My best contribution is still coming. Despite unbelievers and conspiracy theories galore on geoengineering being real, necessary with anything as large as fighting global warming, my supporters in the effort to stabilize the atmospheric environment with a contingency plan will hopefully prevail because of their very wise long term views for this sustainable, non toxic approach which fully contrasts with present practices.
The skeptics and the supporters are going to see that the science is now really conforming to the thinking that the oxygen compounds are a well documented key to fresh healthy air and cannot be ignored. An early party to this of British Monarchy, who once notified of this plan, promptly advised that it was good science but would not fit into planned efforts and it was both too early and a differing way to deal with the problem that can not really be done at the same time as the ones the leaders have chosen.
Our Schumann cavity which has a frequency of 7 HZ is really the heritage that we must unfortunately fight for. This is what we are a key part of; it is our health, our evolution. Never believe that toxifying you will help you mutate and become a better or stronger being. You do that with your own will. Remember that all the stimulants which we have, from VR to caffeine and things like chemicals and electro-smog need to be limited so that you can expand beyond your limits and live well, and find your dreams. There are hard science experiments happening from HAARP to Laser heating of the clouds, to geoengineering along with all of the drugs, chemicals and predators around us. Most if the intentions are not negative. In 1998 when this science was shelved the inventors of the aerosols were offering them and got funded to help with a real problem. As of 2010 there was far too much injection of synthetic materials and in 2018 the world is almost fully awake to these programs and is poising to try to stop them. They need to be replaced with a non toxic technique. Oxygen is the only one I have found after two decades of research that has a real impact for cooling.
Way back in the onset of the cosmic radiation onset of warming ( the solar system is inside a hot interstellar cloud right now) and our realization that we need to clean up our pollution, I corresponded with many politicians and scientists.
A well meaning public figure, Dr. David Suzuki was very honest about his own professional perspectives. Here are two of the hand written fax notes from him to me:
Here is a letter to Dr. Suziki from 2004, well before the Geoengineering spraying was declassified: I conclude this letter back then with a prediction that metallic spraying would cause warming problems- 12 years of further study has -regrettably-validated this as the June 2017 Temperature report is confirming escalating warming.
Viva Cundliffe,#26-330 Fisher Rd.,Golden, B.C., V0A 1H2,PH/Fax: 250-344-7452,
March 31, 2004
Dear Dr. Suzuki,
I saw your Mikisu –Shell Corporation CBC Documentary tonight and I must say, I may have a solution for this group of citizens and others, which I will succinctly share with you. My issue is the overall atmosphere balance, by using the wisdom from pre-industrial times, and the issue I share with you here is seriously obfuscating it. I have now posted a Clean Cloud Factory web site at: http://www.rockies.net/~gomaster. It is a turnkey facility, which brings pre-industrial natural chemistry back into balance for today. There are several endorsements on the web site. Former President Bill Clinton supports this option, and the Canadian Sustainable Development Technology Fund identified it as a “ Noble Cause”, as does Dr. Michael Prather, who affirms that it will assist in raising the oxidizing capacity of the regional area, which will then reverse industrially induced problems such as droughty, or desertification issues, and stagnated air sheds. I have a second paper in preparation to support this facility’s asset as a remedial and restorative tool.
Recently, to my amazement, a fellow named Jim Phelps came forward publicly to confirm that he has been involved in the U.S. Government’s program to spray metallic oxide aerosols at the Oak Ridge National Lab. This fellow has responded with the honest belief that aerosol spraying is a good measure, and has shared some of the “logic” of it with me. Some highlights are copied for you here:
In a message dated 03/08/2004 9:56:49 AM Eastern Standard Time,
<< Perhaps you would have some suggestions on how to convince the DOE and the ORNL good people to correct and change this path of Aerosol-metal oxide spraying to releasing OH* radicals back into the
Atmosphere, where they are 30% depleted and their absence contributes to a Number of cross cutting problems. Of the many emails you receive after your disclosure, I hope that this one will lead to giving you some satisfaction.
Sincerely, Viva M. Cundliffe >>
Do take note that Chemtrails work on two fronts. There are lots of Synergism effects for each chemicals choice. One is in the air directly and the other is in the soils, grass, and animals. In the air, the metals tend to pull out the acid components and induce clouds and rain. In the soil, the action vector is towards the fluoride-metal complexes. The idea is to complex fluorides with titanium, and cut down the activation of the wrong G-protein sites in cells.
If you notice, we are having increasing problems with prions. These come from problems with BBB becoming permeable due to Ache activations. Fluorides cause these effects, and many pesticides. Part of the chemtrail missions are about cutting this effect down, so all the animals’ health effects won’t be so inclined to infect us humans.
OH may well help with the atmosphere equation. This is a really new science and even the national labs have problems with the predictions of interactions. What are your methods for delivery?
Selling a new method depends strongly on cost advantages. Chemtrail methods tend to pay for themselves by lowering airframe chemical erosion and other effects. The metal methods are lite weight and don’t impact the fuel used significantly.
