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New transformation: Human stem cells into functional lung …

By Sykes24Tracey

In computer-based text processing and digital typesetting, a non-breaking space, no-break space or non-breakable space (NBSP) is a variant of the space character that prevents an automatic line break (line wrap) at its position. In certain formats (such as HTML), it also prevents the collapsing of multiple consecutive whitespace characters into a single space. The non-breaking space is also known as a hard space or fixed space. In Unicode, it is encoded at U+00A0 no-break space (HTML:    ).

Text-processing software typically assumes that an automatic line break may be inserted anywhere a space character occurs; a non-breaking space prevents this from happening (provided the software recognizes the character). For example, if the text 100 km will not quite fit at the end of a line, the software may insert a line break between 100 and km. To avoid this undesirable behaviour, the editor may choose to use a non-breaking space between 100 and km. This guarantees that the text 100km will not be broken: if it does not fit at the end of a line it is moved in its entirety to the next line.

A second common application of non-breaking spaces is in plain text file formats such as SGML, HTML, TeX, and LaTeX, which sometimes treat sequences of whitespace characters (space, newline, tab, form feed, etc.) as if they were a single white-space character. Such collapsing of white-space allows the author to neatly arrange the source text using line breaks, indentation and other forms of spacing without affecting the final typeset result.[1][2]

In contrast, non-breaking spaces are not merged with neighboring whitespace characters, and can therefore be used by an author to insert additional visible space in the formatted text. For example, in HTML, non-breaking spaces may be used in conjunction with a fixed-width font to create tabular alignment (courier new font family used):

Column 1Column 2 ---------------- 1.22.3

(note that the use of the pre tag, the whitespace:pre CSS rule, or a table are alternative, if not necessarily better, ways to achieve the same result in HTML)

If ordinary spaces are used instead then the spaces are collapsed when the HTML is rendered and the layout is broken:

Column 1 Column 2 -------- -------- 1.2 2.3

Non-breaking space can also be used to automatically change formatting in a document. This is useful for things like class plans and recipe files where the description of a cell or line may be different from the actual text or title.

Unicode defines several other non-break space characters[3] that differ from the regular space in width:

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New transformation: Human stem cells into functional lung ...

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[International version] Linda van Laake: "We want to work together to improve stem cell treatment" – Video

By Sykes24Tracey


[International version] Linda van Laake: "We want to work together to improve stem cell treatment"
Dr Linda van Laake is assistant professor and specialist registrar in Cardiology at the University Medical Center Utrecht and Hubrecht Institute. She carries...

By: UniversiteitUtrecht

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[International version] Linda van Laake: "We want to work together to improve stem cell treatment" - Video

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Research | Research news | 2012 | Finished heart switches stem …

By LizaAVILA

Finished heart switches stem cells off

Transcription factor Ajuba regulates stem cell activity in the heart during embryonic development

July 12, 2012

It is not unusual for babies to be born with congenital heart defects. This is because the development of the heart in the embryo is a process which is not only extremely complex, but also error-prone. Scientists from the Max Planck Institute for Heart and Lung Research in Bad Nauheim have now identified a key molecule that plays a central role in regulating the function of stem cells in the heart. As a result, not only could congenital heart defects be avoided in future, but new ways of stimulating the regeneration of damaged hearts in adults may be opened up.

Cardiac development out of control: Absence of the transcription factor Ajuba during cardiac development, as is the case in the right-hand photo due to genetic intervention, disrupts development of the heart in the fish embryo. In addition to an increased number of cardiac muscle cells (green with red-stained nuclei), the heart is additionally deformed during development.

Max Planck Institute for Heart and Lung Research

Max Planck Institute for Heart and Lung Research

It's a long road from a cluster of cells to a finished heart. Cell division transforms what starts out as a collection of only a few cardiac stem cells into an ever-larger structure from which the various parts of the heart, such as ventricles, atria, valves and coronary vessels, develop. This involves the stem and precursor cells undergoing a complex process which, in addition to tightly regulated cell division, also includes cell migration, differentiation and specialisation. Once the heart is complete, the stem cells are finally switched off.

Scientists from the Max Planck Institute for Heart and Lung Research in Bad Nauheim have now discovered how major parts of this development process are regulated. Their search initially focused on finding binding partners for transcription factor Isl1. Isl1 is characteristic of a specific group of cardiac stem cells which are consequently also known as Isl1+ cells. During their search, the researchers came across Ajuba, a transcription factor from the group of LIM proteins. "We then took a closer a look at the interaction between these two molecules and came to the conclusion that Ajuba must be an important switch", says Gergana Dobreva, head of the "Origin of Cardiac Cell Lineages" Research Group at the Bad Nauheim-based Max Planck Institute.

Using an animal model, the scientists then investigated the effects of a defective switch on cardiac development. Embryonic development can be investigated particularly effectively in the zebrafish. The Bad Nauheim-based researchers therefore produced a genetically modified fish that lacked a functioning Ajuba protein. Cardiac development in these fishes was in fact severely disrupted. In addition to deformation of the heart, caused by twisting of the cardiac axis, what particularly struck the researchers was a difference in size in comparison with control animals. "In almost all the investigated fish we observed a dramatic enlargement of the heart. If Ajuba is absent, there is clearly no other switch that finally silences the Isl1-controlled part of cardiac development", says Dobreva.

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6. Mending a Broken Heart: Stem Cells and Cardiac Repair [Stem …

By Sykes24Tracey

Charles A. Goldthwaite, Jr., Ph.D.

Cardiovascular disease (CVD), which includes hypertension, coronary heart disease (CHD), stroke, and congestive heart failure (CHF), has ranked as the number one cause of death in the United States every year since 1900 except 1918, when the nation struggled with an influenza epidemic.1 In 2002, CVD claimed roughly as many lives as cancer, chronic lower respiratory diseases, accidents, diabetes mellitus, influenza, and pneumonia combined. According to data from the 19992002 National Health and Nutrition Examination Survey (NHANES), CVD caused approximately 1.4 million deaths (38.0 percent of all deaths) in the U.S. in 2002. Nearly 2600 Americans die of CVD each day, roughly one death every 34 seconds. Moreover, within a year of diagnosis, one in five patients with CHF will die. CVD also creates a growing economic burden; the total health care cost of CVD in 2005 was estimated at $393.5 billion dollars.

Given the aging of the U.S. population and the relatively dramatic recent increases in the prevalence of cardiovascular risk factors such as obesity and type 2 diabetes,2,3 CVD will continue to be a significant health concern well into the 21st century. However, improvements in the acute treatment of heart attacks and an increasing arsenal of drugs have facilitated survival. In the U.S. alone, an estimated 7.1 million people have survived a heart attack, while 4.9 million live with CHF.1 These trends suggest an unmet need for therapies to regenerate or repair damaged cardiac tissue.

