Public release date: 11-Aug-2013 [ | E-mail | Share ]

Contact: Bobbi Nodell bnodell@uw.edu 206-543-8309 University of Washington

Some patients with a rare type of epilepsy called epilepsy aphasia have something else in common. They have mutations in the same gene. Epilepsy aphasia disorders are characterized by seizures and speech abnormalities.

University of Washington researchers headed a recent study on genetic association. Their report, "GRIN2A mutations cause epilepsy-aphasia spectrum disorders," is published in the Aug. 11 issue of Nature Genetics.

The scientists sequenced genes in 519 patients with severe seizure disorders. Within the group, 44 patients had epilepsy aphasia and four of those -- or 10 percent -- and their affected family members had mutations in the GRIN2A gene.

"For a long time, people have debated whether this type of epilepsy had a genetic component, mostly because so few families have the disorder. To find a genetic cause is really interesting," said Gemma Carvill, senior fellow at the UW Department of Pediatrics, Division of Genetic Medicine, and the lead author of the study.

Carvill said to find 10 percent of patients with a genetic mutation for a particular epilepsy disorder "is quite sizable."

"In the families we looked at, multiple individuals were affected with epilepsy aphasia and all had a mutation in GRIN2A," she said.

Heather C. Mefford, assistant professor of pediatrics, said clinical testing for this gene could be done for individuals with epilepsy aphasia disorders who are wondering if they will pass on epilepsy to a child. In families with a mutation in GRIN2A, the risk of passing on a genetic mutation carrying the disorder is 50 percent.

Mefford said two other studies report similar findings.

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Progress made in linking some forms of epilepsy to genetics

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Public release date: 12-Aug-2013 [ | E-mail | Share ]

Contact: Jennifer Sereno jsereno@morgridgeinstitute.org 608-770-8084 University of Wisconsin-Madison

MADISON, Wis. Using human pluripotent stem cells and DNA-cutting protein from meningitis bacteria, researchers from the Morgridge Institute for Research and Northwestern University have created an efficient way to target and repair defective genes.

Writing today (Monday, Aug. 12, 2013) in the Proceedings of the National Academy of Sciences, the team reports that the novel technique is much simpler than previous methods and establishes the groundwork for major advances in regenerative medicine, drug screening and biomedical research.

Zhonggang Hou of the Morgridge Institute's regenerative biology team and Yan Zhang of Northwestern University served as first authors on the study; Dr. James Thomson, director of regenerative biology at the Morgridge Institute, and Erik Sontheimer, professor of molecular biosciences at Northwestern University, served as principal investigators.

"With this system, there is the potential to repair any genetic defect, including those responsible for some forms of breast cancer, Parkinson's and other diseases," Hou said. "The fact that it can be applied to human pluripotent stem cells opens the door for meaningful therapeutic applications."

Zhang said the Northwestern University team focused on Neisseria meningitidis bacteria because it is a good source of the Cas9 protein needed for precisely cleaving damaged sections of DNA.

"We are able to guide this protein with different types of small RNA molecules, allowing us to carefully remove, replace or correct problem genes," Zhang said. "This represents a step forward from other recent technologies built upon proteins such as zinc finger nucleases and TALENs."

These previous gene correction methods required engineered proteins to help with the cutting. Hou said scientists can synthesize RNA for the new process in as little as one to three days compared with the weeks or months needed to engineer suitable proteins.

Thomson, who also serves as the James Kress Professor of Embryonic Stem Cell Biology at the University of WisconsinMadison, a John D. MacArthur professor at UWMadison's School of Medicine and Public Health and a professor in the department of molecular, cellular and developmental biology at the University of California, Santa Barbara, says the discovery holds many practical applications.

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#39;Genetics of Sand #39; May Shed Light on Evolution
An evolutionary ecologist is using "grains of sand" mdash; the fossils of microscopic aquatic creatures mdash; to understand more about the process of evolution. Source:...

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Mini Belted Galloway Bull...Awesome Genetics
This bull produces great calves.

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Beef + Lamb New Zealand is proposing to merge three of its genetic databases into a single $8.8 million tool.

