The Race Card? - Sen. Reid Make Controversial Comments - Michelle Malkin On Hannity
The Race Card? - Sen. Reid Make Controversial Comments - Michelle Malkin On Hannity.

By: Mass Tea Party

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The Race Card? - Sen. Reid Make Controversial Comments - Michelle Malkin On Hannity - Video

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Their creation is part of genetic research aimed at mass-producing medication and treating hereditary illness. And they seem to be in good health, don't worry.

The transgenic bunnies were born last week. They are expected to live long, productive rabbit lives. They are not evil; they just glow bright green under a black light. They do not portend apocalypse, but rather a potential for great good.

The road to their creation began years ago. Dr. Stefan Moisyadi works with transposing DNA vectors at the University of Hawaii School of Medicine, where glowing mice were created in the 1980s. Now he's at the head of the rabbit projectthough this time the birth took place in Istanbul, as part of a collaboration with Turkish researchers.

The idea is that scientists inject genetic material into rabbit embryos, and they want to see that it becomes a part of their genetic makeup. The glowing green is not an end in itself, but a marker that their technique is working. The protein that creates the glow comes from jellyfish DNA (which was injected into the rabbit embryo).

Moisyadi told Hawaii local news channel KHON, "These rabbits are like a light bulb glowing, like an LED light all over their body. And on top of it, their fur is beginning to grow and the greenness is shining right through their fur. Its so intense."

Light bulb, LED lightthe opportunities for creative imagery are numerous. It's like an overflowing bin of potential words.

Since the jellyfish gene codes for a natural protein, Moisyadi et al. don't have reason to suspect that their rabbits are harmed by the experimentation. They live just as long as normal animals do. I can tell you from the mice [which have since been conducted at places like Caltech] they show no ill effects.

If we learned anything from Rudolph (the "red-nosed" reindeer), the transgenic bunnies may be socially excluded at a young age, but the experience will be formative, and they will grow to be celebrated by the rabbit leader.

In 2011, the same technique created glowing kittens as part of an HIV research project. In a collaboration between the Mayo Clinic and Yamaguchi University, the researchers reported in the journal Nature Methods that the cats not only glowed but, more importantly, were resistant to feline immunodeficiency virus (FIV).

They also showed no signs of ill health or evil behavior.

Read this article:
Glowing Bunnies: Why They Matter

Recommendation and review posted by Bethany Smith

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/nd85n7/molecular) has announced the addition of the "Molecular Diagnostics in Genetic Testing" report to their offering.

Molecular diagnostics in genetic testing brings advanced analytical techniques to the diagnosis and treatment of genetic disorders. The confluence of breakthroughs in genomics and proteomics and the development of microarray devices to measure analytes in the blood and various body tissues are driving significant growth in the segment.

Major developments include the integration of specialty labs and gene expression profiling into clinical practice, the introduction and rapid growth of cell-free fetal DNA prenatal testing, the advancement of companion diagnostics for drug development, the widespread installed base of automated instruments for molecular testing and the development of personalized medicine. The genetic testing space is one of the most profitable sectors of molecular diagnostics and is expected to be an area of high growth and corporate change throughout the forecast period.

This report describes the emerging field of molecular diagnostics in genetic testing. This review analyzes the size and growth of the molecular diagnostics in genetic testing market, including the factors that influence the various market segments within it and the dollar volume of sales, both in the United States and worldwide. Moreover, this analysis profiles the leading companies focused on the molecular diagnostics for genetic testing sector.

Companies Mentioned

- Abbott Laboratories

- Beckman Coulter

- CombiMatrix

- EntroGen, Inc

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Research and Markets: Molecular Diagnostics in Genetic Testing - 2013 Study Analyzes the Size and Growth of the ...

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SCHAUMBURG, IL--(Marketwired - August 13, 2013) - Partners of the Cat Health Network (CHN) today released final results of several major research projects that investigated genetic predispositions to disease in cats.

CHN officials reported that, among many significant accomplishments, scientists have

Other studies revealed that, despite scientists' hypotheses, genes involved in white coat color were not also associated with deafness in white cats and that no significant genetic indicator predetermined a cat's response to catnip. For a complete summary of findings, contact Allen Byrne at abyrne@morrisanimalfoundation.org.

These findings will help advance feline medicine and offer veterinarians new ways to improve the health and welfare of cats, said Dr. Roy Smith, president of the American Association of Feline Practitioners (AFP) and liaison to the CHN.

"The CHN funds research efforts that help accelerate advancements in addressing the many problems we face in feline medicine," Dr. Smith said.

Founded in 2011 in response to cats lagging behind dogs in visits to the veterinarian, CHN comprises the American Veterinary Medical Foundation (AVMF), Morris Animal Foundation, Winn Feline Foundation (WFF) and American Association of Feline Practitioners (AFP). Together, the partners are committed to making a substantial difference in the health and welfare of domestic cats by funding targeted health studies.

This research money is critical to advancing feline medicine, said Dr. Wayne Jensen, Morris Animal Foundation's chief scientific officer. "The cat is the most underfunded domestic animal in research," he noted.

Research funded by CHN focuses on feline cancer, chronic renal disease, diabetes mellitus, feline lower urinary tract disease, and pain management. Scientists used gene chips containing feline single nucleotide polymorphisms (SNPs)-variations from the common feline DNA sequence that can be used as markers to track down genes responsible for genetic diseases-to conduct their investigations.

The research conclusions will continue to fill in gaps in knowledge about the cat genome, said Dr. Vicki L. Thayer, president of WFF. "The results from these studies show that genetic mutations do cause many diseases or enhance susceptibility, and tests can now be developed to identify carriers," said Dr. Thayer.

CHN is an initiative of the Animal Health Network, a collaboration of like-minded groups working together toward scientific study of feline, canine and equine health.

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Cat Health Network Announces Discovery of New Feline Gene Mutations, Other Advances in Disease Treatment

Recommendation and review posted by Bethany Smith

Questions Answers 193 - Fasting on Watermelon, Cholesterol, Genetics Experiences
Questions Answers 193 Fasting on Watermelon Cholesterol Genetics Experiences Disclaimer The information given by Robert Morse in these videos are strictl...

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SALT LAKE CITY, Aug. 13, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) today announced financial results for its fiscal fourth quarter and full fiscal year ended June 30, 2013. Revenue for the fiscal fourth quarter increased 31 percent over the same period in the prior year to $174.1 million. Fiscal fourth quarter earnings per diluted share (EPS) were $0.53, an increase of 58 percent over the same period of the prior year.