Ischemic heart failure occurs when cardiac tissue is deprived of oxygen. When the ischemic insult is severe enough to cause the loss of critical amounts of cardiac muscle cells (cardiomyocytes), this loss initiates a cascade of detrimental events, including formation of a non-contractile scar, ventricular wall thinning (see Figure 6.1), an overload of blood flow and pressure, ventricular remodeling (the overstretching of viable cardiac cells to sustain cardiac output), heart failure, and eventual death.4 Restoring damaged heart muscle tissue, through repair or regeneration, therefore represents a fundamental mechanistic strategy to treat heart failure. However, endogenous repair mechanisms, including the proliferation of cardiomyocytes under conditions of severe blood vessel stress or vessel formation and tissue generation via the migration of bone-marrow-derived stem cells to the site of damage, are in themselves insufficient to restore lost heart muscle tissue (myocardium) or cardiac function.5 Current pharmacologic interventions for heart disease, including beta-blockers, diuretics, and angiotensin-converting enzyme (ACE) inhibitors, and surgical treatment options, such as changing the shape of the left ventricle and implanting assistive devices such as pacemakers or defibrillators, do not restore function to damaged tissue. Moreover, while implantation of mechanical ventricular assist devices can provide long-term improvement in heart function, complications such as infection and blood clots remain problematic.6 Although heart transplantation offers a viable option to replace damaged myocardium in selected individuals, organ availability and transplant rejection complications limit the widespread practical use of this approach.

Figure 6.1. Normal vs. Infarcted Heart. The left ventricle has a thick muscular wall, shown in cross-section in A. After a myocardial infarction (heart attack), heart muscle cells in the left ventricle are deprived of oxygen and die (B), eventually causing the ventricular wall to become thinner (C).

2007 Terese Winslow

The difficulty in regenerating damaged myocardial tissue has led researchers to explore the application of embryonic and adult-derived stem cells for cardiac repair. A number of stem cell types, including embryonic stem (ES) cells, cardiac stem cells that naturally reside within the heart, myoblasts (muscle stem cells), adult bone marrow-derived cells, mesenchymal cells (bone marrow-derived cells that give rise to tissues such as muscle, bone, tendons, ligaments, and adipose tissue), endothelial progenitor cells (cells that give rise to the endothelium, the interior lining of blood vessels), and umbilical cord blood cells, have been investigated to varying extents as possible sources for regenerating damaged myocardium. All have been tested in mouse or rat models, and some have been tested in large animal models such as pigs. Preliminary clinical data for many of these cell types have also been gathered in selected patient populations.

However, clinical trials to date using stem cells to repair damaged cardiac tissue vary in terms of the condition being treated, the method of cell delivery, and the primary outcome measured by the study, thus hampering direct comparisons between trials.7 Some patients who have received stem cells for myocardial repair have reduced cardiac blood flow (myocardial ischemia), while others have more pronounced congestive heart failure and still others are recovering from heart attacks. In some cases, the patient's underlying condition influences the way that the stem cells are delivered to his/her heart (see the section, quot;Methods of Cell Deliveryquot; for details). Even among patients undergoing comparable procedures, the clinical study design can affect the reporting of results. Some studies have focused on safety issues and adverse effects of the transplantation procedures; others have assessed improvements in ventricular function or the delivery of arterial blood. Furthermore, no published trial has directly compared two or more stem cell types, and the transplanted cells may be autologous (i.e., derived from the person on whom they are used) or allogeneic (i.e., originating from another person) in origin. Finally, most of these trials use unlabeled cells, making it difficult for investigators to follow the cells' course through the body after transplantation (see the section quot;Considerations for Using These Stem Cells in the Clinical Settingquot; at the end of this article for more details).

Despite the relative infancy of this field, initial results from the application of stem cells to restore cardiac function have been promising. This article will review the research supporting each of the aforementioned cell types as potential source materials for myocardial regeneration and will conclude with a discussion of general issues that relate to their clinical application.

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The heart’s own stem cells play their part in regeneration

By raymumme

Nov. 28, 2013 Up until a few years ago, the common school of thought held that the mammalian heart had very little regenerative capacity. However, scientists now know that heart muscle cells constantly regenerate, albeit at a very low rate. Researchers at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, have identified a stem cell population responsible for this regeneration. Hopes are growing that it will be possible in future to stimulate the self-healing powers of patients with diseases and disorders of the heart muscle, and thus develop new potential treatments.

Some vertebrates seem to have found the fountain of youth, the source of eternal youth, at least when it comes to their heart. In many amphibians and fish, for example, this important organ has a marked capacity for regeneration and self-healing. Some species in the two animal groups have even perfected this capability and can completely repair damage caused to heart tissue, thus maintaining the organ's full functionality.

The situation is different for mammals, whose hearts have a very low regenerative capacity. According to the common school of thought that has prevailed until recently, the reason for this deficit is that the heart muscle cells in mammals cease dividing shortly after birth. It was also assumed that the mammalian heart did not have any stem cells that could be used to form new heart muscle cells. On the contrary: new studies show that aged muscle cells are also replaced in mammalian hearts. Experts estimate, however, that between just one and four percent of heart muscle cells are replaced every year.

Scientists in Thomas Braun's Research Group at the Max Planck Institute for Heart and Lung Research have succeeded in identifying a stem cell population in mice that plays a key role in this regeneration of heart muscle cells. Experiments conducted by the researchers in Bad Nauheim on genetically modified mice show that the Sca1 stem cells in a healthy heart are involved in the ongoing replacement of heart muscle cells. The Sca-1 cells increase their activity if the heart is damaged, with the result that significantly more new heart muscle cells are formed.

Since, in comparison to the large amount of heart muscle cells, Sca-1 stem cells account for just a tiny proportion of the cells in the heart muscle, searching for them is like searching for a needle in a haystack. "We also faced the problem that Sca-1 is no longer available in the cells as a marker protein for stem cells after they have been changed into heart muscle cells. To prove this, we had to be inventive," says project leader Shizuka Uchida. The Max Planck researchers genetically modified the stem cells to such an extent that, in addition to the Sca-1, they produced another visible marker. Even if Sca-1 was subsequently no longer visible, the marker could still be detected permanently.

"In this way, we were able to establish that the proportion of heart muscle cells originating from Sca-1 stem cells increased continuously in healthy mice. Around five percent of the heart muscle cells regenerated themselves within 18 months," says Uchida. Moreover, mice suffering from heart disease triggered by the experiment had up to three times more of these newly formed heart muscle cells.

"The data shows that, in principle, the mammalian heart is able to trigger regeneration and renewal processes. Under normal circumstances, however, these processes are not enough to ultimately repair cardiac damage," says Braun. The aim is to find ways in which the formation of new heart muscle cells from heart stem cells can be improved and thereby strengthen the heart's self-healing powers.