In a message dated 03/08/2004 8:53:07 PM Eastern Standard Time,
I have shared your web page with a number of scientists, in the hope that they will inquire about the oxide spraying, because many of them are skeptical about Chemtrails in their entirety, as I am sure you are aware.
Yes, I well know there are many factors in play there. The US even has a president that likes to corrupt science to the point that global warming effects doesn’t exist, while on the national security compartmented science side of things the problems are considered most severe. The national labs tend to follow suite.
Keep in mind that the major objective for chemtrail methods, or air pharmacology, is the HF effects. Oak Ridge has low-level continuous releases of HF from several operations that allowed us to get a good snap shot of illness responses in the work force. The key is one has to stop the formation of undesirable F-metal complexes. And the only way that works to date is to use metals competition in the organisms and environment, or to reduce the HF emissions. The US likes the cheap coal energy methods and the rates of illnesses.
You appear to be working with the oxygen radical and it is very useful for most applications, but it does not do well against the most highly electronegative element, fluorine. The only way that we have come up with to handle the fluorine atom effect is to use competition effects of metals. It is somewhat like using iodine pills to compensate for I-131 radiation effects—this is a competition effect.
What we do with chemtrails is dump metals into the atmosphere that will dominate the trace metals effects. Chemtrail methods use lots of titanium because this will complex with the fluorine atoms to make neutral F-metal complex molecules that don’t upset cell G-protein effects.
Chemtrails are using Al to induce the cloud formation and the AlFx is one of the undesirable F-metal complexes and to compensate the Ti is introduced. This avoids greatly upsetting the grazing animal health effects.
Oak Ridge has huge liabilities from dumping so much HF into the local air due to its uranium processing. We only caught onto the magnitude of the health effects in the mid-1980’s. By then, lots of the damage was done and hard to correct. The Southern Pine trees of this area are very sensitive to these coal emissions and lots of the South’s Pines are highly damaged from these effects. Oak Ridge looks like someone dumped Agent Orange on all the pine trees. Southern Pines are very sensitive to HF and other acids.
So basically, there will never be any official public release of this problem from ORNL or Oak Ridge. It would put them out of business. Our diffusion process also used three huge TVA fossil fuel thermal plants to power the uranium process, which added to the HF releases from coal combustion.
I will read the information you sent over the next days and see what ideas your presenting. Just keep in mind that we have studied most all the oxygen-based methods and these don’t affect the F problem. F atoms have an affinity with metals and the F atoms electro negativity makes it the driver for the metals selection process. The only way is to use metals competition to compensate. The F atoms will dominate over the oxygen bound metals.
Read up on some of the more recent articles on the web from Europe involving AlFx and G-proteins and you can see a taste of the problem. Then look at the special issue of F in biochemistry and you will see F makes the decisions for metals. And the only way to affect the F decisions is to change the metal dominance factors.
Good point. Source term reduction is the right idea.
The Fluoride Journal is an extremely good publication with some of the better research on fluorides presented. As good as the Fluoride Journal is, the classified research is about 15 years ahead of what is in there. The big issue is how the fluoride-metal complexes upset G-protein signaling in cells. Fluoride bonds to cell sites never clear. It is the high electronegative issue again. Serious problem.
There exist a number of methods to go after the source term for HF and fluorides emissions. Fluidized bed combustors can work well too.
The problem is most of the power utilities like cheep and adding treatment techniques or scrubbers sends up the cost.
The only way to force the hand of these Govt. agencies is to make the problems more public. Which means to expose the purposes of chemtrails and their directions into the fluoride compensation methods. This is one of the prime purposes of my exposing some of these chemtrail effects. The Tennessee Valley Authority is one of the US’s worst polluters from their coal plants. The air quality down here is horrendous in the summers.
The years 94-95 were extreme and the local air was visibly yellow here and the air caused skin irritation.
The way they kept things that way is to keep the HF health effects suppressed. Both Oak Ridge and TVA really don’t want the fluoride related health effects exposed and it goes all the way back to White House policies. If you look, the White House Science advisors are all national lab types. And helping places like Oak Ridge cover up this massive HF health problem.
Science down here has turned into more politics than real freedom of science. Examples follow.
