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.

###

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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Kessler Foundation researchers present findings at September ASCIP Conference

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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

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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

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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

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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.

###

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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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

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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

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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

Recommendation and review posted by Bethany Smith

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

Recommendation and review posted by Bethany Smith

WALTHAM, Mass.--(BUSINESS WIRE)--

Interleukin Genetics,Inc. (ILIU) today announced financial and operational results for the second quarter ended June 30, 2012.

Total revenue for the three months ended June 30, 2012 was $799,000, compared to $797,000 for the same period in the prior year. Revenue in both periods is primarily attributable to sales of our Inherent Health brand of genetic tests sold through our Merchant Network and Channel Partner Agreement with Amway Global.

Research and development expenses were $317,000 for the three months ended June 30, 2012, compared to $360,000 for the same period in the prior year. The Company continues its work in its weight management and periodontal disease programs.

Selling, general, and administrative expenses were $1.2 million for the three months ended June 30, 2012, compared to $1.3 million for the same period in the prior year. The decrease was primarily attributable to lower compensation and sales commissions paid to Amway offset by increased patent related legal fees, consulting and professional fees.

The Company reported a net loss of $1.2 million, or $(0.03) per basic and diluted common share, for the second quarter of 2012 and 2011. On June 30, 2012, the Company had cash and cash equivalents of $3.8 million. On April 13, 2012, the Company drew down the remaining $1.3 million available on its credit facility with Pyxis Innovations, Inc. which becomes due on November 30, 2012. On June 29, 2012, the Company completed an equity transaction with Delta Dental of Michigan, Inc. pursuant to which Delta Dental purchased 500,000 shares of Series B Convertible Preferred Stock for gross proceeds of $3.0 million. Net proceeds to the Company after fees and expenses were $2.75 million.

The Company expects that its current and anticipated financial resources, including the $1.3 million borrowed on April 13, 2012, and the net proceeds from the Preferred Stock sale are adequate to maintain current and planned operations at least through November 30, 2012 and through January 31, 2013 if the debt is extended further than its current November 30, 2012 due date. The Companys independent registered public accounting firm has included an explanatory paragraph in their opinion in connection with the 2011 audit, relating to the Company's ability to continue as a going concern.

Our genetic testing business remains consistent, said Lewis H. Bender, Chief Executive Officer of Interleukin Genetics. We continue to advance our PST clinical utility program with Renaissance Health Service Corporation and the University of Michigan. We are excited by the first set of results received from the University of Michigan announced earlier this month. We shall work to submit a manuscript for peer-review publication and to continue to ramp up the commercialization of our PST genetic test for improved management of dental patients.

Conference Call and Webcast Information

Interleukin Genetics will host a live conference call and webcast today at 4:30 p.m. EDT to review the Companys new business developments and second quarter financial results. To access the live call, dial 877-324-1976 (domestic) or 631-291-4550 (international). The live webcast and replay access will be available on the Investors section of the Companys Website at: http://www.ilgenetics.com.

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Interleukin Genetics Reports Second Quarter 2012 Financial Results

Recommendation and review posted by Bethany Smith

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

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

West Orange, NJ. August 14, 2012. Kessler Foundation has begun testing the upgraded Ekso in individuals unable to walk due to spinal cord injury. Ekso, a wearable, battery-powered robotic exoskeletal device, has been undergoing clinical investigation at Kessler since October 2011, when the research team received the second commercial unit distributed by Ekso Bionics. Gail Forrest, PhD, assistant director of Human Performance and Engineering Research, directs Ekso research at the Foundation, in collaboration with Steven Kirshblum, MD, medical director at Kessler Institute for Rehabilitation.

The upgrade adds important functions, according to Ekso Bionics, which announced the availability of the upgraded Ekso on August 11. Until now, walking in Ekso meant being accompanied by two physical therapists, one of whom triggered each step. Now individuals can gradually progress to independent walking in Ekso by advancing through three levels that enable progressively greater user control. Of interest to researchers is another new feature called EksoPulse. EksoPulse collects usage data for each user and archives it on a secure cloud server, enabling documentation of individuals' progress.

