**********************************************************************
Wednesday, July 31, 2002
Bill Summary - A04209
[EXCERPTS]
This legislation was adapted from model mercury legislation
endorsed
by the New England Governor`s Conference and has been introduced
in
various forms in Vermont, New Hampshire, Massachusetts, Maine,
Rhode
Island, Oregon and is being considered by California and Connecticut.
JUSTIFICATION : Mercury is a known neurotoxin that is linked
to
several cognitive and developmental problems in the brain,
spinal
cord, kidneys, lungs, and liver. There is an especially high risk
for
damage to fetuses and young children. In July 2000, the
National
Academy of Sciences (NAS) released a U.S. Congressionally
mandated
report entitled Toxicological Effects of Methylmercury. The
report
states "over 60,000 children a year are born each year at risk
for
adverse neurodevelopmental effects due to in utero exposure
to
methylmercury."
* Requires a material data safety sheet for the sale of
elemental
mercury.
* Places a ban on mercury
thermometers.
* Places a ban on mercury-containing toys or
games.
* Phases out the use of mercury-added gas
pressure
regulators/manometers for those entities that may use such
equipment
for the purpose of testing pressure, notably natural gas
lines.
* Directs the department of agriculture to establish a program
to
replace existing mercury containing
manometers.
* Requires dental offices to submit an annual amalgam mercury
report.
* Requires dental offices to post notice regarding the health
risks
associated with mercury amalgam.
* Requires informed consent by a person to receive mercury
amalgam
fillings.
* Prohibits any health insurer to discriminate against coverage
of
persons choosing to have dental fillings that do not contain
mercury.
* Requires a permit by DEC to operate a mercury-added lamp
recycling
facility.
* Includes mercury in state universal waste
rules.
* Establishes a State Advisory Committee on mercury pollution
that
must report annually to the legislature and Governor on
matters
concerning mercury pollution and cleanup in the
state.
http://assembly.state.ny.us/leg/?bn=a004209
**********************************************************************
*********
YOUR HELP IS NEEDED!
**********************************************************************
*********
HR 4163 IH
107th CONGRESS
2d Session
H. R. 4163
To prohibit after 2006 the introduction into interstate commerce of
mercury intended for use in a dental filling, and for other purposes.
IN THE HOUSE OF REPRESENTATIVES
APRIL 10, 2002
Ms. WATSON of California (for herself and Mr. BURTON of Indiana)
introduced the following bill; which was referred to the Committee on
Energy and Commerce
----------------------------------------------------------------------
----------
A BILL
To prohibit after 2006 the introduction into interstate commerce of
mercury intended for use in a dental filling, and for other purposes.
Be it enacted by the Senate and House of Representatives of the
United States of America in Congress assembled,
SECTION 1. SHORT TITLE.
This Act may be cited as the `Mercury in Dental Filling Disclosure
and Prohibition Act'.
SEC. 2. FINDINGS.
The Congress finds as follows:
(1) Mercury is a highly toxic element.
(2) A dental amalgam, commonly referred to as a `silver filling',
consists of 43 to 54 percent mercury.
(3) Consumers may be deceived by the use of the term `silver' to
describe a dental amalgam, which contains substantially more mercury
than silver.
(4) Dental amalgam may contain about 1/2 to 3/4 of a gram of mercury,
depending on the size of the filling.
(5) The mercury in a dental amalgam continually emits mercury vapors.
(6) Mercury toxicity is a retention toxicity that builds up over
years of exposure.
(7) According to certain scientific studies, Health Canada, and the
Agency for Toxic Substances and Disease Registry of the Public Health
Service of the Department of Health and Human Services, children and
pregnant women are at particular risk for exposure to mercury
contained in dental amalgam.
(8) According to the Agency for Toxic Substances and Disease
Registry, the mercury from amalgam goes through the placenta of
pregnant women and through the breast milk of lactating women, giving
rise to health risks to an unborn child or a baby.
(9) The Environmental Protection Agency considers removed amalgam
filling and extracted teeth containing amalgam material to be
hazardous waste.
(10) The use of mercury in any product being put into the body is
opposed by many health groups, such as the American Public Health
Association, the California Medical Association, and Health Care
Without Harm.
(11) Consumers and parents have a right to know, in advance, the
risks of placing a product containing a substantial amount of mercury
in their mouths or the mouths of their children.
(12) Alternatives to mercury-based dental fillings exist, but many
publicly and privately financed health plans do not allow consumers
to choose alternatives to mercury amalgam.
SEC. 3. PROHIBITION ON INTRODUCTION OF DENTAL AMALGAM INTO INTERSTATE
COMMERCE.
(a) PROHIBITION- Section 501 of the Federal Food, Drug, and Cosmetic
Act (21 U.S.C. 351) is amended by adding at the end the following:
`(j) Effective January 1, 2007, if it contains mercury intended for
use in a dental filling.'.
(b) TRANSITIONAL PROVISION- For purposes of the Federal Food, Drug,
and Cosmetic Act (21 U.S.C. 301 et seq.), effective July 1, 2002, and
subject to subsection (a), a device that contains mercury intended
for use in a dental filling shall be considered to be misbranded,
unless it bears a label that provides as follows: `Dental amalgam
contains approximately 50 percent mercury, a highly toxic element.
Such product should not be administered to children less than 18
years of age, pregnant women, or lactating women. Such product should
not be administered to any consumer without a warning that the
product contains mercury, which is a highly toxic element, and
therefore poses health risks.'.
END
http://www.bioprobe.com/ReadNews.asp?article=47
http://www.bioprobe.com/ReadNews.asp?article=42
H.R. 4163 -A Bill To Ban Mercury in Dental Fillings
(return to index)
----------------------------------------------------------------------
----------
On April 10, 2002 Representative Diane Watson of California (for
herself and Representative Dan Burton) introduced H.R. 4163, A Bill
that will ban Mercury Dental Amalgam (A copy of the Bill follows). It
is extremely important that you contact your elected representatives
and request that they Co-Sponsor H.R. 4163.
----------------------------------------------------------------------
----------
ELECTED OFFICIALS WILL RESPOND TO THEIR CONSTITUENTS
----------------------------------------------------------------------
----------
The Blue Pages of your telephone directory will have a section titled
Government Offices - U.S. You will find listings of your U.S.
representatives and two U.S. Senators.
If at all possible, pay a personal visit to the local staff and
advise them that you expect your Congress Person to support H.R.
4163. If you cannot make a personal visit then call, fax, write, or e-
mail, to let them know that you want them to support and Co-Sponsor
H.R. 4163.
Emphasize the most important issues: Protecting pregnant women and
their unborn babies, and small children from exposure to the mercury
neurotoxin.
Be sure and state that you will be paying attention to their vote on
this issue.
Tell all your friends about H.R. 4163 and request that they too
participate in contacting their elected Representatives.
See if your local health food store will participate by drafting a
petition of support for H.R. 4163 that all their customers can sign
and which can be forwarded to the U.S. Representative in that
district.
______________________________________________________________________
__________
Congresswoman Diane Watson announces bill to phase-out dental amalgam
(return to index)
Below is Congresswoman Diane Watson's statement concerning the
introduction of her Bill to prohibit the use of mercury in dental
fillings.
Because of the anthrax situation, the congresswoman's office prefers
you e-mail your support for this enormously important Bill. (Snail
mail is now too cumbersome as every letter must now be sanitized to
every Member of Congress.)
Your e-mail should be addressed to Congresswoman Watson:
diane.watson@.... Be sure and include your full mailing
address.
Statement by Congresswoman Diane Watson (D-Los Angeles)
Mercury in Dental Filling Disclosure and Prohibition Act
Los Angeles, California
November 5, 2001
In times like these, there are toxins that we don't know about how
to control them, their source and their impact. But there are toxins
that we DO know about toxins that we know do not belon in our
bodies, toxins that we can do something about. My bill addresses that
very problem.
Mercury is an acute neuro-toxin. It is the most toxic non-radioactive
element and the most volatile heavy metal. In recent years, it has
been, or is being removed from all health care uses, save one.
Antibiotics have replaced oral doses of Mercury. The disinfectant
Mercurochrome is banned. Recently, the Centers for Disease Control
ordered Mercury preservatives removed from childhood vaccines.
Mercury preservatives are no long used in contact lens solutions.
This year, legislatures in California and several other states banned
Mercury thermometers. When Governor Gray Davis signed bills
addressing Mercury in thermometers and in dental fillings, he
said, "Mercury is a persistent and toxic pollutant that
bioaccumulates in the environment." In recent years, the American
Public Health Association, the California Medical Association and
Health Care Without Harm have all called for the elimination of
putting any Mercury in the human body.
Today, I am announcing legislation to disclose and phase-out the last
major use of Mercury in the human body. The fillings that organized
dentistry wrongly calls "silver" are mainly Mercury, not "silver."
Mercury is the major ingredient in each filling, about one-half gram
per. In the words of Professor Boyd Haley of the University of
Kentucky, that is a "colossal" amount of Mercury in scientific terms
as much, in fact, as is in a thermometer. A teenager with six
fillings has six Mercury thermometers worth of Mercury in his or her
mouth.
The Mercury in the fillings is volatile, such that as all
authorities concede poisonous vapors are constantly being emitted
from the fillings, more so when one chews or passes hot liquid over
the teethe. The Agency for Toxic Substances & Disease Registry of the
United States Public Health Service reports that those poisonous
vapors go first to the brain and kidneys. For the developing brain
and by that I mean a child's brain a major health risk exists.
It is in fact children who are at greatest risk from these fillings.
The government of Canada recommended back in 1996 that dentists not
place fillings in the mouths of children or pregnant women. (The 1999
report on Mercury by the Agency for Toxic Substances & Disease
Registry says Mercury passes through the placenta into the developing
child's brain.) In 1997, a major manufacturer of dental amalgam,
Dentsply, said that amalgam is CONTRAINDICATED (translation DO NOT
USE) for children and pregnant women, as well as for those with
braces, Mercury hypersensitivities, or kidney problems. Another
manufacturer, Vivadent, added a contraindication for nursing mothers.
(The 1999 government report says the Mercury goes through the
mother's breast milk into the baby.)
Why don't consumers already know this? The answer is a disappointing
one. Organized dentistry is extremely divided on this issue. My bill,
in fact is supported by the American Academy of Biological Dentistry.
But the American Dental Association tells the public that the
fillings are safe. The ADA does not tell the public that it accepts
payments from the amalgam manufacturers while it pronounces their
product safe. I wish to note that the American Medical Association
has a policy prohibiting the organization from taking money for
product endorsements. The ADA, by contrast, accepts money from the
manufacturers of the products it endorses which certainly hurts its
credibility in my mind.
The public does not know about the presence of Mercury and its risks
for two reasons. First, the fillings are falsely called "silver."
This term is deceptive, because there is much more Mercury than
silver in the product. It's time to call it what it is and quit
hiding the large presence of Mercury.
Second, the ADA has a rule that gags dentists from talking about the
risks of Mercury amalgam, a rule that some dental boards enforce
against dentists who call for the elimination of Mercury in dental
fillings. I understand that rule is being challenged by dentists in
federal court in Maryland based on the First Amendment.
Developments in this area have been quite encouraging this year in my
state. In 1992, as a state Senator, I wrote a law that required the
Dental Board of California to write a "Fact Sheet" about the risks
and efficacies of dental fillings. My goal was to ensure the public
could make informed choices about Mercury dental amalgam. But the
Dental Board continued to ignore the law and, in recent years, defy
the Davis Administration's insistence that it comply with this law.
After an impasse, including the Board refusing to show up for a
hearing in Los Angeles on this issue, the Legislature stepped in and
shut down the Board. I am told that never before has the California
Legislature shut down a board before its Sunset date expired. In
January, a new Dental Board will come into existence.
A major environmental issue exists here. When removed from a
patient's mouth, Mercury amalgam is a hazardous waste, and it is
often improperly disposed of. The more Mercury that goes into
people's teeth, the more of it that will end up in our water supply.
I am delighted, therefore, that San Francisco-based Clean Water
Action is supporting my bill, and I look forward to other
environmental groups joining us in this effort.
The occupational risk is significant. Dental employees are constantly
exposed to the vapors. Women in dental offices have lower fecundity
(pregnancy) rates, more miscarriages, and more problem births.
Mercury exposure is the likely reason. Dentists have the highest
suicide rate of any profession; depression leading to suicide is
consistent with a diagnosis of Mercury toxicity.
Mercury amalgam is dangerous before it is put in the mouth any
dental journal will tell you that and it is considered hazardous
waste after it has been removed. Who can conclusively say it's safe
in between when it is in our bodies?
A major social justice, or environment justice, issue exists here.
While the public lacks informed choice, low- and moderate-income
people have it worse: they have no choice at all. For families on
Medi-Cal, the children get Mercury or nothing. It is outrageous
that low-income Americans are forced to have such a toxic material
put in their mouths. I understand that the Rhode Island legislature
adopted a law this year to provide choice in insurance plans, and
that the state of Maine permits Medicaid children to get alternatives
to amalgam so, yes, we can do it differently.
Mercury, and all other poisons in the body, hurt the body's immune
system its ability to withstand diseases and biologically harmful
agents. If at any time in our nations history we need strong immune
systems, it is now. The stronger our bodies, the more able we are to
fend off biological agents that have so tragically been placed in our
midst.
My bill will protect children, pregnant women, and nursing mothers
immediately regardless of their income. Henceforth, amalgam will
bear warnings that they not be placed in these most vulnerable
people. And there will be health warnings for all consumers of
amalgam, also immediately. Then, there is a five-year phase out of
Mercury amalgam. That will give dentistry plenty of time to shift to
alternatives that exist in today's market resin, porcelain, and
gold or to develop new materials.
Dentistry says amalgam is fine because it has been in ;use for 150
years. This statement, makes no scientific sense. We have abandoned
other remnants of pre-Civil War medicine, and we have abandoned all
other uses of Mercury. It is no longer a question of if, but when.
Mercury dental fillings will be history. I say five more years is
time enough.
______________________________________________________________________
__________
Dr. Haley Rebuts ADA Position on Mercury Amalgam Safety
Dr. Haley Rebuts the American Dental Association Position on Mercury
Amalgam Safety
23 May 2001
The Honorable Dan Burton
Chairman
Committee on Government Reform
U.S. House of Representatives
Washington, D.C.
RE: May 11th letter by Robert M. Anderton, D.D.S., J.D., LL.M. and
President of the ADA, challenging my statement to the Committee on
Government Reform looking at the topic, Autism-Why the Increased
Rates? A One Year Update.
Dear Mr. Chairman:
At the April 25th meeting of your committee I gave testimony that the
President of the American Dental Association (ADA) takes exception to
in a letter sent to you dated 11 May 2001. Quoting from that letter
the testimony the ADA dislikes is "that elementary mercury from
dental amalgam could work synergistically with other ethyl-mercury
sources and have a cumulative toxic effect on the body. Dr. Haley
postulated that this could be a potential cause of autism and
Alzheimer's disease." I stand by my statement as a sensible concern
based on published scientific research regarding synergist toxicities
caused by two very toxic agents, mercury and the organic mercury
compound thimerosal. This concern is elevated since mercury exposure
from amalgams to a pregnant mother concentrates in the fetus and a
single vaccine given to a six-pound newborn is the equivalent of
giving a 180-pound adult 30 vaccinations on the same day. Include in
this the toxic effects of high levels of aluminum and formaldehyde
contained in some vaccines, and the synergist toxicity could be
increased to unknown levels. Further, it is very well known that
infants do not produce significant levels of bile or have adult renal
capacity for several months after birth. Bilary transport is the
major biochemical route by which mercury is removed from the body,
and infants cannot do this very well. They also do not possess the
renal (kidney) capacity to remove aluminum. Additionally, mercury is
a well-known inhibitor of kidney function. Common sense indicates
that the concern I expressed should be taken seriously since we do
not know how combined toxicities effect humans, especially in utero.
