal ileum, preferentially accumulates uranium. The uranium built up in the mesenteric lymph nodes, also.

I suspect that partially misfolded proteins (not prions), just proteins that didn't quite meet the standard and were disposed of as trash - are being transported in the lymphatic system to be dumped, literally. However these partially screwed up protein segments (with a ferrimagnetic metals attached, like manganese or iron) get sequestered by the rogue metal nanoparticles that also are trapped and accummulating in these lymph nodes [like in Vodyanoy's patent application]. Over time, these aggregated, polymerized proteins form fibrils which are more difficult to get rid of. Eventually, they will build up and destroy the white blood cells, clog the lymph glands and dump all the toxic crap back into the body. However, they (fibrils) don't by-pass the blood brain barrier. This may be why many of the positive CWD cases in Alberta, are only positive in the lymph glands and not the brain tissue.

Consequently, in order for the prion fibrils to form in the brain, there must be direct access to the brain by the roque metal nanoparticles - and that usually comes from inhalation or absorption via the eye/optic nerve(gross).

Experimental transmission utilizing homogenized/diseased brain tissue, or laboratory grown strains from yeast or other cells, is absolutely NOT the same as naturally occurring. (note: innoculant is usually "sonicated" just before injection, to break apart the fibrils and super-charge the metal ions).

Anyways, the prion protein (healthy version) is getting more attention, and its benefits as a protector of the cell(s), from oxidative stress, is leading to a better understanding of many disorders. It may even be involved in memory!

Evidence of prion aggregation, may just be a by-stander affect after the fact.

I miss my chats with Mark. His family must miss him terribly.

The whole while I was reading his book, I could hear his voice telling the story...

He certainly had a mischievious side.

Learning about his childhood was kinda neat, it helped to explain his drive.


Toxicology. 2006 Oct 29;227(3):227-39. Epub 2006 Aug 17.
Absorption, accumulation and biological effects of depleted uranium in Peyer's patches of rats.
Dublineau I, Grison S, Grandcolas L, Baudelin C, Tessier C, Suhard D, Frelon S, Cossonnet C, Claraz M, Ritt J, Paquet P, Voisin P, Gourmelon P.
IRSN, Direction de la RadioProtection de l'Homme, Service de Radiobiologie et d'Epidémiologie, Laboratoire de Radiotoxicologie expérimentale, IRSN, BP 17, F-92262 Fontenay-aux-Roses Cedex, France.isabelle.dublineau@irsn.fr

The digestive tract is the entry route for radionuclides following the ingestion of contaminated food and/or water wells. It was recently characterized that the small intestine was the main area of uranium absorption throughout the gastrointestinal tract. This study was designed to determine the role played by the Peyer's patches in the intestinal absorption of uranium, as well as the possible accumulation of this radionuclide in lymphoid follicles and the toxicological or pathological consequences on the Peyer's patch function subsequent to the passage and/or accumulation of uranium. Results of experiments performed in Ussing chambers indicate that the apparent permeability to uranium in the intestine was higher (10-fold) in the mucosa than in Peyer's patches ((6.21 /-1.21 to 0.55 /-0.35)x10(-6)cm/s, respectively), demonstrating that the small intestinal epithelium was the preferential pathway for the transmucosal passage of uranium. A quantitative analysis of uranium by ICP-MS following chronic contamination with depleted uranium during 3 or 9 months showed a preferential accumulation of uranium in Peyer's patches (1355% and 1266%, respectively, at 3 and 9 months) as compared with epithelium (890% and 747%, respectively, at 3 and 9 months). Uranium was also detected in the mesenteric lymph nodes ( approximately 5-fold after contamination with DU). The biological effects of this accumulation of depleted uranium after chronic contamination were investigated in Peyer's patches. There was no induction of the apoptosis pathway after chronic DU contamination in Peyer's patches. The results indicate no change in the cytokine expression (Il-10, TGF-beta, IFN-gamma, TNF-alpha, MCP-1) in Peyer's patches and in mesenteric lymph nodes, and no modification in the uptake of yeast cells by Peyer's patches. In conclusion, this study shows that the Peyer's patches were a site of retention for uranium following the chronic ingestion of this radionuclide, without any biological consequences of such accumulation on Peyer's patch functions.

PMID: 16978755

look up Francois Paquet at Pub Med, he has many papers on how uranium is accumulating in the brain (exposed rats).....

[Kathy]

This Ag Stability "declaration" is only required in Alberta??? hadn't noticed that!

Therefore it is totally unconstitutional, yippie! I was also told, that you did not have to sign the declaration to participate in Agri-Invest.

The folks at AFSC, said that they were only trying to protect the taxpayers money (re: having us sign the declaration). Well, if that's the case, then why don't those who take advantage of Agri-invest, also have to sign the declaration? That's taxpayer money too.

Can you see Cargill or Tyson signing this declaration? Yah right.

[flounder]

mark purdey had it WRONG kathy !


