Archive for the ‘Cardiac Stem Cells’ Category

Cardiac Stem Cells: Making a Difference in Duchenne
Dr Eduardo Marban, Director of the Cedars-Sinai Heart Institute, discusses a possible Cardiac Stem Cell breakthrough for Duchenne muscular dystrophy. Coaliti...

By: CoalitionDuchenne

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Cardiac Stem Cells: Making a Difference in Duchenne - Video

Coronary heart disease is the countrys leading cause of death A new treatment was designed to treat damaged heart muscle The capsule contains stem cells derived from the patients bone marrow

By Roger Dobson for the Daily Mail

Published: 17:33 EST, 9 March 2015 | Updated: 05:45 EST, 10 March 2015

A new treatment using a tiny grow-bag has been designed to treat damaged heart muscle

A tiny grow-bag could be a new way to mend hearts damaged by disease or heart attack.

The capsule, which is pea-sized, contains stem cells that trigger the growth of new cells.

An estimated 2.3 million people in Britain have coronary heart disease the countrys leading cause of death.

It occurs when the arteries supplying the heart become blocked by fatty substances, reducing the flow of blood.

If a bit of this fatty substance breaks off, it can trigger a blood clot, which in turn cuts off the blood supply to heart muscle, causing it to die off. This is what triggers a heart attack.

Heart disease and heart attacks can also lead to heart failure, where the heart becomes too weak to pump blood around the body properly.

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The tiny grow-bag that could mend a heart damaged by disease

Researchers have created a "heart on a chip" using actual cardiac muscles to help test the effects of heart medication.

Anurag Mathur/Healy Lab

A new device could help make drug testing safer, faster, cheaper -- and eliminate the need for animal testing. It's just an inch long, but inside its silicone body is housed a small piece of cardiac muscle that responds to cardiovascular medications in exactly the same way heart muscle does inside a living human body.

"Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy," explained Kevin Healy, UC Berkeley professor of engineering, who led the research team that designed the device.

The problems with using animals to test human heart medication aren't merely ethical -- such concerns about lab animals rarely enter scientific discussions. Rather, there are some serious physiological problems -- namely, that drugs designed for humans will not have the same effect on a species that is biologically different from a human.

"These differences often result in inefficient and costly experiments that do not provide accurate answers about the toxicity of a drug in humans," Healy explained.

"It takes about $5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market."

The chips were created using heart muscle grown in a lab from adult human induced pluripotent stem cells -- stem cells that can be coaxed to grow into many other types of cell. The team then carefully designed the structure to be similar to the geometry and spacing of connective tissue fibre in a living human heart.

Microfluidic channels carved into the silicone on either side of the cell matrix act the same way as blood vessels, mimicking the exchange of nutrients and drugs with human tissue as it would happen in the body.

The cells start beating on their own within 24 hours of being loaded into the chamber at a healthy resting rate of 55 to 80 beats per minute. In order to test the system, the team then administered four well-known cardiovascular drugs -- isoproterenol, E-4031, verapamil and metoprolol. By monitoring the beat rate, the team was able to observe -- and accurately predict -- the chip's response to the drugs. Isoproterenol, for example -- a drug used to treat slow heart rate -- caused the muscle's beat rate to increase from 55 beats per minute to 124 beats per minute half an hour after being administered.

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Human heart on a chip could replace animal drug testing

IMAGE:Professor Paul Robbins and Associate Professor Laura Niedernhofer led research efforts for the new study at Scripps Florida. view more

Credit: Photo courtesy of The Scripps Research Institute.

JUPITER, FL - March 9, 2015 - A research team from The Scripps Research Institute (TSRI), Mayo Clinic and other institutions has identified a new class of drugs that in animal models dramatically slows the aging process--alleviating symptoms of frailty, improving cardiac function and extending a healthy lifespan.

The new research was published March 9 online ahead of print by the journal Aging Cell.

The scientists coined the term "senolytics" for the new class of drugs.

"We view this study as a big, first step toward developing treatments that can be given safely to patients to extend healthspan or to treat age-related diseases and disorders," said TSRI Professor Paul Robbins, PhD, who with Associate Professor Laura Niedernhofer, MD, PhD, led the research efforts for the paper at Scripps Florida. "When senolytic agents, like the combination we identified, are used clinically, the results could be transformative."