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Cardiac regeneration: current therapies—future concepts

By JoanneRUSSELL25

Abstract

Cardiovascular disease (CVD) continues to be one of the main causes of death in the western world. A high burden of disease and the high costs for the healthcare systems claim for novel therapeutic strategies besides current conventional medical care. One decade ago first clinical trials addressed stem cell based therapies as a potential alternative therapeutic strategy for myocardial regeneration and repair. Besides bone marrow derived stem cells (BMCs), adult stem cells from adipose or cardiac tissue have been used in current clinical studies with inconsistent results. Although outcomes in terms of safety and feasibility are generally encouraging, functional improvements were mostly disappointingly low and have failed to reach expectations. In the future, new concepts for myocardial regeneration, especially concerning recovery of cardiomyocyte loss, have to be developed. Transplantation of novel stem or progenitor cell populations with true regenerative potential, direct reprogramming of scar tissue into functional myocardium, tissue engineering or stimulation of endogenous cardiac repair by pharmacological agents are conceivable. This review summarizes current evidence of stem cell based regenerative therapies and discusses future strategies to improve functional outcomes.

KEYWORDS : Myocardial infarction, regenerative medicine, stem cells, tissue engineering, reprogramming

In 2009 cardiovascular disease (CVD) still accounted for 32.3% of all deaths in the United States and therefore continues to be one of the main causes of death (1). From 1999 to 2009, the rate of death due to CVD has declined, but nevertheless the burden of disease remains high. Although improved medical care and acute management of myocardial infarction have led to a considerable reduction of early mortality rate survivors are susceptible to an increased prevalence of chronic heart failure as they develop scarring followed by ventricular remodeling despite optimum medical care (2,3).

Interestingly, cardiovascular operations and interventional procedures increased by 28% from 2000 to 2010 implicating an enormous cost factor for the healthcare system (1). For 2009, it was estimated that the direct and indirect costs of CVD and stroke add up to about $312.6 billion in the United States, which was more than for any other diagnostic group (1).

The main issue of current pharmacological, interventional or operative therapies is their disability to compensate the irreversible loss of functional cardiomyocytes (4). Hence, the future challenge of cardiovascular therapies will be the functional regeneration of myocardial contractility by novel concepts, like cell based therapy, tissue engineering or reprogramming of scar fibroblasts (5,6).

After promising preclinical results using adult stem and precursor cells for cardiac regeneration a rapid clinical translation using autologous bone marrow cells (BMCs) in patients was initiated (7,8). In the last few years numerous clinical trials addressing the transplantation of various adult stem cell populations for cardiac regeneration have been performed. Essential characteristics for the selected adult stem cell populations are the potential to proliferate, migrate and the ability to transdifferentiate into various mature cell types (9). Today, different adult stem cell sources like BMCs, myocardium or adipose tissue derived cells were already used in clinical trials. Beside direct intracoronary or intramyocardial transplantation of adult stem cells into the heart mobilization of autologous progenitor cells by administration of different cytokines [i.e., erythropoietin (EPO) or granulocyte colony stimulating factor (G-CSF)] were also evaluated in first clinical trials (summarized in and ,).

Regenerative therapies and cell sources currently administered in clinical trials. Current clinical trials use BMCs, ADRCs or CPCs to regenerate impaired myocardium after ischemic events. Alternatively cytokines like EPO or G-CSF are employed to mobilize ...

Transplantation of adult stem cells-clinical trials mentioned in the text.

Mobilization of adult stem cells-clinical trials mentioned in the text.

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Endogenous cardiac stem cell – Wikipedia, the free encyclopedia

By Dr. Matthew Watson

Endogenous cardiac stem cells (eCSCs) are tissue-specific stem progenitor cells harboured within the adult mammalian heart.

They were first discovered in 2003 by Bernardo Nadal-Ginard, Piero Anversa and colleagues [1][2] in the adult rat heart and since then have been identified and isolated from mouse, dog, porcine and human hearts.[3][4]

The adult heart was previously thought to be a post mitotic organ without any regenerative capability. The identification of eCSCs has provided an explanation for the hitherto unexplained existence of a subpopulation of immature cycling myocytes in the adult myocardium. Indeed, recent evidence from a genetic fate-mapping study established that stem cells replenish adult mammalian cardiomyocytes lost by cardiac wear and tear and injury throughout the adult life.[5] Moreover, it is now accepted that myocyte death and myocyte renewal are the two sides of the proverbial coin of cardiac homeostasis in which the eCSCs play a central role.[6] These findings produced a paradigm shift in cardiac biology and opened new opportunities and approaches for future treatment of cardiac diseases by placing the heart squarely amongst other organs with regenerative potential such as the liver, skin, muscle, CNS. However, they have not changed the well-established fact that the working myocardium is mainly constituted of terminally differentiated contractile myocytes. This fact does not exclude, but is it fully compatible with the heart being endowed with a robust intrinsic regenerative capacity which resides in the presence of the eCSCs throughout the individual lifespan.

Briefly, eCSCs have been first identified through the expression of c-kit, the receptor of the stem cell factor and the absence of common hematopoietic markers, like CD45. Afterwards, different membrane markers (Sca-1, Abcg-2, Flk-1) and transcription factors (Isl-1, Nkx2.5, GATA4) have been employed to identify and characterize these cells in the embryonic and adult life.[7] eCSCs are clonogenic, self renewing and multipotent in vitro and in vivo,[8] capable of generating the 3 major cell types of the myocardium: myocytes, smooth muscle and endothelial vascular cells.[9] They express several markers of stemness (i.e. Oct3/4, Bmi-1, Nanog) and have significant regenerative potential in vivo.[10] When cloned in suspension they form cardiospheres,[11] which when cultured in a myogenic differentiation medium, attach and differentiate into beating cardiomyocytes.

In 2012, it was proposed that Isl-1 is not a marker for endogenous cardiac stem cells.[12] That same year, a different group demonstrated that Isl-1 is not restricted to second heart field progenitors in the developing heart, but also labels cardiac neural crest.[13] It has also been reported that Flk-1 is not a specific marker for endogenous and mouse ESC-derived Isl1+ CPCs. While some eCSC discoveries have been brought into question, there has been success with other membrane markers. For instance, it was demonstrated that the combination of Flt1+/Flt4+ membrane markers identifies an Isl1+/Nkx2.5+ cell population in the developing heart. It was also shown that endogenous Flt1+/Flt4+ cells could be expanded in vitro and displayed trilineage differentiation potential. Flt1+/Flt4+ CPCs derived from iPSCs were shown to engraft into the adult myocardium and robustly differentiate into cardiomyocytes with phenotypic and electrophysiologic characteristics of adult cardiomyocytes.[14]

With the myocardium now recognized as a tissue with limited regenerating potential,[15] harbouring eCSCs that can be isolated and amplified in vitro [16] for regenerative protocols of cell transplantation or stimulated to replicate and differentiate in situ in response to growth factors,[17] it has become reasonable to exploit this endogenous regenerative potential to replace lost/damaged cardiac muscle with autologous functional myocardium.

