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10 most powerful evidence-based strategies for recovering from
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 CANCER
T he M etabolic D isease U nravelled

M ark S loan
Copyright © 2018 EndAllDisease Publishing
WHY YOU SHOULD READ THIS
BOOK
The official position of the cancer establishment is that cancer is a genetic
disease involving genetically-mutated cells which seek to overwhelm and
kill the patient. This ideology is routinely taught to doctors, nurses and to
the public as if it were fact, yet no scientific evidence has ever suggested it
is true. The prevailing cancer mythology that I like to call ‘the angry cancer
cell’ is how the use of knives, poisons and deadly ionizing radiation are
justified as treatments - and if it were ever acknowledged this theory was
mistaken, the entire cancer industry would crumble.
Backed by evidence from over 1900 scientific and clinical references,
Cancer: The Metabolic Disease Unravelled is the antidote to a disease that
has plagued humanity for centuries.
Groundbreaking cancer research has shown that cancer cells are not the
murderous villains that they were once believed to be. The many
breakthrough scientific discoveries presented in this book will reveal
exactly what a cancer cell is, what causes tumors to form and how to
reverse cancer cells back to normal, healthy cells without harming them.
But the 126 billion dollar cancer industry has no interest in rendering itself
out of business so these findings have never been acknowledged
publically. As a result, mainstream cancer treatments continue killing more
people everyday, including my mother who died when I was 12 years old.
The cancer Industry maintains an un-scientific approach to diagnosing and
treating cancer. Any research that interferes with its ‘official’ position and
the profits that it generates is pushed aside and ignored. It’s time to reveal
the truth to the public once and for all so that humanity can end the disease
of cancer forever.
Prepare to say goodbye to your fear of cancer and say hello to the
confidence in knowing:
EXACTLY what a tumor is
EXACTLY what causes one to form and
Numerous ways to simply and inexpensively heal cancer
Thank you again for supporting my work. I hope you find this book
valuable and that it helps revolutionize the the world’s understanding of the
disease of cancer and ultimately puts an end to what Dr. Siddhartha
Mukherjee has called the emperor of all maladies.
DISCLAIMER
No part of this publication may be reproduced, duplicated, or transmitted in
any form without the expressed written consent of the author. All rights
reserved.
The information presented herein is the opinion of the author and is not
meant to substitute for medical advice.
Statements made in this book regarding conventional and alternative health
treatments have not been evaluated by Health Canada. Do not use this book
to diagnose, treat or cure any illness or health condition. If you have, or
suspect that you have a medical problem, contact your physician or health
care provider.
Neither the author nor the publisher assumes any liability for any injury,
illness or adverse effects caused by the use or misuse of the information
presented herein. Brands, corporations and trademarks are used for
clarification purposes only and have no affiliation with this book.
Under no circumstances will any legal responsibility or blame be held
against the publisher or author for any reparation, damages, or monetary
loss due to the information in this book, either directly or indirectly. The
reader is solely responsible for his or her own actions.
TABLE OF CONTENTS
WHY YOU SHOULD READ THIS BOOK
DISCLAIMER
INTRODUCTION
TARGETING THE TUMOR MICROENVIRONMENT
ORANGES
COCONUT OIL
SODIUM BICARBONATE
UNRAVELING THE MYSTERIES OF CANCER
CONCLUSION
REFERENCES
PLEASE REVIEW THIS!
ABOUT THE AUTHOR
INTRODUCTION
After $500 billion dollars spent on cancer research since 1971, the search
for a cure has been a complete and utter failure.1-3 Nothing about the way
cancer patients are treated has been improved; survival rates have not
improved, cancer diagnostic tests are a public health disaster and
mainstream cancer treatments continue killing far more people than they
help.
“We have a multi-billion dollar industry that is killing people, right and left,
just for financial gain,” wrote Dr. Glen Warner who, like other heroic
doctors, have been doing everything they can for decades to warn the public
of the fraud.
It’s clear that the booming cancer industry is not going to put itself out of
business anytime soon and that if we want a cure for cancer, or even more
reasonable treatments, we are going to have to find them ourselves.
Welcome to book 2 of the Curing Cancer series.
This monumental work has been written in such a way that reading the first
book in this series, The Cancer Industry, is not a prerequisite. However,
that doesn’t mean you shouldn’t read it. I believe that if you’re human and
you have a pulse that you should read it at some point. It exposes in
enormous detail the dismal ‘success’ rates and appalling dangers of cancer
surgery, chemotherapy, radiotherapy and cancer screening tests. It’s been
known for at least 50 years that mainstream cancer treatments do far more
harm than good and The Cancer Industry is the final nail in the coffin.
Equally as important as understanding and acknowledging the fraud of the
cancer establishment is knowing what to replace that void with. It’s the
goal of this work to provide you with an understanding of cancer that will
end any fear you may have of the disease and allow you to easily and
inexpensively prevent or reverse cancer without killing or harming yourself
in the process.
In the first chapter we’re going to dive right into the most crucial area of
cancer research, called the tumor microenvironment. This comprises the
area surrounding a tumor, within which various substances either signal the
tumor to grow and spread or to shrink and resolve itself. Once you’ve read
it you’ll know more than 99.999% of doctors and oncologists about cancer.
The tumor microenvironment is the most accurate scientific framework for
understanding what cancer is and for treating it in a way that is both fully
safe and effective.
The subsequent three chapters are focused on natural medicines – one per
chapter – including oranges, coconut oil and sodium bicarbonate,
respectively. If you’ve ever been curious as to whether these
foods/medicines are effective for treating cancer or other diseases, I think
you will be most satisfied with the results. The interactions of these three
natural medicines with the tumor microenvironment will be explored and
their influences on cancer progression will be recorded. If it’s true that
certain factors within the tumor microenvironment are the mediators of
carcinogenesis and cancer progression, then any downregulation of them by
these natural medicines should either inhibit the progress of cancer or
resolve it. As such, these three chapters are a prime opportunity to either
add validation to or detract from the theory.
As extraordinary as the first four chapters of this book may be, the final
chapter, called Unraveling the Mysteries of Cancer, is on another level. Get
ready for a ride!
In the final chapter, our first task is to question the mainstream somatic
mutations theory of cancer. Captivating lines of research like the cloning of
mice from tumor cell DNA, frog egg tumor transplants and cell cytoplasm-
swapped ‘cybrids’ all present significant problems for cancer’s brittle
genetic theory. As you comprehend this evidence, many of the fractures in
the somatic mutations theory will become evident. The multi-billion dollar
Cancer Genome Atlas Project was the straw that finally broke the camels
back in regards to the genetic theory of cancer. The project’s 2010 results
were a fatal blow to the theory and to the hope of its many exhilarated
supporters, who were left in complete and utter bewilderment.
At this point it will be clear to you what cancer isn’t, and our next task
becomes establishing what cancer is. The case for the metabolic origins of
cancer is then made using scientific evidence, some of which dates back
150 years, and includes the work of the prodigious Nobel Prize laureate Dr.
Otto Warburg and others. Any remaining gaps in Warburg’s understanding
of cancer were filled in by his successors, one of whom was Dr. Konstantin
Buteyko. You’ll learn about Buteyko’s monumental discovery that turned
the medical establishment on its head and how the exact mechanisms
involved in carcinogenesis are implicated in virtually all chronic
degenerative diseases. Suddenly a pinhole of light at the end of a once
seemingly-endless void tears through the fabric of reality – and the end of
cancer and all chronic degenerative diseases is in sight.
Understanding the metabolic differences between a health cell and a cancer
cell is next on the agenda. You’ll learn numerous specific ways to turn a
healthy cell cancerous and vice versa. Dysfunctional metabolism tends to
result in changes within cells that lead to permanent mitochondrial damage.
This is why understanding healing and regeneration in the body – namely,
what inhibits it and what accelerates it – becomes our next task. We begin
our reconnaissance by looking at the physiological role of a number of
factors in the healing process including stem cells, oxygen, carbon dioxide,
inflammation, the tumor microenvironment, the immune system, thyroid,
unsaturated fat, cholesterol and the remarkable phenomenon of scarless
healing that occurs within the human embryo.
It turns out that cancerous tumors have a primary fuel source, but it’s not
what you might think. You’ll learn about the recent groundbreaking
research that has demonstrated one specific energy substrate in particular is
absolutely essential for cancer growth, metastasis and progression. Due to
toxic fragments formed as a byproduct of the utilization of this energy
substrate, stress is amplified rather than alleviated - and the result is a
chronic state of stress which eventually overwhelms the body’s ability to
‘switch’ that stress off. At this point, healing is obstructed and chronic
degenerative diseases of all types, including cancer and aging itself, begin
to occur.
The key to the successful treatment of cancer is to interrupt the vicious
cycle of stress that occurs in the body as a result of years of assimilating
inappropriate food materials. Various ways to interrupt the vicious cycle of
stress, including drugs, medicines, the various forms of carbon dioxide
therapy and a number of dietary interventions are offered.
But the excitement doesn’t end there. Just when you think we’ve reached
the summit and the book couldn’t possibly bestow anymore remarkable
information, the author puts us face to face with a practical method of
literally eradicating not just cancer but all chronic degenerative diseases off
the face of the earth.
My name is Mark Sloan and I am the author of this book. I want to thank
for your supporting my work and I hope that it profoundly changes your life
for the better. If you find it helpful or entertaining in some way, please
remember to leave a quick review on Amazon after you’re done reading. I
read all the reviews myself and your feedback will help this book
tremendously.
Now, let the journey begin.
TARGETING THE TUMOR
MICROENVIRONMENT
The tumor microenvironment is one of the most important areas of cancer
research. Understanding what the tumor microenvironment is and how it
works is critical for understanding the disease of cancer. Despite this, the
concept has never been announced publically and most people are entirely
unaware of it.
The tumor microenvironment is the area surrounding a tumor, which
contains a network of different signaling molecules, hormones and other
factors which are in constant interaction with tumor cells.55 Depending on
which substances are present within the tumor microenvironment, a tumor
will either be signaled to grow and spread to other areas of the body or to
shrink and resolve itself. Put simply, the substances present within the
tumor microenvironment are the ultimate mediators of the fate of a tumor.
If you’ve read my book The Cancer Industry, you’ll recall the detailed
breakdown of the tumor microenvironmental factors in the chapter on
cancer surgery, which included their role in the body and their influence on
carcinogenesis and cancer progression. Due to the significance of that
information I will re-present it and all its details below:
Nitric Oxide - Anytime a tissue has been injured, nitric oxide and other
growth factors are released to signal cells to grow and divide to replace lost
cells.56 In a person with cancer, tumor cells caught in the crossfire of nitric
oxide signaling will also be signaled to grow, which is why nitric oxide is a
well-known promoter of angiogenesis and tumor progression.57-60
Nitric Oxide - Nitric oxide has also been demonstrated to trigger the
adhesion of circulating tumor cells (like the ones released during cancer
surgery) onto body tissues, which is the first step in new tumor formation.61
Vascular Endothelial Growth Factor – Similar to nitric oxide, VEGF is a
protein that signals growth to help repair injured tissues.90 Elevated blood
levels of VEGF have been associated with the growth and progression of
cancer.91
Epidermal Growth Factor – EGF, like nitric oxide and VEGF, enhances
the growth, invasion and metastasis of tumors.92 High levels of EGF are
associated with poor prognosis in cancer patients.93
Free Radicals – Free radicals are highly-reactive molecules that are
balanced by the body’s antioxidant system. In excess, the oxidative damage
caused by free radicals results in aging, cardiovascular disease, cancer and
other chronic diseases.112
Adrenaline – The stress hormone adrenaline is one of the primary triggers
of the breakdown of fat for energy (lipolysis).89 Anytime unsaturated fatty
acids enter the bloodstream, prostaglandins are formed,62 which are
carcinogenic.63
Cortisol - People with cancer have higher cortisol levels than people
without cancer,64 and a number of studies have shown that cancer patients
with the highest levels of cortisol have the greatest risk of dying from the
disease.65,66
Estrogen - The presence of cortisol in the bloodstream leads to increased
production of the hormone estrogen.67-69 The famous 1990’s Women’s
Health Initiative study tested the effects of supplemental estrogen on
women, but was forced to stop early after participants began developing
cardiovascular disease, stroke, dementia and cancer.70
Serotonin - Since cortisol’s basic action is to catabolize muscle tissue and
muscle meat contains high levels of the amino acid tryptophan (a precursor
for serotonin), stress increases serotonin production.71 While most people
think of serotonin as a ‘happy hormone,’ this cultural belief appears
misguided, since serotonin is not a hormone and lowering it can alleviate
depression.87 Serotonin is part of the body’s stress response and has been
shown in numerous studies to promote tumor growth.71-75
Histamine - Histamine is an inflammatory mediator commonly known for
its role in allergic reactions.76-77 Substances that inhibit histamine prevent
cancer growth and progression.78-80
Lactic Acid - Lactic acid is produced by cells that aren’t getting what they
need to produce energy efficiently. Lactic acid suppresses the immune
system,81 promotes cancer growth and metastasis82 and also triggers the
release of cortisol,83 perpetuating the cycle of stress.
Prolactin - Elevated blood concentrations of the hormone prolactin trigger
inflammation by amplifying the production of inflammatory cytokines,84
and promote the formation and progression of numerous types of cancer.85-
86,88

Tumor Necrosis Factor alpha – TNFalpha is an inflammatory cytokine

released by macrophages in response to toxins or other stressors.95 Due to
its extreme toxicity, TNFalpha has been shown to kill cancer cells,96 but the
rest of the body is severely damaged in the process.97-99 TNFalpha promotes
inflammation, is involved in cancer growth and metastasis, and its presence
in the body increases with age,100 like cancer’s.101

Nuclear Factor Kappa b – TNFalpha triggers the production of NFKB,102

which is a protein that signals inflammation103 and plays a key role in tumor
formation, growth and spread.104-105 Many ancient natural medicines found
to be effective against cancer inhibit NFKB.106
Interleukin 6 – IL-6 is a highly-toxic pro-inflammatory cytokine107-108 that
plays a key role in the formation of numerous types of cancer, including
colorectal,94 pancreatic,110 liver111 and prostate.114
High-Mobility Group Box 1 Protein – HMGB1 is a pro-inflammatory
protein that signals immune system activation in response to injury.113
Overexpression of HMGB1 promotes inflammation, carcinogenesis,
angiogenesis and metastasis. “Our studies and those of our colleagues
suggest that HMGB1 is central to cancer.”109
Interestingly, all of the tumor microenvironmental factors we’ve just
outlined tend to rise and fall together and to be self-promoting. Stress
begets more stress. This means health can go downhill faster than one
might think, and conversely, health can also be recovered more quickly than
one might think.
In The Cancer Industry it was established that surgery, chemotherapy and
radiotherapy – whether administered individually or in combination -
significantly elevate all of the aforementioned substances within the tumor
microenvironment. These are the precise biochemical mechanisms that
explain why mainstream cancer treatments ultimately make the health of
cancer patients far worse and often kill them. These findings further
substantiate the conclusions of many reknowned doctors and scientists over
the preceding decades: Treatments that damage the body are the exact
opposite of what a sick person with cancer needs to heal.

Inside The Bodies of Untreated Cancer Patients

Within the tumor microenvironment we know the aforementioned
substances can be found particularly concentrated. But as it turns out, these
same factors can also be found elevated throughout the entire bodies of
cancer patients.
Here’s what scientists have found in the blood and tissues of cancer patients
before receiving any treatments:

Elevated free radicals1-3

Elevated tumor necrosis factor-alpha4-5
Elevated interleukin-15-6
Elevated interleukin-448
Elevated interleukin-65-6
Elevated interleukin-85-6
Elevated nuclear factor-kappa b7
Elevated cortisol8-10
Elevated adrenaline47
Elevated prolactin11-13
 Elevated high mobility group box 1 protein49
Elevated vascular endothelial growth factor50
Elevated epidermal growth factor51
Elevated nitric oxide14-15
Elevated lactic acid16-18
Elevated estrogen10,19
Elevated prostaglandins20-21
Elevated serotonin24-25
Elevated histamine22-23

This means that although the situation is worst in the area surrounding a
tumor, the disease of cancer is not isolated to the tumor itself, and therefore
treatment must then involve direct treatment of the tumor as well as the
entire body as a whole.
The questions that must be asked and answered now are:

Is there anything we can do to safely downregulate the cancer-

promoting substances within the tumor microenvironment of
cancer patients?
And if so, what happens to the health of a cancer patient once
these factors are reduced?
Is reducing these substances the most efficient way to heal cancer?

Downregulating The Tumor Promoting Factors

in Cancer Patients

We all eat food everyday, our lives depend on it. Once consumed, the food
we eat is digested and used by our bodies as base materials to maintain and
regenerate its structure and to power the energy-producing ‘engines’ within
each of our cells, called mitochondria. Based on this, it’s clear that the most
fundamental way to affect human health either positively or negatively is to
alter the types and quantities of food we eat.
If a person is ingesting everything their cells need to be healthy (water, air,
protein, carbohydrates, fat, vitamins and minerals) and avoiding things they
don’t need (chemical poisons), they will be in good health. If they’re not,
the process of disease and degeneration will begin to occur.
Since food is our primary source of nourishment, we will now explore
which foods might act medicinally to downregulate the cancer-promoting
factors within the body and tumor microenvironment.
One of the dietary recommendations Dr. Raymond Peat has been making
for years is that people eat more oranges. After reading a number of studies
on oranges, it became clear that this fruit indeed contains a number of
powerful medicinal ingredients that might make it a good candidate to alter
the tumor microenvironment. I explored the scientific literature to
determine the impact of oranges on the tumor microenvironment and here
are my findings.

Oranges and the Tumor Microenvironment:

Oranges reduce free radicals26-27
Oranges reduce tumor necrosis factor-alpha28
Oranges reduce interleukin-129
Oranges reduce interleukin-430
Oranges reduce interleukin-530
Oranges reduce interleukin-628
Oranges reduce interleukin-831
Oranges reduce interleukin-1330
Oranges reduce nuclear factor kappa-b31
Oranges reduce cortisol32
Oranges reduce adrenaline46
 Oranges reduce prolactin33-34
Oranges reduce high mobility group box 1 protein52
Oranges reduce vascular endothelial growth factor53
Oranges reduce epidermal growth factor54
Oranges reduce nitric oxide35-36
Oranges reduce lactic acid37-38
Oranges reduce estrogen39-41
Oranges reduce prostaglandins35-36
Oranges reduce serotonin44-45
Oranges reduce histamine42-43

It’s clear that oranges can diminish not just one, but all of the previously
outlined cancer-promoting tumor microenvironmental factors within the
human body. Before doing this work I had suspected that oranges would
reduce at least a few of these substances, but to my surprise it seems to be
able to downregulate every single of them. We are off to a great start.
Next we will conduct a thorough scientific investigation into oranges to find
out what they can do in animal and human experiments of cancer.
Following this, similar investigations will be conducted on two other
medicines and then we will return to synthesize the information and unravel
the mysteries of cancer in our final chapter.
ORANGES
Sweet, powerfully refreshing and bursting with flavor; it’s no surprise that
oranges are one of the most popular fruits in the world. Most people are
aware that oranges are a potent source of vitamin C, but there are a number
of other nutrients within an orange that boost its medicinal value
considerably.
In this chapter, we will investigate the therapeutic potential of citrus
flavonoids, modified citrus pectin, vitamin C and orange juice on cancer
and overall health.

Citrus Flavonoids
Flavonoids are naturally occurring substances found in fruits, vegetables,
teas and wines that are responsible for the diversity of colors produced by
plants.1 Epidemiological studies have shown that dietary consumption of
flavonoids can reduce the risk of cardiovascular disease,3 asthma, type 2
diabetes, heart disease, prostate cancer and lung cancer.4
More than 60 flavonoids have been identified in citrus fruit, making them
one of the most concentrated and readily available sources of flavonoids.366
A 2003 study from the UK found that a Sicilian variety of orange called
Tarocco had higher concentrations of citrus flavonoids than 6 other orange
varieties tested.5 Interestingly, flavonoids are found more abundantly in the
peel than in the pulp of citrus fruit.2
Some examples of citrus flavonoids include naringin, naringenin, diosmin,
hesperetin, hesperidin, quercetin, tangeretin, nobiletin. In this section we
will investigate three of them.

Citrus Flavonoids Vs. Cancer

One of the methods used by scientists to test the therapeutic value of
nutrients or drugs against cancer is to add them to a test tube containing
cancer cells and observe the effects. Testing cancer cells outside of living
organisms in this way is called in vitro. Sometimes effects observed in vitro
are not the same as inside living organisms, or in vivo, but many times they
are, as you will see.

Naringin:
In vitro studies have confirmed naringin can inhibit the growth of
stomach,9 cervical,12 breast,14 and colon cancer cells,11 the spread of brain7-8
and bone cancer cells,10 and trigger cancer cell death (apoptosis) in
colon,11,17 pancreatic,17 stomach,17 cervical,12-13,17 liver17 and breast cancer
cells.14, 17
Another popular method used by scientists to determine the value of
nutrients or drugs against cancer is by inducing cancer in animals - usually
by injecting carcinogenic chemicals into them - and then administering the
treatment and observing the outcome.
In vivo studies have confirmed naringin can inhibit the growth of colon,18
oral,19 lung20 and connective tissue tumors,16-17 the spread of skin
tumors20and trigger apoptosis in colon tumors.18

A Closer Look…
In 2012, scientists from Sao Paulo, Brazil, investigated the effects of
naringin on rats bearing connective tissue cancer. Results showed that
a 25mg/kg dose of naringin administered daily for 50 days inhibited
tumor growth by 75%. Naringin also increased survival and notably,
“two rats presented complete tumor regression.”16

One of the most exciting experiments on naringin was conducted in 2016

by Chinese researchers, who added naringin to skin cancer cells to
determine its impact on cellular energy metabolism. One of the key
changes in the metabolism of cancer cells is increased production of lactic
acid, and not only did naringin inhibit lactic acid production in the skin
cancer cells, but it also completely reversed them back into normal cells.
“In summary, we demonstrated that naringin inhibits the malignant
phenotype of A375 cells.” they concluded.15
Perhaps best of all, the beneficial effects of naringin can be obtained
“without adverse side effects.”59
Normally, once a ‘drug’ has proven itself in vitro and in vivo, it would
move on to human testing in clinical trials, but since the average cost of
phase 1 clinical trial in the United States ranges from $1.4 million to $6.6
million dollars;198 and since natural substances found in foods can’t be
patented or sold by drug companies, this type of research doesn’t often
receive funding and is thus rarely performed.
Many times, the only reason in vitro and in vivo studies on food nutrients
are funded is so drug companies can find medicines that work and then
attempt to replicate similar chemicals to patent and sell.

Naringenin:
A 2015 study identified naringenin as one of 10 therapeutic agents “that
may warrant further investigation to target the tumor microenvironment”
for preventing and treating cancer.”64
In vitro experiments have established naringenin can inhibit the growth of
breast,65,73 stomach,71 colon,66,73 skin,68,76 leukemia75 and liver cancer cells,67,77
the spread of breast,65 liver,67 skin,68 bladder,69 pancreatic,70 and stomach
cancer cells,71 and trigger apoptosis in liver,67,77 stomach,71 colon,72-73
breast,73-74 leukemia75 and skin cancer cells.76
Animal experiments have verified naringenin can inhibit the growth of
oral,19 stomach,78 lung81 and brain tumors,80 prevent the spread of breast
tumors79 and trigger apoptosis in brain tumors.82
Synergistic enhancement of the anti-cancer effects of naringenin can be
obtained by combining it with either curcumin83 or vitamin E,84 and one
study reports that nano-encapsulated naringenin exhibits “significantly
higher” antioxidant and anticancer properties than naringenin in free form.86
Naringenin has a “promising safety profile”133 and remarkably, it maintains
its cancer-killing effects even in the presence of the environmental toxin
bisphenol A.85
Hesperidin:
In vitro, hesperidin can inhibit the growth of breast,134-135 immune,138
leukemia,140-141 and lung cancer cells,143 the spread of skin cancer cells,136
and trigger apoptosis in breast,135,144 immune,138 colon,139 leukemia,140-141
liver137,142 and lung cancer cells.143
Animal studies have confirmed hesperidin can inhibit the growth of
colon,145 lung,146 bladder,147 oral,148-149 throat150 and stomach tumors, and
trigger apoptosis in stomach151 and colon tumors.152
One study compared the medicinal potencies of a number of citrus
flavonoids and found that hesperidin exerted a more powerful anti-cancer
effect than neohesperidin, naringin and naringenin.137 With that in mind,
Tunisian researchers reported in 2016 that concentrations of hesperidin
were greater in organically-grown oranges than in oranges grown
conventionally.6
A safety study from 1990 fed rats dietary concentrations of 0%, 1.25% or
5% methyl hesperidin for two years and concluded that the substance
“lacked any carcinogenicity” in rats.193

Additional Health Effects

Antibacterial:

Naringin exerts a “robust antibacterial effect”21

Hesperidin inhibits growth of bifidobacteria153

Antioxidant:

Naringin neutralizes the toxic effects of herbicide paraquat22

Naringin prevents kidney and liver damage from acetaminophen23
and sodium arsenite24
Naringin prevents chemotherapy-induced kidney25 and lung
damage26
 Naringin reverses side effects of HIV medication29-30
Naringenin prevents damage from lead108 and endotoxin87
Hesperidin prevents chemically-induced kidney damage155-158
Hesperidin prevents chemotherapy-induced liver damage161

Antiviral:

Naringin28 and naringenin93 inhibit infection by sindbis virus28

Naringenin reduces hepatitis C virus secretions from infected cells
by 80%92
Hesperidin prevents replication of influenza A virus162
Hesperidin inhibits infection by canine distemper virus163 and
rotavirus164
Hesperidin inhibits combined viral-bacterial infections165

Arthritis:

Naringin prevents inflammation associated with arthritis31-34

Naringenin prevents inflammatory pain in mice94-95
Hesperidin prevents chemically-induced arthritis154,166-167

Asthma:

Naringin significantly reduces coughing (associated with a type of

asthma that causes chronic coughing)63

Bone Health:

Naringin prevents the destruction of cartilage38

Naringin,35-36 naringenin96-99 and hesperidin168-170 prevent bone loss
and accelerate bone formation
Brain Health:

Naringin reverses chemically-induced memory deficits39-41,47

Naringin improves brain function in mice with Alzheimer’s
disease42-43
Naringin prevents brain degeneration in rats with Parkinson’s
disease44-46
Naringin prevents chemically-induced seizures48
Naringenin reduces anxiety caused by lead poisoning89
Naringenin prevents brain damage caused by neurotoxins90 and
iron102
Naringenin prevents Alzheimer’s disease100
Naringenin improves learning and memory in rats with
Alzheimer’s disease101
Naringenin prevents cognitive decline in rats with Parkinson’s
disease103
Hesperidin prevents brain damage from pesticides,171 heavy
metals,172 and other poisons174
Hesperidin prevents cognitive impairment in mice with
Alzheimer’s disease173
Hesperidin prevents brain damage caused by ionizing radiation188

Cooking:

Naringenin prevents toxic acrylamides from forming in food

during high-heat cooking132

Dental Health:

Naringin remineralizes root caries (cavities) in teeth37

Depression:
 Naringenin produces antidepressant-like behavior in rats106-107
Naringenin105 and hesperidin175-177 exert potent antidepressant
effects

Detoxification:

Naringenin chelates lead from the body108

Diabetes:

Naringin prevents scarring of the heart caused by diabetes49

Naringenin prevents kidney damage caused by diabetes52,109
Naringenin improves glucose metabolism110-111
Naringin improves insulin sensitivity50-51
Hesperidin reduces diabetes and its complications178

Digestive Health:

Naringenin an effective treatment for inflammatory bowel

disease120-121
Naringenin prevents defects of the intestinal barrier122

Exercise:

Naringin in combination with treadmill exercise is more effective

at increasing bone strength and density than either therapy alone53
Hesperidin synergistically enhances the health benefits of
exercise179

Eye Health:

Naringenin eye drops prevent chemically-induced retinal damage91

Hesperidin prevents eye damage caused by chemotherapy159
Food Production:

Naringin and Hesperidin fed to chickens elevates antioxidant

levels in chicken meat; are "important additives for both the
consumer and the industry."27

Headaches:

Drynaria quercifolia (a plant containing naringin) alleviates painful

inflammatory conditions, like headache54
Hesperidin may be useful for treating migraines180

Healing:

Naringin55 and hesperidin191 accelerate wound healing

Heart Health:

Naringin56 and naringenin113 prevent arterial plaque formation

Naringinen reduces arterial stiffness112
Naringenin prevents thickening of the heart muscle114

Immune System:

Naringenin boosts the immune system115-116

Naringenin significantly enhances anti-cancer immunity117-119
Hesperidin enhances immune systems of mice181 and irradiated
mice189
Hesperidin enhances immune systems of broiler chickens182

Obesity:

Naringin significantly decreases fat mass57,59

Naringin prevents formation of new fat tissue58
 Naringenin reduces body fat and suppresses weight gain123-125
Hesperidin improves lipid metabolism in humans183-184

Radiation protective:

Naringin protects skin from ultraviolet B radiation61

Naringin60 and naringenin126 prevent genetic damage caused by
ionizing radiation
Naringenin prevents skin aging and wrinkle formation caused by
ultraviolet B radiation127-129
Naringenin added to conventional sunscreen reduces its toxicity130
Hesperidin reduces damage caused by whole-body gamma ray
irradiation185
Hesperidin prevents ultraviolet B radiation damage186-187

Sexual Health:

Naringenin aids the process of conception104

Naringenin prevents testicle damage caused by insecticides88
Hesperidin prevents testicle and sperm damage caused by
chemotherapy160

Skin Health:

Naringin62 and hesperidin192 promote the production of skin-

protective melanin
Naringenin “should be introduced into cosmetic products as
natural tanning agents.”131

Other:

A mixture of citrus flavonoids Hesperidin, Troxerutin, and

Diosmin applied to hemmorhoids reduces pain, bleeding and
 swelling in humans190

Modified Citrus Pectin

Pectin is a complex of sugar molecules (polysaccharide) heavily
concentrated in the pulp and peel of citrus fruit. Because of its gelling
properties, pectin is a traditional ingredient used for making marmalades
and jams.
Pectin’s long-branched chains of polysaccharides make it virtually
indigestible by humans, but researchers have discovered ways to modify
pectin so it can be easily absorbed into the blood stream. Once in the
bloodstream, modified citrus pectin (MCP) has proven useful for treating a
number of conditions, including cancer.317 Although heat treatment and pH
modifications are commonly used to create modified citrus pectin,315 high-
intensity ultrasound is also effective and is said to be more
‘environmentally friendly.’316
“The more we learn about MCP, the more impressive it becomes,” said Dr.
Isaac Eliaz. “With its ability to control aggressive cancers, reduce
inflammation, enhance immunity, chelate heavy metals and work
synergistically with a variety of chemotherapeutic agents, it has earned an
important role within anti-cancer and chronic disease protocols.”367

Modified Citrus Pectin vs. Cancer

Scientists have observed modified citrus pectin prevent the growth of
prostate cancer cells320,322 and trigger apoptosis in lung,321 liver,321 prostate322
and eight other types of cancer cells.323
Co-administration of modified citrus pectin with two herbal products have
revealed synergistic inhibitory effects on the spread of breast and prostate
cancer in vitro.324 Modified citrus pectin can also eliminate chemotherapy
resistance325 and increase the apoptosis-inducing effects of chemotherapy in
cell cultures.326
Modified citrus pectin can prevent the growth of skin327 and sarcoma
tumors in mice; including a 51% reduction in tumor size and increased
survival compared to control mice.323 Another study reported a 70%
reduction in colon tumor size in mice after 20 days of MCP treatment.332
Also in animals, the spread of breast,328 prostate,329 skin330 and colon tumors
can be inhibited by as much as 90% using modified citrus pectin.331
Scientists from the Harry S. Truman Memorial Veteran’s Hospital in
Missouri discovered that MCP prevents cancer metastasis by inhibiting
circulating tumor cells from adhering and establishing themselves onto
distal body tissues.318 Another mechanism behind MCP’s therapeutic
effects is the inhibition of a substance called Galectin-3, which is involved
in inflammation, fibrosis, heart disease, stroke and cancer.319

Studies report modified citrus pectin has no adverse side effects,339

including one study in which 15 grams MCP was administered daily to
humans for 12 consecutive months.340

Additional Health Effects

Antioxidant:

MCP prevents liver fibrosis334

MCP prevents kidney injury335
MCP prevents damage caused by endotoxin336

Arthritis:

MCP is “a therapeutic approach for the treatment of inflammatory

arthritis”337

Detoxification:

MCP dramatically increases urinary excretion of arsenic, cadmium

and lead in humans338
 MCP safely and dramatically detoxifies lead from children339
MCP reduces toxic heavy metal burden in humans by an average
of 74%340

Heart Health:

MCP “may represent a new promising therapeutic option in heart

failure”341
MCP decreases cardiovascular fibrosis and inflammation342-344
Galectin-3 inhibition “causes decreased atherosclerosis”345

Immune System:

MCP enhances anti-cancer immunity346

Inflammation:

MCP reduces inflammation and pain after spinal nerve injury333

Obesity:

MCP prevents production of new fat tissue347

Vitamin C
Although vitamin C (aka ascorbic acid or ascorbate) wasn’t officially
discovered until 1928 by Hungarian biochemist Albert Szent-Gyorgyi,194 the
manifestations of its deficiency, known as scurvy,195 were first documented
by the physician Hippocrates in ancient Greece (460BC-370BC).368 In
1945, scientists from the University of Wisconsin found that when they
deprived monkeys of vitamin C for just a few weeks, various dental issues
including bleeding gums, loosening of the teeth and the formation of heavy
tartar deposits were induced.196
The effects of supplemental vitamin C are highly-dependent on the dose
administered. In low doses, vitamin C behaves as an anti-oxidant, helping
the body neutralize toxins and eliminate waste products. And in high doses,
vitamin C acts as a pro-oxidant that can selectively target unhealthy and
even cancerous cells.197 High-doses of intravenous vitamin C have been
used to treat cancer since the 1970s.200

Vitamin C vs. Cancer

One thing cancer patients all have in common is significantly depleted
levels of vitamin C.222 Remarkably, some researchers have said that vitamin
C might be the most important nutritional factor needed by the body to
resist cancer; “There is increasing recognition that resistance to cancer
depends, to a certain extent, upon the availability of certain nutritional
factors, of which ascorbic acid appears to be the most important,” wrote
scientist Ewan Cameron in 1982.201
An epidemiological study of people in Northern Italy reported that vitamin
C intake has “possible protective activity” against skin cancer202 and greater
consumption of antioxidants was associated with less aggressive prostate
cancer in the United States.203 A 2014 systematic review by Chinese
researchers concluded that low doses of vitamins, specifically vitamins A, C
and E, can significantly reduce the risk of stomach cancer.204
In vitro studies have confirmed vitamin C can trigger apoptosis in colon,206-
207,214
breast,207 skin,208 blood, bone marrow,209 Ehrlich acites carcinoma,205
melanoma220 and four types of malignant mesothelioma cancer cells.213
Co-administration of vitamin C and vitamin B2 can synergistically enhance
apoptosis in multiple types of cancer cells.210 Vitamin C loaded into tiny
bubbles of fat (lipid nanoparticles) was shown to enter into cells more
efficiently than free vitamin C219 and vitamin C affixed to nano-sized
polymer carriers has been shown to trigger apoptosis in brain cancer cells.218
In animals, vitamin C can prevent the growth of lung, skin,211 ovarian,
pancreatic, brain,212 malignant mesothelioma,213 colon214 and sarcoma
tumors,215 and can trigger apoptosis in liver tumors.216 A nutrient mixture
containing lysine, vitamin C, proline, green tea extract and other
micronutrients fed to tumor-bearing mice “demonstrated a potent inhibition
of [cervical] tumor growth.”217

A Closer Look…
An American group of scientists from Kansas administered
500mg/kg/day sodium ascorbate to liver tumor-bearing guinea pigs in
2006. Results showed that “Subcutaneous injections of ascorbate (500
mg/kg/day) inhibited tumor growth by as much as sixty-five percent,
with oral supplementation reducing it by roughly fifty percent.”216

In 1994, researchers from the Oregon Institute of Science and Medicine

induced tumors in mice and treated them with high-doses of vitamin C
along with variations in diet. Results showed that survival could be
increased by up to 20-times simply by adjusting the animal’s nutritional
intake.221
Two-time Nobel Prize winner Linus Pauling and surgeon Ewan Cameron
administered 10 grams/day of vitamin C to terminal cancer patients in 1976
and found that survival was increased “more than 4.2 times” compared to
patients who weren’t given vitamin C.222 Other studies have confirmed
vitamin C can increase survival and significantly improve the quality of life
of terminal cancer patients.223-225
How does vitamin C exert its beneficial effects? When blood levels of
vitamin C are maintained at a consistently high level, it is absorbed into
cancerous tissue where it produces hydrogen peroxide that kills cancer
cells.199

Safety
Thanks to the work of Dr. Frederick R. Klenner, it has been known for over
70 years that vitamin C doses as high as 300,000mg (300 grams) per day in
humans are safe and modern research has confirmed this
finding.205,209,212,224,225,235,260
A Korean study from 2007 acknowledged that vitamin C “is considered a
safe and effective therapy”225 and a 2008 study from the National Institutes
of Health found that high-doses of vitamin C displayed “cytotoxicity
toward a variety of cancer cells in vitro without adversely affecting normal
cells.”212
One thing to be aware of is that vitamin C can increase the absorption of
iron,307-309 which in small amounts is essential, but like all heavy metals,
becomes toxic in excess311 and can diminish the effectiveness of vitamin C
treatment.310 For these reasons, oral supplementation of vitamin C is
probably best without food and to lower existing iron levels in the body,
iron-chelating substances such as tetracycline, doxycycline, minocycline312
or curcumin369 can be used.

Oral vs. Intravenous

There is some controversy surrounding the efficacy of various vitamin C
administration methods. While Dr. Mark Levine of the NIH claims that
"...only injected ascorbate might deliver the concentrations needed to see an
anti-tumor effect,"313 Dr. Steve Hickey has said, "it is not clear that
intravenous vitamin C necessarily provides an advantage over oral
supplements in the treatment of cancer.”314
When the body is given a high enough dose of vitamin C intravenously,
much of it goes unused and is excreted in the urine, according to Dr.
Hickey. Furthermore, he makes the case that high-doses of orally
administered vitamin C might even be more effective.314
While Dr. Levine claims that maximum blood levels of vitamin C are
200μM/L, Dr. Hickey maintains he has been able to generate blood levels of
around 250μM/L with a single 5 gram oral dose of vitamin C and blood
levels above 400μM/L with a single oral dose of liposomal vitamin C.314

Dose
For many people, a single oral dose of 2 grams of vitamin C will cause a
laxative effect and anything more will be eliminated from the body.
Interestingly, bowel tolerance is said to increase dramatically when a person
is ill.314 In other words, a person who would normally be able to tolerate
only 2 grams might be able to tolerate 100-times that amount when sick.
Maximum blood levels of orally-ingested vitamin C can be achieved by
consuming about 3 grams every four hours. Since vitamin C is only active
in the body for a few hours, frequent doses are critical to maintain
consistently high blood levels.

Success Stories
Dr. Victor Marcial, radiation oncologist:
"We studied patients with advanced cancer (stage 4). 40 patients received
40,000-75,000 mg intravenously several times a week. These are patients
that have not responded to other treatments. The initial tumor response rate
was achieved in 75% of patients, defined as a 50% reduction or more in
tumor size... Once you start using IV vitamin C, the effect is so dramatic
that it is difficult to go back to not using it."

Linus Pauling, 2x Nobel Prize Laureate:

"I became interested in vitamin C and cancer in 1971 and began working
with Ewan Cameron, M.B., Ch.B., chief surgeon at Vale of Leven Hospital
in Scotland. Cameron gave 10 grams of vitamin C a day to patients with
untreatable, terminal cancer. These patients were then compared by
Cameron and me to patients with the same kind of cancer at the same
terminal stage who were being treated in the same hospital but by other
doctors-doctors who didn't give vitamin C, but instead just gave
conventional treatments. Cameron's terminal cancer patients lived far
longer compared to the ones who didn't get 10 grams a day of vitamin C.
The other patients lived an average of six months after they were
pronounced terminal, while Cameron's patients lived an average of about
six years."
Dr. Irwin Stone, American biochemist, chemical engineer:
"In one case where complete remission was achieved in myelogenous
leukemia… the patient took 24-42 gms vitamin c per day… it is
inconceivable that no-one appears to have followed this up… without the
scurvy, leukemia may be a relatively benign, non-fatal condition. I wrote a
paper… in an attempt to have the therapy clinically tested… I sent it to 3
cancer journals and 3 blood journals… it was refused by all… Two without
even reading it."

Additional Health Effects

Antioxidant:

Vitamin C is an antidote for snake venom228

Vitamin C cures carbon monoxide poisoning233
Vitamin C cures mushroom poisoning229
Vitamin C prevents damage caused by agricultural fungicides230
and insecticides231
Vitamin C prevents liver damage caused by dexmedetomidine236
Vitamin C prevents damage caused by monosodium glutamate237
Vitamin C prevents damage caused by methylmercury,238
formaldehyde239 and endotoxin241-242,245-246,248
Vitamin C prevents chemically-induced ulcer formation in rats240
Vitamin C prevents septic organ injury in mice243
Vitamin C prevents alcohol-induced liver fibrosis in mice244
Vitamin C prevents the formation of nitric oxide247
Vitamin C prevents kidney249 and liver damage250-251 caused by
chemotherapy

Antiviral:

Vitamin C “kills influenza virus”252

Vitamin C shortens duration of the common cold, pneumonia,
malaria and diarrhea infections253
Vitamin C suppresses HIV replication by infected cells254
 Vitamin C successfully treats polio, hepatitis, mononucleosis,
diphtheria, herpes zoster, herpes simplex, chicken pox, influenza,
measles, mumps and viral pneumonia255-256
Vitamin C successfully treats Epstein-Barr virus257
Vitamin C resolves all symptoms of Chikungunya fever in two
days260

Arthritis:
Elevated free radicals and oxidative stress found in patients with
Rheumatoid Arthritis227

Bone Health:

Vitamin C prevents bone loss261

Vitamin C improves bone mineral density in postmenopausal
women262-264
Vitamin C is “a skeletal anabolic agent”265
Vitamin A, C and E decrease risk of hip fracture266

Brain Health:

Vitamin C prevents brain damage caused by methamphetamine,267

insecticides268-269 and glutamate270
Vitamin C deficiency increases risk of seizures271
Vitamin C (and zinc) deficiencies impair the physical and mental
growth of children287
Vitamin C levels in patients with severe Parkinson’s disease were
“significantly lower”272

Depression:
 Vitamin C reduces anxiety levels in highschool students after 14
days of supplementing 500mg276

Detoxification:

Vitamin C chelates lead from the bloodstream277

Vitamin C reduces blood levels of chemical pollutants232

Diabetes:

Vitamin C reduces fasting blood sugar in diabetics278,280

Vitamin C significantly lowers needed insulin dose for blood sugar
control279

Exercise:

Vitamin C and low-intensity exercise prevent seizures281

Vitamin C has anti-seizure effects in rats performing endurance
swimming282
Vitamin C improves blood flow and oxygen use in muscles283

Food Production:
Vitamin C improves growth performance and enhances stress
resistance in fish303

Headaches:

Vitamin C and Pinus Radiata bark extract ingested for 12 months

reduces headache severity and frequency by 50%284

Healing:

Vitamin C accelerates healing301

 Vitamin C enhances cell survival and DNA repair in human
fibroblasts exposed to x-rays299

Heart Health:

Vitamin C decreases length of hospital stay in patients following

cardiac surgery304

Immune System:

Vitamin C enhances anti-cancer immunity285,289-292

Vitamin C significantly enhances immunity286,288

Inflammation:

Vitamin C reduces inflammation226

Lifespan:

Antioxidant-rich diet extends survival of mice exposed to

endotoxin234
Vitamin C extends lifespan of tetanus patients258-259

Obesity:

Vitamin C intake reduces obesity in women293

Radiation protective:

Vitamin C prevents damage caused by ionizing radiation294,297-298

Vitamin C and vitamin E synergistically prevent damage caused by
ionizing radiation295
Vitamin C and melatonin synergistically prevent damage caused
by ionizing radiation296
Sexual Health:

Vitamin C “significantly improves sperm concentration and

mobility”274
Vitamin C prevents infertility in rats subjected to forced swimming
stress275
Vitamin C promotes a healthy pregnancy273

Sleep:

Vitamin C prevents spatial memory impairment in rats following

sleep deprivation300

Other:

Vitamin C resolves symptoms of burning mouth syndrome in

humans302
Vitamin C diminishes microparticle elevations caused by SCUBA
diving305
Vitamin C prevents complex regional pain syndrome in humans306

Orange Juice
If an orange contains all the medicines we’ve investigated above, then one
would expect orange juice to also have substantial therapeutic value.

Orange Juice vs Cancer

Although studies are limited, scientists have investigated the therapeutic
effects of orange juice on cancer cell cultures and in animals. In vitro
studies have confirmed orange juice can trigger apoptosis in two types of
blood cancer cells.348
In vivo, researchers have experimentally induced tumors in rats and then
replaced their water with orange juice to determine its effects. Results
show that orange juice can inhibit the growth of breast,349 colon,350-352
tongue and lung tumors,352 and can trigger apoptosis in colon tumors.350

A Closer Look…
In 2015, Brazilian researchers incubated two types of blood cancer
cells with orange juice – one with the juice of a red-fleshed sweet
orange and the other with juice from a blond orange - for 24-hours and
observed the results. At the end of the study, both varieties of orange
juice were found to induce apoptosis in the blood cancer cells.348
Mandarin orange juice was tested on rats induced with three types of
cancers in a 2012 Japanese study from the Journal of Biomedicine &
Biotechnology. Citrus juices from the Satsuma mandarin orange were
found to inhibit the formation of chemically-induced colon, tongue and
lung tumors in rats.352
Canadian scientists from Western University in London, Ontario,
chemically-induced breast tumors in rats and fed them orange juice to
determine if it could prevent cancer formation. Published in the
journal Nutrition and Cancer in 1996, results showed that rats given
orange juice “had a smaller tumor burden than controls.”349

Additional Health Effects

Antibacterial:

Tangerine juice concentrate is effective for “controlling unwanted

microbial growth”353

Antioxidant:

Orange juice consumption results in a “marked antioxidant

effect”355-356

Bone Health:

Orange juice increases bone strength in rats358

 Orange juice increases bone mineral density in children and
adults357

Exercise:

Orange juice prevents exercise-induced hypoxia359

Orange juice improves physical performance in overweight
women360

Heart Health:

Fermented orange juice reduces cardiovascular risk factors361

Immune System:

Orange juice enhances the immune system362

Inflammation:

Orange juice reduces inflammation354

Obesity:

Orange juice associated with healthier body composition in

adults363
Orange juice decreases risk of obesity364
Orange juice prevents fatty liver disease365
COCONUT OIL
Coconut is a fruit, a seed and a nut that grows on palm trees in over 90
different countries worldwide.1 Its meat, juice, milk and oil have been
staples in the diets of many cultures for generations.2
The word coconut is derived from the 16th century Portuguese and Spanish
word coco, meaning “head” or “skull,” because the three indentations on its
hairy shell resemble a face.3
Coconut oil consists of about 93% saturated fat, 4% monounsaturated fat
and 3% unsaturated fat.4 Understanding the role of dietary fat in health and
disease is essential for understanding cancer.

Saturated vs. Unsaturated Fat

Due to its high content of saturated fatty acids, coconut oil is stable and
protected from reacting with oxygen (oxidation). Romanian researchers
tested the stability of coconut oil in 2012 by storing it at room temperature
for one full year. When the year was up, they analyzed the coconut oil and
found, “The physic-chemical oxidation of this oil keeped [sic] at room
temperature was negligible.”5 In other words, coconut oil can sit at room
temperature for at least a year without becoming rancid, making it “suitable
for the preservation of medicinal plants and for wound treatment”6 and
desirable to commercial interests such as baking industries, processed
foods, infant formulae, pharmaceuticals and cosmetics.7 Since coconut oil
is one of the least vulnerable dietary oils to oxidation and free-radical
formation, “…it is therefore the safest to use in cooking,” wrote scientists
from Columbia University in 1992.8
Conversely, unsaturated fatty acids are highly unstable and easily react with
oxygen.9 When an unsaturated fatty acid is oxidized, a number of toxic
breakdown products can be formed;10 including prostaglandin E2, which
“dominantly enables progressive tumor growth.”11-12 Unsaturated fats
include oils that are liquid at room temperature like corn, soy, canola, hemp,
flax, sunflower, safflower, peanut and fish oil. In 1990, researchers
demonstrated that feeding 20% corn oil diets to rats produced more
prostaglandin E2 than feeding them diets containing 19% coconut oil and
1% corn oil.13
Interestingly, the most unsaturated of all dietary fats – omega-3 and omega-
6 – are the ones that health ‘authorities’ (and corporations selling them)
claim are essential. In 1981, researchers from the University of Texas
Health Science Center discovered that by not feeding mice any ‘essential’
fatty acids, autoimmune disease was prevented and their lifespans were
increased.14 Looking at the immune system, we find that unsaturated fats
inhibit anti-cancer immunity and saturated fats promote anti-cancer
immunity.95,250
Experiments have shown that unsaturated fatty acids inhibit the growth of
the human fetus15 and, in the absence of omega-3 and omega-6, both short-
term and long-term memory of the fetus are improved.16 In a 2016 study,
Taiwanese scientists reported that ‘essential’ unsaturated fats from fish oil
(omega-3) are toxic to the aging brain,17 and as it turns out: fish oil isn’t
even good for fish! Researchers who fed salmon highly unsaturated fat
diets “enriched” with DHA or EPA in an experiment from 2003 discovered,
“an increased incidence of oxidative stress” in the livers of the fish.18
The detrimental effects of unsaturated fats on the heart build an even
stronger case for its dietary avoidance. “Atherosclerotic plaques readily
incorporate n-3 [omega-3] PUFAs from fish-oil supplementation”19 and
continued consumption leads to a linear increase in arterial plaque
buildup.20 “Men advised to eat oily fish, and particularly those supplied
with fish oil capsules, had a higher risk of cardiac death,”21 reported UK
researchers in 2003.
To put it into perspective, New Zealand researchers conducted a 2014
review on the use of fish oil supplements based on 18 random controlled
trials and 6 meta-analysis’ published between January 2005 and December
2012. Of 16 publications that focused on the relationship between fish oil
supplementation and cardiovascular health, only two reported benefits from
fish oil.22
Saturated Fat Protects the Heart
One of the many popular myths taught in school and on television is that
saturated fat causes heart disease. Examining the diets and subsequent
health of native cultures worldwide reveals a very different reality. People
living in the country of Azerbaijan are famous for being long-lived; the
most famous among them, according to Soviet authorities, was Shirali
Muslimov, who died at the age of 168 in 1973.23 A 1991 study on the
Azerbaijani people revealed their dietary staples were fresh fruit, vegetables
and fermented milk products. Perhaps most importantly, their diets
contained a low ratio of unsaturated to saturated fats.24
The island-dwelling Polynesian populations near the equator known as
Pukapuka and Tokelau obtain 63% and 34% of their nutrition from coconut,
respectively. A 1981 study revealed that despite consumption of large
quantities of saturated fat, their rates of cardiovascular disease were nearly
non-existent. “Vascular disease is uncommon in both populations and there
is no evidence of the high saturated fat intake having a harmful effect in
these populations.”25
In 1978, Sri Lankan’s were consuming coconut oil as their main dietary fat
and had the lowest death rate from ischemic heart disease in the world.26
“All available population studies show that dietary coconut oil does not lead
to high serum cholesterol nor to high coronary heart disease mortality or
morbidity rate,” concluded American and Filipino researchers in 1992.27
For decades, the belief that ‘saturated fat causes heart disease’ has been
echoed as if it were fact, yet scientific studies have never proven a link
between saturated fat intake and cardiovascular disease.28 In 2013,
Cardiologist Dr. Aseem Malhotra of the Croydon University Hospital in
London, England wrote, “The mantra that saturated fat must be removed to
reduce the risk of cardiovascular disease has dominated dietary advice and
guidelines for almost four decades. Yet scientific evidence shows that this
advice has, paradoxically, increased our cardiovascular risks.”29 Two years
later, another study was published in the highly-esteemed British Medical
Journal that concluded, “Saturated fats are not associated with all-cause
mortality, cardiovascular disease, coronary heart disease, stroke, or type 2
diabetes...”30 Dietary saturated fats protect the heart and reduce the risk of
cardiovascular disease.31

Coconut Oil vs. Cancer

It has been known since at least 1945 that unsaturated fats are strong
promoters of tumors and that saturated fats, like coconut oil, protect against
tumor formation. When scientists from the University of Wisconsin fed rats
a 5% corn oil diet for 6 months, 80% of the rats developed tumors. When
they fed another group of rats a diet containing 4.7% hydrogenated (100%
saturated) coconut oil, “no liver tumors developed by 6 months.”32
A few decades later, researchers compared the effects of either 20%
safflower oil or 20% coconut oil diets on tumor growth in mice. After four
months, “the high-oleic safflower oil group had significantly more tumors
than did the coconut oil group.”33 Since then, research has repeatedly
demonstrated that tumor-induced animals fed the least amount of
unsaturated fats formed the least amount of tumors.36,39-42,90-92,95

A Closer Look…
A 1992 review from Michigan State University reported, “as the fat
content of the diet is increased from a low or standard level to a high
level, a consistent and substantial increase in the development of
rodent mammary gland tumors is observed.” This effect was found to
be largely dependent on the type of fat consumed. “High dietary levels
of unsaturated fats (e.g., corn oil, sunflower-seed oil) stimulate this
tumorigenic process more than high levels of saturated fats (e.g., beef
tallow, coconut oil).”40
A group of researchers from the University of South Carolina
examined the effects of high fat diets on rats induced with colon cancer
in 2016. Published in the American Journal of Physiology, “we found
an inverse association between SF [saturated fat] content and tumor
burden.” In other words, the more saturated the fat fed to rats, the less
colon tumors they developed. Furthermore, “we found that high SF
[saturated fat] content was protective,” and “there was a decrease in
 mortality in mice consuming the highest concentration of SFAs
[saturated fatty acids].”42

Both the type and the amount of fat are important considerations when
devising a cancer-preventive diet. Low fat diets and high saturated fat diets
both represent a low intake of unsaturated fat and are therefore similarly
effective in preventing tumor formation; the less unsaturated fat in the diet,
the less likely a tumor will form.
Beginning in 1978, a series of studies were published in the Journal of the
National Cancer Institute that looked at the effects of dietary fat on tumor
growth. Their conclusions were as follows:
1978: “Compared to animals fed diets rich in safflower oil, animals
that ate coconut oil-rich diets survived longer.”34
1981: “…the higher tumor yields were associated with increased
unsaturation of mammary tissue phospholipids.”35
1984: High-fat corn or safflower oil diets produced more colon tumors
in mice than low-fat corn or safflower oil diets. Olive oil, coconut oil
and MCT had “no promoting effect on tumor incidence”37
1986: Rats fed high-fat safflower or corn oil diets “exhibited enhanced
mammary tumor yields” compared to animals fed high-fat olive,
coconut or low-fat diets.38
The National Cancer Institute, “the nation’s leader in cancer research,”251
published these studies in what was at the time their official journal. Why
wasn’t the public notified of these findings? If they had been, tens of
millions of lives could have been saved and the “war on cancer” would be
long over. The blood cannot be washed from their hands.

Success Stories
Entrepreneur Julie Figueroa of Maryland, Ohio was running a computer
company in New York and owned an internet company in the Philippines in
1998. That same year she had an annual checkup with her doctor and was
given a clean bill of health. “A few months later I began feeling a strange
sensation in my breast late October that developed into a sharp pain.” She
went back to her doctor and was immediately referred to an oncologist for
testing. “I was told I had a very aggressive form of breast cancer and
needed surgery immediately.” With no history of cancer in Julie’s family,
this news came as a shock to her. “Before going through with the
mastectomy I wanted a second opinion.”
Julie went to a second specialist but they told her the same thing. She kept
trying to find a doctor who would give her a better option and “finally, the
fifth doctor told it to me straight, ‘you don’t have a choice. We don’t even
know if we can still save you. You are at stage 4, the most serious stage, we
need to do the surgery immediately.’”
Julie went through with the operation to remove her breast and afterwards
underwent several months of chemotherapy. Doctors told her the cancer
was under control but wasn’t completely gone so they kept her on
medication afterwards. Julie decided to go back to the Philippines where
she owned a farm that happened to be filled with coconut palm trees.
In 2011, she began to experience painful headaches; “They became so
severe that I felt like the bones in my skull were being fractured.” She went
to her doctor in the Philippines and had an x-ray taken. When she went
back the next day for her results, several doctors met with her and said they
had never seen anything like the cancer she had. “Almost half my skull
looks like cheese that had been eaten by rats,” described Julie. When she
asked what her chances of survival were, they replied, “In the Philippines,
at your stage… none.”
Julie took the next flight back to the United States and went to see her
doctor that same day, who scheduled her for emergency surgery to remove
the hairline cancer close to the main artery of her brain. Unfortunately,
20% of the cancer was in the back of her skull over her main artery and
could not be removed. “My chances of survival were grim. I knew I’d
better make the most of the time I had remaining.”
After several months of recovery following surgery, Julie returned to her
farm in the Philippines to visit her family. “I was really weak and would
just sit on the hill watching the farmers work among the coconut trees
planting coffee seedlings.” She knew she needed to do something to
strengthen her immune system and wanted to plant a medicinal herb
garden. “I started doing research on what medicinal plants I should grow
that would boost my immune system…Just about that time, I came across
some research on coconut oil.” She read about the clinical trials in the
Philippines where coconut oil was used to cure AIDS patients and figured it
might also work for her.
“I started taking 3 to 4 tablespoons of oil a day plus whatever I used in
preparing my meals,” she explained. “I would add it to my oatmeal in the
morning, put it in my hot chocolate, cook my meals in it. I also snacked on
fresh coconut and drank coconut juice.”
By July, Julie hadn’t been back for a checkup in nearly six months and was
asked to return home. She flew back to the US and to the complete surprise
of her doctors, her cancer was in remission. They asked her what she had
done. “I told them I found a cure: virgin coconut oil.”
As a child, Julie had grown up around coconut trees in the Philippines. Her
grandmother used to make coconut oil from fresh coconuts, but she never
used it because she was told saturated fats were unhealthy. So instead her
family used corn and soybean oil. “I had coconut oil around me all my
life. It took getting cancer and a desperate search for a cure that made me
rediscover this miracle oil.”43

Additional Health Effects

Antibacterial:

Lipolyzed coconut oil inhibits growth of clostridium difficile

bacteria44
Coconut oil inhibits growth of staphylococcus aureus bacteria45

Antifungal:

Coconut oil exhibits “significant antifungal activity”46-47

Antioxidant:

Coconut oil increases antioxidant status in rats48-49

Coconut oil reduces damage caused by numerous poisons,50-52
including chemotherapy53

Antiviral:

Coconut oil reduces viral load of HIV patients54-55

Arthritis:

Coconut oil reduces inflammation in arthritis-induced rats56

Bone Health:

Coconut oil maintains bone structure and prevents bone loss57-58

Brain Health:

Coconut oil improves brain function in patients with Alzheimer’s

disease59
Coconut oil drastically improves life of 74-year-old man with
Parkinson’s60

Dental Health:

Coconut oil pulling decreases plaque formation and gingivitis62,64

Coconut oil pulling inhibits streptococcus mutans in saliva63

Diabetes:

Coconut oil prevents diabetes in rats chemically-induced with

diabetes65
Virgin coconut oil prevents insulin-resistance in rats66
Exercise:

Coconut oil with exercise training improves impaired baroreflex

sensitivity67

Eyes:

Virgin coconut oil can safely be used as eye drops68

Farming:

Coconut oil improves skeletal growth and fecal scores in jersey

calves69
Replacing 75% of dietary soybean oil with coconut oil reduces fat
in broiler chickens70

Food Industry:

Ionizing radiation (used for food preservation) “had little effect on

the fatty acid compositions of saturated fats (lard and coconut
oil)… but caused destruction of 98% of the highly unsaturated
acids…”71

Hair:
Coconut oil prewash conditioner prevents cuticle damage caused
by wet combing72
Coconut oil conditioner prevents hair damage caused by bleaching
and exposing hair to boiling water for 2 hours73
Coconut oil and anise spray “significantly more effective” than the
most commonly used lice shampoo permethrin74

Healing:

Coconut oil applied topically to wounds accelerates healing75

Heart Health:
Coconut oil prevents blood pressure elevation and improves blood
vessel function76

Immune System:

Unsaturated fat inhibits anti-cancer immunity95

Coconut oil maintains anti-cancer immunity95

Liver Health:

Coconut oil protects liver from chemical damage249

Metabolism:

Coconut oil helps maintain a healthy metabolism77

Obesity:

Coconut oil (2 tablespoons per day for 12 weeks) reduces waist

circumference;78-79 body weight, body mass index and neck
circumference80-81

Radiation Protective:

Coconut oil blocks out about 20% of UV rays82

Reproduction:

Coconut oil massage improves weight gain in newborns61

Sexual Health:

Coconut oil increases testosterone253

Skin:

Coconut oil topically treats patients with atopic dermatitis83

Sleep:

Partially-hydrogenated coconut oil diet more-than doubles

sleeping time in sleep-deficient mice84

Tumor Microenvironment:

Coconut oil decreases free radicals259

Coconut oil decreases serum free fatty acids140
Coconut oil decreases prostaglandins254
Coconut oil decreases nitric oxide254
Coconut oil decreases tumor necrosis factor alpha103, 254
Coconut oil decreases interleukin-1260
Coconut oil decreases interleukin-6254
Coconut oil decreases interleukin-8106
Coconut oil decreases nuclear factor kappa b230
Coconut oil decreases estrogen255
Coconut oil decreases lactic acid256
Coconut oil decreases serotonin257
Coconut oil decreases histamine258

Medium-Chain Triglycerides
Depending on growing conditions, anywhere from 55-72% of coconut fat
consists of medium-chain triglycerides (MCTs). The four types of MCTs in
coconut oil are caproic (0-0.8%), caprylic (5-9%), capric (6-10%), and
lauric acids (44-52%).85-86
Medium-chain triglycerides have been described as fats that are rapidly
absorbed and oxidized.87-89 The fact that they can be used by the body as
efficiently as glucose87 makes them a great alternative fuel source.
“Because of their smaller molecular size, MCTs require less bile and
pancreatic juices for digestion and absorption than LCTs [Long Chain
Triglycerides].” Aside from coconut and palm kernel oils, MCTs are found
in only one other place in nature – milk.87

Medium-Chain Triglycerides vs. Cancer

Tumor-bearing mice fed diets high in MCTs were found to have reduced
levels of the enzyme fatty acid synthase and also reduced acetyl CoA,
similar to tumor free mice, suggesting cancer cell metabolism was restored
back to that of normal cells.94
Inflammatory cytokines nuclear factor kappa b (NF-κB) and tumor necrosis
factor alpha (TNF-a) both play major roles in the development of cancer.99-
101
A single dose of corn oil “rapidly activates” NF-κB, which “triggers
production of low levels” of TNF-a.102 Interestingly, replacing just 50% of
unsaturated fatty acids with MCTs is enough to inhibit the production of
TNF-a.103
Interleukin-8 (IL-8), a well-known tumor-growth promoting inflammatory
cytokine104 is “substantially increased” in a number of different types of
cancer cells.105 “We found for the first time that caprylic acid and MCT
suppress IL-8 secretion by Caco-2 cells [colon cancer cells],” reported
Japanese researchers in 2002.106
Up to 90% of patients with advanced cancer are affected by anorexia and
many also suffer from muscle-wasting (cachexia).252 In mice with induced
colon tumors, MCTs shrank tumors and prevented muscle-wasting.91,93
Vitamin D3 dissolved in MCT inhibits the growth of cancer in vitro and in
dogs “significantly greater” than Vitamin D3 alone.96-97
And in cancer patients following surgery for gastrointestinal cancer, MCT
and protein-enriched nutrition enhanced recovery and reduced their length
of hospital stay.98

Safety
Studies suggest that about 25-30 grams of MCTs can be tolerated at a single
meal and that larger amounts may cause gastrointestinal symptoms,
including nausea, vomiting, bloating, gastrointestinal discomfort,
abdominal cramps and diarrhea.222 In MCT-treated patients with
Alzheimer’s disease, “adverse events observed were mild and included
minor gastrointestinal problems such as diarrhea, dyspepsia, and
flatulence.”128
In one study, 56 grams of MCTs were consumed every day for 24 weeks
with no reported side effects,135 and several clinical trials have reported the
safety of MCT consumption as high as 1g/kg.223

Success Stories
A 24-year-old woman had a tumor of her lymph nodes that was
blocking her lymphatic system and resulted in a recurrent milky fluid
leaking into her abdominal cavity (chylous ascites). She was told to
restrict fat in her diet and was supplemented with medium-chain
triglycerides. At the time her case study was published, she was alive
and had been free of abdominal leakage for 2 years.107
Two female brain cancer patients were put on diets containing 60%
medium-chain triglycerides for 8 weeks at the University Hospital of
Cleveland. Within one week, the growth, spread and progression of
cancer in both patients was halted by the diet. “One patient exhibited
significant clinical improvements in mood and new skill development
during the study. She continued the diet for an additional twelve
months and remained free of disease progression.”108

Additional Health Effects

Alcoholism:
 MCTs prevent free radical formation caused by alcohol109
MCTs prevent alcohol-induced liver injury110-111
“A diet enriched in saturated fatty acids effectively reverses
alcohol-induced necrosis, inflammation, and fibrosis despite
continued alcohol consumption.”112

Antibacterial:

MCTs inhibit staphylococcus aureus,113 escherichia coli,113 and

clostridium difficile bacteria114

Antifungal:

MCTs inhibit malassezia fungi116

Antioxidant:
MCTs prevent death caused by lipopolysaccharide (LPS) in rats;
“All rats given corn oil died after LPS administration”117
MCTs reduce oxidative stress caused by surgery118

Antiviral:

MCTs inactivate HIV-1, HIV-2,119 herpes simplex virus type 1,

respiratory syncytial virus, group b streptococcus virus and
haemophilus influenza virus.115
MCTs prevent diarrhea/wasting caused by HIV virus120-121

Autism:

MCTs reduce seizures, obesity, improve brain function and

behavior, increase IQ 70-points and cure child of autism123

Bone Health:
 MCTs improve calcium absorption124-125

Brain Health:

MCTs have “long-lasting cognition-enhancing effects in aged

dogs”126-127
MCTs enhance memory131 and cognition132 in humans
MCTs improve brain function in patients with Alzheimer’s
disease128-130,133

Dental Health:

MCTs inhibit periodontal pathogens135

Detoxification:

MCTs detoxify drugs from bloodstream136

Diabetes:

MCTs improve insulin sensitivity137-139

MCTs stimulate insulin secretion141-143

Exercise:

MCTs and exercise synergistically reduce visceral and

subcutaneous fat accumulation144

Do MCT’s Enhance Exercise Performance?

The effects of MCTs on exercise performance in animals and humans have
been thoroughly tested, yet the results are extraordinarily inconclusive.
Taken before or during endurance exercise and with or without
carbohydrates - three studies showed MCTs increase performance,146-148 four
showed MCTs provide no performance enhancement,148-151 and two showed
MCTs actually have a negative effect on performance.152-153
As I understand it, a healthy person will store carbohydrates in their liver
and muscles (called glycogen), and after carbohydrates in the blood have
been used up during exercise, glycogen stores will be used for fuel. Once
glycogen has been depleted, the body will begin breaking down its own
muscle and fat tissues for fuel. Like strapping a hybrid fuel tank onto a car,
the question is - can MCT ingestion delay the depletion of glycogen and
thereby expand the body’s useable energy supply?
Four studies found that MCT ingestion before or during exercise reduces
glycogen depletion,154-157 and five found that MCT ingestion during exercise
doesn’t reduce glycogen depletion and thus has no additive effect on overall
energy reserves.158-162
South African researchers conducted a review on MCTs for performance
enhancement in 1998 and concluded, “In the search for strategies to
improve athletic performance, recent interest has focused on several
nutritional procedures which may theoretically promote FA [fatty acid]
oxidation, attenuate the rate of muscle glycogen depletion and improve
exercise capacity… At present, there is insufficient scientific evidence to
recommend that athletes either ingest fat, in the form of MCTs, during
exercise…”163

Farming:

Feeding pigs diets containing 15% MCTs “resulted in a lower

mortality of newborns and better development, particularly of
underweight piglets”164

Healing:

MCTs enhance wound healing165

MCTs help young man survive point-blank .32 caliber gunshot
wound166
Heart Health:

MCTs improve heart function168-172

Immune System:

MCTs enhance immune system173-176

MCTs prevent immune system damage caused by soybean oil174-175

Inflammation:

MCTs reduce inflammation caused by fish oil122

Intestinal Health:

MCTs reduce incidence of colitis in mice177-178

MCTs decrease gut inflammation179-180,183
MCTs reduce mortality and improve symptoms of Waldmann’s
disease181-182

Obesity:

MCTs cause weight loss in cats193

MCTs increase satiety and reduce food intake196-197
MCTs reduce body fat accumulation194-195,198,199,200-205

Fat-Burning Effects of MCT’s

Medium-chain triglycerides have been demonstrated to increase resting
energy expenditure (metabolism) in all animal studies184-186 and most human
studies,187-191 for up to 24 hours;192 meaning additional energy will be burnt
for a full 24-hours by doing nothing other than eating MCTs.

Radiation protective:
 MCTs reduce damage caused by ionizing radiation206
MCTs eliminate chylous ascites caused by pelvic irradiation207

Reproduction:

MCTs during pregnancy reduce chances of obesity in offspring

later in life134
MCTs heal cardiomyopathy and normalize liver function in a
newborn baby167
MCTs increase metabolic rate, cheek skin temperature and total
sleep time in newborn babies219

Seizures:

MCTs significantly reduce seizures in animals, children and

adults208-216

Skin:

MCTs increase skin hydration217

Thyroid:

MCTs increase thermogenesis in rodents;87 (thyroid hormone is

responsible for thermogenesis221)

Other:

MCTs stop eye bleeding after retinal surgery220

MCTs preserve dissolved drugs and increase transdermal drug
delivery218

Lauric Acid
While only 2-5% of the fatty acids in cow’s milk are lauric acid, coconut oil
is comprised of almost 50% lauric acid.224-226

Lauric Acid vs. Cancer

All saturated fatty acids have antimicrobial properties to varying degrees;233
and lauric acid has a greater antimicrobial potency than all other saturated
fatty acids found in nature.234
Studies testing lauric acid specifically on cancer are limited, but the ones
that have been conducted are promising. Australian researchers from the
University of Adelaide compared the effects of lauric acid vs. short-chain
fatty acid butyrate (a saturated fat found in butter) on two types of colon
cancer cells in 2013. The results showed, “Lauric acid induced apoptosis in
Caco-2 (p < 0.05) and IEC-6 cells” while butyrate did not.227
In 2012, Chinese researchers from Wuhan University reported that
overexpression of the gene Cytochrome P450 promotes the growth of
human breast cancer cells and that lauric and myristic acid suppress the
overexpression of this gene.228
One method of reducing cancer growth is to inhibit the pro-inflammatory
cytokine nuclear factor kappa b (NF-κB)229 and lauric acid happens to be a
NF-κB inhibitor.230

Additional Health Effects

Acne:

Lauric acid is effective for treating acne231-232

Antibacterial:

Lauric acid inhibits heliobacter pylori235

Antifungal:
 Lauric acid inhibits growth of candida albicans236-237

Antioxidant:

Lauric acid-enriched rice bran oil a more potent antioxidant than

rice bran oil alone238

Antiviral:

Lauric acid inhibits vesicular stomatitis virus239

Lauric acid inhibits junin virus240

Dental Health:

Lauric acid inhibits oral bacteria242

Depression:

Lauric acid reduces depression241

Diabetes:

Lauric acid “may protect against diabetes-induced dyslipidemia”243

Electricity:

Lauric acid enhances sustainable power generation of microbial

fuel cell by 3.9-times244

Farming:

Lauric acid and myristic acid increase breast muscle size of broiler
chickens245
Lauric and oleic acids improve yolk quality of laying hens246

Seizures:
 Lauric, capric, myristic, palmitic and stearic acids prevent
seizures247

Skin:

Lauric acid enhances absorption of medication through shed snake

skin248
SODIUM BICARBONATE
Sodium bicarbonate, also known as baking soda, is a type of salt that can be
found in crystalline rock formations in nature. Bicarbonate, the acid-
neutralizing portion of sodium bicarbonate, is naturally produced by the
human body and used to buffer excess acidity.1
Since one of the metabolic hallmarks of a cancer cell, as first described by
Dr. Otto Warburg in 1930,2 is elevated production of lactic acid,3-8 which
“directly contributes to tumor growth and progression,”9 it seems
reasonable to predict that cancer patients could benefit from additional
bicarbonate.
The fizz that captured our amazement as children after adding baking soda
and vinegar together was sodium bicarbonate rapidly neutralizing the acid
and producing carbon dioxide (CO2) gas as a result. Similarly, once inside
the body, bicarbonate is converted into carbon dioxide;10 so when we’re
talking about sodium bicarbonate, essentially what we’re dealing with is
carbon dioxide, which opens the door to some fascinating lines of research.

The Biology of Carbon Dioxide

The relationship between carbon dioxide and life itself is entirely
misunderstood by most people in the medical profession and by society as a
whole. We’ve been told that carbon dioxide is a toxic environmental
pollutant causing dangerous increases in temperature that threaten the
existence of life on earth. However, like many things we’re told by
politicians and the media, the reality is far different. One of the best ways
to learn about carbon dioxide is to examine what happens to various life
forms when they are exposed to increased concentrations of it.

The Naked Mole Rat

Found naturally in the hot, arid regions of eastern Africa, the naked mole rat
is a type of rodent that lives strictly underground in large colonies.
Remarkably, naked mole rats reproduce for their entire lifespans,12 they
don’t feel pain after being burnt with acid,11 their brains can withstand over
30 minutes without oxygen without damage137 and in their natural habitats,
they are immune to cancer.13 And while the average lifespan for most rats is
less than two years,14-15 the naked mole rat can live an astounding 30
years,16-17 making it the longest-lived rodent known.18
The exceptional longevity and disease resistance of the naked mole rat have
researchers calling it “a true ‘supermodel’ for aging research and resistance
to chronic age-associated diseases.”19 Yet despite decades of research,
scientists still haven’t been able to determine the reasons behind the mole
rat’s longevity, even in the most recent studies.20-22 Perhaps it’s because
they’re searching for a genetic explanation rather than simply examining
the naked mole rat’s natural environment.
“They live in burrows that are kept closed, so the percentage of oxygen is
lower than in the outside air, and the percentage of carbon dioxide ranges
from 0.2% to 5%,” explains Dr. Raymond Peat.23 A 2005 study by Israeli
scientists investigated the oxygen and carbon dioxide content in burrows of
three species of subterranean mole rats and found that maximal CO2 levels
were 6.1% and minimal O2 levels were 7.2%.24

Carbon dioxide Oxygen

Air on Earth 0.04% 20.95%
Mole Rat Burrow 6.1% 7.2%

Researchers at the College of Staten Island in New York re-created these

environmental conditions in their laboratory and examined its effects on a
colony of naked mole rats in 2010. Although they hypothesized the
environment would have a negative impact on the activity, memory and
social interaction of the rats, what they found was the complete opposite.
When the rats were put into an environment of decreased oxygen (hypoxic)
and increased carbon dioxide (hypercapnic) they became more social, had
significantly improved brain function and their overall movements
increased by 76.8%.25
The Queen Bee
In honey bee hives, worker bees carefully regulate the concentration of
carbon dioxide, which can be as high at 6%.26 Remarkably, the lifespan of a
queen bee is more than 40-times that of a worker bee.27 So while the queen
is in the hive, protected by high concentrations of carbon dioxide, the
worker bees are out breathing regular atmospheric air and consuming
pollen, which is high in unsaturated fat and produces large amounts of free
radicals in the absence of carbon dioxide.

The Long-Lived Siberian Bat

Bats are physiologically the same as mice and as such are destined to live
similar lifespans. However, the oldest-surviving bat ever documented is a
tiny bat from Siberia that lived more than 41 years in the wild.28
Researchers measuring the air quality in caves where bats roost have
discovered that carbon dioxide concentrations are significantly higher than
in the outside air. For example, in Drum Cave, Bungonia, New South
Wales, Australia, “the CO2 concentration rises to over 6% in summer when
a nursery colony, which contains more than 1000 unidentified bats, is
present…”29

Humans at High-Altitudes
People living at high altitudes have shown a similar resiliency to the long-
lived creatures above, including reduced rates of heart disease30-34 and
cancer35-39 compared to people living at sea level.
What’s the link between living at altitude and carbon dioxide? The
decrease in oxygen pressure that occurs at elevation means there is less
oxygen pressure pushing carbon dioxide out of cells, allowing the body to
retain more carbon dioxide – a phenomenon known as the Haldane
effect.40,211
In 2009, a Swiss study involving 1.64 million people found that the benefits
of altitude begin at an elevation of about 900m and that for every 1000m
increase in elevation, mortality from heart disease decreases by 22% and
mortality from stroke decreases by 12%.34 San Francisco and Philadelphia
researchers reported a 12.7% drop in the incidence of lung cancer for every
1000m increase in elevation.35

The Plant Kingdom

For over 100 years, carbon dioxide has been used to increase the
productivity of greenhouse crops.41 In 1978, scientists from the University
of British Columbia, Canada, found that tomato plants grown in
greenhouses with enhanced CO2 concentrations, “flowered earlier and
produced more marketable fruit than those grown in normal air.”42
Peanuts,43 rice,44 ginger,45 and lettuce46 have also displayed elevated growth
performance when cultivated in environments enriched with CO2, and these
growth-enhancing benefits also extend to grasses,48 trees,49-51 tobacco,52
hemp,53 roses,54 algae55-56 and indeed all plant life on earth. Reviews of
plant science literature indicate that boosting greenhouse carbon dioxide
levels by just 300 parts per million (ppm) will increase plant growth by
30%.47
Even better, elevated concentrations of carbon dioxide can increase the
nutrient value of food for humans,57-59 while decreasing its nutrient value for
insects. By significantly lowering the radio of nitrogen to carbon in plants,
nutrient availability for predatory insects is significantly limited.
Furthermore, under increased concentrations of CO2, the production of
natural defensive compounds by plants is increased and the growth and
survival of pests are adversely affected.60-61
Better still, carbon dioxide enrichment reduces the water requirements of
plants by enabling them to use water more efficiently;62 it makes them
better able to survive extreme growing conditions like draught,63 high
temperatures,64 and excess salinity;65 it makes them more resistant to
bacterial and fungal infections;66 it suppresses invasive plant species;48 it
increases the number of seeds a plant produces;67 and it also increases the
annual life cycle of plants, extending the growing season.68
Once food crops have fully-ripened, packaging them in containers with
added carbon dioxide can reduce their decay and significantly prolong
shelf-life.69-71
The extraordinary disease resistance, longevity and myriad of other benefits
imparted to animals, humans and plants inhabiting carbon dioxide-enriched
environments have shown us the importance of carbon dioxide. And since
organisms that don’t require oxygen still need carbon dioxide to survive, we
can conclude that carbon dioxide is more fundamental to life than oxygen.72

A Closer Look…
An experiment from 1980 incubated anaerobic bacteria (bacteria that
don’t use oxygen) into jars containing a range of carbon dioxide
concentrations. The study revealed that contrary to established
teaching, “Small supplements of CO2 (0.25%) allowed good growth of
the majority of anaerobes studied.” Furthermore, some anaerobes had
a minimum requirement of at least 1% CO2 for survival and an
anaerobe called B. melaninogenicus “needed an atmospheric content of
10--40% CO2 for optimal growth.”72

Many living creatures, from mole rats to bats to bees, even amphibians like
frogs, which burrow in the mud to accumulate a surplus of carbon dioxide,
inherently understand the essentiality of CO2 and as such have found ways
to intensify their exposures to it. Humans, on the other hand, believe that
carbon dioxide is an environmental waste gas and have actually altered their
behavior to reduce the amount of it in their environment. (Who is smarter -
man or frog?)
There’s one more thing that must be addressed in order to eliminate the
phobia surrounding carbon dioxide.

Is CO2 leading humanity towards climate

catastrophe?

It is the duty of every human being alive to question everything we are told
by those who claim authority over us, especially when the solutions they
advance involve us giving them $226 million more in taxes every year,74 or
when we see the media calling us ‘genocidal mass murderers’ simply for
doing so.73
Anytime the subject of climate change is discussed in the media, we are
presented with the extreme view that elevated CO2 is moving humanity
towards catastrophe and that all scientists agree on this “fact.”209-210
However, when we read the climate science ourselves, we find that not only
is there no consensus among scientists, but there is little to no evidence
suggesting any reason to be alarmed at all. An extensive review of 539
climate change studies published in peer-reviewed scientific journals
between 2004 and 2007 concluded, “Only one paper refers to ‘catastrophic’
climate change, but without offering evidence.”89
So while politicians and the media push their unscientific, alarmist
perspectives about climate change onto the public in support of their own
political and economic interests, scientists, who base their views on
empirical evidence, take into account the large and growing body of
research showing that carbon dioxide has little or nothing to do with the
earth’s surface temperature.75-87 The surge of peer-reviewed studies,
analysis and data error discoveries published in recent years have prompted
Dr. Ian Wilson and many others to declare that the fear surrounding man-
made global warming “bites the dust.”88
Rather than catastrophe, the rising levels of natural and man-made carbon
dioxide in our environment208 are sparking a revolution of intensified plant
growth and abundance that greens the earth and delivers everything needed
by humans and all living creatures to thrive with unprecedented levels of
health, intelligence, compassion and longevity.
Now that we’ve solved all of the world’s problems, let’s find out what
sodium bicarbonate can do for a person with cancer and other diseases.

Sodium Bicarbonate vs Cancer

Many people have claimed that baking soda is a ‘quack’ treatment with no
anti-cancer effects; and if this is your opinion, the research on baking soda
and cancer may surprise you.
Investigations using sodium bicarbonate to treat cancer cells in vitro are
limited, yet promising; published in the World Journal of Pharmacy and
Pharmaceutical Sciences in 2014 by researchers from North Carolina, the
study confirmed that sodium bicarbonate can trigger apoptosis in colon
cancer cells.90
In 2006, Norwegian researchers discovered that an acidic tumor
microenvironment promotes metastasis in mice bearing three different types
of tumors.92 Since sodium bicarbonate mixed in drinking water and
consumed orally can effectively raise the pH of tumors,97 researchers from
the University of Arizona administered it to tumor-bearing mice to see if
cancer metastasis could be prevented. Results confirmed that baking soda
“increases tumor pH and inhibits spontaneous metastases” in mice with
breast and prostate tumors.93
Dr. Robert J. Gillies and his team from the H. Lee Moffitt Cancer Center &
Research Institute in Florida examined the relationship between tumor
microenvironment pH and the growth and spread of cancer in vivo. Results
were published in the journal Cancer Research in 2013 and found that oral
administration of sodium bicarbonate inhibited the growth and spread of
colon and breast tumors. “In every case… the regions of highest tumor
invasion corresponded to areas of lowest pH. Tumor invasion did not occur
into regions with normal or near-normal extracellular pH,” they wrote.94 In
other words, an acidic tumor environment is essential for cancer metastasis
and balancing out the pH using sodium bicarbonate can prevent it from
occurring.
One of the mechanisms behind the anti-metastatic effect of sodium
bicarbonate was discovered by scientists Ian Robey and Lance Nesbit from
the University of Arizona in 2013. Their study found that sodium
bicarbonate treatment reduced the number of circulating tumor cells in the
blood of tumor-bearing mice to less than half. 95
Dr. Gillies and his team discovered another mechanism behind sodium
bicarbonate’s anti-cancer effects in 2016. It is well established that excess
acidity impedes immune system function166-168 and that neutralization of
acidity with sodium bicarbonate can amplify the immune response.169,171
After administering sodium bicarbonate to tumor-bearing mice, the
researchers observed an influx of immune cells into tumors, which
prevented the growth of numerous tumor types.170
One shocking and incredibly rare fact about sodium bicarbonate is that
oncologists actually administer it to cancer patients before, during and after
chemotherapy and radiotherapy to protect them from the extreme toxicity.90
“If you want to see how fast a person can hit the floor during chemotherapy
just forget to mix in the bicarbonate and get out your stopwatch!” exclaimed
Dr. Mark Sircus. “Those who survive the deadly treatment known as
chemotherapy were likely saved by the sodium bicarbonate, and not the
deadly chemotherapy poison pumped into their bodies.”91
26 terminal cancer patients suffering from severe pain and side effects
caused by failed chemotherapy and radiotherapy treatments were
administered sodium bicarbonate dissolved in DMSO intravenously by
Vietnamese researchers in 2011. Results showed the treatment considerably
eased the pain and discomfort of all patients.96

Success Stories
Vernon Johnson
In 2008, Vernon Johnson was diagnosed with stage 4 prostate cancer that
was so advanced it had already metastasized to his bones. Not wanting to
subject himself to toxic cancer therapies, Vernon refused all treatments
recommended by his doctor and followed the advice of his brother instead.
“When Vernon was diagnosed with the disease, I told him to increase the
pH in his body because any type of cancer cannot thrive in an alkaline
environment,” recalled his brother Larry.
Vernon read that a mixture of baking soda and maple syrup was effective
for raising pH, but since he didn’t have any in his kitchen at the time, he
substituted it for molasses and began self-treatment.
After consuming the mixture multiple times a day for 11 days, Vernon
received a medical examination from his doctor and the results showed his
prostate and bone cancers had disappeared completely. Vernon’s success
story made headlines in the California newspaper Valley News in 2009.98

Loredana
Loredana was diagnosed with a breast tumor in 2010. “I took all the tests
requested, and it turned out that I needed to get an operation,” she
explained. Frightened by the prospect of having to undergo chemotherapy
and radiotherapy following surgery, Loredana did some research and found
that she had the option to receive sodium bicarbonate therapy following
surgery instead. “This got me very interested,” exclaimed Loredana.
She found a surgeon willing to follow the sodium bicarbonate protocol of
Italian doctor Tullio Simoncini and had her tumor surgically removed.
Once the tumor was cut from her breast, the area was washed with sodium
bicarbonate and she continued repeating the washes according to the
protocol. One year and multiple checkups, ultrasounds and a mammogram
later, she was completely free of cancer.99

Rod Peterson
In June of 2008, Canadian Rod Peterson was diagnosed with a tumor in his
right kidney. Two months later, Rod had his kidney surgically removed and
about 6 months post-surgery, cancer was found in his lungs. Rod’s
oncologist explained that he could undergo surgery, chemotherapy or
radiation, but none would really work with the type of cancer he had.
“Basically, he told me to go home and enjoy the rest of my life. He gave
me a card for the psychologist if I needed him and I left the office. I was
fairly numb, so to speak.”
Not ready to leave his family behind, Rod started doing some research and
found the work of Dr. Tullio Simoncini. After finding his theories
convincing, Rod flew to Rome to talk with the doctor in person. Impressed
with the meeting and excited to begin, Rod underwent treatment for 6
weeks in August of 2009. “After the treatment I was curious. I came back,
I had my CT Scans, and you could clearly see, from past scans where the
tumors kept constantly growing, all of a sudden they had shrank, some
cases in half. Of course it was very exciting. My oncologist was ecstatic.
He started to say ‘this only happens with 1% of the population. If this
continues, we’re going to have to do a write-up on you.’”
Wanting to see his health improve even more, Rod returned for further
treatments with Dr. Simoncini in January of 2010. “I went back for
treatment with Simoncini. I had a CT Scan to followup with my oncologist,
and after two weeks of a second cycle, my tumors again had shrunk in half.
I continued again with another two weeks of treatment and came back to
Canada. In the CT Scan I got when I returned, the tumors were gone; all
there was left was scar tissue.” After just three cycles of sodium
bicarbonate therapy, doctors confirmed Rod Peterson no longer had cancer.
“Because of Dr. Tullio Simoncini I have a second chance at life, and I
believe everybody should have that. By meeting Dr. Simoncini, I’m still
here today and I am very thankful. I thank God for that.”100

Additional Health Effects

Acidosis:

Sodium bicarbonate cures metabolic acidosis101

Antibacterial:

Sodium bicarbonate inhibits bacterial growth102,104,105

Sodium bicarbonate prevents growth of spoilage microbes on
vegetables106
Sodium bicarbonate and hydrogen peroxide have synergistic
antimicrobial effects107

Antioxidant:

Sodium bicarbonate “is central to the treatment of many

poisonings”108,114,115
 Sodium bicarbonate prevents damage caused by herbicide
glyphosate,109 paraquat,111 amitriptyline,159 yew berry poisoning112
and uranium136
Sodium bicarbonate (topically) reduces redness caused by jellyfish
sting110
Sodium bicarbonate effectively treats near-fatal flecainide
overdose113

Antiviral:

Sodium bicarbonate inhibits calcivirus103

Arthritis:
Sodium bicarbonate and calcium gluconate solution effective for
treating osteoarthritis116

Bone Health:

Sodium bicarbonate prevents bone demineralization caused by

acidosis117

Brain Health:
Sodium bicarbonate corrects mental status abnormalities (i.e.
confusion, slurred speech) caused by acidosis118

Chronic Kidney Disease:

Sodium bicarbonate improves nutritional status and dramatically

slows progression of CKD119-120
Sodium bicarbonate preserves kidney function in patients with
CKD117
Sodium bicarbonate resolves abnormal heart rate in patients with
CKD121
 Sodium bicarbonate mouth rinse restores function of taste buds
and relieves other symptoms of CKD122

Dental Health:

Sodium bicarbonate toothpaste provides a ‘clean mouth feel,’123

whitens teeth,124 enhances plaque removal,126-127 reduces bleeding128
and provides “statistically significant improvements in gingival
health”128
Sodium bicarbonate mouthwash significantly reduces mineral loss
from tooth enamel125,129-132
Sodium bicarbonate chewing gum significantly removes dental
plaque and reduces gingivitis133-135

Detoxification:

Sodium bicarbonate eliminates uranium from the body136

Diabetes:

Bicarbonate-rich mineral water increases insulin sensitivity in

humans138
Sodium bicarbonate treats diabetic acidosis in children139

Environmental Remediation:

Sodium bicarbonate neutralizes high aluminum concentrations in

water141
Sodium bicarbonate removes 92% of uranium from contaminated
soil samples142
Sodium bicarbonate removes chemical pollutant polychlorinated
biphenyl (PCB) from waterways140
"Mixed with sodium bicarbonate, one metric ton of PCB-tainted
soil can be cleansed per hour in a rotary reactor."143
Exercise:

Sodium bicarbonate increases back squat repetitions to failure144

Sodium bicarbonate improves 200m swimming time145
Sodium bicarbonate significantly increases punches landed during
4 rounds of boxing146
Sodium bicarbonate improves cycling performance during
repeated sprints147-148

Farming:
Sodium bicarbonate fed to black belly barbados lambs for 10 days
significantly improves meat quality149
Sodium bicarbonate corrects acidosis and improves hydration in
diarrheal calves150
Sodium bicarbonate improves calcium absorption and eggshell
quality of laying hens153
Sodium bicarbonate promotes growth, photosynthesis and
biochemical composition of marine algae151-152

Healing:

Sodium bicarbonate prevents excessive inflammation and

accelerates healing process154
Bicarbonate-calcium-magnesium water improves skin
regeneration155

Heart Health:

Sodium bicarbonate restores abnormal heart rate caused by crack

cocaine,156,157 bupropion160 and diphenhydramine161
Sodium bicarbonate eliminates seizures and heart abnormalities
caused by antidepressant overdose162,163
 Carbonated water with a meal reduces risk of cardiovascular
disease164,165

Immune System:

Sodium bicarbonate enhances immune system169

Sodium bicarbonate promotes antitumor immunity170,171

Inflammation:

Sodium bicarbonate reduces inflammation154,174

Lifespan:

Sodium bicarbonate significantly increases lifespan of mice172

Metabolism:

Sodium bicarbonate stimulates oxidative metabolism171

Sodium bicarbonate substantially decreases tissue calcification172

Obesity:

Sodium bicarbonate and albumin enhance weight loss effects of

anti-obesity herb fenugreek173

Radiation:

Sodium bicarbonate prevents painful ulceration of the mouth

caused by radiotherapy174

Reproduction:

Bicarbonate “plays critically important roles during virtually the

entire process of reproduction in mammals”175
 Sodium bicarbonate effective for simulating embryonic
environment during in vitro fertilization176
Sodium bicarbonate improves growth of children202

Skin:

Sodium bicarbonate and acetic acid solution (topically) renews

natural immune barrier of skin177
Sodium bicarbonate baths dramatically improve psoriasis in
humans178-179

Sleep:

Sodium bicarbonate improves sleep quality180

Thyroid:

Sodium bicarbonate improves thyroid function181

Tumor Microenvironment:

Sodium bicarbonate reduces free radicals182-183

Sodium bicarbonate reduces tumor necrosis factor-alpha184-185
Sodium bicarbonate reduces interleukin-1beta186,187
Sodium bicarbonate reduces interleukin-6186,188
Sodium bicarbonate reduces interleukin-8187,189
Sodium bicarbonate reduces nuclear factor kappa-b189,190
Sodium bicarbonate reduces cortisol191
Sodium bicarbonate reduces prolactin192,193
Sodium bicarbonate reduces nitric oxide194,195
Sodium bicarbonate reduces lactic acid196,197
Sodium bicarbonate reduces prostaglandins198,199
 Sodium bicarbonate reduces histamine200

Other:

Sodium bicarbonate softens earwax and aids in its removal201

Sodium bicarbonate dissolves uric acid stones203,204 and bladder
stones205
Sodium bicarbonate effective for treating cystic fibrosis206
Sodium bicarbonate decreases mortality in patients treated for
acute respiratory failure207
Sodium bicarbonate increases return of spontaneous circulation
during CPR158

Safety
Considering all the benefits of using sodium bicarbonate therapeutically,
and especially when compared to orthodox cancer treatments, side effects
are few and exceptionally minor.
Some participants in exercise performance-related studies reported upset
stomachs and/or diarrhea at doses of 300mg/kg, which is about 22.5 grams
of sodium bicarbonate for a 75kg (165lb) man or woman. Athletes loading
up on baking soda for performance enhancement have been able to resolve
this issue by consuming sodium bicarbonate in multiple, split-doses.
Vernon Johnson cured himself of metastasized prostate cancer using sodium
bicarbonate and the only side effects he experienced were the occasional
nausea, diarrhea and weakness. All in all, the treatment consisted of less
than half a box of sodium bicarbonate, costing less than $1, and all of his
symptoms went away after the treatment ended - not bad for completely
eliminating his cancer.

Vernon Johnston's Baking Soda & Molasses

Protocol
To give people enough confidence to begin self-treatment with baking soda
if they choose, it’s useful to know the exact protocol used by Vernon
Johnson to cure himself of cancer. Vernon’s protocol involved a mixture of
baking soda, molasses and water over the course of 11 days. Here’s how he
did it:
Days 1-4: Vernon began by consuming 1 cup of water containing 1
teaspoon of baking soda and 1 teaspoon of black strap molasses. Vernon
consumed this mixture once daily for the first four days. After noting that
he felt fine and his pH was 7.0 (saliva) and 7.5 (urine), he decided to
increase his dose.
Day 5: On day five, Vernon doubled his dose and began drinking the same
solution twice per day. After reading that cancer cells become dormant at a
pH of 7 and dead at a pH of 8.0-8.5, his goal was to achieve a saliva and
urine pH between 8.0-8.5 and hold it for four or five days. He used pH test
strips to measure his pH and emphasized the importance of taking both
saliva and urine pH into consideration, since saliva pH can at times be a
poor indicator of blood pH.
Day 6: He continued taking two daily doses of his solution and on day six,
his pH averaged out to be 7.25. On this day he felt slightly nauseous and
his stool had a yellowish tinge.
Day 7: Vernon took 3 teaspoons of baking soda in water with 1 teaspoon of
molasses for his first dose. For his second dose he went back down to the 2
teaspoons of baking soda with molasses in water.
Day 8: Hoping to elevate his pH even more, Vernon took two teaspoons of
baking soda in water and molasses three times over the course of day 8.
Day 9: He noticed a little diarrhea and felt a bit weak on day 9, but said he
"felt oxygen euphoria throughout the day. Like my body was breathing pure
oxygen."
Day 10: Vernon had a persistent headache at this point and noticed body
sweats at night. He took 4 pH readings over the course of the day and they
were all in the mid 8's. He then cut back his dose on this day to a 2
teaspoon sodium bicarbonate solution in molasses and water, twice daily.
Day 11: On the day before returning to his doctor to assess the condition of
his cancerous bones, Vernon experienced diarrhea that was slightly yellow.
He reduced his dose to 1.5 teaspoons of the baking soda, molasses and
water solution and consumed it twice.
"So there you have it. That was my last day before the scan," said Vernon,
before emphasizing the importance of consuming baking soda two hours
before or two hours after a meal to maintain the stomach acidity necessary
for digestion.91
UNRAVELING THE MYSTERIES OF
CANCER
The official position of the cancer establishment is that “cancer is a genetic
disease,”1 whereby a specific set of gene mutations cause a single cell to
turn irreversibly cancerous and multiply out-of-control, until enough of its
mutant clones collectively form a tumor that strives to kill the host.
If this theory is correct, it means that cancer cells are like parasites that
must be eradicated at all costs; even if patients are injured or nearly killed
in the process. It also means that nothing in our environment or the way we
live our lives have any bearing whatsoever on whether or not we develop
cancer. And in this paradigm, since there’s nothing we can do to prevent
cancer from arising or stop it from progressing, if we happen to be one of
the ‘unlucky’ ones who are diagnosed with the disease, we must depend on
people more sophisticated than us for answers.
However, if cancer truly were a genetic disease then you’d think the vast
sums of money spent on genetic cancer research over the past 50 years
would have rendered us at least some progress. It makes you wonder -
maybe researchers have been looking in the wrong place for answers?

Questioning The Genetic Theory of Cancer

In search of another paradigm that could adequately explain the underlying
cause of cancer and why the war on cancer has been such a failure, I
stumbled upon a series of fascinating studies whose conclusions completely
contradicted the genetic theory of cancer. If cancer is a disease of genetic
origin, then none of the following observations would have occurred.

Cloned Mice from Tumor Cell DNA

Researchers from St. Jude Children’s Research Hospital in Memphis,
Tennessee, cloned a mouse using DNA derived from a mouse brain tumor
cell in 2003. Published in the journal Cancer Research, the study found
that the development of the cloned mouse occurred normally without cancer
formation.11

Frog Egg Tumor Transplants

In 1969, a group of researchers transplanted frog tumor cells into frog eggs
and found that despite the mutant cancer DNA contained within the
transplanted tumor cells, from within the eggs emerged healthy, swimming
tadpoles - demonstrating once again that mutated cancer DNA can direct
normal development.10

Cell Cytoplasm-Swapped ‘Cybrids’

Since the 1970’s, scientists have been experimenting with swapping normal
cell cytoplasms (containing the energy-producing mitochondria, not DNA)
with cancer cell cytoplasms and vice versa. They call the resultant cells
‘cybrids.’ When scientists transplanted normal cell cytoplasms into cancer
cells (containing mutated DNA), the cancer cells transformed back into
normal cells,2-8 and when cancer cell cytoplasms were transplanted into
normal cells (containing normal DNA), the cells turned into cancer cells.9
These findings show that mutant cancer DNA doesn’t cause cancer and that
normal DNA doesn’t prevent cancer; the cytoplasm seems to dictate
carcinogenesis.

