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Showing posts with label Aluminum. Show all posts
Showing posts with label Aluminum. Show all posts

Tuesday, April 24, 2012

Chemtrails, nanoaluminum, neurodegenerative and neurodevelopmental effects (mr. professor, you hev dimenticàid the neurodelirium effects)


http://tankerenemy.blogspot.it/2012/04/chemtrails-nanoaluminum.html

Chemtrails, nanoaluminum, neurodegenerative and neurodevelopmental effects

In a recent article, Prof. L. Blaylock warns the people, pointing out the serious dangers associated with the inhalation of aluminum, one of the many metals contained in the so-called "chemtrails": if we are not able to stop these criminal operations, the health of humans and the environmental equilibrium shall be ["SHALL BE"??? STRACATALOL]  irreversibly compromised. We thank Ron for the notice. (LOL)

The Internet is littered with stories of “chemtrails” and geoengineering to combat “global warming” and until recently I took these stories with a grain of salt. One of the main reasons for my skepticism was that I rarely saw what they were describing in the skies. But over the past several years I have notice a great number of these trails and I have to admit they are not like the contrails I grew up seeing in the skies. They are extensive, quite broad, are laid in a definite pattern and slowly evolve into artificial clouds. Of particular concern is that there are now so many­dozens every day are littering the skies.

My major concern is that there is evidence that they are spraying tons of nanosized aluminum compounds. It has been demonstrated in the scientific and medical literature that nanosized particles are infinitely more reactive and induce intense inflammation in a number of tissues. Of special concern is the effect of these nanoparticles on the brain and spinal cord, as a growing list of neurodegenerative diseases, including Alzheimer’s dementia, Parkinson’s disease and Lou Gehrig’s disease (ALS) are strongly related to exposure to environmental aluminum.
Nanoparticles of aluminum are not only infinitely more inflammatory, they also easily penetrate the brain by a number of routes, including the blood and olfactory nerves (the smell nerves in the nose). Studies have shown that these particles pass along the olfactory neural tracts, which connect directly to the area of the brain that is not only most effected by Alzheimer’s disease, but also the earliest affected in the course of the disease. It also has the highest level of brain aluminum in Alzheimer’s cases.

The intranasal route of exposure makes spraying of massive amounts of nanoaluminum into the skies especially hazardous, as it will be inhaled by people of all ages, including babies and small children for many hours. We know that older people have the greatest reaction to this airborne aluminum. Because of the nanosizing of the aluminum particles being used, home filtering system will not remove the aluminum, thus prolonging exposure, even indoors.
In addition to inhaling nanoaluminum, such spraying will saturate the ground, water and vegetation with high levels of aluminum. Normally, aluminum is poorly absorbed from the GI tract, but nanoaluminum is absorbed in much higher amounts. This absorbed aluminum has been shown to be distributed to a number of organs and tissues including the brain and spinal cord. Inhaling this environmentally suspended nanoaluminum will also produce tremendous inflammatory reaction within the lungs, which will pose a significant hazard to children and adults with asthma and pulmonary diseases.

I pray that the pilots who are spraying this dangerous substance fully understand that they are destroying the life and health of their families as well. This is also true of our political officials. Once the soil, plants and water sources are heavily contaminated there will be no way to reverse the damage that has been done.
Steps need to be taken now to prevent an impending health disaster of enormous proportions if this project is not stopped immediately. Otherwise we will see an explosive increase in neurodegenerative diseases occurring in adults and the elderly in unprecedented rates as well as neurodevelopmental disorders in our children. We are already seeing a dramatic increase in these neurological disorders and it is occurring in younger people than ever before.