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Endogenous cardiac stem cell - Wikipedia, the free encyclopedia

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Human neural stem cells could meet the clinical problem of …

By Dr. Matthew Watson

New research has shown human neural stem cells could improve blood flow in critical limb ischemia through the growth of new vessels. Critical limb ischemia (CLI) is a disease that severely obstructs arteries and reduces the blood flow to legs and feet. CLI remains an unmet clinical problem and with an ageing population and the rise in type II diabetes, the incidence of CLI is expected to increase.

The study, led by academics in the University of Bristol's School of Clinical Sciences, is published online in the American Heart Association journal Arteriosclerosis, Thrombosis, and Vascular Biology.

Current stem cell therapy trials for the treatment of CLI have revitalised new hope for improving symptoms and prolonging life expectancy. However, there are limitations on the use of autologous cell therapy. The patient's own stem cells are generally invasively harvested from bone marrow or require purification from peripheral blood after cytokine stimulation. Other sources contain so few stem cells that ex vivo expansion through lengthy bespoke Good Manufacturing Practice processes is required. Ultimately, these approaches lead to cells of variable quality and potency that are affected by the patient's age and disease status and lead to inconsistent therapeutic outcomes.

In order to circumvent the problem a team, led by Professor Paolo Madeddu in the Bristol Heart Institute at the University of Bristol, has used a conditionally immortalised clonal human neural stem cell (hNSC) line to treat animal models with limb ischaemia and superimposed diabetes. The CTX cell line, established by stem cell company ReNeuron, is genetically modified to produce genetically and phenotypically stable cell banks.

Results of the new study have shown that CTX treatment effectively improves the recovery from ischaemia through the promotion of the growth of new vessels. The safety of CTX cell treatment is currently being assessed in disabled patients with stroke [PISCES trial, NCT01151124]. As a result, the same cell product is immediately available for starting dose ranging safety and efficacy studies in CLI patients.

Professor Paolo Madeddu, Chair of Experimental Cardiovascular Medicine and Head of Regenerative Medicine Section in the Bristol Heart Institute at the University of Bristol, said: "Currently, there are no effective drug interventions to treat CLI. The consequences are a very poor quality of life, possible major amputation and a life expectancy of less than one year from diagnosis in 50 per cent of all CLI patients.

"Our findings have shown a remarkable advancement towards more effective treatments for CLI and we have also demonstrated the importance of collaborations between universities and industry that can have a social and medical impact."

Dr John Sinden, Chief Scientific Officer of ReNeuron, added: "The novel idea of using neural stem cells to treat vascular disease arose from a chance discussion with Professor Madeddu. The discussion led to a short pilot study with our cells producing very clear data, which then developed into a further eight experiments exploring different variants of the disease model, the product formulation and dose variation.

"The study also explored the cascade of molecular events that produced vascular and muscle recovery. It is a great example of industry and academia working successfully towards the key goal, clinical translation."

Explore further: UH Case Medical Center launches novel clinical trial using stem cells to prevent amputation

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Cardiac Stem Cells (CSCs) | University of Maryland Medical Center

By JoanneRUSSELL25

For immediate release: September 10, 2012

Baltimore, MD --Researchers at the University of Maryland School of Medicine, who are exploring novel ways to treat serious heart problems in children, have conducted the first direct comparison of the regenerative abilities of neonatal and adult-derived human cardiac stem cells. Among their findings: cardiac stem cells (CSCs) from newborns have a three-fold ability to restore heart function to nearly normal levels compared with adult CSCs. Further, in animal models of heart attack, hearts treated with neonatal stem cells pumped stronger than those given adult cells. The study is published in the September 11, 2012, issue of Circulation.

The surprising finding is that the cells from neonates are extremely regenerative and perform better than adult stem cells, says the study's senor author, Sunjay Kaushal, M.D., Ph.D., associate professor of surgery at the University of Maryland School of Medicine and director, pediatric cardiac surgery at the University of Maryland Medical Center. We are extremely excited and hopeful that this new cell-based therapy can play an important role in the treatment of children with congenital heart disease, many of whom don't have other options.

Dr. Kaushal envisions cellular therapy as either a stand-alone therapy for children with heart failure or an adjunct to medical and surgical treatments. While surgery can provide structural relief for some patients with congenital heart disease and medicine can boost heart function up to two percent, he says cellular therapy may improve heart function even more dramatically. We're looking at this type of therapy to improve heart function in children by 10, 12, or 15 percent. This will be a quantum leap in heart function improvement.

Heart failure in children, as in adults, has been on the rise in the past decade and the prognosis for patients hospitalized with heart failure remains poor. In contrast to adults, Dr. Kaushal says heart failure in children is typically the result of a constellation of problems: reduced cardiac blood flow; weakening and enlargement of the heart; and various congenital malformations. Recent research has shown that several types of cardiac stem cells can help the heart repair itself, essentially reversing the theory that a broken heart cannot be mended.

Stem cells are unspecialized cells that can become tissue- or organ-specific cells with a particular function. In a process called differentiation, cardiac stem cells may develop into rhythmically contracting muscle cells, smooth muscle cells or endothelial cells. Stem cells in the heart may also secrete growth factors conducive to forming heart muscle and keeping the muscle from dying.

To conduct the study, researchers obtained a small amount of heart tissue during normal cardiac surgery from 43 neonates and 13 adults. The cells were expanded in a growth medium yielding millions of cells. The researchers developed a consistent way to isolate and grow neonatal stem cells from as little as 20 milligrams of heart tissue. Adult and neonate stem cell activity was observed both in the laboratory and in animal models. In addition, the animal models were compared to controls that were not given the stem cells.

Dr. Kaushal says it is not clear why the neonatal stem cells performed so well. One explanation hinges on sheer numbers: there are many more stem cells in a baby's heart than in the adult heart. Another explanation: neonate-derived cells release more growth factors that trigger blood vessel development and/or preservation than adult cells.

This research provides an important link in our quest to understand how stem cells function and how they can best be applied to cure disease and correct medical deficiencies, says E. Albert Reece, M.D., Ph.D., M.B.A., vice president for medical affairs, University of Maryland; the John Z. and Akiko K. Bowers Distinguished Professor; and dean, University of Maryland School of Medicine. Sometimes simple science is the best science. In this case, a basic, comparative study has revealed in stark terms the powerful regenerative qualities of neonatal cardiac stem cells, heretofore unknown.

Insights gained through this research may provide new treatment options for a life-threatening congenital heart syndrome called hypoplastic left heart syndrome (HLHS). Dr. Kaushal and his team will soon begin the first clinical trial in the United States to determine whether the damage to hearts of babies with HLHS can be reversed with stem cell therapy. HLHS limits the heart's ability to pump blood from the left side of the heart to the body. Current treatment options include either a heart transplant or a series of reconstructive surgical procedures. Nevertheless, only 50-60 percent of children who have had those procedures survive to age five.

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Stem cell therapy: When will it help the heart? | The Why Files

By JoanneRUSSELL25

Stem cells: When will they heal the heart?

