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Wiring the Brain: The Trouble with Epigenetics (Part 1)

Posted: October 19, 2015 at 5:42 pm

You keep using that word. I do not think it means what you think it means. The insightful Inigo Montoya.

Epigenetics is a word that seems to have caught the public imagination. This is especially true among those, both in science and without, who decry what they see as genetic determinism or at least an overly genocentric point of view. Our genes are not our fate, because epigenetics! Such-and-such disorder is not really genetic, because epigenetics! Acquired characteristics can be inherited, because epigenetics!

This molecular biology definition has really only a loose relationship to Waddingtons usage. It is obviously true that molecular mechanisms of gene regulation effect (as in mediate) the development of an organism. That is what cellular differentiation and coordinated organismal development entail. Genes are turned on, genes are turned off. Epigenetic mechanisms make the profiles of gene expression that define a particular cell type more stable, with different sets of genes held in active or inactive chromatin conformations. These two usages thus relate to very different levels one refers to the profile of gene expression of individual cell types and the other to the emergence of the phenotype of the organism.

Now, clearly, the phenotype of an organism depends largely (though by no means completely) on the profile of gene expression of its constituent cells. And there are indeed a number of examples where the behavioural phenotype of an organism has been linked to the epigenetic state of particular genes in cells in particular brain regions. Importantly, such mechanisms may provide one means whereby environmental factors or particular experiences can have long-lasting effects on an organism, by changing patterns of gene expression in particular cells in a stable manner.

Based on these kinds of examples, epigenetics has become quite a buzz-word in the fields of psychiatric and behavioural genetics, as if it provides a general molecular mechanism for all the non-genetic factors that influence an individuals phenotype.

The fact that environmental factors or extreme experiences can influence an organisms phenotype is not news. In specific cases like those described above, the effects of such factors may indeed be mediated by molecular epigenetic mechanisms. But heres the important thing even though epigenetic mechanisms may be involved in maintaining some stable traits over the lifetime of the animal, they are just that: mechanisms. Not causes. Epigenetics is not a source of variance, it is part of the mechanism whereby certain environmental factors or experiences have their effects. Furthermore, these few examples do not imply that this mechanism is involved in mediating the effects of non-genetic sources of variance more generally.

So, while epigenetic mechanisms may indeed play a role in the stable expression of certain behavioural tendencies (at least in rodents), it remains unclear how general this phenomenon is. In any case, there is no reason to think of epigenetics as a source or cause of phenotypic variance at the level of the organism. And here is a plea: if you are tempted to use the term epigenetic, make it clear which meaning you intend. If you simply mean non-genetic, there is a more precise term for this: non-genetic.

In part 2, I consider a more egregious trend emerging in the literature of late the idea that transgenerational epigenetic inheritance can provide a mechanism of heredity that explains the so-called missing heritability of psychiatric disorders. (It cant).

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Wiring the Brain: The Trouble with Epigenetics (Part 1)

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Stem Cell Therapy | Dr Jeff Bradstreet, MD, MD(H), FAAFP

Posted: October 19, 2015 at 5:44 am

On this blog I have been writing about stem cells, hyperbaric oxygen (HBOT), and some incredible new observations related to reversing brain inflammation. All of the diseases I listed above and a whole bunch more are tied to persistent inflammation. Inflammation itself is very important to the body. In a healthy person it doesnt persist. It comes in response injury or infection cleans that up then stem cells communicate the need to stop the inflammation and heal. To that extent, these chronic persistent inflammatory conditions are the result of a failure of stem cells to do their job to counter inflammation. I will explain what is keeping them out of the process below and in future posts.

As this following picture demonstrates, the balance of inflammation regulation in the brain is complicated, intricate and precarious. But science has reached a point where we understand a large portion of the regulatory pathways.

[Frontiers in Bioscience 14, 5291-5338, June 1, 2009]

