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Post by skyship on Sept 19, 2009 20:18:58 GMT -5
" Superoxide is an anion with the chemical formula O2−. It is important as the product of the one-electron reduction of dioxygen O2, which occurs widely in nature.[1] With one unpaired electron, the superoxide ion is a free radical, and, like dioxygen, it is paramagnetic." en.wikipedia.org/wiki/SuperoxideNow, what is an anion? Anion:"anion The Columbia Encyclopedia, Sixth Edition | 2008 | The Columbia Encyclopedia, Sixth Edition. Copyright 2008 Columbia University Press. (Hide copyright information) Copyright anion , atom or group of atoms carrying a negative charge. The charge results because there are more electrons than protons in the anion. Anions can be formed from nonmetals by reduction (see oxidation and reduction ) or from neutral acids (see acids and bases ) or polar compounds by ionization. Anionic species include Cl - , SO 4-- , and CH 3 COO - . Highly colored intermediates in organic reactions are often radical anions (anions containing an unpaired electron). Salts are made up of anions and cations . See ion . www.encyclopedia.com/topic/anion.aspx... " IonFrom Wikipedia, the free encyclopedia Jump to: navigation, search For other uses, see Ion (disambiguation). An electrostatic potential map of the nitrate ion (NO3−). Areas coloured red are lower in energy than areas colored yellow An ion is an atom or molecule where the total number of electrons is not equal to the total number of protons, giving it a net positive or negative electrical charge. An anion (pronounced /ˈænaɪən/; an-eye-on), from the Greek word ἀνά (ana), meaning 'up', is an ion with more electrons than protons, giving it a net negative charge (since electrons are negatively charged and protons are positively charged). Conversely, a cation (pronounced /ˈkætaɪən/; cat-eye-on), from the Greek word κατά (kata), meaning 'down', is an ion with more protons than electrons.An ion consisting of a single atom is a monatomic ion. If it consists of two or more atoms, it is a polyatomic ion. Polyatomic ions containing oxygen, such as carbonate and sulfate, are called oxyanions.When writing the chemical formula for an ion, its charge is written as a superscript '+' or '−' following a number indicating the difference between the number of protons and the number of electrons. The number is omitted if it is equal to 1. For example, the sodium cation is written as Na+, the '+' indicating that it has one less electron than it has protons. The sulfate anion is written as SO42−, the '2−' indicating that it has two more electrons than it has protons. I f an ion contains unpaired electrons, it is called a radical ion. Just like neutral radicals, radical ions are very reactive."en.wikipedia.org/wiki/Ion========================== Now, the good of Anions: that would be if the electrons are paired, I assume: www.rafrom.com/index.php/en/anion-actskyship
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Post by skyship on Sept 19, 2009 20:51:58 GMT -5
dioxygen
" Dioxygen difluoride is a compound with the formula O2F2. This yellow compound is a strong oxidant and decomposes into OF2 and oxygen even at -160 °C (4% per day).[1] Preparation Dioxygen difluoride can be obtained by subjecting a 1:1 mixture of gaseous fluorine and oxygen at low pressure (7-17 mmHg is optimal)[citation needed] to an electric discharge of 25-30 mA at 2.1-2.4 kV. This is basically the reaction used for the first synthesis by Otto Ruff in 1933.[2]Another synthesis involves mixing O2 and F2 in a stainless steel vessel cooled to −196 °C, followed by exposing the elements to 3 MeV bremsstrahlung for several hours.[citation needed] Structure and electronic descriptionIn O2F2 oxygen is assigned the unusual oxidation state of +1. In most of its other compounds, oxygen has an oxidation state of −2. The structure of dioxygen difluoride resembles that of hydrogen peroxide, H2O2, in its large dihedral angle, which approaches 90°. This geometry conforms with the predictions of VSEPR theory. The O−O bond length is within 2 pm of the 120.7 pm distance for the O=O double bond in dioxygen, O2. Dioxygen difluoride's structureThe bonding within dioxygen difluoride has been the subject of considerable speculation over the years, particularly because of the very short O-O distance and the long O-F distances. Bridgeman has proposed a scheme which essentially has an O-O triple bond and an O-F single bond that is destabilised and lengthened by repulsion between the lone pairs on the fluorine atoms and the π-orbitals of the O-O bond.[3] Repulsion involving the fluorine lone pairs is also responsible for the long and weak covalent bonding in the fluorine molecule. ReactivityThe overarching property of this unstable compound is its oxidizing power, despite the fact that all reactions must be conducted near −100 °C.