Genetic Theory Unlikely

Taken together, it appears that DNA has little (and perhaps nothing) to do
with a cell becoming cancerous. Harry Rubin, Professor Emeritus of Cell
and Developmental Biology from the University of California demonstrated
in 2006 that cells can have hundreds of mutations and still behave normally
within the organism.12
Another apparent flaw in the genetic theory is the claim that cancer cells are
irreversible. There are hoards of studies in which scientists have observed
cancer cells transform back into normal cells.2-8,10,11,13-17,481-493,868 “…our data
suggest quite strongly that nonmalignant tumor populations can be
converted to a more malignant phenotype without additional mutations
taking place and, conversely, malignant populations can be downregulated
to a nontumorigenic phenotype,” wrote researchers from Ohio State
University in 1995.17 But if cancer cells can revert back into normal cells,
how can the cancer establishment justify carving out tumors, scorching
patients with radiation and poisoning them with chemotherapy? They
can’t… and so their only option - if they wish to remain in business - is to
pretend this evidence doesn’t exist.
Despite the many experiments profoundly challenging the genetic theory of
cancer, medical doctors are not presented these controversies in medical
school and are instead taught the genetic theory as if it were fact, which is
unfortunate because as the American Nobel Prize-winning virologist Peyton
Rous said in 1959, “the somatic mutation theory acts like a tranquilizer on
those who believe in it.”18
What better way to resolve the controversies surrounding cancer’s elusive
origins than with the biggest and most comprehensive scientific
investigation ever conducted on the genetics of cancer?

The Cancer Genome Atlas Project

In 2005, the National Cancer Institute launched a giant multi-national
initiative called The Cancer Genome Atlas Project (TCGAP). The goal of
the project was to expand human understanding of cancer genetics and to
pinpoint a common sequence of genetic mutations that drive carcinogenesis
so that new drugs targeting each mutation could be developed.19 If there
ever were a project that could finally either prove or disprove cancer as a
genetic disease, this billion-dollar medical behemoth - spanning more than a
decade - is it.20 As you can imagine, the debut of the project spurred
enormous excitement and hope among its many participants and supporters.
One of the greatest successes of the project, still underway, has been the
accelerated speed at which scientists can fully sequence the genetic code of
a cell. Each cell in our bodies is said to contain around 25,000 genes,21 and
using state-of-the-art technology scientists are now able to churn out the
entire genomic sequence of cells with lightning speed. To date, TCGAP has
compiled data from more than 10,000 tissue samples from over 30 types of
cancer,22 but to the surprise of many, the results have been vastly
disappointing.
Looking at cancer cells from different people with the same type of tumor,
scientists discovered the mutational signatures of cells were so immensely
different that they appeared to occur completely at random.23-25 Scientists
also looked at the genomes of cells from within the very same tumor, but
instead of finding a distinct series of mutations that could explain cancer
initiation, every cell was found to have its own unique set of mutations.26-30
Metastatic cancer cells were also analyzed, and researchers found their
genetic defects were completely different than the genetic defects in cells of
the original tumor.29,31,32 Time and time again, the story was the same: not a
single gene mutation - or any combination of mutations - was found to be
absolutely responsible for initiating the disease.27,33-37
In 2010, researchers from the University of Washington called the results of
the TCGA project ‘sobering’ and conceded, “it is becoming increasingly
difficult to envision how it will be possible to develop a realistic number of
targeted chemotherapies to be directed against a discrete panel of
commonly mutated cancer genes.”26 Dr. David Agus, the University of
California oncologist who treated Steve Jobs, suggested in a recent speech
that cancer is simply too difficult to understand and that we should stop
trying.38
The Cancer Genome Atlas Project - a fascinating milestone in the history of
cancer research - has confirmed to us unequivocally that, above all - cancer
is not a genetic disease. The 81-year-old “father of DNA” James Watson
himself responded publically to these findings in 2013, recommending a
shift in the focus of cancer research from genetics to metabolism.39
Although genetic defects are undeniably ubiquitous features of cancer cells
of all types, they ultimately arise as downstream consequences of
something else occurring first within cells.

The Prime Cause of Cancer

If a scientific observation can be demonstrated repeatedly by many different
people, then it’s probably true. When it comes to the cause of genomic
instability and genetic defects arising in cells, scientists have found that
these events are consistently triggered by the same distinctive conditions
inside cells: insufficient oxygen (hypoxia).40-60 It’s only after a cell is
deprived of oxygen that genetic mutations begin to occur.
Insufficient oxygen, however, is not just the root cause of genomic
instability; it’s also the primary driver of tumor formation,45,61-71 progression
and metastasis;48,51,52,72-80 or said differently, the prime cause of cancer.
What’s particularly striking is that German physiologist, medical doctor and
Nobel Laureate, Dr. Otto Heinrich Warburg first discovered this almost 100
years ago, in 1923. In a presentation to other Nobel Laureates in 1966,
Warburg stated,96

“The cause of cancer is no longer a mystery; we know it occurs

whenever any cell is denied 60% of its oxygen requirements.”

When a cell is deprived of oxygen, it responds by activating hypoxia-

inducible factor-1alpha (HIF-1alpha),67 which can be “found in high levels
in malignant solid tumors, but not in normal tissues or slow-growing
tumors.”81-89 HIF-1alpha then stimulates the release of vascular endothelial
growth factor (VEGF) into the tumor microenvironment,90-95 which signals
cells in its proximity to grow (chapter 1).
Even more extraordinary than Dr. Warburg’s discovery was a statement
made in 1976 by the author of one of the most widely used medical
textbooks in the world:

“All chronic pain, suffering and diseases are caused from a lack of
oxygen at the cell level.”
-Dr. Arthur C. Guyton
Suddenly, our quest to discover how to prevent and cure cancer, we’ve not
only identified cancer’s prime cause, but in doing so we’ve come face-to-
face with the possibility that what cures cancer, cures all diseases. The fact
that all three medicines reviewed in the preceding three chapters accelerate
healing, enhance the immune system, protect the vital organs and are
capable of treating a multitude of diseases and conditions validates
considerably the idea that all diseases have a common origin. And if it is
true, then cancer and all diseases are metabolic in nature, and remarkably,
all are reversible and can be corrected by restoring the efficient use of
oxygen.

Cancer Cell Metabolism

The human body is comprised of an estimated 37.2 trillion cells,97 all of
which require energy to perform the vital functions that make our lives
possible. So while we go about our days not thinking much about it, our
cells are hard at work metabolizing the food we eat into the energy we use
to breathe, move, eat, grow, exercise, regenerate and reproduce.
The metabolism of a healthy cell, put simply, involves a chemical reaction
between glucose and oxygen in the ‘power plants’ of the cell, called
mitochondria.98 The end product of metabolism, often termed ‘the energy
currency of life,’ is a high-energy molecule that provides energy to all our
cells, called adenosine triphosphate (ATP).99
Without getting into all of the complex details, energy metabolism involves
three basic steps – glycolysis, krebs cycle and oxidative phosphorylation.
First, let’s examine the defective metabolism of a cancer cell.

Whereas a normal cell produces energy using cellular respiration (all three
steps; also known as mitochondrial respiration or oxidative metabolism),100
a cancer cell uses glycolysis only, which ferments sugar and produces lactic
acid as a byproduct.101 This metabolic shift from cellular respiration to
glycolysis occurs because – for reasons not yet established – the cell has
lost its ability to use oxygen, and unlike the krebs cycle and oxidative
phosphorylation, glycolysis doesn’t require oxygen.102 The moment a cell
undergoes this metabolic shift, known as the Warburg effect,98 is the
moment it becomes a cancer cell.109

The production of lactic acid is normal during exercise when the

oxygen supply is used up and not adequate to meet energy demands
(anaerobic glycolysis),103-108 but in cancer, lactic acid is produced
even though oxygen is adequately present (aerobic glycolysis).

One of the downsides to using glycolysis for energy production is that it’s
highly inefficient and generates 15-times less ATP than cellular
respiration.110 This means that cancer cells must consume significantly more
glucose in order to generate the same amount of energy111-119 and
consequently, they produce and release large amounts of lactic acid into the
tumor microenvironment.120-125
Aside from the immunosuppressive126 and carcinogenic effects127,128 of lactic
acid, large amounts of lactic acid also cause the breathing rate to increase,
known as hyperventilation,129-132 which quickly lowers the body’s levels of
carbon dioxide.133-138

The Extraordinary Discovery of an Elite

Russian Scientist
While actively engaged in high-level research for the Russian military,
space and sports programs at the First Medical Institute in Moscow, elite
medical scientist Dr. Konstantin Pavlovich Buteyko (1923-2003) claimed to
have made a discovery so vast that it would turn the whole of modern
medicine on its head.139
Motivated by an intense interest in sophisticated medical diagnostics, Dr.
Buteyko used state-of-the-art equipment and facilities to investigate the
physiological and biochemical differences between healthy people and
people with disease. After collecting empirical data from hundreds of
patients, Dr. Buteyko made the extraordinary discovery that all people
suffering from chronic diseases shared one thing in common: a lower than
optimal level of carbon dioxide.
The medical norm of carbon dioxide concentration in the human body is
around 5% (or 35-37mm Hg).140,141 Dr. Buteyko found that people who had
optimal levels of carbon dioxide never suffered from any chronic diseases
and the greater the deficiency of carbon dioxide a person had, the worse
their overall level of health.
Dr. Buteyko went on to develop a system of breathing called The Buteyko
Method, which instructed patients to breathe shallower and less-frequently
to raise their carbon dioxide levels and improve their health. Studies have
confirmed that breathing less can normalize CO2 deficiencies,142,143 and
statistics show that Buteyko’s breathing method has helped more than 1,000
patients suffering from asthma, hypertension or stenocardia fully recover
since 1967.144 To date, eight clinical trials using The Buteyko Method on
human patients suffering from asthma have been conducted and in all
studies, significant reductions in asthmatic symptoms and medication
requirements by patients have been reported.145-152
Dr. Buteyko’s radical discovery and his obsession with it lead him from
being a privileged scientist within the soviet system to being cast a medical
dissident. The medical establishment wanted nothing to do with his
unconventional ideas and obstructed his progress to gain official acceptance
at every turn.
“I was called a charlatan, a schizophrenic and a raving nutter, among other
names,” explained Dr. Buteyko. “They tried to poison me three times, and
organised two car crashes. There were several attempts to put me in a
psychiatric hospital. They physically destroyed my laboratory, which was
unique throughout the world. And all of this because I had discovered a
lever that patients could pull to be free from their piles of pills and
complicated surgical procedures that were far from safe.”153
The fact that Dr. Buteyko publically condemned the use of drug and
surgical-based treatments - on the basis that most of them accelerated the
loss of carbon dioxide and therefore worsened the health of patients - may
have been why health authorities felt so threatened by him and went to such
great lengths to suppress his discovery. Let’s see if we can find any other
evidence to substantiate Dr. Buteyko’s finding that a deficiency of carbon
dioxide occurs in all disease states.
Scientific experiments have determined that people with a wide variety of
diseases are deficient in carbon dioxide, including heart disease,154-162
diabetes,163-167 asthma,168-171 COPD,172-174 sleep apnea,175 cystic fibrosis,176-182
bipolar disorder,183 panic disorder,184 epilepsy,185 and of course, cancer.186-187

A Closer Look…
In 2001, Ukranian medical doctor Sergey Paschenko measured the
CO2 content in the exhaled breath of 120 women with metastasized
breast cancer. Dr. Artour Rakhimov, who translated the study from
Russian to English, reports, “The average value for end-tidal CO2 in
these cancer patients was about 2.9%, while the official medical norm
is about 5.3% that corresponds to 40 mm Hg at sea level.”187

Interestingly, Dr. Rakhimov has graphed data on his website from a large
list of studies showing that overall carbon dioxide levels in people
worldwide have been in a steady, almost-linear decline since the 1920’s.188
In 2015, an international team of scientists led by Dr. Darryl Leong of
McMaster University in Hamilton, Ontario, analyzed the medical records of
almost 140,000 people between the ages of 40 to 70 and discovered that
hand grip strength was a strikingly accurate predictor of all-cause mortality;
and even a more accurate predictor of heart disease than blood pressure.189
A number of similar studies have authenticated the accuracy of grip strength
as a predictor of all-cause mortality.190-193
With these findings in mind, a 2016 study from Winston-Salem State
University in North Carolina found that over the past 30 years, the hand-
grip strength of both men and women living in the US - particularly in
younger people - has declined by 20% on average.194 So while many people
believe ‘people are living longer than ever before,’ given the decline of
carbon dioxide levels and in grip strength in people over the past 100 years,
it seems far more likely that the opposite is true.
Now that we’ve shown how CO2 deficiency can be caused and worsened
by the lactic acid secreted from cancer cells, and provided substantial
supporting evidence for Dr. Buteyko’s groundbreaking discovery that all
chronic disease is caused by a deficiency of carbon dioxide, you may be
wondering: since both oxygen and carbon dioxide are deficient in sick
people – what is the relationship between oxygen and carbon dioxide?

Healthy Cell Metabolism

Unlike a cancer cell, which produces ATP and lactic acid through glycolytic
metabolism, when a normal cell undergoes cellular respiration, in addition
to ATP, it also generates carbon dioxide.
Dr. Buteyko has called carbon dioxide, “the main source of nutrition for any
living matter on earth;” and its physiological effects are two-fold: First,
CO2 dilates blood vessels, increasing bloodflow.195-197 Secondly, oxygen is
transported through the bloodstream by red blood cells (hemoglobin), and
the primary trigger for the release of oxygen from hemoglobin (the Bohr
effect) is carbon dioxide.198-200 In other words, without CO2, oxygen cannot
get into cells.
This has been confirmed by a number of studies looking at oxygen levels in
various tissues following hyperventilation; CO2 deficiency causes hypoxia
in the brain,201-212 heart,213-217 liver,218-220 kidneys,214,220 spleen,214 colon,221 and
indeed in all body tissues.222,223
So while lactic acid is constantly streaming from cancer cells - inhibiting
oxygen use and cellular respiration - carbon dioxide is constantly streaming
from healthy cells - promoting oxygen use and cellular respiration.
Let’s take a closer look at what specifically can cause a cell to turn
cancerous.

Understanding Metabolic Dysfunction

Anything that inhibits the use of oxygen by cells is, by definition,
carcinogenic - and there are two specific ways cellular oxygen can be
inhibited: the first is a nutritional deficiency and the second is chemical
toxicity.

1. Nutritional Deficiency
While carbon dioxide is essential for oxygen to gain entry into cells, there
are a number of other nutrients essential for the production of key enzymes
that power the sequence of chemical reactions during the krebs cycle and
oxidative phosphorylation. The B-series of vitamins are the primary
nutrients that act as co-enzymes for cellular respiration, and include
thiamine (B1), riboflavin (B2), niacinamide (B3), pantothenic acid (B5),
pyridoxine (B6), biotin (B7) and folate (B9).225
Since respiration cannot occur without enzymes produced specifically by
these nutrients, a deficiency in any one of them can inhibit the use of
oxygen and turn a cell cancerous. And conversely, making these nutrients
available to cancer cells can reverse cancer growth.

Foods with the greatest concentrations of B-vitamins include

shellfish (clams, oysters, mussels), liver, caviar, octopus, crab,
lobster, beef, lamb, fish, cheese and eggs.

Thiamine (Vitamin B1):

Thiamine is essential for a number of key metabolic enzymes226 but the one
we’re going to focus on is called pyruvate dehydrogenase, which is critical
because it links glycolysis to the krebs cycle.
Without thiamine and the pyruvate dehydrogenase enzyme made from it, a
cell is forced to metabolize using glycolysis only.227-229 Since glycolysis
increases lactic acid, which lowers carbon dioxide - and since a deficiency
of carbon dioxide can be seen in all disease states - we can expect to see a
thiamine deficiency in many different diseases, including cancer.
This research has been done: Low levels of serum thiamine have been
significantly associated with Parkinson’s disease,230,231 and administering
thiamine to Parkinson’s disease patients improves their brain function and
overall condition.231 Thiamine deficiency is also frequent in patients with
heart disease, and administering thiamine to them improves their heart
function.232-234
A number of studies have shown that a deficiency of thiamine is common in
cancer patients and significantly associated with cancer progression,237-243
and in 1970, Dr. Otto Warburg and his colleagues demonstrated they could
induce cancer in normal cells specifically by depriving them of thiamine.244
The observation that thiamine can lower serum lactate
concentrations228,229,235,236 is evidence that cells are beginning to use oxygen
more efficiently, and scientists from Westminster, California reported in
2013, “A very high dose of thiamine produces a growth-inhibitory effect in
cancer.”237 Additionally, researchers from Kansas State University found
that pyruvate dehydrogenase activation triggered apoptosis in cancer
cells.245
Interestingly, breads, cereals and infant formula in the US and many other
countries are fortified with thiamine,246 so one could argue that people are
getting enough dietary thiamine, except for one thing: most food
manufacturers fortify foods with thiamine in the form of thiamine
mononitrate,247 which cancer patients have a difficult time absorbing248 and
converting249 into the useable form found naturally in certain foods, like
liver,250 called thiamine pyrophosphate. The fact that growing tumor cells
on rat liver tissue makes them revert back to healthy cells suggests that liver
is an important food.
Thiamine can also significantly protect the body from highly-toxic
chemotherapy drugs, which illustrates just how powerful this one single
nutrient can be - and how vital it is for a cell to undergo oxidative
metabolism.251-254 In one study, a patient went completely blind in both eyes
following chemotherapy and after administering daily intravenous thiamine
for just three days, their vision returned. “Symptomatic improvement with
thiamine was rapid, with visual acuity improvement to 20/200 OU in three
days.”255

2. Chemical Toxicity
Environmental toxins can also turn cells cancerous by interfering with the
production of these same critical respiratory enzymes; either by destroying
the nutrients needed to make them or by accelerating their use in an attempt
deal with the toxic insult, ultimately leading to a deficiency.256,257
Cytochrome c oxidase is an essential respiratory enzyme that interacts
directly with oxygen258 and catalyzes the very last step in the process of
oxidative phosphorylation.259,260 The nutrient needed to create this enzyme
is copper261-263 and its activity is amplified by thyroid hormone.264
Foods highest in copper include oysters, lobster, crab, squid, eggs,
beef, lamb, fish, mushrooms and chocolate.

“Defects in cytochrome c oxidase expression induce a metabolic shift to

glycolysis and carcinogenesis,” wrote scientists from the University of
Pennsylvania in 2015.265 A deficiency of cytochrome c oxidase has also
been implicated in tumor progression.266
A number of chemical toxins have been shown to inhibit cytochrome c
oxidase activity; for example, chemotherapy,267 cyanide,268-270 carbon
monoxide,271,272 aluminum phosphide,273 estrogen,274 serotonin,275
endotoxin,276,277 aflatoxin B1,278 UVB radiation,279 X-ray radiation,280,281 and
most notably, unsaturated ‘essential’ fatty acids.282

A Closer Look…
In 1951, researchers investigated the impact of the ‘essential’
unsaturated fatty acids (EFAs) on the respiratory enzyme cytochrome c
oxidase. Results showed that EFAs strongly inhibited cytochrome c
oxidase activity, and when rats were made deficient in the EFAs, both
cytochrome c oxidase activity and cellular respiration were
significantly higher than in normal rats.282

The fact that cigarette smoking inhibits cytochrome c oxidase activity and
smoking cessation restores it283 makes a good case for quitting.
Interestingly, light in the red (622-780nm wavelength) and near-infrared
(700nm-1mm wavelength) spectrums is absorbed by cytochrome c oxidase
and amplifies its activity.284-302 This helps explain why cold and flu season
occurs at the time of year with the least amount of sunlight, and provides a
mechanism behind the incredible healing benefits of red and infrared light
therapies; cognitive enhancement,303-305 accelerated healing,306 increased
bone density,307,308 increased testosterone,309 reduced anxiety and
depression,310 reduced inflammation,311 reduced acne,312 pain relief,314-318 and
hair regrowth,319 to name a few.
Dr. John Harvey Kellogg wrote in his book Light Therapeutics:

“Metabolism is unquestionably stimulated by the reflex action set

out by the light rays impinging upon the nerve endings of the skin
and retina… oxidation of living tissues is increased by the action of
sunlight. In human beings as well as in animals, less carbon
dioxide is emanated at night than during the same number of hours
of daylight.”

Nitric oxide is another toxin320 that inhibits cytochrome c oxidase activity

by binding directly to it.321-323 Remarkably, red and infrared light is capable
of unbinding nitric oxide from cytochrome c oxidase, allowing respiration
and carbon dioxide production to resume.324,325

Rethinking Our Fears Surrounding Cancer

Every day it seems we are inundated with the perception that cancer is some
kind of biological terrorist that’s entirely foreign to our bodies and trying to
kill us - yet from what we’ve learned so far in this final chapter, it seems
cancer is nothing more than a collection of cells not getting what they need
to function properly. As Dr. Ray Peat has said, “The cancer business is
based on something other than science or common sense.”
The metabolic shift of cells to glycolysis that brands a cell cancerous -
induced either by a nutrient deficiency or environmental toxin - causes free
radical electrons to leak from the respiratory chain, which then react with
unsaturated fats342 and ultimately damage cells.343-352 In other words, cancer
cells are not just cells lacking nutrients; they’re cells that have been injured.
German physician, anthropologist, pathologist, prehistorian, biologist,
writer, editor, and politician Rudolph Virchow was the first to notice that
tumors commonly form at sites of chronic injuries. So common do tumors
grow from scars or old injuries that in 1862, Virchow suggested previous
injuries were a precondition for tumor formation.353 Swiss researchers
acknowledged the “remarkable similarities between wound repair and
cancer” in 2008,354 and over the past 150 years, experiments have revealed
there is virtually no difference between a wound and cancer.355-364
So when a doctor looks at a mammographic image and thinks he sees
cancer, he’s actually looking at a collection of injured cells that the body is
trying to heal. A cancer doctor is trained to respond to injury by using
treatments that cause further injury; and for that reason, far scarier than a
diagnosis of cancer is what a doctor will try and do to you if he thinks you
have it.
However, in contrast to a successfully healing wound, the healing process
of a tumor is exaggerated and prolonged; an ‘overhealing’ as Sir Alexander
Haddow put it.354,365-367
Chronic inflammation has been strongly associated with cancer
development and progression368-381 because an inflamed cell is an injured
cell that has lost its ability to respire; it is swollen with water,382 produces
lactic acid,383 and rapidly divides to try and replace itself with a fresh
functioning cell384-385 – the same archetypal characteristics as a cancer cell.
Persistently injured and inflamed cells, like cells within a tumor, are
evidence the body has been unable to properly repair the damage.
So what is preventing the body from completing the healing process in the
case of a tumor? To answer that question, we look to the human embryo.

Scarless Healing of The Human Embryo

The opposite of a wound that won’t heal is a wound that regenerates rapidly
and without scarring. First observed in the 1970’s, the embryos and fetus’
of mice, rats, pigs, monkeys and humans have a remarkable capacity for
healing; when wounded, they repair quickly, scarlessly and “with little or no
inflammation,” wrote Dr. Traci Wilgus at the University of Illinois in
2007.386-402 Yet despite almost 50 years of investigation, researchers are still
baffled by how this scarless healing occurs - admitting as recently as 2014,
“the exact mechanisms of scarless fetal wound healing remain largely
unknown.”386
When investigators from the University of California transplanted adult
sheepskin onto the backs of fetal lambs in 1995, they observed, “The adult-
fetal interface healed without scar formation,”403 suggesting that something
within the embryonic/fetal environment is responsible for its regenerative
capacity.
While arterial blood of a pregnant mother has an oxygen pressure of about
100 mm Hg, the blood that carries oxygen to the fetus through the umbilical
vein is around 35 mm Hg.404-406 This low-oxygen pressure allows the cells
of the fetus to retain more carbon dioxide (the Haldane effect), which
enhances cellular oxygenation and in turn cleans up the wound
microenvironment and facilitates healing.407
Dr. Peat has mentioned another important factor involved in embryonic
scarless healing: the uterus and placenta act as filters that let very little
unsaturated fatty acids into the fetal environment; evidence of this can be
seen in studies showing nearly all newborn babies are born deficient in the
‘essential’ fatty acids.408-412
“It is known that the child is virtually disease-free in the womb of the
mother: only after the birth, do diatheses and all other abnormalities of
metabolism appear,” said Dr. Buteyko in a lecture at Moscow State
University in 1969.413 “After birth, during the first breaths,” he continued,
“there is a sudden increase in blood oxygenation and a sudden drop in
CO2.” This, according to Buteyko, is why babies have been traditionally
tightly swaddled and sometimes even tightened to a wooden plate: “Folk
wisdom understood, that this air, so poisonous for the newborn, requires
gradual adaptation.”
Interestingly, scientists studying the oral soft tissues of adult humans and
pigs have discovered similarly rapid and scarless regenerative capacities;414-
417
“Wound healing in the oral mucosa proceeds faster than in skin and
clinical observations have suggested that mucosal wounds rarely scar,”
wrote Canadian researchers from the University of British Columbia in
2009.418
Just as the mechanisms behind the flawless healing ability of the developing
embryo and fetus remain a mystery in the published literature, scientists are
baffled by this one too. A group of researchers looking at cellular genetics
of oral tissue made the following useful observation: “The striking
difference between these tissues is transient and rapidly resolving
inflammation in oral wounds compared with long-lasting inflammation in
the skin wounds.”414
In 1971, scientists from Boston, Massachusetts measured oxygen levels in
the human mouth and found oxygen pressure was significantly reduced.419
Just like the growing embryo in the womb, oral soft tissues accumulate
increased carbon dioxide, stimulating oxidative metabolism and thus rapid,
scarless regeneration.

Stem Cells & The Healing Process

If we define healing as the repair or replacement of defective cells with
functioning ones, then the process has a lot to do with stem cells. Stem
cells are like the body’s rescue crew; anytime cells are injured they home to
the injured tissue and either repair the damage or differentiate into the
required cells and serve as replacements.386,420-431
Stem cell therapy - where doctors harvest stem cells from the bone marrow
or fat tissue of patients and then administer it back to them – is portrayed by
the media to be a highly-sophisticated medical innovation reserved for
those who can afford the luxury. The irony is that the public is being sold
something that is a normal part of the body’s healing process. "It is well
established that tissue repair depends on stem cells…” wrote researchers
from the United Kingdom in 2012.432
The difference between a wound that heals, like the rapid and flawlessly
healing embryo and adult oral soft tissues and a ‘cancer’ wound that’s
struggling to heal, is the extracellular conditions surrounding the wound
when stem cells arrive.
Stem Cells Meet the Tumor Microenvironment
Interleukin-8,433,434 vascular endothelial growth factor,435 nerve growth
factor,436 hepatocyte growth factor,437 nitric oxide438,439 and estrogen440,441 are
some of the substances released by injured cells that signal the trafficking of
stem cells to a wound.
Normally, the inbound stem cells would repopulate the tissues that have
been damaged or lost, but since stem cells respond to the signals in their
immediate environment,442-445 abnormal substances within the tumor
microenvironment send the wrong instructions and cause them to fail to
complete the task. For example, the presence of toxic heavy metals like
arsenic or cadmium in the tumor microenvironment will transform
incoming stem cells into cancer cells.446,447 Furthermore, all of the
substances located within the tumor microenvironment of untreated cancer
patients also happen to promote carcinogenesis; so just as chemical
carcinogens can induce metabolic dysfunction in arriving stem cells, the
wide range of other stress and inflammatory substances in the tumor
microenvironment also initiate aerobic glycolysis.313,504,869-881

“Cancer, the disease, is much more than a cellular defect. Most of

the cells in a tumor are so defective that they are in the process of
dying, and in that process they recruit replacement cells, which
experience the same damaging conditions. The local and regional
extracellular conditions, and the condition of the host, are just as
central to the disease as the failing mitochondria.”
- Dr. Raymond Peat

Although many people believe tumor growth occurs as a consequence of

rapidly dividing tumor cells, Scottish researchers made a remarkable
discovery in 1972 that revealed an entirely different process. Using
electron microscopes in their laboratory at the University of Aberdeen,
Andrew H. Wyllie and his colleagues found that the rate of cell death in
tumors was enormous; and that cell division alone could only account for
less than 5% of cells present in a growing tumor.448-450
What could account for the other 95% of cells in a tumor?
When conditions surrounding an injury are defective, incoming stem cells
are immediately injured and recruit additional stem cells which also become
injured. As this chronic influx of stem cells and high rate of cell death
continues, cells - both living and dead - begin to accumulate within the
injured region, forming what is commonly referred to as… a tumor.
“Wounding recruits these cells from the follicle to the wound site,…giving
rise to superficial BCC [basal cell carcinoma]-like tumors. These findings
demonstrate that BCC-like tumors can originate from follicular stem cells
and provide an explanation for the association between wounding and
tumorigenesis,” wrote scientists from the Cardiovascular Research Institute
at the University of California in 2011.451
These fairly recent discoveries - that a constant flux of stem cells are
responsible for tumor formation, growth and metastasis - have been
confirmed so thoroughly452-458 that even the cancer establishment has
acknowledged them; except they’ve adapted them to fit in with their
imaginary ‘mutant boogeyman’ theory of cancer, claiming that “cancer stem
cells” are the true “villains” that need to be “eradicated” during cancer
therapy. The fact that scientists would actually suggest killing the body’s
repair cells as a treatment for cancer exposes an astonishing lack of
understanding about the disease.459-474
We’ve seen what happens to tumors when medicines like oranges, sodium
bicarbonate and coconut oil work to normalize the tumor
microenvironment. It’s precisely these alterations that allow homing stem
cells to repair damage and differentiate into healthy replacement cells, just
as they do in a wounded embryo.

Stem Cells Meet the Embryonic

Microenvironment
During the differentiation process of a stem cell into a specific cell type,
some key metabolic changes take place: the number of mitochondria are
increased, the cell begins consuming more oxygen and produces more
energy as a result of the activation of the more efficient, aerobic
metabolism.475 “Cell differentiation is associated with an increase in
mitochondrial content and activity and with a metabolic shift toward
increased oxidative phosphorylation activity.”476 In other words, an
environment that signals cellular respiration is essential for successful stem
cell differentiation.477-479
When a team of international scientists added embryonic stem cells to the
blood serum of cancer patients, the cells transformed into cancer cells,480
and conversely, experiments conducted as early as 1959 have demonstrated
that implanting cancer cells into mouse, zebrafish and chicken embryos
causes them to revert back into healthy, respiring cells.481-492 ”Indeed, our
group and others have elucidated the unique ability of embryonic
microenvironments to normalize aggressive melanoma cells toward a more
benign melanocytic phenotype,” wrote American scientists from
Northwestern University’s Feinberg School of Medicine in 2013.493
The high levels of carbon dioxide within a fetus or embryo - in addition to
rapidly driving oxygen into cells and lowering virtually all of the stress and
inflammatory factors within the wound microenvironment908-925 –
powerfully inhibit the generation of free radicals by keeping cells fully-
oxidizing glucose for energy (preventing ‘free radical’ electron leakage
from the transport chain) and also by preventing accidental free radical
reactions from occurring within the blood; for example, involving
unsaturated fats and heavy metals like iron.494-501 “The results testify to the
fact that CO2 is a powerful inhibitor of reactive oxygen species (ROS)
generation by cells…”502 As a result of this incredibly nurturing CO2-rich
embryonic environment, an embryo is able to withstand exposure to 10x
more chemical toxins than an adult.503
After discovering that inflammation in fetal wound healing is minimal and
resolves rapidly,364,505 scientists looking more closely at the fetal/embryonic
wound environment have observed decreased levels of pro-inflammatory
cytokines interleukin-1,386 interleukin-6,505 interleukin-8,506 tumor necrosis-
factor alpha,386 tumor growth factor beta507 and prostaglandins.508 Tumor
growth factor beta (TGFb), which is absent in fetal wounds and abundant in
tumor microenvironments, metabolically reprograms cells to shift to aerobic
glycolysis (the Warburg effect).509
Most of the inflammatory mediators present in the ‘defective’
microenvironment of a tumor which are absent from the ‘flawless-healing’
fetal wound environment - interleukin-6, interleukin-8, tumor growth factor
beta and prostaglandins - can all be induced by one single dietary
constituent: unsaturated fat.510-515

Cancer and the Immune System

In 1909, German physician and scientist Paul Erhlich first proposed the
existence of an immune ‘surveillance’ system in the body capable of
eliminating transformed cells before they are clinically noticed.535,536 Since
then, it has been confirmed that this system does exist and scientists have
been documenting a consistent association between a malfunctioning
immune system and cancer development in both mice537-542 and humans.543-
550
Epidemiological research has concluded, “Immune-suppressed
populations experience higher rates of cancer than expected.”551
In 1974, American immunologist Dr. George Friou stated the formation of
cancer is not uncommon and cellular defects are overcome by a functional
immune system before they develop into recognizable malignancies.552 And
in 2011, an Italian-American research team wrote, “Occult microscopic
cancers are exceedingly common in the general population and are held in a
dormant state by a balance between cell proliferation and cell death and
also an intact host immune surveillance.”553
Laughter has been shown to enhance the immune systems of cancer
patients554 and also decrease the risk of heart disease.555
Regular exercise of moderate intensity has been shown to boost the immune
system556,557 and reduce the risk of cancer,558-561 while endurance or
excessively intense exercise, both of which significantly elevate lactic acid
production562-564 and cause carbon dioxide loss through hyperventilation,565
have been shown to impair immune function.566-570
For decades, vegetable oil (unsaturated fat) has been recognized as a drug
that can knockout the immune system.571-577 In fact, unsaturated fats are so
potently immunosuppressive that they’ve been used specifically to disable
the immune systems of kidney transplant patients to prevent their bodies
from rejecting the foreign tissue.578-580 One way unsaturated fats do this is by
shrinking the thymus gland; an organ critical for immune function;581 and
they also directly kill white blood cells, which are the most important part
of the immune system.582

Thyroid Hormone, Cholesterol and Cancer

Thyroid hormone is an essential component of cellular respiration; without
it oxygen use and the production of carbon dioxide by cells cannot occur.583-
588
Thyroid hormone exerts two primary actions: First, it rapidly activates
respiration,661-666 which can be seen within minutes of a thyroid hormone
injection, and secondly - within a few days of a thyroid injection - thyroid
hormone stimulates the biogenesis of additional mitochondria within
cells.667-672
Thyroid hormone is also used by the body to produce steroid hormones,
which are some of the most powerful defenders against cancer and diseases
in general. These hormones include pregnenolone, progesterone, DHEA
and testosterone, which all seem to have similar anti-stress, anti-
inflammation, anti-cancer effects mediated by the activation of oxidative
metabolism.589-602,673 The production of these hormones begins with thyroid
hormone converting cholesterol into pregnenolone, and subsequently,
pregnenolone can be converted into all of the other steroids. What’s critical
to understand is that without adequate cholesterol and thyroid hormone,
none of these steroid hormones can be produced.
Impaired memory,604,605 increased aggressive behavior and suicide,606-608 and
increased mortality from cardiovascular disease,609-612 stroke and cancer,613-
616
are all consequences of not having enough cholesterol. The weight of
evidence showing the detrimental effects of low cholesterol has recently
become so titanic, that in 2015, the FDA completely reversed their position
on cholesterol - a position held for over 50 years - officially removing the
‘upper limit’ on cholesterol consumption. In other words, there’s no
amount of dietary cholesterol you can consume that is bad for you.603
With this in mind, one of the primary ways the public has been sold on the
‘essentiality’ of unsaturated fat is that it potently inhibits LDL cholesterol
synthesis.617-620 “Diets rich in omega-3 fatty acids derived from fish oils
lower the plasma concentrations of low density lipoproteins (LDL) and very
low density lipoproteins in humans.”621 If cholesterol was unhealthy, then
lowering it would be a good thing, but the research is exceptionally clear
that inhibiting cholesterol synthesis by eating unsaturated fat (or in any
other way, for example, statin drugs) will eventually lead to cancer and
other degenerative diseases.

Anybody concerned about having high cholesterol should know

that this situation has long been associated with a deficiency of
thyroid (hypothyroidism).622-648 “The thyroid hormone is required
for using and eliminating cholesterol, so cholesterol is likely to be
raised by anything which blocks the thyroid function,” wrote Dr.
Peat. Supplementation with a dessicated thyroid supplement (dry
powdered thyroid gland pressed into a tablet) can be used to
convert cholesterol into valuable hormones.

For decades, Dr. Peat has been saying that unsaturated fats, which include
any oils that are liquid at room temperature, aside from olive oil (which
contains about 11% unsaturated fat650), are potent inhibitors of thyroid
function.649
Unsaturated oils obstruct thyroid hormone at every turn - including its
secretion from the thyroid gland,651 its transport through the blood,652 its
conversation in the liver,653 its uptake by tissues654 and its use inside cells.655
This helps to explain why diets high in unsaturated ‘essential’ fatty acids
promote weight gain and why animals made deficient in unsaturated fats are
leaner and have higher metabolic rates, meaning they produce greater levels
of energy and carbon dioxide as a result of increased oxidative metabolic
activity.656-660
In summary: Thyroid hormone and the anti-aging steroid hormones it
produces are essential for cellular respiration. Both thyroid hormone and
cholesterol are essential for producing these hormones, and unsaturated
fatty acids potently inhibit both thyroid hormone and cholesterol synthesis.

CO2, Unsaturated Fats and Aging

Since our lives begin in the womb with extraordinary health – characterized
by optimal levels of carbon dioxide – and end with disease, characterized
by a deficiency of carbon dioxide, it stands to reason that carbon dioxide
gradually decreases with age. There’s another very important thing that
happens with age.
“We have conducted a systematic literature review of studies reporting the
concentration of LA [Linoleic Acid/omega-6/unsaturated fat] in
subcutaneous adipose tissue of US cohorts. Our results indicate that adipose
tissue LA has increased by 136% over the last half century and that this
increase is highly correlated with an increase in dietary LA intake over the
same period of time,” reported American researchers in 2015.516
It’s no coincidence that as we age, decreasing levels of carbon dioxide are
directly accompanied by an increased accumulation of unsaturated fatty
acids in our tissues.516-526
Scientists have found that cytochrome c oxidase enzyme activity (and thus
carbon dioxide production) in rats also declines with age,527,528 while
simultaneously cardiolipin, a major mitochondrial lipid that interacts
directly with cytochrome c oxidase and plays a pivotal role in cellular
respiration,529-532 becomes increasingly unsaturated.533 Feeding aged rats
hydrogenated peanut oil (100% saturated fat) “completely restored” the
respiratory enzyme activity in their muscles “to 80% of the value observed
in muscles of young animals.”534
In summary: Aging is a consequence of reduced levels of carbon dioxide
in the body caused primarily by the increased accumulation of dietary
unsaturated fatty acids in body tissues.

The Primary Fuel for a Tumor

Discovered nearly 100 years ago by British medical scientist Philip
Randle,690 the Randle effect describes the observation that – similar to an
“on” and “off” switch – having more glucose (sugar) than fat circulating in
the blood will cause cells to metabolize sugar rather than fat, and
reciprocally, having more fatty acids in the blood will cause cells to
metabolize fat rather than sugar.691
While cancer cells do consume large amounts of sugar initially, once the
bloodstream runs low on sugar (hypoglycemia), muscle will be catabolized
into amino acids and fat mobilized from fat stores, which inhibit the use of
glucose (the Randle effect) by cells - so tumor cells rely mostly on fat and
protein for energy.692-696

The Randle effect also explains the metabolism of a person with

diabetes. Like all diseases, excessive stress has mobilized fatty
acids into the bloodstream, shutting off the body’s ability to use
glucose. This situation is so similar to what’s happening in a
person with cancer that the association between diabetes and
cancer has been called ‘a two-way street.’697-704

Aside from chronically elevated stress hormones, some of the adverse

effects of fat and protein metabolism include: fat metabolism produces less
carbon dioxide (per unit of oxygen consumed),964-966 and protein metabolism
results in the production of ammonia - “a highly toxic substance,”705 which
further promotes glycolysis and increases lactic acid production.706-708
Low blood sugar, caused by fasting, starvation, avoiding dietary
carbohydrates, or exercise (unless adequate sugar is consumed during the
workout), stimulates the same stress metabolism as a person with cancer.
This explains why most heart attacks occur in the early morning hours,882
following an overnight ‘fast’ during sleep.
In 2017, researchers from the Barcelona Institute of Science and
Technology in Spain investigated cancer cell metabolism and discovered
that cancer metastasis relies on a single molecule whose function is to allow
cells to absorb fat, called CD36. “The use of neutralizing antibodies to
block CD36 causes almost complete inhibition of metastasis,” they
reported.709 This study indicates that fat is required in order for cancer
metastasis to occur. One year prior to this study, Spanish researchers also
established a similarly remarkable finding: the ability of cancer cells to
grow and proliferate is exclusively dependent on fat, which they called the
“Achilles heel” of cancer.710
Animal experiments have determined that high fat diets of any kind will
increase the frequency of cancer, but that it’s the type of fat that determines
the magnitude;711-723 “Polyunsaturated vegetable oils enhance carcinogenesis
more effectively than saturated fats;”724 “In general, high dietary levels of
unsaturated fats (e.g., corn oil, sunflower-seed oil) stimulate this
tumorigenic process more than high levels of saturated fats (e.g., beef
tallow, coconut oil).”725
Furthermore, the greater the degree of unsaturation, the more carcinogenic
the fat is.726-731

A Closer Look…
In 1998, Netherland researchers from the University of Amsterdam
divided rats into three groups and fed them either - a low fat diet, a fish
oil diet (omega-3), or a safflower oil diet (omega-6) - just three weeks
before injecting colon cancer cells into their veins to induce tumors.
“At 3 weeks after tumor transplantation, the fish oil diet and the
safflower oil diet had induced, respectively, 10- and 4-fold more
metastases (number) and over 1000- and 500-fold more metastases
(size) than were found in the livers of rats on the low-fat diet.”729
 In 1994, researchers from the University of Georgia compared the
effects of feeding rats a high fat fish oil (omega-3) diet with a high fat
corn oil (omega-6) diet. In the group of rats fed omega-3’s - the most
highly-unsaturated fat found in nature730 – researchers found the largest
increase in oxidative stress; “The omega-3 diet showed 675% increase
in basal oxidation, a 2624% increase in auto-oxidation and a 4244%
increase in iron-ascorbate catalyzed oxidation compared to the omega-
6 diet in mammary tissue homogenates.”731

In 1987, Dr. Leonard Sauer and his colleague looked at the effects of
prolonged fasting on the growth of tumors in rats. The researchers found
that tumor growth was increased in proportion to the availability of fat
released from fat stores, substantiating the finding that tumor growth is
dependent on fat.732
Here’s the kicker: No tumor growth occurred in the young rats - only in
the adult rats - meaning the fats deemed essential for tumor growth were
predominantly unsaturated. In other words, unsaturated fat is not only the
primary fuel that drives tumor growth, but a tumor cannot exist without it.
When scientists from the University of Wisconsin fed rats a diet containing
5% corn oil for 6 months - 80% of the rats developed tumors. When they
fed them hydrogenated coconut oil, containing 100% saturated fat, no liver
tumors developed; “The feeding of the fatty acids of hydrogenated coconut
oil lowered the incidence of hepatomas to zero.”733
In rats chemically induced with pancreatic cancer, after 4 months, “Grossly
visible tumors increased significantly in number as the EFA [essential fatty
acid] content of the diet increased,”734 and a number of studies have found
that tumorigenesis could only be induced if a certain amount of unsaturated
fat was included in the diet;735-737 confirming what Dr. Peat has been stating
boldly and repeatedly for decades:

“Cancer cannot exist unless there are unsaturated fatty acids in the
diet.”
 - Dr. Raymond Peat

The Self-Amplifying Stress Response

In life-threatening situations, stress can save our lives by helping us
physically escape danger; but in the modern world where stress is triggered
more frequently, it can eventually result in disease and death.
During a stress response, stress hormones are released to break down
muscle and fat tissues for emergency fuel, and depending on the
composition of fats released into the bloodstream – which depends entirely
on what foods we’ve chosen to eat in our lifetimes - two diametrically
opposing reactions can occur.
Saturated Fat
When mostly saturated free fatty acids enter our bloodstream during stress,
they will be oxidized for energy and at the same time inhibit additional
stress hormones from being produced;674-677 which quickly shuts off the
stress response once the stressful situation is over.
Unsaturated Fat
When mostly unsaturated free fatty acids enter our bloodstream during
stress, they will be oxidized for energy and at the same time – due to their
toxicity - trigger the production of additional stress hormones,678-684 which
cause more unsaturated free fatty acids to be released, causing more stress
hormones to be produced in a vicious circle.
“Various tumor cell-derived and contextual cues feed constantly this vicious
circuitry sustaining inflammation and promoting proliferation,
angiogenesis, invasion and eventually metastasis,” wrote scientists from the
University of Athens Medical School in 2013.689
If our tissues are comprised of mostly saturated fat, our stress response will
be self-limiting, but if our tissues are comprised of mostly unsaturated fat,
then our stress response will be self-amplifying; and when the self-
amplifying stress response overwhelms the body’s ability to deal with it -
the stress will never be switched off; and cancer and diseases will emerge.

Interrupting the Vicious Cycle of Stress

Anytime highly-reactive molecules like unsaturated free fatty acids are put
into an environment rich in oxygen, the two will react - and the fat particles
will be broken down into toxic fragments. And as the temperature of that
oxygen-rich environment is increased, these reactions are enhanced; so
between the toxic excess of oxygen in the air we breathe738,739 and our
relatively high body temperatures, the human body is a perfect setting for
these oxidative reactions to occur.
One class of breakdown products (metabolites), which arise from oxidation
of the unsaturated fat arachidonic acid (omega-6), that are heavily
implicated in cancer growth and progression, are called prostaglandins.740-748
Researchers studying dietary fat have suggested that prostaglandins might
be the underlying reason why unsaturated fats promote tumor formation and
saturated fats don’t.711
Prostaglandins can also at least partly explain why feeding pigs diets
containing unsaturated fat, which is common practice in convention pig
farming, damages their lung function,759 or why heart disease can be
induced by eating unsaturated fat and prevented by adding cocoa butter
(saturated fat) to the diet.760
The direct stimulation of cortisol677-684 and estrogen685-688 by unsaturated fatty
acids as well as the prostaglandins produced from them are probably the
three key factors sustaining the vicious cycle of stress and toxic tumor
microenvironment that prevents stem cells from repairing a tumor wound.
Even if our tissues are brimming with unsaturated fatty acids, as long as
they don’t enter our bloodstream, none of these negative effects will occur,
and therefore, finding ways to prevent unsaturated fatty acids from entering
our bloodstream - so they can be safely detoxified from our tissues by the
liver - is the paramount strategy for interrupting the vicious cycle of stress
sustaining a tumor.
Dietary Considerations
Since unsaturated fatty acids can enter the bloodstream either through
exogenous (eating them) or from endogenous (released from tissues during
stress) sources, the first step in healing a tumor (or preventing one) involves
minimizing consumption of unsaturated fats or ideally, eliminating them
from the diet entirely.
After inducing tumors in mice and amplifying their tumor size by feeding
them high fat corn oil diets - researchers switched the mice to fat-free diets
and after 20 weeks, tumors regressed in about half of the rats, and in some
cases, completely disappeared.761
In the interest of cancer prevention, one strategy that Dr. Peat recommends
for protecting the body when eating at a restaurant or a meal containing
unsaturated fat, is supplemental vitamin E, which is probably based on
evidence showing that vitamin E reduces lipid peroxidation caused by
unsaturated fat,762-764 meaning essentially that it saturates it.

Although consuming saturated fats like coconut oil can dilute the
unsaturated fat content in the blood of a cancer patient and
successfully interrupt the stress response, even coconut oil contains
about 3% unsaturated fat, so a fat-free diet might be a better
strategy. Hydrogenated coconut oil, however, would be a great
medicine for cancer patients since it provides no inhibitory
unsaturated fatty acids.

We’ve previously established that oranges, coconut oil and baking soda
inhibit estrogen, cortisol and prostaglandins - suggesting they inhibit the
movement of free fatty acids into the blood (lipolysis) - and there’s one
medicine in particular that can be used in conjunction with these foods to
inhibit lipolysis probably more effectively than any other known substance.

Cancer Medicine
The enzyme responsible for the production of prostaglandins, which is
highly expressed at sites of inflammation, like wounds and tumors,741,743-
746,765-770
is called COX-2 (cyclooxygenase-2).771 “Cyclooxygenase-2 is
frequently overexpressed in many cancers and is functionally involved in
the pathogenesis of tumours. Therefore, it represents an important target for
pharmaceutical intervention,” wrote Swiss researchers from the Institute of
Cell Biology in Zurich.354
Drugs that inhibit the COX-2 enzyme have been shown to significantly
prevent cancer, including a 40-50% reduction in the incidence of colorectal
cancer in people taking COX-2 inhibitors (which was directly attributed to
decreased prostaglandins) and reduce the growth of existing tumors, in both
animals and in humans.742-744,775-782 And since prostaglandins are one of the
mechanisms by which unsaturated fats knockout the immune system,783-788
anything that inhibits COX-2 will also stimulate the immune system.785
Interestingly, all drugs classified as COX-2 inhibitors, for example,
acetaminophen, ibuprofen, etc., have been shown to be extremely toxic and
increase the risk of heart disease, except one.

Aspirin
Comprised of acetic acid (found in vinegar) and salicylic acid (found in
willow bark, fruit and vegetables789), aspirin (acetylsalicylic acid) is a safe
and inexpensive drug that can effectively inhibit the enzyme COX-2.
Ancient Egyptians used willow bark extract thousands of years ago to help
mothers cope with the pain of childbirth,790 and this same medicine is still
being widely used today for the same and many other purposes.
In 2016, after analyzing the available scientific evidence, the U.S.
Preventive Services Task Force officially began recommending daily low-
dose aspirin for people aged 50 to 69 to prevent heart disease, stroke and
cancer.791 Even the Acting Director of the U.S. National Cancer Institute
Dr. Douglas Lowy publically endorsed the use of daily low-dose aspirin as
a cancer preventive,792 which can reduce the cancer death rate by 30%, heart
disease by 22% and stroke by 17% and save 900,000 lives over the next 20
years, according to a 2016 study from the University of California.793 A
2016 systematic review concluded aspirin was as effective as screening for
preventing colon cancer incidence and mortality; meaning daily low-dose
aspirin can completely replace an annual colonoscopy.794
Aspirin works in part by inhibiting the COX-2 enzyme that converts
unsaturated fatty acids into prostaglandins – but aspirin is far more than just
a COX-2 inhibitor. Aspirin directly inhibits the release of free fatty acids
into the bloodstream (lipolysis)795-797 and it also inhibits the enzyme
responsible for the synthesis of cortisol.798 So while aspirin prevents the
production of prostaglandins, it’s also inhibiting cortisol production and
lipolysis, which cuts off the direct estrogenic, anti-thyroid and
immunosuppressive effects of unsaturated fatty acids.
When you eliminate toxic unsaturated fats from the equation with
medicines like aspirin, the vicious cycle of stress seen in cancer is shut off,
damaged cells are repaired, mitochondrial respiration is restored,799 carbon
dioxide levels rise and amazing things begin to take place.
Aspirin can reduce pain,800 prevent cataracts,801,802 protect the brain from
glutamate803 and nitric oxide toxicity,804 prevent neurodegenerative diseases
like Alzheimer’s, Parkinson’s and Huntington’s diseases,805 improve insulin
sensitivity in diabetics, enhance brain function,806 alleviate depression,807
chelate toxic heavy metal iron,808 prevent damage from ionizing
radiation,809,810 prevent miscarriage,811 improve fertility,812 extend the
lifespan of nematodes by up to 23%;813,814 of mice by 10%;815 and of yeast
by almost 400%; in fact, the active ingredient in aspirin was found to be
more effective at extending lifespans than over 10,000 other plant extracts
tested.816
Highlights of the anti-cancer effects of aspirin in vitro and in animal studies
include stopping the growth of endometrial tumors,817 triggering apoptosis
in gastric cancer cells,818 preventing lung tumor formation819 and shrinking
fibrosarcoma tumors by 30%.820
A groundbreaking study by scientists at the University of Kansas Medical
Center in 2015 administered the human-equivalent dose of a single 325mg
aspirin tablet to mice with breast tumors and found that aspirin not only
prevented tumor growth, but it actually ‘reprogrammed’ stem cells to begin
differentiating and repairing the damage, instead of becoming injured and
maintaining tumor mass.821
Human breast cancer patients were treated with aspirin in a study from the
Bose Institute in Kolkata, India in 2010, and researchers found that aspirin
completely stopped tumor growth in 80% of patients.822 At doses as low as
100mg/day, aspirin can halt the growth of non-metastatic human pancreatic
and colon cancer cells, and at doses between 3-12 grams/day it can halt the
growth of metastatic cancer cells.823
Aspirin’s effects on the tumor microenvironment are significant and include
reductions in free radicals,824,825 tumor necrosis factor-alpha,826,827
interleukin-1,828 interleukin-4,829,830 interleukin-6,831-833 interleukin-8,834-836
interleukin-13,837 nuclear factor kappa-b,828 cortisol,838,839 adrenaline,840-843
high mobility group box 1 protein,844,845 vascular endothelial growth
factor,846 epidermal growth factor,847,848 nitric oxide,849-852 lactic acid,853-855
estrogen856-858 and serotonin.859,860

Aspirin Safety
Mainstream medicine seems devoted to bashing aspirin in the media;
claiming it is a dangerous drug with lethal side effects like bleeding in the
stomach or brain. But like every statement we hear in the media, our first
response is to exert a healthy skepticism until we’ve investigated the subject
for ourselves. So let’s take a look at some evidence and decide if the
concerns surrounding aspirin use are warranted.
An extensive 2015 review looking at the safety of aspirin use in patients
with aneurisms declared, “Aspirin has been found to be a safe in patients
harboring cerebral aneurysms.” The researchers also cited a number of
clinical studies in which aspirin was demonstrated to decrease the overall
chances of rupture/brain bleeding in patients with aneurisms.861
Lebanese researchers examined mortality of patients admitted to hospital
for gastrointestinal bleeding in 2015 and found, “being on aspirin was
protective against in-hospital mortality, rebleeding, and predictive of a
shorter hospital stay.”862
Another well-established benefit of aspirin is that repeated doses actually
protect the stomach from damage caused by strong irritants.866 In 1995,
Polish researchers from the Jagiellonian University School of Medicine
found that administering human-equivalent doses of 1.5 grams of aspirin to
rats for 5 days enhanced their resistance to stomach irritation; “Gastric
adaptation to ASA enhances the mucosal resistance to injury by strong
irritants…” they concluded.867
So how is it possible that aspirin can both prevent stomach and brain
bleeding while simultaneously causing it? The doses used may have a lot to
do with it. Dr. Peat has mentioned that in animal experiments where aspirin
was found to produce stomach ulcers/bleeding, enormous single human-
equivalent doses of anywhere between 10 and 100 aspirin tablets have been
used;864 basically these studies were designed to produce ulcers. So for all
practical purposes, typical doses used by people will not even come close to
having these effects and the evidence seems to substantiate this.
In 2000, researchers from the United Kingdom investigated the effects of
low-dose asprin on the formation of ulcers or stomach damage. Results
showed that low-doses of aspirin caused no increase in intestinal
permeability, ulcers or stomach damage; “Aspirin caused no inflammation
or ulcers.” However, when the researchers tested aspirin use in combination
with the highly-toxic drug dinitrophenol, they found that stomach ulcers did
form.865
Since people often take multiple other drugs together with aspirin, it makes
you wonder if reports of stomach bleeding have been caused by other
medications being used at the same time as aspirin, and yet aspirin has
taken the blame. Contrary to rumors that aspirin can cause deadly stomach
bleeding, a 2016 review and meta-analysis by an international team of
researchers found no evidence of aspirin ever causing fatal stomach
bleeding.863
From my own experience, I’ve read about and experimented with dozens of
different supplements, nutrients and drugs over the past decade and nothing
has even come close to being as helpful for me as aspirin; I feel it has
completely turned my health around, which began when I upped my dose
from 1 to 3 tablets (about 1 gram) per day. For the past 8 months, I’ve been
taking between 3-5 grams of aspirin daily and it’s allowed me to keep my
energy levels high and stress levels low enough to sit, stand and think while
writing this book at an intense pace for usually 8 to 12 hours a day. While I
did notice slight irritation when I first increased my dose of aspirin, I’ve
certainly never experienced any stomach bleeding from it; in fact, my
stomach seemed to adapt rather quickly and I no longer have any issues at
all.
It seems the fears being pushed by the media regarding aspirin use are
vastly overstated and that the decreased risk of heart attack, stroke, cancer
and the many other benefits aspirin delivers greatly outweigh any minor
risk that may exist. The fact that aspirin is unpatented, costs next to
nothing, and has the potential to completely replace everything the cancer
industry has to offer and most of what the drug industry has to offer might
have a lot to do with the deliberate falsehoods and scare tactics being
endorsed in the media.

When purchasing aspirin, be sure to read the ingredients list as

many companies have been adding harmful chemicals to their
tablets. The best options seem to be either pure aspirin
(acetylsalicylic acid) powder or tablets containing only aspirin and
either cornstarch or cellulose. Buy these, boycott the rest, and
drug companies can either clean up their asprin products or go out
of business.

Carbohydrates and Cancer

It’s interesting that for the past half century our society has vilified
saturated fat and now that evidence has overwhelmingly shown that
saturated fat doesn’t ‘clog your arteries’ or have any negative impact on
human health, government food recommendations have switched to
vilifying sugar. Everyone knows sugar makes you fat, right?
Here’s an inconvenient truth: In 2011, Australian researchers compared
sugar consumption and obesity rates in Australia, the UK and USA, and
found that between the years 1980-2003, Australian obesity rates increased
3-fold while sugar consumption decreased by 23%.883

Coconut oil stimulates weight loss by diluting the content of

unsaturated fatty acids in the blood, which is marked by a boost in
thyroid function and increased thermogenesis. Therefore, the
higher your metabolic rate (the more your cells are respiring/the
more carbon dioxide in your body), the leaner and less obese you
will be. It is probable that dietary consumption of unsaturated fat -
a major metabolic inhibitor that can be incredibly difficult to avoid
eating - is the main culprit behind the increased obesity seen in
Australians during this study period.

Since stress hormones are elevated primarily to replenish glucose stores in

the blood, ingesting sugar is one of the quickest and most effective ways to
turn off stress. A 1987 study published in Life Sciences examined the
effects of different diets on hormonal production in men who ate either high
carbohydrate diets (20% fat, 10% protein, 70% carbs) or low carbohydrate
diets (20% fat, 44% protein 35% carbs). The results showed, “Testosterone
concentrations in seven normal men were consistently higher after ten days
on a high carbohydrate diet” and “cortisol concentrations were consistently
lower during the high carbohydrate diet.”884 Another study came to similar
conclusions: Two groups of men were asked to perform three consecutive
days of intensive exercise training while consuming different diets - one
consumed a diet containing 60% carbohydrates and the other 30%
carbohydrates. Blood samples revealed that the men who ate low-
carbohydrate diets had higher cortisol levels and lower testosterone levels
compared to the men who ate high-carbohydrate diets.885 In both studies,
carbohydrates had an androgenic and stress-reducing effect.
One useful way of looking at metabolism is that we have two options – the
relaxed/health metabolism or the stressed/disease metabolism. Which one
we spend the most of our time in is a choice we make everyday, primarily
by the food we eat: either we eat sugar – yes, even plain white sugar - or in
its absence, our body will elevate stress hormones and begin tearing itself
apart in order to make sugar.
The fact that the body is willing to destroy itself to make glucose when it is
lacking reveals how critical dietary consumption of sugar actually is.
“Glucose metabolism in mitochondria through oxidative phosphorylation
(OXPHOS) for generation of adenosine triphosphate (ATP) is vital for cell
function,” wrote scientists in 2015.224
In cancer, since sugar metabolism is switched off by the presence of free
fatty acids in the bloodstream (the Randle effect), inhibiting lipolysis using
medicines like aspirin will effectively switch cells back to metabolizing
sugar. This, in combination with a diet containing adequate protein and
high in carbohydrates, particularly from fruit, like oranges, will elevate the
body’s supply of carbon dioxide, supporting a high metabolic rate and a
disease-free organism.
There are a number of advanced healing technologies that can also be used
as strategies for disease prevention, treatment, athletic performance
enhancement and life extension.

Carbogen
In the 1940’s, fire trucks, police rescue crews and paramedics all across the
United States were equipped with devices called ‘H-H Inhalators,’ which
created a healing mixture of oxygen and carbon dioxide - called carbogen -
that was administered to patients during emergencies.886 The common
practice of using carbogen by emergency response crews was spurred by
the early 19th century work of Yale professor Dr. Yandell Henderson and his
colleagues, whose pioneering research on carbogen uncovered some of the
many virtues of the therapeutic inhalation of carbon dioxide.

The administration of pure oxygen to patients during emergency

situations, which is standard practice today, lowers carbon dioxide
levels (the Haldane effect), which constricts blood vessels887,888 and
ironically, reduces tissue oxygenation201-223 and the overall health
status of patients.889,890 In a 2010 study published in the British
Medical Journal, patients with COPD receiving high-flow oxygen
had significantly increased rates of mortality compared to the
titrated oxygen group.891 A 2016 study published in the Journal of
the American Medical Association found that giving less oxygen to
patients in intensive care units reduced mortality.887 And animals
administered 100% oxygen for just 1 hour had markedly worsened
neurological outcomes than a control group of animals.
Interestingly, the animals administered the excess of oxygen had
increased oxidation of brain lipids (unsaturated fats) and increased
neuronal cell death.892

In 1921, Dr. Henderson and his colleagues found that administering 8%

carbon dioxide in air to patients after major surgical interventions facilitated
a rapid return to consciousness and elimination of anesthetic.893 “The
cutaneous circulation improved. The skin changed in color and temperature,
from blue- gray and cold to pink and warm. The volume of the pulse,
previously thready, rapidly became full; and arterial pressure was restored
to normal… Nausea and vomiting were either greatly reduced or entirely
absent and after the inhalation the patient dropped off to sleep,” wrote
Henderson.
Carbogen can stimulate the breathing of babies in hospitals at birth, and
also the breathing of patients with respiratory failure following severe
alcohol intoxication, drowning, electric shock; it can even reverse a deep
coma caused by severe carbon monoxide poisoning.894-897

“Experience has demonstrated that the return of natural breathing

is considerably aided and accelerated by the administration oxygen
and carbon dioxide from an inhalator, while artificial respiration is
being applied.”
- Dr. Yandell Henderson

In dogs experimentally induced with pneumonia, their lungs were cleared

and their pneumonia cured by putting them in closed chambers containing
about 8% carbon dioxide in air for 12 to 24 hours, according to a study
published in the Archives of Internal Medicine in 1930.898 By 1932, these
findings were widely adopted by the medical community and treatment of
pneumonia in humans with carbogen had become common practice; “Many
cases of pneumonia have now been treated with inhalation of CO2 in O2,”
wrote Dr. Henderson.899
Carbogen has clearly proven itself a highly-effective aid during emergency
situations and in hospital settings and therefore, it’s of high priority that
rescue crews and hospitals worldwide are re-equipped with H-H Inhalators
and the use of carbogen be permanently reinstated.
In addition to helping people in emergency situations, carbogen inhalation
therapy has also been shown to potently suppress seizures in epileptic
patients940 and significantly improve recovery rates in patients with sudden
hearing loss.941 It has also been tested on people with cancer.

Carbon Dioxide Therapy

Carbon dioxide is a potent anti-inflammatory substance901-907 that reverses
cancer growth by rapidly oxygenating cells and lowering carcinogenic
substances within the extracellular matrix of tumors, including interleukin-
1,908 interleukin-1b,909 interleukin-6,908 interleukin-8,908 nuclear factor-kappa
b,910,911 tumor necrosis-factor alpha,912 nitric oxide,913-915 free radicals,916
cortisol,917 prolactin,918,919 lactic acid,920-922 prostaglandins,923,924 and
histamine,925 which in turn allows incoming stem cells to differentiate into
healthy, replacement cells and complete the healing process.
When carbon dioxide levels are increased therapeutically, tumors shrink,326-
328,900
and cancer metastasis - the number one cause of cancer mortality329-336
– is prevented.75-77,337-341 There are a number of ways this can be
accomplished.

Carbon Dioxide Injections

Japanese researchers experimented with carbon dioxide as a treatment for
cancer in 2012 by directly injecting it into rat skin tumors at Kobe
University School of Medicine. Published in the journal PLOS one, carbon
dioxide injections were found to enrich cytochrome c oxidase activity,
multiply the number of mitochondria in cells, trigger apoptosis in tumor
cells and significantly reduce tumor volumes.926 In 2014, researchers from
the same university injected carbon dioxide into another type of skin tumor
- squamous cell carcinoma - and found that it triggered cancer cell
apoptosis and reduced the expression of hypoxia inducible factor 1-alpha
(HIF-1α),337 signifying tumor cells began receiving adequate oxygen.

Carbon Dioxide Baths

The benefits of bathing in naturally carbonated springs or baths infused
with carbon dioxide have long been known in Europe337 and this type of
therapy (balneotherapy) has been in use therapeutically since the Middle
Ages.927 Interestingly, carbon dioxide is readily absorbed through the skin;
100 times more powerfully than water.934
In 1997, German researchers from the University of Freiburg compared the
effects of soaking the lower legs of people in either fresh water or in carbon
dioxide enriched water (1200mg CO2 per kg water). While legs immersed
in fresh water were found to have no increase in circulation and little
increase in oxygen use, researchers discovered that circulation in legs
immersed in carbon dioxide enriched water was enhanced by 300% and
oxygen pressure within tissues was increased by 10%.928 A number of other
studies have confirmed that CO2-enriched baths significantly increase
blood circulation and enhance cellular oxygenation.929-933
Slovakian researchers tested the effects of a series of 20 carbon dioxide
baths on patients and assessed their health after the first, 10th and 20th
sessions. Results confirmed that although the effects of the first bath were
the most pronounced, “a series of carbon dioxide baths had a gradually
improving effect.”935
423 patients with high blood pressure were given a 4-week course of carbon
dioxide baths to determine the effects on blood pressure in 1989. Patients
were randomly assigned to baths containing either high or low
concentrations of carbon dioxide and the results showed, “A significant fall
in blood pressure, both at rest and during exercise was observed in both
groups during the course of treatment.”936
Japanese scientists tested the effects of carbon dioxide baths on the athletic
performance of swimmers. Results showed that swimmers who underwent
carbon dioxide baths prior to swimming had improved muscle performance,
increased endurance and accumulated lower levels of lactic acid during
their swim.937
For those looking to utilize carbon dioxide baths at home, it’s useful to
know that the CO2-enriched bathwater used in many of these studies was
generated by adding products containing sodium bicarbonate and an acid to
water; commonly known as bath bombs.

Carbogen Inhalation Therapy

Scientists experimenting with the use of carbogen on cancer patients have
confirmed its effectiveness for improving tumor oxygenation;942-949 “This
study confirms that breathing 2% CO2 and 98% O2 is well tolerated and
effective in increasing tumour oxygenation.”950 In normal rats and in rats
with implanted brain tumors, inhalation of 5% carbogen was found to
increase brain tissue oxygenation by “at least 100%,”951 and cancer patients
administered 4 minutes of 100% oxygen, followed by 10 minutes of room
air, and then 4 minutes of 5% carbogen had improved tumor oxygenation by
an average of 21-times.952
Most of these studies were testing carbogen to see if it could improve the
‘effectiveness’ of either radiotherapy or chemotherapy, so there are no
reports of the fate of a tumor following carbogen administration on its own
- but by now we’re well aware of what happens when carbon dioxide meets
a tumor and its environment.

Capnometry
In recent years, the revival of Warburg’s finding that cancer cells produce
lactic acid as a result of aerobic glycolysis has inspired some doctors to
begin measuring blood levels of lactic acid as a way of diagnosing cancer.938
Since healthy cells produce carbon dioxide and malfunctioning cells
produce lactic acid - a person who is healthy will have high levels of carbon
dioxide and low levels of lactic acid, while a person who is ill will have low
levels of carbon dioxide and high levels of lactic acid; and therefore, blood
levels of lactic acid and carbon dioxide are the two most accurate indicators
of overall health.
As it turns out, the concentration of carbon dioxide present in the exhaled
breath, which can be measured using a device called a capnometer, is an
accurate way of determining arterial levels of carbon dioxide in the body939
and can therefore be used by anyone, at home, to determine their overall
level of health and as an assessment tool during disease treatment.

Health Rising
If there is a creator of man and all of nature, and there seems to be no
shortage of evidence for this, then it appears our creator has a plan. Prior to
1800, the concentrations of carbon dioxide in Earth’s air were said to have
been 280ppm953 and in 2015, measurements revealed that the rising CO2
levels had officially surpassed the 400ppm (0.04%) mark. Remarkably,
carbon dioxide concentrations in our air are not just rising - they’re rising
exponentially.954-957
And if that news wasn’t good enough - the toxic, excessive levels of oxygen
in our air have simultaneously been in exponential decline; 0.1%
(1000ppm) over the past 100 years, according to a 2016 study by
researchers from Princeton University.958 Oxygen levels in all of the
world’s oceans are dropping at an even faster rate; a 2015 study published
in nature found that oceanic oxygen levels have declined more than 2%
since 1960.959
For those still uncomfortable with the idea that reduced oxygen is
something beneficial for life - remember that less oxygen in our air means
more carbon dioxide in our bodies, which drives oxygen into cells. Here
are a few more fascinating examples to further illustrate this effect.
In the 1980’s, Russian researchers transplanted tumors into rats and then
took them to high altitudes to see the effects of hypoxia (reduced oxygen)
on their recovery. These studies showed that hypoxic high-altitude
environments inhibited tumor growth;960 “It was shown in rat experiments
that high-altitude hypoxia inhibits the growth of transplantable
tumors…”961 Furthermore, some of the rats in these studies were given
chemotherapy, and not only did high-altitude hypoxia help them recover,
but it significantly diminished the toxicity of the chemotherapy drugs.960,961
In 2011, scientists from Harvard Medical School studied the effects of
hypoxia on tumor progression in vivo. After transplanting lung tumors into
rats and then putting them in environments containing 10% oxygen for 14
days, researchers found that tumor growth and cancer metastasis were both
significantly suppressed.962
While the beneficial effects of exponentially increasing carbon dioxide
levels and exponentially decreasing oxygen levels in our environment are
certainly being felt and make for a promising future, like the naked mole
rat, frogs, bats, bees and many other living creatures, I think it’s time we
begin focusing our attention on how to optimize our environment even
further. Identifying the ideal concentration of these two gases in air might
be a good starting point.

The End of All Disease

Current carbon dioxide levels in sea level air are currently only 0.04% and
oxygen levels are 21%963 - an environment that Dr. Buteyko once called
‘poisonous in its composition;’ containing 10-times more oxygen and 250-
times less carbon dioxide than what our bodies need. “…the cells of
animals and humans need about 7% CO2 and only 2% O2 in the
surrounding environment. This is the way our cells live: cells of the heart,
brain, and kidneys,” explained Dr. Buteyko.
Oxygen Carbon Dioxide
Current Concentration 21% 0.04%
Target Concentration 2% 7%

Once the most efficient methods of achieving these environmental

modifications have been realized and implemented, human beings, animals
and nature will be virtually immune to the harmful effects of all
environmental contaminants, and the day will soon follow when humankind
witnesses an end to all suffering and disease.
Until then, that the people now have the understanding needed to heal
themselves, independent of doctors and systems of healthcare, means they
are free.
CONCLUSION
The cancer establishment maintains that cancer is a genetic disease, but the
metabolic nature of cancer was established almost 100 years ago by Dr.
Otto Warburg. Since then the genetic theory of cancer has been disproven
repeatedly and Warburg’s metabolic theory confirmed repeatedly, yet the
cancer industry continues to ignore the truth. To this day, the public
remains ‘officially’ uninformed that cancer is a metabolic disease which is
both preventable and reversible.
Dr. Otto Warburg observed that cancer cells were nothing but normal cells
with malfunctioning mitochondria – not a biological terrorist-type cell that’s
on a killing spree. This observation has been validated numerous times
since Warburg, perhaps most notably by the elite Russian Scientist
Konstantin Buteyko. Buteyko’s conclusion after a lifetime of work in
search of the root cause of disease was that all people with suboptimal
health, including cancer, have one thing in common: A deficiency of carbon
dioxide in the body. This situation arises because in cells with
malfunctioning mitochondria, lactate is rendered as a byproduct of
metabolism instead of carbon dioxide.

Paradigm Shift: A Biological understanding of

cancer

The development of cancer is characterized by a shift inside the body from

high levels of carbon dioxide and low levels of lactate to low levels of
carbon dioxide and high levels of lactate. This altered environment is the
result of cells progressively losing their ability to utilize oxygen and
glucose efficiently. When cells utilize oxygen and glucose efficiently, they
render the healing carbon dioxide that is required for health. When cells
lose their ability to utilize oxygen and glucose efficiently, they render
lactate, which perpetuates the cancer metabolism.
It should be known by all that the most accurate ways to diagnose cancer
are either to test for lactate levels in the blood (or other body fluids) or for
carbon dioxide in the exhaled breath. Many doctors have realized this in
recent years and are beginning to put it into practice.
If elevated lactate or a deficiency of carbon dioxide is found in the body, it
means that a significant number of cells are inefficiently producing energy.
Instead of deriving energy from the complete oxidation of glucose within
the mitochondria of cells, cancer cells derive their energy from the
fermentation of glucose, and then once the body is out of glucose, from the
use of amino acids and fatty acids. This ‘cancer metabolism’ tends to be
self-promoting, and brings about the excessive and prolonged production of
the cancer-promoting hormones and inflammatory substances that have
been identified within the bodies of cancer patients, particularly within the
tumor microenvironment.
Most of the cancer-causing substances within the tumor microenvironment
of cancer patients exist initially as a means to help the body heal the
damaged, ‘cancerous’ tissue. But due to the presence of unsaturated free
fatty acids and the toxic metabolites rendered from their oxidization, the
presence of these cancer-causing substances becomes prolonged and the
body loses its capacity to ‘switch off’ the stress metabolism and complete
the healing process.
If a cancer patient is not thrashed with so-called treatments involving
knives, poison injections and deadly high-dose ionizing radiation they often
heal cancer on their own, which is testament to the remarkable healing
capacity of the human body. And when healing foods and medicines like
oranges, coconut oil, sodium bicarbonate, red light and aspirin are
employed to enhance immunity, protect the body from oxidative damage
and inhibit the self-perpetuating cycle of stress, the tumor
microenvironment and overall environment of the body can be quickly
altered and a reduction of cancer symptoms or a complete resolution of the
disease can occur.

Moving Forward
In book 1 of this series it was established using evidence from existing
scientific publications that cancer treatments are doing far more harm than
good. This has been known for decades, and many doctors and scientists
have done everything they can to warn the public, but to this day their
warnings remain mostly unknown. I hope this series of books plays a
substantial part in making this universally understood. In this exciting age
of information, where communication between people anywhere in the
world is instant and books can be easily self-published, the opportunity to
create real, lasting change in the world has never been greater.
This shift in our understanding of cancer begins with understanding what
the disease truly is and isn’t, which has been the goal of this book. It is
with this understanding that a more rational approach to the prevention and
treatment of cancer can begin.
It can now be said with certainty that cancer is not a disease of genetic
origin, but one of damaged metabolism. And, rather than a disease
involving mutant ‘terrorist’ cells whose goal is to murder the host, cancer
cells are simply normal cells that are damaged from not getting everything
they need to function properly.
A complete evidence-based understanding of all the nutritional and lifestyle
factors that can shift the metabolism to and away from cancer is the final
objective of this book series. An evidence-based protocol for alternative
cancer treatment is all that stands between us and a world without cancer.
If you’ve made it this far in the series, it’s clear that you are willing to
‘carry your own cross’ and take responsibility for your thoughts and for
your existence. The path of seeking truth, of caring about the world around
you and wanting to make a difference can be a difficult path to walk, but
those willing to do so will be rewarded with health and the knowledge and
power to better their lives and change the world.
In the final book of this series, an evidence-based anti-cancer nutritional,
exercise and medicinal protocol will be presented so that all the most
effective healing strategies can be combined in a bulk approach to safely
and effectively prevent and reverse cancer safely and swiftly.
REFERENCES
Introduction
1. THE AMERICAN CANCER SOCIETY. (2017). ALL CANCER
FACTS & FIGURES. AVAILABLE:
HTTPS://WWW.CANCER.ORG/RESEARCH/CANCER-FACTS-
STATISTICS/ALL-CANCER-FACTS-FIGURES.HTML.
[JANUARY 31, 2017]. [BACK]
2. LIZZIE PARRY. (2014). ‘THE WAR ON CANCER MAY NEVER
BE WON’: CURE ‘COULD BE IMPOSSIBLE’ BECAUSE THE
DISEASE IS SO HIGHLY EVOLVED. MAIL ONLINE.
AVAILABLE:
HTTP://WWW.DAILYMAIL.CO.UK/HEALTH/ARTICLE-
2731765/THE-WAR-CANCER-NEVER-WON-CURE-
IMPOSSIBLE-DISEASE-HIGHLY-EVOLVED.HTML.
[JANUARY 31, 2017]. [BACK]
3. KELSEY CAMPBELL-DOLLAGHAN. (2013). INFOGRAPHIC:
HOW PEOPLE DIED IN THE 20TH CENTURY. AVAILABLE:
HTTPS://WWW.FASTCODESIGN.COM/1672161/INFOGRAPH
IC-HOW-PEOPLE-DIED-IN-THE-20TH-CENTURY.
[JANUARY 31, 2017]. [BACK]

Targeting the Tumor Microenvironment

1. SUHAIL N, BILAL N, KHAN HY, ET AL. EFFECT OF
VITAMINS C AND E ON ANTIOXIDANT STATUS OF
BREAST-CANCER PATIENTS UNDERGOING
CHEMOTHERAPY. J CLIN PHARM THER. 2012;37(1):22-6.
[BACK]
2. YUVARAJ S, PREMKUMAR VG, VIJAYASARATHY K,
GANGADARAN SG, SACHDANANDAM P. AUGMENTED
ANTIOXIDANT STATUS IN TAMOXIFEN TREATED
 POSTMENOPAUSAL WOMEN WITH BREAST CANCER ON
CO-ADMINISTRATION WITH COENZYME Q10, NIACIN
AND RIBOFLAVIN. CANCER CHEMOTHER PHARMACOL.
2008;61(6):933-41. [BACK]
3. DE CAVANAGH EM, HONEGGER AE, HOFER E, ET AL.
HIGHER OXIDATION AND LOWER ANTIOXIDANT LEVELS
IN PERIPHERAL BLOOD PLASMA AND BONE MARROW
PLASMA FROM ADVANCED CANCER PATIENTS. CANCER.
2002;94(12):3247-51. [BACK]
4. SHEEN-CHEN SM, CHEN WJ, ENG HL, CHOU FF. SERUM
CONCENTRATION OF TUMOR NECROSIS FACTOR IN
PATIENTS WITH BREAST CANCER. BREAST CANCER RES
TREAT. 1997;43(3):211-5. [BACK]
5. KAMINSKA J, KOWALSKA M, KOTOWICZ B, ET AL.
PRETREATMENT SERUM LEVELS OF CYTOKINES AND
CYTOKINE RECEPTORS IN PATIENTS WITH NON-SMALL
CELL LUNG CANCER, AND CORRELATIONS WITH
CLINICOPATHOLOGICAL FEATURES AND PROGNOSIS. M-
CSF - AN INDEPENDENT PROGNOSTIC FACTOR.
ONCOLOGY. 2006;70(2):115-25. [BACK]
6. KAMINSKA J, NOWACKI MP, KOWALSKA M, ET AL.
CLINICAL SIGNIFICANCE OF SERUM CYTOKINE
MEASUREMENTS IN UNTREATED COLORECTAL CANCER
PATIENTS: SOLUBLE TUMOR NECROSIS FACTOR
RECEPTOR TYPE I--AN INDEPENDENT PROGNOSTIC
FACTOR. TUMOUR BIOL. 2005;26(4):186-94. [BACK]
7. ISMAIL S, MAYAH W, BATTIA HE, ET AL. PLASMA
NUCLEAR FACTOR KAPPA B AND SERUM
PEROXIREDOXIN 3 IN EARLY DIAGNOSIS OF
HEPATOCELLULAR CARCINOMA. ASIAN PAC J CANCER
PREV. 2015;16(4):1657-63. [BACK]
8. SHARMA P, MATHUR K, SHARMA R, ET AL. SERUM
CORTISOL LEVEL IN LUNG CANCER PATIENTS AT
VARIOUS STAGES OF DIAGNOSIS. INTERNATIONAL
 JOURNAL OF BASIC & APPLIED PHYSIOLOGY. 2014.
AVAILABLE:
HTTP://IJBAP.WEEBLY.COM/UPLOADS/1/3/1/4/13145127/10.
PDF . [JANUARY 1, 2016]. [BACK]
9. ZEITZER JM, NOURIANI B, RISSLING MB, ET AL.
ABERRANT NOCTURNAL CORTISOL AND DISEASE
PROGRESSION IN WOMEN WITH BREAST CANCER.
BREAST CANCER RES TREAT. 2016;158(1):43-50. [BACK]
10. FABRE B, GROSMAN H, GONZALEZ D, ET AL. PROSTATE
CANCER, HIGH CORTISOL LEVELS AND COMPLEX
HORMONAL INTERACTION. ASIAN PAC J CANCER PREV.
2016;17(7):3167-71. [BACK]
11. TWOROGER SS, ELIASSEN AH, SLUSS P, HANKINSON SE.
A PROSPECTIVE STUDY OF PLASMA PROLACTIN
CONCENTRATIONS AND RISK OF PREMENOPAUSAL AND
POSTMENOPAUSAL BREAST CANCER. J CLIN ONCOL.
2007;25(12):1482-8. [BACK]
12. BHATAVDEKAR JM, PATEL DD, SHAH NG, ET AL.
PROLACTIN AS A LOCAL GROWTH PROMOTER IN
PATIENTS WITH BREAST CANCER: GCRI EXPERIENCE.
EUR J SURG ONCOL. 2000;26(6):540-7. [BACK]
13. FERNANDEZ I, TOURAINE P, GOFFIN V. PROLACTIN AND
HUMAN TUMOUROGENESIS. J NEUROENDOCRINOL.
2010;22(7):771-7. [BACK]
14. RATAJCZAK-WRONA W, JABLONSKA E, ANTONOWICZ B,
DZIEMIANCZYK D, GRABOWSKA SZ. LEVELS OF
BIOLOGICAL MARKERS OF NITRIC OXIDE IN SERUM OF
PATIENTS WITH SQUAMOUS CELL CARCINOMA OF THE
ORAL CAVITY. INT J ORAL SCI. 2013;5(3):141-5. [BACK]
15. H. HIGASHINO, M. TABUCHI, S. YAMAGATA, T. KURITA, H.
MIYA, H. MUKAI AND Y. MIYA, 2010. SERUM NITRIC
OXIDE METABOLITE LEVELS IN GROUPS OF PATIENTS
WITH VARIOUS DISEASES IN COMPARISON OF HEALTHY
 CONTROL SUBJECTS. JOURNAL OF MEDICAL SCIENCES,
10: 1-11. [BACK]
16. JOHN AP.
DYSFUNCTIONAL MITOCHONDRIA, NOT
OXYGEN INSUFFICIENCY, CAUSE CANCER CELLS TO
PRODUCE INORDINATE AMOUNTS OF LACTIC ACID: THE
IMPACT OF THIS ON THE TREATMENT OF CANCER. MED
HYPOTHESES. 2001;57(4):429-31. [BACK]
17. FISCHER
K, HOFFMANN P, VOELKL S, ET AL. INHIBITORY
EFFECT OF TUMOR CELL-DERIVED LACTIC ACID ON
HUMAN T CELLS. BLOOD. 2007;109(9):3812-9. [BACK]
18. SAN-MILLÁN
I, BROOKS GA. REEXAMINING CANCER
METABOLISM: LACTATE PRODUCTION FOR
CARCINOGENESIS COULD BE THE PURPOSE AND
EXPLANATION OF THE WARBURG EFFECT.
CARCINOGENESIS. 2016. [BACK]
19. WANG
WS, LIU C, LI WJ, ZHU P, LI JN, SUN K.
INVOLVEMENT OF CRH AND HCG IN THE INDUCTION OF
AROMATASE BY CORTISOL IN HUMAN PLACENTAL
SYNCYTIOTROPHOBLASTS. PLACENTA. 2014;35(1):30-6.
[BACK]
20. PUGH
S, THOMAS GA. PATIENTS WITH ADENOMATOUS
POLYPS AND CARCINOMAS HAVE INCREASED COLONIC
MUCOSAL PROSTAGLANDIN E2. GUT. 1994;35(5):675-8.
[BACK]
21. BENNETT A,
CHARLIER EM, MCDONALD AM, SIMPSON
JS, STAMFORD IF, ZEBRO T. PROSTAGLANDINS AND
BREAST CANCER. LANCET. 1977;2(8039):624-6. [BACK]
22. MEDINA VA,
BRENZONI PG, LAMAS DJ, ET AL. ROLE OF
HISTAMINE H4 RECEPTOR IN BREAST CANCER CELL
PROLIFERATION. FRONT BIOSCI (ELITE ED). 2011;3:1042-
60. [BACK]
23. KENNEDY L,
HODGES K, MENG F, ALPINI G, FRANCIS H.
HISTAMINE AND HISTAMINE RECEPTOR REGULATION
 OF GASTROINTESTINAL CANCERS. TRANSL
GASTROINTEST CANCER. 2012;1(3):215-227. [BACK]
24. MCCALL CM,
SHI C, KLEIN AP, ET AL. SEROTONIN
EXPRESSION IN PANCREATIC NEUROENDOCRINE
TUMORS CORRELATES WITH A TRABECULAR
HISTOLOGIC PATTERN AND LARGE DUCT
INVOLVEMENT. HUM PATHOL. 2012;43(8):1169-76. [BACK]
25. NILSSON O, AHLMAN H, ERICSON LE, SKOLNIK G,
DAHLSTRÖM A. RELEASE OF SEROTONIN FROM HUMAN
CARCINOID TUMOR CELLS IN VITRO AND GROWN IN
THE ANTERIOR EYE CHAMBER OF THE RAT. CANCER.
1986;58(3):676-84. [BACK]
26. RANGEL-HUERTA OD, AGUILERA CM, MARTIN MV, ET
AL. NORMAL OR HIGH POLYPHENOL CONCENTRATION
IN ORANGE JUICE AFFECTS ANTIOXIDANT ACTIVITY,
BLOOD PRESSURE, AND BODY WEIGHT IN OBESE OR
OVERWEIGHT ADULTS. J NUTR. 2015;145(8):1808-16.
[BACK]
27. KWATRA M, JANGRA A, MISHRA M, ET AL. NARINGIN
AND SERTRALINE AMELIORATE DOXORUBICIN-
INDUCED BEHAVIORAL DEFICITS THROUGH
MODULATION OF SEROTONIN LEVEL AND
MITOCHONDRIAL COMPLEXES PROTECTION PATHWAY
IN RAT HIPPOCAMPUS. NEUROCHEM RES.
2016;41(9):2352-66. [BACK]
28. BUSCEMIS, ROSAFIO G, ARCOLEO G, ET AL. EFFECTS OF
RED ORANGE JUICE INTAKE ON ENDOTHELIAL
FUNCTION AND INFLAMMATORY MARKERS IN ADULT
SUBJECTS WITH INCREASED CARDIOVASCULAR RISK.
AM J CLIN NUTR. 2012;95(5):1089-95. [BACK]
29. HIRATA M,
MATSUMOTO C, TAKITA M, MIYAURA C,
MASAKI I. NARINGIN SUPPRESSES OSTEOCLAST
FORMATION AND ENHANCES BONE MASS IN MICE.
JOURNAL OF HEALTH SCIENCES. 2009. VOL. 55. [BACK]
30. JIAO
HY, SU WW, LI PB, ET AL. THERAPEUTIC EFFECTS
OF NARINGIN IN A GUINEA PIG MODEL OF OVALBUMIN-
INDUCED COUGH-VARIANT ASTHMA. PULM
PHARMACOL THER. 2015;33:59-65. [BACK]
31. LIU Y,
SU WW, WANG S, LI PB. NARINGIN INHIBITS
CHEMOKINE PRODUCTION IN AN LPS-INDUCED RAW
264.7 MACROPHAGE CELL LINE. MOL MED REP.
2012;6(6):1343-50. [BACK]
32. PETERS EM, ANDERSON R, THERON AJ. ATTENUATION
OF INCREASE IN CIRCULATING CORTISOL AND
ENHANCEMENT OF THE ACUTE PHASE PROTEIN
RESPONSE IN VITAMIN C-SUPPLEMENTED
ULTRAMARATHONERS. INT J SPORTS MED.
2001;22(2):120-6. [BACK]
33. CASANUEVA E,
RIPOLL C, MEZA-CAMACHO C, COUTIÑO
B, RAMÍREZ-PEREDO J, PARRA A. POSSIBLE INTERPLAY
BETWEEN VITAMIN C DEFICIENCY AND PROLACTIN IN
PREGNANT WOMEN WITH PREMATURE RUPTURE OF
MEMBRANES: FACTS AND HYPOTHESIS. MED
HYPOTHESES. 2005;64(2):241-7. [BACK]
34. ARIVAZHAGAN L, SORIMUTHU PILLAI S. TANGERETIN, A
CITRUS PENTAMETHOXYFLAVONE, EXERTS
CYTOSTATIC EFFECT VIA P53/P21 UP-REGULATION AND
SUPPRESSES METASTASIS IN 7,12-
DIMETHYLBENZ(Α)ANTHRACENE-INDUCED RAT
MAMMARY CARCINOMA. J NUTR BIOCHEM.
2014;25(11):1140-53. [BACK]
35. CHAOCL, WENG CS, CHANG NC, LIN JS, KAO ST, HO FM.
NARINGENIN MORE EFFECTIVELY INHIBITS INDUCIBLE
NITRIC OXIDE SYNTHASE AND CYCLOOXYGENASE-2
EXPRESSION IN MACROPHAGES THAN IN MICROGLIA.
NUTR RES. 2010;30(12):858-64. [BACK]
36. RASO
GM, MELI R, DI CARLO G, PACILIO M, DI CARLO R.
INHIBITION OF INDUCIBLE NITRIC OXIDE SYNTHASE
 AND CYCLOOXYGENASE-2 EXPRESSION BY
FLAVONOIDS IN MACROPHAGE J774A.1. LIFE SCI.
2001;68(8):921-31. [BACK]
37. MORAN L, GIRALDEZ FJ, BODAS R, BENAVIDES J, PRIETO
N, ANDRES S. METABOLIC ACIDOSIS CORRECTED BY
INCLUDING ANTIOXIDANTS IN DIETS OF FATTENING
LAMBS. SMALL RUMINANT RESEARCH.2013. VOLUME
109, ISSUES 2-3, PAGES 133–135. [BACK]
38. MURUNGA AN, MIRUKA DO, DRIVER C, NKOMO FS,
COBONGELA SZ, OWIRA PM. GRAPEFRUIT DERIVED
FLAVONOID NARINGIN IMPROVES KETOACIDOSIS AND
LIPID PEROXIDATION IN TYPE 1 DIABETES RAT MODEL.
PLOS ONE. 2016;11(4):E0153241. [BACK]
39. HUANG
Z, FASCO MJ, KAMINSKY LS. INHIBITION OF
ESTRONE SULFATASE IN HUMAN LIVER MICROSOMES
BY QUERCETIN AND OTHER FLAVONOIDS. J STEROID
BIOCHEM MOL BIOL. 1997;63(1-3):9-15. [BACK]
40. BULZOMI P, BOLLI A, GALLUZZO P, LEONE S, ACCONCIA
F, MARINO M. NARINGENIN AND 17BETA-ESTRADIOL
COADMINISTRATION PREVENTS HORMONE-INDUCED
HUMAN CANCER CELL GROWTH. IUBMB LIFE.
2010;62(1):51-60. [BACK]
41. SANDERSON JT, HORDIJK J, DENISON MS, SPRINGSTEEL
MF, NANTZ MH, VAN DEN BERG M. INDUCTION AND
INHIBITION OF AROMATASE (CYP19) ACTIVITY BY
NATURAL AND SYNTHETIC FLAVONOID COMPOUNDS IN
H295R HUMAN ADRENOCORTICAL CARCINOMA CELLS.
TOXICOL SCI. 2004;82(1):70-9. [BACK]
42. KAWAI
M, HIRANO T, HIGA S, ET AL. FLAVONOIDS AND
RELATED COMPOUNDS AS ANTI-ALLERGIC
SUBSTANCES. ALLERGOL INT. 2007;56(2):113-23. [BACK]
43. PARK
HH, LEE S, SON HY, ET AL. FLAVONOIDS INHIBIT
HISTAMINE RELEASE AND EXPRESSION OF
 PROINFLAMMATORY CYTOKINES IN MAST CELLS. ARCH
PHARM RES. 2008;31(10):1303-11. [BACK]
44. RAHMANMS, THOMAS P. INTERACTIVE EFFECTS OF
HYPOXIA WITH ESTRADIOL-17Β ON TRYPTOPHAN
HYDROXYLASE ACTIVITY AND SEROTONIN LEVELS IN
THE ATLANTIC CROAKER HYPOTHALAMUS. GEN COMP
ENDOCRINOL. 2013;192:71-6. [BACK]
45. HIROI
R, MCDEVITT RA, NEUMAIER JF. ESTROGEN
SELECTIVELY INCREASES TRYPTOPHAN
HYDROXYLASE-2 MRNA EXPRESSION IN DISTINCT
SUBREGIONS OF RAT MIDBRAIN RAPHE NUCLEUS:
ASSOCIATION BETWEEN GENE EXPRESSION AND
ANXIETY BEHAVIOR IN THE OPEN FIELD. BIOL
PSYCHIATRY. 2006;60(3):288-95. [BACK]
46. PETERS
EM, ANDERSON R, NIEMAN DC, FICKL H,
JOGESSAR V. VITAMIN C SUPPLEMENTATION
ATTENUATES THE INCREASES IN CIRCULATING
CORTISOL, ADRENALINE AND ANTI-INFLAMMATORY
POLYPEPTIDES FOLLOWING ULTRAMARATHON
RUNNING. INT J SPORTS MED. 2001;22(7):537-43. [BACK]
47. VISTELLE R, GRULET H, GIBOLD C, ET AL. HIGH
PERMANENT PLASMA ADRENALINE LEVELS: A MARKER
OF ADRENAL MEDULLARY DISEASE IN MEDULLARY
THYROID CARCINOMA. CLIN ENDOCRINOL (OXF).
1991;34(2):133-8. [BACK]
48. MOJTAHEDIZ, KHADEMI B, YEHYA A, TALEBI A, FATTAHI
MJ, GHADERI A. SERUM LEVELS OF INTERLEUKINS 4
AND 10 IN HEAD AND NECK SQUAMOUS CELL
CARCINOMA. J LARYNGOL OTOL. 2012;126(2):175-9.
[BACK]
49. TANGD, KANG R, ZEH HJ, LOTZE MT. HIGH-MOBILITY
GROUP BOX 1 AND CANCER. BIOCHIM BIOPHYS ACTA.
2010;1799(1-2):131-40. [BACK]
50. LIU Y,
TAMIMI RM, COLLINS LC, ET AL. THE
ASSOCIATION BETWEEN VASCULAR ENDOTHELIAL
GROWTH FACTOR EXPRESSION IN INVASIVE BREAST
CANCER AND SURVIVAL VARIES WITH INTRINSIC
SUBTYPES AND USE OF ADJUVANT SYSTEMIC THERAPY:
RESULTS FROM THE NURSES' HEALTH STUDY. BREAST
CANCER RES TREAT. 2011;129(1):175-84. [BACK]
51. PFEIFFER
P, CLAUSEN PP, ANDERSEN K, ROSE C. LACK
OF PROGNOSTIC SIGNIFICANCE OF EPIDERMAL
GROWTH FACTOR RECEPTOR AND THE ONCOPROTEIN
P185HER-2 IN PATIENTS WITH SYSTEMICALLY
UNTREATED NON-SMALL-CELL LUNG CANCER: AN
IMMUNOHISTOCHEMICAL STUDY ON CRYOSECTIONS.
BR J CANCER. 1996;74(1):86-91. [BACK]
52. GIL M,
KIM YK, HONG SB, LEE KJ. NARINGIN
DECREASES TNF-Α AND HMGB1 RELEASE FROM LPS-
STIMULATED MACROPHAGES AND IMPROVES
SURVIVAL IN A CLP-INDUCED SEPSIS MICE. PLOS ONE.
2016;11(10):E0164186. [BACK]
53. LUOH, JIANG BH, KING SM, CHEN YC. INHIBITION OF
CELL GROWTH AND VEGF EXPRESSION IN OVARIAN
CANCER CELLS BY FLAVONOIDS. NUTR CANCER.
2008;60(6):800-9. [BACK]
54. WENZEL U,KUNTZ S, DANIEL H. FLAVONOIDS WITH
EPIDERMAL GROWTH FACTOR-RECEPTOR TYROSINE
KINASE INHIBITORY ACTIVITY STIMULATE PEPT1-
MEDIATED CEFIXIME UPTAKE INTO HUMAN
INTESTINAL EPITHELIAL CELLS. J PHARMACOL EXP
THER. 2001;299(1):351-7. [BACK]
55. CATALANO V, TURDO A, DI FRANCO S, DIELI F, TODARO
M, STASSI G. TUMOR AND ITS MICROENVIRONMENT: A
SYNERGISTIC INTERPLAY. SEMIN CANCER BIOL.
2013;23(6 PT B):522-32. [BACK]
56. MORBIDELLIL, DONNINI S, ZICHE M. ROLE OF NITRIC
OXIDE IN THE MODULATION OF ANGIOGENESIS. CURR
PHARM DES. 2003;9(7):521-30. [BACK]
57. MORBIDELLI L, DONNINI S, ZICHE M. ROLE OF NITRIC
OXIDE IN TUMOR ANGIOGENESIS. CANCER TREAT RES.
2004;117:155-67. [BACK]
58. ZICHE
M, MORBIDELLI L. NITRIC OXIDE AND
ANGIOGENESIS. J NEUROONCOL. 2000;50(1-2):139-48.
[BACK]
59. MORBIDELLI L, DONNINI S, ZICHE M. ROLE OF NITRIC
OXIDE IN TUMOR ANGIOGENESIS. CANCER TREAT RES.
2004;117:155-67. [BACK]
60. GALLOO, MASINI E, MORBIDELLI L, ET AL. ROLE OF
NITRIC OXIDE IN ANGIOGENESIS AND TUMOR
PROGRESSION IN HEAD AND NECK CANCER. J NATL
CANCER INST. 1998;90(8):587-96. [BACK]
61. VIDAL MJ,ZOCCHI MR, POGGI A, PELLEGATTA F,
CHIERCHIA SL. INVOLVEMENT OF NITRIC OXIDE IN
TUMOR CELL ADHESION TO CYTOKINE-ACTIVATED
ENDOTHELIAL CELLS. J CARDIOVASC PHARMACOL.
1992;20 SUPPL 12:S155-9. [BACK]
62. SHAVIT Y,
WEIDENFELD J, DEKEYSER FG, ET AL.
EFFECTS OF SURGICAL STRESS ON BRAIN
PROSTAGLANDIN E2 PRODUCTION AND ON THE
PITUITARY-ADRENAL AXIS: ATTENUATION BY
PREEMPTIVE ANALGESIA AND BY CENTRAL
AMYGDALA LESION. BRAIN RES. 2005;1047(1):10-7.
[BACK]
63. WOLFLED. ENHANCEMENT OF CARCINOGEN-INDUCED
MALIGNANT CELL TRANSFORMATION BY
PROSTAGLANDIN F2A. 2003; VOLUME 188, ISSUES 2-3,
PAGES 139-147. [BACK]
64. FABREB, GROSMAN H, GONZALEZ D, ET AL. PROSTATE
CANCER, HIGH CORTISOL LEVELS AND COMPLEX
HORMONAL INTERACTION. ASIAN PAC J CANCER PREV.
2016;17(7):3167-71. [BACK]
65. KIM
HM, HA KS, HWANG IC, AHN HY, YOUN CH.
RANDOM SERUM CORTISOL AS A PREDICTOR FOR
SURVIVAL OF TERMINALLY ILL PATIENTS WITH
CANCER: A PRELIMINARY STUDY. AM J HOSP PALLIAT
CARE. 2016;33(3):281-5. [BACK]
66. COHEN L, COLE SW, SOOD AK, ET AL. DEPRESSIVE
SYMPTOMS AND CORTISOL RHYTHMICITY PREDICT
SURVIVAL IN PATIENTS WITH RENAL CELL CARCINOMA:
ROLE OF INFLAMMATORY SIGNALING. PLOS ONE.
2012;7(8):E42324. [BACK]
67. SCHMIDT
M, LÖFFLER G. INDUCTION OF AROMATASE IN
STROMAL VASCULAR CELLS FROM HUMAN BREAST
ADIPOSE TISSUE DEPENDS ON CORTISOL AND GROWTH
FACTORS. FEBS LETT. 1994;341(2-3):177-81. [BACK]
68. WANG
WS, LIU C, LI WJ, ZHU P, LI JN, SUN K.
INVOLVEMENT OF CRH AND HCG IN THE INDUCTION OF
AROMATASE BY CORTISOL IN HUMAN PLACENTAL
SYNCYTIOTROPHOBLASTS. PLACENTA. 2014;35(1):30-6.
[BACK]
69. WANG
W, LI J, GE Y, ET AL. CORTISOL INDUCES
AROMATASE EXPRESSION IN HUMAN PLACENTAL
SYNCYTIOTROPHOBLASTS THROUGH THE CAMP/SP1
PATHWAY. ENDOCRINOLOGY. 2012;153(4):2012-22. [BACK]
70. WOMEN’SHEALTH INITIATIVE. AVAILABLE:
HTTPS://WWW.NHLBI.NIH.GOV/WHI/ESTRO_ALONE.HTM.
[DECEMBER 1, 2016]. [BACK]
71. SOLL C,JANG JH, RIENER MO, ET AL. SEROTONIN
PROMOTES TUMOR GROWTH IN HUMAN
HEPATOCELLULAR CANCER. HEPATOLOGY.
2010;51(4):1244-54. [BACK]
72. GURBUZN, ASHOUR AA, ALPAY SN, OZPOLAT B. DOWN-
REGULATION OF 5-HT1B AND 5-HT1D RECEPTORS
INHIBITS PROLIFERATION, CLONOGENICITY AND
INVASION OF HUMAN PANCREATIC CANCER CELLS.
PLOS ONE. 2014;9(8):E105245. [BACK]
73. PAI
VP, MARSHALL AM, HERNANDEZ LL, BUCKLEY AR,
HORSEMAN ND. ALTERED SEROTONIN PHYSIOLOGY IN
HUMAN BREAST CANCERS FAVORS PARADOXICAL
GROWTH AND CELL SURVIVAL. BREAST CANCER RES.
2009;11(6):R81. [BACK]
74. SIDDIQUI
EJ, SHABBIR MA, MIKHAILIDIS DP, MUMTAZ
FH, THOMPSON CS. THE EFFECT OF SEROTONIN AND
SEROTONIN ANTAGONISTS ON BLADDER CANCER CELL
PROLIFERATION. BJU INT. 2006;97(3):634-9. [BACK]
75. SUI
H, XU H, JI Q, ET AL. 5-HYDROXYTRYPTAMINE
RECEPTOR (5-HT1DR) PROMOTES COLORECTAL CANCER
METASTASIS BY REGULATING AXIN1/Β-CATENIN/MMP-7
SIGNALING PATHWAY. ONCOTARGET. 2015;6(28):25975-87.
[BACK]
76. KOH KJ, PEARCE AL, MARSHMAN G, FINLAY-JONES JJ,
HART PH. TEA TREE OIL REDUCES HISTAMINE-INDUCED
SKIN INFLAMMATION. BR J DERMATOL. 2002;147(6):1212-
7. [BACK]
77. ADLESIC M, VERDRENGH M, BOKAREWA M, DAHLBERG
L, FOSTER SJ, TARKOWSKI A. HISTAMINE IN
RHEUMATOID ARTHRITIS. SCAND J IMMUNOL.
2007;65(6):530-7. [BACK]
78. LEFRANCF, YEATON P, BROTCHI J, KISS R. CIMETIDINE,
AN UNEXPECTED ANTI-TUMOR AGENT, AND ITS
POTENTIAL FOR THE TREATMENT OF GLIOBLASTOMA
(REVIEW). INT J ONCOL. 2006;28(5):1021-30. [BACK]
79. HSIEH
HY, SHEN CH, LIN RI, ET AL. CYPROHEPTADINE
EXHIBITS ANTITUMOR ACTIVITY IN UROTHELIAL
CARCINOMA CELLS BY TARGETING GSK3Β TO
 SUPPRESS MTOR AND Β-CATENIN SIGNALING
PATHWAYS. CANCER LETT. 2016;370(1):56-65. [BACK]
80. HARRIS AL, SMITH IE. REGRESSION OF CARCINOID
TUMOUR WITH CYPROHEPTADINE. BR MED J (CLIN RES
ED). 1982;285(6340):475. [BACK]
81. CHOISY, COLLINS CC, GOUT PW, WANG Y. CANCER-
GENERATED LACTIC ACID: A REGULATORY,
IMMUNOSUPPRESSIVE METABOLITE?. J PATHOL.
2013;230(4):350-5. [BACK]
82. DHUP S,DADHICH RK, PORPORATO PE, SONVEAUX P.
MULTIPLE BIOLOGICAL ACTIVITIES OF LACTIC ACID IN
CANCER: INFLUENCES ON TUMOR GROWTH,
ANGIOGENESIS AND METASTASIS. CURR PHARM DES.
2012;18(10):1319-30. [BACK]
83. WAHL P,
ZINNER C, ACHTZEHN S, BLOCH W, MESTER J.
EFFECT OF HIGH- AND LOW-INTENSITY EXERCISE AND
METABOLIC ACIDOSIS ON LEVELS OF GH, IGF-I, IGFBP-3
AND CORTISOL. GROWTH HORM IGF RES. 2010;20(5):380-
5. [BACK]
84. BRANDJM, FROHN C, CZIUPKA K, BROCKMANN C,
KIRCHNER H, LUHM J. PROLACTIN TRIGGERS PRO-
INFLAMMATORY IMMUNE RESPONSES IN PERIPHERAL
IMMUNE CELLS. EUR CYTOKINE NETW. 2004;15(2):99-104.
[BACK]
85. TWOROGERSS, ELIASSEN AH, ZHANG X, ET AL. A 20-
YEAR PROSPECTIVE STUDY OF PLASMA PROLACTIN AS
A RISK MARKER OF BREAST CANCER DEVELOPMENT.
CANCER RES. 2013;73(15):4810-9. [BACK]
86. CLEVENGER,
C.V. ROLE OF PROLACTIN/PROLACTIN
RECEPTOR SIGNALING IN HUMAN BREAST CANCER.
BREAST DISEASE. 18(1):75. [BACK]
87. RECCHIONEC, GALANTE E, SECRETO G, CAVALLERI A,
DATI V. ABNORMAL SERUM HORMONE LEVELS IN LUNG
 CANCER. TUMORI. 1983;69(4):293-8. [BACK]
88. CAPURON L, RAVAUD A, NEVEU PJ, MILLER AH, MAES M,
DANTZER R. ASSOCIATION BETWEEN DECREASED
SERUM TRYPTOPHAN CONCENTRATIONS AND
DEPRESSIVE SYMPTOMS IN CANCER PATIENTS
UNDERGOING CYTOKINE THERAPY. MOL PSYCHIATRY.
2002;7(5):468-73. [BACK]
89. COPPACK SW, JENSEN MD, MILES JM. IN VIVO
REGULATION OF LIPOLYSIS IN HUMANS. J LIPID RES.
1994;35(2):177-93. [BACK]
90. LEE
CG, LINK H, BALUK P, ET AL. VASCULAR
ENDOTHELIAL GROWTH FACTOR (VEGF) INDUCES
REMODELING AND ENHANCES TH2-MEDIATED
SENSITIZATION AND INFLAMMATION IN THE LUNG. NAT
MED. 2004;10(10):1095-103. [BACK]
91. MANZOORH, QADIR MI, ABBAS K, ET AL. VASCULAR
ENDOTHELIAL GROWTH FACTOR (VEGF) IN CANCER.
AFRICAN JOURNAL OF PHARMACY AND
PHARMACOLOGY. 2014;8(37):917-923. [BACK]
92. SASAKI T, HIROKI K, YAMASHITA Y. THE ROLE OF
EPIDERMAL GROWTH FACTOR RECEPTOR IN CANCER
METASTASIS AND MICROENVIRONMENT. BIOMED RES
INT. 2013;2013:546318. [BACK]
93. KOENDERS PG, BEEX LV, KIENHUIS CB, KLOPPENBORG
PW, BENRAAD TJ. EPIDERMAL GROWTH FACTOR
RECEPTOR AND PROGNOSIS IN HUMAN BREAST
CANCER: A PROSPECTIVE STUDY. BREAST CANCER RES
TREAT. 1993;25(1):21-7. [BACK]
94. WALDNER MJ, FOERSCH S, NEURATH MF. INTERLEUKIN-
6--A KEY REGULATOR OF COLORECTAL CANCER
DEVELOPMENT. INT J BIOL SCI. 2012;8(9):1248-53. [BACK]
95. LENTZ
EK, CHERLA RP, JASPERS V, WEEKS BR, TESH VL.
ROLE OF TUMOR NECROSIS FACTOR ALPHA IN DISEASE
 USING A MOUSE MODEL OF SHIGA TOXIN-MEDIATED
RENAL DAMAGE. INFECT IMMUN. 2010;78(9):3689-99.
[BACK]
96. MOCELLIN S, ROSSI CR, PILATI P, NITTI D. TUMOR
NECROSIS FACTOR, CANCER AND ANTICANCER
THERAPY. CYTOKINE GROWTH FACTOR REV.
2005;16(1):35-53. [BACK]
97. ULICHTR, DEL CASTILLO J, NI RX, BIKHAZI N, CALVIN L.
MECHANISMS OF TUMOR NECROSIS FACTOR ALPHA-
INDUCED LYMPHOPENIA, NEUTROPENIA, AND BIPHASIC
NEUTROPHILIA: A STUDY OF LYMPHOCYTE
RECIRCULATION AND HEMATOLOGIC INTERACTIONS
OF TNF ALPHA WITH ENDOGENOUS MEDIATORS OF
LEUKOCYTE TRAFFICKING. J LEUKOC BIOL.
1989;45(2):155-67. [BACK]
98. CLARK
GC, TAYLOR MJ. TUMOR NECROSIS FACTOR
INVOLVEMENT IN THE TOXICITY OF TCDD: THE ROLE
OF ENDOTOXIN IN THE RESPONSE. EXP CLIN
IMMUNOGENET. 1994;11(2-3):136-41. [BACK]
99. DEGASPERI
GR, ROMANATTO T, DENIS RG, ET AL. UCP2
PROTECTS HYPOTHALAMIC CELLS FROM TNF-ALPHA-
INDUCED DAMAGE. FEBS LETT. 2008;582(20):3103-10.
[BACK]
100.
HAN D, HOSOKAWA T, AOIKE A, KAWAI K. AGE-
RELATED ENHANCEMENT OF TUMOR NECROSIS
FACTOR (TNF) PRODUCTION IN MICE. MECH AGEING
DEV. 1995;84(1):39-54. [BACK]
101.
SCHMIDLIN K, SPOERRI A, EGGER M, ET AL. CANCER, A
DISEASE OF AGING (PART 1) - TRENDS IN OLDER ADULT
CANCER MORTALITY IN SWITZERLAND 1991-2008. SWISS
MED WKLY. 2012;142:W13637. [BACK]
102.
 PINNA F, SAHLE S, BEUKE K, ET AL. A SYSTEMS
BIOLOGY STUDY ON NFΚB SIGNALING IN PRIMARY
MOUSE HEPATOCYTES. FRONT PHYSIOL. 2012;3:466.
[BACK]
103.
WANG S, LIU Z, WANG L, ZHANG X. NF-KAPPAB
SIGNALING PATHWAY, INFLAMMATION AND
COLORECTAL CANCER. CELL MOL IMMUNOL.
2009;6(5):327-34. [BACK]
104.
SAKAMOTO K, MAEDA S, HIKIBA Y, ET AL.
CONSTITUTIVE NF-KAPPAB ACTIVATION IN
COLORECTAL CARCINOMA PLAYS A KEY ROLE IN
ANGIOGENESIS, PROMOTING TUMOR GROWTH. CLIN
CANCER RES. 2009;15(7):2248-58. [BACK]
105.BHARTI AC, AGGARWAL BB. NUCLEAR FACTOR-
KAPPA B AND CANCER: ITS ROLE IN PREVENTION AND
THERAPY. BIOCHEM PHARMACOL. 2002;64(5-6):883-8.
[BACK]
106.
OLIVIER S, ROBE P, BOURS V. CAN NF-KAPPAB BE A
TARGET FOR NOVEL AND EFFICIENT ANTI-CANCER
AGENTS?. BIOCHEM PHARMACOL. 2006;72(9):1054-68.
[BACK]
107.
WEBER J, YANG JC, TOPALIAN SL, ET AL. PHASE I TRIAL
OF SUBCUTANEOUS INTERLEUKIN-6 IN PATIENTS WITH
ADVANCED MALIGNANCIES. J CLIN ONCOL.
1993;11(3):499-506. [BACK]
108.WEISS GR, MARGOLIN KA, SZNOL M, ET AL. A
PHASE II STUDY OF THE CONTINUOUS INTRAVENOUS
INFUSION OF INTERLEUKIN-6 FOR METASTATIC RENAL
CELL CARCINOMA. J IMMUNOTHER EMPHASIS TUMOR
IMMUNOL. 1995;18(1):52-6. [BACK]
109.
 TANG D, KANG R, ZEH HJ, LOTZE MT. HIGH-MOBILITY
GROUP BOX 1 AND CANCER. BIOCHIM BIOPHYS ACTA.
2010;1799(1-2):131-40. [BACK]
110.
OKADA S, OKUSAKA T, ISHII H, ET AL. ELEVATED
SERUM INTERLEUKIN-6 LEVELS IN PATIENTS WITH
PANCREATIC CANCER. JPN J CLIN ONCOL. 1998;28(1):12-5.
[BACK]
111.
TIAN G, MI J, WEI X, ET AL. CIRCULATING
INTERLEUKIN-6 AND CANCER: A META-ANALYSIS
USING MENDELIAN RANDOMIZATION. SCI REP.
2015;5:11394. [BACK]
112.
LOBO V, PATIL A, PHATAK A, CHANDRA N. FREE
RADICALS, ANTIOXIDANTS AND FUNCTIONAL FOODS:
IMPACT ON HUMAN HEALTH. PHARMACOGN REV.
2010;4(8):118-26. [BACK]
113.
CHEN Q, GUAN X, ZUO X, WANG J, YIN W. THE ROLE OF
HIGH MOBILITY GROUP BOX 1 (HMGB1) IN THE
PATHOGENESIS OF KIDNEY DISEASES. ACTA PHARM SIN
B. 2016;6(3):183-8. [BACK]
114.
NGUYEN DP, LI J, TEWARI AK. INFLAMMATION AND
PROSTATE CANCER: THE ROLE OF INTERLEUKIN 6 (IL-6).
BJU INT. 2014;113(6):986-92. [BACK]

