Elektromedizin - Gary Wade über Rife, Krebs, BX-Virus |
Elektromedizin: welche Geräte gibt es. Welches System kann was?
Zapper
Zapper diverse: Violet-Ray, EMEM, Beck,
F-Scan (englisch)
Clark-Zapper, EMEM, Rife-Bare,
Beck, Doug, Katze mit Tumor (engl.)
Zapper Wade 2127, Rifes Entdeckung
BX/Bestätigung Naessens (engl.)
Zapper 727 und 2128
Zapper III
Zapper Wayne, Diagnose
Zapper Doug
Zapper Weeks-Parker
Zapper EMEM2, EMEM3
Zapper Veja
Zapper Beck Zapper
Beck1
Zapper CES Beck
Brain Tuner
Zapper Clark
Zapper Emor
Pulser Beck
Pulser Superthumpy
Pulser Haining
meine Medizingeräte
Frequenzen finden
Frequenzen finden Doug
Frequenzen finden Michael Prescott
Frequenz-Liste CAFL 2007 englisch
Frequenz-Liste AFCAFL 2016 englisch
Frequenz-Liste ETDFL 2016 englisch
Frequenz-Liste ETDFL 2020 englisch
Frequenz-Liste ETDFL 2020 deutsch
Nebenwirkungen
Entgiftungssymptome bei Rife/Bare-Gerät
|
siehe auch: Elektromedizin Frequenzen
Rife Clark Blitze
Parasiten Unterdrückung |
www.rife.de/cancer/cancer.html
Rife and Cancer
Introduction
Royal Raymond Rife is probably best known for claims
that he discovered an effective treatment for Cancer. Indeed should this be
the case, and there is a lot of circumstantial evidence to support this, then
this would be one of the most significant medical discoveries of the 20th
century.
Here in Europe, there are a number of doctors and clinics openly using the
Rife method for treating patients for cancer and many other diseases.
We also know of a reputable manufacturer of medical equipment in Germany (Onco-Therm
GmbH) that already produces a commercial unit for hospitals that includes
the Rife protocol as part of a comprehensive treatment for cancer and was
presented at the Medica trade fair in 1999! Other companies are known to be
in the process of preparing their own machines for release into the European
market in the near future. Although the medical establishment here in general
is not yet aware of Rife's discovery, there are certainly plenty of signs
that this will be changing in the near future.
To provide you with some serious background information on the subject, here
is an extract from a paper entitled: "
Dr. Rife and the Death of
the Cancer Industry" written by the physicist, Gary Wade.
The Possible Genetic Cause of the Great Majority of Cancer Cases that
are Microbe Induced
In 1931, after seven years of attempting to
isolate a microbe from
over 20.000 cancer tissue samples, Dr. Royal Raymond Rife discovered a
cancer
microbe which finally reached general public notice in 1944. That year
an article entitled
The New Microscopes was published both in
the February issue of The Journal of the Franklin Institute and in the 1944
Annual Report of the Board of Directors of the Smithsonian Institution.
Rife's work was not then and has not yet been appreciated by microbiology,
because microbiology
has a large blind spot, both in its physical visual
view of the living microworld and in its conceptual view of the structure
and life cycles of the living microworld. If you wish to look at living cells,
the best research optical microscopes generally available throughout the world
only reach about
three thousand power.
These microscopes in general
cannot detect viruses, unless a
fluorescence
technique like Rife's fluorescence technique is used. These microscopes
give very limited structural detail about living cell organelles. If the biologist
wants detailed structural information about some cell structure, they use
an electron microscope. However, the electron microscope picture is the
picture
of a dead, often highly degraded and distorted structure.
This is because the sample preparation process, which produces a sample that
can withstand the conditions of high vacuum and bombardment by a high energy
electron beam has degraded and distorted the original living structure. So
at best you end up with a
distorted snap shot of a non living structure.
I do not mean to denigrate the great and marvelous contributions made by the
electron microscope. I have considerable personal experience with the use
and operation of scanning electron microscopes and I hold them and transmission
electron microscopes with high regard. I particularly appreciate the immense
contributions made to the understanding of micro cell structure by the massive
ultra high resolution transmission electron microscopes such as can be found
at the University of Colorado at Boulder, CO. However, all this not withstanding,
I also know the electron microscopes' limitations, both physically and in
its actual use by researchers.