The proposal will mean amalgamating Ovita, Sheep Improvement Ltd (SIL) and the Central Progeny Test (CPT) into a new entity called Beef + Lamb Genetics.

The levy-funded farmer organisation has been working on this project for 15 months, the general manager of Beef + Lamb's farm programme, Richard Wakelin, said.

It will need farmer approval, to be sought in a vote at the organisation's annual meeting in November.

Beef + Lamb hoped to have it up and running by January, Wakelin said.

Beef + Lamb would put up $2.89m and an additional $1.5m would come from industry investors, Wakelin said.

Beef + Lamb has also applied to the Ministry of Business, Innovation and Employment for funding of $4.4m.

"It will be an $8.8m per annum investment for five years," Wakelin said.

Northern North Island director James Parsons said Beef + Lamb spent about $400,000 a year on SIL and the CPT.

About 80 per cent of rams sold by ram breeders are entered into the SIL database, which determines estimated breeding values and other data farmers see in sale catalogues when they buy a ram.

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Aug. 12, 2013 Rice University researchers are making strides toward a set of rules to custom-design Lego-like viral capsid proteins for gene therapy.

A new paper by Rice scientists Junghae Suh and Jonathan Silberg and their students details their use of computational and bioengineering methods to combine pieces of very different adeno-associated viruses (AAVs) to create new, benign viruses that can deliver DNA payloads to specific cells.

The research appears this month in the American Chemical Society journal ACS Synthetic Biology.

AAVs are found in nature and commonly infect humans but cause no disease. That makes them good candidates to serve as carriers that target cells and deliver genes to treat diseases.

The team, which included graduate student and lead author Michelle Ho and undergraduates Benjamin Adler and Michael Torre, wants to define rules to design a variety of viruses that deliver therapeutic genes. They used computer models to find likely AAV candidates for recombination and then tested the model predictions by engineering 17 unique virus capsid proteins and evaluating their ability to fold and assemble into capsid-encased viruses.

Gene therapy shows promise in the treatment of not only genetic disorders but also cancer and cardiovascular diseases, said Suh, an assistant professor of bioengineering at Rice's BioScience Research Collaborative.

"But you need a mechanism to get the correct gene into the human body and to the target cells," she said. "To do that, people use gene vectors, and viruses encompass the largest category of vectors. They've naturally evolved to deliver genes into the body. Our goal is to reprogram them to target specific organs or tissues.

"The big challenge is to go about this in a rational manner," she said. "People have done a lot of work to solve the structure of viruses. We know what they look like. The question is: How can we use that information to guide the design of our viral vectors?"

The team's answer starts with the "SCHEMA" algorithm they adapted to predict how parts of very large viruses can recombine by homing in on the viral protein sequences that work well together.

Silberg, an associate professor of biochemistry and cell biology, said approaches to virus design can lean either toward brute force -- "Let's make 1,000 of them and maybe we'll get lucky" -- or purely computational, where a biophysicist will try to predict the role of small changes to the virus capsid.

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Rules for gene-therapy vectors developed

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IRVINE, CA--(Marketwired - Aug 12, 2013) - MRI Interventions, Inc. (OTCQB: MRIC) today announced treatment of the first patient in a Phase I clinical trial utilizing uniQure B.V.'s glial cell line-derived neurotrophic factor (GDNF) for treatment of Parkinson's disease. This gene therapy holds promise in the battle against the degenerative and debilitating disorder, which affects 1.5 million people in the United States.MRI Interventions' ClearPoint Neuro Intervention System is being used in the clinical trial to enable direct infusion of the gene therapy into an area of the brain affected by Parkinson's disease.

Dr. Krystof Bankiewicz, MD, PhD at University of California, San Francisco (UCSF), and Dr. John D. Heiss, MD at the National Institute for Neurological Disorders and Stroke, part of the National Institutes of Health (NIH), are leading the trial.uniQure B.V., a leader in human gene therapy, is providing the GDNF gene. uniQure made headlines last November by receiving regulatory approval in Europe of a first-in-class gene therapy to treat orphan diseases.