Oranges
1. PATEL K, SINGH GK, PATEL DK. A REVIEW ON
PHARMACOLOGICAL AND ANALYTICAL ASPECTS OF
NARINGENIN. CHIN J INTEGR MED. 2014. [BACK]
2. NAKAJIMA VM, MADEIRA JV, MACEDO GA, MACEDO JA.
BIOTRANSFORMATION EFFECTS ON ANTI LIPOGENIC
 ACTIVITY OF CITRUS EXTRACTS. FOOD CHEM. 2016;197
PT B:1046-53. [BACK]
3. CHANET A, MILENKOVIC D, MANACH C, MAZUR A,
MORAND C. CITRUS FLAVANONES: WHAT IS THEIR ROLE
IN CARDIOVASCULAR PROTECTION?. J AGRIC FOOD
CHEM. 2012;60(36):8809-22. [BACK]
4. KNEKT P, KUMPULAINEN J, JÄRVINEN R, ET AL.
FLAVONOID INTAKE AND RISK OF CHRONIC DISEASES.
AM J CLIN NUTR. 2002;76(3):560-8. [BACK]
5. PROTEGGENTE AR, SAIJA A, DE PASQUALE A, RICE-
EVANS CA. THE COMPOSITIONAL CHARACTERISATION
AND ANTIOXIDANT ACTIVITY OF FRESH JUICES FROM
SICILIAN SWEET ORANGE (CITRUS SINENSIS L. OSBECK)
VARIETIES. FREE RADIC RES. 2003;37(6):681-7. [BACK]
6. LETAIEF H, ZEMNI H, MLIKI A, CHEBIL S. COMPOSITION
OF CITRUS SINENSIS (L.) OSBECK CV «MALTAISE DEMI-
SANGUINE» JUICE. A COMPARISON BETWEEN ORGANIC
AND CONVENTIONAL FARMING. FOOD CHEM.
2016;194:290-5. [BACK]
7. AROUI S, AOUEY B, CHTOUROU Y, MEUNIER AC, FETOUI
H, KENANI A. NARINGIN SUPPRESSES CELL METASTASIS
AND THE EXPRESSION OF MATRIX
METALLOPROTEINASES (MMP-2 AND MMP-9) VIA THE
INHIBITION OF ERK-P38-JNK SIGNALING PATHWAY IN
HUMAN GLIOBLASTOMA. CHEM BIOL INTERACT.
2016;244:195-203. [BACK]
8. AROUI S, NAJLAOUI F, CHTOUROU Y, ET AL. NARINGIN
INHIBITS THE INVASION AND MIGRATION OF HUMAN
GLIOBLASTOMA CELL VIA DOWNREGULATION OF MMP-
2 AND MMP-9 EXPRESSION AND INACTIVATION OF P38
SIGNALING PATHWAY. TUMOUR BIOL. 2016;37(3):3831-9.
[BACK]
9. RAHA S, YUMNAM S, HONG GE, ET AL. NARINGIN
INDUCES AUTOPHAGY-MEDIATED GROWTH INHIBITION
 BY DOWNREGULATING THE PI3K/AKT/MTOR CASCADE
VIA ACTIVATION OF MAPK PATHWAYS IN AGS CANCER
CELLS. INT J ONCOL. 2015;47(3):1061-9. [BACK]
10. TANTW, CHOU YE, YANG WH, HSU CJ, FONG YC, TANG
CH. NARINGIN SUPPRESS CHONDROSARCOMA
MIGRATION THROUGH INHIBITION VASCULAR
ADHESION MOLECULE-1 EXPRESSION BY MODULATING
MIR-126. INT IMMUNOPHARMACOL. 2014;22(1):107-14.
[BACK]
11. VADDER, RADHAKRISHNAN S, REDDIVARI L,
VANAMALA JK. TRIPHALA EXTRACT SUPPRESSES
PROLIFERATION AND INDUCES APOPTOSIS IN HUMAN
COLON CANCER STEM CELLS VIA SUPPRESSING C-
MYC/CYCLIN D1 AND ELEVATION OF BAX/BCL-2 RATIO.
BIOMED RES INT. 2015;2015:649263. [BACK]
12. ZENG L, ZHEN Y, CHEN Y, ET AL. NARINGIN INHIBITS
GROWTH AND INDUCES APOPTOSIS BY A MECHANISM
DEPENDENT ON REDUCED ACTIVATION OF
NF ‑ ΚB/COX ‑ 2 ‑ CASPASE-1 PATHWAY IN HELA
CERVICAL CANCER CELLS. INT J ONCOL. 2014;45(5):1929-
36. [BACK]
13. RAMESHE, ALSHATWI AA. NARINGIN INDUCES DEATH
RECEPTOR AND MITOCHONDRIA-MEDIATED APOPTOSIS
IN HUMAN CERVICAL CANCER (SIHA) CELLS. FOOD
CHEM TOXICOL. 2013;51:97-105. [BACK]
14. LI
H, YANG B, HUANG J, ET AL. NARINGIN INHIBITS
GROWTH POTENTIAL OF HUMAN TRIPLE-NEGATIVE
BREAST CANCER CELLS BY TARGETING Β-CATENIN
SIGNALING PATHWAY. TOXICOL LETT. 2013;220(3):219-28.
[BACK]
15. GUOB, ZHANG Y, HUI Q, WANG H, TAO K. NARINGIN
SUPPRESSES THE METABOLISM OF A375 CELLS BY
INHIBITING THE PHOSPHORYLATION OF C-SRC.
TUMOUR BIOL. 2016;37(3):3841-50. [BACK]
16. CAMARGO CA, GOMES-MARCONDES MC, WUTZKI NC,
AOYAMA H. NARINGIN INHIBITS TUMOR GROWTH AND
REDUCES INTERLEUKIN-6 AND TUMOR NECROSIS
FACTOR Α LEVELS IN RATS WITH WALKER 256
CARCINOSARCOMA. ANTICANCER RES. 2012;32(1):129-33.
[BACK]
17. KANNOS, TOMIZAWA A, HIURA T, ET AL. INHIBITORY
EFFECTS OF NARINGENIN ON TUMOR GROWTH IN
HUMAN CANCER CELL LINES AND SARCOMA S-180-
IMPLANTED MICE. BIOL PHARM BULL. 2005;28(3):527-30.
[BACK]
18. ZHANG YS,
LI Y, WANG Y, ET AL. NARINGIN, A NATURAL
DIETARY COMPOUND, PREVENTS INTESTINAL
TUMORIGENESIS IN APC (MIN/+) MOUSE MODEL. J
CANCER RES CLIN ONCOL. 2016;142(5):913-25. [BACK]
19. MILLEREG, PEACOCK JJ, BOURLAND TC, ET AL.
INHIBITION OF ORAL CARCINOGENESIS BY CITRUS
FLAVONOIDS. NUTR CANCER. 2008;60(1):69-74. [BACK]
20. MENON LG, KUTTAN R, KUTTAN G. INHIBITION OF LUNG
METASTASIS IN MICE INDUCED BY B16F10 MELANOMA
CELLS BY POLYPHENOLIC COMPOUNDS. CANCER LETT.
1995;95(1-2):221-5. [BACK]
21. OZÇELIK
B, KARTAL M, ORHAN I. CYTOTOXICITY,
ANTIVIRAL AND ANTIMICROBIAL ACTIVITIES OF
ALKALOIDS, FLAVONOIDS, AND PHENOLIC ACIDS.
PHARM BIOL. 2011;49(4):396-402. [BACK]
22. BLANCO-AYALA T, ANDÉRICA-ROMERO AC, PEDRAZA-
CHAVERRI J. NEW INSIGHTS INTO ANTIOXIDANT
STRATEGIES AGAINST PARAQUAT TOXICITY. FREE
RADIC RES. 2014;48(6):623-40. [BACK]
23. ADIL M,
KANDHARE AD, GHOSH P, VENKATA S,
RAYGUDE KS, BODHANKAR SL. AMELIORATIVE EFFECT
OF NARINGIN IN ACETAMINOPHEN-INDUCED HEPATIC
 AND RENAL TOXICITY IN LABORATORY RATS: ROLE OF
FXR AND KIM-1. REN FAIL. 2016;:1-14. [BACK]
24. ADIL M,KANDHARE AD, VISNAGRI A, BODHANKAR SL.
NARINGIN AMELIORATES SODIUM ARSENITE-INDUCED
RENAL AND HEPATIC TOXICITY IN RATS: DECISIVE ROLE
OF KIM-1, CASPASE-3, TGF-Β, AND TNF-Α. REN FAIL.
2015;37(8):1396-407. [BACK]
25. CHTOUROU Y, AOUEY B, AROUIS, KEBIECHE M, FETOUI
H. ANTI-APOPTOTIC AND ANTI-INFLAMMATORY
EFFECTS OF NARINGIN ON CISPLATIN-INDUCED RENAL
INJURY IN THE RAT. CHEM BIOL INTERACT. 2016;243:1-9.
[BACK]
26. TURGUTNH, KARA H, ELAGOZ S, DEVECI K, GUNGOR H,
ARSLANBAS E. THE PROTECTIVE EFFECT OF NARINGIN
AGAINST BLEOMYCIN-INDUCED PULMONARY FIBROSIS
IN WISTAR RATS. PULM MED. 2016;2016:7601393. [BACK]
27. GOLIOMYTISM, KARTSONAS N, CHARISMIADOU MA,
SYMEON GK, SIMITZIS PE, DELIGEORGIS SG. THE
INFLUENCE OF NARINGIN OR HESPERIDIN DIETARY
SUPPLEMENTATION ON BROILER MEAT QUALITY AND
OXIDATIVE STABILITY. PLOS ONE. 2015;10(10):E0141652.
[BACK]
28. PAREDES A, ALZURU M, MENDEZ J, RODRÍGUEZ-
ORTEGA M. ANTI-SINDBIS ACTIVITY OF FLAVANONES
HESPERETIN AND NARINGENIN. BIOL PHARM BULL.
2003;26(1):108-9. [BACK]
29. ADEBIYI
OO, ADEBIYI OA, OWIRA PM. NARINGIN
REVERSES HEPATOCYTE APOPTOSIS AND OXIDATIVE
STRESS ASSOCIATED WITH HIV-1 NUCLEOTIDE REVERSE
TRANSCRIPTASE INHIBITORS-INDUCED METABOLIC
COMPLICATIONS. NUTRIENTS. 2015;7(12):10352-68.
[BACK]
30. ADEBIYI
OO, ADEBIYI OA, OWIRA P. NARINGIN
IMPROVES ZIDOVUDINE- AND STAVUDINE-INDUCED
 SKELETAL MUSCLE COMPLICATIONS IN RATS. HUM EXP
TOXICOL. 2016. [BACK]
31. YIN
FM, XIAO LB, ZHANG Y. [RESEARCH PROGRESS ON
DRYNARIA FORTUNEI NARINGIN ON INFLAMMATION
AND BONE ACTIVITY]. ZHONGGUO GU SHANG.
2015;28(2):182-6. [BACK]
32. KAWAGUCHI K, MARUYAMA H, HASUNUMA R,
KUMAZAWA Y. SUPPRESSION OF INFLAMMATORY
RESPONSES AFTER ONSET OF COLLAGEN-INDUCED
ARTHRITIS IN MICE BY ORAL ADMINISTRATION OF THE
CITRUS FLAVANONE NARINGIN. IMMUNOPHARMACOL
IMMUNOTOXICOL. 2011;33(4):723-9. [BACK]
33. AHMAD SF, ZOHEIR KM, ABDEL-HAMIED HE, ET AL.
AMELIORATION OF AUTOIMMUNE ARTHRITIS BY
NARINGIN THROUGH MODULATION OF T REGULATORY
CELLS AND TH1/TH2 CYTOKINES. CELL IMMUNOL.
2014;287(2):112-20. [BACK]
34. LEE
JH, KIM GH. EVALUATION OF ANTIOXIDANT AND
INHIBITORY ACTIVITIES FOR DIFFERENT SUBCLASSES
FLAVONOIDS ON ENZYMES FOR RHEUMATOID
ARTHRITIS. J FOOD SCI. 2010;75(7):H212-7. [BACK]
35. YIN
FM, XIAO LB, ZHANG Y. [RESEARCH PROGRESS ON
DRYNARIA FORTUNEI NARINGIN ON INFLAMMATION
AND BONE ACTIVITY]. ZHONGGUO GU SHANG.
2015;28(2):182-6. [BACK]
36. XU
T, WANG L, TAO Y, JI Y, DENG F, WU XH. THE
FUNCTION OF NARINGIN IN INDUCING SECRETION OF
OSTEOPROTEGERIN AND INHIBITING FORMATION OF
OSTEOCLASTS. EVID BASED COMPLEMENT ALTERNAT
MED. 2016;2016:8981650. [BACK]
37. EPASINGHE
DJ, YIU C, BURROW MF. EFFECT OF
FLAVONOIDS ON REMINERALIZATION OF ARTIFICIAL
ROOT CARIES. AUST DENT J. 2015. [BACK]
38. ZHAO Y,
LI Z, WANG W, ET AL. NARINGIN PROTECTS
AGAINST CARTILAGE DESTRUCTION IN
OSTEOARTHRITIS THROUGH REPRESSION OF NF-ΚB
SIGNALING PATHWAY. INFLAMMATION. 2016;39(1):385-92.
[BACK]
39. CHTOUROU Y, GARGOURI B, KEBIECHE M, FETOUI H.
NARINGIN ABROGATES CISPLATIN-INDUCED
COGNITIVE DEFICITS AND CHOLINERGIC
DYSFUNCTION THROUGH THE DOWN-REGULATION OF
ACHE EXPRESSION AND INOS SIGNALING PATHWAYS IN
HIPPOCAMPUS OF AGED RATS. J MOL NEUROSCI.
2015;56(2):349-62. [BACK]
40. CHTOUROU Y, AOUEY B, KEBIECHE M, FETOUI H.
PROTECTIVE ROLE OF NARINGIN AGAINST CISPLATIN
INDUCED OXIDATIVE STRESS, INFLAMMATORY
RESPONSE AND APOPTOSIS IN RAT STRIATUM VIA
SUPPRESSING ROS-MEDIATED NF-ΚB AND P53
SIGNALING PATHWAYS. CHEM BIOL INTERACT.
2015;239:76-86. [BACK]
41. RAMALINGAYYA GV,NAMPOOTHIRI M, NAYAK PG, ET
AL. NARINGIN AND RUTIN ALLEVIATES EPISODIC
MEMORY DEFICITS IN TWO DIFFERENTIALLY
CHALLENGED OBJECT RECOGNITION TASKS.
PHARMACOGN MAG. 2016;12(SUPPL 1):S63-70. [BACK]
42. WANG DM, YANG YJ, ZHANG L, ZHANG X, GUAN FF,
ZHANG LF. NARINGIN ENHANCES CAMKII ACTIVITY
AND IMPROVES LONG-TERM MEMORY IN A MOUSE
MODEL OF ALZHEIMER'S DISEASE. INT J MOL SCI.
2013;14(3):5576-86. [BACK]
43. WANGD, GAO K, LI X, ET AL. LONG-TERM NARINGIN
CONSUMPTION REVERSES A GLUCOSE UPTAKE DEFECT
AND IMPROVES COGNITIVE DEFICITS IN A MOUSE
MODEL OF ALZHEIMER'S DISEASE. PHARMACOL
BIOCHEM BEHAV. 2012;102(1):13-20. [BACK]
44. KIMHD, JEONG KH, JUNG UJ, KIM SR. NARINGIN
TREATMENT INDUCES NEUROPROTECTIVE EFFECTS IN
A MOUSE MODEL OF PARKINSON'S DISEASE IN VIVO,
BUT NOT ENOUGH TO RESTORE THE LESIONED
DOPAMINERGIC SYSTEM. J NUTR BIOCHEM. 2016;28:140-
6. [BACK]
45. LEEME, NAM JH, JEON MT, ET AL. NARINGIN PROTECTS
THE NIGROSTRIATAL DOPAMINERGIC PROJECTION
THROUGH INDUCTION OF GDNF IN A NEUROTOXIN
MODEL OF PARKINSON'S DISEASE. J NUTR BIOCHEM.
2014;25(7):801-6. [BACK]
46. JUNGUJ, KIM SR. EFFECTS OF NARINGIN, A FLAVANONE
GLYCOSIDE IN GRAPEFRUITS AND CITRUS FRUITS, ON
THE NIGROSTRIATAL DOPAMINERGIC PROJECTION IN
THE ADULT BRAIN. NEURAL REGEN RES. 2014;9(16):1514-
7. [BACK]
47. SACHDEVA AK,
KUHAD A, CHOPRA K. NARINGIN
AMELIORATES MEMORY DEFICITS IN EXPERIMENTAL
PARADIGM OF ALZHEIMER'S DISEASE BY ATTENUATING
MITOCHONDRIAL DYSFUNCTION. PHARMACOL
BIOCHEM BEHAV. 2014;127:101-10. [BACK]
48. GOLECHHA M, SARANGAL V, BHATIA J, CHAUDHRY U,
SALUJA D, ARYA DS. NARINGIN AMELIORATES
PENTYLENETETRAZOL-INDUCED SEIZURES AND
ASSOCIATED OXIDATIVE STRESS, INFLAMMATION, AND
COGNITIVE IMPAIRMENT IN RATS: POSSIBLE
MECHANISMS OF NEUROPROTECTION. EPILEPSY
BEHAV. 2014;41:98-102. [BACK]
49. ADEBIYI OA, ADEBIYI OO, OWIRA PM. NARINGIN
REDUCES HYPERGLYCEMIA-INDUCED CARDIAC
FIBROSIS BY RELIEVING OXIDATIVE STRESS. PLOS ONE.
2016;11(3):E0149890. [BACK]
50. DHANYA R, ARUN
KB, NISHA VM, ET AL.
PRECONDITIONING L6 MUSCLE CELLS WITH NARINGIN
 AMELIORATES OXIDATIVE STRESS AND INCREASES
GLUCOSE UPTAKE. PLOS ONE. 2015;10(7):E0132429.
[BACK]
51. WANGD, YAN J, CHEN J, WU W, ZHU X, WANG Y.
NARINGIN IMPROVES NEURONAL INSULIN SIGNALING,
BRAIN MITOCHONDRIAL FUNCTION, AND COGNITIVE
FUNCTION IN HIGH-FAT DIET-INDUCED OBESE MICE.
CELL MOL NEUROBIOL. 2015;35(7):1061-71. [BACK]
52. CHEN
F, ZHANG N, MA X, ET AL. NARINGIN ALLEVIATES
DIABETIC KIDNEY DISEASE THROUGH INHIBITING
OXIDATIVE STRESS AND INFLAMMATORY REACTION.
PLOS ONE. 2015;10(11):E0143868. [BACK]
53. SUN
X, LI F, MA X, ET AL. THE EFFECTS OF COMBINED
TREATMENT WITH NARINGIN AND TREADMILL
EXERCISE ON OSTEOPOROSIS IN OVARIECTOMIZED
RATS. SCI REP. 2015;5:13009. [BACK]
54. ANUJA GI,
LATHA PG, SUJA SR, ET AL. ANTI-
INFLAMMATORY AND ANALGESIC PROPERTIES OF
DRYNARIA QUERCIFOLIA (L.) J. SMITH. J
ETHNOPHARMACOL. 2010;132(2):456-60. [BACK]
55. KANDHARE AD, ALAM J, PATIL MV, SINHA A,
BODHANKAR SL. WOUND HEALING POTENTIAL OF
NARINGIN OINTMENT FORMULATION VIA REGULATING
THE EXPRESSION OF INFLAMMATORY, APOPTOTIC AND
GROWTH MEDIATORS IN EXPERIMENTAL RATS. PHARM
BIOL. 2016;54(3):419-32. [BACK]
56. CHANET A,
MILENKOVIC D, DEVAL C, ET AL. NARINGIN,
THE MAJOR GRAPEFRUIT FLAVONOID, SPECIFICALLY
AFFECTS ATHEROSCLEROSIS DEVELOPMENT IN DIET-
INDUCED HYPERCHOLESTEROLEMIA IN MICE. J NUTR
BIOCHEM. 2012;23(5):469-77. [BACK]
57. ETXEBERRIA U,
DE LA GARZA AL, MARTÍINEZ JA,
MILAGRO I. BIOCOMPOUNDS ATTENUATING THE
DEVELOPMENT OF OBESITY AND INSULIN RESISTANCE
 PRODUCED BY A HIGH-FAT SUCROSE DIET. NAT PROD
COMMUN. 2015;10(8):1417-20. [BACK]
58. NAKAJIMA VM, MADEIRA JV, MACEDO GA, MACEDO JA.
BIOTRANSFORMATION EFFECTS ON ANTI LIPOGENIC
ACTIVITY OF CITRUS EXTRACTS. FOOD CHEM. 2016;197
PT B:1046-53. [BACK]
59. STOHS
SJ, BADMAEV V. A REVIEW OF NATURAL
STIMULANT AND NON-STIMULANT THERMOGENIC
AGENTS. PHYTOTHER RES. 2016;30(5):732-40. [BACK]
60. MANNA K,
DAS U, DAS D, ET AL. NARINGIN INHIBITS
GAMMA RADIATION-INDUCED OXIDATIVE DNA
DAMAGE AND INFLAMMATION, BY MODULATING P53
AND NF-ΚB SIGNALING PATHWAYS IN MURINE
SPLENOCYTES. FREE RADIC RES. 2015;49(4):422-39.
[BACK]
61. RENX, SHI Y, ZHAO D, ET AL. NARINGIN PROTECTS
ULTRAVIOLET B-INDUCED SKIN DAMAGE BY
REGULATING P38 MAPK SIGNAL PATHWAY. J DERMATOL
SCI. 2016;82(2):106-14. [BACK]
62. TAKEKOSHI
S, NAGATA H, KITATANI K. FLAVONOIDS
ENHANCE MELANOGENESIS IN HUMAN MELANOMA
CELLS. TOKAI J EXP CLIN MED. 2014;39(3):116-21. [BACK]
63. JIAO
HY, SU WW, LI PB, ET AL. THERAPEUTIC EFFECTS
OF NARINGIN IN A GUINEA PIG MODEL OF OVALBUMIN-
INDUCED COUGH-VARIANT ASTHMA. PULM
PHARMACOL THER. 2015;33:59-65. [BACK]
64. CASEY SC, AMEDEI A, AQUILANOK, ET AL. CANCER
PREVENTION AND THERAPY THROUGH THE
MODULATION OF THE TUMOR MICROENVIRONMENT.
SEMIN CANCER BIOL. 2015;35 SUPPL:S199-223. [BACK]
65. SUN Y,
GU J. [STUDY ON EFFECT OF NARINGENIN IN
INHIBITING MIGRATION AND INVASION OF BREAST
CANCER CELLS AND ITS MOLECULAR MECHANISM].
 ZHONGGUO ZHONG YAO ZA ZHI. 2015;40(6):1144-50.
[BACK]
66. SONGHM, PARK GH, EO HJ, ET AL. ANTI-PROLIFERATIVE
EFFECT OF NARINGENIN THROUGH P38-DEPENDENT
DOWNREGULATION OF CYCLIN D1 IN HUMAN
COLORECTAL CANCER CELLS. BIOMOL THER (SEOUL).
2015;23(4):339-44. [BACK]
67. YEN
HR, LIU CJ, YEH CC. NARINGENIN SUPPRESSES TPA-
INDUCED TUMOR INVASION BY SUPPRESSING
MULTIPLE SIGNAL TRANSDUCTION PATHWAYS IN
HUMAN HEPATOCELLULAR CARCINOMA CELLS. CHEM
BIOL INTERACT. 2015;235:1-9. [BACK]
68. MAGGIONI
D, NICOLINI G, RIGOLIO R, ET AL.
MYRICETIN AND NARINGENIN INHIBIT HUMAN
SQUAMOUS CELL CARCINOMA PROLIFERATION AND
MIGRATION IN VITRO. NUTR CANCER. 2014;66(7):1257-67.
[BACK]
69. LIAO AC,
KUO CC, HUANG YC, ET AL. NARINGENIN
INHIBITS MIGRATION OF BLADDER CANCER CELLS
THROUGH DOWNREGULATION OF AKT AND MMP ‑ 2.
MOL MED REP. 2014;10(3):1531-6. [BACK]
70. LOU
C, ZHANG F, YANG M, ET AL. NARINGENIN
DECREASES INVASIVENESS AND METASTASIS BY
INHIBITING TGF-Β-INDUCED EPITHELIAL TO
MESENCHYMAL TRANSITION IN PANCREATIC CANCER
CELLS. PLOS ONE. 2012;7(12). [BACK]
71. BAOL, LIU F, GUO HB, ET AL. NARINGENIN INHIBITS
PROLIFERATION, MIGRATION, AND INVASION AS WELL
AS INDUCES APOPTOSIS OF GASTRIC CANCER SGC7901
CELL LINE BY DOWNREGULATION OF AKT PATHWAY.
TUMOUR BIOL. 2016. [BACK]
72. SONG
HM, PARK GH, EO HJ, JEONG JB. NARINGENIN-
MEDIATED ATF3 EXPRESSION CONTRIBUTES TO
 APOPTOSIS IN HUMAN COLON CANCER. BIOMOL THER
(SEOUL). 2016;24(2):140-6. [BACK]
73. ABAZA MS, ORABI KY, AL-QUATTAN E, AL-ATTIYAH RJ.
GROWTH INHIBITORY AND CHEMO-SENSITIZATION
EFFECTS OF NARINGENIN, A NATURAL FLAVANONE
PURIFIED FROM THYMUS VULGARIS, ON HUMAN
BREAST AND COLORECTAL CANCER. CANCER CELL INT.
2015;15:46. [BACK]
74. AYOB Z, MOHD BOHARI SP, ABD SAMAD A, JAMIL S.
CYTOTOXIC ACTIVITIES AGAINST BREAST CANCER
CELLS OF LOCAL JUSTICIA GENDARUSSA CRUDE
EXTRACTS. EVID BASED COMPLEMENT ALTERNAT MED.
2014. [BACK]
75. LI
RF, FENG YQ, CHEN JH, GE LT, XIAO SY, ZUO XL.
NARINGENIN SUPPRESSES K562 HUMAN LEUKEMIA
CELL PROLIFERATION AND AMELIORATES
ADRIAMYCIN-INDUCED OXIDATIVE DAMAGE IN
POLYMORPHONUCLEAR LEUKOCYTES. EXP THER MED.
2015;9(3):697-706. [BACK]
76. AHAMAD MS, SIDDIQUI S, JAFRI A, AHMAD S, AFZAL M,
ARSHAD M. INDUCTION OF APOPTOSIS AND
ANTIPROLIFERATIVE ACTIVITY OF NARINGENIN IN
HUMAN EPIDERMOID CARCINOMA CELL THROUGH ROS
GENERATION AND CELL CYCLE ARREST. PLOS ONE.
2014;9(10):E110003. [BACK]
77. ARUL D, SUBRAMANIAN P. NARINGENIN (CITRUS
FLAVONONE) INDUCES GROWTH INHIBITION, CELL
CYCLE ARREST AND APOPTOSIS IN HUMAN
HEPATOCELLULAR CARCINOMA CELLS. PATHOL ONCOL
RES. 2013;19(4):763-70. [BACK]
78. EKAMBARAM G, RAJENDRAN P, MAGESH V,
SAKTHISEKARAN D. NARINGENIN REDUCES TUMOR
SIZE AND WEIGHT LOST IN N-METHYL-N'-NITRO-N-
NITROSOGUANIDINE-INDUCED GASTRIC
 CARCINOGENESIS IN RATS. NUTR RES. 2008;28(2):106-12.
[BACK]
79. QIN
L, JIN L, LU L, ET AL. NARINGENIN REDUCES LUNG
METASTASIS IN A BREAST CANCER RESECTION MODEL.
PROTEIN CELL. 2011;2(6):507-16. [BACK]
80. SABARINATHAN D, MAHALAKSHMI P, VANISREE AJ.
NARINGENIN, A FLAVANONE INHIBITS THE
PROLIFERATION OF CEREBRALLY IMPLANTED C6
GLIOMA CELLS IN RATS. CHEM BIOL INTERACT.
2011;189(1-2):26-36. [BACK]
81. BODDULURU LN, KASALA ER, MADHANA RM, ET AL.
NARINGENIN AMELIORATES INFLAMMATION AND CELL
PROLIFERATION IN BENZO(A)PYRENE INDUCED
PULMONARY CARCINOGENESIS BY MODULATING
CYP1A1, NFΚB AND PCNA EXPRESSION. INT
IMMUNOPHARMACOL. 2016;30:102-10. [BACK]
82. SABARINATHAN D, MAHALAKSHMI P, VANISREE AJ.
NARINGENIN PROMOTE APOPTOSIS IN CEREBRALLY
IMPLANTED C6 GLIOMA CELLS. MOL CELL BIOCHEM.
2010;345(1-2):215-22. [BACK]
83. SHI
D, XU Y, DU X, ET AL. CO-TREATMENT OF THP-1
CELLS WITH NARINGENIN AND CURCUMIN INDUCES
CELL CYCLE ARREST AND APOPTOSIS VIA NUMEROUS
PATHWAYS. MOL MED REP. 2015;12(6):8223-8. [BACK]
84. TORRICELLI
P, RICCI P, PROVENZANO B, LENTINI A,
TABOLACCI C. SYNERGIC EFFECT OF Α-TOCOPHEROL
AND NARINGENIN IN TRANSGLUTAMINASE-INDUCED
DIFFERENTIATION OF HUMAN PROSTATE CANCER
CELLS. AMINO ACIDS. 2011;41(5):1207-14. [BACK]
85. BULZOMIP, BOLLI A, GALLUZZO P, ACCONCIA F,
ASCENZI P, MARINO M. THE NARINGENIN-INDUCED
PROAPOPTOTIC EFFECT IN BREAST CANCER CELL LINES
HOLDS OUT AGAINST A HIGH BISPHENOL A
BACKGROUND. IUBMB LIFE. 2012;64(8):690-6. [BACK]
86. KUMARSP, BIRUNDHA K, KAVERI K, DEVI KT.
ANTIOXIDANT STUDIES OF CHITOSAN NANOPARTICLES
CONTAINING NARINGENIN AND THEIR CYTOTOXICITY
EFFECTS IN LUNG CANCER CELLS. INT J BIOL
MACROMOL. 2015;78:87-95. [BACK]
87. FOUAD AA, ALBUALI
WH, JRESAT I. PROTECTIVE
EFFECT OF NARINGENIN AGAINST
LIPOPOLYSACCHARIDE-INDUCED ACUTE LUNG INJURY
IN RATS. PHARMACOLOGY. 2016;97(5-6):224-32. [BACK]
88. MOSTAFA HEL-S, ABD EL-BASET SA, KATTAIA AA, ZIDAN
RA, AL SADEK MM. EFFICACY OF NARINGENIN AGAINST
PERMETHRIN-INDUCED TESTICULAR TOXICITY IN RATS.
INT J EXP PATHOL. 2016;97(1):37-49. [BACK]
89. CHTOUROU Y,
SLIMA AB, GDOURA R, FETOUI H.
NARINGENIN MITIGATES IRON-INDUCED ANXIETY-LIKE
BEHAVIORAL IMPAIRMENT, MITOCHONDRIAL
DYSFUNCTIONS, ECTONUCLEOTIDASES AND
ACETYLCHOLINESTERASE ALTERATION ACTIVITIES IN
RAT HIPPOCAMPUS. NEUROCHEM RES. 2015;40(8):1563-
75. [BACK]
90. SACHDEVA S,PANT SC, KUSHWAHA P, BHARGAVA R,
FLORA SJ. SODIUM TUNGSTATE INDUCED
NEUROLOGICAL ALTERATIONS IN RAT BRAIN REGIONS
AND THEIR RESPONSE TO ANTIOXIDANTS. FOOD CHEM
TOXICOL. 2015;82:64-71. [BACK]
91. LIN
JL, WANG YD, MA Y, ET AL. PROTECTIVE EFFECTS OF
NARINGENIN EYE DROPS ON N-METHYL-N-
NITROSOUREA-INDUCED PHOTORECEPTOR CELL
DEATH IN RATS. INT J OPHTHALMOL. 2014;7(3):391-6.
[BACK]
92. NAHMIAS Y,
GOLDWASSER J, CASALI M, ET AL.
APOLIPOPROTEIN B-DEPENDENT HEPATITIS C VIRUS
SECRETION IS INHIBITED BY THE GRAPEFRUIT
 FLAVONOID NARINGENIN. HEPATOLOGY. 2008;47(5):1437-
45. [BACK]
93. PAREDES A, ALZURU M, MENDEZ J, RODRÍGUEZ-
ORTEGA M. ANTI-SINDBIS ACTIVITY OF FLAVANONES
HESPERETIN AND NARINGENIN. BIOL PHARM BULL.
2003;26(1):108-9. [BACK]
94. PINHO-RIBEIRO
FA, ZARPELON AC, FATTORI V, ET AL.
NARINGENIN REDUCES INFLAMMATORY PAIN IN MICE.
NEUROPHARMACOLOGY. 2016;105:508-519. [BACK]
95. MANCHOPE MF, CALIXTO-CAMPOS C, COELHO-SILVA L,
ET AL. NARINGENIN INHIBITS SUPEROXIDE ANION-
INDUCED INFLAMMATORY PAIN: ROLE OF OXIDATIVE
STRESS, CYTOKINES, NRF-2 AND THE NO-CGMP-PKG-
KATPCHANNEL SIGNALING PATHWAY. PLOS ONE.
2016;11(4). [BACK]
96. ORŠOLIĆ
N, GOLUŽA E, DIKIĆ D, ET AL. ROLE OF
FLAVONOIDS ON OXIDATIVE STRESS AND MINERAL
CONTENTS IN THE RETINOIC ACID-INDUCED BONE LOSS
MODEL OF RAT. EUR J NUTR. 2014;53(5):1217-27. [BACK]
97. LA VD,
TANABE S, GRENIER D. NARINGENIN INHIBITS
HUMAN OSTEOCLASTOGENESIS AND OSTEOCLASTIC
BONE RESORPTION. J PERIODONT RES. 2009;44(2):193-8.
[BACK]
98. MING
LG, LV X, MA XN, ET AL. THE PRENYL GROUP
CONTRIBUTES TO ACTIVITIES OF PHYTOESTROGEN 8-
PRENYNARINGENIN IN ENHANCING BONE FORMATION
AND INHIBITING BONE RESORPTION IN VITRO.
ENDOCRINOLOGY. 2013;154(3):1202-14. [BACK]
99. MINGLG, GE BF, WANG MG, CHEN KM. COMPARISON
BETWEEN 8-PRENYLNARIGENIN AND NARIGENIN
CONCERNING THEIR ACTIVITIES ON PROMOTION OF
RAT BONE MARROW STROMAL CELLS' OSTEOGENIC
DIFFERENTIATION IN VITRO. CELL PROLIF.
2012;45(6):508-15. [BACK]
100.
AMAT-UR-RASOOL H, AHMED M. DESIGNING SECOND
GENERATION ANTI-ALZHEIMER COMPOUNDS AS
INHIBITORS OF HUMAN ACETYLCHOLINESTERASE:
COMPUTATIONAL SCREENING OF SYNTHETIC
MOLECULES AND DIETARY PHYTOCHEMICALS. PLOS
ONE. 2015;10(9). [BACK]
101.
GHOFRANI S, JOGHATAEI MT, MOHSENI S, ET AL.
NARINGENIN IMPROVES LEARNING AND MEMORY IN
AN ALZHEIMER'S DISEASE RAT MODEL: INSIGHTS INTO
THE UNDERLYING MECHANISMS. EUR J PHARMACOL.
2015;764:195-201. [BACK]
102.
CHTOUROU Y, FETOUI H, GDOURA R. PROTECTIVE
EFFECTS OF NARINGENIN ON IRON-OVERLOAD-
INDUCED CEREBRAL CORTEX NEUROTOXICITY
CORRELATED WITH OXIDATIVE STRESS. BIOL TRACE
ELEM RES. 2014;158(3):376-83. [BACK]
103.
ZBARSKY V, DATLA KP, PARKAR S, RAI DK, ARUOMA OI,
DEXTER DT. NEUROPROTECTIVE PROPERTIES OF THE
NATURAL PHENOLIC ANTIOXIDANTS CURCUMIN AND
NARINGENIN BUT NOT QUERCETIN AND FISETIN IN A 6-
OHDA MODEL OF PARKINSON'S DISEASE. FREE RADIC
RES. 2005;39(10):1119-25. [BACK]
104.
LIM W, SONG G. NARINGENIN-INDUCED MIGRATION OF
EMBRYNOIC TROPHECTODERM CELLS IS MEDIATED VIA
PI3K/AKT AND ERK1/2 MAPK SIGNALING CASCADES.
MOL CELL ENDOCRINOL. 2016;428:28-37. [BACK]
105.
YI LT, LI CF, ZHAN X, ET AL. INVOLVEMENT OF
MONOAMINERGIC SYSTEM IN THE ANTIDEPRESSANT-
LIKE EFFECT OF THE FLAVONOID NARINGENIN IN MICE.
PROG NEUROPSYCHOPHARMACOL BIOL PSYCHIATRY.
2010;34(7):1223-8. [BACK]
106.
YI LT, LIU BB, LI J, ET AL. BDNF SIGNALING IS
NECESSARY FOR THE ANTIDEPRESSANT-LIKE EFFECT
OF NARINGENIN. PROG NEUROPSYCHOPHARMACOL
BIOL PSYCHIATRY. 2014;48:135-41. [BACK]
107. YI LT, LI J, LI HC, ET AL. ANTIDEPRESSANT-LIKE
BEHAVIORAL, NEUROCHEMICAL AND
NEUROENDOCRINE EFFECTS OF NARINGENIN IN THE
MOUSE REPEATED TAIL SUSPENSION TEST. PROG
NEUROPSYCHOPHARMACOL BIOL PSYCHIATRY.
2012;39(1):175-81. [BACK]
108.
OZKAYA A, SAHIN Z, DAG U, OZKARACA M. EFFECTS OF
NARINGENIN ON OXIDATIVE STRESS AND
HISTOPATHOLOGICAL CHANGES IN THE LIVER OF LEAD
ACETATE ADMINISTERED RATS. J BIOCHEM MOL
TOXICOL. 2016;30(5):243-8. [BACK]
109.
ROY S, AHMED F, BANERJEE S, SAHA U. NARINGENIN
AMELIORATES STREPTOZOTOCIN-INDUCED DIABETIC
RAT RENAL IMPAIRMENT BY DOWNREGULATION OF
TGF-Β1 AND IL-1 VIA MODULATION OF OXIDATIVE
STRESS CORRELATES WITH DECREASED APOPTOTIC
EVENTS. PHARM BIOL. 2016;:1-12. [BACK]
110.
REN B, QIN W, WU F, ET AL. APIGENIN AND
NARINGENIN REGULATE GLUCOSE AND LIPID
METABOLISM, AND AMELIORATE VASCULAR
DYSFUNCTION IN TYPE 2 DIABETIC RATS. EUR J
PHARMACOL. 2016;773:13-23. [BACK]
111.BHATTACHARYA S, OKSBJERG N, YOUNG JF,
JEPPESEN PB. CAFFEIC ACID, NARINGENIN AND
QUERCETIN ENHANCE GLUCOSE-STIMULATED INSULIN
SECRETION AND GLUCOSE SENSITIVITY IN INS-1E
CELLS. DIABETES OBES METAB. 2014;16(7):602-12.
[BACK]
112.
HABAUZIT V, VERNY MA, MILENKOVIC D, ET AL.
FLAVANONES PROTECT FROM ARTERIAL STIFFNESS IN
POSTMENOPAUSAL WOMEN CONSUMING GRAPEFRUIT
JUICE FOR 6 MO: A RANDOMIZED, CONTROLLED,
CROSSOVER TRIAL. AM J CLIN NUTR. 2015;102(1):66-74.
[BACK]
113.
ORHAN IE, NABAVI SF, DAGLIA M, TENORE GC,
MANSOURI K, NABAVI SM. NARINGENIN AND
ATHEROSCLEROSIS: A REVIEW OF LITERATURE. CURR
PHARM BIOTECHNOL. 2015;16(3):245-51. [BACK]
114.
ZHANG N, YANG Z, YUAN Y, ET AL. NARINGENIN
ATTENUATES PRESSURE OVERLOAD-INDUCED
CARDIAC HYPERTROPHY. EXP THER MED.
2015;10(6):2206-2212. [BACK]
115.
LI YR, CHEN DY, CHU CL, ET AL. NARINGENIN INHIBITS
DENDRITIC CELL MATURATION AND HAS THERAPEUTIC
EFFECTS IN A MURINE MODEL OF COLLAGEN-INDUCED
ARTHRITIS. J NUTR BIOCHEM. 2015;26(12):1467-78.
[BACK]
116. DU G, JIN L, HAN X, SONG Z, ZHANG H, LIANG W.
NARINGENIN: A POTENTIAL IMMUNOMODULATOR FOR
INHIBITING LUNG FIBROSIS AND METASTASIS. CANCER
RES. 2009;69(7):3205-12. [BACK]
117.
QIN L, JIN L, LU L, ET AL. NARINGENIN REDUCES LUNG
METASTASIS IN A BREAST CANCER RESECTION MODEL.
PROTEIN CELL. 2011;2(6):507-16. [BACK]
118.NASR-BOUZAIENE N, SASSI A, BEDOUI A, KRIFA M,
CHEKIR-GHEDIRA L, GHEDIRA K.
IMMUNOMODULATORY AND CELLULAR ANTIOXIDANT
ACTIVITIES OF PURE COMPOUNDS FROM TEUCRIUM
RAMOSISSIMUM DESF. TUMOUR BIOL. 2015. [BACK]
119.KIM JH, LEE JK. NARINGENIN ENHANCES NK CELL
LYSIS ACTIVITY BY INCREASING THE EXPRESSION OF
NKG2D LIGANDS ON BURKITT'S LYMPHOMA CELLS.
ARCH PHARM RES. 2015;38(11):2042-8. [BACK]
120.
FARZAEI MH, RAHIMI R, ABDOLLAHI M. THE ROLE OF
DIETARY POLYPHENOLS IN THE MANAGEMENT OF
INFLAMMATORY BOWEL DISEASE. CURR PHARM
BIOTECHNOL. 2015;16(3):196-210. [BACK]
121.AL-REJAIE SS, ABUOHASHISH HM, AL-ENAZI MM,
AL-ASSAF AH, PARMAR MY, AHMED MM. PROTECTIVE
EFFECT OF NARINGENIN ON ACETIC ACID-INDUCED
ULCERATIVE COLITIS IN RATS. WORLD J
GASTROENTEROL. 2013;19(34):5633-44. [BACK]
122.
AZUMA T, SHIGESHIRO M, KODAMA M, TANABE S,
SUZUKI T. SUPPLEMENTAL NARINGENIN PREVENTS
INTESTINAL BARRIER DEFECTS AND INFLAMMATION IN
COLITIC MICE. J NUTR. 2013;143(6):827-34. [BACK]
123.
CHATTOPADHYAY D, SEN S, CHATTERJEE R, ROY D,
JAMES J, THIRUMURUGAN K. CONTEXT- AND DOSE-
DEPENDENT MODULATORY EFFECTS OF NARINGENIN
ON SURVIVAL AND DEVELOPMENT OF DROSOPHILA
MELANOGASTER. BIOGERONTOLOGY. 2016;17(2):383-93.
[BACK]
124.ASSINI JM, MULVIHILL EE, BURKE AC, ET AL.
NARINGENIN PREVENTS OBESITY, HEPATIC STEATOSIS,
AND GLUCOSE INTOLERANCE IN MALE MICE
INDEPENDENT OF FIBROBLAST GROWTH FACTOR 21.
ENDOCRINOLOGY. 2015;156(6):2087-102. [BACK]
125. KE JY, COLE RM, HAMAD EM, ET AL. CITRUS
FLAVONOID, NARINGENIN, INCREASES LOCOMOTOR
ACTIVITY AND REDUCES DIACYLGLYCEROL
ACCUMULATION IN SKELETAL MUSCLE OF OBESE
OVARIECTOMIZED MICE. MOL NUTR FOOD RES.
2016;60(2):313-24. [BACK]
126.
KUMAR S, TIKU AB. BIOCHEMICAL AND MOLECULAR
MECHANISMS OF RADIOPROTECTIVE EFFECTS OF
NARINGENIN, A PHYTOCHEMICAL FROM CITRUS
FRUITS. J AGRIC FOOD CHEM. 2016;64(8):1676-85. [BACK]
127.
JUNG SK, HA SJ, JUNG CH, ET AL. NARINGENIN
TARGETS ERK2 AND SUPPRESSES UVB-INDUCED
PHOTOAGING. J CELL MOL MED. 2016;20(5):909-19.
[BACK]
128. MARTINEZ RM, PINHO-RIBEIRO FA, STEFFEN VS, ET
AL. TOPICAL FORMULATION CONTAINING NARINGENIN:
EFFICACY AGAINST ULTRAVIOLET B IRRADIATION-
INDUCED SKIN INFLAMMATION AND OXIDATIVE
STRESS IN MICE. PLOS ONE. 2016;11(1):E0146296. [BACK]
129. MARTINEZ RM, PINHO-RIBEIRO FA, STEFFEN VS, ET
AL. NARINGENIN INHIBITS UVB IRRADIATION-INDUCED
INFLAMMATION AND OXIDATIVE STRESS IN THE SKIN
OF HAIRLESS MICE. J NAT PROD. 2015;78(7):1647-55.
[BACK]
130.
KAWAKAMI CM, GASPAR LR. MANGIFERIN AND
NARINGENIN AFFECT THE PHOTOSTABILITY AND
PHOTOTOXICITY OF SUNSCREENS CONTAINING
AVOBENZONE. J PHOTOCHEM PHOTOBIOL B, BIOL.
2015;151:239-47. [BACK]
131.
 NASR BOUZAIENE N, CHAABANE F, SASSI A, CHEKIR-
GHEDIRA L, GHEDIRA K. EFFECT OF APIGENIN-7-
GLUCOSIDE, GENKWANIN AND NARINGENIN ON
TYROSINASE ACTIVITY AND MELANIN SYNTHESIS IN
B16F10 MELANOMA CELLS. LIFE SCI. 2016;144:80-5.
[BACK]
132.
LIU Y, WANG P, CHEN F, ET AL. ROLE OF PLANT
POLYPHENOLS IN ACRYLAMIDE FORMATION AND
ELIMINATION. FOOD CHEM. 2015;186:46-53. [BACK]
133.
KEILER AM, DÖRFELT P, CHATTERJEE N, ET AL.
ASSESSMENT OF THE EFFECTS OF NARINGENIN-TYPE
FLAVANONES IN UTERUS AND VAGINA. J STEROID
BIOCHEM MOL BIOL. 2015;145:49-57. [BACK]
134.
LEE CJ, WILSON L, JORDAN MA, NGUYEN V, TANG J,
SMIYUN G. HESPERIDIN SUPPRESSED PROLIFERATIONS
OF BOTH HUMAN BREAST CANCER AND ANDROGEN-
DEPENDENT PROSTATE CANCER CELLS. PHYTOTHER
RES. 2010;24 SUPPL 1:S15-9. [BACK]
135.
CHOI EJ. HESPERETIN INDUCED G1-PHASE CELL CYCLE
ARREST IN HUMAN BREAST CANCER MCF-7 CELLS:
INVOLVEMENT OF CDK4 AND P21. NUTR CANCER.
2007;59(1):115-9. [BACK]
136.
BRACKE M, VYNCKE B, OPDENAKKER G, FOIDART JM,
DE PESTEL G, MAREEL M. EFFECT OF CATECHINS AND
CITRUS FLAVONOIDS ON INVASION IN VITRO. CLIN EXP
METASTASIS. 1991;9(1):13-25. [BACK]
137.
BANJERDPONGCHAI R, WUDTIWAI B, KHAW-ON P,
RACHAKHOM W, DUANGNIL N, KONGTAWELERT P.
HESPERIDIN FROM CITRUS SEED INDUCES HUMAN
HEPATOCELLULAR CARCINOMA HEPG2 CELL
APOPTOSIS VIA BOTH MITOCHONDRIAL AND DEATH
RECEPTOR PATHWAYS. TUMOUR BIOL. 2016;37(1):227-37.
[BACK]
138.
NAZARI M, GHORBANI A, HEKMAT-DOOST A, JEDDI-
TEHRANI M, ZAND H. INACTIVATION OF NUCLEAR
FACTOR-ΚB BY CITRUS FLAVANONE HESPERIDIN
CONTRIBUTES TO APOPTOSIS AND CHEMO-SENSITIZING
EFFECT IN RAMOS CELLS. EUR J PHARMACOL.
2011;650(2-3):526-33. [BACK]
139.
PARK HJ, KIM MJ, HA E, CHUNG JH. APOPTOTIC EFFECT
OF HESPERIDIN THROUGH CASPASE3 ACTIVATION IN
HUMAN COLON CANCER CELLS, SNU-C4.
PHYTOMEDICINE. 2008;15(1-2):147-51. [BACK]
140.
GHORBANI A, NAZARI M, JEDDI-TEHRANI M, ZAND H.
THE CITRUS FLAVONOID HESPERIDIN INDUCES P53 AND
INHIBITS NF-ΚB ACTIVATION IN ORDER TO TRIGGER
APOPTOSIS IN NALM-6 CELLS: INVOLVEMENT OF PPARΓ-
DEPENDENT MECHANISM. EUR J NUTR. 2012;51(1):39-46.
[BACK]
141. ADAN A, BARAN Y. THE PLEIOTROPIC EFFECTS OF
FISETIN AND HESPERETIN ON HUMAN ACUTE
PROMYELOCYTIC LEUKEMIA CELLS ARE MEDIATED
THROUGH APOPTOSIS, CELL CYCLE ARREST, AND
ALTERATIONS IN SIGNALING NETWORKS. TUMOUR
BIOL. 2015;36(11):8973-84. [BACK]
142.
YUMNAM S, HONG GE, RAHA S, ET AL.
MITOCHONDRIAL DYSFUNCTION AND CA(2+)
OVERLOAD CONTRIBUTES TO HESPERIDIN INDUCED
PARAPTOSIS IN HEPATOBLASTOMA CELLS, HEPG2. J
CELL PHYSIOL. 2016;231(6):1261-8. [BACK]
143.
 BIRSU CINCIN Z, UNLU M, KIRAN B, SINEM BIRELLER E,
BARAN Y, CAKMAKOGLU B. ANTI-PROLIFERATIVE,
APOPTOTIC AND SIGNAL TRANSDUCTION EFFECTS OF
HESPERIDIN IN NON-SMALL CELL LUNG CANCER
CELLS. CELL ONCOL (DORDR). 2015;38(3):195-204. [BACK]
144.
PALIT S, KAR S, SHARMA G, DAS PK. HESPERETIN
INDUCES APOPTOSIS IN BREAST CARCINOMA BY
TRIGGERING ACCUMULATION OF ROS AND ACTIVATION
OF ASK1/JNK PATHWAY. J CELL PHYSIOL.
2015;230(8):1729-39. [BACK]
145.
TANAKA T, MAKITA H, KAWABATA K, ET AL.
CHEMOPREVENTION OF AZOXYMETHANE-INDUCED
RAT COLON CARCINOGENESIS BY THE NATURALLY
OCCURRING FLAVONOIDS, DIOSMIN AND HESPERIDIN.
CARCINOGENESIS. 1997;18(5):957-65. [BACK]
146.
KAMARAJ S, ANANDAKUMAR P, JAGAN S,
RAMAKRISHNAN G, DEVAKI T. MODULATORY EFFECT
OF HESPERIDIN ON BENZO(A)PYRENE INDUCED
EXPERIMENTAL LUNG CARCINOGENESIS WITH
REFERENCE TO COX-2, MMP-2 AND MMP-9. EUR J
PHARMACOL. 2010;649(1-3):320-7. [BACK]
147.
YANG M, TANAKA T, HIROSE Y, DEGUCHI T, MORI H,
KAWADA Y. CHEMOPREVENTIVE EFFECTS OF DIOSMIN
AND HESPERIDIN ON N-BUTYL-N-(4-
HYDROXYBUTYL)NITROSAMINE-INDUCED URINARY-
BLADDER CARCINOGENESIS IN MALE ICR MICE. INT J
CANCER. 1997;73(5):719-24. [BACK]
148.
TANAKA T, MAKITA H, OHNISHI M, ET AL.
CHEMOPREVENTION OF 4-NITROQUINOLINE 1-OXIDE-
INDUCED ORAL CARCINOGENESIS BY DIETARY
CURCUMIN AND HESPERIDIN: COMPARISON WITH THE
PROTECTIVE EFFECT OF BETA-CAROTENE. CANCER
RES. 1994;54(17):4653-9. [BACK]
149.TANAKA T, MAKITA H, OHNISHI M, ET AL.
CHEMOPREVENTION OF 4-NITROQUINOLINE 1-OXIDE-
INDUCED ORAL CARCINOGENESIS IN RATS BY
FLAVONOIDS DIOSMIN AND HESPERIDIN, EACH ALONE
AND IN COMBINATION. CANCER RES. 1997;57(2):246-52.
[BACK]
150.
TANAKA T, MAKITA H, KAWABATA K, ET AL.
MODULATION OF N-METHYL-N-AMYLNITROSAMINE-
INDUCED RAT OESOPHAGEAL TUMOURIGENESIS BY
DIETARY FEEDING OF DIOSMIN AND HESPERIDIN, BOTH
ALONE AND IN COMBINATION. CARCINOGENESIS.
1997;18(4):761-9. [BACK]
151.
ZHANG J, WU D, VIKASH, ET AL. HESPERETIN INDUCES
THE APOPTOSIS OF GASTRIC CANCER CELLS VIA
ACTIVATING MITOCHONDRIAL PATHWAY BY
INCREASING REACTIVE OXYGEN SPECIES. DIG DIS SCI.
2015;60(10):2985-95. [BACK]
152.
SAIPRASAD G, CHITRA P, MANIKANDAN R,
SUDHANDIRAN G. HESPERIDIN INDUCES APOPTOSIS
AND TRIGGERS AUTOPHAGIC MARKERS THROUGH
INHIBITION OF AURORA-A MEDIATED
PHOSPHOINOSITIDE-3-KINASE/AKT/MAMMALIAN
TARGET OF RAPAMYCIN AND GLYCOGEN SYNTHASE
KINASE-3 BETA SIGNALLING CASCADES IN
EXPERIMENTAL COLON CARCINOGENESIS. EUR J
CANCER. 2014;50(14):2489-507. [BACK]
153.
GWIAZDOWSKA D, JUŚ K, JASNOWSKA-MAŁECKA J,
KLUCZYŃSKA K. THE IMPACT OF POLYPHENOLS ON
BIFIDOBACTERIUM GROWTH. ACTA BIOCHIM POL.
2015;62(4):895-901. [BACK]
154.
ABUELSAAD AS, ALLAM G, AL-SOLUMANI AA.
HESPERIDIN INHIBITS INFLAMMATORY RESPONSE
INDUCED BY AEROMONAS HYDROPHILA INFECTION
AND ALTERS CD4+/CD8+ T CELL RATIO. MEDIATORS
INFLAMM. 2014;2014:393217. [BACK]
155.
SIDDIQI A, NAFEES S, RASHID S, SULTANA S,
SAIDULLAH B. HESPERIDIN AMELIORATES
TRICHLOROETHYLENE-INDUCED NEPHROTOXICITY BY
ABROGATION OF OXIDATIVE STRESS AND APOPTOSIS IN
WISTAR RATS. MOL CELL BIOCHEM. 2015;406(1-2):9-20.
[BACK]
156.ANANDAN R, SUBRAMANIAN P. RENAL
PROTECTIVE EFFECT OF HESPERIDIN ON GENTAMICIN-
INDUCED ACUTE NEPHROTOXICITY IN MALE WISTAR
ALBINO RATS. REDOX REP. 2012;17(5):219-26. [BACK]
157. SAHU BD, KUNCHA M, SINDHURA GJ, SISTLA R.
HESPERIDIN ATTENUATES CISPLATIN-INDUCED ACUTE
RENAL INJURY BY DECREASING OXIDATIVE STRESS,
INFLAMMATION AND DNA DAMAGE. PHYTOMEDICINE.
2013;20(5):453-60. [BACK]
158.KAMEL KM, ABD EL-RAOUF OM, METWALLY SA,
ABD EL-LATIF HA, EL-SAYED ME. HESPERIDIN AND
RUTIN, ANTIOXIDANT CITRUS FLAVONOIDS,
ATTENUATE CISPLATIN-INDUCED NEPHROTOXICITY IN
RATS. J BIOCHEM MOL TOXICOL. 2014;28(7):312-9. [BACK]
159.
POLAT N, CIFTCI O, CETIN A, YILMAZ T. TOXIC EFFECTS
OF SYSTEMIC CISPLATIN ON RAT EYES AND THE
PROTECTIVE EFFECT OF HESPERIDIN AGAINST THIS
TOXICITY. CUTAN OCUL TOXICOL. 2016;35(1):1-7. [BACK]
160.
 KAYA K, CIFTCI O, CETIN A, DOĞAN H, BAŞAK N.
HESPERIDIN PROTECTS TESTICULAR AND
SPERMATOLOGICAL DAMAGES INDUCED BY CISPLATIN
IN RATS. ANDROLOGIA. 2015;47(7):793-800. [BACK]
161.
OMAR HA, MOHAMED WR, ARAFA EL-SA, ET AL.
HESPERIDIN ALLEVIATES CISPLATIN-INDUCED
HEPATOTOXICITY IN RATS WITHOUT INHIBITING ITS
ANTITUMOR ACTIVITY. PHARMACOL REP. 2016;68(2):349-
56. [BACK]
162.
SAHA RK, TAKAHASHI T, SUZUKI T. GLUCOSYL
HESPERIDIN PREVENTS INFLUENZA A VIRUS
REPLICATION IN VITRO BY INHIBITION OF VIRAL
SIALIDASE. BIOL PHARM BULL. 2009;32(7):1188-92.
[BACK]
163.
CARVALHO OV, BOTELHO CV, FERREIRA CG, ET AL. IN
VITRO INHIBITION OF CANINE DISTEMPER VIRUS BY
FLAVONOIDS AND PHENOLIC ACIDS: IMPLICATIONS OF
STRUCTURAL DIFFERENCES FOR ANTIVIRAL DESIGN.
RES VET SCI. 2013;95(2):717-24. [BACK]
164.
BAE EA, HAN MJ, LEE M, KIM DH. IN VITRO INHIBITORY
EFFECT OF SOME FLAVONOIDS ON ROTAVIRUS
INFECTIVITY. BIOL PHARM BULL. 2000;23(9):1122-4.
[BACK]
165.
PANASIAK W, WLEKLIK M, ORACZEWSKA A, LUCZAK
M. INFLUENCE OF FLAVONOIDS ON COMBINED
EXPERIMENTAL INFECTIONS WITH EMC VIRUS AND
STAPHYLOCOCCUS AUREUS IN MICE. ACTA MICROBIOL
POL. 1989;38(2):185-8. [BACK]
166.
AHMED YM, MESSIHA BA, ABO-SAIF AA. PROTECTIVE
EFFECTS OF SIMVASTATIN AND HESPERIDIN AGAINST
COMPLETE FREUND'S ADJUVANT-INDUCED
RHEUMATOID ARTHRITIS IN RATS. PHARMACOLOGY.
2015;96(5-6):217-25. [BACK]
167. LI R, CAI L, XIE XF, YANG F, LI J. HESPERIDIN
SUPPRESSES ADJUVANT ARTHRITIS IN RATS BY
INHIBITING SYNOVIOCYTE ACTIVITY. PHYTOTHER RES.
2010;24 SUPPL 1:S71-6. [BACK]
168.
MARTIN BR, MCCABE GP, MCCABE L, ET AL. EFFECT OF
HESPERIDIN WITH AND WITHOUT A CALCIUM
(CALCILOCK) SUPPLEMENT ON BONE HEALTH IN
POSTMENOPAUSAL WOMEN. J CLIN ENDOCRINOL
METAB. 2016;101(3):923-7. [BACK]
169. CHIBA H, KIM H, MATSUMOTO A, ET AL.
HESPERIDIN PREVENTS ANDROGEN DEFICIENCY-
INDUCED BONE LOSS IN MALE MICE. PHYTOTHER RES.
2014;28(2):289-95. [BACK]
170.HABAUZIT V, SACCO SM, GIL-IZQUIERDO A, ET AL.
DIFFERENTIAL EFFECTS OF TWO CITRUS FLAVANONES
ON BONE QUALITY IN SENESCENT MALE RATS IN
RELATION TO THEIR BIOAVAILABILITY AND
METABOLISM. BONE. 2011;49(5):1108-16. [BACK]
171.
TAMILSELVAM K, BRAIDY N, MANIVASAGAM T, ET AL.
NEUROPROTECTIVE EFFECTS OF HESPERIDIN, A PLANT
FLAVANONE, ON ROTENONE-INDUCED OXIDATIVE
STRESS AND APOPTOSIS IN A CELLULAR MODEL FOR
PARKINSON'S DISEASE. OXID MED CELL LONGEV.
2013;2013:102741. [BACK]
172.
KHAN MH, PARVEZ S. HESPERIDIN AMELIORATES
HEAVY METAL INDUCED TOXICITY MEDIATED BY
OXIDATIVE STRESS IN BRAIN OF WISTAR RATS. J TRACE
ELEM MED BIOL. 2015;31:53-60. [BACK]
173.
 WANG D, LIU L, ZHU X, WU W, WANG Y. HESPERIDIN
ALLEVIATES COGNITIVE IMPAIRMENT,
MITOCHONDRIAL DYSFUNCTION AND OXIDATIVE
STRESS IN A MOUSE MODEL OF ALZHEIMER'S DISEASE.
CELL MOL NEUROBIOL. 2014;34(8):1209-21. [BACK]
174.
ANTUNES MS, GOES AT, BOEIRA SP, PRIGOL M, JESSE
CR. PROTECTIVE EFFECT OF HESPERIDIN IN A MODEL
OF PARKINSON'S DISEASE INDUCED BY 6-
HYDROXYDOPAMINE IN AGED MICE. NUTRITION.
2014;30(11-12):1415-22. [BACK]
175.
EL-MARASY SA, ABDALLAH HM, EL-SHENAWY SM, EL-
KHATIB AS, EL-SHABRAWY OA, KENAWY SA. ANTI-
DEPRESSANT EFFECT OF HESPERIDIN IN DIABETIC
RATS. CAN J PHYSIOL PHARMACOL. 2014;92(11):945-52.
[BACK]
176. DONATO F, DE GOMES MG, GOES AT, ET AL.
HESPERIDIN EXERTS ANTIDEPRESSANT-LIKE EFFECTS
IN ACUTE AND CHRONIC TREATMENTS IN MICE:
POSSIBLE ROLE OF L-ARGININE-NO-CGMP PATHWAY
AND BDNF LEVELS. BRAIN RES BULL. 2014;104:19-26.
[BACK]
177.CAI L, LI R, WU QQ, WU TN. [EFFECT OF
HESPERIDIN ON BEHAVIOR AND HPA AXIS OF RAT
MODEL OF CHRONIC STRESS-INDUCED DEPRESSION].
ZHONGGUO ZHONG YAO ZA ZHI. 2013;38(2):229-33.
[BACK]
178.
SHARMA M, AKHTAR N, SAMBHAV K, SHETE G, BANSAL
AK, SHARMA SS. EMERGING POTENTIAL OF CITRUS
FLAVANONES AS AN ANTIOXIDANT IN DIABETES AND
ITS COMPLICATIONS. CURR TOP MED CHEM.
2015;15(2):187-95. [BACK]
179.
 DE OLIVEIRA DM, DOURADO GK, CESAR TB.
HESPERIDIN ASSOCIATED WITH CONTINUOUS AND
INTERVAL SWIMMING IMPROVED BIOCHEMICAL AND
OXIDATIVE BIOMARKERS IN RATS. J INT SOC SPORTS
NUTR. 2013;10:27. [BACK]
180.
DIMPFEL W. DIFFERENT ANTICONVULSIVE EFFECTS OF
HESPERIDIN AND ITS AGLYCONE HESPERETIN ON
ELECTRICAL ACTIVITY IN THE RAT HIPPOCAMPUS IN-
VITRO. J PHARM PHARMACOL. 2006;58(3):375-9. [BACK]
181.
ZANOTTI SIMOES DOURADO GK, DE ABREU RIBEIRO
LC, ZEPPONE CARLOS I, BORGES CÉSAR T. ORANGE
JUICE AND HESPERIDIN PROMOTE DIFFERENTIAL
INNATE IMMUNE RESPONSE IN MACROPHAGES EX
VIVO. INT J VITAM NUTR RES. 2013;83(3):162-7. [BACK]
182.
KAMBOH AA, HANG SQ, KHAN MA, ZHU WY. IN VIVO
IMMUNOMODULATORY EFFECTS OF PLANT
FLAVONOIDS IN LIPOPOLYSACCHARIDE-CHALLENGED
BROILERS. ANIMAL. 2016;:1-7. [BACK]
183.
AMIOT MJ, RIVA C, VINET A. EFFECTS OF DIETARY
POLYPHENOLS ON METABOLIC SYNDROME FEATURES
IN HUMANS: A SYSTEMATIC REVIEW. OBES REV. 2016.
[BACK]
184. ASSINI JM, MULVIHILL EE, HUFF MW. CITRUS
FLAVONOIDS AND LIPID METABOLISM. CURR OPIN
LIPIDOL. 2013;24(1):34-40. [BACK]
185.
PRADEEP K, KO KC, CHOI MH, KANG JA, CHUNG YJ,
PARK SH. PROTECTIVE EFFECT OF HESPERIDIN, A
CITRUS FLAVANOGLYCONE, AGAINST Γ-RADIATION-
INDUCED TISSUE DAMAGE IN SPRAGUE-DAWLEY RATS.
J MED FOOD. 2012;15(5):419-27. [BACK]
 186.
MARTINEZ RM, PINHO-RIBEIRO FA, STEFFEN VS, ET AL.
TOPICAL FORMULATION CONTAINING HESPERIDIN
METHYL CHALCONE INHIBITS SKIN OXIDATIVE STRESS
AND INFLAMMATION INDUCED BY ULTRAVIOLET B
IRRADIATION. PHOTOCHEM PHOTOBIOL SCI.
2016;15(4):554-63. [BACK]
187. MADDUMA HEWAGE SR, PIAO MJ, KANG KA, ET AL.
HESPERIDIN ATTENUATES ULTRAVIOLET B-INDUCED
APOPTOSIS BY MITIGATING OXIDATIVE STRESS IN
HUMAN KERATINOCYTES. BIOMOL THER (SEOUL).
2016;24(3):312-9. [BACK]
188.
SAID UZ, SAADA HN, ABD-ALLA MS, ELSAYED ME,
AMIN AM. HESPERIDIN ATTENUATES BRAIN
BIOCHEMICAL CHANGES OF IRRADIATED RATS. INT J
RADIAT BIOL. 2012;88(8):613-8. [BACK]
189.
LEE YR, JUNG JH, KIM HS. HESPERIDIN PARTIALLY
RESTORES IMPAIRED IMMUNE AND NUTRITIONAL
FUNCTION IN IRRADIATED MICE. J MED FOOD.
2011;14(5):475-82. [BACK]
190.
GIANNINI I, AMATO A, BASSO L, ET AL. FLAVONOIDS
MIXTURE (DIOSMIN, TROXERUTIN, HESPERIDIN) IN THE
TREATMENT OF ACUTE HEMORRHOIDAL DISEASE: A
PROSPECTIVE, RANDOMIZED, TRIPLE-BLIND,
CONTROLLED TRIAL. TECH COLOPROCTOL.
2015;19(6):339-45. [BACK]
191.
MAN G, MAURO TM, ZHAI Y, ET AL. TOPICAL
HESPERIDIN ENHANCES EPIDERMAL FUNCTION IN AN
AGED MURINE MODEL. J INVEST DERMATOL.
2015;135(4):1184-7. [BACK]
192.
 USACH I, TALÉNS-VISCONTI R, MAGRANER-PARDO L,
PERIS JE. HESPERETIN INDUCES MELANIN PRODUCTION
IN ADULT HUMAN EPIDERMAL MELANOCYTES. FOOD
CHEM TOXICOL. 2015;80:80-4. [BACK]
193.
KURATA Y, FUKUSHIMA S, HAGIWARA A, ITO H, OGAWA
K, ITO N. CARCINOGENICITY STUDY OF METHYL
HESPERIDIN IN B6C3F1 MICE. FOOD CHEM TOXICOL.
1990;28(9):613-8. [BACK]
194.
CARPENTER KJ. THE DISCOVERY OF VITAMIN C. ANN
NUTR METAB. 2012;61(3):259-64. [BACK]
195.
PADAYATTY SJ, LEVINE M. VITAMIN C: THE KNOWN,
THE UNKNOWN, AND GOLDILOCKS. ORAL DIS. 2016;
[BACK]
196.
SHAW JH, PHILLIPS PH, ELVEHJEM CA. ACUTE AND
CHRONIC ASCORBIC ACID DEFICIENCIES IN THE
RHESUS MONKEY. J. NUTR. 1945; VOL 29. NO. 6:365-372.
[BACK]
197.
MASTRANGELO D, MASSAI L, LO COCO F, ET AL.
CYTOTOXIC EFFECTS OF HIGH CONCENTRATIONS OF
SODIUM ASCORBATE ON HUMAN MYELOID CELL LINES.
ANN HEMATOL. 2015;94(11):1807-16. [BACK]
198.
SERTKAYA A, WONG HH, JESSUP A, BELECHE T. KEY
COST DRIVERS OF PHARMACEUTICAL CLINICAL TRIALS
IN THE UNITED STATES. SAGE JOURNALS. 2016; VOL 13,
ISSUE 2. [BACK]
199.
PDQ CANCER INFORMATION SUMMARIES – HIGH-DOSE
VITAMIN C. 2015. [AVAILABLE]
HTTP://WWW.NCBI.NLM.NIH.GOV/BOOKS/NBK127724/#C
DR0000742253__1 [MAY 11, 2016]. [BACK]
200.
VENTURELLI S, SINNBERG TW, NIESSNER H, BUSCH C.
MOLECULAR MECHANISMS OF PHARMACOLOGICAL
DOSES OF ASCORBATE ON CANCER CELLS. WIEN MED
WOCHENSCHR. 2015;165(11-12):251-7. [BACK]
201.
CAMERON E. VITAMIN C AND CANCER: AN OVERVIEW.
INT J VITAM NUTR RES SUPPL. 1982;23:115-27. [BACK]
202.
MALAVOLTI M, MALAGOLI C, FIORENTINI C, ET AL.
ASSOCIATION BETWEEN DIETARY VITAMIN C AND RISK
OF CUTANEOUS MELANOMA IN A POPULATION OF
NORTHERN ITALY. INT J VITAM NUTR RES. 2013;83(5):291-
8. [BACK]
203.
VANCE TM, WANG Y, SU LJ, ET AL. DIETARY TOTAL
ANTIOXIDANT CAPACITY IS INVERSELY ASSOCIATED
WITH PROSTATE CANCER AGGRESSIVENESS IN A
POPULATION-BASED STUDY. NUTR CANCER.
2016;68(2):214-24. [BACK]
204.
KONG P, CAI Q, GENG Q, ET AL. VITAMIN INTAKE
REDUCE THE RISK OF GASTRIC CANCER: META-
ANALYSIS AND SYSTEMATIC REVIEW OF RANDOMIZED
AND OBSERVATIONAL STUDIES. PLOS ONE.
2014;9(12):E116060. [BACK]
205.
BENADE L, HOWARD T, BURK D. SYNERGISTIC KILLING
OF EHRLICH ASCITES CARCINOMA CELLS BY
ASCORBATE AND 3-AMINO-1,2,4,-TRIAZOLE. ONCOLOGY.
1969;23(1):33-43. [BACK]
206.
PIRES AS, MARQUES CR, ENCARNAÇÃO JC, ET AL.
ASCORBIC ACID AND COLON CANCER: AN OXIDATIVE
STIMULUS TO CELL DEATH DEPENDING ON CELL
PROFILE. EUR J CELL BIOL. 2016; [BACK]
207.
UETAKI M, TABATA S, NAKASUKA F, SOGA T, TOMITA M.
METABOLOMIC ALTERATIONS IN HUMAN CANCER
CELLS BY VITAMIN C-INDUCED OXIDATIVE STRESS. SCI
REP. 2015;5:13896. [BACK]
208.
SERRANO OK, PARROW NL, VIOLET PC, ET AL.
ANTITUMOR EFFECT OF PHARMACOLOGIC ASCORBATE
IN THE B16 MURINE MELANOMA MODEL. FREE RADIC
BIOL MED. 2015;87:193-203. [BACK]
209.
MASTRANGELO D, MASSAI L, LO COCO F, ET AL.
CYTOTOXIC EFFECTS OF HIGH CONCENTRATIONS OF
SODIUM ASCORBATE ON HUMAN MYELOID CELL LINES.
ANN HEMATOL. 2015;94(11):1807-16. [BACK]
210.
CHEN N, YIN S, SONG X, FAN L, HU H. VITAMIN B ₂
SENSITIZES CANCER CELLS TO VITAMIN-C-INDUCED
CELL DEATH VIA MODULATION OF AKT AND BAD
PHOSPHORYLATION. J AGRIC FOOD CHEM.
2015;63(30):6739-48. [BACK]
211.
CAMPBELL EJ, VISSERS MC, BOZONET S, DYER A,
ROBINSON BA, DACHS GU. RESTORING PHYSIOLOGICAL
LEVELS OF ASCORBATE SLOWS TUMOR GROWTH AND
MODERATES HIF-1 PATHWAY ACTIVITY IN GULO(-/-)
MICE. CANCER MED. 2015;4(2):303-14. [BACK]
212.
CHEN Q, ESPEY MG, SUN AY, ET AL. PHARMACOLOGIC
DOSES OF ASCORBATE ACT AS A PROOXIDANT AND
DECREASE GROWTH OF AGGRESSIVE TUMOR
XENOGRAFTS IN MICE. PROC NATL ACAD SCI USA.
2008;105(32):11105-9. [BACK]
213.
TAKEMURA Y, SATOH M, SATOH K, HAMADA H, SEKIDO
Y, KUBOTA S. HIGH DOSE OF ASCORBIC ACID INDUCES
CELL DEATH IN MESOTHELIOMA CELLS. BIOCHEM
BIOPHYS RES COMMUN. 2010;394(2):249-53. [BACK]
214.
YUN J, MULLARKY E, LU C, ET AL. VITAMIN C
SELECTIVELY KILLS KRAS AND BRAF MUTANT
COLORECTAL CANCER CELLS BY TARGETING GAPDH.
SCIENCE. 2015;350(6266):1391-6. [BACK]
215.
YEOM CH, LEE G, PARK JH, ET AL. HIGH DOSE
CONCENTRATION ADMINISTRATION OF ASCORBIC ACID
INHIBITS TUMOR GROWTH IN BALB/C MICE IMPLANTED
WITH SARCOMA 180 CANCER CELLS VIA THE
RESTRICTION OF ANGIOGENESIS. J TRANSL MED.
2009;7:70. [BACK]
216.
CASCIARI JJ, RIORDAN HD, MIRANDA-MASSARI JR,
GONZALEZ MJ. EFFECTS OF HIGH DOSE ASCORBATE
ADMINISTRATION ON L-10 TUMOR GROWTH IN GUINEA
PIGS. P R HEALTH SCI J. 2005;24(2):145-50. [BACK]
217.
ROOMI MW, CHA J, KALINOVSKY T, ROOMI N,
NIEDZWIECKI A, RATH M. EFFECT OF A NUTRIENT
MIXTURE ON THE LOCALIZATION OF EXTRACELLULAR
MATRIX PROTEINS IN HELA HUMAN CERVICAL CANCER
XENOGRAFTS IN FEMALE NUDE MICE. EXP THER MED.
2015;10(3):901-906. [BACK]
218.
AMBATTU LA, REKHA MR. COLLAGEN SYNTHESIS
PROMOTING PULLULAN-PEI-ASCORBIC ACID
CONJUGATE AS AN EFFICIENT ANTI-CANCER GENE
DELIVERY VECTOR. CARBOHYDR POLYM. 2015;126:52-61.
[BACK]
219.
GÜNEY G, KUTLU HM, GENÇ L. PREPARATION AND
CHARACTERIZATION OF ASCORBIC ACID LOADED
SOLID LIPID NANOPARTICLES AND INVESTIGATION OF
THEIR APOPTOTIC EFFECTS. COLLOIDS SURF B
BIOINTERFACES. 2014;121:270-80. [BACK]
220.
GUSTAFSON CB, YANG C, DICKSON KM, ET AL.
EPIGENETIC REPROGRAMMING OF MELANOMA CELLS
BY VITAMIN C TREATMENT. CLIN EPIGENETICS.
2015;7(1):51. [BACK]
221.
ROBINSON AB, HUNSBERGER A, WESTALL FC.
SUPPRESSION OF SQUAMOUS CELL CARCINOMA IN
HAIRLESS MICE BY DIETARY NUTRIENT VARIATION.
MECH AGEING DEV. 1994;76(2-3):201-14. [BACK]
222.
CAMERON E, PAULING L. SUPPLEMENTAL ASCORBATE
IN THE SUPPORTIVE TREATMENT OF CANCER:
PROLONGATION OF SURVIVAL TIMES IN TERMINAL
HUMAN CANCER. PROC NATL ACAD SCI USA.
1976;73(10):3685-9. [BACK]
223.
RAYMOND YC, GLENDA CS, MENG LK. EFFECTS OF
HIGH DOSES OF VITAMIN C ON CANCER PATIENTS IN
SINGAPORE: NINE CASES. INTEGR CANCER THER. 2015;
[BACK]
224.
VOLLBRACHT C, SCHNEIDER B, LEENDERT V, WEISS G,
AUERBACH L, BEUTH J. INTRAVENOUS VITAMIN C
ADMINISTRATION IMPROVES QUALITY OF LIFE IN
BREAST CANCER PATIENTS DURING
CHEMO-/RADIOTHERAPY AND AFTERCARE: RESULTS OF
A RETROSPECTIVE, MULTICENTRE, EPIDEMIOLOGICAL
COHORT STUDY IN GERMANY. IN VIVO. 2011;25(6):983-90.
[BACK]
225.
YEOM CH, JUNG GC, SONG KJ. CHANGES OF TERMINAL
CANCER PATIENTS' HEALTH-RELATED QUALITY OF LIFE
AFTER HIGH DOSE VITAMIN C ADMINISTRATION. J
KOREAN MED SCI. 2007;22(1):7-11. [BACK]
226.
MIKIROVA N, CASCIARI J, ROGERS A, TAYLOR P. EFFECT
OF HIGH-DOSE INTRAVENOUS VITAMIN C ON
INFLAMMATION IN CANCER PATIENTS. J TRANSL MED.
2012;10:189. [BACK]
227.
MATEEN S, MOIN S, KHAN AQ, ZAFAR A, FATIMA N.
INCREASED REACTIVE OXYGEN SPECIES FORMATION
AND OXIDATIVE STRESS IN RHEUMATOID ARTHRITIS.
PLOS ONE. 2016;11(4):E0152925. [BACK]
228.
MOHAMED R, SHIVAPRASAD HV, JAMEEL NM, SHEKAR
MA, VISHWANATH BS. NEUTRALIZATION OF LOCAL
TOXICITY INDUCED BY VIPERA RUSSELLI
PHOSPHOLIPASE A2 BY LIPOPHILIC DERIVATIVE OF
ASCORBIC ACID. CURR TOP MED CHEM. 2011;11(20):2531-
9. [BACK]
229.
LAING MD. A CURE FOR MUSHROOM POISONING. S AFR
MED J. 1984;65(15):590. [BACK]
230.
PAVLOVIC V, CEKIC S, KAMENOV B, CIRIC M, KRTINIC
D. THE EFFECT OF ASCORBIC ACID ON MANCOZEB-
INDUCED TOXICITY IN RAT THYMOCYTES. FOLIA BIOL
(PRAHA). 2015;61(3):116-23. [BACK]
231.
OZMEN O. ENDOSULFAN SPLENIC PATHOLOGY AND
AMELIORATION BY VITAMIN C IN NEW ZEALAND
RABBIT. J IMMUNOTOXICOL. 2015;:1-6. [BACK]
232.
GUO W, HUEN K, PARK JS, ET AL. VITAMIN C
INTERVENTION MAY LOWER THE LEVELS OF
PERSISTENT ORGANIC POLLUTANTS IN BLOOD OF
HEALTHY WOMEN - A PILOT STUDY. FOOD CHEM
TOXICOL. 2016;92:197-204. [BACK]
233.
RODERIQUE JD, JOSEF CS, NEWCOMB AH, REYNOLDS
PS, SOMERA LG, SPIESS BD. PRECLINICAL EVALUATION
OF INJECTABLE REDUCED HYDROXOCOBALAMIN AS
AN ANTIDOTE TO ACUTE CARBON MONOXIDE
POISONING. J TRAUMA ACUTE CARE SURG. 2015;79(4
SUPPL 2):S116-20. [BACK]
234.
ABE S, TANAKA Y, FUJISE N, ET AL. AN ANTIOXIDATIVE
NUTRIENT-RICH ENTERAL DIET ATTENUATES LETHAL
ACTIVITY AND OXIDATIVE STRESS INDUCED BY
LIPOPOLYSACCHARIDE IN MICE. JPEN J PARENTER
ENTERAL NUTR. 2007;31(3):181-7. [BACK]
235.
BERGER MM, OUDEMANS-VAN STRAATEN HM.
VITAMIN C SUPPLEMENTATION IN THE CRITICALLY ILL
PATIENT. CURR OPIN CLIN NUTR METAB CARE.
2015;18(2):193-201. [BACK]
236.
ARSLAN M, SEZEN SC, TURGUT HC, ET AL. VITAMIN C
AMELIORATES HIGH DOSE DEXMEDETOMIDINE
INDUCED LIVER INJURY. BRATISL LEK LISTY.
2016;117(1):36-40. [BACK]
237.
FAROMBI EO, ONYEMA OO. MONOSODIUM
GLUTAMATE-INDUCED OXIDATIVE DAMAGE AND
GENOTOXICITY IN THE RAT: MODULATORY ROLE OF
VITAMIN C, VITAMIN E AND QUERCETIN. HUM EXP
TOXICOL. 2006;25(5):251-9. [BACK]
238.
MOZHDEGANLOO Z, JAFARI AM, KOOHI MK,
HEIDARPOUR M. METHYLMERCURY-INDUCED
OXIDATIVE STRESS IN RAINBOW TROUT
(ONCORHYNCHUS MYKISS) LIVER: AMELIORATING
EFFECT OF VITAMIN C. BIOL TRACE ELEM RES.
2015;165(1):103-9. [BACK]
239.
GULEC M, GUREL A, ARMUTCU F. VITAMIN E PROTECTS
AGAINST OXIDATIVE DAMAGE CAUSED BY
FORMALDEHYDE IN THE LIVER AND PLASMA OF RATS.
MOL CELL BIOCHEM. 2006;290(1-2):61-7. [BACK]
240.
REZVANJOO B, RASHIDI S, JOUYBAN A, BEHESHTIHA
SH, SAMINI M. EFFECTS OF VITAMIN C AND MELATONIN
ON CYSTEAMINE-INDUCED DUODENAL ULCER IN A
CHOLESTATIC RAT MODEL: A CONTROLLED
EXPERIMENTAL STUDY. CURR THER RES CLIN EXP.
2010;71(5):322-30. [BACK]
241.
KIM SR, HA YM, KIM YM, ET AL. ASCORBIC ACID
REDUCES HMGB1 SECRETION IN
LIPOPOLYSACCHARIDE-ACTIVATED RAW 264.7 CELLS
AND IMPROVES SURVIVAL RATE IN SEPTIC MICE BY
ACTIVATION OF NRF2/HO-1 SIGNALS. BIOCHEM
PHARMACOL. 2015;95(4):279-89. [BACK]
242. TOKUDA Y, MIURA N, KOBAYASHI M, ET AL.
ASCORBIC ACID DEFICIENCY INCREASES ENDOTOXIN
INFLUX TO PORTAL BLOOD AND LIVER INFLAMMATORY
GENE EXPRESSIONS IN ODS RATS. NUTRITION.
2015;31(2):373-9. [BACK]
243.
FISHER BJ, KRASKAUSKAS D, MARTIN EJ, ET AL.
ATTENUATION OF SEPSIS-INDUCED ORGAN INJURY IN
MICE BY VITAMIN C. JPEN J PARENTER ENTERAL NUTR.
2014;38(7):825-39. [BACK]
244.
ABHILASH PA, HARIKRISHNAN R, INDIRA M. ASCORBIC
ACID SUPPRESSES ENDOTOXEMIA AND NF-ΚB
SIGNALING CASCADE IN ALCOHOLIC LIVER FIBROSIS
IN GUINEA PIGS: A MECHANISTIC APPROACH. TOXICOL
APPL PHARMACOL. 2014;274(2):215-24. [BACK]
245.
LOWES DA, WEBSTER NR, GALLEY HF.
DEHYDROASCORBIC ACID AS PRE-CONDITIONER:
PROTECTION FROM LIPOPOLYSACCHARIDE INDUCED
MITOCHONDRIAL DAMAGE. FREE RADIC RES.
2010;44(3):283-92. [BACK]
246. FISHER BJ, SEROPIAN IM, KRASKAUSKAS D, ET AL.
ASCORBIC ACID ATTENUATES LIPOPOLYSACCHARIDE-
INDUCED ACUTE LUNG INJURY. CRIT CARE MED.
2011;39(6):1454-60. [BACK]
247.
MCKINNON RL, LIDINGTON D, TYML K. ASCORBATE
INHIBITS REDUCED ARTERIOLAR CONDUCTED
VASOCONSTRICTION IN SEPTIC MOUSE CREMASTER
MUSCLE. MICROCIRCULATION. 2007;14(7):697-707.
[BACK]
248.
KANTER M, COSKUN O, ARMUTCU F, UZ YH, KIZILAY G.
PROTECTIVE EFFECTS OF VITAMIN C, ALONE OR IN
COMBINATION WITH VITAMIN A, ON ENDOTOXIN-
INDUCED OXIDATIVE RENAL TISSUE DAMAGE IN RATS.
TOHOKU J EXP MED. 2005;206(2):155-62. [BACK]
249.
CHEN MF, YANG CM, SU CM, HU ML. VITAMIN C
PROTECTS AGAINST CISPLATIN-INDUCED
NEPHROTOXICITY AND DAMAGE WITHOUT REDUCING
ITS EFFECTIVENESS IN C57BL/6 MICE XENOGRAFTED
WITH LEWIS LUNG CARCINOMA. NUTR CANCER.
2014;66(7):1085-91. [BACK]
250.
AL-ASMARI AK, KHAN AQ, AL-MASRI N. MITIGATION
OF 5-FLUOROURACIL-INDUCED LIVER DAMAGE IN RATS
BY VITAMIN C VIA TARGETING REDOX-SENSITIVE
TRANSCRIPTION FACTORS. HUM EXP TOXICOL. 2016;
[BACK]
251.PENG LJ, LU DX, QI RB, ZHANG T, WANG Z, SUN Y.
[THERAPEUTIC EFFECT OF INTRAVENOUS HIGH-DOSE
VITAMIN C ON IMPLANTED HEPATOMA IN RATS]. NAN
FANG YI KE DA XUE XUE BAO. 2009;29(2):264-6. [BACK]
252.
CHENG LL, LIU YY, LI B, LI SY, RAN PX. [AN IN VITRO
STUDY ON THE PHARMACOLOGICAL ASCORBATE
TREATMENT OF INFLUENZA VIRUS]. ZHONGHUA JIE HE
HE HU XI ZA ZHI. 2012;35(7):520-3. [BACK]
253.
WINTERGERST ES, MAGGINI S, HORNIG DH. IMMUNE-
ENHANCING ROLE OF VITAMIN C AND ZINC AND
EFFECT ON CLINICAL CONDITIONS. ANN NUTR METAB.
2006;50(2):85-94. [BACK]
254.
HARAKEH S, JARIWALLA RJ. COMPARATIVE STUDY OF
THE ANTI-HIV ACTIVITIES OF ASCORBATE AND THIOL-
CONTAINING REDUCING AGENTS IN CHRONICALLY HIV-
INFECTED CELLS. AM J CLIN NUTR. 1991;54(6
SUPPL):1231S-1235S. [BACK]
255.
DALTON WL. MASSIVE DOSES OF VITAMIN C IN THE
TREATMENT OF VIRAL DISEASES. JOURNAL OF THE
INDIANA STATE MEDICAL ASSOCIATION. 1962. [BACK]
256.RIORDAN CLINIC. HIGH-DOSE INTRAVENOUS
VITAMIN C AS A SUCCESSFUL TREATMENT OF VIRAL
INFECTIONS. [AVAILABLE]
HTTPS://RIORDANCLINIC.ORG/2014/02/HIGH-DOSE-
INTRAVENOUS-VITAMIN-C-AS-A-SUCCESSFUL-
TREATMENT-OF-VIRAL-INFECTIONS [MAY 11, 2016].
[BACK]
257.
 MIKIROVA N, HUNNINGHAKE R. EFFECT OF HIGH DOSE
VITAMIN C ON EPSTEIN-BARR VIRAL INFECTION. MED
SCI MONIT. 2014;20:725-32. [BACK]
258.
JAHAN K, AHMAD K, ALI MA. EFFECT OF ASCORBIC
ACID IN THE TREATMENT OF TETANUS. BANGLADESH
MED RES COUNC BULL. 1984;10(1):24-8. [BACK]
259.HEMILÄ H, KOIVULA TT. VITAMIN C FOR
PREVENTING AND TREATING TETANUS. COCHRANE
DATABASE SYST REV. 2008;(2):CD006665. [BACK]
260.
GONZALEZ MJ, MIRANDA-MASSARI JR, BERDIEL MJ, ET
AL. HIGH DOSE INTRAVENEOUS VITAMIN C AND
CHIKUNGUNYA FEVER: A CASE REPORT. J ORTHOMOL
MED. 2014;29(4):154-156. [BACK]
261.
CHIN KY, IMA-NIRWANA S. VITAMIN C AND BONE
HEALTH: EVIDENCE FROM CELL, ANIMAL AND HUMAN
STUDIES. CURR DRUG TARGETS. 2015; [BACK]
262.
KIM YA, KIM KM, LIM S, ET AL. FAVORABLE EFFECT OF
DIETARY VITAMIN C ON BONE MINERAL DENSITY IN
POSTMENOPAUSAL WOMEN (KNHANES IV, 2009):
DISCREPANCIES REGARDING SKELETAL SITES, AGE,
AND VITAMIN D STATUS. OSTEOPOROS INT.
2015;26(9):2329-37. [BACK]
263.HART A, COTA A, MAKHDOM A, HARVEY EJ. THE
ROLE OF VITAMIN C IN ORTHOPEDIC TRAUMA AND
BONE HEALTH. AM J ORTHOP. 2015;44(7):306-11. [BACK]
264.SUN LL, LI BL, XIE HL, ET AL. ASSOCIATIONS
BETWEEN THE DIETARY INTAKE OF ANTIOXIDANT
NUTRIENTS AND THE RISK OF HIP FRACTURE IN
ELDERLY CHINESE: A CASE-CONTROL STUDY. BR J
NUTR. 2014;112(10):1706-14. [BACK]
265.
 ZHU LL, CAO J, SUN M, ET AL. VITAMIN C PREVENTS
HYPOGONADAL BONE LOSS. PLOS ONE.
2012;7(10):E47058. [BACK]
266.
TORBERGSEN AC, WATNE LO, WYLLER TB, ET AL.
MICRONUTRIENTS AND THE RISK OF HIP FRACTURE:
CASE-CONTROL STUDY. CLIN NUTR. 2015. [BACK]
267.
HUANG YN, YANG LY, WANG JY, LAI CC, CHIU CT, WANG
JY. L-ASCORBATE PROTECTS AGAINST
METHAMPHETAMINE-INDUCED NEUROTOXICITY OF
CORTICAL CELLS VIA INHIBITING OXIDATIVE STRESS,
AUTOPHAGY, AND APOPTOSIS. MOL NEUROBIOL. 2016.
[BACK]
268.
OZKAN F, GÜNDÜZ SG, BERKÖZ M, HUNT AO, YALIN S.
THE PROTECTIVE ROLE OF ASCORBIC ACID (VITAMIN C)
AGAINST CHLORPYRIFOS-INDUCED OXIDATIVE STRESS
IN OREOCHROMIS NILOTICUS. FISH PHYSIOL BIOCHEM.
2012;38(3):635-43. [BACK]
269. ALTUNTAS I, DELIBAS N, SUTCU R. THE EFFECTS
OF ORGANOPHOSPHATE INSECTICIDE METHIDATHION
ON LIPID PEROXIDATION AND ANTI-OXIDANT ENZYMES
IN RAT ERYTHROCYTES: ROLE OF VITAMINS E AND C.
HUM EXP TOXICOL. 2002;21(12):681-5. [BACK]
270.
SHAH SA, YOON GH, KIM HO, KIM MO. VITAMIN C
NEUROPROTECTION AGAINST DOSE-DEPENDENT
GLUTAMATE-INDUCED NEURODEGENERATION IN THE
POSTNATAL BRAIN. NEUROCHEM RES. 2015;40(5):875-84.
[BACK]
271.
WARNER TA, KANG JQ, KENNARD JA, HARRISON FE.
LOW BRAIN ASCORBIC ACID INCREASES
SUSCEPTIBILITY TO SEIZURES IN MOUSE MODELS OF
DECREASED BRAIN ASCORBIC ACID TRANSPORT AND
ALZHEIMER'S DISEASE. EPILEPSY RES. 2015;110:20-5.
[BACK]
272.
IDE K, YAMADA H, UMEGAKI K, ET AL. LYMPHOCYTE
VITAMIN C LEVELS AS POTENTIAL BIOMARKER FOR
PROGRESSION OF PARKINSON'S DISEASE. NUTRITION.
2015;31(2):406-8. [BACK]
273.
SCHJOLDAGER JG, PAIDI MD, LINDBLAD MM, ET AL.
MATERNAL VITAMIN C DEFICIENCY DURING
PREGNANCY RESULTS IN TRANSIENT FETAL AND
PLACENTAL GROWTH RETARDATION IN GUINEA PIGS.
EUR J NUTR. 2015;54(4):667-76. [BACK]
274.
RAFIEE B, MOROWVAT MH, RAHIMI-GHALATI N.
COMPARING THE EFFECTIVENESS OF DIETARY VITAMIN
C AND EXERCISE INTERVENTIONS ON FERTILITY
PARAMETERS IN NORMAL OBESE MEN. UROL J.
2016;13(2):2635-9. [BACK]
275.
VIJAYPRASAD S, BB G, BB N. EFFECT OF VITAMIN C ON
MALE FERTILITY IN RATS SUBJECTED TO FORCED
SWIMMING STRESS. J CLIN DIAGN RES. 2014;8(7):HC05-8.
[BACK]
276.
DE OLIVEIRA IJ, DE SOUZA VV, MOTTA V, DA-SILVA SL.
EFFECTS OF ORAL VITAMIN C SUPPLEMENTATION ON
ANXIETY IN STUDENTS: A DOUBLE-BLIND,
RANDOMIZED, PLACEBO-CONTROLLED TRIAL. PAK J
BIOL SCI. 2015;18(1):11-8. [BACK]
277.
EBUEHI OA, OGEDEGBE RA, EBUEHI OM. ORAL
ADMINISTRATION OF VITAMIN C AND VITAMIN E
AMELIORATES LEAD-INDUCED HEPATOTOXICITY AND
OXIDATIVE STRESS IN THE RAT BRAIN. NIG Q J HOSP
MED. 2012;22(2):85-90. [BACK]
278.
TABATABAEI-MALAZY O, NIKFAR S, LARIJANI B,
ABDOLLAHI M. INFLUENCE OF ASCORBIC ACID
SUPPLEMENTATION ON TYPE 2 DIABETES MELLITUS IN
OBSERVATIONAL AND RANDOMIZED CONTROLLED
TRIALS; A SYSTEMATIC REVIEW WITH META-ANALYSIS.
J PHARM PHARM SCI. 2014;17(4):554-82. [BACK]
279.
MAGED AM, TORKY H, FOUAD MA, ET AL. ROLE OF
ANTIOXIDANTS IN GESTATIONAL DIABETES MELLITUS
AND RELATION TO FETAL OUTCOME: A RANDOMIZED
CONTROLLED TRIAL. J MATERN FETAL NEONATAL MED.
2016;:1-6. [BACK]
280.
MASON SA, DELLA GATTA PA, SNOW RJ, RUSSELL AP,
WADLEY GD. ASCORBIC ACID SUPPLEMENTATION
IMPROVES SKELETAL MUSCLE OXIDATIVE STRESS AND
INSULIN SENSITIVITY IN PEOPLE WITH TYPE 2
DIABETES: FINDINGS OF A RANDOMIZED CONTROLLED
STUDY. FREE RADIC BIOL MED. 2016;93:227-38. [BACK]
281.
KIM HJ, SONG W, JIN EH, ET AL. COMBINED LOW-
INTENSITY EXERCISE AND ASCORBIC ACID
ATTENUATES KAINIC ACID-INDUCED SEIZURE AND
OXIDATIVE STRESS IN MICE. NEUROCHEM RES.
2016;41(5):1035-41. [BACK]
282.
TUTKUN E, ARSLAN G, SOSLU R, AYYILDIZ M, AGAR E.
LONG-TERM ASCORBIC ACID ADMINISTRATION CAUSES
ANTICONVULSANT ACTIVITY DURING MODERATE AND
LONG-DURATION SWIMMING EXERCISE IN
EXPERIMENTAL EPILEPSY. ACTA NEUROBIOL EXP
(WARS). 2015;75(2):192-9. [BACK]
283.
 RICHARDS JC, CRECELIUS AR, LARSON DG, DINENNO
FA. ACUTE ASCORBIC ACID INGESTION INCREASES
SKELETAL MUSCLE BLOOD FLOW AND OXYGEN
CONSUMPTION VIA LOCAL VASODILATION DURING
GRADED HANDGRIP EXERCISE IN OLDER ADULTS. AM J
PHYSIOL HEART CIRC PHYSIOL. 2015;309(2):H360-8.
[BACK]
284.
CHAYASIRISOBHON S. EFFICACY OF PINUS RADIATA
BARK EXTRACT AND VITAMIN C COMBINATION
PRODUCT AS A PROPHYLACTIC THERAPY FOR
RECALCITRANT MIGRAINE AND LONG-TERM RESULTS.
ACTA NEUROL TAIWAN. 2013;22(1):13-21. [BACK]
285.
KIM JE, CHO HS, YANG HS, ET AL. DEPLETION OF
ASCORBIC ACID IMPAIRS NK CELL ACTIVITY AGAINST
OVARIAN CANCER IN A MOUSE MODEL.
IMMUNOBIOLOGY. 2012;217(9):873-81. [BACK]
286.
LI K, WANG J, SHI M, ET AL. PRESCRIPTION CONSISTING
OF VITAMIN C AND BAICALIN INHIBITS TUMOR
GROWTH BY ENHANCING THE ANTIOXIDANT CAPACITY
IN VIVO. J BUON. 2015;20(5):1368-72. [BACK]
287.
MAGGINI S, WENZLAFF S, HORNIG D. ESSENTIAL ROLE
OF VITAMIN C AND ZINC IN CHILD IMMUNITY AND
HEALTH. J INT MED RES. 2010;38(2):386-414. [BACK]
288.
STRÖHLE A, HAHN A. [VITAMIN C AND IMMUNE
FUNCTION]. MED MONATSSCHR PHARM. 2009;32(2):49-54.
[BACK]
289.
HUIJSKENS MJ, WALCZAK M, SARKAR S, ET AL.
ASCORBIC ACID PROMOTES PROLIFERATION OF
NATURAL KILLER CELL POPULATIONS IN CULTURE
SYSTEMS APPLICABLE FOR NATURAL KILLER CELL
THERAPY. CYTOTHERAPY. 2015;17(5):613-20. [BACK]
290.TOLIOPOULOS IK, SIMOS YV, DASKALOU TA,
VERGINADIS II, EVANGELOU AM, KARKABOUNAS SC.
INHIBITION OF PLATELET AGGREGATION AND
IMMUNOMODULATION OF NK LYMPHOCYTES BY
ADMINISTRATION OF ASCORBIC ACID. INDIAN J EXP
BIOL. 2011;49(12):904-8. [BACK]
291. ATASEVER B, ERTAN NZ, ERDEM-KURUCA S,
KARAKAS Z. IN VITRO EFFECTS OF VITAMIN C AND
SELENIUM ON NK ACTIVITY OF PATIENTS WITH BETA-
THALASSEMIA MAJOR. PEDIATR HEMATOL ONCOL.
2006;23(3):187-97. [BACK]
292.KIM JE, CHO HS, YANG HS, ET AL. DEPLETION OF
ASCORBIC ACID IMPAIRS NK CELL ACTIVITY AGAINST
OVARIAN CANCER IN A MOUSE MODEL.
IMMUNOBIOLOGY. 2012;217(9):873-81. [BACK]
293.
CHOI MK, SONG HJ, PAEK YJ, LEE HJ. GENDER
DIFFERENCES IN THE RELATIONSHIP BETWEEN
VITAMIN C AND ABDOMINAL OBESITY. INT J VITAM
NUTR RES. 2013;83(6):377-84. [BACK]
294.
ADARAMOYE O, OGUNGBENRO B, ANYAEGBU O,
FAFUNSO M. PROTECTIVE EFFECTS OF EXTRACTS OF
VERNONIA AMYGDALINA, HIBISCUS SABDARIFFA AND
VITAMIN C AGAINST RADIATION-INDUCED LIVER
DAMAGE IN RATS. J RADIAT RES. 2008;49(2):123-31.
[BACK]
295.
VASILYEVAL IN, BESPALOV VG. [RELEASE OF
EXTRACELLULAR DNA AFTER ADMINISTRATION OF
RADIOPROTECTIVE COMBINATION OF Α-TOCOPHEROL
AND ASCORBIC ACID]. RADIATS BIOL RADIOECOL.
2015;55(5):495-500. [BACK]
 296.
ROSTAMI A, MOOSAVI SA, DIANAT MOGHADAM H,
BOLOOKAT ER. MICRONUCLEI ASSESSMENT OF THE
RADIOPROTECTIVE EFFECTS OF MELATONIN AND
VITAMIN C IN HUMAN LYMPHOCYTES. CELL J.
2016;18(1):46-51. [BACK]
297.
MORTAZAVI SM, RAHIMI S, MOSLEH-SHIRAZI MA, ET
AL. A COMPARATIVE STUDY ON THE LIFE-SAVING
RADIOPROTECTIVE EFFECTS OF VITAMINS A, E, C AND
OVER-THE-COUNTER MULTIVITAMINS. J BIOMED PHYS
ENG. 2015;5(2):59-66. [BACK]
298.DOMINA EA, PYLYPCHUK OP, MIKHAILENKO VM.
DESTABILIZATION OF HUMAN CELL GENOME UNDER
THE COMBINED EFFECT OF RADIATION AND ASCORBIC
ACID. EXP ONCOL. 2014;36(4):236-40. [BACK]
299.
FUJII Y, KATO TA, UENO A, KUBOTA N, FUJIMORI A,
OKAYASU R. ASCORBIC ACID GIVES DIFFERENT
PROTECTIVE EFFECTS IN HUMAN CELLS EXPOSED TO X-
RAYS AND HEAVY IONS. MUTAT RES. 2010;699(1-2):58-61.
[BACK]
300.
MHAIDAT NM, ALZOUBI KH, KHABOUR OF, TASHTOUSH
NH, BANIHANI SA, ABDUL-RAZZAK KK. EXPLORING THE
EFFECT OF VITAMIN C ON SLEEP DEPRIVATION
INDUCED MEMORY IMPAIRMENT. BRAIN RES BULL.
2015;113:41-7. [BACK]
301.
MOHAMMED BM, FISHER BJ, KRASKAUSKAS D, ET AL.
VITAMIN C PROMOTES WOUND HEALING THROUGH
NOVEL PLEIOTROPIC MECHANISMS. INT WOUND J. 2015;
[BACK]
302.
MURRAY EL. BURNING MOUTH SYNDROME RESPONSE
TO HIGH-DOSE VITAMIN C. HEADACHE. 2014;54(1):169.
[BACK]
303.
DAWOOD MA, KOSHIO S, ISHIKAWA M, YOKOYAMA S.
IMMUNE RESPONSES AND STRESS RESISTANCE IN RED
SEA BREAM, PAGRUS MAJOR, AFTER ORAL
ADMINISTRATION OF HEAT-KILLED LACTOBACILLUS
PLANTARUM AND VITAMIN C. FISH SHELLFISH
IMMUNOL. 2016;54:266-275. [BACK]
304.
SADEGHPOUR A, ALIZADEHASL A, KYAVAR M, ET AL.
IMPACT OF VITAMIN C SUPPLEMENTATION ON POST-
CARDIAC SURGERY ICU AND HOSPITAL LENGTH OF
STAY. ANESTH PAIN MED. 2015;5(1):E25337. [BACK]
305.
YANG M, BARAK OF, DUJIC Z, ET AL. ASCORBIC ACID
SUPPLEMENTATION DIMINISHES MICROPARTICLE
ELEVATIONS AND NEUTROPHIL ACTIVATION
FOLLOWING SCUBA DIVING. AM J PHYSIOL REGUL
INTEGR COMP PHYSIOL. 2015;309(4):R338-44. [BACK]
306.
BESSE JL, GADEYNE S, GALAND-DESMÉ S, LERAT JL,
MOYEN B. EFFECT OF VITAMIN C ON PREVENTION OF
COMPLEX REGIONAL PAIN SYNDROME TYPE I IN FOOT
AND ANKLE SURGERY. FOOT ANKLE SURG.
2009;15(4):179-82. [BACK]
307.
LANE DJ, RICHARDSON DR. THE ACTIVE ROLE OF
VITAMIN C IN MAMMALIAN IRON METABOLISM: MUCH
MORE THAN JUST ENHANCED IRON ABSORPTION!. FREE
RADIC BIOL MED. 2014;75:69-83. [BACK]
308.MAY JM, QU ZC, MENDIRATTA S. ROLE OF
ASCORBIC ACID IN TRANSFERRIN-INDEPENDENT
REDUCTION AND UPTAKE OF IRON BY U-937 CELLS.
BIOCHEM PHARMACOL. 1999;57(11):1275-82. [BACK]
309. LANE DJ, CHIKHANI S, RICHARDSON V,
RICHARDSON DR. TRANSFERRIN IRON UPTAKE IS
STIMULATED BY ASCORBATE VIA AN INTRACELLULAR
REDUCTIVE MECHANISM. BIOCHIM BIOPHYS ACTA.
2013;1833(6):1527-41. [BACK]
310.
MOJIĆ M, BOGDANOVIĆ PRISTOV J, MAKSIMOVIĆ-
IVANIĆ D, ET AL. EXTRACELLULAR IRON DIMINISHES
ANTICANCER EFFECTS OF VITAMIN C: AN IN VITRO
STUDY. SCI REP. 2014;4:5955. [BACK]
311.
ANGELUCCI E, PILO F. MANAGEMENT OF IRON
OVERLOAD BEFORE, DURING, AND AFTER
HEMATOPOIETIC STEM CELL TRANSPLANTATION FOR
THALASSEMIA MAJOR. ANN N Y ACAD SCI. 2016; [BACK]
312.
GRENIER D, HUOT MP, MAYRAND D. IRON-CHELATING
ACTIVITY OF TETRACYCLINES AND ITS IMPACT ON THE
SUSCEPTIBILITY OF ACTINOBACILLUS
ACTINOMYCETEMCOMITANS TO THESE ANTIBIOTICS.
ANTIMICROB AGENTS CHEMOTHER. 2000;44(3):763-6.
[BACK]
313.
NATIONAL INSTITUTES OF HEALTH. (2008). VITAMIN C
INJECTIONS SLOW TUMOR GROWTH IN MICE.
[AVAILABLE] HTTPS://WWW.NIH.GOV/NEWS-
EVENTS/NEWS-RELEASES/VITAMIN-C-INJECTIONS-
SLOW-TUMOR-GROWTH-MICE [MAY 11, 2016]. [BACK]
314.
HICKEY, S., & SAUL, A. W. (2008). VITAMIN C: THE REAL
STORY: THE REMARKABLE AND CONTROVERSIAL HEALING
FACTOR. LAGUNA BEACH, CA: BASIC HEALTH
PUBLICATIONS. [BACK]
315.
JACKSON CL, DREADEN TM, THEOBALD LK, ET AL.
PECTIN INDUCES APOPTOSIS IN HUMAN PROSTATE
CANCER CELLS: CORRELATION OF APOPTOTIC
FUNCTION WITH PECTIN STRUCTURE. GLYCOBIOLOGY.
2007;17(8):805-19. [BACK]
316.
ZHANG L, YE X, XUE SJ, ET AL. EFFECT OF HIGH-
INTENSITY ULTRASOUND ON THE PHYSICOCHEMICAL
PROPERTIES AND NANOSTRUCTURE OF CITRUS PECTIN.
J SCI FOOD AGRIC. 2013;93(8):2028-36. [BACK]
317.
LECLERE L, FRANSOLET M, CAMBIER P, ET AL.
IDENTIFICATION OF A CYTOTOXIC MOLECULE IN HEAT-
MODIFIED CITRUS PECTIN. CARBOHYDR POLYM.
2016;137:39-51. [BACK]
318.
GLINSKY VV, RAZ A. MODIFIED CITRUS PECTIN ANTI-
METASTATIC PROPERTIES: ONE BULLET, MULTIPLE
TARGETS. CARBOHYDR RES. 2009;344(14):1788-91.
[BACK]
319.
HUANG ZL, LIU HY. [EXPRESSION OF GALECTIN-3 IN
LIVER METASTASIS OF COLON CANCER AND THE
INHIBITORY EFFECT OF MODIFIED CITRUS PECTIN].
NAN FANG YI KE DA XUE XUE BAO. 2008;28(8):1358-61.
[BACK]
320.
HSIEH TC, WU JM. CHANGES IN CELL GROWTH,
CYCLIN/KINASE, ENDOGENOUS PHOSPHOPROTEINS
AND NM23 GENE EXPRESSION IN HUMAN PROSTATIC
JCA-1 CELLS TREATED WITH MODIFIED CITRUS PECTIN.
BIOCHEM MOL BIOL INT. 1995;37(5):833-41. [BACK]
321.
LECLERE L, FRANSOLET M, COTE F, ET AL. HEAT-
MODIFIED CITRUS PECTIN INDUCES APOPTOSIS-LIKE
CELL DEATH AND AUTOPHAGY IN HEPG2 AND A549
CANCER CELLS. PLOS ONE. 2015;10(3):E0115831. [BACK]
322.
 YAN J, KATZ A. PECTASOL-C MODIFIED CITRUS PECTIN
INDUCES APOPTOSIS AND INHIBITION OF
PROLIFERATION IN HUMAN AND MOUSE ANDROGEN-
DEPENDENT AND- INDEPENDENT PROSTATE CANCER
CELLS. INTEGR CANCER THER. 2010;9(2):197-203. [BACK]
323.
HAO M, YUAN X, CHENG H, ET AL. COMPARATIVE
STUDIES ON THE ANTI-TUMOR ACTIVITIES OF HIGH
TEMPERATURE- AND PH-MODIFIED CITRUS PECTINS.
FOOD FUNCT. 2013;4(6):960-71. [BACK]
324.
JIANG J, ELIAZ I, SLIVA D. SYNERGISTIC AND ADDITIVE
EFFECTS OF MODIFIED CITRUS PECTIN WITH TWO
POLYBOTANICAL COMPOUNDS, IN THE SUPPRESSION OF
INVASIVE BEHAVIOR OF HUMAN BREAST AND
PROSTATE CANCER CELLS. INTEGR CANCER THER.
2013;12(2):145-52. [BACK]
325.
WANG Y, NANGIA-MAKKER P, BALAN V, HOGAN V, RAZ
A. CALPAIN ACTIVATION THROUGH GALECTIN-3
INHIBITION SENSITIZES PROSTATE CANCER CELLS TO
CISPLATIN TREATMENT. CELL DEATH DIS. 2010;1:E101.
[BACK]
326.
HOSSEIN G, KESHAVARZ M, AHMADI S, NADERI N.
SYNERGISTIC EFFECTS OF PECTASOL-C MODIFIED
CITRUS PECTIN AN INHIBITOR OF GALECTIN-3 AND
PACLITAXEL ON APOPTOSIS OF HUMAN SKOV-3
OVARIAN CANCER CELLS. ASIAN PAC J CANCER PREV.
2013;14(12):7561-8. [BACK]
327.
INOHARA H, RAZ A. EFFECTS OF NATURAL COMPLEX
CARBOHYDRATE (CITRUS PECTIN) ON MURINE
MELANOMA CELL PROPERTIES RELATED TO GALECTIN-
3 FUNCTIONS. GLYCOCONJ J. 1994;11(6):527-32. [BACK]
328.
 NANGIA-MAKKER P, HOGAN V, HONJO Y, ET AL.
INHIBITION OF HUMAN CANCER CELL GROWTH AND
METASTASIS IN NUDE MICE BY ORAL INTAKE OF
MODIFIED CITRUS PECTIN. J NATL CANCER INST.
2002;94(24):1854-62. [BACK]
329.
PIENTA KJ, NAIK H, AKHTAR A, ET AL. INHIBITION OF
SPONTANEOUS METASTASIS IN A RAT PROSTATE
CANCER MODEL BY ORAL ADMINISTRATION OF
MODIFIED CITRUS PECTIN. J NATL CANCER INST.
1995;87(5):348-53. [BACK]
330.
PLATT D, RAZ A. MODULATION OF THE LUNG
COLONIZATION OF B16-F1 MELANOMA CELLS BY
CITRUS PECTIN. J NATL CANCER INST. 1992;84(6):438-42.
[BACK]
331.
LIU HY, HUANG ZL, YANG GH, LU WQ, YU NR.
INHIBITORY EFFECT OF MODIFIED CITRUS PECTIN ON
LIVER METASTASES IN A MOUSE COLON CANCER
MODEL. WORLD J GASTROENTEROL. 2008;14(48):7386-91.
[BACK]
332.
HAYASHI A, GILLEN AC, LOTT JR. EFFECTS OF DAILY
ORAL ADMINISTRATION OF QUERCETIN CHALCONE
AND MODIFIED CITRUS PECTIN ON IMPLANTED COLON-
25 TUMOR GROWTH IN BALB-C MICE. ALTERN MED REV.
2000;5(6):546-52. [BACK]
333.
MA Z, HAN Q, WANG X, AI Z, ZHENG Y. GALECTIN-3
INHIBITION IS ASSOCIATED WITH NEUROPATHIC PAIN
ATTENUATION AFTER PERIPHERAL NERVE INJURY. PLOS
ONE. 2016;11(2):E0148792. [BACK]
334.
ABU-ELSAAD NM, ELKASHEF WF. MODIFIED CITRUS
PECTIN STOPS PROGRESSION OF LIVER FIBROSIS BY
INHIBITING GALECTIN-3 AND INDUCING APOPTOSIS OF
STELLATE CELLS. CAN J PHYSIOL PHARMACOL.
2016;94(5):554-62. [BACK]
335.
KOLATSI-JOANNOU M, PRICE KL, WINYARD PJ, LONG
DA. MODIFIED CITRUS PECTIN REDUCES GALECTIN-3
EXPRESSION AND DISEASE SEVERITY IN
EXPERIMENTAL ACUTE KIDNEY INJURY. PLOS ONE.
2011;6(4):E18683. [BACK]
336.
CHEN CH, SHEU MT, CHEN TF, ET AL. SUPPRESSION OF
ENDOTOXIN-INDUCED PROINFLAMMATORY RESPONSES
BY CITRUS PECTIN THROUGH BLOCKING LPS
SIGNALING PATHWAYS. BIOCHEM PHARMACOL.
2006;72(8):1001-9. [BACK]
337.
ARAD U, MADAR-BALAKIRSKI N, ANGEL-KORMAN A,
ET AL. GALECTIN-3 IS A SENSOR-REGULATOR OF TOLL-
LIKE RECEPTOR PATHWAYS IN SYNOVIAL
FIBROBLASTS. CYTOKINE. 2015;73(1):30-5. [BACK]
338.
ELIAZ I, HOTCHKISS AT, FISHMAN ML, RODE D. THE
EFFECT OF MODIFIED CITRUS PECTIN ON URINARY
EXCRETION OF TOXIC ELEMENTS. PHYTOTHER RES.
2006;20(10):859-64. [BACK]
339.
ZHAO ZY, LIANG L, FAN X, ET AL. THE ROLE OF
MODIFIED CITRUS PECTIN AS AN EFFECTIVE CHELATOR
OF LEAD IN CHILDREN HOSPITALIZED WITH TOXIC
LEAD LEVELS. ALTERN THER HEALTH MED.
2008;14(4):34-8. [BACK]
340.
ELIAZ I, WEIL E, WILK B. INTEGRATIVE MEDICINE AND
THE ROLE OF MODIFIED CITRUS PECTIN/ALGINATES IN
HEAVY METAL CHELATION AND DETOXIFICATION--FIVE
CASE REPORTS. FORSCH KOMPLEMENTMED.
2007;14(6):358-64. [BACK]
341.
VERGARO G, PRUD'HOMME M, FAZAL L, ET AL.
INHIBITION OF GALECTIN-3 PATHWAY PREVENTS
ISOPROTERENOL-INDUCED LEFT VENTRICULAR
DYSFUNCTION AND FIBROSIS IN MICE. HYPERTENSION.
2016;67(3):606-12. [BACK]
342.
MARTÍNEZ-MARTÍNEZ E, LÓPEZ-ÁNDRES N, JURADO-
LÓPEZ R, ET AL. GALECTIN-3 PARTICIPATES IN
CARDIOVASCULAR REMODELING ASSOCIATED WITH
OBESITY. HYPERTENSION. 2015;66(5):961-9. [BACK]
343.MARTÍNEZ-MARTÍNEZ E, CALVIER L, FERNÁNDEZ-
CELIS A, ET AL. GALECTIN-3 BLOCKADE INHIBITS
CARDIAC INFLAMMATION AND FIBROSIS IN
EXPERIMENTAL HYPERALDOSTERONISM AND
HYPERTENSION. HYPERTENSION. 2015;66(4):767-75.
[BACK]
344. CALVIER L, MARTINEZ-MARTINEZ E, MIANA M, ET
AL. THE IMPACT OF GALECTIN-3 INHIBITION ON
ALDOSTERONE-INDUCED CARDIAC AND RENAL
INJURIES. JACC HEART FAIL. 2015;3(1):59-67. [BACK]
345.
MACKINNON AC, LIU X, HADOKE PW, MILLER MR,
NEWBY DE, SETHI T. INHIBITION OF GALECTIN-3
REDUCES ATHEROSCLEROSIS IN APOLIPOPROTEIN E-
DEFICIENT MICE. GLYCOBIOLOGY. 2013;23(6):654-63.
[BACK]
346.
RAMACHANDRAN C, WILK BJ, HOTCHKISS A, CHAU H,
ELIAZ I, MELNICK SJ. ACTIVATION OF HUMAN T-
HELPER/INDUCER CELL, T-CYTOTOXIC CELL, B-CELL,
AND NATURAL KILLER (NK)-CELLS AND INDUCTION OF
NATURAL KILLER CELL ACTIVITY AGAINST K562
CHRONIC MYELOID LEUKEMIA CELLS WITH MODIFIED
CITRUS PECTIN. BMC COMPLEMENT ALTERN MED.
2011;11:59. [BACK]
347.
MARTÍNEZ-MARTÍNEZ E, CALVIER L, ROSSIGNOL P, ET
AL. GALECTIN-3 INHIBITION PREVENTS ADIPOSE TISSUE
REMODELLING IN OBESITY. INT J OBES (LOND). 2016;
[BACK]
348.
DOURADO GK, STANILKA JM, PERCIVAL SS, CESAR TB.
CHEMOPREVENTIVE ACTIONS OF BLOND AND RED-
FLESHED SWEET ORANGE JUICE ON THE LOUCY
LEUKEMIA CELL LINE. ASIAN PAC J CANCER PREV.
2015;16(15):6491-9. [BACK]
349.
SO FV, GUTHRIE N, CHAMBERS AF, MOUSSA M,
CARROLL KK. INHIBITION OF HUMAN BREAST CANCER
CELL PROLIFERATION AND DELAY OF MAMMARY
TUMORIGENESIS BY FLAVONOIDS AND CITRUS JUICES.
NUTR CANCER. 1996;26(2):167-81. [BACK]
350.
TANAKA T, KOHNO H, MURAKAMI M, ET AL.
SUPPRESSION OF AZOXYMETHANE-INDUCED COLON
CARCINOGENESIS IN MALE F344 RATS BY MANDARIN
JUICES RICH IN BETA-CRYPTOXANTHIN AND
HESPERIDIN. INT J CANCER. 2000;88(1):146-50. [BACK]
351. MIYAGI Y, OM AS, CHEE KM, BENNINK MR.
INHIBITION OF AZOXYMETHANE-INDUCED COLON
CANCER BY ORANGE JUICE. NUTR CANCER.
2000;36(2):224-9. [BACK]
352.
TANAKA T, TANAKA T, TANAKA M, KUNO T. CANCER
CHEMOPREVENTION BY CITRUS PULP AND JUICES
CONTAINING HIGH AMOUNTS OF Β-CRYPTOXANTHIN
AND HESPERIDIN. J BIOMED BIOTECHNOL.
2012;2012:516981. [BACK]
353.
OIKEH EI, OMOREGIE ES, OVIASOGIE FE, ORIAKHI K.
PHYTOCHEMICAL, ANTIMICROBIAL, AND ANTIOXIDANT
ACTIVITIES OF DIFFERENT CITRUS JUICE
CONCENTRATES. FOOD SCI NUTR. 2016;4(1):103-9.
[BACK]
354.
BUSCEMI S, ROSAFIO G, ARCOLEO G, ET AL. EFFECTS
OF RED ORANGE JUICE INTAKE ON ENDOTHELIAL
FUNCTION AND INFLAMMATORY MARKERS IN ADULT
SUBJECTS WITH INCREASED CARDIOVASCULAR RISK.
AM J CLIN NUTR. 2012;95(5):1089-95. [BACK]
355.
KO SH, CHOI SW, YE SK, CHO BL, KIM HS, CHUNG MH.
COMPARISON OF THE ANTIOXIDANT ACTIVITIES OF
NINE DIFFERENT FRUITS IN HUMAN PLASMA. J MED
FOOD. 2005;8(1):41-6. [BACK]
356. CONSTANS J, BENNETAU-PELISSERO C, MARTIN JF,
ET AL. MARKED ANTIOXIDANT EFFECT OF ORANGE
JUICE INTAKE AND ITS PHYTOMICRONUTRIENTS IN A
PRELIMINARY RANDOMIZED CROSS-OVER TRIAL ON
MILD HYPERCHOLESTEROLEMIC MEN. CLIN NUTR.
2015;34(6):1093-100. [BACK]
357.
LEE SG, YANG M, WANG Y, ET AL. IMPACT OF ORANGE
JUICE CONSUMPTION ON BONE HEALTH OF THE U.S.
POPULATION IN THE NATIONAL HEALTH AND
NUTRITION EXAMINATION SURVEY 2003-2006. J MED
FOOD. 2014;17(10):1142-50. [BACK]
358.
DEYHIM F, GARICA K, LOPEZ E, ET AL. CITRUS JUICE
MODULATES BONE STRENGTH IN MALE SENESCENT
RAT MODEL OF OSTEOPOROSIS. NUTRITION.
2006;22(5):559-63. [BACK]
359.
PITTALUGA M, SGADARI A, TAVAZZI B, ET AL.
EXERCISE-INDUCED OXIDATIVE STRESS IN ELDERLY
SUBJECTS: THE EFFECT OF RED ORANGE
SUPPLEMENTATION ON THE BIOCHEMICAL AND
CELLULAR RESPONSE TO A SINGLE BOUT OF INTENSE
PHYSICAL ACTIVITY. FREE RADIC RES. 2013;47(3):202-11.
[BACK]
360.
APTEKMANN NP, CESAR TB. ORANGE JUICE IMPROVED
LIPID PROFILE AND BLOOD LACTATE OF OVERWEIGHT
MIDDLE-AGED WOMEN SUBJECTED TO AEROBIC
TRAINING. MATURITAS. 2010;67(4):343-7. [BACK]
361.
ESCUDERO-LÓPEZ B, BERNÁ G, ORTEGA Á, ET AL.
CONSUMPTION OF ORANGE FERMENTED BEVERAGE
REDUCES CARDIOVASCULAR RISK FACTORS IN
HEALTHY MICE. FOOD CHEM TOXICOL. 2015;78:78-85.
[BACK]
362.
ZANOTTI SIMOES DOURADO GK, DE ABREU RIBEIRO
LC, ZEPPONE CARLOS I, BORGES CÉSAR T. ORANGE
JUICE AND HESPERIDIN PROMOTE DIFFERENTIAL
INNATE IMMUNE RESPONSE IN MACROPHAGES EX
VIVO. INT J VITAM NUTR RES. 2013;83(3):162-7. [BACK]
363.
WANG Y, LLOYD B, YANG M, ET AL. IMPACT OF ORANGE
JUICE CONSUMPTION ON MACRONUTRIENT AND
ENERGY INTAKES AND BODY COMPOSITION IN THE US
POPULATION. PUBLIC HEALTH NUTR. 2012;15(12):2220-7.
[BACK]
364.
O'NEIL CE, NICKLAS TA, RAMPERSAUD GC, FULGONI
VL. 100% ORANGE JUICE CONSUMPTION IS ASSOCIATED
 WITH BETTER DIET QUALITY, IMPROVED NUTRIENT
ADEQUACY, DECREASED RISK FOR OBESITY, AND
IMPROVED BIOMARKERS OF HEALTH IN ADULTS:
NATIONAL HEALTH AND NUTRITION EXAMINATION
SURVEY, 2003-2006. NUTR J. 2012;11:107. [BACK]
365.
SALAMONE F, LI VOLTI G, TITTA L, ET AL. MORO
ORANGE JUICE PREVENTS FATTY LIVER IN MICE.
WORLD J GASTROENTEROL. 2012;18(29):3862-8. [BACK]
366.
AZIK M. PHYTOCHEMICALS IN CITRUS. FLORIDA
DEPARTMENT OF CITRUS. 2010. AVAILABLE:
HTTP://FDOCGROWER.COM/WP-
CONTENT/UPLOADS/2010/11/FLAVONOIDS_ORANGE.PDF.
[FEBRUARY 5, 2017]. [BACK]
367.
BETTER HEALTH PUBLISHING. NEW RESEARCH:
MODIFIED CITRUS PECTIN – A POTENT ANTI-CANCER
THERAPY. PR NEWSWIRE. 2013. [BACK]
368.
STONE I. ON THE GENETIC ETIOLOGY OF SCURVY.
ACTA GENET MED GEMELLOL (ROMA). 1966;15(4):345-50.
[BACK]
369.
JIAO Y, WILKINSON J, DI X, ET AL. CURCUMIN, A
CANCER CHEMOPREVENTIVE AND
CHEMOTHERAPEUTIC AGENT, IS A BIOLOGICALLY
ACTIVE IRON CHELATOR. BLOOD. 2009;113(2):462-9.
[BACK]

