Vol.1, No.3, 157-165 (2009)
doi:10.4236/ns.2009.13020
SciRes
Copyright © 2009 Openly accessible at http://www.scirp.org/journal/NS/
Natural Science
Steps to the clinic with ELF EMF
Ash Madkan1*, Martin Blank2, Edward Elson3, Kuo-Chen Chou4, Matthew S. Geddis5, Reba
Goodman1
1Department of Pathology, Anatomy and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, USA
2Department of Physiology and Cellular Biophysics, College of Physicians and Surgeons, Columbia University, New York, USA
3Department of Electrical and Computer Engineering, College Park, University of Maryland, MD, USA
4Gordon Life Science Institute, San Diego, California, USA
5Department of Science, Borough of Manhattan Community College-CUNY, New York, NY
Received 10 October 2009; revised 25 October 2009; accepted 27 October 2009.
ABSTRACT
There have been many models to identify and
analyze low-frequency motions in protein and
DNA molecules. It has been successfully used
to simulate various low-frequency collective
motions in protein and DNA molecules. Low-
frequency motions in biomacromolecules origi-
nate from two common and intrinsic character-
istics; i.e., they contain 1) a series of weak
bonds, such as hydrogen bonds, and 2) a sub-
stantial mass distributed over the region of
these weak bonds. Many biological functions
and dynamic mechanisms, including coopera-
tive effects have been reported. In this regard,
some phenomenological theories were estab-
lished. However, differences in experimental
outcomes are expected since many factors
could influence the outcome of experiments in
EMF research. Any effect of EMF has to depend
on the energy absorbed by a biological organ-
ism and on how the energy is delivered in space
and time. Frequency, intensity, exposure dura-
tion, and the number of exposure episodes can
affect the response, and these factors can inter-
act with each other to produce different effects.
In addition, in order to understand the biologi-
cal consequence of EMF exposure, one must
know whether the effect is cumulative, whether
compensatory responses result, and when ho-
meostasis will break down. Such findings will
have great potential for use in translation medi-
cine at the clinical level without being invasive.
Keywords: Electromagnetic Fields; Hsp70;
Interaction Mechanisms; Low-Frequency Collective
Motion
1. INTRODUCTION
Current investigations primarily focus on electromag-
netic fields as electropollutants, e.g. cell phones, with
slight regard to therapy. Electro-pollutants are manifestly
different in field strength and frequency in comparison
to therapeutic applications, yet the FDA fails to address
differences in design, implementation and field strength,
thereby considering them the same and lists therapeutic
devices as ‘‘potentially dangerous’’ by association. The
World Health Organization convened scientists from
around the world and determined that field strengths less
than 20,000 Gauss, which is lower in intensity than mag-
netic resonance imaging, MRI, are free of adverse side
effects [1].
Regardless of device design, EMF technology has
been shown to be clinically effective in bone healing
[2-4], wound repair [2,5] and neural regeneration [5-10].
In terms of clinical application, EMF-induction of ele-
vated levels of hsp70, a stress response protein, also
confers protection against hypoxia [11], aids myocardial
function and survival [12] as well as survival following
ischemia reperfusion [12-14]. Given these results, we are
particularly interested in the translational significance of
effect vs. efficacy. This relationship is generally not in-
vestigated nor reported. More precise description of EM
pulse, field strength intensity and sine wave parameters
will provide consistency and scientific basis in reporting
findings. It is contended that pulsed therapeutic fields
are usually more effective if less than 20 Gauss and fre-
quencies are less than 300 Hz, below which they are
referred to as extremely low frequency (ELF) [15-18].