References

1.Win-Shwe T-T, Fujimaki H. Nanoparticles and Neurotoxicity. In J Mol Sci 2011;12:6267-6280.
2.Krewski D et al. Human health rRevell PA. The biological effects of nanoparticles. Risk assessment for aluminum, aluminum oxide, and aluminum hydroxide. J Toxicol Environ Health B Crit Rev 2007;10(suppl 1): 1-269.
3.Blaylock RL. Aluminum induced immunoexcitotoxicity in neurodevelopmental and neurodegenerative disorders. Curr Inorg Chem 2012;2:46-53.
4.Tomljenovic L. Aluminum and Alzheimer’s disease: after a century, is their a plausible link. J Alzheimer’s Disease 2011;23:567-598.
5.Perl DP, Good PF. Aluminum, Alzheimer’s Disease, and the olfactory system. Ann NY Acad Sci 1991;640:8-13.
6.Shaw CA, Petrik MS. Aluminum hydroxide injections lead to motor deficits and motor neuron degeneration. J Inorg Biochem 2009;103:1555-1562.
7.Braydich-Stolie LK et al. Nanosized aluminum altered immune function. ACS Nano 2010:4:3661-3670.
8.Li XB et al. Glia activation induced by peripheral administration of aluminum oxide nanoparticles in rat brains. Nanomedicine 2009;5:473-479.
9.Exley C, house E. Aluminum in the human brain. Monatsh Chem 2011;142:357-363.
10.Nayak P, Chatterjee AK. Effects of aluminum exposure on brain glutamate and GABA system: an experimental study in rats. Food Chem Toxicol 2001;39:1285-1289.
11.Tsunoda M, Sharma RP. Modulation of tumor necrosis factor alpha expression in mouse brain after exposure to aluminum in drinking water. Arch Toxicol 1999;73:419-426.
12.Matyja E. Aluminum changes glutamate –mediated neurotoxicity in organotypic cultures of rat hippocampus. Folia Neuropathol 2000;38:47-53.
13.Walton JR. Aluminum in hippocampal neurons from human with Alzheimer’s disease. Neurotoxicology 2006;27:385-394.
14.Walton JR. An aluminum-based rat model for Alzheimer’s disease exhibits oxidative damage, inhibition of PP2A activity, hyperphosphorylated tau and granulovacuolar degeneration. J Inorg Biochem 2007;101:1275-1284.
15.Becaria A et al. Aluminum and copper in drinking water enhance inflammatory or oxidative events specifically in brain. J Neuroimmunol 2006;176:16-23.
16.Exley C. A molecular mechanism for aluminum-induced Alzheimer’s disease. J Inorg Biochem 1999;76:133-140.
17.Exley C. The pro-oxidant activity ofnaluminum. Free Rad Biol Med 2004;36:380-387.

Russell L. Blaylock, M.D.
Visiting Professor Biology
Belhaven University
Theoretical Neurosciences Research, LLC

Source: thenhf.com



"Blaylock has endorsed views inconsistent with the scientific consensus, including that food additives such as aspartame and monosodium glutamate (MSG) are excitotoxic in normal doses and that the H1N1 influenza (swine flu) vaccine carries more risk than swine flu itself."
Please, read also notes.

the taigher of the malor


ps: backup http://backupurl.com/7418ds

Monday, September 5, 2011

Ischemic stroke hospitalizations increase among children and young adults in U.S.A.

http://tankerenemy.blogspot.com/2011/09/ischemic-stroke-hospitalizations.html

Ischemic stroke hospitalizations increase among children and young adults in U.S.A.

The article that we publish [forse voleva dire we puBBlish] is about the increase in hospitalizations among people aged 15 to 44 for ischemic stroke. The real cause of this increase is not linked to tobacco and alcool, but to geo-engineering: in fact the problem dates from 1995, the year in which chemtrails became a daily poison for people, animals and plants.

Hospitalizations for stroke increased among children and young adults in the U.S. over 14 years, researchers have found. Investigators from the U.S. Centers for Disease Control and Prevention in Atlanta reported the increase in hospitalizations among people aged 15 to 44 for ischemic stroke, which occurs when a blood vessel supplying the brain is blocked by a clot or by a build-up of fatty deposits called plaque. Stroke is the third leading cause of death in the U.S. and 87 per cent of all cases are attributed to ischemic stroke, according to the American Heart Association.Between 1995 and 2008, hospitalizations for ischemic stroke among those aged five to 14 increased 31 per cent. The rate increased from 3.2 hospitalizations per 10,000 to 4.2 hospitalizations per 10,000.

Among those aged 15 to 34, hospitalizations increased 30 per cent from 5.0 hospitalizations per 10,000 to 6.5 per 10,000, researchers found, informs CBC.ca. In the same 14-year period researchers noted a rise in stroke among youth, they discovered that diabetes, cholesterol and tobacco use "has also increased in adolescents and young adults experiencing stroke," said lead researcher Dr. Mary George, a medical officer in CDC's Division for Heart Disease and Stroke Prevention.