"The prototypes of these senolytic agents have more than proven their ability to alleviate multiple characteristics associated with aging," said Mayo Clinic Professor James Kirkland, MD, PhD, senior author of the new study. "It may eventually become feasible to delay, prevent, alleviate or even reverse multiple chronic diseases and disabilities as a group, instead of just one at a time."

Finding the Target

Senescent cells--cells that have stopped dividing--accumulate with age and accelerate the aging process. Since the "healthspan" (time free of disease) in mice is enhanced by killing off these cells, the scientists reasoned that finding treatments that accomplish this in humans could have tremendous potential.

The scientists were faced with the question, though, of how to identify and target senescent cells without damaging other cells.

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Scripps Research, Mayo Clinic scientists find class of drugs that boosts healthy lifespan

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Newswise JUPITER, FL March 9, 2015 A research team from The Scripps Research Institute (TSRI), Mayo Clinic and other institutions has identified a new class of drugs that in animal models dramatically slows the aging processalleviating symptoms of frailty, improving cardiac function and extending a healthy lifespan.

The new research was published March 9 online ahead of print by the journal Aging Cell.

The scientists coined the term senolytics for the new class of drugs.

We view this study as a big, first step toward developing treatments that can be given safely to patients to extend healthspan or to treat age-related diseases and disorders, said TSRI Professor Paul Robbins, PhD, who with Associate Professor Laura Niedernhofer, MD, PhD, led the research efforts for the paper at Scripps Florida. When senolytic agents, like the combination we identified, are used clinically, the results could be transformative.

The prototypes of these senolytic agents have more than proven their ability to alleviate multiple characteristics associated with aging, said Mayo Clinic Professor James Kirkland, MD, PhD, senior author of the new study. It may eventually become feasible to delay, prevent, alleviate or even reverse multiple chronic diseases and disabilities as a group, instead of just one at a time.

Finding the Target

Senescent cellscells that have stopped dividingaccumulate with age and accelerate the aging process. Since the healthspan (time free of disease) in mice is enhanced by killing off these cells, the scientists reasoned that finding treatments that accomplish this in humans could have tremendous potential.

The scientists were faced with the question, though, of how to identify and target senescent cells without damaging other cells.

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Scripps Research, Mayo Clinic Scientists Find New Class of Drugs that Dramatically Increases Healthy Lifespan

When University of California, Berkeley, bioengineers say they are holding their hearts in the palms of their hands, they are not talking about emotional vulnerability.

Instead, the research team led by bioengineering professor Kevin Healy is presenting a network of pulsating cardiac muscle cells housed in an inch-long silicone device that effectively models human heart tissue, and they have demonstrated the viability of this system as a drug-screening tool by testing it with cardiovascular medications.

This organ-on-a-chip, reported in a study to be published Monday, March 9, in the journal Scientific Reports, represents a major step forward in the development of accurate, faster methods of testing for drug toxicity. The project is funded through the Tissue Chip for Drug Screening Initiative, an interagency collaboration launched by the National Institutes of Health to develop 3-D human tissue chips that model the structure and function of human organs.

"Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy," said Healy.

The study authors noted a high failure rate associated with the use of nonhuman animal models to predict human reactions to new drugs. Much of this is due to fundamental differences in biology between species, the researchers explained. For instance, the ion channels through which heart cells conduct electrical currents can vary in both number and type between humans and other animals.

"Many cardiovascular drugs target those channels, so these differences often result in inefficient and costly experiments that do not provide accurate answers about the toxicity of a drug in humans," said Healy. "It takes about $5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market."

The heart cells were derived from human-induced pluripotent stem cells, the adult stem cells that can be coaxed to become many different types of tissue.

The researchers designed their cardiac microphysiological system, or heart-on-a-chip, so that its 3-D structure would be comparable to the geometry and spacing of connective tissue fiber in a human heart. They added the differentiated human heart cells into the loading area, a process that Healy likened to passengers boarding a subway train at rush hour. The system's confined geometry helps align the cells in multiple layers and in a single direction.

