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Natural Science Forum / Biology / Biology / September 2006



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Methodology-of-Family-Related-Diseases of Alzheimers, Parkinsons, Autism, Prion and the Metal Causation Theory

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a_plutonium - 23 Aug 2006 07:42 GMT
Sorry, I meant to start a new thread with the below since the old one
was too long.

a_plutonium wrote:
> a_plutonium wrote:
> > Last night I went to Google search "autism aluminium" and found this
> > website. Below I quoted what I deemed as a sort of "abstract" of what
> > the entire article was discussing. I wanted to try to keep as many of
> > the specific proteins and points of fact and reference in case the
> > website comes down. Unlike the newsgroups which have a quality of
> > permanence, websites can be altered or taken down easily. And for
> > future readers who may want to search deeper would have those
> > references available.
> >
> > Please see my comments below. And I should start a new thread with this
> > article.
> >
> > --- quoting in part (snipped parts)
> > http://www.mothering.com/articles/growing_child/vaccines/toxic.html ---
> > Toxic Overload: Assessing the Role of Mercury in Autism
> > By Boyd E. Haley
> > Issue 115, November/December 2002
> >
> > From 1996 to 1997, J. Curtis Pendergrass, PhD, did some experiments in
> > my research laboratory at the University of Kentucky that confirmed the
> > toxicity of thimerosal in vaccines. The results appeared on our website
> > (www.altcorp.com), where they attracted the attention of some parents
> > of autistic children.
> >
> > These parents informed me that increased mandatory vaccination of
> > infants was, in their opinion, the cause of an apparent epidemic of
> > autism. ...............................snipped
> > .................................................
> >
> > My laboratory was well experienced in mercury research. We had earlier
> > demonstrated that mercury, when exposed to normal human brain tissue
> > homogenates, is capable of causing many of the same biochemical
> > aberrancies found in Alzheimer's diseased (AD) brains.1-4
> > ......................................................snipped
> > ......................................................................................
> >
> > Therefore, we hypothesized that exposure to mercury is involved in the
> > etiology of AD, or at least would exacerbate this disease. We also
> > proposed that other heavy metals, such as lead and cadmium, which act
> > synergistically to enhance the toxicity of mercury, could be involved.
> > Additionally, we proposed that exposure to organic-mercury compounds
> > like methyl mercury from fish and ethyl mercury from thimerosal would
> > also enhance the toxicity of any exposure to mercury. The early work of
> > Dr. Pendergrass confirmed this with pure thimerosal, with some
> > interesting additional observations. First, in human brain samples the
> > exposure to mercury dramatically reduced the viability of a major brain
> > protein called tubulin, but had little if any effect on another major
> > protein, actin. Both tubulin and actin are critically important for the
> > growth of dendrites or maintenance of axon structures of neurons.
> > Exposing neurons to mercury rapidly results in the stripping of tubulin
> > from the axon structure, leaving bare neurofibrils that form the
> > tangles that are the diagnostic hallmark of AD. Thimerosal, like
> > mercury, also rapidly reduces the viability of tubulin; in addition,
> > however, it abolishes the viability of actin. This likely represents a
> > major difference in the mechanism of mercury versus organic-mercury
> > (more neurotoxic) toxicity. However, both mercury and organic-mercury
> > inhibit tubulin viability and would work in concert to damage neurons
> > of the central nervous
> > system..........................................snipped most all of the
> > rest
> > .....................................................................................................
> >
> > NOTES
> > 1. S. Khatoon et al., "Aberrant GTP-Tubulin Interaction in Alzheimer's
> > Disease," Annals of Neurology 26 (1989): 210-215.
> > 2. S. David et al., "Abnormal Properties of Creatine Kinase in
> > Alzheimer's Disease Brain," Molecular Brain Research 54 (1998):
> > 276-287.
> > 3. E. F. Duhr et al., "HgEDTA Complex Inhibits GTP Interactions with
> > the E-Site of Brain-Tubulin," Toxicology and Applied Pharmacology 122
> > (1993): 273-288.
> > 4. J. C. Pendergrass and B. E. Haley, "Mercury-EDTA Complex
> > Specifically Blocks Brain-Tubulin-GTP Interactions: Similarity to
> > Observations in Alzheimer's Disease," in Status Quo and Perspective of
> > Amalgam and Other Dental Materials, International Symposium
> > Proceedings, L. T. Friberg and G. N. Schrauzer, eds., 98-105 (Stuttgart
> > and New York: Georg Thieme Verlag, 1995).
> > 5. J. C. Pendergrass et al., "Mercury Vapor Inhalation Inhibits Binding
> > of GTP to Tubulin in Rat Brain: Similarity to a Molecular Lesion in
> > Alzheimer's Disease Brain," Neurotoxicology 18, no. 2 (1997): 315-324.
> > 6. G. Olivieri et al., "Mercury Induces Cell Cytotoxicity and Oxidative
> > Stress," J. Neurochemistry 74 (2000): 231-241.
> > 7. C. C. W. Leong et al., "Retrograde Degeneration of Neurite Membrane
> > Structural Integrity and Formation of Neurofibillary Tangles at Nerve
> > Growth Cones Following in Vitro Exposure to Mercury," NeuroReports 12,
> > no. 4 (2001): 733-737.
> >
> > Boyd E. Haley, PhD, is a professor and chair of the department of
> > chemistry at the University of Kentucky, Lexington. His research on
> > biochemical aberrancies in Alzheimer's disease led to his identifying
> > mercury toxicity as a major exacerbating factor, perhaps even a causal
> > factor. Haley has testified before numerous government agencies on the
> > effects of mercury toxicity from dental amalgams and vaccines.
> >
> > --- end quoting in parts
> > http://www.mothering.com/articles/growing_child/vaccines/toxic.html ---
> >
> > The above article totally anticipated this post of mine yesterday where
> > I hypothesized Autism as another form of Alzheimers only in different
> > age groups. Only that Dr. Haley did not go so far as to say that Autism
> > is Alzheimers. And I focused on aluminum whereas Dr. Haley focused on
> > mercury.
> >
> > That is an interesting focus, because we know in the 20th century
> > almost every infant was vaccinated and the use of thimerosal was
> > widespread. But also the fact that many old people in the 20th century
> > got flu shots and other shots in old age in which thimerosal was or
> > could have been used. (And perhaps Ronald Reagan got alot of shots,
> > especially in old age).
> >
> > We know there are forms of speeded up Alzheimers and speeded up Prion
> > disease and speeded up Parkinsons. Perhaps the speeding up form was a
> > too large of a dose of vaccine induced. We know that in England in the
> > 19980s or 1990s was a cluster case of Prion disease of young people.
> > Many think it was something they ate in common. But perhaps it was a
> > vaccine that was too high in mercury.
> >
> > Dr. Haley and others have anticipated me by many years, judging that
> > the above was printed in 2002 (sic).
> >
> > But I do bring something new to the table. What I bring is the
> > Methodology that we categorize similar diseases into one large class
> > and from that we can thence say that if such and such is a factor in
> > one of these diseases, then it is likely factor in every other one of
> > those diseases. I have grouped Alzheimers, Prion, Parkinsons and Autism
> > as members of a one group of disease. So that if one of them has a
> > factor of importance, it is likely to be found in the other three. So
> > if a metal is found to cause say Alzheimers, then a metal is probably
> > the cause of Prion, Parkinsons and Autism.
> >
> > That Methodology was discovered by me in the early years of 2000s.
> >
> > Another one of my discoveries is that I know Prion disease is not
> > explained by the Prusiner Model and that model is a fake. But rather,
> > that whatever is the cause of Alzheimers and Parkinsons and Autism is
> > more likely to be the cause of Prion. No-one in the world, not even
> > Prusiner, would venture to say that what causes Alzheimers and
> > Parkinsons and Autism is a rogue protein that misshapes other protein
> > molecules. But rather instead, what every commonsense person would or
> > might say is that some metal in the environment can cause proteins in
> > the brain to go heywire.
> >
> > This thread is already too long and I will start a new thread with much
> > of the above.
>
> In the above report, it spoke of the combination of thimerosal or
> mercury and of aluminium ions as increasing the toxicity, where the
> metals alone are weak in toxicity the combination makes them overly
> toxic. Likewise for other metals such as lead or cadmium. So I wonder,
> since in Prion disease there are a plethora of types of the diseased
> protein, whether the types are due to different amounts of combinations
> of metals. One combination elicits type/form A prion disease and a
> different metal combination elicits type B prion disease, etcetera.
>
> In the above it spoke of the fact that boys seem to catch Autism about
> 4 times as much as girls. An offered explanation was the difference in
> sex hormones of testosterone to estrogen.
>
> So, now, according to my overarching umbrella theory that these
> diseases are all related as a Family GRoup Diseases would imply that
> hormones affect not only Autism but be seen in Alzheimers and Prion and
> Parkinsons. Not to say that they have to have a strict obeyance of a 4
> to 1 ratio. But that some of them would have evidence of hormones
> affecting the male to female contraction rate. So, do we see some
> imbalance between the sexes in Alzheimers? in Prion? in Parkinsons?
>
> If I am not mistaken, it is mostly males that catch Parkinsons. Prion
> is so rare that maybe no marked data is available. As for Alzheimers, I
> am not aware of any imbalance in numbers between male and female. And
> maybe it has something to do with old age, in that the hormones are
> just not "cooking" so to speak in old age as in younger age.
>
> Archimedes Plutonium
> www.iw.net/~a_plutonium
> whole entire Universe is just one big atom
> where dots of the electron-dot-cloud are galaxies
a_plutonium - 23 Aug 2006 09:23 GMT
> Sorry, I meant to start a new thread with the below since the old one
> was too long.
[quoted text clipped - 172 lines]
> > maybe it has something to do with old age, in that the hormones are
> > just not "cooking" so to speak in old age as in younger age.

