SILVER SPRING, Md., Aug. 16, 2012 (GLOBE NEWSWIRE) -- Nuvilex, Inc. (NVLX), an international biotechnology provider of cell and gene therapy solutions, announced today it has contacted several key members of congress, lending its support to the Pancreatic Cancer Research and Education Act (S. 362/H.R. 733).

The legislation being proposed in H.R. 733, calls for an appropriation of $20 Million and requires the Secretary of Health and Human Services "to establish and implement a pancreatic cancer initiative to assist in coordinating activities to address the high mortality rate associated with pancreatic cancer" through establishing an Interdisciplinary Pancreatic Cancer Coordinating Committee and developing a long-term plan with the National Institutes of Health (NIH), the National Cancer Institute (NCI) and the Centers for Disease Control and Prevention (CDC). Research dedicated to providing possible treatments for pancreatic cancer receives only ~2% of the federal funding from NCI. Finally, there is no national plan designed to improve patient survival, which this bill is designed to initiate.

Since its original introduction in 2009 by Congresswoman Anna Eshoo (D,CA) and reintroduction with Leonard Lance (R,NJ) in 2011 followed by introduction of S. 362 by Senator Sheldon Whitehouse (D,RI) to the Senate, the bill has now received 276 cosponsoring members from the House and 58 from the Senate. In addressing the critical need for this legislation in his letters to Congress, Nuvilex's Chief Executive Dr. Robert Ryan, stressed the importance of funding in order to help bring new pancreatic cancer therapies forward to completion, stating, "...the opportunities for bringing treatments such as Nuvilex's for [pancreatic cancer] to fruition are, and will continue to be, limited by the availability of funding." Dr. Ryan added, "Government funding must be made available to small companies who, like Nuvilex, have demonstrated through preclinical and/or early clinical trials the efficacy of their product in treating high-mortality diseases such as pancreatic cancer." One of the bill's sponsors, Senator Isakson (R,GA), emphasized his deep commitment to this bill stating, "...this bill will go a long way in ensuring that the fight against pancreatic cancer receives its fair share of research and resources."

In providing endorsement of this legislation by Nuvilex, its Board and on behalf of its new wholly-owned subsidiary Austrianova Singapore, Dr. Ryan finished by pointing out, "Nuvilex feels it is critical to endorse S. 362/H.R. 733. It's very important that our Congressional leaders receive the recommendations and support from all constituents, including Nuvilex, in order to help support and stimulate passage of the Pancreatic Cancer Research and Education Act. We believe the completed Phase 1/2 pancreatic cancer trial using our Cell-in-a-Box(R) patented technology will provide an important step toward helping change the poor pancreatic cancer survivor statistics. Nuvilex sees this Congressional Initiative as another potentially critical mechanism to help move our technology forward."

Pancreatic Cancer

Statistics directly show pancreatic cancer is the fourth leading cause of cancer death in the United States. Internationally >250,000 people will die from it this year. At present, there are no standard early detection methods, although recent discoveries suggest a new pancreatic cancer detection method may be on the horizon, there are few effective treatment options and there is no cure. As a result, 74 percent of patients die within a year of diagnosis and only six percent survive beyond five years.

About Nuvilex

Nuvilex, Inc. (NVLX) is an international biotechnology provider of live therapeutically valuable, encapsulated cells and services for research and medicine. A great deal of work is ongoing to move Nuvilex, and in particular its Austrianova Singapore subsidiary, forward. Our company's clinical offerings will include cancer, diabetes and other treatments using the company's cell and gene therapy expertise and live-cell encapsulation technology.

The Nuvilex, Inc. logo is available at http://www.globenewswire.com/newsroom/prs/?pkgid=13494

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Contact: Phil Sahm phil.sahm@hsc.utah.edu 801-581-2517 University of Utah Health Sciences

SALT LAKE CITY Scientists have discovered that poxviruses, which are responsible for smallpox and other diseases, can adapt to defeat different host antiviral defenses by quickly and temporarily producing multiple copies of a gene that helps the viruses to counter host immunity. This discovery provides new insight into the ability of large double-stranded DNA viruses to undergo rapid evolution despite their low mutation rates, according to a study published by University of Utah researchers in the Aug. 17, 2012, issue of Cell.

Poxviruses are a group of DNA-containing viruses that are responsible for a wide range of diseases in both humans and animals, including smallpox. Unlike smaller RNA-containing viruses, such as those that cause influenza and HIV, which are able to evade host immune responses through rapid mutation, poxviruses have larger genomes and low mutation rates and little is known about their adaptive strategies against host defenses.

"Poxviruses encode a variety of genes that help them to counter host immune defenses and promote infection," says Nels Elde, Ph.D., assistant professor of human genetics at the University of Utah School of Medicine and first author on the study. "Despite ample evidence that the poxvirus genome can undergo adaptive changes to overcome evolving host defenses, we still don't know that much about the mechanisms involved in that adaptation."

To determine mechanisms of adaptation, Elde and his colleagues studied the vaccinia virus, a type of poxvirus best known for its role as the vaccine used to eradicate smallpox. Previous research has shown that vaccinia virus encodes two genes, known as K3L and E3L, which inhibit host defenses that normally block viral infection. In this study, Elde and his colleagues started with a strain of vaccinia virus that had been altered to delete the E3L gene and repeatedly propagated this E3L-deficient strain in human cells to see how well the virus would replicate. They found that this E3L-deficient strain was quickly able to increase infectious virus production by selectively increasing the number of copies of the K3L gene in its genome.

"This highly specific and rapid gene amplification was unexpected," says Elde. "Our studies show that increasing K3L copy number leads to increased expression of K3L and enhanced viral replication, providing an immediate evolutionary advantage for those viruses that can quickly expand their genome."

Elde and his colleagues also found that, in addition to K3L copy number amplification, some of the E3L-deficient vaccinia strains also acquired a mutation consisting of a single amino acid substitution in the K3L gene. Both the mutation-bearing and multicopy K3L viruses displayed improved viral fitness, or ability to replicate in the host environment, compared to wild-type vaccinia virus. The emergence of this beneficial amino acid substitution suggests that increasing K3L copy number facilitated the appearance of the variant by providing additional mutational targets, despite the virus' otherwise low mutation rate.

"We were able to demonstrate at least two strategies by which poxviruses are able to adapt diverse mechanisms of host immunity," says Elde. "Our observations reveal that, while poxviruses do undergo gene mutation, their first response to a new, hostile host environment can be rapid gene expansion. We also found evidence that the virus genome can contract after acquiring an adaptive mutation, thus alleviating the potential trade-off of having a larger genome, while leaving a beneficial mutation in place."

Although smallpox was officially eradicated by the World Health Organization in 1980, concerns about the use of smallpox as a bioterrorism agent have spurred renewed interest in the study of vaccinia and other poxviruses. In addition, poxvirus infections, such as monkeypox, can be transmitted from animals to humans and the adaptive strategies of poxviruses may be relevant for other infectious organisms.

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Published: Aug. 16, 2012 at 7:28 AM

DAVIS, Calif., Aug. 16 (UPI) -- A defective gene causes brain changes that lead to the atypical social behavior characteristic of autism, U.S. researchers said.

Cecilia Giulivi, professor of molecular biosciences at the University of California, Davis School of Veterinary Medicine, and a researcher affiliated with the University of California, Davis MIND Institute, said studies in mice showed abnormal action of just one gene disrupted energy use in neurons.