"These upgrades have important implications for clinicians and researchers," noted Dr. Forrest. "Automating data collection and enabling greater independence during therapy are improvements that will advance the pace of our research while enabling greater progress for study participants with spinal cord injury." Data collection also helps provide the documentation necessary to prove the efficacy of Ekso therapy for insurers that reimburse for rehabilitative care.

Dr. Forrest's team also collects key data on the impact of Ekso training on physiological parameters (eg, cardiovascular, muscle activity), quality of life, and chronic pain. "Individuals with spinal cord injury face years of secondary complications, such as pain, pressure ulcers, depression, bowel and bladder dysfunction, and increased risk for cardiovascular disease," noted Dr. Forrest. "That's why we're looking beyond the abilities to stand and walk to the potential long-term effects of these activities on health and well being."

###

About Gail Forrest, PhD

Dr. Forrest conducts mobility research at Kessler Foundation, where in addition to Ekso, she studies the application of a variety of therapies including functional electrical stimulation, activity-based therapy, and the LokomatPro v6 (Hocoma), a robotic treadmill training device. Dr. Forrest is the director of the Kessler NeuroRecovery Network site, a multicenter project of the Reeve Foundation that studies the effect of intensive repetitive locomotor training on mobility in individuals with spinal cord injuries. Dr. Forrest is assistant director of Human Performance & Engineering Research, which is headed by Guang Yue, PhD. She also holds a faculty appointment at the department of physical medicine & rehabilitation at the University of Medicine & Dentistry-New Jersey Medical School in Newark, New Jersey.

About Kessler Foundation

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Kessler Foundation tests upgraded Ekso to advance study of mobility in spinal cord injury

Recommendation and review posted by sam

WINSTON-SALEM, N.C., Aug. 14, 2012 /PRNewswire/ --Tengion, Inc. (TNGN), a leader in regenerative medicine, today reported its financial results for the second quarter ended June 30, 2012 and provided a business update.

"In mid-June we announced significant progress toward delivering on critical value creating milestones for our most advanced product candidate, the Neo-Urinary Conduit, and we are pleased to announce continued advances," said John L. Miclot, President and Chief Executive Officer of Tengion. "The fifth patient is implanted in the Phase 1 clinical trial and we are actively recruiting to enroll the next two patients concurrently. We have also completed our plans to train surgeons on the surgical procedure at four additional clinical sites, allowing the subsequent three patients in this trial to be enrolled in any of the six centers. For our lead preclinical candidate, the Neo-Kidney Augment, with our GLP animal studies currently underway, we are on track to submit an IND filing for this product candidate during the first half of 2013. We are diligently focused on executing on these clinical goals and look forward to updating you on our progress."

Neo-Urinary Conduit Clinical Program UpdateTengion has implanted five patients in the ongoing Phase 1 clinical trial of its most advanced product candidate, the Neo-Urinary Conduit, for use in bladder cancer patients requiring a urinary diversion following bladder removal (cystectomy). The trial is designed to translate the surgical procedure successfully used in preclinical animal models into clinical trials with human patients while assessing the safety and preliminary efficacy of the Neo-Urinary Conduit. The trial is an open-label, single-arm study, which is currently expected to enroll up to ten patients.

Following a positive meeting with the Data Safety Monitoring Board (DSMB), the Company is now actively recruiting in order to proceed with concurrent enrollment of patients six and seven as soon as possible. Assuming appropriate safety data, the Company anticipates commencement of efforts to enroll an additional three patients approximately six weeks after implant of patients six and seven, thereby allowing the Company to achieve its stated objective of completing implantation of up to 10 patients by the end of 2012.

The trial is currently being conducted at the University of Chicago Medical Center and at The Johns Hopkins Hospital in Baltimore, Maryland. In addition to the two original trial sites, the trial has been expanded to include four additional centers for patients seven through ten. The additional trial sites are Memorial Sloan-Kettering Cancer Center in New York, NY; Baylor College of Medicine, Houston, Texas; University of Michigan Comprehensive Cancer Center in Ann Arbor, MI; and a fourth site in Boston, MA.