Caption: Microglia are the primary recipients of peripheral inflammatory signals as they reach the brain. Activated microglia initiate an inflammatory cascade by releasing cytokines, chemokines, prostaglandins and reactive nitrogen and oxygen species (RNS and ROS, respectively). Bi-directional exchanges between microglia and astroglia amplify inflammatory signals within the central nervous system (CNS). Cytokines including interleukin (IL)-1, IL-6, tumor necrosis (TNF)-alpha and interferon (IFN)-gamma induce indoleamine 2,3 dioxygenase (IDO), the enzyme responsible for degrading tryptophan, the primary precursor of serotonin (5-HT), into kynurenine, which is eventually metabolized into quinolinic acid (QUIN), a potent NMDA agonist and stimulator of glutamate (Glu) release. Multiple astrocytic functions are compromised due to the excessive exposure to cytokines, prostaglandins, QUIN and RNS/ROS, ultimately leading to downregulation of glutamate transporters, impaired glutamate reuptake, excessive glutamate release and compromised synthesis and release of neurotrophic factors. Oligodendroglia suffer damage due to toxic overexposure to cytokines such as TNF-alpha, and diminished neurotrophic support, both of which promote apoptosis and demyelination. Copious amounts of glutamate are released from astrocytes in the vicinity of extrasynaptic NMDA receptors, whose activation leads to inhibition of BDNF synthesis. Excessive NMDA activation, caused by QUIN and D-serine, is compounded by diminished glutamate reuptake by astrocytes and oligodendroglia. NMDA-mediated excitotoxicity, combined with a consequent decline in neurotrophic support, and an increase in oxidative stress, synergistically disrupts neural plasticity and induces apoptosis (cell death).

So it doesnt matter if we are talking about autism, post-stroke inflammation, Alzheimers, HIV dementia; the central mechanism is largely the same.

Now this is important to understand: if we have persistent inflammation in the brain, what is driving that signal? The immune system has lots of regulatory steps designed to keep it in balance, but despite all the intrinsic safeguards in the system it has lost control. Why?

Some perspective: About 5 years ago I was sitting on a bus with Professor Thayne Sweeten. We were on our way to dinner to relax after a full day of brainstorming as a group of researchers interested in autism. Thayne is a bright guy. His PhD dissertation was Immune Activation and Autoimmunity in Autism. He explained from everything he had seen regarding the immune system of autism; the CSF observations, the increase in neopterin, etc,, that at least a significant subgroup of children had the immunological footprint of a persistent viral pathogen.

I agreed and I still do agree especially after 5 years of discoveries. And it doesnt have to be a virus: many other pathogenic bacteria and fungi could cause the same response. But for simplicity lets just say virus.

We dont have to agree about which virus is persistent in autism, it actually doesnt matter that much. I am surprised to hear myself say that, but after what I have learned in the last few months, I dont think the actual virus is that important. That is because most do not have a specific anti-viral drug (apart from HIV and some Herpes viruses). Even in those cases the drugs are inadequate and something else is needed.

THE IMMUNE SYSTEM IS BLINDED

The picture depicts the blind miraculously being given sight. I would love to see a miracle of immune unblinding in autism, or any of these other disorders. Absent that we need to give it sight medically.

If you read my blog about this last night I spoke about the problem. We have a raging immune response just like we would expect with a viral infection, except it doesnt go away. Why? The immune cells (particularly macrophages) seem to be blind and cannot find the enemy they are looking for. So while they stumble around, unable to find the viral enemies, the entire system stays turned on. And it will stay turned on until either stem cells say enough its time to heal, or until the virus is eliminated.

The evidence is we dont generate enough stem cell response to regulate this type of immune response presumably because the viruses are still present. Therefore, extra stem cells may help cool the immune fires. BUT, and it is an important but, do we want to down-regulate the immune system if a virus is still present? My belief is no.

What we want is to make the virus go away and with that have the immune response naturally calm down.

To do that we have to give sight to the blind and help the macrophages find their targets.

To do this we are working with some of the finest biotech labs in Europe and we believe we have the solution. More on that to come.

A brief but helpful discussion about TNF alpha is on wikipedia. http://en.wikipedia.org/wiki/Tumor_necrosis_factor-alpha

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STEM CELLS – Wiley Online Library

