If Dr. Doolittle is famous for talking to animals, then here’s a story that might make him hold his tongue: According to new research published online in The FASEB Journal (http://www.fasebj.org), scientists have successfully fused human stem cells …
Fear of free radicals may be exaggerated, according to scientists from the Swedish medical university Karolinska Institutet. A new study, published in the Journal of Physiology, shows that free radicals act as signal substances that cause the heart …
DURHAM, N.C. — Heart tissue and stem cells spring into action to begin repairing muscle damaged in a heart attack, and researchers at Duke University School of Medicine found that a protein naturally produced in the body may potentially play a role…
Menlo Park, Calif. — Calcium regulates many critical processes within the body, including muscle contraction, the heartbeat, and the release of hormones. But too much calcium can be a bad thing. In excess, it can lead to a host of diseases, suc…
PHILADELPHIA – Heart muscle cells do not normally replicate in adult tissue, but multiply with abandoned during development. This is why the loss of heart muscle after a heart attack is so dire — you can’t grow enough new heart muscle to make u…
The disruption of a structural component in heart muscle cells, which is associated with heart failure, appears to occur even before heart function starts to decline, according to a new study by researchers at the University of Iowa Roy J. and L…
People with a certain form of a gene that influences blood flow may have a lower risk of having a heart attack and dying from heart disease, according to a new study in today’s rapid access issue of Circulation: Journal of the American Heart Association. The gene controls variations in beta-2 adrenergic receptors, which are on the surface of heart muscle cells and blood vessel cell walls. When activated by adrenaline and noradrenaline, these receptors set in motion a series of events that dilate the blood vessels and increase heart rate.
Using new DNA microarray technology, researchers have found significant changes in the expression pattern of hundreds of genes in heart muscle cells after mechanical pumps are used to take over from failing hearts. This finding represents a first step, they say, in a line of research that could help predict how heart failure patients will respond when supported by a left ventricular assist device (LVAD). These devices are employed when the heart’s left ventricle — the chamber of the heart that pumps blood throughout the body — is too weak to pump enough blood to nourish the body’s tissues. They have been used as successful short-term “bridges to heart transplant” and are increasingly being considered as long-term heart failure destination therapy, also known as “bridge to recovery.”
Vitamin C helped convert mouse embryonic stem cells growing in the laboratory to heart muscle cells, researchers report. This basic-research discovery could lead to future research on ways to treat people suffering from damaged heart muscle. “Although the findings of this study are very preliminary with respect to their impact on human lives, this line of research has enormous implications for the future care of thousands of patients who develop heart failure each year,” says Robert O. Bonow, M.D., president of the American Heart Association.
An international team of researchers has demonstrated a genetic basis for a fatal form of inherited cardiac arrhythmia that usually strikes young, seemingly healthy people. Basing their research on a French family with a form (Type 4) of inherited Long QT Syndrome (LQTS) and experiments in mice, the researchers found the mutation in a specific gene encoding ankyrin-B, a protein within heart muscle cells. Their discovery identifies what appears to be a novel mechanism for cardiac arrhythmia.
Researchers have determined the molecular machinery that triggers normal cardiac muscle growth and survival, and have linked defects in this complex to an inherited form of human cardiomyopathy, a type of heart failure where an enlarged heart loses its ability to pump blood. Published in the December 27, 2002 issue of the journal Cell, the study also identifies a subset of German cardiomyopathy patients with a specific gene mutation that disrupts the heart muscle’s normal stretch activity. This mutation has apparently been passed down through several generations of Northern Europeans.
