The damage mercury does to brain cells

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bigvince

Posted: Mon Jul 02, 2007 8:14 am

Guest

Some think that the mercury in vaccines has contributed to growing
autism rates. An interesting study from the University of Calgary
shows in real time on video exactly how mercury damages brain cells.Of
course the CDC says it was perfectly safe in vaccines; others
disagree. The video links is here http://video.google.com/videoplay?docid=1745672039422612226&pr=goog-sl
watch for and decide yourself how safe it really is. Thanks Vince

Bryan Heit

Posted: Wed Jul 04, 2007 3:32 pm

Guest

bigvince wrote:

Quote:

Wow, amazing! Its nice to see that people here at work are getting
their research noticed. Now if only you didn't completely mis-interpret
it things would be just dandy. I've forwarded you post to Dr. Syed,
whom I worked with briefly a few years ago; hopefully he'll drop buy to
set you strait.

Anyhow, where to start. Lets see:

1)he was looking at mercury chloride, which is completely different from
the mercury salt used as a preservative in some vaccines. Apples and
oranges. You may as well be claiming that table salt is as toxic as
chlorine gas, on the basis both contain chlorine...

2)he was looking at purified neurons, which unfortunately don't
replicate our brains very well. Had he added water, he would have seen
similar things (due to osmotic stress). It's not hard to kill cells in
a petri dish. In our bodies things are a little different.

3)the concentration of mercury in the micropipette was far, far higher
then what you'd encounter after a vaccine - about 2500x to be specific.
Likewise, the metabolic processing and barrier effects of our bodies
were circumvented.

Not that you'll bother, but that video was produced as a part of this
scientific study:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=11277574&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

If you actually bother to read the paper you'll see just how far off the
mark you really are.

Oh, and while we're on it, the description of the video is way off.
mercury is far from the second most toxic substance on our planet.
There are substances ~500 MILLION more times more toxic (by weight); and
thousands of other chemicals which fall between mercury and that extreme.

Bryan

bigvince

Posted: Thu Jul 05, 2007 1:37 pm

Guest

On Jul 4, 4:32 pm, Bryan Heit <bjh...@NOSPAMucalgary.ca> wrote:

Quote:

bigvince wrote:
Some think that the mercury in vaccines has contributed to growing
autism rates. An interesting study from the University of Calgary
shows in real time on video exactly how mercury damages brain cells.Of
course the CDC says it was perfectly safe in vaccines; others
disagree. The video links is herehttp://video.google.com/videoplay?docid=1745672039422612226&pr=goog-sl
watch for and decide yourself how safe it really is. Thanks Vince

Wow, amazing! Its nice to see that people here at work are getting
their research noticed. Now if only you didn't completely mis-interpret
it things would be just dandy. I've forwarded you post to Dr. Syed,
whom I worked with briefly a few years ago; hopefully he'll drop buy to
set you strait.

Anyhow, where to start. Lets see:

1)he was looking at mercury chloride, which is completely different from
the mercury salt used as a preservative in some vaccines. Apples and
oranges. You may as well be claiming that table salt is as toxic as
chlorine gas, on the basis both contain chlorine...
2)he was looking at purified neurons, which unfortunately don't
replicate our brains very well. Had he added water, he would have seen
similar things (due to osmotic stress). It's not hard to kill cells in
a petri dish. In our bodies things are a little different.

3)the concentration of mercury in the micropipette was far, far higher
then what you'd encounter after a vaccine - about 2500x to be specific.
Likewise, the metabolic processing and barrier effects of our bodies
were circumvented.

bigvince

Posted: Thu Jul 05, 2007 2:26 pm

Guest

On Jul 4, 4:32 pm, Bryan Heit <bjh...@NOSPAMucalgary.ca> wrote:

Quote:

Mercury chloride is the much safer form . From Wikipedia ,,Due to its
low solubility, mercurous chloride is less dangerous than its mercuric
chloride counterpart. From the early 1830s through the 1860s, this
compound was used as a laxative in the U.S. This previous use in
medicine as a diuretic and purgative was discontinued because of its
toxicity.' again from Wikipedia but ...Thiomersal is harmful by
inhalation and ingestion, lethal between 50 and 1000 times[citation
needed][1] the usual intake (hazard symbol T+).[2] It is a
neoplastigen and a teratogen. Thiomersal is also dangerous for the
environment (hazard symbol N).

"Thiomersal causes susceptible bacteria to autolyze (break down their
own cells with self-produced enzymes) via an unknown mechanism.
[citation needed] In the body, it is metabolized to ethylmercury
(C2H5Hg+) and thiosalicylic acid.[3]"

Quote:

Did you actually read the study by Dr.Syed here is some ... . "We
demonstrate that Hg ions
markedly disrupted membrane structure and linear growth rates of
imaged neurites in 77% of all nerve growth cones. When growth cones
were stained with antibodies specific for both tubulin and actin, it
was the tubulin/microtubule structure that disintegrated following Hg
exposure. Moreover, some denuded neurites were also observed to form
neurofibrillary aggregates. In contrast, growth cone exposure to
other
metal ions did not effect growth cone morphology, nor was their
motility rate compromised. To determine the growth suppressive
effects
of Hg ions on neuronal sprouting, cells were cultured either in the
presence or absence of Hg ions. We found that in the presence of Hg
ions, neuronal somata failed to sprout, whereas other metalic ions
did
not effect growth patterns of cultured PeA cells. We conclude that
this visual evidence and previous biochemical data strongly implicate
Hg as a potential etiological factor in neurodegeneration.
PMID: 11277574 [PubMed - indexed for MEDLINE]
Do you see the comparision of the damage Hg ions did to the lack of
damage other metal ions did. It seems it is not hard to kill cells in
a petri dish if mercury is present. Absent mercury much more
difficult.

Quote:

I I read it : perhaps you should. Thanks Vince

Bryan Heit

Posted: Sat Jul 07, 2007 12:03 am

Guest

bigvince wrote:

Quote:

On Jul 4, 4:32 pm, Bryan Heit <bjh...@NOSPAMucalgary.ca> wrote:
bigvince wrote:
Some think that the mercury in vaccines has contributed to growing
autism rates. An interesting study from the University of Calgary
shows in real time on video exactly how mercury damages brain cells.Of
course the CDC says it was perfectly safe in vaccines; others
disagree. The video links is
herehttp://video.google.com/videoplay?docid=1745672039422612226&pr=goog-sl
watch for and decide yourself how safe it really is. Thanks Vince
Wow, amazing! Its nice to see that people here at work are getting
their research noticed. Now if only you didn't completely mis-interpret
it things would be just dandy. I've forwarded you post to Dr. Syed,
whom I worked with briefly a few years ago; hopefully he'll drop buy to
set you strait.

Anyhow, where to start. Lets see:

1)he was looking at mercury chloride, which is completely different from
the mercury salt used as a preservative in some vaccines. Apples and
oranges. You may as well be claiming that table salt is as toxic as
chlorine gas, on the basis both contain chlorine...

Mercury chloride is the much safer form .

No, mercury chloride and mercurIC chloride are the same thing - MgCl2.
You're not even in the correct ball park - you're thinking of mercurous
chloride (Mg2Cl2); which is significantly less toxic then MgCl2, but not
what was used in the study. Thanx for proving that you wouldn't bother
to actually read the research. Guess its easier to ignore things that
would challange your preconceptions.

You obviously didn't even bother reading the entire wikipedia article;
otherwise you'd have seen the part that mentions that mercurous chloride
is nearly insoluble in water, making it virtually impossible to get a
solution to squirt out of a micropipette...

As for my HgCl2, not Hg2Cl2 is used, its simple (aside from the
solubility thing). HgCl2, when dissolved in water, release3s Hg2+ ions
- the same as is released when you inhale/ingest mercury vapor (HgO);
the kind of mercury you would be exposed to in the air, or through some
forms of amalgam fillings. Mercurous chloride does not dissolve into
Hg2+ ions, making it useless for such comparisons.

Quote:

From Wikipedia ,,Due to its
low solubility, mercurous chloride is less dangerous than its mercuric
chloride counterpart. From the early 1830s through the 1860s, this
compound was used as a laxative in the U.S. This previous use in
medicine as a diuretic and purgative was discontinued because of its
toxicity.'

