Archive for the ‘Gene Therapy Research’ Category

LEUVEN, BELGIUM--(Marketwire -08/23/12)- TiGenix NV (EURONEXT:TIG), the European leader in cell therapy, gives an update of its business activities and provides the financial highlights for the half year ending June 30, 2012.

Business highlights

Financial highlights

"The significant progress in all our clinical programs and the commercial ramp up of ChondroCelect in the first half year of 2012 reinforce our position as the European leader in cell therapy," says Eduardo Bravo, CEO of TiGenix. "We continue to consistently deliver on the objectives we set more than a year ago, keeping all key programs on plan, meeting our aggressive targets, and keeping costs under control. In addition, we are in discussions with a number of companies in connection with the US rights to Cx601."

Business update

Commercial roll-out of ChondroCelect continues to gain momentum

ChondroCelect sales for the first half of 2012 amounted to EUR 2.1 million, comprising EUR 1.5 million from 2012 sales, up 115% compared to the same period of last year, and EUR 0.7 million of deferred sales from 2011 as a result of the retroactive reimbursement in the Netherland per January 1, 2011.

Discussions to obtain full national reimbursement keep advancing in Spain, France, and Germany. In addition to the recent important reimbursement success, the Company has obtained a positive decision in the Netherlands by one of the leading private healthcare insurance companies to make treatment with ChondroCelect compulsory for its insured, no longer reimbursing non-ATMP cartilage products. Similarly, two of the large private insurers in the UK expressed their intention to routinely reimburse ChondroCelect going forward.

Positive outcome of ChondroCelect compassionate use program published in leading journal

Positive outcome data from the ChondroCelect compassionate use program (CUP), involving 43 orthopedic centers in 7 European countries, treating 370 patients with ChondroCelect over the span of four years, were published in the June, 2012 issue of Cartilage, the official journal of the International Cartilage Repair Society. The data show that the implantation of ChondroCelect results in a positive benefit/risk ratio when used in an unselected, heterogeneous population, irrespective of the follow-up period, lesion size and type of lesion treated. The study provides TiGenix with a large and unique data set to support the long-term safety and efficacy of ChondroCelect.

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TiGenix Business Update & Financial Highlights for the First Half of 2012

The London Olympics may turn out to be one of the cleanest in history in terms of banned substances but behind the scenes, scientists fear the next big challenge to fair play in sport: gene doping.

Over the past decade, scientific advances in the understanding of how genes control muscle activity have alarmed experts within the World Anti-Doping Agency (Wada) who believe that using genes, rather than drugs, will be the next way illicitly to boost athletic performance without fear of detection.

Although scientists are unanimous in believing that genetically enhanced athletes did not participate in London 2012, they are almost equally unanimous in saying that there will be an attempt to misuse the technology in a future Olympics.

"Is gene doping currently being practised? We don't have any evidence that it is," says Professor Steve Harridge, an expert on muscle physiology at King's College London.

"But in the future, as gene-therapy techniques become more refined, it becomes more likely, although I think we are many years away from that," he adds.

"The attraction of gene doping is that it is much harder to detect. But there are dangers because you don't know what it is going to keep on doing. The overall control of muscles can be brutally changed by the sudden introduction of a gene," he says.

Other experts believe that gene doping will not be so easily dismissed as too difficult or risky by those who are prepared to go to physical and ethical extremes in order to win medals.

"We don't know that gene doping would work, but it's technically feasible," says Andy Miah, a sports ethicist and director of the Creative Futures Research Centre at the University of the West of Scotland.

"If you look at the investment of the Wada over the past 10 years, this is their key issue, and it has been for a decade. It's hard to argue with the view that is real in a lot of sports," Dr Miah says.

Gene doping is defined by Wada as the non-therapeutic use of genes in order to enhance athletic performance, and the Montreal-based agency, which was set up in 1999, has spearheaded a campaign to develop scientific methods of detecting its illicit use in sport.

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The cheat gene: Could the next step in sporting fraud come from manipulating DNA?

TAINAN, Taiwan--(BUSINESSWIRE)-- A National Cheng Kung University (NCKU) research team has discovered Near-Infrared Light-Responsive oligonucleotide-gated Au nanoensembles (Au nanorod complex), a potent new anti-cancer complex that is seen as a promising targeted therapy for curing cancer.

This medical discovery was selected as an important and urgent paper, becoming the image of back cover in the July 2012 issue of Advanced Materials, and has drawn big attention in the academic world and the biotechnology industry as well.

The team, led by Chen-Sheng Yeh, NCKU distinguished professor of Department of Chemistry, focused on the development of NIR light-responsive oligonucleotide-gated Au nanoensembles (Au nanorod complex) for cancer therapy and the result proved that Au nanorod complex could provide better efficiency of cancer therapy by reducing the cancer survival rates by 30%.

Au nanorod complex provides a new platform for cancer therapy, a platform which, depending on different diseases, encapsulates different drugs and small interfering RNA (siRNA) which has special functions to achieve chemotherapy and gene therapy, according to Professor Yeh.

Professor Yeh pointed out that the surface of Au nanorod complex coated with silica can encapsulate anti-cancer drugs.

To avoid the loss of anti-cancer drugs from Au nanorod complex during the delivery process and reduce side effects of anti-cancer drugs, the double-stranded DNA (dsDNA) as a net in covering the surface pores was used to conjugate on the surface pores of silica.

Experimental results show that cancer survival rate can be reduced from 80% to about 50%, confirming the gold nanorods pharmaceutical compound has achieved good therapeutic effect.

The advantage of using NIR light to trigger drug release was that NIR was the biological window, where both blood and soft tissues transmission is optimal due to low energy absorption, providing maximum penetration. Therefore, the developed Au nanorod complex has triggered drug release, maximizing the therapeutic properties of both chemotherapy and gene therapy.

Moreover, the design of the treatment which can be tailored by the medical needs to load the appropriate drug treatment is believed to be a very curative treatment platform, according to Yeh.

Yehs team has applied for patent in Taiwan and the United States, and will continue to conduct animal testing and human trials.

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NCKU Team Discovers New Complex in Treating Cancer

SCIENTISTS say they have developed a strain of rice that grows well in soils lacking the nutrient phosphorus.

It's a feat that could boost crop yields for some farmers by as much as a fifth.

The announcement ends a quest to pinpoint a mystery gene that helps the roots of baby rice plants tease phosphorus from the soil, enabling them to notch up strong, early growth.

The gene has now been transferred to modern varieties of rice using classic methods of cross-breeding, not genetic engineering, said Sigrid Heuer at the International Rice Research Institute (IRRI) in the Philippines.

Next week, national rice breeders from Bangladesh, India, Thailand and India will be briefed on the exciting find, which should benefit small farmers most of all, Heuer said in a phone interview from Manila.