The harmful changes were coupled with anti-social and prolonged repetitive behavior -- traits found in autism, Giulivi said.

"A number of genes and environmental factors have been shown to be involved in autism, but this study points to a mechanism -- how one gene defect may trigger this type of neurological behavior," Giulivi said in a statement. "Once you understand the mechanism, that opens the way for developing drugs to treat the condition."

The research, published in the journal PLoS ONE, showed, when defective, the gene's protein interacts with the protein of a second gene known as p53 to dampen energy production in neurons.

This severe stress leads to a spike in harmful mitochondrial DNA changes and abnormal levels of energy production in the cerebellum and hippocampus -- brain regions critical for social behavior and cognition, Giulivi said.

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Defective gene linked to autism symptoms

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FARMINGTON, Conn., Aug. 16, 2012 /PRNewswire-iReach/ -- "Personalized" cancer care has never had it better, and three drugs have been responsible for confirming their prospects to combat certain common cancers. Of these, two studies have focused on drugs for treating advanced melanoma, and a third study has explored a gene-targeted chemotherapy for a subset of lung cancers. All the three drugs have proved their efficacy in Phase III trials, and tailored medications similar to these are being used in metastasis or cancer settings. Advanced lung cancer and advanced melanoma necessitate targeted therapies that form the standard of care.

(Photo: http://photos.prnewswire.com/prnh/20120816/CG58765)

The past scenario involved doctors administering cancer drugs to patients as a normal course, in the anticipation that response levels in at least some of the patients would be positive. However, with the advent of personalized medicine, this method has taken a back seat, and greater emphasis is being given to patient-centric approaches for targeting therapies towards genetic abnormalities in cancers that are responsible for driving cancer growth.

Global Information, Inc. presents the latest analysis market research published by Industry Experts and the upcoming ADAPT 2012 in Washington, DC.

Market Research: Personalized Medicine - A Global Market Overview

Personalized Medicine product segments analyzed in this study includes Targeted Biologics, Proteomics & Genomics, Genetically Modified (GM) Products, Wellness & Disease Management, Molecular Diagnostics and Self/Other Diagnostics.

Biologics have gained prominence in treating systemic and cutaneous autoimmune diseases, with a design that targets particular components of immune system. Since novel drugs can target proteins in a more precise manner, in addition to having reduced risks of systemic side effects, they offer significant benefits as compared to the erstwhile immunomodulators. For instance, crucial advances have been achieved in developing TNF-alpha blockers for treating psoriasis, psoriatic arthritis, rheumatoid arthritis, Crohn's disease and ankylosing spondylitis in the same manner, B-cell depletion has revolutionized treatment of lupus, pemphigus, certain vasculitides, etc. Having said this, development of these molecules and their clinical usage are as yet in the evolutionary process.

Further categorization of patients' clinical profiles requiring the use of biologics has to reach a culmination point due to the fact that the long-term safety profiles of such agents are largely hidden at present.

Pharmacogenomics is the branch of pharmacology dealing with the influence of genetic variation on drug response in patients through the correlation of gene expression or single-nucleotide polymorphisms with a drug's efficacy or toxicity. This is focused towards developing rational means for optimizing drug therapy relating to the patients' genotype, ensuring maximum efficacy with minimal adverse effects. Pharmacogenomics offers the prospect of advancing personalized medicine to levels where drugs and drug combinations can be optimized for every individual's unique genetic makeup. Pharmacogenomics is the whole genome application of pharmacogenetics, which examines the single gene interactions with drugs.

An Executive Summary of this analysis, full table of contents, and a free sample/whitepaper of the full report are available at http://www.giiresearch.com/report/inde248627-personalized-medicine-global-market-overview.html

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Public release date: 16-Aug-2012 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, August 16, 2012Every year tribal gaming generates billions of dollars in revenue, creates tens of thousands of jobs, and boosts the economies of many Native American communities. In the state of California alone, tribal gaming has brought in $7.5 billion annually. However, because of the aggressive movement to legalize Internet gambling, which effectively would give states the power to regulate and tax online gambling even on reservations, the financial success of these communities could change. In "Native American Off-Reservation Gaming," an expert roundtable published in Gaming Law Review and Economics, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers, panelists discuss and debate the issues of tribal gaming, focusing on the impactboth positive and negativeon both tribes and their surrounding communities. The full tables of content for Gaming Law Review and Economics are available online.

"Though some tribes have been incredibly successful financially from casino and resort businesses, experts have observed that the Native American gaming revenues are already going flat," says Joseph M. Kelly, PhD, JD, Co-Editor-in-Chief of Gaming Law Review and Economics, professor of business law at SUNY College at Buffalo, and co-author of the article, 'Enforcement of Native American Gambling Debts.' "There is concern amongst many of these tribes that state legalization of online gambling might have a negative impact on their revenues. Many tribal experts instead would prefer federal regulation."

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About the Journal

Gaming Law Review and Economics: Regulation, Compliance, and Policy is the only authoritative peer-reviewed journal covering traditional land-based, Internet, and wireless gaming law in one of the fastest growing economic leisure industries. The Journal provides the latest developments in legislative, regulatory, and judicial decisions affecting gaming at both the state and federal level in the U.S. and in more than 75 countries, as well as coverage of economic issues associated with the exponential growth of casinos and gaming practices. Topics include legal aspects of all forms of gaming, including casino games, lotteries, sports books, and horse racing; new regulations in Internet and wireless gaming; legal restrictions on gaming and advertising; gaming license requirements within and across jurisdictions; legal aspects of credit and collection of debts; litigation in application, citing, and employment issues concerning casino operations; gaming tax issues; and intellectual property. Complete tables of content and a sample issue may be viewed online at the Gaming Law Review and Economics: Regulation, Compliance, and Policy website.

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science, biomedical research, and law including Election Law Journal and Biotechnology Law Report. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 70 journals, books, and newsmagazines is available at the Mary Ann Liebert, Inc., publishers website.

Mary Ann Liebert, Inc. 140 Huguenot Street, New Rochelle, NY 10801 http://www.liebertpub.com Phone: (914) 740-2100 (800) M-LIEBERT Fax (914) 740-2101

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Prosperous Native-American tribes grow anxious about legalization of Internet gambling

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15-08-2012 15:37

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USC Institute for Genetic Medicine Art Show - Video

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SAN CLEMENTE, Calif.--(BUSINESS WIRE)--

Metagenics, Inc., a nutrigenomics and lifestyle medicine company dedicated to helping people live happier, healthier lives by realizing their genetic potential, today announced the relocation of its corporate and Americas region headquarters from San Clemente, Calif. to Aliso Viejo, Calif. The modern, efficiently designed, and LEED-certified facility not only supports Metagenics healthy lifestyle vision and mission, but also provides future space to accommodate the companys growth trend and goals. Metagenics will be relocating to its new headquarters beginning August 20.

This move represents the right choice for us at a time when were making plans for the next phase of growth, said Fred Howard, chief executive officer of Metagenics. The new facility accommodates our growing employee base, enabling us to better serve the needs of our customers. Additionally, it provides an ideal environment that represents the healthy balance we strive for in our professional and personal lives.

The facility, located at 25 Enterprise Parkway, is staged to accommodate the companys current office space with room for future growth. The building is certified for Leadership in Energy and Environmental Design (LEED) for more efficient use of resources, which often also provides a healthier work environment.

