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Who wants to be cut opened if
non-surgical treatments can cure
– not even the surgeons.
TRAINED DOCTORS
Artery Clearance
Therapy
(ACT) / Chelation
Therapy
With ACAM(USA)
Protocol
Technical know-how
&
Training from
ARTERIAL DISEASE
CLINIC,
London and Manchester
(UK)
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External Counter
Pulsation (ECP)
Technical know-how &
Training from
World leaders -
CANTON (China)
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Stone Management /
Lithotripsy (ESWL)
Technical know-how &
Training from
Teaching Department of
Direx Ltd,
Israel
DISCLAIMER |
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:: CYTOTRON RESEARCH :: |
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The
scientific research on the therapeutic use of
electromagnetic waves dates back on the 19th
Century and one of the pioneers was the gifted
scientist Nikola Tesla. Tesla saw the healing
potential of high-frequency currents and wrote
an article in titled 1898 article “High
Frequency Oscillators for Electrotherapeutic and
Other Purposes” . Since than several outstanding
scientists evaluated the healing effects of
electromagnetic waves.
Two
time Nobel laurate Albert Szent-Gyorgyi(1960)
wrote that “The living cell is
essentially an electrical device..."
and biochemical explanations alone fail to
explain the role of electricity in cellular
regulation.
Clarence Cone Jr. documented the importance of
transmembrane potential in the regulation of
cell division in his various research papers
such as “Variation of the transmembrane
potential level as a basic mechanism of mitosis
control” or “The role of the surface electrical
transmembrane potential in normal and malignant
mitogenesis”.
Below you find few scientific research papers
regarding the use of electromagnetic waves
for therapeutic purposes especially in the field
of cancer and arthritis, an overview of other
uses and the importance of transmembrane
potential. Thousands of other research documents
are accessible for interested parties.
Effects of pulsed electromagnetic fields on
articular hyaline cartilage: review of
experimental and clinical studies
 Abstract
Osteoarthritis (OA) is the most common
disorder of the musculoskeletal system and
is a consequence of mechanical and
biological events that destabilize tissue
homeostasis in articular joints. Controlling
chondrocyte death and apoptosis, function,
response to anabolic and catabolic stimuli,
matrix synthesis or degradation and
inflammation is the most important target of
potential chondroprotective treatment, aimed
to retard or stabilize the progression of
OA. Although many drugs or substances have
been recently introduced for the treatment
of OA, the majority of them relieve pain and
increase function, but do not modify the
complex pathological processes that occur in
these tissues. Pulsed
electromagnetic fields (PEMFs) have a number
of well-documented physiological effects on
cells and tissues including the upregulation
of gene expression of members of the
transforming growth factor b super family,
the increase in glycosaminoglycan levels,
and an antiinflammatory action. Therefore,
there is a strong rationale supporting the
in vivo use of biophysical stimulation with
PEMFs for the treatment of OA. In
the present paper some recent experimental
in vitro and in vivo data on the effect of
PEMFs on articular cartilage were reviewed.
These data strongly support the clinical use
of PEMFs in OA patients.
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Modification of osteoarthritis by pulsed
electromagnetic field—a morphological study
 Summary
Objective: Hartley
guinea pigs spontaneously develop arthritis
that bears morphological, biochemical, and
immunohistochemical similarities to human
osteoarthritis. It is characterized by the
appearance of superficial fibrillation by 12
months of age and severe cartilage lesions
and eburnation by 18 months of age. This
study examines the effect of treatment with
a pulsed electromagnetic field (PEMF) upon
the morphological progression of
osteoarthritis in this animal model.
Design: Hartley
guinea pigs were exposed to a specific PEMF
for 1 h/day for 6 months, beginning at 12
months of age. Control animals were treated
identically, but without PEMF exposure.
Tibial articular cartilage was examined with
histological / histochemical grading of the
severity of arthritis, by
immunohistochemistry for cartilage
neoepitopes, 3B3(−) and BC-13, reflecting
enzymatic cleavage of aggrecan, and by
immunoreactivity to collagenase (MMP-13) and
stromelysin (MMP-3). Immunoreactivity to
TGFβ, interleukin (IL)-1β, and IL receptor
antagonist protein (IRAP) antibodies was
examined to suggest possible mechanisms of
PEMF activity.
Results: PEMF treatment
preserves the morphology of articular
cartilage and retards the development of
osteoarthritic lesions. This
observation is supported by a reduction in
the cartilage neoepitopes, 3B3(−) and BC-13,
and suppression of the matrix-degrading
enzymes,collagenase and stromelysin. Cells
immunopositive to IL-1 are decreased in
number, while IRAP-positive cells are
increased in response totreatment. PEMF
treatment markedly increases the number of
cells immunopositive to TGFβ.
Conclusions: Treatment with
PEMF appears to be disease-modifying in this
model of osteoarthritis. Since TGFβ
is believed to upregulate gene expression
for aggrecan, downregulate matrix
metalloprotease and IL-1 activity, and
upregulate inhibitors of matrix
metalloprotease,the stimulation of TGFβ may
be a mechanism through which
PEMF
favorably affects cartilage homeostasis.
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