I think some here will take Chris's leap in ill-logic and apply it to
polio.  Children who happen to be in a wheelchair for any reason
following vaccination will be considered to have polio.

On Mar 22, 5:10 pm, mainframetech <flam...@optonline.net> wrote:

This has been hashed, e-hashed, and discussed. Hannah Poling does not
have autism. She was diagnosed with a mitochondrial diosorder that was
aggravated by vaccines, and she developed some autism-like symptoms.
Not enough to be diagnosed with autism, though.
==============
http://www.ncbi.nlm.nih.gov/pubmed/17945343?ordinalpos=2&itool=Entrez...

Histo-cytological responses of Dicentrarchus labrax (L.) following mercury
exposure.
Giari L, Simoni E, Manera M, Dezfuli BS.
Department of Biology and Evolution, University of Ferrara, Via Borsari, 46,
44100 Ferrara, Italy.

This work deals with the damaging effects of mercury (Hg concentrations 251,
355, 501mugl(-1)) on the structure and ultrastructure of gills, liver,
intestine and kidney of farmed European sea bass (Dicentrarchus labrax L.,
1758) acutely treated for 24 and 48h. The histoarchitecture of the gills of
exposed fish was highly modified due to severe oedema, telangiectasia and
secondary lamellar fusion. In hepatocytes and enterocytes hydropic cell
swelling, alterations to the endoplasmic reticulum and mitochondria were
noted, in addition to an abundance of myelinoid bodies which were frequently
encountered following treatment. In the intestine and renal tubules of
exposed European sea bass, rodlet cells (RCs) displayed ultrastructural
modifications. Statistical analyses were conducted on the number and the
size of selected cell types and structures. Following exposure to mercury
for 24 and 48h, the number of chloride cells, RCs and macrophage aggregates
were found to have increased significantly in the gills, the intestine and
the head kidney.

PMID: 17945343 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/17334523?ordinalpos=3&itool=Entrez...

Involvement of glutamate and reactive oxygen species in methylmercury
neurotoxicity.
Aschner M, Syversen T, Souza DO, Rocha JB, Farina M.
Departments of Pediatrics and Pharmacology, Vanderbilt University Medical
Center, B3307 Medical Center North, Nashville, TN 37232, USA.
michael.asch...@vanderbilt.edu

This review addresses the mechanisms of methylmercury (MeHg)-induced
neurotoxicity, specifically examining the role of oxidative stress in
mediating neuronal damage. A number of critical findings point to a central
role for astrocytes in mediating MeHg-induced neurotoxicity as evidenced by
the following observations: a) MeHg preferentially accumulates in
astrocytes; b) MeHg specifically inhibits glutamate uptake in astrocytes; c)
neuronal dysfunction is secondary to disturbances in astrocytes. The
generation of reactive oxygen species (ROS) by MeHg has been observed in
various experimental paradigms. For example, MeHg enhances ROS formation
both in vivo (rodent cerebellum) and in vitro (isolated rat brain
synaptosomes), as well as in neuronal and mixed reaggregating cell cultures.
Antioxidants, including selenocompounds, can rescue astrocytes from
MeHg-induced cytotoxicity by reducing ROS formation. We emphasize that
oxidative stress plays a significant role in mediating MeHg-induced
neurotoxic damage with active involvement of the mitochondria in this
process. Furthermore, we provide a mechanistic overview on oxidative stress
induced by MeHg that is triggered by a series of molecular events such as
activation of various kinases, stress proteins and other immediate early
genes culminating in cell damage.

PMID: 17334523 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/17182013?ordinalpos=4&itool=Entrez...

Brain Res. 2007 Feb 2;1131(1):1-10. Epub 2006 Dec 19.

Methylmercury induces oxidative injury, alterations in permeability and
glutamine transport in cultured astrocytes.
Yin Z, Milatovic D, Aschner JL, Syversen T, Rocha JB, Souza DO, Sidoryk M,
Albrecht J, Aschner M.
Department of Pediatrics, Vanderbilt University Medical Center, TN, USA.

