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Location: BACLIFF, Texas, United States

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS

Saturday, November 02, 2013

OREGON DETECTS SCRAPIE

 
Sent: Saturday, November 02, 2013 12:31 PM
Subject: re-Sheep disease pops up in Douglas County; 300 animals euthanized
 

OREGON DETECTS SCRAPIE
 
 
Sheep disease pops up in Douglas County; 300 animals euthanized
 
 
 
 
 
 
The euthanizing of 300 sheep from a Roseburg ranch shows health officials are vigilant about stopping a livestock disease from spreading, the Oregon state veterinarian said Thursday.
Sheep growers, though, say they received too little information about the state’s first case of scrapie since 2008.
 
“There’s an awful lot of rumors going around. It seems like it would be appropriate to get as much information out about scrapie as possible, because it impacts the market for all of us,” said Oregon Sheep Growers Association President John Fine, a Dixonville rancher.
 
State Veterinarian Brad LeaMaster said Thursday the 300 sheep were from a ranch east of Roseburg, though he declined to identify the rancher.
 
One animal tested positive for scrapie, a fatal brain disease in sheep and goats comparable to mad cow disease, and the sheep were euthanized as a precaution, LeaMaster said.
“It’s not an outbreak. It’s one sheep,” he said. “It’s not a threat to public safety. It’s certainly not a food safety issue.”
 
For the past 10 years in Oregon, the state and the U.S. Department of Agriculture have worked together on a scrapie eradication campaign, said Lyndsay Cole, spokeswoman for the USDA’s Animal and Plant Health Inspection Service.
 
She said the affected Douglas County sheep was identified through a routine sampling of animals at a slaughter plant. Blood tests were taken on the rest of the flock, and the sheep identified as genetically susceptible to scrapie were euthanized.
 
“None of the meat from any of the animals that were depopulated will enter the food chain,” Cole said.
 
LeaMaster said the positive test for scrapie came back in late August, but the federal shutdown in October delayed informing the public.
 
Scrapie has never been known to transfer to people, and it’s not highly contagious, according to a USDA fact sheet.
 
The disease is thought to most commonly spread from ewe to offspring and to other lambs that come in contact with the placenta.
 
Early signs of scrapie include the diseased animal scratching or rubbing against objects, like a fence post.
 
The USDA began an eradication campaign a decade ago, hoping to prevent the economic damage suffered by the beef industry because of mad cow disease.
 
This summer’s case of scrapie was Oregon’s third since 2005.
 
In the past year, the USDA has recorded 18 sheep with scrapie in the U.S., including the one in Douglas County. LeaMaster said testing a live sheep for the disease remains impractical.
 
With about 22,800 ewes valued at roughly $2.6 million, Douglas County is Oregon’s second-largest sheep-producing county. The local sheep population can more than double between December and March, when lambs are born. The American Sheep Industry estimates that every 1,000 head of sheep is responsible for 18 full- or part-time jobs.
 
Dixonville rancher Rancher Jamie Pynch, whose family keeps about 250 head of sheep, said he’s heard talk of scrapie showing up.
 
“It kind of makes you nervous,” he said. “It’s the kind of thing you don’t ever think is going to happen to you.”
 

• You can reach reporter Garrett Andrews at 541-957-4218 or by email at gandrews@nrtoday.com.
 
 
======================
 
>>> Blood tests were taken on the rest of the flock, and the sheep identified as genetically susceptible to scrapie were euthanized.
 
 
really, were NOT slaughtering all scrapie herd cohorts now ???
 
 
nothing surprises me anymore $$$
 
 
 
Hello Garrett and Mr. Ackerman et al,
 
 
I don’t expect any of this to get published, bbbut, you needed to know the rest of this ongoing nightmare.
 
don’t believe everything the USDA INC tells you $$$
 
 
there is, there was, and there has been, evidence to support a risk factor of scrapie transmission to humans. this evidence has been around for decades.
 
but sadly, political science, especially with the TSE prion disease, overrules sound science every day by the industries and legislators, thanks to the USDA and the OIE et al. ...
 
 
NOW, let's look at the evidence brought forth for the potential for transmission of scrapie to humans ;
 
why do we not want to do TSE transmission studies on chimpanzees $
 
snip...
 
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
 
snip...
 
R. BRADLEY
 
 
 
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.
 
snip...
 
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
 
PMID: 6997404
 
 
 
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"
 
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
 
snip...
 
76/10.12/4.6
 
 
 
Nature. 1972 Mar 10;236(5341):73-4.
 
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
 
Gibbs CJ Jr, Gajdusek DC.
 