Microfluidic channels on either side of the cell area serve as models for blood vessels, mimicking the exchange by diffusion of nutrients and drugs with human tissue. In the future, this setup could also allow researchers to monitor the removal of metabolic waste products from the cells.

"This system is not a simple cell culture where tissue is being bathed in a static bath of liquid," said study lead author Anurag Mathur, a postdoctoral scholar in Healy's lab and a California Institute for Regenerative Medicine fellow. "We designed this system so that it is dynamic; it replicates how tissue in our bodies actually gets exposed to nutrients and drugs."

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Bioengineers put human hearts on a chip to aid drug screening

Though it may not look at all like the muscle in your chest, this heart-on-a-chip can beat like the real thing. A blend of microfluidics and biological cells, the device will be used as a more efficient means of testing for drug toxicity.

Developed by a team of bioengineers form University of California, Berkeley, the device is designed to mimic the geometry of fibers in a human heart. Pluripotent stem cellsthe cells that can be nudged to become one of the many different types of tissue present in our bodiesare introduced to a channel which is specially designed to encourage cells to grow in multiple layers in one direction, like real cardiac tissue. Here, they grow in to heart cells.

This section is then perfused with blood from microfluidic channels which act as blood vessels. Within 24 hours of lining the structure with heart cells, the structure began to beat at rate of between 55 to 80 beats per minutejust like a real human heart. Anurag Mathur, one of the researchers, explains to PhysOrg:

"This system is not a simple cell culture where tissue is being bathed in a static bath of liquid. We designed this system so that it is dynamic; it replicates how tissue in our bodies actually gets exposed to nutrients and drugs."

The system has already been used to test established cardiovascular drugs such as isoproterenol, E-4031, verapamil and metoprolol. The team observed effects upon the heart-on-a-chip consistent with those brought about in real humanso, drugs intended to speed up heart rate did exactly that to the cells in the device. The findings are published in Scientific Reports.

It's hoped that the device will be used to screen drugs, model human genetic diseasesand perhaps even link up with other organs-on-a-chip to predict whole-body reactions too. [Scientific Reports via PhysOrg]

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This Heart-on-a-Chip Beats Like the Real Thing

Durham, NC (PRWEB) February 27, 2015

Several studies showing the promise of stem cells for treating patients with heart failure have made headline news recently. However, all these studies dealt with adult patients only. New research appearing in this months STEM CELLS Translational Medicine shows that stem cells may have the same potential in treating children with congenital heart diseases that can lead to heart failure.

The study, undertaken by researchers at the Mayo Clinic in Rochester, Minn., looked at the feasibility and long-term safety of injecting autologous umbilical cord blood cells directly into the heart muscle at the pediatric stage of heart development. The study was conducted on pigs, due to their hearts similarity to human hearts.

The team injected the stem cells directly into the right ventricle of groups of three- and four-week old healthy piglets, and then compared the results to a control group that did not receive any cells. Over the next three months, the animals were monitored to assess cardiac performance and rhythm to determine how safe the procedure would be for humans.

During this follow-up period, we found no significant acute or chronic cardiac injury pattern caused by the injections directly into the heart, said lead author Timothy J. Nelson, M.D., Ph.D., of the Mayo Clinics Department of Medicine, and all the animals hearts appeared to be normal and healthy.

This led us to conclude that autologous stem cells from cord blood can be safely collected and surgically delivered to children. The study also establishes the foundation for cell-based therapy for children and aims to accelerate the science toward clinical trials for helping children with congenital heart disease that could benefit from a regenerative medicine strategy, he added.

The lead author, Susan Cantero Peral, M.D., Ph.D. commented, This work highlights the importance and utility of umbilical cord blood as it can be applied to new applications. Rather than discarding this sample at birth, individuals with congenital heart disease may one day be able to have these cells collected and processed in a specialized way to make them available for cardiac regeneration.

This work was funded by the Todd and Karen Wanek Family Program for Hypoplastic Left Heart Syndrome founded at the Mayo Clinic.

These data help establish the foundation of a cell-based therapy for juvenile hearts by showing that injections of autologous cells from cord blood are safe and feasible, said Anthony Atala, M.D., editor of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine.

