StemCell Therapy

ScienceDaily (Mar. 13, 2012) For the first time, scientists at the University of Wisconsin-Madison have made early retina structures containing proliferating neuroretinal progenitor cells using induced pluripotent stem (iPS) cells derived from human blood.

And in another advance, the retina structures showed the capacity to form layers of cells as the retina does in normal human development and these cells possessed the machinery that could allow them to communicate information. (Light-sensitive photoreceptor cells in the retina along the back wall of the eye produce impulses that are ultimately transmitted through the optic nerve and then to the brain, allowing you to see.) Put together, these findings suggest that it is possible to assemble human retinal cells into more complex retinal tissues, all starting from a routine patient blood sample.

Many applications of laboratory-built human retinal tissues can be envisioned, including using them to test drugs and study degenerative diseases of the retina such as retinitis pigmentosa, a prominent cause of blindness in children and young adults. One day, it may also be possible replace multiple layers of the retina in order to help patients with more widespread retinal damage.

We dont know how far this technology will take us, but the fact that we are able to grow a rudimentary retina structure from a patients blood cells is encouraging, not only because it confirms our earlier work using human skin cells, but also because blood as a starting source is convenient to obtain, says Dr. David Gamm, pediatric ophthalmologist and senior author of the study. This is a solid step forward.

In 2011, the Gamm lab at the UW Waisman Center created structures from the most primitive stage of retinal development using embryonic stem cells and stem cells derived from human skin. While those structures generated the major types of retinal cells, including photoreceptors, they lacked the organization found in more mature retina.

This time, the team, led by Gamm, Assistant Professor of Ophthalmology and Visual Sciences in the UW School of Medicine and Public Health, and postdoctoral researcher and lead author Dr. Joseph Phillips, used their method to grow retina-like tissue from iPS cells derived from human blood gathered via standard blood draw techniques.

In their study, about 16 percent of the initial retinal structures developed distinct layers. The outermost layer primarily contained photoreceptors, whereas the middle and inner layers harbored intermediary retinal neurons and ganglion cells, respectively. This particular arrangement of cells is reminiscent of what is found in the back of the eye. Further, work by Dr. Phillips showed that these retinal cells were capable of making synapses, a prerequisite for them to communicate with one another.

The iPS cells used in the study were generated through collaboration with Cellular Dynamics International (CDI) of Madison, Wis., who pioneered the technique to convert blood cells into iPS cells. CDI scientists extracted a type of blood cell called a T-lymphocyte from the donor sample, and reprogrammed the cells into iPS cells. CDI was founded by UW stem cell pioneer Dr. James Thomson.

We were fortunate that CDI shared an interest in our work. Combining our labs expertise with that of CDI was critical to the success of this study, added Dr. Gamm.

Other members of the research team include:

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Scientists produce eye structures from human blood-derived stem cells

11-03-2012 03:23

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A research lab led by controversial cloning pioneer Hwang Woo-Suk said it would attempt to implant DNA from the extinct mammal into an elephant egg cell to create a new embryo.

They hope it will lead to the birth of a new baby mammoth for the first time since the prehistoric giants last roamed the earth 10,000 years ago.

Sooam Biotech Research Foundation said today it had signed a deal with Russia's North-Eastern Federal University to cooperate on the project.

Scientists will attempt to "restore" cells taken from mammoth remains that were entombed in ice until they were recently uncovered by the thawing permafrost.

First they must find well-preserved tissues with undamaged genes, such as bone marrow. The next step is to replace the nucleus of an Indian elephant egg cell with the mammoth DNA.

If all goes to plan, test tube embryos will be implanted in an elephant's womb and the first woolly mammoth would be born 22 months later.

Sooam researcher Hwang In-Sung said: "The first and hardest mission is to restore mammoth cells.

"This will be a really tough job, but we believe it is possible because our institute is good at cloning animals."

The lab has successfully cloned living animals including a cow, a cat, dogs, a pig and a wolf, but using ancient DNA from a long-extinct species has never been done.