Paper copy provided by Jim Phelps:
Pharmacological implications of aluminofluoride complexes
Charles University, Faculty of Sciences, Department of Physiology and
Developmental Physiology, Prague
Department of Toxicology, Purkynì Military Medical Academy, Hradec
Králové, Czech Republic
Running title: Pharmacological implications of aluminofluoride complexes
Corresponding author: Anna Strunecká
Department of Physiology and Developmental Physiology,
Faculty of Sciences, Charles University, Vinièná
7, 128 00, Prague 2, Czech Republic
Telephone: (42) – 02/21953239
Fax no.: (42) – 02/299713
Aluminofluoride complexes have been widely used in laboratory investigations for stimulation of various guanine nucleotide binding proteins. These fluorometallic complexes cannot be obtained through any catalogue or drug store. They are formed in water solutions containing fluoride and traces of aluminium in the form of the soluble ionic complexes, Aluminofluoride complexes have been recognised to act as phosphate analogues. Reflecting many studies which utilize aluminofluoride complexes in laboratory investigations, the effects of these fluorometallic complexes on various cells and tissues as observed, can be reviewed. With the appearance of acid rain and the use of aluminium in industry, there has been a dramatic increase in the amount of uncomplexed aluminium in ecosystems. In view of the ubiquity of phosphate in cell metabolism, aluminofluoride complexes represent a strong potential danger for living organisms including humans. The possibility of pathophysiological consequences of their long-term action is not fully recognised at this point.
During the last decade aluminofluoride complexes have been widely used in laboratory investigations as the tool for stimulation of various guanine nucleotide binding proteins (G proteins). Knowledge about the role of G proteins in signal transduction has expanded enormously , as over one hundred G protein-coupled receptors have been described (Gilman, 1987). Physiological agonists of these receptors include neurotransmitters and hormones, such as dopamine, epinephrine,norepinephrine, serotonin, acetylcholine, glucagon, vasopressin, neuropeptides, opioids, excitatory aminoacids, prostanoids, purines, photons and odorants. Fluoride anions had been recognised as the activators of the purified guanine nucleotide-binding regulatory component of adenylate cyclase (Rall & Sutherland 1958). Later Sternweis & Gilman (1982) reported that fluoride activation of adenylate cyclase depends on the presence of aluminium traces. The requirement for aluminium is highly specific; of 28 other metal tested, only Be2+ promoted activation of the guanine nucleotide-binding regulatory component of adenylate cyclase by fluoride. [AlF4]- mimics the role of the phosphate only if the phosphate is present and remained unsubstituted. These metallofluoride complexes are only active in conjuction with a bound nucleoside diphosphate.Their effect is more readily seen with G proteins because guanosine diphosphate (GDP) is always tightly bound in the site after the hydrolysis of guanosine triphosphate (GTP).In aqueous solutions, the fluoride anions bind to metal cation and are exchangeable with free fluoride or hydroxyl ions. The complexes are not permanent; equilibria exist between the various possible complexes, and the proportions of multifluorinated species such as AlF3, AlF3(OH) and [AlF4]-, depend on the excess concentration of free F- ions and on the pH of the solution (Bigay et al.1987; Martin 1988; Chabre 1990).
Chabre (1990) explained an important “functional” difference between a phosphate group and the structurally analogous aluminofluoride complexes. In phosphate, oxygen is covalently bound to the phosphorus and does not exchange with oxygen from solvent. In aluminofluoride complexes, ionic bonds are formed between the electropositive aluminium and the highly electronegative fluorine. While the reaction of a bound phosphate compound with orthophosphate is endergonic and slow, the corresponding reaction with [AlF4]- is rapid and spontaneous. Aluminofluoride complexes bind ionically to the terminal oxygen of GDP-phosphate. Enzyme-bound GDP or ADP could therefore form a complex with [AlF4]- that imitates ATP or GTP in its effect on protein conformation. This effect often causes a structural change that locks the site and prevents the dissociation of the trisphosphate. Free phosphates and nucleotides, when present at millimolar concentrations, do bind ionically to all the fluoride complexes. The action of [AlF4 ]- is not therefore restricted only to guanine nucleotides. These fluorometallic complexes influence the activity of a variety of phosphatases, phosphorylases and kinases (Bigay et al. 1987). In view of the ubiquity of phosphate in cell metabolism, aluminofluoride complexes can represent a strong potential danger for living organisms including humans. The possibility of pathophysiological consequences of their long-term action is not fully recognised at this point. But, reflecting many studies which utilise aluminofluoride complexes in laboratory investigations, the effects of these fluorometallic complexes on various cells and tissues as observed, can be reviewed. It might seem difficult to decide if these experiments present a potential toxicological risk for the human population in the future. In this article we review some of the evidence for pathophysiological effects of aluminium and fluoride on living organism.
II. PHYSIOLOGICAL AND BIOCHEMICAL ACTION OF [AlF4]- IN VARIOUS CELLS AND
Isolated parenchymal cells, hepatocytes, maintain responsiveness to hormones and serve as model cells equipped with very complex biochemical pathways. The stimulation of glycolysis by vasopressin, angiotensin II, and 1-adrenergic agonists is mediated in the liver through the increase of the Ca2+ cytosolic level. It has been demonstrated that the phosphoinositide signaling second messenger system is activated and involved in these events (Werve et al.1985).
