Posts Tagged ‘Heart disease’


In ALL ARTICLES, SCIENCE & STEM CELLS on July 9, 2014 at 3:01 pm

Real Life Fight Club… Kind Of
Author: Sarah Hoffman

“Many patients with heart problems – such as heart disease or angina – may need to undergo cardiac surgery in order to restore or improve blood flow. But a new study suggests that the procedure may offer so much more; stem cells in fat discarded during cardiac surgery could be injected back into the patient’s heart to further improve its function.” – Beyond the Dish ‘Heart Function Improved by Injecting Discarded Surgery Fat’

So it looks like Tyler Durden (from Fight Club) was right… kind of. There is a better use for that unwanted, liposuctioned belly fat than just being toxic waste. Scientists have discovered that the belly fat that many of us have (that we really don’t want or need) can be used to improve the functionality of our hearts. This procedure would require liposuction pre-cardiac-surgery, however, scientists are looking into the possibility of using similar fat that builds up around the heart that, conveniently, is removed during the surgery anyway. Wam-Bam-Thank you ma’am

This seems only too fitting, as many young people experiencing cardiac distress may be experiencing it because they have a good amount of this fat to spare. Well, fret no more, because what doesn’t kill us does make us stronger.

All jokes aside this does seem like the circle of life modernized. The fat that could be killing us can be used to save us once it has already begun to kill us. Make sense? No? Well think of it this way… While surgeons are inside of someone’s chest trying to save them from a heart attack, they are also removing excess fat from around the heart– which is part of the reason this person is in this situation to begin with. In the near future doctors may be able to, in one surgery, remove this fat, isolate the stem cells, and inject them back into the heart to have a positive effect post surgery. This could increase blood flow out of the left ventricle and result in “greater ventricular movement”. So the fat that is hurting our heart can now be removed and the stem cells in it put back with basically the opposite effect it had originally. But in the mean time, it seems very likely that we will be able to save some of that liposuctioned fat and use it during cardiac surgery to improve heart function.

Pretty futuristic if you ask me. It’s also nice to know that Tyler Durden wasn’t completely crazy… kind of.

For more on why fat is awesome check THIS out




Stem-Cell Approach Shows Promise for Duchenne Muscular Dystrophy

“Researchers have shown that transplanting stem cells derived from normal mouse blood vessels into the hearts of mice that model the pathology associated with Duchenne muscular dystrophy (DMD) prevents the decrease in heart function associated with DMD.”

Their findings appear in the journal Stem Cells Translational Medicine.

Duchenne muscular dystrophy is a genetic disorder caused by a mutation in the gene for dystrophin, a protein that anchors muscle cells in place when they contract. Without dystrophin, muscle contractions tear cell membranes, leading to cell death. The lost muscle cells must be regenerated, but in time, scar tissue replaces the muscle cells, causing the muscle weakness and heart problems typical of DMD.

The U.S. Centers for Disease Control and Prevention estimates that DMD affects one in every 3,500 males. The disease is more prevalent in males because the dystrophin mutation occurs on the X chromosome; males have one X and one Y chromosome, so a male with this mutation will have DMD, while females have two X chromosomes and must have the mutation on both of them to have the disease. Females with the mutation in one X chromosome sometimes develop muscle weakness and heart problems as well, and may pass the mutation on to their children.  Although medical advances have extended the lifespans of DMD patients from their teens or 20s into their early 30s, disease-related damage to the heart and diaphragm still limits their lifespan.

“Almost 100 percent of patients develop dilated cardiomyopathy,” in which a weakened heart with enlarged chambers prevents blood from being properly pumped throughout the body, said University of Illinois comparative biosciences professor Suzanne Berry-Miller, who led the study. “Right now, doctors are treating the symptoms of this heart problem by giving patients drugs to try to prolong heart function, but that can’t replace the lost or damaged cells,” she said.

In the new study, the researchers injected stem cells known as aorta-derived mesoangioblasts (ADM) into the hearts of dystrophin-deficient mice that serve as a model for human DMD. The ADM stem cells have a working copy of the dystrophin gene.  This stem cell therapy prevented or delayed heart problems in mice that did not already show signs of the functional or structural defects typical of Duchenne muscular dystrophy, the researchers report.

Berry-Miller and her colleagues do not yet know why the functional benefits occur, but proposed three potential mechanisms. They observed that some of the injected stem cells became new heart muscle cells that expressed the lacking dystrophin protein. The treatment also caused existing stem cells in the heart to divide and become new heart muscle cells, and the stem cells stimulated new blood vessel formation in the heart. It is not yet clear which of these effects is responsible for delaying the onset of cardiomyopathy, Berry-Miller said.

“These vessel-derived cells might be good candidates for therapy, but the more important thing is the results give us new potential therapeutic targets to study.  Activating stem cells that are already present in the body to repair tissue would avoid the potential requirement to find a match between donors and recipients and potential rejection of the stem cells by the patients.”

Despite the encouraging results that show that stem cells yield a functional benefit when administered before pathology arises in DMD mouse hearts, a decline in function was seen in mice that already showed the characteristics of dilated cardiomyopathy. One of these characteristics is the replacement of muscle tissue with connective tissue, known as fibrosis.

This difference may occur, Berry-Miller said, as a result of stem cells landing in a pocket of fibrosis rather than in muscle tissue. The stem cells may then become fibroblasts that generate more connective tissue, increasing the amount of scarring and making heart function worse. This shows that the timing of stem cell insertion plays a crucial role in an increase in heart function in mice lacking the dystrophin protein.

She remains optimistic that these results provide a stepping-stone toward new clinical targets for human DMD patients.

“This is the only study so far where a functional benefit has been observed from stem cells in the dystrophin-deficient heart, or where endogenous stem cells in the heart have been observed to produce new muscle cells that replace those lost in DMD, so I think it opens up a new area to focus on in pre-clinical studies for DMD,” Berry-Miller said.

The Illinois Regenerative Medicine Institute supported this research.



Cardiac muscle patches made from stem cells

In VICTORIES & SUCCESS STORIES on June 21, 2012 at 2:01 pm
Old news but good news~!
Cardiac muscle patches made from stem cells

A cutting-edge method developed at the University of Michigan Center for Arrhythmia Research successfully uses stem cells to create heart cells capable of mimicking the heart’s crucial squeezing action.

The cells displayed activity similar to most people’s resting heart rate. At 60 beats per minute, the rhythmic electrical impulse transmission of the engineered cells in the U-M study is 10 times faster than in most other reported stem cell studies.

An image of the electrically stimulated cardiac cells is displayed on the cover of the current issue of Circulation Research, a publication of the American Heart Association.

For those suffering from common, but deadly, heart diseases, stem cell biology represents a new medical frontier…

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