"I would expect to see (an improvement in yield of) around 20 per cent, but it depends so much on the type of the soil and how severe the stress is," Heuer said.

"But realistically, we are talking conservatively of an average of 10-20 per cent, and locally a little more if the (phosphorus) stress is severe," she said.

The breakthrough seeks to address one of the biggest problems facing rice growers from the southeastern United States to South America, Southeast Asia and China.

Many soil types bond tightly to phosphorus, surrendering only a tiny amount of the precious mineral to plant roots.

To get around this, farmers look to phosphorus fertilisers which are spread on the field.

Original post:
Gene boost for rice yields

22 August 2012 Last updated at 18:46 ET By Richard Black Environment correspondent, BBC News

A gene from wild Indian rice plants can significantly raise the yield of common varieties in nutrient-poor soils.

Scientists from the International Rice Research Institute (Irri) identified a gene that helps uptake of phosphorus, nitrogen and potassium, and transferred it into commercial strains.

Their yield was about 60% above normal in phosphorus-poor soils, the team reports in the journal Nature.

Large swathes of Asia have soil that is phosporus-deficient.

The gene came from a variety called Kasalath, native to nutrient-poor soils of eastern India.

About 10 years ago, scientists deduced that Kalasath contained one or more genes that allowed it to grow successfully in low-phosphorus conditions.

It took the Irri team three years to identify the gene responsible, which they have named PSTOL1.

"We got the [DNA] sequence of this region, but the region is very complex and it was very difficult to identify what is an actual gene and what is not," lead researcher Sigrid Heuer told BBC News.

"There's so much work being done on phosphorus pathways and we could never find the genes and the mechanisms, and actually it's very simple - the gene promotes larger root growth, so the plant takes up nutrients more easily."

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Wild rice gene gives yield boost

WASHINGTON Over six frightening months, a deadly germ untreatable by most antibiotics spread in the nations leading research hospital. Pretty soon, a patient a week was catching the bug. Scientists at the National Institutes of Health locked down patients, cleaned with bleach, even ripped out plumbing and still the germ persisted.

By the end, 18 people harbored the dangerous germ, and six died of bloodstream infections from it. Another five made it through the outbreak only to die from the diseases that brought them to NIHs world-famous campus in the first place.

It took gene detectives teasing apart the bacterias DNA to solve the germs wily spread, a CSI-like saga with lessons for hospitals everywhere as they struggle to contain the growing threat of superbugs.

It all stemmed from a single patient carrying a fairly new superbug known as KPC Klebsiella pneumoniae that resists treatment by one of the last lines of defense, antibiotics called carbapenems.

We never want this to happen again, said Dr. Tara Palmore, deputy hospital epidemiologist at the NIH Clinical Center.

Infections at health care facilities are one of the nations leading causes of preventable death, claiming an estimated 99,000 lives a year. Theyre something of a silent killer, as hospitals fearful of lawsuits dont like to publicly reveal when they outfox infection control yet no hospital is immune.

Wednesday, government researchers published an unusually candid account of last years outbreak, with some advice: Fast sequencing of a germs genome, its full DNA, may be essential. It can reveal how drug-resistant bacteria are spreading so that doctors can protect other patients.

This is not an easy story to tell, said Dr. Julie Segre, a senior investigator at NIHs National Human Genome Research Institute. She led the genetic sleuthing that found the bug hiding in sink drains and, most chilling, even in a ventilator that had been cleaned with bleach.

Infection-control specialists at other hospitals called this detailed anatomy of an outbreak, published in the journal Science Translational Medicine, important to share.

They were able to demonstrate that this sneaky little bug was able to stay alive and get transmitted in ways they hadnt quite predicted before they had the detailed genetic information, said Dr. Sara Cosgrove, associate hospital epidemiologist at Johns Hopkins University. Its very revealing.

The rest is here:
Genetic sleuths track down deadly superbug

ScienceDaily (Aug. 22, 2012) Laboratory mice bred without the gene lacked a pro-inflammatory protein called TREM-1 and protected them from developing liver cancer after exposure to carcinogens.

The study, published in Cancer Research, a journal for the American Association for Cancer Research, could lead to drug therapies to target TREM-1, said Dr. Anatolij Horuzsko, an immunologist at the GHSU Cancer Center and principal investigator on the study.

"We have long suspected that chronic inflammation is a very powerful tool in the initiation of cancer, and also in the progression or metastasis of cancer," said Horuzsko. "We [looked] at the molecules that control inflammatory responses to gain a better understanding of how this process works. One important triggering receptor for inflammation is TREM-1."

TREM-1's role in promoting inflammation is useful in cases such as battling viral or bacterial infections and in maintaining normal tissue function. But as Horuzsko's team discovered, in abnormal conditions -- such as liver damage due to alcohol abuse or other irritants -- production of TREM-1 goes haywire. A chronic, low-level state of inflammation is produced as TREM-1 leads to the development of other inflammatory agents, which causes more damage, increases cell production and creates mutated cells. These mutated cells then reproduce -- planting the seeds that can lead to cancer.

During the 14-month study, Horuzsko and his team used mouse studies to gather data on the effect of TREM-1 in the liver cells and identify potential sources for therapies. Because a mouse's life span is about three years, the length of the study mimicked a similar 20- to 30-year cancer progression of liver cancer in humans.

Two sets of mice -- one with the TREM-1 gene removed -- were exposed to the cancer-causing agent diethylnitrosamine, or DEN, which is present in tobacco smoke, chemicals and other products. Within just 48 hours of DEN injection, the control mice were already showing signs of liver cell injury and death and high levels of TREM-1 expression in the liver's Kupffer cells. These specialized liver cells normally destroy bacteria and worn-out red blood cells. Eight months later, these mice also showed massive liver tumors.

But the mice with the gene removed remained healthy, showing very few changes -- and very small, if any, tumors after eight months. The only difference between the two groups was the appearance of TREM-1 in the Kupffer cells.

Horuzko's team hopes the findings -- and their potential in TREM-1-related cancer treatment -- will be applicable to other cancers as well. "TREM-1 could be a target for any inflammation-associated cancer," said Horuzsko. "In the future, we could use a drug to target TREM-1 in the body. We are already working in this direction."

Horuzsko's team also identified another potential target for drug therapy during the study -- a product of liver cell injury and death called HMGB1. HMGB1 is a previously unknown activating ligand, or agent, that stimulates Kupffer cells to produce the TREM-1 protein and start the inflammatory process.

