Death of the Cancer Industry By Gary Wade

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Dr. Rife and the Death of the Cancer Industry By Gary Wade http://educate-yourself.org/gw/rifedeathofcancerindustry%20.shtml Dr. Rife and the Death of the Cancer Industry By Gary Wade http://educate-yourself.org/gw/rifedeathofcancerindustry .shtml The Possible Genetic Cause of the Great Majority of Cancer Casesthat are Microbe Induced In 1931, after seven years of attempting to isolate a microbecause of cancer from over 20.000 cancer tissue samples, Dr. RoyalRaymond Rife did just that. Rife's 1931 discovery of a cancer microbefinally reached general public notice in 1944. That year a articleentitled The New Microscopes was published both in the February issueof The Journal of the Franklin Institute and in the 1944 Annual Reportof the Board of Directors of the Smithsonian Institution. Rife's work was not then and has not yet been appreciated bymicrobiology. because microbiology has a large blind spot, both in itsphysical visual view of the living microworld and in its conceptualview of the structure and life cycles of the living microworld. If youwish to look at living cells, the best research optical microscopesgenerally available throughout the world only reach about threethousand power. These microscopes in general cannot detect viruses,unless a fluorescence technique like Rife's fluorescence technique isused. These microscopes give very limited structural detail aboutliving cell organelles. If the biologist wants detailed structuralinformation about some cell structure, they use an electronmicroscope. However, the electron microscope picture is the picture ofa dead, often highly degraded and distorted structure. This is becausethe sample preparation process, which produces a sample that canwithstand the conditions of high vacuum and bombardment by a highenergy electron beam has degraded and distorted the original livingstructure. So at best you end up with a distorted snap shot of a nonliving structure. I do not mean to denigrate the great and marvelous contributionsmade by the electron microscope. I have considerable personalexperience with the use and operation of scanning electron microscopesand I hold them and transmission electron microscopes with highregard. I particularly appreciate the immense contributions made tothe understanding of micro cell structure by the massive ultra highresolution transmission electron microscopes such as can be found atthe University of Colorado at IBoulder,CO. . However, all this notwithstanding. I also know the electron microscopes' limitations, bothphysically and in its actual use by researchers. If you have ainterest in understanding biological microstructure, go to the troubleof going to a good research library and look up the Feb. 1944 issue ofThe Journal of the Franklin Institute or the 1944 Annual Report of theBoard of Directors of the Smithsonian Institution. In the RE. Seideland M. Elizabeth Winter article, The New Microscopes, look at thephotographic plates. Note the high quality resolution comparable tothat of current electron microscope photographs. The photograph of thetyphoid bacillus was taken with the Rife Universal Microscope at23,000 power and then photographically enlarged to 300,000 power. Note that this photograph has the resolution commonly found intodays high resolution electron microscope pictures of bacteria.Further note that the resolution in this print is not as good as theresolution on the negative it came from do to the limitations inprinting pictures in 1944 and even today. As was explained intechnical detail in Appendix A, Rife had discovered an opticalassembly configuration that effectively suppressed all Fraunhoferdiffraction phenomenon. while at the same time he made the organismlight itself by a natural fluorescence phenomenon. This fluorescencephenomenon was achieved by illuminating the specimen with an intensenarrow wavelength band of light. The particular band of light wasunique to each microbe. Also note that this is a photograph of anintact living bacterium. If you are familiar with currentmicrobiology. you know that little if any time is spent by the greatmajority of researchers watching and studying live microbes. Exceptfor spot optical microscope checks to make sure live cultures are asthey should be or are as assumed they should be. research is carriedout by biochemical techniques the results of which are interpreted inthe light of past perceived research results. In short actually verylittle live observation on microbe life cycles are carried out byresearchers anywhere on the entire planet. This brings us to the other blind spot in biology. Its name ispleomorphism or