Hwang Woo-Suk, who created the world's first cloned dog Snuppy in 2005, was a national hero in South Korea until some of his research into creating human stem cells was found in 2006 to have been faked.

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Woolly mammoths 'will be brought back to life' by cloning

The deal was signed by Vasily Vasiliev, vice rector of North-Eastern Federal University of the Sakha Republic, and controversial cloning pioneer Hwang Woo-Suk of South Korea's Sooam Biotech Research Foundation, on Tuesday.

Hwang was a national hero until some of his research into creating human stem cells was found in 2006 to have been faked. But his work in creating Snuppy, the world's first cloned dog, in 2005, has been verified by experts.

Stem cell scientists are now setting their sights on the extinct woolly mammoth, after global warming thawed Siberia's permafrost and uncovered remains of the animal.

Enlarge

South Korean scientist Hwang Woo-Suk (L) and Vasily Vasiliev (R), vice director of North-Eastern Federal University of Russia's Sakha Republic, exchange agreements during a signing ceremony on joint research at Hwang's office in Seoul. The research collaboration agreement will help Russian and S.Korean scientists to recreate a woolly mammoth which last walked the earth some 10,000 years ago.

The South Korean foundation said it would transfer technology to the Russian university, which has already been involved in joint research with Japanese scientists to bring a mammoth back to life.

"The first and hardest mission is to restore mammoth cells," another Sooam researcher, Hwang In-Sung, told AFP. His colleagues would join Russian scientists in trying to find well-preserved tissue with an undamaged gene.

By replacing the nuclei of egg cells from an elephant with those taken from the mammoth's somatic cells, embryos with mammoth DNA could be produced and planted into elephant wombs for delivery, he said.

Sooam will use an Indian elephant for its somatic cell nucleus transfer. The somatic cells are body cells, such as those of internal organs, skin, bones and blood.

"This will be a really tough job, but we believe it is possible because our institute is good at cloning animals," Hwang In-Sung said.

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S.Korean, Russian scientists bid to clone mammoth

Russian-South Korean project includes participation of disgraced stem cell researcher who faked his results.

Scientists from South Korea and Russia have signed onto a project that sounds like it got lifted off the pages of "Jurassic Park" to bring a woolly mammoth back to life.

This undated handout provided by ExhibitEase LLC shows a 3D computer-generated Image of woolly mammoth emerging from ice block.

Even more controversial than the storyline is the participation of a disgraced cloning expert from South Korea in the project. Hwang Woo-Suk, now with South Korea's Sooam Biotech Research Foundation, was found to have falsified data claiming a stem cell research breakthrough and then forced to resign his post at Seoul National University in 2009.

In 2005, Suk reported in a paper published in the journal Science that his team had come up with a procedure to clone individual stem cell colonies from 11 patients. That built upon a 2004 article which he published. A subsequent investigation by the university found the papers to have been fabrications. Separately, he was later convicted of embezzlement

Still, Suk continues to enjoy notoriety in his native country as the first scientist to clone a dog. Whether he can apply that expertise to reproduce a now-extinct animal may hinge on a variable entirely out of his hands. This isn't the first time scientists have set their sights on cloning a mammoth. Scientists in Russia researching the project have had their progress blocked by not having nuclei with undamaged mammoth genes. That changed last August when paleontologists reported discovering a well-preserved mammoth's thigh bone in Siberia, raising the chances for a successful cloning procedure.

"The first and hardest mission is to restore mammoth cells," another Sooam researcher, Hwang In-Sung, told AFP.

Assuming that the researchers can find nuclei with undamaged genes, they would implant the embryos into elephant wombs for delivery. Although mammoths became extinct about 10,000 years ago, they are considered to be close enough relatives to the modern elephant.

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Scientists sign on to recreate woolly mammoth--just for fun

17-02-2012 10:42 NSCF funds clinical trials to: • Induce drug-free tolerance for transplanted kidneys • Effectively cure inherited red blood cell disorders like sickle cell disease (SCD) and thalassemia •Permanently correct fatal childhood enzyme deficiencies For more information visit nationalstemcellfoundation.org.