I did some scouting around on the Internet and a report from Northern
California gives a rate of contraction of Parkinsons as 2 males per
every 1 female.

Found two sites for Alzheimers statistics. One was from "BC" which I am
guessing is British Columbia and one was from Arizona. Both gave a rate
of 1 male per every 2 females.

I found nothing for gender statistics on Prion disease.

What I surmise from the above data is that these are Metal caused
diseases for which the hormones of testosterone and estrogen play a key
role in the incidences of contraction. In the case of Autism, the male
hormone contributes to the metal toxicity. In the case of Parkinsons
the male hormone hurts but in Alzheimers it helps.

And because the ratios are so integrally-discrete 4 to 1, or, 2 to 1,
or 1 to 2, signifies the action of metals that cause the disease.

And another aspect of these diseases, is that if a metal causes them,
then you would never see a case in which a person has both Parkinsons
and Alzheimers because the metals combine in toxicity so that one
disease materializes.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 23 Aug 2006 20:19 GMT
Autism seems to have a ratio of 4 males to every 1 female. And I was
trying to find out what the ratio is for sheep scrapie or Mad cow
disease, but since these herd animals are selected by sex (few bulls
among many cattle) that there is no observed ratio.

I did happen to find Kuru ratio of 4 females to 1 male given the 3,000
death of Fore people in New Guinea. The alleged mechanism is practiced
cannibalism. But it maybe the case where the brains of one had such a
high concentration of a "bad metal" that it resided in the brain tissue
of many victims. Metal as a causation would still exist in the Fore
society. So the question I have is whether Kuru has been completed
elminated or have cases of Kuru in New Guinea popped up recently? If
metal is the cause then recent cases would show up. If a protein is the
infectious agent (Prusiner Model) then the disease would be totally
eliminated.

So, what is the evidence? Has there been any new Kuru in New Guinea?
And if there has been, then it is likely to be a metal in that tubers
or roots or plants or water or food.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 23 Aug 2006 20:28 GMT
> Autism seems to have a ratio of 4 males to every 1 female. And I was
> trying to find out what the ratio is for sheep scrapie or Mad cow
[quoted text clipped - 15 lines]
> And if there has been, then it is likely to be a metal in that tubers
> or roots or plants or water or food.

Well I did a small search for new cases of Kuru and landed on this
statement quote: "(before the author's initial visit around 1980 and on
his return trip only a few years ago) that the hope that kuru may be
going extinct is still an open question. Cannibalism has been banned
for the better part of a half century, and the cases of kuru all seemed
to be in the dying elderly when Klitzman made his discoveries of the
transmission mode. Yet, there are still new cases, though very few in
number. "

So I need further information and data. If metal is the cause and not
some rogue protein, then Kuru will always exist in New Guinea as it
will always exist in England and parts of Canada where the metal is in
high concentration and accessible to sheep, cattle and humans.

Does anyone have a more detailed update of Kuru than the above
statement by Klitzman?

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
Jason Johnson - 24 Aug 2006 01:45 GMT
> Autism seems to have a ratio of 4 males to every 1 female. And I was
> trying to find out what the ratio is for sheep scrapie or Mad cow
[quoted text clipped - 15 lines]
> And if there has been, then it is likely to be a metal in that tubers
> or roots or plants or water or food.


Well I did a small search for new cases of Kuru and landed on this
statement quote: "(before the author's initial visit around 1980 and on
his return trip only a few years ago) that the hope that kuru may be
going extinct is still an open question. Cannibalism has been banned
for the better part of a half century, and the cases of kuru all seemed
to be in the dying elderly when Klitzman made his discoveries of the
transmission mode. Yet, there are still new cases, though very few in
number. "

So I need further information and data. If metal is the cause and not
some rogue protein, then Kuru will always exist in New Guinea as it
will always exist in England and parts of Canada where the metal is in
high concentration and accessible to sheep, cattle and humans.

Does anyone have a more detailed update of Kuru than the above
statement by Klitzman?

