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Archive for the ‘Cardiac Stem Cells’ Category

Repairing the heart with stem cells – Harvard Health …

Could this experimental treatment reverse damage caused by a heart attack?

The heart muscle relies on a steady flow of oxygen-rich blood to nourish it and keep it pumping. During a heart attack, that blood flow is interrupted by a blockage in an artery. Without blood, the area of heart fed by the affected artery begins to die and scar tissue forms in the area. Over time, this damage can lead to heart failure, especially when one heart attack comes after another.

Though the heart is a tough organ, the damaged portions become unable to pump blood as efficiently as they once could. People who have had a heart attack therefore may face a lifetime of maintenance therapymedications and other treatments aimed at preventing another heart attack and helping the heart work more efficiently.

A new treatment using stem cellswhich have the potential to grow into a variety of heart cell typescould potentially repair and regenerate damaged heart tissue. In a study published last February in The Lancet, researchers treated 17 heart attack patients with an infusion of stem cells taken from their own hearts. A year after the procedure, the amount of scar tissue had shrunk by about 50%.

These results sound dramatic, but are they an indication that we’re getting close to perfecting this therapy? “This is a field where, depending on which investigator you ask, you can get incredibly different answers,” says Dr. Richard Lee, professor of medicine at Harvard Medical School and a leading expert on stem cell therapy.

“The field is young. Some studies show only modest or no improvement in heart function, but others have shown dramatically improved function,” he says. “We’re waiting to see if other doctors can also achieve really good results in other patients.”

Studies are producing such varied outcomes in part because researchers are taking different approaches to harvesting and using stem cells. Some stem cells are taken from the bone marrow of donors, others from the patient’s own heart. It’s not clear which approach is the most promising.

Several different types of approaches are being used to repair damaged heart muscle with stem cells. The stem cells, which are often taken from bone marrow, may be inserted into the heart using a catheter. Once in place, stem cells help regenerate damaged heart tissue.

Like any other therapy, injecting stem cells into the heart can fail or cause side effects. If the stem cells are taken from an unrelated donor, the body’s immune system may reject them. And if the injected cells can’t communicate with the heart’s finely tuned electrical system, they may produce dangerous heart rhythms (arrhythmias). So far, side effects haven’t been a major issue, though, and that has encouraged investigators to push onward.

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Repairing the heart with stem cells – Harvard Health …

What Happens When Stem Cells Go Into My Heart? – Video



What Happens When Stem Cells Go Into My Heart?
Renowned cardiologist, stem cell therapy expert and Okyanos Chief Science Officer Leslie Miller, MD, FACC, explains the importance of generating new blood ve…

By: Okyanos

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What Happens When Stem Cells Go Into My Heart? – Video

In a role reversal, RNAs proofread themselves

10 hours ago Researchers at Cold Spring Harbor Laboratory have uncovered a remarkable, new proofreading mechanism. In general, enzymatic machines are responsible for weeding out and correcting errors. But a team of scientists has found that the CCA-adding enzyme (shown here in blue, green, and pink) doesn’t edit at all. Instead, the RNA (in orange) has a built-in mechanism that allows it to proofread itself. Credit: L. Joshua-Tor, Cold Spring Harbor Laboratory

Building a protein is a lot like a game of telephone: information is passed along from one messenger to another, creating the potential for errors every step of the way. There are separate, specialized enzymatic machines that proofread at each step, ensuring that the instructions encoded in our DNA are faithfully translated into proteins. Scientists at Cold Spring Harbor Laboratory (CSHL) have uncovered a new quality control mechanism along this path, but in a remarkable role reversal, the proofreading isn’t done by an enzyme. Instead, one of the messengers itself has a built-in mechanism to prevent errors along the way.

The building blocks for proteins are carried by molecules known as transfer RNAs (tRNAs). tRNAs work with other cellular machinery to ensure that the building blocks – amino acids – are arranged in the proper order. But before a building block can be loaded onto a tRNA molecule, a three-part chemical sequence that scientists call “CCA” must be added to the tRNA. The letters are added by an appropriately named machine, the CCA-adding enzyme, and they mark the tRNA as a fully functional molecule.

If a tRNA is mutated, the CCA-adding enzyme duplicates its message. The letters now read “CCACCA,” signaling that the tRNA is flawed. The cell rapidly degrades the aberrant tRNA, preventing the flawed message from propagating.

But how does the CCA-adding enzyme distinguish between normal and mutant tRNAs?

CSHL Professor and Howard Hughes Medical Institute Investigator Leemor Joshua-Tor led a team of researchers to investigate how the CCA-adding enzyme makes this distinction. “We used X-ray crystallography – a type of molecular photography – to observe the enzyme at work, and we were surprised to find that the enzyme doesn’t discriminate at all,” explains Joshua-Tor. “In fact, it is the RNA that is responsible for proofreading itself.”

The team used two tRNA-like molecules, called noncoding RNAs, to study the error-correcting mechanism. In previous work, Jeremy Wilusz, PhD, a former CSHL Watson School of Biological Sciences graduate student and an author on this current publication, found a noncoding RNA that is modified with a single CCA group, making it both stable and abundant. Another RNA used in the current study is normally present at negligible levels in cells, and Wilusz and CSHL Professor David Spector found that it is modified with a CCACCA sequence and is rapidly degraded. The difference between the two noncoding RNAs is a simple mutation, and the question the team addressed is how the presence of the mutation affects the addition of “CCA” sequences.

In work published online today in Cell, the team describes a series of molecular photographs of the CCA-adding enzyme bound to the noncoding RNAs. “The CCA-adding enzyme uses a screw-like motion to add each letter of the CCA group to the end of the RNA,” says Claus Kuhn, PhD, lead author on the paper. “Under normal circumstances, after the addition of the final letter A, the enzyme tries to ‘turn’ the molecule again, but can’t.” That increased pressure forces the RNA to pop out of its union with the enzyme – with only a single CCA group attached.

But when an RNA is mutated, the researchers found, the structure becomes more flexible. After a single CCA addition, the mutation allows the RNA to buckle under increased pressure. “That bulge allows the enzyme to add an additional round of “CCA” letters, and only then does the RNA pop out,” says Joshua-Tor.