Posted: October 18, 2015 at 9:49 pm

Pax7 stability is regulated by the proteasome during myogenesis. (A): Proteasome inhibition results in myogenin (Myog) and Pax7 coexpression (arrows) in adult mouse primary myoblasts (pMbs). Syndecan-4 (Sdc-4) expression was used as lineage marker. Scale bar=10 m. Right panel: quantification (three separate experiments; [meanSEM]) of percentage of Myog(+)/Pax7(+) cells from the total Sdc-4(+) population; Student's t-test; *, p <0.005. (B): Western blot analysis of Pax7 and myogenin expression in 48 hours cultured pMbs treated as in (A). (C): Pax7 levels are significantly increased upon proteasome inhibition during differentiation commitment in C2C12 myoblasts. Myogenin (Myog): differentiation marker, tubulin (Tub): loading control. Right panel: quantification of Pax7 fold change (meanSEM) of three separate experiments. One-way analysis of variance (ANOVA); *, p<0.005. (D): Epoxomicin-mediated proteasome inhibition recapitulates Pax7 accumulation in differentiating C2C12 myoblasts. MG132 effect is shown as positive control. Right panel: quantification of Pax7 fold change (meanSEM) of three separate experiments for 1 M epoxomicin and 25 M MG132 treatments. One-way ANOVA; * and **p<0.005. (E): Proteasome inhibition results in Pax7 nuclear accumulation. Pax7 expression was determined by Western blot in cytoplasmic and nuclear fractions: (tubulin: cytoplasmic marker; histone deacetylase 2 [HDAC2]: nuclear marker), Right panel: quantification of Pax7 protein levels normalized to HDAC2 (meanSEM) of three separate experiments. Student's t-test; *, p<0.005. MG132 was used at 25 M in (B), (C), and (E). Abbreviations: DMSO, dimethyl sulfoxide; HDAC2, histone deacetylase 2.

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STEM CELLS - Wiley Online Library

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Ray Kurzweil's Transhumanist Agenda – YouTube

Posted: October 17, 2015 at 5:44 am

Futurist Ray Kurzweil's prediction that humans will be uploading their minds to computers by 2045 and that bodies will be replaced by machines before the end of the century, currently receiving a new wave of media attention, overlooks the fact that such technology will likely be monopolized by the elite as a way of enslaving the rest of humanity on an industrial scale. http://www.prisonplanet.com/the-dark-... [TWITTER] https://twitter.com/RealAlexJones [FACEBOOK] https://www.facebook.com/AlexanderEme... [[[DONATE TO ALEX JONES**]]] $5 or $10 A week. WE NEED YOUR SUPPORT!! http://www.infowars.com/donate/ NEW ITEM** [INFOWARS COMPLETE WATER FILTRATION CENTER] http://www.infowarsshop.com/-Water-Fi... NEW ITEM** [INFOWARS COMPLETE HEALTH & WELLNESS CENTER] http://www.infowarsshop.com/-Health-W...

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Ray Kurzweil's Transhumanist Agenda - YouTube

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Chicago Illinois Office of the American Diabetes Association

Posted: October 16, 2015 at 11:41 pm

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Illinoisans are increasingly feeling the effects of diabetes as thousands of people suffer from the disease, and many others may have diabetes and not know it! It is estimated that one out of every three children born after 2000 in the United States will be directly affected by diabetes.

That is why the American Diabetes Association's Chicago office is so committed to educating the public about how to stop diabetes and support those living with the disease.

We are here to help.

Additional Events

We welcome your help.

Your involvement as an American Diabetes Association volunteer whether on a local or national level will help us expand our community outreach and impact, inspire healthy living, intensify our advocacy efforts, raise critical dollars to fund our mission, and uphold our reputation as the moving force and trusted leader in the diabetes community.

Find volunteer opportunities in our area through the Volunteer Center.

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Chicago Illinois Office of the American Diabetes Association

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Scientists Turn Back the Clock on Adult Stem Cells Aging …

Posted: October 16, 2015 at 7:50 am

Reversing the aging process could lead to medical treatments for many chronic conditions

Researchers have shown they can reverse the aging process for human adult stem cells, which are responsible for helping old or damaged tissues regenerate. The findings could lead to medical treatments that may repair a host of ailments that occur because of tissue damage as people age. A research group led by the Buck Institute for Research on Aging and the Georgia Institute of Technology conducted the study in cell culture, which appears in the September 1, 2011 edition of the journal Cell Cycle.

The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases A research group led by the Buck Institute for Research on Aging in collaboration with the Georgia Institute of Technology, conducted the study that pinpoints what is going wrong with the biological clock underlying the limited division of human adult stem cells as they age.

We demonstrated that we were able to reverse the process of aging for human adult stem cells by intervening with the activity of non-protein coding RNAs originated from genomic regions once dismissed as non-functional genomic junk, said Victoria Lunyak, Ph.D., associate professor at the Buck Institute for Research on Aging.

Adult stem cells are important because they help keep human tissues healthy by replacing cells that have gotten old or damaged. Theyre also multipotent, which means that an adult stem cell can grow and replace any number of body cells in the tissue or organ they belong to. However, just as the cells in the liver, or any other organ, can get damaged over time, adult stem cells undergo age-related damage. And when this happens, the body cant replace damaged tissue as well as it once could, leading to a host of diseases and conditions. But if scientists can find a way to keep these adult stem cells young, they could possibly use these cells to repair damaged heart tissue after a heart attack; heal wounds; correct metabolic syndromes; produce insulin for patients with type 1 diabetes; cure arthritis and osteoporosis and regenerate bone.