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National Stem Cell Foundation - Video

Public release date: 13-Mar-2012 [ | E-mail | Share ]

Contact: Zaal Kokaia zaal.kokaia@med.lu.se 46-705-365-917 Lund University

Stroke and other diseases and injuries to the brain are often followed by inflammation, caused by a reaction of the body's immune system. This reaction has been seen as something that must be combated, but perhaps the immune system could in fact help with recovery following a stroke. A major new EU project, led by Lund University in Sweden and the Weizmann Institute in Israel, is going to study this question.

Stroke is a major public health problem, with 700 000 new cases in the EU and 30 000 new cases in Sweden each year. The EU is now investing EUR 12 million in the project TargetBraIn. The goal of the project is to gain a better understanding of the role of the immune system in stroke.

The immune system protects the body when its tissues are damaged for whatever reason. The cells of the immune system often produce inflammation, which has some negative effects, but which in time helps the original damage to heal.

Stroke is most commonly caused by a cerebral infarction (a blood clot in the brain), which starves the brain of oxygen. It is the damage caused by the lack of oxygen which activates the immune system and leads to inflammation. Until now, this has been seen as a wholly undesirable reaction. To emphasise the positive aspects of the immune system's reaction is therefore something of a paradigm shift in the field. Professor Michal Schwartz and her research group in Israel have pioneered the study of the positive role of the immune system in repairing damaged nerve cells.

Professor Zaal Kokaia, head of the Stem Cell Centre at Lund University, has long worked with stem cell therapy for brain injuries. He led StemStroke, an EU project which researched the possibility of creating new nerve cells after a stroke through transplants or by encouraging the brain to form new cells. Zaal Kokaia and Michal Schwartz are now coordinator and deputy coordinator respectively of TargetBraIn (an acronym which stands for "Targeting Brain Inflammation for Improved Functional Recovery in Acute Neurodegenerative Disorders").

"Within TargetBraIn we want to reinforce the positive effects of inflammation and reduce its negative effects. This could be achieved either by trying to change the immune system's reactions or through stem cell therapy, or both! A combination of the two methods may produce the best results", says Zaal Kokaia.

The research is still at the experimental stage, and the road to general application on patients will be long. However, as the population of Europe ages, stroke is becoming an increasingly costly disease, hence the EU investment in the field.

###

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Could the immune system help recovery from stroke?

By Traci Pedersen Associate News Editor Reviewed by John M. Grohol, Psy.D. on March 11, 2012

A novel explanation of glaucoma is rapidly rising, and it is promoting advances in treatment that may ultimately eliminate the disease. Rather than being viewed solely as an eye disease, top scientists now consider glaucoma to be a neurologic disorder that causes nerve cell death, similar to what happens in Parkinsons disease and Alzheimers.

Treatment advances are being tested in patients or are scheduled to begin clinical trials soon.

The long-standing theory regarding glaucoma was that vision damage was caused by unusually high pressure inside the eye, known as intraocular pressure (IOP). Therefore, lowering IOP was the focus of surgical techniques and medications; developing tests and instruments to measure and track IOP was vital to that effort.

Although measuring a patients IOP is still a key part of glaucoma treatment, it is no longer the only method an ophthalmologist uses to diagnose glaucoma. Even when surgery or medication successfully lowers IOP, some glaucoma patients continue to lose vision.

Also, some patients find it difficult to use eye drop medications as prescribed by their physicians. These problems encouraged researchers to look beyond IOP as a cause of glaucoma and focus of treatment.

The new research model focuses on the damage that occurs in a type of nerve cell called retinal ganglion cells (RGCs), which connect the eye to the brain through the optic nerve and are vital to vision.