And if you had the relevant chemical this would mean something.
Unfortunately, you do not. From the wikipedia article on the correct
compound:

"Mercuric chloride is one of the most toxic forms of mercury because it
easily forms organomercury complexes with proteins."

Quote:

again from Wikipedia but ...Thiomersal is harmful by
inhalation and ingestion, lethal between 50 and 1000 times[citation
needed][1] the usual intake (hazard symbol T+).[2]

Unfortunately they don't have a reference for this, because they are
wrong and I'd like to know where the info came from. Wikipedia is
usually better at these things - I'm quite surprised such an error has
gone uncorrected.

Average thiomersal in a vaccine dose: 50ug (0.05mg) (from the FDA)
LD50 (oral): 75mg/kg
LD50 (IV): 30mg/kg

LD50's from http://physchem.ox.ac.uk/MSDS/TH/thimerosal.html

So here's the math:

Average weight of a human male = 80kg (approx 175lbs).
Lethal IV dose of thiomersal is: 80kg*30mg/kg = 2400mg
Average thiomersal per vaccine dose - 0.05mg

Number of vaccines to reach lethality = 2400mg/0.05mg/dose

= 48,000 - thats right, *forty* *eight* *thousand* vaccines required to
reach a lethal dose.

Now how about a 6mo male child. Average weight (50th percentile) =
7.95kg (17.5lbs).

So doing the same calcs as above we get:

Lethal dose = 238.5mg

Number of vaccines to reach lethality = 4770 vaccines

Far, far higher then what wikipedia reported.

Quote:

It is a
neoplastigen

Fancy way of saying it causes cancer. This is also misleading and not
widely agreed upon - in fact, several groups are researching
thimerosal's apparent ability to kill cancer. It's worth noting that
thiomersal has never been demonstrated to cause cancer in a living animal.

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16624850&ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

In fact, a search of the scientific literature brings up 32 research
papers on the topic of thiomersal & cancer - of those ZERO claim it
causes cancer in living organisms, one (link below) showed it induced
cancer-like changes in an already cancerous cell line (i.e. it made a
cancer "more" cancerous), and the bulk were investigating thimerosal as
a cancer therapeutic.

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=2364396&ordinalpos=26&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Quote:

and a teratogen.

There is no evidence in the medical literature for this claim. A search
for "thiomersal" and "teratogen" brings up zero hits in pubmed. A
simular search in google schoalr brings up 9 hits, of which:

5 are on the subject of thiomersal & other mercury preservatives,
1 is an environmental report on mercury in the environemnt
1 is a laboratory procedure
2 are in German

Obviously the first 5 are the ones we're interested in. Strangely
enough, while all 5 identify methyl mercury as a teratogen (which is
100% correct), those which mention it all specifically state that
thiomersal IS NOT a teratogen.

Check it for yourself - scholar.google.com

Quote:

"Thiomersal causes susceptible bacteria to autolyze (break down their
own cells with self-produced enzymes) via an unknown mechanism.

Hence why it is used as a preservative. Luckily for us, at the doses
used, it doesn't do that to our own cells.

Quote:

[citation needed] In the body, it is metabolized to ethylmercury
(C2H5Hg+) and thiosalicylic acid.[3]"

Which is correct, and contrary to Johns frequent claims, none of those
are methyl mercury, nor do they break down into methyl mercury, and nor
does their toxicity even resemble that of methyl mercury.

Quote:

2)he was looking at purified neurons, which unfortunately don't
replicate our brains very well. Had he added water, he would have seen
similar things (due to osmotic stress). It's not hard to kill cells in
a petri dish. In our bodies things are a little different.

Did you actually read the study by Dr.Syed here is some ... . "We
demonstrate that Hg ions
markedly disrupted membrane structure and linear growth rates of
imaged neurites in 77% of all nerve growth cones. When growth cones
were stained with antibodies specific for both tubulin and actin, it
was the tubulin/microtubule structure that disintegrated following Hg
exposure. Moreover, some denuded neurites were also observed to form
neurofibrillary aggregates. In contrast, growth cone exposure to
other
metal ions did not effect growth cone morphology, nor was their
motility rate compromised. To determine the growth suppressive
effects
of Hg ions on neuronal sprouting, cells were cultured either in the
presence or absence of Hg ions. We found that in the presence of Hg
ions, neuronal somata failed to sprout, whereas other metalic ions
did
not effect growth patterns of cultured PeA cells. We conclude that
this visual evidence and previous biochemical data strongly implicate
Hg as a potential etiological factor in neurodegeneration.
PMID: 11277574 [PubMed - indexed for MEDLINE]

Congratulations, you copied the abstract. 250 words of an article that
is over 20,000 words long. But I'm certain, based on your rather stupid
comments about mercuric chloride above, that you didn't go past the
abstract.

As for the research itself, I am well aware of what they did, and
showed. I was present at the uni when those studies were undertaken,
and as I mentioned I worked briefly with his lab AS THESE EXPERIMENTS
WERE ON GOING. I attended his students/post-docs (who actually
preformed the experiments) research seminars - hell, if I dug though my
notebook I could probably find a few hastily scribbled notes on
experiments they preformed, but which have not been published as yet.

And, as I pointed out above, he's looking at cells in a petri dish.
nothing he saw is definitive - tubulin depolymerization is a common
stress response. It does not indicate toxicity, nor does it indicate
cell death. As I pointed out in my last post, nothing observed in his
study was unexpected - he is using well established methods in order to
try and find out how a toxic substance kills cells. And he did the
exact right first step - he took cells in a petri dish and tried to find
out what happens to them.

But that's all it is - a first step. A petri dish is not a body; nor
does it even come close to replicating the body - if it did we wouldn't
need laboratory animals, something which would make both research
scientists and animal "rights" activists very, very happy.

Quote:

Do you see the comparision of the damage Hg ions did to the lack of
damage other metal ions did.

Yes, which is a critical experiment as it demonstrates that at least
some of the effects they observed were mercury-specific. However,
because they didn't repeat the tubulin experiments under those
conditions we have no evidence that the tubulin defects were the cause
of toxicity.

Plus there is the one thing you are really missing here - he's looking
at mercury ions, which are not release by thiomersal, or thiomersals
break-down products. This is why thiomersal is considered safe, as the
toxic ions are "masked" by the remainder of the thimerosal molecule.

Quote:

It seems it is not hard to kill cells in
a petri dish if mercury is present.

Or too much water, or too much salt, or too much sugar, or too little
surgar, or if you expose them to light, or if the CO2 level goes too far
above 5%, or if the CO2 level goes too far below 5%, or if you sneeze on
them, or if you use too much/too little antibiotic, or if your serum is
off, or if you use the wrong plastic for your dishes.

The trick in growing cells is culture isn't finding ways to kill them 0
its getting them to grow.

Quote:

Absent mercury much more
difficult.

Obviously, you've never cultured cells before. I grow cells on a daily
basis - everything from cancer cells, to bone barrow, to the cells which
line your blood vessels (endothelium to be technical). And if you think
its easy, then you're living on your own little planet. About the only
thing which grows easy is bacteria - and mold.

Bryan

Quote:

Its blatantly obvious you didn't. The abstract isn't the paper.

Quote:

: perhaps you should.

Its blatantly obvious I did - and actually thought about their results.
Maybe you should try that - thinking. Normally I'd ask for
"critically think", but in your case we'll lower the bar. How about we
start with spelling: m-e-r-c-u-r-i-c__c-h-l-o-r-i-d-e

Bryan

bigvince

Posted: Tue Jul 10, 2007 6:42 pm

Guest

On Jul 7, 1:03 am, Bryan Heit <bjh...@nospamucalgary.ca> wrote:

Quote:

bigvince wrote:

On Jul 4, 4:32 pm, Bryan Heit <bjh...@NOSPAMucalgary.ca> wrote: >> bigvince wrote:

Some think that the mercury in vaccines has contributed to growing
autism rates. An interesting study from the University of Calgary
shows in real time on video exactly how mercury damages brain cells.Of
course the CDC says it was perfectly safe in vaccines; others
disagree. The video links is
herehttp://video.google.com/videoplay?docid=1745672039422612226&pr=goog-sl
watch for and decide yourself how safe it really is. Thanks Vince
Wow, amazing! Its nice to see that people here at work are getting
their research noticed. Now if only you didn't completely mis-interpret
it things would be just dandy. I've forwarded you post to Dr. Syed,
whom I worked with briefly a few years ago; hopefully he'll drop buy to
set you strait.