Cell phones are several magnitudes of order larger in
both considerations. Most therapeutic ELF-EMF used
for wound healing and bone repair use field strengths as
small as 50 milliGauss. MRI, a diagnostic EM technol-
ogy, employs static fields from 15,000 to 50,000 Gauss
coupled to radiowaves for tissue penetration. In terms of
molecular effects, concern might be expressed for repeti-
tive transcranial magnetic stimulation (rTMS), an EM
treatment for mental illness employing extremely low
frequencies (ELF) combined with field strengths of sev-
A. Madkan et al. / Natural Science 1 (2009) 157-165
SciRes Copyright © 2009 Openly accessible at http://www.scirp.org/journal/NS/
158
eral thousand Gauss.
This review does not extend to the remainder of the
electromagnetic spectrum (radiofrequency, microwave
or infrared spectrum) though much work on the employ-
ment of these forms of energy in the treatment of neo-
plastic disease is currently under investigation. This re-
search has now been employed as adjunctive therapy in
clinical oncology, e.g. microwave hyperthermia. The
radiofrequency and microwave parts of the spectrum are
used by inserting bulk energy, whereas the ELF-EMF
region is useful by producing electro-mechanical effects
on target tissues, producing specific biochemical reac-
tions.
2. THE PROMISE OF ELF-EMF IN
TREATING CANCER
Since the 1980s a considerable number of reports have
appeared [17,19-22] describing a great variety of cell
culture systems, animal models (mice for the most part),
field sources producing a variety of waveforms and field
strengths, and great variation in exposure protocols.
Many of the invitro (cell culture) studies of tumor-cell
lines report significant cell-killing compared to control
cultures. The studies involving transplantation of tumor
lines into mice, frequently subcutaneously into the ab-
domen, report that magnetic field exposures significantly
reduce the size of transplanted tumors (i.e. cyto-reduc-
tion) compared to controls. Although it is difficult to
compare studies quantitatively, it is interesting that cyto-
reduction occurs across a whole variety of field streng-
ths, wave-forms, pulsed fields versus sinusoidal fields,
and exposure durations. The great challenge for investi-
gators will be to find an optimal exposure regime which
delivers the most efficient cancer-cell-killing with the
most minimal side-effects, to establish the role of ELF-
EMF, whether as adjunctive or primary therapy, to relate
its efficacy to different kinds of cancer and to the stage
and grade of human cancer. This process has not actually
begun but some information from animal studies is al-
ready providing some direction [23-24].
A few studies have been chosen to illuminate the
value of the information they are reporting with regard
to guidelines for human investigations not yet begun. It
should be pointed out that although China and Russia
have reported success in ELF-EMF treatments in human
subjects with cancer, documentation is often weak and
validation by Western science has not occurred. We can
crudely separate the studies into those employing
“weak” magnetic fields, not exceeding tens of micro-
Tesla and those employing “strong” fields, above one
milliTesla and ranging through 100 milliTesla and even
up to several Tesla. This is indeed crude because other
parameters of the fields, such as waveforms, time and
spatial rate of variation of the fields are also critically
important. For reference, the geomagnetic field is about
50 microTesla. Some house-hold appliances produce up
to 1 milliTesla at a distance of 30 cm from the body, but
usually for short periods. A more prolonged exposure is
one to an electric blanket (60 Hertz) in which fields at
the surface run from 2 to 5 microTesla [25]. These am-
bient exposures are considered safe.
One study of extremely low frequency (ELF) pulsed-
gradient magnetic fields inhibited malignant tumor
growth through different biological mechanisms [83]
using a pulsed-gradient magnetic field (0.6-2.0 Tesla,
gradient of 10-100 T/meter, pulse width of 20-200 milli-
seconds, frequency of 0.16-1.34 Hz) to exposed sarco-
mas inoculated into the legs of mice. These normally
rapidly growing tumors showed significant shrinkage
with exposure as compared with a control group. Endo-
thelial cells of tumor blood vessels were swollen and
appeared occluded and morphologic observation and
biochemical tests revealed marked programmed cell
death (apoptosis). Necropsy revealed no abnormalities in
normal tissues.
