This is a far more honest and appropriate video regarding
the vaccine truth situation, editor Costner. Take a look. THIS video is far better than yours!!!!
Animated Video Showing a Typical Conversation Between a
Mother and her Doctor Regarding Autistic Child
VacFacts.info
The Vaccine Damage - Science
More Information:
Thimerosal - MSDS - (Material Safety Data Sheet) A flu vaccine ingredient unless you ask for a single dose vial.
Mother Explains Vaccine Injury, Deteriorating Health, Autism, and Why Not To Vaccinate
Autistic Child Fully Recovered with Biomedical Treatment for
Autism - Holly Riley
Autism Is A Medical Problem And There Is Proven, Effective
Medical Treatment - Dr. Stoller, MD
C’mon Sheeple! Just Hand Your Kids Over to the Doctors.
Doctor in his indoctrinated ignorance attempts to give child 14 vaccines in one day, and when the mother refuses he threatens to all child protective services, ranting ignoranmtly, "your going to kill your child".
http://gaia-health.com/gaia-blog/2012-08-02/cmon-sheeple-just-hand-your-kids-over-to-the-doctors/
CDC Schedules
http://www.cdc.gov/vaccines/schedules/
Vaccine Ingredients
http://www.novaccine.com/vaccine-ingredients/
http://www.informedchoice.info/cocktail.html
Vaccine Package Inserts
http://www.vaccinesafety.edu/package_inserts.htm
Aluminium in vaccines can cause serious polio-like damage, damage motorneuron cells and cause brain damage – possibly leading to Alzheimer’s and other forms of dementia and increasing the risk in children of Autistic Spectrum
Disorders.
From the Transcripts of the US Vaccines and Related
Biological Advisory Committee Meeting (VRBAC) and Scientific Papers
The Experts admitted Ignorance
http://albamora.com/joanmorahomeopatia/pdf/Aluminum%20in%20Vaccines%20-from%20forthcoming%20book.pdf
ASD and Aluminum Toxicity
Brain Res. 2006 Oct 20;1116(1):215-21. Epub 2006 Aug 30.
Aluminum complexing enhances amyloid beta protein
penetration of blood-brain barrier.
Banks WA, Niehoff ML, Drago D, Zatta P.
Source:GRECC, Veterans Affairs Medical Center-St. Louis and
Saint Louis University School of Medicine, Division of Geriatrics, Department
of Internal Medicine, WAB, 915 N. Grand Blvd, St. Louis, MO 63106, USA.
Abstract
A significant co-morbidity of Alzheimer's disease and
cerebrovascular impairment suggests that cerebrovascular dysregulation is an
important feature of dementia. Amyloid beta protein (Abeta), a relevant risk
factor in Alzheimer's disease, has neurotoxic properties and is thought to play
a critical role in the cognitive impairments. Previously, we demonstrated that
the 42mer of Abeta (Abeta42) complexed with aluminum (Al-Abeta42) is much more
cytotoxic than non-complexed Abeta42. The level of Abeta in the brain is a
balance between synthesis, degradation, and fluxes across the blood-brain
barrier (BBB). In the present paper, we determined whether complexing with
aluminum affected the ability of radioactively iodinated Abeta to cross the in
vivo BBB. We found that the rates of uptake of Al-Abeta42 and Abeta42 were
similar, but that Al-Abeta42 was sequestered by brain endothelial cells much
less than Abeta42 and so more readily entered the parenchymal space of the
brain. Al-Abeta42 also had a longer half-life in blood and had increased
permeation at the striatum and thalamus. Brain-to-blood transport was similar
for Al-Abeta42 and Abeta42. In conclusion, complexing with aluminum affects
some aspects of blood-to-brain permeability so that Al-Abeta42 would have more
ready access to brain cells than Abeta42.
--------------------
J Cell Biochem. 2004 Dec 15;93(6):1267-71.
Aluminum decreases the glutathione regeneration by the
inhibition of NADP-isocitrate dehydrogenase in mitochondria.
Murakami K, Yoshino M.
Source
Department of Biochemistry, Aichi Medical University School
of Medicine, Nagakute, Aichi 480-1195, Japan.
Aluminum decreases the glutathione regeneration by the
inhibition of NADP-isocitrate dehydrogenase in mitochondria
------------------------
Mult Scler. 2006 Oct;12(5):533-40.
Elevated urinary excretion of aluminium and iron in multiple
sclerosis.
Exley C, Mamutse G, Korchazhkina O, Pye E, Strekopytov S,
Polwart A, Hawkins C.