RGC-targeted glaucoma treatments now in clinical trials include: medications injected into the eye that deliver survival and growth factors to RGCs; medications known to be useful for stroke and Alzheimers, such as cytidine-5-diphosphocholine; and electrical stimulation of RGCs, delivered through tiny electrodes implanted in contact lenses or other external devices. Human trials of stem cell therapies are in the planning stages.

As researchers turn their attention to the mechanisms that cause retinal ganglion cells to degenerate and die, they are discovering ways to protect, enhance and even regenerate these vital cells, said Jeffrey L Goldberg, M.D., Ph.D., assistant professor of ophthalmology at the Bascom Palmer Eye Institute and Interdisciplinary Stem Cell Institute.

Understanding how to prevent damage and improve healthy function in these neurons may ultimately lead to sight-saving treatments for glaucoma and other degenerative eye diseases.

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Glaucoma: A Neurological Disorder?

TEL AVIV, Israel--(BUSINESS WIRE)--

Orgenesis Inc., (OTCBB: ORGS) (the Company) announced today that pursuant to a licensing agreement dated February 2, 2012 with Tel Hashomer - Medical Research, Infrastructure and Services Ltd. ("Tel Hashomer" or "THM), the Company has an exclusive license to develop and commercialize THM's rights in functional autologous insulin producing cells (AIPC) regeneration technology.

This licensed portfolio is based on the groundbreaking work and two decades of research by the world renowned researcher, Prof. Sarah Ferber conducted at Tel Hashomer.

For the last thirteen years, Prof. Sarah Ferber, Ph.D in Medical Science, the head of the Molecular Endocrinology research unit at theCenter forRegenerative Medicine, Stem Cells and Tissue Engineering, Tel Hashomer, has been developing this unique technology, which seeks to substitute malfunctioning organs with new functional tissues created from the patient's own existing organs. This technology employs a molecular and cellular approach directed at converting liver cells into functional insulin producing cells as a treatment for diabetes.

Prof. Ferber's work has been published in the most highly regarded scientific journals such as Nature Medicine, JBC, PNAS, Hepatology, Journal of Autoimmunity and more. It is the Companys current intention to bring this technology to the clinical stage.

Diabetes Mellitus (DM) is a metabolic disorder resulting in abnormally high blood sugar levels (hyperglycemia) following impaired insulin production by the pancreatic islets' beta cells, which sometimes leads to severe secondary complications such as myocardial infarcts, limb amputations, neuropathies and nephropathies and, in certain circumstances, even death. Currently, the major available treatment modality for an insulin depended diabetes mellitus (IDDM) patient is insulin infusion (injection, pumps or patches). However, the Company believes that these treatments may not prevent, or delay long enough, disease related complications.

A promising therapeutic approach known as pancreatic islet transplantation has been developed as an alternative to insulin injections. Worldwide, there are currently over twenty clinical centers performing pancreatic islet transplantations that are facing formidable obstacles, including a dire shortage of donor insulin producing cells to treat the expanding number of patients with the disease. Furthermore, such transplants require immunosuppressive drugs that may harm the patients and the transplanted cells.

Prof. Ferber states: It is commonly acceptable that the ideal therapy for an IDDM patient is beta cell replacement. I believe that there are three essential steps towards developing a curative treatment:

1) a source of beta cells must be identified;

2) the immune system must be convinced not to attack those cells; and

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Orgenesis Inc. Announces Definitive Agreement to Acquire Autologous Insulin Producing Cells (AIPC) Regeneration ...

09-03-2012 18:23 A company is locked in a battle with the FDA over the use one's own stem cells. The company argues that one has the right to over one's own body? If that's true, why is the FDA blocking this treatment? Find out. Plus, doctors are refusing to treat children that do not get vaccinated. Is this ethical? See more at http://www.pjtv.com

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FDA Blocks Stem Cell Therapy: Is the Government Playing a Cell Game? - Video

WASHINGTON, March 13, 2012 /PRNewswire/ -- TEDMED, http://www.TEDMED.com, the annual gathering where science, medical and technology leaders focus on "imagination, innovation and inspiration" to advance the art of health and medicine, today announced two new programs that will vastly increase the size and scope of its audience.