Blackmore et al. (1985; 1988) demonstrated in their studies that the treatment of isolated hepatocytes with NaF produced the efflux of Ca2+, the rise in free cytosolic Ca2+, the decrease in phosphatidylinositol 4,5-bis-phosphate (PIP2)content and the increase in inositol-1,4,5-trisphosphate (1,4,5-IP3 ) and diacylglycerol. The level of intracellular cyclic adenosine monophosphate (cAMP) was decreased. All these changes were concentration dependent. The effects of low doses of NaF (2-15 mM) were potentiated by AlCl3 and this potentiation was abolished by Al3+ chelator desferoxamine. Fluoride anions in the presence of aluminium thus mimicked the action of Ca2+-mobilizing hormones glucagon and vasopressin in hepatocytes. The effects of submaximal doses of [AlF4]- were potentiated by submaximal doses of vasopressin, angiotensin II, and1-adrenergic agonists. Using phorbol myristate acetate, the activator of protein kinase C, the conclusion was made that [AlF4]- mimics the effects of Ca2+ mobilizing hormones by activating the G protein which couples the hormone receptor to phospholipase C specific to PIP2 (Blackmore & Exton 1986). The phosphate-analogue model of [AlF4]- action is not restricted to guanine nucleotides in the liver.
Blackmore et al. (1985) observed the activation of phosphorylase and inactivation of glycogen synthase after the activation of fluoride in the presence of AlCl3in hepatocytes. [AlF4]- transforms the liver to the organ involved in glycogenolysis, fatty acid oxidation and lipolysis.
G protein-coupled receptors and G protein-mediated cell responses are of key importance in the processes of neurotransmission and intercellular signaling in the brain. Phosphoinositide metabolism is coupled to several neurotransmitter receptors in the central nervous system including cholinergic, adrenergic, dopaminergic and histaminergic receptors. [AlF4]- has been widely used to stimulate phosphoinositide hydrolysis. The ability of [AlF4]- to mimic the effects of Ca2+-mobilizing hormones suggests the coupling of hormone receptors to phosphoinositide breakdown through G proteins (Rana &Hokin 1990). Candura et al. (1991) observed that aluminium salts and NaF mimicked the action of GTP(S) in stimulating phosphoinositide turnover and generation of inositol phosphates in rat cerebral cortical membranes. A much greater hydrolysis of phosphoinositides was observed when AlCl3 and NaF were present together, supporting the concept that [AlF4]- is the active stimulatory species.
Nadakavukaren et al. (1990) demonstrated accumulation of inositol phosphates in the suprachiasmatic nuclei region of rat hypothalamus over a 40 min incubation with [AlF4]-. Hypothalamic suprachiasmatic nuclei were suggested as the site of a biological clock responsible for generation of circadian rhythms. Melatonin receptors are involved in this function. Melatonin can facilitate secretion via a cholera and pertussis toxins-insensitive mechanism which can be inhibited by aluminum fluoride. [AlF4]- blocked the increase in camp stimulation by forskolin, being as effective as melatonin and increased intracellular calcium ( Morgan et al. 1991).
When rat hippocampal slices were exposed to 10 mM NaF and 10 µM AlCl3 for a brief period of time (12-15 min), spike amplitude fell to very low levels. Upon washout, spike amplitude recovered beyond control values and in half of the preparations a prolonged enhancement of spike amplitude (greater than 2 hours) occurred. If AlCl3 was omitted from fluoride-containing saline, enhancement of spike amplitude, when observed, was brief. These experiments show that brief exposure to [AlF4]- induces prolonged enhancement of synaptic transmission in rat hippocampal slices (Publicover 1991).
Tremendous possibilities of multiple molecular interactions of aluminium, fluoride and aluminofluoride complexes probably exist in the brain. Understanding the action of [AlF4]- in the brain warrants further investigation.
The effects of aluminofluoride complexes on the kidney were studied using glomerular mesangial cells, proximal tubular cells, and inner medullary collecting tubule cells of rat kidney. The ion transporting processes are affected by [AlF4]- in kidney tubular cells. [AlF4]- stimulates adenylate cyclase, inhibits amiloride-sensitive Na/H exchange regulated by cAMP-dependent protein kinase, enhances epidermal growth
factor-stimulated prostaglandin production, and mimics vasopressin and bradykinin induced Ca2+ mobilisation. It is suggested that [AlF4]-can affect the activity of many other ion channels and enzymes in the kidney (Zhou et al.1990).
Cells of blood.
[AlF4]- induces shape changes and aggregation in platelets (Rendu et al. 1990). Incubation of platelets with NaF (5-10 mM) induced only slight morphological changes. Addition of 10 µM AlCl3 resulted in aggregation. One min after addition of AlCl3, most of the granules were concentrated in the center of the cell, but some were extruding their contents by direct exocytosis. No myosin light-chain phosphorylation typical for the platelet response was observed after fluoride activation in the presence of aluminium. It has been reported that
[AlF4]- impairs the polymerisation-depolymerisation cycle of tubulin (Chabre1990).