If you have a interest in understanding biological microstructure, go to the
trouble of going to a good research library and look up the Feb. 1944 issue
of "The Journal of the Franklin Institute" or the 1944 "Annual
Report of the Board of Directors of the Smithsonian Institution". In
the RE. Seidel and M. Elizabeth Winter article, "The New Microscopes",
look at the photographic plates.
Note the
high quality resolution comparable to that of current electron
microscope photographs. The photograph of the typhoid bacillus was taken with
the Rife Universal Microscope
at 23,000 power and then photographically
enlarged to
300,000 power. Note that this photograph has the
resolution
commonly found in todays high resolution electron microscope pictures
of bacteria.
Further note that the resolution in this print is not as good as the resolution
on the negative it came from do to the limitations in printing pictures in
1944 and even today. As was explained in technical detail in Appendix A, Rife
had discovered an optical assembly configuration that effectively
suppressed
all Fraunhofer diffraction phenomenon. while at the same time he made
the organism light itself by a
natural fluorescence phenomenon.
This fluorescence phenomenon was achieved by illuminating the specimen with
an intense
narrow wavelength band of light. The particular band of
light was
unique to each microbe. Also note that this is a photograph
of an intact living bacterium. If you are familiar with current microbiology.
you know that little if any time is spent by the great majority of researchers
watching and studying live microbes. Except for spot optical microscope checks
to make sure live cultures are as they should be or are as assumed they should
be.
research is carried out by biochemical techniques the results of
which are interpreted in the light of past perceived research results. In
short actually very little live observation on microbe life cycles are carried
out by researchers anywhere on the entire planet.
This brings us to the other blind spot in biology. Its name is
pleomorphism
or the ability of a microbe to change its physical form. During the later
half of the 19th century and into the early part of this century, a sharply
fought battle over whether or not some microbes could change their physical
form was waged. Those in favor of monomorphism won out and it became "heresy"
to advocate pleomorphism.
After two years of reviewing the research for and against pleomorphism, it
is clear that the monomorphists were wrong. The monomorphists won the argument
because they had political prestige and economic positions of leverage. The
monomorphists used optical microscopes and lab techniques not adequate to
determine the issue due to inadequate magnification power, lack of non-lethal
staining methods, sheer ignorance, and sloppy to lazy research work.
If you go to the trouble of looking up the Feb. 1944 issue of the Franklin
Journal, note that the Rife microscope photograph of the typhoid bacillus
clearly
shows the formation of a filter passing form (the original
operational meaning of the word virus) of the typhoid bacillus, in the top
end of the bacillus.
Rife found that when this
bacillus virus was released by the bacillus,
it had a bacterium flagella and
was motile. Now all of this is just
plain crazy, if you are a currently trained microbiologist. However, no currently
trained microbiologist owns or uses a Rife type optical microscope which could
easily view this and the similar
BX cancer virus, which is
also
a motile virus (ovoid body with bacterium flagella).
The ovoid body dimensions of the BX cancer virus are
750 angstroms
long by
500 angstroms thick. It is propelled by a proton transport
flagella the same as the parent bacterium. This "virus" will easily
fit inside the so called AIDS virus (HIV) outer capsid and is comparable in
size to the inner (HIV) capsid. I now ask you microbiologists reading this:
Will this BX cancer "virus" be recognized in a high power electron
microscope photograph for what it is or will it just be considered another
piece of degraded cellular debris in the prepared cancer cell section 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 been able to observe
and isolate a
microbe from carcinoma cancer tissue. However, upon injection
of concentrations of this microbe into test animals, no cancer was produced.
In 1931, Rife got the idea to expose a sample of card normal breast cancer
tissue to
24 hours of broad band violet to ultraviolet light exposure from
a argon gas discharge tube (see Journal of the Franklin Institute article).
A one half centimeter on a side cube of carcinoma breast cancer tissue was
placed into a test tube containing Kendall medium and incubated at 37 degrees
centigrade. The test tube was then exposed to
24 hours of argon gas discharge
light.
The test tube growth medium was then examined under the Rife Universal microscope
at a magnification of 10.000 diameters. The medium was found to be teeming
with
animated ovoid microbes 1/15 microns long and 1/20 microns thick.
which Rife eventually named the BX cancer virus.