TEDMED is the world's only TED-licensed event focused solely on innovation and breakthrough thinking across all of health and medicine. It will be held at the John F. Kennedy Center for the Performing Arts in Washington, D.C., April 10 - 13.

Speakers, attendee-Delegates and participants will range from biologists (Dr. E.O. Wilson) and writers (Ben Goldacre), to physicists (Albert-Laszlo Barabasi) and public health leaders like the director of the National Institutes of Health (Dr. Francis Collins). Topics to be explored by TEDMED speakers will include neuroscience, microbiology, surgery, oncology, stem cell therapy, bad science, Alzheimer's, robotics, game science, wearable tech, disease evolution, patient choice, virtual anatomy models, the nature of imagination, and dozens more.

For the first time this year, TEDMED will offer a free simulcast, TEDMEDLive, to teaching hospitals, medical schools, research institutions, university life science departments, state and federal government agencies, health-oriented corporations and non-profits across the nation. Participants, forecasted at more than 50,000, will be able to view a high-definition live stream of each presentation and performance. Using the TEDMED Connect mobile app, remote participants can also ask questions of the speakers in real time, which may be answered directly from the TEDMED stage.

Over 2,000 TEDMEDLive simulcast locations will participate, including institutions such as: Case Western Reserve University, Harvard University, University of California (Davis and Irvine), University of Pennsylvania, University of Washington, University of Virginia, Tulane University, Vanderbilt University and Yale University.

Another new TEDMED initiative is the Front-Line Scholarship Program, which offers up to $2 million in half- and full-fee scholarships to those leaders and innovators who are on the front lines of health and medicine. It assists those who would both contribute to the TEDMED conference as attendees, and would greatly benefit from joining the conference in Washington, D.C. in person as a Delegate. The Front-Line Scholarship Program is underwritten by the TEDMED Patron Fund, whose major contributors include Humana and The California Endowment.

"TEDMED is for everyone who is passionate about the future of health and medicine," said Jay Walker, curator of TEDMED."Accordingly, TEDMED is committed to bringing even more expertise and perspective to the table for a national discussion of health and medicine, regardless of ability to pay through our Front-Line Scholarship program. Front-Line Scholarships will permit the broadest possible group of healthcare providers, first responders and other contributors to attend so they can share even more ideas that will save lives."

More than 1,200 TEDMED onsite attendees including researchers, physicians, technologists and policy experts will foster cross-disciplinary collaboration and learning at the Kennedy Center this April. Institutions of excellence represented by speakers and attendees will include The American Cancer Society, The American Red Cross, Biodigital Systems, The Boulis Laboratory, Brandeis University, Brigham and Women's Hospital, The California Institute of Technology, Center for Complex Network Research, The Centers for Disease Control and Prevention, Duke University, Emory University, Harvard University, mc10, Methodist Institute for Technology, Innovation, and Education, The National Institutes of Health, New York University, Penn State University, Quest Diagnostics, The Center for Alzheimer Research and Treatment, Reuters Health, Children's Hospital Boston, The U.S. Department of Health and Human Services, and the Young Professionals Chronic Disease Network.

TEDMED Speaker List (as of 3/12/2012)

Additional speakers will be announced prior to the conference start date.

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TEDMED 2012 Conference Offers $2 Million in Scholarships to Health and Medicine Leaders and Innovators; Free National ...

LOS ANGELES Researchers at the UCLA stem cell center and the departments of chemistry and biochemistry and pathology and laboratory medicine have identified, for the first time, a generic way to correct mutations in human mitochondrial DNA by targeting corrective RNAs, a finding with implications for treating a host of mitochondrial diseases.