[4] With BF3 and PF5, it gives the corresponding dioxygenyl salts:[1][5] 2 O2F2 + 2 PF5 → 2 [O+2]PF−6 + F2 It converts uranium and plutonium oxides into the corresponding hexafluorides.[6]"en.wikipedia.org/wiki/Dioxygen_difluoride===================================== Now, the man who studied this was Otto Ruff: 1933."Otto Ruff was born in Schwäbisch Hall, near Stuttgart. After becoming an pharmacist under the supervision of Carl Magnus von Hell (known from the Hell-Volhard-Zelinsky halogenation) at the University of Stuttgart he joined the group of Hermann Emil Fischer at the University of Berlin. Fischer was noted for his work on carbohydrates (sugars) and so Ruff started his career as organic chemist. In 1898 he published his work on the transformation of d-Glucose to d-Arabinose later called the Ruff degregation. Supported by Fischer Ruff became head of the new inorganic department in Berlin. This drastical change in subject benefited Ruff and during his work on chlorides sulfur compounds. In 1902 he married Meta Richter a pharmacist, from this marriage he had three children. In 1904 he became professor at the University of Danzig and from 1916 he was head of the inorganic department at the University of Breslau. He died three years after his retirement in 1939. His last years of teaching were made miserable by a privatdozent and assistant, Helmut Hartmann, who had joined the Nazi party and became an "insolent politician" who made life unbearable for many. Scientific achievementsOtto Ruff published 290 papers and two books. The books were: "The Chemistry of Fluorine" (published in 1920 by Springer Verlag, Berlin) and "Introduction to Chemical Practicum" (Leipzig 1926, 2nd edition 1937). His papers can be categorized as follows: chemistry of sugars (17 papers), inorganic chemistry of fluorine (86), high temperature chemistry (44), electrolysis of molten salts (9), plastics (10), carbides (20), explosions in mines (7), other fields of inorganic chemistry (72).[1] Along with Svante Arrhenius, Henri Moissan, and Alfred Werner, all of whom received Nobel Prizes, O. Ruff was regarded as the driver of the achievements of inorganic chemistry in first decades of 20 century. See also * Ruff degradation"....... "http://en.wikipedia.org/wiki/Otto_Ruff ============================================ Mentioned above: Hell-Volhard-Zelinsky halogenation: What I am concentrating on here is the carboxy reaction and notice it is negative.The Hell-Volhard-Zelinsky halogenation reaction halogenates carboxylic acids at the α carbon. The reaction is named after three chemists, the German chemists Carl Magnus von Hell (1849-1926) and Jacob Volhard and the Russian chemist Nikolay Zelinsky.[1][2][3][4] The Hell-Volhard-Zelinsky halogenation Scheme
Unlike other halogenation reactions, this reaction takes place in the absence of a halogen carrier. The reaction is initiated by addition of a catalytic amount of PBr3, after which one molar equivalent of Br2 is added. Hell-Volhard-Zelinsky reaction mechanism overallPBr3 replaces the carboxylic OH with a bromide, resulting in a carboxylic acid bromide. The acyl bromide can then tautomerize to an enol, which will readily react with the Br2 to brominate a second time at the α position. In neutral to slightly acidic aqueous solution, hydrolysis of the α-bromo acyl bromide occurs spontaneously, yielding the α-bromo carboxylic acid in an example of a nucleophilic acyl substitution. If an aqueous solution is desirable, a full molar equivalent of PBr3 must be used as the catalytic chain is disrupted. If little nucleophilic solvent is present, reaction of the α-bromo acyl bromide with the carboxylic acid yields the α-bromo carboxylic acid product and regenerates the acyl bromide intermediate. In practice a molar equivalent of PBr3 is often used anyway to overcome the slow reaction kinetics. The mechanism for the exchange between an alkanoyl bromide and a carboxylic acid is at below. The α-bromoalkanoyl bromide has a strongly electrophilic carbonyl carbon because of the electron-withdrawing effects of the two bromides. The carboxylic acid will act as a nucleophile that the carbonyl oxygen of the carboxylic acid has a partial negative charge. en.wikipedia.org/wiki/Hell-Volhard-Zelinsky_halogenation======================================== Carboxylic acid: I have mentioned this before, but, deems repeating here, to get my point across that Our oxygen has been compromised. It is a known fact that due to the aerosol operations and change in protein deletions we are experiencing and change in DNA structures, that something is going on in the very air we breathe, water, hydrogen, oxygen, carbon dioxide.
