Very Funny NW Buck. LMFAO!
Molecular Barriers to Zoonotic Transmission of Prions (CWD, not good for hunters)
Very Funny NW Buck. LMFAO!
TheMadCatter
Well-Known Member
Can't this guy speak English? Maybe an easier format for us to understand? Like maybe say something that I can understand? You're first statement I can understand then I don't know what you're saying.
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I just looked at Flounders posting history. Every single one of his (her?) posts is either about CWD or EHD.
My question to you Flounder9 is...What gives? Do you have some personal issue that prompts you to raise these issues? Or, is JDubs correct in that you are an anti-hunter? I must admit, you live in the wrong state if those are your beliefs. Provided of course you really do live in Texas.
Several times people have asked for clarification but your not giving any. Is there a reason?
My question to you Flounder9 is...What gives? Do you have some personal issue that prompts you to raise these issues? Or, is JDubs correct in that you are an anti-hunter? I must admit, you live in the wrong state if those are your beliefs. Provided of course you really do live in Texas.
Several times people have asked for clarification but your not giving any. Is there a reason?
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Terry Singletary — A retired machinist and high school dropout, Terry Singletary suffered the tragic loss of his mother to “sporadic” Creutzfeldt-Jakob disease (CJD) in 1997. Desperate to find an explanation for his mother’s death, he has devoted himself to the sad and fruitless task of connecting her death to her diet. Various reports confirm that Mrs. Singletary’s life was claimed by the most common sub-type of CJD (one that accounts for 70 percent of “sporadic” cases). Sporadic CJD, unlike its newer “variant,” is not linked to meat.
As the self-appointed international coordinator of CJD Watch, an organization he co-founded with social worker Deborah Oney, Singletary is cited in media reports as an apparent expert on tracking mad cow disease. This despite his lack of formal education and the absence for support from any credible academic, medical or scientific authority. His sensationalist allegations about the safety of U.S. beef have found their way into hundreds of newspapers and broadcasts. Singletary moderates a mad-cow discussion forum run by a vegetarian activist group; his contributions account for more than half the traffic on the “BSE-L” mailing list, which is generally read by real scientists. Animal rights activists and other food-scare artists frequently refer to him as “Dr. Terry Singletary,” apparently an honorary degree as he has yet to finish high school.
Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology
Hope this helps with your questions about Terry the "Flounder"
As the self-appointed international coordinator of CJD Watch, an organization he co-founded with social worker Deborah Oney, Singletary is cited in media reports as an apparent expert on tracking mad cow disease. This despite his lack of formal education and the absence for support from any credible academic, medical or scientific authority. His sensationalist allegations about the safety of U.S. beef have found their way into hundreds of newspapers and broadcasts. Singletary moderates a mad-cow discussion forum run by a vegetarian activist group; his contributions account for more than half the traffic on the “BSE-L” mailing list, which is generally read by real scientists. Animal rights activists and other food-scare artists frequently refer to him as “Dr. Terry Singletary,” apparently an honorary degree as he has yet to finish high school.
Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology
Hope this helps with your questions about Terry the "Flounder"
Shovelbuck
Active Member
thephatchef
PMA Member
Good detective work. Looks fishy to me.
ArcheryIA44
PMA Member
Gentlemen (and any ladies that may be reading)...
Allow me to try to translate (sorry, this has turned out very long). I am not a researcher in prion disease, but I have taught the section relating to prion disease at the University of Iowa in the past and I try to keep up on the topic, both in the popular press and in scientific publications. By chance, my wife's aunt just died of the ultra-aggressive form of prion disease two days after Christmas.
Quick primer...prions are simply misfolded proteins (the protein is called PrP). The word "prion" was coined by Stanley Prusiner and it means infectious protein particle. Prusiner was nearly laughed out of science when he proposed his theory but time proved him right and he was awarded the Nobel Prize in 1997.
How does this protein cause the very serious problems we see with prion disease? It simply mis-folds. Proteins have to be folded into a proper three-dimensional shape in order to function correctly. PrP is unique in that it can assume an incorrect shape that, when it comes into contact with other PrP proteins that start out correctly folded, causes those proteins to change shape into the mis-folded form. This happens in the nervous system and when enough of the proteins are mis-folded, "holes" form in the brain, thus the term spongiform (because the brain looks like a sponge).
