from firstname.lastname@example.org (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
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Out of date, see above.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
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.
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?
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)"
Here's a direct link to Chapter 5, "Testing Blood for Evidence of Agents
of Transmissible Spongiform Encephalopathies" (pp 108 - 124)
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
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.
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
What is it? How does that fit into your calculations of
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.
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.
On Fri, 04 Jun 2004 13:17:55 -0000, email@example.com (Bill Oliver)
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
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
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.
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
"Of what are you afraid, my child?" inquired the kindly teacher.
"Oh, sir! The flowers, they are wild," replied the timid creature.
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.
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.
On Sat, 05 Jun 2004 22:26:06 -0000, firstname.lastname@example.org (Bill Oliver)
Even the FDA has admitted there is no scientific basis for this
decision in the US -- it was purely political, in order to
"reassure" the population.
In fact, this is one example of the BSE hysteria *costing* lives.
The FDA allows fewer and fewer people to donate blood for political
reasons while the demand for blood rises, leading to severe
blood shortages. BSE has cost lives in the US -- because of the
over-reaction to a very small risk.
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