"I was surprised to see the extent of cardiovascular risk factors in this young population," she said. The focus on controlling these risks has usually been among older adults, George said. "We really need to encourage people to lead healthy lifestyles from the time they are very young," she said. "Stroke is largely preventable and eating a healthy diet, getting regular physical activity, avoiding tobacco and alcohol abuse can go a long way to prevent stroke", reports Hispanically Speaking News.

A healthy diet and lifestyle habits can help prevent the onset of stroke and other heart diseases. This includes eating plenty of fruits and vegetables, less salt and saturated fats, not smoking and engaging in regular physical activity.The National Stroke Foundation (Australia) also recommends that people should learn to recognize the signs of strokes, as early detection can make a vast difference in outcome. These include severe headache, changes in speech such as slurring, losing consciousness or feeling dizzy or light-headed, says to PRWire.

Source: Pravda.ru


Saturday, February 6, 2010

Metals and pathologies

http://tankerenemy.blogspot.com/2010/01/metals-and-pathologies.html

Metals and pathologies

Med Hypotheses. 2004;63(5):793-809.

Elevated levels of ferrimagnetic metals in foodchains supporting the Guam cluster of neurodegeneration: do metal nucleated crystal contaminants [corrected] evoke magnetic fields that initiate the progressive pathogenesis of neurodegeneration?
Purdey M.


High Barn Farm, Elworthy, Taunton, Somerset TA4 3PX, UK. tsepurdey@aol.com

Elevated levels of aluminium (Al), strontium (Sr), barium (Ba), iron (Fe), manganese (Mn) cations - combined with deficiencies of magnesium (Mg)/calcium (Ca) - have been observed in the foodchains that traditionally support the Chamorro populations affected by high incidence clusters of Alzheimer (AD), Parkinson-like (PD), motor neurone diseases and multiple sclerosis on the island of Guam. Soils drawn from the cluster region demonstrated an excessive fivefold increase in 'magnetic susceptibility' readings in relation to soils from disease free adjoining regions. A multifactorial aetiological hypothesis is proposed that pivots upon the combined exposure to high levels of natural/industrial sources of ferrimagnetic/ferroelectric compounds incorporating Al, Fe, Mn, Sr, Ba (e.g., via yam/seafood consumption or exposure to world war 2 (WW2) munitions) and to low levels of Mg/Ca in all S. Pacific locations where these clusters of neurodegenerative disease have simultaneously erupted. Once gut/blood brain barrier permeability is impaired, the increased uptake of Al, Fe, Sr, Ba, or Mn into the Mg/Ca depleted brain leads to rogue metal substitutions at the Mg/Ca vacated binding domains on various enzyme/proteoglycan groups, causing a broad ranging disruption in Mg/Ca dependent systems - such as the glutamine synthetase which prevents the accumulation of neurotoxic glutamate. The rogue metals chelate sulphate, disrupting sulphated-proteoglycan mediated inhibition of crystal proliferation, as well as its regulation of the Fibroblast growth factor receptor complex which disturbs the molecular conformation of those receptors and their regulation of transphosphorylation between intracellular kinase domains; ultimately collapsing proteoglycan mediated cell-cell signalling pathways which maintain the growth and structural integrity of the neuronal networks. The depression of Mg/Ca dependent systems in conjunction with the progressive ferrimagnetisation of the CNS due to an overload of rogue ferroelectric/ferrimagnetic metal contaminants, enables 'seeding' of metal-protein crystalline arrays that can proliferate in the proteoglycan depleted brain. The resulting magnetic field emissions initiate a free radical mediated progressive pathogenesis of neurodegeneration. The co-clustering of these various types of disease in select geographical pockets around the world suggests that all of these conditions share a common early life exposure to ferromagnetic metal nucleating agents in their multifactorial aetiology. Factors such as individual genetics, the species of metal involved, etc., dictate which specific class of disease will emerge as a delayed neurotoxic response to these environmental insults.

******

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.

Birchall Centre for Inorganic Chemistry and Materials Science, Lennard-Jones Laboratories, Keele University, Staffordshire, UK. c.exley@chem.keele.ac.uk

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 <> 0.05). 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.


Source: http://www.ncbi.nlm.nih.gov/