Its been 15 years since a University of Wisconsin-Madison researcher isolated embryonic stem cells the do-anything cells that appear in early development. Its been six years since adult human cells were transformed into the related induced pluripotent stem cells.

ENLARGE

Some day, stem cell therapy could restore cells, save hearts, and avoid the need for some heart transplants, such as this one. This heart is ready for its new home.

And yet the early hope to grow spare parts turning stem cells into specialized cells for repairing a failing brain, pancreas or heart, remains mostly promise rather than reality.

Researchers have since found how to transform stem cells into a wide variety of body cells, including heart muscle cells, or cardiomyocytes. But the holy Grail tissue supplementation or replacement remains tantalizingly out of reach.

Last week, Why Files attended a symposium on treating cardiovascular disease with stem cells, at the BioPharmaceutical Technology Center Institute near Madison, Wis. We found the picture unexpectedly complicated: as multiple kinds of stem cells are grown and delivered in a bewildering variety of ways to treat a catalog of conditions.

So far, stem cells have not been approved to treat any heart disease in the United States.

Still, the need remains clear. Disorders of the heart and blood vessels, which deliver oxygen and nutrients to the body, continue to kill. Today, one of every 2.6 Americans will die of some cause related to their heart, writes Columbia University Medical Center.

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UCLA doctors test stem-cell therapy to improve blood flow in …

By daniellenierenberg

Marty Greenfield with UCLA doctors

Marty Greenfield lives with crushing pain every day due to angina, a condition that is caused by an inadequate supply of blood to the heart. He has suffered a heart attack, and a coronary bypass procedure and angioplasty have provided little relief. His doctor referred him to UCLA to be considered for a heart transplant.

Dr. Jonathan Tobis, a UCLA clinical professor of cardiology, performed an angiogram and angioplasty on Greenfield, 64, but found that the patient was not a candidate for a heart transplant because his heart muscle function was still good.

Instead, Tobis suggested that Greenfield consider participating in a Phase 3 clinical trial that uses a patient's own blood-derived stem cells to try to restore circulation to the heart. The procedure uses the latest technology to map the heart in 3-D and guides the doctor to deliver the stem-cell injections to targeted sites in the heart muscle.

On Oct. 17, Greenfield became the first patient at UCLA to participate in the multicenter clinical trial. He said he jumped at the chance to help, even though the study is double blind, which means that neither the patients nor the researchers know who is receiving stem-cell injections and who is receiving placebos.

"This just isn't about me," said Greenfield, a married father of two sons who lives near Las Vegas. "If I can help move this research forward so that it helps just one person, it will be worth it."

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Stem Cell Research at Johns Hopkins Medicine: Repairing Heart Damage

By raymumme

By the time Bill Beatty made it to the Emergency Department in Howard County, he was already several hours into a major heart attack. His physicians performed a series of emergency treatments that included an intra-aortic balloon pump, but the 57-year-old engineers blood pressure remained dangerously low. The cardiologist called for a helicopter to transfer him to Johns Hopkins.

It was fortuitous timing: Beatty was an ideal candidate for a clinical trial and soon received an infusion of stem cells derived from his own heart tissue, making him the second patient in the world to undergo the procedure.

Of all the attempts to harness the promise of stem cell therapy, few have garnered more hope than the bid to repair damaged hearts. Previous trials with other stem cells have shown conflicting results. But this new trial, conducted jointly with cardiologist Eduardo Marbn at Cedars-Sinai Medical Center in Los Angeles, is the first time stem cells come from the patients own heart.

Cardiologist Jeffrey Brinker, M.D., a member of the Hopkins team, thinks the new protocol could be a game-changer. That's based partly on recent animal studies in which scientists at both institutions isolated stem cells from the injured animals hearts and infused them back into the hearts of those same animals. The stem cells formed new heart muscle and blood vessel cells. In fact, says Brinker, the new cells have a pre-determined cardiac fate. Even in the culture dish, he says, theyre a beating mass of cells.

Whats more, according to Gary Gerstenblith, M.D., J.D., the animals in these studies showed a significant decrease in relative infarct size, shrinking by about 25 percent. Based on those and earlier findings, investigators were cleared by the FDA and Hopkins Institutional Review Board to move forward with a human trial.

In Beattys case, Hopkins heart failure chief Stuart Russell, M.D., extracted a small sample of heart tissue and shipped it to Cedars Sinai, where stem cells were isolated, cultured and expanded to large numbers. Hopkins cardiologist Peter Johnston, M.D., says cardiac tissue is robust in its ability to generate stem cells, typically yielding several million transplantable cells within two months.

When ready, the cells were returned to Baltimore and infused back into Beatty through a balloon catheter placed in his damaged artery, ensuring target-specific delivery. Then the watching and waiting began. For the Hopkins team, Beattys infarct size will be tracked by imaging chief Joao Lima, M.D., M.B.A.,and his associates using MRI scans.

Now back home and still struggling with episodes of compromised stamina and shortness of breath, Beatty says his Hopkins cardiologists were fairly cautious in their prognosis, but hell be happy for any improvement.

Nurse coordinator Elayne Breton says Beatty is scheduled for follow-up visits at six months and 12 months, when they hope to find an improvement in his hearts function. But at least one member of the Hopkins team was willing acknowledge a certain optimism. The excitement here, says Brinker, is huge.

The trial is expected to be completed within one to two years.

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Administration of cardiac stem cells in patients with ischemic …

By raymumme

BACKGROUND:

SCIPIO is a first-in-human, phase 1, randomized, open-label trial of autologous c-kit(+) cardiac stem cells (CSCs) in patients with heart failure of ischemic etiology undergoing coronary artery bypass grafting (CABG). In the present study, we report the surgical aspects and interim cardiac magnetic resonance (CMR) results.

A total of 33 patients (20 CSC-treated and 13 control subjects) met final eligibility criteria and were enrolled in SCIPIO. CSCs were isolated from the right atrial appendage harvested and processed during surgery. Harvesting did not affect cardiopulmonary bypass, cross-clamp, or surgical times. In CSC-treated patients, CMR showed a marked increase in both LVEF (from 27.5 1.6% to 35.1 2.4% [P=0.004, n=8] and 41.2 4.5% [P=0.013, n=5] at 4 and 12 months after CSC infusion, respectively) and regional EF in the CSC-infused territory. Infarct size (late gadolinium enhancement) decreased after CSC infusion (by manual delineation: -6.9 1.5 g [-22.7%] at 4 months [P=0.002, n=9] and -9.8 3.5 g [-30.2%] at 12 months [P=0.039, n=6]). LV nonviable mass decreased even more (-11.9 2.5 g [-49.7%] at 4 months [P=0.001] and -14.7 3.9 g [-58.6%] at 12 months [P=0.013]), whereas LV viable mass increased (+11.6 5.1 g at 4 months after CSC infusion [P=0.055] and +31.5 11.0 g at 12 months [P=0.035]).