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies

~~~~~~~~~~~~~~~~~~~~~~~~~

Hello,
You mentioned in another post your theory that hormones may play a role in
related to various disease such as Alzheimers, Parkinsons and autism. Can
genes have an effect upon hormones? I seem to recall learning in a college
genetics class that genes are the cause of MPB (male pattern baldness).
The "MPB" genes cause hormones to be released and the hormones cause
Male Pattern Baldness. The "MPB" genes are NOT in females. In other words,
even if hormones play a role in diseases such as those diseases mentioned
above--it could be because of genes effecting those hormones. The genes that
cause certain diseases may only be in males and not in females in much the same
way that the MPB genes are only in males. You may want to do a google
search on this term: "sex-linked gene".
Jason
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
bae@cs.toronto.no-uce.edu - 24 Aug 2006 02:57 GMT
> Well I did a small search for new cases of Kuru and landed on this
> statement quote: "(before the author's initial visit around 1980 and on
[quoted text clipped - 4 lines]
> transmission mode. Yet, there are still new cases, though very few in
> number. "

This is good support for the fact that kuru is caused by an infectious
agent spread by eating contaminated tissue.  My guess is that while
cannibalism has been banned, it is still practiced to a much smaller
extent, or other funerary customs cause some exposure to infected
tissue.

Note that kuru, IIRC, has a long and variable incubation period, so some
of the new cases may be outliers.

> So I need further information and data. If metal is the cause and not
> some rogue protein, then Kuru will always exist in New Guinea as it
> will always exist in England and parts of Canada where the metal is in
> high concentration and accessible to sheep, cattle and humans.

Kuru does not occur in England or Canada.  It's not a consequence of
any known form of metal poisoning, acute or chronic.

The only reason that BSE has been detected in Canada and not the US is
that Canada has been screening for it for many years now and the US
does not screen at all.  Large numbers of cattle are sold back and
forth across the border.  The transmission pathway of BSE and nvCJD
is pretty well understood -- it's the pattern of a disease caused by
an infectious agent, spread by consumption of infected tissue.  Scrapie
does not occur in Canada because it was kept out by quarantine practices
for imported sheep.  

You have zero evidence for your metal ion theory.  Your reasoning is:
    (1) Hypothesis: metals cause these diseases, not prions
    (2) Prediction: metals will be found where the diseases are found,
       and not elsewhere.
    (4) Conclusion: the diseases are caused by metals

Note that you missed out on step (3), in which you obtain actual facts
about occurrence of these metals in areas where the diseases are found
and where they are not found.  You don't have to be a rocket scientist
to spot the circularity of your so-called argument.

>Hello,
>You mentioned in another post your theory that hormones may play a role in
[quoted text clipped - 9 lines]
>search on this term: "sex-linked gene".
>Jason

You've got the MPB story scrambled.

The MPB genes are in both male and female humans, on the X chromosome.
Scalps of people with the relevant allele respond to testosterone by
becoming bald in middle age.  Castrated men don't become bald. Baldness
is seldom seen in women because unlike men, they have two X
chromosomes, so are more likely to have a non-MPB allele, and of course
they produce much less testosterone.  Women homozygous for this allele
often develop quite thin hair when they are elderly.  It's thin all
over, not in the MPB pattern.  But men in some ethnic groups don't
develop the European pattern -- their hair gets thin all over instead.

And of course genes affect hormones.  There are many genetic conditions
that cause endocrine abnormalities. There's a strong hereditary
component in both Type I and Type II diabetes, for example.  The most
glaring example, however, is the TDF gene on the Y chromosome, which
causes a mammalian embryo to develop as a male instead of a female,
with dramatic differences in the production of sex hormones and in
anatomy and physiology.
a_plutonium - 24 Aug 2006 06:54 GMT
> This is good support for the fact that kuru is caused by an infectious
> agent spread by eating contaminated tissue.  My guess is that while
> cannibalism has been banned, it is still practiced to a much smaller
> extent, or other funerary customs cause some exposure to infected
> tissue.

But to be more logically correct you would have to say either a
infectious protein or a metal associated with that protein. Science has
not yet determined whether it is the protein itself, or a metal inside
the protein or a metal carried along with the protein.

And because geography plays a huge role in the frequency of prion
diseases, the likelihood favors a metal, not the protein.

> Note that kuru, IIRC, has a long and variable incubation period, so some
> of the new cases may be outliers.
[quoted text clipped - 6 lines]
> Kuru does not occur in England or Canada.  It's not a consequence of
> any known form of metal poisoning, acute or chronic.

Just mincing definitions for Kuru is another CJD variant. All the human
prion diseases are variations of one prion disease. Are we going to
call every subtle difference of Alzheimers or Parkinsons with a
different name.

> The only reason that BSE has been detected in Canada and not the US is
> that Canada has been screening for it for many years now and the US
[quoted text clipped - 4 lines]
> does not occur in Canada because it was kept out by quarantine practices
> for imported sheep.

No, I think you are mistaken, for the USA has a very active program of
detecting BSE. So much of what you post is your opinion and not really
factual.

And metal as the cause of prion disease would account for the higher
frequency of Canada because so much metal is in Canada. If you ever
studied geology you would know that Canada is the "shield" of the North
American continent where the most metal can be found.

> You have zero evidence for your metal ion theory.  Your reasoning is:
>     (1) Hypothesis: metals cause these diseases, not prions
[quoted text clipped - 6 lines]
> and where they are not found.  You don't have to be a rocket scientist
> to spot the circularity of your so-called argument.

No, this is a bad thing of you to do to another author. Is to list
(his) reasoning when you yourself is too illogical to understand what
he is doing.

I am still very much active in the "evidence collection phase" of these
4 diseases. And so most of my above is not a reasoning but a collection
of the evidence.

What those 1-4 Reasoning would look like is this:
(1) start with the Methodology that Alzheimers, Parkinsons, Autism,
Prion are members of a Family-Related-Diseases. With that in mind, the
explanation of one disease provides very much the same explanation for
the other 3.
(2) Metals could cause Alzheimers, Parkinsons and Autism, so with that
information we very much have to seriously consider that Prion is
caused by a metal and not a protein. Otherwise, can Alzheimers,
Parkinsons, and Autism be caused by a rogue protein and the answer
would by laughingly no.
(3) Since *Family Related Disease* is the logical structure, and since
Alzheimers comes with a 2female to 1male ratio, and since Parkinsons
comes with a 1female to 2 male ratio and since Autism comes with a 4
male to 1 female ratio. We thence must look to see if Prion has a
ratio.
(4) If Prion has a ratio of say 4female to 1 male, would be indicative
of a particle like nature to the transmission of the disease. That
implies a metal in the environment.

I do not mind if you disagree with what I post, but I do mind when you
never understand what it is I am saying and then construe some
falsehood around me.

You do not have a powerful logical mind as I have for science, and you
should resist on your criticisms. You should be more informative,
rather than critical since you do lack a powerful logic.

Let me give you an example of your deficiency. Above you accept the
Prusiner model, but did you ever consider that to destroy a BSE or CJD
or scrapie agent requires more than boiling water. In fact it requires
acetylene torch to "kill" the infectious agent. Now, you with your
inferior logic never thought about this killing factor. For if you ever
thought about it you would realize that there is no protein that can be
a disease infectious agent if it required heat of acetylene torch.
Where exactly on the temperature scale is Prion disease rendered
harmless or not infectious? Is it over 1000 degrees centigrade? In
other words, if you had put a logical mind to work, you would realize
that because of the heat to render the disease non infectious, implies
that the agent is not a protein. The agent of infection of prion
disease because of the enormous heat to render harmless is a metal
compound or a metal free radical or a toxic metal.

What exactly is the heat to render Prion harmless? Is it the heat that
renders Cu ions or Zn ions into a different atomic or molecular
condition? Is it mercury compounds or manganese compounds for which
that high heat would render harrmless. Is it a metal inside the prion
proteins or a metal in protein solutions?

My criticism of you is not meant to be destructive, but since you
misrepresented my views, I had to come down hard on you. Some
philosopher said he never minded criticism, but hated when people
misunderstood and thus misrepresented him ( I think it was Kant).

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 24 Aug 2006 18:43 GMT
--- quoting
http://www.rcplondon.ac.uk/pubs/journal/journ_34_jul_conf3.htm ---
Journal : vol 34 : Jul/Aug : College Conferences
Infectious diseases

Professor Collinge (Imperial College, London) gave a very
comprehensible overview of prion disease. The transition from normal
prion protein (PrPc) to pathogenic PrPSc is not determined by protein
primary structure but by three-dimensional structural changes, though
the way this is propagated within subjects or transmitted from subject
to subject remains a mystery. Nevertheless, molecular techniques
reflecting glycosylation and structure have shown that the form found
in patients clinically presenting with variant CJD (Creutzfeldt-Jakob
disease) is strikingly similar to that in BSE (bovine spongiform
encephalopathy). Worryingly, new cases of kuru are still appearing,
suggesting an incubation period of up to 40 years for prion disease.
More promisingly, in vitro, it has now proved possible to produce
?-pleated sheets from PrP in the ?-helical form which goes on to form
fibrils, and blockers of this process, which may slow progression of
disease, are being developed.

--- end quoting
http://www.rcplondon.ac.uk/pubs/journal/journ_34_jul_conf3.htm ---

There is no *mystery* in the above if a metal in the environment is the
ultimate cause of prion disease. Whether the metal is inside prion
proteins or in solution alongside the prion proteins. A metal that can
withstand fierce heat. A metal that can be eaten and then migrate to
the brain.

Dr. Collinge did not elaborate on the new cases of Kuru. But if the
metal theory of Prion disease is correct, then there should be new
cases of Kuru and also evidence of a increase in frequency of Kuru as
more people come in contact with the metal in the New Guinea
environment.

Those opposed to the metal theory of prion causation will say that new
cases of Kuru were some leftovers or outlying cases from cannibalism.
The metal theory would say that even though cannibalism has stopped,
new cases of Kuru will arise and sometimes a rise in frequency.
Indicating that the infectious agent is very much present in the
environment-- a metal.

Now, why New Guinea? Are there metal mining in New Guinea? I can
understand England and Canada with their large metal mining and metals
in the environment. But is the geology of New Guinea that of a large
prescence of metals. I need to check on that.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 24 Aug 2006 19:01 GMT
(snipped)

> Now, why New Guinea? Are there metal mining in New Guinea? I can
> understand England and Canada with their large metal mining and metals
> in the environment. But is the geology of New Guinea that of a large
> prescence of metals. I need to check on that.

I checked and New Guinea economics is based mostly on oil and metal
mining. So, now, in the world of prion disease, three locations stand
out in terms of geology and geography of prion disease. They are
England, New Guinea and Saskatchewan region of Canada. Now what type of
metal is present in those 3 places? Is there copper with mercury and
zinc? I know England has alot of tin, but whether New Guinea and
Saskatchewan have alot of tin? Do all three locations have alot of
mercury present?

Now there was a cluster of cases of CJD in Colchester England in the
1990s where five or more young people all contracted CJD and rapidly
died. This is a sign of metal as the cause. Now is the Colchester
region of England in close proximity with tin, mercury, copper mines?

I hear alot about BSE from Saskatchewan Canada region, but is there a
cluster of CJD in that part of Canada?

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
Bob - 25 Aug 2006 02:18 GMT
>No, I think you are mistaken, for the USA has a very active program of
>detecting BSE.

It may be "active", but it is _very_ limited. (At least, has been,
until the fairly recent events.) It was a very thin sampling program.
Critics contended that the purpose of the BSE screening was to make
sure we never found it here.

> but did you ever consider that to destroy a BSE or CJD
>or scrapie agent requires more than boiling water. In fact it requires
>acetylene torch to "kill" the infectious agent.

Who told you that nonsense?

In another recent post you claimed it survived burning. When asked
about that, you had no meaningful response.

We need some civility here. You seem to get your kicks by putting down