"Myriad had an exceptional fourth quarter and delivered strong financial results in fiscal 2013 by successfully growing our existing businesses, and I am proud of the entire Myriad team," said Peter D. Meldrum, President and Chief Executive Officer of Myriad. "We are investing for future growth and expect to launch three exciting new tests in fiscal 2014, including myRisk Hereditary Cancer(TM), myPath Melanoma(TM), and myPlan Lung Cancer(TM), all of which address significant unmet clinical needs. Additionally, we are engaging in several external collaborations, particularly in the area of companion diagnostics and personalized medicine that have the potential to deliver long-term value to our shareholders."

Fiscal Fourth Quarter 2013 Results

Fiscal Year 2013 Results

Business Highlights

Fiscal Year 2014 Financial Targets

The Company expects fiscal year 2014 total revenue of $690 to $710 million representing 13 to 16 percent growth and diluted earnings per share of $1.87 to $1.94 representing 6 to 10 percent growth. Myriad's top-line guidance is consistent with expectations provided at its 2013 Analyst Day calling for low-to-mid, double-digit revenue growth. Our EPS guidance takes into account a projected tax rate of approximately 40 percent in fiscal 2014; the commercial launch of three new molecular diagnostic tests including myRisk Hereditary Cancer, myPath Melanoma, and myPlan Lung Cancer; and an estimated $10 million in higher legal spending associated with recent patent infringement litigation. These projections are forward looking statements and are subject to the risks summarized in the safe harbor statement at the end of this press release. The Company will provide further detail on its business outlook during the conference call it is holding today to discuss its fiscal 2013 fourth-quarter and full-year financial results.

Conference Call and Webcast

A conference call will be held on Tuesday, August 13, 2013, at 4:30 p.m. Eastern Time to discuss Myriad's financial results for the fiscal fourth quarter of 2013. The dial-in number for domestic callers is (800) 404-5245. International callers may dial (303) 223-2688. All callers will be asked to reference reservation number 21668391. An archived replay of the call will be available for seven days by dialing (800) 633-8284 and entering the reservation number above. The conference call also will be available through a live Webcast at http://www.myriad.com.

About Myriad Genetics

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Myriad Genetics Reports Full-Year and Fiscal Fourth-Quarter 2013 Financial Results

Recommendation and review posted by Bethany Smith

RUTHERFORD, N.J., Aug. 13, 2013 (GLOBE NEWSWIRE) -- Cancer Genetics, Inc. (CGIX), a diagnostics company focused on developing genomic-based, oncology tests and services, today announced the pricing of its public offering of 1,500,000 shares of its common stock at a price to the public of $10.00 per share. The gross proceeds to Cancer Genetics from the public offering are expected to be $15,000,000, before underwriting discounts and commissions and other offering expenses payable by Cancer Genetics.

The Company intends to use the net proceeds from the offering to expand sales and marketing, to further product commercialization, to invest in its Mayo Clinic joint venture, to retire mezzanine financing, to continue research and development, and to fund other general working capital needs.

Cancer Genetics also announced that its common stock will begin trading on The NASDAQ Capital Market under the symbol "CGIX" on August 14, 2013. In connection with this listing, Cancer Genetics' common stock will cease trading on the OTC QB.

Cancer Genetics has also granted the representative of the underwriters a 45-day option to purchase up to 225,000 additional shares of common stock from Cancer Genetics to cover over-allotments, if any. The offering is expected to close on August 19, 2013, subject to customary closing conditions.

Aegis Capital Corp. is acting as sole book-running manager for the offering.

Feltl and Company, Inc. is acting as co-lead manager for the offering.

This offering is being made only by means of a prospectus. Copies of the prospectus relating to this offering may be obtained by contacting Aegis Capital Corp., Prospectus Department, 810 Seventh Avenue, 18th Floor, New York, NY 10019, telephone: 212-813-1010, e-mail: prospectus@aegiscap.com.

A registration statement relating to these securities was declared effective by the Securities and Exchange Commission on August 13, 2013. This press release shall not constitute an offer to sell or a solicitation of an offer to buy, nor shall there be any sale of these securities in any state or jurisdiction in which such an offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such state or jurisdiction.

About Cancer Genetics:

Cancer Genetics, Inc. (CGI) is an emerging leader in DNA-based cancer diagnostics and services some of the most prestigious medical institutions in the world. Our tests target cancers that are difficult to diagnose and predict treatment outcomes. These cancers include hematological, urogenital and HPV-associated cancers. We also offer a comprehensive range of non-proprietary oncology-focused tests and laboratory services that provide critical genomic information to healthcare professionals as well as biopharma and biotech. Our state-of-the-art reference lab is focused entirely on maintaining clinical excellence and is both CLIA certified and CAP accredited and has licensure from several states including New York State. CGI has established strong research collaborations with major cancer centers such as Memorial Sloan-Kettering, The Cleveland Clinic, Mayo Clinic and the National Cancer Institute. For further information, please see http://www.cancergenetics.com.

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Cancer Genetics Announces Pricing of Public Offering of 1,500,000 Shares of Common Stock

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Nu step machine for spinal cord injury

By: yolanda salem

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Nu step machine for spinal cord injury - Video

Recommendation and review posted by sam

By: Jet Villa, InterAksyon.com August 13, 2013 8:42 AM

InterAksyon.com The online news portal of TV5

MANILA, Philippines - The Department of Health (DOH) has given all health facilities practicing stem cell therapy and companies importing and producing stem cell products untilAug. 31to apply for accreditation and product registration, respectively.

Nick Lutero, director of the DOH-Bureau of Health Facilities and Services, said it will be considered illegal for facilities to do stem cell procedures if they fail to comply with the requirement.

Papatigil namin ang pag-conduct ng therapy. For those still continuing to practice, I think we have sufficient laws, particularly on the illegal practice of medicine. They could be criminally liable, he said in a chance interview.

Lutero lamented that only five hospitals have applied for registration although the DOH had issued the guidelines on this since March.

We have done preliminary visits sa mga hospitals na ito at mukang based sa initial inspection, merong sufficient compliance sa mga facilities, he said.

Companies importing and producing stem cell products, on the other hand, should apply for registration with the Food and Drug Administration, an agency attached to the DOH.

Products that will not be applied for registration will also be considered illegal after the deadline.