the ability of a microbe to change its physical form.During the later half of the 19th century and into the early part ofthis century, a sharply fought battle over whether or not somemicrobes could change their physical form was waged. Those infavor ofmonomorphism won out and it became "heresy" to advocate pleomorphism.After two years of reviewing the research for and againstpleomorphism, it is clear that the monomorphists were wrong. Themonomorphists won the argument because they had political prestige andeconomic positions of leverage. The monomorphists used opticalmicroscopes and lab techniques not adequate to determine the issue dueto inadequate magnification power, lack of non-lethal stainingmethods, sheer ignorance, and sloppy to lazy research work. If you goto the trouble of looking up the Feb. 1944 issue of the FranklinJournal, note that the Rife microscope photograph of the typhoidbacillus clearly shows the formation of a filter passing form (theoriginal operational meaning of the word virus) of the typhoidbacillus, in the top end of the bacillus. Rife found that when thisbacillus virus was released by the bacillus, it had a bacteriumflagella and was motile. Now all of this is just plain crazy, if youare a currently trained microbiologist. However, no currently trainedmicrobiologist owns or uses a Rife type optical microscope which couldeasily view this and the similar BX cancer virus, which is also amotile virus (ovoid body with bacterium flagella). The ovoid bodydimensions of the BX cancer virus are 750 angstroms long by 500angstroms thick. It is propelled by a proton transport flagella thesame as the parent bacterium. This "virus" will easily fit inside theso called AIDS virus (HIV) outer capsid and is comparable in size tothe inner (HIV) capsid. I now ask you microbiologists reading this:Will this BX cancer "virus" be recognized in a high power electronmicroscope photograph for what it is or will it just be consideredanother piece of degraded cellular debris in the prepared cancer cellsection sample? Much of what you see is what you are trained to see.How are microbiologists trained to see? Rife, using his Rife type microscope, had for seven years beenable to observe and isolate a microbe from carcinoma cancer tissue.However, upon injection of concentrations of this microbe into testanimals, no cancer was produced. In 1931, Rife got the idea to exposea sample of card normal breast cancer tissue to 24 hours of broad bandviolet to ultraviolet light exposure from a argon gas discharge tube(see Journal of the Franklin Institute article). A one half centimeteron a side cube of carcinoma breast cancer tissue was placed into atest tube containing Kendall medium and incubated at 37 degreescentigrade. The test tube was then exposed to 24 hours of argon gasdischarge light. The test tube growth medium was then examined underthe Rife Universal microscope. at a magnification of 10.000 diameters.The medium was found to be teeming with animated ovoid microbes 1/15microns long and 1/20 microns thick. which Rife eventually named theBX cancer virus. This BX cancer virus was then carried throughfourteen transplants from Kendall Medium to Kendall Medium. Theanimated BX cancer virus multiplied and remained of constant form. Thefact that the BX cancer virus could multiply on a sterile non-livinggrowth medium indicated that Rife's BX cancer "virus" was a livingmicroorganism unlike the currently accepted understanding of a virusas a biological structure dependent on cellular metabolism toregenerate (multiply) and propagate its existence. From currentknowledge, we must assume that Rife's BX cancer virus contains withinits structure, a gnome, DNA decoding enzymes, protein digestiveenzymes, transfer RNA, ribosomes, and associated proteins. When concentrations of this BX cancer virus were injected into 426albino rats, all rats developed cancer tumors at the injection releasesite in the animal tissue. Further experiments with the BX cancervirus demonstrated that it can be easily changed from one microbe formto another by means of altering the media upon which it is grown. Rifefound more than six forms, which the BX cancer virus could betransformed into. These included: 1) BY cancer virus, which causedsarcoma cancer tumors. 2) Cryptomyces plemorphia fungi, which Rifefound implicated in rheumatoid arthritis. 