Another study [26] exposed mice with implanted mur-
ine 16/C mammary adenocarcinoma cells to a rectified,
60 Hertz magnetic field for 10 minutes per day at 10,15
and 20 milliTesla for 12 consecutive days after a seven
day period in which the cells produce visible tumors.
Exposure to the fields significantly reduced tumor
growth. On microscopic examination the tumor exhib-
ited marked necrosis and evidence of inhibition of tumor
vascularization. Necropsy revealed no abnormalities in
the remainder of normal tissues.
De Seze et.al., [27] used a 0.8 Hertz square wave 100
mT, 8 hours/day or until death on mice subjected to
chemically induced tumor using benzo(a)pyrene. A sig-
nificant decrease in tumor growth and increase in sur-
vival were observed.
Cameron, et. al. [28] transplanted a human breast can-
cer cell line into athymic nude mice and compared the
effects of a rectified 60 Hz magnetic field signal at 15
milliTesla to that of radiation, 200 cGy of radiation
every other day and found significant cyto-reduction in
radiation and ELF-EMF exposed mice to a roughly
comparable extent. Mice that received either therapy
also had significantly fewer lung metastatic sites than
did untreated mice. Normal tissues were unaffected. This
study raised the question of whether ELF-EMF expo-
sures could achieve the same efficacy as radiation but
without the side effects of radiation.
Although electromagnetic technology was originally
described by Maxwell in 1865, electromagnetic tech-
nology as therapy received little interest from basic sci-
entists or clinicians until the 1980s. It now includes ap-
plications such as mitigation of inflammation (electro-
chemistry) and stimulation of several specific of genes
[15,16]. Studies on DNA have provided an understand-
ing of cell response to low energy EMF inputs via elec-
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159
tromagnetically responsive elements (EMRE; EMF-
sensitive base pairs nCTCTn) [19,20,29,30,84].
3. SELECTING MODEL SYSTEM FOR
TRANSLATIONAL RESEARCH AND
ITS CLINICAL POTENTIAL
Of under rated importance in investigating ELF EMF
reactions, is the model system on which experiments are
based. When extrapolating preclinical testing results to
the intended clinical setting, it is important to recognize
and appreciate both the relevant attributes and the limi-
tations of a selected animal. It is essential to select a
model system that will help provide an understanding of
the interaction mechanism and provide specific markers
for studying the effect of EMF on many diseases/ condi-
tions including regeneration; ischemia-reperfusion, and
tumor suppression. Such model systems include tissue
cultured cells, Platyhelminths (worms), yeast, Diptera
(flies), bacteria, fish and mice.
4. CURRENT THEORIES ON ELF-EMF
INTERACTION MECHANISM
We confine the current discussion to studies of frequen-
cies below 0.3 kHz (commonly defined as the upper
limit of ELF) to magnetic fields with sinusoidal wave-
shapes, studies with simultaneous static magnetic fields,
and studies using pulsed magnetic fields. In the many
studies reported since the 1980s a variety of different
exposure protocols, with variation in such parameters as
magnetic field strength, frequency, duration of exposure
and combined modality applications with chemotherapy
and/or radiation, have been reported. Many studies have
not been replicated, a general weakness of the field. But
the studies taken as a whole still confer great potential
promise on the role of magnetic field therapy, either as
adjunctive therapy (i.e. in addition to chemotherapy or
ionizing radiation) or even potentially as a primary
(stand-alone) therapy for certain neoplastic diseases.
4.1. Basic Mechanisms Underlying the
Efficacy of Elf-Emf Treatments.
Enough is known about the cellular and molecular me-
chanisms of interactions of ELF-EMF to furnish a ra-
tional basis for employing such a therapeutic modality.
We describe several mechanisms for which there is some
documentation and a few proposed models, not verified,
which we believe are worth further investigation.