This is a very unique proofreading mechanism, according to Joshua-Tor. “For the enzyme, there is no difference between the two RNAs – it adds CCA in this screw-like motion regardless of what the sequence is. So it is a mutation in the RNA itself that prevent future errors,” ensuring that proteins are made correctly.

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In a role reversal, RNAs proofread themselves

Cardiac Muscle Derived from Pluripotent Stem Cells – Video



Cardiac Muscle Derived from Pluripotent Stem Cells

By: CK LAB

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Cardiac Muscle Derived from Pluripotent Stem Cells – Video

Hemin improves adipocyte morphology and function by enhancing proteins of regeneration

Scientists at the University of Saskatchewan College of Medicine, Department of Physiology, Saskatoon, Canada, led by Dr. Joseph Fomusi Ndisang have determined that upregulating heme-oxygenase with hemin improves pericardial adipocyte morphology and function. It does so by enhancing the expression of proteins of repair and regeneration such as beta-catenin, Oct3/4, Pax2 as well as the stem/progenitor-cell marker cKit, while concomitantly abating inflammatory/oxidative insults and suppressing extracellular-matrix/profibrotic and remodeling proteins. Visceral adiposity like pericardial fat is correlated to insulin resistance and cardiac disease, and this is amongst the major causes of cardiac complications in obese individuals. By virtue of its anatomical and functional proximity to the coronary circulation, pericardial adiposity can lead to myocardial inflammation, left ventricular hypertrophy and coronary artery disease through paracrine mechanisms that include increased production of inflammatory cytokines, reactive oxygen species and other atherogenic factors.

These findings, which appear in the January 2015 issue of Experimental Biology and Medicine, used a laboratory animal model characterized by obesity, hypertriglyceridemia, hypercholesteromia, insulin resistance, dyslipidemia and excessive pericardial adiposity, all of which are major pathophysiological causes of heart failure and related cardiac complications in patients with obesity. Dr. Ndisang and co-worker underscored the protective role of heme-oxygenase in obesity and related cardiometabolic complications.

“The rising incidence of obesity and related cardiometabolic complications poses a great health challenge of considerable socioeconomic burden with costs that may become unsustainable to healthcare systems. Thus preventive strategies as well as novel therapeutic remedies are needed” states Dr. Ndisang. “In this study, we showed that treatment with the heme-oxygenase inducer, hemin, suppresses hypertriglyceridemia and hypercholesteromia; reduces pericardial adiposity; abates pericardial adipocyte hypertrophy; attenuates adipocyte inflammation and oxidative insults; decreases the excessive levels of profibrotic extracellular matrix; while concomitantly potentiating heme-oxygenase, stem/progenitor cells and proteins of regeneration in the pericardial adipose tissue. These results suggest that substances capable of potentiating heme-oxygenase may be explored for the design of novel remedies against cardiac complications arising from excessive adiposity.”

Future studies are needed to determine if preemptive application of hemin to the animals used in this study will retard/and or delay the manifestation of cardiometabolic complications.

Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine, said “These studies by Dr. Ndisang and colleagues provide promise for the future testing of heme-oxygenase inducers as potential therapeutics to limit cardiac injury related to excess adiposity in obese individuals. As obesity continues to grow globally, in adults and children, better therapies to control the downstream clinical sequelae are desperately needed, in parallel with preemptive education on diet and exercise.”

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Hemin improves adipocyte morphology and function by enhancing proteins of regeneration

Hemin improves adipocyte morphology, function by enhancing proteins of regeneration

Scientists at the University of Saskatchewan College of Medicine, Department of Physiology, Saskatoon, Canada, led by Dr. Joseph Fomusi Ndisang have determined that upregulating heme-oxygenase with hemin improves pericardial adipocyte morphology and function. It does so by enhancing the expression of proteins of repair and regeneration such as beta-catenin, Oct3/4, Pax2 as well as the stem/progenitor-cell marker cKit, while concomitantly abating inflammatory/oxidative insults and suppressing extracellular-matrix/profibrotic and remodeling proteins. Visceral adiposity like pericardial fat is correlated to insulin resistance and cardiac disease, and this is amongst the major causes of cardiac complications in obese individuals. By virtue of its anatomical and functional proximity to the coronary circulation, pericardial adiposity can lead to myocardial inflammation, left ventricular hypertrophy and coronary artery disease through paracrine mechanisms that include increased production of inflammatory cytokines, reactive oxygen species and other atherogenic factors.

These findings, which appear in the January 2015 issue of Experimental Biology and Medicine, used a laboratory animal model characterized by obesity, hypertriglyceridemia, hypercholesteromia, insulin resistance, dyslipidemia and excessive pericardial adiposity, all of which are major pathophysiological causes of heart failure and related cardiac complications in patients with obesity. Dr. Ndisang and co-worker underscored the protective role of heme-oxygenase in obesity and related cardiometabolic complications.

“The rising incidence of obesity and related cardiometabolic complications poses a great health challenge of considerable socioeconomic burden with costs that may become unsustainable to healthcare systems. Thus preventive strategies as well as novel therapeutic remedies are needed” states Dr. Ndisang. “In this study, we showed that treatment with the heme-oxygenase inducer, hemin, suppresses hypertriglyceridemia and hypercholesteromia; reduces pericardial adiposity; abates pericardial adipocyte hypertrophy; attenuates adipocyte inflammation and oxidative insults; decreases the excessive levels of profibrotic extracellular matrix; while concomitantly potentiating heme-oxygenase, stem/progenitor cells and proteins of regeneration in the pericardial adipose tissue. These results suggest that substances capable of potentiating heme-oxygenase may be explored for the design of novel remedies against cardiac complications arising from excessive adiposity.”

Future studies are needed to determine if preemptive application of hemin to the animals used in this study will retard/and or delay the manifestation of cardiometabolic complications.

Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine, said “These studies by Dr. Ndisang and colleagues provide promise for the future testing of heme-oxygenase inducers as potential therapeutics to limit cardiac injury related to excess adiposity in obese individuals. As obesity continues to grow globally, in adults and children, better therapies to control the downstream clinical sequelae are desperately needed, in parallel with preemptive education on diet and exercise.”

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The above story is based on materials provided by Society for Experimental Biology and Medicine. Note: Materials may be edited for content and length.