Mutations in the human mitochondrial genome are implicated in neuromuscular diseases, metabolic defects and aging. There currently are no methods to successfully repair or compensate for these mutations, said study co-senior author Dr. Michael Teitell, a professor of pathology and laboratory medicine and a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Between 1,000 and 4,000 children per year in the United States are born with a mitochondrial disease and up to one in 4,000 children in the U.S. will develop a mitochondrial disease by the age of 10, according to Mito Action, a nonprofit organization supporting research into mitochondrial diseases. In adults, many diseases of aging have been associated with defects of mitochondrial function, including diabetes, Parkinson's disease, heart disease, stroke, Alzheimer's disease and cancer.

"I think this is a finding that could change the field," Teitell said. "We've been looking to do this for a long time and we had a very reasoned approach, but some key steps were missing. Now we have developed this method and the next step is to show that what we can do in human cell lines with mutant mitochondria can translate into animal models and, ultimately, into humans."

The study appears today in the peer-reviewed journal Proceedings of the National Academy of Sciences.

The current study builds on previous work published in 2010 in the peer-reviewed journal Cell, in which Teitell, Carla Koehler, a professor of chemistry and biochemistry and a Broad stem cell research center scientist, and their team uncovered a role for an essential protein that acts to shuttle RNA into the mitochondria, the energy-producing "power plant" of a cell.

Mitochondria are described as cellular power plants because they generate most of the energy supply within a cell. In addition to supplying energy, mitochondria also are involved in a broad range of other cellular processes including signaling, differentiation, death, control of the cell cycle and growth.

The import of nucleus-encoded small RNAs into mitochondria is essential for the replication, transcription and translation of the mitochondrial genome, but the mechanisms that deliver RNA into mitochondria have remained poorly understood.

The study in Cell outlined a new role for a protein called polynucleotide phosphorylase (PNPASE) in regulating the import of RNA into mitochondria. Reducing the expression or output of PNPASE decreased RNA import, which impaired the processing of mitochondrial genome-encoded RNAs. Reduced RNA processing inhibited the translation of proteins required to maintain the mitochondrial electron transport chain that consumes oxygen during cell respiration to produce energy. With reduced PNPASE, unprocessed mitochondrial-encoded RNAs accumulated, protein translation was inhibited and energy production was compromised, leading to stalled cell growth.

The findings from the current study provide a form of gene therapy for mitochondria by compensating for mutations that cause a wide range of diseases, said study co-senior author Koehler.

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Repairing mutations in human mitochondria

Public release date: 12-Mar-2012 [ | E-mail | Share ]

Contact: Kim Irwin kirwin@mednet.ucla.edu 310-206-2805 University of California - Los Angeles Health Sciences

Researchers at the UCLA stem cell center and the departments of chemistry and biochemistry and pathology and laboratory medicine have identified, for the first time, a generic way to correct mutations in human mitochondrial DNA by targeting corrective RNAs, a finding with implications for treating a host of mitochondrial diseases.

Mutations in the human mitochondrial genome are implicated in neuromuscular diseases, metabolic defects and aging. There currently are no methods to successfully repair or compensate for these mutations, said study co-senior author Dr. Michael Teitell, a professor of pathology and laboratory medicine and a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Between 1,000 and 4,000 children per year in the United States are born with a mitochondrial disease and up to one in 4,000 children in the U.S. will develop a mitochondrial disease by the age of 10, according to Mito Action, a nonprofit organization supporting research into mitochondrial diseases. In adults, many diseases of aging have been associated with defects of mitochondrial function, including diabetes, Parkinson's disease, heart disease, stroke, Alzheimer's disease and cancer.

"I think this is a finding that could change the field," Teitell said. "We've been looking to do this for a long time and we had a very reasoned approach, but some key steps were missing. Now we have developed this method and the next step is to show that what we can do in human cell lines with mutant mitochondria can translate into animal models and, ultimately, into humans."

The study appears March 12, 2012 in the peer-reviewed journal Proceedings of the National Academy of Sciences.

The current study builds on previous work published in 2010 in the peer-reviewed journal Cell, in which Teitell, Carla Koehler, a professor of chemistry and biochemistry and a Broad Stem Cell Research Center scientist, and their team uncovered a role for an essential protein that acts to shuttle RNA into the mitochondria, the energy-producing "power plant" of a cell.