One strongly documented mechanism is the activation
of apoptosis, a process characterized as programmed cell
death. In response to many different stimuli, a series of
biochemical cascades are activated within a cell which
results in its death. From a teleological aspect such a
process constitutes a defense of the organism as a whole,
as a damaged cell can undergo the unregulated prolifera-
tion (lack of apoptosis) we regard as a cancerous trans-
formation. Under the microscope such cells can show
fragmentation of nuclei, bizarre appearances of nuclear
chromatin, membrane blebs and cell shrinkage. Bioche-
mically one observes the activation of a family of cys-
teine proteases called caspases which destroy structural
elements of the cell [21]. Caspases are activated by the
BCl-2 family of proteins which cause the release of cy-
tochrome c from mitochondria into the cytoplasm by
altering the mitochondrial membrane potential. Cyto-
chrome c is considered one of the major factors in acti-
vating the caspase cascade. It has been proposed [4] that
ELF-EMF can intervene in this process by affecting
voltage-dependent anion channels which are used in the
BCl-2 activation process. Other processes have also been
described as causing increased intra-cytoplasmic cal-
cium through voltage-activated channels as well [31].
One must bear in mind that the broad picture is far more
complex, as there is a related literature showing that
ELF-EMF fields also play a role in cell proliferation.
Such an effect is generally associated with the weak
fields, 10 microTesla to a few hundred microTesla, as
opposed to higher strength fields, greater than one mil-
liTesla, which can produce cell injury and apoptosis. It
has also been reported that a static field combined with
an ELF field increases apoptosis [31].
A second mechanism which has been reported from
several studies is an effect of ELF-EMF which produces
inhibition of new blood vessel formation. This is most
dramatically observed in histological sections of tumors
exposed to ELF-EMF. Malignant tumors normally ela-
borate angiogenic factors which cause neo-vasculari-
zation of the growing tumor, a proliferation of thin-
walled capillaries branching through the tumor mass to
provide nutrients to the tumor cells. The endothelial cells
which form buds to new vessels from existing vessels
appear to be inhibited during and following ELF-EMF
exposure, a process which most likely plays a role in
tumor cell death.
A few theoretical models have received much discus-
sion over the years. One is the ion cyclotron resonance
(ICR) model of McLeod and Liboff [32]. In this model
free ions move in a cell membrane in a combined static
and ELF magnetic field of the correct “cyclotron” fre-
quency. This motion is thought to trigger cell signals and
disrupt normal cell behavior. Another theory is that of
Lednev [33] and describes the interaction of magnetic
fields with ions bound to channel proteins which influ-
ence the opening and closing of the channels.
A variety of stimulative [4] effects from ELF-EMF
have been found, as opposed to strong field effects de-
scribed as destructive. Utilizing primarily cell culture,
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160
time-varying magnetic fields, sinusoidal or pulsed, with
frequencies in the extremely low frequency (ELF range),
or repetition rates on the order of 1 to 10 Hz, have been
shown to produce up-regulation of early response genes
and stress response genes [4], transcription in several
different cell lines [16] induction of stress response
genes [34], induction of DNA synthesis in fibroblasts
[32] induction of DNA synthesis in frog erythrocytes [35]
and alterations in the mitotic cycle of sea urchin em-
bryos [36]. The literature has been reviewed [25].
The model of gene regulation was believed to be that
the negatively charged DNA was tightly wrapped up in
the nucleus with positively charged histones, and that
most genes were ‘turned off’ most of the time. Of course,
different regions of the DNA code re being read more or
less all the time to replenish essential proteins.
The ability of relatively weak EMF (in the ELF fre-
quency range) to affect movement of electrons has been
demonstrated in several specific biological reactions that
are fundamental to cellular mechanisms; Na, K-ATPase
reaction, the oxidation of cytochrome oxidase, and the
oxidation of malonic acid (the Belousov-Zhabotinsky
reaction) reviewed in [3,4]. Thus, the same fields can
cause electrons to move in DNA, leading to areas of
local charging and local deaggregation of DNA strands.
This would set in motion the biosynthesis associated
with the stresses.