Consider the current epidemic death on birth of over 500 foals from
apparently healthy mares around Lexington, KY. These deaths were
identified as being due to a low level toxicity delivered by
caterpillars eating poison plants and later, on migration, depositing
their waste products on grass being eaten by the mares. The point
being it is the infant in utero that suffered most on exposure to low
level, toxins, not the mother. Combined mercury toxicities can be
devastating as I reference below and in the many references available
on the www.altcorp.com website. What is needed is research by non-
biased scientists to clarify this, something our FDA and NIDCR have
refused to do. As the American public find out what has happened
regarding this issue, they will be quite angry. This is a biomedical
science issue that should have been resolved a long time ago by the
responsible federal agencies.
Below I present detailed and referenced information supporting my
case and respond to various statements made by the ADA President that
I believe to be misleading and sometimes flagrantly wrong. The ADA
seems to think it has the right to select which research it believes
and to trash that research that says it is wrong, even though the
latter represents the bulk of published research. To address the
issues raised by the ADA President in his letter I will go in
sequential order of the comments made in the letter placing the ADA
comments in italics and providing scientific references for my
conclusions.
"There is no scientifically valid evidence linking either autism or
Alzheimer's disease with dental amalgam". First, mercury is a well-
known, potent neurotoxicant, and common sense would lead to the
conclusion that severe neurotoxins would exacerbate all neurological
disorders, including Parkinson's, ALS, MS, autism and AD. Several
research papers in refereed, high quality journals and scientific
publications have shown that mercury inhibits the same enzymes in
normal brain tissues as are inhibited in AD brain samples (1a-c, 2,
3). AD is pathologically confirmed post-mortem by the appearance of
neuro-fibillary tangles (NFTs) and amyloid plaques in brain tissue.
Published research, within the past year, has shown that exposure of
neurons in culture to sub-lethal doses of mercury (much less than is
observed in human brain tissue) causes the formation of NFTs (4), the
increased secretion of amyloid protein and the hyper-phosphorylation
of a protein called Tau (5). All three of these mercury-induced
aberrances are regularly identified as the major diagnostic markers
for AD. In the manuscript published in the J. of Neurochemistry (5)
the authors state "These results indicate that mercury may play a
role in the patho-physiological mechanisms of AD." In most of these
experiments, mercury and only mercury among the several toxic heavy
metals tested, caused the AD related responses reported. Many
medically trained individuals would agree that if something causes
the appearance of the pathological hallmarks confirming the disease
then it likely causes the disease. I at least have limited my claims
to exacerbation of these diseases to err on the side of caution.
Further, consider this about AD. A study of 500 sets of identical
twins from World War II era lead to the conclusion that sporadic AD
which represents 90% of the cases was not a directly inherited
disease. In many cases one twin would get AD and the other would not.
Genetic susceptibility is involved, but a toxic exposure is required
(e.g., if you are genetically susceptible to being an alcoholic you
still need to be exposed to alcohol to become one). The work by
Rose's group at Johns Hopkins University implicates APO-E genotype as
a "risk" factor with APO-E2 being protective and APO-E4 being a major
risk factor. APO-E2 has the ability to protect the brain from mercury
by having two additional thiol-groups to bind mercury appearing in
the cerebrospinal fluid whereas APO-E4 does not have this additional
capability (1). This may explain the proven genetic susceptibility to
AD of the APO-E4 carriers.
NIH has spent hundreds of millions of dollars to find a causal factor
for AD. Yet, no virus, yeast or bacteria has been identified so the
cause remains unknown to general science. The rate of AD per 1,000
population is nearly the same in California, Michigan, Maine, North
Carolina, Florida, Texas, etc. It is not significantly different for
rural versus urban individuals, or factory workers versus those with
outside jobs. So the primary toxicant that may be involved is most
likely not environmental. Therefore, it must be a very personal
toxicant, like what you put in your mouth. Since we place grams of a
neurotoxic metal, mercury, in our mouths in the form of dental
amalgam this makes it a good suspect for the exacerbation of AD---not
that all would be affected, just those that are genetically
susceptible, or those who become ill enough to fall prey to the
toxicity, or those that are also exposed to another synergistic toxin
(see below).
The one fact that ties mercury into a major suspect for AD is the
fact that most of the proteins/enzymes that are inhibited in AD brain
are thiol-sensitive enzymes. Mercury is one of the most potent
chemical inhibitors of thiol-sensitive enzymes and mercury vapor
easily penetrates into the central nervous system (2). Mercury is not
the only toxicant to inhibit thiol-sensitive enzymes. Thimerosal and
lead will do this also as well as reactive oxygen compounds created
in oxidative stress and many other industrial compounds. However,
mercury has been reported to be significantly elevated in AD brain
(14a,b, 15). Mercury is in many mouths being emitted from dental
amalgam and absolutely would exacerbate the clinical condition
identified as AD. Therefore, mercury should be considered as a causal
contributor since mercury can produce the two pathological hallmarks
of the disease and inhibits the same thiol-sensitive enzymes that are
dramatically inhibited in AD brain.
It is documented by a 1991 World Health Organization report that
dental amalgams constitute the major human exposure to mercury. Grams
of mercury are in the mouths of individuals with several amalgam
fillings. Further, the level of blood and urine mercury positively
correlates with the number of amalgam fillings. This was confirmed by
a recently published NIH funded study (6). Therefore, I fail to see
the ADA's viewpoint that there is no scientifically valid evidence
linking mercury from amalgams to exacerbating AD, especially since
mercury produces the diagnostic hallmarks of AD (4,5). The ADA hides
behind the fact that there has not been an epidemiological study to
attempt to correlate mercury exposure and AD. However, absence of
proof is not proof of absence. This also begs the question why the
ADA, the FDA and the National Institutes of Dental Craniofacial
Research (NIDCR) have not pushed for such a study? These agencies
know this would be immensely expensive and only the U.S. government
could afford to support any reliable long-term study. Yet, these same
responsible agencies have failed to confirm as safe the placing into
the mouth of Americans grams of the most toxic heavy metal Americans
are exposed to. The dental branch of the FDA has steadfastly refused
to investigate the toxic potential of dental amalgam.
Look at the references in the ADA letter! Even they must quote
Scandinavian literature to support their contentions of safety, and
even then they have to reference papers on fertility instead of
neurotoxicity! Where is the ADA, FDA and NIDCR supported U.S.
research in this area? Go to the NIH web-sites and look for research
on the safety of mercury from amalgams, or try to find an NIH study
concerning possible mercury involvement in any common neurological
diseases. NIH does support research on methyl-mercury, as we seem to
like beating up on the fishing industry whilst leaving the dental
industry alone. However, according to the NIH study about 90% of the
mercury in our bodies is elemental mercury, not methyl-mercury,
showing the exposure is more likely from dental amalgams rather than
fish (6). Support at NIH has been very sparse for investigating the
relationship of elemental mercury exposure to neurological diseases.
"And there is no scientifically valid evidence demonstrating in vivo
transformation of inorganic mercury into organo mercury species in
individuals occupationally exposed to amalgam mercury vapor". There
was a paper published entitled "Methylation of Mercury from Dental
Amalgam and Mercuric Chloride by Oral Streptococci in vitro" (19).
This strongly indicates that "organo mercury species" are indeed
capable of being made in the human body and may explain the
appearance of methyl-mercury in the blood and urine of individuals
who don't eat seafood.
Further, periodontal disease is considered one of the major risk
factors for stroke, heart and cardiovascular disease and late onset,
insulin independent diabetes. Many studies of the toxicants produced
in periodontal disease have identified hydrogen sulfide (H2S) and
methane-thiol (CH3SH) as major toxic products of infective anerobic
bacteria in the mouth metabolizing the amino acids cysteine and
methionine, respectively. These volatile thiol-compounds are what
cause bad-breath! Methane-thiol (CH3SH) would react immediately and
spontaneously in the mouth with amalgam generated mercury cation to
produce the following two compounds, CH3S-HgCl and CH3S-Hg-SCH3,
which are organo-mercurial compounds (check this out with any
competent chemist). They are also very similar in structure to methyl-
mercury (CH3-HgCl) and dimethyl-mercury (CH3-Hg-CH3), the latter
which caused the highly publicized death of a University of Dartmouth
chemistry professor 10 months after she spilled two drops on her
gloved hand. We have synthesized CH3S-HgCl and CH3-Hg-CH3 in my
laboratory and tested their toxicity in comparison to Hg2+. As
expected, they were both more toxic than Hg2+ and this data is
available on the www.altcorp.com web-site. Therefore, the ADA
President is badly misinformed on this issue. Additionally, I am
amazed that the researchers at the ADA and NIDCR did not previously
report on this obvious chemistry as I would imagine this is the kind
of topic they should be addressing.
"Based on currently available scientific evidence, the ADA believes
that dental amalgam is a safe, affordable and durable material for
all but a handful of individuals who are allergic to one of its
components. It contains a mixture of metals such as silver, copper
and tin, in addition to mercury, which chemically binds these
components into a hard, stable and safe substance." This is a totally
wrong statement unless you underline the "ADA believes" and define
how big is a "handful of individuals". Sensible people
want "believes" replaced with "knows" and a "handful" replaced with
a "hard number". Amalgams emit dangerous levels of mercury and the
ADA absolutely refuses to accept this fact or even to study the
possibility. Otherwise, the ADA administrators seem to be unable to
separate fact from fiction. Consider, if they wanted to destroy my
argument on amalgam toxicity they would reference several solid,
refereed publication showing that mercury is not emitted from dental
amalgams---but they cannot do this with even one article. They always
state the "estimate" is that a very, very, very small amount.
Competent, well-informed researchers don't use the evasive language
used in the ADA President's letter. They would state the amount is so
many micrograms mercury released per centimeter squared amalgam
surface area and a "handful of individuals" would be a percentage of
our population! Lets look at the published literature.
First, careful evaluation of the amount of mercury emitted from a
commonly used dental amalgam in a test tube with 10 ml of water was
presented in an article entitled "Long-term Dissolution of Mercury
from a Non-Mercury-Releasing Amalgam". This study showed that "the
over-all mean release of mercury was 43.5 ± 3.2 micrograms per
cm2/day, and the amount remained fairly constant during the duration
of the experiments (2 years)" (7). This was without pressure, heat or
galvanism as would have occurred if the amalgams were in a human
mouth. Further, research where amalgams containing radioactive
mercury were placed in sheep and monkeys, showed the radioactivity
collecting in all body tissues and especially high in the jaw and
facial bones. (8,9). Another publication, from a major U.S. School of
Dentistry, stated that solutions in which amalgams had been soaked
were "severely cytotoxic initially when Zn release was highest" (13).
Zn is a needed element for body health and is found in very low
percentages in dental amalgams when compared to mercury and why
mercury was not mentioned in the abstract of this publication baffles
me. Why would the statement be true? Because Zn2+ is a synergist that
enhances mercury toxicity! However, does this sound like amalgams are
a safe, stable material? We have repeated similar amalgam soaking
experiments in my laboratory and the results can be seen at
www.altcorp.com. Cadmium (from smoking), lead, zinc and other heavy
metals enhanced mercury toxicity as expected (this research is
currently being prepared for publication).
The ADA claim that a zinc oxide layer is formed on the amalgams that
decreases mercury release is true, if you don't use the teeth. The
zinc oxide layer would be easily removed by slight abrasion such as
chewing food or brushing the teeth. Further, my laboratory has
confirmed that solutions in which amalgams have been soaked can cause
the inhibition of brain proteins that are inhibited by adding mercury
chloride, and these are the same enzymes inhibited in AD brain
samples.
Further, mercury emitting from a dental amalgam can be easily
detected using the same mercury vapor analysis instrument used by
OSHA and the EPA to monitor mercury levels. Anyone who does not
believe mercury is emitted from amalgams should consider doing the
following. Have your local dentist make 10 amalgams using the same
material he/she places in your mouth. Take these 10 amalgams to your
nearest research university's department of chemistry or toxicology
department and have them determine how much mercury is being emitted.
For example, have them calculate how long it would take a single
spill of hardened amalgam to make a gallon of water too toxic to pass
EPA standards as drinking water. You will then have an answer from an
unbiased, solid group of scientists who are trained to do such
determinations. Also, remember the level of mercury they measure
would not include the increase that would occur with amalgams in the
mouth where chewing, grinding your teeth, drinking hot liquids and
galvanism greatly increase the release of mercury. Since this
approach can be easily done by anyone don't you think the ADA, FDA
and other amalgam supporters would have this published by now if the
level of mercury released was below the danger level?
Here is their attempt. According to an ADA spokesman he
has "estimated" that only 0.08 micrograms of mercury per amalgam per
day is taken into the human body. Applying simple math to
this "estimate" of 0.08 micrograms/ day one would divide this amount
by 8,640 (24 hours/day X 60 minutes/hour X 6 ten second
intervals/minute) to determine the amount of mercury in micrograms
available for a ten second mercury vapor analysis. Consider that
somewhere between one-half to five-sixths of the mercury released
would be into the tooth (that area of the amalgam that exists below
the visibly exposed amalgam surface) and not into the oral air. In
addition, some mercury in the oral air would be rapidly absorbed into
the saliva and oral mucosa (mercury loves hydrophobic cell membranes)
and also not be measured by the mercury analyzer. Further, as the
mercury analyzer pulls mercury containing oral air into the analysis
chamber, mercury free ambient air rushes into the oral cavity
decreasing the mercury concentration. Taking all of this into account
you can calculate that most mercury analyzers could not detect
this "estimated" 0.08 micrograms/day level of mercury even if you had
several amalgams. However, the fact is that it is quite easy to
detect mercury emitting from one amalgam using these analyzers.
Therefore, the "estimate" by this ADA spokesman is way to low. Also,
if you gently rub the amalgam with a tooth-brush the amount of
mercury emitted goes up dramatically. This is a test anyone can do
and demonstrate to any group. The ADA spokesmen state that the
mercury vapor analyzer is not accurate at determining oral mercury
levels and they are quite correct. However, using this instrument
would greatly underestimate the amount of mercury exiting the
amalgam. The very fact that the mercury analyzer detects high levels
of oral mercury strongly indicates the emitted amount of mercury is
too high to be acceptable.
Mercury release from dental amalgams is also the reason OSHA has used
this analyzer to make the dentists place unused amalgam in a sealed
container under liquid glycerin. This is done so that the mercury
vapors from the amalgams will not contaminate the dental office
making it an unsafe place to work. This is also the reason the EPA
insists that removed amalgam filling and extracted teeth containing
amalgam material be picked up and disposed of as toxic waste.
Apparently, the only safe place for amalgams is in the human mouth if
you believe what the ADA believes.
"Amalgams have been used for 150 years and, during that time, has
established an extensively reviewed record of safety and
effectiveness." First, what other aspect of industry or medicine is
still using the same basic manufactured material that they used 150
years ago? One has to ask the question as to what has hindered the
progress of development of better and safer dental materials? Also,
consider that in the early 1900s the average life expectancy of most
Americans was about 50 years of age and most of them could not afford
dental fillings. Fifty to sixty years is much less than the average
age of onset of AD. Further, amalgams became more available to most
working class Americans after World War II, or in the early 1950s.
The greatest increase in the use of amalgam occurred at about this
time and these 'baby boomers are the great ongoing amalgam
experiment'. They are now reaching the age where AD appears and have
lived most of their lives carrying amalgam fillings. They also wonder
what is causing their chronic fatigue as the physicians can find
nothing systemically wrong with them. I would encourage all concerned
to contact the health experts on the rate of increase of AD in the
U.S.A. at this time. Consider the cost it will place on the taxpayer
and how much we would save if we could even remove the exacerbation
factors that might speed up the onset of AD. I must point out that
the "extensively reviewed record of safety" mentioned in the ADA
letter was mostly done by dentists and committees dominated by ADA
dentists. Also, much of the "safety opinion" was developed long
before words like Alzheimer's disease and chronic fatigue were
commonplace. Further, these were "reviews" and not carefully
documented studies based on scientific experimentation and done by
unqualified dentists, not medical scientists. Dentists are not
trained to do basic research, nor are they trained in toxicology.
