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The primary toxicological mechanisms of action of the nanoparticles used in nanocomposite materials are mainly due to cholinesterase inhibition. Three main biochemical reactions are responsible for these toxicological effects.

1. Inhibition of cholinesterase activity.

2. Inhibition of neuropathy target esterase (NTE) and development of delayed neuropathy.

3. Release of alkyl groups attached to the phosphorous atom and alkylation’s of macromolecules including RNA and DNA.

On August 2008 Antinuclear Antibody Tests were performed on individual and her result was 25 AU/ml. The ANA test confirms antibodies forming on the cell nuclear membrane. Reviewing the table illustrating the various % cholinesterase inhibitions from initial base line values for the individual, it was determined she had been suffering from severe chronic AChE toxicity as compared to her original baseline functional values for both plasma and RBC parameters. It must be noted, when both values of Plasma and RBC % inhibition are high the individual experiences highly aggressive behavior and when extremely low depression and suicide. The individual has had as high as 59 % cholinesterase inhibition for plasma and 96.4 % for RBC, with a 55.92% annual plasma inhibition value and 61.74 % RBC. Her value from just 3 weeks from July 21, 2009 to August 11, 2009 was 86.2 % cholinesterase inhibition.

During this time period the individual experienced several unique bowel movements that would be diagnosed as fecal incontinence. Thus, confirming as nanoparticles from nano composite materials are broken down and released through FIR Radiant Heat Therapy and appropriate custom nutritional supplementations, AChE values will become a high inhibitory factor. The ANA value, which should be repeated would confirm the alkylation’s of macromolecules of DNA, since ANA is specifically measuring antibodies on the nuclear membrane and the same individual’s had previous genetic testing under toxicogenomics, which showed less Basque values that control groups, which are known to have thicker cellular membranes, thus more superoxide dismutase enzyme would be needed to neutralize neurotoxins. Many of the new nanotubes and nano composite materials would need SOD to neutralize Cu, Cu-C nano contamination via Zn/Cu SOD-1 reactions.

It is important to note that in the formulation of Dragon protein adiptic acid a precursor to aspartame with isoleucine, leucine, lysine and arginine will react with phenylanaline esters.6, 7 Dragon protein has been used as a universal protein to blend DNA plasmids into hydrogels and nanocomposite materials. The individual had measurable amounts of phenylanaline amino acid present in her previous urine tests. The chemical name for aspartame is N-L-alpha-aspartyl-L-phenylalaine-1-methyl ester. Aspartame and its isomers are 160 times sweeter than table sugar.

It is a dipeptide that is prepared from N-benzoyldiester. When this compound is allowed to react with a phenylanaline ester as a food additive or component in many nano synthetic proteins, a displacement of a more reactive compound occurs which is p-nitrophenyl ester? P-nitrophenyl ester is a known excitatory neurotransmitter just as the L-form of aspartic acid is a primary ingredient in the manufacture of aspartame.

Neurotransmitters known to propagate nerve impulses in the receiving neuron are called excitatory neurotransmitters.8 These compounds are synthesized in the nerve’s cell body (the soma) and migrate down the axon to the pre-synaptic terminals. Here they are stored in little packets called vesicles, which fuse with the synaptic membrane like a chain of firecrackers linked to a single fuse. When a depolarizing current (the action potential) is received, these vesicles release their contents into the synaptic cleft.

Phenylalanine is a precursor to the catecholamine neurotransmitters in the brain. Elevated levels in the brain have been associated with seizures and risk of hemorrhagic stroke (when it forms phenyl propanolamine and mixed with aspartame). Aspartic acid can lower seizure thresholds making a seizure more likely in the future. This additive effect of aspartic acid and phenylalanine would significantly increase the likelihood of a seizure, especially under hypoglycemic conditions.

Many different substances effect the transmission of nerve impulse across the synapse and many are falsely called neurotransmitters. Some examples of true excitatory neurotransmitters that relate to an individual exposure are:

• Acetylcholine – peripheral and sensory nerves parasympathetic (maintenance, Diffuse Modulatory excitory forebrain, general excitability, sleep/wake cycle, learning and memory. Disease: Alzheimer’s and multiple sclerosis. MS is increased if an HLA gene mutation exists and Vitamin D deficiency.

• Norepinephrine – sympathetic (stress), Diffuse Modulatory pons, excitory, arousal of brain during interesting external events, increased responsiveness, alarm, attention, readiness, pain, reward, mood, brain metabolism, sleep/wake cycle, and memory. Disease: ADD, ADHA and depression.

