Regenerative Medicine at Advanced Podiatry in Tampa
Advanced Podiatry is a leader in Regenerative Medicine for foot, ankle, leg and knee pain in the Tampa Bay area. We have excellent results and have been usin...

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Improved case of Anky Spondy after PRP and Stem Cell Therapy
stem cell india, stem cell therapy india, stem cell in india, stem cell therapy in india, india stem cell, india stem cell therapy.

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Future of Care: The Future of Stem Cell Therapy Highlights
A few highlights from our October 29, 2014 Future of Care: Future of Stem Cell Therapy event featuring UC San Diego Health System CEO Paul Viviano, Director of Sanford Stem Cell Clinical Center...

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Optogenetics is one of the hottest tools in biomedical research today, a method that uses gene therapy to deliver light-sensitive proteins into specific cells. This new tool allows researchers to interact with a single cell or a network of cells with exquisite precision. Whereas imaging and other technologies allow researchers to watch the brain in action, optogenetics enables them to influence those actions.

With this innovative technique, it is now possible to record neuronal activity during and between seizures, and to test causality and identify potential new therapeutic approaches. Further research could lead to the development of new therapies that could aid more than 300,000 Americans who live with uncontrolled seizures.

A new study that will be featured at the American Epilepsy Society's (AES) 68th Annual Meeting examines the reliability of optogenetics as a method of intervention of temporal lobe seizures, and the role the cerebellum may play in hippocampal function and seizure reduction. Researchers at the University of California Irvine utilized custom-designed software to detect and record chronic, spontaneous seizures in the hippocampus of a mouse model of temporal lobe epilepsy.

Their findings show that when brain cells in the cerebellum were activated by optogenetic lasers in the lateral cerebellar cortex, the duration of temporal lobe seizures decreased significantly. The time between seizures did not dramatically change, indicating the absence of a rebound effect. When light was instead delivered to the midline cerebellum, targeting the vermis, not only were seizures shorter, but there was a significant prolongation of the time between seizures. This reaction far outlasted the duration of the applied light, and was unique to application in the vermis. Optogenetic inhibition, rather than excitation, of brain cells in the cerebellum produced no significant effect on time to next seizure, indicating that activation of these cells is required to see this unique effect on seizure frequency.

"These findings are really exciting," said Dr. Esther Krook-Magnuson, Postdoctoral Scholar at the University of California Irvine. "They demonstrate that two brain structures not typically thought to interact can powerfully influence each other, and that the cerebellum could be a good target for intervention in epilepsy."

The data collected from this study shows the incredible potential for developing novel optogenetics treatments for epilepsy and provides strong support for further research.

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The above story is based on materials provided by American Epilepsy Society (AES). Note: Materials may be edited for content and length.

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Optogenetics: Identifying new targets for intervention

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Scientists at Cold Spring Harbor Laboratory (CSHL) have devised a powerful algorithm that improves the effectiveness of an important research technology harnessing RNA interference, or RNAi.

Discovered in the late 1990s, RNAi is a naturally occurring biological mechanism in which short RNA molecules bind to and "interfere" with messages sent by genes that contain instructions for protein production. Such interference can prevent a gene from being expressed. In addition to helping regulate gene expression, the RNAi pathway in many species, including humans, acts to defend the genome from parasitic viruses and transposons.

Harnessed by scientists since the mid-2000s, RNAi has provided a way to artificially "knock down" the expression of specific genes. By preventing a gene or genes from being activated in a model organism such as a mouse, for instance, much can be learned by inference about gene function. RNAi-based technology also has been extremely useful as tool in drug discovery.

At CSHL, HHMI Professor Gregory Hannon and colleagues have made seminal discoveries over the last decade in elucidating the mechanism through which RNAi operates in nature. They have also pioneered means of harnessing the RNAi pathway, creating comprehensive libraries of small RNA molecules -- called short hairpin RNAs, or shRNAs. These have enabled researchers worldwide to selectively shut down specific genes, for instance, across the entire human and mouse genomes.

In research published ahead of print November 26 in Molecular Cell, a Hannon lab team led by Research Investigator Simon Knott reported the creation of an algorithm that enables researchers to identify shRNAs that will be most effective for shutting down specific genes. Before this work, the sequence determinants responsible for optimizing shRNA efficacy were largely unknown. Thus the new research addresses an important technical issue in using RNAi for gene knockdown. The new algorithm was trained to identify sequence determinants and is able to search across each gene and distinguish the sequence targets that will produce the most effective gene knockdown.