It seems that a control and I believe that a new bill was just introduced into Congress where a sensor would determine our carbon footprint, so as to tax us by what we breathe in or out.
So reducing carbon dioxide we breathe out, one's cap and trade, carbon tax would be lower.
In order to do that our oxygen consumption would have to be lower as well, wouldn't it?
Substituting other forms of oxygen seems to be what is a stake here. This in turn effects our blood. These new forms of oxygen are related to artificial blood hemes.
So, what is the new form of oxygen? Replacing carbon, of which humans are based with another form of oxygen? Artificial as well.
Back to the superoxides:
================================== NADPH:NADPH Oxidase. Neutrophils and other phagocytic cells produce superoxide as part of their bactericidal mechanisms. Superoxide can react to form hydrogen peroxide, HOCl, and perhaps hydroxyl radical. Together, these oxygen-derived species participate in bacterial killing. The enzyme which catalyzes the production of superoxide is the NADPH oxidase or respiratory burst oxidase. The importance of the respiratory burst oxidase is illustrated by the inherited condition Chronic Granulomatous Disease (CGD) in which a component of the respiratory burst oxidase is absent or defective. Affected individuals suffer from recurrent, chronic and severe infections due to the inability of their neutrophils to kill microbes. Similar enzymes in other tissues produce superoxide and hydrogen peroxide, and in non-phagocytic tissues, these species may be involved as signal molecules regulating transcription, apoptosis and cell division. The Lambeth Lab studies the respiratory burst oxidase as a model for a signal transduction effector responses." pathology.emory.edu/Lambeth/nadphpage.htmlIf someone can copy the picture over here, it is self explanatory.
skyship
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Post by skyship on Sept 19, 2009 21:14:05 GMT -5
Chronic granulomatous disease (CGD) (also known as "Bridges–Good syndrome," "Chronic granulomatous disorder," and "Quie syndrome"[1]) is a diverse group of hereditary diseases in which certain cells of the immune system have difficulty forming the reactive oxygen compounds (most importantly, the superoxide radical) used to kill certain ingested pathogens.[2] This leads to the formation of granulomata in many organs.[3] CGD affects about 1 in 200,000 people in the United States, with about 20 new cases diagnosed each year.[4][5] This condition was first discovered in 1954, and in 1957 described as "a fatal granulomatosus of childhood".[6][7] The underlying cellular mechanism that causes chronic granulomatous disease was discovered in 1967, and research since that time has further elucidated the molecular mechanisms underlying the disease.[8] Chronic granulomatous disease is the name for a genetically heterogeneous group of immunodefeciencies. The core defect is a failure of phagocytic cells to kill organisms that they have engulfed because of defects in a system of enzymes that produce free radicals and other toxic small molecules. There are several types, including chronic X-linked disease, chronic b-negative disease, X-linked cytochrome b-positive disease, x-linked variant disease, and atypical granulomatous disease[9]. Symptoms Classically, patients with chronic granulomatous disease will suffer from recurrent bouts of infection due to the decreased capacity of their immune system to fight off disease-causing organisms. The recurrent infections they acquire are specific and are, in decreasing order of frequency: * pneumonia * abscesses of the skin, tissues, and organs * suppurative arthritis * osteomyelitis * bacteremia/fungemia * superficial skin infections such as cellulitis or impetigo Most people with CGD are diagnosed in childhood, usually before age 5.[10] Early diagnosis is important since these people can be placed on antibiotics to ward off infections before they occur. Atypical infections Microscopic image of the fungus, Aspergillus fumigatus, an organism that commonly causes disease in people with chronic granulomatous disease. People with CGD are sometimes infected with organisms that usually do not cause disease in people with normal immune systems. Among the most common organisms that cause disease in CGD patients are: * bacteria (particularly those that are catalase-positive)[11] o Staphylococcus aureus. o Serratia marcescens. o Salmonella species. o Klebsiella species. o Pseudomonas cepacia, a.k.a. Burkholderia cepacia. [12] o Nocardia.[13] * fungi o Aspergillus species. Aspergillus has a propensity to cause infection in people with CGD and of the Aspergillus species, Aspergillus fumigatus seems to be most common in CGD. o Candida species. Genetics Most cases of chronic granulomatous disease are transmitted as a mutation on the X chromosome and are thus called an "X-linked trait".