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TWO SEPARATION PROCEDURES
To cause the cleavage of the pathogen from the host cell’s FCG system at the position alpha to the double bond of the pathogen that activated the integration, be it by an azomethine condensation or a free radical addition, one uses a highly activated Carbonyl group dehydrogenator. The dehydrogenation thus brought about leaves a free radical, which when oxygen is present will add a molecule of molecular oxygen to become a peroxide free radical. This will cause the cleavage leaving a Carbonyl group to restore the FCG, or a Carbonyl group to replace its activating ethylenic linkage that formed the integration. This exchange is to the advantage of a long lasting immunity or resistance of a higher order than the ethylenic linkage had offered formerly, because the Carbonyl group is a richer assembler of electrons than the ethylenic linkage and gives the FCG a higher dehydrogenating power that will start combustion in a wider field of fuel or pathogens that enter the field. This is seen in the Triquinoyl molecule we use as a therapeutic agent. The orbital mechanics of the six Carbonyl groups united in cycle determine such a heavy concentration of electrons at one of the groups that it is actually expellable from the group to make a five-member ring, leuconic acid. It is the electronic saturation of this Carbonyl group that makes it a splendid dehydrogenating agent to serve so satisfactorily as a therapeutic Reagent.
Warburg credited anoxia with the power to produce cancer, and while anoxia is essentially provocative, we have found that in addition, two carcinogenic agents are also necessary.They are the initiating and sustaining carcinogens. One and the same chemical structure may serve in both capacities, as will be seen in the diagrams that follow. However, the initiating carcinogen or allergen may be: a virus, a product of germ activity in the intestine, a mercaptan or other structure carrying a sulfydryl group, or a free radical produced by the sun’s rays on a ripening pollen, or a present in some plastic material. The sustaining allergen or carcinogen is in our experience a product of germ activity. It is brewed in an old scarred in focus of silent infection where enough oxygen is not admitted to burn the free radicals produced in its slow metabolism, thus giving them a chance to polymerize. Both are joined to the energy receiving mechanism of the host cell by free radical addition, and hence, by a single covalent bond. The integration of a virus is with the energy producing mechanism and likewise by a single covalent bond, and so the phenomena associated with viral infection and allergy, including cancer production as well as their reversals, are of the same pattern and may be discussed together.Though the single covalent bond is well known for its easy rotation under environmental influences, it appears fixed for each disease entity, a fact that gives a good clue to the nature of the critical atomic groups, both of the pathogen’s and of the host cell’s energy producing and receiving mechanisms.
A little more discussion should be given to the easy rotation of the single covalent bond, and also its ability to be fixed in one plane by mutual polar attractions and repulsions of component atomic groups in both the host cell and the integrated pathogen. This rigidity exhibited by each species in each of its viral infections has been observed as a constant feature and would be the only explanation available, if we assume that the pathogenic integration takes place by an addition at one position in the host cell’s FCG, and its activating double bond.
The additions of the two pathogens, the initiating and the supporting pathogens, cannot be formulated with exactness as the chemical structures are not known with exactness and we have arrived as far as we have by Postulates and check-up of each Postulate, all of which were based on sound chemical principles. With this reservation in mind, we may also formulate the integration of both pathogens with the critical atomic group of the host cell’s energy producing and receiving mechanisms, as directed by the polarity forces exhibited by the double bond and its substituents. This cannot be claimed to be absolute for we do not know the atomic groupings sufficiently for an absolute diagram. However, any utility in a conclusion reached by postulate is just as good a utility as that reached by cold fact, for it is the utility we need now to face the cancer and viral plagues we fret about or are not willing to tackle. The utility of an explanation is some reward.
We have observed that hog Cholera fails in 100% of cases to respond to the serial system of Carbonyl groups that hog Aftosa, cow Aftosa, and rabies respond to very satisfactorily. Many epidemics of Aftosa in cattle have responded 100% to this Reagent. On the other hand, Aftosa does not respond to Benzoquinone nor does rabies respond to diphenoquinone to which 100% of hog Cholera responds inmore than one epidemic. So the species pathogen-integrate for each disease is set. A diagram in one plane can be given on paper only, and will have to be interpreted by the reader with reference to other planes. The substituent groups R, R’ R” cannot be given in detail for they are not known. However, the signs will have to be understood to carry the polarity values that cause the fixation of the single covalent bond that joins the two parties, as we outlined before. What we can show is how the polarity values of the critical atomic groups of the autonomous host and of the parasitic pathogen favor the pathogenesis and also the separation of the host’s critical atomic group from the pathogen, which undergoes a stepwise oxidation. There is, however, more than one question that is not answered by the diagram. Further data must first be won. The main question answered is how and why the Reducing Agent is successful in all of the pathogenic integrations, regardless of species or viral type. This, one can see, is due to the firmness of the double bond against rotation, since the cleavage is had between its two terminals and they remain fixed with reference to each other. The diagram also indicates the fixation of the single covalent bond that combines the pathogen and host cell, in each specific disease integration, so as to offer steric hindrance to successful attack by certain Reagents, and steric advantage to others, and this is confirmed by clinical experience.
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