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Discussion in 'The Taxidermy Industry' started by John C, Dec 30, 2018.
Hope he didn't get it from eating a CWD deer!
The knee jerk reaction won’t be good if he did.
no...the real truth will be, if he did get it from eating a CWD deer we are all Flocked. every human being is flocked. CWD gets into plants, plants are crops, crops get harvested and put into the food chain and into the stores and into us.
think about that.
OK...i responded bfore i clicked on the link. the doesnt say CWD it says CJD, that has been happening for quite some time now. it doesnt come from deer and its not Chronic Wasting Disease. but when the jump from deer to humans happens, i stand by my statement above.
the aliens from behind pluto are putting this stuff into our food chain to wipe us out reason for all the mutilated livestock a few years back was for reasesrch they want our planet but are not real forceful to nuke us out like was done to the mayans 3,000 years ago they will slowly poison us and then take over earth without the nuclear fallout
why didnt they take it after the mayans.
where did the Mayans go anyhow ? they disappeared like the lost colony of Roanoke, NC
but seriously...if this case of CJD turns out to be CWD....its close to being over for millions of people.
Look, CJD is NOT CWD and thus far there have never been any cases tying the two together. Though it has a common tie with protein prions, CJD has several other forms directly associated with it. Each year in the United States we have about 350 cases and worldwide it's about 1 in 1 million. Seeing as how that many people are effected each year, my biggest concern is as to WHY this man is getting all this news coverage. The very last thing we need is numbnutted taxidermists waving a flag about the tie. Next thing to happen will be Al Gore will blame it on global warming at which point you're more than screwed.
The Mayans were ass holes!
got a link
George it is the same prion 14-3-3. Madcow in humans, Oh wait, same prion 14-3-3 Yes Europe claims it jumped species. Arkansas had 7 cases of vcj last year and three of those did in fact eat deer from the CWD hot zone. I can tell you more but you like some other will say no.
just did a quick search on 14-3-3 it is also associated with parkinsons disease.
Yes and also forms of Alzheimer. I know a family that the son has Parkinsons , the father has Parkinsons, the mother has Alzheimer. The ladies mother died of Alz. they in fact did live right in the hear of Arkansas CWD area. The ladies father died before any of this was being tracked. I do know he had heart problems.
The number of cases of Alz, and Parkinson has been on the rise in this area, espcially with the rural families.
What is Creutzfeldt-Jakob disease?
Creutzfeldt-Jakob disease (CJD) is a rare, degenerative, fatal brain disorder. It affects about one person in every one million per year worldwide; in the United States there are about 350 cases per year. CJD usually appears in later life and runs a rapid course. Typical onset of symptoms occurs at about age 60, and about 70 percent of individuals die within one year. In the early stages of the disease, people may have failing memory, behavioral changes, lack of coordination, and visual disturbances. As the illness progresses, mental deterioration becomes pronounced and involuntary movements, blindness, weakness of extremities, and coma may occur.
There are three major categories of CJD.
In sporadic CJD, the disease appears even though the person has no known risk factors for the disease. This is by far the most common type of CJD and accounts for at least 85 percent of cases.
In hereditary CJD, the person may have a family history of the disease and test positive for a genetic mutation associated with CJD. About 10 to 15 percent of cases of CJD in the United States are hereditary.
In acquired CJD, the disease is transmitted by exposure to brain or nervous system tissue, usually through certain medical procedures. There is no evidence that CJD is contagious through casual contact with someone who has CJD. Since CJD was first described in 1920, fewer than one percent of cases have been acquired CJD. A type of CJD called variant CJD (or vCJD) can be acquired by eating meat from cattle affected by a disease similar to CJD called bovine spongiform encephalopathy (BSE) or, commonly, “mad cow” disease.
CJD belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs) or prion diseases. A prion—derived from “protein” and “infectious”—causes CJD in people and TSEs in animals. Spongiform refers to the characteristic appearance of infected brains, which become filled with holes until they resemble sponges when examined under a microscope. CJD is the most common of the known human TSEs. Other human TSEs include kuru, fatal familial insomnia (FFI), and Gerstmann-Straussler-Scheinker disease (GSS). Kuru was identified in people of an isolated tribe who practiced ritual cannibalisms in Papua, New Guinea and has now almost disappeared. Kuru is considered an acquired prion disease. FFI and GSS are extremely rare hereditary diseases, found in just a few families around the world. To date, about 260 cases of vCJD, mostly in the United Kingdom, have been reported related to consuming beef but none in which the disease was acquired in the U.S. Other TSEs are found in specific kinds of animals. These include BSE, mink encephalopathy, feline encephalopathy, and scrapie, which affects sheep and goats. Chronic wasting disease (CWD) affects elk and deer and is increasingly prevalent in certain areas in the United States.