Lets put your post to some 'critical thinking" First I incorrectly
noted the form of mercury that was used in this experiment.It really
was not important .What the experiment was designed to show was that
mercury ions at low levels cause neurodegenaration. In the film
mercury ions at a low level caused lesions similar to those found in
altheimers.the experiment shows that low level mercury exposure .can
indeed cause damage for this reason any reference to LD50 levels is
moot. The damage being looked for is caused by very low
levels .

Quote:

As no reference was made to thimerosal causing cancer I do not
understand this response. The important question is can thimerosal
produce mercury ions and cause the type of damage shown by the
study.

Quote:

Hence why it is used as a preservative. Luckily for us, at the doses
used, it doesn't do that to our own cells.

Congratulations, you copied the abstract. 250 words of an article that
is over 20,000 words long. But I'm certain, based on your rather stupid
comments about mercuric chloride above, that you didn't go past the
abstract.

Let me reduce that and just paraphrase the conclusions- mercury and
not other metallic ions caused the neurological damage

Quote:

And, as I pointed out above, he's looking at cells in a petri dish.
nothing he saw is definitive - tubulin depolymerization is a common
stress response. It does not indicate toxicity, nor does it indicate
cell death. As I pointed out in my last post, nothing observed in his
study was unexpected - he is using well established methods in order to
try and find out how a toxic substance kills cells. And he did the
exact right first step - he took cells in a petri dish and tried to find
out what happens to them.

From the film produced by the University you attend ' They are looking
at the live neurite isolated from snail tissue and is important to

note that growth cones from all species have identical
characteristics

Quote:

Here you are just plain wrong. Affidavit Of Boyd E. Haley.
Professor And Chair. Department Of Chemistry. University Of Kentucky

Thimerosal Containing Vaccines and Neurodevelopment Outcomes

FORWARD:

Thimerosal or merthiolate is a derivative of thiolsalicylate where
ethyl mercury is attached though the sulfur. It is defined as a
preservative or anti microbial in medical use. This anti microbial
action is dependent on thimerosal breaking down releasing ethyl
mercury that can penetrate cell membranes and bind to intracellular
enzymes, inhibiting them, and causing cell death. Further, in certain
biological environments the ethyl mercury can further break down
releasing mercury cation (Hg2+). Hg2+ is also very reactive with
enzymes and proteins inhibiting their biological functions and causing
cell injury or death. Both ethyl mercury and Hg2+ are very neuro toxic
compounds. However, ethyl mercury is more rapidly partitioned into the
hydrophobic (fatty) tissues of the central nervous system and is a
more potent neuro toxin than Hg2+ based on this "partitioning factor".
It is this partitioning factor that makes organic mercurials such as
dimethyl mercury so neuro toxically lethal (this is the compound that
caused the death of a Dartmouth University chemistry professor after
she was exposed to a drop or two on her gloved hand). The concern with
organic mercurials, such as thimerosal, is that such compounds can be
perceived as "pro toxicants" just as certain pharmaceuticals can be
classified as "pro drugs". This means that the original compound, e.g.
thimerosal, is less reactive giving the compound time to partition
into certain areas of the body before it breaks down releasing the
ethyl mercury and then further releasing Hg2+. However, while
attaching ethyl mercury to thiolsalicylate makes the ethyl mercury
less reactive it most likely allows increased partitioning into the
central nervous system before the ethyl mercury is released and
thereby, increases the neuro toxicity per unit ethyl mercury involved.
Considerable caution must be taken when stating what is the "toxic
level" of mercury and any mercury containing compound. Humans are not
rats in a pristine cage where their environment can be controlled to
ensure that other toxicities and infections are not occurring. The
level of mercury that would cause toxicity in a healthy individual is
much higher than what would be needed to cause a toxic effect in an
individual that is ill or under oxidative stress. This is because
additional stresses lower the amount of protective compounds that bind
mercury and render it less harmful. If an individual is low on these
protective compounds, then less mercury or thimerosal would be needed
to cause a clinical effect. Below I will present my interpretation of
our research and that from other laboratories that focus on the
potential toxicity of injected thimerosal in the vaccine mixture."
Perhaps you disaggree link http://www.vran.org/vaccines/mercury/mer-haley.htm
In your zeal you posted
this
" Thimerosal Induces Apoptosis in a Neuroblastoma Model via the cJun N-
Terminal Kinase Pathway
Michelle L. Herdman*, Aileen Marcelo*, Ying Huang, Richard M. Niles,
Sanjit Dhar and Kinsley Kelley Kiningham*,1
Here a few excepts...... "However, cells transfected with TAM67
showed no changes in those same components. Taken together, these
results indicate that thimerosal-induced neurotoxicity occurs through
the JNK-signaling pathway, independent of cJun activation, leading
ultimately to apoptotic cell death. " strange that you posted an
abstract that links thimerosal and nerotoxicity did you read it? from
the introduction "Thimerosal is an organic mercurial containing
an ethylmercury moiety attached to the sulfur atom of thiosalicylate.
Since the 1930's, thimerosal has been used in many products as an
antiseptic and a preservative. In recent years, controversy has
surrounded the use of thimerosal in vaccines as mercury is a known
neurotoxin and nephrotoxin. Since the controversy began in the late
1990's, much of the thimerosal has been removed from vaccines
administered to children in the United States. " again did you read
the abstart' the text' the headline or none of the above and
furter ... " The present study demonstrates for the first time the
essential role of JNK activation in thimerosal-induced cell death in
an in vitro model. The SK-N-SH cell line was chosen due to cellular
characteristics representative of those in an immature nervous system.
The SK-N-SH cell line, comprised a neuroblast cell type, retains the
capacity to differentiate in vitro, rather than representing a model
of terminal differentiation.".....and concludes ,,,,"Our study is the
first demonstration that thimerosal can induce the activation of JNK
and AP-1 in the SK-N-SH neuroblastoma cell line. We showed that
activation of cJun and AP-1 transcriptional activity following
thimerosal treatment does not appear to be involved in the induction
of apoptosis, as demonstrated with the studies using the cJun dominant
negative. Furthermore, we were able to show that JNK is an essential
upstream component of this pathway through the use of the JNK
inhibitor SP600125. This compound was able to attenuate activation of
downstream components of mitochondrial-mediated cell death and
subsequently protect the cells from apoptosis. These results are
significant because identifying specific signaling pathways activated
in response to thimerosal exposure presents pharmacological targets
for attenuating potential toxicity in patients exposed to thimerosal-
containing products"
http://toxsci.oxfordjournals.org/cgi/content/full/92/1/246 Brian
thanks for that post . I expect you did not read it as it contradicts
every point you made

Quote:

Not that you'll bother, but that video was produced as a part of this
scientific
study:http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView...

If you actually bother to read the paper you'll see just how far off the
mark you really are.

I I read it

Its blatantly obvious you didn't. The abstract isn't the paper.

: perhaps you should.

Its blatantly obvious I did - and actually thought about their results.
Maybe you should try that - thinking. Normally I'd ask for
"critically think", but in your case we'll lower the bar. How about we
start with spelling: m-e-r-c-u-r-i-c__c-h-l-o-r-i-d-e

Bryan

Bryan as the post you gave as a throw away point about cancer is to
quote "The present study demonstrates for the first time the
essential role of JNK activation in thimerosal-induced cell death in
an in vitro model. The SK-N-SH cell line was chosen due to cellular
characteristics representative of those in an immature nervous system.
The SK-N-SH cell line, comprised a neuroblast cell type, retains the
capacity to differentiate in vitro, rather than representing a model
of terminal differentiation" To me it is blatantly obvious you did not
read it before you posted it
http://toxsci.oxfordjournals.org/cgi/content/full/92/1/246
Thanks Vince

Bryan Heit

Posted: Wed Jul 11, 2007 10:10 am

Guest

bigvince wrote:

Quote:

On Jul 7, 1:03 am, Bryan Heit <bjh...@nospamucalgary.ca> wrote:
bigvince wrote:

On Jul 4, 4:32 pm, Bryan Heit <bjh...@NOSPAMucalgary.ca> wrote: >> bigvince wrote:

Some think that the mercury in vaccines has contributed to growing
autism rates. An interesting study from the University of Calgary
shows in real time on video exactly how mercury damages brain cells.Of
course the CDC says it was perfectly safe in vaccines; others
disagree. The video links is
herehttp://video.google.com/videoplay?docid=1745672039422612226&pr=goog-sl
watch for and decide yourself how safe it really is. Thanks Vince
Wow, amazing! Its nice to see that people here at work are getting
their research noticed. Now if only you didn't completely mis-interpret
it things would be just dandy. I've forwarded you post to Dr. Syed,
whom I worked with briefly a few years ago; hopefully he'll drop buy to
set you strait.