Furthermore, the ADA does have a vested interest in keeping amalgam
use legitimate. The ADA was founded on using amalgam technology and
participated in patenting and licensing amalgam technology. One has
to question why there has not been a general outcry by the bulk of
well-meaning dentists and their patients and this question should be
addressed. The International Association of Oral Medicine and
Toxicology, started by American & Canadian dentists, does adamantly
disagree with the ADA on the issue of safety of dental amalgams and
this organization has the mantra of "Show me your science" with
regards to all dental issues.
The ADA, through state dental boards stacked with ADA members, has
instigated a "gag order" preventing dentists from even mentioning to
their patients that amalgams are 50% mercury. Dentists cannot state
that mercury is neurotoxic and emits from amalgams and that the
dental patient should consider this as they select the tooth filling
material they want used. If a dentist informs a patient of these very
truthful facts he will be consider not to be practicing good
dentistry and his license will be in jeopardy. Attacking a person's
freedom of speech because he is telling the truth and causing serious
questions to be asked about the protocols pushed by a bureaucracy
(the ADA) makes me seriously question the commitment the ADA has for
the health of the American people. The negative stand taken by many
state dental boards against even informing the patients about the
mercury content of amalgams and the other filling choices they have
does not speak well for the organized dental profession. What medical
group would give a treatment to a patient without telling them of the
risks involved?
"Issued late in 1997, the FDI World Dental Federation and the World
Health Organization consensus statement on dental amalgam stated "No
controlled studies have been published demonstrating systemic adverse
effects from amalgam restorations."" My first comment would be to
question "who staffed these committees and what percentage were
connected to the ADA though the NIDCR or the FDA dental materials
branch or other relationships?" We appear to have the foxes guarding
the henhouse! Then I would again point out that "absence of proof is
not proof of absence". I would then ask 'have any controlled studies
been done and if not, why not?' If the ADA dentists insist on placing
amalgams in the mouth, are they not required to show it is safe, not
the other way around? Should not the ADA and others concerned push to
require the FDA to prove amalgams are safe instead of totally ducking
this issue. Go to the FDA dental materials web-site and try to find
any evaluation of amalgam safety---you will not succeed. The dental
branch of the FDA refuses to do a safety study on amalgams and this
is shame on our government.
"the small amount of mercury released from amalgam restorations,
especially during placement and removal, has not been shown to cause
anyadverse effects." This increase in mercury exposure has also not
been shown to be safe by proving it does not cause any adverse
effects! Are we to believe this elevated exposure to a toxic metal is
good for us? If one were in a building that caused the rise in
blood/urine mercury that appears after dental amalgam removal, then
OSHA would shut the building down. In fact, no study by the ADA or
NIDCR has been completed that specifically and accurately addresses
this issue. Yet, the ADA leads us to believe that additional exposure
to toxic mercury from these procedures is not dangerous to our
health. Mercury toxicity is a retention toxicity that builds up
during years of exposure. The toxicity of a singular level of mercury
is greatly increased by current or subsequent, low exposures to lead
or other toxic heavy metals (12). Therefore, the damage caused by
amalgams could occur years after initial placement and at mercury
levels now deemed safe by the ADA.
Our ability to protect ourselves from the toxic damage caused by
exposure to mercury depends on the level of protective natural
biochemical compounds (e.g. glutathione, metallothionine) in our
cells and the levels of these protecting agents is dependent upon our
health and age. If we become ill, or as we age, the cellular levels
of glutathione drop and our protection against the toxic effects of
mercury decreases and damage will be done. This is strongly supported
by numerous studies where rodents have been chemically treated to
decrease their cellular levels of protective glutathione and then
treated with mercury, always with dramatic injurious effects when
compared to controls. Therefore, published science indicates that
mercury toxicity is much more pronounced in infants, the very old and
the very ill.
A recent NIH study on 1127 military men showed the major contributor
to human mercury body burden was dental amalgams. The amount of
mercury in the urine increased about 4.5 fold in soldiers with the
average number of amalgams versus the controls with no amalgams. In
extreme cases it was over 8 fold higher. Since the total mercury
included that from diet and industrial pollution are we to expect
that this 4.5 to 8 fold average increase in mercury is not
detrimental to our health? Does this indicate that amalgams are
a "safe and effective restorative material"? Is the public and
Congress expected to be so naοve as to believe that increased
exposure above environmental exposure levels is not damaging? Then
why are pregnant mothers told to limit seafood intake when mercury
exposure from amalgams is much greater? Then why is the EPA pushing
regulations to force the chloro-alkali plants and fossil fuel plants
to clean up their mercury contributions to our environment?
Obviously, from this study most of the human exposure to mercury is
from dental amalgams, not fossil fuel plants. Yet, the FDA lets the
dental profession continue to expose American citizens to even
greater amounts of mercury. They do this by refusing to test amalgam
fillings as a source of mercury exposure. Also, remember that the
amalgam using ADA dentists are a major contributor to mercury in our
water and air through mercury leaving the dental offices, and even
when we are cremated.
"The ADA's Council on Scientific Affairs 1998 report on its review of
the recent scientific literature on amalgam states: "The Council
concludes that, based on available scientific information, amalgam
continues to be a safe and effective restorative material."
and "There currently appears to be no justification for discontinuing
the use of dental amalgam." What would you expect an ADA Council to
say? The ADA, as evidenced in the current letter by the President of
the ADA, only quotes and considers valid the published research that
supports their desire to continue placing mercury containing amalgam
fillings in American citizens. When were dentists trained to evaluate
neurological and toxicological data and manuscripts? What is needed
is an international conference where both the pro- and anti-amalgam
researchers show up and present their data in front of a world-class
scientific committee. I would challenge the ADA to line up their
scientists and supporters to participate in such a conference. This
could be held in Washington, D.C. so the FDA officials could easily
attend. Perhaps we could persuade the FDA to sponsor such a
conference. However, this is unlikely since a recent written request
to have a conference to evaluate the safety of amalgams was rejected
in a letter from the FDA and signed by three FDA/ADA dentists who
presented the ADA line on this issue. Doesn't it seem a bit
fraudulent to have FDA/ADA dentists deciding on whether or not a
safety study should be done on mercury emitting amalgams being placed
in human mouths with the blessing of the ADA? This does seem like a
conflict in interest that Congress should address.
"In an article published in the February 1999 issue of the Journal of
the American Dental Association, researchers report finding "no
significant association of Alzheimer's disease with the number,
surface area or history of having dental amalgam restorations." This
research was lead by a dentist, Dr. Sax. It was submitted to the J.
of the American Medical Association and rejected. It was then
submitted to the New England Journal of Medicine and rejected. It was
then published in the ADA trade journal, JADA, that is not a
refereed, scientific journal. JADA is loaded with commercial
advertisements for dental products. They even called a "press
conference" announcing the release of this article! Calling a press
conference for a twice-rejected publication that is to appear in a
trade journal is playing politics with science at its worst! At this
press conference two of the authors made unbelievable statements that
were not supported by any of the data in the article and conflicted
with numerous major scientific reports, including the 1998 NIH study
(6). Some of these were high-lighted in the side-bars of the ADA
publication. I would suggest that those concerned with this article
visit Medline and look at the publication records of the two
individuals who made these statements. Also, look at the three
earlier excellent publications in refereed journals by some of the
other authors showing significant mercury levels in the brains of AD
subjects compared to controls (14a,b, 15). However, put a dentist in
charge of the project and the data gets reversed!
Apply some common sense. The ancillary comments by some of the
authors and the results of the JADA publication are in total
disagreement with the vast majority of research published that looks
at elevated mercury levels in subjects with amalgam fillings. For
example, the NIH study on military men discussed above showed a very
significant elevation of mercury in the blood that correlated with
number of dental amalgams (6). Another recent publication
demonstrated elevated mercury in the blood of living AD patients in
comparison to age-matched controls (10). These studies clearly show
that there should be increased mercury in your blood if you have
amalgams and especially if you have AD and amalgams (6,10). Does not
the brain have blood in it? This makes it a total mystery as to how
could the authors of the JADA article not find elevated brain mercury
levels in patient with existing amalgams and/or AD. Even cadavers
have brain mercury levels that correlate with the number of amalgam
fillings they had on death.
Further, if you are addressing the contribution of amalgams to brain
mercury and AD wouldn't it be important to divide the AD and control
subjects into those with and without existing amalgams on death? In
the JADA article this was not done and represents a major research
flaw! That this was not done also arouses suspicion. I participated
in submitting a letter pointing out this flaw to editors of JADA but
they refused to acknowledge the letter and did not publish our
comments. It is my opinion that the entire situation around this
singular supportive publication of the ADA position on amalgams,
brain mercury levels and AD represents a weak attempt at controlling
the mind-set of well-meaning dentists, scientists, physicians and
medical research administrators. It definitely impedes honest
scientific debate. It also explains the cavalier attitude of the ADA
and NIDCR about elemental mercury exposure and toxicity when compared
to the more serious approaches taken by the EPA and OSHA.
With regards to the JADA article summary that "no statistically
significant differences in brain mercury levels between subjects with
Alzheimer's disease and control subjects." Here I must quote Mark
Twain on honesty, "There are liars, damned liars and statisticians."
Comparing the level of mercury in the AD versus control alone using
straight-forward statistics previously showed a significant
difference on mercury levels in AD versus control subjects (14a,b,
15). However, there are anomalies, confounders and other factors that
can be considered in this situation, especially if you don't like the
initial results. This allows one to invoke a Bon-Feroni statistical
manipulation. With Bon-Feroni you include the comparison of one pair
of data (that may be statistically significantly different taken
alone, e.g. mercury levels in the brains of AD versus control
subjects) with several other pairs of data rendering the difference
statistically insignificant. One known weakness of the Bon-Feroni
treatment of several coupled pairs of comparisons is that one very
likely will miss a single comparison that is significantly different,
and clever people know this. It is my opinion that application of the
Bon-Feroni manipulation is what happened in this JADA study that
reversed the previous significance of the mercury levels in AD versus
control brain previously reported. Research previously reported by
some of the very same researchers involved in the JADA study
consistently indicated that mercury levels were higher in AD versus
age-matched control brains (14a,b, 15). Only when an ADA dentist
became involved did the results change to being insignificant. I
think the data used in this JADA article and funded by NIH needs to
be re-evaluated by a different statistician if we are to ever really
know if the mercury levels in the AD brains differed significantly
from controls.
The letter from the ADA President then lists four publications as
proof of amalgams having no statistically significant negative
effects. Two of these were published in Scandinavian Journals,
another was a review of the literature in a Dental Journal, and one
was the JADA article mentioned above. Sweden is well known to have
lead the world in the restriction and replacement of dental amalgams
with non-mercury containing materials. Forces are pushing hard to get
the use of amalgams accepted again in Sweden to eliminate this
embarrassment to our ADA. The current situation in Sweden and some
other European countries, Canada and Japan seriously questions the
ADA contention of amalgam safety. What if people in Sweden become
healthier without amalgams?
Additionally, the studies quoted by the ADA President were
epidemiological studies. These are very complex as many confounders
are included which make finding a statistically significant
difference very difficult. So the results are negative, nothing
found, and not surprising. However, they are in disagreement with
numerous other similar reports and appear to be hand-selected to
support the ADA position. One has to wonder, since the ADA President
seemed to visit Swedish journals to support the ADA position, how he
missed the research of the Nylander group in Sweden that showed
increased mercury content in brains and kidneys of humans in
relationship to exposure to dental amalgams (17,18). Also, the
referenced studies in the ADA letter did not involve neurotoxicity,
autism or neurological disease---which is the question at hand.
Rather, they addressed fertility, reproduction and other systemic
illnesses. Could not the ADA find references to focus on
neurotoxiological studies? What about the 1989 study that showed
elevated levels of mercury in 54 individuals with Parkinson's disease
when compared to 95 matched controls (16)? Further, one ought to
consider who was doing these touted ADA studies and any vested
interest they may have in the outcome. I am also aware of studies
done in the U.S.A. by major research universities that would disagree
with the conclusions drawn by the ADA on this subject yet these
articles are not considered in the ADA letter.
At the end of the last publication the quote "Conclusions: No
statistically significant correlation was observed between dental
amalgam and the incidence of diabetes, myocardial infarction, stroke,
or cancer." How does this relate to an article published in the J. of
the American College of Cardiology where the mercury levels in the
heart tissue of individuals who died from Idiopathic Dilated
Cardiomyopathy (IDCM) contained mercury levels 22,000 times that of
individuals who died of other forms of heart disease? Where did this
tremendous amount of mercury come from? Even a Bon-Feroni
manipulation could not make this difference insignificant! Many who
die of IDCM are well-conditioned, young athletes who drop dead during
sporting events---and they live in locations and in economic
environments where sea-food is not a dietary mainstay. Perhaps the
victims of IDCM are within the ADA Presidents "handful of individuals
who are allergic to one of its components."
"The National Institute of Dental and Craniofacial Research is
currently supporting two very large clinical trials on the health
effects of dental amalgam. Studies underway for several years each in
Portugal and the Northeastern United States involve not only direct
neurophysiological measures but also cognitive and functional
assessments." Do we really think that the NIDCR and associated ADA
personnel are going to deliver up a conclusion to American parents
saying "we put a mercury containing toxic material in your child's
mouth that lowered his/her I.Q. and made him more susceptible to
neurological problems in comparison to the children whom we selected
to not get exposed to this toxic material"? It is my opinion that
most bureaucracies don't have a brain or a heart, but they do have a
very strong survival instinct. Therefore, the results presented from
this study will likely follow previously ADA supported research, i.e.
no significant results.
Since the NIDCR started this project only 4 years ago one has to ask
why it took so long for them to get involved since the "amalgam wars"
have been going on for scores of years? Was it the overwhelming
amount of modern science showing mercury from amalgams being a major
part of the daily exposure that forced their hand and they had to
develop a defense? Would I trust the conclusions of this study
without knowing who put it together and who did the statistics? Not
any more than I trust the conclusions of the JADA article mentioned
in the ADA letter that stupendously concludes that mercury from
dental amalgams does not get into the brain.
As was proven by the tobacco situation, trying to find any
significant negative effect of one product (amalgams) related to any
disease through epidemiological studies is very difficult and
complex. To do this with mercury would be difficult because of the
synergistic effect two or more toxic metals or compounds (e.g.
cadmium from smoking) may have on the toxicity of the mercury emitted
from amalgams. For example, one publication showed that combining
mercury and lead both at LD1 levels caused the killing rate to go to
100% or to an LD100 level (12). An LD1 level is where, due to the low
concentrations, the mercury or the lead alone was not very toxic
alone (i.e., killed less than 1% of rats exposed when metal were used
alone). The 100% killing, when addition of 1% plus 1% we would expect
2%, represents synergistic toxicity. Therefore, mixing to non-lethal
levels of mercury plus lead gave an extremely toxic mixture! What
this proves is that one cannot define a "safe level of mercury"
unless you absolutely know what others toxicants the individual is
being exposed to. The combined toxicity of various materials, such as
mercury, thimerosal, lead, aluminum, formaldehyde, etc., is unknown.
The effects various combinations of these toxicants would have is
also not defined except that we know they would be much worse than
any one of the toxicants alone. So how could the ADA take any
exception, based on intellectual considerations, to my contention
that combinations of thimerosal and mercury could exacerbate the
neurological conditions identified with autism and AD? Autism and AD
have clinical and biological markers that correspond to those
observed in patients with toxic mercury exposure. Why would the ADA
take this position? I personally feel like I have been in a ten year
argument with the town drunk on this issue. Facts don't count and
data is only valid if it meets the pro-amalgam agenda.
The ADA was founded on the basis that mercury-containing amalgams are
safe and useful for dental fillings. This may have been an acceptable
position in 1850. However, modern science has proven that amalgams
constantly emit unacceptable levels of mercury. Especially as the
average life span has increased from 50 to 75-78 years of age where
AD and Parkinson's become prevalent diseases. The ADA can try to
verify its position using selected epidemiological studies. But the
bottom line is that amalgams emit significant levels of neurotoxic
mercury that are injurious to human health and would exacerbate the
medical condition of those individuals with neurological diseases
such as ALS, MS, Parkinson's, autism and AD.