To date no transmission of CWD to humans has been reported. (HOW DO WE KNOW THIS?)
What are the symptoms of the disease?
Although sporadic TSE includes five distinct subtypes of sporadic CJD and sporadic fatal insomnia (sFI), overall they are characterized by rapidly progressive dementia. Initially, individuals experience problems with muscle coordination, personality changes (including impaired memory, judgment, and thinking), and impaired vision. People with the disease, especially with FFI, also may experience insomnia, depression, or unusual sensations. As the illness progresses, peoples’ mental impairment becomes severe. They often develop involuntary muscle jerks called myoclonus, and they may go blind. They eventually lose the ability to move and speak, and enter a coma. Pneumonia and other infections often occur in these individuals and can lead to death.
Variant CJD begins primarily with psychiatric symptoms, affects younger individuals than other types of CJD, and has a longer than usual duration from onset of symptoms to death.
Some symptoms of CJD can be similar to symptoms of other progressive neurological disorders, such as Alzheimer’s and Huntington’s disease. However, CJD causes unique changes in brain tissue which can be seen at autopsy. It also tends to cause more rapid deterioration of a person’s abilities than Alzheimer’s disease or most other types of dementia.
Parkinson’s disease (PD) is an age-related neurodegenerative disease characterized by the presence of Lewy bodies and the loss of dopaminergic neurons in the substantia nigra pars compacta (SNc) . 14-3-3 proteins have been associated with PD based on their localization, binding partners, and neuroprotective function.
Lewy body colocalization
Lewy bodies are abnormal protein aggregates developed inside nerve cells in cortical and subcortical regions of PD brains. The main component of Lewy bodies is α-synuclein, a regulator of the MAPK pathway that is involved in dopamine synthesis [24-26]. Several immunohistochemical studies have identified that four of the seven 14-3-3 isoforms (ε, γ, σ, and ζ) are also present in Lewy bodies [21,27,28]. Interestingly, α-synuclein and 14-3-3 proteins share a substantial sequence homology and may interact with each other [29,30]. In transgenic mice overexpressing human wildtype α-synuclein, several 14-3-3 isoforms (γ, τ, ε, and σ) were found to have reduced gene expression . The level of 14-3-3 proteins is also dysregulated in an isoform-specific manner in the α- and β-synuclein double knockout mice . In addition, binding of 14-3-3η to α-synuclein is disrupted by PD-causing mutations of α-synuclein (30P and A53T), suggesting a potential role for this interaction in PD . However, it is not known whether the presence of 14-3-3 proteins in Lewy bodies is mediated by their interactions with α-synuclein.
John that's bull spit. Instead of pandering to the Chicken Little Syndrome crowd and publishing their crap as evidence, you need to study micro biology to understand that particular prion is instrumental in other maladies and miracles. I could give a good damn WHAT the English claim, KJD IS NOT CWD. And there has been no medical PROOF that CWD crosses over. You have a better chance of being gored to death by a whitetail than contracting KJD from eating one.
George, what is it that you claim is "Bull spit"? I'm not sure what you have heard or read but there are many research findings that are not relayed to the masses. I too don't buy into 'The sky is falling" mentality but there is always a chance of it happening and we should be cognizant of that possibility.
all i know for sure is that CWD is here and it can be found in plants. what comes after that...who knows. will it cross ? did it cross ? if it does will they tell us ?
if it does cross and they let the news out i can see real panic setting in. i guess i'll just eat fish and get toxins from them.
This is the best article I have found to share with my micro students. Lots of details and very lengthy. Very interesting thread! Thanks for posting it, John.
and another misleading title. the title says "Will not spread to humans" then you read the article and it says
"Although the CDC has not published information suggesting CWD is not infectious to humans, the center has also stopped short of confirming transmission from cervid animals to humans is possible. “To date, there is no strong evidence for the occurrence of CWD in people, and it is not known if people can get infected with CWD prions. Nevertheless, these experimental studies raise the concern that CWD may pose a risk to people and suggest that it is important to prevent human exposures to CWD.”