"Advanced drug therapies for cancer are a growing field of research, and immune therapies are an important part of our mission," said Dr. Samir N. Khleif, Director of the GHSU Cancer Center. "Studies like Dr. Horuzsko's are leading the way to identify targeted therapies that will become our future standards of care. As we open the door to new scientific discoveries, this enables us to provide better care to patients and families with cancer. "

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Targeting inflammation to prevent, treat cancers

Published on Aug 23, 2012

Workers clean grass from a rice field at Ragas Masigit village in Serang, Indonesia's Banten province, Aug 14, 2012. Scientists on Wednesday said they had developed a strain of rice that grows well in soils lacking the nutrient phosphorus, a feat that could boost crop yields for some farmers by as much as a fifth. -- PHOTO: REUTERS

PARIS (AFP) - Scientists on Wednesday said they had developed a strain of rice that grows well in soils lacking the nutrient phosphorus, a feat that could boost crop yields for some farmers by as much as a fifth.

The announcement ends a quest to pinpoint a mystery gene that helps the roots of baby rice plants tease phosphorus from the soil, enabling them to notch up strong, early growth.

The gene has now been transferred to modern varieties of rice using classic methods of cross-breeding, not genetic engineering, said Dr Sigrid Heuer at the International Rice Research Institute (IRRI) in the Philippines.

Next week, national rice breeders from Bangladesh, India, Thailand and India will be briefed on the exciting find, which should benefit small farmers most of all, Dr Heuer said in a phone interview from Manila.

The rest is here:
Gene breakthrough could boost rice yields by 20%

Public release date: 22-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 22, 2012Mosquito-borne West Nile virus (WNV) caused 26 deaths already this year, and nearly 700 cases had been reported by mid-August according to the Centers for Disease Control and Prevention (CDC). WNV had become "old news" among the public and the media. Furthermore, funding to support research, training and education, and surveillance and vector control had waned. Now there is an urgent imperative to redouble our efforts to understand and control this dangerous virus. Vector-Borne and Zoonotic Diseases, a major peer-reviewed journal from Mary Ann Liebert, Inc., publishers, has published numerous timely and informative studies on WNV, and articles on the topic published since 2007 are available free on the Journal website at http://www.liebertpub.com/vbz through September 10 to help disseminate vital information about this deadly virus that continues to infect and kill people across the U.S. and abroad.

Texas is currently a hotspot for WNV, reporting more than 336 cases and 14 deaths to date, resulting in a state of emergency and aerial spraying for mosquito control in Dallas County, but several other states are also reporting fatal West Nile cases.

"No conclusive explanation has been offered for the increased number of WNV cases, but over the years, many experts have learned that predictions related to West Nile virus should be made with caution," says Stephen Higgs, PhD, Editor-in-Chief of Vector-Borne and Zoonotic Diseases and Associate Vice President for Research, Research Director, Biosecurity Research Institute, Peine Professor of Biosecurity, and Professor of Diagnostic Medicine and Pathobiology, Kansas State University, Manhattan, KS.

"Our journal, Vector-Borne and Zoonotic Diseases, will continue to inform researchers and public health experts and policymakers on all aspects of WNV around the world," adds Dr. Higgs.

###

About the Journal

Vector-Borne and Zoonotic Diseases is an authoritative, monthly peer-reviewed journal published in print and online dedicated to diseases transmitted to humans by insects or animals. The Journal covers a widespread group of vector and zoonotic-borne diseases including bacterial, chlamydial, rickettsial, viral, and parasitic zoonoses and provides a unique platform for basic and applied disease research. The Journal also examines geographic, seasonal, and other risk factors that influence the transmission, diagnosis, management, and prevention of zoonotic diseases that pose a threat to public health worldwide. Vector-Borne and Zoonotic Diseases is the Official Journal of SocZEE, the Society for Zoonotic Ecology and Epidemiology. Tables of content and a sample issue may be viewed on the Vector-Borne and Zoonotic Diseases website at http://www.liebertpub.com/vbz.

About the Publisher

Link:
Deadly outbreak of West Nile virus highlights urgent need for more research, funding

This means that while a 20-year-old man passes on about 25 mutations through his sperm, in an average 40-year-old this will rise to about 65.

Kari Stefansson, senior author of the study by DECODE Genetics, an Icelandic company, said: "All areas of the human genome were a mutation once upon a time, so all human variety is down to a mutation.

"But one interesting aspect of this work is it shows us that the classic focus on the age of the mother and the health of the child is not sufficient.

"The increasing age of the father has a much bigger impact on a child's health in a general way. Women are off the hook and we men are on it."

Dr Allan Pacey, Chairman of the British Fertility Society, said: "It is a surprise to find that men transmit a higher number of mutations to their children than do women.

"Whilst not wanting to scare the children of older fathers, information like this is important to understand and should remind us that nature designed us to have our children at a young age and if at all possible men and women should not delay parenthood if they are in a position not to.

But Prof Darren Griffin, a geneticist at Kent University, said: "There are three billion of letters in the DNA code of humans and the numbers of mutations detected in this study are in the dozens.

"The observed approximate doubling of mutation rate between the ages of 20 and 40 (when most fathers are actively reproducing) is certainly clinically noteworthy but not realistically likely to deter more mature fathers from having children."

In an accompanying opinion piece in Nature, Prof Alexey Kondrashov of Michigan University suggested that younger men ought to bank their sperm to protect their future children from disease.

But Prof Christopher Barrett, an expert in reproductive medicine at Dundee University, said: "Whilst sperm banking is technically feasible, more data would be required to recommend this policy as routine."

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Older fathers pass on more genetic faults

NEW YORK (GenomeWeb News) Genetic testing firm VitaPath Genetics has raised about $5 million toward a financing round targeting $7.3 million, it said in a regulatory document recently.

In a Form D filed with the US Securities and Exchange Commission, the Foster City, Calif.-based company did not disclose how the proceeds would be used or the investors. Among the names listed as related persons are Dennis Gilbert, VitaPath's CEO, who formerly was a chief scientific officer and VP of research at Applied Biosystems; Richard Taylor, its CFO; and Rowan Chapman, a partner in venture capital firm Mohr Davidow and a VitaPath board member.

The types of securities being offered, VitaPath said, are in the form of equity as well as preferred stock which will be converted into common stock.

The company is developing genetic tests to reduce the risk of life-threatening diseases, according to its website. Its first product is a test for identifying risk factors associated with Spina bifida. Last year it inked a licensing deal providing Alere marketing rights for the test.

VitaPath raised $6 million in a round of private financing in September 2009.

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Genetic Test Firm VitaPath Raises $5M

FIVE POINTS, Calif., Aug 22, 2012 /PRNewswire/ -- S&W Seed Company (SANW) today announcedit has purchased the rights to a portfolio of alfalfa varieties suited for colder climate conditions, thereby expanding its alfalfa genetics to include dormant varieties. Since 1980, S&W has focused on breeding and producing non dormant alfalfa seed, known as 8, 9 and 10 dormancies that are suited to warm climates. This purchase is the first time the company has ventured into seed genetics for colder climates, where dormancies of two,three and four dormancies are appropriate.

