Public release date: 15-Oct-2012 [ | E-mail | Share ]

Contact: Michael Turton turtonm@thehastingscenter.org 845-424-4040 x242 The Hastings Center

(Garrison, NY) Personalized genomic medicine is hailed as a revolution that will empower patients to take control of their own health care, but it could end up taking control away from patients and limiting their treatment choices, concludes an article in the Hastings Center Report. A commentary responding to the article, by the editorial director of Health and Family at Consumer Reports, also appears in the journal.

Genomic science provides two categories of data, the authors write: pharmacogenomic information and genomic susceptibility information. Pharmacogenomic information forecasts how an individual might respond to a particular therapy. Genomic susceptibility testing predicts a patient's chances of warding off or succumbing to an environmental threat or disease.

Genomic medicine's stakeholders including direct-to-consumer genetic testing companies, private research centers, and the National Institutes of Health are deeply invested in promoting how this information will benefit patients. The authors call this "empowerment rhetoric." And yet the added knowledge that comes from both pharmacogenomic information and genomic susceptibility information could have a negative impact on how much power a patient really has.

The results gleaned from pharmacogenomic information could pressure patients to comply with physicians' recommendations, the authors suggest, because molecular profiling would allow doctors to give orders with more authority. "In fact, because genomic medicine generates more risk information and makes that information the key lens for approaching health and disease, patients may actually find that they have less ability to influence health care decisions and treatments," the authors state.

The virtues of genomic susceptibility information could also go awry. First, because disease prevention relies heavily on lifestyle changes, responsibility is shifted from doctor to patient. Patients who don't make the "right" choices could be deemed irresponsible, the article says. Second, genomic information can for the time being only reveal the health risks of groups of people. Rather than provide individualized assessments, it classifies people into "genetic superfamilies." The authors argue that "population classification schemes based on racial and ethnic categories can be actively disempowering for individuals, by encouraging potentially prejudicial associations between their group affiliations and health care risks."

Patient empowerment is marketed as a paradigm shift because it puts medical data in the hands of the consumer, not just the doctor. But the authors conclude that the focus on empowerment could clash with the reality of what patients are willing or able to do with the information they receive. "The idea of patient empowerment may run up against not only the limits of patients' control over their health, but also the limits of patient control over health care systems," the article says.

The authors are Eric T. Juengst, director of the Center for Bioethics and professor in the Departments of Social Medicine and Genetics at the University of North Carolina, Chapel Hill; Michael A. Flatt, a doctoral candidate in sociology at Case Western Reserve University; and Richard A. Settersten, Jr., professor of social and behavioral health sciences and endowed director of the Hallie E. Ford Center for Healthy Children and Families in the College of Public Health and Human Sciences at Oregon State University.

In a commentary on the article, Ronni Sandroff, editorial director of Health and Family at Consumer Reports, acknowledges that pharmacogenomics could take control away from a patient if a health insurance company opted not to cover a medicine that was shown to work infrequently in people with a particular genetic makeup. But even an increase in patient empowerment can have downsides if it shifts the responsibility for health care to patients and stigmatizes people who do not, or cannot, make the "right" health choices. Sandroff notes that the greatest challenge in preventive medicine is getting people to eat less, exercise more, and reduce stress. Whether or not genetic susceptibility information will actually empower patients by propelling them toward healthier lifestyles is unknown. "This is a question that needs more serious study," she writes.

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Personalized genomic medicine: How much can it really empower patients?

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ScienceDaily (Oct. 15, 2012) New animal studies provide additional support for investigating stem cell treatments for Parkinson's disease, head trauma, and dangerous heart problems that accompany spinal cord injury, according to research findings released today.

The work, presented at Neuroscience 2012, the annual meeting of the Society for Neuroscience and the world's largest source of emerging news about brain science and health, shows scientists making progress toward using stem cell therapies to repair neurological damage.

The studies focused on using stem cells to produce neurons -- essential, message-carrying cells in the brain and spinal cord. The loss of neurons and the connections they make for controlling critical bodily functions are the chief hallmarks of brain and spinal cord injuries and of neurodegenerative afflictions such as Parkinson's disease and ALS (amyotrophic lateral sclerosis), also known as Lou Gehrig's disease.

Today's new findings show that:

Other recent findings discussed show that:

"As the fields of developmental and regenerative neuroscience mature, important progress is being made to begin to translate the promise of stem cell therapy into meaningful treatments for a range of well-defined neurological problems," said press conference moderator Jeffrey Macklis, MD, of Harvard University and the Harvard Stem Cell Institute, an expert on development and regeneration of the mammalian central nervous system. "Solid, rigorous, and well-defined pre-clinical work in animals can set the stage toward human clinical trials and effective future therapies."

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Realizing the potential of stem cell therapy: Studies report progress in developing treatments for diseases and injuries

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ScienceDaily (Oct. 15, 2012) Research released today demonstrates how new scientific knowledge is driving innovative treatments for spinal cord injuries. Spinal cord damage is debilitating and life-altering, limiting or preventing movement and feeling for millions worldwide, and leading to chronic health conditions and pain.

The new studies suggest potential therapies for managing the aftermath of pain and pressure sores, repairing nervous system damage, and speeding recovery. The findings were presented at Neuroscience 2012, the annual meeting of the Society for Neuroscience and the world's largest source of emerging news about brain science and health.

In the United States, approximately 12,000 people are hospitalized for spinal cord injury (SCI) each year, and at least 270,000 people live with it. The initial injury is usually compounded by a wave of immune activity that can extend the initial nervous system damage, and complications of SCI may include pain and pressure sores that compromise the quality of life. New research is tackling all of these dimensions of SCI.

Today's new findings show that:

"While the damage of SCI can appear to be immediate and dramatic, the biological events that lead to extensive nerve and tissue damage are complex, and injuries evolve over time," said press conference moderator Jacqueline Bresnahan, PhD, of the University of California, San Francisco, an expert on nervous system trauma caused by spinal cord injuries. "Today researchers are finding ways to intervene in the cascade of molecular changes that follow SCI. From understanding immune cell responses to the healing power of social contact, researchers are finding new ways to treat and rehabilitate patients."

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Note: Materials may be edited for content and length. For further information, please contact the source cited above.

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Public release date: 15-Oct-2012 [ | E-mail | Share ]

Contact: Shaun Mason smason@mednet.ucla.edu 310-206-2805 University of California - Los Angeles

Researchers led by Tanya Stoyanova and Dr. Owen Witte of UCLA's Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research have determined how a protein known as Trop2 drives the growth of tumor cells in prostate and other epithelial cancers.

This discovery is important because it may prove essential for creating new therapies that stop the growth of cancer, the researchers said. The study is featured on the cover of the Oct. 15 issue of the journal Genes and Development.

The Trop2 protein is expressed on the surface of many types of epithelial cancer cells cells that form tumors that grow in the skin and the inner and outer linings of organs but little was known about the protein's role in the growth and proliferation of cancer cells. The UCLA researchers discovered that Trop2 controls those processes through a mechanism that leads to the protein being cleaved into two parts, one inside the cell and one outside. This Trop2 division promotes self-renewal of the cancer cells, resulting in tumor growth.