Experimental treatment not for free

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DOH gives health facilities engaged in stem cell therapy until Aug. 31 to register

Recommendation and review posted by simmons

Aug. 13, 2013 A gene variant strongly associated with development of type 2 diabetes appears to interact with a Mediterranean diet pattern to prevent stroke, report researchers from the Jean Mayer USDA Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University and from the CIBER Fisiopatologa de la Obesidad y Nutricin in Spain. Their results, published online today in Diabetes Care, are a significant advance for nutrigenomics, the study of the linkages between nutrition and gene function and their impact on human health, particularly chronic disease risk.

The researchers set out to investigate whether genetics contribute to the cardiovascular benefits seen in the Prevencion con Dieta Mediterranea (PREDIMED) trial. Based in Spain, the randomized, controlled trial enrolled more than 7,000 men and women assigned to either a Mediterranean or low fat control diet and monitored them for cardiovascular disease, stroke and heart attack for almost five years.

"Our study is the first to identify a gene-diet interaction affecting stroke in a nutrition intervention trial carried out over a number of years in thousands of men and women," said senior author Jos M. Ordovs, Ph.D., director of the Nutrition and Genomics Laboratory at the USDA HNRCA at Tufts University. "The PREDIMED study design provides us with stronger results than we have ever had before. With the ability to analyze the relationship between diet, genetics and life-threatening cardiac events, we can begin to think seriously about developing genetic tests to identify people who may reduce their risk for chronic disease, or even prevent it, by making meaningful changes to the way they eat."

Led by Ordovs and corresponding author Dolores Corella, Ph.D., of the CIBER Fisiopatologia de la Obesidad y Nutricin , the researchers focused on a variant in the Transcription Factor 7-Like 2 (TCF7L2) gene, which has been implicated in glucose metabolism but its relationship to cardiovascular disease risk has been uncertain. About 14 percent of the PREDIMED participants were homozygous carriers, meaning they carried two copies of the gene variant and had an increased risk of disease.

"Being on the Mediterranean diet reduced the number of strokes in people with two copies of the variant. The food they ate appeared to eliminate any increased stroke susceptibility, putting put them on an even playing field with people with one or no copies of the variant," explained Ordovs, who is also a professor at the Friedman School of Nutrition Science and Policy at Tufts University. "The results were quite different in the control group following the low fat control diet, where homozygous carriers were almost three times as likely to have a stroke compared to people with one or no copies of the gene variant ."

The Mediterranean diet features olive oil, fish, complex carbohydrates and nuts. To find out how closely the PREDIMED participants adhered to the Mediterranean diet prior to the trial, the authors examined food frequency questionnaires. "Again, we saw that the Mediterranean diet appeared to compensate for genetic influence," said Corella, who is also a scientist in the Genetic and Molecular Epidemiology Unit at the University of Valencia. "If adherence to the diet was high, having two copies of the gene variant had no significant influence on fasting glucose levels. The same was true for three common measures of cardiovascular disease risk: total blood cholesterol, low density lipoprotein and triglycerides. Conversely, these risk factors were considerably higher in homozygous carriers with low adherence to the diet."

The results of the study were not significantly changed by adjusting for variables that could have affected the findings, including type 2 diabetes,body mass index (BMI), and heart and diabetes medications. The authors note more studies are needed to determine what mechanism may be involved in the interaction they observed. They also intend to continue to mine the PREDIMED data for other gene diet interactions that may be associated with stroke as well as heart attacks.

Ordovs is also a member of the Pharmacology & Experimental Therapeutics Faculty at the Sackler of Graduate Biomedical Sciences at Tufts University.

This study was funded by the Spanish Ministry of Health (Institute de Salud Carlos III), the Ministry of Economy and Innovation (Spain) , the Fondo Europeo de Desarrollo Regional, the Generalitat Valenciana (Spain) and by contracts 53-K06-5-10 and 58-1950-9-001 from the USDA.

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Mediterranean diet counteracts a genetic risk of stroke

Recommendation and review posted by Bethany Smith

Public release date: 13-Aug-2013 [ | E-mail | Share ]

Contact: Andrea Grossman 617-636-3728 Tufts University, Health Sciences Campus

BOSTON (August 13, 2013, 10 am EDT) -- A gene variant strongly associated with development of type 2 diabetes appears to interact with a Mediterranean diet pattern to prevent stroke, report researchers from the Jean Mayer USDA Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University and from the CIBER Fisiopatologa de la Obesidad y Nutricin in Spain. Their results , published online today in Diabetes Care, are a significant advance for nutrigenomics, the study of the linkages between nutrition and gene function and their impact on human health, particularly chronic disease risk.

The researchers set out to investigate whether genetics contribute to the cardiovascular benefits seen in the Prevencion con Dieta Mediterranea (PREDIMED) trial. Based in Spain, the randomized, controlled trial enrolled more than 7,000 men and women assigned to either a Mediterranean or low fat control diet and monitored them for cardiovascular disease, stroke and heart attack for almost five years.

"Our study is the first to identify a gene-diet interaction affecting stroke in a nutrition intervention trial carried out over a number of years in thousands of men and women," said senior author Jos M. Ordovs, Ph.D., director of the Nutrition and Genomics Laboratory at the USDA HNRCA at Tufts University. "The PREDIMED study design provides us with stronger results than we have ever had before. With the ability to analyze the relationship between diet, genetics and life-threatening cardiac events, we can begin to think seriously about developing genetic tests to identify people who may reduce their risk for chronic disease, or even prevent it, by making meaningful changes to the way they eat."

Led by Ordovs and corresponding author Dolores Corella, Ph.D., of the CIBER Fisiopatologia de la Obesidad y Nutricin , the researchers focused on a variant in the Transcription Factor 7-Like 2 (TCF7L2) gene, which has been implicated in glucose metabolism but its relationship to cardiovascular disease risk has been uncertain. About 14 percent of the PREDIMED participants were homozygous carriers, meaning they carried two copies of the gene variant and had an increased risk of disease.

"Being on the Mediterranean diet reduced the number of strokes in people with two copies of the variant. The food they ate appeared to eliminate any increased stroke susceptibility, putting put them on an even playing field with people with one or no copies of the variant," explained Ordovs, who is also a professor at the Friedman School of Nutrition Science and Policy at Tufts University. "The results were quite different in the control group following the low fat control diet, where homozygous carriers were almost three times as likely to have a stroke compared to people with one or no copies of the gene variant ."