Today'sacquisition of proprietary alfalfa germ-plasm, will help enable S&W to participate in the marketplaces for dormant alfalfa varieties, particularly in countries which do not currently allow GM (genetically modified) seed. The acquisition also has the potential to help the company produce classically bred,low dormancy, alfalfa seedvarietieswhich might includesalt tolerance or other traits tied to S&W's proprietary alfalfa germ-plasm.As part of the acquisition, the company will also be acquiring select multi leaf alfalfa and orchard grass varieties which the company expects will supplement alfalfa seed sales going forward.S&W expects to commence production on itsfirstdormant seed varietiesthis fall, with seed available for sale in the fall of 2013.

Mark Grewal,chief executive officer of S&W Seed Company, commented, "Today's announcement is a first step into production oflow dormancy, alfalfa seed. We believe that thevarietieswe acquired haveexcellent traits and can be sold internationally and domestically. This acquisitionalso gives us access to additional contract seed growers in the United States and Canada that have been growing these and other dormant varieties for a number of years."

About S&W Seed CompanyFounded in 1980 and headquartered in the Central Valley of California, S&W Seed Company is a leading producer of warm climate, high yield alfalfa seed varieties, including varieties that can thrive in poor, saline soils, as verified over decades of university-sponsored trials. S&W also offers seed cleaning and processing at its 40-acre facility in Five Points, California and has recently launched a business expansion initiative centered on its plan to mass produce stevia leaf in the U.S. in response to growing global demand for the all-natural, zero calorie sweetener from the food and beverage industry. For more information, please visit http://www.swseedco.com.

Safe Harbor StatementThis release contains "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended and such forward-looking statements are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. "Forward-looking statements" describe future expectations, plans, results, or strategies, including statements regarding the potential success of the Company's stevia program, and are generally preceded by words such as "may," "future," "plan" or "planned," "will" or "should," "expected," "anticipates," "draft," "eventually" or "projected." You are cautioned that such statements are subject to a multitude of risks and uncertainties that could cause future circumstances, events, or results to differ materially from those projected in the forward-looking statements, including the risks that actual results may differ materially from those projected in the forward-looking statements as a result of various factors and other risks identified in the Company's 10-K for the fiscal year ended June 30, 2011, and other filings made by the Company with the Securities and Exchange Commission.

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S&W Seed Company Acquires Rights to Dormant Alfalfa Genetics

REYKJAVIK, Iceland--(BUSINESS WIRE)--

deCODE Genetics, a global leader in analyzing and understanding the human genome, in collaboration with Illumina, a global leader in the making of instruments to analyze the genome, reported today in the journal Nature that a fathers age, not a mothers, at the time a child is conceived is the single largest contributor to the passing of new hereditary mutations to offspring. The findings come from the largest whole genome sequencing project to examine associations of diseases with rare variants in the genome.

Strikingly, this study found that a fathers age at the time a child is conceived explains nearly all of the population diversity in new hereditary mutations found in the offspring, said study lead author Kari Stefansson, M.D., Dr. Med., CEO of deCODE Genetics. With the results here, it is now clear that demographic transitions that affect the age at which males reproduce can have a considerable impact on the rate of certain diseases linked to new mutation.

To better understand the cause of new hereditary mutations, the deCODE team sequenced the genomes of 78 Icelandic families with offspring who had a diagnosis of autism or schizophrenia. The team also sequenced the genomes of an additional 1,859 Icelanders, providing a larger comparative population.

On average, the investigators found a two mutation per-year increase in offspring with each one-year increase in age of the father. The average age of the father in the study was 29.7 years old. Also, when specifically examining the genomes of families with autism and schizophrenia, the authors identified in offspring mutations in genes previously implicated in the diseases. They also identified two genes, CUL3 and EPHB2, with mutations in an autism patient subgroup.

Our results all point to the possibility that as a man ages, the number of hereditary mutations in his sperm increases, and the chance that a child would carry a deleterious mutation that could lead to diseases such as autism and schizophrenia increases proportionally, said Dr. Stefansson. It is of interest here that conventional wisdom has been to blame developmental disorders of children on the age of mothers, whereas the only problems that come with advancing age of mothers is a risk of Down syndrome and other rare chromosomal abnormalities. It is the age of fathers that appears to be the real culprit.

Epidemiological studies in Iceland show the risk of both schizophrenia and autism spectrum disorders increases significantly with fathers age at conception, and that the average age of fathers in Iceland (now 33 years-old) at the time a child is conceived is on the rise. The authors noted that demographic change of this kind and magnitude is not unique to Iceland, and it raises the question of whether the reported increase in autism spectrum disorder diagnosis is at least partially due to an increase in the average age of fathers at conception.

About deCODE

Headquartered in Reykjavik, Iceland, deCODE genetics is a global leader in analyzing and understanding the human genome. Using its unique expertise and population resources, deCODE has discovered genetic risk factors for dozens of common diseases ranging from cardiovascular disease to cancer.

In order to most rapidly realize the value of genetics for human health, deCODE partners with life sciences companies to accelerate their target discovery, validation, and prioritization efforts, yielding improved patient stratification for clinical trials and essential companion diagnostics. In addition, through its CLIA- and CAP-certified laboratory, deCODE offers DNA-based tests for gauging risk and empowering prevention of common diseases. deCODE also licenses its tests, intellectual property, and analytical tools to partner organizations. deCODEs corporate information can be found atwww.decode.comwith information about our genetic testing services atwww.decodehealth.comandwww.decodeme.com.

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deCODE Genetics Study Finds Father’s Age—Not Mother’s—Critical to New Mutations Passed to Offspring

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

Viral Genetics (VRAL) published its August 2012 Letter to Shareholders which is available on the company website at: http://www.viralgenetics.com/shareholder-letters/Letter-to-Shareholders-Aug-12.PDF.

In the letter, the companys president, Mr. Haig Keledjian, offers insight into the companys ongoing progress in several key areas:

Additional details on these programs is available by clicking this link.

About Viral Genetics, Inc.

San Marino, California-based Viral Genetics discovers drug therapies from two platform technologies based on over 60 patents: Metabolic Disruption (MDT) and Targeted Peptides (TPT). Founded in 1994, the biotech company is researching treatments for HIV/AIDS, Lyme Disease, Strep, Staph and drug resistant cancer. A majority-owned subsidiary, VG Energy (www.vgenergy.net), is dedicated to exploring biofuel and agricultural applications for the MDT platform. For more information, visit http://www.viralgenetics.com.