"Determining the mechanism of this protein is important for planning treatments that stop the growth of prostate cancer, but it is also overexpressed in so many other types of cancer that it might be a treatment target for many more patients beyond that population," said senior author Witte, director of the Broad Center and a professor in the department of microbiology, immunology, and molecular genetics at UCLA.

The finding may have a critical clinical impact, the researchers said, since preventing the cleavage of Trop2 by mutating those sites on the protein where it splits eliminates the protein's ability to promote tumor cell growth. Using this knowledge, they said, new therapy strategies can be developed that block Trop2 molecular signaling, thus stopping its ability to enhance tumor growth in a variety of epithelial malignancies, including prostate, colon, oral cavity, pancreatic and ovarian cancers, among others.

"The reason I became interested in Trop2 was that it is highly expressed in many epithelial cancers but no one knew precisely how the protein worked to promote the disease," said Stoyanova, the study's first author and a postdoctoral scholar in the department of microbiology, immunology and molecular genetics at UCLA.

###

Funding for the study was provided by the California Institute for Regenerative Medicine Training Grant (TG2-01169), the U.S. Department of Defense Prostate Cancer Research Program (PC110638) and the Howard Hughes Medical Institute.

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SUNRISE, FL--(Marketwire - Oct 15, 2012) - NorthStar Biotech, LLC, a consortium of Bioheart, Inc. ( OTCQB : BHRT ) Directors and Shareholders, led by Managing Director Chuck Hart, has launched a series A private placement financing round and intends to raise a maximum capital of $20 million in exchange for 30% of the company.

"With the intellectual property of Bioheart, NorthStar Biotech is well positioned to become a leader in the field of cardiology. We are also pursuing several opportunities which will make it a leader in regenerative medicine," said Chuck Hart, Managing Director of NorthStar Biotech LLC and a Bioheart Director and longtime shareholder.

Bioheart had previously announced the formation of NorthStar Biotech in August of 2012, a consortium formed by major shareholders and insiders to purchase and protect Bioheart's senior debt that was collateralized with its intellectual property and technology. The primary use of the proceeds raised by the private placement is to fund Bioheart efforts including the Phase II/III MARVEL trial with muscle stem cells, the Phase I REGEN trial with gene modified muscle stem cells and the ANGEL trial with adipose derived stem cells.

Bioheart's cell therapy products address an unmet need in the cardiac market by providing true regenerative medicine where the MyoCell product line may regenerate muscle in areas of scar tissue and the LipiCell product may help reduce inflammation and promote the growth of new blood vessels.

About Bioheart, Inc.

Bioheart is committed to maintaining its leading position within the cardiovascular sector of the cell technology industry delivering cell therapies and biologics that help address congestive heart failure, lower limb ischemia, chronic heart ischemia, acute myocardial infarctions and other issues.Bioheart's goals are to cause damaged tissue to be regenerated, when possible, and to improve a patient's quality of life and reduce health care costs and hospitalizations.

Specific to biotechnology, Bioheart is focused on the discovery, development and, subject to regulatory approval, commercialization of autologous cell therapies for the treatment of chronic and acute heart damage and peripheral vascular disease. Its leading product, MyoCell, is a clinical muscle-derived cell therapy designed to populate regions of scar tissue within a patient's heart with new living cells for the purpose of improving cardiac function in chronic heart failure patients. For more information on Bioheart, visit http://www.bioheartinc.com, or visit us on Facebook: Bioheart and Twitter @BioheartInc.

About NorthStar Biotech, LLC

NorthStar Biotech was founded in 2012 and is focused on the development of regenerative medicine for a variety of degenerative diseases.It maintains an exclusive, international license to the products and intellectual property rights of Bioheart, Inc. ("Bioheart").NorthStar is currently raising sums to complete clinical testing required by Bioheart; to create and oversee an international sales force for Bioheart; and to sell and distribute the Bioheart products and Bioheart IP on an international basis.

Forward-Looking Statements: Except for historical matters contained herein, statements made in this press release are forward-looking statements. Without limiting the generality of the foregoing, words such as "may," "will," "to," "plan," "expect," "believe," "anticipate," "intend," "could," "would," "estimate," or "continue" or the negative other variations thereof or comparable terminology are intended to identify forward-looking statements.

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NorthStar Launches $20 Million Private Placement Round With Proceeds to Fund Bioheart Trials

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ScienceDaily (Oct. 15, 2012) Georgia Health Sciences University researchers have developed a mouse that errs on the side of making bone rather than fat, which could eventually lead to better drugs to treat inflammatory diseases such as rheumatoid arthritis.

Drugs commonly used to treat those types of conditions -- called glucocorticoids -- work by turning down the body's anti-inflammatory response, but simultaneously turn on other pathways that lead to bone loss. The result can lead to osteoporosis and an accumulation of marrow fat, says Dr. Xingming Shi, bone biologist at the GHSU Institute of Molecular Medicine and Genetics.

The key to the body developing bone instead of fat, a small protein called GILZ, was shown in cell cultures in 2008. Now, with work by GHSU Graduate Student Guodong Pan, the work has been replicated in an animal model. Pan received the American Society for Bone and Mineral Research's Young Investigator Award for his work at the society's annual meeting Oct. 12-15 in Minneapolis.

Bone and marrow fat come from the same biological precursor -- mesynchymal stem cells. "The pathways for bone and fat have a reciprocal relationship, so we needed to find the key that disrupts the fat production pathway, which would then instead encourage bone growth," Shi says.

GILZ, Shi and Pan say, was already a known mediator of the anti-inflammatory response of glucocorticoids, and the protein also mediates bone production. Shi's early research had shown that glucocorticoids enhance bone formation in the lab because of a short "burst" of GILZ.

The protein works by inhibiting the way cells regulate fat production and turn on fat-producing genes, Shi says. "When you permanently express GILZ, the fat pathway is suppressed, so the body chooses to produce bone instead."

"We found that when we overexpressed the protein in these mice, it increased bone formation," Pan added. "This supports our original hypothesis that GILZ mediates the body's response to glucocorticoids and encourages bone growth." In fact, the genetically modified mice showed a significant increase in bone mineral density and bone volume as well, he found.

"That means GILZ is a potential new anti-inflammatory drug candidate that could spare people from the harmful effects associated with glucocorticoid therapy," Pan said

Long-term goals, Shi said, are developing the GILZ-like pill that is anti-inflammatory and protects or even increases bone production.

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Public release date: 15-Oct-2012 [ | E-mail | Share ]

Contact: Karen Robinson karobinson@som.umaryland.edu 410-706-7590 University of Maryland Medical Center

A new method of using adult stem cells as a model for the hereditary condition Gaucher disease could help accelerate the discovery of new, more effective therapies for this and other conditions such as Parkinson's, according to new research from the University of Maryland School of Medicine.