Lets put your post to some 'critical thinking" First I incorrectly
noted the form of mercury that was used in this experiment.It really
was not important .

Actually, its hugely important. The form in which mercury takes plays a
huge role in its toxicity. You cannot take the toxicity (mechanism, or
LD50) of one form, and assume its the same as other forms. For example,
this is why your hero Boyd is considered a quack - he claims methyl and
ethylmercury are the same - in the face of overwhelming evidence that
the toxicity, retention, secretion, and mechanism of toxicity are
completely different for the two compounds.

Quote:

What the experiment was designed to show was that
mercury ions at low levels cause neurodegenaration.

No, it was not. The experiment used high levels of mercuric ions (100nM
to be exact). To put this into perspective, assuming mercury spread
evenly throughout your body (which it doesn't, but this keeps the math
simple) to get to this dose would require that the average adult male
inject ~2 LD50's worth of mercury.

That is not a small dose, that is a huge dose which would kill the large
majority of people it is injected into.

As I stated before, what they did was exactly what you do when you're
starting to work out mechanisms of toxicity for any material - you hit
cells with high doses of the material and see what happens. It gives
you an idea of potential mechanisms, and gives you an idea of what you
should look for as you move into more realistic concentrations.

Quote:

In the film
mercury ions at a low level caused lesions similar to those found in
altheimers.

Which right away should act as a warning; alzheimers-like lesions are
not a symptom of mercury toxicity. Which suggests one of two things:

1) Snail neurons (which are what they used) respond to mercury
differently then humans, or

2) The concentration used is not relevant to conventional mercury toxicity

Given that no additional publications have been brought forth in this
area I can't even begin to comment on which of those possibilities are true.

Quote:

the experiment shows that low level mercury exposure .can
indeed cause damage for this reason any reference to LD50 levels is
moot. The damage being looked for is caused by very low
levels .

And, had you actually read the paper, you'd know that they were not
looking at low levels. Permanent neurological damage occurs when brain
levels hit the range of 1-10 nM (i.e. 1/100th to 1/10th the dose used in
this study). Lethal toxicity occurs at about the same dose used in this
study. I'm unsure of how exactly you'd consider lethal toxicity to be a
"low dose".

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=10392564&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=8210224&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Quote:

Actually, you specifically stated that thiomersal causes cancer, hence
why I replied to the statement. Specifically, the reference was made in
your little cut-and-paste from wikipedia. Do you not read the things
you post? Here, I'll refresh your memory:

Message ID: 1183663612.860022.48180@57g2000hsv.googlegroups.com
"Thiomersal is harmful by inhalation and ingestion, lethal between 50
and 1000 times[citation needed][1] the usual intake (hazard symbol
T+).[2] It is a neoplastigen and a teratogen. Thiomersal is also
dangerous for the environment"

Neoplastigen = cancer causing; hence, according to what you wrote,
thiomersal causes cancer.

If you disagree with that statement, then why did you post it?

Quote:

The important question is can thimerosal
produce mercury ions and cause the type of damage shown by the
study.

The answer to which we've known for a very, very long time - a
resounding 'no'. Thomersal breaks town into ethylmercury, which is both
highly stable, and readily excreted from our bodies. And unlike the
more toxic forms of mercury (i.e. ionic, metallic and methylmercury) it
doesn't build up in neural tissues. A small number of studies have
suggested that some Hg2+ may be released. However, it doesn't act like
"pure" ions (i.e. its not retained like Hg2+ normally is), suggesting
that they're not seeing ions, but rather another (unidentified)
breakdown product.

Numerous citations have been posted here in support of these
conclusions. Myself, Mark Probert (sp?) and other frequently post them.
I've included one below.

Quote:

Hardly. At the concentration tested, mercury causes damage to isolated
neurons. No tests were done using animals, isolated pieces of brain, or
any other form of experiment which would have allowed neurological
damage to be assessed.

Once again, a petri dish is not your brain. You're taking discoveries
found in a dish, and extending them to the brain. This is wrong - the
authors of the study did not do this; the closest they came was to say
"this *may* be the mechanism". So if the authors are only that
confident in their findings, what special insight do you have that
extends their observations out of the petri dish?

Quote:

So? That still doesn't guarantee that the mechanisms of toxicity are
the same. Nor does it prove that growth cone loss is the mechanism by
which mercury is toxic within our brains.

For that matter, "stable" neurons - i.e. ones which are not in the
process of growing (as in the bulk of our neurons), do not have growth
cones. Which would lead me to hypothesize that growth cone toxicity (if
it occurs in our body) is only one (and probably minor) mechanism by
which mercury causes neurodegradation.

It's also worth pointing out that other groups disagree with the results
of his studies, and instead believe that it is oxidative damage, not
cytoskeletal changes, which cause toxicity:

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15527868&ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

You'll also notice that like the above study, this paper used a high
dose of mercury...

Quote:

Plus there is the one thing you are really missing here - he's looking
at mercury ions, which are not release by thiomersal, or thiomersals
break-down products. This is why thiomersal is considered safe, as the
toxic ions are "masked" by the remainder of the thimerosal molecule.

Here you are just plain wrong. Affidavit Of Boyd E. Haley.
Professor And Chair. Department Of Chemistry. University Of Kentucky

If you're going to quote someone, you could at least find someone who's
reputable. All of Haley's theories in regards to thiomersal and
ethylmercury have been disproven - again, and again, and again. Lets
not forget that he has ZERO RESEARCH PUBLICATIONS in regards to
thiomerisal toxicity. Hell, you didn't even quote a scientific study,
but rather a court briefing WHICH WAS THROWN OUT BY THE VERY COURT IT
WAS PRESENTED TO.

Apparently, you missed what the court said, after receiving Boyd's
testimony:

"The court…finds that Dr. Haley’s report does not state an expert
opinion that thimerosal causes autism, rather just that he has a theory
about how such a thing could happen. At best, he expressed “strong
belief” that the cause of “neurodevelopmental disorders in infants” is
exposure to an organic-mercury compound such as thimerosal.
Additionally, Plaintiffs proffered the report of Dr. Lucier, who is an
expert in methylmercury and not ethylmercury, which is the substance in
RhoGAM. Dr. Lucier does not offer an opinion that methylmercury causes
autism, but rather that it may cause “developmental disorders.”
Significantly, the Court notes that neither Dr. Haley nor Dr. Lucier
asserts that he is an expert on autism nor are they offered as such. In
any event, the Court finds that neither of the proffered reports of Dr.
Haley nor Dr. Lucier are sufficiently reliable under Daubert on the
general causation issue because neither is relevant to the “task at
hand.” It would be an unacceptable scientific leap to suggest that they
serve as proof, by a preponderance of the evidence, of Plaintiff’s claim
that the thimerosal in RhoGAM can cause autism."

From: http://www.neurodiversity.com/court/rhogam_decision.pdf

So he self-admits that he is not an expert, the court itself
specifically stated that he does not qualify as an expert witness. Gee,
great source for your information.

One of my favorite bits from that particular court case was what was
said about Boyd's bestest-buddy, and greatest supporter, Mark Geier:

"The Court has taken into account…..the fact that Dr. Geier has
testified as an expert witness in about one hundred cases before the
National Vaccine Injury Compensation Program of the United States Court
of Federal Claims. It is noteworthy that in more than ten of these
cases, particularly in some of the more recent cases, Dr. Geier’s
opinion testimony has either been excluded or accorded little or no
weight based upon a determination that he was testifying beyond his
expertise.In this case, subject to the Court’s Daubert analysis"

Ouch!

So instead of quoting a known liar - an individual who's claims have
been throughly disproven by real scientists, and an individual with no
direct experience in the area - why don't you try quoting some
legitimate medical researchers who actually work in the field?

