April 19, 2012 by

Legendary Texas Football Coach and Stem Cell Recipient Sam Harrell Returns to Coaching

Sam Harrell Stem Cell Patient for MS

Coach Sam Harrell at Ennis High School

In 2010, the debilitating effects of multiple sclerosis forced Sam Harrell to retire from his position as Head Football Coach at Ennis High School. But after receiving 3 courses of stem cell therapy at the Stem Cell Institute in Panama, Sam is returing to the gridiron once again.

Brownwood Lion Head Coach, Bob Shipley announced that Harrell will be joining the team as quarterback coach.

Sam coached all three of his sons at Ennis High School, most notably his son Graham Harrell. Graham was a standout quarterback at Texas Tech and now plays for the Green Bay Packers.

During his career at Ennis, Harrell pioneered the spread offense that led the team to three Texas state championships.

“I told the kids this morning,” said Coach Shipley when asked about how he addressed the team, “And I didn’t have to explain who Sam Harrell was, they knew. And they just erupted in applause and they were just looking at each other with their jaws dropped open, like they couldn’t believe that Coach Harrell was going to come and be apart of our staff.”

“Sam just really liked the thought of coming and not being the head coach and not being the offensive coordinator, but just coaching the quarterbacks, which is really what his passion is.”

The Stem Cell Institute was founded in 2005 by Neil Riordan PhD and has treated over 1,500 patients to-date. Find out more about stem cell therapy for MS at www.cellmedicine.com

Filed Under: Multiple Sclerosis, News, Stem Cell Research Tagged With: , , , , , , , ,
April 18, 2012 by

Quality time: Former Ennis coach Sam Harrell is counting his blessings despite having multiple sclerosis

ENNIS, TX — Sam Harrell’s three state football championships are celebrated in his home office. He has pictures, trophies and balls, and even more memories.

For 32 years, Harrell worked in a profession where success is measured by a scoreboard in front of thousands.

These days, life’s little victories — unaccompanied by cheers or Gatorade showers — are just as satisfying.

Harrell can jump up and down in his living room. He can walk across a parking lot without a cane or a walker. He can spend hours at Kolache Depot Bakery without getting fatigued.

Harrell hasn’t beaten multiple sclerosis, but he is successfully living with it.

“It puts everything in perspective,” Harrell said. “Now, I’d rather play catch with my grandson in the back yard than win a state championship. When that gets taken away from you, you realize how precious it is.”

Harrell was 153-51 in 16 seasons at Ennis, winning Class 4A state titles in 2000, ’01 and ’04. He coached all three of his sons — Graham, now a backup quarterback with the Green Bay Packers; Zac, the offensive coordinator at Van High School; and Clark, who finished his college career at Abilene Christian in 2010 and now works as a financial planner.

It was in 2005, while he was on the tennis court, that Harrell’s vision in one eye became blurry. An eye specialist sent him to a neurologist, who, after running tests, gave Harrell the best possible diagnosis: He had MS.

“I didn’t know whether I was supposed to cheer or cry,” Harrell said. “I got the best of the three things it could be, but the bad news is: I have MS.”

Multiple sclerosis is a chronic, unpredictable disease that affects the central nervous system. The immune system eats away the myelin sheath surrounding the nerves. Symptoms vary from person to person. Mild symptoms include numbness in the limbs, weakness, fatigue and blurred vision. Severe symptoms include paralysis and loss of vision.

There is no known cure for MS.

Harrell chose to keep the news a secret from everyone except his wife, Kathy. He didn’t reveal the diagnosis for four years, though, as his condition worsened, those close to Harrell knew something was wrong.

“We’d go to practice, and he had to take a golf cart,” Graham Harrell said in a phone interview after a recent Packers practice. “Sometimes he was off balance a little bit, or shaky walking. So there were times we knew something wasn’t quite right, but we didn’t know exactly what was going on until he finally told us.