Mitochondria are described as cellular power plants because they generate most of the energy supply within a cell. In addition to supplying energy, mitochondria also are involved in a broad range of other cellular processes including signaling, differentiation, death, control of the cell cycle and growth.

The import of nucleus-encoded small RNAs into mitochondria is essential for the replication, transcription and translation of the mitochondrial genome, but the mechanisms that deliver RNA into mitochondria have remained poorly understood.

See more here:
Correcting human mitochondrial mutations

12-03-2012 17:41 Dr.Mark Newkirk is once again on the cutting edge of medicine. Newkirk Family Veterinarians now offer STEM CELL THERAPY for pets. Dr. Mark Newkirk combines traditional medicine and surgery with Holistic Alternatives to access the best of both worlds. As a Veterinarian, Dr. Newkirk has been serving Southern New Jersey for over 25 years. He is extensively trained in medicine and surgery and also is skilled in the care of exotic pets such as reptiles and birds. Dr. Newkirk is also one of only 5 doctors in the country currently undergoing training by the nationally renowned Dr. Martin Goldstein, the author of "The Nature of Animal Healing", and founder of immuno-augmentative therapy for animals, a true alternative cancer therapy. Dr. Newkirk is a member of American Holistic Veterinary Medical Society, the American Veterinary Medical Association, New Jersey Veterinary Medical Association and the Colorado Veterinary Medical Association. For more information check out Stem Cell Therapy on The Animal Planet's dogs 101 http://www.youtube.com

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Stem Cell Therapy at Newkirk Family Veterinarians - Hunter's Story - Video

12-03-2012 20:48 by:www.medicaltourism.hk

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Public release date: 12-Mar-2012 [ | E-mail | Share ]

Contact: Kim Irwin kirwin@mednet.ucla.edu 310-206-2805 University of California - Los Angeles Health Sciences

Researchers at the UCLA stem cell center and the departments of chemistry and biochemistry and pathology and laboratory medicine have identified, for the first time, a generic way to correct mutations in human mitochondrial DNA by targeting corrective RNAs, a finding with implications for treating a host of mitochondrial diseases.

Mutations in the human mitochondrial genome are implicated in neuromuscular diseases, metabolic defects and aging. There currently are no methods to successfully repair or compensate for these mutations, said study co-senior author Dr. Michael Teitell, a professor of pathology and laboratory medicine and a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Between 1,000 and 4,000 children per year in the United States are born with a mitochondrial disease and up to one in 4,000 children in the U.S. will develop a mitochondrial disease by the age of 10, according to Mito Action, a nonprofit organization supporting research into mitochondrial diseases. In adults, many diseases of aging have been associated with defects of mitochondrial function, including diabetes, Parkinson's disease, heart disease, stroke, Alzheimer's disease and cancer.

"I think this is a finding that could change the field," Teitell said. "We've been looking to do this for a long time and we had a very reasoned approach, but some key steps were missing. Now we have developed this method and the next step is to show that what we can do in human cell lines with mutant mitochondria can translate into animal models and, ultimately, into humans."

The study appears March 12, 2012 in the peer-reviewed journal Proceedings of the National Academy of Sciences.

The current study builds on previous work published in 2010 in the peer-reviewed journal Cell, in which Teitell, Carla Koehler, a professor of chemistry and biochemistry and a Broad Stem Cell Research Center scientist, and their team uncovered a role for an essential protein that acts to shuttle RNA into the mitochondria, the energy-producing "power plant" of a cell.

Mitochondria are described as cellular power plants because they generate most of the energy supply within a cell. In addition to supplying energy, mitochondria also are involved in a broad range of other cellular processes including signaling, differentiation, death, control of the cell cycle and growth.

The import of nucleus-encoded small RNAs into mitochondria is essential for the replication, transcription and translation of the mitochondrial genome, but the mechanisms that deliver RNA into mitochondria have remained poorly understood.

See the original post:
Correcting human mitochondrial mutations