Scientists at the University of Maryland School of Medicine reprogrammed stem cells to develop into cells that are genetically similar to and react to drugs in a similar way as cells from patients with Gaucher disease. The stem cells will allow the scientists to test potential new therapies in a dish, accelerating the process toward drug discovery, according to the paper published online in the journal the Proceedings of the National Academy of Sciences (PNAS) on Oct. 15 (Panicker et.al.).

The study was funded with $1.7 million in grants from the Maryland Stem Cell Research Fund; researchers received a start-up grant for $200,000 in 2007 and a larger, five-year grant for $1.5 million in 2009.

"We have created a model for all three types of Gaucher disease, and used stem cell-based tests to evaluate the effectiveness of therapies," says senior author Ricardo Feldman, Ph.D., associate professor of microbiology and immunology at the University of Maryland School of Medicine, and a research scientist at the University of Maryland Center for Stem Cell Biology and Regenerative Medicine. "We are confident that this will allow us to test more drugs faster, more accurately and more safely, bringing us closer to new treatments for patients suffering from Gaucher disease. Our findings have potential to help patients with other neurodegenerative diseases as well. For example, about 10 percent of Parkinson's disease patients carry mutations in the recessive gene for Gaucher disease, making our research possibly significant for Parkinson's disease as well."

Gaucher disease is the most frequent lipid-storage disease. It affects 1 in 50,000 people in the general population. It is most common in Ashkenazi Jews, affecting 1 in 1,000 among that specific population. The disease occurs in three subtypes Type 1 is the mildest and most common form of the disease, causing symptoms such as enlarged livers and spleens, anemia and bone disease. Type 2 causes very serious brain abnormalities and is usually fatal before the age of two, while Type 3 affects children and adolescents.

The condition is a recessive genetic disorder, meaning that both parents must be carriers for a child to suffer from Gaucher. However, said Dr. Feldman, studies have found that people with only one copy of a mutated Gaucher gene those known as carriers are at an increased risk of developing Parkinson's disease.

"This science is a reflection of the mission of the University of Maryland School of Medicine to take new treatments from bench to bedside, from the laboratory to patients, as quickly as possible," says E. Albert Reece, M.D., Ph.D., M.B.A., vice president for medical affairs at the University of Maryland and John Z. and Akiko K. Bowers Distinguished Professor and dean of the University of Maryland School of Medicine. "We are excited to see where this research goes next, bringing new hope to Gaucher patients and their families."

Dr. Feldman and his colleagues used the new reprogramming technology developed by Shinja Yamanaka in Japan, who was recognized with this year's Nobel Prize for Medicine or Physiology. Scientists engineered cells taken from the skin of Gaucher patients, creating human induced pluripotent stem cells, known as hiPSC stem cells that are theoretically capable of forming any type of cell in the body. Scientists differentiated the cells to form white blood cells known as macrophages and neuronal cells.

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University of Maryland School of Medicine scientists develop stem cell model for hereditary disease

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ScienceDaily (Oct. 15, 2012) A new method of using adult stem cells as a model for the hereditary condition Gaucher disease could help accelerate the discovery of new, more effective therapies for this and other conditions such as Parkinson's, according to new research from the University of Maryland School of Medicine.

Scientists at the University of Maryland School of Medicine reprogrammed stem cells to develop into cells that are genetically similar to and react to drugs in a similar way as cells from patients with Gaucher disease. The stem cells will allow the scientists to test potential new therapies in a dish, accelerating the process toward drug discovery, according to the paper published online in the journal the Proceedings of the National Academy of Sciences (PNAS) on Oct. 15.

"We have created a model for all three types of Gaucher disease, and used stem cell-based tests to evaluate the effectiveness of therapies," says senior author Ricardo Feldman, Ph.D., associate professor of microbiology and immunology at the University of Maryland School of Medicine, and a research scientist at the University of Maryland Center for Stem Cell Biology and Regenerative Medicine. "We are confident that this will allow us to test more drugs faster, more accurately and more safely, bringing us closer to new treatments for patients suffering from Gaucher disease. Our findings have potential to help patients with other neurodegenerative diseases as well. For example, about 10 percent of Parkinson's disease patients carry mutations in the recessive gene for Gaucher disease, making our research possibly significant for Parkinson's disease as well."

Gaucher disease is the most frequent lipid-storage disease. It affects 1 in 50,000 people in the general population. It is most common in Ashkenazi Jews, affecting 1 in 1,000 among that specific population. The disease occurs in three subtypes -- Type 1 is the mildest and most common form of the disease, causing symptoms such as enlarged livers and spleens, anemia and bone disease. Type 2 causes very serious brain abnormalities and is usually fatal before the age of two, while Type 3 affects children and adolescents.

The condition is a recessive genetic disorder, meaning that both parents must be carriers for a child to suffer from Gaucher. However, said Dr. Feldman, studies have found that people with only one copy of a mutated Gaucher gene -- those known as carriers -- are at an increased risk of developing Parkinson's disease.

"This science is a reflection of the mission of the University of Maryland School of Medicine -- to take new treatments from bench to bedside, from the laboratory to patients, as quickly as possible," says E. Albert Reece, M.D., Ph.D., M.B.A., vice president for medical affairs at the University of Maryland and John Z. and Akiko K. Bowers Distinguished Professor and dean of the University of Maryland School of Medicine. "We are excited to see where this research goes next, bringing new hope to Gaucher patients and their families."

Dr. Feldman and his colleagues used the new reprogramming technology developed by Shinja Yamanaka in Japan, who was recognized with this year's Nobel Prize for Medicine or Physiology. Scientists engineered cells taken from the skin of Gaucher patients, creating human induced pluripotent stem cells, known as hiPSC -- stem cells that are theoretically capable of forming any type of cell in the body. Scientists differentiated the cells to form white blood cells known as macrophages and neuronal cells.

A key function of macrophages in the body is to ingest and eliminate damaged or aged red blood cells. In Gaucher disease, the macrophages are unable to do so -- they can't digest a lipid present in the red blood cell membrane. The macrophages become engorged with lipid and cannot completely clear the ingested red blood cells. This results in blockage of membrane transport pathways in the macrophages lodged in the bone marrow, spleen and liver. The macrophages that the scientists created from the reprogrammed stem cells exhibited this characteristic hallmark of the macrophages taken from Gaucher patients.

To further test the stem cells, the scientists administered a recombinant enzyme that is effective in treating Gaucher patients with Type 1 disease. When the cells were treated with the enzyme, the function of the macrophages was restored -- they completely cleared the red blood cells.

"The creation of these stem cell lines is a lovely piece of stem cell research," said Curt Civin, M.D., professor of pediatrics and physiology, associate dean for research and founding director of the Center for Stem Cell Biology & Regenerative Medicine at the University of Maryland School of Medicine. "Dr. Feldman is already using these Gaucher patient-derived macrophages to better understand the disease fundamentals and to find novel medicines for Gaucher disease treatment. A major goal of our Center for Stem Cell Biology & Regenerative Medicine is to translate our fundamental discoveries into innovative and practical clinical applications that will enhance the understanding, diagnosis, treatment, and prevention of many human diseases. Clinical applications include not only transplantation of stem cells, but also the use of stem cells for drug discovery as Dr. Feldman's studies so beautifully illustrate."