The hypothesis of the Parkinson's disease trial is that GDNF's neuro-regenerative and protective properties may protect and strengthen brain cells that produce dopamine, a chemical that affects brain function.In Parkinson's disease, dopamine production is reduced in an area of the brain responsible for movement, which leads to the debilitating symptoms experienced by many patients with the disease. The affected area is a tiny spot located deep within the brain, and the ClearPoint System provides the visualization and precision necessary to deliver a desired amount of the gene therapy directly to this very small target without disrupting other critical neurological structures in the process.

"The success of gene therapy in patients requires accuracy in delivery," said Dr. Krys Bankiewicz of UCSF."The ClearPoint System enables this precision, with the safe and accurate infusion of our gene therapy product into a miniscule target in the brain while we observe the procedure and confirm results in real time."

"We are very pleased with our first patient procedure," Dr. Heiss stated. "The ClearPoint System worked exceptionally well, enabling us to achieve precision targeting into the putamen and to observe administration of the therapeutic agent as it occurred."

The ClearPoint navigation platform is the only technology to enable minimally-invasive neurosurgery under continuous MRI guidance, offering surgeons a direct view of the inside of a patient's brain during a procedure.

"We are delighted to be working with UC San Francisco, the National Institutes of Health and uniQure, to help advance a novel treatment for Parkinson's disease," said Kimble Jenkins, CEO of MRI Interventions.

"At uniQure we are convinced that success for gene therapyrequires the most advanced andreliabledelivery technologies," said uniQure CEO Jrn Aldag. "Together with our collaborators at UCSF, the NIH and MRI Interventions, we are paving the way to further advances in the treatment of Parkinson's Disease."

The study, sponsored by the NIH, is a Phase I open-label dose escalation safety study that will include 24 patients over 4 cohorts.The first patient was dosed on May 20 and there have been no safety issues.

About MRI Interventions, Inc.Founded in 1998, MRI Interventions is creating innovative platforms for performing the next generation of minimally invasive surgical procedures in the brain and heart.Utilizing a hospital's existing MRI suite, the company's FDA-cleared and CE-marked ClearPoint system is designed to enable a range of minimally invasive procedures in the brain.MRI Interventions has a co-development and co-distribution agreement with Brainlab, a leader in software-driven medical technology, relating to the ClearPoint system.In partnership with Siemens Healthcare, MRI Interventions is developing the ClearTrace system to enable MRI-guided catheter ablations to treat cardiac arrhythmias, including atrial fibrillation. Building on the imaging power of MRI, the company's interventional platforms strive to improve patient care while reducing procedure costs and times. MRI Interventions is also working with Boston Scientific Corporation to incorporate its MRI-safety technologies into Boston Scientific's implantable leads for cardiac and neurological applications.For more information, please visit http://www.mriinterventions.com.

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What is an Example of Personalized Medicine? Edward Abrahams, Ph.D.
Edward Abrahams, Ph.D., President of the Personalized Medicine Coalition, sits down with Slone Partners at the 8th Annual Personalized Medicine Conference at...

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Who Needs Personalized Medicine Education; Doctors, Patient or Insurers? Edward Abrahams, Ph.D.
Edward Abrahams, Ph.D., President of the Personalized Medicine Coalition, sits down with Slone Partners at the 8th Annual Personalized Medicine Conference at...

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TEDMED - Personalized Medicine and It #39;s Challenges (Part 1), Amy Miller, Ph.D.
Amy Miller PhD, Vice President, Policy, Personalized Medicine Coalition -- Discusses what is personalized medicine and its challenges for 2013 TEDMED Great ...

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TEDMED - Personalized Medicine and It #39;s Challenges (Part 2), Amy Miller, Ph.D.
Amy Miller PhD, Vice President, Policy, Personalized Medicine Coalition -- Discusses what is personalized medicine and its challenges for 2013 TEDMED Great ...

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THE genetic causes of some of the most devastating childhood epilepsies have been revealed in a landmark study jointly led by Australian researchers.

Using advanced gene technology researchers have discovered new genes and new genetic mutations that cause severe childhood epilepsy.

