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On Thursday important research on stem cells and type 1 diabetes, done by professor Doug Melton, was published in the journal Cell. The results of this study have both wide and very personal implications.
Two decades ago, National Geographic reported, the current Harvard professor and stem cell researcher vowed to cure type 1 diabetes. His infant son had just been diagnosed with the disease. Professor Meltons efforts redoubled when, at age 14, his daughter was also diagnosed with the autoimmune disorder.
With the publication of this research he may have taken a step towards helping cure this disease. According to National Geographic, Melton has created a virtually unlimited supply of the cells that are missing in people with type 1 diabetes.
Type 1 diabetes, which is often diagnosed in children or young adults, affects around three million Americans. Type 1 diabetes is a chronic condition in which the pancreas produces little or no insulin, a hormone needed to allow sugar (glucose) to enter cells to produce energy, according to Mayo Clinic. This is due to the fact that the bodys immune system attacks beta cells in the pancreas, which control insulin production.
Professor Melton, along with a whole host of graduate students over 15 years, used stem cells to create replacement beta cells for mice, and human testing will begin in the next two years with government approval.
National Geographic explains:
The researchers started with cells taken from a days-old human embryo. At that point, the cells are capable of turning into any cell in the body. Others have tried to make beta cells from these human embryonic stem cells, but never fully succeeded. Meltons team spent a decade testing hundreds of combinations before finally coaxing the stem cells into becoming beta cells.
The procedure can also be done with non-embryonic stem cells, to avoid the sometimes controversial destruction of an embryo. Adult cells are turned back into stem cells and then into beta cells.
The next step is to create a protective coating for these cells so that the bodys immune system does not attack the beta cells.
MIT professor Daniel Anderson is helping Melton with a method of protection, which would work like an inkjet printer coating the cells with algae that prevents them from being attacked. This device would be implanted into patients. Two other companies are also working on strategies to coat the beta cells.
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Successful stem cell treatment in mice could one day help cure type 1 diabetes
By Alan Mozes HealthDay Reporter
THURSDAY, Oct. 9, 2014 (HealthDay News) -- In what may be a step toward a cure for type 1 diabetes, researchers say they've developed a large-scale method for turning human embryonic stem cells into fully functioning beta cells capable of producing insulin.
Type 1 diabetes, an autoimmune disorder affecting upwards of 3 million Americans, is characterized by the body's destruction of its own insulin-producing pancreatic beta cells. Without insulin, which is needed to convert food into energy, blood sugar regulation is dangerously out of whack.
Currently, people with type 1 diabetes need daily insulin injections to maintain blood sugar control. But "insulin injections don't cure the disease," said study co-author Douglas Melton, of Harvard University. Patients are vulnerable to metabolic swings that can bring about serious complications, including blindness and limb loss, he said at a teleconference this week.
"We wanted to replace insulin injections using nature's own solution, being the pancreatic beta cell," Melton said. Now, "we are reporting the ability to make hundreds of millions of these cells," he added.
Melton ultimately envisions a credit card-sized package of beta cells that can be safely transplanted into a diabetes patient and left in place for a year or more, before needing to be replaced.
But between then and now, human trials must be launched, a venture Melton thinks could begin in about three years.
If that research pans out, the Harvard team's results may prove to be a benchmark in the multi-decade effort to deliver on the promise of stem cell research as a way to access new treatments for all sorts of diseases.
Melton, co-director of the Stem Cell Institute at Harvard, described his work as a "personal quest," given that he has two children with type 1 diabetes.
He and his colleagues outlined the recent results in the Oct. 9 issue of Cell.
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Stem Cell Success Raises Hopes of Type 1 Diabetes Cure
CAMBRIDGE, Mass., Oct. 9 (UPI) -- Patients with type 1 diabetes lack the insulin-producing cells that keep blood glucose levels in check. Currently, these patients must use insulin pumps or daily hormone injections to keep levels stable.
But in a recent breakthrough in laboratories at Harvard University, researchers came upon a new technique for transforming stem cells into pancreatic beta cells that respond to glucose levels and produce insulin when necessary. The breakthrough could lead to new less invasive, more hands-off treatment for diabetes.
Remarkably, the new technique -- a complex process which involves turning on and off specific genes and takes about 40 days and six precise steps to complete -- was replicated not only on embryonic stem cells but also on human skin cells reprogrammed to act in a stem-cell-like manner. This revelation allows scientists to produce millions of insulin-producing cells while avoiding the ethical dilemmas attached to traditional stem cell research.