About VG Energy

VG Energy Inc. is an alternative energy and agricultural biotech company that is a majority-owned subsidiary of Viral Genetics Inc., a biotechnology company researching new treatments and methods of detection for diseases including cancer, HIV/AIDS and others. Using its Metabolic Disruption Technology (MDT), Viral Genetics cancer research led to discoveries with major consequences in a wide variety of other industries, including biofuel, vegetable oils and other high value oils and chemicals. VG Energy holds the exclusive worldwide license to the MDT patent rights for use in the increase of production of various plant-derived oils from algae and seeds. These pivotal discoveries promise to allow the biofuel industry to overcome its major obstacle in the area of production efficiency: namely, an increase in production yields leading to feasible economic returns on investment, allowing renewable biodiesel to be competitive with fossil fuels. For more information, please visit http://www.vgenergy.net.

SAFE HARBOR FOR FORWARD-LOOKING STATEMENTS:

This news release contains forward-looking statements that involve risks and uncertainties associated with financial projections, budgets, milestone timelines, clinical development, regulatory approvals, and other risks described by Viral Genetics, Inc. from time to time in its periodic reports, including statements about its VG Energy, Inc. subsidiary. None of Viral Genetics' drug compounds are approved by the US Food and Drug Administration or by any comparable regulatory agencies elsewhere in the world, nor are any non-pharmaceutical products of VG Energy, Inc. commercialized. While Viral Genetics believes that the forward-looking statements and underlying assumptions reasonable, any of the assumptions could be inaccurate, including, but not limited to, the ability of Viral Genetics to establish the efficacy of any of its drug therapies in the treatment of any disease or health condition, the development of studies and strategies leading to commercialization of those drug compounds in the United States, the obtaining of funding required to carry out the development plan, the completion of studies and tests on time or at all, the successful outcome of such studies or tests, or the successful commercialization of VG Energy, Inc.s non-pharmaceutical products. Therefore, there can be no assurance that the forward-looking statements included in this release will prove to be accurate. In light of the significant uncertainties inherent in the forward-looking statements included herein, the forward-looking statements should not be regarded as a representation by Viral Genetics or any other person that the objectives and plans of Viral Genetics will be achieved.

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Viral Genetics Issues August 2012 Shareholder Update

OWINGS MILLS, Md. and COLUMBIA, Md., Aug. 21, 2012 (GLOBE NEWSWIRE) -- The Foundation Fighting Blindness announces an investment of $2.4 million in eight promising research projects aimed at providing treatments and identifying causes of retinal degenerative diseases including age-related macular degeneration (AMD), retinitis pigmentosa (RP), Leber congenital amaurosis (LCA), and Usher syndrome, among other conditions. The spectrum of funded work spans from innovating gene therapies, to advancing cell transplantation, to understanding AMD risk, to developing new therapies for an inherited condition that causes blindness at birth. Each of the eight investigative teams will receive $300,000 for its three-year research efforts.

"These eight grants are going to a truly outstanding cadre of scientists," says Dr. Stephen Rose, chief research officer, Foundation Fighting Blindness. "The funding will help investigate several approaches to saving sight and provides strong momentum for moving treatments forward, out of the lab and into the clinic."

The projects receiving funding were selected through a rigorous review process conducted by the Foundation's Scientific Advisory Board, a group comprised of the field's leading retinal researchers. A total of 35 proposals were reviewed during the grant allocation process.

Eight New Foundation Fighting Blindness-Funded Projects

Allie Gebhardt

Foundation Fighting Blindness

410-423-0643

AGebhardt@FightBlindness.org

About Foundation Fighting Blindness

The Foundation Fighting Blindness is a national nonprofit driving research that will lead to preventions, treatments and cures for retinitis pigmentosa, macular degeneration, Usher syndrome and the entire spectrum of retinal degenerative diseases that affect more than 10 million Americans. Since 1971, the Foundation has raised over $450 million as the leading non-governmental funder of retinal research. Breakthrough Foundation-funded studies using gene therapy have restored significant vision in children and young adults who were previously blind, paving the way for using this method to treat a variety of retinal degenerative diseases, and proving a cure is in sight. With a network of nearly 50 chapters, the Foundation also provides support and resources to affected individuals and their families in communities across the country.

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Foundation Fighting Blindness Announces $2.4 Million in Funding for Eight New Sight-Saving Research Projects

Destroying genetic diversity

Brad Plumers article on drought-resistant corn follows a pattern suggested in a quotation at the end of the article which states that only 2 percent of the U.S. agricultural-research budget is spent on sustainable farming; in that vein, Plumers article devotes 75 percent of its words to genetic-engineering solutions and just 25 percent to sustainable farming practices that have the same objective [Corn varieties engineered to withstand drought, Business, Aug. 19].

The U.S. Department of Agricultures review of Monsantos own data shows that years of investment into so-called drought-tolerant biotech crops have been nothing more than a risky and very expensive failure. Monsantos new drought-tolerant genetically modified corn variety MON 87460 does not perform any better than non-GMO varieties.

In addition, in the United States and abroad, there are several types of new, drought-tolerant corn grown through natural breeding techniques that are likely to do as well or better than Monsantos corn. Data from U.S. researchers suggest that conventional breeding is producing drought tolerance two to three times faster than genetic engineering.

The danger is that now that MON 87460 has been deregulated, it will inevitably contaminate truly resilient varieties of organic and conventional corn, destroying the rich genetic diversity that the worlds farmers have cultivated in the planets infinitely varied microclimates.

Jeremy Smithson, Seattle

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U.S. drought causes $18 billion in key-crop damages

Doug Heath, a tomato breeder for Monsanto Co., offers visitors juicy slices of 'Cherokee Purple,' a delicate variety with a sweetness and acidity he is trying to replicate in hardier commercial fruit.

"We want to see these in the stores more than one month a year," Heath told visitors this month at his research plot in Woodland (Yolo County). He gave out the tomato slices at Field Days, an annual gathering for farmers and distributors to see new crops from Monsanto's Seminis vegetable seed unit.

Monsanto is accelerating its push to identify thousands of genetic markers in fruits and vegetables as it brings the tools of biotechnology to conventional breeding, giving Heath the ability to select for everything from taste to disease resistance. It's also allowing the world's biggest vegetable-seed producer to develop new varieties in two to four years, down from as many as 10 years. Using the markers is like having "X-ray glasses" that let breeders peer inside a leaf clipping or seed to find what will grow, Heath said.

His efforts are gathering momentum at the St. Louis company, which bought Seminis for $1.4 billion in 2005 and is looking to expand its market share. Monsanto said it has identified about 5,000 genetic markers in peppers, more than 4,000 in tomatoes and thousands more in melons, cauliflower, broccoli, cucumbers and beans. The company plans to identify more vegetable markers this year than in the past 20 years combined.

Food and Water Watch, a consumer advocacy group in Washington that opposes genetic engineering, has raised alarms about the products. It sponsored petitions urging retailers including Walmart not to stock genetically engineered vegetables. Monsanto's sweet corn "hasn't been tested for human safety," according to one online petition.