There are several types. Bovine spongiform encephalopathy (BSE, mad cow), scrapie (in sheep), chronic wasting disease (CWD, deer and elk), Creutzfeldt-Jakob Disease (CJD), variant Creutzfeldt-Jakob Disease (vCJD), among others. CJD happens spontaneously in people, mainly in older people while vCJD usually happens in younger people and is often attributed to the eating of contaminated meat. There are more newly identified forms that are ultra-aggressive.
As was proven in England, eating hamburger from BSE cows resulted in vCJD in people.
Alright, what then are the implications of the current thread and the information posted by Flounder9?
First, this was not the way to give information to this crowd. Dumping a huge pile of scientific jargon at our group is a good way to make the reader skip to the next thread.
I tried to go through the links and other information, but have to admit that I still only saw a subset, but let me give some layperson highlights...
The original report was pretty simple. It showed that in a test tube, the mis-folded PrP protein from deer (from CWD) COULD cause human PrP to change shape into the form that could then cause other human proteins to mid-fold. What does that mean? That CWD from deer has the potential to cause CJD in humans.
The $50,000 question is… do CWD prions cause some form of CJD in humans? Sometimes it seems, yes. But let’s be clear that this is a much more inefficient process relative to what happens with BSE. The scientific paper points out that studies in mice that have been engineered to express the human PrP proteins have shown that they did NOT get prion disease when given proteins from CWD animals (but they did get prion disease when given BSE or CJD prions).
If prions from CWD were efficient at transmitting prion disease to humans, we would have a much higher number of vCJD (the human disease) in endemic areas (starting around the three corners area of Colorado, Wyoming and Nebraska). It might happen sometimes, but it seems to be pretty inefficient.
Scientists who work on prions do so under the most strict research condition (high containment biological laboratories). What did you do the last time you shot a buck? How many times did you cut through the spinal cord while butchering? Did you saw off the top of the head to get the antlers off? Brain matter everywhere!
Okay, the second major point of the information presented by Flounder relates to iatrogenic contamination. WTF does that mean?!?! Iatrogenic is basically causing disease from a medical procedure; making you sick from medical devices or procedures from another person. This is probably the more troubling part of what was presented.
Recent studies have shown that standard decontamination procedures basically do NOTHING to prevent the prion proteins from being transmitted to the next patient. That is HUGE! We really need to use very specific procedures to prevent cross-contamination or use disposable instruments on people that have any remote chance of having prion disease.
Another study that I read even before Flounder presented it here is that scientists have been able to find infectious prion proteins in red blood cells, serum and white blood cells. It has been thought that only nervous tissue was a reservoir of prion protein. This study suggests that even a blood donation could lead to disease in the person receiving the red blood cells or serum. Has that happened? Not yet known.
All this means that we need to be more diligent in our monitoring. Be careful out there!
Allow me to try to translate (sorry, this has turned out very long). I am not a researcher in prion disease, but I have taught the section relating to prion disease at the University of Iowa in the past and I try to keep up on the topic, both in the popular press and in scientific publications. By chance, my wife's aunt just died of the ultra-aggressive form of prion disease two days after Christmas.
Quick primer...prions are simply misfolded proteins (the protein is called PrP). The word "prion" was coined by Stanley Prusiner and it means infectious protein particle. Prusiner was nearly laughed out of science when he proposed his theory but time proved him right and he was awarded the Nobel Prize in 1997.
How does this protein cause the very serious problems we see with prion disease? It simply mis-folds. Proteins have to be folded into a proper three-dimensional shape in order to function correctly. PrP is unique in that it can assume an incorrect shape that, when it comes into contact with other PrP proteins that start out correctly folded, causes those proteins to change shape into the mis-folded form. This happens in the nervous system and when enough of the proteins are mis-folded, "holes" form in the brain, thus the term spongiform (because the brain looks like a sponge).