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Hemin improves adipocyte morphology, function by enhancing proteins of regeneration

Duchenne Muscular Dystrophy May Be Helped With Cardiac Stem Cells – Video



Duchenne Muscular Dystrophy May Be Helped With Cardiac Stem Cells
Study shows cardiac stem cells used to treat heart attacks may also help children with muscular dystrophy. Dr. Bruce Hensel reports for the NBC4 News at 5 on…

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Duchenne Muscular Dystrophy May Be Helped With Cardiac Stem Cells – Video

January 22, 2015

Las Vegas hospital gets tech boost in cardiac care

A tech-savvy procedure involving magnets to fix heart arrhythmias debuted at Desert Springs Hospital Tuesday and is the first of its kind in the state.

Inside the new electrophysiology operating room sit two 2,000-pound rare-earth magnets on either side of an operating table. Across the way is a large glass window that connects to what is, in essence, a command center a small room filled with high-functioning computers where doctors will use heart-mapping software and the magnets to precisely guide catheters to the sources of irregular heartbeats.

The procedure called a cardiac catheter ablation used to be performed manually, with doctors steering the catheters to the problem spots based on electrocardiogram signals. Then the catheters burn the tissue triggering the abnormal impulses, said Lloyd Gauthier, a lead radiologic technologist at Desert Springs.

With the new technology, the catheter is magnetized and doctors use a joystick to guide the catheter to the tissue producing the arrhythmia, Gauthier said.

The manual procedure took two to eight hours to complete, depending on the complexity of the heartbeat abnormalities.

Hopefully, with the new technology of these magnets, it will cut that time down because were able to get exactly where we need to go quicker and more precise, Gauthier said.

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Teenager posed as a doctor at a hospital for a month before anyone noticed

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January 22, 2015

Long-Term Use of Ventricular Assist Devices Induces Heart Muscle Regeneration, Study Finds

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Newswise DALLAS January 21, 2015 Prolonged use of a left ventricular assist device (LVAD) by patients with heart failure may induce regeneration of heart muscle by preventing oxidative damage to a cell-regulator mechanism, UTSouthwestern Medical Center investigators have found.

LVADs are mechanical pumps that are sometimes implanted in patients who are awaiting heart transplants. LVADs substitute for the damaged heart by pumping blood throughout the body.

Dr. Hesham Sadek, Assistant Professor of Internal Medicine at UTSouthwestern, is senior author of the study, which looked at pre- and post-LVAD samples of heart muscle in 10 patients with heart failure. The study authors examined the paired tissue samples for markers of DNA damage and cell proliferation.

Their study builds on earlier work with mice that demonstrated that newborn mammalian hearts are capable of a strong, regenerative response to injury by activating cell division. The earlier studies further showed that the ability to respond to injury is lost due to changes in circulation that occur after birth, which lead to a more oxygenated environment in the heart, ultimately causing oxidative damage to the cellular machinery that controls heart-muscle regeneration.

In the current study, the investigators reasoned that, by assisting the damaged heart, LVADs would alleviate oxidative damage that occurs within the heart-muscle cells.

We looked at markers of what is called the DNA damage response in cardiomyocytes (heart-muscle cells) of these patients, said Dr. Sadek. The response is composed of a cascade of proteins that is activated in response to DNA damage and in turn shuts off the ability of cardiomyocytes to divide. We found that patients who were on LVAD for more than six months had significantly decreased levels of DNA damage response.

Next, the investigators examined the paired tissue samples for markers of cell division. They found that patients who were on LVADs for six months or longer had a significant increase in cardiomyocyte proliferation. The increase in cell proliferation was nearly triple, in fact.

This result shows that patients with mechanical assist devices have the ability to make their muscle cells divide, said Dr. Sadek. And the obvious question now is, Are these hearts regenerating? Could LVADs be used as a cure for heart failure?

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Long-Term Use of Ventricular Assist Devices Induces Heart Muscle Regeneration, Study Finds

Ground-breaking transplant operation gives tragic Gateshead family fresh hope for change

The family of tragic baby Tiarna Middleton are clinging to hope for a change in medical rules after a ground-breaking transplant operation took place in London.

Medical guidelines prevented Tiarna, who died last year, from receiving a donor heart from a newborn baby.

However a six-day-old baby girls kidneys and liver cells have since been given to two separate recipients in an operation being described as a medical milestone in neo-natal care.

Tiarna died aged 18 days after becoming the youngest baby in the world ever to be fitted with a Berlin heart in a world first operation at the Freeman Hospital in Newcastle.

It was hoped the artificial device would keep her alive long enough for a donor heart to become available. But in the UK it is currently recommended that babies under two months old should not become donors due to difficulties in ascertaining whether they are officially brain-stem dead.

Without the availability of a tiny newborn heart, medics had to look to hospitals in France and Spain for help, however Tiarna died before one suitable was found.

Her mum Sharney Gray, of Rowlands Gill in Gateshead, said: I think that this just goes to show though how many lives can be saved if they do change the rules and I do think this operation is a sign that they will change things soon. I think hundreds and hundreds of lives could be saved.

It must have been an incredibly hard decision for that family to make to let their baby become a donor.

The team from the Royal College of Paediatrics and Child Health has spent the past year reviewing current medical guidelines on newborn donations. Their findings are due to be released later this year.

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Ground-breaking transplant operation gives tragic Gateshead family fresh hope for change

Scientists grow first ever contracting human muscle in a lab dish

In a new study, researchers from Duke University in Durham, NC, reveal they have grown the first ever human skeletal muscle that contracts in response to external stimuli, such as electrical impulses and pharmaceuticals. The team says their creation paves the way for testing of new drugs and the study of diseases without having to put a patients heath at risk.

This is a microscopic view of the lab-grown human muscle.

Image credit: Duke University

The beauty of this work is that it can serve as a test bed for clinical trials in a dish, says study leader Nenad Bursac, associate professor of biomedical engineering at Duke.

We are working to test drugs efficacy and safety without jeopardizing a patients health and also to reproduce the functional and biochemical signals of diseases especially rare ones and those that make taking muscle biopsies difficult.

Bursac and his team says there is a strong focus on the development of in vitro models for use in medical research, motivated by ethical factors such as reducing animal testing and the need to improve health outcomes in human patients.