The company says engineered seeds have been used since 1996 and "there has not been one documented case of biotech crops being unsafe for humans or the environment," according to its website. Monsanto said it invests 95 percent of its vegetable research in conventional breeding and 5 percent on genetic engineering.

A lab on Monsanto's Woodland site annually analyzes the genetic makeup of 7 million vegetable samples. The lab can identify genes associated with flavor, appearance, texture and nutrition, as well as traits for disease-resistance and susceptibility.

As recently as five years ago, Monsanto had genetic markers for only a few tomato traits. When Heath started working in 1993 for a predecessor company, there wasn't even a computer.

"We're breeding in a different way now," Heath said. "It's so powerful."

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Genetic markers give Monsanto an edge

Newswise HOUSTON (Aug. 21, 2012) Thanks to a cousins warning that thoracic aortic disease ran in their family, Houstonian Pat Arthur discovered that he carried a genetic defect that could cause his aorta to dissect and rupture with little or no warning. He also learned that this particular defect resulted in an aggressive form of the disease and the growing aneurysm spotted with a scan needed to be surgically corrected sooner than later.

It was life-saving information.

Now a new clinic devoted to integrated care for aortic disease is able to merge personalized genetic information with clinical care at The University of Texas Health Science Center at Houston (UTHealth).

The new clinic will provide state-of-the-art care of patients with aortic and other vascular disease, with a particular emphasis on managing the disease based on the underlying genetic alteration that is causing the disease. This is the epitome of personalized medicine, said Dianna M. Milewicz, M.D., Ph.D., director of the Division of Medical Genetics and the President George H.W. Bush Chair in Cardiovascular Medicine at UTHealth. This is one of the first diseases that we can treat based on the underlying gene causing the disease.

The Multidisciplinary Aortic and Vascular Disease Clinic includes a medical geneticist, genetic counselors, cardiologists, and cardiothoracic and vascular surgeons who specialize in providing care to individuals and families with thoracic aortic aneurysms and dissections, as well as other vascular diseases and cardiac valve abnormalities. Congenital disorders such as bicuspid aortic valve and genetic syndromes such as Marfan syndrome and Loeys-Dietz syndrome can lead to thoracic aortic disease. In addition, thoracic aortic disease can be inherited in families without any features of a syndrome.

Milewicz directs a $12 million grant from the National Heart, Lung & Blood Institute (RO1 HL62594; P50HL083794-01), part of the National Institutes of Health, for collaborative research on thoracic aortic disease. She and her research team at UTHealths John Ritter Research Program in Aortic and Vascular Diseases have discovered four genes that predispose people to familial thoracic aortic aneurysms and dissections and have confirmed that another four contribute to familial disease. Defects in some of these genes also affect other parts of the vascular system and can result in intracranial aneurysms, early onset coronary artery disease, ischemic stroke and Moyamoya disease. If patients know they carry a particular gene defect, they can be treated with medications and monitored for signs of disease. In the case where there appears to be a familial link but the gene defect has not been discovered, family members can undergo regular screening for vascular disease to prevent premature deaths and strokes.

This is translational medicine a direct pipeline from research to the clinic, said cardiologist Siddharth Prakash, M.D., assistant professor of internal medicine at UTHealth. We can look at the risk factors and the long-term survival and tailor that according to the genetic work of Dr. Milewicz and her team.

Surgical care for patients is centered at the Memorial Hermann Heart & Vascular Institute (HVI) in the Texas Medical Center. Hazim Safi, M.D., professor and chair of the Department of Cardiothoracic & Vascular Surgery and chief of cardiothoracic and vascular surgery at HVI, and Anthony Estrera, M.D., are also involved in the care of these patients. The clinic is part of UT Physicians, the clinical practice of the UTHealth Medical School. For more information, call (832) 325-7211.

Link:
UTHealth Research, Clinical Care Merge in Aortic and Vascular Disease Clinic

Newswise ITHACA, N.Y. More than one out of every four cases of breast cancer is associated with a specific, missing gene a finding that could have significant implications for chemotherapy treatments, according a recent study by Cornell University researchers.

The study shows that the lack of a certain gene occurs in almost 28 percent of human breast cancers, playing a role in some 60,000 breast-cancer cases in the United States and 383,000 worldwide this year. Posted online in the journal GENETICS, the study has important clinical implications: It suggests that several existing drugs may be effective in treating breast cancers with the missing gene, called NF1. It also suggests that the commonly used breast cancer drug tamoxifen could make the disease worse in these specific cancers.

The NF1 gene negatively regulates one of the most important oncogenes genes that when mutated or expressed at high levels contribute to turning a normal cell into a cancerous one. This oncogene, called RAS, is involved in signaling inside the cell to control growth. When NF1 is missing or depleted, RAS becomes hyperactivated and can lead to tumor formation.

In the study, Cornell researchers used a mouse model with elevated mutation rates that led to breast cancer in 80 percent of the mice.

These mice almost always get mammary tumors, and when we looked at their genomes, nearly all of them were missing this NF1 gene, said John Schimenti, professor of genetics at Cornells College of Veterinary Medicine and the papers senior author. There are many big cancer studies that identify the most commonly mutated genes, but they dont prove experimentally that those genes are the drivers of cancer.

In humans, there are many causes of breast cancer, and each patients cancer has a slightly different set of natural gene variants as well as new mutations in their tumors, so identifying individual genes that drive cancer can be problematic. But the model mice are inbred and get exactly the same tumor every time. So weve eliminated all the noise, allowing the researchers to identify NF1 as a driver of these tumors, said Schimenti.

In the mouse model, RAS is hyperactivated. Since RAS is one of the most important oncogenes, many drugs have been already developed to interrupt the RAS pathway to treat cancer. If NF1 is missing and it is causing cancer by activating RAS, then these drugs may help, said Schimenti. Therefore, there doesnt need to be any more drug development to test this possibility right now.

The study also suggests that tamoxifen, one of the most common breast cancer treatments, may exacerbate the disease when the missing NF1 is the driver. Another study reported that NF1 protein depletion makes cancer cells resistant to tamoxifen, and tamoxifen-treated patients whose tumors have low NF1 levels had poorer clinical outcomes.

Schimenti and his colleagues plan to test whether they can reverse growth of tumors in mice missing the NF1 gene by inserting a replacement gene. They are also testing how effective RAS inhibitor drugs are at curbing cancer in mice. The paper shows that RAS inhibitors curb growth of these tumor cells in culture.

Marsha Wallace, a graduate student working in Schimentis lab at Cornell, is the papers lead author. Researchers from the University of North Carolina and Sloan Kettering Cancer Center co-authored the study.

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Missing Gene May Drive More Than One in Four Breast Cancers

SAN DIEGO, Aug. 20, 2012 /PRNewswire/ -- HUYA Bioscience International announced today a strategic partnership with one of China's leading research organizations, Tianjin Research Center of Basic Medical Sciences (TJRCBMS). HUYA is an international leader in accelerating the global development of China's pharmaceutical innovations. Their new partnership with TJRCBMS will focus on innovations coming out of this newly formed institution that could meet critical global pharmaceutical pipeline needs.

