Tuesday, July 31, 2007

Genetic Variations Responsible for Heart Disease Identified


The researchers used results from a similar German study to draw comparisons and identify the common genetic variations that led to an increase in the risk for heart disease. They found that changes in the DNA on the chromosomes were responsible for increased risk of developing coronary artery disease and heart attacks. The researchers identified not one or two but six different genetic variations, each linked to a higher risk.

The findings by Dr. Samani and team confirm those of a study earlier this year in which researchers found that mutations on another chromosome increased the risk of heart disease. “Carrying one copy of the genetic change increased the chance of developing heart disease by at least 20 percent, while two copies increased the risk by more than 40 percent” Dr. Samani said.

           



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Monday, July 30, 2007

Stem cells may mend a broken heart


The study, which was done on mice, shows that stem cells play a limited, but significant role in repairing damaged hearts. However, it remains unclear whether it is heart cells that are doing the repair, or cells from elsewhere in the body.


Richard Lee of the Harvard Medical School in Boston and colleagues genetically engineered mice so their heart muscle cells could be stained with a fluorescent protein.


Around 80 per cent of the heart muscle cells in young mice picked up the stain. As the mice aged, this level remained the same, which the researchers say demonstrates that heart muscle cells are not normally replaced in life.


However, when they induced heart attacks in the mice, the number of stained cells dropped to 70 per cent, suggesting that new muscle cells are formed in response to injury.



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This article implies that hearts have a limited ability to regenerate themselves.  More must be found out.


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Saturday, July 21, 2007

Benefits of stem-cell engraftment may not last


The good news is that real, beating cardiomyocytes can be grown from undifferentiated stem cells, and large quantities of these cells with distinctly human characteristics can be obtained from human embryonic stem cells, as Mummery's talk proved. These differentiated cells will permit screens for drugs that bolster the numbers of cardiomyocytes produced and that help cardiomyocytes engraft and survive. Thus, although this progress may not signal the arrival of effective therapies, it may mark the true beginning of their development.


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The good news is also that the real work of heart repair is beginning.  The tough answers are beginning to come out.  Now, we can suspect that varying results might be caused by mis-labeling cells. Now, we know that the heart is a difficult but not impossible place to use stem cells, and that stem cells can form heart cells.



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Tuesday, July 17, 2007

Benefits of stem-cell engraftment may not last

The Article covers some of the road blocks, there seem to be many, to heart repair using stem cells.




Not only do hearts recover poorly after injury, the prevalence of and morbidity from heart damage is high. Not surprisingly, cardiac regeneration is seen as among the most important applications of stem cell research. But although cell replacement therapy, or the successful engraftment of stem cells, works for bone marrow transplantation, this kind of cell therapy will be much more difficult in solid organs, at least according to results, presented at the June 2007 meeting of the ISSCR. Indeed, not only does heart tissue fail to promote integration of transplanted cardiomyocytes, it may even provide a hostile environment.



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