Archive for the ‘Gene Therapy Research’ Category

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

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

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

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

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

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

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

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.

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Gene discovery could improve treatment for acute myeloid leukemia

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

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

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Quintiles Acquires Expression Analysis, Premier Provider of Genomics Services, to Advance Personalized Medicine

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

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:

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NewLink Genetics Corporation Reports Second Quarter 2012 Financial Results

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.

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

Public release date: 13-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 13, 2012Even after being frozen for 18 years, human embryos can be thawed, grown in the laboratory, and successfully induced to produce human embryonic stem (ES) cells, which represent a valuable resource for drug screening and medical research. Prolonged embryonic cryopreservation as an alternative source of ES cells is the focus of an article in BioResearch Open Access, a new bimonthly peer-reviewed open access journal from Mary Ann Liebert, Inc. The article is available free online at the BioResearch Open Access website.

Kamthorn Pruksananonda and coauthors from Chulalongkorn University and Chulalongkorn Memorial Hospital, Bangkok, Thailand, demonstrated that ES cells derived from frozen embryos have a similar ability to differentiate into multiple cell typesa characteristic known as pluripotencyas do ES cells derived from fresh embryos. They present their findings in the article "Eighteen-Year Cryopreservation Does Not Negatively Affect the Pluripotency of Human Embryos: Evidence from Embryonic Stem Cell Derivation."

"The importance of this study is that it identifies an alternative source for generating new embryonic stem lines, using embryos that have been in long-term storage," says Editor-in-Chief Jane Taylor, PhD, MRC Centre for Regenerative Medicine, University of Edinburgh, Scotland.

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About the Journal

BioResearch Open Access is a bimonthly peer-reviewed open access journal that provides a new rapid-publication forum for a broad range of scientific topics including molecular and cellular biology, tissue engineering and biomaterials, bioengineering, regenerative medicine, stem cells, gene therapy, systems biology, genetics, biochemistry, virology, microbiology, and neuroscience. All articles are published within 4 weeks of acceptance and are fully open access and posted on PubMedCentral. All journal content is available online at the BioResearch Open Access website.

About the Publisher

Mary Ann Liebert, Inc., is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Tissue Engineering, Stem Cells and Development, Human Gene Therapy and HGT Methods, and AIDS Research and Human Retroviruses. 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. website.

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Human embryos frozen for 18 years yield viable stem cells suitable for biomedical research

ScienceDaily (Aug. 10, 2012) Duke researchers may have found a promising stem cell therapy for preventing osteoarthritis after a joint injury.

Injuring a joint greatly raises the odds of getting a form of osteoarthritis called post-traumatic arthritis, or PTA. There are no therapies yet that modify or slow the progression of arthritis after injury.

Researchers at Duke University Health System have found a very promising therapeutic approach to PTA using a type of stem cell, called mesenchymal stem cells (MSCs), in mice with fractures that typically would lead to them developing arthritis. Their findings could lead to a therapy that would be used after joint injury and before signs of significant osteoarthritis.

The scientists thought the stem cells would work to prevent PTA by altering the balance of inflammation and regeneration in knee joints, because these stem cells have beneficial properties in other regions of the body.

"The stem cells were able to prevent post-traumatic arthritis," said Farshid Guilak, Ph.D., director of orthopaedic research at Duke and senior author of the study.

The study was published on August 10 in Cell Transplantation.

The researchers also thought that a type of mice bred for their super-healing properties would probably fare better than typical mice, but they were wrong.

"We decided to investigate two therapies for the study, said lead author Brian Diekman, Ph.D., a postdoctoral researcher in the Guilak lab. "We thought that stem cells from so-called superhealer mice would be superior at providing protection, and instead, we found that they were no better than stem cells from typical mice. We thought that maybe it would take stem cells from superhealers to gain an effect as strong as preventing arthritis after a fracture, but we were surprised -- and excited -- to learn that regular stem cells work just as well."

Certain people appear to fall into the superhealer category, too. They bounce back quickly and heal well naturally after a fracture, while other people eventually form cases of arthritis at the fractured joint, said Guilak, who is a professor of orthopaedic surgery and biomedical engineering.

"The ability of the superhealer mice to have superior healing after a fracture may go beyond the properties of their stem cells and be some beneficial factor, like a growth factor, that we don't know about yet," Guilak said.