There are several types. Bovine spongiform encephalopathy (BSE, mad cow), scrapie (in sheep), chronic wasting disease (CWD, deer and elk), Creutzfeldt-Jakob Disease (CJD), variant Creutzfeldt-Jakob Disease (vCJD), among others. CJD happens spontaneously in people, mainly in older people while vCJD usually happens in younger people and is often attributed to the eating of contaminated meat. There are more newly identified forms that are ultra-aggressive.
As was proven in England, eating hamburger from BSE cows resulted in vCJD in people.
Alright, what then are the implications of the current thread and the information posted by Flounder9?
First, this was not the way to give information to this crowd. Dumping a huge pile of scientific jargon at our group is a good way to make the reader skip to the next thread.
I tried to go through the links and other information, but have to admit that I still only saw a subset, but let me give some layperson highlights...
The original report was pretty simple. It showed that in a test tube, the mis-folded PrP protein from deer (from CWD) COULD cause human PrP to change shape into the form that could then cause other human proteins to mid-fold. What does that mean? That CWD from deer has the potential to cause CJD in humans.
The $50,000 question is… do CWD prions cause some form of CJD in humans? Sometimes it seems, yes. But let’s be clear that this is a much more inefficient process relative to what happens with BSE. The scientific paper points out that studies in mice that have been engineered to express the human PrP proteins have shown that they did NOT get prion disease when given proteins from CWD animals (but they did get prion disease when given BSE or CJD prions).
If prions from CWD were efficient at transmitting prion disease to humans, we would have a much higher number of vCJD (the human disease) in endemic areas (starting around the three corners area of Colorado, Wyoming and Nebraska). It might happen sometimes, but it seems to be pretty inefficient.
Scientists who work on prions do so under the most strict research condition (high containment biological laboratories). What did you do the last time you shot a buck? How many times did you cut through the spinal cord while butchering? Did you saw off the top of the head to get the antlers off? Brain matter everywhere!
Okay, the second major point of the information presented by Flounder relates to iatrogenic contamination. WTF does that mean?!?! Iatrogenic is basically causing disease from a medical procedure; making you sick from medical devices or procedures from another person. This is probably the more troubling part of what was presented.
Recent studies have shown that standard decontamination procedures basically do NOTHING to prevent the prion proteins from being transmitted to the next patient. That is HUGE! We really need to use very specific procedures to prevent cross-contamination or use disposable instruments on people that have any remote chance of having prion disease.
Another study that I read even before Flounder presented it here is that scientists have been able to find infectious prion proteins in red blood cells, serum and white blood cells. It has been thought that only nervous tissue was a reservoir of prion protein. This study suggests that even a blood donation could lead to disease in the person receiving the red blood cells or serum. Has that happened? Not yet known.
All this means that we need to be more diligent in our monitoring. Be careful out there!
loneranger
Well-Known Member
With so many diseases and maladies a person can come down with, I am glad I've made it to 61 !
These diseases & problems are actually proven to come from Vegetables. Many well documented studies have proven Vegetable Prions from the planet Krypton have actually came to earth after a horrible explosion many yrs ago. It's infected the very vegetables we eat and contrary to much of this it shows & proves we should be on a sole meat diet. Big cover up if u really want to know the truth.
HorseDoctor
PMA Member
We all got to die of something... 
I choose not to die from worry. Venison (very rare please) remains a staple in my diet.
I choose not to die from worry. Venison (very rare please) remains a staple in my diet.
flounder9
Member
oh heck, you got me there chutch
say there chutch, thanks for posting this old article. sadly though, everything in this old article I stated back then, to date, has come true.
seems every time someone, or some group, i.e. shooting pen owners, supporters, slaughterhouse owners, i.e. 'the industry' cannot dispute what I say with science, they scream ANTI, and they go back to this old article that every thing I said came true, and yes, even a link to Alzheimer's has been proven. so again, thanks for posting this old article. does not make me feel good though. I am saddened by it. it's just ignorance and greed.