Previous attempts to convert stem cells into insulin-producers have proven moderately successful, but these cells mostly produced insulin at will, unable to adjust their output on the fly. The latest techniques -- developed by Douglas Melton, co-director of the Harvard Stem Cell Institute, and his research colleagues -- produce insulin cells that react to glucose spikes by upping production, and lowering insulin output when there's not excess sugar to break down.
The breakthrough has already shown significant promise when used on lab mice. Diabetic mice who received a transplant of the stem cell beta cells had improved blood sugar levels, and were shown to be capable of breaking down sugar.
"We can cure their diabetes right away -- in less than 10 days," Melton told NPR. "This finding provides a kind of unprecedented cell source that could be used for cell transplantation therapy in diabetes."
But there's still one major issue. For reasons doctors still don't understand, the beta cells in humans with diabetes are attacked by the body's immune system. Researchers like Melton still have to figure out a way to protect the new beta cells from being killed -- otherwise the breakthrough won't become anything more than another short-term solution.
"It's taken me 10 to 15 years to get to this point, and I consider this a major step forward," Melton told TIME. "But the longer term plan includes finding ways to protect these cells, and we haven't solved that problem yet."
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Harvard researchers grow insulin-producing stem cells
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9-Oct-2014
Contact: Mark Wheeler mwheeler@mednet.ucla.edu 310-794-2265 University of California - Los Angeles @uclanewsroom
People with autism spectrum disorder often experience a period of accelerated brain growth after birth. No one knows why, or whether the change is linked to any specific behavioral changes.
A new study by UCLA researchers demonstrates how, in pregnant mice, inflammation, a first line defense of the immune system, can trigger an excessive division of neural stem cells that can cause "overgrowth" in the offspring's brain.
The paper appears Oct. 9 in the online edition of the journal Stem Cell Reports.
"We have now shown that one way maternal inflammation could result in larger brains and, ultimately, autistic behavior, is through the activation of the neural stem cells that reside in the brain of all developing and adult mammals," said Dr. Harley Kornblum, the paper's senior author and a director of the Neural Stem Cell Research Center at UCLA's Semel Institute for Neuroscience and Human Behavior.
In the study, the researchers mimicked environmental factors that could activate the immune system such as an infection or an autoimmune disorder by injecting a pregnant mouse with a very low dose of lipopolysaccharide, a toxin found in E. coli bacteria. The researchers discovered the toxin caused an excessive production of neural stem cells and enlarged the offspring's' brains.
Neural stem cells become the major types of cells in the brain, including the neurons that process and transmit information and the glial cells that support and protect them.
Notably, the researchers found that mice with enlarged brains also displayed behaviors like those associated with autism in humans. For example, they were less likely to vocalize when they were separated from their mother as pups, were less likely to show interest in interacting with other mice, showed increased levels of anxiety and were more likely to engage in repetitive behaviors like excessive grooming.
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UCLA study finds link between neural stem cell overgrowth and autism-like behavior in mice
PUBLIC RELEASE DATE:
8-Oct-2014
Contact: Pete Farley peter.farley@ucsf.edu 415-502-6397 University of California - San Francisco @ucsf
Researchers at UC San Francisco and UC Berkeley have teamed up to create an innovative, integrated center for research on neurodegenerative diseases. Supported by a $3 million grant from the Glenn Foundation for Medical Research, the new center aims to pave the way to developing novel treatments for diseases such as Alzheimer's disease and Parkinson's disease by investigating the many ways that proteins can malfunction within cells.
In particular, the center's work will focus on a type of protein called the prion, which displays characteristics of infectious agents and is responsible for "mad cow" disease and a related, devastating human brain disorder known as Creutzfeldt-Jakob disease (CJD).
Stanley B. Prusiner, MD, UCSF professor of neurology, and Andrew Dillin, PhD, the Thomas and Stacey Siebel Distinguished Chair of Stem Cell Research at UCB and a Howard Hughes Medical Institute investigator, will codirect the new inter-campus program, known as the Paul F. Glenn Center for Aging Research. Ten additional researchers from UCSF and 13 from UCB will contribute to the center's work, with more recruitments to come.
"The Glenn Foundation is pleased to welcome UCSF and UC Berkeley to the Glenn Consortium for Research in Aging," said Mark R. Collins, president of the Glenn Foundation for Medical Research, which is based in Santa Barbara, Calif. "I had the pleasure to work with Dr. Dillin previously, when he led the Glenn Center for Aging Research at the Salk Institute for Biological Sciences prior to moving to UC Berkeley. I've known Dr. Prusiner and followed his work for many years and it is a propitious time for us to assist these two leaders in biological research to discover treatments for age-related neurodegenerative disease."