This protective mechanism induces the expression of
stress response genes and refolds damaged proteins to
transport them across cell membranes. Specific DNA
sequences on the promoter of the HSP70 stress gene are
responsive to EMF, and studies with model biochemical
systems suggest that EMF could interact directly with
electrons in DNA. The sensitive base pairs are upstream
on the HSP70 promoter and consist of the nCTCTn con-
sensus sequence. When the EMRE are tranfected into a
reporter gene, which was previously unresponsive to ele-
ctromagnetic fields, they become sensitive. Studies have
shown that the ERK 1-2 protein is phosphorylted when
exposed to electromagnetic radiation (8 mT). A related
model is that of Elson [27] which, like the model of
Blank and Goodman, describes a direct electro-mecha-
nical interaction of ELF-EMF with DNA. These theories
have benefited from the results of a number of studies on
the ability of DNA to conduct electric currents along the
DNA backbone [38]. The phenomenon of DNA conduc-
tivity has been demonstrated in vitro using photo-
chemical techniques and direct measurements of current
flow through DNA strands using nano-techniques [39].
The phenomenon has not been demonstrated in vivo, but
it has been speculated that the motion of charges in DNA
could serve to protect DNA from oxidative damage. The
model advocated by Elson suggests that charge motion
through helical pathways could also serve to open DNA
strands, producing origin sites for DNA replication. This
model also indicates how very strong magnetic fields
could damage DNA, which would send the signal for the
induction of apoptosis. This might constitute yet another
mechanism for the treatment of tumors. The model may
offer an explanation for the finding of DNA strand
breaks produced by electromagnetic fields as reported in
a few studies [40-42].
A final mechanism first described by Dr. K. C. Chou
and subsequently elaborated by both Dr. Chou and Dr.
Glen Gordon [43,44] is the concept of low-frequency
phonons (or internal motion) in proteins. Dr. Chou re-
ported this mechanism in order to solve a perplexing
“free-energy deficit” problem [45], which was encoun-
tered in studying the binding interaction between insulin
and the insulin receptor [46]. According to the inference
elaborated in [45], the wave numbers of the low-frequ-
ency phonons were in the range of 1
10100 cm
31
, cor-
responding to the range of terahertz frequency (to
Hz). In the mean time, the possible biological
functions of low-frequency phonons in proteins were
also discussed [45].
11
0
12
310
Subsequently, low-frequency modes have been indeed
observed by Raman spectroscopy for a number of protein
molecules [47,48] and different types of DNA [49-52].
These observed results have also been further confirmed
by the neutron scattering experiments [53].
To identify and analyze this kind of low-frequency
motion in protein and DNA molecules, the quasi-con-
tinuum model was developed [54-60]. It has been suc-
cessfully used to simulate various low-frequency collec-
tive motions in protein and DNA molecules, such as
accordion-like motion, pulsation or breathing motion, as
reflected by the fact that the low-frequency wave num-
bers thus derived were quite close to the experimental
observations [54-56,59,61]. It was also revealed through
the quasi-continuum model that the low-frequency mo-
tions in biomacromolecules originate from their two
common and intrinsic characteristics; i.e., they usually
contain 1) a series of weak bonds, such as hydrogen
bonds, and 2) a substantial mass distributed over the
region of these weak bonds [62].
The most interesting fact is that many marvelous bio-
logical functions and their profound dynamic mecha-
nisms, such as cooperative effects [60,63], allosteric
transition [64,65], and intercalation of drugs into DNA
[66,67], can be revealed through the low-frequency col-
lective motion or resonance in protein and DNA mole-
cules. In this regard, some phenomenological theories
[57,65,67,68] were established. Meanwhile, the solitary
wave motion was also used to address the internal mo-
tion during microtubule growth [69]. A soliton is a self-
reinforcing solitary wave (a wave packet or pulse) that
maintains its shape while it travels at constant speed.
The relationship between the solitons and the low-fre-
quency phonons in proteins have been discussed in a re-
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161
cent paper [70].