Development of the algorithm, called shERWOOD, was based on a massive parallel assessment of the potency of some 250,000 different shRNAs. In effect, a computer was trained to make very accurate predictions, by learning what distinguished the potent shRNAs within this set from those that were less potent. After this learning process the computer was then able to predict the potency of new sequences.

"We built upon this result to design and construct next-generation shRNA libraries targeting the exomes, or protein-encoding gene set, of mice and humans," says Dr. Knott.

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Making shRNA gene knockdown more effective

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International Centre for Genetic Engineering and Biotechnology (ICGEB)
CGEB is an international organization that operates within the UN Common System and performs cutting edge research and training in molecular biology and gene...

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D27M - Genetic engineering (rock version 2014)
omd cover, rock version 2014. http://www.d27m.fr.mu Created with MAGIX Music Maker 2015.

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D27M - Genetic engineering (rock version 2014) - Video

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Michael Hadjiargyrou, Ph.D., of New York Institute of Technologys College of Arts and Sciences, an expert in engineering new musculoskeletal tissue, is available to discuss advanced bio-science predictions for 2015.

Undoubtedly, next year we will continue to see research advances in the realm of Tissue Engineering/Regenerative Medicine (TERM), says Hadjiargyrou, who specializes in molecular and cell biology, genetic engineering, biomaterials and stem cell research. Specifically, we will witness the formation of more tissues and possibly even organs fabricated in the laboratory with the use of 3D printers (Bioprinters).

Hadjiargyrou specifically identifies the heart valve, blood vessel, trachea, kidney, and liver, as the tissue or organs that will be printed with the use of 3D printers; kidneys, livers and hearts are most in demand.

Additionally, the successful transplantation of some of these laboratory tissues and organs will be achieved, particularly in Europe, as they have been more active in transplantation of biomaterials. With the emergence of such breakthroughs, we will begin to see more and more clinical and even cosmetic applications of TERM.

Hadjiargyrou focuses on studying the molecular mechanisms involved in bone regeneration as a way to better understand the healing of fractures. Hadjiargyrou teaches general biology, genetic engineering, contemporary biotechnology and biomedical research in Old Westbury, NY.

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NYIT Expert Predicts Growth in Demand for 3D Kidneys, Livers and Hearts

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Newswise For a small percentage of cancer patients, treatment aimed at curing the disease leads to a form of leukemia with a poor prognosis. Conventional thinking goes that chemotherapy and radiation therapy induce a barrage of damaging genetic mutations that kill cancer cells yet inadvertently spur the development of acute myeloid leukemia (AML), a blood cancer.

But a new study at Washington University School of Medicine in St. Louis challenges the view that cancer treatment in itself is a direct cause of what is known as therapy-related AML.

Rather, the research suggests, mutations in a well-known cancer gene, P53, can accumulate in blood stem cells as a person ages, years before a cancer diagnosis. If and when cancer develops, these mutated cells are more resistant to treatment and multiply at an accelerated pace after exposure to chemotherapy or radiation therapy, which then can lead to AML, the study indicates.

The teams findings, reported Dec. 8 in the journal Nature, open new avenues for research to predict which patients are at risk of developing therapy-related AML and to find ways to prevent it.

About 18,000 cases of AML are diagnosed in the United States each year, with about 2,000 triggered by previous exposure to chemotherapy or radiation therapy. Therapy-related AML is almost always fatal, even with aggressive treatment.

Until now, weve really understood very little about therapy-related AML and why it is so difficult to treat, said corresponding author Daniel Link, MD, a hematologist/oncologist at Siteman Cancer Center at Washington University and Barnes-Jewish Hospital. This gives us some important clues for further studies aimed at treatment and prevention.

The researchers initially sequenced the genomes of 22 cases of therapy-related AML, finding that those patients had similar numbers and types of genetic mutations in their leukemia cells as other patients who developed AML without exposure to chemotherapy or radiation therapy, an indication that cancer treatment does not cause widespread DNA damage.

This is contrary to what physicians and scientists have long accepted as fact, said senior author Richard K. Wilson, PhD, director of The Genome Institute at Washington University. It led us to consider a novel hypothesis: P53 mutations accumulate randomly as part of the aging process and are present in blood stem cells long before a patient is diagnosed with therapy-related AML.