Rapid and dynamic changes of the actin network are of vital importance for the motility of human neutrophils. Bengtsson et al. (1990) observed [AlF4]- induction of a pronounced and sustained increase in a filamentous form of actin in intact human neutrophils. This effect parallels an increase in cytosolic Ca2+ level, indicating that phospholipase C (PLC) is activated. Shape changes and disorganisation of the spectrin network were observed after addition of 1 mM NaF and 10 µM AlCl3 in human red blood cells (Strunecká et al. 1991). Cells lost their membrane material and became smaller.
Osteoblasts and osteoclasts.
Caverzasio et al. (1996) found that traces of aluminium markedly enhanced the stimulation of inorganic phosphate transport induced by fluoride in osteoblasts, suggesting that a fluoroaluminium complex might be responsible for fluoride -induced regulatory pathway. Analysis of the role of tyrosine phosphorylation in mediating this cellular response indicates that this signal transduction pathway is also involved in the stimulation of inorganic phosphate transport activity by fluoride. Aluminium potentiates the effect of fluoride on tyrosine phosphorylation and osteoblast replication in vitro and bone mass in vivo. The combination of fluoride and aluminium modulates a growth factor-dependent tyrosine kinase pathway enhancing mitogen-activated protein kinase and osteoblastic proliferation. Studies in ewes show that at a low dose fluoride stimulates the recruitment and lifespan of osteoblasts; at higher doses, fluoride decreases osteoblast activity (Chavassieux et al. 1991). The hormone calcitonin inhibits osteoclastic bone resorption. The activation of calcitonin involves two separate effects on the osteoclast: abolition of cell motility and marked cellular retraction. [AlF4]- produces both effects. Calcitonin elicited a biphasic elevation of cytosolic calcium level in isolated osteoclasts. Exposure of osteoclasts to [AlF4]-resulted in a marked concentration-dependent inhibition of bone resorption (Moonga et al. 1993).
ATP generation in mitochondria requires the association of F1 subunit with F0 transmembrane subunit transporting protons. The binding of ADP and Pi in a catalytic site of F1 triggers conformational changes which lock both of them into the site and induce the formation of pyrophosphate bonds by eliminating a water molecule (Chabre 1990). Lunardi et al. (1988) reported the inhibition of mitochondrial ATPase activity in the presence of [AlF4]-. This inhibition is not reversed by elution of fluoride from solution or by addition of strong chelators of aluminium. No significant release of the complex occured over a period of days.
[AlF4]- inhibits many ATPases, phosphatases and phosphorylases. The intervention of aluminofluoride complexes in the energy transformation processes may thus affect the energy metabolism of the entire organism.
III. EVIDENCE FOR IMPLICATION OF ALUMINIUM, FLUORIDE AND ALUMINOFLUORIDE
COMPLEXES IN PATHOLOGY
Elevated aluminium levels have been implicated as the cause of dialysis encephalopathy or dementia in renal failure patients after three to seven years of hemodialysis treatment (Alfrey et al. 1976; Meiri et al. 1991). Speech disorders precede dementia and convulsions. The mode of death has been reported as sudden cardiac arrest usually associated with acute pulmonary oedema (Elliot et al. 1978). Increased serum fluoride concentration and fluoride intoxication have been also observed in chronic hemodialysis patients (Chaleil et al. 1986 ). Arnow et al. (1994) reported that 12 of 15 patients receiving dialysis treatment in one room became acutely ill, with severe pruritus, multiple nonspecific symptoms, and/or fatal ventricular fibrillation (3 patients). Death was associated with longer hemodialysis time and increased age compared with other patients who became ill. Serum concentrations of fluoride in the sick patients were markedly increased to as high as 716 µM. The source of fluoride was the temporary deionization system used to purify water for hemodialysis. NaF is so far clinically used as the potent stimulator of bone formation. However, there are conflicting reports on the effect of fluoride on trabecular bone formation and bone strength. Osteosclerosis in workers exposed to fluoride and aluminium (industrial fluorosis) led to the use of fluoride as a treatment to increase bone mass in osteoporosis patients. Caverzasio et al. (1996) administered fluoride and aluminium subcutaneously to rats for 8 months. Their results suggest that the combination of fluoride and aluminium modulates a growth factor-dependent tyrosine kinase pathway enhancing mitogen-activated protein kinase and osteoblastic proliferation and bone mass. The authors concluded that these effects are consistent with the crucial role of aluminium in osteosclerosis observed in industrial fluorosis. Soyseth et al. (1994) investigated the relation between plasma fluoride levels and bronchial responsiveness in a longitudinal study in aluminium potroom workers who reported work-related asthmatic symptoms. A positive association was found between bronchial responsiveness and plasma fluoride levels. Plasma fluoride levels were associated with the total atmospheric fluoride concentration. The effects of aluminofluoride complexes have been also studied in connection with impairment of blood circulation. As a model for G protein-induced cardiopulmonary dysfunction, fluoride infusion (0.9 mol/l in 0.9% NaCl at 15 µl.kg-1.min-1 for 3 h i.v.) in the presence and absence of AlCl3 (0.6 µg.kg-1.min-1) into pigs anaesthetised with pentobarbital sodium was used (Dodam & Olson, 1995). NaF, with or without AlCl3, induced progressive deterioration of cardiopulmonary function after 1 h of infusion. Recent studies provide evidence that apoptosis of pancreatic cells is important in the early etiology of both type I and type II diabetes mellitus. Lowethet al. (1996) employed fluoride and show that this agent induces apoptosis