I am hoping that the ADA sent this letter to your committee and also
placed it on the ADA web-site to indicate that they are now willing
for a wide-open discussion to take place on the issue of dental
amalgams. I, for one, would welcome a major scientific conference on
this issue. The ADA should feel free to post my letter in response
and address any issue they feel that I am mistaken about. However, in
closing I urge your committee to push forward on the study of the
potential dangers of mercury in our dentistry and medicines. This
includes mercury exposures from amalgams, vaccines and other
medicaments containing thimerosal. The synergistic effects of mercury
with many of the toxicants commonly found in our environment make the
danger unpredictable and possibly quite severe, especially any
mixture containing elemental mercury, organic mercury and other heavy
metal toxicants such as aluminum.
Sincerely,
Boyd E. Haley
Professor and Chair
Department of Chemistry
University of Kentucky
REFERENCES:
1. a. Duhr, E.F., Pendergrass, J. C., Slevin, J.T., and Haley, B.
HgEDTA Complex Inhibits GTP Interactions With The E-Site of Brain b-
Tubulin Toxicology and Applied Pharmacology 122, 273-288 (1993).; b.
Pendergrass, J.C. and Haley, B.E. Mercury-EDTA Complex Specifically
Blocks Brain b-Tubulin-GTP Interactions: Similarity to Observations
in Alzheimer"s Disease. p 98-105 in Status Quo and Perspective of
Amalgam and Other Dental Materials (International Symposium
Proceedings ed. by L. T. Friberg and G. N. Schrauzer) Georg Thieme
Verlag, Stuttgart-New York (1995).; c. Pendergrass, J.C. and Haley,
B.E. Inhibition of Brain Tubulin-Guanosine 5'-Triphosphate
Interactions by Mercury: Similarity to Observations in Alzheimer's
Diseased Brain. In Metal Ions in Biological Systems V34, pp 461-478.
Mercury and Its Effects on Environment and Biology, Chapter 16.
Edited by H. Sigel and A. Sigel. Marcel Dekker, Inc. 270 Madison
Ave., N.Y., N.Y. 10016 (1996).
2. Pendergrass, J. C., Haley, B.E., Vimy, M. J., Winfield, S.A. and
Lorscheider, F.L. Mercury Vapor Inhalation Inhibits Binding of GTP to
Tubulin in Rat Brain: Similarity to a Molecular Lesion in Alzheimer's
Disease Brain. Neurotoxicology 18(2), 315-324 (1997).
3. David, S., Shoemaker, M., and Haley, B. Abnormal Properties of
Creatine kinase in Alzheimer's Diseased Brain: Correlation of Reduced
Enzyme Activity and Active Site Photolabeling with Aberrant Cytosol-
Membrane Partitioning. Molecular Brain Research 54, 276-287 (1998).
4. Leong, CCW, Syed, N.I., and Lorscheider, F.L. Retrograde
Degeneration of Neurite Membrane Structural Integrity and Formation
of Neurofibillary Tangles at Nerve Growth Cones Following In Vitro
Exposure to Mercury. NeuroReports 12 (4): 733-737, 2001.
5. Olivieri, G., Brack, Ch., Muller-Spahn, F., Stahelin, H.B.,
Herrmann, M., Renard, P; Brockhaus, M. and Hock, C. Mercury Induces
Cell Cytotoxicity and Oxidative Stress and Increases b-amyloid
Secretion and Tau Phosphorylation in SHSY5Y Neuroblastoma Cells. J.
Neurochemistry 74, 231-231, 2000.
6. Kingman, A., Albertini, T. and Brown, L.J. Mercury Concentrations
in Urine and Whole-Blood Associated with Amalgam Exposure in a U.S.
Military Population. J. Dental Research 77(3) 461-71, 1998.
7. Chew, C. L., Soh, G., Lee, A. S. and Yeoh, T. S. Long-term
Dissolution of Mercury from a Non-Mercury-Releasing Amalgam. Clinical
Preventive Dentistry 13(3): 5-7, May-June (1991).
8. Hahn, L.J., Kloiber, R., Vimy, M. J., Takahashi, Y. and
Lorscheider, F.L. Dental "Silver" Tooth Fillings: A Source of Mercury
Exposure Revealed by Whole-Body Image Scan and Tissue Analysis. FASEB
J. 3, 2641-2646, 1989.
9. Hahn, L.J., Kloiber, R., Leininger, R.W., Vimy, M. J., and
Lorscheider, F.L. Whole-body Imaging of the Distribution of Mercury
Released from Dental Filling Into Monkey Tissues. FASEB F. 4, 3256-
3260, 1990.
10. Hock, C., Drasch, G., Golombowski, S., Muller-Span, F.,
Willerhausen-Zonnchen, B., Schwarz, P., Hock, U., Growdon, J.H., and
Nitsch, R.M. Increased Blood Mercury Levels in Patients with
Alzheimer's Disease. J. of Neural Transmission v105(1) 59-68, 1998.
11. Frustaci, A., Magnavita, N., Chimenti, C., Caldarulo, M.,
Sabbioni, E., Pietra, R., Cellini. C., Possati, G. F. and Maseri, A.
Marked Elevation of Myocardial Trace Elements in Idiopathic Dilated
Cardiomyopathy Compared With Secondary Dysfunction. J. of the
American College Cardiology v33(6) 1578-1583, 1999,
12. Schubert, J., Riley, E.J., and Tyler, S.A. Combined Effects in
Toxicology-A Rapid Systemic Testing Procedure: Cadmium, Mercury and
Lead. J. of Toxicology and Environmental Health v4, 763-776,1978.
13. Wataha, J. C., Nakajima, H., Hanks, C. T., and Okabe, T.
Correlation of Cytotoxicity with Element Release from Mercury and
Gallium-based Dental Alloys in vitro. Dental Materials 10(5) 298-303,
Sept. (1994)
14. a. Ehmann, W., Markesbery, W., and Alauddin, T., Hossain, E. and
Brubaker, E., Brain Trace Elements in Alzheimer's Disease.
Neurotoxicology 7(1) p197-206, 1986. b. Thompson, C. M., Markesbery,
W.R., Ehmann, W.D., Mao, Y-X, and Vance, D.E. Regional Brain Trace-
Element Studies in Alzheimer's Disease. Neurotoxicology 9, 1-8
(1988).
15. Wenstrup, D., Ehmann, W., and Markesbery, W. Brain Research, 533,
125-131, 1990.
16. Ngim, C.H., Devathasan, G. Epidemiologic Study on the
Assocaiation Between Body Burden Mercury Level and Idiopathic
Parkinson's Disease. Neuroepidemiology, 8, 128-141, 1989.
17. Nylander, M., Friberg, L. and Lind, B. Mercury Concentrations in
the Human Brain and Kidneys in Relation to Exposure from Dental
Amalgam Fillings. Swedish Dentistry J. 11:179-187, 1987.
18. Nylander, M., Friberg, L., Eggleston, D., Bjorkman, L. Mercury
Accumulation in Tissues from Dental Staff and Controls in Relation to
Exposure. Swedish Dental J. 13, 235-243, 1989
19. Heintze, U. Edwardsson, S., Derand, T. and Birkhed, D.
Methylation of Mercury from Dental Amalgam and Mercuric Chloride by
Oral Streptococci in vitro. Scand. J. Dental Research 91(2) 150-152,
1983.
http://www.bioprobe.com/ReadNews.asp?article=36
______________________________________________________________________
__________
Dockets Management Branch (HFA305), Food and Drug Administration,
5630 Fishers Lane,
rm. 1061,
Rockville, MD 20057.
http://www.fda.gov/OHRMS/DOCKETS/98fr/022002a.pdf
http:// www.fda.gov/dockets/ecomment .
FOR FURTHER INFORMATION CONTACT:
Susan Runner,
Center for Devices and Radiological Health (HFZ410),
Food and Drug Administration,
9200 Corporate Blvd.,
Rockville, MD 20850,
3018275283.
In reference to:
Proposed Rules Federal Register 7620 Vol. 67, No. 34
Wednesday, February 20, 2002
DEPARTMENT OF HEALTH AND HUMAN SERVICES Food and Drug Administration
21 CFR Part 872 [Docket No. 01N0067] Dental Devices:
Classification of Encapsulated Amalgam Alloy and Dental Mercury and
Reclassification of Dental Mercury;
Issuance of Special Controls for Amalgam Alloy AGENCY: Food and Drug
Administration, HHS.
Mercury can cause a bewildering variety of problems.
In fact, one of the major criticisms of amalgam illness is that it is
cited as the cause of so many things. But, like the parable of the
blind men and the elephant, mercury can indeed cause many diseases.
Modern physicians are not trained to find the root cause of a sick
person's problems.
They are trained to translate what they see into latin, look it up in
their textbook, and apply a cookbook treatment.
With a toxin that poisons fundamental metabolic processes different
people will experience different symptoms to start off, depending on
their own individual biochemistry. As the poisoning becomes more and
more serious, further symptoms surface and the modern doctor adds
more diagnoses - a patient who starts with depression might later be
considered to have hypothyroidism, allergies and asthma in addition.
But no thought is given to why one person should develop more and
more diseases, when a single diagnosis - chronic mercury poisoning -
could account for them all.
Some of the diseases a modern physician might mistakenly misdiagnose
chronic mercury poisoning as are:
Toxic Encephalopathy, Chronic fatigue Immune Dysfunction Syndrome,
Autoimmune disorders and disease, Multiple chemical sensitivities,
(Environmental illness), Fibromyalgia, Endocrine disorders,
Thyroidsm, Irritable bowel syndrome, High Blood pressure, Rheumatoid
arthritis, Food Sensitivities, Acne, Psoriorisis, Sciatica,
Allergies, Panic attacks, Anxiety, Colitis, Prothralgia, Parkinson's
disease, Amylotrophic lateral sclerosis, Alzheimer's' disease,
Hypothyroidism, Infertility, Neuropathy, Erectile dysfunction
disorder, Polineuropathy, Peripheral neuropathy, Computer vision
Syndrome, Alleged and frequently misdiagnozed misdiagnosed for
MENOPAUSE, Gastritis, Crohn's disease, Addison's disease, Carpal
Tunel, Tersal Tunel, Allergies, Hypogonadism, Ankylosing spondylitis,
Insomnia, Anorexia nervosa, Juvenile arthritis Asthma, RAIDS, RADS,
RUDS, Learning disabilities, Attention deficit hyperactivity
disorder, Lupus erythromatosus, Manic depression, Bipolar disorder,
Multiple sclerosis, Bulimia, Myasthenia gravis, Sleep disorders,
Candidiasis, Yeast syndrome, Pervasive developmental disorder,
Depression, Psychosis, Obsessive-compulsive disorder, Borderline
personality disorder, Schizophrenia.
See damage done by neurotoxicity, and then response to perfumes!
(Jpeg files)
http://home13.inet.tele.dk/mcscphdk/grafik/before.jpg
http://home13.inet.tele.dk/mcscphdk/grafik/after.jpg
Since 1997 I contacted White House, and majority of US senators.
I delt with FDAs own:
1. Leonard, Nancy M.
FDA - Public Health Advisor
1-800-638-2041 ext. 141
US
2. Alderton, Bonnie J.
FDA - CDRH Small Manu. Assistance,
FDA US
3. Auerbach, Jessica B.
FDA, Consumer Section, CDRH (HFZ-210)
301-443-7491, ext.138
US
To be only told bullshit by incompetent FDA employees.
There is NO DOUBT that GULF WAR ILLNESS is caused by MERCURY
poisoniong (dental mercury amalgam reaction with hydrogen sulfide
leaking from OIL WELLS on fire, and additional mercury boost from
vaccines (thimerosal) causing severe brain injury, including
Parkinson's like trembling, and lobar perfussion. Mercury fillings
are the sole cause of Carpal Tunel, erectrile dysfunction alleged
menopause, Fibromyalgia, Chronic Fatigue immune dysfunction syndrome,
Multiple Chemical Sensitivity... and more!
See:
42360 Federal Register / Vol. 59, No. 158 / Wednesday, August 17,
1994 / Notices ENVIRONMENTAL PROTECTION AGENCY [FRL-5050-09]
Final Report: Principles of Neurotoxicity Risk Assessment AGENCY:
U.S. Environmental Protection Agency. ACTION: Final Document.
SUMMARY: The U.S. Environmental Protection Agency is publishing a
document entitled
Final Report: Principles of Neurotoxicity Risk Assessment, which was
prepared by the Working Party on Neurotoxicology under the auspices
of the Subcommittee on Risk Assessment of the Federal Coordinating
Council for Science, Engineering, and Technology (FCCSET).
Industrial Exposure and Control Technologies for OSHA Regulated
Hazardous Substances U.S. Department of Labor Elizabeth Dole,
Secretary March 1989 Volume II of II Substances K-Z and Indices
Occupational Safety and Heath Administration
John A. Pendergrass,
Assistant Secretary
Mercury vapor HEALTH EFFECTS
Lorscheider, F.L., Vimy, M.J., and Summers, A.O.
Mercury Exposure from Silver Tooth Fillings: Emerging Evidence
Questions a Traditional Dental Paradigm. FASEB Journal (April 1995).
Dr. Michael F. Ziff, D.D.S publications Amalgam Illness
Diagnosis and Treatment What you can do to get better
How your doctor can help by Andrew Hall Cutler, PhD,
PE ISBN 0-9676168-0-8
Neurotoxicity: Identifying and Controlling Poisons of the Nervous
System
U.S. Office of Technology Assessment
April 1990 OTA-BA-436
NTIS order #PB90-252511
(361 pages)
http://www.wws.princeton.edu/~ota/disk2/1990/9031_n.html
PENTAGON (General Rostker):
"Summers (1994) has proposed that set of unexplained symptoms in PGW
veterans (skin rashes, chronic fatigue, headaches, sore joints, hair
loss, irritability, insomnia, diarrhea, and depression) are related
to mercury toxicity as result of installation of dental amalgams just
prior to or immediately after service in PGW. This hipotesis asserts
that installation of these amalgams resulted in clinically evident
elemental mercury toxicity that continues as patients have ongoing
exposure to mercury. It is clear that the placement of dental
amalgams results in systemic exposure to mercury (Gross and
Harrisson, 1989;
Researchers suggest that Gulf War veterans and others who meet the
diagnostic criteria for more than one of CFS, FMS and/or MCS may all
be suffering from dental amalgam poisoning but as yet not undefined
common syndrome.
(Summers et al. 1993).
It is also clear that significant exposure to elemental mercury
results in toxic syndrome with complex clinical presentation
(Wyngaarden et al. 1992.)
At the same time, relatively few human studies of adverse effects of
amalgams have been done. Interest in diminishing elemental mercury
exposure has resulted in proposals in Sweden, Denmark and Germany for
restrictions on the use of mercury - containing dental amalgams. To
date, the hypothesis of unexplained symptoms in PGW veterans
associated with the recent installation of dental amalgams has not
been directly investigated to the best of our knowledge. __
It is evident that all, for example, seem to share heightened
sensitivity to a diverse range of stresses, from physical exertion
and infection to environmental exposures. In addition to chemical
sensitivity, they often also report heightened sensitivity to bright
lights, loud noises, hot and/or cold weather, and/or being touched.
Until further research clarifies the nature of this overlap, however,
the majority of physicians, insurers, attorneys and support groups
continue to regard CFS, FMS, MCS and GWS for legal claims are trying
to define as separate and distinct conditions.
http://www.rand.org/publications/MR/MR1018.2/mr1018.2.chap11.html
Gulf War Illness:
Rand Report:
http://www.rand.org/publications/MR/MR1018.2/
The legal position of the American Dental Association (ADA) on the
safety of mercury containing dental amalgam and the use of the
material by dentists in the United States was recently stated as
follows:
The ADA owes no legal duty of care to protect the public from
allegedly dangerous products used by dentists. The ADA did not
manufacture, design, supply or install the mercury-containing
amalgams. The ADA does not control those who do. The ADA's only
alleged involvement in the product was to provide information
regarding its use.
Dissemination of information relating to the practice of dentistry
does not create a duty of care to protect the public from potential
injury.