The study's co-leader Professor Sam Berkovic, Director of the Epilepsy Research Centre at the University of Melbourne and Melbourne's Austin Hospital, said as well as providing a pathway to treating epilepsy the research provides answers to patients and families who previously had little or no idea where epilepsy had come from.

"Parents often have a belief that they've done something wrong that caused this disease," Prof Berkovic said.

"Not knowing why has been one of the most frustrating things ... we've never really had the answer. Now we do.

"This also stops the need for further searching and refines the treatments."

A key aspect of the research has been the ability to sequence the entire human genome, Prof Berkovic said.

"Until now we've had these complex patients and we didn't know what was going on," he said.

"Now all the genes are known and the jigsaw can be completed"

As well as using the latest genetic techniques to sequence and analyse DNA from 4000 epilepsy patients and their relatives, the study known as Epi4Ks shared DNA sequences and patient information among dozens of research institutions.

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Aug. 11, 2013 A decade ago, gene expression seemed so straightforward: genes were either switched on or off. Not both. Then in 2006, a blockbuster finding reported that developmentally regulated genes in mouse embryonic stem cells can have marks associated with both active and repressed genes, and that such genes, which were referred to as "bivalently marked genes," can be committed to one way or another during development and differentiation.

This paradoxical state -- akin to figuring out how to navigate a red and green traffic signal -- has since undergone scrutiny by labs worldwide. What has been postulated is that the control regions (or promoters) of some genes, particularly those critical for development during the undifferentiated state, stay "poised" for plasticity by communicating with both activating and repressive histones, a state biologists term "bivalency."

A study by researchers at the Stowers Institute for Medical Research now revisits that notion. In this week's advance online edition of the journal Nature Structural and Molecular Biology, a team led by Investigator Ali Shilatifard, Ph.D., identifies the protein complex that implements the activating histone mark specifically at "poised" genes in mouse embryonic stem (ES) cells, but reports that its loss has little effect on developmental gene activation during differentiation. This suggests that there is more to learn about interpreting histone modification patterns in embryonic and even cancer cells.

"There has been a lot of excitement over the idea that promoters of developmentally regulated genes exhibit both the stop and go signals," explains Shilatifard. "That work supports the idea that histone modifications could constitute a code that regulates gene expression. However, we have argued that the code is not absolute and is context dependent."

Shilatifard has a historic interest in gene regulation governing development and cancer. In 2001, his laboratory was the first to characterize a complex of yeast proteins called COMPASS, which enzymatically methylates histones in a way that favors gene expression. Later, he discovered that mammals have six COMPASS look-alikes -- two SET proteins (1A and 1B) and four MLL (Mixed-Lineage Leukemia) proteins, the latter so named because they are mutant in some leukemias. The group has since focused on understanding functional differences among the COMPASS methylases. The role of mouse Mll2 in establishing bivalency was the topic of the latest study.

Comprehending the results of the paper requires a brief primer defining three potential methylation states of histone H3. If the 4th amino acid, lysine (K), displays three methyl groups (designated H3K4me3), then this mark is a sign of active transcription from that region of the chromosome. If the 27th residue of histone H3 (also a lysine) is trimethylated (H3K27me3), this mark is associated with the silencing of that region of the chromosome. But if both histone H3 residues are marked by methylation (H3K4me3 and H3K27me3 marks), that gene is deemed poised for activation in the undifferentiated cell state.

The team already knew that an enzyme complex called PRC2 implemented the repressive H3K27me3 mark. To identify which COMPASS family member is involved in this process, the group genetically eliminated all possibilities and came up with Mll2 as the responsible factor. Mll2-deficient cells indeed show H3K4me3 loss, not at all genes, but at the promoters of developmentally regulated genes, such as the Hox genes.

The revelation came when the researchers evaluated behaviors of Mll2-deficient mouse embryonic stem cells. First, the cells continued to display the defining property of a stem cell, the ability to "self-renew," meaning that genes that permit stem cell versatility were undisturbed by Mll2 loss. But remarkably, when cultured with a factor that induces their maturation, Mll2-deficient mouse ES cells showed no apparent abnormalities in gene expression. In fact, expression of the very Hox genes that normally exhibit bivalent histone marks was as timely in Mll2-deficient cells as it was in non-mutant cells.