3) Progenitor cryptocides.4) Bacillus coli. 5) Bacillus typhosus, and 6) Virus of the bacillustyphosus, which can be clearly seen in the photograph of the typhoidbacillus appearing in the article The New Microscopes of Feb.1944. Rife was not the only researcher to find a microbial cause forcancer. Many others have also. Nor was Rife the only one to build anoptical microscope that could see the BX cancer virus. Currently inCanada the biologist Gaston Naessens uses an ultraviolet microscopewhich can easily view the BX cancer virus in living blood from cancerpatients. Naessens' microscope uses an ultraviolet light source whichis first polarized. then focused down and sent through a frequencydoubler crystal and finally sent into a special condenser section fordark field microscopy. Looking at live blood from cancer patients,Naessens has found and made videos of at least sixteen different formsthe BX cancer virus can be transformed into. I have viewed some ofthese videos and the anti mated (motile) BX and BY cancer virues areclearly visible and look just as Rife described them. As for the other researchers who have found the same microbialcause for cancer as Rife, they have all been persecuted, while theirwork has been maimed and discredited by the corrupt higher rulingcircles of what currently passes for legitimate medicine andmicrobiology. Perhaps a brief review of the work of one victim is inorder. Dr. Virginia Livingston-Wheeler in 1947, while studying tumors,found the same organism in all of them. Her findings were published inAugust 1948 by the New York Microscopical Society Bulletin. Later inDec. 1950, Wheeler had an article published in the American Journal ofMedical Sciences on microbes cultures taken from both human and animaltumors. On Sept. 10, 1953 The Washington Post reported the discoveriesof Dr. Wheeler and her team from Rutgers-Presbyterian HospitalLaboratory which were disclosed at the 6 th International Congress ofMicrobiology in Rome. They had found conducive proof of a microbialcause for cancer. When Dr. Wheeler and her group returned from Rome toRutgers-Presbyterian Hospital they found that the funds for theirlaboratory were being cut off. The laboratory was closed. This was thebehind-the-scenes work and doings of Dr. Corneluis P. Rhoads, the headof Memorial Sloan-Kettering Cancer Center. The fear of the cancerindustry elite is and was immense. If the truth about the true causeof cancer becomes known, a cheap cure will be found shortlythereafter. This will kill the cancer goose which lays tens ofbillions of dollars worth of eggs a year. Is there nothing these scumwill not do for their god money? No! The San Diego Union of July 31st, 1949 reported on the work of Dr.Gruner of Mill University, Montreal, Canada and Dr. J.E. Heft ofWindsor, Canada. They were in agreement with and had experimentalproof that Dr.Royal Raymond Rife's discovery that cancer was caused bya microbe was correct. In 1950 Dr. James Hillman of RCA Labs in Princeton, N.J. found theBX cancer virus using an electron microscope. For an in-depth documented overview of the massive suppression byallopathic medicine of real cancer treatment breakthroughs thatworked, I recommend you read: 1) The Cancer Cure That Worked, by BarryLynes, and 2) The Healing of Cancer, by Barry Lynes. Both books areavailable through Marcus Books, P.O. Box 327, Queensville, Ontario,Canada LOG 1 RO. (41 6)-478-2201. I will now share with you some observations about cancer cells anda classic experiment in which they are compared to normal cells, whichsuggests a simple answer to how cells infected with the BX cancervirus become cancerous. It has long been noted that cancer cells actand appear somewhat like undifferentiated embryonic cells.Furthermore, cancer cells apparently have mostly an anaerobic (withoutoxygen) metabolism. Note that the only time in the normal life cycleof mammalian cells in which they are of a undifferentiated embryonicnature and also have an apparent appreciable anaerobic metabolism isthe period between the time the female egg, the ovum, has beenfertilized in the fallopian tube and just before a viable placenta hasdeveloped in the uterus. Geneticists and embryologists have shown thatthe entire development of the fetus from just-fertilized ovum to thefully developed fetus is governed completely by sequentially read andexpressed genetic information. There is an exceedingly complex geneticinterchange and feedback control system in operation. Some of thisgenetic code is used only for a short period of time and is thensealed away not to be read or opened up again in the individualsexistence, except during chromosome copying prior to cell division.Cancer cells act as though they have had some set of embryonic genesequences reactivated. However, in the now mature differentiatedmammalian cells from which this cancer cell has been derived, thecontrol system that normally would have deactivated this embryonicgene sequence(s) is itself long since deactivated. The cancer cell isin a run away catch 22 situation. It has been found that