We saw an enormous amount of opportunity in this decision, commented Willy Pardias, senior vice president and general manager of Metagenics Americas region. This facility provides an inspiring and energizing atmosphere that further supports our companys mission to living healthier lifestyles.

About Metagenics, Inc.

Metagenics, Inc. (www.metagenics.com) is a nutrigenomics and lifestyle medicine company focused on improving health and reversing chronic illness. Founded in 1983, Metagenics serves more than 75,000 healthcare providers worldwide through premium quality, science-based medical foods, nutritional formulas, and lifestyle therapy programs to help their patients achieve a lifetime of good health. Metagenics scientific staffamong the largest in the nutrigenomics industryhas published more than 80 articles in peer-reviewed journals and has been awarded 78 international or domestic patents. The companys educational arm, Metagenics University, collaborates with renowned medical experts to annually deliver more than 200 events designed to help healthcare professionals stay on the leading edge of lifestyle medicine and incorporate nutrition into their clinical practice.

Metagenics will maintain its corporate headquarters in Aliso Viejo, California; R&D headquarters in Gig Harbor, Washington; and operating subsidiaries in Brussels, Belgium and Brisbane, Australia.

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Metagenics to Relocate to New Facility in Aliso Viejo, California

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DETROIT Wayne State University researchers are testing a way to determine the status of fetal chromosomes that could lead to healthier outcomes for mothers and their babies.

Supported by a two-year, $418,000 exploratory/developmental grant from the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health, the researchers will capture human fetal cells for genetic study within the first two months of pregnancy using a newly developed, safe, noninvasive retrieval technique similar to a Pap test.

D. Randall Armant, Ph.D., and Michael P. Diamond, M.D., professors of obstetrics and gynecology in Wayne States School of Medicine, are the principal investigators of the study. Susan Land, Ph.D., associate professor of obstetrics and gynecology, is a co-investigator.

Titled Genetic Analysis of Human First Trimester Trophoblast in Ongoing Pregnancies, the project targets cells called trophoblasts, which surround the blastocyst, a cluster of cells that results from successful fertilization. Researchers are particularly interested in invasive trophoblasts, which attach the blastocyst to the uterine wall; the cells become the placenta and the membranes that nourish and protect the developing organism.

Such cells carry genetic material from the fetus. Armants team will gather them through transcervical sampling, a method that uses a cytobrush inserted into the cervix. Researchers believe the technique is less intrusive than previously used methods, yields intact fetal cells and can be done as early as six to 12 weeks; doctors typically must wait 10 to 14 weeks to use other methods, which can carry more risk to mothers and fetuses.

The earlier you get the information, the more time the doctor has to manage whatever problems are coming up during or after the mothers pregnancy, Armant said. It also gives the parents more time to make decisions about the pregnancy.

Researchers will isolate trophoblasts using immunomagnetic nanotechnology, taking advantage of unique proteins on the surface of fetal cells. Highly sensitive genetic tools capable of analyzing single cells will verify the fetal origin of captured cells before their DNA is analyzed for chromosome number.

Armant said that tests based on fetal cells obtained from the cervix eventually could alert doctors to things like ectopic pregnancy, miscarriage, preterm labor, poor fetal growth, preeclampsia, fetal Rh incompatibility and chromosome number disorders, like Down syndrome. It also could help detect inherited genetic diseases, such as muscular dystrophy, sickle cell anemia and hemophilia.

The goal is to determine if placental cells obtained from the cervix accurately represent the chromosomal status of the fetus.

Development of this diagnostic platform for the detection of chromosome number disorders could establish an innovative approach for prenatal genetic testing that would provide immense opportunities for improving the health of mothers and their babies, Armant said. Continued...

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WAYNE COUNTY: New fetal cell collection method could improve genetic analysis, disorder detection, Wayne State ...

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WEDNESDAY, Aug. 15 (HealthDay News) -- Dogs may soon become man's best friend on a level that goes far beyond companionship and loyalty.

Researchers report that the canine genome, similar in many ways to the human one, is starting to shed light on a wide range of human diseases.

What makes dogs particularly interesting to scientists is their breed structure -- a type of artificial selection -- which creates distinct and diverse lines of animals that range from the muscular German shepherd to the nervous Chihuahua, from the hard-working collie to the perpetually pampered poodle.

According to a review article published Aug. 16 in the New England Journal of Medicine, the fact that most purebred dogs have descended from small, closely related parentage with large litters means recessive diseases are common among them.

To those interested in genetics, that's exciting.

It makes less common recessive diseases (which can't be seen or expressed unless the responsible gene is carried by both parents) more prevalent in these animals. And that opens the window to understanding the genetic underpinnings of a wide range of conditions that humans and dogs share.

"The dog genome is very similar to humans," said review author Elaine Ostrander, chief of the Cancer Genetics Branch of the National Human Genome Research Institute at the U.S. National Institutes of Health. "It's closer to us than the genomes of mice, rats or fruit flies, which are often used in research. Dogs also live side-by-side in our environments with us; they drink the same water, they breathe the same air, they're exposed to the same pesticides and they often even eat some of the same food."

Ostrander said dogs and humans get almost all of the same diseases, including cancer, arthritis, epilepsy, retinal atrophy, autoimmune disorders such as lupus, and psychological problems such as obsessive-compulsive disorder.

There are 400 different breeds, and many are associated with greater risk of getting particular diseases, Ostrander said. "A particular torsion [twisting] of the intestine is the only thing we see in dogs but not in humans."

Cancer is the number one cause of death in dogs, said Dr. Ned Patterson, an associate professor of veterinary medicine and genetics at the University of Minnesota. "Because the mechanism [of the disease] and the therapies are similar, we can really learn a lot about cancer in both directions, even concurrently," he noted.

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Man's Best Friend Points the Way in Genetic Research

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Dog lovers may be interested in an article published this week in the New England Journal of Medicine: It highlights the discoveries scientists are making about diseases that various dog breeds are prone to -- and how those findings can benefit human health as well as that of canines.

Its written by longtime dog genetics researcher Elaine Ostrander of the National Human Genome Research Institute.

The discoveries are possible because of several things: First off, both the human genome and dog genomes have been sequenced. (The breeds chosen for the first round of dog DNA sequencing were a standard poodle and boxer, should you be curious.)

Secondly, dogs have been intensively bred into distinct breeds, and in the case of purebreds (though not my black mutt Nightshade; who knows where she came from?) their pedigrees are very well known. Often, the breeds are descended from just a few animals, so they can be very inbred as well.

The intensive selection over the decades and/or centuries for traits of body shape or hair color has also inadvertently selected for genes that foster diseases. And so Bedlington terriers are prone to copper storage diseases, Doberman pinschers are prone to narcolepsy, and so on.

Here is where some lemonade gets made out of that sad lemon: Its far easier in many cases for scientists to track down genes associated with, say, a cancer or vision disorder in dogs than it is in human beings, Ostrander writes.

Thats especially true when a disease could stem from one of several genetic defects. If you study a bunch of people with the disease, the underlying genes involved will probably be a mix and the results will be too cloudy for scientists to make sense of. But in an inbred dog strain prone to a disorder, the underlying cause is far more likely to be rooted in one specific gene.

And that means scientists can find it. Once theyve found it, they can then go back and see if the same holds true for some human beings.

Some examples Ostrander cites of gene-influenced disorders in dogs shedding light on diseases in human beings:

--A syndrome called RCND that causes kidney cancer and skin growths in German shepherds was pinpointed to versions of a gene called folliculin. That same gene, it turns out, is involved in a human disease called Birt-Hogg-Dube syndrome.