In June last year, Medical News Today reported on the creation of lab-grown miniature human hearts by researchers from Abertay University in the UK, while another study revealed how researchers from the University of Texas successfully grew human lungs from the cells of deceased children.

But Bursac and his team say while much progress has been made in creating in vitro models for liver, lung and cardiac tissues, there has been little progress toward the development of human skeletal muscle.

This is of particular concern as there are a wide range of metabolic, neuromuscular and dystrophic disorders involving skeletal muscle that are under investigation and still lacking therapies, they note.

Lab-grown muscle closely mimics responses of native human muscle

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Scientists grow first ever contracting human muscle in a lab dish

LLY Collaborates With BMY And MRK, CLTX On Watchlist, ZLTQ Continues To Grow

Bristol-Myers Squibb Co. (BMY: Quote) has entered into a clinical collaboration agreement with Eli Lilly and Co. (LLY: Quote) to explore combination regimens from its immuno-oncology portfolio with other mechanisms of action that may accelerate the development of new treatment options for patients.

As per the agreement terms, a phase 1/2 trial will evaluate Bristol-Myers Squibb’s approved immunotherapy Opdivo in combination with Lilly’s investigational Galunisertib as a potential treatment option for patients with advanced (metastatic and/or unresectable) glioblastoma, hepatocellular carcinoma and non-small cell lung cancer.

Opdivo is approved by FDA for intravenous use for the treatment of patients with unresectable or metastatic melanoma while Galunisertib is currently under investigation as an oral treatment for advanced/metastatic malignancies, including phase 2 evaluation in hepatocellular carcinoma, myelodysplastic syndromes (MDS), glioblastoma, and pancreatic cancer.

In other related news, Lilly has also entered into a collaboration agreement with Merck & Co. Inc. (MRK: Quote) to evaluate the safety, tolerability and efficacy of Merck’s KEYTRUDA in combination with Lilly compounds in multiple clinical trials.

Merck’s KEYTRUDA was granted accelerated approval by FDA last September for unresectable or metastatic melanoma with disease progression following Ipilimumab and, if BRAF V600 mutation positive, a BRAF inhibitor.

BMY closed Tuesday’s trading at $63.12, up 1.51%.

Celsus Therapeutics plc (CLTX: Quote) has completed enrollment in its phase II study evaluating the safety and efficacy of MRX-6 cream 2% in a pediatric population with mild to moderate atopic dermatitis.

The topline data from the trial are expected by end-February, 2015.

CLTX closed Tuesday’s trading 10.39% higher at $5.95.

Cellular Dynamics International (ICEL: Quote) has entered into a research collaboration with privately-held Cord Blood Registry to reprogram newborn stem cells into induced pluripotent stem cells.

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LLY Collaborates With BMY And MRK, CLTX On Watchlist, ZLTQ Continues To Grow

Research looks to build organ stockpiles

TUCSON Dr. Zain Khalpey stands next to a ghostly white lung pumping rhythmically on the table next to him. Thats pretty damn good, actually, Khalpey says as he gazes at the data recorded by the lungs ventilator.

The ventilator indicates that the pig lung is inflating and deflating like a normal lung. Experiments such as this bring research a step closer to the operating room.

Khalpey, an associate professor of surgery at the University of Arizona, focuses his research on making more organs available to patients who need a transplant. Every day, 18 people on organ transplant lists die, according to the U.S. Department of Health and Human Services.

In Arizona patients have to wait two to three years for a lung transplant, according to the U.S. National Library of Medicine. This waiting period is emotionally and financially draining for patients.

Khalpey is trying to shrink the wait time. He is taking damaged organs and refurbishing them so they end up in a needy patients body. Other organs too damaged to be refurbished are stripped of their cells and used to grow new organs with the patients stem cells.

In the future, donor organs may not even be needed. Khalpey is working on hybrid organs that are 3-D printed and then seeded with the patients stem cells.

From London

to Tucson

Khalpeys passion for transplant surgery started on a rainy day in 1990s London. A 16-year-old boy lay on the operating table about to undergo a heart-and-lung transplant. Cystic fibrosis caused his lungs to become a breeding ground for infection that whittled away his ability to breathe.

A team of surgeons replaced the boys lungs as well as his heart because he was more likely to survive with donor organs. The medical team rushed the boys viable heart to a second operating room, where it gave new life to another patient.

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Research looks to build organ stockpiles

Cedars-Sinai Medical Tip Sheet for Jan., 2015

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Newswise Researchers Recreate Stem Cells From Deceased Patients to Study Present-Day Illnesses Cedars-Sinai research scientists have developed a novel method to re-create brain and intestinal stem cells from patients who died decades ago, using DNA from stored blood samples to study the potential causes of debilitating illnesses such as inflammatory bowel disease. The lab research, published in the journal STEM CELLS Translational Medicine, could yield new therapies for people who suffer from aggressive motor-neuron and gut-related conditions that proved fatal to the deceased patients who long-ago volunteered their blood samples. CONTACT: Cara Martinez, 310-423-7798; Email cara.martinez@cshs.org

Cedars-Sinai Heart Institute Physician-Researcher Awarded National Heart, Lung, and Blood Institute Grant to Develop Prevention Strategies for Deadly Heart Condition One of medicines most prominent experts in sudden cardiac arrest has received a new $2.36 million grant to study how to better predict the deadly heart condition that kills an estimated 300,000 Americans each year. Over recent years, Sumeet S. Chugh, MD, and his team of researchers in the Cedars-Sinai Heart Institute have identified several risk factors for sudden cardiac arrest, including levels of sex hormones in the blood, genetics and electrical and structural abnormalities of the heart. CONTACT: Sally Stewart, 310-248-6566; Email sally.stewart@cshs.org

Study Shows More Patients With Lou Gehrigs Disease Have Genetic Origin Than Previously Thought Genetics may play a larger role in causing Lou Gehrigs disease than previously believed, potentially accounting for more than one-third of all cases, according to one of the most comprehensive genetic studies to date of patients who suffer from the condition also known as amyotrophic lateral sclerosis, or ALS. The study, conducted by investigators at Cedars-Sinai and Washington University in St. Louis, also showed that patients with defects in two or more ALS-associated genes experience disease onset about 10 years earlier than patients with single-gene mutations. CONTACT: Sandy Van, 808-526-1708; Email sandy@prpacific.com