Neo-Kidney Augment Preclinical Program UpdateTengion's lead preclinical program, the Neo-Kidney Augment, is intended to prevent or delay the need for dialysis or kidney transplant by catalyzing the regeneration of functional kidney tissue in patients with advanced chronic kidney disease (CKD). Tengion scientists have published and presented positive data on the effect of the Company's Neo-Kidney Augment in four different preclinical models of CKD.

Tengion has commenced the good laboratory practice (GLP) animal study program required by the U.S. Food and Drug Administration (FDA) to support an Investigational New Drug (IND) filing and initiation of a Phase 1 clinical trial in CKD patients. These GLP studies are consistent with the preclinical animal models already conducted by Tengion, which yielded positive data demonstrating slowing of kidney disease progression and improved survival.

Tengion anticipates that it will submit an IND filing for the Neo-Kidney Augment during the first half of 2013 and that its Phase 1 trial will provide initial human proof-of-concept data in 2014. Tengion is also exploring an entry strategy in Europe for its Neo-Kidney Augment product candidate using the Advanced Therapy Medicinal Products (ATMP) pathway, an established regulatory route in Europe for advanced cell-based therapies. Tengion plans to define the European regulatory pathway for Neo-Kidney Augment program in the second half of 2012.

Financial UpdateFor the six months ended June 30, 2012, the Company reported an adjusted net loss of $8.9 million, or $3.74 per basic and diluted common share, compared to an adjusted net loss of $13.1 million, or $6.79 per basic and diluted common share, for the same period in 2011. The decreased adjusted net loss for the 2012 period was primarily due to a reduction in compensation and related expenses of $2.5 million and a decrease in depreciation expense of $1.8 million.

The decreased compensation-related expenses during the 2012 period, of which $1.2 million were attributable to research and development personnel and $1.3 million were attributable to general and administrative personnel, were primarily due to lower headcount resulting from the Company's November 2011 restructuring. The decreased depreciation expense during the 2012 period resulted from both a change during the second quarter of 2011 in the estimated useful life of leasehold improvements at the Company's leased facility in Winston-Salem, North Carolina and an impairment during the fourth quarter of 2011 of the carrying value of the Company's leased facility in East Norriton, Pennsylvania.

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Tengion Reports Second Quarter 2012 Financial Results

Recommendation and review posted by sam

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 Bethany Smith

Public release date: 13-Aug-2012 [ | E-mail | Share ]

Contact: Kimberly Newman sciencenews@einstein.yu.edu 718-430-3101 Albert Einstein College of Medicine

August 13, 2012 (BRONX, NY) Scientists at Albert Einstein College of Medicine of Yeshiva University have made a discovery involving mice and humans that could mean that people with acute myeloid leukemia (AML), a rare and usually fatal cancer, are a step closer to new treatment options. Their study results were published online today in Cancer Cell.

"We have discovered that a gene called HLX is expressed at abnormally high levels in leukemia stem cells in a mouse model of AML," said Ulrich Steidl, M.D., Ph.D., assistant professor of cell biology and of medicine at Einstein and senior author of the paper. (Gene expression is the process by which a gene synthesizes the molecule that it codes for; an "over-expressed" gene makes its product in abnormally high amounts.)

According to the National Cancer Institute, AML will be diagnosed in one of every 254 people during their lifetime. Most die within a few years of diagnosis. For the last several decades there has been little improvement in the survival rate for AML patients.

Dr. Steidl and his colleagues found that over-expression of the HLX gene in mice caused blood-forming stem cells to become dysfunctional and develop into abnormal progenitors (biological ancestors) of white blood cells that failed to differentiate into normal blood cells. Instead, those early, abnormal white cells formed duplicates of themselves.

The researchers then analyzed HLX expression data collected from 354 AML patients and found that 87 percent of them were over-expressing HLX compared with HLX expression in healthy individuals. And among patients expressing HLX at high levels in an even larger cohort of 601 patients: the greater their degree of HLX expression, the worse their survival chances.

Importantly, when Dr. Steidl's team used a laboratory technique to "knock down" HLX expression in AML cells taken from a mouse model of AML and from AML patients, proliferation of leukemia cells was greatly suppressed in both cases. And when the researchers knocked down HLX expression in mouse AML cells and human AML cells and then transplanted both types of cancer cells into healthy mice, those mice lived significantly longer compared with mice that received unaltered AML cells.