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How dogs can help unravel genetic diseases in people

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The technique could help patients with currently untreatable diseases such as Huntington's.

RNA Rx: An Alynlam chemist prepares RNA molecules. Alnylam Pharmaceuticals

A biotech company called Alnylam announced today that a small clinical trial for a genetic therapy based on RNA interference, or RNAi, suggests that the technique can have a powerful effect on its target gene. The therapeutic effect lasted for over a month with just one dose. The company is also working with a medical device maker, Medtronic, on a way to deliver RNAi treatment directly to the brain, in order to treat the degenerative brain disease Huntington's.

The patients in the trial have a genetic disorder that originates in the liver and leads to the buildup of protein deposits in many organs. Alnylam, a Cambridge, Massachusetts-based company, says its RNAi therapeutic, given at its highest dose, reduces the amount of the faulty protein that spurs the disease by almost 94 percent.

The positive results add weight to the notion that RNAi therapeutics could eventually help patients with a range of genetic diseases. RNAi therapy involves researchers producing snippets of RNA, a close relative of DNA, that match a portion of a gene of interest. When administered, this so-called small interfering RNA (siRNA) causes the destruction of that gene's products before it can be turned into a protein. The specificity of RNAi for targeting particular genes has attracted a lot of interest from people who want to use it as a clinical treatment (see "Prescription RNA").

"Today's platforms target the protein that causes the disease and bind to that protein. We stop the protein from being made in the first place," says Barry Greene, president and chief operating officer of Alnylam.

But a recurring challenge for the therapeutic RNAi field is how to deliver the siRNAs to the right place in the body. On their own, the small molecules do not survive long in the bloodstream, so simply injecting a patient with a solution of unprotected siRNAs is not effective. "The key technical hurdle is getting the siRNA [inside] the right cells," says Greene.

For several of its projects, Alnylam uses nanoparticles to protect and deliver its siRNAs, which can then be delivered by injection. But for genetic diseases that originate in the brain, the body's own defenses, namely the blood-brain barrier, complicate delivery further. To circumvent the blood-brain barrier, which prevents most molecules from leaving the bloodstream and entering the brain, Alnylam has looked to a different delivery mechanism: direct dosing of unpackaged siRNAs.

Medtronic, a Minneapolis company that designs and manufactures medical devices, has devised a way to allow this. Together, the companies have developed a treatment that combines Alnylam's RNAi therapeutic with Medtronic's drug delivery technology to treat Huntington's.

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Gene Control, Delivered Directly to the Brain

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Lions Park in Mt. Brydges will be rocking this Saturday night as the 7th annual Rockin Wheel in support of spinal cord injury awareness and research is held.

THE TREWS and Bleeker Ridge will be among the top bands performing starting at 2:15 p.m. on Saturday, Aug. 18.

Among the other bands are: Lifeline, Eleven Past One, Two Crown King and Dry County. A special feature this year will be Rockin Idol, started at 2:15, which will include six local karaoke singers ranging in age from 10 to 20-years-old.

Rockin Wheel was started by Ken Allore and has raised $100,000 in the last six years.

It was 20 years ago, that 17-year-old Kenny broke in his neck after being driven into the boards during a playoff hockey game in Belmont.

Ken never walked again, but the devastating injury didnt end his life.

As president of Rockin Wheel for spinal cord research, and ambassador for Shoot for a Cure, Ken feels more needs to be done for people with spinal cord injuries.

Ken has helped implement the stop sign on the back of all Canadian minor hockey player jerseys. The stop sign reminds kids to stop and think before checking from behind.

If we can prevent a needless spinal cord injury from happening to someone else then all our efforts will have been successful, said Ken.

Tickets are available at the door for $25.

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

Contact: Carolann Murphy CMurphy@KesslerFoundation.org 973-324-8382 Kessler Foundation

West Orange, NJ. August 15, 2012. Scientists from Kessler Foundation are presenting recent findings in spinal cord injury research during Beyond Boundaries: the 2012 Conference of the Academy of Spinal Cord Injury Professionals (ASCIP). John DeLuca, PhD, Steven Kirshblum, MD, Trevor Dyson-Hudson, MD, Gail F. Forrest, PhD, Denise Fyffe, PhD, and Rachel Byrne, are addressing a variety of topics at this multidisciplinary conference. Topics include new approaches to improving mobility and cognition, minimizing pain, determining prognosis and addressing health disparities. The ASCIP conference is being held at the Rio All-Suites Hotel and Resort in Las Vegas, Nevada, September 3-6. Attendees represent the ASCIP's membership of clinicians and researchers in medicine, science, psychology, nursing, therapy, and social work.

John DeLuca, PhD, VP of Research & Training at Kessler Foundation is giving the James J. Peters Memorial Lecture, named for the executive director of United Spinal Association who was a tireless advocate for people with spinal cord injury. Dr. DeLuca, a well-known expert in cognitive rehabilitation research, will discuss the cognitive issues that are often under recognized in patients with multiple sclerosis. Dr. Steven Kirshblum's topic for the Jayanthi Lecture is determining prognosis for the individual with acute injury. Drs. Kirshblum and Dyson-Hudson are co-directors of the Northern New Jersey SCI Model System at Kessler Foundation. Dr. Dyson-Hudson is presenting the model system's research on preventing pneumonia after spinal cord injury, as well as results of a pilot study on the use of platelet-rich plasma therapy for shoulder pain in wheelchair users with spinal cord injury.

Dr. Forrest's presentations address the scope of her innovative applications of technological advances for mobility after spinal cord injury. Drs. Forrest, Kirshblum, and colleagues, will discuss their clinical research experience with robotic exoskeletal devices, including their potential for affecting long-term health and well-being in the SCI population. Dr. Fyffe, an expert in health disparities, is an author on two posters: "Qualitative study of the impact of blood pressure dysregulation on quality of life in SCI" and "Self-reported symptoms of blood pressure dysregulation in persons with spinal cord injury." This research is VA funded and conducted in collaboration with researchers at the James J. Peters VA Medical Center.

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About SCI Research at Kessler Foundation

Through the NNJSCIS, funded by the National Institute on Disability and Rehabilitation Research, the Foundation collaborates on research in mobility, secondary medical complications, access to care, and quality of life. The Kessler NRN site is one of 6 centers in the Reeve Foundation's NeuroRecovery Network researching intensive locomotor training in SCI. Innovative studies are also being conducted with Ekso (Ekso Bionics), the bionic exoskeletal device, the LokomatPro v6 (Hocoma), a robotic treadmill training device, and with functional electrical stimulation. Additional funding sources include the National Institutes of Health, New Jersey Commission on Spinal Cord Research, The Craig H. Neilsen Foundation, the Veterans Administration, and Kessler Foundation. The Foundation, which has a model system for traumatic brain injury (NNJTBIS), is also widely known for cognitive rehabilitation research in brain injury, multiple sclerosis and stroke.

About Kessler Foundation

Kessler Foundation is one of the largest public charities in the field of disability. Kessler Foundation Research Center focuses on improving function and quality of life for persons with injuries of the spinal cord and brain, stroke, multiple sclerosis, and other chronic neurological conditions. Kessler Foundation Program Center fosters new approaches to the persistently high rates of unemployment among people disabled by injury or disease. Targeted grantmaking funds promising programs across the nation. Veterans of Iraq and Afghanistan, people recovering from catastrophic injuries and stroke, and young adults striving for independence are among the thousands of people finding jobs and training for careers as a result of the commitment of Kessler Foundation.