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Genetic Errors Linked to Aging Underlie Leukemia That Develops After Cancer Treatment

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PUBLIC RELEASE DATE:

7-Dec-2014

Contact: Glenna Picton picton@bcm.edu 713-798-7973 Baylor College of Medicine @bcmhouston

HOUSTON - (Dec. 7, 2014) - An international consortium of researchers led by Baylor College of Medicine has identified for the first time a gene associated with familial glioma (brain tumors that appear in two or more members of the same family) providing new support that certain people may be genetically predisposed to the disease.

"It is widely thought amongst the clinical community that there is no association between family history and development of glioma. Because we know very little about the contributing genetic factors, when cases occur in two or more family members, it is viewed as coincidental," said Dr. Melissa Bondy, associate director of cancer prevention and population sciences at the NCI-designated Dan L. Duncan Cancer Center at Baylor College of Medicine and lead author of the report that appears in the Journal of the National Cancer Institute today. "By understanding more about the genetic link, we hope that one day we can improve treatments and preventive strategies for those with a family history of glioma."

Bondy estimates that approximately five percent of brain tumors run in families.

The study was conducted through the Gliogene Consortium, a collaborative group of familial brain tumor researchers from around the world, which is primarily supported with funding from the National Cancer Institute.

"I have been researching familial glioma for nearly 30 years, and this study is really the first time we have had a hit when it comes to identifying a gene that is potentially associated with predisposition to the disease," said Bondy, principal investigator of the Gliogene Consortium.

The Gliogene Consortium recruited 435 families in which glioma occurred from 14 centers in the United States, Sweden, Denmark, The United Kingdom and Israel. The recruitment occurred between 2007 and 2011 while Bondy was on faculty at The University of Texas MD Anderson Cancer Center. She joined the Baylor faculty in September 2011.

Once at Baylor, Bondy collaborated with experts in the College's Human Genome Sequencing Center to advance research of the genetics of the disease.

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New study identifies first gene associated with familial glioma

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Genetics of obesity
Obesity is a common problem in the western world. In this video, the students present their findings on the contribution of genes to obesity.

By: GHBiomedicina

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Genetics of obesity - Video

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DNA Genetics @ Cannafest 2014 Prague
Herbies Seeds Interview with Rowan from DNA Genetics @ Cannafest 2014 in Prague, Czech Republic. Buy DNA Genetics Seeds: http://www.herbiesheadshop.com/dna-genetics-seeds Watch Herbies ...

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Let #39;s Play The Sims 3 - Perfect Genetics Challenge - Episode 44
Origin ID - Llandros2012 My Sims 3 Page: http://mypage.thesims3.com/mypage/Llandros2012 My Blog: http://Llandros09.blogspot.com My Facebook: https://www.face...

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What Role Do Genetics Play For Muscle Gains/Fat Loss? Rodzilla Hugo Candid Bodybuilding Talk
http://www.HugoRivera.net - What Role Do Genetics Play For Muscle Gains? Rodney (aka Rodzilla) Hugo Candid Bodybuilding Talk. Hugo Rivera Rodney discuss the role that genetics play in ...

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Seattle Genetics, Inc. ( SGEN ) and Takeda Pharmaceutical Company Limited ( TKPYY ) announced four-year overall survival data from a pivotal phase II study evaluating the efficacy and safety of Adcetris for the treatment of relapsed or refractory systemic anaplastic large cell lymphoma (ALCL). Adcetris showed durable, long-term responses in this treatment setting.

At a median follow-up in the study at 46.3 months, the four-year survival rate was estimated to be 64% (median overall survival (OS) of 55.1 months) with progression-free survival (PFS) of 20 months. In other words, more than 60% of patients suffering from relapsed or refractory ALCL treated with Adcetris were alive at the fourth year of follow-up. One-third of all the patients treated in this study showed complete remission with no evidence of disease after a median follow-up of 46 months.

The company stated that historical outcomes for patients suffering from relapsed T-cell lymphoma, including systemic ALCL have shown a median OS of 5.5 months with a median PFS of 3.1 months.

Meanwhile, Seattle Genetics also announced detailed results from a randomized, double-blind, placebo-controlled phase III study (AETHERA) on Adcetris for the treatment of Hodgkin lymphoma patients with the risk of disease progression following autologous stem cell transplantation (ASCT). PFS was higher in Adcetris-treated patients compared to placebo (43 months versus 24 months).

Earlier, in Sep 2014, the company had already announced that the study met its primary endpoint with a 75% improvement in PFS. Seattle Genetics intends to submit a supplemental biologics license application to the FDA for Adcetris for the above-mentioned indication in the first half of 2015.