Link:
Stem cells may prevent post-injury arthritis

ScienceDaily (Aug. 12, 2012) Genetics researchers have identified a key gene that, when mutated, causes the rare multisystem disorder Cornelia deLange syndrome (CdLS). By revealing how mutations in the HDAC8 gene disrupt the biology of proteins that control both gene expression and cell division, the research sheds light on this disease, which causes intellectual disability, limb deformations and other disabilities resulting from impairments in early development.

"As we better understand how CdLS operates at the level of cell biology, we will be better able to define strategies for devising treatments for CdLS, and possibly for related disorders," said study leader Matthew A. Deardorff, M.D., Ph.D., a pediatric genetics clinician and scientist at The Children's Hospital of Philadelphia. Deardorff also is in the Perelman School of Medicine at the University of Pennsylvania.

Deardorff and co-corresponding author Katsuhiko Shirahige, Ph.D., of the Research Center for Epigenetic Disease at the University of Tokyo, published their study online August 12 in Nature.

The current findings add to previous discoveries by researchers at The Children's Hospital of Philadelphia. A group led by Ian Krantz, M.D., and Laird Jackson, M.D., announced in 2004 that mutations in the NIPBL gene are the primary cause of CdLS, accounting for roughly 60 percent of the "classical" cases of the disease. In 2007, Deardorff joined them to describe mutations in two additional genes, SMC1A and SMC3. First described in 1933, CdLS affects an estimated 1 in 10,000 children.

The CdLS research team at Children's Hospital has focused on the cohesin complex, a group of proteins that form a bracelet-like structure that encircles pairs of chromosomes, called sister chromatids. "Cohesin has two roles," said Deardorff. "It keeps sister chromatids together during cell division, and it allows normal transcription -- the transmission of information from DNA to RNA."

Deardorff added that mutations that perturb normal cohesin function can interfere with normal human development. Such is the case in CdLS, which exemplifies a newly recognized class of diseases called cohesinopathies.

In the current study, the scientists investigated both acetylation -- how an acetyl molecule is attached to part of the cohesin complex -- and deactylation, the removal of that molecule. Normally, deactylation helps recycle cohesin to make it available during successive rounds of cell division. The study team found that mutations in the HDAC8 gene threw off normal cellular recycling of cohesin.

Mutations in the gene cause loss of HDAC8 protein activity, and consequently decrease the amount of "recharged" cohesin available to properly regulate gene transcription. This, in turn, the researchers suggest, impairs normal embryonic development and gives rise to CdLS.

The researchers showed in cell cultures that mutations in HDAC8 lead to a decrease in cohesin binding to genes, similar to that seen for cells deficient in the NIPBL gene. They also identified HDAC8 mutations in approximately 5 percent of patients with CdLS.

Because mothers of children with CdLS may carry mutations in the HDAC8 gene, identifying these mutations will be very useful in accurately counseling families of their recurrence risk -- the likelihood of having a subsequent child with CdLS.

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Mutations disrupt cellular recycling, cause a childhood genetic disease

Public release date: 12-Aug-2012 [ | E-mail | Share ]

Contact: John Ascenzi ascenzi@email.chop.edu 267-426-6055 Children's Hospital of Philadelphia

Genetics researchers have identified a key gene that, when mutated, causes the rare multisystem disorder Cornelia deLange syndrome (CdLS). By revealing how mutations in the HDAC8 gene disrupt the biology of proteins that control both gene expression and cell division, the research sheds light on this disease, which causes intellectual disability, limb deformations and other disabilities resulting from impairments in early development.

"As we better understand how CdLS operates at the level of cell biology, we will be better able to define strategies for devising treatments for CdLS, and possibly for related disorders," said study leader Matthew A. Deardorff, M.D., Ph.D., a pediatric genetics clinician and scientist at The Children's Hospital of Philadelphia. Deardorff also is in the Perelman School of Medicine at the University of Pennsylvania.

Deardorff and co-corresponding author Katsuhiko Shirahige, Ph.D., of the Research Center for Epigenetic Disease at the University of Tokyo, published their study online today in Nature.

The current findings add to previous discoveries by researchers at The Children's Hospital of Philadelphia. A group led by Ian Krantz, M.D., and Laird Jackson, M.D., announced in 2004 that mutations in the NIPBL gene are the primary cause of CdLS, accounting for roughly 60 percent of the "classical" cases of the disease. In 2007, Deardorff joined them to describe mutations in two additional genes, SMC1A and SMC3. First described in 1933, CdLS affects an estimated 1 in 10,000 children.

The CdLS research team at Children's Hospital has focused on the cohesin complex, a group of proteins that form a bracelet-like structure that encircles pairs of chromosomes, called sister chromatids. "Cohesin has two roles," said Deardorff. "It keeps sister chromatids together during cell division, and it allows normal transcriptionthe transmission of information from DNA to RNA."