Source: Legal brief filed in 1995 by attorneys for the ADA in W.H.
Tolhurst vs. Johnson and Johnson Consumer Products, Inc.; Engelhard
Corporation; ABE Dental, Inc.; the American Dental Association, et
al., in the Superior Court of the State of California, in and for the
County of Santa Clara, CA, Case No. 718228.
ADA is being now sued and vigorously is depending themself from
lawsuits by lobbying in Washington DC:
http://www.ada.org/prof/pubs/daily/0206/0621wash.html
It is mandatory that MERCURY WILL BE IMMEDIATELY BANED AS SEVERE
NEUROTOXIC SLOW ACTING POISON, and use of mercury in dentistry must
be criminalized!
http://assembly.state.ny.us/leg/?bn=a004209
http://www.melisa.org
http://www.melisa.org/articles/index.html
http://www.melisa.org/articles/engel-e.pdf
http://www.melisa.org/articles/neuroen.pdf
http://www.melisa.org/articles/biomark.pdf
http://www.melisa.org/articles/biomark2.pdf
http://www.melisa.org/articles/nialler.pdf
http://www.bioprobe.com
http://www.cfspages.com/
http://www.state.hi.us/health/eh/heer/poison.html
http://hometown.aol.com/noamalgam
TESTIMONIALS:
http://www.guestbook.de/yasg.cgi?X=20086&P=1
http://dir.yahoo.com/Health/Medicine/Dentistry/Amalgam/
http://vest.gu.se/~bosse/Mercury/Mouth/amalgamlinks.html
http://hometown.aol.com/Rjj5019/index.html http://www.web-
light.nl/AMALGAM/amalgam.html
http://www.altcorp.com/vimyresponds.htm
http://www.altcorp.com/amalgam.htm
http://www.dentalmercury.com/publications.html
http://lawschool.stanford.edu/library/special/dentalofficerequirements
.html
http://www.toxicteeth.net
http://www.web-light.nl/AMALGAM/EN/SCIENCE/sciencemain.html
http://lawschool.stanford.edu/library/special/dentalofficerequirements
.html
http://www.bioprobe.com/index.asp
http://www.udel.edu/OHS/dartmouth/drtmtharticle.html
Other links:
http://www.sonic.net/kryptox/medicine/mullenix2.htm
http://www.state.hi.us/health/eh/heer/poison.html
http://www.heldref.org/html/Consensus.html
http://www.herc.org/news/mcsarticles/rowat.htm
http://www.california.com/~hawk/MCS-Ammunition.htm
http://home13.inet.tele.dk/mcscphdk/grafik/before.jpg
http://home13.inet.tele.dk/mcscphdk/grafik/after.jpg
http://www.rand.org/publications/MR/MR1018.2/mr1018.2.chap11.html
http://hometown.aol.com/noamalgam/
http://veterans.house.gov/hearings/schedule106/oct99/10-26-
99/miller.htm
http://www.rand.org/publications/MR/MR1018.2/
http://www.cfspages.com/
http://www.mcsrr.org/fedmcsgroup/fedmcsrec.html
http://www.sonic.net/kryptox/medicine/mullenix2.htm
http://www.state.hi.us/health/eh/heer/poison.html
http://www.heldref.org/html/Consensus.html
http://www.herc.org/news/mcsarticles/rowat.htm
http://www.california.com/~hawk/MCS-Ammunition.htm
http://www.wws.princeton.edu/~ota/disk2/1990/9031_n.html
http://hometown.aol.com/noamalgam/
http://veterans.house.gov/hearings/schedule106/oct99/10-26-
99/miller.htm
http://www.rand.org/publications/MR/MR1018.2/
http://www.mcsrr.org/fedmcsgroup/fedmcsrec.html
Norway BAIL OUT with MERCURY fillings!
No more amalgam, Norway's government tells its dentists
The following edited article is from Maryanne Rygg, Norway
A long-awaited breakthrough in the war against amalgam was announced
on 31 May.
The director for the Norwegian Directorate of Health and Social
Welfare said on Norwegian radio that the health authorities now
recommend that dentists no longer use amalgam on their patients. He
said that the new guidelines are based on newer research that has
revealed how mercury leaks from amalgam in the mouth of patients.
The Norwegian Directorate of Health and Social Welfare has announced
that it will be sending its new guidelines for use of dental
materials out for hearing in a couple of weeks, and expects them to
take effect from 1 January 2003.
The announcement was called a "U-turn" by the Norwegian radio. The
current president of the Norwegian Dental Association was also
interviewed, and said that the Norwegian Dental Association was
satisfied that the guidelines stop short of a full ban on amalgam,
and that freedom of choice is still possible. He also said that there
has been controversy around the use of amalgam for 100 years, and
that the Dental Association would not defend amalgam "at any price".
The current president of the Norwegian Dental Association works in an
amalgam-free dental practice, and has not used amalgam for many years.
The ten-page document is still labeled as confidential, until it is
sent out for hearing in a couple of weeks. We have been told that it
will be published (in Norwegian) on the website of the Norwegian
Dental Materials Adverse Reaction Unit
(
http://www.uib.no/bivirkningsgruppen/ ), but it has not appeared
there as
yet. It is expected to be published on the website of the Norwegian
Dental Patient Association (
http://www.tenneroghelse.no ).
It appears that this document contains many statements that the anti-
amalgam movement has claimed for years. Now they have publicly
endorsed the claims, although there are still a few sentences in the
ten-page document that will continue to be disputed. Although the
document states that the overall aim is to phase out the use of
amalgam, the guidelines do stop short of a complete ban. It is
advice, rather than instruction. It will still be possible for adult
patients who insist on amalgam to receive it. However, when the
statements about amalgam which are contained in this document are
made public, it would be a strong disincentive for anyone to choose
to have amalgam installed in their mouth.
http://www.melisa.org/hottopics/newnorway.html
http://www.newstatesman.co.uk/site.php3?
newTemplate=NSArticle_Ideas&newDisplayURN=200207010008
Slide Show!
http://www.altcorp.com/AffinityLaboratory/SlideShows/bacttox/sld001.ht
m
Toxins Produced by Oral Microorganisms and Their Toxic Effects on
Critical Enzymes in the Human Body
Table of Contents
Toxins Produced by Oral Microorganisms and Their Toxic Effects on
Critical Enzymes in the Human Body
"Poison is in everything, and no thing is without poison. The dose
makes it either a poison or a remedy"
3 Types of Bacterial Toxins
Types of Bacterial Toxins
3 Classes of Non-Protein Bacterial Toxins
Evidence for Small Organic (Nonprotein) Bacterial Toxins
Porphyromonas gingivalis, A Common Pathogen in both Periodontal and
Pulpal Infections
Proposed Virulence Factors of Porphyromonas gingivalis
Extracts of Oral Bacteria Are Toxic to Cells in Culture
Reasons for Study
Study Design
Experiments
Results
Conclusions
3 Classes of Non-Protein Bacterial Toxins
Production of Volatile Sulfur Compounds by Oral Bacteria
The Bacterial Enzyme L-Cysteine Desulfhydrase Catalyzes the Breakdown
of L-Cysteine into Hydrogen Sulfide and Ammonium
Mechanism of Methylmercaptan (CH3SH) Production by Anaerobic Oral
Microorganisms
The Bacterial Enzyme L-Methionine-g-Lyase Catalyzes the Breakdown of
the Amino Acid L-Methionine into Methyl Mercaptan
Sources and Levels of VSCs
Mechanisms of Hydrogen Sulfide Toxicity
Mechanisms of Hydrogen Sulfide Toxicity (cont.)
Toxic Effects of H2S and CH3SH on Oral Tissues
Effects of H2S and CH3SH on Membrane Permeability
Toxicity of Hydrogen Sulfide
Human Physiologic Responses to H2S Exposure
The hydrogen sulfide produced by anaerobic bacteria is the same,
chemically speaking, as the hydrogen sulfide produced as a waste
product in over 70 different industrial processes. The toxic
properties of the compound does not differ depending upon the source
of its production.
Neurotoxic Effects of Hydrogen Sulfide
Toxic Effects of Hydrogen Sulfide and Methylmercaptan
Effect of Toxins on Photolabeling of a Mixture of Purified Mammalian
Nucleotide Binding Proteins
Hydrogen Sulfide & Methylmercaptan Inhibit [32P]N3ATP Interactions
with Purified Mammalian Enzymes
3 Classes of Non-Protein Bacterial Toxins
Formation of Polyamines by Oral Bacteria
Relationship Between Polyamines and Periodontitis
Polyamines Produced by Oral Microorganisms
Cadaverine is Produced from Lysine by the Action of the Bacterial
Enzyme Lysine Decarboxylase
Putrescine is Produced from Ornithine by the Action of the Bacterial
Enzyme Ornithine Decarboxylase
Polyamine Bacterial Metabolites Inhibit [32P]N3ATP Interactions with
Purified Mammalian Enzymes
Polyamine Concentrations Measured in Human GCF and Saliva of Persons
with Periodontitis
Polyamines in Gingival Crevicular Fluid
Polyamine Analysis of Infected Root Canal Contents Related to
Clinical Symptoms. Maita & Horiuch (1990). Endod. Dent. Traumatol.
6:213-217.
3 Classes of Non-Protein Bacterial Toxins
Short-Chain Carboxylic Acids (SSCAs) Produced by Oral Microorganisms
Production of Short-Chain Carboxylic Acids by Oral Microorganisms
Common Metabolic Pathways for Production of Short-Chain Carboxylic
Acids by Oral Bacteria
Toxic Effects of Short-Chain Carboxylic Acids
Concentrations of Short-Chain Carboxylic Acids Measured in GCF of
Patients with Periodontitis
Production & Toxicity of Short-Chain Carboxylic Acids
Production & Toxicity of Short-Chain Carboxylic Acids
Short-Chain Carboxylic Acids Inhibit [32P]N3ATP Interactions with
Purified Mammalian Enzymes
Conclusions
Author: Curt Pendergrass
http://www.who.int/pcs/training_material/hazardous_chemicals/section_3
.html
http://www.biosci.ohio-state.edu/~mgonzalez/Micro521/24.html
http://www.biosci.ohio-state.edu/~mgonzalez/Micro521/23.html
http://www.who.int/pcs/training_material/hazardous_chemicals/contents.
htm
More info on MERCURY you can reach clubs:
http://groups.yahoo.com/group/multiplechemicalsensitivity2/
http://groups.yahoo.com/group/adentalmercuryamalgam/
http://groups.yahoo.com/group/amalgamclassaction/
http://groups.yahoo.com/group/attentiondeficitadhd/
http://groups.yahoo.com/group/fibromyalgiaandmyofacial/
http://groups.yahoo.com/group/irritableboweldisease/
http://groups.yahoo.com/group/gulfwarillness/
QUACKS:
http://groups.yahoo.com/group/dangerousdoctors/
One more time MUST read ($ 35):
Amalgam Illness: Diagnosis and Treatment
What you can do to get better
How your doctor can help
by Andrew Hall Cutler, PhD, PE
ISBN 0-9676168-0-8
http://hometown.aol.com/andycutler
______________________________________________________________________
_________
CURRICULUM VITAE
BOYD E. HALEY, Ph.D.
Born 22-09-40 Greensburg, Indiana
ADDRESS: Advanced Science Technology Commercialization Center,
ASTeCC
Room A057
University of Kentucky
Lexington, KY 40506-0286
Laboratory: Telephone; (606) 257-2300 ext 246 FAX; (606) 257-3040
Chemistry Office: Telephone; (606) 257-7082
EDUCATION:
Institution Year Degree/Area
Franklin College 1963 B.A./Chemistry-Physics
University of Idaho 1967 M.S./Organic Chemistry
Washington State University 1971 Ph.D./Chemistry-Biochemistry
Yale University Medical Center 1971-74 Postdoctoral Fellow
RESEARCH AND PROFESSIONAL EXPERIENCE:
1963-1964 Research Scholar, Food and Drug Administration.
1964-1966 U.S. Army Medic
1966-1967 Graduate Student, University of Idaho
1967-1971 Graduate Student, Washington State University
1971-1974 Postdoctoral Scholar, Yale University
1974-1979 Assistant Professor, Department of Biochemistry, University
of Wyoming, Laramie, WY
1979-1981 Associate Professor, Department of Biochemistry, University
of Wyoming, Laramie, WY
1981-1985 Professor, Department of Biochemistry, University of
Wyoming, Laramie, WY
1985-1997 Professor of Medicinal Chemistry, College of Pharmacy,
University of Kentucky, with
joint appointments in Biochemistry & Chemistry
1997-present Chairman & Professor, Department of Chemistry with joint
appointment in College of
Pharmacy
PROFESSIONAL ORGANIZATIONS, SOCIETIES, HONORS AND RESPONSIBILITIES
1959 President's Scholarship, Franklin College, Indiana
1962 Chi Beta Phi, Franklin College
1962 James M. Sprague Award - $400 award to outstanding
undergraduate junior majoring in science.
1963 Kennedy Scholar, Food and Drug Administration,
Washington, D.C.
1970 Sigma Xi
1975 Dreyfus Foundation Visiting Researcher, Enzyme Institute
University of Wisconsin
1977 American Society of Biological Chemists
1981 Biophysical Society
1981 Served on NIH Physiological Chemistry Study Section
1981 Research was presented as a "highlight" in NIH report on
"Cellular and Molecular Basis of Disease Program"
1984 "TOP" Professor Award, University of Wyoming
1982 Served on NIH Physiological Chemistry Study Section
1983 Served on NIH Physiological Chemistry Study Section
1985 Permanent member NIH Biomedical Sciences, Study Section
1991 Honorary Doctorate in Arts & Sciences, Franklin College
1992 Society for Neuroscience
GRANT SUPPORT
1975 - 1978 National Institutes of Health, "Application of
Photoaffinity Nucleotide Analogs", $82,000, Prinicipal Investigator
1975 Research Coordination Committee, University of Wyoming $1,800
1978 - 1981 National Institutes of Health, "Application of
Photoaffinity Nucleotide Analogs", $183,696, Prinicipal Investigator
1978 - 1981 Eleanor Roosevelt Cancer Institute Grant, $11,400
1979 - 1983 PHS Research Career Development Award, $185,000
1981 - 1986 National Institutes of Health, "Application of
Photoaffinity Nucleotide Analogs", $434,000, Prinicipal Investigator
1982 ASBC Travel Award to attend 12th IVB Congress, Perth, Australia
1983 - 1984 National Science Foundation, "Melatonin Photoaffinity
Probe", $84,000, Co-Principal Investigator
1983 - 1985 National Institutes of Health, "Epididymal Sperm
Nucleotide Binding proteins", $190,000, Co-Principal Investigator
1985 - 1988 U.S. Army Mycotoxin Photoprobes, $390,000, Co-Principal
Investigator
1986 - 1989 NIH, "Forskolin Photoaffinity Probes", $170,000, Co-
Principal Investigator
1986 - 1991 NIH, "Application of Photoaffinity Nucleotide Analogs"
$781,661, Principal Investigator
1989 - 1994 NIH, "Nucleotide-Tubulin Interactions in Alzheimer's
Disease", $405,259, Co-Prinicipal Investigator
1990 - 1996 Lexington Clinic Foundation For Medical Education and
Research, "Inhibition of Neoplastic Cell Proliferation Through
Utilization of Photoactive DNA & RNA Synthesis, $100,000, P.I.
1990 - 1993 Eli Lilly, "Development of a Diagnostic Test for
Alzheimer's Disease, $378,000, P.I.
1995 - 1997 Wallace Research Foundation, "Development of Diagnostic
Tests Using Nucleotide Photoaffinity Probes". $109,000 for two years.
1997-1998 Wallace Research Foundation, "Development of Diagnostic
Tests Using Nucleotide Photoaffinity Probes". $74,344.
1997-2000 NIH, "Application of Photoaffinity Nucleotide Analogs",
$378,081, P.I.
1997-1998 Isostent, Inc. "Photoattachment of 32P to angioplastic
ballon cathers" $52,000.