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Study Shows Stem Cells Have Potential to Help Kids Hearts, Too

Albany, NewYork (PRWEB) February 27, 2015

ResearchMoz has announced the addition of a recent study that presents the analysis of the cell culture protein surface coating market across the globe. The research report discusses the current scenario and development prospects of the global cell culture protein surface coating industry for the period of 2015 to 2019.

Read Complete Report With TOC @ http://www.researchmoz.us/global-cell-culture-protein-surface-coating-market-2015-2019-report.html

The research report, titled Global Cell Culture Protein Surface Coating Market, offers an analytical study, providing an in-depth assessment of the industry based on market trends, growth drivers as well as challenges. This is done taking various segments of the market into consideration. The report also forecasts that the worldwide cell culture protein surface coating industry will expand at a CAGR of 12.91% during the forecast period of 2014 to 2019.

Cell culture protein surface coating is defined as the coating process wherein cell culture surfaces are covered with extra-cellular matrix elements or with protein to improve in-vitro linkage and propagation in the cells.

The various kinds of proteins that are available in our surroundings are synthetic proteins, human-derived proteins, plant-derived proteins, and animal-derived proteins. Fibronectin, collagen, laminin, osteopontin, and vitronectin are some of the proteins that are utilized for cell culture protein surface coating. Cell culture protein surface coating assists in the development of several kinds of cells such as epithelial, endothelial, fibroblasts, muscle cells and myoblasts, leukocytes, CHO cell lines, and neurons.

The wide range of applications for cell culture protein surface coatings consist of enhanced adhesion of cells, better propagation and development of cells, cell matrix studies, morphogenesis studies, receptor-ligand binding studies, signal transduction studies, genetic engineering, differentiation of individual cell types, drug screening, and metabolic pathway studies.

Stem cells have high potential for the treatment of severe diseases such as cardiac ailments, neuro degenerative diseases, and even diabetes. This fact has resulted in the increase in demand for highly developed cell culture products for stem cell manufacturing and studies. Cell culture protein surface coating offers enhanced adhesion, propagation, and rapid development of cells during the period of isolation and cultivation.

The main factor that is adding to the growth of the global cell culture protein surface coating industry is increased focus of top market players towards stem cell research. However, the drawbacks of animal-derived protein surface coating is a factor that is soon becoming a matter of concern, hindering the growth of the cell culture protein surface coating market.

Top players of the cell culture protein surface coating industry are EMD Millipore, Thermo Fisher Scientific, Becton, Dickinson and Company, Corning, and Sigma-Aldrich.

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Global Cell Culture Protein Surface Coating Industry: Rising Focus towards Stem Cells Research to Trigger Market Growth

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Newswise LA JOLLA, CA February 25, 2015 A new study led by researchers at The Scripps Research Institute (TSRI) and the University of California (UC), San Diego School of Medicine shows that certain stem cell culture methods are associated with increased DNA mutations. The study points researchers toward safer and more robust methods of growing stem cells to treat disease and injury.

This is about quality control; were making sure these cells are safe and effective, said Jeanne Loring, a professor of developmental neurobiology at TSRI and senior author of the study with Louise Laurent, assistant professor at UC San Diego.

Laurent added, The processes used to maintain and expand stem cell cultures for cell replacement therapies needs to be improved, and the resulting cells carefully tested before use.

The findings were published February 25 in the open-access journal PLOS ONE.

Growing Stem Cells

Because these human stem cells, called "pluripotent stem cells," can differentiate into many types of cells, they could be key to reversing degenerative diseases, such as Parkinsons disease, or repairing injured tissue, such as cardiac muscle after a heart attack. Stem cells are relatively rare in the body, however, so researchers must culture them in dishes.

While all cells run the risk of mutating when they divide, previous research from Loring and her colleagues suggested that stem cell culturing may select for mutations that favor faster cell growth and are sometimes associated with tumors.

Most changes will not compromise the safety of the cells for therapy, but we need to monitor the cultures so that we know what sorts of changes take place, said the papers first author Ibon Garitaonandia, a postdoctoral researcher working in Lorings lab at the time of the study.