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NEW YORK, Aug. 15, 2012 (GLOBE NEWSWIRE) -- Amorcyte, a company of NeoStem, Inc. (NYSE MKT:NBS) ("NeoStem" or the "Company"), a rapidly emerging market leader in the fast growing cell therapy market, today announced that it received on August 9, 2012 approval to continue its PreSERVE AMI Phase 2 clinical trial following its first interim data and safety review by the Data Safety Monitoring Board (DSMB). The PreSERVE trial is a Phase 2, randomized, placebo controlled, double-blind study expected to include 160 patients at more than 40 clinical sites. The trial's product candidate, AMR-001, is designed to prevent major adverse cardiac events following acute myocardial infarction (AMI). Patient enrollment for the PreSERVE trial began in January 2012 and the Company anticipates completing enrollment in 2013 with six months initial data readout near the end of 2013.

"We are pleased that, similar to our Phase 1 trial, the first external review of our Phase 2 trial data confirms that there are no safety signals that would preclude the trial from continuing as planned," said Andrew L. Pecora, M.D. FACP CPE, Chief Medical Officer of NeoStem. "The PreSERVE AMI study to date indicates that multiple National Study sites are capable of acquiring the necessary volume of bone marrow to create the AMR-001 product five to seven days after an AMI in a safe and practical manner, and once created the product can be delivered and administered without a safety signal."

NeoStem management believes that cell therapy is a disruptive technology in the $50 billion worldwide regenerative medicine market. Many key opinion leaders in the scientific, medical and investment communities consider AMR-001 to be best in class. Peak annual worldwide sales of AMR-001 for this indication could exceed $1 billion based upon a conservative market penetration of its qualified target patient population. AMR-001 is protected by two issued and multiple pending U.S. patents with corresponding patent coverage in selected markets around the world. The Amorcyte AMR-001 product development program also extends to congestive heart failure (CHF). The Company is preparing to launch its CHF Phase 1 clinical trials in early 2013. The worldwide CHF patient population is estimated to be four times larger than that of AMI.

About NeoStem, Inc.

NeoStem, Inc. ("we," "NeoStem" or the "Company") continues to develop and build on its core capabilities in cell therapy to capitalize on the paradigm shift that we see occurring in medicine. In particular, we anticipate that cell therapy will have a large role in the fight against chronic disease and in lessening the economic burden that these diseases pose to modern society. Our January 2011 acquisition of Progenitor Cell Therapy, LLC ("PCT") provides NeoStem with a foundation in both manufacturing and regulatory affairs expertise. We believe this expertise, coupled with our existing research capabilities and collaborations, will allow us to achieve our mission of becoming a premier cell therapy company. Our PCT subsidiary's manufacturing base is one of the few current Good Manufacturing Practices ("cGMP") facilities available for contracting in the burgeoning cell therapy industry. Amorcyte, LLC ("Amorcyte"), which we acquired in October 2011, is developing a cell therapy for the treatment of cardiovascular disease. Amorcyte's lead compound, AMR-001, represents NeoStem's most clinically advanced therapeutic and Amorcyte is enrolling patients for a Phase 2 trial to investigate AMR-001's efficacy in preserving heart function after a heart attack. We also expect to begin a Phase 1 clinical trial in 2013 to investigate AMR-001's utility in arresting the progression of congestive heart failure and the associated comorbidities of that disease. Athelos Corporation ("Athelos"), which is approximately 80%-owned by our subsidiary, PCT, is engaged in collaboration with Becton-Dickinson that is exploring the earlier stage clinical development of a T-cell therapy for autoimmune conditions. In addition, our pre-clinical assets include our VSELTM Technology platform as well as our MSC (mesenchymal stem cells) product candidate for regenerative medicine.

For more information on NeoStem, please visit http://www.neostem.com.

Forward-Looking Statements for NeoStem, Inc.

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements reflect management's current expectations, as of the date of this press release, and involve certain risks and uncertainties. Forward-looking statements include statements herein with respect to the successful execution of the Company's business strategy, including with respect to the Company's or its partners' successful development of AMR-001 and other cell therapeutics, the size of the market for such products, its competitive position in such markets, the Company's ability to successfully penetrate such markets and the market for its CDMO business, and the efficacy of protection from its patent portfolio, as well as the future of the cell therapeutics industry in general, including the rate at which such industry may grow. Forward-looking statements also include statements with respect to satisfying all conditions to closing the disposition of Erye, including receipt of all necessary regulatory approvals in the PRC. The Company's actual results could differ materially from those anticipated in these forward-looking statements as a result of various factors, including but not limited to (i) the Company's ability to manage its business despite operating losses and cash outflows, (ii) its ability to obtain sufficient capital or strategic business arrangement to fund its operations, including the clinical trials for AMR-001, (iii) successful results of the Company's clinical trials of AMR-001 and other cellular therapeutic products that may be pursued, (iv) demand for and market acceptance of AMR-001 or other cell therapies if clinical trials are successful and the Company is permitted to market such products, (v) establishment of a large global market for cellular-based products, (vi) the impact of competitive products and pricing, (vii) the impact of future scientific and medical developments, (viii) the Company's ability to obtain appropriate governmental licenses and approvals and, in general, future actions of regulatory bodies, including the FDA and foreign counterparts, (ix) reimbursement and rebate policies of government agencies and private payers, (x) the Company's ability to protect its intellectual property; (xi) the company's ability to successfully divest its interest in Erye, and (xii) matters described under the "Risk Factors" in the Company's Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 20, 2012 and in the Company's other periodic filings with the Securities and Exchange Commission, all of which are available on its website. The Company does not undertake to update its forward-looking statements. The Company's further development is highly dependent on future medical and research developments and market acceptance, which is outside its control.

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NeoStem Reports Data Safety Monitoring Board Recommends Continuation of PreSERVE AMI Phase 2 Trial

Recommendation and review posted by Bethany Smith

Utilizing neuroscience, gene therapy, and optogenetics, a pair of researchers from Cornell University have created a bionic prosthetic eye that can restore almost-normal vision to animals blinded by destroyed retinas.

We have discussed bionic eyes at length, but for the most part these have been dumb prosthetics chips that wire themselves into the ganglion cells behind the retina, which are the interface between the retina and optic nerve. These chips receive optical stimuli (via a CMOS sensor, for example), which they transmit as electrical signals to the ganglion cells. These prosthetic eyes can produce a low-resolution grayscale field that the brain can then interpret which is probably better than being completely blind but they dont actually restore sight.

The Cornell prosthetic eye however, developed by Sheila Nirenberg and Chethan Pandarinath, is a much closer analog to a real eye. Its construction and implementation is rather complex, so bear with me.

First, gene therapy is used to deliver special proteins to the patients damaged retina (i.e. caused by degenerative diseases, such as macular degeneration or diabetic retinopathy). By using optogenetics, these proteins have been modified so that theyre sensitive to light theyre not quite rods and cones, but theyre along the same lines.

The next step is the clever/unique bit. For years now, Nirenberg has been working on decoding the signals sent by the retina to the brain. A year ago, she cracked this code. At the time, she had only cracked the code used by the mouse retina, but now shes cracked the monkey code too and a monkeys retina is very similar to ours.

Thats not the breakthrough here, though: Nirenberg and Pandarinath have now taken the mouse retina code and developed a working prosthetic, completely restoring a mouses vision.