Pending NIH, "Identification of CSF proteins Related to ALS"
NIH, "Photomodification of Antibodies for Diagnostic and Therapeutic
Applications".
TEACHING EXPERIENCE
Introductory Comparative Biochemistry
General Biochemistry
Problems and Topics in Biochemistry
Mercury Toxicity: Chemistry and Biochemistry Involved
Advanced Problems and Topics in Biochemistry
Nucleic Acids and Protein Biosynthesis
Nucleotides in Regulation of Biological Phenomena
Bioenergetics
Medicinal Chemistry
Natural Products and Bio-organics
Graduate level Biochemistry, Protein Chemistry
INVITED LECTURES:
1975 - Sloan Kettering Memorial Cancer Institute, New York
thru Colorado State University (3)
1979 Albert Einstein University, New York
Hoffman-LaRoche Research Institute, Nutley, New Jersey
University of Colorado Medical School Denver (3)
University of Colorado, Boulder (2)
Yale University Medical School (2)
The Salk Institute, San Diego
University of California, Davis
Stanford University Medical School
University of California, San Diego
University of Washington, Seattle
Washington State University
Kansas State University
1979 Symposium Speaker, ASBC Meeting, Dallas, Texas
1979 Symposium Speaker, New York Academy of Sciences Meeting, New York
Department of Molecular Biology, National Jewish Hospital, Denver
University of California, Riverside
Workshop Speaker, ICN-UCLA Conference on Adenylyl Cyclase
1982 Symposium Speaker, 1982 FASEB Meeting, New Orleans
1982 Guest Lecturer and Scientist, German Cancer Research Center,
Institute of Cell and Tumor Biology, Heidelberg, West Germany,
May
1982 Centre National De La Recherche Scientifique, Laboratoire
D'Enzymologie, Gif Sur Yvette, France, June
1982 Workshop Speaker, ASBC Meeting in New Orleans (Photoprobe
utilization, sponsored by Schwarz-Mann)
1982 Symposium Speaker, Society for the Study of Reproduction, Madison
Wisconsin, August
1982 Department of Biochemistry, University of Wisconsin, November
1982 Department of Chemistry, New Mexico State University, November
1982 Department of Chemistry, University of Colorado, December
1983 Institute of Infectious Diseases, U.S. Army Medical Research
Institute, Ft. Detrick, Michigan, January
1983 Department of Biochemistry and Biophysics, Oregon State
University
1983 Department of Biochemistry, Texas Health Science Center, San
Antonio, TX
1983 Department of Biochemistry, University of Mississippi Medical
Center
1984 Department of Biochemistry, University of Kentucky, Lexington, KY
1985 Department of Physiology and Biophysics, Northwestern University
Medical School, Chicago, Illinois
1985 Department of Chemistry, University of Southern California, Los
Angeles, California
1985 Department of Physiology, University of Illionis at Chicago,
Chicago, Illinois
1985 Department of Biochemistry, Ohio State University, Columbus, Ohio
1985 Department of Physiology, Yale University Medical School, New
Haven, Connecticut
1986 Department of Biochemistry, Case Western University, School of
Medicine, Cleveland, Ohio
1986 Department of Biochemistry, Indiana University, School of
Medicine, Indianapolis, Indiana
1986 Department of Biochemistry, Washington University, School of
Medicine, St. Louis, Missouri
1987 Division Fermentation Products Research Division, Eli Lilly
Research Laboratories, Indianapolis, Indiana
1987 Department of Chemistry, University of South Florida, Tampa,
Florida
1987 Department of Molecular Biology and Biochemistry, University of
Wyoming, Laramie, Wyoming
1988 Worcester Foundation, Shrewsbury, Massachusetts
1988 Department of Biochemistry, University of Colorado, Denver,
Colorado
1988 Department of Biochemistry, University of Delaware, Newark,
Delaware
1989 University of California at San Diego
1989 University of California at Los Angeles
1989 Texas College of Osteopathic Medicine, Fort Worth, Texas
1990 Wright State University, Dayton, Ohio
1990 Athena Neurosciences, S. San Francisco, California
1990 Eli Lilly & Co., Indianapolis, Indiana
1990 Connaught Laboratories, Toronto, Canada
1990 University of East Carolina Medical School, Greenville, North
Carolina
1990 Hoffman-LaRoche Research Center, Nutley, New Jersey
1991 Eli Lilly & Co., Indianapolis, Indiana
1991 City University of New York, New York, New York
1991 University of Cincinnati, Cincinnati, Ohio
1991 University of Colorado, Boulder, Colorado
1991 University of Missouri at Kansas, Kansas City, Missouri
1992 Williams College at Williamsburg, Massachusetts
1992 Centre College at Danville, Kentucky
1992 University of Colorado, Boulder, Colorado
1992 Eli Lilly & Co., Indianapolis, Indiana
1992 Merck Laboratories, West Point, Pennsylvania
1993 NIH Rocky Mountain Laboratory, Hamilton, MT
1993 Intern. Acad. Oral & Medical Toxicology, Chicago, IL
1993 Univ. Tenn. at Memphis, Memphis, TN
1993 Penn State University, College Station, PN
1993 University California, Riverside, Riverside, CA
1993 Mayo Clinic, Jacksonville, FL
1993 Washington University, St. Louis, MO
1993 University of Arkansas, Little Rock, AR
1994 European Academy of Science, Otzenhausen, Germany
1994 Intern. Acad. Oral & Medical Toxicology, London, England.
1994 Great Lakes College for Advancement of Medicine, Cincinnati, OH
1995 American College for the Advancement of Medicine, Colorado
Springs, CO.
1995 Pfizer Pharmaceuticals, Groton, CN
1995 Ohio State University, Dept,. Chemistry, Columbus, OH
1996 Intern. Acad. Oral & Medical Toxicology, Tuscon, AZ
1996 University of Wyoming, Laramie WY
1996 American College for the Advancement of Medicine, Colorado
Springs, CO.
1997 American Academy Biological Dentistry, Carmel, CA March 7-9.
1997 International Academy of Oral and Medical Toxicology,
Louisville, KY March 14-16
1997 Washington State University, Dept. of Chemistry and Biophysics,
Pullman, WA, March 27-30.
1997 American Society of Biochemistry and Molecular Biology,
Symposium talk, August 24-28.
1997 Canadian Academy Oral and Medical Toxicology, Toronto, Canada.
September 19-21.
1997 Capital University of Integrative Medicine, Washington, DC,
October 16-18
1997 American Academy Environmental Medicine, San Diego, CA, October
24-26.
1997 University of Missouri at Kansas City, Dept. Biology &
Biophysics, November 20-22.
SERVICE TO DEPARTMENT, COLLEGE AND UNIVERSITY:
1975-1979 Faculty Senate
Biological Interdepartmental Seminar Committee
University Grievance Procedure Committee
College of Agriculture Teaching Improvement Committee
College of Agriculture Academic Planning Committee
Faculty Senate Nominating Committee
Division of Biochemistry Undergraduate Teaching Committee
Division of Biochemistry Graduate Program Committee
University Research Coordination Committee
Chairman of the Graduate Committee, Biochemistry Department
1979-1982 College of Agriculture Tenure and Promotion Committee
1979 College of Agriculture Dean Search Committee
1981 Vice-President for Research Search Committee
1981 College of Human Medicine Evaluation Committee
1981-1982 Biomedical Research Funding Committee
1982 Chairman, Department of Zoology and Physiology Review Committee
1986 Research Committee College of Medicine
Ad Hoc Committee to Review Center on Aging
Ad Hoc Medical Center Research Advisory Committee
Working Group for Biotechnology Center
Center for Pharmaceutical Science and Technology Advisory Committee
College of Pharmacy Graduate Program
College of Pharmacy Research and Seminar
1987 Markey Cancer Center Internal Advisory Committee
College of Medicine Research Committee
Tobacco and Health Advisory Committee
1988 College of Pharmacy BRSG Committee, Tenure and Promotion
1989 Chairman, College of Medicine BRSG Committee
Member, Tobacco & Health Advisory Committee
Member, Markey Cancer Center Advisory Committee
1990 Chairman, College of Medicine BRSG Committee
1991-1992 Member, Intellectual Properties Committee
Member, Search Committee Cancer Center Director
Member, Cancer Center Advisory Committee
Member, Search Committee Diagnostic Radiology Chair
Member, Academic Area Committee, Biological Sciences
1993-1995 Chair, Research and Seminar Committee
Member, Appointment, Tenure and Promotion Committee
1996-1997 Chair, Graduate Program task force, College of Pharmacy
Chair, Physical Plant section, College of Pharmacy self-study
University Chemical Safety Committee
College of Medicine Academic Council
College of Pharmacy Tenure and Promotion Committee
PUBLICATIONS (REFEREED JOURNALS)
1. Haley, B. and Yount, R. Gamma-fluoradenosine
Triphosphate.Synthesis, Properties and Interaction with Myosin and
Heavy Meromyosin. Biochemistry II, 2863-2871 (1972).
2. Haley, B., Yount and Hoffman, J. Selective Inhibition of Divalent
Metal Ion Requiring ATPase Activity of Human Red Cell Ghost by an
Analog of ATP. The Physiologist 16, 333-334 (1973).
3. Haley, B. and Hoffman, J. Interactions of Photo-Affinity ATP
Analog with Cation-Stimulated ATPase Activities of Human Red Cell
Ghost. Proc. Natl. Acad. Sci. 71, 3367-3371 (1974).
4. Staros, J.V., Haley, B. and Richards, F.M. Human Erythrocytes and
Resealed Ghost: A Comparison of Membrane Topology. J. Biol. Chem.
249, 5004-5007 (1974).
5. Pomerantz, A., Rudolph, S.A., Haley, B. and Greengard, P.
Photoaffinity Labeling of a Protein Kinase from Bovine Brain with 8-
Azido-adenosine-3', 5'-monophosphate. Biochemistry 14, 3852-3857
(1975).
6. Haley, B. Photoaffinity Labeling of cAMP Binding Sites of Human
Red Blood Cell Membranes. Biochemistry 14, 3852-3857 (1975).
7. Staros, J.V., Richards, F.M. and Haley, B. Photochemical Labeling
of the Cytoplasmic Surface of the Membranes of Intact Human
Erythrocytes. J. Biol. Chem. 250, 8174-8178 (1975).
8. Malkinson, A.M., Krueger, B.V., Rudolph, S.A., Casnelli, J.E.,
Haley, B. and Greengard, P. Widespread Occurence of a Specific
Protein in Vertebrate Tissues and Regulation by cAMP of its
Endogenous Phosphorylation and Dephosphorylation. Metabolism 24, 331-
341 (1975).
9. Haley, B. Photoaffinity Labeling of Adenosine 3', 5'-Cyclic
Monophosphate Binding Sites. Methods in Enzymology, Jacoby and
Wilchek, Editors. V 46, pp. 339-346 (1976).
10. Owens, J.R. and Haley, B.E. A Study of Adenosine 3', 5'-Cyclic
Monophosphate Binding Sites of Human Erythrocyte Membranes Using 8-
Azido-adenosine-3'-5' Cyclic Monophosphate. J. Supra. Mole. Structure
5, 91-102 (1976).
11. Skare, K., Black, J.L., Pancoe, W.L. and Haley, B. Determination
of the Cellular Location of Cyclic Nucleotide Binding Sites Using 8-
Azido-adenosine-3', 5'-monophosphate, A Photoaffinity Probe. Arch.
Biochem. Biophy. 180, 409-415 (1977).
12. Lau, E., Haley, B. and Barden, R. Interactions of a Photoaffinity
Analog of CoA with CoA Enzymes. Biochemistry 16, 2581-2585 (1977).
13. Owens, J.R. and Haley, B. A Study of Adenosine 3', 5'-Cyclic
Nucleotide Binding Sites of Human Erythrocyte Membranes Using 8-Azido-
adenosine 3'-5'-Cyclic Monophosphate. Cell Shape and Surface
Architecture: Progress in Clinical and Biological Research 17, 65-76
(1977)
14. Lau, E.P., Haley, B. and Barden, R. The 8-Azidoadenine Analog of
S-Benzoyl (3'-dephospho) Coenzyme A-A Photoaffinity Label for Acyl
CoA; Glycine N-Acyltransferase. Biochem. Biophys. Res. Commun 76, 843-
849 (1977).
15. Geahlen, R.T. and Haley, B. Interactions of a Photoaffinity
Analog of GTP with the Proteins of Microtubules. Proc. Natl. Acad.
Sci. 74, 4375-4377 (1977).
16. Owens, J.R. and Haley, B. Use of Photoaffinity Nucleotide Analogs
to Determine the Mechanism of ATP Regulation of a Membrane Bound,
cAMP Activated Protein Kinase. J. Supra. Mole. Structure 9, 57-68
(1978).
17. Czarnecki, J., Geahlen, R.T. and Haley, B. Synthesis and Use of
Azido Photoaffinity Analogs of Adenine and Guanine Nucleotides.
Methods in Enzymology 56, 642-653 (1979).
18. Marcus, F. and Haley, B. Inhibition of Fructose 1,6-biphosphatase
by the Photoreactive AMP Analog, 8-Azido-AMP. J. Biol. Chem. 254, 259-
261 (1979).
19. Geahlen, R., Haley, B. and Krebs, E.G. Synthesis and Use of 8-
azidoguanosine 3', 5'-cyclic Monophosphate as a Photoaffinity Label
for Cyclic GMP-dependent Protein Kinase. Proc. Natl. Acad. Sci. 76,
2213-2217 (1979).
20. Geahlen, R. and Haley, B. Use of GTP Photoaffinity Probe to
Resolve Aspects of the Mechanism of Tubulin Polymerization. J. Biol.
Chem. 254, 11982-11987 (1979).
21. Haley, B. Application of Photoaffinity Nucleotide Analogs to
Biological Membrane Research. Selected Aspects of Cancer-Related
Protein, Carbohydrate, Lipid and other Biochemistry, International
Cancer Research Data Bank, p. 87 (1979).
22. Owens, J. and Haley, B. Mechanism of MgATP Regulation of Membrane
Bound Type I cAMP Activated Protein Kinase. Transmembrane Signaling.
Alan R. Liss, Inc. New York, New York, pp. 149-160 (1979).
23. Forrester, I.T., P.K. Schoff, B.E. Haley and R.G. Atherton.
Determination of Protein Kinase Activity in Intact Mammalian Sperm.
J. of Andrology 1, 70 (1980).
24. Briggs, F. Norman, Al-Jumaily, Walid and Haley, Boyd.
Photoaffinity Labeling of the (Ca+Mg) ATPase of Skeletal and Cardiac
Sarcoplasmic Reticulum with [32P-]-8-Azido ATP. Cell Calcium 1, 205-
215 (1980).
25. Hoyer, P., Owens, J.R. and Haley, B.E. Use of Nucleotide
Photoaffinity Probes to Elucidate Molecular Mechanisms of Nucleotide
Regulated Phenomena. Annals of New York Academy of Science 346, 280-
301 (1980).
26. Takemoto, D.J., B.E. Haley, J. Hanse, P. Pinbett and L.J.
Takemoto. GTPase from Rod Outer Segments: Characterization by
Photoaffinity Labeling and Tryptic Peptide Mapping. Biochem. Biophys.
Res. Commun. 102, 341-347 (1981).
27. Leichtling, B.H., Coffman, D.S., Yaeger, E.S., Rickenberg, H.V.,
Al-Jumaily, W. and Haley, B.E. Occurrence of the Adenylate Cyclase "G-
Protein" in Membranes of Dictyostelium discoidium, Biochem. Biophys.
Res. Commun. 102, 1187-1195 (1981).
28. Schoff, P.K., Forester, I.T., Haley, B.E. and Atherton, R. A
Study of cAMP Binding Proteins on Intact and Distrupted Sperm Cells
Using 8-Azidoadenosine-3', 5'-Cyclic Monophosphate. J. Supra.
Molecular Structure 19, 1-15 (1982).
29. King, M.M., Carlson, G. and Haley, B.E. Photoaffinity-Labeling of
the Subunit of Phosphorylase Kinase by 8-Azidoadenosine-5'-
Triphosphate and its 2', 3' -Dialdehyde Derivative. J. Biol. Chem.