<snippage>

Quote:

In your zeal you posted
this
" Thimerosal Induces Apoptosis in a Neuroblastoma Model via the cJun N-
Terminal Kinase Pathway
Michelle L. Herdman*, Aileen Marcelo*, Ying Huang, Richard M. Niles,
Sanjit Dhar and Kinsley Kelley Kiningham*,1

How nothing to do with zeal, but rather integrity. I'm not hiding the
fact that thiomersal is toxic; you'd be hard pressed to find any
substance which isn't toxic at some level. This paper also doesn't say
anything about thiomersal breaking down into ionic mercury,
methylmercury, or other more toxic forms. So it hardly disproves
anything I claimed.

Ironically, it was also a bit of a trap I set for you - too see if you
actually read and understand these things. I'll give you credit for
reading the paper, unfortunately (thorugh no fault of your own; its
pretty technical stuff) you missed out on some of the more important
details.

Lets look at what this study did:

Cell type used: glioblastoma (brain cancer)
Apopototic dose of thiomersal identified: 2.5-10uM

So we have cells isolated from a brain tumor, and they saw apoptotic
effects at doses of 2.5-10uM. Below that dose nothing happened. What
does that translate into? Well, it translates into about 2000x the
concentration of what is seen in the brain of a child after multiple
vaccinations given over a short period of time:

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16079072&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Now, don't forget that these people are looking at cancer cells. What
happens if we look at normal neurons? Well, someone's done that too:

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16273274&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

As it turns out you get apoptosis and other signs of toxicity as well,
but you need a much higher dose of thiomersal (250uM, rather then
2.5-10uM); as in 100x the dose required to get toxological effects in
the tumor; hence, why thiomersal has been considered a potential cancer
therapeutic. And hence why I posted this article as evidence that
thiomersal may be a potential cancer therapeutic.

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=12773768&ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

<sarcasm> Strange, tumor cells are different then normal cells. How
odd. </sarcasm>

It all comes back to what I was talking about when I posted the
reference. Upon the discovery by studies such as this one, that
thiomersal can kill cancer cells at levels which don't damage normal
cells, it was considered a potential cancer therapeutic. Unfortunately,
the dose required is above the levels considered safe for use. But
those studies do come back to the main point - at the doses used in
vaccines thiomersal is safe.

Quote:

Here a few excepts...... "However, cells transfected with TAM67
showed no changes in those same components.

I'll try not to sound too rude here, as this is one of those technical
things that people outside of the field would be unaware of. That said,
you just completely undermined your own argument. A little advice, if
you don't know what something is, don't try and use it in an argument.

TAM67 is a gene which prevents cancer cells from dividing, or in other
words, is a gene we can add back into cancerous cells that makes those
cells non-cancerous. It is also a commonly mutated gene in cancers -
i.e. loss of this genes normal function will cause a normal cell to
become cancerous. The effect of putting TAM67 into a cancerous cell is
commonly used as a "goal post" of what an anti-cancer drug must achieve
to be effective.

Here's an example:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17477349&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

So the study showed that adding TAM67 prevents thiomersal toxicity - or
in other words, if they made the cancer cells non-cancerous, thiomersal
was no longer toxic.

Now what exactly does that say about thiomersal toxicity in
non-cancerous cells? What does it say about the potential use of
thiomersal as a cancer therapeutic? What does it say about thiomersal
toxicity in those of us who don't have brain tumors?

And keep in mind that the levels of thiomersal they are using is very
high, far, far higher then what is seen in brains after vaccination -
even in young children.

Quote:

Taken together, these
results indicate that thimerosal-induced neurotoxicity occurs through
the JNK-signaling pathway, independent of cJun activation, leading
ultimately to apoptotic cell death. " strange that you posted an
abstract that links thimerosal and nerotoxicity did you read it?

Yes, obviously you didn't, or if you did, you didn't understand it. The
results of the paper were obvious - thiomersal kills cancer cells, but
not non-cancerous cells, at the concentration of thiomersal they used.

What part of that don't you get?

Strangely enough, this very paper is the most-cited paper by those
people who are testing thiomersal for the treatment of cancer. For the
very reason that this paper successfully showed that the toxicity of
thiomersal is much, much higher in cancerous neurons then in
non-cancerous neurons. It isn't the paper that sparked the interest in
thiomersal as a potential anti-cancer drug, but it represents the best
evidence that thiomersal may be useful as an anti-cancer drug.

Quote:

Brian

It's "Bryan", with a 'y'.

Quote:

thanks for that post . I expect you did not read it as it contradicts
every point you made

Hardly, but I'm sure you'll go on believing so, as to actually think
about the data would show that the paper demonstrates exactly what I
claimed it does.

Quote:

Bryan as the post you gave as a throw away point about cancer

Hey, you brought it up. If you didn't want to talk about cancer then
maybe you shouldn't have typed the word "neoplastigen". Although the
irony that you're complaining about me disproving one of your points is
duly noted.

Quote:

is to
quote "The present study demonstrates for the first time the
essential role of JNK activation in thimerosal-induced cell death in
an in vitro model. The SK-N-SH cell line was chosen due to cellular
characteristics representative of those in an immature nervous system.

Really? So kids have cancer in their brains? I'd argue that this
paper, which used neurons from infant mice, would be a much more
accurate model as it is using real neurons and not cancer cells:

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16273274&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

In case you're confused, this is the paper I referred to above, the one
which showed that thiomersal-induced apoptosis occurred at thiomersal
levels 100x those used in this study.

And you were pretty selective in what you posted, what about these parts?

"studies will be needed to determine if either of these events is
occurring in response to thimerosal since SK-N-SH cells treated with the
mercury-containing compound appear unable to successfully process the
toxic insult and thus proceed down an apoptotic pathway"

Or, in other words, the cancer cells they used don't respond the way the
rest of our cells do in response to mercury. Strangely enough, that
throws into doubt any conclusions you make about non-cancerous cells, as
the cancer cells they used as a model for neurons don't behave the same
as real neurons exposed to mercury.

Or how about:
"Our studies are the first to show that proapoptotic Bim levels are
increased in response to thimerosal treatment and are decreased when
cells were pretreated with SP600125 but not when transfected with TAM67"

Yep, the evidence shows that if you make the cell non-cancerous,
thiomersal becomes non-toxic at the dose used. Why does it become
non-toxic? Simple - the very apoptotic pathway that caused the cancer
cells to apoptose doesn't work in non-cancerous cells.

Quote:

to me it is blatantly obvious you did not
read it before you posted it

Bad news for you buddy. Not only have I read this paper, but it makes
up the foundation of a research project we are starting here in our lab.
Not only am I intimately familiar with this paper, their methods, and
their readouts, but I've actually repeated some of their experiments
(using different types of cells, mind you), and we've asked this group
for some of their gene constructs.

If you're wondering, we're not looking at thiomersal; but rather the
signaling pathway they've discovered. Regardless, the pathway they have
identified is very interesting - if it exists in non-cancerous cells. To
date we've only been able to replicate their results in a few
cancer-cell lines, so this may be a cancer-specific signaling pathway.

Now, you want to try going down this road again? Perhaps you'd like to
pull up a paper where they show toxicity in a cancer cell derived from a
monkeys kidney, and claim that its proof that thiomersal is neurotoxic
(that's one of Johns favorite tricks)? Or perhaps you want to pull up a
few papers on methylmercury toxicity, and try to argue that there is
some relevance to thiomersal (Boyds favorite trick? Or perhaps you'd
like to degrade things all the way back to the old arguments about
molecular mass and toxicity?

Or perhaps you'd like to continue to argue that cancer cells and neurons
are the same thing?

Or perhaps you'd like to delve even deeper into my area of expertise; my
entire PhD thesis is on MAP-Kinase signaling (JNK is a MAPK). I'd be
more then happy to blow holes in your claims vis-a-vis JNK-mediated
thiomersal toxicity, JNK mediated apoptosis, and all other things JNK...

Bryan

bigvince

Posted: Thu Jul 12, 2007 12:24 pm

Guest

On Jul 11, 11:10 am, Bryan Heit <bjh...@NOSPAMucalgary.ca> wrote:

Quote:

Or perhaps you'd like to delve even deeper into my area of expertise; my
entire PhD thesis is on MAP-Kinase signaling (JNK is a MAPK). I'd be
more then happy to blow holes in your claims vis-a-vis JNK-mediated
thiomersal toxicity, JNK mediated apoptosis, and all other things JNK...