The neurotoxicity of high levels of methylmercury (MeHg) is well established
both in humans and experimental animals. Astrocytes accumulate MeHg and play
a prominent role in mediating MeHg toxicity in the central nervous system
(CNS). Although the precise mechanisms of MeHg neurotoxicity are
ill-defined, oxidative stress and altered mitochondrial and cell membrane
permeability appear to be critical factors in its pathogenesis. The present
study examined the effects of MeHg treatment on oxidative injury,
mitochondrial inner membrane potential, glutamine uptake and expression of
glutamine transporters in primary astrocyte cultures. MeHg caused a
significant increase in F(2)-isoprostanes (F(2)-IsoPs), lipid peroxidation
biomarkers of oxidative damage, in astrocyte cultures treated with 5 or 10
microM MeHg for 1 or 6 h. Consistent with this observation, MeHg induced a
concentration-dependant reduction in the inner mitochondrial membrane
potential (DeltaPsi(m)), as assessed by the potentiometric dye,
tetramethylrhodamine ethyl ester (TMRE). Our results demonstrate that
DeltaPsi(m) is a very sensitive endpoint for MeHg toxicity, since
significant reductions were observed after only 1 h exposure to
concentrations of MeHg as low as 1 microM. MeHg pretreatment (1, 5 and 10
microM) for 30 min also inhibited the net uptake of glutamine
((3)H-glutamine) measured at 1 min and 5 min. Expression of the mRNA coding
the glutamine transporters, SNAT3/SN1 and ASCT2, was inhibited only at the
highest (10 microM) MeHg concentration, suggesting that the reduction in
glutamine uptake observed after 30 min treatment with lower concentrations
of MeHg (1 and 5 microM) was not due to inhibition of transcription. Taken
together, these studies demonstrate that MeHg exposure is associated with
increased mitochondrial membrane permeability, alterations in
glutamine/glutamate cycling, increased ROS formation and consequent
oxidative injury. Ultimately, MeHg initiates multiple additive or
synergistic disruptive mechanisms that lead to cellular dysfunction and cell
death.

PMID: 17182013 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/16918248?ordinalpos=7&itool=Entrez...

Res Toxicol. 2006 Aug;19(8):1080-5.Methylmercury induces pancreatic
beta-cell apoptosis and dysfunction.Chen YW, Huang CF, Tsai KS, Yang RS, Yen
CC, Yang CY, Lin-Shiau SY, Liu SH.Institute of Toxicology, Department of
Laboratory Medicine, and Departmentof Orthopaedics, College of Medicine,
National Taiwan University, Taipei,Taiwan.Mercury is a well-known toxic
metal, which induces oxidative stress.Pancreatic beta-cells are vulnerable
to oxidative stress. Thepathophysiological effect of mercury on the function
of pancreaticbeta-cells remains unclear. The present study was designed to
investigatethe effects of methylmercury (MeHg)-induced oxidative stress on
the cellviability and function of pancreatic beta-cells. The number of
viable cellswas reduced 24 h after MeHg treatment in a dose-dependent manner
with arange from 1 to 20 microM. 2',7'-Dichlorofluorescein fluorescence as
anindicator of reactive oxygen species (ROS) formation after exposure
ofHIT-T15 cells or isolated mouse pancreatic islets to MeHg
significantlyincreased ROS levels. MeHg could also suppress insulin
secretion in HIT-T15cells and isolated mouse pancreatic islets. After 24 h
of exposure to MeHg,HIT-T15 cells had a significant increase in mercury
levels with adose-dependent manner. Moreover, MeHg displayed several
features of cellapoptosis including an increase of the sub-G1 population and
annexin-Vbinding. Treatment of HIT-T15 cells with MeHg resulted in
disruption of themitochondrial membrane potential and release of cytochrome
c from themitochondria to the cytosol and activation of caspase-3.
AntioxidantN-acetylcysteine effectively reversed the MeHg-induced cellular
responses.Altogether, our data clearly indicate that MeHg-induced oxidative
stresscauses pancreatic beta-cell apoptosis and dysfunction.PMID: 16918248
[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/16764493?ordinalpos=9&itool=Entrez...