“It was hard to watch, obviously, especially with him wanting to coach, and yet not being able to do it like he used to. But recently, he’s seen great improvement, and that’s huge encouragement not only to him, but to us, and hopefully he’ll continue to get better.”

Sam Harrell knew his MS wouldn’t kill him, but he thought not coaching might.

Sam’s father, Jake, established the family business at Seminole, where he spent 20 seasons, including 10 as the head coach. But Sam Harrell’s health forced him to quit coaching before the 2010 season.

“That’s all I’d done my whole life,” Harrell said, “so I was sick about it. I just didn’t know what I was going to do.

“I do wish I could still do it, but I haven’t died from not coaching.”

Harrell, in fact, is alive and well. He credits three trips to Panama for his improved health.

After he retired from coaching, Harrell began researching regenerative medicine. Stem cell treatment is not approved in the United States, but Dr. Neil Riordan, who lives in Trophy Club, is the founder of the Stem Cell Institute in Panama.

Riordan is one of the leading stem cell scientists in the world.

Harrell talked to several of Riordan’s patients, including Richard Humphries, a golf coach out of Diamond Oaks Country Club in Fort Worth. Humphries was diagnosed with MS in 2005. He began stem cell treatments in 2008.

Stem cell treatments introduce new cells, which have regenerative potential, into damaged tissue to treat disease or injury.

“After talking to Richard, I didn’t have the money, but I knew I was going to go,” Harrell said. “I mean, what did I have to lose? I knew where I was headed if I didn’t go. I was going downhill fast. So why wouldn’t I go try this?”

Friends, family and fellow coaches held fundraisers for Harrell’s treatments. Harrell’s first trip to Panama, which was four weeks, cost $40,000. He has been back twice more, the last time in September.

It wasn’t until the third visit that Harrell saw dramatic results.

“MS is like a two-hump camel,” Humphries said. “You can get over the first hump of active T-Cells fairly easily, but the second hump, the memory T-Cells, sometimes bring our MS symptoms back, as it did with Sam.

“He was extremely disappointed for taking the two steps back after three steps forward. I told him it may take another two or three treatments to really get you going again. Needless to say, he could not stop smiling and was greatly relieved. Now, he is seeing the results.”

Harrell is a strong Christian and is quick to credit God and prayer for his recovery. But he also is a big believer in stem cell therapy. Kathy Harrell is a more recent convert.

She was skeptical until seeing the change in Harrell.

“I just feel really grateful that these are good days and good months, and I’m not going to worry about next year,” Kathy Harrell said. “It just makes you thankful that things are good right now, and he’s pretty mobile. This disease reminds you to just be thankful for the day, so that’s what we’re doing. I realize now it can be worse.”

By Charean Williams

Filed Under: Multiple Sclerosis, News, Stem Cell Research Tagged With: , , , ,
April 1, 2012 by

Great Day in Ft. Worth for Stem Cell Team

Stem cell patients and MS walk in Fort Worth

Stem Cell Institute patients participate in MS Walk 2012

Saturday, March 31 was the annual MS Walk in Ft Worth. This year, thanks to the Stem Cell Institute and some of the area stem cell patients, several of us MS sufferers and stem cell patients met for the Walk. Here’s a picture of several of us who have been to Panama, or Costa Rica, for treatments – (from L – R) Richard, Carolyn, Shelley, Carla, Judi, Holly, and me.

We wanted to give the Stem Cell Institute a presence in that sea of MS victims and caregivers. I wish all of them knew that many of us in those blue t-shirts were there walking, actually completing the whole mile, even though we were once unable to do such. I wanted to grab that microphone that the organizers were using and tell all of them “There is HOPE – it doesn’t have to be what you hear from your doctors so often. It can be more than ‘Let’s keep taking this medication so you might get worse at a slower rate’ ”

I personally never heard about the possibility of actually improving when I went to good doctors here in the US – but I chose to try the Stem Cell treatment in Panama, and I walked that mile on Saturday! A year ago, six months ago, I couldn’t have done that – but after my third trip to Panama in September, my walking, my balance, and my stamina all improved dramatically. And many of those in our group on Saturday have a similar story; some results more dramatic than others, but most all of us have seen and felt the changes that give us that Hope that all of those sufferers at the Walk are looking for.