let me make one thing perfectly clear here, I do this for one reason, as i said, I made a promise to my mother, and her death from the hvCJD would not go in vain, and that I would try and stop anymore senseless deaths from the TSE prion, and I don't care what or whom you may eat, I am still a meat eater, although I have slowed. I am pro-hunter and pro-gun. but when folks get so caught up they are blind, don't care about others, and will risk life to others, i.e. iatrogenic, that is not acceptable. let me give you an example of the iatrogenic mode I speak of, you might want to read it twice or three times, it still amazes me every time I read it ;
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. PMID: 8006664 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
however, now that you have brought this old article to light, lets take a better look at it shall we ;
Sunday, September 25, 2011
Mad Cow Scaremongers
Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion
agent 2003-2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html
SO, just who are The Center for Consumer Freedom ;
http://www.consumerfreedom.com/index.cfm
let's take a closer look shall we ;
The Center for Consumer Freedom (CCF) (formerly called the "Guest Choice Network (GCN)") is a front group for the restaurant, alcohol and tobacco industries. It runs media campaigns which oppose the efforts of scientists, doctors, health advocates, environmentalists and groups like Mothers Against Drunk Driving, calling them "the Nanny Culture -- the growing fraternity of food cops, health care enforcers, anti-meat activists, and meddling bureaucrats who 'know what's best for you.'"
CCF is registered as a tax-exempt, non-profit organization under the IRS code 501(c)(3). Its advisory board is comprised mainly of representatives from the restaurant, meat and alcoholic beverage industries.
http://www.sourcewatch.org/index.php?title=Center_for_Consumer_Freedom
http://en.wikipedia.org/wiki/Center_for_Consumer_Freedom
What Is the Center for Consumer Freedom, and Why Is It Attacking PETA?
The Center for Consumer Freedom is a nonprofit corporation run by lobbyist Richard Berman through his Washington, D.C.-based for-profit public relations company, Berman & Co. The Center for Consumer Freedom, formerly known as the Guest Choice Network, was set up by Berman with a $600,000 “donation” from tobacco company Philip Morris.
Berman arranges for large sums of corporate money to find its way into nonprofit societies of which he is the executive director. He then hires his own company as a consultant to these nonprofit groups. Of the millions of dollars “donated” by Philip Morris between the years 1995 and 1998, 49 percent to 79 percent went directly to Berman or Berman & Co.
Richard Berman is an influence peddler. He has worked out a scheme to funnel charitable donations from wealthy corporations into his own pocket. In exchange, he provides a flurry of disinformation, flawed studies, op-ed pieces, letters to the editor, and trade-industry articles, as well as access to his high-level government contacts, who are servants of the industries he represents.
Berman’s name might sound familiar. In 1995, Berman and Norm Brinker, his former boss at Steak and Ale Restaurants, were identified as the special-interest lobbyists who donated the $25,000 that disgraced then-House Speaker Newt Gingrich, who was hauled before the House Ethics Committee for influence-peddling over the money. Berman and Brinker were lobbying against raising the minimum wage.
Richard Berman is a spin doctor. For example, he has argued against a Mothers Against Drunk Driving (MADD) initiative to lower the blood alcohol content (BAC) limit for drivers by claiming that the stricter limits would punish responsible social drinkers. He has claimed that U.S. Centers for Disease Control and Prevention (CDC) warnings about salmonella-related food poisoning are just “whipping up fear over food.”
Here’s how an internal Philip Morris memo described Berman’s spin: “His proposed solution would broaden the focus of the ‘smoking issue,’ and expand into the bigger picture of over-regulation.” Smoking won’t kill you; over-regulation will.
Berman is “a one-man wrecking crew on important issues.” His approach has been described as “misleading” and “despicable.” Berman has been called “a tobacco company whore,” but he’s branched out since then.
Using “freedom of choice” as his battle cry, Berman has now taken on PETA and a number of other groups and organizations whose points of view could have an impact on the profits of his clients by waking consumers up. Berman’s Guest Choice Network has an “advisory panel” whose members in 1998 included officials representing companies ranging from Cargill Processed Meat Products and Outback Steakhouse to Minnesota Licensed Beverage Association and Sutter Home Winery. Berman’s clients are companies with vested interests in low employee wages; cheap, unhealthy restaurant-chain food, particularly meat; and tobacco, soft drink, and alcohol consumption—companies like Ruth’s Chris Steakhouse, Armour Swift, and Philip Morris, whose product line includes Kraft Foods and everything from Marlboro cigarettes to Oscar Meyer wieners and which is a major shareholder in its former subsidiary Miller Brewing, now known as SABMiller.