As stated on the web-page of Vermont Photonics Tech-
nologies Corp. at Vermont
(http://www.sov er.net/~bell/new Frontierp ics.h tm), “Study
of low-frequency (or Terahertz frequency) motions in
biomacromolecules holds a very exciting potential that
could lead to revolutionize biophysics, molecular bio-
logy, and biomedicine.”
For a systematic introduction of the low-frequency col-
lective motion in biomacromolecules and its biological
functions, refer to a comprehensive review article [71].
4.2. Concluding Remarks on Mechanism
Direct effects on electron (or hole) flow in DNA by the
models cited are not proven. It is, however, easy to visu-
alize how ELF-EMF could damage cellular processes
and structures with the documented mechanisms de-
scribed. A cell is an electrolyte rich, dipolar-protein-
filled water-dominated dielectric through which course
many lipid membranes filled with voltage-gated and
other types of channels designed for transmitting bio-
chemical signals. It is easy to visualize how such a sys-
tem could be affected by low frequency, strong time-
varying magnetic fields and their associated electric
fields, and so most attention has been focused on effects
on electrolyte flow, protein dipole responses, and signal
transduction at membranes. One interesting study used
pulsed electric fields (not magnetic fields), a burst of
high voltage, 40 kiloVolt/cm, 300 nanosecond wide
pulses to produce complete destruction of focal mela-
nomas injected subcutaneously into mice [72]. Because
electrodes must be placed on either side of the tumor
there are severe practical restrictions on the applicability
of such a technology to tumors in general, but such an
approach can yield valuable information on the strength
of the fields required to produce tumor destruction. The
general conception has been that it is the electrical fields,
not the magnetic fields per se that couple into biological
structures to produce an effect. Consequently the pulsed
electric field experiment can provide valuable informa-
tion on the magnetic field parameters required to pro-
duce an effective electric field.
One must be cognizant, however, that the studies and
models of Blank, Goodman, and Elson have raised the
possibility that coupling of electromagnetic energy can
occur as well directly through the magnetic fields. This
possibility can be explained by the expressions F = qv X
B and curl E = dB/dt of classical electromagnetism, and
remembering that a cell is filled with currents through
membranes virtually at all times and possibly currents
through DNA as well. The technology is available to
fashion waveforms with far faster rise-times, shorter
pulse-widths, far higher field strengths, varying repeti-
tion rates and burst modes than have been studied. In
view of the fact that no adverse side-effects have been
found and no abnormalities in normal tissue have been
identified to date (possibly a very significant advantage
over chemotherapy and conventional radiation) exciting
opportunities are visible.
In view of these many interesting possibilities, and the
promise communicated by the existing literature, a very
strong case can and should be made for an investment
into the potential of ELF-EMF in cancer therapeutics.
5. EMF-DNA INTERACTION
MECHANISMS: SIGNALING
PATHWAYS
The initial step in transmitting extracellular information
from the plasma membrane to the nucleus of the cell is
by NADH oxidase [73]. NADH then rapidly generates
reactive oxygen species (ROS). These ROS stimulate
matrix metalloproteinases which allows them to cleave
and release heparin binding epidermal growth factor.
This secreted factor actives the epidermal growth recep-
tor which in turn activates the ERK cascade [73].
The major mechanism that regulates transcriptional
activity in response to extracellular stimuli is the activa-
tion of the mitogen-activated protein kinase (MAPK)
signaling cascades. There are three MAPK cascades that
are implicated in exposures to ELF and RF. They are: 1)
extracellular signal regulated kinase 1\2 (ERK), 2)
c-Jun-terminal kinase (JNK), stress actrivated protein
kinase (SAPK) and p38SAPK. Each of the cascades is
composed of three to six tiers of protein kinases and
their signals are transmitted by sequential phosphoryla-
tion and activation of the protein kinases in each of the
tiers. Upon activation the protein kinases in various tiers
phosphorylated and activated a large number of regula-
tory proteins which include a set of transcription factors,
e.g., c-Jun, c-Fos, hsp27 and hsp70. Activation of the
stress response is accompanied by activation of specific
signal transduction cascades involved in regulating cell
proliferation, differentiation and metabolism [74-77].