"This means that Mll2-deficient mouse ES cells that receive a differentiation signal can still activate genes required for maturation, even though they have lost the H3K4me3 mark on bivalent regions" says Deqing Hu, Ph.D., the postdoctoral fellow who led the study. "This work paves the way for understanding what the real function of bivalency is in pluripotent cells and development."

The study's findings also potentially impact oncogenesis, as tumor-initiating "cancer stem cells" exhibit bivalent histone marks at some genes. "Cancer stem cells are resistant to chemotherapy, making them difficult to eradicate," says Hu. "Our work could shed light on how cancer stem cells form a tumor or suggest a way to shut these genes down."

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Rethinking the genetic code

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Public release date: 12-Aug-2013 [ | E-mail | Share ]

Contact: Kathryn Ruehle kruehle@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, August 5, 2013Violent and abusive behavior against women, which can be both physically and emotionally harmful, gain societal acceptance when they are glamorized and normalized in popular culture such as books and movies. The main characters' relationship in the best-selling novel Fifty Shades of Grey, for example, helps perpetuate the problem of intimate partner violence against women, according to an article in Journal of Women's Health, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. To obtain a copy of the article, press contacts should email journalmarketing1@liebertpub.com.

In "'Double Crap!' Abuse and Harmed Identity in Fifty Shades of Grey," Amy Bonomi, PhD, MPH, Lauren Altenburger, BS, and Nicole Walton, MSW from The Ohio State University, Columbus, conducted a systematic analysis of the novel to elucidate patterns consistent with Centers for Disease Control and Prevention (CDC) definitions of interpersonal violence and associated reactions known to occur in abused women. They conclude that the female partner, Anastasia, suffers harm as a result of her relationship with Christian. Specifically, the couple's interactions are emotionally abusive, characterized by stalking, intimidation, and isolation. Sexual violence is pervasive in the novel, including the use of alcohol to impair Anastasia's consent and the use of intimidation. Anastasia suffers stress, altered identity, and disempowerment/entrapment.

At least 25% of women are victims of violence by intimate partners.

"We must be attuned to the way women are treated in books and movies, as such popular culture can perpetuate dangerous violence standards toward women," says Susan G. Kornstein, MD, Editor-in-Chief of Journal of Women's Health, Executive Director of the Virginia Commonwealth University Institute for Women's Health, Richmond, VA, and President of the Academy of Women's Health.

###

About the Journal

Journal of Women's Health, published monthly, is a core multidisciplinary journal dedicated to the diseases and conditions that hold greater risk for or are more prevalent among women, as well as diseases that present differently in women. The Journal covers the latest advances and clinical applications of new diagnostic procedures and therapeutic protocols for the prevention and management of women's healthcare issues. Complete tables of content and a sample issue may be viewed on the Journal of Women's Health website at http://www.liebertpub.com/jwh. Journal of Women's Health is the Official Journal of the Academy of Women's Health and the Society for Women's Health Research.

About the Academy

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Fifty Shades of Grey romanticizes sexual violence and emotional abuse of women

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Aug. 11, 2013 Researchers have identified two new genes and implicated 25 distinct mutations in serious forms of epilepsy, suggesting a new direction for developing tailored treatments of the neurological disorders.

The findings by an international research collaboration, which includes investigators from Duke Medicine, appear Aug. 11 in the journal Nature.

Epileptic encephalopathies are a devastating group of severe brain disorders characterized by the onset of seizures at an early age. The seizures are often accompanied by cognitive and behavioral issues, which can hinder the quality of life of affected children and their families.

The cause of epileptic encephalopathies is largely unknown; while genes are believed to play an important role, specific genes have only been identified in a small number of cases.

"One important aspect of the study is that we identified an unusually large number of distinct disease-causing mutations -- 25 in total, all of which were de novo mutations. These mutations will be an invaluable resource to scientists working to elucidate the underlying causes of the epilepsies," said study author David Goldstein, PhD, director of the Duke Center for Human Genome Variation.