The Mediterranean diet features olive oil, fish, complex carbohydrates and nuts. To find out how closely the PREDIMED participants adhered to the Mediterranean diet prior to the trial, the authors examined food frequency questionnaires. "Again, we saw that the Mediterranean diet appeared to compensate for genetic influence," said Corella, who is also a scientist in the Genetic and Molecular Epidemiology Unit at the University of Valencia. "If adherence to the diet was high, having two copies of the gene variant had no significant influence on fasting glucose levels. The same was true for three common measures of cardiovascular disease risk: total blood cholesterol, low density lipoprotein and triglycerides. Conversely, these risk factors were considerably higher in homozygous carriers with low adherence to the diet."

The results of the study were not significantly changed by adjusting for variables that could have affected the findings, including type 2 diabetes,body mass index (BMI), and heart and diabetes medications. The authors note more studies are needed to determine what mechanism may be involved in the interaction they observed. They also intend to continue to mine the PREDIMED data for other gene diet interactions that may be associated with stroke as well as heart attacks.

###

Link:
Mediterranean diet counteracts a genetic risk of stroke, study reports

Recommendation and review posted by Bethany Smith

Public release date: 13-Aug-2013 [ | E-mail | Share ]

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

New Rochelle, NY, August 13, 2013Employers can have a significant role in improving efforts to prevent and treat diseases such as cancer by introducing and supporting health promotion programs in the workplace. Together, companies can influence health care policies and reimbursement and industry practices to support the fight against cancer. Johnson & Johnson's active role in implementing the CEO Cancer Gold Standard program is described in an article in Population Health Management, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Population Health Management website at http://www.liebertpub.com/pop.

Rachel Henke, PhD and coauthors representing Truven Health Analytics (Cambridge, MA and Washington, DC), Emory University (Atlanta, GA), and Johnson & Johnson (Southwest Ranches, FL, Mansfield, MA, and New Brunswick, NJ), focus on how J&J has incorporated the industry-leading standards developed by the CEO Roundtable on Cancer into its existing Live for Life worksite health promotion program.

In the article "Employers' Role in Cancer Prevention and TreatmentDeveloping Success Metrics for Use by the CEO Roundtable on Cancer," the authors describe the "5 Pillars" of the CEO Cancer Gold Standard program, the framework J&J created to monitor the use and effectiveness of the cancer prevention and treatment enhancement efforts it introduced, and examples of the data collected by the company.

"This nationally prominent group of researchers has once again demonstrated that employers can bend the cost curve and improve outcomes, too," says Editor-in-Chief David B. Nash, MD, MBA, Dean and Dr. Raymond C. and Doris N. Grandon Professor, Jefferson School of Population Health, Philadelphia, PA.

###

About the Journal

Population Health Management is an authoritative peer-reviewed journal published bimonthly in print and online that reflects the expanding scope of health care management and quality. The Journal delivers a comprehensive, integrated approach to the field of population health and provides information designed to improve the systems and policies that affect health care quality, access, and outcomes. Comprised of peer-reviewed original research papers, clinical research, and case studies, the content encompasses a broad range of chronic diseases (such as cardiovascular disease, cancer, chronic pain, diabetes, depression, and obesity) in addition to focusing on various aspects of prevention and wellness. Tables of content and a sample issue may be viewed on the Population Health Management website at http://www.liebertpub.com/pop. Population Health Management is the Official Journal of the Care Continuum Alliance.

About the Publisher

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What role can employers play in cancer prevention and treatment?

Recommendation and review posted by Bethany Smith

Public release date: 13-Aug-2013 [ | E-mail | Share ]

Contact: Sophie Mohin smohin@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, August 13, 2013Recording the sexual orientation and gender identity (SOGI) of individuals in their health records would greatly facilitate identifying the unique health needs and health disparities of LGBT individuals, leading to improved quality and outcomes of their health care. The advantages of reporting this information and the growing support for including it in electronic health records (EHRs) are described in an article in LGBT Health, a new peer-reviewed journal from Mary Ann Liebert, Inc., publishers, launching in fall 2013. The article is available free on the website.

Sean Cahill, PhD and Harvey J. Makadon, MD, The Fenway Institute (Boston, MA), emphasize the need for more data and research on LGBT health and health disparities, as noted in a 2011 Institute of Medicine report that recommended routine collection of SOGI information and its inclusion in EHRs. Ready access to this information could facilitate conversations between clinicians and patients about risk factors and targeted preventive measures. Cahill teaches public policy at New York University (New York, NY) and Makadon is Clinical Professor of Medicine at Harvard Medical School (Boston, MA).

In the article "Sexual Orientation and Gender Identity Data Collection in Clinical Settings and in Electronic Health Records: A Key to Ending LGBT Health Disparities" the authors describe overwhelming support for routine collection of SOGI information among LGBT advocacy groups and HIV/AIDS organizations, as well as the support for SOGI data collection in the Healthy People 2020 initiative, and the Obama administration's Affordable Care Act.

"The Obama Administration has taken significant strides toward increasing LGBT data collection on health surveys," said Cahill. "Right now the federal government is considering whether to include SOGI as standard demographic questions in Stage 3 meaningful use guidelines, which set the standard for data collection in EHRs. We believe that including SOGI measures in these guidelines would dramatically increase our understanding of LGBT health disparities and our ability to address them."

"While there is no question about the benefits of collecting such data, some concern has been raised about the security of the EHR and potential misuses," says Editor-in-Chief, William Byne, MD, PhD, Icahn School of Medicine at Mount Sinai, New York, NY. "In addition to addressing how to best elicit the data, Cahill and Makadon also address such implementation concerns."

###

About the Journal

Spanning a broad array of disciplines LGBT Health brings together the LGBT research, medical, and advocacy communities to address current challenges and improve the health, well-being, and patient outcomes of LGBT populations. The Journal will publish original research, review articles, clinical reports, case studies, legal and policy perspectives, and much more. LGBT Health is published quarterly, online with Open Access options and in print. Sign up today (http://www.liebertpub.com/SubscriptionCenter/default.aspx) to receive email alerts for LGBT Health. A preview issue is available on the LGBT Health website.

Link:
LGBT identity data in health records would improve care, reduce disparities

Recommendation and review posted by Bethany Smith

Washington, Aug 13 (ANI): Researchers have created eight rabbits, which look just like any other white bunnies, but can glow in the dark, in a leap forward for developing medicine for life-threatening genetic diseases.