Coconut Oil
1. RIDGEWAY, S. (2016). DIFFERENT USES FOR A COCONUT.
[ONLINE]. AVAILABLE:
HTTPS://CALORIEBEE.COM/NUTRITION/DIFFERENT-
USES-FOR-A-COCONUT. [NOVEMBER 6, 2016]. [BACK]
2. DEBMANDAL M, MANDAL S. COCONUT (COCOS
NUCIFERA L.: ARECACEAE): IN HEALTH PROMOTION
AND DISEASE PREVENTION. ASIAN PAC J TROP MED.
2011;4(3):241-7. [BACK]
3. DELGADO, S.R. 1982. GLOSSÁRIO LUSO-ASIÁTICO, PART 1.
BUSKE VERLAG. [BACK]
4. MARINA, A.M., CHE MAN, Y.B., NAZIMAH, S.A.H. ET AL.
PHYSICOCHEMICAL PROPERTIES OF VIRGIN COCONUT
OIL EXTRACTED FROM DIFFERENT PROCESSING
METHODS. J AM OIL CHEM SOC. 2009;86: 301. [BACK]
5. MOIGRADEAN D, POIANA MA, GOGOASA I. QUALITY
CHARACTERISTICS AND OXIDATIVE STABILITY OF
COCONUT OIL DURING STORAGE. J AGRO. PROC. &
TECH. 2012; 18(4):272-276. [BACK]
6. SACHS M, VON EICHEL J, ASSKALI F. [WOUND
MANAGEMENT WITH COCONUT OIL IN INDONESIAN
FOLK MEDICINE]. CHIRURG. 2002;73(4):387-92. [BACK]
7. KRISHNA GAG, GAURAV R, SINGH BA, PRASANTH PKK,
PREETI C. COCONUT OIL: CHEMISTRY, PRODUCTION
AND ITS APPLICATIONS – A REVIEW. AGRIS. 2010. [BACK]
8. KAUNITZ H. COCONUT OIL CONSUMPTION AND
CORONARY HEART DISEASE. AGRIS. 1992. [BACK]
9. MARINA AM, CHE MAN YB, NAZIMAH SAH, AMIN I.
CHEMICAL PROPERTIES OF VIRGIN COCONUT OIL. J.
AMER. OIL. CHEM. SOC. 2009; 86(4):301-307. [BACK]
10. SRIVASTAVA KC, AWASTHI KK, LINDEGÅRD P, TIWARI KP.
EFFECT OF SOME SATURATED AND UNSATURATED
FATTY ACIDS ON PROSTAGLANDIN BIOSYNTHESIS IN
WASHED HUMAN BLOOD PLATELETS FROM (1-14
C)ARACHIDONIC ACID. PROSTAGLANDINS LEUKOT
MED. 1982;8(3):219-37. [BACK]
11. ZELENAY S,REIS E SOUSA C. REDUCING
PROSTAGLANDIN E2 PRODUCTION TO RAISE CANCER
 IMMUNOGENICITY. ONCOIMMUNOLOGY.
2016;5(5):E1123370. [BACK]
12. BELLAMKONDA K,CHANDRASHEKAR NK, OSMAN J,
SELVANESAN BC, SAVARI S, SJÖLANDER A. THE
EICOSANOIDS LEUKOTRIENE D4 AND PROSTAGLANDIN
E2 PROMOTE THE TUMORIGENICITY OF COLON
CANCER-INITIATING CELLS IN A XENOGRAFT MOUSE
MODEL. BMC CANCER. 2016;16:425. [BACK]
13. BIBBY DC, GRIMBLE RF. TUMOUR NECROSIS FACTOR-
ALPHA AND ENDOTOXIN INDUCE LESS
PROSTAGLANDIN E2 PRODUCTION FROM
HYPOTHALAMI OF RATS FED COCONUT OIL THAN FROM
HYPOTHALAMI OF RATS FED MAIZE OIL. CLIN SCI.
1990;79(6):657-62. [BACK]
14. HURDER, JOHNSTON JM, OKITA JR, MACDONALD PC,
ZIFF M, GILLIAM JW. PREVENTION OF
GLOMERULONEPHRITIS AND PROLONGED SURVIVAL IN
NEW ZEALAND BLACK/NEW ZEALAND WHITE F1
HYBRID MICE FED AN ESSENTIAL FATTY ACID-
DEFICIENT DIET. J CLIN INVEST. 1981;67(2):476-85.
[BACK]
15. DIRIX
CE, KESTER AD, HORNSTRA G. ASSOCIATIONS
BETWEEN TERM BIRTH DIMENSIONS AND PRENATAL
EXPOSURE TO ESSENTIAL AND TRANS FATTY ACIDS.
EARLY HUM DEV. 2009;85(8):525-30. [BACK]
16. DIRIX
CE, HORNSTRA G, NIJHUIS JG. FETAL LEARNING
AND MEMORY: WEAK ASSOCIATIONS WITH THE EARLY
ESSENTIAL POLYUNSATURATED FATTY ACID STATUS.
PROSTAGLANDINS LEUKOT ESSENT FATTY ACIDS.
2009;80(4):207-12. [BACK]
17. HSU YM, YIN MC. EPA OR DHA ENHANCED OXIDATIVE
STRESS AND AGING PROTEIN EXPRESSION IN BRAIN OF
D-GALACTOSE TREATED MICE. BIOMEDICINE (TAIPEI).
2016;6(3):17. [BACK]
18. KJAER
MA, TODORCEVIĆ M, TORSTENSEN BE,
VEGUSDAL A, RUYTER B. DIETARY N-3 HUFA AFFECTS
MITOCHONDRIAL FATTY ACID BETA-OXIDATION
CAPACITY AND SUSCEPTIBILITY TO OXIDATIVE STRESS
IN ATLANTIC SALMON. LIPIDS. 2008;43(9):813-27. [BACK]
19. THIES
F, GARRY JM, YAQOOB P, ET AL. ASSOCIATION OF
N-3 POLYUNSATURATED FATTY ACIDS WITH STABILITY
OF ATHEROSCLEROTIC PLAQUES: A RANDOMISED
CONTROLLED TRIAL. LANCET. 2003;361(9356):477-85.
[BACK]
20. RAPP JH,
CONNOR WE, LIN DS, PORTER JM. DIETARY
EICOSAPENTAENOIC ACID AND DOCOSAHEXAENOIC
ACID FROM FISH OIL. THEIR INCORPORATION INTO
ADVANCED HUMAN ATHEROSCLEROTIC PLAQUES.
ARTERIOSCLER THROMB. 1991;11(4):903-11. [BACK]
21. BURRML, ASHFIELD-WATT PA, DUNSTAN FD, ET AL.
LACK OF BENEFIT OF DIETARY ADVICE TO MEN WITH
ANGINA: RESULTS OF A CONTROLLED TRIAL. EUR J
CLIN NUTR. 2003;57(2):193-200. [BACK]
22. GREY A,BOLLAND M. CLINICAL TRIAL EVIDENCE AND
USE OF FISH OIL SUPPLEMENTS. JAMA INTERN MED.
2014;174(3):460-2. [BACK]
23. GASIMOV,C., HASHIMOVA, U., ABBASOV, A.,
ISMAYILOVA, A. (1994). CENTENARIANS IN AZERBAIJAN.
[ONLINE]. AVAILABLE:
HTTP://WWW.AZER.COM/AIWEB/CATEGORIES/MAGAZIN
E/23_FOLDER/23_ARTICLES/23_CENTENARIANS.HTML.
[NOVEMBER 6, 2016]. [BACK]
24. GRIGOROV
IUG, KOZLOVSKAIA SG, SEMES'KO TM,
ASADOV SHA. [CHARACTERISTICS OF ACTUAL
NUTRITION OF THE LONG-LIVED POPULATION OF
AZERBAIJAN]. VOPR PITAN. 1991;(2):36-40. [BACK]
25. PRIOR
IA, DAVIDSON F, SALMOND CE, CZOCHANSKA Z.
CHOLESTEROL, COCONUTS, AND DIET ON POLYNESIAN
 ATOLLS: A NATURAL EXPERIMENT: THE PUKAPUKA AND
TOKELAU ISLAND STUDIES. AM J CLIN NUTR.
1981;34(8):1552-61. [BACK]
26. KAUNITZ
H. MEDIUM CHAIN TRIGLYCERIDES (MCT) IN
AGING AND ARTERIOSCLEROSIS. J ENVIRON PATHOL
TOXICOL ONCOL. 1986;6(3-4):115-21. [BACK]
27. KAUNITZ H. COCONUT OIL CONSUMPTION AND
CORONARY HEART DISEASE. PHILLIP. J. INT. MED.
1992;30(3):165-171. [BACK]
28. SIRI-TARINO PW, SUN Q, HU FB, KRAUSS RM. META-
ANALYSIS OF PROSPECTIVE COHORT STUDIES
EVALUATING THE ASSOCIATION OF SATURATED FAT
WITH CARDIOVASCULAR DISEASE. AM J CLIN NUTR.
2010;91(3):535-46. [BACK]
29. MALHOTRA A. SATURATED FAT IS NOT THE MAJOR
ISSUE. BMJ. 2013;347:F6340. [BACK]
30. DE
SOUZA RJ, MENTE A, MAROLEANU A, ET AL. INTAKE
OF SATURATED AND TRANS UNSATURATED FATTY
ACIDS AND RISK OF ALL CAUSE MORTALITY,
CARDIOVASCULAR DISEASE, AND TYPE 2 DIABETES:
SYSTEMATIC REVIEW AND META-ANALYSIS OF
OBSERVATIONAL STUDIES. BMJ. 2015;351:H3978. [BACK]
31. MOZAFFARIAND, RIMM EB, HERRINGTON DM. DIETARY
FATS, CARBOHYDRATE, AND PROGRESSION OF
CORONARY ATHEROSCLEROSIS IN POSTMENOPAUSAL
WOMEN. AM J CLIN NUTR. 2004;80(5):1175-84. [BACK]
32. KLINE
BE, MILLER JA. THE CARCINOGENICITY OF P-
DIMETHYLAMINOAZOBENZENE IN DIETS CONTAINING
THE FATTY ACIDS OF HYDROGENATED COCONUT OIL
OR OF CORN OIL. CANCER RES. 1946;6:1-4. [BACK]
33. DAYTON
S, HASHIMOTO S, WOLLMAN J. EFFECT OF
HIGH-OLEIC AND HIGH-LINOLEIC SAFFLOWER OILS ON
MAMMARY TUMORS INDUCED IN RATS BY 7,12-
 DIMETHYLBENZ(ALPHA)ANTHRACENE. J NUTR.
1977;107(8):1353-60. [BACK]
34. BURNS CP, LUTTENEGGER DG, SPECTOR AA. EFFECT OF
DIETARY FAT SATURATION ON SURVIVAL OF MICE WITH
L1210 LEUKEMIA. J NATL CANCER INST. 1978;61(2):513-5.
[BACK]
35. HOPKINS GJ, KENNEDY TG, CARROLL KK.
POLYUNSATURATED FATTY ACIDS AS PROMOTERS OF
MAMMARY CARCINOGENESIS INDUCED IN SPRAGUE-
DAWLEY RATS BY 7,12-
DIMETHYLBENZ[A]ANTHRACENE. J NATL CANCER INST.
1981;66(3):517-22. [BACK]
36. IP C,
SINHA DK. ENHANCEMENT OF MAMMARY
TUMORIGENESIS BY DIETARY SELENIUM DEFICIENCY
IN RATS WITH A HIGH POLYUNSATURATED FAT INTAKE.
CANCER RES. 1981;41(1):31-4. [BACK]
37. REDDY BS,MAEURA Y. TUMOR PROMOTION BY
DIETARY FAT IN AZOXYMETHANE-INDUCED COLON
CARCINOGENESIS IN FEMALE F344 RATS: INFLUENCE
OF AMOUNT AND SOURCE OF DIETARY FAT. J NATL
CANCER INST. 1984;72(3):745-50. [BACK]
38. COHEN LA, THOMPSON DO, MAEURA Y, CHOI K, BLANK
ME, ROSE DP. DIETARY FAT AND MAMMARY CANCER. I.
PROMOTING EFFECTS OF DIFFERENT DIETARY FATS ON
N-NITROSOMETHYLUREA-INDUCED RAT MAMMARY
TUMORIGENESIS. J NATL CANCER INST. 1986;77(1):33-42.
[BACK]
39. COHEN LA. FAT AND ENDOCRINE-RESPONSIVE CANCER
IN ANIMALS. PREV MED. 1987;16(4):468-74. [BACK]
40. WELSCH CW. DIETARY FAT, CALORIES, AND MAMMARY
GLAND TUMORIGENESIS. ADV EXP MED BIOL.
1992;322:203-22. [BACK]
41. CRAIG-SCHMIDT M, WHITE MT, TEER P, JOHNSON J,
LANE HW. MENHADEN, COCONUT, AND CORN OILS AND
MAMMARY TUMOR INCIDENCE IN BALB/C VIRGIN
FEMALE MICE TREATED WITH DMBA. NUTR CANCER.
1993;20(2):99-106. [BACK]
42. ENOSRT, VELÁZQUEZ KT, MCCLELLAN JL, ET AL. HIGH-
FAT DIETS RICH IN SATURATED FAT PROTECT AGAINST
AZOXYMETHANE/DEXTRAN SULFATE SODIUM-
INDUCED COLON CANCER. AM J PHYSIOL
GASTROINTEST LIVER PHYSIOL. 2016;310(11):G906-19.
[BACK]
43. FIGUEROA, J. (2015). COCONUT OIL CURES CANCER.
[ONLINE]. AVAILABLE: HTTP://REVELATION12.CA/?
P=2110 . [NOVEMBER 6, 2016]. [BACK]
44. SHILLING
M, MATT L, RUBIN E, ET AL. ANTIMICROBIAL
EFFECTS OF VIRGIN COCONUT OIL AND ITS MEDIUM-
CHAIN FATTY ACIDS ON CLOSTRIDIUM DIFFICILE. J MED
FOOD. 2013;16(12):1079-85. [BACK]
45. VERALLO-ROWELL VM, DILLAGUE KM, SYAH-
TJUNDAWAN BS. NOVEL ANTIBACTERIAL AND
EMOLLIENT EFFECTS OF COCONUT AND VIRGIN OLIVE
OILS IN ADULT ATOPIC DERMATITIS. DERMATITIS.
2008;19(6):308-15. [BACK]
46. SHINO
B, PEEDIKAYIL FC, JAIPRAKASH SR, AHMED
BIJAPUR G, KOTTAYI S, JOSE D. COMPARISON OF
ANTIMICROBIAL ACTIVITY OF CHLORHEXIDINE,
COCONUT OIL, PROBIOTICS, AND KETOCONAZOLE ON
CANDIDA ALBICANS ISOLATED IN CHILDREN WITH
EARLY CHILDHOOD CARIES: AN IN VITRO STUDY.
SCIENTIFICA (CAIRO). 2016;2016:7061587. [BACK]
47. OGBOLU DO, ONI AA, DAINI OA, OLOKO AP. IN VITRO
ANTIMICROBIAL PROPERTIES OF COCONUT OIL ON
CANDIDA SPECIES IN IBADAN, NIGERIA. J MED FOOD.
2007;10(2):384-7. [BACK]
48. MARINA AM, MAN YB, NAZIMAH SA, AMIN I.
ANTIOXIDANT CAPACITY AND PHENOLIC ACIDS OF
VIRGIN COCONUT OIL. INT J FOOD SCI NUTR. 2009;60
SUPPL 2:114-23. [BACK]
49. YEAP SK,
BEH BK, ALI NM, ET AL. ANTISTRESS AND
ANTIOXIDANT EFFECTS OF VIRGIN COCONUT OIL IN
VIVO. EXP THER MED. 2015;9(1):39-42. [BACK]
50. OTUECHERE CA, MADARIKAN G, SIMISOLA T, BANKOLE
O, OSHO A. VIRGIN COCONUT OIL PROTECTS AGAINST
LIVER DAMAGE IN ALBINO RATS CHALLENGED WITH
THE ANTI-FOLATE COMBINATION, TRIMETHOPRIM-
SULFAMETHOXAZOLE. J BASIC CLIN PHYSIOL
PHARMACOL. 2014;25(2):249-53. [BACK]
51. NAIR
SS, MANALIL JJ, RAMAVARMA SK, SUSEELA IM,
THEKKEPATT A, RAGHAVAMENON AC. VIRGIN COCONUT
OIL SUPPLEMENTATION AMELIORATES
CYCLOPHOSPHAMIDE-INDUCED SYSTEMIC TOXICITY IN
MICE. HUM EXP TOXICOL. 2016;35(2):205-12. [BACK]
52. SHADNIA S, RAHIMI M, PAJOUMAND A, RASOULI MH,
ABDOLLAHI M. SUCCESSFUL TREATMENT OF ACUTE
ALUMINIUM PHOSPHIDE POISONING: POSSIBLE
BENEFIT OF COCONUT OIL. HUM EXP TOXICOL.
2005;24(4):215-8. [BACK]
53. LAWKS, AZMAN N, OMAR EA, ET AL. THE EFFECTS OF
VIRGIN COCONUT OIL (VCO) AS SUPPLEMENTATION ON
QUALITY OF LIFE (QOL) AMONG BREAST CANCER
PATIENTS. LIPIDS HEALTH DIS. 2014;13:139. [BACK]
54. COCONUT OIL IN HEALTH AND DISEASE: ITS AND
MONOLAURIN’S POTENTIAL AS CURE FOR AIDS.
UNKNOWN JOURNAL. DATE UNKNOWN. AVAILABLE:
HTTPS://WWW.RESEARCHGATE.NET/PUBLICATION/23723
3256_COCONUT_OIL_IN_HEALTH_AND_DISEASE_ITS_AN
D_MONOLAURIN%27S_POTENTIAL_AS_CURE_FOR_HIVA
IDS_BY. [FEBRUARY 15, 2017]. [BACK]
55. INTERVIEWS AND ANECDOTAL REPORTS. POSIT HEALTH
NEWS. 1998;(NO 16):13-5. [BACK]
56. VYSAKH A,RATHEESH M, RAJMOHANAN TP, ET AL.
POLYPHENOLICS ISOLATED FROM VIRGIN COCONUT
OIL INHIBITS ADJUVANT INDUCED ARTHRITIS IN RATS
THROUGH ANTIOXIDANT AND ANTI-INFLAMMATORY
ACTION. INT IMMUNOPHARMACOL. 2014;20(1):124-30.
[BACK]
57. HAYATULLINA Z,
MUHAMMAD N, MOHAMED N,
SOELAIMAN IN. VIRGIN COCONUT OIL
SUPPLEMENTATION PREVENTS BONE LOSS IN
OSTEOPOROSIS RAT MODEL. EVID BASED
COMPLEMENT ALTERNAT MED. 2012;2012:237236. [BACK]
58. ABUJAZIA MA,MUHAMMAD N, SHUID AN, SOELAIMAN
IN. THE EFFECTS OF VIRGIN COCONUT OIL ON BONE
OXIDATIVE STATUS IN OVARIECTOMISED RAT. EVID
BASED COMPLEMENT ALTERNAT MED. 2012;2012:525079.
[BACK]
59. HU YANGI, DE LA RUBIA ORTÍ JE, SELVI SABATER P, ET
AL. [COCONUT OIL: NON-ALTERNATIVE DRUG
TREATMENT AGAINST ALZHEIMER’S DISEASE]. NUTR
HOSP. 2015;32(6):2822-7. [BACK]
60. NEWPORT, S. (2013). COCONUT OIL HAS IMPROVED MY
LIFE. [ONLINE]. AVAILABLE:
HTTPS://HEALTHUNLOCKED.COM/PARKINSONSMOVEME
NT/POSTS/1170627/COCONUT-OIL-HAS-IMPROVED-MY-
LIFE [NOVEMBER 6, 2016]. [BACK]
61. SANKARANARAYANAN K, MONDKAR JA, CHAUHAN
MM, MASCARENHAS BM, MAINKAR AR, SALVI RY. OIL
MASSAGE IN NEONATES: AN OPEN RANDOMIZED
CONTROLLED STUDY OF COCONUT VERSUS MINERAL
OIL. INDIAN PEDIATR. 2005;42(9):877-84. [BACK]
62. PEEDIKAYIL FC,
SREENIVASAN P, NARAYANAN A.
EFFECT OF COCONUT OIL IN PLAQUE RELATED
 GINGIVITIS - A PRELIMINARY REPORT. NIGER MED J.
2015;56(2):143-7. [BACK]
63. KAUSHIK
M, REDDY P, SHARMA R, UDAMESHI P, MEHRA
N, MARWAHA A. THE EFFECT OF COCONUT OIL PULLING
ON STREPTOCOCCUS MUTANS COUNT IN SALIVA IN
COMPARISON WITH CHLORHEXIDINE MOUTHWASH. J
CONTEMP DENT PRACT. 2016;17(1):38-41. [BACK]
64. SINGLA N, ACHARYA S,
MARTENA S, SINGLA R. EFFECT
OF OIL GUM MASSAGE THERAPY ON COMMON
PATHOGENIC ORAL MICROORGANISMS - A
RANDOMIZED CONTROLLED TRIAL. J INDIAN SOC
PERIODONTOL. 2014;18(4):441-6. [BACK]
65. HOUSSAY BA,MARTÍNEZ C. EXPERIMENTAL DIABETES
AND DIET. SCIENCE. 1947;105(2734):548-9. [BACK]
66. NARAYANANKUTTY A, MUKESH RK, AYOOB SK, ET AL.
VIRGIN COCONUT OIL MAINTAINS REDOX STATUS AND
IMPROVES GLYCEMIC CONDITIONS IN HIGH FRUCTOSE
FED RATS. J FOOD SCI TECHNOL. 2016;53(1):895-901.
[BACK]
67. ALVESNF, PORPINO SK, MONTEIRO MM, GOMES ER,
BRAGA VA. COCONUT OIL SUPPLEMENTATION AND
PHYSICAL EXERCISE IMPROVES BAROREFLEX
SENSITIVITY AND OXIDATIVE STRESS IN
HYPERTENSIVE RATS. APPL PHYSIOL NUTR METAB.
2015;40(4):393-400. [BACK]
68. MUTALIBHA, KAUR S, GHAZALI AR, CHINN HOOI N,
SAFIE NH. A PILOT STUDY: THE EFFICACY OF VIRGIN
COCONUT OIL AS OCULAR REWETTING AGENT ON
RABBIT EYES. EVID BASED COMPLEMENT ALTERNAT
MED. 2015;2015:135987. [BACK]
69. BOWEN YOHOWS, SWANK VA, EASTRIDGE ML, O'DIAM
KM, DANIELS KM. JERSEY CALF PERFORMANCE IN
RESPONSE TO HIGH-PROTEIN, HIGH-FAT LIQUID FEEDS
 WITH VARIED FATTY ACID PROFILES: INTAKE AND
PERFORMANCE. J DAIRY SCI. 2013;96(4):2494-506. [BACK]
70. WANG J, WANG X, LI J, CHEN Y, YANG W, ZHANG L.
EFFECTS OF DIETARY COCONUT OIL AS A MEDIUM-
CHAIN FATTY ACID SOURCE ON PERFORMANCE,
CARCASS COMPOSITION AND SERUM LIPIDS IN MALE
BROILERS. ASIAN-AUSTRALAS J ANIM SCI.
2015;28(2):223-30. [BACK]
71. HAMMER CT, WILLS ED. THE EFFECT OF IONIZING
RADIATION ON THE FATTY ACID COMPOSITION OF
NATURAL FATS AND ON LIPID PEROXIDE FORMATION.
INT J RADIAT BIOL RELAT STUD PHYS CHEM MED.
1979;35(4):323-32. [BACK]
72. RELE AS,
MOHILE RB. EFFECT OF MINERAL OIL,
SUNFLOWER OIL, AND COCONUT OIL ON PREVENTION
OF HAIR DAMAGE. J COSMET SCI. 2003;54(2):175-92.
[BACK]
73. RELE AS,MOHILE RB. EFFECT OF COCONUT OIL ON
PREVENTION OF HAIR DAMAGE. PART 1. J. COSMET. SCI.
1999; 50:327-339. [BACK]
74. BURGESSIF, BRUNTON ER, BURGESS NA. CLINICAL
TRIAL SHOWING SUPERIORITY OF A COCONUT AND
ANISE SPRAY OVER PERMETHRIN 0.43% LOTION FOR
HEAD LOUSE INFESTATION, ISRCTN96469780. EUR J
PEDIATR. 2010;169(1):55-62. [BACK]
75. NEVIN
KG, RAJAMOHAN T. EFFECT OF TOPICAL
APPLICATION OF VIRGIN COCONUT OIL ON SKIN
COMPONENTS AND ANTIOXIDANT STATUS DURING
DERMAL WOUND HEALING IN YOUNG RATS. SKIN
PHARMACOL PHYSIOL. 2010;23(6):290-7. [BACK]
76. NURUL-IMAN BS, KAMISAH Y, JAARIN K, QODRIYAH HM.
VIRGIN COCONUT OIL PREVENTS BLOOD PRESSURE
ELEVATION AND IMPROVES ENDOTHELIAL FUNCTIONS
IN RATS FED WITH REPEATEDLY HEATED PALM OIL.
 EVID BASED COMPLEMENT ALTERNAT MED.
2013;2013:629329. [BACK]
77. DEOL P,
EVANS JR, DHAHBI J, ET AL. SOYBEAN OIL IS
MORE OBESOGENIC AND DIABETOGENIC THAN
COCONUT OIL AND FRUCTOSE IN MOUSE: POTENTIAL
ROLE FOR THE LIVER. PLOS ONE. 2015;10(7):E0132672.
[BACK]
78. ASSUNÇÃO ML, FERREIRA HS, DOS SANTOS AF, CABRAL
CR, FLORÊNCIO TM. EFFECTS OF DIETARY COCONUT
OIL ON THE BIOCHEMICAL AND ANTHROPOMETRIC
PROFILES OF WOMEN PRESENTING ABDOMINAL
OBESITY. LIPIDS. 2009;44(7):593-601. [BACK]
79. LIAUKM, LEE YY, CHEN CK, RASOOL AH. AN OPEN-
LABEL PILOT STUDY TO ASSESS THE EFFICACY AND
SAFETY OF VIRGIN COCONUT OIL IN REDUCING
VISCERAL ADIPOSITY. ISRN PHARMACOL.
2011;2011:949686. [BACK]
80. CARDOSO DA, MOREIRA AS, DE OLIVEIRA GM, RAGGIO
LUIZ R, ROSA G. A COCONUT EXTRA VIRGIN OIL-RICH
DIET INCREASES HDL CHOLESTEROL AND DECREASES
WAIST CIRCUMFERENCE AND BODY MASS IN
CORONARY ARTERY DISEASE PATIENTS. NUTR HOSP.
2015;32(5):2144-52. [BACK]
81. LAWRENCEGD. DIETARY FATS AND HEALTH: DIETARY
RECOMMENDATIONS IN THE CONTEXT OF SCIENTIFIC
EVIDENCE. ADV NUTR. 2013;4(3):294-302. [BACK]
82. KORAĆRR, KHAMBHOLJA KM. POTENTIAL OF HERBS IN
SKIN PROTECTION FROM ULTRAVIOLET RADIATION.
PHARMACOGN REV. 2011;5(10):164-73. [BACK]
83. EVANGELISTA MT, ABAD-CASINTAHAN F, LOPEZ-
VILLAFUERTE L. THE EFFECT OF TOPICAL VIRGIN
COCONUT OIL ON SCORAD INDEX, TRANSEPIDERMAL
WATER LOSS, AND SKIN CAPACITANCE IN MILD TO
MODERATE PEDIATRIC ATOPIC DERMATITIS: A
 RANDOMIZED, DOUBLE-BLIND, CLINICAL TRIAL. INT J
DERMATOL. 2014;53(1):100-8. [BACK]
84. ALOIA RC,
MLEKUSCH W. THE EFFECT OF A SATURATED
FAT DIET ON PENTOBARBITAL INDUCED SLEEPING TIME
AND PHOSPHOLIPID COMPOSITION OF MOUSE BRAIN
AND LIVER. PHARMAZIE. 1988;43(7):496-8. [BACK]
85. CHEMPRO. TOP-NOTCH TECHNOLOGY IN PRODUCTION
OF OILS AND FATS. AVAILABLE AT:
HTTP://WWW.CHEMPRO.IN/FATTYACID.HTM. [FEBRUARY
6, 2016]. [BACK]
86. MAGALHÃES MS, FECHINE FV, MACEDO RN, ET AL.
EFFECT OF A COMBINATION OF MEDIUM CHAIN
TRIGLYCERIDES, LINOLEIC ACID, SOY LECITHIN AND
VITAMINS A AND E ON WOUND HEALING IN RATS. ACTA
CIR BRAS. 2008;23(3):262-9. [BACK]
87. BACH AC, BABAYAN VK. MEDIUM-CHAIN
TRIGLYCERIDES: AN UPDATE. AM J CLIN NUTR.
1982;36(5):950-62. [BACK]
88. BACH A,
PHAN T, METAIS P. INFLUENCE OF A LONG OR
MEDIUM CHAIN TRIGLYCERIDE DIET ON
INTERMEDIARY HEPATIC METABOLISM OF THE RAT.
NUTR METAB. 1975;19(1-2):103-10. [BACK]
89. BACH A,SCHIRARDIN H, WERYHA A, BAUER M.
KETOGENIC RESPONSE TO MEDIUM-CHAIN
TRIGLYCERIDE LOAD IN THE RAT. J NUTR.
1977;107(10):1863-70. [BACK]
90. COHEN LA, THOMPSON DO, MAEURA Y, WEISBURGER
JH. INFLUENCE OF DIETARY MEDIUM-CHAIN
TRIGLYCERIDES ON THE DEVELOPMENT OF N-
METHYLNITROSOUREA-INDUCED RAT MAMMARY
TUMORS. CANCER RES. 1984;44(11):5023-8. [BACK]
91. TISDALE
MJ, BRENNAN RA, FEARON KC. REDUCTION OF
WEIGHT LOSS AND TUMOUR SIZE IN A CACHEXIA
 MODEL BY A HIGH FAT DIET. BR J CANCER. 1987;56(1):39-
43. [BACK]
92. COHEN LA, THOMPSON DO. THE INFLUENCE OF
DIETARY MEDIUM CHAIN TRIGLYCERIDES ON RAT
MAMMARY TUMOR DEVELOPMENT. LIPIDS.
1987;22(6):455-61. [BACK]
93. TISDALE
MJ, BRENNAN RA. A COMPARISON OF LONG-
CHAIN TRIGLYCERIDES AND MEDIUM-CHAIN
TRIGLYCERIDES ON WEIGHT LOSS AND TUMOUR SIZE
IN A CACHEXIA MODEL. BR J CANCER. 1988;58(5):580-3.
[BACK]
94. TISDALE
MJ, LEUNG YC. CHANGES IN HOST LIVER
FATTY ACID SYNTHASE IN TUMOUR-BEARING MICE.
CANCER LETT. 1988;42(3):231-5. [BACK]
95. KIMOTO Y,
TANJI Y, TAGUCHI T, ET AL. ANTITUMOR
EFFECT OF MEDIUM-CHAIN TRIGLYCERIDE AND ITS
INFLUENCE ON THE SELF-DEFENSE SYSTEM OF THE
BODY. CANCER DETECT PREV. 1998;22(3):219-24. [BACK]
96. POURGHOLAMI MH, AKHTER J, MORRIS DL. IN VITRO
ANTIPROLIFERATIVE ACTIVITY OF A MEDIUM-CHAIN
TRIGLYCERIDE SOLUTION OF 1,25-DIHYDROXYVITAMIN
D3 IN HEPG2 CELLS. ANTICANCER RES. 2000;20(6B):4257-
60. [BACK]
97. KAEWSAKHORN T, KISSEBERTH WC, CAPEN CC, HAYES
KA, CALVERLEY MJ, INPANBUTR N. EFFECTS OF
CALCITRIOL, SEOCALCITOL, AND MEDIUM-CHAIN
TRIGLYCERIDE ON A CANINE TRANSITIONAL CELL
CARCINOMA CELL LINE. ANTICANCER RES.
2005;25(4):2689-96. [BACK]
98. WANGX, PAN L, ZHANG P, ET AL. ENTERAL NUTRITION
IMPROVES CLINICAL OUTCOME AND SHORTENS
HOSPITAL STAY AFTER CANCER SURGERY. J INVEST
SURG. 2010;23(6):309-13. [BACK]
99. NOMURA A,MAJUMDER K, GIRI B, ET AL. INHIBITION OF
NF-KAPPA B PATHWAY LEADS TO DEREGULATION OF
EPITHELIAL-MESENCHYMAL TRANSITION AND NEURAL
INVASION IN PANCREATIC CANCER. LAB INVEST. 2016.
[BACK]
100.WU L, ZHANG X, ZHANG B, ET AL. EXOSOMES
DERIVED FROM GASTRIC CANCER CELLS ACTIVATE NF-
ΚB PATHWAY IN MACROPHAGES TO PROMOTE CANCER
PROGRESSION. TUMOUR BIOL. 2016;37(9):12169-12180.
[BACK]
101. WANG X, LIN Y. TUMOR NECROSIS FACTOR AND
CANCER, BUDDIES OR FOES?. ACTA PHARMACOL SIN.
2008;29(11):1275-88. [BACK]
102.
RUSYN I, BRADHAM CA, COHN L, ET AL. CORN OIL
RAPIDLY ACTIVATES NUCLEAR FACTOR-KAPPAB IN
HEPATIC KUPFFER CELLS BY OXIDANT-DEPENDENT
MECHANISMS. CARCINOGENESIS. 1999;20(11):2095-100.
[BACK]
103.
GOGOS CA, ZOUMBOS N, MAKRI M, KALFARENTZOS F.
MEDIUM- AND LONG-CHAIN TRIGLYCERIDES HAVE
DIFFERENT EFFECTS ON THE SYNTHESIS OF TUMOR
NECROSIS FACTOR BY HUMAN MONONUCLEAR CELLS
IN PATIENTS UNDER TOTAL PARENTERAL NUTRITION. J
AM COLL NUTR. 1994;13(1):40-4. [BACK]
104.
BUSSARD KM, MUTKUS L, STUMPF K, GOMEZ-
MANZANO C, MARINI FC. TUMOR-ASSOCIATED
STROMAL CELLS AS KEY CONTRIBUTORS TO THE
TUMOR MICROENVIRONMENT. BREAST CANCER RES.
2016;18(1):84. [BACK]
105.
HA NH, PARK DG, WOO BH, ET AL. PORPHYROMONAS
GINGIVALIS INCREASES THE INVASIVENESS OF ORAL
CANCER CELLS BY UPREGULATING IL-8 AND MMPS.
CYTOKINE. 2016;86:64-72. [BACK]
106.
HOSHIMOTO A, SUZUKI Y, KATSUNO T, NAKAJIMA H,
SAITO Y. CAPRYLIC ACID AND MEDIUM-CHAIN
TRIGLYCERIDES INHIBIT IL-8 GENE TRANSCRIPTION IN
CACO-2 CELLS: COMPARISON WITH THE POTENT
HISTONE DEACETYLASE INHIBITOR TRICHOSTATIN A.
BR J PHARMACOL. 2002;136(2):280-6. [BACK]
107.
CALABRESE PR, FRANK HD, TAUBIN HL.
LYMPHANGIOMYOMATOSIS WITH CHYLOUS ASCITES:
TREATMENT WITH DIETARY FAT RESTRICTION AND
MEDIUM CHAIN TRIGLYCERIDES. CANCER.
1977;40(2):895-7. [BACK]
108.
NEBELING LC, MIRALDI F, SHURIN SB, LERNER E.
EFFECTS OF A KETOGENIC DIET ON TUMOR
METABOLISM AND NUTRITIONAL STATUS IN PEDIATRIC
ONCOLOGY PATIENTS: TWO CASE REPORTS. J AM COLL
NUTR. 1995;14(2):202-8. [BACK]
109.
KONO H, ENOMOTO N, CONNOR HD, ET AL. MEDIUM-
CHAIN TRIGLYCERIDES INHIBIT FREE RADICAL
FORMATION AND TNF-ALPHA PRODUCTION IN RATS
GIVEN ENTERAL ETHANOL. AM J PHYSIOL
GASTROINTEST LIVER PHYSIOL. 2000;278(3):G467-76.
[BACK]
110.
ZHONG W, LI Q, XIE G, ET AL. DIETARY FAT SOURCES
DIFFERENTIALLY MODULATE INTESTINAL BARRIER
AND HEPATIC INFLAMMATION IN ALCOHOL-INDUCED
LIVER INJURY IN RATS. AM J PHYSIOL GASTROINTEST
LIVER PHYSIOL. 2013;305(12):G919-32. [BACK]
111. RONIS MJ, KOROURIAN S, ZIPPERMAN M, HAKKAK
R, BADGER TM. DIETARY SATURATED FAT REDUCES
ALCOHOLIC HEPATOTOXICITY IN RATS BY ALTERING
FATTY ACID METABOLISM AND MEMBRANE
COMPOSITION. J NUTR. 2004;134(4):904-12. [BACK]
112.
NANJI AA, JOKELAINEN K, TIPOE GL, RAHEMTULLA A,
DANNENBERG AJ. DIETARY SATURATED FATTY ACIDS
REVERSE INFLAMMATORY AND FIBROTIC CHANGES IN
RAT LIVER DESPITE CONTINUED ETHANOL
ADMINISTRATION. J PHARMACOL EXP THER.
2001;299(2):638-44. [BACK]
113.
KHORAMNIA A, EBRAHIMPOUR A, GHANBARI R,
AJDARI Z, LAI OM. IMPROVEMENT OF MEDIUM CHAIN
FATTY ACID CONTENT AND ANTIMICROBIAL ACTIVITY
OF COCONUT OIL VIA SOLID-STATE FERMENTATION
USING A MALAYSIAN GEOTRICHUM CANDIDUM.
BIOMED RES INT. 2013;2013:954542. [BACK]
114.
SHILLING M, MATT L, RUBIN E, ET AL. ANTIMICROBIAL
EFFECTS OF VIRGIN COCONUT OIL AND ITS MEDIUM-
CHAIN FATTY ACIDS ON CLOSTRIDIUM DIFFICILE. J MED
FOOD. 2013;16(12):1079-85. [BACK]
115.
ISAACS CE, LITOV RE, THORMAR H. ANTIMICROBIAL
ACTIVITY OF LIPIDS ADDED TO HUMAN MILK, INFANT
FORMULA, AND BOVINE MILK. J NUTR BIOCHEM.
1995;6(7):362-366. [BACK]
116.
PAPAVASSILIS C, MACH KK, MAYSER PA. MEDIUM-
CHAIN TRIGLYCERIDES INHIBIT GROWTH OF
MALASSEZIA: IMPLICATIONS FOR PREVENTION OF
SYSTEMIC INFECTION. CRIT CARE MED. 1999;27(9):1781-
6. [BACK]
117.
 KONO H, FUJII H, ASAKAWA M, ET AL. PROTECTIVE
EFFECTS OF MEDIUM-CHAIN TRIGLYCERIDES ON THE
LIVER AND GUT IN RATS ADMINISTERED ENDOTOXIN.
ANN SURG. 2003;237(2):246-55. [BACK]
118.
LIN MT, YEH SL, KUO ML, ET AL. EFFECTS OF MEDIUM-
CHAIN TRIGLYCERIDE IN PARENTERAL NUTRITION ON
RATS UNDERGOING GASTRECTOMY. CLIN NUTR.
2002;21(1):39-43. [BACK]
119.
ISAACS CE, KIM KS, THORMAR H. INACTIVATION OF
ENVELOPED VIRUSES IN HUMAN BODILY FLUIDS BY
PURIFIED LIPIDS. ANN N Y ACAD SCI. 1994;724:457-64.
[BACK]
120.
WANKE C. SINGLE-AGENT/COMBINATION THERAPY OF
HUMAN IMMUNODEFICIENCY VIRUS-RELATED
WASTING. SEMIN ONCOL. 1998;25(2 SUPPL 6):98-103.
[BACK]
121. WANKE CA, PLESKOW D, DEGIROLAMI PC, LAMBL
BB, MERKEL K, AKRABAWI S. A MEDIUM CHAIN
TRIGLYCERIDE-BASED DIET IN PATIENTS WITH HIV AND
CHRONIC DIARRHEA REDUCES DIARRHEA AND
MALABSORPTION: A PROSPECTIVE, CONTROLLED
TRIAL. NUTRITION. 1996;12(11-12):766-71. [BACK]
122.
CARLSON SJ, NANDIVADA P, CHANG MI, ET AL. THE
ADDITION OF MEDIUM-CHAIN TRIGLYCERIDES TO A
PURIFIED FISH OIL-BASED DIET ALTERS
INFLAMMATORY PROFILES IN MICE. METAB CLIN EXP.
2015;64(2):274-82. [BACK]
123.
HERBERT MR, BUCKLEY JA. AUTISM AND DIETARY
THERAPY: CASE REPORT AND REVIEW OF THE
LITERATURE. J CHILD NEUROL. 2013;28(8):975-82. [BACK]
 124.
KEHAYOGLOU K, HADZIYANNIS S, KOSTAMIS P,
MALAMOS B. THE EFFECT OF MEDIUM-CHAIN
TRIGLYCERIDE ON 47 CALCIUM ABSORPTION IN
PATIENTS WITH PRIMARY BILIARY CIRRHOSIS. GUT.
1973;14(8):653-6. [BACK]
125.KEHAYOGLOU AK, WILLIAMS HS, WHIMSTER WF,
HOLDSWORTH CD. CALCIUM ABSORPTION IN THE
NORMAL, BILE-DUCT LIGATED, AND CIRRHOTIC RAT,
WITH OBSERVATIONS ON THE EFFECT OF LONG- AND
MEDIUM-CHAIN TRIGLYCERIDES. GUT. 1968;9(5):597-603.
[BACK]
126.
PAN Y, LARSON B, ARAUJO JA, ET AL. DIETARY
SUPPLEMENTATION WITH MEDIUM-CHAIN TAG HAS
LONG-LASTING COGNITION-ENHANCING EFFECTS IN
AGED DOGS. BR J NUTR. 2010;103(12):1746-54. [BACK]
127. MANTECA X. NUTRITION AND BEHAVIOR IN
SENIOR DOGS. TOP COMPANION ANIM MED.
2011;26(1):33-6. [BACK]
128.
SHARMA A, BEMIS M, DESILETS AR. ROLE OF MEDIUM
CHAIN TRIGLYCERIDES (AXONA®) IN THE TREATMENT
OF MILD TO MODERATE ALZHEIMER'S DISEASE. AM J
ALZHEIMERS DIS OTHER DEMEN. 2014;29(5):409-14.
[BACK]
129. OHNUMA T, TODA A, KIMOTO A, ET AL. BENEFITS
OF USE, AND TOLERANCE OF, MEDIUM-CHAIN
TRIGLYCERIDE MEDICAL FOOD IN THE MANAGEMENT
OF JAPANESE PATIENTS WITH ALZHEIMER'S DISEASE: A
PROSPECTIVE, OPEN-LABEL PILOT STUDY. CLIN INTERV
AGING. 2016;11:29-36. [BACK]
130. CUNNANE SC, COURCHESNE-LOYER A, ST-PIERRE
V, ET AL. CAN KETONES COMPENSATE FOR
DETERIORATING BRAIN GLUCOSE UPTAKE DURING
AGING? IMPLICATIONS FOR THE RISK AND TREATMENT
OF ALZHEIMER'S DISEASE. ANN N Y ACAD SCI.
2016;1367(1):12-20. [BACK]
131.
REBELLO CJ, KELLER JN, LIU AG, JOHNSON WD,
GREENWAY FL. PILOT FEASIBILITY AND SAFETY STUDY
EXAMINING THE EFFECT OF MEDIUM CHAIN
TRIGLYCERIDE SUPPLEMENTATION IN SUBJECTS WITH
MILD COGNITIVE IMPAIRMENT: A RANDOMIZED
CONTROLLED TRIAL. BBA CLIN. 2015;3:123-5. [BACK]
132.
PAGE KA, WILLIAMSON A, YU N, ET AL. MEDIUM-CHAIN
FATTY ACIDS IMPROVE COGNITIVE FUNCTION IN
INTENSIVELY TREATED TYPE 1 DIABETIC PATIENTS AND
SUPPORT IN VITRO SYNAPTIC TRANSMISSION DURING
ACUTE HYPOGLYCEMIA. DIABETES. 2009;58(5):1237-44.
[BACK]
133.
REGER MA, HENDERSON ST, HALE C, ET AL. EFFECTS
OF BETA-HYDROXYBUTYRATE ON COGNITION IN
MEMORY-IMPAIRED ADULTS. NEUROBIOL AGING.
2004;25(3):311-4. [BACK]
134.
DONG YM, LI Y, NING H, WANG C, LIU JR, SUN CH. HIGH
DIETARY INTAKE OF MEDIUM-CHAIN FATTY ACIDS
DURING PREGNANCY IN RATS PREVENTS LATER-LIFE
OBESITY IN THEIR OFFSPRING. J NUTR BIOCHEM.
2011;22(8):791-7. [BACK]
135.
LAVERTY G, GILMORE BF, JONES DS, COYLE L, FOLAN
M, BREATHNACH R. ANTIMICROBIAL EFFICACY OF AN
INNOVATIVE EMULSION OF MEDIUM CHAIN
TRIGLYCERIDES AGAINST CANINE AND FELINE
PERIODONTOPATHOGENS. J SMALL ANIM PRACT.
2015;56(4):253-63. [BACK]
136.
 DHANIKULA AB, KHALID NM, LEE SD, ET AL. LONG
CIRCULATING LIPID NANOCAPSULES FOR DRUG
DETOXIFICATION. BIOMATERIALS. 2007;28(6):1248-57.
[BACK]
137.
HAN J, HAMILTON JA, KIRKLAND JL, CORKEY BE, GUO
W. MEDIUM-CHAIN OIL REDUCES FAT MASS AND DOWN-
REGULATES EXPRESSION OF ADIPOGENIC GENES IN
RATS. OBES RES. 2003;11(6):734-44. [BACK]
138.ECKEL RH, HANSON AS, CHEN AY, BERMAN JN,
YOST TJ, BRASS EP. DIETARY SUBSTITUTION OF
MEDIUM-CHAIN TRIGLYCERIDES IMPROVES INSULIN-
MEDIATED GLUCOSE METABOLISM IN NIDDM
SUBJECTS. DIABETES. 1992;41(5):641-7. [BACK]
139. YOST TJ, ECKEL RH. HYPOCALORIC FEEDING IN
OBESE WOMEN: METABOLIC EFFECTS OF MEDIUM-
CHAIN TRIGLYCERIDE SUBSTITUTION. AM J CLIN NUTR.
1989;49(2):326-30. [BACK]
140.
GOLA A, BOCHENEK W, MOLIN I. EFFECTS OF MEDIUM
CHAIN TRIGLYCERIDES ON PLASMA FREE FATTY ACIDS
IN NORMAL SUBJECTS. ARCH IMMUNOL THER EXP
(WARSZ). 1974;22(6):797-802. [BACK]
141.
PERRET JP, GUIFFRAY N, MOTTAZ P. [STIMULATION OF
INSULIN SECRETION BY MEDIUM-CHAIN FATTY ACIDS
IN THE DIET OF YOUNG RABBITS]. ANN NUTR METAB.
1983;27(2):153-61. [BACK]
142. GREENBERGER NJ, TZAGOURNIS M, GRAVES TM.
STIMULATION OF INSULIN SECRETION IN MAN BY
MEDIUM CHAIN TRIGLYCERIDES. METAB CLIN EXP.
1968;17(9):796-801. [BACK]
143. VALLS E, HERRERA E, DÍAZ M, BARREIRO P, VALLS
A. [MODIFICATIONS OF INSULIN AND GROWTH
HORMONE AFTER MEDIUM CHAIN TRIGLYCERIDES
INGESTION (AUTHOR'S TRANSL)]. AN ESP PEDIATR.
1978;11(10):675-82. [BACK]
144.
OOYAMA K, WU J, NOSAKA N, AOYAMA T, KASAI M.
COMBINED INTERVENTION OF MEDIUM-CHAIN
TRIACYLGLYCEROL DIET AND EXERCISE REDUCES
BODY FAT MASS AND ENHANCES ENERGY
EXPENDITURE IN RATS. J NUTR SCI VITAMINOL.
2008;54(2):136-41. [BACK]
145. FUSHIKI T, MATSUMOTO K, INOUE K, KAWADA T,
SUGIMOTO E. SWIMMING ENDURANCE CAPACITY OF
MICE IS INCREASED BY CHRONIC CONSUMPTION OF
MEDIUM-CHAIN TRIGLYCERIDES. J NUTR.
1995;125(3):531-9. [BACK]
146.
VAN ZYL CG, LAMBERT EV, HAWLEY JA, NOAKES TD,
DENNIS SC. EFFECTS OF MEDIUM-CHAIN TRIGLYCERIDE
INGESTION ON FUEL METABOLISM AND CYCLING
PERFORMANCE. J APPL PHYSIOL. 1996;80(6):2217-25.
[BACK]
147. NOSAKA N, SUZUKI Y, NAGATOISHI A, KASAI M, WU
J, TAGUCHI M. EFFECT OF INGESTION OF MEDIUM-
CHAIN TRIACYLGLYCEROLS ON MODERATE- AND HIGH-
INTENSITY EXERCISE IN RECREATIONAL ATHLETES. J
NUTR SCI VITAMINOL. 2009;55(2):120-5. [BACK]
148.
MISELL LM, LAGOMARCINO ND, SCHUSTER V, KERN M.
CHRONIC MEDIUM-CHAIN TRIACYLGLYCEROL
CONSUMPTION AND ENDURANCE PERFORMANCE IN
TRAINED RUNNERS. J SPORTS MED PHYS FITNESS.
2001;41(2):210-5. [BACK]
149.ANGUS DJ, HARGREAVES M, DANCEY J, FEBBRAIO
MA. EFFECT OF CARBOHYDRATE OR CARBOHYDRATE
PLUS MEDIUM-CHAIN TRIGLYCERIDE INGESTION ON
CYCLING TIME TRIAL PERFORMANCE. J APPL PHYSIOL.
2000;88(1):113-9. [BACK]
150.GOEDECKE JH, ELMER-ENGLISH R, DENNIS SC,
SCHLOSS I, NOAKES TD, LAMBERT EV. EFFECTS OF
MEDIUM-CHAIN TRIACLYGLYCEROL INGESTED WITH
CARBOHYDRATE ON METABOLISM AND EXERCISE
PERFORMANCE. INT J SPORT NUTR. 1999;9(1):35-47.
[BACK]
151. SATABIN P, PORTERO P, DEFER G, BRICOUT J,
GUEZENNEC CY. METABOLIC AND HORMONAL
RESPONSES TO LIPID AND CARBOHYDRATE DIETS
DURING EXERCISE IN MAN. MED SCI SPORTS EXERC.
1987;19(3):218-23. [BACK]
152.
GOEDECKE JH, CLARK VR, NOAKES TD, LAMBERT EV.
THE EFFECTS OF MEDIUM-CHAIN TRIACYLGLYCEROL
AND CARBOHYDRATE INGESTION ON ULTRA-
ENDURANCE EXERCISE PERFORMANCE. INT J SPORT
NUTR EXERC METAB. 2005;15(1):15-27. [BACK]
153.JEUKENDRUP AE, THIELEN JJ, WAGENMAKERS AJ,
BROUNS F, SARIS WH. EFFECT OF MEDIUM-CHAIN
TRIACYLGLYCEROL AND CARBOHYDRATE INGESTION
DURING EXERCISE ON SUBSTRATE UTILIZATION AND
SUBSEQUENT CYCLING PERFORMANCE. AM J CLIN
NUTR. 1998;67(3):397-404. [BACK]
154.
LAMBERT EV, HAWLEY JA, GOEDECKE J, NOAKES TD,
DENNIS SC. NUTRITIONAL STRATEGIES FOR
PROMOTING FAT UTILIZATION AND DELAYING THE
ONSET OF FATIGUE DURING PROLONGED EXERCISE. J
SPORTS SCI. 1997;15(3):315-24. [BACK]
155. BEHREND AM, HARDING CO, SHOEMAKER JD, ET
AL. SUBSTRATE OXIDATION AND CARDIAC
PERFORMANCE DURING EXERCISE IN DISORDERS OF
LONG CHAIN FATTY ACID OXIDATION. MOL GENET
METAB. 2012;105(1):110-5. [BACK]
156. JEUKENDRUP AE, SARIS WH, SCHRAUWEN P,
BROUNS F, WAGENMAKERS AJ. METABOLIC
AVAILABILITY OF MEDIUM-CHAIN TRIGLYCERIDES
COINGESTED WITH CARBOHYDRATES DURING
PROLONGED EXERCISE. J APPL PHYSIOL. 1995;79(3):756-
62. [BACK]
157.HAWLEY JA. EFFECT OF INCREASED FAT
AVAILABILITY ON METABOLISM AND EXERCISE
CAPACITY. MED SCI SPORTS EXERC. 2002;34(9):1485-91.
[BACK]
158.
AUCLAIR E, SATABIN P, SERVAN E, GUEZENNEC CY.
METABOLIC EFFECTS OF GLUCOSE, MEDIUM CHAIN
TRIGLYCERIDE AND LONG CHAIN TRIGLYCERIDE
FEEDING BEFORE PROLONGED EXERCISE IN RATS. EUR
J APPL PHYSIOL OCCUP PHYSIOL. 1988;57(1):126-31.
[BACK]
159. HOROWITZ JF, MORA-RODRIGUEZ R, BYERLEY LO,
COYLE EF. PREEXERCISE MEDIUM-CHAIN
TRIGLYCERIDE INGESTION DOES NOT ALTER MUSCLE
GLYCOGEN USE DURING EXERCISE. J APPL PHYSIOL.
2000;88(1):219-25. [BACK]
160.JEUKENDRUP AE, SARIS WH, BROUNS F, HALLIDAY
D, WAGENMAKERS JM. EFFECTS OF CARBOHYDRATE
(CHO) AND FAT SUPPLEMENTATION ON CHO
METABOLISM DURING PROLONGED EXERCISE. METAB
CLIN EXP. 1996;45(7):915-21. [BACK]
161. DÉCOMBAZ J, ARNAUD MJ, MILON H, ET AL.
ENERGY METABOLISM OF MEDIUM-CHAIN
TRIGLYCERIDES VERSUS CARBOHYDRATES DURING
EXERCISE. EUR J APPL PHYSIOL OCCUP PHYSIOL.
1983;52(1):9-14. [BACK]
162.MASSICOTTE D, PÉRONNET F, BRISSON GR,
HILLAIRE-MARCEL C. OXIDATION OF EXOGENOUS
MEDIUM-CHAIN FREE FATTY ACIDS DURING
PROLONGED EXERCISE: COMPARISON WITH GLUCOSE. J
APPL PHYSIOL. 1992;73(4):1334-9. [BACK]
163.
HAWLEY JA, BROUNS F, JEUKENDRUP A. STRATEGIES
TO ENHANCE FAT UTILISATION DURING EXERCISE.
SPORTS MED. 1998;25(4):241-57. [BACK]
164.
ZENTEK J, BUCHHEIT-RENKO S, FERRARA F, VAHJEN W,
VAN KESSEL AG, PIEPER R. NUTRITIONAL AND
PHYSIOLOGICAL ROLE OF MEDIUM-CHAIN
TRIGLYCERIDES AND MEDIUM-CHAIN FATTY ACIDS IN
PIGLETS. ANIM HEALTH RES REV. 2011;12(1):83-93.
[BACK]
165.
STEINBRENNER I, HOUDEK P, POLLOK S, BRANDNER
JM, DANIELS R. INFLUENCE OF THE OIL PHASE AND
TOPICAL FORMULATION ON THE WOUND HEALING
ABILITY OF A BIRCH BARK DRY EXTRACT. PLOS ONE.
2016;11(5):E0155582. [BACK]
166.
RUDICH MD, ROWLAND MC, SEIBEL RW, BORDER J.
SURVIVAL FOLLOWING A GUNSHOT WOUND OF THE
ABDOMINAL AORTA AND INFERIOR VENA CAVA. J
TRAUMA. 1978;18(7):548-9. [BACK]
167.
DURAN M, WANDERS RJ, DE JAGER JP, ET AL. 3-
HYDROXYDICARBOXYLIC ACIDURIA DUE TO LONG-
CHAIN 3-HYDROXYACYL-COENZYME A
DEHYDROGENASE DEFICIENCY ASSOCIATED WITH
SUDDEN NEONATAL DEATH: PROTECTIVE EFFECT OF
MEDIUM-CHAIN TRIGLYCERIDE TREATMENT. EUR J
PEDIATR. 1991;150(3):190-5. [BACK]
168.
 FINCK BN, HAN X, COURTOIS M, ET AL. A CRITICAL
ROLE FOR PPARALPHA-MEDIATED LIPOTOXICITY IN
THE PATHOGENESIS OF DIABETIC CARDIOMYOPATHY:
MODULATION BY DIETARY FAT CONTENT. PROC NATL
ACAD SCI USA. 2003;100(3):1226-31. [BACK]
169.FOOTITT EJ, STAFFORD J, DIXON M, ET AL. USE OF
A LONG-CHAIN TRIGLYCERIDE-RESTRICTED/MEDIUM-
CHAIN TRIGLYCERIDE-SUPPLEMENTED DIET IN A CASE
OF MALONYL-COA DECARBOXYLASE DEFICIENCY
WITH CARDIOMYOPATHY. J INHERIT METAB DIS. 2010;33
SUPPL 3:S253-6. [BACK]
170. LABARTHE F, KHAIRALLAH M, BOUCHARD B,
STANLEY WC, DES ROSIERS C. FATTY ACID OXIDATION
AND ITS IMPACT ON RESPONSE OF SPONTANEOUSLY
HYPERTENSIVE RAT HEARTS TO AN ADRENERGIC
STRESS: BENEFITS OF A MEDIUM-CHAIN FATTY ACID.
AM J PHYSIOL HEART CIRC PHYSIOL. 2005;288(3):H1425-
36. [BACK]
171. SHIMOJO N, MIYAUCHI T, IEMITSU M, ET AL.
EFFECTS OF MEDIUM-CHAIN TRIGLYCERIDE (MCT)
APPLICATION TO SHR ON CARDIAC FUNCTION,
HYPERTROPHY AND EXPRESSION OF ENDOTHELIN-1
MRNA AND OTHER GENES. J CARDIOVASC PHARMACOL.
2004;44 SUPPL 1:S181-5. [BACK]
172. IEMITSU M, SHIMOJO N, MAEDA S, ET AL. THE
BENEFIT OF MEDIUM-CHAIN TRIGLYCERIDE THERAPY
ON THE CARDIAC FUNCTION OF SHRS IS ASSOCIATED
WITH A REVERSAL OF METABOLIC AND SIGNALING
ALTERATIONS. AM J PHYSIOL HEART CIRC PHYSIOL.
2008;295(1):H136-44. [BACK]
173.
KONO H, FUJII H, ASAKAWA M, ET AL. MEDIUM-CHAIN
TRIGLYCERIDES ENHANCE SECRETORY IGA
EXPRESSION IN RAT INTESTINE AFTER
ADMINISTRATION OF ENDOTOXIN. AM J PHYSIOL
GASTROINTEST LIVER PHYSIOL. 2004;286(6):G1081-9.
[BACK]
174.
SEDMAN PC, SOMERS SS, RAMSDEN CW, BRENNAN TG,
GUILLOU PJ. EFFECTS OF DIFFERENT LIPID EMULSIONS
ON LYMPHOCYTE FUNCTION DURING TOTAL
PARENTERAL NUTRITION. BR J SURG. 1991;78(11):1396-9.
[BACK]
175.GOGOS CA, KALFARENTZOS FE, ZOUMBOS NC.
EFFECT OF DIFFERENT TYPES OF TOTAL PARENTERAL
NUTRITION ON T-LYMPHOCYTE SUBPOPULATIONS AND
NK CELLS. AM J CLIN NUTR. 1990;51(1):119-22. [BACK]
176. HINTON PS, PETERSON CA, MCCARTHY DO, NEY
DM. MEDIUM-CHAIN COMPARED WITH LONG-CHAIN
TRIACYLGLYCEROL EMULSIONS ENHANCE
MACROPHAGE RESPONSE AND INCREASE MUCOSAL
MASS IN PARENTERALLY FED RATS. AM J CLIN NUTR.
1998;67(6):1265-72. [BACK]
177.
KONO H, FUJII H, ISHII K, HOSOMURA N, OGIKU M.
DIETARY MEDIUM-CHAIN TRIGLYCERIDES PREVENT
CHEMICALLY INDUCED EXPERIMENTAL COLITIS IN
RATS. TRANSL RES. 2010;155(3):131-41. [BACK]
178. MAÑÉ J, PEDROSA E, LORÉN V, ET AL. PARTIAL
REPLACEMENT OF DIETARY (N-6) FATTY ACIDS WITH
MEDIUM-CHAIN TRIGLYCERIDES DECREASES THE
INCIDENCE OF SPONTANEOUS COLITIS IN
INTERLEUKIN-10-DEFICIENT MICE. J NUTR.
2009;139(3):603-10. [BACK]
179.
CABRÉ E, GASSULL MA. NUTRITIONAL AND
METABOLIC ISSUES IN INFLAMMATORY BOWEL
DISEASE. CURR OPIN CLIN NUTR METAB CARE.
2003;6(5):569-76. [BACK]
180.CABRÉ E, DOMÈNECH E. IMPACT OF
ENVIRONMENTAL AND DIETARY FACTORS ON THE
COURSE OF INFLAMMATORY BOWEL DISEASE. WORLD J
GASTROENTEROL. 2012;18(29):3814-22. [BACK]
181.
EISENBERH BC. CONGENITAL LYMPHANGIECTASIA
AND ATOPY. ANN ALLERGY. 1976;36(5):342-50. [BACK]
182.DESAI AP, GUVENC BH, CARACHI R. EVIDENCE FOR
MEDIUM CHAIN TRIGLYCERIDES IN THE TREATMENT OF
PRIMARY INTESTINAL LYMPHANGIECTASIA. EUR J
PEDIATR SURG. 2009;19(4):241-5. [BACK]
183.
LI R, MA J, YU K, WANG L. DIETARY OR ENTERAL
MEDIUM-CHAIN TRIGLYCERIDE USAGE IN A CHINESE
GENERAL HOSPITAL. ASIA PAC J CLIN NUTR.
2015;24(3):387-93. [BACK]
184.
LASEKAN JB, RIVERA J, HIRVONEN MD, KEESEY RE,
NEY DM. ENERGY EXPENDITURE IN RATS MAINTAINED
WITH INTRAVENOUS OR INTRAGASTRIC INFUSION OF
TOTAL PARENTERAL NUTRITION SOLUTIONS
CONTAINING MEDIUM- OR LONG-CHAIN TRIGLYCERIDE
EMULSIONS. J NUTR. 1992;122(7):1483-92. [BACK]
185. MABAYO RT, FURUSE M, MURAI A, OKUMURA J.
INTERACTIONS BETWEEN MEDIUM-CHAIN AND LONG-
CHAIN TRIACYLGLYCEROLS IN LIPID AND ENERGY
METABOLISM IN GROWING CHICKS. LIPIDS.
1994;29(2):139-44. [BACK]
186. ROTHWELL NJ, STOCK MJ. STIMULATION OF
THERMOGENESIS AND BROWN FAT ACTIVITY IN RATS
FED MEDIUM CHAIN TRIGLYCERIDE. METAB CLIN EXP.
1987;36(2):128-30. [BACK]
187.
SCALFI L, COLTORTI A, CONTALDO F. POSTPRANDIAL
THERMOGENESIS IN LEAN AND OBESE SUBJECTS AFTER
MEALS SUPPLEMENTED WITH MEDIUM-CHAIN AND
LONG-CHAIN TRIGLYCERIDES. AM J CLIN NUTR.
1991;53(5):1130-3. [BACK]
188. SEATON TB, WELLE SL, WARENKO MK, CAMPBELL
RG. THERMIC EFFECT OF MEDIUM-CHAIN AND LONG-
CHAIN TRIGLYCERIDES IN MAN. AM J CLIN NUTR.
1986;44(5):630-4. [BACK]
189. HILL JO, PETERS JC, YANG D, ET AL.
THERMOGENESIS IN HUMANS DURING OVERFEEDING
WITH MEDIUM-CHAIN TRIGLYCERIDES. METAB CLIN
EXP. 1989;38(7):641-8. [BACK]
190. WHITE MD, PAPAMANDJARIS AA, JONES PJ.
ENHANCED POSTPRANDIAL ENERGY EXPENDITURE
WITH MEDIUM-CHAIN FATTY ACID FEEDING IS
ATTENUATED AFTER 14 D IN PREMENOPAUSAL WOMEN.
AM J CLIN NUTR. 1999;69(5):883-9. [BACK]
191. KASAI M, NOSAKA N, MAKI H, ET AL. COMPARISON
OF DIET-INDUCED THERMOGENESIS OF FOODS
CONTAINING MEDIUM- VERSUS LONG-CHAIN
TRIACYLGLYCEROLS. J NUTR SCI VITAMINOL.
2002;48(6):536-40. [BACK]
192.
DULLOO AG, FATHI M, MENSI N, GIRARDIER L.
TWENTY-FOUR-HOUR ENERGY EXPENDITURE AND
URINARY CATECHOLAMINES OF HUMANS CONSUMING
LOW-TO-MODERATE AMOUNTS OF MEDIUM-CHAIN
TRIGLYCERIDES: A DOSE-RESPONSE STUDY IN A
HUMAN RESPIRATORY CHAMBER. EUR J CLIN NUTR.
1996;50(3):152-8. [BACK]
193.
MACDONALD ML, ROGERS QR, MORRIS JG. AVERSION
OF THE CAT TO DIETARY MEDIUM-CHAIN
TRIGLYCERIDES AND CAPRYLIC ACID. PHYSIOL BEHAV.
1985;35(3):371-5. [BACK]
 194.
LEE YY, TANG TK, AB KARIM NA, ALITHEEN NB, LAI
OM. SHORT TERM AND DOSAGE INFLUENCES OF PALM
BASED MEDIUM- AND LONG-CHAIN
TRIACYLGLYCEROLS ON BODY FAT AND BLOOD
PARAMETERS IN C57BL/6J MICE. FOOD FUNCT.
2014;5(1):57-64. [BACK]
195.GELIEBTER A, TORBAY N, BRACCO EF, HASHIM SA,
VAN ITALLIE TB. OVERFEEDING WITH MEDIUM-CHAIN
TRIGLYCERIDE DIET RESULTS IN DIMINISHED
DEPOSITION OF FAT. AM J CLIN NUTR. 1983;37(1):1-4.
[BACK]
196.
COLEMAN H, QUINN P, CLEGG ME. MEDIUM-CHAIN
TRIGLYCERIDES AND CONJUGATED LINOLEIC ACIDS IN
BEVERAGE FORM INCREASE SATIETY AND REDUCE
FOOD INTAKE IN HUMANS. NUTR RES. 2016;36(6):526-33.
[BACK]
197. ST-ONGE MP, MAYRSOHN B, O'KEEFFE M, KISSILEFF
HR, CHOUDHURY AR, LAFERRÈRE B. IMPACT OF
MEDIUM AND LONG CHAIN TRIGLYCERIDES
CONSUMPTION ON APPETITE AND FOOD INTAKE IN
OVERWEIGHT MEN. EUR J CLIN NUTR. 2014;68(10):1134-
40. [BACK]
198.
MATSUO T, MATSUO M, KASAI M, TAKEUCHI H.
EFFECTS OF A LIQUID DIET SUPPLEMENT CONTAINING
STRUCTURED MEDIUM- AND LONG-CHAIN
TRIACYLGLYCEROLS ON BODYFAT ACCUMULATION IN
HEALTHY YOUNG SUBJECTS. ASIA PAC J CLIN NUTR.
2001;10(1):46-50. [BACK]
199.
NOSAKA N, MAKI H, SUZUKI Y, ET AL. EFFECTS OF
MARGARINE CONTAINING MEDIUM-CHAIN
TRIACYLGLYCEROLS ON BODY FAT REDUCTION IN
HUMANS. J ATHEROSCLER THROMB. 2003;10(5):290-8.
[BACK]
200.
ST-ONGE MP, BOSARGE A. WEIGHT-LOSS DIET THAT
INCLUDES CONSUMPTION OF MEDIUM-CHAIN
TRIACYLGLYCEROL OIL LEADS TO A GREATER RATE OF
WEIGHT AND FAT MASS LOSS THAN DOES OLIVE OIL.
AM J CLIN NUTR. 2008;87(3):621-6. [BACK]
201.HAINER V, KUNESOVÁ M, STICH V, ZÁK A,
PARIZKOVÁ J. [THE ROLE OF OILS CONTAINING
TRIACYLGLYCEROLS AND MEDIUM-CHAIN FATTY
ACIDS IN THE DIETARY TREATMENT OF OBESITY. THE
EFFECT ON RESTING ENERGY EXPENDITURE AND
SERUM LIPIDS]. CAS LEK CESK. 1994;133(12):373-5.
[BACK]
202. KROTKIEWSKI M. VALUE OF VLCD
SUPPLEMENTATION WITH MEDIUM CHAIN
TRIGLYCERIDES. INT J OBES RELAT METAB DISORD.
2001;25(9):1393-400. [BACK]
203.ST-ONGE MP, ROSS R, PARSONS WD, JONES PJ.
MEDIUM-CHAIN TRIGLYCERIDES INCREASE ENERGY
EXPENDITURE AND DECREASE ADIPOSITY IN
OVERWEIGHT MEN. OBES RES. 2003;11(3):395-402. [BACK]
204.XUE C, LIU Y, WANG J, ET AL. CONSUMPTION OF
MEDIUM- AND LONG-CHAIN TRIACYLGLYCEROLS
DECREASES BODY FAT AND BLOOD TRIGLYCERIDE IN
CHINESE HYPERTRIGLYCERIDEMIC SUBJECTS. EUR J
CLIN NUTR. 2009;63(7):879-86. [BACK]
205. HAN JR, DENG B, SUN J, ET AL. EFFECTS OF
DIETARY MEDIUM-CHAIN TRIGLYCERIDE ON WEIGHT
LOSS AND INSULIN SENSITIVITY IN A GROUP OF
MODERATELY OVERWEIGHT FREE-LIVING TYPE 2
DIABETIC CHINESE SUBJECTS. METAB CLIN EXP.
2007;56(7):985-91. [BACK]
 206.
BOUNOUS G, LE BEL E, SHUSTER J, GOLD P, TAHAN WT,
BASTIN E. DIETARY PROTECTION DURING RADIATION
THERAPY. STRAHLENTHERAPIE. 1975;149(5):476-83.
[BACK]
207.
SIPES SL, NEWTON M, LURAIN JR. CHYLOUS ASCITES: A
SEQUEL OF PELVIC RADIATION THERAPY. OBSTET
GYNECOL. 1985;66(6):832-5. [BACK]
208.
LAW TH, DAVIES ES, PAN Y, ZANGHI B, WANT E, VOLK
HA. A RANDOMISED TRIAL OF A MEDIUM-CHAIN TAG
DIET AS TREATMENT FOR DOGS WITH IDIOPATHIC
EPILEPSY. BR J NUTR. 2015;114(9):1438-47. [BACK]
209. ROSENTHAL E, WEISSMAN B, KYLLONEN K. USE OF
PARENTERAL MEDIUM-CHAIN TRIGLYCERIDE
EMULSION FOR MAINTAINING SEIZURE CONTROL IN A
5-YEAR-OLD GIRL WITH INTRACTABLE DIARRHEA. JPEN
J PARENTER ENTERAL NUTR. 1990;14(5):543-5. [BACK]
210.CALANDRE L, MARTÍNEZ MARTÍN P, CAMPOS
CASTELLÓ J. [TREATMENT OF LENNOX SYNDROME
WITH MEDIUM CHAIN TRIGLYCERIDES (AUTHOR'S
TRANSL)]. AN ESP PEDIATR. 1978;11(3):189-94. [BACK]
211.SCHIFF Y, LERMAN-SAGIE T. [KETOGENIC DIET--AN
ALTERNATIVE THERAPY FOR EPILEPSY IN ADULTS].
HAREFUAH. 1998;134(7):529-31, 591. [BACK]
212.ROS PÉREZ P, ZAMARRÓN CUESTA I, APARICIO
MEIX M, SASTRE GALLEGO A. [EVALUATION OF THE
EFFECTIVENESS OF THE KETOGENIC DIET WITH
MEDIUM-CHAIN TRIGLYCERIDES, IN THE TREATMENT
OF REFRACTORY EPILEPSY IN CHILDREN. APROPOS OF
A SERIES OF CASES]. AN ESP PEDIATR. 1989;30(3):155-8.
[BACK]
213.SILLS MA, FORSYTHE WI, HAIDUKEWYCH D,
MACDONALD A, ROBINSON M. THE MEDIUM CHAIN
TRIGLYCERIDE DIET AND INTRACTABLE EPILEPSY.
ARCH DIS CHILD. 1986;61(12):1168-72. [BACK]
214. CHOMTHO K, SUTEEROJNTRAKOOL O, CHOMTHO
S. EFFECTIVENESS OF MEDIUM CHAIN TRIGLYCERIDE
KETOGENIC DIET IN THAI CHILDREN WITH
INTRACTABLE EPILEPSY. J MED ASSOC THAI.
2016;99(2):159-65. [BACK]
215.MAK SC, CHI CS, WAN CJ. CLINICAL EXPERIENCE
OF KETOGENIC DIET ON CHILDREN WITH REFRACTORY
EPILEPSY. ACTA PAEDIATR TAIWAN. 1999;40(2):97-100.
[BACK]
216.AZZAM R, AZAR NJ. MARKED SEIZURE REDUCTION
AFTER MCT SUPPLEMENTATION. CASE REP NEUROL
MED. 2013;2013:809151. [BACK]
217.
WIEDERSBERG S, LEOPOLD CS, GUY RH. EFFECTS OF
VARIOUS VEHICLES ON SKIN HYDRATION IN VIVO. SKIN
PHARMACOL PHYSIOL. 2009;22(3):128-30. [BACK]
218.
KOGAN A, GARTI N. MICROEMULSIONS AS
TRANSDERMAL DRUG DELIVERY VEHICLES. ADV
COLLOID INTERFACE SCI. 2006;123-126:369-85. [BACK]
219.
TELLIEZ F, BACH V, LEKE A, CHARDON K, LIBERT JP.
FEEDING BEHAVIOR IN NEONATES WHOSE DIET
CONTAINED MEDIUM-CHAIN TRIACYLGLYCEROLS:
SHORT-TERM EFFECTS ON THERMOREGULATION AND
SLEEP. AM J CLIN NUTR. 2002;76(5):1091-5. [BACK]
220.
AURIOL S, MAHIEU L, BROUSSET P, MALECAZE F,
MATHIS V. SAFETY OF MEDIUM-CHAIN TRIGLYCERIDES
USED AS AN INTRAOCULAR TAMPONADING AGENT IN
AN EXPERIMENTAL VITRECTOMY MODEL RABBIT.
RETINA (PHILADELPHIA, PA). 2013;33(1):217-23. [BACK]
221.
BROEDERS EP, VIJGEN GH, HAVEKES B, ET AL.
THYROID HORMONE ACTIVATES BROWN ADIPOSE
TISSUE AND INCREASES NON-SHIVERING
THERMOGENESIS--A COHORT STUDY IN A GROUP OF
THYROID CARCINOMA PATIENTS. PLOS ONE.
2016;11(1):E0145049. [BACK]
222.
JEUKENDRUP AE, ALDRED S. FAT SUPPLEMENTATION,
HEALTH, AND ENDURANCE PERFORMANCE. NUTRITION.
2004;20(7-8):678-88. [BACK]
223.
TRAUL KA, DRIEDGER A, INGLE DL, NAKHASI D.
REVIEW OF THE TOXICOLOGIC PROPERTIES OF
MEDIUM-CHAIN TRIGLYCERIDES. FOOD CHEM
TOXICOL. 2000;38(1):79-98. [BACK]
224.
NONAKA Y, TAKAGI T, INAI M, ET AL. LAURIC ACID
STIMULATES KETONE BODY PRODUCTION IN THE KT-5
ASTROCYTE CELL LINE. J OLEO SCI. 2016;65(8):693-9.
[BACK]
225. FACIOLA AP, BRODERICK GA. EFFECTS OF FEEDING
LAURIC ACID OR COCONUT OIL ON RUMINAL
PROTOZOA NUMBERS, FERMENTATION PATTERN,
DIGESTION, OMASAL NUTRIENT FLOW, AND MILK
PRODUCTION IN DAIRY COWS. J DAIRY SCI.
2014;97(8):5088-100. [BACK]
226.LIEBERMAN S, ENIG MG, PREUSS HG. A REVIEW OF
MONOLAURIN AND LAURIC ACID. ALT. & COMPLEM.
THER. 2006. [BACK]
227.
FAUSER JK, MATTHEWS GM, CUMMINS AG, HOWARTH
GS. INDUCTION OF APOPTOSIS BY THE MEDIUM-CHAIN
LENGTH FATTY ACID LAURIC ACID IN COLON CANCER
CELLS DUE TO INDUCTION OF OXIDATIVE STRESS.
CHEMOTHERAPY. 2013;59(3):214-24. [BACK]
228.
YU W, CHAI H, LI Y, ET AL. INCREASED EXPRESSION OF
CYP4Z1 PROMOTES TUMOR ANGIOGENESIS AND
GROWTH IN HUMAN BREAST CANCER. TOXICOL APPL
PHARMACOL. 2012;264(1):73-83. [BACK]
229.
SACCANI A, SCHIOPPA T, PORTA C, ET AL. P50 NUCLEAR
FACTOR-KAPPAB OVEREXPRESSION IN TUMOR-
ASSOCIATED MACROPHAGES INHIBITS M1
INFLAMMATORY RESPONSES AND ANTITUMOR
RESISTANCE. CANCER RES. 2006;66(23):11432-40. [BACK]
230.
HUANG WC, TSAI TH, CHUANG LT, LI YY, ZOUBOULIS
CC, TSAI PJ. ANTI-BACTERIAL AND ANTI-
INFLAMMATORY PROPERTIES OF CAPRIC ACID AGAINST
PROPIONIBACTERIUM ACNES: A COMPARATIVE STUDY
WITH LAURIC ACID. J DERMATOL SCI. 2014;73(3):232-40.
[BACK]
231.
YANG D, PORNPATTANANANGKUL D, NAKATSUJI T, ET
AL. THE ANTIMICROBIAL ACTIVITY OF LIPOSOMAL
LAURIC ACIDS AGAINST PROPIONIBACTERIUM ACNES.
BIOMATERIALS. 2009;30(30):6035-40. [BACK]
232.NAKATSUJI T, KAO MC, FANG JY, ET AL.
ANTIMICROBIAL PROPERTY OF LAURIC ACID AGAINST
PROPIONIBACTERIUM ACNES: ITS THERAPEUTIC
POTENTIAL FOR INFLAMMATORY ACNE VULGARIS. J
INVEST DERMATOL. 2009;129(10):2480-8. [BACK]
233.
HUANG CB, ALIMOVA Y, MYERS TM, EBERSOLE JL.
SHORT- AND MEDIUM-CHAIN FATTY ACIDS EXHIBIT
ANTIMICROBIAL ACTIVITY FOR ORAL
MICROORGANISMS. ARCH ORAL BIOL. 2011;56(7):650-4.
[BACK]
234.
KABARA JJ, SWIECZKOWSKI DM, CONLEY AJ, TRUANT
JP. FATTY ACIDS AND DERIVATIVES AS ANTIMICROBIAL
AGENTS. ANTIMICROB AGENTS CHEMOTHER.
1972;2(1):23-8. [BACK]
235.
PETSCHOW BW, BATEMA RP, FORD LL. SUSCEPTIBILITY
OF HELICOBACTER PYLORI TO BACTERICIDAL
PROPERTIES OF MEDIUM-CHAIN MONOGLYCERIDES
AND FREE FATTY ACIDS. ANTIMICROB AGENTS
CHEMOTHER. 1996;40(2):302-6. [BACK]
236.
SOUZA JL, DA SILVA AF, CARVALHO PH, PACHECO BS,
PEREIRA CM, LUND RG. ALIPHATIC FATTY ACIDS AND
ESTERS: INHIBITION OF GROWTH AND EXOENZYME
PRODUCTION OF CANDIDA, AND THEIR CYTOTOXICITY
IN VITRO: ANTI-CANDIDA EFFECT AND CYTOTOXICITY
OF FATTY ACIDS AND ESTERS. ARCH ORAL BIOL.
2014;59(9):880-6. [BACK]
237.TAKAHASHI M, INOUE S, HAYAMA K, NINOMIYA K,
ABE S. [INHIBITION OF CANDIDA MYCELIA GROWTH BY
A MEDIUM CHAIN FATTY ACIDS, CAPRIC ACID IN VITRO
AND ITS THERAPEUTIC EFFICACY IN MURINE ORAL
CANDIDIASIS]. MED MYCOL J. 2012;53(4):255-61. [BACK]
238.
SENGUPTA A, GHOSH M, BHATTACHARYYA DK. IN
VITRO ANTIOXIDANT ASSAY OF MEDIUM CHAIN FATTY
ACID RICH RICE BRAN OIL IN COMPARISON TO NATIVE
RICE BRAN OIL. J FOOD SCI TECHNOL. 2015;52(8):5188-95.
[BACK]
239.
HORNUNG B, AMTMANN E, SAUER G. LAURIC ACID
INHIBITS THE MATURATION OF VESICULAR STOMATITIS
VIRUS. J GEN VIROL. 1994;75 ( PT 2):353-61. [BACK]
240.
BARTOLOTTA S, GARCÍA CC, CANDURRA NA,
DAMONTE EB. EFFECT OF FATTY ACIDS ON
ARENAVIRUS REPLICATION: INHIBITION OF VIRUS
PRODUCTION BY LAURIC ACID. ARCH VIROL.
2001;146(4):777-90. [BACK]
241.IRMISCH G, SCHLÄFKE D, RICHTER J.
RELATIONSHIPS BETWEEN FATTY ACIDS AND
PSYCHOPHYSIOLOGICAL PARAMETERS IN DEPRESSIVE
INPATIENTS UNDER EXPERIMENTALLY INDUCED
STRESS. PROSTAGLANDINS LEUKOT ESSENT FATTY
ACIDS. 2006;74(2):149-56. [BACK]
242.
SHAPIRO S. THE INHIBITORY ACTION OF FATTY ACIDS
ON ORAL BACTERIA. ORAL MICROBIOL IMMUNOL.
1996;11(5):350-5. [BACK]
243.
KOCHIKUZHYIL BM, DEVI K, FATTEPUR SR. EFFECT OF
SATURATED FATTY ACID-RICH DIETARY VEGETABLE
OILS ON LIPID PROFILE, ANTIOXIDANT ENZYMES AND
GLUCOSE TOLERANCE IN DIABETIC RATS. INDIAN J
PHARMACOL. 2010;42(3):142-5. [BACK]
244.
RAJESH PP, NOORI MT, GHANGREKAR MM.
CONTROLLING METHANOGENESIS AND IMPROVING
POWER PRODUCTION OF MICROBIAL FUEL CELL BY
LAURIC ACID DOSING. WATER SCI TECHNOL.
2014;70(8):1363-9. [BACK]
245.
ZEITZ JO, FENNHOFF J, KLUGE H, STANGL GI, EDER K.
EFFECTS OF DIETARY FATS RICH IN LAURIC AND
MYRISTIC ACID ON PERFORMANCE, INTESTINAL
MORPHOLOGY, GUT MICROBES, AND MEAT QUALITY IN
BROILERS. POULT SCI. 2015;94(10):2404-13. [BACK]
246.
GOLDBERG EM, RYLAND D, GIBSON RA, ALIANI M,
HOUSE JD. DESIGNER LAYING HEN DIETS TO IMPROVE
EGG FATTY ACID PROFILE AND MAINTAIN SENSORY
QUALITY. FOOD SCI NUTR. 2013;1(4):324-35. [BACK]
247.
NAKAMURA J, MIWA T, SASAKI H, SHIBASAKI J,
KANETO H. EFFECT OF STRAIGHT CHAIN FATTY ACIDS
ON SEIZURES INDUCED BY PICROTOXIN AND
PENTYLENETETRAZOLE IN MICE. J PHARMACOBIO-
DYN. 1990;13(1):76-81. [BACK]
248.
KOUCHAK M, HANDALI S. EFFECTS OF VARIOUS
PENETRATION ENHANCERS ON PENETRATION OF
AMINOPHYLLINE THROUGH SHED SNAKE SKIN.
JUNDISHAPUR J NAT PHARM PROD. 2014;9(1):24-9.
[BACK]
249.
OTUECHERE CA, MADARIKAN G, SIMISOLA T,
BANKOLE O, OSHO A. VIRGIN COCONUT OIL PROTECTS
AGAINST LIVER DAMAGE IN ALBINO RATS
CHALLENGED WITH THE ANTI-FOLATE COMBINATION,
TRIMETHOPRIM-SULFAMETHOXAZOLE. J BASIC CLIN
PHYSIOL PHARMACOL. 2014;25(2):249-53. [BACK]
250.
WALLACE FA, NEELY SJ, MILES EA, CALDER PC.
DIETARY FATS AFFECT MACROPHAGE-MEDIATED
CYTOTOXICITY TOWARDS TUMOUR CELLS. IMMUNOL
CELL BIOL. 2000;78(1):40-8. [BACK]
251.
AMERICAN CANCER SOCIETY. HOMEPAGE SLIDER.
(2016). AVAILABLE AT: HTTPS://WWW.CANCER.GOV
[NOVEMBER 28TH, 2016]. [BACK]
252.
REUTER SE, MARTIN JH. PHARMACOKINETICS OF
CANNABIS IN CANCER CACHEXIA-ANOREXIA
SYNDROME. CLIN PHARMACOKINET. 2016;55(7):807-12.
[BACK]
253.
VOLEK JS, KRAEMER WJ, BUSH JA, INCLEDON T,
BOETES M. TESTOSTERONE AND CORTISOL IN
RELATIONSHIP TO DIETARY NUTRIENTS AND
RESISTANCE EXERCISE. JOURNAL OF APPLIED
PHYSIOLOGY (BETHESDA, MD. : 1985). 82(1):49-54. 1997.
[BACK]
254.
VYSAKH A, RATHEESH M, RAJMOHANAN TP, ET AL.
POLYPHENOLICS ISOLATED FROM VIRGIN COCONUT
OIL INHIBITS ADJUVANT INDUCED ARTHRITIS IN RATS
THROUGH ANTIOXIDANT AND ANTI-INFLAMMATORY
ACTION. INT IMMUNOPHARMACOL. 2014;20(1):124-30.
[BACK]
255.
MONTEIRO R, AZEVEDO I, CALHAU C. MODULATION OF
AROMATASE ACTIVITY BY DIET POLYPHENOLIC
COMPOUNDS. J AGRIC FOOD CHEM. 2006;54(10):3535-40.
[BACK]
256.
OTUECHERE CA, MADARIKAN G, SIMISOLA T,
BANKOLE O, OSHO A. VIRGIN COCONUT OIL PROTECTS
AGAINST LIVER DAMAGE IN ALBINO RATS
CHALLENGED WITH THE ANTI-FOLATE COMBINATION,
TRIMETHOPRIM-SULFAMETHOXAZOLE. J BASIC CLIN
PHYSIOL PHARMACOL. 2014;25(2):249-53. [BACK]
257.
YEAP SK, BEH BK, ALI NM, ET AL. ANTISTRESS AND
ANTIOXIDANT EFFECTS OF VIRGIN COCONUT OIL IN
VIVO. EXP THER MED. 2015;9(1):39-42. [BACK]
258.
JING H, WANG Z, CHEN Y. EFFECT OF OESTRADIOL ON
MAST CELL NUMBER AND HISTAMINE LEVEL IN THE
 MAMMARY GLANDS OF RAT. ANAT HISTOL EMBRYOL.
2012;41(3):170-6. [BACK]
259.
YEAP SK, BEH BK, ALI NM, ET AL. ANTISTRESS AND
ANTIOXIDANT EFFECTS OF VIRGIN COCONUT OIL IN
VIVO. EXP THER MED. 2015;9(1):39-42. [BACK]
260.
SADEGHI S, WALLACE FA, CALDER PC. DIETARY LIPIDS
MODIFY THE CYTOKINE RESPONSE TO BACTERIAL
LIPOPOLYSACCHARIDE IN MICE. IMMUNOLOGY.
1999;96(3):404-10. [BACK]