PETA’s recent successes in gaining fast-food industry concessions for more humane conditions for farm animals have sent ripples of fear through the food and beverage service industry. About the same time that McDonald’s buckled to PETA’s demands, Richard Berman changed his front group’s name and stepped up his attacks.
The key to Berman’s aggressive strategy is, in his own words, “to shoot the messenger ... we’ve got to attack their credibility as spokespersons,”—an interesting remark from someone whose background and funding so severely challenge his own credibility.
http://www.consumerdeception.com/index.asp
please see full text ;
Thursday, December 23, 2010
Alimentary prion infections: Touch-down in the intestine, Alzheimer, Parkinson disease and TSE mad cow diseases $ The Center for Consumer Freedom
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Proposal ID: 29403
http://betaamyloidcjd.blogspot.com/2012/05/alzheimers-disease-and-transmissible.html
Tuesday, November 26, 2013
Transmission of multiple system atrophy prions to transgenic mice
http://proteinopathies.blogspot.com/2013/11/transmission-of-multiple-system-atrophy.html
Singeltary to be continued...
flounder9
Member
Singeltary continued...part 2
Re: vCJD in the USA * BSE in U.S.
15 November 1999
Terry S Singeltary, NA
CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997. So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie.
It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses.
http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...
2 January 2000 Terry S Singeltary
The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."
A few more factors to consider, page 15;
"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."
"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."
"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."
Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.
To be continued...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA
Competing interests: None declared
http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well
Letters
JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr Bacliff, Tex
Since this article does not have an abstract, we have provided the first 150 words of the full text.
KEYWORDS: creutzfeldt-jakob disease, diagnosis. To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
http://jama.ama-assn.org/content/285/6/733.extract
Published March 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
Terry S. Singeltary, retired (medically)
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?
Published March 26, 2003
http://www.neurology.org/content/60/2/176/reply#neurology_el_535
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
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 ...
http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/%20fulltext
http://www.thelancet.com/journals/laninf/issue/vol3no8/PIIS1473-3099(00)X0025-4
SEE FULL TEXT ;
-------- Original Message --------
Subject: Tracking spongiform encephalopathies in North America
LANCET INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003
Date: Tue, 29 Jul 2003 17:35:30 –0500
From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
Volume 3, Number 8 01 August 2003
Previous
Next
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 hunterstwo of whom were friendswho 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
Singeltary submission to PLOS ;
No competing interests declared.
see full text ;
http://www.plosone.org/annotation/listThread.action?root=363
14th ICID International Scientific Exchange Brochure - Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary Bacliff, TX, USA
Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods: 12 years independent research of available data
Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
FSIS, USDA, REPLY TO SINGELTARY
http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
http://madcowusda.blogspot.com/2013/12/fda-part-589-substances-prohibited-from.html
layperson,
kindest regards, terry
Terry S. Singeltary Sr.
Bacliff, Texas USA 77518
flounder9@verizon.net
Re: vCJD in the USA * BSE in U.S.
15 November 1999
Terry S Singeltary, NA
CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997. So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie.
It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses.
http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...
2 January 2000 Terry S Singeltary
The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."
A few more factors to consider, page 15;
"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."
"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."
"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."
Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.
To be continued...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA
Competing interests: None declared
http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well
Letters
JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr Bacliff, Tex
Since this article does not have an abstract, we have provided the first 150 words of the full text.
KEYWORDS: creutzfeldt-jakob disease, diagnosis. To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
http://jama.ama-assn.org/content/285/6/733.extract
Published March 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
Terry S. Singeltary, retired (medically)
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?