Located on the Tianjin Medical University campus, TJRCBMS is a nonprofit research institution founded by the municipal government of Tianjin. Its mission is to be on the global biomedical research frontiers and serve China's strategic development needs. Since its opening in 2005, it has recruited high-caliber principal investigators from China as well as from overseas to establish laboratories and conduct cutting-edge research in areas such as translational cancer biology, neural information processing, and gene therapy. Many of these investigators are well established in their respective research areas and have published extensively in peer-reviewed scientific journals.

The new partnership between HUYA and TJRCBMS will enable both parties to collaborate to promote new drug development in China and worldwide. TJRCBMS will be able to consult with HUYA's team of experts in drug development and globalization. In turn, HUYA will have the first opportunity to evaluate certain research and development projects conducted at TJRCBMS, and provide support and assistance as needed.

"Working with Tianjin Research Center of Basic Medical Sciences puts us at the cutting edge of biomedical research in China," said Clement Gingras, HUYA's Chief Technical Officer and COO, China. "We are very excited about this opportunity and look forward to fruitful collaborations in the years to come."

Professor Ning Zhang, the Director for TJRCBMS also expressed his optimism about this new partnership: "HUYA can provide their expertise on pharmaceutical development to help accelerate the global reach of our innovative research."

ABOUT HUYA BIOSCIENCE INTERNATIONAL

HUYA is one of the first companies to have recognized China's potential to help meet the global demand for new preclinical and clinical stage compounds. The company's strategy is to facilitate and promote the global development and commercialization of new drug compounds originating in China. With eight offices strategically located across China, the most comprehensive Chinese compound portfolio in the world, and a growing number of collaboration agreements with premier Chinese research and development organizations, HUYA occupies a unique position with regards to the China bio-pharmaceutical industry. Its strategy to identify and license novel Chinese compounds, and to offer Western pharmaceutical companies efficient and comprehensive access to therapeutic innovation in China, means the Company can enable efficient global development. HUYA has become a champion in guiding China's biomedical innovations into the worldwide marketplace. HUYA is jointly headquartered in Shanghai and in San Diego, California. More information is available at http://www.huyabio.com.

ABOUT TIANJIN RESEARCH CENTER OF BASIC MEDICAL SCIENCES

With initial funding of 30 million RMB from the municipal government of Tianjin, Tianjin Research Center of Basic Medical Sciences was established as a non-profit research institution to advance the biomedical research and serve China's strategic development needs. With its innovative open recruiting strategy and supportive management policies, TJRCBMS has attracted top talent globally to establish laboratories to conduct research in areas covering translational cancer biology, pharmaceutical sciences, neural information processing, epigenetics and tumorigenesis, molecular and populational genetics, gene therapy, molecular immunology as well as immunology and inflammation. For more information, please visit http://202.113.48.12/cn/expcenter/chinese.html.

CONTACT

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HUYA Bioscience Announces New Partnership With Tianjin Research Center of Basic Medical Sciences

ScienceDaily (Aug. 21, 2012) Research on a unique vertebrate called the sea lamprey shows that more than a thousand genes are shed during its early development. These genes are paradoxically lost all throughout the developing embryo except in a specialized compartment called "primordial germ cells" or PGCs. The PGCs can be thought of as embryonic stem cells and are used, ultimately, for making the next generation of lampreys. Based on computational analysis, a significant number of genes that are lost in the embryo have signatures of "pluripotency," which suggests that they could also have undesirable effects if they were inadvertently turned on in the body. In effect, by undergoing programmed genome rearrangement and gene loss during embryogenesis, the sea lamprey "seals" the genes away in the small germline compartment so they cannot be misexpressed and thereby create untoward problems (such as development of cancer, for example).

The study was completed at the Benaroya Research Institute at Virginia Mason (BRI) and recently published as a featured article in Current Biology, along with an outside commentary.

The article authors are Jeramiah Smith, PhD, former postdoctoral fellow at BRI and now Assistant Professor of Biology at the University of Kentucky; Chris Amemiya, PhD, Principal Investigator at BRI and Professor of Biology, University of Washington; Evan Eichler, PhD, University of Washington Genome Sciences Professor; and Carl Baker, Research Scientist, University of Washington.

The discovery builds on the group's previous work published in the Proceedings of the National Academy of Sciences in 2009. "Our new research confirms that lampreys experience rampant programmed genome rearrangement and losses during early development," says Dr. Amemiya. "The genes are restricted to the germline compartment suggesting a deeper biological strategy in order to regulate the genome for highly precise, normal functioning. The strategy removes the possibility that the genes will be expressed in deleterious ways. Humans, on the other hand, must contain these genes through other "epigenetic" mechanisms that are not fool-proof.

There are several implications of this work:

Sea lampreys are "basal" vertebrates that lack jaws and have unique properties that are of interest to scientists. This includes a completely different genetic toolkit for their adaptive immune system, which was also discovered, in part, by Amemiya's group, as well as remarkable powers of regeneration that allow them to completely recover from a severed spinal cord.

High throughput genomic sequencing, computational analysis and other state-of-the-art scientific advances made this research possible. Grant funding was provided by the National Science Foundation, National Institutes of Health and Howard Hughes Medical Institute.

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Unique solution to gene regulation

Public release date: 21-Aug-2012 [ | E-mail | Share ]

Contact: Kay Branz kbranz@benaroyaresearch.org 206-342-6903 Immune Tolerance Network

SEATTLE - (August 21, 2012) Research on a unique vertebrate called the sea lamprey shows that more than a thousand genes are shed during its early development. These genes are paradoxically lost all throughout the developing embryo except in a specialized compartment called "primordial germ cells" or PGCs. The PGCs can be thought of as embryonic stem cells and are used, ultimately, for making the next generation of lampreys. Based on computational analysis, a significant number of genes that are lost in the embryo have signatures of "pluripotency," which suggests that they could also have undesirable effects if they were inadvertently turned on in the body. In effect, by undergoing programmed genome rearrangement and gene loss during embryogenesis, the sea lamprey "seals" the genes away in the small germline compartment so they cannot be misexpressed and thereby create untoward problems (such as development of cancer, for example). The study was completed at the Benaroya Research Institute at Virginia Mason (BRI) and recently published as a featured article in Current Biology, along with an outside commentary highlighting its biological importance.

The article authors are Jeramiah Smith, PhD, former postdoctoral fellow at BRI and now Assistant Professor of Biology at the University of Kentucky; Chris Amemiya, PhD, Principal Investigator at BRI and Professor of Biology, University of Washington; Evan Eichler, PhD, University of Washington Genome Sciences Professor; and Carl Baker, Research Scientist, University of Washington.