257, 14058-14065 (1982).
30. Potter, R. and Haley, B.E. Photoaffinity Labeling of Nucleotide
Binding Sites with 8-Azidopurine Analogs. Meth. Enzymol. 91, 613-633
(1982).
31. Hoyer, P.B. and Haley, B.E. Utilization of Nucleotide
Photoaffinity Probes to Study Protein-Nucleotide Interactions in Cell
Fractions. J. Cellular Biochemistry, submitted. (1983)
32. Haley, Boyd. Development and Utilization of 8-Azidopurine
Nucleotide Photoaffinity Probes. Federation Proceedings 42, 2831-2836
(1983).
33. Khatoon, S., Atherton, R. Al-Jumaily, W. and Haley, B.E. Use of
Nucleotide Photoaffinity Probes to Study Hormone Action. Biology of
Reproduction 28, 61-73 (1983).
34. Kaiser, I.I., Kladianos, D.M., Van Kirk, E.A., and Haley, B.E.
Photoaffinity Labeling of catechol-o-methyltransferase with 8'-Azido-
S-adenosylmethionine. J. Biol. Chem. 258, 1747-1751 (1983).
35. Abraham, K., Haley, B. and Modak, M. Biochemistry of Terminal
Deoxynucleotidyl Transferase: 8-Azido ATP as A Substrate Binding Site-
Directed Photoaffinity Labeling Prob. Biochemistry 22, 4197-4203
(1983).
36. Haley, B.E., Ponstingl, H. and Doenges, K.H. Photoaffinity
Labeling of Pure Tubulin Using 8-Azidoguanosine triphosphate at the b-
Subunit. Hoppe-Seylers J. Physiol. Chem. 364, 1137 (1983).
37. Woody, A.M., Vader, C.R., Woody, R.W. and Haley, B.E.
Photoaffinity Labeling of DNA-dependent RNA polymerase from E. coli
with 8-azidoadenosine-5'-triphosphate. Biochemistry 23, 2843-2848
(1984).
38. Owens, J.R. and Haley, B.E. Synthesis and Utilization of [5'-32P]-
8-Azidoguanosine-3'-phosphate-5'-phosphate: Photoaffinity Studies on
Cytosolic Proteins of E. coli. J. Biol. Chem. 259, 14843-14848
(1984).
39. Pfister, K.K. , Haley, B.E. and Witman, G.B. The Photoaffinity
Probe 8-azidoadenosine-5'-triphosphate. Selectivity Labels the Heavy
Chain of Chlamydomonas 12S Dynein. J. Biol. Chem. 259, 8499-8504
(1984).
40. Atherton, R.W., Khatoon, S., Schoff, P.K. and Haley, B.E. A Study
of Rat Epididymal Sperm Adenosine-3', 5'-monophosphate-dependent
Protein Kinase: Maturation Differences and Cellular Location. Biol.
of Reproduction 32, 155-172 (1985).
41. McMurray, M.M., Hansen, J.S., Haley, B.E., Takemoto, D.J. and
Takemoto, L.J. Interspecies Conservation of Retinal Guanosine-5'-
triphosphatase: Characterization by Photoaffinity Labeling and
Tryptic Peptide Mapping. Biochemical Journal 225, 227-232 (1985).
42. Khatoon, S., Haley, B.E. and Atherton, R.W. A Comparative
Analysis of cAMP-dependent Protein Kinase Regulatory Subunits in Sea
Urchin and Rat Sperm. J. Andrology 6, 251-260 (1985).
43. DeBortoli, M.E., Issa, H.A., Haley, B.E. and Cho-Chung, Y.S.
Elevated Levels of p2l ras Protein in Hormone-Dependent Mammary
Carcinomas of Humans and Rodents. Bioch. Biophys. Res. Commun. 127,
699-709 (1985).
44. Evans, R., Haley, B. and Roth, D. Photoaffinity Labeling of a
Viral Induced Protein from Tobacco. J. Biol. Chem. 260, 7800-7804
(1985).
45. Nunamaker, R.A., Wilson, W.T. and Haley, B.E. Electrophoretic
Detection of Africanized Honey Bees (Apis mellifera scutellata) in
Guatemala and Mexico Based on Malate Dehydrogenase Allozyme Patterns.
Journal of the Entomological Society 57, 622-631 (1985).
46. Pfister, K.K., Haley, B.E. and Witman, G.B. Labeling of
Chlamydomonas 18S Dynein Polypeptides by 8-Azidoadenosine 5'-
Triphosphate, a Photoaffinity Analog of ATP. J. Biol. Chem. 260,
12844-12850 (1985).
47. Hoyer, P.B., Fletcher, P. and Haley, B.E. Synthesis of 2', 3'-0-
(2,4,6,-trinitrocyclohexadienylidine) guanosine 5'-Triphosphate and
study of its Inhibitory Properties with Adenylate Cyclase. Arch.
Biochem. Biophys. 245, 368-378 (1986).
48. Evans, R.K., Johnson, J.D. and Haley, B.E. 5'-Azido-2'-
deoxyuridine-5'-triphosphate: A Novel Photoaffinity Labeling Reagent
and Tool for the Enzymatic Synthesis of Photoactive DNA. Proc. Natl.
Acad. Sci. USA. 83, pp. 5382-5386 (1986).
49. Jeganathan, A., Richardson, S.K., Mani, R.S., Haley, B.E. and
Watt, D.S. Selective Reactions of Azide-substituted a-Diazoamides
with Olefins and Alcohols Using Rhodium (II) Catalysts. J. Org. Chem.
51, 5362-5367 (1986).
50. Malkinson, A.M., Haley, B.E., Macintyre, B.E. and Buthy, M.S.
Changes in Pulmonary Adenosine Triphosphate Binding Proteins Detected
by Nucleotide Photoaffinity Labeling Following Treatment of Mice with
the Tumor-Modulatory Agent Butylated Hydroxytoluene. Cancer Res. 46,
4626-4630 (1986).
51. Evans, R.K. and Haley, B.E. Synthesis and Biological Properties
of 5-Azido-2'-deoxyuridine-5'-triphosphate: A Photoactive Nucleotide
Suitable for Making Light Sensitive DNA. Biochemistry 26, 269-276
(1987).
52. Richardson, S.K., Jeganathan, A., Mani, R.S., Haley, B.E. and
Watt, D.S. Synthesis and Biological Activity of C-4 and C-15 Aryl
Azide Derivatives of Anguidine. Tetrahedron Letters 43, 2925 (1987).
53. Droms, K.A., Haley, B.E. and Malkinson, A.M. Decreased
Incorporation of the Photoaffinity Probe [g3232P]-8N3 GTP into a 45KD
Protein in Lung Tumors. Bioch. Biophys. Res. Commun. 144, 591-597
(1987).
54. Karpel, R.L., Levin, V.Y. and Haley, B.E. Photoaffinity Labeling
of T4 Bacteriophage 32Protein. J.Biol.Chem. 262, 9359-66 (1987).
55. Suhadolnik, R.J., Li, Shi Wu, Sobol, Jr. R.W., and Haley, B.E. 2-
and 8-Azido Photoaffinity Probes. II. Studies on the Binding Process
of 2-5A Synthetase. Biochemistry 27, 8846-8851 (1988).
56. Suhadolnik, R.J., Kariko, K., Sobol, Jr., R.W., Shi Wu,
Richenbach, N.L. and Haley, B.E. 2- and 8-Azido Photoaffinity Probes.
I. Enzymatic Synthesis, Characterization and Biological Properties of
2- and 8-Azido Photoprobes of 2-5A & Photolabeling of 2-5A Binding
Proteins. Biochemistry 27, 8840-8846 (1988).
57. Droms, K.A., Haley, B.E., Smith, G.J. and Malkinson, A.M.
Decreased Photolabeling of Gsa With [a-32P]8N3-GTP in Tumorigenic
Lung Epithelial Cell Lines: Association with Decreased Hormone
Responsiveness and Loss of Contact-Inhibited Growth. Experimental
Cell Research 182, 330-339 (1989).
58. Francis, B., Overmeyer, J., John, W., Marshall, E. and Haley, B.
Prevalence of Nucleoside Diphosphate Kinase Autophosphorylation in
Human Colon Carcinoma versus Normal Colon Homogenates. Molecular
Carcinogenesis 2, 168-178 (1989).
59. King, S.M., Haley, B.E. and Witman, G.B. Structure of the a and b
Heavy Chains of the Outer Arm Dynein from Chlamydomonas Flagella. J.
Biol. Chem. 264, 10210-10218 (1989).
60. Khatoon, S., Campbell, S.R., Haley, B.E. and Slevin, J.T.
Aberrant GTP b-Tubulin Interaction in Alzheimer's Disease. Annals of
Neurology 26, 210-215 (1989).
61. Lawson, S.G., Mason, T.L., Sabin, R.D., Sloan, M.E., Drake, R.R.,
Haley, B.E. and Wasserman, B.P. UDP-Glucose: (1,3)-B-Glucan Synthase
from Daucas carota L.: Characterization, Photoaffinity Labeling and
Solubilization. Journal of Plant Physiology 90, 101-108 (1989).
62. Lewis, C.T., Haley, B.E. and Carlson, G.M. Formation of an
Intramolecular Cystine Disulfide During the Reaction of 8-Azido-GTP
with Cytosolic Phosphoenolpyruvate Carboxykinase (GTP) Causes
Inactivation without Photolabeling. Biochemistry 28, 9248-9255 (1989).
63. Ho, L.T., Nie, Z.M., Mende, T.J., Richardson, S., Chavan, A.,
Kolaczkowska, E., Watt, D.S., Haley, B.E. and Ho, R.J. Modification
of Adenylate Cyclase by Photoaffinity Analogs of Forskolin. J. Second
Messengers and Phosphoproteins 12, 209-223 (1989).
64. Wasserman, B.P., Read, S.M., Frost, D.J., Mason, T.L., Drake,
R.R. and Haley, B.E. Potential use of Affinity Labels in Subunit
Identification Studies of (1,3)-b-Glucan Synthase. J.Applied Polymer
Science Symposium (Proceeding of the Tenth Cellulose Conference,
Syracuse, NY). C. Schuerch and T. Timell, Eds. 43, 827-837 (1989).
65. Drake, R.R., Evans, R.K., Wolf, M.J. and Haley, B.E. Synthesis
and Properties of 5-Azido-UDP-Glucose: Development of Photoaffinity
Probes for Nucleotide Diphosphate Sugar Binding Sites. J. Biol. Chem.
264, 11928-11933 (1989).
66. Dholakia, J.N., Francis, B.R., Haley, B.E. and Wahba, A.
Photoaffinity Labeling of the Rabbit Reticulocyte Guanine Nucleotide
Exchange Factor and Eukaryotic Initiation Factor 2 with 8-Azidopurine
Nucleotides. J. Biol. Chem. 264, 20638-20642 (1989).
67. Campbell,S., Kim, H., Doukas, M. and Haley, B. Photoaffinity
Labeling of ATP and NAD+ Binding Sites on Recombinant Human
Interleukin-2. Proc. Natl. Acad. Sci. 87, 1243-1246 (1990).
68. Kim, H. and Haley, B. Synthesis and Properties of 2-Azido-NAD+: A
Study of Interactions with Glutamate Dehydrogenase. J. Biol. Chem.
265, 3636-3641 (1990).
69. Drake, R., Palamarczyk, G., Haley, B. and Lennarz, W.J. Evidence
for the Involvement of a 35-kDa Membrane Protein in the Synthesis of
Glucosylphosphoryldolichol. Bioscience Reports 10, 61-68 (1990).
70. Marchase, R.B., Richardson, K.L., Srisomsap, C., Drake, R. and
Haley, B.E. Resolution of Phosphoglucomutase and the 62 kDa Acceptor
for the Glucosylphosphotransferase. Arch. Biochim. Biophys. 280, 122-
129. (1990).
71. Salvucci, M.E. and Haley, B.E. Photoaffinity Labeling of Ribulose
Bisphosphate Carboxylase/Oxygenase With 8-Azidoadenosine 5'-
Triphosphate. Planta 181, 287-295 (1990).
72. Salvucci, M.E., Drake, R., Broadbent, K.P., Haley, B.E., Hanson,
K.R. and McHale, N.A. Identification of the 64 Kilodalton Chloroplast
Stromal Phosphoprotein as Phosphoglucomutase. Plant Physiology 93,
105-109 (1990).
73. Frost, D.J., Read, S.M., Drake, R., Haley, B.E. and Wasserman,
B.P. Identification of the UDPG Binding Polypeptide of (1,3)-b-Glucan
Synthase From A Higher Plant by Photoaffinity Labeling with 5-
AzidoUDP-Glucose. J. Biol. Chem. 265, 2162-2167 (1990).
74. Lin, F.C., Brown, R.M. Jr., Drake, R.R. and Haley, B.E.
Characterization of Cellulose Synthase Catalytic Subunit of
Acetobacter xylinum Using 5-Azido-UDP-glc, A Photoaffinity Probe. J.
Biol. Chem. 265, 4782-4784 (1990).
75. Salvucci, M.E., Drake, R.R., and Haley, B.E. Purification and
Photoaffinity Labeling of Sucrose Phosphate Synthase from Spinach
Leaves. Arch. Biochem. Biophys. 281, 212-218 (1990).
76. Chavan, A.J., Kim, H., Haley, B.E., and Watt, D.S. A Photoactive
Phosphonamide Derivative of GTP for the Identification of the GTP
Binding Domain of b-Tubulin. Bioconjugate Chemistry, 1, No. 5, 337-
344 (1990).
77. Kwiatkowski, S., Crocker, P.J., Chavan, A.J., Nobuyuki, I.,
Haley, B.E. and Watt, D.S. Thiazolidine and Thiazoline Derivatives of
3-Aryl 3-Trifluormethyl Diazirines for the Preparation of Fluorescent
or 35S-Radiolabeled Photoaffinity Probes. Tetrahedron Lett, 31, 2093-
2096 (1990).
78. Palamarczyk, G., Drake, R., Haley, B. and Lennarz, W.J. Evidence
that the Synthesis of Glucosylphosphoryl Dolichol in Yeast Involves a
35 kDa Membrane Protein. Proc. Natl. Acad. Sci. 87, 2666-2670 (1990).
79. King, S., Kim, H., and Haley, B. Strategies and Reagents for
Photoaffinity Labeling of Mechanochemical Proteins. Meth. Enzymol.
196, 449-466 (1991).
80. Kim, H. and Haley, B. Identification of Peptides in the Adenine
Ring Binding Domain of Glutamate and Lactate Dehydrogenase Using 2-
AzidoNAD+. Bioconjugate Chemistry 2, 1142-147 (1991).
81. Mann, D., Haley, B., and Greenberg, R. Photoaffinity Labeling of
Atrial Natriurtic Factor Analog Atriopeptin III woith [g32P]8N3GTP.
Peptide Research 4, #2, 79-83 (1991).
82. Drake, R.R., Zimniak, P., Haley, B.E., Lester, R., Elbein, A.D.
and Radominska, A. Synthesis and Characterization of5-Azido-UDP-
Glucuronic Acid. J. Biol. Chem., 266, 23257-23260 (1991).
83. Drake, R.R., Zimniak, P., Haley, B.E., Lester, R., Elbein, A.D.
and Radominska, A. Synthesis and Characterization of5-Azido-UDP-
Glucuronic Acid. J. Biol. Chem., 266, 23257-23260 (1991).
84. Hiestand, D., Haley, B., and Kindy, M. Role of Calcium
inInactivation of Calcium/Calmodulin Dependent Protein Kinase II
After Cerebral Ischemia. Journal of the Neurological Sciences, 113,
31-37 (1992).
85. Salvucci, M., Chavan, A. and Haley, B. Identification of Peptides
for the Adenine Binding Domains of ATP and AMP in Adenylate Kinase:
Isolation of Photoaffinity Labeled Peptides by Metal Chelate
Chromatography. Biochemistry 31 4479-4487 (1992).