Adcetris is already approved in more than 45 countries for the treatment of Hodgkin lymphoma after failure of ASCT or after failure of at least two prior multi-agent chemotherapy regimens in non-ASCT patients and the treatment of sALCL after failure of at least one prior multi-agent chemotherapy regimen.

Additionally, Seattle Genetics reported data from two ongoing phase I studies on SGN-CD19A for the treatment of B-cell malignancies including non-Hodgkin lymphoma and acute lymphoblastic leukemia. SGN-CD19A showed multiple objective responses without significant myelosuppression or neuropathy. Based on this data, the company plans to initiate a randomized phase II study on SGN-CD19A for this indication in 2015.

The above data was presented at the annual meeting of the American Society of Hematology (ASH).

Seattle Genetics holds a Zacks Rank #2 (Buy). Some better-ranked stocks in the biotech sector are Biogen Idec Inc. ( BIIB ) and Amgen Inc. ( AMGN ). Both carry a Zacks Rank #1 (Strong Buy).

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Research in action at Marquette University | Spinal cord injuries
Dr. Murray Blackmore is an assistant professor of biomedical sciences in the College of Health Sciences at Marquette University. Dr. Blackmore #39;s research focuses on the use of gene therapy...

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Research in action at Marquette University | Spinal cord injuries - Video

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SAN FRANCISCO (TheStreet) -- Bluebird Bio (BLUE) has now treated seven beta-thalassemia patients with its experimental, one-time gene therapy. Four of the patients -- all followed for longer than three months -- are producing enough oxygen-carrying hemoglobin on their own to eliminate the need for chronic blood transfusions.

Two of these super-responding beta-thalassemia patients -- followed for a year and nine months, respectively -- have hemoglobin levels of healthy adults. At this point, a single infusion of Bluebird's gene therapy has essentially cured them of this serious, inherited blood disease.

The remaining three beta-thalassemia patients were infused with Bluebird's gene therapy around one month ago so it's too early to assess their response. A single patient with sickle cell disease was also just treated within the past month.

It's still unreasonable to expect an equivalent strong response in every patient, but Bluebird is learning that as its therapy replaces the defective gene causing beta-thalassemia (or sickle cell disease) with a gene that is fully functional, the patient's ability to produce normal-functioning hemoglobin improves over time, said CEO Nick Leschly.

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Bluebird Gene Therapy Inducing Durable Cures in Blood Disorder Patients

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2:46

Researchers have discovered five genes play a role in controlling human susceptibility to severe malaria.

US health officials are investigating nine cases of muscle weakness or paralysis in Colorado children.

Researchers say a drug developed by Roche to treat a form of breast cancer has been shown to extend lives.

The World Health Organisation has said experimental vaccines to treat Ebola could be ready for use in 2015.

A new survey has found organ donation can 'bring comfort' to families who have experienced a death.

A study from NZ has found paracetamol taken when pregnant increases the risk of children developing ADHD.

Health experts from 16 European countries have urged 'all possible resources' are needed to fight Ebola.

Research has shown calcium in the blood could provide an early warning of cancers, especially in men.

A third of patients who undergo surgery to remove cancerous tumours end up with microscopic pieces left.

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Gene therapy offers hope for the blind

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LONDON Pfizer Inc. is moving into the gene therapy space in the latest sign that the technology for fixing faulty genes may finally be ready for prime time, following earlier setbacks.

The U.S. drugmaker said on Monday it was establishing a gene therapy platform to study potential treatments, led by a top UK expert, and had struck a deal with privately owned U.S. biotech firm Spark Therapeutics to develop a treatment for hemophilia.

The Spark program is expected to enter early-stage clinical trials for hemophilia B in the first half of 2015. Spark will be responsible for the early Phase I/II tests, with Pfizer taking over late-stage studies, any regulatory approvals and potential commercialization.

Spark will get $20 million upfront and be eligible for additional payments based on product success worth up to $260 million.

Pfizer's research effort in gene therapy will be led by Michael Linden, a professor from King's College London and director of the University College London Gene Therapy Consortium. Linden is joining Pfizer on a two-year secondment.

Gene therapy has seen more than 20 years of experiments but research has been dogged by a series of disappointments and safety concerns.

Now, however, scientists have solved some of the earlier problems and treatments are starting to reach the clinic, with a the Western world's first gene therapy set to go on sale in Germany to treat and ultra-rare blood disease.

"The fundamental understanding of the biology of hereditary rare diseases, coupled with advances in the technology to harness disarmed viruses as gene delivery vehicles, provide a ripe opportunity to investigate the next wave of potential life-changing therapies for patients," said Pfizer research head Mikael Dolsten.

