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Common chemical prevents heart failure
in mice with muscular dystrophy
A study led by U-M Center for Integrative Genomics director and
CVC member Joseph Metzger, Ph.D., has received international media
attention from British Broadcasting Corporation (BBC), Nature, and beyond.
Metzger team focused on a common chemical used in the manufacturing
and pharmaceutical industries that can repair damage to cardiac muscle
cell membranes and prevent heart failure in mice with the genetic mutation
that causes Duchenne muscular dystrophy. The mutation in the dystrophin
gene causes the progressive deterioration of skeletal muscles seen in
people with muscular dystrophy. But the mutation affects cardiac muscle,
too. This study is important because it is the first to show what happens
to heart muscle cells called myocytes in the absence of dystrophin. It
is also the first study to demonstrate a new, promising approach to repair
the damage. However, Metzger emphasizes that several years of additional
animal research will be required before the treatment could be tested
in human patients. Read
the full story.
U-M studies indicate possible cause of abdominal aortic aneurysms
Two papers from U-M CVC researchers led by vascular surgeon Gilbert
Upchurch, Jr., M.D., are shedding light on the cause of deadly
abdominal aortic aneurysms (AAA). In a recent issue of Circulation,
U-M researchers
report that a certain type of white blood cell called a neutrophil
appears to be crucial to AAA formation. The two papers show for
the first time
that neutrophils are important in the very early stages of AAA
formation, when the aorta wall begins to weaken and bulge. The
researchers think
the cell may somehow act in combination with other AAA risk factors
such as smoking, high blood pressure and inherited genetic vulnerability.
The
U-M researchers made the findings in laboratory experiments on
mice that had been treated to wipe out their neutrophils temporarily,
and in rats
that lacked the protein that lets neutrophils attach to tissue.
In both cases, the rodents that had low neutrophil levels or no
neutrophil-attaching protein developed little or no sign of aneurysm.
Meanwhile, an
induced
injury to the aorta wall prompted the rapid formation of aneurysms
in the normal rodents. Read
the full story.
More is better: Angioplasty study shows patients still do better
with doctors who do more procedures
According to a paper published in the Journal of the American College
of Cardiology, researchers from the CVC and the Blue Cross Blue
Shield of Michigan Cardiovascular Consortium have found that the
risk of major
cardiovascular problems was 63 percent higher among patients treated
by doctors who performed less than 90 angioplasty procedures each
year compared
with those who did more than 90 a year. However, the study found
no difference in the risk of death before leaving the hospital
among patients treated
by low- and high-volume doctors. It also found that some doctors
who performed fewer angioplasties each year still had very good
patient outcomes, suggesting
that “practice makes perfect” is not the whole story for the
minimally invasive procedures known as percutaneous coronary interventions
or PCI. While previous studies using older data have shown major
differences in rates of complications and death depending on how
many artery-clearing
procedures doctors have done, the new study suggests that the playing
field is leveling. According to lead author Mauro Moscucci, M.D.,
the bottom line is still that more is better, for the most part.
Moscucci, who directs the U-M cardiac catheterization laboratory, leads the multi-hospital
project funded by BCBSM tfoundation hat provided the new data. Read
the full story.
Carbon monoxide: Poison gas or the body’s
natural anti-inflammatory drug?
According to research from the CVC, deadly carbon monoxide could
turn out to be a lifesaver for patients recovering from organ transplants,
strokes or heart attacks. U-M scientists found that inhaling small
amounts of carbon monoxide (CO) for several weeks after transplant
surgery prevented the development of a lethal inflammatory reaction in experimental
mice receiving transplanted trachea, or windpipes. The findings,
made by U-M chief of Cardiovascular Medicine David J. Pinsky, M.D., and his
team, suggest that a patient's chances of living or dying after
a lung transplant
depend mostly on the outcome of an internal power struggle between
two enzymes that control cellular production of carbon monoxide
and nitric oxide (NO). Results of the U-M study were published
in the July 18 issue of the Journal of Experimental Medicine (JEM). Pinsky's research
team previously published evidence for the therapeutic efficacy
of CO inhalation in mice recovering from the type of cardiovascular injuries caused
by blood clots to the lungs. Pinsky says that the balancing act
between CO and NO is an important factor in transplant rejection after heart
transplants and in recovery after other types of damage to the
cardiovascular system.
Read
the full story.
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