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
 
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
 
C. J. GIBBS jun. & D. C. GAJDUSEK
 
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
 
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
 
 
 
 
 
Suspect symptoms
 
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
 
28 Mar 01
 
Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
 
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
 
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
 
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.
 
Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.
 
Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.
 
As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.
 
"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.
 
But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.
 
People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.
 
But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."
 
There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.
 
Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.
 
 
 
Wednesday, February 16, 2011
 
IN CONFIDENCE
 
SCRAPIE TRANSMISSION TO CHIMPANZEES
 
IN CONFIDENCE
 
 
 
Sunday, December 12, 2010
 
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010
 
 
 
Sunday, April 18, 2010
 
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
 
 
 
AND ATYPICAL NOR-98 SCRAPIE IS EVEN MORE OF A CONCERN FOR TRANSMISSION TO HUMANS, AND THE ATYPICAL NOR-98 HAS SPREAD FROM COAST TO COAST HERE IN THE USA ;
 
Thursday, March 29, 2012
 
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
 
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
 
 
 
AND WHAT HAVE THE PRION GODS SAID OF THE ATYPICAL NOR-98, AND IT'S POTENTIAL FOR TRANSMISSION TO HUMANS ;
 
A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes
 
Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations
 
*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway
 
***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)
 
Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice.
 
*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
 
 
 
OR
 
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
 
 
 
OR
 
*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
 
 
 
 
 
*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
 
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $
 
OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles
 
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA
 
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.
 
Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
 
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.
 
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.
 
Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
 
The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
 
 
 
Monday, January 14, 2013
 
Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe
 
 
 
Saturday, July 6, 2013
 
Small Ruminant Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy
 
Research Article
 
 
 
Monday, August 9, 2010
 
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more Prionbaloney ?
 
 
 
Wednesday, March 28, 2012
 
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $
 
OR-10 15:25 - 15:40 VARIABLY PROTEASE-SENSITIVE PRIONOPATHY IS TRANSMISSIBLE IN BANK VOLES Nonno
 
 
 
 
DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)
 
The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why???? than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!!
 
Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....
 
Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any action........it is ALL gonna be sporadic!!!
 
And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...
 
Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"
 
again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.
 
You need to watch your back........but keep picking at them.......like a buzzard to the bone...you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)
 
 
END...TSS
 
 
Tuesday, October 29, 2013
 
VARIANT CJD PRESENTS DIFFERENTLY IN OLDER PATIENTS
 
 
 
 
bought and paid for by your local cattle dealers. ...
 
 


Wednesday, October 30, 2013

SPECIFIED RISK MATERIAL (SRM) CONTROL VERIFICATION TASK FSIS NOTICE 70-13 10/30/13
http://madcowusda.blogspot.com/2013/10/specified-risk-material-srm-control.html
 
 
 
Saturday, November 2, 2013
 
APHIS Finalizes Bovine Import Regulations in Line with International Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type disease around the Globe
 
 


SPREADING IT ALL AROUND


Saturday, October 19, 2013

***A comparative study of modified confirmatory techniques and additional immuno-based methods for non-conclusive autolytic Bovine spongiform encephalopathy cases
http://transmissiblespongiformencephalopathy.blogspot.com/2013/10/a-comparative-study-of-modified.html


Wednesday, September 25, 2013

Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE PRION 2013
http://madcowusda.blogspot.com/2013/09/inspections-compliance-enforcement-and.html



Wednesday, October 09, 2013

*** WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY, £41,078,281 in compensation REVISED
http://creutzfeldt-jakob-disease.blogspot.com/2013/10/why-ukbsenvcjd-only-theory-is-so.html

Thursday, October 10, 2013

*** CJD REPORT 1994 increased risk for consumption of veal and venison and lamb ***
http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-report-1994-increased-risk-for.html


Sunday, August 11, 2013

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010
http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html

Sunday, October 13, 2013

CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-tse-prion-disease-cases-in-texas-by.html

Tuesday, September 24, 2013

NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow TSE prion Contamination Suit Cethrin(R)

*** Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1 of 15 ***
http://creutzfeldt-jakob-disease.blogspot.com/2013/09/nordion-us-inc-and-bioaxone-biosciences.html

Saturday, July 6, 2013

*** Small Ruminant Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy

Research Article
http://nor-98.blogspot.com/2013/07/small-ruminant-nor98-prions-share.html
 
 
just saying...
 
 
kind regards,
terry
 
layperson, mom dead dod 12/14/97 confirmed ‘hvCJD’...TEXAS
 
 
 

1 Comments:

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