J Prev Med Pub Health. 2006 May;39(3):199-204.[Mercuric chloride induces
apoptosis in MDCK cells][Article in Korean]Lee JH, Youm JH, Kwon
KS.Department of Preventive Medicine and Public Health, School of
MedicineChonbuk National University.OBJECTIVES: Mercury is a hazardous
organ-specific environmental contaminant.It exists in a wide variety of
physical and chemical states, each of whichhas unique characteristics for
the target organ specificity. Exposure tomercury vapor and to organic
mercury compounds specifically affects the CNS,while the kidney is the
target organ for inorganic Hg compounds. METHODS: Inthis study, mercury
chloride (HgCl2) was studied in a renal derived cellsystem, i.e., the
tubular epithelial Madin-Darby canine kidney (MDCK) cellline, which has
specific sensitivity to the toxic effect of mercury. MDCKcells were cultured
for 6-24 hr in vitro in various concentrations (0.1-100M) of HgCl2, and the
markers of apoptosis or cell death were assayed,including DNA fragmentation,
caspase-3 activity andwestern blotting ofcytochrome c. The influence of the
metal on cell proliferation and viabilitywere evaluated by the conventional
MTT test. RESULTS: The cell viability wasdecreased in a time and
concentration dependent fashion: decreases werenoted at 6, 12 and 24 hr
after HgCl2 exposure. The increases of DNAfragmentation were also observed
in the concentrations from 0.1 to 10 M ofHgCl2 at 6 hr after exposure.
However, we could not observe DNAfragmentation in the concentrations more
than 25 M because the cells rapidlyproceeded to necrotic cell death. The
activation of caspase-3 was alsoobserved at 6 hr exposure in the HgCl2
concentrations from 0.1 to 10 M. Therelease of cytochrome c from the
mitochondria into the cytosol, which is aninitiator of the activation of the
caspase cascade, was also observed in theHgCl2-treated MDCK cells.
CONCLUSIONS: These results suggest that theactivation of caspase-3 was
involved in HgCl2-induced apoptosis. The releaseof cytochrome c from the
mitochondria into the cytosol was also observed inthe HgCl2-treated MDCK
cells. These findings indicate that in MDCK cells,HgCl2 is a potent inducer
of apoptosis via cytochrome c release from themitochondria.PMID: 16764493
[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/16457873?ordinalpos=11&itool=Entre...

