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NEWS: Mad Cow Disease Is Found In Goat

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posted on Feb, 1 2005 @ 02:34 PM
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...OR - once these little guys are created by a sort of "electro-immune suppression," and they're not killed off, but are released into the environment, are they then "infectious"?

AND - my research shows clearly that fibromuscular dysplasia is the original prion disease - and that it first appeared in the early 1900's. ...Does your hypothesis accommodate this early appearance?


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posted on Feb, 1 2005 @ 03:31 PM
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That's a pretty interesting theory Dr H. With all of the species, including the fish, that have been found with this disease, are there any reports of them dying from it.
Think of all of the weird things that have been happening to wildlife recently. From whales, and dolphins beaching themselves, Pelicans crashing into the ground, etc....
Is it possible that there is some sort of link? BSE basically turns the brain into mush doesn't it? That would have to show some signs of mental breakdown wouldn't it?
If this is a man made "bug" that is targeted to a specific group, and a specific incubation time - did we actually witness testing?



posted on Feb, 1 2005 @ 05:03 PM
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Originally posted by superdude
That's a pretty interesting theory Dr H. With all of the species, including the fish, that have been found with this disease, are there any reports of them dying from it.
Think of all of the weird things that have been happening to wildlife recently. From whales, and dolphins beaching themselves, Pelicans crashing into the ground, etc....
Is it possible that there is some sort of link?




My research says there is - much of what's happening at the cellular level in diseased animals involves "fibroblasts" - the stem cells for connective tissue. These stem cells mutate into myofibroblasts because the cell-building proteins are hijacked by a prion called "a-smooth muscle actin."




BSE basically turns the brain into mush doesn't it? That would have to show some signs of mental breakdown wouldn't it?



True - but that's only the end stage of the disease. ...It travels through the body through the lymph and blood vessels, and can inffect virtually any body part, system or organ before it gets there...




If this is a man made "bug" that is targeted to a specific group, and a specific incubation time - did we actually witness testing?



.....Who knows? But we're definitely watching it spread and mutate before our eyes...



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posted on Feb, 2 2005 @ 05:11 AM
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"Scrapie in a cow: 1883 full text
24 Mar 98 webmaster
Below is the full text of the 1881 case of 'scrapie in a cow' of 8 years age from an 1883 French medical veterinary journal article. It has no list of citations at the end as was typical for scientific articles until after WWI. I have no idea when peer review came into play as we understand it today. A professional translation to English is being appended.
Did this cow in fact exhibit symptoms of a bovine TSE? What favors this over Aujeszky's disease (pseudorabies)? The quality of supporting evidence is open for discussion. Please let us not fault the veterinarian for not doing a western blot, electron micrsoscopy, or prion gene sequencing.

If yes, did it have an origin in scrapie? One scenario is that the cow was exposed to scrapie in co-pastured sheep, ie, horizontal transmission. This may have occured earlier in the herd with subsequent cow-to-cow transmission so that the cow of the article was not the primary passage. This might be called scrapie-BSE or scrapie-in-a-cow to indicate origin, keeping in mind that the cow prion causes the problem, not the long-gone sheep prion of different sequence. It is not scrapie any more, scrapie is a disease only sheep can get.

A second scenario is a validation of the Gibbs Principle, familial bovine TSE, that is, the cow had a familial CJD-type mutation in its prion gene as expected from the one per million background mutational rate. Other variants are somatic mutation bovine TSE or sporadic bovine TSE. These might be called familial BSE or sporadic BSE, keeping in mind that:

Neither scenario makes the ailment of this cow equivalent to either modern day UK BSE or Stetsonville BSE. This would be an unlikely coincidence because of the many possible strain types. Both scenarios are supportive, but certainly not proof, of the concept that some sporadic CJD in humans might long have had a dietary origin. "

www.mad-cow.org...

Otto von Guericke invented the first static electric generator in 1675, while the first current generator was made by Alosio Galvani in 1780. But except for some supposed medicinal applications, electricity had little use.

Communication, the first of the great uses for electricity, began with the telegraph invented by Samuel Morse around 1840, to be followed by the telephone, radio and television. Thomas Edison added lighting in 1880, which was soon followed by working electric motors and electric heating. Most recently has come electronics and the computer revolution. In all electricity has fundamentally transformed the way we live.

www.bydesign.com...



posted on Feb, 2 2005 @ 05:44 AM
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Xenopus prion
31 May 01 Xenopus laevis cDNA clone BG813008 from eye. WashU Xenopus EST project
Average insert size 2.3 kb. High quality sequence stops at base 436.

This 5' EST appeared today at GenBank. It did not emerge from prion research per se but rather a Xenopus genomic transcriptome project. This very important sequence pushes back the earliest known prion protein to the time of divergence of the amphibians, to 360 million years ago (Kumar and Hedges: Nature 392:917 1998).
This is a partial sequence containing 131 bp of upstream sequence followed by 387 bp of coding sequence, of which 22 codons are signal peptide and 107 mature protein coding. Because the sequence stops at the second residue of the second beta strand (both are perfectly conserved), it provides no information about helices B and C, disulfides, glycosylation sites, or GPI anchor.

This is definitely a prion protein, bearing 41% blast identity (higher without repeat gap penalties) equally to avian and mammalian prions. It bears little resemblance to doppel, again suggesting that the gene doubling event was very ancient -- the reconstructed ancestral amniote protein has not converged to any plausible ancestral doppel. If the sequence could be extended to the complete coding region, a single disulfide pair in prion position would probably be affirmed. Thus, unless there was lineage-specific loss, xenopus also will have a doppel.