other people, who try to introduce real facts into the discussion.
When all else fails, criticize the other person's character. Please,
learn to behave decently in a public forum. This is a good place to
discuss ideas, even odd ones, but surely we can do so respectfully.

bob
lucasea@sbcglobal.net - 25 Aug 2006 02:58 GMT
>> but did you ever consider that to destroy a BSE or CJD
>>or scrapie agent requires more than boiling water. In fact it requires
[quoted text clipped - 4 lines]
> In another recent post you claimed it survived burning. When asked
> about that, you had no meaningful response.

Well, I hate to find myself agreeing with AP, but I thought I had heard
something similar, although not as extreme.  What I thought I remembered was
that the "prion" was essentially the global minimum conformation of the
protein, and was thus very refractory to conditions that would denature
other less stable local-minimum conformations.  Essentially, the only thing
that would destroy the protein was conditions that would break covalent
bonds--i.e., from peptide hydrolysis up to an including outright combustion.
Since amide hydrolysis is slow even at 100 C at biological pH, I wouldn't
think the "survive boiling water" would be an inapt description.  In fact,
when we're talking about cooking food, it's awfully difficult to heat it up
to > 100 C, so applying a blowtorch wouldn't be a bad method to use.  I
think I also remember hearing concern in GB during the BSE outbreak about 10
years ago, that cremation of infected carcasses entailed the risk of
unaltered prions being carried airborne in aerosols and soot particles.
Since cremation at hotter temperatures lessens this likelihood, use of an
extremely hot flame like oxyacetylene would minimize the risk.  This could
have given some less-than-critical thinkers who are too focused on their own
pet hypotheses the impression that the prions could survive fire.

However, I'm a physical organic chemist by trade, not a biochemist, and the
last time I had read anything on prion diseases in the scientific literature
was on the order of 10 years ago.  Is this no longer consistent with the
current state of understanding?

Eric Lucas
Bob - 25 Aug 2006 05:01 GMT
>>> but did you ever consider that to destroy a BSE or CJD
>>>or scrapie agent requires more than boiling water. In fact it requires
[quoted text clipped - 28 lines]
>was on the order of 10 years ago.  Is this no longer consistent with the
>current state of understanding?

There are a couple of ways to look at this. One is in terms of the
structure, and the other is empirical data. The structure is certainly
interesting, but empirical data may address the question better for
the moment.

As you suggest above re the cremation procedure, one needs to be
careful in describing the result. Kill curves are (idealized)
exponentials. So any statement that a treatment does or does not kill
is weak (unless the kill rate is zero). It is one thing to say that a
particular treatment does not result in "complete" destruction
(sterilization) -- a result with practical implications. Yet sometimes
it is said that the treatment did not kill, when in fact, several logs
of killing were obtained.

I don't have much real data with me at the moment, but will look for
some when I get a chance.

My recollection is that prions are killed by autoclaving -- but not
very well. That is, ordinary autoclaving is not very good for
sterilization, but that should not be translated as saying the prion
is stable under autoclave conditions. Also, remember that it is not
particularly uncommon to find that bacterial spores survive
autoclaving, at a low level -- especially if there are problems of
heat transfer thru the sample.

An interesting paper, which got a lot of attention, is:
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival
after ashing at 600°C suggests an inorganic template of replication
Paul Brown, Edward H. Rau, Bruce K. Johnson, Alfred E. Bacote,
Clarence J. Gibbs, Jr., and D. Carleton Gajdusek
PNAS 97(7): 3418-3421, 3/28/00.

This should be freely available online.

They study the use of dry heat to reduce the infectivity of prions.
The key data of concern to them is that a small amount of infectivity
is seen after treatment at 600 C for 15 min. Taken at face value, this
represents about 7 logs of kill. Interestingly, no residual
infectivity was seen at the 5 minute point! [With 150 C, they estimate
2 logs of kill in 15 min. This with dry heat, and crude biological
material (ie, poor heat penetration).]

So, even if there is a residual infectivity from the high T treatment,
it is also important that the work shows killing even with 150 C heat.
No one would consider 15 min of 150 C dry heat to be even close to
sterilization conditions for bacteria, so their results here are
unremarkable.

(As to the residual infectivity... I find the quality of the data
rather bad, and have looked for follow-up work; as of a  year or so
ago, I found nothing published that addressed the residual
infectivity.)

As to the structure... I think it might be making a bit much of it to
make arguments about a global energy well -- of apparently magnificent
proportions. It may be sufficient that the infectious agent is an
aggregated protein, less accessible to agents attacking it. There are
multiple "strains" of prions (of same primary sequence). It has been
shown that these represent different conformations of the protein. But
a recent elaboration of this suggested that part of the difference is
how the subunits are joined together in the "aggregate". That makes
sense, and emphasizes that the active agent is "big" -- a feature
which in itself may promote resistance.

bob
a_plutonium - 25 Aug 2006 06:09 GMT
> >>> but did you ever consider that to destroy a BSE or CJD
> >>>or scrapie agent requires more than boiling water. In fact it requires
[quoted text clipped - 95 lines]
>
> bob

I do not know what the temperature would have to be to break the
covalent bonds.
So I guessed 1000 degrees C.

I could not find any temperature in any report that renders infectious
prion disease as noninfectious. So the above 600 C for 15 minutes is
the first noteworthy data.

No-one has researched this issue of what temperature and for how long
to render noninfectious. Because no-one had any alternate theory that
the infectious agent was a metal inside the prion protein or a metal
alongside the prion proteins (metal in protein solutions).

So this testing of what temperature and for how long to render
noninfectious would be a deciding experiment to differentiate between
the Prusiner Model and the Metal Causation Model.

It maybe the case that if a metal is the cause of prion disease, that
increasing the temperature may increase infectivity, not reduce
infectivity. So if the experiments find that there is no "high"
temperature that eliminates infectivity, would be proof that metal is
the cause of prion diseases. And if the high temperature does
accomplish noninfectivity that also would point to a metal as the
underlying cause of prion diseases.

It maybe the case that mercury attaches to the copper atoms in prion
molecules and is the mechanism of changing the shape of other prion
molecules. So the burning off of the mercury would disinfect the
disease. Does mercury burn off at about 600 C for 15 minutes?

At what temperature and time does it require to remove all the atoms of
a prion molecule leaving only the copper ?

I must see if alpha synuclein in Parkinsons or beta amyloid in
Alzheimers have metals in their composition.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 25 Aug 2006 07:17 GMT
Bob wrote about autoclaving as disinfectant, but there are some reports
of prions surviving after 600 degrees C for 15 minutes.

If the Metal Cause Model is correct, then there should be a simple
chemical solution which destroys the infectivity of Prion Molecules. I
am guessing it is a combination of copper and mercury and zinc that
causes prion disease. So I wonder, what physical test a solution of
prion disease can be subjected to that will render the copper, mercury
and zinc atoms into a different form.

Instead of autoclaving of high pressure and high temperature. There
should be a chemical means of altering the metals, but not altering the
other atoms of the protein prion molecule.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 25 Aug 2006 18:40 GMT
--- quoting from Journal of Neurochemistry ---
Volume 78 Page 1400  - September 2001
doi:10.1046/j.1471-4159.2001.00522.xVolume 78 Issue 6  Aberrant metal
binding by prion protein in human prion diseaseBoon-Seng Wong,* Shu G.
Chen,* Monica Colucci,*,1 Zhiliang Xie,* Tao Pan,* Tong Liu,* Ruliang
Li,* Pierluigi Gambetti,* Man-Sun Sy* and David R. Brown

Human prion diseases are characterized by the conversion of the normal
prion protein (PrPC) into a pathogenic isomer (PrPSc). Distinct PrPSc
conformers are associated with different subtypes of prion diseases.
PrPC binds copper and has antioxidation activity. Changes in metal-ion
occupancy can lead to significant decline of the antioxidation activity
and changes in conformation of the protein. We studied the trace
element status of brains from patients with sporadic
Creutzfeldt-Jakob disease (sCJD). We found a decrease of up to 50% of
copper and an increase in manganese of approximately 10-fold in the
brain tissues from sCJD subjects. We have also studied the metal
occupancy of PrP in sCJD patients. We observed striking elevation of
manganese and, to a lesser extent, of zinc accompanied by significant
reduction of copper bound to purified PrP in all sCJD variants,
determined by the PrP genotype and PrPSc type, combined. Both zinc and
manganese were undetectable in PrPC preparations from controls. Copper
and manganese changes were pronounced in sCJD subjects homozygous for
methionine at codon 129 and carrying PrPSc type-1. Anti-oxidation
activity of purified PrP was dramatically reduced by up to 85% in the
sCJD variants, and correlated with increased in oxidative stress
markers in sCJD brains. These results suggest that altered metal-ion
occupancy of PrP plays a pivotal role in the pathogenesis of prion
diseases. Since the metal changes differed in each sCJD variants, they
may contribute to the diversity of PrPSc and disease phenotype in sCJD.
Finally, this study also presented two potential approaches in the
diagnosis of CJD; the significant increase in brain manganese makes it
potentially detectable by MRI, and the binding of manganese by PrP in
sCJD might represent a novel diagnostic marker.
--- end quoting from Journal of Neurochemistry ---

In the literature, 600 degrees C for 15 minutes was applied to prion
proteins to make sterile. This is "ash material" after such high heat.
Yet this ash still had residual infectivity. Logically, this indicates
the protein is not the agent of infection, but rather, some metal.

I do not know if mercury can amalgamate with copper atoms situated in a
protein molecule. The melting point of copper is 1085 C and the melting
point of mercury is -39 C and boils at 357C.

I do not know the heat-of-reaction (enthalpy) is for a mercury to
copper association.

I think it is mercury that is the agent of prion disease, and not
manganese.

And I think that mercury is mainly to blame for Alzheimers and
Parkinsons. And the reason Prion is so common in animals but rare in
humans is because animals do not catch Alzheimers or Parkinsons but
catch only prion disease. If humans were animals then all cases of
Alzheimers and Parkinsons would be viewed as a prion disease.

This also makes sense in the fact that these diseases occur in old age,
after the accumulation of metals such as mercury in the brain tissue.

And it makes sense with Autism in that infants exposed to a high dosage
of mercury in vaccines destroys the part of the brain that makes for
"socialization".

Now there is a curious study as to the amount of prion infection agent
to be of a level high enough to start the disease. If the level is
below this amount, no disease. This indicates that a specific amount of
mercury has to be present to start Prion or start Alzheimers or start
Autism.

Now in well-water bacteria that have been implicated in Parkinsons, I
wonder if that water was also containing of mercury, for there are some
bacteria that live in high concentrated mercury environments. Perhaps,
even, these bacteria carry mercury atoms in a high concentration and
thus, when the bacteria entire a human body they deposit the mercury.

And this may go to explain the high numbers of Prion disease in England
with its connection to the oceans and seas of fish and fish meal for
plants and animals. And fish with high amount of mercury which is fed
to the sheep and cattle as protein supplement. And explain why Canada
and New Guinea are high in prion-related diseases is the fish meal.

P.S. it is interesting to note that the above abstract mentions
manganese, able to be measured by MRI. So I wonder if anyone
followed-up on that experiment.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 25 Aug 2006 18:58 GMT
There is not much knowledge about how copper and mercury react in brain
tissue with respect to amalgamation. It is a fact that the ability of
Prion infectivity corresponds to the amount of agent present. If below
a level, no disease. This reminds me of the toxicity of mercury. If
below a level, not toxic.

So, now, in Prion disease, since it requires heat of 600 degrees C for
15 minutes to make sterile, yet still a residue of infectivity
remaining.

Makes me think that the process of the Prion disease is a amalgam of
mercury atoms attached to the copper bond of prion proteins.

That what causes the shape change of prion molecules is the attached
amalgam of mercury atoms to prion proteins.

Could it be that the mercury atoms thence replace the copper atoms in
the prion molecule?

And that the high heat of 600 degrees C for 15 minutes required to
sterilize is the stripping of the prion molecule of its mercury atom
bond.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
lucasea@sbcglobal.net - 25 Aug 2006 19:09 GMT