Deardorff added that mutations that perturb normal cohesin function can interfere with normal human development. Such is the case in CdLS, which exemplifies a newly recognized class of diseases called cohesinopathies.

In the current study, the scientists investigated both acetylationhow an acetyl molecule is attached to part of the cohesin complexand deactylation, the removal of that molecule. Normally, deactylation helps recycle cohesin to make it available during successive rounds of cell division. The study team found that mutations in the HDAC8 gene threw off normal cellular recycling of cohesin.

Mutations in the gene cause loss of HDAC8 protein activity, and consequently decrease the amount of "recharged" cohesin available to properly regulate gene transcription. This, in turn, the researchers suggest, impairs normal embryonic development and gives rise to CdLS.

View post:
Mutations disrupt cellular recycling and cause a childhood genetic disease

The Korea Herald/Asia News Network Friday, Aug 10, 2012

South Korea - A local team of scientists has discovered genes closely involved in regulating feeding behaviour, opening new possibilities for treating obesity and metabolic disorders.

Led by Yu Kweon, principal researcher at Korea Research Institute of Bioscience and Biotechnology's Aging Research Center, the team found that the fruit fly gene minibrain, or mnb, and mammalian functional equivalent DYRK1a gene control the expression of neuropeptides - proteins that transmit signals from nerve cells - involved in food intake regulation.

The results were published in the August issue of the peer-review journal PLoS Genetics.

In fruit flies, the mnb gene controls the expression of short neuropeptide F, or sNPF, while DYRK1a controls that of neuropeptide Y, or NPY.

Yu's research showed that the fruit fly and mammalian genes stimulate the production of the relevant proteins.

In the experiments, fruit flies with artificially enhanced mnb gene expression had 60 per cent larger daily food intake than control insects. In contrast, the food intake of flies with reduced mnb gene expression was about 30 per cent lower than those with normal levels of gene expression.

Similar results were also obtained in mice, with subjects with enhanced DYRK1a gene expression eating 20 per cent more.

In addition, Yu found that while DYRK1a acts in a positive feedback loop where NPY expression is increased with the rise in DYRK1a expression, the same process is dampened by insulin, the lack of which is the cause of Type 1 diabetes.

Although the involvement of sNPF and neuropeptide Y in food intake control has been known for some time, Yu and his team were the first to discover that the food intake-related genes are controlled by other genes.

Excerpt from:
Korean scientists find key gene in eating behavior

BAR HARBOR Advances in genetic medicine are proceeding at such a rapid clip that solutions to some of humanitys most intractable medical problems could be present within the decade, Jackson Laboratory President and CEO Edison Liu, M.D. said Monday. Dr. Liu was speaking before a crowd of 150 gathered at the Bar Harbor Club for the annual meeting of the Mount Desert Island Hospital.

If we can push the envelope, we will cure cancer by the year 2020, Dr. Liu said in his keynote address. If Jackson Lab, on the little island on MDI, can win the Nobel Prize, we can beat breast cancer.

Advances in technology and in knowledge of the human genome have risen so much in the past decade that what we imagined just a few years ago is now reality, Dr. Liu said.

Today, we have high-resolution understanding of your genetics and your genome. We dont have to guess anymore, he said. We havent seen anything like this since the development of the motherboard in electronics.

In typical cancer treatment, a 30 percent response rate is considered a good outcome. But, with the growing ability to tailor drugs to each individual, the field of personalized medicine now promises the ability to increase that rate greatly, if not eliminate mortality from the disease altogether.

Link:
Cancer Cure Close, Liu Says

Copyright 2012 National Public Radio. For personal, noncommercial use only. See Terms of Use. For other uses, prior permission required.

IRA FLATOW, HOST:

This is SCIENCE FRIDAY, I'm Ira Flatow. Earlier this week, yet another potential cure for Alzheimer's failed. Pfizer called off additional studies of its intravenous drug bapineuzumab, an antibody designed to seek and destroy plaques that build up in the brains of people with Alzheimer's.

The thinking was that if you clear the plaques, maybe the dementia will improve or go away. Unfortunately, the drug did not seem to do that. But it's not the only possibility. Researchers are testing other types of antibodies. They're testing hormones. They're trying gene therapy. What are the chances that these approaches will pan out? Might we see an Alzheimer's vaccine someday? That's what we're going to be talking about, a status check on Alzheimer's research.