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New Study Shows Safer Methods for Stem Cell Culturing

Posted by Richard Dietman (@rdietman) 3 day(s) ago

Mayo Clinic Radio: Cardiac Regeneration/Stop-Smoking Drug/Juicing

On this weeks Mayo Clinic Radio,fixing a broken heart. Cardiac regeneration uses the bodys own stem cells to repair damage done by heart disease. Mayo Clinic cardiologist Dr. Atta Behfar explains. Also on the program, nicotine dependency expert Dr. Richard Hurt discusses results of a new study about the stop-smoking drug varenicline (Chantix). And Mayo Clinic registered dietitian Katherine Zeratsky explains the risks of juice-only diets.

Myth or Matter-of-Fact: Cardiac regeneration may someday replace the need for surgery to repair heart damage.

To listen to the program at 9 a.m. Saturday, February 21, clickhere.

Follow#MayoClinicRadioand tweet your questions.

Mayo Clinic Radio is available oniHeartRadio.

Mayo Clinic Radiois a weeklyone-hour radio program highlighting health and medical informationfrom Mayo Clinic.

To find and listen toarchived shows,click here.

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Mayo Clinic Radio: Cardiac Regeneration/Stop-Smoking Drug/Juicing

DALLAS, February 19, 2015 /PRNewswire/ --

The Global Cell Culture Protein Surface Coating Market 2015-2019 research report available with LifeScienceIndustryResearch.com provides information on the usage of different types of proteins derived from various sources for cell culture protein surface coating: Animal-derived protein, Human-derived protein, Synthetic protein and Plant-derived protein.

The Global Cell Culture Protein Surface Coating Market is expected to post 12.91% CAGR from 2014-2019, thanks to the wide range of applications for protein surface coatings include improved adhesion of cells, better proliferation and growth of cells, receptor-ligand binding studies, cell matrix studies, signal transduction studies, morphogenesis studies, differentiation of individual cell types, genetic engineering, metabolic pathway studies and drug screening. The high potential of stem cells in the treatment of severe diseases, including neurodegenerative diseases, cardiac diseases, and even diabetes, has resulted in demand for advanced cell culture products for stem cell production and study. Cell culture protein surface coating products help researchers improve the adhesion, proliferation, and growth of cultured cells. Complete report is available at http://www.lifescienceindustryresearch.com/global-cell-culture-protein-surface-coating-market-2015-2019.html .

Biopharmaceuticals are protein-based products such as vaccines, somatic cells, allergenics, and recombinant therapeutic proteins that are derived through cell culture. There has been increased demand for biopharmaceuticals, since they can be used to treat diseases and injuries more effectively than conventional drugs. Several big biopharmaceutical companies such as Roche, Novo Nordisk, and EMD Millipore are involved in biopharmaceutical production, and they require high accuracy and efficiency in their cell culture applications. Since cell culture protein surface coating has been shown to facilitate cell adhesion, and delivers high productivity in cell culture activities, these products are now in high demand in the biopharmaceuticals sector.

Cell culture protein surface coating is a procedure in which the cell culture surfaces are coated with proteins or extracellular matrix components to enhance the adhesion and proliferation of the cells in vitro. The following are the different types of available proteins: human-derived proteins, animal-derived proteins, plant-derived proteins, and synthetic proteins. Proteins such as fibronectin, laminin, collagen, vitronectin, and osteopontin are used for cell culture protein surface coating. Protein surface coating helps in the growth of various types of cells such as endothelial, epithelial, fibroblasts, leukocytes, myoblasts and muscle cells, neurons, and CHO cell lines. Cell culture protein surface coating provides improved adhesion, proliferation, and rapid growth of cells during isolation and cultivation.

This report covers the present scenario and the growth prospects of Global Cell Culture Protein Surface Coating market for the period 2015-2019. To calculate the market size, the report considers revenue generated from the sales of cell culture protein surface coating products including consumables and instruments.

Companies like Becton, Dickinson and Company, Corning, EMD Millipore, Sigma-Aldrich, Thermo Fisher Scientific, Abcam, BioMedTech Laboratories, Bio-Techne, Cedarlane Laboratories, Cell Guidance Systems, Cytoskeleton, Full Moon BioSystems, Greiner Bio-One, neuVitro, Orla Protein Technologies, Pall, PerkinElmer, PROGEN Biotechnik, PromoCell, RayBiotech, Sartorius Stedim Biotech, SouthernBiotech, Trevigen and Viogene BioTek are mentioned in this research available for purchase at http://www.lifescienceindustryresearch.com/purchase?rname=34847 .