Computer System More Effective Than Doctors at Producing Comprehensive Patient Reports A computer system was more effective than doctors at collecting information about patient symptoms, producing reports that were more complete, organized and useful than narratives generated by physicians during office visits, according to a Cedars-Sinai study. Investigators said the research, published in the American Journal of Gastroenterology, highlights the potential of computers to enhance the quality of medical care and improve outcomes by harnessing accurate and thorough patient information. CONTACT: Duke Helfand, 310-248-6608; Email: duke.helfand@cshs.org

Double Lung Transplant Patient Pays Tribute to Donors Family in the Rose Parade Hours before receiving a lung transplant he thought would never happen, Michael Adams told his surgical team at Cedars-Sinai that hed be happy to live just one more year. Adams, 51, had suffered from cystic fibrosis since he was a baby. Hed been in and out of hospitals for as long as he could remember. By Thanksgiving of 2002, the former wheelchair company worker had end-stage disease. His lungs barely worked. Even eight liters of oxygen left him gasping for air. Then Adams received the call that saved his life: Two healthy lungs had suddenly become available. They belonged to a 15-year-old boy who had been shot and killed on the steps of his church 78 miles away in San Bernardino. Adams was transferred immediately to Cedars-Sinai, where he underwent a double lung transplant. He and his transplant surgeons are available for interviews CONTACT: Laura Coverson, 310-423-5215 Email: laura.coverson@cshs.org

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Stem Cell Treatment for Heart Disease

At Stem Cell Treatment Institute advanced stem cell procedures are performed at some of the most scientifically advanced hospitals in the world. Our Heart Disease treatment differs from standard methods by attacking the root cause inside the heart. Stem cell therapy is focused on affecting physical changes in the heart that can improve a patient’s quality of life.

Most Heart Failure patients are treated by IV; injecting the stem cells into the blood which transports them up the heart.

Another procedure, by which the stem cells are surgically implanted directly into the heart, with angiography is also available.

Treatment using Bone Marrow Stem Cells First bone marrow is collected from the patient’s iliac crest (hip bone) using thin-needle puncture under local anesthesia. Once the bone marrow collection is complete, patients may return to their hotel and go about normal activities.

The stem cells are then processed in a state-of-the-art laboratory. In the lab, both the quantity and quality of the stem cells are measured.

The stem cells are then implanted back into the patient by IV or surgical implantation.

Cost: Stem cell treatments begin around $13,500 (adults).

To contact us and learn more Click Here >>>

As we age our stem cells become less prolific and less effective. For this reason younger cells are often preferred. We do not need to go all the way back to an early stage embryo to get young cells. Young cells can be used from The Placenta, or Umbilical Cord (cord blood cells), and other young sources. These young cells are more likely than stem cells found in adult sources like bone marrow and adipose tissue (fat) to have proliferative properties. This means that stem cells found in placenta and cord blood have a greater ability to regenerate. In some counrties (US and Europe) requlations limit access to these advanced stem cell sources. Fortunately our International Health Department Permit, a COFEPRIS, is on a Presidential level, insuring access to the highest level of quality stem cells.

Begin the evaluation and scheduling process now! Click Here >>>

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Stem Cell Treatment for Heart Disease

heart disease helped with own Adult Stem Cells and Stem …

HEART DISEASE & HEART ATTACK Helped With Your OWN STEM CELLS Watch these Heart Repair VIDEOS .. and Review All your Stem Cell Options for Heart Attacks

Heart disease can be helped and controlled with your own Stem Cells. REVIEW and Investigate All your NATURAL Adult Stem cell Options.

Just 2 Patented Stem Cell Enhancer capsules, release 3 to 4 Million New STEM CELLS into your blood stream within 60 Minutes.. Your very OWN Adult Stem Cells can Help prevent and repair Heart Attacks with NO Injections.. NO Surgery .. NO Controversy .. No Hospitals…

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Heart disease patients with clogged arteries and severe chest pain who were injected with stem cells from their own bone marrow had a small improvement in blood flow and the pumping ability of their hearts, along with an easing of pain, researchers found.

Doctors in the Netherlands drew bone marrow from the hips of heart disease patients in the study. After isolating the stem cells, they injected them back into the patients hearts and monitored their progress. The results were published in the Journal of the American Medical Association.(JAMA)

Go HERE and see a VIDEO of HOW your OWN Adult Stem cells repair your Body)…

FACT : To treat a range of conditions, and several thousand heart disease patients have been treated with adult stem cells, those found in mature organs. While some cardiologists originally hoped bone marrow cells might generate new heart muscle to replace damaged tissue, that hasnt been found to occur, said Warren Sherman, a cardiologist at Columbia University in New York.

The focus has shifted, said Sherman, in a telephone interview today. Cardiologists are now hoping that bone marrow stem cells can promote the growth of new blood vessels and improve the quality of life and level of chest pain patients have. The new study, in 50 heart disease patients, showed that adult stem cells can improve blood flow and ease chest pain, Sherman said. In the study, half of the heart disease patients got their own stem cells and the others got a simulated treatment. The cardiologists used a catheter, a thin wire threaded through their arteries that also carried a small camera to guide the injections. Go Review and investigate healthy heart and heart wellness stem cell options HERE

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Adult Stem Cell Technology Center, LLCs Director Sherley's Address on Whats Holding Back Regenerative Medicine …

Boston, MA (PRWEB) December 23, 2014

Earlier this year in a June 24 international conference presentation, Dr. James L. Sherley, director of the Adult Stem Cell Technology Center, LLC (ASCTC) focused attention on an often overlooked and under appreciated unique property of adult tissue stem cells. His title Asymmetric Self-Renewal by Distributed Stem Cells: Misunderstood in the Past, Important for the Future, embodied the essence of his message to congress participants. He gave the address at the 4th World Congress on Cell Science and Stem Cell Research in Valencia, Spain.

The international congress was organized by the Omics Group as a part of its mission to foster the dissemination of leading discoveries and advances in life sciences research. Their posting this month of the slides from Dr. Sherley’s June 24 keynote address now provides worldwide open access to life sciences investigators – stem cell biologists in particular – of the concepts that he emphasized.