This BX cancer virus was then carried through
fourteen transplants
from Kendall Medium to Kendall Medium. The animated BX cancer virus multiplied
and
remained of constant form. The fact that the BX cancer virus could
multiply on a sterile non-living growth medium indicated that Rife's BX cancer
"virus"
was a living microorganism unlike the currently accepted
understanding of a virus as a biological structure dependent on cellular metabolism
to regenerate (multiply) and propagate its existence. From current knowledge,
we must assume that Rife's BX cancer virus contains within its structure,
a genome, DNA decoding enzymes, protein digestive enzymes, transfer RNA, ribosomes,
and associated proteins.
When concentrations of this BX cancer virus were
injected into 426 albino
rats, all rats developed cancer tumors at the injection release site in
the animal tissue. Further experiments with the BX cancer virus demonstrated
that it can be easily
changed from one microbe form to another by means
of altering the media upon which it is grown.
Rife found
more than six forms, which the BX cancer virus could be
transformed into. These included:
1) BY cancer virus, which caused sarcoma cancer tumors.
2) Cryptomyces plemorphia fungi, which Rife found implicated in rheumatoid
arthritis.
3) Progenitor cryptocides.
4) Bacillus coli.
5) Bacillus typhosus, and
6) Virus of the bacillus typhosus, which can be clearly seen in the photograph
of the typhoid bacillus appearing in the article 'The New Microscopes' of
february 1944.
Rife was not the only researcher to find a microbial cause for cancer. Many
others have also. Nor was Rife the only one to build an optical microscope
that could see the BX cancer virus.
Currently in Canada the biologist Gaston
Naessens
uses an ultraviolet microscope
which can easily view the BX cancer virus
in living blood from cancer patients. Naessens' microscope uses an
ultraviolet
light source which is
+ first polarized, then
+ focused down and
+ sent through a frequency doubler crystal and finally
+ sent into a special condenser section for dark field microscopy.
Looking at live blood from cancer patients, Naessens has found and made
videos
of at least sixteen different forms the BX cancer virus can be transformed
into.
I have viewed some of these videos and the animated
(motile) BX and BY cancer virues are clearly visible and look just as Rife
described them.
As for the other researchers who have found the same microbial cause for cancer
as Rife,
they have all been persecuted, while their work has been maimed
and discredited by the corrupt higher ruling circles of what currently passes
for legitimate medicine and microbiology. Perhaps a brief review of the work
of one victim is in order.
Dr. Virginia Livingston-Wheeler in 1947, while studying tumors, found the
same organism in all of them. Her findings were published in August 1948 by
the New York Microscopical Society Bulletin. Later in Dec. 1950, Wheeler had
an article published in the American Journal of Medical Sciences on microbes
cultures taken from both human and animal tumors.
On Sept. 10, 1953 The Washington Post reported the discoveries of Dr. Wheeler
and her team from Rutgers-Presbyterian Hospital Laboratory which were disclosed
at the 6 th International Congress of Microbiology in Rome. They had
found
conducive proof of a microbial cause for cancer.
When Dr. Wheeler and her group returned from Rome to Rutgers-Presbyterian
Hospital they found that the
funds for their laboratory were being cut
off. The laboratory was closed. This was the behind-the-scenes work and
doings of Dr. Cornelius P. Rhoads, the head of Memorial Sloan-Kettering Cancer
Center.
The fear of the cancer industry elite is and was immense. If the truth about
the true cause of cancer becomes known, a cheap cure will be found shortly
thereafter. This will kill the cancer goose which lays tens of billions of
dollars worth of eggs a year. Is there nothing these scum will 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. Hett of Windsor, Canada.
They were in agreement with and had experimental proof that Dr. Royal Raymond
Rife's discovery that cancer was caused by a microbe was correct.
In 1950 Dr. James Hillier of RCA Labs in Princeton, N.J.
found the BX cancer
virus using an electron microscope.
For an in-depth documented overview of the massive suppression by allopathic
medicine of real cancer treatment breakthroughs that worked, I recommend you
read:
1)
Lynes:
'The Cancer Cure That Worked', by Barry Lynes, and
2)
Lynes: 'The Healing of Cancer', by Barry Lynes (Marcus Books, Queensville, Ontario,
Canada)
I will now share with you some observations about cancer cells and a classic
experiment in which they are compared to normal cells, which suggests a simple
answer to
how cells infected with the BX cancer virus become cancerous.