Sodium Bicarbonate
1. SCIALLA JJ, APPEL LJ, ASTOR BC, ET AL. ESTIMATED NET
ENDOGENOUS ACID PRODUCTION AND SERUM
BICARBONATE IN AFRICAN AMERICANS WITH CHRONIC
KIDNEY DISEASE. CLIN J AM SOC NEPHROL.
2011;6(7):1526-32. [BACK]
2. SEMENZA GL, ARTEMOV D, BEDI A, ET AL. 'THE
METABOLISM OF TUMOURS': 70 YEARS LATER.
NOVARTIS FOUND SYMP. 2001;240:251-60. [BACK]
3. GOGVADZE V, ORRENIUS S, ZHIVOTOVSKY B.
MITOCHONDRIA IN CANCER CELLS: WHAT IS SO
SPECIAL ABOUT THEM?. TRENDS CELL BIOL.
2008;18(4):165-73. [BACK]
4. BOAG JM, BEESLEY AH, FIRTH MJ, ET AL. ALTERED
GLUCOSE METABOLISM IN CHILDHOOD PRE-B ACUTE
LYMPHOBLASTIC LEUKAEMIA. LEUKEMIA.
2006;20(10):1731-7. [BACK]
5. SEYFRIED TN, MUKHERJEE P. TARGETING ENERGY
METABOLISM IN BRAIN CANCER: REVIEW AND
HYPOTHESIS. NUTR METAB (LOND). 2005;2:30. [BACK]
6. RISTOW M. OXIDATIVE METABOLISM IN CANCER
GROWTH. CURR OPIN CLIN NUTR METAB CARE.
2006;9(4):339-45. [BACK]
7. GATENBY RA, GILLIES RJ. WHY DO CANCERS HAVE
HIGH AEROBIC GLYCOLYSIS?. NAT REV CANCER.
2004;4(11):891-9. [BACK]
8. TANNOCK IF, ROTIN D. ACID PH IN TUMORS AND ITS
POTENTIAL FOR THERAPEUTIC EXPLOITATION. CANCER
RES. 1989;49(16):4373-84. [BACK]
9. DHUP S, DADHICH RK, PORPORATO PE, SONVEAUX P.
MULTIPLE BIOLOGICAL ACTIVITIES OF LACTIC ACID IN
CANCER: INFLUENCES ON TUMOR GROWTH,
ANGIOGENESIS AND METASTASIS. CURR PHARM DES.
2012;18(10):1319-30. [BACK]
10. GOTO K. A STUDY OF THE ACIDOSIS, BLOOD UREA, AND
PLASMA CHLORIDES IN URANIUM NEPHRITIS IN THE
DOG, AND OF THE PROTECTIVE ACTION OF SODIUM
BICARBONATE. J EXP MED. 1917;25(5):693-719. [BACK]
11. SMITH ES, OMERBAŠIĆ D, LECHNER SG, ANIRUDHAN G,
LAPATSINA L, LEWIN GR. THE MOLECULAR BASIS OF
ACID INSENSITIVITY IN THE AFRICAN NAKED MOLE-
RAT. SCIENCE. 2011;334(6062):1557-60. [BACK]
12. EDREY YH, PARK TJ, KANG H, BINEY A, BUFFENSTEIN R.
ENDOCRINE FUNCTION AND NEUROBIOLOGY OF THE
LONGEST-LIVING RODENT, THE NAKED MOLE-RAT. EXP
GERONTOL. 2011;46(2-3):116-23. [BACK]
13. LIANG S, MELE J, WU Y, BUFFENSTEIN R, HORNSBY PJ.
RESISTANCE TO EXPERIMENTAL TUMORIGENESIS IN
CELLS OF A LONG-LIVED MAMMAL, THE NAKED MOLE-
RAT (HETEROCEPHALUS GLABER). AGING CELL.
2010;9(4):626-35. [BACK]
14. ASDELL SA, DOORNENBAL H, JOSHI SR, SPERLING GA.
THE EFFECTS OF SEX STEROID HORMONES UPON
 LONGEVITY IN RATS. J REPROD FERTIL. 1967;14(1):113-20.
[BACK]
15. SUTER
P, LUETKEMEIER H, ZAKOVA N, CHRISTEN P,
SACHSSE K, HESS R. LIFESPAN STUDIES ON MALE AND
FEMALE MICE AND RATS UNDER SPF-LABORATORY
CONDITIONS. ARCH TOXICOL SUPPL. 1979;(2):403-7.
[BACK]
16. BUFFENSTEIN
R. THE NAKED MOLE-RAT: A NEW LONG-
LIVING MODEL FOR HUMAN AGING RESEARCH. J
GERONTOL A BIOL SCI MED SCI. 2005;60(11):1369-77.
[BACK]
17. O'CONNORTP, LEE A, JARVIS JU, BUFFENSTEIN R.
PROLONGED LONGEVITY IN NAKED MOLE-RATS: AGE-
RELATED CHANGES IN METABOLISM, BODY
COMPOSITION AND GASTROINTESTINAL FUNCTION.
COMP BIOCHEM PHYSIOL, PART A MOL INTEGR
PHYSIOL. 2002;133(3):835-42. [BACK]
18. CSISZAR A,
LABINSKYY N, OROSZ Z, XIANGMIN Z,
BUFFENSTEIN R, UNGVARI Z. VASCULAR AGING IN THE
LONGEST-LIVING RODENT, THE NAKED MOLE RAT. AM J
PHYSIOL HEART CIRC PHYSIOL. 2007;293(2):H919-27.
[BACK]
19. EDREY YH,
HANES M, PINTO M, MELE J, BUFFENSTEIN R.
SUCCESSFUL AGING AND SUSTAINED GOOD HEALTH IN
THE NAKED MOLE RAT: A LONG-LIVED MAMMALIAN
MODEL FOR BIOGERONTOLOGY AND BIOMEDICAL
RESEARCH. ILAR J. 2011;52(1):41-53. [BACK]
20. LEWISKN, MELE J, HORNSBY PJ, BUFFENSTEIN R.
STRESS RESISTANCE IN THE NAKED MOLE-RAT: THE
BARE ESSENTIALS - A MINI-REVIEW. GERONTOLOGY.
2012;58(5):453-62. [BACK]
21. KIM
EB, FANG X, FUSHAN AA, ET AL. GENOME
SEQUENCING REVEALS INSIGHTS INTO PHYSIOLOGY
 AND LONGEVITY OF THE NAKED MOLE RAT. NATURE.
2011;479(7372):223-7. [BACK]
22. LEWISKN, ANDZIAK B, YANG T, BUFFENSTEIN R. THE
NAKED MOLE-RAT RESPONSE TO OXIDATIVE STRESS:
JUST DEAL WITH IT. ANTIOXID REDOX SIGNAL.
2013;19(12):1388-99. [BACK]
23. PEAT
R. PROTECTIVE CO2 AND AGING. [ONLINE].
AVAILABLE:
HTTP://RAYPEAT.COM/ARTICLES/ARTICLES/CO2.SHTML.
[FEBRUARY 15, 2017]. [BACK]
24. SHAMS
I, AVIVI A, NEVO E. OXYGEN AND CARBON
DIOXIDE FLUCTUATIONS IN BURROWS OF
SUBTERRANEAN BLIND MOLE RATS INDICATE
TOLERANCE TO HYPOXIC-HYPERCAPNIC STRESSES.
COMP BIOCHEM PHYSIOL, PART A MOL INTEGR
PHYSIOL. 2005;142(3):376-82. [BACK]
25. BERKOVITSR, BOFFA N, DELUCA V. THE EFFECTS OF
HYPERCAPNIC HYPOXIA ON NAKED MOLE RAT
ACTIVITY LEVELS, MEMORY, AND SOCIAL
INTERACTION. 2010. AVAILABLE:
HTTPS://MACAULAY.CUNY.EDU/EPORTFOLIOS/NEWYOR
KCITYONTHEBRAIN/FILES/2010/12/NMR-POSTER.PDF
[FEBRUARY 15, 2017]. [BACK]
26. BAHREINI R, CURRIE RW. THE POTENTIAL OF BEE-
GENERATED CARBON DIOXIDE FOR CONTROL OF
VARROA MITE (MESOSTIGMATA: VARROIDAE) IN
INDOOR OVERWINTERING HONEY BEE (HYMENOPTERA:
APIDAE) COLONIES. J ECON ENTOMOL. 2015;108(5):2153-
67. [BACK]
27. REMOLINA SC,
HUGHES KA. EVOLUTION AND
MECHANISMS OF LONG LIFE AND HIGH FERTILITY IN
QUEEN HONEY BEES. AGE (DORDR). 2008;30(2-3):177-85.
[BACK]
28. PODLUTSKY AJ, KHRITANKOV AM, OVODOV ND,
AUSTAD SN. A NEW FIELD RECORD FOR BAT
LONGEVITY. J GERONTOL A BIOL SCI MED SCI.
2005;60(11):1366-8. [BACK]
29. HOWARTHFG, STONE FD. 1990. ELEVATED CARBON
DIOXIDE LEVELS IN BAYLISS CAVE, AUSTRALIA:
IMPLICATIONS FOR THE EVOLUTION OF OBLIGATE
CAVE SPECIES. PAC SCI 44(3): 207-218. [BACK]
30. FAEHD, MOSER A, PANCZAK R, ET AL. INDEPENDENT AT
HEART: PERSISTENT ASSOCIATION OF ALTITUDE WITH
ISCHAEMIC HEART DISEASE MORTALITY AFTER
CONSIDERATION OF CLIMATE, TOPOGRAPHY AND BUILT
ENVIRONMENT. J EPIDEMIOL COMMUNITY HEALTH.
2016;70(8):798-806. [BACK]
31. MORTIMER EA, MONSON RR, MACMAHON B.
REDUCTION IN MORTALITY FROM CORONARY HEART
DISEASE IN MEN RESIDING AT HIGH ALTITUDE. N ENGL J
MED. 1977;296(11):581-5. [BACK]
32. VOORS AW,
JOHNSON WD. ALTITUDE AND
ARTERIOSCLEROTIC HEART DISEASE MORTALITY IN
WHITE RESIDENTS OF 99 OF THE 100 LARGEST CITIES IN
THE UNITED STATES. J CHRONIC DIS. 1979;32(1-2):157-62.
[BACK]
33. BURTSCHER M. EFFECTS OF LIVING AT HIGHER
ALTITUDES ON MORTALITY: A NARRATIVE REVIEW.
AGING DIS. 2014;5(4):274-80. [BACK]
34. FAEHD, GUTZWILLER F, BOPP M. LOWER MORTALITY
FROM CORONARY HEART DISEASE AND STROKE AT
HIGHER ALTITUDES IN SWITZERLAND. CIRCULATION.
2009;120(6):495-501. [BACK]
35. SIMEONOV KP, HIMMELSTEIN DS. LUNG CANCER
INCIDENCE DECREASES WITH ELEVATION: EVIDENCE
FOR OXYGEN AS AN INHALED CARCINOGEN. PEERJ.
2015;3:E705. [BACK]
36. YOUK AO,BUCHANICH JM, FRYZEK J, CUNNINGHAM M,
MARSH GM. AN ECOLOGICAL STUDY OF CANCER
MORTALITY RATES IN HIGH ALTITUDE COUNTIES OF
THE UNITED STATES. HIGH ALT MED BIOL. 2012;13(2):98-
104. [BACK]
37. AMSEL J, WATERBOR JW, OLER J, ROSENWAIKE I,
MARSHALL K. RELATIONSHIP OF SITE-SPECIFIC CANCER
MORTALITY RATES TO ALTITUDE. CARCINOGENESIS.
1982;3(5):461-5. [BACK]
38. WEINBERGCR, BROWN KG, HOEL DG. ALTITUDE,
RADIATION, AND MORTALITY FROM CANCER AND
HEART DISEASE. RADIAT RES. 1987;112(2):381-90. [BACK]
39. HARTJ. CANCER MORTALITY IN SIX LOWEST VERSUS
SIX HIGHEST ELEVATION JURISDICTIONS IN THE U.S.
DOSE RESPONSE. 2010;9(1):50-8. [BACK]
40. KLOCKE
RA. MECHANISM AND KINETICS OF THE
HALDANE EFFECT IN HUMAN ERYTHROCYTES. J APPL
PHYSIOL. 1973;35(5):673-81. [BACK]
41. TRIPP KE,PEET MM, PHARR DM, WILLITS DH, NELSON
PV. CO(2)-ENHANCED YIELD AND FOLIAR
DEFORMATION AMONG TOMATO GENOTYPES IN
ELEVATED CO(2) ENVIRONMENTS. PLANT PHYSIOL.
1991;96(3):713-9. [BACK]
42. HINKLETONPR, JOLIFFE PA. EFFECTS OF GREENHOUSE
CO2 ENRICHMENT ON THE YIELD AND
PHOTOSYNTHETIC PHYSIOLOGY OF TOMATO PLANTS.
CAN J. PLANT SCI. 1977;58:801-817. [BACK]
43. SRINIVASA RAO
M, MANIMANJARI D, VANAJA M, ET AL.
IMPACT OF ELEVATED CO ₂ ON TOBACCO
CATERPILLAR, SPODOPTERA LITURA ON PEANUT,
ARACHIS HYPOGEA. J INSECT SCI. 2012;12:103. [BACK]
44. CHENG
W, SAKAI H, YAGI K, HASEGAWA T.
INTERACTIONS OF ELEVATED [CO2] AND NIGHT
 TEMPERATURE ON RICE GROWTH AND YIELD.
AGRICULTURAL AND FOREST METEOROLOGY; VOL.149,
ISSUE 1:51-58. [BACK]
45. GHASEMZADEH A,
JAAFAR HZ. EFFECT OF CO(2)
ENRICHMENT ON SYNTHESIS OF SOME PRIMARY AND
SECONDARY METABOLITES IN GINGER (ZINGIBER
OFFICINALE ROSCOE). INT J MOL SCI. 2011;12(2):1101-14.
[BACK]
46. BECKERC, KLÄRING HP. CO ₂ ENRICHMENT CAN
PRODUCE HIGH RED LEAF LETTUCE YIELD WHILE
INCREASING MOST FLAVONOID GLYCOSIDE AND SOME
CAFFEIC ACID DERIVATIVE CONCENTRATIONS. FOOD
CHEM. 2016;199:736-45. [BACK]
47. IDSOSB, KIMBALL BA, ANDERSON MG, MAUNEY JR.
EFFECTS OF ATMOSPHERIC CO2 ENRICHMENT ON
PLANT GROWTH: THE INTERACTIVE ROLE OF AIR
TEMPERATURE. AG ECO AND ENVI. 1987; VOL 20, ISSUE
1:1-10. [BACK]
48. ZELIKOVA TJ,
BLUMENTHAL DM, WILLIAMS DG, ET AL.
LONG-TERM EXPOSURE TO ELEVATED CO2 ENHANCES
PLANT COMMUNITY STABILITY BY SUPPRESSING
DOMINANT PLANT SPECIES IN A MIXED-GRASS PRAIRIE.
PROC NATL ACAD SCI USA. 2014;111(43):15456-61. [BACK]
49. TEMPERTON VM, GRAYSTON SJ, JACKSON G, BARTON
CV, MILLARD P, JARVIS PG. EFFECTS OF ELEVATED
CARBON DIOXIDE CONCENTRATION ON GROWTH AND
NITROGEN FIXATION IN ALNUS GLUTINOSA IN A LONG-
TERM FIELD EXPERIMENT. TREE PHYSIOL.
2003;23(15):1051-9. [BACK]
50. JACH
EM, CEULEMANS R. EFFECTS OF ELEVATED
ATMOSPHERIC CO2 ON GROWTH AND CROWN
STRUCTURE OF SCOTS PINE (PINUS SYLVESTRIS)
SEEDLINGS AFTER TWO YEARS OF EXPOSURE IN THE
FIELD. TREE PHYSIOL. 1999;19(45):289-300. [BACK]
51. BOND WJ, MIDGLEY GF. CARBON DIOXIDE AND THE
UNEASY INTERACTIONS OF TREES AND SAVANNAH
GRASSES. PHILOS TRANS R SOC LOND, B, BIOL SCI.
2012;367(1588):601-12. [BACK]
52. CAMPBELL, C. D., SAGE, R. F., KOCACINAR, F. AND WAY,
D. A. (2005), ESTIMATION OF THE WHOLE-PLANT CO2
COMPENSATION POINT OF TOBACCO (NICOTIANA
TABACUM L.). GLOBAL CHANGE BIOLOGY, 11: 1956–1967.
[BACK]
53. ESCONDIDON. (2014). CULTIVATION CLINIC: CO2 CAN
INCREASE YIELDS 40%. HIGH TIMES. [ONLINE].
AVAILABLE:
HTTP://HIGHTIMES.COM/GROW/CULTIVATION-CLINIC-
CO2-CAN-INCREASE-YIELDS-40. [FEBRUARY 15, 2017].
[BACK]
54. HOLLEY WD,GOLDSBERRY KL. CARBON DIOXIDE
INCREASES GROWTH OF GREENHOUSE ROSES.
COLORADO STATE UNIVERSITY. 1961. AVAILABLE:
HTTPS://HORTSCANS.CES.NCSU.EDU/UPLOADS/C/A/CAR
BON_D_534D6D760C4ED.PDF [FEBRUARY 15, 2017].
[BACK]
55. SINGH
SP, SINGH P. EFFECT OF CO2 CONCENTRATION ON
ALGAL GROWTH: A REVIEW. RENEWABLE AND
SUSTAINABLE ENERGY REVIEWS. 2014; 38:172-179.
[BACK]
56. ROBERTS
DA, DE NYS R, PAUL NA. THE EFFECT OF CO2
ON ALGAL GROWTH IN INDUSTRIAL WASTE WATER FOR
BIOENERGY AND BIOREMEDIATION APPLICATIONS.
PLOS ONE. 2013;8(11):E81631. [BACK]
57. GHASEMZADEH A,JAAFAR HZ, RAHMAT A. ELEVATED
CARBON DIOXIDE INCREASES CONTENTS OF
FLAVONOIDS AND PHENOLIC COMPOUNDS, AND
ANTIOXIDANT ACTIVITIES IN MALAYSIAN YOUNG
 GINGER (ZINGIBER OFFICINALE ROSCOE.) VARIETIES.
MOLECULES. 2010;15(11):7907-22. [BACK]
58. STILING,
P. AND CORNELISSEN, T. HOW DOES ELEVATED
CARBON DIOXIDE (CO2) AFFECT PLANT–HERBIVORE
INTERACTIONS? A FIELD EXPERIMENT AND META-
ANALYSIS OF CO2-MEDIATED CHANGES ON PLANT
CHEMISTRY AND HERBIVORE PERFORMANCE. GLOBAL
CHANGE BIOLOGY, 13: 1823–1842. [BACK]
59. PENUELAS J, ESTIARTE M, KIMBALL BA, IDSO SB,
PINTER JR PJ, WALL GW, GARCIA RL, HANSAKER DJ,
LAMORTE RL, HENDRIX DL. VARIETY OF RESPONSES OF
PLANT PHENOLIC CONCENTRATION TO CO2
ENRICHMENT. J EXPER BOT. 1996;VOL. 47, 302: 1463-1467.
[BACK]
60. PAPITCHAYA T,
CHEN WT, SRIPONTAN Y, HWANG SY.
ELEVATED CO2 CONCENTRATION PROMOTES TOMATO
PLANT GROWTH BUT IMPAIRS SPODOPTERA LITURA
PERFORMANCE. J ZOO SCI. 2015. [BACK]
61. COVIELLA CE, STIPANOVIC RD, TRUMBLE JT. PLANT
ALLOCATION TO DEFENSIVE COMPOUNDS:
INTERACTIONS BETWEEN ELEVATED CO(2) AND
NITROGEN IN TRANSGENIC COTTON PLANTS. J EXP BOT.
2002;53(367):323-31. [BACK]
62. PRIOR
SA, RUNION GB, MARBLE SC, ROGERS HH,
GILLIAM CH, TORBERT HA. A REVIEW OF ELEVATED
ATMOSPHERIC CO@ EFFECTS ON PLANT GROWTH AND
WATER RELATIONS: IMPLICATIONS FOR HORTICULTURE.
HORTSCIENCE. 2011;46(2). [BACK]
63. ABDELGAWAD H, FARFAN-VIGNOLO ER, DE VOS D,
ASARD H. ELEVATED CO ₂ MITIGATES DROUGHT AND
TEMPERATURE-INDUCED OXIDATIVE STRESS
DIFFERENTLY IN GRASSES AND LEGUMES. PLANT SCI.
2015;231:1-10. [BACK]
64. IDSOSB, ALLEN SG, ANDERSON MG, KIMBALL BA.
ATMOSPHERIC CO2 ENRICHMENT ENHANCES SURVIVAL
OF AZOLLA AT HIGH TEMPERATURES. ENV & EXP BOT.
1989; 29(3):337-341. [BACK]
65. ABDELGAWAD H, ZINTA G, BEEMSTER GT, JANSSENS IA,
ASARD H. FUTURE CLIMATE CO2 LEVELS MITIGATE
STRESS IMPACT ON PLANTS: INCREASED DEFENSE OR
DECREASED CHALLENGE?. FRONT PLANT SCI.
2016;7:556. [BACK]
66. MHAMDI A,
NOCTOR G. HIGH CO2 PRIMES PLANT
BIOTIC STRESS DEFENCES THROUGH REDOX-LINKED
PATHWAYS. PLANT PHYSIOL. 2016;172(2):929-942. [BACK]
67. HARTWELL JR AL,BAKER JT, BOOTE KJ. THE CO2
FERTILIZATION EFFECTS: HIGHER CARBOHYDRATE
PRODUCTION AND RETENTION AS BIOMASS AND SEED
YIELD. AVAILABLE:
HTTP://WWW.FAO.ORG/DOCREP/W5183E/W5183E06.HTM
[FEBRUARY 15, 2017]. [BACK]
68. REYES-FOX M, STELTZER H, TRLICA MJ, ET AL.
ELEVATED CO2 FURTHER LENGTHENS GROWING
SEASON UNDER WARMING CONDITIONS. NATURE.
2014;510(7504):259-62. [BACK]
69. CHOI
HJ, BAE YS, LEE JS, PARK MH, KIM GJ. EFFECTS OF
CARBON DIOXIDE TREATMENT AND MODIFIED
ATMOSPHERE PACKAGING ON THE QUALITY OF LONG
DISTANCE TRANSPORTING “MAEHYANG”
STRAWBERRIES. AG SCI. 2016; 7:813-821. [BACK]
70. RAMAYYA N, NIRANJAN K, DUNCAN E. EFFECTS OF
MODIFIED ATMOSPHERE PACKAGING ON QUALITY OF
'ALPHONSO' MANGOES. J FOOD SCI TECHNOL.
2012;49(6):721-8. [BACK]
71. ALMENAR E, HERNÁNDEZ-MUÑOZ P, LAGARÓN JM,
CATALÁ R, GAVARA R. CONTROLLED ATMOSPHERE
 STORAGE OF WILD STRAWBERRY FRUIT (FRAGARIA
VESCA L.). J AGRIC FOOD CHEM. 2006;54(1):86-91. [BACK]
72. REILLY S.THE CARBON DIOXIDE REQUIREMENTS OF
ANAEROBIC BACTERIA. J MED MICROBIOL.
1980;13(4):573-9. [BACK]
73. BARRETT,
J. CNN HOST LINKS CLIMATE ‘DENIERS’ TO
GENOCIDAL MASS MURDERERS. DAILY WIRE. [ONLINE].
AVAILABLE:
HTTP://WWW.DAILYWIRE.COM/NEWS/11152/CNN-
CORRESPONDENT-LINKS-CLIMATE-DENIERS-
GENOCIDAL-JAMES-BARRETT. [FEBRUARY 15, 2017].
[BACK]
74. THE
CANADIAN FREE PRESS. (2017). CARBON TAX NOT
NEUTRAL. CASTANET. [ONLINE]. AVAILABLE:
HTTP://WWW.CASTANET.NET/NEWS/BC/189019/CARBON-
TAX-NOT-NEUTRAL. [FEBRUARY 15, 2017]. [BACK]
75. ESSEX C, MCKITRICK R, ANDRESEN B. DOES A GLOBAL
TEMPERATURE EXIST? J. NON-EQUILIBRIUM THERMO.
2006. [BACK]
76. GRAY,
L. J., ET AL. (2010), SOLAR INFLUENCES ON
CLIMATE, REV. GEOPHYS. 48, RG4001. [BACK]
77. CAMP,
C. D., AND K. K. TUNG (2007), SURFACE WARMING
BY THE SOLAR CYCLE AS REVEALED BY THE
COMPOSITE MEAN DIFFERENCE PROJECTION,
GEOPHYS. RES. LETT., 34, L14703. [BACK]
78. SCHWARTZ SE. HEAT CAPACITY, TIME CONSTANT, AND
SENSITIVITY OF EARTH’S CLIMATE SYSTEM. J. GEO RES.
2007. [BACK]
79. TECH-KNOW-GROUP. DOZENS OF UNPUBLISHED
SCIENTIFIC PAPERS OPEN FOR PEER REVIEW. [BACK]
80. LU
QB. COSMIC-RAY-DRIVEN REACTION AND
GREENHOUSE EFFECT OF HALOGENATED MOLECULES:
CULPRITS FOR ATMOSPHERIC OZONE DEPLETION AND
 GLOBAL CLIMATE CHANGE. INT. J. MOD. PHYS.
2013;27:1350073. [BACK]
81. CARTERRM. PUBLIC MISPERCEPTIONS OF HUMAN-
CAUSED CLIMATE CHANGE: THE ROLE OF THE MEDIA.
2006 TESTIMONY BEFORE THE COMMITTEE ON
ENVIRONMENT AND PUBLIC WORKS. AVAILABLE:
HTTPS://WWW.EPW.SENATE.GOV/109TH/CARTER_TESTIM
ONY.PDF [FEBRUARY 15, 2017]. [BACK]
82. TSONIS, A. A.,
K. SWANSON, AND S. KRAVTSOV (2007), A
NEW DYNAMICAL MECHANISM FOR MAJOR CLIMATE
SHIFTS, GEOPHYS. RES. LETT. 34, L13705. [BACK]
83. SPENCERRW. SATELLITE AND CLIMATE MODEL
EVIDENCE AGAINST SUBSTANTIAL MANMADE CLIMATE
CHANGE (SUPERCEDES “HAS THE CLIMATE
SENSITIVITY HOLY GRAIL BEEN FOUND?”) 2008. [BACK]
84. SPENCERRW. GLOBAL WARMING AS A NATURAL
RESPONSE TO CLOUD CHANGES ASSOCIATED WITH THE
PACIFIC DECADAL OSCILLATION (PDO). 2008. [BACK]
85. MACKEY R. RHODES FAIRBRIDGE AND THE IDEA THAT
THE SOLAR SYSTEM REGULATES THE EARTH’S
CLIMATE. J. CTL RES. 2007;50:955-968. [BACK]
86. SHAN LZ, XIAN S. MULTI-SCALE ANALYSIS OF GLOBAL
TEMPERATURE CHANGES AND TREND OF A DROP IN
TEMPERATURE IN THE NEXT 20 YEARS. ATMOS. PHYS.
2007; 95:115. [BACK]
87. MANUEL OK.
EARTH’S HEAT SOURCE – THE SUN.
ENERGY & ENVIRONMENT. 2009; 20:131-144. [BACK]
88. CARUBA, A.
(2007). THE YEAR THE GLOBAL WARMING
HOAX DIED. CANADA FREE PRESS. [ONLINE].
AVAILABLE:
HTTP://CANADAFREEPRESS.COM/2007/CARUBA090307.H
TM. [FEBRUARY 15, 2017]. [BACK]
89. SCHULTE
M-K. SCIENTIFIC CONSENSUS ON CLIMATE
CHANGE? ENERGY & ENVIRONMENT. 2008; 19(2). [BACK]
90. AL-ACHI A,
MEDURI RT. AN IN VITRO STUDY OF
MODULATORY EFFECTS OF SODIUM BICARBONATE ON
HUMAN COLON ADENOCARCINOMA CELL (CACO-2).
WORLD J. PHAR. & PHAR. SCI. 2014;3(3):228-244. [BACK]
91. SIRCUS,
M. 2014. SODIUM BICARBONATE: NATURE’S
UNIQUE FIRST AID REMEDY. SQUARE ONE. 224 PPS.
[BACK]
92. ROFSTAD EK, MATHIESEN B, KINDEM K, GALAPPATHI K.
ACIDIC EXTRACELLULAR PH PROMOTES
EXPERIMENTAL METASTASIS OF HUMAN MELANOMA
CELLS IN ATHYMIC NUDE MICE. CANCER RES.
2006;66(13):6699-707. [BACK]
93. ROBEY IF,BAGGETT BK, KIRKPATRICK ND, ET AL.
BICARBONATE INCREASES TUMOR PH AND INHIBITS
SPONTANEOUS METASTASES. CANCER RES.
2009;69(6):2260-8. [BACK]
94. ESTRELLA V,
CHEN T, LLOYD M, ET AL. ACIDITY
GENERATED BY THE TUMOR MICROENVIRONMENT
DRIVES LOCAL INVASION. CANCER RES. 2013;73(5):1524-
35. [BACK]
95. ROBEY IF,
NESBIT LA. INVESTIGATING MECHANISMS OF
ALKALINIZATION FOR REDUCING PRIMARY BREAST
TUMOR INVASION. BIOMED RES INT. 2013;2013:485196.
[BACK]
96. HOANGBX, TRAN DM, TRAN HQ, ET AL. DIMETHYL
SULFOXIDE AND SODIUM BICARBONATE IN THE
TREATMENT OF REFRACTORY CANCER PAIN. J PAIN
PALLIAT CARE PHARMACOTHER. 2011;25(1):19-24.
[BACK]
97. RAGHUNAND
N, HE X, VAN SLUIS R, ET AL.
ENHANCEMENT OF CHEMOTHERAPY BY
 MANIPULATION OF TUMOUR PH. BR J CANCER.
1999;80(7):1005-11. [BACK]
98. FASSA,
P. (2009). BICARBONATE OF SODA USED TO CURE
STAGE FOUR PROSTATE CANCER. NATURAL NEWS.
[ONLINE]. AVAILABLE:
HTTP://WWW.NATURALNEWS.COM/027481_PROSTATE_C
ANCER_BAKING_SODA.HTML. [FEBRUARY 15, 2017].
[BACK]
99. LOREDANA.
SEOLEOINT. (2012). BREAST CANCER
TREATMENT WITH SODIUM BICARBONATE. AVAILABLE:
HTTPS://WWW.YOUTUBE.COM/WATCH?V=7FAK-56WCDG.
[FEBRUARY 15, 2017]. [BACK]
100.
PETERSON R. SEOLEOINT. (2012). DR. SIMONCINI –
PATIENT KIDNEY CANCER RCC. AVAILABLE:
HTTPS://WWW.YOUTUBE.COM/WATCH?
V=KGA3ZHQUQEK. [FEBRUARY 15, 2017]. [BACK]
101.
BRUNKHORST R. [MINERAL AND BONE DISORDER IN
CHRONIC KIDNEY DISEASE : CRITICAL APPRAISAL OF
PHARMACOTHERAPY]. INTERNIST (BERL).
2014;55(3):334-9. [BACK]
102.
WOLINSKY LE, LOTT T. EFFECTS OF THE INORGANIC
SALTS SODIUM CHLORIDE, SODIUM BICARBONATE, AND
MAGNESIUM SULFATE UPON THE GROWTH AND
MOTILITY OF TREPONEMA VINCENTII. J PERIODONTOL.
1986;57(3):172-5. [BACK]
103.
MALIK YS, GOYAL SM. VIRUCIDAL EFFICACY OF
SODIUM BICARBONATE ON A FOOD CONTACT SURFACE
AGAINST FELINE CALICIVIRUS, A NOROVIRUS
SURROGATE. INT J FOOD MICROBIOL. 2006;109(1-2):160-3.
[BACK]
104.
 NEWBRUN E. THE USE OF SODIUM BICARBONATE IN
ORAL HYGIENE PRODUCTS AND PRACTICE. COMPEND
CONTIN EDUC DENT SUPPL. 1997;18(21):S2-7. [BACK]
105.
DRAKE DR, VARGAS K, CARDENZANA A, SRIKANTHA R.
ENHANCED BACTERICIDAL ACTIVITY OF ARM AND
HAMMER DENTAL CARE. AM J DENT. 1995;8(6):308-12.
[BACK]
106.
PINTO L, IPPOLITO A, BARUZZI F. CONTROL OF SPOILER
PSEUDOMONAS SPP. ON FRESH CUT VEGETABLES BY
NEUTRAL ELECTROLYZED WATER. FOOD MICROBIOL.
2015;50:102-8. [BACK]
107.
MIYASAKI KT, GENCO RJ, WILSON ME. ANTIMICROBIAL
PROPERTIES OF HYDROGEN PEROXIDE AND SODIUM
BICARBONATE INDIVIDUALLY AND IN COMBINATION
AGAINST SELECTED ORAL, GRAM-NEGATIVE,
FACULTATIVE BACTERIA. J DENT RES. 1986;65(9):1142-8.
[BACK]
108.
NEAVYN MJ, BOYER EW, BIRD SB, BABU KM. SODIUM
ACETATE AS A REPLACEMENT FOR SODIUM
BICARBONATE IN MEDICAL TOXICOLOGY: A REVIEW. J
MED TOXICOL. 2013;9(3):250-4. [BACK]
109.
BANDO H, MURAO Y, AOYAGI U, HIRAKAWA A, IWASE
M, NAKATANI T. [EXTREME HYPERKALEMIA IN A
PATIENT WITH A NEW GLYPHOSATE POTASSIUM
HERBICIDE POISONING: REPORT OF A CASE]. CHUDOKU
KENKYU. 2010;23(3):246-9. [BACK]
110.
DECLERCK MP, BAILEY Y, CRAIG D, ET AL. EFFICACY
OF TOPICAL TREATMENTS FOR CHRYSAORA CHINENSIS
SPECIES: A HUMAN MODEL IN COMPARISON WITH AN IN
VITRO MODEL. WILDERNESS ENVIRON MED.
2016;27(1):25-38. [BACK]
111.
REN A, REN S, JIAN X, ZHANG Q. [THE PREVENTION
AND THERAPEUTICS EFFECT OF SODIUM BICARBONATE
WITH GASTRIC LAVAGE, ATOMIZATION INHALATION
AND INTRAVENOUS INJECTION ON THE PATIENTS WITH
PARAQUAT POISONING AND PULMONARY FIBROSIS
INDUCED BY PARAQUAT POISONING]. ZHONGHUA LAO
DONG WEI SHENG ZHI YE BING ZA ZHI. 2015;33(9):693-4.
[BACK]
112.
PIEROG J, KANE B, KANE K, DONOVAN JW.
MANAGEMENT OF ISOLATED YEW BERRY TOXICITY
WITH SODIUM BICARBONATE: A CASE REPORT IN
TREATMENT EFFICACY. J MED TOXICOL. 2009;5(2):84-9.
[BACK]
113.
JANG DH, HOFFMAN RS, NELSON LS. A CASE OF NEAR-
FATAL FLECAINIDE OVERDOSE IN A NEONATE
SUCCESSFULLY TREATED WITH SODIUM BICARBONATE.
J EMERG MED. 2013;44(4):781-3. [BACK]
114.
ZHAO B, YANG L, XIAO L, ET AL. [THE INFLUENCE OF
SODIUM BICARBONATE COMBINED WITH ULINASTATIN
ON CHOLINESTERASE ACTIVITY FOR PATIENTS WITH
ACUTE PHOXIM PESTICIDE POISONING]. ZHONGHUA
LAO DONG WEI SHENG ZHI YE BING ZA ZHI.
2016;34(1):53-5. [BACK]
115.
STEFANOVIC D, ANTONIJEVIC B, BOKONJIC D,
STOJILJKOVIC MP, MILOVANOVIC ZA, NEDELJKOVIC M.
EFFECT OF SODIUM BICARBONATE IN RATS ACUTELY
POISONED WITH DICHLORVOS. BASIC CLIN
PHARMACOL TOXICOL. 2006;98(2):173-80. [BACK]
116.
 GARCÍA-PADILLA S, DUARTE-VÁZQUEZ MA,
GONZALEZ-ROMERO KE, CAAMAÑO MDEL C, ROSADO
JL. EFFECTIVENESS OF INTRA-ARTICULAR INJECTIONS
OF SODIUM BICARBONATE AND CALCIUM GLUCONATE
IN THE TREATMENT OF OSTEOARTHRITIS OF THE KNEE:
A RANDOMIZED DOUBLE-BLIND CLINICAL TRIAL. BMC
MUSCULOSKELET DISORD. 2015;16:114. [BACK]
117.
RAPHAEL KL. APPROACH TO THE TREATMENT OF
CHRONIC METABOLIC ACIDOSIS IN CKD. AM J KIDNEY
DIS. 2016;67(4):696-702. [BACK]
118.
BAKHRU MR, KUMAR A, ANEJA A. A 58-YEAR-OLD
WOMAN WITH MENTAL STATUS CHANGES. CLEVE CLIN
J MED. 2007;74(6):457-62. [BACK]
119.
DE BRITO-ASHURST I, VARAGUNAM M, RAFTERY MJ,
YAQOOB MM. BICARBONATE SUPPLEMENTATION
SLOWS PROGRESSION OF CKD AND IMPROVES
NUTRITIONAL STATUS. J AM SOC NEPHROL.
2009;20(9):2075-84. [BACK]
120.JEONG J, KWON SK, KIM HY. EFFECT OF
BICARBONATE SUPPLEMENTATION ON RENAL
FUNCTION AND NUTRITIONAL INDICES IN PREDIALYSIS
ADVANCED CHRONIC KIDNEY DISEASE. ELECTROLYTE
BLOOD PRESS. 2014;12(2):80-7. [BACK]
121.
ROUMELIOTI ME, RANPURIA R, HALL M, ET AL.
ABNORMAL NOCTURNAL HEART RATE VARIABILITY
RESPONSE AMONG CHRONIC KIDNEY DISEASE AND
DIALYSIS PATIENTS DURING WAKEFULNESS AND SLEEP.
NEPHROL DIAL TRANSPLANT. 2010;25(11):3733-41.
[BACK]
122.
 MANLEY KJ. WILL MOUTH WASH SOLUTIONS OF
WATER, SALT, SODIUMBICARBONATE OR CITRIC ACID
IMPROVE UPPER GASTROINTESTINAL SYMPTOMS IN
CHRONIC KIDNEY DISEASE. NEPHROLOGY (CARLTON).
2017;22(3):213-219. [BACK]
123.
ASH A, WILDE PJ, BRADSHAW DJ, KING SP, PRATTEN JR.
STRUCTURAL MODIFICATIONS OF THE SALIVARY
CONDITIONING FILM UPON EXPOSURE TO SODIUM
BICARBONATE: IMPLICATIONS FOR ORAL LUBRICATION
AND MOUTHFEEL. SOFT MATTER. 2016;12(10):2794-801.
[BACK]
124.
GHASSEMI A, HOOPER W, VORWERK L, DOMKE T,
DESCISCIO P, NATHOO S. EFFECTIVENESS OF A NEW
DENTIFRICE WITH BAKING SODA AND PEROXIDE IN
REMOVING EXTRINSIC STAIN AND WHITENING TEETH. J
CLIN DENT. 2012;23(3):86-91. [BACK]
125.
CHARIG A, WINSTON A, FLICKINGER M. ENAMEL
MINERALIZATION BY CALCIUM-CONTAINING-
BICARBONATE TOOTHPASTES: ASSESSMENT BY
VARIOUS TECHNIQUES. COMPEND CONTIN EDUC DENT.
2004;25(9 SUPPL 1):14-24. [BACK]
126.
PUTT MS, MILLEMAN KR, GHASSEMI A, ET AL.
ENHANCEMENT OF PLAQUE REMOVAL EFFICACY BY
TOOTH BRUSHING WITH BAKING SODA DENTIFRICES:
RESULTS OF FIVE CLINICAL STUDIES. J CLIN DENT.
2008;19(4):111-9. [BACK]
127.GHASSEMI A, VORWERK LM, HOOPER WJ, PUTT MS,
MILLEMAN KR. A FOUR-WEEK CLINICAL STUDY TO
EVALUATE AND COMPARE THE EFFECTIVENESS OF A
BAKING SODA DENTIFRICE AND AN ANTIMICROBIAL
DENTIFRICE IN REDUCING PLAQUE. J CLIN DENT.
2008;19(4):120-6. [BACK]
128.
LOMAX A, PATEL S, WANG N, KAKAR K, KAKAR A,
BOSMA ML. A RANDOMIZED CONTROLLED TRIAL
EVALUATING THE EFFICACY OF A 67% SODIUM
BICARBONATE TOOTHPASTE ON GINGIVITIS. INT J DENT
HYG. 2016. [BACK]
129.
MESSIAS DC, TURSSI CP, HARA AT, SERRA MC. SODIUM
BICARBONATE SOLUTION AS AN ANTI-EROSIVE AGENT
AGAINST SIMULATED ENDOGENOUS EROSION. EUR J
ORAL SCI. 2010;118(4):385-8. [BACK]
130.KASHKET S, YASKELL T. EFFECTS OF A HIGH-
BICARBONATE DENTIFRICE ON INTRAORAL
DEMINERALIZATION. COMPEND CONTIN EDUC DENT
SUPPL. 1997;18(21):S11-6. [BACK]
131.TURSSI CP, VIANNA LM, HARA AT, DO AMARAL FL,
FRANÇA FM, BASTING RT. COUNTERACTIVE EFFECT OF
ANTACID SUSPENSIONS ON INTRINSIC DENTAL
EROSION. EUR J ORAL SCI. 2012;120(4):349-52. [BACK]
132.ALVES MDO S, MANTILLA TF, BRIDI EC, ET AL.
RINSING WITH ANTACID SUSPENSION REDUCES
HYDROCHLORIC ACID-INDUCED EROSION. ARCH ORAL
BIOL. 2016;61:66-70. [BACK]
133.
KLEBER CJ, PUTT MS, MILLEMAN JL, DAVIDSON KR,
PROSKIN HM. AN EVALUATION OF SODIUM
BICARBONATE CHEWING GUM IN REDUCING DENTAL
PLAQUE AND GINGIVITIS IN CONJUNCTION WITH
REGULAR TOOTHBRUSHING. COMPEND CONTIN EDUC
DENT. 2001;22(7A):4-12. [BACK]
134.KLEBER CJ, DAVIDSON KR, RHOADES ML. AN
EVALUATION OF SODIUM BICARBONATE CHEWING
GUM AS A SUPPLEMENT TO TOOTHBRUSHING FOR
REMOVAL OF DENTAL PLAQUE FROM CHILDREN'S
TEETH. COMPEND CONTIN EDUC DENT. 2001;22(7A):36-
42. [BACK]
135.SHARMA NC, GALUSTIANS JH, QAQISH JG. AN
EVALUATION OF A COMMERCIAL CHEWING GUM IN
COMBINATION WITH NORMAL TOOTHBRUSHING FOR
REDUCING DENTAL PLAQUE AND GINGIVITIS.
COMPEND CONTIN EDUC DENT. 2001;22(7A):13-7. [BACK]
136.
OHMACHI Y, IMAMURA T, IKEDA M, ET AL. SODIUM
BICARBONATE PROTECTS URANIUM-INDUCED ACUTE
NEPHROTOXICITY THROUGH URANIUM-
DECORPORATION BY URINARY ALKALINIZATION IN
RATS. J TOXICOL PATHOL. 2015;28(2):65-71. [BACK]
137.
LARSON J, PARK TJ. EXTREME HYPOXIA TOLERANCE
OF NAKED MOLE-RAT BRAIN. NEUROREPORT.
2009;20(18):1634-7. [BACK]
138.
SCHOPPEN S, SÁNCHEZ-MUNIZ FJ, PÉREZ-GRANADOS
M, ET AL. DOES BICARBONATED MINERAL WATER RICH
IN SODIUM CHANGE INSULIN SENSITIVITY OF
POSTMENOPAUSAL WOMEN?. NUTR HOSP. 2007;22(5):538-
44. [BACK]
139.
REDDY CM, ORTI E. INSULIN AND SODIUM
BICARBONATE TREATMENT IN DIABETIC
KETOACIDOSIS IN CHILDREN. J NATL MED ASSOC.
1977;69(5):355-7. [BACK]
140.
YAN T, LAPARA TM, NOVAK PJ. THE EFFECT OF
VARYING LEVELS OF SODIUM BICARBONATE ON
POLYCHLORINATED BIPHENYL DECHLORINATION IN
HUDSON RIVER SEDIMENT CULTURES. ENVIRON
MICROBIOL. 2006;8(7):1288-98. [BACK]
141.
NEAL C, ROWLAND P, NEAL M, ET AL. ALUMINIUM IN
UK RIVERS: A NEED FOR INTEGRATED RESEARCH
RELATED TO KINETIC FACTORS, COLLOIDAL
TRANSPORT, CARBON AND HABITAT. J ENVIRON MONIT.
2011;13(8):2153-64. [BACK]
142.
PHILLIPS, E.J.P., LANDA, E.R. & LOVLEY, D.R.
REMEDIATION OF URANIUM CONTAMINATED SOILS
WITH BICARBONATE EXTRACTION AND MICROBIAL
U(VI) REDUCTION. JOURNAL OF INDUSTRIAL
MICROBIOLOGY (1995) 14: 203. [BACK]
143.
POPULAR SCIENCE. RECIPE FOR PCB DESTRUCTION:
ADD BAKING SODA. AUGUST 1993;25. [BACK]
144.
DUNCAN MJ, WELDON A, PRICE MJ. THE EFFECT OF
SODIUM BICARBONATE INGESTION ON BACK SQUAT
AND BENCH PRESS EXERCISE TO FAILURE. J STRENGTH
COND RES. 2014;28(5):1358-66. [BACK]
145.
LINDH AM, PEYREBRUNE MC, INGHAM SA, BAILEY DM,
FOLLAND JP. SODIUM BICARBONATE IMPROVES
SWIMMING PERFORMANCE. INT J SPORTS MED.
2008;29(6):519-23. [BACK]
146.
SIEGLER JC, HIRSCHER K. SODIUM BICARBONATE
INGESTION AND BOXING PERFORMANCE. J STRENGTH
COND RES. 2010;24(1):103-8. [BACK]
147.
MILLER P, ROBINSON AL, SPARKS SA, BRIDGE CA,
BENTLEY DJ, MCNAUGHTON LR. THE EFFECTS OF
NOVEL INGESTION OF SODIUM BICARBONATE ON
REPEATED SPRINT ABILITY. J STRENGTH COND RES.
2016;30(2):561-8. [BACK]
148.EGGER F, MEYER T, SUCH U, HECKSTEDEN A.
EFFECTS OF SODIUM BICARBONATE ON HIGH-
INTENSITY ENDURANCE PERFORMANCE IN CYCLISTS: A
DOUBLE-BLIND, RANDOMIZED CROSS-OVER TRIAL.
PLOS ONE. 2014;9(12):E114729. [BACK]
149.
JALLOW DB, HSIA LC. EFFECT OF SODIUM
BICARBONATE SUPPLEMENTATION ON CARCASS
CHARACTERISTICS OF LAMBS FED CONCENTRATE
DIETS AT DIFFERENT AMBIENT TEMPERATURE LEVELS.
ASIAN-AUSTRALAS J ANIM SCI. 2014;27(8):1098-103.
[BACK]
150.
BOOTH AJ, NAYLOR JM. CORRECTION OF METABOLIC
ACIDOSIS IN DIARRHEAL CALVES BY ORAL
ADMINISTRATION OF ELECTROLYTE SOLUTIONS WITH
OR WITHOUT BICARBONATE. J AM VET MED ASSOC.
1987;191(1):62-8. [BACK]
151.
ZHOU W, SUI Z, WANG J, ET AL. EFFECTS OF SODIUM
BICARBONATE CONCENTRATION ON GROWTH,
PHOTOSYNTHESIS, AND CARBONIC ANHYDRASE
ACTIVITY OF MACROALGAE GRACILARIOPSIS
LEMANEIFORMIS, GRACILARIA VERMICULOPHYLLA,
AND GRACILARIA CHOUAE (GRACILARIALES,
RHODOPHYTA). PHOTOSYN RES. 2016;128(3):259-70.
[BACK]
152. SARAT CHANDRA T, DEEPAK RS, MANEESH KUMAR
M, ET AL. EVALUATION OF INDIGENOUS FRESH WATER
MICROALGA SCENEDESMUS OBTUSUS FOR FEED AND
FUEL APPLICATIONS: EFFECT OF CARBON DIOXIDE,
LIGHT AND NUTRIENT SOURCES ON GROWTH AND
BIOCHEMICAL CHARACTERISTICS. BIORESOUR
TECHNOL. 2016;207:430-9. [BACK]
153.
JIANG MJ, ZHAO JP, JIAO HC, WANG XJ, ZHANG Q, LIN H.
DIETARY SUPPLEMENTATION WITH SODIUM
BICARBONATE IMPROVES CALCIUM ABSORPTION AND
EGGSHELL QUALITY OF LAYING HENS DURING PEAK
PRODUCTION. BR POULT SCI. 2015;56(6):740-7. [BACK]
154.
YUAN Z, ZHAO J, CHEN Y, YANG Z, CUI W, ZHENG Q.
REGULATING INFLAMMATION USING ACID-RESPONSIVE
ELECTROSPUN FIBROUS SCAFFOLDS FOR SKIN
SCARLESS HEALING. MEDIATORS INFLAMM.
2014;2014:858045. [BACK]
155.
FAGA A, NICOLETTI G, GREGOTTI C, FINOTTI V, NITTO
A, GIOGLIO L. EFFECTS OF THERMAL WATER ON SKIN
REGENERATION. INT J MOL MED. 2012;29(5):732-40.
[BACK]
156.
ERZOUKI HK, BAUM I, GOLDBERG SR, SCHINDLER CW.
COMPARISON OF THE EFFECTS OF COCAINE AND ITS
METABOLITES ON CARDIOVASCULAR FUNCTION IN
ANESTHETIZED RATS. J CARDIOVASC PHARMACOL.
1993;22(4):557-63. [BACK]
157.
MIRANDA CH, PAZIN-FILHO A. CRACK COCAINE-
INDUCED CARDIAC CONDUCTION ABNORMALITIES ARE
REVERSED BY SODIUM BICARBONATE INFUSION. CASE
REP MED. 2013;2013:396401. [BACK]
158.
KIM J, KIM K, PARK J, ET AL. SODIUM BICARBONATE
ADMINISTRATION DURING ONGOING RESUSCITATION IS
ASSOCIATED WITH INCREASED RETURN OF
SPONTANEOUS CIRCULATION. AM J EMERG MED.
2016;34(2):225-9. [BACK]
159.
PAKSU MS, ZENGIN H, ILKAYA F, ET AL. CAN EMPIRICAL
HYPERTONIC SALINE OR SODIUM BICARBONATE
TREATMENT PREVENT THE DEVELOPMENT OF
CARDIOTOXICITY DURING SERIOUS AMITRIPTYLINE
POISONING? EXPERIMENTAL RESEARCH. CARDIOVASC J
AFR. 2015;26(3):134-9. [BACK]
160.
FRANCO V. WIDE COMPLEX TACHYCARDIA AFTER
BUPROPION OVERDOSE. AM J EMERG MED.
2015;33(10):1540.E3-5. [BACK]
161.
JANG DH, MANINI AF, TRUEGER NS, ET AL. STATUS
EPILEPTICUS AND WIDE-COMPLEX TACHYCARDIA
SECONDARY TO DIPHENHYDRAMINE OVERDOSE. CLIN
TOXICOL (PHILA). 2010;48(9):945-8. [BACK]
162.
HODES D. SODIUM BICARBONATE AND
HYPERVENTILATION IN TREATING AN INFANT WITH
SEVERE OVERDOSE OF TRICYCLIC ANTIDEPRESSANT.
BR MED J (CLIN RES ED). 1984;288(6433):1800-1. [BACK]
163.
CLEMENT A, RANEY JJ, WASSERMAN GS, LOWRY JA.
CHRONIC AMITRIPTYLINE OVERDOSE IN A CHILD. CLIN
TOXICOL (PHILA). 2012;50(5):431-4. [BACK]
164.
TOXQUI L, PÉREZ-GRANADOS AM, BLANCO-ROJO R,
VAQUERO MP. A SODIUM-BICARBONATED MINERAL
WATER REDUCES GALLBLADDER EMPTYING AND
POSTPRANDIAL LIPAEMIA: A RANDOMISED FOUR-WAY
CROSSOVER STUDY. EUR J NUTR. 2012;51(5):607-14.
[BACK]
165.
PÉREZ-GRANADOS AM, NAVAS-CARRETERO S,
SCHOPPEN S, VAQUERO MP. REDUCTION IN
CARDIOVASCULAR RISK BY SODIUM-BICARBONATED
MINERAL WATER IN MODERATELY
HYPERCHOLESTEROLEMIC YOUNG ADULTS. J NUTR
BIOCHEM. 2010;21(10):948-53. [BACK]
166.
RIEMANN A, WUSSLING H, LOPPNOW H, FU H, REIME S,
THEWS O. ACIDOSIS DIFFERENTLY MODULATES THE
INFLAMMATORY PROGRAM IN MONOCYTES AND
MACROPHAGES. BIOCHIM BIOPHYS ACTA.
2016;1862(1):72-81. [BACK]
167. LANGFELDER A, OKONJI E, DECA D, WEI WC,
GLITSCH MD. EXTRACELLULAR ACIDOSIS IMPAIRS P2Y
RECEPTOR-MEDIATED CA(2+) SIGNALLING AND
MIGRATION OF MICROGLIA. CELL CALCIUM.
2015;57(4):247-56. [BACK]
168.SHIELDS EJ, LAM CJ, COX AR, ET AL. EXTREME
BETA-CELL DEFICIENCY IN PANCREATA OF DOGS WITH
CANINE DIABETES. PLOS ONE. 2015;10(6):E0129809.
[BACK]
169.
ORI Y, ZINGERMAN B, BERGMAN M, BESSLER H,
SALMAN H. THE EFFECT OF SODIUM BICARBONATE ON
CYTOKINE SECRETION IN CKD PATIENTS WITH
METABOLIC ACIDOSIS. BIOMED PHARMACOTHER.
2015;71:98-101. [BACK]
170.
PILON-THOMAS S, KODUMUDI KN, EL-KENAWI AE, ET
AL. NEUTRALIZATION OF TUMOR ACIDITY IMPROVES
ANTITUMOR RESPONSES TO IMMUNOTHERAPY.
CANCER RES. 2016;76(6):1381-90. [BACK]
171.
SINGER RB, DEERING RC, CLARK JK. THE ACUTE
EFFECTS IN MAN OF A RAPID INTRAVENOUS INFUSION
OF HYPERTONIC SODIUM BICARBONATE SOLUTION. II.
CHANGES IN RESPIRATION AND OUTPUT OF CARBON
DIOXIDE. J CLIN INVEST. 1956;35(2):245-53. [BACK]
172.
LEIBROCK CB, VOELKL J, KOHLHOFER U,
QUINTANILLA-MARTINEZ L, KURO-O M, LANG F.
BICARBONATE-SENSITIVE CALCIFICATION AND
LIFESPAN OF KLOTHO-DEFICIENT MICE. AM J PHYSIOL
RENAL PHYSIOL. 2016;310(1):F102-8. [BACK]
173.
DAKAM W, SHANG J, AGBOR G, OBEN J. EFFECTS OF
SODIUM BICARBONATE AND ALBUMIN ON THE IN
VITRO WATER-HOLDING CAPACITY AND SOME
PHYSIOLOGICAL PROPERTIES OF TRIGONELLA FOENUM
GRAECUM L. GALACTOMANNAN IN RATS. J MED FOOD.
2007;10(1):169-74. [BACK]
174.
MALLICK S, BENSON R, RATH GK. RADIATION INDUCED
ORAL MUCOSITIS: A REVIEW OF CURRENT LITERATURE
ON PREVENTION AND MANAGEMENT. EUR ARCH
OTORHINOLARYNGOL. 2016;273(9):2285-93. [BACK]
175.
LIU Y, WANG DK, CHEN LM. THE PHYSIOLOGY OF
BICARBONATE TRANSPORTERS IN MAMMALIAN
REPRODUCTION. BIOL REPROD. 2012;86(4):99. [BACK]
176.
QUINN P, COOKE S. EQUIVALENCY OF CULTURE MEDIA
FOR HUMAN IN VITRO FERTILIZATION FORMULATED TO
HAVE THE SAME PH UNDER AN ATMOSPHERE
CONTAINING 5% OR 6% CARBON DIOXIDE. FERTIL
STERIL. 2004;81(6):1502-6. [BACK]
177.
KURGAN DM, KOKORUZ MV, KURGAN MG, NOVAK VL.
[THE DYNAMICS OF IMMUNOLOGICAL RESULTS OF
PATIENTS WITH T-CELL SKIN LYMPHOMAS AND
PSORIASIS BY THE THERAPY OF ACTIVATION
MECHANISMS SANOGENESIS METHODS]. LIK SPRAVA.
2015;(3-4):31-8. [BACK]
178.
 SAMSOEN M. SODIUM BICARBONATE BATH AND
PSORIASIS. FIRST OPEN STUDY IN A SINGLE CENTER.
2007. AVAILABLE:
HTTPS://WWW.RESEARCHGATE.NET/PUBLICATION/29027
9882_SODIUM_BICARBONATE_BATH_AND_PSORIASIS_FI
RST_OPEN_STUDY_IN_A_SINGLE_CENTER. [FEBRUARY
15, 2017]. [BACK]
179. VERDOLINI R, BUGATTI L, FILOSA G, MANNELLO B,
LAWLOR F, CERIO RR. OLD FASHIONED SODIUM
BICARBONATE BATHS FOR THE TREATMENT OF
PSORIASIS IN THE ERA OF FUTURISTIC BIOLOGICS: AN
OLD ALLY TO BE RESCUED. J DERMATOLOG TREAT.
2005;16(1):26-30. [BACK]
180.
AFSAR B, ELSURER R. ASSOCIATION BETWEEN SERUM
BICARBONATE AND PH WITH DEPRESSION, COGNITION
AND SLEEP QUALITY IN HEMODIALYSIS PATIENTS. REN
FAIL. 2015;37(6):957-60. [BACK]
181.
DISTHABANCHONG S, TREERUTTANAWANICH A. ORAL
SODIUM BICARBONATE IMPROVES THYROID FUNCTION
IN PREDIALYSIS CHRONIC KIDNEY DISEASE. AM J
NEPHROL. 2010;32(6):549-56. [BACK]
182.
BROWN JR, BLOCK CA, MALENKA DJ, O’CONNOR GT,
SCHOOLWERTH AC, THOMPSON CA. SODIUM
BICARBONATE PLUS N-ACETYLCYSTEINE
PROPHYLAXIS : A META-ANALYSIS. JACC.
2009;2(11):1116-1124. [BACK]
183. MERTEN GJ, BURGESS WP, RITTASE RA, KENNEDY
TP. PREVENTION OF CONTRAST-INDUCED
NEPHROPATHY WITH SODIUM BICARBONATE: AN
EVIDENCE-BASED PROTOCOL. CRIT PATHW CARDIOL.
2004;3(3):138-43. [BACK]
184.
 MONTALTO AS, BITTO A, IRRERA N, ET AL. CO2
PNEUMOPERITONEUM IMPACT ON EARLY LIVER AND
LUNG CYTOKINE EXPRESSION IN A RAT MODEL OF
ABDOMINAL SEPSIS. SURG ENDOSC. 2012;26(4):984-9.
[BACK]
185.DE SMET HR, BERSTEN AD, BARR HA, DOYLE IR.
HYPERCAPNIC ACIDOSIS MODULATES INFLAMMATION,
LUNG MECHANICS, AND EDEMA IN THE ISOLATED
PERFUSED LUNG. J CRIT CARE. 2007;22(4):305-13. [BACK]
186.
KIMURA D, TOTAPALLY BR, RASZYNSKI A,
RAMACHANDRAN C, TORBATI D. THE EFFECTS OF CO2
ON CYTOKINE CONCENTRATIONS IN ENDOTOXIN-
STIMULATED HUMAN WHOLE BLOOD. CRIT CARE MED.
2008;36(10):2823-7. [BACK]
187.
GAO W, LIU DD, LI D, CUI GX. EFFECT OF THERAPEUTIC
HYPERCAPNIA ON INFLAMMATORY RESPONSES TO
ONE-LUNG VENTILATION IN LOBECTOMY PATIENTS.
ANESTHESIOLOGY. 2015;122(6):1235-52. [BACK]
188.
COOKER LA, LUNEBURG P, HOLMES CJ, JONES S,
TOPLEY N. INTERLEUKIN-6 LEVELS DECREASE IN
EFFLUENT FROM PATIENTS DIALYZED WITH
BICARBONATE/LACTATE-BASED PERITONEAL DIALYSIS
SOLUTIONS. PERIT DIAL INT. 2001;21 SUPPL 3:S102-7.
[BACK]
189.
TAKESHITA K, SUZUKI Y, NISHIO K, ET AL.
HYPERCAPNIC ACIDOSIS ATTENUATES ENDOTOXIN-
INDUCED NUCLEAR FACTOR-[KAPPA]B ACTIVATION. AM
J RESPIR CELL MOL BIOL. 2003;29(1):124-32. [BACK]
190.
TAWFIK AMIN A, SHIRAISHI N, NINOMIYA S, TAJIMA M,
INOMATA M, KITANO S. ACTIVATION OF NUCLEAR
FACTOR KAPPA B AND INDUCTION OF MIGRATION
INHIBITORY FACTOR IN TUMORS BY SURGICAL STRESS
OF LAPAROTOMY VERSUS CARBON DIOXIDE
PNEUMOPERITONEUM: AN ANIMAL EXPERIMENT. SURG
ENDOSC. 2010;24(3):578-83. [BACK]
191.
MAURER M, RIESEN W, MUSER J, HULTER HN, KRAPF R.
NEUTRALIZATION OF WESTERN DIET INHIBITS BONE
RESORPTION INDEPENDENTLY OF K INTAKE AND
REDUCES CORTISOL SECRETION IN HUMANS. AM J
PHYSIOL RENAL PHYSIOL. 2003;284(1):F32-40. [BACK]
192.
ROJAS VEGA S, STRÜDER HK, WAHRMANN BV, BLOCH
W, HOLLMANN W. BICARBONATE REDUCES SERUM
PROLACTIN INCREASE INDUCED BY EXERCISE TO
EXHAUSTION. MED SCI SPORTS EXERC. 2006;38(4):675-80.
[BACK]
193.
STRÜDER HK, HOLLMANN W, DONIKE M, PLATEN P,
WEBER K. EFFECT OF O2 AVAILABILITY ON
NEUROENDOCRINE VARIABLES AT REST AND DURING
EXERCISE: O2 BREATHING INCREASES PLASMA
PROLACTIN. EUR J APPL PHYSIOL OCCUP PHYSIOL.
1996;74(5):443-9. [BACK]
194.
CAPELLINI VK, RESTINI CB, BENDHACK LM, EVORA PR,
CELOTTO AC. THE EFFECT OF EXTRACELLULAR PH
CHANGES ON INTRACELLULAR PH AND NITRIC OXIDE
CONCENTRATION IN ENDOTHELIAL AND SMOOTH
MUSCLE CELLS FROM RAT AORTA. PLOS ONE.
2013;8(5):E62887. [BACK]
195.
PEDOTO A, CARUSO JE, NANDI J, ET AL. ACIDOSIS
STIMULATES NITRIC OXIDE PRODUCTION AND LUNG
DAMAGE IN RATS. AM J RESPIR CRIT CARE MED.
1999;159(2):397-402. [BACK]
196.
SABATINI S, KURTZMAN NA. BICARBONATE THERAPY
IN SEVERE METABOLIC ACIDOSIS. J AM SOC NEPHROL.
2009;20(4):692-5. [BACK]
197.
MALOV IUS, KULIKOV AN. [BICARBONATE DEFICIENCY
AND DUODENAL PEPTIC ULCER]. TER ARKH.
1998;70(2):28-32. [BACK]
198.
HAYLOR J, TONER JM, JACKSON PR, RAMSAY LE, LOTE
CJ. IS THE URINARY EXCRETION OF PROSTAGLANDIN E
IN MAN DEPENDENT ON URINE PH?. CLIN SCI.
1985;68(4):475-7. [BACK]
199.
PEPELKO WE. THE EFFECT OF CORTISOL UPON
LIPOLYSIS DURING CYPERCAPNIA AND AFTER BETA-
ANDRENERGIC BLOCKADE. ANAT & PHYS PHARMAC.
1971. AVAILABLE: HTTP://OAI.DTIC.MIL/OAI/OAI?
VERB=GETRECORD&METADATAPREFIX=HTML&IDENTI
FIER=AD0731124. [FEBRUARY 15, 2017]. [BACK]
200.
STRIDER JW, MASTERSON CG, DURHAM PL.
TREATMENT OF MAST CELLS WITH CARBON DIOXIDE
SUPPRESSES DEGRANULATION VIA A NOVEL
MECHANISM INVOLVING REPRESSION OF INCREASED
INTRACELLULAR CALCIUM LEVELS. ALLERGY.
2011;66(3):341-50. [BACK]
201.
SOY FK, OZBAY C, KULDUK E, DUNDAR R, YAZICI H,
SAKARYA EU. A NEW APPROACH FOR CERUMENOLYTIC
TREATMENT IN CHILDREN: IN VIVO AND IN VITRO
STUDY. INT J PEDIATR OTORHINOLARYNGOL.
2015;79(7):1096-100. [BACK]
202.
SHARMA AP, SINGH RN, YANG C, SHARMA RK, KAPOOR
R, FILLER G. BICARBONATE THERAPY IMPROVES
GROWTH IN CHILDREN WITH INCOMPLETE DISTAL
RENAL TUBULAR ACIDOSIS. PEDIATR NEPHROL.
2009;24(8):1509-16. [BACK]
203.
HESS B. METABOLIC SYNDROME, OBESITY AND
KIDNEY STONES. ARAB J UROL. 2012;10(3):258-64. [BACK]
204.
CICERELLO E, MERLO F, MACCATROZZO L. URINARY
ALKALIZATION FOR THE TREATMENT OF URIC ACID
NEPHROLITHIASIS. ARCH ITAL UROL ANDROL.
2010;82(3):145-8. [BACK]
205.
VIVIEN P, ALLANNIC H, TURPIN J, PRUNIER P,
LEBORGNE P, LOUSSOUARN J. [A CASE OF VOLUMINOUS
CYSTINE LITHIASIS CURED WITH HIGH DOSES OF
SODIUM BICARBONATE]. THERAPIE. 1971;26(1):121-7.
[BACK]
206.
STIGLIANI M, MANNIELLO MD, ZEGARRA-MORAN O, ET
AL. RHEOLOGICAL PROPERTIES OF CYSTIC FIBROSIS
BRONCHIAL SECRETION AND IN VITRO DRUG
PERMEATION STUDY: THE EFFECT OF SODIUM
BICARBONATE. J AEROSOL MED PULM DRUG DELIV.
2016;29(4):337-45. [BACK]
207.
PIÑERO-ZAPATA M, CINESI-GÓMEZ C, LUNA-
MALDONADO A. [MORTALITY IN PATIENTS WITH ACUTE
RESPIRATORY FAILURE ON CHRONIC TREATMENT WITH
BENZODIAZEPINES]. ENFERM CLIN. 2013;23(3):89-95.
[BACK]
208.
NATIONAL SCIENCE FOUNDATION. (2004). "IMPACT OF
EARTH'S RISING ATMOSPHERIC CARBON DIOXIDE
FOUND IN WORLD OCEANS." SCIENCEDAILY.
[ONLINE].AVAILABLE:
 WWW.SCIENCEDAILY.COM/RELEASES/2004/07/0407190928
07.HTM.[APRIL 2,2017]. [BACK]
209.
POBEREZHSKAYA M. MEDIA COVERAGE OF CLIMATE
CHANGE IN RUSSIA: GOVERNMENTAL BIAS AND
CLIMATE SCIENCE. PUBLIC UNDERSTANDING OF
SCIENCE. 2014;24(1). [BACK]
210.SHAPIRO JM. SPECIAL INTERESTS AND THE MEDIA:
THEORY AND AN APPLICATION TO CLIMATE CHANGE. J.
PUBLIC ECON. 2016;144:91-108. [BACK]
211.
ABDO WF, HEUNKS LM. OXYGEN-INDUCED
HYPERCAPNIA IN COPD: MYTHS AND FACTS. CRIT CARE.
2012;16(5):323. [BACK]