In 1997, Prusiner, director of UCSF's Institute for Neurodegenerative Diseases, received the Nobel Prize in Physiology or Medicine for his discovery of prions, which he demonstrated were an abnormally folded form of normal proteins that set up a template for replication in the brain. According to Prusiner, recent work provides persuasive evidence that, in addition to mad cow disease and CJD, many common neurodegenerative diseases, including Alzheimer's and Parkinson's, are caused by abnormally folded forms of normal proteins functioning as prions.
Dillin agrees that prions are ideal targets for research and novel therapeutic approaches. "The Glenn Foundation's confidence to support our hypothesis is greatly appreciated," he said, adding that the combination of UCSF's medical mission with the strong basic research traditions of both campuses will make the new Glenn Center's work uniquely powerful.
Proteins are crucial for many of a cell's normal functions, but as people age, cells' quality-control mechanisms become less efficient. Normally these systems ensure that proteins are properly formed, and target badly formed or "worn-out" proteins for destruction. But as the effectiveness of cellular quality control wanes over time, improperly formed proteins, including prions, can begin to accumulate.
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UCSF, UC Berkeley scientists join forces in new Glenn Center for Aging Research
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Newswise People with autism spectrum disorder often experience a period of accelerated brain growth after birth. No one knows why, or whether the change is linked to any specific behavioral changes.
A new study by UCLA researchers demonstrates how, in pregnant mice, inflammation, a first line defense of the immune system, can trigger an excessive division of neural stem cells that can cause overgrowth in the offsprings brain.
The paper appears Oct. 9 in the online edition of the journal Stem Cell Reports.
We have now shown that one way maternal inflammation could result in larger brains and, ultimately, autistic behavior, is through the activation of the neural stem cells that reside in the brain of all developing and adult mammals, said Dr. Harley Kornblum, the papers senior author and a director of the Neural Stem Cell Research Center at UCLAs Semel Institute for Neuroscience and Human Behavior.
In the study, the researchers mimicked environmental factors that could activate the immune system such as an infection or an autoimmune disorder by injecting a pregnant mouse with a very low dose of lipopolysaccharide, a toxin found in E. coli bacteria. The researchers discovered the toxin caused an excessive production of neural stem cells and enlarged the offsprings brains.
Neural stem cells become the major types of cells in the brain, including the neurons that process and transmit information and the glial cells that support and protect them.
Notably, the researchers found that mice with enlarged brains also displayed behaviors like those associated with autism in humans. For example, they were less likely to vocalize when they were separated from their mother as pups, were less likely to show interest in interacting with other mice, showed increased levels of anxiety and were more likely to engage in repetitive behaviors like excessive grooming.
Kornblum, who also is a professor of psychiatry, pharmacology and pediatrics at the David Geffen School of Medicine at UCLA, said there are many environmental factors that can activate a pregnant womans immune system.
Read more from the original source:
Study Finds Link Between Neural Stem Cell Overgrowth and Autism-Like Behavior in Mice
We are now just one pre-clinical step away from the finish line, said Prof Melton.
Asked about his childrens reaction he said: "I think like all kids, they always assumed that if I said I'd do this, I'd do it,
"It was gratifying to know that we can do something that we always thought was possible.
The stem cell-derived beta cells are presently undergoing trials in animal models, including non-human primates, where they are still producing insulin after several months, Prof Melton said.
Type 1 diabetes is an autoimmune condition that causes the pancreas to stop producing insulin - the hormone that regulates blood glucose levels.
If the amount of glucose in the blood is too high it can seriously damage the body's organs over time.
While diabetics can keep their glucose levels under general control by injecting insulin, that does not provide the fine tuning necessary to properly control metabolism, which can lead to devastating complications such as blindness or loss of limbs.
Around 10 per cent of all diabetes is Type 1, but it is the most common type of childhood diabetes. 29,000 youngsters suffer in Britain.
The team at Harvard used embryonic stem cells to produce human insulin-producing cells equivalent in almost every way to normally functioning cells in vast quantities.
Chris Mason, Professor of Regenerative Medicine, University College London, said it was potentially a major medical breakthrough.
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Cure for Type 1 diabetes imminent after Harvard stem-cell breakthrough
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Newswise Four scientists from the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA have received a National Institutes of Health (NIH) Director's New Innovator Award that will forward revolutionary stem cell and neuro-science in medicine. The four UCLA researchers were among only 50 scientists nationwide to receive the New Innovator Award, the most of any institution represented.