These findings suggest that targeting elevated HLX expression may be a promising novel strategy for treating AML.

"HLX is clearly a key factor in causing the over-production of white cells that occurs in AML," said Dr. Steidl. "Our research is still in its early stages, but we're looking towards developing drugsso we can improve treatment for AML and possibly other types of cancer." Einstein has filed a patent application related to this research. The HLX technology is available for licensing.

Link:
Gene discovery could improve treatment for acute myeloid leukemia

Recommendation and review posted by Bethany Smith

ScienceDaily (Aug. 14, 2012) Two papers that will appear in the journal Molecular Psychiatry, both receiving advance online release, may help identify gene variants that contribute to the risks of developing obsessive-compulsive disorder (OCD) or Tourette syndrome (TS). Both multi-institutional studies were led by Massachusetts General Hospital (MGH) investigators, and both are the first genome-wide association studies (GWAS) in the largest groups of individuals affected by the conditions.

"Previous studies of these disorders have demonstrated that both TS and OCD are strongly heritable and may have shared genetic risk factors, but identification of specific genes has been a huge challenge," says Jeremiah Scharf, MD, PhD, of the Psychiatric and Neurodevelopmental Genetics Unit (PNGU) in the MGH Departments of Psychiatry and Neurology, a co-lead author of both papers and co-chair of the Tourette Syndrome Association International Consortium for Genetics. "These new studies represent major steps towards understanding the underlying genetic architecture of these disorders."

An anxiety disorder characterized by obsessions and compulsions that disrupt patients' lives, obsessive-compulsive disorder (OCD) is the fourth most common psychiatric illness. Tourette syndrome, a chronic disorder characterized by motor and vocal tics, usually begins in childhood and is often accompanied by conditions like OCD or attention-deficit hyperactivity disorder. Both conditions have a high risk of recurrence in close relatives of affected individuals, but previous studies that compared affected and unaffected individuals were not large enough to identify specific genes or areas of the genome that contribute to risk.

Since many gene variants probably contribute to risk for both conditions, the research teams undertook GWAS investigations, which analyze hundreds of thousands of gene variants called SNPs (single-nucleotide polymorphisms) in thousands of individuals with and without the condition of interest. The International OCD Foundation Genetic Collaborative, consisting of more than 20 research groups in nine countries, analyzed almost 480,000 SNPs in 1,465 individuals with OCD, more than 5,500 controls and from 400 trio samples consisting of an OCD patient and both parents. The Tourette Syndrome Association International Consortium for Genetics and the TS GWAS Consortium, representing 22 groups across seven countries, analyzed 484,000 SNPs across almost 1,500 cases and more than 5,200 controls.

The OCD study -- led by Evelyn Stewart, MD, of the MGH-PNGU, who is now based at the University of British Columbia, and David Pauls, PhD, MGH-PNGU -- identified possible associations close to a gene called BTBD3, which is closely related to a gene that may be involved in Tourette Syndrome, and within DLGAP1, a close relative of a gene that produces OCD-like symptoms in mice if it is deleted. The Tourette study was led by Scharf and Pauls and found evidence of a possible association with a gene called COL27A1, which may be expressed in the cerebellum during development, and with variants that help regulate gene expression in the frontal cortex.

None of these or other identified SNPs reached the high threshold of genome-wide significance, which would indicate that the associations represented true risk factors, and the authors stress that additional, larger studies are required. "Although GWAS analysis allows much more comprehensive examination of the entire genome than do studies focused on particular families or candidate genes, these two studies are still underpowered and should be interpreted with caution," says Pauls, a co-senior author of both papers. "The current results are interesting and provide us with a starting point for analyzing future studies that must be done to replicate and extend these findings."

Scharf adds that the next steps should include testing the SNPs identified by these studies in other groups of patients and controls, analyzing both study groups together to identify genes that contribute to the risk of both disorders, and expanding international collaborations to increase the size and power of patient samples for both OCD and TS. "If future studies confirm that some of these variants do contribute to risk -- either directly or by altering the function of other risk genes -- that would suggest both novel disease mechanisms and might give us new treatment targets," he says.