Bryan

Perhaps All from the text ...".The cJun N-terminal kinase (JNK)-
signaling pathway is activated in response to a variety of stimuli,
including environmental insults, and has been implicated in neuronal
apoptosis. In this study, we investigated the role that the JNK
pathway plays in neurotoxicity caused by thimerosal, an ethylmercury-
containing
preservative" .........
and " To assess which components are essential to apoptosis,
cells were treated with a cell-permeable JNK inhibitor II (SP600125)
or transfected with TAM67, and the downstream effectors of apoptosis
were analyzed. Cells pretreated with SP600125 showed decreases in
activation of caspases 9 and 3, decreases in degradation of poly(ADP-
ribose) polymerase (PARP), and decreased levels of proapoptotic Bim,
in comparison to cells treated with thimerosal alone. However, cells
transfected with TAM67 showed no changes in those same components.
Taken together, these results indicate that thimerosal-induced
neurotoxicity occurs through the JNK-signaling pathway, independent of
cJun activation, leading ultimately to apoptotic cell death."

The whole point of the study is that thimerosal to occurs through the
JNK pathway . Or are you claiming that the JNK pathway only occurs in
cancer cells? Back to the
text
" By using a cell-permeable JNK inhibitor (SP600125) to block the
pathway, we demonstrate that JNK activation is an essential component
of thimerosal-induced cell death. However, through the use of a cJun
dominant negative, we show that cJun activation is not required for
cell death in SK-N-SH cells treated with thimerosal. To our knowledge,
this is the first study to show that thimerosal activates JNK, leading
to cell death in a cJun-independent manner. These results are
significant because they establish a signaling pathway that could be
targeted pharmacologically to decrease toxicity in patients exposed to
thimerosal."

Let me emphasis the reason this study is important from the text....
" These results are significant because they establish a signaling
pathway that could be targeted pharmacologically to decrease toxicity
in patients exposed to thimerosal. " http://toxsci.oxfordjournals.org/cgi/content/full/92/1/246

Bryan your argument is with the study authors they conclude that this
study may help decrease the damage {toxicity} done by thimerosal. As
the video presented earlier shows the the nerolocical damage I
encourage people to view it ..Bryan critical thinking requires that
one be able to grasp the essential ellements and not be misled by non
crital pieces of information you did a fairly good of trying to
confuse this. This studies main points 1 Thimerosol is neurotoxic. 2.
JNk pathway plays a role in it's neurotoxic effects. The study also
supports DR. Haleys physical desciption of mercury being stored in the
brain from the text " Kunimoto (1994) showed that primary cultures of
rat cerebellar neurons undergo apoptosis when exposed to low
concentrations of methylmercury but undergo necrotic cell death when
exposed to higher concentrations. Additionally, several studies have
shown that once organic mercurials enter the body, they can be
converted to inorganic mercury, which has a much longer half-life than
the parent compound (Friberg and Mottet, 1989 ; Norseth and Clarkson,
1970 ; Suda et al., 1991). Several studies have indicated that both
inorganic and organic mercurials induce apoptosis in vitro as well as
in vivo (Guo et al., 1998 ; Shenker et al., 1999 , 2000). At the organ
level, one of the primary targets for mercurials is the brain. Studies
using Wistar rats exposed to methylmercury demonstrated that
cerebellar granule cells underwent apoptotic cell death (Nagashima et
al., 1996). Baskin et al. (2003) demonstrated that thimerosal induced
changes in membrane permeability, DNA damage, and caspase 3 activation
in both cultured human cerebral cortical neurons and fibroblasts. It
has been known for 30 years that mercury accumulates in rabbit brain
tissue following the application of thimerosal-containing ophthalmic
medications (Gassett et al., 1975 ) and that inorganic mercury
accumulates in monkey brain tissue following daily administration of
thimerosal (Blair et al., 1975). Recent studies have shown that
mercury accumulates in the brain tissue of neonatal mice given
intramuscular injections of thimerosal, and the levels did not
decrease at 7 days after treatment (Harry et al., 2004 ). Hornig et
al. (2004) used an autoimmune disease-sensitive mouse model (SJL/J) to
show that some populations may have a genetic predisposition for
sensitivity to thimerosal-induced neurotoxicity. However, specific
signaling pathways in thimerosal-induced neurotoxicity have not been
established in animal or tissue culture models. "
Thanks Vince

Bryan Heit

Posted: Thu Jul 12, 2007 2:27 pm

Guest

bigvince wrote:

Quote:

On Jul 11, 11:10 am, Bryan Heit <bjh...@NOSPAMucalgary.ca> wrote:

Or perhaps you'd like to delve even deeper into my area of expertise; my
entire PhD thesis is on MAP-Kinase signaling (JNK is a MAPK). I'd be
more then happy to blow holes in your claims vis-a-vis JNK-mediated
thiomersal toxicity, JNK mediated apoptosis, and all other things JNK...

Bryan

Perhaps All from the text ...".The cJun N-terminal kinase (JNK)-
signaling pathway is activated in response to a variety of stimuli,

But thats the key - Jnk is activated by nearly anything you can name -
hormones which support cell survival, control metabolism, and control
cell differentiation also activate Jnk. Jnk itself is pretty
non-specific in what it does - there is a whole range of transcription
factors which Jnk activates, which result in the activation of a variety
of genes that have all kinds of different purposes.

Think of it as a "master on/off switch" - it turns lots of things on and
off, but is not overly specific.

What determines specificity is what else is going on in the cell at the
time - if the cell is heading towards apopotosis, Jnk will give it an
extra shove in that direction. If a cell is migrating Jnk will help out
with that too - its all dependent on what else the cell is doing at the
time, and what other genes are active.

Quote:

The whole point of the study is that thimerosal to occurs through the
JNK pathway .

Actually, that is the least interesting thing that they showed. As I
pointed out above, showing Jnk is doing something isn't too exciting -
as jnk will affect pretty much every cellular process you can name.

The exciting part of the paper - the reason why my lab is interested in
it - and the reason why cancer researchers are interested in it is a bit
more then showing Jnk is involved. Rather, the big news is that Jnk is
interacting with another pathway - specifically that Jnk was interacting
with the Bim pathway.

That is unprecedented. That Jnk affects apoptosis is a well known fact.
That it can impact on Bim has never been reported before, and absed on
what we know of Jnk signaling, was totally unexpected. And while it
would be difficult to explain why that is exciting without writing a
book on cell biology, lets just say that this observation is very,very
exciting to many scientists. Myself included; in fact, if this pathway
functions in non-cancerous cells it would explain an outstanding problem
we've been unable to explain for about 3 years.

But in regards to the whole thiomersal causes neurotoxicity question
this paper falls short. As I pointed out previously, in real neurons
(not cancerous ones) thiomersal doesn't become active until you hit much
higher doses. Likewise, the entier toxic effect they say with
thiomersal disappears when TAM67 is transfected into the cell -
suggesting that the toxicity of thiomersal may be linked to cell
division, or some other aspect of cancer, which is eliminated by TAM67's
function.

Most importantly though, from a clinical perspective, is that these
cancer cells are somewhere between 10 and 100x more sensitive to
thiomersal then are normal neurons. And even so, you don't see
activation of Jnk, or the Jnk-assocaited toxicity in these cancerous
cells until you hit levels of thiomeral much, much higher then that seen
in the brains of people who have received multiple vaccines.

Or, in other words, it demonstrates that even in cells with
hypersensitivity to thiomersal, that no significant signs of toxicity
can be observed until you hit concentrations far, far above what you see
in the real world.

Quote:

Or are you claiming that the JNK pathway only occurs in
cancer cells?

Don't be stupid. But the protein-protein interactions which allow for
Jnk to impinge on Bim function may be unique to cancer. Or, far more
likely, the cellular changes which occur when cells become cancerous may
enhance an otherwise insignificant Jnk-Bim interaction that normally is
not detectable in cells.

Quote:

Back to the
text
" By using a cell-permeable JNK inhibitor (SP600125) to block the
pathway, we demonstrate that JNK activation is an essential component
of thimerosal-induced cell death. However, through the use of a cJun
dominant negative, we show that cJun activation is not required for
cell death in SK-N-SH cells treated with thimerosal.

All this means is that the normal pathway by which Jnk is activated
(i.e. how a hormone would activate Jnk) is not used. Instead, Jnk is
probably being activated (although they didn't do the experiment to show
this) by some form of intracellular stress reporter protein. Which in
plain english means that thoimersal is probably not acting via a direct
mechanisms, but rather by doing something to the cell which causes
stress, thereon leading to Jnk activation by one of the cells "stress
reporter proteins".

