Bone/ Blood Meal and Mad Cow Disease

Like billbo is a shill?

Acts of creation are ordinarily reserved for gods and poets. To plant a pine, one need only own a shovel.

-- Aldo Leopold

Reply to
Tom Jaszewski
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oh billbo please stick to gardening, oops then we get Monsanto shill diatribes......

Acts of creation are ordinarily reserved for gods and poets. To plant a pine, one need only own a shovel.

-- Aldo Leopold

Reply to
Tom Jaszewski

On Thu, 03 Jun 2004 01:20:37 -0000, I found this from snipped-for-privacy@radix.net (Bill Oliver) :

Who did you say you wrked for?

Reply to
Will

The message from snipped-for-privacy@radix.net (Bill Oliver) contains these words:

The risk of eating BSE-infected beef in Britain, has gone down since then. That is not the same as saying, that the incidence of nv CJD infection will decrease, because a) virtually all the meat-eating population of the UK was exposed to BSE for at least a decade and B) we still don't know the incubation period, or what other factors activate a dormant infection.

You've misinterpreted the above statement and got it back to front.

It says that because of the lack of statistics, any assurances about lack of blood-transmission are tentative and infirm.

That 2000 research has been overtaken by events in the UK. Of the

140-odd UK cases of nv CJD, 15 were blood donors. The recipients of their donations are monitored, and since 2000, one of those recipients has developed nv CJD.

Those forms of CJD are not related to BSE. The concern is about the new variant of CJD. \/\/\/\/\/\

Out of date, see above.

Furthermore, the presence of infectivity in

However, it does pose the problem of human cross-contamination by surgical instruments, since the prions are not susceptible to sterilisation techniques.

You're conflating statistics. There are only 15 *known* nv-CJD infected human blood donors; their blood never reached "millions and millions" of recipients. One case of infection from only 15 donors is rather more worrying.

The "decade ago", is not yet grounds for complacency either, since we still don't know the full range of the incubation period. Recent research on discarded appendixes and tonsils showed that some of the UK population are still carrying the prions.

Janet.

Reply to
Janet Baraclough..

But you do know the prevalance of symptomatic disease, and that is decreasing. You also know a good deal about conventional CJD and you know that the route of transmission and pertinent vectors are essentially the same. In order for the hysterical view to be correct, you would not only have to posit not only that "we still don't know the incubation period" but

*also* that this unknown incubation period is actively *increasing* in order to explain the decrease in the symptomatic cohort. Otherwise, a constant percentage of infected people would become symptomatic. Since fewer people are becoming symptomatic, either the number of infections is decreasing or the incubation period is magically increasing.

You know that the exposure is decreasing, the prevalence of symptomatic disease is decreasing, you know that there is no evidence of significant other methods of transmission, and you have no rational reason to believe that the decrease in symptomatic patients is because there is a large reservoir of disease that is busily increasing its dormancy period simply to stay hidden.

Unless you believe in magic the risk is decreasing, and the

1996 calculations provide an upper bound.

Well, no. I entered this because a respondent used the ban on donors as evidence of risk. It is not. And the millions and millions of recipients apply to that. Further, your claim provides its own problem. There were only 15 known vCJD donors in this study. Are you now positing that there are not many, many untested prion-positive donors? In fact, and if you really want, I can provide you with articles that provide good evidence that *lots* of people with prions have given blood. Where are *those* cases of vCJD?

Right. And you posit that this incubation period is *increasing* because those clever prions just don't want to get caught. That's why the number of patients with disease is decreasing, right?

billo

Reply to
Bill Oliver

Oh, good. The crazies are coming out of the woodwork. My favorite anti-science netstalker returns. Still peddling hysteria for personal gain, Tom?

Take your your sock puppets, your aliases, and your multiple personalities and stalk someone else for awhile.

billo

Reply to
Bill Oliver

I didn't. Not only is it irrelevant, but my opinions are my own and do not necessarily reflect those of my employer, or any official, Office, Agency or similar entity.

billo

Reply to
Bill Oliver

Here's a homework assignment for you. There is good evidence to believe that most people (who are not Japanese) are simply immune to vCJD. *One hundred percent* of people who have acquired vCJD have one specific thing in common, which is found in only 37% of Caucasians (and, alas, in 95% of Japanese).

What is it? How does that fit into your calculations of risk?

billo

Reply to
Bill Oliver

Ignore the freaking ideologue.