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Public release date: 15-Oct-2012 [ | E-mail | Share ]

Contact: Kat Snodgrass 202-962-4090 Society for Neuroscience

NEW ORLEANS New animal studies provide additional support for investigating stem cell treatments for Parkinson's disease, head trauma, and dangerous heart problems that accompany spinal cord injury, according to research findings released today. The work, presented at Neuroscience 2012, the annual meeting of the Society for Neuroscience and the world's largest source of emerging news about brain science and health, shows scientists making progress toward using stem cell therapies to repair neurological damage.

The studies focused on using stem cells to produce neurons essential, message-carrying cells in the brain and spinal cord. The loss of neurons and the connections they make for controlling critical bodily functions are the chief hallmarks of brain and spinal cord injuries and of neurodegenerative afflictions such as Parkinson's disease and ALS (amyotrophic lateral sclerosis), also known as Lou Gehrig's disease.

Today's new findings show that:

Other recent findings discussed show that:

"As the fields of developmental and regenerative neuroscience mature, important progress is being made to begin to translate the promise of stem cell therapy into meaningful treatments for a range of well-defined neurological problems," said press conference moderator Jeffrey Macklis, MD, of Harvard University and the Harvard Stem Cell Institute, an expert on development and regeneration of the mammalian central nervous system. "Solid, rigorous, and well-defined pre-clinical work in animals can set the stage toward human clinical trials and effective future therapies."

###

This research was supported by national funding agencies such as the National Institutes of Health, as well as private and philanthropic organizations.

Todd Bentsen, (202) 962-4086

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Realizing the potential of stem cell therapy

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The Grekos hearing is scheduled to begin at 9 a.m. Tuesday. The location has changed to the Collier County Courthouse in room 4-D, according to a case filing Monday.

The hearing before J. Lawrence Johnson, an administrative law judge from Tallahassee, will begin at 9 a.m. The hearing is scheduled to last four days. The Collier County Courthouse is located at 3315 U.S. 41 E.

Photo by Allie Garza

Zannos Grekos

BONITA SPRINGS Bonita Springs physician Zannos Grekos, whose license is in jeopardy for controversial stem cell therapy, is getting his day before a judge.

Barring a last-minute delay or settlement, an administrative hearing is scheduled to begin Tuesday in Naples for the 47-year-old. He is fighting to get his license back in good standing from a suspension order, while the state Department of Health is pursuing more discipline and potentially revocation of his license.

Trained as a cardiologist, he's been licensed in Florida since 1996.

The trial-like proceeding, without a jury, is scheduled for four days before an administrative law judge. The proceeding is open to the public. The case against Grekos has garnered considerable media attention, including CNN and inquiries from European media.

A Texas father, Jimmy Bell, will be tracking what happens. Last year, he paid $57,000 upfront for his 5-year-old son, Jason, to undergo stem cell therapy to fight pulmonary hypertension. Despite pleas that his boy was weakening by the day, the treatment was never scheduled and Jason died. Bell received a $10,000 refund.

"He's taking advantage of people and it's more for personal gain," Bell said. "I'd like to see that stopped."

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ScienceDaily (Oct. 15, 2012) Soybean cyst nematode (SCN) does hundreds of millions of dollars' worth of damage each year. Matt Hudson and Brian Diers, crop sciences researchers at the University of Illinois and Andrew Bent at the University of Wisconsin, think they may have found a way to strengthen plant resistance. The research has just been published in Science Express.

Diers and Hudson, with researchers at Wisconsin and the University of Nebraska, have been studying an area on chromosome 18 called Rhg1 (Resistance to H. glycines) that is known to be the location of the main source of SCN resistance. Rhg1 disrupts the formation and maintenance of potential nematode-feeding sites on plant roots.

Most SCN-resistant soybeans in the Midwest are bred to contain Rhg1, but no one knew the DNA sequence of the gene that was responsible for the resistance. Diers wanted to find it.

"You could say it's a billion-dollar gene because it's in many varieties, it's widely used, and it's protecting varieties against these nematodes," he explained.

Using fine mapping, which is a technique that involves mapping genes in a very constrained area, Diers narrowed the search down to a few gene candidates. At that point, Hudson and Bent got involved in the analysis.

By then, the soybean genome sequence had been completed, greatly facilitating their research. "It became possible to know which genes were within the genetic intervals that people had historically used to confer traits like nematode resistance," Hudson said.

"When we had the genome sequenced, most people were shocked by how many genes there were in regions that people considered to be one gene," he continued. "By doing these fine-mapping experiments, you could get it down to a smaller number of possible genes."

There was, however, one big problem: the soybean that had been sequenced was not nematode-resistant.

"So, however many genes there were in the Rhg1 interval, we knew that the gene that actually makes the plants nematode-resistant wasn't there," Hudson said.

They went back to the nematode-resistant line and sequenced the genome in the interval. When they finished, they saw something very unusual. Rather than finding a gene in the resistant line that was not present in the susceptible line or changes in a gene that was present in both, they saw that a group of four genes had been replicated several times.

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Dundee University experts said P34 played a key role in causing the disease punctate PPK, which gives sufferers dots of hard, thickened skin which can cause pain and discomfort.

Irwin McLean, professor of human genetics in the Centre for Dermatology and Genetic Medicine at the university, said: "We have not only found this gene but we have been able to figure out how it works, which is very important.

"When the gene is disrupted or knocked out, the cells in the skin grow too fast and this results in these hard, thick, painful lesions which can be quite debilitating. When the gene is working properly then the skin forms normally.

"Knowing about this gene and what it does makes it easier for us to diagnose this form of skin disease and look towards developing new therapies.

"The pathway where this gene functions is a possible drug target although it will need more work to identify how we can take advantage of that."

Punctate PPK is one of a whole family of PPK skin diseases, each of which are relatively rare. It is estimated to affect around one in every 15,000 people in the UK.

The find was made possible by the use of next generation sequencing technology, which allows researchers to screen large amounts of genome data in a short space of time.

"This is a notable step forward in diagnosing skin diseases and the genetic causes behind them as this is research that we simply could not have done just a few years ago, We are now able to spot faulty genes and track their behaviour far more effectively," said Mr McLean.

The research is published in the journal Nature Genetics.

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Scientists have identified a soybean gene responsible for making some varieties resistant to the cyst nematode, a pest responsible for $1 billion in annual crop losses.

The gene wards off nematodes by making an enzyme that starves the pest or acts as a natural pesticide, according to a paper released today in the journal Nature. The study is the first to identify the gene and its mechanism for creating resistance, said lead authors Melissa Mitchum of the University of Missouri in Columbia and Khalid Meksem of Southern Illinois University in Carbondale.

The soybean cyst nematode can cut crop yields 50 percent and cause $1 billion in losses in the $42.2 billion annual U.S. crop, making it the top soybean pathogen, Greg Tylka, a plant pathology professor at Iowa State University. Knowing which gene is responsible for natural resistance will help breeders identify the hardiest varieties and could lead to genetically modified soybeans with complete resistance, he said.