In a 2008 publication [Breast Disease 29, 37-46, 2008], Sherley coined the new term distributed stem cells (DSCs) as a biology-based name for all natural tissue stem cells that are not embryonic in origin. Adult stem cells are included under the DSC heading. DSCs do not make every cell in the body. Their nature is to produce only a limited tissue-specific or organ-specific distribution of the total possible mature cell types. So, for example, liver DSCs make mature liver cells, but not mature cells found in other organs like the lungs.

Since 2001 and the start of “the stem cell debate,” Sherley has insisted that only DSCs can be effective for developing new cellular therapies. In his keynote address, he explained to attendees why the counterparts of DSCs human embryonic stem cells (hESCs) and more recently developed induced pluripotent stem cells (iPSCs) could not.

Though many stem cell scientists recognize and acknowledge the genetic defects, incomplete differentiation, and tumor formation problems of hESCs and iPSCs – which their proponents suggest can be solved – few appreciate their greater problem, which cannot be solved. Unlike DSCs, hESCs and iPSCs lack the property of asymmetric self-renewal.

Sherleys main message is that asymmetric self-renewal, which is the gnomonic for DSCs the very property that defines DSCs is essential for effective cellular therapies. Asymmetric self-renewal means that DSCs can actively multiply with simultaneous reproduction of themselves and production of mature cells. This ability allows DSCs to replenish mature cells, which are continuously lost from tissues and organs, but not lose their genetic blueprint required for tissue and organ renewal and repair.

The asymmetric self-renewal of DSCs is a crucial consideration for all aspects of their study and use. Sherley argues that overlooking it is holding back progress in regenerative medicine. Asymmetric self-renewal is the factor that limits the production of DSCs; but it is so unique to them that it can also be used to identify DSCs, which are notorious for being elusive. The ASCTCs patented technologies for producing and counting DSCs for research and clinical development are grounded in the companys special research and bioengineering expertise for DSC asymmetric self-renewal.

Asymmetric self-renewal may even play a role in the efficient production of iPSCs. At the end of his address, Sherley announced the approval of a new ASCTC patent. The patent covers the invention of a method to make iPSCs from DSCs that were produced by regulating their asymmetric self-renewal (U.S. Patent and Trademark Office No. 8,759,098).

The ASCTC anticipates that despite the new technologys origin in DSC research, it will advance human disease research based on iPSCs. Although iPSCs are not suitable for cell therapy applications, they are uniquely able to provide disease research models for hard to obtain cell types found in patients (e.g., brain cells from autism patients, cardiac cells from heart disease patients).

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Adult Stem Cell Technology Center, LLCs Director Sherley's Address on Whats Holding Back Regenerative Medicine …

Stem Cell Treatment Heart Disease – ASCI – Asian Stem Cell …

Cardiovascular diseases remain the biggest cause of deaths worldwide, though over the last two decades, cardiovascular mortality rates have declined in many high-income countries but have increased at an astonishingly fast rate in low- and middle-income countries. The percentage of premature deaths from cardiovascular disease range from 4% in high-income countries to 42% in low-income countries. More than 17 million people died from cardiovascular diseases in 2008. Each year, heart disease kills more Americans than cancer. In recent years, cardiovascular risk in women has been increasing and has killed more women than breast cancer.

Measures to prevent cardiovascular disease may include:

A fairly recent emphasis is on the link between low-grade inflammation that hallmarks atherosclerosis and its possible interventions. C-reactive protein (CRP) is a common inflammatory marker that has been found to be present in increased levels in patients at risk for cardiovascular disease. Also osteoprotegerin which is involved with regulation of a key inflammatory transcription factor called NF-B has been found to be a risk factor of cardiovascular disease and mortality. Studies have shown that Stem Cells have shown the ability to reduce inflammation.

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Stem Cell Treatment Heart Disease – ASCI – Asian Stem Cell …

Stem Cell Research: Heart Stem Cells May Help Heal Hearts …

Two men in landmark heart stem cell study tell their stories.

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Jim Dearing of Louisville, Ky., one of the first men in the world to receive heart stem cells, might have helped start a medical revolution that could lead to a cure for heart failure.

Three years after getting the experimental stem cell procedure, following two heart attacks and heart failure, Dearings heart is working normally.

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The difference is clear and dramatic — and it’s lasting, according to findings now being made public for the first time.

Dearing first showed “completely normal heart function” on an echocardiogram done in 2011, says Roberto Bolli, MD, who is leading the stem cell trial at the University of Louisville. Those results have not been published before.

That was still true in July 2012, when Dearing again showed normal heart function on another echocardiogram.

Based on those tests, Bolli says, “Anyone who looks at his heart now would not imagine that this patient was in heart failure, that he had a heart attack, that he was in the hospital, that he had surgery, and everything else.”

It’s not just Dearing who has benefited. His friend, Mike Jones, who had even more severe heart damage, also got the stem cell procedure in 2009. Since then, scarred regions of his heart have shrunk. His heart now appears leaner and stronger than it was before.

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Stem Cell Research: Heart Stem Cells May Help Heal Hearts …

New UQ platform aids stem cell research

Researchers at The University of Queensland are part of a global team that has identified a new type of artificial stem cell.

UQ Associate Professor Christine Wells (right) said Project Grandiose had revealed it could track new ways to reprogram a normal adult cell, such as skin cells, into cells similar to those found in an early embryo.

The development is expected to help researchers explore ways to arrive at new cell types in the laboratory, with important implications for regenerative medicine and stem cell science.

Associate Professor Wells, who leads the Stemformatics stem cell research support unit at UQs Australian Institute for Bioengineering and Nanotechnology, said the project involved a consortium of 50 researchers from Canada, Australia, Korea, the USA and the Netherlands

We all come from just one cell the fertilised egg and this cell contains within its DNA a series of instruction manuals to make all of the many different types of cells that make up our body, AIBN Associate Professor Wells said.

These very early stage cells can now be made in the lab by reversing this process of development.

Our research reveals the new instructions imposed on a cell when this developmental process is reversed.

Project Grandiose is a large-scale research effort to understand what happens inside a cell as it reverts to an artificial stem cell.

The role of the Stemformatics.org group was to help the researchers have access to the vast information and data they generated from the project, Associate Professor Wells said.

Our online data platform is designed to let non-specialists view the genes involved and the many ways they are regulated during cell formation.