Copper deficiency in the young bovine results in dramatic decreases in brain copper concentration but does not alter brain prion protein biology

L. R. Legleiter, J. W. Spears and H. C. Liu Department of Animal Science and Interdepartmental Nutrition Program, North Carolina State University, Raleigh, NC

Jerry_Spears@ncsu.edu

Abstract

A manganese (Mn) for copper (Cu) substitution on cellular prion proteins (PrPc) in the brain that results in biochemical changes to PrPc has been implicated in the pathogenesis of transmissible spongiform encephalopathies. Recent research in the mature bovine does _NOT_ support this theory. The present study tested this hypothesis using progeny from gestating cows receiving Cu-deficient diets or Cu-deficient diets coupled with high dietary Mn. Copper-adequate cows (n = 39) were assigned randomly to treatments: 1) control (adequate in Cu and Mn), 2) Cu-deficient (-Cu), and 3) Cu-deficient plus high dietary Mn (-Cu Mn). Cows assigned to treatments -Cu and -Cu Mn received no supplemental Cu and were supplemented with molybdenum (Mo) to further induce Cu deficiency. The -Cu Mn treatment also received 500 mg supplemental Mn/kg dietary DM. Calves were weaned at 180 d and maintained on the same treatments as their respective dams for 260 d. Copper-deficient calves (-Cu and -Cu Mn) had decreased (P = 0.001) brain (obex) Cu and tended to have increased (P = 0.09) obex Mn relative to controls. Obex Mn/Cu ratios were substantially increased (P < 0.001) in calves receiving -Cu and -Cu Mn treatments compared to controls and were higher (P < 0.001) in -Cu Mn calves than in -Cu calves. Obex prion protein characteristics, including proteinase K degradability, superoxide dismutase (SOD)-like activity, and glycoform distributions, were largely unaffected. Obex tissue antioxidant capacity was not compromised by perturbations in brain metals, but Cu-deficient calves tended to have decreased (P = 0.06) Cu/Zn SOD activity and increased (P = 0.06) Mn SOD activity. Although obex copper was decreased due to Cu deficiency and Mn increased due to exposure to high dietary Mn, the obex metal imbalance had minimal effects on PrPc functional characteristics in the calves.

http://jas.fass.org/cgi/content/abstract/jas.2007-0403v1

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

a) As regards the involvement of organophosphates in the origin of BSE, no new scientific information providing evidence or supporting the hypothesis by valid data became available after the adoption of the last opinion of the SSC on this issue. Consequently there is no reason for modifying the existing opinions.

b) Regarding the possibility of OP poisoning, the European legislation for registration of plant protection products and veterinary medicines – addressed in the enquiries – provide the basis for safe use of registered compounds and their formulations. Regarding the alleged intoxication cases reported and OP exposure it must be concluded that safety measures may not have been strictly followed.

References

Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R., Fraser, P.E., Kruck, T., von Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar, H. (1997) The Cellular Prion Protein Binds Copper In Vivo, Nature, 390, 684-7. Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs Demonstrate Excesses of the Radical- Generating Divalent Cation Manganese and Deficiencies of Antioxidant Co-Factors Cu, Se, Fe, Zn Medical Hypotheses, 54, 278-306. Scientific Steering Committee, 1998. Opinion on possible links between BSE and Organophosphates. Adopted on 25-26 June 1998 Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and transmission of BSE. Adopted on 29-30 November 2001.

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

OP'S MEETING WITH PURDEY

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

P04.27

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route

Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany

Background:

In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.

Aims:

The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.

Methods:

Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).

Results:

In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.

Conclusions:

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.

The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

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 int****ritoneal.

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

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

2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 7 Terry S. Singeltary Sr. Vol #: 1

Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 -0500 From: "Terry S. Singeltary Sr." To: fdadockets@oc.fda.gov

snip...

Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097, USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit, Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax 1 970 491 0523. e-mail ehoover@lamar.colostate.edu

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.

snip...

These results indicate that mule deer fawns develop detectable PrP res after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node. He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings support oral exposure as a natural route of CWD infection in deer and support oral inoculation as a reasonable exposure route for experimental studies of CWD.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757

Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-L To: BSE-L

8420-20.5% Antler Developer For Deer and Game in the wild Guaranteed Analysis Ingredients / Products Feeding Directions

snip...

_animal protein_

http://www.surefed.com/deer.htm

BODE'S GAME FEED SUPPLEMENT #400 A RATION FOR DEER NET WEIGHT 50 POUNDS 22.6 KG.

snip...

_animal protein_

http://www.bodefeed.com/prod7.htm

J Infect Dis. 2004 Aug 1;190(3):653-60.

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.

http://www.ncbi.nlm.nih.gov/

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

Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST

snip... see listings and references of enormous amounts of banned mad cow protein 'in commerce' in 2006 and 2005 ;

see full text ;

Friday, April 25, 2008

Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46

http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html

SPECIFIED RISK MATERIALS

http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html

Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the United States of America (USA) Question number: EFSA-Q-2003-083

EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.

http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_v2_en1,0.pdf

TSS

[Kathy]

I'm feel very sorry for you flounder. You cannot understand that Mark Purdey was a bloody genius, and yes, dear, he had it absolutely right.

I wish I could enlighten the beef production board on everything I have read over the last 5 years, but that's impossible.

I do however, have very good sources for some information which I cannot discuss openly on the board, right now. It points directly to radiological metals causing prion diseases. Whether directly attached, or as a by-stander effect on near-by cells.

The nature of this disease is multifactoral. And as you know, Dr. Spears is looking at metals in specific manners which eliminate the development of prions. All he needs to do is expose the pregnant cow and fetus to some radiation (be it internalized radionuclides, or external radiation with internal rogue metal partners).

I have enough now to fully convince me this is due to ionizing radiation. Chow!