in clonal pancreatic cells and also in the cells of normal rat islets of Langerhans. The process may reflect the formation of [AlF4]- since it was inhibited by the aluminum chelator deferoxamine. Conroy et al. (1995) reported that treatment of thymic lobes cells with fluoroaluminate provoked apoptosis of a wider range of thymocyte subtypes. Oguro et al. (1990) studied the cytotoxicity of NaF on fibroblast-like cells from 5 Japanese whole foetuses and found that the growth of the cells was markedly impaired by fluoride. In a living organism, fibroblasts must be able to move into areas of newly forming tissue and to secrete molecules that helps glue together the tissue. Laboratory investigations clearly indicate that both production of extracellular matrix and cell movement can be affected by the action of [AlF4]-. Because a higher amount of aluminium was found in the human brain with Alzheimer’s disease (AD) than in brains of age-matched healthy controls, the hypothesis that the accumulation of toxic amounts of aluminium in the brain is the cause of neurofibrillary changes and dementia has been discussed very often (McDermott et al. 1979; Zatta et al. 1988; Patoka et al. 1996). A positive correlation between the incidence of Alzheimer’s disease and concentrations of aluminium in drinking water was reported by some authors (Martyn et al. 1989; Flaten 1990). Neither the increased content of aluminium in the brain nor the results of ecological studies can explain why aluminium constitutes a risk. Aluminium is currently regarded as the putative risk factor for the etiology of this disease. The recent fundamental research of pathogenesis of AD has brought evidence that this disease is connected with the alterations in neurotransmission, amyloid production, plaque formation, and cytoskeletal abnormalities in brain tissue. We suggest that some of pathologic changes are not raised by aluminium alone, but by the aluminofluoride complexes (Strunecká 1999).
AD could be an example demonstrating the diversified and multidimensional nature of the integration of the nervous system. However, aluminofluoride complexes may act as the initial signal stimulating impairment of homeostasis, degeneration and death of the cells. By influencing energy metabolism these complexes can accelerate the aging and impair the functions of the nervous system. In respect to the etiology of AD, the long term action of [AlF4]- may represent a serious and powerful risk factor for the development of this devastating disease.
Aluminofluoride complexes appear as a new class of phosphate analogues for laboratory investigations. Experimental data clearly indicate that aluminofluoride complexes may mimic or potentiate the action of numerous extracellular signals and significantly affect many cellular responses. The principle of amplification of the initial signal during its conversion into the functional response has been a widely accepted tenet in cell physiology. Aluminofluoride complexes may therefore act with powerful pharmacological efficacy. The interpretation of laboratory investigations using isolated animal and human cells or tissues on the intact human organism could be discussed. It seems that, in an evolutionary sense, the natural barrier systems such as low aluminium absorption in the gastrointestinal tract, and various physiological ligands, such as transferrin, citrate, phosphate and silicic acid, were efficient buffers preventing the increased intake of this metal in natural conditions (Wilhelm et al. 1990). With the appearance of acid rains and due to the use of aluminium in industry, there has been a dramatic increase in the amount of aluminium appearing in ecosystems, nourishment and water sources (Cooke & Gould 1991). The increasing content of aluminium and fluorides in environment and food chains has raised the possibility that the near future will supply us with more data about the danger of aluminofluoride complexes for the human race. Supported by Grant Agency of Charles University, Prague (Grant No.113/1998/BBio/P?F).
©Anna Strunecká & Jirí Patocka
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At this point, I contacted your Foundation with this comment:
Hello, Dr. Suzuki. You may be aware of the presence of some of these compounds; however, the pervasiveness of their presence may be compounding by what I term a deviant arm of science termed geological pharmacology, or atmospheric pharmacology. This vein of science has evolved based on the premise that Flourides, Aluminums, and other oxides are firstly, the Aluminas are very concentrated in low grade coal which is used by the United States and allowed to pass through the pollution stream into the air, or secondly the Alumina and Titanium Oxides are being used to counteract the released Flourides through spraying operations. As you are a Geneticist by training, Dr. Suzuki, I think that this information below, which I have obtained from an educated and formerly high security clearance Whistleblower in the United States over the past ten days, might interest you seriously. This gentleman was involved in developing metal oxide sprays to counteract the HF problem caused by coal combustion in the United States, and came to the realization that this area of “science” is fundamentally wrong because the Flouride problem can be treated at source, but for cost reasons, which are really not a barrier, government has found it expedient to look the other way, and see what kind of “pharmacology” instead would be attempted. I understand thus far, that the Oak Ridge National Laboratory, the Lawrence Livermore National Laboratory, funded by the Department of Defence are stakeholders in this apparent”special access only” hush hush work….Dr. Suzuki, I tool out my Guyton Textbook while reading this submission. The primacy of the Flouride as a deeply embedded intracellular receptor mimicker in such important processes, as this paper suggests, could point to so many modern health problems.