The transgenic bunnies were born last week at a university in Istanbul, Turkey. But the scientific process behind the glowing wonders started with mice at the University of Hawaii more than a decade ago, KHON2.com reported.

Biogenesis researcher Dr. Stefan Moisyadi said that these rabbits are like a light bulb glowing, like an LED light all over their body, and on top of it, their fur is beginning to grow and the greenness is shining right through their fur.

Moisyadi said that they live just as long as normal animals do.

"In mice, I can tell you that from mice, and they show no ill effects," he said.

To produce the glow, researchers injected fluorescent protein from jellyfish DNA into eight rabbit embryos in a lab. The embryos were then re-inserted into the mother rabbit and two were born with the "glowing gene."

Moisyadi said that the goal is to eventually produce larger transgenic animals including sheep, cows and even pigs.

He said that the benefits in doing it in large animals are to create bio-reactors that basically produce pharmaceuticals that can be made a lot cheaper.

Moisyadi said this research could also lead to cures for human illnesses caused by genetic deficiencies. (ANI)

Link:
Scientists create 'glow-in-dark bunnies' to battle life-threatening genetic diseases

Recommendation and review posted by Bethany Smith

A startup called Genome Liberty is developing a consumer genetics test to gauge an individuals ability to metabolize prescription drugs.

A personal genetics startup thinks that there is one set of DNA variants that everyone should know: the ones that help determine how you respond to drugs.

Genome Liberty, a New Jersey-based startup, wants to provide a $99 test that will tell customers, based on their genetics, if they should take a nonstandard dose of a drug because their body will break it down faster or slower than most people. In some cases the test might suggest a particular drug someone should take or avoid. The idea is to give you a card to keep in your wallet, or an iPhone app, which says which medications you shouldnt take, says cofounder Jeffrey Rosenfeld, a genome scientist at Rutgers University.

The company would offer these tests directly to consumers, who could then relay any relevant information to their doctors, Rosenfeld says.

Genome Liberty isnt the first company to offer such tests. The consumer genetics company 23andMe also offers some drug response tests in its genome scan, which also includes tests for things like eye color and the genetic risk for developing serious diseases. Rosenfeld says Genome Liberty wanted a more focused test. The idea is to provide information that is usable, that you can act on, he says.

Consumers who get the Genome Liberty drug response test would send a sample of saliva to the companys lab. The company scans the genome for DNA variations in 11 liver enzyme genes, which are a subset of the dozens of genes encoding enzymes for drug metabolism. Enzymes in the liver process drugs and can either deactivate or activate drugs, depending on the compound. Different people carry different versions or amounts of many of these enzymes, which can affect how they respond to drugs. Some patients may process a drug more quickly, more slowly, or perhaps not at all.

Genome Liberty says that variants in those 11 enzymes can affect the activity of nearly 80 drugs in the body. The test will tell people which medications they should take and which they should avoid based on markers in their DNA, says Rosenfeld.

The company is using a crowdfunding site to raise money to develop its test, which is available for pre-order. The recent U.S. Supreme Court decision that limited the patent claims that companies can make on genes (see U.S. Supreme Court Says Natural Human Genes May Not Be Patented) helped spur Genome Liberty to launch. We were worried about whether we could start this company or not, says Rosenfeld. Until that decision, he says, most genes were covered by a patent.

It is still not clear whether genetic tests sold directly to consumers will come under regulatory scrutiny. In 2010, the FDA warned 23andMe and other consumer genetics companies that their services amount to medical devices and thus need regulatory approval. But since then, the U.S. government has not come up with clear rules for these companies. Nevertheless, 23andMe applied for regulatory approval for portions of its test last year (see Personal Genetics Company Seeks Regulatory Approval).

Another question is whether doctors will make use of information from a consumer genetics test. Physicians dont always trust the results of direct-to-consumer tests and may not have clear medical guidelines for how to use it (see Why We Have a Right to Consumer Genetics). But the connections between the liver enzyme variants and drug response are well-supported, says Rosenfeld. If a doctor doesnt want to accept these results, he says, then find a different doctor.

Original post:
Consumer Genetic Test Can Predict Your Drug Response

Recommendation and review posted by Bethany Smith

Aug. 13, 2013 A study investigating the function of the recently discovered enhancer RNA molecules may open new avenues for gene therapy. According to the study researchers, altering the production and function of these molecules could affect the expression of genes and, in consequence, possibly also the progression of various diseases.

Published in Molecular Cell on 8 August, the study was carried out in collaboration between the University of California, San Diego and the University of Eastern Finland.

Besides promoters located in the beginning of genes, gene expression is also regulated by enhancers which may be located as far as thousands of base pairs away from the gene they regulate. Enhancers have been shown to be responsible for cell-specific gene regulation. Previously, it was thought that the number of enhancer sequences in a differentiated cell is static; however, recent findings are starting to disprove the idea. In 2010, it was discovered that non-coding RNA molecules were being produced from the enhancer regions. The first observations relating to the biological function of these enhancer RNAs, or eRNAs, were published earlier this year. However, no study to date has addressed the question of whether enhancer transcription is of functional importance.

In the study researchers used genome-wide approaches to demonstrate that inflammation response causes the emergence of novel enhancers in primary macrophage cells. For the first time ever, the study used this formation of novel enhancer regions to describe the selection of enhancers and the progression of the activation from transcription factor binding to histone acetylation and eRNA transcription, finally leading to the mono- and dimethylation of histone H3 lysine 4 (H3K4me1/2). The H3K4me1 and H3K4me2 histone modifications are the very markers generally used to identify the location of enhancer regions on DNA. This type of histone methylation enables the function of these regions as enhancer sequences, i.e. as marks that can be identified by specific proteins which boost gene transcription.

The study showed that the direction and extent of eRNA transcription and H3K4me1/2 regions show strong correlation and that the inhibition of eRNA transcription with polymerase inhibitors inhibited histone methylation and thus also the emergence of novel enhancer sequences. Furthermore, the study showed that histone methyltransferases Mll1, Mll2/4 and Mll3 play a key role in de novo H3K4 methylation.

The results show that enhancer transcription causes long-term epigenetic changes in cells. Furthermore, besides offering valuable insight into the function of this novel RNA type, the researchers also believe that the findings will open new avenues for novel treatments in which cell-specific enhancer sequences can be targeted to alter gene expression. In June, this same group of researchers published a study in Nature, reporting for the first time reduction in target gene expression using eRNA knockdown in experimental animals.