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Gene variants that increase risk of obsessive-compulsive disorder and Tourette syndrome identified

Recommendation and review posted by Bethany Smith

RESEARCH TRIANGLE PARK, N.C.--(BUSINESS WIRE)--

To help biopharmaceutical companies dramatically improve drug development productivity and deliver greater value, Quintiles today announced the acquisition of Expression Analysis, Inc. (EA), a premier provider of genomics testing and analysis to biopharma, academic, government and non-profit customers.

Terms of the transaction were not disclosed. This is the latest in a series of acquisitions and alliances designed to help Quintiles customers leverage the power of genomics to better understand diseases; develop diagnostic tools; and deliver safer, more effective therapies based on the genetic makeup of the disease and the patient.

The addition of EAs Genomic Know-How to Quintiles is another step forward in our efforts to bring personalized medicine into mainstream drug development, said Thomas Wollman, Senior Vice President, Quintiles Global Laboratories. Its expertise in genetic sequencing and advanced bioinformatics is essential to understanding diseases and drugs at the molecular level. Thats a huge step in creating more value across the healthcare spectrum.

EA has about 77 employees, most based in its offices near Research Triangle Park.

Steve McPhail, EA President and Chief Executive Officer, said: The combination of Quintiles Global Laboratories and EA genomic technology excellence will facilitate worldwide access to resources and expertise to drive improvements in the diagnosis, treatment and management of complex disease. EA can now play a global role in helping biopharma succeed in the New Health.

This is the right move for our company and our employees. Our mission perfectly fits Quintiles strategy to use genomic data and advanced informatics to yield actionable insights and more effective personalized treatments.

EA provides whole genome to focused-set gene expression and genotyping assays, along with next-generation sequencing services, sequence enrichment technologies and bioinformatics support. It offers a broad range of services across multiple platforms. Its quality system follows CLSI guidelines and its CLIA-registered laboratory supports GLP compliance.

Quintiles Global Laboratories supports trials worldwide with wholly owned facilities in the U.S., Europe, South Africa, India, China, Singapore and Japan, and a tightly coordinated network of affiliate laboratories in Argentina and Brazil. All Quintiles laboratories operate with uniform instrumentation and standard operating procedures, delivering high quality, harmonized data.

About Quintiles

The rest is here:
Quintiles Acquires Expression Analysis, Premier Provider of Genomics Services, to Advance Personalized Medicine

Recommendation and review posted by Bethany Smith

LOS ANGELES, Aug. 14, 2012 /PRNewswire/ -- Response Genetics, Inc. (RGDX), a company focused on the development and sale of molecular diagnostic tests for helping determine a patient's response to cancer therapy, today announced its consolidated financial results for the second quarter ended June 30, 2012.

Total revenues for the quarter ended June 30, 2012 were $3.84 million, compared to $3.98 million for the quarter ended March 31, 2012 and $6.70 million for the quarter ended June 30, 2011. The decrease relative to last year was largely a result of the expected decrease in pharmaceutical client revenue. The Company's ResponseDX revenue decreased slightly by $151 thousand and the pharmaceutical client revenue decreased by $2.72 million relative to the quarter ended June 30, 2011.

The Company's net loss for the quarter ended June 30, 2012 was $2.7 million compared to a net loss of $3.1 million for the quarter ended March 31, 2012 and a net loss of $0.1 million for the quarter ended June 30, 2011. This is the second consecutive quarter the Company decreased its net loss.

The Company also increased its gross margin in two consecutive quarters from approximately 25% for the fourth quarter of 2011, to approximately 32% for the quarter ended March 31, 2012 to approximately 37% for the quarter ended June 30, 2012. Gross margin is defined as net revenue less cost of revenue.

Excluding cost of revenue, total operating expenses for the second quarter were $4.1 million, compared to $4.4 million for the quarter ended March 31, 2012 and $4.0 million for the same period last year.

"We have made many changes in the Company since the beginning of the year and we believe we have made great strides, both financially and strategically. Since the fourth quarter of 2011, gross margins have increased, expenses have been reduced, and losses have subsequently decreased," said Thomas Bologna, the Company's Chairman & Chief Executive Officer. "Additionally, we expect our third quarter operating results to continue this favorable trend, and in fact, we believe the results will be better based on additional actions that we have taken since the end of the second quarter."