It has long been noted that
cancer cells act and appear somewhat like undifferentiated
embryonic cells. Furthermore, cancer cells apparently have mostly an anaerobic
(without oxygen) metabolism. Note that the only time in the normal life cycle
of mammalian cells in which they are of a undifferentiated embryonic nature
and also have an apparent appreciable anaerobic metabolism is the period between
the time the female egg, the ovum, has been fertilized in the fallopian tube
and just before a viable placenta has developed in the uterus.
Geneticists and embryologists have shown that the entire development of the
fetus from just-fertilized ovum to the fully developed fetus is governed completely
by sequentially read and expressed genetic information. There is an
exceedingly
complex genetic interchange and feedback control system in operation.
Some of this genetic code is
used only for a short period of time and
is then sealed away not to be read or opened up again in the individuals existence,
except during chromosome copying prior to cell division.
Cancer
cells act as though they have had some set of embryonic gene sequences reactivated.
However, in the now mature
differentiated mammalian cells from which
this cancer cell has been derived, the control system that normally would
have deactivated this embryonic gene sequence(s) is itself long since deactivated.
The cancer cell is in a run away catch 22 situation.
It has been found that many genes occur in sequenced sets in which none of
the genes in the sequence can be read and expressed unless the first gene
in the sequence has been opened to be read. Just in front of that first gene
there is a DNA code sequence which has to have a promoter protein bound to
it so that the DNA code sequence reading enzyme can temporarily attach to
this promoter protein and then begin reading/translating the DNA code of the
gene sequences into messenger RNA for protein synthesis by ribosomes.
For this promoter protein to attach to its DNA coupling sequence at the beginning
of the gene sequence, this sequence must be in the normal B-DNA right handed
double helix form (see Figures 1 and 3). If the coupling site code sequence
or the DNA code sequence immediately in front of it has a blocking protein
attached or is in the form of the left handed Z-DNA double helix (see Figure
2), the promoter protein can not bind/couple with its DNA code sequence and
therefore the entire sequence of genes will not be read and expressed. The
Z-DNA double helix form is a very compact form of the double helix. It has
no major grove structure like the B-DNA double helix which allows a promoter
protein to physically match up with a specific DNA code sequence which will
manifest itself in the unique molecular structure of the surface of the major
grove for that unique DNA code sequence. The Z-DNA double helix structure
gives very little information about what the DNA code sequence is in its core.
For a left handed Z-DNA double helix associated with a specific DNA code sequence
to convert itself into a right handed B-DNA double helix, so that the promoter
protein can attach, the concentrations of various ions in the cell nucleus
must be in certain specific ranges for that specific Z-DNA sequence. The specific
concentrations and ratios of ions in the nucleus is determined by the actions
of ion gates and pumps in the cell outer membrane. These ion gates and pumps
are controlled by messenger proteins and compounds from both inside and outside
the cell membrane. What this means is that the cell genetic expression can
be greatly influenced and controlled by the genetic expression of other cells
and cell sets (organs). And of coarse during embryonic development this external
cell influence is in dominant control of the whole cell system of membrane
ion gates and pumps.
Now that some of the basic genetic control process has been stated, several
questions need to be asked. Can one or more microbe proteins or chemical compounds
be
generated and released inside a mammalian cell
by a parasitic
microbe? Can these proteins or compounds act as a messenger to open up
or close down cell membrane ion gates or pumps? Can this opening or dosing
of ion gates and or pumps cause a gene sequence which is normally only open
during early embryonic development to open up again and thereby cause the
cell to go cancerous? I believe the answer to all these questions is yes.
Of course there are many other possibilities i.e. some of these protein fragments
may act as promoter proteins or combine with and remove blocker proteins,
thereby allowing a promoter protein to attach to a DNA sequence and thereby
initiate DNA transcription.
Dr. Robert Becker, M.D. has written a book
'The
Body Electric' in which he goes into great detail about tissue regeneration
processes and their electrical and ionic connection to genetic expression.
I will now use information distilled from Becker's book which supports my
above suppositions.
In 1948 Dr. Meryl S. Rose performed a mile stone experiment
on salamanders. Rose transplanted frog kidney cancer tumor tissue onto a salamander's
hind limb. These
frog tumors were virus induced.