Our number is 1-800-989-8255. You can tweet us @scifri, and you can also go to our website at sciencefriday.com.

Dr. Ronald Petersen is director of the Mayo Alzheimer's Disease Research Center at the Mayo Clinic in Rochester, Minnesota. Welcome to SCIENCE FRIDAY, Dr. Petersen.

RONALD PETERSEN: Thanks very much, Ira.

FLATOW: First give us a little inside baseball on what happened with the Pfizer drug. Did it not clear the plaques? Do we know? Do we know why it failed?

PETERSEN: Well, it was a preliminary report regarding the clinical findings, meaning that the memory, the functional changes in these patients with the mild to moderate state of the dementia of Alzheimer's disease, the clinical features did not improve.

What we don't know yet, they haven't announced yet, is whether the drug actually had an impact on the underlying biological process. So there was no clinical improvement, but we're still waiting for data on the biological signal. Did the antibody do what it was supposed to do in the brain?

Read more from the original source:
Attacking Alzheimer's With Antibodies, Hormones

Actress Rachel Weisz interviewed researchers to develop her scientist role in The Bourne Legacy. Image courtesy Universal Pictures

In The Bourne Legacy, Jeremy Renner plays Aaron Cross, a superspy whos been pharmaceutically tweaked to jump higher, think faster, punch harder, hear better and tolerate extreme cold. The surprising thing is, this type of gene-doped warrior is not a total figment of filmmaker Tony Gilroys imagination.

Filmmaker Tony Gilroy researched viral delivery systems while scripting The Bourne Legacy. Image courtesy Universal Pictures

Charged with devising a new storyline to extend the Bourne franchise beyond Matt Damons amnesiac spy character, the Bourne Legacy writer-director thoroughly researched what he calls the United States espionocracy.

Gilroy became fascinated with behavior modification through gene-doping, and now says the idea that government-funded scientists have gone far beyond steroids to produce a new breed of hypertough warriors isnt as far-fetched as it seems.

Im not a scientist but Im a real good idiot screenwriter and layman reader of science, Gilroy told Wired in a phone interview. There are different ways to introduce chromosomal changes to affect genomics. You can hijack a virus, put in what you want and use that as the delivery system. I got really interested in this idea of genomic alteration, where you go in on a chromosomal level.

To vet the films viral-modification premise, Gilroy and actress Rachel Weisz whose Bourne Legacy character tests viruses on black-ops agents met with scientists working in the biotech industry. We wanted reassurance that we werent doing anything too far-fetched, Gilroy said. We had some really cool conversations with someone who had a CV very similar to Rachels character, and this person confirmed a lot of what we were doing in the film.

Jeremy Renner plays gene-doped guinea pig Aaron Cross. Image courtesy Universal Pictures

Ive been staggered to see articles where you have the Olympics main drug-testing guy saying they dont know if theyll be able to test for gene-doping, Gilroy said. Im going, Holy shit! This is the cutting edge of athletic enhancement. Theres a legitimate fear in the sports world that gene doping is going to be the next turn of the wheel.

Eager to avoid sci-fi extravagance in favor of reported fact, Gilmore read bioethicist Jonathan Moreno, bookmarked Wireds Danger Room blog, studied the Washington Posts Top Secret America series, monitored Darpas ongoing supersoldier experiments and surveyed the teeming biotech corridor anchored by Marylands Fort Detrick research center.

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Bourne Legacy' s Gene-Doped Superspies Aren't as Far-Fetched as They Sound

SACRAMENTO Scientists affiliated with the UC Davis MIND Institute have discovered how a defective gene causes brain changes that lead to the atypical social behavior characteristic of autism. The research offers a potential target for drugs to treat the condition.

Earlier research already has shown 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 online today (Aug. 10) 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, professor of molecular biosciences in the UC Davis School of Veterinary Medicine and a researcher affiliated with the UC Davis MIND Institute.

"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 cell's molecular energy factories called mitochondria.

In the research, a gene called pten was tweaked in the mice so that neurons lacked the normal amount of pten's protein. The scientists detected malfunctioning mitochondria in the mice as early as four to six weeks after birth.

By 20 to 29 weeks, DNA damage in the mitochondria and disruption of their function had increased dramatically. At this time the mice began to avoid contact with their litter mates and engage in repetitive grooming behavior. Mice without the single gene change exhibited neither the mitochondria malfunctions nor the behavioral problems.

The antisocial behavior was most pronounced in the mice at an age comparable in humans to the early teenage years, when schizophrenia and other behavioral disorders become most apparent, Giulivi said.