The team began by hypothesizing that DNA damage in the genome of adult stem cells would look very different from age-related damage occurring in regular body cells. They thought so because body cells are known to experience a shortening of the caps found at the ends of chromosomes, known as telomeres. But adult stem cells are known to maintain their telomeres. Much of the damage in aging is widely thought to be a result of losing telomeres. So there must be different mechanisms at play that are key to explaining how aging occurs in these adult stem cells, they thought.

Researchers used adult stem cells from humans and combined experimental techniques with computational approaches to study the changes in the genome associated with aging. They compared freshly isolated human adult stem cells from young individuals, which can self-renew, to cells from the same individuals that were subjected to prolonged passaging in culture. This accelerated model of adult stem cell aging exhausts the regenerative capacity of the adult stem cells. Researchers looked at the changes in genomic sites that accumulate DNA damage in both groups.

We found the majority of DNA damage and associated chromatin changes that occurred with adult stem cell aging were due to parts of the genome known as retrotransposons, said King Jordan, Ph.D., associate professor in the School of Biology at Georgia Tech.

Retroransposons were previously thought to be non-functional and were even labeled as junk DNA, but accumulating evidence indicates these elements play an important role in genome regulation, he added.

While the young adult stem cells were able to suppress transcriptional activity of these genomic elements and deal with the damage to the DNA, older adult stem cells were not able to scavenge this transcription. New discovery suggests that this event is deleterious for the regenerative ability of stem cells and triggers a process known as cellular senescence.

By suppressing the accumulation of toxic transcripts from retrotransposons, we were able to reverse the process of human adult stem cell aging in culture, said Lunyak.

Furthermore, by rewinding the cellular clock in this way, we were not only able to rejuvenate aged human stem cells, but to our surprise we were able to reset them to an earlier developmental stage, by up-regulating the pluripotency factors the proteins that are critically involved in the self-renewal of undifferentiated embryonic stem cells. she said.

Next the team plans to use further analysis to validate the extent to which the rejuvenated stem cells may be suitable for clinical tissue regenerative applications.

The study was conducted by a team with members from the Buck Institute for Research on Aging, the Georgia Institute of Technology, the University of California, San Diego, Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, International Computer Science Institute, Applied Biosystems and Tel-Aviv University.

Citation: Inhibition of activated pericentromeric SINE/Alu repeat transcription in senescent human adult stem cells reinstates self-renewal. Cell Cycle, Volume 10, Issue 17, September 1, 2011

About the Buck Institute for Research on Aging The Buck Institute is the first freestanding institute in the United States that is devoted solely to basic research on aging and age-associated disease. The Institute is an independent nonprofit organization dedicated to extending the healthspan, the healthy years of each individuals life. Buck Institute scientists work in an innovative, interdisciplinary setting to understand the mechanisms of aging and to discover new ways of detecting, preventing and treating conditions such as Alzheimers and Parkinsons disease, cancer, cardiovascular disease and stroke. Collaborative research at the Institute is supported by new developments in genomics, proteomics and bioinformatics technology. For more information: http://www.thebuck.org.

About the Georgia Institute of Technology The Georgia Institute of Technology is one of the world's premier research universities. Ranked seventh amongU.S. News & World Report's top public universities, Georgia Tech has more than 20,000 students enrolled in its Colleges of Architecture, Computing, Engineering, Liberal Arts, Management and Sciences and is among the nation's top producers of women and minority engineers.The Institute offers research opportunities to both undergraduate and graduate students and is home to more than 100 interdisciplinary units plus the Georgia Tech Research Institute. For more information: http://www.gatech.edu.

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Scientists Turn Back the Clock on Adult Stem Cells Aging ...

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The Power of Stem Cells | California's Stem Cell Agency

Posted: October 16, 2015 at 7:46 am

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Myles Brown, MD – DF/HCC

Posted: October 16, 2015 at 1:46 am

Dana-Farber Cancer Institute EDUCATIONAL TITLES

Dr. Brown's research laboratory focuses on elucidating the epigenetic factors underlying the action of steroid hormones. This work has important implications both for normal physiology and for the treatment of hormone dependent malignancies including breast and prostate cancer. He is recognized for three seminal discoveries. His lab opened the steroid receptor coregulator field, illuminated the dynamic nature of receptor and coregulator interaction with the genome and elucidated the importance of epigenetically determined distant cis-regulatory steroid receptor binding sites. His contributions have uniquely reformulated the understanding of steroid hormone action in normal physiology and in hormone-dependent cancer.