Among other major pharmaceutical companies, Bayer AG struck a gene therapy deal with Dimension Therapeutics in June, while Novartis AG recently established a new cell and gene therapies unit, and Sanofi SA has a long-standing tie-up with Oxford BioMedica.

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Pfizer Bets On Gene Therapy

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WRC NBC Washington, D.C. - Gary Coetzee, Spinal Cord Injury MedStar NRH
WRC NBC Washington, D C - Gary Coetzee, Spinal Cord Injury Patient - MedStar NRH Dec. 2, 2014.

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Sarah Heilshorn, Materials that Heal
Sarah Heilshorn, Materials that Heal Watch, learn and connect: https://stanfordconnects.stanford.edu/ Scientists created a bionic man by pulling together p...

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Asymmetrex
Technologies For Stem Cell Medicine.

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Asymmetrex - Video

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Future of Care: The Future of Stem Cell Therapy (Full Presentation)
Watch our October 29, 2014 Future of Care presentation on the future of stem cell therapy featuring Dr. David Brenner, Vice Chancellor, UC San Diego Health Sciences, Paul Viviano, Chief Executive...

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Future of Care: The Future of Stem Cell Therapy (Full Presentation) - Video

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A team of scientists that included researchers from UCLA has discovered a novel mechanism of RNA regulation in embryonic stem cells. The findings are strong evidence that a specific chemical modification, or "tag," on RNA plays a key role in determining the ability of embryonic stem cells to adopt different cellular identities.

The team also included scientists from Harvard Medical School, Massachusetts General Hospital and Stanford University.

Published in the journal Cell Stem Cell, the research reveals that depleting or knocking out a key component of the machinery that places this chemical tag -- known both as m6A and N6-methyladenosine -- on RNA significantly blocks embryonic stem cells from differentiating into more specialized types of cells.

A key property of embryonic stem cells is their ability to differentiate into many specialized types of cells. However, instead of marching toward a specific fate when prompted by signals to differentiate, embryonic stem cells that have reduced ability to place m6A become stuck in a sort of suspended animation, even though they appear healthy.

Yi Xing, a UCLA associate professor of microbiology, immunology and molecular genetics, led the informatics analyses and was a co-corresponding author of the paper. Other corresponding authors were Dr. Cosmas Giallourakis, an assistant professor of medicine at Harvard Medical School and Massachusetts General Hospital, and Dr. Howard Chang, a professor of Stanford University's School of Medicine and a Howard Hughes Medical Institute investigator.

The study of naturally occurring chemical modifications on RNAs is part of an emerging field known as epitranscriptomics. The m6A tag is the most commonly occurring modification known to scientists; it is found on RNAs of thousands of protein-coding genes and hundreds of non-coding genes in a typical cell type. The tags may help regulate RNA metabolism by marking them for destruction.

Little was known about the dynamics, conservation and function of m6A in human or mouse embryonic stem cells when the authors began the project. The authors analyzed which RNAs were tagged with m6A and the location of the m6A modifications along RNAs in mouse and human embryonic stem cells.

"Our analysis revealed a high level of conservation of m6A patterns between mice and humans, suggesting that m6A has conserved functions in human and mouse embryonic stem cells," Xing said. "Moreover, RNAs with m6A tags were degraded more rapidly and lived a shorter life in the cell than those without."

The investigators then found a strikingly conserved requirement for the presence of normal levels of m6A for differentiating embryonic stem cells into multiple cell types. Depletion of METTL3, a gene encoding the enzyme that places the m6A tag on RNAs, severely blocked human embryonic stem cells from differentiating into the gut or neural precursors. Deletion of the mouse METTL3 gene also led to a severe block in the ability of embryonic stem cells to differentiate into neural and cardiac lineages.

The study suggests that m6A modifications on RNA make the transition between cell states possible by instructing the cells to physically degrade those RNAs marked by m6A in embryonic stem cells, to allow the cells to become another cell type. However, if the cells can no longer tag RNA for destruction, the cells lose the ability to change. This discovery sheds new light on gene regulation in stem cells.

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Loss of a chemical tag on RNA keeps embryonic stem cells in suspended animation

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Sir Martin Evans - Investing with Cell Therapy Ltd
Sir Martin Evans shares his enthusiasm regarding CTL #39;s crowdfunding with professional investment platform - Crowdcube.

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Sir Martin Evans - Investing with Cell Therapy Ltd - Video

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