The research showed that, when defective, pten'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.

More here:
Gene defect linked to autism-like behavior

Published: Aug. 10, 2012 at 11:58 PM

GLASGOW, Scotland, Aug. 10 (UPI) -- Colon cancer was two to three times more likely to develop in mice with a faulty APC gene and fed high amounts of iron, researchers in Britain and Scotland say.

Researchers at Cancer Research UK at the University of Birmingham and the Beatson Institute for Cancer Research in Glasgow, Scotland, said mice with a faulty APC gene fed a diet low in iron did not develop bowel cancer.

"We've made a huge step in understanding how bowel cancer develops. The APC gene is faulty in around eight out of 10 bowel cancers but until now we haven't known how this causes the disease," Owen Sansom of the Beatson Institute for Cancer Research in Glasgow said in a statement. "It's clear that iron is playing a critical role in controlling the development of bowel cancer in people with a faulty APC gene."

The study might also explain why foods such as red meat, which have high levels of iron, are linked to an increased risk of bowel cancer.

In mice fed a diet with no iron, cells with a faulty APC gene were killed and bowel cancers did not develop, the study said. But, mice with a fully functioning APC gene did not develop bowel cancers, even when fed a diet high in iron, the researchers said.

The study was published in Cell Reports.

Read more here:
Iron, faulty gene cause bowel cancer

ScienceDaily (Aug. 10, 2012) Singing mice (scotinomys teguina) are not your average lab rats. Their fur is tawny brown instead of the common white albino strain; they hail from the tropical cloud forests in the mountains of Costa Rica; and, as their name hints, they use song to communicate.

University of Texas at Austin researcher Steven Phelps is examining these unconventional rodents to gain insights into the genes that contribute to the unique singing behavior -- information that could help scientists understand and identify genes that affect language in humans.

"We can choose any number of traits to study but we try and choose traits that are not only interesting for their own sake but also have some biomedical relevance," said Phelps. "We take advantage of the unique property of the species."

The song of the singing mouse song is a rapid-fire string of high-pitched chirps called trills used mostly used by males in dominance displays and to attract mates. Up to 20 chirps are squeaked out per second, sounding similar to birdsong to untrained ears. But unlike birds, the mice generally stick to a song made up of only a single note.

"They sound kind of soft to human ears, but if you slow them down by about three-fold they are pretty dramatic," said Phelps.

Most rodents make vocalizations at a frequency much too high for humans to hear. But other rodents typically don't vocalize to the extent of singing mice, which use the song to communicate over large distances in the wild, said Andreas George, a graduate student working in Phelps' lab.

Within the last year Phelps research on the behavior of the mouse has appeared in the journals Hormones and Behavior and Animal Behavior. But one of his newest research projects is looking deeper: examining the genetic components that influence song expression. Center stage is a special gene called FOXP2.

"FOXP2 is famous because it's the only gene that's been implicated in human speech disorders specifically," said Phelps.

Having at least one mutated copy of the gene has been associated with a host of language problems in humans, from difficulty understanding grammar to an inability to make the precise mouth movements needed to speak a clear sentence.

The FOXP2 gene is remarkably similar overall between singing mice, lab mice and humans, said Phelps. To find parts of the gene that may contribute to the singing mouse's songs, Phelps is searching for sequences unique to the singing mouse and testing them for evidence of natural selection, which weeds out mutations with no likely observable effect from those that are likely to contribute to singing behavior.

Read the original:
Of mice and melodies: Research on language gene seeks to uncover the origins of the singing mouse

Public release date: 10-Aug-2012 [ | E-mail | Share ]

Contact: Phyllis Brown phyllis.brown@ucdmc.ucdavis.edu 916-734-9023 University of California - Davis Health System

Scientists affiliated with the UC Davis MIND Institute have discovered how a defective gene causes brain changes that lead to the atypical social behavior characteristic of autism. The research offers a potential target for drugs to treat the condition.

Earlier research already has shown 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 online today 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, professor of molecular biosciences in the UC Davis School of Veterinary Medicine and a researcher affiliated with the UC Davis MIND Institute.

"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 cell's molecular energy factories called mitochondria.

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

By 20 to 29 weeks, DNA damage in the mitochondria and disruption of their function had increased dramatically. At this time the mice began to avoid contact with their litter mates and engage in repetitive grooming behavior. Mice without the single gene change exhibited neither the mitochondria malfunctions nor the behavioral problems.

See more here:
Research shows gene defect's role in autism-like behavior