A de novo mutation is a new alteration in a gene that appears for the first time in a family, and results from a genetic mutation in a parent's germ cell (egg or sperm).

Learning more about the disorders' origin will guide development of effective therapies, which is the goal of Epi4K, an international research consortium funded by the National Institute of Neurological Diseases and Stroke (NINDS).

"This research focusing on epileptic encephalopathies is the first large-scale project of Epi4K," said study author Erin Heinzen, PhD, assistant professor of medicine in the Division of Medical Genetics at Duke. "The study was designed to identify de novo mutations and search for ones that contribute to risk."

The Epi4K researchers partnered with the Epilepsy Phenome/Genome Project, another NINDS-funded group working to unlock the mysteries of epilepsy. Led by Daniel Lowenstein, M.D., professor of neurology at the University of California, San Francisco, the researchers in the Epilepsy Phenome/Genome Project gathered genetic information on 264 children with epileptic encephalopathies and their parents.

The Epi4K researchers then focused on identifying all new mutations in the children using next-generation sequenced data, which looks at the part of genome that encodes protein. The Center for Human Genome Variation at Duke conducted this analysis, and confirmed 329 de novo mutations. Most of these mutations had no connection to the risk of disease, but the researchers showed that a fraction of them strongly influence risk.

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Washington, Aug 11 (IANS) Children born with genetic birth defects like Down's syndrome are at an increased risk of developing childhood cancer, says a study.

Scientists have said that children born with non-chromosomal birth defects have a two-fold higher risk of cancer before age 15, compared to children born without birth defects.

However, cancer risk varies by the specific type of birth defect, and is not significantly increased in many of the more common birth defects, Science Daily reported citing the study published in July in PLOS ONE.

Birth defects are an increasing health concern worldwide, and in 2010 the World Health Organisation identified birth defect prevention and care as a global priority.

"There is a large body of evidence for increased cancer risk in children with Down's syndrome, a genetic birth defect caused by the presence of an extra copy of chromosome 21," says Lorenzo Botto, professor of paediatrics at the University of Utah School of Medicine and an author of the study.

"However, studies to date have provided inconsistent findings on cancer risk in children with structural birth defects that are not caused by chromosome abnormalities."

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Genetic birth defects may lead to childhood cancer

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Public release date: 11-Aug-2013 [ | E-mail | Share ]

Contact: Eric Peters petersem@vcu.edu 804-828-0563 Virginia Commonwealth University

An international consortium has shown for the first time evidence of substantial overlap of genetic risk factors shared between bipolar disorder, major depressive disorder and schizophrenia and less overlap between those conditions and autism and attention deficit-hyperactivity disorder (ADHD), according to a study published this week in Nature Genetics' Advance Online publication.

The root cause of psychiatric illnesses such as bipolar disorder, major depressive disorder schizophrenia, autism and ADHD is not fully understood. For more than 125 years, clinicians have based diagnosis on a collection of symptoms observed in patients.

But, scientists have since identified that the five psychiatric disorders share a common genetic link and are now moving toward understanding the molecular underpinnings of psychiatric illness. The precise degree to which these disorders share common ground has remained unknown, until now.

The project is led by the Cross-Disorder Group of the Psychiatric Genomics Consortium and is the largest genetic study of psychiatric illness to date.

The findings provide insight into the biological pathways that may predispose an individual to disease and could ultimately lead to the development of new therapeutic avenues to treat the five major psychiatric illnesses.

"This is a very large scale study using a new, innovative statistical method," said study co-senior author Kenneth S. Kendler, M.D., professor of psychiatry, and human and molecular genetics in the Virginia Commonwealth University School of Medicine, and an internationally recognized psychiatric geneticist.

"Prior to this model, we have not been able to address these questions. These results give us by far the clearest picture available to date of the degree of genetic similarity between these key psychiatric disorders. We hope that this will help us both in developing a more scientifically based diagnostic system and understanding the degree of sharing of the biological foundation these illnesses," he said.

The study builds on findings published earlier this year in The Lancet, which reported that specific single nucleotide polymorphisms, or SNPs, are associated with a range of psychiatric disorders that can occur during childhood or adulthood.