The prosthetic contains a camera pointed forward, a Texas Instruments OMAP 3530 SoC (system-on-a-chip), and a tiny DLP pico projector. The SoC converts the cameras output into encoded data that the mouses brain can understand, and then the projector is used to beam that data to the optogenetic proteins that were earlier placed in the retina using gene therapy. The optogenetic proteins then transmit the encoded signal to the brain, via the ganglion cells and optic nerve. Voila: restored (grayscale) vision.

In the image above you can see just how effective Nirenberg and Pandarinaths prosthetic eye is. The top row is what a normal mouse eye would see (just before it gets eaten, seemingly), and the second row shows the images produced by the prosthetic eye. The bottom right corner shows the image your eye would see if it had only received the optogenetic gene therapy, and none of the fancy camera/neural-encoding tricks.

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Scientists reverse engineer animal brains to create bionic prosthetic eyes

Recommendation and review posted by Bethany Smith

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

Contact: Proffesor Dr. Gunther Meinlschmidt gunther.meinlschmidt@rub.de 49-234-507-73173 Ruhr-University Bochum

Acute stress alters the methylation of the DNA and thus the activity of certain genes. This is reported by researchers at the Ruhr-Universitt Bochum together with colleagues from Basel, Trier and London for the first time in the journal Translational Psychiatry. "The results provide evidence how stress could be related to a higher risk of mental or physical illness", says Prof. Dr. Gunther Meinlschmidt from the Clinic of Psychosomatic Medicine and Psychotherapy at the LWL University Hospital of the RUB. The team looked at gene segments which are relevant to biological stress regulation.

Epigenetics - the "second code" - regulates gene activity

Our genetic material, the DNA, provides the construction manual for the proteins that our bodies need. Which proteins a cell produces depends on the cell type and the environment. So-termed epigenetic information determines which genes are read, acting quasi as a biological switch. An example of such a switch is provided by methyl (CH3) groups that attach to specific sections of the DNA and can remain there for a long time - even when the cell divides. Previous studies have shown that stressful experiences and psychological trauma in early life are associated with long-term altered DNA methylation. Whether the DNA methylation also changes after acute psychosocial stress, was, however, previously unknown.

Two genes tested

To clarify this issue, the research group examined two genes in particular: the gene for the oxytocin receptor, i.e. the docking site for the neurotransmitter oxytocin, which has become known as the "trust hormone" or "anti-stress hormone"; and the gene for the nerve growth factor Brain-Derived Neurotrophic Factor (BDNF), which is mainly responsible for the development and cross-linking of brain cells. The researchers tested 76 people who had to participate in a fictitious job interview and solve arithmetic problems under observation - a proven means for inducing acute stress in an experiment. For the analysis of the DNA methylation, they took blood samples from the subjects before the test as well as ten and ninety minutes afterwards.

DNA methylation changes under acute psychosocial stress

Stress had no effect on the methylation of the BDNF gene. In a section of the oxytocin receptor gene, however, methylation already increased within the first ten minutes of the stressful situation. This suggests that the cells formed less oxytocin receptors. Ninety minutes after the stress test, the methylation dropped below the original level before the test. This suggests that the receptor production was excessively stimulated.

Possible link between stress and disease

Originally posted here:
Acute stress alters control of gene activity

Recommendation and review posted by Bethany Smith

ScienceDaily (Aug. 15, 2012) Acute stress alters the methylation of the DNA and thus the activity of certain genes. This is reported by researchers at the Ruhr-Universitt Bochum together with colleagues from Basel, Trier and London for the first time in the journal Translational Psychiatry. "The results provide evidence how stress could be related to a higher risk of mental or physical illness," says Prof. Dr. Gunther Meinlschmidt from the Clinic of Psychosomatic Medicine and Psychotherapy at the LWL University Hospital of the RUB. The team looked at gene segments which are relevant to biological stress regulation.

Epigenetics -- the "second code" -- regulates gene activity

Our genetic material, the DNA, provides the construction manual for the proteins that our bodies need. Which proteins a cell produces depends on the cell type and the environment. So-termed epigenetic information determines which genes are read, acting quasi as a biological switch. An example of such a switch is provided by methyl (CH3) groups that attach to specific sections of the DNA and can remain there for a long time -- even when the cell divides. Previous studies have shown that stressful experiences and psychological trauma in early life are associated with long-term altered DNA methylation. Whether the DNA methylation also changes after acute psychosocial stress, was, however, previously unknown.

Two genes tested

To clarify this issue, the research group examined two genes in particular: the gene for the oxytocin receptor, i.e. the docking site for the neurotransmitter oxytocin, which has become known as the "trust hormone" or "anti-stress hormone"; and the gene for the nerve growth factor Brain-Derived Neurotrophic Factor (BDNF), which is mainly responsible for the development and cross-linking of brain cells. The researchers tested 76 people who had to participate in a fictitious job interview and solve arithmetic problems under observation -- a proven means for inducing acute stress in an experiment. For the analysis of the DNA methylation, they took blood samples from the subjects before the test as well as ten and ninety minutes afterwards.

DNA methylation changes under acute psychosocial stress

Stress had no effect on the methylation of the BDNF gene. In a section of the oxytocin receptor gene, however, methylation already increased within the first ten minutes of the stressful situation. This suggests that the cells formed less oxytocin receptors. Ninety minutes after the stress test, the methylation dropped below the original level before the test. This suggests that the receptor production was excessively stimulated.

Possible link between stress and disease

Stress increases the risk of physical or mental illness. The stress-related costs in Germany alone amount to many billions of Euros every year. In recent years, there have been indications that epigenetic processes are involved in the development of various chronic diseases such as cancer or depression. "Epigenetic changes may well be an important link between stress and chronic diseases" says Prof. Meinlschmidt, Head of the Research Department of Psychobiology, Psychosomatics and Psychotherapy at the LWL University Hospital. "We hope to identify more complex epigenetic stress patterns in future and thus to be able to determine the associated risk of disease. This could provide information on new approaches to treatment and prevention." The work originated within the framework of an interdisciplinary research consortium with the University of Trier, the University of Basel and King's College London. The German Research Foundation and the Swiss National Science Foundation supported the study.

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Acute stress alters control of gene activity: Researchers examine DNA methylation

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By Rick Nauert PhD Senior News Editor Reviewed by John M. Grohol, Psy.D. on August 13, 2012

In a new mouse study, University of California, Davis, researchers have found that a defective gene is responsible for brain changes that lead to the disrupted social behavior that accompanies autism.

Investigators believe the discovery could lead to the development of medications to treat the condition.

Prior research had determined that the gene is defective in children with autism, but its effect on neurons in the brain was not known.

The new studies in mice show that abnormal action of just this one gene disrupted energy use in neurons. The harmful changes were coupled with antisocial and prolonged repetitive behavior traits found in autism.

The research is published in the scientific journal PLoS ONE.

A number of genes and environmental factors have been shown to be involved in autism, but this study points to a mechanism how one gene defect may trigger this type of neurological behavior, said study senior author Cecilia Giulivi, Ph.D.

Once you understand the mechanism, that opens the way for developing drugs to treat the condition, she said.

The defective gene appears to disrupt neurons use of energy, Giulivi said, the critical process that relies on the cells molecular energy factories called mitochondria.

In the research, a gene called pten was modififed in the mice so that neurons lacked the normal amount of ptens protein. The scientists detected malfunctioning mitochondria in the mice as early as 4 to 6 weeks after birth.