Xenopus prion completely lacks a repeat region (as predicted here years ago from the discordance between marsupial, placental, avian/turtle repeats). There are no possibilites for copper binding: no histidines whatsoever in 129 residues. Therefore it cannot function as a superoxide dismutase. The globular domain must have a self-contained, distinct function likely having nothing to do with oxidative stress.

Like doppels, xenopus prion has post-signal region, here of 34 residues, that strongly retains the character and composition of flanking regions of mammalian repeats. The remarkable conservation of this region for 360 million years in another protein lineage strongly refutes the notion of an unstructured extended peptide. Note the WGQ tripeptide conserved in prions and doppels in all species -- this involves a billion years of "round-trip" evolutionary time, requiring a compelling reason. This region is probably folded back over the main domain making it more globular; some hints of this have come from nmr and modelling; however, there is no hint of helix or sheet in its predicted secondary structure [see below].

www.mad-cow.org...

Why, after so many years of existence in the world have Prions "suddenly" become infectious? What 'changed".



posted on Feb, 2 2005 @ 06:18 AM
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Originally posted by DrHoracid

Why, after so many years of existence in the world have Prions "suddenly" become infectious? What 'changed".




Good stuff DrH.


1. Your link to electro-magnetic fields -electricity- looks good. Electro-magnetic fields cause normal prions to mutate into infectious forms - plus they damage the immune system, making people and animals more susceptible to the infection.

2.
Didn't know about the 1881 scrapie in a cow case - and yes, it may have been horizontal transmission. Good find. ...Of course, there were idiots messing around with creating bioweapons back then... They just didn't know what they were really messing with.

3. This jibes with my findings that FMD first appeared in the early 1900's. ...Both cow and sheep products are used to mass-produce vaccines - the first mass-vaccinations ocurred around 1914, in American soldiers being sent to the front for WWI. ....So the manufacturing process likely created new strains, and vaccines became a major vector for wide spread transmission.


.....Prions respond to environmental change by changing their form or 'mutating' and creating a new strain. 'Environmental change' includes a lot in our "modern" world - chemical contamination, electricity, heating and cooling in factory food processing, processing in laboratory centrifuges.


...Most mutation-causing factors are also highly efficient "prion-manufacturing" processes, and excellent vehicles for transmission...



.



posted on Feb, 2 2005 @ 08:11 AM
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So with all of this being said, I have to congratulate both Soficrow, and DrHoracid for their amazing analysis.

Here's a question to ponder. A mother is carrying these prions during her incubation period. She gets pregnant and has a baby. Is this baby now infected? Is this baby immune?



posted on Feb, 2 2005 @ 09:39 AM
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There is also speculation that the original polio vaccine was prion contaminated which may have caused simeon crossover of HIV into humans. Prions from all the data I have are kinda "blank" building blocks similar to "stem" cells. W/O nuclei of course. The protein stucture is easily coopted by virus and perhaps provides a natural "sheild" against the imune systems.



posted on Feb, 3 2005 @ 04:39 AM
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Originally posted by soficrow
My research says there is - much of what's happening at the cellular level in diseased animals involves "fibroblasts" - the stem cells for connective tissue. These stem cells mutate into myofibroblasts because the cell-building proteins are hijacked by a prion called "a-smooth muscle actin."



Soficrow - do you have any more information about this A-sma, particularly regarding when a person tests positive for this blood test? It seems that this blood test is sometimes positive when a person has hepatitis, but when a person who definately doesn't have hepatitis gets a positive, the Drs. consider it an unknown/insignificant finding.



posted on Feb, 3 2005 @ 10:13 AM
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Originally posted by Relentless

soficrowThese stem cells mutate into myofibroblasts because the cell-building proteins are hijacked by a prion called "a-smooth muscle actin."



Soficrow - do you have any more information about this A-sma, particularly regarding when a person tests positive for this blood test? It seems that this blood test is sometimes positive when a person has hepatitis, but when a person who definately doesn't have hepatitis gets a positive, the Drs. consider it an unknown/insignificant finding.



...Fibromuscular dysplasia is only diagnosed when the protein build-up creates life-threatening fibrosis in the arteries - the tests used are arteriography, magnetic resonance imaging with an angio (MRA) or other less effective imaging technologies - most involve radiation and are dangerous. ...the only ones who pay attention to the a-SMA are geneticists and molecular biologists - pathologists and doctors ignore it.


...Fibroblast testing is done from a skin scraping (not a blood test) - the test is not generally used because even when it's positive. the test doesn't show which particular proteins or cells are infected or where the disease might be located in the body - or what stage it has progressed to.

...Any positive test results should lead to a battery of follow-up immunology, hormone, molecular biology, and proteomic tests to identify exactly how the individual's body is reacting to the infection(s). The treatment is then tailored to the individual case. ....This is called "personalized medicine" - and isn't covered by any insurance.

....Block buster drugs don't work - they just turn every patient into a guinea pig...


Scroll back up and look at my post "Self-help for Prion Defense"

...if it's not here, look at
www.abovetopsecret.com...

and check out
www.abovetopsecret.com...


.



posted on Feb, 25 2006 @ 09:27 AM
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It's caused by cannibalism. When a chicken is fed chicken, prions develop. Same with cows or any other animal. I think eating organic meat probably is the best answer since organic farmers don't practice cannibalism with their livestock. Agribusiness, however, does.

-Forstlady



posted on Feb, 25 2006 @ 11:54 AM
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Geeze is nothing sacred,just when I was getting used to eating goat meat too



posted on Oct, 7 2016 @ 11:36 AM
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a reply to: Oldtimer2

this is all so very interesting..and scary....we'll have tosee what else comes aout about this,,,,great topic to discuss



posted on Oct, 7 2016 @ 05:12 PM
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posted on Oct, 18 2016 @ 06:39 PM
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Somehow this 11 year old thread has become a spam magnet.

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