[10] The affected gene on the X chromosome codes for the gp91 protein p91-PHOX (p is the weight of the protein in kDa; the g means glycoprotein). CGD can also be transmitted in an autosomal recessive fashion (via CYBA and NCF1) and affects other PHOX proteins. The type of mutation that causes both types of CGD are varied and may be deletions, frame-shift, nonsense, and missense.[14][15] A low level of NADPH, the cofactor required for superoxide synthesis, can lead to CGD. This has been reported in women who are homozygous for the genetic defect causing glucose-6-phosphate dehydrogenase deficiency (G6PD), which is characterised by reduced NADPH levels. Pathophysiology Two neutrophils among many red blood cells. Neutrophils are one type of cell affected by chronic granulomatous disease. Phagocytes (i.e., neutrophils, monocytes, and macrophages) require an enzyme to produce reactive oxygen species to destroy bacteria after they ingest the bacteria in a process called phagocytosis, a process known as the respiratory burst. This enzyme is termed "phagocyte NADPH oxidase" (PHOX). The initial step in this process involves the one-electron reduction of molecular oxygen to produce superoxide anion, a free radical. Superoxide then undergoes a further series of reactions to produce products such as hydrogen peroxide, hydroxyl radical and hypochlorite (bleach). The reactive oxygen species this enzyme produces are toxic to bacteria and help the phagocyte kill them once they are ingested. In particular, individuals are vulnerable to infections with catalase positive organisms. Defects in one of the four essential subunits of this enzyme can all cause CGD of varying severity, dependent on the defect. There are over 410 known possible defects in the PHOX enzyme complex that can lead to chronic granulomatous disease[3]. Diagnosis The nitroblue-tetrazolium (NBT) test is the original and most widely-known test for chronic granulomatous disease.[16] It is negative in CGD, and positive in normal individuals. This test depends upon the direct reduction of NBT by superoxide free radical to form an insoluble formazan. This test is simple to perform and gives rapid results, but only tells whether or not there is a problem with the PHOX enzymes, not how much they are affected. A similar test uses dihydrorhodamine (DHR); whole blood is stained with DHR, incubated, and stimulated produce superoxide radicals which reduce DHR to rhodamin in cells with normal function. An advanced test called the cytochrome C reduction assay tells physicians how much superoxide a patient's phagocytes can produce. Once the diagnosis of CGD is established, a genetic analysis may be used to determine exactly which mutation is the underlying cause. Treatment Management of chronic granulomatous disease revolves around two goals: 1) diagnose the disease early so that antibiotic prophylaxis can be given to keep an infection from occurring, and 2) educate the patient about his or her condition so that prompt treatment can be given if an infection occurs. Antibiotics Physicians often prescribe the antibiotic trimethoprim-sulfamethoxazole to prevent bacterial infections.[17] This drug also has the benefit of sparing the normal bacteria of the digestive tract. Fungal infection is commonly prevented with itraconazole,[18] although a newer drug of the same type called voriconazole may be more effective.[19] The use of this drug for this purpose is still under scientific investigation. Immunomodulation Interferon, in the form of interferon gamma-1b (Actimmune) is approved by the Food and Drug Administration for the prevention of infection in CGD. It has been shown to prevent infections in CGD patients by 70% and to reduce their severity. Although its exact mechanism is still not entirely understood, it has the ability to give CGD patients more immune function and therefore, greater ability to fight off infections. This therapy has been standard treatment for CGD for several years.[20] Hematopoietic stem cell transplantation (HSCT) Hematopoietic stem cell transplantation from a matched donor is potentially curative. The procedure is controversial, and not without significant risk [21] Prognosis There are currently no studies detailing the long term outcome of chronic granulomatous disease with modern treatment. Without treatment children often die in the first decade of life. Available data indicates that X linked CGD is more severe, with most treated patients dying in the third or fourth decade of life [22]. Epidemiology CGD affects about 1 in 200,000 people in the United States, with about 20 new cases diagnosed each year.[4][5] Chronic granulomatous disease affects all people of all races, however, little information on prevalence outside of the United States is available. One survey in Sweden reported an incidence of 1 in 220,000 people [22]. en.wikipedia.org/wiki/Chronic_granulomatous_diseaseNow, what is interesting here about this CGD is that all of a sudden Superoxide appears. However, it is related to x-linked carriers of certain diseases, as lilsissy and I discussed a while back.