• Dopamine – Diffuse Modulatory substantial Nigra, voluntary movement VTA,
Assign value to adaptive behaviors, and attention reward system. Disease:
Schizophrenia, Wain’s cats, novelty seeking, Parkinson’s, and reflective-orderly disorder.

• Serotonin – Diffuse Modulatory inhibition Raphe Nuclei, modulate pain-relief, mood, emotional behavior, satiety, self-esteem, balance, things are OK, sleep/wake, sleep stages, arousal. Disease: bipolar and synesthesia.

• Peptides – opioid; 4-joy, analgesia, and breathing. Disease: Autism.

• Glutamate – 70% of brain neurons, learning, and memory. Disease: epilepsy and nerve cell death.7

Carboxyhemoglobin values and ammonia levels were present. These materials are the degradation products of silicon nanotube/composites and the coatings applied to them as found in Acrylin™ and silicon nanotubes.

It is very important to note that excessive quantities of AChE as shown in the individual’s baseline comparative values accumulate at peripheral ganglionic and central nerve endings (synapses in effector organs, elevated concentrations occur in plasma and intestinal fluid. The intoxication effects connected with the excitement of M- and N-choline receptors (present on nerve terminals of effector organs) are as follows:

• Muscarine effect due to postganglionic cholinergic nerve impulses exciting the M-choline receptors of the lungs, gastrointestinal system, heart, kidneys, sweat glands, pupils and muscles.

• Nicotinic effect on the receptors of ganglionic synapses and motoric plates, the medular part of glandular subrenalis, and carotic nodules.

• Central effect of AChE due to nerve cells or AChE accumulation directly impacting the choline receptors, with parallel inhibition of other enzymes by nano particles or specific cholinesterase inhibitors (pesticides and polymers)
Such as lipase, cholesterol esterase, proteinase, monoaminooxidase, and other nonspecific esterase.

The duration of symptoms depends partly on the rate of AChE reactivation. Spontaneous reactivation depends on the chemical structure attached to the enzyme. The reactivation of the inhibited enzyme can be facilitated considerably by special compounds (oxymes). Several of these compounds have become important antidotes in the treatment of pesticide poisonings.

The inhibition enzyme may also be transformed into a state where no spontaneous reactivation occurs and where oximes are no longer capable of reactivating it. The phenomenon is called “aging” and is characterized by removal of one of the alkyl groups form the phosphoryl groups attached to the enzymes. The rapidity of inhibited AChE aging depends on the chemical nature of the phosphorylating materials. It must be noted that in the materials previously found by other patients exposed to advance nanomicrobic materials/nano particles phosphorus was present in other exposed individuals.

Over the last year the individual has experienced the following classical AChE symptoms with the appropriate site of action (target organ system):

Site of Action Signs and Symptoms

Eyes Increased lacrimation, slight myosis (occasional unequal, later
marked, blurred vision, eye pain when focusing, frontal headaches,
conjunctive hyperemia.

Respiratory System Rhinorrhea, hyperemia (local exposure), tightness in chest,
Prolonged wheezing, bronchoconstriction, increased secretion,
dispnea (not enough air), slight chest pain, cough, edema of the
lung.

Gastrointestinal System Increased salivation, anorexia, vomiting, abdominal
Cramps, epigastric and substernal tightness (cardiospasm) with
“heartburn” and eructation, diarrhea, tenesumus, involuntary
defection (fecal incontinence).

Sweat Glands Increased sweating.

Striated Muscles Easy fatigue, mild weakness, twitching, fasciculation’s (more
Pronounced at the side of exposure), cramps, generalized weakness
including respiratory muscles, dispnea, cyanosis.

Central Nervous System Giddiness, tension, anxiety, tremor, restlessness,
emotional labiality, excessive dreaming, insomnia, nightmares,
headache, tremor, apathy, withdrawal, and depression, slow wave
burst of elevated voltage in EEG (especially on hyperventilation),
drowsiness, concentration difficulty, slow recall, confusion, slurred
speech, ataxia, generalized weakness, coma with absence of reflexes,
Cheyne-Strokes respiration, convulsions, respiratory and circulatory
centers depression, dispnea, fall in blood pressure.

Circulatory System Brandycardia, decreased cardiac output, cardiac arrest,
vasomotor center paralysis.

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