Source:Birchall Centre for Inorganic Chemistry and Materials
Science, Lennard-Jones Laboratories, Keele University, Staffordshire, UK. c.exley@chem.keele.ac.uk
Abstract
Multiple sclerosis (MS) is a chronic, immune-mediated,
demyelinating disease of the central nervous system of as yet unknown
aetiology. A consensus of opinion has suggested that the disorder is the result
of an interplay between environmental factors and susceptibility genes. We have
used a battery of analytical techniques to determine if the urinary excretion
of i) markers of oxidative damage; ii) iron and iii) the environmental toxin
aluminium and its antagonist, silicon, are altered in relapsing-remitting
(RRMS) and secondary progressive MS (SPMS). Urinary concentrations of oxidative
biomarkers, MDA and TBARS, were not found to be useful indicators of
inflammatory disease in MS. However, urinary concentrations of another
potential marker for inflammation and oxidative stress, iron, were
significantly increased in SPMS (P<0.01) and insignificantly increased in
RRMS (P>0.05). Urinary concentrations of aluminium were also significantly
increased in RRMS (P<0.001) and SPMS (P <0.05) such that the levels of
aluminium excretion in the former were similar to those observed in individuals
undergoing metal chelation therapy. The excretion of silicon was lower in MS
and significantly so in SPMS (P<0.05). Increased excretion of iron in urine
supported a role for iron dysmetabolism in MS. Levels of urinary aluminium
excretion similar to those seen in aluminium intoxication suggested that
aluminium may be a hitherto unrecognized environmental factor associated with
the aetiology of MS. If aluminium is involved in MS then an increased dietary
intake of its natural antagonist, silicon, might be a therapeutic option.
Aluminum decreases the glutathione regeneration by the
inhibition of NADP-isocitrate dehydrogenase in mitochondria.
Murakami K, Yoshino M.
Source
Department of Biochemistry, Aichi Medical University School
of Medicine, Nagakute, Aichi 480-1195, Japan.
Aluminum decreases the glutathione regeneration by the
inhibition of NADP-isocitrate dehydrogenase in mitochondria
J Inorg Biochem. 2007 Sep;101(9):1275-84. Epub 2007 Jun 12.
An aluminum-based rat model for Alzheimer's disease exhibits
oxidative damage, inhibition of PP2A activity, hyperphosphorylated tau, and
granulovacuolar degeneration.
Walton JR.
Source: Australian Institute for Biomedical Research,
Sydney, NSW, Australia.
Abstract
In Alzheimer's disease (AD), oxidative damage leads to the
formation of amyloid plaques while low PP2A activity results in
hyperphosphorylated tau that polymerizes to form neurofibrillary tangles. We
probed these early events, using brain tissue from a rat model for AD that
develops memory deterioration and AD-like behaviors in old age after
chronically ingesting 1.6 mg aluminum/kg bodyweight/day, equivalent to the high
end of the human dietary aluminum range. A control group consumed 0.4 mg
aluminum/kg/day. We stained brain sections from the cognitively-damaged rats
for evidence of amyloid plaques, neurofibrillary tangles, aluminum, oxidative
damage, and hyperphosphorylated tau. PP2A activity levels measured 238.71+/-17.56
pmol P(i)/microg protein and 580.67+/-111.70 pmol P(i)/microg protein
(p<0.05) in neocortical/limbic homogenates prepared from cognitively-damaged
and control rat brains, respectively. Thus, PP2A activity in
cognitively-damaged brains was 41% of control value. Staining results showed:
(1) aluminum-loading occurs in some aged rat neurons as in some aged human
neurons; (2) aluminum-loading in rat neurons is accompanied by oxidative
damage, hyperphosphorylated tau, neuropil threads, and granulovacuolar degeneration;
and (3) amyloid plaques and neurofibrillary tangles were absent from all rat
brain sections examined. Known species difference can reasonably explain why
plaques and tangles are unable to form in brains of genetically-normal rats
despite developing the same pathological changes that lead to their formation
in human brain. As neuronal aluminum can account for early stages of plaque and
tangle formation in an animal model for AD, neuronal aluminum could also
initiate plaque and tangle formation in humans with AD.
KURODA, Y. and KAWAHARA, M. Aggregation of Amyloid
-Protein and Its Neurotoxicity: Enhancement by
Aluminum and Other Metals.
Brain Res Bull. 2001 May 15;55(2):211-7.