Sci Total Environ. 2006 Aug 1;366(2-3):627-37. Epub 2006 Feb 7Accumulation
of mercury, selenium and their binding proteins in porcinekidney and liver
from mercury-exposed areas with the investigation of theirredox
responses.Chen C, Qu L, Zhao J, Liu S, Deng G, Li B, Zhang P, Chai Z.Key
Laboratory of Nuclear Analytical Techniques and Institute of High
EnergyPhysics, Chinese Academy of Sciences, P. O. Box 918, Beijing 100039,
PRChina. chen...@mail.ihep.ac.cnThe subcellular localization of Se and Hg
and their cytosolic bindingproteins, including cellular oxidative status, in
porcine liver and kidneyhave been studied by using samples from a chronic
Hg-contaminated area and anon-Hg-contaminated area. Coaccumulation and
redistribution of Se and Hg insubcellular fractions due to mercury exposure
were found. The Hg and Seconcentrations in tissues from Hg-exposed porcine
were 80 fold and 5-20 foldhigher than controls, respectively. Interestingly,
the retention of both Seand Hg increased 10% in mitochondria, while
decreased 10% in cytosol ofHg-exposed pig liver. Mercury was mainly in the
form of MTs in the cytosolof the non-Hg-exposed porcine kidney. MT binds Hg
in the cytosol withlimited capacity, and the rest Hg was redistributed to
the high molecularweight (MW) proteins (80-100 kDa) in the Hg-exposed group.
Thecoaccumulation of Hg and Se was also found in high MW proteins, where
theirmolar ratio tended to be 1:1. Moreover, the Se-containing polypeptides
(3-6kDa) increased significantly both in hepatic and renal cytosol of
theHg-exposed pigs. Se-dependent GSH-Px and SOD activity were increased to
copewith Hg-induced oxidative stress. In previous studies, the roles of Se
andMTs were generally taken into account separately; we discussed
theircombining roles in the case of high Hg exposure. The present results
werebeneficial to understand the existing states of Hg in vivo and evaluate
theinteraction of toxic and essential elements.PMID: 16457873 [PubMed -
indexed for
MEDLINE]http://www.ncbi.nlm.nih.gov/pubmed/17182013?ordinalpos=1&itool=Entr­ezSystem2.PE
ntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum1:
Brain Res. 2007 Feb 2;1131(1):1-10. Epub 2006 Dec 19.  LinksMethylmercury
induces oxidative injury, alterations in permeability andglutamine transport
in cultured astrocytes.Yin Z, Milatovic D, Aschner JL, Syversen T, Rocha JB,
Souza DO, Sidoryk M,Albrecht J, Aschner M.Department of Pediatrics,
Vanderbilt University Medical Center, TN, USA.The neurotoxicity of high
levels of methylmercury (MeHg) is well establishedboth in humans and
experimental animals. Astrocytes accumulate MeHg and playa prominent role in
mediating MeHg toxicity in the central nervous system(CNS). Although the
precise mechanisms of MeHg neurotoxicity areill-defined, oxidative stress
and altered mitochondrial and cell membranepermeability appear to be
critical factors in its pathogenesis. The presentstudy examined the effects
of MeHg treatment on oxidative injury,mitochondrial inner membrane
potential, glutamine uptake and expression ofglutamine transporters in
primary astrocyte cultures. MeHg caused asignificant increase in
F(2)-isoprostanes (F(2)-IsoPs), lipid peroxidationbiomarkers of oxidative
damage, in astrocyte cultures treated with 5 or 10microM MeHg for 1 or 6 h.
Consistent with this observation, MeHg induced aconcentration-dependant
reduction in the inner mitochondrial membranepotential (DeltaPsi(m)), as
assessed by the potentiometric dye,tetramethylrhodamine ethyl ester (TMRE).
Our results demonstrate thatDeltaPsi(m) is a very sensitive endpoint for
MeHg toxicity, sincesignificant reductions were observed after only 1 h
exposure toconcentrations of MeHg as low as 1 microM. MeHg pretreatment (1,
5 and 10microM) for 30 min also inhibited the net uptake of
glutamine((3)H-glutamine) measured at 1 min and 5 min. Expression of the
mRNA codingthe glutamine transporters, SNAT3/SN1 and ASCT2, was inhibited
only at thehighest (10 microM) MeHg concentration, suggesting that the
reduction inglutamine uptake observed after 30 min treatment with lower
concentrationsof MeHg (1 and 5 microM) was not due to inhibition of
transcription. Takentogether, these studies demonstrate that MeHg exposure
is associated withincreased mitochondrial membrane permeability, alterations
inglutamine/glutamate cycling, increased ROS formation and
consequentoxidative injury. Ultimately, MeHg initiates multiple additive
orsynergistic disruptive mechanisms that lead to cellular dysfunction and
celldeath.PMID: 17182013 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/16366737?ordinalpos=2&itool=Entr­ezSystem2.
PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSumNeurodegenerati­on from
mitochondrial insufficiency: nutrients, stem cells,growth factors, and
prospects for brain rebuilding using integrativemanagement.Kidd
PM.University of California, Berkeley, USA. dock...@dockidd.comDegenerative
brain disorders (neurodegeneration) can be frustrating for bothconventional
and alternative practitioners. A more comprehensive,integrative approach is
urgently needed. One emerging focus for interventionis brain energetics.
Specifically, mitochondrial insufficiency contributesto the etiopathology of
many such disorders. Electron leakages inherent tomitochondrial energetics
generate reactive oxygen free radical species thatmay place the ultimate
limit on lifespan. Exogenous toxins, such as mercuryand other environmental
contaminants, exacerbate mitochondrial electronleakage, hastening their
demise and that of their host cells. Studies of thebrain in Alzheimer's and
other dementias, Down syndrome, stroke, Parkinson'sdisease, multiple
sclerosis, amyotrophic lateral sclerosis, Huntington'sdisease, Friedreich's
ataxia, aging, and constitutive disorders demonstrateimpairments of the
mitochondrial citric acid cycle and oxidativephosphorylation (OXPHOS)
enzymes. Imaging or metabolic assays frequentlyreveal energetic
insufficiency and depleted energy reserve in brain tissuein situ.
Orthomolecular nutrients involved in mitochondrial metabolismprovide
clinical benefit. Among these are the essential minerals and the Bvitamin
group; vitamins E and K; and the antioxidant and energetic
cofactorsalpha-lipoic acid (ALA), ubiquinone (coenzyme Q10; CoQ10), and
nicotinamideadenine dinucleotide, reduced (NADH). Recent advances in the
area of stemcells and growth factors encourage optimism regarding brain
regeneration.The trophic nutrients acetyl L-carnitine (ALCAR),
glycerophosphocholine(GPC), and phosphatidylserine (PS) provide
mitochondrial support andconserve growth factor receptors; all three
improved cognition indouble-blind trials. The omega-3 fatty acid
docosahexaenoic acid (DHA) isenzymatically combined with GPC and PS to form
membrane phospholipids fornerve cell expansion. Practical recommendations
are presented forintegrating these safe and well-tolerated orthomolecular
nutrients into acomprehensive dietary supplementation program for brain
vitality andproductive lifespan.PMID: 16366737 [PubMed - indexed for
MEDLINE]