THANKS STEM CELL INSTITUTE!

Sam Harrell
Sam in Panama

Filed Under: Adult Stem Cells, Multiple Sclerosis, News, Stem Cell Research Tagged With: , , , , , , ,
February 2, 2012 by

Autologous mesenchymal stem cells for the treatment of secondary progressive multiple sclerosis: an open-label phase 2a proof-of-concept study

Connick P, Kolappan M, Crawley C, Webber DJ, Patani R, Michell AW, Du MQ, Luan SL, Altmann DR, Thompson AJ, Compston A, Scott MA, Miller DH, Chandran S.

Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.

Abstract

BACKGROUND:
More than half of patients with multiple sclerosis have progressive disease characterised by accumulating disability. The absence of treatments for progressive multiple sclerosis represents a major unmet clinical need. On the basis of evidence that mesenchymal stem cells have a beneficial effect in acute and chronic animal models of multiple sclerosis, we aimed to assess the safety and efficacy of these cells as a potential neuroprotective treatment for secondary progressive multiple sclerosis.

METHODS:
Patients with secondary progressive multiple sclerosis involving the visual pathways (expanded disability status score 5·5-6·5) were recruited from the East Anglia and north London regions of the UK. Participants received intravenous infusion of autologous bone-marrow-derived mesenchymal stem cells in this open-label study. Our primary objective was to assess feasibility and safety; we compared adverse events from up to 20 months before treatment until up to 10 months after the infusion. As a secondary objective, we chose efficacy outcomes to assess the anterior visual pathway as a model of wider disease. Masked endpoint analyses was used for electrophysiological and selected imaging outcomes. We used piecewise linear mixed models to assess the change in gradients over time at the point of intervention. This trial is registered with ClinicalTrials.gov, number NCT00395200.

FINDINGS:
We isolated, expanded, characterised, and administered mesenchymal stem cells in ten patients. The mean dose was 1·6×10(6) cells per kg bodyweight (range 1·1-2·0). One patient developed a transient rash shortly after treatment; two patients had self-limiting bacterial infections 3-4 weeks after treatment. We did not identify any serious adverse events. We noted improvement after treatment in visual acuity (difference in monthly rates of change -0·02 logMAR units, 95% CI -0·03 to -0·01; p=0·003) and visual evoked response latency (-1·33 ms, -2·44 to -0·21; p=0·020), with an increase in optic nerve area (difference in monthly rates of change 0·13 mm(2), 0·04 to 0·22; p=0·006). We did not identify any significant effects on colour vision, visual fields, macular volume, retinal nerve fibre layer thickness, or optic nerve magnetisation transfer ratio.

INTERPRETATION:
Autologous mesenchymal stem cells were safely given to patients with secondary progressive multiple sclerosis in our study. The evidence of structural, functional, and physiological improvement after treatment in some visual endpoints is suggestive of neuroprotection.

FUNDING:
Medical Research Council, Multiple Sclerosis Society of Great Britain and Northern Ireland, Evelyn Trust, NHS National Institute for Health Research, Cambridge and UCLH Biomedical Research Centres, Wellcome Trust, Raymond and Beverly Sackler Foundation, and Sir David and Isobel Walker Trust.

Filed Under: Multiple Sclerosis, News, Stem Cell Research Tagged With: , , , , , , ,
January 18, 2012 by

Umbilical cord stem cells may lead to new spinal cord injury and multiple sclerosis treatments

Researchers in Florida have accomplished converting umbilical cord stem cells into other cell types. According to University of Central Florida bioengineer James Hickman, it’s the first time that non-embryonic cells have accomplished this feat. His research group published this work in the January 18th issue of ACS Chemical Neuroscience.