Oh, excuse me! That's "Dr. Freaking Ideologue." Hmmm .... gotta be an aging "M.D." ;-)

For those who are interested in a SCIENTIFIC review of the state of prion SCIENCE and its attendant issues in the U.S., here's a link to the most recent Institute of Medicine (part of the Nat'l Academies of Science) report, "Advancing Prion Science: Guidance for the National Prion Research Program (2004)"

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's a direct link to Chapter 5, "Testing Blood for Evidence of Agents of Transmissible Spongiform Encephalopathies" (pp 108 - 124)

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Reply to
Ermalina

And, interestingly enough, not one single statement in it contradicts anything I have written, though it *does* contradict much of what you have claimed -- including your ludicrous doubly false claim that studies involving CJD are irrelevant because vCJD is not related.

It notes that not one case of transmission of CJD by blood has been validated. It notes that there has not been an increase in CJD cases in the face of increasing use of blood products. It notes that case controlled studies have failed to show a connection between blood transfusion and CJD. Note particularly the table on page 113.

Note the lookback studies on page 114, as well as the studies on what one would expect to be high risk patients such as hemophiliacs (again page 114).

Perhaps you should read these things before you refer to them. You wouldn't look so silly. Indeed. Ignore the freaking ideologue. The one running around claiming the sky is falling.

billo

Reply to
Bill Oliver

Ouch!

So hurtful!

imagine that, the good doctor victim of so many personal attacks is actually just another nut following the same path.....

Interesting that anyone daring to reveal your real world links to the same entities wishing to peddle pseudo science for corporate gain is considered stalking! I suppose next we'll here Nixon and was also a victims of stalkers.....

Acts of creation are ordinarily reserved for gods and poets. To plant a pine, one need only own a shovel.

-- Aldo Leopold

Reply to
Tom Jaszewski

It's nice to know that people spend hours and hours reading through my old posts from years ago. And it's good to know that what I write holds up over time.

But really, Tom, pull up your pants and wash your hands. You really shouldn't be doing that kind of thing in public.

Your obsession is flattering in some ways, but you really are getting kinda creepy.

billo

Reply to
Bill Oliver

Gad damn what a fatuous little troll you inevitably make of yourself.

Reply to
paghat

Uh huh. As opposed to people like you an Tommy, who follow posters around doing nothing but personal attacks? You and your obsessive little buddy go stalk someone else.

billo

Reply to
Bill Oliver

I'm assuming your show of a deep & profound paranoia is a put-on & you're not actually as severely mentally ill as you continuously portray yourself. I still view you as purely & exclusively "Trolly trolly trolly," though obviously a certifiable fruitcake might occasionally be mistaken for a mere troll. If you DO believe this kind of I'm Being Netstalked crap, my sincere condolences to your family, who must suffer daily due to such fantastical delusions of persecution -- for as an authentic paranoid you would not restrict your weird beliefs to just the one lunatic conviction you're being stalked whenever your usual trolly antics gain you no more or less than is entirely merited.

-paghat the ratgirl

Reply to
paghat

I'll tell you what, paghat, instead of obsessing with chasing me around newsgroups in order to insult me, why don't you try addressing the issue. Show us your knowledge and insight into the subject.

I have challenged the hysterics to find a fact about vCJD. Let's see if you are up to the task. There's something that *all* victims of vCJD have in common that only about 37% of Caucasians have in common. What is that thing, and how does it fit into your risk calculation?

Or, you can continue to obsess about my posts and continue to follow me around from thread to thread and newsgroup to newsgroup.

Your choice, of course.

billo

Reply to
Bill Oliver

It seems that the hysterics either don't know the answer, or don't want to acknowledge it. So here it is. If, as is almost certainly the case, vCJD is a prion disease (there are still those who think it's a virus), then as a prion it has characteristics somewhere between a classic poison and a classic infection. In particular, the prion does not work by modifying DNA directly or indirectly. Instead, it is a protein that acts as an enzyme to modify normal versions of the same protein to work like itself. Enzymes are essentially small machines that perform specific tasks; they are what nanotechnology wants to be.