Mr. Bologna added, "We appreciate that we need to work the top line as well and as noted in our recent Form 8-K, we are pleased to have extended/replaced our existing Amended and Restated Master Services Agreement with GlaxoSmithKline Biologicals S.A. (GSK), which expired on May 15, 2012. The Second Amended and Restated Master Services Agreement enables us to continue to provide services to GSK for up to an additional two and a half years and to continue to derive revenues from those services. We are also pleased to report that we recently achieved a milestone under our existing Non-Exclusive License Agreement with GSK, dated March 10, 2010, which has resulted in us receiving a $500,000 milestone payment last week."

Total revenues for the six months ended June 30, 2012 were $7.8 million compared to $12.6 million for the six months ended June 30, 2011, the decrease largely a result of the expected decrease in pharmaceutical client revenue of $4.5 million from $6.5 million for the six months ended June 30, 2011 to $2.0 million for the six months ended June 30, 2012. The Company's ResponseDX revenue was $5.8 million for the six months ended June 30, 2012, compared to $6.1 million for the six months ended June 30, 2011.

The Company's net loss for the six months ended June 30, 2012 was $5.9 million, compared with a net loss of $0.4 million for the six months ended June 30, 2011.

Excluding cost of revenue, total operating expenses for the six months were $8.5 million, compared to $7.5 million for the same period last year. The increase in total operating expense of $1.0 million was due to an increase in general and administrative expenses of $0.1 million and an increase in research and development expenses of $0.9 million.

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Response Genetics, Inc. Announces Second Quarter Financial Results

Recommendation and review posted by Bethany Smith

AMES, Iowa, Aug. 14, 2012 (GLOBE NEWSWIRE) -- NewLink Genetics Corporation (NLNK), a biopharmaceutical company focused on discovering, developing and commercializing cancer therapeutics, today reported consolidated financial results for the second quarter of 2012, and provided an update on the progress of its clinical development programs.

"Data from the Phase 2 study of our HyperAcute pancreatic cancer immunotherapy was successfully presented at two major conferences and continues to support our Phase 3 study design," commented Dr. Charles Link, Chairman and Chief Executive Officer of NewLink. "We are well past the halfway point in our pivotal trial in pancreatic cancer and we expect to reach the triggering point for our first interm analysis in the first quarter of 2013 and to complete patient enrollment in 2013."

Dr. Nicholas Vahanian NewLink's President and Chief Medical Officer added; "Recent positive data from Phase 2 studies in three different HyperAcute cancer immunotherapies have given us confidence to move forward aggressively in the clinical development of multiple therapies derived from this platform."

The second quarter 2012 Financial Results

Financial Guidance

NewLink is maintaining its financial guidance and continues to expect to end 2012 with about $20 million in cash, cash equivalents and marketable securities.

Recap of Data From Phase-2 HyperAcute(R) Pancreas (algenpantucel-L) Immunotherapy Trial:

Treated patients demonstrated statistically significant improvement in 12-month disease free survival and there was a strong suggestion of improvements in 12 month overall survival (OS) (observed 86% v. predicted 63% indicating a 37% improvement). Kaplan-Meier analysis suggests the improvement in OS increases over time with the 2-year and 3-year observed survival rates of 51% and 42% suggesting relative improvement of 59% and 121% in comparison to expected survival of 32% and 19% predicted by nomogram analysis.

Upcoming Activities

NewLink expects to present at the following investor conferences:

Link:
NewLink Genetics Corporation Reports Second Quarter 2012 Financial Results

Recommendation and review posted by Bethany Smith

CLEARWATER, FL--(Marketwire -08/13/12)- Biostem U.S., Corporation (HAIR) (HAIR) (Biostem, the Company) is a fully reporting public company in the stem cell regenerative medicine sciences sector. President, John Satino announced today that the Pizarro Hair Restoration Clinic in Orlando, Florida is now equipped and ready to begin offering The Biostem Method of hair re-growth using the patient's own adult cells in a minimally invasive, painless procedure. In addition, Biostem Medical Director and Trainer, Dr. Marina Pizarro is ready to offer onsite training to new Biostem affiliates.