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Post by skyship on Sept 19, 2009 22:05:42 GMT -5
Now we get into the Cytochromes: notice that the baculovirus is being talked about over on LB. Mutations in the CYBB gene:" Cytochrome b558 was expressed in Sf9 insect cells coinfected with recombinant baculoviruses carrying cDNAs for p22phox and gp91phox [5]."....www.wikigenes.org/e/gene/e/1536.htmlThe p22phox and the gp91phox are involved with the NADPH. oxidase burst. in insects, and in Humans? Sf9 insect cells: tissue from army worms. This is getting sicker and sicker. Haven't got to the blood from pigs yet. www.orbigen.com/objects/catalog/product/extras/CEL-10002.pdfcDNAs for p22phox and gp91phox
goes through the fric.... blood cell wall. A gp91phox Containing NADPH Oxidase Selectively Expressed in Endothelial Cells Is a Major Source of Oxygen Radical Generation in the Arterial Wall.Abstract—Reactive oxygen species (ROS) play an important role in regulating vascular tone and intracellular signaling; the enzymes producing ROS in the vascular wall are, however, poorly characterized. We investigated whether a functionally active NADPH oxidase similar to the leukocyte enzyme, ie, containing the subunits p22phox and gp91phox, is expressed in endothelial cells (ECs) and smooth muscle cells (SMCs). Phorbol 12-myristate 13-acetate (PMA), a stimulus for leukocyte NADPH oxidase, increased ROS generation in cultured ECs and endothelium-intact rat aortic segments, but not in SMCs or endothelium-denuded arteries. NADPH enhanced chemiluminescence in all preparations. p22phox mRNA and protein was detected in ECs and SMCs, whereas the expression of gp91phox was confined to ECs. Endothelial gp91phox was identical to the leukocyte form as determined by sequence analysis. In contrast, mitogenic oxidase-1 (mox1) was expressed in SMCs, but not in ECs. To determine the functional relevance of gp91phox expression, experiments were performed in aortic segments from wild-type, gp91phox-/-, and endothelial NO synthase (eNOS)-/- mice. PMA-induced ROS generation was comparable in aortae from wild-type and eNOS-/- mice, but was attenuated in segments from gp91phox-/- mice. Endothelium-dependent relaxation was greater in aortae from gp91phox-/- than from wild-type mice. The ROS scavenger tiron increased endothelium-dependent relaxation in segments from wild-type, but not from gp91phox-/- mice. These data demonstrate that ECs, in contrast to SMCs, express a gp91phox-containing leukocyte-type NADPH oxidase. This enzyme is a major source for arterial ROS generation and affects the bioavailability of endothelium-derived NO. (Circ Res. 2000;87:26-32.) Key Words: oxygen radicals • endothelial function • smooth muscle cells • p22phox circres.ahajournals.org/cgi/content/abstract/87/1/26Does this not sound like tissue from the worm is being used as seed for oxygen generation in the arterial wall?
skyship
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Post by skyship on Sept 19, 2009 22:16:47 GMT -5
But, can you see what is happening?
Taking tissue from insects, animals and interacting it with human tissues.
this symbiosis with animals is really sick, isn't it?
And to think that by using the word Evolution, it gave these scientists full rein to use tissue from anything as seed for growth in the epithelial cells or any cells, so we are forced to become symbiotic with everything else, thereby eliminating the the pure natural state of the human, separate from insects, animals and plants.
Pissed is not the work. f mad..................!
And we know they did not stop at just that:
Biomineralization where even geology is part of the equation.
Biometallization where even metals are part of the equation
SS where even solid state physics is part of the equation
Bioilluminence and Radiance become united where there is no zero point, there is no soul, we are one with nature, we are nature, nature is us. We are pigs, cows, squash, corn, wireless. We are electrical and the chemistry of oxydative bursts, hydrogen becomes part of our DNA as well.
However, they will have a helluva time trying to separate SOUL from SPIRIT.
more on this later, but seems a new cytochrome has been introduced and forms the heterodimers, and dimers that replace our nerves. Our nerves become electrical units.
Skyship
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Post by aqt on Sept 25, 2009 14:49:20 GMT -5
perhaps through the use of the bioelectromagnetism?
the form of energy already found in us....conducting our muscles and nerves?
aqt
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Post by aqt on Sept 25, 2009 14:54:53 GMT -5
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Post by aqt on Sept 25, 2009 14:58:43 GMT -5
LA JOLLA, CA, June 19, 2009Researchers at The Scripps Research Institute, the University of California, San Diego, and Ohio State University have used a very sensitive fluorescence technique to find that a bacterial protein thought to exist in one "natural" three-dimensional structure (shape), can actually twist itself into a second form, depending on the protein's chemical environment. One folded form is active and the other is inactive, but the protein can easily morph from one state to anotherwww.bio-medicine.org/biology-news-1/Researchers-observe-single-protein-dimers-wavering-between-two-symmetrically-opposed-structures-8934-1/The group of Scripps Research Associate Professor Ashok Deniz has conducted a series of studies that use novel fluorescence methods to show that both simple and complex proteins can swiftly change their structures. In March, Deniz and his Scripps Research team published a study, also in PNAS, demonstrating how a simple protein associated with development of Parkinson's disease can switch shapes back and forth between different structures, depending on its binding to molecular partners.