Two major benefits of umbilical cord-derived stem cells are that they have not been shown to cause adverse immune system reactions and they pose no ethical issues since they come from a source that would be naturally discarded anyway.

Hedvika Davis, a post-doc researcher and lead author of the paper, had to search for the right chemical to coax the stem cells into becoming oligodendrocytes, which are cells that insulate nerves residing in the brain and spinal cord.

Other researchers had already shown that oligodendrocytes bind with a hormone called norepinephrine and Davis theorized that this could be the key. So she used norepinephrine and other growth factors to induce the cells to differentiate into oligodendrocytes. The only problem was that the cells were not sufficiently developed as they would be in the body.

So Davis devised a novel approach of approximating the body’s environment in the lab. By growing the cells on top of a slide, with another slide on top, Davis was able to simulate a 3-dimensional environment and grow mature oligodendrocytes.

Because oligodendrocytes produce myelin, researcher believe that this discovery might lead to treatments for multiple sclerosis, spinal cord injury and diabetic neuropathy.

Filed Under: Adult Stem Cells, Cord Blood Stem Cells, Multiple Sclerosis, News, Spinal Cord Injury, Stem Cell Research Tagged With: , , , , , ,
January 16, 2012 by

Blood from young mice helps older mice with multiple sclerosis

A new mouse study has shown that blood from young mice helps old mice to heal damage caused by MS.

MS causes myelin, which insulates nerve cells electrically, to become damaged. Stem cells can produce myelin but they lose efficiency in older patients.

Researchers in the UK have found a way to reverse this age-related efficiency loss. By linking the bloodstreams of young mice to old mice with myelin damage, the older stem cells were reactivated and boosted myelin production.

White blood cells from the young mice called macrophages were found at myelin damage sites in the old mice. These cells engulf and destroy pathogens and debris, including destroyed myelin.

Amy Wagers, from Harvard University says, “We know this debris inhibits regeneration, so clearing it up is important.”

Filed Under: Multiple Sclerosis, News, Stem Cell Research Tagged With: , , , , ,
January 6, 2012 by

Stem Cells May Reverse Age-Related Multiple Sclerosis Effects

Proof-of-principle study provides hope for stimulating remyelination

Scientists at Joslin Diabetes Center, Harvard University, and the University of Cambridge have found that the age-related impairment of the body’s ability to replace protective myelin sheaths, which normally surround nerve fibers and allow them to send signals properly, may be reversible, offering new hope that therapeutic strategies aimed at restoring efficient regeneration can be effective in the central nervous system throughout life.

In a proof-of-principle study published in the journal Cell Stem Cell, the researchers report that defects in the regeneration of the myelin sheaths surrounding nerves, which are lost in diseases such as multiple sclerosis may be at least partially corrected following exposure of an old animal to the circulatory system of a young animal. Myelin is a fatty substance that protects nerves and aids in the quick transmission of signals between nerve cells.

Using a surgical technique, the researchers introduced an experimental demyelinating injury in the spinal cord of an old mouse, creating small areas of myelin loss, and then exposed those areas to cells found the blood of a young mouse. By doing so, they found that the influx of certain immune cells, called macrophages, from the young mouse helped resident stem cells restore effective remyelination in the old mouse’s spinal cord. This “rejuvenating” effect of young immune cells was mediated in part by the greater efficiency of the young cells in clearing away myelin debris created by the demyelinating injury. Prior studies have shown that this debris impedes the regeneration of myelin.

“Aging impairs regenerative potential in the central nervous system,” says author Amy J. Wagers, PhD, an associate professor of stem cell and regenerative biology at Harvard University and Joslin, who co-led the study with Professor Robin Franklin, director of the MS Society’s Cambridge Centre for Myelin Repair at the University of Cambridge. “This impairment can be reversed, however, suggesting that the eventual development of cell-based or drug-based interventions that mimic the rejuvenation signals found in our study could be used therapeutically.”