This could speed up breeding for soybean cyst nematode resistance by a quantum leap, Tylka, who wasnt involved with the Nature study, said today by telephone from Ames, Iowa. It will allow traditional breeding to be very precise.

The soybean cyst nematode starts life as a microscopic worm that burrows into soybean roots, where the female feeds and swells into a leathery, lemon-sized cyst full of eggs. The eggs are time released, hatching over the course of a decade or more, so rotation with other crops does little to eradicate the pests from a field, Tylka said.

Soybeans have been bred to resist the cyst nematode, an import from Asia, since it was first discovered in the U.S. in 1954, Tylka said. Resistant varieties remain imperfect, with damage occurring to varying degrees depending on the plant and the type of cyst nematode in the field, he said.

Identification of a second soybean gene for cyst nematode resistance is needed before plants can be created that offer complete resistance, Tylka said. In the near term, researchers may want to focus on how the newly discovered enzyme-producing gene confers resistance.

In addition to breeding soybeans for resistance to nematodes, Monsanto Co. (MON), the worlds biggest seed company, has an early-stage research project on a bean that is genetically modified to resist the pest, Sara E. Miller, a spokeswoman for the St. Louis-based company, said in an e-mail. Monsanto, which in 2008 made public its sequence of the soybean cyst nematode genome, also is developing a seed treatment to control nematodes, she said.

To contact the reporter on this story: Jack Kaskey in Houston at jkaskey@bloomberg.net

To contact the editor responsible for this story: Simon Casey at scasey4@bloomberg.net

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Soybean Gene Find May Ward Off $1 Billion Pest

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MELBOURNE researchers may have found a way to block a gene that fuels the growth of tumours in about a quarter of stomach cancer cases, paving the way for a new treatment for one of the world's deadliest cancers.

Researchers from the Monash Institute of Medical Research found a gene that produces a protein called toll-like receptor 2 was overactivated in about 25 per cent of cancer patients, after noticing a similar trend in animals.

In the study published today in the journal Cancer Cell, they found the protein was causing tumour cells to grow, and that antibodies could counteract it in mice.

Senior researcher Brendan Jenkins said: "It was quite remarkable, over a 10-week period the antibodies actually stopped these tumours from growing."

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The antibody treatment is expected to move into human trials within the next couple of years, and would be offered in addition to existing treatments such as chemotherapy before and after surgery.

"We will identify patients who have increasing amounts of this protein, and treat them with the antibody together with the current standard treatment," Associate Professor Jenkins said.

"Our belief is that by doing that we can stop or slow down the growth of tumours, and reduce the chance they will spread to other parts of the body."

Associate Professor Jenkins said screening for the protein could also be used to capture stomach cancer in its early stages, allowing for more effective treatment.

He said the finding might be relevant to other cancers in which chronic inflammation could lead to the development of cancer, such as colon, liver and lung cancers.

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ScienceDaily (Oct. 15, 2012) Preventing activity of a key enzyme in potatoes could help boost potato quality by putting an end to cold-induced sweetening, according to U.S. Department of Agriculture (USDA) scientists.

Cold-induced sweetening, which occurs when potatoes are put in long-term cold storage, causes flavor changes and unwanted dark colors in fried and roasted potatoes. But long-term cold storage is necessary to maintain an adequate supply of potatoes throughout the year.

Agricultural Research Service (ARS) scientists found that during cold storage, an enzyme called invertase causes changes in potato sugars -- more accumulation of sucrose and a corresponding increase in the amount of glucose and fructose in tubers stored at very low temperatures.

At the ARS Vegetable Crops Research Unit in Madison, Wis., plant physiologist Paul Bethke, geneticist Shelley Jansky, and technician Andy Hamernik used a recently developed technology to show that decreasing the activity of invertase is sufficient to enable cold storage of potatoes without compromising the appearance of potato chips or the growth characteristics of the potato plants.

Bethke and his colleagues are using molecular tools to improve understanding of what is controlling the process of cold-induced sweetening. Potatoes are sensitive to their environment and highly sensitive to low temperatures, and respond to these temperatures by producing certain sugars called "reducing sugars," primarily glucose and fructose. When chips or fries are made from these potatoes, they tend to be dark-colored and bitter. The scientists' research paper in Plant Physiology provides a proof of concept that the invertase enzyme is critically important in the process.

However, invertase's level of importance has never been clear, because there are other biochemical steps that might also contribute, according to Bethke.

Read more about this research in the October 2012 issue of Agricultural Research magazine: http://www.ars.usda.gov/is/AR/archive/oct12/fruits1012.htm

ARS is USDA's principal intramural scientific research agency, and the research supports the USDA priority of promoting international food security.

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Gene suppression can reduce cold-induced sweetening in potatoes

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The pitter-patter of tiny feet could announce the arrival of tomorrow's landmine detectors lab mice genetically engineered by humans to sniff out TNT explosives.

The idea became reality in a New York City lab that already created and bred the special breed of mice. Such mice have a sense of smell 500 times better than normal at detecting DNT, a chemical cousin of TNT, and they may alert humans to the presence of landmines by possibly falling down in an epileptic seizure.

"Whatever their behavior is going to be, we think we will be able to track their change in behavior using a sort of microchip implanted under their skin that would indeed wirelessly report back to a computer," said Charlotte D'Hulst, a bioengineer at Hunter College, City University of New York.

The mice could go a long way toward saving human lives in a world where landmines kill 15,000 to 20,000 people every year, according to the United Nations. A Belgian nonprofit has already trained giant African pouched rats to sniff out landmine explosives in a matter of hours compared with days for humans using metal detectors.

But the rats require nine months of training based on banana food rewards. The genetically modified mice could prove faster to breed and would require much shorter training, D'Hulst said. She presented her research at the Neuroscience 2012 conference in New Orleans on Oct. 14.

"The major advantage of the approach is that we will have created animals with an inherent super sensitivity to DNT, which will make the training significantly quicker," D'Hulst told TechNewsDaily. "Mice are smaller, cheaper and very easy to breed in large numbers, so one could get more animals do the job simultaneously (about 500, for example)."

Recent research suggests the mice may fall down and undergo epileptic seizures in response to the smell of TNT the result of all the sensory neurons firing off in their hypersensitive noses and flooding the brain with signals. But whatever their response, researchers anticipate using the implanted microchips implanted microchips to detect whether the mice had found explosive material.

D'Hulst and her colleagues still need to test how the mice react to DNT in the lab and on the field. But she expects that the mice could be ready for action in five years if all goes well. [Genetically Engineered Cell Shoots Out First-Ever Biological Laser]

The MouSensor Project, funded by the National Institutes of Health, could also eventually lead to mice genetically modified with special noses for other jobs sniffing out tuberculosis in humans, identifying contaminated water, or perhaps helping rescue workers locate survivors of natural disasters.

Researchers created the special mice for the landmine detection job by injecting genetically modified DNA into a fertilized mouse egg, so that the embryos could be surgically implanted in a female mouse. The female mice were tricked into becoming "pseudopregant" by mating them with male mice who had undergone vasectomies to prevent them from breeding.