The way I came upon concerning you with this topic is that it goes back to coal-and it is well known that you are a Geneticist, which makes this major DNA/RNA physiology disturber very petrinent to your expertise.
Back to coal; I may have made some major inroads in completely curbing CO2 at large emitter sites, and actually transforming it back into helpful OH radicals, which would be plentifully released to abate atmospheric Methane. The work is being well received, and one benefit may be the pairing up of Thermonuclear Fusion with coal plants because I have modeled a situation where they actually require one another to achieve their successful continuation of operation and development-free energy is necessary to supplement.
We must be guardians of living tissues at all levels at present or the mass extinction warnings now coming out from scientists across the full spectrum will become a reality.
Please note that I have been a full skeptic of Chemical Spraying operations until I received contact with Mr. Jim Phelps, who is the whistleblower from the Oak ridge National Lab., and other areas of the US government. I am giving you his email point of contact in the event that you would like to confer with him directly. Magnu96196@aol.com
Chemical spraying has a long intellectual history, with the father patent from 1918 and numerous others, available for you right on this link: http://users.ev1.net/~seektress/patlist.htm . With so much Intellectual property having been generated, I don’t think it is a great leap to be concerned that there has been a defacto market for these ideas. There seems to be two categories of spraying, firstly military using Barium oxides to improve or alter radio and radar transmissions in war/conflict theatres; and, domestic spraying using Aluminium and Titanium oxides to counteract Fluoride compounds released by industry.
Mr. Jim Phelps is willing to shed as much light on this problem as he can. Thank you for your interest, and unquestionable dedication as always, Viva Cundliffe
In a message dated 03/14/2004 2:40:41 PM Eastern Standard Time,
March 15th, 2004 << #19 my comment is that co-emission techniques are two fundamental “wrongs”being put together. (chemtrail technology versus emissions)
Good observation. Basically, that is right. Now, if we had an ideal world—we might be there. If we did not pollute so excessively, we would not need pharmacy so much to offset health effects. All “air pharmacology” idea did was combine the two ideas.
The industrial age means pollution and only in recent time have the ideas of scrubbers and reducing emissions become part of the industrial operation equations. Many coal plants continue to pollute. But as you said once, it is fixable. One has to bring it into the political forefront. Which is part of what this is about also. The fixes will cost money and influence the industry bottom line, and also the bottom line for medicine, health, etc. Lots of politics in play around this.
Oak Ridge is a toxic zone to work in and in this zone one can notice synergism effects from varied emissions. For instance, Oak Ridge has tons of heavy metal emissions and those that worked near CN- emission sources fared better than those that did not.
Other odd things happened like those exposed to the low level cumulative HF emissions and also drank lots of beer—–did not get sick. Those that were tea-totlers mostly came down with health effects sometimes like CFS in the long run. There became some interesting truths in the alchemical origins for beer. And really even for wine also. Wine has some interesting anti-aging enzymes.
Oak Ridge even did some experiments with the local DOE incinerator to include CN- emissions from burning train car loads of acetyl nitrile. This was to do some lung and body retention experiments related to the laetrile effect.
When we found the problems with low level HF in the local air from the K-25 plant emissions, this exposed another massive problem linked to coal emissions of HF and etc. So, it became a tough choice. Cut out electric generation from coal or pull some tricks to change the outcomes.The national security system really likes the tricks ideas. But they can only help for so long.
We had some ideas to modify the local air effects, but to handle the coal emissions problems, we needed some global methods. This is how the jet planes come into effect as delivery systems.
NASA had been showing that jet black soot emissions were affecting global warming, so the little idea on adding aluminum spikes into the fuel could change this by making some white clouds, absorbing some the Sulfuric acid, etc. This offset the jet plane black particle soot effects. It also pulls some of the HF down. As Star Wars entered the picture we gained some funding mechanisms for some of the greater research projects on the issues of modification of the potential gradient to change the storm formation potentials. This is how the barium got into the chemtrail equation.
The F–metal complex is why the titanium is added. Titanium is in lots of things these days. Vitamins, bread, pharmacy, etc. Ti offsets the F-metal negative effects. So, some little ideas became great in the world of national security cover up and special Star Wars weapons. It became a question of trying to compensate for the problems while changes were made to the global energy equation. Problem now is the national security system is so corrupted by the BUSH gangs interests in OIL and NWO dominance that one hand in this system does not know what the others are doing.