The presence of developed healthcare infrastructure and government funding for companies is encouraging extensive R&D in the Global Cell Culture Surface Coating Market. Big pharmaceutical and biotechnology companies are investing extensively in R&D to develop innovative products to meet customer demand. High-end cell culture protein surface coating products can be used in many applications such as drug development, cell biology, tissue engineering, and biopharmaceutical production to increase efficiency and productivity.

The Global Cell Culture Protein Surface Coating Market 2015-2019 research report has been prepared based on an in-depth market analysis with inputs from industry experts. The report covers the Americas, and the EMEA and APAC regions; it also covers the Global Cell Culture Protein Surface Coating market landscape and its growth prospects in the coming years. The report includes a discussion of the key vendors operating in this market.

Other newly published research reports on the biotechnology market available with LifeScienceIndustryResearch.com can be accessed at http://www.lifescienceindustryresearch.com/category/biotechnology .

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Biopharma Demand Driving Cell Culture Protein Surface Coating Market Growth Globally, Along with Synthetic Proteins ...

Kansas City, MO (PRWEB) February 09, 2015

One in five Americans will develop heart failure in their lifetime. It is the number one cause of hospitalization for adults over 65. The cost to treat heart failure is $32 billion and expected to double by 2030. There is no doubt heart failure is a significant health problem. The good news is proper care and treatment can dramatically improve a patients outcome and potentially promising new treatments are on the horizon.

February 8-14, 2015 is National Heart Failure Awareness Week. Saint Lukes Mid America Heart Institute, in Kansas City, Missouri specializes in treating heart failure and other complex cardiovascular conditions and has long been one of the leaders in cardiovascular care not only in the Midwest, but across the country.

Heart failure occurs when the heart is unable to efficiently move blood to the rest of the body either due to thickening or weakness. Onset can come from a variety of causes including heart attack, viral illness, abnormal heart valves, genetic traits and even after pregnancy. Symptoms can be subtle; shortness of breath, fatigue, dizziness, swelling in the legs and or stomach.

The good news is a variety of treatments are available and proper care and treatment can dramatically improve symptoms and quality of life for patients.

Treatments include:

The exciting news for patients is we have promising treatments currently in the research phase of development, said Bethany Austin, M.D., Associate Medical Director of the Advanced Heart Failure Program at Saint Lukes Mid America Heart Institute. These treatments range from clinical trials involving catheter based treatments, treatment of sleep apnea, and gene therapy with stem cells for damaged heart muscles. In addition, there is a new medication which has shown in recent trials to provide significant benefit to heart failure patients compared to standard therapy although it is not yet commercially available. All of these offer new hope to heart failure patients.

Saint Lukes offers a multidisciplinary heart team, including the regions only team of cardiologists board certified in Advanced Heart Failure and Cardiac Transplant, cardiothoracic surgeons, and critical care anesthesiologists.

The Saint Lukes Heart Failure Program also features:

In 2014, The Joint Commission awarded Saint Lukes Hospital Advanced Certification in Heart Failure. Only 53 other hospitals in the United States currently have Advanced Heart Failure Certification. Saint Lukes Hospital also received the Get With The GuidelinesHeart Failure Gold-Plus Quality Achievement Award for implementing specific quality improvement measures outlined by the American Heart Association/American College of Cardiology Foundation secondary prevention guidelines for heart failure patients.

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Saint Lukes Mid America Heart Institute Offers Tips & Treatments For Heart Failure Awareness Week 2015

Late-Breaking Basic Science Research Presented at American Heart Association Scientific Sessions Shows Stem Cell Treatment Restores Heart Function Damaged by Muscular Disease

Contact: Sally Stewart Email: sally.stewart@cshs.org

Los Angeles - Nov. 17, 2014 Researchers at the Cedars-Sinai Heart Institute have found that injections of cardiac stem cells might help reverse heart damage caused by Duchenne muscular dystrophy, potentially resulting in a longer life expectancy for patients with the chronic muscle-wasting disease.