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New patterns found in the genetic relationship of 5 major psychiatric disorders

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Participants Learn Their Risk for Complex Diseases

Doni Bloomfield

To Know or Not To Know: Dr Kroenthal holds a vial of DNA

An email popped up in Hershel Richmans inbox. Your new personalized risk report is now available through the CPMC web portal! the email cheerfully informed him. Its contents were tactfully vague: some talk of genetic counselors and a medicine collaborative. But this wasnt some credit report spam, or a Nigerian phishing scam. No, Richman, a retired environmental lawyer and former president of Jewish Learning Venture, a not-for-profit based in Pennsylvania, was about to find out his relative likelihood of developing macular degeneration, one of the leading causes of blindness in the United States.

Richman had given the New Jerseybased Coriell Institute his family history, his medical history, his diet and exercise routines and his DNA as one of 7,500 volunteers seeking to help advance mankinds understanding of the genetic basis for disease. The genetics lab had scanned his genes, crunched the numbers, weighed his odds and were ready to tell him how likely he was to go blind.

Im the type of guy who wants to go to the bottom line, says Richman, and so he breezed past information about the disease, declined to speak to a genetic counselor immediately, agreed to see the results, assured the computer that he really was ready to see the results and got to the numbers. As always, he was eager to find out his risks. Coriell had previously informed him about his risk for heart disease, type 2 diabetes and adverse reactions to the anticoagulant coumadin, as scientists linked genes to these conditions.

Along with his fellow participants, Richman had become accustomed to periodically learning his odds for contracting various grave illnesses. In a way, Coriells study makes all its participants betting men and women.

The Coriell Institute was founded 60 years ago by Dr. Lewis Coriell, a researcher who helped make Jonas Salks polio vaccine reproducible on a mass scale. In 2009, it launched an ambitious new project: the Coriell Personalized Medicine Collaborative. The CPMC seeks to enroll 10,000 volunteers, scan selected sites of their genome, look over their family history and current lifestyle, inform them of their medical risks for common illnesses and track what they do with the information.

Are people able to fend off their genetic predispositions? Will they overreact? Do nothing? With the price of sequencing falling and the emergence of new genetic scanning firms, understanding the pros and cons of knowing ones genetic risks is increasingly urgent. Whether patients take genetic profiles as destiny or discard them as meaningless may decide the future of personalized medicine.

Were not talking about diseases like Tay-Sachs or cystic fibrosis where one gene [leads to] one disease, says Erynn Gordon, director of genetic counseling at Coriell. Thats kind of the classical model of genetics that most people think of the peas and Mendel. Indeed, because the CPMC focuses on complex genetic conditions, it doesnt even screen for most single-gene diseases, deadly as some may be.

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Coriell Institute Gives Patients a Genetic Crystal Ball — With Consequences

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Genetics - Just The Two of Us @ The Aggie Theatre
Feat Nick Dalessandro on sax and Josh Voegler on percussion.

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Omics Group Hereditary Genetics Current Research 2161 1041 1 112

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Hendrix Genetics corporate video, Chinese version

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#39;Spiritual Genetics #39; by Pastor Apollo C. Quiboloy on Give Us This Day - SMNI
Powerline: August 8, 2013 What is Spirit and truth? The Spirit that we talk about here is the spirit of obedience to His Will that makes us connected to the...

By: Sonshine Media Network International

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How to Say or Pronounce Genetics
Get those medical secrets: http://www.health101.pw/Medical-Secrets.shtml This video shows you how to say or pronounce Genetics. Audio is from cancer.gov.

By: Dorsey Anderson

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#39;Spiritual Genetics - Part 2 #39; by Pastor Apollo C. Quiboloy on Give Us This Day - SMNI
Powerline: August 9, 2013 wit special guest Senator Paolo Benigno "BAM" Aquino IV. What is Spirit and truth? The Spirit that we talk about here is the spiri...

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Familial/Genetics and PAH
From PHA #39;s 2012 International PH Conference What is familial pulmonary arterial hypertension? Learn about what is known about the genetic basis of pulmonary ...

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