86. Shoemaker, M., Lin, P.C., and Haley, B. Identification of the
Guanine Binding Domain Peptide of the GTP Binding Site of Glucagon.
Protein Science 1, 884-891 (1992).
87. Doukas, M., Chavan, A., Gass, C., Boone, T. and Haley, B.
Identification and charaterization of a Nucleotide Binding Site on
Recombinant Murine Granulocyte/Macrophage-Colony Stimulating Factor.
Bioconjugate Chemistry 3, 484-492 (1992).
88. Segal, A., West, I., Wientjes, F., Nugent, J., Chavan, A., Haley,
B., Garcia, R., Rosen, H. and Scrace, G. Cytochrome b-245 is a
Flavocytochrome Containing FAD and the NADPH Binding Site of the
Microbicidal Oxidase of Phagocytes. Biochem. J. 284, 781-788 (1992).
89. Hammond, D., Haley, B. and Lesnaw, J. Identification and
Characterization of Serine/Threonine Protein Kinase ActivityIntrinsic
to the L Protein of Vesicular Stomatitis Virus New Jersey. Journal of
General Virology 73, 67-75 (1992)
90. Chavan, A., Nemoto, Y., Narumiya, S., Kozaki, S., and Haley, B.
NAD+ Binding Site of Clostridium botulinum C3 ADP-ribosyltransferase:
Identification of Peptide in the Adenine Ring Binding Domain using 2-
Azido NAD+. J. Biol. Chem. 267, 14866-14870 (1992).
91. Gunnersen, D.J. and Haley, B.E. Detection of Glutamine Synthetase
in the Cerebrospinal Fluid of Alzheimer's Diseased Patients: A
Potential Diagnostic Biochemical Marker. Proc. Natl. Acad. Sci. USA,
89 pp. 11949-11953 (1992).
92. Shoemaker, M., and Haley, B. Identification of a Guanine Binding
Domain Peptide of the GTP Binding Site of Glutamate Dehydrogenase:
Isolation with Metal-Chelate Affinity Chromatography. Biochemistry
32, 1883-1890 (1993).
93. Churn, S.B., Sankaran, B., Haley, B.E. and Delorenzo, R.J.
Ischemic Brain Injury Selectively Alters ATP Binding of Calcium and
Calmodulin-Dependent Protein Kinase-II. Biochem. Biophys. Res. Comm.
193:3, 934-940 (1993).
94. Salvucci, M., Rajagopalan, K., Sievert, G., Haley, B. and Watt,
D. Photoaffinity Labeling of Rubisco Activase with ATP-g-
benzophenone: Identification of the ATP g-Phosphate Binding Domain J.
Biol. Chem. 268, 14239-14244 (1993).
95. Rajagopalan, K., Chavan, A., Haley, B. and Watt, D. Bidentate
Cross-Linking Reagents: Non-Hydrolyzable Nucleotide Photoaffinity
Probes with Two Photoactive Groups J. Biol. Chem. 268, 14245-14253
(1993).
96. Trad, C., Chavan, A., Clemens, J., and Haley, B. Identification
and Characterization of an NADH Binding Site of Prolactin with 2-
Azido-NAD+ Arch. Biochem. Biophys. 304, 58-64 (1993).
97. Chavan, A., Ensor, C., Wu, P., Haley, B. and Tai, H.
Photoaffinity Labeling of Human Placental NAD+-Linked 15-
Hydroxyprostaglandin Dehydrogenase with [a32P]-2N3NAD+:
Identification of a Peptide in the Adenine Ring Binding Domain J.
Biol. Chem. 268, 16437-16442 (1993).
98. Chavan, A., Richardson, S., Kim, H., Haley, B. and Watt, D.
Forskolin Photoaffinity Probes for the Evaluation of Tubulin Binding
Sites Bioconjugate Chem. 4, 268-274 (1993).
99. Duhr, E.F., Pendergrass, J. C., Slevin, J.T., and Haley, B.
HgEDTA Complex Inhibits GTP Interactions With The E-Site of Brain b-
Tubulin Toxicology and Applied Pharmacology 122, 273-288 (1993).
100. Jayaram, B. and Haley, B. Identification of Peptides Within the
Base Binding Domains of the GTP and ATP Specific Binding Sites of
Tubulin. J. Biol. Chem. 269 (5) 3233-3242 (1994).
101. A. Chavan, B. Haley, D. Volkin, K. Marfia, A. Verticelli, M.
Bruner, J. Draper, C. Burke and R. Middaugh. Interaction of
Nucleotides with Acidic Fibroblast Growth Factor (FGF-1).
Biochemistry 33,7193-7202 (1994).
102. Logan, J., Hiestand, D., Daram, P., Huang, Z., Muccio, D.,
Hartman, J., Haley, B., Cook, W., and Sorscher, E. Cystic Fibrosis
Transmembrane Conductance Regulator Mutations That Disrupt Nucleotide
Binding. J. Clin. Invest. 94, 228-236 (1994).
103. Olcott, M. and Haley, B. Identification of Two Peptides From the
ATP-Binding Domain of Creatine Kinase. Biochemistry, 33, 11935-11941
(1994).
104. Bhattacharyya, A., Chavan, A., Shuffett, M., Haley, B. and
Collins, D. Photoaffinity Labeling of Rat Liver Microsomal 5a-
Reductase by 2-Azido-NADP+. Steroids 59, 634-641 (1994).
105. Salvucci, M., Chavan, A., Klein, R., Rajagopalan, K. and Haley,
B. Photoaffinity Labeling of the ATP Binding Domain of Rubisco
Activase and a Separate Domain Involved in the Activation of Ribulose-
1,5-Bisphosphate Carboxylase/Oxygenase. Biochemistry 33, 14879-14886
(1994).
106. Pendergrass, J.C. and Haley, B.E. Mercury-EDTA Complex
Specifically Blocks Brain b-Tubulin-GTP Interactions: Similarity to
Observations in Alzheimer"s Disease. pp98-105 in Status Quo and
Perspective of Amalgam and Other Dental Materials (International
Symposium Proceedings ed. by L. T. Friberg and G. N. Schrauzer) Georg
Thieme Verlag, Stuttgart-New York (1995).
107. Doukas, M., Chavan, A., Gass, C., Nickel, P., Boone, T. and
Haley, B. Inhibition of GM-CSF Activity by Suramine and Suramin
Analogues is Correlated to Interaction with the GM-CSF Nucleotide
Binding Site. Cancer Research 55:5161-5163 (1995).
108. Bhattacharyya, A. K., Chavan, A.J., Haley, B., Taylor, M.F., and
Collins, D.C. Identification of the NADP(H) Binding Site of Rat Liver
Microsomal 5a-Reductase (Isozyme-1): Purification of a Photolabeled
Peptide Corresponding to the Adenine Binding Domain. Biochemistry 34,
3663-3669 (1995)
109. Chavan, A., Gass, C., Haley, B., Boone, T. and Doukas, M. A.
Identification of N-Terminus Peptide of Human Granulocyte/Macrophage
Colony Stimulating Factor as the Site of Nucleotide Interaction.
Biochem. Biophys. Res. Commun. 208,#1 390-396 (1995).
110. Shoemaker, M., and Haley, B. Identification of the Adenine
Binding Domain Peptides of the ADP Binding Site of Glutamate
Dehydrogenase. Bioconjugate Chemistry 7, 302-310 (1996).
111. Rajagopalan, K., Pavlinkova, G., Levy, S., Pokkuluri, R.,
Schiffer, M., Haley, B., and Kohler, H. Novel Unconventional Binding
Site in the Variable Region of Immunoglobulins. Proc. Natl. Acad.
Sci. 93, 6019-6024 (1996).
112. Pavlinkova, G., Rajagopalan, K., Muller, S., Chavan, A.,
Sievert, G., Lou, D., O'Tolle, C., Haley, B., and Kohler, H. Site-
Specific Photobiotinylation of Immunoglobins, Fragments and Light
Chain Dimers. J. Immunological Methods 201, 77-88 (1997).
113. Pendergrass, J.C. and Haley, B.E. Inhibition of Brain Tubulin-
Guanosine 5'-Triphosphate Interactions by Mercury: Similarity to
Observations in Alzheimer's Diseased Brain. In Metal Ions in
Biological Systems V34, Mercury and Its Effects on Environment and
Biology, Chapter 16. Edited by H. Sigel and A. Sigel. Marcel Dekker,
Inc. 270 Madison Ave., N.Y., N.Y. 10016 (1996).
114. McGuire, M., Carroll, L. J., Yankie, L., Thrall, S. H., Dunaway-
Mariano, D., Hertzberg, O., Jayaram, B. and Haley, B. Determination
of the Nucleotide Binding Site within Clostridium symbiosum Pyruvate
Phosphate Dikinase by Photoaffinity Labeling, Site-Directed
Mutagenesis, and Structural Analysis. Biochemistry 35, 8544-8552
(1996).
115. Kohler, H., Pavlinkova, G., and Haley, B. Immunoglobulin
Nucleotide Binding Site: A Possible Superantigen Receptor. In Human B
Cell Superantigens, edited by Moncei Zouali, Chapter 13, pp 189-194
(1996).
116. Sankaran, B., Chavan, A. and Haley, B. Identification of Adenine
Binding Domain Peptides of the NADP+ Active Site within Porcine Heart
NADP+-Dependent Isocitrate Dehydrogenase. Biochemistry 35, 13501-
13510 (1996).
117. Sankaran, B., Clemens, J., and Haley, B. A Comparison of Changes
in Nucleotide-Protein Interactions in the Striatal, Hippocampus and
Paramedian Cortex After Cerebral Ischemia and Reperfusion:
Correlations to Regional Vulnerability. Molecular Brain Research 47,
237-250 (1997).
118. Hensley, K., Cole, P. ,Aksenov, M., Aksenova, M., Bummer, P.E.,
Carney, J.M., Haley, B.E., and Butterfield, D.A. Oxidatively-Induced
Structural Alteration of Glutamine Synthetase Assessed by Analysis of
Spin Label Incorporation Kinetics. J. of Neurochemistry 68, 2451-2457
(1997).
119. Pendergrass, J. C., Haley, B.E., Vimy, M. J., Winfield, S.A. and
Lorscheider, F.L. Mercury Vapor Inhalation Inhibits Binding of GTP to
Tubulin in Rat Brain: Similarity to a Molecular Lesion in Alzheimer's
Disease Brain. Neurotoxicology 18(2), 315-324 (1997).
120. Olcott, M.C. and Haley, B.E. Identification of an Adenine-
nucleotide Binding Site on Interferon-a2. Eur. J. Biochem. 247/3, 762-
769 (1997).
121. David, S., Shoemaker, M., and Haley, B. Abnormal Properties of
Creatine kinase in Alzheimer's Disease Brain: Correlation of Reduced
Enzyme Activity and Active Site Photolabeling with Aberrant Cytosol-
Membrane Partitioning. Molecular Brain Research accepted (1997).
RESEARCH PAPERS (ABSTRACTS)
1. Haley, B. and Yount, R. Inhibition of Myosin by Gamma-
Fluoroadenosine Triphosphate, Abstracts Pacific Slope Biochemistry
Conference, Seattle, Washington (1969).
2. Haley, B. Synthesis of Photoaffinity Analogs of ATP and AMP and
Their Use as Membrane Probes. Mount Sinai School of Medicine &
Rockefeller University School of Medicine, (Invited paper)(1974)
3. Haley, B. and Hoffman, J. Photoaffinity Labeling of ATP Binding
Sites of Human Erythrocyte Membrane, FASEB Meeting, Atlantic City
(1974).
4. Haley, B. Photoaffinity Labeling of cAMP Binding Sites of Human
Erythrocyte Membranes, Abstracts 1975 ICN-UCLA Biochemistry
Conference on Energy Transduction (1975).
5. Haley, B. Photoaffinity Labeling of Human Red Cell Membrane
Binding Sites Using 8-Azido-cAMP, Abstracts 1975 FASEB Meeting,
Atlantic City (1975).
6. Owens, J.R. and Haley, B. A Study of cAMP Stimulated
Phosphorylation and cAMP Binding Sites of Human Erythrocyte Membrane
Proteins using 32P-8-Azido-cAMP, a Photoaffinity Probe. ICN-UCLA
Conference on Molecular and Cellular Biology (1975).
7. Owens, J. and Haley, B. Properties of cAMP Binding Proteins of the
Human Erythrocyte Membrane, Abstracts 1976 ICN-UCLA Biochemistry
Conference on Cell Shape and Surface Architecture (1976).
8. Seery, V. and Haley, B. Activation of Glycogen Phosphorylase by 8-
Azidoadenosine 5'-Monophosphate, Abstracts ASBC Meeting, San
Francisco (1976).
9. Waterson, R. and Haley, B. Interactions of Photoaffinity AMP and
ATP Analogs with E. coli Aminoacyl-tRNA Synthetases, Abstracts ASBC
Meeting, San Francisco (1976).
10. Fletcher, P., Kaltenback, C. and Haley, B. Photoaffinity Labeling
of Adenosine-3', 5' Cyclic Monophosphate Binding Sites in Ovine
Corpus Lutea. Abstracts, Society for the Study of Reproduction,
Philadelphia, Pennsylvania (1976).
11. Geahlen, R.L., Moore, V.G., Kaiser, I.I. and Haley, B.E.
Synthesis and Biological Activity of Photoactive 8-Azidoguanosine
Nucleotide Analogs. Abstracts, 1977 FASEB Meeting, Chicago (1977).
12. Owens, J. and Haley, B. Mechanism of Action of Membrane Bound
cAMP Activated Protein Kinase. 1977 ICN-UCLA Conference on Molecular
Aspects of Membrane Transport (1977).
13. Hahn, G.L., Metz, K.W., Atherton, R.W. and Haley, B.E. Labeling
of a Surface Cyclic-AMP Receptor Site on Rabbit Sperm Utilizing a
Photoaffinity Analog. American Society of Andrology, Nashville,
Tennessee (1978).
14. Owens, J. and Haley, B.E. Mechanism of Mg-ATP Regulation of
Membrane Bound Type 1 cAMP Activated Protein Kinase, Transmembrane
Signaling, ICN-UCLA Symposia (1978).
15. Czarnecki, J. and Haley, B. Interaction of 8-Azido-2'-
Deoxyadenosine-5'-Triphosphate, A Photoaffinity Label, with a DNA-
Dependent DNA Polymerase. ASBC Meeting, Atlanta (1978).
16. Hoyer, P.B. and Haley, B.E. Partial Characterization of Rat Brain
cAMP Binding Proteins: Cellular Location, Molecular Weights, and
Nucleotide Effects. 1979 ICN-UCLA Conference on Covalent Modification
of Proteins (1979).
17. Schoff, P., Atherton, R.W. and Haley, B.E. A Study of the cAMP
Receptor Proteins of Human Ejaculated Sperm Using a Photoaffinity
Analog. 1979 Soc. Study of Reproduction (1979).
18. Briggs, F.N., Al-Jumaily, W. and Haley, B.E. Interactions of the
Photoaffinity Analog of ATP, 8-Azido-ATP, 8-Azido-ATP, with Vesicles
of Skeletal and Cardiac Sarcoplasmic Reticulum (1980).
19. Hoyer, P.B. and Haley, B.E. Use of Photoaffinity Probes to Study
cAMP Dependent Membrane Partitioning of ATP Binding and
Phosphorylated Proteins (1980).
20. Owens, J.R. and Haley, B.E. Photoaffinity Labeling of Guanosine
Polyphosphate (Magic Spot) Binding Proteins. Fed. Proc. 40, St.
Louis, Missouri (1981).
21. Khatoon, S., Schoff, P.L., Haley, B.E. and Atherton, R.W. A
Comparative Study of Sperm cAMP Dependent Protein Kinases by a
Photoaffinity Analysis. American Society of Andrology Meeting, New
Orleans, Louisiana (1981).
22. Woody, A-Young, M., Vader, C.R., Reisbig, R.R., Woody,
(Message over 64k, truncated.)
Having problems with message search?
Fill out this form to ensure your group is one of the first to be migrated to the new message search system.
Offline 
