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HEALTH TIPS WEEKLY - Thursday, May 8, 2008
"News That Keeps You Healthy"
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Botulism neurotoxin antidote is sought
UPTON, N.Y., -- U.S. government scientists say they've taken
the first step toward designing an effective antidote to the
most potent form of Botulinum neurotoxin. The neurotoxin
isn't only responsible for the deadly food poisoning disease
botulism but it can also be used as a biological weapon.
When ingested or inhaled, less than one-one billionth of an
ounce can cause muscle paralysis and death, researchers
said. Although experimental vaccines administered prior to
exposure can inhibit the destructive action of the neurotox-
in -- the most deadly protein known to humans -- no effect-
ive pharmacological treatment exists. Now, scientists at the
U.S. Department of Energy's Brookhaven National Laboratory
and the U.S. Army Medical Research Institute of Infectious
Diseases report finding they can trick the toxin to bypass
its normal binding protein, thereby blocking its deadly act-
ion. "We have found a highly efficient inhibitor of botul-
inum neurotoxin type A -- the most potent of seven neurotox-
ins produced by the bacterium Clostridium botulinum. This
finding can lead to a very effective drug to stop the devas-
tating effects of the toxin," said Brookhaven biologist Sub-
ramanyam Swaminathan, the study's co-principal investigator.
The research is reported in the online issue of the Journal
of Biological Chemistry.
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Tumor cell 'destruct triggers' studied
GAINESVILLE, Fla.,-- U.S. geneticists say tumor cells might
be able to escape death from radiation or chemotherapy bec-
ause of a blockage in their self-destruct mechanisms. Univ-
ersity of Florida researchers studying fruit fly cells dis-
covered that slight changes in the protein scaffolds suppor-
ting the genes "reaper" and "hid" cause the cells to become
naturally resistant to X-rays during early development. "It
turns out that a piece of DNA that is required for mediating
this process of cell death is blocked," Associate Professor
Lei Zhou. "When it is blocked, the cells just don't die,
even when subjected to heavy doses of radiation. This may be
what is happening in some resistant cancer cells. The pro-
apoptotic genes cannot be induced to cause cell death." The
researchers said their findings might be the first to link
apoptosis -- the gene-driven process that leads to the nec-
essary destruction of old, damaged, or infected cells --
with epigenetics, the study of how gene function changes
even when the genes themselves don't change. The research
was reported in a recent issue of the journal Developmental
Cell.
Infectious disease study takes new tack
GENOA, Italy, -- Italian scientists have discovered a new
perspective in the study of infectious disease that reveals
how an organism can cause an illness. Normally, such studies
are based upon laboratory research that looks at an organism
and how it works within the human body. But Carla Pruzzo,
Luigi Vezzulli and Rita Colwell of the University of Genoa
studied an environmental bacteria and its interaction with
the environment and found that method provided them with
vast amounts of information about how the organism they
studied -- Vibrio cholerae -- causes cholera. They discov-
ered that in the aquatic environment the bacteria interacts
with chitin, a naturally-occurring compound found in the
cell walls of fungi and in crustaceans and insects. The int-
eraction was found to play a large part in determining how
the organism survives, how it is spread and how it infects
humans. "This knowledge provides a new framework for the
understanding of the role of the non-human environment in
affecting the spread of environmental disease-causing bac-
teria, their evolutionary derivation and the way they infect
humans to cause disease," Vezzulli said. The study was rec-
ently published in the journal Environmental Microbiology.
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Genetic map of a cancerous bladder created
HOUSTON, -- U.S.-led cancer researchers have created a phy-
sical-genetic map depicting a cancerous bladder's molecular
journey from normal cells to malignancy. Scientists at The
University of Texas M.D. Anderson Cancer Center said by geo-
graphically relating an organ's varied tissues to their und-
erlying genetic variation or regulation, the team also iden-
tified a crucial new category of genes that launches the
process of cancer development. "These 'forerunner genes' are
the ignition key that starts the engine of carcinogenesis,"
said senior author Dr. Bogdan Czerniak. "Discovery of fore-
runner genes opens an entirely new field of investigation to
identify biomarkers for the early detection and prevention
of cancer. Inactivation of these genes occurs during can-
cer's invisible stage, when it is undetectable by traditio-
nal means." The research model can be used to study other
cancers of the epithelium -- the tissue that lines the sur-
faces and cavities of the body's organs, the researchers
said. Epithelial cancers, or carcinomas, make up 80 percent
of all cancers. The 29-page paper will take up half of the
space devoted to original research in the July issue of the
journal Laboratory Investigation.
Study discovers how moles become cancerous
STATE COLLEGE, Pa., -- U.S. scientists say they've discov-
ered how a mole develops into melanoma by showing the inter-
action of two proteins involved in up to 70 percent of
tumors. "We have shown that when two proteins (B-Raf and
Akt3) communicate with one another in a mole, they cooper-
ate, leading to the development of melanoma," said Penn
State University Associate Professor Gavin Robertson, lead
author of the study. "We have also shown that effective
therapies for melanoma need to target both these proteins,
which essentially eliminates the tumors." Melanoma is the
most deadly form of skin cancer because it metastasizes so
quickly, the scientists said. In general, people with adva-
nced-stage melanoma only have months to live. B-Raf is the
most mutated gene in melanoma. The mutant protein, (V600E)B-
Raf, produced by that gene is important in helping mole
cells survive and grow but it is unable to form melanomas
on its own, the scientists said Robertson and his colleag-
ues found a second protein -- produced by Akt3 -- regulates
the activity of mutated B-Raf, which aids melanoma develop-
ment. The research that included Mitchell Cheung, Arati
Sharma and SubbaRao Madhunapantula is reported in the jour-
nal Cancer Research.
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Drug compound lowers blood pressure
GAINESVILLE, Fla., -- U.S. scientists say they've created a
drug compound that lowers blood pressure and prevents heart
and kidney damage in rats with persistent hypertension. The
University of Florida researchers said their findings could
lead to a new class of antihypertensive drugs designed to
address two major problems associated with cardiovascular
disease: high blood pressure and the tissue damage associ-
ated with it, known as fibrosis. "When people have heart
attacks (or suffer from hypertension) the blood vessels get
more rigid," said Assistant Professor David Ostrov. "We dis-
covered a compound that reverses the fibrosis that makes the
blood vessels more rigid." He said the discovery, in itself,
is significant because no one has ever specifically identif-
ied a compound that enhances the activity of an enzyme -- in
this case ACE2 -- using a rational structure-based approach.
"In other words, no one has ever done this before on pur-
pose," he said. "People have discovered molecules that en-
hance the activity of enzymes by trial and error but no
group has ever done it in a specifically pointed way like
this." Additional research, he said, will continue to exp-
lore the compound's effectiveness in animals and humans.
The findings appear in the journal Hypertension.
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