Effects of aluminum on the neurotoxicity of primary cultured
neurons and on the aggregation of beta-amyloid protein.
Kawahara M, Kato M, Kuroda Y.
-----------------
Toxicol In Vitro. 2007 Feb;21(1):16-24. Epub 2006 Aug 5.
Aluminum toxicity triggers the nuclear translocation of
HIF-1alpha and promotes anaerobiosis in hepatocytes.
Mailloux RJ, Appanna VD.
Source:Department of Chemistry and Biochemistry, Laurentian
University, Sudbury, Ont., Canada P3E 2C6.
Excerpted: HPLC analyses confirmed increased glycolytic ATP
production in Al-exposed hepatocytes. These findings reveal the ability of Al
to create a hypoxic environment that promotes the translocation of HIF-1alpha
to the nucleus and stimulates the anaerobic metabolism of D-glucose.
-----------------
J Trace Elem Med Biol. 2001;15(2-3):139-41.
Inhibitory effect of aluminum on dopamine beta-hydroxylase
from bovine adrenal gland.
Excerpt: Aluminum is a well known neurotoxic agent that is
overaccumulated in the substantia nigra of patients affected by Parkinson's
disease as well as in certain cerebral areas of other neurodegenerative
pathologies such as Alzheimer's disease. Although the role of aluminum in
neurodegenerative diseases is yet to be clearly understood, the metal ion is
known to substantially alter the activity of several key enzymes in the central
nervous system.
The potential implications of aluminum in the
etiopathogenesis of neurological disorders are discussed.
-------------
[Toxic effects of aluminum on human embryonic cerebral
neurocytes in vitro studies].
Huang G, Kang J, Zhang W, Liu L, Yu M, Mei M, Dong Y.
Excerpt: CONCLUSIONS:
The growth, development and function of human embryonic
cerebral neurocytes was inhibited in the high Al group. The neurotoxicity of Al
may be caused by lipid peroxidation and the damage of cell membrane.
--------------
J Inorg Biochem. 2003 Sep 15;97(1):132-42.
Aluminium-induced impairment of Ca2+ modulatory action on
GABA transport in brain cortex nerve terminals.
Cordeiro JM, Silva VS, Oliveira CR, Gonçalves PP.
Source:Centre for Environmental and Marine Studies,
Department of Biology, University of Aveiro, 3810-193 Aveiro, Portugal.
Excerpt: In conclusion, aluminium-induced relief of Ca(2+)
modulatory action on GABA transporter may contribute significantly to modify
GABAergic signalling during neurotoxic events in response to aluminium
exposure.
---------------
J Biochem Mol Toxicol. 2006;20(4):198-208.
Aluminum toxicity elicits a dysfunctional TCA cycle and
succinate accumulation in hepatocytes.
Mailloux RJ, Hamel R, Appanna VD.
Source:Department of Chemistry and Biochemistry, Laurentian
University, Sudbury, Ontario, Canada, P3E 2C6.
In conclusion, these results suggest that Al toxicity
promotes a dysfunctional TCA cycle and impedes ATP production, events that may
contribute to various Al-induced abnormalities.
---------------
Aluminum modulates brain amyloidosis through oxidative
stress in APP transgenic mice.
Praticò D, Uryu K, Sung S, Tang S, Trojanowski JQ, Lee VM.
Source: Center for Experimental Therapeutics and Department
of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia,
Pennsylvania
Excerpt: These results indicate that dietary Al can modulate
in vivo AD-like amyloidosis in Tg2576 by increasing brain oxidative stress.
Toxicol Ind Health. 2006 Feb;22(1):39-46.
Possible peripheral markers for chronic aluminium toxicity
in Wistar rats.
Kaur A, Gill KD.
Source:Department of Biochemistry, Post Graduate Institute
of Medical Education and Research, Chandigarh, India.
Abstract
This investigation gives detailed analysis of peripheral
marker enzymes as well as neurobehavioral tests following chronic aluminium
(Al) exposure (10 mg/kg b.w. for 12 weeks intragastrically). We observed a
significant decrease in the levels of serum cholinesterase after toxicity. The
enzymatic activity of cytochrome oxidase (CO), the terminal enzyme of the
electron transport chain, was significantly diminished and that of
glucose-6-phosphate dehydrogenase (G-6-PD) was significantly enhanced.
Neuromuscular co-ordination was assessed using motor and memory function tests.
Deficits were observed suggesting a probable model for chronic Al
neurotoxicity.
--------------------------------
J Cell Biochem. 2004 Dec 15;93(6):1267-71.