According to Satino, "This week, Dr. Pizarro treated her first two patients using The Biostem Method of hair re-growth in her Orlando office. This paves the way for Biostem to start offering affiliate agreements throughout the country in response to the many inquiries from physicians who want to offer this transplant alternative to their patients. We are making plans to open affiliate offices in major cities soon, after which we will expand the services to rural and international locations focusing first on Europe and Asia."

As a side note, Satino stated that, "While the industry typically sees more males requesting hair transplant for hair re-growth solutions, it is interesting that the first two treatments Dr. Pizarro performed were on women. Statistics do show that women suffer hair loss in significant numbers, yet are less likely to go through the transplant procedure. The Biostem Method finally offers women as well as men, a viable and proven alternative."

About Biostem U.S. Corporation Biostem U.S., Corporation (HAIR) is a fully reporting Nevada corporation with offices in Clearwater, Florida. Biostem U.S. is a technology licensing company with proprietary technology centered on providing hair re-growth using human stem cells. The company also intends to train and license selected physicians to provide Regenerative Cellular Therapy treatments to assist the body's natural approach to healing tendons, ligaments, joints and muscle injuries by using the patient's own stem cells. Biostem U.S. is seeking to expand its operations worldwide through licensing of its proprietary technology and acquisition of existing stem cell related facilities. The company's goal is to operate in the international biotech market, focusing on the rapidly growing regenerative medicine field, using ethically sourced adult stem cells to improve the quality and longevity of life for all mankind.

The company's Board of Directors is headed by Chairman, Scott Crutchfield, who also acts as Senior Vice President of World Wide Operations for Crocs, Inc. (CROX) and includes Crocs, Inc. original member, Steve Beck.

More information on Biostem U.S., Corporation can be obtained through http://www.biostemus.com or by contacting Fox Communications Group at 310-974-6821.

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Gene mutation responsible of inherited ataxia found through sophisticated genetic analysis of Asian, European & American families

Newswise ANN ARBOR, Mich. A global hunt for the cause of a crippling inherited nerve disorder has found its target. The discovery opens the door for better diagnosis and treatment of this particular disease but also for better understanding of why nerves in the brains movement-controlling center die, and how new DNA-mapping techniques can find the causes of other diseases that run in families.

In a new paper in the Annals of Neurology, a team from Taiwan, France and the University of Michigan Health System report that mutations in the gene KCND3 were found in six families in Asia, Europe and the United States that have been haunted by the same form of a disease called spinocerebellar ataxia or SCA. The disease causes progressive loss of balance, muscle control and ability to walk.

The new paper finds the disease gene in a region of chromosome 1 where a Dutch group had previously shown linkage with a form of SCA called SCA19, and the Taiwanese group on the new paper had shown similar linkage in a family for a form of the disease that was then called SCA22.

The Dutch group has just published results in the same issue of the journal, zeroing in on the same gene as the U-M/Taiwanese/French groups.

The gene governs the production of a protein that allows nerve cells to talk to one another through the flow of potassium. Pinpointing its role as a cause of ataxia will now allow more people with ataxia to learn the exact cause of their disease, give a very specific target for new treatments, and perhaps allow the families to stop the disease from affecting future generations.

But the findings also have significance beyond ataxia. The researchers also show that when KCND3 is mutated, it causes not only poor communication between nerve cells in the cerebellum but also the death of those cells. Its information that could aid research on other neurological disorders involving balance and movement.

Margit Burmeister, Ph.D., the U-M geneticist who helped lead the work, notes that the gene could not have been found without a great deal of DNA detective work and the cooperation of the families who volunteered to let researchers map all the DNA of multiple members of their family tree.

We combined traditional genetic linkage analysis in families with inherited diseases with whole exome sequencing of an individuals DNA, allowing us to narrow down and ultimately identify the mutation, she says. This new type of approach has already resulted in many new gene identifications, and will bring in many more.

U-M neurologist Vikram Shakkottai, M.D., Ph.D., an ataxia specialist and co-author on the paper, notes that the new genetic information will help patients find out the specific cause of their disease a reassuring thing in itself.

Read more:
Three Continents, One Gene: DNA Detectives Track Down Nerve Disorder Cause

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