DF/HCC members that share similar concepts* with Myles Brown, MD but have yet to coauthor a publication with this researcher.

ARTHUR B. PARDEE, PH.D. Dana-Farber Cancer Institute

DENNIS C. SGROI, MD Massachusetts General Hospital

BREAST CANCER, CANCER GENETICS

IRENE KUTER, DPHIL, MD Massachusetts General Hospital

BREAST CANCER

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Myles Brown, MD - DF/HCC

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Knee Stem Cell Therapy – Surgery & Replacement Alternative

Posted: October 15, 2015 at 3:49 pm

Regenexx Knee Stem Cell Therapy for Injuries and ArthritisChris Centeno2015-08-07T15:30:40+00:00

The Regenexx family ofnon-surgical stem cell and blood platelet procedures offer next-generation injection treatments for those who are suffering from knee pain or may be facing knee surgery or knee replacement due to common tendon, ligament and bone injuries, arthritis and other degenerative conditions.

As an alternative to knee surgery or knee replacement, Regenexx procedures may help alleviate knee pain and the conditions that cause it with a same-day office injection procedure. Unlike traditional surgery, Regenexx patients are typically encouraged to walk the same day, and most patients experience very little down time from the procedure.

Knee Patient Results | Regenexx SD Procedure Overview | ACL Injuries | Meniscus Tears

This is not a complete list of conditions treated, but the most common knee conditions we have treated throughout the years. If you are experiencing knee pain, injury, or arthritis, please contact us or complete the candidacy form below to learn more about whether the Regenexx Procedures are right for you.

This Regenexx-SD (same-day) bone marrow derived stem cell treatment outcome data analysis is part of the Regenexx data download of patients who were tracked in the Regenexx advanced patient registry.

This Regenexx-SD (same-day) bone marrow derived stem cell treatment outcome data analysis is part of the Regenexx data download of patients who were tracked in the Regenexx advanced patient registry following treatment for Meniscus Tears.

This data utilizes LEFS (Lower Extremity Functional Scale) data from our knee arthritis patients treated with stem cell injections. Functional questionnaires ask the patients questions such as how well they can walk, run, climb stairs, etc. The improvements following the Regenexx-SD procedure are highly statistically significant.

If you are considering a knee replacement, watch the video in the sidebar of this page and read about how stem cells stack up against knee replacements.

BioMed Research International;Volume 2014, Article ID 370621,.Centeno CJ.

Introduction. We investigated the use of autologous bone marrow concentrate (BMC) with and without an adipose graft, fortreatment of knee osteoarthritis (OA). Methods. Treatment registry data for patients who underwent BMC procedures with andwithout an adipose graft were analyzed. Pre- and posttreatment outcomes of interest included the lower extremity functional scale(LEFS), the numerical pain scale (NPS), and a subjective percentage improvement rating. Multivariate analyses were performedto examine the effects of treatment type adjusting for potential confounding factors. The frequency and type of adverse events(AE) were also examined. Results. 840 procedures were performed, 616 without and 224 with adipose graft. The mean LEFS scoreincreased by 7.9 and 9.8 in the two groups (out of 80), respectively, and the mean NPS score decreased from 4 to 2.6 and from 4.3to 3 in the two groups, respectively. AE rates were 6% and 8.9% in the two groups, respectively. Although pre- and posttreatmentimprovements were statistically significant, the differences between the groups were not. Conclusion. BMC injections for knee OAshowed encouraging outcomes and a low rate of AEs. Addition of an adipose graft to the BMC did not provide a detectible benefitover BMC alone.

Two time Super Bowl Champ Jarvis Greens story. From a young boy struggling to get through a football practice, to a 2X Super Bowl Champion, Jarvis tells his story of pain and struggle following knee surgeries, and his return to form following a Regenexx Stem Cell Procedure.

If you are interested in learning whether you are a good candidate for the Regenexx Procedure, please complete the Regenexx Procedure Candidate Form below or call us at 888-525-3005.