many genes occur in sequenced sets in whichnone of the genes in the sequence can be read and expressed unless thefirst gene in the sequence has been opened to be read. Just in frontof that first gene there is a DNA code sequence which has to have apromoter protein bound to it so that the DNA code sequence readingenzyme can temporarily attach to this promoter protein and then beginreading/translating the DNA code of the gene sequences into messengerRNA for protein synthesis by ribosomes. For this promoter protein toattach to its DNA coupling sequence at the beginning of the genesequence, this sequence must be in the normal B-DNA right handeddouble helix form (see Figures 1 and 3). If the coupling site codesequence or the DNA code sequence immediately in front of it has ablocking protein attached or is in the form of the left handed Z-DNAdouble helix (see Figure 2), the promoter protein can not bind/couplewith its DNA code sequence and therefore the entire sequence of geneswill not be read and expressed. The Z-DNA double helix form is a verycompact form of the double helix. It has no major grove structure like the B-DNA double helix whichallows a promoter protein to physically match up with a specific DNAcode sequence which will manifest itself in the unique molecularstructure of the surface of the major grove for that unique DNA codesequence. The Z-DNA double helix structure gives very littleinformation about what the DNA code sequence is in its core. For aleft handed Z-DNA double helix associated with a specific DNA codesequence to convert itself into a right handed B-DNA double helix, sothat the promoter protein can attach, the concentrations of variousions in the cell nucleus must be in certain specific ranges for thatspecific Z-DNA sequence. The specific concentrations and ratios ofions in the nucleus is determined by the actions of ion gates andpumps in the cell outer membrane. These ion gates and pumps arecontrolled by messenger proteins and compounds from both inside andoutside the cell membrane. What this means is that the cell geneticexpression can be greatly influenced and controlled by the geneticexpression of other cells and cell sets (organs). And of coarse duringembryonic development this external cell influence is in dominantcontrol of the whole cell system of membrane ion gates and pumps. Now that some of the basic genetic control process has beenstated, several questions need to be asked. Can one or more microbeproteins or chemical compounds be generated and released inside amammalian cell by a parasitic microbe? Can these proteins or compoundsact as a messenger to open up or close down cell membrane ion gates orpumps? Can this opening or dosing of ion gates and or pumps cause agene sequence which is normally only open during early embryonicdevelopment to open up again and thereby cause the cell to gocancerous? I believe the answer to all these questions is yes. Ofcourse there are many other possibilities i.e. some of these proteinfragments may act as promoter proteins or combine with and removeblocker proteins, thereby allowing a promoter protein to attach to aDNA sequence and thereby initiate DNA transcription. Dr. Robert 0. Becker, M.D. has written a book The Body Electric inwhich he goes into great detail about tissue regeneration processesand their electrical and ionic connection to genetic expression. Iwill now use information distilled from Becker's book which supportsmy above suppositions. In 1948 Dr. Meryl S. Rose performed a milestone experiment on salamanders. Rose transplanted frog kidney cancertumor tissue onto a salamander's hind limb. These frog tumors werevirus induced. The results of his experiment, however are the sameeven if the tumor is carcinogen induced, which was done later. Thetransplanted tumors would grow and spread, leading to the salamander'sdeath, if no intervention was taken. However, if Rose amputated thelimb below or through the middle of the tumor, the salamander wouldregrow the limb and in the process the tumor(s) would disappear, evenif the tumor had already spread to other body locations. Tissuebiopsies of the wound region during regeneration showed that bothsalamander cells as well as cancerous frog kidney cellsdedifferentiated into embryonic cell forms during the blastemaformation process as the wound healed. Even more amazing, as the blastema propagated forward,regenerating the limb, both embryonic frog and embryonic salamandercells of the blastema multiplied (devided). They differentiated intothe cell types needed to form the new limb tissue, i.e. muscle cells,cartilage cells, capillary cells, etc. In later years researchers suchas Becker demonstrated that it was the near unique ability of