> There is not much knowledge about how copper and mercury react in brain
> tissue with respect to amalgamation.

Amalgamation is a meaningless concept in this context.  Amalgamation is a
bulk phenomenon (it's basically a solid solution), not an single-atom
phenomenon.  Metals bind to proteins one atom/ion at a time, with a few
notable exceptions of two, three or four atoms/ions per protein.  You could
as meaningfully ask how well a single sodium ion dissolves in a single water
molecule.

So, reasking the question in a meaningful way...how do single copper ions
(not atoms--not in biological systems) interact with single mercury ions or
atoms?  They don't.

Have you ever even heard of Ockham's Razor?

Eric Lucas
a_plutonium - 25 Aug 2006 22:16 GMT
> > There is not much knowledge about how copper and mercury react in brain
> > tissue with respect to amalgamation.
>
> Amalgamation is a meaningless concept in this context.  Amalgamation is a

It happens to be the best concept in the literature, close to or
nearby, to the phenomenon of the 4 diseases I am discussing. Amalgam,
in physics, (something you are very weak in) ultimately is a electrical
force between atoms of mercury and copper. ( I remember in High School
of coating a copper penny with mercury).

Anyway, there is a force if enough mercury atoms conglomerate that when
nearby to prion molecules of their copper atom interiors would force a
*shape change* of the prion molecule. And if enough mercury atoms
conglomerate, call it a blob, which then attracts other prion molecules
into a Amalgam Bond.

There is a electrical force of attraction of mercury atoms to copper
atoms when in close proximity. I simply call it the Amalgam force bond.

> bulk phenomenon (it's basically a solid solution), not an single-atom
> phenomenon.  Metals bind to proteins one atom/ion at a time, with a few
[quoted text clipped - 9 lines]
>
> Eric Lucas

This is why you are a failure in science. Too rigid, and not flexible.
You read something and you never look for the kernels of truth but
rather search for some spot of tarnish and then dismiss the entire
exposition. No wonder you can never accomplish anything in science. No
wonder you never have any new ideas for you waste your time in
criticism over those who do have new ideas.

There is a Force of Conglomeration involved with Alzheimers, with
Prion, perhaps with Parkinsons although questionable; and perhaps with
Autism although questionable also. Because both Alzheimers and Prion
have conglomeration of proteins, unwanted proteins, perhaps this
conglomeration is started by the amalgam of mercury in the brain in
close proximity to alot of copper ions in solution.

Perhaps the plaques and fibrils in all these diseases is initiated by
this mercury amalgam force for copper.

Has anyone run a Mass Spectrometer on Alzheimers plaques for mercury
abundance? Has anyone run a Mass Spectrometer on Prion victims for
mercury abundance.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
lucasea@sbcglobal.net - 25 Aug 2006 22:59 GMT
>  blah, blah, blah

Yeah, whatever.

Eric Lucas
lucasea@sbcglobal.net - 25 Aug 2006 23:20 GMT
> This is why you are a failure in science. Too rigid, and not flexible.
> You read something and you never look for the kernels of truth but
> rather search for some spot of tarnish and then dismiss the entire
> exposition.

Yes, I admit it, my failing is insisting that theories be tested against
actual data, and aren't just based on imagined phenomena from the mental
vomitus of a megalomaniacal netkook.  Believe me, I look hard for kernels of
truth in everything I read...it's just that, in your blather, there are none
to find.  That says far more about your writing than it does about me.

Eric Lucas
a_plutonium - 26 Aug 2006 06:33 GMT
I think I hit a grand slam homerun here.

I was looking for pictures of prion proteins, the normal and rogue ones
to see if I can fit mercury atoms in-between the two. So that the shape
change is because of a mercury atom that causes the shape change.

I did not quite find that, but I did find something that is even more
intriguing and further evidence in favor of the Metal Causation Theory.

I found out what the role or function of prion proteins was. And I am
quite ashamed of myself for not insisting on knowing the function of
prion proteins in order to develop a correct theory of prion disease. I
mean, the likelihood of me finding the correct theory of prion disease
without knowing the role or function of what the prion protein does or
its reason for existence, is a low likelihood.

Well, I am glad to announce that from reading this website:
--- quoting http://srs.dl.ac.uk/Annual_Reports/AnRep00_01/prion.htm ---
The research indicates that the normal isoform of PrP has the
necessary properties, in the form of histidine residues 96 and 111, to
transport copper from outside the cell through the process known as
endocytic cycling.
--- end quoting ---

That the function of prion proteins is *surprize* the transportation of
copper.

All of a sudden the Metal Causation theory becomes a million times more
easy and becomes very much more the true theory.

So it is not the rogue protein changing the shape of other normal
proteins. Rather instead, it is a toxic metal that passes through
normal prion proteins, bends and misshapes the normal prion protein
into that of a rogue prion protein.

One protein is not altering the shape of another protein, but rather
instead, a metal transported through prion proteins is altering the
shape. I am not sure what metal that would be. It could be a rare form
of copper itself. It could be mercury.

So what is needed at this time, is a mass spectroscopy of disease prion
proteins to try to find some METAL that could cause this disease.

And it brings up the interesting question, going back to the
Foundational Methodology of these 4 diseases as
family-related-diseases. What is the role or function of the amyloid
proteins in Alzheimers? Is its function that of transporting aluminum
or the transport of something else? And that the disease of Alzheimers
is caused by a metal that gums up the working of the APP-scissors?

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 26 Aug 2006 06:58 GMT
Since the role or function or reason-of-existence of the prion protein
is copper transport, one can see that the geometry of the prion protein
is like a pipe where copper enters one end and is transported to the
other end.

And so the Prion diseases of scrapie, CJD, BSE, are diseases in which a
metal particle that passes through the prion protein and destroys the
piping. As it passes through it changes the shape of the original prion
protein.

Here we need mass spectroscopy to find out what candidate metals would
do such a thing. I suspect mercury. Some have suggested magnetic
manganese.

The England Colchester cluster of about 4 to 5 young people who caught
CJD and quickly died is suggestive of what metal it could be. And the
fact that autoclaving to sterilize the disease requires more than 600
degrees C for 15 minutes. And the speed of  illness of the Colchester
cluster (early 1990s ??) suggests that the metal is mercury. But I
could be very much wrong on what metal it would be.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 26 Aug 2006 19:53 GMT
> Well, I am glad to announce that from reading this website:
> --- quoting http://srs.dl.ac.uk/Annual_Reports/AnRep00_01/prion.htm ---
[quoted text clipped - 9 lines]
> All of a sudden the Metal Causation theory becomes a million times more
> easy and becomes very much more the true theory.

>From that website above it is mentioned that superoxide dismutase
closely resembles prion proteins. Even the geometry of the molecules
resemble one another.

The function of superoxide dismutase is to oxidize the copper ions from
say +2 and +1.

But this brings up an interesting question as to what the "infectious
agent" would be in prion disease, since superoxide dismutase is
related. The most reactive alkalis effect superoxide dismutase such as
cesium and rubidium.

How much cesium or rubidium in an animal body before it is toxic?

All along I am thinking it is mercury that is corrupting the prion
proteins. Perhaps I should look into these most reactive of alkali
metals.

And another reference says that infectious prion proteins are
sterilized by autoclaving at 600 degrees C for 15 minutes. I looked up
the boiling point of cesium and rubidium which are 671 degrees C and
688 degrees C respectively.

So is cesium or rubidium in tiny quantity in the brain the causing
agent of Prion diseases, and not mercury?

The above researchers used some fancy X-ray scanning. I wonder if that
same method can reveal whether diseased brain of a CJD victim
contains-- mercury, or cesium or rubidium?

What modern day instrumentation would best take a diseased BSE or
scrapie or CJD and tell us the amounts of metals in the brain tissue?
Is it mass spectroscopy or some form of X-ray diffraction?

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 26 Aug 2006 20:20 GMT
> So is cesium or rubidium in tiny quantity in the brain the causing
> agent of Prion diseases, and not mercury?
[quoted text clipped - 6 lines]
> scrapie or CJD and tell us the amounts of metals in the brain tissue?
> Is it mass spectroscopy or some form of X-ray diffraction?

I notice that prion disease is fairly well geographically dependent. It
occurs most often in places like England and Canada and New Guinea
(kuru flair up).

So I went to check to see if England and Canada and New Guinea have
alot of caesium cesium and rubidium prevalent in the environment.

--- quoting the titles of a Google search for caesium in UK ---

BBC - h2g2 - The Elements: Names and Origins - AE
Access keys help · bbc.co.uk ... Cesium - the internationally-accepted
spelling is caesium - was ... Copper-mining dates back to prehistoric
times. ...
www.bbc.co.uk/dna/h2g2/A3768672 - 60k - Aug 24, 2006 - Cached - Similar
pages

Bibliography of Cesium 137 Studies Related to Erosion And Sediment ...
Fixation of Cs-137 by soil and sediment in the Esk estuary, Cumbria,
UK. ... Dating of mine waste in lacustrine sediments using cesium-137.
...
hydrolab.arsusda.gov/cesium137bib.htm - 508k - Cached - Similar pages

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Using the high-sensitivity cesium magnetometer he was involved with and
... Chairman of the National Association of Mining History
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--- end quoting ---

I also looked to see if Canada mines cesium and it said Manitoba with
pegmatites.

Also wanted to see if cesium and rubidium ores are present in New
Guinea in connection with Kuru and that is an affirmative.

So what would happen if a human eats a small quantity of cesium or
rubidium bonded with copper? Would it find its way into the brain
tissue? Would it then start corrupting normal prion molecules into
deformed prion molecules? Or in sheep? Is the location of the world's
highest scrapie infection in the sites mentioned above? Does cesium and
rubidium compounds available in the sheep pastures of England, and
where sheep can easily intake those compounds?

The frequency of Mad Cow disease in Canada, does it coincide with the
geography of cesium and rubidium in the soil?

The cases of Kuru in New Guinea, does it coincide with the leaching or
water supply of cesium and rubidium compounds?

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
Jason Johnson - 27 Aug 2006 02:04 GMT


> So is cesium or rubidium in tiny quantity in the brain the causing
> agent of Prion diseases, and not mercury?
[quoted text clipped - 6 lines]
> scrapie or CJD and tell us the amounts of metals in the brain tissue?
> Is it mass spectroscopy or some form of X-ray diffraction?


I notice that prion disease is fairly well geographically dependent. It
occurs most often in places like England and Canada and New Guinea
(kuru flair up).

So I went to check to see if England and Canada and New Guinea have
alot of caesium cesium and rubidium prevalent in the environment.

--- quoting the titles of a Google search for caesium in UK ---

BBC - h2g2 - The Elements: Names and Origins - AE
Access keys help =B7 bbc.co.uk ... Cesium - the internationally-accepted
spelling is caesium - was ... Copper-mining dates back to prehistoric
times. ...
www.bbc.co.uk/dna/h2g2/A3768672 - 60k - Aug 24, 2006 - Cached - Similar
pages

Bibliography of Cesium 137 Studies Related to Erosion And Sediment ...
Fixation of Cs-137 by soil and sediment in the Esk estuary, Cumbria,
UK. ... Dating of mine waste in lacustrine sediments using cesium-137.
.=2E.
hydrolab.arsusda.gov/cesium137bib.htm - 508k - Cached - Similar pages

The Management Committee
Using the high-sensitivity cesium magnetometer he was involved with and
.=2E. Chairman of the National Association of Mining History
Organisations and has ...
www.bradford.ac.uk/archsci/archprospection/ManCom/ - 21k - Cached -
Similar pages

PSIgate Timeline - Physics
This information will be of use within UK further and higher education
for ... at the National Physical Laboratory, Teddington More about:
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--- end quoting ---

I also looked to see if Canada mines cesium and it said Manitoba with
pegmatites.

Also wanted to see if cesium and rubidium ores are present in New
Guinea in connection with Kuru and that is an affirmative.

So what would happen if a human eats a small quantity of cesium or
rubidium bonded with copper? Would it find its way into the brain
tissue? Would it then start corrupting normal prion molecules into
deformed prion molecules? Or in sheep? Is the location of the world's
highest scrapie infection in the sites mentioned above? Does cesium and
rubidium compounds available in the sheep pastures of England, and
where sheep can easily intake those compounds?

The frequency of Mad Cow disease in Canada, does it coincide with the
geography of cesium and rubidium in the soil?

The cases of Kuru in New Guinea, does it coincide with the leaching or
water supply of cesium and rubidium compounds?

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies

~~~~~~~~~~~~~~~~~~~~~~~~~~~

Hello,
What would happen if you done an experiment making use of two separate
groups of sheep. Feed one group of sheep a diet that includes high amounts
of cesium and and rubidium componds. The other group of sheep would be
used as a control group and would have a diet that did NOT contain any
cesium and rubidum compounds.
If your theory is correct, the first group of sheep should develop Prion
disease. Do you think the experiment would help you reach a conclusion?
Jason
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
a_plutonium - 27 Aug 2006 04:08 GMT
> Hello,
> What would happen if you done an experiment making use of two separate
[quoted text clipped - 5 lines]
> disease. Do you think the experiment would help you reach a conclusion?
> Jason

I think it would be easier to just look for metals in scrapie sheep
compared to normal sheep. To induce a prion disease takes a long time.
And besides it may not be cesium,  rubidium or mercury but some other
metal and we would not know what form the cesium is in; if it causes
the disease.

So all in all, the route of simply looking for any suspicious metal in
scrapie tissue would be more productive, in my estimation, then to do
yours above.

If Autism or Alzheimers or Parkinsons can be simulated in mice which
have a quick time rate of catching the disease, then it maybe pragmatic
to try out some metals to see if the disease is induced. There is a
good chance that mercury causes Autism and Alzheimers. So if mice are
hurry-up able to catch the disease, then okay.

If a metal is found to cause prion disease, then I think your above
experiment would be a pragmatic follow-up experiment.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 27 Aug 2006 13:22 GMT
> > Hello,
> > What would happen if you done an experiment making use of two separate
[quoted text clipped - 24 lines]
> If a metal is found to cause prion disease, then I think your above
> experiment would be a pragmatic follow-up experiment.

I was looking for any reports of cesium (caesium) found in prion
diseased animals. Found a report from White Sands New Mexico where a
cluster of deer were smitten by the prion disease. They tested for
metals and found alot of cesium.

Because of the autoclaving to sterilize Prion disease is 600 degrees C
for 15 minutes with residual infectivity remaining, and since the
boiling point of cesium is 671 degrees centigrade, that cesium is at
this moment my very best candidate as the cause of all prion diseases.

The past 3 decades of prion research have never focused on an accurate
analysis of the metals in the brains of victims. The New Mexico deer
analysis is one of the few that attempted to look for metals.

Mercury boiling point is 357 degrees C and so the autoclaving would
rule out mercury.

So that leaves me with either cesium or rubidium. What is needed now is
a thorough and accurate analysis for the brain tissue of prion victims
for metal amounts.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 27 Aug 2006 13:51 GMT
I made an attempt to find out if England has the world's highest
density of caesium in the soil and environment. There were some
search-hits but unable to open pdf file.

So anyone have data as to whether England has alot of caesium in the
environment? And what would that abundance be attributed to? Would it
be attributed to the large coal  and fossil fuels in England? Would
burning of coal release more caesium into the environment?

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 27 Aug 2006 14:09 GMT
> I made an attempt to find out if England has the world's highest
> density of caesium in the soil and environment. There were some
[quoted text clipped - 4 lines]
> be attributed to the large coal  and fossil fuels in England? Would
> burning of coal release more caesium into the environment?

If mercury is the metal culprit that causes Alzheimers, Parkinsons or
Autism, then one would expect people living down-wind of coal fired
power plants to have increasing cases of these diseases, since the
burning of coal releases alot of mercury into the air we breathe.

I know the Midwest leading into Chicago used to be coal fired power
plants and this Midwest had the highest frequency of Parkinsons
disease. It has been long speculated that some farming chemical is the
cause.

Is there increased frequency to Autism near a coal fired power plant?

Have there been clusters of Alzheimers,Parkinsons, Autism down-wind of
coal fired power plants?

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 27 Aug 2006 19:52 GMT
I was looking for reported links between mercury and Autism and
apparently scientists from U. Texas have made such a study.

The epidemic increase in Autism can be linked with the global pollution
of mercury begot from coal fired power stations.

The mercury comes from those coal fired smokestacks and eventually fish
accumulate the methylmercury. We in turn eat the fish.

But the direct exposure downwind to mercury such as the state of Utah
downwind of Nevada mining operations would result in increasing cases
of prenatal exposure from the air breathed and increasing Autism.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
a_plutonium - 27 Aug 2006 20:12 GMT
You see I tackle the problem of what causes diseases by first grouping
them into one Family Related Diseases. So I take Prion and Alzheimers
and Parkinsons and Autism and call them one Family Related Disease.
This is important because progress in solving one of those diseases
implies the same or similar underpinning mechanisms in the other 3
diseases.

This is the failure of Mr. Prusiner is that he never grouped Prion into
a family-related-group of diseases. If Prusiner had done that in the
1980s, he would never have gotten into trouble now with having a dud
and false model of Prion disease and a ludicrous mechanism that a
protein alters the shape of other proteins. Prusiner would have seen
that if a metal causes Autism or Alzheimers or Parkinsons, then, you
can bet that a metal probably causes the other diseases of the
family-related-group diseases. What is found true in one disease of a
group, is likely to be found in the other 3.