Isolation of CSCs from cardiac tissue obtained in the operating room is feasible and does not alter practices during CABG surgery. CMR shows that CSC infusion produces a striking improvement in both global and regional LV function, a reduction in infarct size, and an increase in viable tissue that persist at least 1 year and are consistent with cardiac regeneration.

This study is registered with clinicaltrials.gov, trial number NCT00474461.

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Bone-Derived Stem Cells for Heart Repair | Worldhealth.net Anti …

By NEVAGiles23

Stem cell therapy for heart disease has demonstrated safety and efficacy in clinical trials, but a key for better clinical outcomes is to determine the optimal stem cell type best suited for cardiac regeneration, Steven B. Houser, from Temple University (Pennsylvania, USA), and colleagues report that cortical bone-derived stem cells (CBSCs) may be superior to cardiac stem cells, for the regeneration of heart tissue. The researchers collected CBSCs from mouse tibias. The particular mice used had been engineered with green fluorescent protein (GFP), which meant that the CBSCs carried a green marker to allow for their later identification. The cells were then expanded in petri dishes in the laboratory before being injected directly into the hearts of non-GFP mice that had suffered heart attacks. Some mice received cardiac stem cells instead of CBSCs. In the following weeks, as the team monitored the progress of the mice, they found that the youthfulness of the CBSCs had prevailed. The cells had triggered the growth of new blood vessels in the injured tissue, and six weeks after injection, they had differentiated, or matured, into heart muscle cells. While generally smaller than native heart cells, the new cells had the same functional capabilities, and overall they had improved survival and heart function. The study authors submit that: CBSCs improve survival, cardiac function, and attenuate remodeling through the following 2 mechanisms: (1) secretion of proangiogenic factors that stimulate endogenous neovascularization, and (2) differentiation into functional adult myocytes and vascular cells.

Duran JM, Makarewich CA, Sharp TE, Starosta T, Zhu F, Hoffman NE, Houser SR, et al. Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms. Circ Res. 2013 Aug 16;113(5):539-52.

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Bone-Derived Stem Cells for Heart Repair | Worldhealth.net Anti ...

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Stem-Cell Therapy and Repair after Heart Attack and Heart Failure

By raymumme

Stem Cell Therapy: Helping the Body Heal Itself

Stem cells are natures own transformers. When the body is injured, stem cells travel the scene of the accident. Some come from the bone marrow, a modest number of others, from the heart itself. Additionally, theyre not all the same. There, they may help heal damaged tissue. They do this by secreting local hormones to rescue damaged heart cells and occasionally turning into heart muscle cells themselves. Stem cells do a fairly good job. But they could do better for some reason, the heart stops signaling for heart cells after only a week or so after the damage has occurred, leaving the repair job mostly undone. The partially repaired tissue becomes a burden to the heart, forcing it to work harder and less efficiently, leading to heart failure.

Initial research used a patients own stem cells, derived from the bone marrow, mainly because they were readily available and had worked in animal studies. Careful study revealed only a very modest benefit, so researchers have moved on to evaluate more promising approaches, including:

No matter what you may read, stem cell therapy for damaged hearts has yet to be proven fully safe and beneficial. It is important to know that many patients are not receiving the most current and optimal therapies available for their heart failure. If you have heart failure, and wondering about treatment options, an evaluation or a second opinion at a Center of Excellence can be worthwhile.

Randomized clinical trials evaluating these different approaches typically allow enrollment of only a few patients from each hospital, and hence what may be available at the Cleveland Clinic varies from time to time. To inquire about current trials, please call 866-289-6911 and speak to our Resource Nurses.

Cleveland Clinic is a large referral center for advanced heart disease and heart failure we offer a wide range of therapies including medications, devices and surgery. Patients will be evaluated for the treatments that best address their condition. Whether patients meet the criteria for stem cell therapy or not, they will be offered the most advanced array of treatment options.

Reviewed: 04/13

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Study to infuse stem cells into coronary artery to regenerate …

By Sykes24Tracey

Medical investigators are embarking on a study that involves infusing 10 million stem cells directly into a coronary artery of heart attack patients in an effort to regenerate tissue that otherwise would be forever damaged.

Regeneration has been an ongoing theme in science fiction and a goal of real-life scientists.

Dr. Luis Gruberg, of the Stony Brook Heart Institute, and Dr. Allen Jeremias, director of the intensive care unit, led a team late last month in a novel case, which they describe as a clinical trial designed to harvest, and then inject, a patient's own stem cells into the blocked artery responsible for the attack.

"This is a post-heart attack procedure and it is for patients who have had a large heart attack," said Gruberg, director of interventional cardiology research.

In patients whose attacks are severe, vast portions of the heart are irreparably damaged, resulting in cardiac tissue that no longer performs efficiently.

Every year about 715,000 Americans have a heart attack. Of those, 525,000 are a first heart attack and 190,000 are repeat episodes. Every 44 seconds someone in the United States dies of a heart attack, according to federal data.

If stem cells can aid in the remodeling of the heart, regenerating healthy tissue, then medicine can offer patients a new lease on life, the doctors said.

Arriving at a point when such a treatment can be offered, Gruberg added, requires research. The gold standard of clinical study in Western medicine is the placebo-controlled randomized clinical trial, which means some of the Stony Brook heart patients will receive a stem cell transplant, others, a placebo.

Doctors began their study, part of a larger national investigation, abruptly late last month because they had been awaiting the perfect patient.

That person, a 66-year-old man who had been visiting Long Island from the Midwest, arrived at Stony Brook University Hospital as a transfer from Southampton Hospital.

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Stem cell therapy – Wikipedia, the free encyclopedia

By JoanneRUSSELL25

This article is about the medical therapy. For the cell type, see Stem cell.

Stem cell therapy is an intervention strategy that introduces new adult stem cells into damaged tissue in order to treat disease or injury. Many medical researchers believe that stem cell treatments have the potential to change the face of human disease and alleviate suffering.[1] The ability of stem cells to self-renew and give rise to subsequent generations with variable degrees of differentiation capacities,[2] offers significant potential for generation of tissues that can potentially replace diseased and damaged areas in the body, with minimal risk of rejection and side effects.

A number of stem cell therapies exist, but most are at experimental stages, costly or controversial,[3] with the notable exception of bone-marrow transplantation.[citation needed] Medical researchers anticipate that adult and embryonic stem cells will soon be able to treat cancer, Type 1 diabetes mellitus, Parkinson's disease, Huntington's disease, Celiac disease, cardiac failure, muscle damage and neurological disorders, and many others.[4] Nevertheless, before stem cell therapeutics can be applied in the clinical setting, more research is necessary to understand stem cell behavior upon transplantation as well as the mechanisms of stem cell interaction with the diseased/injured microenvironment.[4]

For over 30 years, bone-marrow, and more recently, umbilical-cord blood stem cells, have been used to treat cancer patients with conditions such as leukemia and lymphoma.[5][6] During chemotherapy, most growing cells are killed by the cytotoxic agents. These agents, however, cannot discriminate between the leukaemia or neoplastic cells, and the hematopoietic stem cells within the bone marrow. It is this side effect of conventional chemotherapy strategies that the stem cell transplant attempts to reverse; a donor's healthy bone marrow reintroduces functional stem cells to replace the cells lost in the host's body during treatment.