Many poisons work in an enzymatic manner, though not to replicate but to destroy. One famous such is ricin, a product of castor beans, that achieved fame for being placed in a small metal bead and injected into a Bulgarian dissident, Georgi Markov, by poking him with an umbrella at a London bus stop. Ricin enzymatically modifies the RNA that makes up the ribosome in a cell which is part of the machinery of translating information in DNA into cellular constituents. Since this is essentially a mechanical effect, the ricin is not destroyed and can affect another ribosome, until the translation machinery of the cell is destroyed and the cell dies. Since it just keeps moving along like a little machine, one molecule of ricin inactivates up to 1500 ribosomes per minute, and can kill an entire cell. Many of the lectin poisons, such as ricin, abrin, and modeccin work in similar ways.

The prion in vCJD is another such little machine. It is a malformed version of a normal cellular protein and instead of breaking apart cellular components, works by changing the normal version into the malformed version, which in turn changes other normal versions, etc. The interesting thing about how it works, though, is that instead of modifying the structure of the normal version, it modifies the

*shape.* Enzymes work in a way analogous to a socket wrench, and fitting the substrate to the enzyme is a function of charge and shape, among other things.

The interesting thing about the prion structure is that the normal form may work in a way proposed by some people thinking about organic computers -- having one molecule shaped in one way for a "0" and different shape for a "1." This is a good way to do things because these conformational changes can be very fast and it means that each molecule can contain one bit of information.

Recent research suggests that the normal form of the prion protein may work in a similar way -- that the change in conformation (shape) of the normal protein is a way of making memory. See: HELEN PEARSON, Prion proteins may store memories: Study hints at vital job for two-faced proteins. Nature, 30 Dec 2003 for a short review or Si, K. et al. A neuronal isoform of CPEB regulates local protein synthesis and stablizes synapse-specific long-term facilitation in Aplysia. Cell,

115, 879 - 891, (2003). for the full article.

Thus, the action of the malformed prion protein is similar to the normal mechanics of the normal prion protein -- to change shape under certain circumstances and to encourage surrounding prion proteins to do likewise. This may well be an example of the cellular machinery that we use to create memory going bad.

But if the enzyme works a little like a socket-wrench, what would happen if you changed the shape of the substrate? The enzyme would either work less well or not work at all. Even though the hysterics in this group refuse to believe that classic CJD is related to variant CJD (vCJD), in fact studies with CJD are illuminating. It turns out that if you take the prion protein and change one amino acid, you make it resistant to the malformed prion's attack. If it is partially resistant, then you increase the time it takes for the patient to become symptomatic. If it is completely resistant, then it is, well, completely resistant. If you change it a different way, you make the victim more susceptible.

Normal populations have multiple forms of the same enzyme -- some work better than others, but mutations along the way have caused some diversity. Since we have two copies of each chomosome, some people have two copies of the same version, and some have one copy each of two versions. This genetic variation, called polymorphism, is the basis for much of what is called "DNA fingerprinting" for identification.

Enzymes are proteins, which means they are largely strings of amino acids all folded up. Two common variations of the prion protein is to have the amino acid valine at one position (coded for by the genes of codon 129) and the other is to have a different amino acid called methionine. Since we have two copies of the gene, a person can have two copies of the methionine version (MM), one copy of each (MV) or two copies of the Valine version (VV). Interestingly enough, this gene is associated with other wierd things -- mutations of the prion protein at codon 178 are associated with Fatal Familial Insomnia, for instance. Gerstmann-Straussler-Scheinker syndrome, related to Alzheimers, is associated with mutations at codons 105, 117, 145, and 198. Cerebellar ataxia is associated with mutations at codon 102. Alzheimer's patients often have mutations at codon 200.

It turns out that *all* of the people who have acquired vCJD are homozygous for *one* version of prion protein -- they are "MM" at codon

129. *No* person who is MV or VV has contracted mad cow disease.

The good news is that only 37% of Caucasians are MM, though over 90% of Japanese are MM. The bad news is that people who have valine (MV and VV) may be resistant to vCJD, but are *more* susceptible to Alzheimers, and Down's Syndrome subjects who are MV or VV have an accelerated decline in cognitive function when compared with MM subjects.

For the purposes of the Mad Cow hysteria, however, it may well be that most people are resistant.

billo

Reply to
Bill Oliver

Actually a simple google search and several minutes are enough. But you know that.

Revealling your inconsistencies is really pretty key to understanding your trolling on diseases and chemical issues in rec.gardenst.

A simple search conclusively demonstrates you ONLY troll this group.

Reply to
tomjasz

""Honestly, the chances of getting killed using a rototiller are a lot greater." "

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Reply to
michaelanthony207

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