thesalamander's nervous system to drastically change the ionicenvironment around blastema cells, along with hormone secretions fromnerve dendrites, which allowed blastema cells to dedifferentiate intoembryonic cells and then to red differentiate into the new cell typesof the regenerating limb. Becker and other researchers were able toget rats to regrow most of, or all of a amputated limb. They implanteda negative current source that produced a negative electric potentialdistribution inside the limb directly behind the amputation site. Thisclosely mimicked what a salamander would have at that site if it werescaled up to the rats size. To understand what is happening here, youneed to know that in a rat just as in a salamander the myelin sheathcells coating the motor nerve fibers carry an electron current throughcollagen fibers which are N-type semi-conductors. This current is deposited mostly into the body's electrolyticsolution surrounding the cells near where the nerve fiber ends. Themyelin sheath cells coating the sensor nerve fibers carry an electroncurrent on their collagen fibers away from where the sensor nervefiber ends. The motor nerve fibers are essentially all in the bodyinterior and the sensor nerve fibers are essentially all on the bodysurface. As a amputation wound heals over with skin, surface sensornerve fibers cover over what is normally a motor nerve fiber region.In a short period of time the cells under the new forming skin layercan be converted into dedifferentiated embryonic cells under theinfluence or control of the external cell membrane ionic environmentat the wound site as determined by the electric currentipotential ofthe combined sensor and motor nerve sheaths activity in the wound area( blastema formation zone). I can not here go into all of thewonderful detail of Becker's book. However, I hope I have given thereader at least an understanding of how cancer can possibly come aboutby a simple change in the ion environment in the cell nucleus. If youare interested in tissue regeneration or are aserious biologist. I cannot recommend Becker's book enough. Particularly the last chapter,Postcript: Political Science. This chapter with great clarity andskill, clearly shows why we as a nation need to dismantle allcentralized cesspools of corruption as exemplified by the NationalInstitutes Of Health. The NIH needs to be replaced by regionalinstitutes which are government funded, but ran and controlled bydemocratically elected administrators elected by the research community. Before ending this appendix, a warning and an explanation of whyX-ray radiation should never be used to treat cancer. Rife was able toisolate the BX cancer virus from cancer tumor tissue samples. He thenexposed these viruses to 24 hours of ultra violet light exposure. Thisvirus obtained in this manner was 100% effective in inducing cancer inlab animals. His form of the BX cancer virus was exceedingly virulent.Other researchers who apparently isolated the same BX cancer virus, ora form of it, and inoculated test animals by similar methods only hadapproximately 25% cancer induction rates. A possible simple answer forthe discrepancy is that the ultraviolet light from the argon dischargecaused some of the adjacent thimine DNA base codes to dimerize(chemically bond together). When the DNA reader enzyme whichtranslates the DNA base code into messenger RNA for protein synthesiscomes across a dimerized thimine base code pair, it stops RNAsynthesis. The reader enzyme then breaks into two fragments. One fragment stays at the dimerization site to mark it and theother fragment initiates a complex set of enzyme reactions to removethe dimerized pair and replace them with a new undimerized pair.During this repair process the messenger RNA generated fragment isreleased. If this messenger RNA fragment contains the genetic RNA basecode sequence for ribosome attachment, it will be read by theribosomes and a protein fragment will be generated and released. Inparticular, if the RNA fragment is fed into a cluster of ribosomes(polyribosomes) which are located on or associated with theintercellular matrix web intersections, we can expect many copies ofthe coded protein fragment to be generated and released Furthermore,since the RNA fragment does not contain the normal stop synthesis codeand message RNA end sequence base code, the RNA fragment is not likelyto be immediately dismantled after polyribosome reading and proteinsynthesis like regular messenger RNA is. This fragment is likely to beread over again and again. Now. if the generated protein fragmenthappens to be an activator or suppressor of a cell membrane ionchannel or ion pump you have the potential beginnings of a cancerproducing