The study results were presented today at a Breaking Basic Science presentation during the American Heart Association Scientific Sessions in Chicago. After laboratory mice with Duchenne muscular dystrophy were infused with cardiac stem cells, the mice showed steady, marked improvement in heart function and increased exercise capacity.

Duchenne muscular dystrophy, which affects 1 in 3,600 boys, is a neuromuscular disease caused by a shortage of a protein called dystrophin, leading to progressive muscle weakness. Most Duchenne patients lose their ability to walk by age 12. Average life expectancy is about 25. The cause of death often is heart failure because the dystrophin deficiency leads to cardiomyopathy, a weakness of the heart muscle that makes the heart less able to pump blood and maintain a regular rhythm.

"Most research into treatments for Duchenne muscular dystrophy patients has focused on the skeletal muscle aspects of the disease, but more often than not, the cause of death has been the heart failure that affects Duchenne patients," said Eduardo Marbn, MD, PhD, director of the Cedars-Sinai Heart Institute and study leader. "Currently, there is no treatment to address the loss of functional heart muscle in these patients."

During the past five years, the Cedars-Sinai Heart Institute has become a world leader in studying the use of stem cells to regenerate heart muscle in patients who have had heart attacks. In 2009, Marbn and his team completed the world's first procedure in which a patient's own heart tissue was used to grow specialized heart stem cells. The specialized cells were then injected back into the patient's heart in an effort to repair and regrow healthy muscle in a heart that had been injured by a heart attack. Results, published in The Lancet in 2012, showed that one year after receiving the experimental stem cell treatment, heart attack patients demonstrated a significant reduction in the size of the scar left on the heart muscle.

Earlier this year, Heart Institute researchers began a new study, called ALLSTAR, in which heart attack patients are being infused with allogeneic stem cells, which are derived from donor-quality hearts. Recently, the Heart Institute opened the nations first Regenerative Medicine Clinic, designed to match heart and vascular disease patients with appropriate stem cell clinical trials being conducted at Cedars-Sinai and other institutions.

"We are committed to thoroughly investigating whether stem cells could repair heart damage caused by Duchenne muscular dystrophy," Marbn said.

In the study, 78 lab mice were injected with cardiac stem cells. Over the next three months, the lab mice demonstrated improved pumping ability and exercise capacity in addition to a reduction in heart inflammation. The researchers also discovered that the stem cells work indirectly, by secreting tiny fat droplets called exosomes. The exosomes, when purified and administered alone, reproduce the key benefits of the cardiac stem cells.

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Cardiac Stem Cell Therapy May Heal Heart Damage Caused by ...

LA JOLLA (CNS) - Two scientists with UC San Diego were awarded a combined $2.7 million in grants from the California Institute for Regenerative Medicine to pursue their studies on stem cell therapies, the school announced Monday.

Shyni Varghese, an associate professor in the Department of Bioengineering and director of the Bio-Inspired Materials and Stem Cell Engineering Laboratory, received a $1.4 CIRM grant to improve the function of transplanted stem cells.

Shaochen Chen, a professor in the Department of Nanoengineering in the Jacobs School of Engineering and a member of UCSD's Institute of Engineering in Medicine, received $1.3 million to develop three-diminensional bioprinting techniques that use heart muscle cells derived from human embryonic stem cells to create new cardiac tissue.

The awards were part of almost $30 million in grants announced at CIRM's monthly meeting in San Francisco, according to UCSD.

"Sometimes even the most promising therapy can be derailed by a tiny problem," said Jonathan Thomas, chairman of the CIRM Board of Directors. "These awards are designed to help find ways to overcome those problems, to bridge the gaps in our knowledge and ensure that the best research is able to keep progressing and move out of the lab and into clinical trials in patients."

Varghese's lab focuses on the interactions of cells with their surrounding micro-environment, and how the conditions necessary to promote normal, healthy survival and growth occur, according to UCSD.

Chen's studies focus on using stem cells to create new heart tissue that would help patients when transplants aren't immediately available.

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UCSD scientists awarded $2.7M grants for stem cell research

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?
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

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

By: CK LAB

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Cardiac Muscle Derived from Pluripotent Stem Cells - Video

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

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
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...

By: CoalitionDuchenne

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

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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January 22, 2015

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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

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