This could be particularly useful, she adds, in treating MS, which typically spans many decades of life, and thus is likely to be influenced by age-dependent reductions in the ability of myelin to regenerate. In MS, the body’s own immune system attacks the myelin sheath and prevents nerve fibers in the brain from sending signals properly, which can cause mild symptoms such as limb numbness or more serious ones like losing the ability to walk or speak. As people with MS age, remyelination decreases significantly, eventually causing permanent loss of nerve fibers.

“For MS sufferers,” says Franklin, “this means that, in theory, regenerative therapies will work throughout the duration of the disease. Specifically, it means that remyelination therapies do not need to be based on stem cell transplantation since the stem cells already present in the brain and spinal cord can be made to regenerate myelin, regardless of a person’s age.”

Other Joslin co-authors of the study were Tata Nageswara Rao and Jennifer L. Shadrach.

About Joslin Diabetes Center
Joslin Diabetes Center, located in Boston, Massachusetts, is the world’s preeminent diabetes research and clinical care organization. Joslin is dedicated to ensuring that people with diabetes live long, healthy lives and offers real hope and progress toward diabetes prevention and a cure. Joslin is an independent, nonprofit institution affiliated with Harvard Medical School.

Filed Under: Multiple Sclerosis, Multiple Sclerosis, News, Stem Cell Research, Stem Cell Therapy Tagged With: , , , , , , , , ,
April 12, 2011 by