But here I reached a point of noncongruence or noncompliance in that
Parkinsons was recently found to have a "cause" from certain bacteria
found in well-water. So if it is bacteria that causes Parkinsons, does
not agree with metal as causing Autism, Prion and Alzheimers. So you
see, I have a bit of a sticking point here of a problem.

I could say that Parkinsons is sufficiently different from Alzheimers,
Prion and Autism  and so different that even though a metal causes the
other 3, that bacteria could cause Parkinsons. For in Parkinsons there
is no accumulated waste of a protein in the brain. And perhaps no
accumulated waste of a protein in Autism either.

But maybe this recent report may come to my rescue over Parkinsons.

--- quoting from a Internet website ---
US mercury pollution more pervasive than realized

19 March 2005
>From New Scientist Print Edition.

MERCURY pollution in the north-eastern US is much more pervasive than
scientists had realised. The discovery of high levels of the most toxic
form of mercury in a mountain songbird has stunned scientists and will
heat up the spat between environmentalists and the Bush administration
over how best to control smokestack emissions.

Terrestrial ecosystems, such as that of the Bicknell thrush, were not
thought to be affected by mercury fallout from coal-fired power
stations. Researchers believed an aquatic bacterium was needed to
convert mercury from power plants into its most harmful form, methyl
mercury. This then passes up the aquatic food chain to fish. Because of
this, 44 US states warn children and women of child-bearing age not to
eat certain fish.
--- end quoting ---

So I wonder, I just wonder, whether the bacteria in well-water,
implicated in Parkinsons is a bacteria that interacts with mercury. And
whether the cause of Parkinsons is ultimately linked to mercury.

So I am torn between whether Parkinsons is sufficiently different from
the other 3 diseases and has a different cause-- bacteria from the
cause of the other 3 as that of metal poisoning. Or, whether bacteria
alter the form of mercury and have concentrated mercury in the
bacterium-body which causes the Parkinsons disease.

I have to use the METHODOLOGY-THEORY to unravel the mystery of these 4
diseases, but I am aware that sometimes, differences are large
differences and that what is a mechanism of 3 of the diseases fails to
be a mechanism of the 4th.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
Jason Johnson - 27 Aug 2006 21:14 GMT
You see I tackle the problem of what causes diseases by first grouping
them into one Family Related Diseases. So I take Prion and Alzheimers
and Parkinsons and Autism and call them one Family Related Disease.
This is important because progress in solving one of those diseases
implies the same or similar underpinning mechanisms in the other 3
diseases.

This is the failure of Mr. Prusiner is that he never grouped Prion into
a family-related-group of diseases. If Prusiner had done that in the
1980s, he would never have gotten into trouble now with having a dud
and false model of Prion disease and a ludicrous mechanism that a
protein alters the shape of other proteins. Prusiner would have seen
that if a metal causes Autism or Alzheimers or Parkinsons, then, you
can bet that a metal probably causes the other diseases of the
family-related-group diseases. What is found true in one disease of a
group, is likely to be found in the other 3.

But here I reached a point of noncongruence or noncompliance in that
Parkinsons was recently found to have a "cause" from certain bacteria
found in well-water. So if it is bacteria that causes Parkinsons, does
not agree with metal as causing Autism, Prion and Alzheimers. So you
see, I have a bit of a sticking point here of a problem.

I could say that Parkinsons is sufficiently different from Alzheimers,
Prion and Autism  and so different that even though a metal causes the
other 3, that bacteria could cause Parkinsons. For in Parkinsons there
is no accumulated waste of a protein in the brain. And perhaps no
accumulated waste of a protein in Autism either.

But maybe this recent report may come to my rescue over Parkinsons.

--- quoting from a Internet website ---
US mercury pollution more pervasive than realized

19 March 2005
>From New Scientist Print Edition.

MERCURY pollution in the north-eastern US is much more pervasive than
scientists had realised. The discovery of high levels of the most toxic
form of mercury in a mountain songbird has stunned scientists and will
heat up the spat between environmentalists and the Bush administration
over how best to control smokestack emissions.

Terrestrial ecosystems, such as that of the Bicknell thrush, were not
thought to be affected by mercury fallout from coal-fired power
stations. Researchers believed an aquatic bacterium was needed to
convert mercury from power plants into its most harmful form, methyl
mercury. This then passes up the aquatic food chain to fish. Because of
this, 44 US states warn children and women of child-bearing age not to
eat certain fish.
--- end quoting ---

So I wonder, I just wonder, whether the bacteria in well-water,
implicated in Parkinsons is a bacteria that interacts with mercury. And
whether the cause of Parkinsons is ultimately linked to mercury.

So I am torn between whether Parkinsons is sufficiently different from
the other 3 diseases and has a different cause-- bacteria from the
cause of the other 3 as that of metal poisoning. Or, whether bacteria
alter the form of mercury and have concentrated mercury in the
bacterium-body which causes the Parkinsons disease.

I have to use the METHODOLOGY-THEORY to unravel the mystery of these 4
diseases, but I am aware that sometimes, differences are large
differences and that what is a mechanism of 3 of the diseases fails to
be a mechanism of the 4th.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

You may want to visit the PubMed site and conduct searches on these terms:

1st search: Alzheimer Disease/aluminum
2nd search: Autism/mercury
3rd search: Parkinson Disease/aluminum
4th search: Parkinson Disease/mercury
5th search: Prion Disease
6th search: Alzheimer Disease/autopsy
a_plutonium - 28 Aug 2006 22:27 GMT
> You may want to visit the PubMed site and conduct searches on these terms:
>
[quoted text clipped - 4 lines]
> 5th search: Prion Disease
> 6th search: Alzheimer Disease/autopsy

Yes, I have already done some of that.

FAMILY-RELATED-DISEASE-METHODOLOGY-THEORY
coupled with
Metal-Causation-theory

Alzheimers   (concensus is that it is aluminum) I think it maybe a
combination of mercury and aluminum. Little is known about combinations
of metals

Autism (concensus is that it is mercury from vaccines and coal fired
power plants)
I think mercury is the best bet here, since mercury easily penetrates
into the brain tissue and at such a young age would do alot of damage.

Parkinsons (no concensus here) It was found that well-water bacteria
can induce the disease. But whether those bacteria have mercury is
unknown.

Prion (concensus here is that it is manganese since CJD was first known
in the 1920s which coincides with the rise of industrial manganese) I
think it is *cesium/caesium* based on the incineration heat required to
disinfect which is about 700 degrees C

Trouble is that there is no uniform research of experiments all based
on the Metal Causation theory. Where diseased tissue is inspected for
the prescence of abnormal amounts of metals.

Where we can say things like this in PUBMED:
Autopsy of diseased Alzheimers tissue always shows abnormal aluminum
and both mercury amounts of such and such a quantity.

Autopsy of diseased Autism tissue always shows abnormal mercury amounts
of such and such a quantity.

Autopsy of diseased Parkinsons tissue always shows abnormal amounts of
mercury of such and such a quantity

Autopsy of diseased Prion tissue always shows abnormal amounts of
(manganese) and or (caesium/cesium) of such and such a quantity.

The literature of full of reports of metals as the cause of the above
but we need to consolidate and make more firm the case and experimental
results.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
Jason Johnson - 29 Aug 2006 00:14 GMT
Jason Johnson wrote:


> You may want to visit the PubMed site and conduct searches on these terms:
>
[quoted text clipped - 4 lines]
> 5th search: Prion Disease
> 6th search: Alzheimer Disease/autopsy

Yes, I have already done some of that.

FAMILY-RELATED-DISEASE-METHODOLOGY-THEORY
coupled with
Metal-Causation-theory

Alzheimers   (concensus is that it is aluminum) I think it maybe a
combination of mercury and aluminum. Little is known about combinations
of metals

Autism (concensus is that it is mercury from vaccines and coal fired
power plants)
I think mercury is the best bet here, since mercury easily penetrates
into the brain tissue and at such a young age would do alot of damage.

Parkinsons (no concensus here) It was found that well-water bacteria
can induce the disease. But whether those bacteria have mercury is
unknown.

Prion (concensus here is that it is manganese since CJD was first known
in the 1920s which coincides with the rise of industrial manganese) I
think it is *cesium/caesium* based on the incineration heat required to
disinfect which is about 700 degrees C

Trouble is that there is no uniform research of experiments all based
on the Metal Causation theory. Where diseased tissue is inspected for
the prescence of abnormal amounts of metals.


Where we can say things like this in PUBMED:
Autopsy of diseased Alzheimers tissue always shows abnormal aluminum
and both mercury amounts of such and such a quantity.

Autopsy of diseased Autism tissue always shows abnormal mercury amounts
of such and such a quantity.

Autopsy of diseased Parkinsons tissue always shows abnormal amounts of
mercury of such and such a quantity

Autopsy of diseased Prion tissue always shows abnormal amounts of
(manganese) and or (caesium/cesium) of such and such a quantity.