Postdoctoral Researcher Minna U. Kaikkonen at A.I. Virtanen Institute for Molecular Sciences at the University of Eastern Finland was one of the two lead authors of the current study, carried out under Professor Christopher Glass. Dr Kaikkonen completed her post doc study in Professor Glass' research group at the University of California, San Diego in 2009-2012. Besides Dr Kaikkonen, the UEF contributors to the earlier study from June also include Postdoctoral Researcher Hanna P. Lesch.

The main funders of the study are Fondation Leducq, Sigrid Juslius Foundation, the Academy of Finland, ASLA Fulbright, the Finnish Foundation for Cardiovascular Research, the Finnish Cultural Foundation (North Savo Regional Fund), Orion-Farmos Research Foundation and the US National Institutes of Health grants DK091183, CA17390, and DK063491.

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Enhancer RNAs may open new avenues for gene therapy

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In 1980, though, he opened up the journal Science and suddenly understood how doctors might someday cure Lesch-Nyhan, along with thousands of other genetic disorders that had once seemed incurable. Two Stanford biologists, Richard Mulligan and Paul Berg, had figured out a way to transplant genes into cells, effectively rewriting their DNA. The phrase gene therapy had been floating around medical circles for decades, but Wilson realized that its time had come. As soon as he finished his degrees, he and his wife moved to Boston so he could learn about gene transplantation from Mulligan, now at MIT. After nearly three years under Mulligans tutelage, he headed back to Michigan to set up his own lab.

The first disease that Wilson targeted was called familial hypercholesterolemia, in which the patient lacks the gene that produces receptors for grabbing bad cholesterol, or LDL, from the blood, which the liver normally filters out. Vessels become so badly clogged that many sufferers have heart attacks in their forties and fifties, and sometimes even before age 30.

Wilson figured out how to make a vector to attack the conditiona virus with a working version of the gene loaded on it. He first tested it on a type of rabbit genetically prone to high levels of LDL, and the gene therapy lowered those levels considerably. For a human trial in 1992, he and his colleagues chose a 28-year-old woman from Canada. Surgeons removed part of her liver, and then Wilson and his colleagues infected its cells with the virus, which delivered a working version of the defective gene. Finally, Wilson and his colleagues injected those cells back into the womans liver, where they took hold and grew. The womans LDL levels dropped by 23 percent.

The result, published in 1994, was a milestone in the young field. GENE EXPERIMENT TO REVERSE INHERITED DISEASE IS WORKING, The New York Times reported, noting that Wilsons paper was the first to report any therapeutic benefits of human gene therapy. Thanks to this study and others, the FDA gave the green light to more clinical trials every year, jumping from zero in 1989 to 91 in 1999. Universities set up gene therapy programs to stake a claim in the new field.

One of those was the Institute for Human Gene Therapy at the University of Pennsylvania. At age 38, Wilson became the institutes head, overseeing a staff that soon grew to more than 200. They launched new clinical trials, including a sequel to Wilsons study on familial hypercholesterolemia and on another genetic disorder in the liver: OTCD. Wilson now wanted to take the surgery out of gene therapy, so he and his colleagues searched the scientific literature for a virus that could seek out liver cells in the body.

They settled on a virus known as an adenovirus. Adenoviruses are best known for causing the common cold, but other scientists had found that they were very good at delivering genes into cells. Everything seemed to be moving forward nicelyuntil Jesse Gelsinger checked into Childrens Hospital of Philadelphia.

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The Fall and Rise of Gene Therapy

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Manila, Philippines -- Hospitals and health facilities offering stem cell therapy have until August 31 to apply for accreditation from the Department of Health (DoH).

DoH Secretary Enrique T. Ona said a number of hospitals in Metro Manila have already applied for accreditation to perform this "innovative" treatment that has not yet been accepted as standard mode of care in the country since it needs further tests and several more layers of research.

In the first mid-year convention of the Philippine Society for Stem Cell Medicine at the Manila Hotel yesterday, Ona reiterated that stem cell therapy is "the future of medicine."

"Stem cell therapy is not a cure-all medical treatment. Patients have yet to be presented first with standard of treatment, and in many cases, stem cell treatments have to be done in conjunction with other standard modalities of treatment," he said.

The Bureau of Health Facilities and Services (BHFS) of the DoH is accepting the applications for accreditation while a bio-ethics committee and a hospital-based review board will go over the applications and decide on their approval.

Five big hospitals in Metro Manila have already applied for accreditation, said Nick Lutero, chief of the BHFS.

Lutero said initial checks have revealed that these hospitals possess the required equipment needed for the treatment but they would still have to check on requirements set by the Food and Drug Administration (FDA) in relation to the practice.

Lutero said institutions that are offering stem cell treatments can still perform the procedures pending the approval of applications. However, once formal accreditations are already given, unaccredited institutions should cease offering stem cell therapy.

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DOH sets deadline for stem cell therapy accreditation

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

Contact: Elizabeth Allen allenea@uthscsa.edu 210-450-2020 University of Texas Health Science Center at San Antonio

SAN ANTONIO -- Adding to the picture of what prompts breast cancers to form, researchers from the Cancer Therapy & Research Center (CTRC) at The University of Texas Health Science Center San Antonio today announced that "distant estrogen response elements" (DEREs) can act independently of oncogenes to spur tumor development.

DEREs appear to be depots or hubs that remotely and simultaneously control multiple target genes in response to estrogen stimulation, said Pei-Yin Hsu, Ph.D., lead author of the paper in Cancer Cell. As such, they are prime targets for the study of novel therapies for breast cancer and could also be useful in diagnosis.

Copy numbers

Where DEREs are multiplied or present in abnormal numbers, this contributes to tumor development, especially in estrogen receptor-positive breast cancers, said study senior author Tim Hui-Ming Huang, Ph.D., deputy director of the CTRC.

Decreasing the number of DERE copies could have therapeutic potential to treat women with this aggressive form of cancer, Dr. Huang said.

DEREs at 2 sites

The researchers analyzed two DERE clusters on human chromosomes 17 and 23. They found that the DEREs induce pro-growth factors and inhibit growth-suppressing genes. "It is worthwhile to note that DERE-DERE interactions, instead of DERE interactions with genes, may also contribute to tumor development," Dr. Hsu said.