Quote:

To our knowledge,
this is the first study to show that thimerosal activates JNK, leading
to cell death in a cJun-independent manner.

And, AFAIK, this statement is 100% true, and even today their paper
still (AFAIK) remains the only paper showing this link.

Quote:

These results are
significant because they establish a signaling pathway that could be
targeted pharmacologically to decrease toxicity in patients exposed to
thimerosal."

Maybe. Problem is that Jnk is so broad-acting that its any inhibitor of
the pathway would probably have such severe side effects as to make any
use of the inhibitor meaningless.

It would be like targeting insulin to get rid of diabetes - it would
probably work, but you'd kill the patient.

Quote:

Let me emphasis the reason this study is important from the text....
" These results are significant because they establish a signaling
pathway that could be targeted pharmacologically to decrease toxicity
in patients exposed to thimerosal. " http://toxsci.oxfordjournals.org/cgi/content/full/92/1/246

I'm going to let you into one of sciences nasty little secrets - in
order to get our studies published we often need to make dramatic
statements like the one above. It works especially well when a topic is
"hot". The above is nothing more then that. And its pretty easy to
prove - through a variety of accidental exposures several people have
been exposed to hundreds, even thousands of times the "safe" dose of
thiomersal, and yet none of them have experience any signs of toxicity.
Which makes one wonder what toxicity they're proposing we deal with:

Example - 2,250ug/ml blood concentration - i.e 1000x what it took to see
toxicity in cancer cells. Symptoms - none.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16431248&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

In fact, of the dozen case reports I found only one reported case where
toxic symptoms were observed - in a suicide attempt. A man consumed
over 60 grams of thiomersal, and not too surprising got very sick. To
put that into perspective, that's equivalent to ~120,000 (yes, one
hundred and twenty *thousand*) thiomersal-containing vaccinations all at
once. And even after consuming an absolutely stupid amount of
thiomersal he survived, with no apparent long-term neurological damage.
More impressively, his brain saw saw ~2500 times the toxic dose of
thiomersal observed in the cancerous neuron study, and yet he suffered
no neurological problems:

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=8699562&ordinalpos=17&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Oh, and cause I know John has a hard-on for chelation therapy, its worth
noting that it was tested in this man, and did not help remove the
thiomersal from his body.

So I ask again - what toxicity? If you consumed 60 grams of table salt
in one go you'd experience symptoms very similar (though shorter lived)
to what he experienced - certainty you aren't proposing we begin
treating people with drugs every time they put salt on their food?

Probably the last thing worth pointing out is that the only significant
medical effect we see as a result of normal thiomersal exposure (i.e. a
few vaccines worth) is hypersensitivity - AKA allergy. And inhibiting
Jnk in that situation is the very last thing you want to do. After all,
Jnk is an important signaling molicule which plays a pretty important
role in controlling immune responses. And if your #1 side effect of a
treatment is an immune response (which allergy is), the very last thing
you want to do is begin fiddling with the immune system.

Quote:

Bryan your argument is with the study authors they conclude that this
study may help decrease the damage {toxicity} done by thimerosal.

I have no argument with them. They used the discussion section of their
paper in the same way everyone else does - to "sell" the paper to the
editors of the journal. Unfortunately, it is common practice. It's
also why most of us don't even bother reading the discussion - if you're
familiar with the field you are able to put things into context without
the paper authors spoon-feeding you. It also gets you away from the
sale pitch that we all have to do to get our work published.

Quote:

As
the video presented earlier shows the the nerolocical damage I
encourage people to view it ..Bryan critical thinking requires that
one be able to grasp the essential ellements and not be misled by non
crital pieces of information

But its also important to put singular facts into context of other
facts. Critical thinking also involved actually thinking about results
- not just accepting them at face value. The video, and all your
commentary thereof is a perfect example of not critically thinking. Why
- easy, we know for a fact that:

a) thiomersal does not release significant amounts of mercury ions upon
degradation in the body. Rather, it degrades to ethylmercury; which is
rapidly excreted and not associated with neurological damage.

b) even if thiomersal were to release all of its mercury, it does not
reach levels anywhere near those used in the video

c) thiomersal itself has a toxicological profile completely different
from ionic mercury. Therefore making any conclusion on the safety of
thiomersal-containing products, based on that video, absolutely
meaningless - not to mention just plain stupid.

Quote:

you did a fairly good of trying to
confuse this.

Hey, if you didn't want to talk about cancer then you shouldn't have
brought it up.

Quote:

This studies main points 1 Thimerosol is neurotoxic.

You're missing the "critical" part of the "critical thinking" thing.
You forgot to add "at concentrations far higher then those seen in
people who receive vaccines and other thiomersal-containing products".

Quote:

2.
JNk pathway plays a role in it's neurotoxic effects.

I never claimed otherwise. But the critical thinking bit again forces
us to ask exactly what that means & why. The why is via interactions
with bim. These interactions with bim are not seen in non-cancerous
neurons. The "what that means" is that cancer cells appear to have a
unique pathway which increases their sensitivity to thiomersal.

You see, the "critical" part of the "critical thinking" is putting
together all the details into a concrete picture. Single facts on their
own are meaningless - in combination with other facts they tell you a lot.

Quote:

The study also
supports DR. Haleys physical desciption of mercury being stored in the
brain from the text " Kunimoto (1994) showed that primary cultures of
rat cerebellar neurons undergo apoptosis when exposed to low
concentrations of methylmercury but undergo necrotic cell death when
exposed to higher concentrations.

Well, at least you tried to be critical here. unfortuantly, thiomersal
does not degrade into methylmercury or mercury ions; nor does is it
retained in the brain.

These are well established facts. These facts also make any comparison
to methylmercury meaningless in context of thiomersal. You may as well
be comparing to plutonium.

Quote:

Additionally, several studies have
shown that once organic mercurials enter the body, they can be
converted to inorganic mercury, which has a much longer half-life than
the parent compound (Friberg and Mottet, 1989 ; Norseth and Clarkson,
1970 ; Suda et al., 1991).

However, none of those looked at thiomersal, or ethylmercury. More
recent studies have shown that this does not appear to be the case for
thiomersal:

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17582588&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16079072&ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

To quote the last study:

"The results indicate that MeHg is not a suitable reference for risk
assessment from exposure to thimerosal-derived Hg. Knowledge of the
toxicokinetics and developmental toxicity of thimerosal is needed to
afford a meaningful assessment of the developmental effects of
thimerosal-containing vaccines."

So why are you using methylmercury as an example - remeber that critical
thinking bit. The "critical" part should tell you that using apples, to
understand oranges, is doomed to failure...

Quote:

Several studies have indicated that both
inorganic and organic mercurials induce apoptosis in vitro as well as
in vivo (Guo et al., 1998 ; Shenker et al., 1999 , 2000).

All using methylmercury, or ionic mercury. Neither of which comes from
thiomersal breakdown. So the relevance is. . .nothing.

Quote:

At the organ
level, one of the primary targets for mercurials is the brain.

No. Ionic and methylmercury concentrate in the brain. Thiomersal and
ethylmercury do not.

Once again, you're looking at apples, but making conclusions about
oranges. Not exactly "critical thinking".

Quote:

Studies
using Wistar rats exposed to methylmercury

God, I htae repeating myself. If you haven't figured out that
methylmercury is not the same as thiomersal or thiomersals breakdown
product by this point, then you'll never understand...

Quote:

Why don't you try something newer, like the links I posted above? Not
to be too rude to those scientists, but the technology, as well as
chemical purity they had to work with led them to a lot of incorrect
results. Strangely enough, we cannot replicate those results today -
see my links above for examples.

Also, if you're going to try and make a serious scientific argument, kin
the field of biology, you should try to stick to the last decade. We've
done a pretty good job recently of disproving much of what we believed
to be true at the end of the 1980's - if you're quoting the 1970's
chances are pretty good the science was wrong...

Quote:

Recent studies have shown that
mercury accumulates in the brain tissue of neonatal mice given
intramuscular injections of thimerosal, and the levels did not
decrease at 7 days after treatment (Harry et al., 2004 ).