The results of his experiment, however are the same even if the tumor is carcinogen
induced, which was done later. The transplanted tumors would grow and spread,
leading to the salamander's death, if no intervention was taken. However,
if Rose
amputated the limb below or through the middle of the tumor,
the salamander would regrow the limb and in the process the
tumor(s)
would disappear, even if the tumor had already spread to other body
locations.
Tissue biopsies of the wound region during regeneration showed that both salamander
cells as well as cancerous frog kidney cells
dedifferentiated into embryonic
cell forms during the blastema formation process as the wound healed.
Even more amazing, as the blastema propagated forward, regenerating the limb,
both embryonic frog and embryonic salamander cells of the blastema multiplied
(divided).
They differentiated into the cell types needed to form the new limb tissue,
i.e. muscle cells, cartilage cells, capillary cells, etc.
In later years researchers such as Becker demonstrated that it was the near
unique ability of the salamander's nervous system to
drastically change
the ionic environment around blastema cells, along with hormone secretions
from nerve dendrites, which allowed blastema cells to
dedifferentiate into
embryonic cells and then to
redifferentiate into the new cell types
of the regenerating limb.
Becker and other researchers were able to
get rats to regrow most of, or all of a amputated limb. They implanted a negative current
source that produced a negative electric potential distribution inside the
limb directly behind the amputation site. This closely mimicked what a salamander
would have at that site if it were scaled up to the rats size.
To understand what is happening here, you need to know that in a rat just
as in a salamander the myelin sheath cells coating the motor nerve fibers
carry an electron current through collagen fibers which are N-type semiconductors.
This current is deposited mostly into the body's electrolytic solution surrounding
the cells near where the nerve fiber ends. The myelin sheath cells coating
the sensor nerve fibers carry an electron current on their collagen fibers
away from where the sensor nerve fiber ends.
The motor nerve fibers are essentially all in the body interior and the sensor
nerve fibers are essentially all on the body surface. As a amputation wound
heals over with skin, surface sensor nerve fibers cover over what is normally
a motor nerve fiber region. In a short period of time the cells under the
new forming skin layer can be converted into dedifferentiated embryonic cells
under the influence or control of the external cell membrane ionic environment
at the wound site as determined by the electric current potential of the combined
sensor and motor nerve sheaths activity in the wound area (blastema formation
zone). I can not here go into all of the wonderful detail of Becker's book.
However, I hope I have given the reader at least an understanding of how cancer
can possibly come about by a simple change in the ion environment in the cell
nucleus. If you are interested in tissue regeneration or are aserious biologist.
I can not recommend Becker's book enough.
Particularly the last chapter, Postcript:
Political Science. This chapter
with great clarity and skill, clearly shows why we as a nation need to dismantle
all centralized cesspools of corruption as exemplified by the National Institutes
Of Health. The NIH needs to be replaced by regional institutes which are government
funded, but ran and controlled by democratically elected administrators elected
by the research community.
Before ending this appendix, a warning and an explanation of
why X-ray
radiation should never be used to treat cancer. Rife was able to isolate
the BX cancer virus from cancer tumor tissue samples. He then
exposed these
viruses to 24 hours of ultra violet light exposure.
This virus obtained in this manner was
100% effective in inducing cancer
in lab animals. His form of the BX cancer virus was exceedingly virulent.
Other researchers who apparently isolated the same BX cancer virus, or a form
of it, and inoculated test animals by similar methods only had approximately
25% cancer induction rates.
A possible simple answer for the discrepancy is that the
ultraviolet light
from the argon discharge caused some of the adjacent thimine DNA base
codes to dimerize (chemically bond together). When the DNA reader enzyme which
translates the DNA base code into messenger RNA for protein synthesis comes
across a dimerized thimine base code pair, it stops RNA synthesis. The reader
enzyme then breaks into two fragments. One fragment stays at the dimerization
site to mark it and the other fragment initiates a complex set of enzyme reactions
to remove the dimerized pair and replace them with a new undimerized pair.
During this repair process the messenger RNA generated fragment is released.
