Source of aberrant bone growth discovered
Tuesday, March 10th, 2009Gizmorama -
“The Cutting Edge of Science Fact and Science Possibilities”
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Good Morning,
A U.S. study has identified the source of immature
cells that spur heterotopic ossification — misplaced
bone growth.
Until Tomorrow,
Erin
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Gene modifies cystic fibrosis lung disease
U.S. medical scientists involved in an international
study say they’ve identified a gene that modifies
lung disease severity in people with cystic fibrosis.
Wake Forest University Baptist Medical Center research-
ers said the research is the first published study to
search the entire genome looking for genes that modify
the severity of cystic fibrosis lung disease. Carl
Langefeld, a study co-author and Wake Forest University
School of Medicine researcher, said the findings might
“help in the identification of targets for drug develop-
ment and the development of tools for the earlier
diagnosis of individuals with cystic fibrosis who are
susceptible to severe lung disease.” After analyzing
the genetic makeup of nearly 3,000 cystic fibrosis
patients, researchers found small genetic differences
in a gene called IFRD1 correlate with lung disease
severity. They discovered the protein encoded by IFRD1
is particularly abundant in a type of white blood cell
called neutrophils, and that it regulates their func-
tion. “Neutrophils … are important to the immune sys-
tem’s response to bacterial infection,” said senior
investigator Dr. Christopher Karp of Cincinnati
Children’s Hospital Medical Center. “In cystic fibrosis,
however, neutrophilic airway inflammation is dys-
regulated, eventually destroying the lung.” The study
was reported in the Feb. 25 online edition of the
journal Nature in advance of print publication.
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Malaria drug can kill two lethal viruses
U.S. medical scientists say they’ve discovered two
lethal viruses that cause encephalitis and respiratory
disease are susceptible to chloroquine treatment. Re-
searchers at the Weill Cornell Medical College in New
York said chloroquine, a drug used to prevent and
treat malaria, kills the Hendra virus and the Nipah
virus — both harbored by fruit bats. The viruses that
emerged during the 1990s in Australia and Southeast
Asia can produce a 75 percent fatality rate in humans.
“The fact that chloroquine is safe and widely used in
humans means that it may bypass the usual barriers
associated with drug development and move quickly into
clinical trials,” said Professor Anne Moscona, the
study’s senior author. “Chloroquine stands a good
chance of making it through the development process in
time to prevent further outbreaks of these deadly in-
fections.” Hendra and Nipah are zoonotic pathogens.
That means they originate in certain animals, but can
jump between animal species and between animals and
humans. There are currently no vaccines or treatments
against the two henipaviruses, which are listed by the
U.S. government as possible bioterrorism agents, the
researchers said. The study appears online in the
Journal of Virology in advance of the journal’s April
print issue.
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Source of aberrant bone growth discovered
Researchers at the University of Pennsylvania School
of Medicine and the University of Connecticut said
they discovered the major repository of bone-forming
cells originates in blood vessels deep within skeletal
muscle and other connective tissues, and not from
muscle stem cells themselves. That finding, said the
scientists, shows cells important in the inflammatory
response to injury trigger skeleton-stimulating pro-
teins to transform muscle tissue into bone. Understand-
ing that process, they said, has important implications
for understanding the formation of bone, not only in
fibrodysplasia ossificans progressive — a rare disease
known as FOP in which patients’ muscle cells literally
metamorphose to bone — but also in many common dis-
orders of misplaced bone growth such as thouse follow-
ing head, athletic and spinal cord injuries. “We always
knew that heterotopic, or misplaced, bone growth was
supplied by a rich vasculature, but we never suspected
that cells from the blood vessels … could undergo a
metamorphosis that becomes a second skeleton,” said Dr.
Frederick Kaplan, the study’s senior author. “When
these components interact pathologically, as in the
rare disease FOP, devastating results occur. We want
to fix that.” The findings are reported in the Journal
of Bone & Joint Surgery.