Immune Cells Killing Stem Cells and Stem Cells Killing Immune Cells

Knight et al. J Neurol Sci.
Several studies have demonstrated that stem cells are useful in the treatment of multiple sclerosis. The Cellmedicine clinic published previously in collaboration with the University of California San Diego that 3 patients treated with their own fat derived stem cells entered remission. Other studies are ongoing, including a study at the Cleveland Clinic in which bone marrow stem cells differentiated into mesenchymal stem cells are being administered into patients with multiple sclerosis. Unfortunately the mechanisms by which therapeutic effects occur are still largely unknown. One general school of thought believes that stem cells are capable of differentiating into damaged brain cells. The other school of thought believes that stem cells are capable of producing numerous growth factors, called trophic factors, that mediate therapeutic activity of the stem cells. Yet another school of thought propagates the notion that stem cells are merely immune modulatory cells. Before continuing, it is important to point out that stem cell therapy for multiple sclerosis involving autologous hematopoietic transplants is different than what we are discussing here. Autologous (your own) hematopoietic stem cell therapy is not based on regenerating new tissues, but to achieve the objective of extracting cells from a patients, purifying blood making (hematopoietic) stem cells, destroying the immune system of the recipient so as to wipe out the multiple sclerosis causing T cells, and subsequently readministering the patient’s own cells in order to regenerate the immune system. This approach, which was made popular by Dr. Richard Burt from Northwestern University.
In order to assess mechanisms of how stem cells work in multiple sclerosis it is necessary to induce the disease in animals. The most widely used animal model of multiple sclerosis is the experimental allergic encephalomyelitis model. This disease is induced in female mice that are genetically bred to have a predisposition to autoimmunity. These animals are immunized with myelin basic protein or myelin oligodendrocyte protein. Both of these proteins are components of the myelin sheath that protects the axons. In multiple sclerosis immune attack occurs against components of the myelin sheath. Therefore immunizing predisposed animals to components of the myelin sheath induces a disease similar to multiple sclerosis. The EAE model has been critical in development of some of the currently used treatments for multiple sclerosis such as copaxone and interferon.
Original studies have demonstrated that administration of bone marrow derived mesenchymal stem cells protects mice from development of EAE. This protection was associated with regeneration on oligodendrocytes as well as shifts in immune response. Unfortunately these studies did not decipher whether the protective effects of the stem cells were mediated by immune modulation, regeneration, or a combination of both. Other studies have shown that MSC derived from adipose tissue had a similar effect. One interesting point of these studies was that the stem cell source used was of human origin and the recipient mice were immune competent. One would imagine that administration of human cells into a mouse would result in rapid rejection. This did not appear to be the case since the human cells were found to persist and also to differentiated into human neural tissues in the mouse. One mechanism for this “immune privilege” of MSC is believed to be their low expression of immune stimulatory molecules such as HLA antigens, costimulatory molecules (CD80/86) and cytokines capable of stimulating inflammatory responses such as IL-12. Besides not being seen by the immune system, it appears that MSC are involved in actively suppressing the immune system. In one study MSC were demonstrated to naturally home into lymph nodes subsequent to intravenous administration and “reprogram” T cells so as to suppress delayed type hypersensitive reactions. In those experiments scientists found that the mechanism of MSC-mediated immune inhibition was via secretion of nitric oxide. Other molecules that MSC use to suppress the immune system include soluble HLA-G, Leukemia Inhibitor Factor (LIF), IL-10, interleukin-1 receptor antagonist, and TGF-beta. MSC also indirectly suppress the immune system by secreting VEGF which blocks dendritic cell maturation and thus prevents activation of mature T cells.
While a lot of work has been performed investigating how MSC suppress the immune system, relatively little is known regarding if other types of stem cells, or immature cells, inhibit the immune system. This is very relevant because there are companies such as Stem Cells Inc that are using fetally-derived progenitor cells therapeutically in a universal donor fashion. There was a paper from an Israeli group demonstrating that neural progenitors administered into the EAE model have a therapeutic effect that is mediated through immune modulation, however, relatively little work has been performed identifying the cell-to-cell interactions that are associated with such immune modulation.
Recently a paper by Knight et al. Cross-talk between CD4(+) T-cells and neural stem/progenitor cells. Knight et al. J Neurol Sci. 2011 Apr 12 attempted to investigate the interaction between immune cells and neural stem cells and vice versa. The investigators developed an in vitro system in which neural stem cells were incubated with CD 4 cells of the Th1 (stimulators of cell mediated immunity), Th2 (stimulators of antibody mediated immunity) and Th17 (stimulators of inflammatory responses) subsets. In order to elucidate the impact of the death receptor (Fas) and its ligand (FasL), the mouse strains lpr and gld, respectively, were used.
The investigators showed that Th1 type CD4 cells were capable of directly killing neural stem cells in vitro. Killing appeared to be independent of Fas activation on the stem cells since gld derived T cells or lpr derived neural stem cells still participated in killing. Interestingly, neural stem cells were capable of stimulating cell death in Th1 and Th17 cells but not in the Th2 cells. Killing was contact dependent and appeared to be mediated by FasL expressed on the neural stem cells. This is interesting because some other studies have demonstrated that FasL found on hematopoietic stem cells appears to kill activated T cells. In the context of hematopoietic stem cells this phenomena may be used to explain clinical findings that transplanting high numbers of CD34 cells results in a higher engraftment, mediated in part by killing of recipient origin T cells.
The finding that neural stem cells express FasL and selectively kill inflammatory cells (Th1 and Th17) while sparing anti-inflammatory cells (Th2) indicates that the stem cells themselves may be therapeutic by exerting an immune modulatory effect. One thing that the study did not do is to see if differentiated neural stem cells would mediate the same effect. In other words, it is essentially to know if the general state of cell immaturity is associated with inhibition of inflammatory responses, or whether this is an activity specific to neurons. As mentioned above, previous studies have demonstrated that mesenchymal stem cells (MSC) are capable of eliciting immune modulation through a similar means. Specifically, MSC have been demonstrated to stimulate selective generation of T regulatory cells. This cell type was not evaluated in the current study, however some activities of Th2 cells are shared with Treg cells in that both are capable of suppressing T cytotoxic cell activation. In the context of explaining biological activities of stem cell therapy studies such as this one stimulate the believe that stem cells do not necessarily mediate their effects by replacing damaged cells, but by acting on the immune system. Theoretically, one of the reasons why immature cells are immune modulatory in the anti-inflammatory sense may be because inflammation is associated with oxidative stress. Oxidative stress is associated with mutations. Conceptually, the body would want to preferentially protect the genome of immature cells given that the more immature the cells are, the more potential they have for stimulation of cancer. Mature cells have a limited self renewal ability, whereas immature cells, given they have a higher potential for replication are more likely to accumulate genomic damage and neoplastically transform.