Once again, you need to rad more. More resent studies have cataloged
thiomersal clearance over longer periods of time and shown that
thiomersal is indeed cleared from the barins of young animals. It takes
longer then 7 days - one of the studies I linked to above did just that,
and in monkeys, pretty much disproving your attempted claim that
thiomersal isn't cleared, or that thiomersal is retained like methylmercury.

Quote:

Hornig et
al. (2004) used an autoimmune disease-sensitive mouse model (SJL/J) to
show that some populations may have a genetic predisposition for
sensitivity to thimerosal-induced neurotoxicity.

That mouse has lupus. If you think that has any relevance to the rest
of us, then you've got some serious problems. Also, it was previously
shown that the response they observed was an immune response against
thiomersal in those mice (Tsai WM et al. J Immunol vol 149(6)).

Bryan

bigvince

Posted: Sun Jul 15, 2007 9:20 am

Guest

On Jul 12, 3:27 pm, Bryan Heit <bjh...@NOSPAMucalgary.ca> wrote:

Quote:

However, none of those looked at thiomersal, or ethylmercury. More
recent studies have shown that this does not appear to be the case for
thiomersal:

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView...http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView...

To quote the last study:

"The results indicate that MeHg is not a suitable reference for risk
assessment from exposure to thimerosal-derived Hg. Knowledge of the
toxicokinetics and developmental toxicity of thimerosal is needed to
afford a meaningful assessment of the developmental effects of
thimerosal-containing vaccines."

" Lets quote a little more of that study ... ." Brain concentrations
of total Hg were significantly lower by approximately 3-fold for the
thimerosal-exposed monkeys when compared with the MeHg infants,
whereas the average brain-to-blood concentration ratio was slightly
higher for the thimerosal-exposed monkeys (3.5 +/- 0.5 vs. 2.5 +/-
0.3). A higher percentage of the total Hg in the brain was in the form
of inorganic Hg for the thimerosal-exposed monkeys (34% vs. 7%). The
results indicate that MeHg is not a suitable reference for risk
assessment from exposure to thimerosal-derived Hg. Knowledge of the
toxicokinetics and developmental toxicity of thimerosal is needed to
afford a meaningful assessment of the developmental effects of
thimerosal-containing vaccines."

As no one recommends the routine administration of MeHg to infants
the fact that it produced higher blood concentrations of mercury does
not show that the levels produced by thimerosal are safe. This study
also shows that thimerosal tend to partition to the brain; partial
confirmation of Dr. Halleys work. Note the blood brain
concentrations.. lets look at Haleys
statement
Affidavit Of Boyd E. Haley. Professor And Chair. Department Of
Chemistry. University Of Kentucky

Thimerosal Containing Vaccines and Neurodevelopment Outcomes

FORWARD:

Thimerosal or merthiolate is a derivative of thiolsalicylate where
ethyl mercury is attached though the sulfur. It is defined as a
preservative or anti microbial in medical use. This anti microbial
action is dependent on thimerosal breaking down releasing ethyl
mercury that can penetrate cell membranes and bind to intracellular
enzymes, inhibiting them, and causing cell death. Further, in certain
biological environments the ethyl mercury can further break down
releasing mercury cation (Hg2+). Hg2+ is also very reactive with
enzymes and proteins inhibiting their biological functions and causing
cell injury or death. Both ethyl mercury and Hg2+ are very neuro toxic
compounds. However, ethyl mercury is more rapidly partitioned into the
hydrophobic (fatty) tissues of the central nervous system and is a
more potent neuro toxin than Hg2+ based on this "partitioning factor".
It is this partitioning factor that makes organic mercurials such as
dimethyl mercury so neuro toxically lethal (this is the compound that
caused the death of a Dartmouth University chemistry professor after
she was exposed to a drop or two on her gloved hand). The concern with
organic mercurials, such as thimerosal, is that such compounds can be
perceived as "pro toxicants" just as certain pharmaceuticals can be
classified as "pro drugs". This means that the original compound, e.g.
thimerosal, is less reactive giving the compound time to partition
into certain areas of the body before it breaks down releasing the
ethyl mercury and then further releasing Hg2+. However, while
attaching ethyl mercury to thiolsalicylate makes the ethyl mercury
less reactive it most likely allows increased partitioning into the
central nervous system before the ethyl mercury is released and
thereby, increases the neuro toxicity per unit ethyl mercury involved.
Considerable caution must be taken when stating what is the "toxic
level" of mercury and any mercury containing compound. Humans are not
rats in a pristine cage where their environment can be controlled to
ensure that other toxicities and infections are not occurring. The
level of mercury that would cause toxicity in a healthy individual is
much higher than what would be needed to cause a toxic effect in an
individual that is ill or under oxidative stress. This is because
additional stresses lower the amount of protective compounds that bind
mercury and render it less harmful. If an individual is low on these
protective compounds, then less mercury or thimerosal would be needed
to cause a clinical effect. Below I will present my interpretation of
our research and that from other laboratories that focus on the
potential toxicity of injected thimerosal in the vaccine mixture.

Note the partitioning into the brain and the ability to produce
Mercury catons .Key points as you do not care for Haley here a
different
source
" Organic mercury metabolism in humans '

Limited human toxicologic and pharmacokinetic data are available for
ethylmercury, particularly from episodic, low-dose, intramuscular
exposure. Comparison is made to methylmercury, for which
gastrointestinal exposure in particular has been studied more
extensively(1,19,25,29). Although methylmercury binds with cysteine to
form a complex that readily crosses the blood-brain barrier and enters
neurons, it is unknown if a similar transport mechanism exists for
ethylmercury(45). The biologic half-life of methylmercury in humans is
about 70 days(25,29), but it is likely less for ethylmercury due to
more rapid conversion in the lungs, liver and red blood cells to
inorganic mercury -which does not cross the blood-brain barrier as
readily(20,46-4 Cool

. On the other hand, once in the brain, ethylmercury
is converted to its inorganic form, resulting in higher cumulative
neural exposure to mercury, again due to less efficient inorganic
mercury transport across the blood-brain barrier(20). Organic mercury
also binds to glutathione, which may play a protective role in
transporting mercury out of cells, as well as to metallothionein and
other plasma proteins(19). The metabolic and toxicologic effects of
these mercury-containing complexes are poorly understood(19). " Source
CCDR http://www.phac-aspc.gc.ca/publicat/ccdr-rmtc/02vol28/dr2809ea.html

Quote:

So why are you using methylmercury as an example - remember that
critical
thinking bit. The "critical" part should tell you that using apples, to
understand oranges, is doomed to failure...

The key here is; in terms of nerologic damage does ethel mercury
accumulate in the brain; does it clear rapadly once there and can it
cause damage the evidence shows it does accumulate it does not clear
rapidly and it can do damage. Critical thinking requires that
evidence ; not ones perconcieved ideas are key

Quote:

All using methylmercury, or ionic mercury. Neither of which comes
from
thiomersal breakdown.

Reread last section.

Quote:

At the organ
level, one of the primary targets for mercurials is the brain.

No. Ionic and methylmercury concentrate in the brain. Thiomersal and
ethylmercury do not.

Reread last section pay attention to the Canadian CDR report and the
pummed link you posted both say exactly the opposite as does Dr.
Halleys work let me help from CCDR " On the other hand, once in the
brain, ethylmercury is converted to its inorganic form, resulting in
higher cumulative neural exposure to mercury, again due to less
efficient inorganic mercury transport across the blood-brain
barrier(20). Organic mercury also binds to glutathione, which may play
a protective role in transporting mercury out of
cells"

Quote:

God, I htae repeating myself. If you haven't figured out that
methylmercury is not the same as thiomersal or thiomersals breakdown
product by this point, then you'll never understand...

So do I reread previous paragraphs

Quote:

It
has been known for 30 years that mercury accumulates in rabbit brain
tissue following the application of thimerosal-containing ophthalmic
medications (Gassett et al., 1975 ) and that inorganic mercury
accumulates in monkey brain tissue following daily administration of
thimerosal (Blair et al., 1975).

Why don't you try something newer, like the links I posted above? Not
to be too rude to those scientists, but the technology, as well as
chemical purity they had to work with led them to a lot of incorrect
results. Strangely enough, we cannot replicate those results today -
see my links above for examples.

The link you posted noted the higher ratio of brain to blood mercury
produced by thimerosal in monkeys > to be true at the end of the
1980's - if you're quoting the 1970's

Quote:

chances are pretty good the science was wrong...

Reread previous section all in last decade
Thanks
Vince

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