Unravelling The Mysteries of Cancer

1. CANADIAN CANCER SOCIETY. WHAT IS CANCER?
[ONLINE]. AVAILABLE:
HTTPS://WWW.CANCER.GOV/ABOUT-
CANCER/UNDERSTANDING/WHAT-IS-CANCER. [MARCH
1ST, 2017]. [BACK]

2. SHAY JW, WERBIN H. CYTOPLASMIC SUPPRESSION OF

TUMORIGENICITY IN RECONSTRUCTED MOUSE CELLS.
CANCER RES. 1988;48(4):830-3. [BACK]

3. ISRAEL BA, SCHAEFFER WI. CYTOPLASMIC

SUPPRESSION OF MALIGNANCY. IN VITRO CELL DEV
BIOL. 1987;23(9):627-32. [BACK]
4. HOWELL AN, SAGER R. TUMORIGENICITY AND ITS
SUPPRESSION IN CYBRIDS OF MOUSE AND CHINESE
HAMSTER CELL LINES. PROC NATL ACAD SCI USA.
1978;75(5):2358-62. [BACK]
5. SHAY JW, LIU YN, WERBIN H. CYTOPLASMIC
SUPPRESSION OF TUMOR PROGRESSION IN
RECONSTITUTED CELLS. SOMAT CELL MOL GENET.
1988;14(4):345-50. [BACK]
6. GIGUÈRE L, MORAIS R. ON SUPPRESSION OF
TUMORIGENICITY IN HYBRID AND CYBRID MOUSE
CELLS. SOMATIC CELL GENET. 1981;7(4):457-71. [BACK]
7. KOURA M, ISAKA H, YOSHIDA MC, TOSU M, SEKIGUCHI
T. SUPPRESSION OF TUMORIGENICITY IN INTERSPECIFIC
RECONSTITUTED CELLS AND CYBRIDS. GAN.
1982;73(4):574-80. [BACK]
8. SHAY JW, LORKOWSKI G, CLARK MA. SUPPRESSION OF
TUMORIGENICITY IN CYBRIDS. J SUPRAMOL STRUCT
CELL BIOCHEM. 1981;16(1):75-82. [BACK]
9. ISRAEL BA, SCHAEFFER WI. CYTOPLASMIC MEDIATION
OF MALIGNANCY. IN VITRO CELL DEV BIOL.
1988;24(5):487-90. [BACK]
10. MCKINNELL RG, DEGGINS BA, LABAT DD.
TRANSPLANTATION OF PLURIPOTENTIAL NUCLEI FROM
TRIPLOID FROG TUMORS. SCIENCE. 1969;165(3891):394-6.
[BACK]
11. LI L, CONNELLY MC, WETMORE C, CURRAN T, MORGAN
JI. MOUSE EMBRYOS CLONED FROM BRAIN TUMORS.
CANCER RES. 2003;63(11):2733-6. [BACK]
12. RUBIN H. WHAT KEEPS CELLS IN TISSUES BEHAVING
NORMALLY IN THE FACE OF MYRIAD MUTATIONS?.
BIOESSAYS. 2006;28(5):515-24. [BACK]
13. NIKOLAOU N, GREEN CJ, GUNN PJ, HODSON L,
TOMLINSON JW. OPTIMIZING HUMAN HEPATOCYTE
MODELS FOR METABOLIC PHENOTYPE AND FUNCTION:
EFFECTS OF TREATMENT WITH DIMETHYL SULFOXIDE
(DMSO). PHYSIOL REP. 2016;4(21). [BACK]
14. WEAVER
VM, PETERSEN OW, WANG F, ET AL.
REVERSION OF THE MALIGNANT PHENOTYPE OF
HUMAN BREAST CELLS IN THREE-DIMENSIONAL
CULTURE AND IN VIVO BY INTEGRIN BLOCKING
ANTIBODIES. J CELL BIOL. 1997;137(1):231-45. [BACK]
15. BRINSTER
RL. THE EFFECT OF CELLS TRANSFERRED
INTO THE MOUSE BLASTOCYST ON SUBSEQUENT
DEVELOPMENT. J EXP MED. 1974;140(4):1049-56. [BACK]
16. MINTZB, ILLMENSEE K. NORMAL GENETICALLY
MOSAIC MICE PRODUCED FROM MALIGNANT
TERATOCARCINOMA CELLS. PROC NATL ACAD SCI USA.
1975;72(9):3585-9. [BACK]
17. MILO
GE, SHULER CF, LEE H, CASTO BC. A CONUNDRUM
IN MOLECULAR TOXICOLOGY: MOLECULAR AND
BIOLOGICAL CHANGES DURING NEOPLASTIC
TRANSFORMATION OF HUMAN CELLS. CELL BIOL
TOXICOL. 1995;11(6):329-45. [BACK]
18. ROUS
P. SURMISE AND FACT ON THE NATURE OF
CANCER. NATURE. 1959;183(4672):1357-61. [BACK]
19. TOMCZAK K, CZERWIŃSKA P, WIZNEROWICZ M. THE
CANCER GENOME ATLAS (TCGA): AN IMMEASURABLE
SOURCE OF KNOWLEDGE. CONTEMP ONCOL (POZN).
2015;19(1A):A68-77. [BACK]
20. KAISERJ. GENOMICS. BILLION-DOLLAR CANCER
MAPPING PROJECT STEPS FORWARD. SCIENCE.
2008;321(5885):26-7. [BACK]
21. POETHIG RS. LIFE WITH 25,000 GENES. GENOME RES.
2001;11(3):313-6. [BACK]
22. LEE
JS. EXPLORING CANCER GENOMIC DATA FROM THE
CANCER GENOME ATLAS PROJECT. BMB REP.
2016;49(11):607-611. [BACK]
23. GREENMANC, STEPHENS P, SMITH R, ET AL. PATTERNS
OF SOMATIC MUTATION IN HUMAN CANCER GENOMES.
 NATURE. 2007;446(7132):153-8. [BACK]
24. LOEBLA. A MUTATOR PHENOTYPE IN CANCER. CANCER
RES. 2001;61(8):3230-9. [BACK]
25. PARSONS DW, JONES S, ZHANG X, ET AL. AN
INTEGRATED GENOMIC ANALYSIS OF HUMAN
GLIOBLASTOMA MULTIFORME. SCIENCE.
2008;321(5897):1807-12. [BACK]
26. SALK
JJ, FOX EJ, LOEB LA. MUTATIONAL
HETEROGENEITY IN HUMAN CANCERS: ORIGIN AND
CONSEQUENCES. ANNU REV PATHOL. 2010;5:51-75.
[BACK]
27. GIBBS
WW. UNTANGLING THE ROOTS OF CANCER. SCI
AM. 2003;289(1):56-65. [BACK]
28. STEEG
PS. HETEROGENEITY OF DRUG TARGET
EXPRESSION AMONG METASTATIC LESIONS: LESSONS
FROM A BREAST CANCER AUTOPSY PROGRAM. CLIN
CANCER RES. 2008;14(12):3643-5. [BACK]
29. WU
JM, FACKLER MJ, HALUSHKA MK, ET AL.
HETEROGENEITY OF BREAST CANCER METASTASES:
COMPARISON OF THERAPEUTIC TARGET EXPRESSION
AND PROMOTER METHYLATION BETWEEN PRIMARY
TUMORS AND THEIR MULTIFOCAL METASTASES. CLIN
CANCER RES. 2008;14(7):1938-46. [BACK]
30. GABORMIKLOS GL. THE HUMAN CANCER GENOME
PROJECT--ONE MORE MISSTEP IN THE WAR ON CANCER.
NAT BIOTECHNOL. 2005;23(5):535-7. [BACK]
31. STOECKLEIN NH, HOSCH SB, BEZLER M, ET AL. DIRECT
GENETIC ANALYSIS OF SINGLE DISSEMINATED CANCER
CELLS FOR PREDICTION OF OUTCOME AND THERAPY
SELECTION IN ESOPHAGEAL CANCER. CANCER CELL.
2008;13(5):441-53. [BACK]
32. THE
PATTERNS AND DYNAMICS OF GENOMIC
INSTABILITY IN METASTATIC PANCREATIC CANCER.
 NATURE. 2010;467(7319):1109. [BACK]
33. SEYFRIEDTN, SHELTON LM. CANCER AS A METABOLIC
DISEASE. NUTR METAB (LOND). 2010;7:7. [BACK]
34. THE
CANCER GENOME. NATURE. 2009;458(7239):719.
[BACK]
35. MANDINOVA A,
LEE SW. THE P53 PATHWAY AS A TARGET
IN CANCER THERAPEUTICS: OBSTACLES AND PROMISE.
SCI TRANSL MED. 2011;3(64):64RV1. [BACK]
36. GRAVENDEEL LA,KOUWENHOVEN MC, GEVAERT O, ET
AL. INTRINSIC GENE EXPRESSION PROFILES OF
GLIOMAS ARE A BETTER PREDICTOR OF SURVIVAL
THAN HISTOLOGY. CANCER RES. 2009;69(23):9065-72.
[BACK]
37. DANG
L, WHITE DW, GROSS S, ET AL. CANCER-
ASSOCIATED IDH1 MUTATIONS PRODUCE 2-
HYDROXYGLUTARATE. NATURE. 2009;462(7274):739-44.
[BACK]
38. AGUS,
D. [TED]. (2010). DAVID AGUS: A NEW STRATEGY
IN THE WAR AGAINST CANCER. AVAILABLE:
HTTPS://WWW.YOUTUBE.COM/WATCH?
V=IRXGDMSP9GS.[MARCH 1, 2017]. [BACK]
39. BEGLEY,
S. (2013). DNA PIONEER JAMES WATSON TAKES
AIM AT “CANCER ESTABLISHMENTS”. [ONLINE].
AVAILABLE: HTTP://WWW.REUTERS.COM/ARTICLE/US-
USA-CANCER-WATSON-IDUSBRE90805N20130109.
[MARCH 1, 2017]. [BACK]
40. LUOTO
KR, KUMARESWARAN R, BRISTOW RG. TUMOR
HYPOXIA AS A DRIVING FORCE IN GENETIC
INSTABILITY. GENOME INTEGR. 2013;4(1):5. [BACK]
41. KUMARESWARAN R, LUDKOVSKI O, MENG A, SYKES J,
PINTILIE M, BRISTOW RG. CHRONIC HYPOXIA
COMPROMISES REPAIR OF DNA DOUBLE-STRAND
 BREAKS TO DRIVE GENETIC INSTABILITY. J CELL SCI.
2012;125(PT 1):189-99. [BACK]
42. TAIAKINA D,
DAL PRA A, BRISTOW RG. INTRATUMORAL
HYPOXIA AS THE GENESIS OF GENETIC INSTABILITY
AND CLINICAL PROGNOSIS IN PROSTATE CANCER. ADV
EXP MED BIOL. 2014;772:189-204. [BACK]
43. SCANLON SE, GLAZER PM. MULTIFACETED CONTROL OF
DNA REPAIR PATHWAYS BY THE HYPOXIC TUMOR
MICROENVIRONMENT. DNA REPAIR (AMST). 2015;32:180-
9. [BACK]
44. CHAN
N, KOCH CJ, BRISTOW RG. TUMOR HYPOXIA AS A
MODIFIER OF DNA STRAND BREAK AND CROSS-LINK
REPAIR. CURR MOL MED. 2009;9(4):401-10. [BACK]
45. CHAN N, ALI M, MCCALLUM GP, ET AL. HYPOXIA
PROVOKES BASE EXCISION REPAIR CHANGES AND A
REPAIR-DEFICIENT, MUTATOR PHENOTYPE IN
COLORECTAL CANCER CELLS. MOL CANCER RES.
2014;12(10):1407-15. [BACK]
46. MENG AX,
JALALI F, CUDDIHY A, ET AL. HYPOXIA
DOWN-REGULATES DNA DOUBLE STRAND BREAK
REPAIR GENE EXPRESSION IN PROSTATE CANCER
CELLS. RADIOTHER ONCOL. 2005;76(2):168-76. [BACK]
47. BRISTOW
RG, HILL RP. HYPOXIA AND METABOLISM.
HYPOXIA, DNA REPAIR AND GENETIC INSTABILITY. NAT
REV CANCER. 2008;8(3):180-92. [BACK]
48. CHANN, BRISTOW RG. "CONTEXTUAL" SYNTHETIC
LETHALITY AND/OR LOSS OF HETEROZYGOSITY:
TUMOR HYPOXIA AND MODIFICATION OF DNA REPAIR.
CLIN CANCER RES. 2010;16(18):4553-60. [BACK]
49. BINDRA RS,
CROSBY ME, GLAZER PM. REGULATION OF
DNA REPAIR IN HYPOXIC CANCER CELLS. CANCER
METASTASIS REV. 2007;26(2):249-60. [BACK]
50. BINDRA RS,
SCHAFFER PJ, MENG A, ET AL. DOWN-
REGULATION OF RAD51 AND DECREASED
HOMOLOGOUS RECOMBINATION IN HYPOXIC CANCER
CELLS. MOL CELL BIOL. 2004;24(19):8504-18. [BACK]
51. BINDRA RS,SCHAFFER PJ, MENG A, ET AL. ALTERATIONS
IN DNA REPAIR GENE EXPRESSION UNDER HYPOXIA:
ELUCIDATING THE MECHANISMS OF HYPOXIA-
INDUCED GENETIC INSTABILITY. ANN N Y ACAD SCI.
2005;1059:184-95. [BACK]
52. CHAN N, PIRES IM, BENCOKOVA Z, ET AL. CONTEXTUAL
SYNTHETIC LETHALITY OF CANCER CELL KILL BASED
ON THE TUMOR MICROENVIRONMENT. CANCER RES.
2010;70(20):8045-54. [BACK]
53. CHAN N, MILOSEVIC M, BRISTOW RG. TUMOR HYPOXIA,
DNA REPAIR AND PROSTATE CANCER PROGRESSION:
NEW TARGETS AND NEW THERAPIES. FUTURE ONCOL.
2007;3(3):329-41. [BACK]
54. BINDRA RS,
GLAZER PM. GENETIC INSTABILITY AND
THE TUMOR MICROENVIRONMENT: TOWARDS THE
CONCEPT OF MICROENVIRONMENT-INDUCED
MUTAGENESIS. MUTAT RES. 2005;569(1-2):75-85. [BACK]
55. WIGERUP C,
PÅHLMAN S, BEXELL D. THERAPEUTIC
TARGETING OF HYPOXIA AND HYPOXIA-INDUCIBLE
FACTORS IN CANCER. PHARMACOL THER. 2016;164:152-
69. [BACK]
56. GLAZER PM, HEGAN DC, LU Y, CZOCHOR J, SCANLON SE.
HYPOXIA AND DNA REPAIR. YALE J BIOL MED.
2013;86(4):443-51. [BACK]
57. YOO YG,HAYASHI M, CHRISTENSEN J, HUANG LE. AN
ESSENTIAL ROLE OF THE HIF-1ALPHA-C-MYC AXIS IN
MALIGNANT PROGRESSION. ANN N Y ACAD SCI.
2009;1177:198-204. [BACK]
58. NOWELL PC.
THE CLONAL EVOLUTION OF TUMOR CELL
POPULATIONS. SCIENCE. 1976;194(4260):23-8. [BACK]
59. KAISER
J. COMBINING TARGETED DRUGS TO STOP
RESISTANT TUMORS. SCIENCE. 2011;331(6024):1542-5.
[BACK]
60. SONNENSCHEIN C, SOTO AM. SOMATIC MUTATION
THEORY OF CARCINOGENESIS: WHY IT SHOULD BE
DROPPED AND REPLACED. MOL CARCINOG.
2000;29(4):205-11. [BACK]
61. RYAN
HE, LO J, JOHNSON RS. HIF-1 ALPHA IS REQUIRED
FOR SOLID TUMOR FORMATION AND EMBRYONIC
VASCULARIZATION. EMBO J. 1998;17(11):3005-15. [BACK]
62. RYANHE, POLONI M, MCNULTY W, ET AL. HYPOXIA-
INDUCIBLE FACTOR-1ALPHA IS A POSITIVE FACTOR IN
SOLID TUMOR GROWTH. CANCER RES. 2000;60(15):4010-
5. [BACK]
63. ACKERT, PLATE KH. A ROLE FOR HYPOXIA AND
HYPOXIA-INDUCIBLE TRANSCRIPTION FACTORS IN
TUMOR PHYSIOLOGY. J MOL MED. 2002;80(9):562-75.
[BACK]
64. HARRIS AL.
HYPOXIA--A KEY REGULATORY FACTOR IN
TUMOUR GROWTH. NAT REV CANCER. 2002;2(1):38-47.
[BACK]
65. PULLAMSETTISS, BANAT GA, SCHMALL A, ET AL.
PHOSPHODIESTERASE-4 PROMOTES PROLIFERATION
AND ANGIOGENESIS OF LUNG CANCER BY CROSSTALK
WITH HIF. ONCOGENE. 2013;32(9):1121-34. [BACK]
66. THIENPONTB, STEINBACHER J, ZHAO H, ET AL.
TUMOUR HYPOXIA CAUSES DNA HYPERMETHYLATION
BY REDUCING TET ACTIVITY. NATURE. 2016;537(7618):63-
68. [BACK]
67. DAYAN
F, MAZURE NM, BRAHIMI-HORN MC,
POUYSSÉGUR J. A DIALOGUE BETWEEN THE HYPOXIA-
 INDUCIBLE FACTOR AND THE TUMOR
MICROENVIRONMENT. CANCER MICROENVIRON.
2008;1(1):53-68. [BACK]
68. AYYASAMY V, OWENS KM, DESOUKI MM, ET AL.
CELLULAR MODEL OF WARBURG EFFECT IDENTIFIES
TUMOR PROMOTING FUNCTION OF UCP2 IN BREAST
CANCER AND ITS SUPPRESSION BY GENIPIN. PLOS ONE.
2011;6(9):E24792. [BACK]
69. SEOANE
M, MOSQUERA-MIGUEL A, GONZALEZ T, FRAGA
M, SALAS A, COSTOYA JA. THE MITOCHONDRIAL
GENOME IS A "GENETIC SANCTUARY" DURING THE
ONCOGENIC PROCESS. PLOS ONE. 2011;6(8):E23327.
[BACK]
70. THE
METABOLISM OF TUMORS. JAMA OTOLARYNGOL
HEAD NECK SURG. 2015;141(5):428. [BACK]
71. ROSKELLEY RC, MAYER N, HORWITT BN, SALTER WT.
STUDIES IN CANCER. VII. ENZYME DEFICIENCY IN
HUMAN AND EXPERIMENTAL CANCER. J CLIN INVEST.
1943;22(5):743-51. [BACK]
72. BRIZEL DM,
SCULLY SP, HARRELSON JM, ET AL. TUMOR
OXYGENATION PREDICTS FOR THE LIKELIHOOD OF
DISTANT METASTASES IN HUMAN SOFT TISSUE
SARCOMA. CANCER RES. 1996;56(5):941-3. [BACK]
73. KUNZ
M, IBRAHIM SM. MOLECULAR RESPONSES TO
HYPOXIA IN TUMOR CELLS. MOL CANCER. 2003;2:23.
[BACK]
74. DE
JAEGER K, KAVANAGH MC, HILL RP. RELATIONSHIP
OF HYPOXIA TO METASTATIC ABILITY IN RODENT
TUMOURS. BR J CANCER. 2001;84(9):1280-5. [BACK]
75. DENKO NC, FONTANA LA, HUDSON KM, ET AL.
INVESTIGATING HYPOXIC TUMOR PHYSIOLOGY
THROUGH GENE EXPRESSION PATTERNS. ONCOGENE.
2003;22(37):5907-14. [BACK]
76. SEMENZA GL. HYPOXIA-INDUCIBLE FACTORS:
MEDIATORS OF CANCER PROGRESSION AND TARGETS
FOR CANCER THERAPY. TRENDS PHARMACOL SCI.
2012;33(4):207-14. [BACK]
77. BURROUGHS SK, KALUZ S, WANG D, WANG K, VAN MEIR
EG, WANG B. HYPOXIA INDUCIBLE FACTOR PATHWAY
INHIBITORS AS ANTICANCER THERAPEUTICS. FUTURE
MED CHEM. 2013;5(5):553-72. [BACK]
78. ONNISB, RAPISARDA A, MELILLO G. DEVELOPMENT OF
HIF-1 INHIBITORS FOR CANCER THERAPY. J CELL MOL
MED. 2009;13(9A):2780-6. [BACK]
79. XIA Y,
CHOI HK, LEE K. RECENT ADVANCES IN HYPOXIA-
INDUCIBLE FACTOR (HIF)-1 INHIBITORS. EUR J MED
CHEM. 2012;49:24-40. [BACK]
80. MELILLO G. INHIBITING HYPOXIA-INDUCIBLE FACTOR 1
FOR CANCER THERAPY. MOL CANCER RES. 2006;4(9):601-
5. [BACK]
81. MARÍN-HERNÁNDEZ A, GALLARDO-PÉREZ JC, RALPH SJ,
RODRÍGUEZ-ENRÍQUEZ S, MORENO-SÁNCHEZ R. HIF-
1ALPHA MODULATES ENERGY METABOLISM IN CANCER
CELLS BY INDUCING OVER-EXPRESSION OF SPECIFIC
GLYCOLYTIC ISOFORMS. MINI REV MED CHEM.
2009;9(9):1084-101. [BACK]
82. PORPORATO PE, DHUP S, DADHICH RK, COPETTI T,
SONVEAUX P. ANTICANCER TARGETS IN THE
GLYCOLYTIC METABOLISM OF TUMORS: A
COMPREHENSIVE REVIEW. FRONT PHARMACOL.
2011;2:49. [BACK]
83. GUZY RD,
SCHUMACKER PT. OXYGEN SENSING BY
MITOCHONDRIA AT COMPLEX III: THE PARADOX OF
INCREASED REACTIVE OXYGEN SPECIES DURING
HYPOXIA. EXP PHYSIOL. 2006;91(5):807-19. [BACK]
84. FAVIERJ, BRIÈRE JJ, BURNICHON N, ET AL. THE
WARBURG EFFECT IS GENETICALLY DETERMINED IN
INHERITED PHEOCHROMOCYTOMAS. PLOS ONE.
2009;4(9):E7094. [BACK]
85. SEMENZA GL.
HIF-1 MEDIATES THE WARBURG EFFECT
IN CLEAR CELL RENAL CARCINOMA. J BIOENERG
BIOMEMBR. 2007;39(3):231-4. [BACK]
86. DANG
CV, SEMENZA GL. ONCOGENIC ALTERATIONS OF
METABOLISM. TRENDS BIOCHEM SCI. 1999;24(2):68-72.
[BACK]
87. DENKO NC. HYPOXIA, HIF1 AND GLUCOSE METABOLISM
IN THE SOLID TUMOUR. NAT REV CANCER. 2008;8(9):705-
13. [BACK]
88. VANDER
HEIDEN MG, CANTLEY LC, THOMPSON CB.
UNDERSTANDING THE WARBURG EFFECT: THE
METABOLIC REQUIREMENTS OF CELL PROLIFERATION.
SCIENCE. 2009;324(5930):1029-33. [BACK]
89. SEMENZA GL.
OXYGEN-DEPENDENT REGULATION OF
MITOCHONDRIAL RESPIRATION BY HYPOXIA-
INDUCIBLE FACTOR 1. BIOCHEM J. 2007;405(1):1-9.
[BACK]
90. FANGJ, YAN L, SHING Y, MOSES MA. HIF-1ALPHA-
MEDIATED UP-REGULATION OF VASCULAR
ENDOTHELIAL GROWTH FACTOR, INDEPENDENT OF
BASIC FIBROBLAST GROWTH FACTOR, IS IMPORTANT IN
THE SWITCH TO THE ANGIOGENIC PHENOTYPE DURING
EARLY TUMORIGENESIS. CANCER RES. 2001;61(15):5731-
5. [BACK]
91. TSUZUKI Y,
FUKUMURA D, OOSTHUYSE B, KOIKE C,
CARMELIET P, JAIN RK. VASCULAR ENDOTHELIAL
GROWTH FACTOR (VEGF) MODULATION BY TARGETING
HYPOXIA-INDUCIBLE FACTOR-1ALPHA--> HYPOXIA
RESPONSE ELEMENT--> VEGF CASCADE
DIFFERENTIALLY REGULATES VASCULAR RESPONSE
 AND GROWTH RATE IN TUMORS. CANCER RES.
2000;60(22):6248-52. [BACK]
92. MAZURENM, BRAHIMI-HORN MC, POUYSSÉGUR J.
PROTEIN KINASES AND THE HYPOXIA-INDUCIBLE
FACTOR-1, TWO SWITCHES IN ANGIOGENESIS. CURR
PHARM DES. 2003;9(7):531-41. [BACK]
93. VANDENBUNDER B. [HYPOXIA AND TUMORS: DOES HIF-
1 TRANSCRIPTION FACTOR FAVOR TUMOR GROWTH OR
HYPOXIA?]. BULL CANCER. 1998;85(10):843-5. [BACK]
94. BÜCHLER P, REBER HA, BÜCHLER M, ET AL. HYPOXIA-
INDUCIBLE FACTOR 1 REGULATES VASCULAR
ENDOTHELIAL GROWTH FACTOR EXPRESSION IN
HUMAN PANCREATIC CANCER. PANCREAS. 2003;26(1):56-
64. [BACK]
95. CHOIKS, BAE MK, JEONG JW, MOON HE, KIM KW.
HYPOXIA-INDUCED ANGIOGENESIS DURING
CARCINOGENESIS. J BIOCHEM MOL BIOL. 2003;36(1):120-
7. [BACK]
96. FRANCIS,
R. 2011. NEVER FEAR CANCER AGAIN: HOW TO
PREVENT AND REVERSE CANCER. HCI. 384PS. [BACK]
97. BIANCONI
E, PIOVESAN A, FACCHIN F, ET AL. AN
ESTIMATION OF THE NUMBER OF CELLS IN THE HUMAN
BODY. ANN HUM BIOL. 2013;40(6):463-71. [BACK]
98. JANG
M, KIM SS, LEE J. CANCER CELL METABOLISM:
IMPLICATIONS FOR THERAPEUTIC TARGETS. EXP MOL
MED. 2013;45:E45. [BACK]
99. JURTSHUK,P JR. 1996. MEDICAL MICROBIOLOGY: 4TH
EDITION. THE UNIVERSITY OF TEXAS MEDICAL
BRANCH AT GALVESTON. [BACK]
100.
ZHENG J. ENERGY METABOLISM OF CANCER:
GLYCOLYSIS VERSUS OXIDATIVE PHOSPHORYLATION
(REVIEW). ONCOL LETT. 2012;4(6):1151-1157. [BACK]
 101.
ROGATZKI MJ, FERGUSON BS, GOODWIN ML, GLADDEN
LB. LACTATE IS ALWAYS THE END PRODUCT OF
GLYCOLYSIS. FRONT NEUROSCI. 2015;9:22. [BACK]
102.
CARPENTER KLH, JALLOH I, HUTCHINSON JP.
GLYCOLYSIS AND THE SIGNIFICANT OF LACTATE IN
TRAUMATIC BRAIN INJURY. FRONT. NEURO. 2015.
[BACK]
103.
SAHLIN K, KATZ A, HENRIKSSON J. REDOX STATE AND
LACTATE ACCUMULATION IN HUMAN SKELETAL
MUSCLE DURING DYNAMIC EXERCISE. BIOCHEM J.
1987;245(2):551-6. [BACK]
104. KATZ A, SAHLIN K. REGULATION OF LACTIC ACID
PRODUCTION DURING EXERCISE. J APPL PHYSIOL.
1988;65(2):509-18. [BACK]
105. SAHLIN K. MUSCLE ENERGETICS DURING
EXPLOSIVE ACTIVITIES AND POTENTIAL EFFECTS OF
NUTRITION AND TRAINING. SPORTS MED. 2014;44 SUPPL
2:S167-73. [BACK]
106. ISHII H, NISHIDA Y. EFFECT OF LACTATE
ACCUMULATION DURING EXERCISE-INDUCED MUSCLE
FATIGUE ON THE SENSORIMOTOR CORTEX. J PHYS THER
SCI. 2013;25(12):1637-42. [BACK]
107. GHOSH AK. ANAEROBIC THRESHOLD: ITS CONCEPT
AND ROLE IN ENDURANCE SPORT. MALAYS J MED SCI.
2004;11(1):24-36. [BACK]
108.FAUDE O, KINDERMANN W, MEYER T. LACTATE
THRESHOLD CONCEPTS: HOW VALID ARE THEY?.
SPORTS MED. 2009;39(6):469-90. [BACK]
109.
WARBURG O. UBER DEN STOFFWECHSEL DER
HEFE.PP252-254. [BACK]
 110.
ALBERTS B, JOHNSON A, LEWIS J, ET AL. 2002.
MOLECULAR BIOLOGY OF THE CELL: 4TH EDITION.
NEW YORK. GARLAND SCIENCE. [BACK]
111.
ARCHETTI M. EVOLUTIONARY DYNAMICS OF THE
WARBURG EFFECT: GLYCOLYSIS AS A COLLECTIVE
ACTION PROBLEM AMONG CANCER CELLS. J THEOR
BIOL. 2014;341:1-8. [BACK]
112. PHAN LM, YEUNG SC, LEE MH. CANCER
METABOLIC REPROGRAMMING: IMPORTANCE, MAIN
FEATURES, AND POTENTIALS FOR PRECISE TARGETED
ANTI-CANCER THERAPIES. CANCER BIOL MED.
2014;11(1):1-19. [BACK]
113.CHEN X, QIAN Y, WU S. THE WARBURG EFFECT:
EVOLVING INTERPRETATIONS OF AN ESTABLISHED
CONCEPT. FREE RADIC BIOL MED. 2015;79:253-63. [BACK]
114. GANAPATHY-KANNIAPPAN S, GESCHWIND JF.
TUMOR GLYCOLYSIS AS A TARGET FOR CANCER
THERAPY: PROGRESS AND PROSPECTS. MOL CANCER.
2013;12:152. [BACK]
115. GATENBY RA, GILLIES RJ. WHY DO CANCERS HAVE
HIGH AEROBIC GLYCOLYSIS?. NAT REV CANCER.
2004;4(11):891-9. [BACK]
116.GATENBY RA, GAWLINSKI ET. THE GLYCOLYTIC
PHENOTYPE IN CARCINOGENESIS AND TUMOR
INVASION: INSIGHTS THROUGH MATHEMATICAL
MODELS. CANCER RES. 2003;63(14):3847-54. [BACK]
117. LINCET H, ICARD P. HOW DO GLYCOLYTIC
ENZYMES FAVOUR CANCER CELL PROLIFERATION BY
NONMETABOLIC FUNCTIONS?. ONCOGENE.
2015;34(29):3751-9. [BACK]
118.MASSON N, RATCLIFFE PJ. HYPOXIA SIGNALING
PATHWAYS IN CANCER METABOLISM: THE IMPORTANCE
OF CO-SELECTING INTERCONNECTED PHYSIOLOGICAL
PATHWAYS. CANCER METAB. 2014;2(1):3. [BACK]
119. POLIAKOV E, MANAGADZE D, ROGOZIN IB.
GENERALIZED PORTRAIT OF CANCER METABOLIC
PATHWAYS INFERRED FROM A LIST OF GENES
OVEREXPRESSED IN CANCER. GENET RES INT.
2014;2014:646193. [BACK]
120.
LIPID METABOLIC REPROGRAMMING IN CANCER
CELLS. ONCOGENESIS. 2016;5(1):E189. [BACK]
121. DART A. TUMOUR METABOLISM: LACTIC ACID:
NOT JUST A WASTE PRODUCT?. NAT REV CANCER.
2016;16(11):676-677. [BACK]
ANNIBALDI A, WIDMANN C. GLUCOSE
122.
METABOLISM IN CANCER CELLS. CURR OPIN CLIN
NUTR METAB CARE. 2010;13(4):466-70. [BACK]
123.CANTOR JR, SABATINI DM. CANCER CELL
METABOLISM: ONE HALLMARK, MANY FACES. CANCER
DISCOV. 2012;2(10):881-98. [BACK]
124. WARD PS, THOMPSON CB. METABOLIC
REPROGRAMMING: A CANCER HALLMARK EVEN
WARBURG DID NOT ANTICIPATE. CANCER CELL.
2012;21(3):297-308. [BACK]
125. PHAN LM, YEUNG SC, LEE MH. CANCER
METABOLIC REPROGRAMMING: IMPORTANCE, MAIN
FEATURES, AND POTENTIALS FOR PRECISE TARGETED
ANTI-CANCER THERAPIES. CANCER BIOL MED.
2014;11(1):1-19. [BACK]
126.
FISCHER K, HOFFMANN P, VOELKL S, ET AL.
INHIBITORY EFFECT OF TUMOR CELL-DERIVED LACTIC
ACID ON HUMAN T CELLS. BLOOD. 2007;109(9):3812-9.
[BACK]
127.
 MOTHERSILL C, SEYMOUR CB, MORIARTY M. LACTATE-
MEDIATED CHANGES IN GROWTH MORPHOLOGY AND
TRANSFORMATION FREQUENCY OF IRRADIATED C3H
10T1/2 CELLS. CELL BIOL INT REP. 1983;7(11):971-80.
[BACK]
128.
SAN-MILLÁN I, BROOKS GA. REEXAMINING CANCER
METABOLISM: LACTATE PRODUCTION FOR
CARCINOGENESIS COULD BE THE PURPOSE AND
EXPLANATION OF THE WARBURG EFFECT.
CARCINOGENESIS. 2016. [BACK]
129.
OLSSON M, HO HP, ANNERBRINK K, THYLEFORS J,
ERIKSSON E. RESPIRATORY RESPONSES TO
INTRAVENOUS INFUSION OF SODIUM LACTATE IN MALE
AND FEMALE WISTAR RATS.
NEUROPSYCHOPHARMACOLOGY. 2002;27(1):85-91.
[BACK]
130.LIEBOWITZ MR, GORMAN JM, FYER AJ, ET AL.
LACTATE PROVOCATION OF PANIC ATTACKS. II.
BIOCHEMICAL AND PHYSIOLOGICAL FINDINGS. ARCH
GEN PSYCHIATRY. 1985;42(7):709-19. [BACK]
131.GORMAN JM, COHEN BS, LIEBOWITZ MR, FYER AJ,
ROSS D, DAVIES SO, KLEIN DF. BLOOD GAS CHANGES
AND HYPOPHOSPHATEMIA IN LACTATE-INDUCED
PANIC. ARCH GEN PSYCHIATRY. 1986;43(11):1067-1071.
[BACK]
132.JACK M. GORMAN, RAYMOND R. GOETZ, JUDY UY,
DONALD ROSS, JOSE MARTINEZ, ABBY J. FYER,
MICHAEL R. LIEBOWITZ, DONALD F. KLEIN.
HYPERVENTILATION OCCURS DURING LACTATE-
INDUCED PANIC. JOURNAL OF ANXIETY DISORDERS,
VOLUME 2, ISSUE 3, PAGES 193-202. [BACK]
133.
 RAICHLE ME, PLUM F. HYPERVENTILATION AND
CEREBRAL BLOOD FLOW. STROKE. 1972;3(5):566-75.
[BACK]
134. NASCHITZ JE, MUSSAFIA-PRISELAC R, PECK ER, ET
AL. HYPERVENTILATION AND AMPLIFIED BLOOD
PRESSURE RESPONSE: IS THERE A LINK?. J HUM
HYPERTENS. 2005;19(5):381-7. [BACK]
135.HAYASHI K, FUJIKAWA M, SAWA T.
HYPERVENTILATION-INDUCED HYPOCAPNIA CHANGES
THE PATTERN OF ELECTROENCEPHALOGRAPHIC
BICOHERENCE GROWTH DURING SEVOFLURANE
ANAESTHESIA. BR J ANAESTH. 2008;101(5):666-72. [BACK]
136. CHIN LM, LEIGH RJ, HEIGENHAUSER GJ, ROSSITER
HB, PATERSON DH, KOWALCHUK JM.
HYPERVENTILATION-INDUCED HYPOCAPNIC
ALKALOSIS SLOWS THE ADAPTATION OF PULMONARY
O2 UPTAKE DURING THE TRANSITION TO MODERATE-
INTENSITY EXERCISE. J PHYSIOL (LOND). 2007;583(PT
1):351-64. [BACK]
137. MEURET AE, RITZ T. HYPERVENTILATION IN PANIC
DISORDER AND ASTHMA: EMPIRICAL EVIDENCE AND
CLINICAL STRATEGIES. INT J PSYCHOPHYSIOL.
2010;78(1):68-79. [BACK]
138.TER AVEST E, PATIST FM, TER MAATEN JC, NIJSTEN
MW. ELEVATED LACTATE DURING PSYCHOGENIC
HYPERVENTILATION. EMERG MED J. 2011;28(4):269-73.
[BACK]
139.
LEARN BUTEYKO. (2011). LEARN BUTEYKO
PRESENTATION PART 1. AVAILABLE:
HTTPS://WWW.YOUTUBE.COM/WATCH?V=H-
WVOFFGMZS.[MARCH 1, 2017]. [BACK]
140.
 PUYBASSET L, STEWART T, ROUBY JJ, ET AL. INHALED
NITRIC OXIDE REVERSES THE INCREASE IN
PULMONARY VASCULAR RESISTANCE INDUCED BY
PERMISSIVE HYPERCAPNIA IN PATIENTS WITH ACUTE
RESPIRATORY DISTRESS SYNDROME.
ANESTHESIOLOGY. 1994;80(6):1254-67. [BACK]
141.
LAM AM, ARTRU AA. AUTOREGULATION OF CEREBRAL
BLOOD FLOW IN RESPONSE TO ADENOSINE-INDUCED
HYPOTENSION IN DOGS. J NEUROSURG ANESTHESIOL.
1992;4(2):120-7. [BACK]
142.
BUTEYKO KP & SHURGAL SI, FUNCTIONAL
DIAGNOSTIC OF CORONARY DISEASE. IN: SURGICAL
TREATMENT OF THE CORONARY DISEASE (IN RUSSIAN),
MOSCOW, 1965: P. 117-118. [BACK]
143.
SINICHENKO VV, LESCHENKO GY, MELEKHIN VD,
EMOTIONAL-VOLITIONAL TRAINING IN COMPLEX
TREATMENT OF PATIENTS WITH RHEUMATOID
ARTHRITIS (IN RUSSIAN), THERAP ARCH 1990, 62: P. 58-
61. [BACK]
144.
BREATHING RETRAINING CENTER. HISTORY OF THE
BUTEYKO BREATHING TECHNIQUE. [ONLINE].
AVAILABLE:
HTTP://WWW.BREATHINGRETRAININGCENTER.COM/HIS
TORY-OF-BUTEYKO.PHP.[MARCH 1, 2017]. [BACK]
145.
BOWLER SD, GREEN A, MITCHELL CA. BUTEYKO
BREATHING TECHNIQUES IN ASTHMA: A BLINDED
RANDOMISED CONTROLLED TRIAL. MED J AUST.
1998;169(11-12):575-8. [BACK]
146. MCHUGH P, AITCHESON F, DUNCAN B, HOUGHTON
F. BUTEYKO BREATHING TECHNIQUE FOR ASTHMA: AN
EFFECTIVE INTERVENTION. N Z MED J.
2003;116(1187):U710. [BACK]
147.COOPER S, OBORNE J, NEWTON S, ET AL. EFFECT
OF TWO BREATHING EXERCISES (BUTEYKO AND
PRANAYAMA) IN ASTHMA: A RANDOMISED
CONTROLLED TRIAL. THORAX. 2003;58(8):674-9. [BACK]
148.MCHUGH P, DUNCAN B, HOUGHTON F. BUTEYKO
BREATHING TECHNIQUE AND ASTHMA IN CHILDREN: A
CASE SERIES. N Z MED J. 2006;119(1234):U1988. [BACK]
149. COWIE RL, CONLEY DP, UNDERWOOD MF, READER
PG. A RANDOMISED CONTROLLED TRIAL OF THE
BUTEYKO TECHNIQUE AS AN ADJUNCT TO
CONVENTIONAL MANAGEMENT OF ASTHMA. RESPIR
MED. 2008;102(5):726-32. [BACK]
150.HASSAN ZM, RIAD NM, AHMED FH. EFFECT OF
BUTEYKO BREATHING TECHNIQUE ON PATIENTS WITH
BRONCHIAL ASTHMA. 2012;61(4):235-241. [BACK]
151. RAVINDER N, BHADURI SN, AJITA M. A STUDY OF
THE EFFECTS OF BUTEYKO BREATHING TECHNIQUE ON
ASTHMATIC PATIENTS. IND. J. PHYS. & OCC. THER.
2012;6(4):224-228. [BACK]
152. ADELOLA OA, OOSTHUIZEN JC, OOSTHUIVEN JC,
FENTON JE. ROLE OF BUTEYKO BREATHING TECHNIQUE
IN ASTHMATICS WITH NASAL SYMPTOMS. CLIN
OTOLARYNGOL. 2013;38(2):190-1. [BACK]
153.
ALTUKHOV, S. (2009). 150 DISEASES OF DEEP
BREATHING. DOCTOR BUTEYKO’S DISCOVERY
TRILOGY. [ONLINE]. AVAILABLE:
HTTP://WWW.DOCTORBUTEYKODISCOVERYTRILOGY.CO
M/150-DISEASES-OF-DEEP-BREATHING.PHP.[MARCH 1,
2017]. [BACK]
154.
 MATSUMOTO A, ITOH H, ETO Y, ET AL. END-TIDAL CO2
PRESSURE DECREASES DURING EXERCISE IN CARDIAC
PATIENTS: ASSOCIATION WITH SEVERITY OF HEART
FAILURE AND CARDIAC OUTPUT RESERVE. J AM COLL
CARDIOL. 2000;36(1):242-9. [BACK]
155. DIMOPOULOU I, TSINTZAS OK, ALIVIZATOS PA,
TZELEPIS GE. PATTERN OF BREATHING DURING
PROGRESSIVE EXERCISE IN CHRONIC HEART FAILURE.
INT J CARDIOL. 2001;81(2-3):117-21. [BACK]
156. JOHNSON BD, BECK KC, OLSON LJ, ET AL.
VENTILATORY CONSTRAINTS DURING EXERCISE IN
PATIENTS WITH CHRONIC HEART FAILURE. CHEST.
2000;117(2):321-32. [BACK]
157.FANFULLA F, MORTARA A, MAESTRI R, ET AL. THE
DEVELOPMENT OF HYPERVENTILATION IN PATIENTS
WITH CHRONIC HEART FAILURE AND CHEYNE-STROKES
RESPIRATION: A POSSIBLE ROLE OF CHRONIC HYPOXIA.
CHEST. 1998;114(4):1083-90. [BACK]
158. CLARK AL, VOLTERRANI M, SWAN JW, COATS AJ.
THE INCREASED VENTILATORY RESPONSE TO EXERCISE
IN CHRONIC HEART FAILURE: RELATION TO
PULMONARY PATHOLOGY. HEART. 1997;77(2):138-46.
[BACK]
159. BANNING AP, LEWIS NP, NORTHRIDGE DB, ELBORN
JS, HENDERSEN AH. PERFUSION/VENTILATION
MISMATCH DURING EXERCISE IN CHRONIC HEART
FAILURE: AN INVESTIGATION OF CIRCULATORY
DETERMINANTS. BR HEART J. 1995;74(1):27-33. [BACK]
160. CLARK AL, CHUA TP, COATS AJ. ANATOMICAL
DEAD SPACE, VENTILATORY PATTERN, AND EXERCISE
CAPACITY IN CHRONIC HEART FAILURE. BR HEART J.
1995;74(4):377-80. [BACK]
161. BULLER NP, POOLE-WILSON PA. MECHANISM OF
THE INCREASED VENTILATORY RESPONSE TO EXERCISE
IN PATIENTS WITH CHRONIC HEART FAILURE. BR HEART
J. 1990;63(5):281-3. [BACK]
162.ELBORN JS, RILEY M, STANFORD CF, NICHOLLS DP.
THE EFFECTS OF FLOSEQUINAN ON SUBMAXIMAL
EXERCISE IN PATIENTS WITH CHRONIC CARDIAC
FAILURE. BR J CLIN PHARMACOL. 1990;29(5):519-24.
[BACK]
163.
BOTTINI P, DOTTORINI ML, CRISTINA CORDONI M,
CASUCCI G, TANTUCCI C. SLEEP-DISORDERED
BREATHING IN NONOBESE DIABETIC SUBJECTS WITH
AUTONOMIC NEUROPATHY. EUR RESPIR J. 2003;22(4):654-
60. [BACK]
164.TANTUCCI C, BOTTINI P, FIORANI C, ET AL.
CEREBROVASCULAR REACTIVITY AND HYPERCAPNIC
RESPIRATORY DRIVE IN DIABETIC AUTONOMIC
NEUROPATHY. J APPL PHYSIOL. 2001;90(3):889-96. [BACK]
165.MANCINI M, FILIPPELLI M, SEGHIERI G, ET AL.
RESPIRATORY MUSCLE FUNCTION AND HYPOXIC
VENTILATORY CONTROL IN PATIENTS WITH TYPE I
DIABETES. CHEST. 1999;115(6):1553-62. [BACK]
166. TANTUCCI C, SCIONTI L, BOTTINI P, ET AL.
INFLUENCE OF AUTONOMIC NEUROPATHY OF
DIFFERENT SEVERITIES ON THE HYPERCAPNIC DRIVE
TO BREATHING IN DIABETIC PATIENTS. CHEST.
1997;112(1):145-53. [BACK]
167.TANTUCCI C, BOTTINI P, DOTTORINI ML, ET AL.
VENTILATORY RESPONSE TO EXERCISE IN DIABETIC
SUBJECTS WITH AUTONOMIC NEUROPATHY. J APPL
PHYSIOL. 1996;81(5):1978-86. [BACK]
168.
CHALUPA DC, MORROW PE, OBERDÖRSTER G, UTELL
MJ, FRAMPTON MW. ULTRAFINE PARTICLE DEPOSITION
IN SUBJECTS WITH ASTHMA. ENVIRON HEALTH
PERSPECT. 2004;112(8):879-82. [BACK]
169. JOHNSON BD, SCANLON PD, BECK KC.
REGULATION OF VENTILATORY CAPACITY DURING
EXERCISE IN ASTHMATICS. J APPL PHYSIOL.
1995;79(3):892-901. [BACK]
170. KASSABIAN J, MILLER KD, LAVIETES MH.
RESPIRATORY CENTER OUTPUT AND VENTILATORY
TIMING IN PATIENTS WITH ACUTE AIRWAY (ASTHMA)
AND ALVEOLAR (PNEUMONIA) DISEASE. CHEST.
1982;81(5):536-43. [BACK]
171. MCFADDEN ER, LYONS HA. ARTERIAL-BLOOD GAS
TENSION IN ASTHMA. N ENGL J MED. 1968;278(19):1027-
32. [BACK]
172.
PALANGE P, VALLI G, ONORATI P, ET AL. EFFECT OF
HELIOX ON LUNG DYNAMIC HYPERINFLATION,
DYSPNEA, AND EXERCISE ENDURANCE CAPACITY IN
COPD PATIENTS. J APPL PHYSIOL. 2004;97(5):1637-42.
[BACK]
173.SINDERBY C, SPAHIJA J, BECK J, ET AL.
DIAPHRAGM ACTIVATION DURING EXERCISE IN
CHRONIC OBSTRUCTIVE PULMONARY DISEASE. AM J
RESPIR CRIT CARE MED. 2001;163(7):1637-41. [BACK]
174. STULBARG MS, WINN WR, KELLETT LE. BILATERAL
CAROTID BODY RESECTION FOR THE RELIEF OF
DYSPNEA IN SEVERE CHRONIC OBSTRUCTIVE
PULMONARY DISEASE. PHYSIOLOGIC AND CLINICAL
OBSERVATIONS IN THREE PATIENTS. CHEST.
1989;95(5):1123-8. [BACK]
175.
RADWAN L, MASZCZYK Z, KOZIOROWSKI A, ET AL.
CONTROL OF BREATHING IN OBSTRUCTIVE SLEEP
APNOEA AND IN PATIENTS WITH THE OVERLAP
SYNDROME. EUR RESPIR J. 1995;8(4):542-5. [BACK]
176.
FAUROUX B, NICOT F, BOELLE PY, ET AL. MECHANICAL
LIMITATION DURING CO2 REBREATHING IN YOUNG
PATIENTS WITH CYSTIC FIBROSIS. RESPIR PHYSIOL
NEUROBIOL. 2006;153(3):217-25. [BACK]
177.BROWNING IB, D'ALONZO GE, TOBIN MJ.
IMPORTANCE OF RESPIRATORY RATE AS AN INDICATOR
OF RESPIRATORY DYSFUNCTION IN PATIENTS WITH
CYSTIC FIBROSIS. CHEST. 1990;97(6):1317-21. [BACK]
178.WARD SA, TOMEZSKO JL, HOLSCLAW DS, PAOLONE
AM. ENERGY EXPENDITURE AND SUBSTRATE
UTILIZATION IN ADULTS WITH CYSTIC FIBROSIS AND
DIABETES MELLITUS. AM J CLIN NUTR. 1999;69(5):913-9.
[BACK]
179. DODD JD, BARRY SC, BARRY RB, GALLAGHER CG,
SKEHAN SJ, MASTERSON JB. THIN-SECTION CT IN
PATIENTS WITH CYSTIC FIBROSIS: CORRELATION WITH
PEAK EXERCISE CAPACITY AND BODY MASS INDEX.
RADIOLOGY. 2006;240(1):236-45. [BACK]
180. MCKONE EF, BARRY SC, FITZGERALD MX,
GALLAGHER CG. ROLE OF ARTERIAL HYPOXEMIA AND
PULMONARY MECHANICS IN EXERCISE LIMITATION IN
ADULTS WITH CYSTIC FIBROSIS. J APPL PHYSIOL.
2005;99(3):1012-8. [BACK]
181.BELL SC, SAUNDERS MJ, ELBORN JS, SHALE DJ.
RESTING ENERGY EXPENDITURE AND OXYGEN COST
OF BREATHING IN PATIENTS WITH CYSTIC FIBROSIS.
THORAX. 1996;51(2):126-31. [BACK]
182.TEPPER RS, SKATRUD JB, DEMPSEY JA.
VENTILATION AND OXYGENATION CHANGES DURING
SLEEP IN CYSTIC FIBROSIS. CHEST. 1983;84(4):388-93.
[BACK]
183.
MACKINNON DF, CRAIGHEAD B, HOEHN-SARIC R.
CARBON DIOXIDE PROVOCATION OF ANXIETY AND
RESPIRATORY RESPONSE IN BIPOLAR DISORDER. J
AFFECT DISORD. 2007;99(1-3):45-9. [BACK]
184.
PAIN MC, BIDDLE N, TILLER JW. PANIC DISORDER, THE
VENTILATORY RESPONSE TO CARBON DIOXIDE AND
RESPIRATORY VARIABLES. PSYCHOSOM MED.
1988;50(5):541-8. [BACK]
185.
ESQUIVEL E, CHAUSSAIN M, PLOUIN P, PONSOT G,
ARTHUIS M. PHYSICAL EXERCISE AND VOLUNTARY
HYPERVENTILATION IN CHILDHOOD ABSENCE
EPILEPSY. ELECTROENCEPHALOGR CLIN
NEUROPHYSIOL. 1991;79(2):127-32. [BACK]
186.
TRAVERS J, DUDGEON DJ, AMJADI K, ET AL.
MECHANISMS OF EXERTIONAL DYSPNEA IN PATIENTS
WITH CANCER. J APPL PHYSIOL. 2008;104(1):57-66.
[BACK]
187.
PASCHENKO SN. STUDY OF APPLICATION OF THE
SHALLOW BREATHING METHOD IN COMBINED
TREATMENT OF BREAST CANCER. ONCOLOGY.
2001;3(1):77-78. [BACK]
188.
RAKHIMOV, A. REFERENCES FOR TABLE (MINUTE
VENTILATION IN NORMAL SUBJECTS). [ONLINE].
AVAILABLE:
HTTP://WWW.NORMALBREATHING.COM/REFER-TABLE-
NORMALS.PHP.[MARCH 1, 2017]. [BACK]
189.
LEONG DP, TEO KK, RANGARAJAN S, ET AL.
PROGNOSTIC VALUE OF GRIP STRENGTH: FINDINGS
FROM THE PROSPECTIVE URBAN RURAL
EPIDEMIOLOGY (PURE) STUDY. LANCET.
2015;386(9990):266-73. [BACK]
190.
VOGT BP, BORGES MCC, DE GOES CR, COSTA J,
CARAMORI T. HANDGRIP STRENGTH IS AN
INDEPENDENT PREDICTOR OF ALL-CAUSE MORTALITY
IN MAINTENANCE DIALYSIS PATIENTS. CLINICAL
NUTRITION. 2016;35(6):1429-1433. [BACK]
191. RANTANEN T, VOLPATO S, FERRUCCI L, HEIKKINEN
E, FRIED LP, GURALNIK JM. HANDGRIP STRENGTH AND
CAUSE-SPECIFIC AND TOTAL MORTALITY IN OLDER
DISABLED WOMEN: EXPLORING THE MECHANISM. J AM
GERIATR SOC. 2003;51(5):636-41. [BACK]
192. RANTANEN T, HARRIS T, LEVEILLE SG, ET AL.
MUSCLE STRENGTH AND BODY MASS INDEX AS LONG-
TERM PREDICTORS OF MORTALITY IN INITIALLY
HEALTHY MEN. J GERONTOL A BIOL SCI MED SCI.
2000;55(3):M168-73. [BACK]
193. METTER EJ, TALBOT LA, SCHRAGER M, CONWIT R.
SKELETAL MUSCLE STRENGTH AS A PREDICTOR OF
ALL-CAUSE MORTALITY IN HEALTHY MEN. J GERONTOL
A BIOL SCI MED SCI. 2002;57(10):B359-65. [BACK]
194.
FAIN E, WEATHERFORD C. COMPARATIVE STUDY OF
MILLENNIALS' (AGE 20-34 YEARS) GRIP AND LATERAL
PINCH WITH THE NORMS. J HAND THER. 2016;29(4):483-
488. [BACK]
195.
RAICHLE ME, POSNER JB, PLUM F. CEREBRAL BLOOD
FLOW DURING AND AFTER HYPERVENTILATION. ARCH
NEUROL. 1970;23(5):394-403. [BACK]
ALTERATIONS IN CEREBRAL BLOOD FLOW AND
196.
OXYGEN CONSUMPTION DURING PROLONGED
HYPOCARBIA. PEDIATRIC RESEARCH. 1986;20(2):147.
[BACK]
197.VOORS AW, JOHNSON WD. ALTITUDE AND
ARTERIOSCLEROTIC HEART DISEASE MORTALITY IN
WHITE RESIDENTS OF 99 OF THE 100 LARGEST CITIES IN
THE UNITED STATES. J CLIN. EPID. 1979;32(1-2):157-162.
[BACK]
198.
POYART CF, BURSAUX E. [CURRENT CONCEPTION OF
THE BOHR EFFECT]. POUMON COEUR. 1975;31(4):173-7.
[BACK]
199. TYUMA I. THE BOHR EFFECT AND THE HALDANE
EFFECT IN HUMAN HEMOGLOBIN. JPN J PHYSIOL.
1984;34(2):205-16. [BACK]
200.KILMARTIN JV. THE BOHR EFFECT OF HUMAN
HEMOGLOBIN. TRENDS IN BIO. SCI. 1977;2(11):247-249.
[BACK]
201.
BROWN EB, PHYSIOLOGICAL EFFECTS OF
HYPERVENTILATION 1953, PHYSIOI REV 33:445-471.
[BACK]
202. KENNEALY JA, MCLENNAN JE, LOUDON RG,
MCLAURIN RL, HYPERVENTILATION-INDUCED
CEREBRAL HYPOXIA, AM REV RESPIR DIS 1980, 122: P.
407-412. [BACK]
203.WILSON DF, PASTUSZKO A, DIGIACOMO JE,
PAWLOWSKI M, SCHNEIDERMAN R, DELIVORIA-
PAPADOPOULOS M. EFFECT OF HYPERVENTILATION ON
OXYGENATION OF THE BRAIN CORTEX OF NEWBORN
PIGLETS. J APPL PHYSIOL. 1991;70(6):2691-6. [BACK]
204.LIEM KD, KOLLEE LA, HOPMAN JC, DE HAAN AF,
OESEBURG B, THE INFLUENCE OF ARTERIAL CARBON
DIOXIDE ON CEREBRAL OXYGENATION AND
HEMODYNAMICS DURING ECMO IN NORMOXAEMIC
AND HYPOXAEMIC PIGLETS, ACTA ANAESTHESIOLICA
SCANDANAVICA SUPPLEMENT, 1995; 107: P.157-164.
[BACK]
205. LUM LC, HYPERVENTILATION: THE TIP AND THE
ICEBERG, JOURNAL OF PSYCHOSOMATIC RESEARCH,
1975, VOL. 19, PP. 375-383. [BACK]
206. LUM LC, HYPERVENTILATION AND ANXIETY
STATE, JOURNAL OF THE ROYAL SOCIETY OF MEDICINE,
1981 (74) 1-4. [BACK]
207. MACEY PM, WOO MA, HARPER RM, HYPEROXIC
BRAIN EFFECTS ARE NORMALIZED BY ADDITION OF
CO2, PLOS MEDICINE, 2007 MAY; 4(5): P. E173. [BACK]
208. LITCHFIELD PM, A BRIEF OVERVIEW OF THE
CHEMISTRY OF RESPIRATION AND THE BREATHING
HEART WAVE, CALIFORNIA BIOFEEDBACK, 2003 SPRING,
19(1). [BACK]
209. SANTIAGO T V & EDELMAN NH, BRAIN BLOOD
FLOW AND CONTROL OF BREATHING, IN HANDBOOK OF
PHYSIOLOGY, SECT ION 3: THE RESPIRATORY SYSTEM,
VOL. II, ED. BY AP FISHMAN. AMERICAN
PHYSIOLOGICAL SOCIETY, BETHEDA, MARYLAND, 1986,
P.163-179. [BACK]
210. SKIPPEN P, SEEAR M, POSKITT K, ET AL. EFFECT OF
HYPERVENTILATION ON REGIONAL CEREBRAL BLOOD
FLOW IN HEAD-INJURED CHILDREN. CRIT CARE MED
1997, 25: P. 1402-1409. [BACK]
211.STARLING E & LOVATT EC, PRINCIPLES OF HUMAN
PHYSIOLOGY, 14TH ED., 1968, LEA & FEBIGER,
PHILADELPHIA. [BACK]
212.TSUDA Y, KIMURA K, YONEDA S, HARTMANN A,
ETANI H, HASHIKAWA K, KAMADA T, EFFECT OF
HYPOCAPNIA ON CEREBRAL OXYGEN METABOLISM
AND BLOOD FLOW IN ISCHEMIC CEREBROVASCULAR
DISORDERS, EUR NEUROL. 1987; 27(3): P.155-163. [BACK]
213.
FOEX P, RYDER WA, EFFECT OF CO2 ON THE SYSTEMIC
AND CORONARY CIRCULATIONS AND ON CORONARY
SINUS BLOOD GAS TENSIONS, BULLETIN OF EUROPEAN
PHYSIOPATHOLOGY AND RESPIROLOGY, 1979 JUL-AUG;
15(4): P.625-638. [BACK]
214.
KARLSSON T, ST JERNSTRÖM EL, ST JERNSTRÖM H,
NORLÉN K, WIKLUND L, CENTRAL AND REGIONAL
BLOOD FLOW DURING HYPERVENTILATION. AN
EXPERIMENTAL STUDY IN THE PIG, ACT A
ANAESTHESIOL SCAND. 1994 FEB; 38(2): P.180-186.
[BACK]
215. OKAZAKI K, HASHIMOTO K, OKUTSU Y, OKUMURA
F, EFFECT OF ARTERIAL CARBON DIOXIDE TENSION ON
REGIONAL MYOCARDIAL TISSUE OXYGEN TENSION IN
THE DOG [ARTICLE IN JAPANESE], MASUI, 1991 NOV;
40(11): P. 1620-1624. [BACK]
216. OKAZAKI K, HASHIMOTO K, OKUTSU Y, OKUMURA
F, EFFECT OF CARBON DIOXIDE (HYPOCAPNIA AND
HYPERCAPNIA) ON REGIONAL MYOCARDIAL TISSUE
OXYGEN TENSION IN DOGS WITH CORONARY STENOSIS
[ARTICLE IN JAPANESE], MASUI, 1992 FEB; 41(2): P. 221-
224. [BACK]
217. WEXELS JC, MYHRE ES, MJOS OD, EFFECTS OF
CARBON DIOXIDE AND PH ON MYOCARDIAL BLOOD-
FLOW AND METABOLISM IN THE DOG, CLIN PHYSIOL.
1985 DEC; 5(6): P.575-588. [BACK]
218.
FUJITA Y, SAKAI T, OHSUMI A, TAKAORI M, EFFECTS OF
HYPOCAPNIA AND HYPERCAPNIA ON SPLANCHNIC
CIRCULATION AND HEPATIC FUNCTION IN THE BEAGLE,
ANESTHESIA AND ANALGESIA, 1989 AUG; 69(2): P. 152-
157. [BACK]
219. HUGHES RL, MATHIE RT, FITCH W, CAMPBELL D,
LIVER BLOOD FLOW AND OXYGEN CONSUMPTION
DURING HYPOCAPNIA AND IPPV IN THE GREYHOUND,
JOURNAL OF APPLIED PHYSIOLOGY, 1979 AUG; 47(2): P.
290-295. [BACK]
220.
OKAZAKI K, OKUTSU Y, FUKUNAGA A, EFFECT OF
CARBON DIOXIDE (HYPOCAPNIA AND HYPERCAPNIA)
ON TISSUE BLOOD FLOW AND OXYGENATION OF LIVER,
KIDNEYS AND SKELETAL MUSCLE IN THE DOG, MASUI,
1989 APR, 38 (4): P. 457-464. [BACK]
221.
GUZMAN JA, KRUSE JA. GUT MUCOSAL-ARTERIAL
PCO2 GRADIENT AS AN INDICATOR OF SPLANCHNIC
PERFUSION DURING SYSTEMIC HYPO- AND
HYPERCAPNIA, CRIT CARE MED 1999; 27: P. 2760-2765.
[BACK]
222.
LAFFEY JG & KAVANAGH BP, HYPOCAPNIA, NEW
ENGLAND JOURNAL OF MEDICINE 2002, 347(1) 43-53.
[BACK]
223.
NUNN JF. APPLIED RESPIRATORY PHYSIOLOGY, 1987,
3RD ED. LONDON: BUTTERWORTHS. [BACK]
224.
ZHANG S, YANG C, YANG Z, ET AL. HOMEOSTASIS OF
REDOX STATUS DERIVED FROM GLUCOSE METABOLIC
PATHWAY COULD BE THE KEY TO UNDERSTANDING THE
WARBURG EFFECT. AM J CANCER RES. 2015;5(3):928-44.
[BACK]
225.
ZASTRE JA, SWEET RL, HANBERRY BS, YE S. LINKING
VITAMIN B1 WITH CANCER CELL METABOLISM.
CANCER METAB. 2013;1(1):16. [BACK]
226.
RASCHKE M, BÜRKLE L, MÜLLER N, ET AL. VITAMIN B1
BIOSYNTHESIS IN PLANTS REQUIRES THE ESSENTIAL
IRON SULFUR CLUSTER PROTEIN, THIC. PROC NATL
ACAD SCI USA. 2007;104(49):19637-42. [BACK]
227.
NAITO E, ITO M, YOKOTA I, SAIJO T, OGAWA Y, KURODA
Y. DIAGNOSIS AND MOLECULAR ANALYSIS OF THREE
MALE PATIENTS WITH THIAMINE-RESPONSIVE
PYRUVATE DEHYDROGENASE COMPLEX DEFICIENCY. J
NEUROL SCI. 2002;201(1-2):33-7. [BACK]
228.
NAITO E, ITO M, YOKOTA I, ET AL. THIAMINE-
RESPONSIVE PYRUVATE DEHYDROGENASE DEFICIENCY
IN TWO PATIENTS CAUSED BY A POINT MUTATION
(F205L AND L216F) WITHIN THE THIAMINE
PYROPHOSPHATE BINDING REGION. BIOCHIM BIOPHYS
ACTA. 2002;1588(1):79-84. [BACK]
229.
LEE EH, AHN MS, HWANG JS, RYU KH, KIM SJ, KIM SH. A
KOREAN FEMALE PATIENT WITH THIAMINE-
RESPONSIVE PYRUVATE DEHYDROGENASE COMPLEX
DEFICIENCY DUE TO A NOVEL POINT MUTATION
(Y161C)IN THE PDHA1 GENE. J KOREAN MED SCI.
2006;21(5):800-4. [BACK]
230.
LU'O'NG KV, NGUYÊN LT. THIAMINE AND PARKINSON'S
DISEASE. J NEUROL SCI. 2012;316(1-2):1-8. [BACK]
231.
LUONG KV, NGUYỄN LT. THE BENEFICIAL ROLE OF
THIAMINE IN PARKINSON DISEASE. CNS NEUROSCI
THER. 2013;19(7):461-8. [BACK]
232.
DINICOLANTONIO JJ, NIAZI AK, LAVIE CJ, O'KEEFE JH,
VENTURA HO. THIAMINE SUPPLEMENTATION FOR THE
TREATMENT OF HEART FAILURE: A REVIEW OF THE
LITERATURE. CONGEST HEART FAIL. 2013;19(4):214-22.
[BACK]
233. DINICOLANTONIO JJ, LAVIE CJ, NIAZI AK, O'KEEFE
JH, HU T. EFFECTS OF THIAMINE ON CARDIAC
FUNCTION IN PATIENTS WITH SYSTOLIC HEART
FAILURE: SYSTEMATIC REVIEW AND METAANALYSIS OF
RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED
TRIALS. OCHSNER J. 2013;13(4):495-9. [BACK]
234. SELIGMANN H, HALKIN H, RAUCHFLEISCH S, ET
AL. THIAMINE DEFICIENCY IN PATIENTS WITH
CONGESTIVE HEART FAILURE RECEIVING LONG-TERM
FUROSEMIDE THERAPY: A PILOT STUDY. AM J MED.
1991;91(2):151-5. [BACK]
235.
ROUZET P, RUBIE H, ROBERT A, ET AL. [SEVERE
HYPERLACTACIDEMIA IN 2 CHILDREN TREATED FOR
MALIGNANT TUMORS. ROLE OF VITAMIN B1]. ARCH FR
PEDIATR. 1991;48(6):423-6. [BACK]
236.
ROVELLI A, BONOMI M, MURANO A, LOCASCIULLI A,
UDERZO C. SEVERE LACTIC ACIDOSIS DUE TO
THIAMINE DEFICIENCY AFTER BONE MARROW
TRANSPLANTATION IN A CHILD WITH ACUTE
MONOCYTIC LEUKEMIA. HAEMATOLOGICA.
1990;75(6):579-81. [BACK]
237.
LU'O'NG KV, NGUYỄN LT. THE ROLE OF THIAMINE IN
CANCER: POSSIBLE GENETIC AND CELLULAR
SIGNALING MECHANISMS. CANCER GENOMICS
PROTEOMICS. 2013;10(4):169-85. [BACK]
238.VAN ZAANEN HC, VAN DER LELIE J. THIAMINE
DEFICIENCY IN HEMATOLOGIC MALIGNANT TUMORS.
CANCER. 1992;69(7):1710-3. [BACK]
239. TREBUKHINA RV, OSTROVSKY YM, SHAPOT VS,
MIKHALTSEVICH GN, TUMANOV VN. TURNOVER OF
[14C]THIAMIN AND ACTIVITIES OF THIAMIN
PYROPHOSPHATE-DEPENDENT ENZYMES IN TISSUES OF
MICE WITH EHRLICH ASCITES CARCINOMA. NUTR
CANCER. 1984;6(4):260-73. [BACK]
240.BARTLEY JC, MCGRATH H, ABRAHAM S. GLUCOSE
AND ACETATE UTILIZATION BY HYPERPLASTIC,
ALVEOLAR NODULE OUTGROWTHS AND
ADENOCARCINOMAS OF MOUSE MAMMARY GLAND.
CANCER RES. 1971;31(5):527-37. [BACK]
241. BASU TK, DICKERSON JW, RAVEN RW, WILLIAMS
DC. THE THIAMINE STATUS OF PATIENTS WITH CANCER
AS DETERMINED BY THE RED CELL TRANSKETOLASE
ACTIVITY. INT J VITAM NUTR RES. 1974;44(1):53-8.
[BACK]
242. SELIGMANN H, LEVI R, KONIJN AM, PROKOCIMER
M. THIAMINE DEFICIENCY IN PATIENTS WITH B-
CHRONIC LYMPHOCYTIC LEUKAEMIA: A PILOT STUDY.
POSTGRAD MED J. 2001;77(911):582-5. [BACK]
243. KAUL L, HESHMAT MY, KOVI J, ET AL. THE ROLE OF
DIET IN PROSTATE CANCER. NUTR CANCER. 1987;9(2-
3):123-8. [BACK]
244.
WARBURG O, GEISSLER AW, LORENZ S. [GENESIS OF
TUMOR METABOLISM BY VITAMIN B1 DEFICIENCY
(THIAMINE DEFICIENCY)]. Z NATURFORSCH B.
1970;25(3):332-3. [BACK]
245.
ROCHE TE, HIROMASA Y. PYRUVATE DEHYDROGENASE
KINASE REGULATORY MECHANISMS AND INHIBITION
IN TREATING DIABETES, HEART ISCHEMIA, AND
CANCER. CELL MOL LIFE SCI. 2007;64(7-8):830-49. [BACK]
246.
 BETTENDORFF L. THIAMIN. IN: ERDMAN JW,
MACDONALD IA, ZEISEL SH, EDS. PRESENT
KNOWLEDGE IN NUTRITION. 10TH ED. WASHINGTON,
DC: WILEY-BLACKWELL; 2012:261-79. [BACK]
247.
SAID HM. THIAMIN. IN: COATES PM, BETZ JM,
BLACKMAN MR, ET AL., EDS. ENCYCLOPEDIA OF
DIETARY SUPPLEMENTS. 2ND ED. LONDON AND NEW
YORK: INFORMA HEALTHCARE; 2010:748-53. [BACK]
248.
DE REUCK JL, SIEBEN GJ, SIEBEN-PRAET MR,
NGENDAHAYO P, DE COSTER WJ, VANDER EECKEN HM.
WERNICKE'S ENCEPHALOPATHY IN PATIENTS WITH
TUMORS OF THE LYMPHOID-HEMOPOIETIC SYSTEMS.
ARCH NEUROL. 1980;37(6):338-41. [BACK]
249.
BASU TK, DICKERSON JW. THE THIAMIN STATUS OF
EARLY CANCER PATIENTS WITH PARTICULAR
REFERENCE TO THOSE WITH BREAST AND BRONCHIAL
CARCINOMAS. ONCOLOGY. 1976;33(5-6):250-2. [BACK]
250.
GOETHART G. THE THIAMINE PYROPHOSPHATE
CONTENT OF CENTRIFUGALLY-PREPARED FRACTIONS
OF RAT LIVER HOMOGENATE; THE INFLUENCE OF A
THIAMINE-DEFICIENT DIET. BIOCHIM BIOPHYS ACTA.
1952;8(4):479-80. [BACK]
251.
TURAN MI, SILTELIOGLU TURAN I, MAMMADOV R,
ALTINKAYNAK K, KISAOGLU A. THE EFFECT OF
THIAMINE AND THIAMINE PYROPHOSPHATE ON
OXIDATIVE LIVER DAMAGE INDUCED IN RATS WITH
CISPLATIN. BIOMED RES INT. 2013;2013:783809. [BACK]
252. TURAN MI, CAYIR A, CETIN N, SULEYMAN H,
SILTELIOGLU TURAN I, TAN H. AN INVESTIGATION OF
THE EFFECT OF THIAMINE PYROPHOSPHATE ON
CISPLATIN-INDUCED OXIDATIVE STRESS AND DNA
DAMAGE IN RAT BRAIN TISSUE COMPARED WITH
THIAMINE: THIAMINE AND THIAMINE PYROPHOSPHATE
EFFECTS ON CISPLATIN NEUROTOXICITY. HUM EXP
TOXICOL. 2014;33(1):14-21. [BACK]
253. MOORE DH, FOWLER WC, CRUMPLER LS. 5-
FLUOROURACIL NEUROTOXICITY. GYNECOL ONCOL.
1990;36(1):152-4. [BACK]
254.TURAN MI, CETIN N, TURAN IS, SULEYMAN H.
EFFECTS OF THIAMINE AND THIAMINE
PYROPHOSPHATE ON OXIDATIVE STRESS BY
METHOTREXATE IN THE RAT BRAIN. LATIN AM. J.
PHARM. 2013;32(2):203-207. [BACK]
255.
ZENG KL, KURUVILLA S, SANATANI M, LOUIE AV.
BILATERAL BLINDNESS FOLLOWING CHEMORADIATION
FOR LOCALLY ADVANCED OROPHARYNGEAL
CARCINOMA. CUREUS. 2015;7(10):E352. [BACK]
256.
BASU TK, AKSOY M, DICKERSON JW. EFFECTS OF 5-
FLUOROURACIL ON THE THIAMIN STATUS OF ADULT
FEMALE RATS. CHEMOTHERAPY. 1979;25(2):70-6. [BACK]
257.
GONZALEZ MJ, MIRANDA MASSARI JR, DUCONGE J, ET
AL. THE BIO-ENERGETIC THEORY OF CARCINOGENESIS.
MED HYPOTHESES. 2012;79(4):433-9. [BACK]
258.
YONETANI T, KIDDER GW. STUDIES ON CYTOCHROME
OXIDASE. J BIO CHEM. 1963;238(1). [BACK]
259.
LI Y, PARK JS, DENG JH, BAI Y. CYTOCHROME C
OXIDASE SUBUNIT IV IS ESSENTIAL FOR ASSEMBLY
AND RESPIRATORY FUNCTION OF THE ENZYME
COMPLEX. J BIOENERG BIOMEMBR. 2006;38(5-6):283-91.
[BACK]
 260.
HERRMANN PC, HERRMANN EC. OXYGEN
METABOLISM AND A POTENTIAL ROLE FOR
CYTOCHROME C OXIDASE IN THE WARBURG EFFECT. J
BIOENERG BIOMEMBR. 2007;39(3):247-50. [BACK]
261.
EKICI S, TURKARSLAN S, PAWLIK G, ET AL.
INTRACYTOPLASMIC COPPER HOMEOSTASIS
CONTROLS CYTOCHROME C OXIDASE PRODUCTION.
MBIO. 2014;5(1):E01055-13. [BACK]
262.KAKO K, TAKEHARA A, ARAI H, ET AL. A
SELECTIVE REQUIREMENT FOR COPPER-DEPENDENT
ACTIVATION OF CYTOCHROME C OXIDASE BY COX17P.
BIOCHEM BIOPHYS RES COMMUN. 2004;324(4):1379-85.
[BACK]
263.NAIR PM, MASON HS. RECONSTITUTION OF
CYTOCHROME C OXIDASE FROM A COPPER-DEPLETED
ENZYME AND CU. J BIOL CHEM. 1967;242(7):1406-15.
[BACK]
264.
STEVENS RJ, NISHIO ML, HOOD DA. EFFECT OF
HYPOTHYROIDISM ON THE EXPRESSION OF
CYTOCHROME C AND CYTOCHROME C OXIDASE IN
HEART AND MUSCLE DURING DEVELOPMENT. MOL
CELL BIOCHEM. 1995;143(2):119-27. [BACK]
265.
DONG DW, SRINIVASAN S, GUHA M, AVADHANI NG.
DEFECTS IN CYTOCHROME C OXIDASE EXPRESSION
INDUCE A METABOLIC SHIFT TO GLYCOLYSIS AND
CARCINOGENESIS. GENOM DATA. 2015;6:99-107. [BACK]
266.
SRINIVASAN S, GUHA M, DONG DW, ET AL. DISRUPTION
OF CYTOCHROME C OXIDASE FUNCTION INDUCES THE
WARBURG EFFECT AND METABOLIC REPROGRAMMING.
ONCOGENE. 2016;35(12):1585-95. [BACK]
 267.
HASINOFF BB, DAVEY JP, O'BRIEN PJ. THE ADRIAMYCIN
(DOXORUBICIN)-INDUCED INACTIVATION OF
CYTOCHROME C OXIDASE DEPENDS ON THE PRESENCE
OF IRON OR COPPER. XENOBIOTICA. 1989;19(2):231-41.
[BACK]
268.
STANNARD JN, HORECKER BL. THE IN VITRO
INHIBITION OF CYTOCHROME OXIDASE BY AZIDE AND
CYANIDE. J BIOL. CHEM. 1948;172:599-608. [BACK]
269.WILSON MT, ANTONINI G, MALATESTA F, SARTI P,
BRUNORI M. PROBING THE OXYGEN BINDING SITE OF
CYTOCHROME C OXIDASE BY CYANIDE. J BIO
CHEM.1994;269(39):24114-24119. [BACK]
270. JENSEN P, WILSON MT, AASA R, MALMSTRÖM BG.
CYANIDE INHIBITION OF CYTOCHROME C OXIDASE. A
RAPID-FREEZE E.P.R. INVESTIGATION. BIOCHEM J.
1984;224(3):829-37. [BACK]
271.
MIRÓ O, CASADEMONT J, BARRIENTOS A, URBANO-
MÁRQUEZ A, CARDELLACH F. MITOCHONDRIAL
CYTOCHROME C OXIDASE INHIBITION DURING ACUTE
CARBON MONOXIDE POISONING. PHARMACOL
TOXICOL. 1998;82(4):199-202. [BACK]
272.
ALONSO JR, CARDELLACH F, LÓPEZ S, CASADEMONT J,
MIRÓ O. CARBON MONOXIDE SPECIFICALLY INHIBITS
CYTOCHROME C OXIDASE OF HUMAN MITOCHONDRIAL
RESPIRATORY CHAIN. PHARMACOL TOXICOL.
2003;93(3):142-6. [BACK]
273.
SINGH S, BHALLA A, VERMA SK, KAUR A, GILL K.
CYTOCHROME-C OXIDASE INHIBITION IN 26 ALUMINUM
PHOSPHIDE POISONED PATIENTS. CLIN TOXICOL
(PHILA). 2006;44(2):155-8. [BACK]
274.
KOTWICKA M, SKIBINSKA I, JENDRASZAK M,
JEDRZEJCZAK P. 17Β-ESTRADIOL MODIFIES HUMAN
SPERMATOZOA MITOCHONDRIAL FUNCTION IN VITRO.
REPROD BIOL ENDOCRINOL. 2016;14(1):50. [BACK]
275.
HARVEY AT, PRESKORN SH. CYTOCHROME P450
ENZYMES: INTERPRETATION OF THEIR INTERACTIONS
WITH SELECTIVE SEROTONIN REUPTAKE INHIBITORS.
PART II. J CLIN PSYCHOPHARMACOL. 1996;16(5):345-55.
[BACK]
276.
LEVY RJ, VIJAYASARATHY C, RAJ NR, AVADHANI NG,
DEUTSCHMAN CS. COMPETITIVE AND
NONCOMPETITIVE INHIBITION OF MYOCARDIAL
CYTOCHROME C OXIDASE IN SEPSIS. SHOCK.
2004;21(2):110-4. [BACK]
277.
NAGAI N, ITO Y. DYSFUNCTION IN CYTOCHROME C
OXIDASE CAUSED BY EXCESSIVE NITRIC OXIDE IN
HUMAN LENS EPITHELIAL CELLS STIMULATED WITH
INTERFERON-Γ AND LIPOPOLYSACCHARIDE. CURR EYE
RES. 2012;37(10):889-97. [BACK]
278.
MOHAPATRA NK, ROBERTS JF. IN VITRO EFFECT OF
AFLATOXIN B1 ON RAT LIVER MACROPHAGES (KUFFER
CELLS). TOXICOL LETT. 1985;29(2-3):177-81. [BACK]
279.
ORIOWO O, SIVAK J, BOLS N. UVB-RADIATION
ATTENUATION OF CYTOCHROME C OXIDASE ENZYME
IN OCULAR LENS-UV CATARACT IMPLICATION. AM.
ACAD. OPT. 2003. [BACK]
280.
WARBURG O. ON THE ORIGIN OF CANCER CELLS.
SCIENCE. 1956;123(3191):309-14. [BACK]
281.
 ZHONG J, RAJARAM N, BRIZEL DM, ET AL. RADIATION
INDUCES AEROBIC GLYCOLYSIS THROUGH REACTIVE
OXYGEN SPECIES. RADIOTHER ONCOL. 2013;106(3):390-6.
[BACK]
282.
KUNKEL, H. O., AND WILLIAMS, J. N., JR., J. BIOL.
CHEM., 189, 755 (1951). [BACK]
283.
CARDELLACH F, ALONSO JR, LÓPEZ S, CASADEMONT J,
MIRÓ O. EFFECT OF SMOKING CESSATION ON
MITOCHONDRIAL RESPIRATORY CHAIN FUNCTION. J
TOXICOL CLIN TOXICOL. 2003;41(3):223-8. [BACK]
284.
HAMBLIN MR. MECHANISMS OF LOW LEVEL LIGHT
THERAPY. PHOTOBIOLOGY. HARVARD MEDICAL
SCHOOL. [BACK]
285. KARU T, TIPHLOVA O, ESENALIEV R, LETOKHOV V.
TWO DIFFERENT MECHANISMS OF LOW-INTENSITY
LASER PHOTOBIOLOGICAL EFFECTS ON ESCHERICHIA
COLI. J PHOTOCHEM PHOTOBIOL B, BIOL. 1994;24(3):155-
61. [BACK]
286.MORIMOTO Y, ARAI T, KIKUCHI M, NAKAJIMA S,
NAKAMURA H. EFFECT OF LOW-INTENSITY ARGON
LASER IRRADIATION ON MITOCHONDRIAL
RESPIRATION. LASERS SURG MED. 1994;15(2):191-9.
[BACK]
287. PASSARELLA S, OSTUNI A, ATLANTE A,
QUAGLIARIELLO E. INCREASE IN THE ADP/ATP
EXCHANGE IN RAT LIVER MITOCHONDRIA IRRADIATED
IN VITRO BY HELIUM-NEON LASER. BIOCHEM BIOPHYS
RES COMMUN. 1988;156(2):978-86. [BACK]
288.GRECO M, GUIDA G, PERLINO E, MARRA E,
QUAGLIARIELLO E. INCREASE IN RNA AND PROTEIN
SYNTHESIS BY MITOCHONDRIA IRRADIATED WITH
HELIUM-NEON LASER. BIOCHEM BIOPHYS RES
COMMUN. 1989;163(3):1428-34. [BACK]
289.KARU T, PYATIBRAT L, KALENDO G. IRRADIATION
WITH HE-NE LASER INCREASES ATP LEVEL IN CELLS
CULTIVATED IN VITRO. J PHOTOCHEM PHOTOBIOL B,
BIOL. 1995;27(3):219-23. [BACK]
290. PASTORE D, DI MARTINO C, BOSCO G, PASSARELLA
S. STIMULATION OF ATP SYNTHESIS VIA OXIDATIVE
PHOSPHORYLATION IN WHEAT MITOCHONDRIA
IRRADIATED WITH HELIUM-NEON LASER. BIOCHEM
MOL BIOL INT. 1996;39(1):149-57. [BACK]
291. PASTORE D, GRECO M, PASSARELLA S. SPECIFIC
HELIUM-NEON LASER SENSITIVITY OF THE PURIFIED
CYTOCHROME C OXIDASE. INT J RADIAT BIOL.
2000;76(6):863-70. [BACK]
292. KARU T. PRIMARY AND SECONDARY MECHANISMS
OF ACTION OF VISIBLE TO NEAR-IR RADIATION ON
CELLS. J PHOTOCHEM PHOTOBIOL B, BIOL. 1999;49(1):1-
17. [BACK]
293.EELLS JT, HENRY MM, SUMMERFELT P, ET AL.
THERAPEUTIC PHOTOBIOMODULATION FOR
METHANOL-INDUCED RETINAL TOXICITY. PROC NATL
ACAD SCI USA. 2003;100(6):3439-44. [BACK]
294. KARU TI, PYATIBRAT LV, RYABYKH TP. MELATONIN
MODULATES THE ACTION OF NEAR INFRARED
RADIATION ON CELL ADHESION. J PINEAL RES.
2003;34(3):167-72. [BACK]
295.KARU TI, PYATIBRAT LV, KALENDO GS.
PHOTOBIOLOGICAL MODULATION OF CELL
ATTACHMENT VIA CYTOCHROME C OXIDASE.
PHOTOCHEM PHOTOBIOL SCI. 2004;3(2):211-6. [BACK]
296.EELLS JT, WONG-RILEY MT, VERHOEVE J, ET AL.
MITOCHONDRIAL SIGNAL TRANSDUCTION IN
ACCELERATED WOUND AND RETINAL HEALING BY
NEAR-INFRARED LIGHT THERAPY. MITOCHONDRION.
2004;4(5-6):559-67. [BACK]
297.KARU TI, PYATIBRAT LV, AFANASYEVA NI.
CELLULAR EFFECTS OF LOW POWER LASER THERAPY
CAN BE MEDIATED BY NITRIC OXIDE. LASERS SURG
MED. 2005;36(4):307-14. [BACK]
298. KARU TI, PYATIBRAT LV, KOLYAKOV SF,
AFANASYEVA NI. ABSORPTION MEASUREMENTS OF A
CELL MONOLAYER RELEVANT TO PHOTOTHERAPY:
REDUCTION OF CYTOCHROME C OXIDASE UNDER NEAR
IR RADIATION. J PHOTOCHEM PHOTOBIOL B, BIOL.
2005;81(2):98-106. [BACK]
299. KARU TI, KOLYAKOV SF. EXACT ACTION SPECTRA
FOR CELLULAR RESPONSES RELEVANT TO
PHOTOTHERAPY. PHOTOMED LASER SURG.
2005;23(4):355-61. [BACK]
300. WONG-RILEY MT, LIANG HL, EELLS JT, ET AL.
PHOTOBIOMODULATION DIRECTLY BENEFITS PRIMARY
NEURONS FUNCTIONALLY INACTIVATED BY TOXINS:
ROLE OF CYTOCHROME C OXIDASE. J BIOL CHEM.
2005;280(6):4761-71. [BACK]
301.YEAGER RL, FRANZOSA JA, MILLSAP DS, ET AL.
SURVIVORSHIP AND MORTALITY IMPLICATIONS OF
DEVELOPMENTAL 670-NM PHOTOTHERAPY: DIOXIN CO-
EXPOSURE. PHOTOMED LASER SURG. 2006;24(1):29-32.
[BACK]
302.LIANG HL, WHELAN HT, EELLS JT, ET AL.
PHOTOBIOMODULATION PARTIALLY RESCUES VISUAL
CORTICAL NEURONS FROM CYANIDE-INDUCED
APOPTOSIS. NEUROSCIENCE. 2006;139(2):639-49. [BACK]
303.
GONZALEZ-LIMA F, BARRETT DW. AUGMENTATION OF
COGNITIVE BRAIN FUNCTIONS WITH TRANSCRANIAL
LASERS. FRONT SYST NEUROSCI. 2014;8:36. [BACK]
304.HWANG J, CASTELLI DM, GONZALEZ-LIMA F.
COGNITIVE ENHANCEMENT BY TRANSCRANIAL LASER
STIMULATION AND ACUTE AEROBIC EXERCISE. LASERS
MED SCI. 2016;31(6):1151-60. [BACK]
305.BARRETT DW, GONZALEZ-LIMA F. TRANSCRANIAL
INFRARED LASER STIMULATION PRODUCES
BENEFICIAL COGNITIVE AND EMOTIONAL EFFECTS IN
HUMANS. NEUROSCIENCE. 2013;230:13-23. [BACK]
306.
HOPKINS JT, MCLODA TA, SEEGMILLER JG, DAVID
BAXTER G. LOW-LEVEL LASER THERAPY FACILITATES
SUPERFICIAL WOUND HEALING IN HUMANS: A TRIPLE-
BLIND, SHAM-CONTROLLED STUDY. J ATHL TRAIN.
2004;39(3):223-229. [BACK]
307.
DE SOUZA MERLI LA, DE MEDEIROS VP, TOMA L, ET AL.
THE LOW LEVEL LASER THERAPY EFFECT ON THE
REMODELING OF BONE EXTRACELLULAR MATRIX.
PHOTOCHEM PHOTOBIOL. 2012;88(5):1293-301. [BACK]
308.
SAAD A, EL YAMANY M, ABBAS O, YEHIA M. POSSIBLE
ROLE OF LOW LEVEL LASER THERAPY ON BONE
TURNOVER IN OVARIECTOMIZED RATS. ENDOCR
REGUL. 2010;44(4):155-63. [BACK]
309.
AHN JC, KIM YH, RHEE CK. THE EFFECTS OF LOW
LEVEL LASER THERAPY (LLLT) ON THE TESTIS IN
ELEVATING SERUM TESTOSTERONE LEVEL IN RATS.
BIOMED RES. 2013;24(1):28-32. [BACK]
310.
SCHIFFER F, JOHNSTON AL, RAVICHANDRAN C, ET AL.
PSYCHOLOGICAL BENEFITS 2 AND 4 WEEKS AFTER A
SINGLE TREATMENT WITH NEAR INFRARED LIGHT TO
THE FOREHEAD: A PILOT STUDY OF 10 PATIENTS WITH
MAJOR DEPRESSION AND ANXIETY. BEHAV BRAIN
FUNCT. 2009;5:46. [BACK]
311.
GOMES LE, DALMARCO EM, ANDRÉ ES. THE BRAIN-
DERIVED NEUROTROPHIC FACTOR, NERVE GROWTH
FACTOR, NEUROTROPHIN-3, AND INDUCED NITRIC
OXIDE SYNTHASE EXPRESSIONS AFTER LOW-LEVEL
LASER THERAPY IN AN AXONOTMESIS EXPERIMENTAL
MODEL. PHOTOMED LASER SURG. 2012;30(11):642-7.
[BACK]
312.
AZIZ-JALALI MH, TABAIE SM, DJAVID GE. COMPARISON
OF RED AND INFRARED LOW-LEVEL LASER THERAPY IN
THE TREATMENT OF ACNE VULGARIS. INDIAN J
DERMATOL. 2012;57(2):128-30. [BACK]
313.
SHI DY, XIE FZ, ZHAI C, STERN JS, LIU Y, LIU SL. THE
ROLE OF CELLULAR OXIDATIVE STRESS IN
REGULATING GLYCOLYSIS ENERGY METABOLISM IN
HEPATOMA CELLS. MOL CANCER. 2009;8:32. [BACK]
314.
BJORDAL JM, JOHNSON MI, IVERSEN V, AIMBIRE F,
LOPES-MARTINS RA. LOW-LEVEL LASER THERAPY IN
ACUTE PAIN: A SYSTEMATIC REVIEW OF POSSIBLE
MECHANISMS OF ACTION AND CLINICAL EFFECTS IN
RANDOMIZED PLACEBO-CONTROLLED TRIALS.
PHOTOMED LASER SURG. 2006;24(2):158-68. [BACK]
315.FALAKI F, NEJAT AH, DALIRSANI Z. THE EFFECT OF
LOW-LEVEL LASER THERAPY ON TRIGEMINAL
NEURALGIA: A REVIEW OF LITERATURE. J DENT RES
DENT CLIN DENT PROSPECTS. 2014;8(1):1-5. [BACK]
316.SUMEN A, SARSAN A, ALKAN H, YILDIZ N, ARDIC F.
EFFICACY OF LOW LEVEL LASER THERAPY AND
INTRAMUSCULAR ELECTRICAL STIMULATION ON
MYOFASCIAL PAIN SYNDROME. J BACK
MUSCULOSKELET REHABIL. 2015;28(1):153-8. [BACK]
317. YOUSEFI-NOORAIE R, SCHONSTEIN E, HEIDARI K,
ET AL. LOW LEVEL LASER THERAPY FOR NONSPECIFIC
LOW-BACK PAIN. COCHRANE DATABASE SYST REV.
2008;(2):CD005107. [BACK]
318.CHOW RT, JOHNSON MI, LOPES-MARTINS RA,
BJORDAL JM. EFFICACY OF LOW-LEVEL LASER
THERAPY IN THE MANAGEMENT OF NECK PAIN: A
SYSTEMATIC REVIEW AND META-ANALYSIS OF
RANDOMISED PLACEBO OR ACTIVE-TREATMENT
CONTROLLED TRIALS. LANCET. 2009;374(9705):1897-908.
[BACK]
319.
AVCI P, GUPTA GK, CLARK J, WIKONKAL N, HAMBLIN
MR. LOW-LEVEL LASER (LIGHT) THERAPY (LLLT) FOR
TREATMENT OF HAIR LOSS. LASERS SURG MED.
2014;46(2):144-51. [BACK]
320.
BARRY WEINBERGER, DEBRA L. LASKIN, DIANE E.
HECK, JEFFREY D. LASKIN; THE TOXICOLOGY OF
INHALED NITRIC OXIDE. TOXICOL SCI 2001; 59 (1): 5-16.
[BACK]
321.
BROWN GC, COOPER CE. NANOMOLAR
CONCENTRATIONS OF NITRIC OXIDE REVERSIBLY
INHIBIT SYNAPTOSOMAL RESPIRATION BY COMPETING
WITH OXYGEN AT CYTOCHROME OXIDASE. FEBS LETT.
1994;356(2-3):295-8. [BACK]
322. BOLAÑOS JP, PEUCHEN S, HEALES SJ, LAND JM,
CLARK JB. NITRIC OXIDE-MEDIATED INHIBITION OF
THE MITOCHONDRIAL RESPIRATORY CHAIN IN
CULTURED ASTROCYTES. J NEUROCHEM. 1994;63(3):910-
6. [BACK]
323. CLEETER MW, COOPER JM, DARLEY-USMAR VM,
MONCADA S, SCHAPIRA AH. REVERSIBLE INHIBITION
OF CYTOCHROME C OXIDASE, THE TERMINAL ENZYME
OF THE MITOCHONDRIAL RESPIRATORY CHAIN, BY
NITRIC OXIDE. IMPLICATIONS FOR
NEURODEGENERATIVE DISEASES. FEBS LETT.
1994;345(1):50-4. [BACK]
324.
BROWN GC, BORUTAITE V. NITRIC OXIDE,
CYTOCHROME C AND MITOCHONDRIA. BIOCHEM SOC
SYMP. 1999;66:17-25. [BACK]
325.
HAMBLIN M. THE ROLE OF NITRIC OXIDE IN LOW
LEVEL LIGHT THERAPY. 2008;6846. [BACK]
326.
RISTOW M, CUEZVA JM. OXIDATIVE
PHOSPHORYLATION AND CANCER: THE ONGOING
WARBURG HYPOTHESIS. 2008;1-18. [BACK]
327. GOGVADZE V, ORRENIUS S, ZHIVOTOVSKY B.
MITOCHONDRIA IN CANCER CELLS: WHAT IS SO
SPECIAL ABOUT THEM?. TRENDS CELL BIOL.
2008;18(4):165-73. [BACK]
328.CUEZVA JM, ORTEGA AD, WILLERS I, SÁNCHEZ-
CENIZO L, ALDEA M, SÁNCHEZ-ARAGÓ M. THE TUMOR
SUPPRESSOR FUNCTION OF MITOCHONDRIA:
TRANSLATION INTO THE CLINICS. BIOCHIM BIOPHYS
ACTA. 2009;1792(12):1145-58. [BACK]
329.
CHAMBERS AF, GROOM AC, MACDONALD IC.
DISSEMINATION AND GROWTH OF CANCER CELLS IN
METASTATIC SITES. NAT REV CANCER. 2002;2(8):563-72.
[BACK]
330.POSTE G, FIDLER IJ. THE PATHOGENESIS OF
CANCER METASTASIS. NATURE. 1980;283(5743):139-46.
[BACK]
331. CHAFFER CL, WEINBERG RA. A PERSPECTIVE ON
CANCER CELL METASTASIS. SCIENCE.
2011;331(6024):1559-64. [BACK]
332. WELCH DR. DO WE NEED TO REDEFINE A CANCER
METASTASIS AND STAGING DEFINITIONS?. BREAST DIS.
2006;26:3-12. [BACK]
LAZEBNIK Y. WHAT ARE THE HALLMARKS OF
333.
CANCER?. NAT REV CANCER. 2010;10(4):232-3. [BACK]
334.TARIN D. COMPARISONS OF METASTASES IN
DIFFERENT ORGANS: BIOLOGICAL AND CLINICAL
IMPLICATIONS. CLIN CANCER RES. 2008;14(7):1923-5.
[BACK]
335.BACAC M, STAMENKOVIC I. METASTATIC CANCER
CELL. ANNU REV PATHOL. 2008;3:221-47. [BACK]
HANAHAN D, WEINBERG RA. THE HALLMARKS OF
336.
CANCER. CELL. 2000;100(1):57-70. [BACK]
337.
TAKEDA D, HASEGAWA T, UEHA T, ET AL.
TRANSCUTANEOUS CARBON DIOXIDE INDUCES
MITOCHONDRIAL APOPTOSIS AND SUPPRESSES
METASTASIS OF ORAL SQUAMOUS CELL CARCINOMA IN
VIVO. PLOS ONE. 2014;9(7):E100530. [BACK]
338. KAMARAJUGADDA S, STEMBOROSKI L, CAI Q, ET
AL. GLUCOSE OXIDATION MODULATES ANOIKIS AND
TUMOR METASTASIS. MOL CELL BIOL. 2012;32(10):1893-
907. [BACK]
LU J, TAN M, CAI Q. THE WARBURG EFFECT IN
339.
TUMOR PROGRESSION: MITOCHONDRIAL OXIDATIVE
METABOLISM AS AN ANTI-METASTASIS MECHANISM.
CANCER LETT. 2015;356(2 PT A):156-64. [BACK]