Each recipient received a $2.3M award for their respective projects. These included Dr. Reza Ardehali, assistant professor of cardiology, for his research investigating novel ways to use stem cells to regenerate heart tissue; Dr. Elissa Hallem, assistant professor of microbiology, immunology and molecular genetics, for her work studying interactions between animal parasites and their hosts to foster the further understanding of human parasitic diseases; Dr. Sririam Kosuri, assistant professor of chemistry and biochemistry, for his project developing new biological system technologies to solve outstanding problems in gene regulation; and Dr. Lili Yang, assistant professor of microbiology, immunology and molecular genetics, for her work developing a new method to track special immune cells for use in new cellular therapies.
"These New Innovator Award grants are an important acknowledgement of our cutting-edge research and will help our faculty drive the revolutionary advances we are seeing in stem cell and neuro-science," said Dr. Owen Witte, professor and director of the Broad Stem Cell Research Center. "Every cellular therapy that reaches patients must begin in the laboratory with novel ideas and experiments that will lead us in new directions in medicine and ultimately improve human life. That makes these awards invaluable to our research effort."
The NIH Director'sNew Innovator Award is designed specifically to support unusually creative investigators with highly innovative research ideas at an early stage of their career. The award seeks to support exceptionally creative new scientists whose research complements ongoing efforts by NIH.
Dr. Reza Ardehali: Unlocking the Secrets to Regenerating Heart Tissue
Dr. Ardehali's cutting-edge work focuses on both human embryonic stem cells and induced pluripotent stem cells, known as human pluripotent stem cells (hPSC), to provide insights into the mechanisms involved in the differentiation and specification of heart cells. hPSC have the unique ability to become any cell type in the body. His lab recently identified several novel surface markers that can highly enrich early cardiovascular progenitor cells. When delivered into functioning human hearts that are transplanted in laboratory conditions, the progenitor cells integrate structurally and functionally into the host myocardium. These studies established the basis for future hPSC-based cardiac therapy.
Dr. Ardehali and his colleagues were also the first to directly measure limited division in the cells that make up heart muscle (cardiomyocytes), proving that cardiomyocytes divide and that such cell division is rare. This discovery resolves an important controversy over whether the heart muscle has the power to regenerate and is critical for future research that may lead to regenerating heart tissue to repair damage caused by disease or heart attack.
His 2013, California Institute for Regenerative Medicine (CIRM), the state's stem cell research agency, New Faculty Physician Scientist Translational Research Award allowed Dr. Ardehali to initiate the preclinical studies on stem cell based therapies for heart disease that were pivotal for his success in the 2014 New Innovator Award competition. The NIH grant affirms the critical success of the project-to-date, and emphasizes the creativity of Dr. Ardehali's research and its potential to have a significant impact on the creation of novel regenerative approaches to treat heart disease.
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Four UCLA Scientists Receive Prestigious Innovator Award for Pioneering Research Using Stem Cells
10.10.2014 - (idw) Fraunhofer-Gesellschaft
From 9-10 October 2014 around 200 scientists met at the Leipzig Fraunhofer Institute for Cell Therapy and Immunology for the ninth Fraunhofer Life Science Symposium. Held every two years, this year the event focused on the theme "Medicinal Cell Products and Stem Cells for Medicinal Applications". In recent years biomedical research has revealed numerous promising new approaches for the prevention and treatment of serious illnesses. The issue of stem cells plays a key role in this. With the symposium the Fraunhofer IZI offers international scientists a platform on which they can discuss the latest developments in this field.
The scientific program encompasses three major subject areas: production, manufacture and application. In the first section a paper presented by Sarah Ferber (Centre for Stem Cells, Regenerative Medicine and Tissue Engineering, Sheba Medical Center, Tel Hashomer, Israel) was one major point of interest: "Reprogramming the endocrine pancreas; autologous cell replacement therapy for diabetic patients". She spoke about the possibilities for transforming liver cells into insulin-producing cells. In the future this method could possibly be used to help patients with type 1 diabetes, where the misdirected immune system destroys the body's own insulin-producing beta cells of the pancreas.
The Fraunhofer Life Science Symposium brings together up to 200 participants from academic and clinical institutions to discuss the various focal points concerning new technologies, trends and developments. It is organized by the Fraunhofer Institute for Cell Therapy and Immunology IZI. For further information see http://www.fs-leipzig.com. Weitere Informationen:http://www.fs-leipzig.comhttp://www.izi.fraunhofer.de
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Experts discuss new developments in the field of stem cell research and cell therapy