So, it is time to break it all out into the open and play fair.
Bush and his interests don’t care about doing right things; they have positioned their interests to make money from pharmacy and huge health effects. They get rich by keeping the secrets, denying that Kyoto points to a growing real problem. The chemtrails and other methods were originally intended to buy some time, but now the corrupted influences are going beyond that. They want to lower the population in a sort of slow process. Only way to get the balance back is take it into the open as quickly as possible.
[ Here, clearly, Phelps believes the chemtrails are beneficial]
In a message dated 03/30/2004 12:54:35 PM Eastern Standard Time,
<< I have already been in contact with Dr. Castle. In your opinion, what is the mechanism that is causing the pH shift in the soils? Is it the deposition of the metals as Castle describes.
The big issue on soil Ph is acid rain from coal emissions. The acid rain leaches the trace metals from the soils and this is upsetting the health. Coal derived acid rain is lots of Sulfuric, HCl, and HF.
One of the seridipitous effects of the metal chemtrail methods is to react with these acids (particularly the Sulfuric) in the atmosphere and convert them into metal sulfates, and this also does cloud seeding to reflect some of the IR for global cooling. There are multiple factors in play.Chemtrail methods actually slow down these negative soil effects. They are even desired to cut down on airplane aluminum erosion that sets airframe lifetimes. Chemtrail methods use titanium to offset the negative toxic effects of things like Al and Ba. The real big issue with soils is the trace metals depeletion effects. It is partly driven by Ph, partly by overplanting, and highly by poor fertilizer methods. One of the big things in fertilizer is the volcanic ash methods that are being tested in the UK. Here the soils have been highly affected by hundreds of years of coal use, overfarming, and improper fertilizers. The phosphate fertilzers are a problem because they add lots of F, and these actually have to be cooked to reduce the F in the “as mined” phosphates.
This upsets the trace metals too. See the article below for what happens when the balance gets restored. The loss of these benefcial trace elements from the food chain highly affects human health. jp
[Now, March 30th, I have included Dr. Mike R. Castle in these exchanges]
Solar radiation coming in on Right, Infrared on Left.
Dear Jim, I would suggest at point B on this picture, that essentially chemtrails are an artificial roof which more than anything, traps IR to its interior, as proven in any greenhouse. At point A, there would then
be less venting. This logic is Totally counterintuitive. Points C & D are where Photolysis for O2 to O (1) D and OH to O3 are occurring, but are having 1) water hijacked by artificial aerosols, a loss of a natural source of HO for H2O Photolysis which promotes venting; 2) A disturbance in the natural regulated formation of O3. At point E a buildup of H20, which is now reported to be at 15% above normal, I suggest it is being stagnated, and when conditions allow for it to be relieved or released, abrupt climate events occur with the addition of
heavier CCN and other particles generated by artificial aerosols, which would magnify the power of those events. At point F, a nominal amount of IF reflection by creating an artificial lithosphere with aerosols has
been created and its real effect is to create an accumulation of IF below it. Sulfates are not the problem they once were due to the increase in source capture. Nature is extremely intelligent, far more than our collective
Understanding of it. Regards, Viva Cundliffe
[Dr. Castle provided a positive review of my proposed H202 Release Technique in March 2004]
Thanks for copying me on the communiqué with Jim.
I’m just beginning to understand the dynamics of the Model. It appears functional and many of the forces you point out are reality. The chemical Moisture Scavengers from the in-situ formation of Barium
Hydroxide occurs every two to three days in the US Midwest. Identifying the region of preferences by the dispensary-fleet, diagonal upper Minnesota straight Southwest to Western Iowa, this chemical aerosolized heavy-metal particulates use the Great Lakes Region of the US to stage Weather-Modification events through-out the Midwest and East and South to the Eastern Seaboard. This are is highly irradiated with Microwave, ELF/VLF from HAARPS source. We discovered that HAARPS has been responsible for punching massive holes in the Ozone Layer, since 1994. Dr. Eastlund had to place “Ozone Hole Remediation into the scope of operations at HAARPS. This is accomplished aerially by the selective dispensement of a mixture of
Selenium and Hydrocarbons to form ozone in-situ….a massive patch circling the upper latitudes, if you were looking down from the North Pole. All these regions of the Northern extremities suffer massive UV
Radiation events and penetration. This event and other figure prominently with your theory, as well as
Dr. Michael Castle
Summary for Dr. Suzuki
I am concerned that there may be a lot of truth to these activities of spraying, as suggested by the existence of numerous patents for this purpose, and Mr. Jim Phelps genuine support of aspects of aerosol spraying.
My main position is that we should set the atmospheric bar of cleanliness to as close to pre industrial as possible. I see this “deviant arm of chemistry”, as a collection of human wisdom trying to alter the fundamental and sweeping wisdom of the natural system we inherited.
Perhaps you will be interested in pursuing this subject further, and if you are, feel free to contact me at your convenience. Yours Truly,