The MAPK pathways have been characterized in several
cell types [74,78-81]. Exposure to nonthermal EMF as
well as RF affects the expression of many cellular pro-
teins [73-75].
The initial step in transmitting extracellular informa-
tion from the plasma membrane to the nucleus of the cell
is by NADH oxidase [73]. NADH then rapidly generates
reactive oxygen species (ROS). These ROS stimulate
matrix metalloproteinnases which allows them to cleave
and release heparin binding epidermal growth factor.
This secreted factor activates the epidermal growth re-
ceptor which in turn activates the ERK cascade [73].
Both EMF and RF activate the upregulation of the
HSP70 gene and the induction of elevated levels of the
hsp70 protein. This effect on RNA transcription and
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162
protein stability is controlled by specific protein tran-
scription factors which are elements of the mitogen-acti-
vated-phospho-kinase (MAPK) cascade.
EMF also stimulate serum response factor which
binds to the serum response element (SRE) through
ERKmapk activation and is associated with injury and
repair in in vivo and in vitro. The SRE site is on the
promoter of an early response gene, c-fos, which under
specific cellular circumstances has oncogenic properties.
The c-fos promoter is EMF-sensitive; a 20 min exposure
to 60Hz 80mG sinusoidal fields significantly increased
c-fos gene expression [82]. The SRE accessory protein,
Elk-1, contains a growth-regulated transcriptional acti-
vation domain. ERK phosphorylation potentiates Elk-1
and transactivation at the c-fos SRE [8]. ELF-EMF ex-
posure may also control protein regulation through the
PI3-kinase pathway as inhibition results in an upregula-
tion of collagen in response to ELF-EMF, suggesting an
inhibitory role for PI3K in ELF-EMF induction. Fur-
thermore, the role of nitric oxide/ cGMP signaling path-
way has been implicated in pulsed EMF induced chon-
drocyte proliferation.
In studying human disorders, such as cancer, a strong-
er emphasis should be placed on model systems and
noninvasive techniques for patient safety and ease of
application for the treating physician. Information from
the laboratory bench on non-human model organisms is
under appreciated and very important.
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Literature Cited
Legend: To facilitate an understanding of mechanisms, defi-
nition of the following terms should be helpful.
Wave - A wave is a disturbance traveling through a medium
by which energy is transferred from one particle of the medium
to another without causing any permanent displacement of the
medium itself. The peaks of the wave are the maximum amount
of energy.
Longitudinal Wave - a longitudinal wave is like a sound wave in
air, where the pulse travels parallel to the direction of disturbance.
Transverse Wave - a transverse wave is like a leaf
floating in a lake. When a wave comes, the leaf goes
up and then back down. So a transverse wave is
where the motion is perpendicular to the direction of
disturbance.
Wavelength – A wavelength is the distance between
any two repeating points, as shown in the diagram.
Rise Time: The speed with which a pulse goes from
zero to peak
Measurement of field strength: Tesla/Gauss measure:
1 Tesla equals 10,000 gauss
Frequency – The frequency of a wave is the number
of times a point repeats in a certain amount of time.
While EMF signals come in various shapes (sine and square,
pulsed etc.) through a sine wave or a series of sine waves.
The delivery system of an electromagnetic field can be single
pulse, repetive pulse and can be through Helmholtz and other
coil configureation.
To understand the impact of EMF on cells and tissues it is
important to understand specific acronyms. These include
pulsed electromagnetic field (PEMF), time varying electro-
magnetic field (TVEMF) to pulsed electric stimulation (PES)
and pulsed electromagnetic therapy (PEMT). The need to spe-
cifically design pulse and/or static field for maximal bio-effi-
cacy.