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Public release date: 15-Oct-2012 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, October 15, 2012In addition to the obvious benefit of eliminating the need for an injection, new vaccine delivery methods via the lungs offer particular advantages for protecting against infectious agents that enter the body through the respiratory track. A comprehensive review article that presents the current status, challenges, and opportunities of pulmonary vaccine delivery is published in Journal of Aerosol Medicine and Pulmonary Drug Delivery, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free online on the Journal of Aerosol Medicine and Pulmonary Drug Delivery website.

In "Pulmonary Vaccine Delivery: A Realistic Approach?" Wouter Tonnis and coauthors from University of Groningen and National Institute for Public Health and the Environment (Bilthoven), The Netherlands, describe the unique physiology and immune responsiveness of the respiratory track that make pulmonary vaccine delivery such an attractive alternative to traditional injections. Although pulmonary vaccination is still a young field, with much more research needed, evidence suggests administration of a vaccine to the lungs can induce a local immune response more effectively than conventional types of vaccine delivery, in addition to stimulating antibody production throughout the body. This could be especially important for combating pathogens that cause pulmonary diseases.

"The lung is an immunologic powerhouse that remains largely unexplored. Theoretically we should be able to avoid needles and simply inhale our vaccines," says Editor-in-Chief Gerald C. Smaldone, MD, PhD, Professor and Chief, Division of Pulmonary and Critical Care Medicine at SUNY-Stony Brook.

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About the Journal

Journal of Aerosol Medicine and Pulmonary Drug Delivery is an authoritative peer-reviewed journal published bimonthly in print and online. It is the Official Journal of the International Society for Aerosols in Medicine. The Journal is the only authoritative publication delivering innovative articles on the health effects of inhaled aerosols and delivery of drugs through the pulmonary system. Topics covered include airway reactivity and asthma treatment, inhalation of particles and gases in the respiratory tract, toxic effects of inhaled agents, and aerosols as tools for studying basic physiologic phenomena. Complete tables of content and a sample issue may be viewed on the Journal of Aerosol Medicine and Pulmonary Drug Delivery website.

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Pediatric Allergy, Immunology, and Pulmonology, High Altitude Medicine & Biology, and Microbial Drug Resistance. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 70 journals, books, and newsmagazines is available online on the Mary Ann Liebert, Inc., publishers website.

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Can vaccines be delivered via the lungs instead of by injection?

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Re: your Oct. 14 editorial, The propositions:

The Star believes that agencies at the federal and state levels should make sure foods are safe and properly labeled, but they are not doing. So, it is now up to the people to take food safety matters into their own hands when it comes to genetic engineering and the resulting effect on our health and the health of our families.

Proposition 37 is neither complicated nor technical, and rather than properly managing genetic engineering, federal and state agencies are leaving it in the hands of the chemical companies to assure us that our food is safe when it comes to genetic engineering.

Proposition 37 requires labeling of products that contain first generation genetically modified organisms - plain and simple. If these chemical companies, big agriculture, etc., are so proud of their laboratory created, genetically modified food, we say they should be proud to put a label on them so we know what we are buying, or not.

We have a right to know what we are eating, just like the citizens of the 50 other countries that already label genetically engineered food.

- Cyndi and Jude Egold,

Moorpark

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Food labeling regulations

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Public release date: 15-Oct-2012 [ | E-mail | Share ]

Contact: Anita Srikameswaran 412-578-9193 University of Pittsburgh Schools of the Health Sciences

PITTSBURGH, Oct. 15, 2012 An increased risk of autism spectrum disorders (ASD) could result from an accumulation of many small, common genetic variations rather than large-effect, rare changes in the genetic code, according to a multicenter team led by researchers at the University of Pittsburgh School of Medicine. Their findings, published today in Molecular Autism, provide new insights into the genetic factors that underlie the neurodevelopmental condition.

Scientists have debated about the genetic contributions that lead to ASD in families where only one individual is affected, called simplex, versus those that have multiple affected family members, called multiplex, said senior author Bernie Devlin, Ph.D., associate professor, Department of Psychiatry, University of Pittsburgh School of Medicine.

"Our team compared simplex, multiplex and unaffected families using sophisticated quantitative genetic techniques," he said. "In families where only one child has an ASD, 40 percent of the risk is inherited while in families with more than one affected child, the risk rises to 60 percent."

For the project, the team examined thousands of DNA samples from families in the Simons Simplex Collection, in which one child but no parent or sibling had an ASD; the Autism Genome Project, in which more than one child had an ASD; and unaffected families enrolled in the HealthABC Program.

In addition to reviewing nearly 1 million gene variations, called single nucleotide polymorphisms (SNPs), to look for inheritance patterns associated with ASD, they also ran computer simulations to plot family trees using 1,000 SNPs that appear to impact the risk of ASD.

"These small gene changes can add up even though individually they do little harm," Dr. Devlin said. "This might explain why parents who do not have autism traits can have children who do."

Other research has shown that autism and related disorders also can arise from spontaneous variations in parental genes prior to conception as well as rare mutations of larger effect that are passed on, he noted. The multiple inheritance patterns could help explain the range of symptoms in the disorder.

The team included researchers from Yale University, the University of Michigan, University of California Los Angeles, Emory University, Harvard University and others. The effort was funded by grants from the Simons Foundation and National Institutes of Health grant MH057881.

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Additive effect of small gene variations can increase risk of autism spectrum disorders

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MOUNTAIN VIEW, Calif., Oct. 15, 2012 /PRNewswire/ --In a new theoretical study, 23andMe, the leading personal genetics company, developed a mathematical model which shows that family history and genetic tests offer different strengths. The study results suggest that both family history and genetics are best used in combination to improve disease risk prediction. The full results of the study have now been published online in the journal PLOS Genetics.

Family history is most useful in assessing risks for highly common, heritable conditions such as coronary artery disease. However, for diseases with moderate or low frequency, such as Crohn's disease, family history accounts for less than four percent of disease heritability and is substantially less predictive than genetic factors in the overall population. The study results indicate single nucleotide polymorphism (SNP)-based genetic tests can reveal extreme likelihood ratios for a relatively large percentage of individuals, thus providing potentially valuable evidence in differential diagnoses.

"Both family history and genetics are important tools for assessing an individual's risk for disease," 23andMe CEO and co-founder Anne Wojcicki said. "We believe it will become increasingly important for individuals and physicians to know both family history and genetic profile to provide optimal healthcare."

Lead author and 23andMe scientist Chuong Do, Ph.D, worked with 23andMe senior medical director Uta Francke, M.D., and principal scientists David Hinds, Ph.D., and Nicholas Eriksson Ph.D. to make a comprehensive comparison of family health histories and genetic testing to assess risk for 23 different conditions. These conditions included coronary artery and heart diseases, type 1 and 2 diabetes, prostate cancer, Alzheimer's disease, breast cancer, lung cancer, Crohn's and celiac disease, ovarian cancer, melanoma, bipolar disease and schizophrenia among others.