Filed Under: Adult Stem Cells, Multiple Sclerosis, Multiple Sclerosis, News, Stem Cell Research, Stem Cell Therapy Tagged With: , , , , , , , , , , , ,
December 30, 2009 by

Stem Cells Might Reverse Heart Damage From Chemo

One of the great findings of regenerative medicine was that organs previously believed to be incapable of healing themselves actually contain stem cells that in response to injury cause some degree of healing. The problem being that these "endogenous healing mechanisms" are usually too small to mediate effects that are visible at the clinical level. For example, the brain was considered to have very limited ability to heal itself after damage. Recent studies that have allowed for observation of brain cells after experimental strokes have led to the discovery of brain stem cells in the dendate gyrus and subventricular zones of the brain, stem cells that start to multiple after a stroke. Interestingly, various hormones such as human chonrionic gonadotropin, are capable of stimulating brain stem cell multiplication. This is currently being used in clinical trials for stroke by the company Stem Cell Therapeutics.

In the area of heart failure, it was also believed that once cardiac tissue is damaged, the only repair process that the body performs is production of scar tissue, which is pathological to the patient. While this scar tissue is found in the majority of the injured area, molecular studies have revealed the existence of cardiac specific stem cells, which start to multiply after injury and serve to repair, albeit in small amounts, the infarct area.

One way to augment endogenous repair processes is to administer stem cells from the bone marrow, which are known to produce various growth factors that assist the tissue-specific stem cell in mediating its activity. Another way is to physically extract the tissue specific stem cells, expand them outside of the body and reimplant them into the damaged area.

In a recent publication in the journal Circulation, Piero Anversa, M.D., director, Center for Regenerative Medicine, Departments of Anesthesia and Medicine and Cardiovascular Division, Brigham and Women’s Hospital, Boston and Roberto Bolli, M.D., chief, cardiology, and director, Institute of Molecular Cardiology, University of Louisville, Kentucky, describe the use of cardiac specific stem cells in treatment of animals whose hearts of been damaged by the chemotherapeutic drug doxorubicin.
Doxorubicin is a chemotherapeutic drug that is mainly used in the treatment of breast, ovarian, lung, and thyroid cancers, as well as for neuroblastoma, lymphoma and leukemia. One of the main limiting factors to increasing the dose of doxorubicin to levels that can lead to tumor eradication is that it causes damage to the heart muscle, the myocardium.

In the published study, the investigators expanded the cardiac specific stem cells from rats, gave the rats high doses of doxorubicin and in some rats injected back cardiac specific stem cells, whereas other rats received control cells. The rats that received the cardiac specific stem cells had both preservation of cardiac function, and also regeneration of the damaged heart tissue. This is an important finding since the type of damage that doxorubicin does to the heart is different from other types of heart damage that have been studies, such as the damage that occurs after a heart attack. These data seem to suggest that stem cell therapy may be useful in a variety of injury situations.