The literature of full of reports of metals as the cause of the above
but we need to consolidate and make more firm the case and experimental
results.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Hello,
Excellent post. I continue to believe that genes play a role related to
many of these metal related diseases. Otherwise, almost everyone would
develop these diseases. A great example is autism. 1000 children could
receive the same vaccines (that contain thimerosal) and less than 5 of
them would develop autism. The reason is probably because their bodies
could not process the mercury (due to defective genes) and remove it from
their bodies. The mercury ends up in the brains of those 5 children and
they develop autism. This theory could also explain the other metal
related diseases but different metals may be involved in those diseases.
You could do PubMed searches (mentioned above) and use the term "genes" to
replace the names of metals.
Jason
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
John Savage - 09 Sep 2006 02:15 GMT
On the topic of Alzheimers, it apparently is not necessarily predestined.

Research studies claim that supplements of Vit E can reduce the incidence
by 40%

Last weekend there was a report (of, I think, a Swedish study) showing
that drinking a combination fresh whole-fruit and vegetable juice can
reduce the likelihood of Alzheimers by 75% if consumed at a rate of some-
thing like 3 or more cupsful per week. (Possibly it was 'per day', I just
forget. :-))

The theory stated is that the active ingredient must be a component in the
skins of these foods.
--
John Savage                   (my news address is not valid for email)
a_plutonium - 09 Sep 2006 06:28 GMT
> On the topic of Alzheimers, it apparently is not necessarily predestined.
>
[quoted text clipped - 11 lines]
> --
> John Savage

Yes, I mentioned phenols in those foods is the active ingredient. In
the Metals Causing theory of Alzheimers, Autism, Prion, Parkinsons,
Schizophrenia, the diet can thwart any of these diseases because the
diet can clean out the metals such as mercury. So that if persons who
eat alot of fresh fruit happen to get mercury in their bodies can clean
it out better than those who seldom eat fruit.

Linus Pauling was correct when he subscribed to a megadoses of citric
acid and fruits.

Someday I need to research how citric acid and vitamin C combat foreign
metals that get inside our bodies and how they help to expel these
metals. Of course it would not be practical to submit babies to
megadoses of vit C and citric acid to ward against Autism. One of the
reasons Autism is so abundant is that the concentration of metal needs
to be small and tiny to ruin the life of a child. Whereas the old age
diseases of Alzheimers, Parkinsons, Prion, Schizophrenia can be
combatted by megadoses of citrus fruits.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
lucasea@sbcglobal.net - 09 Sep 2006 18:50 GMT
> Yes, I mentioned phenols in those foods is the active ingredient. In
> the Metals Causing theory of Alzheimers, Autism, Prion, Parkinsons,
> Schizophrenia, the diet can thwart any of these diseases because the
> diet can clean out the metals such as mercury. So that if persons who
> eat alot of fresh fruit happen to get mercury in their bodies can clean
> it out better than those who seldom eat fruit.

And how, exactly, is that supposed to happen?  Or is this another of those
"it happens because I say it does" theories?  If I told you there's a
fundamental reason it won't happen, would you have the faintest clue what it
might be?  Do you even know what it takes to remove mercury?

> Linus Pauling was correct when he subscribed to a megadoses of citric
> acid and fruits.

If you're going to quote a fellow crackpot, at least do it right.  It was
ascorbic acid, not citric acid or fruits.  At least fruits would have been
healthy.  There is not one shred of evidence that what Pauling was
proselytizing, megadoses of ascorbic acid, do one whit of good for anybody,
and may even be harmful for the kidneys.  Pauling was a great mind, and very
well deserved both of his Nobel prizes, but I saw him give a "lecture" at
OSU in 1985, and it was truly sad to see such a great mind turned into a
doddering, proselytizing old fool with Wheatena for brains.  Nobody will cry
for you, however, Archie.  You started out as a doddering fool.

> Someday I need to research how citric acid and vitamin C combat foreign
> metals that get inside our bodies and how they help to expel these
> metals.

I could answer the question for you right now, and I could tell you exactly
what types of chemicals you specifically need to remove mercury.  But first
you would have to learn at least a tiny modicum of actual chemistry to
understand why.

> Of course it would not be practical to submit babies to
> megadoses of vit C and citric acid to ward against Autism. One of the
> reasons Autism is so abundant is that the concentration of metal needs
> to be small and tiny to ruin the life of a child.

Is *that* what happened to you.  "Oh, looky, such a pretty clear candy stick
with a bright shiny silvery center!  Yummy, yummy!"

Eric Lucas
Marvin - 10 Sep 2006 19:29 GMT
>>Yes, I mentioned phenols in those foods is the active ingredient. In
>>the Metals Causing theory of Alzheimers, Autism, Prion, Parkinsons,
[quoted text clipped - 39 lines]
>
> Eric Lucas

You may not know that you are trying to reply sensibly to
"archie-poo", who has a long-established reputation as one
of the most persistent nuts on the Internet.

I didn't see his posting that you are responding to because
I have his messages blocked.  I recommend that you do the same.
a_plutonium - 25 Aug 2006 08:28 GMT
> An interesting paper, which got a lot of attention, is:
> New studies on the heat resistance of hamster-adapted scrapie agent:
[quoted text clipped - 24 lines]
> ago, I found nothing published that addressed the residual
> infectivity.)

Let us assume for the moment that the above was all very accurate and
well done. That the quality was superb.

Then the above favors the Metal Model and disfavors the Prusiner Model.
For what the above suggests is that some metal could alternate in
increasing infectivity and decreasing infectivity as the temperature
rises. Making some metal ions more infectious. In the Metal Model,
infectivity can fluctuate as temperature and pressure rise. As in the
above where 5 minutes had a larger affect than 15 minutes.

With the Prusiner Model, as heat and pressure rise, infectivity should
be linearly decreasing.

Now I wonder if anyone has performed experiments on mice who have the
potential of catching Alzheimers and Parkinsons, whether if fed with
the beta amyloid or alpha synuclein, respectively, show signs of coming
down with the diseases. The idea is that the metal causing them is
transfered.

Archimedes Plutonium
www.iw.net/~a_plutonium
whole entire Universe is just one big atom
where dots of the electron-dot-cloud are galaxies
Bob - 28 Aug 2006 02:59 GMT
>Well, I hate to find myself agreeing with AP, but I thought I had heard
>something similar, although not as extreme.  What I thought I remembered was
[quoted text clipped - 7 lines]
>when we're talking about cooking food, it's awfully difficult to heat it up
>to > 100 C, so applying a blowtorch wouldn't be a bad method to use.  

Here is  a bit more...

From a recent paper:
Incubation for 60 min at indicated T. 100 or 110 C, no effect. 140,
total inactivation. Intermediate result at 120. (This is wet heat.)
(I'm a little confused about details. One place seems to say 20 min,
another 60 min. Doesn't really matter for now. I didn't try hard to
resolve this.)

Castilla et al, In Vitro Generation of Infectious Scrapie Prions.
Cell, Vol. 121, 195–206, April 22, 2005.

Thus this stability is reasonable for a protein -- though at the
higher end. There is nothing "extraordinary" about it.

Practical sterilization requires "many" logs of killing -- a severe
criterion. Further, the physical nature of the material, esp when dry,
makes heat penetration and probably some chemical penetration
difficult. These reflect inaccessibility of the material, not extreme
stability.

bob
lucasea@sbcglobal.net - 28 Aug 2006 04:53 GMT
> Here is  a bit more...
>
[quoted text clipped - 16 lines]
> difficult. These reflect inaccessibility of the material, not extreme
> stability.

Of course, none of this negates any of the "observations" that I remembered
reading about--wet heat and dry heat are very different as regards their
ability to penetrate and transfer heat to solid masses.

Thanks for injecting a little actual data into the discussion.    Archie-Poo
has never been one to let a little actual data stand in the way of a
beautiful theory.  And whenever anyone points that out, he gets quite
belligerent, insulting and, oddly, self-superior.

Eric Lucas
Beverly Erlebacher - 28 Aug 2006 12:55 GMT
>> Here is  a bit more...
>>
[quoted text clipped - 20 lines]
>reading about--wet heat and dry heat are very different as regards their
>ability to penetrate and transfer heat to solid masses.

Definitely.  Just from a common sense perspective, consider that for
home canning of non-acid foods, an hour or more at 15psi is usually
recommended depending on size of container, because the spores of
Clostridium botulinum are so heat-stable.  But killing those spores
doesn't mean that every protein in the jar or spore is denatured,
just that enough are to kill almost any microbe.

Bacteria in hot springs may conduct their entire lives at temperatures
near boiling, and those in deep-sea vents at temperatures substantially
above 100C.  That means that not only some, but all their proteins are
stable under these conditions.

With the problem of disposing of contaminated material, consider
that incinerating all those cattle is far more practical than any
other method, and converting all that organic matter to ash and
carbon dioxide is sure to destroy every protein, even if it's
overkill from the theoretical point of view.

>Thanks for injecting a little actual data into the discussion.    Archie-Poo
>has never been one to let a little actual data stand in the way of a
>beautiful theory.  And whenever anyone points that out, he gets quite
>belligerent, insulting and, oddly, self-superior.

It isn't possible to reason with him.  He has a serious personality
disorder, and he isn't going to change.
lucasea@sbcglobal.net - 28 Aug 2006 14:13 GMT
> In article <gNtIg.3784$yO7.3456@newssvr14.news.prodigy.com>,