The team found a correlation between a subset of DERE-regulated genes and tamoxifen resistance. Tamoxifen is a widely prescribed hormone therapy for breast cancer. It may be possible to evaluate how a woman will respond to tamoxifen by measuring DERE activity, Dr. Hsu said.

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Estrogen enhancers tied to aggressive breast cancer

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Javascript is currently disabled in your web browser. For full site functionality, it is necessary to enable Javascript. In order to enable it, please see these instructions. 12 hours ago Rice University researchers adapted a computer algorithm to find the parts of two distantly related adeno-associated viruses that could be recombined into new and useful viruses for gene therapy. They intend to determine the rules by which custom viruses can easily be designed for therapies. Credit: Benjamin Adler/Rice University

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.

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Writing rules for gene-therapy vectors: Researchers compute, then combine benign viruses to fight disease

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Aug. 12, 2013 More than 50 million people worldwide have epilepsy, with a third of these being children. The most common forms of epilepsy in children occur without any apparent trigger and only affect certain regions of the brain. This condition is known as idiopathic focal epilepsy (IFE). The hallmark of IFE is the origin of the fit being in what is termed the rolandic region of the brain. Now, thanks to the considerable input of MedUni Vienna researchers, two pan-European research networks have successfully identified the first disease gene for IFE.

The gene concerned is known as GRIN2A. Changes to this gene cause one of the key ion channels in the brain to malfunction, affecting the electrical excitation of nerve cells. This explains the increased number of electrical discharges in the brain and therefore the manifestation of epileptic fits. The results of the study, which were obtained through the two research networks EuroEPINOMICS and IonNeurOnet, have now been published in the journal Nature Genetics.

The research project came into being from collaboration between numerous groups of researchers in Europe who shared a common goal: to understand the genetic causes of this type of childhood epilepsy. "What was crucial for our breakthrough was the close cooperation of doctors carrying out clinical research with theoretical researchers," explains Fritz Zimprich from the University Department of Neurology at the MedUni Vienna, who coordinated the researchers involved in the project from Vienna, Graz and Innsbruck. "A third of the patients investigated with state-of-the-art genetic methods come from Austria.

All in all, genetic material from 400 patients with IFE was analysed. In 7.5 per cent of sufferers, the scientists found changes in the GRIN2A gene. In "rolandic epilepsy," which accounts for 15 per cent of cases of childhood epilepsy and therefore makes it the most common form of the condition, these mutations disrupt the function of the NMDA receptor, one of the brain's key ion channels. The flow of ions in this type of channel influences and determines the nerve cells' electrical excitation.

It is however still not yet fully understood how the mutation in the gene on the NMDA receptor leads to epilepsy. Says Zimprich: "We only see the condition as a result of the mutations; we haven't yet fully discovered the mechanisms behind it." The next target is to understand these mechanisms. This is also an essential step in the development of more effective and more tolerable anticonvulsant medications.

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Disease gene discovered for frequent epilepsy in childhood

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SOURCE: Cystinosis Research Foundation

IRVINE, CA--(Marketwired - Aug 12, 2013) - Six grants totaling $1,295,377 were issued to cystinosis researchers investigating better treatments and a cure for the disease by the Cystinosis Research Foundation in its first round of proposals in 2013. Included is funding for additional research on stem cell and gene therapy, which holds the greatest promise to cure the rare, deadly metabolic and genetic disease.Cystinosis afflicts about 500 children and young adults in the United States and 2,000 worldwide.

"A cure is within sight.These new studies will accelerate the research process and will provide the critical data we need to realize our goal of finding a cure for cystinosis.CRF funded research has led to new research discoveries and treatments for cystinosis and as an unexpected, positive result, helped other more prevalent diseases such as Parkinson's and Huntington's disease.We believe that there will be an autologous stem cell trial for patients with cystinosis within three to four years.We are committed to continue to fund research until we find the cure," said Nancy Stack, CRF Trustee and President.

The CRF's spring grants were awarded to research programs at hospitals and universities in the United States and Canada.In the last 11 years the CRF has raised more than $22 million and has funded 108 studies and fellowships in 11 countries. The CRF is the only funding source for bench and clinical investigations of cystinosis worldwide.

"CRF is guided by a Scientific Review Board, a world renowned group of cystinosis experts and scientists who evaluate every research application we receive.Their expertise and leadership ensures that CRF funds only the most promising research studies. These new research projects are important in the sequence of solving the mysteries of this disease," Stack said.The scientific panel is headed by Dr. Corinne Antignac, a Paris researcher who first identified the CTNS gene in 1998.

Dr. Stphanie Cherqui, assistant professor Department of Pediatrics, University of California, San Diego, was on Dr. Antignac's team that discovered the cystinosis gene. She is a member of the Scientific Review Board and chairs the CRF Cystinosis Gene Therapy Consortium.Dr. Cherqui's work, in 2009 reversed the disease and halted tissue damage in mice.

Cystinosis is a metabolic disease that slowly destroys every organ in the body, including the liver, kidneys, eyes, muscles, thyroid and brain. There is a medicine, cysteamine that prolongs the children's lives, but there is no cure.

CRF's mission to find a better treatment for cystinosis was realized with the discovery of delayed-release cysteamine by researchers at UC San Diego. In 2008, Raptor Pharmaceuticals bought the worldwide license for the CRF-funded research and completed the necessary clinical trials to bring the drug to market and after years of waiting, Raptor received FDA approval on April 30, 2013.The drug will be sold under the name Procysbi.In addition, cysteamine and its delayed-release formula is being used in clinical trials for Huntington's disease and NASH, a progressive liver disease.

The CRF also has launched the Cure Cystinosis International Registry (CCIR), whose purpose is to consolidate information about cystinosis patients into a single data repository which will help advance research and clinical trials leading to future treatments and cures.

Stack and her husband, Geoffrey, a managing director of the SARESREGIS Group, an Irvine real estate company, have a daughter, Natalie, 22, with cystinosis.

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Cystinosis Research Foundation Awards $1.29 Million in Grants to Find a Cure for Deadly Genetic Disease

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

Contact: Rachel Steinhardt rsteinhardt@licr.org 212-450-1582 Ludwig Institute for Cancer Research

August 12, 2013, New York, NY Loss of a gene required for stem cells in the brain to turn into neurons may underlie the most severe forms of neuroblastoma, a deadly childhood cancer of the nervous system, according to a Ludwig Cancer Research study. Published in Developmental Cell today, the findings also provide clues about how to improve the treatment of this often-incurable tumor.