Stroke and traumatic brain injury lead to cell death, characterized by a loss of neurons and oligodendrocytes within the brain. Healthy adult brains contain neural stem cells which divide to maintain general stem cell numbers, or become progenitor cells. In healthy adult animals, progenitor cells migrate within the brain and function primarily to maintain neuron populations for olfaction (the sense of smell). In pregnancy and after injury, this system appears to be regulated by growth factors and can increase the rate at which new brain matter is formed.[citation needed] Although the reparative process appears to initiate following trauma to the brain, substantial recovery is rarely observed in adults, suggesting a lack of robustness.[7]

Stem cells may also be used to treat brain degeneration, such as in Parkinson's and Alzheimer's disease.[8][9]

Pharmacological activation of an endogenous population of neural stem cells / neural precursor cells by soluble factors has been reported to induce powerful neuroprotection and behavioral recovery in adult rat models of neurological disorder through a signal transduction pathway involving the phosphorylation of STAT3 on the serine residue and subsequent Hes3 expression increase (STAT3-Ser/Hes3 Signaling Axis).[10][11][12]

Stem cell technology gives hope of effective treatment for a variety of malignant and non-malignant diseases through the rapid developing field that combines the efforts of cell biologists, geneticists and clinicians. Stem cells are defined as totipotent progenitor cells capable of self-renewal and multi-lineage differentiation. Stem cells survive well and show steady division in culture which then causes them the ideal targets for vitro manipulation. Research into solid tissue stem cells has not made the same progress as haematopoietic stem cells because of the difficulty of reproducing the necessary and precise 3D arrangements and tight cell-cell and cell-extracellular matrix interactions that exist in solid organs. Yet, the ability of tissue stem cells to assimilate into the tissue cytoarchitecture under the control of the host microenvironment and developmental cues, makes them ideal for cell replacement therapy. [3] [13]

The development of gene therapy strategies for treatment of intra-cranial tumours offers much promise, and has shown to be successful in the treatment of some dogs;[14] although research in this area is still at an early stage. Using conventional techniques, brain cancer is difficult to treat because it spreads so rapidly. Researchers at the Harvard Medical School transplanted human neural stem cells into the brain of rodents that received intracranial tumours. Within days, the cells migrated into the cancerous area and produced cytosine deaminase, an enzyme that converts a non-toxic pro-drug into a chemotheraputic agent. As a result, the injected substance was able to reduce the tumor mass by 81 percent. The stem cells neither differentiated nor turned tumorigenic.[15]

Some researchers believe that the key to finding a cure for cancer is to inhibit proliferation of cancer stem cells. Accordingly, current cancer treatments are designed to kill cancer cells. However, conventional chemotherapy treatments cannot discriminate between cancerous cells and others. Stem cell therapies may serve as potential treatments for cancer.[16] Research on treating lymphoma using adult stem cells is underway and has had human trials. Essentially, chemotherapy is used to completely destroy the patients own lymphocytes, and stem cells injected, eventually replacing the immune system of the patient with that of the healthy donor.

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Cardiac Stem Cell Research – Cedars-Sinai

By raymumme

Results from a ground-breaking Cedars-Sinai Heart Institute clinical trial show that an infusion of cardiac stem cells helps damaged hearts regrow healthy muscle.

The first-in-man clinical trial, based on technologies and discoveries made by Eduardo Marbn, MD, PhD, and led by Raj Makkar, MD, explored the safety of harvesting, growing and giving patients their own cardiac stem cells to repair heart tissue injured by heart attack.

The studys findings, published in The Lancet, show that heart attack patients who received stem cell treatment demonstrated a significant reduction in the size of the scar left on the heart muscle; this is a pioneering stem cell result, says Marban, who notes the study shows actual regeneration of tissues. With support from the California Institute for Regenerative Medicine, the Heart Institute team is now planning future clinical trials to treat advanced heart disease patients with stem cells.

The process to grow cardiac-derived stem cells involved in the study was developed earlier by Marbn when he was on the faculty of Johns Hopkins University. The university has filed for a patent on that intellectual property, and has licensed it to a company in which Marbn has a financial interest. No funds from that company were used to support the clinical study. All funding was derived from the National Institutes of Health and Cedars-Sinai Medical Center.

Since the Cedars-Sinai team completed the worlds first cardiac stem cell infusion in 2009, additional insights have emerged from this and related work, including the discovery in animals that iron-infused cardiac stem cells can be guided with a magnet to damaged areas of the heart, dramatically increasing their retention and healing potential.

Another finding to emerge from Marbns cardiac stem cell lab may have implications for many peoples health: Stem cells exposed to high doses of supplemental antioxidants can develop genetic abnormalities that predispose them to cancer formation.

Click here to watch a CBS Evening News story about the clinical trials results.

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9. Can Stem Cells Repair a Damaged Heart? [Stem Cell Information]

By daniellenierenberg

Heart attacks and congestive heart failure remain among the Nation's most prominent health challenges despite many breakthroughs in cardiovascular medicine. In fact, despite successful approaches to prevent or limit cardiovascular disease, the restoration of function to the damaged heart remains a formidable challenge. Recent research is providing early evidence that adult and embryonic stem cells may be able to replace damaged heart muscle cells and establish new blood vessels to supply them. Discussed here are some of the recent discoveries that feature stem cell replacement and muscle regeneration strategies for repairing the damaged heart.

For those suffering from common, but deadly, heart diseases, stem cell biology represents a new medical frontier. Researchers are working toward using stem cells to replace damaged heart cells and literally restore cardiac function.

Today in the United States, congestive heart failurethe ineffective pumping of the heart caused by the loss or dysfunction of heart muscle cellsafflicts 4.8 million people, with 400,000 new cases each year. One of the major contributors to the development of this condition is a heart attack, known medically as a myocardial infarction, which occurs in nearly 1.1 million Americans each year. It is easy to recognize that impairments of the heart and circulatory system represent a major cause of death and disability in the United States [5].

What leads to these devastating effects? The destruction of heart muscle cells, known as cardiomyocytes, can be the result of hypertension, chronic insufficiency in the blood supply to the heart muscle caused by coronary artery disease, or a heart attack, the sudden closing of a blood vessel supplying oxygen to the heart. Despite advances in surgical procedures, mechanical assistance devices, drug therapy, and organ transplantation, more than half of patients with congestive heart failure die within five years of initial diagnosis. Research has shown that therapies such as clot-busting medications can reestablish blood flow to the damaged regions of the heart and limit the death of cardiomyocytes. Researchers are now exploring ways to save additional lives by using replacement cells for dead or impaired cells so that the weakened heart muscle can regain its pumping power.