"Theoretically, patients could be rescued using their own stem cells," said study author Dr. Piero Anversa, director of the Center for Regenerative Medicine at Brigham and Women’s Hospital in Boston. Dr. Aversa is one of the original discoverers of the cardiac specific stem cell when he published experiments in dogs demonstrating multiplication of cells in the myocardium that seem to have ability to generate new tissue after damage (Linke et al. Stem cells in the dog heart are self-renewing, clonogenic, and multipotent and regenerate infarcted myocardium, improving cardiac function. Proc Natl Acad Sci U S A. 2005 Jun 21;102(25):8966-71).

"A Phase 1 clinical trial using a similar procedure in people is already under way", said Dr. Roberto Bolli, chief of cardiology and director of the Institute of Molecular Cardiology at the University of Louisville in Kentucky, who is heading the trial. The FDA has approved a Phase I clinical trial using cardiac specific stem cells in 30 patients who have congestive heart failure due to disseminated atherosclerosis. "In the trial, participants’ cardiac tissue will be harvested, the stem cells isolated and then expanded in vitro from about 500 cells to 1 million cells over several weeks", Bolli explained. "Several months after the patient has undergone bypass surgery, the stem cells will be re-injected." A similar clinical trial is being performed at Cedars Sinai in Los Angeles.

While the problems of tissue extraction (which is performed by an invasive procedure requiring biopsy of heart tissue) and cost of expansion are still formidable hurdles to widespread implementation, it is believed that the clinical evidence of a therapeutic response will open the door to other avenues of expanding tissue specific stem cells, such as administration of growth factors that can accomplish this without need for cell extraction outside of the body.

Filed Under: Adult Stem Cells, Multiple Sclerosis, News, Stem Cell Research, Stem Cells, Uncategorized Tagged With: , , , , ,
December 11, 2009 by

Stem Cell Therapy Aids the Return of Lava Man

Lava Man is a race horse that has had quite a career: he has earned more than $5.2 million and was considered one of the top racehorses in North America. Unfortunately, the recent past has not been to kind to him. Last year he finished last in the 2008 Eddie Read Handicap at Del Mar, and previous to that he has lost a series of six races in a row. Lava Man had arthritis in the joints in his ankles and a small fracture in his left front leg, Being 7 years old at that time, his owners decided it was time for Lava Man to retire.

However it seems like Lava Man’s fortunes may have changed. 17 months after his last race, he is scheduled to make a come-back this Saturday at Hollywood Park in the Native Diver Handicap. The horse was treated with his own fat derived stem cells by Dr. Doug Herthel, who stated:

"The trainer is the only one who can tell you how he’s going to run Saturday, but as far as the way he looks and based on our experience with other horses, theoretically, he should be much better than he was," said Dr. Doug Herthel, who treated Lava Man at the Alamo Pintado Equine Medical Center in Los Olivos, Calif.

"We think of those stem cells as little paramedics," Herthel said. "They go in and they help; they enhance the health of the cartilage." Dr. Herthel stated that significant improvements have occurred in Lava Man following stem cell therapy. He also stated that if Lava Man makes a triumphant return due to stem cells, this would not be the first case of this occurring. He cited the example of Ever A Friend , a 6-year-old horse, who was injured in May 2008, received the same type of fat derived stem cells as Lava Man and returned to win an allowance race and finish second in the Grade I Citation Handicap.

The fat derived stem cells that are being used in the treated of horses appear to work through several mechanisms. On the one hand they can become new cartilage and bone tissue directly, while on the other hand the stem cells producing various growth factors that accelerate the process of healing. Another method, that is more debated amongst scientists, is that the stem cells can actually produce enzymes that degrade scar tissue and allow replacement with functional tissue.

Human use of fat stem cells has been performed for multiple sclerosis (Riordan et al. Non-expanded adipose stromal vascular fraction cell therapy for multiple sclerosis. J Transl Med. 2009 Apr 24;7:29) and is currently being investigated for other conditions such as heart failure and rheumatoid arthritis.

Filed Under: Adult Stem Cells, Multiple Sclerosis, News, Stem Cell Research, Stem Cells, Uncategorized Tagged With: , , , , ,
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