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Post by skyship on Sept 25, 2009 20:42:20 GMT -5
The above link says this: ......"Such a powerful mechanism has lots of clinical implications," Deniz says. "Small mutations in proteins could throw off the delicate balance of energy that is needed between conformational structures of proteins in a cell, leading to disease. If so, a drug might be able to reverse those kinds of imbalances." Notice that mutations in "proteins could throw off the delicate balance of energy"...... so, bioset works to set it right for the correct balance so disease can be altered itself? sounds like if the energy level is corrected, the disease will have less chance of settling in. So for the conformational structure to remain intack despite what the proteins are doing sounds like what Bioset can do. ============================== Also the dimers in alzheimers, I figured it. Aldrich Sigma makes the products that make the dimer, dendrimers, and heter and homo dimers. will see what their web page is saying nowdays. Here is the web page. I had introduced this before, but, many could not grasp it. I even had a hard time, because it looks like they might be good for fixing things, like genes, or rearranging them The tools of the trade, so to speak. tinyurl.com/ycv92ctwww.sigmaaldrich.com/etc/medialib/docs/Aldrich/Acta/al_acta_37_2.Par.0001.File.tmp/al_acta_37_2.pdf Bioelectromagnetism and dendrimers: I wonder if Duchenne was doing the same thing that the Bioset folks do? " Guillaume Duchenne: The Father of Electrotherapy and Neuropathology Born: 17 September 1806 Died: 15 September 1875 The search for ways to use electricity for medical treatment is well rooted in history. Peter Christian Abildgaard suggested the possibilities in a bizarre way in 1775, when he discovered that he could render a chicken unconscious with an electric shock, and then revive it the same way. In 1780, Luigi Galvani noticed that his static-electricity generator caused the muscles in a frog’s leg to contract. And between the late 1700s and early 1840s, when it first became known that each beat of the heart was accompanied by an electrical pulse, there was an explosion of interest in using electricity either to study or cure the body. One of the key researchers during this period was French physician Guillaume Duchenne (1806-1875). Born in the coastal town of Boulogne-sur-Mer, he was not interested in following the path of his mariner father and instead pursued a career in medicine. This career was nearly derailed when his wife died during childbirth, leading to a depression in which he almost abandoned the field of science. At the age of 36, Duchenne moved to Paris and developed a fascination with the ability of electricity, when applied to a patient’s skin, to cause muscle contractions. " www.ieeeghn.org/wiki/index.php/Guillaume_Duchenneright up there with Rife and Priore. ....... great article. skyship
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Post by skyship on Sept 25, 2009 20:57:48 GMT -5
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Post by skyship on Sept 25, 2009 21:13:04 GMT -5
Will try to concentrate on this, I noticed that the bucky balls which are in chemtrails are listed here as well. Vorticell was mentioned: this ties in with the Tardegrade, but notice his mention of lead, I am thinking tin as well, tin roofs, metal roofs. and these things living with the metal. ? Vorticella the wheel like animal, ties in with the wheel like caricatures left by some ancestors in caves, Indians as well. the wheel is always shown, may not mean industrialization, may mean the "wheel animal" as E. Darwin called it. He talks of this in this paragraph found here: tinyurl.com/yaj97smbooks.google.com/books?id=Epyc1v7SrAcC&pg=PA146&lpg=PA146&dq=vorticella+and+Erasmus+darwin&source=bl&ots=tNmNYI17pk&sig=kZVEAJG3EB4 FxvwjaiZSUpQLpCI&hl=en&ei=fXe9Sr_DLNrg8Ab1xuWuAQ&sa=X&oi=book_result&ct= result&resnum=1#v=onepage&q=&f=false skyship
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Post by skyship on Sept 25, 2009 21:21:01 GMT -5
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Post by aqt on Sept 26, 2009 4:43:28 GMT -5
wow...you NEVER cease to amaze me
off to work for 12 hours....will read more when I get home
keep pluggin'/ don't stop
aqt
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