The discovery builds on the group's previous work published in the Proceedings of the National Academy of Sciences in 2009. "Our new research confirms that lampreys experience rampant programmed genome rearrangement and losses during early development," says Dr. Amemiya. "The genes are restricted to the germline compartment suggesting a deeper biological strategy in order to regulate the genome for highly precise, normal functioning. The strategy removes the possibility that the genes will be expressed in deleterious ways. Humans, on the other hand, must contain these genes through other "epigenetic" mechanisms that are not fool-proof.

There are several implications of this work:

Sea lampreys are "basal" vertebrates that lack jaws and have unique properties that are of interest to scientists. This includes a completely different genetic toolkit for their adaptive immune system, which was also discovered, in part, by Amemiya's group, as well as remarkable powers of regeneration that allow them to completely recover from a severed spinal cord.

High throughput genomic sequencing, computational analysis and other state-of-the-art scientific advances made this research possible. Grant funding was provided by the National Science Foundation, National Institutes of Health and Howard Hughes Medical Institute.

###

About Benaroya Research Institute at Virginia Mason

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Research reveals unique solution to gene regulation

ScienceDaily (Aug. 20, 2012) Algae are high on the genetic engineering agenda as a potential source for biofuel, and they should be subjected to independent studies of any environmental risks that could be linked to cultivating algae for this purpose, two prominent researchers say.

Writing in the August 2012 issue of the journal BioScience, the researchers argue that ecology experts should be among scientists given independent authority and adequate funding to explore any potential unintended consequences of this technological pursuit.

A critical baseline concern is whether genetically engineered algae would be able to survive in the wild, said Allison Snow, professor of evolution, ecology and organismal biology at Ohio State University and lead author of the paper.

"If they're grown in big, open ponds, which is mainly what were talking about, could the newer types of microalgae get out into nature and mingle? We need to know if they can survive and whether they can hybridize or evolve to become more prolific when they get out of a controlled environment," Snow said.

"If they can survive, we also need to know whether some types of genetically engineered blue-green algae, for example, could produce toxins or harmful algal blooms -- or both," Snow noted.

And because algae are so small and could be dispersed by rough weather or wildlife activity, biologists worry that any transgenes they contain to enhance their growth and strength could be transferred to other species in a way that could upset a fragile ecosystem.

"The applications are new and the organisms are less well-known. They range from being very tame 'lab rats' that won't survive in nature to wild organisms that can presumably cross with each other unless some measures are taken to prevent crossing. It's a very new situation," Snow said.

Snow co-authored the article with aquatic ecologist Val Smith, a professor in the Department of Ecology and Evolutionary Biology at the University of Kansas.

Snow has a history in this area of research. She led a study in 2002 that was the first to show that a gene artificially inserted into crop plants to fend off pests could migrate to weeds in a natural environment and make the weeds stronger. She also has served on national panels that monitor and make recommendations about the release of genetically engineered species into the environment.

There are a lot of unknowns about this area of research and development in microalgae, and that's largely because algae don't have the breeding history that, say, corn and soybeans have, Snow said. In addition, few details are publicly available because much of this information remains confidential as businesses compete to be the first to commercialize their genetically altered algae.

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Genetically engineered algae for biofuel pose potential risks

Public release date: 21-Aug-2012 [ | E-mail | Share ]

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

New Rochelle, NY, August 21, 2012For the millions of people worldwide with type 1 diabetes who cannot produce sufficient insulin, the potential to transplant insulin-producing cells could offer hope for a long-term cure. The discovery of a marker to help identify and isolate stem cells that can develop into insulin-producing cells in the pancreas would be a critical step forward and is described in an article in BioResearch Open Access, a new bimonthly peer-reviewed open access journal from Mary Ann Liebert, Inc. (http://www.liebertpub.com) The article is available free online at the BioResearch Open Access website (http://www.liebertpub.com/biores).

Pancreatic stem cells, the precursors of insulin-producing cells, have not yet been identified in humans or animals, and there is much debate about where they may reside. Ivka Afrikanova, Ayse Kayali, Ana Lopez, and Alberto Hayek, University of California, San Diego, CA, have identified a biochemical markerstage-specific embryonic antigen 4 (SSEA4)that they propose can be used to identify and purify human pancreatic stem cells. The article "Is Stage-Specific Embryonic Antigen 4 a Marker for Human Ductal Stem/Progenitor Cells" (http://online.liebertpub.com/doi/full/10.1089/biores.2012.0235) reports that when grown in culture with high levels of glucose and B27, these SSEA4+ stem cells can differentiate into insulin-producing pancreatic cells.

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About the Journal

BioResearch Open Access (http://www.liebertpub.com/biores) 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 (http://www.liebertpub.com/biores).

About the Publisher

Mary Ann Liebert, Inc., publishers (http://www.liebertpub.com) 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 (http://www.liebertpub.com).

Mary Ann Liebert, Inc. 140 Huguenot St., New Rochelle, NY 10801-5215 http://www.liebertpub.com Phone: (914) 740-2100 (800) M-LIEBERT Fax: (914) 740-2101

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New marker for identifying precursors to insulin-producing cells in pancreas

Public release date: 20-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 20, 2012Major depression affects as many as 16% of reproductive-aged women in the U.S. Yet pregnant women have a higher rate of undiagnosed depression than nonpregnant women, according to a study published in Journal of Women's Health, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Women's Health website at http://www.liebertpub.com/jwh.

Jean Ko, PhD and coauthors from the Centers for Disease Control and Prevention (CDC), Atlanta, GA, found that more than 1 in 10 women ages 18-44 years had a major depressive event during the previous yearrepresenting about 1.2 million U.S. womenbut more than half of those women did not receive a diagnosis of depression and nearly half did not receive any mental health treatment. The article "Depression and Treatment among U.S. Pregnant and Nonpregnant Women of Reproductive Age, 2005-2009," further reports that disparities in receiving a diagnosis and treatment were associated with younger age, belonging to a racial/ethnic minority, and insurance status.

The accompanying Editorial entitled "Depression: Is Pregnancy Protective?" by Jennifer Payne, MD, Johns Hopkins School of Medicine, Baltimore, MD, explores the ongoing challenges in the adequate diagnosis and treatment of major depression, the additional factors that come into play during pregnancy, and the implications of the Ko et al. study results.

"As health care providers, we simply must do a better job at diagnosing depression and referring women for mental health treatment. Reproductive health care visits provide an opportune time to address this ," says Susan G. Kornstein, MD, Editor-in-Chief of Journal of Women's Health, Executive Director of the Virginia Commonwealth University Institute for Women's Health, Richmond, VA, and President of the Academy of Women's Health.

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About the Journal

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

About the Society

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How well is depression in women being diagnosed and treated?