340.LIU W, BECK BH, VAIDYA KS, ET AL. METASTASIS
SUPPRESSOR KISS1 SEEMS TO REVERSE THE WARBURG
EFFECT BY ENHANCING MITOCHONDRIAL BIOGENESIS.
CANCER RES. 2014;74(3):954-63. [BACK]
341. RISTOW M. OXIDATIVE METABOLISM IN CANCER
GROWTH. CURR OPIN CLIN NUTR METAB CARE.
2006;9(4):339-45. [BACK]
342.
ADDABBO F, MONTAGNANI M, GOLIGORSKY MS.
MITOCHONDRIA AND REACTIVE OXYGEN SPECIES.
HYPERTENSION. 2009;53(6):885-92. [BACK]
343.
NAVIAUX RK. OXIDATIVE SHIELDING OR OXIDATIVE
STRESS?. J PHARMACOL EXP THER. 2012;342(3):608-18.
[BACK]
344. BRAND MD, AFFOURTIT C, ESTEVES TC, ET AL.
MITOCHONDRIAL SUPEROXIDE: PRODUCTION,
BIOLOGICAL EFFECTS, AND ACTIVATION OF
UNCOUPLING PROTEINS. FREE RADIC BIOL MED.
2004;37(6):755-67. [BACK]
345.KORSHUNOV SS, SKULACHEV VP, STARKOV AA.
HIGH PROTONIC POTENTIAL ACTUATES A MECHANISM
OF PRODUCTION OF REACTIVE OXYGEN SPECIES IN
MITOCHONDRIA. FEBS LETT. 1997;416(1):15-8. [BACK]
346.SRINIVASAN S, AVADHANI NG. CYTOCHROME C
OXIDASE DYSFUNCTION IN OXIDATIVE STRESS. FREE
RADIC BIOL MED. 2012;53(6):1252-63. [BACK]
347. TURRENS JF. MITOCHONDRIAL FORMATION OF
REACTIVE OXYGEN SPECIES. J PHYSIOL (LOND).
2003;552(PT 2):335-44. [BACK]
348.JOHN AP. DYSFUNCTIONAL MITOCHONDRIA, NOT
OXYGEN INSUFFICIENCY, CAUSE CANCER CELLS TO
PRODUCE INORDINATE AMOUNTS OF LACTIC ACID: THE
IMPACT OF THIS ON THE TREATMENT OF CANCER. MED
HYPOTHESES. 2001;57(4):429-31. [BACK]
349.SRINIVASAN S, AVADHANI NG. CYTOCHROME C
OXIDASE DYSFUNCTION IN OXIDATIVE STRESS. FREE
RADIC BIOL MED. 2012;53(6):1252-63. [BACK]
350. PINHEIRO CH, SILVEIRA LR, NACHBAR RT, VITZEL
KF, CURI R. REGULATION OF GLYCOLYSIS AND
EXPRESSION OF GLUCOSE METABOLISM-RELATED
GENES BY REACTIVE OXYGEN SPECIES IN
CONTRACTING SKELETAL MUSCLE CELLS. FREE RADIC
BIOL MED. 2010;48(7):953-60. [BACK]
351.SULLIVAN LB, CHANDEL NS. MITOCHONDRIAL
REACTIVE OXYGEN SPECIES AND CANCER. CANCER
METAB. 2014;2:17. [BACK]
352.SZATROWSKI TP, NATHAN CF. PRODUCTION OF
LARGE AMOUNTS OF HYDROGEN PEROXIDE BY HUMAN
TUMOR CELLS. CANCER RES. 1991;51(3):794-8. [BACK]
353.
VIRCHOW, R. AETIOLOGIE DER NEOPLASTISCHEN
GESCHWULSTE/PATHOGENIE DER NEOPLASTISCHEN
GESCHWULSTE. (VERLAG VON AUGUST HIRSCHWALD,
BERLIN, GERMANY, 1863. [BACK]
354.
SCHÄFER M, WERNER S. CANCER AS AN OVERHEALING
WOUND: AN OLD HYPOTHESIS REVISITED. NAT REV
MOL CELL BIOL. 2008;9(8):628-38. [BACK]
355.
MOKBEL K, PRICE RK, CARPENTER R. RADIAL SCARS
AND BREAST CANCER. NEJM. 1999;341:210. [BACK]
356. SLOANE JP, MAYERS MM. CARCINOMA AND
ATYPICAL HYPERPLASIA IN RADIAL SCARS AND
COMPLEX SCLEROSING LESIONS: IMPORTANCE OF
LESION SIZE AND PATIENT AGE. HISTOPATHOLOGY.
1993;23(3):225-31. [BACK]
357. FROUGE C, TRISTANT H, GUINEBRETIÈRE JM, ET
AL. MAMMOGRAPHIC LESIONS SUGGESTIVE OF RADIAL
SCARS: MICROSCOPIC FINDINGS IN 40 CASES.
RADIOLOGY. 1995;195(3):623-5. [BACK]
358.MENG X, RIORDAN NH. CANCER IS A FUNCTIONAL
REPAIR TISSUE. MED HYPOTHESES. 2006;66(3):486-90.
[BACK]
359. MORGAN C, SHAH ZA, HAMILTON R, ET AL. THE
RADIAL SCAR OF THE BREAST DIAGNOSED AT CORE
NEEDLE BIOPSY. PROC (BAYL UNIV MED CENT).
2012;25(1):3-5. [BACK]
360. KENNEDY M, MASTERSON AV, KERIN M,
FLANAGAN F. PATHOLOGY AND CLINICAL RELEVANCE
OF RADIAL SCARS: A REVIEW. J CLIN PATHOL.
2003;56(10):721-4. [BACK]
361.NASSAR A, CONNERS AL, CELIK B, JENKINS SM,
SMITH CY, HIEKEN TJ. RADIAL SCAR/COMPLEX
SCLEROSING LESIONS: A CLINICOPATHOLOGIC
CORRELATION STUDY FROM A SINGLE INSTITUTION.
ANN DIAGN PATHOL. 2015;19(1):24-8. [BACK]
362.LV M, ZHU X, ZHONG S, ET AL. RADIAL SCARS AND
SUBSEQUENT BREAST CANCER RISK: A META-
ANALYSIS. PLOS ONE. 2014;9(7):E102503. [BACK]
363.DUNHAM LJ. CANCER IN MAN AT SITE OF PRIOR
BENIGN LESION OF SKIN OR MUCOUS MEMBRANE: A
REVIEW. CANCER RES. 1972;32(7):1359-74. [BACK]
364.
ENNIS WJ, SUI A, BARTHOLOMEW A. STEM CELLS AND
HEALING: IMPACT ON INFLAMMATION. ADV WOUND
CARE (NEW ROCHELLE). 2013;2(7):369-378. [BACK]
365.
DVORAK HF. TUMORS: WOUNDS THAT DO NOT HEAL.
SIMILARITIES BETWEEN TUMOR STROMA GENERATION
AND WOUND HEALING. N ENGL J MED. 1986;315(26):1650-
9. [BACK]
366. MENG X, ZHONG J, LIU S, MURRAY M, GONZALEZ-
ANGULO AM. A NEW HYPOTHESIS FOR THE CANCER
MECHANISM. CANCER METASTASIS REV. 2012;31(1-
2):247-68. [BACK]
367. HADDOW A. MOLECULAR REPAIR, WOUND
HEALING, AND CARCINOGENESIS: TUMOR PRODUCTION
A POSSIBLE OVERHEALING?. ADV CANCER RES.
1972;16:181-234. [BACK]
368.
COUSSENS LM, WERB Z. INFLAMMATION AND CANCER.
NATURE. 2002;420(6917):860-7. [BACK]
369.RAKOFF-NAHOUM S. WHY CANCER AND
INFLAMMATION?. YALE J BIOL MED. 2006;79(3-4):123-30.
[BACK]
370.BONOMI M, PATSIAS A, POSNER M, SIKORA A. THE
ROLE OF INFLAMMATION IN HEAD AND NECK CANCER.
ADV EXP MED BIOL. 2014;816:107-27. [BACK]
371.BORRELLO MG, DEGL'INNOCENTI D, PIEROTTI MA.
INFLAMMATION AND CANCER: THE ONCOGENE-DRIVEN
CONNECTION. CANCER LETT. 2008;267(2):262-70. [BACK]
372. ALLAVENA P, GARLANDA C, BORRELLO MG, SICA
A, MANTOVANI A. PATHWAYS CONNECTING
INFLAMMATION AND CANCER. CURR OPIN GENET DEV.
2008;18(1):3-10. [BACK]
373. KUNDU JK, SURH YJ. INFLAMMATION: GEARING
THE JOURNEY TO CANCER. MUTAT RES. 2008;659(1-2):15-
30. [BACK]
374. MANTOVANI A. MOLECULAR PATHWAYS LINKING
INFLAMMATION AND CANCER. CURR MOL MED.
2010;10(4):369-73. [BACK]
375.DOBROVOLSKAIA MA, KOZLOV SV.
INFLAMMATION AND CANCER: WHEN NF-KAPPAB
AMALGAMATES THE PERILOUS PARTNERSHIP. CURR
CANCER DRUG TARGETS. 2005;5(5):325-44. [BACK]
376. KEIBEL A, SINGH V, SHARMA MC. INFLAMMATION,
MICROENVIRONMENT, AND THE IMMUNE SYSTEM IN
CANCER PROGRESSION. CURR PHARM DES.
2009;15(17):1949-55. [BACK]
377.SHACTER E, WEITZMAN SA. CHRONIC
INFLAMMATION AND CANCER. ONCOLOGY (WILLISTON
PARK, NY). 2002;16(2):217-26, 229. [BACK]
378.COLOTTA F, ALLAVENA P, SICA A, GARLANDA C,
MANTOVANI A. CANCER-RELATED INFLAMMATION, THE
SEVENTH HALLMARK OF CANCER: LINKS TO GENETIC
INSTABILITY. CARCINOGENESIS. 2009;30(7):1073-81.
[BACK]
379.MANTOVANI A, SICA A. MACROPHAGES, INNATE
IMMUNITY AND CANCER: BALANCE, TOLERANCE, AND
DIVERSITY. CURR OPIN IMMUNOL. 2010;22(2):231-7.
[BACK]
380. HANAHAN D, WEINBERG RA. HALLMARKS OF
CANCER: THE NEXT GENERATION. CELL. 2011;144(5):646-
674. [BACK]
381. KARIN M. NUCLEAR FACTOR-KAPPAB IN CANCER
DEVELOPMENT AND PROGRESSION. NATURE.
2006;441(7092):431-6. [BACK]
382.
ZHEJIANG UNIVERSITY. ISCHEMIC AND HYPOXIC
INJURY. [ONLINE]. AVAILABLE:
HTTP://JPCK.ZJU.EDU.CN/JCYXJP/FILES/GE/03/MT/0365.PD
F. [MARCH 30, 2017]. [BACK]
383.
HAAS R, SMITH J, ROCHER-ROS V, ET AL. LACTATE
REGULATES METABOLIC AND PRO-INFLAMMATORY
CIRCUITS IN CONTROL OF T CELL MIGRATION AND
EFFECTOR FUNCTIONS. PLOS BIOL. 2015;13(7):E1002202.
[BACK]
384.
KIRALY O, GONG G, OLIPITZ W, MUTHUPALANI S,
ENGELWARD BP. INFLAMMATION-INDUCED CELL
PROLIFERATION POTENTIATES DNA DAMAGE-INDUCED
MUTATIONS IN VIVO. PLOS GENET. 2015;11(2):E1004901.
[BACK]
385. BOSCHETTI G, KANJARAWI R, BARDEL E, ET AL.
GUT INFLAMMATION IN MICE TRIGGERS
PROLIFERATION AND FUNCTION OF MUCOSAL FOXP3+
REGULATORY T CELLS BUT IMPAIRS THEIR
CONVERSION FROM CD4+ T CELLS. J CROHNS COLITIS.
2017;11(1):105-117. [BACK]
386.
LARSON BJ, LONGAKER MT, LORENZ HP. SCARLESS
FETAL WOUND HEALING: A BASIC SCIENCE REVIEW.
PLAST RECONSTR SURG. 2010;126(4):1172-80. [BACK]
387.WILGUS TA. REGENERATIVE HEALING IN FETAL
SKIN: A REVIEW OF THE LITERATURE. OSTOMY WOUND
MANAGE. 2007;53(6):16-31. [BACK]
388.COLWELL AS, LONGAKER MT, LORENZ HP.
MAMMALIAN FETAL ORGAN REGENERATION. ADV
BIOCHEM ENG BIOTECHNOL. 2005;93:83-100. [BACK]
389.MACKOOL RJ, GITTES GK, LONGAKER MT.
SCARLESS HEALING. THE FETAL WOUND. CLIN PLAST
SURG. 1998;25(3):357-65. [BACK]
390.LORENZ HP, ADZICK NS. SCARLESS SKIN WOUND
REPAIR IN THE FETUS. WEST J MED. 1993;159(3):350-5.
[BACK]
391. BULLARD KM, LONGAKER MT, LORENZ HP. FETAL
WOUND HEALING: CURRENT BIOLOGY. WORLD J SURG.
2003;27(1):54-61. [BACK]
392.ROLFE KJ, GROBBELAAR AO. A REVIEW OF FETAL
SCARLESS HEALING. ISRN DERMATOL. 2012;2012:698034.
[BACK]
393. LO DD, ZIMMERMANN AS, NAUTA A, LONGAKER
MT, LORENZ HP. SCARLESS FETAL SKIN WOUND
HEALING UPDATE. BIRTH DEFECTS RES C EMBRYO
TODAY. 2012;96(3):237-47. [BACK]
394. DANG C, TING K, SOO C, LONGAKER MT, LORENZ
HP. FETAL WOUND HEALING CURRENT PERSPECTIVES.
CLIN PLAST SURG. 2003;30(1):13-23. [BACK]
395. BLEACHER JC, ADOLPH VR, DILLON PW, KRUMMEL
TM. FETAL TISSUE REPAIR AND WOUND HEALING.
DERMATOL CLIN. 1993;11(4):677-83. [BACK]
396. STELNICKI EJ, CHIN GS, GITTES GK, LONGAKER
MT. FETAL WOUND REPAIR: WHERE DO WE GO FROM
HERE?. SEMIN PEDIATR SURG. 1999;8(3):124-30. [BACK]
397.KATHJU S, GALLO PH, SATISH L. SCARLESS
INTEGUMENTARY WOUND HEALING IN THE
MAMMALIAN FETUS: MOLECULAR BASIS AND
THERAPEUTIC IMPLICATIONS. BIRTH DEFECTS RES C
EMBRYO TODAY. 2012;96(3):223-36. [BACK]
398.FERGUSON MW, O'KANE S. SCAR-FREE HEALING:
FROM EMBRYONIC MECHANISMS TO ADULT
THERAPEUTIC INTERVENTION. PHILOS TRANS R SOC
LOND, B, BIOL SCI. 2004;359(1445):839-50. [BACK]
399.JUN Q, JI-HONG Z. MECHANISM OF SCARLESS
HEALING OF EMBRYONIC SKIN. J CLIN. REHAB. TISS.
ENG. RES. 2005;9(22):228-230. [BACK]
400.LEE YS, WYSOCKI A, WARBURTON D, TUAN TL.
WOUND HEALING IN DEVELOPMENT. BIRTH DEFECTS
RES C EMBRYO TODAY. 2012;96(3):213-22. [BACK]
401.SAMUELS P, TAN AK. FETAL SCARLESS WOUND
HEALING. J OTOLARYNGOL. 1999;28(5):296-302. [BACK]
402.YATES CC, HEBDA P, WELLS A. SKIN WOUND
HEALING AND SCARRING: FETAL WOUNDS AND
REGENERATIVE RESTITUTION. BIRTH DEFECTS RES C
EMBRYO TODAY. 2012;96(4):325-33. [BACK]
403.
SULLIVAN KM, MEULI M, MACGILLIVRAY TE, ADZICK
NS. AN ADULT-FETAL SKIN INTERFACE HEALS WITHOUT
SCAR FORMATION IN SHEEP. SURGERY. 1995;118(1):82-6.
[BACK]
404.
RESNIK, R, CREASY, RK. LOCKWOOD, CJ, MOORE, T,
GREENE MF. 2013. CREASY AND RESNIK’S MATERNAL-
FETAL MEDICINE: PRINCIPLES AND PRACTISE.
ELSEVIER CANADA: 7TH EDITION. 1320 PPS. [BACK]
405.RODESCH F, SIMON P, DONNER C, JAUNIAUX E.
OXYGEN MEASUREMENTS IN ENDOMETRIAL AND
TROPHOBLASTIC TISSUES DURING EARLY PREGNANCY.
OBSTET GYNECOL. 1992;80(2):283-5. [BACK]
406.JAUNIAUX E, GULBIS B, BURTON GJ. THE HUMAN
FIRST TRIMESTER GESTATIONAL SAC LIMITS RATHER
THAN FACILITATES OXYGEN TRANSFER TO THE
FOETUS--A REVIEW. PLACENTA. 2003;24 SUPPL A:S86-93.
[BACK]
407.
KLOTH LC. ELECTRICAL STIMULATION FOR WOUND
HEALING: A REVIEW OF EVIDENCE FROM IN VITRO
STUDIES, ANIMAL EXPERIMENTS, AND CLINICAL
TRIALS. INT J LOW EXTREM WOUNDS. 2005;4(1):23-44.
[BACK]
408.
AL MD, HORNSTRA G, VAN DER SCHOUW YT, BULSTRA-
RAMAKERS MT, HUISJES HJ. BIOCHEMICAL EFA STATUS
OF MOTHERS AND THEIR NEONATES AFTER NORMAL
PREGNANCY. EARLY HUM DEV. 1990;24(3):239-48. [BACK]
409. OTTO SJ, HOUWELINGEN AC, ANTAL M, ET AL.
MATERNAL AND NEONATAL ESSENTIAL FATTY ACID
STATUS IN PHOSPHOLIPIDS: AN INTERNATIONAL
COMPARATIVE STUDY. EUR J CLIN NUTR. 1997;51(4):232-
42. [BACK]
410. HORNSTRA G, VAN HOUWELINGEN AC, SIMONIS M,
GERRARD JM. FATTY ACID COMPOSITION OF
UMBILICAL ARTERIES AND VEINS: POSSIBLE
IMPLICATIONS FOR THE FETAL EFA-STATUS. LIPIDS.
1989;24(6):511-7. [BACK]
411.RUMP P, MENSINK RP, KESTER AD, HORNSTRA G.
ESSENTIAL FATTY ACID COMPOSITION OF PLASMA
PHOSPHOLIPIDS AND BIRTH WEIGHT: A STUDY IN TERM
NEONATES. AM J CLIN NUTR. 2001;73(4):797-806. [BACK]
412. HORNSTRA G, AL MD, VAN HOUWELINGEN AC,
FOREMAN-VAN DRONGELEN MM. ESSENTIAL FATTY
ACIDS IN PREGNANCY AND EARLY HUMAN
DEVELOPMENT. EUR J OBSTET GYNECOL REPROD BIOL.
1995;61(1):57-62. [BACK]
413.
RAKHIMOV, A. 1969. DR. BUTEYKO LECTURE IN THE
MOSCOW STATE UNIVERSITY ON 9 DECEMBER 1969.
AVAILABLE:
HTTP://WWW.NORMALBREATHING.COM/BOOK-
LECTURE.PHP.[MARCH 1, 2017]. [BACK]
414.
LARJAVA H, WIEBE C, GALLANT-BEHM C, HART DA,
HEINO J, HÄKKINEN L. EXPLORING SCARLESS HEALING
OF ORAL SOFT TISSUES. J CAN DENT ASSOC. 2011;77:B18.
[BACK]
415. HARRISON JW. HEALING OF SURGICAL WOUNDS IN
ORAL MUCOPERIOSTEAL TISSUES. J ENDOD.
1991;17(8):401-8. [BACK]
416.GLIM JE, VAN EGMOND M, NIESSEN FB, EVERTS V,
BEELEN RH. DETRIMENTAL DERMAL WOUND HEALING:
WHAT CAN WE LEARN FROM THE ORAL MUCOSA?.
WOUND REPAIR REGEN. 2013;21(5):648-60. [BACK]
417.MAK K, MANJI A, GALLANT-BEHM C, ET AL.
SCARLESS HEALING OF ORAL MUCOSA IS
CHARACTERIZED BY FASTER RESOLUTION OF
INFLAMMATION AND CONTROL OF MYOFIBROBLAST
ACTION COMPARED TO SKIN WOUNDS IN THE RED
DUROC PIG MODEL. J DERMATOL SCI. 2009;56(3):168-80.
[BACK]
418.
WONG JW, GALLANT-BEHM C, WIEBE C, ET AL. WOUND
HEALING IN ORAL MUCOSA RESULTS IN REDUCED
SCAR FORMATION AS COMPARED WITH SKIN:
EVIDENCE FROM THE RED DUROC PIG MODEL AND
HUMANS. WOUND REPAIR REGEN. 2009;17(5):717-29.
[BACK]
419.
ESKOW RN, LOESCHE WJ. OXYGEN TENSIONS IN THE
HUMAN ORAL CAVITY. ARCH ORAL BIOL. 1971;16(9):1127-
8. [BACK]
420.
KØRBLING M, ESTROV Z. ADULT STEM CELLS FOR
TISSUE REPAIR - A NEW THERAPEUTIC CONCEPT?. N
ENGL J MED. 2003;349(6):570-82. [BACK]
421.HENNESSY B, KÖRBLING M, ESTROV Z.
CIRCULATING STEM CELLS AND TISSUE REPAIR.
PANMINERVA MED. 2004;46(1):1-11. [BACK]
422. MIZUNO H. ADIPOSE-DERIVED STEM CELLS FOR
TISSUE REPAIR AND REGENERATION: TEN YEARS OF
RESEARCH AND A LITERATURE REVIEW. J NIPPON MED
SCH. 2009;76(2):56-66. [BACK]
423. HU MS, RENNERT RC, MCARDLE A, ET AL. THE
ROLE OF STEM CELLS DURING SCARLESS SKIN WOUND
HEALING. ADV WOUND CARE (NEW ROCHELLE).
2014;3(4):304-314. [BACK]
424. ROUBELAKIS MG, TROHATOU O, ROUBELAKIS A,
ET AL. PLATELET-RICH PLASMA (PRP) PROMOTES FETAL
MESENCHYMAL STEM/STROMAL CELL MIGRATION AND
WOUND HEALING PROCESS. STEM CELL REV.
2014;10(3):417-28. [BACK]
425. TAGHAVI S, GEORGE JC. HOMING OF STEM CELLS
TO ISCHEMIC MYOCARDIUM. AM J TRANSL RES.
2013;5(4):404-11. [BACK]
426.PYTLÍK R, RENTSCH C, SOUKUP T, ET AL. EFFICACY
AND SAFETY OF HUMAN MESENCHYMAL STROMAL
CELLS IN HEALING OF CRITICAL-SIZE BONE DEFECTS IN
IMMUNODEFICIENT RATS. PHYSIOL RES. 2016. [BACK]
427.COVACU R, BRUNDIN L. ENDOGENOUS SPINAL
CORD STEM CELLS IN MULTIPLE SCLEROSIS AND ITS
ANIMAL MODEL. J NEUROIMMUNOL. 2016. [BACK]
428.COLLINS JN, COLLINS JJ. TISSUE DEGENERATION
FOLLOWING LOSS OF SCHISTOSOMA MANSONI CBP1 IS
ASSOCIATED WITH INCREASED STEM CELL
PROLIFERATION AND PARASITE DEATH IN VIVO. PLOS
PATHOG. 2016;12(11):E1005963. [BACK]
429.CHENG CW, ADAMS GB, PERIN L, ET AL.
PROLONGED FASTING REDUCES IGF-1/PKA TO PROMOTE
HEMATOPOIETIC-STEM-CELL-BASED REGENERATION
AND REVERSE IMMUNOSUPPRESSION. CELL STEM
CELL. 2014;14(6):810-23. [BACK]
430. WAGERS AJ, CHRISTENSEN JL, WEISSMAN IL. CELL
FATE DETERMINATION FROM STEM CELLS. GENE THER.
2002;9(10):606-12. [BACK]
431.HARDY D, BESNARD A, LATIL M, ET AL.
COMPARATIVE STUDY OF INJURY MODELS FOR
STUDYING MUSCLE REGENERATION IN MICE. PLOS
ONE. 2016;11(1):E0147198. [BACK]
432.
ARWERT EN, HOSTE E, WATT FM. EPITHELIAL STEM
CELLS, WOUND HEALING AND CANCER. NAT REV
CANCER. 2012;12(3):170-80. [BACK]
433.
LATERVEER L, LINDLEY IJ, HAMILTON MS, WILLEMZE
R, FIBBE WE. INTERLEUKIN-8 INDUCES RAPID
MOBILIZATION OF HEMATOPOIETIC STEM CELLS WITH
RADIOPROTECTIVE CAPACITY AND LONG-TERM
MYELOLYMPHOID REPOPULATING ABILITY. BLOOD.
1995;85(8):2269-75. [BACK]
434.
LATERVEER L, LINDLEY IJ, HEEMSKERK DP, ET AL.
RAPID MOBILIZATION OF HEMATOPOIETIC PROGENITOR
CELLS IN RHESUS MONKEYS BY A SINGLE
INTRAVENOUS INJECTION OF INTERLEUKIN-8. BLOOD.
1996;87(2):781-8. [BACK]
435.
WESTENBRINK BD, LIPSIC E, VAN DER MEER P, ET AL.
ERYTHROPOIETIN IMPROVES CARDIAC FUNCTION
THROUGH ENDOTHELIAL PROGENITOR CELL AND
VASCULAR ENDOTHELIAL GROWTH FACTOR MEDIATED
NEOVASCULARIZATION. EUR HEART J. 2007;28(16):2018-
27. [BACK]
436.
MELONI M, CAPORALI A, GRAIANI G, ET AL. NERVE
GROWTH FACTOR PROMOTES CARDIAC REPAIR
FOLLOWING MYOCARDIAL INFARCTION. CIRC RES.
2010;106(7):1275-84. [BACK]
437.
ROTA M, PADIN-IRUEGAS ME, MISAO Y, ET AL. LOCAL
ACTIVATION OR IMPLANTATION OF CARDIAC
PROGENITOR CELLS RESCUES SCARRED INFARCTED
MYOCARDIUM IMPROVING CARDIAC FUNCTION. CIRC
RES. 2008;103(1):107-16. [BACK]
438.
II M, NISHIMURA H, IWAKURA A, ET AL. ENDOTHELIAL
PROGENITOR CELLS ARE RAPIDLY RECRUITED TO
MYOCARDIUM AND MEDIATE PROTECTIVE EFFECT OF
ISCHEMIC PRECONDITIONING VIA "IMPORTED" NITRIC
OXIDE SYNTHASE ACTIVITY. CIRCULATION.
2005;111(9):1114-20. [BACK]
439.
TAGHAVI S, GEORGE JC. HOMING OF STEM CELLS TO
ISCHEMIC MYOCARDIUM. AM J TRANSL RES.
2013;5(4):404-11. [BACK]
440.
RUIFROK WP, DE BOER RA, IWAKURA A, ET AL.
ESTRADIOL-INDUCED, ENDOTHELIAL PROGENITOR
CELL-MEDIATED NEOVASCULARIZATION IN MALE MICE
WITH HIND-LIMB ISCHEMIA. VASC MED. 2009;14(1):29-36.
[BACK]
441.
IWAKURA A, SHASTRY S, LUEDEMANN C, ET AL.
ESTRADIOL ENHANCES RECOVERY AFTER
MYOCARDIAL INFARCTION BY AUGMENTING
INCORPORATION OF BONE MARROW-DERIVED
ENDOTHELIAL PROGENITOR CELLS INTO SITES OF
ISCHEMIA-INDUCED NEOVASCULARIZATION VIA
ENDOTHELIAL NITRIC OXIDE SYNTHASE-MEDIATED
ACTIVATION OF MATRIX METALLOPROTEINASE-9.
CIRCULATION. 2006;113(12):1605-14. [BACK]
442.
BERGSLAND M, COVACU R, PEREZ ESTRADA C,
SVENSSON M, BRUNDIN L. NITRIC OXIDE-INDUCED
NEURONAL TO GLIAL LINEAGE FATE-CHANGE DEPENDS
ON NRSF/REST FUNCTION IN NEURAL PROGENITOR
CELLS. STEM CELLS. 2014;32(9):2539-49. [BACK]
443.DRUMMOND-BARBOSA D. STEM CELLS, THEIR
NICHES AND THE SYSTEMIC ENVIRONMENT: AN AGING
NETWORK. GENETICS. 2008;180(4):1787-97. [BACK]
444.TOWNS CR, JONES DG. STEM CELLS, EMBRYOS,
AND THE ENVIRONMENT: A CONTEXT FOR BOTH
SCIENCE AND ETHICS. J MED ETHICS. 2004;30(4):410-3.
[BACK]
445.GATTAZZO F, URCIUOLO A, BONALDO P.
EXTRACELLULAR MATRIX: A DYNAMIC
MICROENVIRONMENT FOR STEM CELL NICHE. BIOCHIM
BIOPHYS ACTA. 2014;1840(8):2506-19. [BACK]
446.
TOKAR EJ, DIWAN BA, WAALKES MP. ARSENIC
EXPOSURE TRANSFORMS HUMAN EPITHELIAL
STEM/PROGENITOR CELLS INTO A CANCER STEM-LIKE
PHENOTYPE. ENVIRON HEALTH PERSPECT.
2010;118(1):108-15. [BACK]
447.
XU Y, TOKAR EJ, PERSON RJ, ORIHUELA RG, NGALAME
NN, WAALKES MP. RECRUITMENT OF NORMAL STEM
CELLS TO AN ONCOGENIC PHENOTYPE BY
NONCONTIGUOUS CARCINOGEN-TRANSFORMED
EPITHELIA DEPENDS ON THE TRANSFORMING
CARCINOGEN. ENVIRON HEALTH PERSPECT.
2013;121(8):944-50. [BACK]
448.
LOWE SW, LIN AW. APOPTOSIS IN CANCER.
CARCINOGENESIS. 2000;21(3):485-95. [BACK]
449. WYLLIE AH, KERR JF, CURRIE AR. CELL DEATH:
THE SIGNIFICANCE OF APOPTOSIS. INT REV CYTOL.
1980;68:251-306. [BACK]
450.KERR JF, WYLLIE AH, CURRIE AR. APOPTOSIS: A
BASIC BIOLOGICAL PHENOMENON WITH WIDE-
RANGING IMPLICATIONS IN TISSUE KINETICS. BR J
CANCER. 1972;26(4):239-57. [BACK]
451.
WONG SY, REITER JF. WOUNDING MOBILIZES HAIR
FOLLICLE STEM CELLS TO FORM TUMORS. PROC NATL
ACAD SCI USA. 2011;108(10):4093-8. [BACK]
452.
HOUGHTON J, STOICOV C, NOMURA S, ET AL. GASTRIC
CANCER ORIGINATING FROM BONE MARROW-DERIVED
CELLS. SCIENCE. 2004;306(5701):1568-71. [BACK]
453.KASPER M, JAKS V, ARE A, ET AL. WOUNDING
ENHANCES EPIDERMAL TUMORIGENESIS BY
RECRUITING HAIR FOLLICLE KERATINOCYTES. PROC
NATL ACAD SCI USA. 2011;108(10):4099-104. [BACK]
454. GRACHTCHOUK M, PERO J, YANG SH, ET AL. BASAL
CELL CARCINOMAS IN MICE ARISE FROM HAIR
FOLLICLE STEM CELLS AND MULTIPLE EPITHELIAL
PROGENITOR POPULATIONS. J CLIN INVEST.
2011;121(5):1768-81. [BACK]
455.DONOVAN J. REVIEW OF THE HAIR FOLLICLE
ORIGIN HYPOTHESIS FOR BASAL CELL CARCINOMA.
DERMATOL SURG. 2009;35(9):1311-23. [BACK]
456. HUTCHIN ME, KARIAPPER MS, GRACHTCHOUK M,
ET AL. SUSTAINED HEDGEHOG SIGNALING IS REQUIRED
FOR BASAL CELL CARCINOMA PROLIFERATION AND
SURVIVAL: CONDITIONAL SKIN TUMORIGENESIS
RECAPITULATES THE HAIR GROWTH CYCLE. GENES
DEV. 2005;19(2):214-23. [BACK]
GUPTA S, TAKEBE N, LORUSSO P. TARGETING THE
457.
HEDGEHOG PATHWAY IN CANCER. THER ADV MED
ONCOL. 2010;2(4):237-50. [BACK]
CATALANO V, TURDO A, DI FRANCO S, DIELI F,
458.
TODARO M, STASSI G. TUMOR AND ITS
MICROENVIRONMENT: A SYNERGISTIC INTERPLAY.
SEMIN CANCER BIOL. 2013;23(6 PT B):522-32. [BACK]
459.
HONG M, TAN HY, LI S, ET AL. CANCER STEM CELLS:
THE POTENTIAL TARGETS OF CHINESE MEDICINES AND
THEIR ACTIVE COMPOUNDS. INT J MOL SCI. 2016;17(6).
[BACK]
460.DRAGU DL, NECULA LG, BLEOTU C, DIACONU CC,
CHIVU-ECONOMESCU M. THERAPIES TARGETING
CANCER STEM CELLS: CURRENT TRENDS AND FUTURE
CHALLENGES. WORLD J STEM CELLS. 2015;7(9):1185-201.
[BACK]
461.BAEK SJ, ISHII H, TAMARI K, ET AL. CANCER STEM
CELLS: THE POTENTIAL OF CARBON ION BEAM
RADIATION AND NEW RADIOSENSITIZERS (REVIEW).
ONCOL REP. 2015;34(5):2233-7. [BACK]
462. HONG IS, LEE HY, NAM JS. CANCER STEM CELLS:
THE 'ACHILLES HEEL' OF CHEMO-RESISTANT TUMORS.
RECENT PAT ANTICANCER DRUG DISCOV. 2015;10(1):2-22.
[BACK]
463. VOCHEM R, EINENKEL J, HORN LC, RUSCHPLER P.
[IMPORTANCE OF THE TUMOR STEM CELL HYPOTHESIS
FOR UNDERSTANDING OVARIAN CANCER]. PATHOLOGE.
2014;35(4):361-70. [BACK]
464.CHHABRA R. CERVICAL CANCER STEM CELLS:
OPPORTUNITIES AND CHALLENGES. J CANCER RES CLIN
ONCOL. 2015;141(11):1889-97. [BACK]
465.AHMED N, ABUBAKER K, FINDLAY JK. OVARIAN
CANCER STEM CELLS: MOLECULAR CONCEPTS AND
RELEVANCE AS THERAPEUTIC TARGETS. MOL ASPECTS
MED. 2014;39:110-25. [BACK]
466.AHMED N, ABUBAKER K, FINDLAY J, QUINN M.
CANCEROUS OVARIAN STEM CELLS: OBSCURE
TARGETS FOR THERAPY BUT RELEVANT TO
CHEMORESISTANCE. J CELL BIOCHEM. 2013;114(1):21-34.
[BACK]
467.BAR JK, GRELEWSKI P, LIS-NAWARA A,
DROBNIKOWSKA K. [THE ROLE OF CANCER STEM
CELLS IN PROGRESSIVE GROWTH AND RESISTANCE OF
OVARIAN CANCER: TRUE OR FICTION?]. POSTEPY HIG
MED DOSW (ONLINE). 2015;69:1077-86. [BACK]
468. CHEN K, HUANG YH, CHEN JL. UNDERSTANDING
AND TARGETING CANCER STEM CELLS: THERAPEUTIC
IMPLICATIONS AND CHALLENGES. ACTA PHARMACOL
SIN. 2013;34(6):732-40. [BACK]
469.OGAWA K, YOSHIOKA Y, ISOHASHI F, SEO Y,
YOSHIDA K, YAMAZAKI H. RADIOTHERAPY TARGETING
CANCER STEM CELLS: CURRENT VIEWS AND FUTURE
PERSPECTIVES. ANTICANCER RES. 2013;33(3):747-54.
[BACK]
470.ZHANG Q, FENG Y, KENNEDY D. MULTIDRUG-
RESISTANT CANCER CELLS AND CANCER STEM CELLS
HIJACK CELLULAR SYSTEMS TO CIRCUMVENT
SYSTEMIC THERAPIES, CAN NATURAL PRODUCTS
REVERSE THIS?. CELL MOL LIFE SCI. 2017;74(5):777-801.
[BACK]
471.CHEN LS, WANG AX, DONG B, PU KF, YUAN LH, ZHU
YM. A NEW PROSPECT IN CANCER THERAPY:
TARGETING CANCER STEM CELLS TO ERADICATE
CANCER. CHIN J CANCER. 2012;31(12):564-72. [BACK]
HU Y, FU L. TARGETING CANCER STEM CELLS: A
472.
NEW THERAPY TO CURE CANCER PATIENTS. AM J
CANCER RES. 2012;2(3):340-56. [BACK]
473.KIM YJ, SIEGLER EL, SIRIWON N, WANG P.
THERAPEUTIC STRATEGIES FOR TARGETING CANCER
STEM CELLS. J CANCER METASTA TREAT 2016;2:233-42.
[BACK]
474. UNDERSTANDING AND TARGETING CANCER STEM
CELLS: THERAPEUTIC IMPLICATIONS AND
CHALLENGES. ACTA PHARMACOLOGICA SINICA.
2013;34(6):732. [BACK]
475.
FACUCHO-OLIVEIRA JM, ST JOHN JC. THE
RELATIONSHIP BETWEEN PLURIPOTENCY AND
MITOCHONDRIAL DNA PROLIFERATION DURING EARLY
EMBRYO DEVELOPMENT AND EMBRYONIC STEM CELL
DIFFERENTIATION. STEM CELL REV. 2009;5(2):140-58.
[BACK]
476.
WANET A, ARNOULD T, NAJIMI M, RENARD P.
CONNECTING MITOCHONDRIA, METABOLISM, AND
STEM CELL FATE. STEM CELLS DEV. 2015;24(17):1957-71.
[BACK]
477.
HARRIS H. THE ANALYSIS OF MALIGNANCY BY CELL
FUSION: THE POSITION IN 1988. CANCER RES.
1988;48(12):3302-6. [BACK]
478.SZENT-GYÖRGYI A. THE LIVING STATE AND
CANCER. PROC NATL ACAD SCI USA. 1977;74(7):2844-7.
[BACK]
479.SOTO AM, SONNENSCHEIN C. THE SOMATIC
MUTATION THEORY OF CANCER: GROWING PROBLEMS
WITH THE PARADIGM?. BIOESSAYS. 2004;26(10):1097-107.
[BACK]
480.
ABDOUH M, ZHOU S, ARENA V, ET AL. TRANSFER OF
MALIGNANT TRAIT TO IMMORTALIZED HUMAN CELLS
FOLLOWING EXPOSURE TO HUMAN CANCER SERUM. J
EXP CLIN CANCER RES. 2014;33:86. [BACK]
481.
GERSCHENSON M, GRAVES K, CARSON SD, WELLS RS,
PIERCE GB. REGULATION OF MELANOMA BY THE
EMBRYONIC SKIN. PROC NATL ACAD SCI USA.
1986;83(19):7307-10. [BACK]
482. POSTOVIT LM, MARGARYAN NV, SEFTOR EA,
HENDRIX MJ. ROLE OF NODAL SIGNALING AND THE
MICROENVIRONMENT UNDERLYING MELANOMA
PLASTICITY. PIGMENT CELL MELANOMA RES.
2008;21(3):348-57. [BACK]
483. ZHOU S, ABDOUH M, ARENA V, ARENA M, ARENA
GO. REPROGRAMMING MALIGNANT CANCER CELLS
TOWARD A BENIGN PHENOTYPE FOLLOWING
EXPOSURE TO HUMAN EMBRYONIC STEM CELL
MICROENVIRONMENT. PLOS ONE. 2017;12(1):E0169899.
[BACK]
484. ABBOTT DE, POSTOVIT LM, SEFTOR EA,
MARGARYAN NV, SEFTOR RE, HENDRIX MJ. EXPLOITING
THE CONVERGENCE OF EMBRYONIC AND
TUMORIGENIC SIGNALING PATHWAYS TO DEVELOP
NEW THERAPEUTIC TARGETS. STEM CELL REV.
2007;3(1):68-78. [BACK]
485.D'ANGELO RC, WICHA MS. STEM CELLS IN
NORMAL DEVELOPMENT AND CANCER. PROG MOL BIOL
TRANSL SCI. 2010;95:113-58. [BACK]
486. VERNEY EL, PIERCE GB, DIXON FJ. THE BIOLOGY
OF TESTICULAR CANCER. III. HETEROTRANSPLANTED
CHORIOCARCINOMAS. CANCER RES. 1959;19(6, PART
1):633-7. [BACK]
487. POSTOVIT LM, SEFTOR EA, SEFTOR RE, HENDRIX
MJ. TARGETING NODAL IN MALIGNANT MELANOMA
CELLS. EXPERT OPIN THER TARGETS. 2007;11(4):497-505.
[BACK]
488.HENDRIX MJ, SEFTOR EA, KIRSCHMANN DA,
QUARANTA V, SEFTOR RE. REMODELING OF THE
MICROENVIRONMENT BY AGGRESSIVE MELANOMA
TUMOR CELLS. ANN N Y ACAD SCI. 2003;995:151-61.
[BACK]
489. HENDRIX MJ, SEFTOR EA, SEFTOR RE, KASEMEIER-
KULESA J, KULESA PM, POSTOVIT LM.
REPROGRAMMING METASTATIC TUMOUR CELLS WITH
EMBRYONIC MICROENVIRONMENTS. NAT REV CANCER.
2007;7(4):246-55. [BACK]
490. DÍEZ-TORRE A, ANDRADE R, EGUIZÁBAL C, ET AL.
REPROGRAMMING OF MELANOMA CELLS BY
EMBRYONIC MICROENVIRONMENTS. INT J DEV BIOL.
2009;53(8-10):1563-8. [BACK]
491.LEE LM, SEFTOR EA, BONDE G, CORNELL RA,
HENDRIX MJ. THE FATE OF HUMAN MALIGNANT
MELANOMA CELLS TRANSPLANTED INTO ZEBRAFISH
EMBRYOS: ASSESSMENT OF MIGRATION AND CELL
DIVISION IN THE ABSENCE OF TUMOR FORMATION. DEV
DYN. 2005;233(4):1560-70. [BACK]
492.SEFTOR EA, BROWN KM, CHIN L, ET AL.
EPIGENETIC TRANSDIFFERENTIATION OF NORMAL
MELANOCYTES BY A METASTATIC MELANOMA
MICROENVIRONMENT. CANCER RES. 2005;65(22):10164-9.
[BACK]
493.
POSTOVIT LM, SEFTOR EA, SEFTOR RE, HENDRIX MJ.
INFLUENCE OF THE MICROENVIRONMENT ON
MELANOMA CELL FATE DETERMINATION AND
PHENOTYPE. CANCER RES. 2006;66(16):7833-6. [BACK]
494.
VESELÁ A, WILHELM J. THE ROLE OF CARBON DIOXIDE
IN FREE RADICAL REACTIONS OF THE ORGANISM.
PHYSIOL RES. 2002;51(4):335-9. [BACK]
SQUADRITO GL, PRYOR WA. OXIDATIVE
495.
CHEMISTRY OF NITRIC OXIDE: THE ROLES OF
SUPEROXIDE, PEROXYNITRITE, AND CARBON DIOXIDE.
FREE RADIC BIOL MED. 1998;25(4-5):392-403. [BACK]
496. KOGAN AKH, GRACHEV SV, ELISEEVA SV,
BOLEVICH S. [ABILITY OF CARBON DIOXIDE TO INHIBIT
GENERATION OF SUPEROXIDE ANION RADICAL IN
CELLS AND ITS BIOMEDICAL ROLE]. VOPR MED KHIM.
1996;42(3):193-202. [BACK]
497. KOGAN AKH, MANUĬLOV BM, GRACHEV SV,
BOLEVICH S, TSYPIN AB, DANILIAK IG. [CO2--A
NATURAL INHIBITOR OF ACTIVE OXYGEN FORM
GENERATION BY PHAGOCYTES]. BIULL EKSP BIOL MED.
1994;118(10):395-8. [BACK]
498. KOGAN AKH, GRACHEV SV, ELISEEVA SV,
BOLEVICH S. [CARBON DIOXIDE--A UNIVERSAL
INHIBITOR OF THE GENERATION OF ACTIVE OXYGEN
FORMS BY CELLS (DECIPHERING ONE ENIGMA OF
EVOLUTION)]. IZV AKAD NAUK SER BIOL. 1997;(2):204-
17. [BACK]
499. BOLJEVIC S, KOGAN AH, GRACEV SV, JELISEJEVA
SV, DANILJAK IG. [CARBON DIOXIDE INHIBITS THE
GENERATION OF ACTIVE FORMS OF OXYGEN IN HUMAN
AND ANIMAL CELLS AND THE SIGNIFICANCE OF THE
PHENOMENON IN BIOLOGY AND MEDICINE].
VOJNOSANIT PREGL. 1996;53(4):261-74. [BACK]
500. BAEV VI, VASIL'EVA IV, L'VOV SN, SHUGALEĬ IV.
[THE UNKNOWN PHYSIOLOGICAL ROLE OF CARBON
DIOXIDE]. FIZIOL ZH IM I M SECHENOVA. 1995;81(2):47-
52. [BACK]
501. KOGAN AKH, BOLEVICH S, DANILIAK IG.
[COMPARATIVE STUDY OF THE EFFECT OF CARBON
DIOXIDE ON THE GENERATION OF ACTIVE FORMS OF
OXYGEN BY LEUKOCYTES IN HEALTH AND IN
BRONCHIAL ASTHMA]. PATOL FIZIOL EKSP TER. 1995;
(3):34-40. [BACK]
502.
BOLEVICH S, KOGAN AH, ZIVKOVIC V, ET AL.
PROTECTIVE ROLE OF CARBON DIOXIDE (CO2) IN
GENERATION OF REACTIVE OXYGEN SPECIES. MOL
CELL BIOCHEM. 2016;411(1-2):317-30. [BACK]
503.
SANDULACHE VC, PAREKH A, LI-KOROTKY HS, DOHAR
JE, HEBDA PA. PROSTAGLANDIN E2 DIFFERENTIALLY
MODULATES HUMAN FETAL AND ADULT DERMAL
FIBROBLAST MIGRATION AND CONTRACTION:
IMPLICATION FOR WOUND HEALING. WOUND REPAIR
REGEN. 2006;14(5):633-43. [BACK]
504.
VAUGHAN RA, GARCIA-SMITH R, TRUJILLO KA, BISOFFI
M. TUMOR NECROSIS FACTOR ALPHA INCREASES
AEROBIC GLYCOLYSIS AND REDUCES OXIDATIVE
METABOLISM IN PROSTATE EPITHELIAL CELLS.
PROSTATE. 2013;73(14):1538-46. [BACK]
505.
LIECHTY KW, ADZICK NS, CROMBLEHOLME TM.
DIMINISHED INTERLEUKIN 6 (IL-6) PRODUCTION
DURING SCARLESS HUMAN FETAL WOUND REPAIR.
CYTOKINE. 2000;12(6):671-6. [BACK]
506.
LIECHTY KW, CROMBLEHOLME TM, CASS DL, MARTIN
B, ADZICK NS. DIMINISHED INTERLEUKIN-8 (IL-8)
PRODUCTION IN THE FETAL WOUND HEALING
RESPONSE. J SURG RES. 1998;77(1):80-4. [BACK]
507.
ADZICK NS, LORENZ HP. CELLS, MATRIX, GROWTH
FACTORS, AND THE SURGEON. THE BIOLOGY OF
SCARLESS FETAL WOUND REPAIR. ANN SURG.
1994;220(1):10-8. [BACK]
508.
WILGUS TA, BERGDALL VK, TOBER KL, ET AL. THE
IMPACT OF CYCLOOXYGENASE-2 MEDIATED
INFLAMMATION ON SCARLESS FETAL WOUND
HEALING. AM J PATHOL. 2004;165(3):753-61. [BACK]
509.
GUIDO C, WHITAKER-MENEZES D, CAPPARELLI C, ET
AL. METABOLIC REPROGRAMMING OF CANCER-
ASSOCIATED FIBROBLASTS BY TGF-Β DRIVES TUMOR
GROWTH: CONNECTING TGF-Β SIGNALING WITH
"WARBURG-LIKE" CANCER METABOLISM AND L-
LACTATE PRODUCTION. CELL CYCLE. 2012;11(16):3019-
35. [BACK]
510.
CHO JS, HAN IH, LEE HR, LEE HM. PROSTAGLANDIN E2
INDUCES IL-6 AND IL-8 PRODUCTION BY THE EP
RECEPTORS/AKT/NF-ΚB PATHWAYS IN NASAL POLYP-
DERIVED FIBROBLASTS. ALLERGY ASTHMA IMMUNOL
RES. 2014;6(5):449-57. [BACK]
511. HINSON RM, WILLIAMS JA, SHACTER E. ELEVATED
INTERLEUKIN 6 IS INDUCED BY PROSTAGLANDIN E2 IN
A MURINE MODEL OF INFLAMMATION: POSSIBLE ROLE
OF CYCLOOXYGENASE-2. PROC NATL ACAD SCI USA.
1996;93(10):4885-90. [BACK]
512.CARISTI S, PIRAINO G, CUCINOTTA M, VALENTI A,
LODDO S, TETI D. PROSTAGLANDIN E2 INDUCES
INTERLEUKIN-8 GENE TRANSCRIPTION BY ACTIVATING
C/EBP HOMOLOGOUS PROTEIN IN HUMAN T
LYMPHOCYTES. J BIOL CHEM. 2005;280(15):14433-42.
[BACK]
513. YU Y, CHADEE K. PROSTAGLANDIN E2 STIMULATES
IL-8 GENE EXPRESSION IN HUMAN COLONIC
EPITHELIAL CELLS BY A POSTTRANSCRIPTIONAL
MECHANISM. J IMMUNOL. 1998;161(7):3746-52. [BACK]
514.RAMIREZ-YAÑEZ GO, HAMLET S, JONARTA A,
SEYMOUR GJ, SYMONS AL. PROSTAGLANDIN E2
ENHANCES TRANSFORMING GROWTH FACTOR-BETA 1
AND TGF-BETA RECEPTORS SYNTHESIS: AN IN VIVO
AND IN VITRO STUDY. PROSTAGLANDINS LEUKOT
ESSENT FATTY ACIDS. 2006;74(3):183-92. [BACK]
515.RICCIOTTI E, FITZGERALD GA. PROSTAGLANDINS
AND INFLAMMATION. ARTERIOSCLER THROMB VASC
BIOL. 2011;31(5):986-1000. [BACK]
516.
GUYENET SJ, CARLSON SE. INCREASE IN ADIPOSE
TISSUE LINOLEIC ACID OF US ADULTS IN THE LAST
HALF CENTURY. ADV NUTR. 2015;6(6):660-4. [BACK]
517. NOUROOZ-ZADEH J, PEREIRA P. AGE-RELATED
ACCUMULATION OF FREE POLYUNSATURATED FATTY
ACIDS IN HUMAN RETINA. OPHTHALMIC RES.
1999;31(4):273-9. [BACK]
518. LEE J, YU BP, HERLIHY JT. MODULATION OF
CARDIAC MITOCHONDRIAL MEMBRANE FLUIDITY BY
AGE AND CALORIE INTAKE. FREE RADIC BIOL MED.
1999;26(3-4):260-5. [BACK]
519.SMÍDOVÁ L, BASE J, MOUREK J, CECHOVÁ I.
PROPORTION OF INDIVIDUAL FATTY ACIDS IN THE NON-
ESTERIFIED (FREE) FATTY ACID (FFA) FRACTION IN THE
SERUM OF LABORATORY RATS OF DIFFERENT AGES.
PHYSIOL BOHEMOSLOV. 1990;39(2):125-34. [BACK]
520.SCHÄFER L, OVERVAD K, THORLING EB,
VELANDER G. ADIPOSE TISSUE LEVELS OF FATTY ACIDS
AND TOCOPHEROL IN YOUNG AND OLD WOMEN. ANN
NUTR METAB. 1989;33(6):315-22. [BACK]
521. LAGANIERE S, YU BP. MODULATION OF
MEMBRANE PHOSPHOLIPID FATTY ACID COMPOSITION
BY AGE AND FOOD RESTRICTION. GERONTOLOGY.
1993;39(1):7-18. [BACK]
522.QI K, HALL M, DECKELBAUM RJ. LONG-CHAIN
POLYUNSATURATED FATTY ACID ACCRETION IN BRAIN.
CURR OPIN CLIN NUTR METAB CARE. 2002;5(2):133-8.
[BACK]
523.GUERRA A, DEMMELMAIR H, TOSCHKE AM,
KOLETZKO B. THREE-YEAR TRACKING OF FATTY ACID
COMPOSITION OF PLASMA PHOSPHOLIPIDS IN HEALTHY
CHILDREN. ANN NUTR METAB. 2007;51(5):433-8. [BACK]
524. CROWE FL, SKEAFF CM, GREEN TJ, GRAY AR.
SERUM N-3 LONG-CHAIN PUFA DIFFER BY SEX AND AGE
IN A POPULATION-BASED SURVEY OF NEW ZEALAND
ADOLESCENTS AND ADULTS. BR J NUTR. 2008;99(1):168-
74. [BACK]
525.LAGANIERE S, YU BP. ANTI-LIPOPEROXIDATION
ACTION OF FOOD RESTRICTION. BIOCHEM BIOPHYS RES
COMMUN. 1987;145(3):1185-91. [BACK]
526. WALKER CG, BROWNING LM, MANDER AP, ET AL.
AGE AND SEX DIFFERENCES IN THE INCORPORATION OF
EPA AND DHA INTO PLASMA FRACTIONS, CELLS AND
ADIPOSE TISSUE IN HUMANS. BR J NUTR. 2014;111(4):679-
89. [BACK]
527.
PARADIES G, RUGGIERO FM, PETROSILLO G,
QUAGLIARIELLO E. AGE-DEPENDENT DECLINE IN THE
CYTOCHROME C OXIDASE ACTIVITY IN RAT HEART
MITOCHONDRIA: ROLE OF CARDIOLIPIN. FEBS LETT.
1997;406(1-2):136-8. [BACK]
528.
PARADIES G, PETROSILLO G, GADALETA MN,
RUGGIERO FM. THE EFFECT OF AGING AND ACETYL-L-
CARNITINE ON THE PYRUVATE TRANSPORT AND
OXIDATION IN RAT HEART MITOCHONDRIA. FEBS LETT.
1999;454(3):207-9. [BACK]
529.
ORRENIUS S, ZHIVOTOVSKY B. CARDIOLIPIN
OXIDATION SETS CYTOCHROME C FREE. NAT CHEM
BIOL. 2005;1(4):188-9. [BACK]
530.IVERSON SL, ORRENIUS S. THE CARDIOLIPIN-
CYTOCHROME C INTERACTION AND THE
MITOCHONDRIAL REGULATION OF APOPTOSIS. ARCH
BIOCHEM BIOPHYS. 2004;423(1):37-46. [BACK]
531.PARADIES G, PARADIES V, DE BENEDICTIS V,
RUGGIERO FM, PETROSILLO G. FUNCTIONAL ROLE OF
CARDIOLIPIN IN MITOCHONDRIAL BIOENERGETICS.
BIOCHIM BIOPHYS ACTA. 2014;1837(4):408-17. [BACK]
532.HANSKE J, TOFFEY JR, MORENZ AM, BONILLA AJ,
SCHIAVONI KH, PLETNEVA EV. CONFORMATIONAL
PROPERTIES OF CARDIOLIPIN-BOUND CYTOCHROME C.
PROC NATL ACAD SCI USA. 2012;109(1):125-30. [BACK]
533.
LEE HJ, MAYETTE J, RAPOPORT SI, BAZINET RP.
SELECTIVE REMODELING OF CARDIOLIPIN FATTY
ACIDS IN THE AGED RAT HEART. LIPIDS HEALTH DIS.
2006;5:2. [BACK]
534.
BRONNIKOV GE, KULAGINA TP, ARIPOVSKY AV.
DIETARY SUPPLEMENTATION OF OLD RATS WITH
HYDROGENATED PEANUT OIL RESTORES ACTIVITIES OF
MITOCHONDRIAL RESPIRATORY COMPLEXES IN
SKELETAL MUSCLES. BIOCHEMISTRY MOSC.
2010;75(12):1491-7. [BACK]
535.
EHRLICH P. UEBER DEN JETZIGEN STAND DER
KARZINOMFORSCHUNG. NED TIJDSCHR GENEESKD.
1909;5:73–290. [BACK]
536.
KIM R, EMI M, TANABE K. CANCER IMMUNOEDITING
FROM IMMUNE SURVEILLANCE TO IMMUNE ESCAPE.
IMMUNOLOGY. 2007;121(1):1-14. [BACK]
537.
 SHANKARAN V, IKEDA H, BRUCE AT, ET AL. IFNGAMMA
AND LYMPHOCYTES PREVENT PRIMARY TUMOUR
DEVELOPMENT AND SHAPE TUMOUR
IMMUNOGENICITY. NATURE. 2001;410(6832):1107-11.
[BACK]
538.GIRARDI M, OPPENHEIM DE, STEELE CR, ET AL.
REGULATION OF CUTANEOUS MALIGNANCY BY
GAMMADELTA T CELLS. SCIENCE. 2001;294(5542):605-9.
[BACK]
539. DUNN GP, BRUCE AT, SHEEHAN KC, ET AL. A
CRITICAL FUNCTION FOR TYPE I INTERFERONS IN
CANCER IMMUNOEDITING. NAT IMMUNOL. 2005;6(7):722-
9. [BACK]
540. KAPLAN DH, SHANKARAN V, DIGHE AS, ET AL.
DEMONSTRATION OF AN INTERFERON GAMMA-
DEPENDENT TUMOR SURVEILLANCE SYSTEM IN
IMMUNOCOMPETENT MICE. PROC NATL ACAD SCI USA.
1998;95(13):7556-61. [BACK]
541. STREET SE, TRAPANI JA, MACGREGOR D, SMYTH
MJ. SUPPRESSION OF LYMPHOMA AND EPITHELIAL
MALIGNANCIES EFFECTED BY INTERFERON GAMMA. J
EXP MED. 2002;196(1):129-34. [BACK]
542. SMYTH MJ, THIA KY, STREET SE, MACGREGOR D,
GODFREY DI, TRAPANI JA. PERFORIN-MEDIATED
CYTOTOXICITY IS CRITICAL FOR SURVEILLANCE OF
SPONTANEOUS LYMPHOMA. J EXP MED. 2000;192(5):755-
60. [BACK]
543.
HAYWARD AR, LEVY J, FACCHETTI F, ET AL.
CHOLANGIOPATHY AND TUMORS OF THE PANCREAS,
LIVER, AND BILIARY TREE IN BOYS WITH X-LINKED
IMMUNODEFICIENCY WITH HYPER-IGM. J IMMUNOL.
1997;158(2):977-83. [BACK]
544. MUELLER BU, PIZZO PA. CANCER IN CHILDREN
WITH PRIMARY OR SECONDARY IMMUNODEFICIENCIES.
J PEDIATR. 1995;126(1):1-10. [BACK]
545. VAN DER MEER JW, WEENING RS, SCHELLEKENS
PT, VAN MUNSTER IP, NAGENGAST FM. COLORECTAL
CANCER IN PATIENTS WITH X-LINKED
AGAMMAGLOBULINAEMIA. LANCET.
1993;341(8858):1439-40. [BACK]
546.GATTI RA, GOOD RA. OCCURRENCE OF
MALIGNANCY IN IMMUNODEFICIENCY DISEASES. A
LITERATURE REVIEW. CANCER. 1971;28(1):89-98. [BACK]
547. KINLEN LJ, WEBSTER AD, BIRD AG, ET AL.
PROSPECTIVE STUDY OF CANCER IN PATIENTS WITH
HYPOGAMMAGLOBULINAEMIA. LANCET.
1985;1(8423):263-6. [BACK]
548. SALAVOURA K, KOLIALEXI A, TSANGARIS G,
MAVROU A. DEVELOPMENT OF CANCER IN PATIENTS
WITH PRIMARY IMMUNODEFICIENCIES. ANTICANCER
RES. 2008;28(2B):1263-9. [BACK]
549. SCHREIBER RD, OLD LJ, SMYTH MJ. CANCER
IMMUNOEDITING: INTEGRATING IMMUNITY'S ROLES IN
CANCER SUPPRESSION AND PROMOTION. SCIENCE.
2011;331(6024):1565-70. [BACK]
550.BOSHOFF C, WHITBY D, TALBOT S, WEISS RA.
ETIOLOGY OF AIDS-RELATED KAPOSI'S SARCOMA AND
LYMPHOMA. ORAL DIS. 1997;3 SUPPL 1:S129-32. [BACK]
551.
MUELLER N. OVERVIEW OF THE EPIDEMIOLOGY OF
MALIGNANCY IN IMMUNE DEFICIENCY. J ACQUIR
IMMUNE DEFIC SYNDR. 1999;21 SUPPL 1:S5-10. [BACK]
552.
GEORGE J. FRIOU, M.D., “RELATIONSHIP OF
MALIGNANCY, AUTOIMMUNITY, AND IMMUNOLOGICAL
DISEASE,” ANNALS OF THE NEW YORK ACADEMY OF
SCIENCES, MARCH 18, 1974, 44-45, 48. [BACK]
553.
GOLDSTEIN MR, MASCITELLI L. SURGERY AND
CANCER PROMOTION: ARE WE TRADING BEAUTY FOR
CANCER?. QJM. 2011;104(9):811-5. [BACK]
554.
SAKAI Y, TAKAYANAGI K, OHNO M, INOSE R, FUJIWARA
H. A TRIAL OF IMPROVEMENT OF IMMUNITY IN CANCER
PATIENTS BY LAUGHTER THERAPY. JPN HOSP. 2013;
(32):53-9. [BACK]
555.
HAYASHI K, KAWACHI I, OHIRA T, KONDO K, SHIRAI K,
KONDO N. LAUGHTER IS THE BEST MEDICINE? A CROSS-
SECTIONAL STUDY OF CARDIOVASCULAR DISEASE
AMONG OLDER JAPANESE ADULTS. J EPIDEMIOL.
2016;26(10):546-552. [BACK]
556.
FAIREY AS, COURNEYA KS, FIELD CJ, MACKEY JR.
PHYSICAL EXERCISE AND IMMUNE SYSTEM FUNCTION
IN CANCER SURVIVORS: A COMPREHENSIVE REVIEW
AND FUTURE DIRECTIONS. CANCER. 2002;94(2):539-51.
[BACK]
557.
GLEESON M. IMMUNE FUNCTION IN SPORT AND
EXERCISE. J APPL PHYSIOL. 2007;103(2):693-9. [BACK]
558.
FRIEDENREICH CM, CUST AE. PHYSICAL ACTIVITY AND
BREAST CANCER RISK: IMPACT OF TIMING, TYPE AND
DOSE OF ACTIVITY AND POPULATION SUBGROUP
EFFECTS. BR J SPORTS MED. 2008;42(8):636-47. [BACK]
559. GIOVANNUCCI E, ASCHERIO A, RIMM EB, COLDITZ
GA, STAMPFER MJ, WILLETT WC. PHYSICAL ACTIVITY,
OBESITY, AND RISK FOR COLON CANCER AND
ADENOMA IN MEN. ANN INTERN MED. 1995;122(5):327-34.
[BACK]
560.GIOVANNUCCI E, COLDITZ GA, STAMPFER MJ,
WILLETT WC. PHYSICAL ACTIVITY, OBESITY, AND RISK
OF COLORECTAL ADENOMA IN WOMEN (UNITED
STATES). CANCER CAUSES CONTROL. 1996;7(2):253-63.
[BACK]
561. THUNE I, FURBERG AS. PHYSICAL ACTIVITY AND
CANCER RISK: DOSE-RESPONSE AND CANCER, ALL
SITES AND SITE-SPECIFIC. MED SCI SPORTS EXERC.
2001;33(6 SUPPL):S530-50. [BACK]
562.
BANG O. THE LACTATE CONTENT OF BLOOD DURING
AND AFTER MUSCULAR EXERCISE IN MAN. SCAND.
ARCH. PHYSIOL. 1936;74:51–82. [BACK]
563. OWLES WH. ALTERATIONS IN THE LACTIC ACID
CONTENT OF THE BLOOD AS A RESULT OF LIGHT
EXERCISE, AND ASSOCIATED CHANGES IN THE CO(2)-
COMBINING POWER OF THE BLOOD AND IN THE
ALVEOLAR CO(2) PRESSURE. J PHYSIOL (LOND).
1930;69(2):214-37. [BACK]
564. GHOSH AK. ANAEROBIC THRESHOLD: ITS CONCEPT
AND ROLE IN ENDURANCE SPORT. MALAYS J MED SCI.
2004;11(1):24-36. [BACK]
565.
MEYER T, FAUDE O, SCHARHAG J, URHAUSEN A,
KINDERMANN W. IS LACTIC ACIDOSIS A CAUSE OF
EXERCISE INDUCED HYPERVENTILATION AT THE
RESPIRATORY COMPENSATION POINT?. BR J SPORTS
MED. 2004;38(5):622-5. [BACK]
566.
NIEMAN DC. IS INFECTION RISK LINKED TO EXERCISE
WORKLOAD?. MED SCI SPORTS EXERC. 2000;32(7
SUPPL):S406-11. [BACK]
567.NIEMAN DC. IMMUNONUTRITION SUPPORT FOR
ATHLETES. NUTR REV. 2008;66(6):310-20. [BACK]
568. GLEESON M. IMMUNE SYSTEM ADAPTATION IN
ELITE ATHLETES. CURR OPIN CLIN NUTR METAB CARE.
2006;9(6):659-65. [BACK]
569. JEURISSEN A, BOSSUYT X, CEUPPENS JL, HESPEL P.
[THE EFFECTS OF PHYSICAL EXERCISE ON THE IMMUNE
SYSTEM]. NED TIJDSCHR GENEESKD. 2003;147(28):1347-
51. [BACK]
570.MACKINNON LT. CHRONIC EXERCISE TRAINING
EFFECTS ON IMMUNE FUNCTION. MED SCI SPORTS
EXERC. 2000;32(7 SUPPL):S369-76. [BACK]
571.
SHAIKH SR, EDIDIN M. IMMUNOSUPPRESSIVE EFFECTS
OF POLYUNSATURATED FATTY ACIDS ON ANTIGEN
PRESENTATION BY HUMAN LEUKOCYTE ANTIGEN
CLASS I MOLECULES. J LIPID RES. 2007;48(1):127-38.
[BACK]
572. HUGHES DA, PINDER AC. N-3 POLYUNSATURATED
FATTY ACIDS INHIBIT THE ANTIGEN-PRESENTING
FUNCTION OF HUMAN MONOCYTES. AM J CLIN NUTR.
2000;71(1 SUPPL):357S-60S. [BACK]
573. GEYEREGGER R, ZEYDA M, ZLABINGER GJ,
WALDHÄUSL W, STULNIG TM. POLYUNSATURATED
FATTY ACIDS INTERFERE WITH FORMATION OF THE
IMMUNOLOGICAL SYNAPSE. J LEUKOC BIOL.
2005;77(5):680-8. [BACK]
574. SHAIKH SR, EDIDIN M. POLYUNSATURATED FATTY
ACIDS, MEMBRANE ORGANIZATION, T CELLS, AND
ANTIGEN PRESENTATION. AM J CLIN NUTR.
2006;84(6):1277-89. [BACK]
575. VAN DER HEIDE JJ, BILO HJ, DONKER JM, WILMINK
JM, TEGZESS AM. EFFECT OF DIETARY FISH OIL ON
RENAL FUNCTION AND REJECTION IN CYCLOSPORINE-
TREATED RECIPIENTS OF RENAL TRANSPLANTS. N
ENGL J MED. 1993;329(11):769-73. [BACK]
576.IZGÜT-UYSAL VN, TAN R, BÜLBÜL M, DERIN N.
EFFECT OF STRESS-INDUCED LIPID PEROXIDATION ON
FUNCTIONS OF RAT PERITONEAL MACROPHAGES. CELL
BIOL INT. 2004;28(7):517-21. [BACK]
577. MASCIOLI EA, BISTRIAN BR, BABAYAN VK,
BLACKBURN GL. MEDIUM CHAIN TRIGLYCERIDES AND
STRUCTURED LIPIDS AS UNIQUE NONGLUCOSE
ENERGY SOURCES IN HYPERALIMENTATION. LIPIDS.
1987;22(6):421-3. [BACK]
578.
BENNETT WM, CARPENTER CB, SHAPIRO ME, ET AL.
DELAYED OMEGA-3 FATTY ACID SUPPLEMENTS IN
RENAL TRANSPLANTATION. A DOUBLE-BLIND,
PLACEBO-CONTROLLED STUDY. TRANSPLANTATION.
1995;59(3):352-6. [BACK]
579. MERTIN J. LETTER: UNSATURATED FATTY ACIDS
AND RENAL TRANSPLANTATION. LANCET.
1974;2(7882):717. [BACK]
580.MCHUGH MI, WILKINSON R, ELLIOTT RW, ET AL.
IMMUNOSUPPRESSION WITH POLYUNSATURATED
FATTY ACIDS IN RENAL TRANSPLANTATION.
TRANSPLANTATION. 1977;24(4):263-7. [BACK]
581.
GUIMARÃES AR, SITNIK RH, CURI CM, CURI R.
POLYUNSATURATED AND SATURATED FATTY ACIDS-
RICH DIETS AND IMMUNE TISSUES. 2. MAXIMAL
ACTIVITIES OF KEY ENZYMES OF GLUTAMINOLYSIS,
GLYCOLYSIS, PENTOSE-PHOSPHATE-PATHWAY AND
KREBS CYCLE IN THYMUS, SPLEEN AND MESENTERIC
LYMPH NODES. BIOCHEM INT. 1990;22(6):1015-23. [BACK]
582.
 C. J. MEADE AND J. MARTIN, ADV. LIPID RES., 127, 1978.
[BACK]
583.
POPOVICI D, MIHAI N, URBANAVICIUS V.
ABNORMALITIES OF OXIDATIVE PHOSPHORYLATION
DUE TO EXCESS OF DEFICIENCY OF THYROID
HORMONES. ENDOCRINOLOGIE. 1980;18(3):143-7. [BACK]
584.MARTINEZ B, DEL HOYO P, MARTIN MA, ARENAS J,
PEREZ-CASTILLO A, SANTOS A. THYROID HORMONE
REGULATES OXIDATIVE PHOSPHORYLATION IN THE
CEREBRAL CORTEX AND STRIATUM OF NEONATAL
RATS. J NEUROCHEM. 2001;78(5):1054-63. [BACK]
585. HARPER ME, SEIFERT EL. THYROID HORMONE
EFFECTS ON MITOCHONDRIAL ENERGETICS. THYROID.
2008;18(2):145-56. [BACK]
586. LANNI A, MORENO M, GOGLIA F. MITOCHONDRIAL
ACTIONS OF THYROID HORMONE. COMPR PHYSIOL.
2016;6(4):1591-1607. [BACK]
587. YEHUDA-SHNAIDMAN E, KALDERON B, BAR-TANA
J. THYROID HORMONE, THYROMIMETICS, AND
METABOLIC EFFICIENCY. ENDOCR REV. 2014;35(1):35-58.
[BACK]
588. VERHOEVEN AJ, KAMER P, GROEN AK, TAGER JM.
EFFECTS OF THYROID HORMONE ON MITOCHONDRIAL
OXIDATIVE PHOSPHORYLATION. BIOCHEM J.
1985;226(1):183-92. [BACK]
589.
SINGHAL H, GREENE ME, TARULLI G, ET AL. GENOMIC
AGONISM AND PHENOTYPIC ANTAGONISM BETWEEN
ESTROGEN AND PROGESTERONE RECEPTORS IN
BREAST CANCER. SCI ADV. 2016;2(6):E1501924. [BACK]
590. BEHERA MA, DAI Q, GARDE R, SANER C, JUNGHEIM
E, PRICE TM. PROGESTERONE STIMULATES
MITOCHONDRIAL ACTIVITY WITH SUBSEQUENT
INHIBITION OF APOPTOSIS IN MCF-10A BENIGN BREAST
EPITHELIAL CELLS. AM J PHYSIOL ENDOCRINOL METAB.
2009;297(5):E1089-96. [BACK]
591.KALRA PS, KALRA SP. PROGESTERONE
STIMULATES TESTOSTERONE SECRETION IN MALE
RATS. NEUROENDOCRINOLOGY. 1980;30(3):183-6. [BACK]
592. SCHWEIZER MT, ANTONARAKIS ES, WANG H, ET
AL. EFFECT OF BIPOLAR ANDROGEN THERAPY FOR
ASYMPTOMATIC MEN WITH CASTRATION-RESISTANT
PROSTATE CANCER: RESULTS FROM A PILOT CLINICAL
STUDY. SCI TRANSL MED. 2015;7(269):269RA2. [BACK]
593.VALLÉE M, VITIELLO S, BELLOCCHIO L, ET AL.
PREGNENOLONE CAN PROTECT THE BRAIN FROM
CANNABIS INTOXICATION. SCIENCE. 2014;343(6166):94-8.
[BACK]
594. PATEL MA, KATYARE SS.
DEHYDROEPIANDROSTERONE (DHEA) TREATMENT
STIMULATES OXIDATIVE ENERGY METABOLISM IN THE
CEREBRAL MITOCHONDRIA FROM DEVELOPING RATS.
INT J DEV NEUROSCI. 2006;24(5):327-34. [BACK]
595. PATEL MA, MODI HR, KATYARE SS. STIMULATION
OF OXIDATIVE ENERGY METABOLISM IN LIVER
MITOCHONDRIA FROM OLD AND YOUNG RATS BY
TREATMENT WITH DEHYDROEPIANDROSTERONE
(DHEA). A COMPARATIVE STUDY. AGE (DORDR).
2007;29(1):41-9. [BACK]
596.PATEL MA, KATYARE SS. TREATMENT WITH
DEHYDROEPIANDROSTERONE (DHEA) STIMULATES
OXIDATIVE ENERGY METABOLISM IN THE LIVER
MITOCHONDRIA FROM DEVELOPING RATS. MOL CELL
BIOCHEM. 2006;293(1-2):193-201. [BACK]
597.PATEL MA, KATYARE SS. TREATMENT WITH
DEHYDROEPIANDROSTERONE (DHEA) STIMULATES
OXIDATIVE ENERGY METABOLISM IN THE CEREBRAL
MITOCHONDRIA. A COMPARATIVE STUDY OF EFFECTS
IN OLD AND YOUNG ADULT RATS. NEUROSCI LETT.
2006;402(1-2):131-6. [BACK]
598.CLEARY MP. EFFECT OF
DEHYDROEPIANDROSTERONE TREATMENT ON LIVER
METABOLISM IN RATS. INT J BIOCHEM. 1990;22(3):205-10.
[BACK]
599.MUTHUSAMY T, MURUGESAN P, SRINIVASAN C,
BALASUBRAMANIAN K. SEX STEROIDS INFLUENCE
GLUCOSE OXIDATION THROUGH MODULATION OF
INSULIN RECEPTOR EXPRESSION AND IRS-1 SERINE
PHOSPHORYLATION IN TARGET TISSUES OF ADULT
MALE RAT. MOL CELL BIOCHEM. 2011;352(1-2):35-45.
[BACK]
600.TORO-URREGO N, GARCIA-SEGURA LM,
ECHEVERRIA V, BARRETO GE. TESTOSTERONE
PROTECTS MITOCHONDRIAL FUNCTION AND
REGULATES NEUROGLOBIN EXPRESSION IN
ASTROCYTIC CELLS EXPOSED TO GLUCOSE
DEPRIVATION. FRONT AGING NEUROSCI. 2016;8:152.
[BACK]
601.WANG F, YANG J, SUN J, ET AL. TESTOSTERONE
REPLACEMENT ATTENUATES MITOCHONDRIAL
DAMAGE IN A RAT MODEL OF MYOCARDIAL
INFARCTION. J ENDOCRINOL. 2015;225(2):101-11. [BACK]
602. PARTHASARATHY C, RENUKA VN,
BALASUBRAMANIAN K. SEX STEROIDS ENHANCE
INSULIN RECEPTORS AND GLUCOSE OXIDATION IN
CHANG LIVER CELLS. CLIN CHIM ACTA. 2009;399(1-2):49-
53. [BACK]
603.
TINKER, B. (2015). CHOLESTEROL IN FOOD NOT A
CONCERN, REPORT SAYS. CNN. [ONLINE]. AVAILABLE:
HTTP://WWW.CNN.COM/2015/02/19/HEALTH/DIETARY-
GUIDELINES.[MARCH 1, 2017]. [BACK]
604.
SINGH-MANOUX A, GIMENO D, KIVIMAKI M, BRUNNER
E, MARMOT MG. LOW HDL CHOLESTEROL IS A RISK
FACTOR FOR DEFICIT AND DECLINE IN MEMORY IN
MIDLIFE: THE WHITEHALL II STUDY. ARTERIOSCLER
THROMB VASC BIOL. 2008;28(8):1556-62. [BACK]
605.
HUANG X, AUINGER P, EBERLY S, ET AL. SERUM
CHOLESTEROL AND THE PROGRESSION OF
PARKINSON'S DISEASE: RESULTS FROM DATATOP. PLOS
ONE. 2011;6(8):E22854. [BACK]
606.
ENGELBERG H. LOW SERUM CHOLESTEROL AND
SUICIDE. LANCET. 1992;339(8795):727-9. [BACK]
607. BOSCARINO JA, ERLICH PM, HOFFMAN SN. LOW
SERUM CHOLESTEROL AND EXTERNAL-CAUSE
MORTALITY: POTENTIAL IMPLICATIONS FOR RESEARCH
AND SURVEILLANCE. J PSYCHIATR RES. 2009;43(9):848-
54. [BACK]
608. HAWTHON K, COWEN P, OWENS D, BOND A,
ELLIOTT M. LOW SERUM CHOLESTEROL AND SUICIDE.
BR J PSYCHIATRY. 1993;162:818-25. [BACK]
609.
HORWICH TB, HAMILTON MA, MACLELLAN WR,
FONAROW GC. LOW SERUM TOTAL CHOLESTEROL IS
ASSOCIATED WITH MARKED INCREASE IN MORTALITY
IN ADVANCED HEART FAILURE. J CARD FAIL.
2002;8(4):216-24. [BACK]
610. BAE JM, YANG YJ, LI ZM, AHN YO. LOW
CHOLESTEROL IS ASSOCIATED WITH MORTALITY FROM
CARDIOVASCULAR DISEASES: A DYNAMIC COHORT
STUDY IN KOREAN ADULTS. J KOREAN MED SCI.
2012;27(1):58-63. [BACK]
611. FROOM P, KRISTAL-BONEH E, MELAMED S, HARARI
G, BENBASSAT J, RIBAK J. SERUM TOTAL CHOLESTEROL
AND CARDIOVASCULAR MORTALITY IN ISRAELI
MALES: THE CORDIS STUDY. CARDIOVASCULAR
OCCUPATIONAL RISK FACTOR DETERMINATION IN
ISRAELI INDUSTRY. ISR MED ASSOC J. 2000;2(9):668-71.
[BACK]
612.RAVNSKOV U, DIAMOND DM, HAMA R, ET AL.
LACK OF AN ASSOCIATION OR AN INVERSE
ASSOCIATION BETWEEN LOW-DENSITY-LIPOPROTEIN
CHOLESTEROL AND MORTALITY IN THE ELDERLY: A
SYSTEMATIC REVIEW. BMJ OPEN. 2016;6(6):E010401.
[BACK]
613.
KNEKT P, REUNANEN A, AROMAA A, HELIÖVAARA M,
HAKULINEN T, HAKAMA M. SERUM CHOLESTEROL AND
RISK OF CANCER IN A COHORT OF 39,000 MEN AND
WOMEN. J CLIN EPIDEMIOL. 1988;41(6):519-30. [BACK]
614. NAGO N, ISHIKAWA S, GOTO T, KAYABA K. LOW
CHOLESTEROL IS ASSOCIATED WITH MORTALITY FROM
STROKE, HEART DISEASE, AND CANCER: THE JICHI
MEDICAL SCHOOL COHORT STUDY. J EPIDEMIOL.
2011;21(1):67-74. [BACK]
615. BEHAR S, GRAFF E, REICHER-REISS H, ET AL. LOW
TOTAL CHOLESTEROL IS ASSOCIATED WITH HIGH
TOTAL MORTALITY IN PATIENTS WITH CORONARY
HEART DISEASE. THE BEZAFIBRATE INFARCTION
PREVENTION (BIP) STUDY GROUP. EUR HEART J.
1997;18(1):52-9. [BACK]
616.EICHHOLZER M, STÄHELIN HB, GUTZWILLER F,
LÜDIN E, BERNASCONI F. ASSOCIATION OF LOW
PLASMA CHOLESTEROL WITH MORTALITY FOR CANCER
AT VARIOUS SITES IN MEN: 17-Y FOLLOW-UP OF THE
PROSPECTIVE BASEL STUDY. AM J CLIN NUTR.
2000;71(2):569-74. [BACK]
617.
ILLINGWORTH DR, HARRIS WS, CONNOR WE.
INHIBITION OF LOW DENSITY LIPOPROTEIN SYNTHESIS
BY DIETARY OMEGA-3 FATTY ACIDS IN HUMANS.
ARTERIOSCLEROSIS. 1984;4(3):270-5. [BACK]
618. CONNOR WE, DEFRANCESCO CA, CONNOR SL. N-3
FATTY ACIDS FROM FISH OIL. EFFECTS ON PLASMA
LIPOPROTEINS AND HYPERTRIGLYCERIDEMIC
PATIENTS. ANN N Y ACAD SCI. 1993;683:16-34. [BACK]
619. KARANTH S, TRAN VM, KUBERAN B, SCHLEGEL A.
POLYUNSATURATED FATTY ACYL-COENZYME AS ARE
INHIBITORS OF CHOLESTEROL BIOSYNTHESIS IN
ZEBRAFISH AND MICE. DIS MODEL MECH. 2013;6(6):1365-
77. [BACK]
620. SPADY DK. REGULATORY EFFECTS OF INDIVIDUAL
N-6 AND N-3 POLYUNSATURATED FATTY ACIDS ON LDL
TRANSPORT IN THE RAT. J LIPID RES. 1993;34(8):1337-46.
[BACK]
621.
ILLINGWORTH DR, HARRIS WS, CONNOR WE.
INHIBITION OF LOW DENSITY LIPOPROTEIN SYNTHESIS
BY DIETARY OMEGA-3 FATTY ACIDS IN HUMANS.
ARTERIOSCLEROSIS. 1984;4(3):270-5. [BACK]
622.
O'BRIEN T, KATZ K, HODGE D, NGUYEN TT, KOTTKE BA,
HAY ID. THE EFFECT OF THE TREATMENT OF
HYPOTHYROIDISM AND HYPERTHYROIDISM ON
PLASMA LIPIDS AND APOLIPOPROTEINS AI, AII AND E.
CLIN ENDOCRINOL (OXF). 1997;46(1):17-20. [BACK]
623. CANARIS GJ, MANOWITZ NR, MAYOR G, RIDGWAY
EC. THE COLORADO THYROID DISEASE PREVALENCE
STUDY. ARCH INTERN MED. 2000;160(4):526-34. [BACK]
624.TURNER KB, STEINER A. A LONG TERM STUDY OF
THE VARIATION OF SERUM CHOLESTEROL IN MAN. J
CLIN INVEST. 1939;18(1):45-9. [BACK]
625. FELD S, DICKEY RA. AN ASSOCIATION BETWEEN
VARYING DEGREES OF HYPOTHYROIDISM AND
HYPERCHOLESTEROLEMIA IN WOMEN: THE THYROID-
CHOLESTEROL CONNECTION. PREV CARDIOL.
2001;4(4):179-182. [BACK]
626. ORIBE H. [CLINICAL STUDIES ON LIPID
METABOLISM IN HYPERTHYROIDISM AND
HYPOTHYROIDISM--EVALUATION OF SERUM
APOLIPOPROTEIN LEVELS BEFORE AND AFTER
TREATMENT]. NIHON NAIBUNPI GAKKAI ZASSHI.
1989;65(8):781-93. [BACK]
627.MULS E, BLATON V, ROSSENEU M, LESAFFRE E,
LAMBERIGTS G, DE MOOR P. SERUM LIPIDS AND
APOLIPOPROTEINS A-I, A-II, AND B IN
HYPERTHYROIDISM BEFORE AND AFTER TREATMENT. J
CLIN ENDOCRINOL METAB. 1982;55(3):459-64. [BACK]
628.KUNG AW, PANG RW, LAUDER I, LAM KS, JANUS ED.
CHANGES IN SERUM LIPOPROTEIN(A) AND LIPIDS
DURING TREATMENT OF HYPERTHYROIDISM. CLIN
CHEM. 1995;41(2):226-31. [BACK]
629. DIEKMAN MJ, ANGHELESCU N, ENDERT E, BAKKER
O, WIERSINGA WM. CHANGES IN PLASMA LOW-DENSITY
LIPOPROTEIN (LDL)- AND HIGH-DENSITY LIPOPROTEIN
CHOLESTEROL IN HYPO- AND HYPERTHYROID
PATIENTS ARE RELATED TO CHANGES IN FREE
THYROXINE, NOT TO POLYMORPHISMS IN LDL
RECEPTOR OR CHOLESTEROL ESTER TRANSFER
PROTEIN GENES. J CLIN ENDOCRINOL METAB.
2000;85(5):1857-62. [BACK]
MEIER C, STAUB JJ, ROTH CB, ET AL. TSH-
630.
CONTROLLED L-THYROXINE THERAPY REDUCES
CHOLESTEROL LEVELS AND CLINICAL SYMPTOMS IN
SUBCLINICAL HYPOTHYROIDISM: A DOUBLE BLIND,
PLACEBO-CONTROLLED TRIAL (BASEL THYROID
STUDY). J CLIN ENDOCRINOL METAB. 2001;86(10):4860-6.
[BACK]
631.IQBAL A, JORDE R, FIGENSCHAU Y. SERUM LIPID
LEVELS IN RELATION TO SERUM THYROID-
STIMULATING HORMONE AND THE EFFECT OF
THYROXINE TREATMENT ON SERUM LIPID LEVELS IN
SUBJECTS WITH SUBCLINICAL HYPOTHYROIDISM: THE
TROMSØ STUDY. J INTERN MED. 2006;260(1):53-61.
[BACK]
632.KUNG AW, PANG RW, JANUS ED. ELEVATED SERUM
LIPOPROTEIN(A) IN SUBCLINICAL HYPOTHYROIDISM.
CLIN ENDOCRINOL (OXF). 1995;43(4):445-9. [BACK]
633.MIKHAIL GS, ALSHAMMARI SM, ALENEZI MY,
MANSOUR M, KHALIL NA. INCREASED ATHEROGENIC
LOW-DENSITY LIPOPROTEIN CHOLESTEROL IN
UNTREATED SUBCLINICAL HYPOTHYROIDISM. ENDOCR
PRACT. 2008;14(5):570-5. [BACK]
634. DANESE MD, LADENSON PW, MEINERT CL, POWE
NR. CLINICAL REVIEW 115: EFFECT OF THYROXINE
THERAPY ON SERUM LIPOPROTEINS IN PATIENTS WITH
MILD THYROID FAILURE: A QUANTITATIVE REVIEW OF
THE LITERATURE. J CLIN ENDOCRINOL METAB.
2000;85(9):2993-3001. [BACK]
635. SHIN DJ, OSBORNE TF. THYROID HORMONE
REGULATION AND CHOLESTEROL METABOLISM ARE
CONNECTED THROUGH STEROL REGULATORY
ELEMENT-BINDING PROTEIN-2 (SREBP-2). J BIOL CHEM.
2003;278(36):34114-8. [BACK]
636. THOMPSON GR, SOUTAR AK, SPENGEL FA, JADHAV
A, GAVIGAN SJ, MYANT NB. DEFECTS OF RECEPTOR-
MEDIATED LOW DENSITY LIPOPROTEIN CATABOLISM IN
HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA
AND HYPOTHYROIDISM IN VIVO. PROC NATL ACAD SCI
USA. 1981;78(4):2591-5. [BACK]
637. PUGSLEY LI. THE EFFECT OF THYROTROPIC
HORMONE UPON SERUM CHOLESTEROL. BIOCHEM J.
1935;29(3):513-6. [BACK]
638.JUNG CH, SUNG KC, SHIN HS, ET AL. THYROID
DYSFUNCTION AND THEIR RELATION TO
CARDIOVASCULAR RISK FACTORS SUCH AS LIPID
PROFILE, HSCRP, AND WAIST HIP RATIO IN KOREA.
KOREAN J INTERN MED. 2003;18(3):146-53. [BACK]
639. LUBOSHITZKY R, AVIV A, HERER P, LAVIE L. RISK
FACTORS FOR CARDIOVASCULAR DISEASE IN WOMEN
WITH SUBCLINICAL HYPOTHYROIDISM. THYROID.
2002;12(5):421-5. [BACK]
640. PESIĆ M, ANTIĆ S, KOCIĆ R, RADOJKOVIĆ D,
RADENKOVIĆ S. [CARDIOVASCULAR RISK FACTORS IN
PATIENTS WITH SUBCLINICAL HYPOTHYROIDISM].
VOJNOSANIT PREGL. 2007;64(11):749-52. [BACK]
641. WALSH JP, BREMNER AP, BULSARA MK, ET AL.
THYROID DYSFUNCTION AND SERUM LIPIDS: A
COMMUNITY-BASED STUDY. CLIN ENDOCRINOL (OXF).
2005;63(6):670-5. [BACK]
642. SERTER R, DEMIRBAS B, KORUKLUOGLU B, CULHA
C, CAKAL E, ARAL Y. THE EFFECT OF L-THYROXINE
REPLACEMENT THERAPY ON LIPID BASED
CARDIOVASCULAR RISK IN SUBCLINICAL
HYPOTHYROIDISM. J ENDOCRINOL INVEST.
2004;27(10):897-903. [BACK]
643. MILIONIS HJ, TAMBAKI AP, KANIOGLOU CN, ELISAF
MS, TSELEPIS AD, TSATSOULIS A. THYROID
SUBSTITUTION THERAPY INDUCES HIGH-DENSITY
LIPOPROTEIN-ASSOCIATED PLATELET-ACTIVATING
FACTOR-ACETYLHYDROLASE IN PATIENTS WITH
SUBCLINICAL HYPOTHYROIDISM: A POTENTIAL
ANTIATHEROGENIC EFFECT. THYROID. 2005;15(5):455-60.
[BACK]
644. ARINZON Z, ZUTA A, PEISAKH A, FELDMAN J,
BERNER Y. EVALUATION RESPONSE AND
EFFECTIVENESS OF THYROID HORMONE
REPLACEMENT TREATMENT ON LIPID PROFILE AND
FUNCTION IN ELDERLY PATIENTS WITH SUBCLINICAL
HYPOTHYROIDISM. ARCH GERONTOL GERIATR.
2007;44(1):13-9. [BACK]
645.MIURA S, IITAKA M, YOSHIMURA H, ET AL.
DISTURBED LIPID METABOLISM IN PATIENTS WITH
SUBCLINICAL HYPOTHYROIDISM: EFFECT OF L-
THYROXINE THERAPY. INTERN MED. 1994;33(7):413-7.
[BACK]
646.DZUGAN SA, ARNOLD SMITH R.
HYPERCHOLESTEROLEMIA TREATMENT: A NEW
HYPOTHESIS OR JUST AN ACCIDENT?. MED
HYPOTHESES. 2002;59(6):751-6. [BACK]
647.ALTHAUS BU, STAUB JJ, RYFF-DE LÈCHE A,
OBERHÄNSLI A, STÄHELIN HB. LDL/HDL-CHANGES IN
SUBCLINICAL HYPOTHYROIDISM: POSSIBLE RISK
FACTORS FOR CORONARY HEART DISEASE. CLIN
ENDOCRINOL (OXF). 1988;28(2):157-63. [BACK]
648. THORELL B, SVÄRDSUDD K. MYOCARDIAL
INFARCTION RISK FACTORS AND WELL-BEING AMONG
50-YEAR-OLD WOMEN BEFORE AND AFTER THE
MENOPAUSE. THE POPULATION STUDY "50-YEAR-OLD
PEOPLE IN KUNGSÖR". SCAND J PRIM HEALTH CARE.
1993;11(2):141-6. [BACK]
649.
ALTINTERIM B. ANTI-THYROID EFFECTS OF PUFAS
(POLYUNSATURATED FATS) AND HERBS. 2012. [BACK]
650.
 THE CONSCIOUS LIFE. FAT COMPOSITION OF OLIVE
OIL. [ONLINE]. AVAILABLE:
HTTPS://THECONSCIOUSLIFE.COM/FOODS/OLIVE-OIL-
04053.HTM.[MARCH 1, 2017]. [BACK]
651.
FUKUSEN N, KIDO H, KATUNUMA N. INHIBITION OF
CHYMASE ACTIVITY BY PHOSPHOGLYCERIDES. ARCH
BIOCHEM BIOPHYS. 1985;237(1):118-23. [BACK]
652.
TABACHNICK M, KORCEK L. EFFECT OF LONG-CHAIN
FATTY ACIDS ON THE BINDING OF THYROXINE AND
TRIIODOTHYRONINE TO HUMAN THYROXINE-BINDING
GLOBULIN. BIOCHIM BIOPHYS ACTA. 1986;881(2):292-6.
[BACK]
653.
CHOPRA IJ, HUANG TS, BEREDO A, SOLOMON DH, CHUA
TECO GN, MEAD JF. EVIDENCE FOR AN INHIBITOR OF
EXTRATHYROIDAL CONVERSION OF THYROXINE TO
3,5,3'-TRIIODOTHYRONINE IN SERA OF PATIENTS WITH
NONTHYROIDAL ILLNESSES. J CLIN ENDOCRINOL
METAB. 1985;60(4):666-72. [BACK]
654.
WIERSINGA WM, CHOPRA IJ, TECO GN. INHIBITION OF
NUCLEAR T3 BINDING BY FATTY ACIDS. METAB CLIN
EXP. 1988;37(10):996-1002. [BACK]
655.
RAFAEL J, PATZELT J, SCHÄFER H, ELMADFA I. THE
EFFECT OF ESSENTIAL FATTY ACID DEFICIENCY ON
BASAL RESPIRATION AND FUNCTION OF LIVER
MITOCHONDRIA IN RATS. J NUTR. 1984;114(2):255-62.
[BACK]
656.
WESSON LG, BURR GO. THE METABOLIC RATE AND
RESPIRATORY QUOTIENTS OF RATS ON A FAT-DEFICIENT
DIET. J. BIOL. CHEM. 1931;91:525-539. [BACK]
657.BURR GO, BEBER AJ. METABOLISM STUDIES WITH
RATS SUFFERING FROM FAT DEFICIENCY: SIX FIGURES. J
NUTR. 1937;14:553-566. [BACK]
658. GOUBERN M, YAZBECK J, SENAULT C, PORTET R.
NON-SHIVERING THERMOGENESIS AND BROWN
ADIPOSE TISSUE ACTIVITY IN ESSENTIAL FATTY ACID
DEFICIENT RATS. ARCH INT PHYSIOL BIOCHIM.
1990;98(4):193-9. [BACK]
659.RAFAEL J, PATZELT J, ELMADFA I. EFFECT OF
DIETARY LINOLEIC ACID AND ESSENTIAL FATTY ACID
DEFICIENCY ON RESTING METABOLISM,
NONSHIVERING THERMOGENESIS AND BROWN
ADIPOSE TISSUE IN THE RAT. J NUTR. 1988;118(5):627-32.
[BACK]
660.YAZBECK J, GOUBERN M, SENAULT C, CHAPEY MF,
PORTET R. THE EFFECTS OF ESSENTIAL FATTY ACID
DEFICIENCY ON BROWN ADIPOSE TISSUE ACTIVITY IN
RATS MAINTAINED AT THERMAL NEUTRALITY. COMP
BIOCHEM PHYSIOL A COMP PHYSIOL. 1989;94(2):273-6.
[BACK]
661.
O'REILLY I, MURPHY MP. STUDIES ON THE RAPID
STIMULATION OF MITOCHONDRIAL RESPIRATION BY
THYROID HORMONES. ACTA ENDOCRINOL.
1992;127(6):542-6. [BACK]
662.LOMBARDI A, MORENO M, DE LANGE P, IOSSA S,
BUSIELLO RA, GOGLIA F. REGULATION OF SKELETAL
MUSCLE MITOCHONDRIAL ACTIVITY BY THYROID
HORMONES: FOCUS ON THE "OLD" TRIIODOTHYRONINE
AND THE "EMERGING" 3,5-DIIODOTHYRONINE. FRONT
PHYSIOL. 2015;6:237. [BACK]
663.WEITZEL JM, IWEN KA, SEITZ HJ. REGULATION OF
MITOCHONDRIAL BIOGENESIS BY THYROID HORMONE.
EXP PHYSIOL. 2003;88(1):121-8. [BACK]
 WRUTNIAK-CABELLO C, CASAS F, CABELLO G.
664.
THYROID HORMONE ACTION IN MITOCHONDRIA. J MOL
ENDOCRINOL. 2001;26(1):67-77. [BACK]
665. VERHOEVEN AJ, KAMER P, GROEN AK, TAGER JM.
EFFECTS OF THYROID HORMONE ON MITOCHONDRIAL
OXIDATIVE PHOSPHORYLATION. BIOCHEM J.