How might stem cells play a part in repairing the heart? To answer this question, researchers are building their knowledge base about how stem cells are directed to become specialized cells. One important type of cell that can be developed is the cardiomyocyte, the heart muscle cell that contracts to eject the blood out of the heart's main pumping chamber (the ventricle). Two other cell types are important to a properly functioning heart are the vascular endothelial cell, which forms the inner lining of new blood vessels, and the smooth muscle cell, which forms the wall of blood vessels. The heart has a large demand for blood flow, and these specialized cells are important for developing a new network of arteries to bring nutrients and oxygen to the cardiomyocytes after a heart has been damaged. The potential capability of both embryonic and adult stem cells to develop into these cells types in the damaged heart is now being explored as part of a strategy to restore heart function to people who have had heart attacks or have congestive heart failure. It is important that work with stem cells is not confused with recent reports that human cardiac myocytes may undergo cell division after myocardial infarction [1]. This work suggests that injured heart cells can shift from a quiescent state into active cell division. This is not different from the ability of a host of other cells in the body that begin to divide after injury. There is still no evidence that there are true stem cells in the heart which can proliferate and differentiate.

Researchers now know that under highly specific growth conditions in laboratory culture dishes, stem cells can be coaxed into developing as new cardiomyocytes and vascular endothelial cells. Scientists are interested in exploiting this ability to provide replacement tissue for the damaged heart. This approach has immense advantages over heart transplant, particularly in light of the paucity of donor hearts available to meet current transplantation needs.

What is the evidence that such an approach to restoring cardiac function might work? In the research laboratory, investigators often use a mouse or rat model of a heart attack to study new therapies (see Figure 9.1. Rodent Model of Myocardial Infarction). To create a heart attack in a mouse or rat, a ligature is placed around a major blood vessel serving the heart muscle, thereby depriving the cardiomyocytes of their oxygen and nutrient supplies. During the past year, researchers using such models have made several key discoveries that kindled interest in the application of adult stem cells to heart muscle repair in animal models of heart disease.

Figure 9.1. Rodent Model of Myocardial Infarction.

( 2001 Terese Winslow, Lydia Kibiuk)

Recently, Orlic and colleagues [9] reported on an experimental application of hematopoietic stem cells for the regeneration of the tissues in the heart. In this study, a heart attack was induced in mice by tying off a major blood vessel, the left main coronary artery. Through the identification of unique cellular surface markers, the investigators then isolated a select group of adult primitive bone marrow cells with a high capacity to develop into cells of multiple types. When injected into the damaged wall of the ventricle, these cells led to the formation of new cardiomyocytes, vascular endothelium, and smooth muscle cells, thus generating de novo myocardium, including coronary arteries, arterioles, and capillaries. The newly formed myocardium occupied 68 percent of the damaged portion of the ventricle nine days after the bone marrow cells were transplanted, in effect replacing the dead myocardium with living, functioning tissue. The researchers found that mice that received the transplanted cells survived in greater numbers than mice with heart attacks that did not receive the mouse stem cells. Follow-up experiments are now being conducted to extend the posttransplantation analysis time to determine the longer-range effects of such therapy [8]. The partial repair of the damaged heart muscle suggests that the transplanted mouse hematopoietic stem cells responded to signals in the environment near the injured myocardium. The cells migrated to the damaged region of the ventricle, where they multiplied and became "specialized" cells that appeared to be cardiomyocytes.

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Grant Funds Research Into Cardiac Stem Cells as Treatment for Heart Disease Related to Duchenne Muscular Dystrophy

By LizaAVILA

Newswise LOS ANGELES May 30, 2013 Newport Beach-based nonprofit Coalition Duchenne has awarded a $150,000 grant to a Cedars-Sinai Heart Institute team investigating whether an experimental cardiac stem cell treatment could be used to treat Duchenne muscular dystrophy patients who have developed heart disease.

Coalition Duchenne is led by Catherine Jayasuriya, a mother whose 20-year-old son, Dusty Brandom, has cardiomyopathy associated with Duchenne muscular dystrophy. She was inspired to underwrite cardiac stem cell research at Cedars-Sinai after reading about a successful clinical trial led by Eduardo Marbn, MD, PhD, director of the Cedars-Sinai Heart Institute and the Mark S. Siegel Family Professor.

The experimental stem cell therapy, developed by Marbn, is the only treatment shown in clinical trials to regenerate healthy heart muscle. In the clinical trial, patients underwent biopsies during which doctors removed a piece of heart muscle about the size of half a raisin. The heart tissue was then used to grow specialized heart stem cells, which then were injected back into the patients heart. Results published in The Lancet showed that patients experienced an average 50 percent reduction in muscle damaged by heart attack.

I immediately sensed the potential for applying this rapidly evolving treatment to Duchenne, said Jayasuriya. I made it my personal quest to help get this kind of therapy for Duchenne patients.

Jayasuriyas commitment was further cemented when she discovered that Ron Victor, MD, associate director of the Cedars-Sinai Heart Institute, has been working with Duchenne patients as part of his investigation of the cardiac benefits of sildenafil (Viagra) and tadalafil (Cialis).

We know that boys with Duchenne are born with a small scar in the base of their heart, said Victor, the Burns and Allen Chair in Cardiology Research at the Cedars-Sinai Heart Institute. The damage to hearts in boys with Duchenne increases over time. If we can use stem cells to slow or stop heart damage, it could help stall progression of the disease.

The first step in the study is to examine the effect of injecting cardiac stem cells into the hearts of mice with Duchenne. If the data is positive, the experimental treatment could be rapidly approved for use in humans with Duchenne because of cardiac stem cell treatments have been approved for other patient populations, including those with advanced heart disease.

Each year, 20,000 boys are born with Duchenne, Jayasuriya said, who founded Coalition Duchenne in 2010 to raise global awareness for Duchenne muscular dystrophy, fund research and find a cure for Duchenne. Many do not live into their 20s and we lose many to cardiac issues. We need to focus on changing the course of the disease. We hope that working with cardiac stem cells is one way we will eventually change that outcome.

Duchenne muscular dystrophy is a progressive muscle-wasting disease and the most common fatal disease that affects children. Duchenne occurs in one in 3,500 male births, across all races, cultures and countries. Duchenne is caused by a defect in the gene that produces the protein dystrophin, which helps connect the muscle fiber to the cell membranes. Without dystrophin, muscle cells become unstable, are weakened and lose their functionality. Life expectancy of boys and young men with Duchenne ranges from the mid-teens to the mid-20s. Their minds are unaffected.

The Cedars-Sinai Heart Institute is internationally recognized for outstanding heart care built on decades of innovation and leading-edge research. From cardiac imaging and advanced diagnostics to surgical repair of complex heart problems to the training of the heart specialists of tomorrow and research that is deepening medical knowledge and practice, the Cedars-Sinai Heart Institute is known around the world for excellence and innovations.

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