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Knee Stem Cell Therapy - Surgery & Replacement Alternative

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Arthritic Dogs Healed With New Stem Cell Therapy – ABC News

Posted: October 15, 2015 at 3:49 pm

A couple of years ago, Brad Perry's dogs started having joint problems. Cowboy, the golden retriever, developed a severe case of arthritis, while Mr. Jones, the mutt, tore the ligaments in both of his knees during some overenthusiastic play.

"It was so sad. They wouldn't even come to the door to greet me they were in so much pain. It just broke my heart," recalled Perry, a tractor-trailer driver from Alexandria, Ky.

Perry gave the dogs all sorts of medications, but nothing worked, and he knew such medications could result in kidney and liver damage. The dogs' suffering became so great, Perry considered putting the pets down. But late last year he heard about a veterinarian in his area who performed stem cell therapy on dogs to regenerate and repair their joints and figured it was worth a try.

Cowboy underwent the procedure first. Mr. Jones followed a few months later. Perry said that within 10 days of receiving treatment the dogs were like puppies again, chasing his kids, running around in the park and swimming in the lake.

The treatment Perry's dogs received was developed by MediVet America of Lexington, Ky., one of several companies that sell equipment and training to veterinary clinics around the world. MediVet has more than a thousand clinics. Participating vets have performed more than 10,000 stem cell procedures about 7,000 of them in the past 12 months.

An operation like the one Cowboy and Mr. Jones underwent takes several hours. To start, the vet harvests a few tablespoons of fat cells from the pet's abdomen or shoulder, then spins the cells in a centrifuge to separate out the stem cells that are naturally present in fat. Next, the cells are mixed with special enzymes to "digest" any residual fat and connective tissue, and are then "activated" by mixing them with "plasma rich platelets" extracted from the animal's blood cells. The mixture is stimulated under a LED light for 20 minutes or so to further concentrate the stem cells. Finally, the newly awakened cells are injected back into the damaged joint.

Jeremy Delk, MediVet's chief executive officer, said that the therapy works because stem cells are the only cells in the body that have the ability to transform themselves into other types of specialized cells -- such as cartilage -- making them a potent tool for repairing damaged and deteriorating joints. There are 50 to 1,000 times more stem cells in the fat than bone marrow, a source that was more consistently used in animal and human -- stem cell therapy until the fat method started becoming more popular.

"As we age, humans and animals alike, our stem cells are starting to die off so we have fewer. What we are able to do with these techniques is isolate the cells in very large numbers, wake them up and put them back into the area that needs help," he explained.

While still largely unavailable to their owners, stem cell therapy from fat cells has been offered to our furry friends for several years. With fewer regulatory hoops to jump through in veterinary medicine and no contentious religious debates, experimental procedures are often tested and perfected on animals decades before they're green-lighted for use on humans.

One of the things veterinarians and owners alike praise about the procedure is it can be completed in one day, and all at the vet's office. Stem cells can also be banked for future injection so the animal does not have to endure extraction again.

John Sector, the owner of Shelby St. Veterinarian Hospital in Florence, who performed the surgery on Cowboy and Mr. Jones, had high praise for the therapy.

"This is potentially a game changer. We're seeing incredible results in the joints. We also see some unexpected improvements in other things, like skin conditions," he said.

Stem cell therapy is not just for pets who curl up on couches or ride in the backseat either. Delk said horses, donkeys, zebras and lions are also regular stem cell patients. He and his team recently traveled to the Middle East to perform the therapy on some prized racing camels.

However, stem cell remedies, even for animals, are still considered experimental. Shila Nordone, the chief scientific officer at the AKC Canine Health Foundation, a nonprofit group that funds health research for dogs, said that its use for joint regenerative purposes is exciting, but that the lower regulatory bar in animal medicine is both good and bad.

"It's good because we can do things sooner for our patients without 10 years of expensive clinical trials, but bad because we are still in the process of establishing best practices to ensure the procedures are the safest and most effective possible," she said.

Studies funded by the Health Foundation and others have been promising. One study of more than 150 dogs found improvements in joint stiffness, mobility and other joint health indicators in nearly 95 percent of arthritic cases. In some patients, improvements were seen in as little as a week while others took up to 90 days and required multiple injections.

The cost of a single procedure is $1800-$3,000, depending on the area of the country, the species of animal and severity of joint damage. Even those with pet insurance can expect to pay out of pocket.

Owners like Perry believe it is worth every penny.

"They are completely different dogs. It absolutely changed their lives," he said of Cowboy and Mr. Jones. "It changed mine too -- I got my dogs back."

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Arthritic Dogs Healed With New Stem Cell Therapy - ABC News

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