Aluminum decreases the glutathione regeneration by the
inhibition of NADP-isocitrate dehydrogenase in mitochondria.
Murakami K, Yoshino M.
Source:Department of Biochemistry, Aichi Medical University
School of Medicine, Nagakute, Aichi 480-1195, Japan.
Abstract
Effect of aluminum on the NADPH supply and glutathione
regeneration in mitochondria was analyzed. Reduced glutathione acted as a
principal scavenger of reactive oxygen species in mitochondria. Aluminum
inhibited the regeneration of glutathione from the oxidized form, and the
effect was due to the inhibition of NADP-isocitrate dehydrogenase the only
enzyme supplying NADPH in mitochondria. In cytosol, aluminum inhibited the
glutathione regeneration dependent on NADPH supply by malic enzyme and
NADP-isocitrate dehydrogenase, but did not affect the glucose 6-phosphate
dehydrogenase dependent glutathione formation. Aluminum can cause oxidative
damage on cellular biological processes by inhibiting glutathione regeneration
through the inhibition of NADPH supply in mitochondria, but only a little
inhibitory effect on the glutathione generation in cytosol.
--------------------------------
J Enzyme Inhib Med Chem. 2004 Aug;19(4):317-25.
The effect of cations on the amidase activity of human
tissue kallikrein: 1-linear competitive inhibition by sodium, potassium,
calcium and magnesium. 2-linear mixed inhibition by aluminium.
De Sousa MO, Santoro MM, De Souza Figueiredo AF.
Source:Departamento de Análises Clínicas e Toxicológicas,
Faculdade de Farmácia, Universidade Federal de Minas Gerais, C. P. 689,
30123-970 Belo Horizonte, MG, Brazil.
Excerpt: Aluminium is not a physiological cation, but is a
known neurotoxicant for animals and humans. The neurotoxic actions of aluminium
may relate to neuro-degenerative diseases.
Proc Soc Exp Biol Med. 2000 Apr;223(4):397-402.
Aluminum increases levels of beta-amyloid and ubiquitin in
neuroblastoma but not in glioma cells.
Excerpted: These data suggest that one of the mechanisms by
which Al may play a role in AD is by promoting the formation of Abeta and
ubiquitin in neurons.
The MMR vaccine is made by use of aborted fetal tissue; more
specifically, MRC-5 and WI-38.
Computational Detection of Homologous Recombination Hotspots
in X-Chromosome Autism-Associated Genes
Vaccine Ingredients:
Here is a little more information, and a list of vaccines
that have been made with human diploid cells, (shocking).
Vaccines, Abortion, & Fetal Tissue
"Designer" Cells as Substrates, (What the FDA
clearly knows)
for the Manufacture of Viral Vaccines
How would THIS be possible, if all the vaccines are actually
purified during that said step process? What has actually been improved since
the days of SV-40 contasmination in the polio vaccines? Not much, it surely
does not appear to be/
Gardasil Vaccine Found to be Contaminated
SEPTEMBER 10, 2011
Gardasil victim found to have HPV DNA in her blood 2 Years
Post-Vaccination
13 different vaccine vials – 13 different lots of Gardasil
from around the world tested
Results – 100% contamination with HPV Recombinant DNA.
Contaminated Gardasil Vaccine May Be Infectious –
Potentially Causing Millions More to Become Sick via Blood Transference – Merck
Doctor Admits Contaminant Does Not Belong in the Vaccine
Gardasil Vaccine rDNA Introduced at Coroner’s Inquest
Bombshell Interview Reveals DNA Fragments Discovered 6
Months After Vaccination, (Gardasil)
Science 14 February 1975:
Vol. 187 no. 4176 pp. 522-523
DOI: 10.1126/science.187.4176.522
Phage in Live Virus Vaccines: Are They Harmful to People?
And since 1975, do you think anything has changed to correct
that situation? The answer is clearly, no.
Autism Epidemic, Is Foreign DNA in MMR II Vaccine
Responsible? CBCD Suggests CDC Study Microcompetition Theory
The Center for the Biology of Chronic Disease (CBCD)
believes that the cause of the epidemic is the foreign DNA in the MMR II
vaccine.
Foreign DNA Fragments Cause Major Diseases
Vaccine Contamination Pig Virus DNA Found in Rotarix April
7, 2010
Corrupted Rotavirus Vaccine Contains Pig Virus (Part 1 of 6)
http://www.youtube.com/watch?v=d2tqttvy9ig