The analysis confirms that family history is most useful for highly common, heritable conditions and for single-gene (Mendelian) disorders with high penetrance, where the specific genetic cause is not yet known. For relatively common diseases that may have many contributing genetic and environmental factors, such as coronary artery disease, knowing that your father had the disease is helpful at predicting whether or not you might be at risk for the same condition.

For less common diseases involving many weak genetic, such as Crohn's disease, knowing family history seldom helps in making a risk prediction, in part, because these diseases are uncommon enough that they would rarely show up in the immediate family health history. When family histories are uninformative, genetic testing may still reveal the genetic variants that would put an individual at a higher or lower risk for the condition. For example, Crohn's disease might not show up in a family history, but the risk prediction from a genetic test can be relatively more informative.

"These results indicate that for a broad range of diseases, already identified SNP associations may be better predictors of risk than their family history-based counterparts, despite the large fraction of missing heritability that remains to be explained," stated lead researcher Chuong Do, Ph.D. "They also suggest that in some cases, individuals may benefit from supplementing their family medical history with genetic data, in particular, as genetic tests are improving and more risk factors are discovered."

"This study addresses the false division between these two diagnostic tools, genetic testing versus family health histories, where the approaches have traditionally been portrayed as competing alternatives," explained Uta Francke, M.D., senior medical director. "Physicians rely on a variety of tools such as a stethoscope or a thermometer both are useful in their own way. Similarly, family health histories and genetics both offer different but equally valuable information to inform patient care."

"Using genetic testing or SNP-association based methods to estimate risk for some rare complex diseases is as good as family histories can be at estimating risk for common heritable conditions," Dr. Francke continued, "and for individuals who don't have access to their family health history, genetic testing can alert them to risks they wouldn't be aware of otherwise."

The authors use their theoretical model to demonstrate the limits of predictive testing while also outlining specific areas where genetic tests have the potential to be medically useful. These results, which provide a cautiously optimistic outlook on the future of genetic testing, contrast with the conclusions reached in an independent study published earlier this year in Science Translational Medicine.

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FIVE POINTS, Calif., Oct.15, 2012 /PRNewswire/ --S&W Seed Company (Nasdaq:SANW)today announced that Dan Gardnerhas joined S&W as Vice President of Seed Breeding and Genetics. Mr. Gardner joins S&W from a leadership position in breeding and international sales at Dairyland Seed Co., a Dow AgroSciences subsidiary, where he served for 18 years. Mr. Gardner,aUC Davis educated scientist and seedsman, is well known and respected in the alfalfa seed industry.

"It's no coincidence that Dan is joining our seniormanagement so soon after the acquisition of Imperial Valley Seeds," said Mark Grewal, chief executive officer of S&W Seed Company. "The leadership at S&W and IVS has long known Dan as a world class seed breeder. To say we are 'charged up' that Dan is joining us now -- after our acquisition of Imperial Valley Seeds -- would be a real understatement. It's perfect timing for him to come on board."

Dan Gardner's most recent position was asInternational Distribution ManagerfortheDairylandSeed Co., a subsidiary ofDowAgroSciences.In that capacity, Mr. Gardner was tasked withincreasing sales ofDairylandSeed's non-dormant alfalfa varieties in California, Saudi Arabia, Morocco, South Africa, Mexico, Argentina, and France.At the same time, Mr. Gardnerwasthe Alfalfa Breeding Leader and Field Station Leader for a multiple location team of breeders with testing locations in both North and South America.Duringhisyears as an alfalfa seed breeder, Mr. Gardner was responsible for Dairyland releasing 12 certified non-dormant and semi-dormant varieties plus the first "four"semi-dormant hybrids and the only non-dormant hybrid alfalfa in the world.Mr. Gardnergraduated from UCDavis in 1989 with a BS degree in Genetics and from the UCDavis Plant Breeding Academy in 2008. Mr. Gardner currently serves on the board of the California Seed Association.

S&W anticipates that Mr. Gardner will be intimately involved with the design and implementation of the company's plant breeding activities.S&W recently announced the expansion into the biotech segment through its intellectual property licensing and breeding agreements with Monsanto and Forage Genetics, Inc. (FGI).S&W has previously announced the expansion of its alfalfa seed breeding program to include dormant varieties.In addition, S&W is seeking to expand the stevia breeding program which it launched in 2009.

Dan Gardner, S&W's new Vice President of Breeding and Genetics, commented, "I look forward to continuing the S&W tradition of providing growers with the highest yielding alfalfa varieties, both in terms of seed yield and forage yield. My experience has prepared me to take existing S&W germplasm to the next level of yield performance, as well as broadening the range of S&W varieties to meet the expanding geography of S&W customers."

About S&W Seed CompanyFounded in1980 and headquartered in the Central Valley of California, S&W Seed Company is a leading producer of warm climate, high yield alfalfa seed varieties, including varieties that can thrive in poor, saline soils, as verified over decades of university-sponsoredtrials.S&WSeedalso offers seed cleaning and processing at its 40-acre facility in Five Points, Californiaand, in 2011,began the commercial launch of its California-basedsteviabusinessin response tothe growing global demand for the all-natural, zero calorie sweetenerfrom the food and beverage industry. For more information, please visitwww.swseedco.com.

Safe Harbor StatementThis release contains "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended and such forward-looking statements are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. "Forward-looking statements" describe future expectations, plans, results, or strategies and are generally preceded by words such as "may," "future," "plan" or "planned," "will" or "should," "expected," "anticipates," "draft," "eventually" or "projected." You are cautioned that such statements are subject to a multitude of risks and uncertainties that could cause future circumstances, events, or results to differ materially from those projected in the forward-looking statements, including the risks that actual results may differ materially from those projected in the forward-looking statements as a result of various factors and other risks identified in the Company's 10-K for thefiscal year ended June 30, 2012, and other filings made by the Company with the Securities and Exchange Commission.

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Dan Gardner Joins S&W as Vice President of Breeding and Genetics

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SALT LAKE CITY, Oct. 15, 2012 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) today announced that it will issue financial results for the first fiscal quarter 2013 following the close of market on Monday, November 5, 2012.

The Company will also host a conference call on Monday, November 5, 2012 at 4:30 P.M. Eastern to review the financial results. Participating on the call will be: Peter Meldrum, President and Chief Executive Officer, Mark Capone, President of Myriad Genetic Laboratories, Inc. and Jim Evans, Chief Financial Officer.

To listen to the call, interested parties may dial 800-354-6885 or 303-223-2680. All callers will be asked to reference reservation number 21607424.

The conference call will also be available through a live webcast at http://www.myriad.com.

A replay of the call will be available two hours after the end of the call for seven days and may be accessed by dialing 800-633-8284 or 402-977-9140 and entering reservation number 21607424.

About Myriad Genetics

Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patient's lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's portfolio of molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com

Myriad, the Myriad logo, BRACAnalysis, Colaris, Colaris AP, Melaris, TheraGuide, Prezeon, OnDose, Panexia and Prolaris are trademarks or registered trademarks of Myriad Genetics, Inc. in the United States and foreign countries. MYGN-F, MYGN-G

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Myriad Genetics to Announce First Fiscal Quarter 2013 Results on Monday, November 5, 2012

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Newswise BETHESDA, MD -- October 15, 2012 -- The Genetics Society of America (GSA) is pleased to announce its 2013 award recipients. The five individuals honored are recognized by their peers for their outstanding achievements and contributions to the community of geneticists. They will receive their awards at GSA conferences during 2013.