situation as discussed above. This protein fragment(s) might also act as a promoter protein thatenables the DNA reader enzyme to attach to and read a gene sequence.Or this protein fragment may combine with a blocker protein on arepressor gene at the front of a DNA gene sequence and remove it,thereby allowing a promoter protein to combine with a DNA sequence andthen facilitating attachment of the DNA reader enzyme (RNApolymerase). All of this is not the normal "plan" of the normal cellmetabolism. An excellent example of this sort of defective proteinproduction and its cancerous consequences is the genetic diseasexeroderma pigmentosum. In it the individual has an inherited defect intheir ability to repair the aforementioned DNA base code dimerizationdamage. They are hypersensitive to sun light exposure and developpre-cancerous and cancerous skin conditions. They usually die of skincancer before their twentieth birthday. Now what does this have to dowith massive cellular tissue damage suffered by cancer patients whileunder going standard allopathic medical X-ray treatment for cancer? Asstated in Appendix B. Rife's normal treatment for cancer patients wasthree minutes of exposure once every three days to his frequencyinstrument. This frequency instrument, when treating cancer, probably producedrepeating packets of 11,780,000 or 23.560,000 light pulses per second.These light pulses in turn produced ultra low intensity ultra sound inthe patient's body of a frequency of 11.780.000 or 23.560.000 cyclesper second, which is the approximate mechanical structural resonancefrequency of the BX cancer viruses. The Bx viruses disintegrated. Inthe normal carcinoma cancer cell, there are thousands of BX cancerviruses. When these BX cancer viruses all disintegrate together at thesame time, they release their gnome, digestive enzymes, ribosomes,assorted proteinslenzymes, etc. into the cell. The cancer cell isoverwhelmed, dies, and promptly disintegrates. When using Rife'scancer treatment method on a cancer patient that has undergoneextensive allopathic medical X-ray damage, there is the highpossibility of an encounter with a new kind of cancer cell whichRife's treatment method won't work on. Allopathic medical X-ray treatment causes significant ultravioletlight, ionization, and free radical production both in tumor tissueand adjacent normal tissue. With this ultraviolet light, ionizationand free radical production, there is the associated dimerization ofadjacent DNA base code molecular pairs. Both cancer cells and adjacentnon cancer cells suffer significant cell membrane integrity damagefrom the X-ray radiation. All of this culminates in the possibility ofa heavily radiation damaged BX cancer virus penetrating the cellmembrane of a non cancerous cell and instigating production of cancercausing protein fragments as discussed above. But its own gnome sobadly damaged that it can not propagate itself. If this were to occur,then a cancer cell could be created which was not infested with the BXcancer virus and therefore not treatable by Rife's frequencyinstrument or ultra sound of 11.789,000 or 23.560.000 cycles persecond. Of coarse the X-ray radiation alone could generate a cancercell that the original Rife's treatment method would not cure. Well we have skimmed over a lot of technical data in thisappendix. however, I hope the reader now has a conceptual frame workin which to begin questioning the current allopathic medicine approachto cancer causes, treatments, and cures. Only by honest researchersgoing back and looking at the suppressed results of past honest cancerresearchers can we hope to find honest valid answers about cancercauses and cures. Gary Wade "An important scientific innovation rarely makes its way bygradually winning over and converting its opponents: it rarely happensthat Saul becomes Paul. What does happen is that its opponentsgradually die out and that the growing generation is familiarized withthe idea from the beginning." Max Planck Taken from: DR. RIFE AND THE DEATH OF THE CANCER INDUSTRY. a paperby physicist Gary Wade. P.S. - It is now empirically known that many types of cancer canbe easily and quickly killed by exposure to pressure square waves of afrequency of approximately 2127 cycles per second. It appears that oneor more of the higher frequency hidden fourier sine wave components.i.e. 3 x 2127Hz = 6381Hz; 5 x 2127Hz = 10,635Hz; 7 x 2127Hz = 14,889Hz; 9 x 2127Hz = 19,143 Hz, etc. , etc. opens up ion gates on thecancer cells' membrane and radically changes the ionic conditionsinside the cancer cell such that it drops the bi-lipid layer potentialdifference below some critical value below which the cancer cell cannot recover and it dies.