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Gene Related to Autism Behavior ID’d in Mice Study

Recommendation and review posted by Bethany Smith

STURGEON BAY, Wis. - Stored inside a nondescript building and greenhouse in Door County is the equivalent of much of the world's potato blueprints.

Wisconsin is home to many things, but it's safe to say that few people know the globe's largest collection of wild and cultivated potato species are here.

Most folks traveling past the Peninsular Agriculture Research Station just outside Sturgeon Bay have no idea the potato chips or French fries they gobbled at lunch were most likely developed through the efforts of the U.S. Potato Genebank. Potato germ plasm is sent from Sturgeon Bay to researchers throughout the world who are trying to figure out how to make potatoes more frost- and pest-resistant, easier to digest and even various colors.

"Part of our business is to find things, characterize them as unusual, determine if there's interest, publish and see if anyone wants to run with it," said John Bamberg, director of the gene bank.

The gene bank is a repository of thousands of seeds and cultivars collected throughout the U.S. and world over more than six decades. The oldest potato seeds at the facility, which was established by Wisconsin potato farmers in 1948, date to the early 1950s.

The Sturgeon Bay site, part of the National Plant Germplasm System preserving the genetic diversity of plants, is the only gene bank based in Wisconsin. Gene banks are scattered across the country, including facilities for rice in Arkansas, soybeans and maize in Illinois, wheat in Idaho and tomatoes in California.

The gene banks are used to acquire, preserve and evaluate plant varieties and then distribute them free to researchers. The potato facility houses about 5,000 seed populations and 1,000 clonal varieties. U.S. scientists and breeders outnumber international researchers seeking germ plasm 3 to 2. Plus horticulturists from companies such as Frito-Lay work with potato germ plasm from the gene bank.

Scientists like Shelley Jansky need access to genetic diversity to develop varieties that are resistant to pests and extreme weather. She's working on solving the problem of verticillium wilt, a common fungus in the soil. To solve the problem, potato farmers must inject chemicals in their fields before planting.

Through the potato gene bank, Jansky has found a wild species of potato from South America that's mostly immune to verticillium wilt.

"It's a tremendous resource that's right at my fingertips. I call them and say, 'Can you send me this, this and this?' and they send me seeds in the mail," said Jansky, a U.S. Department of Agriculture research scientist and associate professor of horticulture at the University of Wisconsin, Madison.

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Potato gene bank stores world's varieties

Recommendation and review posted by Bethany Smith

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

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

New Rochelle, NY, August 15, 2012Childhood Obesity, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers, has published a special issue dedicated to the role that schools can and should play in providing and encouraging healthy nutrition and good eating habits to help stem the tide of the obesity epidemic in children and adolescents. The special issue provides comprehensive coverage of food policy, systems, and programs to improve food culture, practices, and nutrition standards in the school environment, and is available free on the Childhood Obesity website at http://www.liebertpub.com/chi.

Efforts to improve school nutrition have been limited mainly "by a relative absence of evidence," says David L. Katz, MD, MPH, Editor-in-Chief of Childhood Obesity and Director of Yale University's Prevention Research Center. "Standards for school food should be set high, and our society should do what it takes to get there from here," writes Dr. Katz in his editorial.

The issue contains multiple Perspectives including an article in which authors from the U.S. Department of Agriculture (USDA), Washington, DC, advocate replacing less healthful competitive foods with healthier options without compromising food service revenues. A team comprised of authors from the Centers for Disease Control and Prevention (CDC), Atlanta, GA, Food Family Farming Foundation, Boulder, CO, United Fresh Produce Association, Washington, DC, and Whole Foods Market, Inc., Austin, TX, describes the progress to date of the LMSB2S model for introducing salad bars in schools, launched in 2010 in support of First Lady Michelle Obama's Let's Move! initiative, in the article "Let's Move Salad Bars to Schools: A Public-Private Partnership to Increase Student Fruit and Vegetable Consumption." The article "Causal Pathways Linking Farm to School to Childhood Obesity Prevention" presents a framework for developing an evidence base to support a link between Farm to School programs and prevention of childhood obesity.

In the interview entitled "Salad Bars in Schools," Rodney Taylor, Director of Nutrition Services at Riverside, CA, Unified School District, discusses how his Farm to School salad bar model is unique, offering an option to the traditional hot lunch, and has been shown to yield a sustainable improvement in health and nutritional behaviors in children.

Original research articles include "School Lunches and Lunches Brought from Home: A Comparative Analysis," in which authors from Baylor College of Medicine and The Cluthe & William B. Oliver Foundation, Houston, TX, examine differences in nutritional quality between school lunches and home-prepared lunches. "Local Wellness Policy Strength and Perceived Implementation of School Nutrition Standards across Three States," evaluating the influence of federally mandated local wellness policies on reimbursable school meals and nutritional guidelines for competitive foods, was coauthored by a team of researchers from Iowa State University (Ames), Pennsylvania State University (University Park), and University of California, Berkeley.

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This special issue of Childhood Obesity was funded by a grant from the W.K. Kellogg Foundation to ensure that the Journal is accessible as widely as possible, and to provide a framework that addresses the social and environmental conditions that influence opportunities for children to have access to healthy, affordable food and safe places to play and be physically active.

About the Journal

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School food -- on the front line in the fight against childhood obesity

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

Contact: Mary Jane Gore mary.gore@duke.edu 919-660-1309 Duke University Medical Center

DURHAM, N.C. Researchers at Duke University Medical Center may finally have discovered why people with sickle cell disease get milder cases of malaria than individuals who have normal red blood cells.

In a finding that has eluded scientists for years, Duke researchers discovered that genetic material in red blood cells may help alter parasite activity via a novel mechanism that alters parasite gene regulation.

"One of the most interesting findings in our study is that the human microRNA (very small units of genetic material) found in sickle red cells directly participate in the gene regulation of malaria parasites," said Dr. Jen-Tsan Chi, M.D., Ph.D., senior author and associate professor in the Duke Institute for Genome Sciences and Policy and Department of Molecular Genetics and Microbiology. "These microRNAs enriched in the sickle red cells reduce the parasite's ability to propagate, so that certain people stay more protected."

MicroRNAs are small units of RNA, which come from DNA. MicroRNAs are only 20-25 nucleotides long and help to regulate gene expression.

The scientists also showed that when two different microRNAs were introduced at higher levels in normal red cells, the parasite growth also was decreased.

The findings appear in the journal Cell Host and Microbe.

"This finding should lead to greater understanding of the host-parasite interaction and parasite lifecycle, which may eventually develop into a new approach to therapy for malaria, which up to 500 million people develop each year worldwide," Chi said.

Every year about 1.5 to 3 million people die from the disease, most of them children, according to the World Health Organization (WHO). Between 1,000 and 2,000 cases occur in the United States.

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Duke scientists discover genetic material in blood cells that may affect malaria parasites

Recommendation and review posted by Bethany Smith

ScienceDaily (Aug. 15, 2012) Researchers at Duke University Medical Center may finally have discovered why people with sickle cell disease get milder cases of malaria than individuals who have normal red blood cells.

In a finding that has eluded scientists for years, Duke researchers discovered that genetic material in red blood cells may help alter parasite activity via a novel mechanism that alters parasite gene regulation.