This years award winners are an outstanding group of individuals who have all contributed in such powerful ways to the field of genetics in research, in education, and in fostering the genetics community. The GSA awards provide an opportunity for the genetics community as a whole to say a heartfelt thank you and to recognize those whose impressive achievements have advanced the science of genetics, said Phil Heiter, PhD, President of GSA.

The recipients of the 2013 GSA Awards are as follows:

Thomas D. Petes, PhD (Duke University) is awarded the Thomas Hunt Morgan Medal for lifetime contributions in the field of genetics.

Elaine A. Ostrander, PhD (National Institutes of Health, National Human Genome Research Institute) is awarded the Genetics Society of America Medal for outstanding contributions to the field of genetics in the last 15 years.

R. Scott Hawley, PhD (Stowers Institute for Medical Research) is awarded the George W. Beadle Award for outstanding contributions to the community of genetics researchers.

A. Malcolm Campbell, PhD (Davidson College) is awarded the Elizabeth W. Jones Award for Excellence in Education, which recognizes significant and sustained impact in genetics education.

Jonathan K. Pritchard, PhD (HHMI and University of Chicago) is awarded the Edward Novitski Prize, which recognizes an extraordinary level of creativity and intellectual ingenuity in solving a significant problem in genetics research. Additional information about each of the awards and the recipients achievement is listed below.

Recipient: Thomas D. Petes, PhD, Duke University Award: The Thomas Hunt Morgan Medal

Dr. Petes is the Minnie Geller Professor in Genetics in the Department of Molecular Genetics and Microbiology at Duke University Medical Center in Durham, NC. He has made seminal research contributions that have furthered the understanding of the mechanisms of DNA damage and repair using the yeast Saccharomyces cerevisiae as a model system. His insights into comprehending genome stability and instability extend far beyond this model system, laying the foundation for much of our knowledge about how human cells replicate, protect, repair and combine their chromosomes. This has provided crucial understanding in identifying the gene defects of the most common form of hereditary colon cancer and in other human diseases.

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Contact: Karen Robinson karobinson@som.umaryland.edu 410-706-7590 University of Maryland Medical Center

A new method of using adult stem cells as a model for the hereditary condition Gaucher disease could help accelerate the discovery of new, more effective therapies for this and other conditions such as Parkinson's, according to new research from the University of Maryland School of Medicine.

Scientists at the University of Maryland School of Medicine reprogrammed stem cells to develop into cells that are genetically similar to and react to drugs in a similar way as cells from patients with Gaucher disease. The stem cells will allow the scientists to test potential new therapies in a dish, accelerating the process toward drug discovery, according to the paper published online in the journal the Proceedings of the National Academy of Sciences (PNAS) on Oct. 15 (Panicker et.al.).

The study was funded with $1.7 million in grants from the Maryland Stem Cell Research Fund; researchers received a start-up grant for $200,000 in 2007 and a larger, five-year grant for $1.5 million in 2009.

"We have created a model for all three types of Gaucher disease, and used stem cell-based tests to evaluate the effectiveness of therapies," says senior author Ricardo Feldman, Ph.D., associate professor of microbiology and immunology at the University of Maryland School of Medicine, and a research scientist at the University of Maryland Center for Stem Cell Biology and Regenerative Medicine. "We are confident that this will allow us to test more drugs faster, more accurately and more safely, bringing us closer to new treatments for patients suffering from Gaucher disease. Our findings have potential to help patients with other neurodegenerative diseases as well. For example, about 10 percent of Parkinson's disease patients carry mutations in the recessive gene for Gaucher disease, making our research possibly significant for Parkinson's disease as well."

Gaucher disease is the most frequent lipid-storage disease. It affects 1 in 50,000 people in the general population. It is most common in Ashkenazi Jews, affecting 1 in 1,000 among that specific population. The disease occurs in three subtypes Type 1 is the mildest and most common form of the disease, causing symptoms such as enlarged livers and spleens, anemia and bone disease. Type 2 causes very serious brain abnormalities and is usually fatal before the age of two, while Type 3 affects children and adolescents.

The condition is a recessive genetic disorder, meaning that both parents must be carriers for a child to suffer from Gaucher. However, said Dr. Feldman, studies have found that people with only one copy of a mutated Gaucher gene those known as carriers are at an increased risk of developing Parkinson's disease.

"This science is a reflection of the mission of the University of Maryland School of Medicine to take new treatments from bench to bedside, from the laboratory to patients, as quickly as possible," says E. Albert Reece, M.D., Ph.D., M.B.A., vice president for medical affairs at the University of Maryland and John Z. and Akiko K. Bowers Distinguished Professor and dean of the University of Maryland School of Medicine. "We are excited to see where this research goes next, bringing new hope to Gaucher patients and their families."

Dr. Feldman and his colleagues used the new reprogramming technology developed by Shinja Yamanaka in Japan, who was recognized with this year's Nobel Prize for Medicine or Physiology. Scientists engineered cells taken from the skin of Gaucher patients, creating human induced pluripotent stem cells, known as hiPSC stem cells that are theoretically capable of forming any type of cell in the body. Scientists differentiated the cells to form white blood cells known as macrophages and neuronal cells.

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Public release date: 15-Oct-2012 [ | E-mail | Share ]

Contact: Kat Snodgrass 202-962-4090 Society for Neuroscience

NEW ORLEANS New animal studies provide additional support for investigating stem cell treatments for Parkinson's disease, head trauma, and dangerous heart problems that accompany spinal cord injury, according to research findings released today. The work, presented at Neuroscience 2012, the annual meeting of the Society for Neuroscience and the world's largest source of emerging news about brain science and health, shows scientists making progress toward using stem cell therapies to repair neurological damage.

The studies focused on using stem cells to produce neurons essential, message-carrying cells in the brain and spinal cord. The loss of neurons and the connections they make for controlling critical bodily functions are the chief hallmarks of brain and spinal cord injuries and of neurodegenerative afflictions such as Parkinson's disease and ALS (amyotrophic lateral sclerosis), also known as Lou Gehrig's disease.

Today's new findings show that:

Other recent findings discussed show that:

"As the fields of developmental and regenerative neuroscience mature, important progress is being made to begin to translate the promise of stem cell therapy into meaningful treatments for a range of well-defined neurological problems," said press conference moderator Jeffrey Macklis, MD, of Harvard University and the Harvard Stem Cell Institute, an expert on development and regeneration of the mammalian central nervous system. "Solid, rigorous, and well-defined pre-clinical work in animals can set the stage toward human clinical trials and effective future therapies."

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This research was supported by national funding agencies such as the National Institutes of Health, as well as private and philanthropic organizations.

Todd Bentsen, (202) 962-4086

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Realizing the potential of stem cell therapy

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