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New UQ platform aids stem cell research

Loss of a chemical tag on RNA keeps embryonic stem cells in suspended animation

A team of scientists that included researchers from UCLA has discovered a novel mechanism of RNA regulation in embryonic stem cells. The findings are strong evidence that a specific chemical modification, or “tag,” on RNA plays a key role in determining the ability of embryonic stem cells to adopt different cellular identities.

The team also included scientists from Harvard Medical School, Massachusetts General Hospital and Stanford University.

Published in the journal Cell Stem Cell, the research reveals that depleting or knocking out a key component of the machinery that places this chemical tag — known both as m6A and N6-methyladenosine — on RNA significantly blocks embryonic stem cells from differentiating into more specialized types of cells.

A key property of embryonic stem cells is their ability to differentiate into many specialized types of cells. However, instead of marching toward a specific fate when prompted by signals to differentiate, embryonic stem cells that have reduced ability to place m6A become stuck in a sort of suspended animation, even though they appear healthy.

Yi Xing, a UCLA associate professor of microbiology, immunology and molecular genetics, led the informatics analyses and was a co-corresponding author of the paper. Other corresponding authors were Dr. Cosmas Giallourakis, an assistant professor of medicine at Harvard Medical School and Massachusetts General Hospital, and Dr. Howard Chang, a professor of Stanford University’s School of Medicine and a Howard Hughes Medical Institute investigator.

The study of naturally occurring chemical modifications on RNAs is part of an emerging field known as epitranscriptomics. The m6A tag is the most commonly occurring modification known to scientists; it is found on RNAs of thousands of protein-coding genes and hundreds of non-coding genes in a typical cell type. The tags may help regulate RNA metabolism by marking them for destruction.

Little was known about the dynamics, conservation and function of m6A in human or mouse embryonic stem cells when the authors began the project. The authors analyzed which RNAs were tagged with m6A and the location of the m6A modifications along RNAs in mouse and human embryonic stem cells.

“Our analysis revealed a high level of conservation of m6A patterns between mice and humans, suggesting that m6A has conserved functions in human and mouse embryonic stem cells,” Xing said. “Moreover, RNAs with m6A tags were degraded more rapidly and lived a shorter life in the cell than those without.”

The investigators then found a strikingly conserved requirement for the presence of normal levels of m6A for differentiating embryonic stem cells into multiple cell types. Depletion of METTL3, a gene encoding the enzyme that places the m6A tag on RNAs, severely blocked human embryonic stem cells from differentiating into the gut or neural precursors. Deletion of the mouse METTL3 gene also led to a severe block in the ability of embryonic stem cells to differentiate into neural and cardiac lineages.

The study suggests that m6A modifications on RNA make the transition between cell states possible by instructing the cells to physically degrade those RNAs marked by m6A in embryonic stem cells, to allow the cells to become another cell type. However, if the cells can no longer tag RNA for destruction, the cells lose the ability to change. This discovery sheds new light on gene regulation in stem cells.

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Loss of a chemical tag on RNA keeps embryonic stem cells in suspended animation

Advances reshape stem cell research

A decade ago, a dream team of researchers from Pittsburgh to South Korea claimed a medical invention that promised to reshape a culture war.

The scientists said they custom-designed stem cells from cloned human embryos. The scientific breakthrough was celebrated around the globe.

Then the bottom fell out.

A scandal erupted over fabricated data, and University of Pittsburgh biologist Gerald Schatten was forced to pull back the findings. Critics cast the 2004 discovery as a farce, a high-profile fraud that forced the journal Science into a rare retraction in January 2006.

Eight years later, the push to use stem cells as a medical treatment continues, but scholars balk at the suggestion that anyone is trying to make genetically identical individuals.

We’re not here to clone human beings, for gosh sakes, said John Gearhart, a stem cell researcher and University of Pennsylvania professor in regenerative medicine. Instead, he said, scholars are working to manipulate stem cells to produce heart cells for cardiac patients, brain cells for neurological patients and other custom transplants that could match a person’s genetic makeup.

Schatten’s work continues at the Magee-Womens Research Institute at Pitt, where university officials cleared him of scientific misconduct, and he remains a vice chairman for research development. He focuses on educating and training physician-scientists and other scientists, a school spokeswoman wrote in a statement. She said Schatten was traveling and was unable to speak with the Tribune-Review.

Researchers have turned the onetime myth of developing stem cells into reality.

At the Oregon Health and Science University, researchers succeeded by blending unfertilized human eggs with body tissue to mold stem cells. Scholars say the cells could let doctors grow customized organs for transplants and other therapies.

The approach engineered by biologist Shoukhrat Mitalipov’s research team last year in Portland is among two that scientists are using to forge laboratory-made stem cells the so-called master cells that can transform into other body parts without relying on donated human embryos. Federal law tightly controls the use of taxpayer money for embryonic research.

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Stem Cell Treatment Congestive Heart Failure | CHF Stem …

Congestive Heart Failure Treatment Using Stem Cells

Congestive Heart Failureor CHF is a state wherein the heart does not have the capability to properly function as a pump. As a result of the cardiac-malfunction the oxygen pumped into the body is insufficient. Congestive heart failure is generally caused bysimultaneousillnesses. Illnesses that weaken the heart muscle,or diseases that trigger the heart muscles to become stiff, or illnesses that create an increase in oxygen demands for the body which consequently increases the supply for fresh oxygen by the body when the heart is incapable of producing oxygen-rich blood at the level needed.

Congestive heart failure and ishchemic heart disease can have an impact on numerous organs in the body. For instance, the injured areas of the heart directly affected by the sickness does not have the capability to produce enough blood for the kidneys, which then affect their capability to excrete water and salt (sodium). The distressed kidney function may cause the body to retain more fluids than needed by the body. The lungs also may develop pulmonary edema (PE).

PE occurs when the fluid in the lungs diminishes a persons ability to exercise normally. Fluid might likewise accumulate inside the liver, which directly affects it function by impairing the livers capability to create important proteins and also in helping clear the body of harmful elements and/ortoxins. The intestines might also turn out to be much less effective in being able to absorb the vitamins, nutrients and medicines a human needs. The fluids in the body can also accumulate quickly which could result to edema (severe swelling) of the ankles and feet.