"One of the most interesting findings in our study is that the human microRNA (very small units of genetic material) found in sickle red cells directly participate in the gene regulation of malaria parasites," said Dr. Jen-Tsan Chi, M.D., Ph.D., senior author and associate professor in the Duke Institute for Genome Sciences and Policy and Department of Molecular Genetics and Microbiology. "These microRNAs enriched in the sickle red cells reduce the parasite's ability to propagate, so that certain people stay more protected."

MicroRNAs are small units of RNA, which come from DNA. MicroRNAs are only 20-25 nucleotides long and help to regulate gene expression.

The scientists also showed that when two different microRNAs were introduced at higher levels in normal red cells, the parasite growth also was decreased.

The findings appear in the journal Cell Host and Microbe.

"This finding should lead to greater understanding of the host-parasite interaction and parasite lifecycle, which may eventually develop into a new approach to therapy for malaria, which up to 500 million people develop each year worldwide," Chi said.

Every year about 1.5 to 3 million people die from the disease, most of them children, according to the World Health Organization (WHO). Between 1,000 and 2,000 cases occur in the United States.

"I think this work will expand our understanding of the interaction between the malaria parasite and its human host, given that this is a completely new mode of interaction between them, and will give us a far greater understanding of the parasite life cycle," said lead author Greg LaMonte, a scientist in the Chi laboratory.

The malaria parasites grow in the human red cells, cells that scientists thought lacked any genetic material. Many scientists had looked for the components in sickle cells that could help them resist the parasite, but the Duke researchers found one component by thinking outside of scientific norms.

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Genetic material in blood cells may affect malaria parasites

Recommendation and review posted by Bethany Smith

MANILA, Philippines Celebrity hairstylist Ricky Reyes, talent manager and host Lolit Solis, actress Lorna Tolentino and even former President Joseph Estrada are only among the prominent Filipinos who swear by the healing effects of fresh cell therapy, which involves the injection of live animal cells into the body.

Reyes, who used to suffer from a rare disease which he called reading eye epilepsy, said he went to Germany last June for fresh cell therapy.

After a number of sessions, the celebrity hairstylist can now read newspapers without suffering a seizure.

It was gone immediately, he said. Pati arthritis ko. Naalis yung sakit, tapos gaganda at babata ka pa.

Solis, 65, had fresh cell therapy after experiencing knee pain, and 75-year-old Estrada opted to undergo the procedure in Germany to keep healthy.

Before them, several other well-known figures worldwide are said to have tried fresh cell treatments, among them the late English actor Charlie Chaplin.

So how is this procedure done? Dr. Robert Janson-Muller, who runs a fresh cell therapy clinic in Germany, is in town to give Filipinos the lowdown on this decades-long treatment.

Not stem cell treatment

Before starting his lecture for members of the local media on Tuesday, Janson-Muller made it clear that fresh cell therapy is different from the now controversial stem cell treatment, which aims to replace damaged organs in the body or create one from scratch.

He stressed that his methods, which do not promise miracles, have been proven effective by his predecessors for the past 60 years.

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Fresh cell therapy promises better health, sex and more

Recommendation and review posted by simmons

Public release date: 14-Aug-2012 [ | E-mail | Share ]

Contact: Todd Kluss tkluss@geron.org 202-587-2839 The Gerontological Society of America

The Gerontological Society of America (GSA) and the National Center for Creative Aging (NCCA) have chosen Bruce L. Miller, MD, of the University of California, San Francisco (UCSF) as the 2012 recipient of the Gene D. Cohen Research Award in Creativity and Aging.

This award recognizes and honors the seminal work of Gene Cohen, MD, whose research in the field of creativity and aging shifted the conceptual focus from a problem paradigm to one of promise and potential. Cohen inspired individuals to approach longevity asking what wonders can be achieved, not in spite of age, but because of age. The award is presented annually to a professional whose research in the field of creativity and aging demonstrates these positive attributes.

The award presentation will take place at GSA's 65th Annual Scientific Meeting, which will be held from November 14 to 18 in San Diego. This conference is organized to foster interdisciplinary collaboration among researchers, educators, and practitioners who specialize in the study of the aging process. Visit http://www.geron.org/annualmeeting for further details.

Miller is a professor of neurology and psychiatry at UCSF, where he also holds the A.W. & Mary Margaret Clausen Distinguished Chair and serves as the director of the Memory and Aging Center. He is a behavioral neurologist with a special interest in brain and behavior relationships, and has focused his work in the area of dementia. He actively is involved in patient care at the UCSF clinics and hospital, and teaches extensively in the medical school.

He also is the principal investigator of the National Institutes of Health-sponsored Alzheimer's Disease Research Center, and directs a program project on frontotemporal dementia (FTD). His work with FTD has emphasized both the behavioral and emotional deficits that characterize these patients, while simultaneously noting the visual creativity that can emerge in the setting of FTD.

Miller is author of the books "The Human Frontal Lobes" and "The Behavioral Neurology of Dementia," and has extensive publications regarding dementia diagnosis and treatment. He has been featured on programs such as "The PBS NewsHour" and "Charlie Rose." For nearly three decades, Miller has been the scientific director for the philanthropic organization The John Douglas French Alzheimer's Foundation, a private philanthropic organization that funds basic science research in Alzheimer's disease. He also runs the Behavioral Neurology Fellowship at UCSF.

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The Gerontological Society of America (GSA) is the nation's oldest and largest interdisciplinary organization devoted to research, education, and practice in the field of aging. The principal mission of the Society and its 5,400+ members is to advance the study of aging and disseminate information among scientists, decision makers, and the general public. GSA's structure also includes a policy institute, the National Academy on an Aging Society, and an educational branch, the Association for Gerontology in Higher Education.

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Miller to receive 2012 Gene D. Cohen Award

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SALT LAKE CITY, Aug. 14, 2012 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) today announced results for its fourth quarter and fiscal year ending June 30, 2012. Revenue for the fourth fiscal quarter increased 24 percent over the same period in the prior year to $133.0 million and resulted in fiscal year 2012 revenue of $496.0 million, an increase of 23 percent over fiscal 2011. Fourth fiscal quarter diluted earnings per share were $0.34, an increase of 14 percent over the same period of the prior year. Fiscal 2012 diluted earnings per share equaled $1.30, an increase of 18 percent year-over-year.

"Myriad achieved record revenue and operating profits last year," said Peter D. Meldrum, President and Chief Executive Officer of Myriad Genetics, Inc. "We are committed to building on this strong performance in fiscal 2013 as we continue to execute on our strategic directives: to grow existing tests and markets, to expand internationally and to launch new tests, including companion diagnostics, across a diverse set of major disease indications."

Fourth Fiscal Quarter 2012 Results

Fiscal Year 2012 Results

Business Highlights of Fiscal Year 2012

Fiscal Year 2013 Outlook

The Company expects fiscal year 2013 total revenue of $550 million to $565 million and diluted earnings per share of $1.44 to $1.48. 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 results for the fourth fiscal quarter and fiscal year 2012 financial results.

Conference Call and Webcast

A conference call will be held on Tuesday, August 14, 2012, at 4:30 p.m. Eastern Time to discuss Myriad's financial results for the fourth fiscal quarter of 2012 and fiscal 2012. The dial-in number for domestic callers is (800) 403-7802. International callers may dial (303) 223-2680. All callers will be asked to reference reservation number 21600202. 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 will also be available through a live Webcast at http://www.myriad.com.

About Myriad Genetics

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Myriad Genetics Reports Fourth Quarter and Fiscal Year 2012 Results

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