1985;226(1):183-92. [BACK]
666. HOCH FL, LIPMANN F. THE UNCOUPLING OF
RESPIRATION AND PHOSPHORYLATION BY THYROID
HORMONES. PROC NATL ACAD SCI USA. 1954;40(10):909-
21. [BACK]
667.
WOOTEN WL, CASCARANO J. THE EFFECT OF THYROID
HORMONE ON MITOCHONDRIAL BIOGENESIS AND
CELLULAR HYPERPLASIA. J BIOENERG BIOMEMBR.
1980;12(1-2):1-12. [BACK]
668.LESMANA R, SINHA RA, SINGH BK, ZHOU J, OBHA
K, WU Y, YAU WWY, BAY BH, YEN PM. THYROID
HORMONE STIMULATION OF AUTOPHAGY IS ESSENTIAL
FOR MITOCHONDRIAL BIOGENESIS ACTIVITY IN
SKELETAL MUSCLE. ENDOCRINOLOGY. 2015;157(1).
[BACK]
669.WEITZEL JM, IWEN KA. COORDINATION OF
MITOCHONDRIAL BIOGENESIS BY THYROID HORMONE.
MOL CELL ENDOCRINOL. 2011;342(1-2):1-7. [BACK]
670.MARÍN-GARCÍA J. THYROID HORMONE AND
MYOCARDIAL MITOCHONDRIAL BIOGENESIS. VASCUL
PHARMACOL. 2010;52(3-4):120-30. [BACK]
671.CIOFFI F, SENESE R, LANNI A, GOGLIA F. THYROID
HORMONES AND MITOCHONDRIA: WITH A BRIEF LOOK
AT DERIVATIVES AND ANALOGUES. MOL CELL
ENDOCRINOL. 2013;379(1-2):51-61. [BACK]
672.NELSON BD. THYROID HORMONE REGULATION OF
MITOCHONDRIAL FUNCTION. COMMENTS ON THE
MECHANISM OF SIGNAL TRANSDUCTION. BIOCHIM
BIOPHYS ACTA. 1990;1018(2-3):275-7. [BACK]
673.
POTTINGER TG, CARRICK TR, HUGHES SE, BALM PH.
TESTOSTERONE, 11-KETOTESTOSTERONE, AND
ESTRADIOL-17 BETA MODIFY BASELINE AND STRESS-
INDUCED INTERRENAL AND CORTICOTROPIC ACTIVITY
IN TROUT. GEN COMP ENDOCRINOL. 1996;104(3):284-95.
[BACK]
674.
KATOH K, ASARI M, ISHIWATA H, SASAKI Y, OBARA Y.
SATURATED FATTY ACIDS SUPPRESS
ADRENOCORTICOTROPIC HORMONE (ACTH) RELEASE
FROM RAT ANTERIOR PITUITARY CELLS IN VITRO.
COMP BIOCHEM PHYSIOL, PART A MOL INTEGR
PHYSIOL. 2004;137(2):357-64. [BACK]
675.OH YT, KIM J, KANG I, YOUN JH. REGULATION OF
HYPOTHALAMIC-PITUITARY-ADRENAL AXIS BY
CIRCULATING FREE FATTY ACIDS IN MALE WISTAR
RATS: ROLE OF INDIVIDUAL FREE FATTY ACIDS.
ENDOCRINOLOGY. 2014;155(3):923-31. [BACK]
676. JANKORD R, GANJAM VK, TURK JR, HAMILTON MT,
LAUGHLIN MH. EXERCISE TRAINING ALTERS EFFECT OF
HIGH-FAT FEEDING ON THE ACTH STRESS RESPONSE IN
PIGS. APPL PHYSIOL NUTR METAB. 2008;33(3):461-9.
[BACK]
677.
VAN SCHALKWIJK DB, PASMAN WJ, HENDRIKS HF, ET
AL. DIETARY MEDIUM CHAIN FATTY ACID
SUPPLEMENTATION LEADS TO REDUCED VLDL
LIPOLYSIS AND UPTAKE RATES IN COMPARISON TO
LINOLEIC ACID SUPPLEMENTATION. PLOS ONE.
2014;9(7):E100376. [BACK]
678.
 GOODFRIEND TL, BALL DL, RAFF H, BRUDER ED,
GARDNER HW, SPITELLER G. OXIDIZED PRODUCTS OF
LINOLEIC ACID STIMULATE ADRENAL
STEROIDOGENESIS. ENDOCR RES. 2002;28(4):325-30.
[BACK]
679.BRUDER ED, BALL DL, GOODFRIEND TL, RAFF H.
AN OXIDIZED METABOLITE OF LINOLEIC ACID
STIMULATES CORTICOSTERONE PRODUCTION BY RAT
ADRENAL CELLS. AM J PHYSIOL REGUL INTEGR COMP
PHYSIOL. 2003;284(6):R1631-5. [BACK]
680.ABOU-SAMRA AB, CATT KJ, AGUILERA G. ROLE OF
ARACHIDONIC ACID IN THE REGULATION OF
ADRENOCORTICOTROPIN RELEASE FROM RAT
ANTERIOR PITUITARY CELL CULTURES.
ENDOCRINOLOGY. 1986;119(4):1427-31. [BACK]
681.MONTERO D, TEROVA G, RIMOLDI S, ET AL.
MODULATION OF ADRENOCORTICOTROPHIN HORMONE
(ACTH)-INDUCED EXPRESSION OF STRESS-RELATED
GENES BY PUFA IN INTER-RENAL CELLS FROM
EUROPEAN SEA BASS (DICENTRARCHUS LABRAX). J
NUTR SCI. 2015;4:E16. [BACK]
682. GANGA R, BELL JG, MONTERO D, ET AL.
ADRENOCORTICOTROPHIC HORMONE-STIMULATED
CORTISOL RELEASE BY THE HEAD KIDNEY INTER-
RENAL TISSUE FROM SEA BREAM (SPARUS AURATA)
FED WITH LINSEED OIL AND SOYABEAN OIL. BR J NUTR.
2011;105(2):238-47. [BACK]
683. GANGA R, TORT L, ACERETE L, MONTERO D,
IZQUIERDO MS. MODULATION OF ACTH-INDUCED
CORTISOL RELEASE BY POLYUNSATURATED FATTY
ACIDS IN INTERRENAL CELLS FROM GILTHEAD
SEABREAM, SPARUS AURATA. J ENDOCRINOL.
2006;190(1):39-45. [BACK]
684.WON JG, ORTH DN. ROLE OF LIPOXYGENASE
METABOLITES OF ARACHIDONIC ACID IN THE
REGULATION OF ADRENOCORTICOTROPIN SECRETION
BY PERIFUSED RAT ANTERIOR PITUITARY CELLS.
ENDOCRINOLOGY. 1994;135(4):1496-503. [BACK]
685.
REED MJ, BERANEK PA, CHENG RW, JAMES VH. FREE
FATTY ACIDS: A POSSIBLE REGULATOR OF THE
AVAILABLE OESTRADIOL FRACTIONS IN PLASMA. J
STEROID BIOCHEM. 1986;24(2):657-9. [BACK]
686. BRUNING PF, BONFRER JM. POSSIBLE RELEVANCE
OF STEROID AVAILABILITY AND BREAST CANCER. ANN
N Y ACAD SCI. 1988;538:257-64. [BACK]
687. BENASSAYAG C, RIGOURD V, MIGNOT TM, ET AL.
DOES HIGH POLYUNSATURATED FREE FATTY ACID
LEVEL AT THE FETO-MATERNAL INTERFACE ALTER
STEROID HORMONE MESSAGE DURING PREGNANCY?.
PROSTAGLANDINS LEUKOT ESSENT FATTY ACIDS.
1999;60(5-6):393-9. [BACK]
688. REED MJ, DUNKLEY SA, SINGH A, THOMAS BS,
HAINES AP, CRUICKSHANK JK. THE ROLE OF FREE
FATTY ACIDS IN REGULATING THE TISSUE
AVAILABILITY AND SYNTHESIS OF SEX STEROIDS.
PROSTAGLANDINS LEUKOT ESSENT FATTY ACIDS.
1993;48(1):111-6. [BACK]
689.
VAIOPOULOS AG, ATHANASOULA KCH, PAPAVASSILIOU
AG. NF-ΚB IN COLORECTAL CANCER. J MOL MED.
2013;91(9):1029-37. [BACK]
690.
DENTON RM, ASHCROFT SJ. A TRIBUTE TO THE LIFE
AND WORK OF PHILIP RANDLE. DIABETOLOGIA.
2007;50(7):1359-61. [BACK]
691.
 RANDLE PJ. REGULATORY INTERACTIONS BETWEEN
LIPIDS AND CARBOHYDRATES: THE GLUCOSE FATTY
ACID CYCLE AFTER 35 YEARS. DIABETES METAB REV.
1998;14(4):263-83. [BACK]
692.
HOSIOS AM, HECHT VC, JOHNSON M, RATHMELL JC,
MANALIS SR, VANDER HEIDEN MG. AMINO ACIDS
RATHER THAN GLUCOSE ACCOUNTS FOR THE
MAJORITY OF CELL MASS IN RAPIDLY PROLIFERATING
MAMMALIAN CELLS. MOLECULAR CANCER RESEARCH.
2016;14(1):A36. [BACK]
693.RAJAGOPALAN KN, EGNATCHIK RA, CALVARUSO
MA, ET AL. METABOLIC PLASTICITY MAINTAINS
PROLIFERATION IN PYRUVATE DEHYDROGENASE
DEFICIENT CELLS. CANCER METAB. 2015;3:7. [BACK]
694.SEYFRIED TN. IS MITOCHONDRIAL GLUTAMINE
FERMENTATION A MISSING LINK IN THE METABOLIC
THEORY OF CANCER? 2012. PP. 133-144. [BACK]
695. GU Y, CHEN T, FU S, ET AL. PERIOPERATIVE
DYNAMICS AND SIGNIFICANCE OF AMINO ACID
PROFILES IN PATIENTS WITH CANCER. J TRANSL MED.
2015;13:35. [BACK]
696. DEREZIŃSKI P, KLUPCZYNSKA A, SAWICKI W,
PAŁKA JA, KOKOT ZJ. AMINO ACID PROFILES OF SERUM
AND URINE IN SEARCH FOR PROSTATE CANCER
BIOMARKERS: A PILOT STUDY. INT J MED SCI.
2017;14(1):1-12. [BACK]
697.
ANDERSEN DK. DIABETES AND CANCER: PLACING THE
ASSOCIATION IN PERSPECTIVE. CURR OPIN
ENDOCRINOL DIABETES OBES. 2013;20(2):81-6. [BACK]
698.CUI Y, ANDERSEN DK. DIABETES AND PANCREATIC
CANCER. ENDOCR RELAT CANCER. 2012;19(5):F9-F26.
[BACK]
699.SALVATORE T, MARFELLA R, RIZZO MR, SASSO FC.
PANCREATIC CANCER AND DIABETES: A TWO-WAY
RELATIONSHIP IN THE PERSPECTIVE OF
DIABETOLOGIST. INT J SURG. 2015;21 SUPPL 1:S72-7.
[BACK]
700. MUNIRAJ T, CHARI ST. DIABETES AND PANCREATIC
CANCER. MINERVA GASTROENTEROL DIETOL.
2012;58(4):331-45. [BACK]
701. SCIACCA L, VIGNERI R, TUMMINIA A, ET AL.
CLINICAL AND MOLECULAR MECHANISMS FAVORING
CANCER INITIATION AND PROGRESSION IN DIABETIC
PATIENTS. NUTR METAB CARDIOVASC DIS.
2013;23(9):808-15. [BACK]
702.TORIOLA AT, STOLZENBERG-SOLOMON R,
DALIDOWITZ L, LINEHAN D, COLDITZ G. DIABETES AND
PANCREATIC CANCER SURVIVAL: A PROSPECTIVE
COHORT-BASED STUDY. BR J CANCER. 2014;111(1):181-5.
[BACK]
703. ROSTA A. [DIABETES AND CANCER RISK:
ONCOLOGIC CONSIDERATIONS]. ORV HETIL.
2011;152(29):1144-55. [BACK]
704. BUYSSCHAERT M, SADIKOT S. DIABETES AND
CANCER: A 2013 SYNOPSIS. DIABETES METAB SYNDR.
2013;7(4):247-50. [BACK]
705.
MCDERMOTT WV. METABOLISM AND TOXICITY OF
AMMONIA. N ENGL J MED. 1957;257(22):1076-81. [BACK]
706.
LEKE R, BAK LK, ANKER M, ET AL. DETOXIFICATION OF
AMMONIA IN MOUSE CORTICAL GABAERGIC CELL
CULTURES INCREASES NEURONAL OXIDATIVE
METABOLISM AND REVEALS AN EMERGING ROLE FOR
RELEASE OF GLUCOSE-DERIVED ALANINE. NEUROTOX
RES. 2011;19(3):496-510. [BACK]
707. KALA G, HERTZ L. AMMONIA EFFECTS ON
PYRUVATE/LACTATE PRODUCTION IN ASTROCYTES--
INTERACTION WITH GLUTAMATE. NEUROCHEM INT.
2005;47(1-2):4-12. [BACK]
708.MUNTZ JA, HURWITZ J. EFFECT OF POTASSIUM
AND AMMONIUM IONS UPON GLYCOLYSIS CATALYZED
BY AN EXTRACT OF RAT BRAIN. ARCH BIOCHEM
BIOPHYS. 1951;32(1):124-36. [BACK]
709.
PASCUAL G, AVGUSTINOVA A, MEJETTA S, MARTIN M,
CASTELLANOS A, ATTOLINI SO, BERENGUER A, PRATS N,
TOLL A, HUETO JA, BESCOS C, DI CROCE L, BENITAH SA.
TARGETING METASTASIS-INTITATING CELLS THROUGH
THE FATTY ACID RECEPTOR CD36. NATURE. 2017;541:41-
45. [BACK]
710.
SLEBE F, ROJO F, VINAIXA M, ET AL. FOXA AND LIPG
ENDOTHELIAL LIPASE CONTROL THE UPTAKE OF
EXTRACELLULAR LIPIDS FOR BREAST CANCER
GROWTH. NAT COMMUN. 2016;7:11199. [BACK]
711.
COHEN LA. FAT AND ENDOCRINE-RESPONSIVE CANCER
IN ANIMALS. PREV MED. 1987;16(4):468-74. [BACK]
712.RAO CV, HIROSE Y, INDRANIE C, REDDY BS.
MODULATION OF EXPERIMENTAL COLON
TUMORIGENESIS BY TYPES AND AMOUNTS OF DIETARY
FATTY ACIDS. CANCER RES. 2001;61(5):1927-33. [BACK]
713.ZUSMAN I, GUREVICH P, MADAR Z, ET AL. TUMOR-
PROMOTING AND TUMOR-PROTECTIVE EFFECTS OF
HIGH-FAT DIETS ON CHEMICALLY INDUCED MAMMARY
CANCER IN RATS. ANTICANCER RES. 1997;17(1A):349-56.
[BACK]
CARROLL KK. NEUTRAL FATS AND CANCER.
714.
CANCER RES. 1981;41(9 PT 2):3695-9. [BACK]
715.CHAN PC, FERGUSON KA, DAO TL. EFFECTS OF
DIFFERENT DIETARY FATS ON MAMMARY
CARCINOGENESIS. CANCER RES. 1983;43(3):1079-83.
[BACK]
716. DAYTON S, HASHIMOTO S, WOLLMAN J. EFFECT OF
HIGH-OLEIC AND HIGH-LINOLEIC SAFFLOWER OILS ON
MAMMARY TUMORS INDUCED IN RATS BY 7,12-
DIMETHYLBENZ(ALPHA)ANTHRACENE. J NUTR.
1977;107(8):1353-60. [BACK]
717. CARROLL KK, HOPKINS GJ. DIETARY
POLYUNSATURATED FAT VERSUS SATURATED FAT IN
RELATION TO MAMMARY CARCINOGENESIS. LIPIDS.
1979;14(2):155-8. [BACK]
718. KARMALI RA, DONNER A, GOBEL S, SHIMAMURA T.
EFFECT OF N-3 AND N-6 FATTY ACIDS ON 7,12
DIMETHYLBENZ (A) ANTHRACENE-INDUCED
MAMMARY TUMORIGENESIS. ANTICANCER RES.
1989;9(4):1161-7. [BACK]
719. AYLSWORTH CF, JONE C, TROSKO JE, MEITES J,
WELSCH CW. PROMOTION OF 7,12-
DIMETHYLBENZ[A]ANTHRACENE-INDUCED MAMMARY
TUMORIGENESIS BY HIGH DIETARY FAT IN THE RAT:
POSSIBLE ROLE OF INTERCELLULAR COMMUNICATION.
J NATL CANCER INST. 1984;72(3):637-45. [BACK]
720. COHEN LA, THOMPSON DO, MAEURA Y, CHOI K,
BLANK ME, ROSE DP. DIETARY FAT AND MAMMARY
CANCER. I. PROMOTING EFFECTS OF DIFFERENT
DIETARY FATS ON N-NITROSOMETHYLUREA-INDUCED
RAT MAMMARY TUMORIGENESIS. J NATL CANCER INST.
1986;77(1):33-42. [BACK]
721. KUNO T, HIROSE Y, YAMADA Y, ET AL. PROMOTING
EFFECTS OF HIGH-FAT CORN OIL AND HIGH-FAT MIXED
LIPID DIETS ON 7,12-DIMETHYLBENZ[A]ANTHRACENE-
INDUCED MAMMARY TUMORIGENESIS IN F344 RATS.
ONCOL REP. 2003;10(3):699-703. [BACK]
722. COHEN LA, THOMPSON DO, CHOI K, KARMALI RA,
ROSE DP. DIETARY FAT AND MAMMARY CANCER. II.
MODULATION OF SERUM AND TUMOR LIPID
COMPOSITION AND TUMOR PROSTAGLANDINS BY
DIFFERENT DIETARY FATS: ASSOCIATION WITH TUMOR
INCIDENCE PATTERNS. J NATL CANCER INST.
1986;77(1):43-51. [BACK]
723. HOPKINS GJ, KENNEDY TG, CARROLL KK.
POLYUNSATURATED FATTY ACIDS AS PROMOTERS OF
MAMMARY CARCINOGENESIS INDUCED IN SPRAGUE-
DAWLEY RATS BY 7,12-
DIMETHYLBENZ[A]ANTHRACENE. J NATL CANCER INST.
1981;66(3):517-22. [BACK]
724.
CARROLL KK. DIETARY FAT IN RELATION TO
MAMMARY CARCINOGENESIS. INT SYMP PRINCESS
TAKAMATSU CANCER RES FUND. 1985;16:255-63. [BACK]
725.
WELSCH CW. DIETARY FAT, CALORIES, AND MAMMARY
GLAND TUMORIGENESIS. ADV EXP MED BIOL.
1992;322:203-22. [BACK]
726.
OYAIZU N, MORII S, SAITO K, KATSUDA Y, MATSUMOTO
J. MECHANISM OF GROWTH ENHANCEMENT OF 7,12-
DIMETHYLBENZ[A]-ANTHRACENE-INDUCED
MAMMARY TUMORS IN RATS GIVEN HIGH
POLYUNSATURATED FAT DIET. JPN J CANCER RES.
1985;76(8):676-83. [BACK]
727. SELENSKAS SL, IP MM, IP C. SIMILARITY BETWEEN
TRANS FAT AND SATURATED FAT IN THE MODIFICATION
OF RAT MAMMARY CARCINOGENESIS. CANCER RES.
1984;44(4):1321-6. [BACK]
728. COHEN LA, CHOI K, WEISBURGER JH, ROSE DP.
EFFECT OF VARYING PROPORTIONS OF DIETARY FAT ON
THE DEVELOPMENT OF N-NITROSOMETHYLUREA-
INDUCED RAT MAMMARY TUMORS. ANTICANCER RES.
1986;6(2):215-8. [BACK]
729.
GRIFFINI P, FEHRES O, KLIEVERIK L, ET AL. DIETARY
OMEGA-3 POLYUNSATURATED FATTY ACIDS PROMOTE
COLON CARCINOMA METASTASIS IN RAT LIVER.
CANCER RES. 1998;58(15):3312-9. [BACK]
730.
TWINING, C. W., BRENNA, J. T., HAIRSTON, N. G. AND
FLECKER, A. S. (2016), HIGHLY UNSATURATED FATTY
ACIDS IN NATURE: WHAT WE KNOW AND WHAT WE
NEED TO LEARN. OIKOS, 125: 749–760. [BACK]
731.
MEHTA RS, GUNNETT CA, HARRIS SR, BUNCE OR,
HARTLE DK. HIGH FISH OIL DIET INCREASES OXIDATIVE
STRESS POTENTIAL IN MAMMARY GLAND OF
SPONTANEOUSLY HYPERTENSIVE RATS. CLIN EXP
PHARMACOL PHYSIOL. 1994;21(11):881-9. [BACK]
732.
SAUER LA, DAUCHY RT. BLOOD NUTRIENT
CONCENTRATIONS AND TUMOR GROWTH IN VIVO IN
RATS: RELATIONSHIPS DURING THE ONSET OF AN
ACUTE FAST. CANCER RES. 1987;47(4):1065-8. [BACK]
733.
KLINE BE, MILLER JA. THE CARCINOGENICITY OF P-
DIMETHYLAMINOAZOBENZENE IN DIETS CONTAINING
THE FATTY ACIDS OF HYDROGENATED COCONUT OIL
OR OF CORN OIL. CANCER RES. 1946;6:1-4. [BACK]
734.
ROEBUCK BD, LONGNECKER DS, BAUMGARTNER KJ,
THRON CD. CARCINOGEN-INDUCED LESIONS IN THE
RAT PANCREAS: EFFECTS OF VARYING LEVELS OF
ESSENTIAL FATTY ACID. CANCER RES. 1985;45(11 PT
1):5252-6. [BACK]
735.
CARROLL KK. SUMMATION: WHICH FAT/HOW MUCH
FAT--ANIMALS. PREV MED. 1987;16(4):510-5. [BACK]
736. HOPKINS GJ, CARROLL KK. RELATIONSHIP
BETWEEN AMOUNT AND TYPE OF DIETARY FAT IN
PROMOTION OF MAMMARY CARCINOGENESIS INDUCED
BY 7,12-DIMETHYLBENZ[A]ANTHRACENE. J NATL
CANCER INST. 1979;62(4):1009-12. [BACK]
737. IP C, CARTER CA, IP MM. REQUIREMENT OF
ESSENTIAL FATTY ACID FOR MAMMARY
TUMORIGENESIS IN THE RAT. CANCER RES.
1985;45(5):1997-2001. [BACK]
738.
SINGER MM, WRIGHT F, STANLEY LK, ROE BB,
HAMILTON WK. OXYGEN TOXICITY IN MAN. A
PROSPECTIVE STUDY IN PATIENTS AFTER OPEN-HEART
SURGERY. N ENGL J MED. 1970;283(27):1473-8. [BACK]
739.
BAEYENS DA, HOFFERT JR, FROMM PO. A
COMPARATIVE STUDY OF OXYGEN TOXICITY IN THE
RETINA, BRAIN AND LIVER OF THE TELEOST,
AMPHIBIAN AND MAMMAL. COMP BIOCHEM PHYSIOL A
COMP PHYSIOL. 1973;45(4):925-32. [BACK]
740.
BROWN JR, DUBOIS RN. CYCLOOXYGENASE AS A
TARGET IN LUNG CANCER. CLIN CANCER RES.
2004;10(12 PT 2):4266S-4269S. [BACK]
741.
RIEDL K, KRYSAN K, PÕLD M, ET AL. MULTIFACETED
ROLES OF CYCLOOXYGENASE-2 IN LUNG CANCER.
DRUG RESIST UPDAT. 2004;7(3):169-84. [BACK]
742.
 HARRIS RE. CYCLOOXYGENASE-2 (COX-2) AND THE
INFLAMMOGENESIS OF CANCER. SUBCELL BIOCHEM.
2007;42:93-126. [BACK]
743.
SANDLER AB, DUBINETT SM. COX-2 INHIBITION AND
LUNG CANCER. SEMIN ONCOL. 2004;31(2 SUPPL 7):45-52.
[BACK]
744.SPANO JP, CHOUAHNIA K, MORÈRE JF.
[CYCLOOXYGENASE 2 INHIBITORS AND LUNG
CARCINOMA]. BULL CANCER. 2004;91 SPEC NO:S109-12.
[BACK]
745. ZELENAY S, REIS E SOUSA C. REDUCING
PROSTAGLANDIN E2 PRODUCTION TO RAISE CANCER
IMMUNOGENICITY. ONCOIMMUNOLOGY.
2016;5(5):E1123370. [BACK]
746.FUJITA H, KOSHIDA K, KELLER ET, ET AL.
CYCLOOXYGENASE-2 PROMOTES PROSTATE CANCER
PROGRESSION. PROSTATE. 2002;53(3):232-40. [BACK]
747. CARROLL KK, BRADEN LM. DIETARY FAT AND
MAMMARY CARCINOGENESIS. NUTR CANCER.
1984;6(4):254-9. [BACK]
748. JIANG J, DINGLEDINE R. PROSTAGLANDIN
RECEPTOR EP2 IN THE CROSSHAIRS OF ANTI-
INFLAMMATION, ANTI-CANCER, AND
NEUROPROTECTION. TRENDS PHARMACOL SCI.
2013;34(7):413-23. [BACK]
749.WANG MT, HONN KV, NIE D. CYCLOOXYGENASES,
PROSTANOIDS, AND TUMOR PROGRESSION. CANCER
METASTASIS REV. 2007;26(3-4):525-34. [BACK]
750. CASTELLONE MD, TERAMOTO H, WILLIAMS BO,
DRUEY KM, GUTKIND JS. PROSTAGLANDIN E2
PROMOTES COLON CANCER CELL GROWTH THROUGH A
GS-AXIN-BETA-CATENIN SIGNALING AXIS. SCIENCE.
2005;310(5753):1504-10. [BACK]
751. WU WK, SUNG JJ, LEE CW, YU J, CHO CH.
CYCLOOXYGENASE-2 IN TUMORIGENESIS OF
GASTROINTESTINAL CANCERS: AN UPDATE ON THE
MOLECULAR MECHANISMS. CANCER LETT.
2010;295(1):7-16. [BACK]
752.CASTELLONE MD, TERAMOTO H, GUTKIND JS.
CYCLOOXYGENASE-2 AND COLORECTAL CANCER
CHEMOPREVENTION: THE BETA-CATENIN CONNECTION.
CANCER RES. 2006;66(23):11085-8. [BACK]
753.WANG D, DUBOIS RN. EICOSANOIDS AND CANCER.
NAT REV CANCER. 2010;10(3):181-93. [BACK]
754. HIRAGA T, MYOUI A, CHOI ME, YOSHIKAWA H,
YONEDA T. STIMULATION OF CYCLOOXYGENASE-2
EXPRESSION BY BONE-DERIVED TRANSFORMING
GROWTH FACTOR-BETA ENHANCES BONE METASTASES
IN BREAST CANCER. CANCER RES. 2006;66(4):2067-73.
[BACK]
755.SINGH B, BERRY JA, SHOHER A, AYERS GD, WEI C,
LUCCI A. COX-2 INVOLVEMENT IN BREAST CANCER
METASTASIS TO BONE. ONCOGENE. 2007;26(26):3789-96.
[BACK]
756.SINGH B, BERRY JA, SHOHER A, LUCCI A. COX-2
INDUCES IL-11 PRODUCTION IN HUMAN BREAST
CANCER CELLS. J SURG RES. 2006;131(2):267-75. [BACK]
757.FOSSLIEN E. REVIEW: MOLECULAR PATHOLOGY OF
CYCLOOXYGENASE-2 IN CANCER-INDUCED
ANGIOGENESIS. ANN CLIN LAB SCI. 2001;31(4):325-48.
[BACK]
758.GATELY S, KERBEL R. THERAPEUTIC POTENTIAL OF
SELECTIVE CYCLOOXYGENASE-2 INHIBITORS IN THE
MANAGEMENT OF TUMOR ANGIOGENESIS. PROG EXP
TUMOR RES. 2003;37:179-92. [BACK]
759.
 WOLFE RR, MARTINI WZ, IRTUN O, HAWKINS HK,
BARROW RE. DIETARY FAT COMPOSITION ALTERS
PULMONARY FUNCTION IN PIGS. NUTRITION. 2002;18(7-
8):647-53. [BACK]
760.
KRAMER JK, FARNWORTH ER, THOMPSON BK, CORNER
AH, TRENHOLM HL. REDUCTION OF MYOCARDIAL
NECROSIS IN MALE ALBINO RATS BY MANIPULATION
OF DIETARY FATTY ACID LEVELS. LIPIDS. 1982;17(5):372-
82. [BACK]
761.
DAVIDSON MB, CARROLL KK. INHIBITORY EFFECT OF A
FAT-FREE DIET ON MAMMARY CARCINOGENESIS IN
RATS. NUTR CANCER. 1982;3(4):207-15. [BACK]
762.
BUCKINGHAM KW. EFFECT OF DIETARY
POLYUNSATURATED/SATURATED FATTY ACID RATIO
AND DIETARY VITAMIN E ON LIPID PEROXIDATION IN
THE RAT. J NUTR. 1985;115(11):1425-35. [BACK]
763. JENKINSON AM, COLLINS AR, DUTHIE SJ, WAHLE
KW, DUTHIE GG. THE EFFECT OF INCREASED INTAKES
OF POLYUNSATURATED FATTY ACIDS AND VITAMIN E
ON DNA DAMAGE IN HUMAN LYMPHOCYTES. FASEB J.
1999;13(15):2138-42. [BACK]
764.DEBRY G. POLYUNSATURATED FATTY ACIDS AND
VITAMIN E : THEIR IMPORTANCE IN HUMAN NUTRITION.
ANN NUTR ALIMENT. 1980;34(2):337-50. [BACK]
765.
DUBOIS RN, ABRAMSON SB, CROFFORD L, ET AL.
CYCLOOXYGENASE IN BIOLOGY AND DISEASE. FASEB J.
1998;12(12):1063-73. [BACK]
766. CHAN TA. PROSTAGLANDINS AND THE COLON
CANCER CONNECTION. TRENDS MOL MED.
2006;12(6):240-4. [BACK]
767.BUCHANAN FG, DUBOIS RN. CONNECTING COX-2
AND WNT IN CANCER. CANCER CELL. 2006;9(1):6-8.
[BACK]
768.ROELOFS HM, TE MORSCHE RH, VAN HEUMEN BW,
NAGENGAST FM, PETERS WH. OVER-EXPRESSION OF
COX-2 MRNA IN COLORECTAL CANCER. BMC
GASTROENTEROL. 2014;14:1. [BACK]
769.BODEY B, SIEGEL SE, KAISER HE.
CYCLOOXYGENASE-2 (COX-2) OVEREXPRESSION IN
CHILDHOOD BRAIN TUMORS. IN VIVO. 2006;20(4):519-25.
[BACK]
770. PETKOVA DK, CLELLAND C, RONAN J, ET AL.
OVEREXPRESSION OF CYCLOOXYGENASE-2 IN NON-
SMALL CELL LUNG CANCER. RESPIR MED.
2004;98(2):164-72. [BACK]
771.
TURINI ME, DUBOIS RN. CYCLOOXYGENASE-2: A
THERAPEUTIC TARGET. ANNU REV MED. 2002;53:35-57.
[BACK]
772. DEMPKE W, RIE C, GROTHEY A, SCHMOLL HJ.
CYCLOOXYGENASE-2: A NOVEL TARGET FOR CANCER
CHEMOTHERAPY?. J CANCER RES CLIN ONCOL.
2001;127(7):411-7. [BACK]
773.HARRIS RE. CYCLOOXYGENASE-2 (COX-2)
BLOCKADE IN THE CHEMOPREVENTION OF CANCERS
OF THE COLON, BREAST, PROSTATE, AND LUNG.
INFLAMMOPHARMACOLOGY. 2009;17(2):55-67. [BACK]
774.WILLIAMS CS, MANN M, DUBOIS RN. THE ROLE OF
CYCLOOXYGENASES IN INFLAMMATION, CANCER, AND
DEVELOPMENT. ONCOGENE. 1999;18(55):7908-16. [BACK]
775.
SPINELLA F, ROSANÒ L, DI CASTRO V, NICOTRA MR,
NATALI PG, BAGNATO A. INHIBITION OF
CYCLOOXYGENASE-1 AND -2 EXPRESSION BY
TARGETING THE ENDOTHELIN A RECEPTOR IN HUMAN
OVARIAN CARCINOMA CELLS. CLIN CANCER RES.
2004;10(14):4670-9. [BACK]
776. GRIDELLI C, MAIONE P, AIROMA G, ROSSI A.
SELECTIVE CYCLOOXYGENASE-2 INHIBITORS AND
NON-SMALL CELL LUNG CANCER. CURR MED CHEM.
2002;9(21):1851-8. [BACK]
777.SAWAOKA H, TSUJI S, TSUJII M, ET AL.
CYCLOOXYGENASE INHIBITORS SUPPRESS
ANGIOGENESIS AND REDUCE TUMOR GROWTH IN VIVO.
LAB INVEST. 1999;79(12):1469-77. [BACK]
778.TSUJI S, TSUJII M, KAWANO S, HORI M.
CYCLOOXYGENASE-2 UPREGULATION AS A
PERIGENETIC CHANGE IN CARCINOGENESIS. J EXP CLIN
CANCER RES. 2001;20(1):117-29. [BACK]
779. LIU XH, KIRSCHENBAUM A, YAO S, LEE R,
HOLLAND JF, LEVINE AC. INHIBITION OF
CYCLOOXYGENASE-2 SUPPRESSES ANGIOGENESIS AND
THE GROWTH OF PROSTATE CANCER IN VIVO. J UROL.
2000;164(3 PT 1):820-5. [BACK]
780.YOSHIDA S, AMANO H, HAYASHI I, ET AL. COX-
2/VEGF-DEPENDENT FACILITATION OF TUMOR-
ASSOCIATED ANGIOGENESIS AND TUMOR GROWTH IN
VIVO. LAB INVEST. 2003;83(10):1385-94. [BACK]
781. CHU J, LLOYD FL, TRIFAN OC, KNAPP B, RIZZO MT.
POTENTIAL INVOLVEMENT OF THE CYCLOOXYGENASE-
2 PATHWAY IN THE REGULATION OF TUMOR-
ASSOCIATED ANGIOGENESIS AND GROWTH IN
PANCREATIC CANCER. MOL CANCER THER. 2003;2(1):1-7.
[BACK]
782.ROZIC JG, CHAKRABORTY C, LALA PK.
CYCLOOXYGENASE INHIBITORS RETARD MURINE
MAMMARY TUMOR PROGRESSION BY REDUCING
TUMOR CELL MIGRATION, INVASIVENESS AND
ANGIOGENESIS. INT J CANCER. 2001;93(4):497-506.
[BACK]
783.
GOLDYNE ME. PROSTAGLANDINS AND THE
MODULATION OF IMMUNOLOGICAL RESPONSES. INT J
DERMATOL. 1977;16(9):701-12. [BACK]
784.MUTHUSWAMY R, OKADA NJ, JENKINS FJ, ET AL.
EPINEPHRINE PROMOTES COX-2-DEPENDENT IMMUNE
SUPPRESSION IN MYELOID CELLS AND CANCER
TISSUES. BRAIN BEHAV IMMUN. 2017;62:78-86. [BACK]
785.
GOODWIN JS, CEUPPENS J. REGULATION OF THE
IMMUNE RESPONSE BY PROSTAGLANDINS. J CLIN
IMMUNOL. 1983;3(4):295-315. [BACK]
786.LANGHENDRIES JP, MATON P, FRANÇOIS-ADANT A,
CHANTRAIN C, BURY F, PHILIPPET P. [PROSTAGLANDINS
AND THE IMMUNE RESPONSE AT THE INTESTINAL
SUBMUCOSAL LEVEL. A POTENTIAL SITE FOR
INTERFERENCE WITH THE REPEATED USE OF
PARACETAMOL AND IBUPROFEN AT A YOUNG AGE?].
ARCH PEDIATR. 2015;22(3):311-9. [BACK]
787.REMES LENICOV F, VARESE A, MERLOTTI A,
GEFFNER J, CEBALLOS A. PROSTAGLANDINS IN SEMEN
COMPROMISE THE IMMUNE RESPONSE AGAINST
SEXUALLY TRANSMITTED PATHOGENS. MED
HYPOTHESES. 2014;83(2):208-10. [BACK]
788. BARONE J, HEBERT JR. DIETARY FAT AND NATURAL
KILLER CELL ACTIVITY. MED HYPOTHESES.
1988;25(4):223-6. [BACK]
789.
ROBERTSON GL, KERMODE WJ. SALICYLIC ACID IN
FRESH AND CANNED FRUIT AND VEGETABLES. J. SCI.
FOOD. AG. 1981;32(8):833-836. [BACK]
790.
 SPENCER, B. (2016). HOW LIQUID ASPIRIN COULD HELP
FIGHT BRAIN CANCER. DAILYMAIL. [ONLINE].
AVAILABLE:
HTTP://WWW.DAILYMAIL.CO.UK/SCIENCETECH/ARTICLE
-3663188/HOW-LIQUID-ASPIRIN-HELP-FIGHT-BRAIN-
CANCER-SPECIAL-VERSION-DRUG-TEN-TIMES-
EFFECTIVE-KILLING-CANCER-CELLS-
CHEMOTHERAPY.HTML.[MARCH 2, 2017]. [BACK]
791.
US PREVENTIVE SERVICES TASK FORCE. (2016). ASPIRIN
USE TO PREVENT CARDIOVASCULAR DISEASE AND
COLORECTAL CANCER: PREVENTIVE MEDICATION.
[ONLINE]. AVAILABLE:
HTTPS://WWW.USPREVENTIVESERVICESTASKFORCE.OR
G/PAGE/DOCUMENT/UPDATESUMMARYFINAL/ASPIRIN-
TO-PREVENT-CARDIOVASCULAR-DISEASE-AND-
CANCER.[MARCH 1, 2017]. [BACK]
792.
UYTTEBROUCK, O. (2016). DEATH RATES FOR MOST
CANCERS IN DECLINE. ALBUQUERQUE JOURNAL.
[ONLINE]. AVAILABLE:
HTTPS://WWW.ABQJOURNAL.COM/754139/DEATH-RATES-
FOR-MOST-CANCERS-IN-DECLINE.HTML.[MARCH 1,
2017]. [BACK]
793.
AGUS DB, GAUDETTE É, GOLDMAN DP, MESSALI A. THE
LONG-TERM BENEFITS OF INCREASED ASPIRIN USE BY
AT-RISK AMERICANS AGED 50 AND OLDER. PLOS ONE.
2016;11(11):E0166103. [BACK]
794.
EMILSSON L, HOLME Ø, BRETTHAUER M, ET AL.
SYSTEMATIC REVIEW WITH META-ANALYSIS: THE
COMPARATIVE EFFECTIVENESS OF ASPIRIN VS.
SCREENING FOR COLORECTAL CANCER PREVENTION.
ALIMENT PHARMACOL THER. 2017;45(2):193-204. [BACK]
795.
 SCHÖNHÖFER PS, SOHN J, PETERS HD, DINNENDAHL V.
EFFECTS OF SODIUM SALICYLATE AND
ACETYLSALICYLIC ACID ON THE LIPOLYTIC SYSTEM OF
FAT CELLS. BIOCHEM PHARMACOL. 1973;22(5):629-37.
[BACK]
796.HUNDAL RS, PETERSEN KF, MAYERSON AB, ET AL.
MECHANISM BY WHICH HIGH-DOSE ASPIRIN IMPROVES
GLUCOSE METABOLISM IN TYPE 2 DIABETES. J CLIN
INVEST. 2002;109(10):1321-6. [BACK]
797.MEESTER WD, SCHUT GE, HAMP JA, SEKHAR NC.
EFFECT OF ASPIRIN ON EPINEPHRINE-INDUCED
LIPOLYSIS AND PLATELET AGGREGATION IN RATS. RES
COMMUN CHEM PATHOL PHARMACOL. 1972;4(2):405-11.
[BACK]
798.
NIXON M, WAKE DJ, LIVINGSTONE DE, ET AL.
SALICYLATE DOWNREGULATES 11Β-HSD1 EXPRESSION
IN ADIPOSE TISSUE IN OBESE MICE AND IN HUMANS,
MEDIATING INSULIN SENSITIZATION. DIABETES.
2012;61(4):790-6. [BACK]
799.
DE CRISTÓBAL J, CÁRDENAS A, LIZASOAIN I, ET AL.
INHIBITION OF GLUTAMATE RELEASE VIA RECOVERY
OF ATP LEVELS ACCOUNTS FOR A NEUROPROTECTIVE
EFFECT OF ASPIRIN IN RAT CORTICAL NEURONS
EXPOSED TO OXYGEN-GLUCOSE DEPRIVATION.
STROKE. 2002;33(1):261-7. [BACK]
800.
SINGH AK, ZAJDEL J, MIRRASEKHIAN E, ET AL.
PROSTAGLANDIN-MEDIATED INHIBITION OF
SEROTONIN SIGNALING CONTROLS THE AFFECTIVE
COMPONENT OF INFLAMMATORY PAIN. J CLIN INVEST.
2017. [BACK]
801.
 COTLIER E. SENILE CATARACTS: EVIDENCE FOR
ACCELERATION BY DIABETES AND DECELERATION BY
SALICYLATE. CAN J OPHTHALMOL. 1981;16(3):113-8.
[BACK]
802.
COTLIER E. ASPIRIN EFFECT ON CATARACT
FORMATION IN PATIENTS WITH RHEUMATOID
ARTHRITIS ALONE OR COMBINED WITH DIABETES. INT
OPHTHALMOL. 1981;3(3):173-7. [BACK]
803.
GOMES I. ASPIRIN: A NEUROPROTECTIVE AGENT AT
HIGH DOSES?. NATL MED J INDIA. 1998;11(1):14-7. [BACK]
804.
ASANUMA M, NISHIBAYASHI-ASANUMA S, MIYAZAKI I,
KOHNO M, OGAWA N. NEUROPROTECTIVE EFFECTS OF
NON-STEROIDAL ANTI-INFLAMMATORY DRUGS BY
DIRECT SCAVENGING OF NITRIC OXIDE RADICALS. J
NEUROCHEM. 2001;76(6):1895-904. [BACK]
805.
CHOI HW, TIAN M, MANOHAR M, ET AL. HUMAN GAPDH
IS A TARGET OF ASPIRIN'S PRIMARY METABOLITE
SALICYLIC ACID AND ITS DERIVATIVES. PLOS ONE.
2015;10(11):E0143447. [BACK]
806.
SMITH JW, AL-KHAMEES O, COSTALL B, NAYLOR RJ,
SMYTHE JW. CHRONIC ASPIRIN INGESTION IMPROVES
SPATIAL LEARNING IN ADULT AND AGED RATS.
PHARMACOL BIOCHEM BEHAV. 2002;71(1-2):233-8.
[BACK]
807.
GUAN XT, SHAO F, XIE X, CHEN L, WANG W. EFFECTS OF
ASPIRIN ON IMMOBILE BEHAVIOR AND ENDOCRINE
AND IMMUNE CHANGES IN THE FORCED SWIMMING
TEST: COMPARISON TO FLUOXETINE AND IMIPRAMINE.
PHARMACOL BIOCHEM BEHAV. 2014;124:361-6. [BACK]
808.
 SCHWARZ KB, AREY BJ, TOLMAN K, MAHANTY S. IRON
CHELATION AS A POSSIBLE MECHANISM FOR ASPIRIN-
INDUCED MALONDIALDEHYDE PRODUCTION BY
MOUSE LIVER MICROSOMES AND MITOCHONDRIA. J
CLIN INVEST. 1988;81(1):165-70. [BACK]
809.
VERHEIJ M, STEWART FA, OUSSOREN Y, WEENING JJ,
DEWIT L. AMELIORATION OF RADIATION NEPHROPATHY
BY ACETYLSALICYLIC ACID. INT J RADIAT BIOL.
1995;67(5):587-96. [BACK]
810.
WANG HF, LI XD, CHEN YM, YUAN LB, FOYE WO.
RADIATION-PROTECTIVE AND PLATELET AGGREGATION
INHIBITORY EFFECTS OF FIVE TRADITIONAL CHINESE
DRUGS AND ACETYLSALICYLIC ACID FOLLOWING
HIGH-DOSE GAMMA-IRRADIATION. J
ETHNOPHARMACOL. 1991;34(2-3):215-9. [BACK]
811.
SJAARDA LA, RADIN RG, SILVER RM, MITCHELL E,
MUMFORD SL, WILCOX B, GALAI N, PERKINS NJ,
WACTAWSKI-WENDE J, STANFORD JB, SCHISTERMAN EF.
PRECONCEPTION LOW-DOSE ASPIRIN RESTORES
DIMINISHED PREGNANCY AND LIVE BIRTH RATES IN
WOMEN WITH LOW GRADE INFLAMMATION: A
SECONDARY ANALYSIS OF A RANDOMIZED TRIAL. J
CLIN. ENDOCRINOL. METAB. JC.2016-2917. [BACK]
812.
WADA I, HSU CC, WILLIAMS G, MACNAMEE MC,
BRINSDEN PR. THE BENEFITS OF LOW-DOSE ASPIRIN
THERAPY IN WOMEN WITH IMPAIRED UTERINE
PERFUSION DURING ASSISTED CONCEPTION. HUM
REPROD. 1994;9(10):1954-7. [BACK]
813.
WAN QL, ZHENG SQ, WU GS, LUO HR. ASPIRIN EXTENDS
THE LIFESPAN OF CAENORHABDITIS ELEGANS VIA
AMPK AND DAF-16/FOXO IN DIETARY RESTRICTION
PATHWAY. EXP GERONTOL. 2013;48(5):499-506. [BACK]
814.
AYYADEVARA S, BHARILL P, DANDAPAT A, ET AL.
ASPIRIN INHIBITS OXIDANT STRESS, REDUCES AGE-
ASSOCIATED FUNCTIONAL DECLINES, AND EXTENDS
LIFESPAN OF CAENORHABDITIS ELEGANS. ANTIOXID
REDOX SIGNAL. 2013;18(5):481-90. [BACK]
815.
STRONG R, MILLER RA, ASTLE CM, ET AL.
NORDIHYDROGUAIARETIC ACID AND ASPIRIN
INCREASE LIFESPAN OF GENETICALLY
HETEROGENEOUS MALE MICE. AGING CELL.
2008;7(5):641-50. [BACK]
816.
LUTCHMAN, VICKY; MEDKOUR, YOUNES; SAMSON,
EUGENIE; ARLIA-CIOMMO, ANTHONY; DAKIK, PAMELA;
CORTES, BERLY; FELDMAN, RACHEL; MOHTASHAMI,
SADAF; MCAULEY, MÉLISSA; CHANCHAROEN, MARISA;
RUKUNDO, BELISE; SIMARD, ÉRIC; TITORENKO,
VLADIMIR I. DISCOVERY OF PLANT EXTRACTS THAT
GREATLY DELAY YEAST CHRONOLOGICAL AGING AND
HAVE DIFFERENT EFFECTS ON LONGEVITY-DEFINING
CELLULAR PROCESSES. ONCOTARGET. 7(13):16542.
[BACK]
817.
ARANGO HA, ICELY S, ROBERTS WS, CAVANAGH D,
BECKER JL. ASPIRIN EFFECTS ON ENDOMETRIAL
CANCER CELL GROWTH. OBSTET GYNECOL.
2001;97(3):423-7. [BACK]
818.
REDLAK MJ, POWER JJ, MILLER TA. ASPIRIN-INDUCED
APOPTOSIS IN HUMAN GASTRIC CANCER EPITHELIAL
CELLS: RELATIONSHIP WITH PROTEIN KINASE C
SIGNALING. DIG DIS SCI. 2007;52(3):810-6. [BACK]
819.
 RIOUX N, CASTONGUAY A. PREVENTION OF NNK-
INDUCED LUNG TUMORIGENESIS IN A/J MICE BY
ACETYLSALICYLIC ACID AND NS-398. CANCER RES.
1998;58(23):5354-60. [BACK]
820.
VALDÉZ JC, PERDIGÓN G. PIROXICAM, INDOMETHACIN
AND ASPIRIN ACTION ON A MURINE FIBROSARCOMA.
EFFECTS ON TUMOUR-ASSOCIATED AND PERITONEAL
MACROPHAGES. CLIN EXP IMMUNOL. 1991;86(2):315-21.
[BACK]
821.
MAITY G, DE A, DAS A, BANERJEE S, SARKAR S,
BANERJEE SK. ASPIRIN BLOCKS GROWTH OF BREAST
TUMOR CELLS AND TUMOR-INITIATING CELLS AND
INDUCES REPROGRAMMING FACTORS OF
MESENCHYMAL TO EPITHELIAL TRANSITION. LAB
INVEST. 2015;95(7):702-17. [BACK]
822.
MITRAL, P. (2016). ASPIRIN LIFELINE FOR END-STAGE
CANCER. TIMES OF INDIA. [ONLINE]. AVAILABLE:
HTTP://TIMESOFINDIA.INDIATIMES.COM/CITY/KOLKATA/
ASPIRIN-LIFELINE-FOR-END-STAGE-
CANCER/ARTICLESHOW/53407589.CMS.[MARCH 1, 2017].
[BACK]
823.
MITRUGNO A, SYLMAN JL, NGO AT, ET AL. ASPIRIN
THERAPY REDUCES THE ABILITY OF PLATELETS TO
PROMOTE COLON AND PANCREATIC CANCER CELL
PROLIFERATION: IMPLICATIONS FOR THE
ONCOPROTEIN C-MYC. AM J PHYSIOL, CELL PHYSIOL.
2017;312(2):C176-C189. [BACK]
824.
SAINI T, BAGCHI M, BAGCHI D, JAEGER S, HOSOYAMA
S, STOHS SJ. PROTECTIVE ABILITY OF
ACETYLSALICYLIC ACID (ASPIRIN) TO SCAVENGE
RADIATION INDUCED FREE RADICALS IN J774A.1
MACROPHAGE CELLS. RES COMMUN MOL PATHOL
PHARMACOL. 1998;101(3):259-68. [BACK]
825.
SHI X, DING M, DONG Z, ET AL. ANTIOXIDANT
PROPERTIES OF ASPIRIN: CHARACTERIZATION OF THE
ABILITY OF ASPIRIN TO INHIBIT SILICA-INDUCED LIPID
PEROXIDATION, DNA DAMAGE, NF-KAPPAB
ACTIVATION, AND TNF-ALPHA PRODUCTION. MOL CELL
BIOCHEM. 1999;199(1-2):93-102. [BACK]
826.
BECKMANN I, BEN-EFRAIM S, VERVOORT M,
WALLENBURG HC. RELEASE OF TUMOR NECROSIS
FACTOR-ALPHA AND PROSTANOIDS IN WHOLE BLOOD
CULTURES AFTER IN VIVO EXPOSURE TO LOW-DOSE
ASPIRIN. MEDIATORS INFLAMM. 2001;10(2):81-8. [BACK]
827.
SHACKELFORD R, ALFORD PB, XUE Y, THAI SF, ADAMS
DO, PIZZO S. ASPIRIN INHIBITS TUMOR NECROSIS
FACTOR-Α GENE EXPRESSION IN MURINE TISSUE
MACROPHAGES. MOLECULAR PHARMACOLOGY.
1997;52(3):421. [BACK]
828.
VERVOORDELDONK MJ, PINEDA TORRA IM, AARSMAN
AJ, VAN DEN BOSCH H. ASPIRIN INHIBITS EXPRESSION
OF THE INTERLEUKIN-1BETA-INDUCIBLE GROUP II
PHOSPHOLIPASE A2. FEBS LETT. 1996;397(1):108-12.
[BACK]
829.
MARSHALL H. ASPIRIN INHIBITS IL-4 PRODUCTION.
TRENDS IMMUNOL. 2001;22(5):242. [BACK]
830.
CIANFERONI A, SCHROEDER JT, KIM J, ET AL.
SELECTIVE INHIBITION OF INTERLEUKIN-4 GENE
EXPRESSION IN HUMAN T CELLS BY ASPIRIN. BLOOD.
2001;97(6):1742-9. [BACK]
831.
 HOVENS MM, SNOEP JD, GROENEVELD Y, FRÖLICH M,
TAMSMA JT, HUISMAN MV. EFFECTS OF ASPIRIN ON
SERUM C-REACTIVE PROTEIN AND INTERLEUKIN-6
LEVELS IN PATIENTS WITH TYPE 2 DIABETES WITHOUT
CARDIOVASCULAR DISEASE: A RANDOMIZED PLACEBO-
CONTROLLED CROSSOVER TRIAL. DIABETES OBES
METAB. 2008;10(8):668-74. [BACK]
832.KIM SR, BAE MK, KIM JY, WEE HJ, YOO MA, BAE SK.
ASPIRIN INDUCES APOPTOSIS THROUGH THE
BLOCKADE OF IL-6-STAT3 SIGNALING PATHWAY IN
HUMAN GLIOBLASTOMA A172 CELLS. BIOCHEM
BIOPHYS RES COMMUN. 2009;387(2):342-7. [BACK]
833. OGSTON NC, KARASTERGIOU K, HOSSEINZADEH-
ATTAR MJ, ET AL. LOW-DOSE ACETYLSALICYLIC ACID
INHIBITS THE SECRETION OF INTERLEUKIN-6 FROM
WHITE ADIPOSE TISSUE. INT J OBES (LOND).
2008;32(12):1807-15. [BACK]
834.
GOLDSTEIN SL, LEUNG JC, SILVERSTEIN DM. PRO- AND
ANTI-INFLAMMATORY CYTOKINES IN CHRONIC
PEDIATRIC DIALYSIS PATIENTS: EFFECT OF ASPIRIN.
CLIN J AM SOC NEPHROL. 2006;1(5):979-86. [BACK]
835. WU D, SHEU JS, LIU HC, ET AL. INCREASE OF TOLL-
LIKE RECEPTOR 4 BUT DECREASE OF INTERLEUKIN-8
MRNA EXPRESSION AMONG ISCHEMIC STROKE
PATIENTS UNDER ASPIRIN TREATMENT. CLIN BIOCHEM.
2012;45(16-17):1316-9. [BACK]
836. YANG YY, HU CJ, CHANG SM, TAI TY, LEU SJ.
ASPIRIN INHIBITS MONOCYTE CHEMOATTRACTANT
PROTEIN-1 AND INTERLEUKIN-8 EXPRESSION IN TNF-
ALPHA STIMULATED HUMAN UMBILICAL VEIN
ENDOTHELIAL CELLS. ATHEROSCLEROSIS.
2004;174(2):207-13. [BACK]
837.
 PEREZ-G M, MELO M, KEEGAN AD, ZAMORANO J.
ASPIRIN AND SALICYLATES INHIBIT THE IL-4- AND IL-
13-INDUCED ACTIVATION OF STAT6. J IMMUNOL.
2002;168(3):1428-34. [BACK]
838.
BHATT S, PUNDARIKAKSHUDU K, PATEL P, ET AL.
BENEFICIAL EFFECT OF ASPIRIN AGAINST INTERFERON-
Α-2B-INDUCED DEPRESSIVE BEHAVIOR IN SPRAGUE
DAWLEY RATS. CLIN EXP PHARMACOL PHYSIOL.
2016;43(12):1208-1215. [BACK]
839.
DI LUIGI L, ROSSI C, SGRÒ P, ET AL. DO NON-
STEROIDAL ANTI-INFLAMMATORY DRUGS INFLUENCE
THE STEROID HORMONE MILIEU IN MALE ATHLETES?.
INT J SPORTS MED. 2007;28(10):809-14. [BACK]
840.
SCHÖNHÖFER PS, SOHN J, PETERS HD, DINNENDAHL V.
EFFECTS OF SODIUM SALICYLATE AND
ACETYLSALICYLIC ACID ON THE LIPOLYTIC SYSTEM OF
FAT CELLS. BIOCHEM PHARMACOL. 1973;22(5):629-37.
[BACK]
841. MAHARAJ H, MAHARAJ DS, SARAVANAN KS,
MOHANAKUMAR KP, DAYA S. ASPIRIN CURTAILS THE
ACETAMINOPHEN-INDUCED RISE IN BRAIN
NOREPINEPHRINE LEVELS. METAB BRAIN DIS. 2004;19(1-
2):71-7. [BACK]
842.HUNDAL RS, PETERSEN KF, MAYERSON AB, ET AL.
MECHANISM BY WHICH HIGH-DOSE ASPIRIN IMPROVES
GLUCOSE METABOLISM IN TYPE 2 DIABETES. J CLIN
INVEST. 2002;109(10):1321-6. [BACK]
843.MEESTER WD, SCHUT GE, HAMP JA, SEKHAR NC.
EFFECT OF ASPIRIN ON EPINEPHRINE-INDUCED
LIPOLYSIS AND PLATELET AGGREGATION IN RATS. RES
COMMUN CHEM PATHOL PHARMACOL. 1972;4(2):405-11.
[BACK]
844.
YANG H, PELLEGRINI L, NAPOLITANO A, ET AL. ASPIRIN
DELAYS MESOTHELIOMA GROWTH BY INHIBITING
HMGB1-MEDIATED TUMOR PROGRESSION. CELL DEATH
DIS. 2015;6:E1786. [BACK]
845.
CHOI HW, TIAN M, SONG F, ET AL. ASPIRIN'S ACTIVE
METABOLITE SALICYLIC ACID TARGETS HIGH
MOBILITY GROUP BOX 1 TO MODULATE
INFLAMMATORY RESPONSES. MOL MED. 2015;21:526-35.
[BACK]
846.
NADAR S, BLANN AD, LIP GY. EFFECTS OF ASPIRIN ON
INTRA-PLATELET VASCULAR ENDOTHELIAL GROWTH
FACTOR, ANGIOPOIETIN-1, AND P-SELECTIN LEVELS IN
HYPERTENSIVE PATIENTS. AM J HYPERTENS.
2006;19(9):970-7. [BACK]
847.
ZANDOMENEGHI R, SERRA L, PAVESI C, BAUMGARTL U,
POPPI C, MONTANARI P. EFFECT OF ASPIRIN AND
INDOMETHACIN ON EPIDERMAL GROWTH FACTOR
SECRETION IN DUODENAL TISSUE FRAGMENTS
CULTIVATED IN VITRO. DIGESTION. 1992;51(1):37-41.
[BACK]
848.
CHIOW KH, TAN Y, CHUA RY, ET AL. SNX3-DEPENDENT
REGULATION OF EPIDERMAL GROWTH FACTOR
RECEPTOR (EGFR) TRAFFICKING AND DEGRADATION
BY ASPIRIN IN EPIDERMOID CARCINOMA (A-431) CELLS.
CELL MOL LIFE SCI. 2012;69(9):1505-21. [BACK]
849.
AMIN AR, VYAS P, ATTUR M, ET AL. THE MODE OF
ACTION OF ASPIRIN-LIKE DRUGS: EFFECT ON
INDUCIBLE NITRIC OXIDE SYNTHASE. PROC NATL ACAD
SCI USA. 1995;92(17):7926-30. [BACK]
850. CARVALHO-FILHO MA, ROPELLE ER, PAULI RJ, ET
AL. ASPIRIN ATTENUATES INSULIN RESISTANCE IN
MUSCLE OF DIET-INDUCED OBESE RATS BY INHIBITING
INDUCIBLE NITRIC OXIDE SYNTHASE PRODUCTION
AND S-NITROSYLATION OF IRBETA/IRS-1 AND AKT.
DIABETOLOGIA. 2009;52(11):2425-34. [BACK]
851. CHEN B, ZHAO J, ZHANG S, WU W, QI R. ASPIRIN
INHIBITS THE PRODUCTION OF REACTIVE OXYGEN
SPECIES BY DOWNREGULATING NOX4 AND INDUCIBLE
NITRIC OXIDE SYNTHASE IN HUMAN ENDOTHELIAL
CELLS EXPOSED TO OXIDIZED LOW-DENSITY
LIPOPROTEIN. J CARDIOVASC PHARMACOL.
2012;59(5):405-12. [BACK]
852. CARNOVALE DE, FUKUDA A, UNDERHILL DC,
LAFFAN JJ, BREUEL KF. ASPIRIN DOSE DEPENDENTLY
INHIBITS THE INTERLEUKIN-1 BETA-STIMULATED
INCREASE IN INDUCIBLE NITRIC OXIDE SYNTHASE,
NITRIC OXIDE, AND PROSTAGLANDIN E(2) PRODUCTION
IN RAT OVARIAN DISPERSATES CULTURED IN VITRO.
FERTIL STERIL. 2001;75(4):778-84. [BACK]
853.
DE CRISTÓBAL J, CÁRDENAS A, LIZASOAIN I, ET AL.
INHIBITION OF GLUTAMATE RELEASE VIA RECOVERY
OF ATP LEVELS ACCOUNTS FOR A NEUROPROTECTIVE
EFFECT OF ASPIRIN IN RAT CORTICAL NEURONS
EXPOSED TO OXYGEN-GLUCOSE DEPRIVATION.
STROKE. 2002;33(1):261-7. [BACK]
854.ASHOORI MR, BATHAIE SZ, HEIDARZADEH H.
LONG-TERM, HIGH-DOSE ASPIRIN THERAPY INCREASES
THE SPECIFIC ACTIVITY OF COMPLEX III OF
MITOCHONDRIAL RESPIRATORY CHAIN IN THE KIDNEY
OF DIABETIC RATS. PHYS. PHARM. 2015; 158-166. [BACK]
855.CHESHIRE RM, PARK MV. THE INHIBITION OF
LACTATE DEHYDROGENASE BY SALICYLATE. INT. J.
BIO. 1977; 8(9):637-643. [BACK]
856.
HARRIS RE, ROBERTSON FM, ABOU-ISSA HM, FARRAR
WB, BRUEGGEMEIER R. GENETIC INDUCTION AND
UPREGULATION OF CYCLOOXYGENASE (COX) AND
AROMATASE (CYP19): AN EXTENSION OF THE DIETARY
FAT HYPOTHESIS OF BREAST CANCER. MED
HYPOTHESES. 1999;52(4):291-2. [BACK]
857.TERRY MB, GAMMON MD, ZHANG FF, ET AL.
ASSOCIATION OF FREQUENCY AND DURATION OF
ASPIRIN USE AND HORMONE RECEPTOR STATUS WITH
BREAST CANCER RISK. JAMA. 2004;291(20):2433-40.
[BACK]
858. GATES MA, TWOROGER SS, ELIASSEN AH, MISSMER
SA, HANKINSON SE. ANALGESIC USE AND SEX STEROID
HORMONE CONCENTRATIONS IN POSTMENOPAUSAL
WOMEN. CANCER EPIDEMIOL BIOMARKERS PREV.
2010;19(4):1033-41. [BACK]
859.
SHEN L, SHEN J, PU J, HE B. ASPIRIN ATTENUATES
PULMONARY ARTERIAL HYPERTENSION IN RATS BY
REDUCING PLASMA 5-HYDROXYTRYPTAMINE LEVELS.
CELL BIOCHEM BIOPHYS. 2011;61(1):23-31. [BACK]
860.
DAYA S, ANOOPKUMAR-DUKIE S. ACETAMINOPHEN
INHIBITS LIVER TRYTOPHAN-2,3-DIOXYGENASE
ACTIVITY WITH A CONCOMITANT RISE IN BRAIN
SEROTONIN LEVELS AND A REDUCTION IN URINARY 5-
HYDROXYINDOLE ACETIC ACID. LIFE SCI. 2000;67(3):235-
40. [BACK]
861.
STARKE RM, CHALOUHI N, DING D, HASAN DM.
POTENTIAL ROLE OF ASPIRIN IN THE PREVENTION OF
ANEURYSMAL SUBARACHNOID HEMORRHAGE.
CEREBROVASC DIS. 2015;39(5-6):332-42. [BACK]
862.
WEHBEH A, TAMIM HM, ABU DAYA H, ET AL. ASPIRIN
HAS A PROTECTIVE EFFECT AGAINST ADVERSE
OUTCOMES IN PATIENTS WITH NONVARICEAL UPPER
GASTROINTESTINAL BLEEDING. DIG DIS SCI.
2015;60(7):2077-87. [BACK]
863.
ELWOOD PC, MORGAN G, GALANTE J, ET AL.
SYSTEMATIC REVIEW AND META-ANALYSIS OF
RANDOMISED TRIALS TO ASCERTAIN FATAL
GASTROINTESTINAL BLEEDING EVENTS ATTRIBUTABLE
TO PREVENTIVE LOW-DOSE ASPIRIN: NO EVIDENCE OF
INCREASED RISK. PLOS ONE. 2016;11(11):E0166166.
[BACK]
864.
PEAT, R. ASPIRIN, BRAIN AND CANCER. [ONLINE].
AVAILABLE:
HTTP://RAYPEAT.COM/ARTICLES/AGING/ASPIRIN-BRAIN-
CANCER.SHTML. [MARCH 1, 2017]. [BACK]
865.
SOMASUNDARAM S, SIGTHORSSON G, SIMPSON RJ, ET
AL. UNCOUPLING OF INTESTINAL MITOCHONDRIAL
OXIDATIVE PHOSPHORYLATION AND INHIBITION OF
CYCLOOXYGENASE ARE REQUIRED FOR THE
DEVELOPMENT OF NSAID-ENTEROPATHY IN THE RAT.
ALIMENT PHARMACOL THER. 2000;14(5):639-50. [BACK]
866.
BRZOZOWSKI T, KONTUREK PC, KONTUREK SJ,
STACHURA J. GASTRIC ADAPTATION TO ASPIRIN AND
STRESS ENHANCES GASTRIC MUCOSAL RESISTANCE
AGAINST THE DAMAGE BY STRONG IRRITANTS. SCAND
J GASTROENTEROL. 1996;31(2):118-25. [BACK]
867.
BRZOZOWSKI T, KONTUREK PC, KONTUREK SJ, ERNST
H, STACHURA J, HAHN EG. GASTRIC ADAPTATION TO
INJURY BY REPEATED DOSES OF ASPIRIN STRENGTHENS
MUCOSAL DEFENCE AGAINST SUBSEQUENT EXPOSURE
TO VARIOUS STRONG IRRITANTS IN RATS. GUT.
1995;37(6):749-57. [BACK]
868.
COLEMAN WB, WENNERBERG AE, SMITH GJ, GRISHAM
JW. REGULATION OF THE DIFFERENTIATION OF DIPLOID
AND SOME ANEUPLOID RAT LIVER EPITHELIAL
(STEMLIKE) CELLS BY THE HEPATIC
MICROENVIRONMENT. AM J PATHOL. 1993;142(5):1373-82.
[BACK]
869.YOSHIMURA K. BIPHASIC ACTIVATION OF
NUCLEAR FACTOR-KAPPA B IN CHONDROCYTE DEATH
INDUCED BY INTERLEUKIN-1BETA: THE EXPRESSION OF
INDUCIBLE NITRIC OXIDE SYNTHASE AND
PHAGOCYTE-TYPE NADPH OXIDASE THROUGH
IMMEDIATE AND MONOCARBOXYLATE TRANSPORTER-
1-MEDIATED LATE-PHASE ACTIVATION OF NUCLEAR
FACTOR-KAPPA B. 2016; 58(2):39-44. [BACK]
870.ANDO M, UEHARA I, KOGURE K, ET AL.
INTERLEUKIN 6 ENHANCES GLYCOLYSIS THROUGH
EXPRESSION OF THE GLYCOLYTIC ENZYMES
HEXOKINASE 2 AND 6-PHOSPHOFRUCTO-2-
KINASE/FRUCTOSE-2,6-BISPHOSPHATASE-3. J NIPPON
MED SCH. 2010;77(2):97-105. [BACK]
871. KAWAUCHI K, ARAKI K, TOBIUME K, TANAKA N.
P53 REGULATES GLUCOSE METABOLISM THROUGH AN
IKK-NF-KAPPAB PATHWAY AND INHIBITS CELL
TRANSFORMATION. NAT CELL BIOL. 2008;10(5):611-8.
[BACK]
872. VAUGHAN OR, DAVIES KL, WARD JW, DE BLASIO
MJ, FOWDEN AL. A PHYSIOLOGICAL INCREASE IN
MATERNAL CORTISOL ALTERS UTEROPLACENTAL
METABOLISM IN THE PREGNANT EWE. J PHYSIOL
(LOND). 2016;594(21):6407-6418. [BACK]
873.BLECHER M. EFFECTS OF CORTISOL ON THE
METABOLISM OF GLUCOSE BY LYMPHOID TISSUE. J
BIOL CHEM. 1964;239:1299-300. [BACK]
874. LAURENT D, PETERSEN KF, RUSSELL RR, CLINE
GW, SHULMAN GI. EFFECT OF EPINEPHRINE ON MUSCLE
GLYCOGENOLYSIS AND INSULIN-STIMULATED MUSCLE
GLYCOGEN SYNTHESIS IN HUMANS. AM J PHYSIOL.
1998;274(1 PT 1):E130-8. [BACK]
875. SHI, S., XU, J., ZHANG, B., JI, S., XU, W., LIU, J., ... YU,
X. (2016). VEGF PROMOTES GLYCOLYSIS IN PANCREATIC
CANCER VIA HIF1Α UP-REGULATION. CURRENT
MOLECULAR MEDICINE, 16(4), 394-403. [BACK]
876. SUMI S, ICHIHARA K, KONO N, NONAKA K, TARUI S.
INSULIN AND EPIDERMAL GROWTH FACTOR
STIMULATE GLYCOLYSIS IN QUIESCENT 3T3
FIBROBLASTS WITH NO CHANGES IN KEY GLYCOLYTIC
ENZYME ACTIVITIES. ENDOCRINOL JPN. 1984;31(2):117-
25. [BACK]
877. CANEBA CA, YANG L, BADDOUR J, CURTIS R, WIN J,
HARTIG S, MARINI J, NAGRATH D. NITRIC OXIDE IS A
POSITIVE REGULATOR OF THE WARBURG EFFECT IN
OVARIAN CANCER CELLS. CELL DEATH & DISEASE.
2014;5(6):E1302. [BACK]
878. THOMAS M, MONET JD, BRAMI M, ET AL.
COMPARATIVE EFFECTS OF 17 BETA-ESTRADIOL,
PROGESTIN R5020, TAMOXIFEN AND RU38486 ON
LACTATE DEHYDROGENASE ACTIVITY IN MCF-7
HUMAN BREAST CANCER CELLS. J STEROID BIOCHEM.
1989;32(2):271-7. [BACK]
879.IWAI M, JUNGERMANN K. LEUKOTRIENES
INCREASE GLUCOSE AND LACTATE OUTPUT AND
DECREASE FLOW IN PERFUSED RAT LIVER. BIOCHEM
BIOPHYS RES COMMUN. 1988;151(1):283-90. [BACK]
880. KOREN-SCHWARTZER N, CHEN-ZION M, BEN-
PORAT H, BEITNER R. SEROTONIN-INDUCED DECREASE
IN BRAIN ATP, STIMULATION OF BRAIN ANAEROBIC
GLYCOLYSIS AND ELEVATION OF PLASMA
HEMOGLOBIN; THE PROTECTIVE ACTION OF
CALMODULIN ANTAGONISTS. GEN PHARMACOL.
1994;25(6):1257-62. [BACK]
881.
NOVAK M, HALL CL, BLACKBURN BJ. A NUCLEAR
MAGNETIC RESONANCE STUDY OF THE GLUCOSE
METABOLISM OF HYMENOLEPIS DIMINUTA EXPOSED
TO HISTAMINE AND SEROTONIN IN VITRO. INT J
PARASITOL. 1991;21(5):589-96. [BACK]
882.
BRAGGION-SANTOS MF, VOLPE GJ, PAZIN-FILHO A,
MACIEL BC, MARIN-NETO JA, SCHMIDT A. SUDDEN
CARDIAC DEATH IN BRAZIL: A COMMUNITY-BASED
AUTOPSY SERIES (2006-2010). ARQ BRAS CARDIOL.
2015;104(2):120-7. [BACK]
883.
BARCLAY AW, BRAND-MILLER J. THE AUSTRALIAN
PARADOX: A SUBSTANTIAL DECLINE IN SUGARS INTAKE
OVER THE SAME TIMEFRAME THAT OVERWEIGHT AND
OBESITY HAVE INCREASED. NUTRIENTS. 2011;3(4):491-
504. [BACK]
884.
ANDERSON KE, ROSNER W, KHAN MS, ET AL. DIET-
HORMONE INTERACTIONS: PROTEIN/CARBOHYDRATE
RATIO ALTERS RECIPROCALLY THE PLASMA LEVELS OF
TESTOSTERONE AND CORTISOL AND THEIR RESPECTIVE
BINDING GLOBULINS IN MAN. LIFE SCI. 1987;40(18):1761-
8. [BACK]
885.
LANE AR, DUKE JW, HACKNEY AC. INFLUENCE OF
DIETARY CARBOHYDRATE INTAKE ON THE FREE
TESTOSTERONE: CORTISOL RATIO RESPONSES TO
SHORT-TERM INTENSIVE EXERCISE TRAINING. EUR J
APPL PHYSIOL. 2010;108(6):1125-31. [BACK]
886.
HENDERSON, Y. CARBON DIOXIDE. [ONLINE].
AVAILABLE:
HTTP://WWW.LEARNBUTEYKO.ORG/INFORMATION-
ABOUT-LEARNBUTEYKOORG/CARBON-DIOXIDE-BY-
YANDELL-HENDERSON. [MARCH 1, 2017]. [BACK]
887.
GIRARDIS M, BUSANI S, DAMIANI E, ET AL. EFFECT OF
CONSERVATIVE VS CONVENTIONAL OXYGEN THERAPY
ON MORTALITY AMONG PATIENTS IN AN INTENSIVE
CARE UNIT: THE OXYGEN-ICU RANDOMIZED CLINICAL
TRIAL. JAMA. 2016;316(15):1583-1589. [BACK]
888.
YIP K, ALONZI R. CARBOGEN GAS AND RADIOTHERAPY
OUTCOMES IN PROSTATE CANCER. THER ADV UROL.
2013;5(1):25-34. [BACK]
889.
FERGUSON ND. OXYGEN IN THE ICU: TOO MUCH OF A
GOOD THING?. JAMA. 2016;316(15):1553-1554. [BACK]
890.
KAVANAGH B. NORMOCAPNIA VS HYPERCAPNIA.
MINERVA ANESTESIOL. 2002;68(5):346-50. [BACK]
891.
AUSTIN MA, WILLS KE, BLIZZARD L, WALTERS EH,
WOOD-BAKER R. EFFECT OF HIGH FLOW OXYGEN ON
MORTALITY IN CHRONIC OBSTRUCTIVE PULMONARY
DISEASE PATIENTS IN PREHOSPITAL SETTING:
RANDOMISED CONTROLLED TRIAL. BMJ. 2010;341:C5462.
[BACK]
892.
LIU Y, ROSENTHAL RE, HAYWOOD Y, MILJKOVIC-LOLIC
M, VANDERHOEK JY, FISKUM G. NORMOXIC
VENTILATION AFTER CARDIAC ARREST REDUCES
OXIDATION OF BRAIN LIPIDS AND IMPROVES
NEUROLOGICAL OUTCOME. STROKE. 1998;29(8):1679-86.
[BACK]
893.
LUNDY JS. CARBON DIOXIDE AS AN AID IN GENERAL
ANESTHESIA. JAMA. 1925;85(25):1953-1955. [BACK]
894.
HENDERSON Y. RESUSCITATION: FROM CARBON
MONOXIDE ASPHYXIA, FROM ETHER OR ALCOHOL
INTOXICATION, AND FROM RESPIRATORY FAILURE DUE
TO OTHER CAUSES; WITH SOME REMARKS ALSO ON
THE USE OF OXYGEN IN PNEUMONIA, AND
INHALATIONAL THERAPY IN GENERAL. JAMA.
1924;83(10):758-764. [BACK]
895. FISHER JA, ISCOE S, FEDORKO L, DUFFIN J. RAPID
ELIMINATION OF CO THROUGH THE LUNGS: COMING
FULL CIRCLE 100 YEARS ON. EXP PHYSIOL.
2011;96(12):1262-9. [BACK]
896.HENDERSON, Y., AND HAGGARD, H.W., J.
PHARMACOL. AND EXP. THERAP., 16, 11 (1920). [BACK]
897.HENDERSON, Y., AND HAGGARD, H.W., J.AM. MED.
ASSN.,79, 1137 (1922). [BACK]
898.
HENDERSON, Y., HAGGARD, H.W., CORYLLOS, P.N.,
BIRNBAUM, G.L., AND RADLOFF, E.M., ARCH. INT. MED.,
45, 72 (1930). [BACK]
899.
HENDERSON Y. REASONS FOR THE USE OF CARBON
DIOXIDE WITH OXYGEN IN THE TREATMENT OF
PNEUMONIA. N ENGL. J. MED. 1932; 206:151-155. [BACK]
900.
FOSSLIEN E. CANCER MORPHOGENESIS: ROLE OF
MITOCHONDRIAL FAILURE. ANN CLIN LAB SCI.
2008;38(4):307-29. [BACK]
901.
 BRIVA A, LECUONA E, SZNAJDER JI. [PERMISSIVE AND
NON-PERMISSIVE HYPERCAPNIA: MECHANISMS OF
ACTION AND CONSEQUENCES OF HIGH CARBON
DIOXIDE LEVELS]. ARCH BRONCONEUMOL.
2010;46(7):378-82. [BACK]
902. CURLEY G, LAFFEY JG, KAVANAGH BP. BENCH-TO-
BEDSIDE REVIEW: CARBON DIOXIDE. CRIT CARE.
2010;14(2):220. [BACK]
903.O'CROININ D, NI CHONGHAILE M, HIGGINS B,
LAFFEY JG. BENCH-TO-BEDSIDE REVIEW: PERMISSIVE
HYPERCAPNIA. CRIT CARE. 2005;9(1):51-9. [BACK]
904.ISMAIEL NM, HENZLER D. EFFECTS OF
HYPERCAPNIA AND HYPERCAPNIC ACIDOSIS ON
ATTENUATION OF VENTILATOR-ASSOCIATED LUNG
INJURY. MINERVA ANESTESIOL. 2011;77(7):723-33. [BACK]
905. ROGOVIK A, GOLDMAN R. PERMISSIVE
HYPERCAPNIA. EMERG MED CLIN NORTH AM.
2008;26(4):941-52, VIII-IX. [BACK]
906. BAUTISTA AF, AKCA O. HYPERCAPNIA: IS IT
PROTECTIVE IN LUNG INJURY?. MED GAS RES.
2013;3(1):23. [BACK]
907.LAFFEY JG, KAVANAGH BP. CARBON DIOXIDE AND
THE CRITICALLY ILL--TOO LITTLE OF A GOOD THING?.
LANCET. 1999;354(9186):1283-6. [BACK]
908.
GAO W, LIU DD, LI D, CUI GX. EFFECT OF THERAPEUTIC
HYPERCAPNIA ON INFLAMMATORY RESPONSES TO
ONE-LUNG VENTILATION IN LOBECTOMY PATIENTS.
ANESTHESIOLOGY. 2015;122(6):1235-52. [BACK]
909.
NARDELLI LM, RZEZINSKI A, SILVA JD, ET AL. EFFECTS
OF ACUTE HYPERCAPNIA WITH AND WITHOUT
ACIDOSIS ON LUNG INFLAMMATION AND APOPTOSIS IN
EXPERIMENTAL ACUTE LUNG INJURY. RESPIR PHYSIOL
NEUROBIOL. 2015;205:1-6. [BACK]
910.
NI CHONGHAILE M, HIGGINS B, LAFFEY JG.
PERMISSIVE HYPERCAPNIA: ROLE IN PROTECTIVE
LUNG VENTILATORY STRATEGIES. CURR OPIN CRIT
CARE. 2005;11(1):56-62. [BACK]
911.
CONTRERAS M, MASTERSON C, LAFFEY JG.
PERMISSIVE HYPERCAPNIA: WHAT TO REMEMBER.
CURR OPIN ANAESTHESIOL. 2015;28(1):26-37. [BACK]
912.
DE SMET HR, BERSTEN AD, BARR HA, DOYLE IR.
HYPERCAPNIC ACIDOSIS MODULATES INFLAMMATION,
LUNG MECHANICS, AND EDEMA IN THE ISOLATED
PERFUSED LUNG. J CRIT CARE. 2007;22(4):305-13. [BACK]
913.
BANNENBERG GL, GIAMMARRESI C, GUSTAFSSON LE.
INHALED CARBON DIOXIDE INHIBITS LOWER AIRWAY
NITRIC OXIDE FORMATION IN THE GUINEA PIG. ACTA
PHYSIOL SCAND. 1997;160(4):401-5. [BACK]
914. BROGAN TV, HEDGES RG, MCKINNEY S,
ROBERTSON HT, HLASTALA MP, SWENSON ER.
PULMONARY NO SYNTHASE INHIBITION AND INSPIRED
CO2: EFFECTS ON V'/Q' AND PULMONARY BLOOD FLOW
DISTRIBUTION. EUR RESPIR J. 2000;16(2):288-95. [BACK]
915. ADDING LC, AGVALD P, PERSSON MG, GUSTAFSSON
LE. REGULATION OF PULMONARY NITRIC OXIDE BY
CARBON DIOXIDE IS INTRINSIC TO THE LUNG. ACTA
PHYSIOL SCAND. 1999;167(2):167-74. [BACK]
916.
NICHOL AD, O'CRONIN DF, NAUGHTON F, HOPKINS N,
BOYLAN J, MCLOUGHLIN P. HYPERCAPNIC ACIDOSIS
REDUCES OXIDATIVE REACTIONS IN ENDOTOXIN-
INDUCED LUNG INJURY. ANESTHESIOLOGY.
2010;113(1):116-25. [BACK]
917.
MAURER M, RIESEN W, MUSER J, HULTER HN, KRAPF R.
NEUTRALIZATION OF WESTERN DIET INHIBITS BONE
RESORPTION INDEPENDENTLY OF K INTAKE AND
REDUCES CORTISOL SECRETION IN HUMANS. AM J
PHYSIOL RENAL PHYSIOL. 2003;284(1):F32-40. [BACK]
918.
ROJAS VEGA S, STRÜDER HK, WAHRMANN BV, BLOCH
W, HOLLMANN W. BICARBONATE REDUCES SERUM
PROLACTIN INCREASE INDUCED BY EXERCISE TO
EXHAUSTION. MED SCI SPORTS EXERC. 2006;38(4):675-80.
[BACK]
919.
STRÜDER HK, HOLLMANN W, DONIKE M, PLATEN P,
WEBER K. EFFECT OF O2 AVAILABILITY ON
NEUROENDOCRINE VARIABLES AT REST AND DURING
EXERCISE: O2 BREATHING INCREASES PLASMA
PROLACTIN. EUR J APPL PHYSIOL OCCUP PHYSIOL.
1996;74(5):443-9. [BACK]
920.
NIELSEN FU, DAUGAARD P, BENTZEN L, ET AL. EFFECT
OF CHANGING TUMOR OXYGENATION ON GLYCOLYTIC
METABOLISM IN A MURINE C3H MAMMARY
CARCINOMA ASSESSED BY IN VIVO NUCLEAR
MAGNETIC RESONANCE SPECTROSCOPY. CANCER RES.
2001;61(13):5318-25. [BACK]
921.SABATINI S, KURTZMAN NA. BICARBONATE
THERAPY IN SEVERE METABOLIC ACIDOSIS. J AM SOC
NEPHROL. 2009;20(4):692-5. [BACK]
922.MALOV IUS, KULIKOV AN. [BICARBONATE
DEFICIENCY AND DUODENAL PEPTIC ULCER]. TER
ARKH. 1998;70(2):28-32. [BACK]
923.
 PEPELKO WE. THE EFFECT OF CORTISOL UPON
LIPOLYSIS DURING CYPERCAPNIA AND AFTER BETA-
ANDRENERGIC BLOCKADE. ANAT & PHYS PHARMAC.
1971. AVAILABLE: HTTP://OAI.DTIC.MIL/OAI/OAI?
VERB=GETRECORD&METADATAPREFIX=HTML&IDENTI
FIER=AD0731124. [FEBRUARY 15, 2017]. [BACK]
924.
HAYLOR J, TONER JM, JACKSON PR, RAMSAY LE, LOTE
CJ. IS THE URINARY EXCRETION OF PROSTAGLANDIN E
IN MAN DEPENDENT ON URINE PH?. CLIN SCI.
1985;68(4):475-7. [BACK]
925.
STRIDER JW, MASTERSON CG, DURHAM PL.
TREATMENT OF MAST CELLS WITH CARBON DIOXIDE
SUPPRESSES DEGRANULATION VIA A NOVEL
MECHANISM INVOLVING REPRESSION OF INCREASED
INTRACELLULAR CALCIUM LEVELS. ALLERGY.
2011;66(3):341-50. [BACK]
926.
ONISHI Y, KAWAMOTO T, UEHA T, ET AL.
TRANSCUTANEOUS APPLICATION OF CARBON DIOXIDE
(CO2) INDUCES MITOCHONDRIAL APOPTOSIS IN HUMAN
MALIGNANT FIBROUS HISTIOCYTOMA IN VIVO. PLOS
ONE. 2012;7(11):E49189. [BACK]
927.
PAGOURELIAS ED, ZOROU PG, TSALIGOPOULOS M,
ATHYROS VG, KARAGIANNIS A, EFTHIMIADIS GK.
CARBON DIOXIDE BALNEOTHERAPY AND
CARDIOVASCULAR DISEASE. INT J BIOMETEOROL.
2011;55(5):657-63. [BACK]
928.
HARTMANN BR, BASSENGE E, PITTLER M. EFFECT OF
CARBON DIOXIDE-ENRICHED WATER AND FRESH
WATER ON THE CUTANEOUS MICROCIRCULATION AND
OXYGEN TENSION IN THE SKIN OF THE FOOT.
ANGIOLOGY. 1997;48(4):337-43. [BACK]
 929.
HARTMANN B, DREWS B, BURNUS C, BASSENGE E.
[INCREASE IN SKIN BLOOD CIRCULATION AND
TRANSCUTANEOUS OXYGEN PARTIAL PRESSURE OF
THE TOP OF THE FOOT IN LOWER LEG IMMERSION IN
WATER CONTAINING CARBON DIOXIDE IN PATIENTS
WITH ARTERIAL OCCLUSIVE DISEASE. RESULTS OF A
CONTROLLED STUDY COMPARED WITH FRESH WATER].
VASA. 1991;20(4):382-7. [BACK]
930.HARTMANN B, DREWS B, BASSENGE E. [CO2-
INDUCED ACRAL BLOOD FLOW AND THE OXYGEN
PARTIAL PRESSURE IN ARTERIAL OCCLUSIVE DISEASE].
DTSCH MED WOCHENSCHR. 1991;116(43):1617-21. [BACK]
931. HARTMANN BR, BASSENGE E, HARTMANN M.
EFFECTS OF SERIAL PERCUTANEOUS APPLICATION OF
CARBON DIOXIDE IN INTERMITTENT CLAUDICATION:
RESULTS OF A CONTROLLED TRIAL. ANGIOLOGY.
1997;48(11):957-63. [BACK]
932. RESCH KL, JUST U. [POSSIBILITIES AND LIMITS OF
CO2 BALNEOTHERAPY]. WIEN MED WOCHENSCHR.
1994;144(3):45-50. [BACK]
933. SATO M, KANIKOWSKA D, IWASE S, ET AL. EFFECTS
OF IMMERSION IN WATER CONTAINING HIGH
CONCENTRATIONS OF CO2 (CO2-WATER) AT
THERMONEUTRAL ON THERMOREGULATION AND
HEART RATE VARIABILITY IN HUMANS. INT J
BIOMETEOROL. 2009;53(1):25-30. [BACK]
934.
SCHMIDT KL. CARBON DIOXIDE BATH (CARBON
DIOXIDE SPRING). CENTER FOR CLINICAL RESEARCH IN
RHEUMATOLOGY, PHYSICAL MEDICINE AND
BALNEOTHERAPY, GERMANY. AVAILABLE:
HTTP://WWW.MESOTHERAPYWORLDWIDE.COM/IMAGES
/PDF/CARBON_DIOXIDE_BATH.PDF. [APRIL 1, 2017].
[BACK]
935.
STREC V, DUKÁT A, AKSAMITOVÁ K, ADOLF P,
STALMASEKOVÁ B. [RESPONSE TO A SERIES OF
CARBON DIOXIDE BATHS]. VNITR LEK. 1992;38(2):148-54.
[BACK]
936.
HARTMANN B, POHL U, WOHLTMANN D, HOLTZ J,
BASSENGE E. [THE EFFECT OF CARBON DIOXIDE BATHS
ON BLOOD PRESSURE OF BORDERLINE HYPERTENSIVE
PATIENTS]. Z KARDIOL. 1989;78(8):526-31. [BACK]
937.
AKAMINE T, TAGUCHI N. EFFECTS OF AN ARTIFICIALLY
CARBONATED BATH ON ATHLETIC WARM-UP. J HUM
ERGOL (TOKYO). 1998;27(1-2):22-9. [BACK]
938.
MIAO P, SHENG S, SUN X, LIU J, HUANG G. LACTATE
DEHYDROGENASE A IN CANCER: A PROMISING TARGET
FOR DIAGNOSIS AND THERAPY. IUBMB LIFE.
2013;65(11):904-10. [BACK]
939.
MCSWAIN SD, HAMEL DS, SMITH PB, ET AL. END-TIDAL
AND ARTERIAL CARBON DIOXIDE MEASUREMENTS
CORRELATE ACROSS ALL LEVELS OF PHYSIOLOGIC
DEAD SPACE. RESPIR CARE. 2010;55(3):288-93. [BACK]
940.
TOLNER EA, HOCHMAN DW, HASSINEN P, ET AL. FIVE
PERCENT CO ₂ IS A POTENT, FAST-ACTING INHALATION
ANTICONVULSANT. EPILEPSIA. 2011;52(1):104-14. [BACK]
941.
LEE HJ, PARK CY, LEE JH, ET AL. THERAPEUTIC
EFFECTS OF CARBOGEN INHALATION AND LIPO-
PROSTAGLANDIN E1 IN SUDDEN HEARING LOSS.
YONSEI MED J. 2012;53(5):999-1004. [BACK]
942.
GRIFFITHS JR, TAYLOR NJ, HOWE FA, ET AL. THE
RESPONSE OF HUMAN TUMORS TO CARBOGEN
BREATHING, MONITORED BY GRADIENT-RECALLED
ECHO MAGNETIC RESONANCE IMAGING. INT J RADIAT
ONCOL BIOL PHYS. 1997;39(3):697-701. [BACK]
943. TAYLOR NJ, BADDELEY H, GOODCHILD KA, ET AL.
BOLD MRI OF HUMAN TUMOR OXYGENATION DURING
CARBOGEN BREATHING. J MAGN RESON IMAGING.
2001;14(2):156-63. [BACK]
944. BADDELEY H, BRODRICK PM, TAYLOR NJ, ET AL.
GAS EXCHANGE PARAMETERS IN RADIOTHERAPY
PATIENTS DURING BREATHING OF 2%, 3.5% AND 5%
CARBOGEN GAS MIXTURES. BR J RADIOL.
2000;73(874):1100-4. [BACK]
945.MCSHEEHY PM, PORT RE, RODRIGUES LM, ET AL.
INVESTIGATIONS IN VIVO OF THE EFFECTS OF
CARBOGEN BREATHING ON 5-FLUOROURACIL
PHARMACOKINETICS AND PHYSIOLOGY OF SOLID
RODENT TUMOURS. CANCER CHEMOTHER
PHARMACOL. 2005;55(2):117-28. [BACK]
946.TEICHER BA, SCHWARTZ GN, DUPUIS NP, ET AL.
OXYGENATION OF HUMAN TUMOR XENOGRAFTS IN
NUDE MICE BY A PERFLUOROCHEMICAL EMULSION
AND CARBOGEN BREATHING. ARTIF CELLS BLOOD
SUBSTIT IMMOBIL BIOTECHNOL. 1994;22(4):1369-75.
[BACK]
947. ALONZI R, PADHANI AR, MAXWELL RJ, ET AL.
CARBOGEN BREATHING INCREASES PROSTATE CANCER
OXYGENATION: A TRANSLATIONAL MRI STUDY IN
MURINE XENOGRAFTS AND HUMANS. BR J CANCER.
2009;100(4):644-8. [BACK]
948. KHAN N, LI H, HOU H, ET AL. TISSUE PO2 OF
ORTHOTOPIC 9L AND C6 GLIOMAS AND TUMOR-
SPECIFIC RESPONSE TO RADIOTHERAPY AND
HYPEROXYGENATION. INT J RADIAT ONCOL BIOL PHYS.
2009;73(3):878-85. [BACK]
949. KHAN N, MUPPARAJU S, HEKMATYAR SK, ET AL.
EFFECT OF HYPEROXYGENATION ON TISSUE PO2 AND
ITS EFFECT ON RADIOTHERAPEUTIC EFFICACY OF
ORTHOTOPIC F98 GLIOMAS. INT J RADIAT ONCOL BIOL
PHYS. 2010;78(4):1193-200. [BACK]
950.
POWELL ME, COLLINGRIDGE DR, SAUNDERS MI,
HOSKIN PJ, HILL SA, CHAPLIN DJ. IMPROVEMENT IN
HUMAN TUMOUR OXYGENATION WITH CARBOGEN OF
VARYING CARBON DIOXIDE CONCENTRATIONS.
RADIOTHER ONCOL. 1999;50(2):167-71. [BACK]
951.
HOU H, KRISHNAMURTHY NEMANI V, DU G, ET AL.
MONITORING OXYGEN LEVELS IN ORTHOTOPIC HUMAN
GLIOMA XENOGRAFT FOLLOWING CARBOGEN
INHALATION AND CHEMOTHERAPY BY IMPLANTABLE
RESONATOR-BASED OXIMETRY. INT J CANCER.
2015;136(7):1688-96. [BACK]
952.
AQUINO-PARSONS C, GREEN A, MINCHINTON AI.
OXYGEN TENSION IN PRIMARY GYNAECOLOGICAL
TUMOURS: THE INFLUENCE OF CARBON DIOXIDE
CONCENTRATION. RADIOTHER ONCOL. 2000;57(1):45-51.
[BACK]
953.
CORE WRITING TEAM, PACHAURI, R.K. AND REISINGER,
A. 2007. CLIMATE CHANGE 2007: SYNTHESIS REPORT.
IPCC, GENEVA, SWITZERLAND. PP 104. [BACK]
954.
VALENTINO FL, LEUENBERGER M, UGLIETTI C AND
STABURM P. MEASUREMENTS AND TREND ANALYSIS OF
O2, CO2 AND FROM HIGH ALTITUDE RESEARCH STATION
JUNFGRAUJOCH, SWITZERLND – A COMPARISON WITH
THE OBSERVATIONS FROM THE REMOTE SITE PUY DE
DÔME, FRANCE. SCIENCE OF THE TOTAL ENVIRONMENT
2008, 203-10. [BACK]
955.SIRIGNANO C, NEUBERT REM, JEIJER HAJ AND
RŐDENBECK C. ATMOSPHERIC OXYGEN AND CARBON
DIOXIDE OBSERVATIONS FROM TWO EUROPEAN
COASTAL STATIONS 2000-2005: CONTINENTAL
INFLUENCE TREND CHANGES AND APO CLIMATOLOGY.
ATMOS CHEM PHY DISCUSS 2008, 8, 20113-54. [BACK]
956.TOHJIMA Y, MUAI H, MACHIDA T, NOJIRI Y. GAS-
CHROMATOGRAPHIC MEASUREMENTS OF THE
ATMOSPHERIC OXYGEN/NITROGEN RATIO AT
HATERUMNA ISLAND AND CAPE OCHI-ISHI, JAPAN.
GEOPHYS RES LETT 2003, 30, 1653. [BACK]
957.EARTH SYSTEM RESEARCH LABORATORY. 2017.
TRENDS IN ATMOSPHERIC CARBON DIOXIDE. [ONLINE].
AVAILABLE:
HTTPS://WWW.ESRL.NOAA.GOV/GMD/CCGG/TRENDS/GL
OBAL.HTML.[MARCH 1, 2017]. [BACK]
958.
KELLY, M. (2016). ICE CORES REVEAL A SLOW DECLINE
IN ATMOSPHERIC OXYGEN OVER THE LAST 800,000
YEARS. PRINCETON UNIVERSITY [ONLINE]. AVAILABLE:
HTTPS://BLOGS.PRINCETON.EDU/RESEARCH/2016/09/23/I
CE-CORES-REVEAL-A-SLOW-DECLINE-IN-
ATMOSPHERIC-OXYGEN-OVER-THE-LAST-800000-
YEARS-SCIENCE/.[MARCH 1, 2017]. [BACK]
959.
SCHMIDTKO S, STRAMMA L, VISBECK M. DECLINE IN
GLOBAL OCEANIC OXYGEN CONTENT DURING THE
PAST FIVE DECADES. NATURE. 2015;542:335-339. [BACK]
960.
KULISH OP. [EFFECT HIGH-ALTITUDE CONDITIONS ON
THE ANTITUMOR ACTIVITY OF CYCLOPHOSPHANE AND
ITS ACTION ON LYMPHOID TISSUE CELLS]. EKSP ONKOL.
1985;7(3):60-3. [BACK]
961.
 KULISH OP, GALKINA KA. [EFFECT OF HIGH-ALTITUDE
HYPOXIA ON THE EFFECTIVENESS OF CHEMOTHERAPY
IN TUMORS]. BIULL EKSP BIOL MED. 1983;95(2):33-5.
[BACK]
962.
YU L, HALES CA. LONG-TERM EXPOSURE TO HYPOXIA
INHIBITS TUMOR PROGRESSION OF LUNG CANCER IN
RATS AND MICE. BMC CANCER. 2011;11:331. [BACK]
963.
BASCIANO L, NEMOS C, FOLIGUET B, ET AL. LONG
TERM CULTURE OF MESENCHYMAL STEM CELLS IN
HYPOXIA PROMOTES A GENETIC PROGRAM
MAINTAINING THEIR UNDIFFERENTIATED AND
MULTIPOTENT STATUS. BMC CELL BIOL. 2011;12:12.
[BACK]
964.
BENEDICT, F.G., AND HIGGINS, H.L.: AM. J. PHYSIOL.
30:217, 1912. [BACK]
965.HIGGINS, H.L., PEABODY, F.W., AND FITZ, R.: J. M.
RESEARCH. 29:263, 1916. [BACK]
HAWLEY, E.E.; JOHNSON, C.W., AND MURLIN, J.R.: J.
966.
NUTRITION. 6:523, 1933. [BACK]
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