If this messenger RNA fragment contains the genetic RNA base code sequence
for ribosome attachment, it will be read by the ribosomes and a protein fragment
will be generated and released. In particular, if the RNA fragment is fed
into a cluster of ribosomes (polyribosomes) which are located on or associated
with the intercellular matrix web intersections, we can expect many copies
of the coded protein fragment to be generated and released Furthermore, since
the RNA fragment does not contain the normal stop synthesis code and message
RNA end sequence base code, the RNA fragment is not likely to be immediately
dismantled after polyribosome reading and protein synthesis like regular messenger
RNA is. This fragment is likely to be read over again and again. Now if the
generated protein fragment happens to be an activator or suppressor of a cell
membrane ion channel or ion pump you have the potential beginnings of a cancer
producing situation as discussed above. This protein fragment(s) might also
act as a promoter protein that enables the DNA reader enzyme to attach to
and read a gene sequence. Or this protein fragment may combine with a blocker
protein on a repressor gene at the front of a DNA gene sequence and remove
it, thereby allowing a promoter protein to combine with a DNA sequence and
then facilitating attachment of the DNA reader enzyme (RNA polymerase).
All of this is not the normal "plan" of the normal cell metabolism.
An excellent example of this sort of defective protein production and its
cancerous consequences is the genetic disease xeroderma pigmentosum. In it
the individual has an inherited defect in their ability to repair the aforementioned
DNA base code dimerization damage. They are
hypersensitive to sun light
exposure and develop pre-cancerous and cancerous skin conditions. They
usually die of skin cancer before their twentieth birthday.
Now what does this have to do with
massive cellular tissue damage suffered
by cancer patients while under going standard allopathic
medical X-ray
treatment for cancer?
As stated in Appendix B. Rife's normal treatment for cancer patients was
three
minutes of exposure once every three days to his frequency instrument.
This frequency instrument, when treating cancer, probably produced repeating
packets of
11,780,000 or 23.560,000 light pulses per second. These
light
pulses in turn produced
ultra low intensity
ultra sound in the patient's body of a frequency of 11.780.000 or 23.560.000
cycles per second, which is the approximate
mechanical structural resonance
frequency of the BX cancer viruses. The BX viruses disintegrated.
In the normal carcinoma cancer cell,
there are thousands of BX cancer viruses.
When these BX cancer viruses all disintegrate together at the same time, they
release their genome, digestive enzymes, ribosomes, assorted proteinslenzymes,
etc. into the cell. The cancer cell is overwhelmed, dies, and promptly disintegrates.
When using Rife's cancer treatment method on a cancer patient that has undergone
extensive allopathic medical X-ray damage, there is the
high possibility
of an encounter with a new kind of cancer cell which Rife's treatment
method won't work on. Allopathic medical X-ray treatment causes significant
ultraviolet light, ionization, and free radical production both in tumor tissue
and adjacent normal tissue. With this ultraviolet light, ionization and free
radical production, there is the associated dimerization of adjacent DNA base
code molecular pairs. Both cancer cells and adjacent non cancer cells suffer
significant cell membrane integrity damage from the X-ray radiation. All of
this culminates in the possibility of a heavily radiation damaged BX cancer
virus penetrating the cell membrane of a non cancerous cell and instigating
production of cancer causing protein fragments as discussed above.
But its own gnome so badly 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 BX cancer virus and therefore
not treatable by Rife's frequency
instrument or ultra sound of 11.789,000 or 23.560.000 cycles per second.
Of coarse the X-ray radiation alone could generate a cancer cell that the
original Rife's treatment method would not cure.
Well we have skimmed over a lot of technical data in this appendix. however,
I hope the reader now has a conceptual frame work in which to begin questioning
the current allopathic medicine approach to cancer causes, treatments, and
cures. Only by honest researchers going back and looking at the suppressed
results of past honest cancer researchers can we hope to find honest valid
answers about cancer causes and cures.
"An important scientific innovation rarely makes its way by gradually
winning over and converting its opponents: it rarely happens that Saul becomes
Paul. What does happen is that its opponents gradually die out and that the
growing generation is familiarized with the idea from the beginning."
Max Planck
Taken from: DR. RIFE AND THE DEATH OF THE CANCER INDUSTRY. a paper by physicist
Gary Wade.
P.S. - It is now empirically known that many types of cancer can be easily
and quickly killed by
exposure to pressure square waves of a frequency
of approximately
2127 cycles per second. It appears that
one or
more of the higher frequency hidden fourier sine wave components. i.e.
3(2127), 5(2127), 7(2127), 9(2127), etc. opens up ion gates on the cancer
cells' membrane and radically changes the ionic conditions inside the cancer
cell such that it drops the bi-lipid layer potential difference below some
critical value below which the cancer cell can not recover and it dies.