An Ejection fraction of 20% would be considered a dangerous level and therefore indicates a highly advanced stage of heart failure. Healthy people usually have ejection fractions in between 52% and 68%.

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Stem Cell Treatment Congestive Heart Failure | CHF Stem …

Delivering stem cells into heart muscle may enhance cardiac repair and reverse injury

PUBLIC RELEASE DATE:

19-Nov-2014

Contact: Lauren Woods lauren.woods@mountsinai.org 646-634-0869 The Mount Sinai Hospital / Mount Sinai School of Medicine @mountsinainyc

Delivering stem cell factor directly into damaged heart muscle after a heart attack may help repair and regenerate injured tissue, according to a study led by researchers from Icahn School of Medicine at Mount Sinai presented November 18 at the American Heart Association Scientific Sessions 2014 in Chicago, IL.

“Our discoveries offer insight into the power of stem cells to regenerate damaged muscle after a heart attack,” says lead study author Kenneth Fish, PhD, Director of the Cardiology Laboratory for Translational Research, Cardiovascular Research Center, Mount Sinai Heart, Icahn School of Medicine at Mount Sinai.

In the study, Mount Sinai researchers administered stem cell factor (SCF) by gene transfer shortly after inducing heart attacks in pre-clinical models directly into damaged heart tissue to test its regenerative repair response. A novel SCF gene transfer delivery system induced the recruitment and expansion of adult c-Kit positive (cKit+) cardiac stem cells to injury sites that reversed heart attack damage. In addition, the gene therapy improved cardiac function, decreased heart muscle cell death, increased regeneration of heart tissue blood vessels, and reduced the formation of heart tissue scarring.

“It is clear that the expression of the stem cell factor gene results in the generation of specific signals to neighboring cells in the damaged heart resulting in improved outcomes at the molecular, cellular, and organ level,” says Roger J. Hajjar, MD, senior study author and Director of the Cardiovascular Research Center at Mount Sinai. “Thus, while still in the early stages of investigation, there is evidence that recruiting this small group of stem cells to the heart could be the basis of novel therapies for halting the clinical deterioration in patients with advanced heart failure.”

cKit+ cells are a critical cardiac cytokine, or protein receptor, that bond to stem cell factors. They naturally increase after myocardial infarction and through cell proliferation are involved in cardiac repair.

According to researchers there has been a need for the development of interventional strategies for cardiomyopathy and preventing its progression to heart failure. Heart disease is the number one cause of death in the United States, with cardiomyopathy or an enlarged heart from heart attack or poor blood supply due to clogged arteries being the most common causes of the condition. In addition, cardiomyopathy causes a loss of cardiomyocyte cells that control heartbeat, and changes in heart shape, which lead to the heart’s decreased pumping efficiency.

“Our study shows our SCF gene transfer strategy can mobilize a promising adult stem cell type to the damaged region of the heart to improve cardiac pumping function and reduce myocardial infarction sizes resulting in improved cardiac performance and potentially increase long-term survival and improve quality of life in patients at risk of progressing to heart failure,” says Dr. Fish.

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Delivering stem cells into heart muscle may enhance cardiac repair and reverse injury

Delivery of Stem Cells into Heart Muscle After Heart Attack May Enhance Cardiac Repair and Reverse Injury

New York, NY (PRWEB) November 19, 2014

Delivering stem cell factor directly into damaged heart muscle after a heart attack may help repair and regenerate injured tissue, according to a study led by researchers from Icahn School of Medicine at Mount Sinai presented November 18 at the American Heart Association Scientific Sessions 2014 in Chicago, IL.

Our discoveries offer insight into the power of stem cells to regenerate damaged muscle after a heart attack, says lead study author Kenneth Fish, PhD, Director of the Cardiology Laboratory for Translational Research, Cardiovascular Research Center, Mount Sinai Heart, Icahn School of Medicine at Mount Sinai.

In the study, Mount Sinai researchers administered stem cell factor (SCF) by gene transfer shortly after inducing heart attacks in pre-clinical models directly into damaged heart tissue to test its regenerative repair response. A novel SCF gene transfer delivery system induced the recruitment and expansion of adult c-Kit positive (cKit+) cardiac stem cells to injury sites that reversed heart attack damage. In addition, the gene therapy improved cardiac function, decreased heart muscle cell death, increased regeneration of heart tissue blood vessels, and reduced the formation of heart tissue scarring.

It is clear that the expression of the stem cell factor gene results in the generation of specific signals to neighboring cells in the damaged heart resulting in improved outcomes at the molecular, cellular, and organ level, says Roger J. Hajjar, MD, senior study author and Director of the Cardiovascular Research Center at Mount Sinai. Thus, while still in the early stages of investigation, there is evidence that recruiting this small group of stem cells to the heart could be the basis of novel therapies for halting the clinical deterioration in patients with advanced heart failure.

cKit+ cells are a critical cardiac cytokine, or protein receptor, that bond to stem cell factors. They naturally increase after myocardial infarction and through cell proliferation are involved in cardiac repair.

According to researchers there has been a need for the development of interventional strategies for cardiomyopathy and preventing its progression to heart failure. Heart disease is the number one cause of death in the United States, with cardiomyopathy or an enlarged heart from heart attack or poor blood supply due to clogged arteries being the most common causes of the condition. In addition, cardiomyopathy causes a loss of cardiomyocyte cells that control heartbeat, and changes in heart shape, which lead to the hearts decreased pumping efficiency.

Our study shows our SCF gene transfer strategy can mobilize a promising adult stem cell type to the damaged region of the heart to improve cardiac pumping function and reduce myocardial infarction sizes resulting in improved cardiac performance and potentially increase long-term survival and improve quality of life in patients at risk of progressing to heart failure, says Dr. Fish.

This study adds to the emerging evidence that a small population of adult stem cells can be recruited to the damaged areas of the heart and improve clinical outcomes, says Dr. Hajjar.

Other study co-authors included Kiyotake Ishikawa, MD, Jaume Aguero, MD, Lisa Tilemann, MD, Dongtak Jeong, PhD, Lifan Liang, PhD, Lauren Fish, Elisa Yaniz-Galende, PhD, and Krisztina Zsebo, PhD.

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Delivery of Stem Cells into Heart Muscle After Heart Attack May Enhance Cardiac Repair and Reverse Injury

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