Neuroblastoma can appear in nervous tissue in the abdomen, chest and spine, among other regions of the body, and can spawn body-wracking metastasis. The most severe tumors respond poorly to treatment, and the disease accounts for 15 percent of cancer deaths in children.

Johan Holmberg, PhD, at the Ludwig Institute for Cancer Research Stockholm took a close look at the role of the CHD5 tumor suppressor during normal nervous system development. Previous studies had shown that the gene CHD5 is often inactivated in the most severe forms of neuroblastoma, but little was known about its function in healthy tissue or how it operates. The study, which was conducted in close collaboration with colleagues at Trinity College, Dublin, Ireland, addressed these two key issues.

The researchers found that CHD5 is required for the cellular transition from a stem cell to a mature neuron. In one experiment, the researchers knocked down the CHD5 gene by injecting a small RNA into the brains of fetal mice while in the womb.

"The result was a complete absence of neurons," says Ludwig researcher Holmberg who is based at the Karolinska Institutet. "Instead of becoming neurons, the cells with CHD5 knocked down stayed in a limbo-like state between an actively-dividing stem cell and a mature nerve cell. It was a very robust effect," added Holmberg.

The researchers also dissected how CHD5 operates, showing that it sticks to certain modifications of histone proteins. These modifications help control how genes are turned on and off. In the absence of CHD5, key stem cell genes are not turned off, and genes required for neuronal maturation are not turned on. The findings highlight how the failure of a cell to properly mature into its terminal state can underlie cancer, a relatively understudied area of research.

"It is necessary for cells in the healthy nervous tissue to be able to go from stem cells to neurons," explains Holmberg. "If you lose this capacity, these cells become locked in an immature state, which might yield quite dangerous tumor cells, especially in combination with additional cancer-promoting cellular events."

The research could also lead to new ways to treat neuroblastoma, perhaps using currently approved drugs. One component of neuroblastoma treatment is retinoic acid, a drug that can drive neuronal maturation. Holmberg and his colleagues found that knocking down the expression of CHD5 in more benign neuroblastoma cells blocked their capacity to mature in response to retinoic acid treatment. "These cells were completely insensitive to treatment, no matter how much we gave them, mirroring the same unresponsiveness to retinoic acid in the more malignant CHD5-negative neuroblastoma cells," says Holmberg.

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

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

New Rochelle, NY -- Body mass index (BMI) or a change in BMI is often the sole measure used to evaluate whether an intervention intended to combat childhood obesity is effective. But a new study clearly shows that an intervention can have beneficial effects on other health outcomes, such as cardiovascular fitness, regardless of its effect on BMI. Focusing on a single factor like the degree of BMI change is restrictive and can overlook other important outcomes, according to an article published in Childhood Obesity, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Childhood Obesity website at http://www.liebertpub.com/chi.

Maria Kolotourou and a team of authors involved in the Mind, Exercise, Nutrition...Do It! (MEND) trial from University of London, University College London, and Mytime MEND gathered data from a group of obese children before they participated in the MEND childhood obesity intervention and again at 6- and 12-month follow-up intervals. The researchers measured BMI, degree of change in BMI, waist circumference, cardiovascular fitness, physical activity, sedentary behaviors, and self-esteem.

In the article "Is BMI Alone a Sufficient Outcome to Evaluate Interventions for Child Obesity?" the authors report improvements, in several of the parameters measured, independent of whether a child's BMI decreased, increased, or remained the same.

"Good interventions aimed at helping overweight children lose weight should be equally directed at helping them to find health. This article suggests that health benefits may be seen independent of weight change, per se, and we are thus better served by evaluation strategies that encompass an array of relevant and important measures," says David L. Katz, MD, MPH, Editor-in-Chief of Childhood Obesity and Director of Yale University's Prevention Research Center.

###

About the Journal

Childhood Obesity is a bimonthly journal, published in print and online, and the journal of record for all aspects of communication on the broad spectrum of issues and strategies related to weight management and obesity prevention in children and adolescents. The Journal includes peer-reviewed articles documenting cutting-edge research and clinical studies, opinion pieces and roundtable discussions, profiles of successful programs and interventions, and updates on task force recommendations, global initiatives, and policy platforms. It reports on news and developments in science and medicine, features programs and initiatives developed in the public and private sector, and includes a Literature Watch. Tables of content and a sample issue may be viewed on the Childhood Obesity website at http://www.liebertpub.com/chi.

About the Publisher

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Child obesity interventions -- is change in BMI a good measure of success?

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Robert Preidt HealthDay News Posted: Sunday, August 11, 2013, 2:00 PM

SUNDAY, Aug. 11 (HealthDay News) -- Five major mental disorders share common inherited genetic variations, a new study finds.

The overlap is highest between schizophrenia and bipolar disorder (15 percent), moderate between bipolar disorder and depression and between attention-deficit/hyperactivity disorder (ADHD) and depression (about 10 percent), and lowest between schizophrenia and autism (3 percent).

Overall, common genetic variations accounted for 17 percent to 28 percent of risk for the five mental disorders, according to the study published in the Aug. 11 issue of the journal Nature Genetics, which the researchers say is the largest genome-wide study of its kind.

The project involved more than 300 scientists at 80 research centers in 20 countries and was supported by the U.S. National Institute of Mental Health (NIMH).

The investigators analyzed the genomes of several thousand people with the five mental disorders and people without the disorders.

"Since our study only looked at common gene variants, the total genetic overlap between the disorders is likely higher," study co-leader Naomi Wray, of the University of Queensland in Australia, said in an NIMH news release. "Shared variants with smaller effects, rare variants, mutations, duplications, deletions, and gene-environment interactions also contribute to these illnesses."

The genetic overlap between schizophrenia and depression could prove important in terms of research and diagnosing patients, according to the study authors. They expected to see more overlap between ADHD and autism, but said the moderate overlap between schizophrenia and autism is consistent with emerging evidence.

"Such evidence quantifying shared genetic risk factors among traditional psychiatric diagnoses will help us move toward classification that will be more faithful to nature," said Bruce Cuthbert, director of the NIMH's adult translational research and treatment development division. Cuthbert is also the coordinator of an NIMH project that is working to develop a mental disorders classification system for research based more on underlying causes.

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Genetic overlap seen in five mental disorders

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