Published March 26, 2003
http://www.neurology.org/content/60/2/176/reply#neurology_el_535
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
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 ...
http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/%20fulltext
http://www.thelancet.com/journals/laninf/issue/vol3no8/PIIS1473-3099(00)X0025-4
SEE FULL TEXT ;
-------- Original Message --------
Subject: Tracking spongiform encephalopathies in North America
LANCET INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003
Date: Tue, 29 Jul 2003 17:35:30 –0500
From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
Volume 3, Number 8 01 August 2003
Previous
Next
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 hunterstwo of whom were friendswho 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
Singeltary submission to PLOS ;
No competing interests declared.
see full text ;
http://www.plosone.org/annotation/listThread.action?root=363
14th ICID International Scientific Exchange Brochure - Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary Bacliff, TX, USA
Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods: 12 years independent research of available data
Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
FSIS, USDA, REPLY TO SINGELTARY
http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
http://madcowusda.blogspot.com/2013/12/fda-part-589-substances-prohibited-from.html
layperson,
kindest regards, terry
Terry S. Singeltary Sr.
Bacliff, Texas USA 77518
flounder9@verizon.net
flounder9
Member
Singeltary continued...part 3
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/cwd-tse-prion-in-cervids-to-htgmice.html
Friday, August 16, 2013
*** Creutzfeldt-Jakob disease (CJD) biannual update August 2013 U.K. and Contaminated blood products induce a highly atypical prion disease devoid of PrPres in primates
http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-biannual.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
Subtype 1: (sCJDMM1 and sCJDMV1)
This subtype is observed in patients who are MM homozygous or MV heterozygous at codon 129 of the PrP gene (PRNP) and carry PrPSc Type 1. Clinical duration is short, 3‑4 months.32 The most common presentation in sCJDMM1 patients is cognitive impairment leading to frank dementia, gait or limb ataxia, myoclonic jerks and visual signs leading to cortical blindness (Heidenhain’s syndrome)...
https://www.landesbioscience.com/pdf/06Ahmad_Liberski.pdf
Animals injected with iatrogenic Creutzfeldt–Jakob disease MM1 and genetic Creutzfeldt–Jakob disease MM1 linked to the E200K mutation showed the same phenotypic features as those infected with sporadic Creutzfeldt–Jakob disease MM1 prions...
http://brain.oxfordjournals.org/content/early/2010/09/07/brain.awq234.full.pdf
*** our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions. ***
http://www.jbc.org/cgi/content/abstract/M704597200v1?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Cross-sequence+transmission+of+sporadic+Creutzfeldt-Jakob+disease+creates+a+new+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
snip...see full text ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html
o.k. folks, every one has to make your own minds up, but now, you have a bit more science to do it with. ...
Stay warm, have a Great, Safe hunt !!!
kind regards,
terry
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/cwd-tse-prion-in-cervids-to-htgmice.html
Friday, August 16, 2013
*** Creutzfeldt-Jakob disease (CJD) biannual update August 2013 U.K. and Contaminated blood products induce a highly atypical prion disease devoid of PrPres in primates
http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-biannual.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
Subtype 1: (sCJDMM1 and sCJDMV1)
This subtype is observed in patients who are MM homozygous or MV heterozygous at codon 129 of the PrP gene (PRNP) and carry PrPSc Type 1. Clinical duration is short, 3‑4 months.32 The most common presentation in sCJDMM1 patients is cognitive impairment leading to frank dementia, gait or limb ataxia, myoclonic jerks and visual signs leading to cortical blindness (Heidenhain’s syndrome)...
https://www.landesbioscience.com/pdf/06Ahmad_Liberski.pdf
Animals injected with iatrogenic Creutzfeldt–Jakob disease MM1 and genetic Creutzfeldt–Jakob disease MM1 linked to the E200K mutation showed the same phenotypic features as those infected with sporadic Creutzfeldt–Jakob disease MM1 prions...
http://brain.oxfordjournals.org/content/early/2010/09/07/brain.awq234.full.pdf
*** our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions. ***
http://www.jbc.org/cgi/content/abstract/M704597200v1?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Cross-sequence+transmission+of+sporadic+Creutzfeldt-Jakob+disease+creates+a+new+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
snip...see full text ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html
o.k. folks, every one has to make your own minds up, but now, you have a bit more science to do it with. ...
Stay warm, have a Great, Safe hunt !!!
kind regards,
terry
Last edited: